- •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
Management of Carotid |
32 |
Bifurication Disease |
Wesley S. Moore
A 72-year-old white male was referred for evaluation and management following the finding of an asymptomatic carotid bruit, picked up on routine physical examination by his primary-care physician. The patient was asymptomatic with respect to ocular or hemispheric ischaemic events. His risk factors included a 30-year history of smoking one pack of cigarettes a day, which he quit a year ago. He had hypertension that was controlled well by two drugs. He had no history of coronary artery disease, diabetes mellitus, or symptoms of peripheral vascular disease. On physical examination, his temporal pulses were equal. His carotid pulses were full and equal, but there was a loud bruit over the right carotid bifurcation. His femoral, popliteal, dorsalis paedis and posterior tibial pulses were normally palpable bilaterally.
Question 1
What should the next step in this patient’s evaluation be?
A. Counseling with respect to the nature of carotid territory ischaemic attacks B. Start the patient on an antiplatelet drug, such as aspirin, and a statin
C. Counsel the patientwith respect totheimportance of refraining from cigarettesmoking and careful control of blood pressure
D. Obtain bilateral carotid duplex scanning E. All of the above
The patient underwent a bilateral carotid duplex scan. [Q1: D] The scan demonstrated a category 60–79% right carotid bulb stenosis. The plaque characteristic was one of mixed consistency, a mildly irregular surface, and minimal calcification. The left carotid bulb showed a category 20–59% stenosis. Both vertebral arteries were imaged with normal antegrade flow velocities.
W.S. Moore
Division of Vascular Surgery, UCLA, Los Angeles, CA, USA
G. Geroulakos and B. Sumpio (eds.), Vascular Surgery, |
331 |
DOI: 10.1007/978-1-84996-356-5_32, © Springer-Verlag London Limited 2011 |
|
332 |
W.S. Moore |
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|
Question 2
What would be appropriate management for this patient?
A. Elective carotid endarterectomy B. Full Coumadin anticoagulation
C. Aspirin antiplatelet management, a statin, and risk factor control
Thepatientwasplacedonaspirinantiplatelettherapy,begunonastatin,9 counseledregarding the importance of good blood pressure control including the use of a beta blocker or ACE inhibitor, and given an appointment for a return visit in 6 months time for a repeat carotid duplex scan to see whether there was any evidence of progression. The patient was also counseled regarding the importance of calling the vascular service should he develop ocular or hemispheric transient ischaemic attacks within the 6-month interval before his return appointment. [Q2: C]
The patient did quite well for the next 4 months; then one afternoon, he noted the onset of an episode of numbness and weakness of his left hand. The hand was not totally paralyzed, but it was clearly numb, weak and uncoordinated. This cleared completely within a period of 10 min. The patient thought that this might have been related to his arm position and chose to do nothing further until the next day, when the same event occurred. At this point, he called his physician and was advised to return immediately. An emergent carotid duplex scan was ordered. The scan now showed progression to a category 80–99% stenosis with plaque once again of mixed consistency.
Question 3
What is the best management for this patient?
A. Clopidogrel antiplatelet therapy B. Full Coumadin anticoagulation
C. Schedule elective carotid endarterectomy 1 month from now D. Urgent right carotid endarterectomy
The patient now had two clear indications for proceeding with carotid endarterectomy: the onset of symptoms in the territory of the carotid lesion, and progression of the lesion to an 80–99%stenosis.Twoadditionaldecisionsalsohadtobeconsidered:thetimingofoperation andwhetherbrainimagingwasindicated.Inviewofthefactthatthepatienthadanappropriate carotid artery lesion, and the symptoms were typical for hemispheric transient ischaemic events in the distribution of the carotid lesion, information gained from brain imaging such as computed tomography (CT) or magnetic resonance imaging (MRI) would be of limited value.Therefore,thecost/benefitratioforbrainimagingwasclearlyunfavorable.Thetiming of carotid endarterectomy was urgent. The patient had a new onset of transient ischaemic attacks and evidence of plaque progression. Therefore, the patient was now at highest risk of a hemispheric stroke. The optimum management for this patient would be emergent admission to the hospital and rapid evaluation for operation, including the patient’s cardiac status.10,11
32 Management of Carotid Bifurication Disease |
333 |
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While this was taking place, it would be appropriate to start the patient on intravenous heparinanticoagulation.Onceclearedfromacardiacstandpoint,plansshouldbemadetoproceed with operation either that day or the next morning. [Q3: D]
The patient was admitted as an emergency to the hospital and started on intravenous heparin with a loading dose of 5,000 units and a continuing dose of 1,000 units/h. He was seen in cardiology consultation, an electrocardiogram (ECG) was obtained and a stressecho study was performed. In the absence of any symptoms of coronary disease, a relatively normal ECG, and a stress-echo study showing a 55% ejection fraction, the patient was cleared for operation.
Question 4
What should the next step in this patient’s management be?
A. Aortic arch angiogram with selected carotid arteriograms B. Magnetic resonance angiogram (MRA)
C. CT angiogram
D. Proceed with operation on the basis of a duplex scan of diagnostic quality in an accredited laboratory
The patient was taken to the operating room the next morning. Before this, EEG electrodes were placed for intraoperative monitoring. An arterial line was placed for blood pressure monitoring, and general anaesthesia was administered. A vertical incision along the anterior border of the sternomastoid muscle was made. The facial vein was divided, and the common carotid, carotid bifurcation, internal and external carotid arteries were fully mobilized. There was a posterior plaque present in the common carotid artery, which was nonocclusive. The major plaque build-up was in the bulb of the internal carotid artery, which went a short distance beyond the bulb into the internal carotid artery distally. Beyond this point, the vessel was circumferentially soft. The distal internal carotid artery was somewhat collapsed, and no distal pulse was noted. Since the patient had experienced only transient symptoms and not a completed stroke, it was our plan to use an internal shunt only if there were electroencephalogram (EEG) changes with trial clamping. A bolus of 5,000 units of heparin was administered, and the internal, external and common carotid arteries were clamped. The EEG was observed: there were no changes. The amplitude and frequency of the EEG wave form were maintained. A longitudinal arteriotomy was made in the common carotid artery and extended through a very tight carotid stenosis. The plaque within the carotid bulb showed evidence of recent intraplaque haemorrhage. As we passed through the plaque, we emerged into an unencumbered internal carotid artery distally. A bifurcation endarterectomy was then performed with clean endpoints in the internal, external and common carotid arteries. The intimectomised surface was then irrigated with heparinised saline, and small bits of medial debris were removed carefully. The intimal endpoint was adherentto the media.Once we were satisfied that there was no evidence of intimal flap and all of the loose bits of medial debris were removed, attention was turned to closure.
334 |
W.S. Moore |
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Question 5
Closure of the arteriotomy should be:
A. A primary, carefully placed closure with 6–0 prolene B. Closure with a patch angioplasty
The patient’s arteriotomy was closed with a patch angioplasty using a collagenimpregnated knitted Dacron patch that was cut to length and beveled at each end. Upon completion of the closure, blood flow was begun first to the external then to the internal carotid artery. Excellent pulsation in all vessels was noted. We then carried out a completion angiogram by placing a small needle in the patch and injecting contrast into the carotid bifurcation using a portable cine-fluoro unit. The carotid bifurcation was imaged, and there was an excellent technical result with no evidence of residual stenosis or intimal flap. Intracranial imaging was also carried out, and excellent flow into the carotid siphon and the anterior and middle cerebral arteries was confirmed. After meticulous haemostasis was achieved, a 7.0-mm Jackson Pratt drain was placed in the wound and brought out through a separate stab wound. The platysmal layer was closed with an absorbable suture, and the skin was closed with a subcuticular absorbable suture. An adhesive plastic dressing was applied directly to the skin, and the patient was returned to the recovery room. The patient awoke at his neurological baseline with no evidence of cerebral or cranial nerve deficit. His blood pressure was monitored carefully and was noted to be stable at 150/80 mmHg.
Question 6
After an appropriate stay in the recovery room, to where should the patient be transferred?
A. An intensive care unit with continual monitoring overnight
B. A step-down unit with 3 : 1 nursing coverage and monitoring capability C. The patient should be left in the recovery room overnight
D. A regular hospital room
Since the patient was neurologically intact and was maintaining his normal blood pressure, he was transferred to a regular hospital room for routine overnight care. The patient spent an uneventful night in a regular hospital room. The following morning, we removed the dressing and drain. The patient was ambulatory and on a regular diet and was discharged home on the first postoperative day.1 This management is typical of the so-called “fasttrack” management of carotid bifurcation disease. Patients are usually admitted electively on the morning of operation, undergo carotid endarterectomy, spend a period of 2–3 h of observation in the recovery room, transfer to a regular hospital room, and are discharged the following morning. Thus, carotid endarterectomy has become extremely cost-effective in the overall medical economic environment. The patient was instructed to return for a routine visit in 3 weeks. At that time, we obtained a right carotid duplex scan to confirm the result of carotid endarterectomy and to establish a new baseline for future comparison. The next visit will be in 6 months, at which time a bilateral carotid duplex scan will be performed. The objective will be to look for evidence of intimal hyperplasia and recurrent