- •Vascular Surgery
- •SECTION AND BOARD OF VASCULAR SURGERY
- •Foreword to the First Edition
- •Preface to the First Edition
- •Preface to the Second Edition
- •Preface to the Third Edition
- •Contents
- •Contributors
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •1.1 Commentary
- •1.2 Beta-Adrenergic Antagonists
- •1.3 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitors (Statins)
- •1.4 Percutaneous Revascularization
- •1.5 Coronary Artery Bypass Grafting
- •References
- •2: Abdominal Aortic Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •2.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •Question 12
- •Question 13
- •Question 14
- •3.1 Commentary
- •3.2 Case Analysis Quiz
- •References
- •4: Ruptured Abdominal Aortic Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •4.1 Commentary
- •References
- •5: Thoracoabdominal Aortic Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •5.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •Question 12
- •Question 13
- •6.1 Commentary
- •References
- •7: Aortic Dissection
- •7.1 Dissection: Stanford A
- •Question 1
- •Question 2
- •Question 3
- •7.2 Dissection: Stanford B
- •Question 4
- •Question 5
- •7.3 Commentary
- •References
- •8: Popliteal Artery Aneurysms
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •8.1 Popliteal Artery Aneurysm
- •References
- •9: Renal Artery Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •9.1 Commentary
- •References
- •10: Anastomotic Aneurysms
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •10.1 Commentary
- •10.2 Indications for Intervention
- •10.3 Treatment for Anastomotic Aneurysms
- •10.4 Infection in Anastomotic Aneurysms
- •10.5 Outcome
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •11.1 Commentary
- •References
- •12: Acute Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •12.1 Commentary
- •References
- •13: Arterial Embolism
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •13.1 Commentary
- •References
- •14: Blast Injury to the Lower Limb
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •14.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •15.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Smoking
- •Antiplatelet Agents
- •Blood Pressure (BP)
- •Glucose Status
- •Lipids
- •Emerging Risk Factors
- •Question 4
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •17.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •18.1 Commentary
- •18.2 Clinical Assessment
- •18.3 Imaging Techniques
- •18.4 Revascularization Options
- •18.5 Aortobifemoral Bypass
- •18.6 Iliac Angioplasty and Stenting
- •18.7 Iliac Stenting Combined with Profunda Femoris Artery Revascularization
- •18.8 Rationale for Angioplasty of “Donor” Iliac Artery Prior to Femorofemoral Crossover Bypass
- •18.10 Supervision and Follow-up of the Patient
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •Question 12
- •19.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •20.1 Commentary
- •References
- •21: Bypass to the Popliteal Artery
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •21.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •22.1 Commentary
- •References
- •23: Popliteal Artery Entrapment
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •23.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •24.1 Commentary
- •References
- •25: The Obturator Foramen Bypass
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •25.1 Commentary
- •25.2 Preoperative Measures
- •25.3 The Concept of the Obturator Foramen Bypass
- •25.4 Obturator Foramen Bypass Technique
- •References
- •26: Diabetic Foot
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •26.1 Commentary
- •References
- •27: Chronic Visceral Ischemia
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •27.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •28.1 Commentary
- •References
- •29: Renovascular Hypertension
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •29.1 Commentary
- •29.4 Intra-arterial Angiography
- •29.5 Duplex Ultrasonography (DU)
- •29.6 Treatment
- •29.6.1 Medical Treatment
- •29.6.2 Revascularization
- •29.7 Prognosis
- •References
- •30: Midaortic Syndrome
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •30.1 Commentary
- •References
- •31: Management of Portal Hypertension
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •31.1 Commentary
- •31.2 General Considerations
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •32.1 Commentary
- •References
- •33: The Carotid Body Tumor
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •33.1 Commentary
- •33.2 Clinical Presentation
- •33.3 Treatment
- •33.4 Summary
- •References
- •Question 1
- •Question 2
- •Question 3
- •34.1 Commentary
- •34.2 Vertebrobasilar Ischemia: Low-Flow Mechanism
- •Question 1
- •Question 2
- •34.3 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •35.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •36.1 Commentary
- •References
- •37: Acute Axillary/Subclavian Vein Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •37.1 Commentary
- •References
- •38: Raynaud’s Phenomenon
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •38.1 Commentary
- •References
- •39: Aortofemoral Graft Infection
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •39.1 Commentary
- •References
- •40: Aortoenteric Fistulas
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •40.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •41.1 Commentary
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Questions 7 and 8
- •Question 9
- •Question 10
- •Comment
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •42.1 Commentary
- •References
- •43: Amputations in an Ischemic Limb
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •43.1 Commentary
- •References
- •44: Congenital Vascular Malformation
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •44.1 Clinical Evaluation
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •44.2 Commentary
- •References
- •45: Klippel-Trenaunay Syndrome
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •45.1 Commentary
- •Clinical Presentation
- •Evaluation
- •Treatment
- •References
- •46: Deep Venous Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •46.1 Commentary
- •References
- •47: Endoluminal Ablation of Varicose Veins
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •47.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •48.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •50.1 Commentary
- •References
- •51: Iliofemoral Venous Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •50.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •52.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •53.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •54.1 Commentary
- •References
- •Index
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Renovascular Hypertension |
29 |
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Constantina Chrysochou and Philip A. Kalra |
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A 55-year-old male is referred for investigation of lower limb claudication pains. His past medical history includes long standing hypertension and a previous myocardial infarction 3 years previously with subsequent coronary angioplasty and stenting. He is a life long smoker, but rarely takes any alcohol. His symptomatic claudication arises after walking for approximately 200 m on the level. He is receiving an angiotensin converting enzyme inhibitor (ACE-I), which, according to the General Practitioner’s letter, was commenced about 2 months before referral, and he also receives a diuretic and a calcium antagonist at full dosage to optimize his blood pressure. On examination he is noted to have bilateral ilio-femoral bruits but palpable pedal pulses. His blood pressure remains sub-optimally controlled at 170/90 mmHg. He is commenced on an alpha-blocker (Doxazosin).
Following the clinic visit you review his blood results and notice that there has been a deterioration in his renal function with the serum creatinine increasing from 120 to 180 mmol/L and estimated glomerular filtration rate (eGFR) decreasing from 58 to 36 mL/min since the time of referral.
Question 1
Which of the following statements support your suspicion that the patient has renovascular disease contributing to his poorly controlled blood pressure?
A. Longstanding hypertension
B. There is difficulty in controlling the blood pressure with three different anti-hypertensive drugs
C. There was a relatively rapid deterioration of renal function between the time of referral and the first clinic visit
D. He is an arteriopath with symptoms of lower limb claudication pains
C. Chrysochou ( )
Department of Renal Medicine, Salford Royal Hospital and University of Manchester,
Manchester, UK
G. Geroulakos and B. Sumpio (eds.), Vascular Surgery, |
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DOI: 10.1007/978-1-84996-356-5_29, © Springer-Verlag London Limited 2011 |
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C. Chrysochou and P.A. Kalra |
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Question 2
What would be the most appropriate investigation(s) to decide whether the hypertension has a renovascular origin?
A. Direct intra-arterial angiography
B. Renography with captopril provocation C. Magnetic resonance angiography (MRA)
D. Computerized tomography angiogram (CTA) E. Duplex ultrasound of the renal arteries
In this patient, magnetic resonance imaging showed diffuse aorto-iliac disease. There was a 90% stenosis with post stenotic dilatation at the ostium of the left renal artery and the kidney was 10 cm in length. On the right hand side there were two renal arteries, the smaller of these exhibited a 50% renal artery stenosis (RAS). The kidney measured 11 cm in length.
In view of the deterioration in renal function and the poorly controlled hypertension it is decided to stop the ACE-inhibitor and to proceed to intervention.
Question 3
What is the most appropriate revascularization approach for the renal artery stenosis?
A. Aortorenal bypass
B. Thromboendarterectomy
C. Percutaneous transluminal angioplasty (PTA) with stent D. PTA alone
E. Nephrectomy
Question 4
Which are the most frequent serious complications seen after renal artery PTA?
A. Arterial rupture B. Occlusion
C. Cholesterol microembolisation
D. Contrast-related Acute kidney injury E. Groin haematoma
The patient underwent percutaneous angioplasty with bare-metal stent placement in the left renal artery. The right renal artery was not amenable to endovascular intervention. The procedure progressed without complications and the patient was sent home the day after treatment in good condition.
29 Renovascular Hypertension |
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He was reviewed again after 2 weeks at which stage his creatinine had improved to 140 mmol/L (eGFR 49 mL/min). His blood pressure (165/90) control had improved to some extent.
Question 5
Which of the following would be most appropriate for his future management?
A. Regular clinic review with attention to medical control of blood pressure, and vasculoprotective therapy
B. Repeat renal artery imaging with possible repeat left renal artery stenting C. Right renal artery PTA and stenting
D. Surgical revascularization of the left kidney
29.1 Commentary
Renovascular disease is common, and atheromatous renovascular disease (ARVD) accounts for 90% of renal artery stenosis (RAS) in western populations. The remainder is mainly due to fibromuscular disease (FMD) which usually presents as hypertension in younger patients.
There has been a steady increase in the number of patients diagnosed with ARVD in the last 2 decades.1 ARVD is a disease of ageing just as is the case with other traditional macrovascular atheromatous diseases, and it is strongly associated with coronary artery disease (CAD), congestive cardiac failure, aorto-iliac and more distal peripheral vascular disease (PVD) and cerebrovascular disease. The finding of ARVD during investigation and management of one of these other vascular diseases can be of detrimental prognostic importance.2,3 For example, 15–30% of patients with CAD have evidence of ARVD, with RAS >50% detectable in about 5%.4 A close relationship exists between the number of diseased CAD vessels and severity of RAS.4 In turn, prospective observational studies have shown that the presence and severity of RAS confer a negative impact upon survival in these CAD patients.5 Due to anatomic proximity, aorto-iliac disease is very frequently associated with ARVD, most studies showing that around 40–45% of patients referred for investigation of PVD have the disease.6
ARVD can be identified in about 2% of selected hypertensive populations.7 Conversely, around 90% of patients with ARVD have hypertension, but whether this hypertension is the direct result of ARVD, rather than simply an association, is often difficult to determine. A strict definition of “renovascular hypertension” necessitates that the hypertension is cured or substantially improved following correction of the RAS (usually with revascularization). Renovascular hypertension has been listed as the primary cause of end stage renal
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disease (ESRD) in 5.2%8 of the US dialysis population. With an increasingly ageing population, the incidence of ARVD is likely to continue to rise, as will the related cardiological and renal burden on the healthcare system.
Clinical features which would lead a clinician to suspect ARVD include:
•Patients with cardiovascular risk factors, e.g., smokers, type 2 diabetics, evidence of atheroma in other vascular beds
•Rapid onset of hypertension in young people (FMD)
•Rapid deterioration of previously well-controlled essential hypertension
•Malignant/accelerated hypertension or hypertensive crises
•Three-drug- (or more) resistant hypertension
•Hypertension and deteriorated renal function
•Impaired renal function on commencement of renin angiotensin blocking (RAB) therapy (ACE inhibitors, angiotensin receptor blockers or renin inhibitors)
•Flash pulmonary oedema
•Epigastric, flank or back bruit
•Discrepancy of >1.5 cm between kidney sizes on imaging
In our patient, the presence of concomitant vascular disease and marked smoking history provided a higher suspicion for ARVD. The sudden deterioration in renal function with RAB and poorly controlled hypertension supported investigation for renovascular hypertension. [Q1: B, C, D]
Many radiological techniques have been used to investigate the presence of RAS. All these methods have their advantages and disadvantages. The three most commonly used radiological methods are magnetic resonance angiography (MRA), computerized tomography angiography (CTA) and duplex sonography as they are non-invasive and they can provide a reasonable estimation of the degree of RAS. The most appropriate radiological method will depend on availability, and the patient’s level of kidney function – due to the risks posed by nephrogenic systemic fibrosis (NSF) and contrast induced nephropathy in those with severe renal dysfunction (see below). The various investigational methods are briefly considered below:
29.2 MRA
Advantages: Contrast enhanced MRA with gadolinium (Gd) provides a non-invasive, rapid and accurate investigation of the degree of RAS9–11 with high specificity and sensitivity (Fig. 29.1). MR imaging (MRI) has the potential to assess the functional and morphological characteristics within the renal parenchyma.
Disadvantages: Gd-enhanced MRI has been implicated in causing cases of NSF in patients with moderate to severe renal impairment,12,13 the condition being characterized by skin thickening, systemic fibrosis and even death. Guidance from the UK Commission on Human Medicines recommends that certain types of Gd containing agents should not be used in patients with advanced CKD with the result that MRA is now performed with