Noninvasive Peripheral Arterial Diagnosis · Ali F. AbuRahma John J. Bergan Editors Noninvasive Peripheral Arterial Diagnosis Editors AliF.AbuRahma,MD,FACS,FRCS,RVT,RPVI JohnJ.Bergan,MD,FACS,HonFRCS Professor UCSDSchoolofMedicine Chief,Vascular/EndovascularSurgery LaJolla,CA DepartmentofSurgery USA RobertC.ByrdHealthSciencesCenter WestVirginiaUniversity and MedicalDirector,VascularLaboratory Co-Director,VascularCenterofExcellence CharlestonAreaMedicalCenter Charleston,WV,USA ISBN978-1-84882-954-1 e-ISBN978-1-84882-955-8 DOI10.1007/978-1-84882-955-8 SpringerLondonDordrechtHeidelbergNewYork BritishLibraryCataloguinginPublicationData AcataloguerecordforthisbookisavailablefromtheBritishLibrary LibraryofCongressControlNumber:2010920020 (cid:2)c Springer-VerlagLondonLimited2010 Firstpublishedin2000aspartofNoninvasiveVascularDiagnosis,editedbyAliF.AbuRahmaandJohnJ.Bergan, ISBN1-85233-128-3,2ndeditionpublished2007,ISBN978-1-84628-446-5 Apartfromanyfairdealingforthepurposesofresearchorprivatestudy,orcriticismorreview,aspermittedunderthe Copyright,DesignsandPatentsAct1988,thispublicationmayonlybereproduced,storedortransmitted,inanyform orbyanymeans,withthepriorpermissioninwritingofthepublishers,orinthecaseofreprographicreproductionin accordancewiththetermsoflicensesissuedbytheCopyrightLicensingAgency.Enquiriesconcerningreproduction outsidethosetermsshouldbesenttothepublishers. Theuseofregisterednames,trademarks,etc.,inthispublicationdoesnotimply,evenintheabsenceofaspecific statement,thatsuchnamesareexemptfromtherelevantlawsandregulationsandthereforefreeforgeneraluse. Thepublishermakesnorepresentation,expressorimplied,withregardtotheaccuracyoftheinformationcontained inthisbookandcannotacceptanylegalresponsibilityorliabilityforanyerrorsoromissionsthatmaybemade. Printedonacid-freepaper SpringerispartofSpringerScience+BusinessMedia(www.springer.com) Table of Contents 1. Overview of Peripheral Arterial Disease of the Lower Extremity ...................................................................................... 1 Ali F. AbuRahma 2. Overview of Noninvasive Vascular Techniques in Peripheral Arterial Disease............................................................... 15 Ali F. AbuRahma 3. Segmental Doppler Pressures and Doppler Waveform Analysis in Peripheral Vascular Disease of the Lower Extremities.............................................................................................................…..… 25 Ali F. AbuRahma and Kimberly S. Jarrett 4. Pulse Volume Recording in the Diagnosis of Peripheral Vascular Disease ..................................................................... 39 Jeffrey K. Raines and Jose I. Almeida 5. Duplex Scanning for Lower Extremity Arterial Disease .................................................................................................. 47 Paul A. Armstrong and Dennis F. Bandyk 6. Duplex Surveillance of Infrainguinal Bypass Grafts ….................................................................................................... 57 Patrick A. Stone and Dennis F. Bandyk 7. Rationale and Benefits of Surveillance After Prosthetic Infrainguinal Bypass Grafts ...................................................... 69 Stephen Kolakowski, Jr., Keith D. Calligaro, Sandy McAffe-Benett, Kevin J. Doerr, Kathy Mueller, and Matthew J. Dougherty 8. Rationale and Benefits of Surveillance After Percutaneous Transluminal Angioplasty and Stenting of Iliac and Femoral Arteries .................................................................................................. 75 Evan C. Lipsitz and George L. Berdejo 9. Duplex Ultrasound in the Diagnosis and Treatment of Femoral Pseudoaneurysms ......................................................... 83 Patrick A. Stone 10. Lower Extremity Arterial Mapping: Duplex Ultrasound as an Alternative to Arteriography Prior to Femoral and Popliteal Reconstruction …..................................................................................... 89 Enrico Ascher, Sergio X. Salles-Cunha, Natalie Marks, and Anil Hingorani 11. Preoperative Saphenous Vein Mapping ........................................................................................................................... 99 Benjamin B. Chang, Ann Marie Kupinski, R. Clement Darling III, Philip S.K. Paty, Paul B. Kreienberg, Sean P. Roddy, Kathleen J. Ozsvath, Manish Mehta, and Dhiraj M. Shah 12. Noninvasive Diagnosis of Upper Extremity Vascular Disease ….................................................................................. 109 Jocelyn A. Segall and Gregory L. Moneta 13. Ultrasound Imaging of Upper Extremity Arteries: Clinical Applications ….................................................................. 123 Sergio X. Salles-Cunha 14. Protocol and Technique of Dialysis Ultrasound Surveillance ….................................................................................... 133 Niten Singh, Cameron M. Akbari, and Anton N. Sidawy v vi Table of Contents 15. Noninvasive Evaluation for Congenital Arteriovenous Fistulas and Malformation ….................................................. 141 Robert B. Rutherford 16. Clinical Implications of the Vascular Laboratory in the Diagnosis of Peripheral Arterial Disease …........................... 149 Ali F. AbuRahma Index .....................................................................................................................................................................................169 1 Overview of Peripheral Arterial Disease of the Lower Extremity Ali F.AbuRahma Introduction artery,which continues inferiorly to become the popliteal arteryat its point of entry into the adductor canal. As the population continues to grow in average age, The popliteal artery then continues below the knee, chronic lower extremity ischemia is becoming more where the anterior tibial artery branches, piercing the prevalent. Recently, Dormandy et al.1 reported the interosseous membrane to supply the anterior compart- weighted mean incidence of intermittent claudication ment of the lower leg.The tibioperoneal trunk then con- from five large population-based studies.The incidence tinues briefly,where the posteriortibialarterybranches to ranged from two per 1000 men per year in the 30- to 54- course in a plane deep to the soleus muscle.The vessel year-old group to seven per 1000 in those over 65 years then continues inferiorly as the peronealartery.The pos- of age.In a recent summary of large population studies terior tibial artery is divided into lateral and medial from Italy,Britain,Holland,and Finland,the prevalence plantar arteries below the medial malleolus to supply the of intermittent claudication increases gradually from sole of the foot. <1% in 30-year-old men to 3% in 55- to 59-year-old men. Ultimately,the anterior tibial artery continues on to the The prevalence also increases starting at age 60,from 3% dorsum of the foot,where it becomes the dorsalis pedis to over 7% in those 70 years old and older.2It is believed artery.Here it anastomoses with branches of the posterior that the overall incidence and prevalence of peripheral tibial and peroneal arteries to form the plantararch.4On arterial disease are likely to increase significantly with the the dorsum of the foot,the dorsalis pedis artery forms two aging of the population, and it has been estimated that branches: the dorsal metatarsal and the deep plantar the number of individuals aged ≥65 will grow by 70% in arteries.The deep plantar artery penetrates into the sole the United States between 2010 and 2030.3 of the foot and joins the lateral plantar artery (branch of the posterior tibial artery) to form the plantar arch. Anatomy of the Lower Extremity Collateral Circulation Vascular System In the event of chronic obstruction of major arterial The arterial anatomy relevant to the lower extremity cir- vessels,collateral pathways exist that allow preservation culation is demonstrated in Figure 1–1. of sufficient distal blood flow to maintain viability of the At its most distal aspect, the aorta branches to form tissues distally.The degree of adequacy of these pathways paired common iliac arteries.These continue retroperi- determines what degree of functional disability results. toneally to the pelvic brim, at which the common iliac With obstruction at the level of the distal aorta and vessels branch to form paired internal and external iliac common iliac arteries,a variety of pathways for collateral arteries.The internaliliac(or hypogastric) arteriesprovide circulation exist (Figure 1–2). Communications may blood supply to the pelvic structures, while the external exist between the lumbar and circumflex iliac or hypogas- iliac courses inferior to the inguinal ligament to become tric arteries. Other communications may exist between thecommonfemoral artery. the gluteal branches of the hypogastric arteries and recur- The common femoral artery then bifurcates early in its rent branches of the common femoral or profunda course to form the profunda femoris artery, which sup- femoris arteries. Visceral–parietal communications may plies the thigh musculature, and the superficial femoral also exist at this level between the inferior mesenteric A.F. Aburahma, J.J. Bergan (eds.), Noninvasive Peripheral Arterial Diagnosis, DOI 10.1007/978-1-84882-955-8_1, 1 © Springer-Verlag London Limited 2010 2 A.F.AbuRahma Figure1–1. A normal right arterial tree (except for occlusion of the right common iliac artery) beginning with the common R L iliac artery down to the pedal branches. The left side shows occlusion of the left common iliac artery, stenosis of the left Common iliac artery external iliac artery,and occlusion of the left superficial femoral artery,popliteal artery,and diseased tibioperoneal trunk. Internal iliac artery External iliac artery Common femoral artery Deep femoral artery Superfical femoral artery R L Superior mesenteric artery Lumbar artery Inferior mesenteric artery Common iliac artery Popliteal artery Deep circumflex iliac artery Internal iliac External iliac artery artery Common femoral artery Medial femoral Lateral femoral circumflex artery circumflex artery Anterior tibial artery Superficial Deep femoral artery femoral artery Peroneal artery Posterior tibial artery Descending geniculate artery (superior) Popiteal artery Dorsalis pedis artery Middle geniculate artery Ascending genicu- Plantar arch late artery (inferior) Anterior tibial artery Peroneal artery Posterior tibial artery Dorsalis pedis artery Plantar arch A Figure 1–2. (A) Collateral circulation of the left lower extremity secondary to occlusion of the major arterial segments as noted in Figure 1–1. (B) Arteriogram showing complete occlusion of the left common iliac artery (arrow).Note the col- lateral circulation around the obstruction. This also shows extensive disease of both right and left external iliac arteries. B 1. Overview of Peripheral Arterial Disease of the Lower Extremity 3 and internal iliac vessels via hemorrhoidal branches at has been estimated to be as low as 20cm/s in the femoral the level of the rectum. artery.A diameter reduction of >90% would be required More distally,with obstruction of the common femoral for a stenotic lesion at these rates to be considered hemo- artery, collateral circulation around the hip is provided dynamically significant.However,the metabolic require- via communication of the inferior epigastric and deep ments in the distal tissue of an exercising or active circumflex branches of the external iliac arteries with the individual are higher, and the femoral artery velocities internal pudendal and obturator branches of the internal may increase up to 150cm/s,and at this velocity level,a iliac arteries (Figure 1–2B). stenosis of 50% can cause significant pressure and flow With chronic obstruction of the superficial femoral gradient leading to inadequate oxygen delivery. In artery,collateral circulation to the popliteal artery is pro- general,patients with mild intermittent claudication typ- vided by communications with the profunda femoris ically have a single segment disease,which is often asso- artery via the geniculate arteries, as well as descending ciated with well-developed collateral circulation, in branches of the lateral femoral circumflex arteries.With contrast to patients with severe claudication or critical popliteal occlusion,it is these geniculate arteries that are limb ischemia,which is associated with multilevel disease. responsible for the filling of the more distal tibial vessels The hemodynamic abnormalities of peripheral arterial as well (Figure 1–2B).More distally,branches of the per- occlusive disease reflected in ankle-brachial index (ABI) oneal, anterior tibial, and posterior tibial arteries all measurements or direct measurement of calf blood flow provide collateral supply to the plantar arch vessels.4,5 do not necessarily correlate with walking performance or severity of the claudication symptoms.8 Biochemical changes and microcirculatory changes induced by the Normal Structure of the Arterial Wall cycle of ischemia and reperfusion have been suggested as evidence of this observation. This may lead to skeletal Before discussion of any pathologic process affecting the muscle injury due to distal axonal degeneration, which, arterial wall,it is important to understand the basic struc- in turn,may cause muscle atrophy,further compromising tural anatomy of the normal blood vessel.The artery is exercise tolerance.This injury may be mediated at the cel- composed of three major layers known as the intima, lular level through increased oxidative stress,generation media,andadventitia. of oxygen-free radicals,and lipid peroxidation that occurs The intima,the innermost layer,consists of a layer of during reperfusion of ischemic tissue. Several studies endothelium that lines the luminal surface and overlies have demonstrated the accumulation of several meta- one or more layers of smooth muscle. These are then bolic intermediates,such as acylcarnitines,impaired syn- covered by a layer of connective tissue known as the thesis of phosocreatinine, and supranormal levels of internalelasticlamina. adenosine diphosphates.9Patients with advanced chronic Just beyond the internal elastic lamina begins the peripheral arterial disease have an abundance of these media, which is bounded by the internal and external antimetabolic compounds,which signify well-established elastic lamina.The media is composed of smooth muscle metabolic myopathy. Increased acylcarnitine accumula- cells arranged in layers and lying in a matrix of proteo- tion has been noted to correlate well with decreased glycan substance. Collagen and elastin fibers are also treadmill exercise performance.10 present within this layer. The basic underlying disease process affecting the arte- The adventitiais the outermost layer of the arterial wall rial wall, and the one responsible for the clinical mani- and the layer responsible for the majority of the vessel’s festations of lower extremity peripheral arterial disease, strength.It is composed of connective tissue,fibroblasts, is atherosclerosis.Simply put,atherosclerosis is a disease capillaries, neural fibers, and occasional leukocytes. In of medium to large arterial vessels that causes lumi- large vessels a microvasculature known as the vasa nal narrowing, thrombosis, and occlusion resulting in vasorumis present within the adventitial layer,serving to ischemia of the end organ involved.The process of ath- nourish the adventitia and outermost layers of the media.6 erosclerosis is extremely complex and is the subject of continuous investigation within the medical and surgical Atherosclerosis community. In addition to lower extremity vascular disease,atherosclerosis is known to produce many other clinical events of importance including,but not limited to, Pathophysiology myocardial infarction,stroke,mesenteric vascular insuf- Intermittent claudication as a symptom of peripheral ficiency,and aortic aneurysm formation.11 arterial disease can be caused by flow limiting stenosis, Atherosclerosis is primarily a disease of the intima which is almost secondary to atherosclerosis.Whether or characterized by the proliferation of smooth muscle cells not a stenotic lesion is flow limiting depends on both flow and the accumulation of lipid material.The earliest lesion velocities and the degree of stenosis.7Flow velocity at rest appears to be that of the fatty streak.In this lesion,lipid