Conclusions: For locally advanced bladder carcinoma,ncoadjuvantchcmotherapy significantly reduces tumour volume which

is associated with improved survival.

PROSTATE CANCER

10 YrOutcomesAfter Monitoring. HEJM 2016;375|15|:1415-1424

Surgery,or Radiotherapy for

Localized Prostate Cancer

Title:10 Yr Outcomes After Monitoring,Surgery,or Radiotherapy for localizedProstate Cancer

Purpose:To evaluate the effectiveness of active monitoring,radical prostatectomy,and radiotherapy inrelabon tomortality

and the incidence of metastases and disease progression.

Methods:1643 men randomized into active monitoring,surgery,andradiotherapy. The primary outcome was prostatecancer mortality at median 10 yr of follow-up and the secondary outcomes were rale of disease progression,metastases,and

all-cause deaths.

Results: Ho significant difference among groups in prostate-cancer-specific deaths and in thenumbers ol deaths from any

cause. Metastases developed more in the active monitoring group (33 men) vs. surgery group (13 men)or radiotherapy group

(16 men) (P-0.004).Higher rates of disease progression in active-monitoring group (112 events) vs.surgery group (46 events)

or radiotherapy group (46 events)|P

‘

0.001).

Conclusions:At 10 yr,prostate-cancer-specific mortality was low regardless of the treatment,with no significant difference

among treatments.Surgery andradiotherapy were associated with lower incidences of disease progression and metastasis

compared to active monitoring.

Title:Screening and Prostate-Cancer Mortality in a Randomized European Study

Purpose:To determine the reduction of prostate-cancer mortality byPSA-based screening.

Methods:Participants were randomized to a group that received PSA screening an average of once every 4 yr or to a control

group that did not receive such screening.The primary outcome v/as the rate of death from prostate cancer.

Results:The incidence of prostate cancer was higher in the screening group than in the control group (8.2% vs.4.2%).The

absolute risk difference was 0.71deaths/1000 men.meaning that 1410 men would need to be screened and 48 additional

cases of prostate cancer would need to be treated to prevent one death from prostate cancer.

Conclusions:PSA-based screening reduced the rate of mortality from prostate cancer by 20% but was associated with a high

risk of overdiagnosis.

Title:Chemohormonal Therapy in Metastatic Hormone-Sensitive Prostate Cancer

Purpose:To assess whether concomitant treatment with Androgen-deprivation therapy (ADT) plus docetaxel would result in

longer overall survival than that with ADT alone.

Methods:Patients with metastatic,hormone-sensitive prostate cancer were randomized toreceive either ADT plusdocetaxel

or ADT alone.The primary objective was overall survival.

Results:After a median follow-up of 28.9 months,the median overall survival was13.6 months longer in the combination

therapy group than within the ADT-alone group|P‘

0.001).The median time to progression was 20.2 months in the

combination group and 11.7 months in the ADT- alone group (P‘

0.001).

Conclusions:Combination ol docetaxel and ADT lor hormone-sensitive metastatic prostate cancer resulted in significantly

longer overall survival than that with ADT alone.

ERSPC HJEM 2009:360:1320-1328

CHAARTED NJEM 2015:373(8):737-46

References

General Information

American Joint Commitlee on Cancer.AJCC Cancer StalmgManual.Eighth Edition.Available from:http://cancerslaging.org/.

American Urological Association.Available Irom:http://www.auanet.org/guidclincv/.

Canadian Urological Association. Available from:http://www.cua.org/cn/9uidclincs/.

Ferri F.Practical guide to the careolIhe medical patient,6lhed.St. Louis:Mosby,2006.

Goldman L.Ausiello 0.Cecil textbook of medicine.23ided.Philadelphia:WB Saunders.2007.

Macfarlane MT. House officer scries:urology. 3rd ed. Philadelphia:lippincoll.2001.

Montague OK. Jarow J.Broderick GA.etal.Guidclmeon the management ol priapism.American Urological Association Education and Research.Inc. 2003 Available from:http://www.auancl.oig/cducation/

guidelines/priaplsm.cfm.

Tanagho EA,McAninch JW.Smith's generalurology.17th ed. New York:McGraw Hill. 2007.

Wcin AJ.Kavoussi Ut.Hovick AC.ct al.Campbell's urology. 10th ed.Philadelphia: W8 Saunders. 2011.

Wieder JA. Pocket guide to urology.4th ed.Oakland:Wicder.2010.

Common PresentingProblems

AbramsP.Artibani W, Cardozo L.etal.Reviewing theICS 2002 terminology report:The ongoing debate. Hcutout ol Urodynam 2002:21:167-178.

Alshar K.Dos Santos J.BlaisAS.ft at. Canadian Urological Association guideline for the managemenl olbladder and bowel dysfunction inchildren.CUAJ.2021:15(2).

Anger J.leeU.Ackerman AL.etal.Recurrent Uncomplicated Urinary TradInfcctionsin Women:AUAiCUA/SUFU Guideline. J Urol 2019:202|6):1273-1274.

Assimos D.Krambeck A,Miller HI. etal.Surgical managementol stones:AUAEndourology society guidelines. J Urol 2016:196(4):1153 60.

Bettez M. Tu LM. Carlson K.et al.2012 Update:Guidelines for Adult Urinary Incontinence Collaborative Consensus Document for IheCanadian UrologicalAssociation. CUAJ 2012:6:354 363.

Bowman C.Goldberg JM.Care of the patient undergoing sex reassignment surgery.International Journal olIransgenderism.Ini. J. Transgend.Health 2006:9(3 4|:135-16S.

Bremnor JO,Sadovsky R.Evaluation of dysuria inadults.Am Earn Phys 2002:65:1589-1597.

+

Activate Windows

Go to Settings to activateWindows.

U50 Urology Toronto Notes 2023

Bryson C.Honiq SC.Genitourinary Complications of Gender-Affirming Surgery.Curr.Urol.Rep 2019;6:20-31.

Capohcchio JP. Braga IH.Stymanski KM.Canadian UrologicalAssocialioni

'Pcdiatric Urologists of Canada guideline on the investigation and managcmcntol antcnalally detected hydronephrosis. Can.Urol.Assoc.

J 2018 Apr;12(4) 85.

Cohen RA.Brown RS.Microscopic hematuria. NEJM 2003;348:2330-2338.

Cooper TG.Noonan E.Von Echardstem S,etal.World Health Organization reference values for human semen characteristics.Hum Reprod Update 2010;16|3):231-245.

Cox A,Golda N.Nadeau G.etal. CUA guideline:Diagnosis and treatment of interstitial cystitis/bladder pain syndrome.CUAJ 2016;10:E136 -E155.

Dason S,Dason JT.Kapoor A.Guidelines for thediagnosis andmanagement ofrecurrent urinary tract infection inwomen.CUAJ.2011;5|5):316-322.

Djordjevic ML.Stojanovic B.Bizic M.Metoidioplasty:techniques and outcomes.Transl.Androl.Urol.2019;8(3):248.

Evans SM. Bandarage VP,Kronborg C.clal.Gleason group concordancebetween biopsy and radical prostatectomy specimens:Acohort study from Prostate Cancer Outcome Registry - Victoria.Prostate Int

2016:4(41:145 151.

Gofiit ON.Kate R.Shapiro A. clal,Gross Hematuria in Patients withProslate Cancer:Etiology and Management.ISRN Surgery. 2013.

Kavanagh A, Baverstock R,Campeaul.etal.CUAguidelinc:Diagnosis,management,and surveillance of neurogenic lower urinary tract dysfunction. CMAJ 2019;13|6):1S6 165.

Kassouf W,TraboulsaSL.Kulkarni GS.et al.CUA guidelines on the management of non-muscle invasive bladder cancer.CUAJ 2015:9:E690-E704.

Kulkarni GS,Black PC.Sridhar SS,et al.Canadian Urological Association guideline:Muscle-invasive bladder cancer.CUAJ 2019;13|8):230.

Mahmood J,Shamah AA,Creed TM, etal.Radiation-induced erectile dysfunction:Recent advances and future directions.Adv.Radial.Oncol.2016;1(3):161-169.

Minami,H„Furukawa.S..Sakai, et al.Physical activity and prevalence of erectile dysfunction inJapanese patients with type 2 diabetes mellitus:The DogoStudy.J.DiabetesInvestig 2018;9|1(.193-198.

Morrison SD,Shakir A.Vyas KS.cl al.Phalloplasty:a review of techniques and outcomes.Plast.Reconstr.Surg 2016;138|3):S94-615.

Mtiilon AR.Iliescu EA. Wilson JWL. Nephrology:investigation andtreatment of recurrent kidney stones. CMAJ 2002:166:213- 218.

Nguyen HI. Benson C8,Bromley B, elal. Multidisciplinary consensus on the classification of prenatal and postnatal urinary tract dilation (UI0 classification system). J.Pedialr. Urol. 2014:10(61:982-98.

Nickel JC.Prostabls.CUAJ 2011;5:306-315.

Pearle MS.Goldfarb DS.Assimos DG.etal.Medical management of kidney stones:AUA guideline.J Urol 2014;192|2):316- 324.

Rashid M.Tamimy MS.Phalloplasty:the dream and the reality.Indian journal of plastic surgery:official publication of the Association of Plastic Sugeonsof India.2013 May:46|2):283.

Rendon RA.Mason RJ.Marzouk K.et al.Canadian Urological Association recommendations on prostate cancer screeningand early diagnosis.CUAJ 2017;11:298-309.

Rourke KF.Welk B,Kodama R.et al.Canadian Urological Association guideline on male urethral stricture. Can.Urol.Assoc.J.2020:14(10).

Saad f, Apnkian A.Finelli A. et al. 2021Canadian Urological Association (CUA)

-Canadian Uro Oncology Group (CUOG) guideline:Managements castration-resistant prostate cancel (CRPC).Can.Urol. Assoc.J

2021:15!2):E81.

Santucci RA Urethral compticalionsalter transgender phalloplasty: strategies to treat them and minimue their occurrence.Clin Anal 2018:31(2) 187 190

So A.Chi K.Danielson 8.et al.Canadian Urological Association-Canadian Urologic Oncology Group guideline on metastatic castration-naive and castration-sensitive prostate cancer.CUAJ 2020:14(2).

TeichmanJMH.Acute renal colic from ureteral calculus. NEJM 2004:350:684-693.

Verta W.Oosterlinck W.Spinoit AF.etal.A ComprehensiveReview Emphasizing Anatomy,Etiology.Diagnosis,and Treatment of Male Urethral Stricture Disease.Biomed Res Int 2019;2019.

Zini A,Grantmyre J.Chan P.CUA guideline:Vasectomy.CUAJ 2016 Jultl0(7-8):E2 74.

Overactivc Bladder

Ouslander JG.Management of overactivc bladder. NEJM 2004:250:786 799.

Yazdany 1,Jakus -Waldman S,Jeppson PC.el al.American Urogynecologic Society Systematic Review:The Impact of Weight loss Intervention on lower Urinary Tract Symptoms and Urinary Incontinence in

Overweight and Obese Women.FemalePelvic Med Reconstr Surg 2020:26|1):16 29.

Benign RenalNeoplasm

Israel GM,Bosniak MA.An update of Bosniak renal cyst classification system.Urology 2005;66:484-488.

Richard P0. Violette PD.Jewett MAS,etal.CUA guideline on the management of cystic renal lesions.CUAJ 2017:11:E66-E73.

Jewett MAS.Rendon R.lacombcl. et al.Canadian guidelines lor the management of smallrenal masses.CUAJ 2015:9(5 6);160- 3.

Urological Emergencies

Galcjs LE.Diagnosis and treatment of the acute scrotum. Ain Fam Phys 1999:5:817-824.

Infertility and Andrology

Grober ED.Krakovrsky Y.Khera M.etal.Canadian Urological Association guideline on testosterone deficiency inmen:Evidence-basedOSA.Can.Urol.Assoc. J 2021:15|5):E234.

Medications

Bill-Axelson A,Holmbcrgl,Ruutu M,etal.SPCG 4 Investigators.Radical prostatectomy vs.watchful waitingIn early prostate cancer. NEJM 2011:364:1708 1717.

Compendium of Pharmaceuticals and Specialties.Available from:http://www.ethcrapcutic5.ca.

Micromedex health care series. Available from:http:i7www.rnicromedex.com.

Rini B.Halabi S.Rosenberg J,et.al.Bevacizumab plus interferon alia compared with interferon alia monotherapy inpatients with metastatic renal cell carcinoma:CAIGB 90206 trial. J Clin Oncol 2008:26:5422-

5428.

EBM

Bill-Axelson A. Holmberg L,Ruutu M.et al.Radical prostatectomy vs. watchful waiting in early prostate cancer.HEJM 2011:364:1708-1717.

Campschroer T.2hu X,Vemooij RW,el al.Alpha-blockers as medical expulsive therapy lor ureteral stones. Cochrane 0B Syst Rev 2018;4:C0008509.

Carter HB.Albertscn PC.Barry MJ el al:Early detection ol prostatecancer: AUA guideline.J Urol 2013;190:419.

Coelho RF.Rocco 8.Patel MB.etal. Retropubic,laparoscopic,and robot-assisted radical prostatectomy:a criticalreview oloutcomes reportedbyhigh-volume centers.JEndourol 2010:24:2003 2015.

Escudier B,EisenI.Stadler WM, et al.Sorafemb in advanced dear- cellrenal-cell carcinoma.NEJM 2007;356:125-134.

Grossman H8.Natale RB. Tangen CM.et al.Neoadjuvantchemotherapy plus cystectomy comparedwith cystectomy alone for locally advanced bladder cancer.NEJM 2003;349:859-866.

Hoffman RM.Monga M.Elliott SP,et al.Microwave thermotherapy for benign prostatic hyperplasia.Cochrane D8 Syst Rev 2012;9:CD004135.

Ilic D.Evans SM,Allan CA,et al.laparoscopic and robolic-assisted vs.open radical prostatectomy for the treatmentof localised prostate cancer.Cochrane DB Syst Rev 2017:9:CD009625.

James ND. Hussain SA.Hall E,et al. Radiotherapy wilh or without chemotherapy inmuscle-invasive bladder cancer. NEJM 2012;366:1477-1488.

Kim SC.Sco KK.Efficacy and safety ol fluoxetine,sertraline and clomipramine inpatients with premature ejaculation:a double-blind, placebo controlled study. J Urol 1998:159:425-427.

McDonnell JD,Rochrborn CG. Bautista 0M.ct al. The long term effect of doxazosin,finasteride,and combination therapy on the clinical progression of benign prostalic hyperplasia. NEJM 2003:349:2387- 2398.

Motzer RJ,Escudier B. Tomczak P,et al. Axitimb vs.soraiemb as second- line treatment for advancedrenal cell carcinoma: overall survival analysis and updated results from a randomizedphase 3 trial,lancet

Oncol 2013:14:552-562.

Parsons JK,Hergan LA.Sakamoto K.etal.Efficacy of alpha-biockersfor the treatment of ureteral stones.J Urol 2007:177:983-987.

Schroder FH.Hugosson J,Roobol MJ. etal.Screening and prostate- cancer mortality in a randomized European study.NEJM 2009:360:1320-1328.

Wiysonge CS.Kongnyuy EJ.Shey M,et al.Malecircumcision for prevention of heterosexual acquisition of HIV in men.Cochrane DB Syst Rev 2011:6:00007496.

lacklind J.Fink HA.Macdonald R, et al.Finasteride for benign prostatic hyperplasia.Cochrane 0B Syst Rev 2010:10:00006015.

Wiesenthal JD.Ghiculcte 0. D'A Honey R J.clal.A comparison of treatment modalities for renal calculi between 100 and 300 mm2: are shockwave lithotripsy,urcleroscopy.andpercutaneous nephrolithotomy

equivalent? JEndourol 2011:25:481 485.

Will1J.Brawer MK,JonesKM,etal. Radical prostatectomy vs. observation for localized prostate cancer.NEJM 2012:367:203-213.

r-i

LJ

+

Activate Windows

Go to Settings to activate Windows.

Vascular Surgery

Kauniil V. Patel and George Hlzawy, chapter editors

Chunyi Christie Tan and Vrati Mehra, associate editors

Arjan S. Dhoot, EBM editor

Dr. Elisa Greco and Dr. George Orcopoulos, staff editors

Acronyms VS2

Arterial Disease

Acute LimbIschemia

Peripheral Arterial Disease

Aortic Disease

Aortic Dissection

Aortic Aneurysm

Carotid Stenosis

Venous Disease

Venous Thromboembolism

Chronic Venous Insufficiency

Lymphedema

Landmark Vascular Surgery Trials.

References

VS2

VS6

VS9

VS10

VS11

VS12

.VS13

ri

LJ

+

VSI Vascular Surgery Toronto Notes 2023

Activate Windows

Go to Settings to activate Windows.

VS2 Vascular Surgery Toronto Xotes 2023

Acronyms

abdominal aortic aneurysm

ankle- brachial index

angiotensin converting enzyme

inhibitor

acute kidney injury

acute limb ischemia

angiotensin II receptor blocker

best medical therapy

carotid artery angioplasty +

stenting

calcium channel blocker

carotid endarterectomy

CEAP clinical, etiological,

anatomical, pathophysiological Echo

(classification of venous disease) EVAR

chronic limb threatening

ischemia

computed tomography

angiography

cerebrovascular accident

cerebrovascular disease

chronic venous insufficiency

disseminated intravascular LV

coagulation

deep vein thrombosis

DUS duplex U/S

echocardiogram

endovascular aortic aneurysm

repair

heparin- induced

thrombocytopenia with

thrombosis

international normalized ratio

low-density lipoprotein

cholesterol

left ventricular

magnetic resonance

angiography

MSK musculoskeletal

PAD peripheral arterial disease

PFO patentforamen ovale

prothrombin time

PIT partial thromboplastin time (i.e.

aPIT)

TAA thoracic aortic aneurysm

TBI toe-brachial index

TEE transesophageal

echocardiography

TEVAR thoracic endovascular aortic

repair

TIA transient ischemic attack

AAA

ABI

ACEI

CLTI PI

AKI HITT

All CTA

ARB

BMT CVA INR

CAS CVD LDL-C

CVI

CCB DIC

CEA MRA

DVT

Arterial Disease

Anterior Posterior

1\

Abdominal aorta & IVC

Common iliac a.& v.

Internal iliac a. & v.

/:

i

-

\

V

— External iliac a. & v

— Inguinal ligament

• Common femoral a.& v.

Deep femoral a.& v. -

Superficial fomoral a. & v.

— Great saphenous v. — — Adductor hiatus

Popliteal a. & v, —

— Tibioperoneal trunk —

I I

:

:

<

- Small saphenous v.-

" Anterior tibial a. & v.

Posterior tibial a & v.

Fibular (peroneal) a. & v.

Dorsalis pedis a. & v.

O ©Kim Nipp 2019

Figure 1. Peripheral vascular anatomy

Acute Limb Ischemia

Definition

• acute occlusion of a peripheral artery that often threatenslimb viability with symptom duration <2

wk - clinical presentation usually within h to d

urgent management required asskeletal muscle can tolerate 6 h of total ischemia before

irreversible damage

< exception is acute-on-chronic occlusion, where previously developed collaterals provide minimal

perfusion

• tends to be lower extremity > upper extremity;femoropopliteal > aortoiliac

• paralysis with complete loss of sensation is sign of late ischemia

Etiology and Risk Factors

• the most common causes of AL1 is cardiac embolism;other causes include:thrombosis, peripheral

artery aneurysm, dissection, and traumatic artery injury

• embolism

• cardiac: arrhythmias ( most common cause is atrial fibrillation), endocarditis, Ml, LV aneurysm,

myxoma/cardiac tumour, paradoxical embolism with PTO, valvular heart disease

non-cardiac: mural thrombus within arterial aneurysms, atheroemholism, ulcerated plaque with

distal embolism

• thrombosis(in situ)

progression of high-grade atherosclerotic plaque to acute occlusion

bypass graft: occlusion (most common etiology of arterial thrombosis in setting of previous open

or endovascular reconstruction)

hypercoagutable states

hypercoagulability, low arterial flow, or hyperviscosity

HITT

r i

L J

+

Activate Windows

Go to Settings to activate Windows.

VS3 Vascular Surgery Toronto Notes 2023

aortic or arterial dissection

aortic dissection typically caused by hypertensive crisis

isolated arterial dissection of vessels supplying lower limbs is uncommon but can occur from

trauma or collagen disorders

• trauma (e.g. arterial transection, compression)

vasospasm/vasculitis

iatrogenic (e.g.occlusion at arterial accesssite)

•differentiating between embolism and thrombosis

embolism is more common than thrombosis

embolus typically lodges at arterial bifurcations, where the vessel narrows naturally

embolism due to plaque rupture generally results in greater degree of ischemia due to relative lack

of collaterals

•suspect embolism in patients with the following features:

• acute onset (patient able to accurately recall the moment of the event)

history of embolism

• known embolic source (e.g. cardiac arrhythmias), lapse in prescribed anticoagulation

no prior history of intermittent claudication

normal pulse and Doppler U/S or DUS in unaffected limb

•suspect in-situ thrombus in patients with the following features:

prior history of intermittent claudication

prior vascular intervention/bypass

abnormal pulse examination of the unaffected limb

Viischow'sTriad

• Hypercoagulability

• Stasis of flow

,

Endothelial injury

Clinical Features

•6 Ps- may not all be present

Polar/Poikilothermia: cold

leg becomes cold

• Pallor: pale

within a few h becomes mottled cyanosis

Pain

may be constant or elicited by passive movement

absent in 20% of cases

Pulselessness

helpful to determine site of occlusion

• Paresthesia (late sign of ischemia)

light touch lost first then other sensory modalities

Paralysis/ Power loss (late sign of ischemia):

most important; heralds impending non-salvageable limb

HypercoagulableStates

Congenital

• Group I (reduced anticoagulants)

• Antithrombin

• Protein C

• Protein S

• Group II (increased coagulants)

• Factor V leiden

. Prothrombin

• Factor VIII

• Other

. Sickle cell disease

. Hyperhomocysteinemia

Investigations

•history and physical exam are essential:depending on degree of ischemia one may have to forego

investigations and go straight to the OR (i.e.an immediately threatened limb)

•DUS: bilateral ultrasound examination; greater accuracy than pulse examination alone; absent

arterial signal indicates threatened limb

•determine Rutherford classification (see Table I. VS4) based on physical findings and Doppler U/S or

DUS signals

•AB1: extension of physical exam, easily performed at bedside

•RCG, troponin:rule out recent MI or arrhythmia

•CBC:rule out leukocytosis, thrombocytosis,or thrombocytopenia in patients receiving heparin (may

suggest HITT)

•P'

l

'

/INR, PTT: patient anticoagulated/sub-therapeutic INR

•echo: Identify wall motion abnormalities, intracardiac thrombus, valvular disease, or aortic dissection

(Type A) (see Aortic Dissection, VS6)

•not part of immediate work- up to decide on operative management unlike other testslisted

•CT'

A:most often used but not a requirement for decision making and sometimes performed after

operative intervention;identify underlying atherosclerosis,aneurysm, aortic dissection;embolic

source;other end organs with emboli (e.g.splenic/renal infarcts);identify level of the occlusion and

extent

•angiography:can be obtained in OR as part of intervention or for treatment

Acquired

• Age

• Obesity

• Smoking

• Immobility

• Cancer

• Pregnancy/systemic hormonal

contraceptives

• Antiphospholipid antibody syndrome

• Inflammatory disorders

. Myeloproliferative disorders

• Nephrotic syndrome (acquired deficit

in Protein C and S)

r T

L J

+

Activate Windows

Go to Settings to activate Windows,

VS4 Vascular Surgery Toronto Notes 2023

Table 1. Rutherford ALI Classification

Category Description/

Prognosis

Findings Doppler Signals

Sensory Loss Muscle Weakness Arterial Venous

IViable Not immediately

threatened

None None Audible Audible

II Threatened

lla Marginally Salvageable If Minimal (toes)or none None

promptly treated

Salvageable

with immediate

revascularization pain

Major tissue lossor

permanent nerve

damage inevitable

Inaudible Audible

lib Immediately More than toes. Mild,moderate

associated with rest

Inaudible Audible

III Irreversible Profound, anesthetic Profound,paralysis Inaudible

(rigor)

Inaudible

Adopted from:Rutherford RB,Baker JD.Ernst C.et al.Recommended standards tor reportsdealing with lower extremity ischemia:revised version.

JVascSurg.«97:26:517-38.

Treatment

• immediate unfractionated heparinization with weight-based bolus (70-100 lU/kg) and continuous

infusion to titrate PTT to 70-90

• IV fluids, urine output monitoring, analgesia,supplemental O:

• if impaired neurovascularstatus: emergent revascularization (Rutherford category 11b)

• if intact neurovascularstatus:may have time for workup (including CTA)

• identify and treat underlying cause

embolus: embolectomy

thrombus:thrombectomy ± bypass graft ± endovascular therapy

irreversible ischemia (i.e. Rutherford category 111): primary amputation or palliation

arterial aneurysm: bypass/stent graft

• continue heparin postoperatively;start oral anticoagulant postoperatively wh

longer depending on underlying etiology and other comorbidities

note unfractionated heparin carries a greater risk for heparin induced thrombocytopenia than

low molecular weight heparin

Complications

• local:compartmentsyndrome secondary to reperfusion (see Orthopaedic Surgery, OR10) with

prolonged ischemia;requires 4-compartment (anterior/lateral/superficial and deep posterior)

fasciotomy in calf

• heart: risk of arrhythmia, Ml, cardiac arrest, and death with reperfusion injury

• kidneys/other organs: renal failure and multi

-organ failure due to toxic metabolites from ischemic

muscle, rhabdomyolysis

• up to 10% chance of metachronous embolism

Prognosis

• 12-15% mortality rate

• 5-40% morbidity rate (amputation)

en stable x3 mo or

Peripheral Arterial Disease

Distinction between CLTI and AU

Definition

• chronic ischemia due to inadequate arterial supply to meet cellular metabolic demands during

walking (claudication) or at rest (CLTI)

Etiology and Risk Factors

• predominantly due to atherosclerosis (for pathogenesis,see Cardiology and Cardiac Surgery,C30);

primarily occurs in the lower extremities

• modifiable risk factors:smoking, DM, hyperlipidemia, HTN,obesity, and sedentary lifestyle

• nnn- modifiahle risk factors: advanced age, and PMHx or l

:MHx of PAD/CAD/CVD

Clinical Features

• claudication:

1. pain with exertion:usually in calves or any exercising muscle group

2. relieved by short rest:less than 5 min and no postural changes necessary

3. reproducible:same distance or time to elicit pain, same location of pain,same amount of rest

to relieve pain

the presence of the preceding features differentiates vascular claudication from neurogenic

claudication or MSK pain

1. includes rest pain, night pain, and/or tissue loss (ulceration or gangrene) in a patient with

existing PAD for at least 2 wk

2. pain most commonly over the forefoot/toes, waking person from sleep, and often relieved by

hanging foot off bed

ALI:A precipitous decrease and/

or cessation in blood flow to a limb

threatening viability. Typically,due to

arterial embolism or thrombosis, or other

acute cause.Characterized by rapidly

worsening leg pain that is present for

<2 wk (usually h to d) in patients with no

history of claudication

CLTI:Severe manifestation of PAD

where blood flow to the extremities is

markedly reduced. Defined asischemic

foot pain at rest or at night occurring

>2 wk.wounds, or gangrene in patients

who may have a history of claudication

Acute Aortoiliac Occlusion

If a patient presents with new onset

bilateral ALI,suspect possible occlusion

of the aorta or aortoiliac segment.

Etiologies include thrombosis or rupture

of AAA. aortic dissection, or large saddle

embolism

. CLTI: +

Activate Windows

Go to Settings to activate Windows.

VS5Vascular Surgery Toronto Notes 2023

3. ankle pressure 50 mmHg, toe pressure <30 mmHg, and/or ABI <0.40

distal pulses are absent

signs of poor perfusion: hair loss, hypertrophic nails,shiny skin, atrophic muscle,

ulcerations and infections,slow capillary'refill, prolonged pallor with elevation and

rubor on dependency, and venous troughing (Buerger’

ssign/Buerger’

s angle) (collapse of

superficial veins of foot)

4. high-risk of 1 yr limb amputation (25%) and mortality (25%)

5. usually the result of multilevel occlusive arterial disease in the lower extremity

Investigations

•routine blood work, fasting metabolic profile

•ankle pressure and ABI: highest ankle pressure (dorsalis pedis or posterior tibial) for each side divided

by highest brachial pressure (see Table 2 for cut-offs)

•toe pressure and TB1:highest pressure in the great toe for each side divided by highest brachial

pressure; useful in patients with non-compressible vessels

•ABI and/or a1BI study are recommended to confirm diagnosis of PAD

•arterial DUS: combines b-modc and Doppler U/S to visualize blood vessels and characterize flow and

plaques

•non-invasive:CTA and MRA excellent for large arteries (aorta, iliac, femoral, popliteal) but may have

difficulty with tibial arteries (especially in the presence ofsignificant wall calcification)

requires IV injection of iodinated contrast for CTA (contrast-induced nephropathy risk),

gadolinium for MRA (avoid in patients with severe renal failure)

used primarily for planning interventions

•invasive: arteriography

superior resolution to CTA/MRA, better for tibial arteries,can be done intraoperatively as part of

intervention

• can be diagnostic and/or therapeutic

<§>

Leriche Syndrome

Chronic aortoiliac occlusive disease

presenting with a triad of:

1.Claudication (ol buUocks and thighs)

2.Decreased femoral pulses

3.Erectile dysfunction/impotence

Subclavian Steal Syndrome

A chronic arterial disease of the upper

limb where stenosisor occlusion of

the proximal subclavian artery results

in retrograde flow from the vertebral

artery, compromising vertebrobasilar

circulation. Patients can present with

pre/syncope and neurological deficits

especially upon exertion of the limb

(rare),though most usually exhibit

diminished BP with an associated finding

of retrograde vertebral artery flow

Differential Diagnosis of Lower

Extremity Pain

Vascular

• Atherosclerotic disease

• Fibromuscular dysplasia

• Popliteal entrapmentsyndrome

• Venous claudication/hypertension

Table 2. Ankle-Brachial Index Cut-Offs

ABI Recording Degree of PAD

>130 Non-compressible vessel (e.g.wall calcification,common in DM)

0.91-1.30 Normal

0.71-0.90

0.50-0.70

Neurogenic

• Neurospinal disease (e.g. spinal

stenosis)

• Complex regional pain syndrome

• Radiculopathies

• Diabetic neuropathy

Mild

Moderate

<0.5 Severe

Treatment

• goals MSK

• Osteoarthritis

• Rheumatoid arthritis/connective

tissue disease

• Remote trauma

• Medial tibial stresssyndrome

• Sprain/straln

• preserve viability (save the leg)

• preserve life (avoid complicated procedures in sick patients)

improve function and alleviate symptoms

• prevent deterioration and recurrence

• conservative

• risk factor modification (smoking cessation,glucose control, treatment of HTN and

hyperlipidemia)

structured exercise program (30-45 min 3x/wk):improves collateral circulation and muscle

oxygenation

• foot care (especially in DM):trim toenails, check between toes for skin breaks, wear socks and

shoes, dear shoes of any debris, keep wounds clean/dry, avoid trauma and pressure on wounds

• pharmacotherapy

for global cardiovascular protection since patients with PAD are at increased risk for CAD and

CVD

• antiplatelet agents (e.g. ASA, clopidogrel)

• anticoagulants (e.g. low-dose rivaroxaban)

statin ± icosapent ethyl

- ACEI/ARB

« SGLT-2 inhibitor if type 2 diabetic

• surgical

indications:severe lifestyle impairment, vocational impairment, CLTI

revascularization

endovascular (angioplasty ± stenting)

endarterectomy:removal of plaque and repair with patch (usually distal aorta or common/

deep femoral)

bypass graft sites:

- anatomic: aortofemora), femoropopliteal, popliteal

-tiblal bypass

- extra-anatomic:axillofemoral, femorofemoral,femorotibial bypass

graft choices:saphenous vein graft (reversed or in situ),synthetic (polytetrafluoroethvlene

graft, e.g. Gore-Tex* or Dacron*),cryo-preserved homograft

not offered to asymptomatic patients

• amputation: if not anatomically suitable for revascularization, persistent serious infections/gangrene,

unremitting rest pain that is poorly controlled with analgesics, medically unfit for revascularization

Treating PAD

Note that symptoms do not necessarily

correlate with ABI measurement.

e.g.a patient with ABI of 0.45 may

be asymptomatic.Intervention is

guided mainly by the patient'

s clinical

presentation

The ABCDEs of PAD Treatment

A ANTI

-PLATELET (ASA, clopidogrel),

anti-coagulant (if indicated), ACEI/

ARB

B BP control; targetsBP <140 mmHg,

p- blocker (if indicated)

C Cholesterol management (statin):

target LDL-C <2 mmol/ L,smoking

cessation

D Diabetic control;target HbA1c <7%.

diet/wclght management

E Exercise (3x/wk.30-45 min per

session)

n

L J

+

Activate Windows

Go to Settings to activate Windows.

VS6 Vascular Surgery Toronto Notes 2023

’Aorta CLTI

’Aortofomoral I

Bypass

Axillary A.

Limb not

salvageable

Limb

salvage

•Femoral A.

Axillofemoral

Bypass

—Aorta

Femoral A.

Femoral A I .

Occlusion Femoropopliteal

Bypass Pationt

moribund

[ Arteriography

or duplex

J

scanning

Pationt

L fi!

Aortic

Occlusion Femoral A.

Occlusion

^

Analgesiaj^

Popliteal A

Amputation )

t

'—Femoral A

^

ngioplosty)#-

^

lr

)

Bypass

ndarterectoniy

I

S

OL

C!Sona Sato altar Kaieandra Havichandiran j

Figure 3. Treatment options for CLTI

Modified(

tom Beufd JO. Chronic lower limb

ischemia.BMJ 2000;320:854-857

Aurtulemofal Bypass Axillofemoral Bypass Femoropopliteal Bypass a

Figure 2. Aortofemoral bypass, axillofemoral bypass, and femoropopliteal bypass

Prognosis

•claudication: conservative therapy: 60-80% improve, 20-30% stay the same, 5-10% deteriorate, 5% will

require intervention within 5 yr, <4% will require amputation

•for patients with CLTI, at 1 yr: 25% risk of mortality (secondary to CVA/M1), 25% risk of major

amputation, 50% alive with two limbs, 33% 5 yr survival rate

Aortic Disease

y

\

2

External elastic membrane

..Smooth muscle

Tunlcamedla R

J ^ .2

Basement membrane CO ’ I

Nerve Endothelium 5

3

Vasavasorurn

I

Tunica adventitia oa

2

5

cr. Internal elastic

membrane

Lamina propria

(smootti muscle and connecbve tissue)

Tunica

intima I

'

e.

T

->

Figure 4. Arterial structure

Aortic Dissection

Definition

• tear in aortic intima allowing blood to dissect into the media

• Stanford classification:Type A (involve the ascending aorta) vs.Type B (distal to left subclavian artery)

• acute <2 wk (initial mortality 1% per h for Type A dissections)

• chronic >2 wk

Etiology

• most common: chronic and/or uncontrolled HTN

• other: connective tissue disease (e.g. Marfan syndrome, Hhlers-Danlos type IV syndrome), cystic

medial necrosis, atherosclerosis, congenital conditions (e.g. coarctation of aorta, bicuspid aortic

valves, patent ductus arteriosus), infection (e.g.syphilis), trauma, arteritis (e.g. Takayasu’s)

Epidemiology

• M:l

;

=3:l

• small increased incidence in African-Canadians (related to higher incidence of HTN); lowest

incidence in Asians

• peak incidence: ages 50-65; ages 20-40 with connective tissue diseases

Figure 5. Stanford classification of

aortic dissection r n \

L J

+

Activate Windows

Go to Settings to activate Windows.

VS7 Vascular Surgery Toronto Notes 2023

Clinical Features

• sudden onset tearing chest or back pain that radiates distally or between the scapulae with:

-

HTN

ischemic syndromes due to occlusion of aortic branches: coronary (Ml), carotids(ischemic stroke,

partial Horner’s syndrome),splanchnic (mesenteric ischemia), renal (AKI), peripheral (ischemic

leg), intercostal vessels (spinal cord ischemia)

“unseating"

of aortic valve cusps(new diastolic murmur in 20-30%) in Type A dissection can lead

to severe aortic insufficiency

rupture into pleura (dyspnea, hemoptysis), retroperitoneum (hypotension,shock),or pericardium

(cardiac tamponade in Type A dissection)

syncope

Investigations

• CTA is the mainstay for both diagnosis and determining the type and extent of dissection:M RA may

also be used if CTA is contraindicated

• EC(j to rule out cardiac causes: LV hypertrophy ± ischemic changes, pericarditis, heart block, MI

• CXR: widened mediastinum, hemothorax if ruptured, apical pleural cap

• TEE:can visualize aortic valve and thoracic aorta but not abdominal aorta; rule out intra-cardiac

thrombus

. consider:lactate (elevated in ischemic gut,shock), amylase (rule out pancreatitis), troponin (rule out

Ml), CBC, electrolytes, creatinine (renal failure), LETs (shock, liver)

Treatment

• Type A dissection needs referral to cardiac surgeon for urgent repair

resection of segment with intimal tear; reconstitution of flow through true lumen; replacement of

the affected aorta with prosthetic graft

postoperative complications:renal failure,intestinal ischemia,stroke, paraplegia, persistent leg

ischemia,death

• 2/3 of patients die of operative or postoperative complications

initial mortality rale without surgery is 1% per h for first 24 h, 30% 1 wk, 80% 2 wk

• Type B dissection is usually managed medically in the absence of spinal/mesentcric/limb

maiperfusion syndrome

<10-20% require urgent operation for complications

acute therapy is typically with intravenous antihypertensivestitrated to sBP of 100-120 mmHg

measured by arterial line and HR of 50-65 bpm in critical care setting

may transition to oral meds after initial control

a and (1-blocker to lower BP and decrease cardiac contractility (e.g. labetalol);

nondihydropyridine CCB (e.g. diltiazem) if clear contraindications to p-blockers, and assecondline therapy; IV nitroglycerin also used assecond-line agent

AC.

'

EI and/or other vasodilators if insufficient BP or HR control

selective intervention (endovascular orsurgical) for complications or refractory symptoms/

progression despite medical therapy

may be a subset of patients who could be well treated with early aortic stent-grafting after initial

medical stabilization

with treatment,60% 5 yr survival, 40% 10 yr survival

long term complications include aneurysmal degeneration of the

• Type B dissection with spinal/mesenteric/renal/limb maiperfusion and/or aortic rupture may be

treated with TEVAR or open surgical repair

True Aneurysm

Saccular

aorta

Fusiform

Aortic Aneurysm

Definition

• localized dilatation of an artery >l.5x normal diameter (3 cm and larger for abdominal aorta)

• true aneurysm:involves all vessel wall layers (intima, media, adventitia)

• false aneurysm (pseudoaneurysm):does not involve all layers; breach in intima/ntedia that allows

blood to collect between media and adventitia

• aneurysms can rupture, thrombose, embolize, erode, and fistulize

Pseudo-Aneurysm

Figure 6. Classification of aneurysms

Classification

• shape

fusiform:concentric; involves full circumference of vessel wall

saccular: eccentric; involves only a portion of vessel wall (theoretical higher risk of rupture due to

unequal distribution of pressure)

%

Ruptured AAA

Classic Triad

• Hypotcnsion/collapse

• Back/abdominal pain

• Palpable, pulsatile abdominal mass

(caution In patients with raised BMI)

• location

TAA: ascending, transverse arch,descending

• thoracoabdominal

AAA:90-98% are infrarenal

suprarenal:starts above the renal arteries but does not involve the thoracic aorta

pararenal:starts at the renal arteries but the superior mesenteric artery origin is not

aneurysmal

Initial Management +

• Intravenous access with two

peripheral large bore IVs

• Permissive hypotension (sBP enough

to maintain mental status)

Activate Windows

Go to Settings to activate Windows,

VS8Vascular Surgery Toronto Notes 2023

juxtarenal:startsimmediately distal to renal arteries (there is no normal aorta immediately

distal to the origin of the renal arteries);renal artery origin is not aneurysmal

infrarenal;starts distal to the renal arteries(there issome normal aorta immediately distal to

the origin of the renal arteries)

Etiology and Risk Factors

•risk factors:smoking (current or prior), advanced age,male sex, White race, l-

'

MHx, presence of other

large vessel aneurysms, HTN

•degenerative

•traumatic

« mycotic (Salmonella,Staphylococcus, usually suprarenal aneurysms)

•connective tissue disorder (Marfan syndrome, Loeys-Dietz syndrome, Ehlers-Danlos type IV

syndrome)

•vasculitis

•infectious (syphilis,fungal)

•ascending thoracic aneurysms are associated with bicuspid aortic valve

•aortic dissection

•congenital (e.g.Turner’s syndrome)

Clinical Features

•75% asymptomatic

•most commonly in the abdominal aorta

•common presentation:due to acute expansion or rupture

syncope

• pain (chest, abdominal, flank, back)

• hypotension

• palpable pulsatile mass above the umbilicus

airway or esophageal obstruction, hoarseness(left recurrent laryngeal nerve paralysis),

hemoptysis,or hematemesis (indicatesthoracic or thoracoabdominal aortic aneurysm)

• distal pulses may be intact

Canadian Society of Vascular Surgery

2018 AAA Screening Guidelines

Recommend:

• One time screening ultrasound for

. Men age 65-80

• Women age 65-80 with smoking

history or cardiovascular disease

• First degree relatives after age 55

• Repeat ultrasound 10 yr after initial

screening if aortic diameter >2.5cm

and <3cm

Investigations

•blood work:CBC, electrolytes, urea, creatinine, PIT, INR, blood type,and crossmatch

•abdominal U/S (approaching 100% sensitivity, up to ± 0.6 cm accuracy in size determination) - useful

for screening and surveillance

•CT with contrast (accurate anatomic visualization,size determination, EVAR planning)

•peripheral arterial DUS (rule out aneurysms elsewhere, e.g. popliteal)

Treatment

•conservative (for asymptomatic aneurysms that do not meet the size threshold for repair;see below)

• cardiovascular risk factor reduction:smoking cessation; control of H'

l

'

N, DM, hyperlipidemia,

regular exercise, watchful waiting, U/S surveillance with frequency depending on size and

location

•surgical

indications

ruptured

symptomatic (tenderness on palpation of the aneurysm)

AAA:size >5.5 cm (men) or >5.0 cm (women )

rapid growth greater than 0.5 cni/6 mo or I cm/yr

risk of rupture depends on:size,family history of rupture,rate of enlargement (>1 cm/yr in

diameter),symptoms,and comorbidities(HTN,COPD, dissection),smoking

• surgical options for AAA

open surgery (laparotomy or retroperitoneal)

- complications

- early:renal failure,spinal cord injury (paraparesis or paraplegia), impotence,

arterial

- thrombosis, anastomotic rupture or bleeding, peripheral emboli, ischemia

- late: graft infection/thrombosis, aortoenteric fistula, anastomotic (pseudo)aneurysm

- death (2-5%)

EVAR

- newer procedure

- advantages: preferred to open surgery in higher risk patients with suitable anatomy;

decreased perioperative morbidity and mortality, procedure time, need for transfusion,

1CU admissions,length of hospitalization, and recovery time

- disadvantages:endoleak rates as high as 20-50%,device failure increasing aslonger

follow-up periods are achieved, re-intervention rates 10-30%, cost

-effectiveness is an

issue, radiation exposure (especially in younger patients due to need for life-long followri

L J

up) +

- complications

- early: immediate conversion to open repair (<1%), groin hematoma, arterial

thrombosis, iliac artery rupture and throinboemboli, renal failure, impotence,

ischemia

Activate Windows

Go to Settings to activate Windows.

VS9 Vascular Surgery Toronto Notes 2023

- late:endoleak,graft kinking,stent fracture, device componentseparation and

migration, thrombosis, rupture of aneurysm, complications of radiation exposure

- death (1-2%, though may be up to 10% in elective advanced endovascular repair

especially with proximal aortic and thoracoabdominal repairs)

Carotid Stenosis

Definition

• narrowing of the internal carotid artery lumen due to atherosclerotic plaque formation, usually near

common carotid bifurcation into internal and external carotids (carotid bulb)

Risk Factors

• HTN,smoking, DM,CVD or CAD, dyslipidemia, older age

Clinical Features

• maybe asymptomatic

• if symptomatic -T1A, ischemic stroke; may be hemispheric presentation (deficits contralateral to

carotid lesion) or ocular presentation (deficits ipsilateral to carotid lesion - amaurosis fugax or retinal

artery ischemia)

• physical exam

fundoscopy: cholesterol emboli in retinal vessels (Hollenhorst plaques)

Investigations

• CBC, PT/INR,PIT (hypercoagulable states)

• ECG, echo (rule out other causes of stroke)

• carotid duplex U/S or DUS:determines severity of disease (mild/moderate/severe stenosis or

occlusion)

• angiography:CTA, MRA

Treatment

• generally the decision to treat with BMT alone vs. BMT + surgical management depends on whether

stenosis is asymptomatic or symptomatic (see Table 3,VS10);size of infarct, patient functional

recovery, life expectancy, and comorbidities are important in decision-making

• symptomatic carotid stenosis is defined asfocal neurologic deficits referable to carotid artery

distribution occurring within the past 6 mo with >50% stenosis;ideally surgical treatment should be

done within the first 48 h to 2 wk of symptom onset

• lifestyle modifications:smoking cessation, weight loss,dietary changes, exercise

1.medical management

• anti-hyperglycemlcs:if concomitant DM

• anti

-hypertensives: target BP <140/90 or <140/85 if concomitant DM

• statins: aggressive management to achieve LDL-C reduction; plaque stabilization effect

• anti-platelet agents (ASA ± clopidogrel): confer-25% relative risk reduction

2.surgical management

• CTA or CAS for symptomatic carotid stenosis

• CHA:generally mainstay of treatment

• CAS: indicated if poor surgical access, radiation-induced stenosis, or comorbidities that increase risk

of surgery/anesthesia

• aggregate risk of death,stroke,or Ml in periprocedural period is notsignificantly different between

CHA or CAS

• higher risk of periprocedural stroke in CAS

higher risk of Ml and temporary cranial nerve palsy in CHA

10 Yi Stroke Prevention after Successful Carotid

Endarterectomy for Asymptomatic Stenosis

(ACST-1): A Multicentre Randomised Trial

Lancet 2010:376:1074-1084

Study: Asymptomatic Carotid Surgery Trial (ACSI), an

RCT with lollow-up at 10 yrr.

Patients: 1110 asymptomatic patients wiUs

significant carotd artery stenovs(126 centres m

30 countries) were randomized equally between

immediate CEA and indefinite deferral of CEA and

weie followed for up until dealt or to a median of 5 yi

among sjrnrors(IRO 6-11 ).

Main Outcome: Perioperative mortality and

morbidity (death or stroke witbin 30 d) a nd nonperioperalive stroke.

Conclusions: In asymptomatic patients under age IS

with significant carotid artery stenosis, successful CEA

reducesthe 10 yr stroke risk,let benefit dependson

risks from uaoperated carotid leskms,future surgical

risks, and whether life expectancy exceeds M yr.

Second Asymptomatic Carotid Surgery Trial

(ACST-2): Atandomized Comparison ol Carotid

Artery Stenting Versus Carotid Endarterectomy

Lancet 2021:3981065-10)3

Patients: 362S asymptomatic patientswithcarotid

artery stenosisfrom 33countries were randomized

equally between CAS and CEA with mean follow-up

ol 4.9 years.

Main Outcome: Procedural mortality and morbidly,

non-procedural stioke subdivided by severity.

Conclusions: Occurrence of setiouscomplications

after CAS and CEA issimilarand uncommon, and both

procedures ban similar long-term effects on fatal

and disabling stroke.

r -i

LJ

+

Activate Windows

Go to Settings to activate Windows.

VS10 Vascular Surgery Toronto Notes 2023

Table 3. Indications for Medical vs. Surgical Management of Carotid Stenosis

Stenosis Asymptomatic Symptomatic

«50% BMT BMT

50-60%

60- 70%

BM1

BM1 BMT

Surgical management if:

• Progression of disease

• Young and otherwise healthy

• Ocular ischemic syndrome

• life expectancy >5yr

• Surgeon's perioperative morbidity/mortality

risk <3%

Surgical management if:

Surgeon'

s perioperative morbidity/mortality

risk «3%

50-70% stenosis:ARR-4.6%. HNT-22

60-99% stenosis:AMM-3%; H NT-33

70-99% BMT BMT

Surgical management if:

Surgeon'

s perioperative morbidity/mortality

risk <3%

Surgical management if:

Surgeon'sperioperative morbidity/mortality

risk <3%

ARR-1-3%; NHT

-33 ARR-16%: NNT--6

100% BMT BMT

No surgical intervention No surgical intervention

ARR -* absolute risk reduction:NNT * number needed to treat

Venous Disease

Venous Thromboembolism

• see Hematology.H36

Chronic Venous Insufficiency

Definition

• wide spectrum of chronic venous disease with advancing symptoms of edema,skin changes,

varicosities, or leg ulcers

Epidemiology

• primary venous insufficiency is the most common venous disorder of the lower extremities

• 65% of North American adult population developssome degree of venous insufficiency

Etiology

• spectrum of chronic venous disease involving deep and superficial lower extremity veins caused by

calf muscle pump dysfunction, venous obstruction, and chronic valvular incompetence (reflux) due to

phlebitis, varicosities,or DVT

• final common pathway is development of venous hypertension, leading to histologic and physiologic

inflammatory changes

• primary (99% of cases) venous insufficiency:venous valve incompetence or obstruction

• suspected risk factors: increasing age,systemic hormonal contraceptive use, prolonged standing,

pregnancy, obesity

• secondary venous insufficiency: DVT,malignant pelvic tumours with venous compression, congenital

anomalies, arteriovenousfistulae, trauma, pregnancy

Clinical Features and Complications

• pain (most common) described as fullness/tightness and aching; worst at end of the day

• telangiectasias or reticular veins: dilated intradermal and subdermal veins,respectively (<3mm in

diameter) (CHAP classification Cl,Table 4)

• varicose veins:visible, long, dilated, and tortuoussuperficial veins (great or small saphenous veins

and tributaries) resulting from incompetent valves in the deep,superficial, or perforator systems(>3

mm in diameter) (CEAP C2)

• ankle and calf edema;relieved by foot elevation (CEAP C3)

• burning, aching,fullness/tightness

• skin changes:

eczema,stasis dermatitis, pruritus, brownish hyperpigmentation (hemosiderin deposits) (CEAP

C4a)

• subcutaneous fibrosis if chronic (lipodermatosclerosis or “inverted champagne bottle legs"),

atrophie blanche (CEAP C4b)

ri

L J

+

Activate Windows

Go to Settings to activate Windows.

VSll Vascular Surgery Toronto Notes 2023

• ulceration:shallow, above medial malleolus (gaiter area), weeping (wet), painless, irregular outline:

healed venous ulcer (CEAPC5)

active venous ulcer (CEAP C6)

• recurrentsuperficial thrombophlebitis and DVT

• bleeding or hematoma of varicosities secondary to trauma

Table 4. CEAP Classification of Venous Disease

Clinical Etiological Anatomical Pathophysiological

CO Congenital

Primary

As Superficial veins Pr Reflux

Ap Perforating veins Po Obstruction

No dinicalsigns of disease £c

Telangiectasia or reticular Ep

veins

Varicoseveins

Edema

Cl

C2 Es Secondary

No etiology

Identified

Pr.o Reflux * obstruction

An No venouslocation Pn No pathophysiology identified

identified

Ad Deep veins

C3 En

Cd: Skin changes:

Enema, pigmentation

lipodermatosderosisor

atrophic blanche

Healed venous ulcers

Active venous ulcers

Symptomatic

Asymptomatic

C 4a

C4b

CS

C6

S

A

Investigations

• AB1 ( pre-compression to ensure no arterial disease)

. venous Doppler U/S or DUS

Treatment

• conservative

elastic compression stockings, ambulation, periodic rest-elevation, avoid prolonged standing

• ulcers:wound care using multilayer compression bandage ± antibiotics ± debridement PRN

medical treatments are variable, e.g. pentoxifylline for venous ulcer healing, (lavonoids (e.g.

diosmin) for pain, etc.

• surgical

surgical destruction of vein with partial or complete removal; techniques include vein ligation/

stripping, phlebectomy, perforator ligation

• indications forsurgery:

• documented rellux at the saphenofemoral or saphenopopliteal junction by DUS or Doppler U/S

• failed trial of conservative treatment for >3 mo

signs of CVI (eczema, pigmentation, lipodermatosclerosis, ulceration) or complications associated

with varicosities (ulceration due to venousstasis, hemorrhage from superficial varicosity,

recurrent superficial thrombophlebitis,stasis dermatitis, varicose eczema, lipodermatosclerosis,

unremitting edema/pain affecting quality of life and requiring chronic analgesia)

• 10 yr postoperative recurrence of 20%

• endovenous:laser therapy, radiofrequency ablation, foam/liquid/glue sclerotherapy

Lymphedema

Definition

• impaired lymphatic drainage resulting in accumulation of interstitial fluid and fibroadipose tissue

Etiology

• primary

congenital lymphedema (e.g.Milroy disease, Turnersyndrome): presents age <2

lymphedema praecox (75% of primary cases):presents in adolescence at onset of puberty

lymphedema tarda: presents age >35

• secondary

infection:filariasis (roundworm parasitic infection;leading cause worldwide), cellulitis,

lymphadenitis, tuberculosis

inflammation:rheumatoid arthritis, dermatitis, psoriasis,sarcoidosis

malignant infiltration/obstruction:axillary,groin or intrapelvic,pressure from large tumours

iatrogenic:radiation/surgery (axillary,groin lymphadenectomy) (leading cause in North

America),vein surgery'

,lymph node dissection,scarring

patients who develop lymphedema after axillary lymph node dissection are at increased risk

for developing angiosarcoma

• traumatic injury and burns

venous disease:CVI

n

L J

+

Activate Windows

Go to Settings to activate Windows.

VS12 Vascular Surgery Toronto Notes 2023

Clinical Features

• classically non-pitting edema and hyperkeratotic cutaneous/subcutaneous changes with progressive- disease

• impaired limb mobility, discomfort/pain, psychological distress

• positive Stemmer sign (sensitive): examiner unable to lift skin of thickened skin fold at the base of

second toe or finger

• lipodermatosclerosis

• ulcerations

nvestigations

lymphoscintigraphy: most definitive test

secondary causes of lymphedema must be evaluated and treated appropriately if found

Treatment

conservative measures: avoid limb injury, treat skin infections early,skin hygiene, limb elevation,

avoid prolonged sitting/standing/crossing legs

external support: intensive (compression bandages) vs. maintenance (compression garments)

exercise: gentle daily exercise of affected limb, gradually increasing range of motion (must wear

compression garment while exercising)

massage: manual lymph drainage therapysurgical: physiological (early disease:increase lymphatic drainage) lymphovenous bypass vs.reductive

(advanced disease: remove fibroadipose deposits)

Landmark Vascular Surgery Trials

Trial Name Reference Clinical Trial Details

ARTERIAL DISEASE

BASIL J Vase Surg 2010;S1|S

Suppl):SS-17S

Title:Bypass vs. Angioplasty in Severe Ischemia ol the leg (BASIL) trial:An Intention-to-Treat Analysis ol Amputation Free and Overall Survrval

In Patients Randomized to a Bypass Surgery|BSX|- First or a Balloon Angioplasty (BAP} First Rcvasculariialion Strategy

Purpose: Determine Ihe optimal lust tine rcvasculariialion surgery between bypasssurgeiy and balloon angioplasty in severe leg ischemia.

Methods: 4S2 enrolled patients in 27 United Kingdom hospitals, hall were randomised lo BSX-lirst and hall to BAP-first.All palienls were

monitored lor 3yr and mote than half were monitored for »

5 yr.

Results: AFS (Amputation Free Survival) and OS (Overall Survival) did not differ between treatments during follow up. BSX-first patients who

survived 2 yr post randomiiation had a reduced hazard ratio for subseguenl AFS ol 0.85% (Cl.0.5 to1.07; P'0.108) and for subseguent OS of 0.61%

(95% Cl.0.50 lo 0.75:P'0.009) in an adjusted time dependent Con proportional hazards model.

Conclusions: No significant difference in amputation-free survival and overallsurvival between severe limb ischemia patients treated with

bypass surgery and those treated with balloon angioplasty.

Title:Rivaroiaban in Peripheral Artery Disease after Revascularization

Purpose:To investigate the efficacy and safety of rivaroxaban for patients with PAD who have undergone lower extremity revascularization.

Methods:Patients with PAD whD had undergone revascularization were randomized lo receive rivaroxaban plus Aspirin!

or placebo plus

Aspirin -.Ihe primary efficacy outcome was a combination of acute limb ischemia,major amputation, myocardial infarction, ischemic stroke,or

death.The primary safety outcome was major bleeding.

Results: The 3-yv incidence of Ihe primary efficacy outcome was17.3% and19.9% (hazard ratio.0.85. 95% Cl. 0.76 lo 0.96: P"

0.009)in the

rivaroxaban and the placebo group,respectively. Ihe primary safety outcome occurred in 2.65% and 1.87% (hazard ratio.1.43:95% Cl. 0.97 to

2.10:P'

0.07) ol Ihe rivaroiaban and the placebo group, respectively.

Conclusions:In patients with PAD. there wassignificantly lower mortality and morbidity in patients treated with ASA and rivaroxaban than those

treated with ASA alone.

VOYAGER NEJM 2020:382:1994-

2004

AORTIC DISEASE

NEJM 2010:362:1863 Title: Endovascular vs. Open Repair of Abdominal Aortic Aneurysm

Purpose: To evaluate the long-term outcome ol EVAR compared with open repair of taigc aneurysms.

Methods: Between 1999 to 2004,1252 patients with large AAA (:5.5 cm in diameter) were randomized to undergo either EVAR or open repair.

Patients were followed for rates of death, graft-related complications,reintervenlions. and resource use until end of 2009.

Results:Ihe 30- day operative mortality was1.8% in the EVAR group and 4.3% in Ihe open- repair group (odds ratio, 0.39;95% Cl.0.18 to 0.87:

P'

0.02). but by Ihe end ol the study there was no significant difference in the rate of death from any cause (hazard ratio.1.03:95% Cl.0.86 to

1.23: P'0.72).The rates of graft-related complications and reintervenlionswere 3-4 limes higher in the EVAR group.

Conclusions:In patients with large AAAs. there was nosignificant difference in mortality in patients treated with open surgical repair and those

treated with EVAR.Patients treated with EVAR had lower operative mortality but a higher incidence of graft-related complications,graft-related

reintervenlions, and healthcare costs.

Title:Comparative Clinical Effectiveness and Cost Effectiveness of Endovascular Strategy vs.Open Repair for Ruptured Abdominal Aortic

Aneurysm:3-yr Results of the IMPROVE Randomised Trial

Purpose: To compare the clinical outcomes and cost effectiveness of endovascular repair vs. open repair for patients with suspected ruptured

AAA.

Methods: 502 palienls who underwent emergency repair lor rupture were randomized to endovascular strategy or open repair.

Results:Similar mortality between strategies by 90 days.There was lower mortality (48% vs. 56%). improved OALYs of 0.17 (95% confidence

interval 0.00 lo 0.33). and lower average costs of C2605 (95% confidence interval-(5966 lo (702) in the endovascular strategy than the open

repair group at 3 yr.

Conclusions: At 3 yr.endovascular strategy for suspected AAA was associated with belter outcomes and was more cost-effective than open

repair.

EVAR1

1871

IMPROVE BMJ 2017;359:j4859

+

Activate Windows

Go to Settings to activate Windows.

VS13 Vascular Surgery Toronto Notes 2023

Trial Name Reference Clinical Trial Details

CAROTID DISEASE

lancet 2004:364:331-337 Title:Aspirin

*

andClopidogrel Compared with Clopidogrel Alone after Recent Ischaemic Stroke or Transient Ischaemic Attack inHigh-Risk

Patients (MATCH):Randomised.Doable-Blind.Placebo-Controlled Trial

Purpose: Tocompate the benefits of adding ASA to clopidogrel vs.clopidogrel alone inprevention of vascular events with higher bleeding risk.

Methods: 7599 patients with recent ischaemic stroke or TIA with vascular risk factors) that were already receiving clopidogrel were randomized

to either ASA or placebo.The primary endpoint was the first occurrence of an event in the amalgamation of ischaemic stroke andrelatedvascular

complications.

Results:15.7% of patients in the ASA and clopidogrel group aeguired primary endpoint,comparedwith16.7% in the clopidogrel alone group

(relative risk reduction 6.4%.(95% Cl -4.6 to 16.3):absolute risk reduction1% (-0.6 to 2.7)).Major and life-threatening bleedings were higher in

the ASA and clopidogrel group compared to clopidogrel alone group but there wasno difference inmortality.

Conclusions:The addition ol ASA to clopidogrelmonotherapy in patients withprior ischemic stroke or TIA did notprevent recurrence ofischemic

stroke.TIA.or related complications.Dual therapy was associatedwith a greater risk of major hemorrhage.

Title:Stenting vs.Endarterectomy for Treatment of Carotid-Artery Stenosis

Purpose:To compare outcomes of CAS vs. CEA lor patients with symptomatic or asymptomatic entracranial carotid artery stenosis.

Methods:Patients with symptomatic or asymptomatic carotid stenosis were randomly assigned to CAS or CEA.The primary endpoint was a

composite of stroke,myocardial infarction,or death from any cause during theperioperative period or any ipsilateral stroke in the followtrg 4 yr.

Results:The estimated 4-yr rates of the primary endpoint between the stenting group and the endarterectomy group were 7.2% and 6.8%.

respectively (hazard ratio with stenting.1.11:95% confidence interval.0.81to 1.51:P‘0.51),with no differential treatment effectbased on

symptomatic status|P*0.84).

Conclusions:In patients with asymptomatic or symptomatic carotid artery stenosis,there were no significant drfferences in the combined risk

of stroke.Ml.or death between those who underwentCEA compared to those who underwent CAS.CEA was associated with a greater risk of ML

while CAS was associated with a greater risk of strokeinthepostprocedural period.

MATCH

CREST NEJM 2010;363:11-23

VENOUS DISEASE

ESCHAR1 BrJSurg 2005:92:291- Title:Randomized Clinical Trial of CompressionPlus Surgery vs.Compression Alone in Chronic Venous Ulceratron (ESCHAR Study)-Haemodynamic

and Anatomical Changes

Purpose:Toevaluate the effects of superficial venoussurgery and compression on legs with chronic venous ulceration.

Methods: Patients with open or recentlyhealed leg venous ulceration and saphenous reflux were randomized to either compression bandagng

or superficial venous surgery plus compression.Venous refill times (VRTs) were catenated via photoplethysmography before treatment and atl

yr later.

Results:Out of 214 legs.112 underwent compression bandaging and102underwent compression plus surgery.Saphenous surgery eliminated

deep reflux in10/ 22 legs with segmental deep reflux and 3/17 with total deep reflux.Median VRT increased from10 to15 seconds1yr later

(P<0.001).

Conclusions:Superficial venous surgery was effective in improving venous hemodynamics in patients with active or healed venous ulceration.

Title:long Term Results of Compression TherapyAlone vs.Compression Plus Surgery in Chronic VenousUlceration(ESCHAR):Randomised

Controlled Trial

Purpose:Toevaluate whether superficial venous surgery in addition to compression bandaging prevents recurrent legulcers.

Methods: Patients with open or recentlyhealed leg ulcers and superficial venous reflux underwent either compression plus saphenous surgery or

compression alone.Primary outcomes were ulcer healing and ulcer recurrence.

Results:At three yr. ulcer healing rates were 93% for the compression plus surgery group and 89% for the compression alone group (P^0-73).At

four yr.the rales of ulcer recurrence were 31% for the compression plus surgery group and 56% for the compression alone group (P<0.01|.

Conclusions:Superficial venous surgery and compressionbandaging was effective inreducing the recurrence of venous ulcers compared to

compression bandaging alone.Superficial venous surgery and compression bandaging did not reduce thehealing time of venous ulcers compared

to compression bandaging alone.

2 %'

ESCHAR2 BMJ 2007:335:83

References

Arterial Disease

Aboyans V. Ricco J-B. Barlelink M- LEL. et al.2017 ESC guidelines on the diagnosis and treatment of peripheral arterial diseases,in collaboration with theEuropean Society for Vascular Surgery (ESVS).Eur Heart J

2018;39:763-816.

Ackermann M.Verleden SE,Kuehnel M.et al.Pulmonary vascular endolhelialitis.thrombosis,and angiogenesis inCOVID-19.NEJM 2020:383|2):120.

Bilaloglu S.Aphinyanaphongs V.JonesS.et al.Thrombosis in hospitalized patients with COVID-19 in a new york city health system.JAMA 2020:324|8):799.

BjorckM,Earnshaw JJ.Acosta S. etal.Editor's choice -European Society for Vascular Surgery (ESVS) 2020 clinical practice guidelines on the management of acute limb ischaemia.Eur JVaseEndovascSurg

2020;59:173-218.

Bonaca MP. Bauersachs RM.Anand SS,etal.Rivaroxaban in peripheral artery disease after revascularization.NEJM 2020;382:1994-2004.

Bovrlesl,Platton S.Yartey H. et al.Lupus anticoagulant and abnormal coagulation tests inpatients with COVID-19.NEJM 2020;3S3(3):288.

Conte MS.Bradbury AW.Kohl P. et al.Global vascular guidelines on the management of chronic limb-threatening ischemia.J VascSurg 2019;69:3S-125S.

Dormandy JA,Rutherford RB.Management of peripheral arterial disease (PAD).TASC Working Group.TransAtlantic Inter-Society Consensus (TASC).JVaseSurg 2000:31(1Pt 2)41-S296.

Eikelboom JW.Bosch CJ,Dagenais GR.etal.Rivaroxaban with or without aspirin in stable cardiovascular disease.NEJM 2017;377:1319-1330.

Gerhard-Herman MD.Gornik HI.Barrett C,etal. 2016 AHA,

'ACC guideline on the managementof patients withlower extremity peripheral artery disease:A report of theAmerican College of Cardiology American

Heart Association Task force on ClinicalPractice Guidelines.Circulation 2017;135:e686- ?25.

Grip 0,WanhainenA, Bjorck M.Acute aortic occlusion:Nationwide cohort study.Circulation 2019:139(2)392-294.

Leriche R.Morel A.The syndrome of thromboticobliteration of the aortic bifurcation.Ann Surg 1948;127(2):191

Ochoa VM.Yeghiazarians Y.Subclavian artery stenosis:a review for the vascular medicine practitioner.Vase Med 2010;16|1):29-34.

Norgren L.Hiatt WR.Dormandy JA.et al.Inter-Society consensusfor the management of peripheralarterial disease (TASC II).JVascSurg 2007;45|SupplS):SS-S67.

Rutherford RB.Baker JD,Ernst C,et al.Recommendedstandards for reports dealing with lower extremity ischemia revised version.J VaseSurg 1997:26:517-538.

Westin GG,Armstrong EJ,Bang H.et al.Associationbetween statin medications and mortality,major adverse cardiovascular event,and amputation-free survivalm patients withcritical limb ischemia.J Am Coil

Cardiol 2014;63|7):682-690.

Abramson Bl,Al Orman M.Anand SS.et al.Canadian Cardiovascular Society 2022 Guidelines for Peripheral Arterial Disease.CanJCardiol 2022;38|5):560 587.

Aortic Disease

Boodhwani M.Andelfinger G.Leipsic J.elal.Canadian Cardiovascular Society position statement on the managementof thoracic aortic disease.CanJ Cardiol 2014;30:577-589.

Canadian Task Force on Preventive Health Care.Recommendations on screening for abdominal aortic aneurysminprimary care.CMAJ 2017:189:61137-1145.

Chaikof El. Dalman RL,Eskandari MK,el al.The Society for Vascular Surgery practice guidelines on the care of patients withan abdominal aortic aneurysm.J Vase Surg 20T8:67(1):2- 77.e2.

Creager MA, Kaufman JA. Conte MS.Acutelimb ischemia.NEJM 2012:366:2198-2206.

Erbel R,Aboyans V,BoileauC,etal.2014 ESC Guidelines on the diagnosis and treatment of aortic diseases:Document covering acute and chronic aortic diseases of the thoracic and abdominalaorta of theadulL

The Task force for the Diagnosis and Treatment of Aortic Diseases of the European Society of Cardiology (ESC).Eur Heart J 2014;35|41|:2873-2926.

Farber A.Chronic limb-threatening ischemia.NEJM 2018:379171-180.

Hiratzka IF. Bakris Gl. Beckman JA. et al. 2010 ACCF/AHA/AATSi’ACRfASA.'SCAr'SCAI/SIR.

'

SIS.'SVM guidelines for the diagnosis andmanagement of patients with thoracic aortic disease.J Am CollCardiol

2010;55:e27-129.

IMPROVE Trial Investigators.Comparative clinical effectiveness and cost effectiveness of endovascular strategy v open repair for rupturedabdominal aortic aneurysm:3yr results of the IMPROVE randomizedtrie.

BMJ 2017;359:j4859.

+

Activate Windows

Go to Settings to 3Ctivste Window

VS14 Vascular Surgery Toronto Xotes 2023

Kapila V.Jetty P.Wooster D.et aL 2018 Screening for abdominal aneurysms inCanada:Revised position statement from the Canadian Society of Vascular Surgery.CanadianSociety for Vascular Surgery 2018:1-9.

Lai BK.Zhou W.Li Z,et at.Predictors and outcomesof endoleaks inthe Veterans Affairs Open vs.Endovascular Repair (OVER) trialof abdominal aortic aneurysms.J Vase Surg 2015:62:1394-1404.

Yang B,Norton E.Hobbs R.etal.Short- and long-term outcomes of aortic root repair and replacement inpatients undergoing acute type A aortic dissection repair:20-year experience.J Ihorac Cardiovasc Surg

2019:157(6):2125-36.

Carotid Stenosis

Barnett HJM.Taylor OW.Haynes RB.etal.Beneftcial effect of carotid endarterectomy in symptomatic patients with high-grade carotidstenosis.NEJM 1991:325:445- 453.

Brott TG.Howard G.Roubin GS.etal.Long-term results of stentingvs.endarterectomy for carotid-artery stenosis.NEJM 2016:374:1021-1031.

Brott IG.HalperinJL.AbbaraS.etal.2011ASAfACCF.'

AHAi'AANNi'AANS/ACR/ASNRi

'CNS'

SAIP/SCAIlSIRi'SNIS/SVIil

'

SVS guideline on the management of patients with extracranial carotid andvertebral artery disease.J

Am Coll Cardiol 2011:57:e16-e94.

Halliday A.Harrison M.Hayter E,et al.10-year stroke prevention after successful carotid endarterectomy for asymptomatic stenosis|ACST-1):a multicentre randomised trial.Lancet 2010:376:1074-1084.

MRC European Carotid Surgery trial:interim results for symptomatic patients withsevere (70-99%) or with mild (0-29%) carotid stenosis.European Carotid Surgery Trialists'Collaborative Group.Lancet

1991:337:1235-1243.

Naylor AR.RiccoJ-B.de Borst GJ.etal.Editor's choice - Management of atherosclerotic carotid and vertebral artery disease:2017 clinical practice guidelines of the EuropeanSociety for VascularSurgery (ESVS).

Eur JVaseEndovasc Surg 2018;55|1):3-81.

Ricotla JJ.AbuRahma A.Ascher E.et al.Updated Society for Vascular Surgery guidelines for management of extracranial carotid disease.J Vase Surg 2011:54:e1-e31.

AbuRahma AF.Avgerinos ED.Chang RW.etal.Society for Vascular Surgery clinical practice guidelines for management of extracranial cerebrovasculardisease.J Vase Surg 2022c75-4S-22S.

Sardar P.ChatterjeeS.Aronow H.et al.Carotid artery stenting vs.endarterectomy for stroke prevention. J Am Coll Cardiol 2018:69:2266-2275.

Peripheral Venous Disease

Butros SR.Liu R.Oliveira GR. et al.Venous compression syndromes:clinical features,imaging findings andmanagement.Br J Radiol 2013:86|1030):20130284.

EberhardtRT.RaffettoJD.Chronic venous insufficiency.Circulation 2014:130:333-346.

Scallon C.Bell-Syer SE,AzizZ.Flavonoids for treating venous leg ulcers.Cochrane Database Syst Rev 2013;(5):CDO06477.

Widens C.Davies AH.Bskgaard N. et al.Management of chronic venous disease:Clinical practice guidelines of the European Society for Vascular Surgery|ESVS).Eur J VaseEndovasc Surg 2015:49:678-737.

Lymphedema

Hassanein AH.Madellan RA.Grant ED,etal.Diagnostic accuracy of lymphoscintigraphy for lymphedema and analysisof false-negative tests. Plast Reconstr Surg GlobOpen 2017:5(7):e1396.

Greene AK.Obesity-induced lymphedema.In:Lymphedema Presentation,Diagnosis,and Treatment. Greene AK.Slavin SA.Brorson H (Eds).Switzerland:Springer.2015.

InternationalSociety of Lymphology.The diagnosis and treatment of peripheral lymphedema:2016 consensus document of the International Society of Lymphology.Lymphology 2016:49:170-184.

Kerchner K.Fleischer A.Yosipovitch G.Lower extremity lymphedema update:pathophysiology,diagnosis,and treatment guidelines.J Am Acad Dermatol 2008:59:324-331.

Lawenda BD.Mondry IE,Johnstone PA.Lymphedema:a primer on theidenlifrcation and management of a chronic condition in oncologic treatment. CA Cancer J Clin 2009:59:8-24.

Szuba A,Rockson SG.Lymphedema:classification,diagnosis andtherapy.Vase Med 1998:3(2):145-15G.

Vascular Surgery Textbook

Cronenwett JL, Johnston W (editors).Rutherford's vascular surgery, 7th ed. Philadelphia:Saunders/Elsevier. 2014.