The Osler Institute Excellence in Continuing Medical Education

“The Best of Series” Vascular Surgery Syllabus DISC 3

DISC 1 Renovascular Disorders I

Ahmed Mahmoud

Visceral Artery Aneurysms

Paul Lajos

Renovascular Disorders II

Ahmed Mahmoud

Lower Extremity Aneurysms

Paul Lajos

Vascular Graft Infections

Ahmed Mahmoud

Thoracic Outlet Syndrome

Ahmed Mahmoud

Lower Extremity Arterial Occlusions

Paul Lajos

Carotid Artery Occlusions

Marvin Atkins

Aortoiliac Occlusive Disease

Chad Jacobs

Venous Disease

Marvin Atkins

Endovascular Therapies

Marvin Atkins

Upper Extremity Arterial Occlusions

Chad Jacobs

Chronic Limb Ischemia

Chad Jacobs

Non-Atherosclerotic Vascular Disease I and II

Chad Jacobs

DISC 2 Thoracic Aorta Aneurysms

Amy Coulter

Aortoiliac Aneurysms

Amy Coulter

Visceral ischemic Syndromes

Amy Coulter

Acute limb Ischemia

Amy Coulter

Popliteal entrapment

Natalie Weger

Vascular Labs

Natalie Weger

Lymphedema

Natalie Weger

Vascular Trauma

Paul Lajos

Questions or comments on this or any other Osler products please contact us at (800)356-7537 or [email protected]

The Osler Institute Excellence in Continuing Medical Education

“The Best of Series” Vascular Surgery Syllabus

Marvin D. Atkins, Jr. , MD Texas A & M Health Science Center Assistant Professor of Surgery Amy H. Coulter , MD Louisiana State University Assistant Professor of Surgery Chad Elliot Jacobs , MD Rush Medical College of Rush University Assistant Professor of Surgery Paul Lajos , MD Icahn School of Med at Mount Sinai, NY, NY

Assistant Professor of Surgery

Ahmed Mahmoud , MD University of California, Davis Clinical Associate Professor of Surgery Natalie S. Weger , DO Surgeon

Medical Centers of Central GA and Coliseum Med Ctr Practicing Vascular

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Renovascular Disorders

Ahmed Mahmoud, MD University of California, Davis

Presentation Outline Introduction & classification Pathophysiology and natural history Renovascular hypertension Ischemic nephropathy

Clinical evaluation Indications for intervention Treatment - surgical vs. endovascular Miscellaneous

Classification of Hypertension Primary (essential, “benign”, idiopathic): > 90% of all cases of hypertension

Secondary (e.g. we know what’s causing it): < 10% of all cases of hypertension Conn’s syndrome (hyperaldosteronism) Renal artery stenosis Pheochromocytoma Coarctation of aorta Primary Renal Disease Endocrine (i.e., Cushing’s syndrome)

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Kidney 0.5% of the total body weight Receives about 25% of the C.O. Converts >1700 L blood per day into about 1 L of urine Excretes the waste products Regulates body’s concentration of water and salt Maintains the acid balance. Serves as an endocrine organ Erythropoietin Renin Prostaglandins

Epidemiology Hypertension affect 60 million Americans 1-5% patients has secondary hypertension Renal vascular hypertension accounts for the majority of parents with secondary hypertension Not all renal artery stenosis is associated with RVH

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Presentation Outline Introduction & classification Pathophysiology and natural history Renovascular hypertension Ischemic nephropathy

Clinical evaluation Indications for intervention Treatment - surgical vs. endovascular Miscellaneous

Renovascular Hypertension ‘Renovascular hypertension’ refers to de-novo development or acceleration of hypertension produced by high-grade vascular renal artery stenosis. Activation of the renin-angiotensin system occurs when renal artery perfusion falls. Mechanisms differ between one- and two-kidney forms of renovascular hypertension, depending upon the ability of the contralateral kidney to excrete sodium.

Pathophysiology of Renovascular Hypertension RENAL ARTERY STENOSIS DECREASED RENAL PERFUSION

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Renovascular Hypertension Systemic hypertension affects 20% of the adult population. Renal artery occlusive disease is present in 5% of the hypertensive population. Most common cause of correctable hypertension Renovascular disease may be an important cause of renal insufficiency in up to 15% of patients with dialysis-dependent ESRD.

Normal Physiology Decreased renal blood flow: renin release Renin catalyzes production of Angiotensin I Angiotensin I is converted to Angiotensin II, a potent vasoconstrictor Angiotensin II stimulates release of Aldosterone: sodium and water

Unilateral Renal Artery Stenosis ↓ blood flow to involved kidney stimulates release of Renin Renin increases Angiotensin II and Aldosterone, resulting in vasoconstriction and sodium and water retention Normal kidney responds to increased blood pressure with natriuresis Compensatory natriuresis limits negative feedback on Renin, perpetuating renin-induced vasoconstriction hypertension

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Bilateral Renal Artery Stenosis Decreased renal blood flow: Renin is released Elevated Aldosterone causes sodium retention and volume expansion The opposite kidney cannot compensate Volume expansion inhibits Renin release, decreasing Angiotensin II and vasoconstriction Hypertension is primarily due to volume

Ischemic Nephropathy Requires high-grade stenoses of both main renal arteries Recovery of function is unlikely with longstanding renal failure May be possible with recent, rapid deterioration of excretory function

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A 56 year old male who has chronic hypertension and bilateral renal artery stenosis with renal insufficiency suddenly developed an acute onset pulmonary edema. His fluid overload is due to: a. Volume-dependent aldosterone effect b. Acute myocardial infarction c. Non compliant left ventricle d. renin-dependent hypertensive effect

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Etiology of Renovascular Disease Atherosclerosis >70% Fibromuscular Disease Renal Artery Aneurysm Takayasu’s Disease Atheroemboli / Thromboemboli Renal Artery Dissection AVM’s Trauma Neurofibromatosis Retroperitoneal Fibrosis

A 56 year old male who has chronic hypertension and bilateral renal artery stenosis with renal insufficiency suddenly developed an acute onset pulmonary edema. His fluid overload is due to: a. Volume-dependent aldosterone effect b. Acute myocardial infarction c. Non compliant left ventricle d. renin-dependent hypertensive effect

Renal Artery Stenosis

Renal Artery Stenosis (RAS)

Atherosclerosis 70-85% of all renovascular lesions Usually systemic disease (80%): Aorta, coronary, carotid, or PAD Ostium or proximal 1-2 cm of renal artery (20%) High mortality rate: 29.7% at 3 yrs. 38% at 2 yrs. due to fatal cardiac events

Prevalence of RAS with associated diseases Peripheral Arterial Disease 22-59% Coronary Disease “Clues” RAS Bilateral Disease

Renal Artery Stenosis Drive by aortograms “Screening” Abdominal Aortograms in 3987 patients undergoing cardiac catheterization > 50% RAS 9.1% (362) > 75% RAS 4.8% (191)

Atherosclerosis

20% bilateral

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30% 70% 44%

Renal Artery Stenosis (RAS) Fibromuscular Dysplasia

Atherosclerosis Affect up to 0.5% of the general population Prevalence in the population with elevated blood pressure is low (~2% to 5%). More common in women (25-50 yrs. old) Involves distal 2/3 of artery. 80% is Medial Fibroplasia

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Renal Artery Stenosis

Renal Artery Stenosis

Fibromuscular Dysplasia Classification

Frequency

Clinical Findings

Angiographic Appearance

Intimal Fibroplasia

5%

Children & young adults both sexes equally

Concentric focal band Long smooth narrowing

Medial Hyperplasia

< 1%

Women 30-50 y/o

Concentric smooth stenoses Midportion of main RA

Medial Fibroplasia

85%

White women 30-40 y/o 55% bilateral 80% right 25% branch vessels

“string of beads”

Paramedial Dysplasia

10%

Younger women

“Beading” “beads” are smaller than artery diameter

Medial Fibrodysplasia 85% of renal artery dysplasia Mostly women, 4th decade Series of stenoses with intervening aneurysms Involves distal main artery; first order branches in 25% Bilateral 55%, right 75%, left 10%

Renal Artery Stenosis

Renal Artery Stenosis

Intimal Fibrodysplasia

Paramedial Fibrodysplasia

5% of renal artery dysplasia Male = Female Infants, children, and young adults Smooth focal stenosis of main renal artery

Renal Artery Stenosis Prognosis of RAS A major consideration in both the dx and Rx of RAS is the potential for progressive RA occlusion Rates of progression are highly variable Advanced stenosis results in renal atrophy, arterial occlusion, fibrosis, and irreversible parenchymal injury

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10% of renal artery dysplasia Exclusively in women 4th or 5th decade

Focal or multiple stenoses of main renal artery without intervening aneurysms

Renal Artery Stenosis Progression of RAS Serial DUS (q 6 month) demonstrate the potential for RA atherosclerosis to develop to more severe vascular occlusion Progression defined as rise in Doppler velocity by 100cm/s Those most likely to progress had the most severe ( >60%) stenosis from the outset Factors predictive of disease progression included sBP levels, ABI and DM

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Renal Artery Stenosis Progression of RAS

Renal Artery Stenosis Progression of RAS

Progression from normal to > 75% stenosis associated with increase in creatinine Lesion progression more likely with more severe stenosis Crowley JJ. Am J Heart, 1998

Renal Artery Stenosis Multivariate analysis of risk factors associated with progression of RAS

VARIABLE

OR (95% CI)

P value

Female sex

1.9 (1.5-2.2)

.002

Increased age

1.6 (1.4-1.8)

.0001

CAD

1.3 (1.2-1.4)

.004

Time between angiograms

1.3 yrs. (1.2-1.4 yrs.)

.0001 Crowley JJ. Am J Heart, 1998

Renal Artery Stenosis 4 year survival for incidental asymptomatic RAS at C. Cath

Severity of incidental RAS

Four year survival

No RAS

90%

50-75%

70%

75-95%

68%

>95%

48%

Renal Artery Stenosis Clinical endpoints of RAS 41 Patients with RAS & renovascular HTN Mean F/U 28 months 46% with ↑Cr from 25 to 120 % GFR decreased in 29% 37% with decrease in kidney length > 10%

Renal Artery Stenosis ESRD resulting from RAS

683 patients followed 12% progression to ESRD Renal Survival @ 2 years - 97.3% with unilateral RAS - 82% with bilateral RAS - 45% with RAS in solitary kidney Mailloux, AM J Kid Dis 1994

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Renal Artery Stenosis Survival on Dialysis 65 y/o avg. survival is 2.7 yrs. Patients with RAS have decreased survival 2 year survival 56% 5 year survival 18% 10 year survival 5% PCKD avg. is 133mo Mailloux, AM J Kid Dis 1994

EVALUATION OF RENOVASCULAR HYPERTENSION A high index of suspicion along with a careful history and clinical examination will continue to provide the initial guidepost in determining whether additional anatomic or functional studies are warranted.

CLINICAL MANIFESTATIONS OF RENAL ARTERY STENOSIS Asymptomatic ‘incidental RAS’ Renovascular hypertension Ischemic nephropathy Accelerated CV disease: CHF Stroke Secondary aldosteronism

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EVALUATION OF RENOVASCULAR HYPERTENSION The primary motivation for screening symptomatic patients for renovascular occlusive disease and for pursuing catheteror surgical-based interventions is the benefit derived from possible improved control of hypertension and preservation of renal function

Presentation Outline Introduction & classification Pathophysiology and natural history Renovascular hypertension Ischemic nephropathy

Clinical evaluation Indications for intervention Treatment - surgical vs. endovascular Miscellaneous

IDENTIFYING SUSCEPTIBLE PATIENT POPULATIONS Hypertension onset age 1.5cm) Unexplained renal dysfunction Deterioration of renal function precipitated by ACE inhibitor Unexplained CHF Pulmonary vascular congestion: ‘flash pulmonary edema’ Atherosclerosis in other arterial beds i.e. coronary, carotid, and extremities (~20%)

Renal Duplex Scanning

EVALUATION OF RENOVASCULAR HYPERTENSION Anatomy

Functional

Presence of a renal artery stenosis Duplex scanning Spiral CT / MRA Arteriography

Renin-angiotensin system Renal vein renin levels Captopril scintigraphy

Bilateral renal artery disease limits the usefulness of all functional studies of renovascular hypertension

DUPLEX ULTRASONOGRAPHY Combines B-mode imaging (luminal anatomy) with Doppler measurement (hemodynamic assessment) 2 to 3 MHz probe Identify landmarks Left renal vein Celiac axis Superior mesenteric artery

Left renal artery and spectral waveform

Flank approach to main renal artery origins

Components of a Renal Duplex Scan

Angle of insonation is uncertain index renal artery velocities to aortic velocity

DUPLEX ULTRASONOGRAPHY Advantages

Scan abdominal aorta (inflow velocity) Locate origins of main renal arteries Scan proximal, middle, distal segments Locate sites of stenosis (peak velocity) Search for accessory/polar arteries Measure renal length Parenchymal signals (resistance) Renal veins

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Noninvasive and inexpensive No need to alter antihypertensive medications No risk to residual excretory renal function Overall accuracy is not affected adversely by concomitant aortoiliac disease

Disadvantages Inability to interrogate entire length of renal artery Multiple/polar arteries poorly visualized Only 40% of accessory renal arteries can be identified ( present in ~30% patients ) 17% of patients with renovascular HTN have polar RA disease; constitutes sole source in 11% Study limited by fat and bowel gas

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Diagnostic Criteria RAR: Renal-Aortic Ratio =PSVStenosis PSVAorta PSV: Peak Systolic Velocity EDV: End-Diastolic Velocity

PSVStenosis

PSVAorta

EDV EDR: End-Diastolic Ratio (parenchyma) =

CRITERIA FOR SIGNIFICANT ( ≥ 60% ) RENAL ARTERY STENOSIS RA PSV > 180 cm/sec (se 84-98%, sp 62-99%) Ratio of RA PSV /Aortic PSV > 3.5 Turbulent flow in post-stenotic area Arterial occlusion is indicated by failure to obtain a Doppler signal from imaged ( B-mode ) renal artery EDV > 150cm/sec ≥ 80% stenosis

PSV

CPSV: Cortical PSV CEDV: Cortical EDV

Renal Duplex Diagnostic Criteria Renal Artery Diameter Reduction Normal

Renal Artery PSV

RAR

< 180 cm/s

< 3.5

< 60%

≥ 180 cm/s

< 3.5

≥ 60%

≥ 180 cm/s

≥ 3.5

Occlusion

No signal

No signal

Anatomical Evaluation

DUPLEX ULTRASONOGRAPHY Resistive Index = (PSV – EDV) / PSV NL RI < 0.70 : no parenchymal disease RI > 0.80 : parenchymal disease i.e.. nephrosclerosis or glomerulosclerosis RI > 0.80 = predictor of poor benefit from surgery or angioplasty

COMPUTED TOMOGRAPHIC ARTERIOGRAPHY Advantages Noninvasive ≥ 50% stenosis detected in main and accessory renal arteries with se of 96% and sp of 99% Ability to determine renal size, cortical thickness, and renal perfusion No need to discontinue antihypertensive medications

CT Angio

MRA

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Contrast Arteriography

Disadvantages Expensive Limited by calcification Overestimates degree of RAS ( false-positives) Difficult to interpret branch artery stenoses Large amount of iodinated contrast required (120 – 180cc) Reformatting and image reconstruction is timeconsuming Inability to image patients >125kg

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MAGNETIC RESONANCE ANGIOGRAPHY Advantages Noninvasive Extensively evaluated Produces angiographic images not affected by calcific plaques No need to discontinue antihypertensive medications Not require nephrotoxic agents Physiologic parameters can also be measured 100% se and 97% sp (RAS ≥ 50%) with breath-holding 3D gadolinium-enhanced method

Disadvantages Expensive Can overestimate degree of stenosis (false-positives) Images do not strictly correlate with luminal anatomy Not useful in FMD Patients with claustrophobia may not tolerate the procedure Contraindicated in patents with pacemakers, cerebral aneurysm clips, or intraocular metal devices

ARTERIOGRAPHY Advantages Gold standard Identifies accessory and polar arteries, and associated aortic disease or aneurysms The only imaging modality capable of adequately visualizing branch vessel stenoses Offers opportunity to measure arterial pressures and dimensions across the stenosis Intervention can be performed concomitantly

Disadvantages Expensive and invasive Limited role in preliminary screening for RAS Groin puncture complications: hematomas and psuedoaneurysms Contrast-induced nephropathy ~3% (0-7%). ↑ risk (20-50%) with dehydration, renal insufficiency and DM Atheroembolism ~ 1.4%. ↑ susceptibility with widespread atherosclerotic disease and pre-existing renal insufficiency

Renal Artery Anatomy L1-L2 interspace in 75% Between T12 to L2

Renal arteries are single in 70% 10% accessory 20% aberrant Two equal-sized arteries in 10%

Atherosclerosis

Upper pole artery 7% Lower pole artery 6% Both upper and lower pole arteries 1% Three renal arteries 3% Four or more renal arteries 1%

Fibromuscular dysplasia

Anatomic Variations Accessory: enter kidney at hilus 98% from aorta, 2% from common iliac artery

Aberrant: enter kidney outside of the hilus Upper pole arteries usually arise from main renal artery Lower pole arteries usually arise from aorta

Rare origins SMA, IMA, median sacral, intercostal, lumbar, adrenal, inferior phrenic, right hepatic, right colic, supraceliac aorta, and lower thoracic aorta

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TREATMENT PROTOCOL FOR PATIENTS WITH RENAL DYSFUNCTION Pre-procedure hydration N-Acetylcysteine

600mg PO bid, given pm prior and am of procedure, or 150mg/kg 30 minutes prior with 50mg/kg gtt for 4hr post procedure Minimize amount of contrast Dilute contrast agent Combine contrast study with gadopentetic dimeglumine or CO2 Post-procedure hydration Evaluate renal function after procedure

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RENAL VEIN RENIN ASSAYS RVH and unilateral RAS Hypersecretion of renin from ischemic kidney Renin secretion should be suppressed in normal, contralateral kidney

Sample from both renal veins and IVC simultaneously Positive study: Lateralization Ratio > 1.4: 1 Predictive of positive outcome

RENAL VEIN RENIN ASSAYS Advantages Correlation between RVR’s and favorable response to surgery may exist

Ratio > 1.5 and Hypertension < 5 years Cure Rate 95% Specific, but not sensitive

Captopril renography Direct test of renovascular hypertension Isotope renogram before and after ACE inhibitor Compares RA flow and excretion ACE inhibitors cause acute decrease in renal function in kidney ipsilateral to RAS, while the nonstenotic side is unaffected

Disadvantages Not a screening study Invasive, involves catheterization of the renal veins Requires antihypertensive drug free period Limited role when bilateral RAS or solitary kidney Absence of a significant difference in RVR’s does not always correlate with lack of benefit of RA revascularization (57% with negative test still had improvement)

RENAL SCINTIGRAPHY Hydrate, hold ACE-I Baseline scan 25-50 mg of Captopril PO or Enalaprilat 50ug/kg Images repeated after 60 minutes Positive for renovascular hypertension ↓ renal function (DTPA) ↑ cortical retention (MAG3) Angiotensin II-induced vasoconstriction of efferent arteriole is reduced, resulting in decreased GFR in kidney affected with RAS Affected kidney with decreased GFR (compared with baseline study), NL kidney with increased perfusion

Less reliable in patients with significant parenchymal disease or bilateral RAS

RENAL SCINTIGRAPHY: CRITERIA FOR RAS > 50% Delayed time to maximal uptake (>11 minutes) in affected kidney Significant asymmetry in uptake between kidneys Cortical retention of radionuclide with captopril Marked reduction of GFR after captopril Se of 91% and sp 94% for detection RAS >50%

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Captopril Renography for RVH Good sensitivity and specificity when disease is unilateral Limited use in bilateral disease or with solitary functioning kidney

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RENAL SCINTIGRAPHY Advantages

Positive study suggests a high likelihood of renovascular HTN in subjects with preserved renal function

Disadvantages

Noninvasive Not a screening study Limited role when azotemia, bilateral RAS or solitary kidney

Presentation Outline

Classification of Hyperaldosteronism Secondary Hypertension Primary hyperaldosteronism Increased aldosterone secretion Aldosterone / renin ratio > 400 Conn’s syndrome (adrenal adenoma) vs. bilateral adrenal hyperplasia

Secondary hyperaldosteronism Increased renin production due to decreased renal artery perfusion Renin / aldosterone ratio > 50; renin vein renin ratio > 1.5 RAS; FMD; Takayasu arteritis

TREATMENT OF RAS

Introduction & classification Pathophysiology and natural history Renovascular hypertension Ischemic nephropathy

Clinical evaluation Indications for intervention Treatment - surgical vs. endovascular Miscellaneous

TREATMENT OF RENOVASCULAR DISEASE Few prospective randomized trials comparing available treatment options In the absence of level one data advocates of medical management, percutaneous transluminal renal angioplasty, or operative intervention cite selective clinical data to support their particular views

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TREATMENT OF RENOVASCULAR DISEASE Medical treatment

Atherosclerotic renovascular disease is associated with systemic vascular disease High mortality rates (38% @ 2yrs) are predominantly a result of cardiac events Medical therapy goals are to prevent or retard further progression of AS

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TREATMENT OF RENOVASCULAR DISEASE

ENDOVASCULAR TREATMENT OF RENOVASCULAR DISEASE FMD

Medical treatment

Lifestyle modification: smoking cessation, weight loss (BMI < 25), ↑ exercise

Blood Pressure control 70% diameter reduction) Fibromuscular dysplasia lesion Gradient > 20 mm Hg Kidney size > 8 cms Affected/unaffected kidney renin ratio of > 1:5/1

Clinical Refractory or rapidly progressive hypertension Hypertension associated with flash pulmonary edema without CAD Rapidly progressive deterioration in renal function Intolerance to medications

Contraindications to stenting Absolute Diffuse intrarenal vascular disease Noncompliant lesion Vessel rupture during PTRA

Relative Branch vessel disease Lesion length greater than 2 cm Renal artery size less than 3 mm

Percutaneous Renal Angioplasty

Results vary with the etiology, location, and severity of occlusive disease Fibrodysplastic disease Medial fibroplasia responded better than intimal and subadventitial fibrodysplasia Short term benefit 95%, long term 90% Cure rate 39%-66%

Atherosclerotic disease Technical success 73%-83% 6 months cure rates 3%-11%, improvement rate78%-87%

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Percutaneous Renal Angioplasty Takayasu disease Controversial More resistant to dilation and require highpressure balloon Technical success rate 85-90% Clinical benefit 80-90% at 1-2 year follow-up

Predictors of Improved Renal Function

Restenosis

More frequent in patients with ostial and branch lesions than with main artery lesions (35% versus 12%) 50% of the stenosis are within 6 months of initial angioplasty, 75% of the stenosis are within one year. Stent placement may reduce the restenosis rate-1/3 of the restenosis are within 6 months

Renal Artery Disease Treatment - Minimally Invasive Techniques

215 patients with ostial stenosis >70% PTA and Stent Predictors for good outcome Acute increase in serum creatinine Good LV function Female sex High baseline MAP Normal renal parenchymal thickness/resistance Zeller, et al, Circulation, 2003

Technique Pigtail catheter

Aortogram

AP for left renal artery 15-30° LAO for right renal artery

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Technique Selective catheterization of renal artery 5 Fr diagnostic catheter Renal double curve (RDC), Simmons, Multipurpose Glide, Cobra 2, Hockey stick.

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Technique

Technique

Technique

Technique Selective angiography via 5 Fr diag. cath. Before wires passage give NTG 100-200 µg Guidewire passage across the lesion .035” Bentson or Wholly 180 cm .014” Platinum plus 180cm

Technique Guiding catheter 6 Fr 55 cm (Tuohy-Borst) Renal guiding catheter (BSV) Brite-tip Multipurpose, (Cordis, RDC-1)

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• Once the diagnostic catheter is across the lesion, a stiffer exchange wire is used • • • •

0.035, 0.018, or 0.014 SV-5, V-18 or Platinum 0.018 TAD II (0.018 to 0.035) Rosen 0.035

• Give systemic heparin 5,000 U IV

Technique Ostial lesion Predilection recommended 4 mm x 2 cm balloon Inflation time 30 to 60 seconds Pressure 4 –12 mm Hg (> 12 mm Hg for FMD) Balloon-expand. stent (5.0-7.0 mm x 2 cm balloon)

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Technique

Non-ostial lesion Attempt PTA 5-6 mm x 2 cm balloon Stent is not mandatory if good result with PTA PTA considered adequate if < 30% residual stenosis & the systolic pressure gradient < 10 mm Hg.

Technique stenting Advance the guide cath. across lesion Track over the PTA deflated balloon. Advance stent to desired location

Technique Consider road-mapping Guiding cath. is retracted to the renal A. origin Puff contrast via the guide cath. & fire the stent Angiogram to access deployment

Post-procedural Management Remove sheath once the ACT < 180 sec (Bedrest overnight) Groin closure device (Perclose – bedrest 3 hour) Oral aspirin 325 mg lifelong. Adjust the antihypertensive agents as necessary Role of Plavix load 300 mg and 75 mg qd for 6 months.

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Pearls For bilateral disease attempt the PTA on the side with larger kidney first, if all goes well than do the other side. Check peak systolic pressure gradient across the stenosis. A significant gradient is > 10%. Sizing the balloon diameter approximately 10% larger than the estimated “normal” size. Can use a 4 Fr balloon system over a 0.018 / 0.014 wire. Once PTA is done avoid recrossing the site with a wire. Risk of renal failure high? Consider dilute contrast, CO2, or gadolinium based contrast. Stent should extend into aorta ~2-3 mm

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Presentation Outline Introduction & classification Pathophysiology and natural history Renovascular hypertension Ischemic nephropathy

Clinical evaluation Indications for intervention Treatment endovascular surgical

Surgical Renal Artery Revascularization Indication Renovascular hypertension Ischemic nephropathy Adjunctive to aortic reconstruction Failed percutaneous angioplasty Lesion associated renal artery aneurysms Osteal lesions and lesions involve branches

Miscellaneous

Surgical options Techniques Aortorenal bypass Extra-anatomic bypass Hepatorenal bypass Splenorenal bypass Thoracic aortorenal Ilio renal

Endarterectomy Aortorenal endarterectomy Trap-door aortic endarterectomy (viscerals)

Renal a reimplantation Ex-vivo reconstruction No prospective randomized trial comparing different surgical techniques

Surgical options Techniques Thromboendarterectomy AS of renal +- visceral arteries Combined with AAA or aortoiliac occlusive dz

Renal a re-implantation Orifice RAS and sufficient length RA and vein Re-implant inferiorly

Nephrectomy Goldblatt kidney Non-reconstructible vessels

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Surgical options Techniques Aortorenal bypass RSVG > 4mm Hypogastric a pediatric 6mm Dacron/PTFE

Extra-anatomic bypasses Avoids aortic cross-clamping Need pre-op angio to confirm patency

Surgical options Techniques Ex-vivo reconstruction Distal RA disease Indications Complications/stent failure FMD/aneurysms Stenoses/occlusion/dissection branches Congenital AVF Degeneration RA bypass graft Reconstruction lasting > 30 minutes

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Surgical Renal Artery Revascularization Pearls

Surgical Renal Artery Revascularization Pearls

Left RA bypass: Retroperitoneal approach with kidney up makes left renal bypass straight forward Distal left renal a exposure via midline approach requires mobilization of left colon! Splenorenal is technically challenging

Surgical Renal Artery Revascularization

Right RA bypass: Usually easier to distal R RA with graft routed under IVC Ileo-renal can be routed lateral to the cava Hepatorenal easier than splenorenal

Aortorenal bypass

Pearls Both right and left revascularizations: Bilateral RA endarterectomy is harder than it sounds Midline with both kidneys down

Bilateral RA bypass is easier and less risky Prosthetic for adults (Dacron easier than PTFE) End-end easier than end to side Hypogastric artery for children

Aortorenal Endarterectomy

Aortorenal Endarterectomy

RAS secondary due to spillover of aortic plaque (65% of atherosclerotic RAS) Focal eccentric or concentric narrowing within the proximal 1.5 cm of the artery (30% of arthro sclerotic RAS)

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Aortorenal Endarterectomy

AAA repair with concomitant aortorenal bypass

R. hepatorenal bypass

Right medial visceral rotation

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Aortorenal Endarterectomy

Aortorenal bypass with saphenous vein graft

R. hepatorenal bypass

Kocher maneuver with duodenal mobilization

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R. hepatorenal bypass

R. hepatorenal bypass Isolation of common hepatic artery and right renal artery

Kocher maneuver with duodenal mobilization

R. hepatorenal bypass

Left splenorenal bypass

R. hepatorenal bypass

Left splenorenal bypass Left medial visceral rotation including the pancreas, stomach and spleen

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Left splenorenal bypass Mobilization of left splenic artery from the hilum

Trap door aortic endarterectomy Aorta must be clampable at supraceliac & infrarenal levels. •CA & SMA disease not extend beyond first 2 cm.

Left splenorenal bypass Completion splenorenal bypass with end-to-side splenic-renal artery anastomosis

Trap door aortic endarterectomy A rectangular aortotomy is made, midline approach with kidney down

Trap door aortic endarterectomy Endarterectomy of all 4 vessels can be performed

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Aortotomy is closed following a complete endarterectomy.

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