Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3711_Библиотеки_им_академика_М_И_Перельмана
.pdf
214
https://t.me/med1917
J. D. Newman et al.
extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular
Surgery/Society for Vascular Surgery, Society for Cardiovascular
Angiography and Interventions, Society for Vascular Medicine
and Biology, Society of Interventional Radiology, and the ACC/
AHA Task Force on Practice Guidelines (Writing Committee
to Develop Guidelines for the Management of Patients With
Peripheral Arterial Disease): endorsed by the American
Association of Cardiovascular and Pulmonary Rehabilitation;
National Heart, Lung, and Blood Institute; Society for Vascular
Nursing; TransAtlantic Inter-Society Consensus; and Vascular
Disease Foundation. Circulation. 2006;113(11):e463–654.
26. Lederle FA, Simel DL. The rational clinical examination.
Does this patient have abdominal aortic aneurysm? JAMA.
1999;281(1):77–82.
27. Fink HA, Lederle FA, Roth CS, Bowles CA, Nelson DB, Haas
MA.The accuracy of physical examination to detect abdominal
aortic aneurysm. Arch Intern Med. 2000;160(6):833–6.
28. Wilson WR, Bower TC, Creager MA, Amin-Hanjani S, O’Gara
PT, Lockhart PB, etal. Vascular graft infections, mycotic aneurysms, and endovascular infections: a scientic statement from the
American Heart Association. Circulation. 2016;134(20):e412–60.
29. Mix J, Pitta S, Schwartz J, Tuchek J, Dieter R, Freeman
M.Abdominal aorta. In: Dieter R, Dieter RJ, Dieter RI, editors.
Peripheral arterial disease. New York: McGraw-Hill Education;
2008. p.569–92.
30. Davis PM, Gloviczki P, Cherry KJ Jr, Toomey BJ, Stanson AW,
Bower TC, etal. Aorto-caval and ilio-iliac arteriovenous stulae.
Am J Surg. 1998;176(2):115–8.
31. Salo JA, Verkkala KA, Ala-Kulju KV, Heikkinen LO, Luosto
RV.Hematuria is an indication of rupture of an abdominal aortic
aneurysm into the vena cava. J Vasc Surg. 1990;12(1):41–4.
32. Kent KC.Clinical practice. Abdominal aortic aneurysms. N Engl
J Med. 2014;371(22):2101–8.
33. Hong H, Yang Y, Liu B, Cai W. Imaging of abdominal aortic aneurysm: the present and the future. Curr Vasc Pharmacol.
2010;8(6):808–19.
34. Beales L, Wolstenhulme S, Evans JA, West R, Scott
DJ.Reproducibility of ultrasound measurement of the abdominal
aorta. Br J Surg. 2011;98(11):1517–25.
35. Jaakkola P, Hippelainen M, Farin P, Rytkonen H, Kainulainen S,
Partanen K.Interobserver variability in measuring the dimensions
of the abdominal aorta: comparison of ultrasound and computed
tomography. Eur J Vasc Endovasc Surg. 1996;12(2):230–7.
36. Chiu KW, Ling L, Tripathi V, Ahmed M, Shrivastava V.Ultrasound
measurement for abdominal aortic aneurysm screening: a direct
comparison of the three leading methods. Eur J Vasc Endovasc
Surg. 2014;47(4):367–73.
37. Sprouse LR 2nd, Meier GH 3rd, Lesar CJ, Demasi RJ, Sood J,
Parent FN, et al. Comparison of abdominal aortic aneurysm
diameter measurements obtained with ultrasound and computed
tomography: is there a difference? J Vasc Surg. 2003;38(3):466–
71; discussion 471–2.
38. Reed MJ, Cheung LT. Emergency department led emergency
ultrasound may improve the time to diagnosis in patients presenting with a ruptured abdominal aortic aneurysm. Eur J Emerg Med.
2014;21(4):272–5.
39. Chien DK, Chang WH, Yeh YH.Radiographic ndings of a ruptured
abdominal aortic aneurysm. Circulation. 2010;122(18):1880–1.
40. Dalrymple N, Oliphant M, Leyendecker J.Imaging evaluation of
acute abdominal pain. In: Dalrymple N, editor. Problem solving
in abdominal imaging. 1st ed. Philadelphia: Mosby Inc; 2009.
p.147–83.
41. Thammaroj J, Vungtal S, Srinakarin J. Predictive CT features
in ruptured abdominal aortic aneurysm. J Med Assoc Thail.
2006;89(4):434–40.
42. Lin MP, Chang SC, Wu RH, Chou CK, Tzeng WS.A comparison
of computed tomography, magnetic resonance imaging, and digital subtraction angiography ndings in the diagnosis of infected
aortic aneurysm. J Comput Assist Tomogr. 2008;32(4):616–20.
43. Litmanovich DE, Yildirim A, Bankier AA.Insights into imaging
of aortitis. Insights Imaging. 2012;3(6):545–60.
44. Nordon IM, Hinchliffe RJ, Malkawi AH, Taylor J, Holt PJ, Morgan
R, etal. Validation of DynaCT in the morphological assessment of
abdominal aortic aneurysm for endovascular repair. J Endovasc
Ther. 2010;17(2):183–9.
45. Shabana WM, Cohan RH, Ellis JH, Hussain HK, Francis IR, Su
LD, etal. Nephrogenic systemic brosis: a report of 29 cases. AJR
Am J Roentgenol. 2008;190(3):736–41.
46. Choke E, Cockerill G, Wilson WR, Sayed S, Dawson J, Loftus I,
etal. A review of biological factors implicated in abdominal aortic
aneurysm rupture. Eur J Vasc Endovasc Surg. 2005;30(3):227–44.
47. Kotze C, Menezes L, Endozo R, Groves A, Ell P, Yusuf S.Increased
metabolic activity in abdominal aortic aneurysm detected by
18F-uorodeoxyglucose (18F-FDG) positron emission tomography/computed tomography (PET/CT). Eur J Vasc Endovasc Surg.
2009;38(1):93–9.
48. Reeps C, Essler M, Pelisek J, Seidl S, Eckstein HH, Krause
BJ.Increased 18F-uorodeoxyglucose uptake in abdominal aortic
aneurysms in positron emission/computed tomography is associated with inammation, aortic wall instability, and acute symptoms. J Vasc Surg. 2008;48(2):417–23; discussion 424.
49. Lindholt JS, Norman P.Screening for abdominal aortic aneurysm
reduces overall mortality in men. A meta-analysis of the mid- and
long-term effects of screening for abdominal aortic aneurysms.
Eur J Vasc Endovasc Surg. 2008;36(2):167–71.
50. Final Recommendation Statement: Abdominal Aortic Aneurysm:
Screening. U.S. Preventive Services Task Force. 2014; Available
at: https://www.uspreventiveservicestaskforce.org/Page/Document/
RecommendationStatementFinal/abdominal-aortic-aneurysmscreening. Accessed 3 Dec 2016.
51. LeFevre ML, U.S. Preventive Services Task Force. Screening
for abdominal aortic aneurysm: U.S. Preventive Services
Task Force recommendation statement. Ann Intern Med.
2014;161(4):281–90.
52. Lederle FA, Johnson GR, Wilson SE, Chute EP, Littooy FN,
Bandyk D, etal. Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection
and Management (ADAM) Veterans Affairs Cooperative Study
Group. Ann Intern Med. 1997;126(6):441–9.
53. Scott RA, Wilson NM, Ashton HA, Kay DN.Inuence of screening on the incidence of ruptured abdominal aortic aneurysm:
5-year results of a randomized controlled study. Br J Surg.
1995;82(8):1066–70.
54. Lederle FA, Wilson SE, Johnson GR, Reinke DB, Littooy FN,
Acher CW, et al. Immediate repair compared with surveillance of small abdominal aortic aneurysms. N Engl J Med.
2002;346(19):1437–44.
55. Lederle FA, Johnson GR, Wilson SE, Ballard DJ, Jordan WD
Jr, Blebea J, etal. Rupture rate of large abdominal aortic aneurysms in patients refusing or unt for elective repair. JAMA.
2002;287(22):2968–72.
56. Powell JT, Brown LC, Forbes JF, Fowkes FG, Greenhalgh
RM, Ruckley CV, etal. Final 12-year follow-up of surgery versus surveillance in the UK Small Aneurysm Trial. Br J Surg.
2007;94(6):702–8.
57. Chaikof EL, Brewster DC, Dalman RL, Makaroun MS, Illig KA,
Sicard GA, etal. SVS practice guidelines for the care of patients
with an abdominal aortic aneurysm: executive summary. J Vasc
Surg. 2009;50(4):880–96.
58. United Kingdom Small Aneurysm Trial Participants. Longterm outcomes of immediate repair compared with surveil-

14 Abdominal Aortic Aneurysms
https://t.me/med1917
215
lance of small abdominal aortic aneurysms. N Engl J Med.
2002;346(19):1445–52.
59. Cao P, De Rango P, Verzini F, Parlani G, Romano L, Cieri E, etal.
Comparison of surveillance versus aortic endografting for small
aneurysm repair (CAESAR): results from a randomised trial. Eur
J Vasc Endovasc Surg. 2011;41(1):13–25.
60. Ouriel K, Clair DG, Kent KC, Zarins CK. Positive Impact of
Endovascular Options for treating Aneurysms Early (PIVOTAL)
Investigators. Endovascular repair compared with surveillance
for patients with small abdominal aortic aneurysms. J Vasc Surg.
2010;51(5):1081–7.
61. Hendy K, Gunnarson R, Golledge J. Growth rates of small
abdominal aortic aneurysms assessed by computerised
tomography--a systematic literature review. Atherosclerosis.
2014;235(1):182–8.
62. Titus J, Butler B. Endoleak management. In: Dieter R, Dieter
RJ, Dieter RI, editors. Endovascular interventions: a case based
approach. NewYork: Springer Science + Business Media; 2014.
p.373–81.
63. Harris PL, Vallabhaneni SR, Desgranges P, Becquemin JP, van
Marrewijk C, Laheij RJ.Incidence and risk factors of late rupture,
conversion, and death after endovascular repair of infrarenal aortic
aneurysms: the EUROSTAR experience. European Collaborators
on Stent/graft techniques for aortic aneurysm repair. J Vasc Surg.
2000;32(4):739–49.
64. Manning BJ, O’Neill SM, Haider SN, Colgan MP, Madhavan P,
Moore DJ. Duplex ultrasound in aneurysm surveillance following endovascular aneurysm repair: a comparison with computed
tomography aortography. J Vasc Surg. 2009;49(1):60–5.
65. Bredahl KK, Taudorf M, Lonn L, Vogt KC, Sillesen H, Eiberg
JP.Contrast enhanced ultrasound can replace computed tomography angiography for surveillance after endovascular aortic
aneurysm repair. Eur J Vasc Endovasc Surg. 2016;52(6):729–34.
66. Ashoke R, Brown LC, Rodway A, Choke E, Thompson MM,
Greenhalgh RM, etal. Color duplex ultrasonography is insensitive
for the detection of endoleak after aortic endografting: a systematic review. J Endovasc Ther. 2005;12(3):297–305.
67. Raman KG, Missig-Carroll N, Richardson T, Muluk SC,
Makaroun MS. Color-ow duplex ultrasound scan versus computed tomographic scan in the surveillance of endovascular aneurysm repair. J Vasc Surg. 2003;38(4):645–51.
68. Habets J, Zandvoort HJ, Reitsma JB, Bartels LW, Moll FL, Leiner
T, etal. Magnetic resonance imaging is more sensitive than computed tomography angiography for the detection of endoleaks
after endovascular abdominal aortic aneurysm repair: a systematic
review. Eur J Vasc Endovasc Surg. 2013;45(4):340–50.
69. Garg T, Baker LC, Mell MW. Postoperative surveillance and
long-term outcomes after endovascular aneurysm repair among
Medicare beneciaries. JAMA Surg. 2015;150(10):957–63.
70. Hoornweg LL, Storm-Versloot MN, Ubbink DT, Koelemay
MJ, Legemate DA, Balm R.Meta analysis on mortality of ruptured abdominal aortic aneurysms. Eur J Vasc Endovasc Surg.
2008;35(5):558–70.
71. Kent K.Clinical practice. Abdominal aortic aneurysms. NEJM.
2014;371:2101–8.
72. Kent KC, Zwolak RM, Egorova NN, Riles TS, Manganaro A,
Moskowitz AJ, etal. Analysis of risk factors for abdominal aortic
aneurysm in a cohort of more than 3 million individuals. J Vasc
Surg. 2010;52(3):539–48.
73. Tenforde AS, Cheng CP, Suh GY, Herfkens RJ, Dalman RL,
Taylor CA. Quantifying invivo hemodynamic response to exercise in patients with intermittent claudication and abdominal
aortic aneurysms using cine phase-contrast MRI.J Magn Reson
Imaging. 2010;31(2):425–9.
74. Nakahashi TK, Hoshina K, Tsao PS, Sho E, Sho M, Karwowski
JK, et al. Flow loading induces macrophage antioxidative gene
expression in experimental aneurysms. Arterioscler Thromb Vasc
Biol. 2002;22(12):2017–22.
75. Myers J, McElrath M, Jaffe A, Smith K, Fonda H, Vu A, etal.
A randomized trial of exercise training in abdominal aortic aneurysm disease. Med Sci Sports Exerc. 2014;46(1):2–9.
76. Best PJ, Tajik AJ, Gibbons RJ, Pellikka PA.The safety of treadmill exercise stress testing in patients with abdominal aortic aneurysms. Ann Intern Med. 1998;129(8):628–31.
77. Propanolol Aneurysm Trial Investigators. Propranolol for small
abdominal aortic aneurysms: results of a randomized trial. J Vasc
Surg. 2002;35(1):72–9.
78. Sweeting MJ, Thompson SG, Brown LC, Greenhalgh RM, Powell
JT.Use of angiotensin converting enzyme inhibitors is associated
with increased growth rate of abdominal aortic aneurysms. J Vasc
Surg. 2010;52(1):1–4.
79. Takagi H, Matsui M, Umemoto T. A meta-analysis of clinical
studies of statins for prevention of abdominal aortic aneurysm
expansion. J Vasc Surg. 2010;52(6):1675–81.
80. Bailey MA, Dunne JA, Grifn KJ, Coughlin PA, Scott
DJ.Systematic review and meta-analysis of the effects of statin
therapy on abdominal aortic aneurysms (Br J Surg 2011; 98: 362-
353). Br J Surg. 2011;98(5):744–5; author reply 745.
81. Meijer CA, Stijnen T, Wasser MN, Hamming JF, van Bockel JH,
Lindeman JH, et al. Doxycycline for stabilization of abdominal aortic aneurysms: a randomized trial. Ann Intern Med.
2013;159(12):815–23.
82. Thompson A, Cooper JA, Fabricius M, Humphries SE, Ashton
HA, Hafez H.An analysis of drug modulation of abdominal aortic
aneurysm growth through 25 years of surveillance. J Vasc Surg.
2010;52(1):55–61.e2.
83. Sieunarine K, Lawrence-Brown MM, Goodman MA.Comparison
of transperitoneal and retroperitoneal approaches for infrarenal aortic surgery: early and late results. Cardiovasc Surg.
1997;5(1):71–6.
84. Annambhotla S, Kibbe M. Infrarenal abdominal aortic aneurysm: EVAR.In: Dieter RS, Dieter Jr RA, Dieter III RA, editors.
Endovascular interventions: a case-based approach. New York:
Springer Science+Business Media; 2014. p.355–65.
85. Aziz F.Endovascular abdominal aortic aneurysm repair for ruptured abdominal aortic aneurysm. In: Dean S, Satiani B, Abraham
W, editors. Color atlas of vascular diseases. NewYork: McGrawHill; 2015.
86. Prinssen M, Verhoeven EL, Buth J, Cuypers PW, van Sambeek
MR, Balm R, etal. A randomized trial comparing conventional
and endovascular repair of abdominal aortic aneurysms. N Engl J
Med. 2004;351(16):1607–18.
87. Blankensteijn JD, de Jong SE, Prinssen M, van der Ham AC, Buth
J, van Sterkenburg SM, etal. Two-year outcomes after conventional or endovascular repair of abdominal aortic aneurysms. N
Engl J Med. 2005;352(23):2398–405.
88. De Bruin JL, Baas AF, Buth J, Prinssen M, Verhoeven EL, Cuypers
PW, etal. Long-term outcome of open or endovascular repair of
abdominal aortic aneurysm. N Engl J Med. 2010;362(20):1881–9.
89. EVAR trial participants. Endovascular aneurysm repair versus open
repair in patients with abdominal aortic aneurysm (EVAR trial 1):
randomised controlled trial. Lancet. 2005;365(9478):2179–86.
90. Greenhalgh RM, Brown LC, Kwong GP, Powell JT, Thompson
SG, EVAR trial participants. Comparison of endovascular aneurysm repair with open repair in patients with abdominal aortic
aneurysm (EVAR trial 1), 30-day operative mortality results: randomised controlled trial. Lancet. 2004;364(9437):843–8.
91. Patel R, Sweeting MJ, Powell JT, Greenhalgh RM, EVAR trial
investigators. Endovascular versus open repair of abdominal aortic aneurysm in 15-years’ follow-up of the UK endovascular aneurysm repair trial 1 (EVAR trial 1): a randomised controlled trial.
Lancet. 2016;388(10058):2366–74.

216
https://t.me/med1917
J. D. Newman et al.
92. Lederle FA, Freischlag JA, Kyriakides TC, Padberg FT Jr,
Matsumura JS, Kohler TR, etal. Outcomes following endovascular vs open repair of abdominal aortic aneurysm: a randomized
trial. JAMA. 2009;302(14):1535–42.
93. Lederle FA, Freischlag JA, Kyriakides TC, Matsumura JS,
Padberg FT Jr, Kohler TR, etal. Long-term comparison of endovascular and open repair of abdominal aortic aneurysm. N Engl J
Med. 2012;367(21):1988–97.
94. The UK Small Aneurysm Trial Participants. Mortality results
for randomised controlled trial of early elective surgery or
ultrasonographic surveillance for small abdominal aortic aneurysms. Lancet. 1998;352(9141):1649–55.
95. Moll FL, Powell JT, Fraedrich G, Verzini F, Haulon S, Waltham
M, et al. Management of abdominal aortic aneurysms clinical
practice guidelines of the European society for vascular surgery.
Eur J Vasc Endovasc Surg. 2011;41(Suppl 1):S1–S58.
96. Rooke TW, Hirsch AT, Misra S, Sidawy AN, Beckman JA,
Findeiss L, etal. Management of patients with peripheral artery
disease (compilation of 2005 and 2011 ACCF/AHA Guideline
Recommendations): a report of the American College of
Cardiology Foundation/American Heart Association Task Force
on Practice Guidelines. J Am Coll Cardiol. 2013;61(14):1555–70.
97. Karthikesalingram A, Vidal-Diez A, Holt P, Loftus I,
Schermerhorn M, Soden P, etal. Thresholds for abdominal aortic
aneurysm repair in England and the United States. N Engl J Med.
2016;375:2051–9.
98. Haulon S, Amiot S, Magnan PE, Becquemin JP, Lermusiaux P,
Koussa M, etal. An analysis of the French multicentre experience
of fenestrated aortic endografts: medium-term outcomes. Ann
Surg. 2010;251(2):357–62.
99. Coscas R, Kobeiter H, Desgranges P, Becquemin JP.Technical
aspects, current indications, and results of chimney grafts for juxtarenal aortic aneurysms. J Vasc Surg. 2011;53(6):1520–7.
100. Leon L, Ihnat D, Mills J.Native arterial infections. In: Hallett J,
Mills J, Earnshaw J, Reekers J, editors. Comprehensive vascular
and endovascular surgery. 2nd ed. Philadelphia: Elsevier; 2009.
101. Leon LR Jr, Mills JLS. Diagnosis and management of aortic
mycotic aneurysms. Vasc Endovasc Surg. 2010;44(1):5–13.
102. Kan CD, Lee HL, Yang YJ.Outcome after endovascular stent graft
treatment for mycotic aortic aneurysm: a systematic review. J Vasc
Surg. 2007;46(5):906–12.
103. Hart T, Milner R.Surgical versus endovascular aortic aneurysm
repair: evidence to guide the optimal approach for the individual
patient. Curr Atheroscler Rep. 2016;18(12):76.
104. Paravastu SC, Ghosh J, Murray D, Farquharson FG, SerracinoInglott F, Walker MG.A systematic review of open versus endovascular repair of inammatory abdominal aortic aneurysms. Eur
J Vasc Endovasc Surg. 2009;38(3):291–7.

Abdominal Aortic Occlusive Disease
https://t.me/med1917
SunghoLim andPaulR.Crisostomo
15
Introduction
Atherosclerosis of the abdominal aorta or iliac arteries is one
of the most common causes of lower extremity ischemia.
The rst implication of the disease was uncovered in the late
eighteenth century by British anatomist John Hunter.
However, two more centuries passed before Rene Leriche
described a patient with claudication and erectile dysfunction in 1948, ultimately linking clinical symptoms with
pathophysiology and anatomy [1].
Surgical revascularization of aortoiliac artery was rst
described by Wylie etal. in San Francisco in 1952 [2]. Since
then, tremendous advances have occurred in synthetic graft
conduits, tissue engineering, and, most recently, percutaneous endovascular devices which allow a wide range of treatment options based on patient morbidity and anatomic
defect. This chapter will review clinical characteristics of
abdominal aortic occlusive disease and contemporary
management.
Epidemiology
The majority of patients with aortic occlusive disease present
with diffuse disease involving multi-level peripheral vasculature including femoropopliteal or infrapopliteal vessels. This
subset of patients with diffuse multi-level disease are typically older, more likely male, with a higher prevalence of diabetes and hypertension and with concomitant coronary artery
disease, cerebrovascular disease, and visceral atherosclerosis
[3, 4]. Such patients with multi-vessel disease often present
with ischemic pain, tissue loss, or gangrene. Not surprisingly,
S. Lim
Surgery, Loyola University Medical Center, Maywood, IL, USA
P. R. Crisostomo (
Department of Surgery, Division of Vascular and Endovascular
Therapy, Loyola University Chicago, Stritch School of Medicine,
Maywood, IL, USA
*)
their life expectancy is lower than their age- matched counterpart [5]. In contrast, patients with isolated aortoiliac disease
are generally younger and more likely female with a high
prevalence of smoking or dyslipidemia [6].
“Hypoplastic aortic syndrome” or “small aorta syndrome”
is a particularly virulent form of aortic atherosclerosis often
found in young, small stature women who smoke [6]. This
disease particularly involves the infrarenal aorta proximal to
the aortic bifurcation. Radiographic ndings are typically
atretic or narrowed vasculature with diffuse calcic atherosclerosis. Due to the diminutive size of the aorta and iliac
vessels, durability of either endovascular intervention or
local endarterectomy is generally inferior, particularly in the
presence of continued cigarette use.
Pathophysiology
Aortoiliac atherosclerosis typically starts at the iliac bifurcation and extends proximally and distally. Degree of the progression may vary but ultimately could occlude aortic blood
ow over time. Starrett et al. demonstrated one-third of
patients experienced proximal disease progression up to the
level of renal artery in the period of 6–10years [7]. In the
same study, they also demonstrated a 30–40% chance of profunda femoris or supercial femoral artery distal involvement [7].
Due to the relatively slow progression of atherosclerosis,
collateral circulation often develops. The primary compensatory vessels to the lower extremity include the internal thoracic artery (mammary) to the inferior epigastric artery and
the intercostal and lumbar artery to the deep circumex
artery. Additional colonic collaterals arise from the SMA to
the IMA via the marginal artery of Drummond and the arc of
Riolan. Pelvic collaterals from the IMA to the hypogastric
include the superior rectal to the middle rectal, the iliolumbar to the lumbar, and the lateral sacral to the median sacral
artery. It is important to recognize these compensatory pathways and to preserve them during reconstruction.
© Springer Nature Switzerland AG 2019
R. S. Dieter et al. (eds.), Diseases of the Aorta, https://doi.org/10.1007/978-3-030-11322-3_15
217

218
8
Prevalence (%)
Age-group
https://t.me/med1917
S. Lim and P. R. Crisostomo
Clinical Presentation
Chronic atherosclerosis of the aortoiliac segment often
accompanies infrainguinal arterial disease. Thus, this disease
most frequently manifests as lower extremity arterial insufciency. Symptoms vary widely depending on location of
concomitant disease and degree of collateralization.
Patients with multi-level disease can present with typical lower extremity arterial insufciency symptoms such as
leg claudication, tissue loss, or gangrene. In contrast,
patients with isolated aortoiliac segment disease may present with pelvic or buttock claudication. In male aortoiliac
disease patients, up to 30% experience difculty achieving
and maintaining an erection owing to decreased perfusion
of the internal pudendal artery. The constellation of symptoms associated with distal aortic occlusion, including pelvic claudication, atrophy of the leg muscles, impotence,
and decreased femoral pulses, is known as Leriche’s syndrome [1].
Diagnosis
Patient History
Conducting a complete history and identifying cardiovascular risk factors are important in the diagnosis.
Atherosclerosis is a pathologic process related with aging
(Fig.15.1). Hypertension, diabetes, dyslipidemia, chronic
kidney disease, and cigarette smoking are classic risk factors that must be identied and addressed. It is critical to
control these modiable factors to slow the progression of
the atherosclerosis.
Male gender and non-Hispanic black race are known
unmodiable risk factors for atherosclerosis. In patients who
lack these classic risk factors, hyperhomocysteinemia,
hypercoagulability, and hyperbrinogenemia should be
investigated.
Risk Factors for Atherosclerosis [8]
• Advanced age.
• Race (non-Hispanic blacks).
• Male gender.
• Hyperbrinogenemia.
• Diabetes mellitus.
• Hyperhomocysteinemia.
• Smoking.
• Hypercoagulability.
• Hypertension.
• Elevated C-reactive protein.
• Dyslipidemia.
• Chronic renal insufciency.
Physical Examination
Physical examination begins with inspection. Aortoiliac disease may cause ischemic changes of the pelvis/buttocks and/
or the lower extremities. Visual signs of ischemia include
pallor, muscular atrophy, and cyanosis or skin mottling.
Palpation and comparison of femoral pulses is the quickest
and the most important way to diagnose aortoiliac occlusive
disease. Grading a pulse is subjective, simply described as (1)
normal, diminished, or absent and (2) symmetric versus
asymmetric. If a pulse is not palpable, further assessment
using Doppler should be pursued. The Doppler signal can be
described as triphasic, biphasic, or monophasic. Palpation of
the lower extremity is also helpful to assess the level of skin
temperature and neurologic (motor and sensory) status.
Fig. 15.1 Prevalence of
symptomatic peripheral
arterial disease. (From
Norgren etal. [8]. Reprinted
with permission from
Elsevier)
7
6
5
4
3
2
1
0
30–34
35–39
40–44
45–49
50–54
55–59
60–64
65–69
70–74

15 Abdominal Aortic Occlusive Disease
https://t.me/med1917
219
Auscultation of the abdomen commonly reveals bruits
when signicant stenosis of the aorta or its branch is present.
Middle to lower abdominal bruits may present with aortoiliac occlusive disease, whereas epigastric or paramedian
bruits can indicate visceral vessel stenosis or renal artery stenosis, respectively.
Patients with aortoiliac occlusive disease and robust collateral formation may have a deceiving lack of distinct physical examination ndings. In that case, an exercise trial may
augment changes in pulses or bruit. Lumbar disc herniation,
spinal stenosis, or arthritis of the hip or knee joint should be
included in the differential diagnosis. Discomfort related
with certain positions, or prolonged standing in elderly often
arises from neurogenic or musculoskeletal origins.
Vascular Laboratory
Non-invasive hemodynamic vascular laboratory testing
begins with ankle-brachial index (ABI). Segmental systolic
blood pressure measurement and pulse volume recording
(PVR) may aid inlocating the area of concern. A difference
of systolic blood pressure between the upper arm and proximal thigh more than 20mmHg reects signicant stenosis in
the aortoiliac or proximal femoral arteries. Further reduction
of blood pressure in the distal segments or decreased PVR or
ABI indicates concomitant outow disease. The combination of a thorough history and physical examination with
vascular laboratory testing often provides sufcient clinical
data to decide upon the necessity of revascularization.
Duplex ultrasound (DUS) is the most commonly used
diagnostic imaging study for delineating extremity vascular
abnormalities. However, evaluation of aortoiliac, renal, and
visceral arteries is somewhat limited mainly due to overlying
bowel gas. Patient factors such as obesity or tortuosity of the
vessel also complicate visualization and make it difcult to
determine the precise anatomic location of the disease and its
severity.
Axial Imaging
with sensitivity and specicity near 95% [10]. MRA can
even be obtained without contrast, utilizing time of ight.
MRA can be a reliable guide for percutaneous or open intervention of the aortoiliac disease. However, MRA has a tendency to overestimate the degree of stenosis and has limited
evaluation of the severity of calcic disease. In addition,
MRI cannot be utilized for patients with certain metallic
implants such as cardiac pacemaker or debrillator.
Arteriography
Despite recent technical advances in CT or MRI with
increased speed and accuracy, diagnostic catheter-based
arteriography remains a valuable tool in a physician’s armamentarium. Femoral approach is the preferred way in our
institution; however, brachial approach may be necessary in
long-segment, near-occlusive, or occlusive aortic or bi-iliac
disease. Real-time angiographic imaging utilizing lateral or
oblique views may delineate the contribution of accessory
renal vessels (Can they be sacriced?), IMA vs SMA perfusion (IMA reimplantation?), and lumbar vessels for spinal
perfusion (risk of paralysis?) and/or clarify whether radiographic stenosis are truly hemodynamically signicant. For
example, the presence of superior mesenteric artery occlusion, hypogastric occlusion, or prominent inferior mesenteric artery may require preservation of the inferior
mesenteric artery during aortic reconstruction to avoid bowel
ischemia.
Treatment Modalities
Conservative Management
Smoking
Smoking cessation is without question desirable in aortic
occlusive disease to slow down the progression of atherosclerosis. Smoking cessation is associated with reduced risks
of amputation, myocardial infarction, and mortality in this
patient population [11, 12].
Computed tomographic angiography (CTA) is the gold standard imaging modality for aortoiliac disease in our institution. CTA is a non-invasive alternative to standard angiography
and can be obtained quickly [9]. With recent advances in
multi-detector CT scan, high-quality images with sub-millimeter spatial resolution are now available. Disadvantages of
CT scan include radiation exposure, risk of contrast-induced
nephropathy, and hypersensitivity to iodine contrast.
In some institutions, magnetic resonance angiography
(MRA) has become the imaging study of choice. MRA is an
excellent diagnostic study for aortoiliac occlusive disease
Dyslipidemia
Use of statin has demonstrated a signicant reduction of
adverse cardiovascular event in patient with atherosclerosis
[13–15]. Low-density lipoprotein cholesterol should be
controlled under 100mg/dL or to 70mg/dL in very high-risk
patients [16].
Diabetes
It is unclear whether aggressive diabetic control decreases
adverse cardiovascular events. However, atherosclerosis
tends to be more complicated, and amputation rate is higher

220
https://t.me/med1917
S. Lim and P. R. Crisostomo
in diabetic patient. This may be related to susceptibility to
infection in this population and higher prevalence of distal
sensory neuropathy from poor diabetic control.
Hypertension
Hypertension is recognized as a risk factor of atherosclerosis; however, relative risk for atherosclerosis is less for
hypertension than dyslipidemia or smoking. Treatment for
hypertension is associated with low cardiovascular complications, stroke, or death [17].
Antiplatelet Therapy
The American Heart Association and the Society for Vascular
Surgery recommend the use of an antiplatelet agent in
peripheral arterial occlusive disease [16, 18]. The same can
be applied to aortoiliac atherosclerotic disease. Dual antiplatelet therapy can be applied at the physician’s discretion,
but there is a lack of evidence to date that combination therapy is more effective than a single-agent therapy [19].
Supervised Exercise Therapy
Exercise therapy may improve intermittent claudication. A
meta-analysis of 1200 patients demonstrated overall
improvement of walking distance without improvement of
ankle-brachial index [20]. The precise mechanism of action
is still unknown, but it is thought to be related with nitric
oxide-related vasodilation and improved bioenergetics of
skeletal muscle. However, severe cardiopulmonary disease
or arthritis may preclude adequate exercise participation.
Medical Therapy
Medical therapy aims for symptomatic relief of claudication.
There are two Food and Drug Administration (FDA)approved medications – pentoxifylline and cilostazol –
whereas the Royal College of Physicians in the UK identied
naftidrofuryl as the drug of choice over those two drugs.
Naftidrofuryl is widely available in the European countries
but has not been FDA approved in the USA.
Pharmacodynamics of pentoxifylline includes reducing
blood viscosity and enhancing peripheral perfusion and tissue oxygenation. Multicenter prospective randomized trial
proved its efcacy over placebo [21]. Pentoxifylline can be
begun at 400mg three times daily with maximum dose of
1800mg/day. Side effects of this medication include hypertension, nausea, vomiting, and headache.
Cilostazol is a phosphodiesterase inhibitor that induces
vasodilation and suppresses platelet aggregation. In addition
to routine antiplatelet therapy, cilostazol (100 mg twice
daily) can contribute to increased overall pain-free ambulatory distance in as short as 4weeks [22]. However, this agent
can exacerbate congestive heart failure and is contraindicated in a patient with any level of heart failure.
A multicenter, randomized, double-blind, parallel-group
study compared cilostazol and pentoxifylline and found that
while cilostazol signicantly improved walking distance, pentoxifylline was not signicantly different than placebo [23].
Decision-Making toIntervention
The natural history of atherosclerosis in aortoiliac disease is
a slow arterial process that impairs walking ability. With
maximum medical treatment and exercise therapy, the
chance of developing severe ischemic symptoms such as rest
pain or tissue loss is relatively low (<5%) [8, 24]. Thus, the
majority of patients need just reassurance from their physician. However, patients with advanced ischemic symptoms
or claudication that signicantly impacts their daily living or
occupation should be under consideration for intervention.
It is important to recognize that determining the degree of
functional impairment is not straightforward. Patient perception of functional impairment may vary according to their
baseline activity. For example, mild to moderate claudication
in an active man may have a greater impact, while severe
claudication in a sedentary patient may be less signicant.
Patient morbidity is another important aspect to be considered. Patients with severe arthritis or spinal degenerative disease might not benet from invasive vascular intervention,
whereas patients with severe coronary artery disease or pulmonary compromise may suffer from postoperative signicant morbidity or mortality.
Open revascularization has traditionally demonstrated
improved patency over endovascular intervention at the
expense of higher morbidity and mortality although supporting data comparing the two strategies are still poor. The
TransAtlantic Inter Society Consensus (TASC) document
rst in 2000, then in 2007, and most recently updated in
2015, classied anatomic patterns of disease severity from
types A through D for aortoiliac, femoropopliteal, and infrapopliteal segments [25] (Fig. 15.2). Initially, the TASC
working group advocated endovascular intervention for
TASC type A lesions and open surgical treatment for TASC
type D lesions. However, the latest TASC II update in 2015
recognized that with modern advances in endovascular
instruments and practitioner skill, an endovascular rst
approach has become the predominant modality when revascularization is decided. Moreover, hybrid open and endovascular procedures may be suitable for complex anatomy.
Endovascular Intervention
Arterial Access
Lesions at the aortic bifurcation or common iliac arteries
can be treated with the usual retrograde approach from the
common femoral arteries. Occlusions that cannot be crossed

T
T
• Shor
• Unilateral CIA occlusion
• Single or multiple stenosis totaling 3-10 cm in
• Unilateral EIA occlusion not in
• Bilateral CIA occlusions
• Bilateral EIA stenoses 3–10 cm long not e
• Unilateral EIA stenosis e
• Unilateral EIA occlusion that in
• Hea
• Infra-renal aor
• Diffuse disease in
• Diffuse multiple stenoses in
• Unilateral occlusions of both CIA and EIA
• Bilateral occlusions of EIA
• Iliac stenoses in patients with AAA requir
15 Abdominal Aortic Occlusive Disease
https://t.me/med1917
ype A lesions
• Unilateral or bilateral stenoses of CIA
• Unilateral or bilateral single short (≤3 cm) stenosis of EIA
Type B lesions:
t (≤3cm) stenosis of infrarenal aorta
221
EIA not extending into the CFA
internal iliac or CFA
ype C lesions
the CFA
xtending into the CFA
internal iliac and/or CFA
vily calcified unilateral EIA occlusion with or without
involvement of origins of internal iliac and/or CFA
Type D lesions
volving the
volving the origins of
xtending into
volves the origins of
requiring treatment
EIA, and CFA
and not amenable to endograft placement or other
lesions requiring open aortic or iliac surgery
toiliac occlusion
volving the aorta and both iliac arteries
Fig. 15.2 TransAtlantic Inter-Societal Classication of aortoiliac lesions. (From Norgren etal. [8]. Reprinted with permission from Elsevier)
from the ipsilateral femoral retrograde approach may require
contralateral femoral artery or brachial artery access and
subsequent antegrade approach. A left brachial artery
approach may also decrease the risk of an aortic dissection,
but this patient population not infrequently exhibits con-
volving the unilateral CIA,
ing treatment
comitant left subclavian artery stenosis that may require
pretreatment prior to aortoiliac intervention.
After access is obtained, a diagnostic angiographic evaluation should be performed prior to intervention. Aortogram
and pelvic images are essential to evaluate extent of the dis-

222
ab
https://t.me/med1917
S. Lim and P. R. Crisostomo
ease. A contralateral oblique view opens the iliac bifurcation, whereas an ipsilateral oblique view helps to clarify the
femoral bifurcation. Infrainguinal runoffs also should be
evaluated prior to intervention in case of distal embolization
during the course of intervention.
Crossing theLesion
An angled GLIDEWIRE (Terumo Medical Corp, Somerset,
NJ) and angled support catheter are the prototypical methods
for crossing an iliac stenosis. Chronic total occlusions (CTO)
often require a variety of wires, catheters, and sheath support. The most difcult part of the occlusion is the proximal
cap. After the wire is fully crossed over, true lumen location
should be conrmed with contrast injection. Blood draw as
conrmation may be false. A variety of CTO devices exist,
some of which allow re-entry from a subintimal plane to the
true lumen (Fig.15.3).
Aortic Bifurcation Disease
Lesions at the aortic bifurcation traditionally are treated
with kissing iliac balloon and stent placement. Even in scenarios with unilateral disease, if the lesion is close to the
aortic bifurcation, simultaneous bilateral intervention has
been advocated to prevent contralateral iliac dissection or
thrombus dislodgement and subsequent embolism.
Contralateral prophylactic treatment has also been recommended in order to treat spill over plaque originating from
the aorta [26, 27]. However, a retrospective of 175 patients
with unilateral iliac artery lesions treated with unilateral
method revealed about 1% risk of contralateral extremity
complications [28].
Selection ofBalloon andStent
Plain old balloon angioplasty (POBA) is inferior in patency
to balloon angioplasty and stent within the aortoiliac system
[29–31]. The optimal vessel diameter is often derived from
the normal equivalent segment on the contralateral side. A
calibration imaging system can also be useful to facilitate
measuring size and length of the lesion. Balloons and stents
should be large enough to cover the diseased segment completely but small enough not to injure normal vessels and
aortic branches. Five to ten percent oversize of the balloon
and stent is recommended except for a heavily calcied
lesion that may rupture with larger devices.
A variety of stents are commercially available which fall
into two main deployment categories: balloon-expandable
and self-expanding. Selection of a stent often depends on
device availability and the operator’s familiarity. However,
it is noteworthy that a balloon-expandable stent is advantageous when precise stent placement is necessary. Such is the
case in bilateral common iliac lesions which need kissing
stents to be deployed precisely at the same level to allow
equal opposition. In contrast, when the stent must follow a
tortuous path or is to be placed from the contralateral side, a
self-expanding stent provides greater exibility. The external iliac artery often benets from self-expanding stent
placement.
A covered stent graft is a metal stent covered with Dacron
or polytetrauorethylene (PTFE) which initially was developed for exclusion of an aneurysmal segment or treatment of
an iatrogenic perforation or rupture. Covered stents exclude
the diseased segments from the circulation and, theoretically,
may reduce in-stent restenosis. Although limited studies
Fig. 15.3 Reentry catheters.
(a) Pioneer catheter with
needle deployed. (b) Outback
LTD catheter. (Right: with
needle retracted. Left: with
needle deployed). (From
Jacobs etal. [42]. Reprinted
with permission from
Elsevier)

Patency (%)
15 Abdominal Aortic Occlusive Disease
https://t.me/med1917
223
100
80
60
95%
40
89%
20
0
01020
Primary assisted patency
Primary patency
Fig. 15.4 Comparison of primary patency between stents and stent
grafts. (From Chang et al. [32]. Reprinted with permission from
Elsevier)
95%
80%
30
Time (months)
40 50 60
95%
80%
have been conducted in patients with aortoiliac atherosclerotic disease, primary and primary-assisted patency rate at
5years are 80% and 95% which are superior to bare-metal
stents [32] (Fig.15.4).
Drug-eluting stents (DES) were initially developed for
the treatment of coronary artery disease. A drug such as
paclitaxel or sirolimus delivered via stent inhibits restenosis and improves long-term patency. DES and drug-coated
balloons (DCB) have similarly been FDA approved for the
treatment of femoropopliteal artery disease [33–35]. These
newer-generation balloons and stents have been recommended over their nondrug coated counterparts but may
require extended dual antiplatelet therapy [36]. Although
these newer drug-coated devices have been used off label in
the external iliac artery, data for the aortoiliac segment is
lacking.
Concomitant Femoral Artery Disease
With coexisting severe common femoral artery disease, the
artery can be accessed utilizing a hybrid femoral open cut
down allowing arterial puncture under direct visualization.
At the end of the intervention, proximal and distal control is
obtained and the femoral artery can be endarterectomized
using a longitudinal arteriotomy and closed with a patch
angioplasty. This will improve inow perfusion to the ipsilateral leg and better maintain graft patency [32].
Postoperative Care
Aspirin therapy should be initiated and continued indenitely. Dual antiplatelet is recommended for at least 30days.
Clinical surveillance with physical exam, ABI, and duplex
ultrasonography should be performed immediate postop
(30days) and every 6months at least 1year and annually
thereafter.
Results ofEndovascular Revascularization
The technical success rate of endovascular interventions in
the aortoiliac segment is very high in many reports. However,
maintaining long-term patency requires dedicated surveillance and may need multiple secondary interventions.
Although a variety of factors can affect the outcome, the
TASC classication well represents outcomes referencing
disease location and severity [37]. Endovascular long-term
outcomes are better in TASC A and B lesions compared to
TASC C or D lesions. Cumulative primary patency of all
lesions was 83% at 5years (Fig.15.5). Although many TASC
D lesions can be treated successfully with an endovascular
approach, open surgical revascularization especially in
patients suitable for the procedure should be discussed.
Open Surgical Revascularization
In general, open surgical repair carries a higher perioperative
morbidity and mortality compared to minimally invasive
endovascular revascularization. Thus, cardiopulmonary
comorbidities and renal function have to be assessed and
optimized prior to operation. Coagulation prole should be
checked routinely. Preoperative coronary evaluation may be
necessary and is an important modiable risk factor in
patients undergoing open vascular procedures. Preoperative
nuclear cardiac stress test has been used in our institution
frequently given most of aortic occlusive patients cannot
complete an exercise stress test and are at high risk for postoperative myocardial infarction. Full assessment of the
peripheral vasculature is indicated because the condition of
the distal runoffs inuence the outcome of the aortoiliac
intervention. Sometimes, concurrent distal bypass may be
indicated.
Intraoperatively, appropriate antibiotic prophylaxis
should be administered before the incision and through the
perioperative period. Invasive arterial blood pressure monitoring is routine in many hospitals.
Direct Surgical Revascularization (AortoBifemoral Bypass)
Initial Approach andGroin Dissection
The patient is placed in supine position. Bilateral groin incisions are made. The choices of groin incisions are predominated by preoperative ndings and patient factors. Oblique
Соседние файлы в папке Библиотека им академика М.И. Перельмана
