Current Therapy in Vascular and Endovascular Surgery [5 ed.] 9781455709847, 2014002164, 9780323315265, 9781455759620, 1455709840

Table of contents :
Front Matter
Copyright
Contributors
Preface
Cerebrovascular Disease
1 Cerebrovascular Disease
Pathology of Carotid
Artery Atherosclerosis
Geometry of
The Carotidbifurcation
Hemodynamic Conditions At Thecarotid Bifurcation
Carotid Bifurcation Atherosclerosis
2
Carotid and Vertebral Artery Fibrodysplasia
Carotid Artery Fibrodysplasia
Vertebral Artery Fibrodysplasia
3
Carotid Artery Dissections
Clinical Pathophysiology
Diagnosis
Treatment
Outcomes
4
Carotid Artery Kinks and Coils
ETIOLOGY
EPIDEMIOLOGY
IMAGING AND DIAGNOSIS
MANAGEMENT AND TREATMENT
5
Giant Cell Arteritis
PATHOPHYSIOLOGY
CLINICAL FEATURES
DIAGNOSIS
MEDICAL TREATMENT
SURGICAL TREATMENT
PROGNOSIS
6
Arteriographic Evaluation of Cerebrovascular Disease
INDICATIONS FOR CATHETER-BASED ANGIOGRAPHY
Diagnostic Indications
Intraoperative Indications
Surveillance
ANGIOGRAPHIC PROCEDURES
Access to the Arterial System
Sheath and Catheter Principles
Contrast Agents
Vessel Selection
Catheter Positioning
Angiographic Images
Angiographic Anatomy
Embolic Precautions
Injection Rates
Sedation and Anesthesia Requirements
Postangiography Orders
COMPLICATIONS OF CEREBRAL ANGIOGRAPHY
Neurologic Complications
Nonneurologic Complications
7
Computed Tomography in Cerebrovascular Disease
8
Magnetic Resonance Imaging and Positron Emission Tomography in the Evaluation of Cerebrovascular Disease
MAGNETIC RESONANCE IMAGING
POSITRON EMISSION TOMOGRAPHY
CONCLUSION
9
Duplex Scanning and Spectral Analysis of Carotid Bifurcation Atherosclerotic Disease
IMPORTANT CONCEPTS
GRADING OF STENOSIS
Use of Velocity Criteria
Limitations of Duplex Velocity Criteria
Other Methods of Grading ICA Stenosiswith Ultrasound
DUPLEX SCANNING AND STROKE RISK STRATIFICATION: FUTURE PERSPECTIVES
10
Transcranial Doppler in the Evaluation of Cerebrovascular Disease
TECHNIQUE
CLINICAL INDICATIONS
Cerebral Ischemia
Vasomotor Reactivity
Cerebral Embolization
Subarachnoid Hemorrhage
Sickle Cell Disease
Cerebral Circulatory Arrest
FUNCTIONAL TRANSCRANIAL DOPPLER
THERAPEUTIC TRANSCRANIAL DOPPLER
SUMMARY
11
Medical Treatment to Prevent Transient Ischemic Attacks and Ischemic Stroke
MODIFICATION OF RISK FACTORS
Hypertension
Tobacco Abuse
Diabetes Mellitus
Hyperlipidemia
Antiplatelet Medication
Lifestyle Interventions to Prevent Stroke
CARDIOEMBOLIC STROKE PREVENTION
Atrial Fibrillation
Carotid Artery Stenosis
STROKE PREVENTION IN SPECIAL PATIENT POPULATION
SECONDARY PREVENTION OF TRANSIENT ISCHEMIC ATTACKAND STROKE
SECONDARY PREVENTION OF CARDIOEMBOLIC STROKE
Antiplatelet Agents for Secondary Preventionof Stroke or Transient Ischemic Attack
CONCLUSION
12
Medical Therapy Including Fibrinolytic Therapy of Acute Ischemic Stroke
DIAGNOSIS
TREATMENT
PREVENTING FUTURE STROKES
Strokes of Unknown Onset and Wake-up Strokes
INTRAARTERIAL THROMBOLYSIS
13
Diabetes as a Risk Factor in Atherosclerotic Cerebrovascular Disease
DIABETES AND CEREBROVASCULAR DISEASE
Stroke Characteristics in Diabetes
Pathophysiology of Stroke in Diabetes and Hyperglycemia
PREVENTION OF STROKE IN PATIENTS WITH DIABETES
Glycemic Control
Antihypertensive Therapy
Lipid-Lowering Therapy
Antiplatelet and Anticoagulation Therapy
DIABETES AND SURGICAL INTERVENTION FOR CEREBROVASCULAR DISEASES
GLYCEMIC CONTROL IN THE SETTING OF ACUTE ISCHEMIC STROKE
CONCLUSION
14
Selection of Patients for Carotid Endarterectomy versus Carotid Artery Stenting
CAROTID STENTING VERSUS ENDARTERECTOMY: MAJORTRIAL DATA
TREATMENT OF ASYMPTOMATIC CAROTID ARTERY STENOSIS
TREATMENT OF SYMPTOMATIC CAROTID ARTERY STENOSIS
LIMITATIONS OF TRANSFEMORAL CAROTID ARTERY STENTING WITH DISTAL FILTER PROTECTION
15
Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease
PREPROCEDURAL EVALUATION
ARTERIAL ACCESS
CAROTID IMAGING AND SHEATH ACCESS
Aortic Arch Angiogram
Selective Common Carotid Catheterization
Carotid Sheath Access
CEREBRAL PROTECTION
Technique for Using Distal Filters
Proximal Occlusion and Flow-Reversal Devices
ANGIOPLASTY AND STENTING
COMPLETION ANGIOGRAM
MANAGEMENT OF THE ACCESS SITE
POSTOPERATIVE CARE ANDFOLLOW-UP
16
Reversal of Cerebral Blood Flow to Prevent Stroke during Percutaneous Carotid Artery Angioplasty and Stenting
IMPACT OF EMBOLIZATION
PRINCIPLES OF FLOW REVERSAL
CLINICAL RESULTS WITH THEFIRST-GENERATION FLOW-REVERSAL SYSTEM
SECOND-GENERATION FLOW-REVERSAL SYSTEM AND EMPIRE TRIAL
17
Embolic Protection Devices to Prevent Stroke during Percutaneous Angioplasty and Stenting
DEVICE CHARACTERISTICS
SELECTION OF DEVICES
TECHNIQUE
CLINICAL TRIAL RESULTS
CONCLUSIONS
18
Blood Pressure Instability after Percutaneous Carotid Angioplasty and Stenting
PATHOPHYSIOLOGY OF HEMODYNAMIC INSTABILITY ASSOCIATED WITH CAROTID INTERVENTIONS
HEMODYNAMIC INSTABILITY TRIGGERED BY CAROTID ARTERY INTERVENTIONS
FACTORS PREDICTING HEMODYNAMIC INSTABILITY DURING CAROTID INTERVENTIONS
MANAGEMENT OF HEMODYNAMIC INSTABILITY INDUCED BY CAROTID ANGIOPLASTY AND STENTING
19
Cerebral Hyperperfusion Syndrome After Carotid Endarterectomy and Carotid Stenting
PATHOPHYSIOLOGY
INCIDENCE
RISK FACTORS
CLINICAL MANIFESTATIONS
DIAGNOSIS
TREATMENT
20
Treatment of Recurrent Carotid Artery Stenosis After Percutaneous Angioplasty and Stenting
INCIDENCE
DIAGNOSIS
NATURAL HISTORY
CLINICAL SIGNIFICANCE
TREATMENT
CONCLUSION
21
Technical Aspects of Conventional Carotid Endarterectomy for Atherosclerotic Disease
SURGICAL TECHNIQUE
POSTOPERATIVE CARE
POSTOPERATIVE RESULTS
22
Technical Aspects of Eversion Carotid Endarterectomy for Atherosclerotic Disease
METHODS
SHUNTING AND EVERSION ENDARTERECTOMY
UNUSUAL PROBLEMS AND TROUBLESHOOTING
23
Patch Graft Closure with Carotid Endarterectomy
PATCH CLOSURE VERSUS PRIMARY CLOSURE
ROLE OF SELECTIVE PATCHING
CHOICE OF PATCH MATERIAL
CONCLUSIONS
24
Management of the Infected Carotid Artery Patch
INFECTING MICROORGANISMS
CLINICAL PRESENTATION
RELATIONSHIP WITH PERIOPERATIVE INFECTION
INVESTIGATION OF PROSTHETIC PATCH INFECTION
MANAGEMENT OF PROSTHETIC PATCH INFECTION
CONCLUSION
25
Role of Shunting During Carotid Endarterectomy
SELECTIVE SHUNTING
Awake Carotid Endarterectomy
Carotid Back Pressure Measurement
Electroencephalographic Monitoring
Transcranial Doppler
Cerebral Oximetry
ROUTINE SHUNTING
CONCLUSIONS
26
Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy
ANGIOGRAPHY
DOPPLER STUDIES
DUPLEX SCANNING
FOLLOW-UP STUDIES
CURRENT RECOMMENDATIONS
27
Intraoperative Recognition and Treatment of Cerebral Ischemia During Carotid Endarterectomy
REGIONAL ANESTHESIA
GENERAL ANESTHESIA
INTRAOPERATIVE TREATMENT
Hypoperfusion
Embolization
Fronds
Dissection
Thrombosis
28
Early Postoperative Recognition and Management of Acute Stroke After Carotid Endarterectomy
EVALUATION
Portable Duplex Sonography
Magnetic Resonance Imaging andComputed Tomography
Angiography
SURGICAL REEXPLORATION
ENDOVASCULAR NEURORESCUE
MEDICAL MANAGEMENT
CEREBRAL HYPERPERFUSION VERSUS MICROEMBOLIC SHOWERS
29
Regional and Local Anesthesia for Carotid Endarterectomy
30 Carotid Endarterectomy or Stenting for Evolving Stroke Secondary
to Carotid Artery Atherosclerosis
THROMBOLYSIS AND CAROTID ENDARTERECTOMY IN ACUTE CERVICAL CAROTID OCCLUSION
CAROTID ARTERY STENTING IN ACUTE CERVICAL CAROTID OCCLUSION
CAROTID ARTERY STENTING FOR EMERGENT REVASCULARIZATION FOR ACUTE ISCHEMIC STROKE
CONCLUSION
31
Timing of Carotid Endarterectomy After Fixed Stroke Secondary to Carotid Artery Atherosclerosis
32
Carotid Occlusion and Near-Carotid Occlusion of the Extracranial Internal Carotid Artery
INTERNAL CAROTID ARTERY OCCLUSION
Acute Occlusion, Asymptomatic
Acute Occlusion, Symptomatic
Chronic Occlusion, Asymptomatic
Chronic Occlusion, Symptomatic
CAROTID STRING SIGN
SUMMARY
33
Blood Pressure Instability After Carotid Endarterectomy
INCIDENCE
ETIOLOGY
TREATMENT
34
Relevance of External Carotid Artery Disease in Internal Carotid Artery Occlusion
ANATOMY OF CEREBRAL COLLATERAL CIRCULATION
EVALUATION OF THE PATIENT WITH SYMPTOMATIC OCCLUSION OF THE INTERNAL CAROTID ARTERY
CURRENT INDICATIONS AND RESULTS OF SURGICAL TREATMENT
TECHNIQUE OF EXTERNAL CAROTID ENDARTERECTOMY
RECOMMENDATIONS
35
Intracranial Occlusive Disease and Aneurysms: Influence on Carotid Revascularization Outcomes
INTRACRANIAL OCCLUSIVE DISEASE
INTRACRANIAL ANEURYSMS
36
Pathology of Carotid Artery Restenosis
DESCRIPTIVE PATHOLOGY
PATHOGENESIS
Cell Proliferation
Extracellular Matrix Synthesis
Thrombus Organization
Artery Wall Remodeling
Predictors of Carotid Restenosis after Endarterectomy
37
Treatment of Recurrent Stenosis After Previous Carotid Endarterectomy
OPTIMAL IMAGING FOR ASSESSMENT OF CAROTID RESTENOSIS
TREATMENT OPTIONS FOR RECURRENT CAROTID ARTERY STENOSIS
Repeat CEA for Recurrent Carotid Stenosis
Other Surgical Options for RecurrentCarotid Stenosis
Endovascular Procedures
Carotid Endarterectomy versus Carotid Artery Stenting
38
Management of Concomitant Carotid and Coronary Arterial Disease
CARDIAC RISK STRATIFICATION PRIOR TO CAROTID ENDARTERECTOMY
CAUSES OF STROKE FOLLOWING CORONARY REVASCULARIZATION
RELATIONSHIP OF CAROTID STENOSIS TO PERIOPERATIVE STROKE
TIMING OF CAROTID AND CORONARY OPERATIONS
CONCOMITANT CAROTID AND CORONARY ARTERY OPERATIONS
STAGED VERSUS COMBINED CAROTID AND CORONARY ARTERY OPERATIONS
CONCLUSION
39
The Role of Extracranial–Intracranial Bypass in Current Practice
HISTORICAL PERSPECTIVE
PROCEDURAL CHARACTERISTICS
Preoperative Evaluation
Procedural Considerations
Postprocedural Follow-up and Management
CURRENT DATA
CONCLUSIONS
40
Open Surgical Treatment of Fibromuscular Dysplasia of the Carotid Artery
OPERATIVE TECHNIQUES
Open Dilation
Resection and Interposition Graft Reconstruction
SURGICAL RESULTS
41
Endovascular Treatment of Fibromuscular Dysplasia of the Carotid Artery
INDICATIONS
TECHNIQUE
RESULTS
SUMMARY
42
Vertebral Artery Reconstruction for Vertebrobasilar Ischemia
PATIENT EVALUATION
INDICATIONS FOR OPERATION
SURGICAL REPAIR
Transposition of the Proximal VA to the Common
Carotid Artery
Proximal Subclavian–Vertebral Bypass
Distal VA Reconstruction (Bypass)
Reconstruction and Decompressionof the VA of the C0–C1 Level
43
Endovascular Angioplasty and Stenting for Proximal Subclavian Artery Stenosis
CLINICAL EVALUATION AND DIAGNOSIS
INDICATIONS FOR TREATMENT
TECHNICAL PRINCIPLES OF ENDOVASCULAR THERAPY
RESULTS OF SUBCLAVIAN ARTERY ANGIOPLASTY AND STENTING
ENDOVASCULAR VERSUS SURGICAL INTERVENTION
CONCLUSION
44
Subclavian to Carotid Arterial Transposition
45
Carotid–Subclavian Bypass and Other Nonanatomic Revascularizations for Proximal Subclavian Artery Stenosis
ANATOMY
CAROTID–SUBCLAVIAN BYPASS
OTHER NONANATOMIC SUBCLAVIAN ARTERY RECONSTRUCTIONS
46
Conventional Surgical and Endovascular Treatment of Innominate Artery Atherosclerosis
CLINICAL PRESENTATION
DIAGNOSIS
TREATMENT
Surgical Techniques
Endovascular Techniques
CONCLUSIONS
47
Extracranial Carotid Artery Aneurysms
TRUE CAROTID ARTERY ANEURYSMS
Incidence
Manifestations
Treatment
TRAUMATIC FALSE ANEURYSMS OF THE CAROTID ARTERY
Incidence
Treatment
FALSE ANEURYSMS FOLLOWING CAROTID ARTERY ENDARTERECTOMY
Incidence
Treatment
48
Carotid Body Tumors
CLINICAL PRESENTATION
DIAGNOSIS
PREOPERATIVE EMBOLIZATION
SURGICAL INDICATIONS
SURGICAL APPROACH
SURGICAL RESULTS
49
Radiation-Induced Arteritis
COMPARISON WITH ARTERIOSCLEROSIS
PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS
Subclavian–Axillary Lesions
Extracranial Cervical Lesions
Abdominal Aorta and Its Branches
MANAGEMENT
Carotid Lesions
Subclavian–Axillary Lesions
Lesions of the Abdominal Aorta and Its Branches
SURVEILLANCE AND PREVENTION
50
Surgical Treatment of Takayasu Arteritis
CLINICAL FEATURES
MEDICAL TREATMENT
SURGICAL TREATMENT
Transluminal Angioplasty
Arterial Reconstruction
Surgical Results
Upper Extremity
Arterial Disease
51
Pathology of Upper Extremity Arterial Disease
VASOSPASM
INTRINSIC ARTERIAL DISEASE
Atherosclerosis
Inflammatory Diseases
Connective Tissue Disorders
Aneurysms
EMBOLISM
TRAUMA
Iatrogenic Injuries
Occupational Trauma
Athletic Injuries
MEDICAL CONDITIONS
52
Upper Extremity Revascularization
DIAGNOSTIC EVALUATION
ENDOVASCULAR TREATMENT
SURGICAL TREATMENT
COMMON APPROACHES TO THE UPPER EXTREMITY VESSELS
Subclavian Artery and Proximal Axillary Artery
Distal Axillary Artery
Brachial, Proximal Radial, and Ulnar Arteries
Distal Arteries
SURGICAL RESULTS
53
Diagnosis and Treatment of Upper Extremity Vasospastic Disease
RAYNAUD’S SYNDROME
Primary Raynaud’s Syndrome
Secondary Raynaud’s Syndrome
Disorders That Mimic Raynaud’s Syndrome
TREATMENT
Conservative Therapy
Pharmacologic Therapy
Lumbar Sympathectomy
54
Extremity Causalgia: Reflex Sympathetic Dystrophy
DIFFERENTIAL DIAGNOSIS
MEDICAL THERAPY
SUMMARY
55
Thoracic Sympathectomy
ANATOMY OF THE CERVICAL AND THORACIC SYMPATHETIC GANGLIA
PHYSIOLOGY OF SYMPATHETIC NERVOUS SYSTEM
Indications for Cervicodorsal Sympathectomy
THERAPEUTIC OPTIONS
Medical Therapy
Surgical Therapy
Conclusion
56
Etiology and Anatomic Pathology of Thoracic Outlet Syndrome
ANATOMY
PATHOPHYSIOLOGY
Neurogenic Thoracic Outlet Syndrome
Venous Thoracic Outlet Syndrome
Arterial Thoracic Outlet Syndrome
SUMMARY
57
Diagnosis of Thoracic Outlet Syndrome
NEUROGENIC THORACIC OUTLET SYNDROME
Clinical Presentation
Physical Examination
VENOUS THORACIC OUTLET SYNDROME
Clinical Presentation
ARTERIAL THORACIC OUTLET SYNDROME
Clinical Presentation
Management and Indications for Surgery
58
Conservative Treatment for Thoracic Outlet Syndrome
ASSESSMENT FOR PHYSICAL THERAPY
COMMENT
59
Transaxillary Operative Management of Thoracic Outlet Syndrome
OPERATIVE TECHNIQUE
60
Supraclavicular Operative Approach for Thoracic Outlet Syndrome
MANAGEMENT OF NEUROGENIC THORACIC OUTLET SYNDROME
Positioning and Initial Exposure
Mobilization of the Scalene Fat Pad
Anterior Scalenectomy
Brachial Plexus Mobilization
Middle Scalenectomy
Division of the Posterior First Rib
Division of the Anterior First Rib
Cervical Rib Resection
Pectoralis Minor Tenotomy
MANAGEMENT OF VENOUS THORACIC OUTLET SYNDROME
MANAGEMENT OF ARTERIAL THORACIC OUTLET SYNDROME
CLOSURE, POSTOPERATIVE CARE, AND RECOVERY
61
Treatment of Arterial Complications in Thoracic Outlet Syndrome
ANATOMIC FEATURES
CLINICAL PRESENTATION
DIAGNOSIS
TREATMENT
62
Subclavian and Axillary Artery Aneurysms
SUBCLAVIAN ARTERY ANEURYSMS
ABCDABERRANT SUBCLAVIAN ARTERY ANEURYSMS
AXILLARY ARTERY ANEURYSMS
DIAGNOSIS AND EVALUATION
OPERATIVE TREATMENT
ENDOVASCULAR REPAIR
RESULTS
63
Buerger’s Disease
DIAGNOSIS
NONOPERATIVE MANAGEMENT
Patient Education
Smoking Cessation
Pharmacologic Therapy
Pain Control
Local Wound Care
OPERATIVE MANAGEMENT
Arterial Reconstruction
Sympathectomy
Amputation
64
Ergotism
PHARMACOLOGY
CLINICAL PRESENTATION OF ERGOTISM
ERGOT ALKALOIDS AND DRUG INTERACTIONS
TREATMENT
65
Hypothenar Hammer Syndrome
PREVALENCE OF DISEASE
ANATOMY AND PATHOPHYSIOLOGY
DIAGNOSTIC EVALUATION
MANAGEMENT
Aortic Aneurysm
66
Pathogenesis of Abdominal Aortic Aneurysms
BIOMECHANICAL WALL STRESS ANDSTRUCTURAL PATHOLOGY
INTRALUMINAL THROMBUS
MATRIX METALLOPROTEINASES AND ENDOGENOUS PROTEASES
AORTIC MEDIAL DECOMPENSATION
INFLAMMATION AND AUTOIMMUNITY
PATHOGEN INVOLVEMENTAND AUTOIMMUNITY
OXIDATIVE STRESS
ADVENTITIAL MODIFICATION
MODELS OF ABDOMINAL AORTIC ANEURYSM AND FUTURE RESEARCH
SUMMARY
67
Genetics of Abdominal Aortic Aneurysms
THE HERITABILITY OF ABDOMINAL AORTIC ANEURYSMS VERSUS THORACIC AORTIC ANEURYSMS
INHERITANCE OF ABDOMINAL AORTIC ANEURYSM
IDENTIFYING GENES ASSOCIATED WITH ABDOMINAL AORTIC ANEURYSMS
LINKAGE STUDIES
GENOME-WIDE ASSOCIATION STUDIES
FUTURE RESEARCH
CONCLUSION
68
Pathogenesis of Inflammatory Aortic Aneurysms
PATHOLOGY
ETIOLOGY
A Severe Variant of Aortic Aneurysm
A Generalized Autoimmune Process
An Immunoglobulin G4–Related Systemic Disease
CONCLUSION
69
Pathophysiology of Aortic Dissection
EARLY ANATOMIC CHANGESIN AORTIC DISSECTION
ISCHEMIC COMPLICATIONSOF AORTIC DISSECTION
FALSE LUMEN EXPANSION
70
Arteriomegaly and Aneurysmosis
ETIOLOGY
CLASSIFICATION
SURGICAL MANAGEMENT
CONCLUSION
71
Vascular Complications of Marfan Syndrome, Ehlers–Danlos Syndrome, and Loeys–Dietz Syndrome
MARFAN SYNDROME
Affected Organ Systems
Treatment
EHLERS–DANLOS SYNDROME
Affected Organ Systems
Treatment
Prognosis
LOEYS–DIETZ SYNDROME
Affected Organ Systems
Treatment
72
Ultrasonography in the Evaluation of Abdominal Aortic Aneurysms
SCREENING FOR ABDOMINAL AORTIC ANEURYSM
ULTRASONOGRAPHIC FOLLOW-UP OF ABDOMINAL AORTIC ANEURYSM
Abdominal Aortic and Iliac Artery Aneurysms
Follow-up after Endovascular Aneurysm Repair
73
Angiography in the Evaluation of Abdominal Aortic Aneurysm
INDICATIONS FOR CATHETER-BASED ARTERIOGRAPHY
PLANNING ABDOMINAL AORTIC ANEURYSM REPAIR
74
Magnetic Resonance Imaging in the Evaluation of Abdominal Aortic Aneurysm
75
Computed Tomography and Computed Tomographic Arteriography in the Evaluation of Abdominal Aortic Aneurysms
DATA SETS
SCAN PARAMETERS
RECONSTRUCTION
INITIAL AORTIC ASSESSMENT
ANALYSIS OF DISEASE EXTENT
ANEURYSM SIZE
ASSESSMENT OF THE PROXIMAL AND DISTAL NECKS
TORTUOSITY
AORTIC BRANCH ASSESSMENT
RELATIONAL BRANCH VESSEL GEOMETRY
AORTIC COMPUTED TOMOGRAPHY AFTER OPEN OR ENDOVASCULAR TREATMENT
76
Selection of Patients with Aortic Aneurysms for Open Surgical or Endovascular Repair
OPEN REPAIR OF ABDOMINAL AORTIC ANEURYSM
ENDOVASCULAR ANEURYSM REPAIR
OPEN VERSUS ENDOVASCULAR ANEURYSM REPAIR: THE DATA
Endovascular versus Open Repair of Abdominal Aortic Aneurysm Trial
Dutch Randomized Endovascular Aneurysm Management Trial
Open Versus Endovascular Repair Trial
The Medicare Population
INTEGRATION OF TRIAL DATA INTO CLINICAL DECISION MAKING
Mortality
Rates of Reintervention
Cost
Quality of Life
EVAR VERSUS MEDICAL MANAGEMENT IN PATIENTSAT TOO-HIGH RISK FOR OPEN REPAIR
SUMMARY
77
Management of Small Abdominal Aortic Aneurysms
RUPTURE RISK
LIFE EXPECTANCY
OPERATIVE RISK
OPERATIVE DECISION MAKING
GROWTH AND MEDICAL MANAGEMENT
SURVEILLANCE RECOMMENDATIONS
78
Endovascular Treatment of Nonruptured Infrarenal Aortic and Aortoiliac Aneurysms
PROCEDURAL PLANNING AND ANATOMIC MEASUREMENTS
DEVICE OVERSIZING
ENDOVASCULAR STENT DEPLOYMENT TECHNIQUES
Imaging
Access
Anatomic Aims
Aortic Neck
Contralateral Limb Cannulation
Iliac Anatomy
LONG-TERM DATA AND FUTURE DIRECTIONS
79
Endovascular Treatment of Pararenal and Suprarenal Abdominal Aortic Aneurysms
TECHNIQUE
LIMITATIONS
PUBLISHED RESULTS
EVOLUTION
80
Endovascular Treatment of Inflammatory Abdominal Aortic Aneurysms
CLINICAL FEATURES
ENDOVASCULAR MANAGEMENT
RUPTURED INFLAMMATORY ABDOMINAL AORTIC ANEURYSMS
SUMMARY
81
Endovascular Treatment of Ruptured Infrarenal Aortic Aneurysms
THEORETICAL CONSIDERATIONS
A SINGLE CENTER EXPERIENCE
COLLECTED WORLD EXPERIENCE
WHY ARE RESULTS VARIABLE?
Standard Approach or Protocol
Fluid Restriction (Hypotensive Hemostasis)
Treatment Site
Anesthesia and Catheter-Guidewire Placement
Supraceliac Aortic Sheath Placementand Balloon Control
Endograft Type and Configuration
Abdominal Compartment Syndrome
Endovascular Aneurysm Repair for Highest-Risk Patients
IS A RANDOMIZED, CONTROLLED COMPARISON OF ENDOVASCULAR AND OPEN REPAIR NEEDED
82
Management of Coexistent Splanchnic and Renal Artery Occlusive Disease
SPLANCHNIC OCCLUSIVE DISEASE AND ENDOVASCULAR ANEURYSM REPAIR
RENAL ARTERY OCCLUSIVE DISEASE AND ENDOVASCULAR ANEURYSM REPAIR
83
Internal Iliac Artery Embolization as an Adjunct to Endovascular Aneurysm Repair
RELEVANT ANATOMY
EMBOLIZATION TOOLS
Pushable Coils
Detachable Coils
Vascular Occlusion Plug
TECHNIQUE
Embolization of Internal Iliac Arteries
COMPLICATIONS
84
Endovascular Iliac Branch Devices for Iliac Aneurysms
RATIONALE
DEVICE DESIGN
DEVICE DEPLOYMENT
RESULTS
DISCUSSION
85
Iliac Artery Conduits for Endovascular Access
ILIAC ARTERY ACCESS
REMOTE FEMORAL ARTERY ACCESS
86
Conversion to Open Surgical Treatment After Failed Endovascular Aortic Aneurysm Repair
INDICATIONS
PREOPERATIVE CONSIDERATIONS
OPERATIVE TECHNIQUES
POSTOPERATIVE CONSIDERATIONS
87 Treatment of Endovascular Leaks After Aortic Endografting
TYPE I ENDOLEAK
TYPE II ENDOLEAK
TYPE III ENDOLEAK
TYPE IV ENDOLEAK
TYPE V ENDOLEAK
CONCLUSIONS
88
Management of Acute Limb Ischemia Complicating Aortic Reconstruction
SCOPE OF THE PROBLEM
ETIOLOGY
PREVENTION
DIAGNOSIS
MANAGEMENT
Medical
Interventional
Open Surgical
89
Intestinal and Renal Ischemia Complicating Open and Endovascular Abdominal Aortic Reconstructions
RENAL COMPLICATIONS
Open Repair
Endovascular Repair
INTESTINAL COMPLICATIONS
Open Repair
Endovascular Repair
90
Neurologic Complications after Open and Endovascular Aortic Surgery
SPINAL CORD INJURY
STROKE
DIRECT NERVE INJURY
Retrograde Ejaculation
Peripheral Neuropathy
91
Postoperative Surveillance of Thoracic and Abdominal Aortic Endografts
RATIONALE FOR POSTOPERATIVE SURVEILLANCE
ELEMENTS OF COMPLETE SURVEILLANCE
Computed Tomography Angiography
Magnetic Resonance Angiography
Multiview Radiographs
Duplex Ultrasound with or without Contrast
Intravascular Pressure Sensor
FOLLOW-UP SCHEDULE
92
Treatment of Aortic Endograft Migration
DEFINITION
INCIDENCE
RISK FACTORS FOR MIGRATION
TREATMENT
Endovascular Treatment
Hybrid Treatment
Open Treatment
93
Open Transperitoneal Surgical Treatment of Nonruptured Infrarenal Aortic Aneurysms
ANATOMIC PREOPERATIVE PLANNING
TECHNIQUE
Exposure
Clamping
Aneurysmorrhaphy
Unclamping
Closure
POSTOPERATIVE CARE
Myocardial Infarction
Bleeding
Acute Pulmonary Decompensation Resulting in Reintubation
Deep Vein Thrombosis
Kidney Dysfunction
Ischemic Colitis
Lower Extremity Ischemia
EARLY SURVIVAL
94
Open Surgical Treatment of Ruptured Infrarenal Aortic Aneurysms
DIAGNOSIS
PROCEDURE
OUTCOMES
95
Surgical Treatment of Infected Abdominal Aortic Aneurysms
DIAGNOSIS
MANAGEMENT
OUTCOMES
96
Surgical Treatment of Inflammatory Abdominal Aortic Aneurysms
CLINICAL PRESENTATION
OPERATIVE MANAGEMENT
97
Open Surgical Treatment of Pararenal and Suprarenal Abdominal Aortic Aneurysms
PRESENTATION AND DIAGNOSIS
OPERATIVE CONSIDERATIONS
OUTCOMES
98
Retroperitoneal Approach for Elective Abdominal Aortic Aneurysmectomy
INDICATIONS AND CONTRAINDICATIONS
SURGICAL TECHNIQUES
Left Posterolateral Retroperitoneal Approach
Right Retroperitoneal Approach
Retroperitoneal Exposure for Failed Endovascular Aneurysm Repair
OUTCOMES
99
Autotransfusion in Aortic Reconstruction
AUTOLOGOUS PREOPERATIVE DEPOSIT
INTRAOPERATIVE AUTOTRANSFUSION IN ELECTIVE AND EMERGENCY AORTIC PROCEDURES
INDICATIONS FOR TRANSFUSION
100
Surgical Treatment of Abdominal Aortic Aneurysm–Inferior Vena Cava Fistula
CLINICAL PRESENTATION
SURGICAL TREATMENT
101
Management of Primary Aortoenteric Fistulas
ETIOLOGY
DIAGNOSIS
TREATMENT
102
Renal Ectopia and Renal Fusion in Patients Requiring Abdominal Aortic Operations
EMBRYOLOGY
ANATOMIC SUBGROUPS OF RENAL ECTOPIA
Ipsilateral Renal Ectopia
Horseshoe Kidney
Crossed Renal Ectopia
PREOPERATIVE IMAGING
THERAPEUTIC ALTERNATIVES
Open Surgical Approach
Open Surgical Technique
Endovascular Approaches
COMPLICATIONS AND RESULTS
103
Venous Anomalies Encountered During Aortic Reconstruction
RETROAORTIC OR CIRCUMAORTIC LEFT RENAL VEIN
TRANSPOSED OR DUPLICATE INFERIOR VENA CAVA
104
Open and Endovascular Repair of Abdominal Aortic Aneurysms in Kidney Transplant Patients
INDICATIONS
RENAL PROTECTION
Preoperative Measures
Intraoperative Techniques
OPEN AORTIC RECONSTRUCTION
Technique
Complications
Follow-up
ENDOVASCULAR AORTIC RECONSTRUCTION
Technique
Complications
Follow-up
RUPTURED ABDOMINAL AORTIC ANEURYSM IN KIDNEY TRANSPLANT PATIENTS
105
Open Abdominal Aortic Aneurysm Repair and Concurrent Nonvascular Disease
SYNCHRONOUS DISEASE
GALLBLADDER AND HEPATOBILIARY DISEASE
PANCREATIC DISEASE
UPPER GASTROINTESTINAL TRACT
LOWER GASTROINTESTINAL TRACT
GENITOURINARY TRACT
GYNECOLOGIC DISEASE
RARE TUMORS AND SPINE DISORDERS
ABDOMINAL WALL
106
Recognition and Treatment of Abdominal Compartment Syndrome Following Ruptured Abdominal Aortic Aneurysm Repair
DETECTION
PATHOPHYSIOLOGY
Cardiovascular Derangements
Pulmonary Derangements
Renal Derangements
Gastrointestinal Derangements
Hepatic Derangements
Central Nervous System Derangements
Abdominal Wall Derangements
RISK FACTORS
CLINICAL PRESENTATION
CURRENT MANAGEMENT
Nonsurgical Management
Surgical Management
Outcome after Surgical Management
107
Endovascular Treatment of Thoracic Aortic Aneurysms
STENT GRAFTS
INDICATIONS
TECHNIQUE
RESULTS
108
Endovascular Graft Completion of Elephant Trunk Thoracic Aneurysm Repair
SECOND-STAGE ENDOVASCULAR PROCEDURE
RESULTS
109
Thoracic and Abdominal Aortic Debranching in the Endovascular Treatment of Thoracoabdominal Aortic Aneurysms
AORTIC ARCH AND PROXIMAL DESCENDING AORTIC ANEURYSM DEBRANCHING
ASCENDING, ARCH, AND MORE EXTENSIVE ANEURYSMS
DEBRANCHING OF THORACOABDOMINAL ANEURYSMS
Thoracoceliac with Thoracomesenteric–Left Renal Bypass (Antegrade Bypass)
Iliomesenteric Reconstructions (Retrograde Bypass)
Complete Visceral Revascularization (Retrograde)
POSTOPERATIVE CONSIDERATIONS
110
Endograft (VORTEC) Reconstruction of Aortic Branches Allowing Endovascular Treatment of Aortic Aneurysms
ORIGINAL TECHNIQUE
INCISION AND TRANSECTION TECHNIQUES
RESULTS
DISCUSSION
111
Multibranched Endovascular Repair of Thoracoabdominal Aortic Aneurysm
MULTIBRANCHED THORACOABDOMINAL STENT GRAFTS
STANDARDIZATION
STANDARD STENT GRAFT
PLANNING THE REPAIR
ADJUNCTIVE PROCEDURES
STENT GRAFT IMPLANTATION
RADIATION SAFETY
RESULTS
112
Open Surgical Treatment of Thoracic Aortic Aneurysms
INDICATIONS FOR REPAIR
OPERATIVE PLANNING
Comorbidity Assessment
MEASURES FOR END-ORGAN PROTECTION
Extracorporeal Circulation by Atriofemoral Perfusion
Hypothermic Arrest
Alternative Perfusion Techniques
Spinal cord protection
SURGICAL TECHNIQUE
POSTOPERATIVE MANAGEMENT
SURGICAL RESULTS
113
Open Surgical Treatment of Thoracoabdominal Aortic Aneurysms
CLASSIFICATION OF THORACOABDOMINAL AORTIC ANEURYSMS
CLINICAL MANIFESTATIONS
OPEN SURGICAL TECHNIQUE
RISK OF IMMEDIATE NEUROLOGIC DEFICIT
RISK OF DELAYED NEUROLOGIC DEFICIT
RISK OF KIDNEY DYSFUNCTION
POSTOPERATIVE GASTROINTESTINAL COMPLICATIONS
SURVIVAL AND LONG-TERM OUTCOMES
114
Paraplegia Prevention in Thoracic and Thoracoabdominal Aortic Aneurysm Repair
ASSISTED CIRCULATION
INTERCOSTAL REIMPLANTATION
MOTOR EVOKED POTENTIALS
HYPOTHERMIA
CEREBROSPINAL FLUID DRAINAGE
ENDOGRAFT THORACIC AND THORACOABDOMINAL AORTIC ANEURYSM REPAIR
115
Nonoperative Medical Management of Acute Aortic Dissection
EPIDEMIOLOGY
CLINICAL SIGNS AND SYMPTOMS
INITIAL MEDICAL THERAPY
ASCENDING AORTA
DESCENDING AORTA
LONG-TERM FOLLOW-UP
116 Endovascular Treatment of Aortic Dissection
ROLE OF IMAGING
VASCULAR ACCESS
EXCLUDING THE FALSE LUMEN
MALPERFUSION
CHRONIC AORTIC DISSECTION
117
Open Surgical Treatment of Aortic Dissection
CLASSIFICATION
OPERATIVE TREATMENT
Surgery for Acute Proximal Aortic Dissection
Surgery for Chronic Proximal Aortic Dissection
Surgery for Acute Distal Aortic Dissection
Surgery for Chronic Distal Aortic Dissection
POSTOPERATIVE CARE
118
Natural History and Open Treatment of Isolated Iliac Artery Aneurysms
EPIDEMIOLOGY
CLINICAL FINDINGS
DIAGNOSIS
NATURAL HISTORY
INDICATIONS FOR TREATMENT
TREATMENT
POSTOPERATIVE CARE
119
Endovascular Management of Isolated Iliac Artery Aneurysms
PREOPERATIVE PLANNING AND IMAGING
OPERATIVE TECHNIQUE
RESULTS
ISOLATED INTERNAL ILIAC ARTERY ANEURYSMS
FUTURE THERAPY
120
Long-Term Alterations in Large-Caliber Arterial Prostheses Used for Aortic Repair
EARLY HOST RESPONSES TO IMPLANTED MATERIALS
Protein Deposition
Platelet Deposition and Coagulation
Inflammation
Mesenchymal Cell Infiltration
MID- TO LONG-TERM PROSTHETIC HEALING
LONG-TERM PHYSICAL ALTERATIONS
Dilatation
Other Changes
121 Surgical Treatment
of Pediatric Abdominal Aortic Aneurysms
ETIOLOGIES
SURGICAL OPTIONS
Lower Extremity
Aneurysm
122 Arteriosclerotic
Femoral Artery Aneurysms
PATHOGENESIS
PATTERN OF DISEASE
NATURAL HISTORY
CLINICAL PRESENTATION
DIAGNOSIS
MANAGEMENT
RESULTS
123
Infected Femoral Artery False Aneurysms
ETIOLOGY
PRESENTATION AND DIAGNOSIS
TREATMENT
Ligation
Reconstruction
124
Obturator Foramen Bypass Grafts in Groin Sepsis
PATIENT SELECTION
OPERATIVE PROCEDURE: ANATOMIC CONSIDERATIONS
RESULTS
125
Open Surgical Treatment of Popliteal Artery Aneurysms
CLINICAL PRESENTATION
DIAGNOSIS AND IMAGING
SURGICAL MANAGEMENT
SURVEILLANCE
126
Endovascular Treatment of Popliteal Artery Aneurysms
PREOPERATIVE EVALUATION
CONTRAINDICATIONS FOR ENDOVASCULAR REPAIR
STENT GRAFTS
ENDOVASCULAR PROCEDURE AND FOLLOW-UP
RESULTS OF ENDOVASCULAR REPAIR
Aortoiliac
Occlusive Disease
127 Conventional Arteriography, Magnetic Resonance Angiography, and Computed Tomographic Arteriography of
Aortoiliac Occlusive Disease
DIGITAL SUBTRACTIONARTERIOGRAPHY
COMPUTED TOMOGRAPHY ANGIOGRAPHY
MAGNETIC RESONANCE ANGIOGRAPHY
CONCLUSION
128
Physiologic and Noninvasive Studies to Document Severity and Extent of Aortoiliac Occlusive Disease
SYMPTOMS AND SIGNS
EXTREMITY PRESSURE MEASUREMENTS AND DOPPLER ANALYSIS
DUPLEX ULTRASONOGRAPHY
129
Selecting Treatment for Patients with Aortoiliac Occlusive Disease
CONSERVATIVE MEDICAL TREATMENT
CRITERIA INFLUENCING CHOICE OF REVASCULARIZATION TECHNIQUES
Patient Factors
Operator and Resource Factors
Anatomic and Technical Factors
CONCLUSIONS
130
Percutaneous Arterial Angioplasty with and without Stenting for Atherosclerotic Aortic and Iliac Artery Occlusive Disease
INDICATIONS
TECHNIQUE
RESULTS
131
Aortofemoral Bypass for Atherosclerotic Aortoiliac Occlusive Disease
PROCEDURE SELECTION
OPERATIVE MANAGEMENT
Operative Approach
Tunnel Construction
Proximal Graft Anastomosis
Femoral Anastomosis
RESULTS OF AORTOFEMORAL BYPASS GRAFTS
132
Endarterectomy for Atherosclerotic Aortoiliac Occlusive Disease
OPERATIVE TECHNIQUE
RESULTS
133
Management of Juxtarenal Aortic Occlusive Disease by Retroperitoneal and Transperitoneal Exposure of the Pararenal and Suprarenal Aorta
TRANSPERITONEAL EXPOSURE OF THE SUPRACELIAC AORTA AND CELIAC ARTERY
TRANSPERITONEAL APPROACH TO SUPERIOR MESENTERIC ARTERY AND PARARENAL AORTA
LEFT RETROPERITONEAL APPROACH TO THE ABDOMINAL AORTA
TRANSPERITONEAL APPROACH TO THE COMPLETE ABDOMINAL AORTA WITH LEFT MEDIAL VISCERAL ROTATION
DISCUSSION
134
Acute Aortic Occlusion
ETIOLOGY
CLINICAL PRESENTATION AND DIAGNOSIS
PRINCIPLES OF MANAGEMENT
PREOPERATIVE EVALUATION
OPERATIVE PLANNING
THROMBOEMBOLECTOMY
AXILLOBIFEMORAL AND AORTOBIFEMORAL BYPASS
PERCUTANEOUS ENDOVASCULAR TREATMENT
ADEQUACY OF REVASCULARIZATION AND ADJUNCTIVE PROCEDURES
ISCHEMIA AND REPERFUSION INJURY
OUTCOME
135
Aortic Graft Limb Occlusion
ETIOLOGY
CLINICAL PRESENTATION
MANAGEMENT
Open Surgical Treatment
Surgical Technique
Interventional Management
RESULTS
136
Open and Endovascular Treatment of Anastomotic Aneurysms after Aortoaortic, Aortoiliac, and Aortofemoral Bypass
INCIDENCE
PATHOPHYSIOLOGY
PRESENTATION
EVALUATION AND DIAGNOSIS
OPEN SURGICAL TREATMENT
ENDOVASCULAR TREATMENT
RESULTS
137
Combined Laparoscopic and Endovascular Treatment of Aortic Diseases
OPERATIVE TECHNIQUE
LAPAROSCOPIC REMODELLING OF THE AORTA AFTER ENDOVASCULAR ANEURYSM REPAIR
EXCLUSION CRITERIA FOR LAPAROSCOPIC REMODELING AFTER ENDOVASCULAR ANEURYSM REPAIR
LAPAROSCOPY-ASSISTED THORACIC ENDOVASCULAR ANEURYSM REPAIR
RESULTS OF HYBRID PROCEDURES AND LAPAROSCOPIC TECHNIQUES AFTER ENDOVASCULAR ANEURYSM REPAIR
DISCUSSION
THE ROLE OF LAPAROSCOPIC AORTIC SURGERY
138
Abdominal Aortic Coarctation and Hypoplasia
ETIOLOGY
CLINICAL MANIFESTATIONS
MANAGEMENT
RESULTS
139
Descending Thoracic Aorta to Femoral Bypass
INDICATIONS
SURGICAL TECHNIQUE
RESULTS
140
Axillofemoral Bypass
GENERAL PRINCIPLES AND PATIENT SELECTION
PREOPERATIVE EVALUATION
TECHNIQUE
POSTOPERATIVE CARE ANDFOLLOW-UP
RESULTS AND INFLUENCE OF PATIENT AND GRAFT FACTORS
CONTINUING EVOLUTION OF THE ROLE OF AXILLOFEMORAL BYPASS
141
Unilateral Retroperitoneal Iliofemoral Bypass
TREATMENT ALGORITHM FOR ILIAC OCCLUSIVE DISEASE
RETROPERITONEAL ILIOFEMORAL BYPASS: SURGICAL TECHNIQUE
RESULTS
142
Femorofemoral Bypass for Aortoiliac Occlusive Disease
GENERAL PRINCIPLES AND PATIENT SELECTION
PREOPERATIVE EVALUATION
TECHNIQUE
POSTOPERATIVE CARE ANDFOLLOW-UP
RESULTS AND INFLUENCE OF PATIENT AND GRAFT FACTORS
CONTINUING EVOLUTION OF THE ROLE OF FEMOROFEMORAL BYPASS
143
Diagnosis of Aortic Graft Infection
PRESENTATION
DIAGNOSISThe diagnosis of aortic graft
Computed Tomography
Magnetic Resonance Imaging
Sinography
Endoscopy
Other Techniques
CONCLUSIONS
144
Treatment of Aortic Graft Infection with Autologous Femoral Vein
GRAFT EXCISION
OPTIONS FOR RECONSTRUCTION
Extraanatomic Reconstruction
In-Situ Reconstruction
PREOPERATIVE EVALUATION
SURGICAL MANAGEMENTAND TECHNIQUE
POSTOPERATIVE CARE ANDFOLLOW-UP
145
In-Situ Treatment of Aortic Graft Infection with Prosthetic Grafts and Allografts
ANTIBIOTIC OR SILVER-COATED PROSTHETIC GRAFTS
CRYOPRESERVED ARTERIAL ALLOGRAFTS
PROSTHETIC GRAFT PRESERVATION
146
Aortic Graft–Enteric Fistula
PRESENTATION
PREOPERATIVE EVALUATION
MANAGEMENT
The Stable Patient
The Unstable Patient
147
Vasculogenic and Postoperative Neurogenic Impotence
NORMAL ERECTILE AND EJACULATORY FUNCTION
VASCULOGENIC ERECTILE DYSFUNCTION
CORRELATION BETWEEN ERECTILE DYSFUNCTION AND CARDIOVASCULAR DISEASE
THE METABOLIC SYNDROME AND ERECTILE DYSFUNCTION
POSTOPERATIVE NEUROGENIC SEXUAL DYSFUNCTION
CONCLUSION
148
Drug Therapy of Erectile Dysfunction
BASIC PRINCIPLES
PHOSPHODIESTERASE 5 INHIBITORS
PENILE INJECTION THERAPY
INTRAURETHRAL ALPROSTADIL
TESTOSTERONE
NONDRUG TREATMENTS FOR ERECTILE DYSFUNCTION
Vacuum Constriction Devices
Penile Implants
THE PRINCETON GUIDELINES
149
Management of Groin Lymphocele and Lymph Fistula
INCIDENCE
CLINICAL PRESENTATION AND DIAGNOSIS
PREVENTION
TREATMENT
Treatment Options
Operative Technique
150
Management of Chyloperitoneum and Chylothorax after Aortic Reconstruction
LYMPHATIC ANATOMY IN THE ABDOMEN AND THORAX
DIAGNOSIS OF CHYOPERIOTNEUM AND CHYLOTHORAX
MANAGEMENT OF CHYLOPERITONEUM AND CHYLOTHORAX
SUMMARY
151
Coronary Artery Disease in Patients with Aortoiliac Occlusive Disease and Abdominal Aortic Aneurysm
IMPORTANCE OF CORONARY ARTERY DISEASE
PREOPERATIVE CARDIAC RISK ASSESSMENT
POSTOPERATIVE CARE
152
Pulmonary Risks in Patients Being Treated for Aortic Aneurysms and Occlusive Disease
PULMONARY COMPLICATIONS OF OPEN VASCULAR SURGERY
IMPACT OF PULMONARY COMPLICATIONS FOLLOWING OPEN ABDOMINAL AORTIC ANEURYSM REPAIR ON PATIENT OUTCOMES
APPROACHES TO REDUCE PULMONARY COMPLICATIONS VASCULAR SURGERY
Endovascular Repair
Anesthesia Technique
Administration of Prophylactic Noninvasive Perioperative Ventilation
RISK FACTORS FOR PULMONARY COMPLICATIONS
MODIFICATION OF RISK FACTORS
CONCLUSIONS
153
The Metabolic Syndrome in the Modern World
DEFINITION
ETIOLOGY
Obesity
Hypertension: The Role of Adipocytes
Atherosclerosis: Disturbed Endothelium andthe Inflammatory Process
TREATMENT
Hypertension
Hyperlipidemia
Insulin Resistance
154
Smoking as a Risk Factor in Atherosclerotic Cardiovascular Disease
PATHOPHYSIOLOGY
Vasomotor Dysregulation
Inflammation
Thrombosis
Metabolism
EVIDENCE IN CARDIOVASCULAR DISEASE
Coronary Heart Disease
Cerebrovascular Disease
Aortic Aneurysm
Peripheral Arterial Disease
SMOKING CESSATION
CONCLUSIONS
155
Smoking Cessation
IDENTIFYING SMOKERS
MOTIVATING PATIENTS TO QUIT
HELPING THOSE WHO WISH TO QUIT
SUCCESSFUL STRATEGIES
156
Treatment of Dyslipidemia and Hypertriglyceridemia
RISK ASSESSMENT AND LDL CHOLESTEROL GOALS
GOALS FOR NON-HDL CHOLESTEROL
DIET AND EXERCISE GUIDELINES AND RECOMMENDATIONS
PHARMACOTHERAPY FOR HIGH LDL CHOLESTEROL
PHARMACOTHERAPY FOR LOWNON-HDL CHOLESTEROL
ADVERSE EFFECTS OF LIPID TREATMENT
157
Hypertension as a Risk Factor in Atherosclerotic Cardiovascular Disease
MEASUREMENT OF BLOOD PRESSURE IN THE OFFICE
MEASUREMENT OF BLOOD PRESSURE IN THE HOSPITAL
HYPERTENSION AND CARDIOVASCULAR RISK
TREATMENT OF HYPERTENSION
Initial Treatment
Combination Therapies
Therapeutic Blood Pressure Targets
158
Homocysteine as a Risk Factor in Atherosclerotic Cardiovascular Disease
NOMENCLATURE
PATHOPHYSIOLOGY
HOMOCYSTEINE AND PERIPHERAL VASCULAR DISEASE EXPRESSION
Aortic Disease
Cervical Artery Disease
Peripheral Artery Occlusive Disease
TREATMENT
159
Nitric Oxide and Vascular Disease
PHYSIOLOGY OF NITRIC OXIDE IN THE VASCULATURE
PATHOPHYSIOLOGY OF NITRIC OXIDE IN THE VASCULATURE
Atherosclerosis
Restenosis
Hypertension
Angiogenesis
CONCLUSIONS
160
Integrative Therapies in Vascular Disease
DIET
EXERCISE
SMOKING CESSATION
MIND–BODY CONNECTION
NATURAL PRODUCTS FOR PERIPHERAL ARTERIAL DISEASE
Ginkgo biloba Leaf Extract
Inositol Nicotinate
Propionyl-l-Carnitine
Padma 28
Policosanol
l-Arginine
Mesoglycan
Others
NATURAL PRODUCTS FOR PERIPHERAL VENOUS DISEASE
Hesperidin
Horse Chestnut Seed Extract (Aesculus hippocastanum)
Grape Seed Extract (Vitis vinifera)
Rutin
Gotu Kola Extract (Centella asiatica)
Pycnogenol (Pinus pinaster)
Others
SURGICAL ISSUES RELATED TO NATURAL PRODUCTS
Coagulation Issues
Sedative–Hypnotic Interactions
Drug–Herb Interactions
CARDIAC EFFECTS OF NONCARDIAC HERBS
CONCLUSION
Lower Extremity
Occlusive Disease
161
Magnetic Resonance Arteriography for Assessment of Infrainguinal Occlusive Disease
FUNDAMENTAL PRINCIPLESOF MAGNETIC RESONANCEARTERIOGRAPHY
CLINICAL EXPERIENCE WITHMAGNETIC RESONANCEARTERIOGRAPHY
162
Doppler Pressure Evaluation of Infrainguinal Occlusive Disease
PHYSIOLOGY OF ARTERIAL OBSTRUCTION
TECHNIQUE
ANKLE PRESSURE MEASUREMENT
SEGMENTAL LIMB PRESSURE MEASUREMENT
EXERCISE TESTING
TOE PRESSURES
LIMITATIONS
SUMMARY
163
Duplex Imaging of Infrainguinal Occlusive Disease
EQUIPMENT AND TECHNIQUE
VELOCITY WAVEFORMS AND CRITERIA DEFINING STENOSES
CLINICAL APPLICATIONS
Color Flow Duplex Scanning in Preparationfor Endovascular Therapy
Arterial Duplex Mapping Instead of Arteriography before Operation
Arterial Duplex-Guided Endovascular Therapy
164
Intravascular Ultrasound for Imaging of Diseased Arteries
INTRAVASCULAR ULTRASOUND IMAGING
CLINICAL UTILITY
ANGIOPLASTY
ATHERECTOMY
STENT DEPLOYMENT
ABDOMINAL ENDOLUMINAL GRAFTS
THORACIC ENDOLUMINAL GRAFTS
165
Selecting Patients for Open Surgical or Endovascular Treatment of Lower Extremity Occlusive Disease
PATIENT SELECTION FOR TREATMENT AND THERAPEUTIC OPTIONS
ENDOVASCULAR INTERVENTIONS
OPEN SURGICAL PROCEDURES
166
Percutaneous Angioplasty With and Without Stenting for Lower Extremity Occlusive Disease
SUPERFICIAL FEMORAL ARTERY
Angioplasty
Angioplasty with Stenting
POPLITEAL ARTERY
Angioplasty
Stenting
INFRAPOPLITEAL ARTERIES
Angioplasty
Stenting
167
Subintimal Recanalization for Lower Limb Occlusive Disease
TECHNIQUE
OUTCOMES
168
Endovascular Grafts in the Treatment of Lower Extremity Occlusive Disease
INDICATIONS
TECHNIQUE
RESULTS
169
Percutaneous Cryoplasty and Laser Treatment of Lower Extremity Occlusive Disease
LASER PHYSICS
LASER EFFECTS ON TARGET TISSUE
SPECIFIC LASER SYSTEMS
Yttrium–Aluminum–Garnet Laser
Argon Laser
CO2 Laser
Excimer Laser
CLINICAL APPLICATION OF LASER ANGIOPLASTY
CRYOPLASTY
170
Duplex-Guided Balloon Angioplasty for Infrainguinal Arterial Occlusive and Aneurysmal Disease
DUPLEX-GUIDED INFRAINGUINAL ARTERIAL ANGIOPLASTY
Preoperative Evaluation
Technique
Technical Success and Predictors of Technical Failure
Thromboembolic Complications
Adjunctive Infrapopliteal Balloon Angioplasty
Follow-up, Patency, and Limb Salvage
DUPLEX-GUIDED ENDOVASCULAR REPAIR OF POPLITEAL ARTERY ANEURYSMS
Technique
Follow-up, Patency, Morbidity, and Mortality
CONCLUSION
171
Reversed and Nonreversed Transposed Autogenous Vein Grafting for Atherosclerotic Lower Extremity Occlusive Disease
PATIENT SELECTION AND PREOPERATIVE EVALUATION
OPERATIVE TECHNIQUE
POSTOPERATIVE CARE
RESULTS
172
Short Vein Grafts from the Distal Superficial Femoral, Popliteal, or Infrapopliteal Arteries to More Distal Arteries for Limb Salvage
GENERAL CONSIDERATIONS
IMPROVED GRAFT PATENCY RATES
DECREASED INCIDENCEOF VEIN GRAFT STENOSES
INCREASED VEIN UTILIZATION
FEWER VEIN HARVEST COMPLICATIONS
OTHER ADVANTAGES
DISADVANTAGES
173
In-Situ Saphenous Vein Graft for Lower Extremity Occlusive Disease
OPERATIVE TECHNIQUE
Preparation
Equipment
Procedure
TECHNICAL COMMENTARY
POSTOPERATIVE FOLLOW-UP
174
Arm Veins for Lower Extremity Arterial Reconstruction
ANATOMY
PREOPERATIVE ASSESSMENT
INDICATIONS AND CONTRAINDICATIONSFOR ARM VEIN GRAFTS
OPERATIVE TECHNIQUE
Harvesting of the Vein
Implantation
RESULTS
COMPLICATIONS AND MANAGEMENT
COMMENTS
175
Composite Sequential Bypass for Lower Extremity Occlusive Disease
INDICATIONS
TECHNIQUE
RESULTS
176
Expanded Polytetrafluoroethylene and Dacron Grafts for Atherosclerotic Lower Extremity Occlusive Disease
INDICATIONS FOR PROSTHETIC BYPASS
DATA
TECHNICAL CONSIDERATIONS
CONCLUSIONS
177
Human Umbilical Vein and Other Biografts for Atherosclerotic Lower Extremity Occlusive Disease
HUMAN UMBILICAL VEIN GRAFTS
Technical Features
Patency Data
Comparative Studies
Complications
CRYOPRESERVED VASCULAR CONDUITS
Preparation of the Allograft
Immunology
Clinical Outcomes
Complications
Infected Field
COLD-PRESERVED VESSELS
BOVINE GRAFTS
CONCLUSIONS
178
Deep Femoral Patch Angioplasty for Atherosclerotic Occlusive Disease of the Lower Extremity
INDICATIONS
TECHNIQUES
179
Superficial Femoral Artery Endarterectomy for Atherosclerotic Lower Extremity Occlusive Disease
OPEN ENDARTERECTOMY
SEMICLOSED ENDARTERECTOMY
COMPARISON OF ENDARTERECTOMY TO BYPASS
ENDARTERECTOMY IN PERSPECTIVE
INDICATIONS
180
Percutaneous Mechanical Thrombectomy and Fibrinolytic Therapy for Acute Thrombosis of Lower Extremity Arteries and Grafts
PERCUTANEOUS MECHANICAL THROMBECTOMY DEVICES
MECHANISMS OF CLOT FORMATION AND DISSOLUTION
FIBRINOLYTIC AGENTS
INDICATIONS FOR THROMBOLYTIC THERAPY
Patient Selection
Lesion Selection
TECHNIQUES OF THROMBOLYSIS
Initiation of Thrombolytic Therapy
RESULTS
COMPLICATIONS
181
Operative Thrombectomy for Acute Thrombosis of Lower Extremity Bypass Grafts
PREOPERATIVE PLANNING
TECHNIQUE
182
Surveillance of Lower Extremity Bypass Grafts
MECHANISMS AND HEMODYNAMICS OF GRAFT FAILURE
ESSENTIALS OF GRAFT SURVEILLANCE
183
Open Surgery and Endovascular Management of Failing Infrainguinal Bypass Graft
PATHOLOGY OF THE FAILING VEIN GRAFT
FACTORS INFLUENCING REPAIR CHOICE
Time after Graft Implantation
Stenosis Length
Lesion Location
Graft Occlusion
TECHNICAL CONSIDERATIONSFOR REPAIR
Endovascular Repair
Open Operation
OUTCOMES
CONCLUSIONS
184
Complications and Treatment of Persistent Sciatic Arteries
CLINICAL CHARACTERISTICS
DIAGNOSTIC CONSIDERATIONS
TREATMENT
185
Popliteal Artery Adventitial Cystic Disease
ETIOLOGY
CLINICAL PRESENTATION
DIAGNOSIS
TREATMENT
186
Chronic Compartment Syndrome and Functional Popliteal Artery Entrapment
EVALUATION
TREATMENT
Chronic Compartment Syndrome
Popliteal Entrapment
Recovery
RESULTS AND DISCUSSION
187
Exercise in Peripheral Arterial Disease
SYSTEMIC DISEASES ALWAYS REQUIRE SYSTEMIC CARE
EFFICACY OF EXERCISE TRAINING
SCIENCE AND MECHANISMS OF EXERCISE BENEFIT
Blood Flow
Change in Muscle Metabolism
Inflammation and Muscle Injury
Changes in Microcirculation and Endothelial Function
Hemorheologic Response
Walking Economy
CLAUDICATION TRAINING TREATMENT PROTOCOL
EFFECT OF EXERCISE ON ATHEROSCLEROSIS RISK FACTORS
ALL CLAUDICATION THERAPIES ARE EFFECTIVE AND CAN BE USED TOGETHER
POTENTIAL OBSTACLES TO THERAPEUTIC SUCCESS
CONCLUSIONS
188
Pharmacologic Management of Intermittent Claudication
NATURE OF THE PROBLEM
CONCOMITANT CORONARY ARTERY DISEASE
RHEOLOGIC AGENTS
VASODILATOR THERAPY
ADDRESSING ENDOTHELIAL DYSFUNCTION
CONCLUSION
189
Cutaneous Ulcers in the Neuroischemic Diabetic Foot
ETIOLOGY AND PATHOPHYSIOLOGY
DISTRIBUTION
CLASSIFICATION OF DIABETICFOOT ULCERS
REVASCULARIZATION
ACHIEVING ULCER CLOSURE
190
Lumbar Sympathectomy for Lower Extremity Ischemic Ulcers
ANATOMY AND PHYSIOLOGY
CLINICAL RESULTS
INDICATIONS AND PATIENT SELECTION
SURGICAL TECHNIQUE
COMPLICATIONS
RECOMMENDATIONS
191
Biologic Therapies for Patients with Critical Limb Ischemia
GENE THERAPY TRIALS
STEM CELL THERAPY TRIALS
SUMMARY
192
Bone Marrow Stem Cell Treatment for Critical Limb Ischemia
CELL BIOLOGY OF VASCULOGENESIS
PIONEERING WORK
CURRENT CLINICAL TRIALS
193
Prothrombotic States and Vascular Thromboses
ANTITHROMBIN III DEFICIENCY
PROTEIN C AND S DEFICIENCY
ANTIPHOSPHOLIPID SYNDROME
FACTOR V LEIDEN
PROTHROMBIN G20210A MUTATION
HEPARIN-INDUCED THROMBOCYTOPENIA AND THROMBOSIS
GUIDELINES
194
Role of Antithrombotic Drugs in Maintaining Graft Patency
PLATELET INHIBITORS
Cilostazol
Aspirin
Thienopyridines
Clopidogrel
Glycoprotein IIb/IIIa Antagonists
Dextran-like Compounds
Bleeding Risks with Antiplatelet Agents
ANTICOAGULATION
Vitamin K Antagonists
Vitamin K Antagonists Plus Aspirin
CONCLUSION
195
Complications of Heparin Anticoagulation Therapy
NONBLEEDING COMPLICATIONS
Heparin-Induced Thrombocytopenia
Heparin-Induced Osteoporosis
Heparin-Induced Skin Lesions
BLEEDING COMPLICATIONS
CONCLUSIONS
Embolic Diseases of
the Extremities
196 Arterial Macroembolism
DIAGNOSIS AND ANATOMY
PERIOPERATIVE AND POSTOPERATIVE MEDICAL THERAPY
OPERATIVE SETTING AND TECHNIQUES
POSTOPERATIVE MANAGEMENT AND COMPLICATIONS
197
Paradoxical Embolism
PATHOPHYSIOLOGY
DIAGNOSIS
TREATMENT
198
Atheroembolism
PATHOGENESIS
CLINICAL SYNDROMES
CLINICAL PICTURES
EVALUATION
TREATMENT
199
Operative Revascularization for Trash Foot
CLINICAL PRESENTATIONAND DIAGNOSIS
MEDICAL THERAPY AND THROMBOLYSIS
PEDAL AND PERIMALLEOLAR THROMBOEMBOLECTOMY
PEDAL ARTERY BYPASS
200
Anticoagulant and Lytic Therapy for Arterial Thromboembolism in Extremities
PERIOPERATIVE MANAGEMENT
THROMBOLYSIS AND RESULTS
Pharmacology of Fibrinolytic Agents
Outcome Studies of Thrombolysis versusPrimary Operation
New-Generation Fibrinolytics
THROMBECTOMY DEVICES
POSTINTERVENTION TREATMENT
CONCLUSIONS
201
Balloon Catheter Embolectomy for Macroembolization in the Extremities
PREOPERATIVE DIAGNOSIS AND MANAGEMENT
OPERATIVE TECHNIQUE
OPERATIVE ADJUNCTS
OUTCOMES
202
Noninvasive Methods of Diagnosing Cardiac and Noncardiac Sources of Macroemboli
ECHOCARDIOGRAPHY
DIAGNOSTIC VASCULAR LABORATORY STUDIES
COMPUTED TOMOGRAPHY AND MAGNETIC RESONANCE IMAGING
DIAGNOSTIC APPROACH TOA PATIENT WITH PERIPHERAL ARTERIAL EMBOLI
Amputation
203
Minor Amputations
INDICATIONS
SURGICAL TECHNIQUE
Transphalangeal Toe Amputation
Transmetatarsal (Ray) Toe Amputation
Transmetatarsal Foot Amputation
POSTOPERATIVE MANAGEMENT
COMPLICATIONS
OUTCOMES
204
Below-Knee Amputation
DETERMINING AMPUTATION LEVEL
SURGICAL TECHNIQUE
POSTOPERATIVE CARE
RESULTS AND COMPLICATIONS
205
Above-Knee Amputation and Hip Disarticulation
ABOVE-KNEE AMPUTATION
Indications
Operative Technique
Postoperative Care and Perioperative Outcome
Long-Term Outcome
HIP DISARTICULATION
206
Upper Extremity Amputations
SHOULDER DISARTICULATION
TRANSHUMERAL AMPUTATION
TRANSRADIAL AMPUTATION
KRUKENBERG AMPUTATION
WRIST DISARTICULATION
207
Rehabilitation of the Amputee
BEFORE AMPUTATION
AMPUTATION LEVEL
POSTOPERATIVE RESIDUAL LIMB MANAGEMENT AND THERAPY
PROSTHETIC RESTORATION
Vascular Trauma
208 Conventional and
Computed Tomographic Arteriography in Penetrating Vascular Injuries
IMAGING FOR PENETRATINGVASCULAR INJURIES OF THE NECK
IMAGING FOR PENETRATINGVASCULAR INJURIES OF THE THORAX
IMAGING FOR PENETRATINGVASCULAR INJURIES OF THEABDOMEN
IMAGING FOR PENETRATING VASCULAR INJURIES OF THE EXTREMITIES
209
Nonarteriographic Diagnosis of Penetrating Vascular Trauma
HISTORICAL BACKGROUND
ARTERIAL PRESSURE MEASUREMENTS
DUPLEX ULTRASONOGRAPHY
MINIMAL ARTERIAL INJURY
ROLE OF THE SERIAL PHYSICAL EXAMINATION
210
Penetrating and Blunt Injuries of the Carotid Artery
PENETRATING CAROTID ARTERY INJURIES
Operative Approach
Outcomes
BLUNT CAROTID ARTERY INJURIES
Treatment
Outcomes
211 Penetrating and
Blunt Injuries ofthe Vertebral Artery
ETIOLOGY
TREATMENT
212
Blunt Arterial Injuries of the Shoulder: Open and Endovascular Therapy
PRESENTATION AND DIAGNOSIS
OPEN OPERATIVE MANAGEMENT
ENDOVASCULAR MANAGEMENT
213
Penetrating Injuries to the Aortic Arch and Intrathoracic Great Vessels
ARTERIAL INJURIES IN THE MEDIASTINUM
Epidemiology
Clinical Presentation
Diagnosis
Management
Outcomes
SPECIFIC ARTERIAL INJURIES
Innominate Injury
Subclavian Injury
Common Carotid Injury
214
Open and Endovascular Management of Blunt and Penetrating Nonaortic Abdominal Vascular Injury
ZONES OF INJURY
VENA CAVA INJURIES
CELIAC ARTERY INJURIES
HEPATIC ARTERY INJURIES
PORTAL VEIN INJURIES
SUPERIOR MESENTERIC ARTERY INJURIES
RENAL ARTERY INJURIES
215
Aortic Injury
INCIDENCE
PATHOPHYSIOLOGY
PRESENTATION AND DIAGNOSIS
TIMING OF REPAIR
OPERATIVE REPAIR
Open Thoracic Technique
Open Abdominal Technique
Endovascular Technique
CHANGE IN PARADIGM
216
Complications of Upper and Lower Extremity Percutaneous Arterial Puncture and Catheterization
COMPLICATIONS OF LOWER EXTREMITY ARTERIAL PUNCTURES
Bleeding
Pseudoaneurysm
Arteriovenous Fistula
Thrombosis, Dissection, and Distal Embolization
Femoral Neuropathy
Vascular Closure Devices
COMPLICATIONS OF UPPER EXTREMITY PUNCTURES
217
Open and Endovascular Treatment of Penetrating Extremity Arterial Injuries
RESUSCITATION AND SURGICAL ASSESSMENT
OPEN OPERATIVE MANAGEMENT
ENDOVASCULAR MANAGEMENT
COMPLETION IMAGING
POSTOPERATIVE CONSIDERATIONS
218
Blunt Popliteal Artery Injuries
DIAGNOSIS
Physical Examination
Imaging
TREATMENT
Vascular Repair
Fasciotomy
Orthopedic and Soft Tissue Injury
Postoperative Management
OUTCOME
219
Fasciotomy for Compartmental Hypertension and Acute Compartment Syndrome
PATHOPHYSIOLOGY
CLINICAL PRESENTATION AND DIAGNOSIS
OBJECTIVE TESTS IN THE DIAGNOSIS OF COMPARTMENTAL HYPERTENSION
FASCIOTOMY
Indications
Techniques
Immediate and Late Effects
220
Ischemia-Induced Muscle Myonecrosis, Myoglobinuria, and Secondary Kidney Failure
PATHOPHYSIOLOGY
DIAGNOSIS
MANAGEMENT
221
Vascular Injury Secondary to Drug Abuse
ARTERIAL INJURY
Pathophysiology
Presentation
Evaluation and Diagnosis
Treatment
VENOUS INJURY
Superficial Thrombophlebitis
Deep Vein Thrombophebitis
Mycotic Venous Aneurysm
Chronic Venous Disease
222
Cold Injury
HYPOTHERMIA
FROSTBITE
NONFREEZING INJURIES
TREATMENT
223
Pediatric Iatrogenic Vascular Injury
LOWER EXTREMITY AND FEMORAL ARTERY
UPPER EXTREMITY AND BRACHIAL ARTERY
ABDOMINAL AORTA
CERVICAL AND CAROTID ARTERY
Mesenteric
Vascular Disease
224 Arteriography
Evaluation of Splanchnic Artery Occlusive Disease
VASCULAR ANATOMY
Celiac Artery
Superior Mesenteric Artery
Inferior Mesenteric Artery
TECHNIQUE
ARTERIOGRAPHY DIAGNOSIS
Occlusive Disease at the Origins ofthe Splanchnic Arteries
Occlusive Disease of Splanchnic Artery Branches
Distal Splanchnic Arterial Occlusive Disease
Nonocclusive Mesenteric Ischemia
225
Duplex Scanning in the Diagnosis of Splanchnic Artery Occlusive Disease
TECHNIQUE OF MESENTERIC DUPLEX SCANNING
FASTING DOPPLER MESENTERIC ARTERY WAVEFORMS
FASTING DUPLEX CRITERIA FOR MESENTERIC ARTERY STENOSIS
POSTPRANDIAL MESENTERIC DUPLEX SCANNING
EVALUATION OF MESENTERIC ARTERY BYPASS GRAFTS
EVALUATION OF STENTED SUPERIOR MESENTERIC ARTERIES
INTERMITTENT CELIAC AXIS COMPRESSION
226
Acute Embolic and Thrombotic Mesenteric Ischemia
CLINICAL PRESENTATION
Acute Embolic Mesenteric Ischemia
Acute Thrombotic Mesenteric Ischemia
DIAGNOSIS
TREATMENT
Surgical Treatment
Endovascular Treatment
Surgical versus Endovascular Therapy for Acute Mesenteric Embolus and Thrombosis
227 Endovascular Therapy for Chronic Mesenteric Ischemia
DIAGNOSIS
TREATMENT
Selection
Techniques
RESULTS
Symptom Relief
Morbidity and Mortality
Restenosis, Symptom Recurrence,and Reintervention
Survival
228
Transaortic Splanchnic Endarterectomy for Chronic Mesenteric Ischemia
DIAGNOSIS AND EVALUATION OF CHRONIC MESENTERIC ISCHEMIA
TECHNIQUE OF TRANSAORTIC SPLANCHNIC ENDARTERECTOMY
OUTCOME
PATIENT SELECTION
229
Arterial Bypass for Chronic Mesenteric Ischemia
TREATMENT OPTIONS
ANTEGRADE VERSUS RETROGRADE BYPASS
SINGLE- VERSUS MULTI-VESSEL BYPASS
TECHNICAL DETAILS
SURGICAL RESULTS
230
Operative Treatment of Pediatric Splanchnic Arterial Occlusive Disease
CLINICAL PRESENTATION
ETIOLOGY OF SPLANCHNIC ARTERIAL OCCLUSIVE LESIONS
OPERATIVE THERAPY
OUTCOMES
231
Celiac Artery Compression Syndrome
CLINICAL MANIFESTATIONS
ANATOMIC BASIS OF ARTERIAL ENTRAPMENT
PHYSIOLOGIC CONSEQUENCESOF ARTERIAL ENTRAPMENT
DIAGNOSTIC EVALUATION
OPERATIVE TREATMENT
Conventional Open Surgical Approach
Laparoscopic and Endoscopic Surgical Approaches
Endovascular Management
SURGICAL OUTCOMES
232
Nonocclusive Mesenteric Ischemia
PATHOPHYSIOLOGY
CLINICAL PRESENTATION
DIAGNOSIS
MANAGEMENT
233
Venous Thrombosis Within the Splanchnic Circulation
MESENTERIC VEIN THROMBOSIS
Epidemiology
Risk Factors
Clinical Presentation
Diagnosis
Medical Management
Surgical and Interventional Management
Outcomes
PORTAL VEIN THROMBOSIS
SPLENIC VEIN THROMBOSIS
BUDD–CHIARI SYNDROME
234
Celiac, Hepatic, and Splenic Artery Aneurysms
CELIAC ARTERY ANEURYSMS
Clinical Presentation
Management
HEPATIC ARTERY ANEURYSMS
Clinical Presentation
Management
SPLENIC ARTERY ANEURYSMS
Clinical Presentation
Management
235
Mesenteric Artery Aneurysms
SUPERIOR MESENTERIC ARTERY ANEURYSMS
INFERIOR MESENTERIC ARTERY ANEURYSMS
JEJUNAL, ILEAL, AND COLIC ARTERY ANEURYSMS
236
Gastroduodenal and Pancreaticoduodenal Artery Aneurysms
PSEUDOANEURYSMS
Clinical Manifestations
Diagnosis
TREATMENT
TRUE ANEURYSMS
Diagnosis
Clinical Manifestations
Treatment
237
Vascular Malformations and Arteriovenous Fistulas of the Gastrointestinal Tract
ARTERIOVENOUS FISTULAS
VASCULAR MALFORMATIONS
Renovascular
Disease
238 Pathology of
Arteriosclerotic, Fibrodysplastic, and Developmental Renal Artery Occlusive Disease
RENAL ARTERY FIBRODYSPLASIA
Intimal Fibroplasia
Medial Fibroplasia
Perimedial Dysplasia
DEVELOPMENTAL RENAL ARTERY STENOSES
RENAL ARTERY ARTERIOSCLEROSIS
239
Conventional Arteriographic and Computed Tomography Arteriographic Diagnosis of Renovascular Hypertension
CATHETER ANGIOGRAPHY
COMPUTED TOMOGRAPHY ARTERIOGRAPHY
240
Magnetic Resonance Angiographic Diagnosis of Renovascular Disease
PATIENT PREPARATION
INTERPRETING THE IMAGE
241
Duplex Scanning in the Evaluation of Renal Arterial Occlusive Disease
SCANNING TECHNIQUE
INTERPRETATION
CLINICAL APPLICATIONS
242
Renovascular Hypertension and Renal Artery Occlusive Disease
PATHOPHYSIOLOGY OF RENOVASCULAR HYPERTENSION
CLINICAL EVIDENCE OF RENIN–ANGIOTENSIN ACTIVATION
243
Renal Insufficiency and Renal Artery Occlusive Disease
PATHOPHYSIOLOGY
PREVALENCE
NATURAL HISTORY
DIAGNOSIS
MANAGEMENT
Selected References
244
Selection of Patients for Open Surgical or Endovascular Treatment of Renal Artery Arteriosclerotic Disease
CONDITIONS IN FAVOR OF OPEN RENAL ARTERY REVASCULARIZATION
CONDITIONS IN FAVOR OF ENDOVASCULAR RENAL ARTERY REVASCULARIZATION
CONCLUSION
Selected References
245
Percutaneous Arterial Dilation and Stenting for Arteriosclerotic Renovascular Hypertension and Ischemic Nephropathy
PATIENT SELECTION
TECHNIQUES OF RENAL ARTERY STENTING
ASTRAL AND STAR TRIALS
RESULTS OF RETROSPECTIVE OBSERVATIONAL STUDIES OFRENAL ARTERY STENTING
Selected References
246
Percutaneous Arterial Dilation for Fibrodysplastic Renovascular Hypertension
TREATMENT
OUTCOMES
247
Transaortic Renal Artery Endarterectomy for Renal Artery Atherosclerosis
OPERATIVE TECHNIQUE
Exposure
Axial Aortorenal Endarterectomy
Transaortic Renal Artery Endarterectomy
Direct Renal Artery Endarterectomy
POSTOPERATIVE CARE
248
Aortorenal Bypass for Renovascular Hypertension in Adults
PREOPERATIVE PREPARATION
OPERATIVE MANAGEMENT
Surgical Strategy
Operative Exposure
Renal Artery Bypass
Operative Duplex Sonography
OUTCOMES
249
Alternative Renal Artery Reconstruction Techniques: Hepatorenal, Splenorenal, Iliorenal, and Mesorenal Bypass Procedures
SPLENORENAL BYPASS
HEPATORENAL AND GASTRODUODENAL BYPASS
ILIORENAL BYPASS
MESORENAL BYPASS
250
Ex Vivo Arterial Repair for Renovascular Hypertension Secondary to Fibrodysplasia
THERAPY
SURGICAL TECHNIQUE
Incision
Nephrectomy
Ex Vivo Reconstruction
Autotransplantation of the Kidney
RESULTS
Complications
251
Operative Evaluation of Renal and Visceral Arterial Reconstructions Using Duplex Sonography
252
Surgical Treatment of Renovascular Hypertension in Children
OPERATIVE THERAPY
Types of Surgery
General Tenets
Concomitant Nonrenal Procedures
DISCUSSION
OUTCOMES
253
Renal Artery Dissection
ENDOVASCULAR PROCEDURE-INDUCED DISSECTION
BLUNT TRAUMA–RELATED DISSECTION
SPONTANEOUS DISSECTION
254
Renal Artery Atheroembolism
ETIOLOGY
DIAGNOSIS
TREATMENT
255
Renal Vein Thrombosis
PATHOPHYSIOLOGY
CLINICAL PRESENTATION
DIAGNOSIS
TREATMENT
Neonates
Adults
256
Treatment of Renal Artery Aneurysms
PATHOGENESIS
CLINICAL PRESENTATION
TREATMENT
Indications
Surgical Exposure
Specific Interventions
OUTCOMES
257
Renal Arteriovenous Malformations And Arteriovenous Fistulas
CLASSIFICATION
INCIDENCE
CLINICAL FEATURES
ANGIOGRAPHIC DIAGNOSIS
MANAGEMENT
Congenital Arteriovenous Malformations
Arteriovenous Fistula
Traumatic Arteriovenous Fistula
258
Endovascular Renal Denervation
RESISTANT HYPERTENSION ANDTHE ROLE OF SYMPATHETIC NERVOUS SYSTEM
ENDOVASCULAR RENAL DENERVATION
CLINICAL EVALUATION OF RENAL DENERVATION
ALTERNATIVE APPROACHESTO RENAL DENERVATION
EFFECT OF RENAL DENERVATION ON PHYSIOLOGIC PARAMETERS
SAFETY OF THE PROCEDURE
RENAL DENERVATION FOR OTHER CONDITIONS
Arteriovenous Fistulas and
Arteriovenous Malformations
259
Classification of Peripheral Arteriovenous and Venous Malformations
260
Imaging of Peripheral Vascular Fistulas and Arteriovenous Malformations
IMAGING MODALITIES
MAGNETIC RESONANCE IMAGING AND MAGNETIC RESONANCE ANGIOGRAPHY
ULTRASONOGRAPHY
COMPUTED TOMOGRAPHY
IMAGING FEATURES OF VASCULAR ANOMALIES
Capillary Malformations
Venous Malformations
Lymphatic Malformations
Arteriovenous Malformations
Mixed Malformations and Syndromes
Vascular Tumors
Arteriovenous Fistulas
261
Treatment of Congenital Vascular Malformations in Children and Adults
TREATMENT GUIDELINES
Surgical Treatment
Endovascular Treatment
262
Treatment of Traumatic Arteriovenous Fistulas
ETIOLOGY AND PATHOPHYSIOLOGY
CLINICAL PRESENTATION AND DIAGNOSIS
TREATMENT
Management Options
Treatment at Specific Sites
Angioaccess Surgery
263
External Methods of Angioaccess
INDICATIONS FOR CENTRAL VENOUSACCESS
Chemotherapy
Hemodialysis
TYPES OF CENTRAL VENOUSCATHETERS
Acute-Care Devices
Transition Access Devices
Tunneled Catheters
Implanted Ports
TECHNIQUES FOR INSERTION
Internal Jugular Approach
Subclavian Vein Approach
Femoral Vein Approach
Other Approaches
COMPLICATIONS OF CENTRAL VENOUS CATHETERIZATION
Pneumothorax
Vascular Injury
Arrhythmia
Air Embolism
Infection
Mechanical Complications
264
Direct Arteriovenous Communication Angioaccess
PREOPERATIVE EVALUATION
LOCATION OF THE FISTULA
TECHNIQUE
COMPLICATIONS
Graft Stenosis
Steal Syndrome with Hand Ischemia
Central Vein Stenosis
MATURATION OF THE FISTULA
FOLLOW-UP
265
Bridge Grafts for Angioaccess
PREOPERATIVE CONSIDERATIONS
BRIDGE GRAFTS
SURGERY
266
Role of Surveillance for Hemodialysis Access
JUSTIFICATION
CLINICAL MONITORING AND SURVEILLANCE TECHNIQUES
RECOMMENDATIONS FROM NATIONAL GUIDELINES
EVIDENCE TO SUPPORT SURVEILLANCE
PRACTICAL RECOMMENDATIONS
267
Thrombotic Complications of Arteriovenous Access
RISK FACTORS FOR THROMBOSISOF ARTERIOVENOUS ACCESS
Inflow Disease
Anastomotic Factors
Complications with the Type of Conduit
Systemic Factors
Intradialytic Factors
CLINICAL PRESENTATION
MANAGEMENT
Patient Selection
Contraindications to Thrombectomy
TREATMENT TECHNIQUES
Standard Percutaneous Technique
Standard Open Technique
Thrombolysis
Mechanical Thrombectomy
Balloon Angioplasty
Stent and Stent-Graft Placement
COMPLICATIONS OF THROMBOLYSIS AND THROMBECTOMY
Local Complications
Distant Complications
Systemic Complications
268
Ambulatory Treatment of Dialysis Access Stenosis
TECHNIQUE OF ULTRASOUND-GUIDED FISTULA TREATMENT
OFFICE-BASED MANAGEMENT OF ARTERIOVENOUS ACCESS UNDER FLUOROSCOPIC GUIDANCE
FOLLOW-UP
Venous Disease
269
Coagulation Cascade and Thrombosis
BASIC COAGULATION PATHWAYS
NATURAL ANTICOAGULANTS BALANCE THROMBOSIS
PHYSIOLOGIC THROMBOLYSIS
ORGAN HEMOSTASIS: ENDOTHELIUM
INFLAMMATION AND THROMBOSIS
863RESOLUTION OF THROMBOSIS
INTERPLAY OF ARTERIAL AND VENOUS THROMBOSIS
FACTORS THAT INCREASE RISK OF VENOUS THROMBOEMBOLISM
BIOMARKERS FOR VENOUS THROMBOEMBOLISM
270
Pathophysiology of Acute Venous Thrombosis
RISK FACTORS FOR ACUTE VENOUS THROMBOEMBOLISM
PATHOPHYSIOLOGY OF ACUTE VENOUS THROMBOEMBOLISM
SUMMARY
271
Ultrasonography for the Diagnosis of Venous Disease
EVALUATION OF REFLUX
EVALUATION OF OBSTRUCTION
EVALUATION OF CONGENITAL MALFORMATION
272
Computed Tomographic Venography and Magnetic Resonance Venography
COMPUTED TOMOGRAPHY VENOGRAPHY
MAGNETIC RESONANCE VENOGRAPHY
273
Invasive Methods of Diagnosing Acute and Chronic Venous Disease
INTRAVASCULAR ULTRASONOGRAPHY
CONTRAST VENOGRAPHY
IMAGING OF ACUTE AND CHRONIC VENOUS THROMBOSIS
274
Natural History of Acute Venous Thrombosis
VENOUS THROMBOGENESIS ANDTHE EARLY NATURAL HISTORY OF DEEP VEIN THROMBOSIS
COMPLICATIONS OF ACUTE DEEP VEIN THROMBOSIS
CLINICAL IMPLICATIONS OF NATURAL HISTORY STUDIES
SUMMARY
275
Nonoperative Treatment of Acute Lower Extremity Venous Thrombosis
PATIENTS WITH DEEP VEIN THROMBOSIS
PATIENTS WITH THE POST-THROMBOTIC SYNDROME
276
New and Alternative Anticoagulants
FONDAPARINUX
APIXABAN
RIVAROXABAN
EDOXABAN
DABIGATRAN
FUTURE ANTICOAGULANTS
277
Warfarin-Induced Skin Necrosis
CLINICAL PRESENTATION
LABORATORY PRESENTATION
PATHOPHYSIOLOGY
PREVENTION AND MANAGEMENT
PROGNOSIS
278
Endovascular Thrombolysis and Mechanical Clot Removal for Acute Symptomatic Lower Extremity Deep Vein Thrombosis
MECHANISM OF THROMBOLYSIS
EVALUATION
ENDOVASCULAR STRATEGIESOF THROMBUS REMOVAL
QUALITY OF LIFE, VEIN VALVE FUNCTION, AND RECURRENCE
CONCLUSION
279
Open Surgical Treatment of Acute Iliofemoral and Inferior Vena Cava Thrombosis
INDICATIONS FOR INTERVENTION
SURGICAL THROMBECTOMY
COMPLICATIONS AND RESULTSOF SURGICAL THROMBECTOMY
NEW DEVELOPMENTS TO IMPROVE SURGICAL VENOUS THROMBECTOMY
280
Treatment of Acute Upper Extremity Venous Occlusion
CATHETER-ASSOCIATED DEEP VEIN THROMBOSIS OF THE UPPER EXTREMITY
TREATMENT
COMPLICATIONS
281
Lower Extremity Superficial Vein Thrombophlebitis
282
Pathology and Classification of Chronic Venous Disease
IN SEARCH OF COMPLETEAND ACCURATE DIAGNOSIS
CLUES TO CHRONIC VENOUS DISEASE
SKIN PATHOLOGY AND CLINICAL CLASSIFICATION
REFINEMENT IN C, E, A, AND P:2004 CONSENSUS
VENOUS CLINICAL SEVERITY SCORING
DISABILITY SCORE
QUALITY OF LIFE
SUMMARY
283
Endovascular Treatment of Chronic Venous Occlusion
PATHOPHYSIOLOGY
DIAGNOSIS
TREATMENT
RESULTS
284
Endovascular Laser Treatment of Varicose Veins
PATIENT SELECTION
TECHNIQUE
FOLLOW-UP
COMPLICATIONS
CLINICAL EXPERIENCE
285
Endovascular Radiofrequency Treatment of Varicose Veins
PROCEDURE
POST-TREATMENT CARE
RESULTS
286
Injection Treatment of Lower Extremity Varicose Veins
SCLEROSANTS
LIQUID SCLEROTHERAPY
FOAM SCLEROTHERAPY
SCLEROTHERAPY FOR SUPERFICIAL VARICES AND TELANGIECTASES
SAPHENOUS SCLEROTHERAPY
RESULTS OF CLINICAL TRIALS
SYSTEMIC COMPLICATIONS
287
Excision of Varicose Veins
IMPORTANCE OF TREATING TRUNCAL INCOMPETENCE
PRINCIPLES OF TREATING VARICOSITIES
EXCISION OF VARICOSE VEINS
288
Open Surgical Treatment of Chronic Venous Insufficiency
INDICATIONS FOR DETAILED VENOUS EVALUATIONS
PRIMARY VENOUS INSUFFICIENCY
SECONDARY VENOUS INSUFFICIENCY
RESULTS
COMPLICATIONS
CONCLUSION
289
Nonoperative Management of Chronic Venous Insufficiency
COMPRESSION THERAPY
Elastic Stockings
Paste Boots
Compressive Bandages
Legging Orthosis
Pneumatic Compression Devices
PHARMACOLOGIC THERAPIES
Diuretics
Zinc
Fibrinolytic Agents
Phlebotrophic Agents
Hemorheologic Agents
Prostaglandins
TOPICAL THERAPIES
290
Pathophysiology of Venous Varicosities and Venous Ulcers
MACROSCOPIC ALTERATIONS
MICROSCOPIC ALTERATIONS
EXTRACELLULAR MATRIX ALTERATIONS
CYTOKINE REGULATION AND TISSUE FIBROSIS
MATRIX METALLOPROTEINASES AND THEIR INHIBITORS IN VENOUS ULCER HEALING
REGULATION OF VENOUS ULCER FORMATION AND HEALING
SUMMARY
291
Open Surgical, Endoscopic, and Endovascular Treatment of Perforating Veins
ANATOMY AND FUNCTION OF PERFORATORS
New Nomenclature
Common Sites of Perforating Veins
PATHOPHYSIOLOGY
DIAGNOSIS OF PERFORATOR INCOMPETENCE
CLINICAL OUTCOMES FOLLOWING PERFORATOR ABLATION
Determining the Role of and Indication for Ablation
Effect of Interrupting ICPVs on Ulcer Healingand Recurrence
Effect of Treating GSV Incompetence Aloneon Ulcer Healing and Recurrence
NEWER TECHNIQUES FOR ICPV ABLATION
Sclerotherapy
Endovenous Ablation
Radiofrequency Ablation for Venous Ulcer
CURRENT APPROACH
292
Nonoperative Treatment of Venous Ulcers
COMPRESSION THERAPY AND CHRONIC VENOUS ULCERWOUND THERAPY
PHARMACOLOGIC TREATMENT
TREATMENT WITH TOPICAL GROWTH FACTORS
THERAPEUTIC MODULATION OF MATRIX METALLOPROTEINASE
HUMAN SKIN EQUIVALENTS AND BIOLOGIC MATRICES
293
Renal Vein Entrapment: The Nutcracker Syndrome
ANATOMIC FEATURES
CLINICAL FEATURES
DIAGNOSTIC STUDIES
TREATMENT
Surgical Treatment
Endovascular Treatment
294
Pelvic Venous Flow Disorder
VENOUS ANATOMY OF THE PELVIS
PATHOPHYSIOLOGY
SYMPTOMS
DIAGNOSIS
TREATMENT
RESULTS AND OUTCOMES
295
Endovascular Treatment of Vena Cava Occlusion
CLINICAL PRESENTATION
IMAGING EVALUATION
VASCULAR ACCESS FOR ENDOVASCULAR TREATMENT
TECHNIQUE OF VENOUS RECANALIZATION
TREATMENT ENDPOINTS
SPECIAL CASES
POSTOPERATIVE FOLLOW-UP
AREAS OF UNCERTAINTY AND OPPORTUNITY FOR FUTURE DEVELOPMENT
296
Open Surgical Treatment of Thrombotic Vena Cava Occlusion
SUPERIOR VENA CAVA SYNDROME
Clinical Presentation
Surgical Technique
Results
INFERIOR VENA CAVA THROMBOSIS
Clinical Presentation
Open Surgical Treatment
Results
297
Primary and Secondary Vena Cava Tumors
TUMOR TYPES
CLINICAL PRESENTATION
EVALUATION
TREATMENT
OUTCOMES
298
Nonoperative Treatment of Acute Pulmonary Embolism
RISK STRATIFICATION
TREATMENT STRATEGIES
Systemic Fibrinolysis
Catheter-Directed Therapy
Local Fibrinolytic Therapy
Pigtail Fragmentation
Rheolytic Thrombectomy
Rotational Thrombectomy
Ultrasound-Accelerated Thrombolysis
PRACTICAL PERSPECTIVE
299
Surgical Treatment of Acute and Chronic Pulmonary Embolism
ACUTE PULMONARY EMBOLISM
CHRONIC PULMONARY EMBOLISM
CONCLUSION
300
Permanent and Temporary Inferior Vena Cava Filters
INDICATIONS FOR PLACING FILTERS
TYPES OF FILTERS
PLACING THE FILTER
RETRIEVING THE FILTER
COMPLICATIONS OF FILTER PLACEMENT
PROPHYLACTIC FILTER PLACEMENT
301
Venous Aneurysms
POPLITEAL VENOUS ANEURYSMS
ANEURYSMS OF THE SUPERFICIAL VEINS OF THE EXTREMITIES
VENOUS ANEURYSMS OF THE DEEP VEINS OF THE EXTREMITIES
VENOUS ANEURYSMS OF THE VEINS OF THE NECK AND FACE
THORACIC VENOUS ANEURYSMS
AZYGOS VEIN ANEURYSMS
SUBCLAVIAN AND INNOMINATE VENOUS ANEURYSMS
ABDOMINAL VENOUS ANEURYSMS
Lymphatic Disease
302
Lymphedema
ANATOMY AND PHYSIOLOGY
PATHOPHYSIOLOGY
CLASSIFICATION
EVALUATION AND DIAGNOSIS
TREATMENT
303
Lymphedema: Medical and Physical Therapy
STRUCTURE AND FUNCTION OF THE LYMPHATIC SYSTEM
PATHOPHYSIOLOGY
PRIMARY AND SECONDARY LYMPHEDEMA
GRADES OF LYMPHEDEMA
TREATMENT
REHABILITATIVE TREATMENT
Elevation
Skin Hygiene
Exercise
Specialized Massage
Compression
Intermittent Vasopneumatic Compression
304
Surgical Treatment of Lymphedema
INDICATIONS FOR SURGICAL TREATMENT
EXCISIONAL OPERATIONS
MICROSURGICAL LYMPH VESSEL RECONSTRUCTIONS
LYMPHATIC GRAFTING
CONCLUSION

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current therap y in vascul ar and end ovascul ar surgery

5

th

edition J ames C. S tanley , MD Handleman Professor of Surgery Director, Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan

F rank J. V eith , MD Professor of Surgery New York University New York, New York; Professor of Surgery and William J. von Liebig Chair in Vascular Surgery Cleveland Clinic and Lerner College of Medicine of Case Western Reserve Cleveland, Ohio

T homas W. W akefield , MD Stanley Professor of Surgery Head, Section of Vascular Surgery Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899 Current Therapy in Vascular and Endovascular Surgery, Fifth Edition     ISBN: 978-1-4557-0984-7 Copyright © 2014 by Saunders, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher's permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data Current therapy in vascular surgery (Ernst)   Current therapy in vascular and endovascular surgery / [edited by] James C. Stanley, Frank J. Veith, Thomas W. Wakefield. -- 5th edition.    p. ; cm.   Preceded by: Current therapy in vascular surgery / editors, Calvin B. Ernst, James C. Stanley. 4th ed. 2001.   Includes bibliographical references and index.   ISBN 978-1-4557-0984-7 (hardcover : alk. paper)   I. Stanley, James C., editor of compilation. II. Veith, Frank J., 1931- editor of compilation. III. Wakefield, Thomas W., editor of compilation. IV. Title.   [DNLM: 1. Vascular Surgical Procedures. WG 170]  RD598.5  617.4'13--dc23 2014002164

Executive Content Strategist: Michael Houston Content Development Specialist: Laura Schmidt Publishing Services Manager: Deborah L. Vogel Project Manager: John W. Gabbert Designer: Steve Stave

Cover image from Computed Tomography and Computed Tomographic ­Arteriography in the Evaluation of Abdominal Aortic Aneurysms chapter by Roy K. Greenberg. Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1

contributors

Jihad Abbas, MD, FACS Vascular Surgeon The University of Toledo Medical Center Toledo, Ohio Ali F.  AbuRahma, MD Professor of Surgery Chief, Vascular & Endovascular Surgery Robert C. Byrd Health Sciences Center West Virginia University Charleston, West Virginia Shadi J. Abu-Hamilah, MD Vascular Surgeon Charleston Area Medical Center Charleston, West Virginia Charles W.  Acher, MD Professor Department of Surgery University of Wisconsin Madison, Wisconsin Mark A.  Adelman, MD Chief, Vascular and Endovascular Surgery Vascular and Endovascular Surgery NYU Langone Medical Center New York, New York Ibrahim Akin, MD, PhD Department of Medicine Division of Cardiology at the University Hospital Rockstock Rockstock, Germany Cary W. Akins, MD Cardiac Surgeon Massachusetts General Hospital Boston, Massachusetts Matthew T.  Allemang, MD Division of Vascular Surgery and ­Endovascular Therapy Department of General Surgery University Hospitals of Case Medical Center Cleveland, Ohio

Jose I.  Almeida, MD, FACS, RPVI, RVT Voluntary Associate Professor Department of Surgery University of Miami-Jackson Memorial Hospital; Medical Director, Vascular Surgery Miami Vein Center Miami, Florida Daniel M.  Alterman, MD Vascular Surgery Fellow Division of Vascular Surgery The University of Tennessee Graduate School of Medicine Knoxville, Tennessee Parth B.  Amin, MD Department of Surgery University of Iowa Carver College of Medicine Iowa City, Iowa Javier E.  Anaya-Ayala, MD Vascular Research Fellow Department of Cardiovascular Surgery Methodist DeBakey Heart and Vascular Center The Methodist Hospital Houston, Texas George Andros, MD Medical Director Amputation Prevention Center Valley Presbyterian Hospital Van Nuys, California Margaret W.  Arnold, MD Assistant Professor of Surgery and ­Radiology Department of Surgery Mount Sinai School of Medicine New York, New York Shipra Arya, MD Assistant Professor of Surgery and Endovascular Therapy Emory University Atlanta, Georgia

Enrico Ascher, MD Chief, Vascular and Endovascular Surgery Lutheran Medical Center Brooklyn, New York Joseph C. Babrowicz Jr., MD Assistant Professor of Surgery Division of Vascular Surgery, Department of Surgery George Washington University Washington, DC Dennis F. Bandyk, MD Section Chief Department of Vascular and Endovascular Surgery University of California San Diego San Diego, California Donal T. Baril, MD Vascular Surgeon University of Pittsburgh Physicians Pittsburgh, Pennsylvania Hisham S. Bassiouny, MD, FACS Director, Vascular Surgery and ­Endotherapy Dar Al Fouad Hospital Giza, Egypt Charudatta Bavare, MD, MPH Fellow Department of Vascular Surgery Methodist Debakey Heart and Vascular Center Houston, Texas B. Timothy Baxter, MD, FACS Professor Department of Surgery Division of General Surgery - Vascular Surgery University of Nebraska Medical Center Omaha, Nebraska v

vi CONTRIBUTORS Mazen Bazzi, DO Vascular Surgeon St. John Providence Health System Detroit, Michigan

John D. Bisognano, MD, PhD Professor of Medicine University of Rochester Medical Center Rochester, New York

Adam W. Beck, MD Vascular Surgeon University of Florida Health Gainesville, Florida

Haraldur Bjarnason, MD Professor of Radiology Division of Vascular and Inerventional Radiology Mayo Clinic Rochester, Minnesota

Ronald J. Belczyk, DPM Co-director Amputation Prevention Center Valley Presbyterian Hospital Van Nuys, California Michael Belkin, MD Division Chief Vascular and Endovascular Surgery Brigham & Women's Hospital Boston, Massachusetts Phillip J. Bendick, PhD Technical Director Peripheral Vascular Diagnostic Center Beaumont Health System Royal Oak, Michigan Rodney P. Bensley, MD Beth Israel Deaconess Medical Center Harvard Medical School Boston, Massachusetts Scott A. Berceli, MD, PhD Professor of Surgery Department of Surgery University of Florida Chief, Vascular Surgery North Florida/South Georgia Veterans Health System Gainesville, Florida David Bergqvist, MS, PhD Professor Emeritus Department of Surgical Sciences Section of Surgery Uppsala University Uppsala, Sweden Ramon Berguer, MD, PhD Frankel Professor of Vascular Surgery Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Todd L. Berland, MD Department of Surgery New York University Medical Center New York, New York

John Blebea, MD, MBA Professor of Surgery Chair, Department of Surgery University of Oklahoma Tulsa, Oklahoma Aaron S. Blom, DO, MBA Clinical Fellow Vascular Surgery Pennsylvania Hospital Philadelphia, Pennsylvania Cristal Boatright, MMS, PA-C Director Nuvena Vein Center Fort Wayne, Indiana Timothy W. Bodnar, MD Fellow Department of Internal Medicine Division of Metabolism, Endocrinology, and Diabetes University of Michigan Ann Arbor, Michigan Amman Bolia, MBChB, DMRD Consultant Vascular Radiologist Department of Imaging and Interventions University Hospitals of Leicester NHS Trust Leicester, United Kingdom Balasz Botos, MD Department of Vascular and Endovascular Surgery Klinikum Nürnberg Süd Nürnberg, Germany Thomas C. Bower, MD Professor of Surgery Mayo Medical School; Chair, Department of Vascular and Endovascular Surgery Mayo Clinic Rochester, Minnesota

Matthew J. Bown, MB BCh, MD Senior Lecturer in Vascular Surgery Department of Cardiovascular Sciences University of Leicester Leicester, United Kingdom David C. Brewster, MD Clinical Professor of Surgery Harvard Medical School Division of Vascular and Endovascular Surgery Massachusetts General Hospital Boston, Massachusetts Robert D. Brook, MD Associate Professor, Department of Internal Medicine Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Thomas E. Brothers, MD Professor of Surgery Medical University of South Carolina Chief of Vascular Surgery Ralph H. Johnson Department of Veterans Affairs Medical Center Charleston, South Carolina Jack Brownrigg, MD, ChB Academic Clinical Fellow, Vascular Surgery St George's Vascular Institute St George's Hospital London, United Kingdom Jan S. Brunkwall, MD, PhD Professor Chairman, Department of Vascular Surgery University of Cologne Cologne, Germany Keith D. Calligaro, MD Clinical Professor of Surgery University of Pennsylvania School of Medicine Chief, Section of Vascular Surgery Pennsylvania Hospital Clinical Professor of Surgery Philadelphia, Pennsylvania Richard P. Cambria, MD Chief, Division of Vascular and ­Endovascular Surgery Department of Surgery Massachusetts General Hospital Boston, Massachusetts

CONTRIBUTORS vii

James E. Carpenter, MD Professor and Chair Department of Orthopaedic Surgery University of Michigan Ann Arbor, Michigan Jeffrey P. Carpenter, MD Professor and Chairman Department of Surgery Cooper Medical School of Rowan ­University Camden, New Jersey Robert Carter, MD Assistant Professor of Surgery University of Missouri Kansas City, Missouri Sherrie Cavanaugh, MD Resident Department of Surgery Cedars-Sinai Medical Center Los Angeles, California Neal S. Cayne, MD Associate Professor of Surgery New York University Director, Endovascular Surgery Department of Vascular Surgery New York University Medical Center New York, New York Rabih A. Chaer, MD, MSc Assistant Professor of Surgery Division of Vascular Surgery The University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania Ronil V. Chandra, MMed Interventional Neuroradiology Unit ­Department of Diagnostic Imaging Monash Medical Centre Melbourne, Australia Alexander T. Chang, MD Fellow Department of Vascular Surgery University Hospitals of Case Medical Center Cleveland, Ohio Benjamin B. Chang, MD Associate Professor of Surgery Albany Medical College Albany, New York

Catherine K. Chang, MD Assistant Professor of Surgery University of Florida Health Gainesville, Florida Kristofer M. Charlton-Ouw, MD, FACS Assistant Professor Department of Cardiothoracic and ­Vascular Surgery University of Texas Medical School at Houston Memorial Hermann Heart and Vascular Institute – Texas Medical Center Houston, Texas Kenneth J. Cherry, MD Division of Vascular and Endovascular Surgery University of Virginia Charlottesville, Virginia Kyung J. Cho, MD Martel Professor of Radiology Department of Radiology Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan M. Chung Resident Brooklyn Hospital Center New York, New York Timothy A.M. Chuter, BM, DM Professor of Surgery Division of Vascular Surgery University of California San Francisco San Francisco, California G. Patrick Clagett, MD Division of Vascular and Endovascular Surgery Department of Surgery The University of Texas Southwestern Medical Center Dallas Dallas, Texas

Anthony J. Comerota, MD Adjunct Professor of Surgery Vascular Surgery University of Michigan Ann Arbor, Michigan; Director, Jobst Vascular Center The Toledo Hospital Toledo, Ohio Michael S. Conte, MD Professor Chief, Division of Vascular and Endovascular Surgery University of California, San Francisco San Francisco, California Joseph S. Coselli, MD Professor and Cullen Foundation Endowed Chair Division of Cardiothoracic Surgery Michael E. DeBakey Department of Surgery Baylor College of Medicine; Chief, Section of Adult Cardiac Surgery The Texas Heart Institute at St. Luke's Episcopal Hospital, Houston, Texas Enrique Criado, MD Pfeifer Professor of Surgery Section of Vascular Surgery Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Jack L. Cronenwett, MD Department of Vascular Surgery Dartmouth-Hitchcock Medical Center Lebanon, New Hampshire Ronald L. Dalman, MD Professor of Surgery Division of Vascular and Endovascular Surgery Stanford University Stanford, California

Daniel G. Clair, MD Department of Vascular Surgery Cleveland Clinic Cleveland, Ohio

Michael C. Dalsing, MD Director of Vascular Surgery Department of Surgery Indiana University Indianapolis, Indiana

Dawn M. Coleman, MD Assistant Professor Section of Vascular Surgery Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan

R. Clement Darling III, MD Professor of Surgery Albany Medical Center; Chief, Division of Vascular Surgery Albany Medical Center Albany, New York

viii CONTRIBUTORS Narasimham L. Dasika, MD Associate Professor Department of Radiology Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Alun H. Davies, MA, DM Professor Department of Vascular Surgery Imperial College Heathcare London, United Kingdom Mark G. Davies, MD, PhD Weill Medical College at Cornell University New York, New York; Senior Investigator The Methodist Hospital Research Institute Houston, Texas Gert Jan de Borst, MD, PhD Department of Vascular Surgery University Medical Center Utrecht, Netherlands Ralph G. DePalma, MD, FACS Professor of Surgery Uniformed Services University of the Health Sciences Bethesda, Maryland; Special Operations Officer Office of Research and Development Department of Veterans Affairs Washington, DC Florian Dick, MD Division of Cardiovascular Surgery Swiss Cardiovascular Center University Hospital Berne, Switzerland Manuel Doblas, MD Vascular Surgeon Complejo Hospitalario de Toledo Toledo, Spain

Matthew J. Dougherty, MD Clinical Professor of Surgery University of Pennsylvania Pennsylvania Hospital Philadelphia, Pennsylvania Paul J. Dougherty, MD Clinical Associate Professor Orthopaedic Surgery Wayne State University Detroit, Michigan; Adjunct Clinical Associate Professor Orthopaedic Surgery University of Michigan Ann Arbor, Michigan Maciej Dryjsk, MD, PhD Associate Professor Department of Surgery Buffalo General Medical Center Buffalo, New York

Jonathan L. Eliason, MD Associate Professor Lindenauer Professor of Surgery Section of Vascular Surgery Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Jennifer Ellis, MD Associate Professor of Surgery University of Rochester Medical Center Rochester, New York Eric D. Endean, MD Professor Department of Surgery University of Kentucky Lexington, Kentucky

Yazan Duwayri, MD Assistant Professor Vascular Surgery and Endovascular Therapy Emory University School of Medicine Atlanta, Georgia

Tod C. Engelhardt, MD Associate Professor of Surgery Department of Thoracic surgery Tulane University Medical School New Orleans, Louisiana; Chairman Cardiovascular and Thoracic Surgery East Jefferson General Hospital Metairie, Louisiana

Kathryn S. Dyhdalo, MD Fellow Pathology and Laboratory Medicine Cleveland Clinic Cleveland, Ohio

Sean J. English, MD Resident Department of Surgery University of Michigan Ann Arbor, Michigan

Kim Eagle, MD Albion Walter Hewlett Professor of Internal Medicine Chief, Clinical Cardiovascular Medicine Director, Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan

Guillermo A. Escobar, MD Assistant Professor of Surgery University of Arkansas for Medical Sciences Little Rock, Arkansas

John F. Eidt, MD Greenville Memorial Hospital Greenville, South Carolina

Konstantinos P. Donas, MD, PhD Department of Vascular Surgery St. Franziskus Hospital Münster Münster University Hospital Münster, Germany

Bo G. Eklof, MD, PhD Emeritus Professor Department of Surgery University of Hawaii Honolulu, Hawaii

Qian Dong, MD Assistant Professor of Radiology University of Michigan Health System Ann Arbor, Michigan

Steve Elias, MD Director, Division of Vascular Surgery Vein Programs Department of Vascular Surgery Columbia University Medical Center New York, New York

Mark K. Eskandari, MD Vascular Surgeon Bluhm Cardiovascular Institute Northwestern Memorial Hospital Chicago, Illinois Anthony L. Estrera, MD Professor Chief, Division of Adult Cardiac Surgery Department of Cardiothoracic and ­Vascular Surgery University of Texas Medical School at Houston Memorial Hermann Heart and Vascular Institute – Texas Medical Center Houston, Texas

CONTRIBUTORS ix

Andres Fajardo, MD Assistant Professor of Surgery Vascular Surgery Indiana University Section Chief, Vascular Surgery Wishard Memorial Hospital Indianapolis, Indianapolis Grant T. Fankhauser, MD Instructor in Surgery Department of Surgery Division of Vascular Surgery Mayo Clinic Arizona Scottsdale, Arizona Mark A. Farber, MD Professor Departments of Radiology and Surgery Director, Aortic Disease Management University of North Carolina School of Medicine Chapel Hill, North Carolina Peter L. Faries, MD Franz W. Sichel Professor of Surgery Chief, Division of Vascular Surgery Mount Sinai School of Medicine New York, New York Steven M. Farley, MD Vascular Surgery University of California Los Angeles Los Angeles, California Robert J. Feezor, MD Vascular Surgeon University of Florida Health Gainesville, Florida Cindy L. Felty, MSN Director, Vascular Ulcer/Wound Healing Clinic Gonda Vascular Center Rochester, Minnesota D. Preston Flanigan, MD Medical Director St. Joseph Hospital Vascular Institute Orange, California William R. Flinn, MD Professor of Surgery Division of Vascular Surgery University of Maryland Baltimore, Maryland Mikkel Fode, MD Faculty of Health Science University of Copenhagen Copenhagen, Denmark

Juan Fontcuberta, MD, PhD Vascular and Endovascular Surgery Hospital de la Zarzuela y Hospital de la Moraleja. Sanitas - Madrid Madrid, Spain Charles J. Fox, MD Associate Professor of Surgery Department of Surgery Uniformed Services University of the Health Sciences Bethesda, Maryland; Chief, Vascular Surgery Department of Surgery Denver Health Medical Center Denver, Colorado Marc Friedman, MD Senior Radiologist Cedars-Sinai Medical Center Los Angeles, California James B. Froehlich, MD, MPH Director, Vascular Medicine Division of Cardiovascular Medicine Department of Internal Medicine Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Santhi K. Ganesh, MD Assistant Professor Division of Cardiovascular Medicine Department of Internal Medicine Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Nitin Garg, MD Assistant Professor of Surgery Wake Forest Baptist Medical Center Winston-Salem, North Carolina Nicholas J. Gargiulo, III, MD Professor of Surgery Associate Chief of Vascular Surgery Hofstra University School of Medicine, and New York Institute of Osteopathic Medicine Professor Emeritus Albert Einstein College of Medicine New York, New York Brandon T. Garland, MD Resident University of Washington Medicine Department of Surgery Seattle, Washington

Jonathan P. Gertler, MD, MBA Senior Partner Back Bay Life Science Advisors Boston, Massachussets; Lecturer Massachusetts Institute of Technology Cambridge, Massachussets Bruce L. Gewertz, MD Chair and Vice-President of Interventional Services Department of Surgery Cedars-Sinai Medical Center Los Angeles, California Roma Gianchandani, MD Clinical Assistant Professor Department of Internal Medicine University of Michigan Ann Arbor, Michigan Peter Gloviczki, MD Joe M. and Ruth Roberts Professor of Surgery Mayo Medical School Chair Emeritus Division of Vascular and Endovascular Surgery Mayo Clinic Rochester, Minnesota Manj S. Gohel, MD, FRCS Honorary Clinical Lecturer Department of Surgery and Cancer Imperial College London Department of Vascular Surgery Imperial Vascular Unit St. Mary's Hospital London, United Kingdom Mitchell H. Goldman, MD Professor and Chairman Department of Surgery Assistant Dean for Research The University of Tennessee Graduate School of Medicine Knoxville, Tennessee Jerry Goldstone, MD Professor Department of Surgery Case Western Reserve University Chief Emeritus, Vascular Surgery & Endovascular Therapy University Hospitals of Case Medical Center Cleveland, Ohio

x CONTRIBUTORS Wadi Gomero-Cure, MD Resident Vascular Surgery Washington Hospital Center Georgetown University Hospital Washington, DC David Gordon, MD Professor Department of Pathology University of Michigan Ann Arbor, Michigan Alan M. Graham, MD Professor of Vascular Surgery Robert Wood Johnson University Hospital New Brunswick, New Jersey Linda M. Graham, MD Professor of Surgery Cleveland Clinic Lerner College of Medicine of Case Western Reserve University Department of Vascular Surgery Cleveland Clinic Cleveland, Ohio Richard M. Green, MD Chairman, Department of Surgery Lenox Hill Hospital New York, New York Roy K. Greenberg, MD (Deceased, 2013) Director, Endovascular Research Vascular Surgery Cleveland Clinic; Associate Professor Department of Surgery Cleveland Clinic Learner College of Medicine; Associate Professor Biomedical Engineering Case School of Engineering Case Western Reserve University Cleveland, Ohio Andreas Greiner, MD European Vascular Centre University Hospital RWTH Aachen, Aachen, Germany Howard P. Greisler, MD Professor Department of Cell Biology and Department of Surgery Loyola University Medical Center Maywood, Illinois

Maura Griffin, PhD Vascular Noninvasive Diagnostic Centre London, United Kingdom Jochen Grommes, MD Department of Vascular Surgery, University Hospital Aachen, Germany Ankur Gupta, MD Resident Department of Surgery Cedars-Sinai Health System Medical Center Los Angeles, California Hitinder S. Gurm, MD Associate Professor Department of Internal Medicine Division of Cardiovascular Medicine University of Michigan Ann Arbor, Michigan John W. Hallett, Jr., MD Clinical Professor of Surgery Medical Director, Roper St Francis Heart and Vascular Center Charleston, South Carolina Kimberley J. Hansen, MD Professor of Surgery Wake Forest University Winston-Salem, North Carolina Linda M. Harris, MD Associate Professor of Surgery Chief, Division of Vascular Surgery University at Buffalo, SUNY Buffalo, New York Robert W. Harris, MD Vascular Surgeon (retired) Encino, California Peter K. Henke, MD Doan Professor of Surgery Section of Vascular Surgery Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Santiago Herrera, MD Vascular Surgeon Jobst Vascular Center Toledo, Ohio

Norman R. Hertzer, MD Emeritus Chairman Department of Vascular Surgery The Cleveland Clinic Cleveland, Ohio Anil Hingorani, MD Vascular Surgeon Total Vascular Care New York, New York Alan T. Hirsch, MD Professor of Medicine, Epidemiology and Community Health Vascular Medicine Program, Cardiovascular Division University of Minnesota Medical School Minneapolis, Minnesota Joshua A. Hirsch, MD Associate Professor of Radiology Harvard Medical School Department of Radiology Massachusetts General Hospital Boston, Massachussets Karen J. Ho, MD Brigham and Women's Hospital Boston, Massachussets Kelley Hodgkiss-Harlow, MD Department of Vascular and Endovascular Surgery University of California San Diego San Diego, California Larry H. Hollier, MD Chancellor Louisiana State University Health Sciences Center New Orleans, Louisiana Douglas B. Hood, MD Department of Surgery Southern Illinois University School of Medicine Springfield, Illinois L. Nelson Hopkins, MD Professor Department of Neurosurgery and Department of Radiology University at Buffalo, State University of New York, Director, Toshiba Stroke Research Center Buffalo, New York; Department of Neurosurgery Millard Fillmore Gates Circle Hospital, Kaleida Health Buffalo, New York

CONTRIBUTORS xi

Joe Huang, MD Section of Vascular Surgery University of Medicine and Dentistry of New Jersey Newark, New Jersey Thomas S. Huber, MD, PhD Professor and Chief, Division of Vascular and Endovascular Surgery Department of Surgery Universityof Florida College of Medicine Gainesville, Florida Russell D. Hull, MBBS, MSc Professor of Medicine University of Calgary Calgary, Alberta Misty D. Humphries, MD Fellow Division of Vascular Surgery University of Utah Salt Lake City, Utah Justin Hurie, MD Assistant Professor Department of Vascular Surgery Wake Forest University Winston-Salem, North Carolina Rob Hurks, MD, PhD Harvard Medical School Beth Israel Deaconess Medical Center Harvard Medical School Boston, Massachusetts Niamh Hynes, MD Vascular Clinical Lecturer National University of Ireland Galway Galway, Ireland Karl A. Illig, MD Professor of Surgery Director, Division of Vascular Surgery University of South Florida College of Medicine Tampa, Florida Elizabeth A. Jackson, MD, MPH Assistant Professor Division of Cardiovascular Medicine Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Michael J. Jacobs, MD University of Rochester Medical Center School of Medicine and Dentistry Rochester, New York

Michael R. Jaff, DO Associate Professor of Medicine Harvard Business School; Medical Director, Vascular Center Massachusetts General Hospital Boston, Massachusetts Shady Jahshan, MD Fellow Department of Neurosurgery School of Medicine and Biomedical ­Sciences University at Buffalo, State University of New York Department of Neurosurgery Millard Fillmore Gates Hospital, Kaleida Health, Buffalo, New York Stuart W. Jamieson, MD Head, Cardiovascular and Thoracic Surgery Chair and Distinguished Professor of Surgery University of California, San Diego La Jolla, California Juan Carlos Jimenez, MD Associate Clinical Professor of Surgery Division of Vascular Surgery-Gonda ­(Goldschmied) Vascular Center David Geffen School of Medicine at University of California, Los Angeles Los Angeles, California Kaj H. Johansen, MD, PhD Clinical Professor of Surgery University of Washington School of Medi­cine; Chief of Vascular Surgery, Swedish Medical Center Seattle, Washington K. Wayne Johnston, MD Professor Department of Surgery University of Toronto Toronto, Canada Peter G. Kalman, MD Private Surgical Practice Toronto, Ontario Peter Kan, MD, MPH Department of Neurosurgery School of Medicine and Biomedical Sciences University at Buffalo, State University of New York Department of Neurosurgery Millard Fillmore Gates Circle Hospital, Kaleida Health Buffalo, New York

Edward P. Kang, MD Vascular Fellow University of Minnesota Vascular Surgery University of Minnesota Minneapolis, Minnesota Joseph Karam, MD Resident Department of Surgery Henry Ford Hospital Detroit, Michigan Omar Kass-Hout, MD Department of Neurology School of Medicine and Biomedical Sciences University at Buffalo, State University of New York Millard Fillmore Gates Circle Hospital, Kaleida Health Buffalo, New York Vikram Kashyap, MD Division Chief, Vascular Surgery University Hospitals Case Medical Center Cleveland, Ohio Blair A. Keagy, MD Professor of Surgery Department of Surgery University of North Carolina Chapel Hill, North Carolina Brian M. Kelly, DO Associate Professor Department of Physical Medicine and Rehabilitation University of Michigan Ann Arbor, Michigan Rebecca L. Kelso, MD Department of Vascular Surgery Cleveland Clinic Cleveland, Ohio K. Craig Kent, MD Chair, Department of Surgery University of Wisconsin Hospital and Clinics Madison, Wisconsin Tanaz A. Kermani, MD Assistant Professor Division of Rheumatology Department of Medicine Mayo Clinic Rochester, Minnesota

xii CONTRIBUTORS Melina R. Kibbe, MD Professor and Vice Chair of Research Department of Surgery Northwestern University; Co-Chief, Peripheral Vascular Service Department of Surgery Jesse Brown VA Medical Center Chicago, Illinois Stephan Kische, MD Department of Medicine Division of Cardiology at the University Hospital Rockstock Rockstock, Germany Robert L. Kistner, MD Clinical Professor of Surgery Department of Surgery University of Hawaii Kistner Vein Clinic Honolulu, Hawaii Jordan Knepper, MD Vascular Surgery Resident Section of Vascular Surgery Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Ralf R. Kolvenbach, MD, PhD Professor Vascular Centre Catholic Clinics Duesseldorf, Augusta Hospital Duesseldorf, Germany George Kopchok, BS Los Angeles Biomedical Research institute Harbor UCLA Medical Center Torrance, California Paul B. Kreienberg, MD Associate Professor of Surgery Albany Medical College Albany, New York Timothy F. Kresowik, MD Professor of Surgery University of Iowa Carver College of Medicine Iowa City, Iowa Marcus R. Kret, MD General Surgeon Oregon Health & Science University Portland, Oregon

Gentian Kristo, MD Division of Cardiac Surgery Brigham & Women's Hospital Harvard Medical School Boston, Massachusetts Nicos Labropoulos, PhD Professor of Surgery Department of Surgery, Division of Vascular Surgery Stony Brook University Medical Center Stony Brook, New York Mario Lachat, MD Professor, Head of Vascular Surgery Clinic for Cardiovascular Surgery University Hospital Zurich Zurich, Switzerland Brajesh K. Lal, MD Director, Center for Vascular Diagnostics Associate Professor Vascular Surgery and Biomedical Engineering University of Maryland Medical School Chief, Vascular Surgery Veterans Affairs Medical Center Baltimore, Maryland Glenn M. LaMuraglia, MD Associate Professor of Surgery Harvard Medical School Division of Vascular and Endovascular Surgery Massacusetts General Hospital Boston, Massachusetts Robert T. Lancaster, MD, MPH Fellow Division of Vascular and Endovascular Surgery Massachusetts General Hospital Boston, Massachusetts James Laredo, MD, PhD Associate Professor of Surgery Division of Vascular Surgery George Washington University Washington, DC Ignacio Leal, MD Vascular Surgeon Complejo Hospitalario de Toledo Toledo, Spain Frank A. Lederle, MD Medicine Service Veterans Affairs Medical Center Minneapolis, Minnesota

Byung-Boong Lee, MD, PhD Professor of Surgery Division of Vascular Surgery, Department of Surgery George Washington University Clinical Professor of Surgery Georgetown University, Washington, DC W. Anthony Lee, MD Director, Endovascular Program Christine E. Lynn Heart and Vascular Institute Boca Raton, Florida Scott A. LeMaire, MD Professor of Surgery Baylor College of Medicine Houston, Texas James A. Leonard Jr, MD Clinical Professor, Medical Director ­Orthotics and Prosthetics Department of Physical Medicine and Rehabilitation University of Michigan Ann Arbor, Michigan Thabele M. Leslie-Mazwi, MD Interventional Neuroradiology/Endovascular Neurosurgery Massachusetts General Hospital Boston, Massachusetts Elad I. Levy, MD Professor Department of Neurosurgery and Department of Radiology School of Medicine and Biomedical Sciences University at Buffalo, State University of New YorkCo-Director, Toshiba Stroke Research and Vascular Center Director, Interventional Stroke Services Kaleida Health Buffalo, New York Timothy K. Liem, MD Associate Professor of Surgery Oregon Health & Science University Portland, Oregon Peter H. Lin, MD Professor of Surgery Chief of Vascular Surgery Michael E. DeBakey Department of Surgery Baylor College of Medicine Houston, Texas

CONTRIBUTORS xiii

Peter S. Liu, MD Assistant Professor of Radiology and ­Vascular Surgery Department of Radiology and Section of Vascular Surgery Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Ying Wei Lum, MD Assistant Professor Division of Vascular Surgery and Endovascular Therapy Johns Hopkins Hospital Baltimore, Maryland; Section Director for Anatomy Perdana University Graduate School of Medicine Serdang, Selangor, Malaysia Alan B. Lumsden, MD Professor and Chairman Cardiovascular Surgery The Methodist Hospital Houston, Texas Sean P. Lyden, MD Associate Professor Vascular Surgery Cleveland Clinic Foundation Cleveland, Ohio Harry Ma, MD, PhD Fellow Vascular Surgery Tufts Medical Center Boston, Massachusetts William C. Mackey, MD Professor of Surgery Cardiovascular Center Tufts University School of Medicine Boston, Massachusetts Jason MacTaggart, MD Assistant Professor of Surgery Department of Surgery University of Nebraska Omaha, Nebraska Michael Madani, MD Professor of Surgery University of California, San Diego La Jolla, California Michel S. Makaroun, MD Professor of Surgery Division of Vascular Surgery University of Pittsburgh Pittsburgh, Pennsylvania

Adel M. Malek, MD, PhD Associate Professor Neurosurgery, Radiology and Neurology Tufts University School of Medicine; Director, Cerebrovascular and Endovascular Division Department of Neurosurgery Tufts Medical Center Boston, MA Rafael D. Malgor, MD Resident Division of Vascular Surgery Stony Brook Medical Center Stony Brook, New York Kirti Malhotra, MD Department of Internal Medicine George Washington University Washington, DC George Manis, MD Clinical Assistant Professor Vascular Surgery University of Medicine & Dentistry of New Jersey Newark, New Jersey Michael L. Marin, MD Professor and Chair, Vascular ­Surgery Mount Sinai Hospital New York, New York Nickolay P. Markov, MD General Surgeon Brooke Army Medical Center San Antonio, Texas Natalie Marks, MD Vascular and Internal Medicine Physician Total Vascular Care New York, New York S. Martindale Resident Brooklyn Hospital Center New York, New York Jon S. Matsumura, MD Professor of Surgery Chairman, Division of Vascular Surgery University of Wisconsin Madison, Wisconsin Dieter Mayer, MD Clinic for Cardiovascular Surgery The University Hospital of Zurich Zurich, Switzerland

Walter McCarthy, MD, MS Chief, Section of Vascular Surgery Rush University Medical School Chicago, Illinois Kenneth E. McIntyre Jr, MD Professor of Surgery Chief, Division of Vascular Surgery University of Nevada Las Vegas, Nevada James T. McPhee, MD Vascular Surgery Fellow Vascular and Endovascular Surgery Brigham & Women's Hospital Boston, Massachusetts Manish Mehta, MD, MPH Associate Professor of Surgery Albany Medical Center Albany, New York Mark H. Meissner, MD Professor of Surgery Department of Surgery University of Washington Seattle, Washington Keith C. Menes, MD Fellow Division of Vascular Surgery Henry Ford Hospital Detroit, Michigan Louis M. Messina, MD Chief, Division of vascular and Endovascular Surgery University of Massachusetts Worcester, Massachusetts Joseph L. Mills Sr, MD Professor of Surgery Chief, Vascular and Endovascular Surgery University of Arizona Health Sciences Center Tucson, Arizona Erica Mitchell, MD Associate Professor of Surgery Oregon Health & Science University Portland, Oregon J. Gregory Modrall, MD Professor of Surgery Division of Vascular and Endovascular Surgery Unversity of Texas Southwestern Medical Center Dallas, Texas

xiv CONTRIBUTORS Frans L. Moll, MD, PhD Department of Vascular Surgery University Medical Center Utrecht Utrecht, Netherlands Gregory L. Moneta, MD Professor and Chief Division of Vascular Surgery Oregon Health and Science University Portland, Oregon Samuel R. Money, MD, MBA Professor of Surgery Division of Vascular Surgery Mayo Clinic Arizona Scottsdale, Arizona Wesley S. Moore, MD Professor and Chief Emeritus Division of Vascular Surgery University of California, Los Angeles Medical Center Los Angeles, California Mark D. Morasch, MD John Marquardt Clinical Research Professor in Vascular Surgery Division of Vascular Surgery Northwestern University Feinberg School of Medicine Chicago, Illinois Edward S. Moreira, PhD Division of Vascular Surgery Northwestern University Chicago, Illinois Antonio Orgaz, MD Vascular Surgeon Complejo Hospitalario de Toledo Toledo, Spain Nick Morrison, MD Co-Founder, Medical Director Morrison Vein Institute Scottsdale, Arizona Albeir Y. Mousa, MD Associate Professor Robert C. Byrd Health Sciences Center West Virginia University Charleston, West Virginia Palaniappan Muthappan, MD Fellow Division of Cardiovascular Medicine Department of Internal Medicine University of Michigan Ann Arbor, Michigan

Daniel D. Myers Jr, DVM, MPH Associate Professor Section of Vascular Surgery Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan

Paula Novelli, M.D. Assistant Professor Department of Radiology Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan

Stuart I. Myers, MD Chief of Vascular Surgery Bryan LGH Health System Lincoln, Nebraska

Timothy J. Nypaver, MD Clinical Assistant Professor of Surgery Wayne State University School of ­Medicine Senior Staff Surgeon Henry Ford Hospital Detroit, Michigan

A. Ross Naylor, MBChB, MD Professor Department of Vascular Surgery Leicester Royal Infirmary Leicester, United Kingdom Justin K. Nelms, MD Clinical Assistant Professor University of Maryland School of Medicine Baltimore, Maryland David G. Neschis, MD Vascular Surgeon Maryland Vascular Center Glen Burnie, Maryland Richard F. Neville, MD Professor, Chief of Vascular Surgery George Washington University Washington, DC Bao-Ngoc Nguyen, MD Assistant Professor of Surgery George Washington University Washington, DC Rachael Nicholson, MD Assistant Professor Department of Surgery University of Iowa Carver School of Medicine Iowa City, Iowa Andrew N. Nicolaides, MS Emeritus Professor of Vascular Surgery Imperial College, London University London, United Kingdom; Special Scientist Biological Sciences University of Cyprus Nicosia, Cyprus Christoph A. Nienaber, MD Division of Cardiology Department of Internal Medicine I University of Rostock Rostock, Germany

Gavin C. O'Brien, RPAH Consultant Vascular & Endovascular Surgeon Mercy University Cork, Ireland Christian J. Ochoa, MD Assistant Professor of Surgery Division of Vascular Surgery University of Southern California Los Angeles, California David J. O'Connor, MD Vascular Surgery Fellow Department of Surgery Mount Sinai Medical Center New York, New York Gustavo S. Oderich, MD Associate Professor of Surgery Division of Vascular and Endovascular Surgery Mayo Clinic College of Medicine Director of Endovascular Therapy Mayo Clinic Rochester, Minnesota Thomas F. O'Donnell Jr, MD Benjamin Andrews Emeritus Professor of Surgery Tufts University School of Medicine Boston, Massachusetts Daniel C. Oh, MD Department of Interventional Neuroradiology and Endovascular Neurosurgery Massachusetts General Hospital Boston, Massachusetts Patrick J. O'Hara, MD, FACS Professor of Surgery Cleveland Clinic Lerner College of ­Medicine Department of Vascular Surgery Cleveland Clinic Foundation Cleveland, Ohio

CONTRIBUTORS xv

Dana A. Ohl, MD Professor of Urology Head of Division of Sexual and Reproductive Medicine Department of Urology University of Michigan Ann Arbor, Michigan George D. Oreopoulos, MD Assistant Professor Division of Vascular Surgery University of Toronto Division of Vascular Interventional Radiology, Joint Department of Medical Imaging University Health Network Toronto, Ontario David Orion, MD Department of Neurosurgery, School of Medicine and Biomedical Sciences University at Buffalo, State University of New York Millard Fillmore Gates Circle Hospital, Kaleida Health Buffalo, New York Nicholas H. Osborne, MD Vascular Surgery Fellow University of Michigan Health System Ann Arbor, Michigan C. Keith Ozaki, MD Associate Professor Department of Surgery Harvard Medical School Brigham & Women's Hospital Boston, Massachusetts Kathleen J. Ozsvath, MD Albany Memorial Hospital Albany, New York Frank T. Padberg Jr, MD Professor of Vascular Surgery Department of Surgery Rutgers, New Jersey Medical School Chief, Section of Vascular Surgery Veterans Affairs New Jersey Health Care System East Orange, New Jersey Peter J. Pappas, MD Clinical Professor of Surgery Weill Cornell Medical College New York, New York; Chair, Department of Surgery Brooklyn Hospital Center Brooklyn, New York

Ezequiel Parodi, MD Department of Vascular Surgery University of South Florida Tampa, Florida Juan Parodi, MD Department of Vascular Surgery University of Buenos Aires Buenos Aires, Argentina Himanshu J. Patel, MD Associate Professor of Cardiac Surgery University of Michigan Health System Cardiovascular Center Ann Arbor, Michigan Madhukar S. Patel, MD, MBA Resident Department of Surgery Massachusetts General Hospital Boston, Massuchesetts

Bruce A. Perler, MD, MBA Julius H Jacobson II Professor Department of Surgery The Johns Hopkins University School of Medicine Chief Emeritus, Division of Vascular Surgery and Endovascu­lar Therapy Frankel Cardiovascular Center The Johns Hopkins Hospital Baltimore, Maryland Brian G. Peterson, MD Associate Professor of Surgery Department of Surgery Saint Louis University St. Louis, Missouri Mun Jye Poi, MD Assistant Professor of Surgery Baylor College of Medicine Houston, Texas

Mitul Suresh Patel, MD Department of Surgery Cooper University Hospital Camden, New Jersey

Frank B. Pomposelli, Jr, MD Chairman, Department of Surgery St. Elizabeth's Medical Center Brighton, Massuchesetts

Virendra I. Patel, MD, MPH Assistant Professor Harvard Medical School Division of Vascular and Endovascular Surgery Massachusetts General Hospital Boston, Massuchesetts

Shahin Pourrabbani, MD University of Southern California Health Center Los Angeles, California

Philip S.K. Paty, MD Professor of Surgery Albany Medical College Albany, New York Thomas Pfammatter, EBIR Radiologist University Hospital Zurich Zurich, Switzerland William H. Pearce, MD Violet R. and Charles A. Baldwin Professor of Vascular Surgery Division of Vascular Surgery Northwestern University Chicago, Illinois Felice Pecoraro, MD Vascular Surgeon University of Palermo Palermo, Italy

Janet T. Powell, PhD, MD Professor Imperial College London, United Kingdom Richard J. Powell, MD Professor of Surgery Geisel School of Medicine at Dartmouth Chief, Section of Vascular Surgery Dartmouth-Hitchcock Medical Center Lebanon, New Hampshire Adam H. Power, MD, MPhil Fellow Vascular and Endovascular Surgery Mayo Clinic Rochester, Minnesota Victor Pretorius, MBchB Assistant Clinical Professor University of California San Diego San Diego, California

xvi CONTRIBUTORS Martin R. Prince, MD, PhD Professor of Radiology Weill Cornell Medical College Columbia College of Physicians and S­ urgeons New York, New York

John E. Rectenwald, MD, MS Associate Professor of Surgery Section of Vascular Surgery University of Michigan Ann Arbor, Michigan

Askin G. Rivera, MD Attending Vascular and Endovascular Surgeon Jacobi Medical Center New York, New York

Raffi A. Qasabian, MBBS Royal Prince Alfred Hospital Sydney, Australia

Daniel J. Reddy, MD Clinical Assistant Professor Department of Surgery Wayne State University School of Medicine Detroit, Michigan

William P. Robinson, III, MD Vascular Surgeon University of Massachusetts Memorial Medical Center Worcester, Massachusetts

Tim C. Rehders, MD Department of Medicine Division of Cardiology at the University Hospital Rockstock Rockstock, Germany

Caron B. Rockman, MD Associate Professor of Surgery Division of Vascular Surgery New York University New York, New York

Boudewijn L. Reichmann, MD, PhD Department of Vascular Surgery University Medical Center Utrecht, Netherlands

Sean P. Roddy, MD Associate Professor of Surgery Department of Surgery Albany Medical College Albany, New York

Susanne A. Quallich, MSN Adjunct Clinical Instructor in Nursing University of Michigan Ann Arbor, Michigan William J. Quinones-Baldrich, MD Professor of Surgery University of California, Los Angeles Los Angeles, California Joseph Raffetto, MD, MS Associate Professor of Surgery Harvard Medical School Brigham & Women's Hospital Boston, Massachusetts; Chief, Vascular Surgery Veterans Affairs Boston Healthcare System West Roxbury, Massachusetts Rodeen Rahbar, MD Assistant Professor Department of Radiology The George Washington University Washington, DC Saum A. Rahimi, MD Assistant Professor Division of Vascular Surgery University of Medicine & Dentistry of New Jersey-Robert Wood Johnson Medical School New Brunswick, New Jersey Seshadri Raju, MD The RANE Center Jackson, Mississippi Zoran Rancic, PhD Senior Physician - Vascular Surgery University Hospital Zurich Zurich, Switzerland Todd E. Rasmussen, MD Professor of Surgery Uniformed Services University Deputy Director US Combat Casualty Care Research ­Program Bethesda, Maryland

Linda M. Reilly, MD Professor of Surgery University of California, San Francisco San Francisco, California Norman M. Rich, MD Leonard Heaton and David Packard ­Professor Norman M. Rich Department of Surgery F. Edward Hébert School of Medicine Uniformed Services University of the Health Sciences Bethesda, Maryland John J. Ricotta, MD Professor Department of Surgery Georgetown University; Harold H. Hawfield Chair Department of Surgery Washington Hospital Center Washington, DC Thomas S. Riles, MD Professor of Surgery New York University New York, New York Wolfgang Ritter, MD Department of Radiology Klinikum Nürnberg Süd Nürnberg, Germany

Heron E. Rodriguez, MD Associate Professor Division of Vascular Surgery Northwestern University Feinberg School of Medicine Chicago, Illinois Lee Rogers, DPM Assistant Professor College of Podiatric Medicine Western University of Health Sciences Pomona, California Thom W. Rooke, MD Krehbiel Professor of Vascular Medicine Mayo Clinic Rochester, Minnesota Vincent L. Rowe, MD Professor of Surgery Department of Surgery Keck School of Medicine at University of Southern California Los Angeles, California Connie Ryjewski, APN, CNS Department of Surgery Advocate Lutheran General Hospital Park Ridge, Illinois Mikel Sadek, MD Fellow Division of Vascular Surgery New York University New York, New York

CONTRIBUTORS xvii

Hazim J. Safi, MD Professor and Chairman Department of Cardiothoracic and ­Vascular Surgery The University of Texas Health Science Center at Houston Memorial Hermann Heart and Vascular Institute – Texas Medical Center Houston, Texas Steven M. Santilli, MD, PhD, MBA Professor and Chief Division of Vascular Surgery University of Minnesota; Chief, Vascular Surgery Veterans Affairs Medical Center Minneapolis, Minnesota Timur P. Sarac, MD Professor of Surgery The Cleveland Clinic Lerner School of Medicine of Case Western Reserve University Cleveland, Ohio Mohammad Sarraf, MD John F Kennedy Medical Center Edison, New Jersey Salvatore T. Scali, MD Assistant Professor of Surgery University of Florida Health Gainesville, Florida Marc L. Schermerhorn, MD Department of Surgery Beth Israel Deaconess Medical Center Boston, Massachusetts Alvin H. Schmaier, MD Robert W. Kellermeyer Professor of ­Hematology and Oncology Department of Medicine Case Western Reserve University Cleveland, Ohio Joseph R. Schneider, M.D., Ph.D. Professor of Surgery, Northwestern University Vascular and Interventional Program of Cadence Health Winfield and Geneva, Illinois Peter A. Schneider, MD Chief, Division of Vascular Therapy Kaiser Foundation Hospital Honolulu, Hawaii

Stefan Schoenberg, MD Professor and Chairman Department of Clinical Radiology and Nuclear Medicine University Medical Center Mannheim Mannheim, Germany

James Shields, MD Assistant Professor Department of Radiology Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan

Claudio J. Schonholz, MD Professor Interventional Radiology, Heart and Vascular Center Medical University of South Carolina Charleston, South Carolina

Gregario A. Sicard, MD Section of Vascular Surgery Washington University School of Medicine Saint Louis, Missouri

Dhiraj M. Shah, MD Professor of Surgery Albany Medical College Albany, New York Sherene Shalhub, MD, MPH Assistant Professor Cardiothoracic and Vascular Surgery The University of Texas Medical School Houston, Texas Murray L. Shames, MD Professor of Surgery and Radiology Division of Vascular and Endovascular Surgery University of South Florida Morsani School of Medicine Tampa, Florida Melhem J. Sharafuddin, MD Associate Professor Division of Vascular Surgery University of Iowa Carver School of Medicine Iowa City, Iowa Evelyn M. Shea Section of Vascular Surgery University of Michigan Ann Arbor, Michigan Claudie M. Sheahan, MD Vascular Surgeon Oschner Baptist New Orleans, Louisiana Malachi G. Sheahan III, MD Assistant Professor of Surgery and Radiology Louisiana State University Health Sciences Center New Orleans, Louisiana Alexander D. Shepard, MD Professor of Surgery Wayne State University School of Medicine Head, Division of Vascular Surgery Henry Ford Hospital Detroit, Michigan

Anton N. Sidawy, MD, MPH Professor and Chairman Department of Surgery George Washington University Washington, DC Adnan H. Siddiqui, MD, PhD Department of Neurosurgery and Department of Radiology School of Medicine and Biomedical Sciences University at Buffalo, State University of New York; Toshiba Stroke Research Center Department of Neurosurgery Millard Fillmore Gates Circle Hospital, Kaleida Health Buffalo, New York Thomas H. Sisson, MD Associate Professor Department of Internal Medicine University of Michigan Ann Arbor, Michigan Brigitte K. Smith, MD Division of Vascular Surgery University of Wisconsin Hospital and Clinics Madison, Wisconsin Christopher J. Smolock, MD Vascular Surgery Fellow Department of Cardiovascular Surgery Methodist DeBakey Heart and Vascular Center,The Methodist Hospital Houston, Texas Jens Sonksen, MD Department of Urology University of Copenhagen Copenhagen, Denmark Thomas A. Sos, MD Professor Department of Radiology Weill Cornell Medical College Presbyterian Hospital New York, New York

xviii CONTRIBUTORS Fredrick N. Southern, MD Mary Immaculate Hospital Newport News, Virginia

Mark D. Stoneham, MA, MB, BChir Oxford University Hospitals NHS Trust Headington, United Kingdom

Sunita Srivastava, MD Department of Vascular Surgery Cleveland Clinic Cleveland, Ohio

David Strick, PhD Physical Medicine and Rehabilitation Mayo Clinic Rochester, Minnesota

Gregory A. Stanley Assistant Professor of Clinical Surgery Section of Vascular Surgery and Endovascular Interventions New York - Presbyterian Hospital Columbia University Medical Center New York, New York

Sherif Sultan, MB, BCh, MCh, MD Consultant, Vascular and Endovascular Surgeon University College Hospital; Honorary Senior Clinical Lecturer National University of Ireland; Consultant, Vascular and Endovascular Surgery Galway Clinic; Chairman, Western Vascular Institute Galway, Ireland

James C. Stanley, MD Handleman Professor of Surgery Director, Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Anthony W. Stanson, MD Mayo Clinic Rochester Rochester, New York Courtney Stellar, DO Obstetrician and Gynecologist Advocate Lutheran General Hospital Park Ridge, Illinois W. Charles Sternbergh, III, MD Chief, Vascular and Endovascular Surgery Vice Chair for Research, Department of Surgery Ochsner Clinic Foundation; Professor of Surgery University of Queensland School of Medicine New Orleans, Louisiana David H. Stone, MD Assistant Professor of Surgery Section of Vascular Surgery Dartmouth-Hitchcock Medical Center Lebanon, New Hampshire Patrick A. Stone, MD Vascular Surgeon Charleston Area Medical Center Charleston, West Virginia William M. Stone, MD Professor of Surgery Division of Vascular Surgery Mayo Clinic Arizona Scottsdale, Arizona

Lars G. Svensson, MD, PhD Director, Aorta Center Marfan and Connective Tissue Disorder Clinic; Professor of Surgery Thoracic and Cardiovascular Surgery Cleveland Clinic Cleveland, Ohio Ryan M. Svoboda, MD Department of Vascular Surgery Dartmouth Hitchcock Medical Center Lebanon, New Hampshire Andrew L. Tambyraja, MD Consultant Edinburgh Vascular Service Royal Infirmary of Edinburgh Edinburgh, Scotland Wael Tawfick, MB, BCh Western Vascular Institue Galway, Ireland Nyali E. Taylor, MD, MPH Division of Vascular and Endovascular Surgery Albert Einstein Health Network Philadelphia, Pennsylvania Janice Thai, MD Vascular Surgery Resident University of Arizona Health Sciences Center Tucson, Arizona

Matthew M. Thompson, MD Professor of Vascular Surgery St George's Vascular Institute St George's Hospital London, United Kingdom Robert W. Thompson, MD Professor of Surgery Radiology, Cell Biology, and Physiology Washington University School of Medicine; Director, Center for Thoracic Outlet Syndrome Washington University School of Medicine and Barnes-Jewish Hospital St. Louis, Missouri Ignace F.J. Tielliu, MD, PhD Division of Vascular Surgery Department of Surgery University Medical Center Groningen Groningen, Netherlands Jessica M. Titus, MD Fellow Vascular Surgery Cleveland Clinic Foundation Cleveland, Ohio Bruce Torrance, MD Assistant Professor of Clincal Surgery Department of Surgery Louisiana State University School of Medicine New Orleans, Louisiana Giovanni Torsello, MD, PhD Director, Center for Vascular and Endovascular Surgery University Hospital Munster Munster, Germany Gerald S. Treiman, MD Professor Section of Vascular Surgery Department of Surgery University of Utah Veteran Affairs Health Care System Salt Lake City, Utah Richard L. Treiman, MD Emeritus Clinical Professor of Surgery University of Southern California School of Medicine; Emeritus Adjunct Professor of Surgery University of Los Angeles, California Los Angeles, California Magdiel Trinidad-Hernandez, MD Assistant Professor of Surgery Vascular and Endovascular Surgery University of Arizona Tucson, Arizona

CONTRIBUTORS xix

William Turnipseed, MD Professor of Surgery Division of Vascular Surgery Department of Surgery University of Wisconsin Madison, Wisconsin Areck A. Ucuzian, MD Loyola University Medical Center Maywood, Illinois Gilbert R. Upchurch Jr, MD Professor and Chief Division of Vascular and Endovascular Surgery University of Virginia Charlottesville, Virginia

Frank J.Veith, MD Professor of Surgery Department of Surgery New York University, New York, New York; The William J. von Liebig Chair in Vascular Surgery Professor of Surgery The Clevelad Clinic Cleveland, Ohio Chandu Vemuri, MD Assistant Professor Washington University School of Medicine St. Louis, Missouri

Anatolie Usatii, MD Altru Health System Grand Forks, North Dakota

Eric L.G.Verhoeven, MD, PhD Department of Vascular and Endovascular Surgery Klinikum Nürnberg Süd Nürnberg, Germany

J. Hajo van Bockel, MD, PhD Professor of Surgery Department of Surgery Leiden University Medical Center Leiden, Netherlands

J. Leonel Villavicencio, MD Distinguished Professor of Surgery Uniformed Services University School of Medicne Bethesda, Maryland

Jos C. van den Berg, MD, PhD Head, Service of Interventional Radiology Ospedale Regionale di Lugano, sede Civico Lugano, Switzerland

Michel J.T.Visser, MD, PhD Department of Surgery Leiden University Medical Center Leiden, Netherlands

Frank C.Vandy, MD Minneapolis Vascular Physicians Minneapolis, Minnesota

David L.Vogel, MD Vascular Surgeon Surgical Center of the Heartland Omaha, Nebraska

Lina M.Vargas, MD Vascular Surgery Resident Cleveland Clinic, Case Western Reserve University Cleveland, Ohio Manish Varma, MD Radiologist Advanced Radiology Services Grand Rapids, Michigan Shant M.Vartanian, MD Assistant Professor of Surgery Division of Vascular and Endovascular Surgery University of California San Francisco San Francisco, California Melina Vega de Céniga, MD Department of Angiology and Vascular Surgery Hospital de Galdakao-Usansolo Galdakao, Bizkaia, Spain

Daynene Vykoukal, PhD Department of Cardiovascular Surgery Methodist DeBakey Heart and Vascular Center The Methodist Hospital Houston, Texas Thomas W. Wakefield, MD Stanley Professor of Surgery Head, Section of Vascular Surgery Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Daniel B. Walsh, MD Professor of Surgery Section of Vascular Surgery Dartmouth-Hitchcock Medical Center Lebanon, New Hampshire

Sara L. Warber, MD Associate Professor Department of Family Medicine University of Michigan; Director, University of Michigan Integrative Medicine Ann Arbor, Michigan Kenneth Warrington, MD Associate Professor of Medicine Mayo Clinic Rochester, Minnesota Peadar Waters, MB, BCh Postgraduate Surgical Researcher NUI Galway Galway, Ireland Fred A. Weaver, MD, MMM Professor and Chief Division of Vascular Surgery and Endovascular Therapy University of Southern California Los Angeles, California Mitchell R. Weaver, MD Assistant Clinical Professor Wayne State University School of Medicine Department of Vascular Surgery Henry Ford Hospital Detroit, Michigan Alan B. Weder, MD Professor Department of Internal Medicine Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Ido Weinberg, MD, MSc, MHA Fellow, Cardiology Vascular Medicine Massachusetts General Hospital Boston, Massachusetts David R. Welling, MD Professor of Surgery Uniformed Services University of the Health Sciences Bethesda, Maryland Geoffrey H. White, MD (Deceased, 2012) Royal Prince Alfred Hospital Sydney, Australia

xx CONTRIBUTORS John V. White, MD Clinical Professor Department of Surgery University of Illinois Chicago, Illinois; Chairman, Department of Surgery Advocate Lutheran General Hospital Park Ridge, Illinois Rodney A. White, MD Professor of Surgery University of California, Los Angeles Los Angeles, California Anthony D. Whittemore, MD Chief Medical Officer Brigham & Woman's Hospital Boston, Massachusetts David M. Williams, MD Professor of Radiology Department of Radiology Frankel Cardiovascular Center University of Michigan Ann Arbor, Michigan Russell A. Williams, MD Vascular and Endovascular Surgery University of California Irvine Irvine, California Samuel E. Wilson, MD Vascular and Endovascular Surgery University of California Irvine Irvine, California Edward Y. Woo, MD Chief, Vascular Surgery Medstar Washington Hospital Center and Medstar Georgetown University Hospital Washington, DC

Karen Woo, MD Division of Vascular Surgery and Endovascular Therapy University of Southern California Los Angeles, California

Christopher K. Zarins, MD Chidester Professor of Surgery, Emeritus Stanford University Stanford, California

Martha M. Wynn, MD Department of Anesthesiology University of Wisconsin Madison, Wisconsin

Mohamed A. Zayed, MD, PhD Resident Division of Vascular Surgery Department of Surgery Stanford University Stanford, California

Thomas R. Wyss, MD Vascular Surgery Research Group Imperial College Charing Cross Hospital London, United Kingdom

Gerald B. Zelenock, MD Professor and Chairman Department of Surgery University of Toledo College of Medicine Toledo, Ohio

Chengpei Xu, MD, PhD Principal Scientist Medtronic Cardiovascular Santa Rosa, California

R. Eugene Zierler, MD Professor Department of Surgery University of Washington; Medical Director D. E. Strandness Jr. Vascular Laboratory University of Washington Medical Center and Harborview Medical Center Seattle, Washington

James S.T.Yao, MD, PhD Professor of Education in Vascular Surgery Division of Vascular Surgery Northwestern University Feinberg School of Medicine Chicago, Illinois Albert J.Yoo, MD Assistant Professor Department of Radiology Harvard Medical School Massachusetts General Hospital Boston, Massachusetts Phillip M.Young, MD Associate Professor Chair, Division of Body Magnetic Resonance Imaging Department of Radiology Mayo Clinic Rochester, Minnesota

preface

The 302 chapters of the Fifth Edition of Current Therapy in Vascular and Endovascular Surgery reflect the extensive breadth of diseases affecting the arterial, venous, and lymphatic circulations. More than half of the chapters address new topics, the majority of which describe advances in endovascular interventions. The newfound clarity regarding the value of many new technologies is balanced by up-to-date presentations on those historically essential modalities that are the foundation of contemporary clinical practice. The earlier editions of this textbook—published in 1987, 1991, 1995, and 2001—were written by a collection of extraordinarily accomplished physicians and scientists, and the current work continues the tradition. Physicians and scientists from around the globe are among the 424 authors who committed their wisdom to this book. Tabular and illustrative materials have been expanded, particularly to enhance the technical aspects of contemporary care. Each chapter provides a succinct approach to a specific topic with information

intended to serve as a no-nonsense source for practitioners to obtain a creditable expert opinion. The editors are grateful to our contributors who have made this work possible, and we are most appreciative of the assistance of our publisher, Elsevier, and especially Arlene Chapelle, Laura Schmidt, and John Gabbert for bringing it all to print. We are very indebted to Calvin B. Ernst, who was the lead editor of the first four editions. We want to particularly recognize Duwana Villemure, administrative assistant to the Senior Editor, for the dedication she put forth in managing the more than 3,500 manuscript pages submitted for this volume. It is hoped that busy established clinicians as well as younger trainees—and, most importantly, patients in need with vascular ­infirmities—will benefit from the knowledge imparted in the pages of this book. James C. Stanley, MD Frank J. Veith, MD Thomas W. Wakefield, MD

xxi

Cerebrovascular Disease

Pathology of Carotid Artery Atherosclerosis Christopher K. Zarins and Chengpei Xu

Atherosclerosis is associated with a number of well-recognized systemic risk factors such as hyperlipidemia, hypertension, cigarette smoking, and diabetes mellitus. Atherosclerotic plaque formation is a localized rather than diffuse process, however, and preferentially affects certain segments of the arterial tree such as the carotid, coronary, and lower extremity arteries, while sparing others such as the upper extremity vessels. Arteriosclerotic plaques in the carotid circulation usually form at the origin of the common carotid artery as it arises from the aortic arch, at the bifurcation of the common carotid artery in the neck, or intracranially in the siphon portion of the internal carotid artery. Most clinically significant carotid plaques are localized in the carotid bifurcation, making surgical treatment by endarterectomy possible. Little plaque formation occurs in the common carotid artery proximal to the bifurcation or in the internal carotid artery distal to the carotid sinus. The unique and focal pattern of plaque formation in the arterial tree at branch points and bends has been attributed to local hemodynamic conditions and to differences in artery wall susceptibility, and these have been studied most extensively at the carotid bifurcation.

GEOMETRY OF THE CAROTID BIFURCATION Certain geometric features of the carotid bifurcation make it particularly prone to plaque formation. It is a branching point, and as such, it is vulnerable to plaque formation, as are other branching points in the arterial tree. In addition, the carotid bifurcation is unique in that the proximal portion of the internal carotid artery is enlarged to form the carotid bulb. The cross-sectional diameter of the carotid bulb is twice that of the distal internal carotid artery, and this enlargement results in more enhanced and prominent hemodynamic alterations than are found at other branchings. The carotid bulb and the associated hemodynamic alterations might exist to permit the carotid sinus and the carotid body to carry out their functions as baroreceptors and chemoreceptors better. These functions may be particularly important early in life, but the hemodynamic conditions can predispose to plaque formation later in life.

HEMODYNAMIC CONDITIONS AT THE CAROTID BIFURCATION A number of flow field changes occur at arterial branch points, and these are greatly accentuated in the carotid bifurcation owing to the presence of the carotid bulb. Hydrogen bubble flow visualization studies and quantitative flow field descriptions in model carotid bifurcations have revealed that blood flow in the common carotid artery is laminar. In the carotid bifurcation, flow separates at the flow divider between the internal and external carotid branches. Flow streamlines are compressed toward the flow divider, and flow remains laminar with high velocity and wall shear stress. Along the outer wall of the widened carotid bulb there is a large area of flow separation and stasis with nonlaminar flow, low flow velocity, and low wall shear stress (Figure 1). In the region of flow separation, a reversal of axial flow and slow fluid movement upstream, with complex secondary and tertiary flow patterns with counter-rotating helical trajectories, often occurs. In the distal, tapering portion of the bulb and in the distal internal carotid artery, flow reattaches to the wall, and velocity and shear stress increase. The flow profile again becomes laminar. Dye-washout and particle-tracking studies reveal rapid clearance along the inner wall of the internal carotid but very slow clearance from the outer sinus region, where flow separation occurs. Particles in the region of flow separation thus have an increased residence time and a greater opportunity to interact with the vessel wall. In this regard, time-dependent lipid particle vessel wall interactions would be facilitated in the region of slow flow, making plaque formation more likely to occur. In addition, bloodborne cellular elements that may be involved in atherogenesis are likely to have an increased probability of deposition on or adhesion to the vessel wall in regions of increased residence time. Radiographic and ultrasonographic studies in patients have confirmed the presence of flow separation and stasis in the outer wall region of the carotid bifurcation, where early plaques are most likely to form. In vivo human and animal studies have confirmed the relationship between low endothelial shear stress and atherosclerotic plaque localization. The presence of the carotid bulb also results in a fluctuating change in the direction of blood flow along the outer wall of the sinus, with oscillation or change in the direction of shear stress during the cardiac pulse cycle. This shear stress oscillation has been shown to correlate strongly with early plaque formation in the carotid bifurcation. Endothelial cells normally align in the direction of flow in an overlapping arrangement. The oscillating shear stress pattern can alter the orientation of intercellular overlapping junctions and result in an increase in endothelial permeability through these junctions. Oscillation of shear stress direction also may be important because it is a systolic event and thus is directly related to the heart rate. Heart rate has been shown to be an independent risk factor for coronary atherosclerosis in humans and an important factor in coronary and carotid atherosclerosis in primates. 1

2

CEREBROVASCULAR DISEASE

FIGURE 1  Hydrogen bubble flow visualization in a glass model

carotid bifurcation. Flow is laminar along the inner wall of the internal carotid artery (arrow), where velocity and shear stress are high. The cross-sectional diameter of the carotid bulb is twice that of the distal internal carotid artery, which results in a larger area of flow separation and stasis, low shear stress, increased particle residence time, and oscillation of shear stress direction (*). These hemodynamic features are associated with plaque deposition in this region of the carotid bifurcation.  (Reproduced with permission from Zarins CK, Giddens DP, Bharadvaj BK, et al. Carotid bifurcation atherosclerosis: quantitative correlation of plaque localization with flow velocity profiles and wall shear stress. Circ Res 53:502–514, 1983.)

CAROTID BIFURCATION ATHEROSCLEROSIS Quantitative morphologic studies of early human carotid atherosclerosis have revealed that early plaques localize in the carotid bulb along the outer wall in the region of low wall shear stress, flow separation, flow stasis, increased particle residence time, and shear stress oscillation. Early plaques do not form along the inner wall of the internal carotid artery, where shear stress is high, flow is laminar and unidirectional, and particle residence time is short. Intimal thickening and early plaque formation along the outer wall of the carotid bulb are common and constant features in most carotid bifurcations. Most carotid plaques are smooth, nonstenotic, and fibrous; possess a well-formed fibrous cap; and are clinically insignificant. Plaques that become clinically significant because they cause stenosis, occlusion, or embolization form in the same location as early fibrous plaques; however, they are more complex (Figure 2) and are characterized by intimal cellular proliferation, lipid accumulation, calcification, hemorrhage, and necrosis. The necrotic core is usually covered by a fibrous cap, which serves to isolate the advanced lesion from the lumen. As plaques enlarge, arteries can respond by enlarging to maintain a

FIGURE 2  Sagittal section of a complex plaque removed during

carotid endarterectomy. Probe is in the lumen of the internal carotid artery. There is a large plaque along the outer wall of the carotid sinus. This is the same region in which flow separation, low shear stress, oscillation of shear, and increased particle residence time occur in model flow studies. The necrotic core of the plaque is covered by a thin fibrous cap, which is prone to ulceration and breakdown.  (Reproduced with permission from Zarins CK. Hemodynamics in atherogenesis. In Moore WW (ed). Vascular surgery:  A comprehensive review. Orlando, 1986, Grune & Stratton, Inc.)

normal or adequate lumen caliber. Such enlargement can occur in the carotid bifurcation as well as in the coronary arteries. If lumen caliber is sufficient to provide cerebral blood flow and the fibrous cap remains intact, symptoms do not develop despite the presence of a complex, advanced lesion. Breakdown of the endothelial cell surface and fibrous cap exposes the underlying intima and necrotic core to the blood stream. This can result in platelet deposition, thrombosis, and embolization. It is not clear that endothelial cell disruption alone, without concomitant erosion of the fibrous cap, will result in these processes. Mechanisms that underlie progression of atherosclerotic carotid plaques to critical stenosis or to surface disruption, ulceration, and embolization are poorly understood. Intraplaque hemorrhage and plaque dissection have been implicated in the development of cerebrovascular symptoms, and ulceration and hemorrhage are prominent features of symptomatic carotid plaques. Ulceration or breakdown of the fibrous cap can result from hemodynamic alterations caused by a developing stenosis. As the lumen becomes narrower, blood flow velocity and shear stress increase. High shear stress in the early stages of plaque development acts to inhibit plaque formation, and under normal circumstances, shear stress is never high enough to cause endothelial cell damage. Very high levels of shear, such as occur in a critical stenosis, can promote erosion of the endothelial cell surface and fibrous cap, however. The fibrous cap can become thin or focally disrupted, resulting in embolization of the necrotic core or the



Carotid and Vertebral Artery Fibrodysplasia

3

formation of thrombus on the surface. Alternatively, blood can penetrate through the fibrous cap erosion into the lesion so as to produce a plaque dissection or hemorrhage. Intraplaque hemorrhage also can result from disruption of vasa vasora} within the plaque because advanced atherosclerotic lesions are known to contain abundant vasa vasora that arise from the adventitial layer. Intraplaque hemorrhage is a feature of both symptomatic and asymptomatic high-grade stenotic plaques. Critical carotid stenoses are characterized by a significantly higher incidence of ulceration, thrombosis, and lumen irregularity than nonstenotic lesions. These features are found in 80% of stenotic plaques. The disruptive processes that underlie plaque instability appear to be closely related to plaque size and the degree of stenosis rather than to the lipid and chemical composition of the plaque. Many complex stenotic plaques demonstrate evidence of foam cell accumulation and chronic inflammatory processes in areas of thinning and erosion of the fibrous cap. Large areas of plaque necrosis are commonly found in close proximity to the luminal surface. Leukocyte infiltration on the surface of a plaque can modulate progression and necrosis of the lesion through the release of various mediators such as proteases, free oxygen radicals, mitogenic factors, and tissue necrosis factors. These mediators can help to determine the structural integrity of the plaque. The interaction between focal, potent hemodynamic stresses and components of the plaque and artery wall in the area of a stenosis may be important determinants of plaque disruption, ulceration, and thrombosis. An increased understanding of the interactions among hemodynamic, cellular, metabolic, and structural features of carotid plaques is needed to identify factors that lead to plaque breakdown and the clinical complications of carotid atherosclerosis.

Selected References

Carotid and Vertebral Artery Fibrodysplasia

of neurologic complications is unpredictable. For instance, stroke has been described in 6% to 28% of patients with this disease, and transient ischemic attacks have been reported in 7% to 67% of these patients. Pancerebral ischemic episodes form multiple-vessel disease manifest by dizziness, and nonfocal events have been described in 2% to 50% of patients with carotid fibrodysplasia. The reported range of these events is so great as to prevent any firm conclusion as to the risk in an individual patient. Medial fibroplasia of the extracranial internal carotid artery was initially reported in 1964. A decade later this entity was reported to affect 0.42% of 3600 patients undergoing cerebral arteriographic examinations at the University of Michigan. On the basis of arteriographic examinations, others have reported similar incidences; however, most of these studies were performed for suspected cerebrovascular disease. Thus, the true incidence of carotid fibrodysplasia in the general population is undoubtedly less. The disease has been diagnosed most often during the fourth and fifth decades of life, although in some series the mean age at the time of recognition has been in the sixth decade. Although cumulative data on all types of carotid dysplasia reveal that 85% occur in women, classic medial fibrodysplasia with its string-of-beads appearance has rarely been encountered in men. Progression of medial fibroplasia in the carotid artery approaches 30%, but the exact rate of progression and factors contributing to it have yet to be defined. It is believed to be more progressive in women during their active reproductive years than after menopause. Medial fibroplasia usually involves a 2- to 6-cm segment of the internal carotid artery adjacent to the second and third cervical vertebrae (Figure 1). Bilateral medial fibrodysplastic disease occurs in approximately 65% of patients. Multiple stenoses in series with intervening mural dilations are characteristic of this disease entity. These stenoses often appear as serial narrowings on external examination

James C. Stanley

CAROTID ARTERY FIBRODYSPLASIA Extracranial carotid fibrodysplasia represents a heterogeneous nonatherosclerotic, noninflammatory vascular disease. Principal forms of carotid arterial fibrodysplasia include medial fibroplasias and intimal fibroplasia. These two entities represent distinctly different pathologic processes. Combinations of these occlusive lesions exist, as do other less easily categorized dysplastic derangements of the vessel wall. Most patients with carotid artery fibrodysplasia are likely to be asymptomatic, although the number of asymptomatic cases described in the literature is small because most reports are surgical experiences encompassing more advanced disease. Clinical complications of carotid fibrodysplasia when they do occur are related to the encroachment on the lumen, causing flow reductions, occasional collection of thrombi within the cul-de-sacs that embolize, dissections, and on rare occasions rupture with arteriovenous formation. The most catastrophic complication of carotid fibrodysplasia is a stroke from embolization or acute occlusion of the dysplastic vessel with subsequent cerebral infarction. Unfortunately, the actual risk

Beere PA, Glagov S, Zarins CK: Retarding effect of lowered heart rate on coronary atherosclerosis, Science 226:180–182, 1984. Chatzizisis YS, Jonas M, Coskun AU, et al: Prediction of the localization of high-risk coronary atherosclerotic plaques on the basis of low endothelial shear stress: an intravascular ultrasound and histopathology natural history study, Circulation 117:993–1002, 2008. Glagov S, Weisenberg E, Kolettis G, et al: Compensatory enlargement of human atherosclerotic coronary arteries, N Engl J Med 316:1371–1375, 1987. Imparato AM, Riles TS, Gorstein F: Carotid bifurcation plaque: pathologic findings associated with cerebral ischemia, Stroke 10:238–245, 1979. Ku DN, Giddens DP, Zarins CK, et al: Pulsatile flow and atherosclerosis in the human carotid bifurcation: positive correlation between plaque localization and low and oscillating shear stress, Arteriosclerosis 5:293–302, 1985. Lusby RJ, Ferrell LD, Ehrenfeld WK, et al: Carotid plaque hemorrhage: its role in production of cerebral ischemia, Arch Surg 117:1479–1488, 1982. Zarins CK: Hemodynamics in atherogenesis. In Moore WS, editor: Vascular surgery: a comprehensive review, Orlando, 1986, Grune & Stratton. Zarins CK, Bomberger RA, Glagov S: Local effects of stenoses: increased flow velocity inhibits atherogenesis, Circulation 64(Suppl II):221–227, 1981. Zarins CK, Giddens DP, Bharadvaj BK, et al: Carotid bifurcation atherosclerosis: quantitative correlation of plaque localization with flow velocity profiles and wall shear stress, Circ Res 53:502–514, 1983. Zarins CK, Weisenberg E, Kolettis G, et al: Differential enlargement of artery segments in response to enlarging atherosclerotic plaques, J Vasc Surg 7:386–394, 1988.



Carotid and Vertebral Artery Fibrodysplasia

3

formation of thrombus on the surface. Alternatively, blood can penetrate through the fibrous cap erosion into the lesion so as to produce a plaque dissection or hemorrhage. Intraplaque hemorrhage also can result from disruption of vasa vasora} within the plaque because advanced atherosclerotic lesions are known to contain abundant vasa vasora that arise from the adventitial layer. Intraplaque hemorrhage is a feature of both symptomatic and asymptomatic high-grade stenotic plaques. Critical carotid stenoses are characterized by a significantly higher incidence of ulceration, thrombosis, and lumen irregularity than nonstenotic lesions. These features are found in 80% of stenotic plaques. The disruptive processes that underlie plaque instability appear to be closely related to plaque size and the degree of stenosis rather than to the lipid and chemical composition of the plaque. Many complex stenotic plaques demonstrate evidence of foam cell accumulation and chronic inflammatory processes in areas of thinning and erosion of the fibrous cap. Large areas of plaque necrosis are commonly found in close proximity to the luminal surface. Leukocyte infiltration on the surface of a plaque can modulate progression and necrosis of the lesion through the release of various mediators such as proteases, free oxygen radicals, mitogenic factors, and tissue necrosis factors. These mediators can help to determine the structural integrity of the plaque. The interaction between focal, potent hemodynamic stresses and components of the plaque and artery wall in the area of a stenosis may be important determinants of plaque disruption, ulceration, and thrombosis. An increased understanding of the interactions among hemodynamic, cellular, metabolic, and structural features of carotid plaques is needed to identify factors that lead to plaque breakdown and the clinical complications of carotid atherosclerosis.

Selected References

Carotid and Vertebral Artery Fibrodysplasia

of neurologic complications is unpredictable. For instance, stroke has been described in 6% to 28% of patients with this disease, and transient ischemic attacks have been reported in 7% to 67% of these patients. Pancerebral ischemic episodes form multiple-vessel disease manifest by dizziness, and nonfocal events have been described in 2% to 50% of patients with carotid fibrodysplasia. The reported range of these events is so great as to prevent any firm conclusion as to the risk in an individual patient. Medial fibroplasia of the extracranial internal carotid artery was initially reported in 1964. A decade later this entity was reported to affect 0.42% of 3600 patients undergoing cerebral arteriographic examinations at the University of Michigan. On the basis of arteriographic examinations, others have reported similar incidences; however, most of these studies were performed for suspected cerebrovascular disease. Thus, the true incidence of carotid fibrodysplasia in the general population is undoubtedly less. The disease has been diagnosed most often during the fourth and fifth decades of life, although in some series the mean age at the time of recognition has been in the sixth decade. Although cumulative data on all types of carotid dysplasia reveal that 85% occur in women, classic medial fibrodysplasia with its string-of-beads appearance has rarely been encountered in men. Progression of medial fibroplasia in the carotid artery approaches 30%, but the exact rate of progression and factors contributing to it have yet to be defined. It is believed to be more progressive in women during their active reproductive years than after menopause. Medial fibroplasia usually involves a 2- to 6-cm segment of the internal carotid artery adjacent to the second and third cervical vertebrae (Figure 1). Bilateral medial fibrodysplastic disease occurs in approximately 65% of patients. Multiple stenoses in series with intervening mural dilations are characteristic of this disease entity. These stenoses often appear as serial narrowings on external examination

James C. Stanley

CAROTID ARTERY FIBRODYSPLASIA Extracranial carotid fibrodysplasia represents a heterogeneous nonatherosclerotic, noninflammatory vascular disease. Principal forms of carotid arterial fibrodysplasia include medial fibroplasias and intimal fibroplasia. These two entities represent distinctly different pathologic processes. Combinations of these occlusive lesions exist, as do other less easily categorized dysplastic derangements of the vessel wall. Most patients with carotid artery fibrodysplasia are likely to be asymptomatic, although the number of asymptomatic cases described in the literature is small because most reports are surgical experiences encompassing more advanced disease. Clinical complications of carotid fibrodysplasia when they do occur are related to the encroachment on the lumen, causing flow reductions, occasional collection of thrombi within the cul-de-sacs that embolize, dissections, and on rare occasions rupture with arteriovenous formation. The most catastrophic complication of carotid fibrodysplasia is a stroke from embolization or acute occlusion of the dysplastic vessel with subsequent cerebral infarction. Unfortunately, the actual risk

Beere PA, Glagov S, Zarins CK: Retarding effect of lowered heart rate on coronary atherosclerosis, Science 226:180–182, 1984. Chatzizisis YS, Jonas M, Coskun AU, et al: Prediction of the localization of high-risk coronary atherosclerotic plaques on the basis of low endothelial shear stress: an intravascular ultrasound and histopathology natural history study, Circulation 117:993–1002, 2008. Glagov S, Weisenberg E, Kolettis G, et al: Compensatory enlargement of human atherosclerotic coronary arteries, N Engl J Med 316:1371–1375, 1987. Imparato AM, Riles TS, Gorstein F: Carotid bifurcation plaque: pathologic findings associated with cerebral ischemia, Stroke 10:238–245, 1979. Ku DN, Giddens DP, Zarins CK, et al: Pulsatile flow and atherosclerosis in the human carotid bifurcation: positive correlation between plaque localization and low and oscillating shear stress, Arteriosclerosis 5:293–302, 1985. Lusby RJ, Ferrell LD, Ehrenfeld WK, et al: Carotid plaque hemorrhage: its role in production of cerebral ischemia, Arch Surg 117:1479–1488, 1982. Zarins CK: Hemodynamics in atherogenesis. In Moore WS, editor: Vascular surgery: a comprehensive review, Orlando, 1986, Grune & Stratton. Zarins CK, Bomberger RA, Glagov S: Local effects of stenoses: increased flow velocity inhibits atherogenesis, Circulation 64(Suppl II):221–227, 1981. Zarins CK, Giddens DP, Bharadvaj BK, et al: Carotid bifurcation atherosclerosis: quantitative correlation of plaque localization with flow velocity profiles and wall shear stress, Circ Res 53:502–514, 1983. Zarins CK, Weisenberg E, Kolettis G, et al: Differential enlargement of artery segments in response to enlarging atherosclerotic plaques, J Vasc Surg 7:386–394, 1988.

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FIGURE 1  Medial fibroplasia of the extracranial internal carotid

artery adjacent to the second and third cervical vertebrae, with characteristic serial stenoses alternating with mural aneurysms.  (Reproduced with permission from Stanley JC, Fry WJ, Seeger JF, et al: Extracranial internal carotid and vertebral artery fibrodysplasia, Arch Surg 109:213–222, 1974).

of the artery. Within the interior of the vessel, a stenosis appears as an irregular luminal lining composed of linear ridges of hyperplasticlike tissue. The area of the carotid bulb has not been observed to be involved with typical medial fibroplasia. Carotid arteries that exhibit medial fibrodysplasia are often elongated, causing obvious kinking and critical narrowings in approximately 5% of patients (Figure 2). Typical medial fibroplastic disease of the intracranial arteries has been observed but is very rare. Although the stenotic ridges of medial fibroplasias can cause stagnation of blood flow, thrombus formation in the intervening aneurysmal cul-de-sacs is a more important event. Similarly, dissections are an unusual accompaniment of medial fibroplasia. The precise incidence of the latter complication is unknown but certainly occurs in less than 10% of patients. On the other hand, dissections can obscure the underlying fibrodysplastic process, and many patients who experienced this complication might have been classified erroneously as having spontaneous dissections. Medial fibroplastic stenoses are characterized by replacement of the media by disorganized secretory cells, considered to be modified smooth muscle cells, which appear to be myofibroblasts (Figure 3). These cells are surrounded by excess fibrous connective tissue, including considerable amounts of collagen and amorphous ground substance. Between these stenoses are aneurysmal dilations that result from a scarcity of vascular smooth muscle and medial thinning in areas of advanced disease. In most instances of medial fibroplasia, the intima and internal elastic lamina are relatively unaffected, although continuity of the external elastic lamina is often lost. Secondary intimal fibroplasia can occur in areas of advanced disease and is considered a potential adaptive response to altered flow patterns and abnormal blood-surface interactions. The etiology of carotid medial fibroplasia is poorly understood but seems to be nearly identical to that occurring in similarly diseased renal arteries. Three factors appear to contribute to this form of arterial dysplasia: unusual physical stretching, vessel wall ischemia, and estrogen effects on the arterial smooth muscle cell. Peculiar tractionstretch stresses, occurring with hyperextension and extreme rotation

FIGURE 2  Medial fibroplasia of the extracranial internal carotid

artery with angulation (arrow) affecting a tortuous elongated segment.  (Reproduced with permission from Stanley JC, Fry WJ, Seeger JF, et al: Extracranial internal carotid and vertebral artery fibrodysplasia, Arch Surg 109:213–222, 1974).

FIGURE 3  Medial fibroplasia manifested by regions of excessive medial fibroproliferation, with intervening areas of medial thinning. Masson stain × 30 (longitudinal section).

of the neck, can transmit forces to the vascular smooth muscle that cause its transformation from a contractile state to a secretory state. Mechanical forces such as these are thought to be responsible for the excess production and accumulation of ground substances within the media of these vessels. Experimental evidence exists that such secretory events occur within smooth muscle subjected to physical stretching in vitro.

PATHOLOGY OF CAROTID ARTERY ATHEROSCLEROSIS

FIGURE 4  A, Medial fibroplasia of vertebral artery manifest by irregular stenoses (arrows).  (Reproduced with permission from Stanley JC, Wakefield TW: Arterial fibrodysplasia. In Rutherford RB [ed]: Vascular surgery, 3rd ed. Philadelphia, 1989, WB Saunders).  B, Medial fibroplasia of vertebral artery exhibiting multiple lesions (arrows), suggesting dissections and aneurysm formation.  (Reproduced with permission from Stanley JC, Fry WJ, Seeger JF, et al: Extracranial internal carotid and vertebral artery fibrodysplasia, Arch Surg 109:215–222, 1974).

A

Ischemia of the vessel wall itself as a result of a paucity of vasa vasora, which usually have their origins at branchings of muscular arteries, is a second factor suspected to be important in carotid medial fibroplasia. It is theorized that because of its few branches, the internal carotid artery has a paucity of intrinsic vasa vasora compared with other similarly sized vessels and that any further compromise of these nutrient vessels, such as may accompany physical stretching, might produce mural ischemia. Impaired medial blood flow in these circumstances is a probable cause of smooth muscle transformation to myofibroblasts. The unusual predilection of carotid fibroplasia for women, especially during their later reproductive years, could reflect the effects of estrogen on increasing the synthesis of proteinaceous material by the transformed smooth muscle cells of the media. Again, there is clear experimental evidence that smooth muscle becomes secretory when exposed to estrogens in the tissue culture environment, and such is likely to also occur in vivo. Medial fibroplasia might represent a systemic disease. For instance, renal artery dysplasia is known to occur in at least 25% of patients with carotid artery medial fibroplasia. The incidence of simultaneous carotid and renal artery dysplasia may be even higher, having been noted in 50% of patients undergoing arteriographic examinations of both vessels in one series. Dysplastic lesions of the external iliac and superior mesenteric arteries also have been noted in patients having carotid fibrodysplasia. In some respects, this simultaneous occurrence appears to represent a generalized arteriopathy that occurs primarily in hormonally active women, with a predilection for involvement of vessels subjected to unusual physical forces, such as renal and internal carotid arteries. Intracranial aneurysms have been reported in select series to occur in 15% to 25% of patients with carotid medial fibroplasia. The actual incidence is probably closer to 7%. These aneurysms often occur on the ipsilateral side of the extracranial dysplastic disease. They do not necessarily develop within an obviously diseased vessel; however, they can evolve as part of a generalized dysplastic process, manifest by vessel weakening at arterial branching. The anatomic distribution of these aneurysms among patients with medial fibroplasia is the same as berry aneurysms in patients unaffected by carotid dysplasia.

5

B

Intimal fibroplasia of the extracranial internal carotid artery, when associated with elongation, kinking, or coiling of the vessel, usually represents a secondary process rather than a primary dysplastic disease. Intimal fibroplastic lesions of the carotid artery occur most often as smooth focal or tubular narrowings and on rare occasions as isolated webs affecting the proximal vessel. Many of these intimal lesions likely represent the sequelae of focal trauma, an earlier arteritis, or some other noninflammatory arteriopathy with organization and cellular invasion of surface thrombus.

VERTEBRAL ARTERY FIBRODYSPLASIA Arterial fibrodysplasia of the vertebral vessels occurs most often as a stenotic disease (Figure 4A), and less frequently as nonocclusive mural aneurysms (see Figure 4B). It is an uncommon entity. Most of these lesions are asymptomatic, although an occasional patient has symptoms of posterior cerebral ischemia. In these instances both emboli from the diseased artery or occlusion are operative; occlusion is often associated with positional changes leading to kinking of the artery. Most vertebral artery fibrodysplastic lesions appear similar to medial fibrodysplasia noted in other vessels. Dysplastic changes of the vertebral arteries are seen in approximately 20% of patients with carotid artery medial fibrodysplasia. Stenoses develop most often in the lower vertebral artery adjacent to the fifth cervical vertebrae or higher, at the second cervical vertebral level. These dysplastic arteries exhibit marked irregularities and eccentric mural aneurysms. They do not manifest the typical serial stenoses and intervening mural aneurysms characteristic of carotid artery fibroplasia. Microtrauma may be an important causative factor in vertebral artery fibrodysplasia. In fact, unrecognized adventitial bleeding caused by vertebral artery injury has been noted during birth, and similar trauma can contribute to the development of vertebral artery dysplastic lesions in adulthood. Repetitive stretching, mural ischemia, and hormonal influences on vascular smooth muscle, as is the case with carotid artery fibroplasia, may be important in the pathogenesis of vertebral artery dysplasia.

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CEREBROVASCULAR DISEASE

Selected References Cloft HJ, Kallmes DF, Kallmes MH, et al: Prevalence of cerebral aneurysms in patients with fibromuscular dysplasia: a reassessment, J Neurosurg 88:436–440, 1998. Kimura H, Hosoda K, Hara Y: A very unusual case of fibromuscular dysplasia with multiple aneurysms of the vertebral artery and posterior inferior cerebellar artery. Case report, J Neurosurg 109:1108–1112, 2008. Mettinger KL: Fibromuscular dysplasia and the brain. II. Current concept of the disease, Stroke 13:53–58, 1982. Mettinger KL, Ericson K: Fibromuscular dysplasia and the brain. Observations on angiographic, clinical and genetic characteristics, Stroke 13:46–52, 1982. Olin JW, Sealove BA: Diagnosis, management, and future developments of fibromuscular dysplasia, J Vasc Surg 53:826–836, 2011.

So EL, Toole JE, Dalal P, et al: Cephalic fibromuscular dysplasia in 32 patients. Clinical findings and radiologic features, Arch Neurol 38:619–622, 1981. Stanley JC, Fry WJ, Seeger JF, et al: Extracranial internal carotid and vertebral artery fibrodysplasia, Arch Surg 109:215–222, 1974. Stanley JC, Gewertz BL, Bove EL, et al: Arterial fibrodysplasia. Histopathologic character and current etiologic concepts, Arch Surg 110:561–566, 1975. Stewart MT, Moritz MW, Smith RB III, et al: The natural history of carotid fibromuscular dysplasia, J Vasc Surg 3:305–310, 1986. Van Damme H, Sakalihasan N, Limet R: Fibromuscular dysplasia of the internal carotid artery: personal experience with 13 cases and literature review, Acta Chir Belg 99:163–168, 1999.

Carotid Artery Dissections Gerald B. Zelenock and Jihad Abbas

Carotid artery dissections have been increasingly recognized over the last several decades. Their precise incidence is hard to estimate, but it ranges from 2.5 to 3/100,000 population. They account for 2% to 3% of first-time strokes but up to 20% of strokes in patients younger than 30 years. They have been reported in children and at times are bilateral. In the setting of major trauma with liberal use of computed tomography (CT) scanning, they are recognized in 1.7% of cases. Diagnosis is often considered late after a neurologic event or not at all. Treatment remains problematic. Carotid artery dissection is sometimes thought to be a spontaneous event, which merely means that we have not yet fully understood the pathophysiology of this problem.

CLINICAL PATHOPHYSIOLOGY Carotid artery dissection can occur as a result of clear-cut stretch– traction–rotation injury (Figure 1) or direct compression between the angle of the jaw and the transverse vertebral processes (Figure 2). In the setting of significant trauma, such as a motor vehicle accident or a direct blow to the neck, cranial–cervical CT images are typically obtained and a rapid diagnosis follows. However, repetitive stress injury, whereby minor stresses of a subcritical nature accumulate and cause a dissection, is often associated with a delay in diagnosis. A number of precipitating events have been cited in case reports, including violent coughing, forceful emesis, heavy exercise, looking over one’s shoulder while driving, and chiropractic manipulation. Such reports are anecdotal at best. Intraoral trauma, typically in a child falling with a pencil or other object in his or her mouth, also has been reported. Certain diseased arteries, such as in patients with fibrodysplasia or connective tissue disorders, have a propensity to dissect. Many other arteriopathies and conditions are occasionally noted in conjunction with carotid artery dissections (Box 1). The intimal disruption leading to an intramural hematoma can narrow the lumen and reduce flow or totally occlude the carotid artery. The disrupted intima can also serve as a nidus for deposit of platelet fibrin, which can subsequently embolize. Finally, the dissected and weakened artery can produce a pseudoaneurysm.

FIGURE 1  Stretch–traction–rotation forces cause intimal injury as

the postbulbus internal carotid artery crosses the transverse processes of the second and third cervical vertebrae.  (Reproduced with permission from Zelenock GB, Kazmers A, Whitehouse WM Jr., et al: Extracranial internal carotid dissections: noniatrogenic traumatic lesions, Arch Surg 117:425–432, 1982.)

Pseudoaneurysm typically occurs in the distal internal carotid artery at the skull base. Regardless of the etiology, dissected carotid arteries remain an important clinical entity and are often associated with significant diagnostic and therapeutic challenges.

DIAGNOSIS Clinical diagnosis of carotid artery dissection is often delayed. Some dissections are asymptomatic, but some patients have minor nonspecific symptoms. In its full-blown picture, carotid dissection manifests in a young patient with typical or atypical signs of stroke or transient

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Selected References Cloft HJ, Kallmes DF, Kallmes MH, et al: Prevalence of cerebral aneurysms in patients with fibromuscular dysplasia: a reassessment, J Neurosurg 88:436–440, 1998. Kimura H, Hosoda K, Hara Y: A very unusual case of fibromuscular dysplasia with multiple aneurysms of the vertebral artery and posterior inferior cerebellar artery. Case report, J Neurosurg 109:1108–1112, 2008. Mettinger KL: Fibromuscular dysplasia and the brain. II. Current concept of the disease, Stroke 13:53–58, 1982. Mettinger KL, Ericson K: Fibromuscular dysplasia and the brain. Observations on angiographic, clinical and genetic characteristics, Stroke 13:46–52, 1982. Olin JW, Sealove BA: Diagnosis, management, and future developments of fibromuscular dysplasia, J Vasc Surg 53:826–836, 2011.

So EL, Toole JE, Dalal P, et al: Cephalic fibromuscular dysplasia in 32 patients. Clinical findings and radiologic features, Arch Neurol 38:619–622, 1981. Stanley JC, Fry WJ, Seeger JF, et al: Extracranial internal carotid and vertebral artery fibrodysplasia, Arch Surg 109:215–222, 1974. Stanley JC, Gewertz BL, Bove EL, et al: Arterial fibrodysplasia. Histopathologic character and current etiologic concepts, Arch Surg 110:561–566, 1975. Stewart MT, Moritz MW, Smith RB III, et al: The natural history of carotid fibromuscular dysplasia, J Vasc Surg 3:305–310, 1986. Van Damme H, Sakalihasan N, Limet R: Fibromuscular dysplasia of the internal carotid artery: personal experience with 13 cases and literature review, Acta Chir Belg 99:163–168, 1999.

Carotid Artery Dissections Gerald B. Zelenock and Jihad Abbas

Carotid artery dissections have been increasingly recognized over the last several decades. Their precise incidence is hard to estimate, but it ranges from 2.5 to 3/100,000 population. They account for 2% to 3% of first-time strokes but up to 20% of strokes in patients younger than 30 years. They have been reported in children and at times are bilateral. In the setting of major trauma with liberal use of computed tomography (CT) scanning, they are recognized in 1.7% of cases. Diagnosis is often considered late after a neurologic event or not at all. Treatment remains problematic. Carotid artery dissection is sometimes thought to be a spontaneous event, which merely means that we have not yet fully understood the pathophysiology of this problem.

CLINICAL PATHOPHYSIOLOGY Carotid artery dissection can occur as a result of clear-cut stretch– traction–rotation injury (Figure 1) or direct compression between the angle of the jaw and the transverse vertebral processes (Figure 2). In the setting of significant trauma, such as a motor vehicle accident or a direct blow to the neck, cranial–cervical CT images are typically obtained and a rapid diagnosis follows. However, repetitive stress injury, whereby minor stresses of a subcritical nature accumulate and cause a dissection, is often associated with a delay in diagnosis. A number of precipitating events have been cited in case reports, including violent coughing, forceful emesis, heavy exercise, looking over one’s shoulder while driving, and chiropractic manipulation. Such reports are anecdotal at best. Intraoral trauma, typically in a child falling with a pencil or other object in his or her mouth, also has been reported. Certain diseased arteries, such as in patients with fibrodysplasia or connective tissue disorders, have a propensity to dissect. Many other arteriopathies and conditions are occasionally noted in conjunction with carotid artery dissections (Box 1). The intimal disruption leading to an intramural hematoma can narrow the lumen and reduce flow or totally occlude the carotid artery. The disrupted intima can also serve as a nidus for deposit of platelet fibrin, which can subsequently embolize. Finally, the dissected and weakened artery can produce a pseudoaneurysm.

FIGURE 1  Stretch–traction–rotation forces cause intimal injury as

the postbulbus internal carotid artery crosses the transverse processes of the second and third cervical vertebrae.  (Reproduced with permission from Zelenock GB, Kazmers A, Whitehouse WM Jr., et al: Extracranial internal carotid dissections: noniatrogenic traumatic lesions, Arch Surg 117:425–432, 1982.)

Pseudoaneurysm typically occurs in the distal internal carotid artery at the skull base. Regardless of the etiology, dissected carotid arteries remain an important clinical entity and are often associated with significant diagnostic and therapeutic challenges.

DIAGNOSIS Clinical diagnosis of carotid artery dissection is often delayed. Some dissections are asymptomatic, but some patients have minor nonspecific symptoms. In its full-blown picture, carotid dissection manifests in a young patient with typical or atypical signs of stroke or transient



Carotid Artery Dissections

7

FIGURE 2  Direct internal carotid artery injury results from com-

pression of the artery between the angle of the mandible and the upper cervical vertebrae.  (Reproduced with permission from Zelenock GB, Kazmers A, Whitehouse WM Jr., et al: Extracranial internal carotid dissections: noniatrogenic traumatic lesions, Arch Surg 117:425–432, 1982).

BOX 1:  Arteriopathies and Conditions Associated with Carotid Artery Dissection • Fibrodysplasia • Ehlers–Danlos syndrome type IV • Marfan’s syndrome • α1-Antitrypsin deficiency • Type 1 collagen point mutation • Migraine • Cystic medial necrosis • Low-lying carotid bifurcation • Coils, kinks, loops • Giant cell arteritis • Temporal arteritis • Irradiated blood vessels • Moyamoya disease • Neck manipulation ischemic attack, hemicranias, and unilateral Horner’s syndrome. Ischemic neurologic symptoms are described in almost 80% of patients. They may be transient or permanent. Typically, neurologic symptoms have been preceded by local symptoms such as ipsilateral head or neck pain (hemicrania) or Horner’s syndrome. These symptoms in a young patient do not appear to change outcomes. The head and neck pain associated with dissection is not itself specific enough to allow early diagnosis. It is typically noted at or after diagnosis and is often described as having a throbbing character. Horner’s syndrome results from the disruption of sympathetic nerve fibers in the arterial wall. Cranial nerve XII involvement is most common, but virtually all cranial nerves except for the olfactory (I) have been reported involved with these

FIGURE 3  Classic tapered narrowing of the internal carotid artery

beyond the bifurcation and bulb. An extremely narrowed lumen (string sign) with associated thrombus is noted.  (Reproduced with permission from Zelenock GB, Kazmers A, Whitehouse WM Jr., et al: Extracranial internal carotid dissections: noniatrogenic traumatic lesions, Arch Surg 117:425–432, 1982).

dissections. The mechanism of cranial nerve involvement appears to be direct compression by the dissected internal carotid artery or compromise of the blood supply to the vasonervorum of the cranial nerve. Rarely, unilateral facial sweating or tinnitus suggests the diagnosis. Definitive diagnosis requires catheter-angiographic imaging, CT angiography, or magnetic resonance angiography (MRA). Carotid duplex ultrasonography can also suggest the diagnosis in selected circumstances, especially when high-resistance flow is noted or blunted waveforms or absent flow are detected, but it is not the imaging modality of choice when this diagnosis is being considered. Likewise, angiography, the previous gold standard, has given way to CT angiography or MRA. Several distinct pictures are characteristic of carotid artery dissection. Typically, the carotid bulb is spared and a tapered narrowing of the distal bulb and proximal internal carotid artery are noted (Figure 3). There may or may not be extension to the base of the skull or even intracranially. Late diagnosis results in the production of pseudoaneurysms typically located in the high internal carotid artery at the base of the skull (Figure 4). Such lesions can be a source of emboli or can cause thrombosis of the internal carotid artery.

TREATMENT Once carotid artery dissection is recognized, treatment is initiated. Virtually all authorities agree that use of antiplatelet agents and anticoagulants is appropriate. However, neither treatment has received

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CEREBROVASCULAR DISEASE

treated as would be other aneurysms, recognizing they pose a threat of further neurologic injury from embolization, thrombosis, or rupture. For selected lesions with severe stenosis or occlusion, treating the pseudoaneurysm with a covered stent or embolic occlusion has been described with acceptable results. Endovascular therapies pose the potential for benefit in properly selected patients; however, clinical series showing demonstrated improvement are not convincing. Medical treatment including antiplatelet and anticoagulation therapy is the current standard for most carotid dissections; however, a recent Cochrane review noted, “There were no randomized trials comparing either anticoagulants or antiplatelet drugs with control. . . . There were no randomized studies comparing antiplatelet agents to anticoagulants and the non-randomized studies did not show any evidence of a significant difference between the two.”

OUTCOMES Dissections diagnosed while patients are asymptomatic or mildly symptomatic tend to have a reasonable prognosis, with up to 90% of patients having a full functional recovery with healing or maturation of the dissection. Patients presenting with a fixed neurologic deficit have a variable and less optimistic course: fully 20% can die within about a week, and half of survivors have a significant residual disability, with only 40% ultimately making a good recovery. The dissections associated with significant trauma have a prognosis dictated by the associated injuries and the degree of shock.

Selected References

FIGURE 4  Saccular pseudoaneurysm of the distal internal carotid

artery at the skull base.  (Reproduced with permission from Zelenock GB, Kazmers A, Whitehouse WM Jr., et al: Extracranial internal carotid dissections: noniatrogenic traumatic lesions, Arch Surg 117:425–432, 1982).

universal acceptance and neither is completely effective in eliminating the risk of stroke. With a dissection resulting from significant systemic trauma, anticoagulants and antiplatelet medications may be contraindicated. Direct surgical interventions are rarely, if ever, advantageous and can produce adverse outcomes from thrombosis or embolization. The exceptions are the persistently symptomatic lesion amenable to intervention and the large or enlarging pseudoaneurysm. The latter are

Fleck SK, Langner S, Baldauf J, et al: Incidence of blunt craniocervical artery injuries: use of whole-body computed tomography trauma imaging with adapted computed tomography angiography, Neurosurgery 69:615–624, 2011. Lyrer P, Engelter S: Antithrombotic drugs for carotid artery dissection, Cochrane Database Syst Rev. Oct 6;(10):CD000255, 2010. Ohta H, Natarajan SK, Hauck EF, et al: Endovascular stent therapy for extracranial and intracranial carotid artery dissection: single-center experience, J Neurosurg 115:91–100, 2011. Pham MH, Rahme RJ, Arnaout O, et al: Endovascular stenting of extracranial carotid and vertebral artery dissections: a systematic review of the literature, Neurosurgery 68(4):856–866, 2011. Rao AS, Makaroun MS, Marone LK, et al: Long-term outcomes of internal carotid artery dissection, Vasc Surg 54:370–375, 2011. Schievink WI: Spontaneous dissection of the carotid and vertebral arteries, N Engl J Med 344:898–906, 2011. Stapf MC, Elkind SV, Mohr JP: Carotid artery dissection, Ann Rev Med 51:329–347, 2000. Yin W, Li Y, Fan X, et al: Feasibility and safety of stenting for symptomatic carotid arterial dissection, Cerebrovasc Dis 32(Suppl 1):11–15, 2011. Zelenock GB, Kazmers A, Whitehouse WM Jr, et al: Extracranial internal carotid dissections: noniatrogenic traumatic lesions, Arch Surg 117:425–432, 1982.



9

Carotid Artery Kinks and Coils

Carotid Artery Kinks and Coils Christopher J. Smolock, Javier E.  Anaya-Ayala, Daynene V   ykoukal,  Alan B. Lumsden, and Mark G. Davies

Most anatomic descriptions of the cervical carotid artery note a straight course to the skull base free of branches. Although angulated cervical carotid arteries, especially the internal carotid artery (ICA), are a relatively common finding in adults (∼25%), the excessive elongation of the internal carotid artery in a confined space results in a curvature termed coiling. Kinking of the internal carotid artery also results from elongation of the vessel, but it is defined as an angulation of the vessel of 90 degrees or less. Kinks are often associated with stenoses of the vessel and have been linked with arterial wall degeneration and loss of elasticity. Coiling and kinking of the vessels may also be associated with the formation of an actual looped vessel. This can result in the formation of single or double vessel loops. Metz and colleagues and Weibel and Fields have each proposed a grading system (Figure 1). Togay-Isikay modified and combined these grading systems into a single set of criteria (Table 1).

interpretation of such studies is imperative because treatment decisions, which include medical therapy, carotid operations, and interventions, are often based solely on ultrasound data. Velocity criteria are used to define carotid stenosis. Hoskins and coworkers, among others, have investigated carotid kinks and coils and the associated technical and interpretive errors using the standard approach to duplex imaging of the carotid artery. Lawrence’s group conducted a study that accounted for carotid artery curvature and tortuosity through a series of protractor angle measurements. These angle measurements were then considered along the length of the carotid artery studied so that the Doppler angle of insonation could be periodically adjusted to maintain 60 degrees before or after the apex of a curvature, but 0 degrees at the apex or any location where a 50- to 60-degree range cannot be maintained. Hemodynamically significant ICA disease was present in 15% of a study group of 200 consecutive carotid duplex patients who were not participants in follow-up studies, not endarterectomy patients, and not carotid stent patients. Disease is often proximal to areas of acute angulation. In total, only a small percentage (∼2%) of the tortuous arteries demonstrated more than 50% ICA stenosis. This suggests that there is little, if any, association between atherosclerotic

Classification of Kinks According to Severity Grade I

Grade II

Grade III

ETIOLOGY Controversy exists as to the possible etiologies of vessel elongation and the resultant conditions. Whether these are sequelae of atherosclerosis, post–carotid endarterectomy changes, fibromuscular dysplasia, age-related degeneration, or simply normal variation or developmental differences remains a matter of debate. Observation of kinks and coils in fetuses and infants support the argument that at least a portion of these phenomena arise from congenital anatomic variation and are not simply acquired. Of note, such an aberrant course and variable location can place the ICA at risk during certain pharyngeal and cervical procedures. The otolaryngology literature discusses tortuous internal carotid arteries manifesting as pharyngeal masses.

EPIDEMIOLOGY The incidence of cervical ICA anatomic variations, such as those described earlier, ranges from 10% to 40%, and most cases are bilateral. Several older studies with biased sample groups that are not representative of the general population put prevalence of carotid artery tortuosity at 30% to 35%, with 5% kinks and 6% coils. A majority of these are seen in female patients. An association exists between extracranial carotid kinks and coils and intracranial arterial aneurysms. More recently, a study population was found to have ICA tortuosity in 22% of vessels. Fifty percent of patients demonstrated bilateral tortuosity. Occurrence is typically 2 to 3 cm distal to the carotid bifurcation. A higher incidence of tortuosity in female patients was also reported. However, the true incidence and prevalence of carotid artery kinks and coils is more difficult to determine given that most patients with this condition are believed to be asymptomatic and are therefore never evaluated.

IMAGING AND DIAGNOSIS Duplex ultrasound is routinely used to screen for and investigate cervical carotid disease. Accuracy regarding the performance and

< 60 < 90

< 30 FIGURE 1  Classification of kinks according to severity.

TABLE 1:  Modified Criteria of Metz and Weibel-Fields by Togay-Isikay Malformation

Description

Tortuosity

S- or C-shaped elongation or undulation of ICA course

Mild kinking

Acute angulation of ICA between segments forming kink ≥60 degrees

Moderate kinking

Acute angulation of ICA between segments forming kink 30–60 degrees

Severe kinking

Acute angulation of ICA between segments forming kink 110 mm Hg) • Evidence of active bleeding on examination • Acute bleeding diathesis, including but not limited to the ­following: • Platelet count 1.7 or prothrombin time >15 seconds • Blood glucose concentration 1⁄3 cerebral hemisphere)

Relative Exclusion Criteria and Contraindications

• Only minor or rapidly improving stroke symptoms (clearing spontaneously) • Seizure at onset with postictal residual neurologic impairments • Major surgery or serious trauma within previous 14 days • Recent gastrointestinal or urinary tract hemorrhage (within previous 21 days) • Recent acute myocardial infarction (within previous 3 months)

Additional Characteristics for 3 to 4.5 Hours from Symptom Onset Inclusion Criteria

• Ischemic stroke diagnosis causing measurable neurologic deficit • Symptom onset 3 to 4.5 hours before beginning treatment

Exclusion Criteria

• Age >80 years • Severe stroke (NIHSS >25) • Taking an oral anticoagulant, regardless of international ­normalized ratio • History of both diabetes and previous stroke rtPA, Recombinant tissue plasminogen activator.

Box compiled from Jauch EC, Cucchiara B, Adeoye O, et al: Part 11: Adult Stroke: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, Circulation 122:S818–S828, 2010.

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Acute ischemic stroke and brain CT scan negative for bleed

Time of onset 37.5°C), evaluation of the patient’s swallowing and speech, and physical therapy. Blood pressure management differs depending on whether the patient is a candidate for rtPA, as discussed previously. Although hyperglycemia is associated with worse stroke outcome, the benefit of tight glucose control for a better stroke outcome is yet to be shown (Glucose Insulin in Stroke Trial [GIST]; U.K. Glucose Insulin in Stroke Trial [GIST-UK]). The American Stroke Association recommends the use of insulin in acute strokes for serum glucose levels of 185 mg/dL and greater. The usefulness of using insulin for serum glucose levels less than 185 mg/dL is unclear. The use of antiepileptic medications in stroke for early or isolated seizures is not recommended. Patients who develop recurrent early or late seizures after a stroke generally require pharmacologic treatment.

PREVENTING FUTURE STROKES Prevention of future strokes in stroke survivors is a major part in the management of this condition. Hospital admissions provide optimal settings in which to act on identifying and modifying the patients’ risk factors, such as obesity, smoking, dyslipidemia, diabetes mellitus, hypertension, and arrhythmias. For stroke patients with atrial fibrillation, the risks and benefits associated with anticoagulation therapy

Consider IA thrombolysis

management paradigm. DM, Diabetes mellitus; IA, intraarterial; NIHSS, National Institutes of Health Stroke Scale score; rtPA, recombinant tissue plasminogen activator.

should be weighed to decide on starting the patient on warfarin or dabigatran. Stroke patients who are not eligible for anticoagulation therapy should be on a daily regimen of antiplatelet agents, unless there is a frank contraindication for their use. The use of statins in stroke survivors is recommended. The Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) study showed that 80 mg of atorvastatin daily in patients with a recent stroke or transient ischemic attack reduced the overall incidence of strokes.

Strokes of Unknown Onset and Wake-up Strokes Strokes of unknown onset and strokes upon awakening from sleep (wake-up strokes) represent a challenge in the management of acute strokes. Multiple clinical trials are ongoing to study the value of using modern brain–blood perfusion imaging options (magnetic resonance perfusion imaging and CT perfusion imaging) to validate rtPA therapy on the basis of brain tissue viability in the absence of an exact known time of onset. Early results from such studies, including the Reperfusion Therapy in Acute Ischemic Stroke with Unclear Onset trial (RESTORE; NCT01138059), are promising.

INTRAARTERIAL THROMBOLYSIS Theoretically, intraarterial thrombolysis with recombinant prourokinase has several advantages compared with intravenous thrombolysis because it is given locally proximal to the clot, which in turn allows a higher local concentration with a smaller dose of thrombolytic agent and potentially fewer systemic side effects. Several clinical trials showed a higher rate of recanalization with intraarterial therapy (than with IV therapy alone). For example, in the Prolyse in Acute Cerebral Thromboembolism (PROACT) II trial, up to 66% of patients in the intraarterial group had recanalization, compared with 18% in the control group, but with a higher rate of symptomatic intracranial hemorrhage (10% vs. 2%), along with better outcomes for that group. Patients in whom intravenous therapy has failed or is contraindicated may be treated with intraarterial therapy alone or in combination with mechanical thrombectomy outside the window of 4.5 hours and up to 6 hours (Figure 1).

Selected References Amarenco P, Bogousslavsky J, Callahan A 3rd, et al: High-dose atorvastatin after stroke or transient ischemic attack, N Engl J Med 355:549–559, 2006. Camilo O, Goldstein LB: Seizures and epilepsy after ischemic stroke, Stroke 35:1769–1775, 2004.

Medical Therapy Including Fibrinolytic Therapy of Acute Ischemic Stroke

37

Furlan A, Higashida R, Wechsler L, et al: Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in acute cerebral thromboembolism, JAMA 282:2003–2011, 1999. Graham GD: Tissue plasminogen activator for acute ischemic stroke in clinical practice: a meta-analysis of safety data, Stroke 34:2847–2850, 2003. Hacke W, Kaste M, Bluhmki E, et al: Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke, N Engl J Med 359:1317–1329, 2008. Hill MD, Buchan AM: Thrombolysis for acute ischemic stroke: results of the canadian alteplase for stroke effectiveness study, CMAJ 172:1307–1312, 2005.

Jauch EC, Cucchiara B, Adeoye O, et al: Part 11: adult stroke: 2010 american heart association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care, Circulation 122:S818–S828, 2010. Marler JR, Tilley BC, Lu M, et al: Early stroke treatment associated with better outcome: the NINDS rt-PA stroke study, Neurology 55:1649–1655, 2000. Saver JL: Time is brain—quantified, Stroke 37:263–266, 2006. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group: Tissue plasminogen activator for acute ischemic stroke, N Engl J Med 333:1581–1587, 1995.

Diabetes as a Risk Factor in Atherosclerotic Cerebrovascular Disease

Stroke Characteristics in Diabetes

Tim Bodnar

Diabetes mellitus (DM) has been described as an epidemic in progress. By 2050 its prevalence among adults in the United States is predicted to increase from 1 in 10 to 1 in 5. Additionally, in the adolescent population its incidence is on the rise. DM results from either the absolute deficiency of insulin (type 1 [T1DM]) or resistance to the action of insulin (type 2 [T2DM]). The diagnosis of T2DM is confirmed by two levels of fasting blood glucose (BG) higher than 126 mg/dL, by a 2-hour postprandial glucose of 200 mg/dL, and by the newer criteria of hemoglobin A1c (A1c) 6.5% or higher. Two different abnormal criteria together can also make the diagnosis. In stroke, as with other medical or surgical illnesses, high BG levels can occur without a history of DM. In the recent VISTA (Virtual International Stroke Trials Archive) analysis, 43% of stroke patients had admission hyperglycemia and 36% of those with elevated BG levels had no history of DM. This stress hyperglycemia is postulated to be either a protective mechanism during early stroke or an epiphenomenon that reflects the size and severity of a stroke. Conversely, numerous reports link hyperglycemia to poor stroke outcome in both DM and stress hyperglycemia. The health burden of DM is related to its microvascular and macrovascular complications. Cardiovascular disease (CVD) is increased two- to threefold in persons with DM, independent of other risk factors, and stroke and coronary artery disease are major causes of death and morbidity, especially in those older than 65 years. In T1DM, CVD occurs 10 to 12 years after the initial diagnosis, but in T2DM it can occur as early as in the prediabetes stage. Although CVD is not as extensively studied in T1DM, its presence is often reported with nephropathy. In T2DM the presentation spectrum is wide.

DIABETES AND CEREBROVASCULAR DISEASE Patients with DM have an increased risk of cerebral infarctions. Prospective epidemiologic data have found the incidence of ischemic stroke to be two- to threefold higher in DM, independent of other risk factors. Other risk factors include hypertension, hyperlipidemia, atrial fibrillation, and obesity and are found to be additive. Women with DM have a higher stroke risk than men.

In both T1DM and T2DM, the commonest stroke phenotype is an ischemic stroke. The lacunar (small cerebral artery) subtype is consistently the most common, especially multiple lacunar strokes. Hemorrhagic strokes are six times less common, and subarachnoid hemorrhages are rare in this population. Although carotid and basilar artery occlusion are a complication of the heavy burden of atherosclerotic disease in DM, large-vessel infarcts are less common. In some studies A1c is independently related to the severity of carotid occlusion as well as to macroalbuminuria. The incidence of transient ischemic attacks (TIAs) in DM is variably reported, though the majority find a low incidence. It is postulated that irreversible and permanent damage caused by hyperglycemic neuronal changes lead to strokes rather than TIAs. Ischemic strokes in the setting of hyperglycemia are at high risk for hemorrhagic transformation, especially with reperfusion therapy. Various BG cutoffs ranging over 150 mg/dL are reported to increase this risk. DM patients also have a high incidence of stroke mortality, early recurrence, and physical disability, especially with brain stem or cerebellar infarction.

Pathophysiology of Stroke in Diabetes and Hyperglycemia Although classified as a macrovascular complication, DM causes both extracranial atherosclerotic and cortical microangiopathic changes. Carotid occlusion is common, especially in the elderly. Endothelial damage from subclinical inflammation of the vessel wall (high levels of interleukin [IL]-6, tumor necrosis factor [TNF], and TNF-α), oxidative stress increasing reactive oxygen species, lipoprotein oxidation, altered platelet aggregation, inhibition of fibrinolysis, and hypercoagulability are some vasculature features in DM. Prolonged hyperglycemia increases permanent glycosylation end products. Vessel wall reactivity to nitric oxide (NO) and free radical production is altered. The brain microvasculature is also damaged by hyalinosis and altered glucose oxidation, all these factors contributing to arterial damage. An acute ischemic event is usually mitigated by collateral circulation. The irreversibly damaged central area is surrounded by the hypoperfused penumbra within which viable cells switch to anaerobic respiration. Early hyperglycemia is favorable to this process, but if perfusion is not restored, continued production and accumulation of lactate leads to cell death, enlarging the infarct. Initial use of intravenous insulin is reported to have multifactorial benefits that include stress hormone reduction and vessel wall relaxation, which lower blood pressure (BP).

PREVENTION OF STROKE IN PATIENTS WITH DIABETES In DM, primary and secondary prevention of cerebrovascular disease requires a multifactorial approach. The STENO-2 study has unequivocally shown that controlling BG and additional risk factors

Medical Therapy Including Fibrinolytic Therapy of Acute Ischemic Stroke

37

Furlan A, Higashida R, Wechsler L, et al: Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in acute cerebral thromboembolism, JAMA 282:2003–2011, 1999. Graham GD: Tissue plasminogen activator for acute ischemic stroke in clinical practice: a meta-analysis of safety data, Stroke 34:2847–2850, 2003. Hacke W, Kaste M, Bluhmki E, et al: Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke, N Engl J Med 359:1317–1329, 2008. Hill MD, Buchan AM: Thrombolysis for acute ischemic stroke: results of the canadian alteplase for stroke effectiveness study, CMAJ 172:1307–1312, 2005.

Jauch EC, Cucchiara B, Adeoye O, et al: Part 11: adult stroke: 2010 american heart association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care, Circulation 122:S818–S828, 2010. Marler JR, Tilley BC, Lu M, et al: Early stroke treatment associated with better outcome: the NINDS rt-PA stroke study, Neurology 55:1649–1655, 2000. Saver JL: Time is brain—quantified, Stroke 37:263–266, 2006. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group: Tissue plasminogen activator for acute ischemic stroke, N Engl J Med 333:1581–1587, 1995.

Diabetes as a Risk Factor in Atherosclerotic Cerebrovascular Disease

Stroke Characteristics in Diabetes

Tim Bodnar

Diabetes mellitus (DM) has been described as an epidemic in progress. By 2050 its prevalence among adults in the United States is predicted to increase from 1 in 10 to 1 in 5. Additionally, in the adolescent population its incidence is on the rise. DM results from either the absolute deficiency of insulin (type 1 [T1DM]) or resistance to the action of insulin (type 2 [T2DM]). The diagnosis of T2DM is confirmed by two levels of fasting blood glucose (BG) higher than 126 mg/dL, by a 2-hour postprandial glucose of 200 mg/dL, and by the newer criteria of hemoglobin A1c (A1c) 6.5% or higher. Two different abnormal criteria together can also make the diagnosis. In stroke, as with other medical or surgical illnesses, high BG levels can occur without a history of DM. In the recent VISTA (Virtual International Stroke Trials Archive) analysis, 43% of stroke patients had admission hyperglycemia and 36% of those with elevated BG levels had no history of DM. This stress hyperglycemia is postulated to be either a protective mechanism during early stroke or an epiphenomenon that reflects the size and severity of a stroke. Conversely, numerous reports link hyperglycemia to poor stroke outcome in both DM and stress hyperglycemia. The health burden of DM is related to its microvascular and macrovascular complications. Cardiovascular disease (CVD) is increased two- to threefold in persons with DM, independent of other risk factors, and stroke and coronary artery disease are major causes of death and morbidity, especially in those older than 65 years. In T1DM, CVD occurs 10 to 12 years after the initial diagnosis, but in T2DM it can occur as early as in the prediabetes stage. Although CVD is not as extensively studied in T1DM, its presence is often reported with nephropathy. In T2DM the presentation spectrum is wide.

DIABETES AND CEREBROVASCULAR DISEASE Patients with DM have an increased risk of cerebral infarctions. Prospective epidemiologic data have found the incidence of ischemic stroke to be two- to threefold higher in DM, independent of other risk factors. Other risk factors include hypertension, hyperlipidemia, atrial fibrillation, and obesity and are found to be additive. Women with DM have a higher stroke risk than men.

In both T1DM and T2DM, the commonest stroke phenotype is an ischemic stroke. The lacunar (small cerebral artery) subtype is consistently the most common, especially multiple lacunar strokes. Hemorrhagic strokes are six times less common, and subarachnoid hemorrhages are rare in this population. Although carotid and basilar artery occlusion are a complication of the heavy burden of atherosclerotic disease in DM, large-vessel infarcts are less common. In some studies A1c is independently related to the severity of carotid occlusion as well as to macroalbuminuria. The incidence of transient ischemic attacks (TIAs) in DM is variably reported, though the majority find a low incidence. It is postulated that irreversible and permanent damage caused by hyperglycemic neuronal changes lead to strokes rather than TIAs. Ischemic strokes in the setting of hyperglycemia are at high risk for hemorrhagic transformation, especially with reperfusion therapy. Various BG cutoffs ranging over 150 mg/dL are reported to increase this risk. DM patients also have a high incidence of stroke mortality, early recurrence, and physical disability, especially with brain stem or cerebellar infarction.

Pathophysiology of Stroke in Diabetes and Hyperglycemia Although classified as a macrovascular complication, DM causes both extracranial atherosclerotic and cortical microangiopathic changes. Carotid occlusion is common, especially in the elderly. Endothelial damage from subclinical inflammation of the vessel wall (high levels of interleukin [IL]-6, tumor necrosis factor [TNF], and TNF-α), oxidative stress increasing reactive oxygen species, lipoprotein oxidation, altered platelet aggregation, inhibition of fibrinolysis, and hypercoagulability are some vasculature features in DM. Prolonged hyperglycemia increases permanent glycosylation end products. Vessel wall reactivity to nitric oxide (NO) and free radical production is altered. The brain microvasculature is also damaged by hyalinosis and altered glucose oxidation, all these factors contributing to arterial damage. An acute ischemic event is usually mitigated by collateral circulation. The irreversibly damaged central area is surrounded by the hypoperfused penumbra within which viable cells switch to anaerobic respiration. Early hyperglycemia is favorable to this process, but if perfusion is not restored, continued production and accumulation of lactate leads to cell death, enlarging the infarct. Initial use of intravenous insulin is reported to have multifactorial benefits that include stress hormone reduction and vessel wall relaxation, which lower blood pressure (BP).

PREVENTION OF STROKE IN PATIENTS WITH DIABETES In DM, primary and secondary prevention of cerebrovascular disease requires a multifactorial approach. The STENO-2 study has unequivocally shown that controlling BG and additional risk factors

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addressed later results in a greater reduction of cerebrovascular events and overall CV mortality.

Glycemic Control Although there is strong evidence for a reduction in microvascular complications (nephropathy, neuropathy, and retinopathy) with intensive glycemic control in T1DM and T2DM, true benefit in preventing macrovascular complications (coronary artery disease, stroke, and peripheral arterial disease) is less certain. Intensive BG control is reported to have some long-term benefit in minimizing macrovascular complications only if it is implemented early in the course of T1DM and possibly for T2DM. However, intensive control in older adults with T2DM was not clearly shown to prevent CV outcomes. In fact, studies raise the concern for a high rate of hypoglycemia and increased mortality, although the two were not definitively linked. The American Diabetes Association (ADA) therefore suggests target A1c of less than 7% for most adults with DM but an appropriately lower A1c goal of less than 8% for adults with advanced microvascular or macrovascular disease, the elderly, and those with significant comorbidities and/or a limited life expectancy. Therefore, stroke patients (focusing on secondary prevention) with DM should have a target A1c between 7% and 8%. T1DM BG targets are achieved with intensive insulin therapy: either multiple daily injections (one injection of basal insulin [glargine, detemir, NPH] and multiple injections of prandial insulin [lispro, aspart and glulisine]) or a continuous subcutaneous insulin infusion (insulin pump), both ideally managed by an endocrinologist. T2DM BG targets are usually achieved with a combination of oral and injectable agents. Some agents are preferable in stroke patients. Studies have linked metformin to CV benefits, independent of its BG-lowering ability. It is now considered first-line therapy for T2DM, but kidney function must be evaluated before metformin is used. When metformin monotherapy becomes inadequate, addition of a second oral agent, either a sulfonylurea, dipeptidyl peptidase 4 (DPP-4) inhibitor, or thiazolidinedione (TZD), can achieve further A1c reduction (roughly 1% for each additional medication). Sulfonylureas are effective but can cause prolonged hypoglycemia and therefore must be used cautiously in the elderly. Pioglitazone, a TZD, might have additional benefits in secondary prevention of CV events; however, weight gain, edema, and growing concern about increased risk of fractures and bladder cancer limit its use. The other TZD, rosiglitazone, was withdrawn in Europe and is highly restricted in the United States because of elevated risk of myocardial infarction. DPPIV inhibitors are newer drugs and when used alone have a low risk of hypoglycemia, but they are contraindicated in pancreatic disorders. Initiating insulin therapy in T2DM need not wait for failure of BG control on multiple oral agents. Insulin may be added to an oral agent, and a stepwise progression is recommended, starting with basal insulin and later adding short-acting insulin at one meal (basal plus), then at multiple meals as required for controlling hyperglycemia.

Antihypertensive Therapy In the Hypertension in Diabetes Study (HDS), it was well demonstrated that treatment of hypertension prevents cerebrovascular events in DM adults. Out of the larger UKPDS (United Kingdom Prospective Diabetes Study) cohort, 1148 hypertensive DM patients were randomized to receive either tight BP control (70%) and 15 asymptomatic (>80%) stenotic ICAs. The PAES was positioned in all 30 patients, although access for flow reversal was not successful in two of them. One patient had onset of aphasia after flow reversal, necessitating balloon deflation between subsequent stages of the procedure. There were no strokes or neurologic deficits at 30 days. Bates and coworkers reported on a series of 62 patients, including 27 (44%) with restenotic lesions after remote CEA and 11 (18%) who had previously undergone radical neck surgery and external-beam radiation therapy for cancer. There were no strokes or TIAs during the CAS procedure or follow-up. Intolerance to ICA flow arrest or reversal occurred in five patients, but the procedures were completed in stages, without sequelae. Independent neurologic evaluations detected no important changes in National Institutes of Health Stroke Scale (NIHSS) status. Rabe’s group reported results of CAS using reversal of flow in 56 patients. The procedure was technically successful in all cases. There were no strokes or deaths during the intervention. Of the 56 patients, 55 (98.2%) had a full recovery, with no change in NIHSS status,

A

B

C

D

49

immediately after deflation of the occlusion balloons. One patient had a TIA and became unconscious for 1 minute and aphasic for 3 minutes because of the strong suction required to remove a thrombus at the lesion site. These symptoms resolved completely at the end of the procedure, and postprocedure cerebral MRI showed no evidence of a new ischemic lesion or bleeding. Cerebral MRI or CT scanning was performed before CAS in 54 of the 56 patients (96.4%) in this series. The imaging studies showed that 15 of the patients (27.7%) had ipsilateral ischemic lesions and 13 (24.1%) had contralateral ischemic lesions. After CAS, cerebral MRI or CT scanning was performed in 46 of the 56 patients (82.1%), and no new ipsilateral or contralateral ischemic lesions were found.

SECOND-GENERATION FLOWREVERSAL SYSTEM AND EMPIRE TRIAL Significant improvements in the device were made in 2004, including a profile reduction from 11 Fr to 9 Fr outer diameter, when W. L. Gore acquired the flow-reversal technology from ArteriA. Hemostasis at the catheter hub was improved, and labeled ports are present in the new design (see Figure 4). This second-generation device was used during the FDA phase II EMPiRE (Embolic Protection with Reverse Flow) clinical trial. The purpose of the EMPiRE clinical trial was to assess the safety and effectiveness of the Gore Flow Reversal System to provide cerebral embolic protection during CAS procedures. The study was designed as a prospective, non-randomized, single arm clinical trial. The study objective was to compare the 30-day safety and efficacy of the GORE Flow Reversal System used with FDA-approved stents to an objective performance criterion derived from trials using distal embolic protection. The primary endpoint was a composite major adverse event rate of death, any stroke, TIA, and MI at 30 days after the procedure. Fifty-six training cases and 245 pivotal subjects were enrolled at 29 sites (Figures 5 and 6). The patient population consisted of patients with carotid artery stenosis requiring revascularization and at high risk for carotid endarterectomy (one or more anatomic or comorbid conditions). The mean age for study participants was 70 years; 16% (38 patients) were octogenarians and 165 were male. Seventy-eight (32%) were symptomatic and 167 (68%) were asymptomatic. In terms of medical history, 31% were current tobacco users, 35% had diabetes, 38% had respiratory ailments, 42% had coronary disease, 82% had hyperlipidema, and 87% suffered from hypertension. The mean procedure time was 80 minutes (25 minimum and 345 maximum),

E

F

G

FIGURE 5  EMPiRE trial case performed at the Medical University of South Carolina. A, Left carotid

arteriogram showing high-grade internal carotid artery stenosis. B, Balloon sheath and balloon wire are positioned at the common and external carotid arteries. C, Balloon wire is inflated to occlude the external carotid artery. D, Balloon sheath is inflated and flow reversal is started. At that point, the lesion was crossed and predilation was performed with a 4-mm angioplasty balloon. E, The stent is in position before delivery. F, Follow-up angiogram after stent delivery. G, Final angiogram showing satisfactory result without residual stenosis.

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were deflated. The failure rate of 3.7% (nine patients) was because of such factors as device failure, poor selection, and inadequate anatomy, such as balloon sheath rupture, tortuous anatomy, inability to position the device, and the patient’s inability to tolerate flow reversal. Flow reversal provides embolic protection prior to crossing the lesion and provides continuous protection during the critical stages of the carotid stenting procedure.

Selected References

FIGURE 6  Multiple particles were observed in the external filter at

the end of the procedure.

with a mean flow-reversal time of 15 minutes. The mean hospital stay was 1 day (24 days maximum). The EMPiRE clinical study met the primary, major adverse event endpoint. The 30-day stroke, death, and MI rate was 3.7 percent (4.5 percent including TIA) and the death or any stroke rate was low, at 2.9 percent, as compared with other embolic protection trials. Importantly, the study also showed encouraging results in some of the most challenging patient populations, with a low death, stroke, and MI rate of 2.6 percent for octogenarians and 3.8 percent for symptomatic patients. The Gore Flow Reversal System itself had a technical success rate of 96.3% (236 patients). Just six subjects (2.4%) were unable to tolerate the procedure, but there were no permanent neurologic deficits, and intolerance was resolved when the balloons

Embolic Protection Devices to Prevent Stroke during Percutaneous Angioplasty and Stenting David J. O’Connor and Peter L. Faries

The use of a cerebral protection device during carotid angioplasty and stenting (CAS) has been a component of most trials demonstrating the safety and efficacy of CAS, thereby suggesting that use of cerebral protection devices is standard practice. Currently, there are two basic mechanisms to provide cerebral embolic protection: interpose a distal protection device between the lesion and the cerebral vasculature to interrupt embolic debris dislodged during angioplasty and institute proximal cessation or reversal of flow in the internal carotid

Adami CA, Scuro A, Spinamano L, et al: Use of the Parodi anti-embolism system in carotid stenting: Italian trial results, J Endovasc Ther 9:147–154, 2002. Bates MC, Molano J, Pauley ME: Internal carotid artery flow arrest/reversal cerebral protection techniques, W V Med J 100:60–63, 2004. Jaeger HJ, Mathias KD, Hauth E, et al: Cerebral ischemia detected with diffusion-weighted MR imaging after stent implantation in the carotid artery, Am J Neuroradiol 23:200–207, 2002. Parodi JC: Is flow reversal the best method of protection during carotid stenting? J Endovasc Ther 12:414–415, 2005. Parodi JC, Ferreira LM, Sicard G, et al: Cerebral protection during carotid stenting using flow reversal, J Vasc Surg 41:416–422, 2006. Parodi JC, Schönholz C, Ferreira LM, et al: “Seat belt and air bag” technique for cerebral protection during carotid stenting, J Endovasc Ther 9:20–24, 2002. Parodi JC, Schönholz C, Parodi FE, et al: Initial 200 cases of carotid artery stenting using a reversal-of-flow cerebral protection device, J Cardiovasc Surg 48:117–124, 2007. Rabe K, Sugita J, Godel H, Sievert H: Flow-reversal device for cerebral protection during carotid artery stenting—acute and long term results, J Interv Cardiol 19:55–62, 2006. Schönholz CJ, Uflacker R, Mendaro E, et al: Techniques for carotid artery stenting under cerebral protection, J Cardiovasc Surg (Torino) 46:201–217, 2005. Vermeer SE, Prins ND, den Heijer T, et al: Silent brain infarcts and the risk of dementia and cognitive decline, N Engl J Med 348:1215–1222, 2003.

artery. The disadvantage of a filter protection device is that it requires crossing the atherosclerotic lesion without protection. The major advantage of filters, however, is that they preserve antegrade flow and perfusion to the brain. This chapter focuses on the use of the distal embolic protection, including the microporous filter and temporary occlusion balloon, during carotid angioplasty and stenting.

DEVICE CHARACTERISTICS Microporous filters are designed to catch embolic debris that is liberated during CAS before it reaches the cerebral circulation. A delivery sheath constrains the filter until it is positioned in a nondiseased segment of the internal carotid artery distal to the area to be stented. Once the filter is deployed, antegrade cerebral perfusion is maintained through the filter throughout the procedure. Embolic material dislodged during balloon angioplasty becomes trapped within the filter and is removed when the filter is reconstrained at the completion of the procedure (Figure 1). Pore sizes for filters range from 100 to 165 μm, allowing capture of particulate debris larger than the pore size yet preserving blood flow through the filter. A variety of filters are now FDA approved for clinical use in the United States and are delivered either with the filter as a component of the angiographic wire or with separate delivery over an angiographic wire already positioned into the distal internal carotid artery. Filters that are delivered attached to a fixed wire include the Angioguard XP (Cordis, Johnson & Johnson, Miami Lakes, FL), FilterWire EZ (Boston Scientific, Natick, MA), and Accunet (Abbott Laboratories,

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were deflated. The failure rate of 3.7% (nine patients) was because of such factors as device failure, poor selection, and inadequate anatomy, such as balloon sheath rupture, tortuous anatomy, inability to position the device, and the patient’s inability to tolerate flow reversal. Flow reversal provides embolic protection prior to crossing the lesion and provides continuous protection during the critical stages of the carotid stenting procedure.

Selected References

FIGURE 6  Multiple particles were observed in the external filter at

the end of the procedure.

with a mean flow-reversal time of 15 minutes. The mean hospital stay was 1 day (24 days maximum). The EMPiRE clinical study met the primary, major adverse event endpoint. The 30-day stroke, death, and MI rate was 3.7 percent (4.5 percent including TIA) and the death or any stroke rate was low, at 2.9 percent, as compared with other embolic protection trials. Importantly, the study also showed encouraging results in some of the most challenging patient populations, with a low death, stroke, and MI rate of 2.6 percent for octogenarians and 3.8 percent for symptomatic patients. The Gore Flow Reversal System itself had a technical success rate of 96.3% (236 patients). Just six subjects (2.4%) were unable to tolerate the procedure, but there were no permanent neurologic deficits, and intolerance was resolved when the balloons

Embolic Protection Devices to Prevent Stroke during Percutaneous Angioplasty and Stenting David J. O’Connor and Peter L. Faries

The use of a cerebral protection device during carotid angioplasty and stenting (CAS) has been a component of most trials demonstrating the safety and efficacy of CAS, thereby suggesting that use of cerebral protection devices is standard practice. Currently, there are two basic mechanisms to provide cerebral embolic protection: interpose a distal protection device between the lesion and the cerebral vasculature to interrupt embolic debris dislodged during angioplasty and institute proximal cessation or reversal of flow in the internal carotid

Adami CA, Scuro A, Spinamano L, et al: Use of the Parodi anti-embolism system in carotid stenting: Italian trial results, J Endovasc Ther 9:147–154, 2002. Bates MC, Molano J, Pauley ME: Internal carotid artery flow arrest/reversal cerebral protection techniques, W V Med J 100:60–63, 2004. Jaeger HJ, Mathias KD, Hauth E, et al: Cerebral ischemia detected with diffusion-weighted MR imaging after stent implantation in the carotid artery, Am J Neuroradiol 23:200–207, 2002. Parodi JC: Is flow reversal the best method of protection during carotid stenting? J Endovasc Ther 12:414–415, 2005. Parodi JC, Ferreira LM, Sicard G, et al: Cerebral protection during carotid stenting using flow reversal, J Vasc Surg 41:416–422, 2006. Parodi JC, Schönholz C, Ferreira LM, et al: “Seat belt and air bag” technique for cerebral protection during carotid stenting, J Endovasc Ther 9:20–24, 2002. Parodi JC, Schönholz C, Parodi FE, et al: Initial 200 cases of carotid artery stenting using a reversal-of-flow cerebral protection device, J Cardiovasc Surg 48:117–124, 2007. Rabe K, Sugita J, Godel H, Sievert H: Flow-reversal device for cerebral protection during carotid artery stenting—acute and long term results, J Interv Cardiol 19:55–62, 2006. Schönholz CJ, Uflacker R, Mendaro E, et al: Techniques for carotid artery stenting under cerebral protection, J Cardiovasc Surg (Torino) 46:201–217, 2005. Vermeer SE, Prins ND, den Heijer T, et al: Silent brain infarcts and the risk of dementia and cognitive decline, N Engl J Med 348:1215–1222, 2003.

artery. The disadvantage of a filter protection device is that it requires crossing the atherosclerotic lesion without protection. The major advantage of filters, however, is that they preserve antegrade flow and perfusion to the brain. This chapter focuses on the use of the distal embolic protection, including the microporous filter and temporary occlusion balloon, during carotid angioplasty and stenting.

DEVICE CHARACTERISTICS Microporous filters are designed to catch embolic debris that is liberated during CAS before it reaches the cerebral circulation. A delivery sheath constrains the filter until it is positioned in a nondiseased segment of the internal carotid artery distal to the area to be stented. Once the filter is deployed, antegrade cerebral perfusion is maintained through the filter throughout the procedure. Embolic material dislodged during balloon angioplasty becomes trapped within the filter and is removed when the filter is reconstrained at the completion of the procedure (Figure 1). Pore sizes for filters range from 100 to 165 μm, allowing capture of particulate debris larger than the pore size yet preserving blood flow through the filter. A variety of filters are now FDA approved for clinical use in the United States and are delivered either with the filter as a component of the angiographic wire or with separate delivery over an angiographic wire already positioned into the distal internal carotid artery. Filters that are delivered attached to a fixed wire include the Angioguard XP (Cordis, Johnson & Johnson, Miami Lakes, FL), FilterWire EZ (Boston Scientific, Natick, MA), and Accunet (Abbott Laboratories,

Embolic Protection Devices to Prevent Stroke during Percutaneous Angioplasty and Stenting

51

or stiffness of the filter component. In these instances, a free-wire filter system or proximal balloon occlusion should be considered. Advancing a guidewire initially, independent from the filter, provides greater flexibility. Once the wire is positioned in the internal carotid artery distal to the target, the filter can be delivered over the wire with greater ease. Filters and distal occlusion balloons should be deployed in a straight and nondiseased segment of the internal carotid artery that is of a sufficient distance distally to allow angioplasty and stent insertion, bearing in mind that the lead component of the balloon and stent delivery system might extend beyond the working component. Proximal balloon occlusion is an option when the internal carotid does not have a satisfactory distal landing zone. Consideration of sufficient collateral circulation and the patient’s ability to tolerate temporary cessation of antegrade cerebral perfusion should also be a factor in selecting an embolic protection device. A microporous filter is a viable option in patients with poor collateral circulation.

TECHNIQUE

FIGURE 1  Captured embolic material in a Filterwire.

Abbott Park, IL). Emboshield NAV6 (Abbott Laboratories) and SpiderFx (EV3, Plymouth, MN) are delivered using a wire positioned independently from the filter. The PercuSurge GuardWire (Medtronic) is a temporary occlusion balloon originally developed for use in the treatment of saphenous vein coronary artery bypass grafts. It has been adapted for use in CAS, where it prevents distal embolization by occluding blood flow in the internal carotid artery distal to the lesion. The balloon is a component of an angiographic wire and is inflated through the hypotube within the core of the wire. Similar to filter devices, the balloon is inflated in a normal segment of the internal carotid artery after passage through the lesion. An Export Catheter (Medtronic) is used to aspirate the debris and standing column of blood in the internal carotid artery between the angioplasty site and the occlusion balloon. An advantage of this device is the lower device-crossing profile and greater flexibility compared to filters; however, of necessity, cerebral perfusion is temporarily interrupted during the procedure.

SELECTION OF DEVICES There are no randomized trials comparing the advantages of one cerebral protection device against another; however, certain characteristics of patients and anatomy can help guide the choice of the best device on an individual patient basis. Particular attention should be focused on the carotid bifurcation lesion and the distal internal carotid artery. The anatomy of the access vessels, aortic arch, and common and external carotid arteries can also affect the selection of the embolic protection device, particularly if a larger-caliber proximal occlusion device is being considered. Proximal balloon occlusion should be avoided in the presence of a diseased aortic arch or proximal common carotid artery, because passage of the larger sheath and balloon inflation in the common carotid can lead to vessel damage or embolization. Characteristics of the lesion at the carotid bifurcation are also important in selecting a device. A tight, calcified lesion can make passage of a fixed-wire filter system difficult as a result of its larger profile. Extensive tortuosity of the vessel at or immediately distal to the target lesion can also increase the difficulty of advancing a protection device that is attached to the guidewire because of the inflexibility

Placement of a distal embolic protection device is preceded by obtaining femoral access; performing diagnostic aortic arch, carotid, and cerebral angiography; and placing a 6-Fr sheath in the common carotid artery proximal to the target lesion. Attention should be paid to the characteristics of the aortic arch, the complexity of the lesion at the carotid bifurcation, the distal internal carotid landing zone, and the presence of cerebral collateral circulation (see “Selection of Devices”). The patient is anticoagulated with intravenous heparin to an activated clotting time of 250 sec or greater. If a fixed-wire filter system is chosen, the wire with the filter inside the delivery system is advanced past the lesion under fluoroscopic visualization into a straight segment of internal carotid artery a few centimeters distal to the proposed level of stent placement. Deployment of the filter in an arterial segment in which the walls are parallel allows optimal apposition of the filter to the luminal surface of the internal carotid artery. The delivery system is removed, resulting in deployment of the self-expanding filter. Angiography is performed to confirm proper placement, adequate wall apposition, and preservation of antegrade cerebral blood flow (Figure 2). If difficulty is encountered in passing the delivery system as a result of vessel tortuosity, a 0.010- or 0.014-inch buddy wire can first be advanced past the lesion, with subsequent passage of the filter system. The buddy wire can provide support for passage by helping to straighten the tortuous vessel. It has far greater flexibility and torquability and so can be advanced through tortuous segments or critically stenosed lesions more readily. If the filter still will not cross the lesion, proximal protection or carotid endarterectomy (CEA) should be considered, because dilating the carotid lesion before placing the filter is not advisable owing to the high risk of embolism. With the filter in position, predilation balloon angioplasty, stent deployment, and postdilation angioplasty are all performed over the wire attached to the filter. If a buddy wire is used, it should be removed before the stent is deployed to avoid it trapping between the stent and the arterial wall. Before the filter is retrieved, contrast should be observed to flow through the filter. If not, the filter may be filled with debris, or the flow may be obstructed by spasm of the internal carotid artery at the location of the filter. In the absence of flow through the filter mechanism, embolic debris will no longer be captured within the filter and may be suspended freely in the standing column of blood between the lesion and the embolic protection device, analogous to the circumstance encountered when using an occlusion balloon for embolic protection. Under such conditions, an export catheter may be employed to evacuate the standing column of blood and the debris suspended within it. The retrieval system is then advanced forward over the filter, collapsing and reconstraining the filter and the embolic debris

52

A

CEREBROVASCULAR DISEASE

B

C

FIGURE 2  Angiography demonstrating Filterwire embolic protection.

A, The Filterwire is deployed distal to the internal carotid artery stenosis. B, The stent is positioned after angioplasty balloon predilation. C, Angiography after carotid angioplasty and stenting, demonstrating resolution of the stenosis. The filter is then reconstrained and withdrawn.

trapped within it. Care should be taken at to avoid pulling back on the filter, because this can cause the internal carotid artery to spasm or dissect. It can also cause spillage of debris. The use of a free-wire filter system is similar to that of the fixed system with the exception that a guidewire is passed first alone through the lesion into the distal internal carotid artery. With the Spider device, the delivery system with the device constrained within it is advanced over the 0.014-inch wire. The device is then advanced through the system and delivered. At the conclusion of the procedure it is then recaptured. The Emboshield NAV6 filter is used with the BareWire Filter Delivery Wire, which is passed through the lesion. This wire has a bead at the tip, and the filter is advanced independently over the wire. The bead prevents the filter from coming off the distal end of the wire. This system has the advantage of allowing the filter and wire to move independently. Removal of the NAV6 is similar to that for other filter systems. The retrieval system is advanced over the BareWire and the proximal aspect of the filter, which collapses and reconstrains the filter. The filter may then be withdrawn. The PercuSurge occlusion balloon is advanced as part of the wire system into the distal internal carotid in a similar fashion as the fixed wire filter system. The balloon, however, has a lower crossing profile and greater flexibility than the fixed-wire filter systems. This provides easier maneuverability through tortuous vessels and severely stenosed, calcified lesions. Once the balloon is in position in the internal carotid, it is inflated with dilute contrast to allow visualization using a device that attaches to the wire and instills dilute contrast through the hypotube into the occlusion balloon. Angiography is then performed to confirm occlusion of the internal carotid (Figure 3). Balloon predilation, stent insertion, and postdilation occur while the balloon is inflated. At each step, cessation of flow past the balloon should be confirmed, and the patient should be monitored for any adverse effects from temporary cessation of antegrade flow in the internal carotid artery. Once angioplasty and stenting are completed, the export catheter is advanced into the internal carotid and the standing column of blood is aspirated. The balloon is subsequently deflated and removed, and antegrade flow to the cerebral circulation is restored.

A

B

C

FIGURE 3  Angiography demonstrating use of the PercuSurge occlu-

sion balloon. A, A distal segment of internal carotid artery is chosen for placement of the balloon. B, The PercuSurge balloon is inflated, and flow in the internal carotid artery ceases subsequently. C, After carotid angioplasty and stenting, the standing column of blood is aspirated via the export catheter and the PercuSurge balloon is deflated.

CLINICAL TRIAL RESULTS There are now several randomized, controlled trials comparing outcomes of CEA and CAS for treatment of both symptomatic and asymptomatic patients. Beginning with the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial, the most recent trials have used an embolic protection device in the carotid stent treatment arms. These individual trials demonstrated the clinical efficacy of embolic protection and helped lead to FDA approval of the studied device. The SAPPHIRE trial randomized 334 patients at increased risk for CEA with either a greater than 50% symptomatic stenosis or a greater than 80% asymptomatic stenosis to either CAS or CEA. Patients treated with CAS had mandatory cerebral protection using the Angioguard filter. The study concluded that CAS using an embolic protection device is not inferior to CEA. This is based upon a 30-day periprocedural adverse event rate of 4.8% in the stent group and 9.8% in the surgical group (p = .09 for intention-to-treat analysis); at 1 year, the major adverse event rate was 12.2% for those undergoing stenting and 20.1% in those undergoing endarterectomy (p = .05). Much of the higher event rate in the endarterectomy cohort was the result of the higher rate of non–Q wave myocardial infarction, and this has fueled considerable debate regarding this trial. The Carotid Revascularization Using Endarterectomy or Stenting Systems (CaRESS) trial was a nonrandomized multicenter prospective trial aimed to prove equivalence between CEA and CAS using the Monorail Wallstent (Boston Scientific) and the GuardWire Plus (Medtronic) temporary occlusion balloon distal protection device. The study included high- and low-risk symptomatic (>50% stenosis) and asymptomatic (>75% stenosis) patients treated by either endarterectomy or stenting. Primary endpoints including death and stroke at 30 days and 1-year death, stroke, and myocardial infarction rates revealed no difference at 30 days (3.6% endarterectomy vs. 2.1% stenting) or at 1 year (13.6% endarterectomy vs. 10.0% stenting). More recently, the ICSS (International Carotid Stenting Study) and CREST (Carotid Revascularization Endarterectomy versus

53

Embolic Protection Devices to Prevent Stroke during Percutaneous Angioplasty and Stenting

Stenting) trials have reported results of randomization to either CEA or CAS. The ICSS trial left stent and filter selection to the practitioner’s discretion in the carotid stent treatment arm, with 72% of procedures using a distal embolic protection device. At 120 days, the incidence of stroke, death, or procedural myocardial infarction was 8.5% in the stenting group versus 5.2% in the endarterectomy group. CREST randomized 2502 asymptomatic and symptomatic patients to either stenting or endarterectomy. The use of the Accunet filter during stenting was mandatory. There was no difference in the aggregate rate of stroke, death, and myocardial infarction at 4 years (7.2% in the stented group and 6.8% in the endarterectomy group, p = 0.51). Further analysis revealed a higher stroke rate in the stented group (4.1% vs. 2.3%, p = .01) and a higher rate of myocardial infarction in the endarterectomy group (1.1 vs. 2.3%, p = .03). The Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) trial randomized CAS to CEA in patients with a symptomatic carotid stenosis of at least 60%, with the primary endpoint of stroke or death at 30 days after treatment. An important feature of this trial is the availability of comparative results of CAS with and without embolic protection, because embolic protection devices were not required initially and were used in 92% of patients. The data safety monitoring board enforced mandatory use of an embolic protection device after identifying significantly higher stroke rates in patients undergoing CAS without embolic protection. Patients who underwent CAS with cerebral protection had a lower 30-day stroke or death rate compared with those treated without cerebral protection (7.9% vs. 25%; p = .03). In addition to the comparative trials, several carotid registries have prospectively evaluated the safety and efficacy of CAS with individual distal embolic protection devices. These registries include, among others, the MAVErIC, CABERNET, CREATE, ARCHeR, and SECuRITY studies (Table 1). MAVErIC I and II evaluated the GuardWire and the Medtronic Exponent stent, finding a 30-day major adverse event rate of 5.4% and a 1-year event rate of 12.5% in 498 patients. The Interceptor Filter System was used during the MAVErIC III study (Evaluation of the Medtronic AVE Self-Expanding Carotid Stent System with distal protection In the treatment of Carotid stenosis). High-risk patients with either a greater than 50% symptomatic or a greater than 80% asymptomatic stenosis were treated with the Medtronic Exponent Carotid Stent and the Interceptor filter. Major adverse events rates, including death, stroke, and myocardial infarction, were 5.9% at 30 days, 5.9% at 6 months, and 11.8% at 1 year. The CABERNET study (carotid artery revascularization using the Boston Scientific FilterWire EX/EZ and the EndoTex NexStent) enrolled 454 high-risk patients with greater than 50% symptomatic and greater than 60% asymptomatic lesions by angiography. The major adverse event rates (death, ipsilateral stroke, and myocardial infarction) at 30 days and 1 year were 4.7% and 11.6%, respectively. The authors concluded that these results demonstrated that CAS is noninferior to CEA historical controls. CREATE (Carotid Revascularization with Ev3 Arterial Technology Evolution) established a 6.2% major adverse event rate and an all-stroke rate of 3.3% with the use of the Protégé stent and Spider embolic protection system. The ARCHeR (ACCULINK for Revascularization of Carotids in High-Risk patients) trial used the Acculink carotid stent with the Accunet filter, and it reported a 30-day stroke or death rate of 6.9% and 1-year composite rate of stroke, death, or myocardial infarction of 9.6%. Finally, SECuRITY is a multicenter prospective registry evaluating the Xact carotid stent with the Emboshield filter, which has reported a 30-day rate of death, stroke, or myocardial infarction of 7.2%.

TABLE 1:  Rates of Major Adverse Events during Carotid Angioplasty and Stenting in the Cerebral Protection Registries Adverse Event

MAVERiC CREATE (PercuSurge) (Spider) (%) (%)

CABERNET ARCHeR (Filterwire) (Accunet) (%) (%)

Major stroke

2.0

1.1

1.4

1.5

All stroke

3.3

3.3

3.4

5.5

Death + MI + stroke at 30 days

5.3

6.2

3.9

8.3

Death + MI + stroke at 1 year

6.4

NR

4.5

9.6

MI, Myocardial infarction; NR, not reported.

CONCLUSIONS CAS is effective and safe in appropriately selected patients. Embolic protection devices improve CAS results compared with not using them at all. Technical limitations persist, and these should be considered in the decision to perform CAS and to use specific embolic protection devices.

Selected References Brott TG, Hobson RW, Howard G, et al: Stenting versus endarterectomy for treatment of carotid-artery stenosis, N Eng J Med 363:11–23, 2010. CaRESS Steering Committee: Carotid revascularization using endarterectomy or stenting systems (CaRESS) phase I clinical trial: 1-year results, J Vasc Surg 42:213–219, 2005. Gray WA, Hopkins LN, Yadav S, et al: Protected carotid stenting in high-­ surgical-risk patients: the ARCHeR results, J Vasc Surg 44:258–269, 2006. Hill MD, Morrish W, Soulez G, et al: Multicenter evaluation of a selfexpanding carotid stent system with distal protection in the treatment of carotid stenosis, Am J Neuroradiol 27:759–765, 2006. Hopkins LN, Myla S, Grube E, et al: Carotid artery revascularization in high surgical risk patients with the NexStent and the FilterWire EX/EZ: 1-year results in the CABERNET trial, Catheter Cardiovasc Interv 71:950–960, 2008. International Carotid Stenting Study Investigators: Carotid artery stenting compared with endarterectomy in patients with symptomatic carotid stenosis (International Carotid Stenting Study): an interim analysis of a randomized controlled trial, Lancet 375:985–997, 2010. Mas JL, Chatellier G, Beyssen B, et al: Endarterectomy versus stenting in patients with symptomatic severe carotid stenosis, N Eng J Med 355:1660–1671, 2006. Safian RD, Bresahan JF, Jaff MR, et al: Protected carotid stenting in high-risk patients with severe carotid artery stenosis, J Am Coll Cardiol 47: 2384–2389, 2006. Whitlow P: SECuRITY investigators SECuRITY: multicenter evaluation of carotid stenting with a distal protection filter. Available at: http://www.tct md.com/csportal/appmanager/tctmd/main?Nfpb=true&pageLabel=TCT MDContent&hdCon=862459Accessed on June 1, 2011. Yadav JS, Wholey MH, Kuntz RE, et al: Protected carotid-artery stenting versus endarterectomy in high-risk patients, N Eng J Med 351(15): 1493–1501, 2004.

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CEREBROVASCULAR DISEASE

Blood Pressure Instability after Percutaneous Carotid Angioplasty and Stenting Mun Jye Poi and Peter H. Lin

Endovascular treatment of carotid stenosis by way of balloon angioplasty and carotid artery stenting (CAS) may be accompanied by bradycardia or hypotension. The incidence of CAS-induced bradycardia varies widely in the literature, ranging from 5% to 76%. Similarly, the incidence of hypotension resulting from endovascular carotid interventions showed a wide range from 14% to 28%, based on available reports. The wide disparity in the reported incidence of CAS-induced hemodynamic instability may be due in part to the lack of uniformity with regard to the definitions of hemodynamically significant bradycardia or hypotension. Considering all available reports, most researchers agree that hypotension is defined as a decrease of baseline systolic blood pressure by 30 mm Hg after carotid intervention. Persistent hypotension is defined as blood pressure reduction lasting more than 1 hour following carotid interventions. The significance of these conditions have been associated with adverse clinical outcomes following catheter-based carotid interventions.

PATHOPHYSIOLOGY OF HEMODYNAMIC INSTABILITY ASSOCIATED WITH CAROTID INTERVENTIONS The causative factor contributing to CAS-related hemodynamic instability is the physical stimulation of the carotid sinus baroreceptors brought on by dilation of an angioplasty balloon catheter or deployment of an intravascular stent. Baroreceptors are located within cardiovascular structures that respond to blood pressure alteration and provide instant feedback information to the brain in response to changes in arterial blood pressure. The baroreceptor nerve endings are located primarily in the adventitia of arteries, predominantly in the region of the carotid sinus and aortic arch. Baroreceptors can also be found in other arterial regions including the brachiocephalic artery and pulmonary artery. The baroreceptor sensory nerves in the carotid sinus are part of the glossopharyngeal nerve, and the other baroreceptor sensory nerves are part of the vagus nerve. The carotid sinus and aortic arch baroreceptors are tonically active at normal levels of arterial pressure, and they increase or decrease their rate of firing in response to the mean level as well as the pulsatile component of arterial pressure. The frequency of baroreceptor firing is directly proportional to the mean arterial pressure and the rate of change in pressure. This afferent input controls a variety of reflex responses encompassing autonomic and endocrine adjustments, each toward maintaining cardiovascular homeostasis. Impulses are propagated through the glossopharyngeal and vagus nerves to the nucleus tractus solitarius of the medulla, with resultant activation of parasympathetic nuclei and inhibition of sympathetic nuclei. From the nucleus, second-order

neurons pass to the caudal portion of the ventrolateral medulla. From there, third-order inhibitory neurons pass to the rostral ventrolateral medulla, the location where the cell bodies of the neurons control blood pressure. The axons of these neurons descend into the spinal cord and innervate the cell bodies of the blood pressure–regulating preganglionic sympathetic neurons in the intermediolateral gray column of the spinal cord. The axons of the preganglionic neurons leave the spinal cord and synapse on the postganglionic neurons in the ganglionic chain and collateral ganglia and the catecholaminesecreting cells in the adrenal medulla. The axons of the postganglionic noradrenergic neurons innervate the blood vessels and the heart. Impulses from the carotid sinus also initiate excitatory impulses from the nucleus tractus solitarius to the nucleus ambiguus and dorsal vagal nucleus. The increase in vagal activity results in a decrease in heart rate. Baroreceptor sensitivity is a physiologic measure of the ability of the cardiovascular autonomic system to buffer acute fluctuation in blood pressure. It is defined as changes in the heart rate in response to changes in systolic blood pressure. This value generally decreases with age and can differ widely among individuals, ranging from 2 and 30 ms/mm Hg. Low baroreceptor sensitivity has been reported in experimental atheromatous animal models as well as in patients with unilateral or bilateral carotid stenosis. Rigid atheroma in the carotid sinus and proximal internal carotid artery are believed to be associated with decreased baroreceptor sensitivity. Therefore, with the removal of the thickened atheroma by carotid endarterectomy, improvement in baroreceptor sensitivity through greater stimulation of the stretched baroreceptors may be expected. However, reports on clinical outcomes following carotid endarterectomy reveal conflicting alterations in blood pressure with baroreceptor stimulation. In this regard, it has been postulated that chronic hypertension can lead to desensitization of baroreceptors, which can diminish response to baroreceptor stimulation following carotid endarterectomy.

HEMODYNAMIC INSTABILITY TRIGGERED BY CAROTID ARTERY INTERVENTIONS Hemodynamic instability is often seen during CAS procedures, primarily at the time of inflation of an angioplasty balloon catheter. Modification of the elasticity or compliance of the arterial wall during balloon angioplasty and stent placement can alter the sensitivity of carotid baroreceptors. Balloon dilatation causes stretching of a vessel wall, resulting in superficial splitting of the intima and atherosclerotic plaque. Retraction of the intima and distention of the media results in a permanent increase in vessel diameter. It has been demonstrated in a canine model that balloon angioplasty of nondiseased carotid arteries increases the sensitivity of carotid sinus baroreceptors. This has been attributed to increased sensitivity to changes in the mechanical properties of the carotid sinus, such as greater compliance and increased diameter for a given arterial blood pressure. Enlargement of the canine carotid sinus diameter by balloon angioplasty or vein patch grafting has also produced decreases in blood pressure in normal and hypertensive dogs that persisted for days in the presence of normally active arterial baroreceptors at other sites. Adaptation of carotid sinus receptors to changes in mechanical properties in that setting appears slow and incomplete. Long-term and short-term changes in autonomic activity after CAS have also been observed. Some researchers have postulated that the presence of a carotid stent could cause persistent stimulation of the carotid sinus, causing continuous vagal stimulation during the periprocedural period. Others have reported that CAS could change an expansile artery to a relatively rigid tube, causing dysfunction of the adventitial baroreceptors and decrease of baroreceptor sensitivity. In one study, baroreceptor sensitivity is found to be decreased for



Blood Pressure Instability after Percutaneous Carotid Angioplasty and Stenting

1 month after CAS and resumed to near-baseline level at 6 months after intervention. However, this observation may be a result of the compensatory ability of the aortic and contralateral carotid baroreceptors that contribute partially to the recovery of baroreceptor sensitivity after CAS on one side.

FACTORS PREDICTING HEMODYNAMIC INSTABILITY DURING CAROTID INTERVENTIONS Profound bradycardia and hypotension associated with CAS can result in severe hemodynamic instability, which can have neurologic sequelae. Understanding of the clinical significance and potential predisposing factors of CAS-related hemodynamic instability is critical in improving the procedural safety and minimizing potential complications. Predisposing conditions associated with hemodynamic instability include advanced age, coronary artery disease, low ejection fraction, history of myocardial infarct, female sex, involvement of the carotid bulb, plaque calcification, contralateral carotid stenosis, and baseline bradycardia. When CAS is performed in elderly patients with age-related cardiac dysfunction, these patients can have poor cardiac compensation caused by depressed cardiac output state secondary to low blood volume and compromised diastolic ventricular dysfunction. These patients can also lack full cerebral autoregulatory response to bradycardia or hypotension owing to age-related neuronal impairment. As a consequence, older patients or those with compromised cardiac reserve are vulnerable to hypotensive episodes after CAS. Patients with impaired cardiac function are also at an increased risk for hemodynamic depression after CAS. Studies have also demonstrated increased sensitivity of carotid artery baroreceptors in patients with coronary artery disease. The mechanism underlying increased responsiveness to carotid sinus stimulation is not known. Activation or sensitization of the vagal nerve by receptors located in the atrial or ventricular region or the atrioventricular node caused by chronic or acute coronary ischemia has been implicated in the exaggerated carotid sinus response. Increased baroreceptor sensitivity in conjunction with a history of myocardial infarction might have predisposed some patients to postprocedural hypotension after CAS. Extensive plaque involving the carotid bulb also carries an increased risk for developing hemodynamic depression after CAS. Gupta and associates reviewed the incidence and predictors of bradycardia and hypotension in 500 consecutive patients. Plaques at the carotid bifurcation as well as calcified and ulcerated plaques were associated with a significantly higher risk of hemodynamic instability. The association of hemodynamic depression and carotid plaque characteristics was similarly demonstrated by Leisch and colleagues, who reported that transient asystole and hypotension developed in 40% of their patients. That study showed that the most important predictor of hemodynamic instability was a lesion involving the carotid bifurcation and that the plaque characters associated with hemodynamic instability after CAS are isolated internal carotid artery calcification and an ostial lesion. Intraprocedural hemodynamic instability has been shown to be an important determinant of postprocedural hemodynamic complications. Dangas observed that 44% of patients who had hypotension after CAS had intraprocedural hypotension. Only 10.4% of their patients without post-CAS hypotension had evidence of intraprocedural hypotension. Qureshi and colleagues also found intraprocedural hypotension to be the strongest predictor of postprocedural hypotension. Gupta and associates reported findings that diabetes mellitus and a history of smoking reduced the risk of hemodynamic instability after CAS. They postulated that long-term smoking impairs the carotid baroreceptor response and augments the sympathetic tone, which raises the blood pressure and heart rate. Similarly,

55

diabetes mellitus is known to impair cardiovascular autonomic response by attenuating parasympathetic nerve function, which might attenuate the carotid baroreceptor stimulation triggered by carotid intervention. In contrast, we reported a series of 416 veteran patients who developed hemodynamic alteration following CAS. In these patient cohorts who have a high prevalence of smoking and diabetes, our study found that diabetes mellitus and a history of smoking were not protective toward hemodynamic instability during CAS. Many reports, including ours, showed that patients who had postendarterectomy-related carotid stenosis and who underwent CAS were less likely to develop hemodynamic depression after CAS. In patients who have had a prior carotid endarterectomy, the carotid sinus or the carotid sinus nerve, which lies in the vicinity of the carotid bulb, has been routinely divided or interrupted surgically. As a result, the carotid adventitial baroreceptors or the afferent nerve fibers are unable to send impulses to the medulla when triggered by balloon dilatation, which likely accounts for the low incidence of CAS-induced bradycardia in patients with carotid stenosis following carotid endarterectomy.

MANAGEMENT OF HEMODYNAMIC INSTABILITY INDUCED BY CAROTID ANGIOPLASTY AND STENTING Most of the hemodynamic instability events during and after CAS are transient and self-limiting. Most patients experienced transient bradycardia with or without asystole that resolved after balloon deflation and intravenous administration of glycopyrrolate or atropine. Most events resolve at the conclusion of the intensive care unit monitoring period, in less than 48 hours. Conservative management with intravenous fluids and medications, such as atropine or glycopyrrolate, is often sufficient treatment and confers no increased periprocedural risk. Persistent hemodynamic depression requiring vasopressor support develops in up to 17% of patients. This phenomenon is associated with an increased risk of developing major periprocedural adverse clinical events or stroke. Patients in this group also have longer stays in the intensive care unit and hospital compared with patients with transient hemodynamic instability. Persistent hypotension, not hypotension alone, is associated with an increased risk of adverse clinical outcome. In our practice, we administer intravenous atropine only when bradycardia is triggered by carotid instrumentation. We have adapted our practice by paying particular attention to hemodynamic variables during endovascular carotid interventions whereby a nurse or technician would call out the heart rate on the basis of an electrocardiogram tracing during carotid balloon angioplasty or carotid stent deployment. This practice allows the physician to remain focused on the fluoroscopic monitor while receiving an audible feedback on the patient’s heart rate and enables a clear communication among all personnel about the decision of atropine administration. Although we have reported a potential adjunctive role of temporary transfemoral cardiac pacing to treat bradycardia during CAS, we have found that prompt administration of atropine in selective cases is effective in reversing CAS-induced bradycardia. Others have advocated prophylactic atropine administration in all patients undergoing CAS. It should be emphasized that prophylactic treatment with atropine is not without potential harmful effects. Qureshi and colleagues reported a paradoxical finding of a higher risk of postprocedural bradycardia associated with prophylactic use of atropine in patients undergoing CAS. Other side effects of atropine include tachycardia, confusion, urinary retention, and arrhythmias. With resultant tachycardia and arrhythmia, there is an increased cardiac oxygen demand and added myocardial workload that can lead to adverse cardiac events, particularly because many of these patients are elderly and have underlying coronary artery disease.

56

CEREBROVASCULAR DISEASE

The risk factors of hemodynamic instability after CAS should be recognized. Postprocedural monitoring and management in the intensive care unit can facilitate the identification of hemodynamic complications and prompt intervention. We recommend postprocedural monitoring of blood pressure and electrocardiographic changes in patients undergoing CAS, particularly in patients who have intraoperative hemodynamic instability.

Selected References Bush RL, Lin PH, Bianco CC, et al: Reevaluation of temporary transvenous cardiac pacemaker usage during carotid angioplasty and stenting: a safe and valuable adjunct, Vasc Endovascular Surg 38:229–235, 2004. Cayne NS, Faries PL, Trocciola SM, et al: Carotid angioplasty and stentinduced bradycardia and hypotension: impact of prophylactic atropine administration and prior carotid endarterectomy, J Vasc Surg 41:956–961, 2005. Dangas G, Laird JR Jr, Satler LF, et al: Postprocedural hypotension after ­carotid artery stent placement: predictors and short- and long-term ­clinical outcomes, Radiology 215:677–683, 2000.

Cerebral Hyperperfusion Syndrome After Carotid Endarterectomy and Carotid Stenting Thomas S. Riles and Caron B. Rockman

Cerebral hyperperfusion syndrome (CHS) and intracerebral hemorrhage are perhaps the most feared complications of carotid endarterectomy (CEA) and carotid angioplasty and stenting (CAS). Although relatively uncommon, such complications can have devastating and often fatal sequelae and remain a significant cause of neurologic morbidity after carotid interventions. Intracerebral hemorrhage (ICH) after cerebral revascularization was recognized as early as 1964 by Wylie and colleagues and was found to be associated with patients who underwent CEA or carotid thrombectomy for an acute stroke. In these patients it was proposed that removal of an obstructing plaque or thrombus and subsequent cerebral reperfusion converted an ischemic infarct into a hemorrhagic one, most likely because of capillary and arteriolar damage caused by the original ischemic insult. In 1984, Bernstein and associates reported the first CEA patient with postoperative unilateral head, face, and eye pain, classic symptoms of CHS. This patient went on to have seizures and eventually died of a delayed ICH that occurred in the absence of other risk factors.

PATHOPHYSIOLOGY It is generally hypothesized that the cause of intracranial hemorrhage after CEA or CAS is postoperative hyperperfusion, that is, increased blood flow and/or increased pressure in the intracranial vessels. Schroeder and colleagues reported that even after uncomplicated

Feng B, Li BY, Nauman EA, et al: Theoretical and electrophysiological evidence for axial loading about aortic baroreceptor nerve terminals in rats, Am J Physiol Heart Circ Physiol 293:H3659–H3672, 2007. Gupta R, Abou-Chebl A, Bajzer CT, et al: Rate, predictors, and consequences of hemodynamic depression after carotid artery stenting, J Am Coll Cardiol 47:1538–1543, 2006. Leisch F, Kerschner K, Hofmann R, et al: Carotid sinus reactions during carotid artery stenting: predictors, incidence, and influence on clinical outcome, Catheter Cardiovasc Interv 58:516–523, 2003. Lin PH, Zhou W, Kougias P, et al: Factors associated with hypotension and bradycardia after carotid angioplasty and stenting, J Vasc Surg 46:846–853, 2007. McKevitt FM, Sivaguru A, Venables GS, et al: Effect of treatment of carotid artery stenosis on blood pressure: a comparison of hemodynamic disturbances after carotid endarterectomy and endovascular treatment, Stroke 34:2576–2581, 2003. Nano G, Dalainas I, Bianchi P, et al: Ballooning-induced bradycardia during carotid stenting in primary stenosis and restenosis, Neuroradiology 48:533–536, 2006. Qureshi AI, Luft AR, Sharma M, et al: Frequency and determinants of postprocedural hemodynamic instability after carotid angioplasty and stenting, Stroke 30:2086–2093, 1999.

CEA there is a pronounced increase in cerebral blood flow, as much as 37% in the ipsilateral and 33% in the contralateral hemisphere. The increase was most pronounced 2 to 4 days after surgery. After the initial rise, the blood flow gradually returned to normal. Jansen and coworkers documented increased transcranial Doppler blood flow velocity measurements after CEA. The increases of peak blood flow velocities and pulsatility indices in patients who developed ICH were significantly higher than in patients who did not. Riegel and colleagues noted that when electroencephalography (EEG) was performed in patients with classic hyperperfusion syndrome, periodic lateralizing epileptiform discharges (PLEDs) were invariably noted ipsilateral to the endarterectomy site. These discharges denote an acute, localized cerebral focus of irritability. Several groups have documented intracranial changes in the specimens of patients who died from ICH after CEA that closely resembled histologic changes seen in malignant hypertension. Interestingly, hemorrhage occasionally occurred within healthy brain tissue, not simply in areas of previous infarction. Postoperative ICH appears to result from certain events. Patients with chronic severe carotid occlusive disease and relative cerebral hypoperfusion and ischemia experience maximal vascular dilatation as a protective measure, and this in turn likely causes paralysis of normal vascular autoregulatory mechanisms. When CEA or CAS is performed, this lack of autoregulation results in an increased perfusion pressure supplying an area in which vessels are fixed in dilation. This pathophysiologic mechanism is analogous to reperfusion injuries of ischemic limbs and other tissues. In less severe forms, hyperperfusion can result in mild cerebral edema, headache, and seizures. When an abnormal hyperperfused vessel ruptures, intracerebral hemorrhage results.

INCIDENCE The true incidence of CHS is difficult to ascertain because postoperative hypertension and headache are not uncommon after CEA. A review by Bouri and colleagues found the reported incidence in 36 studies to be approximately 1% of all cases; ICH, much easier to document, occurred in 0.5% of the reported cases they reviewed. In a review of data from the National Inpatient Sample by Timaran and associates, among 135,903 cases of carotid revascularization reported in 2005, the incidence of ICH among the CEA patients was 0.016%, and incidence among CAS patients was 0.15%. Because

56

CEREBROVASCULAR DISEASE

The risk factors of hemodynamic instability after CAS should be recognized. Postprocedural monitoring and management in the intensive care unit can facilitate the identification of hemodynamic complications and prompt intervention. We recommend postprocedural monitoring of blood pressure and electrocardiographic changes in patients undergoing CAS, particularly in patients who have intraoperative hemodynamic instability.

Selected References Bush RL, Lin PH, Bianco CC, et al: Reevaluation of temporary transvenous cardiac pacemaker usage during carotid angioplasty and stenting: a safe and valuable adjunct, Vasc Endovascular Surg 38:229–235, 2004. Cayne NS, Faries PL, Trocciola SM, et al: Carotid angioplasty and stentinduced bradycardia and hypotension: impact of prophylactic atropine administration and prior carotid endarterectomy, J Vasc Surg 41:956–961, 2005. Dangas G, Laird JR Jr, Satler LF, et al: Postprocedural hypotension after ­carotid artery stent placement: predictors and short- and long-term ­clinical outcomes, Radiology 215:677–683, 2000.

Cerebral Hyperperfusion Syndrome After Carotid Endarterectomy and Carotid Stenting Thomas S. Riles and Caron B. Rockman

Cerebral hyperperfusion syndrome (CHS) and intracerebral hemorrhage are perhaps the most feared complications of carotid endarterectomy (CEA) and carotid angioplasty and stenting (CAS). Although relatively uncommon, such complications can have devastating and often fatal sequelae and remain a significant cause of neurologic morbidity after carotid interventions. Intracerebral hemorrhage (ICH) after cerebral revascularization was recognized as early as 1964 by Wylie and colleagues and was found to be associated with patients who underwent CEA or carotid thrombectomy for an acute stroke. In these patients it was proposed that removal of an obstructing plaque or thrombus and subsequent cerebral reperfusion converted an ischemic infarct into a hemorrhagic one, most likely because of capillary and arteriolar damage caused by the original ischemic insult. In 1984, Bernstein and associates reported the first CEA patient with postoperative unilateral head, face, and eye pain, classic symptoms of CHS. This patient went on to have seizures and eventually died of a delayed ICH that occurred in the absence of other risk factors.

PATHOPHYSIOLOGY It is generally hypothesized that the cause of intracranial hemorrhage after CEA or CAS is postoperative hyperperfusion, that is, increased blood flow and/or increased pressure in the intracranial vessels. Schroeder and colleagues reported that even after uncomplicated

Feng B, Li BY, Nauman EA, et al: Theoretical and electrophysiological evidence for axial loading about aortic baroreceptor nerve terminals in rats, Am J Physiol Heart Circ Physiol 293:H3659–H3672, 2007. Gupta R, Abou-Chebl A, Bajzer CT, et al: Rate, predictors, and consequences of hemodynamic depression after carotid artery stenting, J Am Coll Cardiol 47:1538–1543, 2006. Leisch F, Kerschner K, Hofmann R, et al: Carotid sinus reactions during carotid artery stenting: predictors, incidence, and influence on clinical outcome, Catheter Cardiovasc Interv 58:516–523, 2003. Lin PH, Zhou W, Kougias P, et al: Factors associated with hypotension and bradycardia after carotid angioplasty and stenting, J Vasc Surg 46:846–853, 2007. McKevitt FM, Sivaguru A, Venables GS, et al: Effect of treatment of carotid artery stenosis on blood pressure: a comparison of hemodynamic disturbances after carotid endarterectomy and endovascular treatment, Stroke 34:2576–2581, 2003. Nano G, Dalainas I, Bianchi P, et al: Ballooning-induced bradycardia during carotid stenting in primary stenosis and restenosis, Neuroradiology 48:533–536, 2006. Qureshi AI, Luft AR, Sharma M, et al: Frequency and determinants of postprocedural hemodynamic instability after carotid angioplasty and stenting, Stroke 30:2086–2093, 1999.

CEA there is a pronounced increase in cerebral blood flow, as much as 37% in the ipsilateral and 33% in the contralateral hemisphere. The increase was most pronounced 2 to 4 days after surgery. After the initial rise, the blood flow gradually returned to normal. Jansen and coworkers documented increased transcranial Doppler blood flow velocity measurements after CEA. The increases of peak blood flow velocities and pulsatility indices in patients who developed ICH were significantly higher than in patients who did not. Riegel and colleagues noted that when electroencephalography (EEG) was performed in patients with classic hyperperfusion syndrome, periodic lateralizing epileptiform discharges (PLEDs) were invariably noted ipsilateral to the endarterectomy site. These discharges denote an acute, localized cerebral focus of irritability. Several groups have documented intracranial changes in the specimens of patients who died from ICH after CEA that closely resembled histologic changes seen in malignant hypertension. Interestingly, hemorrhage occasionally occurred within healthy brain tissue, not simply in areas of previous infarction. Postoperative ICH appears to result from certain events. Patients with chronic severe carotid occlusive disease and relative cerebral hypoperfusion and ischemia experience maximal vascular dilatation as a protective measure, and this in turn likely causes paralysis of normal vascular autoregulatory mechanisms. When CEA or CAS is performed, this lack of autoregulation results in an increased perfusion pressure supplying an area in which vessels are fixed in dilation. This pathophysiologic mechanism is analogous to reperfusion injuries of ischemic limbs and other tissues. In less severe forms, hyperperfusion can result in mild cerebral edema, headache, and seizures. When an abnormal hyperperfused vessel ruptures, intracerebral hemorrhage results.

INCIDENCE The true incidence of CHS is difficult to ascertain because postoperative hypertension and headache are not uncommon after CEA. A review by Bouri and colleagues found the reported incidence in 36 studies to be approximately 1% of all cases; ICH, much easier to document, occurred in 0.5% of the reported cases they reviewed. In a review of data from the National Inpatient Sample by Timaran and associates, among 135,903 cases of carotid revascularization reported in 2005, the incidence of ICH among the CEA patients was 0.016%, and incidence among CAS patients was 0.15%. Because



Cerebral Hyperperfusion Syndrome After Carotid Endarterectomy and Carotid Stenting

the data are based on discharge diagnosis and not postdischarge follow-up, it is likely these figures underestimate the actual incidence. The data do suggest, however, that the risk is higher with CAS than with CEA. Although the cause of perioperative stroke in most large series of CEAs is less than 2%, ICH represents a significant component of those strokes. In a study by Ouriel and coworkers of 1471 CEAs, ICH accounted for 35% of the 31 perioperative neurologic events. Massive hemorrhage and death occurred in four of their patients. Others have reported a similarly high mortality for ICH. Considering the severe morbidity of this particular complication, it is important to recognize which patients are at increased risk.

RISK FACTORS A number of risk factors have been identified that appear to predispose patients toward the development of CHS. The most commonly recognized of these are a preoperative stroke, especially if recent, a high-grade stenosis of the ipsilateral artery (>90%), severe intraoperative and postoperative hypertension, anticoagulant use, chronic cerebral ischemia, and perhaps contralateral carotid artery occlusion. In the study by Ouriel and coworkers, 11 patients who suffered intracranial hemorrhage after CEA were compared with 50 control patients who had no postoperative hemorrhage. Five factors were associated with an increased risk of ICH: increased age, a history of hypertension, significant ipsilateral stenosis, significant contralateral stenosis, and contralateral carotid occlusion. The patients who sustained ICH had a mean ipsilateral stenosis of 92% compared with 77% in the 50 patients without hemorrhage. Factors identified in this study as not being significantly associated with perioperative ICH included gender, operative indication, smoking, diabetes, and the use of antiplatelet therapy or perioperative heparin therapy. The vast majority of patients undergoing CEA or CAS have one or more of the above-mentioned risk factors and do not develop CHS or ICH. Carotid intervention for the appropriate indications should not be denied a patient who has these risk factors. However, the presence of one or more of these risk factors should serve to alert the surgeon or interventionalist of the possible development of the syndrome so that the diagnosis can be made and treatment can instituted as early as possible. Dalman and associates have shown that an increased in intracranial blood flow during CEA, determined by intraoperative transcranial Doppler measurements, correlates with postoperative CHS. Whether this is an independent predictor or an expected finding in a patient undergoing CEA or CAS for a high-grade stenosis is unclear.

CLINICAL MANIFESTATIONS The most common symptom of CHS is headache followed by seizures and hemiparesis. Postoperative hypertension, although not a symptom, is almost universally present. In the literature review by Bouri and associates, 36% of the patients presented with seizures, 31% with hemiparesis, and 33% with both. The incidence of postoperative hypertension in CHS patients compared with controls was significant (p < .001). Those with CHS had a mean systolic blood pressure of 189 mm Hg. Unlike other complications of CEA and CAS, symptoms of CHS often do not manifest until several days after the procedure. In a report by Reigel and associates of 10 patients with uncomplicated CHS, the mean interval between the CEA and onset of headaches was 3 days. Among their patients, nine developed focal seizures and six had transient focal neurologic deficits. All patients fully recovered. In the review by Bouri and associates, 92% of the patients developed symptoms during the first postoperative week, but the mean interval between surgery and symptoms was 5 days. Like CHS, ICH can occur in the early postoperative period, but it is more commonly is delayed. In the report by Ouriel and coworkers,

57

the median interval between surgery and ICH was 3 days. In a series from our institution, five of 2024 patients undergoing CEA developed ICH, and three occurred on postoperative day 4 or later. When a patient develops a postoperative neurologic deficit, it is important to differentiate among an ischemic thromboembolic episode (usually from the endarterectomy site), CHS, and intracranial bleed. The management of these complications is quite different. Anticoagulation and immediate reexploration may be appropriate for intraarterial thrombus formation, whereas these measures would not be appropriate for CHS and ICH. It has been our experience that neurologic deficits related to CHS and ICH not only occur later in the postoperative course but also are commonly associated with severe headache, seizures, and some degree of obtundation; however, these deficits are unreliable for making a definitive diagnosis. These symptoms and a duplex scan showing normal flow in the recently reconstructed carotid artery can lead the surgeon to order an emergent computed tomography (CT) scan of the brain before proceeding with anticoagulation and reoperation.

DIAGNOSIS The diagnosis of uncomplicated cerebral hyperperfusion syndrome is often clinical and rests heavily on the surgeon’s suspicion in a patient with appropriate risk factors. Certainly any patient with severe postCEA or post-CAS headache should be thoroughly evaluated. Frank seizures are an obvious sign as well. CT scanning is the test of choice to evaluate for intracerebral hemorrhage or simple edema that can occur with CHS. An EEG can show periodic lateralizing epileptiform discharges (PLEDs) or frank seizure activity. The patient with a focal neurologic deficit corresponding to the side of operation, especially when this develops early in the postoperative course, can be more puzzling. These patients must undergo prompt evaluation to document absence of thrombosis or technical deficits causing embolization from the site of endarterectomy or stent placement. Depending on the particular situation and the surgeon’s suspicion, this could be performed by duplex scan at the bedside, arteriography, or surgical reexploration. Once patency of the endarterectomy site has been confirmed, CT scanning of the brain and neck should be expeditiously performed.

TREATMENT Because it is difficult to predict which patients will develop CHS, there is no effective prophylactic measure to prevent this complication other than control of intraoperative and postoperative hypertension, a routine measure for any CEA or CAS. Continuous arterial monitoring is necessary to achieve this goal. If a patient has specific risk factors such as a preoperative stroke and high-grade stenosis, a discussion with the anesthesiologist emphasizing potential risk and the importance of blood pressure control may be worthwhile. Mild headaches after CEA or CAS are common and usually require only simple analgesic therapy. For those with severe headaches, other manifestations of CHS and hypertension, some evidence suggests that aggressive management of the hypertension can reduce the risk of ICH and other complications. Frank seizures are often difficult to control. If cerebral edema is thought to be significant, use of diuretics and antiinflammatory medications becomes appropriate. If mental status changes or neurologic deficits evolve, CT scanning of the brain is mandatory to evaluate for the development of hemorrhage. If petechial or small cerebral hemorrhages occur, the measures described often suffice. Anticoagulants, if used at all, must be used only for clear indications. If massive hemorrhage occurs, neurosurgical intervention should be considered to avoid herniation and death. Nevertheless, in all reported series, the prognosis of massive intracerebral hemorrhage after CEA and CAS is exceedingly poor.

CEREBROVASCULAR DISEASE

Selected References Bernstein M, Fleming JFR, Deck JHN: Cerebral hyperperfusion after carotid endarterectomy: a cause of cerebral hemorrhage, Neurosurgery 15:50–56, 1984. Bouri S, Thapar A, Shalhoub J, et al: Hypertension and the post-carotid endarterectomy cerebral hyperperfusion syndrome, Euro J Vasc Endovasc Surg 41:229–237, 2011. Dalman JE, Beenakkers IC, Moll FL, et al: Transcranial Doppler monitoring during carotid endarterectomy helps to identify patients at risk of postoperative hyperperfusion, Euro J Vasc Endovasc Surg 18:222–227, 1999. Ouriel K, Shortell DK, Illig KA, et al: Intracerebral hemorrhage after carotid endarterectomy: incidence, contribution to neurologic morbidity, and predictive factors, J Vasc Surg 29:82–87, 1999. Reigel MM, Hollier LH, Sundt TM Jr, et al: Cerebral hyperperfusion syndrome: a cause of neurologic dysfunction after carotid endarterectomy, J Vasc Surg 5:628–634, 1987.

Treatment of Recurrent Carotid Artery Stenosis After Percutaneous Angioplasty and Stenting Brajesh K. Lal and Jon S. Matsumura

Carotid endarterectomy (CEA) has been proved effective at reducing the risk of stroke in large-scale landmark clinical trials. These randomized trials have established indications for CEA in selected patients with symptomatic stenosis of 50% or more and asymptomatic stenosis of 60% or more. The emergence of carotid artery stenting (CAS) has been accompanied by much deliberation. Carotid artery stenting has become an alternative to reoperation in the management of carotid restenosis after prior CEA. This approach is also recommended in the management of other subgroups of patients with carotid stenosis, including patients with significant medical comorbidities, anatomically inaccessible lesions above C2, and radiationinduced stenoses. Endovascular management of these high-risk subsets is based on acceptable post-procedural complications as well as long-term outcomes. Among many questions that arise in the evaluation of any new technology, there is specific concern about the durability of the carotid stent in the neck, where motion occurs in several dimensions. Although the final role of CAS in carotid revascularization continues to evolve on the basis of results of recently reported and other ongoing randomized, controlled trials, it is clear that stenting will continue to be performed in subgroups of patients with carotid stenoses. Therefore, it is anticipated that there will be a corresponding increase in in-stent restenosis (ISR) cases after CAS. Considerable controversy exists regarding the clinical significance, natural history, threshold for retreatment, and appropriate intervention of recurrent carotid stenosis after stenting.

INCIDENCE Coronary stenting is associated with significantly lower rates of angiographic and clinical restenosis than angioplasty alone. This salutary

Riles TS, Imparato AM, Jacobowitz GJ, et al: The cause of perioperative stroke after carotid endarterectomy, J Vasc Surg 19:206–216, 1994. Schoser BGH, Heesen C, Eckert B, et al: Cerebral hyperperfusion injury after percutaneous transluminal angioplasty of extracranial arteries, J Neurol 244:101–104, 1997. Schroeder T, Sillesen H, Sorensen O, et al: Cerebral hyperperfusion following carotid endarterectomy, J Neurosurg 66:824–829, 1987. Timaran CH, Veith FJ, Rosero EB, et al: Intracranial hemorrhage after carotid endarterectomy and carotid stenting in the United States in 2005, J Vasc Surg 49:623–628, 2009. Wagner WH, Cossman DV, Farber A, et al: Hyperperfusion syndrome after carotid endarterectomy, Ann Vasc Surg 19:479–486, 2005.

effect may be a result of the stent’s ability to provide predictably larger arterial lumens. However, myointimal hyperplasia accompanies virtually every stent placement in the coronary, iliac, or carotid system. Intimal hyperplastic recurrence has been observed after coronary stenting in 16% to 59% of cases and after iliac stenting in 13% to 39% of reported series. A valid concern has been that CAS could be associated with similarly high rates of ISR during follow-up. Most existing studies have relatively short follow-up periods, resulting in underreporting of ISR rates. Life-table analysis provides specific information on ISR after CAS (Figure 1). Over a follow-up period of 1 to 74 months, only five patients demonstrated high-grade ISR (≥80%), and the projected 5-year recurrence rate for ISR of 80% or more was 6.4%. In the Carotid Revascularization, Endarterectomy versus Stent Trial (CREST), of the 1086 patients receiving CAS, only 58 patients developed 70% or greater ISR, for a 2-year recurrence rate of 6.0%. The Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial, Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS), Stent-Protected Angioplasty versus Carotid Endarterectomy (SPACE) study, and the Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) trial, each reported similarly low recurrence rates ranging from 2.8% over 3 years to 10.5% over 5 years. Therefore, although ISR does not appear to occur at the high rates associated with bare-metal stenting of the coronary arteries, a substantial number of patients can be anticipated to progress to moderate and high-grade ISR.

Percent CAS interventions free of ISR 80%

58

100

97.3%

93.6%

80 60 40 20 0

N= SE =

0 122 0

12 64 1.9

24

36

36 3.6

21 5.0

48 10 6.8

60

72

4 9.6

Months of follow-up FIGURE 1  Kaplan Meier life table graph of freedom from in-stent

restenosis after carotid artery stenting.

1 38.3

CEREBROVASCULAR DISEASE

Selected References Bernstein M, Fleming JFR, Deck JHN: Cerebral hyperperfusion after carotid endarterectomy: a cause of cerebral hemorrhage, Neurosurgery 15:50–56, 1984. Bouri S, Thapar A, Shalhoub J, et al: Hypertension and the post-carotid endarterectomy cerebral hyperperfusion syndrome, Euro J Vasc Endovasc Surg 41:229–237, 2011. Dalman JE, Beenakkers IC, Moll FL, et al: Transcranial Doppler monitoring during carotid endarterectomy helps to identify patients at risk of postoperative hyperperfusion, Euro J Vasc Endovasc Surg 18:222–227, 1999. Ouriel K, Shortell DK, Illig KA, et al: Intracerebral hemorrhage after carotid endarterectomy: incidence, contribution to neurologic morbidity, and predictive factors, J Vasc Surg 29:82–87, 1999. Reigel MM, Hollier LH, Sundt TM Jr, et al: Cerebral hyperperfusion syndrome: a cause of neurologic dysfunction after carotid endarterectomy, J Vasc Surg 5:628–634, 1987.

Treatment of Recurrent Carotid Artery Stenosis After Percutaneous Angioplasty and Stenting Brajesh K. Lal and Jon S. Matsumura

Carotid endarterectomy (CEA) has been proved effective at reducing the risk of stroke in large-scale landmark clinical trials. These randomized trials have established indications for CEA in selected patients with symptomatic stenosis of 50% or more and asymptomatic stenosis of 60% or more. The emergence of carotid artery stenting (CAS) has been accompanied by much deliberation. Carotid artery stenting has become an alternative to reoperation in the management of carotid restenosis after prior CEA. This approach is also recommended in the management of other subgroups of patients with carotid stenosis, including patients with significant medical comorbidities, anatomically inaccessible lesions above C2, and radiationinduced stenoses. Endovascular management of these high-risk subsets is based on acceptable post-procedural complications as well as long-term outcomes. Among many questions that arise in the evaluation of any new technology, there is specific concern about the durability of the carotid stent in the neck, where motion occurs in several dimensions. Although the final role of CAS in carotid revascularization continues to evolve on the basis of results of recently reported and other ongoing randomized, controlled trials, it is clear that stenting will continue to be performed in subgroups of patients with carotid stenoses. Therefore, it is anticipated that there will be a corresponding increase in in-stent restenosis (ISR) cases after CAS. Considerable controversy exists regarding the clinical significance, natural history, threshold for retreatment, and appropriate intervention of recurrent carotid stenosis after stenting.

INCIDENCE Coronary stenting is associated with significantly lower rates of angiographic and clinical restenosis than angioplasty alone. This salutary

Riles TS, Imparato AM, Jacobowitz GJ, et al: The cause of perioperative stroke after carotid endarterectomy, J Vasc Surg 19:206–216, 1994. Schoser BGH, Heesen C, Eckert B, et al: Cerebral hyperperfusion injury after percutaneous transluminal angioplasty of extracranial arteries, J Neurol 244:101–104, 1997. Schroeder T, Sillesen H, Sorensen O, et al: Cerebral hyperperfusion following carotid endarterectomy, J Neurosurg 66:824–829, 1987. Timaran CH, Veith FJ, Rosero EB, et al: Intracranial hemorrhage after carotid endarterectomy and carotid stenting in the United States in 2005, J Vasc Surg 49:623–628, 2009. Wagner WH, Cossman DV, Farber A, et al: Hyperperfusion syndrome after carotid endarterectomy, Ann Vasc Surg 19:479–486, 2005.

effect may be a result of the stent’s ability to provide predictably larger arterial lumens. However, myointimal hyperplasia accompanies virtually every stent placement in the coronary, iliac, or carotid system. Intimal hyperplastic recurrence has been observed after coronary stenting in 16% to 59% of cases and after iliac stenting in 13% to 39% of reported series. A valid concern has been that CAS could be associated with similarly high rates of ISR during follow-up. Most existing studies have relatively short follow-up periods, resulting in underreporting of ISR rates. Life-table analysis provides specific information on ISR after CAS (Figure 1). Over a follow-up period of 1 to 74 months, only five patients demonstrated high-grade ISR (≥80%), and the projected 5-year recurrence rate for ISR of 80% or more was 6.4%. In the Carotid Revascularization, Endarterectomy versus Stent Trial (CREST), of the 1086 patients receiving CAS, only 58 patients developed 70% or greater ISR, for a 2-year recurrence rate of 6.0%. The Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial, Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS), Stent-Protected Angioplasty versus Carotid Endarterectomy (SPACE) study, and the Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) trial, each reported similarly low recurrence rates ranging from 2.8% over 3 years to 10.5% over 5 years. Therefore, although ISR does not appear to occur at the high rates associated with bare-metal stenting of the coronary arteries, a substantial number of patients can be anticipated to progress to moderate and high-grade ISR.

Percent CAS interventions free of ISR 80%

58

100

97.3%

93.6%

80 60 40 20 0

N= SE =

0 122 0

12 64 1.9

24

36

36 3.6

21 5.0

48 10 6.8

60

72

4 9.6

Months of follow-up FIGURE 1  Kaplan Meier life table graph of freedom from in-stent

restenosis after carotid artery stenting.

1 38.3

Treatment of Recurrent Carotid Artery Stenosis After Percutaneous Angioplasty and Stenting

TABLE 1:  Suggested Duplex Ultrasound Threshold Velocity Criteria Defining Clinically Important Stenoses in the Stented Carotid Artery (University of Maryland Criteria) Percent Stenosis

Peak Systolic Velocity Threshold (cm/sec)

50%) restenosis after CEA. It remains to be seen whether restenosis after CAS follows the same pattern of low risk of stroke as that associated with restenosis after CEA. Long-term follow-up data on stroke rates in patients with and without ISR after CAS will be forthcoming through 2016 from the CREST long-term follow-up study. However, in the absence of such data, several clinical centers and trials have established their own criteria for reintervention and methodology of target lesion revascularization. A review of their experience can provide insight into the general trends in CAS practices.

TREATMENT We have elected to re-treat all asymptomatic patients who reached a threshold ISR of at least 80% diameter reduction. In one published series we treated patients with single repeat angioplasty (n = 3), three different angioplasties (n = 1), and restenting (n = 1) without complications. Embolic protection was used in all patients. One of these patients developed occlusion 1 year after reintervention. In another center, asymptomatic ISR of at least 80% was treated with single repeat angioplasty (n = 4), cutting balloon angioplasty (n = 1), and restenting (n = 1) without neurologic complications. Reimers and colleagues have treated 32 cases of ISR. Seven patients were symptomatic with at least 50% symptomatic restenosis or at least 70% asymptomatic restenosis. Angioplasty alone was used in 22 procedures (5.5–7.0 mm diameter, 10–40 mm length) and cutting balloon in 10 procedures. Ten (31%) patients had repeat stenting. All procedures used embolic protection, and balloon inflations were 6 to 12 atmospheres for a mean of 20 seconds. Seventyone percent of the filters had macroscopic debris, and microscopic analysis showed that it was primarily thrombotic material, although fibrous hypercellular debris was occasionally noted. There were no neurologic complications, access problems, or deaths within 30 days. After 17 months’ mean follow-up, no deaths or strokes occurred; one patient developed another restenosis after 3 months, and this was treated with angioplasty without recurrence in the subsequent 12 months. Multicenter registries for CAS have also reported their experience with re-interventions. The ACCULINK for Revascularization of Carotids in High-Risk patients (ARCHeR) long-term follow-up study reported an annualized non-periprocedural ipsilateral stroke rate of 1.2% in the first 36 months after CAS in patients at high risk for CEA. The clinically driven repeat intervention rate was 4.3% at 36 months. The Registry Study to Evaluate the Neuroshield Bare Wire Cerebral Protection System (SECURITY) evaluated 305 high-risk patients undergoing CAS and found a repeat intervention rate of 0.65% at 1 year after the primary procedure. In the Carotid Revascularization using Endarterectomy or Stenting Systems (CARESS) study, 397 patients were treated in a nonrandomized study with CEA

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(n = 254) and CAS (n = 143). Person-year rates at 1 year for repeat carotid revascularization was 1.0% in CEA patients and 1.8% in CAS patients (p = .627). CAVATAS compared outcomes between endovascular treatment mostly with angioplasty alone and CEA. In this trial, restenosis was defined as at least 70% diameter reducing stenosis after revascularization. The SAPPHIRE trial defined restenosis as at least 80% diameter reduction, and these patients underwent reintervention with either angioplasty or, in a small number of instances, restenting. At 1080 days, repeat revascularization was performed in 3.0% of CAS patients.

CONCLUSION Each of the aforementioned studies has strengths and weaknesses in regard to study design, patient selection, subject heterogeneity, CAS methodology, follow-up methodology and compliance, restenosis definition, and treatment. Taken together, the repeat revascularization rates after CAS are about 1% to 2% per year after CAS, but they are higher after angioplasty alone. These rates compare favorably with CEA in studies of patients at high risk for CEA. Additional information on long-term follow-up from the large randomized studies incorporating CAS and CEA will provide definitive data on the natural history and clinical significance of restenosis after CAS and relative to CEA. Pooled data will be necessary to identify risk factors for restenosis and evaluate optimal management of in-stent restenosis after CAS because it is so uncommon.

Technical Aspects of Conventional Carotid Endarterectomy for Atherosclerotic Disease Norman R. Hertzer

Carotid endarterectomy (CEA) is a conceptually simple but technically unforgiving surgical procedure. Although other factors like patient selection and preoperative antiplatelet therapy also play an important role, a good clinical outcome after CEA probably is related most directly to the technical perfection of the operation itself. Provided they are accurate, data from the Nationwide Inpatient Sample suggest that as many as 90% of the CEAs in the United States were done for asymptomatic carotid stenosis from 2005 to 2007. If for no other reason, therefore, the prevention of technical complications has never been more important. There is more than one way to perform CEA safely, but the following remarks describe the strategy the author adopted during almost 30 years at the Cleveland Clinic.

SURGICAL TECHNIQUE The author has previously reported a personal series of 2262 CEAs, nearly all being done under general anesthesia with routine carotid shunting and, during the last 20 years, patch angioplasty preferentially

Selected References Arquizan C, Trinquart L, Touboul P-J, et al: Restenosis is more frequent after carotid stenting than after endarterectomy, Stroke 42:1015–1020, 2011. Bonati LH, Ederle J, McCabe DJH, et al: Long-term risk of carotid restenosis in patients randomly assigned to endovascular treatment or endarterectomy in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS): long-term follow-up of a randomised trial, Lancet Neurol 8:908–917, 2009. CARESS Steering Committee: Carotid revascularization using endarterectomy or stenting systems (CARESS): phase I clinical trial: 1 year results, J Vasc Surg 42:213–219, 2005. Eckstein H-H, Ringleb P, Allenberg J-R, et al: Results of the Stent-protected Angioplasty versus Carotid Endarterectomy (SPACE) study to treat symptomatic stenoses at 2 years: a multinational, prospective, randomised trial, Lancet Neurol 7:893–902, 2008. Gurm HS, Yadav JS, Fayad P, et al: Long-term results of carotid stenting versus endarterectomy in high-risk patients, N Engl J Med 358:1572–1579, 2008. Lal BK, Beach KW, Roubin GS, et al; for the CREST Investigators: Restenosis after carotid artery stenting and endarterectomy: a secondary analysis of CREST, a randomised controlled trial, Lancet Neurology 11(9):755–763, 2012. Lal BK, Hobson RW II, Goldstein J, et al: In-stent recurrent stenosis after carotid artery stenting: life table analysis and clinical relevance, J Vasc Surg 38:1162–1168, 2003. Lal BK, Hobson RW II, Goldstein J, et al: Carotid artery stenting: is there a need to revise ultrasound velocity criteria? J Vasc Surg 39:58–66, 2004. Lal BK, Hobson RW II, Tofighi B, et al: Duplex ultrasound velocity criteria for the stented carotid artery, J Vasc Surg 47:63–73, 2008. Reimers B, Tubler T, de Donato G, et al: Endovascular treatment of in-stent restenosis after carotid artery stenting: immediate and midterm results, J Endovasc Ther 13:429–435, 2006.

using the saphenous vein. The principal technical steps of the procedure became standardized (Figure 1). After the patient is positioned on a shoulder roll, the neck, the upper chest, and the groin from which the greater saphenous vein is to be harvested are prepared and draped in a standard fashion. The cervical incision is made parallel and slightly anterior to the course of the sternocleidomastoid muscle, its length being determined by the level of the carotid bifurcation on preoperative imaging studies. If an especially high incision is necessary, it is angled posterior to the earlobe to avoid the parotid gland. The platysma layer is divided with the cutting mode of the electrocautery unit, and complete hemostasis is maintained throughout the operation, which generally is conducted within avascular planes. The internal jugular vein is reflected laterally with minimal exposure, ligating the common facial vein with a 5–0 suture before it is divided. The carotid sheath is opened longitudinally over the common carotid artery (CCA), being sure to avoid the vagus nerve if it happens to take an anomalous course anterior to the artery. In fact, the identification and preservation of several cranial nerves are cardinal features to the remainder of the dissection (see Figure 1). The vagus nerve ordinarily lies within the carotid sheath posterior or slightly posterolateral to the CCA, may be closely adherent to the carotid bulb, and becomes nearly confluent with the hypoglossal nerve near the styloid process. To avoid at least temporary paralysis of the ipsilateral vocal cord, the vagus nerve should be protected from injury during the placement of self-retaining retractors, the application of a proximal arterial clamp, and the use of electrocautery. The hypoglossal nerve often is shrouded by small veins that never should be clamped and divided indiscriminately. This nerve probably is more likely to be injured by retraction than by full mobilization and, for this reason, structures tethering it in place—such as the artery and vein to the sternocleidomastoid muscle, the descending hypoglossal branch to the ansa cervicalis, and less commonly, the occipital artery—might require division to elevate the nerve for distal exposure of the internal

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(n = 254) and CAS (n = 143). Person-year rates at 1 year for repeat carotid revascularization was 1.0% in CEA patients and 1.8% in CAS patients (p = .627). CAVATAS compared outcomes between endovascular treatment mostly with angioplasty alone and CEA. In this trial, restenosis was defined as at least 70% diameter reducing stenosis after revascularization. The SAPPHIRE trial defined restenosis as at least 80% diameter reduction, and these patients underwent reintervention with either angioplasty or, in a small number of instances, restenting. At 1080 days, repeat revascularization was performed in 3.0% of CAS patients.

CONCLUSION Each of the aforementioned studies has strengths and weaknesses in regard to study design, patient selection, subject heterogeneity, CAS methodology, follow-up methodology and compliance, restenosis definition, and treatment. Taken together, the repeat revascularization rates after CAS are about 1% to 2% per year after CAS, but they are higher after angioplasty alone. These rates compare favorably with CEA in studies of patients at high risk for CEA. Additional information on long-term follow-up from the large randomized studies incorporating CAS and CEA will provide definitive data on the natural history and clinical significance of restenosis after CAS and relative to CEA. Pooled data will be necessary to identify risk factors for restenosis and evaluate optimal management of in-stent restenosis after CAS because it is so uncommon.

Technical Aspects of Conventional Carotid Endarterectomy for Atherosclerotic Disease Norman R. Hertzer

Carotid endarterectomy (CEA) is a conceptually simple but technically unforgiving surgical procedure. Although other factors like patient selection and preoperative antiplatelet therapy also play an important role, a good clinical outcome after CEA probably is related most directly to the technical perfection of the operation itself. Provided they are accurate, data from the Nationwide Inpatient Sample suggest that as many as 90% of the CEAs in the United States were done for asymptomatic carotid stenosis from 2005 to 2007. If for no other reason, therefore, the prevention of technical complications has never been more important. There is more than one way to perform CEA safely, but the following remarks describe the strategy the author adopted during almost 30 years at the Cleveland Clinic.

SURGICAL TECHNIQUE The author has previously reported a personal series of 2262 CEAs, nearly all being done under general anesthesia with routine carotid shunting and, during the last 20 years, patch angioplasty preferentially

Selected References Arquizan C, Trinquart L, Touboul P-J, et al: Restenosis is more frequent after carotid stenting than after endarterectomy, Stroke 42:1015–1020, 2011. Bonati LH, Ederle J, McCabe DJH, et al: Long-term risk of carotid restenosis in patients randomly assigned to endovascular treatment or endarterectomy in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS): long-term follow-up of a randomised trial, Lancet Neurol 8:908–917, 2009. CARESS Steering Committee: Carotid revascularization using endarterectomy or stenting systems (CARESS): phase I clinical trial: 1 year results, J Vasc Surg 42:213–219, 2005. Eckstein H-H, Ringleb P, Allenberg J-R, et al: Results of the Stent-protected Angioplasty versus Carotid Endarterectomy (SPACE) study to treat symptomatic stenoses at 2 years: a multinational, prospective, randomised trial, Lancet Neurol 7:893–902, 2008. Gurm HS, Yadav JS, Fayad P, et al: Long-term results of carotid stenting versus endarterectomy in high-risk patients, N Engl J Med 358:1572–1579, 2008. Lal BK, Beach KW, Roubin GS, et al; for the CREST Investigators: Restenosis after carotid artery stenting and endarterectomy: a secondary analysis of CREST, a randomised controlled trial, Lancet Neurology 11(9):755–763, 2012. Lal BK, Hobson RW II, Goldstein J, et al: In-stent recurrent stenosis after carotid artery stenting: life table analysis and clinical relevance, J Vasc Surg 38:1162–1168, 2003. Lal BK, Hobson RW II, Goldstein J, et al: Carotid artery stenting: is there a need to revise ultrasound velocity criteria? J Vasc Surg 39:58–66, 2004. Lal BK, Hobson RW II, Tofighi B, et al: Duplex ultrasound velocity criteria for the stented carotid artery, J Vasc Surg 47:63–73, 2008. Reimers B, Tubler T, de Donato G, et al: Endovascular treatment of in-stent restenosis after carotid artery stenting: immediate and midterm results, J Endovasc Ther 13:429–435, 2006.

using the saphenous vein. The principal technical steps of the procedure became standardized (Figure 1). After the patient is positioned on a shoulder roll, the neck, the upper chest, and the groin from which the greater saphenous vein is to be harvested are prepared and draped in a standard fashion. The cervical incision is made parallel and slightly anterior to the course of the sternocleidomastoid muscle, its length being determined by the level of the carotid bifurcation on preoperative imaging studies. If an especially high incision is necessary, it is angled posterior to the earlobe to avoid the parotid gland. The platysma layer is divided with the cutting mode of the electrocautery unit, and complete hemostasis is maintained throughout the operation, which generally is conducted within avascular planes. The internal jugular vein is reflected laterally with minimal exposure, ligating the common facial vein with a 5–0 suture before it is divided. The carotid sheath is opened longitudinally over the common carotid artery (CCA), being sure to avoid the vagus nerve if it happens to take an anomalous course anterior to the artery. In fact, the identification and preservation of several cranial nerves are cardinal features to the remainder of the dissection (see Figure 1). The vagus nerve ordinarily lies within the carotid sheath posterior or slightly posterolateral to the CCA, may be closely adherent to the carotid bulb, and becomes nearly confluent with the hypoglossal nerve near the styloid process. To avoid at least temporary paralysis of the ipsilateral vocal cord, the vagus nerve should be protected from injury during the placement of self-retaining retractors, the application of a proximal arterial clamp, and the use of electrocautery. The hypoglossal nerve often is shrouded by small veins that never should be clamped and divided indiscriminately. This nerve probably is more likely to be injured by retraction than by full mobilization and, for this reason, structures tethering it in place—such as the artery and vein to the sternocleidomastoid muscle, the descending hypoglossal branch to the ansa cervicalis, and less commonly, the occipital artery—might require division to elevate the nerve for distal exposure of the internal

Technical Aspects of Conventional Carotid Endarterectomy for Atherosclerotic Disease

External carotid a Baroreceptor n Hypoglossal n

Internal carotid a

A

Vagus n

Common carotid a

Internal jugular v

B

C

D

E

F

G

61

H

carotid artery (ICA). The superior laryngeal nerve is located medial to the ICA, distributes branches that wrap around the superior thyroid artery, and can potentially be injured while controlling either of these two vessels. The glossopharyngeal nerve crosses the ICA near the base of the skull, often is filamentous and difficult to identify, and is best protected by maintaining dissection very close to the anterior surface of the artery. Finally, excessive or prolonged retraction at the upper aspect of the incision can cause at least temporary compression injuries laterally to the greater auricular nerve or medially to the marginal mandibular branch of the facial nerve. It is well known that exposure should be obtained with minimal manipulation of the carotid bifurcation to avoid cerebral embolization. There should be no hesitancy in dividing the posterior belly of the digastric muscle superiorly, or the omohyoid muscle inferiorly, to facilitate atraumatic dissection and a subsequent arteriotomy that adequately encompasses the diseased segment of the carotid artery. Dissection near the baroreceptor nerve of Hering occasionally provokes bradycardia with associated hypotension, but this usually can be promptly controlled by the injection of 1 to 2 mL of local anesthetic into the carotid sinus at the notch of the bifurcation. A syringe containing 1% lidocaine should be available on the instrument table for this purpose.

FIGURE 1 Schematic illustration of some of the technical aspects of carotid endarterectomy described in the text.  (From Brewster DC (ed): Common problems in vascular surgery, Chicago, 1989, Year Book Medical.)

Once the exposure has been completed and the patient has been systemically heparinized, traction is placed on the elastic vessel loops surrounding the external carotid and superior thyroid arteries. The proximal CCA then is controlled with an angled Hydrogrip clamp, after which a smaller clamp is applied to the distal ICA. The arteriotomy is begun with a No. 15 or No. 11 scalpel blade on the anterolateral aspect of the distal CCA. Using Potts scissors, the arteriotomy then is extended a sufficient distance proximally and distally to expose the full extent of the atherosclerotic plaque shown by preoperative imaging. Because of their eccentric calcification, some plaques promote a spiral arteriotomy through the internal carotid bulb unless care is taken to avoid it. Some thickening of the medial layer in the posterior wall of the CCA is not uncommon and can extend all the way to the innominate artery or the aortic arch. This generally should not be pursued, but further exposure of the CCA may be warranted if the lower end of an unexpectedly thick plaque can be palpated near the clavicle. The distal end of a flexible loop shunt is then inserted into the ICA, retaining it with a small ring clamp. After all air is vented from the shunt, and the cul-de-sac of the CCA is filled with blood, the proximal end of the shunt is placed well into the CCA, temporarily preventing flow in the shunt by digital compression. After a proximal ring clamp has been positioned, the Hydrogrip clamp is

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FIGURE 2  The endarterectomy is performed in the subadventitial

plane, removing all circular smooth muscle fibers of the medial layer.

removed by an assistant, and any potential debris is briefly flushed through the CCA around the shunt before the surgeon tightens the ring clamp and releases digital compression of the shunt. Another elastic vessel loop should be placed on slight traction around the CCA above the proximal ring clamp to prevent dislodgment of the shunt during the remainder of the procedure (see Figure 1). Any annoying backbleeding from the external carotid artery (ECA) usually can be controlled by applying a small hemostatic clip to an ascending pharyngeal branch hidden within the soft tissue of the carotid sinus. The endarterectomy is begun using a Cannon blade or a Freer elevator and entering the alabaster subadventitial plane to excise all circular fibers of the media (Figures 1 and 2). The CCA endarterectomy is terminated about 1 cm above the proximal end of the arteriotomy. After the specimen is divided at this level, it can be elevated under full vision while the endarterectomy is continued upward into the carotid bulb. A plaque extending only a short distance into the ICA may be teased medially toward the origin of the ECA to achieve an adequate endpoint. More often, it is simpler to divide the plaque in the bulb so that the ICA and ECA endarterectomies can be done independently. Once the plaque has been divided and the elastic vessel loop has been loosened around the ECA, the ECA endarterectomy is performed with slight traction on the plaque to evert the artery until an appropriate endpoint has been attained. The ECA then is gently explored with the tips of a small curved (mosquito) hemostat to remove any loose intimal fragments. If the carotid bifurcation is located unusually low in the neck and the main branchless stem of the ECA is correspondingly long, a separate arteriotomy in the ECA may also be required to complete its endarterectomy. The remainder of the divided plaque then is removed from the ICA, feathering the plaque to its transition into normal intima. Although it is unusual for a plaque to extend above the level of the distal clamp if an adequate length of the ICA has been opened, two solutions are available when this situation occurs. First, the plaque can be transected below its unseen endpoint, secured with interrupted 7–0 tacking sutures, and compensated by the application of a generous patch during closure of the arteriotomy. Preferably, however, additional exposure of the ICA should be obtained, the distal clamp advanced upward, the arteriotomy extended toward the clamp, and the endarterectomy completed under direct vision. Under exceptional circumstances in the past when a plaque reached nearly to the level of the styloid process, the author sometimes had to temporarily remove the shunt, control retrograde bleeding from the ICA with a small balloon catheter, complete the endarterectomy, and then reinsert the shunt. At present, lesions like this might be better suited to carotid stenting.

FIGURE 3  After the endarterectomy is completed, interrupted 7–0

tacking sutures may be necessary to secure the intima of the distal internal carotid artery.

FIGURE 4  Recurrent stenosis at the lower end of the arteriotomy

may be prevented by dividing residual thickening above this level, securing it with tacking sutures, and covering it with a patch.

After the endarterectomy is completed, all residual medial fibers are excised owing to their potential contribution to cerebral embolization or recurrent hyperplastic stenosis (see Figure 1). Pulsed saline irrigation and loupe magnification are indispensable for this purpose. When the endarterectomy site seems to be rough or pitted after the removal of deeply ulcerated plaques, an intravenous infusion of low-molecular-weight dextran is initiated and continued at least for several hours. Investigators at the Leicester Royal Infirmary have reported that dextran reduces the incidence of early postoperative platelet embolization as measured by transcranial Doppler (TCD) monitoring, but they now employ dextran much less often because TCD has detected so few microemboli in patients receiving dual preoperative antiplatelet therapy with aspirin plus a single dose of ­clopidogrel (75 mg) on the night before CEA. Unless it is entirely imperceptible, the intimal endpoint in the ICA ordinarily is secured with 7–0 tacking sutures (Figures 1 and 3). According to conventional wisdom, the proximal extent of the endarterectomy in the CCA does not require tacking sutures because it theoretically should not be elevated by antegrade blood flow. Archie has found this proximal shelf to be a nidus for recurrent stenosis, however, and the author has had a similar experience. Therefore, current technique departs from that shown in Figure 1 in the sense that tacking sutures are now routinely used, and the proximal extent of the CCA endarterectomy is terminated above the lower end of the arteriotomy so that it can be covered by a patch (Figure 4).

Technical Aspects of Conventional Carotid Endarterectomy for Atherosclerotic Disease

63

Patch Angioplasty Until the mid-1980s, the author employed primary arteriotomy closure with 6–0 polypropylene suture, reserving patch angioplasty for the approximately 10% of patients who had small ICAs. In 1987, however, a prospective nonrandomized study at the Cleveland Clinic indicated that vein patching was superior to primary closure with respect to the risks for perioperative stroke, ICA thrombosis, and recurrent carotid stenosis. Counsell and associates also found that routine patch angioplasty was accompanied by significantly lower stroke rates in their systematic review of six randomized trials in 1997, and a Cochrane review of 10 randomized trials by Rerkasem and Rothwell again concluded in 2009 that patching was associated with significantly lower risks for ipsilateral stroke, perioperative occlusion, and late restenosis. Although synthetic patches are more convenient, the author has always preferred the saphenous vein because it can encourage endothelial regeneration at the endarterectomy site. The vein should always be obtained from the groin to avoid the rare but catastrophic complication of central patch rupture. After an appropriate length of saphenous vein has been harvested, it is gently distended to establish its true diameter. The vein then is opened longitudinally with Potts scissors along an axis that will permit excision of any ligated branches when it is trimmed to a width of about 10 mm, depending on the size of the artery. The diameter of the vein must be tailored to achieve a streamlined patch that complements the contour of the carotid bifurcation, thus discouraging turbulence and the formation of mural thrombus. Valve leaflets are excised from the vein, allowing it to be applied to the arteriotomy in a reversed or nonreversed fashion. Using double-armed 6–0 polypropylene, the patch first is secured to the proximal end of the arteriotomy and cut to a length that will conform to the slight curve that usually is present in the ICA just above its origin. The apical suture then is placed, followed by a quadrant suture at the midpoint of each side of the anastomosis (see Figure 1). The dimensions of either a venous or synthetic patch must be continuously refined by adjusting how much patch and artery are incorporated into the suture line, leaving a small opening in the anastomosis for subsequent venting (Figures 1 and 5). To remove the shunt, the elastic vessel loop around the proximal carotid artery is advanced upward to a point just below the vein patch. It then is placed on sufficient traction to retain the shunt in the artery while the lower ring clamp is removed, the bulbous end of the shunt is advanced to the level of the vessel loop, and the Hydrogrip clamp is replaced across the CCA. The vessel loop is discarded, and the proximal end of the shunt is withdrawn from the artery using digital compression of the shunt to prevent retrograde bleeding through it. Once the distal ring clamp has been removed, an occluding clamp is repositioned across the ICA above the patch. This clamp is not applied until the shunt has been withdrawn, thus permitting a brief burst of retrograde bleeding from the ICA. The two polypropylene sutures still remaining in the near side of the suture line then are elevated, residual air is vented from the endarterectomy site by filling the site with heparinized saline, and the anastomosis is completed. Protamine sulfate can now be administered, conceding that systemic heparin reversal after CEA is a matter of modest debate. After momentary release of the distal ICA clamp to encourage any residual air to return to the center of the intact patch, the CCA clamp is opened and the elastic vessel loop surrounding the ECA is relaxed. After several pulse beats, the ICA clamp finally is opened and removed (see Figure 1). It is exceedingly important not to allow any retrograde flow from the ECA into the patched area after the arteriotomy has been completely closed, because loose intimal debris could conceivably still be present in the ECA following its essentially blind endarterectomy. Complete hemostasis is obtained before closing the incision, being certain not to employ the electrocautery near any of the cranial nerves. Although a temporary silicone-elastic vacuum drain is

FIGURE 5  The arteriotomy has been repaired using a patch of

greater saphenous vein harvested from the groin.

not inappropriate after autogenous arteriotomy closure, an external drain probably ought not be used after synthetic patching because of a potential risk for patch infection.

POSTOPERATIVE CARE Patients are awakened in the operating room to establish that no neurologic deficits have occurred. They then are transferred to the postanesthetic care unit, where their perioperative aspirin therapy is continued in the form of a rectal suppository. They are closely observed there for approximately 6 hours, because any delayed neurologic deficits caused by platelet aggregation with cerebral embolization and/or ICA thrombosis most often occur within this period. The hospital stay usually is no longer than a day, the sutures are removed within a week, and a follow-up appointment is scheduled in about a month. Patients are then placed under long-term surveillance with annual duplex scans for 3 years, after which scans can be repeated biannually if no recurrent stenosis has been discovered on the operated side and there is no serious occlusive disease in the contralateral carotid artery.

POSTOPERATIVE RESULTS In addition to technical considerations, the complication rate of CEA also is influenced by the clinical setting in which it is done. In the personal series of 2262 CEAs mentioned earlier, vein patch angioplasty was employed in 1232 (54%), synthetic patches in 247 (11%), and primary arteriotomy closure in 783 (35%). However, only 1775 (78%) of these operations involved CEA alone. The remaining 487 operations were done as either staged (n = 184, 8.1%) or simultaneous (n = 303, 13%) procedures in conjunction with coronary bypass surgery, and the combined stroke and/or mortality rate (CSM) for staged (5.4%) and simultaneous (8.9%) CEAs was significantly higher than for CEA alone (2.4%, p < .001). Moreover, the CSM was only 1.4% in the 621 asymptomatic patients who underwent CEA alone and received vein patches. No statistical differences were identified between vein patching and synthetic patching, but patching of any kind was associated with significantly lower risks than primary closure for ipsilateral perioperative stroke (1.3% vs. 2.8%, p = .011) and for recurrent stenosis of 60% or greater at a median follow-up of approximately 5 years (odds ratio 0.61, p = .019). Such findings seem important in an era in which an overwhelming majority of CEAs appears to be done for asymptomatic stenosis in the United States. Although there are other ways to perform this operation safely, they undoubtedly share many of the technical aspects described in this chapter.

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Selected References Archie JP: The endarterectomy-produced common carotid artery step: a harbinger of early emboli and later restenosis, J Vasc Surg 23:932–939, 1996. Counsell CE, Salinas R, Naylor R, et al: A systematic review of the randomized trials of carotid patch angioplasty in carotid endarterectomy, Eur J Vasc Endovasc Surg 13:345–354, 1997. Eslami MH, McPhee JT, Simons JP, et al: National trends in utilization and postprocedure outcomes for carotid artery revascularization 2005 to 2007, J Vasc Surg 53:307–315, 2011. Hertzer NR: The Nationwide Inpatient Sample may contain inaccurate data for carotid endarterectomy and carotid stenting, J Vasc Surg 55:263–267, 2012. Hertzer NR, Beven EG, O’Hara PJ, et al: A prospective study of vein patch angioplasty during carotid endarterectomy, Ann Surg 206:628–635, 1987.

Technical Aspects of Eversion Carotid Endarterectomy for Atherosclerotic Disease Dhiraj M. Shah, R. Clement Darling III, Benjamin B. Chang, Paul B. Kreienberg, Philip S.K. Paty, Kathleen J. Ozsvath, Sean P. Roddy, and Manish Mehta

All methods of arterial closure following a standard carotid endarterectomy (CEA) are associated with appreciable rates of persistent or recurrent internal carotid artery (ICA) stenoses, of which some are related to technical issues in closing the artery. Eversion endarterectomy of the ICA is an alternative technique that had its origins in the United States and recent resurgence in Europe. The eversion technique, as currently conceived, involves complete transection of the ICA at its origin from the carotid bifurcation. This procedure should be distinguished from the eversion endarterectomy involving division of the distal common carotid artery (CCA) as described by DeBakey and colleagues in 1959. The latter method is only of historical interest, because lengthy disease of the ICA is difficult to treat with this method. Current eversion endarterectomy facilitates the removal of plaque higher up in the ICA. More importantly, this method appears to improve upon standard endarterectomy in two and possibly three ways. First, because the endpoint is fully visualized and generally not sutured, it is easier to detect intimal flaps. Second, and most clearly, the reanastomosis of the ICA to the bulb is technically simple and obviates the risk of narrowing a primary closure of the ICA during conventional endarterectomy or the need for patching. Third, this method has been associated with a decrease in later restenosis.

Hertzer NR, Mascha EJ: A personal experience with coronary artery bypass grafting, carotid patching, and other factors influencing the outcome of carotid endarterectomy, J Vasc Surg 43:959–968, 2006. Lennard N, Smith J, Dumville J, et al: Prevention of postoperative thrombotic stroke after carotid endarterectomy: the role of transcranial Doppler ultrasound, J Vasc Surg 26:579–584, 1997. O’Hara PJ, Hertzer NR, Krajewski LP, et al: Saphenous vein patch rupture after carotid endarterectomy, J Vasc Surg 15:504–509, 1992. Rerkasem K, Rothwell PM: Patch angioplasty versus primary closure for carotid endarterectomy, Cochrane Database Syst Rev (4):CD000160, 200910.1002/14651858.CD000160.pub3. Sharpe RY, Dennis MJS, Nasim A, et al: Dual antiplatelet therapy prior to carotid endarterectomy reduces post-operative embolisation and thromboembolic events: post-operative transcranial Doppler monitoring is now unnecessary, Eur J Vasc Endovasc Surg 40:162–167, 2010.

addition, if desired, this dissection may be completed after crossclamping, but this increases the cross-clamp time unnecessarily. After the carotid arteries are isolated, heparin sodium is administered and the arteries are clamped. At this time, the ICA is transected obliquely, with the line of division running from the crotch of the carotid to a point more proximal on the lateral (internal) side of the CCA. The specific angle of division is not critical, but a 10- to 15-mm opening should be left in the CCA. Doing so aids visualization of disease in the bulb and facilitates reanastomosis of the arteries. After division, the ICA almost always is redundant. Because of this, it may be spatulated, further increasing the diameter of the eventual suture line. If this is done, the common carotid arteriotomy is extended caudad a similar amount (Figure 1). Endarterectomy of the ICA is begun by circumferentially elevating the plaque from the arterial wall. It is important to remove both the intima and media, and if done, the adventitia may be grasped with two fine forceps while the assistant holds the plaque. The adventitia is then pulled or rolled like a sock until the end of the plaque is reached (Figure 2). If the endarterectomy plane is too shallow and appreciable media remains, the artery will be too stiff to easily evert. At this time, the specimen usually spontaneously divides at the endpoint. If not, the plaque is sharply divided at its termination. This process usually requires less than 30 seconds. At this point, the assistant holds the luminal side of the adventitia as near as possible to the endpoint. This task can require the surgeon to move the ICA clamp more cephalad. The operator may then inspect the entire circumference of the endpoint, removing loose fragments and making sure the distal intima is adherent. It is critically important for the operator to see the entire endpoint clearly at this

METHODS Surgeons adopting eversion endarterectomy need not change much of their conventional CEA technique. Initial dissection and isolation of the carotid artery are identical. However, after the artery is exposed, it is important to circumferentially isolate the ICA and the bulb. The need for more extensive dissection is a common criticism of this technique, but in reality it has not produced an increase in complications, most particularly, an injury of the vagus nerve. In

FIGURE 1  Internal carotid artery divided from bulb.

64

CEREBROVASCULAR DISEASE

Selected References Archie JP: The endarterectomy-produced common carotid artery step: a harbinger of early emboli and later restenosis, J Vasc Surg 23:932–939, 1996. Counsell CE, Salinas R, Naylor R, et al: A systematic review of the randomized trials of carotid patch angioplasty in carotid endarterectomy, Eur J Vasc Endovasc Surg 13:345–354, 1997. Eslami MH, McPhee JT, Simons JP, et al: National trends in utilization and postprocedure outcomes for carotid artery revascularization 2005 to 2007, J Vasc Surg 53:307–315, 2011. Hertzer NR: The Nationwide Inpatient Sample may contain inaccurate data for carotid endarterectomy and carotid stenting, J Vasc Surg 55:263–267, 2012. Hertzer NR, Beven EG, O’Hara PJ, et al: A prospective study of vein patch angioplasty during carotid endarterectomy, Ann Surg 206:628–635, 1987.

Technical Aspects of Eversion Carotid Endarterectomy for Atherosclerotic Disease Dhiraj M. Shah, R. Clement Darling III, Benjamin B. Chang, Paul B. Kreienberg, Philip S.K. Paty, Kathleen J. Ozsvath, Sean P. Roddy, and Manish Mehta

All methods of arterial closure following a standard carotid endarterectomy (CEA) are associated with appreciable rates of persistent or recurrent internal carotid artery (ICA) stenoses, of which some are related to technical issues in closing the artery. Eversion endarterectomy of the ICA is an alternative technique that had its origins in the United States and recent resurgence in Europe. The eversion technique, as currently conceived, involves complete transection of the ICA at its origin from the carotid bifurcation. This procedure should be distinguished from the eversion endarterectomy involving division of the distal common carotid artery (CCA) as described by DeBakey and colleagues in 1959. The latter method is only of historical interest, because lengthy disease of the ICA is difficult to treat with this method. Current eversion endarterectomy facilitates the removal of plaque higher up in the ICA. More importantly, this method appears to improve upon standard endarterectomy in two and possibly three ways. First, because the endpoint is fully visualized and generally not sutured, it is easier to detect intimal flaps. Second, and most clearly, the reanastomosis of the ICA to the bulb is technically simple and obviates the risk of narrowing a primary closure of the ICA during conventional endarterectomy or the need for patching. Third, this method has been associated with a decrease in later restenosis.

Hertzer NR, Mascha EJ: A personal experience with coronary artery bypass grafting, carotid patching, and other factors influencing the outcome of carotid endarterectomy, J Vasc Surg 43:959–968, 2006. Lennard N, Smith J, Dumville J, et al: Prevention of postoperative thrombotic stroke after carotid endarterectomy: the role of transcranial Doppler ultrasound, J Vasc Surg 26:579–584, 1997. O’Hara PJ, Hertzer NR, Krajewski LP, et al: Saphenous vein patch rupture after carotid endarterectomy, J Vasc Surg 15:504–509, 1992. Rerkasem K, Rothwell PM: Patch angioplasty versus primary closure for carotid endarterectomy, Cochrane Database Syst Rev (4):CD000160, 200910.1002/14651858.CD000160.pub3. Sharpe RY, Dennis MJS, Nasim A, et al: Dual antiplatelet therapy prior to carotid endarterectomy reduces post-operative embolisation and thromboembolic events: post-operative transcranial Doppler monitoring is now unnecessary, Eur J Vasc Endovasc Surg 40:162–167, 2010.

addition, if desired, this dissection may be completed after crossclamping, but this increases the cross-clamp time unnecessarily. After the carotid arteries are isolated, heparin sodium is administered and the arteries are clamped. At this time, the ICA is transected obliquely, with the line of division running from the crotch of the carotid to a point more proximal on the lateral (internal) side of the CCA. The specific angle of division is not critical, but a 10- to 15-mm opening should be left in the CCA. Doing so aids visualization of disease in the bulb and facilitates reanastomosis of the arteries. After division, the ICA almost always is redundant. Because of this, it may be spatulated, further increasing the diameter of the eventual suture line. If this is done, the common carotid arteriotomy is extended caudad a similar amount (Figure 1). Endarterectomy of the ICA is begun by circumferentially elevating the plaque from the arterial wall. It is important to remove both the intima and media, and if done, the adventitia may be grasped with two fine forceps while the assistant holds the plaque. The adventitia is then pulled or rolled like a sock until the end of the plaque is reached (Figure 2). If the endarterectomy plane is too shallow and appreciable media remains, the artery will be too stiff to easily evert. At this time, the specimen usually spontaneously divides at the endpoint. If not, the plaque is sharply divided at its termination. This process usually requires less than 30 seconds. At this point, the assistant holds the luminal side of the adventitia as near as possible to the endpoint. This task can require the surgeon to move the ICA clamp more cephalad. The operator may then inspect the entire circumference of the endpoint, removing loose fragments and making sure the distal intima is adherent. It is critically important for the operator to see the entire endpoint clearly at this

METHODS Surgeons adopting eversion endarterectomy need not change much of their conventional CEA technique. Initial dissection and isolation of the carotid artery are identical. However, after the artery is exposed, it is important to circumferentially isolate the ICA and the bulb. The need for more extensive dissection is a common criticism of this technique, but in reality it has not produced an increase in complications, most particularly, an injury of the vagus nerve. In

FIGURE 1  Internal carotid artery divided from bulb.

Technical Aspects of Eversion Carotid Endarterectomy for Atherosclerotic Disease

65

FIGURE 2  Eversion of plaque from divided internal carotid artery.

time. If a loose flap is found, it can usually be removed. Rarely, tacking sutures may be employed, and these are best performed using doublearmed fine sutures inserted from the luminal side and tied externally. After the endpoint is secured, the artery is unrolled and the interior is inspected for loose bodies. Irrigation with heparinized saline into the lumen allows any loose fragments to float away from the wall to aid in their removal. Any persistent stenosis or flap is then corrected. This is the most critical point of the operation and should be done carefully. After the ICA endarterectomy is completed, the distal CCA and the external carotid artery (ECA) are examined. If there is no significant disease, the arteries may be reanastomosed. More often an extended endarterectomy is performed. The plaque is elevated in the bulb and carried up the ECA and proximally into the CCA as dictated by the extent of the disease. Division of the plaque in its midportion allows the surgeon to deal with each artery separately. Endarterectomy of the ECA is performed by standard methods. Endarterectomy of the CCA may also be performed with a combination of direct elevation of exposed plaque and proximal eversion of more extensive plaque. Rarely, if the CCA plaque extends very proximally, the arteriotomy in the distal CCA can be extended inferiorly. The CCA is then primarily reapproximated or the ICA is opened further, to encompass the expanded CCA arteriotomy. After the endarterectomy is completed, the ICA is reapproximated to the CCA. Because the original line of incision was oblique and both arteries were further opened, the anastomosis is usually 10 to 30 mm in length. Thus closure of the artery is much easier with the eversion technique, and there is little chance that the arteries will be narrowed during closure. A continuous suture of 6–0 polypropylene is started at the most cephalad portion of the internal carotid arteriotomy. Because the walls of the arteries are now redundant, fairly large bites may be taken with the suture with little fear of causing a stenosis. Following completion of the anastomosis, antegrade blood flow is reinstituted in the usual manner.

SHUNTING AND EVERSION ENDARTERECTOMY A common although misplaced criticism of eversion endarterectomy is that it precludes the use of a shunt. This is clearly not the case, although the surgeon might need to modify the method of shunt insertion slightly. Pruitt-Inahara–type shunts or Javid shunts held in place with shunt clamps (not vessel loops) are ideal, whereas straight (Edwards-type) shunts are less satisfactory. If a shunt is used, the ICA is obliquely transected as previously described. At this time, the plaque most often obscures the lumen,

FIGURE 3  Alternative arteriotomy for nonredundant internal carotid

artery.

and shunt insertion might not be possible. However, the distal lumen of the ICA may be rapidly revealed by either spatulating the artery past the endpoint of the plaque (useful when the ICA is redundant) or by quickly everting and removing the bulk of the internal plaque. A shunt can always be inserted in a safe and expeditious fashion. Insertion of the shunt into the CCA can similarly require an extension of the common carotid arteriotomy to expose open lumen. Interestingly, after shunt insertion is completed, the presence of the shunt actually facilitates the examination of the endpoint. If the shunt clamp or balloon is sufficiently cephalad, the shaft of the shunt serves as a mandrel over which the ICA is everted. After the endarterectomy is completed, reanastomosis is performed in the usual fashion. The shunt is removed and the arteries are clamped before the final two or three sutures are placed.

UNUSUAL PROBLEMS AND TROUBLESHOOTING If the plaque extends without visible termination despite the most cephalad dissection possible, neither standard nor eversion endarterectomy will produce a reliably satisfactory result. Furthermore, at times the endpoint of the plaque looks shaggy or otherwise unsuitable. In these cases, the operator may consider performing a bypass with either autogenous vein or polytetrafluoroethylene (preferred) from the CCA. The ICA should be transected sharply above the unsatisfactory endpoint and the bypass anastomosed at this level. The sutures tack down any residual plaque and diminish the chance of embolization or occlusion. In cases with extensive plaque, it may be difficult to keep everting the artery to the endpoint of the plaque. An alternative to bypass is to extend the ICA endarterectomy until the endpoint is clearly visualized. If the ICA is not especially redundant, the CCA endarterectomy may be extended up the ECA. The ICA and ECA are then used to patch each other to minimize the chance of stenosis. This method results in a more cephalad arterial bifurcation (bifurcation advancement) (Figure 3). Eversion endarterectomy is the procedure of choice for carotid kinks or loops. After transection, the redundant artery may be resected. The remainder of the procedure may then be performed without further modification. Recurrent carotid stenoses may sometimes be treated with eversion techniques. Late-occurring stenoses are more likely to be

66

CEREBROVASCULAR DISEASE

atheromatous and amenable to eversion. Earlier, more fibrous lesions may be less well treated by attempted eversion. Eversion endarterectomy is capable of generating excellent results. As of August 2005, 7001 CEAs had been performed with the eversion technique, including 456 during combined carotid and coronary artery bypass grafting (CABG) procedures. There was a 0.7% incidence of stroke in this group. The combined stroke–mortality rate was 1.2%. Although use of this method does not necessarily guarantee an improvement in results, it is an effective, reliable technique for treating carotid artery arteriosclerotic occlusive disease.

Selected References Archie JP: Prevention of early restenosis and thrombosis-occlusion after carotid endarterectomy by saphenous vein patch angioplasty, Stroke 17:901–905, 1986. Clagett GP, Rich NR, McDonald PT, et al: Etiologic factors for recurrent carotid artery stenosis, Surgery 93:313–318, 1983.

Patch Graft Closure with Carotid Endarterectomy Ali F.  AbuRahma

Stroke is the third leading cause of death in the United States. Approximately 15% to 52% of all ischemic strokes are caused by extracranial cerebrovascular atherosclerotic lesions. It has also been estimated that 103,000 carotid endarterectomies (CEAs) were done in the United States in 2005. Few procedures have been scrutinized as thoroughly as CEA during the last 2 decades. The Society of Vascular Surgery, in a special communication, and based on the results of several prospective randomized trials in North America and Europe that were designed to compare the safety and efficacy of CEA versus medical therapy, published outlines for managing atherosclerotic carotid artery disease that details recommendations for medical therapy versus CEA and carotid stenting for both symptomatic and asymptomatic carotid artery stenosis. Collectively, the data from these prospective trials have confirmed that CEA offers significantly better protection from ipsilateral strokes than medical therapy in a substantial number of patients presenting with either symptomatic or asymptomatic carotid artery disease.

PATCH CLOSURE VERSUS PRIMARY CLOSURE The type of closure after a CEA, primary versus patch closure, remains controversial. Most authorities agree that in a small carotid artery (≤4 mm), particularly in the presence of technical difficulties at the internal carotid artery (ICA) end of the arteriotomy, closing with a patch can prevent restenosis. It is not uncommon for lateral tears to occur at the apex of the ICA after the linear arteriotomy is made, and patching can prevent narrowing during primary closure of the arteriotomy. In patients with excessive thickening of the intima of the distal ICA, patching can smooth the transition zone from the CEA site to the residual artery beyond. Patching might also be advisable in patients with kinked arteries, and it can help maintain the lumen and

DeBakey ME, Crawford ES, Cooley DA, et al: Surgical considerations of occlusive disease of innominate, carotid, subclavian and vertebral arteries, Ann Surg 149:690–710, 1959. Entz L, Jarany ZS, Nemes A: Eversion endarterectomy in the surgery of the internal carotid artery, Cardiovasc Surg 4:190–194, 1996. Hertzer NR, Beven EG, O’Hara PJ, et al: A prospective study of vein patch angioplasty during carotid endarterectomy: three year results for 801 patients and 917 operations, Ann Surg 206:628–635, 1987. Kasprzak PM, Raithel D: Eversion carotid endarterectomy: technique and early results, J Cardiovas Surg 30:495, 1989. Koskas F, Kieffer E, Bahnini A: Carotid eversion endarterectomy: short-and long-term results, Ann Vasc Surg 9:9–15, 1995. Mehta M, Roddy SP, Darling RC III, et al: Safety and efficacy of eversion carotid endarterectomy for the treatment of recurrent stenosis: 20-year experience, Ann Vasc Surg 19:492–498, 2005. Ouriel K, Green RM: Appropriate frequency of carotid duplex testing following carotid endarterectomy, Am J Surg 170:144–147, 1995. Reigner B, Reveilleau P, Gayral M, et al: Eversion endarterectomy of the internal carotid artery: mid-term results of a new technique, Ann Vasc Surg 9:141–246, 1995.

prevent postoperative occlusion. Patching should also be routinely used for redo CEA. CEA with patch angioplasty is generally believed to decrease the chance of technical errors and has been shown by multiple clinical trials to be more effective than CEA with primary closure in decreasing the incidence of perioperative carotid thrombosis, perioperative stroke, and late restenosis. However, many others believe that inclusion of a patch prolongs the operative time and clamp or shunt time, makes the procedure technically more demanding, and is unnecessary in some patients. In 1996, we published the largest prospective randomized trial comparing CEA with primary closure versus patching, where 264 CEAs were done with patching (130 vein patch closures and 134 polytetrafluoroethylene [PTFE] patch closures) and 135 CEAs were done with primary closure. The perioperative stroke or death rates were 2.3% for patching versus 6.7% for primary closure (odds ratio [OR], 0.3; 95% confidence interval [CI], 0.1–0.88), and the 50% or greater restenosis rates at 30 months were 5.3% for patching versus 33% for primary closure (OR, 0.11; CI, 0.06–0.19). In another unique randomized trial, we analyzed 74 patients undergoing bilateral sequential CEAs. Patients were randomized to either patching in the first CEA then primary closure in the second CEA or primary closure in the first and patching in the second; that is, each patient was his or her own control. Primary closure had an ipsilateral stroke rate of 4% versus 0% for CEA with patching, and at a late mean follow-up of 29 months, the incidence of at least 80% restenosis was significantly higher in the primary closure group. Several randomized, controlled trials (Level I evidence) have been published since the 1990s comparing CEA with patch angioplasty versus primary closure. Table 1 summarizes the results of these randomized, controlled trials. As noted in this table, these trials showed the superiority of patch closure over primary closure in reducing the perioperative stroke or death and the incidence of significant restenosis. In addition, there were two meta-analyses of the randomized, controlled carotid trials by the Cochrane Collaboration in 2000 and 2004. In an earlier Cochrane meta-analysis of randomized carotid trials, the early postoperative thrombosis, postoperative stroke, and at least 50% restenosis were superior for patching, in contrast to primary closure. In an update of the Cochrane Collaboration meta-analysis in 2004, Bond and colleagues reported the outcome for 1281 patients, including seven controlled carotid trials. Patch angioplasty was associated with a reduction in ipsilateral stroke (1.6% versus 4.8% for primary closure, p = .001), any stroke (1.6% vs. 4.5%, p = .004), stroke or death (2.5% vs. 6.1%, p = .007), arterial occlusion

66

CEREBROVASCULAR DISEASE

atheromatous and amenable to eversion. Earlier, more fibrous lesions may be less well treated by attempted eversion. Eversion endarterectomy is capable of generating excellent results. As of August 2005, 7001 CEAs had been performed with the eversion technique, including 456 during combined carotid and coronary artery bypass grafting (CABG) procedures. There was a 0.7% incidence of stroke in this group. The combined stroke–mortality rate was 1.2%. Although use of this method does not necessarily guarantee an improvement in results, it is an effective, reliable technique for treating carotid artery arteriosclerotic occlusive disease.

Selected References Archie JP: Prevention of early restenosis and thrombosis-occlusion after carotid endarterectomy by saphenous vein patch angioplasty, Stroke 17:901–905, 1986. Clagett GP, Rich NR, McDonald PT, et al: Etiologic factors for recurrent carotid artery stenosis, Surgery 93:313–318, 1983.

Patch Graft Closure with Carotid Endarterectomy Ali F.  AbuRahma

Stroke is the third leading cause of death in the United States. Approximately 15% to 52% of all ischemic strokes are caused by extracranial cerebrovascular atherosclerotic lesions. It has also been estimated that 103,000 carotid endarterectomies (CEAs) were done in the United States in 2005. Few procedures have been scrutinized as thoroughly as CEA during the last 2 decades. The Society of Vascular Surgery, in a special communication, and based on the results of several prospective randomized trials in North America and Europe that were designed to compare the safety and efficacy of CEA versus medical therapy, published outlines for managing atherosclerotic carotid artery disease that details recommendations for medical therapy versus CEA and carotid stenting for both symptomatic and asymptomatic carotid artery stenosis. Collectively, the data from these prospective trials have confirmed that CEA offers significantly better protection from ipsilateral strokes than medical therapy in a substantial number of patients presenting with either symptomatic or asymptomatic carotid artery disease.

PATCH CLOSURE VERSUS PRIMARY CLOSURE The type of closure after a CEA, primary versus patch closure, remains controversial. Most authorities agree that in a small carotid artery (≤4 mm), particularly in the presence of technical difficulties at the internal carotid artery (ICA) end of the arteriotomy, closing with a patch can prevent restenosis. It is not uncommon for lateral tears to occur at the apex of the ICA after the linear arteriotomy is made, and patching can prevent narrowing during primary closure of the arteriotomy. In patients with excessive thickening of the intima of the distal ICA, patching can smooth the transition zone from the CEA site to the residual artery beyond. Patching might also be advisable in patients with kinked arteries, and it can help maintain the lumen and

DeBakey ME, Crawford ES, Cooley DA, et al: Surgical considerations of occlusive disease of innominate, carotid, subclavian and vertebral arteries, Ann Surg 149:690–710, 1959. Entz L, Jarany ZS, Nemes A: Eversion endarterectomy in the surgery of the internal carotid artery, Cardiovasc Surg 4:190–194, 1996. Hertzer NR, Beven EG, O’Hara PJ, et al: A prospective study of vein patch angioplasty during carotid endarterectomy: three year results for 801 patients and 917 operations, Ann Surg 206:628–635, 1987. Kasprzak PM, Raithel D: Eversion carotid endarterectomy: technique and early results, J Cardiovas Surg 30:495, 1989. Koskas F, Kieffer E, Bahnini A: Carotid eversion endarterectomy: short-and long-term results, Ann Vasc Surg 9:9–15, 1995. Mehta M, Roddy SP, Darling RC III, et al: Safety and efficacy of eversion carotid endarterectomy for the treatment of recurrent stenosis: 20-year experience, Ann Vasc Surg 19:492–498, 2005. Ouriel K, Green RM: Appropriate frequency of carotid duplex testing following carotid endarterectomy, Am J Surg 170:144–147, 1995. Reigner B, Reveilleau P, Gayral M, et al: Eversion endarterectomy of the internal carotid artery: mid-term results of a new technique, Ann Vasc Surg 9:141–246, 1995.

prevent postoperative occlusion. Patching should also be routinely used for redo CEA. CEA with patch angioplasty is generally believed to decrease the chance of technical errors and has been shown by multiple clinical trials to be more effective than CEA with primary closure in decreasing the incidence of perioperative carotid thrombosis, perioperative stroke, and late restenosis. However, many others believe that inclusion of a patch prolongs the operative time and clamp or shunt time, makes the procedure technically more demanding, and is unnecessary in some patients. In 1996, we published the largest prospective randomized trial comparing CEA with primary closure versus patching, where 264 CEAs were done with patching (130 vein patch closures and 134 polytetrafluoroethylene [PTFE] patch closures) and 135 CEAs were done with primary closure. The perioperative stroke or death rates were 2.3% for patching versus 6.7% for primary closure (odds ratio [OR], 0.3; 95% confidence interval [CI], 0.1–0.88), and the 50% or greater restenosis rates at 30 months were 5.3% for patching versus 33% for primary closure (OR, 0.11; CI, 0.06–0.19). In another unique randomized trial, we analyzed 74 patients undergoing bilateral sequential CEAs. Patients were randomized to either patching in the first CEA then primary closure in the second CEA or primary closure in the first and patching in the second; that is, each patient was his or her own control. Primary closure had an ipsilateral stroke rate of 4% versus 0% for CEA with patching, and at a late mean follow-up of 29 months, the incidence of at least 80% restenosis was significantly higher in the primary closure group. Several randomized, controlled trials (Level I evidence) have been published since the 1990s comparing CEA with patch angioplasty versus primary closure. Table 1 summarizes the results of these randomized, controlled trials. As noted in this table, these trials showed the superiority of patch closure over primary closure in reducing the perioperative stroke or death and the incidence of significant restenosis. In addition, there were two meta-analyses of the randomized, controlled carotid trials by the Cochrane Collaboration in 2000 and 2004. In an earlier Cochrane meta-analysis of randomized carotid trials, the early postoperative thrombosis, postoperative stroke, and at least 50% restenosis were superior for patching, in contrast to primary closure. In an update of the Cochrane Collaboration meta-analysis in 2004, Bond and colleagues reported the outcome for 1281 patients, including seven controlled carotid trials. Patch angioplasty was associated with a reduction in ipsilateral stroke (1.6% versus 4.8% for primary closure, p = .001), any stroke (1.6% vs. 4.5%, p = .004), stroke or death (2.5% vs. 6.1%, p = .007), arterial occlusion

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Patch Graft Closure with Carotid Endarterectomy

TABLE 1:  Results of Randomized, Controlled Trials of Carotid Endarterectomy with Patch Closure versus Primary Closure

Odds Ratio (95% CI)

≥50% Restenosis Rate (%) Patch/ Primary

Odds Ratio (95% CI)

Follow-Up (mo.)

0/0

N/A

1.1/10.7

0.1 (0.0–0.8)

12

66/60

4.5/6.7

0.67 (0.15–3.06)

11.9/27.4

0.37 (0.16–0.89)

60

Lord, 1989

90/50

1.1/6.0*

0.2 (0.0–1.7)

N/A

N/A

Hospital discharge

Ranaboldo, 1993

96/91

3.2/7.7

0.41 (0.11–1.45)

5.5/16.3

0.33 (0.14–0.77)

12

Myers, 1994

46/48

0/2.1

0.14 (0.00–7.12)

3.2/3.1

1.03 (0.14–7.51)

54

Katz, 1994

43/44

2.3/4.5

0.52 (0.05–5.11)

0/5.9

0.14 (0.01–1.33)

29

AbuRahma, 1998

264/135

2.3/6.7

0.3 (0.10–0.88)

5.3/33.3

0.11 (0.06–0.19)

30

AbuRahma, 1999

74/74

0/4.0

NA

7/45

0.09 (0.03–0.25)

29

Bond, 2004† (Cochrane review)

515/378

2.5/6.1

0.40 (0.2–0.8)

4.8/18.6

0.22 (0.1–0.3)

N/A

Al-Rawi, 2006

153/175

4.0/2.9

1.39 (0.42–4.64)

3.3/1.7‡

1.9 (0.46–8.24)

12

No. Patch/ Primary

Perioperative Stroke/Death (%) Patch/ Primary

De Vleeschauwer, 1987

90/84

Eikelboom, 1988

Reference

*Includes 30-day risk of ipsilateral stroke only. †This is a meta-analysis of several randomized trials. ‡Carotid occlusion only (not ≥50% restenosis). CI, Confidence interval; N/A, not available or not applicable. AbuRahma AF, Robinson PA, Saiedy S, et al: Prospective randomized trial of carotid endarterectomy with primary closure and patch a­ ngioplasty with saphenous vein, jugular vein, and polytetrafluoroethylene: long-term follow-up, J Vasc Surg 27:222–234, 1998. AbuRahma AF, Robinson PA, Saiedy S, et al: Prospective randomized trial of bilateral carotid endarterectomies: primary closure versus patching, Stroke 30:1185–1189, 1999. Bond R, Rerkasem K, Naylor AR, et al: Systematic review of randomized controlled trials of patch angioplasty versus primary closure and ­different patch materials during carotid endarterectomy, J Vasc Surg 40:1126–1135, 2004. Lord RSA, Raj TB, Stary DL, et al: Comparison of saphenous vein patch, polytetrafluoroethylene patch, and direct arteriotomy c­ losure after carotid endarterectomy. Part I: perioperative results, J Vasc Surg 9:521–529, 1989.

(0.5% vs. 3.6%, p = .0001), and return to the operating room (1.1% vs. 3.1%, p = .01). In long-term follow-up, patch angioplasty was also superior to primary closure in the reduction of ipsilateral stroke (1.6% vs. 4.8%, p = .001), any stroke (1.9% vs. 5.9%, p = .0009), stroke or death (14.6% vs. 24%, p = .004), and late restenosis (4.8% vs. 18.6%, p < .0001) (Figure 1). One interesting article in support of primary closure has been published. In this study, primary closure was performed with an operating microscope and compared to patch closure with Dacron. Three hundred twenty-eight patients (153 patches vs. 175 primary closures) were compared. All CEAs were performed by a single surgeon. The 30-day perioperative stroke rate was 2.9% for primary closure versus 3.9% for patch closure. Unfortunately, this study was stopped after 328 patients, on the basis of futility. The authors concluded that there was no difference in vessel patency and clinical outcome after microscopic patch angioplasty and direct arteriotomy repair. The authors also concluded that there was no benefit from the routine use of patch angioplasty in microscopic CEA. It is generally believed that this study did not have the statistical power to support their conclusions. Other nonrandomized trials with level 2 to 4 evidence have been published that support patching over primary closure. Rockman and coworkers reported the results of a nonrandomized trial of 1972

CEAs by 81 surgeons in two states. These included 233 patients with primary closure and 1377 with patch angioplasty. Primary closure had a 5.6% stroke rate versus 2.2% for patch closure (p = .006). The authors strongly recommended abandonment of primary closure. Kresowik’s group performed a hospital review of a random sample of 10,000 Medicare patients undergoing CEA in 10 Midwestern states during a 12-month period in 1995 to 1996 and in 1998 to 1999. They concluded that stroke and mortality rates were lower in the second period than in the first period (5% vs. 5.6%, p < .05), and two factors were considered responsible for this improvement: patch closure and the increased use of antiplatelet agents (p < .05).

ROLE OF SELECTIVE PATCHING Selective patching in CEA has been proposed, that is, using it for patients with tortuous or exceptionally small carotid arteries. There is no level 1 evidence supporting selective patching versus primary closure or routine patching. Pappas and coworkers reported the results of a retrospective study of 133 CEAs where 77 patients were closed primarily and 56 patients were patched. Primary closure was done if the arteriotomy could be closed over a Javid shunt without tension; otherwise the carotid arteries were patched. The stroke rate

68

CEREBROVASCULAR DISEASE Patch Closure Subgroup

Events/Patients

Primary Closure Events/ Odds Patients Ratio 95% CI

Significance

30-Day Results Ipsilateral stroke

10/625 (1.6)

23/480 (4.8)

0.32

0.2-0.7

p = .001

All death

5/577 (0.9)

5/442 (1.1)

0.76

0.2-2.7

p = .6

Fatal stroke

1/577 (0.2)

2/442 (0.5)

0.38

0.0-4.2

p = .5

Any stroke

9/577 (1.6)

20/442 (4.5)

0.33

0.2-0.7

p = .004

Stroke or death

13/515 (2.5)

23/378 (6.1)

0.40

0.2-0.8

p = .007

Return to theater

8/731 (1.1)

17/550 (3.1)

0.35

0.1-0.8

p = .01

Arterial occlusion

3/641 (0.5)

17/468 (3.6)

0.12

0.0-0.4

p = .0001

Cranial nerve injury

8/375 (2.1)

7/250 (2.8)

0.76

0.3-2.1

p = .7

Long-Term Follow-Up

FIGURE 1  Summary esti-

mates of treatment effect from all meta-analysis outcomes from seven trials that compared patch angioplasty versus primary closure. Review included 1193 patients (1281 operations).  (Reprinted with permission from Bond R, Rerkasem K, Naylor AR, et al: Systematic review of randomized controlled trials of patch angioplasty versus primary closure and different patch materials during carotid endarterectomy, J Vasc Surg 40:1126–1135, 2004.)

Ipsilateral stroke

10/641 (1.6)

24/500 (4.8)

0.31

0.1-0.7

p = .001

All death

65/577 (11.3)

69/442 (15.6)

0.69

0.5-1.0

p = .1

Fatal stroke

1/577 (0.2)

4/442 (0.9)

0.19

0.0-1.7

p = .2

Any stroke

11/577 (1.9)

26/442 (5.9)

0.31

0.2-0.6

p = .0009

Stroke or death

75/515 (14.6)

91/378 (24.1)

0.54

0.4-0.8

p = .004

Restenosis

31/641 (4.5)

93/500 (18.6)

0.22

0.1-0.3

p < .0001

for patched arteries was 3.6%, versus 0% for primary closure (not significant), with no difference in long-term restenosis. The findings of this study were expected given the overall low incidence of stroke and the small patient numbers. Golledge and colleagues, from the Charing Cross group in London, reported their experience with selective patching of carotid arteries that were less than 5 to 6 mm. These authors found no significant difference in stroke or restenosis and advocated selective patching of carotid arteries.

CHOICE OF PATCH MATERIAL Selection of CEA patch material is also controversial, with supporters for vein patches (saphenous or neck veins) and for synthetic patches (PTFE or Dacron) (Table 2). Existing data from randomized, controlled trials suggest that the type of patch, whether vein or prosthetic, has no effect on short- or long-term results. Proponents of vein patch angioplasty (saphenous vein patch) state that the theoretical benefits include an increase in luminal size and provision of endothelialized tissue to the endarterectomy site. Others cite that they prefer an autogenous vein over prosthetic materials because the luminal surface is less thrombogenic and more resistant to infection. Opponents to synthetic patches also fear bleeding through the patch material and thrombus formation. Although many authorities prefer vein patching, several issues have been raised with respect to availability, increased operative time, morbidity related to harvesting, vein patch rupture, and late aneurysmal dilatation. Because of patients’ complaints about ankle harvest

0.1 Patch closure better

1

10 Primary closure better

incisions, some authorities recommended the abandonment of vein in favor of prosthesis (Dacron). The long saphenous vein is the most common autogenous source for carotid vein patch angioplasty, but it is also in demand for coronary artery bypass grafting and lower extremity revascularization. To save the saphenous vein for these procedures, the internal jugular vein has been proposed as an alternative for carotid vein patch angioplasty. Some have advocated the use of everted external jugular veins, where the vein is turned inside out to provide a tube of vein with intima on the outside. This double-walled patch can then be used, which is thought to be stronger and more resistant to rupture than a single-walled saphenous vein patch. The Cochrane Database update by Bond and colleagues reported on seven randomized clinical trials with 1280 patients. In spite of this large number, there were insufficient data to enable definite conclusions about the optimal patch material, because the adverse events were so small. The authors concluded that there were no obvious differences in the perioperative stroke or death rate in patients receiving vein or synthetic patch, and there was also no difference in the longterm follow-up to support either patch. The risk of major arterial complications, such as rupture or infection, was less than 1% in both groups. Three out of 348 (0.9%) had vein patch blowout, one of which was fatal, in contrast to two out of 359 (0.6%) with synthetic patches that sustained rupture, one of which was also fatal. A Cochrane update included 13 trials involving a total of 2083 operations; seven trials compared vein closure with PTFE closure, and six compared Dacron grafts with other synthetic materials. There were no significant differences in the outcomes between vein

Patch Graft Closure with Carotid Endarterectomy

69

TABLE 2:  Results of Randomized Controlled Trials of CEA Comparing Various Patch Materials

Odds Ratio (95% CI)

≥50% Restenosis/ Occlusion Rate (%) @ 1 yr.

Odds Ratio (95% CI)

Dacron/ Vein Patch

Dacron/ Vein Patch

Dacron/ Vein Patch

Dacron/ Vein Patch

107/100

2.8/1.0

2.9 (0.3 to >10)

N/A

N/A

Hayes, 2001

135/136

2.2/2.2

1.0 (0.2–5.1)

N/A

N/A

O’Hara, 2002

94/101

3.2/3.9

0.8 (0.2–3.7)

6.3/4.3

1.0 (0.3–3.1)

Naylor, 2004

136/137

2.2/3.7

0.6 (0.14–2.54)

12.4/7.2

1.8 (0.8–4.1)

ePTFE/ Vein Patch

ePTFE/ Vein Patch

ePTFE/ Vein Patch

ePTFE/ Vein Patch

ePTFE/ Vein Patch

Lord, 1989

47/43

2.1/0

N/A

N/A

N/A

Gonzalez-Fajardo, 1994

39/35

5.1/0

199 (0.0 to >10)

4/0

19.7 (0.0 to >50)

AbuRahma, 1998

134/130

2.2/2.3

1.0 (0.2–4.9)

2.2/8.5

0.2 (0.1–0.9)

Dacron/ ePTFE Patch

Dacron/ ePTFE Patch

Dacron/ ePTFE Patch

Dacron/ ePTFE Patch

Dacron/ ePTFE Patch

AbuRahma, 2003*

100/100

7/0

N/A

12/2

6.68 (1.46–30.69)

AbuRahma, 2008†

100/100

2/2

1.0 (0.14–7.24)

4/0

N/A

No.

Perioperative Stroke/Death (%)

Dacron/ Vein Patch

Katz, 1996

Reference

*Conventional PTFE vs. collagen-impregnated Dacron patch (Hemashield). †ACUSEAL vs Finesse (Ultrathin Dacron) (PTFE). CI, Confidence interval; N/A, not available or not applicable. AbuRahma AF, Hopkins ES, Robinson PA, et al: Prospective randomized trial of carotid endarterectomy with polytetrafluoroethylene versus collagen-­ impregnated Dacron (Hemashield) patching: late follow-up, Ann Surg 237:885–893, 2003. AbuRahma AF, Robinson PA, Saiedy S, et al: Prospective randomized trial of carotid endarterectomy with primary closure and patch a­ ngioplasty with saphenous vein, jugular vein, and polytetrafluoroethylene: long-term follow-up, J Vasc Surg 27:222–234, 1998. AbuRahma AF, Stone PA, Elmore M, et al: Prospective randomized trial of ACUSEAL (Gore-Tex) vs Finesse (Hemashield) patching during carotid endarterectomy: long-term outcome, J Vasc Surg 48:99–103, 2008. Katz SG, Kohl RD: Does the choice of material influence early morbidity in patients undergoing carotid patch angioplasty? Surgery 119:297–301, 1996. Lord RSA, Raj TB, Stary DL, et al: Comparison of saphenous vein patch, polytetrafluoroethylene patch, and direct arteriotomy c­ losure after carotid endarterectomy. Part I: perioperative results, J Vasc Surg 9:521–529, 1989. Naylor R, Hayes PD, Payne DA, et al: Randomized trial of vein versus Dacron patching during carotid endarterectomy: long-term results, J Vasc Surg 39:985–993, 2004. O’Hara PJ, Hertzer NR, Mascha EJ, et al: A prospective randomized study of saphenous vein patching versus synthetic patching during carotid endarterectomy, J Vasc Surg 35:324–332, 2002.

patches and synthetic materials apart from pseudoaneurysms, where there were fewer associated with synthetic patches than vein patches (OR, 0.09; CI, 0.02–0.49). However, the sample size was small and the clinical significance of this finding was uncertain. Compared with other synthetic patches, Dacron was associated with a higher risk of combined perioperative stroke and transient ischemic attack (p = .03), restenosis at 30 days (p = .004), perioperative carotid thrombosis (p = .1), and perioperative stroke (p = .07). During follow-up for more than 1 year, there were also significantly more stroke or death (p = .02), strokes (p = .03), and restenoses (p < .0001) with Dacron. The authors concluded that the number of outcome events was too small to allow reliable conclusions to be drawn, and more trial data are required to establish whether any differences do exist. Nevertheless, there was some evidence that other synthetic (e.g., PTFE) patches may be superior to collagen-impregnated Dacron grafts in

terms of perioperative stroke rates and restenosis. Pseudoaneurysm formation may be more common after use of a vein patch compared with a synthetic patch. O’Hara and colleagues reported the results of a randomized clinical trial of saphenous vein patching (101) versus knitted Dacron patching (94). The stroke rates were similar in both groups (3% for vein patching versus 2.1% for Dacron). The recurrent stenosis rates were also similar (4.3% versus 6.3%). The authors concluded that CEA can be safely performed with either patch. Naylor and coworkers also reported the results of a randomized trial, comparing thinwalled Dacron patch closure (136) versus vein patch closure (137). The stroke or death rate was 2.2% for Dacron versus 3.7% for vein. They noted that the Dacron patch had a significantly higher incidence of carotid restenosis; however, none of the 11 patients with greater than 70% restenosis were symptomatic.

70

CEREBROVASCULAR DISEASE

Initially, carotid patching was performed using conventional Dacron patches or PTFE patches. However, one of the main criticisms of the conventional PTFE patch was a prolonged hemostasis time, and therefore a new modified PTFE patch was introduced (ACUSEAL, Gore, Flagstaff, AZ), which is claimed to have better hemostatic properties. Similarly, a new ultrathin Dacron patch was introduced to minimize thrombosis (Finesse, Boston Scientific, Natick, MA). We reported the results of a prospective randomized clinical trial of CEA using the conventional PTFE (100) versus conventional collagen-impregnated Dacron-Hemashield (100). The perioperative stroke rate was 0% for PTFE versus 7% for Dacron (p = .02). The combined stroke and transient ischemic attacks (TIAs) were also higher in the Hemashield group (p = .03). There were five incidences of perioperative carotid thrombosis in the Dacron group versus none in the PTFE group. The restenosis rate was also higher in patients with Dacron (p < .001). However, the intraoperative needle-hole bleeding time for PTFE was longer. We also reported the results of a prospective randomized trial of 200 CEA patients (100 ACUSEAL and 100 Finesse). The perioperative stroke rates for both groups were comparable (2%). The long-term follow-up of the same study showed that the strokefree survival rates were comparable for both patches; however, the freedom from at least 70% restenosis at 1, 2, and 3 years was 98%, 96%, and 98% for ACUSEAL versus 92%, 85%, and 79% for the Finesse patch (p = .04). The difference between the 5-minute hemostasis time for the ACUSEAL patch and the 3.7-minute hemostasis time for the Finesse patch was significant; however, its clinical ­significance is debatable. Based on several randomized trials conducted at our institution, we strongly believe that synthetic patches, particularly the ACUSEAL PTFE and the Finesse Dacron patch, have comparable early and late clinical outcomes to saphenous vein patching. Our experience with the use of bovine pericardial patching has been limited for the last few years, but a few recently published studies have confirmed a favorable clinical outcome using this patch after CEA. Marien’s group reported the results of a prospective randomized study comparing bovine pericardium (51 CEAs) versus Dacron patch (44 CEAs). The perioperative stroke rates were comparable (2% for bovine patch versus 0% for Dacron patch, p = .55). However, suture bleeding at 4 minutes was present in 4% with the bovine patch versus 30% with the Dacron patch (p = .001).

CONCLUSIONS At present, there are still some vascular surgeons who do not use carotid patching routinely in all patients undergoing CEA; however, based on the data presented in this review, there is level I evidence to support a recommendation (grade A) in favor of routine carotid

patching. Meanwhile, there is no level 1 evidence to support selective patching for CEA, but a grade D recommendation may be used to recommend that primary closure can be safely practiced in a large ICA (>6 mm). There is also no difference between the preferential use of various patch materials, namely, saphenous vein or external jugular vein versus synthetic (PTFE or Dacron) patches. However, autogenous saphenous vein patching usually performs better than the old conventional collagen-impregnated Dacron patch. It is also believed that a grade A recommendation can be made that the conventional PTFE patch performs better than the conventional collagen-impregnated Dacron patch in decreasing perioperative stroke/carotid thrombosis and carotid restenosis. Meanwhile, there were no differences in early perioperative strokes between the new PTFE patch (ACUSEAL) and the new ultrathin Dacron patch (Finesse); however, late restenosis rates were better for the ACUSEAL patch.

Selected References AbuRahma AF, Hopkins ES, Robinson PA, et al: Prospective randomized trial of carotid endarterectomy with polytetrafluoroethylene versus collagen-impregnated Dacron (Hemashield) patching: late follow-up, Ann Surg 237:885–893, 2003. AbuRahma AF, Robinson PA, Saiedy S, et al: Prospective randomized trial of carotid endarterectomy with primary closure and patch angioplasty with saphenous vein, jugular vein, and polytetrafluoroethylene: long-term follow-up, J Vasc Surg 27:222–234, 1998. AbuRahma AF, Robinson PA, Saiedy S, Richmond BK, Khan J: Prospective randomized trial of bilateral carotid endarterectomies: primary closure versus patching, Stroke 30:1185–1189, 1999. AbuRahma AF, Stone PA, Elmore M, et al: Prospective randomized trial of ACUSEAL (Gore-Tex) vs Finesse (Hemashield) patching during carotid endarterectomy: long-term outcome, J Vasc Surg 48:99–103, 2008. Bond R, Rerkasem K, Naylor AR, et al: Systematic review of randomized controlled trials of patch angioplasty versus primary closure and different patch materials during carotid endarterectomy, J Vasc Surg 40:1126–1135, 2004. Katz SG, Kohl RD: Does the choice of material influence early morbidity in patients undergoing carotid patch angioplasty? Surgery 119:297–301, 1996. Lord RSA, Raj TB, Stary DL, Nash PA, et al: Comparison of saphenous vein patch, polytetrafluoroethylene patch, and direct arteriotomy closure after carotid endarterectomy. Part I: perioperative results, J Vasc Surg 9:521–529, 1989. Naylor R, Hayes PD, Payne DA, et al: Randomized trial of vein versus Dacron patching during carotid endarterectomy: long-term results, J Vasc Surg 39:985–993, 2004. O’Hara PJ, Hertzer NR, Mascha EJ, et al: A prospective randomized study of saphenous vein patching versus synthetic patching during carotid endarterectomy, J Vasc Surg 35:324–332, 2002. Rerkasem K, Rothwell PM: Patches of different types for carotid patch angioplasty, Cochrane Database Syst Rev (3):CD000071, 2010, doi: 10.1002/14651858.CD000071.pub3.

71

Management of the Infected Carotid Artery Patch

Management of the Infected Carotid Artery Patch A. Ross Naylor

It is likely that everyone performing carotid endarterectomy (CEA) is aware of prosthetic patch infection, but only 123 cases have been reported in the world literature from 29 published series (18 of which reported a single case). Accordingly, because surgeons only tend to publish good outcomes, it is likely that the procedural risks and longer-term rates of reinfection (or other adverse outcomes) may be considerably underestimated. This should be borne in mind when interpreting discussions on this subject. The majority of vascular surgeons use patches either selectively or routinely, and many prefer to use prosthetic patches because they are accessible and because using them avoids groin wound complications and retains the long saphenous vein for future use. Unfortunately, prosthetic carotid patches are vulnerable to infection. The true prevalence of patch infection is unknown, but it is likely to be 1% or less.

INFECTING MICROORGANISMS Out of the 123 patients known to have patch infection, 11 (9%) had no mention of whether a culture had been taken. Of the 112 where a culture was reported, 25 (20%) had no growth, and 87 (71%) yielded a positive growth for Staphylococcus sp. (n = 79, 91%), Streptococcus sp., Bacteroides sp. (n = 3, 2%), Pseudomonas sp. (n = 3, 2%), and Proteus sp. (in the remaining patient). Overall, 11 patients culturing staphylococci (16%) grew methicillin-resistant Staphylococcus aureus (MRSA), and overall, 91% of all positive cultures grew either staphylococci or streptococci.

CLINICAL PRESENTATION There was a biomodal pattern of symptoms in the 123 patients with patch infection (Table 1). Thirty-six patients (29%) presented within 2 months of their primary CEA, and 78 (63%) presented after 6 months or more had elapsed. Patients presenting within 2 months were more likely to present with an abscess or complex wound infection (20/36, 56%) or patch rupture (6/36, 17%). A minority presented with false aneurysm formation (3/36, 8%). By contrast, patients presenting after more than 6 months had elapsed since their CEA were significantly more likely to present with false aneurysm (22/78, 28%) or chronic sinus discharge (28/78, 36%) and were unlikely to present with either a wound abscess (12/78, 15%) or patch rupture (6/78, 8%). Overall, only four of the 123 patients (3%) presented with either a transient ischemic attack (TIA) or stroke.

RELATIONSHIP WITH PERIOPERATIVE INFECTION It is usually accepted that most prosthetic infections begin at the time of surgery. In the review of 123 cases, it was possible to correlate timing of onset of symptoms with the presence or absence of wound complications in the perioperative period in the majority of patients

TABLE 1:  Mode of Presentation of 75 Cases of Prosthetic Patch Infection Relative to Timing after Surgery Lesion

6 mo

Total

20

1

12

33

Patch rupture

6

1

6

13

False aneurysm

3

2

22

27

Sinus discharge

6

3

28

37*

Sinus + false aneurysm

0

2

6

8

TIA/stroke

1

0

1

2†

Swelling

0

0

0

3

36

9

78

123

Wound infection or abscess

Total

*Two of these patients presented with TIA as well. †Paper did not specify any other presentation but recorded positive cultures. TIA, Transient ischemic attack.

TABLE 2: Wound Complications 30 Days after Carotid Endarterectomy and Their Relationship with Prosthetic Patch Infection TIMING OF PRESENTATION WITH PATCH INFECTION Complication 6 mo

Total

No data provided

5

2

39

46

Wound infection

19

3

1

23

Hematoma

7

0

2

9

No wound problem

5

4

36

45

Fraction with a wound complication

26/31 (84%) 3/7 (43%) 3/39 (8%) 32/77 (42%)

(Table 2). No information was provided in 46 patients. Out of the remaining 77, 32 (42%) reported either a wound infection or hematoma in the perioperative period. However, the prevalence varied according to the delay to presentation, with 26 of 31 (84%) and 3 of 7 (43%) of patients presenting at less than 2 months or 2 to 6 months (respectively), having documented evidence of a wound complication in the perioperative period compared with only 3 of 39 (8%) patients presenting late.

INVESTIGATION OF PROSTHETIC PATCH INFECTION Patients presenting with massive neck hemorrhage have little time to undergo detailed investigations before going to the operating room. However, only eight patch ruptures secondary to prosthetic infection

72

CEREBROVASCULAR DISEASE

FIGURE 1  Color duplex ultrasound scan showing jet of blood enter-

ing a false aneurysm. The electronic cursor (white arrow) is insonating the flow into the false aneurysm, producing the flow waveform (bottom).

There is no role for routine intraarterial subtraction angiography. Computed tomography angiography (CTA) and magnetic resonance angiography (MRA) may be helpful in evaluating patch infections, revealing the upper extent of any inflammatory process, patency or tortuosity of the distal carotid artery, proximal inflow disease, and angulated or tortuous innominate or common carotid arteries. In the modern era, the latter information can enable the surgeon to determine whether there might be an endovascular option (e.g., insertion of a covered stent). If an open surgical approach is to be considered, CTA or MRA will also advise the surgeon if adjunctive access measures might be required to facilitate distal exposure. It could be catastrophic if the surgeon started an already difficult redo operation only to find that the inflammatory or infective process extended into the upper reaches of the neck. Finally, on a practical note, it is worth reviewing the original case notes. Important points to actively look for include whether the original surgeon encountered problems with distal access at the first operation. If so, it is likely that further access problems will be encountered at any redo surgery. If the first operation was done under locoregional anesthesia, did the patient suffer a focal neurologic deficit following test clamping? If yes, this patient will not tolerate carotid ligation. How high up the carotid artery did the patch extend? A 2to 3-cm patch is obviously be easier to treat than a 4- to 6-cm one, and the approach to the distal internal carotid artery will be different. Consider the potential for cranial nerve injury, especially in patients who have undergone a contralateral CEA, neck dissection, or thyroid surgery. Bilateral recurrent laryngeal nerve palsies can be fatal. If there is any doubt, check the vocal cords preoperatively.

MANAGEMENT OF PROSTHETIC PATCH INFECTION

FIGURE 2  Intraoperative view of a partially disrupted carotid patch.

Note the irregular, corrugated appearance of the patch, with partial dehiscence associated with an extruding thrombus (white arrow). A duplex scan had shown evidence of patch corrugation preoperatively (inset). Patch corrugation on duplex ultrasound can precede the onset of symptoms of infection by up to 11 months.  (From Naylor AR, Moir A: An aid to accessing the distal internal carotid artery, J Vasc Surg 49: 1345–1347, 2009.)

have been reported in the world literature, and it is likely that most patients present in a nonemergency situation. First is the need to take microbiologic tissue for culture because this can influence management decisions. For example, recognition of the presence of MRSA can make the surgeon consider carotid ligation (if the patient is able to tolerate this) because ongoing MRSA sepsis is more likely to cause a secondary anastomotic disruption. The literature contains conflicting recommendations regarding how best to investigate patients with suspected patch infection. The first-line investigations are usually duplex ultrasound to identify or exclude bleeding into a false aneurysm (Figure 1), patch corrugation (Figure 2), distal and proximal carotid patency, and extent of periarterial inflammation. Interestingly, patch corrugation can precede onset of more overt signs and symptoms of patch infection by up to 11 months. If patch corrugation is demonstrated, a high index of suspicion should be maintained over the ensuing months of follow-up. Radionuclide-labeled white cell scans are rarely undertaken unless there is an index of suspicion in selected patients with equivocal findings. A positive scan makes the diagnosis of infection more likely, but a negative scan is merely nondiagnostic.

The management strategies used in the 123 patients along with their early and late outcomes are diverse (Table 3). Twenty-three patients were treated with débridement (no patch excision) plus either oral antibiotics, antibiotic irrigation, sternomastoid flap coverage, or simple abscess drainage. There were no deaths, but three patients developed reinfection. Six were treated by no débridement plus either systemic then oral antibiotics or insertion of a covered stent. None of these patients died or suffered a stroke in the perioperative period and none developed a reinfection. These patients probably represent highly selected cases with good outcomes that then encouraged the authors to publish. It is likely that a much larger cohort of patients who have been treated in this more conservative manner have encountered much poorer outcomes and their cases have not been published. Only five patients in the world literature have undergone insertion of a covered stent to treat a proven patch infection. All had universally good outcomes, but follow-up was only for 3-39 months, respectively. Insertion of a covered stent is an attractive alternative to redo carotid surgery, but data are insufficient to be able to advise if they are likely to become reinfected in the future. Insertion of a covered stent could, however, be invaluable in the actively bleeding patient following acute disruption of the patch. Similarly, insertion of a balloon catheter via the femoral artery or proximal common carotid artery might be useful in arresting hemorrhage during an open dissection. The largest cohort of patients underwent patch excision plus either carotid ligation (n = 7), autologous vein patching or bypass (n = 67), or prosthetic reconstruction (n = 10). Carotid ligation was tolerated in six of seven patients; one patient suffered a fatal stroke. One died and two suffered a perioperative stroke after prosthetic reconstruction; five of the seven survivors developed reinfection. There is no easy way to determine who will or will not tolerate ligation. In the Leicester Vascular Unit, no patient would be considered for carotid ligation if the mean middle cerebral artery blood flow was less than 15 cm/sec during test clamping.

Management of the Infected Carotid Artery Patch

73

TABLE 3:  Management Strategies and Their Outcomes in 75 Patients with Prosthetic Patch Infection Number 30-Day of Patients Death

30-Day Stroke

30-Day Death and Stroke

LTFU No after 30 Days Reinfection

Reinfection

3

0

0

0

—

1

2

Postoperative antibiotic irrigation 1

0

0

0

—

1

—

Sternomastoid flap

2

0

0

0

—

2

—

Abscess drainage

2

0

0

0

—

Systemic or oral antibiotics

1

0

0

0

—

1

—

Insertion of covered stent

3

0

0

0

—

3

—

Carotid ligation

7

1 (17%) 1 (17%)

1 (17%)

1

5

—

Autologous reconstruction

46

1 (2%)

5 (11%)

5 (11%)

7

34 (89%) at 4 (3 at 1 mo and 1 at mean of 27 mo 2 mo after surgery)

Prosthetic material

10

1 (10%) 2 (20%)

2 (20%)

2

2

Procedure Débridement plus

Postoperative oral antibiotics

2

No débridement plus

Débridement, patch excision plus

5 (at 2, 12, 13, 16, and 24 mo)

LTFU, Long-term follow-up.

Ten patients were treated by patch excision plus prosthetic reconstruction. Two died or suffered a stroke in the perioperative period, and five of the seven survivors with follow-up data developed reinfection. The largest cohort of patients in the review (n = 46) underwent patch excision and reconstruction using autologous vein. The 30-day death or stroke rate was 11% (5/46), but 34 of 38 survivors (89%) with follow-up were free of infection at a mean of 27 months. Four patients developed an early reinfection. Three presented within 30 days, and the fourth developed a recurrent infection at 2 months. No patient undergoing autologous reconstruction has suffered a late reinfection after 2 months. Patch excision and replacement with autologous vein is the preferred treatment in Leicester, and the procedure is usually done in conjunction with an otolaryngologist to facilitate access to the upper reaches of the carotid artery if needed. The first step is to achieve proximal control of the common carotid artery and then distal control of the internal carotid artery. In patients with a partially disrupted patch, control of the distal internal carotid artery should be achieved before reopening the original wound. Each patient needs to be treated on individual merits. The frail, unfit patient may be better treated conservatively or with insertion of a covered stent. The fitter patient should be considered for definitive treatment, which should include patch excision and autologous reconstruction. The main lesson from this review was that patch excision followed by prosthetic reconstruction should be avoided. In the future, it is likely that more information will be forthcoming on the role of inserting a covered stent. It is, however, essential that not only the good results get published because this will bias interpretation of the literature. Insertion of covered stents can save lives (where catastrophic hemorrhage has occurred), but as with their role in other vascular beds, one needs to know whether these are temporary bridging procedures (pending a more definitive reconstruction) or whether they offer a longer infection-free prognosis. One thing is clear, however: It will definitely be more difficult to remove a

secondarily reinfected stent at a later stage because distal access will be a major problem.

CONCLUSION Prosthetic patch infection is a well-recognized, but grossly underreported complication of carotid surgery. Two thirds of patients present after 6 months, and these presentations are not usually associated with early wound complications. One third present early, and the majority report wound complications in the perioperative period. The vast majority of patch infections (90%) follow staphylococcal or streptococcal infections, and only seven cases of MRSA patch infection have been reported in the world literature. Investigations depend on the urgency of intervention, and the surgeon should use the available time to develop a management strategy that combines the principles of eradication of infection, minimizing morbidity and mortality, and minimizing the risk of reinfection. Thirty-day rates of death or stroke are higher than after primary CEA and can require access to the upper reaches of the internal carotid artery. Moreover, real-world results are likely to be much worse than in the published literature. Accordingly, this is not the type of case for an inexperienced vascular surgeon. Although insertion of a covered stent might prove to be an attractive alternative to redo surgery (especially in the presence of massive hemorrhage), there are no data regarding long-term freedom from reinfection. This is essential information to acquire in the future. For the moment, the majority of patients should probably undergo patch excision plus autologous vein reconstruction. Insertion of prosthetic material should be avoided. There is no consensus as to how long targeted antibiotic therapy should be continued. Based on the lack of reinfection after 2 months in patients treated by patch excision and autologous reconstruction, this should probably be 3 months. It should probably be longer in patients treated by insertion of a covered stent.

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Selected References Lazaris A, Sayers RD, Thompson MM, et al: Patch corrugation on duplex ultrasonography may be an early warning of prosthetic patch infection, Eur J Vascular Vasc Endovasc Surg 29:91–92, 2005. Naylor AR, Moir A: An aid to accessing the distal internal carotid artery, J Vasc Surg 49:1345–1347, 2009.

Role of Shunting During Carotid Endarterectomy Steven M. Farley and Wesley S. Moore

Temporary clamping of the internal carotid during carotid endarterectomy (CEA) interrupts antegrade blood flow to the brain in the distribution of the ipsilateral middle and anterior cerebral artery. The consequence of clamping the internal carotid artery is of critical importance to the patient and has been the subject of debate for more than 50 years. In a 1998 editorial, Denton Cooley wrote, “No consensus concerning the proper conduct of this procedure exists, or probably ever will.” In describing their first carotid endarterectomy, Cooley and colleagues fabricated a shunt from polyvinyl tubing with large-bore needles at each end. The same patient underwent adjunctive cerebral protection measures including hypercarbia, cooling the head in ice, and barbiturate use. Interestingly, for most of his career, Cooley argued for a no-shunt approach. Few modern surgeons argue that no patients should undergo shunt placement to reestablish antegrade flow during endarterectomy. Therefore, the question is not if to shunt but when to shunt: selectively or routinely? Because little level I evidence exists, a Cochrane report summarized insufficient evidence is available to support the superiority of either method. Therefore, this chapter discusses the techniques and the proposed advantages and disadvantages of both approaches.

SELECTIVE SHUNTING The impetus for selective shunting originates from the agreed observation that a majority of patients tolerate carotid clamping, and therefore shunting offers no benefit to most patients. Also, routine carotid shunting has several disadvantages, further weakening the argument for universal shunt placement. A selective approach offers the potential advantages of a shorter operative time and unobstructed inspection of the distal endpoint, and it avoids any risks associated with shunt placement for a majority of patients. Identification of the minority of patients who benefit from shunting remains the challenge. In particular, patients with history of stroke or contralateral carotid occlusion have been reported as high-risk patients. However, the use of preoperative risk factors alone has not proved reliable in identifying patients at risk for ischemic stroke following carotid clamping. The traditional intraoperative techniques for identifying patients for shunt insertion—awake CEA, carotid back pressure measurement, and electroencephalographic (EEG) monitoring are relevant. Transcranial Doppler and cerebral oximetry are newer and less-validated methods to assess the need for shunting.

Naylor AR, Payne D, Thompson MM, et al: Prosthetic patch infection after carotid endarterectomy, Eur J Vascular Vasc Endovasc Surg 23:11–16, 2002. Rerkasem K, Rothwell PM: Systematic review of randomized controlled trials of patch angioplasty versus primary closure during carotid endarterectomy, Stroke 41:e55–e56, 2010.

Awake Carotid Endarterectomy Most agree that awake CEA is the gold standard for neurologic monitoring during carotid clamping. The technique involves intraarterial blood pressure monitoring, frequent neurologic checks, and cervical block for analgesia. Patients who develop neurologic changes after test clamping are shunted. Interestingly, many authors report immediate reversal of neurologic symptoms after the establishment of a working shunt, suggesting the value of shunting. Awake CEA has low rates of shunt insertion, with rates around 5%, and reported stroke rates of 1%. An important disadvantage of awake CEA remains: Not all surgeons are trained to perform the operation under cervical block anesthesia. From a metabolic standpoint, awake CEA has been reported to increase the metabolic demands of the brain when compared with general anesthesia. Therefore, patients undergoing an awake CEA may be at greater risk of ischemic injury when compared with those receiving general anesthesia. Another disadvantage is not all patients tolerate the operation for reasons including claustrophobia, pain, cervical arthritis, and redo neck surgery. Without another method for selective shunting, the surgeon may elect to shunt patients routinely.

Carotid Back Pressure Measurement During the development of CEA in the 1960s, carotid back pressure was investigated as a surrogate marker of cerebral perfusion after clamping. To measure back pressure, the common and external carotid arteries are clamped. A needle is inserted into the common carotid artery and the pressure is transduced. A patient with a high carotid back pressure should have adequate cerebral collaterals, should tolerate clamping, and, in theory, does not need a shunt. An important advantage of carotid back pressure measurement over other methods for selective shunting is that back pressures do not require advanced training or expensive equipment, making it an option for any surgeon. Studies support equivalent outcomes when compared with routine shunting. The optimal threshold for back pressure has been intensely studied and been reported from 25 to 50 mm Hg. In general, the back pressure cutoff has become more conservative in an attempt to yield a high sensitivity and not miss patients who might benefit from shunting. Comparing back pressure with EEG, a back pressure of less than 50 mm Hg is sensitive in identifying 97% of patients with EEG changes. AbuRahma and colleagues randomized routine shunting versus selective shunting using a threshold of less than 40 mm Hg. In the selective shunting group, 38% of patients were shunted, and there was no statistically significant difference in the stroke rate. The lower specificity of carotid back pressure results in shunt insertion rates of around 40%. When compared with the shunt insertion rate of 4% to 7% for awake patients, the use of back pressure with a higher threshold of 50 mm Hg likely results in unnecessary shunting in many patients. The potential benefit of shunting may be lost by unnecessarily exposing some patients to the risks of shunting. Also, back pressure accuracy can be questioned. In series of awake patients or with EEG monitoring, patients with back pressures greater than 50 mm Hg can demonstrate signs of cerebral ischemia. Another concern

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CEREBROVASCULAR DISEASE

Selected References Lazaris A, Sayers RD, Thompson MM, et al: Patch corrugation on duplex ultrasonography may be an early warning of prosthetic patch infection, Eur J Vascular Vasc Endovasc Surg 29:91–92, 2005. Naylor AR, Moir A: An aid to accessing the distal internal carotid artery, J Vasc Surg 49:1345–1347, 2009.

Role of Shunting During Carotid Endarterectomy Steven M. Farley and Wesley S. Moore

Temporary clamping of the internal carotid during carotid endarterectomy (CEA) interrupts antegrade blood flow to the brain in the distribution of the ipsilateral middle and anterior cerebral artery. The consequence of clamping the internal carotid artery is of critical importance to the patient and has been the subject of debate for more than 50 years. In a 1998 editorial, Denton Cooley wrote, “No consensus concerning the proper conduct of this procedure exists, or probably ever will.” In describing their first carotid endarterectomy, Cooley and colleagues fabricated a shunt from polyvinyl tubing with large-bore needles at each end. The same patient underwent adjunctive cerebral protection measures including hypercarbia, cooling the head in ice, and barbiturate use. Interestingly, for most of his career, Cooley argued for a no-shunt approach. Few modern surgeons argue that no patients should undergo shunt placement to reestablish antegrade flow during endarterectomy. Therefore, the question is not if to shunt but when to shunt: selectively or routinely? Because little level I evidence exists, a Cochrane report summarized insufficient evidence is available to support the superiority of either method. Therefore, this chapter discusses the techniques and the proposed advantages and disadvantages of both approaches.

SELECTIVE SHUNTING The impetus for selective shunting originates from the agreed observation that a majority of patients tolerate carotid clamping, and therefore shunting offers no benefit to most patients. Also, routine carotid shunting has several disadvantages, further weakening the argument for universal shunt placement. A selective approach offers the potential advantages of a shorter operative time and unobstructed inspection of the distal endpoint, and it avoids any risks associated with shunt placement for a majority of patients. Identification of the minority of patients who benefit from shunting remains the challenge. In particular, patients with history of stroke or contralateral carotid occlusion have been reported as high-risk patients. However, the use of preoperative risk factors alone has not proved reliable in identifying patients at risk for ischemic stroke following carotid clamping. The traditional intraoperative techniques for identifying patients for shunt insertion—awake CEA, carotid back pressure measurement, and electroencephalographic (EEG) monitoring are relevant. Transcranial Doppler and cerebral oximetry are newer and less-validated methods to assess the need for shunting.

Naylor AR, Payne D, Thompson MM, et al: Prosthetic patch infection after carotid endarterectomy, Eur J Vascular Vasc Endovasc Surg 23:11–16, 2002. Rerkasem K, Rothwell PM: Systematic review of randomized controlled trials of patch angioplasty versus primary closure during carotid endarterectomy, Stroke 41:e55–e56, 2010.

Awake Carotid Endarterectomy Most agree that awake CEA is the gold standard for neurologic monitoring during carotid clamping. The technique involves intraarterial blood pressure monitoring, frequent neurologic checks, and cervical block for analgesia. Patients who develop neurologic changes after test clamping are shunted. Interestingly, many authors report immediate reversal of neurologic symptoms after the establishment of a working shunt, suggesting the value of shunting. Awake CEA has low rates of shunt insertion, with rates around 5%, and reported stroke rates of 1%. An important disadvantage of awake CEA remains: Not all surgeons are trained to perform the operation under cervical block anesthesia. From a metabolic standpoint, awake CEA has been reported to increase the metabolic demands of the brain when compared with general anesthesia. Therefore, patients undergoing an awake CEA may be at greater risk of ischemic injury when compared with those receiving general anesthesia. Another disadvantage is not all patients tolerate the operation for reasons including claustrophobia, pain, cervical arthritis, and redo neck surgery. Without another method for selective shunting, the surgeon may elect to shunt patients routinely.

Carotid Back Pressure Measurement During the development of CEA in the 1960s, carotid back pressure was investigated as a surrogate marker of cerebral perfusion after clamping. To measure back pressure, the common and external carotid arteries are clamped. A needle is inserted into the common carotid artery and the pressure is transduced. A patient with a high carotid back pressure should have adequate cerebral collaterals, should tolerate clamping, and, in theory, does not need a shunt. An important advantage of carotid back pressure measurement over other methods for selective shunting is that back pressures do not require advanced training or expensive equipment, making it an option for any surgeon. Studies support equivalent outcomes when compared with routine shunting. The optimal threshold for back pressure has been intensely studied and been reported from 25 to 50 mm Hg. In general, the back pressure cutoff has become more conservative in an attempt to yield a high sensitivity and not miss patients who might benefit from shunting. Comparing back pressure with EEG, a back pressure of less than 50 mm Hg is sensitive in identifying 97% of patients with EEG changes. AbuRahma and colleagues randomized routine shunting versus selective shunting using a threshold of less than 40 mm Hg. In the selective shunting group, 38% of patients were shunted, and there was no statistically significant difference in the stroke rate. The lower specificity of carotid back pressure results in shunt insertion rates of around 40%. When compared with the shunt insertion rate of 4% to 7% for awake patients, the use of back pressure with a higher threshold of 50 mm Hg likely results in unnecessary shunting in many patients. The potential benefit of shunting may be lost by unnecessarily exposing some patients to the risks of shunting. Also, back pressure accuracy can be questioned. In series of awake patients or with EEG monitoring, patients with back pressures greater than 50 mm Hg can demonstrate signs of cerebral ischemia. Another concern



Role of Shunting During Carotid Endarterectomy

regarding back pressures is that unlike EEG or neurologic examination, it does not directly monitor the perfusion of the brain. Back pressures likely do not identify possible intracranial arterial lesions that can make areas of the brain dependent on antegrade flow at risk. Also, poststroke patients have areas of relative hypoperfusion in the healed, collateralized postischemic penumbra. These areas are sensitive to hypoperfusion, and back pressures do not identify these areas. Similarly, back pressures represent a snapshot of cerebral pressure and do not continuously monitor brain function. If physiologic changes occur after clamping, the perfusion status of the brain remains unknown.

Electroencephalographic Monitoring EEG monitoring offers several advantages. First of all, the operation can be done under general anesthesia. Second, EEG monitoring allows continuous monitoring of the bilateral hemispheres of the brain. Unlike carotid back pressure, which measures the patient’s back pressure at one point in time, continuous EEG monitoring can detect hypoperfusion from hypotension, shunt malfunction, or even distal embolization. Most importantly, EEG monitoring has been shown in several studies to be safe and effective. The reported stroke and shunt insertion rates using EEG for selective shunting have been of 0.8% and 14%, respectively. EEG requires more equipment and technical expertise, limiting the application of the technology. Several authors have noted the increased cost to the health care system and have argued that the expense has not been justified by superior outcomes. In general, shunt insertion rates have been reported as 14% to 20%. In comparison to awake CEA, these insertion rates are higher and suggest EEG is overly sensitive. Also, EEG is not specific for all patients. Because the technology measures electrical activity of the cerebral cortex, ischemic changes in the deep white matter may be undetected. Also, patients with previous stroke might have focal areas of relative cerebral ischemia, which might not be detectable by EEG. In many series, patients with prior stroke have been routinely shunted and not included in selective shunting reports.

Transcranial Doppler Transcranial Doppler (TCD) offers continuous, noninvasive intraoperative monitoring of the middle cerebral artery velocity. Various criteria for shunt insertion have been proposed and in general involve a mean flow reduction of 50%. TCD also offers additional data not provided by other monitoring such as detection of emboli or cerebral hyperperfusion, a potential cause of perioperative stroke. The technical aspects of transcranial Doppler are a major disadvantage to its use for cerebral monitoring. Ten to twenty percent of patients do not have a sufficient temporal bone window. Because of the positional nature of the probe, frequent repositioning and monitoring of the probe may be required intraoperatively. As a whole, the technique requires significant expertise not available in all hospitals. Moreover, the reported sensitivity and specificity of 75% when compared with awake CEA would seem inferior.

Cerebral Oximetry A probe is positioned over the ipsilateral parietotemporal area of the brain, just above the temporal muscle, and uses near-infrared spectroscopy to measure cerebral oxygen saturation. Reduction in cerebral oxygenation after carotid clamping suggests cerebral hypoperfusion. Near-infrared oximetry is an attractive technology for several reasons. It requires little training and no particular expertise. The probe pads are easily placed and provide continuous, noninvasive monitoring.

75

Oximetry is still in an investigational stage. Cutoffs for sensitivity and specificity for cerebral ischemia are not standardized and are not validated in a large series of patients. Another concern is that the probe measures oxygenation of the frontal lobe only and does not provide data regarding other regions of the brain. Other drawbacks include the need for shaving the head and the cost of materials.

ROUTINE SHUNTING Would you want your carotid artery clamped? Routine carotid shunting is satisfying at an intuitive level. By placing a shunt, the surgeon alters the natural flow of blood to the brain for the least possible time, providing maximum protection against an ischemic stroke. In the rare event of a stroke, the patient, family, and surgeon can be comforted by the fact that the surgeon did everything possible to prevent it. If shunting were risk-free, likely all vascular surgeons would support routine shunting. However, shunt placement is not without its drawbacks. Those using shunts routinely acknowledge that a small but significant percentage of carotid endarterectomy patients develop symptoms of cerebral ischemia with carotid clamping. Studies of selective shunting suggest shunt insertion rates from 4% to 40% depending on the form of cerebral monitoring employed. Surgeons, who routinely shunt, state that identification of these patients can be unavailable, costly, inaccurate, and stressful. Also, they argue that shunting, in practiced hands, is technically straightforward and adds minimal risk to the operation. Intraoperative cerebral monitoring is not available to all surgeons. Many surgeons did not train or are not comfortable with awake CEA, eliminating one method of cerebral monitoring. EEG, a second method of cerebral monitoring, requires highly skilled technologists to monitor the patients intraoperatively. Not all hospitals can provide this expert addition to the operating room. Also, EEG monitoring adds significant cost to the operation. Back pressures can be viewed as a crude test of cerebral collateral blood flow, and high back-pressure thresholds result in high rates of shunt insertion. Those using shunts routinely comment that the time for flow interruption is minimized and the stress of the operation is reduced by shunt placement. Selective shunters who perform awake CEA can relate anecdotal stories of stressful shunt placement. With clamping, a patient can become agitated and confused. If a patient is unable to lie still or to follow commands, the patient becomes a difficult candidate for shunt placement. Another scenario is the awake patient who becomes aphasic, hemiplegic, or unresponsive after the artery is already open. The need for expedient shunt placement is real and again stressful. Some surgeons prefer the relaxed feeling of a working shunt. With blood flowing through the shunt to the brain, the clock is not ticking while the surgeon is performing the endarterectomy, freeing the surgeon to perform a more meticulous operation. Also, the routine shunter maintains his or her skill at shunt placement. In every case, adequate exposure is achieved, and the operative team is ready with the shunt and shunt clamps on the field. Many selective shunters can relate not expecting to and then needing to shunt, only to find the shunt is unavailable or the surgical exposure is inadequate for shunt placement. Moreover, the steps to shunt placement may be less familiar to the selective surgeon. Shunting is not without risk. Green and colleagues reported in a series of 562 that CEA technical problems were more common (5%) among shunted patients and concluded, “the act of shunting introduces a risk of stroke due to technical error that at least equals the risk of stroke due to hemodynamic ischemia.” Proper technique in shunt placement is critical. First of all, shunt placement can require more exposure of the artery. Particularly in high carotid bifurcations or in patients with disease extending up the internal carotid artery, adequate exposure for shunt placement and endarterectomy may be associated with longer operative times and places the patient at increased risk of cranial nerve injury. In some patients, shunt placement may be technically impossible.

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Once surgical exposure for shunt placement is completed, the shunt is placed after opening the artery. Meticulous attention to detail to prevent embolism is critical. Shunt-induced air emboli or atheromatous emboli are possible. Using transcranial Doppler data, Spencer suggested higher stroke rates because of embolization among shunted patients. Moreover, during positioning, shunt tips can dissect either the distal or proximal arteries. Despite careful placement and de-airing the shunt line, shunt performance is not guaranteed. Manipulating the shunt during endarterectomy can result in tip opposition to the artery wall and, unbeknownst to the surgeon, can significantly reduce shunt flow. Worse yet, shunts can thrombose during surgery. The shunt can also obscure the endarterectomy, especially the critical distal endpoint, and compromise the technical integrity of the operation.

CONCLUSIONS In general, vascular surgeons have decided to either selectively shunt or routinely shunt. Those routinely shunting believe that the risk of stroke as a result of cerebral ischemia during clamping is greater than the risks of shunt of placement. They point to the relative ease of shunt placement, especially when performed for every case. Those who selectively use shunts argue that a small percentage of patients exhibit changes in cerebral perfusion during clamping, and routine shunt placement unnecessarily subjects a majority of patients to the risks of shunt placement. Evidence supports low stroke rates and excellent results using either approach.

Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy D. Preston Flanigan

Improving the results of carotid endarterectomy (CEA) through technical excellence will likely further establish the known effectiveness of the procedure. Technical errors, which can lead to perioperative stroke, include arterial strictures, intraluminal thrombi, intimal flaps, and arterial kinks. These defects can be diagnosed by the proper use of intraoperative testing. It is logical to assume that correction of these defects before completing the procedure should decrease the incidence of perioperative stroke.

ANGIOGRAPHY Blaisdell and colleagues were the first to recognize the potential of intraoperative testing to decrease the morbidity of carotid endarterectomy. They found a 26% incidence of technical error using completion arteriography, with most of the defects being strictures. Others have also found technical errors following carotid endarterectomy, and the rate of reoperation when completion arteriography has been used has ranged from 2.4% to 26%.

Selected References AbuRahma AF, Stone PA, Hass SM, et al: Prospective randomized trial of routine versus selective shunting in carotid endarterectomy based on stump pressure, J Vasc Surg 51:1133–1138, 2010. Ali AM, Green D, Zayed H, et al: Cerebral monitoring in patients undergoing carotid endarterectomy using a triple assessment technique, Interact Cardiovasc Thorac Surg 12:454–457, 2011. Cooley DA: Carotid endarterectomy: from first recorded case to present, Tex Heart Inst 15:139–141, 1988. Green RM, Messick WJ, Riccota JJ, et al: Benefits, shortcomings and costs of EEG monitoring, Ann Surg 201:785–792, 1985. Lawrence PF, Alves JC, Jicha D, et al: Incidence, timing, and causes of cerebral ischemic during carotid endarterectomy with regional anesthesia, J Vasc Surg 27:329–334, 1998. Moore WS, Hall AD: Carotid artery back pressure—A test of cerebral ­tolerance to temporary carotid occlusion, Arch Surg 99:702–710, 1969. Pennekamp CWA, Bots ML, Kappelle LJ, et al: The value of near-infrared spectroscopy measured cerebral oximetry during carotid endarterectomy in perioperative stroke prevention. A review, Eur J Vasc Endovasc Surg 38:539–545, 2009. Rerkasem K, Rothwell PM: Routine or selective carotid artery shunting for carotid endarterectomy (and different method of monitoring in selective shunting), Cochrane Database Syst Rev(4)CD000190, 2009. Spencer MP: Transcranial Doppler monitoring and causes of stroke from carotid endarterectomy, Stroke 28:685–691, 1997. Tan TW, Garcia-Toca M, Marcaccio EJ, et al: Predictors of shunt during carotid endarterectomy with routine electroencephalography monitoring, J Vasc Surg 49:1374–1378, 2009.

Owing to the relatively low stroke rate associated with carotid endarterectomy, it has been difficult to demonstrate that the use of intraoperative arteriography actually decreases the complication rate because of the large number of patients required to assure a statistically reliable result. An exception is the report by Scott’s group, which showed a significant difference in the stroke rate when 146 procedures in which intraoperative arteriography was not used were compared with 137 endarterectomies in which intraoperative arteriography was used. These authors found that the stroke rate was reduced from 6.8% to 3.8%, and the mortality rate was reduced from 4.8% to 1.5% when intraoperative completion arteriography was employed. However, the groups were concurrent rather than randomized. Another potential benefit of using intraoperative arteriography is the prevention of recurrent disease. Courbier and colleagues demonstrated that defects that were seen on intraoperative arteriography and that were not corrected led to a higher than usual incidence of recurrent disease. By performing arteriography a mean of 19.2 months postoperatively, Courbier and colleagues documented disease recurrence in only 3% of internal carotid arteries that had normal intraoperative arteriographic studies. This rate was considerably less than the 28% recurrence rate of when residual defects were left uncorrected. Intraoperative completion carotid arteriography is performed before reversing the heparin effect, so that any defect that requires correction can be repaired without the need to administer heparin to the patient again. An x-ray cassette is placed under the patient’s head and neck. The head is maintained in the turned position to allow optimal separation of the internal and external carotid arteries in the anteroposterior view. The common carotid artery is punctured with a 19-gauge needle attached to a long extension tubing and a 25-mL syringe. It is most important to be sure that no air bubbles or other debris are present in the line. Just before injection, the common carotid artery is clamped as far proximal as the wound edge allows. The surgeon, standing behind a lead shield, injects 12 mL of full-strength contrast medium, and the film is exposed. The common carotid artery clamp is then removed. The needle is usually

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Once surgical exposure for shunt placement is completed, the shunt is placed after opening the artery. Meticulous attention to detail to prevent embolism is critical. Shunt-induced air emboli or atheromatous emboli are possible. Using transcranial Doppler data, Spencer suggested higher stroke rates because of embolization among shunted patients. Moreover, during positioning, shunt tips can dissect either the distal or proximal arteries. Despite careful placement and de-airing the shunt line, shunt performance is not guaranteed. Manipulating the shunt during endarterectomy can result in tip opposition to the artery wall and, unbeknownst to the surgeon, can significantly reduce shunt flow. Worse yet, shunts can thrombose during surgery. The shunt can also obscure the endarterectomy, especially the critical distal endpoint, and compromise the technical integrity of the operation.

CONCLUSIONS In general, vascular surgeons have decided to either selectively shunt or routinely shunt. Those routinely shunting believe that the risk of stroke as a result of cerebral ischemia during clamping is greater than the risks of shunt of placement. They point to the relative ease of shunt placement, especially when performed for every case. Those who selectively use shunts argue that a small percentage of patients exhibit changes in cerebral perfusion during clamping, and routine shunt placement unnecessarily subjects a majority of patients to the risks of shunt placement. Evidence supports low stroke rates and excellent results using either approach.

Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy D. Preston Flanigan

Improving the results of carotid endarterectomy (CEA) through technical excellence will likely further establish the known effectiveness of the procedure. Technical errors, which can lead to perioperative stroke, include arterial strictures, intraluminal thrombi, intimal flaps, and arterial kinks. These defects can be diagnosed by the proper use of intraoperative testing. It is logical to assume that correction of these defects before completing the procedure should decrease the incidence of perioperative stroke.

ANGIOGRAPHY Blaisdell and colleagues were the first to recognize the potential of intraoperative testing to decrease the morbidity of carotid endarterectomy. They found a 26% incidence of technical error using completion arteriography, with most of the defects being strictures. Others have also found technical errors following carotid endarterectomy, and the rate of reoperation when completion arteriography has been used has ranged from 2.4% to 26%.

Selected References AbuRahma AF, Stone PA, Hass SM, et al: Prospective randomized trial of routine versus selective shunting in carotid endarterectomy based on stump pressure, J Vasc Surg 51:1133–1138, 2010. Ali AM, Green D, Zayed H, et al: Cerebral monitoring in patients undergoing carotid endarterectomy using a triple assessment technique, Interact Cardiovasc Thorac Surg 12:454–457, 2011. Cooley DA: Carotid endarterectomy: from first recorded case to present, Tex Heart Inst 15:139–141, 1988. Green RM, Messick WJ, Riccota JJ, et al: Benefits, shortcomings and costs of EEG monitoring, Ann Surg 201:785–792, 1985. Lawrence PF, Alves JC, Jicha D, et al: Incidence, timing, and causes of cerebral ischemic during carotid endarterectomy with regional anesthesia, J Vasc Surg 27:329–334, 1998. Moore WS, Hall AD: Carotid artery back pressure—A test of cerebral ­tolerance to temporary carotid occlusion, Arch Surg 99:702–710, 1969. Pennekamp CWA, Bots ML, Kappelle LJ, et al: The value of near-infrared spectroscopy measured cerebral oximetry during carotid endarterectomy in perioperative stroke prevention. A review, Eur J Vasc Endovasc Surg 38:539–545, 2009. Rerkasem K, Rothwell PM: Routine or selective carotid artery shunting for carotid endarterectomy (and different method of monitoring in selective shunting), Cochrane Database Syst Rev(4)CD000190, 2009. Spencer MP: Transcranial Doppler monitoring and causes of stroke from carotid endarterectomy, Stroke 28:685–691, 1997. Tan TW, Garcia-Toca M, Marcaccio EJ, et al: Predictors of shunt during carotid endarterectomy with routine electroencephalography monitoring, J Vasc Surg 49:1374–1378, 2009.

Owing to the relatively low stroke rate associated with carotid endarterectomy, it has been difficult to demonstrate that the use of intraoperative arteriography actually decreases the complication rate because of the large number of patients required to assure a statistically reliable result. An exception is the report by Scott’s group, which showed a significant difference in the stroke rate when 146 procedures in which intraoperative arteriography was not used were compared with 137 endarterectomies in which intraoperative arteriography was used. These authors found that the stroke rate was reduced from 6.8% to 3.8%, and the mortality rate was reduced from 4.8% to 1.5% when intraoperative completion arteriography was employed. However, the groups were concurrent rather than randomized. Another potential benefit of using intraoperative arteriography is the prevention of recurrent disease. Courbier and colleagues demonstrated that defects that were seen on intraoperative arteriography and that were not corrected led to a higher than usual incidence of recurrent disease. By performing arteriography a mean of 19.2 months postoperatively, Courbier and colleagues documented disease recurrence in only 3% of internal carotid arteries that had normal intraoperative arteriographic studies. This rate was considerably less than the 28% recurrence rate of when residual defects were left uncorrected. Intraoperative completion carotid arteriography is performed before reversing the heparin effect, so that any defect that requires correction can be repaired without the need to administer heparin to the patient again. An x-ray cassette is placed under the patient’s head and neck. The head is maintained in the turned position to allow optimal separation of the internal and external carotid arteries in the anteroposterior view. The common carotid artery is punctured with a 19-gauge needle attached to a long extension tubing and a 25-mL syringe. It is most important to be sure that no air bubbles or other debris are present in the line. Just before injection, the common carotid artery is clamped as far proximal as the wound edge allows. The surgeon, standing behind a lead shield, injects 12 mL of full-strength contrast medium, and the film is exposed. The common carotid artery clamp is then removed. The needle is usually



Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy N

S

F

T

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FIGURE 1 Intraoperative

sonograms from canine aortas demonstrating a normal aorta without defects (N), a stricture following arterial closure (S, arrows), an intimal flap (F, arrow), and an intraluminal thrombus (T, arrow).  (Reproduced with permission from Coelho JCU, Sigel B, Flanigan DP, et al: Detection of arterial defects by real-time ultrasound scanning during vascular surgery: an experimental study, J Surg Res 32:130–137, 1981.)

left in place until a satisfactory film has been obtained. A figure-ofeight suture is placed at the needle base, and the needle is removed as the suture is tied. Numerous variations of the technique have been described, most of which give satisfactory results. The use of a dental film placed within the wound also has been shown to be satisfactory.

DOPPLER STUDIES Doppler spectrum analysis was one of the first noninvasive techniques to be used in evaluating carotid artery disease. Barnes and others have demonstrated that the technique also is useful intraoperatively to detect technical errors. Initially, continuous-wave devices were employed for this purpose, but subsequently it has been demonstrated that pulsed Doppler is probably more sensitive. Highfrequency pulsed Doppler allows the sampling of small volumes of blood flow within the vessel being insonated. Although tight stenoses may be detected by the audible interpretation of the Doppler frequency shift, hard copy spectral analysis is much more sensitive. Zierler and coworkers demonstrated that pulsed Doppler, using a 20-MHz pulsed device, was as accurate as arteriography in detecting intraoperative defects in internal carotid arteries. The Doppler probe is a 20-MHz pulsed device mounted in a 16-gauge needle. The sample volume is very small and can be positioned at discrete points within the vessel. The probe is connected to a real-time, fast-Fourier transform spectrum analyzer that puts out a visual spectrum. The probe is held at a 60-degree angle to the vessel, and saline is placed in the wound for acoustic coupling. Examination is performed both before and after endarterectomy. Velocity patterns are measured at several sites in the common, external, and internal carotid arteries. Flow abnormalities are classified into three categories. Mild disturbances show peak systolic frequencies up to 16 kHz and spectral broadening in late systole only. Also, any spectrum with minimal

spectral broadening is characterized as a mild disturbance. Moderate disturbances show peak systolic frequency up to 16 kHz and spectral broadening throughout most of systole. Severe flow disturbances show peak systolic frequency above 16 kHz and spectral broadening throughout most of systole. It is important to realize that these criteria are only good for the incident frequency (20 MHz) used. Although pulsed Doppler is very sensitive in detecting flow disturbances, it is not able to identify the defect responsible for the disturbance, and it thus requires the addition of an imaging test to identify the defect and to assist the surgeon in the decision to reopen the vessel to correct the defect.

DUPLEX SCANNING The advent of high-resolution imaging ultrasonography was a major advance in the noninvasive evaluation of carotid artery disease. It is not surprising that the technique was quickly adopted for intraoperative evaluation during carotid endarterectomy. Duplex scanning, which combines both imaging ultrasonography and pulsed Doppler, has been used more recently. Before ultrasonic imaging was used in the operating room the utility of the technique was assessed in the canine laboratory. At the University of Illinois, Coelho and colleagues created technical defects consisting of strictures, thrombi, intimal flaps, and intimal dissections in the aortas of dogs and then imaged the defects using a highresolution small parts scanner (Figure 1). Scans were interpreted by observers who were blinded to the defects. The observers were able to identify all but 1-mm intimal flaps 100% of the time. The 1-mm flaps were correctly identified 67% of the time. The correlation between real and measured flap size was r = .84. In a follow-up study, Coelho and colleagues then compared ultrasonographic imaging to singleplane and biplane portable arteriography. Both ultrasonography and arteriography were accurate in detecting arterial strictures; however,

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I E

flaps (73%). In every artery the defect identified on ultrasound was identified when the vessel was reopened. No wound infection was associated with the procedure. An additional 442 carotid endarterectomies performed using intraoperative duplex scanning was reported by the author in 2007. In this latter study the incidence of significant defects requiring reopening the artery for correction was 6.3%. In a study from the Mayo Clinic published in 2001, Panneton reported that 11% of arteries studied had significant defects requiring correction.

FOLLOW-UP STUDIES C

FIGURE 2  Intraoperative sonogram of a normal carotid artery bifur-

cation following endarterectomy. E, External carotid artery; I, internal carotid artery; C, common carotid artery.  (Reproduced with permission from Flanigan DP, Douglas DJ, Machi J, et al: Intraoperative ultrasonic imaging of the carotid artery during carotid endarterectomy, Surgery 100:893–898, 1986.)

ultrasonography was superior to both single-plane and biplane arteriography in detecting intimal flaps and intraluminal thrombi. With the safety and accuracy of intraoperative ultrasonographic imaging assured, the technique was next employed in the operating room. High resolution is obtainable with intraoperative carotid ultrasonography (Figure 2). The technique of duplex imaging is used after the carotid arteriotomy is closed and blood flow is reestablished. The surgeon does the actual scanning while the ultrasound machine is controlled by an ultrasound technician. A hand-held probe is placed into a sterile plastic sheath into which acoustic jelly has already been added. The sheath is 6 feet long to allow manipulation of the probe without risk of contamination by the cable. The wound is filled with sterile saline solution for acoustic coupling. The entire endarterectomy site is insonated, as is the artery above and below the endarterectomy site within the operative wound. Each vessel is visualized in multiple transverse and saggital planes. Pulsed Doppler measurements are performed at the endarterectomy endpoints in the internal, external, and common carotid arteries. Figure 3 shows an intimal flap with subflap thrombus imaged in both the saggital and transverse planes. Intraoperative ultrasonic images are not difficult to interpret. The high resolution of the technique and the limited number of defects make interpretation easy even for the first-time reader (see Figures 1 and 2). Normal vessel lumens are easily identified because the intimal surface is smooth and regular. Arterial strictures are easily identified by luminal narrowing (see Figure 1). Thrombi are identified by intraluminal filling defects fixed to the arterial wall. Intimal flaps are linear structures that are attached to the arterial wall at one end while the other end moves back and forth from the arterial wall with the pulsations of blood flow (Figures 3 and 4). Combined lesions show thrombus under intimal flaps. These complex lesions are often more difficult to identify, but their complexity and size always mandate reexploration of the artery. The author considers a velocity greater than 130 cm/sec to be abnormal, but does not use this velocity as the sole criterion for reexploration. In the original 200 carotid endarterectomy procedures in which completion duplex scanning was used by the author 28% of the arteries were found to have technical errors. Six arteries had more than one defect. In only 28% of the arteries were the defects judged sufficiently dangerous to warrant reopening the vessel to correct the defect (8% of all arteries scanned). The vast majority of defects found were intimal

The high sensitivity of intraoperative ultrasonography creates a problem of deciding which defects should be repaired and which defects can be left unrepaired. The author's approach has been to correct all but the most minimal of defects in the internal carotid artery while being less concerned with minor defects in the external and common carotid arteries. To evaluate the immediate effects of this approach, the author, in 1989, studied three groups of patients: those with normal intraoperative ultrasonography studies, those having defects repaired, and those with minor defects that were left uncorrected. The incidence of stroke was greatest in the normal group (3.8%), whereas those who had defects corrected had no perioperative strokes. Patients with uncorrected minor defects had a stroke rate similar to those with normal study results (3.3%). The low stroke rate does not allow the demonstration of significant differences between the groups. The data tend to support the criteria used to select defects for repair. Reopening the carotid artery to repair a defect was not associated with morbidity in this study. The late findings reported by Courbier and colleagues using arteriography raises concern about leaving even minor defects uncorrected. Although the defects left uncorrected were more significant defects than in the author’s series, the demonstration of recurrent disease in such patients suggests that even minor defects should be corrected. Such an approach would need to be justified, however, because reopening the carotid artery to correct defects in a large number of patients can increase the possibility of perioperative stroke. The author studied the question of which defects should be corrected by performing carotid duplex scans in the early postoperative period and again at regular intervals during the subsequent postoperative period. This protocol was carried out successfully in 80 carotid arteries. Sixty-two arteries were normal intraoperatively, and 18 had 21 minor defects that were left uncorrected. These defects included nine common, four internal, and eight external carotid artery lesions consisting of 1- to 3-mm intimal flaps (19) or mild stenoses. Sixteen of the 19 intimal flaps were not seen on the first postoperative study, indicating healing of the flaps. Both minor stenoses were undetected by postoperative duplex scanning. There was no statistically significant relationship between the presence of a minor residual defect on intraoperative ultrasonic imaging and the subsequent development of recurrent plaque, stenosis, or occlusion in any of the vessels assessed. Further analysis of these data indicated that minor stenoses (50% vs. >70% lumenal diameter narrowing, and variable times of study after the surgical intervention). Some restenotic lesions also undergo later regression for unclear reasons.

David Gordon

Restenosis at the site of previous atherosclerotic plaque removal or dilatation commonly accompanies mechanical methods to reopen an artery. This often follows balloon angioplasty, atherectomy, endarterectomy, or arterial stenting. In arterial stenting, tissue grows inside the stent, causing a luminal stenosis. In general, the pathologic basis of restenosis appears to be a substantial increase in intimal volume of the affected artery with secondary luminal narrowing. In arteries not stented, some form of artery wall contraction occurs. Both phenomena can result in a vessel that is hemodynamically narrowed. A number of reports on the histopathology of this lesion following a carotid endarterectomy (CEA) or following carotid angioplasty with stenting (CAS) have been published. However, compared with the coronary arteries, there is generally less experience with the carotid lesion, partly because most restenotic cases are asymptomatic, and as such, their surgical removal is usually not indicated. Thus existing pathologic studies are likely to be heavily skewed toward the symptomatic lesions or lesions obtained at autopsy. The estimated rates of restenosis are generally higher for the coronary arteries than for the carotid arteries. In the coronary arteries,

Selected References Badruddin A, Teleb MS, Abraham MG: Safety and feasibility of simultaneous ipsilateral proximal carotid artery stenting and cerebral aneurysm coiling, Front Neurol 1:120, 2010. Cohen JE, Gomori J, Grigoriadis S: Single-staged sequential endovascular stenting in patients with in tandem carotid stenoses, Neurol Res 30:262–267, 2008. Gock SL, Mitchell PJ, Field PL: Tandem lesions of the carotid circulation: combined extracranial endarterectomy and intracranial transluminal angioplasty, Australas Radiol 45:320–325, 2001. Kappelle LJ, Eliasziw M, Fox AJ: Small, unruptured intracranial aneurysms and management of symptomatic carotid artery stenosis. North American Symptomatic Carotid Endarterectomy Trial Group, Neurology 55:307–309, 2000. Ladowski JS, Webster MW, Yonas HO: Carotid endarterectomy in patients with asymptomatic intracranial aneurysm, Ann Surg 200:70–73, 1984. Mackey WC, O'Donnell TF Jr, Callow AD: Carotid endarterectomy in patients with intracranial vascular disease: short-term risk and long-term outcome, J Vasc Surg 10:432–438, 1989. Mattos MA, van Bemmelen PS, Hodgson KJ: The influence of carotid siphon stenosis on short- and long-term outcome after carotid endarterectomy, J Vasc Surg 17:902–910, 1993. discussion 910–911. Orecchia PM, Clagett GP, Youkey JR: Management of patients with symptomatic extracranial carotid artery disease and incidental intracranial berry aneurysm, J Vasc Surg 2:158–164, 1985. Schuler JJ, Flanigan DP, Lim LT: The effect of carotid siphon stenosis on stroke rate, death, and relief of symptoms following elective carotid endarterectomy, Surgery 92:1058–1067, 1982. Siddiqui FM, Hassen AE, Tariq N: Endovascular management of symptomatic extracranial stenosis associated with secondary intracranial tandem stenosis. A multicenter review, J Neuroimaging 22:243–248, 2012.

DESCRIPTIVE PATHOLOGY Although several animal model systems have been used to study mechanically induced arterial intimal thickening, the dynamic, human in  vivo mechanisms leading to recurrent stenosis remain incompletely understood. In general, some degree of acute mural thrombus formation and acute inflammation can be seen after CEA. Within the first few weeks to months of the arterial manipulation, the restenotic lesion is described as intimal tissue composed of numerous smooth muscle cells, much proteoglycan-rich and collagen-rich extracellular matrix, and a few monocyte/macrophages, and possibly other inflammatory cells. This early-stage lesion thus resembles the diffuse intimal thickening seen in many adult arteries and is best mimicked by animal models of angioplasty-induced arterial injury. After several months to years, the lesion is generally richer in monocyte/macrophages and might contain a necrotic core, with occasional features of thrombosis and hemorrhage. This later lesion thus better resembles the atherosclerotic plaque, which was the type

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and three elective aneurysm clippings. Of the 44 patients in these three reports, only one (2.3%) had rupture of an intracranial aneurysm, and this large aneurysm was in the posterior circulation. In addition, Adams in 1977 reported a single case of fatal subarachnoid hemorrhage 7 months after carotid endarterectomy. Although rupture of intracranial aneurysms can occur at any time, the relationship of intracranial aneurysm rupture and prior carotid revascularization remains unproved. A combined treatment of extracranial carotid stenosis and an intracranial aneurysm by an endovascular approach has recently been reported. Using different approaches, Iwata and colleagues and Espinosa and colleagues demonstrated in case reports the ability to treat both the aneurysm and the stenosis endovascularly in separate staged procedures. Alternatively, Badruddin and coauthors demonstrated in a series of 10 patients that simultaneous endovascular aneurysm coiling and CAS was effective and safe. In this study, the technical success rate was 100% for stenting and coiling, without incidence of immediate postoperative complications. Mean follow-up time was 7.5 ± 5.5 months and no stroke, TIA, or aneurysmal bleeding was noted. An incidentally discovered intracranial aneurysm in a patient with recurrent episodes of transient ischemic attacks caused by a critical carotid stenosis is most appropriately treated by a CEA or CAS first (Figure 3A to C). The patient may have the aneurysm treated later (Figure 3D). Because there is little added perioperative risk and no clear relationship to late postoperative aneurysm enlargement or rupture, CEA or CAS should not be denied to appropriate candidates because of the incidental finding of an asymptomatic intracranial aneurysm. In cases where an intracerebral aneurym is found in conjunction with a carotid stenosis, the symptomatic lesion should be treated first. If the proximal hemodynamic limiting carotid stenosis is proximally in tandem to a large aneurysm, there could be clinical concern for securing the aneurysm soon following carotid revascularization

given the possibility that increased cerebral blood flow could result in increased shear forces or high flow volumes to the aneurysm, theoretically increasing risk of rupture.

Pathology of Carotid Artery Restenosis

with restenosis rates up to 30%, this has become a significant clinical problem. Published rates for restenosis following a CEA are 1% to 4% for symptomatic restenosis. However, if noninvasive methods of serial patient follow-up such as Doppler ultrasound are used, restenosis rates as high as 31% are seen. A significant problem in studying restenosis rates is the lack of a uniform definition of "restenosis," (e.g., >50% vs. >70% lumenal diameter narrowing, and variable times of study after the surgical intervention). Some restenotic lesions also undergo later regression for unclear reasons.

David Gordon

Restenosis at the site of previous atherosclerotic plaque removal or dilatation commonly accompanies mechanical methods to reopen an artery. This often follows balloon angioplasty, atherectomy, endarterectomy, or arterial stenting. In arterial stenting, tissue grows inside the stent, causing a luminal stenosis. In general, the pathologic basis of restenosis appears to be a substantial increase in intimal volume of the affected artery with secondary luminal narrowing. In arteries not stented, some form of artery wall contraction occurs. Both phenomena can result in a vessel that is hemodynamically narrowed. A number of reports on the histopathology of this lesion following a carotid endarterectomy (CEA) or following carotid angioplasty with stenting (CAS) have been published. However, compared with the coronary arteries, there is generally less experience with the carotid lesion, partly because most restenotic cases are asymptomatic, and as such, their surgical removal is usually not indicated. Thus existing pathologic studies are likely to be heavily skewed toward the symptomatic lesions or lesions obtained at autopsy. The estimated rates of restenosis are generally higher for the coronary arteries than for the carotid arteries. In the coronary arteries,

Selected References Badruddin A, Teleb MS, Abraham MG: Safety and feasibility of simultaneous ipsilateral proximal carotid artery stenting and cerebral aneurysm coiling, Front Neurol 1:120, 2010. Cohen JE, Gomori J, Grigoriadis S: Single-staged sequential endovascular stenting in patients with in tandem carotid stenoses, Neurol Res 30:262–267, 2008. Gock SL, Mitchell PJ, Field PL: Tandem lesions of the carotid circulation: combined extracranial endarterectomy and intracranial transluminal angioplasty, Australas Radiol 45:320–325, 2001. Kappelle LJ, Eliasziw M, Fox AJ: Small, unruptured intracranial aneurysms and management of symptomatic carotid artery stenosis. North American Symptomatic Carotid Endarterectomy Trial Group, Neurology 55:307–309, 2000. Ladowski JS, Webster MW, Yonas HO: Carotid endarterectomy in patients with asymptomatic intracranial aneurysm, Ann Surg 200:70–73, 1984. Mackey WC, O'Donnell TF Jr, Callow AD: Carotid endarterectomy in patients with intracranial vascular disease: short-term risk and long-term outcome, J Vasc Surg 10:432–438, 1989. Mattos MA, van Bemmelen PS, Hodgson KJ: The influence of carotid siphon stenosis on short- and long-term outcome after carotid endarterectomy, J Vasc Surg 17:902–910, 1993. discussion 910–911. Orecchia PM, Clagett GP, Youkey JR: Management of patients with symptomatic extracranial carotid artery disease and incidental intracranial berry aneurysm, J Vasc Surg 2:158–164, 1985. Schuler JJ, Flanigan DP, Lim LT: The effect of carotid siphon stenosis on stroke rate, death, and relief of symptoms following elective carotid endarterectomy, Surgery 92:1058–1067, 1982. Siddiqui FM, Hassen AE, Tariq N: Endovascular management of symptomatic extracranial stenosis associated with secondary intracranial tandem stenosis. A multicenter review, J Neuroimaging 22:243–248, 2012.

DESCRIPTIVE PATHOLOGY Although several animal model systems have been used to study mechanically induced arterial intimal thickening, the dynamic, human in  vivo mechanisms leading to recurrent stenosis remain incompletely understood. In general, some degree of acute mural thrombus formation and acute inflammation can be seen after CEA. Within the first few weeks to months of the arterial manipulation, the restenotic lesion is described as intimal tissue composed of numerous smooth muscle cells, much proteoglycan-rich and collagen-rich extracellular matrix, and a few monocyte/macrophages, and possibly other inflammatory cells. This early-stage lesion thus resembles the diffuse intimal thickening seen in many adult arteries and is best mimicked by animal models of angioplasty-induced arterial injury. After several months to years, the lesion is generally richer in monocyte/macrophages and might contain a necrotic core, with occasional features of thrombosis and hemorrhage. This later lesion thus better resembles the atherosclerotic plaque, which was the type

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of lesion originally treated. However, there is much variation in the reported histology, and no definite transition time from the former to the latter is evident. Features of both can also coexist in the same primary or restenotic lesion. For example, although some descriptions of regions of restenotic tissue have focused on features such as stellate smooth muscle cells, a proteoglycan-rich matrix, and occasional organizing thrombi, it is important to remember that all of these features can be seen in primary atherosclerotic lesions that have never undergone interventional procedures. Intimal neovascularization can also be seen in both types of lesions. Features of carotid lesions that produce symptoms are also not fully clarified. With the primary atherosclerotic plaque, several studies have suggested that in addition to the degree of stenosis, the presence of plaque complications such as ulceration and thrombus formation are important for producing ipsilateral symptoms. Based on correlations between B-mode ultrasound imaging and pathology, many such complicated lesions are described as heterogeneous on ultrasound imaging, whereas many of the early restenotic lesions are described as both asymptomatic and having a homogeneous ultrasound appearance. This homogeneous character is often correlated with diffuse intimal thickening, which is generally devoid of plaque ulcerations or thrombus formation. One is tempted to speculate therefore that the absence of plaque ulcerations and thrombus formation accounts for the lack of symptoms in most carotid restenosis lesions.

PATHOGENESIS Based on the author's knowledge of experimental artery wall reactions to injury and results from clinical studies employing ultrasound methods, the presumed processes leading to arterial restenosis can be categorized as follows, although this is likely not a complete listing: smooth muscle cell proliferation, extracellular matrix synthesis, thrombus organization, and artery wall remodeling. These processes can occur to varying degrees in the affected arteries.

Cell Proliferation The initial major focus in this disease was on cell proliferation after either the mechanical balloon dilatation or endarterectomy of the atherosclerotic artery. In the case of endarterectomy, the artery is opened longitudinally from the adventitia, usually through to the lumen. The atherosclerotic intima is removed in the segment, and variable amounts of the underlying media are removed as well. The artery thus has mechanical injury to all layers of the artery wall, resulting with media and the cut ends of the proximal and distal intima exposed to the blood elements. Such exposure of collagen and possibly tissue factor promotes platelet adhesion to this injured surface, as well as variable amounts of fibrin deposition. Platelet deposition and release of growth factors, smooth muscle necrosis, and fibrin deposition as a scaffold for subsequent mesenchymal cell migration all result from the initial injury. These factors act to induce smooth muscle proliferation, migration, and extracellular matrix synthesis, which in turn are all visible aspects of the restenotic lesion. Speculation about subsequent arterial wall repair has been heavily influenced by detailed studies of the reactions of normal arteries to balloon dilatation injury. They are best described in the rat carotid artery model. Here endothelial denudation is accompanied by variable degrees of medial smooth muscle cell injury and death, followed in 1 to 3 days by a brisk smooth muscle proliferative response, reaching proliferative indices of about 30% to 50% and higher. Modulated smooth muscle–derived cells that have lost most of their smooth muscle–distinguishing features eventually repopulate the media, migrate into the intima, and continue their proliferation and intimal expansion for weeks thereafter, albeit with

a gradually decreasing proliferative index. These smooth muscle– derived cells also synthesize much extracellular matrix, proteoglycans and collagen in particular, and thereby greatly expand the volume of the intima further. This general sequence of events is presumed to occur in human atherosclerotic arteries as well, and somewhat similar sequences of events have been described in some animal models of angioplasty injury to preexisting atherosclerotic arteries. Such proliferative indices tend to peak at later times after injury, with somewhat decreased proliferative indices when compared with the rat carotid model. However, this sequence of events for human restenosis was originally called into question based on measurements of actual proliferative indices in human restenotic tissue obtained by atherectomy catheter. The authors’ laboratory first studied human coronary arterial samples obtained from the atherectomy catheter in both primary atherosclerotic plaques and restenoses after previous angioplasty/atherectomy resection. Using proliferating cell nuclear antigen (PCNA), the authors found proliferative indices in the 0% to 2% range for both classes of lesions, with no significant differences between the two. This has been confirmed by others using PCNA and the Ki-67 proliferation marker. Other studies using PCNA immunolabeling on human iliac and femoral arterial plaques and restenosis lesions have reported average PCNA labeling indices on the order of 3.6% in primary atherosclerotic lesions and 15.2% in restenosis lesions. The reason for these reportedly higher labeling indices is not clear. It is possible that restenosis biology differs in the iliac, femoral, and possibly carotid arteries compared with coronary lesions. The larger lower extremity arteries, when they have restenoses, might allow an enrichment of actual restenotic tissue samples, whereas the smaller coronary arteries are more likely to yield a mixture of primary lesion and restenotic tissue. Most of these studies have looked at restenotic tissue several weeks after the initial surgical intervention, a time at which animal models indicate that the cell proliferation rate has returned to low levels.

Extracellular Matrix Synthesis One feature characteristic of restenotic tissue is intimal masses of stellate-appearing smooth muscle cells within a proteoglycan-rich extracellular matrix. However, such regions also can be found in primary atherosclerotic plaques without previous mechanical injury, and when found in restenotic tissue, they do not have significantly higher proliferative indices than other regions. Indeed, as with primary plaques, the volume of restenotic intima attributable to extracellular matrix far exceeds that attributable to cell mass, possibly suggesting that extracellular matrix synthesis is more important to the volume growth of restenotic tissue than is cell proliferation. Based on studies of coronary atherectomy samples, considerable type I collagen synthesis occurs in human coronary restenosis tissues. The best predictors of type I collagen synthesis in either primary or restenotic coronary tissue appear to be the presence of organizing thrombus, penetrating microvessels, and regions of smooth muscle– like cells with a stellate morphology. Type I collagen synthesis has also been documented in restenotic carotid lesions. Thus much extracellular matrix production occurs in the evolution of the restenosis lesion, as well as remodeling of this matrix. The synthesis of other collagen types is likely as well. The importance of extracellular matrix expansion in the intima was also highlighted in the rat carotid balloon injury model. In this study, after 2 weeks during which cell proliferative activity was returning to control levels and intimal cell number remained constant, the intima continued to enlarge markedly. Indeed the percentage of intimal volume composed of essentially of smooth muscle dropped from 41% at 2 weeks to 20% at 8 weeks. Conversely, the proportion of extracellular matrix increased from approximately 59% to 80%, of which collagen constituted a large proportion. Thus during the

Pathology of Carotid Artery Restenosis

short-lived proliferative phase, and predominantly thereafter, much intimal enlargement occurs by extracellular matrix expansion, largely owing to presumed synthesis by the previously proliferating smooth muscle cells. Other studies of the rat carotid artery have shown that collagen gene expression is up-regulated after balloon injury, and this change is preceded by increases in transforming growth factor beta (TGFβ) type 1 mRNA and protein. Because it is known that TGF-β and platelet-derived growth factor (PDGF) are potent stimulators of ­ smooth muscle collagen synthesis and are potent smooth muscle mitogens, it is conceivable that the in vivo role of these growth factors lies more with collagen and extracellular matrix gene expression than with cell proliferation in human arterial lesions. The real importance of cell proliferation after angioplasty or endarterectomy may be the production of a few smooth muscle–like cells that can later go on to generate vast amounts of extracellular matrix. It may be appropriate to generate therapies that inhibit such matrix production.

Thrombus Organization Not much is known about thrombus organization during the evolution of human restenosis. It seems likely that the initial angioplasty or endarterectomy injury disrupts atherosclerotic plaques, which are rich in tissue factor, and that variable amounts of mural thrombus with platelet deposition occurs. However, despite good control of acute procedure-related thrombosis of the injured artery, the true incidence of subsequent, nonocclusive mural thrombus that might occur days to weeks after the angioplasty in human arteries is unknown. Noninvasive imaging techniques with improved resolution need to be developed to clearly distinguish thrombus from solid intima. Thrombus formation can be seen in some restenotic lesions, and variable degrees of thrombus formation have been reported after endarterectomy or after angioplasty with stent deployment. It is conceivable that much of the restenotic intima in several cases could have an initial thrombus template and that this thrombus later organizes into solid intima. Certainly the features of intimal vascularization and much proteoglycan production, which are commonly seen in restenotic tissue, can be produced as a consequence of thrombus organization.

Artery Wall Remodeling Artery wall remodeling is usually defined as a change in artery wall size resulting in luminal narrowing, without a change in artery wall mass, although operational definitions differ with different studies. The general concept is that after the arterial dilatation caused by the angioplasty or plaque resection, there can be a slow constriction of the artery occurring over days, weeks, or months that results in a restenotic lumen. This condition can occur without having to invoke significant contributions from the processes of intimal cell proliferation, extracellular matrix synthesis, and thrombus organization. Human evidence for this restenosis phenomenon has largely come from intravascular coronary ultrasound studies comparing the immediate results of angioplasty and the subsequent restenotic artery weeks to months later. Some studies have indicated that the majority of the luminal narrowing at the site of human coronary restenosis was a result of such artery wall remodeling. Again, this could explain why anti­proliferative therapies have generally failed for this disease. As for carotid arteries after endarterectomy, the contribution of such arterial remodeling is unclear. Certainly, the adventitia undergoes some fibrosis, and this could impart a constrictive tendency on the operated artery. It

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has also been noted that women tend to have smaller carotid artery diameters than men, and some have suggested that this plays a role in the increased carotid restenotic rates seen in women, where a little constriction and a little neointima presumably is more likely to cause significant lumen narrowing in a smaller artery. Finally, because arterial stents have been shown to decrease the human coronary restenosis rate, their use in human carotid artery disease has increased. The sequence of events in the less common restenosis that occurs in the presence of such stents needs to be further elucidated (although some ultrasound follow-up studies have been performed, the detailed correlation between the ultrasound features seen and actual histopathology needs further study). Stents do appear to largely eliminate the problem of artery wall contraction after angioplasty. Thus restenosis in such situations is likely to be mostly caused by intimal mass growth through the stent wires, although the relative contributions of cell proliferation, extracellular matrix, synthesis, and thrombus organization have yet to be carefully defined in human studies of the carotid artery. Similar to the coronary and other arterial setting, carotid stent restenosis is likely to evolve with similar smooth muscle proliferation and extracellular matrix synthesis, and/or mural thrombus organization.

Predictors of Carotid Restenosis after Endarterectomy Although a full discussion of the clinical correlates with restenosis is beyond the scope of this pathology discussion, certain clinical features appear to be correlated with restenosis. These include female gender and primary closure of the artery after an endarterectomy versus the use of a vascular patch to enlarge the arterial segment. Of interest, histopathologic studies have suggested that endarterectomies in which the primary atherosclerotic plaque has a large lipid core or that has significant macrophage infiltration are somewhat less likely to be followed by restenotic lesions. Further pathologic studies might elucidate the proposed mechanisms underlying this correlation.

Selected References Bond R, Rerkasem K, Naylor AR, et al: Systematic review of randomized controlled trials of patch angioplasty versus primary closure and different types of patch materials during carotid endarterectomy, J Vasc Surg 40:1126–1135, 2004. Callow AD: Recurrent stenosis after carotid endarterectomy, Arch Surg 117:1082–1085, 1982. Clowes AW, Reidy MA, Clowes MM: Kinetics of cellular proliferation after arterial injury. I. Smooth muscle growth in the absence of endothelium, Lab Invest 49:327–333, 1983. Clowes AW, Reidy MA, Clowes MM: Mechanisms of stenosis after arterial injury, Lab Invest 49:208–215, 1983. Gordon D, Rekhter MD: The growth of human atherosclerosis: cell proliferation and collagen synthesis, Cardiovasc Pathol 6:103–116, 1997. Hellings WE, Moll FL, de Vries JPM, et al: Atherosclerotic plaque composition and occurrence of restenosis after carotid endarterectomy, JAMA 299:547–554, 2008. Hunter GC: The clinical and pathologic spectrum of recurrent carotid stenosis, Am J Surg 174:583–588, 1997. Lattimer CR, Burnand KG: Recurrent carotid stenosis after carotid endarterectomy, Br J Surg 84:1206–1219, 1997. Rekhter MD, O’Brien E, Shah N, et al: The importance of thrombus organization and stellate cell phenotype in collagen I gene expression in human coronary atherosclerotic and restenotic lesions, Cardiovasc Res 32:496–502, 1996. Willfort-Ehringer A, Ahmadi R, Gschwandtner MEHaumer A, Heinz G, Lang W, Ehringer H: Healing of carotid stents: a prospective duplex ultrasound study, J Endovasc Ther 10:636–642, 2003.

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Treatment of Recurrent Stenosis After Previous Carotid Endarterectomy Boudewijn L. Reichmann, Gert Jan de Borst, and Frans L. Moll

Carotid endarterectomy (CEA) is the gold standard in the treatment of carotid occlusive disease and prevention of stroke. However, the benefit of carotid revascularization is hampered by restenosis, which is associated with a modestly increased risk for stroke. Symptomatic recurrent stenosis has been reported to range between 0.6% and 3.6%, and asymptomatic restenosis, based on noninvasive studies, ranges from 8.8% to 19%. A systematic review in 1998 concluded that the risk of developing restenosis after CEA was 10% in the first year, 3% in the second year, and only 1% per year thereafter. The potential of a carotid restenosis to cause a stroke seems to be highly variable, but in general it is smaller than that of the primary lesion. The optimal treatment strategy for recurrent stenosis, especially when asymptomatic, remains a challenge. Symptomatic patients with a recurrent stenosis greater than 70% or asymptomatic patients with a recurrent stenosis greater than 80% may be considered for reintervention. The site of recurrent stenosis is primarily situated at the ends of or within the confines of the original endarterectomy site and the suture lines. The recurrence lesion therefore is located in the internal carotid artery (ICA), the distal common carotid artery (CCA), or both. The majority (70%) of lesions are localized within the origin of the ICA. Some regions of the artery wall are exposed simultaneously to low wall shear stress and high mechanical stress, and these regions correspond to the areas where atherosclerotic lesions develop. It makes the carotid bulb a focus for disease because of its geometry coupled with pulsatile flow that produces low shear rates, which in turn promotes atherosclerosis.

OPTIMAL IMAGING FOR ASSESSMENT OF CAROTID RESTENOSIS In the distant past, conventional angiography was required to determine the degree of a carotid stenosis. However, an accurate alternative with no need to use intra arterial contrast agents was found in duplex ultrasonography. The severity of a stenosis has been defined using specific threshold velocities, including the peak systolic velocity (PSV), the end diastolic velocity (EDV), and/or the ICA/CCA PSV ratio. Most vascular laboratories use the (modified) Strandness criteria to grade restenosis after CEA. However, these criteria, established for evaluating primary carotid stenosis, might not be applicable in grading recurrent stenosis because of hemodynamic changes in the treated vessel. Closing the arteriotomy with a patch widens the carotid diameter and decreases the stiffness of the arterial wall. This phenomenon is known as the dilatation or pantaloon effect following CEA. Hirschl and colleagues conducted a study to determine if patch angioplasty or direct closure of the ICA after CEA resulted in any hemodynamic or pathologic differences. Patients undergoing carotid patching with broadened bulb lumen exhibited statistically elevated turbulent flow disturbances with increased flow velocity in the ICA just distal to

the patch. However, quantitative flow volume measurement did not reveal any differences between the two groups. Several papers have proposed new and revised ultrasound criteria, but there is still no consensus on the optimal criteria for grading recurrent carotid artery stenosis. It is therefore helpful to combine ultrasonography with an additional diagnostic modality, such as magnetic resonance imaging (MRI) or computed tomography (CT), to accurately evaluate the degree of stenosis.

TREATMENT OPTIONS FOR RECURRENT CAROTID ARTERY STENOSIS Whether recurrent carotid stenosis must be treated or not remains arbitrary. However, most authors agree that symptomatic restenoses warrant repeated intervention because of the risk of subsequent cerebrovascular events. Unfortunately, there are no reliable prognostic tests to differentiate between which highly stenotic lesions will cause a stroke and which will not. Most institutions therefore follow the consensus that reintervention should be considered in symptomatic patients with a recurrent stenosis of more than 70%, asymptomatic patients with a recurrent stenosis of more than 80%, patients with severe four-vessel disease, or patients with a contralateral occlusion. A second open procedure or endovascular intervention requires that the proposed treatment has a low periprocedural risk and provides long-term freedom from further cerebrovascular events.

Repeat CEA for Recurrent Carotid Stenosis Repeat CEA for recurrent carotid stenosis in experienced hands can be performed with approximately the same complication rates as primary CEA. However, published complication rates for redo surgery vary. In guidelines by the American Heart Association, a stroke and death rate of less than 6% for symptomatic and less than 3% for asymptomatic patients have been considered acceptable for primary CEA versus a remarkable 10% threshold for repeat CEA. A major concern during redo surgery is the feared possibility of injuring adjacent structures such as cranial nerves and the internal jugular vein. The mandibular branch of the facial, vagus, glossopharyngeal, and hypoglossal nerves are all at risk. The structures tend to become adherent to the previous dissection plane and therefore can be harder to dissect during redo surgery. Reported rates of cranial nerve injury during repeat CEA are 0% to 7%; however, most of these injuries are transient. Such complications are within ranges suggested for primary carotid surgery. If the site of the restenosis is predominantly situated in the distal part of the ICA, obtaining cephalad control may be very difficult. Mandibular subluxation or resection of the styloid process might be necessary in order to accurately place the clamp distal of the stenotic lesion. If the use of a Javid shunt is inevitable because of changes or asymmetry on cerebral monitoring, obtaining control of the distal ICA is of key importance. It is important to continue the dissection until 1 to 2 cm of uninvolved artery are circumferentially mobilized both proximally and distally. In most cases, the restenotic plaque can be removed en toto through the cleavage plane that was used during primary surgery. The neointima and atherosclerotic plaque are usually not very adherent to the arterial wall. Most authors agree that the arteriotomy during redo surgery should not be closed primarily, but a patch closure should be performed. De Borst and coworkers published a series of 73 consecutive procedures in 72 patients in which redo CEA was performed. The cumulative freedom from all stroke was 98% and from ipsilateral stroke 100% during a follow-up of 5 years. The cumulative freedom

111

Treatment of Recurrent Stenosis After Previous Carotid Endarterectomy

TABLE 1:  Studies on Redo Carotid Endarterectomy as Treatment for Recurrent Stenosis

Reference

AbuRahma (2010)

Patients

CEA

Periop Sympt (%) Stroke (%)

Cranial Stroke-free Periop Nerve Injury Hematoma Follow-up Restenosis Survival ±5 MI (%) (%) (%) (mo) >50% (50) yr (%)

192

72

72

3

0

14

1

NS

9

97

Attigah (2010)

79

41

42

5

3

0

7

70

17

100

De Borst (2007)

72

73

39

0

1.4

1.4

4.1

52

14

98

Jain (2007)

80

84

40

0

1.2

7.2

3.6

51

NS

98

Bettendorf (2007)

67

46

44

2.2

0

4.3

2.2

38

14

NS

145

153

36

1.9

0

1.3

3.2

53

9

96

Cho (2004)

64

66

50

3.1

5.0

6.0

3.0

52

9

92

Archie (2001)

66

69

52

2.9

0

4.3

NS

50

13

90

199

206

43

3.4

1.0

1.0

NS

52

6

82

Stoner (2005)

O’Hara

CEA, Carotid endarterectomy; NS, not significant; periop, perioperative. AbuRahma AF, Abu-Halimah S, Hass SM, et al: Carotid artery stenting outcomes are equivalent to carotid endarterectomy outcomes for patients with post– carotid endarterectomy stenosis, J Vasc Surg 52:1180–1187, 2010. de Borst GJ, Ackerstaff RG, de Vries JP, et al: Carotid angioplasty and stenting for postendarterectomy stenosis: long-term follow-up, J Vasc Surg 45:118–123, 2007.

of re-restenosis (≥50%) was 85%, with five patients needing a tertiary carotid reconstruction. Other authors have also published large series (Table 1) with excellent long-term results (stroke-free survival 83%–100% and restenosis-free survival 84%–95% during long-term follow-up) and concluded that repeat CEA as a treatment for recurrent stenosis is a feasible, durable, and safe option.

Other Surgical Options for Recurrent Carotid Stenosis Treiman and colleagues described a series of 57 redo CEAs with concomitant carotid bifurcation resection in toto, including the stenotic lesion with placement of a venous interposition graft to restore blood flow. The perioperative stroke rate was 3.5%, and during a mean follow-up of 35 months the graft patency was 93%. In another series, 31 interposition grafts, 18 subclavian–carotid grafts, and 11 carotid– carotid grafts were reported that had acceptable perioperative stroke rates. These techniques are generally reserved for secondary or even tertiary restenosis or cases of near occlusion in patients who have severe four-vessel cerebrovascular disease. These techniques can also be undertaken when the carotid artery is not amenable for a redo CEA.

Endovascular Procedures Although reoperative CEA is an accepted treatment for recurrent carotid stenosis, some have proposed an endovascular intervention in the management of this condition. As in treatment of lesions in other vascular beds, it is currently recommended that carotid endovascular procedures use standardized stenting. Completion angiography of the extra- and intracranial vessels should always be performed to evaluate the result of the procedure and quantify any residual stenosis.

Several studies on carotid angioplasty and stenting (CAS) of recurrent carotid stenosis showed excellent 30-day results, with stroke rates comparable to those following the surgical treatment of primary lesions. However, De Borst and coworkers and AbuRahma and colleagues showed that the cumulative rate of restenosis-free survival after 4 years was 76% and 72%, respectively. These results show that CAS for carotid restenosis could be a feasible, safe, and durable option. In-stent restenosis following CAS is, however, an ongoing phenomenon that requires long-term follow-up.

Carotid Endarterectomy versus Carotid Artery Stenting As stated earlier, there are numerous options in the treatment of recurrent carotid stenosis (Table 2). One of these questions is whether the interval between primary CEA and the redo procedure affects outcome. Some authors recommend that lesions that require treatment within 2 years after the primary procedure be treated with CAS. However, as a result of plaque characteristics, these patients might be susceptible to higher complication rates. An open approach might be preferable to an endovascular approach in patients with an interval longer than 2 years between the primary treatment and the occurrence of symptomatic restenosis. Both CEA and CAS seem to be feasible and durable options for treating restenosis; however, the incidence of secondary recurrence or even tertiary recurrence is illdefined as a result of the scarcity of data. Arguments in favor of endovascular or operative management should be based on the clinician’s experience. In general, the decision to operate on an asymptomatic patient with a recurrent carotid stenosis should be individualized and based on several factors, including the degree and rate of progression of the stenosis, the condition of the remainder of the cerebral circulation, and the age, sex, and overall medical condition of the patient. A randomized clinical trial is necessary to determine the role of CAS compared with operative management of post-CEA restenosis.

112

NUMBER OF PATIENTS

PERIOP STROKE (%)

PERIOP MI (%)

Reference

Total

CEA

CAS

CEA

CAS

CEA

AbuRahma (2010)

192

72

120

2.8

0.8

0

Attigah (2010)

79

41

45

9.7

2.2

Bettendorf

75

46

45

2.2

Bowser (2003)

77

27

50

AbuRahma (2001)

81

58

25

CAS

CRANIAL NERVE INJURY (%)

HEMATOMA (%)

CEA

CAS

CEA

0

13.9

0

1.4

2.4

0

0

0

3.0

0

3.0

4.6

3.7

3.8

0

0

3.4

16

NS

NS

CAS

FOLLOW-UP (MO) CEA

CAS

0

33

24

7.3

2.2

70

0

2.3

0

3.7

0

3.7

17.2

0

1.7

RESTENOSIS >50% (50) CEA

STROKE-FREE SURVIVAL ±5 yr) (%)

CAS

CEA

CAS

5

28

97

98

25

NS

NS

89

95

39

12

6

14

NS

NS

3.8

39

26

26

34

89

89

4.0

NS

NS

0

56

82

79

Note: Bold indicates p < .05. CAS, Carotid artery stenting; CEA, carotid endarterectomy; NS, not significant; periop, perioperative. AbuRahma AF, Abu-Halimah S, Hass SM, et al: Carotid artery stenting outcomes are equivalent to carotid endarterectomy outcomes for patients with post–carotid endarterectomy stenosis, J Vasc Surg 52: 1180–1187, 2010.

CEREBROVASCULAR DISEASE

TABLE 2:  Studies of Carotid Endarterectomy versus Carotid Artery Stenting as Treatment for Recurrent Stenosis.

Management of Concomitant Carotid and Coronary Arterial Disease

Selected References Abou-Zamzam AM Jr, Moneta GL, Edwards JM, et al: Extrathoracic arterial grafts performed for carotid artery occlusive disease not amenable to endarterectomy, Arch Surg 134:952–956, 1999. discussion 956–957. AbuRahma AF, Abu-Halimah S, Hass SM, et al: Carotid artery stenting outcomes are equivalent to carotid endarterectomy outcomes for patients with post–carotid endarterectomy stenosis, J Vasc Surg 52:1180–1187, 2010. AbuRahma AF, Robinson PA, Saiedy S, et al: Prospective randomized trial of carotid endarterectomy with primary closure and patch angioplasty with saphenous vein, jugular vein, and polytetrafluoroethylene: long-term follow-up, J Vasc Surg 27:222–232, 1998. discussion 233–224. de Borst GJ, Ackerstaff RG, de Vries JP, et al: Carotid angioplasty and stenting for postendarterectomy stenosis: long-term follow-up, J Vasc Surg 45:118–123, 2007. de Borst GJ, Zanen P, de Vries JP, et al: Durability of surgery for restenosis after carotid endarterectomy, J Vasc Surg 47:363–371, 2008.

Management of Concomitant Carotid and Coronary Arterial Disease Virendra I. Patel, Cary W. Akins, and Richard P. Cambria

The management of patients with coexistent carotid and coronary artery disease (CAD) depends upon the circumstances of clinical presentation. Most surgeons would agree that symptomatic carotid stenosis requires prompt, if not urgent, surgical therapy based on presentation. In such patients, concurrent CAD should be managed with maximal medical therapy in the perioperative setting. A more controversial issue is the management of patients who require coronary artery bypass grafting (CABG) and who have asymptomatic carotid artery occlusive disease. The management of such patients varies widely, and there is no consensus among practitioners regarding optimal management. Of the potential causes of perioperative stroke after cardiac surgery, carotid stenosis is the one situation that may be eliminated before the cardiac procedure. Because carotid stenosis is a significant risk factor for perioperative stroke, the need to define carotid disease before coronary artery grafting becomes obvious. The logical extension that surgical correction of carotid stenosis can decrease the risk of stroke has been the basis of our approach for many years. The reported safety of the combined operative approach as well as level I evidence supporting this approach is key to its continued application.

CARDIAC RISK STRATIFICATION PRIOR TO CAROTID ENDARTERECTOMY An assessment of CAD before vascular reconstruction has several purposes. These include preventing perioperative cardiac ischemic complication and assessing long-term prognosis because natural history implicates CAD as the principal cause of late mortality in patients following carotid endarterectomy (CEA). Several studies have highlighted the prevalence of CAD and its short- and long-term

113

Frericks H, Kievit J, van Baalen JM, et al: Carotid recurrent stenosis and risk of ipsilateral stroke: a systematic review of the literature, Stroke 29:244–250, 1998. Hirschl M, Bernt RA, Hirschl MM: Carotid endarterectomy (CE) of the internal carotid artery (ICA) with and without patch angioplasty: comparison of hemodynamical and morphological parameters, Int Angiol 8:10–15, 1989. International Carotid Stenting Study Investigators: Carotid artery stenting compared with endarterectomy in patients with symptomatic carotid stenosis (International Carotid Stenting Study): an interim analysis of a randomized controlled trial, Lancet 20:985–997, 2010. New G, Roubin GS, Iyer SS, et al: Safety, efficacy, and durability of carotid artery stenting for restenosis following carotid endarterectomy: a multicenter study, J Endovasc Ther 7:345–352, 2000. Treiman GS, Jenkins JM, Edwards WH, et al: The evolving surgical management of recurrent carotid stenosis, J Vasc Surg 16:354–362, 1992; discussion 362–353.

implications for patients treated with CEA. Hertzer and colleagues performed routine preoperative coronary angiography in 506 carotid endarterectomy patients and found that the severity of coronary artery disease was normal in 7%, mild to moderate in 28%, advanced and compensated in 30%, severe and correctable in 28%, and inoperable in 7%. Mackey and colleagues found that 53% of patients undergoing CEA had evidence of CAD by clinical history or electrocardiographic studies. CEA patients with clinical CAD had an operative mortality of 1.5% and a rate of myocardial infarction (MI) of 4.3% compared with 0% mortality and 0.5% MI rates in patients without CAD. They reported the 5- and 10-year survival rates of patients with CAD to be 68.6% and 44.9%, respectively, versus 86.4% and 72.3% for patients without CAD. Urbinati and colleagues found that 25% of 106 patients undergoing CEA had significant defects on thallium exercise testing. They noted 7-year freedom from cardiac events after CEA was 51% for patients with silent myocardial ischemia versus 98% for patients with normal stress tests. In our own’ cohort of more than 2000 CEA patients (1990–1999), the rate of perioperative MI was 1.2%, and 10-year actuarial survival was 45%. Among variables associated with increased late mortality, concomitant CAD (odds ratio [OR] 1.4; p = .0002) figured prominently. Improved perioperative care and adjunctive medical therapy have substantially lowered the risk of coronary ischemic events complicating CEA. Recent American College of Cardiology and American Heart Association (ACC/AHA) guidelines on perioperative cardiovascular evaluation for noncardiac surgery designated CEA as a low- to intermediate-risk procedure. The guidelines suggest that in the absence of active coronary ischemia, clinical profiling based on cardiovascular risk factors and functional capacity is the mainstay of cardiac risk stratification for such procedures. Patients undergoing noncardiac surgery in the absence of active coronary ischemia are best treated with continuance of β-blockers, statins, and aspirin and might benefit from perioperative use of these medications if they are not already taking them. Indeed, Perler and coworkers have reported the favorable role of statin therapy with respect to postoperative stroke (three fold reduction) and cardiovascular mortality (five fold reduction) following CEA.

CAUSES OF STROKE FOLLOWING CORONARY REVASCULARIZATION Next to operative mortality, permanent stroke is the most dreaded complication following coronary revascularization because of the devastating consequences to the patient as well as the increased

Management of Concomitant Carotid and Coronary Arterial Disease

Selected References Abou-Zamzam AM Jr, Moneta GL, Edwards JM, et al: Extrathoracic arterial grafts performed for carotid artery occlusive disease not amenable to endarterectomy, Arch Surg 134:952–956, 1999. discussion 956–957. AbuRahma AF, Abu-Halimah S, Hass SM, et al: Carotid artery stenting outcomes are equivalent to carotid endarterectomy outcomes for patients with post–carotid endarterectomy stenosis, J Vasc Surg 52:1180–1187, 2010. AbuRahma AF, Robinson PA, Saiedy S, et al: Prospective randomized trial of carotid endarterectomy with primary closure and patch angioplasty with saphenous vein, jugular vein, and polytetrafluoroethylene: long-term follow-up, J Vasc Surg 27:222–232, 1998. discussion 233–224. de Borst GJ, Ackerstaff RG, de Vries JP, et al: Carotid angioplasty and stenting for postendarterectomy stenosis: long-term follow-up, J Vasc Surg 45:118–123, 2007. de Borst GJ, Zanen P, de Vries JP, et al: Durability of surgery for restenosis after carotid endarterectomy, J Vasc Surg 47:363–371, 2008.

Management of Concomitant Carotid and Coronary Arterial Disease Virendra I. Patel, Cary W. Akins, and Richard P. Cambria

The management of patients with coexistent carotid and coronary artery disease (CAD) depends upon the circumstances of clinical presentation. Most surgeons would agree that symptomatic carotid stenosis requires prompt, if not urgent, surgical therapy based on presentation. In such patients, concurrent CAD should be managed with maximal medical therapy in the perioperative setting. A more controversial issue is the management of patients who require coronary artery bypass grafting (CABG) and who have asymptomatic carotid artery occlusive disease. The management of such patients varies widely, and there is no consensus among practitioners regarding optimal management. Of the potential causes of perioperative stroke after cardiac surgery, carotid stenosis is the one situation that may be eliminated before the cardiac procedure. Because carotid stenosis is a significant risk factor for perioperative stroke, the need to define carotid disease before coronary artery grafting becomes obvious. The logical extension that surgical correction of carotid stenosis can decrease the risk of stroke has been the basis of our approach for many years. The reported safety of the combined operative approach as well as level I evidence supporting this approach is key to its continued application.

CARDIAC RISK STRATIFICATION PRIOR TO CAROTID ENDARTERECTOMY An assessment of CAD before vascular reconstruction has several purposes. These include preventing perioperative cardiac ischemic complication and assessing long-term prognosis because natural history implicates CAD as the principal cause of late mortality in patients following carotid endarterectomy (CEA). Several studies have highlighted the prevalence of CAD and its short- and long-term

113

Frericks H, Kievit J, van Baalen JM, et al: Carotid recurrent stenosis and risk of ipsilateral stroke: a systematic review of the literature, Stroke 29:244–250, 1998. Hirschl M, Bernt RA, Hirschl MM: Carotid endarterectomy (CE) of the internal carotid artery (ICA) with and without patch angioplasty: comparison of hemodynamical and morphological parameters, Int Angiol 8:10–15, 1989. International Carotid Stenting Study Investigators: Carotid artery stenting compared with endarterectomy in patients with symptomatic carotid stenosis (International Carotid Stenting Study): an interim analysis of a randomized controlled trial, Lancet 20:985–997, 2010. New G, Roubin GS, Iyer SS, et al: Safety, efficacy, and durability of carotid artery stenting for restenosis following carotid endarterectomy: a multicenter study, J Endovasc Ther 7:345–352, 2000. Treiman GS, Jenkins JM, Edwards WH, et al: The evolving surgical management of recurrent carotid stenosis, J Vasc Surg 16:354–362, 1992; discussion 362–353.

implications for patients treated with CEA. Hertzer and colleagues performed routine preoperative coronary angiography in 506 carotid endarterectomy patients and found that the severity of coronary artery disease was normal in 7%, mild to moderate in 28%, advanced and compensated in 30%, severe and correctable in 28%, and inoperable in 7%. Mackey and colleagues found that 53% of patients undergoing CEA had evidence of CAD by clinical history or electrocardiographic studies. CEA patients with clinical CAD had an operative mortality of 1.5% and a rate of myocardial infarction (MI) of 4.3% compared with 0% mortality and 0.5% MI rates in patients without CAD. They reported the 5- and 10-year survival rates of patients with CAD to be 68.6% and 44.9%, respectively, versus 86.4% and 72.3% for patients without CAD. Urbinati and colleagues found that 25% of 106 patients undergoing CEA had significant defects on thallium exercise testing. They noted 7-year freedom from cardiac events after CEA was 51% for patients with silent myocardial ischemia versus 98% for patients with normal stress tests. In our own’ cohort of more than 2000 CEA patients (1990–1999), the rate of perioperative MI was 1.2%, and 10-year actuarial survival was 45%. Among variables associated with increased late mortality, concomitant CAD (odds ratio [OR] 1.4; p = .0002) figured prominently. Improved perioperative care and adjunctive medical therapy have substantially lowered the risk of coronary ischemic events complicating CEA. Recent American College of Cardiology and American Heart Association (ACC/AHA) guidelines on perioperative cardiovascular evaluation for noncardiac surgery designated CEA as a low- to intermediate-risk procedure. The guidelines suggest that in the absence of active coronary ischemia, clinical profiling based on cardiovascular risk factors and functional capacity is the mainstay of cardiac risk stratification for such procedures. Patients undergoing noncardiac surgery in the absence of active coronary ischemia are best treated with continuance of β-blockers, statins, and aspirin and might benefit from perioperative use of these medications if they are not already taking them. Indeed, Perler and coworkers have reported the favorable role of statin therapy with respect to postoperative stroke (three fold reduction) and cardiovascular mortality (five fold reduction) following CEA.

CAUSES OF STROKE FOLLOWING CORONARY REVASCULARIZATION Next to operative mortality, permanent stroke is the most dreaded complication following coronary revascularization because of the devastating consequences to the patient as well as the increased

114

CEREBROVASCULAR DISEASE

cost of hospitalization and post-hospital care. Major reported risk factors associated with stroke following coronary revascularization include age, ascending aortic atherosclerosis, long cardiopulmonary bypass time, perioperative hypotension, and preexisting cerebrovascular disease. Intracranial hemorrhage can lead to neurologic injury following cardiopulmonary bypass, but this a rare event, despite the degree of anticoagulation necessary for cardiopulmonary bypass. Neurologic injury can also result from inadequate perfusion pressure on cardiopulmonary bypass, and adequate perfusion is especially important in the presence of carotid stenosis or occlusion. Some investigators have shown a linear relationship between the degree of carotid stenosis and the risk of perioperative stroke; in such analyses, patients with total internal carotid artery (ICA) occlusion are typically the subgroup at highest risk for stroke. Yet carotid revascularization is not possible in the circumstance of total ICA occlusion. When there is occlusion of carotid or intracerebral arteries, brain blood flow depends on collateral circulation, which, in turn, depends on perfusion pressure. Atheroemboli or thromboemboli remain the most common causes of stroke following CABG. Intracardiac emboli emanate from mural thrombus associated with MI, valvular disease, arrhythmias, surgical suture lines, or, in rare instances, trapped air. Cannulation of the ascending aorta for bypass, aortic cross-clamp application, and intra aortic cardioplegia delivery devices can dislodge existing atherosclerotic material from the aorta. Thus, numerous investigators have identified aortic atherosclerosis as a risk factor for perioperative stroke. Use of preoperative computed tomography angiography (CTA) or intraoperative echocardiography to identify and avoid aortic atherosclerosis during clamping and cannulation has resulted in a reduced stroke risk.

RELATIONSHIP OF CAROTID STENOSIS TO PERIOPERATIVE STROKE Virtually all studies have emphasized that the patient’s age is the single highest risk variable for the presence of carotid artery disease in patients undergoing CABG. In 1986, Gardner and colleagues found the risk of stroke to be a direct function of the patient’s age. Patients younger than 45 years had a stroke rate of 0.2%, which rose to 3.0% for patients in their 60s and to 8.0% for patients older than 75 years. At our institution, the mean age of CABG patients rose from 56 years in 1980 to older than 67 years in 2007. In 1980 only 6% of patients were 70 years or older, whereas by 2007 more than 41% were 70 years or older, and 10% were 80 years or older. Berens and colleagues, using routine carotid artery scanning in 1087 cardiac surgery candidates 65 years or older (91% with coronary disease), found that 186 (17.0%) had a greater than 50% carotid stenosis and 65 (5.9%) had a greater than 80% carotid stenosis. Predictors of carotid artery disease were female gender, peripheral vascular disease, history of transient ischemic attacks (TIAs) or stroke, smoking history, and left main CAD. D’Agostino and coworkers, using noninvasive testing in 1279 CABG candidates, found that 262 (20.5%) had greater than 50% stenosis in at least one carotid artery and 23 (1.8%) had bilateral stenoses greater than 80%. Significant multivariable predictors of carotid disease were age, diabetes, female sex, left main CAD, prior stroke, peripheral vascular disease, and smoking. The presence of carotid stenosis in patients referred for CABG has been shown to significantly increase the risk of postoperative stroke. Brener and colleagues studied 4047 cardiac surgical patients and found a 9.2% rate of stroke or transient ischemic attack in patients with asymptomatic carotid stenosis, significantly greater than the 1.3% rate in patients with no carotid stenosis. Faggioli and colleagues in 1990 reported that routine carotid noninvasive testing in CABG patients with no ischemic neurologic symptoms yielded

an odds ratio for stroke of 9.9 with greater than 75% carotid stenosis. In patients older than 60 years with greater than 75% carotid stenosis, the stroke rate was 15%, versus 0.6% for patients of the same age with no carotid disease. Using routine carotid duplex scanning for cardiac surgical patients 65 years of age or older, Berens and colleagues found that the risk of stroke was 2.5% for carotid stenoses greater than 50%, 7.6% for carotid stenoses greater than 50%, 10.9% for carotid stenoses greater than 80%, and 10.9% for unilateral carotid artery occlusion. Thus, adequate evidence exists that significant carotid artery stenosis is an important incremental risk factor for the development of perioperative neurologic injury following CABG.

TIMING OF CAROTID AND CORONARY OPERATIONS If one accepts that uncorrected carotid stenosis increases the risk of stroke for patients with severe carotid and CAD who have only isolated CABG, carotid endarterectomy is the indicated treatment for severe symptomatic and asymptomatic carotid stenosis, CAD increases the early and late risk of death for carotid endarterectomy patients, and CABG is an indicated treatment for CAD, then the important question becomes not the indication for but the timing of the two operative procedures. One approach is to perform the carotid endarterectomy and CABG operations as staged procedures. By convention, doing the carotid endarterectomy before CABG is referred to as a staged procedure, whereas doing the CABG before the carotid artery operation is called a reverse staged procedure. Most advocates of a sequential operative approach to patients with severe combined disease usually do the carotid endarterectomy first if the patient is hemodynamically stable and without active coronary ischemia. Improvements in patient management, especially use of regional anesthesia, often allow safe initial isolated CEA. Depending on the timing of the two procedures, practical considerations, such as imminent need for the large doses of heparin required for cardiopulmonary bypass, airway and/or neck swelling, and the risk of perioperative coronary ischemic events, remain real issues. For unstable cardiac patients, particularly those with asymptomatic carotid stenosis, some cardiac surgeons opt to perform initial myocardial revascularization followed by an interval carotid endarterectomy. The principal risk with this approach is the potential for neurologic complications either during or shortly after the myocardial revascularization. Clearly the principal clinical variable to be considered is the stability, or lack thereof, of the CAD. Currently, we advocate concomitant carotid and coronary artery operations for virtually all patients with severe combined disease. However, in patients with severe bilateral carotid stenosis, a staged approach may be appropriate, especially if the patient is stable. We occasionally treat the more severe of the two carotid artery lesions with initial isolated endarterectomy, followed by combined CABG and CEA of the other carotid artery within a few days.

CONCOMITANT CAROTID AND CORONARY ARTERY OPERATIONS The strategy of performing both operative procedures during one anesthetic is based on the premise that such an approach to severe combined disease minimizes cardiac events that often complicate isolated CEA and neurologic events that complicate isolated CABG. Some groups have reported on the perceived advantages of cardiopulmonary bypass, namely, heparinization, hypothermia, and hemodynamic control, to perform carotid endarterectomy. Theoretically,

Management of Concomitant Carotid and Coronary Arterial Disease

hypothermia on cardiopulmonary bypass provides an extra margin of ischemic protection for the brain during the carotid endarterectomy and avoids the need for intravascular shunting. Performing the carotid and coronary artery operations on cardiopulmonary bypass prolongs aortic occlusion and cardiopulmonary bypass times, which most cardiac surgeons prefer to avoid. The usual technique for concomitant CEA and CABG has been to perform the CEA during harvesting of CAD conduits before cardiopulmonary bypass. At our institution, the carotid operation is performed by vascular surgeons as the cardiac surgical team harvests whatever saphenous vein or other conduits may be needed. We use routine electroencephalographic monitoring, selective shunting, and either eversion endarterectomy (presuming no need for a shunt), or patch closure. After the CEA is completed, the neck incision is loosely approximated over a sponge. Final closure, usually over a plastic drain, is performed after cardiopulmonary bypass is completed and heparinization is reversed. Since the late 1970s, we have taken an aggressive approach to patients with combined carotid disease and CAD, using concomitant operation as the standard approach. Our first report in 1989 noted a 2% risk of stroke or death. In 1995 we published the results of our first 200 consecutive combined operations (1979–1993) with a hospital mortality of 3.5%, MI of 2.5%, and perioperative stroke of 4.0%. More recently, we published results of concomitant operation between 1979 and 2001 (N = 500). Mean patient age was 69 years (6 years older than CABG-only patients). Three quarters of the patients had unstable angina pectoris, and 53% had prior MI. The distribution of single-, double-, and triple-vessel coronary disease was at 4%, 21%, and 75%, respectively, with 42% of patients having significant left main disease. Of the 500 patients, 329 (66%) were neurologically asymptomatic, 21% had TIAs, and 13% had a prior stroke. Unilateral severe carotid stenosis (>70%) was found in 336 patients (67%); 32% had disease in the contralateral carotid artery. Urgent or emergency operations were required in 54% of patients. Hospital mortality was 3.6%, MI was 2.0%, and stroke occurred in 4.6%. Twenty-three patients had strokes, of which 12 were ipsilateral to the CEA and 11 were contralateral or bilateral, suggesting that concomitant carotid endarterectomy and CABG have neutralized the impact of carotid stenosis as a risk factor for stroke following CABG in our experience. Multivariate predictors of hospital death were preoperative TIAs, preoperative MI, and urgent operation. Peripheral vascular disease independently predicted postoperative stroke. Late follow-up of combined operations revealed the following 10-year freedom from late events: death, 43%; MI, 87%; coronary angioplasty, 92%; redo CABG, 96%; any stroke, 85%; and ipsilateral stroke, 90%. These favorable results contrast to reports using administrative data. Brown’s group reported a 17.7% stroke risk for combined operations in Medicare patients in Midwestern states. In a Canadian study the combined risk of stroke and death for CABG alone was 4.9% versus 13% for combined carotid and coronary artery operations. However, data from the New York State Registry indicate that such results can be explained largely by the disparate cardiac risk profiles of the two patient groups. Accordingly, Ricotta and colleagues, using propensity scoring to match case and control patients based on risk factors, found no difference in combined stroke and death risk for the two operations in the matched cohorts.

STAGED VERSUS COMBINED CAROTID AND CORONARY ARTERY OPERATIONS Two prospective randomized studies have highlighted the utility of the combined operation over the reversed staged operation. Hertzer and colleagues randomized subgroups of patients with unstable coronary syndromes and incidental asymptomatic carotid stenosis. Over

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5 years they treated 275 patients with severe combined disease. Their criteria for carotid endarterectomy was symptomatic and/or severe (>70%) carotid artery disease. Only 24 (9%) of the patients had CAD that was stable enough to allow carotid endarterectomy before CABG. Of those 24 patients, 1 (4.2%) suffered a perioperative stroke after the carotid endarterectomy and died of an MI awaiting CABG. Symptomatic or severe bilateral carotid artery disease in 122 patients was treated with combined carotid and coronary artery operation, with an operative mortality rate of 6.1% and a perioperative stroke rate of 7.1%. The remaining 129 patients with unstable coronary symptoms and severe unilateral asymptomatic carotid stenoses were randomized to either a combined or a reversed staged operation. Patients having concomitant carotid and coronary operations had a mortality rate of 4.2% versus a combined rate of 5.3% for the two operations in the staged patients. Stroke rate in the concomitant operations was 2.8%, significantly lower than the 14% risk of the reversed staged operations (6.9% during the isolated CABG and 7.5% during the delayed isolated carotid endarterectomy). Illuminati and colleagues prospectively randomized patients who were candidates for CABG (three-vessel or left main coronary artery disease) and who were found to have asymptomatic severe (>70%) carotid stenosis. Patients were randomized to a staged (CEA before CABG) or combined procedure (Group A; n = 94) or to a reverse staged procedure (Group B; n = 91). The majority of Group A (n = 79, 84%) patients were treated with a combined procedure. Patients were excluded if they required urgent or emergent surgery, if they required associated cardiac procedures, or if significant aortic atheroma was present on preoperative CTA, thus isolating stroke risk to ipsilateral carotid stenosis. Operative mortality was similar (n = 1) between the two groups (1% Group A vs. 1.1% Group B; p = not significant), whereas ipsilateral stroke was significantly increased in reversed staged patients (seven ipsilateral strokes vs. none). The combined stroke and death rate therefore favored a combined approach (1% Group A vs. 8.8% Group B; P = .02). Multivariate analysis identified delayed CEA (OR 14.2; 95% CI, 1.32–152; p = .03) and length of cardiopulmonary bypass (OR 1.06; 95% CI, 1.02–1.11; p = .004) as independent predictors of postoperative stroke or death. Both randomized studies emphasize the advantage of concomitant operations over reversed staged procedures.

CONCLUSION The risk of perioperative stroke following myocardial revascularization rises with increasing patient age, and increasing age is accompanied by an increased incidence of carotid artery disease. Several studies have defined severe, uncorrected carotid stenosis as a major risk factor for perioperative stroke. Patients with carotid bruits, patients with a history of ischemic neurologic events, or patients 65 years old or older should have noninvasive carotid artery evaluation prior to CABG. Randomized trials have established the safety and efficacy of carotid endarterectomy as the most appropriate treatment for both symptomatic and asymptomatic severe carotid stenosis. Additionally, two randomized studies have demonstrated the advantage of concomitant CEA and CABG over reversed staged operations. Thus, we advocate combined carotid and coronary artery operations for virtually all patients with severe concomitant coronary and carotid artery disease.

Selected References Akins CW, Hilgenberg AD, Vlahakes GJ, et al: Late results of combined carotid and coronary surgery using actual versus actuarial methodology, Ann Thorac Surg 80:2091–2097, 2005. Akins CW, Moncure AC, Daggett WM, et al: Safety and efficacy of concomitant carotid and coronary artery operations, Ann Thorac Surg 60:311–317, 1995.

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Brener BJ, Brief DK, Alpert J, et al: The risk of stroke in patients with asymptomatic carotid stenosis undergoing cardiac surgery: a follow-up study, J Vasc Surg 5:269–279, 1987. Brown KR, Kresowik TF, Chin MH, et al: Multistate population-based outcomes of combined carotid endarterectomy and coronary artery bypass, J Vasc Surg 37:32–39, 2003. Cambria RP, Ivarsson BL, Akins CW, et al: Simultaneous carotid and coronary disease: safety of the combined approach, J Vasc Surg 9:56–64, 1989. Faggioli GL, Curl GR, Ricotta JJ: The role of carotid screening before coronary artery bypass, J Vasc Surg 12:724–729, 1990. Hertzer NR, Loop FD, Beven EG, et al: Surgical staging for simultaneous

coronary and carotid disease: a study including prospective randomization, J Vasc Surg 9:455–463, 1989. Hill MD, Shrive FM, Kennedy J, et al: Simultaneous carotid endarterectomy and coronary bypass surgery in Canada, Neurology 641:1435–1437, 2005. Illuminati G, Ricco JB, Calio F, et al: Short-term results of a randomized trial examining timing of carotid endarterectomy in patients with severe asymptomatic unilateral carotid stenosis undergoing coronary artery bypass grafting, J Vasc Surg 54:993–999, 2011. Ricotta JJ, Wall LP, Blackstone E: The influence of concurrent endarterectomy on coronary bypass: a case-controlled study, J Vasc Surg 41:397–401, 2005.

The Role of Extracranial–Intracranial Bypass in Current Practice

as well, especially in patients with poor collateral circulation. One study demonstrated that in 49 patients who presented with an ICA occlusion, treatment that included performing an EC-IC bypass was particularly effective for patients who were symptomatic or who had significant contralateral carotid artery stenosis. Two randomized trials have been performed since the inception of the procedure. The first and larger was the EC-IC Bypass Study Group trial that was conducted in the mid-1980s. The EC-IC Bypass Study Group trial was designed as an international multicenter prospective randomized trial that evaluated the use of EC-IC bypass for treating symptomatic cerebrovascular stenosis or occlusion. Patients were evaluated who presented with one or more transient ischemic attacks (TIAs), or strokes with associated stenosis, or occlusion in the affected ICA or MCA distributions. Cerebrovascular lesions were stratified according to the following anatomic landmarks: ICA occlusion, stenosis of the ICA above the second cervical vertebrae (C2), and MCA stenosis or occlusion. A total of 1377 patients were randomized to either EC-IC bypass (n = 714) or best medical management (n = 663). Best medical management at the time consisted of acetylsalicylic acid (325 mg up to four times per day) with appropriate control of hypertension. The mean follow-up interval was 56 months. In the surgical group, postprocedural angiographic patency was achieved in 96% of patients. Within the surgical group, the postoperative mortality and stroke rates were 0.6% and 2.5%, respectively. There was a nonsignificant trend toward increased nonfatal and fatal strokes in the surgical group as compared with the medically treated group. Subset analyses suggested that patients with severe MCA stenosis or occlusion of the ICA fared worse. Regardless, statistical significance was not achieved for any of the primary outcomes within the study. The study concluded that EC-IC bypass failed to demonstrate benefit in preventing ischemic events postoperatively as compared with medical management. The most recently completed randomized trial was the Japanese EC-IC bypass trial (JET). The trial studied 195 patients who were symptomatic and who exhibited cerebrovascular hemodynamic compromise as measured by functional imaging; these patients were randomized to EC-IC bypass or to best medical care. The average follow-up was 25 months, and mortality rates were low for both groups (surgery, n = 2; medical, n = 1). Moreover, there were no significant differences between the surgical and medical treatment groups in all other adverse events measured. The trial concluded that there were no significant differences in outcomes between the surgical and medical groups. Multiple criticisms were raised against both trials. The EC-IC Bypass Study Group was criticized for having inadequate randomization with regard to baseline criteria. Only stable low-risk patients were included in the study, which did not necessarily reflect the group that was being treated in the general population. In addition, there was no stratification for cerebrovascular hemodynamic

Mark A. Adelman and Mikel Sadek

Multiple indications exist for constructing an extracranial– intracranial (EC-IC) bypass. The indications that are encountered most frequently in contemporary practice are symptomatic occlusion of the internal carotid artery (ICA), stenosis or occlusion of the intracranial vasculature, usually at the level of the carotid siphon or middle cerebral artery (MCA), and intracranial aneurysms that are not amenable to endovascular treatment or to open ligation. Patients with an ipsilateral ICA occlusion have an annual stroke risk of 5% to 7% as well as an annual risk of ipsilateral stroke of 2% to 6%. Moreover, 15% of patients with anterior circulation ischemia are found to have ipsilateral occlusion of the ICA. Cerebral ischemia can occur secondary to thromboembolism from the distal occluded stump or to diminished cerebral blood flow. Anticoagulation or antiplatelet therapy is considered ineffective in the treatment of ICA occlusion, and performing an ipsilateral EC-IC bypass can prevent recurrent cerebral ischemic events in a subset of symptomatic patients. In patients who elect conservative management initially, an EC-IC bypass may be constructed if symptoms develop or progress despite maximal medical therapy. Other indications that require the consideration for an EC-IC bypass include ischemic ocular syndromes, moyamoya disease, vertebrobasilar insufficiency, oncologic resections, and chronic low-­ perfusion syndromes.

HISTORICAL PERSPECTIVE The first EC-IC bypass was reported by Donaghy and colleagues in 1967, and the procedure was in widespread use during the following decade. The most commonly performed variation was the superficial temporal artery–to–MCA bypass. Initial nonrandomized retrospective and prospective studies supported the safety and efficacy of the procedure. In addition to studies demonstrating an improvement in cerebral hemodynamics following EC-IC bypass based on functional imaging, improved clinical outcomes were demonstrated

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CEREBROVASCULAR DISEASE

Brener BJ, Brief DK, Alpert J, et al: The risk of stroke in patients with asymptomatic carotid stenosis undergoing cardiac surgery: a follow-up study, J Vasc Surg 5:269–279, 1987. Brown KR, Kresowik TF, Chin MH, et al: Multistate population-based outcomes of combined carotid endarterectomy and coronary artery bypass, J Vasc Surg 37:32–39, 2003. Cambria RP, Ivarsson BL, Akins CW, et al: Simultaneous carotid and coronary disease: safety of the combined approach, J Vasc Surg 9:56–64, 1989. Faggioli GL, Curl GR, Ricotta JJ: The role of carotid screening before coronary artery bypass, J Vasc Surg 12:724–729, 1990. Hertzer NR, Loop FD, Beven EG, et al: Surgical staging for simultaneous

coronary and carotid disease: a study including prospective randomization, J Vasc Surg 9:455–463, 1989. Hill MD, Shrive FM, Kennedy J, et al: Simultaneous carotid endarterectomy and coronary bypass surgery in Canada, Neurology 641:1435–1437, 2005. Illuminati G, Ricco JB, Calio F, et al: Short-term results of a randomized trial examining timing of carotid endarterectomy in patients with severe asymptomatic unilateral carotid stenosis undergoing coronary artery bypass grafting, J Vasc Surg 54:993–999, 2011. Ricotta JJ, Wall LP, Blackstone E: The influence of concurrent endarterectomy on coronary bypass: a case-controlled study, J Vasc Surg 41:397–401, 2005.

The Role of Extracranial–Intracranial Bypass in Current Practice

as well, especially in patients with poor collateral circulation. One study demonstrated that in 49 patients who presented with an ICA occlusion, treatment that included performing an EC-IC bypass was particularly effective for patients who were symptomatic or who had significant contralateral carotid artery stenosis. Two randomized trials have been performed since the inception of the procedure. The first and larger was the EC-IC Bypass Study Group trial that was conducted in the mid-1980s. The EC-IC Bypass Study Group trial was designed as an international multicenter prospective randomized trial that evaluated the use of EC-IC bypass for treating symptomatic cerebrovascular stenosis or occlusion. Patients were evaluated who presented with one or more transient ischemic attacks (TIAs), or strokes with associated stenosis, or occlusion in the affected ICA or MCA distributions. Cerebrovascular lesions were stratified according to the following anatomic landmarks: ICA occlusion, stenosis of the ICA above the second cervical vertebrae (C2), and MCA stenosis or occlusion. A total of 1377 patients were randomized to either EC-IC bypass (n = 714) or best medical management (n = 663). Best medical management at the time consisted of acetylsalicylic acid (325 mg up to four times per day) with appropriate control of hypertension. The mean follow-up interval was 56 months. In the surgical group, postprocedural angiographic patency was achieved in 96% of patients. Within the surgical group, the postoperative mortality and stroke rates were 0.6% and 2.5%, respectively. There was a nonsignificant trend toward increased nonfatal and fatal strokes in the surgical group as compared with the medically treated group. Subset analyses suggested that patients with severe MCA stenosis or occlusion of the ICA fared worse. Regardless, statistical significance was not achieved for any of the primary outcomes within the study. The study concluded that EC-IC bypass failed to demonstrate benefit in preventing ischemic events postoperatively as compared with medical management. The most recently completed randomized trial was the Japanese EC-IC bypass trial (JET). The trial studied 195 patients who were symptomatic and who exhibited cerebrovascular hemodynamic compromise as measured by functional imaging; these patients were randomized to EC-IC bypass or to best medical care. The average follow-up was 25 months, and mortality rates were low for both groups (surgery, n = 2; medical, n = 1). Moreover, there were no significant differences between the surgical and medical treatment groups in all other adverse events measured. The trial concluded that there were no significant differences in outcomes between the surgical and medical groups. Multiple criticisms were raised against both trials. The EC-IC Bypass Study Group was criticized for having inadequate randomization with regard to baseline criteria. Only stable low-risk patients were included in the study, which did not necessarily reflect the group that was being treated in the general population. In addition, there was no stratification for cerebrovascular hemodynamic

Mark A. Adelman and Mikel Sadek

Multiple indications exist for constructing an extracranial– intracranial (EC-IC) bypass. The indications that are encountered most frequently in contemporary practice are symptomatic occlusion of the internal carotid artery (ICA), stenosis or occlusion of the intracranial vasculature, usually at the level of the carotid siphon or middle cerebral artery (MCA), and intracranial aneurysms that are not amenable to endovascular treatment or to open ligation. Patients with an ipsilateral ICA occlusion have an annual stroke risk of 5% to 7% as well as an annual risk of ipsilateral stroke of 2% to 6%. Moreover, 15% of patients with anterior circulation ischemia are found to have ipsilateral occlusion of the ICA. Cerebral ischemia can occur secondary to thromboembolism from the distal occluded stump or to diminished cerebral blood flow. Anticoagulation or antiplatelet therapy is considered ineffective in the treatment of ICA occlusion, and performing an ipsilateral EC-IC bypass can prevent recurrent cerebral ischemic events in a subset of symptomatic patients. In patients who elect conservative management initially, an EC-IC bypass may be constructed if symptoms develop or progress despite maximal medical therapy. Other indications that require the consideration for an EC-IC bypass include ischemic ocular syndromes, moyamoya disease, vertebrobasilar insufficiency, oncologic resections, and chronic low-­ perfusion syndromes.

HISTORICAL PERSPECTIVE The first EC-IC bypass was reported by Donaghy and colleagues in 1967, and the procedure was in widespread use during the following decade. The most commonly performed variation was the superficial temporal artery–to–MCA bypass. Initial nonrandomized retrospective and prospective studies supported the safety and efficacy of the procedure. In addition to studies demonstrating an improvement in cerebral hemodynamics following EC-IC bypass based on functional imaging, improved clinical outcomes were demonstrated

The Role of Extracranial–Intracranial Bypass in Current Practice

compromise. More specifically, patients with embolic strokes but adequate collateral flow from the contralateral circulation as evidenced by functional imaging were not differentiated from stroke patients with compromised cerebrovascular hemodynamics. Despite these criticisms, EC-IC bypass procedure volume diminished significantly in subsequent years. The Carotid Occlusion Surgery Study (COSS) is a randomized control trial that is under way to reassess outcomes for EC-IC bypass. The study is designed to evaluate patients specifically with cerebrovascular hemodynamic compromise ipsilateral to a symptomatic carotid occlusion as measured by oxygen extraction fraction using positron emission tomography (PET). The hypothesis is that patients with impaired hemodynamics, whose strokes result from a low-flow state, might benefit preferentially from an EC-IC bypass.

PROCEDURAL CHARACTERISTICS Preoperative Evaluation The goal of the preoperative evaluation is to diagnose and characterize the pathology being treated as well as to differentiate who will tolerate vascular occlusion as a sole therapeutic option and who will require the construction of an EC-IC bypass. In general, contrast imaging is required preoperatively to delineate the anatomy. This may be performed using computed tomography angiography (CTA), magnetic resonance angiography (MRA), or digital subtraction angiography (DSA). In addition, a brain-perfusion scan or balloon occlusion test may be obtained to assess for adequacy of direct and collateral cerebral blood flow. The balloon occlusion test might produce no change in blood flow, a mild decrease in global blood flow, or a marked asymmetric decrease in blood flow, suggesting significant cerebrovascular hemodynamic compromise.

Procedural Considerations The creation of an EC-IC bypass follows the same tenets as the creation of vascular bypasses elsewhere in the periphery: inflow, outflow, and conduit. The inflow can vary depending on the clinical situation. Possible inflow vessels include the common carotid artery (CCA), the internal carotid artery (ICA), the external carotid artery (ECA), or a branch off of the ECA. If given the option, the surgeon should select the inflow vessel in the following order or preference: ECA preferred to CCA preferred to ICA. The preferential use of the ECA or CCA as the inflow vessel diminishes the risk of cerebral ischemia secondary to a low-flow state during clamping of the proximal anastomosis. Two commonly used outflow vessels include the ICA or MCA. The latter is accessed through a pretragal (zygoma) tunnel. Other options exist for the outflow vessel, and the choice depends on the location of the pathology being treated. With regard to the conduit, the common options include the saphenous vein or the radial artery. The radial artery graft is used preferentially at our institution owing to a better size match resulting in a theoretical improvement in flow dynamics. In addition, the use of distal vein requires valvular lysis, because it needs to be used in a nonreversed fashion to minimize size discrepancy. Successful harvesting of the radial artery depends on appropriate preoperative planning and selection. In general, the nondominant arm should be used. Pulse volume recordings and compression studies should be performed to assess adequacy of collateral flow to the hand. Most significantly, digital pulse volume recordings or

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angiography should be used to confirm the presence of a patent palmar arch. Following appropriate preoperative planning, the procedure is conducted in three stages. The first stage consists of performing the usual exposure and isolation of the CCA, ICA, and ECA using an incision along the anterior sternocleidomastoid. The target intracerebral vessel is exposed and isolated using a pterional craniotomy. The final component of the exposure consists of isolating the radial artery. This is carried out in a standard fashion with care to preserve the radial nerve. The harvested artery is flushed using a combination of heparin (1000 U), papaverine (20 mg), and nitroglycerine (1 mg) in 1 L of a crystalloid solution. At this point, a pretragal soft-tissue tunnel with a furrow at the base of the zygoma is created, and an arteriovenous graft tunneler is used to tunnel the conduit. The second stage of the procedure consists of performing the distal anastomosis. This is performed before the proximal anastomosis to allow additional maneuverability of the graft. The patient is heparinized (100 U/kg), and dexamethasone and barbiturates are administered until cerebral activity is suppressed adequately as monitored by electroencephalogram (EEG). A 5-mm arteriotomy is made in the target vessel, and an end-to-side anastomosis is constructed using interrupted 8–0 or 9–0 Prolene sutures. The conduit is drained and air is removed, after which the conduit is clamped and the intracerebral vessel is reperfused. The third stage of the procedure consists of performing the proximal anastomosis. At this point an end-to-side anastomosis is performed at the desired site, usually using a 6–0 Prolene suture. Before the ICA is ligated, the ICA is accessed using a 20-gauge angiocatheter. The native artery is clamped, and the bypass patency is assessed using DSA. Evoked potentials are used to assess for hypoperfusion before the ICA is ligated. Once adequacy of flow is confirmed, the ICA is suture ligated at its origin or immediately distal to the proximal anastomosis. Protamine is used at the end of the procedure for reversal of anticoagulation. Aspirin is initiated postoperatively and continued indefinitely.

Postprocedural Follow-up and Management Because so few of these procedures are being performed, followup regimens are not standardized. At our institution, the patient is monitored postoperatively using serial neurovascular checks and bedside Doppler evaluations of the graft. Repeat cerebral angiography is performed at 48 hours. Duplex surveillance is then performed at 3 months and 6 months and then annually thereafter. Systolic flow velocities of greater than 400 cm/sec or less than 40 cm/sec warrant additional evaluation and possible intervention when indicated.

CURRENT DATA One of the more comprehensive reviews of the current data on EC-IC bypass for occlusive carotid artery disease comes from the Cochrane database. Twenty-one trials were evaluated for a total of 2591 patients, including the two randomized, controlled trials mentioned previously. The goal of the review was to assess whether or not the EC-IC bypass might be beneficial to a subgroup of symptomatic patients with ICA occlusion who suffer from significant cerebrovascular hemodynamic compromise. Separate analyses were performed for the randomized, controlled trials and the remaining retrospective studies. With regard to the combined data from the randomized, controlled trials (EC-IC Bypass Study Group and JET), there were no significant differences for the majority of primary or secondary endpoints. The primary outcomes comparing treatment with control groups

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included death from all causes (odds ratio [OR], 0.81), any stroke during follow-up (OR, 0.79), and death or dependency (OR, 0.94). The measurable secondary outcomes included vascular death (OR, 0.96) and myocardial infarction (OR, 0.78). The one outcome that proved to be significant was the composite outcome of stroke, serious vascular event, or vascular death, whereby there was a statistically significant benefit in favor of surgery (OR, 0.68; 95% confidence interval [CI], 0.51–0.91; p = .009). With regard to the retrospective studies, the combined data showed that there were no significant differences in the majority of primary or secondary endpoints evaluated. Data obtained from 11 trials (524 patients) regarding the endpoint of transient ischemic attack or amaurosis fugax demonstrated a significant benefit in favor of surgery (OR, 0.34; CI, 0.16–0.69; p = .003). Moreover, there were trends favoring surgery regarding the endpoint of ischemic stroke (OR, 0.72) and the composite endpoint of stroke, serious vascular events, or vascular death (OR, 0.69). An additional review was performed for the treatment of cerebral aneurysms using exclusion and EC-IC bypass. Twenty trials were evaluated for a total of 408 patients. The mean follow-up across all studies was 39 months, and functional cerebrovascular impairment was identified in 21% of the study population. A total of 19 deaths were identified, with six secondary to stroke, four secondary to cerebral hemorrhage, and the remainder secondary to nonneurologic and noncardiac causes. Within the 30-day perioperative period, seven TIAs and two strokes were identified. Six TIAs and 17 strokes were identified on later follow-up. The annual postprocedural risk for mortality and stroke were 1.5% and 1.6%, respectively. Graft patency was noted to be 93% in total, with a 2.3% failure rate per year after the first year. These results were deemed favorable, in particular for patients with cerebral aneurysms that were otherwise not amenable to endovascular treatment or to open ligation. Our current institutional experience relates primarily to the treatment of giant intracranial aneurysms that are not amenable to endovascular coiling or surgical clipping. Twenty-nine patients with giant intracranial aneurysms were evaluated retrospectively, with a mean follow-up duration of 62 months. The procedures performed consisted of an EC-IC bypass with concomitant occlusion of the parent vessel. Graft occlusions occurred in two patients. Three patients sustained strokes, and one of these patients died secondary to a large cerebral infarction. The conclusion borne from the data was that the procedure was safe and effective for the treatment of giant intracranial aneurysms. Nevertheless, patients required close long-term observation because of the possibility of perforating vessel thrombosis following the altered hemodynamics that resulted from occlusion of the parent vessel.

CONCLUSIONS The EC-IC bypass is a procedure that was once in widespread use but is now less common as a result of a lack of level I evidence to support its benefit. For symptomatic carotid artery occlusion, the trials thus far have demonstrated neither superiority nor inferiority when comparing surgery with medical management. However, the current body of literature has not adequately stratified patients for preoperative differences in cerebral hemodynamics. Additional evaluation in the setting of a randomized, controlled trial, such as the ongoing COSS trial, is required to assess whether the theoretical advantage of a bypass in patients with carotid occlusion and concomitant impaired cerebrovascular circulation is clinically significant. At this time, the EC-IC bypass should be used in the setting of a clinical trial or for select pathologies, such as giant cerebral aneurysms, that are not otherwise amenable to conventional treatment modalities.

Selected References Danaila L, Olarescu A, Gheorghitescu L, et al: Extra–intracranial anastomosis between the superficial temporal artery and a cortical branch of the middle cerebral artery, Neurologie et Psychiatrie 22:251–261, 1984. Donaghy RMP: Patch and bypass in microangional surgery. In Donaghy RMP, Yasargil MG, (eds): Microvascular surgery, St. Louis, 1967, CV Mosby, pp 75–86. Fluri F, Engelter S, Lyrer P: Extracranial–intracranial arterial bypass surgery for occlusive carotid artery disease, Cochrane Database Syst Rev (2):CD005953, 2010. Heilbrun MP: Overall management of vascular lesions considered treatable with extracranial–intracranial bypass: part 1. Internal carotid occlusion, Neurosurgery 11(2):239–246, 1982. Meyer JS, Nakajima S, Okabe T, et al: Redistribution of cerebral blood flow following STA-MCA bypass in patients with hemispheric ischemia, Stroke 13:774–784, 1982. Ogasawara K, Ogawa A: Japanese EC-IC bypass trial, Nippon Rinsho 64(Suppl 7):524–527, 2006. The EC/IC Bypass Study Group: Failure of extracranial–intracranial arterial bypass to reduce the risk of ischemic stroke. Results of an international randomized trial, N Engl J Med 313:1191–1200, 1985. Tsuda Y, Kimura K, Iwata Y, et al: Improvement of cerebral blood flow and/ or CO2 reactivity after superficial temporal artery–middle cerebral artery bypass in patients with transient ischemic attacks and watershed-zone infarctions, Surg Neurol 22(6):595–604, 1984. Yonas H, Gur D, Good BC, Latchaw RE, et al: Stable xenon CT blood flow mapping for evaluation of patients with extracranial–intracranial bypass surgery, J Neurosurg 62(3):324–333, 1985. Yonekura M, Austin G, Hayward W: Long-term evaluation of cerebral blood flow, transient ischemic attacks, and stroke after STA-MCA anastomosis, Surg Neurol 18(2):123–130, 1982.



Open Surgical Treatment of Fibromuscular Dysplasia of the Carotid Artery

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Open Surgical Treatment of Fibromuscular Dysplasia of the Carotid Artery James C. Stanley

FIGURE 1  Operative exposure of artery revealing external beaded

appearance representing serial narrowings caused by medial fibroplasia.  (From Stanley JC,Wakefield TW: Arterial fibrodysplasia. In Rutherford RB, (ed): Vascular surgery, 3rd ed. Philadelphia, 1989,WB Saunders, pp 245–265).

Most patients with carotid artery fibrodysplasia are likely to be asymptomatic, although the number reported without symptoms is small because most reported series are surgical experiences encompassing more advanced disease. Complications of this disease include embolization, dissections, and rupture with formation of an arteriovenous fistula. The most catastrophic clinical complication is stroke, and prophylactic interventions in asymptomatic patients are directed at reducing or eliminating this sequela of the disease. The risk of stroke or other related neurologic events varies widely and is unpredictable. Once clinical manifestations of this entity have arisen, operative intervention appears justified.

OPERATIVE TECHNIQUES Open surgical therapy for extracranial internal carotid artery fibrodysplasia includes resection of the diseased vessel with interposition grafting, angioplasty with patch grafts for focal lesions, and graduated intraluminal dilation. Operative exposure of the carotid vessel in these cases usually requires dissection of the entire internal carotid artery to within a few centimeters of the base of the skull (Figure 1). Care must be used not to cause injury to cranial nerves IX, X, XI, and XII. Extended exposure of the internal carotid artery at the upper cervical levels may be facilitated by subluxation of the mandible. In the author’s experience, intermittent traction on the mandible, with an external clamp inserted into the angle of the mandible, facilitates the subluxation. Others have advocated fixed traction with placement of arch bars, as well as transection of the mandibular ramus. Patients undergoing open procedures are placed on preoperative antiplatelet agents. They are systemically anticoagulated intraoperatively with intravenous heparin before the carotid vessels are occluded, and unless incessant bleeding is present after restoring antegrade carotid flow, the heparin effect is not reversed.

back bleeding as the dilation proceeds, as a means of flushing out any debris that arises as the dysplastic septa are fractured. Completion arteriography is not routinely performed, but if concerns arise regarding the adequacy of the dilation, then arteriography should be undertaken. Intraoperative duplex sonography may be useful, but the high cervical regions are usually difficult to insonate, and this technology is often wanting in these circumstances. Patients subjected to dilation should receive antiplatelet agents for 3 months postoperatively, until the dysplastic arterial segment has been completely remodeled.

Resection and Interposition Graft Reconstruction Certain complex cases of carotid fibrodysplasia exhibiting extensive mural aneurysms, septae with adherent thrombus, and elongation with acute angulations may be at greater risk for complications if treated by open dilation or percutaneous balloon angioplasty. In this setting, resection of the diseased segment and reconstruction of the artery with an interposition vein graft or synthetic conduit is appropriate. Exposure for these procedures is more extensive than for open dilation given the usual location of dysplastic lesions at the second and third cervical vertebral level. In these reconstructive procedures, anterior subluxation of the mandible improves exposure at the upper cervical level and lessens the risk of cranial nerve stretch injuries caused by the forcefulness of retractors that may be required with more limited exposures. Anastomosis of a graft to the internal carotid artery when performed near the skull base requires great care. Back bleeding may be best controlled with an intraluminal balloon rather than a microvascular clamp, which can compromise adequate visualization of the anastomotic site. Interrupted sutures rather than a continuous suture may be necessary to safely complete the distal anastomosis. Vein conduits are preferred over synthetic prostheses for technical reasons, as well as a concern that synthetic prostheses may be more likely to be complicated by late thromboembolic events or infection.

Open Dilation Graduated intraluminal dilation of the diseased internal carotid artery is usually accomplished by advancing rigid olive-tip dilators through an arteriotomy placed in the proximal carotid bulb. These are then passed the full length of the internal carotid artery to the base of the skull. Initial dilators range in diameter from 1.5 to 2.5 mm, with subsequent passage of increasingly larger dilators up to a maximum of 5.0 to 5.5 mm in diameter. Use of larger dilators should be avoided, in that they are likely to cause deep dissections within the vessel wall. Balloon catheters have been preferred by some. Because of a balloon’s radial dilation, they may be less likely to cause a dissection of the dysplastic artery when compared with longitudinal dilation by metal devices. Arterial perforation is a rare complication, but such can accompany overzealous dilation. It is important to allow

SURGICAL RESULTS Operative outcomes in properly selected patients have been very good (Figure 2). More than 170 reported patients have been treated by open surgical procedures. Excellent outcomes without early or late neurologic complications have been reported in 90% of cases. However, approximately 5% of patients undergoing open dilation experience perioperative strokes and 1% die. Sporadic follow-up studies suggest that approximately 2% of treated patients develop late transient ischemic attacks, and an additional 2% experience late strokes. Unfortunately, natural history data in patients who received antiplatelet agents and who were not subjected to operation have been inconsistently reported, and such precludes direct comparisons with open operative interventions.

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FIGURE 2  Preoperative appearance of medical fibrodysplasia of the external carotid and internal carotid arteries. Postoperative appearance following graduated intraluminal dilation of the external carotid and internal carotid arteries using rigid dilators.  (From Stanley JC, Fry WJ, Seeger JF, et al: Extracranial internal carotid and vertebral artery fibrodysplasia, Arch Surg 109: 215–222, 1974).

Selected References Chiche L, Bahnini A, Koskas F, et al: Occlusive fibromuscular disease of arteries supplying the brain: results of surgical treatment, Ann Vasc Surg 11:496–504, 1997. Collins GJ Jr, Rich NM, Clagett GP, et al: Fibromuscular dysplasia of the internal carotid arteries. Clinical experience and follow-up, Ann Surg 194:89–96, 1981. Effeney DJ, Ehrenfeld WK, Stoney RJ, et al: Why operate on carotid fibromuscular dypsplasia? Arch Surg 115:1261–1265, 1980. Ehrenfeld WK, Wylie EJ: Fibromuscular dysplasia of the internal carotid artery, Arch Surg 109:676–681, 1974. Moreau P, Albar B, Thevenet A: Fibromuscular dysplasia of the internal carotid artery: long-term surgical results, J Cardiovasc Surg 34:463–472, 1993.

Endovascular Treatment of Fibromuscular Dysplasia of the Carotid Artery Gustavo S. Oderich and Peter A. Schneider

Treatment of carotid fibromuscular dysplasia (FMD) in the past has been open graduated rigid carotid dilatation for symptomatic stenoses or segmental resection with saphenous vein interposition for aneurysms. The results of contemporary open surgical reports have shown the risk of stroke to be 1.4% to 2.8% and that of transient ischemic attack (TIA) to be 1.4% to 7.7%. Because high surgical exposure up to the first and second cervical vertebrae may be needed to ensure that safe dilatation is carried out under direct vision, rates of cranial nerve injury are higher (5.1% up to 58%) than those reported for carotid endarterectomy. Endovascular treatment of renal FMD with balloon angioplasty has gained widespread acceptance. It is safe, effective, and durable. The enthusiasm for using endovascular techniques to treat carotid

Stanley JC, Fry WJ, Seeger JF, et al: Extracranial internal carotid and vertebral artery fibrodysplasia, Arch Surg 109:215–222, 1974. Starr DS, Lawrie GM, Morris GJ Jr: Fibromuscular dysplasia of carotid arteries: long-term results of graduated internal dilatation, Stroke 12:196–199, 1981. Stewart MT, Moritz MW, Smith RB III, et al: The natural history of carotid fibromuscular dysplasia, J Vasc Surg 3:305–310, 1986. Touze E, Oppenheim C, Trystram D, et al: Fibromuscular dysplasia of cervical and intracranial arteries, Int J Stroke 5:296–305, 2010. van Damme H, Sakalihasan N, Limet R: Fibromuscular dysplasia of the internal carotid artery. Personal experience with 13 cases and literature review, Acta Chir Belg 99:163–168, 1999.

FMD lesions has been fueled by the higher morbidity rates of open surgery in some reports and by recent improvements in endovascular carotid stent technology.

INDICATIONS The choice of open or endovascular treatment takes into consideration the clinical syndrome, the characteristics of the lesion, and the institutional experience. Endovascular treatment is an excellent choice in patients without excessive tortuosity of the aortic arch and carotid arteries and who have FMD lesions that spare at least 1 or 2 cm of distal cervical internal carotid artery (ICA).

TECHNIQUE The same principles used to treat atherosclerotic carotid bifurcation lesions are applied to FMD lesions, with a few important modifications. Pharmacologic prevention of cerebrovascular events starts before the procedure with oral aspirin and clopidogrel. Dual antiplatelet therapy is continued for 4 to 6 weeks, followed by aspirin alone, except for patients treated by covered stents who receive dual antiplatelet regimen indefinitely. The procedure is usually performed using the transfemoral approach, with monitored anesthesia care. Intravenous heparin (100 units/kg) is administered to achieve a target activated clotting time of longer than 250 seconds before any catheters are manipulated in

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FIGURE 2  Preoperative appearance of medical fibrodysplasia of the external carotid and internal carotid arteries. Postoperative appearance following graduated intraluminal dilation of the external carotid and internal carotid arteries using rigid dilators.  (From Stanley JC, Fry WJ, Seeger JF, et al: Extracranial internal carotid and vertebral artery fibrodysplasia, Arch Surg 109: 215–222, 1974).

Selected References Chiche L, Bahnini A, Koskas F, et al: Occlusive fibromuscular disease of arteries supplying the brain: results of surgical treatment, Ann Vasc Surg 11:496–504, 1997. Collins GJ Jr, Rich NM, Clagett GP, et al: Fibromuscular dysplasia of the internal carotid arteries. Clinical experience and follow-up, Ann Surg 194:89–96, 1981. Effeney DJ, Ehrenfeld WK, Stoney RJ, et al: Why operate on carotid fibromuscular dypsplasia? Arch Surg 115:1261–1265, 1980. Ehrenfeld WK, Wylie EJ: Fibromuscular dysplasia of the internal carotid artery, Arch Surg 109:676–681, 1974. Moreau P, Albar B, Thevenet A: Fibromuscular dysplasia of the internal carotid artery: long-term surgical results, J Cardiovasc Surg 34:463–472, 1993.

Endovascular Treatment of Fibromuscular Dysplasia of the Carotid Artery Gustavo S. Oderich and Peter A. Schneider

Treatment of carotid fibromuscular dysplasia (FMD) in the past has been open graduated rigid carotid dilatation for symptomatic stenoses or segmental resection with saphenous vein interposition for aneurysms. The results of contemporary open surgical reports have shown the risk of stroke to be 1.4% to 2.8% and that of transient ischemic attack (TIA) to be 1.4% to 7.7%. Because high surgical exposure up to the first and second cervical vertebrae may be needed to ensure that safe dilatation is carried out under direct vision, rates of cranial nerve injury are higher (5.1% up to 58%) than those reported for carotid endarterectomy. Endovascular treatment of renal FMD with balloon angioplasty has gained widespread acceptance. It is safe, effective, and durable. The enthusiasm for using endovascular techniques to treat carotid

Stanley JC, Fry WJ, Seeger JF, et al: Extracranial internal carotid and vertebral artery fibrodysplasia, Arch Surg 109:215–222, 1974. Starr DS, Lawrie GM, Morris GJ Jr: Fibromuscular dysplasia of carotid arteries: long-term results of graduated internal dilatation, Stroke 12:196–199, 1981. Stewart MT, Moritz MW, Smith RB III, et al: The natural history of carotid fibromuscular dysplasia, J Vasc Surg 3:305–310, 1986. Touze E, Oppenheim C, Trystram D, et al: Fibromuscular dysplasia of cervical and intracranial arteries, Int J Stroke 5:296–305, 2010. van Damme H, Sakalihasan N, Limet R: Fibromuscular dysplasia of the internal carotid artery. Personal experience with 13 cases and literature review, Acta Chir Belg 99:163–168, 1999.

FMD lesions has been fueled by the higher morbidity rates of open surgery in some reports and by recent improvements in endovascular carotid stent technology.

INDICATIONS The choice of open or endovascular treatment takes into consideration the clinical syndrome, the characteristics of the lesion, and the institutional experience. Endovascular treatment is an excellent choice in patients without excessive tortuosity of the aortic arch and carotid arteries and who have FMD lesions that spare at least 1 or 2 cm of distal cervical internal carotid artery (ICA).

TECHNIQUE The same principles used to treat atherosclerotic carotid bifurcation lesions are applied to FMD lesions, with a few important modifications. Pharmacologic prevention of cerebrovascular events starts before the procedure with oral aspirin and clopidogrel. Dual antiplatelet therapy is continued for 4 to 6 weeks, followed by aspirin alone, except for patients treated by covered stents who receive dual antiplatelet regimen indefinitely. The procedure is usually performed using the transfemoral approach, with monitored anesthesia care. Intravenous heparin (100 units/kg) is administered to achieve a target activated clotting time of longer than 250 seconds before any catheters are manipulated in



121

Endovascular Treatment of Fibromuscular Dysplasia of the Carotid Artery

the aortic arch. Any abnormal or possibly abnormal arterial segments of the carotid, vertebral, and cerebrovascular anatomy identified by computed tomographic angiography (CTA) or magnetic resonance angiography (MRA) should be evaluated with angiography. In patients with type I arch, a simple catheter (e.g., JB1, vertebral) is preferred; curved catheters (e.g., Simmons II, Vitek) are used in patients with difficult arches (types II and III). Selective catheterization of the mid-distal common carotid artery (CCA) is performed over a stiff 0.035-inch angled glide wire using the Shuttle select system. If flow reversal, balloon occlusion, or a larger (>7 Fr) sheath is used, advancement of the sheath requires placement of an exchange length 0.035-inch stiff glide wire into the terminal branches of the external carotid artery. It is important to maintain sheath access to the CCA, realizing that once the 0.035-inch stiff wire and dilator are removed, support is provided solely by the sheath. Fibromuscular dysplasia lesions are by nature more prone to dissection, are longer than atherosclerotic lesions, can harbor small debris, and often extend to the distal ICA. Filter wires are typically not very steerable to navigate the tortuous membranous segments of FMD. In addition, the filter needs to be deployed within an uninvolved straight segment of cervical ICA, which is not always available. In these cases the use of flow reversal or balloon occlusion can decrease risk of embolization, which can occur during unprotected guidewire manipulations. It is preferable to cross the lesion with a soft 0.018-inch glide wire and microcatheter. After the lesion is crossed and true lumen access is confirmed, the interventional 0.014-inch guidewire of choice is positioned. The Gore Flow Reversal system (WL Gore, Flagstaff, AZ) has a 6-Fr working sheath compatible with most small-profile, rapid-exchange angioplasty balloons and self-expandable stents. A small-profile (0.018inch) 5- or 6-mm Gore Viabahn stent graft (WL Gore, Flagstaff, AZ) may be used over a 6-Fr sheath to treat aneurysms or FMD lesions that have large outpouchings. If a larger stent graft (7 or 8 mm) is needed, the sheath size must be increased to 7 Fr. In these cases, the technique is modified and a 0.014-inch filter wire with long (>300 cm) working length is used. A larger delivery system can require direct surgical exposure of the carotid arteries, which allows flow reversal by clamping the CCA and external carotid artery. Performing angioplasty alone or in conjunction with a stent or stent graft is somewhat controversial given the small number of patients reported in the literature. Although primary angioplasty has been shown to be safe and durable for renal FMD, it leaves multiple small intimal flaps, membranes, and debris that pose an ongoing risk of embolization during or after carotid interventions. Our preference is to use self-expanding stents (Figure 1) to scaffold the affected ICA segment, unless this cannot be done safely because of tortuosity or other anatomic constraints. For aneurysms or larger outpouches with beaded dilatations that may contain embolic material, low profile stent-grafts are used (Figure 2). For excessively tortuous or focal lesions, primary angioplasty is used. Administration of atropine (0.5– 1 mg) may be considered for de novo lesions as prophylaxis against bradycardia during balloon inflation in the carotid artery.

B D

A

C

E

F

FIGURE 1  Treatment of multiple high-grade stenoses associated with

fibromuscular dysplasia of the internal carotid artery. A and B, In these cases, the use of reversal of flow can decrease the risk of embolization of small thrombi or debris lodged in the membranes and outpouches. C, The lesion should be crossed with a soft 0.018-inch wire and microcatheter to minimize risk of dissection. D, E, and F, After confirmation of true lumen access using small injection of contrast, the i­nterventional 0.014inch wire is placed and a self-expandable stent is deployed. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

0.018 0.035

RESULTS Reports of endovascular interventions for carotid FMD are limited, as a result of the small number of patients treated by a variety of techniques with mixed indications (stenoses, dissections, and aneurysms) and limited follow-up. Preliminary results indicate that in selected patients, endovascular treatment is safe and effective. The first reports of open balloon angioplasty from the 1980s used direct carotid exposure. Ballard and associates reported 11 cases treated by open balloon angioplasty with no perioperative events or cranial nerve injuries. Olin reported four patients treated by primary percutaneous angioplasty for carotid FMD causing debilitating headaches, with relief of symptoms in all patients. Most reports have used self-expandable stents for carotid dissections, including those

A

B

FIGURE 2  Carotid fibromuscular dysplasia associated with aneu-

rysms and large outpouches is ideally treated using self-expandable stent grafts. A small-profile stent graft may be delivered using a reversal of flow device (6 Fr). A, However, if a larger-diameter stent graft is needed, a filter wire is used for embolic protection. B, The stent graft is deployed into normal distal internal carotid artery. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

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CEREBROVASCULAR DISEASE

caused by FMD. Fava and associates reported 12 patients treated with Wallstents (Boston Scientific, Freemont, CA) for symptomatic carotid dissections refractory to anticoagulation therapy. Adjuvant thrombolysis was used in patients with occlusions. Acute symptoms resolved in 66% and stabilized in 34%. All stents were patent at 24 months. Edgell and colleagues reported symptomatic improvement in seven patients treated with angioplasty and stenting of 12 dissected carotid arteries, five of which were caused by FMD. Self-expanding stent grafts offer a promising alternative to treating patients with carotid aneurysms or symptomatic FMD lesions with irregular membranes and large outpouches. The availability of lowprofile self-expanding stent grafts has allowed treatment of patients who have more difficult anatomy. Assadian and colleagues reported the use of Viabahn stent grafts to treat carotid FMD lesions complicated by dissections, stenoses, and aneurysms. In this series, which predated flow-reversal devices and low-profile delivery, direct exposure of the carotid artery was used to induce flow reversal, which was used during stent-graft deployment. There was one post-procedure TIA and no strokes or cranial nerve injuries. All stent grafts remained patent, and there were no recurrent symptoms at a mean follow-up of 4 years. A systematic review of 224 patients treated for carotid aneurysms by stent grafts showed in-hospital mortality of 4% and 30-day stroke rate of 1.8%. Primary stent-graft patency was 93% at mean follow-up of 15 months. Cohen and associates reported the use of smaller 4-mm self-expanding covered stents (Symbiotic stent, Boston Scientific, Bloomington, MN). The use of flow-diversion stents, which have been approved to treat intracranial aneurysms, has not yet been reported for FMD lesions but may be of use in selected cases.

made endovascular treatment of these lesions effective, with lowprofile balloons and stents using embolic protection devices. Our preference is to employ reversal of flow for embolic protection and revascularization with self-expanding stents or stent grafts.

Selected References Assadian A, Senekowitsch C, Assadian O, et al: Combined open and endovascular stent grafting of internal carotid artery fibromuscular dysplasia: long term results, Eur J Vasc Endovasc Surg 29:345–349, 2005. Ballard JL, Guinn JE, Killeen JD, et al: Open operative balloon angioplasty of the internal carotid artery: a technique in evolution, Ann Vasc Surg 390–393, 1995. Cohen JE, Grigoriadis S, Gomori JM, et al: Petrous carotid artery pseudoaneurysm in bilateral carotid fibromuscular dysplasia: treatment by means of self-expanding covered stents, Surgical Neurology 68:216–220, 2007. Edgell RC, Abou-Chebl A, Yadav JS: Endovascular management of spontaneous carotid artery dissection, J Vasc Surg 42:854–860, 2005. Effeney DJ, Krupski WC, Stoney RJ, et al: Fibromuscular dysplasia of the carotid artery, Aust N Z J Surg 53:527–531, 1983. Fava M, Meneses L, Loyola S, et al: Carotid artery dissection: endovascular treatment in 12 patients, Cath Cardiovasc Interv 71:694–700, 2008. Li Z, Chang G, Yao C, et al: Endovascular stenting of extracranial carotid artery aneurysm: a systematic review, Eur J Vasc Endovasc Surg 42:419–426, 2011. Muller BT, Luther B, Hort W, et al: Surgical treatment of 50 carotid dissections: Indications and results, J Vasc Surg 31:980–398, 2000. Olin JW, Sealove BA: Diagnosis, management, and future developments of fibromuscular dysplasia, J Vasc Surg 53:826–836, 2011. Schneider PA: Endovascular and surgical management of extracranial carotid fibromuscular arterial dysplasia. In Cronenwett JL, Johnston KW, (eds): Rutherford’s vascular surgery, 7th ed, Philadelphia, 2010, Saunders, pp.1487–1496

SUMMARY Indications for endovascular treatment of carotid FMD are the presence of symptoms or aneurysm. Technological improvements have

Vertebral Artery Reconstruction for Vertebrobasilar Ischemia Ramon Berguer

Vertebrobasilar ischemia (VBI) is a syndrome with different etiologies. The term insufficiency, which is still commonly used, should be abandoned because it implies only a low-flow condition affecting the vertebrobasilar territory and ignores the important mechanism of microembolization that constitutes approximately a third of the VBI pathology. Low-flow VBI is more often than not caused by a drop in systemic blood pressure, but it can also be the result of a mild drop in central aortic pressure compounded with severe stenosis or occlusion of the vertebral or basilar arteries. A patient may have a severe vertebral artery (VA) stenosis or occlusion but be free of symptoms because of flow compensation from the opposite vertebral artery or from the internal or external carotid arteries. Symptoms caused by vertebral artery dissection can be a result of both the

low-flow mechanism (collapse of the true lumen by the dissecting hematoma) or microembolization (reentry of fragments of the dissecting hematoma into the true lumen through the distal tear of the dissection). When considering low-flow VBI, it is important to bear in mind that a cause-and-effect relationship between the VA stenosis and the syndrome cannot be presumed until a number of medical entities have been ruled out as being causative factors. Treatment of low-flow VBI requires consideration of the different possible etiologies of this clinical entity, and to rule them out, the collaboration of a cardiologist, an otolaryngologist, and a neurologist are often needed. Once the common medical causes of VBI have been ruled out, a computed tomography arteriogram (CTA) or a conventional arteriography is indicated. When an arteriogram is needed, special techniques and views are required. The VA is conventionally divided into four segments:   

1. The first segment (VI) extends from the origin of the VA in the subclavian artery to the point where the VA enters the cervical spine, usually at the level of the transverse process of C6. 2. The V2 segment is the bony cervical course from C6 to the top of C2. 3. The third segment (V3) begins at the top of the transverse process of V2 and ends at the atlanto-occipital membrane, where the VA starts its intradural course. 4. The fourth segment (V4) covers the intradural course of the artery from the atlanto-occipital membrane to the point where it joins the opposite VA to form the basilar artery.

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CEREBROVASCULAR DISEASE

caused by FMD. Fava and associates reported 12 patients treated with Wallstents (Boston Scientific, Freemont, CA) for symptomatic carotid dissections refractory to anticoagulation therapy. Adjuvant thrombolysis was used in patients with occlusions. Acute symptoms resolved in 66% and stabilized in 34%. All stents were patent at 24 months. Edgell and colleagues reported symptomatic improvement in seven patients treated with angioplasty and stenting of 12 dissected carotid arteries, five of which were caused by FMD. Self-expanding stent grafts offer a promising alternative to treating patients with carotid aneurysms or symptomatic FMD lesions with irregular membranes and large outpouches. The availability of lowprofile self-expanding stent grafts has allowed treatment of patients who have more difficult anatomy. Assadian and colleagues reported the use of Viabahn stent grafts to treat carotid FMD lesions complicated by dissections, stenoses, and aneurysms. In this series, which predated flow-reversal devices and low-profile delivery, direct exposure of the carotid artery was used to induce flow reversal, which was used during stent-graft deployment. There was one post-procedure TIA and no strokes or cranial nerve injuries. All stent grafts remained patent, and there were no recurrent symptoms at a mean follow-up of 4 years. A systematic review of 224 patients treated for carotid aneurysms by stent grafts showed in-hospital mortality of 4% and 30-day stroke rate of 1.8%. Primary stent-graft patency was 93% at mean follow-up of 15 months. Cohen and associates reported the use of smaller 4-mm self-expanding covered stents (Symbiotic stent, Boston Scientific, Bloomington, MN). The use of flow-diversion stents, which have been approved to treat intracranial aneurysms, has not yet been reported for FMD lesions but may be of use in selected cases.

made endovascular treatment of these lesions effective, with lowprofile balloons and stents using embolic protection devices. Our preference is to employ reversal of flow for embolic protection and revascularization with self-expanding stents or stent grafts.

Selected References Assadian A, Senekowitsch C, Assadian O, et al: Combined open and endovascular stent grafting of internal carotid artery fibromuscular dysplasia: long term results, Eur J Vasc Endovasc Surg 29:345–349, 2005. Ballard JL, Guinn JE, Killeen JD, et al: Open operative balloon angioplasty of the internal carotid artery: a technique in evolution, Ann Vasc Surg 390–393, 1995. Cohen JE, Grigoriadis S, Gomori JM, et al: Petrous carotid artery pseudoaneurysm in bilateral carotid fibromuscular dysplasia: treatment by means of self-expanding covered stents, Surgical Neurology 68:216–220, 2007. Edgell RC, Abou-Chebl A, Yadav JS: Endovascular management of spontaneous carotid artery dissection, J Vasc Surg 42:854–860, 2005. Effeney DJ, Krupski WC, Stoney RJ, et al: Fibromuscular dysplasia of the carotid artery, Aust N Z J Surg 53:527–531, 1983. Fava M, Meneses L, Loyola S, et al: Carotid artery dissection: endovascular treatment in 12 patients, Cath Cardiovasc Interv 71:694–700, 2008. Li Z, Chang G, Yao C, et al: Endovascular stenting of extracranial carotid artery aneurysm: a systematic review, Eur J Vasc Endovasc Surg 42:419–426, 2011. Muller BT, Luther B, Hort W, et al: Surgical treatment of 50 carotid dissections: Indications and results, J Vasc Surg 31:980–398, 2000. Olin JW, Sealove BA: Diagnosis, management, and future developments of fibromuscular dysplasia, J Vasc Surg 53:826–836, 2011. Schneider PA: Endovascular and surgical management of extracranial carotid fibromuscular arterial dysplasia. In Cronenwett JL, Johnston KW, (eds): Rutherford’s vascular surgery, 7th ed, Philadelphia, 2010, Saunders, pp.1487–1496

SUMMARY Indications for endovascular treatment of carotid FMD are the presence of symptoms or aneurysm. Technological improvements have

Vertebral Artery Reconstruction for Vertebrobasilar Ischemia Ramon Berguer

Vertebrobasilar ischemia (VBI) is a syndrome with different etiologies. The term insufficiency, which is still commonly used, should be abandoned because it implies only a low-flow condition affecting the vertebrobasilar territory and ignores the important mechanism of microembolization that constitutes approximately a third of the VBI pathology. Low-flow VBI is more often than not caused by a drop in systemic blood pressure, but it can also be the result of a mild drop in central aortic pressure compounded with severe stenosis or occlusion of the vertebral or basilar arteries. A patient may have a severe vertebral artery (VA) stenosis or occlusion but be free of symptoms because of flow compensation from the opposite vertebral artery or from the internal or external carotid arteries. Symptoms caused by vertebral artery dissection can be a result of both the

low-flow mechanism (collapse of the true lumen by the dissecting hematoma) or microembolization (reentry of fragments of the dissecting hematoma into the true lumen through the distal tear of the dissection). When considering low-flow VBI, it is important to bear in mind that a cause-and-effect relationship between the VA stenosis and the syndrome cannot be presumed until a number of medical entities have been ruled out as being causative factors. Treatment of low-flow VBI requires consideration of the different possible etiologies of this clinical entity, and to rule them out, the collaboration of a cardiologist, an otolaryngologist, and a neurologist are often needed. Once the common medical causes of VBI have been ruled out, a computed tomography arteriogram (CTA) or a conventional arteriography is indicated. When an arteriogram is needed, special techniques and views are required. The VA is conventionally divided into four segments:   

1. The first segment (VI) extends from the origin of the VA in the subclavian artery to the point where the VA enters the cervical spine, usually at the level of the transverse process of C6. 2. The V2 segment is the bony cervical course from C6 to the top of C2. 3. The third segment (V3) begins at the top of the transverse process of V2 and ends at the atlanto-occipital membrane, where the VA starts its intradural course. 4. The fourth segment (V4) covers the intradural course of the artery from the atlanto-occipital membrane to the point where it joins the opposite VA to form the basilar artery.



Vertebral Artery Reconstruction for Vertebrobasilar Ischemia

PATIENT EVALUATION The syndrome of VBI is well defined even though its clinical manifestations are more ambiguous and less precise than those caused by ischemia of the anterior circulation. Standard neurologic textbooks give a detailed description. A brief listing of symptoms includes any or several of the following: dizziness, vertigo, diplopia, blurring of vision, tinnitus, perioral numbness, alternating paresthesias, and drop attacks. The history should clarify the precise sequence of events that results in VBI. In most patients, the symptoms, particularly lightheadedness, appear on orthostatism when rising from bed or from a chair. Although this does not rule out a VA lesion as etiology, it draws attention to the possibility that one may be dealing with poor peripheral vasomotor control as seen in diabetics or in patients taking antihypertensive drugs experiencing autonomic dysfunction. Concurrence of palpitation during attacks of VBI suggests a cardiac arrhythmia causing a temporary drop in cardiac output and hypotension. Vertigo or syncope triggered by neck rotation or extension suggest extrinsic compression of a VA in its bony cervical course (segments V2 and V3) and requires a specific arteriography technique—dynamic angiography—to demonstrate this mechanism. Carotid symptoms are uncommon in patients experiencing VBI. When they do occur, it is usually a case of bilateral internal carotid artery (ICA) occlusion and an anterior circulation dependent on posterior (basilar) inflow. Examination of the patient must include the taking of bilateral brachial pressures. A difference greater than 25 mm Hg suggests a subclavian artery stenosis or occlusion and the possibility of subclavian steal syndrome. A drop in brachial pressure after the patient stands briskly shows that an orthostatic component is present. A 25 mm Hg drop in systolic pressure after briskly standing up is the arbitrary indicator of significant orthostatic hypotension. Supraclavicular bruits can suggest subclavian or VA disease but have no specificity, and the absence of bruits has no clinical significance. A dampened and delayed radial pulse in one wrist is evidence of a lengthened and narrowed pulse pathway associated with a subclavian steal syndrome. Vertigo and nystagmus provoked by brisk head rotation to both sides suggests labyrinthine dysfunction. Slow rotation to one side that, after a delay of 1 to 2 seconds, results in dizziness, dysequilibrium, or syncope suggests external compression of the VA by bone (bow hunter syndrome). Duplex scanning of both carotid and vertebral arteries is indicated in all cases. Holter monitoring of cardiac rhythm is indicated if cardiac arrhythmia is suspected. The antihypertensive drugs the patient is taking and their dosage should be reviewed. In specific cases (symptoms induced by brisk shaking of the head), labyrinthine function tests are indicated. The primary imaging tool for vertebral artery disease is a CTA of the head and neck. CTA displays stenosis, dissection, occlusion, and false aneurysm of the VA and will give information on the status of the posterior communicating and basilar arteries. The search for infarctions in the brain stem or cerebellum requires magnetic resonance imaging (MRI) because computed tomography (CT) cannot resolve the small infarcts occurring in the brain stem. The brain stem is surrounded by dense bone that causes diffraction artifacts. The standard arteriogram includes at least an intraarterial digital view of the arch in both the right and the left posterior oblique projections and selective injections of both carotids and the left subclavian arteries. The vertebrobasilar system must be displayed in its entirety from the origin of the VA to the top of the basilar artery. There is no reason to selectively catheterize a VA, a procedure that can result in a dissection. Arch views will document if the left VA originates from the arch (7%). The point of entrance of the VA into the cervical vertebral canal should be determined because this information is relevant to the choice of operation. Vertebral arteries are usually of different size, and deciding which one is dominant is important because the latter will

123

be the one chosen for reconstruction in patients with low-flow symptoms. The left VA is more commonly the dominant one. Incomplete or hypoplastic vertebrals that terminate in a posteroinferior cerebellar artery are not uncommon (7%). These arteries do not contribute to basilar flow. When quantifying disease in both VA in order to make a surgical decision, these incomplete arteries are considered occluded. The most common and most easily missed atherosclerotic lesion of the VA is a short and severe stenosis at its origin. The entire lesion may be obscured by the superimposition of the subclavian artery. This requires additional oblique views to throw off the first segment of the subclavian artery that obscures the origin of the VA. If one or both vertebral arteries are occluded, demonstration of their reconstitution at V3 is sought in subtracted and delayed views. This provides essential information in the planning stage of a VA reconstruction because demonstration of reconstituted V3 and V4 segments distal to a proximally occluded VA makes it technically possible to bypass the artery at the C2–C1 level to provide new basilar artery inflow. At, or just distal to, the level of the atlanto-occipital membrane, the VA can have a short stenosis difficult to discern in the usual arteriographic views. It is important not to overlook these stenoses because, when they are critical, they contraindicate a proximal VA reconstruction. The basilar artery in the lateral projection is overlain by the temporal bone and in the Towne anteroposterior (AP) projection is foreshortened. Its normalcy needs to be assessed because severe disease of the basilar artery contraindicates any VA reconstruction. In patients with rotational symptoms, additional views (dynamic arteriography) are indicated. These are done by selective subclavian injections with rotation-extension of the head while inducing axial compression of the latter to show the interruption of VA flow, usually in the V3 segment (bow hunter syndrome).

INDICATIONS FOR OPERATION For patients with symptoms of distal microembolization, the VA with the lesion likely to be the source of emboli (false aneurysm, ulcerated plaque, dissection) is selected for reconstruction. For patients with low-flow VBI, the lesion in the dominant VA is the one selected. When critical stenoses are present bilaterally, the dominant VA is chosen for reconstruction. Critical VA stenosis exists when both arteries are narrowed by 75 percent of their cross-sectional area or, in the case of a clearly dominant or single VA, when its lumen is narrowed by the same percentage. A normal VA of appropriate size perfusing the basilar artery contraindicates an operation for low-flow VBI on the opposite VA, regardless of the severity of the lesions of the latter. A positive dynamic arteriogram finding consists in flow stoppage or severe restriction in a dominant VA during rotation–extension of the head concomitant with the appearance of symptoms.

SURGICAL REPAIR For proximal lesions (V1 segment), the author's preferred technique is the transposition of the VA to the common carotid artery. A second option, used rarely, is a subclavian–vertebral bypass.

Transposition of the Proximal VA to the Common Carotid Artery The incision starts at the head of the clavicle and follows a line that bisects the angle formed by the clavicle and the anterior edge of the sternomastoid muscle. The two heads of the sternomastoid are separated. The underlying omohyoid is the only muscle that needs to be divided. The common carotid is exposed and retracted medially while the internal jugular vein and vagus nerve are retracted laterally

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CEREBROVASCULAR DISEASE

by means of soft neurosurgical malleable retractors. Dissection stays medial to the scalenus anticus and the prescalene fat pad. On the left side the thoracic duct is identified and divided between ligatures without transfixion. The dissection proceeds posterior to the common carotid artery, and the sympathetic chain is identified. The vertebral vein is identified and after its division, the VA can be found beneath it. The V1 segment of the VA is freed from the overlying intermediate cervical sympathetic ganglion and its rami. It is now possible to estimate how much length of healthy VA is available and how it would best fit when transposed to the common carotid artery. After the adventitia is excised, the spot selected for reimplantation in the common carotid is marked with methylene blue. The patient is given systemic heparin sodium. A Heifetz microsurgical clip is placed in the distal portion of the V1 segment and the origin of the VA is suture-ligated proximally and, in addition, secured with a hemoclip. The artery is then divided above its origin, and the distal mouth of the VA is inspected. If the free end contains a fragment of plaque in its edge, the plaque can be removed by eversion, leaving a clean breakoff. The artery is spatulated and trimmed, preparing it for anastomosis. The carotid artery is clamped using a baby Satinsky clamp that immobilizes the area of anastomosis but allows an assistant to displace the common carotid artery toward the VA to avoid tension during the anastomosis. The carotid arteriostomy is made with a 5-mm aortic punch. The anastomosis is done with continuous 7–0 polypropylene, using an open suture technique. The arteries are individually backbled into the wound. Flow is resumed first into the VA and then into the distal common carotid artery.

Proximal Subclavian–Vertebral Bypass The subclavian artery is approached by a transverse supraclavicular incision, which progresses through the scalene fat pad, preserving the phrenic nerve and exposing the subclavian artery after the scalenus anticus is divided. The VA is identified under the vertebral vein and dissected up to the point where it disappears under the longus colli muscle. The intermediate ganglion is left intact. If the VA is elongated, there may be enough length to reimplant it into another spot in the wall of the subclavian artery or into a thyrocervical stump. A vein bypass is placed between the subclavian artery and the distal VA. A segment of vein from the ankle usually approximates the diameter of the VA. End-to-end distal anastomosis is performed using 7–0 polypropylene to the trimmed distal segment of VA. The proximal anastomosis is end-to-side to the subclavian artery. It is important not to leave any slack in the graft.

Distal VA Reconstruction (Bypass) Severe disease or occlusion in the V2 segment is corrected by means of a distal (V3) vein bypass, preferably from the common carotid artery and occasionally from the external carotid artery. The distal bypass operation is the standard operation for any critical VA lesion at or above C6. The artery is bypassed to the level of C2–C1. This is the best site for reconstructing the distal VA because it is the widest of the bony gaps between the transverse processes of the cervical spine. This level is also above the points where the VA is compressed by osteophytes. Another advantage of this intertransverse space is that when the VA is occluded proximally it reconstitutes at the level of C2. The incision is similar to that used for ICA endarterectomy. The space between the internal jugular vein and the posterior edge of the sternomastoid muscle is dissected, identifying the spinal accessory nerve, which is then freed upward. As the nerve is dissected cranially, an index finger slid under the digastric muscle can feel the nerve in front of the sharp prominence of the transverse

process of C1. The digastric muscle is divided. The exposed transverse process of C1 constitutes the upper limit of the surgical field. The anterior and posterior edges of the levator scapula muscle are exposed, and the C2 ramus is identified as it exits below the medial edge of the levator. The levator scapulae is divided over the C2 ramus. Once the ramus is exposed, the closely attached VA can be seen crossing below and perpendicular to it. The C2 ramus is divided where it is still a single trunk before it divides into three branches. The artery is then exposed. Dissection around the artery requires bipolar coagulation of the surrounding venous plexus and care to avoid injuring any arterial collateral entering its posteromedial wall, usually an anastomotic connection with the occipital artery. With the artery exposed and secured with a silicone–elastic loop, the common carotid artery is dissected. The site for the proximal anastomosis of the graft is chosen below and clear of the bifurcation so that the clamp used to isolate the segment of common carotid artery does not crush any atheroma that may be present in the bifurcation. The saphenous vein graft is usually taken from the thigh. The VA is cross-clamped with an specially designed short baby J clamp. The vein graft is anastomosed to the VA end-to-side with 7-0 polypropilene. The graft is channeled under the jugular vein and its proximal end is anastomosed to a 5-mm punch arteriotomy to the common carotid artery in end-to-side fashion. Other possible arrangements to revascularize the distal VA are: (1) transposing the distal VA to the ipsilateral postbulbar ICA (a technique that should not be used if the contralateral internal carotid is occluded) and (2) traansposing the external carotid artery to the distal VA providing the origin of the former is free of disease.

Reconstruction and Decompression of the VA of the C0–C1 Level In patients presenting with the bow-hunter syndrome, the compression of the VA with rotation can occur at C1 or above C1 between its lamina and the occipital bone in the proatlantal segment of the VA. To access the VA at this level and to remove the bone element of compression, the approach is posterior, through the suboccipital space. The patient is either prone or in the park-bench position. The incision is horizontal below the occipital ridge and is prolonged in a racket fashion toward the posterior belly of the sternomastoid muscle for about an inch. The posterior nuchal muscles are divided. The sharp edge of the posterior lamina of C1 is identified and exposed using a periosteal elevator. The VA above the lamina is covered with a dense venous plexus. If the operation requires a bypass at this level, the plexus is controlled with bipolar coagulation. If no reconstruction of the artery is needed, the artery and its surrounding venous plexus are retracted superiorly and protected by a small malleable retractor. A segment of approximately 2 cm of the posterior lamina is exposed for laminectomy. At this stage there is bleeding from the epidural plexus of veins in the ventral aspect of the lamina that is controlled by mild elevation of the head of the table and small cottonoids. The lamina is divided using a high-speed drill while the artery is protected and lifted with a small retractor. The sharp ends of the divided posterior arch are rounded off with a rongeur. If, as may be the case, there is no need to reconstruct the artery at this level, the operation concludes at this time. In some cases the integrity of the artery has been disrupted by a dissection that reaches the C1 level. In this rare situation a bypass can be constructed from the internal carotid artery. The internal carotid artery can be approached posteriorly through the same operative field after gently mobilizing cranial nerves IX, X, and XII, which cover the posterior aspect of the internal carotid artery at the entrance of the temporal canal.



Endovascular Angioplasty and Stenting for Proximal Subclavian Artery Stenosis

Selected References Berguer R: Distal vertebral artery bypass: technique, the occipital connection and potential uses, J Vasc Surg 2:621–626, 1985. Berguer R: Suboccipital approach to the distal vertebral artery, J Vasc Surg 30:344–349, 1999. Berguer R, Andaya LV, Bauer RB: Vertebral artery bypass, Arch Surg 111:976–979, 1976. Berguer R, Feldman AJ: Surgical reconstruction of the vertebral artery, Surgery 93:670, 1983.

Endovascular Angioplasty and Stenting for Proximal Subclavian Artery Stenosis Ali F. AbuRahma and Patrick A. Stone

The prevalence of atherosclerotic stenotic disease involving the proximal brachiocephalic arteries is significantly less than that in the extracranial carotid arteries. Additionally, only 10% of patients with hemodynamically significant proximal subclavian artery stenoses develop symptoms. This probably reflects the robust collateral network distal to ostial subclavian artery stenosis, including the vertebral and internal mammary arteries. Unfortunately, there is a paucity of data on the natural history of untreated proximal subclavian artery stenosis. The incidence of subclavian steal syndrome was evaluated in more than 7881 patients undergoing carotid artery duplex scanning. A pressure difference of more than 20 mm Hg, indicating subclavian artery stenosis, was found in 514 (6.5%); however, symptoms were only present in 38 patients, with the majority being related to the posterior circulation. Patients with a difference of greater than 40 mm Hg in the extremities were more likely to have associated symptoms. In patients undergoing evaluation for coronary artery disease, 2.5% were found to have significant proximal left subclavian artery stenosis. The MESA study (Multi-Ethnic Study of Atherosclerosis) evaluated 6743 patients and reported that 4.6% of patients had subclavian stenosis, as defined by a systolic blood pressure difference of 15 mm Hg. There was also a higher prevalence in women (5.1%) compared with African Americans and men (3.9%).

CLINICAL EVALUATION AND DIAGNOSIS Most patients with subclavian stenosis are asymptomatic. Patients are often referred for evaluation by primary care physicians after they find asymmetry in the upper extremity blood pressures. A brachial blood pressure difference exceeding 15 to 20 mm Hg is considered a significant finding. Symptoms of subclavian artery stenosis can occur either in the form of exertional ischemia of the extremity (limb fatigue or pain) or, rarely, digital embolization, which can manifest as ulcerations

125

Berguer R, Higgins RF, Nelson R: Noninvasive diagnosis of reversal of vertebral artery flow, N Engl J Med 302:1349–1351, 1980. Berguer R, Morasch MD, Kline RA: A review of 100 consecutive reconstructions of the distal vertebral artery for embolic and hemodynamic disease, J Vasc Surg 27:852–859, 1998. Caplan L, Tettenborn B: Embolism in the posterior circulation. In Berguer R, Caplan L, (eds): Vertebrobasilar arterial disease, St Louis, 1992, Quality Medical, pp. 52–65.

or nonhealing wounds. Vertebrobasilar symptoms can occur in patients with reversal of flow in the vertebral artery, and this is referred to as subclavian steal syndrome. Angina or acute myocardial infarction can occur in patients with a previously placed internal mammary bypass and hemodynamically significant proximal subclavian stenosis. Rarely, patients present with pseudohypotension and are found to have severe bilateral subclavian artery stenoses. Physical examination should include an inspection of the hand and digits for evidence of embolic phenomena; palpation of the brachial, radial, and ulnar arteries; auscultation of the supraclavicular fossa for bruits; and a recording of bilateral brachial artery pressures. Duplex examination should be the first imaging modality to assess patients with suspected symptomatic disease. Standard imaging of the extracranial carotid arteries should be performed to assess for concomitant disease affecting these vessels, as well as an indirect assessment of the proximal carotid arteries by waveform and velocity analysis. A duplex examination of the subclavian and axillary arteries can suggest significant proximal subclavian artery disease in the presence of elevated peak systolic velocities or monophasic waveforms. However, no recognized duplex criteria have been widely accepted in assessing these arteries. A duplex examination of the vertebral artery should include direction of blood flow: antegrade, bidirectional, or reversed. Bidirectional or reversed flow suggests high-grade subclavian stenosis or occlusion or disease of the innominate artery. Conventional subtraction angiography is the gold standard for establishing the diagnosis of a subclavian arterial stenosis and has the added benefit of an optional therapeutic intervention during the diagnostic procedure. Computed tomography and magnetic resonance arteriography have limited utility for evaluating subclavian artery stenosis before conventional angiography.

INDICATIONS FOR TREATMENT We consider asymptomatic, good-risk patients with severe bilateral subclavian artery disease for treatment in order to facilitate accurate ambulatory blood pressure measurements. Additionally, asymptomatic patients with severe proximal left subclavian artery stenosis should be considered for intervention before coronary artery bypass grafting if the left internal mammary artery is to be used as a conduit. Symptomatic patients with exertional arm ischemia, vertebrobasilar symptoms such as subclavian steal, or angina related to a previous left internal mammary artery bypass are also offered treatment. Patients with vertebrobasilar symptoms or symptoms of subclavian steal with concomitant significant carotid artery stenosis should undergo carotid reconstruction prior to subclavian reconstruction, which may relieve their symptoms. Endovascular treatment of subclavian artery stenosis can be performed with local sedation and minimal morbidity, but the threshold for intervention should not be lower than that of open surgical therapy. Additionally, although endovascular techniques have continued



Endovascular Angioplasty and Stenting for Proximal Subclavian Artery Stenosis

Selected References Berguer R: Distal vertebral artery bypass: technique, the occipital connection and potential uses, J Vasc Surg 2:621–626, 1985. Berguer R: Suboccipital approach to the distal vertebral artery, J Vasc Surg 30:344–349, 1999. Berguer R, Andaya LV, Bauer RB: Vertebral artery bypass, Arch Surg 111:976–979, 1976. Berguer R, Feldman AJ: Surgical reconstruction of the vertebral artery, Surgery 93:670, 1983.

Endovascular Angioplasty and Stenting for Proximal Subclavian Artery Stenosis Ali F. AbuRahma and Patrick A. Stone

The prevalence of atherosclerotic stenotic disease involving the proximal brachiocephalic arteries is significantly less than that in the extracranial carotid arteries. Additionally, only 10% of patients with hemodynamically significant proximal subclavian artery stenoses develop symptoms. This probably reflects the robust collateral network distal to ostial subclavian artery stenosis, including the vertebral and internal mammary arteries. Unfortunately, there is a paucity of data on the natural history of untreated proximal subclavian artery stenosis. The incidence of subclavian steal syndrome was evaluated in more than 7881 patients undergoing carotid artery duplex scanning. A pressure difference of more than 20 mm Hg, indicating subclavian artery stenosis, was found in 514 (6.5%); however, symptoms were only present in 38 patients, with the majority being related to the posterior circulation. Patients with a difference of greater than 40 mm Hg in the extremities were more likely to have associated symptoms. In patients undergoing evaluation for coronary artery disease, 2.5% were found to have significant proximal left subclavian artery stenosis. The MESA study (Multi-Ethnic Study of Atherosclerosis) evaluated 6743 patients and reported that 4.6% of patients had subclavian stenosis, as defined by a systolic blood pressure difference of 15 mm Hg. There was also a higher prevalence in women (5.1%) compared with African Americans and men (3.9%).

CLINICAL EVALUATION AND DIAGNOSIS Most patients with subclavian stenosis are asymptomatic. Patients are often referred for evaluation by primary care physicians after they find asymmetry in the upper extremity blood pressures. A brachial blood pressure difference exceeding 15 to 20 mm Hg is considered a significant finding. Symptoms of subclavian artery stenosis can occur either in the form of exertional ischemia of the extremity (limb fatigue or pain) or, rarely, digital embolization, which can manifest as ulcerations

125

Berguer R, Higgins RF, Nelson R: Noninvasive diagnosis of reversal of vertebral artery flow, N Engl J Med 302:1349–1351, 1980. Berguer R, Morasch MD, Kline RA: A review of 100 consecutive reconstructions of the distal vertebral artery for embolic and hemodynamic disease, J Vasc Surg 27:852–859, 1998. Caplan L, Tettenborn B: Embolism in the posterior circulation. In Berguer R, Caplan L, (eds): Vertebrobasilar arterial disease, St Louis, 1992, Quality Medical, pp. 52–65.

or nonhealing wounds. Vertebrobasilar symptoms can occur in patients with reversal of flow in the vertebral artery, and this is referred to as subclavian steal syndrome. Angina or acute myocardial infarction can occur in patients with a previously placed internal mammary bypass and hemodynamically significant proximal subclavian stenosis. Rarely, patients present with pseudohypotension and are found to have severe bilateral subclavian artery stenoses. Physical examination should include an inspection of the hand and digits for evidence of embolic phenomena; palpation of the brachial, radial, and ulnar arteries; auscultation of the supraclavicular fossa for bruits; and a recording of bilateral brachial artery pressures. Duplex examination should be the first imaging modality to assess patients with suspected symptomatic disease. Standard imaging of the extracranial carotid arteries should be performed to assess for concomitant disease affecting these vessels, as well as an indirect assessment of the proximal carotid arteries by waveform and velocity analysis. A duplex examination of the subclavian and axillary arteries can suggest significant proximal subclavian artery disease in the presence of elevated peak systolic velocities or monophasic waveforms. However, no recognized duplex criteria have been widely accepted in assessing these arteries. A duplex examination of the vertebral artery should include direction of blood flow: antegrade, bidirectional, or reversed. Bidirectional or reversed flow suggests high-grade subclavian stenosis or occlusion or disease of the innominate artery. Conventional subtraction angiography is the gold standard for establishing the diagnosis of a subclavian arterial stenosis and has the added benefit of an optional therapeutic intervention during the diagnostic procedure. Computed tomography and magnetic resonance arteriography have limited utility for evaluating subclavian artery stenosis before conventional angiography.

INDICATIONS FOR TREATMENT We consider asymptomatic, good-risk patients with severe bilateral subclavian artery disease for treatment in order to facilitate accurate ambulatory blood pressure measurements. Additionally, asymptomatic patients with severe proximal left subclavian artery stenosis should be considered for intervention before coronary artery bypass grafting if the left internal mammary artery is to be used as a conduit. Symptomatic patients with exertional arm ischemia, vertebrobasilar symptoms such as subclavian steal, or angina related to a previous left internal mammary artery bypass are also offered treatment. Patients with vertebrobasilar symptoms or symptoms of subclavian steal with concomitant significant carotid artery stenosis should undergo carotid reconstruction prior to subclavian reconstruction, which may relieve their symptoms. Endovascular treatment of subclavian artery stenosis can be performed with local sedation and minimal morbidity, but the threshold for intervention should not be lower than that of open surgical therapy. Additionally, although endovascular techniques have continued

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to improve since the turn of the century with lower-profile delivery systems, better stent design, and other advances, we do not agree that endovascular intervention is the first line of treatment in all patients or lesions. Nevertheless, most centers pursue angioplasty and stent placement, particularly in the management of subclavian and proximal carotid artery pathology.

TECHNICAL PRINCIPLES OF ENDOVASCULAR THERAPY Arterial access for diagnostic procedures and interventions on the proximal subclavian artery may be obtained through the femoral, brachial, or radial arteries. The preferred approach is the femoral artery. Brachial access has been fraught with more access-related complications when compared with the femoral access. Others gaining access through the radial artery have reported excellent technical success with limited access complications. Once access is achieved, arch angiography at 30 degrees left anterior oblique is performed with a pigtail catheter. Contrast injections at 15 to 20 mL/second, for a total injection of 30 to 40 mL, are routine. Evaluation of the great vessels should include type of aortic arch, degree of aortic disease, and status of contralateral vertebral artery. The length and severity of subclavian artery stenosis should be assessed, along with the proximity of the lesion to the vertebral and internal mammary arteries (Figure 1). Selective catheterization can be performed with a variety of catheters, based on the preference of the interventionalist and the type of aortic arch. Stenoses of greater than 75% are crossed with a hydrophilic wire after administration of 3000 to 5000 IU of unfractionated heparin. Purchase of the hydrophilic wire is achieved in the brachial artery. The diagnostic catheter is advanced and exchanged over a stiff wire; our preference is a 0.35-inch, 300-cm Hi Torque SupraCore Wire (Abbott Vascular, Calif.). The short 5-Fr sheath can be exchanged over the stiff wire for a long 6-Fr sheath in preparation for an intervention. Critical ostial stenosis should be predilated to allow safe advancement of a balloon-expandable stent across the lesion. The sheath should then be advanced just distal to the lesion (Figure 2). Ostial lesions are best treated with balloon-expandable stents and should be sized 1:1 with the native artery. Oversizing in this setting can result in arterial perforation. If the surgeon is unsure of the size of the native artery, intravascular ultrasound can be used to obtain a measurement. After the balloon-expandable stent is advanced to the end of the sheath, the sheath is withdrawn into the aortic arch, leaving the stent across the lesion. Only 2 mm of the proximal stent should protrude within the arch of the aorta. If the protrusion of the proximal stent is too long, this can limit future repeat interventions and can pose a hazard with future coronary catheterizations. Currently, there is no Federal Drug Administration–approved stent for use specifically in the subclavian artery, and off-label use is required if primary stenting is chosen or needed if an inadequate angioplasty is achieved. Occlusions of the subclavian artery can also be treated by endovascular techniques; however, understanding the anatomy in such cases is paramount to prevent complications (Figure 3). Flush occlusions typically require brachial access, and sometimes combined femoral access, to successfully cross the obstruction. When ostial occlusions are crossed, care must be taken to safely reenter the aorta. Creation of a subintimal plane can result in arch dissection, which can be fatal. Standard techniques commonly used in the femoral arteries can be used in the subclavian artery, including subintimal angioplasty, reentry devices, and others. Technical success in most series is nearly 100% for stenotic lesions, and ranges from 60% to 100% when treating occlusions. In most series, the ratio of cases treated for stenosis versus occlusions exceeds 3–4:1. Access-related complications account for the majority of morbidity in the perioperative period, including access site hematomas, false

FIGURE 1  Proximal subclavian artery stenosis before treatment.

FIGURE 2  Selective left subclavian angiogram: sheath advanced distal

to lesion.

aneurysms, and vessel thrombosis, among other problems. Ulcerative plaques with associated thrombus should be treated with caution, and embolic protection devices have been used in several case reports to limit vertebral or extremity embolic complications. When the vertebral artery has retrograde flow, embolic events to the posterior circulation are less likely (Figure 4). It has been reported to take minutes for flow to reverse to an antegrade direction after subclavian artery stenting. Our group, as well as others, advocates exercise of the left arm by squeezing a ball to augment flow in the brachial artery, which potentially reduces the risk of posterior circulation events. Neurologic complications can also occur secondary to catheter manipulation within the aortic arch. Interventions of the right subclavian are associated with a higher incidence of neurologic events secondary to the catheter crossing the arch vessels. Other rare complications include stent infections, arterial rupture, and aortic dissection. Understanding the pitfalls of endovascular treatment is imperative to minimize patient morbidity. Patients with hostile groins and small brachial arteries are at high risk of access-related complications. Patients with severe atherosclerotic aortic arch disease, ulcerative lesions, mural thrombus, and flush occlusions are at higher risk for atheroembolic complications. Treatment of lengthy stenoses in proximity to the vertebral and internal mammary arteries is more apt to compromise these branches.



Endovascular Angioplasty and Stenting for Proximal Subclavian Artery Stenosis

FIGURE 3  Left subclavian artery occlusion during arch angiography.

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FIGURE 4  Retrograde filling of left subclavian artery via left verte-

bral artery during arch angiography.

RESULTS OF SUBCLAVIAN ARTERY ANGIOPLASTY AND STENTING Historically, subclavian endovascular treatment was initially by angioplasty alone (PTA). Because most ostial lesions are the result of aortic spillover disease, plain balloon angioplasty fared poorly. In the early 1990s, Hebrang and colleagues reported the results of 52 patients with ostial subclavian artery stenosis or occlusions treated with PTA alone. A 93% primary patency rate was achieved at 4 years, with approximately a 50% primary patency rate in those treated for occlusions. Several other series have found similar results that imply inferiority of angioplasty alone for occlusions of the subclavian artery, compared to those treated for stenotic lesions. De Vries and coworkers analyzed a series of 110 patients treated with PTA with adjunct stenting of the subclavian artery and reported an 89% primary patency rate at 5 years. These results have provided evidence of long-term durability following stent placement. Additional series have shown similar results with greater than 90% technical success with stenosis and occlusions, as well as patency rates exceeding 70% at 5 years (Table 1). Factors influencing long-term outcomes of subclavian artery stenting were studied by our group. Over a 9-year period with a mean follow-up of 36 months, 91 patients had 101 stents placed. The primary patency decreased from 93% at 1 year to 72% at 5 years. There were no statistically significant predictors of restenosis, but there was a trend toward more in-stent stenosis in women. The presence of hypothyroidism and increasing age were strongly correlated with decreasing patient survival. Several series have specifically examined the results of subclavian artery PTA and stenting in patients who were scheduled to undergo coronary artery bypass grafting (CABG) or who previously underwent CABG using the left internal mammary artery as a conduit. Westerband and colleagues reported the results of 14 patients during a 4-year period. Nine patients presented with angina or heart failure after CABG, and five patients were treated before CABG. Thirteen patients were treated with PTA and/or stenting, and one was treated with carotid–subclavian bypass. During a mean follow-up of 29 months, in-stent stenosis was identified in two symptomatic patients. They reported an assisted patency rate of 100%. Similarly, Hwang’s group treated 20 patients with

angioplasty of the subclavian artery before or after CABG and reported patency rates at 2 and 5 years of 100% and 85%, respectively. Only one series has reported on endovascular treatment of failing brachiocephalic surgical reconstructions. Twenty-two patients with 24 symptomatic stenoses of previously placed Dacron bypass grafts were treated with balloon-expandable stents. Eleven patients were treated previously with carotid–subclavian bypass for isolated subclavian artery stenosis. The mean time from initial surgical reconstruction to symptomatic restenosis was 25 months. Two of the 11 patients developed recurrent in-stent stenosis at a mean follow-up of 29 months; both cases of stenosis were symptomatic and were subsequently treated with repeat endovascular therapy, with no major complications.

ENDOVASCULAR VERSUS SURGICAL INTERVENTION Unfortunately, no prospective randomized trials have been performed to compare endovascular and open surgical treatment strategies. Furthermore, only a few series have directly compared the results of subclavian artery PTA and stenting with surgical reconstruction (Table 2). In 1989, Farina and colleagues compared PTA alone with a carotid–subclavian bypass or transposition procedure. The mean follow-up exceeded 30 months in both groups, with similar 1-year patency rates. Late patency was inferior in the PTA group at 54%, versus 87% with surgical reconstruction. Similar findings were reported by Palchik and coworkers; however, the PTA group had adjunct stent placement. That series compared 67 stented subclavian arteries to 70 bypass and transposition procedures over a 14-year period. The assisted patency rate was 76% at 5 years, compared to a 90% primary patency rate with surgical reconstruction. Additional findings in this study were improved patency rates, based on the indication for intervention. Patients presenting with vertebrobasilar symptoms had improved patency rates, in comparison to those treated for arm claudication symptoms. The largest series of brachiocephalic reconstruction, comparing operative and endovascular management of single-vessel disease,

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TABLE 1:  Published Data on Subclavian Artery Percutaneous Transluminal Angioplasty and Stenting Reference

Arteries

Technical Success (%)

Stenosis and Occlusion (%)

Mean Follow-up (mo)

Henry et al.

237

192/192 (100)

31/45 (69)

65

67% PTA 89% PTA + stent at 120 mo

Patel et al.

177

155/156 (99)

19/21 (90)

35

83% at 66 mo

De Vries et al.*

110

89/89 (100)

13/20 (65)

40

89% at 60 mo

36

72% at 60 mo

13

92% at 18 mo

Bates

91

89/91(98)

Rodriguez-Lopez

70

50/53 (94)

17/17 (100)

Primary Patency

*In this study, 59 patients had stent placement, and the other patients had percutaneous transluminal angioplasty alone.

TABLE 2:  Published Series Comparing Subclavian Artery Stenosis and Occlusions Treated by Endovascular or Surgical Reconstruction PRIMARY PATENCY (%) Mean Follow-up 1 Yr

Reference

Treatment

5 Yr

Takach et al.

Stenting, n = 160 CSBG, n = 214

3.3 5.2

95 95

84 93

AbuRahma et al.

Stenting, n = 121 CSBG, n = 51

3.4 7.7

93 100

70 96

Palchik et al.

Stenting n = 67 CSBG/transp. n = 70

5 10

78 95

62 90

Farina et al.

PTA, n = 21 CSBG/transp., n = 15

2.5 3.3

91 87

54 87

CSBG, Carotid–subclavian bypass graft; PTA, percutaneous transluminal angioplasty; transp., subclavian–carotid transposition.

included nearly 400 procedures. When comparing the freedom from graft intervention or failure at 5 years, surgical bypass was superior to endovascular treatment: 93% versus 84%. That study also incorporated a satisfaction questionnaire that was completed by patients with both procedures, with a similar satisfaction rate for both groups exceeding 95%. Our group also compared carotid–subclavian bypass versus primary stenting for isolated subclavian artery disease in 121 patients treated with endovascular techniques and 51 patients with carotid– subclavian prosthetic bypass grafts. The early 30-day primary patency rate was 100% for the bypass group and 99% for the PTA and stent group. The 5-year primary patency rate was 96% for the carotid– subclavian bypass graft and 70% for PTA and stenting (p < .0001). Major complications in the surgical patients were limited to two phrenic nerve injuries that recovered over a 2-month period and one nonfatal myocardial infarction. In comparison, complications in the endovascular group included two embolic complications and one

death following coronary artery bypass grafting within 30 days of the stenting procedure. There was no significant difference in survival between both groups at 3 and 5 years.

CONCLUSION Endovascular treatment is recommended as the initial management of most symptomatic subclavian artery lesions. Patients with failed endovascular interventions, lesions that risk coverage of the vertebral artery, ostial occlusions, and those without an ostial stump may be considered for open surgical reconstructions as the initial procedure. Transcatheter treatment of the subclavian artery offers a minimally invasive procedure with acceptable short- and long-term results.

Selected References Aboyans V, Kamineni A, Allison MA, et al: The epidemiology of subclavian stenosis and its association with markers of subclinical atherosclerosis: the Multi-Ethnic Study of Atherosclerosis (MESA), Atherosclerosis 211:266–270, 2010. AbuRahma AF, Bates MC, Stone PA, et al: Angioplasty and stenting versus carotid–subclavian bypass for the treatment of isolated subclavian artery disease, J Endovasc Ther 14:698–704, 2007. Bates MC, Broce M, Lavigne PS, et al: Subclavian artery stenting: factors influencing long-term outcome, Catheter Cardiovasc Inter 61:5–11, 2004. de Vries Jean-Paul PM, Jager LC, van den Berg JC, et al: Durability of percutaneous transluminal angioplasty for obstructive lesions of proximal subclavian artery: long-term results, J Vasc Surg 41:19–23, 2005. Farina C, Mingoli A, Schultz RD, et al: Percutaneous transluminal angioplasty versus surgery for subclavian arterial disease, Am J Surg 158:511–514, 1989. Henry M, Henry I, Polydorou A, et al: Percutaneous transluminal angioplasty of the subclavian arteries, Int Angiol 26:324–340, 2007. Labropoulos N, Nandivada P, Bekelis K: Prevalence and impact of the subclavian steal syndrome, Ann Surg 252:166–170, 2010. Palchik E, Bakken AM, Wolford HY, et al: Subclavian artery revascularization: an outcome analysis based on mode of therapy and presenting symptoms, Ann Vasc Surg 22:70–78, 2008. Patel SN, White CJ, Collins TJ, et al: Catheter-based treatment of subclavian and innominate arteries, Catheter Cardiovasc Inter 7:963–968, 2008. Takach TJ, Duncan JM, Livesay JJ, et al: Brachiocephalic reconstruction. II: operative and endovascular management of single-vessel disease, J Vasc Surg 42:55–61, 2005.



Subclavian to Carotid Arterial Transposition

Subclavian to Carotid Arterial Transposition Mark D. Morasch

Cervical reconstruction of the subclavian artery is most commonly performed by a transposition onto or a bypass originating from the ipsilateral common carotid artery. There are advantages and disadvantages to both approaches, and the decision which to pursue often depends upon anatomic considerations and surgeon expertise. When performed by experienced surgeons, both procedures carry very low risk for complications. Although the long-term patency rate for arterial transposition is virtually 100%, the long-term patency rates for a bypass are commonly reported to be 10% to 15% poorer than for transposition. On the other hand, arterial transpositions might not be possible when the vertebral artery takes off early from the subclavian artery or when the atherosclerotic process extends far distally beyond the vertebral origin. Another indication for carotid–subclavian bypass, as opposed to a transposition, would be in the patient with a patent internal mammary artery–coronary artery graft. With the use of a cervical bypass, the arterial clamps can be placed beyond the internal mammary artery to avoid myocardial ischemia. Cervical reconstruction by a transposition should be considered the surgical technique of choice for single proximal occlusive lesions involving the subclavian artery. In addition, with the advent of endovascular therapy for thoracic aortic disease, surgical manipulation of the supra-aortic trunks to prepare patients with thoracic and thoracoabdominal aortic aneurysms, dissections, or traumatic tears have become accepted and commonplace (Figure 1). Subclavian artery reconstruction is now commonly performed to preserve vertebral and left upper extremity flow while extending the proximal neck landing zone before deploying an endograft. Many consider an aggressive approach to pre-­endograft revascularization of the left subclavian to optimize posterior brain, spinal cord, and upper extremity circulation to be imperative. Not

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only is preservation of the vertebral artery critical but it is equally important to mobilize and preserve the valuable internal mammary artery. Transposition of the left subclavian clearly has a prominent role, and when there is a usable ipsilateral source vessel, an arterial transposition should be the first choice. When performed properly, transposition not only preserves arm, vertebral, and mammary flow, it also obviates the need for proximal subclavian ligation or transcatheter embolization of the vessel to prevent the development and persistence of a large retrograde type II endoleak, as would occur following bypass. Arterial transpositions are completed through a short, transverse cervical incision above the clavicle. The incision is placed more medially than for bypass and is positioned to overlie the space between the two heads of the sternocleidomastoid muscle. The surgical dissection itself is carried out between the two heads of the sternocleidomastoid muscle. This is an important contradistinction to performing a bypass where the dissection is carried out lateral to the entire sternocleidomastoid muscle. For a transposition, after dividing the omohyoid muscle between ligatures or with electrocautery, the jugular vein is reflected laterally and the common carotid is reflected medially along with the vagus nerve. It is important to point out the difference in approach when compared to a bypass procedure. During a bypass, the jugular vein and vagus nerve are reflected medially to expose the common carotid beneath them. During a transposition, the medially reflected carotid is mobilized circumferentially with the dissection carried out deeply toward the mediastinum. On the left side, the thoracic duct and small identifiable lymphatics are identified, ligated, and divided (Figure 2). On the right, multiple cervical lymphatic channels must also be tied. After the vertebral vein is divided (Figure 3), the subclavian artery and its proximal branches can be identified behind the clavicle. If the vessel is patent, digital palpation can help with localization. Care must be taken when isolating and controlling the vertebral artery because it originates from an awkward position on the posterior aspect of the subclavian artery. The medial border of the anterior scalene muscle may be encountered with more lateral dissection. Again, in contradistinction from bypass, the anterior scalene is never divided for a transposition. Only slight lateral reflection of this muscle may be necessary to obtain control of the subclavian vessel distal to the thyrocervical trunk. For a bypass, the more distal

FIGURE 1  Images before and after

endograft deployment in a patient who has had subclavian transposition.  (Reprinted from Morasch M: Cervical transposition procedures. In Pearce WH, Matsumura JS,Yao JST (eds): Vascular surgery in the endovascular era, 2008, Greenwood Academic, pp. 452–456.)

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middle third of the subclavian artery is commonly exposed by dividing the anterior scalene muscle. During a bypass, care must be taken to avoid injury to the phrenic nerve during this more lateral approach. For transposition, the subclavian artery is dissected as far proximally as possible, also well into the mediastinum. During proximal

FIGURE 2  Ligation and division of the thoracic duct.  (Reprinted from

Repair of the supraaortic trunks. In Berguer R, Keiffer E (eds): Surgery of the arteries to the head, New York, 1992, Springer-Verlag pp. 84-107.)

FIGURE 3  Ligation and division of the vertebral

vein.  (Reprinted from Repair of the supraaortic trunks. In Berguer R, Keiffer E (eds): Surgery of the arteries to the head, New York, 1992, Springer-Verlag, pp. 84–107.)

subclavian dissection there is the potential to enter the pleural space anteriorly. This can be avoided by keeping the dissection close to the arterial wall. Care should also be taken to avoid disrupting sympathetic branches that cross anterior to the subclavian and ascend in the neck along side the vertebral artery. If multiple sympathetic fibers are cut, the patient can develop Horner’s syndrome, although it is usually only temporary. Once heparin anticoagulation has been established, the subclavian and its proximal branches are controlled. The vertebral, mammary, and thryocervical trunk are temporarily occluded with small microbulldog-type clamps. The distal subclavian can be controlled with loops or, preferably, with a profunda clamp. The proximal subclavian is then transected beyond a right-angled clamp or stapled with a vascular load stapler. It is important to secure the proximal stump of a patent subclavian immediately after the diseased artery has been divided; if control of the transected stump is lost in the chest or mediastinum, the consequences can be devastating. This specific risk does not accompany a bypass procedure. The carotid artery is then slightly rotated to expose the posterior aspect. It is clamped proximally and distally. A Satinsky clamp usually facilitates obtaining proximal control well behind the clavicle. A punch arteriotomy is created in the side of the donor carotid, and the end-to-side anastomosis is completed without tension. Occasionally some redundant subclavian must be resected to avoid a kink. The anastomosis is facilitated by using a parachute technique and by starting the suture line on the posterior wall (Figure 4). Rarely is the subclavian too short to reach to the side of the carotid. If this problem is encountered, more carotid can be mobilized to swing it farther laterally over to the subclavian. The vessel is flushed, the clamps are removed, and flow is reestablished into the vertebral artery last (Figure 5). A drain is useful to collect lymphatic fluid. The wound is closed by reapproximating the platysma muscle and skin. Transposition procedures carry very low risk for complications, and their durability is unsurpassed. Potential complications include bleeding, thrombosis, infection, stroke, pneumothorax, lymphatic or thoracic duct leak, recurrent laryngeal nerve palsy from vagus stretch, and Horner’s syndrome.



Subclavian to Carotid Arterial Transposition

FIGURE 4  Subclavian stump and transposition suture line.  (Reprinted

from Repair of the supraaortic trunks. In Berguer R, Keiffer E (eds): Surgery of the arteries to the head, New York, 1992, Springer-Verlag, pp. 84-107.)

A

B FIGURE 5  Completed transposition.  (A reprinted from Repair of the supraaortic trunks. In Berguer R, Keiffer E (eds): Surgery of the arteries to the head, New York, 1992, Springer-Verlag, pp. 84-107; B from Morasch M: Cervical transposition procedures. In Pearce WH, Matsumura JS,Yao JST (eds): Vascular surgery in the endovascular era, 2008, Greenwood Academic, pp. 452–456.)

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Selected References Berguer R, Morasch MD, Kline RA, et al: Friedland MS. Cervical reconstruction of the supra-aortic trunks: a 16-year experience, J Vasc Surg 29:239–246, 1999. discussion 246–238. Cina CS, Safar HA, Lagana A, et al: Subclavian carotid transposition and bypass grafting: consecutive cohort study and systematic review, J Vasc Surg 35:422–429, 2002.

Lee WA, Matsumura JS, Mitchell RS, et al: Endovascular repair of traumatic thoracic aortic injury: clinical practice guidelines of the Society for Vascular Surgery, J Vasc Surg 53:187–192, 2011. Peterson BG, Eskandari MK, Gleason TG, et al: Utility of left subclavian artery revascularization in association with endoluminal repair of acute and chronic thoracic aortic pathology, J Vasc Surg 43:433–439, 2006. Schardey HM, Meyer G, Rau HG, et al: Subclavian carotid transposition: an analysis of a clinical series and a review of the literature, Eur J Vasc Endovasc Surg 12:431–436, 1996.

Carotid–Subclavian Bypass and Other Nonanatomic Revascularizations for Proximal Subclavian Artery Stenosis

Carotid a. Vertebral a. Subclavian a.

John F. Eidt and Fredrick N. Southern Internal mammary a.

In the past, subclavian revascularization was most often performed to relieve either vertebrobasilar symptoms or exertional arm pain associated with subclavian steal syndrome. Currently, subclavian revascularization is increasingly undertaken to extend the proximal landing zone during endovascular management of thoracic aortic conditions including aneurysm, dissection, and trauma. Additionally, subclavian revascularization may be appropriate to maintain or restore normal inflow to the mammary artery used in coronary artery bypass (Figure 1). Surgical correction of subclavian steal syndrome is recommended for patients with severe, repetitive symptoms that affect lifestyle, increase the risk of injury from falling, or threaten the ability of the patient to live independently. In addition, carotid subclavian bypass is one of several techniques used to restore perfusion pressure to an internal mammary artery bypass used in a coronary artery revascularization. Bilateral brachial blood pressures should be checked in all patients before internal mammary bypass and reassessed if angina recurs at follow-up. Emergence of endovascular treatment for a variety of thoracic aortic conditions has led to a significant increase in the need for subclavian revascularization to extend the proximal landing zone and preserve spinal cord blood supply (Figure 2). While the role of subclavian revascularization continues to evolve, the Society for Vascular Surgery practice guidelines currently recommend routine preoperative subclavian revascularization in elective cases and in cases in which coverage of the subclavian artery would compromise perfusion of critical organs. In particular, subclavian revascularization is recommended in the settings of a dominant left vertebral artery, a left vertebral artery terminating in the posterior inferior cerebellar artery (PICA), or extensive coverage of the thoracic aorta, which could compromise spinal cord blood flow.

ANATOMY The subclavian artery travels laterally between the anterior and middle scalene muscles. Three segments of the subclavian artery

FIGURE 1  Subclavian steal. Because of decreased pressure distal to

subclavian artery stenosis or occlusion, blood flow may be reversed in the vertebral and internal mammary arteries to provide collateral circulation to the arm. Flow reversal may be present at all times or may be intermittent during arm exertion or neck movements that compress other cervical vessels.

A

B

FIGURE 2  Subclavian revascularization may be required to extend

the landing zone for thoracic endografting. A, Subclavian–carotid transposition. B, Carotid–subclavian bypass with synthetic graft  (Figure from Riesenman PJ, Farber MA, Mendes RR, et al: Coverage of the left subclavian artery during thoracic endovascular aortic repair, J Vasc Surg 45:90–95, 2007.)

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Selected References Berguer R, Morasch MD, Kline RA, et al: Friedland MS. Cervical reconstruction of the supra-aortic trunks: a 16-year experience, J Vasc Surg 29:239–246, 1999. discussion 246–238. Cina CS, Safar HA, Lagana A, et al: Subclavian carotid transposition and bypass grafting: consecutive cohort study and systematic review, J Vasc Surg 35:422–429, 2002.

Lee WA, Matsumura JS, Mitchell RS, et al: Endovascular repair of traumatic thoracic aortic injury: clinical practice guidelines of the Society for Vascular Surgery, J Vasc Surg 53:187–192, 2011. Peterson BG, Eskandari MK, Gleason TG, et al: Utility of left subclavian artery revascularization in association with endoluminal repair of acute and chronic thoracic aortic pathology, J Vasc Surg 43:433–439, 2006. Schardey HM, Meyer G, Rau HG, et al: Subclavian carotid transposition: an analysis of a clinical series and a review of the literature, Eur J Vasc Endovasc Surg 12:431–436, 1996.

Carotid–Subclavian Bypass and Other Nonanatomic Revascularizations for Proximal Subclavian Artery Stenosis

Carotid a. Vertebral a. Subclavian a.

John F. Eidt and Fredrick N. Southern Internal mammary a.

In the past, subclavian revascularization was most often performed to relieve either vertebrobasilar symptoms or exertional arm pain associated with subclavian steal syndrome. Currently, subclavian revascularization is increasingly undertaken to extend the proximal landing zone during endovascular management of thoracic aortic conditions including aneurysm, dissection, and trauma. Additionally, subclavian revascularization may be appropriate to maintain or restore normal inflow to the mammary artery used in coronary artery bypass (Figure 1). Surgical correction of subclavian steal syndrome is recommended for patients with severe, repetitive symptoms that affect lifestyle, increase the risk of injury from falling, or threaten the ability of the patient to live independently. In addition, carotid subclavian bypass is one of several techniques used to restore perfusion pressure to an internal mammary artery bypass used in a coronary artery revascularization. Bilateral brachial blood pressures should be checked in all patients before internal mammary bypass and reassessed if angina recurs at follow-up. Emergence of endovascular treatment for a variety of thoracic aortic conditions has led to a significant increase in the need for subclavian revascularization to extend the proximal landing zone and preserve spinal cord blood supply (Figure 2). While the role of subclavian revascularization continues to evolve, the Society for Vascular Surgery practice guidelines currently recommend routine preoperative subclavian revascularization in elective cases and in cases in which coverage of the subclavian artery would compromise perfusion of critical organs. In particular, subclavian revascularization is recommended in the settings of a dominant left vertebral artery, a left vertebral artery terminating in the posterior inferior cerebellar artery (PICA), or extensive coverage of the thoracic aorta, which could compromise spinal cord blood flow.

ANATOMY The subclavian artery travels laterally between the anterior and middle scalene muscles. Three segments of the subclavian artery

FIGURE 1  Subclavian steal. Because of decreased pressure distal to

subclavian artery stenosis or occlusion, blood flow may be reversed in the vertebral and internal mammary arteries to provide collateral circulation to the arm. Flow reversal may be present at all times or may be intermittent during arm exertion or neck movements that compress other cervical vessels.

A

B

FIGURE 2  Subclavian revascularization may be required to extend

the landing zone for thoracic endografting. A, Subclavian–carotid transposition. B, Carotid–subclavian bypass with synthetic graft  (Figure from Riesenman PJ, Farber MA, Mendes RR, et al: Coverage of the left subclavian artery during thoracic endovascular aortic repair, J Vasc Surg 45:90–95, 2007.)



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Carotid–Subclavian Bypass and Other Nonanatomic Revascularizations

are defined by their relation to the anterior scalene muscle. The internal mammary artery, the vertebral artery, and the thyrocervical trunk arise from the first part of the subclavian artery medial to the anterior scalene muscle. The thyrocervical trunk gives rise to the inferior thyroid artery, the suprascapular artery, and the transverse cervical artery, which may be safely ligated if necessary. The costocervical trunk typically originates from the second part of the subclavian artery deep to the anterior scalene muscle and divides into the superior (supreme) intercostal artery and the deep cervical artery. The deep cervical artery can represent a significant ascending collateral vessel in the setting of ipsilateral vertebral occlusive disease. The third segment of the subclavian artery gives rise to the dorsal scapular artery, typically at the lateral border of the first rib, marking the distal boundary of the subclavian artery. Substantial variation in the branches of the subclavian artery are common and must be anticipated to avoid bothersome bleeding.

Sternocleidomastoid m.

Anterior scalene m. Internal jugular v. Phrenic n. Common carotid a. Vertebral a.

CAROTID–SUBCLAVIAN BYPASS General anesthesia is preferred for carotid–subclavian bypass. The patient is positioned with the head turned to the opposite side. Prophylactic antibiotics are administered. A transverse incision is made a fingerbreadth above the medial third of the clavicle (Figure 3). The platysma and clavicular head of the sternocleidomastoid are divided. To make the graft as short as possible, we mobilize the scalene fat pad medially. The phrenic nerve is identified on the surface of the anterior scalene muscle coursing diagonally from lateral to medial. The anterior scalene muscle is divided, taking care to avoid injury to the phrenic nerve. The thoracic duct may be ligated and divided near the point that it enters the venous system at the junction of the internal jugular and subclavian veins to prevent a postoperative lymph leak. The subclavian artery lies just deep to the anterior scalene muscle. The thyrocervical trunk, internal mammary artery, and vertebral artery are identified. The vertebral vein may be divided, if needed. The lower cords of the brachial plexus are located posterolateral at this level. The sympathetic chain lies just deep to the origin of the vertebral artery, and injury at this level will result in Horner’s syndrome (ptosis, miosis, and anhydrosis). The internal jugular vein is retracted medially, and the common carotid artery (CCA) is dissected circumferentially, taking care to avoid injury to the vagus nerve. The proposed anastomotic site is marked with ink on the lateral wall of the common carotid artery (Figure 4). After systemic anticoagulation with heparin sodium (100 U/kg), the common carotid is occluded between vascular clamps and rotated anteriorly to provide easy access to the planned anastomotic site. An arteriotomy is made in the lateral wall of the CCA with a No. 11 blade and enlarged appropriately with a cardiac punch. It is important to avoid an anastomosis on the anterior surface of the CCA because this can cause a kink in the graft. The authors do not routinely use a shunt, but a shunt may be appropriate in the setting of contralateral carotid occlusion. The arteriotomy is relatively low in the neck so that the graft lies parallel to the apex of the subclavian artery and is as short as possible (2–4 cm). We prefer to use an 8-mm woven polyester graft for the bypass, but the size should be chosen to match the subclavian outflow. An end-to-side anastomosis is made between the end of the graft and the side of the CCA with 5–0 polypropylene suture. The common carotid artery must be carefully back bled and forward flushed before carotid flow is restored to prevent embolism of air or thrombotic debris. The graft is routed posterior to the jugular vein. The anastomosis to the subclavian artery is placed distal to the origin of the vertebral artery in an easily accessible location. The subclavian artery has a welldeserved reputation for lacking structural integrity, and care must be taken to follow the curve of the needle to avoid tearing the artery with aggressive needle placement. Small branches of the subclavian artery, including the costocervical trunk, may be ligated to facilitate placement of the anastomosis (see Figure 4). There is no evidence that carotid–subclavian bypass steals blood from the internal carotid

Thoracic duct Thyrocervical trunk Subclavian v. & a. FIGURE 3  Surgical exposure of the left subclavian artery and com-

mon carotid artery through a supraclavicular incision. Sternocleidomastoid m.

Anterior scalene m. Internal jugular v.

Phrenic n.

Common carotid a. Vertebral a.

Thoracic duct Carotid subclavian bypass Subclavian v. & a. FIGURE 4  Synthetic carotid–subclavian bypass graft. The graft is

placed as proximal as possible on the common carotid artery to reduce the risk of the graft’s kinking. The distal anastomosis may be proximal or distal to the origin of the vertebral artery, depending on the individual anatomic considerations.

artery in the absence of occlusive disease in the CCA proximal to the origin of the bypass. In patients with coexisting subclavian steal and significant carotid occlusive disease, carotid endarterectomy (CEA) alone can relieve the cerebral symptoms by increasing collateral blood flow through the

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FIGURE 5  Total aortic debranching. Increasingly, novel extraanatomic

bypasses have been used to debranch all or part of the aortic arch in conjunction with thoracic endovascular aneurysm repair (TEVAR). In the figure, a femoral to axillary bypass is used as the origin for complete aortic debranching in association with carotid–carotid and carotid–subclavian bypass.

posterior communicating arteries and obviating the need for direct revascularization of the posterior circulation. If CEA is elected as a combined procedure with carotid subclavian bypass, a separate skin incision is used to expose the carotid bifurcation. We prefer to perform a CEA immediately after completing the carotid–subclavian bypass. A shunt is typically used during the CEA. A single graft from the endarterectomized carotid bifurcation to the subclavian artery is not recommended because it is prone to kinking, especially with neck movement. Carotid–subclavian bypass is a safe and relatively simple procedure. In a review of results of this procedure from our institution, there were no strokes or permanent neurologic deficits and only one perioperative death in 124 patients. Carotid–subclavian bypass was effective in relieving both the cerebral and arm symptoms in patients with subclavian steal syndrome. Dizziness persisted or recurred in three patients despite patent grafts, reinforcing the importance of considering all possible causes of dizziness before vascular reconstruction. The primary patency rate of carotid–subclavian bypass was 94%, and the symptom-free survival was 87% at 10 years by life-table analysis. The major complications associated with carotid–subclavian bypass include injury to the thoracic duct with development of either lymph fistula or chylothorax, injury to sympathetic or cranial nerves, graft infection, and graft occlusion.

OTHER NONANATOMIC SUBCLAVIAN ARTERY RECONSTRUCTIONS Axilloaxillary bypass may be useful in the setting of previous extensive neck surgery or radiation. General anesthesia is preferred, but

this procedure can be performed with local anesthesia and light sedation if cardiopulmonary comorbidities dictate. The axillary arteries are exposed through bilateral infraclavicular incisions. The pectoralis minor tendon may be divided to improve access to the artery. A 6- to 8-mm externally supported synthetic graft is tunneled in a subcutaneous plane. The long-term durability of axilloaxillary bypass is inferior to either carotid–subclavian bypass or subclavian–carotid transposition, but the procedure is relatively simple and can be performed under local anesthesia. This bypass should be avoided in patients who might need a subsequent sternotomy for cardiac disease, because the graft is vulnerable to direct injury. The contralateral common carotid artery may be used for inflow in unusual circumstances. We prefer to route the graft in a retropharyngeal plane, though a more superficial pretracheal path may be an alternative. We have treated a pretracheal carotid–carotid bypass that eroded through the skin just above the sternal notch. An ipsilateral femoral-to-axillary artery bypass may be appropriate in selected patients when no other cervical inflow vessel is available (Figure 5). The configuration is identical to the more common axillary–femoral bypass, which is described in more detail in another chapter. An 8-mm externally supported polytetrafluoroethylene (PTFE) graft is typically chosen. The axillary anastomosis should be placed as proximal as possible to prevent tethering on the graft and potential avulsion when the arm is raised. Other configurations of subclavian bypass are limited only by the surgeon’s imagination. In all cases, steal from the donor artery is rare in the absence of stenosis in the inflow vessel. Care must be taken to ensure that the donor vessel is free from occult occlusive disease that could jeopardize the patency of the bypass. Percutaneous transluminal angioplasty (PTA) and stenting of subclavian artery occlusive disease, despite its popularity, has not been shown to be superior to carotid–subclavian bypass as measured by durability of the reconstruction. Carotid subclavian bypass continues to be an appropriate intervention for symptomatic occlusive disease, as well as for the endovascular management of complex aortic conditions necessitating coverage of the left subclavian artery.

Selected References Bornstein N, Norris J: Subclavian steal: a harmless haemodynamic phenomenon? Lancet 328:303–305, 1986. Bryan F, Allen R, Lumsden A: Coronary–subclavian steal syndrome: report of five cases, Ann Vasc Surg 9:115–122, 1995. Eidt J, Moursi M: Direct reconstruction of the aortic arch branches. In ­Fischer JE, (eds): Mastery of surgery, 5th ed, Philadelphia, 2007, ­Lippincott Williams & Wilkins, pp 1984–1992. Harper C, Cardullo P, Weyman A, et al: Transcranial Doppler ultrasonography of the basilar artery in patients with retrograde vertebral artery flow, J Vasc Surg 48:859–864, 2008. Inoue K, Kawachi K, Oyama C, et al: Usefulness of femoro(ilio)–axillary bypass surgery for the treatment of subclavian steal syndrome, Heart Vessels 10:111–115, 1995. Labropoulos N, Nandivada P, Bekelis K: Prevalence and impact of the subclavian steal syndrome, Ann Surg 252:166–170, 2010. Matsumura J, Lee A, Mitchell R, et al: The Society for Vascular Surgery Practice Guidelines: management of the left subclavian artery with thoracic endovascular aortic repair, JVasc Surg 50:1155–1158, 2009. Perkins J, Magee T, Hands L, et al: The long-term outcome after axilloaxillary bypass grafting for proximal subclavian artery disease, Eur J Vasc Endovasc Surg 19:52–55, 2000. Spittell P: Subclavian steal syndrome. In Eidt J, Mills J, eds, Jan 2011. ed: UpToDate, 2011. Vitti M, Thompson B, Read R, et al: Carotid subclavian bypass: a twenty two year experience, J Vasc Surg 20:411–418, 1994.



Conventional Surgical and Endovascular Treatment of Innominate Artery Atherosclerosis

Conventional Surgical and Endovascular Treatment of Innominate Artery Atherosclerosis Mark K. Eskandari

The arterial blood supply to the upper extremities and brain is based on the supra-aortic trunk vessels, which include the innominate, left common carotid, and left subclavian arteries. The innominate artery is unique in that it is solely responsible for the circulation to the right arm and entire right hemisphere of the brain. Although a variety of pathologic disease processes are known to affect the innominate artery, atherosclerotic occlusive disease is the most common. Typically, atherosclerotic involvement represents spillover from a diseased aortic arch and is generally isolated to the ostium of the vessel.

CLINICAL PRESENTATION Patients with significant innominate arterial occlusive disease may be free of symptoms or can present with right-sided cerebrovascular and upper extremity symptoms. With a significant innominate artery stenosis in a right-handed patient, complaints of early-onset arm fatigue may be evident, as well as vertebrobasilar insufficiency. Alternatively, plaque rupture of an innominate artery lesion and distal embolization can lead to a clinical presentation of right upper extremity ischemia and/or a stroke, transient ischemic attack (TIA), or amaurosis fugax.

DIAGNOSIS The diagnosis of an innominate artery stenosis or occlusion is best achieved using noninvasive radiographic imaging. Duplex ultrasound can provide indirect evidence of an innominate arterial lesion by detecting reduced flow velocities in the right common carotid and subclavian arteries, but direct assessment is best achieved with either contrast-enhanced computed tomography angiography (CTA) or magnetic resonance angiography (MRA). Duplex ultrasound is hampered by the inability to directly image the innominate artery in the chest, whereas CTA and MRA provide cross-sectional, sagittal, coronal, and three-dimensional views of the innominate artery. Moreover, CTA and MRA provide additional detail of the plaque morphology and characteristics of the atherosclerotic lesion. Contraindications to CTA are the risk of radiation exposure and sequelae of intravenous iodinated contrast administration. MRA is generally avoided in cases of claustrophobia and preexisting ferromagnetic elements such as a pacemaker. If noninvasive imaging is not feasible, then conventional angiography can be used to accurately assess the innominate artery.

TREATMENT Medical therapy remains a cornerstone for atherosclerotic innominate artery disease. In certain instances, additional surgical or

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endovascular treatment is advocated. Although this particular disease has not been as well studied as extracranial carotid artery disease with randomized studies, the guidelines for proceeding with surgical or endovascular treatment are similar: symptomatic disease with at least 50% stenosis or asymptomatic disease with at least 80% stenosis.

Surgical Techniques Traditional open surgical treatment of atherosclerotic innominate artery disease is typically divided into transthoracic bypass, transthoracic endarterectomy, or extra-anatomic cervical bypass. The transthoracic bypass is considered the gold standard, but all three are effective and durable therapies. An extra-anatomic bypass is generally reserved for patients deemed unable to undergo a median sternotomy for definitive treatment owing to a prior sternotomy, severe cardiopulmonary disease, or extensive ascending or aortic arch disease. The primary risks associated with these approaches are cranial nerve injuries, stroke, and myocardial infarction. Transthoracic Bypass Preoperative cardiopulmonary assessment is necessary before a transthoracic aortic–innominate artery bypass. Generally, noninvasive cardiac imaging is sufficient. However, if there exists any concern about underlying coronary artery or significant valvular disease that could require surgical treatment, it is best to determine this before proceeding with the median sternotomy. Because the bypass inflow is typically based off the ascending aorta, it is important to evaluate the size and quality of the aorta in this location. Heavy calcification or extensive intraluminal thrombus is a contraindication caused by the increased risks of stroke and localized injury to the aorta during clamping under these conditions. A standard median sternotomy is used to access the ascending aorta and innominate artery. The thymus is divided and the innominate vein is preserved. The pericardial sac is opened and the ascending aorta is exposed. Next, the innominate artery is dissected above the innominate vein up to the bifurcation into the right common and subclavian arteries, taking care not to injure the recurrent laryngeal nerve. After the intravenous administration of weight-based systemic heparin sulfate, the right lateral wall of the ascending aorta is clamped with a side-biting clamp (i.e., Lomel-Strong clamp). Pharmacologic lowering of the systemic blood pressure by the anesthetic team during this time is helpful. The proximal anastomosis is performed in a beveled fashion to the ascending aorta using a 10- or 12-mm prosthetic graft (i.e., polyester or polytetrafluoroethylene) and 3–0 or 4–0 polypropylene sutures. The graft is then clamped and the side-biting clamp is removed. Next, the innominate artery is controlled with vascular clamps and transected above the offending lesion, and the proximal portion of the artery is oversewn. The graft is positioned anterior to the innominate vein and sewn end-to-end to the distal innominate artery with 4–0 or 5–0 polypropylene sutures (Figure 1). At the conclusion of the vascular reconstruction, hemostasis is achieved and protamine sulfate is administered. The pericardial sac is left open. Chest and/or mediastinal tubes are placed and the sternum is closed with wires in the usual fashion. Transthoracic Endarterectomy Transthoracic endarterectomy is less commonly employed for a number of reasons, but it is usually most suitable for focal lesions involving the midsection of the innominate artery. Preoperative assessment and case planning is similar to that for an aortic–innominate artery bypass. However, a crucial tenet to the success of this operation is that the lesion is short, discrete, and focal, with minimal disease in the aortic arch and distal innominate artery.

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Surgical exposure of the aorta and innominate artery is conducted as described for the transthoracic bypass. After systemic heparin sulfate is given, the distal innominate artery is clamped above and below the offending lesion. The vessel is opened longitudinally, and the endarterectomy is performed in a standard manner. Generally, the vessel size is significant enough that a primary closure of the arteriotomy with 5–0 polypropylene is required. This approach should be avoided if there is ostial involvement or significant aortic arch disease. Extra-Anatomic Cervical Bypass An extra-anatomic cervical bypass is an appropriate alternative for patients who require innominate artery revascularization but who have severe oxygen-dependent pulmonary disease, severe left ventricular dysfunction, prior external-beam chest irradiation, extensive aortic arch atherosclerotic disease, or a prior sternotomy. Again, a thorough cardiac workup is recommended. Because this operation is

typically based off the left common carotid artery, an assessment of the extracranial carotid circulation is required. Surgical exposure of both the right and left common carotid arteries is done through two separate neck incisions, taking care to preserve the vagus nerve. Next, a retropharyngeal tunnel is developed low in the neck. After systemic anticoagulation, the left proximal common carotid artery is controlled with vascular clamps and a 6or 8-mm prosthetic graft is sewn end-to-side to the medial side of the left common carotid artery. The graft is then passed through the retropharyngeal tunnel and sewn to the right common carotid artery in a similar fashion. This configuration provides adequate flow to the cerebrovascular circulation as well as to the right arm via retrograde flow into the distal innominate artery and into the right subclavian artery. Complications of Traditional Open Surgery The primary risks associated with traditional open surgical reconstruction of innominate artery disease include myocardial infarction, stroke, TIA, and cranial nerve injuries. In experienced centers, the perioperative risks are low and the long-term patency is high.

Endovascular Techniques Endoluminal interventions to alleviate vascular lesions of the innominate artery have been reported with good early success, yet their durability remains in question. In general, short-segment, less calcified stenotic lesions respond better to endovascular techniques than long-segment heavily calcified or occluded innominate artery. Access to the innominate artery is generally achieved from a percutaneous femoral approach. However, brachial or right common carotid artery approaches have also been used. In all cases, angioplasty alone is usually insufficient, and placement of a bare metal stent is generally recommended (Figure 2). As expected, the primary risk associated with this approach is distal cerebral embolization, which can manifest clinically as a TIA or stroke. Transfemoral Approach

FIGURE 1  Intraoperative view of a completed transthoracic aortic–

innominate artery bypass with a polytetrafluoroethylene graft via a median sternotomy.

As with many endovascular interventions, a traditional percutaneous transfemoral approach under conscious sedation is most commonly employed for treatment of supra-aortic trunk disease. Once access to the common femoral artery has been secured with a 5- or 6-Fr sheath, a diagnostic catheter is placed in the aortic arch. With the image intensifier positioned in a 30- or 40-degree left anterior oblique

FIGURE 2  Conventional angio-

graphic views of an innominate artery stenosis treated with stenting. A, Arch aortogram in a 30-degree left anterior oblique projection. B, Angiogram after stenting from a retrograde open trans­ carotid approach.

Arch view

A

B



Conventional Surgical and Endovascular Treatment of Innominate Artery Atherosclerosis

angle and using a power injector to administer high-flow contrast, the aortic arch and the origin of the arch vessels can be imaged. In treating most innominate arterial occlusive lesions, either a long 6-Fr sheath (75–100 cm) or 8-Fr guiding catheter is placed at the origin of the vessel to provide a stable platform for the delivery of the embolic protection device (EPD) and the intended intervention. At this point, the patient is given either systemic intravenous heparin sulfate or bivalirudin to achieve an activated clotting time of at least 300 seconds. Next, a distal filter EPD is passed across the stenosis and deployed. With the EPD in place, the stenotic lesion is then primarily stented with an appropriately sized balloon-expandable stent with protrusion of 1 to 2 mm of the stent into the aorta. Care must be taken to cover the origin of the right subclavian artery orifice, best seen in a right anterior oblique projection. Predilating the lesion with an angioplasty balloon and using selfexpanding stents are techniques for carotid bifurcation disease, but they are usually not needed for innominate arterial disease. A balloon-expandable stent allows accurate placement of the stent across the lesion and provides more outward radial force than most selfexpanding stents. After a successful technical result is confirmed, the EPD and sheath are removed. Recovery is similar to that for most percutaneous femoral interventions: manual pressure on the arteriotomy site or the use of an arterial closure device. Dual antiplatelet therapy is generally advocated for at least 4 weeks using aspirin (325 mg) and clopidogrel (75 mg). Transbrachial Approach In some instances, antegrade access to the innominate artery is required as a result of either excessive aortic arch disease or tortuosity or inadequate femoral access. Although the use of an EPD for the intervention by a brachial approach has been occasionally described, it is cumbersome and rarely employed. The steps for intervention are similar to what was described earlier for a transfemoral approach. Transcarotid Approach A good alternative to a transbrachial approach is a retrograde transcarotid approach that can be performed either percutaneously or, more commonly, through an open surgical exposure of the right common carotid artery. The latter method affords the opportunity to provide embolic protection by clamping the common carotid artery distal to the sheath and then aspirating the stagnant column of blood after stent placement to retrieve any released debris. Complications of Endoluminal Therapy The primary periprocedural risks associated with innominate artery stenting include stroke, TIA, and dissection. A unique complication to the transbrachial approach is the risk of a brachial sheath hematoma after removal, which does not manifest with an expanding hematoma but rather with hand paresthesias in the median nerve distribution. This complication requires emergent surgical decompression. As expected, the risk of cerebral events is

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FIGURE 3  Radiography 1 year after placement of an innominate

artery stent showing a complex type IV stent fracture.

increased for lesions with complete occlusions or heavily calcified lesions. Long-term risks include in-stent restenosis and stent fractures (Figure 3).

CONCLUSIONS Innominate artery occlusive disease is encountered relatively infrequently. Indications for its treatment are similar to extracranial carotid bifurcation disease. Traditional open surgical reconstruction is known to be effective and durable, but the morbidity is greater than with endovascular techniques. Although innominate artery stenting has been shown to be effective in the short term, the development of late stent fatigue and restenosis needs to be better understood. Endovascular treatment appears to be most suitable for patients with short-segment focal innominate stenoses without significant calcification and those who have had prior chest or neck external beam irradiation or surgery that makes open surgery hazardous.

Selected References Berguer R, Morasch MD, Kline RA: Transthoracic repair of innominate and common carotid artery disease: immediate and long-term outcome for 100 consecutive surgical reconstructions, J Vasc Surg 27:34–41, 1998. Berguer R, Morasch MD, Kline RA, et al: Cervical reconstruction of the supra-aortic trunks: a 16-year experience, J Vasc Surg 29:239–246, 1999. Peterson BG, Resnick SA, Morasch MD, et al: Aortic arch vessel stenting: a single-center experience using cerebral protection, Arch Surg 141: 560–563, 2006. Sullivan TM, Gray BH, Bacharach JM, et al: Angioplasty and primary stenting of the subclavian, innominate, and common carotid arteries in 83 patients, J Vasc Surg 28:1059–1065, 1998. Usman AA, Resnick SA, Benzuly KH, et al: Late stent fractures after endoluminal treatment of ostial supraaortic trunk arterial occlusive lesions, J Vasc Interv Radiol 21:1364–1369, 2010.

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Extracranial Carotid Artery Aneurysms James C. Stanley

Extracranial carotid artery aneurysms represent an important but uncommon disease. Certain of these aneurysms are associated with thromboembolic complications causing stroke. Rupture of an aneurysm, especially in the case of a false aneurysm following carotid artery endarterectomy, represents a surgical emergency. Clinical manifestations and treatment vary, depending upon the type, size, and location of the aneurysm, warranting individual discussion of true aneurysms, traumatic false aneurysms, and false aneurysms following carotid artery endarterectomy.

TRUE CAROTID ARTERY ANEURYSMS Incidence

FIGURE 1  True arteriosclerotic aneurysm of the carotid artery bulb

True aneurysms account for a little more than half of all reported extracranial carotid artery aneurysms. These aneurysms affect men twice as often as women. The average age at recognition is 60 years. Although most true carotid aneurysms exhibit arteriosclerosis, arteriosclerosis is considered a secondary event rather than a primary etiologic factor. The carotid artery bulb is the site of true aneurysms in more than 95% of cases (Figures 1 and 2). Bilateral aneurysms are noted in 12% of cases, and no predilection exists for right- or left-sided involvement in patients with unilateral aneurysms. Because the normal carotid bulb is usually 40% greater in diameter than the more distal internal carotid artery, it requires very little expansion to reach the 50% dilation level. The latter is a generally accepted definition of an aneurysm. However, given the normal dilation of the carotid bulb, it becomes difficult to define the natural history of borderline-sized aneurysms. Because of concerns over one’s ability to differentiate a generous-sized carotid bulb from a small aneurysm, it has been proposed that an aneurysm only exists when the carotid bulb dilation at least is 200% greater than the extracranial internal carotid artery diameter or 150% of the common carotid artery diameter. Although true arteriosclerotic aneurysms have been encountered in the common carotid artery and the more distal internal carotid artery, trauma or some other vascular insult has likely preceded aneurysm development at these latter sites. Aneurysms affecting other arteries in patients with carotid artery aneurysms have been observed in nearly 25% of cases.

FIGURE 2  True aneurysm of the internal carotid artery of undeter-

Manifestations The natural history of true carotid artery aneurysms is poorly defined. Most aneurysms are likely to be asymptomatic, although the surgical literature does not support such a statement. Among patients described in surgical reports, approximately 60% have experienced transient ischemic attacks, including 33% with amaurosis and 21% with hemispheric symptoms. Frank strokes affected an additional 8% of patients. Rupture of a true carotid aneurysm is rare, having been reported in fewer than a dozen patients. However, acute expansion of true carotid artery aneurysms does occur, and it can cause secondary cranial nerve dysfunction, such as hoarseness related to pressure on the recurrent

with involvement of both the internal and external carotid arteries.

mined etiology with evidence of secondary arteriosclerosis documented in the resected specimen.  (From Zwolak RM, Whitehouse WM Jr, Knake JE, et al: Atherosclerotic extracranial carotid artery aneurysms, J Vasc Surg 1:415–422, 1984).

laryngeal nerve. Severe hemicrania, often with Horner’s syndrome, can accompany acute expansion of an aneurysm, although such is more often caused by a carotid artery dissection. These aneurysms manifest as nontender cervical masses in a third of patients, and in some patients they may be mistaken for a deep peritonsillar abscess when they expand medially and encroach on the retropharyngeal space. More than 80% of patients with these aneurysms present with



a pulsatile mass that may be difficult to distinguish from a tortuous artery or lymphadenopathy overlying a normal carotid bulb. Duplex ultrasonography is adequate to define the size and extent of low-lying carotid artery aneurysms. However, computed tomography is necessary to define the relationship between high-lying aneurysms and surrounding structures above the angle of the mandible. Conventional cerebral arteriography or computed tomographic arteriography should be performed in all patients with suspected carotid aneurysms before proceeding to open operative or endovascular therapy. Arteriography is particularly useful to differentiate carotid artery aneurysms from carotid artery kinks and loops.

Treatment Open operative or endovascular intervention should be undertaken for symptomatic true carotid artery aneurysms with manifestations related to cerebral ischemia, cranial nerve dysfunction, or local cervical neck discomfort. Operative indications for asymptomatic aneurysms are controversial because the risks of their remaining untreated are not well known. Nevertheless, surgical treatment is recommended for all asymptomatic aneurysms greater than 2 cm in diameter, presuming that the patient is otherwise a reasonable operative candidate. Surgical exposure for true carotid bifurcation aneurysms is similar to that for an elective carotid endarterectomy. Most of these aneurysms are best treated by their resection with reconstruction of the artery using an interposition carotid–carotid saphenous vein graft. The reversed vein is anastomosed in an end-to-end fashion to the common carotid artery, with a distal end-to-end anastomosis to the normal internal carotid artery. The external carotid artery is commonly ligated but may be implanted into the vein graft. Saphenous vein grafts are preferred over synthetic conduits for these reconstructions, although Dacron or polytetrafluoroethylene (PTFE) grafts are appropriate when adequate vein is unavailable. In young children and adolescents the internal iliac artery is favored as a graft. Spatulation of the distal internal carotid artery and graft provides for creation of a generous ovoid anastomosis. Back bleeding from the distal internal carotid artery is usually controlled with small microvascular clamps, although rigid intraluminal dilators or balloon catheters are used when high lesions or further dissection might make clamp placement hazardous or difficult. Intraluminal shunts are used if there is evidence of impaired intracranial collateral blood flow or if the patient has experienced a prior ipsilateral stroke. Some believe shunting should be used in all patients. Markedly tortuous carotid arteries with limited aneurysmal involvement occasionally are treated by simple aneurysm resection and primary reanastomosis or reimplantation of the carotid artery. Open aneurysmorrhaphy to reduce the carotid artery diameter may be performed in select patients with fusiform aneurysms, although the longterm success of such has not been established. Operative ligation of the internal carotid artery is rarely undertaken in managing accessible true carotid artery aneurysms. If such appears necessary then one should consider using an implantable clamp device to gradually occlude the carotid artery. In instances where immediate ligation is required, postoperative anticoagulation might lessen the risks of perioperative stroke as a result of intracranial extension of carotid thrombus. The most morbid complications accompanying treatment of true aneurysms relate to strokes caused by dislodgment of aneurysmal debris with distal embolization. This might be suspected given the fact that intra-aneurysmal thrombus affects 20% of these aneurysms. Injury of the cranial nerves, especially nerves X and XII, contribute to significant postoperative morbidity in 5% of these patients, and transection of the carotid sinus nerve and loss of its baroreceptor function in an occasional patient can result in neurogenic hypertension, if the opposite sinus or aortic baroreceptors are not functional. Cautious dissection of these aneurysms should lessen the high perioperative stroke rate reported in earlier surgical experiences. Current outcomes accompanying aneurysmectomy and carotid

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artery reconstruction include less than a 2% operative mortality rate and a stroke rate of approximately 5%. Ligation alone carries a 25% stroke risk and 20% chance of death. Carotid artery aneurysms not subjected to surgical therapy should be followed with duplex ultrasonography or some other imaging modality, and patients and their families should be well informed as to the warnings of cerebrovascular accidents and the need to seek medical attention immediately if such occur. Endovascular stenting of extracranial aneurysms has evolved into an accepted alternative to open surgical therapy. More than 50 patients with true extracranial aneurysms have been successfully treated by stenting. Covered stents have been used in the majority of cases, and patencies of more than 90% at follow-up average a little more than a year. Endoleaks have accompanied 8% of stent placements, and conversion from an endovascular intervention to an open procedure occurred in 7% of cases. The procedural stroke rate neared 2%, and the mortality approached 5%. Late stent thrombosis or stenoses affected a little more than 5% of patients.

TRAUMATIC FALSE ANEURYSMS OF THE CAROTID ARTERY Incidence False aneurysms of the carotid artery caused by noniatrogenic injury are uncommon, with fewer than 500 blunt or penetrating traumarelated aneurysm reported in the literature (Figure 3). Men slightly outnumber women with both types of these aneurysms. The management of traumatic false carotid artery aneurysms is quite different from that for true aneurysms. The clinical manifestations range from asymptomatic swellings to local pain and cerebral ischemic symptoms.

Treatment False carotid artery aneurysms associated with penetrating trauma should be managed as other vascular injuries are. Open surgery with local repair may be possible if the injury is limited, or a formal arterial reconstruction may be required with more extensive arterial disruption. Rarely is it necessary to ligate the internal carotid artery for an injured artery, although such may be appropriate when distal occlusion already exists in a neurologically intact patient. In other circumstances where ligation is necessary and the patient is at risk for cerebral infarction, treatment should be as noted in the earlier discussion on ligation for true aneurysms. The location of a penetrating carotid artery traumatic aneurysm may be anywhere from the origin of the common carotid artery to the base of the skull, and the operative exposure must be tailored for such. Surgical approaches range from a sternotomy in the treatment of low-lying common carotid artery aneurysms to resection of the mastoid process or subluxation of the mandible when treating highlying internal carotid artery aneurysms. Treatment of penetrating injury-related false aneurysms carries up to a 15% mortality and a 20% stroke rate among survivors. Arterial disruption and actual false aneurysm formation as a result of direct blunt or stretch trauma to the neck is not as common as the development of a dissection-related mural aneurysm. Dissecting aneurysms usually involve the distal internal carotid arteries and are discussed elsewhere in this text. Direct blunt injury to the carotid artery occurs most often in the mid portion of the artery. Management of these lower-lying aneurysms is similar to that of true carotid artery aneurysms. Treatment of accessible aneurysms induced by blunt injury carries similar morbidity and mortality risks as with true carotid artery aneurysms. Endovascular stenting has a particularly useful role in the treatment of trauma-related false aneurysms of the carotid artery. More than half

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FIGURE 3  False aneurysm of the proximal internal carotid artery

following blunt trauma to the neck.  (From Stanley JC: Aneurysms of the extracranial carotid and vertebral arteries. In Cameron JL (ed): Current surgical therapy, 6th ed. St. Louis, 1998, Mosby Year Book, pp. 761–767.)

the cases of extracranial carotid stenting for aneurysm have involved carotid injuries. The risks attending endovascular interventions for dissections parallel those when treating true aneurysms.

FALSE ANEURYSMS FOLLOWING CAROTID ARTERY ENDARTERECTOMY Incidence False aneurysms following carotid endarterectomy have been reported in fewer than 200 patients. Nearly 20% of these postendarterectomy aneurysms exhibit infection. This infectious complication occurs in less than 0.3% of all carotid endarterectomies, often being associated with a prosthetic patch closure (Figure 4). Staphylococcal organisms are the most common infectious agent in these cases. Infected false aneurysms usually manifest with a tender mass and fever. Hemorrhage is the most serious complication attending these aneurysms, whether they are infected or not. Early operative therapy is warranted once the diagnosis is established.

Treatment Postendarterectomy false aneurysms without obvious evidence of infection are usually treated by excision and arterial reconstruction with an interposition carotid–carotid graft using an autogenous vein or synthetic prosthesis. In select cases, endovascular placement of a covered stent graft may be appropriate. Under such circumstances, prophylactic antibiotics should be used for at least 2 months to lessen the potential of reinfection, should an unrecognized occult aneurysm infection exist. Management of infected postendarterectomy aneurysms requires excision of the involved arteries, with a reconstruction usually using autologous saphenous vein. If the carotid bulb is spared, a different approach may be feasible, in which the external carotid artery is

FIGURE 4  False aneurysm of the carotid artery bulb secondary to

a disrupted infected prosthetic patch placed during a previous carotid endarterectomy.  (From Stanley JC: Aneurysms of the extracranial carotid and vertebral arteries. In Cameron JL (ed): Current surgical therapy, 6th ed. St. Louis, 1998, Mosby Year Book, pp. 761–767.)

transected and anastomosed end-to-end to the more normal distal internal carotid artery above the site of false aneurysm. Simple ligation of the internal carotid artery involved with an infected postendarterectomy false aneurysm causes the patient’s death in 40% of cases. In survivors, ligation carries a high risk of stroke. If ligation becomes unavoidable, the patient should be anticoagulated with heparin at the time of the operation and then maintained on a course of warfarin (Coumadin) anticoagulation for a period of weeks postoperatively, to lessen the likelihood of extracranial thrombus propagation into the intracranial circulation. The adequacy of the intracranial collateral circulation in these patients may be assessed by preoperative PET studies during temporary catheter balloon occlusion of the carotid artery. Failure to tolerate such a test occlusion precludes safe ligation. Patients failing this test are candidates for an extracranial–intercranial bypass as the first of a staged treatment program, with the second stage being removal of the infected extracranial carotid vessel.

Selected References Aleksic M, Heckenkamp J, Gawenda M, et al: Differentiated treatment of aneurysms of the extracranial carotid artery, J Cardiovasc Surg 46:19–23, 2005. Attigah N, Kulkens S, Zausig N, et al: Surgical therapy of extracranial carotid artery aneurysms: long-term results over a 24-year period, Eur J Vasc Endovasc Surg 37:127–133, 2009. Blanco E, Serrano FJ, Reina R: Saccular aneurysms of the extracranial internal carotid artery. Experience and review of the literature, J Cardiovasc Surg 49:73–78, 2008. Faggioli GL, Freyrie A, Stella A, et al: Extracranial internal carotid artery aneurysms: results of a surgical series with long-term follow-up, J Vasc Surg 23:587–595, 1996. Li Z, Chang G, Yao C, et al: Endovascular stenting of extracranial carotid artery aneurysm: a systematic review, Eur J Vasc Endovasc Surg 42:419–426, 2011. May J, White GH, Waugh R, et al: Endoluminal repair of internal carotid artery aneurysm: a feasible but hazardous procedure, J Vasc Surg 31:713–723, 2000.



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Raptis S, Baker SR: Infected false aneurysms of the carotid arteries after carotid endarterectomy, Eur J Vasc Endovasc Surg 11:148–152, 1966. Rosset E, Albertini J-N, Magnan PE: Surgical treatment of extracranial internal carotid artery aneurysm: a feasible but hazardous procedure, J Vasc Surg 26:1055–1060, 1997.

Zhou W, Lin PH, Bush RL: Carotid artery aneurysm: evolution of management over two decades, J Vasc Surg 43:493–496, 2006. Zwolak RM, Whitehouse WM Jr, Knake JE, et al: Atherosclerotic extracranial carotid artery aneurysms, J Vasc Surg 1:415–422, 1984.

Carotid Body Tumors

secretions causing catecholamine-related symptoms, such as headache, flushing, and diaphoresis. Tumors that are at least 3 cm may be appreciated on physical examination as a bulging lump in the anterior triangle of the neck. The tissue is rubbery, firm, and noncompressible. The lump can be displaced laterally but not vertically, and lateral displacement results in movement of the carotid pulse in the same direction, known as Fontaine’s sign. Generally, a thrill or a bruit is not present. Cranial nerve deficits are rarely present unless the tumor is larger than 5 cm, if there is an associated cervical paraganglioma, or if the tumor is malignant. Other causes of neck mass are commonly confused with a carotid body tumor. These causes include benign nodal inflammation or hypertrophy, metastatic cancer to a cervical node, a branchial cleft cyst, low parotid tumors, or a glomus jugulare tumor. They can be differentiated from carotid aneurysms by the pulsatile and expansile nature of an aneurysm, which is not present with a carotid body tumor.

Adam H. Power and John W. Hallett, Jr.

Carotid body tumors are the most common form of paraganglioma in the head and neck. These tumors are difficult to resect because of impressive vascularity, arterial adherence, and local cranial nerve involvement. Stroke and cranial nerve dysfunction remain sobering risks of surgical resection. However, advances in diagnostic imaging and surgical technique have reduced perioperative complications to a reassuringly low level. The carotid body is located in the adventitia of the common carotid artery at its bifurcation. It consists of chemoreceptors that aid in homeostasis by increasing the ventilatory rate when stimulated by hypoxia, hypercapnia, and acidosis. These tumors have an extremely high blood flow and oxygen consumption, more than either the brain or the heart. Its blood supply runs through a thin strand of adventitia, known as Meyer’s ligament, and arises from the external carotid artery (ECA) through multiple feeder vessels, with the ascending pharyngeal artery typically being the largest. The carotid body is innervated by the nerve of Hering, which originates from the afferent ganglion of the glossopharyngeal nerve. Carotid body tumors, also known as cervical paragangliomas, chemodectomas, or glomus caroticum tumors, are of both mesodermal and neuroectodermal origin. They are generally well circumscribed, splay the carotid bifurcation, and adhere to the adventitial surface of the artery. Carotid body tumors are characteristically extremely vascular, secrete catecholamines on rare occasions, and are usually benign. When malignant, they can metastasize to local lymph nodes, liver, lung, bone, and occasionally the brain, although metastases occur in no more than 5% of cases. Carotid body tumors tend to be sporadic but are familial in 10% to 20% of cases, with succinate dehydrogenase (SDH) B, C, and D germline mutations being predominant. Familial tumors are often bilateral, occurring in a synchronous or metachronous fashion, and may be associated with other cervical paragangliomas, such as glomus vagale or jugulare tumors. Current controversy in the diagnosis and management of carotid body tumors centers on determining if a carotid body tumor is in need of resection, the necessary preoperative tests, the role of preoperative embolization and the technical steps that will allow complete tumor resection with minimal neurovascular complications.

DIAGNOSIS The extensive vascularity of carotid body tumors precludes percutaneous needle aspiration or incisional biopsy, and therefore the diagnosis relies heavily on radiologic imaging techniques. Color-flow carotid duplex scanning is extraordinarily accurate in detecting the presence of a carotid body tumor and coexistent atherosclerotic disease in the carotid artery. Characteristically, the tumor is localized to the carotid bifurcation as a well-defined, solid, and hypoechoic mass. With color Doppler imaging, hypervascularity with a low-resistance flow pattern is evident. The limitation of color-flow duplex ultrasonography is its inability to image the low or high neck for other paragangliomas. Cross-sectional imaging of these tumors, in the form of either computed tomography angiography (CTA) or magnetic resonance angiography (MRA), has become the preferred diagnostic modality. CTA is an excellent method to define the size and extent of a carotid body tumor, as well as the relation of the tumor to bony landmarks in the neck, which can modify the surgical approach (Figure 1). It can also easily identify contralateral tumors and other associated paragangliomas of the neck.

CLINICAL PRESENTATION Carotid body tumors usually manifest as an asymptomatic anterior neck mass. Patients commonly note the sensation of a lump in the neck, sometimes before a mass is detectable by palpation. Most patients appreciate a slow increase in the size of the mass over several years. A third of patients note some discomfort in the area of the mass, whereas a minority of patients complain of dysphagia or voice change. Carotid body tumors have been reported to be more prevalent in patients who live at high altitudes, with chronic hypoxia causing carotid body cell hyperplasia. Rarely, they produce neuroendocrine

A

B

FIGURE 1  A, Computed tomography angiography reformatted images of right carotid body tumor splaying the bifurcation of the right internal and external carotid arteries. B, A three-dimensional reconstruction. Coronal view.



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141

Raptis S, Baker SR: Infected false aneurysms of the carotid arteries after carotid endarterectomy, Eur J Vasc Endovasc Surg 11:148–152, 1966. Rosset E, Albertini J-N, Magnan PE: Surgical treatment of extracranial internal carotid artery aneurysm: a feasible but hazardous procedure, J Vasc Surg 26:1055–1060, 1997.

Zhou W, Lin PH, Bush RL: Carotid artery aneurysm: evolution of management over two decades, J Vasc Surg 43:493–496, 2006. Zwolak RM, Whitehouse WM Jr, Knake JE, et al: Atherosclerotic extracranial carotid artery aneurysms, J Vasc Surg 1:415–422, 1984.

Carotid Body Tumors

secretions causing catecholamine-related symptoms, such as headache, flushing, and diaphoresis. Tumors that are at least 3 cm may be appreciated on physical examination as a bulging lump in the anterior triangle of the neck. The tissue is rubbery, firm, and noncompressible. The lump can be displaced laterally but not vertically, and lateral displacement results in movement of the carotid pulse in the same direction, known as Fontaine’s sign. Generally, a thrill or a bruit is not present. Cranial nerve deficits are rarely present unless the tumor is larger than 5 cm, if there is an associated cervical paraganglioma, or if the tumor is malignant. Other causes of neck mass are commonly confused with a carotid body tumor. These causes include benign nodal inflammation or hypertrophy, metastatic cancer to a cervical node, a branchial cleft cyst, low parotid tumors, or a glomus jugulare tumor. They can be differentiated from carotid aneurysms by the pulsatile and expansile nature of an aneurysm, which is not present with a carotid body tumor.

Adam H. Power and John W. Hallett, Jr.

Carotid body tumors are the most common form of paraganglioma in the head and neck. These tumors are difficult to resect because of impressive vascularity, arterial adherence, and local cranial nerve involvement. Stroke and cranial nerve dysfunction remain sobering risks of surgical resection. However, advances in diagnostic imaging and surgical technique have reduced perioperative complications to a reassuringly low level. The carotid body is located in the adventitia of the common carotid artery at its bifurcation. It consists of chemoreceptors that aid in homeostasis by increasing the ventilatory rate when stimulated by hypoxia, hypercapnia, and acidosis. These tumors have an extremely high blood flow and oxygen consumption, more than either the brain or the heart. Its blood supply runs through a thin strand of adventitia, known as Meyer’s ligament, and arises from the external carotid artery (ECA) through multiple feeder vessels, with the ascending pharyngeal artery typically being the largest. The carotid body is innervated by the nerve of Hering, which originates from the afferent ganglion of the glossopharyngeal nerve. Carotid body tumors, also known as cervical paragangliomas, chemodectomas, or glomus caroticum tumors, are of both mesodermal and neuroectodermal origin. They are generally well circumscribed, splay the carotid bifurcation, and adhere to the adventitial surface of the artery. Carotid body tumors are characteristically extremely vascular, secrete catecholamines on rare occasions, and are usually benign. When malignant, they can metastasize to local lymph nodes, liver, lung, bone, and occasionally the brain, although metastases occur in no more than 5% of cases. Carotid body tumors tend to be sporadic but are familial in 10% to 20% of cases, with succinate dehydrogenase (SDH) B, C, and D germline mutations being predominant. Familial tumors are often bilateral, occurring in a synchronous or metachronous fashion, and may be associated with other cervical paragangliomas, such as glomus vagale or jugulare tumors. Current controversy in the diagnosis and management of carotid body tumors centers on determining if a carotid body tumor is in need of resection, the necessary preoperative tests, the role of preoperative embolization and the technical steps that will allow complete tumor resection with minimal neurovascular complications.

DIAGNOSIS The extensive vascularity of carotid body tumors precludes percutaneous needle aspiration or incisional biopsy, and therefore the diagnosis relies heavily on radiologic imaging techniques. Color-flow carotid duplex scanning is extraordinarily accurate in detecting the presence of a carotid body tumor and coexistent atherosclerotic disease in the carotid artery. Characteristically, the tumor is localized to the carotid bifurcation as a well-defined, solid, and hypoechoic mass. With color Doppler imaging, hypervascularity with a low-resistance flow pattern is evident. The limitation of color-flow duplex ultrasonography is its inability to image the low or high neck for other paragangliomas. Cross-sectional imaging of these tumors, in the form of either computed tomography angiography (CTA) or magnetic resonance angiography (MRA), has become the preferred diagnostic modality. CTA is an excellent method to define the size and extent of a carotid body tumor, as well as the relation of the tumor to bony landmarks in the neck, which can modify the surgical approach (Figure 1). It can also easily identify contralateral tumors and other associated paragangliomas of the neck.

CLINICAL PRESENTATION Carotid body tumors usually manifest as an asymptomatic anterior neck mass. Patients commonly note the sensation of a lump in the neck, sometimes before a mass is detectable by palpation. Most patients appreciate a slow increase in the size of the mass over several years. A third of patients note some discomfort in the area of the mass, whereas a minority of patients complain of dysphagia or voice change. Carotid body tumors have been reported to be more prevalent in patients who live at high altitudes, with chronic hypoxia causing carotid body cell hyperplasia. Rarely, they produce neuroendocrine

A

B

FIGURE 1  A, Computed tomography angiography reformatted images of right carotid body tumor splaying the bifurcation of the right internal and external carotid arteries. B, A three-dimensional reconstruction. Coronal view.

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CTA is especially helpful in classifying the Shamblin group of tumor (Figure 2). Shamblin’s classification divides carotid body tumors into three groups that relate to the difficulty of resection and the likelihood of local neurovascular complications. Group I tumors are small and readily resected from the carotid bifurcation. Group II are larger tumors that are densely adherent to the carotid arteries and can partially surround them. Group III tumors encase the carotid artery or adjacent nerves. MRA is also excellent at characterizing carotid body tumors, although it is more time consuming and expensive than CTA. MRA can estimate the size of the tumor and clearly delineate the adjacency and involvement of the carotid vessels. Gadolinium enhancement helps to define the arterial blood supply to the tumor and also reveals any associated atherosclerotic changes that may be present. In the past, the classic diagnosis of a carotid body tumor was by arteriography. An arteriogram provides the image of a very vascular mass splaying the carotid bifurcation, also known as the lyre sign (Figure 3A). Standard arteriography is mainly necessary for patients who are selected for preoperative embolization of the blood supply to the tumor.

highly selective catheter embolization, usually the ascending pharyngeal branch of the external carotid artery, to reduce intraoperative hemorrhage (see Figure 3). The major risk is embolization of the polyvinyl alcohol (PVA) particles into the brain, causing transient ischemic attacks or a stroke, although this is exceedingly rare with current neurointerventional techniques. In general, preoperative embolization is not necessary for small Shamblin I tumors. There is now strong evidence that in larger Shamblin II and III tumors, preoperative embolization simplifies the carotid body tumor resection and reduces blood loss. Preoperative embolization may also be useful in tumors with locations at or above the angle of the jaw. However, these benefits are balanced by the requirement of an additional outpatient procedure, greater expense, and no significant impact on the most common complication, cranial nerve injury. The theoretical increase in difficulty of the resection from the peritumoral inflammatory response secondary to embolization is largely unfounded, especially if resection occurs within 24 hours of the embolization.

SURGICAL INDICATIONS

PREOPERATIVE EMBOLIZATION Since the 1990s, one of the controversies in the preoperative preparation of patients with a carotid body tumor has been the role of preoperative embolization of the tumor’s blood supply. Because these tumors are extraordinarily vascular, some surgeons have advocated

In general, all carotid body tumors in healthy patients should be resected. Surgical resection provides the only reliable cure. Although radiation therapy has provided excellent palliation in certain unresected or recurrent tumors, it is not curative. Resection of carotid body Superior laryngeal n. ECA XII N.

N. X ICA

XII N. FIGURE 2  Shamblin classification of

carotid body tumors for difficulty of surgical resection. Group I tumors are localized and easily resected. Group II tumors adhere to or partially surround the carotid arteries. Group III completely surrounds or encases at least one of the arteries.  (From Hallett JW Jr, Nora JD, Hollier LH, et al: Trends in the neurovascular complications of surgical management for carotid body and cervical paragangliomas: a 50-year experience with 153 tumors, J Vasc Surg 7:284–291, 1988.)

Superior laryngeal n.

N. X

FIGURE 3  A, Preoperative embolization of right carotid body tumor. B, Lateral cervical angiogram from the right common carotid artery demonstrates splaying of the internal and external carotid arteries. C, Superselective injections of the ascending pharyngeal artery shows significant contributions to the tumor vascularity. There is significant reduction in the tumor vascularity following embolization with polyvinyl alcohol (PVA) particles measuring 255 to 350 μm.

Type II

Type I

A

B

Type III

C



Carotid Body Tumors

saphenous vein harvest site should be prepared if needed for possible arterial repair or replacement. Carotid shunts should also be ready. Most patients (90%) require no arterial repair or a simple lateral suture repair of the carotid artery. More complicated arterial reconstruction (patch, graft, or end-to-end anastomosis) may be necessary in 10% to 25%. A carotid shunt is required very rarely if continuous EEG is used. The risk of neurovascular complications, however, is significantly higher in patients who require any type of arterial repair. In fact, nearly all strokes occur in patients who have arterial repair or replacement during tumor excision. The cervical incision must provide clear and adequate exposure for both vascular control and cranial nerve preservation. For small tumors, less than 3 to 4 cm in diameter, the best incision is along the anterior border of the sternocleidomastoid muscle, an approach that is relatively standard for carotid endarterectomy. In contrast, larger tumors are more safely approached through a modified T radial neck incision. Both incisions generally result in a satisfactory cosmetic appearance with healing. A systematic dissection around the tumor can minimize the risk of cranial nerve injury. Dissection can be completed sequentially in three anatomic steps or zones (Figure 4). Zone I includes the common carotid artery, its bifurcation, and adjacent vagus nerve. The initial step in the dissection is to identify the common carotid artery at the level of the omohyoid muscle and carefully dissect away the adjacent vagus nerve. Near the carotid bifurcation, a myriad of small veins draining the tumor can be controlled with bipolar electrocautery. Zone II encompasses territory of the external carotid artery and the overlying hypoglossal nerve, the underlying superior laryngeal nerve, and the more superficial marginal mandibular branch of the facial nerve. Although these nerves can appear incorporated in the tumor, they usually can be separated from the surface and preserved. Zone III contains the ICA and the confluence of several cranial nerves: the proximal hypoglossal nerve, the upper vagus nerve, the pharyngeal branch of the vagus nerve, the spinal accessory nerve, and the glossopharyngeal nerve. Most serious cranial nerve injuries occur in this crowded zone. An experienced head and neck surgeon can be an invaluable assistant in safely resecting large tumors that extend high into zone III. One of the most important instruments for safe tumor resection is bipolar electrocautery. The standard electrocautery allows a zone of

tumors when they are small is the best method to ensure long-term cure and to minimize the risk of any neurovascular injury. Observation is not recommended, except in the very elderly or debilitated patient.

SURGICAL APPROACH The major risks in surgical resection of carotid body tumors remain cranial nerve injury and, to a much lesser degree, stroke. The risk of stroke has declined dramatically from approximately 25% between 1935 and 1965 to approximately 1% more recently. Most strokes are associated with large tumors requiring vascular repair or replacement. The incidence of cranial nerve dysfunction has changed little in the past few decades and still affects up to 40% of patients. Most of these deficits are temporary. Nevertheless, permanent cranial nerve dysfunction occurs in approximately 5% of cases. Some tumors involve cranial nerves, and postoperative dysfunction is predictable with curative resection. However, surgical dissection can affect the marginal mandibular branch of the facial nerve, the hypoglossal nerve, the superior laryngeal nerve, the vagus nerve, and the glossopharyngeal nerve. The risk of cranial nerve deficit is related to the size of the tumor and its location in the neck, with larger and higher tumors leading to more injuries. General nasotracheal anesthesia is preferable. A nasotracheal tube allows greater displacement of the floor of the mouth during retraction and dissection beneath the mandible. Although seldom necessary, subluxation of the mandible can improve exposure of large tumors that extend toward the base of the skull. Continuous electroencephalographic (EEG) monitoring provides a sensitive method to detect hemispheric ischemia, if internal carotid artery (ICA) blood flow is interrupted for any reason (e.g., kinking by retraction, severe spasm with thrombosis or clamping during arterial repair). In the authors' experience, EEG has immediately indicated the presence of an ICA thrombosis, which occurs occasionally with large tumors and manipulation of the ICA without systemic anticoagulation. In the past, carotid artery ligation was used to control hemorrhage and allow complete tumor resection, which led to a perioperative stroke rate that approached 25%. Therefore, ICA blood flow is now protected and maintained throughout the procedure, and some patients require arterial repair or replacement. Consequently, a

Mandibular br. of facial n. VII

ZONE III

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ZONE II

Spinal accessory n.

Ext. carotid a.

Pharyngeal br. of X Hypoglossal n. XII

Hypoglossal n. XII

Int. carotid a. Sup. laryngeal n.

Vagus n. X

Bifurcation

FIGURE 4  Anatomic zones of dissection for a Common carotid a.

Vagus n. X ZONE I

carotid body tumor.  (From Hallett JW Jr, Nora JD, Hollier LH, et al: Trends in the neurovascular complications of surgical management for carotid body and cervical paragangliomas: a 50-year experience with 153 tumors, J Vasc Surg 7:284–291, 1988.)

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Mobilization of hypoglossal n.

Distal internal carotid a. control

Proximal ext. carotid a. control Common carotid a. control Hypoglossal n. FIGURE 5  Resection of smaller carotid body

tumors, less than 3 to 4 cm. Proximal and distal control of the common and internal carotid arteries is the first step in safe resection. Hypoglossal and vagus nerves should be carefully dissected from the tumor surface. Bipolar cautery can control bothersome surface bleeding while dissection with fine scissors continues in the periadventitial plane. Temporary anticoagulation and carotid clamping allows safer and easier tumor dissection of the carotid bifurcation. Once the tumor is freed from the bifurcation, the superior laryngeal nerve can be identified posteriorly. Tumor dissection can continue up along the internal carotid artery in the periadventitial plane.

Periadventitial plane Bipolar cautery dissection

Temporary carotid a. clamping

heat conduction around the cautery tip. Such heat can injure adjacent cranial nerves. Conversely, the bipolar cautery only conducts energy between the tips of the bipolar forceps and can allow nearly bloodless dissection along the tumor surface as the surgeon attempts to dissect it away from the adjacent arteries and nerves. The tumor should be dissected in the periadventitial plane and not in the mistakenly recommended and treacherous subadventitial plane (Figure 5). Subadventitial dissection either leads to an intraoperative hemorrhage as the surgeon ventures into the arterial lumen or leaves a weakened spot on the artery that is prone to disastrous carotid blowout. Temporary carotid clamping after a small dose of heparin, 2500 units, may be necessary for safe resection of tumors that are densely adherent to the carotid bifurcation. This area can be easier to dissect when the carotid bifurcation is not pulsating (see Figure 5). This part of the tumor resection is often the most difficult point of dissection in an area where carotid injury is relatively common. Clamp time can be relatively short (5–10 minutes), and EEG changes seldom occur. Consequently, a carotid shunt is usually not necessary. A small dose of heparin generally does not increase bleeding and is also useful when the ICA develops intense spasm. Such spasm is relatively common in younger patients and can be so intense that it causes local thrombosis or thromboembolism. Several maneuvers may be necessary to resect large tumors greater than 5 to 6 cm. Adequate superior tumor exposure can require identification of the facial nerve and its marginal mandibular branch, some parotid gland elevation, division of the digastric and stylohyoid muscles, and, occasionally, submandibular gland resection. Mandibular subluxation is an additional maneuver that can enhance high carotid exposure. Ligation of the external carotid artery is necessary in approximately 15% of patients with these large tumors. Such ligation decreases tumor vascularity in size, reduces bleeding, and facilitates complete removal and dissection away from the ICA. The ICA in such cases is usually stretched and pushed laterally but not encased by the tumor. The ICA may be so tortuous after

Sup. laryngeal n.

tumor resection that segmental resection and reanastomosis may be necessary. A generous dead space is often left after resection of large tumors. Accumulation of blood or fluid in this dead space can cause some difficulty with the airway and also with swallowing. Consequently, a closed suction drain should be placed for 24 to 48 hours.

SURGICAL RESULTS Almost all carotid body tumors can be completely resected. Perioperative mortality rates are less than 1%, and postoperative stroke is unusual, affecting only 1% to 2% of patients. About 5% of patients develop a permanent cranial nerve deficit, but temporary cranial nerve deficits can occur in up to 40% of patients, usually involving the hypoglossal or marginal mandibular nerves. These temporary deficits often improve with time and are usually secondary to excessive retraction intraoperatively. The survival of patients after complete carotid body or cervical paraganglioma resection is encouraging. Survival rates are essentially equivalent to that of sex- and age-matched control subjects. Metastatic disease develops in less than 5% of patients. Recurrence has been noted in approximately 5% to 10%. In most series, recurrent tumors have been observed in patients with multiple or familial cervical paragangliomas. Routine follow-up imaging is recommended, especially in patients with multiple paragangliomas, positive family history, or a confirmed succinate dehydrogenase (SDH) mutation.

Selected References Hallett JW Jr, Nora JD, Hollier LH, et al: Trends in neurovascular complications of surgical management for carotid body and cervical paragangliomas: a fifty-year experience with 153 tumors, J Vasc Surg 7:284–291, 1988. Kafie FE, Freischlag JA: Carotid body tumors: the role of preoperative embolization, Ann Vasc Surg 15:237–242, 2001.



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Kruger AJ, Walker PJ, Foster WJ, et al: Important observations made managing carotid body tumors during a 25-year experience, J Vasc Surg 52:1518–1523, 2010. Li J, Wang S, Zee C, et al: Preoperative angiography and transarterial embolization in the management of carotid body tumor: a single-center, 10-year experience, Neurosurgery 67:941–948, 2010. Nora JD, Hallett JW Jr, O'Brien PC, et al: Surgical resection of carotid body tumors: long-term survival, recurrence, and metastasis, Mayo Clin Proc 63:348–352, 1988. Power A, Cloft H, Kallmes D, et al: Impact of preoperative embolization on outcomes of Shamblin II and III carotid body tumor resections, SVS Meeting, 2011. Abstract.

Sajid MS, Hamilton G, Baker DM: A multicenter review of carotid body tumour management, Eur J Vasc Endovasc Surg 34:127–130, 2007. Shamblin WR, ReMine WH, Sheps SG, et al: Carotid body tumor (chemodectoma). Clinicopathologic analysis of ninety cases, Am J Surg 122: 732–729, 1971. van der Bogt KE, Vrancken Peeters MP, van Baalen JM, et al: Resection of carotid body tumors: results of an evolving surgical technique, Ann Surg 247:877–884, 2008. Zeitler DM, Glick J, Har-El G: Preoperative embolization in carotid body tumor surgery: is it required? Ann Otol Rhinol Laryngol 119:279–283, 2010.

Radiation-Induced Arteritis

there may be an external carotid stenosis rather than the more prevalent bifurcation and internal carotid involvement. Clinically important upper extremity ischemia following radiation therapy for breast carcinoma usually results from poorly collateralized, often ulcerated occlusive lesions near the subclavian–axillary junction. In contrast, arteriosclerosis usually arises proximally at the subclavian artery origin, not infrequently with an associated steal syndrome. Additional sites of atypical arterial stenosis include isolated renal artery lesions after abdominal irradiation for Hodgkin’s disease, external iliac artery lesions after uterine or prostate cancer treatment, superficial femoral artery occlusion many years after successful radiation of lower extremity sarcoma, and midaortic and visceral artery stenosis decades after external irradiation to the midabdomen for a variety of neoplasms. The clinical syndromes of radiation arteritis tend to present 10 to 15 years earlier than those of arteriosclerosis. This relative prematurity has been observed for both carotid and subclavian–axillary occlusions. The coexistence of risk factors for arteriosclerosis, such as hyperlipidemia, male gender, smoking, and hypertension, also predisposes to radiation arteritis. For example, 26 of the 28 patients in our study were smokers. The microscopic similarity of arteriosclerosis and radiation-induced lesions suggests possible shared pathogenic mechanisms. It is believed that superimposed arteriosclerosis can accelerate the development of stenosing or aneurysmal lesions initiated by irradiation.

George Andros, Peter A. Schneider, and Robert W. Harris

With the expanded application of the radiation therapy of malignancies has come the increased recognition of radiation-induced arteritis. Because ensuing vascular complications often develop insidiously, presenting as chronic ischemic syndromes, the role of earlier radiation is often overlooked. Radiation-associated arteriopathy is often misconstrued to be the more widely prevalent arteriosclerosis. Both are diseases of the elderly and are seen most often in technologically advanced societies, arteriosclerosis with its multiple risk factors and postirradiation arterial degenerative lesions many years after the treatment of neoplasms. A synergistic effect with arteriosclerosis is suggested in that the predisposing factors of arteriosclerosis appear to potentiate the injurious effects that radiation therapy has on major arteries. We have treated 28 patients with radiation-induced arterial lesions. This experience underscores the importance of understanding the similarities and diversities of these lesions; current concepts of the pathophysiology of the vascular lesions; the various clinical syndromes seen in different segments of the arterial system; therapeutic interventions that are safe, effective, and durable; and the role of arterial surveillance and possible techniques for prevention.

COMPARISON WITH ARTERIOSCLEROSIS Radiation-associated arterial lesions and arteriosclerosis are both segmental in nature, although the latter can be diffuse. It is axiomatic that the vessels affected by radiation lie within the field of treatment. Similarly, vessels outside the irradiated field are essentially disease-free. Associated injuries to adjacent tissue such as skin, muscle, lung, rectum, bladder, and other tissues can occur. However, venous injury is rare, and we have not observed clinically relevant damage to nerves adjacent to radiation-injured arteries. The sites of radiation arteritis are atypical compared with the segmental distribution of arteriosclerotic lesions. In the cerebrovascular circulation, one or both common carotid arteries may be affected while the bifurcation is spared. Subjacent vertebral arteries often are narrowed not at their origins but distally, corresponding to the radiation portal. When carotid bifurcation disease is identified by a bruit,

PATHOPHYSIOLOGY Early and late sequelae of arterial irradiation have been characterized clinically and histopathologically. The severity of the arterial injury is related to radiation dose. Smaller doses cause lesser degrees of cellular damage, whereas larger doses may be acutely or subacutely necrotizing. Macroscopic radiation effects include arterial spasm and epithelial denudation. Within 24 hours, intimal disruption, subintimal edema, and internal elastic membrane fragmentation are widespread. This is followed by degeneration of collagen and smooth muscle. Subsequently, adventitial fibrosis, hemorrhage, and lymphocytic infiltration occur. The sensitivity of elastic tissue to irradiation damage, in particular, might partially account for the preferential occurrence of rupture in affected elastic arteries. Signs of healing tend to occur along with myointimal fibrous proliferation and luminal resurfacing with nonendothelial cells. The resultant artery, with its altered architecture, can undergo subsequent arteriosclerotic degeneration with foam cell deposition and plaque formation. Diminished fibrinolytic activity, endothelium-derived plasminogen activator activity, and prostacylin synthesis have been reported. Among early lesions (2.5 cm) common iliac artery, allowing treatment of significantly more patients, particularly female and Asian patients.

RESULTS More than 1000 IBDs have been implanted worldwide, yet such numbers are not represented in the published literature. The first reported series by Greenberg and associates in 2006 included 21 patients with three technical failures (14%), all related to the inability to visualize the origin of the internal iliac artery as a result of significant stenosis. Ziegler and associates analyzed 46 patients treated with S-IBDs; the first 26 patients were treated using an early-generation unibody configuration, and the last 20 used the S-IBD system. Technical success improved from 58% with the early-generation device to 85% with the current S-IBD. There were no perioperative deaths, and of the 35 IBDs successfully implanted, none developed endoleak, component separations, or migration. There were four branch occlusions after a mean follow-up of 26 months. Haulon and colleagues reported on 52 patients treated in Lille, France, or at the Cleveland Clinic. Technical success occurred 94% of the time, and during the mean follow-up of 14 months there were no conversions, ruptures, or aneurysm-related deaths. Verzini and associates from Perugia, Italy, reported the only comparative analysis of IBDs versus hypogastric exclusion in 74 patients. In that study, there were no differences in procedure time, contrast use, and technical success, and there were no early deaths. However, there was a trend toward more endoleaks (19% vs. 4%) and pelvic ischemic symptoms (22% vs. 4%) among patients treated with coil embolization when compared with patients treated with iliac branch devices. Karthikesalingam and associates published a conglomerate analysis of nine studies involving 196 patients treated with IBDs. Technical success ranged from 85% to 100%. There were no aneurysm-related deaths. Only one patient with patent IBD complained of buttock claudication. However, late thrombosis of the IBD occurred in 24 patients (12%) and resulted in buttock claudication in 12 (50%) of these patients, implying the importance of antegrade internal iliac artery flow. Endoleak rates were exceedingly low, with only one type I (0.5%) and two type III endoleaks (1%). Type II endoleaks were treated conservatively and were not associated with sac expansion. Reinterventions were required in 12 patients (6%), including five with occlusion stent graft limbs to the external iliac artery. The anatomic suitability for IBD was not detailed in most studies, but in one study (Tielliu and colleagues) the applicability of the repair was criticized for being acceptable in only 52% of their potential IBD candidates. The same group compared open repair of CIA aneurysms to EVAR with an IBD and found that endovascular procedures had fewer complications and similar patency to open repair. An update from Cao’s group reported 100 patients treated with 95% technical success and 81% patency at 5 years. Growth was noted in only 4% of the patients, and there were three device-related endoleaks (one type III and two distal type I) that required treatment. The latest report from the Cleveland Clinic included 138 devices in 130 patients. Technical success was 95% and patency at 5 years was 82%. There were no patients with aneurysmal growth following IBD placement in this series. In this paper, anatomic challenges were stratified such that separate analyses were conducted for a small common iliac artery, the presence of an internal iliac artery aneurysm mandating seal within one of the later artery’s trunks, and tight ostial stenosis of the internal iliac artery. None of these factors had any affect on patency or endoleaks, and only endoleak was associated with a lower

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technical success rate than experienced in patients without concomitant internal iliac artery occlusive disease.

DISCUSSION The most common cause of technical failures resulted from an inability to visualize the target internal iliac artery following introduction of the IBD delivery system. This occurs in the setting of small external iliac arteries and diseased internal iliac artery origins, and it results from compression of the internal iliac artery origin by the IBD delivery system. The initial technical failures were potentially avoidable by using a modified delivery technique. After the IBD sheath is introduced, if the internal iliac artery origin is not visualized, the preloaded wire is snared, and the constrained IBD device (still entirely within the delivery sheath) is withdrawn into the external iliac artery. The contralateral sheath is advanced up and over, and the target internal iliac artery is cannulated while the IBD delivery system remains distal to the internal iliac artery origin. A balloon (4–6 mm) is placed into the internal iliac artery and inflated. The IBD is advanced while the internal iliac artery balloon remains inflated, akin to a kissing balloon technique. When this technique is used, the internal iliac artery can be visualized and accessed more readily following IBD deployment. Additional causes of technical failure can result from iatrogenic dissections that occur during implantation. The distal internal iliac artery bed is always tortuous and often fragile. We now obtain access into a distal gluteal branch with a gentle steerable catheter and wire system, and then we place a stiff wire through the catheter. The self-expanding stent graft generally passes easily, and the likelihood of iatrogenic injury is minimized when the wire is placed into the distal circulation rather than into the common trunk or proximal divisions. Caution must be taken when advancing large sheaths through an implanted IBD. Dislodgement of the IBD can occur and is preventable by stabilization of the internal iliac artery branch with a balloon from the contralateral side, or using an alternative access to introduce sheaths that are larger than 20 Fr. There is a learning curve associated with procedure planning. Before the B-IBD device was developed, many patients were excluded as a result of common iliac artery length. With the advent of a device that simplifies the use of IBDs in patients with a common iliac artery of 6 cm or less, the need for H-IBD or S-IBD devices has declined, and these devices have been modified to mitigate some of the theoretical complications that can occur as a result of limited overlap between the limb bridging the IBD repair with the AAA repair. An additional stent has been placed proximal to the branch, providing a longer segment of overlap, resulting in the need for a longer common iliac artery. Thus, currently patients with a common iliac artery longer than 6 cm are treated with and H-IBD or S-IBD and all others with the B-IBD. Iliac branch technology represents one of the methods by which complex anatomy can be treated with an endovascular approach in a manner analogous to open repair. The principles of antegrade pelvic blood flow are maintained, and patients are encouraged to exercise following their repair. The techniques required for implantation of IBDs are similar to techniques required to do other complex procedures, such as thoracoabdominal branches and supraaortic trunk branch repairs. The iliac bed is an appealing region to perfect such techniques, because a technical failure in the setting of an iliac aneurysm most commonly results in an occluded internal iliac artery, which is how most aneurysms are managed today. The use of such devices do require longer procedure times and potentially more contrast and radiation, and thus they must be employed judiciously in the context of a risk and benefit to such patients. In our practice this translates into reserving IBD for patients who ambulate enough to be affected by claudication and for all patients considered to be at risk for spinal cord ischemia as a result of more proximal aortic disease. The option for unilateral or bilateral internal iliac artery preservation with IBDs further advances the potential advantages of

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endovascular repairs. The procedure can be performed with high technical success rates and with acceptable long-term patency results, without any considerable increase to the risks of the standard endovascular aneurysm repair. The use of these devices in difficult anatomies must be carefully considered. Short internal iliac arteries appear to be well managed by the development of the B-IBD, yet extreme calcification and ostial disease of the vessel remain challenging. However, widespread use of IBD still faces several challenges including regulatory approval, physician training, and an evaluation of the late results of IBDs including device integrity, reinterventions, and occlusion rates.

Selected References Donas KP, Torsello G, Pitoulias GA, et al: Surgical versus endovascular repair by iliac branch device of aneurysms involving the iliac bifurcation, J Vasc Surg 53:1223–1229, 2011. Greenberg RK, Lu Q, Roselli EE, et al: Contemporary analysis of descending thoracic and thoracoabdominal aneurysm repair: A comparison of endovascular and open techniques, Circulation 118:808–817, 2008. Greenberg RK, West K, Pfaff K, et al: Beyond the aortic bifurcation: Branched endovascular grafts for thoracoabdominal and aortoiliac aneurysms, J Vasc Surg 43:879–886, 2006. discussion 886–877.

Iliac Artery Conduits for Endovascular Access Brian G. Peterson and Jon S. Matsumura

Iliac artery occlusive disease or small-caliber vessels often make endovascular abdominal aortic aneurysm repair (EVAR) and thoracic endovascular aortic repair (TEVAR) from remote femoral access difficult. In fact, limitation in access was one of the most common reasons for conversion to open aneurysm repair in the European Collaborators on Stent-graft Techniques for Aortic Aneurysm Repair (EUROSTAR) registry of patients undergoing attempted EVAR, and access-related complications were seen in 13% of the registry patients. Likewise, iliac conduits were used in 9% to 21% of TEVAR patients in industry-­ sponsored trials owing to access limitations. Various adjunctive techniques have been developed to overcome access-related complications.

ILIAC ARTERY ACCESS One of the most commonly used conduits in the setting of endovascular aortic repair is the surgically created conduit approached through a retroperitoneal exposure to the common iliac artery or distal aorta. Preoperative imaging helps to determine which side is chosen, taking into account the vessel’s size and calcification. A standard incision is made in an oblique, slightly curvilinear fashion two fingerbreadths from the anterior superior iliac spine, starting at or slightly above the level of the umbilicus. The external oblique, internal oblique, and transversalis muscles are divided with electrocautery, exposing the peritoneum. The retroperitoneal space is exposed by gently mobilizing the peritoneum with a sponge stick. The ureter is identified, and if the left side is chosen, care is taken to avoid manipulating the nerve plexus draped over the common iliac artery. A self-retaining retractor is useful to maintain exposure while the conduit is created. After systemic anticoagulation, depending on the patient’s anatomy, two vascular clamps or a side-biting clamp is placed on the

Haulon S, Greenberg RK, Pfaff K, et al: Branched grafting for aortoiliac aneurysms, Eur J Vasc Endovasc Surg 33:567–574, 2007. Karthikesalingam A, Hinchliffe RJ, Holt PJ, et al: Endovascular aneurysm repair with preservation of the internal iliac artery using the iliac branch graft device, Eur J Vasc Endovasc Surg 39:285–294, 2010. Oderich GS, Greenberg RK: Endovascular iliac branch devices for iliac aneurysms, Perspect Vasc Surg Endovasc Ther 23:166–172, 2011. Parlani G, Verzini F, De Rango P, et al: Long-term results of iliac aneurysm repair with iliac branched endograft: A 5-year experience on 100 consecutive cases, Eur J Vasc Endovasc Surg 43:287–292, 2012. Verzini F, Parlani G, Romano L, et al: Endovascular treatment of iliac aneurysm: Concurrent comparison of side branch endograft versus hypogastric exclusion, J Vasc Surg 49:1154–1161, 2009. Wong S, Greenberg RK, Brown CR, Mastracci TM, Bena J, Eagleton MJ: Endovascular repair of aortoiliac aneurysmal disease with the helical iliac bifurcation device and the bifurcated-bifurcated iliac bifurcation device, J Vasc Surg 58(4):861-9, 2013 Oct. Ziegler P, Avgerinos ED, Umscheid T, et al: Branched iliac bifurcation: 6 years experience with endovascular preservation of internal iliac artery flow, J Vasc Surg 46:204–210, 2007.

iliac artery, and a 10-mm polyester graft is sewn in an end-to-side fashion to the vessel using a running monofilament suture (Figure 1). A graft of this size will accommodate both the delivery sheath and a 5-Fr sheath used for passage of a diagnostic angiogram catheter (Figure 2). This allows single-sided access in the setting of TEVAR. The anastomosis can be reinforced with a felt cuff in patients with friable vessels, and it can be marked with a radiopaque clip so that the level of the anastomosis can be visualized fluoroscopically during later sheath passage. In obese patients or in deep wounds, the graft is often tunneled out the abdominal wall through a separate stab incision in the skin to keep the sheath from entering into the native vessel at a steep angle. The open end of the graft is clamped, the side of the conduit is punctured with an entry needle, and the sheaths are inserted through the side of the graft to avoid unnecessary blood loss if sheath exchanges are required. The tip of the delivery sheath should be advanced through the anastomosis so that the anastomosis is not disrupted with multiple device exchanges. Manual stabilization of the anastomosis as the delivery sheath passes through the anastomosis can also aid in preventing disruption. After the endovascular portion of the procedure is completed, the sheaths are removed from the conduit, the graft is transected, and the remaining small cuff is oversewn or transected and closed with a vascular stapler. Presence of this cuff should be noted because it can lead to some confusion on postoperative imaging. Alternatively, in the setting of symptomatic iliac occlusive disease, the graft can be tunneled under the inguinal ligament and can be used as an iliofemoral bypass. In either case, the patient has a prosthetic graft that is susceptible to infection. Another option for endovascular access is direct aortic or iliac access. This can be performed through the retroperitoneal approach described earlier or through a transperitoneal approach if the patient is undergoing simultaneous exploratory laparotomy (e.g., trauma patients). This option avoids leaving behind prosthetic material prone to infection, or if too large a cuff is left behind, it may be a source of distal embolization. Some describe puncturing the artery in the middle of a purse-string suture placed in the common iliac artery or distal aorta and cinching down the adventitial suture after removing the sheath. Although this technique and the standard iliac conduit technique overcome iliac artery limitations, both require retroperitoneal dissection, which can add to the morbidity of endovascular aortic procedures. The retroperitoneal approach, in comparison to the femoral approach used during endovascular aortic procedures, has been shown to lead to a 2.6-fold greater blood loss, 1.5-day longer hospital

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endovascular repairs. The procedure can be performed with high technical success rates and with acceptable long-term patency results, without any considerable increase to the risks of the standard endovascular aneurysm repair. The use of these devices in difficult anatomies must be carefully considered. Short internal iliac arteries appear to be well managed by the development of the B-IBD, yet extreme calcification and ostial disease of the vessel remain challenging. However, widespread use of IBD still faces several challenges including regulatory approval, physician training, and an evaluation of the late results of IBDs including device integrity, reinterventions, and occlusion rates.

Selected References Donas KP, Torsello G, Pitoulias GA, et al: Surgical versus endovascular repair by iliac branch device of aneurysms involving the iliac bifurcation, J Vasc Surg 53:1223–1229, 2011. Greenberg RK, Lu Q, Roselli EE, et al: Contemporary analysis of descending thoracic and thoracoabdominal aneurysm repair: A comparison of endovascular and open techniques, Circulation 118:808–817, 2008. Greenberg RK, West K, Pfaff K, et al: Beyond the aortic bifurcation: Branched endovascular grafts for thoracoabdominal and aortoiliac aneurysms, J Vasc Surg 43:879–886, 2006. discussion 886–877.

Iliac Artery Conduits for Endovascular Access Brian G. Peterson and Jon S. Matsumura

Iliac artery occlusive disease or small-caliber vessels often make endovascular abdominal aortic aneurysm repair (EVAR) and thoracic endovascular aortic repair (TEVAR) from remote femoral access difficult. In fact, limitation in access was one of the most common reasons for conversion to open aneurysm repair in the European Collaborators on Stent-graft Techniques for Aortic Aneurysm Repair (EUROSTAR) registry of patients undergoing attempted EVAR, and access-related complications were seen in 13% of the registry patients. Likewise, iliac conduits were used in 9% to 21% of TEVAR patients in industry-­ sponsored trials owing to access limitations. Various adjunctive techniques have been developed to overcome access-related complications.

ILIAC ARTERY ACCESS One of the most commonly used conduits in the setting of endovascular aortic repair is the surgically created conduit approached through a retroperitoneal exposure to the common iliac artery or distal aorta. Preoperative imaging helps to determine which side is chosen, taking into account the vessel’s size and calcification. A standard incision is made in an oblique, slightly curvilinear fashion two fingerbreadths from the anterior superior iliac spine, starting at or slightly above the level of the umbilicus. The external oblique, internal oblique, and transversalis muscles are divided with electrocautery, exposing the peritoneum. The retroperitoneal space is exposed by gently mobilizing the peritoneum with a sponge stick. The ureter is identified, and if the left side is chosen, care is taken to avoid manipulating the nerve plexus draped over the common iliac artery. A self-retaining retractor is useful to maintain exposure while the conduit is created. After systemic anticoagulation, depending on the patient’s anatomy, two vascular clamps or a side-biting clamp is placed on the

Haulon S, Greenberg RK, Pfaff K, et al: Branched grafting for aortoiliac aneurysms, Eur J Vasc Endovasc Surg 33:567–574, 2007. Karthikesalingam A, Hinchliffe RJ, Holt PJ, et al: Endovascular aneurysm repair with preservation of the internal iliac artery using the iliac branch graft device, Eur J Vasc Endovasc Surg 39:285–294, 2010. Oderich GS, Greenberg RK: Endovascular iliac branch devices for iliac aneurysms, Perspect Vasc Surg Endovasc Ther 23:166–172, 2011. Parlani G, Verzini F, De Rango P, et al: Long-term results of iliac aneurysm repair with iliac branched endograft: A 5-year experience on 100 consecutive cases, Eur J Vasc Endovasc Surg 43:287–292, 2012. Verzini F, Parlani G, Romano L, et al: Endovascular treatment of iliac aneurysm: Concurrent comparison of side branch endograft versus hypogastric exclusion, J Vasc Surg 49:1154–1161, 2009. Wong S, Greenberg RK, Brown CR, Mastracci TM, Bena J, Eagleton MJ: Endovascular repair of aortoiliac aneurysmal disease with the helical iliac bifurcation device and the bifurcated-bifurcated iliac bifurcation device, J Vasc Surg 58(4):861-9, 2013 Oct. Ziegler P, Avgerinos ED, Umscheid T, et al: Branched iliac bifurcation: 6 years experience with endovascular preservation of internal iliac artery flow, J Vasc Surg 46:204–210, 2007.

iliac artery, and a 10-mm polyester graft is sewn in an end-to-side fashion to the vessel using a running monofilament suture (Figure 1). A graft of this size will accommodate both the delivery sheath and a 5-Fr sheath used for passage of a diagnostic angiogram catheter (Figure 2). This allows single-sided access in the setting of TEVAR. The anastomosis can be reinforced with a felt cuff in patients with friable vessels, and it can be marked with a radiopaque clip so that the level of the anastomosis can be visualized fluoroscopically during later sheath passage. In obese patients or in deep wounds, the graft is often tunneled out the abdominal wall through a separate stab incision in the skin to keep the sheath from entering into the native vessel at a steep angle. The open end of the graft is clamped, the side of the conduit is punctured with an entry needle, and the sheaths are inserted through the side of the graft to avoid unnecessary blood loss if sheath exchanges are required. The tip of the delivery sheath should be advanced through the anastomosis so that the anastomosis is not disrupted with multiple device exchanges. Manual stabilization of the anastomosis as the delivery sheath passes through the anastomosis can also aid in preventing disruption. After the endovascular portion of the procedure is completed, the sheaths are removed from the conduit, the graft is transected, and the remaining small cuff is oversewn or transected and closed with a vascular stapler. Presence of this cuff should be noted because it can lead to some confusion on postoperative imaging. Alternatively, in the setting of symptomatic iliac occlusive disease, the graft can be tunneled under the inguinal ligament and can be used as an iliofemoral bypass. In either case, the patient has a prosthetic graft that is susceptible to infection. Another option for endovascular access is direct aortic or iliac access. This can be performed through the retroperitoneal approach described earlier or through a transperitoneal approach if the patient is undergoing simultaneous exploratory laparotomy (e.g., trauma patients). This option avoids leaving behind prosthetic material prone to infection, or if too large a cuff is left behind, it may be a source of distal embolization. Some describe puncturing the artery in the middle of a purse-string suture placed in the common iliac artery or distal aorta and cinching down the adventitial suture after removing the sheath. Although this technique and the standard iliac conduit technique overcome iliac artery limitations, both require retroperitoneal dissection, which can add to the morbidity of endovascular aortic procedures. The retroperitoneal approach, in comparison to the femoral approach used during endovascular aortic procedures, has been shown to lead to a 2.6-fold greater blood loss, 1.5-day longer hospital



Iliac Artery Conduits for Endovascular Access

FIGURE 1  A 10-mm polyester graft anastomosed to the common

iliac artery in an end-to-side fashion.  (From Peterson BG: Conduits and endoconduits, percutaneous access, J Vasc Surg 52:60S–64S, 2010.)

FIGURE 2  A conduit used during thoracic endovascular aortic repair.

Notice that the end of the conduit is controlled with a clamp and that two sidewall punctures permit simultaneous passage of a 5-Fr sheath for diagnostic purposes and a 24-F sheath for device delivery.  (From Peterson BG: Conduits and endoconduits, percutaneous access, J Vasc Surg 52:60S–64S, 2010.)

stay, 82% longer procedure time, and a 21% incidence of retroperitoneal hematoma. Nevertheless, surgical conduits or direct arterial access through a retroperitoneal exposure are excellent options for overcoming iliac artery size and tortuosity limitations. These options require involvement of physicians with surgical expertise and stringent adherence to sterile techniques as can be found in the operation room setting.

REMOTE FEMORAL ARTERY ACCESS In an effort to avoid the added morbidity of retroperitoneal exposures, various adjunctive techniques can be employed to allow endovascular aortic procedures to be performed through a femoral approach. When mild iliac artery occlusive disease is present, balloon angioplasty alone may be enough to allow sheath passage. Alternatively, the sequential passage of hydrophilic dilators of increasing size can be used. Isolated distal external iliac artery disease can often

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be addressed with retrograde endarterectomy from a standard groin exposure. A less commonly used option is in situ sheath dilatation. This technique involves using a sheath smaller than that typically needed for device delivery, followed by balloon angioplasty within the sheath using a noncompliant balloon, stretching the sheath to allow passage of the device. These techniques are all viable options when faced with mild occlusive disease, but care must still be taken to avoid vessel disruption or dissection. Recognizing the potential for iliac artery injury associated with these adjunctive maneuvers, a novel technique of creating an endoluminal iliofemoral bypass conduit has been described. This involves suturing a prosthetic graft to a bare metal stent, which is then loaded into a sheath. The device is deployed with the bare metal stent across the origin of the hypogastric artery and the graft portion of the device extending down to the level of the femoral access. The external iliac artery can then be dilated with a noncompliant angioplasty balloon from within the graft up to a diameter large enough for the delivery sheath to be passed through the graft. After the endovascular aortic procedure is completed, the end of the graft is anastomosed to the femoral artery. This ingenious technique allows femoral access to the aorta despite unfavorable external iliac artery anatomy. Much like the endoluminal iliofemoral bypass technique, use of an endoconduit overcomes most iliac artery limitations, avoids retroperitoneal dissections, and allows open or percutaneous femoral access during aortic endovascular procedures. Unlike the endoluminal iliofemoral bypass, the endoconduit uses readily available prefabricated stent grafts and can be used to overcome disease in both the common and external iliac arteries. With this technique, the endoconduit is advanced through the diseased iliac segment (occasionally after predilatation with a small-profile angioplasty balloon), and the stent graft is deployed from the common iliac artery into the distal external iliac artery or proximal common femoral artery. Iliac limb devices or other commercially available covered stents can be used off label as endoconduits. Devices designed as iliac limbs are often tapered, with the large-diameter portion of the graft placed in the common iliac and the smaller-diameter portion positioned in the distal external iliac or proximal common femoral artery. The commercially available covered stents are usually lower profile compared to the iliac limbs and have more flexibility, which may be beneficial in tortuous iliac arteries, but the large delivery sheaths seem to pass through the iliac limb endoprostheses without internal stents more smoothly. After deployment across the iliac segment, the proximal and distal ends of the endoconduit are ballooned to create a seal. The midportion of the covered stent is then aggressively angioplastied with a noncompliant balloon, creating a controlled rupture of the vessel and allowing passage of the delivery sheath through the endoconduit (Figure 3). Angioplasty with a 10-mm balloon is required for passage of sheaths with an inner diameter up to 22 Fr, whereas a 12-mm noncompliant balloon is required for larger sheaths. Endoconduits are an excellent option for overcoming unfavorable iliac artery anatomy, but several potential complications and a few tips deserve mentioning. Patency of the hypogastric artery must be noted on preoperative imaging or initial angiogram at the time of the endovascular procedure. With all else being similar, choose the iliac system with an occluded or more stenotic hypogastric artery as the side on which to use the endoconduit. In this setting, patients are more likely to tolerate coverage of the hypogastric artery if the contralateral vessel is widely patent. While devastating complications of decreased pelvic perfusion are possible and include paraplegia, gluteal necrosis, and colonic ischemia, these have not been seen with endoconduit use. More commonly, patients report transient buttock claudication, which is usually responsive to cilostazol. Back bleeding from a patent hypogastric into the area of controlled iliac rupture is also a theoretical concern. If the most diseased portion of the iliac system is adjacent to a patent hypogastric artery, then preemptive coil embolization of the hypogastric before endoconduit placement may be worthwhile to prevent hemorrhage analogous to a type II endoleak in this area. The setting where significant bleeding

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FIGURE 4  Extravasation of contrast (large arrow) from disruption of FIGURE 3  Delivery sheath (24-Fr) passing through the endoconduit

after ballooning with a 12-mm noncompliant balloon.  (From Peterson BG, Matsumura JS: Internal endoconduit: An innovative technique to address unfavorable iliac artery anatomy encountered during thoracic endovascular aortic repair, J Vasc Surg 47:441–445, 2008.)

the intervening segment of artery between the end of the endoconduit (small arrow) and the tip of the delivery sheath.

Selected References has occurred has been when the distal end of the endoconduit is not brought down to at least the inguinal ligament. There have been ruptures of the intervening segment between the end of the endoconduit and the femoral access site (Figure 4). These have been repaired with a short interposition graft from the end of the endoconduit to the common femoral artery, but this type of repair can be cumbersome and is likely avoided by bringing the endoconduit closer to the access site. Another option when using open femoral artery exposure (not possible with percutaneous repair) would be to use a long stent graft as the endoconduit such that it extends out the femoral artery and after completing the aortic repair, perform an anastomosis to the femoral artery much like the endoluminal iliofemoral bypass. Regardless of the technique used to overcome unfavorable iliac anatomy from the femoral approach, it is imperative to maintain wire access across the iliac system until the delivery sheaths are removed. Hemorrhage and resultant hypotension from an iliac artery rupture is profound, and being able to control the vessel with a balloon while the rupture is addressed endovascularly or surgically can be life-saving. Despite improvements in aortic stent-graft technology, large delivery sheaths are still required for EVAR and TEVAR, and accessrelated issues remain common. A variety of techniques exist to address unfavorable iliac artery anatomy, each with its own advantages and disadvantages.

Carpenter JP: Delivery of endovascular grafts by direct sheath placement into the aorta or iliac arteries, Ann Vasc Surg 16:787–790, 2002. Criado FJ: Iliac arterial conduits for endovascular access: Technical considerations, J Endovasc Ther 14:347–351, 2007. Etezadi V, Katzen BT, Benenati JF, et al: Retroperitoneal versus direct femoral artery approach for thoracic endovascular aortic repair access: A case-control study, Ann Vasc Surg 25:340–344, 2011. Fairman RM, Criado F, Farber M, et al: Pivotal results of the Medtronic Vascular Talent Stent Graft System: The VALOR trial, J Vasc Surg 48:546–554, 2008. Lee WA, Berceli SA, Huber TS, et al: Morbidity with retroperitoneal procedures during endovascular abdominal aortic aneurysm repair, J Vasc Surg 38:459–465, 2003. Makaroun MS, Dillavou ED, Kee ST, et al: Endovascular treatment of thoracic aortic aneurysms: Results of the phase II multicenter trial of the GORE TAG thoracic endoprosthesis, J Vasc Surg 41:1–9, 2005. Matsumura JS, Cambria RP, Dake MD, et al: International controlled clinical trial of thoracic endovascular aneurysm repair with the Zenith TX2 endovascular graft: 1-year results, J Vasc Surg 47:247–257, 2008. Peterson BG, Matsumura JS: Internal endoconduit: An innovative technique to address unfavorable iliac artery anatomy encountered during thoracic endovascular aortic repair, J Vasc Surg 47:441–445, 2008. von Segesser LK, Marty B, Tozzi PG, et al: In situ introducer sheath dilatation for complex aortic access, Eur J Cardio Thor Surg 22:316–318, 2002. Yano OJ, Faries PL, Morrissey N, et al: Ancillary techniques to facilitate endovascular repair of aortic aneurysms, J Vasc Surg 34:69–75, 2001.



Conversion to Open Surgical Treatment After Failed Endovascular Aortic Aneurysm Repair

Conversion to Open Surgical Treatment After Failed Endovascular Aortic Aneurysm Repair Rebecca L. Kelso and Sean P. Lyden

Endovascular aneurysm repair (EVAR) has proved to be safe and effective for the primary treatment of aortic aneurysms. However, endoleaks, endotension, migration, and stent fracture can lead to aneurysm growth and rupture if not treated in a timely fashion. Although transition to newer-generation material and technology has improved the durability of EVAR, complications still occur. Despite the success rate of secondary interventions, patients who are not candidates for an endovascular repair or have unsuccessful interventions require conversion and explant of their endograft. As the length of follow-up increases, studies have also shown that all devices remain susceptible to the risk of removal. The overall conversion rate is 0% to 9% based on published literature within various EVAR series. The true risk of conversion is difficult to ascertain because many patients are lost to follow-up or report to a different institution for removal. Devices that are placed outside of the instructions for use have been found to carry a higher risk of endograft failure and subsequent removal. Differences exist between early and late conversions, which are defined as occurring before and after 30 days, respectively. A systematic literature review found that the incidence of early conversion is 0.3% to 5.9%, with a decrease in recent years. For late conversions they found that the incidence averaged 0.4% to 6.3%. In either situation, conversion to open surgery and endograft explant requires careful planning and technical skill.

INDICATIONS The indications for early conversion are often technical from failure of deployment as a result of anatomic or contralateral gate difficulties, inadvertent coverage of renal arteries, or vessel rupture. In these circumstances, conversion is usually related to poor planning, use of devices outside of the instructions for use (IFU), or lack of technical expertise. The indications for late explant of an aortic endograft are primarily related to device failure. This may be related to one of the many types of endoleaks with or without an enlarging aneurysm sac or migration. With the exception of a type IV endoleak, all types of endoleaks and endotension have been reported causes of aneurysm rupture. The need for explant may also be urgent or emergent as related to graft infection, including aortoduodenal fistulas, or rupture. Limb complications (such as thrombosis caused by stenoses or kinking) can also be a reason for removal when other endoluminal or surgical revascularization options do not exist. Close monitoring of EVAR patients with secondary interventions has helped identify and, in many cases, successfully treat complications. Not all endoleaks are equal in terms of risk to the patient, and literature supports early management of type I and III endoleaks to prevent aneurysm rupture. Although endovascular salvage of EVAR

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complications and even recurrent rupture is a viable and often successful option for many patients, conversion is required for those that fail.

PREOPERATIVE CONSIDERATIONS Preoperative evaluation deserves mention for a few factors including overall patient health, as well as preoperative imaging and preparation. The preoperative strategy is not considerably different from other patients undergoing open aneurysm surgery, including those with rupture or infection. Medical optimization of cardiac and pulmonary status is critical because many patients have been deemed high risk before the initial endograft implant. Knowledge of the type and placement of the graft before explant is also useful and can be found in the patient’s previous medical records as well as determined by plain abdominal film and computed tomography (CT) imaging. Contrast-enhanced spiral CT imaging enables a three-dimensional (3-D) reconstruction, which usually helps identify the cause of endograft failure and thus plan the surgical options, including clamping positions and reconstruction options.

OPERATIVE TECHNIQUES At its most basic, explant of an endograft is approached like that of an open aneurysm repair. Technical challenges encountered during removal of endografts include management of suprarenal components, incorporation of stents from endografts into the vessel wall, presence of external stents or barbs, and periaortic inflammation. In terms of exposure, both retroperitoneal and midline approaches have been used. There are advocates for each approach; however, devices with suprarenal fixation have been more commonly approached by a retroperitoneal approach in most series. Both approaches are equally effective, with the key being the anticipated proximal clamp location. Cases without a suprarenal component and long aortic neck are suitable for infrarenal clamping. Early papers advocated infrarenal clamping, with a temporary release to pull out more proximal portions. However, the ability to temporarily place a higher clamp is of critical importance because releasing the proximal fixation from the aorta can be difficult. In obtaining supravisceral aortic control without an aortoduodenal fistula, it should be the surgeon’s preference and expertise to use a transperitoneal incision with or without medial visceral rotation versus retroperitoneal incision and exposure. In general, endografts with proximal fixation problems are more likely to be approached from the retroperitoneum with a supravisceral clamp. Once the graft has been removed, the clamp position can be moved a location to limit the renal and visceral ischemic insult. Distal exposure can require the ability to access the external and internal iliac arteries, especially if the entire device is to be removed. An alternative strategy may employ balloon occlusion of the endograft limbs once the aorta is opened and the graft is transected. Some have suggested the use of endoluminal proximal balloon occlusion; however, we find this approach to be cumbersome and unhelpful. To date there is no association between clamp positions (suprarenal vs. infrarenal) and perioperative kidney failure. Periaortic inflammation can increase the difficulty of the exposure. It has been identified in grafts with both active and passive fixation and grafts with internal and external stents. This finding is unpredictable and not always present—even within similar graft types. Some devices have intimal overgrowth of stents exposed to the vessel wall (e.g., AneuRx, Medtronic, Santa Rosa, CA), and removal of these stents can produce an uncontrolled endarterectomy of the area involved. To aid in removing incorporated portions of endografts we recommend secure control of the aorta above the area in

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question. The distal device can then be removed in segments when necessary or incorporated into a hybrid open repair when the EVAR device is very adherent to the native vessel wall. Once the proximal juxtarenal, supravisceral (if needed), and distal control is complete, we recommend opening the aortic sac without clamping unless there is a proximal endoleak. Opening the midportion of the aneurysm sac allows for the evaluation of the positioning of the graft and source of failure. This provides confirmation of the type of endoleak and identifies areas of the graft that are secure in case complete removal is not possible. Managing and treating the endoleaks without graft explantation may be reasonable when a patient might not physiologically tolerate aortic clamping and complete removal. External suture fixation for type I endoleaks using transaortic to graft sutures has been successfully performed. Some have sutured through felt wrapping for reinforcement of the proximal sealing stent. There are also reports of ligation of lumbar arteries or inferior mesenteric arteries (IMA) responsible for type II endoleaks. Unfortunately, there are also anecdotal reports of continued failures of buttressed grafts with proximal migration as well as development of new types of endoleaks. Choosing this type of open secondary intervention compared to a complete removal with synthetic graft replacement should be carefully weighed

FIGURE 1 The top stent is collapsed into a 20-mL syringe, retracting the hooks from the wall of the aorta without damaging the aorta.  (Used with permission from Koning OH, Hinnen JW, van Baalen JM: Technique for safe removal of an aortic endograft with suprarenal fixation, J Vasc Surg 43:855–857, 2006.)

in light of the patient’s physiologic status. If the procedure fails, the risk of repeat open surgery would be much higher. There are many helpful maneuvers to assist in successful removal of the aortic stent graft. The most commonly used is a traditional clamp-and-pull method. In stents with proximal barbs it is helpful to collapse the proximal stent. A technique we have used for removing suprarenal fixation devices with barbs involves collapsing the device into a 20-mL syringe (Figure 1). By cutting off the closed end of a syringe, the syringe cylinder can be then used as a type of short sheath to recapture and separate the proximal stent safely from the aortic wall. For endografts with nitinol stents, iced saline has been suggested to help reduce diameter and ease removal, but we have not found this effective in most circumstances. Metal wire cutters are a necessary instrument to have in the operating room because they can help transect the device at any point with metal. They can usually be found with instruments used for open heart procedures because they are used to cut sternal wires. They can be used to facilitate the removal of uncovered suprarenal fixation. When plans include leaving portions of well-incorporated devices in situ, metal wire cutters are invaluable to facilitate creating a place to safely suture to the remaining components. Large balloon-expandable stainless steel stents within the aortic neck can be crushed with a Kelly clamp or divided with metal cutters to aid in their atraumatic removal. Although removing the proximal device seems to concern most surgeons, removal of the distal limbs can be equally difficult. When a long length of the limb remains in a normal iliac artery it can be just as difficult to remove. Difficulty can also be encountered when a distal balloon-expandable stent has been placed. When control is possible distal to the end of the endograft limbs, transection of the native artery and sewing at this level is the simplest solution. When the limbs are not removable or extend far down into the external iliac artery, it is usually easier to do a hybrid reconstruction by leaving some of the endograft limb in place. The last option is to bypass to an artery distal to the end of the stent, such as the femoral artery. Regardless of the type of reconstruction, it is important to try to maintain pelvic flow to minimize the risk of colonic ischemia. Initial publications recommended against using a transected endograft as a part of the anastomosis because of concern regarding future pseudoaneurysm; however, to date this problem has not been reported. When portions of an endograft have been incorporated into the repair, tight closure of the aortic sac around the device can minimize potential device migration. Complete removal of the endograft should be the goal of the procedure. In a series of 41 patients treated with conversion at our center, stent grafts were not completely removed owing to aneurysmal

FIGURE 2  Hybrid reconstruction: Exam-

A

B

C

ples incorporating residual endografts into the aortic reconstruction. A, Incorporated proximal Zenith endograft into distal aortobiiliac repair. B, Proximal Dacron graft with distal AneuRx limbs. C, Beveled proximal Dacron graft with left renal implant anastomosed to distal Talent endograft.  (Used with permission from Kelso RL, Lyden SP, Butler B, et al: Late conversion of aortic stent grafts, J Vasc Surg 49:589–595, 2009.)



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Conversion to Open Surgical Treatment After Failed Endovascular Aortic Aneurysm Repair

progression of the suprarenal segment with abdominal aortic aneurysm (AAA) exclusion and good distal fixation, difficulty removing a well-incorporated endograft both proximally and distally, and isolated limb problem with good proximal fixation. Hybrid reconstructions were performed in these patients (Figure 2). Important factors when deciding when not to remove the entire endograft include location of the endograft problem (proximal or distal), extent of the problem, and prevention of injury to the native tissue. Using sections of well-incorporated graft potentially improves mortality by limiting the technical challenges of a more extensive operation. Patients who have in situ retention of a portion of the endograft still require lifelong CT surveillance because future complications of the remaining EVAR elements remains a possibility. The rate of aortic graft infection has been estimated in a metaanalysis by Sharif and coworkers to be 0.16% at 2 years after EVAR. There have been reports of aortoduodenal fistulas even in cases without large aneurysm sacs. The mechanism of the aortoduodenal fistula is unclear in EVAR because the graft is always covered by the aortic wall; the fistula may be related to the radial forces of the stent or primary or secondary infection. Further management of the infected graft is no different than primary management of infected aortic grafts or aortoduodenal fistulas. The concepts of removing infected material, managing the stump, and débriding infected tissue are unchanged. A hybrid reconstruction is not an option because the presence of infection requires complete removal of all portions of the endograft.

In most instances, a bifurcated aortoiliac graft reconstruction is performed. When the distal aorta and iliacs are normal, a tube graft repair may be appropriate. In cases of infection there are several options for reconstruction, including extra-anatomic or anatomic. If anatomic reconstruction is used, the choice of conduit can be homograft, rifampin-soaked graft, or deep femoral vein. In circumstances where the renal arteries are involved or iliac vessels are injured beyond repair, additional bypasses may be necessary.

POSTOPERATIVE CONSIDERATIONS Compared to open primary aortic repair, the postoperative management is similar. Cardiopulmonary and renal complications are the biggest risks. A large meta-analysis also compared rates of conversion and mortality in both early and late explants. In 178 patients undergoing early conversion, the mortality rate was 12.4%. The mortality in late conversion (279 patients) was similar at 10%. When further extrapolated in reviewing cases that underwent emergent late conversion as a result of rupture, the average mortality was increased to 25.6% (Table 1). This increase in mortality is a consistent finding among other studies. It is related not only to the emergent nature of the surgery but also to the increased cardiovascular risk of these patients, complexity of removal, and blood loss. Both the EUROSTAR (EUROpean Collaboration on Stent/graft Techniques for Aortic aneurysm Repair) registry and our own study found that patients experiencing rupture after

TABLE 1:  Late Conversions to Open Surgery: Incidence and Mortality Late Conversions Reference

Perioperative Mortality

Ruptures

Perioperative Mortality

No. of Patients

No.

%

No.

%

No.

%

No.

Lipsitz (2003)

386

11

2.8

2

18.2

7

1.8

1

14.3

Terramani (2003)

319

9

2.8

1

11.1

2

0.6

—

—

Verhoeven (2004)

308

9

2.9

0

0.0

1

0.3

0

0.0

Dalaines (2004)

186

4

2.2

0

0.0

—

—

—

—

Kong (2005)

594

16

2.7

1

6.3

1

0.2

1

100.0

2664

28

1.1

0

0.0

—

—

—

—

649

29

4.5

0

0.0

4

0.6

0

0.0

2846

40

1.4

6

15.0

5

0.2

—

—

Brewster (2006)

873

20

2.3

4

20.0

5

0.6

2

40.0

Tiesenhausen (2006)

117

26

22.2

3

11.5

6

5.1

3

50.0

Jimenez (2007)

574

12

2.1

0

0.0

—

—

—

—

AURC (2008)

1588

20

1.3

3

15.0

8

0.5

2

25.0

Coppi (2008)

205

5

2.4

—

—

2

1.0

—

—

Kelso (2009)

1606

41

2.6

7

17.1

6

0.4

4

66.7

Pitoulias (2009)

625

9

6.2

4

10.3

4

0.6

1

25.0

Brinster (2010)

1273

21

1.6

0

0.0

1

0.1

0

0.0

14813

330

2.2

31

10.0

52

0.4

14

31.8

Life Registry (2005) Verzini (2006) EUROSTAR (2006)

Total

%

Kelso RL, Lyden SP, Butler B, et al: Late conversion of aortic stent grafts, J Vasc Surg 49:589–595, 2009. Lipsitz EC, Ohki T, Veith FJ, et al: Delayed open conversion following endovascular aortoiliac aneurysm repair: Partial (or complete) endograft preservation as a useful adjunct, J Vasc Surg 38:1191–1198, 2003.

264

AORTIC ANEURYSM

EVAR had either type I or type III endoleaks and migration. We suggest that patients with these problems have higher risk and should be considered for expedited conversion if they fail endovascular options. Elective conversion is recommended when endovascular salvage procedures have failed or are not possible in patients with type I or III endoleaks, migration, and type II endoleaks with an enlarging aneurysm. With improving operative technique, the mortality for elective late EVAR AAA-related conversion has been reduced from the initial report of 43% to similar to the rate for primary open repair. Although endograft conversion is technically more challenging, it can be performed with acceptable results with proper planning and execution.

Selected References Harris PL, Vallabhaneni SR, Desgranges P, et al: Incidence and risk factors of late rupture, conversion, and death after endovascular repair of infrarenal aortic aneurysms: The EUROSTAR experience. European Collaborators on Stent/graft techniques for aortic aneurysm repair, J Vasc Surg 32:739–749, 2000.

Treatment of Endovascular Leaks After Aortic Endografting Rabih A. Chaer and Michel S. Makaroun

Endovascular abdominal aortic aneurysm repair (EVAR) is predicated on complete exclusion of the aneurysm from the arterial circulation. An endoleak, or continued arterial perfusion of the aneurysm sac after endovascular treatment, can compromise the effectiveness of EVAR. There are five major categories of endoleaks (Table 1). Some appear to be an unavoidable consequence of placing a stent graft inside an aneurysm sac with patent outflow vessels, some are the result of poor seal at the proximal or distal fixation sites or between the graft components, and others occur as a result of graft material failure. Endoleaks are associated with a variable increase in intrasac pressure that depends on the type of endoleak, which determines its severity and clinical significance.

TYPE I ENDOLEAK Type I endoleak continues to be a major cause of rupture after EVAR and should be considered a failure of the treatment. They are best prevented by proper patient and device selection. The incidence of type I endoleak increases with difficult anatomic situations, typically when devices are used outside the manufacturer’s instructions for use, such as short or angulated necks and landing zones with heavy calcifications. Type I endoleak is associated with significant pressure elevation in the aneurysm sac and has been linked to a continued risk of rupture, with a high of 22% mortality from rupture reported in earlier series. The risk of rupture from an untreated type I endoleak has been reported to be 3.4% at 15 months in the EUROSTAR (EUROpean Collaboration on Stent/graft Techniques for Aortic aneurysm Repair) registry, similar to

Jacobowitz GR, Lee AM, Riles TS: Immediate and late explantation of endovascular aortic grafts: The endovascular technologies experience, J Vasc Surg 29:309–316, 1999. Kelso RL, Lyden SP, Butler B, et al: Late conversion of aortic stent grafts, J Vasc Surg 49:589–595, 2009. Koning OH, Hinnen JW, van Baalen JM: Technique for safe removal of an aortic endograft with suprarenal fixation, J Vasc Surg 43:855–857, 2006. Lipsitz EC, Ohki T, Veith FJ, et al: Delayed open conversion following endovascular aortoiliac aneurysm repair: Partial (or complete) endograft preservation as a useful adjunct, J Vasc Surg 38:1191–1198, 2003. Lyden SP, McNamara JM, Sternbach Y, et al: Technical considerations for late removal of aortic endografts, J Vasc Surg 36:674–678, 2002. May J, White GH, Harris JP: Techniques for surgical conversion of aortic endoprosthesis, Eur J Vasc Endovasc Surg 18:284–289, 1999. Moulakakis KG, Dalainas I, Mylonas S, et al: Conversion to open repair after endografting for abdominal aortic aneurysm: A review of causes, incidence, results, and surgical techniques of reconstruction, J Endovasc Ther 17:694–702, 2010. Sharif MA, Lee B, Lau LL, et al: Prosthetic stent graft infection after endovascular abdominal aortic aneurysm repair, J Vasc Surg 46: 442–448, 2007.

the risk of rupture of an untreated abdominal aortic aneurysm (AAA). Whenever feasible, all type I endoleaks should be corrected promptly because spontaneous resolution, though possible, is not typical, and treatment can be simple with endovascular means. The initial treatment of procedural type I endoleak typically involves reballooning of the fixation sites, although additional aortic cuffs or iliac limb extensions, or placement of a balloon-expandable Palmaz stent (Cordis, Johnson & Johnson, Warren, NJ) are sometimes required. Late type I endoleaks can occur as a result of graft migration, aneurysmal degeneration of the aortic neck, enlargement of the iliac arteries, or severe angulation at the fixation site that can disengage the stent graft from the aortic wall as the sac starts to shrink. The treatment of late type I endoleaks can be more challenging, but it usually also involves ballooning, stent graft extension (Figure 1), or use of Palmaz stent to increase the graft radial force and apposition to the aortic wall. In situations where visceral branches preclude graft extension, glue or coil deposition in the track between the stent graft and the aortic wall may be successful. At the proximal attachment site, the edge of the graft can be probed with a reverse or simple-curve catheter, depending on the approach. Unless the leak is a result of gross undersizing or severe neck angulation, it often consists of a small channel alongside the graft leading to the perigraft space. A microcatheter can be advanced into this channel and embolization can be performed with microcoils, glue, or other embolic agents. It is essential to initially perform angiography of the aneurysm sac to rule out a combined type I and type II endoleak, which is not uncommon. In the case of a combined endoleak, the feeding vessel should be embolized with microcoils before the attachment site leak is treated, in order to optimize the seal and prevent adverse events from end organ damage from embolization to the colon or spinal cord. Embolization is less often required for distal type I endoleaks because a distal seal can be achieved with graft extension, and a variety of surgical or endovascular maneuvers are available to preserve hypogastric perfusion. Open conversion is almost never required at the time of the initial EVAR, but it is sometimes required for delayed endoleak. It can be associated with increased morbidity and mortality, although several series report results that are comparable to de novo open AAA repair. This can be performed by way of a transperitoneal or retroperitoneal approach, with the initial proximal aortic control often at the supraceliac or suprarenal location, depending on the graft location and the presence of suprarenal fixation. Stepwise distal clamping is performed to reduce ischemic time, with complete or partial endograft removal. Partial explantation with in situ replacement can be

264

AORTIC ANEURYSM

EVAR had either type I or type III endoleaks and migration. We suggest that patients with these problems have higher risk and should be considered for expedited conversion if they fail endovascular options. Elective conversion is recommended when endovascular salvage procedures have failed or are not possible in patients with type I or III endoleaks, migration, and type II endoleaks with an enlarging aneurysm. With improving operative technique, the mortality for elective late EVAR AAA-related conversion has been reduced from the initial report of 43% to similar to the rate for primary open repair. Although endograft conversion is technically more challenging, it can be performed with acceptable results with proper planning and execution.

Selected References Harris PL, Vallabhaneni SR, Desgranges P, et al: Incidence and risk factors of late rupture, conversion, and death after endovascular repair of infrarenal aortic aneurysms: The EUROSTAR experience. European Collaborators on Stent/graft techniques for aortic aneurysm repair, J Vasc Surg 32:739–749, 2000.

Treatment of Endovascular Leaks After Aortic Endografting Rabih A. Chaer and Michel S. Makaroun

Endovascular abdominal aortic aneurysm repair (EVAR) is predicated on complete exclusion of the aneurysm from the arterial circulation. An endoleak, or continued arterial perfusion of the aneurysm sac after endovascular treatment, can compromise the effectiveness of EVAR. There are five major categories of endoleaks (Table 1). Some appear to be an unavoidable consequence of placing a stent graft inside an aneurysm sac with patent outflow vessels, some are the result of poor seal at the proximal or distal fixation sites or between the graft components, and others occur as a result of graft material failure. Endoleaks are associated with a variable increase in intrasac pressure that depends on the type of endoleak, which determines its severity and clinical significance.

TYPE I ENDOLEAK Type I endoleak continues to be a major cause of rupture after EVAR and should be considered a failure of the treatment. They are best prevented by proper patient and device selection. The incidence of type I endoleak increases with difficult anatomic situations, typically when devices are used outside the manufacturer’s instructions for use, such as short or angulated necks and landing zones with heavy calcifications. Type I endoleak is associated with significant pressure elevation in the aneurysm sac and has been linked to a continued risk of rupture, with a high of 22% mortality from rupture reported in earlier series. The risk of rupture from an untreated type I endoleak has been reported to be 3.4% at 15 months in the EUROSTAR (EUROpean Collaboration on Stent/graft Techniques for Aortic aneurysm Repair) registry, similar to

Jacobowitz GR, Lee AM, Riles TS: Immediate and late explantation of endovascular aortic grafts: The endovascular technologies experience, J Vasc Surg 29:309–316, 1999. Kelso RL, Lyden SP, Butler B, et al: Late conversion of aortic stent grafts, J Vasc Surg 49:589–595, 2009. Koning OH, Hinnen JW, van Baalen JM: Technique for safe removal of an aortic endograft with suprarenal fixation, J Vasc Surg 43:855–857, 2006. Lipsitz EC, Ohki T, Veith FJ, et al: Delayed open conversion following endovascular aortoiliac aneurysm repair: Partial (or complete) endograft preservation as a useful adjunct, J Vasc Surg 38:1191–1198, 2003. Lyden SP, McNamara JM, Sternbach Y, et al: Technical considerations for late removal of aortic endografts, J Vasc Surg 36:674–678, 2002. May J, White GH, Harris JP: Techniques for surgical conversion of aortic endoprosthesis, Eur J Vasc Endovasc Surg 18:284–289, 1999. Moulakakis KG, Dalainas I, Mylonas S, et al: Conversion to open repair after endografting for abdominal aortic aneurysm: A review of causes, incidence, results, and surgical techniques of reconstruction, J Endovasc Ther 17:694–702, 2010. Sharif MA, Lee B, Lau LL, et al: Prosthetic stent graft infection after endovascular abdominal aortic aneurysm repair, J Vasc Surg 46: 442–448, 2007.

the risk of rupture of an untreated abdominal aortic aneurysm (AAA). Whenever feasible, all type I endoleaks should be corrected promptly because spontaneous resolution, though possible, is not typical, and treatment can be simple with endovascular means. The initial treatment of procedural type I endoleak typically involves reballooning of the fixation sites, although additional aortic cuffs or iliac limb extensions, or placement of a balloon-expandable Palmaz stent (Cordis, Johnson & Johnson, Warren, NJ) are sometimes required. Late type I endoleaks can occur as a result of graft migration, aneurysmal degeneration of the aortic neck, enlargement of the iliac arteries, or severe angulation at the fixation site that can disengage the stent graft from the aortic wall as the sac starts to shrink. The treatment of late type I endoleaks can be more challenging, but it usually also involves ballooning, stent graft extension (Figure 1), or use of Palmaz stent to increase the graft radial force and apposition to the aortic wall. In situations where visceral branches preclude graft extension, glue or coil deposition in the track between the stent graft and the aortic wall may be successful. At the proximal attachment site, the edge of the graft can be probed with a reverse or simple-curve catheter, depending on the approach. Unless the leak is a result of gross undersizing or severe neck angulation, it often consists of a small channel alongside the graft leading to the perigraft space. A microcatheter can be advanced into this channel and embolization can be performed with microcoils, glue, or other embolic agents. It is essential to initially perform angiography of the aneurysm sac to rule out a combined type I and type II endoleak, which is not uncommon. In the case of a combined endoleak, the feeding vessel should be embolized with microcoils before the attachment site leak is treated, in order to optimize the seal and prevent adverse events from end organ damage from embolization to the colon or spinal cord. Embolization is less often required for distal type I endoleaks because a distal seal can be achieved with graft extension, and a variety of surgical or endovascular maneuvers are available to preserve hypogastric perfusion. Open conversion is almost never required at the time of the initial EVAR, but it is sometimes required for delayed endoleak. It can be associated with increased morbidity and mortality, although several series report results that are comparable to de novo open AAA repair. This can be performed by way of a transperitoneal or retroperitoneal approach, with the initial proximal aortic control often at the supraceliac or suprarenal location, depending on the graft location and the presence of suprarenal fixation. Stepwise distal clamping is performed to reduce ischemic time, with complete or partial endograft removal. Partial explantation with in situ replacement can be



Treatment of Endovascular Leaks After Aortic Endografting

TABLE 1:  Classification of Endoleaks and Endotension Endoleak Type

Source of Perigraft Flow

I

Attachment site Ia

Proximal, aortic end

Ib

Distal, iliac end

Ic

Iliac occluder

II

the aortic neck was required in 14 patients, and type I endoleaks in eight patients sealed spontaneously and did not require any further intervention. Two postoperative deaths (3.9%) were reported, one from an aortoenteric fistula that developed as a procedural complication after translumbar coil embolization, and one after graft explant with aortoiliac reconstruction in a patient with prior stent graft and a Palmaz stent. Most patients can therefore be managed by endovascular means, and open conversion is sometimes required with acceptable overall morbidity and mortality.

TYPE II ENDOLEAK

Branch leaks

IIa

Simple: one patent branch

IIb

Complex: two or more patent branches

III

265

Stent graft defect

IIIa

Junctional leak or modular disconnect

IIIb

Fabric holes

IV

Stent graft porosity 25% baseline), although the incidence is usually quoted to be about 1%. As in other scenarios of exposure to contrast dye, it is known that the risk factors for this complication include advanced age, preexisting kidney failure, diabetes, and high doses of contrast dye. In EVAR, the dose of contrast may be the most important risk factor for kidney dysfunction. In our institution, we prefer to use carbon dioxide as our primary (or only) contrast agent to minimize use of contrast dye during EVAR, even in cases of ruptured AAA. Another strategy used in our practice is diluting the injector contrast concentration to half, which allows procedures that require multiple injections (such as fenestrated endograft) to use far less total contrast with minimal loss of resolution.

INTESTINAL COMPLICATIONS Complications involving the intestines during open aortic surgery or EVAR range from those directly caused by the surgeon during the approach to the aorta, those induced by the purposeful ligation or occlusion of the inferior mesenteric artery (IMA), and those attributed to the idiopathic effects on intestinal function integrity after surgery. A review of the Nationwide Inpatient Sample database of more than 89,867 patients treated for all types of AAA repair revealed an incidence of intestinal ischemia of approximately 2.2%. This was statistically more common after treating ruptured aneurysms (8.9%) when compared to both elective open repair (2.2%) and EVAR (0.5%). In addition, having colonic ischemia after AAA repair led to a sobering fourfold increase in mortality (37.8% vs. 6.7%), three times the length of stay, and a dramatic increase in costs, all of which highlight the importance of avoiding intestinal ischemia after AAA repair whenever possible. The most dreaded enteric complication after either open aortic reconstructions or EVAR is graft–enteric fistula. This uncommon morbidity can occur at almost any time after either aortic intervention. Although graft–enteric fistula is more commonly described after open aortic procedures, endografts can also erode into the bowel even though they are by definition placed within the aorta. Graft–enteric fistulas can manifest as infections, hemorrhage, or a combination of both. Some patients present with only vague constitutional symptoms with or without fever, and they may be like this for months before the diagnosis is made with imaging or duodenoscopy. Others have epigastric pain and fevers with overt septic shock. Those with hemorrhagic complications can present with chronic anemia of unknown origin or with a sentinel bleed with symptomatic hypotension that is soon followed by hemorrhagic shock. Any patient with an aortic graft and evidence of upper gastrointestinal bleeding mandates suspicion of an aorto-enteric fisulta and requires emergent intervention. The management of graft-enteric fistula is discussed in detail in another chapter, but ultimately it requires explantation and reestablishing flow to the lower extremities, or it may be managed palliatively with an endograft to just stop acute blood loss. These fistulas

272

AORTIC ANEURYSM

can be avoided in open aortic interventions by wrapping the aneurysm sac over the graft and with the liberal use of pedicled omental flaps placed between the graft and the bowel. No clear, preventable risk factors have been described with endovascular repair because it remains a very uncommonly reported complication.

Open Repair Intestinal injuries during open repair can occur from direct trauma to the bowel during access to the aortoiliac system from the moment the peritoneal cavity is entered. This is magnified (as in any laparotomy) when patients have had prior abdominal surgery. Retroperitoneal incisions allowing access to the aorta are the ideal method in cases of previous abdominal surgery because it avoids all contact with intraabdominal adhesions. If a laparotomy is chosen for access, traumatic injury to the bowel can be best avoided with a careful evaluation of the CT scan to locate an area in the anterior abdomen where the bowel is not directly below the initial incision. A transperitoneal incision made over an area of the abdomen that had not been previously violated, either more cephalad or caudad to the previous incision, can also help in cases where no imaging is available. Enterotomies can lead to a devastating outcome because they are usually detected late, after the postoperative ileus has resolved. In addition, contamination of the prosthetic graft is a primary concern after an enterotomy. Injuries to the intestine during tunneling for an aortofemoral anastomosis might not be detected early on, especially if the graft limb itself is driven through and through the bowel. These cases can even simply manifest as an indolent illness with fever of unknown origin and vague gastrointestinal symptoms for months or even years after the anastomosis was done! The incidence of clinically diagnosed mesenteric ischemia after elective open AAA repair is about 2% to 3% (more than double this in cases of ruptured AAA), and this complication has been well recognized since the dawn of open repair of AAA in the 1950s. More than 60 years of medical advances aside, the mortality from mesenteric ischemia after aortic reconstructions occurs in one half to two thirds of cases. Ischemic colitis is thought to be a consequence of the routine ligation of the IMA in patients with inappropriate collateral flow from the superior mesenteric artery (SMA) to the sigmoid. Patients who are thought to be at special risk are those with previous colon resections, and normal collateral pathways may be interrupted during the division of the mesocolon. This may be particularly concerning when there is limited flow or no flow into the internal iliac arteries. It should be routine practice during open AAA repair to examine the sigmoid colon before and after the AAA repair to compare the appearance of the colon. Intestinal ischemia always manifests first at the level of the mucosa, so even a well-appearing colon in the operating room can manifest some degree of ischemic colitis that might or might not need further intervention. If obvious signs of ischemia are detected, either reimplantation of the inferior mesenteric artery into the graft or a end-to-end bypass with prosthetic may be indicated; treatment usually resolves the ischemia, or even, in the absence of cure, can minimize the severity so it can be managed medically. In cases of suspected intestinal ischemia in the first 48 hours after AAA repair, sigmoidoscopy can reveal early ischemic colitis and help direct its management. If ischemia is mild, it may be able to be managed with supportive care, avoidance of hypotension, and antibiotics. Ultimately, if the ischemia is transmural or the patient is progressively doing poorly, early exploratory laparotomy and timely colectomy can be lifesaving in cases of severe ischemic colitis. One must recall that mesenteric ischemia always begins in the mucosa (seen on endoscopy) before it is visualized in the serosa (seen at laparotomy). If a laparotomy is done expeditiously owing to a patient's poor clinical status, and the exploration of the bowel seems unremarkable, then a second-look laparotomy a few hours later can reveal the affected segment of bowel.

Endovascular Repair The incidence of acute intestinal ischemia after EVAR is uncommon and is thought to occur in approximately 0.5% to 1.5% of cases. It is particularly concerning because almost half of cases take more than 30 days after the EVAR to be diagnosed. However, when large bowel ischemia is detected after EVAR, its appearance is linked to a statistically higher mortality than open AAA repair (73% vs. 51% respectively; p < .01). The higher mortality in EVAR is likely caused by a delay in its diagnosis, secondary to its low incidence and early discharge after elective EVAR. As in open repair, there is decreased flow into the inferior mesenteric artery (IMA) after the endograft excludes it from antegrade aortic flow. Endovascular treatment of AAA can therefore also lead to sigmoid and rectal ischemia. This can be especially concerning when there is concomitant coverage (or purposeful embolization), of the internal iliac arteries during the EVAR. This theoretical risk notwithstanding, bilateral internal iliac artery embolization in conjunction with EVAR does not necessarily condemn the patient to intestinal ischemia, and staged approaches do not seem to change the incidence of ischemic complications. Embolization to the mesenteric vessels during graft deployment or from wire manipulations of thrombus was described very early in the history of EVAR and still leads to significant morbidity and mortality. Even in patients with patent internal iliac arteries or an occluded IMA, atheroembolism to the small or large bowel can result in fatal outcomes. Mural thrombus burden must therefore always be considered while reviewing a CT scan of a potential EVAR candidate or while performing repeated wire manipulations to avoid this complication. A high index of suspicion and liberal use of sigmoidoscopy should be common practice in any patient with progressive lower abdominal pain or unexpected systemic inflammatory response syndrome after EVAR. Mild cases diagnosed with a sigmoidoscope can usually be managed with supportive care and antibiotics, but as mentioned earlier, urgent laparotomy and bowel resection can dramatically change the outcome of a patient with severe ischemic colitis.

FIGURE 2  Unrecognized importance of the inferior mesenteric

artery (IMA) in a patient treated with endovascular aneurysm repair (EVAR). She immediately developed symptoms of chronic mesenteric ischemia after EVAR accompanied by purposeful coil embolization of the IMA (dashed arrow showing CT scatter). High-grade stenosis of the superior mesenteric artery (SMA) and celiac arteries (solid arrows) is apparent. The patient was treated with a angioplasty with stent placement in the SMA.



Neurologic Complications after Open and Endovascular Aortic Surgery

The most uncommon and devastating etiology of acute mesenteric ischemia with EVAR is inadvertent coverage of the SMA during deployment. A more subtle version of this (and often overlooked) is covering the IMA with an EVAR before considering that it may be providing the majority of flow to the intestines. Preoperative planning for EVAR must include a careful evaluation of all of the abdominal aortic branches and not just the aortic neck and the iliac landing zones. A perfectly placed infrarenal EVAR in cases where both the SMA and celiac artery have high-grade stenosis (or occlusion) can lead to acute mesenteric ischemia or new-onset chronic mesenteric ischemia syndrome that may be misdiagnosed for months after the EVAR (Figure 2). These patients require some form of mesenteric revascularization (open or endovascular) in an emergent or semi-elective manner according to the severity of the case.

Selected References Boules TN, Stanziale SF, Chomic A, et al: Predictors of diffuse renal microembolization following endovascular repair of abdominal aortic aneurysms, Vascular 15:18–23, 2007. Chong T, Nguyen L, Owens CD, et al: Suprarenal aortic cross-clamp position: A reappraisal of its effects on outcomes for open abdominal aortic aneurysm repair, J Vasc Surg 49:873–880, 2009.

Neurologic Complications after Open and Endovascular Aortic Surgery Richard M. Green

Neurologic complications after aortic surgery can range from minor irritants to life-threatening problems. It is important to recognize that the majority, but certainly not all, can be avoided by careful preoperative planning and meticulous intraoperative technique.

SPINAL CORD INJURY The devastating neurologic injury following aortic surgery is spinal cord ischemia (SCI). This is true for open and endovascular procedures on the abdominal or thoracic aorta. Much has been written on the cause and avoidance of SCI after operations on the thoracic and thoracoabdominal aorta, and outcomes have improved since the 1980s. The ultimate risk depends on the presentation, the extent of aortic involvement and replacement, kidney function, and the experience of the surgical team. Among other variables, cerebrospinal fluid (CSF) drainage and distal aortic perfusion are considered important technical adjuncts by a number of surgeons with extensive experience in this area. These techniques as well as others, such as spinal cord cooling, sequential aortic clamping, and reimplantation of intercostal arteries, all increase the tolerance of the spinal cord to clamp-induced ischemia.

273

Donas KP, Lachat M, Rancic Z, et al: Early and midterm outcome of a novel technique to simplify the hybrid procedures in the treatment of thoracoabdominal and pararenal aortic aneurysms, J Vasc Surg 50:1280–1284, 2009. Grant SW, Grayson AD, Grant MJ, et al: What are the risk factors for renal failure following open elective abdominal aortic aneurysm repair? Eur J Vasc Endovasc Surg 43:182–187, 2012. Knipp BS, Escobar GA, English S, et al: Endovascular repair of ruptured aortic aneurysms using carbon dioxide contrast angiography, Ann Vasc Surg 24:845–850, 2010. Koksoy C, LeMaire SA, Curling PE, et al: Renal perfusion during thoracoabdominal aortic operations: Cold crystalloid is superior to normothermic blood, Ann Thorac Surg 73:730–738, 2002. Mehta T, Wade RG, Clarke JM: Is it safe to ligate the left renal vein during open abdominal aortic aneurysm repair? Ann Vasc Surg 24:758–761, 2010. Miller A, Marotta M, Scordi-Bello I, et al: Ischemic colitis after endovascular aortoiliac aneurysm repair: A 10-year retrospective study, Arch Surg 144:900–903, 2009. Miller CC 3rd, Villa MA, Sutton J, et al: Serum myoglobin and renal morbidity and mortality following thoracic and thoraco-abdominal aortic repair: Does rhabdomyolysis play a role? Eur J Vasc Endovasc Surg 37:388–394, 2009. Moulakakis KG, Dalainas I, Mylonas S, et al: Conversion to open repair after endografting for abdominal aortic aneurysm: A review of causes, incidence, results, and surgical techniques of reconstruction, J Endovasc Ther 17:694–702, 2010.

A nonrandomized but representative series by Safi and his colleagues comparing patients with CSF drainage and distal aortic perfusion against a group of patients without demonstrated a significantly lower neurologic complication rate (9% vs. 19%). Intraoperative spinal cord monitoring is used in some centers to predict whether intercostal artery reimplantation is necessary. Loss of somatosensory evoked potentials within 15 minutes of aortic cross clamping indicates poor collateralization and mandates prompt restoration of spinal cord blood supply. This can improve with release of the proximal clamp or can require reimplantation of the intercostal arteries. While the broad range of thoracic aortic pathologies are not currently treated with endografts (TEVAR), our limited experience indicates that paraplegia following thoracic endovascular aneurysm repair (TEVAR) ranges from 1.2% to 12.5%. There are two studies that compare the incidence of spinal cord ischemia after TEVAR and open repair. One of the two studies showed a reduction in SCI after TEVAR to 3%, as compared to 14% after open repair. Whether or not TEVAR provides protection against SCI is an unresolved issue. The difficulty in resolving this issue largely relates to the heterogeneity of the cohorts with regard to the extent of the aorta treated and clinical presentation. In the EUROSTAR (EUROpean Collaboration on Stent/graft Techniques for Aortic aneurysm Repair) series, in the group of patients with SCI following TEVAR, 40% had the left subclavian artery (LSA) covered without revascularization, and 19% underwent preoperative revascularization. Multivariate analysis of the European experience determined that four factors are associated with paraplegia: coverage of the LSA without revascularization, kidney failure, prior or concomitant open abdominal aortic surgery, and three or more stent grafts used, indicating the amount of aortic coverage. The area around T10 appears to be most susceptible to SCI. A review and meta-analysis of 51 observational TEVAR studies was performed under the aegis of the Committee on Thoracic Aortic Disease from the Society for Vascular Surgery to evaluate the outcome of LSA coverage. The findings documented that LSA coverage without revascularization was associated with a significant increase in arm ischemia (odds ratio [OR], 47.69) and vertebrobasilar



Neurologic Complications after Open and Endovascular Aortic Surgery

The most uncommon and devastating etiology of acute mesenteric ischemia with EVAR is inadvertent coverage of the SMA during deployment. A more subtle version of this (and often overlooked) is covering the IMA with an EVAR before considering that it may be providing the majority of flow to the intestines. Preoperative planning for EVAR must include a careful evaluation of all of the abdominal aortic branches and not just the aortic neck and the iliac landing zones. A perfectly placed infrarenal EVAR in cases where both the SMA and celiac artery have high-grade stenosis (or occlusion) can lead to acute mesenteric ischemia or new-onset chronic mesenteric ischemia syndrome that may be misdiagnosed for months after the EVAR (Figure 2). These patients require some form of mesenteric revascularization (open or endovascular) in an emergent or semi-elective manner according to the severity of the case.

Selected References Boules TN, Stanziale SF, Chomic A, et al: Predictors of diffuse renal microembolization following endovascular repair of abdominal aortic aneurysms, Vascular 15:18–23, 2007. Chong T, Nguyen L, Owens CD, et al: Suprarenal aortic cross-clamp position: A reappraisal of its effects on outcomes for open abdominal aortic aneurysm repair, J Vasc Surg 49:873–880, 2009.

Neurologic Complications after Open and Endovascular Aortic Surgery Richard M. Green

Neurologic complications after aortic surgery can range from minor irritants to life-threatening problems. It is important to recognize that the majority, but certainly not all, can be avoided by careful preoperative planning and meticulous intraoperative technique.

SPINAL CORD INJURY The devastating neurologic injury following aortic surgery is spinal cord ischemia (SCI). This is true for open and endovascular procedures on the abdominal or thoracic aorta. Much has been written on the cause and avoidance of SCI after operations on the thoracic and thoracoabdominal aorta, and outcomes have improved since the 1980s. The ultimate risk depends on the presentation, the extent of aortic involvement and replacement, kidney function, and the experience of the surgical team. Among other variables, cerebrospinal fluid (CSF) drainage and distal aortic perfusion are considered important technical adjuncts by a number of surgeons with extensive experience in this area. These techniques as well as others, such as spinal cord cooling, sequential aortic clamping, and reimplantation of intercostal arteries, all increase the tolerance of the spinal cord to clamp-induced ischemia.

273

Donas KP, Lachat M, Rancic Z, et al: Early and midterm outcome of a novel technique to simplify the hybrid procedures in the treatment of thoracoabdominal and pararenal aortic aneurysms, J Vasc Surg 50:1280–1284, 2009. Grant SW, Grayson AD, Grant MJ, et al: What are the risk factors for renal failure following open elective abdominal aortic aneurysm repair? Eur J Vasc Endovasc Surg 43:182–187, 2012. Knipp BS, Escobar GA, English S, et al: Endovascular repair of ruptured aortic aneurysms using carbon dioxide contrast angiography, Ann Vasc Surg 24:845–850, 2010. Koksoy C, LeMaire SA, Curling PE, et al: Renal perfusion during thoracoabdominal aortic operations: Cold crystalloid is superior to normothermic blood, Ann Thorac Surg 73:730–738, 2002. Mehta T, Wade RG, Clarke JM: Is it safe to ligate the left renal vein during open abdominal aortic aneurysm repair? Ann Vasc Surg 24:758–761, 2010. Miller A, Marotta M, Scordi-Bello I, et al: Ischemic colitis after endovascular aortoiliac aneurysm repair: A 10-year retrospective study, Arch Surg 144:900–903, 2009. Miller CC 3rd, Villa MA, Sutton J, et al: Serum myoglobin and renal morbidity and mortality following thoracic and thoraco-abdominal aortic repair: Does rhabdomyolysis play a role? Eur J Vasc Endovasc Surg 37:388–394, 2009. Moulakakis KG, Dalainas I, Mylonas S, et al: Conversion to open repair after endografting for abdominal aortic aneurysm: A review of causes, incidence, results, and surgical techniques of reconstruction, J Endovasc Ther 17:694–702, 2010.

A nonrandomized but representative series by Safi and his colleagues comparing patients with CSF drainage and distal aortic perfusion against a group of patients without demonstrated a significantly lower neurologic complication rate (9% vs. 19%). Intraoperative spinal cord monitoring is used in some centers to predict whether intercostal artery reimplantation is necessary. Loss of somatosensory evoked potentials within 15 minutes of aortic cross clamping indicates poor collateralization and mandates prompt restoration of spinal cord blood supply. This can improve with release of the proximal clamp or can require reimplantation of the intercostal arteries. While the broad range of thoracic aortic pathologies are not currently treated with endografts (TEVAR), our limited experience indicates that paraplegia following thoracic endovascular aneurysm repair (TEVAR) ranges from 1.2% to 12.5%. There are two studies that compare the incidence of spinal cord ischemia after TEVAR and open repair. One of the two studies showed a reduction in SCI after TEVAR to 3%, as compared to 14% after open repair. Whether or not TEVAR provides protection against SCI is an unresolved issue. The difficulty in resolving this issue largely relates to the heterogeneity of the cohorts with regard to the extent of the aorta treated and clinical presentation. In the EUROSTAR (EUROpean Collaboration on Stent/graft Techniques for Aortic aneurysm Repair) series, in the group of patients with SCI following TEVAR, 40% had the left subclavian artery (LSA) covered without revascularization, and 19% underwent preoperative revascularization. Multivariate analysis of the European experience determined that four factors are associated with paraplegia: coverage of the LSA without revascularization, kidney failure, prior or concomitant open abdominal aortic surgery, and three or more stent grafts used, indicating the amount of aortic coverage. The area around T10 appears to be most susceptible to SCI. A review and meta-analysis of 51 observational TEVAR studies was performed under the aegis of the Committee on Thoracic Aortic Disease from the Society for Vascular Surgery to evaluate the outcome of LSA coverage. The findings documented that LSA coverage without revascularization was associated with a significant increase in arm ischemia (odds ratio [OR], 47.69) and vertebrobasilar

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insufficiency (OR, 10.78). There was a strong trend but an insignificant increase in SCI and anterior circulation stroke. As a result, the SVS has put forward three recommendations with regard to TEVAR and the LSA:   

n For elective TEVAR where LSA coverage is required for a

proximal seal, preoperative revascularization is suggested. n For cases where LSA perfusion is vital (e.g., patent left internal mammary artery bypass or termination of vertebral artery into the posterior inferior cerebellar artery), preoperative revascularization is indicated. n For emergent TEVAR, a decision regarding preoperative revascularization should be individualized.

  

The LSA is not the only important source of arterial perfusion of the spinal cord. The alarming sevenfold increase in SCI after prior abdominal aortic aneurysm repair indicates the importance of the lumbar arteries in spinal cord perfusion. Other factors of significance in this analysis by Schlosser and coworkers are preoperative renal insufficiency (OR, 29.5), increase in length of aortic coverage (OR, 1.1 per centimeter increase), and the time interval between TEVAR and infrarenal repair (OR, 1.2 per year increase). Although the benefit of CSF drainage is not as clear with endovascular repair as it is with open repair, most experts recommend drainage when long segments of the aorta are covered and particularly when the area around T10 is involved. The guidelines from the Society for Vascular Surgery recommend, regardless of technique (open vs. EVAR), that blood be preserved to at least one hypogastric artery. Failure to do so can result in pelvic ischemia, colonic ischemia, or spinal cord ischemia. Perfusion of the distal spinal cord is derived from the hypogastric artery via the lumbar, iliolumbar, and lateral sacral arteries. These vessels become significant when perfusion from the greater radicular artery is compromised or eliminated by coverage by an endograft.

STROKE Data from the EUROSTAR registry indicate that the incidence of stroke following TEVAR is 3.1%. This was a heterogeneous population, and one can postulate a number of possible etiologies including coverage of a brachiocephalic trunk, occlusion of a trunk caused by dissection, embolization from manipulation of the device and/ or wires in a diseased proximal aorta, air embolism or hypotension, and preexisting cerebrovascular disease. The incidence of stroke after TEVAR in a 10-year review of 530 patients at the University of Pennsylvania was 3.8%. All the strokes were embolic and were associated with a greater in-hospital mortality rate (20.0% vs. 5.7% for patients without stroke). The diagnosis of stroke was made within 24 hours of operation in one half of the patients and shortly thereafter in the others. This pattern is consistent with the hypothesis that the underlying pathology is related to the manipulation of plaque within the aorta by the wires and/or devices. Significant risk factors for any stroke were chronic renal insufficiency (OR, 4.65) and a history of prior stroke (OR, 7.67). There were cause and outcome differences between strokes involving the anterior and posterior circulations. The significant risk factor for anterior-circulation strokes was a prior stroke, and 75% recovered fully without any mortality. Risk factors for posterior-circulation strokes were age, prior stroke, zone 2 coverage, and penetrating ulcer. The mortality rate in this group was 33%. Other authors have corroborated the incidence and danger of posteriorcirculation strokes after TEVAR. There were no significant differences between the no-stroke and stroke groups in aortic pathology (degenerative vs. dissection), acuity, preoperative LSA revascularization, or number of stents used. Intuitively, one would expect that preoperative LSA revascularization would reduce the incidence of posterior-circulation stroke. There are data that show LSA coverage

to be an independent risk factor for stroke, but preoperative revascularization does not alter this risk.

DIRECT NERVE INJURY Retrograde Ejaculation Exposure of the distal aorta and common iliac arteries may be associated with the phenomenon of retrograde ejaculation. This is the result of injury to the efferent sympathetic pathways (superior hypogastric nervous plexus) supplying the bladder neck, vas deferens, and prostate. The neural tissue is located in the retroperitoneal space, coursing anterior to the aorta and left common iliac vein. Early series of operations documented an incidence as high as 50%, but more recently with refined dissections the incidence has come down significantly. Most of the data regarding ejaculation-preserving dissections come from the urologic oncology literature. On that basis, an aortic exposure that begins laterally and creates a plane by dividing the lateral splanchnic nerves on the left side of the aorta allows one to mobilize the neural tissues on the anterior aspect of the aorta without dividing it, thereby reducing the incidence of erectile dysfunction. Recommending endovascular therapy to a sexually active male patient may be the deciding factor in determining the choice of procedure.

Peripheral Neuropathy Injury to peripheral nerves can occur with either percutaneous or open groin procedures. Fortunately, they are infrequent. Symptoms can vary from mild sensory neuropathy to disabling motor paralysis. Femoral neuropathy is the most common neurologic complication after percutaneous intervention. The etiology is usually a hematoma, but direct trauma to the nerve can occur from the actual puncture or from excessive compression at the time the sheath is removed. Severe pain usually precedes the diagnosis of neuropathy. Localized groin hematomas produce anterior displacement of the medial and intermediate cutaneous branches of the femoral nerve and result in sensory loss or dysesthesias along the anterior medial thigh. Patients with hematomas extending into the retroperitoneum can develop weakness of the psoas and quadriceps muscles. These situations can require operative decompression based upon the size of the hematoma, its rate of growth, the degree of associated pain, the condition of the overlying skin, and the neurologic deficit. The sensory abnormalities tend to resolve completely, but the motor deficit might only recover partially regardless of drainage. The lateral femoral cutaneous nerve is located lateral to the femoral vessels and passes either through or under the inguinal ligament. A spontaneous neuropathy, meralgia paresthetica, manifests with numbness or pain along the lateral thigh. The sensory findings never go below the knee, and the diagnosis can be confirmed by EMG studies. The same syndrome can be caused by trauma to the nerve in groin dissections that stray laterally. For that reason, particularly in obese patients, the femoral vessels should be marked using ultrasound when the pulse is difficult to palpate in order to be sure that the dissection starts in the proper place. Operative trauma usually results in a permanent problem without remedy. The genitofemoral nerve is at risk during retroperitoneal exposure of the aorta. It courses over the psoas muscle and is easily recognizable and avoided in the unoperated retroperitoneum. The nerve divides into a femoral branch that supplies the skin in the upper part of the femoral triangle and a genital branch that supplies the cremaster muscle and skin of the scrotum. As with the other peripheral neuropathies, injury manifests with excessive pain and sensorimotor symptoms in the distribution of the nerve.



Postoperative Surveillance of Thoracic and Abdominal Aortic Endografts

Selected References Bavaria J, Appoo JJ, Makaroun M, et al: Endovascular stent grafting versus open surgical repair of descending thoracic aortic aneurysms in lowrisk patients: A multicenter comparative trial, J Thorac Cardiovasc Surg 133:369–377, 2007. Buth J, Harris PL, Hobb R, et al: Neurologic complications associated with endovascular repair of thoracic aortic pathology: Incidence, risk factors. A Study from European Collaborators on Stent/Graft Techniques for Aortic aneurysm Repair (EUROSTAR) Registry, J Vasc Surg 46:1103–1111, 2007. Chaikof EL, Brewster DC, Dalman RL, et al: The care of patients with an abdominal aortic aneurysm: The society for vascular surgery practice guidelines, J Vasc Surg 50(Suppl):S2–S49, 2009. Kent KC, Moscucci M, Gallagher SG, et al: Neuropathy after cardiac catheterization: Incidence, clinical patterns, and long-term outcome, J Vasc Surg 19:1008–1114, 1994.

Postoperative Surveillance of Thoracic and Abdominal Aortic Endografts W. Anthony Lee

Postoperative surveillance is an integral part of the overall treatment strategy after endovascular aortic repair, and failure of surveillance can be considered tantamount to no treatment at all. Indeed, suspected noncompliance to follow-up during preoperative evaluation of a potential endovascular candidate can even be construed as a relative contraindication to the therapy. Lifelong follow-up after endovascular repair is one of the necessary burdens that the patient must bear in exchange for the benefits of a minimally invasive procedure and earlier recovery. That said, the optimal surveillance schedule and diagnostic testing remain controversial and in evolution. Most follow-up protocols are applicable for both thoracic and abdominal aortic endovascular repairs.

Matsumura JS, Rizvi AZ: Left subclavian artery revascularization: Society for vascular surgery practice guidelines, J Vasc Surg 52:65S–70S, 2010. Picone AL, Green RM, Ricotta JR, et al: Spinal cord ischemia following operations on the abdominal aorta, J Vasc Surg 3:94–103, 1986. Safi HJ, Hess KR, Randel M, et al: Cerebrospinal fluid drainage and distal aortic perfusion: Reducing neurologic complications in repair of thoracoabdominal aortic aneurysm types I and II, J Vasc Surg 23:223–229, 1996. Svensson LG, Crawford ES, Hess KR, et al: Experience with 1509 patients undergoing thoraco-abdominal aortic operations, J Vasc Surg 17: 357–370, 1993. Ullery BW, McGarvey M, Cheung AT, et al: Vascular distribution of stroke and its relationship to perioperative mortality and neurologic outcome after thoracic endovascular aortic repair, J Vasc Surg 56:1510–1517, 2012. Van Schaik J, van Baalen JM, Visser MJT, et al: Nerve-preserving aortoiliac reconstruction surgery: Anatomical study and surgical approach, J Vasc Surg 33:983–989, 2001.

is safer and easier to manage than intervention after the fact. Therefore, the purpose of postoperative surveillance is timely detection of impending problems and prevention of serious complications before they occur.

ELEMENTS OF COMPLETE SURVEILLANCE Proper surveillance after endovascular aortic repair shares many features of any postoperative evaluation after a major surgical procedure. In the first postoperative visit, history-taking should focus on fevers and other systemic symptoms, new-onset claudication, hypertension, and azotemia, which could suggest iliac or renovascular compromise. Physical examination should be directed at the groins and other vascular access sites, femoral pulses, and aortic pulsatility in cases of abdominal aortic aneurysms. While pulsatility in isolation is a relatively nonspecific finding, a change from a nonpulsatile to a pulsatile examination during follow-up often indicates a new type I or III endoleak (Figure 1). Any serious access site problems such as infections, seromas, or pseudoaneurysms will manifest themselves within the first 30 days.

RATIONALE FOR POSTOPERATIVE SURVEILLANCE Late adverse events after endovascular repair are part of the natural history of the therapy and a well-recognized complication. The incidence is time dependent, meaning that the longer the period of observation, the greater the likelihood of an event. Adverse events can be broadly categorized as device-related and anatomic. Device-related events are self-explanatory, and they include material fatigue (graft tears or erosions, stent fractures) and stent graft kinking, compression, or infolding leading to thrombosis or vascular compromise. Anatomic issues include endoleaks, degeneration or enlargement of landing zones, obstruction of branch vessels, and/ or continued expansion of the sac. Although fortunately many of the device-related events occur less often than they used to with early generation devices, they have not been completely eliminated. For most of these complications, prophylactic intervention before a clinically symptomatic event such as rupture or end-organ ischemia

275

FIGURE 1  Type III endoleak from fabric tear in an iliac limb

12 months after implant.



Postoperative Surveillance of Thoracic and Abdominal Aortic Endografts

Selected References Bavaria J, Appoo JJ, Makaroun M, et al: Endovascular stent grafting versus open surgical repair of descending thoracic aortic aneurysms in lowrisk patients: A multicenter comparative trial, J Thorac Cardiovasc Surg 133:369–377, 2007. Buth J, Harris PL, Hobb R, et al: Neurologic complications associated with endovascular repair of thoracic aortic pathology: Incidence, risk factors. A Study from European Collaborators on Stent/Graft Techniques for Aortic aneurysm Repair (EUROSTAR) Registry, J Vasc Surg 46:1103–1111, 2007. Chaikof EL, Brewster DC, Dalman RL, et al: The care of patients with an abdominal aortic aneurysm: The society for vascular surgery practice guidelines, J Vasc Surg 50(Suppl):S2–S49, 2009. Kent KC, Moscucci M, Gallagher SG, et al: Neuropathy after cardiac catheterization: Incidence, clinical patterns, and long-term outcome, J Vasc Surg 19:1008–1114, 1994.

Postoperative Surveillance of Thoracic and Abdominal Aortic Endografts W. Anthony Lee

Postoperative surveillance is an integral part of the overall treatment strategy after endovascular aortic repair, and failure of surveillance can be considered tantamount to no treatment at all. Indeed, suspected noncompliance to follow-up during preoperative evaluation of a potential endovascular candidate can even be construed as a relative contraindication to the therapy. Lifelong follow-up after endovascular repair is one of the necessary burdens that the patient must bear in exchange for the benefits of a minimally invasive procedure and earlier recovery. That said, the optimal surveillance schedule and diagnostic testing remain controversial and in evolution. Most follow-up protocols are applicable for both thoracic and abdominal aortic endovascular repairs.

Matsumura JS, Rizvi AZ: Left subclavian artery revascularization: Society for vascular surgery practice guidelines, J Vasc Surg 52:65S–70S, 2010. Picone AL, Green RM, Ricotta JR, et al: Spinal cord ischemia following operations on the abdominal aorta, J Vasc Surg 3:94–103, 1986. Safi HJ, Hess KR, Randel M, et al: Cerebrospinal fluid drainage and distal aortic perfusion: Reducing neurologic complications in repair of thoracoabdominal aortic aneurysm types I and II, J Vasc Surg 23:223–229, 1996. Svensson LG, Crawford ES, Hess KR, et al: Experience with 1509 patients undergoing thoraco-abdominal aortic operations, J Vasc Surg 17: 357–370, 1993. Ullery BW, McGarvey M, Cheung AT, et al: Vascular distribution of stroke and its relationship to perioperative mortality and neurologic outcome after thoracic endovascular aortic repair, J Vasc Surg 56:1510–1517, 2012. Van Schaik J, van Baalen JM, Visser MJT, et al: Nerve-preserving aortoiliac reconstruction surgery: Anatomical study and surgical approach, J Vasc Surg 33:983–989, 2001.

is safer and easier to manage than intervention after the fact. Therefore, the purpose of postoperative surveillance is timely detection of impending problems and prevention of serious complications before they occur.

ELEMENTS OF COMPLETE SURVEILLANCE Proper surveillance after endovascular aortic repair shares many features of any postoperative evaluation after a major surgical procedure. In the first postoperative visit, history-taking should focus on fevers and other systemic symptoms, new-onset claudication, hypertension, and azotemia, which could suggest iliac or renovascular compromise. Physical examination should be directed at the groins and other vascular access sites, femoral pulses, and aortic pulsatility in cases of abdominal aortic aneurysms. While pulsatility in isolation is a relatively nonspecific finding, a change from a nonpulsatile to a pulsatile examination during follow-up often indicates a new type I or III endoleak (Figure 1). Any serious access site problems such as infections, seromas, or pseudoaneurysms will manifest themselves within the first 30 days.

RATIONALE FOR POSTOPERATIVE SURVEILLANCE Late adverse events after endovascular repair are part of the natural history of the therapy and a well-recognized complication. The incidence is time dependent, meaning that the longer the period of observation, the greater the likelihood of an event. Adverse events can be broadly categorized as device-related and anatomic. Device-related events are self-explanatory, and they include material fatigue (graft tears or erosions, stent fractures) and stent graft kinking, compression, or infolding leading to thrombosis or vascular compromise. Anatomic issues include endoleaks, degeneration or enlargement of landing zones, obstruction of branch vessels, and/ or continued expansion of the sac. Although fortunately many of the device-related events occur less often than they used to with early generation devices, they have not been completely eliminated. For most of these complications, prophylactic intervention before a clinically symptomatic event such as rupture or end-organ ischemia

275

FIGURE 1  Type III endoleak from fabric tear in an iliac limb

12 months after implant.

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2

3

H

2

4

H

3

4

1 5

1

2

5

3

4 5

1 6

6 7

F

Pre D/C

F

12 M

24 M

FIGURE 2  Component separation of two thoracic stent grafts: left, before discharge; center, at

12 months after surgery; right, at 24 months after surgery.

Unique to endovascular repair are types of imaging that form an integral part of the surveillance regimen. Available imaging modalities include computed tomography angiography (CTA), magnetic resonance angiography (MRA), plain multiview x-ray, duplex ultrasound with or without sonographic contrast, and intrasaccular pressure monitoring. No single modality is sufficient or necessary for each follow-up, and each should be considered complementary depending on the segment of the aorta treated, the pathology, the device’s construction, and the patient’s physiology. The purpose of imaging includes measurement of aortic size and detection of endoleak or device migration (Figure 2) and impaired endograft patency (including kinking and/or compression) and device integrity. Secondary findings include associated vascular problems such as iliac stenosis or dissection, branch vessel compromise or graft infection, and nonvascular pathologies that can masquerade as aortic symptoms and malignancies. Regardless of which modality, any new finding or serial dimensional measurement (e.g., length, distance, diameter) should be compared or performed using the same modality performed the same way, such as aneurysm diameter measured on orthogonal centerline reconstruction.

Computed Tomography Angiography The CT angiogram remains the gold standard for postoperative surveillance after endovascular aortic repair. This is a result of its widespread availability, familiarity with interpretation of vascular structures by nonradiologists, turnkey consistency in producing quality images, spatial resolution, and data acquisition speed using multidetector array scanners. It is relatively more resistant to metallic artifact, especially nitinol, and the study is not restricted by any type of body implants. As three-dimensional (3-D) postprocessing software becomes more commonplace, images can be rendered into a variety of formats such as multiplanar reformat (MPR) and maximumintensity projection (MIP) to look for intravascular abnormalities and stent morphology and integrity. Principal disadvantages are radiation exposure, whose cumulative lifetime dose for a younger patient may be significant, and risk of contrast nephropathy, especially in those with mild to moderate chronic kidney disease and/or diabetes.

Typical acquisition technique should include chest–abdomen– pelvis after thoracic repair, abdomen–pelvis after abdominal repair, and a three-phase scan consisting of noncontrast (5-mm collimation), arterial-phase (intravenous timed-bolus contrast infusion at ≤2-mm collimation), and delayed phase (60 to 90 seconds at 5-mm collimation). Ideally, the dataset should be stored in DICOM format digital media to be able to be viewed on a personal or PACS workstation so that the contrast and brightness can be properly adjusted (windowing) and direct dimensional analysis can be performed using digital measurement tools.

Magnetic Resonance Angiography MR imaging is slightly less readily available than CT scanning and typically is more expensive. Main advantages include absence of radiation and ability to detect certain perfusion and time-resolved events using native volumetric acquisition. Investigational protocols have been established in certain centers that have used these techniques to detect intermittent endoleaks and characterize the inflow and outflow of indeterminate endoleaks. Disadvantages include exclusion of patients with magnetic implants, high variability of image quality depending on acquisition technique, relative contraindication for contrast enhancement (reduced spatial resolution) in patients with severe chronic kidney disease, and nonvisualization of stent components of the endograft. Recent attention directed at the rare occurrence of nephrogenic systemic fibrosis in patients with kidney failure after gadolinium infusion has virtually eliminated the utility of MRA as an alternative contrast study in patients who are at increased risk for contrast nephropathy after conventional CTA.

Multiview Radiographs Plain x-ray used to be one of the mainstays of postoperative imaging. It was rapid, simple, inexpensive, and widely available. It allowed very detailed and high-quality examination of the metallic components of the endograft and, therefore, many of the stent fracture and component separation problems that affected



Postoperative Surveillance of Thoracic and Abdominal Aortic Endografts

X-ray

MIP

277

Type 2 endoleak

FIGURE 3  Comparison of the stent structure using plain x-ray (left)

FIGURE 4  Color-flow duplex ultrasound showing a type II endoleak

and maximum-intensity projection (MIP) (right) imaging.

after endovascular repair of an abdominal aortic aneurysm.

early-generation devices were detected using this modality alone. However, it was limited by ability to view the endograft in only certain projections and, owing to parallax, only gross movements or conformational changes of the endograft could be seen. Furthermore, endografts that were not fully stented throughout were difficult to visualize, even with radiographic markers. Although the role of the plain x-ray cannot be completely eliminated from the diagnostic armamentarium, using postprocessing techniques such as CT-MIP, metallic elements can be visualized with great detail and analyzed in 3-D, and its role in current surveillance strategy is limited (Figure 3).

regional differences in pressure and wall stress over the surface area of the aneurysm and inconsistent transmission of pressure through a thrombus make data obtained from these sensors difficult to interpret. Similar to the pulsatility of an endografted aneurysm sac on physical examination, an acute increase in the sac pressure might indicate a problem, but the absence of pressure change does not rule out an acute change in the status of the repair. One fundamental problem that cannot be overlooked is the fact that this modality is only useful after an obvious late event—most commonly a new type I or III endoleak from a device failure and repressurization of the sac—has already taken place. Unlike other image-based modalities, it cannot detect early changes so that preventive measures can be taken before a catastrophic complication occurs.

Duplex Ultrasound with or without Contrast Duplex ultrasound is a very useful imaging modality that is complementary with other surveillance methods. Advantages are that it is completely noninvasive, painless, and relatively inexpensive and it can detect real-time flow. Disadvantages include the fact that it is highly technique dependent, quality can be limited by body habitus and bowel gas, and it is useless for thoracic aortic imaging because of surrounding lung tissue. Accuracy and reliability of aortic size measurements and sensitivity and specificity of endoleak detection and characterization are dependent on patient and technician factors (Figure 4). The sensitivity and specificity of endoleak detection may be increased by use of sonographic contrast agents, but this introduces another order of complexity, invasiveness, and risk to the study. Similar to the plain x-ray, subtle migrations and morphologic alterations are not easily detected using this modality.

Intravascular Pressure Sensor Implantable pressure sensors are now available that allow direct measurement of the end hemodynamic result of aneurysm exclusion by the endograft—that is, reduction of the sac pressure. The sensor is implanted into the sac using a catheter-based delivery system, and it is powered and controlled using an external radiofrequencybased hand-held unit. However, benchtop experimental evidence of

FOLLOW-UP SCHEDULE A critical question relates to the optimum schedule that will minimize follow-up while maximizing detection of adverse events. In the early days of this therapy, standard of care consisted of a CT and x-ray before discharge and then at 1, 6, and 12 months and every 6 months thereafter. With increased collective experience, better understanding of the natural history of the therapy, and improved devices, the trend has been toward eliminating a number of these time points. Although opinions on which ones should or can be eliminated are quite divided, there has been a near unanimity in doing away with predischarge imaging. From a practical standpoint, because patients are now often discharged in less than 24 hours, it would have been logistically difficult to schedule the scan without delaying the discharge, and more importantly, elimination of the study saved the patient from receiving another major contrast load. Today, one version of a follow-up schedule can consist of imaging at 1, (6), 12, 24, (36), 48, (60), 72 months, and so on. Pending the findings of the baseline postoperative scan at 1 month, namely, presence of an endoleak and/or other abnormalities that do not require immediate intervention, the 6-month scan can be optional. Similarly, if the endograft (position, conformation, etc.), aneurysm sac, and endoleak appear stable and favorable by 24 months, the follow-up interval can be lengthened to every other year. In certain situations

278

AORTIC ANEURYSM

where patients must travel from a distance, after the first year, if the CT angiogram can be performed locally using the protocol described earlier, the dataset (single word) may be simply sent on digital media to the original operator for review, obviating the need for a face-toface visit unless the patient complains of new-onset aorta-, device- or procedure-related symptoms. The issue of which of the imaging modalities, either alone or in combination, to employ at one or more of the time points suggested is a very complex issue that does not submit easily to a succinct discussion. It depends on the availability of a given technology, local expertise, and operator bias. This is especially true of modalities that rely on technique to produce high-quality images. For example, given the widespread availability of an accredited noninvasive laboratory in most vascular practices, operators have either alternated CT scans with duplex ultrasounds or have used duplex ultrasounds exclusively, using CT angiogram only to clarify new abnormal duplex findings, after performing baseline studies of both modalities. The basic tenet of postoperative surveillance after endovascular repair has always assumed that it is lifelong. As the population ages and patients with aortic disease become older, disease awareness and detection increases, and minimally invasive treatments are being offered to those previously excluded from any type of repair, the issue of how long to follow these patients versus end-of-life issues relating to futility of care becomes real and not simply one of medical ethics. Lifelong follow-up should not be taken literally, but instead, operators should ask at each follow-up whether, given the current health status of the patient, any significant finding on subsequent follow-up will change therapy given the magnitude of the intervention and the ability for the patient to tolerate a secondary procedure. If the answer is “no,” follow-up should stop. Postoperative surveillance is an integral component to the overall therapeutic strategy after endovascular aortic repair. The optimal

schedule of follow-up and diagnostic testing remains in evolution as endovascular devices, collective technical skill, and our understanding of the natural history of the therapy improve. Regardless of what methodology is chosen, it must be tailored to the local referral patterns to encourage compliance with follow-up, ensure local technical expertise in performing and interpreting a particular diagnostic study, and minimize long-term cumulative risks of radiation and contrast exposure.

Treatment of Aortic Endograft Migration

a mean time to treatment of 3 to 4 years after EVAR. The reported incidence of endograft migration is widely variable, ranging from 1% to 35% at 5 years. The reasons for such variance are multifactorial. Because endograft migration is time dependent, its true incidence must be calculated with life-table (Kaplan–Meier) analysis. Failure to use this methodology will significantly underestimate the true incidence.

W. Charles Stenbergh III

Caudal movement of the proximal aspect of an aortic endograft is a significant late failure of endovascular aneurysm repair (EVAR). This endograft migration can cause type Ia endoleak and enlargement and rupture of an abdominal aortic aneurysm (AAA). Thus, surveillance for and timely treatment of significant endograft migration is important in maximizing the long-term safety of EVAR.

DEFINITION Caudal movement of 10 mm or more, or any movement causing symptoms, is considered to be significant endograft migration as defined by the Society for Vascular Surgery (SVS) reporting standards. However, investigators have used variable definitions including a stricter movement limit of 5 mm or more, or movement twice the width of the reconstructed CT slice.

INCIDENCE Endograft migration is a time-dependent phenomenon that generally occurs later in follow-up. Most reported series demonstrate that clinically significant migration is unusual in the first 1 to 2 years, with

Selected References Bakken AM, Illig KA: Long-term follow-up after endovascular aneurysm repair: Is ultrasound alone enough? Perspect Vasc Surg Endovasc Ther 22:145–151, 2010. Brown LC, Greenhalgh RM, Powell JT, et al: Use of baseline factors to predict complications and reinterventions after endovascular repair of abdominal aortic aneurysm, Br J Surg 97:1207–1217, 2010. Houbballah R, Majewski M, Becquemin JP: Significant sac retraction after endovascular aneurysm repair is a robust indicator of durable treatment success, J Vasc Surg 52:878–883, 2010. Ishibashi H, Ishiguchi T, Ohta T, et al: Intraoperative sac pressure measurement during endovascular abdominal aortic aneurysm repair, Cardiovasc Intervent Radiol 33:939–942, 2010. Karthikesalingam A, Holt PJ, Hinchliffe RJ, et al: Risk of reintervention after endovascular aortic aneurysm repair, Br J Surg 97:657–663, 2010. Kopp R, Zürn W, Weidenhagen R, et al: First experience using intraoperative contrast-enhanced ultrasound during endovascular aneurysm repair for infrarenal aortic aneurysms, J Vasc Surg 51:1103–1110, 2010. Patel MS, Carpenter JP: The value of the initial post-EVAR computed tomography angiography scan in predicting future secondary procedures using the Powerlink stent graft, J Vasc Surg 52:1135–1139, 2010. Wyss TR, Brown LC, Powell JT, et al: Rate and predictability of graft rupture after endovascular and open abdominal aortic aneurysm repair: Data from the EVAR trials, Ann Surg 252:805–812, 2010.

RISK FACTORS FOR MIGRATION Many factors are responsible for endograft migration (Box 1). Disadvantaged aortic neck anatomy is likely the single greatest risk factor for later migration. Zarins and other investigators have conclusively demonstrated that the risk of migration increases as the aortic neck fixation length decreases. Severe aortic angulation and a conical neck have also been associated with increased migration. Patients with multiple anatomic limitations of the aortic neck are at particularly high risk for subsequent endograft migration. Adhering to the instructions for use (IFU) recommendations for acceptable aortic neck anatomy lessens the late migration risk. However, large population-based studies suggest that 30% to 50% of EVARs performed in the United States are performed on patients who do not have IFUsuitable anatomy. Pushing the anatomic envelope should be done on a case-by-case basis after weighing the relative early and long-term risks of endovascular repair, open repair, and continued observation. Excessive endograft oversizing of more than 30% has been demonstrated by Sternbergh and colleagues to be associated with an increased risk of endograft migration in patients treated with Zenith or AneuRx endografts. Such excessive oversizing can cause pleating of the endograft fabric, thus impairing graft apposition to the aortic wall. Bench studies by Kratzberg and colleagues have subsequently demonstrated that barb penetration is also adversely affected by more

278

AORTIC ANEURYSM

where patients must travel from a distance, after the first year, if the CT angiogram can be performed locally using the protocol described earlier, the dataset (single word) may be simply sent on digital media to the original operator for review, obviating the need for a face-toface visit unless the patient complains of new-onset aorta-, device- or procedure-related symptoms. The issue of which of the imaging modalities, either alone or in combination, to employ at one or more of the time points suggested is a very complex issue that does not submit easily to a succinct discussion. It depends on the availability of a given technology, local expertise, and operator bias. This is especially true of modalities that rely on technique to produce high-quality images. For example, given the widespread availability of an accredited noninvasive laboratory in most vascular practices, operators have either alternated CT scans with duplex ultrasounds or have used duplex ultrasounds exclusively, using CT angiogram only to clarify new abnormal duplex findings, after performing baseline studies of both modalities. The basic tenet of postoperative surveillance after endovascular repair has always assumed that it is lifelong. As the population ages and patients with aortic disease become older, disease awareness and detection increases, and minimally invasive treatments are being offered to those previously excluded from any type of repair, the issue of how long to follow these patients versus end-of-life issues relating to futility of care becomes real and not simply one of medical ethics. Lifelong follow-up should not be taken literally, but instead, operators should ask at each follow-up whether, given the current health status of the patient, any significant finding on subsequent follow-up will change therapy given the magnitude of the intervention and the ability for the patient to tolerate a secondary procedure. If the answer is “no,” follow-up should stop. Postoperative surveillance is an integral component to the overall therapeutic strategy after endovascular aortic repair. The optimal

schedule of follow-up and diagnostic testing remains in evolution as endovascular devices, collective technical skill, and our understanding of the natural history of the therapy improve. Regardless of what methodology is chosen, it must be tailored to the local referral patterns to encourage compliance with follow-up, ensure local technical expertise in performing and interpreting a particular diagnostic study, and minimize long-term cumulative risks of radiation and contrast exposure.

Treatment of Aortic Endograft Migration

a mean time to treatment of 3 to 4 years after EVAR. The reported incidence of endograft migration is widely variable, ranging from 1% to 35% at 5 years. The reasons for such variance are multifactorial. Because endograft migration is time dependent, its true incidence must be calculated with life-table (Kaplan–Meier) analysis. Failure to use this methodology will significantly underestimate the true incidence.

W. Charles Stenbergh III

Caudal movement of the proximal aspect of an aortic endograft is a significant late failure of endovascular aneurysm repair (EVAR). This endograft migration can cause type Ia endoleak and enlargement and rupture of an abdominal aortic aneurysm (AAA). Thus, surveillance for and timely treatment of significant endograft migration is important in maximizing the long-term safety of EVAR.

DEFINITION Caudal movement of 10 mm or more, or any movement causing symptoms, is considered to be significant endograft migration as defined by the Society for Vascular Surgery (SVS) reporting standards. However, investigators have used variable definitions including a stricter movement limit of 5 mm or more, or movement twice the width of the reconstructed CT slice.

INCIDENCE Endograft migration is a time-dependent phenomenon that generally occurs later in follow-up. Most reported series demonstrate that clinically significant migration is unusual in the first 1 to 2 years, with

Selected References Bakken AM, Illig KA: Long-term follow-up after endovascular aneurysm repair: Is ultrasound alone enough? Perspect Vasc Surg Endovasc Ther 22:145–151, 2010. Brown LC, Greenhalgh RM, Powell JT, et al: Use of baseline factors to predict complications and reinterventions after endovascular repair of abdominal aortic aneurysm, Br J Surg 97:1207–1217, 2010. Houbballah R, Majewski M, Becquemin JP: Significant sac retraction after endovascular aneurysm repair is a robust indicator of durable treatment success, J Vasc Surg 52:878–883, 2010. Ishibashi H, Ishiguchi T, Ohta T, et al: Intraoperative sac pressure measurement during endovascular abdominal aortic aneurysm repair, Cardiovasc Intervent Radiol 33:939–942, 2010. Karthikesalingam A, Holt PJ, Hinchliffe RJ, et al: Risk of reintervention after endovascular aortic aneurysm repair, Br J Surg 97:657–663, 2010. Kopp R, Zürn W, Weidenhagen R, et al: First experience using intraoperative contrast-enhanced ultrasound during endovascular aneurysm repair for infrarenal aortic aneurysms, J Vasc Surg 51:1103–1110, 2010. Patel MS, Carpenter JP: The value of the initial post-EVAR computed tomography angiography scan in predicting future secondary procedures using the Powerlink stent graft, J Vasc Surg 52:1135–1139, 2010. Wyss TR, Brown LC, Powell JT, et al: Rate and predictability of graft rupture after endovascular and open abdominal aortic aneurysm repair: Data from the EVAR trials, Ann Surg 252:805–812, 2010.

RISK FACTORS FOR MIGRATION Many factors are responsible for endograft migration (Box 1). Disadvantaged aortic neck anatomy is likely the single greatest risk factor for later migration. Zarins and other investigators have conclusively demonstrated that the risk of migration increases as the aortic neck fixation length decreases. Severe aortic angulation and a conical neck have also been associated with increased migration. Patients with multiple anatomic limitations of the aortic neck are at particularly high risk for subsequent endograft migration. Adhering to the instructions for use (IFU) recommendations for acceptable aortic neck anatomy lessens the late migration risk. However, large population-based studies suggest that 30% to 50% of EVARs performed in the United States are performed on patients who do not have IFUsuitable anatomy. Pushing the anatomic envelope should be done on a case-by-case basis after weighing the relative early and long-term risks of endovascular repair, open repair, and continued observation. Excessive endograft oversizing of more than 30% has been demonstrated by Sternbergh and colleagues to be associated with an increased risk of endograft migration in patients treated with Zenith or AneuRx endografts. Such excessive oversizing can cause pleating of the endograft fabric, thus impairing graft apposition to the aortic wall. Bench studies by Kratzberg and colleagues have subsequently demonstrated that barb penetration is also adversely affected by more



Treatment of Aortic Endograft Migration

BOX 1:  Risk Factors for Endograft Migration Disadvantaged preoperative aortic neck • Length 60 degrees • Conical or reverse conical morphology Endograft oversizing >30% Late aortic neck dilatation Use of endograft without active or anatomic fixation • Incomplete iliac fixation

than 30% oversizing, further explaining the increased risk of migration. Endografts should be oversized 10% to 20% in relation to the minor axis of the aortic neck. Late aortic neck dilatation is an intuitive risk factor for late migration. If the aortic neck dilates beyond the size of the endograft, there may be loss of seal and/or fixation. More controversial are the risk factors for such late aortic neck dilatation. Short, conical necks are more likely to dilate over time than long and straight necks. Largerdiameter aortic necks (>25–28 mm) have been associated with an increased risk of late dilatation in some studies. Excessive oversizing can contribute to subsequent neck dilatation, although the literature is conflicting in this regard. The relative risk of endograft migration is device dependent. Although all endografts have the potential to migrate, those without active barb or hook fixation or anatomic fixation at the iliac bifurcation have been demonstrated in multiple studies to have a higher incidence of late migration. This increased risk is particularly heightened in patients with disadvantaged aortic necks. The increase in late mortality in patients treated with such a device (AneuRx) prompted the FDA to issue a clinical warning in 2008 to ensure that the device is implanted only in patients with IFU-acceptable anatomy. Finally, the relative length of distal iliac fixation in devices without active proximal fixation has been postulated to modulate the risk of late migration. Because these devices (AneuRx, Talent) also rely partially on longitudinal columnar support, it has been suggested that routinely extending the iliac limbs to the common iliac artery bifurcation reduces late migration. There are no data suggesting a similar phenomenon in devices with active fixation. In that the manufacturer of these devices (Medtronic) has now essentially replaced them with a new endograft incorporating active proximal fixation (Endurant), the issue of optimizing iliac limb length is largely moot.

TREATMENT Treatment options are listed in Box 2.

Endovascular Treatment Cuff Placement The simplest endovascular treatment of endograft migration is the addition of a proximal aortic cuff. This option is acceptable if the distance of migration is not excessive (50%) common femoral artery stenoses are present, we recommend surgical repair or a hybrid ­endovascular–surgical approach (Figure 2). The common femoral artery and its bifurcation is exposed and is treated with endarterectomy and patch repair with concurrent iliac (and sometimes also superficial femoral artery) angioplasty and stenting. Whereas angioplasty and even stenting of the common femoral artery has been reported, we believe that evidence suggests poor patency rates. Stenting of the



Selecting Treatment for Patients with Aortoiliac Occlusive Disease

A

413

B

FIGURE 2  A, Computed tomography angiogram (CTA) of patient with critical ischemia of the right foot revealing near occlusion of the right common femoral artery. B, CTA of the same patient with calcified proximal common iliac arteries and moderate to severe right common iliac artery stenosis requiring hybrid repair with iliac artery angioplasty and stenting and concurrent right common femoral repair.

common femoral artery has a higher risk of stent fracture as a result of the mobility of the hip. Also, there is the risk of compromising the profunda femoris artery, a vessel critical to maintaining viability of the extremity in the setting of a superficial artery occlusion. Profunda Femoris Artery as Outflow for Reconstruction When the common femoral arteries are occluded or severely diseased, direct bypass from the abdominal aorta, axillary artery, contralateral femoral artery, or thoracic aorta onto the profunda femoris is employed. Small External Iliac Arteries We also consider an open surgical approach in patients with small external iliac arteries with bilateral long segment severe stenoses or occlusions. These patients are candidates for direct reconstruction (ABF or iliofemoral bypass) or extra-anatomic bypass (axillofemoral bypass). Previous Failed Attempt at Revascularization A hybrid approach can also be used after a failed iliac artery recanalization. A femorofemoral bypass is employed, often with angioplasty and stenting on the inflow side (Figure 3).

FIGURE 3  Hybrid procedure with femoral sheath inserted for

angioplasty and stenting of inflow iliac system with femorofemoral bypass.

aneurysm repair that is not amenable to endovascular repair, or a cardiac surgical procedure (Figure 4).

High-Risk Lesion for Distal Embolization Patients with ulcerated plaques, especially in the pararenal segment of the aorta, are at higher risk for embolization with endovascular treatment, and they may be better served with open surgery in an effort to decrease the risk of embolic complications. Need for Concomitant Procedures An open surgical approach is sometimes employed when concomitant surgical procedures are required, for example in the case of patients requiring bypass to the superior mesenteric or renal arteries, revascularization of a transplanted organ, abdominal aortic

CONCLUSIONS Despite a relative lack of scientific evidence, there has been a paradigm shift in the treatment of AIOD toward an endovascular-first strategy. However, there still remains a role for open surgical repair by direct or extra-anatomic bypass, and the practitioner must consider a variety of factors when selecting the most appropriate treatment for patients with AIOD in whom revascularization is indicated. The interplay among these factors is complex, and hopefully future studies will provide better evidence on which to base treatment decisions.

414

AORTOILIAC OCCLUSIVE DISEASE

FIGURE 4  Ascending aorta-to-femoral bypass in a patient with a

severely calcified infrarenal aorta, requiring concurrent aortic valve replacement and coronary artery bypass.

Selected References Giles KA, Hamdan AD, Pomposelli FB, et al: Body mass index: Surgical site infections and mortality after lower extremity bypass from the National Surgical Quality Improvement Program 2005–2007, Ann Vasc Surg 24:48–56, 2010. Hertzer NR, Bena JF, Karafa MT, et al: A personal experience with direct reconstruction and extraanatomic bypass for aortoiliofemoral occlusive disease, J Vasc Surg 45:527–535, 2007.

Percutaneous Arterial Angioplasty with and without Stenting for Atherosclerotic Aortic and Iliac Artery Occlusive Disease Douglas B. Hood

The comparative ease and success of endovascular management of aortoiliac occlusive disease (AIOD) has greatly reduced the need for its open surgical repair. Factors such as reduced patient morbidity, discomfort, and length of convalescence have resulted not only in increased acceptance by patients but often in patients’ insistence on this mode of therapy. Potential cost savings is another factor favoring

Hirsch AT, Haskal ZJ, Hertzer NR, et al: ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): Executive summary. A collaborative report from the American Association for Vascular Surgery/ Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease) endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation, J Am Coll Cardiol 47:1239–1312, 2006. Indes JE, Tuggle CT, Mandawat A, et al: Age-stratified outcomes in elderly patients undergoing open and endovascular procedures for aortoiliac occlusive disease, Surgery 148:420–428, 2010. Jacobs DL, Cox DE, Motaganahalli R: Crossing chronic total occlusions of the iliac and femoral–popliteal vessels and the use of true lumen reentry devices, Perspect Vasc Surg Endovasc Ther 18:31–37, 2006. Murphy TP, Hirsch AT, Cutlip DE, et al: Claudication: Exercise vs endoluminal revascularization (CLEVER) study update, J Vasc Surg 50:942–945, 2009. Norgren L, Hiatt WR, Dormandy JA, et al: Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II), J Vasc Surg (45 Suppl S):S5–S67, 2007. Pulli R, Dorigo W, Fargion A, et al: Early and long-term comparison of endovascular treatment of iliac artery occlusions and stenosis, J Vasc Surg 53:92–98, 2011. Stirling MJ, Miller MJ, Smith TP, et al: Subintimal stent graft reconstruction of an infrarenal aortic occlusion, Semin Intervent Radiol 24:10–14, 2007. Taylor SM, Kalbaugh CA, Healty MG: Do current outcomes justify more liberal use of revascularization for vasculogenic claudication? A single center experience of 1,000 consecutively treated limbs, J Am Coll Surg 206:1053–1062, 2008.

endovascular treatments, although the expense of the necessary endovascular devices and implants and the not uncommon need for repeat interventions to treat recurrent disease can negate this potential advantage.

INDICATIONS Endovascular treatment of AIOD should be considered for patients with disabling claudication or critical limb ischemia who have lesions with favorable expected results. The Trans-Atlantic Inter-Society Consensus (TASC) classification scheme, which stratifies patients into four groups according to the anatomic pattern of occlusive lesions, is useful to select patients for these interventions (Box 1). Patients with type A lesions (focal stenosis of the common or external iliac arteries) have the best results, and endovascular therapy is the treatment of choice for this group. Open surgical reconstruction is recommended for patients with the most severe pattern of disease (type D lesions). Comorbidities, patient’s preference, and the operator’s experience should be considered when choosing endovascular or open techniques for managing patients with types B and C lesions, with the majority of these patients currently treated with endovascular intervention. Treatment guidelines also recommend that patients with critical limb ischemia and combined aortoiliac and infrainguinal occlusive disease should have the AIOD addressed first. Infrainguinal intervention should then be performed in patients with persistent ischemia

414

AORTOILIAC OCCLUSIVE DISEASE

FIGURE 4  Ascending aorta-to-femoral bypass in a patient with a

severely calcified infrarenal aorta, requiring concurrent aortic valve replacement and coronary artery bypass.

Selected References Giles KA, Hamdan AD, Pomposelli FB, et al: Body mass index: Surgical site infections and mortality after lower extremity bypass from the National Surgical Quality Improvement Program 2005–2007, Ann Vasc Surg 24:48–56, 2010. Hertzer NR, Bena JF, Karafa MT, et al: A personal experience with direct reconstruction and extraanatomic bypass for aortoiliofemoral occlusive disease, J Vasc Surg 45:527–535, 2007.

Percutaneous Arterial Angioplasty with and without Stenting for Atherosclerotic Aortic and Iliac Artery Occlusive Disease Douglas B. Hood

The comparative ease and success of endovascular management of aortoiliac occlusive disease (AIOD) has greatly reduced the need for its open surgical repair. Factors such as reduced patient morbidity, discomfort, and length of convalescence have resulted not only in increased acceptance by patients but often in patients’ insistence on this mode of therapy. Potential cost savings is another factor favoring

Hirsch AT, Haskal ZJ, Hertzer NR, et al: ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): Executive summary. A collaborative report from the American Association for Vascular Surgery/ Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease) endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation, J Am Coll Cardiol 47:1239–1312, 2006. Indes JE, Tuggle CT, Mandawat A, et al: Age-stratified outcomes in elderly patients undergoing open and endovascular procedures for aortoiliac occlusive disease, Surgery 148:420–428, 2010. Jacobs DL, Cox DE, Motaganahalli R: Crossing chronic total occlusions of the iliac and femoral–popliteal vessels and the use of true lumen reentry devices, Perspect Vasc Surg Endovasc Ther 18:31–37, 2006. Murphy TP, Hirsch AT, Cutlip DE, et al: Claudication: Exercise vs endoluminal revascularization (CLEVER) study update, J Vasc Surg 50:942–945, 2009. Norgren L, Hiatt WR, Dormandy JA, et al: Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II), J Vasc Surg (45 Suppl S):S5–S67, 2007. Pulli R, Dorigo W, Fargion A, et al: Early and long-term comparison of endovascular treatment of iliac artery occlusions and stenosis, J Vasc Surg 53:92–98, 2011. Stirling MJ, Miller MJ, Smith TP, et al: Subintimal stent graft reconstruction of an infrarenal aortic occlusion, Semin Intervent Radiol 24:10–14, 2007. Taylor SM, Kalbaugh CA, Healty MG: Do current outcomes justify more liberal use of revascularization for vasculogenic claudication? A single center experience of 1,000 consecutively treated limbs, J Am Coll Surg 206:1053–1062, 2008.

endovascular treatments, although the expense of the necessary endovascular devices and implants and the not uncommon need for repeat interventions to treat recurrent disease can negate this potential advantage.

INDICATIONS Endovascular treatment of AIOD should be considered for patients with disabling claudication or critical limb ischemia who have lesions with favorable expected results. The Trans-Atlantic Inter-Society Consensus (TASC) classification scheme, which stratifies patients into four groups according to the anatomic pattern of occlusive lesions, is useful to select patients for these interventions (Box 1). Patients with type A lesions (focal stenosis of the common or external iliac arteries) have the best results, and endovascular therapy is the treatment of choice for this group. Open surgical reconstruction is recommended for patients with the most severe pattern of disease (type D lesions). Comorbidities, patient’s preference, and the operator’s experience should be considered when choosing endovascular or open techniques for managing patients with types B and C lesions, with the majority of these patients currently treated with endovascular intervention. Treatment guidelines also recommend that patients with critical limb ischemia and combined aortoiliac and infrainguinal occlusive disease should have the AIOD addressed first. Infrainguinal intervention should then be performed in patients with persistent ischemia

Percutaneous Arterial Angioplasty with and without Stenting for Atherosclerotic

after inflow revascularization. If it is unclear whether or not a particular lesion is hemodynamically significant, a pressure gradient across the lesion should be performed before and after the administration of a vasodilator. A peak systolic gradient of 5 to 10 mm Hg before or 10 to 15 mm Hg after vasodilatation is considered significant.

BOX 1: TASC Classification of Aortoiliac Lesions

Type A Lesions

• Unilateral or bilateral stenoses of SFA • Unilateral or bilateral single short (≤3 cm) stenosis of EIA

Type B Lesions

• Short (≤3 cm) stenosis of infrarenal aorta • Unilateral CIA occlusion • Single or multiple stenosis totaling 3–10 cm involving the EIA not extending into the CFA • Unilateral EIA occlusion not involving the origins of internal iliac or CFA

Type C Lesions

• Bilateral CIA occlusions • Bilateral EIA stenoses 3–10 cm long not extending into the CFA • Unilateral EIA stenosis extending into the CFA • Unilateral EIA occlusion that involves the origins of internal iliac and/or CFA • Heavily calcified unilateral EIA occlusion with or without involvement of origins of internal iliac and/or CFA

Type D Lesions

• Infrarenal aortoiliac occlusion • Diffuse disease involving the aorta and both iliac arteries requiring treatment • Diffuse multiple stenoses involving the unilateral CIA, EIA, and CFA • Unilateral occlusions of both CIA and EIA • Bilateral occlusions of EIA • Iliac stenoses in patients with AAA requiring treatment and not amenable to endograft placement or other lesions requiring open aortic or iliac surgery AAA, Abdominal aortic aneurysm; CFA, common femoral artery; CIA, common iliac artery; EIA, external iliac artery; SFA, superficial femoral artery; TASC, Trans-Atlantic Inter-Society Consensus.

FIGURE 1  A, Diagnostic arteriogram showing serial stenoses of left common and external iliac arteries. B, Completion study after stent placement.Vascular access achieved via retrograde puncture of the contralateral common femoral artery. The guidewire can be seen crossing aortic bifurcation.

A

415

TECHNIQUE Endovascular interventions for common and proximal external iliac artery lesions are most easily performed through an ipsilateral retrograde femoral approach. If necessary or desirable, however, many interventions can be performed through a contralateral femoral puncture, with over-the-top contralateral access across the aortic bifurcation (Figure 1). Upper extremity vascular access is also technically feasible, but it is not preferred. Guidewire and catheter manipulations are more difficult over the longer working distance from the arm, and the larger-diameter sheath required for many interventional devices increases the likelihood of puncture site complications in the smaller arm vessels. Aortic lesions near its bifurcation should be considered complex lesions involving the distal aorta and both common iliac arteries. Safe and effective intervention in this situation typically requires the use of two balloons or stents, one in each iliac artery and projecting partway into the aorta so that they kiss in the distal aorta. Aortic lesions distant from the bifurcation or other critical branches are otherwise treated similarly to that described for iliac stenoses. Successful navigation of guidewires and catheters across the target lesion from the access site can require considerable skill and experience. Failure to achieve successful traversal is one reason for initial technical failure of the procedure. Navigation across a complete occlusion, with reentry into the true lumen of the vessel beyond the lesion, can be especially challenging. This maneuver is most often accomplished using angled hydrophilic guidewires and/or catheters (Figure 2). If reentry cannot be achieved from the chosen point of vascular access (e.g., ipsilateral common femoral), an attempt may be made from a new access site (e.g., contralateral common femoral or brachial). For more challenging cases, reentry devices such as the Outback (Cordis Corp., Bridgewater, NJ) or Pioneer (Medtronic, Fridley, MN) catheters can be used. Once a lesion is successfully crossed with a guidewire, the operator must decide on the method of intervention: an initial attempt at balloon angioplasty alone with stenting reserved for technical failure or primary stenting. Transluminal atherectomy has not been widely adopted for the management of AIOD. Typical balloon or stent diameters are 8 to 10 mm for the common iliac arteries and 6 to 8 mm for the external iliac arteries. Angioplasty balloon or stent length is selected to completely cover the offending lesion, with minimal coverage of the adjacent normal vessel. Elastic recoil of atherosclerotic plaque and flow-limiting dissections are the principal causes of early failure of balloon angioplasty alone. In most instances, the deployment of a stent can successfully

B

416

AORTOILIAC OCCLUSIVE DISEASE

A

D

B

E

C

F

FIGURE 2  A, Diagnostic arteriogram showing complete occlusion of the right common iliac artery beginning close to the aortic bifurcation. B, After the occlusion has been successfully traversed using a ­hydrophilic wire and angled catheter, contrast injection through the catheter confirms reentry into the true lumen of the aorta. C, Guidewires are placed into the aorta from bilateral femoral access sites. D, ­After kissing stents are placed into both common iliac arteries, a persistent intraluminal filling defect is seen in the distal right common iliac artery. E, Unsubtracted image showing placement of an additional stent across the defect noted in D. F, Arteriographic image showing resolution of the defect noted in D.

address these issues. Long-term failure generally results from intimal hyperplasia causing recurrent stenosis at the site of dilation or from progression of proximal or distal atherosclerotic disease. Repeat endovascular intervention is often all that is required in these situations. Metallic stents have been widely adopted as an adjunct to balloon angioplasty in the treatment of AIOD. Stents serve as intraluminal scaffolds to oppose postangioplasty elastic recoil of the media and adventitia of the artery. They are also highly effective means of sealing dissection planes within the atherosclerotic plaque resulting from the angioplasty procedure. By tacking down the dissection planes, a more laminar pattern of blood flow through the treated lesion is produced, and exposure of the arterial media to the circulating promoters of intimal hyperplasia is limited. The availability of

stents increased the initial success rates of endovascular intervention by serving as a salvage method to treat lesions with persistent residual stenosis after balloon angioplasty alone. Lastly, stents can improve the long-term results of balloon angioplasty by reducing the incidence of significant restenosis within the dilated site. Several stents have received U.S. Food and Drug Administration (FDA) approval for placement in the iliac arteries. Features include self-expanding versus balloon-expandable deployment and bare-metal versus covered designs. No stent has demonstrated clear superiority, and the choice of a particular design remains at the discretion of the operator and local availability. In general, the author prefers to use balloon-expandable stents in the common iliac arteries owing to the increased radial force of this design compared to the self-­expanding varieties.

Percutaneous Arterial Angioplasty with and without Stenting for Atherosclerotic

A self-expanding stent is often chosen for placement in the external iliac arteries, where the increased longitudinal flexibility of this design may be beneficial for placement in more tortuous vessels. Covered stents may be preferred to reduce distal embolization from particularly irregular or ulcerated lesions or to limit intimal hyperplasia between the interstices of a bare-metal stent. Balloon-expandable stents are premounted onto an angioplasty balloon; a variety of stent lengths and balloon diameters are available. A diameter is selected that produces slight overdilation to a diameter 10% to 15% greater than the adjacent normal native artery. The stent is deployed and released by simply inflating the balloon. Oversizing that can result in vessel injury is to be avoided; slight undersizing can be managed by further expanding the stent after deployment using a larger balloon. Self-expanding stents are packaged on a proprietary delivery system, with the stent usually constrained by a retractable outer sheath. The delivery system is passed over a guidewire to the intended site of stent placement, the outer sheath of the delivery catheter is retracted, and the stent is freed to assume its expanded form. Postdeployment balloon angioplasty is commonly performed to achieve full stent expansion and apposition of the stent to the vessel wall. Similar to balloon-expandable stents, a self-expanding stent is chosen that is 10% to 15% larger than the adjacent normal vessel. A smaller-­ diameter stent should not be chosen, because self-expanding stents cannot be dilated beyond their nominal diameter. Covered stents are available in balloon-expandable (iCast, Atrium Medical Corp., Hudson, NH) and self-expanding (Viabahn, W.L. Gore & Associates, Flagstaff, AZ) platforms. When deploying a covered stent, care must be taken so that critical side branches are not excluded from flow. Iliac artery stents are most clearly indicated for lesions that are incompletely treated with balloon angioplasty alone. A suboptimal result after angioplasty is defined as a persistent diameter reduction of 30% or more as assessed by arteriography or intravascular ultrasound, or as a persistent blood pressure gradient across the treated lesion. If completion arteriography alone is to be used, multiple views in anteroposterior and oblique planes may be necessary to completely exclude residual stenosis. Contrast arteriography alone, however, provides only morphologic information and is not sufficient to assess the hemodynamic significance of any residual lesions. This is best evaluated by measurement of a blood pressure gradient across the lesion, which is simple to perform and may be more sensitive than completion arteriography alone. A resting mean blood pressure gradient of 5 mm Hg or greater or a systolic blood pressure gradient exceeding 5 to 10 mm Hg is considered significant. Provocative testing with pharmacologic vasodilation may be necessary. As many as 75% of patients found to have a significant blood pressure gradient after pharmacologic vasodilation had no significant blood pressure gradient when measured at rest. This test is performed by injecting 100 to 200 μg of nitroglycerin or 25 mg of papaverine directly into the involved extremity distal to the lesion, which produces nearly immediate distal arterial dilation that simulates exercise. Placement of iliac artery stents is also clearly indicated for the acute management of extensive dissections that sometimes occur after balloon angioplasty or other interventions. Although limited dissections occur after virtually all instances of balloon angioplasty, in some the dissection extends beyond the angioplasty site and causes significant narrowing, or even occlusion, of the arterial lumen. If a guidewire is still in place across the angioplastied lesion, this complication can be quickly treated by deploying a stent to tack down the dissection. If no guidewire remains across the area of dissection, a cautious attempt at recrossing the lesion with the guidewire may be made as a prelude to stent placement, but this maneuver must be performed with great care to avoid subintimal passage of the wire and worsening of the dissection. Other relative indications for iliac artery stent placement include the treatment of eccentric plaque, which tends to resist fracture, and of recanalized arterial occlusions. In the latter circumstance, a brief

417

trial of thrombolysis or mechanical thrombectomy may be helpful in patients with relatively acute symptomatic deterioration as a means to minimize the length of artery undergoing dilation, as well as the risk of embolization of unstable thrombus. Less commonly, stenting is performed for the endovascular treatment of ulcerated atherosclerotic plaques that are felt to be the source of distal emboli. Angioplasty alone of an ulcerated lesion can increase the risk of further embolization; stenting without preliminary angioplasty can minimize this risk. Lastly, restenosis after balloon angioplasty alone may be better treated with stenting than with repeat angioplasty only.

RESULTS Results of iliac artery angioplasty alone were prospectively analyzed and reported by Johnston and colleagues in 1987. Included in this report were 684 aortoiliac angioplasty procedures, 88.4% of which were performed for intermittent claudication. Arterial stenoses were present in 87.9% of patients, and occlusions were present in 12.1%. The average translesional pressure gradient fell from 41.8 ± 27.3 mm Hg before angioplasty to 7.0 ± 10.9 mm Hg after angioplasty. Initial success, defined as a combination of clinical factors and ankle Doppler data, was achieved in 88.6%, with continued success in 48.2% at 60 months. Predictors of success included indication (intermittent claudication vs. limb salvage), site of angioplasty (common iliac artery vs. other), lesion severity (stenosis vs. occlusion), and the status of the runoff circulation. From their data, these authors predicted clinical success at 5 years in 63% of patients after angioplasty of a common iliac stenosis in patients with claudication and good runoff. Bosch and Hunink reported a meta-analysis of the results of balloon angioplasty and stenting of the iliac arteries. Immediate technical success was higher in the stent group (96%) than in the angioplasty group (91%), although for occlusions, the immediate technical success was equivalent (80%). The systemic complication rate (1%), local complication rate (9%–10%), and rate of major complications that required treatment (4%–5%) were similar between groups. Excluding technical failures, the overall 4-year primary patency rate was 64% after angioplasty alone and 77% after stent placement. The risk of long-term failure was reduced by 39% after stent placement compared with angioplasty. If initial technical failures were excluded, treatment of an occlusion versus a stenosis was not a significant variable affecting long-term success. The degree of ischemia (intermittent claudication vs. critical ischemia) did affect success, with less severely affected patients faring better. Patients’ gender, disease pattern, disease severity, lesion type, and site (common iliac vs. other) were not significant variables. Primary patency at 4 years, with technical failures included, was not affected by the type of stent placed. The role of primary stenting for the management of AIOD has also been addressed in a prospective multicenter randomized trial of patients undergoing iliac artery intervention (Dutch Iliac Stent Trial). In this study, 279 patients were randomized into two groups. The first group was assigned to primary stent placement. The second group underwent primary angioplasty, with stenting performed only for patients with a persistent mean translesional pressure gradient of 10 mm Hg or more. In this second group, stents ultimately were placed in 43%. Baseline clinical (e.g., risk factors, indication, ankle-to-brachial index [ABI]) and angiographic (e.g., site, percentage of stenosis, runoff) characteristics were similar in the two groups. Based on clinical, hemodynamic, and duplex assessments, there was no difference between the groups at 2 years. Patency at 2 years as measured by duplex was 71.3% in the primary stent group and 69.9% in the primary angioplasty group, not a significant difference. These authors suggested that angioplasty followed by stent placement for failures may be preferred over primary iliac stenting. However, primary stenting has been adopted by many practitioners and remains an acceptable therapeutic strategy.

418

AORTOILIAC OCCLUSIVE DISEASE

Covered stents to treat AIOD have been proposed as a method to reduce restenosis caused by intimal hyperplasia after iliac interventions, and this approach is supported by a recently reported multicenter randomized trial (Covered versus Balloon Expandable Stent Trial [COBEST]). Patients received either a bare-metal stent or a covered balloon-expandable stent. At 18 months, freedom from restenosis greater than 50% was significantly higher in the covered-stent group, with a hazard ratio of 0.35. Subgroup analysis showed significant improvement for TASC C and D lesions, but not for TASC B lesions.

Selected References Bosch JL, Hunink MGM: Meta-analysis of the results of percutaneous transluminal angioplasty and stent placement for aortoiliac occlusive disease, Radiology 204:87–96, 1997. Chen BL, Holt HR, Day JD, et al: Subintimal angioplasty of chronic total ­occlusion in iliac arteries: a safe and durable option, J Vasc Surg 53: 367–373, 2011. Johnston KW, Rae M, Hogg-Johnston SA, et al: Five-year results of a prospective study of percutaneous transluminal angioplasty, Ann Surg 206:403–413, 1987. Kashyap VS, Pavkov ML, Bena JF, et al: The management of severe aortoiliac occlusive disease: Endovascular therapy rivals open reconstruction, J Vasc Surg 48:1451–1457, 2008.

Aortofemoral Bypass for Atherosclerotic Aortoiliac Occlusive Disease David C. Brewster

Aortoiliac disease (AOID) is usually segmental in distribution and therefore amenable to effective treatment. Even in patients with multilevel disease, successful correction of hemodynamically significant inflow disease often provides adequate revascularization of the extremities and satisfactory clinical relief of ischemic symptoms.

PROCEDURE SELECTION Numerous options exist for revascularization in patients with AOID. Selection of the most appropriate method depends largely on two factors: the patient’s surgical risk and the extent and distribution of occlusive disease. Aortobifemoral grafting is elected for patients who are relatively free of serious comorbid medical conditions that would make them a high or prohibitive risk for direct abdominal aortic reconstruction. Thus careful preoperative evaluation is important. For patients with relatively limited areas of disease, particularly unilateral iliac disease, alternative lesser procedures such as percutaneous transluminal angioplasty (PTA) with or without stenting, femorofemoral bypass, or unilateral iliofemoral grafting may be considered. For high-risk patients with bilateral iliac disease or those with relative contraindications to direct aortic reconstruction as a result of technical considerations, such as heavy retroperitoneal scarring or contamination, axillobifemoral extra-anatomic bypass may be chosen. The lower long-term patency rate of these grafts is accepted as a compromise to achieve revascularization in high-risk situations.

Mwipatayi BP, Thomas S, Wong J, et al: A comparison of covered vs bare expandable stents for the treatment of aortoiliac occlusive disease, J Vasc Surg 54:1561–1570, 2011. Norgren L, Hiatt WR, Dormandy JA, et al: TASC II Working Group. InterSociety Consensus for the Management of Peripheral Arterial Disease (TASC II), J Vasc Surg 45(Suppl S):S5–S67, 2007. Park KB, Do YS, Kim DI, et al: The Trans-Atlantic Intersociety Consensus (TASC) classifications system in iliac arterial stent placement: Long-term patency and clinical limitations, J Vasc Intervent Radiol 18:193–201, 2007. Rooke TW, Hirsch AT, Misra S, et al: 2011 ACCF/AHA focused update of the guideline for the management of patients with peripheral artery disease (updating the 2005 guideline): A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, Circulation 124:2020–2045, 2011. Tetteroo E, van Engelen AD, Spithoven JH, et al: Stent placement after iliac angioplasty: Comparison of hemodynamic and angiographic criteria, Radiology 201:155–159, 1996. Tetteroo E, van der Graaf Y, Bosch JL, et al: Randomised comparison of primary stent placement versus primary angioplasty followed by selective stent placement in patients with iliac-artery occlusive disease. Dutch Iliac Stent Trial Study Group, Lancet 351:1153–1159, 1998.

Although all of the alternative methods may be helpful or appropriate choices in selected circumstances, aortobifemoral grafting clearly provides superior long-term results in terms of durability and sustained relief of symptoms and thus should be properly regarded as the preferred treatment or gold standard for the management of atherosclerotic AOID, as well as the yardstick to which the results of alternative therapies must be measured. Aortoiliac endarterectomy formerly was employed in many such patients. Although excellent results may be obtained in patients whose AOID is confined to the distal aorta and common iliac vessels, the majority of patients have diffuse disease and are better managed with aortofemoral graft insertion, which is more expedient and effective in such circumstances.

OPERATIVE MANAGEMENT A broad-spectrum prophylactic antibiotic, such as cefazolin 1 g, is administered intravenously 1 to 2 hours before the operation and continued for 1 or 2 days postoperatively. In patients with an infected open ischemic lesion of an extremity or any other possible source of bacteremia, culture-specific antibiotics are best started several days before the operation. A radial artery cannula is inserted in all patients for continuous blood pressure monitoring and arterial blood gas determinations. A Swan–Ganz catheter is used in many, but not all, patients, depending on preoperative assessment of cardiac and renal status. Most patients undergoing aortic reconstruction on the author's vascular unit and in many other centers undergo anesthesia by a combination of epidural narcotics and inhalation agents (combined general and epidural technique). Continuation of epidural analgesia in the early postoperative period for pain control has been a significant advance in limiting administration of systemic narcotics and in reducing associated respiratory complications following aortic reconstruction.

Operative Approach The infrarenal abdominal aorta may be exposed for aortofemoral reconstruction by a variety of approaches. A long midline vertical

418

AORTOILIAC OCCLUSIVE DISEASE

Covered stents to treat AIOD have been proposed as a method to reduce restenosis caused by intimal hyperplasia after iliac interventions, and this approach is supported by a recently reported multicenter randomized trial (Covered versus Balloon Expandable Stent Trial [COBEST]). Patients received either a bare-metal stent or a covered balloon-expandable stent. At 18 months, freedom from restenosis greater than 50% was significantly higher in the covered-stent group, with a hazard ratio of 0.35. Subgroup analysis showed significant improvement for TASC C and D lesions, but not for TASC B lesions.

Selected References Bosch JL, Hunink MGM: Meta-analysis of the results of percutaneous transluminal angioplasty and stent placement for aortoiliac occlusive disease, Radiology 204:87–96, 1997. Chen BL, Holt HR, Day JD, et al: Subintimal angioplasty of chronic total ­occlusion in iliac arteries: a safe and durable option, J Vasc Surg 53: 367–373, 2011. Johnston KW, Rae M, Hogg-Johnston SA, et al: Five-year results of a prospective study of percutaneous transluminal angioplasty, Ann Surg 206:403–413, 1987. Kashyap VS, Pavkov ML, Bena JF, et al: The management of severe aortoiliac occlusive disease: Endovascular therapy rivals open reconstruction, J Vasc Surg 48:1451–1457, 2008.

Aortofemoral Bypass for Atherosclerotic Aortoiliac Occlusive Disease David C. Brewster

Aortoiliac disease (AOID) is usually segmental in distribution and therefore amenable to effective treatment. Even in patients with multilevel disease, successful correction of hemodynamically significant inflow disease often provides adequate revascularization of the extremities and satisfactory clinical relief of ischemic symptoms.

PROCEDURE SELECTION Numerous options exist for revascularization in patients with AOID. Selection of the most appropriate method depends largely on two factors: the patient’s surgical risk and the extent and distribution of occlusive disease. Aortobifemoral grafting is elected for patients who are relatively free of serious comorbid medical conditions that would make them a high or prohibitive risk for direct abdominal aortic reconstruction. Thus careful preoperative evaluation is important. For patients with relatively limited areas of disease, particularly unilateral iliac disease, alternative lesser procedures such as percutaneous transluminal angioplasty (PTA) with or without stenting, femorofemoral bypass, or unilateral iliofemoral grafting may be considered. For high-risk patients with bilateral iliac disease or those with relative contraindications to direct aortic reconstruction as a result of technical considerations, such as heavy retroperitoneal scarring or contamination, axillobifemoral extra-anatomic bypass may be chosen. The lower long-term patency rate of these grafts is accepted as a compromise to achieve revascularization in high-risk situations.

Mwipatayi BP, Thomas S, Wong J, et al: A comparison of covered vs bare expandable stents for the treatment of aortoiliac occlusive disease, J Vasc Surg 54:1561–1570, 2011. Norgren L, Hiatt WR, Dormandy JA, et al: TASC II Working Group. InterSociety Consensus for the Management of Peripheral Arterial Disease (TASC II), J Vasc Surg 45(Suppl S):S5–S67, 2007. Park KB, Do YS, Kim DI, et al: The Trans-Atlantic Intersociety Consensus (TASC) classifications system in iliac arterial stent placement: Long-term patency and clinical limitations, J Vasc Intervent Radiol 18:193–201, 2007. Rooke TW, Hirsch AT, Misra S, et al: 2011 ACCF/AHA focused update of the guideline for the management of patients with peripheral artery disease (updating the 2005 guideline): A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, Circulation 124:2020–2045, 2011. Tetteroo E, van Engelen AD, Spithoven JH, et al: Stent placement after iliac angioplasty: Comparison of hemodynamic and angiographic criteria, Radiology 201:155–159, 1996. Tetteroo E, van der Graaf Y, Bosch JL, et al: Randomised comparison of primary stent placement versus primary angioplasty followed by selective stent placement in patients with iliac-artery occlusive disease. Dutch Iliac Stent Trial Study Group, Lancet 351:1153–1159, 1998.

Although all of the alternative methods may be helpful or appropriate choices in selected circumstances, aortobifemoral grafting clearly provides superior long-term results in terms of durability and sustained relief of symptoms and thus should be properly regarded as the preferred treatment or gold standard for the management of atherosclerotic AOID, as well as the yardstick to which the results of alternative therapies must be measured. Aortoiliac endarterectomy formerly was employed in many such patients. Although excellent results may be obtained in patients whose AOID is confined to the distal aorta and common iliac vessels, the majority of patients have diffuse disease and are better managed with aortofemoral graft insertion, which is more expedient and effective in such circumstances.

OPERATIVE MANAGEMENT A broad-spectrum prophylactic antibiotic, such as cefazolin 1 g, is administered intravenously 1 to 2 hours before the operation and continued for 1 or 2 days postoperatively. In patients with an infected open ischemic lesion of an extremity or any other possible source of bacteremia, culture-specific antibiotics are best started several days before the operation. A radial artery cannula is inserted in all patients for continuous blood pressure monitoring and arterial blood gas determinations. A Swan–Ganz catheter is used in many, but not all, patients, depending on preoperative assessment of cardiac and renal status. Most patients undergoing aortic reconstruction on the author's vascular unit and in many other centers undergo anesthesia by a combination of epidural narcotics and inhalation agents (combined general and epidural technique). Continuation of epidural analgesia in the early postoperative period for pain control has been a significant advance in limiting administration of systemic narcotics and in reducing associated respiratory complications following aortic reconstruction.

Operative Approach The infrarenal abdominal aorta may be exposed for aortofemoral reconstruction by a variety of approaches. A long midline vertical



Aortofemoral Bypass for Atherosclerotic Aortoiliac Occlusive Disease

incision is employed most often and is generally preferred because it is rapidly made, is easy to close, and affords maximal exposure and technical flexibility in most patients. A retroperitoneal approach may also be used, if desired. For this method, the patient is positioned with the shoulders and torso rotated approximately 45 degrees toward the right, while the hips and extremities are maintained as horizontal as possible to facilitate exposure of the femoral arteries in each groin. An oblique left flank incision beginning at the tip of the twelfth rib and carried toward the midline just below the umbilicus is used. A retroperitoneal approach is potentially advantageous in patients who have had multiple prior abdominal operations or, particularly, for reoperative aortic procedures. This approach is also often useful for obese patients or those with right-sided intestinal stomas. Advocates also believe that a retroperitoneal approach causes less postoperative ileus, decreased fluid losses, and reduced cardiopulmonary stresses postoperatively. However, many of these potential benefits are not conclusively established. The author prefers a transperitoneal midline approach, primarily because of the easier and generally superior exposure of the femoral arteries that it allows. A retroperitoneal approach is reserved for some of the specific technical indications outlined earlier. Bilateral groin incisions are made to expose both femoral arteries. Any lymph nodes or lymphatic tissue is best divided between clamps and then suture ligated to minimize the possibility of a postoperative lymphatic leak with its associated risk of wound or graft infection. The posterior aspect of the inguinal ligament is partially divided directly over the femoral artery to ensure ample space for tunneling the graft without compression. Dissection is carried to just beyond the femoral artery bifurcations, and the proximal aspect of both superficial and deep femoral artery branches are encircled with silicone elastic (Silastic) loops. If preoperative arteriograms or palpation at the time of operation suggests significant occlusive disease involving the proximal deep femoral artery branch, more distal exposure of this vessel for at least another 2 to 3 cm is required to allow concomitant profundaplasty at the time of distal graft anastomosis. This method usually necessitates dividing and ligating one or more branches of the deep femoral vein that typically cross the anterior surface of the proximal profunda femoris artery.

Tunnel Construction After the aortic and femoral artery dissection are completed, retroperitoneal tunnels between the two fields of dissection are made for subsequent passage of each graft limb. Such tunnels are best made by gentle blunt dissection with the index finger of each hand simultaneously from the groins and the area of the aortic bifurcation (Figure 1). Dissection should be kept on a plane directly anterior to the common and external iliac vessels to ensure that the graft is subsequently placed posterior to the ureter. This detail is important because passage of graft anterior to the ureter can lead to later compression and obstruction of the ureter and hydronephrosis. After appropriate tunnels have been created to both groins, a long blunt-tipped clamp is placed through the tunnel, and a Penrose drain is drawn through the tunnel. Elevation on both ends of this facilitates later passage of the graft limbs to the site of distal graft anastomosis. After the proximal and distal anastomotic sites are dissected and controlled, the patient is systemically heparinized with 5000 to 7500 units of intravenous heparin sodium, and the aorta is clamped just distal to the left renal vein.

Proximal Graft Anastomosis For most patients, an end-to-end aortic anastomosis is preferred for several reasons (Figure 2). First, because all blood flows through the graft with an end-to-end reconstruction, there is less chance of competitive flow through the native aortoiliac vessels, which can lead to a higher incidence of graft limb thrombosis. Second, an end-to-end

419

Ureter

A

B FIGURE 1  A, Retroperitoneal tunneling is performed by blunt

finger dissection on the anterior surface of the iliac arteries to ensure passage of graft posterior to the ureter. B, Placement of a rubber sling through each tunnel facilitates later passage of graft to each groin. (From Brewster DC: Aortofemoral bypass. In Fischer JF, Bland KI (eds): Mastery of surgery, 5th ed, Philadelphia, 2007, Wolters Kluwer/Lippincott Williams &Wilkins, pp 2063–2074.)

anastomosis is theoretically a superior hemodynamic configuration, with less perianastomotic turbulence and thereby potentially less chance of development of recurrent atheroma or anastomotic aneurysm. In addition, an end-to-end anastomosis is less likely to cause distal atheromatous embolization (trash foot), and is easier to cover with retroperitoneal tissue after implantation than a forward-­ protruding end-to-side anastomosis. This consideration can reduce the potential for late formation of a graft–enteric fistula. It is important to resect a short segment of the diseased aorta (see Figure 2). If the surgeon then uses an aortic graft with a short body, the graft can be positioned in the native aortic bed, greatly facilitating adequate graft coverage by retroperitoneal tissues. The transected distal aorta is oversewn in two layers with a 3–0 vascular suture. If the lumen of the proximal infrarenal aorta is significantly compromised by thickened and diseased intimal and medial layers, the author often favors thromboendarterectomy of the aortic stump up to the level of the proximal clamp. The remaining adventitial layer usually holds sutures well and permits construction of an excellent aortic anastomosis, but it is thin, and the author prefers to use an interrupted mattress suture technique, with each suture bolstered by a Teflon pledget. Although an end-to-end graft-to-aorta anastomosis is preferred in the majority of patients, certain anatomic patterns of disease are encountered that make an end-to-side configuration potentially advantageous. These include a sizable accessory renal artery arising from the infrarenal aorta or a patent inferior mesenteric artery that is thought desirable to maintain (Figure 3). Although such branch vessels may be preserved by reimplanting them into the body of an end-to-end graft, it is clearly easier to achieve this objective by an end-to-side aortic anastomosis, which maintains native aortic blood flow into these vessels.

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AORTOILIAC OCCLUSIVE DISEASE

C A FIGURE 2  End-to-end aortofemo-

B

D

ral graft. A, Schematic of preoperative aortogram. B, Segment of diseased aorta is resected, and the distal aortic stump is oversewn. C, End-to-end anastomosis, using a short body or stem of prosthetic bifurcation graft. D, Completed reconstruction. (From Brewster DC: Direct reconstruction for aortoiliac occlusive disease. In Rutherford RB (ed): Vascular surgery, 6th ed, Philadelphia, 2005, Elsevier Saunders, pp 1106–1136.)

Inf. mesenteric a. Accessory renal a.

B

A More commonly, however, an end-to-side or onlay graft is elected patients in whom the majority of occlusive disease is located in both external iliac arteries (see Figure 3A). In many such patients, the aorta and common iliac arteries are relatively well preserved, with good blood flow into the internal iliac (hypogastric) branches, which have a rich collateral pattern developed to maintain extremity perfusion. With such a pattern of disease, the normally anticipated retrograde blood flow up the external iliac arteries to maintain pelvic circulation cannot occur, and construction of an end-to-end proximal graft anastomosis will likely result in considerable devascularization of the pelvic area. The potential hemodynamic consequences include impotence in male patients, a higher risk of postoperative colonic ischemia, and even instances of lower extremity neurologic dysfunction caused by lumbosacral spinal or cauda equina ischemia. Hence, an end-to-side graft configuration that maintains the pelvic

FIGURE 3  End-to-side proximal anastomosis.

C

A, Patterns of disease favoring preservation of native aortic flow. B, Beveled end-of-graft to side-of-aorta anastomosis. C, Schematic representation of preserved flow into patent branch vessels and pelvis. (From Brewster DC: Aortofemoral bypass. In Fischer JF, Bland KI (eds): Mastery of surgery, 5th ed, Philadelphia, 2007, Wolters Kluwer/Lippincott Williams &Wilkins, pp 2063–2074.)

circulation by way of the hypogastric systems is clearly desirable in these circumstances (see Figure 3C).

Femoral Anastomosis After the proximal graft anastomosis is completed, the previously placed Penrose drains in the graft tunnels are elevated, and a long blunt-tipped, slightly curved clamp, such as a large DeBakey aortic cross clamp, is passed from each groin incision to the region of the aorta through the previously created graft tunnels. The distal end of each femoral graft limb is then grasped with the clamp, under direct vision, and each graft limb is pulled down through the tunnel to the femoral area (Figure 4A). Care must be taken to avoid twisting the graft limbs.



Aortofemoral Bypass for Atherosclerotic Aortoiliac Occlusive Disease

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C

B

A

A

B D

FIGURE 5  Femoral anastomosis in a patient with proximal profunda

C

D

E

FIGURE 4  A, Passage of graft limbs through the retroperitoneal tunnels. Elevation of Penrose drain sling greatly facilitates proper passage and positioning. B, Location of femoral arteriotomy if the profunda femoris is free of significant disease. C through E, Graft is cut to appropriate length and end-to-side femoral anastomosis is performed. (From Brewster DC: Aortofemoral bypass. In Fischer JF, Bland KI (eds): Mastery of surgery, 5th ed, Philadelphia, 2007, Wolters Kluwer/Lippincott Williams &Wilkins, pp 2063–2074.)

Performance of a flawless femoral anastomosis is likely the most important technical aspect of aortobifemoral bypass and the most important determinant of late graft patency. It is particularly critical to ensure unimpeded blood flow into the profunda femoris artery on each side. Thus the surgeon must carefully evaluate profunda femoris runoff, both on preoperative arteriograms and also by direct inspection and gentle passage of graduated vascular dilators at the time of operation. The profunda femoral orifice should accept a 3.5- to to 4-mm probe in normal circumstances. In the absence of any significant profunda femoris disease, a standard anastomosis confined to the common femoral artery can be made with running 5–0 monofilament suture (see Figure 4B to E). If, however, stenotic disease of the proximal profunda is encountered, the femoral arteriotomy should be carried down into the profunda (Figure 5A and B) across the stenosis to establish reliable graft outflow runoff. In most circumstances, profundaplasty can be adequately achieved by the long beveled tip of the graft (see Figure 5C). When the tip of the graft anastomosis is placed in the profunda, three to five interrupted mattress sutures are recommended, all placed under direct vision before any are tied (see Figure 5D). This optimizes accurate placement and minimizes any constriction of the critical outflow vessel.

RESULTS OF AORTOFEMORAL BYPASS GRAFTS Excellent early and late results of aortobifemoral grafts can be anticipated and are achievable at highly acceptable rates of morbidity and mortality. A consensus of several large series in the modern

disease. A and B, Common femoral arteriotomy is carried into the proximal profunda femoris, extending beyond the origin stenosis. C, Distal graft limb is cut with a long beveled hood, and anastomosis is begun at the heel of the graft on the common femoral artery. D, Femoral anastomosis is completed, with the beveled graft tip creating a patch profundaplasty. Three to five interrupted sutures are first placed at the tip of the anastomosis but are not tied down until all are inserted, thereby optimizing visualization and accurate placement, without constriction of the runoff tract. (From Brewster DC: Direct reconstruction for aortoiliac occlusive disease. In Rutherford RB (ed): Vascular surgery, 6th ed, Philadelphia, 2005, Elsevier Saunders, pp 1106–1136.)

era clearly supports this outcome, indicating that it is reasonable to expect approximately 85% to 90% graft patency at 5 years, and 70% to 75% at 10 years. Perioperative mortality rates well under 5% are now common in many centers. The mortality risk in patients with relatively localized AOID can be expected to be extremely low, whereas patients with multilevel disease and associated occlusive lesions in coronary and visceral vessels naturally have somewhat greater mortality risk. Advances in anesthetic management, perioperative hemodynamic monitoring, and postoperative intensive care have contributed to significant reduction of cardiopulmonary morbidity in high-risk patients in current practice. However, long-term survival of these patients continues to be compromised. The cumulative long-term survival rate for patients undergoing aortoiliac reconstruction remains 10 to 15 years less than that anticipated for a normal age- and sex-matched population. Overall, approximately 35% to 40% of patients will be dead at 5 years and 50% to 60% at 10 years. Not unexpectedly, the majority of late deaths are attributable to atherosclerotic heart disease. Patients with localized AOID, who have a lesser incidence of coronary artery disease, distal occlusive disease, or diabetes, appear to have a more favorable long-term prognosis, approaching that of a normal population at risk.

Selected References Brewster DC: Aortofemoral bypass. In Fischer JF, Bland KI, (eds): Mastery of Surgery, ed 5, Philadelphia, 2007, Wolters Kluwer/Lippincott Williams &Wilkins, pp 2063–2074. Brewster DC: Clinical and anatomic considerations for surgery in aortoiliac disease and results of surgical treatment, Circulation 83(Suppl I):42–52, 1991. Brewster DC: Current controversies in the management of aortoiliac occlusive disease, J Vasc Surg 25:367–379, 1997. Brewster DC: Direct reconstruction for aortoiliac occlusive disease. In Rutherford RB, (eds): Vascular Surgery, ed 6, Philadelphia, 2005, Elsevier Saunders, pp 1106–1136.

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Brewster DC, Darling RC: Optimal methods of aortoiliac reconstruction, Surgery 84:739–748, 1978. Brewster DC, Perler BA, Robison JG, et al: Aortofemoral graft for multilevel occlusive disease: Predictors of success and need for distal bypass, Arch Surg 117:1593–1600, 1982. Burke CR, Henke PK, Hernandez R, et al: A contemporary comparison of aorto-femoral bypass and aortoiliac stenting in the treatment of aortoiliac occlusive disease, Ann Vasc Surg 24:4–13, 2010.

Chiu KW, Davies RS, Nightingale PG, et al: Review of direct anatomical open repair of atherosclerotic aortoiliac occlusive disease, Eur J Vasc Endovasc Surg 39:460–471, 2010. deVries SO, Hunick MGM: Results of aortic bifurcation grafts for aortoiliac occlusive disease: A meta-analysis, J Vasc Surg 26:558–569, 1997. Hertzer NR, Bena JF, Karafa MT: A personal experience with direct reconstruction and extra-anatomic bypass for aortobifemoral occlusive disease, J Vasc Surg 45:527–535, 2007.

Endarterectomy for Atherosclerotic Aortoiliac Occlusive Disease

technique in patients who have symptomatic atheroembolism resulting from an aortic lesion if an open technique is used to treat it.

Louis M. Messina and Andres Schanzer

Thromboendarterectomy was the first technique used to treat aortoiliac occlusive disease. Dos Santos performed the first femoral endarterectomy in Lisbon in 1947. Wylie performed the first successful aortoiliac thromboendarterectomy in the United States in 1951. Over the ensuing decades, aortobifemoral bypass grafting using synthetic grafts and, more recently, endovascular stenting have replaced thromboendarterectomy as the primary surgical technique to manage aortoiliac occlusive disease. Nonetheless, aortoiliac endarterectomy can still play an important role in managing these patients under specific clinical circumstances. Thromboendarterectomy is feasible technically because of the pathologic distribution of atherosclerosis in the arterial wall and relies on the principle that the strength and integrity of the arterial wall depends on the outermost layer of adventitia. Atherosclerotic lesions are confined to the intima and inner media of the arterial wall. In general, the cleavage plane within the deep media is identified relatively easily. To complete an endarterectomy, the transition zone of the plaque from its position within the intima and media to the point at which it resides exclusively within the intima must be identified to feather the distal endpoint. Aortoiliac endarterectomy has certain distinct advantages over synthetic grafting. It is an autogenous tissue technique. Therefore it is not vulnerable to graft infection. The technique of aortoiliac endarterectomy also permits direct revascularization of the internal iliac arteries in patients who have internal iliac artery stenoses or occlusions and have impotence or buttock claudication. Finally, endarterectomy can also be applied when there is a compelling indication for revascularization, such as critical limb ischemia in the presence of a contaminated operative field. The primary contraindication to aortoiliac endarterectomy is the existence of a degenerated or aneurysmal aortic wall. Optimal outcome after aortoiliac endarterectomy depends on appropriate patient selection. Ideally, this technique is applied in patients whose aortoiliac occlusive disease terminates at or near the common iliac bifurcation. This pattern of disease is often referred to as type A disease, which is found in 5% to 10% of patients requiring aortic reconstruction for occlusive disease. The type A pattern of occlusive disease is particularly common in young women who have a history of tobacco use. Aortoiliac endarterectomy is also a favored

OPERATIVE TECHNIQUE Operative exposure is obtained thorough a standard xiphoid-to-pubis midline abdominal incision. The incision in the retroperitonum over the aorta is placed toward the right of the midline and continued down along the right common iliac artery. The dissection is undertaken to preserve the periaortic nervi erigentes, which course along the left side of the aorta and left common iliac artery (Figure 1A). Aortoiliac endarterectomy requires complete mobilization of the aorta and iliac artery branches, including all of the lumbar arteries (see Figure 1B). This mobilization must be accomplished relatively atraumatically to minimize the risk of atheroembolization during the procedure. Typically, the iliac artery disease extends into the first 1 to 2 cm of the external iliac artery. Therefore mobilization should proceed from the aorta to the middle of the external iliac artery. When undertaking the endarterectomy, atraumatic vascular clamps are placed on the distal external iliac arteries and on the aorta at the level of the renal arteries. Bulldog clamps are placed on the lumbar and inferior mesenteric arteries. The aorta is incised longitudinally on the right side, and the aortotomy is carried from its proximal point down to the level of the aortic bifurcation. The endarterectomy plane is identified within the deep media, and the endarterectomy is developed further by pushing the aortic wall away from the lesion. The proximal lesion is transected at the level of the aortic clamp, using Metzenbaum scissors to retract the aortic wall and simultaneously transect the lesion. The distal endpoint is obtained through a transverse arteriotomy made just proximal to the common iliac artery bifurcation (Figure 2). This technique allows the tip of the atheroma to be lifted with a Beaver blade. A plane is then developed circumferentially around the lesion within the common iliac artery. The approach to circumferential mobilization of the common iliac artery plaque can be undertaken in a number of different ways. This is often accomplished with dural elevators, but alternatives such as using a hand-held oscillating endarterectomy blade can be applied expeditiously. Specialized angled extraction clamps are ideal for removing the residual core of iliac atheroma. If the external iliac artery lesion extends beyond the area exposed throughout the common iliac arteriotomy, a second, more distal transverse incision in the external iliac artery can be made, and a Beaver blade can be used to develop an appropriate endpoint (Figure 3). Extraction endarterectomy of the internal iliac artery is accomplished after developing the distal endpoint in the external iliac artery. Typically, the atheroma extends to the first bifurcation of the internal iliac artery. Specialized angled extraction clamps facilitate this maneuver (Figure 4). After thorough irrigation of the aorta with heparinized saline and appropriate backbleeding, as well as forward flushing of the aorta, the aortotomy is closed with a continuous 4–0 suture, and the iliac artery is closed with multiple interrupted 5–0 sutures. Although more technically demanding than synthetic bypass grafting, aortoiliac

422

AORTOILIAC OCCLUSIVE DISEASE

Brewster DC, Darling RC: Optimal methods of aortoiliac reconstruction, Surgery 84:739–748, 1978. Brewster DC, Perler BA, Robison JG, et al: Aortofemoral graft for multilevel occlusive disease: Predictors of success and need for distal bypass, Arch Surg 117:1593–1600, 1982. Burke CR, Henke PK, Hernandez R, et al: A contemporary comparison of aorto-femoral bypass and aortoiliac stenting in the treatment of aortoiliac occlusive disease, Ann Vasc Surg 24:4–13, 2010.

Chiu KW, Davies RS, Nightingale PG, et al: Review of direct anatomical open repair of atherosclerotic aortoiliac occlusive disease, Eur J Vasc Endovasc Surg 39:460–471, 2010. deVries SO, Hunick MGM: Results of aortic bifurcation grafts for aortoiliac occlusive disease: A meta-analysis, J Vasc Surg 26:558–569, 1997. Hertzer NR, Bena JF, Karafa MT: A personal experience with direct reconstruction and extra-anatomic bypass for aortobifemoral occlusive disease, J Vasc Surg 45:527–535, 2007.

Endarterectomy for Atherosclerotic Aortoiliac Occlusive Disease

technique in patients who have symptomatic atheroembolism resulting from an aortic lesion if an open technique is used to treat it.

Louis M. Messina and Andres Schanzer

Thromboendarterectomy was the first technique used to treat aortoiliac occlusive disease. Dos Santos performed the first femoral endarterectomy in Lisbon in 1947. Wylie performed the first successful aortoiliac thromboendarterectomy in the United States in 1951. Over the ensuing decades, aortobifemoral bypass grafting using synthetic grafts and, more recently, endovascular stenting have replaced thromboendarterectomy as the primary surgical technique to manage aortoiliac occlusive disease. Nonetheless, aortoiliac endarterectomy can still play an important role in managing these patients under specific clinical circumstances. Thromboendarterectomy is feasible technically because of the pathologic distribution of atherosclerosis in the arterial wall and relies on the principle that the strength and integrity of the arterial wall depends on the outermost layer of adventitia. Atherosclerotic lesions are confined to the intima and inner media of the arterial wall. In general, the cleavage plane within the deep media is identified relatively easily. To complete an endarterectomy, the transition zone of the plaque from its position within the intima and media to the point at which it resides exclusively within the intima must be identified to feather the distal endpoint. Aortoiliac endarterectomy has certain distinct advantages over synthetic grafting. It is an autogenous tissue technique. Therefore it is not vulnerable to graft infection. The technique of aortoiliac endarterectomy also permits direct revascularization of the internal iliac arteries in patients who have internal iliac artery stenoses or occlusions and have impotence or buttock claudication. Finally, endarterectomy can also be applied when there is a compelling indication for revascularization, such as critical limb ischemia in the presence of a contaminated operative field. The primary contraindication to aortoiliac endarterectomy is the existence of a degenerated or aneurysmal aortic wall. Optimal outcome after aortoiliac endarterectomy depends on appropriate patient selection. Ideally, this technique is applied in patients whose aortoiliac occlusive disease terminates at or near the common iliac bifurcation. This pattern of disease is often referred to as type A disease, which is found in 5% to 10% of patients requiring aortic reconstruction for occlusive disease. The type A pattern of occlusive disease is particularly common in young women who have a history of tobacco use. Aortoiliac endarterectomy is also a favored

OPERATIVE TECHNIQUE Operative exposure is obtained thorough a standard xiphoid-to-pubis midline abdominal incision. The incision in the retroperitonum over the aorta is placed toward the right of the midline and continued down along the right common iliac artery. The dissection is undertaken to preserve the periaortic nervi erigentes, which course along the left side of the aorta and left common iliac artery (Figure 1A). Aortoiliac endarterectomy requires complete mobilization of the aorta and iliac artery branches, including all of the lumbar arteries (see Figure 1B). This mobilization must be accomplished relatively atraumatically to minimize the risk of atheroembolization during the procedure. Typically, the iliac artery disease extends into the first 1 to 2 cm of the external iliac artery. Therefore mobilization should proceed from the aorta to the middle of the external iliac artery. When undertaking the endarterectomy, atraumatic vascular clamps are placed on the distal external iliac arteries and on the aorta at the level of the renal arteries. Bulldog clamps are placed on the lumbar and inferior mesenteric arteries. The aorta is incised longitudinally on the right side, and the aortotomy is carried from its proximal point down to the level of the aortic bifurcation. The endarterectomy plane is identified within the deep media, and the endarterectomy is developed further by pushing the aortic wall away from the lesion. The proximal lesion is transected at the level of the aortic clamp, using Metzenbaum scissors to retract the aortic wall and simultaneously transect the lesion. The distal endpoint is obtained through a transverse arteriotomy made just proximal to the common iliac artery bifurcation (Figure 2). This technique allows the tip of the atheroma to be lifted with a Beaver blade. A plane is then developed circumferentially around the lesion within the common iliac artery. The approach to circumferential mobilization of the common iliac artery plaque can be undertaken in a number of different ways. This is often accomplished with dural elevators, but alternatives such as using a hand-held oscillating endarterectomy blade can be applied expeditiously. Specialized angled extraction clamps are ideal for removing the residual core of iliac atheroma. If the external iliac artery lesion extends beyond the area exposed throughout the common iliac arteriotomy, a second, more distal transverse incision in the external iliac artery can be made, and a Beaver blade can be used to develop an appropriate endpoint (Figure 3). Extraction endarterectomy of the internal iliac artery is accomplished after developing the distal endpoint in the external iliac artery. Typically, the atheroma extends to the first bifurcation of the internal iliac artery. Specialized angled extraction clamps facilitate this maneuver (Figure 4). After thorough irrigation of the aorta with heparinized saline and appropriate backbleeding, as well as forward flushing of the aorta, the aortotomy is closed with a continuous 4–0 suture, and the iliac artery is closed with multiple interrupted 5–0 sutures. Although more technically demanding than synthetic bypass grafting, aortoiliac



Endarterectomy for Atherosclerotic Aortoiliac Occlusive Disease

A

423

B FIGURE 1  A, Incision in the retroperitoneum on the surface of the aorta is made to the right of the

midline and extended onto the anterior surface of the right common iliac artery to avoid both the inferior mesenteric artery and the nervi erigentes, which cross the proximal left common iliac artery as they descend into the pelvis. B, Complete atraumatic mobilization of the aorta is fundamental to the successful aortoiliac endarterectomy. This includes full mobilization of the posterior aorta and lumbar arteries. A linear aortotomy is made extending just below the renal arteries up to the aortic bifurcation. The aortic atheroma is resected proximally with Metzenbaum scissors and distally at the aortic bifurcation.  (From Wylie EJ, Stoney RJ, Ehrenfeld WK: Manual of vascular surgery, New York, 1980, Springer-Verlag.)

endarterectomy is technically satisfying and provides durable relief of symptoms of aortoiliac occlusive disease.

RESULTS In appropriately selected patients, the 5-year patency rates after aortoiliac endarterectomy are 80% to 90%. Long-term degeneration of the aortic or iliac artery walls after endarterectomy, although of theoretical concern during the initial application of this technique, has

not been documented in long-term follow-up. Failure, as a result of recurrent aortoiliac stenosis, can be managed successfully with endovascular techniques or with aortobifemoral bypass grafting. When the surgery is performed properly, the risk of sexual dysfunction should be no greater than that after aortobifemoral bypass grafting. Aortoiliac endarterectomy remains an important although infrequently applied surgical technique for managing atherosclerotic aortoiliac occlusive disease. Refinements in technique and application of new instrumentation have simplified the endarterectomy technique and thereby minimized procedural complications.

424

AORTOILIAC OCCLUSIVE DISEASE

A

B

FIGURE 2  Management of the distal endpoint during

C

aortoiliac endarterectomy. A, Transverse arteriotomy is made in the common iliac artery just proximal to its bifurcation. The tip of atheroma extending into the external iliac artery is elevated with the tip of a Beaver blade. B, The dissection plane is then developed proximally into the common iliac artery first by spreading and developing a circumferential plane around the atheroma with the tips of a right-angle clamp. Once the circumferential plane has been developed, the remainder of the endarterectomy can be accomplished using a hand-held oscillating endarterectomy blade that can be passed both proximally and distally. C, Elongated extraction clamps can be used to facilitate retrieval of the atheroma.  (From Wylie EJ, Stoney RJ, Ehrenfeld WK: Manual of vascular surgery, New York, 1980, Springer-Verlag.)



Endarterectomy for Atherosclerotic Aortoiliac Occlusive Disease

425

FIGURE 3  If the external iliac artery lesion extends beyond the common iliac arteriotomy, a more distal transverse arteriotomy is made beyond the palpable extent of the atheroma, and the area of normal intima is incised carefully, lifting the tip with the Beaver blade.  (From Wylie EJ, Stoney RJ, Ehrenfeld WK: Manual of vascular surgery, New York, 1980, Springer-Verlag.)

Selected References Brewster DC, Darling RC: Optimal methods of aortoiliac reconstruction, Surgery 84:739–748, 1978. Dos Santos JC: Sur la désobstruction des thrombus artérielles anciennes, Mem Acad Chir 73:404–411, 1947. Inahara T: Evaluation of endarterectomy for aortoiliac and aortoiliofemoral occlusive disease, Arch Surg 110:458–464, 1975. van der Akker PJ, van Schulfgaarde R, Brand R, et al: Long-term results of prosthetic and nonprosthetic reconstruction for obstructive aortoiliac disease, Eur J Vasc Surg 6:53–61, 1992. Wylie EJ: Thromboendarterectomy for arteriosclerotic thrombus of major arteries, Surgery 32:275–292, 1952.

FIGURE 4  Internal iliac artery endarterectomy is accomplished by

developing a circumferential plane around the plaque and extracting it through the common iliac artery arteriotomy using angled extraction clamps. The distal endpoint is usually located at the first bifurcation, and residual fragments are removed with an angled extraction clamp guided by a finger placed behind the artery.  (From Wylie EJ, Stoney RJ, Ehrenfeld WK: Manual of vascular surgery, New York, 1980, Springer-Verlag.)

426

AORTOILIAC OCCLUSIVE DISEASE

Management of Juxtarenal Aortic Occlusive Disease by Retroperitoneal and Transperitoneal Exposure of the Pararenal and Suprarenal Aorta Adam W. Beck and Thomas S. Huber

The perivisceral aorta can be involved in a variety of pathologic conditions. These diverse conditions include atherosclerotic occlusive disease of the aorta and its visceral branches, aneurysmal degeneration, trauma (both penetrating and blunt), and congenital problems (e.g., midabdominal coarctation). The exposure of the paravisceral aorta is also relevant for reoperative aortic surgery such as open conversion after failed endovascular aneurysm repair or failed aortobifemoral bypass. Adequate exposure of the paravisceral aorta is tantamount to the successful conduct of the operation, regardless of the indication for the procedure. The exposure of the paravisceral aorta can be technically challenging, particularly in the reoperative setting and for obese patients, although the various approaches are within the skill set of experienced modern vascular surgeons. Indeed, the majority of the open aortic procedures currently performed at our tertiary care medical centers involve the paravisceral aorta, and it is our expectation that this trend will continue given the advances in the endovascular approach for most aortic pathologies. There is no one universal approach to the paravisceral aorta that is adequate for all indications. The specific choice or approach should be dictated by the underlying condition, the treatment goals for reconstruction, the presence of arterial or venous anatomic variants, the presence of associated injuries in the case of trauma, and any prior incisions. The various approaches include the transperitoneal approach to the celiac artery and supraceliac aorta, the transperitoneal approach to the superior mesenteric artery (SMA) and pararenal aorta (including the right medial visceral rotation), the retroperitoneal approach to the complete abdominal aorta, and the transperitoneal approach to the complete abdominal aorta using left medial visceral rotation. Given the current quality of computed tomography (CT) imaging, a safe preoperative plan can usually be developed that is rarely altered by the intraoperative findings.

TRANSPERITONEAL EXPOSURE OF THE SUPRACELIAC AORTA AND CELIAC ARTERY The exposure of the supraceliac aorta and the celiac artery is required for antegrade bypass to the visceral vessels (both SMA and celiac artery) in the setting of mesenteric ischemia and for the more

common scenario when proximal control of the abdominal aorta is required as in the case of a ruptured infrarenal or juxtarenal abdominal aortic aneurysm. The origin of the celiac artery and a 5- to 8-cm segment of the aorta caudal to its origin may be exposed using this approach, although a more limited approach and dissection is usually sufficient if the objective is only to apply a proximal aortic clamp. The supraceliac aorta is usually relatively free of atherosclerotic occlusive disease and therefore is a good inflow source for antegrade visceral bypass. The exposure of the segment of aorta caudal to the celiac artery is somewhat limited through this approach given the overlying anatomic structures and should be exposed through an alternative approach. The procedure can be performed using either a midline or bilateral subcostal incision; the choice is contingent upon the surgeon’s preference and the patient’s body habitus. The midline incision is slightly easier to close, although a bilateral subcostal incision with a midline extension to the xiphoid provides optimal exposure of the upper abdomen. A lumbar bump can augment the aortic exposure for all of the transperitoneal approaches. After a general exploration of the abdomen, the left triangular ligament of the liver is incised and the left lateral segment of the liver is reflected to the patient’s right side using a self-retaining retractor such as a Bookwalter. Care should be exercised during incision of the triangular ligament to avoid injuring the hepatic veins. The gastrohepatic ligament is then incised, although caution should be exercised during this maneuver because a replaced left hepatic artery, a common anatomic variant, passes through the ligament. The esophagus and stomach are then retracted to the patient’s left, and identification of the esophagus is facilitated by palpation of the nasogastric tube or transesophageal echocardiography probe. The exposure can be facilitated at this point by placing the patient in a significant amount of reverse Trendelenburg, allowing the abdominal structures to retract caudally by gravity.

SMA

FIGURE 1  The supraceliac aorta and the origin of the celiac artery

are shown. Note that the right lobe of the liver has been retracted to the right and the esophagus has been retracted to the left. The median arcuate ligament and the crus of the diaphragm have been incised to expose the aorta. The dense neural plexus surrounding the celiac artery has also been dissected free.  (Reproduced with permission from Kazmers A: Operative management of chronic mesenteric ischemia, Ann Vasc Surg 12:299–308, 1998.)



Management of Juxtarenal Aortic Occlusive Disease by Retroperitoneal and Transperitoneal

The median arcuate ligament and the crus of the diaphragm are incised to expose the underlying aorta; this can be facilitated by incising the muscle fibers between the jaws of a large right-angle clamp using electrocautery (Figure 1). The dissection of the aorta cephalad to the celiac artery can be exposed relatively quickly, although care should be exercised in the segment adjacent to the celiac artery to avoid inadvertent injury to the vessel. Additionally, a dense neural plexus, further complicating the dissection, encases the origin of the celiac artery. The extent of the aortic dissection required is dictated by the clinical situation. It is not usually necessary to dissect the aorta circumferentially, but it can be helpful to place an umbilical tape around the aorta to serve as a handle should difficulties arise. Importantly, the intercostal vessels come off the posterior aspect of the aorta at this location and can be easily injured. Occasionally the pleura of the lung is entered during the dissection. This is usually obvious and of little consequence, although a chest radiograph should be obtained in the immediate postoperative period to confirm that the lungs are fully expanded. Vascular control of the supraceliac aorta can be obtained very expeditiously if necessary (e.g., unstable patient with ruptured aneurysm) by bluntly dissecting the crus of the diaphragm with the index and long fingers and using them as a guide to position an aortic clamp.

TRANSPERITONEAL APPROACH TO SUPERIOR MESENTERIC ARTERY AND PARARENAL AORTA The aorta can be exposed from the origin of the SMA to its first branching through a transperitoneal approach similar to the generic approach used for most open infrarenal abdominal aortic aneurysm repairs. The exposure of the aorta from the origin of the renal arteries to the base of the SMA is complicated by the adjacent anatomic structures including the crus of the diaphragm, the pancreas, and the left renal vein. The following approach is used commonly for aortorenal bypass, retrograde aorta–SMA bypass, juxtarenal aortic aneurysm repair, and aortobifemoral bypass in the setting of an infrarenal aortic occlusion. A midline or some type of transverse abdominal incision may be used. Our preferred incision is a transverse one, with a bilateral subcostal incision positioned approximately three fingerbreadths below

427

the margin of the ribs. After initial abdominal exposure, the ligament of Treitz is incised and the duodenum is reflected to the right. A selfretaining retractor is placed to facilitate exposure with the transverse colon retracted cephalad. The inferior mesenteric vein is ligated at the base of the mesentery to prevent inadvertent injury during retraction, although it is important to palpate the adjacent tissue to confirm that there is no accompanying meandering artery, which would function as an important collateral for patients with visceral artery occlusive disease. The retroperitoneum over the aorta is incised, with the caudal extension dictated by the underlying pathology and indication for the procedure. The left renal vein is completely mobilized and retracted using a vessel loop. This is facilitated by ligating and transecting its lumbar, adrenal, and gonadal branches; preferably ligating them with both a suture ligature and a hemostatic clip. Alternatively, the left renal vein itself can be transected at its confluence with the inferior vena cava, although it is important to preserve the three collateral veins in this setting (i.e., adrenal, lumbar, gonadal). Although somewhat inelegant, ligating the left renal vein is likely safe in terms of its impact on kidney function provided that the collaterals are persevered. The pararenal aorta and the renal arteries themselves may then be exposed by retracting the left renal vein cephalad and caudad as necessary. The suprarenal aorta can then be exposed to the base of the SMA by retracting the pancreas cephalad and incising the investing dense neural plexus. The origin of the SMA and its proximal few centimeters can be exposed with this approach, and it is our preferred approach for retrograde bypasses to this vessel provided that the occlusive disease is limited to its orifice (Figure 2). Alternatively, the SMA may be exposed through the lesser space at the caudal border of the pancreas or at the base of the mesocolon after caudal retraction of the transverse colon. Exposure of the suprarenal aorta can be further facilitated by incising the crus of the diaphragm that passes on its lateral aspects, and this can be particularly helpful to facilitate applying an aortic clamp. Additional exposure of the retroperitoneal structures caudal to the SMA, including the inferior vena cava, can be obtained by mobilizing the right colon (i.e., medial visceral rotation). This can be facilitated by extending the retroperitoneal incision over the aorta onto that overlying the right common iliac vessels and then connecting this with the incision over the peritoneal reflection of the right colon. The right colon and small bowel may then be completely mobilized and retracted cephalad, ultimately tethered on the SMA.

Adrenal vein

Lumbar renal vein

B

FIGURE 2  Exposure of the suprarenal aorta and superior

mesenteric artery (SMA). Note that the retroperitoneum over the infrarenal and pararenal aorta has been incised. The adrenal, lumbar, and gonadal venous branches of the left renal vein have been ligated, thereby allowing the renal vein to be retracted both cephalad and caudad. The dense neural plexus surrounding the SMA has been dissected free. Lateral retraction of the inferior vena cava requires ligating the lumbar branches, although this is rarely necessary.  (Reproduced with permission from Godshall CJ, Hansen KJ: Renovascular disease: open surgical treatment. In Cronenwett JL, Johnston KW (eds): Rutherford’s vascular surgery, Philadelphia, 2010, Saunders, p 2203.)

Lumbar veins

A

Gonadal vein

C

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AORTOILIAC OCCLUSIVE DISEASE

This essentially exposes the whole retroperitoneum below the SMA and to the right of the aorta. It can be particularly helpful for patients requiring bilateral aortorenal bypass or those with combined aortic and caval injuries, although it has been our anecdotal impression that it can result in moderate operative bowel edema.

LEFT RETROPERITONEAL APPROACH TO THE ABDOMINAL AORTA The complete abdominal aorta can be exposed using the left retroperitoneal approach. This incision can be extended further into the chest to expose the thoracic aorta for combined thoracoabdominal aortic pathologies. The origins of both the celiac artery and the SMA can be exposed using this approach, although it is difficult to dissect too far out onto either vessel given the overlying visceral structures. The left renal artery can be dissected completely free using this approach, although it is difficult to expose the right renal artery, particularly for patients with large suprarenal aneurysms, because it courses away from the operative field. Similarly, the exposure of the distal right common iliac artery and its bifurcation can be difficult. The retroperitoneal approach is ideal for complex aortic pathologies involving the suprarenal aorta, open conversions after endovascular aneurysm repair, and redo aortic procedures when the initial approach was transperitoneal. The patient is placed on the operating room table with the anterior superior iliac crest positioned at the break. The patient’s shoulders are rotated approximately 30 to 45 degrees while the hips are kept as flat as possible to facilitate exposure of the femoral vessels, if necessary. Positioning is facilitated using a beanbag. The left arm and shoulder are immobilized using an armrest. Notably, an axillary roll is not usually required on the right side, and we do not usually use a double-lumen endotracheal tube because the lung can usually be adequately retracted with the blades of a fixed retractor if the chest is entered. The patient’s position is accentuated by breaking the table at its midportion, thereby accentuating the distance between the costal margin and the iliac crest (the rooftop position). The bed is rotated to the patient’s right and placed in a moderate degree of Trendelenburg (i.e., head down). An incision is made in a curvilinear fashion starting in the midline halfway between the umbilicus and pubic bone and extending in the intercostal space (Figure 3). The appropriate intercostal space is dictated by the anticipated proximal extent of the dissection and the patient’s body habitus. The 8th or 9th intercostal space is usually adequate for exposure of the pararenal aorta. Notably, the anticipated incision is marked on the patient after positioning and before the skin is prepped. The abdominal wall musculature is incised and the retroperitoneal space is entered, usually near the costal margin. It is not necessary to incise the abdominal rectus muscle because adequate medial exposure can usually be obtained by simply incising the rectus fascia and reflecting the rectus muscle to the patient’s right. The retroperitoneal space is then dissected bluntly until the aorta is encountered. Several small venous branches from the abdominal wall are encountered during the dissection and should be cauterized or ligated. The dissection plane should follow the course of the lateral abdominal wall, deep to the kidney. The peritoneum can be particularly difficult to separate from the diaphragm and near the abdominal wall at the midline, although inadvertent entry in the peritoneal cavity is inconsequential and easily repaired. After the visceral structures are mobilized and reflected medially, a fixed retractor is positioned to further facilitate exposure, but caution should be exercised to avoid injuring the underlying spleen. Additional exposure can be obtained by extending the incision in the intercostal space and incising the diaphragm. Indeed, we routinely enter the chest cavity, although we try to limit the dissection to the abdominal cavity alone in patients with significant ­pulmonary disease. The orientation of the diaphragm incision is dictated by the extent of the exposure required, ranging from a short radial incision

FIGURE 3  The incision for the left retroperitoneal approach is

marked on the skin. The patient is positioned on the operating room table with the hips flat and the left shoulder rotated to the right approximately 30 degrees. The table is elevated at the mid portion to accentuate the distance between the iliac crest and the costal margin. Additionally, the table is rotated to the right side and placed in the Trendelenburg to position the planned incision in the center of the operative field. The incision extends in a curvilinear fashion from the midpoint between the umbilicus and the pubic bone to the ninth intercostal space.

that is essentially a continuation of the intercostal incision to a circumferential incision extending from the intercostal incision to the crus of the diaphragm, leaving a cuff of diaphragm attached to the chest wall to facilitate the subsequent closure. Alternatively, a limited radial incision may be made and a Penrose drain may be placed around the diaphragm after the incision of the crus, thereby allowing it to be retracted outside the operative field (both cephalad and caudad). Although this approach can minimize the injury to the diaphragm and the resultant respiratory compromise, it is somewhat cumbersome. The aorta and visceral vessels are exposed by incising the left crus of the diaphragm along the lateral aspect of the aorta (Figure 4). This can be facilitated by using a large right-angle clamp and cauterizing the muscle between its spread jaws. Care must be exercised to avoid injuring the underlying aorta and intercostal vessels. The origins of the celiac artery and the SMA can then be dissected free. It is important to realize that the orientation of these vessels is directed to the patient’s right side, given the patient’s position on the operating table. The left renal artery and vein are fairly easy to identify and can actually serve as landmarks for the more proximal visceral vessels. Importantly, the lumbar vein drapes over the aorta and needs to be transected and suture ligated to facilitate exposure of the infrarenal aorta and to avoid inadvertent injury. The right renal artery is oriented approximately 180 degrees from the left one and can be difficult to expose using the retroperitoneal approach, particularly in patients with large pararenal aneurysms. The left iliac vessels are easily identified in the operative field and serve as a landmark for the viscera reflection during the initial retroperitoneal dissection. The proximal aspect of the right common iliac vessels can be dissected at the aortic bifurcation, and an adequate length can usually be exposed for the application of a vascular clamp. Additional exposure of the right iliac vessels can be obtained by ligating the inferior mesenteric artery, thereby allowing the viscera to be further reflected to the patient’s right side. The right iliac vessels can also be exposed using a separate right lower quadrant abdominal incision and a retroperitoneal dissection, although this is rarely necessary. A tunnel to assist passing the right limb of an aortofemoral bypass graft can usually be created in the standard fashion with the retroperitoneal approach, although this is somewhat more difficult



Management of Juxtarenal Aortic Occlusive Disease by Retroperitoneal and Transperitoneal

429

Inferior mesenteric a. (ligated)

FIGURE 4  The retroperitoneal exposure of the

abdominal aorta and left common iliac artery is shown. The crus of the diaphragm has been incised to facilitate exposure of the celiac axis and the superior mesenteric artery. The visceral structures have been reflected to the patient’s right. The Bookwalter retractor is used to facilitate exposure.  (Reproduced with permission from Wind GG,Valentine RJ: Anatomic exposures in vascular surgery, Baltimore, 1991, Williams & Wilkins, p 231.)

given the orientation of the patient, and it often requires using an aortic clamp.

TRANSPERITONEAL APPROACH TO THE COMPLETE ABDOMINAL AORTA WITH LEFT MEDIAL VISCERAL ROTATION The complete abdominal aorta can also be exposed through a transperitoneal approach using a left medial visceral rotation. The anatomic limitations of this approach are essentially the same as those associated with the retroperitoneal approach outlined earlier, although access to the peritoneal approach provides several advantages, particularly in the setting of trauma with combined vascular and intestinal injuries. A midline bilateral subcostal incision or a midline incision with an extension into the left intercostal space in a hockey stick configuration can be used; the choice is dictated by the surgeon’s preference and the likelihood of additional intraabdominal pathology in the case of the trauma. The visceral structures are reflected to the patient’s right side in the retroperitoneal plane deep to the colon and left kidney. This is facilitated by incising the peritoneal reflection of the left colon and requires taking down the splenophrenic and ­splenorenal ligaments to mobilize the spleen. Once the retroperitoneal plane is entered, the dissection is similar to that outlined for the retroperitoneal approach.

DISCUSSION The approaches outlined provide complete exposure of the abdominal aorta and visceral vessels. Unfortunately, no single approach is sufficient for all paravisceral aortic pathologies, and safe, effective treatment requires facility with all of the techniques. However, given the current quality of CT-based imaging, it is possible to match the operative approach with the aortic pathology and achieve the desired or optimal outcome. We prefer the left retroperitoneal approach for reconstruction of the paravisceral aorta in the setting of both aneurysmal and occlusive disease. Although the transperitoneal approaches are possible and useful in certain scenarios, we find that the retroperitoneal approach provides better exposure and is significantly easier in the majority of cases. Indeed, the visceral structures can be reflected in the

Diaphragm

retroperitoneal plane relatively expeditiously and the full extent of the abdominal aorta widely visualized. This facilitates the placement of an aortic clamp above the visceral vessels (i.e., suprarenal, supraSMA or supraceliac) and an unobstructed view of the aorta for construction of the anastomosis. This flexibility in positioning the aortic clamp is helpful in the setting of conversion after endovascular repair, particularly for devices with suprarenal fixation. Notably, it can be somewhat challenging to construct an aortorenal bypass on the left through the retroperitoneal approach given the anterior location of the kidney and given the tendency of the graft to kink when the retractors are removed and the kidney returned to its anatomic position. This can be avoided by reimplanting the left renal artery itself on the new aortic graft or by making the renal graft as short as possible. The presence of a retroaortic left renal vein can also complicate the retroperitoneal approach as detailed earlier. The options in this setting include leaving the left kidney in its anatomic position by dissecting in the retroperitoneal plane anterior to it or by tunneling the aortic graft beneath the renal vein after completing the proximal anastomosis (in the scenario that the kidney is elevated as described earlier). The left retroperitoneal approach is particularly beneficial for reoperative aortic surgery when the original procedure was performed transperitoneally. In the case of a redo aortobifemoral bypass, the retroperitoneal approach simplifies identification of the left ureter and the creation of the tunnels for the femoral limbs. Specifically, the left limb of the redo aortofemoral graft can be tunneled through the retroperitoneal space created by the dissection while the right limb is passed in the preperitoneal space adjacent to the bladder, or the bypass can be configured as a left aortofemoral bypass with a crossover femorofemoral limb. One downside to the retroperitoneal approach is that patients often develop a fullness or laxity in the incision secondary to the denervation of the abdominal wall, which can be confused with ventral hernia. Additionally, this can also result in chronic pain, presumably secondary to a neuropathy. We prefer antegrade bypass to the celiac artery and SMA for patients requiring open bypass for chronic mesenteric ischemia using the approach to the supraceliac aorta outlined earlier. We favor the retrograde iliac-to-SMA bypass for patients with acute mesenteric ischemia and approach the reconstruction in this setting by mobilizing the duodenum and exposing its proximal aspect. Notably, we usually transect the SMA at its base and have found that this facilitates a better course for the graft that courses both caudad to cephalad and posterior to anterior.

430

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Selected References Darling III RC, Shah DM, Chang BB, et al: Retroperitoneal approach for bilateral renal and visceral artery revascularization, Am J Surg 168:148–151, 1994. Huber TS, Lee WA: Chronic ischemia. In Cronenwett JL, Johnston KW, (eds): Rutherford's vascular surgery, ed 7, Philadelphia, 2010, Saunders Elsevier. pp 2273–2288. Reilly LM, Ramos TK, Murray SP, et al: Optimal exposure of the proximal abdominal aorta: A critical appraisal of transabdominal medial visceral rotation, J Vasc Surg 19:375–389, 1994. Ryan SV, Calligaro KD, McAffee-Bennett S, et al: Management of juxtarenal aortic aneurysms and occlusive disease with preferential suprarenal clamping via a midline transperitoneal incision: Technique and results, Vasc Endovascular Surg 38:417–422, 2004.

Acute Aortic Occlusion

Shepard AD, Tollefson DF, Reddy DJ, et al: Left flank retroperitoneal exposure: A technical aid to complex aortic reconstruction, J Vasc Surg 14:283–291, 1991. West Jr CA, Johnson LW, Doucet L, et al: A contemporary experience of open aortic reconstruction in patients with chronic atherosclerotic occlusion of the abdominal aorta, J Vasc Surg 52:1164–1172, 2010. Wind GG, Valentine RJ: Anatomic exposures in vascular surgery, Baltimore, 1991, Williams & Wilkins.

hospital setting. A small number of interesting collections of case reports have described several additional rare etiologies.

Salvatore T. Scali and Thomas S. Huber

CLINICAL PRESENTATION AND DIAGNOSIS Acute aortic occlusion is a true vascular emergency associated with significant morbidity and mortality secondary to the underlying etiology, the related comorbidities, and the ischemia–reperfusion injury resulting from revascularization. Indeed, the morbidity and mortality rates are comparable to those associated with a ruptured abdominal aortic aneurysm (AAA). The optimal management requires early recognition and definitive treatment, similar to most vascular surgical emergencies. Despite the evolution of various percutaneous therapies, open surgical reconstruction remains the cornerstone of treatment. Fortunately, acute aortic occlusion is a relatively uncommon problem and, not surprisingly, the published experience with it is quite limited.

ETIOLOGY The leading causes of an acute aortic occlusion are an embolus originating from the heart and in-situ thrombosis in the setting of severe aortoiliac occlusive disease. Review of the largest published series (Table 1) suggests that the incidence of these two events are comparable and somewhat series dependent. Emboli usually occlude the aortic bifurcation as a saddle embolus with retrograde propagation of thrombus to the next patent vessel, usually the lowest renal artery. A variety of cardiac conditions and pathologies can result in peripheral emboli, including atrial fibrillation, acute myocardial infarction, valve diseases, prosthetic valves, dilated cardiomyopathy, congestive heart failure, and ventricular aneurysms. Massive or saddle emboli can also originate from aortic aneurysms, although this is distinctly less common. In-situ thrombosis in the setting of severe aortoiliac occlusive disease is often precipitated by an exacerbating event such as dehydration or diminished cardiac output from a myocardial infarction. Similar to the scenario with saddle emboli, the thrombotic process usually extends to the level of the renal arteries, with rare suprarenal extension of the thrombus. A number of other mechanisms have been implicated and should be considered in the differential diagnosis of an acute aortic occlusion given the appropriate clinical setting (Table 2). These include acute aortic dissections, thrombosis secondary to a hypercoaguable state, trauma, and postoperative complications after aortic reconstruction. Among the hypercoagulable states, heparin-induced thrombocytopenia merits consideration given the high prevalence of exogenous heparin use in the

Patients with an acute aortic occlusion usually present with sudden lower torso and extremity ischemia as reflected by some or all of the classic six Ps of acute limb ischemia (pulseless, pallor, poikilothermia, pain, paresthesia, paralysis). The severity and extent of the ischemia ranges over a wide spectrum and is contingent upon the thrombus burden, presence of distal embolization, and adequacy of the collateral network. Indeed, patients without peripheral vascular disease might recall the exact moment when their symptoms began, whereas the presentation may be more subtle in patients with long-standing occlusive disease. Pain is usually the predominant complaint, although the skin pallor and/or mottling may be quite impressive, extending to the level of the umbilicus in up to 30% of patients. The spectrum of neurologic deficits can range from mild numbness to paresthesia and frank paralysis. Notably, these clinical findings are likely secondary to peripheral nerve or lumbar plexus ischemic injury rather than frank spinal cord ischemia. Inappropriate focus on the neurologic complaints during the initial presentation can lead to inadvertent delays in diagnosis and definitive treatment. Indeed, several reports have documented initial referral to various specialists for evaluation of the neurologic deficit in patients with classic symptoms of their aortic occlusion. Patients with visceral and/ or renal artery involvement can experience anuria, hypertensive crisis, and/or abdominal pain. The diagnosis of an acute aortic occlusion can usually be made by history and physical examination and confirmed with the appropriate imaging study if there is any question about the diagnosis or the initial treatment approach. Computed tomography (CT) arteriography has emerged as the definitive diagnostic test for acute aortic occlusion (Figure 1). CT arteriography image acquisition times are rapid, and the quality of the images with the newer-generation multi-slice technology is excellent. Furthermore, it overcomes many of the limitations of catheter-based arteriography in the setting of an acute aortic occlusion, including the need to cannulate the brachial artery and the potential limited contrast delivery for vessel visualization below the aortic occlusion. Admittedly, the decision to obtain a confirmatory imaging study must be balanced by the additional risk in terms of the potential delay of the definitive treatment and the associated contrast nephrotoxicity. Given the relative ease of obtaining a CT arteriogram in our center, we have a low threshold for obtaining such a study in the setting of a presumed aortic occlusion, particularly if there is any concern about visceral and/or renal involvement. The slight risk or delay appears justified by the additional anatomic information provided by the study.

430

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Selected References Darling III RC, Shah DM, Chang BB, et al: Retroperitoneal approach for bilateral renal and visceral artery revascularization, Am J Surg 168:148–151, 1994. Huber TS, Lee WA: Chronic ischemia. In Cronenwett JL, Johnston KW, (eds): Rutherford's vascular surgery, ed 7, Philadelphia, 2010, Saunders Elsevier. pp 2273–2288. Reilly LM, Ramos TK, Murray SP, et al: Optimal exposure of the proximal abdominal aorta: A critical appraisal of transabdominal medial visceral rotation, J Vasc Surg 19:375–389, 1994. Ryan SV, Calligaro KD, McAffee-Bennett S, et al: Management of juxtarenal aortic aneurysms and occlusive disease with preferential suprarenal clamping via a midline transperitoneal incision: Technique and results, Vasc Endovascular Surg 38:417–422, 2004.

Acute Aortic Occlusion

Shepard AD, Tollefson DF, Reddy DJ, et al: Left flank retroperitoneal exposure: A technical aid to complex aortic reconstruction, J Vasc Surg 14:283–291, 1991. West Jr CA, Johnson LW, Doucet L, et al: A contemporary experience of open aortic reconstruction in patients with chronic atherosclerotic occlusion of the abdominal aorta, J Vasc Surg 52:1164–1172, 2010. Wind GG, Valentine RJ: Anatomic exposures in vascular surgery, Baltimore, 1991, Williams & Wilkins.

hospital setting. A small number of interesting collections of case reports have described several additional rare etiologies.

Salvatore T. Scali and Thomas S. Huber

CLINICAL PRESENTATION AND DIAGNOSIS Acute aortic occlusion is a true vascular emergency associated with significant morbidity and mortality secondary to the underlying etiology, the related comorbidities, and the ischemia–reperfusion injury resulting from revascularization. Indeed, the morbidity and mortality rates are comparable to those associated with a ruptured abdominal aortic aneurysm (AAA). The optimal management requires early recognition and definitive treatment, similar to most vascular surgical emergencies. Despite the evolution of various percutaneous therapies, open surgical reconstruction remains the cornerstone of treatment. Fortunately, acute aortic occlusion is a relatively uncommon problem and, not surprisingly, the published experience with it is quite limited.

ETIOLOGY The leading causes of an acute aortic occlusion are an embolus originating from the heart and in-situ thrombosis in the setting of severe aortoiliac occlusive disease. Review of the largest published series (Table 1) suggests that the incidence of these two events are comparable and somewhat series dependent. Emboli usually occlude the aortic bifurcation as a saddle embolus with retrograde propagation of thrombus to the next patent vessel, usually the lowest renal artery. A variety of cardiac conditions and pathologies can result in peripheral emboli, including atrial fibrillation, acute myocardial infarction, valve diseases, prosthetic valves, dilated cardiomyopathy, congestive heart failure, and ventricular aneurysms. Massive or saddle emboli can also originate from aortic aneurysms, although this is distinctly less common. In-situ thrombosis in the setting of severe aortoiliac occlusive disease is often precipitated by an exacerbating event such as dehydration or diminished cardiac output from a myocardial infarction. Similar to the scenario with saddle emboli, the thrombotic process usually extends to the level of the renal arteries, with rare suprarenal extension of the thrombus. A number of other mechanisms have been implicated and should be considered in the differential diagnosis of an acute aortic occlusion given the appropriate clinical setting (Table 2). These include acute aortic dissections, thrombosis secondary to a hypercoaguable state, trauma, and postoperative complications after aortic reconstruction. Among the hypercoagulable states, heparin-induced thrombocytopenia merits consideration given the high prevalence of exogenous heparin use in the

Patients with an acute aortic occlusion usually present with sudden lower torso and extremity ischemia as reflected by some or all of the classic six Ps of acute limb ischemia (pulseless, pallor, poikilothermia, pain, paresthesia, paralysis). The severity and extent of the ischemia ranges over a wide spectrum and is contingent upon the thrombus burden, presence of distal embolization, and adequacy of the collateral network. Indeed, patients without peripheral vascular disease might recall the exact moment when their symptoms began, whereas the presentation may be more subtle in patients with long-standing occlusive disease. Pain is usually the predominant complaint, although the skin pallor and/or mottling may be quite impressive, extending to the level of the umbilicus in up to 30% of patients. The spectrum of neurologic deficits can range from mild numbness to paresthesia and frank paralysis. Notably, these clinical findings are likely secondary to peripheral nerve or lumbar plexus ischemic injury rather than frank spinal cord ischemia. Inappropriate focus on the neurologic complaints during the initial presentation can lead to inadvertent delays in diagnosis and definitive treatment. Indeed, several reports have documented initial referral to various specialists for evaluation of the neurologic deficit in patients with classic symptoms of their aortic occlusion. Patients with visceral and/ or renal artery involvement can experience anuria, hypertensive crisis, and/or abdominal pain. The diagnosis of an acute aortic occlusion can usually be made by history and physical examination and confirmed with the appropriate imaging study if there is any question about the diagnosis or the initial treatment approach. Computed tomography (CT) arteriography has emerged as the definitive diagnostic test for acute aortic occlusion (Figure 1). CT arteriography image acquisition times are rapid, and the quality of the images with the newer-generation multi-slice technology is excellent. Furthermore, it overcomes many of the limitations of catheter-based arteriography in the setting of an acute aortic occlusion, including the need to cannulate the brachial artery and the potential limited contrast delivery for vessel visualization below the aortic occlusion. Admittedly, the decision to obtain a confirmatory imaging study must be balanced by the additional risk in terms of the potential delay of the definitive treatment and the associated contrast nephrotoxicity. Given the relative ease of obtaining a CT arteriogram in our center, we have a low threshold for obtaining such a study in the setting of a presumed aortic occlusion, particularly if there is any concern about visceral and/or renal involvement. The slight risk or delay appears justified by the additional anatomic information provided by the study.



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TABLE 1:  Series of Acute Aortic Occlusions ETIOLOGY Author

Patients

Embolus (%)

Thrombus (%)

Mortality (%)

Morbidity (%)

Limb Salvage (%) 5-Year Survival (%)*

Littooy & Baker 1986

18

56

44

50

67

100

NA

Tapper et al. 1992

26

50

50

31

37

NA

56

Dossa et al. 1994

46

65

35

34

74

95

70

Babu et al. 1995

48

8

92

52

NA

NA

NA

Surowiec et al. 1998

33

16

17

21

63

88

NA

*Among those surviving the acute event. NA, Not available. Babu SC, Shah PM, Nitahara J: Acute aortic occlusion—factors that influence outcome, J Vasc Surg 21:567–572, 1995; Dossa CD, Shepard AD, Reddy DJ, et al: Acute aortic occlusion. A 40-year experience, Arch Surg 129:603–607, 1994; Littooy FN, Baker WH: Acute aortic occlusion—a multifaceted catastrophe, J Vasc Surg 4:211–216, 1986; Surowiec SM, Isiklar H, Sreeram S, et al: Acute occlusion of the abdominal aorta, Am J Surg 176:193–197, 1998; Tapper SS, Jenkins JM, Edwards WH, et al: Juxtarenal aortic occlusion, Ann Surg 215:443–449, 1992.

TABLE 2:  Reported Causes of Acute Aortic Occlusions Category

Example

Embolic

Cardiogenic (e.g., Afib, valve disease)

In-situ thrombosis

PAD, plaque rupture, AAA

Dissection

Type B aortic dissection

Postsurgical

Bypass graft thrombosis (e.g., ABF), endograft collapse (i.e., TEVAR/EVAR, iliac stents)

Metabolic

Diabetic ketoacidosis

Infectious

Aspergillus spp, Candida spp

Inflammatory

Arteritis

Low-flow state

Dehydration, CHF, diarrhea, vomiting

Hypercoagulable state

HIT, thrombophilic state (e.g., cancer)

Trauma

Aortic transection (e.g., lap belt injury)

Miscellaneous

Umbilical artery catheterization, tension pneumoperitoneum, lymphoma, SBO

AAA, Abdominal aortic aneurysm; ABF, aortobifemoral bypass; Afib, atrial fibrillation or other cardiac arrhythmia; CHF, congestive heart failure; HIT, heparin-induced thrombocytopenia; PAD, peripheral artery disease; SBO, small bowel obstruction; TEVAR/EVAR, thoracic or abdominal aortic stent graft.

PRINCIPLES OF MANAGEMENT The treatment goals for patients with acute aortic occlusions are to stop the thrombotic process and restore blood flow to the lower torso and extremities, while limiting the ischemia–reperfusion

injury. Unfortunately, the variable presentations and common failure to make the appropriate initial diagnosis often lead to significant delays before definitive treatment can be provided. There is no true golden period for limb or life salvage. However, the duration, extent, and severity of the ischemia needs to be factored into the treatment algorithm. All patients should be anticoagulated once the diagnosis of acute limb ischemia is made, provided that there are no contraindications. We typically use unfractionated heparin with a bolus of 80 units/ kg followed by infusion of 18 units/kg unless there is a concern about heparin-induced thrombocytopenia. The restoration of blood flow to the ischemic tissues has traditionally required open operative intervention. However, several reports have described successful outcomes with percutaneous endovascular approaches. The role of the complete endovascular approach remains to be determined given the inherent delays to complete revascularization, and it is likely only appropriate for high-risk patients with minimal ischemic symptoms.

PREOPERATIVE EVALUATION The preoperative evaluation should be performed in an expeditious manner and limited to the extent necessary to safely proceed to the operating room. Intravenous access should be established with a large-bore cannula, and a Foley catheter should be inserted. A blood specimen should be obtained for a cross match, complete blood count, coagulation profile, blood gas, serum lactate, serum myoglobin, electrolytes, and liver function tests (particularly if visceral ischemia is suspected). Fluid resuscitation should be initiated with an isotonic crystalloid solution; patients with acute aortic occlusions are often dehydrated and volume contracted. Additional invasive monitoring is dictated by the underlying comorbidities and cardiac dysfunction, although we usually insert an arterial catheter for continuous blood pressure monitoring. Patients are anticoagulated with unfractionated heparin as outlined earlier (if not already done), unless there is some concern about heparin-induced thrombocytopenia. Strategies (sodium bicarbonate, mannitol, acetylcysteine) to reduce the potential kidney injury from any contrast agent and urine myoglobin are usually initiated.

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B

A

FIGURE 1  A, Preoperative three-dimensional (3-D) computed tomography (CT) arteriogram and intraoperative CT arteriogram with 3-D reconstructions in a patient with a 5-hour history of bilateral leg pain and mottling of his lower torso demonstrated an acute aortic occlusion at the level of the renal arteries, with reconstitution of the iliac and femoral system. Note the large epigastric vessels that suggest presence of a significant amount of preexisting underlying arterial occlusive disease. B, A catheter-based arteriogram performed in the operating room confirmed the findings on the CT. An aortobifemoral bypass with bilateral fasciotomies was performed. The patient’s postoperative course was complicated by an acute lung and renal injury, which required prolonged mechanical ventilation and hemodialysis, respectively.

OPERATIVE PLANNING The operative approach includes catheter or pharmacomechanical thromboembolectomy, extra-anatomic bypass, axillobifemoral bypass, and direct aortic reconstruction. Patients with an acute aortic occlusion from an embolus are usually successfully treated with bilateral transfemoral thromboembolectomy. In contrast, thromboembolectomy alone is usually insufficient for patients with an acute aortic occlusion secondary to in-situ thrombosis. Notably, Littooy and colleagues documented that thromboembolectomy was successful in nine of 10 patients presenting with embolic events but in none of the eight patients experiencing in-situ thromboses. Regardless, patients with a presumed occlusion secondary to an in-situ thrombosis should likely undergo an attempted thromboembolectomy as the initial procedure with the choice of definitive revascularization (endovascular, extra-anatomic, direct) based upon the extent of aortoiliac occlusive disease on the intraoperative arteriogram, severity of the ischemia, potential need for additional procedures, and their comorbidities. In the endovascular era, many patients with an acute aortic occlusion secondary to in-situ thrombosis can be treated in a timely fashion with initial thromboembolectomy and a combination of angioplasty and stenting of the aortoiliac segments. The long-standing question about the optimal open surgical procedure in this setting still remains unresolved, although the alternative approaches (extra-anatomic vs. direct aortic reconstruction) should likely be viewed as complementary. The extra-anatomic approach is easier and safer in terms of both its physiologic impact and mortality rate. These concerns are particularly relevant given the common delays in diagnosis of these patients and their disadvantaged physiologic states. Patients with acute aortic occlusion secondary to in-situ thrombosis often require simultaneous infrainguinal revascularization, thereby further justifying the extra-anatomic approach, given the significant mortality rates reported for combined direct aortoiliac

(inflow) and infrainguinal (outflow) reconstruction in the elective setting. These concerns were highlighted by Babu and coworkers, who reported that 60% of their patients with an acute aortic occlusion required additional procedures: 19 required infrainguinal bypass, three bowel resection, six fasciotomy, and nine major amputation. Disadvantages of the extra-anatomic bypass include the inferior longterm patency and the potential for aortic clot propagation proximal to the renal and mesenteric vessels. We favor extra-anatomic bypass in the majority of patients and reserve direct aortic reconstruction for younger, healthier patients who have minimal ischemic symptoms and who are in good physiologic condition. Patients with renal and mesenteric involvement require direct revascularization. However, the mortality rate in this setting is extremely high, and renal salvage, in the absence of extensive preformed collaterals, is poor.

THROMBOEMBOLECTOMY Balloon thromboembolectomy can be performed using either transverse or longitudinal femoral arteriotomy, although we favor the latter because it affords greater flexibility in the event that an inflow procedure or a common femoral endarterectomy is required. Admittedly, this usually requires a patch angioplasty, but the slight increase in time required seems to be offset by the increased flexibility. We extend the arteriotomy to the common femoral bifurcation to allow access to the orifices of the profunda and superficial femoral arteries, and we place vessel loops around all three femoral vessels to facilitate control, thereby limiting retrograde bleeding after clot removal. A 3-Fr and a 4-Fr Fogarty thromboembolectomy catheter are used for the profunda and superficial femoral arteries, respectively, and anywhere from a 4-Fr to a 6-Fr balloon are used for the aortoiliac segment. Thromboembolectomy can be performed under fluoroscopic guidance using half-strength contrast to inflate the balloon. This



Acute Aortic Occlusion

technique is particularly helpful if there is concern about renal or visceral artery involvement because it allows a better assessment of the location of the thrombus (and/or embolus) and adequacy of clot removal. A second contrast-filled balloon can be positioned in the contralateral common iliac artery (after the clot has been removed) to prevent inadvertent embolization of any further thrombus during the final passes of the thromboembolectomy catheter. We have found the graft thrombectomy catheter (Edwards Life Sciences, Irvine, CA) to be helpful in the setting of an acute aortic occlusion after an aortobifemoral bypass. Importantly, the various steps of the thrombectomy should be coordinated with the anesthesiologists, and every attempt should be made to minimize blood loss. It is not uncommon to lose a moderate amount of blood during the aortoiliac thrombectomy, and this can be problematic given the physiologic derangements commonly seen in patients with these aortic occlusions. The adequacy of arterial inflow can be assessed after the thromboembolectomy by the quantity of the bleeding and the character of the pulse. Admittedly, this is somewhat qualitative, although it is adequate in most situations. If there is any uncertainty about the adequacy of the arterial inflow, arterial pressure measurements and/or an arteriogram can be obtained by cannulating the common femoral artery (or the patch used to close the arteriotomy). Any pressure differential greater than a 15% drop in pressure after administration of a vasodilator (typically papaverine 30 mg) between the radial and femoral arteries suggests an inflow stenosis not detected by the resting pressure measurements. We have a very low threshold for obtaining an arteriogram and treating all significant inflow lesions.

AXILLOBIFEMORAL AND AORTOBIFEMORAL BYPASS The axillobifemoral and aortobifemoral bypass procedures may be performed using fairly standard techniques. The axillary artery with the greatest brachial pressure is used as the donor artery. An arteriogram can be obtained at the time of the procedure if there is any question about the adequacy of the donor axillary artery. The axillobifemoral bypass is performed using 8-mm ringed expanded polytetrafluoroethylene (ePTFE) graft, with the axillofemoral component tunneled through the subcutaneous plane in the anterior axillary line and the femorofemoral component tunneled in the subfascial plane. The axillary anastomosis is constructed in a tension-free fashion medially on the axillary artery, with the graft essentially sitting on the chest wall as a way to keep the anastomosis from being disrupted during vigorous activity. The graft can be tunneled either anterior or posterior to the axillary vein; the choice is usually dictated by the orientation that looks the best. In the case of an aortobifemoral bypass for an acute aortic occlusion, proximal aortic control usually needs to be obtained above the level of the renal arteries, given the extent of the thrombus, with the typical options being immediately above the renal arteries or above the celiac artery. We prefer to obtain control immediately above the renal arteries to minimize the duration of visceral ischemia, although this requires mobilizing the renal vein by suture ligating the gonadal, lumbar, and adrenal branches when using the transperitoneal approach. The aortic clamp can be repositioned below the renal arteries after removing the offending thrombus or completing the aortic anastomosis. When the thrombus extends to the level of the visceral vessels, supraceliac control is required, and we prefer a retroperitoneal approach in this setting.

PERCUTANEOUS ENDOVASCULAR TREATMENT A percutaneous endovascular approach may be considered as part of the treatment algorithm, although this procedure is usually reserved for patients with subcritical ischemia. Successful treatment

433

has been reported using catheter-directed thrombolysis, direct ­pharmacomechanical lysis with thrombectomy, and/or adjunctive angioplasty and intraluminal stent placement. Mertens and coworkers successfully treated eight patients with acute aortic occlusions using a combination of pulse spray pharmacomechanical thrombolysis and low-dose urokinase, concluding that it was the “treatment of choice for long, multi-level occlusive disease because it simplifies therapy and reduces the need for surgery.” Despite their bold conclusion, our enthusiasm for the complete percutaneous endovascular approach has been ­limited given the paucity of reports and the multiple potential pitfalls including time to reperfusion, completeness of thrombus resolution, contrast load, need for multiple procedures, and long-term durability.

ADEQUACY OF REVASCULARIZATION AND ADJUNCTIVE PROCEDURES The adequacy of revascularization after thromboembolectomy or bypass is assessed by examination of the feet and insonation of the pedal vessels with continuous-wave Doppler. If the feet appear to be viable and pedal signals are present, the revascularization was likely initially sufficient to reverse the ischemic process. Bilateral fasciotomies should be performed in most cases, and it has been our maxim that if a fasciotomy is even considered in the treatment algorithm then it should likely be performed. The wound morbidity associated with fasciotomy can be reduced by lacing a vessel loop through staples across the open wound, although it is relatively simple to close the wounds postoperatively at the bedside with interrupted sutures if there is not a lot of swelling. Unlike with elective revascularization, we do not routinely perform a completion lower extremity arteriogram if the character of the pedal Doppler signals sound adequate. All patients with acute aortic occlusion from an embolus should be anticoagulated, throughout the postoperative period and long term, although we usually wait a few days to initiate this therapy, in an attempt to reduce the incidence of wound hematomas. In the event that the feet do not appear viable after the initial aortoiliac revascularization, further intervention is required. There are several options in the decision algorithm, including obtaining an arteriogram, repeating the femoral thromboembolectomy, and/or performing a tibial thrombectomy through the below-knee popliteal artery. Although the choice is usually predicated on the clinical scenario, our general approach is to repeat the thromboembolectomy of the femoral vessels and the inflow source first. If the feet are still concerning, the popliteal artery below the knee is explored, and a thromboembolectomy of the tibial vessels is performed by directing a 3-Fr Fogarty catheter down each of the three vessels under direct vision. This can be facilitated through an arteriotomy starting in the popliteal artery near the origin of the anterior tibial artery and extending onto the tibioperoneal trunk. The arteriotomy is closed with a vein patch after the thromboembolectomy, and a completion arteriogram is obtained. If the feet remain ischemic and/or nonviable, lower extremity bypass is performed as dictated by the findings on the arteriogram. Unfortunately, the need for simultaneous infrainguinal bypass and aortoiliac revascularization in patients with acute aortic occlusion is common, occurring in 40% of patients in the series reported by Babu and colleagues. Perhaps the most difficult clinical situation arises when the feet appear to be ischemic, yet viable, and the quality of the pedal signals is poor or nonexistent. Provided that there is an arterial signal at the popliteal fossa, we have been willing to accept a less-than-perfect initial outcome given the uncertainty about the extent of the infrainguinal occlusive disease, the potential contribution of reversible vasospasm, the concerns about further prolonging the operative procedure, and the physiologic duress associated with the initial aortic occlusion. However, these patients need to be monitored very closely in the early postoperative period and returned to the operating room

434

AORTOILIAC OCCLUSIVE DISEASE

for definitive revascularization within 4 to 6 hours if they do not improve. They should likely be anticoagulated unless there is a specific contraindication.

ISCHEMIA AND REPERFUSION INJURY Revascularization of the ischemic lower extremities and lower torso is associated with a predictable reperfusion injury whose magnitude depends upon the extent and duration of the initial ischemic insult. This restoration of blood flow leads to the release of hydrogen ions, metabolic breakdown products, potassium, and a variety of other inflammatory mediators that can lead to hypotension, myocardial dysfunction, arrhythmias, and ultimately multiorgan failure. It is important to anticipate these reperfusion events and communicate with the anesthesia team to minimize their impact to the extent possible. The reperfusion should occur in a series of small steps (controlled limb reperfusion) to mitigate the impact of the metabolic washout and the associated hypotension from the expanded volume of distribution similar to that seen with the removal of the aortic clamp after an infrarenal aneurysm repair. Fortunately, this can usually be accomplished by restoring perfusion to a specific blood vessel (e.g., right hypogastric, right profunda femoral) or anatomic region (e.g., right buttock, right thigh), with the sequence and options dictated by the underlying problem and patent vessels. Sodium bicarbonate may be administered preemptively, with the dosing regimen based on serum pH on the arterial blood gas. Any resultant hyperkalemia can be temporized with sodium bicarbonate, glucose, insulin, and calcium and definitively treated with forced diuresis, potassium-binding agents, and/or dialysis, with the last three approaches generally reserved for the postoperative period. A variety of techniques have been described to mitigate ischemia– reperfusion injury, including aspirating blood from the femoral vein to capture the initial bolus of ischemic metabolites, using intraoperative hemofiltration, and administering oxygen free radical scavengers such as mannitol. Not surprisingly, the sequelae of the ischemia– reperfusion injury extends beyond the operating room into the postoperative period and often results in multiple organ dysfunction. This should be anticipated and all appropriate supportive measures should be implemented. The breakdown of the ischemic muscle by rhabdomyolysis can result in myoglobinuria, leading to renal dysfunction; volume expansion, alkalinization of the urine with sodium bicarbonate, and forced diuresis with mannitol may be beneficial in this setting.

Aortic Graft Limb Occlusion Robert T. Lancaster and Glenn M. LaMuraglia

Aortofemoral bypass (AFB) has been recognized as a durable and effective form of vascular reconstruction for aortoiliac occlusive disease. With the advent of balloon angioplasty and intraluminal stents in the last 20 years, there has been a decrease in the number of patients treated by AFB procedures. However, it is still the treatment

OUTCOME The morbidity and mortality after revascularization for an acute aortic occlusion remains high, despite the improvements in surgical care over the past several decades, with the adverse outcomes related to the underlying etiologies and comorbidities. The reported mortality rates have ranged from 20% to 50%. The majority of the deaths in these patients are related to cardiac events, although multiple organ dysfunction is common. Notably, Babu and colleagues reported an overall mortality rate of 52% in their 48-patient series, with 85% of the patients developing left ventricular dysfunction after a successful revascularization. The mortality rates for patients with suprarenal aortic occlusions and those with hypercoaguable states appear to be increased, although the limited data preclude definitive conclusions. The corresponding morbidity rates are also significant, with Dossa and coworkers reporting a 75% complication rate among 46 patients. Fortunately, both the limb-salvage and neurologic recovery rates are good; limb-salvage rates range from 88% to 95%. Notably, the incidence of recurrent arterial emboli is significant, with rates up to 17% in the early postoperative period and 27% to 37% over the long term, thereby underscoring the importance of long-term anticoagulation. As a result of the limited published data, the long-term survival after an acute aortic occlusion remains poorly defined, with 5-year rates ranging from 56% to 70%.

Selected References Babu SC, Shah PM, Nitahara J: Acute aortic occlusion—factors that influence outcome, J Vasc Surg 21:567–572, 1995. Busuttil RW, Keehn G, Milliken J, et al: Aortic saddle embolus. A twentyyear experience, Ann Surg 197:698–706, 1983. Dossa CD, Shepard AD, Reddy DJ, et al: Acute aortic occlusion. A 40-year experience, Arch Surg 129:603–607, 1994. Krajcer Z, Gilbert JH, Dougherty KM, et al: Successful treatment of aortic endograft thrombosis with rheolytic thrombectomy, J Endovasc Ther 9:756–764, 2002. Littooy FN, Baker WH: Acute aortic occlusion—a multifaceted catastrophe, J Vasc Surg.4211–216, 1986. Mestres CA, Castella M, Barriuso C, et al: Acute thrombotic occlusion of the suprarenal aorta: Importance of early diagnosis and treatment, Br J Surg 82:502–504, 1995. Mertens H, Van Holsbeeck B, Gryspeerdt SG, et al: Percutaneous treatment of acute multiple limb ischemia, JBR-BTR 83:238–242, 2000. Mozingo JR, Denton Jr IC: The neurological deficit associated with sudden occlusion of abdominal aorta due to blunt trauma, Surgery 77:118–125, 1975. Surowiec SM, Isiklar H, Sreeram S, et al: Acute occlusion of the abdominal aorta, Am J Surg 176:193–197, 1998. Tapper SS, Jenkins JM, Edwards WH, et al: Juxtarenal aortic occlusion, Ann Surg 215:443–449, 1992.

of choice for selected patients with extensive bilateral and calcific aortoiliac occlusive disease. The most common complication occurring after the placement of an AFB graft is thrombotic occlusion of one of its limbs. This can occur early after bypass grafting, but it manifests with increasing frequency during long-term follow-up. The incidence of primary thrombosis of an AFB limb is reported to be approximately 10% within the first 5 years and up to 20% after 10 years. Among late failures, the average time from placement of the graft to limb thrombosis was 34 months. Those with limb thrombosis after an AFB are usually high-risk patients, often arriving at the hospital on an urgent basis with an ischemic lower extremity, multiple comorbidities, and generalized extensive arteriosclerotic occlusive disease. These patients pose multiple management and operative challenges that require careful clinical assessment and judgment.

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for definitive revascularization within 4 to 6 hours if they do not improve. They should likely be anticoagulated unless there is a specific contraindication.

ISCHEMIA AND REPERFUSION INJURY Revascularization of the ischemic lower extremities and lower torso is associated with a predictable reperfusion injury whose magnitude depends upon the extent and duration of the initial ischemic insult. This restoration of blood flow leads to the release of hydrogen ions, metabolic breakdown products, potassium, and a variety of other inflammatory mediators that can lead to hypotension, myocardial dysfunction, arrhythmias, and ultimately multiorgan failure. It is important to anticipate these reperfusion events and communicate with the anesthesia team to minimize their impact to the extent possible. The reperfusion should occur in a series of small steps (controlled limb reperfusion) to mitigate the impact of the metabolic washout and the associated hypotension from the expanded volume of distribution similar to that seen with the removal of the aortic clamp after an infrarenal aneurysm repair. Fortunately, this can usually be accomplished by restoring perfusion to a specific blood vessel (e.g., right hypogastric, right profunda femoral) or anatomic region (e.g., right buttock, right thigh), with the sequence and options dictated by the underlying problem and patent vessels. Sodium bicarbonate may be administered preemptively, with the dosing regimen based on serum pH on the arterial blood gas. Any resultant hyperkalemia can be temporized with sodium bicarbonate, glucose, insulin, and calcium and definitively treated with forced diuresis, potassium-binding agents, and/or dialysis, with the last three approaches generally reserved for the postoperative period. A variety of techniques have been described to mitigate ischemia– reperfusion injury, including aspirating blood from the femoral vein to capture the initial bolus of ischemic metabolites, using intraoperative hemofiltration, and administering oxygen free radical scavengers such as mannitol. Not surprisingly, the sequelae of the ischemia– reperfusion injury extends beyond the operating room into the postoperative period and often results in multiple organ dysfunction. This should be anticipated and all appropriate supportive measures should be implemented. The breakdown of the ischemic muscle by rhabdomyolysis can result in myoglobinuria, leading to renal dysfunction; volume expansion, alkalinization of the urine with sodium bicarbonate, and forced diuresis with mannitol may be beneficial in this setting.

Aortic Graft Limb Occlusion Robert T. Lancaster and Glenn M. LaMuraglia

Aortofemoral bypass (AFB) has been recognized as a durable and effective form of vascular reconstruction for aortoiliac occlusive disease. With the advent of balloon angioplasty and intraluminal stents in the last 20 years, there has been a decrease in the number of patients treated by AFB procedures. However, it is still the treatment

OUTCOME The morbidity and mortality after revascularization for an acute aortic occlusion remains high, despite the improvements in surgical care over the past several decades, with the adverse outcomes related to the underlying etiologies and comorbidities. The reported mortality rates have ranged from 20% to 50%. The majority of the deaths in these patients are related to cardiac events, although multiple organ dysfunction is common. Notably, Babu and colleagues reported an overall mortality rate of 52% in their 48-patient series, with 85% of the patients developing left ventricular dysfunction after a successful revascularization. The mortality rates for patients with suprarenal aortic occlusions and those with hypercoaguable states appear to be increased, although the limited data preclude definitive conclusions. The corresponding morbidity rates are also significant, with Dossa and coworkers reporting a 75% complication rate among 46 patients. Fortunately, both the limb-salvage and neurologic recovery rates are good; limb-salvage rates range from 88% to 95%. Notably, the incidence of recurrent arterial emboli is significant, with rates up to 17% in the early postoperative period and 27% to 37% over the long term, thereby underscoring the importance of long-term anticoagulation. As a result of the limited published data, the long-term survival after an acute aortic occlusion remains poorly defined, with 5-year rates ranging from 56% to 70%.

Selected References Babu SC, Shah PM, Nitahara J: Acute aortic occlusion—factors that influence outcome, J Vasc Surg 21:567–572, 1995. Busuttil RW, Keehn G, Milliken J, et al: Aortic saddle embolus. A twentyyear experience, Ann Surg 197:698–706, 1983. Dossa CD, Shepard AD, Reddy DJ, et al: Acute aortic occlusion. A 40-year experience, Arch Surg 129:603–607, 1994. Krajcer Z, Gilbert JH, Dougherty KM, et al: Successful treatment of aortic endograft thrombosis with rheolytic thrombectomy, J Endovasc Ther 9:756–764, 2002. Littooy FN, Baker WH: Acute aortic occlusion—a multifaceted catastrophe, J Vasc Surg.4211–216, 1986. Mestres CA, Castella M, Barriuso C, et al: Acute thrombotic occlusion of the suprarenal aorta: Importance of early diagnosis and treatment, Br J Surg 82:502–504, 1995. Mertens H, Van Holsbeeck B, Gryspeerdt SG, et al: Percutaneous treatment of acute multiple limb ischemia, JBR-BTR 83:238–242, 2000. Mozingo JR, Denton Jr IC: The neurological deficit associated with sudden occlusion of abdominal aorta due to blunt trauma, Surgery 77:118–125, 1975. Surowiec SM, Isiklar H, Sreeram S, et al: Acute occlusion of the abdominal aorta, Am J Surg 176:193–197, 1998. Tapper SS, Jenkins JM, Edwards WH, et al: Juxtarenal aortic occlusion, Ann Surg 215:443–449, 1992.

of choice for selected patients with extensive bilateral and calcific aortoiliac occlusive disease. The most common complication occurring after the placement of an AFB graft is thrombotic occlusion of one of its limbs. This can occur early after bypass grafting, but it manifests with increasing frequency during long-term follow-up. The incidence of primary thrombosis of an AFB limb is reported to be approximately 10% within the first 5 years and up to 20% after 10 years. Among late failures, the average time from placement of the graft to limb thrombosis was 34 months. Those with limb thrombosis after an AFB are usually high-risk patients, often arriving at the hospital on an urgent basis with an ischemic lower extremity, multiple comorbidities, and generalized extensive arteriosclerotic occlusive disease. These patients pose multiple management and operative challenges that require careful clinical assessment and judgment.



Aortic Graft Limb Occlusion

ETIOLOGY Causes of aortic graft limb occlusion can be best conceptualized as early or late. Early postoperative thrombosis of an AFB graft limb most commonly results from a technical problem. Such problems most often occur with either the handling of the graft or the construction of the distal anastomosis at the time of AFB graft placement. Generally, inflow from the aorta is not a problem, provided that a major clamp injury or dissection has not occurred. Correct handling of the graft includes its proper placement without twisting through the retroperitoneal tunnel to the femoral position. Proper graft length is critical because redundant graft near either anastomosis tends to kink and obstruct blood flow (Figures 1 and 2). Extended graft body versus limb length can also cause a kink at the origin of the limb as it traverses the pelvis to the inguinal ligament. Proper technical execution of the distal anastomosis requires careful clamping of an often diseased superficial femoral artery (SFA) or profunda femoral artery (PFA) to avoid creating intimal flaps. Adequate intraprocedural anticoagulation and ample flushing of the graft and vessels of air or thrombus that have accumulated in the graft during construction of the anastomoses is also important. It is also relevant to properly assess the extent of outflow disease, to be assured of adequate outflow to maintain graft limb patency. It is important to recognize the relevance of a significant stenosis of the PFA origin in a patient with an SFA that is severely diseased or occluded. Occasionally, the PFA does not have the blood flow capacity to maintain patency of the AFB limb. A distal bypass might need to be performed in conjunction with the AFB graft in this setting. Late thrombosis of an AFB limb generally occurs secondary to progressive intimal hyperplasia or progression of outflow atherosclerotic disease at the distal anastomosis. In the first few years after graft placement, luminal narrowing can result from intimal hyperplasia from a clamp injury or turbulent flow from a large-diameter prosthetic graft anastomosed to diminutive artery. Late thrombosis results primarily from progression of distal arteriosclerotic disease. This may also be associated with an anastomotic aneurysm (Figure 3).

The anastomotic aneurysm, upon enlarging, develops luminal thrombus, resulting in a thrombogenic milieu that can precipitate graft limb occlusion. Rarely, a proximal aortic stenosis occurs and leads to aortic graft limb thrombosis (Figure 4). This condition is best avoided by placing the proximal graft-to-aorta anastomosis as close as possible to the origins of the renal arteries. Other causes of aortic graft limb occlusion are unusual. It is rare to have a hypercoagulable state by itself cause occlusion of a single limb of a graft. Other contributing causes such as impaired cardiac

FIGURE 2  Redundancy of the distal limb of the aortofemoral graft in

the groin (arrow).

FIGURE 1  Aortogram performed on a patient with early recurring

thromboses of both limbs of the aortofemoral graft. Note at the proximal anastomosis the kinking of both limbs at their origin from the body of the graft (arrows).

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FIGURE 3  Anastomotic aneurysm at the femoral anastomosis

(arrows). The actual aneurysm was significantly larger, reflecting nonvisualized intraluminal thrombus.

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AORTOILIAC OCCLUSIVE DISEASE

FIGURE 4  Proximal anastomotic stenosis of an aortofemoral graft

FIGURE 5  Aortogram of thrombosed left limb of an aortofemoral

(arrow).

graft. Note the presence of thrombus in the body of the graft on the ipsilateral side and early thrombus development at the origin of the right limb (arrows).

function or high doses of vasopressors could lead to bilateral limb occlusion and aortic thrombosis, but this is unusual. However, with vascular disease causing a degree of obstruction to blood flow, these other factors can contribute to graft limb thromboses. In addition, because the femoral artery or distal anastomosis is an important access site to the vascular tree for vascular or cardiac interventions, thrombosis of a limb can follow a local injury, overzealous compression of the access site after sheath removal, or inadequate anticoagulation with the placement of a catheter or a larger device such as an intraaortic balloon pump.

CLINICAL PRESENTATION Patients with an AFB limb occlusion usually come to the hospital with acute symptoms of lower extremity ischemia. Less often, with slowly progressive arteriosclerotic disease, enough collaterals develop so that symptoms manifest as progressive intermittent claudication. Characteristically, patients complain of greater symptoms of lower extremity ischemia than existed when they required their original operation.

MANAGEMENT Certain important anatomic information, usually evident on computed tomography arteriography (CTA), is very helpful for determining the optimal treatment options. The aortic anastomosis must be visualized to determine whether there is adequate inflow to the graft, the presence of thrombus in the body of the graft or the contralateral limb, or the suggestion of an aortic anastomotic aneurysm (Figures 5 and 6). It is also important to visualize the contralateral limb to determine whether intrinsic graft degeneration may be occurring, although it is unusual in grafts today. In some instances, there is poor visualization of the reconstituted vessels on the affected side of the occluded graft limb as a result of poor collateral filling with CT contrast bolus. Poor or nonvisualization of the reconstituted vessels should not discourage attempted reconstruction because patent vessels may be identified with intraoperative arteriography at the time of surgery. In fact, direct opacification

FIGURE 6  Aortogram of an occluded right limb of aortofemoral

graft. Note the short meniscus present at the origin of the limb (arrowhead). The left, patent limb shows the development of multiple intraluminal defects as a preocclusive finding (white arrows).

of the PFA provides better identification of distal runoff vessels should a distal bypass be necessary. Upon arrival to the hospital, candidates for urgent surgical intervention with severe limb-threatening ischemia are anticoagulated with intravenous heparin unless this anticoagulation is contraindicated. To facilitate intraoperative arteriography, the procedure is best performed on a radiolucent operating table. The type of anesthesia



employed depends on the individual patient’s circumstances, but early anticoagulation contraindicates epidural puncture, and general anesthesia is commonly the default.

Open Surgical Treatment Revascularization in a patient with a thrombosed AFB graft limb requires restoration of inflow to the limb and provision of reliable outflow to maintain graft patency. However, the specifics of that strategy remain controversial, especially for the optimal method for restoring inflow and how often a concomitant distal bypass is necessary to maintain outflow. Because there is no single standard approach, the surgical procedure must be customized to the patient at hand. When both limbs of an AFB graft occlude, a direct aortic approach is necessary for adequate thrombectomy of the body and both limbs of the graft. Distal anastomosis exposure and thrombectomy beyond the distal anastomosis are also required. In these circumstances, the findings will likely reveal either a proximal aortic problem or severe bilateral distal anastomotic occlusive disease. If there is a pathologic condition at the proximal aortic anastomosis, a direct approach to the aorta or an appropriate extra-anatomic reconstruction is necessary. If there is thrombus extending into the body of the graft from the thrombosed limb, thrombectomy of the affected limb can occasionally result in contralateral limb embolism. Further, the thrombotic material in the body of the graft can be difficult to extract. Therefore in this circumstance, if the contralateral limb is free of pathologic findings, a femorofemoral bypass may be the most appropriate alternative to provide inflow. With no documented pathologic condition at the proximal aortic anastomosis and a patent, normal-appearing contralateral limb, retrograde graft limb thrombectomy is the procedure of choice. The results of establishing inflow in this fashion and performing a concomitant outflow procedure to maintain patency have a reported 90% success rate. Careful inspection of the graft and the anastomoses is necessary to determine if an underlying infection contributed to the graft limb thrombosis. Intraoperative Gram staining and cultures of perigraph tissue and graft material are pursued when the prosthesis is not incorporated or when an anastomotic aneurysm is identified. If the graft was not incorporated by surrounding tissue and the Gram stain is negative, a sartorius muscle flap can be considered to cover the graft reconstruction with well-vascularized tissue to optimize healing. Once inflow has been established, the success of the vascular reconstruction depends on ensuring adequate outflow. Because the SFA is occluded in most of these patients, careful examination of the PFA is necessary. With an adequate main PFA, a profundaplasty or extension of the graft beyond the prior anastomosis into the profunda can restore adequate outflow. The evidence that SFA occlusion has any influence on the patency of a limb of an AFB graft is controversial. Although many studies have documented that the SFA can help maintain patency, others have documented the sufficient capacity of the profunda system to maintain patency of an AFB graft. When the PFA is very diseased or distally occluded, an outflow bypass to the popliteal or distal artery may be necessary.

Surgical Technique The challenge of perivascular scarring complicating repeated vascular operations cannot be overstated. It is important that the patient be widely prepped and draped to include the entire abdomen, both groins, and the entire involved limb. If a femorofemoral bypass is not considered an option, alternative inflow sources such as the axillary artery means that the arm and shoulder should be prepped into the field. The prior groin incision is reopened, and the inguinal ligament at the level of the femoral artery is dissected and divided to make

Aortic Graft Limb Occlusion

437

identification of the occluded AFB limb easier, and to encircle it with a vessel loop in the retroperitoneum. Collateral branches should be preserved as much as possible but not to the extent that surgical exposure is compromised. The graft limb is then divided just proximal to the femoral anastomosis. This facilitates dissection and control of the remaining vessels. Systemic anticoagulation is maintained while No. 4-Fr and 5-Fr embolectomy catheters are sequentially advanced proximally, inflated, and removed. This is performed in a progressive fashion up to 22 to 25 cm, at which point they are beyond the bifurcation. This sequential extraction opens the lumen to permit mobilized thrombus adherent to the graft to flush down the graft and not reflux up into the body of the graft, with potential embolization to the contralateral limb. Once the proximal cap of thrombus is retrieved and identified, vigorous inflow should be concomitantly obtained. Occasionally, balloon catheter embolectomy proves inadequate to remove densely organized material from the limb of the graft, especially the proximal cap. Various other techniques have been developed to ensure adequate clot retrieval. The most common methods include loop endarterectomy strippers and the Fogarty graft thrombectomy catheter. This latter device uses collapsible wire loops attached perpendicular to the distal end of a catheter, the profile of which can be modified. After it is placed in the graft, the wire loop profile is increased from 6 to 18 mm, and the surgeon engages the walls of the graft, pulling the device down the graft limb, shearing thrombus off the graft as it is removed. With completion of the limb thrombectomy, the adequacy of the thrombectomy should be assessed. This can be done by using an angioscope in conjunction with occluding the origin of the limb of the AFB graft with a balloon catheter. Other assessments include measuring the force of the arterial inflow, measuring the arterial pressure in the limb after completion of the vascular reconstruction, or performing a retrograde arteriogram. If inflow cannot be restored through the limb of the AFB graft, alternative approaches need to be employed. The most common is the placement of a femorofemoral bypass. Other types of extra-anatomic bypasses, such as an axillofemoral bypass, can also be used. Proximal aortic graft thromboendarterectomy or repeated AFB grafting is also possible. However, repeated aortic surgery is technically very challenging and fraught with risks and complications, and it should be reserved for extreme cases such as prosthetic graft degeneration. The limb of the AFB graft is infused with a heparin–saline solution while the limb is clamped during the reconstruction of the distal anastomotic outflow. Generally, a short interposition prosthetic graft is sutured proximally to the limb of the AFB graft and distally to the PFA. If the SFA is still patent, even for a short segment, it is recommended to preserve its patency. If the external iliac artery is still patent, efforts should be made to maintain retrograde flow into the pelvis. There are multiple options for reconstructing the femoral arteries (Figure 7). The simplest include incorporating the heel of the distal anastomosis to the proximal patent vessel. If there is a proximal stenosis of the PFA, the toe of the graft should extend at least several centimeters beyond the vessel’s origin. Other options include endarterectomy with or without patch repair, incising the middle of the graft toe to provide a short patch to both the SFA and PFA, or placing an additional short graft to bypass a longer stenosis of the outflow vessel. Methods for determining the adequacy of the PFA to maintain patency of the AFB limb include the acceptance of a 4-mm probe and the measurement of its length to 20 to 25 cm by a noninflated embolectomy catheter. Distal bypass may be necessary if the PFA is small or does not meet the aforementioned criteria. Concomitant distal bypass grafting has been reported by some to be necessary 30% to 50% of the time. However, others believe that distal bypass grafting is rarely necessary unless the PFA is very small or heavily diseased. Even if distal bypass grafting is performed, the importance of preserving blood flow to the PFA cannot be overstated.

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AORTOILIAC OCCLUSIVE DISEASE

SFA

B A

PFA

artery access with preformed catheters placed in the thrombosed limb to infuse thrombolytic drugs. Catheters are advanced and repositioned over time to ensure optimal delivery of the drugs until patency is restored. The disadvantages of lytic therapy include the common necessity of a subsequent surgical reconstructive procedure, the length of time a catheter is indwelling in the contralateral prosthetic limb, and the theoretical possibility of bleeding through the interstices of the graft into the retroperitoneum. With the advance of ultrasonic probes, clot aspiration, and spray delivery catheters, more options are available to recanalize thrombosed grafts more efficiently. Treatment of proximal aortic pathologic conditions with interventional techniques deserves mention. The availability of largediameter stents and stent grafts provides the option to stent kinks in the graft and allows the treatment of proximal nonanastomotic aortic stenosis with stent grafts. The unusual nature of these clinical entities makes experience with these novel techniques difficult to accumulate, but they should be considered in individual patients.

RESULTS Operative mortality rates reported for treatment of aortic graft limb occlusions are low (0%–2.6%) considering the comorbid conditions in this group of patients. Long-term secondary patency can be expected to be 78% to 85%, whereas 26% of patients require repetitive operations to maintain graft limb patency. There are no good data supporting the use of full anticoagulation to maintain graft limb patency of aortofemoral grafts.

C

D

FIGURE 7  Alternatives for femoral artery reconstruction. Each

can be done in conjunction with an endarterectomy. A, Extended ­profundaplasty with patent superficial femoral artery (SFA) or ­significant femoral collaterals. B, Combined patch reconstruction of both ­profunda femoral arteries (PFA) and superficial femoral arteries. C, Ligation of the occluded superficial femoral artery and distal profunda femoral reconstruction. D, Bypass to both profunda and superficial femoral artery. This can be done at proximal or more distal patent ­segments of the arteries involved.

It should be included as part of every reconstruction even if the vessel appears to be diminutive and relatively inconsequential.

Interventional Management With the continued advances in percutaneous techniques for the treatment of vascular disease, it is important to determine what role they might have in the treatment of a thrombosed AFB limb. Local infusions of thrombolytic agents have been reported to be successful in recanalizing thrombosed limbs of AFB grafts. This method can only be performed in a patient without profound lower extremity ischemia because of the length of time necessary to dissolve the thrombus. The technique involves contralateral limb or left brachial

Selected References Brewster DC, Meier GH, Darling RC, et al: Reoperation for aortofemoral graft limb occlusion: Optimal methods and long-term results, J Vasc Surg 5:363–374, 1987. Erdoes LS, Bernhard VM, Berman SS: Aortofemoral graft occlusion: strategy and timing of reoperation, Cardiovasc Surg 3:277–283, 1995. Hyde GL, McCready RA, Schwartz RW, et al: Durability of thrombectomy of occluded aortofemoral graft limbs, Surgery 94:748–751, 1983. LaMuraglia GM, Brewster DC, Moncure AC, et al: Angioscopic evaluation of unilateral aortic graft limb thrombectomy: Is it helpful? J Vasc Surg 17:1069–1074, 1993. Nevelsteen A, Suy R: Graft occlusion following aortofemoral Dacron bypass, Ann Vasc Surg 5:32–37, 1991. Nolan KD, Benjamin ME, Murphy TJ, et al: Femorofemoral bypass for aortofemoral graft limb occlusion: A ten-year experience, J Vasc Surg 19:851–856, 1994. Pedrini L, Pisano E, Donato Di Paola M, et al: Late occlusion of ­aortobifemoral bypass graft: Surgical treatment, Cardiovasc Surg 2:763–766, 1994. Seabrook GR, Mewissen MW, Schmitt DD, et al: Percutaneous intraarterial thrombolysis in the treatment of thrombosis of lower extremity arterial reconstructions, J Vasc Surg 13:646–651, 1991. Sharafuddin MJ, Hicks ME, Jenson ML, et al: Rheolytic thrombectomy with use of the Angiojet-F105 catheter: Preclinical evaluation of safety, J Vasc Interv Radiol 8:939–945, 1997. Szilagyi DE, Elliott Jr JP, Smith RF, et al: A thirty-year survey of the reconstructive surgical treatment of aortoiliac occlusive disease, J Vasc Surg 3:421–436, 1986.



Open and Endovascular Treatment of Anastomotic Aneurysms

Open and Endovascular Treatment of Anastomotic Aneurysms after Aortoaortic, Aortoiliac, and Aortofemoral Bypass Misty D. Humphries, Gerald S. Treiman, and Richard L. Treiman

Anastomotic aneurysms result from a disruption of the native artery–to–graft anastomosis. They are characterized by type (true or false), location (aortic, iliac, or femoral), and etiology (mycotic or nonmycotic). The majority are false aneurysms (pseudoaneurysms), with blood extravasation contained by periarterial tissue. True aneurysms can develop as the native artery itself dilates. Retroperitoneal anastomotic aneurysms often lead to life-threatening complications because of potential for rupture, and in the absence of major contraindications to intervention, they should be repaired. Several endovascular and open surgical options exist, but they are often complex and technically challenging.

INCIDENCE The overall incidence of aortic and iliac anastomotic aneurysm formation is likely underestimated by retrospective reviews because long-term graft surveillance is not the standard of care. These aneurysms are usually asymptomatic and, given their retroperitoneal location, are difficult to diagnose with physical examination. Studies using routine ultrasound surveillance to identify anastomotic abdominal aortic aneurysms estimate the incidence somewhere between 5% after 8 years and up to 27% after 15 years. Retrospective data on iliac anastomotic aneurysms estimate the incidence to be 6.3% at 15 years. Femoral anastomotic aneurysms after aortofemoral bypass are c­ ommon, with an incidence in some reports as high as 24% at 15 years.

PATHOPHYSIOLOGY The development of a true or false anastomotic aneurysm is influenced by the indication for the initial arterial reconstruction. Patients treated for aneurysmal disease are more likely to develop true anastomotic aneurysms than patients treated for occlusive disease. In a study of 49 true anastomotic aneurysms, histologic evaluation of 28 resected arterial segments showed degeneration, with replacement of the media smooth muscle with acellular fibrous connective tissue, decrease or absence of elastic fibers, and hyaline degeneration of the adventitia. Patients with the connective tissue disorders Ehlers–Danlos syndrome, α1-antitrypsin deficiency, and Marfan’s syndrome or with systemic vasculitis such as Beçhet’s or Takayasu’s arteritis are

439

predisposed to develop true anastomotic aneurysms owing to abnormalities of the native arterial wall. Technical factors contributing to the development of anastomotic aneurysms include creation of the anastomosis in residual aneurysmal tissue, use of an oversized graft in relation to native arteries, endto-side anastomosis, use of a Dacron graft, and endarterectomy of the arterial wall. Several etiologies have been proposed for the development of anastomotic false aneurysms. Historically, the use of braided or silk suture was thought to be the main factor in their development. As an antigenic material, these sutures elicited an inflammatory response that destroys the suture over time. Widespread use of monofilament suture has made such an event no longer an issue. Other suggested causes of pseudoaneurysm formation include suture failure from overmanipulation or knotting, aggressive arterial wall endarterectomy, mismatch in the compliance of the vessel and graft, graft dilation, and, most importantly, infection. Occult infection as a nidus of anastomotic aneurysms, especially of the femoral arteries, is commonly underestimated. After repair of 45 femoral pseudoaneurysms with no clinical sign of infection, 60% of the resected prosthetic graft specimens cultured were found to be positive for Staphylococcus species. Others have found graft infection rates as high as 80% after repair. The incidence of infection is unknown because microbiology laboratories often do not subject vascular graft material to ultrasonication to separate bacteria from the interstices of the material before culture. This likely led to erroneous reports of negative culture results. A postoperative wound infection with complete healing has been shown to increase the relative risk of femoral pseudoaneurysm formation by ninefold at 5 years.

PRESENTATION Anastomotic aneurysms have been diagnosed as early as a few months and as late as 23 years postoperatively. Allen found that 35% presented within 5 years. Factors associated with early d ­ evelopment of anastomotic aneurysms are connective tissue disorders and graft infection. True aneurysms tend to occur late owing to the time needed for continued arterial wall degradation or graft material dilation. The mean time for development of all anastomotic aneurysms is approximately 8 years. Although aortic and iliac anastomotic aneurysms are often asymptomatic, when symptoms develop, they are often insidious and include nonspecific abdominal pain, back pain, fatigue, and general malaise. Given their retroperitoneal location, aortic and iliac anastomotic aneurysms can grow to the point of palpation before symptoms develop. Nevertheless, in the largest series of aortic anastomotic aneurysms, 66% were identified in asymptomatic patients by computed tomography (CT) during workup for other conditions. Increased size leads to risk of serious complications, including rupture or erosion into surrounding structures. Retrospective series have reported up to a 10% incidence of aortoenteric graft erosion following development of an aortic anastomotic aneurysm. Patients with aortoenteric fistula often come to the hospital with life-­ threatening gastrointestinal bleeding, and historically the mortality has approached 50%. Endovascular techniques have improved mortality by allowing intraaortic balloon occlusion to provide time for resuscitation and controlled open surgical repair. Femoral anastomotic aneurysms typically manifest as a pulsatile groin mass that may be tender. A bruit or thrill may be present. As the aneurysm grows, patients can develop lower extremity edema or neuropathy from compression of the surrounding femoral vein and nerve. Rarely do these become large enough to rupture, but

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AORTOILIAC OCCLUSIVE DISEASE

development of intraluminal thrombus in the aneurysm can lead to distal embolization, graft limb occlusion, or even acute limb-threatening ischemia. Typically, graft limb occlusion results in symptoms of claudication, with loss of the femoral pulse.

EVALUATION AND DIAGNOSIS Initial evaluation begins with a thorough history and systematic physical examination, including palpation of the abdomen and/or groin for a pulsatile mass, examination of distal pulses, and assessment for distal emboli. Diagnosis of an aneurysm at one anastomosis should prompt evaluation of other graft anastomoses given the 36% incidence of concurrent anastomotic aneurysms. Abdominal duplex scan may be useful in evaluating aortic and iliac anastomotic aneurysms, but its accuracy depends on the ability of the technologist, depth of the vessels, presence of gas in the gastrointestinal tract, and girth of the patient. Limitations of history and physical examination to make the diagnosis, combined with the severity of potential complications of intraabdominal anastomotic aneurysms, have prompted some authors to recommend yearly duplex surveillance even though its cost-effectiveness has not been established. In patients in whom femoral anastomotic aneurysm is suspected, a duplex scan should be the initial diagnostic modality because it is easily obtained, avoids radiation, does not need contrast enhancement, and can accurately determine size and the presence of intraluminal thrombus. Cross-sectional imaging of the aorta and iliac arteries with magnetic resonance angiography (MRA) or CT angiography (CTA) is the mainstay of surgical planning and should be obtained in all patients with confirmed or suspected aortic and iliac anastomotic aneurysms. MRA and CTA can diagnose the presence of the aneurysm, identify surrounding infection, delineate the relationship to surrounding structures, suggest a graft enteric fistula, and help plan operative reconstruction. Both provide detailed information about the relative proximity of the aneurysm to the surrounding arterial branches. Because MRA requires a dedicated radiologist to establish specific protocols and monitor image acquisition, the adequacy of MRA is particularly center-specific. CTA is much more widely available but requires administration of an ionizing contrast agent. The rapid acquisition of CTA also makes it more favorable in cases where hemorrhage or rupture is suspected. Traditional angiography, although rarely needed, may be necessary for operative planning when CT images are obscured by arterial calcification or metallic hardware in the area of a planned intervention. Because angiography can only see the lumen of the vessel, identifying the exact location of the anastomosis may be limited in patients with true aneurysms and intraluminal thrombus. In cases where infection is suspected but not confirmed by cross-sectional imaging, technetium-labeled white blood cell scanning or combined positive emission tomography (PET)/CT may be able to identify an infected anastomotic aneurysm.

OPEN SURGICAL TREATMENT Treatment of all retroperitoneal anastomotic aneurysms is indicated unless the patient has major contraindications to intervention. Mortality from such aneurysms if they rupture approaches 70%. Although few natural history studies are available, progressive enlargement leading to rupture is almost inevitable without intervention. Open surgical repair of aortic and iliac anastomotic aneurysms requires careful preoperative planning and detailed cross-sectional imaging with coronal and sagittal reconstructions. All attempts to rule out infection must be made prior to operative intervention. Operative treatment for graft infection when encountered is best

managed with complete graft excision and in-situ reconstruction or extraanatomic bypass. Either a transabdominal or retroperitoneal approach can be used, with the decision for one exposure over the other based on the surgeon’s discretion. In cases where treatment of concomitant right iliac or femoral anastomotic aneurysms is required, the transabdominal approach allows better exposure. Retroperitoneal exposure is advantageous if the patient has undergone multiple abdominal operations and in cases where the proximal reconstruction might necessitate visceral vessel reimplantation. Visceral patches should be limited in diameter to reduce the risk of aneurysm recurrence. Isolated iliac anastomotic aneurysms may be treated with a retroperitoneal approach as well. When aortic anastomotic aneurysms are treated, the replacement graft is usually sutured in close proximity to the renal arteries, which often necessitates suprarenal or supraceliac aortic clamping for proximal control. In Allen’s series of 29 open reconstructions for anastomotic aortic aneurysms, nine needed supraceliac and two required suprarenal aortic control. The majority were accomplished with infrarenal clamping. If the aneurysmal segment is limited to the aorta, reconstruction can often be accomplished with a tube graft sutured distally to the previous graft. If the anastomotic aneurysm involves iliac arteries, a bifurcated graft must be used. Attempts to preserve the internal iliac artery with reimplantation or a short interposition graft should be made if reasonable to do so. However, these operations are often extensive, with significant blood loss and prolonged lower extremity ischemia. Adjunctive procedures are undertaken only if the patient’s condition allows. Repair of femoral anastomotic aneurysms may be accomplished with resection of the aneurysmal segment (Figure 1) and interposition grafting from the original bypass graft end-to-side to the nondiseased common femoral artery. Alternatively, the proximal common femoral can be ligated with an end-to-end interposition graft reconstruction to the distal common femoral artery. Care should be taken to match the size of the original graft, so typically 8- or 10-mm Dacron or polytetrafluoroethylene (PTFE) grafts are used. If the anastomotic aneurysm extends to the superficial femoral or profunda femoris artery, the femoral bifurcation can be reconstructed with focused effort to preserve the patency of the profunda artery. The most direct way to accomplish this is with creation of an end-to-end interposition graft from the common femoral to the profunda femoris artery, with either reimplantation of the superficial femoral artery or a jump graft to the superficial femoral artery.

ENDOVASCULAR TREATMENT Improvements in technique have made endovascular treatment, when possible, the preferred approach for elective and emergent treatment of aortic and iliac anastomotic aneurysms. The main technical advantage for the surgeon is avoidance of a difficult dissection in a scarred field with a lower incidence of injury to other structures, less hemodynamic instability, and shorter operative time. Need for blood transfusion, postoperative intubation, and intensive care unit stay; postoperative pain; and length of hospitalization are all improved with endovascular repairs. Preoperative planning for endovascular repair begins with contrastenhanced cross-sectional imaging reconstructed in the coronal and sagittal planes. In cases where fenestration or snorkel techniques are being considered, additional reconstructions with centerline measurements are helpful. The initial type of aortic reconstruction determines the endovascular options. Patients with tube graft aortic reconstructions are candidates for bifurcated endoprosthesis placement. Patients with an initial bifurcated open repair likely do not have enough length from the base of the lowest renal artery to the flow divider of the graft to place a commercially available bifurcated endoprosthesis. In these cases, if adequate aortic neck length is present, an aortic cuff can be used to exclude the anastomotic aneurysm. Suprarenal fixation should be considered in all cases of proximal aortic anastomotic aneurysm



Open and Endovascular Treatment of Anastomotic Aneurysms

441

inguinal ligament and the repetitive forces exerted on the artery during ambulation. Stent fracture, migration, and thrombosis are complications that can lead to limb-threatening ischemia. Currently, stent graft insertion for femoral anastomotic aneurysm is only described in case reports of singular instances under unique circumstances and is not advocated in the routine management of these aneurysms.

RESULTS

A

B

C

D

FIGURE 1  Options for reconstruction of a femoral anastomotic an-

eurysm. A, Before resection of the aneurysm. B, After resection of the aneurysm but before reconstruction. C, Reconstruction with ligation of the common femoral artery and end-to-end interposition graft. D, Reconstruction with an end-to-side graft.  (Adapted from Crownenwett and Johnston, Local Complications: Anastamotic Aneurysms, page 682, from Rutherford’s vascular surgery 7th edition, Elsevier, Philadelphia, 2010.)

repair, preventing graft migration and subsequent endoleak that can lead to late aneurysm rupture. If a concomitant iliac anastomotic aneurysm is present, a unilateral aortoiliac device can be used. This requires revascularization of the contralateral side, usually with a femorofemoral bypass graft. Additionally, the hypogastric arteries need to be closely evaluated. Embolization of the hypogastric artery may be required to completely exclude an iliac anastomotic aneurysm and prevent an endoleak. In this event, efforts to preserve the contralateral hypogastric artery should be made to prevent buttock claudication. If the anastomotic aneurysm involves the renal or visceral vessels, a hybrid approach with debranching and aortic endografting may be required. Historically, the procedures have been staged, but the availability of high-quality fixed imaging in the operating room has allowed a single combined operation. The debranching procedure is undertaken first to minimize any ischemic time to the vital organs. Alternatively, a completely endovascular approach using snorkel or endograft fenestration is also possible. Both of these are advanced techniques and should be done with superior fixed imaging by surgeons experienced with endovascular interventions. Common femoral anastomotic aneurysms are rarely amenable to endovascular treatment as a result of the vessel course under the

Recurrence rate after repair of an aortic or iliac anastomotic aneurysm in the largest reported series was 9.5% at 5 years. Factors that predict recurrence include postoperative infection and early development of the initial anastomotic aneurysm. Morbidity and mortality associated with repair of retroperitoneal aneurysms depends of the type and urgency of the repair. Morbidity associated with open elective repair ranges from 17% to 40%. Major complications include limb loss, kidney failure, and intestinal ischemia. Minor complications include transient kidney failure, abdominal dehiscence, and lymphocele development. Endovascular repair, when possible, is preferred because it provides comparable or superior effectiveness with lower morbidity. Thirty-day mortality for open elective repair is approximately 5%, versus 3% after endovascular repair. The incidence of complications associated with endovascular repair of an aortic or iliac anastomotic aneurysm is also less and ranges from 5% to 10%. Most complications are late and include acute graft limb thrombosis, proximal anastomotic disruption, femoral artery pseudoaneurysm after postoperative groin infection, graft infection, and proximal type I endoleak. In the largest series of endovascular repair, 6% of patients developed a proximal type I endoleak. The majority of these patients required subsequent open surgical repair because of limited proximal neck length, and the mortality rate was 66%. Five-year patency after open repair of femoral anastomotic aneurysms is 85%, with a recurrence rate of 1.9% per year. Studies to identify predictors of recurrence have shown continued smoking and postoperative wound infection to be the greatest risk factors. Femoral anastomotic aneurysm repair is associated with a morbidity of 7.6% and a mortality of 2%.

Selected References Allen RC, Schneider J, Longenecker L, et al: Paraanastamotic aneurysms of the abdominal aorta, J Vasc Surg 18:424–432, 1993. Dardik A, Perler BA, Roseborough GS, et al: Aneurysmal expansion of the visceral patch after thoracoabdominal aortic replacement: An argument for limiting patch size? J Vasc Surg 34:405–410, 2001. Gawenda M, Zaehringer M, Brunkwall J: Open versus endovascular repair of para-anastomotic aneurysms in patients who were morphological candidates for endovascular treatment, J Endovasc Ther 10:745–751, 2003. Hallet JW, Marshall DM, Petterson TM, et al: Graft Related complications after abdominal aortic aneurysm repair: Reassurance from a 36 year population-based experience, J Vasc Surg 25:277–284, 1997. Sachdev U, Baril DT, Morrissey NJ, et al: Endovascular repair of para-anastamotic aortic aneurysms, J Vasc Surg 46:636–641, 2007. Seabrook GR, Schmitt DD, Bandyk DF, et al: Anastomotic femoral pseudoaneurysm: An investigation of occult infection as in etiologic factor, J Vasc Surg 11:629–634, 1990. Skourtis G, Bountouris I, Papacharalambous G, et al: Anastomotic pseudoaneurysms: Our experience with 49 cases, Ann Vasc Surg 20:582–589, 2006. Yasuda K, Murashita T, Takigami T, et al: Experience of reoperations followed by repairs of abdominal aortic aneurysms, Rinsho Kyobu Geka 14:480–485, 1994. Ylönen K, Biancari F, Leo E, et al: Predictors of development of anastomotic femoral pseudoaneurysms after aortobifemoral reconstruction for abdominal aortic aneurysm, Am J Surg 187:83–87, 2004.

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Combined Laparoscopic and Endovascular Treatment of Aortic Diseases Ralf R. Kolvenbach

Endoleaks, endotension, and graft migration are the major problems of endovascular aneurysm repair (EVAR) when treating abdominal aortic aneurysms (AAAs). There are patients with endotension and aneurysms that increase in diameter without any evidence of patent lumbar arteries or a patent inferior mesenteric artery (IMA). Endovascular coiling of patent lumbar arteries or of the IMA is cumbersome, often requiring several treatment sessions by experienced interventionists. Laparoscopy offers a minimal invasive and expeditious alternative to graft explantation as well as to the time-consuming endovascular approach to treat type II endoleaks and endotension. Laparoscopic treatment options for patients with endograft complications include clipping of the IMA and of lumbar arteries to treat type II leaks, laparoscopic downsizing of large aneurysms, laparoscopy-guided direct vascular access, and total laparoscopic conversion after failed EVAR and laparoscopy to facilitate complex total laparoscopic aortic procedures. Laparoscopic techniques can be used to treat patients with type II endoleaks after EVAR. Lumbar arteries as well as the IMA can be occluded with clips. Yet the major advantage is that the aneurysm after EVAR can be remodeled laparoscopically. For example, the thrombus can be removed, which permits wrapping of the endograft as in a Creech procedure. Considering that thrombus is not an inert substance but a place for macrophages generating free oxygen radicals, which further weaken the aortic wall, the removal of thrombus material as occurs in open surgery can potentially enhance graft incorporation. Using special suturing techniques, the endoprosthesis

can be attached to the aortic wall, preventing graft migration. This can be combined with a banding procedure to enlarge the landing zone and to prevent neck dilatation.

OPERATIVE TECHNIQUE A pneumoperitoneum is established and the abdomen is inspected. A transperitoneal retrocolic access combined with medial mobilization of the left kidney is preferred (Figure 1). Alternatively, the left kidney can be left in situ. For more complex total laparoscopic operations like conversion after EVAR, up to eight trocars are required. The retrorenal access described permits complete transperitoneal exposure of the abdominal aorta and, when necessary, suprarenal clamping. When an endograft has been in place for several months, there is quite often a dense inflammatory retroperitoneal reaction. In very rare cases under these circumstances a transperitoneal approach must be chosen. The origin of the IMA is identified and the artery is divided between clips. When clips are too small to safely occlude the IMA, a vascular stapler is used. This facilitates further mobilization of the aorta. The aneurysm and the aortic neck are identified. As many lumbar arteries as are accessible are clipped on the left side of the aorta. Because access to the right-sided lumbar arteries is often very difficult because of the inflammatory changes, we now prefer a more direct approach, stitching lumbar arteries from inside as is done during open surgery.

LAPAROSCOPIC REMODELLING OF THE AORTA AFTER ENDOVASCULAR ANEURYSM REPAIR The principal laparoscopic steps are performed without clamping the aorta because this would damage the endograft. Instead, transfemorally under fluoroscopic guidance, an aortic balloon occlusion catheter is introduced from the groin through a hemostatic sheath. This balloon is inflated before the sac of the aneurysm is incised to stabilize the graft inside the aorta. The balloon is inflated to prevent dislodging the endograft when taking out the thrombus.

FIGURE 1  Transperitoneal medial visceral ­rotation.

The spleen is left in situ and the left kidney is mobilized medially. The patient is placed on a beanbag, which permits an almost 90-degree right decubital position.



Combined Laparoscopic and Endovascular Treatment of Aortic Diseases

443

repair, like the placement of extension cuffs or angioplasty as well as graft limb thrombectomy. Another contraindication are patients with a hostile abdomen, in whom laparoscopic exposure of the retroperitoneum cannot be accomplished. Hybrid techniques can facilitate complex total laparoscopic procedures. Total laparoscopic techniques can be used to perform more complex operations like conversion after failed stent graft exclusion, using balloon catheters to prevent back bleeding from iliac arteries. If necessary, transfemorally placed balloons can be inserted through hemostatic 11-Fr sheaths that are placed percutaneously over the wire through the abdominal wall into the peritoneal cavity. This technique avoids gas loss and permits direct and rapid access to the iliac arteries. Laparoscopic conversion after stent graft placement is facilitated by leaving part of the iliac extensions in place and by suturing the Dacron graft to the remnants of the stent graft.

LAPAROSCOPY-ASSISTED THORACIC ENDOVASCULAR ANEURYSM REPAIR

FIGURE 2 An H-shaped incision of the sac of the abdominal aortic

aneurysm after endovascular repair to remove the thrombus and to obtain access to the lumbar arteries.

FIGURE 3  Laparoscopic inspection of the endograft after evacuation

of thrombus material.

The sac of the aneurysm is incised and opened with laparoscopic scissors in an H-shaped configuration (Figure 2). The graft is inspected using the magnification of the 30-degree endoscope to exclude any damage of the fabric or stents. Laparoscopic graspers and a 10-mm suction–irrigation device are used to remove the thrombus material. Patent lumbar arteries are stitched from within using Vicryl sutures. The surgeon is standing on the right side of the patient. In addition to these steps, bioglues can be injected into the sac of the aneurysm to accelerate graft incorporation and to prevent any backbleeding from the lumbar arteries (Figure 3). With a laparoscopic running suture (2–0 Prolene), the sac of the aneurysm is closed, wrapping the aorta tightly around the endograft.

EXCLUSION CRITERIA FOR LAPAROSCOPIC REMODELING AFTER ENDOVASCULAR ANEURYSM REPAIR Laparoscopic remodeling should not be used in cases with extensive graft migration, even with the balloon catheter in place. However, this technique has been used in combination with endovascular

Limitations of thoracic endografting include the anatomic morphology of the aneurysm and tortuous or stenotic access arteries. The femoral artery is the most commonly used access vessel, but the common iliac artery or abdominal aorta can be used in case of anatomic problems. The 21- to 22-Fr introducer sheaths make deployment in patients with aortoiliac occlusive disease often difficult or impossible. An extra-anatomic exposure of the aorta or iliac arteries significantly increases the invasiveness of the procedure. The intent is to use a regular bypass graft as a conduit to obtain a safe and durable access to the iliac arteries or to the aorta as well as a bypass graft to treat the occlusive disease. This could easily be accomplished by tunneling the Dacron graft to the groin and subsequently performing an anastomosis with the femoral artery after introducing the stent graft. A maximum number of six ports are required in this setting to expose the aorta or the iliac artery (Figures 4 and 5). In these cases the Dacron graft was exteriorized (Figure 6) with a 10-mm preclotted graft (see Figure 5). Two running sutures secured at the end with a felt pledget, as described by Coggia, are used to perform the anastomosis. At the end of the procedure, after the graft is deployed the graft is tunneled to the groin and anastomosed with the femoral artery. For thoracic endograft deployment, the Dacron graft may be assessed with a 5-Fr sheath after direct puncture and a superstiff wire placed in the ascending aorta. The patient is repositioned, and C-arm fluoroscopy was used to obtain multiple oblique angles of the proximal landing zone. Without removing the trocars, the endograft is inserted through the Dacron graft and deployed. Simultaneously passage of the graft through the anastomosis is controlled with the laparoscopic camera. After deployment of the thoracic endograft, the Dacron prosthesis is cut to length, and after tunneling to the groin, the distal anastomosis with the femoral artery is performed. Totally laparoscopic assisted graft implantation in aorta or iliac arteries provides a safe and effective access for the endovascular delivery system.

RESULTS OF HYBRID PROCEDURES AND LAPAROSCOPIC TECHNIQUES AFTER ENDOVASCULAR ANEURYSM REPAIR Indication for a laparoscopic hybrid procedure is an increase of the aortic diameter after EVAR or a failure of the aneurysm to shrink in patients with aneurysms larger than 6 cm in diameter. In all cases, type I endoleaks were ruled out before we undertook a laparoscopic procedure.

444

AORTOILIAC OCCLUSIVE DISEASE

80°

Dacron graft FIGURE 4  Intraoperative arrangement of trocars

for deployment in a total laparoscopic-assisted thoracic endovascular aneurysm repair.

FIGURE 6 Dacron graft was exteriorized.

DISCUSSION FIGURE 5  Laparoscopic end-to-side anastomosis of a 10-mm

­Dacron graft with the left iliac artery.

During the mean follow-up period of 36 months after the laparoscopic procedure, we have not detected further increase in aneurysm diameter. In all cases, at the grafts were found intact at surgery. There was always a substantial decrease of the diameter of the AAA after intraluminal thrombus was removed laparoscopically. There have been no major complications and no graft dislodgement when incising the sac of the AAA as a result of the standardized approach with transfemoral balloon insertion. We have not had to cross clamp the infrarenal aorta in either case. It was easier to clip lumbar arteries on the left side compared to the right side

In open surgery, aortic thrombus is removed to enhance incorporation of the Dacron graft into the aortic wall; this is a proven technique with outstanding long-term results. The amount of thrombus can play a role, particularly in large aneurysms with a diameter larger than 6 cm. Thrombus is not an inert substance. Macrophages generating oxygen free radicals in the canaliculi of the intraluminal thrombus can cause further degeneration of the aortic wall by enhancing tissue hypoxia. Thrombus transmits pressure that can further complicate the differentiation between type II endoleaks and endotension. Theoretically there is a fear that removal of thrombus can weaken the outer shell of the aneurysm. However, in cases with endotension in patients with an aneurysm that has increased in diameter, partial wrapping of the endograft has accelerated incorporation of the graft and prevented migration of the device. The indication for treating type II endoleaks is not yet absolutely clear. The intraoperative injection of contrast dye into the sac of the



Abdominal Aortic Coarctation and Hypoplasia

aneurysm after graft deployment as well as a delayed contrast computed tomography (CT) or modern pressure-sensor technology might define who is a suitable candidate for a laparoscopic postinterventional exploration. EVAR replaces open surgery in most aneurysm cases, and as a consequence there is an increasing demand for repair techniques to improve long-term performance of aortic endografts. Hybrid techniques combining laparoscopy and endovascular procedures can offer an all–minimally invasive approach to most patients. Patients who are primarily treated using a laparoscopic assisted or total approach also benefit from a combination of endovascular and videoendoscopic hybrid procedures.

THE ROLE OF LAPAROSCOPIC AORTIC SURGERY The reasons to pursue laparoscopic interventions are inferior durability of endovascular therapy compared with open repair and the need for lifelong surveillance and frequent reinterventions, although endovascular interventions remain an easier, less invasive, and safe alternative to laparoscopic interventions. Compared with laparoscopic repair of AIOD, laparoscopic repair of aneurysms is more involved and technically demanding. Some patients, however, are unsuitable for EVAR owing to neck anatomy and vascular access limitations. These patients can benefit from the minimally invasive aspect and durable results of laparoscopic repair. Questions remain despite the demonstrated safety and feasibility of laparoscopic surgery. The reports in the literature are from centers and surgeons who have a dedicated interest in laparoscopic surgery, and for the most part, the patients being treated are carefully selected. The data are observational, noncomparative, and prone to selection bias. Although there are reports of reduced hospital stay, decreased pain, and earlier ambulation and resumption of diet, there are technical difficulties that must be overcome and a need for reliable data before wide implementation of these techniques can be justified by the majority of vascular surgeons. The role that laparoscopic surgery will play in vascular surgery must be determined in the context of randomized clinical trials. At

Abdominal Aortic Coarctation and Hypoplasia James C. Stanley, Dawn M. Coleman, and Jonathan L. Eliason

Focal developmental narrowings of the distal thoracic and abdominal aorta are rare anomalies accounting for less than 2% of all aortic coarctations. Most physicians have limited experience with the management of these unusual lesions. Abdominal aortic coarctations are categorized by the most superior extent of the aortic narrowing. Among these aortic coarctations, 69% are suprarenal (Figure 1). Narrowings originating in the intrarenal aorta occur in 23% of patients (Figure 2) and in the infrarenal aorta in 8% of patients (Figure 3). Diffuse involvement of the entire abdominal aorta is usually classified in the suprarenal category (Figure 4).

445

present, it is not realistic to believe that laparoscopic surgery will be widely adopted and implemented by the vascular surgical community because of other alternatives that are easier to perform and have a low morbidity. The potential to avoid the cost and inconvenience of lifelong surveillance that is required to monitor and address complications that develop following endovascular interventions is enticing. New laparoscopic instruments and technology that make intracorporeal suturing, hemostasis, and clamping easier are needed to help spur continued interest in laparoscopic vascular surgery and facilitate performance of these techniques by more vascular surgeons.

Selected References Coggia M, DiCenta I, Javerliat I, et al: Total laparoscopic aortic surgery: Transperitoneal left retrorenal approach, Eur J Vasc Endovasc Surg 28:619–622, 2004. Dion Y-M, Gracia CR: A new technique for laparoscopic aortobifemoral grafting in occlusive aortoiliac disease, J Vasc Surg 26:685–692, 1997. Dion Y-M, Gracia CR, Ben El Kadi HH: Totally laparoscopic abdominal aortic aneurysm repair, J Vasc Surg 33:181–185, 2001. Edoga JK, Asgarian K, Singh D, et al: Laparoscopic surgery for abdominal aortic aneurysm: Technical elements of the procedure and a preliminary report of the first 22 patients, Surg Endosc 12:1064–1072, 1998. Kolvenbach R, Pinter L, Raghunandan M, et al: Laparoscopic remodeling of abdominal aortic aneurysm after endovascular exclusion: A technical description, J Vasc Surg 36:1267–1270, 2002. Kolvenbach R, Schwierz E, Wasilljew S, et al: Total laparoscopically and robotically assisted aortic aneurysm surgery: A critical evaluation, J Vasc Surg 39:771–776, 2004. Lee JT, Lee J, Aziz I, et al: Stent-graft migration following endovascular repair of aneurysm with large proximal necks: anatomical risk factors and long-term sequelae, J Endovasc Ther 9:652–664, 2002. Piergiorgio C, Verzini F, Zannetti S, et al: Device migration after endoluminal abdominal aortic aneurysm repair: Analysis of 113 cases with a minimum follow up period of 2 years, J Vasc Surg 35:229–235, 2002. Veith FJ, Baum RA, Ohki T, et al: Nature and significance of endoleaks and endotension: Summary of opinions expressed at an international conference, J Vasc Surg 35:1029–1035, 2002. Wisselink W, Cuesta AM, Berends FJ, et al: Retroperitoneal endoscopic ligation of lumbar and inferior mesenteric arteries as a treatment of persistent endoleak after endoluminal aortic aneurysm repair, J Vasc Surg 31:1240–1244, 2000.

Aortoiliac hypoplasia occurs in a distinct subgroup of patients, mostly younger women, with atherosclerosis often affecting the narrowed aorta and iliac arteries. In fact, approximately 2% of women with arteriosclerotic aortoiliac occlusive disease manifest this entity. Regardless of the particular nomenclature used, most evidence suggests that both aortic coarctation and aortoiliac hypoplasia represent a spectrum of developmental abnormalities. Variations in their clinical presentation relate more to different anatomic locations and secondary pathologic events than the underlying etiologic differences. An exception exists with aortic narrowings caused by an inflammatory aortoarteritis such as occurs in Takayasu’s syndrome, in which other systemic manifestations may be more prominent than the vascular symptoms.

ETIOLOGY The most widely accepted hypothesis as to the cause of the developmental narrowings relates to abnormal fetal events, including faulty fusion of the two primitive dorsal aortas during intrauterine life. Indirect evidence in support of this is derived from the fact that multiple renal arteries occur in 70% of patients with narrowings of the midabdominal aorta. This is two to three times the expected



Abdominal Aortic Coarctation and Hypoplasia

aneurysm after graft deployment as well as a delayed contrast computed tomography (CT) or modern pressure-sensor technology might define who is a suitable candidate for a laparoscopic postinterventional exploration. EVAR replaces open surgery in most aneurysm cases, and as a consequence there is an increasing demand for repair techniques to improve long-term performance of aortic endografts. Hybrid techniques combining laparoscopy and endovascular procedures can offer an all–minimally invasive approach to most patients. Patients who are primarily treated using a laparoscopic assisted or total approach also benefit from a combination of endovascular and videoendoscopic hybrid procedures.

THE ROLE OF LAPAROSCOPIC AORTIC SURGERY The reasons to pursue laparoscopic interventions are inferior durability of endovascular therapy compared with open repair and the need for lifelong surveillance and frequent reinterventions, although endovascular interventions remain an easier, less invasive, and safe alternative to laparoscopic interventions. Compared with laparoscopic repair of AIOD, laparoscopic repair of aneurysms is more involved and technically demanding. Some patients, however, are unsuitable for EVAR owing to neck anatomy and vascular access limitations. These patients can benefit from the minimally invasive aspect and durable results of laparoscopic repair. Questions remain despite the demonstrated safety and feasibility of laparoscopic surgery. The reports in the literature are from centers and surgeons who have a dedicated interest in laparoscopic surgery, and for the most part, the patients being treated are carefully selected. The data are observational, noncomparative, and prone to selection bias. Although there are reports of reduced hospital stay, decreased pain, and earlier ambulation and resumption of diet, there are technical difficulties that must be overcome and a need for reliable data before wide implementation of these techniques can be justified by the majority of vascular surgeons. The role that laparoscopic surgery will play in vascular surgery must be determined in the context of randomized clinical trials. At

Abdominal Aortic Coarctation and Hypoplasia James C. Stanley, Dawn M. Coleman, and Jonathan L. Eliason

Focal developmental narrowings of the distal thoracic and abdominal aorta are rare anomalies accounting for less than 2% of all aortic coarctations. Most physicians have limited experience with the management of these unusual lesions. Abdominal aortic coarctations are categorized by the most superior extent of the aortic narrowing. Among these aortic coarctations, 69% are suprarenal (Figure 1). Narrowings originating in the intrarenal aorta occur in 23% of patients (Figure 2) and in the infrarenal aorta in 8% of patients (Figure 3). Diffuse involvement of the entire abdominal aorta is usually classified in the suprarenal category (Figure 4).

445

present, it is not realistic to believe that laparoscopic surgery will be widely adopted and implemented by the vascular surgical community because of other alternatives that are easier to perform and have a low morbidity. The potential to avoid the cost and inconvenience of lifelong surveillance that is required to monitor and address complications that develop following endovascular interventions is enticing. New laparoscopic instruments and technology that make intracorporeal suturing, hemostasis, and clamping easier are needed to help spur continued interest in laparoscopic vascular surgery and facilitate performance of these techniques by more vascular surgeons.

Selected References Coggia M, DiCenta I, Javerliat I, et al: Total laparoscopic aortic surgery: Transperitoneal left retrorenal approach, Eur J Vasc Endovasc Surg 28:619–622, 2004. Dion Y-M, Gracia CR: A new technique for laparoscopic aortobifemoral grafting in occlusive aortoiliac disease, J Vasc Surg 26:685–692, 1997. Dion Y-M, Gracia CR, Ben El Kadi HH: Totally laparoscopic abdominal aortic aneurysm repair, J Vasc Surg 33:181–185, 2001. Edoga JK, Asgarian K, Singh D, et al: Laparoscopic surgery for abdominal aortic aneurysm: Technical elements of the procedure and a preliminary report of the first 22 patients, Surg Endosc 12:1064–1072, 1998. Kolvenbach R, Pinter L, Raghunandan M, et al: Laparoscopic remodeling of abdominal aortic aneurysm after endovascular exclusion: A technical description, J Vasc Surg 36:1267–1270, 2002. Kolvenbach R, Schwierz E, Wasilljew S, et al: Total laparoscopically and robotically assisted aortic aneurysm surgery: A critical evaluation, J Vasc Surg 39:771–776, 2004. Lee JT, Lee J, Aziz I, et al: Stent-graft migration following endovascular repair of aneurysm with large proximal necks: anatomical risk factors and long-term sequelae, J Endovasc Ther 9:652–664, 2002. Piergiorgio C, Verzini F, Zannetti S, et al: Device migration after endoluminal abdominal aortic aneurysm repair: Analysis of 113 cases with a minimum follow up period of 2 years, J Vasc Surg 35:229–235, 2002. Veith FJ, Baum RA, Ohki T, et al: Nature and significance of endoleaks and endotension: Summary of opinions expressed at an international conference, J Vasc Surg 35:1029–1035, 2002. Wisselink W, Cuesta AM, Berends FJ, et al: Retroperitoneal endoscopic ligation of lumbar and inferior mesenteric arteries as a treatment of persistent endoleak after endoluminal aortic aneurysm repair, J Vasc Surg 31:1240–1244, 2000.

Aortoiliac hypoplasia occurs in a distinct subgroup of patients, mostly younger women, with atherosclerosis often affecting the narrowed aorta and iliac arteries. In fact, approximately 2% of women with arteriosclerotic aortoiliac occlusive disease manifest this entity. Regardless of the particular nomenclature used, most evidence suggests that both aortic coarctation and aortoiliac hypoplasia represent a spectrum of developmental abnormalities. Variations in their clinical presentation relate more to different anatomic locations and secondary pathologic events than the underlying etiologic differences. An exception exists with aortic narrowings caused by an inflammatory aortoarteritis such as occurs in Takayasu’s syndrome, in which other systemic manifestations may be more prominent than the vascular symptoms.

ETIOLOGY The most widely accepted hypothesis as to the cause of the developmental narrowings relates to abnormal fetal events, including faulty fusion of the two primitive dorsal aortas during intrauterine life. Indirect evidence in support of this is derived from the fact that multiple renal arteries occur in 70% of patients with narrowings of the midabdominal aorta. This is two to three times the expected

446

AORTOILIAC OCCLUSIVE DISEASE

A

B

FIGURE 1  A, Suprarenal abdominal aortic coarctation (bracket) with superior mesenteric artery stenosis (arrow). B, Bilateral renal artery ostial stenosis (arrows). Note common trunk of lower lumbar artery (arrow). Preoperative computed tomography angiography, anterior and posterior projections, respectively.  (From Stanley JC, Criado E, Eliason JL, et al: Abdominal aortic coarctation: Surgical treatment of 53 patients with a thoracoabdominal bypass, patch aortoplasty, or interposition aortoaortic graft, J Vasc Surg 48:1073–1082, 2008).

FIGURE 3  Infrarenal abdominal aortic coarctation (arrows).  (From

Stanley JC, Wakefield TW: Arterial fibroplasia. In Rutherford RB (ed): Vascular surgery, 3rd ed, Philadelphia, 1989, WB Saunders, pp 245–265.)

FIGURE 2  Intrarenal abdominal aortic coarctation with bilateral

artery stenosis). Preoperative aortogram.  (From Stanley JC, Criado E, Eliason JL, et al: Abdominal aortic coarctation: Surgical treatment of 53 patients with a thoracoabdominal bypass, patch aortoplasty, or interposition aortoaortic graft, J Vasc Surg 48:1073–1082, 2008). FIGURE 4  Diffuse aortic hypoplasia extending from the level of the

incidence of multiple renal arteries in the general population. The basis for this is complex. During normal development in most embryos, fusion of the paired dorsal aortas occurs simultaneously with regression of all but one dominant metanephric vessel to each kidney around day 25 of embryonic life. It is speculated that development of a single renal artery to each kidney occurs because of its obligate hemodynamic advantage over adjacent metanephric vessels. By creating local blood flow disturbances with an aortic fusion abnormality, this obligate hemodynamic advantage is lost and additional metanephric channels persist. Support for an overfusion of the two aortas comes from the finding of a single bifurcating distal lumbar artery in up to 55% of

celiac artery to the infrarenal aorta. Severe renal arterial occlusive disease is most apparent, affecting the ostial of two left renal arteries.  (From Graham LM, Zelenock GB, Erlandson EE, et al: Abdominal aortic coarctation and segmental hypoplasia, Surgery 86:519–529, 1979; with permission).

patients with abdominal aortic coarctations and aortoiliac hypoplasia (see Figure 1), compared to less than 5% in normal persons. Multiple renal arteries are less likely to develop when the aortic coarctation is distant from the central abdominal aorta. Theoretically, any event that alters the normal transition or organization of fetal mesenchymal cells into vascular smooth muscle can result in narrowing of the aorta as well as splanchnic and renal



Abdominal Aortic Coarctation and Hypoplasia

FIGURE 5  A, Suprarenal coarctation (bracket) with superior mesenteric artery stenosis (arrow). Preoperative magnetic resonance angiography (MRA). B, Thoracoabdominal bypass (broad arrow) with aortic implantation of the superior mesenteric artery (arrow). Postoperative computed tomography angiography.  (From Stanley JC, Criado E, Eliason JL, et al: Abdominal aortic coarctation: Surgical treatment of 53 patients with a thoracoabdominal bypass, patch aortoplasty, or interposition aortoaortic graft, J Vasc Surg 48:1073– 1082, 2008).

A

arterial stenoses. This might explain the existence of aortic coarctation or hypoplasia following cytocidal viral infections such as gestational rubella. A genetic alteration in the growth and development of vascular smooth muscle has also been implicated in abdominal aortic coarctation and hypoplasia associated with neurofibromatosis 1 and Williams syndrome. Coincident with the aortic narrowings in patients with Williams syndrome are the common occurrence of renal and splanchnic arterial narrowings. These arteries at their aortic origins are truly diminutive. It is more than happenstance that among our patients with midabdominal aortic narrowings, renal arterial stenoses were seen in 87% and splanchnic arterial occlusive disease in 62%.

CLINICAL MANIFESTATIONS Developmental narrowings of the distal thoracic and midabdominal aorta generally become evident during the first or second decade of life, with a mean age at initial diagnosis of 12 years. There appears to be a slight male gender predilection. The classic triad in these young patients consists of severe hypertension, diminished or absent femoral pulses, and an abdominal bruit. Symptomatic lower extremity ischemia and intestinal angina affect less than 10% of these children. The natural history of patients with developmental narrowings of the more cephalic abdominal aorta above the renal vessels is directly related to the severity of their renin-mediated hypertensive vascular disease. The prognosis for untreated patients is dismal, and most patients die in early adulthood from cardiac failure or cerebrovascular accidents. In one earlier review, 55% of untreated patients died at a mean age of 34 years. Thus, all patients with coarctation or segmental hypoplasia of the distal thoracic or central abdominal aorta must be considered at risk for serious complications of their disease. Infrarenal abdominal aortic narrowings, unlike those above the renal arteries, usually become symptomatic in the fourth or fifth decade of life as a result of secondary atherosclerotic occlusive disease. These patients often come to the hospital with lower extremity fatigue and less often with claudication. There is a generally recognized predilection for women to exhibit hypoplastic aortoiliac narrowings. Although the genetic basis for this phenomenon is unknown, anecdotal evidence suggests a higher incidence among women with red hair. Their usual presentation is lower extremity claudication.

447

B

MANAGEMENT The surgical approach to these complex developmental anomalies must be individualized, based on the aortic pathology, the extent of renal and splanchnic arterial disease, and the patient’s age. A singlestaged reconstruction is currently favored if both aortic and visceral artery reconstructions are needed. Such will avoid the technical difficulties that can accompany secondary operations at a later time. Extensive anatomic exposure of the distal thoracic and midabdominal aorta is essential to achieve an optional vascular reconstruction. Exposure of the supraceliac aorta is facilitated by a thoracoabdominal incision through the left sixth or seventh intercostal space. This incision is generally extended from the left posterior axillary line across the costal margin, either to the right of the umbilicus or along the midline to the suprapubic region. In other cases where only the central abdominal aorta needs exposure, a transverse supraumbilical abdominal incision extended laterally to the midaxillary lines is combined with medial rotation of the viscera. This approach is preferred to a midline incision and transmesenteric approach. Prior to aortic clamping, systemic anticoagulation is achieved with intravenous heparin sodium (150 U/kg), and a diuresis is established with the administration of intravenous mannitol before interrupting renal blood flow. Thoracoabdominal bypasses are necessary when the coarcted segment of aorta is too small to accommodate a patch reconstruction. In these cases, an expanded polytetrafluoroethylene (ePTFE) prosthesis is preferred over a Dacron prosthesis. Dacron grafts exhibit a propensity to undergo aneurysmal dilation after long periods of implantation. Such has not been observed with ePTFE prostheses. These procedures are often performed in conjunction with renal and splanchnic arterial revascularizations (Figure 5). The proximal aortic anastomosis above the level of the coarctation is constructed first, in an end-to-side fashion using a continuous cardiovascular suture. The bypass graft is then occluded and the aortic clamps are removed to restore flow through the native aorta, following which the graft is tunneled through the posterior hemidiaphragm behind the left kidney to the level of the infrarenal aorta. The distal end-to-side aortic anastomosis is subsequently constructed in a fashion similar to the proximal anastomosis. In younger patients the graft diameter should be chosen to be as big as possible, short of being so large that excessive luminal thrombus

448

AORTOILIAC OCCLUSIVE DISEASE

would accumulate. The intent is always to oversize grafts compared to the aorta, with anticipated growth potentially resulting a in a graft that otherwise may be too small to maintain normal distal pressures and flow. In the ideal circumstance, one should use a graft whose size would not represent an energy-consuming constriction as the patient grows into maturity. This means having a conduit at least 60% or 70% the size of the predicted adult aorta. This translates into using 8- to 12-mm grafts in young children, 12- to 16-mm grafts for early adolescents, and 14- to 20-mm grafts in late adolescents and adults. In the very young child, use of large conduits might not be possible. In these cases a second aortic reconstruction will be required later. Graft length is a nonissue in older children and adolescents, with axial growth from the diaphragm to pelvis being minimal after age 9 or 10 years in late childhood. An aortoplasty employing an ePTFE patch, combined with bypass or direct aortic reimplantation of the normal splanchnic or renal arteries beyond their diseased segments, is preferred in treating younger patients whenever feasible (Figure 6). In these patients the aorta and its visceral branches are controlled and the patch is sewn into place before undertaking the renal or splanchnic arterial reimplantations. Performing patch aortoplasty before branch artery revascularization can limit kinking or tension that could occur if branches are revascularized first, followed by the patch, which could rotate or distort the aortic segment from which the revascularized branches arise. The patch, as is the case with bypass grafts, should be generous enough to accommodate normal growth without causing a restenosis but not so large as to accumulate mural thrombus that might embolize. In female patients with symptomatic infrarenal aortoiliac hypoplasia complicated by arteriosclerosis, medical management should center around arteriosclerotic risk factor reduction. The primary goal of operative therapy in this subgroup of patients is improvement of lower extremity perfusion and alleviation of disabling intermittent claudication. Percutaneous transluminal angioplasty is often the primary intervention in these cases, but success may be limited as a result of the unyielding nature of the vascular hypoplasia. Intraluminal stents can obviate certain of these failures. Aortofemoral bypass is generally considered the operative treatment of choice in these patients. Bifurcated ePTFE grafts are preferred for these reconstructions. A proximal end-to-end aortic-to-graft anastomosis is favored. The distal femoral artery anastomoses are constructed in

a conventional end-to-side manner. An aortoiliac endarterectomy with a patch closure may be successful in treating limited narrowings affecting the distal aorta in carefully selected patients. Current endovascular technologies appear to allow the safe treatment of focal and weblike aortic stenoses remote from the splanchnic and renal arteries. Stenting is usually required to overcome the rigidity of these hypoplastic and highly fibrotic aortic narrowings. Unfortunately, balloon dilation with placement of stents in this subset of patients may be followed by early restenosis caused by proliferative neointimal hyperplasia. This is particularly relevant in young women and children. One must remain cautious at accepting the long-term benefits of endoluminal treatment of abdominal aortic coarctation, except in adults or late adolescents having very focal narrowings distant from their splanchnic and renal arteries. Given the high incidence with which these visceral arteries are affected in abdominal aortic coarctation, especially in the younger, growing patient, the number of these coarctations amenable to endovascular repair are likely to be limited. No role exists for long-term medical management of patients with severe hypertension secondary to developmental narrowings of the distal thoracic and midabdominal aorta. Conventional drug interventions for control of hypertension have been mostly unsuccessful, and angiotensin-converting enzyme inhibitors have potentially deleterious effects on kidney function in these patients.

RESULTS Surgical treatment of midabdominal aortic coarctation and hypoplasia provides excellent results. At the University of Michigan Medical Center, more than 70 patients with abdominal aortic coarctations have undergone a thoracoabdominal bypass or patch aortoplasty, often combined with visceral arterial reconstructions. Excellent results were obtained in more than 90% of patients treated for these developmental aortic lesions. There have been no operative deaths in this experience. It is important to recognize that these complex reconstructions can require reoperation, as occurred in nearly 10% of our series, with half related to the predicted inadequacy of the original operation as the child grew and the remainder a result of the narrowing of the aortic–graft anastomosis, except for one case of aneurysmal changes

FIGURE 6  A, Suprarenal coarcta-

A

B

tion (bracket) with bilateral renal artery ostial stenosis. Preoperative magnetic resonance angiography. B, Patch aortoplasty (broad arrow) with aortic diameter exceeding that of uninvolved proximal and distal aorta. Reimplantation of the renal arteries accompanied the aortic reconstruction. Postoperative computed tomographic angiography.  (From Stanley JC, Criado E, Eliason JL, et al: Abdominal aortic coarctation: Surgical treatment of 53 patients with a thoracoabdominal bypass, patch aortoplasty, or interposition aortoaortic graft, J Vasc Surg 48:1073–1082, 2008).



Descending Thoracic Aorta to Femoral Bypass

associated with an extensive patch aortoplasty. All the secondary procedures were successful. An aortofemoral bypass or an occasional endarterectomy with patch closure in female patients with aortoiliac hypoplasia complicated by secondary atherosclerosis carry a 90% patency at 5 years, despite the tiny caliber of the outflow vessels.

Selected References Cronenwett JL, Garrett HE: Arteriographic measurement of the abdominal aorta, iliac, and femoral arteries in women with atherosclerotic occlusive disease, Radiology 148:389–392, 1983. DeLaurentis DA, Friedmann SO, Wolferth Jr CC: Atherosclerosis and the hypoplastic aortoiliac system, Surgery 83:27–37, 1978. Delis KT, Gloviczki P: Middle aortic syndrome: From presentation to contemporary open surgical and endovascular treatment. (Editorial comment by JC Stanley included), Persp Vasc Surg Endovasc Ther 17:187–206, 2005. Eliason JL, Passman MA, Guzman RJ, et al: Durability of percutaneous angioplasty and stent implantation for the treatment of abdominal aortic coarctation: A case report, Vasc Surg 35:397–401, 2001.

Descending Thoracic Aorta to Femoral Bypass Peter Hunt and Walter J. McCarthy

The descending thoracic aorta–to–femoral artery bypass can be defined as a bypass from the aorta just proximal to the diaphragmatic hiatus with either a bifurcated or tube graft reaching the iliac or femoral arterial system. This operation was first performed in 1956 by Sauvage, who used an aortic homograft for a patient who had standard aortoiliac graft failure. In 1961, Blaisdell used the thoracofemoral bypass for reconstruction after removing an infected infrarenal aortic prosthesis. Increasing acceptance of this operation by the surgical community is reflected by reports of 166 similar cases in the literature by the early 1990s and many more since.

INDICATIONS This operation is simple in concept but should be restricted to very special settings in which conventional arterial grafting configurations are inadequate. As a general rule, if simpler or more commonly used operations can achieve the same end, they should be used in preference to the thoracofemoral bypass. Thus, although the thoracic aorta provides excellent inflow for treatment of an infrarenal aortic occlusion, the routine intraabdominal approach remains preferred. Although the thoracofemoral operation has been described for situations of acute aortic infection, one might more reasonably use an axillofemoral bypass instead. The reason is that in the septic patient, if the extra-anatomic repair were to become infected, the axillarybased graft is easier to manage than one anastomosed to the descending thoracic aorta. Therefore, in the relatively common setting of infected infrarenal aortic bypass removal, an axillofemoral bypass is still recommended. Three specific indications have evolved. The first indication is the rare situation of a hostile abdomen, usually after either extensive previous operations or radiation in the periaortic region. Circumstances including inflammatory bowel disease or abdominal wall deficiencies

449

Ghazi P, Haji-Zeinali A-M, Shafiee N, et al: Endovascular abdominal aortic stenosis treatment with the OptiMed self-expandable nitinol stent, Catheter Cardiovasc Interv 74:634–641, 2009. Graham LM, Zelenock GB, Erlandson EE, et al: Abdominal aortic coarctation and segmental hypoplasia, Surgery 86:519–529, 1979. Hallett Jr JW, Brewster DC, Darling RC, et al: Coarctation of the abdominal aorta. Current options in surgical management, Ann Surg 190:430–437, 1980. Messina LM, Reilly LM, Goldstone J, et al: Middle aortic syndrome. Effectiveness and durability of complex arterial revascularization techniques, Ann Surg 204:331–339, 1986. Stanley JC, Criado E, Eliason JL, et al: Abdominal aortic coarctation: Surgical treatment of 53 patients with a thoracoabdominal bypass, patch aortoplasty, or interposition aortoaortic graft, J Vasc Surg 48:1073–1082, 2008. Upchurch Jr GR, Henke PK, Eagleton MJ, et al: Pediatric splanchnic arterial occlusive disease: Clinical relevance and operative treatment, J Vasc Surg 35:860–867, 2002.

can enter into this decision. In such patients, aortic inflow from the left chest may be less traumatic than an abdominal exploration. The second indication is for repeated failure of abdominal aortic grafting. As a general rule, failure after a single aortofemoral bypass is appropriately managed with another intraabdominal aortic graft. After two failures, one may reasonably consider moving to the thoracic aorta for inflow. Finally, the thoracofemoral bypass has been useful for patients with multiple failed extra-anatomic bypasses. They include patients with axillopopliteal and axillofemoral grafts having had multiple graft thrombectomy operations. Many of these patients were first seen at the time of infected aortic graft removal, and reconstruction was performed in the usual way with axillary-based inflow grafts. Following removal of their infected grafts, many such patients enjoy a potentially long life and are gravely affected by their repeated axillary graft thromboses. A reconstruction providing an uninhibited inflow source such as the descending thoracic aorta and the intracavitary tunnel of the thoracofemoral bypass seems reasonable in this setting.

SURGICAL TECHNIQUE The patient is positioned to maintain adequate surgical access to both femoral arteries. The pelvis is left reasonably flat, with a rotation of the thorax to about 30 degrees (Figure 1). A thoracotomy incision is made in the sixth or seventh intercostal space and brought across the costal cartilage for several centimeters onto the abdominal wall. Remove 1 or 2 centimeters of costal cartilage with the curved Mayo scissors for a less painful closure. After the thoracic cavity is entered, the diaphragm is incised for several centimeters in a radial fashion. Later, the bypass graft will pass through this short incision. Left lung retraction with either conventional retractors or selective deflation with a double-lumen endotracheal tube is followed by incision of the inferior pulmonary ligament to expose the aorta. The aorta is circumferentially dissected above the diaphragm to allow placement of a bypass graft several centimeters above the diaphragmatic hiatus. Avoid placing the anastomosis too close to the diaphragm to prevent kinking. A nasogastric tube allows identification of the esophagus by palpation during this dissection, and an silicone elastic sling is left around the aorta for control should the side-biting aortic clamp be dislodged. Tunnels are formed from the retroperitoneum just beneath the costal cartilage incision to the left groin. This process is aided by



Descending Thoracic Aorta to Femoral Bypass

associated with an extensive patch aortoplasty. All the secondary procedures were successful. An aortofemoral bypass or an occasional endarterectomy with patch closure in female patients with aortoiliac hypoplasia complicated by secondary atherosclerosis carry a 90% patency at 5 years, despite the tiny caliber of the outflow vessels.

Selected References Cronenwett JL, Garrett HE: Arteriographic measurement of the abdominal aorta, iliac, and femoral arteries in women with atherosclerotic occlusive disease, Radiology 148:389–392, 1983. DeLaurentis DA, Friedmann SO, Wolferth Jr CC: Atherosclerosis and the hypoplastic aortoiliac system, Surgery 83:27–37, 1978. Delis KT, Gloviczki P: Middle aortic syndrome: From presentation to contemporary open surgical and endovascular treatment. (Editorial comment by JC Stanley included), Persp Vasc Surg Endovasc Ther 17:187–206, 2005. Eliason JL, Passman MA, Guzman RJ, et al: Durability of percutaneous angioplasty and stent implantation for the treatment of abdominal aortic coarctation: A case report, Vasc Surg 35:397–401, 2001.

Descending Thoracic Aorta to Femoral Bypass Peter Hunt and Walter J. McCarthy

The descending thoracic aorta–to–femoral artery bypass can be defined as a bypass from the aorta just proximal to the diaphragmatic hiatus with either a bifurcated or tube graft reaching the iliac or femoral arterial system. This operation was first performed in 1956 by Sauvage, who used an aortic homograft for a patient who had standard aortoiliac graft failure. In 1961, Blaisdell used the thoracofemoral bypass for reconstruction after removing an infected infrarenal aortic prosthesis. Increasing acceptance of this operation by the surgical community is reflected by reports of 166 similar cases in the literature by the early 1990s and many more since.

INDICATIONS This operation is simple in concept but should be restricted to very special settings in which conventional arterial grafting configurations are inadequate. As a general rule, if simpler or more commonly used operations can achieve the same end, they should be used in preference to the thoracofemoral bypass. Thus, although the thoracic aorta provides excellent inflow for treatment of an infrarenal aortic occlusion, the routine intraabdominal approach remains preferred. Although the thoracofemoral operation has been described for situations of acute aortic infection, one might more reasonably use an axillofemoral bypass instead. The reason is that in the septic patient, if the extra-anatomic repair were to become infected, the axillarybased graft is easier to manage than one anastomosed to the descending thoracic aorta. Therefore, in the relatively common setting of infected infrarenal aortic bypass removal, an axillofemoral bypass is still recommended. Three specific indications have evolved. The first indication is the rare situation of a hostile abdomen, usually after either extensive previous operations or radiation in the periaortic region. Circumstances including inflammatory bowel disease or abdominal wall deficiencies

449

Ghazi P, Haji-Zeinali A-M, Shafiee N, et al: Endovascular abdominal aortic stenosis treatment with the OptiMed self-expandable nitinol stent, Catheter Cardiovasc Interv 74:634–641, 2009. Graham LM, Zelenock GB, Erlandson EE, et al: Abdominal aortic coarctation and segmental hypoplasia, Surgery 86:519–529, 1979. Hallett Jr JW, Brewster DC, Darling RC, et al: Coarctation of the abdominal aorta. Current options in surgical management, Ann Surg 190:430–437, 1980. Messina LM, Reilly LM, Goldstone J, et al: Middle aortic syndrome. Effectiveness and durability of complex arterial revascularization techniques, Ann Surg 204:331–339, 1986. Stanley JC, Criado E, Eliason JL, et al: Abdominal aortic coarctation: Surgical treatment of 53 patients with a thoracoabdominal bypass, patch aortoplasty, or interposition aortoaortic graft, J Vasc Surg 48:1073–1082, 2008. Upchurch Jr GR, Henke PK, Eagleton MJ, et al: Pediatric splanchnic arterial occlusive disease: Clinical relevance and operative treatment, J Vasc Surg 35:860–867, 2002.

can enter into this decision. In such patients, aortic inflow from the left chest may be less traumatic than an abdominal exploration. The second indication is for repeated failure of abdominal aortic grafting. As a general rule, failure after a single aortofemoral bypass is appropriately managed with another intraabdominal aortic graft. After two failures, one may reasonably consider moving to the thoracic aorta for inflow. Finally, the thoracofemoral bypass has been useful for patients with multiple failed extra-anatomic bypasses. They include patients with axillopopliteal and axillofemoral grafts having had multiple graft thrombectomy operations. Many of these patients were first seen at the time of infected aortic graft removal, and reconstruction was performed in the usual way with axillary-based inflow grafts. Following removal of their infected grafts, many such patients enjoy a potentially long life and are gravely affected by their repeated axillary graft thromboses. A reconstruction providing an uninhibited inflow source such as the descending thoracic aorta and the intracavitary tunnel of the thoracofemoral bypass seems reasonable in this setting.

SURGICAL TECHNIQUE The patient is positioned to maintain adequate surgical access to both femoral arteries. The pelvis is left reasonably flat, with a rotation of the thorax to about 30 degrees (Figure 1). A thoracotomy incision is made in the sixth or seventh intercostal space and brought across the costal cartilage for several centimeters onto the abdominal wall. Remove 1 or 2 centimeters of costal cartilage with the curved Mayo scissors for a less painful closure. After the thoracic cavity is entered, the diaphragm is incised for several centimeters in a radial fashion. Later, the bypass graft will pass through this short incision. Left lung retraction with either conventional retractors or selective deflation with a double-lumen endotracheal tube is followed by incision of the inferior pulmonary ligament to expose the aorta. The aorta is circumferentially dissected above the diaphragm to allow placement of a bypass graft several centimeters above the diaphragmatic hiatus. Avoid placing the anastomosis too close to the diaphragm to prevent kinking. A nasogastric tube allows identification of the esophagus by palpation during this dissection, and an silicone elastic sling is left around the aorta for control should the side-biting aortic clamp be dislodged. Tunnels are formed from the retroperitoneum just beneath the costal cartilage incision to the left groin. This process is aided by

450

AORTOILIAC OCCLUSIVE DISEASE

FIGURE 1  Rotation of the left chest to 30 degrees allows level positioning of the femoral regions.  (From

McCarthy WJ, Rubin JR, Flinn WR, et al: Descending thoracic aorta-to-femoral artery bypass, Arch Surg 121:681–688, 1986; with permission.)

FIGURE 2  Blunt index finger dissection allows atraumatic tunneling along the anterior or midaxillary

line.  (From McCarthy WJ, Rubin JR, Flinn WR, et al: Descending thoracic aorta-to-femoral artery bypass, Arch Surg 121:681–688, 1986; with permission.)

transecting the left inguinal ligament and is achieved with blunt bimanual index finger dissection. Remarkably, finger dissection with both hands usually provides enough length for this tunnel (Figure 2). The tunnel is beneath the lateral abdominal musculature but extraperitoneally along the anterior or midaxillary line (Figure 3). After systemic anticoagulation with heparin, the proximal aortic anastomosis is performed after partial occlusion of the aorta. Selection of just the right J-shaped clamp from the instrument tray can require some experimentation. Patients are well served with a ring-supported 10-mm graft, but 8- or 12-mm ringed grafts may be used, depending upon patient size. Suture with 3–0 or 4–0 polypropylene or polytetrafluoroethylene is appropriate. Chest tube drainage for 1 or 2 days is instituted after standard closure of the thoracotomy. Tunneling techniques differ among surgeons. The aforementioned method is the simplest available and allows tunneling anterior to the left kidney and spleen (Figure 4). Perfusion of the right lower extremity is provided by standard femorofemoral grafting based from the thoracofemoral graft, with the tunnel anterior to the rectus muscle. Alternative tunneling techniques involve using a more posterior tunnel, often

with a bifurcated aortic graft. The posterior tunnel method can require a left flank counterincision and some blind tunneling to reach the right femoral region. Either approach should yield a good result. The thoracic cavity lends itself well to endoscopic surgery. With the advance of videoscopic assisted thoracscopy (VATS), usually for lung cancer surgery, several authors have used this method for the proximal anastomosis. Recently small series have been published emphasizing the advantage of less postoperative chest wall pain and shorter lengths of stay. We developed a canine model and then used the technique in a few selected patients. While possible, the method involves advanced skills and is more challenging than open anastomosis. It should be used only where special surgical expertise is available.

RESULTS The 5-year patency characteristics for several series range from 72% patency at 2 years to 85% patency at 5 years. Not all recent studies have been published with standard life table techniques, but it seems that



Descending Thoracic Aorta to Femoral Bypass

FIGURE 3  The 10-mm graft is visible retroperitoneally along the

midaxillary line anterior to the kidney and spleen.

451

the expected patency at 5 years is consistently in the lower 80% range. This is slightly lower than what is reported for standard aortofemoral bypass grafting, but it is achieved in patients who are almost always undergoing reoperation rather than primary repair. A review of 166 patients reported in the literature documents a perioperative mortality rate of 6.6%. Many of these patients died of septic complications. Patient survival data are unavailable from most reports but was 65% at 60 months for 21 patients in the Northwestern University experience. Six of their eight patients who died in the follow-up period had myocardial infarction at a mean of 39 months after their operation. Review of the functional outcome for the 21 patients in the former study documented that additional arterial operations were eventually necessary for limb salvage. In this group, 15 subsequent infrainguinal surgical procedures were required. These included five femoropopliteal, three femorotibial, and two operations involving the deep femoral artery. There were two femorofemoral bypass operations, and three patients underwent leg amputation but never because of failed arterial inflow. Patients require careful postoperative surveillance and particular attention to cardiac risk factors for longterm success after this operation.

Selected References Alimi YS, Hartung O, Boufi M, et al: Thoracoscopic aortofemoral bypass: Early and mid-term results, Surg Laparosc Endosc Percutan Tech 15:49–52, 2005. Blaisdell FW, DeMattei GA, Gauder PJ: Extraperitoneal thoracic aorta to femoral bypass graft as replacement for an infected aortic bifurcation prosthesis: Case reports, Am J Surg 102:583–585, 1961. Branchereau A, Magnan P-E, Moracchini P, et al: Use of descending thoracic aorta for lower limb revascularisation, Eur J Vasc Surg 6:255–262, 1992. Fukui S, Paraskevas N, Soury P, et al: Totally videoendoscopic descending thoracic aorta to femoral artery bypass, J Vasc Surg 37:191–193, 2003. McCarthy WJ, Mesh CL, McMillan WD, et al: Descending thoracic aorta to femoral bypass: Ten years’ experience with a durable procedure, J Vasc Surg 17:336–348, 1993. McCarthy WJ, Rubin JR, Flinn WR, et al: Descending thoracic aorta-tofemoral artery bypass, Arch Surg 121:681–688, 1986. McMillan WD, McCarthy WJ: Thoracoscopically-assisted thoraco-femoral bypass in a canine model, Cardiovasc Surg 7:247–250, 1999. McMillan WD, McCarthy WJ: Minimally invasive thoracoscopic thoracofemoral bypass: A case report, Cardiovasc Surg 7:251–254, 1999. Passam MA, Farber MA, Criado E, et al: Descending thoracic aorta to iliofemoral artery bypass grafting: A role for primary revascularization for aortoiliac occlusive disease? J Vasc Surg 29:249–258, 1999. Stevenson JK, Sauvage LR, Harkins HN: A bypass homograft from thoracic aorta to femoral arteries for occlusive vascular disease: Case report, Ann Surg 27:632–637, 1961.

FIGURE 4  The bypass graft is visible coursing over the diaphragm

and along the lateral abdominal wall retroperitoneally. This patient had undergone removal of an infected aortic graft 2 years previously.

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Axillofemoral Bypass Joseph R. Schneider

Axillofemoral bypass (AxFB), a bypass graft from one axillary artery to one or both femoral arteries, was first performed in the early 1960s in patients at high cardiopulmonary risk for surgery as an alternative to the more direct reconstructive operation, an aortofemoral bypass (AFB). Initially, AxFBs were placed in patients with bilateral iliac artery occlusive disease, but the operation was quickly extended to reconstruction in patients with aortic infection (mycotic aneurysm), infected aortic prostheses, and other intraabdominal infections or otherwise hostile abdomens. At first the operation was most likely viewed as a technique to be used for limb salvage only in patients with critical limb ischemia or in those whose normal axial flow was expected to be interrupted by aortic ligation or removal of an aortic prosthesis. As the operation became familiar to surgeons, it was in some cases extended to patients with ischemic claudication. A primary area of controversy in the 1970s to 1990s was whether this operation is in fact appropriate for patients with claudication. This question is complex. Claudicants tend to have less systemic atherosclerotic and other serious disease, they tend to live longer and enjoy better graft patency, and series dominated by claudicants tend to have more favorable results as measured by long-term graft patency and patient survival. On the other hand, series composed primarily of patients with chronic critical limb ischemia and certainly those with a large fraction of patients with aortic and aortic prosthetic infection are associated with less favorable patient survival. Patients with critical limb ischemia have less favorable graft patency. It is the author’s perspective that the claudication question has never been settled, at first because patient selection was clearly so different among reported case series and more recently because endovascular techniques can be effectively applied in a significant fraction of patients who would have been considered for an AxFB in the past. Even aortic infection or an infected aortic prosthesis is a less secure indication for an AxFB because many of these patients have been successfully managed with in situ aortic graft replacement using antibiotic-treated prosthetic grafts, autologous superficial femoral veins, or arterial homografts.

GENERAL PRINCIPLES AND PATIENT SELECTION Successful AxFB depends on the ability of one axillosubclavian artery to supply adequate blood for the arm and one or both legs. In general, the evidence is that in the absence of an occlusive process in the axillosubclavian arterial system, this concept is sound and the operation will provide adequate resting perfusion to both legs without causing harm to the arm. However, some patients have overt or occult disease in the inflow to the donor axillary artery, most often at the origin of the brachiocephalic or subclavian artery. One group has recommended routine arch and axillosubclavian angiography before performing an AxFB. We have not found this to be necessary in practice and are satisfied with demonstration of a normal triphasic Doppler waveform in the brachial artery and no more than a 10 mm Hg lower systolic blood pressure in the proposed donor-side arm compared to the contralateral arm. AxFB is most often considered for high-risk patients with aortoiliac arterial occlusive disease who cannot be treated by endovascular techniques or with bypass from the contralateral femoral or other, closer donor artery. Endovascular techniques for arterial occlusive disease have advanced dramatically since the 1990s, and in most

patients and most practices these endovascular techniques would now be primary treatment for these patients, if feasible. The concept of prohibitive risk, usually a result of advanced cardiopulmonary disease, is not well defined. Furthermore it is likely that many patients who would in the past have been considered to be at prohibitive risk as a result of cardiopulmonary or other systemic disease would now be viewed as average risk in vascular surgery practice. However, unreconstructed coronary artery disease with recent myocardial infarction, angina, or abnormal stress testing would certainly be considered high risk for AFB. Compromised pulmonary function with FEV1.0 less than 1 L would also be considered very high risk for AFB. With respect to hostile abdomen, this would generally include problems of intraabdominal infection such as peritonitis or abscess, the presence of an intestinal or urinary stoma, or previous infection or prior surgery with adhesions, and these are potential indications for an AxFB. It is likely that the majority of patients with infrarenal aortic infection or infected aortic prosthetic grafts are still managed with aortic débridement and ligation with excision of the infected graft and AxFB, although there is no way to determine this with certainty, and there are some alternatives in such cases.

PREOPERATIVE EVALUATION In addition to blood pressure check and Doppler interrogation of the proposed donor-side brachial artery, a lower extremity arterial segmental Doppler waveform and pressure study with toe pressures should be obtained. This study helps confirm the diagnosis and calibrate the severity and also serves as a baseline to allow assessment of the results of any intervention. An angiogram, most often either computed tomography (CT) angiogram or conventional transfemoral or transbrachial catheter angiogram, is required for planning the intervention. In most cases an angiogram will have been performed before an AxFB is even considered. General medical evaluation, often including some sort of cardiac stress testing, is performed to better assess risk and guide the choice of intervention.

TECHNIQUE The operation is performed with the patient supine and the arm on the donor side abducted to 90 degrees, nearly always with general anesthesia. Towels, gel pads, intravenous fluid bags wrapped in towels, or other suitable padding is placed between the patient and the operating table on the side of the axillofemoral component to elevate the flank and lower chest. The patient is prepped from the neck to the lower anterior thighs including the intervening abdomen, ipsilateral flank, and chest including the sternum to allow entry to the abdomen and ipsilateral chest or a sternotomy (although none of these has ever been required in the author’s practice). Perioperative prophylactic antibiotics are administered and continued for 24 hours. Specific antibiotic coverage is administered as necessary in cases of an established remote infection when surgery cannot be delayed in an attempt to clear the infection. The donor axillary artery is exposed using a transverse incision inferior to the middle of the ipsilateral clavicle, splitting of the pectoralis major muscle fibers, and division of the deep fascia. Exposure and control of the axillary artery is in most cases facilitated by ligation and division of at least one large crossing vein. Care must be taken to avoid injury to the adjacent axillosubclavian vein and brachial plexus elements. The axillary artery is less robust than the more familiar femoral artery and must be treated with great care to avoid injury. The author does not divide the pectoralis minor muscle as some have recommended. A critical technical point is to keep the graft anastomosis as medial as possible on the axillary artery to reduce the tendency for later arm abduction to disrupt the anastomosis. Leaving the pectoralis minor intact forces the surgeon to keep



Axillofemoral Bypass

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FIGURE 1  Axillobifemoral bypass graft, in this case from the right

axillary donor artery to the right femoral artery and from the right to the left femoral artery. The intermediate incision in the right lower chest or upper flank is generally unnecessary if an appropriate tunneler is used.  (From Schneider JR: Aortoiliac disease: Extra-anatomic bypass. In Cronenwett J, Johnston KW (eds): Rutherford's Vascular Surgery, 7th ed, Philadelphia, 2010, Saunders, pp 1633–1652.)

the anastomosis medial. One or both femoral arteries are exposed through standard groin incisions. A longitudinal groin incision is used most often because it allows more flexibility depending on findings at inspection of the target arteries. The axillofemoral graft is tunneled from the axillary artery ­exposure to the femoral exposure, which is nearly always ipsilateral (Figure 1). Circumstances requiring bypass from one axillary artery to a single contralateral femoral target are rare. The author’s team’s practice is to tunnel the graft posterior to the pectoralis minor muscle, but the graft may be tunneled anterior to the pectoralis minor, or the pectoralis minor may be divided, and there is no evidence that this affects outcome. The graft should be tunneled in the subcutaneous tissue in the midaxillary line to prevent kinking during subsequent patient torsoflexion and compression/angulation of the graft by the costal margin, which tends to be more prominent anteriorly. Classic descriptions of the operation have included an intermediate incision in the flank to facilitate tunneling, but we prefer to use a long enough tubular tunneler that allows tunneling without any intermediate incision. Venous and other autografts would be used for AxFB only in the case of active infection. Prosthetic grafts are the norm. We prefer externally supported extended polytetrafluoroethylene (ePTFE) grafts, but there is no evidence that one graft material is superior to another or even that a supported graft is superior in this application. We prefer an 8-mm-diameter axillofemoral graft in most cases, and there are theoretical reasons why a larger graft may be more prone to thrombosis. A 6-mm-diameter graft may be appropriate for an axillounifemoral graft, particularly in the rare circumstance when the graft is to be extended to the popliteal artery. In cases of axillobifemoral bypass, a graft is also tunneled from one groin incision to the other groin incision just as with standard femorofemoral bypass described elsewhere in this text. We prefer a 6-mm-diameter supported ePTFE graft for the femorofemoral component, but there is no evidence that one graft type is superior to another in this application. A suitable dose of heparin or other anticoagulant is administered before clamps are placed. The axillary artery is controlled with suitable vascular clamps, and a longitudinal axillary arteriotomy is performed as medially as possible. This also results in a very acute angle that is desired between the axillary artery and the graft at the anastomosis. The graft is spatulated and an end-to-side, graft-to-axillary anastomosis is performed with running 5–0 or 6–0 polypropylene or ePTFE suture. A surplus length of graft is maintained in the area of the axillary exposure. These three principles (medial anastomosis, acute angle at the axillary artery anastomosis, and redundant graft in the axillary exposure) are employed to attempt to reduce the likelihood of tension and disruption of the axillary anastomosis during arm abduction. Femoral artery control is by means of clamps and Potts vessel loops as appropriate based on the local anatomy. If the construction

FIGURE 2  Right axillobifemoral graft. The distal end of the axil-

lofemoral component is anastomosed to the anterior side of the femoral artery, the right end of a right-to-left femorofemoral graft is anastomosed to the distal axillofemoral graft hood, and the left end of the femorofemoral graft is anastomosed to the left femoral arterial system. In a common alternative that the author favors, a conventional femorofemoral bypass graft is placed, after which the distal end of the axillofemoral component is anastomosed to the ipsilateral hood of the femorofemoral component. The target artery for both the axillofemoral and femorofemoral components depends on disease in the artery determined from imaging and local inspection at surgery and by geometry depending on patient’s habitus and other patient characteristics.  (From Schneider JR: Aortoiliac disease: Extra-anatomic bypass. In Cronenwett J, Johnston KW (eds): Rutherford's Vascular Surgery, 7th ed, Philadelphia, 2010, Saunders, pp 1633–1652.)

is axillounifemoral, then the distal anastomosis is between the axillofemoral graft and the common femoral, superficial femoral, or deep femoral artery or some combination thereof. The surgeon should review preoperative arterial images and decide on the distal anastomotic site based on local disease, the patient’s individual geometry, and the patient’s habitus. In the case of axillobifemoral bypass, there are multiple approaches to the femoral anastomosis. One of the most common options is to complete the anastomosis between the axillofemoral component and the target femoral artery, then excise an appropriate-sized oval portion of the anastomotic hood of that axillofemoral graft, and then perform an anastomosis between that graft and the spatulated ipsilateral end of the femorofemoral graft component (Figure 2). A second common option, and our preferred choice, is to place a standard femorofemoral graft as described elsewhere in this text and then perform the anastomosis between the distal end of the axillofemoral component and the ipsilateral anastomotic hood of the femorofemoral component. There are unique geometric challenges in femorofemoral bypass that apply equally to the femorofemoral component of axillobifemoral grafts. There are at least two and more often three separate surgical exposures, and in the case of axillobifemoral bypass there are four anastomoses, and the operation can be facilitated by having two surgeons who may work independently. The most efficient approach to this with two surgeons is to have one surgeon performing the axillary and the other the first ipsilateral femoral anastomosis, after which one surgeon moves to the other side of the table and then one surgeon performs the second ipsilateral femoral and the second surgeon the contralateral femoral anastomosis. The system is then flushed of air and possible debris before the final anastomosis is completed. Clamps are removed and acceptable flow is then confirmed in donor inflow and bilateral outflow arteries using a sterile continuouswave Doppler. The radial pulse and hand perfusion on the axillary

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donor side are assessed to be certain that there has been no technical problem, unsuspected axillosubclavian inflow lesion, or anything else that would compromise the perfusion of the distal arm on the donor side. The feet are inspected, and flow to the feet is interrogated with a continuous-wave Doppler at the ankles to ensure that perfusion is adequate. An AxFB virtually never results in a palpable pulse at the ankle and foot. Once the surgeon is satisfied with hemostasis and arterial flow is confirmed to be as expected, wounds are closed per surgeon preference (we generally use a running absorbable subcutaneous closure and then skin staples), but as with any femoral artery exposure, a careful inspection for lymphatic leaks should be performed before closure.

POSTOPERATIVE CARE AND FOLLOW-UP AxFBs are well tolerated by patients. Postoperative surgical site pain is usually easily controlled with analgesics. We target a hospital stay of 2 days, rarely if ever with any time in the intensive care unit. AxFB is generally performed in older patients with advanced comorbidities who have little reserve and can require longer acute care convalescence. Patients are encouraged to walk by the first postoperative day, with the help of physical therapists as necessary. Patients are asked to limit activity at home for a few days and then advance activity as tolerated. Overactivity is virtually never a problem with these generally older, often sedentary patients. Noninvasive surveillance examination is performed at the time of the patient’s first return visit about 2 weeks after surgery. This examination includes standard ankle (posterior tibial and dorsal pedal) blood pressure measurements with ankle-brachial indices and Doppler waveforms, great toe photoplethysmography waveforms and blood pressures, and a graft duplex scan with pulsed-Doppler waveform inspection and velocity estimation at several sites within the axillofemoral and femorofemoral graft components and at the recipient anastomoses and outflow vessels. We repeat the clinical examination and surveillance noninvasive studies every 3 months for the first year, consistent with our protocol for infrainguinal bypass grafts. We acknowledge that the evidence is less clear that this surveillance predicts impending graft failure than is the case for infrainguinal bypass grafts.

RESULTS AND INFLUENCE OF PATIENT AND GRAFT FACTORS Clinical series of patients undergoing an AxFB have reported remarkably different results. Reported late patency has ranged from the mid30% to the 80% range, clearly one of the largest ranges for any common vascular reconstruction. Furthermore, inclusion of even a small fraction of claudicants is associated with significantly better patency estimates for reasons discussed earlier. Thus, it is difficult to provide a useful composite estimate for late primary AxFB patency. However, previous publications with a few notable exceptions have reported patency to be less than that of AFB. Publications in the late 1960s and 1970s favored routine use of axillobifemoral configurations. Patency was observed to be better for axillobifemoral than for axillounifemoral grafts. However subsequent publications, including one from the group that was the first to champion axillobifemoral configurations, have observed no patency benefit for axillobifemoral configuration. These bypasses are likely still performed in the axillobifemoral configuration in most patients, but decisions must be individualized based on anatomic factors and patient factors. Axillounifemoral bypasses are likely to remain a less common procedure because if the contralateral iliac system is sufficient to maintain viability of the contralateral limb, then in most cases it is good enough—or can be improved with endovascular techniques to make it good enough—to serve as a donor for a less extensive procedure like a femorofemoral bypass.

An ankle-brachial index of about 0.7 is predicted after an AxFB with completely normal infrainguinal outflow. This compares to a predicted ankle-brachial index of slightly greater than 1.0 after AFB with normal infrainguinal outflow. Thus an AxFB is associated with adequate resting perfusion to allow limb salvage in most cases, although further infrainguinal intervention, surgical or endovascular, may be necessary if there is significant concomitant infrainguinal occlusive disease. A reasonable composite estimate of predicted 5-year primary patency for an AxFB is in the range of 50% to 60%, at least among series of patients with critical limb ischemia. In this regard we recommend against an AxFB for non–limb threatening claudication as a result of bilateral iliac artery disease because an AFB is a more effective and durable procedure. The patency results are actually significantly better among patients undergoing an AxFB for an aortic infection or prosthetic aortic graft infection. Furthermore, with thrombosis of an AxFB, operative thrombectomy is relatively easy in most cases, and secondary patency is significantly better than primary patency. Thus in most cases an AxFB supports limb salvage and has a significantly lower impact on these typically very ill patients.

CONTINUING EVOLUTION OF THE ROLE OF AXILLOFEMORAL BYPASS There have been no major changes regarding AxFB technique in many years. The population continues to age, and with this increase in age comes increasingly diffuse disease that is less amenable to endovascular techniques. These progressively more aged patients may be better served by an AxFB unless endovascular techniques improve the results in patients with very diffuse iliac artery disease. With respect to the role of AxFB for patients with aortic infection and infected aortic prostheses, in situ aortic replacement with autologous superficial femoral vein or aortic homograft have emerged as the first choice in many patients. Thus, there has almost certainly been a decline in AxFB since the turn of the century. However, the procedure remains an important alternative that should be familiar to any surgeon dealing with aortoiliac arterial occlusive disease as well as aortic infection and infected aortic prostheses.

Selected References Angle N, Dorafshar AH, Farooq MM, et al: The evolution of the axillofemoral bypass over two decades, Ann Vasc Surg 16:742–745, 2002. Clagett GP, Valentine RJ, Hagino RT, et al: Autogenous aortoiliac/femoral reconstruction from superficial femoral–popliteal veins: Feasibility and durability, J Vasc Surg 25:255–270, 1997. El-Massry S, Saad E, Sauvage LR, et al: Axillofemoral bypass with externally supported, knitted Dacron grafts: A follow-up through twelve years, J Vasc Surg 17:107–115, 1993. Johnson WC, Lee KK: Comparative evaluation of externally supported Dacron and polytetrafluoroethylene prosthetic bypasses for femorofemoral and axillofemoral arterial reconstructions. Veterans Affairs Cooperative Study #141, J Vasc Surg 30:1077–1083, 1999. Kieffer E, Bahnini A, Koskas F, et al: In situ allograft replacement of infected infrarenal aortic prosthetic grafts: Results in forty-three patients, J Vasc Surg 17:349–356, 1993. Musicant SE, Giswold ME, Olson CJ, et al: Postoperative duplex scan surveillance of axillofemoral bypass grafts, J Vasc Surg 37:54–61, 2003. O'Hara PJ, Hertzer NR, Beven EG, et al: Surgical management of infected abdominal aortic grafts: Review of a 25-year experience, J Vasc Surg 3:725–731, 1986. Passman MA, Taylor LM, Moneta GL, et al: Comparison of axillofemoral and aortofemoral bypass for aortoiliac occlusive disease, J Vasc Surg 23:263–271, 1996. Schneider JR, McDaniel MD, Walsh DB, et al: Axillofemoral bypass: Outcome and hemodynamic results in high-risk patients, J Vasc Surg 15:952–963, 1992. Yeager RA, Taylor Jr LM: Axillary artery anastomosis to avoid axillofemoral bypass disruption, Semin Vasc Surg 13:74–76, 2000.



Unilateral Retroperitoneal Iliofemoral Bypass

Unilateral Retroperitoneal Iliofemoral Bypass Peter G. Kalman

The typical patient with isolated iliac occlusive disease generally has intermittent claudication. Critical ischemia in the form of rest pain, ulceration, or gangrene is usually absent unless multilevel disease exists. There are several management options for symptomatic patients with unilateral iliac occlusive disease ranging from conservative medical management to endovascular catheter-based intervention or open operation.

TREATMENT ALGORITHM FOR ILIAC OCCLUSIVE DISEASE The initial approach for management of localized iliac disease, if feasible, is usually balloon dilation with percutaneous transluminal angioplasty (PTA). There is little evidence to support routine primary stenting after successful iliac PTA other than for a few specific indications, such as lesion recoil, an eccentric lesion, or a dissection following dilation. In general, the results with PTA are less satisfactory than after open surgical reconstruction, but considering the low morbidity and the option of repeating the procedure, PTA is justified for localized iliac stenoses or short occlusions. The only lesion not amenable to PTA is the less common focal iliac coral-reef plaque, which is best managed by endarterectomy. Extensive iliac endarterectomy is rarely performed in contemporary practice since those times when it was more routinely pursued in the 1960s. The long-term results for localized endarterectomy are excellent; however, most patients with localized disease previously treated by endarterectomy are now treated by PTA. Extensive endarterectomy is tedious and time consuming, and it is associated with greater blood loss than bypass grafting and a risk of sexual dysfunction in male patients. Although aortobifemoral bypass is the gold standard for managing patients with diffuse aortoiliac occlusive disease, other suitable options exist for those with unilateral iliac disease. A femorofemoral bypass is often indicated with extensive unilateral iliac disease in the presence of a normal donor iliac artery in patients in all risk categories. An axillofemoral bypass is indicated in patients with a high anesthetic risk for which a femorofemoral bypass is not possible because of the extent of donor iliac disease. A unilateral iliofemoral bypass is a third option, provided that the aorta and ipsilateral common iliac artery are normal or only minimally diseased.

RETROPERITONEAL ILIOFEMORAL BYPASS: SURGICAL TECHNIQUE The patient is positioned supine and a wide field, including the abdomen, both groins, and lower extremities, is prepped and draped with the feet are covered in clear plastic bags. The common femoral, superficial femoral, and profunda arteries are isolated through a vertical groin incision and preoperative arteriogram. Exposure of the iliac artery is facilitated by slightly tilting the table with the operative side upward. The retroperitoneal incision for

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exposure of the iliac artery extends obliquely from the anterior axillary line, in line with the tip of the 10th rib, to the midline approximately 3 to 4 cm below the umbilicus. The medial extent of the incision often can be shortened to the midrectus level in patients with a wide costal margin. Keeping the incision high at this level facilitates ample exposure all the way up to the aortic bifurcation, if necessary. The anterior rectus sheath and rectus muscle are divided using cautery, followed by transection of the external and internal oblique muscles. The retroperitoneal exposure is developed, beginning laterally in the flank after splitting the transversus abdominus muscle in the line of its fibers. The peritoneum is then stripped posteriorly and anteriorly, and the entire envelope of peritoneum is retracted medially, with retraction maintained using a table retractor. The ureter is identified as it crosses the bifurcation of the common iliac artery and is carefully mobilized and retracted medially. Before vascular reconstruction, the patient is systematically anticoagulated with intravenous heparin (75–100 U/kg). Generally, an 8-mm graft is selected for the conduit in normal-sized adults. The proximal anastomosis is performed end to side at a suitable location on the common iliac artery using a running 4–0 or 5–0 polypropylene monofilament suture with a parachute technique. The graft is tunneled under the inguinal ligament, and the distal anastomosis is performed to the selected outflow artery. After reversal of the heparin anticoagulation with protamine and other satisfactory hemostasis is evident, the abdominal wall and groin incisions are closed in a standard fashion.

RESULTS A unilateral iliofemoral bypass graft can be considered as an option in patients with significant unilateral symptoms, provided that the aorta and ipsilateral common iliac artery are normal or only minimally diseased. Earlier reports recommended that retroperitoneal iliofemoral bypass be reserved primarily for elderly, poor-risk patients who appeared too ill to withstand a major transabdominal approach. However, given that the patency is excellent, the indications for iliofemoral bypass can be extended to include patients of low operative risk as well. The reason these bypasses are relatively uncommon is that unilateral iliac disease with sparing of the common iliac artery is infrequently found and in contemporary times most can be treated by PTA. Although the patency rates for unilateral iliofemoral and femorofemoral bypass have been reported as equivalent, there appears to be a small patency advantage for iliofemoral bypass in most reports. The cumulative patency at 3 years has been reported to be more than 90%, and excellent results at 4 and 5 years were noted in 84% and 82% of patients, respectively. The main advantage of iliofemoral bypass compared with femorofemoral bypass is the avoidance of a second groin incision with the risk of lymphatic complications and potential for infection. Other advantages include a generally shorter length of graft than with a femorofemoral bypass and the deeper anatomic position of the tunneled graft.

Selected References Beard JD: Comparison of iliofemoral and femorofemoral crossover bypass in the treatment of unilateral iliac artery occlusive disease, Br J Surg 79:181, 1992 letter. Cham C, Myers KA, Scott DF, et al: Extraperitoneal unilateral iliac artery bypass for chronic lower limb ischaemia, Aust N Z J Surg 58:859–863, 1988. Darling RC, Leather RP, Chang BB, et al: Is the iliac artery a suitable inflow conduit for iliofemoral occlusive disease: An analysis of 514 aortoiliac reconstructions, J Vasc Surg 17:15–19, 1993. Hanafy M, McLoughlin GA: Comparison of iliofemoral and femorofemoral crossover bypass in the treatment of unilateral iliac arterial occlusive disease, Br J Surg 78:1001–1002, 1991.

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Kalman PG, Hosang M, Johnston KW, et al: Unilateral iliac disease: The role of iliofemoral bypass, J Vasc Surg 6:139–143, 1987. Kalman PG, Johnston KW: Aortoiliac occlusive disease. In Ritchie WP, (eds): General Surgery, Philadelphia, 1995, JB Lippincott, pp 643–653. Kalman PG, Johnston KW, Sniderman KW: Indications and results of balloon angioplasty for arterial occlusive lesions, World J Surg 20:630–634, 1996.

Lorenzi G, Domanin M, Costantini A, et al: Role of bypass, endarterectomy, extra-anatomic bypass and endovascular surgery in unilateral iliac occlusive disease: A review of 1257 cases, Cardiovasc Surg 2:370–373, 1994. Rutherford RB: Aortobifemoral bypass, the gold standard: Technical considerations, Semin Vasc Surg 7:11–16, 1994. Sidawy AN, Menzoian JO, Cantelmo NL, et al: Retroperitoneal inflow procedures for iliac occlusive vascular disease, Arch Surg 120:794–796, 1985.

Femorofemoral Bypass for Aortoiliac Occlusive Disease

donor artery? Is there reasonable common, deep, and/or superficial femoral artery target runoff on the ipsilateral side?

Joseph R. Schneider

Femorofemoral bypass was first performed in the early 1950s as an alternative to the more direct aortofemoral bypass (AFB). Femorofemoral bypass, as with axillofemoral bypass, was initially employed primarily as a lower-risk alternative to AFB in high-risk patients with critical limb ischemia. It was quickly extended as a method to reconstruct patients with claudication, intraabdominal infection, or an otherwise hostile abdomen. As the vascular surgical experience evolved and more rigorous approaches to outcome assessment became the norm, it became apparent that a femorofemoral bypass was not associated with the same excellent outcomes as an AFB. Consequently, questions arose regarding the appropriateness of this bypass for the treatment of claudication. This question is complex because claudicants tend to live longer than patients with critical limb ischemia, and this can lead to an inaccurate assessment of patency when the results in one group are used to predict outcomes in another group.

GENERAL PRINCIPLES AND PATIENT SELECTION The primary indication for performing a femorofemoral bypass is the presence of symptomatic unilateral iliac artery occlusive disease. A more recent indication is completing a reconstruction after an aorto-uni-iliac endovascular graft placement for abdominal aortic aneurysm. The threshold for high risk and the decision to choose a femorofemoral bypass over an AFB are certainly not well defined, and criteria are likely to be somewhat different from surgeon to surgeon. The less satisfactory patency and hemodynamic performance of a femorofemoral bypass compared to an AFB makes the author much less likely to recommend its use in claudicants, who are generally lower risk and likely to live longer than those with critical limb ischemia. A femorofemoral bypass depends on the ability of one iliac artery to supply adequate blood for both legs without causing a decline in flow to the donor leg. The surgical literature has confirmed that this concept is correct, at least when the patient is at rest as long as there is no significant disease in the donor iliac arterial system. If needed, a suboptimal donor iliac artery can often be improved using endovascular techniques to make it satisfactory for use as a donor vessel. Thus the primary considerations from an anatomic standpoint are: Does the patient have ipsilateral iliac artery disease that does not appear favorable for endovascular treatment? Is the contralateral iliac arterial system free of hemodynamically significant disease, and if not, can it be improved with endovascular techniques to make it a suitable

PREOPERATIVE EVALUATION A lower extremity segmental arterial noninvasive examination should be performed to calibrate the severity of disease and to serve as a baseline to which post-reconstruction studies may be compared. A good-quality CT angiogram may be sufficient for determining suitability for a femorofemoral bypass and operative planning. However, resolution might not be adequate to determine the level of disease in the common and external iliac arteries, particularly if there is significant calcification, which significantly degrades resolution. In such cases, a conventional transfemoral angiogram is preferred. In some cases it may be useful to perform a vasodilator (papaverine)enhanced measurement of the pressure gradient between the aorta and the donor side femoral artery to determine the physiologic significance of any suspect donor iliac arterial lesion. Significant occlusive disease of the aorta itself is unusual in the face of at least one patent common iliac artery, but if the aorta is occluded, the occlusion must be addressed (endovascular in many cases) or another procedure must be considered.

TECHNIQUE The operation is performed with the patient supine. The operation may be performed with general, regional, or even local anesthesia. Perioperative prophylactic antibiotics are administered and continued for 24 hours. Specific antibiotic coverage is administered as necessary in cases with established remote infection and critical limb ischemia such that surgery cannot be delayed for a period to attempt to clear infection. Femoral arteries are exposed through a longitudinal groin incision most often, because this allows more flexibility depending on findings at inspection of the target arteries. The graft is tunneled in the subcutaneous tissue from one groin incision to the other. The general strategy is to try to maximize the radius of curvature of any changes in the direction of the graft to prevent graft kinking. The tunnel forms an inverted U and should be brought well above the level of the groin incisions to prevent acute angulation of the graft at any point (Figure 1). Care must be taken to keep the graft anterior to the anterior abdominal fascia in most cases. The tunnel may be created using a tubular tunneler if one is available or with a combination of finger dissection and a large clamp. Special care must be taken when tunneling through areas of scarring from previous incisions where there might even be herniated abdominal contents at risk of injury during tunneling. Grafts are placed in the preperitoneal potential space only in very unusual circumstances, such as a uniquely thin subcutaneous layer or an abnormal abdominal wall (from radiation, scarring, etc.). The first reported femorofemoral bypass was actually performed with a disobliterated superficial femoral artery autograft, and many have been performed with venous autografts. However, prosthetic grafts, usually expanded polytetrafluoroethylene (ePTFE) or polyester textile, are used unless there is local or remote infection, which

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Kalman PG, Hosang M, Johnston KW, et al: Unilateral iliac disease: The role of iliofemoral bypass, J Vasc Surg 6:139–143, 1987. Kalman PG, Johnston KW: Aortoiliac occlusive disease. In Ritchie WP, (eds): General Surgery, Philadelphia, 1995, JB Lippincott, pp 643–653. Kalman PG, Johnston KW, Sniderman KW: Indications and results of balloon angioplasty for arterial occlusive lesions, World J Surg 20:630–634, 1996.

Lorenzi G, Domanin M, Costantini A, et al: Role of bypass, endarterectomy, extra-anatomic bypass and endovascular surgery in unilateral iliac occlusive disease: A review of 1257 cases, Cardiovasc Surg 2:370–373, 1994. Rutherford RB: Aortobifemoral bypass, the gold standard: Technical considerations, Semin Vasc Surg 7:11–16, 1994. Sidawy AN, Menzoian JO, Cantelmo NL, et al: Retroperitoneal inflow procedures for iliac occlusive vascular disease, Arch Surg 120:794–796, 1985.

Femorofemoral Bypass for Aortoiliac Occlusive Disease

donor artery? Is there reasonable common, deep, and/or superficial femoral artery target runoff on the ipsilateral side?

Joseph R. Schneider

Femorofemoral bypass was first performed in the early 1950s as an alternative to the more direct aortofemoral bypass (AFB). Femorofemoral bypass, as with axillofemoral bypass, was initially employed primarily as a lower-risk alternative to AFB in high-risk patients with critical limb ischemia. It was quickly extended as a method to reconstruct patients with claudication, intraabdominal infection, or an otherwise hostile abdomen. As the vascular surgical experience evolved and more rigorous approaches to outcome assessment became the norm, it became apparent that a femorofemoral bypass was not associated with the same excellent outcomes as an AFB. Consequently, questions arose regarding the appropriateness of this bypass for the treatment of claudication. This question is complex because claudicants tend to live longer than patients with critical limb ischemia, and this can lead to an inaccurate assessment of patency when the results in one group are used to predict outcomes in another group.

GENERAL PRINCIPLES AND PATIENT SELECTION The primary indication for performing a femorofemoral bypass is the presence of symptomatic unilateral iliac artery occlusive disease. A more recent indication is completing a reconstruction after an aorto-uni-iliac endovascular graft placement for abdominal aortic aneurysm. The threshold for high risk and the decision to choose a femorofemoral bypass over an AFB are certainly not well defined, and criteria are likely to be somewhat different from surgeon to surgeon. The less satisfactory patency and hemodynamic performance of a femorofemoral bypass compared to an AFB makes the author much less likely to recommend its use in claudicants, who are generally lower risk and likely to live longer than those with critical limb ischemia. A femorofemoral bypass depends on the ability of one iliac artery to supply adequate blood for both legs without causing a decline in flow to the donor leg. The surgical literature has confirmed that this concept is correct, at least when the patient is at rest as long as there is no significant disease in the donor iliac arterial system. If needed, a suboptimal donor iliac artery can often be improved using endovascular techniques to make it satisfactory for use as a donor vessel. Thus the primary considerations from an anatomic standpoint are: Does the patient have ipsilateral iliac artery disease that does not appear favorable for endovascular treatment? Is the contralateral iliac arterial system free of hemodynamically significant disease, and if not, can it be improved with endovascular techniques to make it a suitable

PREOPERATIVE EVALUATION A lower extremity segmental arterial noninvasive examination should be performed to calibrate the severity of disease and to serve as a baseline to which post-reconstruction studies may be compared. A good-quality CT angiogram may be sufficient for determining suitability for a femorofemoral bypass and operative planning. However, resolution might not be adequate to determine the level of disease in the common and external iliac arteries, particularly if there is significant calcification, which significantly degrades resolution. In such cases, a conventional transfemoral angiogram is preferred. In some cases it may be useful to perform a vasodilator (papaverine)enhanced measurement of the pressure gradient between the aorta and the donor side femoral artery to determine the physiologic significance of any suspect donor iliac arterial lesion. Significant occlusive disease of the aorta itself is unusual in the face of at least one patent common iliac artery, but if the aorta is occluded, the occlusion must be addressed (endovascular in many cases) or another procedure must be considered.

TECHNIQUE The operation is performed with the patient supine. The operation may be performed with general, regional, or even local anesthesia. Perioperative prophylactic antibiotics are administered and continued for 24 hours. Specific antibiotic coverage is administered as necessary in cases with established remote infection and critical limb ischemia such that surgery cannot be delayed for a period to attempt to clear infection. Femoral arteries are exposed through a longitudinal groin incision most often, because this allows more flexibility depending on findings at inspection of the target arteries. The graft is tunneled in the subcutaneous tissue from one groin incision to the other. The general strategy is to try to maximize the radius of curvature of any changes in the direction of the graft to prevent graft kinking. The tunnel forms an inverted U and should be brought well above the level of the groin incisions to prevent acute angulation of the graft at any point (Figure 1). Care must be taken to keep the graft anterior to the anterior abdominal fascia in most cases. The tunnel may be created using a tubular tunneler if one is available or with a combination of finger dissection and a large clamp. Special care must be taken when tunneling through areas of scarring from previous incisions where there might even be herniated abdominal contents at risk of injury during tunneling. Grafts are placed in the preperitoneal potential space only in very unusual circumstances, such as a uniquely thin subcutaneous layer or an abnormal abdominal wall (from radiation, scarring, etc.). The first reported femorofemoral bypass was actually performed with a disobliterated superficial femoral artery autograft, and many have been performed with venous autografts. However, prosthetic grafts, usually expanded polytetrafluoroethylene (ePTFE) or polyester textile, are used unless there is local or remote infection, which

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operating simultaneously. In either case, the donor-side anastomosis is completed first and the entire system is flushed of air and possible debris before the recipient-side anastomosis is completed. Acceptable flow is then confirmed in donor inflow and bilateral outflow arteries using continuous-wave Doppler with a sterile Doppler probe. The feet are inspected, and pulses are palpated or flow to the feet is interrogated as necessary to ensure that perfusion is adequate.

POSTOPERATIVE CARE AND FOLLOW-UP

FIGURE 1  Standard inverted-U configuration of femorofemoral

bypass graft. In this case both anastomoses have been made to the common femoral arteries, but the site of donor and target artery anastomoses will vary depending on imaging and the patient’s anatomy and habitus.

would increase the risk of graft infection. The author prefers supported ePTFE grafts, but there is no evidence that favors one graft material or external support. A 6-mm-diameter graft is sufficient. A key technical point is that the choice of the artery to which the graft will be anastomosed can have a profound impact on the geometry of the reconstruction. This cannot be predicted with certainty until the arteries have been explored. In some cases, the graft has a satisfactory geometry with anastomoses confined to the common femoral arteries. However, anastomosis at least in part to the deep femoral artery tends to reduce the requirement to bring the graft into a sagittal plane parallel to the common femoral artery and can thereby reduce the tendency for the graft to kink adjacent to the anastomosis. In patients with unusually protuberant abdominal walls, the plane of the graft tunnel may be tipped unusually forward. This can cause buckling of the graft opposite the heel of the end-to-side anastomosis, with a posterior indentation of the anterior wall of the graft at this point. This can compromise the graft lumen and increase the risk of stasis and thrombosis. Such a problem may be ameliorated by making an unusually short graft-to-artery anastomosis or by choosing a more distal artery for anastomosis. The superficial femoral artery may also be used as a target if it has no significant disease. The extent of exposure and control of the femoral arteries (common, superficial, and deep femoral) depend on where the surgeon determines the most favorable anastomosis can be made. Local endarterectomy is not desirable because the risk of anastomotic pseudoaneurysm may be increased, but endarterectomy may be performed as necessary to improve the donor and recipient arteries. Once the donor and recipient arteries have been selected and the graft has been tunneled, the patient is anticoagulated and a longitudinal arteriotomy is then made on the appropriate femoral artery or combination of femoral artery branches. The graft is spatulated to allow an anastomotic hood slightly longer than the arteriotomy, and the anastomosis is created between the side of the artery and the end of the graft with running 5–0 or 6–0 polypropylene or PTFE suture. A 3.5-mm-diameter arterial dilator is passed through the toe (the inferior end) of the anastomosis into the outflow vessels before the anastomosis is completed, and this dilator must pass without difficulty to ensure that outflow will be adequate. The contralateral anastomosis is performed in the same manner. The donor anastomosis is generally performed first, but it may be performed simultaneously with the recipient if two surgeons are

Patients are encouraged to walk by the first postoperative day, with the help of physical therapy as necessary. They are asked to limit activity at home for a few days and then advance activity as tolerated. Overactivity is virtually never a problem with these generally older, often sedentary patients with multiple comorbidities. We perform a noninvasive surveillance examination at the time of the patient’s first return visit about 2 weeks after surgery. This examination includes standard ankle (posterior tibial and dorsal pedal) blood pressure measurements and Doppler waveforms, great toe photoplethysmographic waveforms and blood pressures, and a graft duplex scan with pulsed-Doppler waveform inspection and velocity estimation at the native inflow above the donor anastomosis, at the donor anastomosis, at several sites within the graft, at the recipient anastomosis, and at the outflow vessels on both donor and recipient sides. We repeat the clinical examination and surveillance noninvasive studies every 3 months for the first year, consistent with our protocol for infrainguinal bypass grafts. We acknowledge that there is less clear evidence that this surveillance predicts impending graft failure than is the case for infrainguinal bypass grafts, but this has not been adequately studied for femorofemoral bypass follow-up.

RESULTS AND INFLUENCE OF PATIENT AND GRAFT FACTORS Earlier reports of series of femorofemoral bypass provided fairly good patency rates. However, older methods of calculating and estimating patency were not consistent with today’s reporting standards. A fair composite estimate of 5-year primary patency using current reporting standards is about 60% to 70%. The impact of outflow disease, most often disease of the superficial femoral artery, is a continuing area of controversy. Some authors have found that superficial femoral artery disease, especially occlusion, negatively affects femorofemoral graft patency. Others (including us) have found that superficial femoral artery disease does not negatively affect femorofemoral graft patency as long as there is good outflow to the deep femoral artery. An ankle-brachial index of about 0.8 is predicted after a femorofemoral bypass with completely normal infrainguinal outflow. This compares to a predicted ankle-brachial index of slightly greater than 1.0 after performing an AFB with normal infrainguinal outflow.

CONTINUING EVOLUTION OF THE ROLE OF FEMOROFEMORAL BYPASS Conventional bypass is a mature procedure with no major changes in recommendations regarding technique in many years. With respect to the indications, it is impossible to determine from the literature what fraction of patients undergo a femorofemoral bypass versus an AFB. It is likely that a large fraction of patients who previously have undergone a femorofemoral bypass are now treated with endovascular techniques. The fact is that a femorofemoral bypass as part of endovascular aortic aneurysm repair has emerged as one of the most common indications for this procedure.

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Selected References Brener BJ, Brief DK, Alpert J, et al: Femorofemoral bypass: A twenty-five year experience. In Yao JST, Pearce WH, (eds): Long-term results in vascular surgery, East Norwalk, 1993, Appleton & Lange, pp 385–393. Davis RC, O'Hara ET, Mannick JA, et al: Broadened indications for femorofemoral grafts, Surgery 72:990–994, 1972. Flanigan DP, Ryan TJ, Williams LR, et al: Aortofemoral or femoropopliteal revascularization? A prospective evaluation of the papaverine test, J Vasc Surg 1:215–223, 1984. Harris JP, Flinn WR, Rudo ND, et al: Assessment of donor limb hemodynamics in femorofemoral bypass for claudication, Surgery 90:764–773, 1981. Kretschmer G, Niederle B, Schemper M, et al: Extra-anatomic femoro-­ femoral crossover bypass (FF) vs. unilateral orthotopic ilio-femoral bypass (IF): An attempt to compare results based on data matching, Eur J Vasc Surg 5:75–82, 1991.

Diagnosis of Aortic Graft Infection Linda M. Reilly

The incidence of infection affecting a prosthetic aortic graft varies from less than 1% to about 4%, depending on whether the vascular prosthesis is entirely intrathoracic (1%–2%), is retroperitoneal (25 cm). However, it has since fallen out of favor for several reasons. First, it was regarded as too time-consuming and tedious. Closure of a long arteriotomy required a long incision, and it required both potential sacrifice of long segments of vein (that could be otherwise used for a bypass). Lastly, this technique sometimes resulted in aneurysmal dilation of the patch, creating the potential for thromboembolic complications or the need for an additional surgical revision. Consequently, this technique was abandoned for long-segment occlusions of the SFA. Short-segment focal SFA lesions, by contrast, may still be amenable to endarterectomy techniques, particularly among patients who have failed endovascular revascularization or who have poor conduit options for a conventional bypass. Inahara and Scott initially described their results using this technique among 100 patients (85% for claudication), emphasizing good patient selection (lesion length 14 days) are less responsive to fibrinolytic therapy than young clots (2) had a significantly lower 4-year patency of 57% compared to 83% observed in normal grafts. Intervention, based on a duplex surveillance protocol, has resulted in 5-year assisted primary patency rates of 82% to 93%, significantly higher than the 30% to 50% secondary patency rates of thrombosed vein grafts. Clinical studies indicate that routine infrainguinal bypass surveillance can enhance long-term patency by at least 15% to 20%. In regard to repair techniques, a duplex finding of a focal (2) had a significantly lower 4-year patency of 57% compared to 83% observed in normal grafts. Intervention, based on a duplex surveillance protocol, has resulted in 5-year assisted primary patency rates of 82% to 93%, significantly higher than the 30% to 50% secondary patency rates of thrombosed vein grafts. Clinical studies indicate that routine infrainguinal bypass surveillance can enhance long-term patency by at least 15% to 20%. In regard to repair techniques, a duplex finding of a focal (70% diameter reduction) stenosis: PSV > 300 cm/sec and Vr > 3.5. These lesions have a damped velocity waveform downstream of the stenosis and reduction in MGV; the MGV is calculated

as the average of graft PSV measured at two or three nonstenotic graft segments of less than 30 cm/sec compared to levels when no graft stenosis was present. A decrease in the ankle-to-brachial index (ABI) also predicts an acquired graft lesion, but it is associated with a low positive predictive value for graft thrombosis. In selected patients, such as those with a high-grade stenosis identified in the body of the graft or at an anastomosis and a low graft flow velocity or ABI, duplex scanning can supplant arteriography for clinical decision making and the need for graft revision. Serial duplex testing beginning in the early postoperative period, repeated within 1 to 2 months, and then at 6-month intervals if no graft abnormality is detected offers several advantages. It predicts initial technical success, identifies the graft with residual stenosis, and detects deterioration in graft functional patency, so developing occlusive lesions can be easily managed by elective surgical revision or percutaneous transluminal angioplasty. A wide range of duplex-derived blood flow velocities can be measured in infrainguinal grafts after successful bypass grafting. In general, PSV in mid and distal graft segments exceeds 40 to 45 cm/sec unless the conduit diameter is greater than 6 mm or the graft runoff is limited to an isolated tibial artery segment or dorsalis pedis artery. The graft PSV varies with luminal diameter, and it is recommended that duplex surveillance be performed using diameter-specific criteria. Belkin and colleagues found graft flow velocity was lower (p < .04) in inframalleolar grafts (59 cm/sec) compared to tibial (77 cm/sec) and popliteal (71 cm/sec) grafts. Only four of 72 grafts, all to inframalleolar arteries, had a measured PSV below 45 cm/sec. Arm vein or varicose saphenous segment grafts were also associated with low graft conduit flow velocity. Lower limb prosthetic bypasses have an MGV of 50 to 70 cm/sec, axillofemoral bypass has an MGV greater than 150 cm/sec, and femorofemoral bypass has an MGV greater than 100 cm/sec. Thus, the hemodynamic parameter by itself does not predict impending thrombosis but can guide decision making regarding the potential benefit of instituting postoperative oral anticoagulation. A low graft flow velocity because of poor runoff is an infrequent finding. Management of low-flow grafts caused by poor runoff is controversial, but options include anticoagulation, sequential bypass grafting, or adjunctive distal arteriovenous fistulas, the last two modalities being constructed to augment graft flow. Interpretation of vascular laboratory testing allows the bypass graft to be classified as normal or abnormal (Figure 1, Table 1). Normal graft hemodynamics in limbs revascularized for critical ischemia have a low-resistance graft blood-flow pattern, with antegrade flow throughout the pulse cycle reflecting hyperemic flow. Within days to several weeks, the hyperemic graft flow dissipates, and the velocity waveform gradually changes to a triphasic configuration typical of normal peripheral artery blood flow and ABI. If the normal triphasic graft velocity waveform changes to a monophasic configuration, coupled with an MGV decrease, a graft stenosis should be suspected. The reduction in waveform pulsatility and the presence of a diastolic blood flow component indicates a pressure-reducing stenosis and compensatory arteriolar dilatation. The site of graft stenosis may be proximal or distal to the recording site. A monophasic waveform with low MGV has been observed in approximately 40% of grafts with stenoses. All patients were asymptomatic, and resting ABI varied from 0.7 to 0.9. Typically, the severity of stenosis was classified in the 50% to 75% diameterreduction category by both duplex scanning and arteriography. An uncommon (6% of abnormal grafts) but ominous waveform demonstrated a staccato velocity spectral pattern representing to-and-fro motion of blood within the compliant venous conduit with each pulse cycle (Figure 2). This waveform was always associated with a high-grade distal stenosis and was a harbinger of graft thrombosis. The minimal antegrade blood flow in these grafts complicates angiographic visualization of the distal graft and anastomosis, causing some clinicians to refer to this condition as “pseudoocclusive graft failure.”



Surveillance of Lower Extremity Bypass Grafts

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FIGURE 1  Duplex surveillance proto-

col and interpretation criteria for normal and abnormal bypasses. ABI, Ankle-tobrachial index; Abn, abnormal; PSV, peak systolic velocity.

TABLE 1:  Normal and Abnormal Duplex Ultrasound Categories of Bypass Graft Blood Flow Duplex Category

Velocity Spectra (Waveform) Characteristics

Normal

Normal PVR

Triphasic configuration Vp > 45 cm/sec at mid to distal graft recording site Applicable for graft diameter 3–6 mm

Low PVR

Biphasic configuration End-diastolic flow velocity >0 Vp > 45 cm/second An expected waveform at operation and in the early postoperative period caused by revascularization hyperemia

Abnormal Low Graft Flow Velocity

High PVR

Monophasic configuration No diastolic forward flow Vp 3.5) has uniformly correlated with an arteriographically detected lesion that warranted correction. Duplex scanning and surveillance is of the utmost importance in the high-risk group, whether that relates to conduit type, vein diameter, or poor inflow and outflow considerations. The PREVENT (Proliferation REduction with Vascular ENergy Trial) III database provided data that showed that high-risk conduits (vein diameter 2 yr

Atherosclerosis

2%/yr

Presenting Symptoms*

Hemodynamic Characteristics of Repaired Stenoses

*Identified by surveillance program using duplex scanning and Doppler-derived pressure measurements. ABI, Ankle-to-brachial index.

Common to all reports dealing with graft surveillance is a caveat stating that symptomatic limb ischemia should not be a requisite criterion for graft revision. Because graft type, luminal diameter, configuration, and runoff vary widely, the surveillance protocol should not be based on rigid criteria applied at a single point in time, but rather it should be designed to detect changes from baseline graft and limb hemodynamics measured at operation or in the perioperative period once an initially successful bypass is apparent. The combined velocity and pressure changes allow detection of low-flow, abnormal grafts, a hemodynamic state that commonly precedes graft failure (positive predictive value, 60%–70%; negative predictive value, 95%). Interpretation of graft surveillance studies must consider that the magnitude

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Open Surgery and Endovascular Management of Failing Infrainguinal Bypass Graft Scott A. Berceli

Originally described in 1984, failing bypass grafts now include any stenosis or abnormal hemodynamics determined by clinical examination, duplex scanning, or arteriography. Although clinical examination provides an initial assessment for vein graft patency, this approach in isolation fails to identify up to 70% of significant lesions. Duplex ultrasound has evolved into the test of choice to identify significant vein graft lesions.

PATHOLOGY OF THE FAILING VEIN GRAFT Multicenter prospective data demonstrate that only 50% of patients with infrainguinal vein grafts are free from clinically significant stenosis, revision, or major amputation at 1 year. The highest rate of graft failure occurs in the 3 months following implantation, where 15% of grafts are lost or require repair. Technical or judgment errors at the time of graft insertion dominate the underlying etiology for these early problems, with graft torsion, retained valves, unrecognized conduit abnormalities, and anastomotic narrowing being the most common. Progressive loss of primary graft patency in the 6- to 18-month time frame occurs predominantly through intimal hyperplasia development in the perianastomotic (53% incidence) or midgraft (30% incidence) regions. After 2 years, graft loss is reduced to about 4% per year and results from either delayed intimal hyperplasia or progressive atherosclerosis in the proximal and distal arterial segments. Development of optimal strategies for treating the failing graft has been hampered by the heterogeneity of lesion pathology. Although a specific open surgical or endovascular approach may be appropriate for pathologies observed within the initial month after implantation, this same treatment approach can have limited durability when applied to hyperplastic lesions that are observed in the range of 9 to 18 months postoperatively. Unfortunately, few published studies have sufficient statistical power to adequately examine the influence of lesion pathology on the success or failure of a specific treatment strategy.

FACTORS INFLUENCING REPAIR CHOICE Open surgical revision can be adapted to encompass the full spectrum of potential graft pathologies, but the durability of endovascular treatments for the failing vein graft are inherently linked to the characteristics of the lesion. Time after implantation, lesion location, stenosis length, and graft occlusion have been identified as important surrogates for lesion pathology that significantly influence the

intermediate and long-term success of endovascular interventions, and they thus become important factors in directing the choice between open and endovascular revision (Figure 1).

Time after Graft Implantation Flow-limiting lesions identified within the initial 3 months are usually secondary to technical or judgment issues at the time of graft implantation. Delayed identification of kinks, twists, and external constricting bands that result from creating the graft tunnel present a variety of technical challenges to endovascular therapies and are best approached with open surgical revision. Intraluminal pathologies such as retained valves or intraluminal webs are more amenable to endovascular interventions, and small series have described the use of atherectomy devices to treat these lesions. Despite the promising results in this select group of patients, direct excision and vein patch angioplasty remain the standard treatment for preexisting vein pathology. Selection of a suboptimal distal target with reductions in graft flow presents an early risk for vein graft failure. Although advances in endovascular technologies have improved our ability to treat infrageniculate lesions, creation of a distal jump graft likely offers the most durable solution in patients with available autogenous conduit and a suitable distal target. Although these early lesions encompass a variety of underlying etiologies, in aggregate they present significant challenges to endovascular revisions, supported by numerous reports documenting a high failure rate for these less invasive approaches.

Stenosis Length Stenosis length is well described as an important risk factor for influencing durability following endovascular interventions. Such less invasive therapies used in the treatment of lesions less than 2 cm in length are significantly more durable than those aimed at longsegment disease, with an approximate threefold increase in the need Vein Graft Stenosis Requiring Revision

Less than 3 months since implantation yes

no Greater than 2 cm in length or multiple stenoses no

yes

Open Surgical Revision yes

Failed two previous endovascular revisions no Endovascular Revision FIGURE 1  Treatment algorithm for patients who come to the hospi-

tal with a vein graft stenosis.



Open Surgery and Endovascular Management of Failing Infrainguinal Bypass Graft

for reintervention in these longer lesions. Similarly, vein grafts undergoing endovascular treatment for tandem lesions are prone to earlier failure, with a 2.5-fold increase in the failure rate following an intervention to treat multiple lesions.

Lesion Location The role of endovascular therapies in the treatment of perianastomotic lesions is less well established. Theoretically, the nonuniform geometries and abnormal flow dynamics, major components for the development of these lesions, are not improved by endovascular revision, and the forces leading to augmented hyperplastic growth remain unchanged. Studies examining this issue, however, have been mixed, with some suggesting an increased restenosis rate but others failing to demonstrate this association. On a practical level, endovascular repair of lesions located a short distance from the anastomosis likely respond similar to midgraft lesions, whereas those extending into the suture line are constrained by the local geometry and are at increased risk for failure.

Graft Occlusion The significant pathology and extensive injury that result from graft thrombosis present notable hurdles in attempted endovascular interventions for occluded grafts. Poor outcomes following such interventions in these difficult situations have been well documented. In patients coming to the hospital with graft thrombosis, endovascular interventions are only marginally successful at restoring patency, and if they are successful, early failure rates are exceedingly high.

TECHNICAL CONSIDERATIONS FOR REPAIR Endovascular Repair The principal technique used in endovascular revision of the failing vein graft is percutaneous transluminal angioplasty. Access may be obtained using either a retrograde and contralateral or an antegrade and ipsilateral femoral approach. A contralateral approach is often preferred because it offers a comfortable working length from the arterial entry site to the origin of the bypass graft. This crossover technique, however, may be limited by previous placement of a bifurcated aortic graft or in some cases an insufficient catheter length to reach the most distal tibial lesions in the contralateral limb. In these instances, the ipsilateral antegrade approach is a reasonable alternative, but it may be untenable in the obese patient or unsuitable for treating proximal vein graft lesions. Brachial access or direct graft puncture may be used in these situations. Angioplasty balloon size should be chosen by the apparent normal diameter of the proximal or distal graft. Hyperplastic lesions typically encountered in the vein graft tend to be quite firm, and high-pressure balloons with extended inflation times are commonly required to fully efface these narrowings. Cutting balloon angioplasty has been proposed as a solution to reduce recurrent stenosis following treatment of hyperplastic vein graft lesions. Nevertheless, results using this technique have been mixed. It is conceptually attractive that a controlled series of longitudinal lacerations into the lesion would facilitate effacement using a conventional angioplasty balloon. However, initial reports failed to demonstrate any improvement in primary patency when using a cutting balloon to either improve a suboptimal result or intentionally predilate a stenosis. Subsequent reports have presented a contrasting view. Marked improvements in stenosis-free patency were reported with the use of a cutting balloon versus conventional angioplasty (62% vs. 34% at 4 years), and these results approached the stenosis-free patency observed following open surgical repair (74% at 4 years).

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Stenting and directional atherectomy have also been described in several small series as potential adjunct interventions for the failing vein graft. In one study of eight patients, patency 1 year following stent placement was low, at only 25%. The results of atherectomy in a larger study of 35 patients have been more promising, with a stenosisfree patency of 79% at 3 years. However, complication rates associated with atherectomy are relatively high, with major complications reported in approximately 10% of the cases.

Open Operation Surgical procedures used for graft revision vary with the location, length, and number of lesions. Focal lesions less than 2 cm in length, often with underlying intimal hyperplasia or a sclerotic valve leaflet, are commonly repaired using a patch angioplasty technique. Highly focal lesions may be amenable to excision and reanastomosis, but this is technically feasible in only a minority of cases where there is local redundancy in the vein graft. More extensive midgraft lesions, often demonstrating diffuse luminal narrowing or tandem lesions in close proximity, are best treated with interposition grafting. Hyperplastic lesions at the anastomosis or atherosclerotic lesions involving the graft runoff arteries are most suitable for sequential (or jump) bypass grafting. The optimal conduit for graft revision has not been fully established and is subject to the individual surgeon’s preference. Arm vein, and in particular the basilic vein, can be an attractive option because it is usually spared during the initial operation, is amenable to a two-team operative approach, and preserves the continuity of the contralateral leg vein for future use. Challenging the conventional bias toward autogenous reconstructions, a small retrospective review by Veith and colleagues documented an 83% primary patency rate for ePTFE prosthetic interposition graft repair, which was not notably different from their parallel experience with autogenous repairs. ePTFE thus seems a reasonable alternative for surgical revision in patients lacking autogenous conduit.

OUTCOMES The vast majority of the published literature examines either endovascular or surgical interventions independently, and only a few studies provide a direct comparison of the two types of repair. Review of these studies suggests a second reintervention procedure occurs in approximately 25% to 35% of vein grafts within the first year, with permanent graft loss in 10% to 15%. There is a continued need for intervention between 1 and 5 years, leading to progressive decline in primary patency, but the majority of these procedures are successful in maintaining graft patency. No clear difference in the durability of endovascular versus open surgical repair is apparent from the available aggregate data. In the absence of randomization, a direct assessment of the superiority between the two repair types is difficult. Despite its limitations, probably the best direct comparison of endovascular and surgical vein graft revision can be extracted from PREVENT III (Project of Ex Vivo graft Engineering via Transfection), a large multicenter trial designed to evaluate the efficacy of edifoligide in reducing vein graft failure. Enrolling more than 1400 patients who required 313 grafts revisions, this multicenter study eliminates single-institution bias and provides a modern approach to this problem. These data demonstrated that an open surgical revascularization imparted an improved graft survival over an endovascular intervention, and endovascular approaches more commonly required multiple procedures to maintain graft patency. These data were balanced by the perceived benefit of reduced morbidity and mortality that endovascular revisions held over open surgical interventions. Interestingly, neither hospital length of stay nor global quality of life, which one might postulate would benefit by endovascular intervention, was significantly different between endovascular and open surgical procedures in this study.

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In general, patient comorbidities appear to have limited influence on the durability of open surgical or endovascular revisions. Among the exceptions may be hypertension, which seems to be associated with reduced failure following surgical revisions (hazard ratio [HR], 0.3). Although the underlying reason for this observation is not readily apparent, the concomitant medications used for control of hypertension might have positively influenced the durability. However, among the strongest effect from medications is observed from HMG-CoA reductase inhibitors (statins), where statin administration has been associated with a significant improvement in primary patency following open revision (HR, 0.4).

CONCLUSIONS Open surgical revisions appear to offer a modest benefit in primary patency, but likely at the cost of increased periprocedural morbidity. Although endovascular revisions are more prone to failure, recurrent lesions following this therapy are usually amenable to reintervention so that the secondary patency rates for both endovascular and open interventions are essentially equivalent. Given this, endovascular intervention as an initial treatment modality seems reasonable for favorable lesions. Exceptions to this approach are stenotic lesions longer than 2 cm, multiple stenoses, lesions occurring within 3 months of graft placement, or interventions for graft thrombosis, where endovascular failures are high and open surgery as an initial approach is warranted.

Complications and Treatment of Persistent Sciatic Arteries David J O’Connor, Nicholas J Gargiulo III, and Frank J Veith

The persistent sciatic artery (PSA), first described by Green in 1832, is a rare congenital anomaly resulting from the failure of regression of the sciatic artery during the embryonal period. Diagnosis can be difficult, and life-and limb-threatening complications are well recognized. Descriptions and management of PSAs have been limited to several isolated case reports in the literature. The reported incidence of this condition has been estimated to occur in only 0.025% to 0.05% of the general population.

CLINICAL CHARACTERISTICS During embryonal development, the sciatic artery is the main blood supply to the lower extremity until the 6th week of gestation. Beyond this period, the artery begins to regress, and its remnants contribute to the formation of the inferior gluteal, deep femoral, popliteal, peroneal, and pedal arteries. The sciatic artery can fail to involute in either complete or incomplete forms. A complete sciatic artery, occurring in 63% to 79% of cases, provides the main blood flow to the lower extremity. It originates off the internal iliac artery, courses through the greater sciatic foramen, runs

Selected References Avino AJ, Bandyk DF, Gonsalves AJ, et al: Surgical and endovascular intervention for infrainguinal vein graft stenosis, J Vasc Surg 29:60–71, 1999. Berceli SA, Hevelone ND, Lipsitz SR, et al: Surgical and endovascular revision of infrainguinal vein bypass grafts: Analysis of midterm outcomes from the PREVENT III trial, J Vasc Surg 46:1173–1179, 2007. Hoksbergen AWJ, Legemate DA, Reekers JA, et al: Percutaneous transluminal angioplasty of peripheral bypass stenoses, Cardiovasc Intervent Radiol 22:282–286, 1999. Mills JL, Fujitani RM, Taylor SM: The characteristics and anatomic distribution of lesions that cause reversed vein graft failure: A five-year prospective study, J Vasc Surg 17:195–204, 1993. Nguyen LL, Conte MS, Menard MT, et al: Infrainguinal vein bypass graft revision: Factors affecting long-term outcome, J Vasc Surg 40:916–923, 2004. Sanchez LA, Suggs WD, Marin ML, et al: Is percutaneous balloon angioplasty appropriate in the treatment of graft and anastomotic lesions responsible for failing vein bypasses? Am J Surg 168:97–101, 1994. Sanchez LA, Suggs WD, Marin ML, et al: The merit of polytetrafluoroethylene extensions and interposition grafts to salvage failing infrainguinal vein bypasses, J Vasc Surg 23:329–335, 1996. Simosa HF, Pomposelli FB, Dahlberg S, et al: Predictors of failure after angioplasty of infrainguinal vein bypass grafts, J Vasc Surg 49:117–121, 2009. Sullivan J, Welch HJ, Iafrati MD, et al: Clinical results of common strategies used to revise infrainguinal vein grafts, J Vasc Surg 24:909–919, 1996. Whittemore AD, Donaldson MC, Polak JF, et al: Limitations of balloon angioplasty for vein graft stenosis, J Vasc Surg 14:340–345, 1991.

along the adductor magnus muscle, and joins the popliteal artery distally lateral to the insertion of the adductor magnus. The superficial femoral artery is often hypoplastic and terminates in the thigh. The incomplete PSA is hypoplastic and ends in the thigh, and the superficial femoral artery provides the main blood supply to the popliteal artery (Figure 1). Bilateral PSAs occur in about 20% of cases. Associated venous anomalies are present and can include a persistent sciatic vein or large communicating veins between the deep femoral vein and the popliteal vein. PSAs are asymptomatic in up to 40% of patients. However, they are prone to early atherosclerosis and aneurysm formation. This is thought to be partially caused by congenital hypoplasia of the wall as well as repetitive traumatic forces to the artery during sitting and hip flexion and extension. The presence of a mass in the buttock, claudication, acute ischemia, gangrene, and sciatica are all reported symptoms that can develop. Aneurysms are the most common cause of symptoms in patients with a PSA, and patients with aneurysms have a high associated rate of complications and limb loss. The estimated incidence of PSA aneurysm formation is between 15% and 44%. They form posteriorly at the level of the greater trochanter and are often palpable. Distal embolization, thrombosis, and rupture into the gluteal region are possible complications. With larger aneurysms, compression of the adjacent sciatic nerve can lead to sciatica, foot drop, or progressive loss of function of the extremity. Progressive atherosclerosis can also occur in a sciatic artery as in any lower extremity artery. The resulting arterial insufficiency can range from claudication to tissue loss and gangrene.

DIAGNOSTIC CONSIDERATIONS Detection of a PSA by physical examination alone can be difficult. Cowie’s sign, the classic finding, is the absence of a femoral pulse with intact popliteal and pedal pulses. It has only been reported in five

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In general, patient comorbidities appear to have limited influence on the durability of open surgical or endovascular revisions. Among the exceptions may be hypertension, which seems to be associated with reduced failure following surgical revisions (hazard ratio [HR], 0.3). Although the underlying reason for this observation is not readily apparent, the concomitant medications used for control of hypertension might have positively influenced the durability. However, among the strongest effect from medications is observed from HMG-CoA reductase inhibitors (statins), where statin administration has been associated with a significant improvement in primary patency following open revision (HR, 0.4).

CONCLUSIONS Open surgical revisions appear to offer a modest benefit in primary patency, but likely at the cost of increased periprocedural morbidity. Although endovascular revisions are more prone to failure, recurrent lesions following this therapy are usually amenable to reintervention so that the secondary patency rates for both endovascular and open interventions are essentially equivalent. Given this, endovascular intervention as an initial treatment modality seems reasonable for favorable lesions. Exceptions to this approach are stenotic lesions longer than 2 cm, multiple stenoses, lesions occurring within 3 months of graft placement, or interventions for graft thrombosis, where endovascular failures are high and open surgery as an initial approach is warranted.

Complications and Treatment of Persistent Sciatic Arteries David J O’Connor, Nicholas J Gargiulo III, and Frank J Veith

The persistent sciatic artery (PSA), first described by Green in 1832, is a rare congenital anomaly resulting from the failure of regression of the sciatic artery during the embryonal period. Diagnosis can be difficult, and life-and limb-threatening complications are well recognized. Descriptions and management of PSAs have been limited to several isolated case reports in the literature. The reported incidence of this condition has been estimated to occur in only 0.025% to 0.05% of the general population.

CLINICAL CHARACTERISTICS During embryonal development, the sciatic artery is the main blood supply to the lower extremity until the 6th week of gestation. Beyond this period, the artery begins to regress, and its remnants contribute to the formation of the inferior gluteal, deep femoral, popliteal, peroneal, and pedal arteries. The sciatic artery can fail to involute in either complete or incomplete forms. A complete sciatic artery, occurring in 63% to 79% of cases, provides the main blood flow to the lower extremity. It originates off the internal iliac artery, courses through the greater sciatic foramen, runs

Selected References Avino AJ, Bandyk DF, Gonsalves AJ, et al: Surgical and endovascular intervention for infrainguinal vein graft stenosis, J Vasc Surg 29:60–71, 1999. Berceli SA, Hevelone ND, Lipsitz SR, et al: Surgical and endovascular revision of infrainguinal vein bypass grafts: Analysis of midterm outcomes from the PREVENT III trial, J Vasc Surg 46:1173–1179, 2007. Hoksbergen AWJ, Legemate DA, Reekers JA, et al: Percutaneous transluminal angioplasty of peripheral bypass stenoses, Cardiovasc Intervent Radiol 22:282–286, 1999. Mills JL, Fujitani RM, Taylor SM: The characteristics and anatomic distribution of lesions that cause reversed vein graft failure: A five-year prospective study, J Vasc Surg 17:195–204, 1993. Nguyen LL, Conte MS, Menard MT, et al: Infrainguinal vein bypass graft revision: Factors affecting long-term outcome, J Vasc Surg 40:916–923, 2004. Sanchez LA, Suggs WD, Marin ML, et al: Is percutaneous balloon angioplasty appropriate in the treatment of graft and anastomotic lesions responsible for failing vein bypasses? Am J Surg 168:97–101, 1994. Sanchez LA, Suggs WD, Marin ML, et al: The merit of polytetrafluoroethylene extensions and interposition grafts to salvage failing infrainguinal vein bypasses, J Vasc Surg 23:329–335, 1996. Simosa HF, Pomposelli FB, Dahlberg S, et al: Predictors of failure after angioplasty of infrainguinal vein bypass grafts, J Vasc Surg 49:117–121, 2009. Sullivan J, Welch HJ, Iafrati MD, et al: Clinical results of common strategies used to revise infrainguinal vein grafts, J Vasc Surg 24:909–919, 1996. Whittemore AD, Donaldson MC, Polak JF, et al: Limitations of balloon angioplasty for vein graft stenosis, J Vasc Surg 14:340–345, 1991.

along the adductor magnus muscle, and joins the popliteal artery distally lateral to the insertion of the adductor magnus. The superficial femoral artery is often hypoplastic and terminates in the thigh. The incomplete PSA is hypoplastic and ends in the thigh, and the superficial femoral artery provides the main blood supply to the popliteal artery (Figure 1). Bilateral PSAs occur in about 20% of cases. Associated venous anomalies are present and can include a persistent sciatic vein or large communicating veins between the deep femoral vein and the popliteal vein. PSAs are asymptomatic in up to 40% of patients. However, they are prone to early atherosclerosis and aneurysm formation. This is thought to be partially caused by congenital hypoplasia of the wall as well as repetitive traumatic forces to the artery during sitting and hip flexion and extension. The presence of a mass in the buttock, claudication, acute ischemia, gangrene, and sciatica are all reported symptoms that can develop. Aneurysms are the most common cause of symptoms in patients with a PSA, and patients with aneurysms have a high associated rate of complications and limb loss. The estimated incidence of PSA aneurysm formation is between 15% and 44%. They form posteriorly at the level of the greater trochanter and are often palpable. Distal embolization, thrombosis, and rupture into the gluteal region are possible complications. With larger aneurysms, compression of the adjacent sciatic nerve can lead to sciatica, foot drop, or progressive loss of function of the extremity. Progressive atherosclerosis can also occur in a sciatic artery as in any lower extremity artery. The resulting arterial insufficiency can range from claudication to tissue loss and gangrene.

DIAGNOSTIC CONSIDERATIONS Detection of a PSA by physical examination alone can be difficult. Cowie’s sign, the classic finding, is the absence of a femoral pulse with intact popliteal and pedal pulses. It has only been reported in five



Complications and Treatment of Persistent Sciatic Arteries Common iliac a.

Common iliac a.

Common iliac a.

Common iliac a.

Common femoral a.

Common femoral a.

595

Internal iliac a.

Femoral a. Sciatic a.

Sciatic a.

Sciatic a.

Profunda a.

Profunda a.

Popliteal a.

Popliteal a.

Foot plexus

A

Superficial femoral a.

Superficial femoral a.

Femoral a.

B

C

Sciatic a.

D

FIGURE 1  The embryologic development of the lower extremity arterial circulation. A, Complete sciatic

artery. B, An early femoral artery and regression of the sciatic artery. C, Continued femoral artery growth. D, Normal femoral artery and former sciatic artery (dotted line) showing the sciatic artery’s contribution to the internal iliac, profunda, and popliteal arteries.  (From Williams LR, Flanigan DP, O’Connor RJ, et al: Persistent sciatic artery: Clinical aspects and operative management, Am J Surg 145:687–693, 1983, with permission.)

cases. In patients with an aneurysm of the sciatic artery, a palpable pulsatile mass can sometimes be felt over the buttock with an associated audible bruit. When a persistent sciatic artery is suspected, arteriography has been the primary diagnostic modality. The course of the artery, presence of aneurysmal or atherosclerotic disease, and the status of distal runoff to the lower extremity can be assessed with such studies. Characteristic associated findings include enlargement of the internal iliac artery with or without a hypoplastic superficial femoral artery. Aortography with lower extremity runoff should be performed, because unilateral femoral arteriography can fail to identify a PSA. A selective injection with the catheter tip placed in the orifice of the internal iliac artery should also be performed for best visualization of the sciatic artery. The use of computed tomography angiography (CTA) and magnetic resonance angiography (MRA) has recently been reported for diagnostic use and surgical planning. A detailed examination of the PSA is possible, allowing evaluation for aneurysm size, intramural thrombus burden, visualization of the contralateral side, and demonstration of totally occluded vessels that cannot be visualized on conventional arteriography. Another advantage of CTA and MRA is visualization of the PSA in relation to surrounding nerves, venous anomalies, and the musculoskeletal structure. These modalities are particularly helpful when planning an operative approach.

TREATMENT Treatment of patients with PSAs is reserved for those who develop complications or aneurysmal disease. The presence of an aneurysm, even without symptoms, warrants treatment because of an up to 25%

rate of limb loss if untreated. The course of treatment depends on the presence of an aneurysm and whether the sciatic artery is complete versus incomplete. Open surgical procedures have been traditionally performed, but recent reports have described endovascular techniques as the sole or adjunctive therapy. The goal of treatment is to prevent rupture and distal embolization. Several methods have been described for treating aneurysms, including ligation, aneurysmorrhaphy, coil embolization, and covered stent placement. In the incomplete type of PSA, ligation or embolization of the aneurysm is adequate treatment because the sciatic artery does not provide distal perfusion to the extremity. In the setting of a complete type of a PSA, an adjunctive revascularization procedure is required if ligation or embolization of the aneurysm is employed, in order to maintain lower extremity circulation. Fundamental to the treatment of PSA aneurysms is exclusion of flow to the aneurysm sac. This is necessary to prevent rupture and distal embolization. Traditionally, open surgical ligation has been used. For proximal control, this requires a retroperitoneal exposure or high ligation of the sciatic artery by a transgluteal approach. Distal ligation at the level of the sciatic or popliteal artery is employed to prevent retrograde flow into the aneurysm or distal embolization. Both approaches to proximal ligation can be challenging, and endovascular techniques have gained favor for excluding the aneurysmal segment. Coil embolization or Amplatzer plug (St. Jude Medical, St. Paul, MN) placement proximal and distal to the aneurysm have been used for successful cessation of blood flow to the aneurysm (Figure 2). Ruptured aneurysms with large hematomas or those causing compressive nerve symptoms treated by endovascular embolization usually require adjunctive surgical decompression.

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be challenging as a result of adjacent bony structures. This can be aided by the use of a lower abdominal incision with retroperitoneal control of the iliac artery. Posterior interposition graft placement, however, can ultimately result in graft thrombosis from repeated compression with sitting. Obturator and a standard iliofemoral–popliteal bypass have also been used with success in the setting of hypoplastic femoral arteries to avoid the difficulty of a transgluteal surgical approach to bypass. Transcatheter placement of covered stents has been used to exclude PSA aneurysm flow and to maintain perfusion to the distal sciatic artery. This has allowed an entirely endovascular approach to the treatment of aneurysms with complete sciatic arteries. However, this approach has only been limited to a few case reports, and the long-term success of these interventions is not known. Transcatheter access to the aneurysm usually requires contralateral retrograde access over the aortic bifurcation. A significant amount of vessel tortuosity or the presence of bilateral sciatic arteries can preclude this method of access. Retrograde access through the ipsilateral popliteal artery has been used as a method of straight-line access to the aneurysm. We have reported the use of a direct transgluteal puncture of the sciatic artery for access. With the patient in the prone position, an antegrade puncture can be performed and allows easy access to the distal sciatic artery and the popliteal and tibial arteries. This approach is useful in patients who have distal atherosclerotic disease and who need endovascular intervention. FIGURE 2  Angiogram demonstrating ruptured persistent sciatic

artery aneurysm with exclusion of outflow using an Amplatzer vascular plug (arrow).  (From Rezayat C, Sambol E, Goldstein L, et al: Ruptured persistent sciatic artery aneurysm managed by endovascular embolization, Ann Vasc Surg 24:115.e5–115.e9, 2010, with permission.)

In cases where the PSA is incomplete or the superficial femoral artery provides distal arterial flow, a revascularization procedure is not necessary after exclusion of the aneurysm. For complete sciatic arteries and conditions where the superficial femoral artery is hypoplastic, preservation of flow in the distal sciatic artery or the popliteal artery becomes necessary to maintain blood flow to the lower extremity. This can be accomplished with a bypass procedure or sciatic aneurysmorrhaphy with interposition graft placement. Common femoral-to-popliteal artery bypass procedures have traditionally been used in many instances because of their familiarity and relative feasibility. In instances where the common femoral artery is too diseased or hypoplastic to provide inflow, the sciatic artery proximal to the aneurysm can be approached through a posterolateral buttock curvilinear incision, with splitting of the gluteus maximus muscle in the direction of its fibers. Careful dissection is necessary to avoid adjacent sciatic nerve injury, especially near the aneurysm. Gaining proximal control in this area can

Popliteal Artery Adventitial Cystic Disease Justin K. Nelms, David G. Neschis, and William R. Flinn

Adventitial cystic disease of the popliteal artery is a relatively rare cause of lower limb ischemia in which single or multiloculated cysts develop within the adventitial layer of the wall of the popliteal artery.

Selected References Gargiulo NJ, O’Connor DJ, Phangureh V, et al: Management of persistent sciatic artery embolization to the lower extremity using covered stent through a transgluteal approach, Am Surg 77:366–368, 2011. Jung AY, Lee W, Chung JW, et al: Role of computed tomographic angiography in the detection and comprehensive evaluation of persistent sciatic artery, J Vasc Surg 42:678–683, 2005. Noblet D, Gasmi T, Mikati A, et al: Persistent sciatic artery: Case report, anatomy, and review of the literature, Ann Vasc Surg 2:390–396, 1988. Rezayat C, Sambol E, Goldstein L, et al: Ruptured persistent sciatic artery aneurysm managed by endovascular embolization, Ann Vasc Surg 24:115. e5–115.e9, 2010. Urayama H, Tamura M, Ohtake H, et al: Exclusion of a sciatic artery aneurysm and an obturator bypass, J Vasc Surg 26:697–699, 1997. Van Hooft IM, Zeebregts CJ, van Sterkenburk WR, et al: The persistent sciatic artery, Eur J Vasc Endovasc Surg 37:585–591, 2009. Wijeyaratne SM, Wijewardene N: Endovascular stenting of a persistent sciatic artery aneurysm via retrograde popliteal approach: A durable option, Eur J Vasc Endovasc Surg 38:91–92, 2009. Williams LR, Flanigan DP, O’Connor RJ, et al: Persistent sciatic artery: clinical aspects and operative management, Am J Surg 145:687–693, 1983. Wolf YG, Gibbs BF, Guzzetta VJ, et al: Surgical treatment of aneurysm of the persistent sciatic artery, J Vasc Surg 17:218–221, 1993.

As the typical gelatinous secretions of the intramural adventitial cyst accumulate, the cyst produces progressive obliteration of the adjacent arterial lumen. The reduction of arterial flow leads to the subsequent development of ischemic symptoms, most often intermittent claudication. The term adventitial cystic disease has been almost universally associated with the popliteal artery, but the first case of adventitial cystic disease was actually observed in the external iliac artery by Atkins and Key in 1947. They observed a 7-cm cystic lesion reminiscent of a sausage and thought it to be a myxomatous tumor of the adventitia. The first description of adventitial cystic disease of the popliteal artery was that of Ejrup and Heirtonn in 1954. They reported the incision of a mass filled with gelatinous material in a thickened area of the popliteal artery, which they believed at the time represented mucoid degeneration of the media. Subsequently, more

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LOWER EXTREMITY OCCLUSIVE DISEASE

be challenging as a result of adjacent bony structures. This can be aided by the use of a lower abdominal incision with retroperitoneal control of the iliac artery. Posterior interposition graft placement, however, can ultimately result in graft thrombosis from repeated compression with sitting. Obturator and a standard iliofemoral–popliteal bypass have also been used with success in the setting of hypoplastic femoral arteries to avoid the difficulty of a transgluteal surgical approach to bypass. Transcatheter placement of covered stents has been used to exclude PSA aneurysm flow and to maintain perfusion to the distal sciatic artery. This has allowed an entirely endovascular approach to the treatment of aneurysms with complete sciatic arteries. However, this approach has only been limited to a few case reports, and the long-term success of these interventions is not known. Transcatheter access to the aneurysm usually requires contralateral retrograde access over the aortic bifurcation. A significant amount of vessel tortuosity or the presence of bilateral sciatic arteries can preclude this method of access. Retrograde access through the ipsilateral popliteal artery has been used as a method of straight-line access to the aneurysm. We have reported the use of a direct transgluteal puncture of the sciatic artery for access. With the patient in the prone position, an antegrade puncture can be performed and allows easy access to the distal sciatic artery and the popliteal and tibial arteries. This approach is useful in patients who have distal atherosclerotic disease and who need endovascular intervention. FIGURE 2  Angiogram demonstrating ruptured persistent sciatic

artery aneurysm with exclusion of outflow using an Amplatzer vascular plug (arrow).  (From Rezayat C, Sambol E, Goldstein L, et al: Ruptured persistent sciatic artery aneurysm managed by endovascular embolization, Ann Vasc Surg 24:115.e5–115.e9, 2010, with permission.)

In cases where the PSA is incomplete or the superficial femoral artery provides distal arterial flow, a revascularization procedure is not necessary after exclusion of the aneurysm. For complete sciatic arteries and conditions where the superficial femoral artery is hypoplastic, preservation of flow in the distal sciatic artery or the popliteal artery becomes necessary to maintain blood flow to the lower extremity. This can be accomplished with a bypass procedure or sciatic aneurysmorrhaphy with interposition graft placement. Common femoral-to-popliteal artery bypass procedures have traditionally been used in many instances because of their familiarity and relative feasibility. In instances where the common femoral artery is too diseased or hypoplastic to provide inflow, the sciatic artery proximal to the aneurysm can be approached through a posterolateral buttock curvilinear incision, with splitting of the gluteus maximus muscle in the direction of its fibers. Careful dissection is necessary to avoid adjacent sciatic nerve injury, especially near the aneurysm. Gaining proximal control in this area can

Popliteal Artery Adventitial Cystic Disease Justin K. Nelms, David G. Neschis, and William R. Flinn

Adventitial cystic disease of the popliteal artery is a relatively rare cause of lower limb ischemia in which single or multiloculated cysts develop within the adventitial layer of the wall of the popliteal artery.

Selected References Gargiulo NJ, O’Connor DJ, Phangureh V, et al: Management of persistent sciatic artery embolization to the lower extremity using covered stent through a transgluteal approach, Am Surg 77:366–368, 2011. Jung AY, Lee W, Chung JW, et al: Role of computed tomographic angiography in the detection and comprehensive evaluation of persistent sciatic artery, J Vasc Surg 42:678–683, 2005. Noblet D, Gasmi T, Mikati A, et al: Persistent sciatic artery: Case report, anatomy, and review of the literature, Ann Vasc Surg 2:390–396, 1988. Rezayat C, Sambol E, Goldstein L, et al: Ruptured persistent sciatic artery aneurysm managed by endovascular embolization, Ann Vasc Surg 24:115. e5–115.e9, 2010. Urayama H, Tamura M, Ohtake H, et al: Exclusion of a sciatic artery aneurysm and an obturator bypass, J Vasc Surg 26:697–699, 1997. Van Hooft IM, Zeebregts CJ, van Sterkenburk WR, et al: The persistent sciatic artery, Eur J Vasc Endovasc Surg 37:585–591, 2009. Wijeyaratne SM, Wijewardene N: Endovascular stenting of a persistent sciatic artery aneurysm via retrograde popliteal approach: A durable option, Eur J Vasc Endovasc Surg 38:91–92, 2009. Williams LR, Flanigan DP, O’Connor RJ, et al: Persistent sciatic artery: clinical aspects and operative management, Am J Surg 145:687–693, 1983. Wolf YG, Gibbs BF, Guzzetta VJ, et al: Surgical treatment of aneurysm of the persistent sciatic artery, J Vasc Surg 17:218–221, 1993.

As the typical gelatinous secretions of the intramural adventitial cyst accumulate, the cyst produces progressive obliteration of the adjacent arterial lumen. The reduction of arterial flow leads to the subsequent development of ischemic symptoms, most often intermittent claudication. The term adventitial cystic disease has been almost universally associated with the popliteal artery, but the first case of adventitial cystic disease was actually observed in the external iliac artery by Atkins and Key in 1947. They observed a 7-cm cystic lesion reminiscent of a sausage and thought it to be a myxomatous tumor of the adventitia. The first description of adventitial cystic disease of the popliteal artery was that of Ejrup and Heirtonn in 1954. They reported the incision of a mass filled with gelatinous material in a thickened area of the popliteal artery, which they believed at the time represented mucoid degeneration of the media. Subsequently, more

Popliteal Artery Adventitial Cystic Disease

than 400 case reports have been published in the world literature that describe adventitial cystic disease in the radial, ulnar, and femoral arteries, but the vast majority of cases have involved the popliteal artery. There have also been rare reports of adventitial cystic disease involving the iliofemoral and saphenous veins.

ETIOLOGY The precise cause of popliteal artery adventitial cystic disease remains uncertain. Disparate reports of the findings from surgical exploration and from pathologic examination of cysts have resulted in several different theories. The first was the theory of microtrauma, in which repetitive stretch injury to the arterial wall or injury from surrounding musculotendinous structures was thought to cause cystic myxomatous degeneration of the adventitia. Past reports have noted that the young men afflicted were often heavy laborers or were athletically active. However, if trauma alone were the cause, it would be expected that the condition would be seen more often. Cases of adventitial cystic disease have also been reported in children in whom chronic trauma as a primary cause would be unlikely. A second theory proposed an extraarterial origin for the adventitial cysts. Adventitial cysts closely resemble ganglion cysts and can originate from pericapsular joint tissue and then extend outward to involve the arterial wall. Advocates of this theory have noted that adventitial cystic disease has always been found adjacent to joint spaces and never in the mid thigh or mid calf. A ganglion arising from the tibiofibular joint has been reported to extend to and compress the lateral popliteal nerve, indicating the potential for these articular lesions to involve anatomically proximate structures. Some cases of adventitial disease of the popliteal artery have been reported to have a communication to the knee joint documented by an arthrogram or discovered at the time of surgical exploration. More evidence has emerged to contradict the extraarterial or ganglion theory. The cyst contents in adventitial cystic disease of the popliteal artery are essentially identical to that of typical ganglion cysts. The viscid, gel-like material is rich in mucopolysaccharides with a high content of hyaluronic acid and is markedly dissimilar to synovial fluid. A microanalysis of a cystic adventitial lesion performed by Oi and colleagues detected only one of the two types of synoviocytes that compose normal synovium, suggesting that the lesion was not derived from synovial fluid. Additionally, in most reported cases, microscopic examination has not identified a lining of synovial cells in the adventitial cyst. This has led many investigators to doubt an extraarterial origin of adventitial cysts from adjacent joint tissue. A third theory of pathogenesis for adventitial cystic disease suggests a systemic process. Adventitial cysts are thought to develop as a result of spontaneous ganglionic degeneration of the intrinsic tissue within the adventitia of the artery itself. This theory has fallen out of favor because pathologic and epidemiologic supporting evidence has been scarce, and multicentric disease has proved to be extremely rare. A final proposed etiology is the developmental theory, which at this time appears to have the most widespread acceptance and supporting evidence. The theory suggests that mucin-secreting mesenchymal cells from nearby joints are inadvertently deposited in the adventitia of vessels during embryogenesis and then secrete mucin later in life. Levien and coworkers recognized that all reported cases of adventitial cystic disease occurred in nonaxial vessels that are formed adjacent to developing joint structures in gestational weeks 15 to 22. During this time, mesenchymal tissue destined to form joints can become trapped in nearby developing nonaxial vessels and proceed to secrete mucoid material years later. Whatever the precise origin of these unusual lesions, they appear to have a relatively benign clinical source overall. Once accurately diagnosed, most have been successfully treated. The cyst wall can be resected in most patients. When involvement of the artery is extensive

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or arterial thrombosis has occurred, resection with vein graft interposition has been successful. Recurrence of these cysts is infrequent, and limb loss or other serious morbidity is rare.

CLINICAL PRESENTATION Adventitial cystic disease of the popliteal artery characteristically occurs in young, healthy, nonsmoking men without evidence of atherosclerosis or other vascular disease. Previous reviews of this disorder have noted a 5:1 predominance of men over women and a mean age of approximately 40 years. The typical patient has a relatively sudden onset of intermittent, unilateral calf claudication. Severe limb-threatening ischemia has been rare. Patients usually report symptoms of claudication early because of the abrupt onset and relatively disabling nature in these young men who have previously been very active in work or athletics. However, because of their young age and the absence of other risk factors, symptoms are often initially interpreted to be neurogenic or musculoskeletal, which can delay definitive diagnosis. The clinical picture may be further confused by the spontaneous resolution of symptoms and the disappearance of abnormal physical findings in the some patients. In young adults with intermittent claudication or symptoms suggesting claudication, adventitial cystic disease should be considered because there are now reliable noninvasive methods available to confirm the diagnosis in most patients.

DIAGNOSIS Physical examination of patients with symptomatic adventitial cystic disease of the popliteal artery reveals reduced or absent pedal pulses on the affected side with a normal ipsilateral femoral pulse and normal pedal pulses in the asymptomatic leg. In contrast, patients with popliteal entrapment (another rare pathology seen in young claudicants) typically have normal pedal pulses at rest. Also, adventitial cystic disease is almost always unilateral, in contrast to popliteal entrapment, which is often bilateral. Distal pulses in patients with adventitial cystic disease may be obliterated by sharp flexion of the knee (Ishikawa’s sign). This too could help differentiate this condition from popliteal entrapment, where pedal pulses are obliterated by knee extension and contraction of the gastrocnemius muscle. A bruit over the popliteal fossa has been described. In the past, the diagnosis of adventitial cystic disease was made most often with standard contrast arteriography. If the adventitial cystic disease does not cause occlusion of the popliteal artery, the intramural cyst produces a focal, eccentric, smooth stenosis—the scimitar sign—on arteriography (Figure 1). If the cyst compresses the arterial lumen circumferentially, an hourglass deformity is seen. Multiplanar arteriographic images should be obtained to ensure that such a lesion is not overlooked. When adventitial cystic disease of the popliteal artery has produced occlusion, accurate diagnosis by arteriography alone is unreliable. Indirect findings include the location of the occlusion distal to the adductor hiatus, the lack of other evidence of atherosclerotic arterial occlusive disease, and the young age of the patient. Patients with popliteal arterial thrombosis produced by adventitial cystic disease may be treated initially with thrombolytic therapy, after which the characteristic arteriographic deformity might be documented, but modern adjunctive imaging techniques should be able to establish the diagnosis even in the face of thrombosis. Duplex ultrasound scanning combines arterial imaging with simultaneous detection of flow abnormalities and may be a useful initial diagnostic modality for evaluating patients with suspected adventitial cystic disease. Duplex scanning may be able to detect an avascular, sonolucent mass lesion producing an arterial stenosis. Kaufman and colleagues made the diagnosis of adventitial cystic disease based upon the B-mode image, but no flow disturbance was identifiable. Duplex ultrasound can also differentiate between

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FIGURE 1  Arteriogram in a young athlete with calf claudication dem-

onstrates a classic scimitar sign (arrows), which is virtually diagnostic of adventitial cystic disease in a patient with no evidence of atherosclerosis.

these cysts from popliteal aneurysms and is a useful postoperative surveillance tool. Computed tomography angiography (CTA) is probably the modern imaging technique of choice for the diagnosis of adventitial cystic disease of the popliteal artery and other uncommon popliteal arteriopathies. CTA provides imaging of the arterial lumen and examination of periarterial soft tissue anatomy. This direct imaging provides a significant benefit for evaluating rare disorders like popliteal entrapment or adventitial cystic disease (Figure 2). Magnetic resonance imaging (MRI) also is diagnostic and requires no contrast media or ionizing radiation. A case series by Maged’s group detailed three consecutive patients with adventitial cystic disease in whom MRI identified a cyst originating from the involved vessel wall as well as a connection with the adjacent joint. CT and MRI may be particularly helpful to establish the accurate diagnosis of adventitial cystic disease if the lesion has produced occlusion of the popliteal artery and the classic arteriographic signs are absent.

TREATMENT With the expanding application of endovascular procedures, it has become almost routine to consider percutaneous transluminal angioplasty (PTA) for treatment of focal arterial stenosis in a patient with disabling claudication. However, most attempts at endovascular treatment for adventitial cystic disease have not resulted in durable success. Initial success may be achieved by a forceful but temporary redistribution of the cyst’s contents within the wall of the artery. The response to this trauma may be the production of more cystic fluid and prompt return of symptoms. Needle aspiration of the cyst’s contents under ultrasound or CT guidance has been reported but has not provided reliable restoration of distal arterial perfusion or permanent relief of symptoms. It would appear that as long as the cyst wall remains intact there is a high likelihood that cyst contents will reaccumulate and produce a recurrence of ischemic symptoms. Surgery remains the treatment of choice for adventitial cystic disease of the popliteal artery, and when diagnosis and treatment are

A

B FIGURE 2  A, Arteriogram in a patient who demonstrated no significant occlusive lesion but had marked medial deviation of the popliteal artery, which might be suggestive of an entrapment syndrome. B, Imaging of the popliteal fossa by computed tomography demonstrated that the medial deviation in this case was produced by an adventitial cyst of the popliteal artery (arrow).

initiated before cystic disease has produced arterial thrombosis, the operative procedure is simplified. Accurate diagnosis using modern imaging techniques (duplex, CT, or MRI) allows selection of a posterior approach to the popliteal fossa rather than the standard medial approach used for femoropopliteal bypass. The posterior approach is performed with the patient prone and an S-shaped incision extending from medially above to laterally below the crease of the knee joint. This allows exposure of the involved area, which is most often directly behind the knee joint, an area that is relatively inaccessible using a medial approach unless extensive musculotendinous division is employed (Figure 3). Because the uninvolved arterial segments are normal, surgical treatment can be easily accomplished in most patients with the somewhat more limited arterial exposure afforded by the posterior approach. With careful attention to the tibial and peroneal nerves, the morbidity should be minimal and recovery shortened with this approach. The small number of patients in any single experience and the variety of treatments employed to date make it difficult to espouse a



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When arterial thrombosis has occurred, restoration of normal arterial morphology and biology is probably not possible with simple thrombectomy combined with cyst evacuation or cyst wall resection. Resection of the involved popliteal artery with interposition graft replacement is recommended under these circumstances. Autogenous vein is the preferred graft material. Prosthetic grafts have been used successfully but ideally are avoided in young patients.

Selected References

FIGURE 3  The posterior surgical approach allows exposure of the

mid portion of the popliteal artery containing a small adventitial cyst (arrow). In this case, evacuation of the cyst contents and resection of the cyst wall resulted in a return of normal distal arterial flow without grafting.

definitive surgical treatment for adventitial cystic disease. However, in most patients the cyst’s contents can be evacuated and the wall of the cyst can be resected. This restores normal luminal diameter to the popliteal artery and maintains an intact native arterial wall and endothelium. Resection of the cyst necessitates resection of at least part of the adventitia, but this does not appear to predispose to aneurysm formation. Arteriograms have been normal in patients so treated more than 9 years postoperatively, and other forms of noninvasive surveillance have continued to document the durability of this approach. Cyst resection appears to be the most direct and effective surgical treatment and is recommended whenever anatomically possible.

Chronic Compartment Syndrome and Functional Popliteal Artery Entrapment William D. Turnipseed

Atypical claudication symptoms in adolescents and young adults are often associated with athletic overuse injuries and are clinically manifested by isolated muscle group cramping and focal paresthesias on the dorsal or plantar surface of the feet. These complaints commonly have a delayed onset with exercise and last for an extended period after exercise. Atypical claudication symptoms that occur in the absence of obvious vascular disease or musculoskeletal injury can indicate the presence of chronic recurrent exertional compartment syndrome (CRECS) or functional popliteal entrapment syndrome (FPAES). These conditions are often confused with each other because the complaints are similar in quality and anatomic location and commonly overlap. CRECS and FPAES require distinctly

Fox RL, Kahn M, Adler J, et al: Adventitial cystic disease of the popliteal artery: Failure of percutaneous transluminal angioplasty as a therapeutic modality, J Vasc Surg 2:464–467, 1985. Jay GD, Ross FL, Mason RA, et al: Clinical and chemical characterization of an adventitial popliteal cyst, J Vasc Surg 9:448–451, 1989. Kaufman JL, Kupinski AM, Shah DM, et al: The diagnosis of ­adventitial cystic disease of the popliteal artery by duplex scanning, J Vasc Technol 11:132–135, 1987. Levien L, Benn C: Adventitial cystic disease: A unifying hypothesis, J Vasc Surg 28:193–205, 1998. Maged I, Turba U, Housseini A, et al: High spatial resolution magnetic ­resonance imaging of cystic adventitial disease of the popliteal artery, J Vasc Surg 51:471–474, 2010. Melliere D, Ecollan P, Kassab M, et al: Adventitial cystic disease of the popliteal artery: Treatment by cyst removal, J Vasc Surg 8:638–642, 1988. Oi K, Yoshida T, Shinohara N: Rapid recurrence of cystic adventitial disease in femoral artery and an etiologic consideration for the cyst, J Vasc Surg 53:1702–1706, 2011. Rai S, Davies R, Vohra R, et al: Failure of endovascular stenting for adventitial cystic disease, Ann Vasc Surg 23:410.e1–410.e5, 2009. Rizzo RJ, Flinn WR, Yao JST, et al: Computed tomography for evaluation of arterial disease in the popliteal fossa, J Vasc Surg 11:112–119, 1990. Tsilimparis N, Hanck U, Yousefi S, et al: Cystic adventitial disease of the popliteal artery: An argument for the developmental theory, J Vasc Surg 45:1249–1252, 2007.

different surgical procedures for successful cure. This chapter describes the clinical presentation, diagnostic testing, and treatment differences in patients with CRECS and FPAES.

EVALUATION Over the past few decades, referral patterns have changed. Previously, most patients were sent from orthopedic or sports medicine consultants because of persistent muscular cramping and pain without obvious vascular or orthopedic origins. However, as awareness of overuse syndromes, such as CRECS and FPAES, has spread, coaches, trainers, teammates, and parents searching the Internet have been consistent referral sources. Claudication complaints in these patients are atypical because symptoms affect isolated muscle groups (anterior lateral, posterior superficial, distal deep) in the lower leg, with occasional plantar or dorsal pedal paresthesias. Symptoms are associated with fixed but long exercise distances, often measured in miles, and commonly take hours to resolve after exercise. These symptoms develop in the absence of obvious vascular or musculoskeletal abnormalities. The workup of these patients includes a detailed history, physical examination, and selective noninvasive vascular imaging. The history is often more revealing than a physical examination because most are healthy adolescents or young adults actively engaged in sports activities. All patients have screening ankle-to-brachial indices (ABIs) and stress positional plethysmography using the Flow



Chronic Compartment Syndrome and Functional Popliteal Artery Entrapment

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When arterial thrombosis has occurred, restoration of normal arterial morphology and biology is probably not possible with simple thrombectomy combined with cyst evacuation or cyst wall resection. Resection of the involved popliteal artery with interposition graft replacement is recommended under these circumstances. Autogenous vein is the preferred graft material. Prosthetic grafts have been used successfully but ideally are avoided in young patients.

Selected References

FIGURE 3  The posterior surgical approach allows exposure of the

mid portion of the popliteal artery containing a small adventitial cyst (arrow). In this case, evacuation of the cyst contents and resection of the cyst wall resulted in a return of normal distal arterial flow without grafting.

definitive surgical treatment for adventitial cystic disease. However, in most patients the cyst’s contents can be evacuated and the wall of the cyst can be resected. This restores normal luminal diameter to the popliteal artery and maintains an intact native arterial wall and endothelium. Resection of the cyst necessitates resection of at least part of the adventitia, but this does not appear to predispose to aneurysm formation. Arteriograms have been normal in patients so treated more than 9 years postoperatively, and other forms of noninvasive surveillance have continued to document the durability of this approach. Cyst resection appears to be the most direct and effective surgical treatment and is recommended whenever anatomically possible.

Chronic Compartment Syndrome and Functional Popliteal Artery Entrapment William D. Turnipseed

Atypical claudication symptoms in adolescents and young adults are often associated with athletic overuse injuries and are clinically manifested by isolated muscle group cramping and focal paresthesias on the dorsal or plantar surface of the feet. These complaints commonly have a delayed onset with exercise and last for an extended period after exercise. Atypical claudication symptoms that occur in the absence of obvious vascular disease or musculoskeletal injury can indicate the presence of chronic recurrent exertional compartment syndrome (CRECS) or functional popliteal entrapment syndrome (FPAES). These conditions are often confused with each other because the complaints are similar in quality and anatomic location and commonly overlap. CRECS and FPAES require distinctly

Fox RL, Kahn M, Adler J, et al: Adventitial cystic disease of the popliteal artery: Failure of percutaneous transluminal angioplasty as a therapeutic modality, J Vasc Surg 2:464–467, 1985. Jay GD, Ross FL, Mason RA, et al: Clinical and chemical characterization of an adventitial popliteal cyst, J Vasc Surg 9:448–451, 1989. Kaufman JL, Kupinski AM, Shah DM, et al: The diagnosis of ­adventitial cystic disease of the popliteal artery by duplex scanning, J Vasc Technol 11:132–135, 1987. Levien L, Benn C: Adventitial cystic disease: A unifying hypothesis, J Vasc Surg 28:193–205, 1998. Maged I, Turba U, Housseini A, et al: High spatial resolution magnetic ­resonance imaging of cystic adventitial disease of the popliteal artery, J Vasc Surg 51:471–474, 2010. Melliere D, Ecollan P, Kassab M, et al: Adventitial cystic disease of the popliteal artery: Treatment by cyst removal, J Vasc Surg 8:638–642, 1988. Oi K, Yoshida T, Shinohara N: Rapid recurrence of cystic adventitial disease in femoral artery and an etiologic consideration for the cyst, J Vasc Surg 53:1702–1706, 2011. Rai S, Davies R, Vohra R, et al: Failure of endovascular stenting for adventitial cystic disease, Ann Vasc Surg 23:410.e1–410.e5, 2009. Rizzo RJ, Flinn WR, Yao JST, et al: Computed tomography for evaluation of arterial disease in the popliteal fossa, J Vasc Surg 11:112–119, 1990. Tsilimparis N, Hanck U, Yousefi S, et al: Cystic adventitial disease of the popliteal artery: An argument for the developmental theory, J Vasc Surg 45:1249–1252, 2007.

different surgical procedures for successful cure. This chapter describes the clinical presentation, diagnostic testing, and treatment differences in patients with CRECS and FPAES.

EVALUATION Over the past few decades, referral patterns have changed. Previously, most patients were sent from orthopedic or sports medicine consultants because of persistent muscular cramping and pain without obvious vascular or orthopedic origins. However, as awareness of overuse syndromes, such as CRECS and FPAES, has spread, coaches, trainers, teammates, and parents searching the Internet have been consistent referral sources. Claudication complaints in these patients are atypical because symptoms affect isolated muscle groups (anterior lateral, posterior superficial, distal deep) in the lower leg, with occasional plantar or dorsal pedal paresthesias. Symptoms are associated with fixed but long exercise distances, often measured in miles, and commonly take hours to resolve after exercise. These symptoms develop in the absence of obvious vascular or musculoskeletal abnormalities. The workup of these patients includes a detailed history, physical examination, and selective noninvasive vascular imaging. The history is often more revealing than a physical examination because most are healthy adolescents or young adults actively engaged in sports activities. All patients have screening ankle-to-brachial indices (ABIs) and stress positional plethysmography using the Flow

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Laboratory Pulse Volume Recorder (Parks Medical Electronics, Aloha, OR) to screen for arterial occlusive disorders and popliteal entrapment. Duplex imaging is only used when the patient comes to the hospital with chronic limb swelling in order to rule out postphlebitis syndrome or venous valvular incompetence. Duplex imaging is also helpful when a popliteal mass is present to rule out popliteal aneurysm or Baker’s cyst. Occasionally, three-phased nucleotide bone scanning is performed in patients with chronic medial tibial bone pain to rule out the presence of periostitis or microcortical fractures. Popliteal entrapment screening is done with stress positional testing using a 10-cm cuff inflated to 60 mm Hg with the patient supine, the knees extended, and the foot in neutral, forced plantarflexion, and dorsiflexion positions. Abnormal stress position testing consists of an ABI decrease greater than 30% or flattening of the plethysmographic waveforms with plantarflexion or dorsiflexion, or both. My group does not routinely use stress positional duplex imaging unless there is a clinical suggestion that venous impingement is the basis for suspected symptoms. We found that plethysmography or duplex imaging by themselves are not useful for determining whether abnormal musculotendinous anomalies are responsible for popliteal impingement. We prefer magnetic resonance angiography (MRA) to evaluate patients with suspected popliteal entrapment. The combination of stress positional T2-weighted magnetic resonance imaging (MRI) and MRA allows definition of normal and abnormal muscular tendinous structures within the popliteal fossa as well as accurate arterial imaging in younger healthy patients. Compartment pressures are routinely measured using the Stryker computer system (Stryker Surgical, Kalamazoo, MI) when claudication symptoms are referable to the anterior lateral or posterior superficial muscle groups. Resting pressures are measured bilaterally, even if complaints are unilateral. Pressures after exercise are only measured if patients had been inactive for longer than 1 month before examination because a prolonged period of inactivity results in loss of muscle tone and compartment pressures that do not accurately reflect the active physiologic status of the conditioned athlete. When exercise testing is required, the patients run outside the clinic until symptoms develop, thereby more accurately duplicating conditions under which they normally exercise. Pressures normally return to baseline level within 3 to 5 minutes after exercise. With this in mind, compartment pressures are measured at least 10 minutes after exercise. In our practice we consider normal resting pressures to be between 15 and 17 mm Hg. Pressures in excess of 25 mm Hg exceed venous closing pressure and are considered abnormal.

TREATMENT Chronic Compartment Syndrome The surgical treatment for CRECS is fasciectomy performed using local anesthesia with sedation. The most commonly released compartments in order of prevalence are the anterior lateral (47%), the posterior superficial (44%), and the distal deep posterior (9%). Anterior lateral and distal deep posterior compartment releases are done with the patient in the supine position, and the posterior superficial compartment releases are usually done with the patient prone. Drains are rarely used postoperatively for anterior lateral releases unless there is evidence of soft tissue bleeding, whereas in the posterior superficial compartment releases they are routinely used owing to the tendency to accumulate postoperative subcutaneous serum collections. Postoperative seromas and/or hematomas are the most common cause of recurrence in our surgical series, and using the drain is our best effort to prevent such complications. Drains are left in from 2 to 5 days to minimize the risk of surgical infection.

Popliteal Entrapment The popliteal entrapment releases are the only procedures routinely done under general anesthesia. The more traditional anatomic entrapments are treated using a posterior knee approach with resection of the offending musculotendinous band and vascular reconstruction when necessary. The functional popliteal entrapment release is done quite differently and requires supine positioning and a medial calf incision similar to that used to expose the distal popliteal artery. Through this incision the fascial attachments of the gastrocnemius and soleus muscles to the medial tibia are excised along with a large posterior flap of fascia covering these muscles. The plantaris tendon and distal third of the plantaris muscle located between the gastrocnemius and soleus muscles is transected and excised. The muscular attachments of the soleus muscle to the posteromedial surface of the tibia are taken down with electrocautery, and the rigid band of anterior soleus fascia that forms the distal outlet of the popliteal fossa is excised from its tibia attachments laterally to the fibula. This fibrous band is the fulcrum against which the neurovascular bundle is laterally compressed, causing the symptoms of functional popliteal entrapment syndrome.

Recovery Postoperatively, patients are placed in compression dressings and kept at rest with bathroom privileges for 48 hours. Crutches are used for 3 or 4 days or until the drains are removed if they have been placed. At 1 week, patients are started on a nonimpact aerobic rehabilitation program that includes swimming and using a stationary bike, cross-country ski exercise machine, and stairstep exerciser. Patients are instructed to stretch before exercise and to ice over the surgical wounds afterward. If no problems develop with nonimpact aerobic conditioning, patients are started on an injured runner’s program at 4 to 6 weeks after surgery. After completing this rehabilitation requirement, patients are allowed to resume full athletic activity.

RESULTS AND DISCUSSION Since the 1990s the demographics for these overuse syndromes changed. Initially the interval between onset of symptoms and surgical treatment was more than 24 months. With greater awareness, the interval now is less than 1 year. These syndromes were originally associated with running sports such as cross country and track, and it occurred equally between genders (male, 51%; female, 49%). Since Title IX legislation, there has been a tremendous increase in women’s sports activity and a dramatic shift in gender prevalence (male, 30%; female, 70%). Soccer is the sport most commonly associated with overuse injury in female athletes. In the 1980s the anterior lateral (70%), posterior superficial (17%), and deep posterior (13%) compartments were most commonly affected. Since the late 1990s the distribution has changed: anterior lateral 47%, posterior superficial 44%, and deep posterior 9%. This has created a diagnostic problem because the symptoms of the posterior superficial compartment can coexist with or mimic those of the functional popliteal entrapment syndrome. To make matters more confusing, up to 30% of patients evaluated for atypical claudication complaints have positive entrapment screening tests. However, only 3% of all patients treated for atypical claudication actually have symptoms that are associated with this finding. There are symptomatic differences between posterior superficial chronic compartment syndrome and functional popliteal entrapment. The posterior superficial compartment patients often have symmetric cramping in the medial and/or lateral gastrocnemius muscle belly, and they rarely, if ever, experience plantar paresthesias. On the other hand, patients with functional popliteal entrapment often have unilateral complaints of deep soleus muscle cramping and



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pain made worse by running on inclines or repetitive jumping, and they commonly have plantar paresthesias. The vascular imaging of FPAES patients demonstrates long segment compression of the neurovascular bundle laterally against the popliteal fossa margin. This is unlike findings encountered with anatomic impingement, where the neurovascular bundle is displaced medially and compressed by an anomalous muscle strip or tendon. Since the 1970s, 1700 patients have been treated for atypical claudication symptoms caused by CRECS or FPAES; 2500 fasciectomies have been performed for compartment syndrome and 51 releases have been performed for functional popliteal entrapment syndrome. The collective recurrence rate for these procedures is 6.4%, most commonly the result of postoperative wound complications such as seroma or hematoma. Sensory nerve irritation (saphenous, sural, superficial peroneal) occurred in 2.2%. The majority of patients were able to return to previous levels of athletic activity. Those who did not, suffered from other musculotendinous sports injuries or new or recurrent compartment symptoms. The major issue is to properly diagnose the etiology for atypical claudication, particularly when the complaints affect the upper posterior calf muscles. It is critically important to measure the posterior superficial compartment pressures even if the popliteal entrapment screening tests are positive. In our experience, less than 15% of all patients with a positive popliteal entrapment screening study actually had symptoms consistent with functional popliteal entrapment syndrome. The large majority of these patients with atypical claudication have chronic compartment syndrome and not a popliteal entrapment problem. It is important, however, to remember that these conditions

can coexist, as manifest by the fact that more than 50% of all patients with popliteal entrapment also have compartment release surgery done at some time.

Exercise in Peripheral Arterial Disease

and to preventing its progression in asymptomatic patients. Current care guidelines provide no pathways that define an effective approach to improve outcomes in patients with atypical leg pain. Such patients are often relegated to a challenging attempt to deliver care that might focus on lumbar spine disease; hip, knee, and ankle arthritis; neuropathy; and deconditioning. Most current vascular specialists internationally receive training in revascularization, but not didactic or clinical training in the biology of leg function, and they do not receive mentorship in delivering effective behavioral therapies to improve leg ambulatory function. Any lower extremity PAD health system based on revascularization alone cannot fully address patient autonomy and treatment preference, might not fully balance clinical risk and benefit, and likely cannot achieve the mandate to offer an economically sustainable health care delivery approach to a common disease.

Mohammad Sarraf and Alan T. Hirsch

Atherosclerotic lower extremity peripheral arterial disease (PAD) represents one of the most common manifestations of systemic atherosclerosis and is known to affect approximately 5% of the adult population and more than 20% of patients older than 70 years. As for any atherosclerotic disease, key clinical goals include preserving life and limb, which are best accomplished by creating individualized treatment programs supported by evidence-based clinical care guidelines that encompass the translation of best science into clinical practice. Current evidence-based guidelines recognize five clinical syndromes that define the presentation of patients with lower extremity PAD. These syndromes encompass patients who are asymptomatic (or who could not express a concise symptom limitation, even though most such patients are objectively limited); who experience atypical leg pain, defined as limb discomfort that is present at both rest and with exercise, and that includes impediments to ambulatory function that are, in part, nonvascular in origin; who have classic claudication, which is present in only 8% to 12% of the total population of patients with PAD; who have acute critical limb ischemia; and who experience chronic critical limb ischemia. Past care pathways and national health care reimbursement schemes were rarely based on an accurate understanding of the patients’ health or the symptom burden of PAD. Thus, negligible resources have been applied to preventing PAD in healthy populations

Selected References Erdoes LS, Devin JJ, Bernhard VM, et al: Popliteal vascular compression in a normal population, J Vasc Surg 20:978–986, 1994. Mubarak SJ, Hargens AR: Exertional compartment syndromes. In Mack RP, editor: AAOS Symposium on the foot and leg in running sports, St. Louis, 1982, Mosby, pp 141–159. Pham TT, Kapur R, Harwood MI: Exertional leg pain: Teasing out arterial entrapments, Curr Sports Med Rep 6:371–375, 2007. Rignault DP, Pailler JL, Lunel F: The “functional” popliteal entrapment syndrome, Int Angiol 4:341–343, 1985. Turnipseed WD: Atypical claudication associated with overuse injury in patients with chronic compartment, functional entrapment, and medial tibial stress syndromes, Cardiovasc Surg 11:421–423, 2003. Turnipseed WD: Clinical review of patients treated for atypical claudication: A 28-year experience, J Vasc Surg 40:79–85, 2004. Turnipseed WD: Functional popliteal entrapment or chronic compartment syndrome: Which is it? How do I tell?. In Eskandari MK, Morasch MD, Pearce WH, Yao JST, (eds): New findings in vascular surgery, Shelton, CT, 2011, People’s Medical Publishing House—USA, pp 47–52. Turnipseed WD, Pozniak M: Popliteal entrapment as a result of neurovascular compression by the soleus and plantaris muscles, J Vasc Surg 15:285–294, 1992. Turnipseed WD: Functional popliteal artery entrapment syndrome: A poorly understood and often missed diagnosis that is frequently mistreated, J Vasc Surg 49:1189–1195, 2009.

SYSTEMIC DISEASES ALWAYS REQUIRE SYSTEMIC CARE Patients with PAD have systemic atherosclerosis and they have risk factors for progressive atherosclerosis and major ischemic events (e.g., heart attack, stroke, death) that are similar to those for patients with coronary artery disease (CAD). Low health-related quality of life is defined, in large part, by the limitation in functional status. Functional status is defined by the ability of the patient to perform independent ambulation, and it is usually best defined with objective treadmill testing. Quality of life is defined by a more complex interplay of functional status and leg symptoms on the perceived ability of the patient to accomplish key life goals. Patients with PAD are characterized by a very low functional status and variable impact on health-related quality of life. Community-derived patients with PAD were assessed in the Peripheral Arterial Disease Awareness, Risk, and Treatment (PARTNERS) program, in which the impact of PAD



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pain made worse by running on inclines or repetitive jumping, and they commonly have plantar paresthesias. The vascular imaging of FPAES patients demonstrates long segment compression of the neurovascular bundle laterally against the popliteal fossa margin. This is unlike findings encountered with anatomic impingement, where the neurovascular bundle is displaced medially and compressed by an anomalous muscle strip or tendon. Since the 1970s, 1700 patients have been treated for atypical claudication symptoms caused by CRECS or FPAES; 2500 fasciectomies have been performed for compartment syndrome and 51 releases have been performed for functional popliteal entrapment syndrome. The collective recurrence rate for these procedures is 6.4%, most commonly the result of postoperative wound complications such as seroma or hematoma. Sensory nerve irritation (saphenous, sural, superficial peroneal) occurred in 2.2%. The majority of patients were able to return to previous levels of athletic activity. Those who did not, suffered from other musculotendinous sports injuries or new or recurrent compartment symptoms. The major issue is to properly diagnose the etiology for atypical claudication, particularly when the complaints affect the upper posterior calf muscles. It is critically important to measure the posterior superficial compartment pressures even if the popliteal entrapment screening tests are positive. In our experience, less than 15% of all patients with a positive popliteal entrapment screening study actually had symptoms consistent with functional popliteal entrapment syndrome. The large majority of these patients with atypical claudication have chronic compartment syndrome and not a popliteal entrapment problem. It is important, however, to remember that these conditions

can coexist, as manifest by the fact that more than 50% of all patients with popliteal entrapment also have compartment release surgery done at some time.

Exercise in Peripheral Arterial Disease

and to preventing its progression in asymptomatic patients. Current care guidelines provide no pathways that define an effective approach to improve outcomes in patients with atypical leg pain. Such patients are often relegated to a challenging attempt to deliver care that might focus on lumbar spine disease; hip, knee, and ankle arthritis; neuropathy; and deconditioning. Most current vascular specialists internationally receive training in revascularization, but not didactic or clinical training in the biology of leg function, and they do not receive mentorship in delivering effective behavioral therapies to improve leg ambulatory function. Any lower extremity PAD health system based on revascularization alone cannot fully address patient autonomy and treatment preference, might not fully balance clinical risk and benefit, and likely cannot achieve the mandate to offer an economically sustainable health care delivery approach to a common disease.

Mohammad Sarraf and Alan T. Hirsch

Atherosclerotic lower extremity peripheral arterial disease (PAD) represents one of the most common manifestations of systemic atherosclerosis and is known to affect approximately 5% of the adult population and more than 20% of patients older than 70 years. As for any atherosclerotic disease, key clinical goals include preserving life and limb, which are best accomplished by creating individualized treatment programs supported by evidence-based clinical care guidelines that encompass the translation of best science into clinical practice. Current evidence-based guidelines recognize five clinical syndromes that define the presentation of patients with lower extremity PAD. These syndromes encompass patients who are asymptomatic (or who could not express a concise symptom limitation, even though most such patients are objectively limited); who experience atypical leg pain, defined as limb discomfort that is present at both rest and with exercise, and that includes impediments to ambulatory function that are, in part, nonvascular in origin; who have classic claudication, which is present in only 8% to 12% of the total population of patients with PAD; who have acute critical limb ischemia; and who experience chronic critical limb ischemia. Past care pathways and national health care reimbursement schemes were rarely based on an accurate understanding of the patients’ health or the symptom burden of PAD. Thus, negligible resources have been applied to preventing PAD in healthy populations

Selected References Erdoes LS, Devin JJ, Bernhard VM, et al: Popliteal vascular compression in a normal population, J Vasc Surg 20:978–986, 1994. Mubarak SJ, Hargens AR: Exertional compartment syndromes. In Mack RP, editor: AAOS Symposium on the foot and leg in running sports, St. Louis, 1982, Mosby, pp 141–159. Pham TT, Kapur R, Harwood MI: Exertional leg pain: Teasing out arterial entrapments, Curr Sports Med Rep 6:371–375, 2007. Rignault DP, Pailler JL, Lunel F: The “functional” popliteal entrapment syndrome, Int Angiol 4:341–343, 1985. Turnipseed WD: Atypical claudication associated with overuse injury in patients with chronic compartment, functional entrapment, and medial tibial stress syndromes, Cardiovasc Surg 11:421–423, 2003. Turnipseed WD: Clinical review of patients treated for atypical claudication: A 28-year experience, J Vasc Surg 40:79–85, 2004. Turnipseed WD: Functional popliteal entrapment or chronic compartment syndrome: Which is it? How do I tell?. In Eskandari MK, Morasch MD, Pearce WH, Yao JST, (eds): New findings in vascular surgery, Shelton, CT, 2011, People’s Medical Publishing House—USA, pp 47–52. Turnipseed WD, Pozniak M: Popliteal entrapment as a result of neurovascular compression by the soleus and plantaris muscles, J Vasc Surg 15:285–294, 1992. Turnipseed WD: Functional popliteal artery entrapment syndrome: A poorly understood and often missed diagnosis that is frequently mistreated, J Vasc Surg 49:1189–1195, 2009.

SYSTEMIC DISEASES ALWAYS REQUIRE SYSTEMIC CARE Patients with PAD have systemic atherosclerosis and they have risk factors for progressive atherosclerosis and major ischemic events (e.g., heart attack, stroke, death) that are similar to those for patients with coronary artery disease (CAD). Low health-related quality of life is defined, in large part, by the limitation in functional status. Functional status is defined by the ability of the patient to perform independent ambulation, and it is usually best defined with objective treadmill testing. Quality of life is defined by a more complex interplay of functional status and leg symptoms on the perceived ability of the patient to accomplish key life goals. Patients with PAD are characterized by a very low functional status and variable impact on health-related quality of life. Community-derived patients with PAD were assessed in the Peripheral Arterial Disease Awareness, Risk, and Treatment (PARTNERS) program, in which the impact of PAD

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on quality of life was prospectively measured, demonstrating that health-related quality of life was as low or lower in all PAD patients compared to patients with other cardiovascular diseases, such as CAD and/or stroke. As each nation provides resources to preserve health (prevention), to lower suffering (quality-of-life interventions), and lower mortality, the role of intervention for PAD claudication provides an example of where central improvements must occur. Current estimates of the United States health economic cost of PAD care suggest that more than $21 billion is now expended annually, and much of this cost is associated with invasive procedures. The annual medical cost to Medicare for PAD patients is estimated to be at least 5% higher than for other cardiovascular diseases. Unfortunately, there is little evidence that this expenditure prevents PAD, improves quality of life, or decreases amputation or death on a population scale. An evidence-based, guideline-supported approach to the treatment of claudication in both individual patients and populations would, therefore, include the use of each proven intervention (supervised exercise, claudication pharmacotherapies, and revascularization) in alignment with the science establishing their efficacy and the mandate to include the choice of the individual patient. This approach should be undertaken in a population-sustainable manner. Exercise interventions are effective, safe, and cost-effective, and they protect the autonomy of the patient with PAD.

EFFICACY OF EXERCISE TRAINING The benefit of exercise training to improve claudication symptoms in patients with PAD was recognized as early as 1966. This database of efficacy and safety has continued to strengthen every decade through 2013. Several observational studies of patients who had claudication and who were offered access to therapeutic exercise training programs have consistently demonstrated improvements in both pain-free and maximum walking distances, with an associated improvement in quality of life. The 1995 claudication exercise meta-analysis by Gardner and colleagues included 18 nonrandomized and three randomized clinical trials. This meta-analysis revealed that exercise training was associated with a 179% increase in pain-free walking distance and a 122% increase in maximum walking distance. The most recent 2008 Cochrane Collaboration systematic review included 22 randomized trials of exercise versus usual care, medical intervention, or surgical intervention in 1200 participants with stable claudication and provided an analysis of efficacy for variable periods of follow-up that spanned 2 weeks to 2 years. Improvements in functional capacity were achieved despite the lack of change of measured ankle-to-brachial index (ABI) values between the groups. Exercise training improved maximal walking time by a mean of 5.12 minutes and achieved an overall improvement in walking ability of approximately 50% to 200% compared with patients not offered such care. Pain-free walking distance improved by 82 meters and maximum walking distance by 113 meters, and these improvements were durable for at least 2 years. Such improvements in pain-free and maximal walking distances have been reproducibly achieved whether the treatment effect has been assessed in randomized or nonrandomized trials. This improvement is one of exercise science’s most consistent proven outcomes and is unambiguous, consistently achieved, reproducible in every health system studied, and observed regardless of PAD anatomy, PAD severity (e.g., baseline ABI), or baseline functional status. As for any behavioral, pharmacologic, or invasive therapy, there is a well-defined dose–response relation that predicts clinical benefit. The benefit of exercise training for PAD has usually been observed to require training sessions that last more than 30 minutes and occur at least 2 or 3 times per week. Beneficial responses are observed as early as 1 month, are consistently increased at 3 months, and continue to improve for at least 6 months after the exercise program has begun.

Despite persistent clinical anecdotes, there is no scientific or clinical experiential evidence that functional gains diminish at the conclusion of the supervised phase of an exercise program.

SCIENCE AND MECHANISMS OF EXERCISE BENEFIT The leg is a complex end-organ whose function is not defined by arterial anatomy alone. Excellent ambulatory function is plastic and can be achieved by way of its effects on muscle function, neurologic function, arterial perfusion, and orthopedic and podiatric function. Every health professional who has observed the impact of hospitalbased deconditioning is aware that limb function markedly changes (declines and improves) in patients with normal leg blood flow, as it also does in patients with severe PAD.

Blood Flow In normal adults, the common femoral artery blood flow measured at rest by a dye dilution technique is approximately 500 mL/min and can decrease at rest to 300 mL/min in patients with claudication. During exercise, leg blood flow in healthy persons can increase 30-fold to the working lower extremity muscles, but in patients with PAD this blood flow might not increase beyond two to three times basal flow rates. This supply-and-demand mismatch is only one cause of ischemic claudication symptoms. Other causes coexist, such as muscle deconditioning, denervation, and loss of skeletal myocytes, which also contribute to the inability to sustain functional performance. In animal studies, limb blood flow can return to baseline within a year after femoral artery ligation owing to the development of robust collaterals. Such collaterals also occur in patients with PAD, but collateral flow does not support normal exercise perfusion. Exercise training does not cause either conduit artery blood flow or collateral circulation flow to increase to normal levels. This strongly demonstrates that other mechanism(s) of action underpin the dramatic improvement of symptoms and walking distance. In response to training, flow may be preferentially shunted from minimally active muscles (low oxygen-extraction rate) to exercising muscles (high oxygen-extraction rate). What is proved is that improvement in major conduit artery blood flow is not a prerequisite for the success of an exercise program for PAD patients.

Change in Muscle Metabolism Skeletal muscle function depends on a continuous supply of adenosine triphosphate (ATP), which serves as an immediately available form of energy. The ATP stored in muscle is sufficient for only a short period of activity, and much larger amounts of energy are stored as creatine phosphate, which can be rapidly converted to ATP (Figure 1). During rest or light exercise, skeletal muscles use fatty acids as the main source of energy. These can only be used by the oxidative processes in the mitochondria. Increasing the exercise intensity leads to glycolysis of carbohydrate. When compared with glucose, fatty acid oxidation generates more ATP, but at a higher oxygen cost. Trained adaptation after endurance training is manifested by the ability to use fatty acids more effectively, as demonstrated by trained athletes. In patients with PAD, aerobic generation of ATP becomes inadequate and anaerobic metabolism predominates. This results in an increase in lactic acid production and depletion of ATP and creatine phosphate, leading to pain, a slower recovery of high-energy phosphate substrate in the muscles, poor physical tolerance of exercise, and a prolonged recovery time. There are two types of skeletal muscle fibers: type I and type II. Type I fibers have more mitochondria and higher oxidative capacity and are specialized for sustained activity such as walking or distance



Exercise in Peripheral Arterial Disease Systemic Atherosclerosis

PAD

PAD

Claudication/symptoms

Claudication symptoms

Supervised exercise training

Altered muscle function Muscle strength Walking economy Muscle metabolism

Limitation of physical activity Low quality of life Increased depression Self-limitation of exertion

1. Improved pain threshold 2. Improved muscle metabolism 3. Increased muscle strength 4. Improved quality of life 5. Increased walking economy

Worsening of atherosclerotic risk factors - Increased incidence of BW, DM, HLP, HTN

A

603

- Increased claudication time - Increased physical activity - Improved risk factor modification of BW, DM, HLP, HTN

Improved symptoms

B FIGURE 1  A, Relation between atherosclerosis, muscle pathophysiology, quality of life, and risk factors.

B, Multiplicity of mechanisms by which supervised exercise improves claudication symptoms.

running. These muscle fibers require an uninterrupted blood flow to supply the large amounts of ATP that can be produced only by oxidative (aerobic) metabolism. For type II fibers, on the other hand, a limited supply of ATP can be generated from phosphocreatine and by anaerobic glycolysis and do not depend on oxidative metabolism. Thus, in these fibers the rate of energy expenditure can exceed that of energy production, with an associated oxygen debt and lactic acid production. Some studies have suggested a more preferential loss of type II fibers in patients with severe PAD that leads to a higher concentration of type I fibers than type II. Chronic ischemia also affects other specialized cells such as those of the peripheral nervous system. In most patients with mild to moderate disease, changes caused by denervation and reinnervation are seen in both motor and sensory nerves, as reflected by the fact that 88% of patients with claudication have sensory impairment and 56% have motor weakness, with detrimental effects on walking biomechanics. Patients with PAD have an increase in oxidative enzymes such as citrate synthase and cytochrome oxidase in the calf muscles, which is reversed following vascular bypass procedures. In animal studies, hypoxia per se does not induce an increase in the metabolic capacity of muscles; a combination of hypoxia and physical activity is required to stimulate enzyme production. Patients with claudication who exercise infrequently and athletes who stop training share the same histological findings. The requirement for ATP in patients with claudication is twice as high as in normal controls for a standard workload. This metabolic inefficiency is supported by the finding of an accumulation of acylcarnitine, a marker of muscle metabolic rate. Therefore, inefficient muscle function is produced by a multiplicity of proven mechanisms, regardless of blood flow.

Patients with PAD have higher neutrophil counts in the venous blood of the affected limb, higher complement levels, and free oxygen radicals that could cause damage to the vascular endothelium. These inflammatory effects represent systemic disease, because increased endothelial permeability and microalbuminuria have been observed in the glomeruli of patients with PAD. The urinary albumin loss is accentuated by exercise in a manner that is not observed in healthy persons, and this observation may be reversed by revascularization. However, exercise-trained PAD patients manifest an attenuation of the post-exercise albumin excretion that is not observed in control subjects. In adequately trained patients with PAD, the level of albuminuria, C-reactive protein, serum amyloid A protein, blood viscosity, and red blood cell filterability all significantly improve.

Changes in Microcirculation and Endothelial Function Investigation of animal models of PAD suggest that exercise significantly improves endothelium-dependent vasodilation. These studies also demonstrate that elevated shear stress, as occurs from exercise-induced augmentation of blood flow, stimulates vasodilatation by increasing the vascular expression of nitric oxide synthase. These results from animal studies have been observed in human trials, although inconsistently. Incomplete normalization of endothelial function may be expected in human studies because the human disease is invariably associated with other factors, including smoking, hypertension, diabetes mellitus, and hyperlipidemia. Despite risk factor–induced endothelial dysfunction, patients with heart failure, diabetes mellitus, and the metabolic syndrome can improve endothelial-dependent vasodilation by exercise training. Thus, exercise serves as a potent mechanism to provide improved muscle blood flow.

Inflammation and Muscle Injury Atherosclerosis is a chronic inflammatory disease, and ischemia contributes to local muscle inflammation. Patients with claudication can experience repeated episodes of low-grade inflammation. Furthermore, the resting phase can promote an inflammation that is more severe than the initial insult, owing to a process of reperfusion injury. The exercise associated with training to improve claudication results in activation of the inflammation cascade. Although this process could, in theory, have deleterious effects, none are observed over the long term.

Hemorheologic Response Hemorheology is defined by the interaction of plasma and blood elements with the vessel wall and surrounding tissues. Exercise training is known to improve the observed abnormal hemorheology of patients with PAD, leading to improved limb blood oxygenation, increased filterability, and decreased blood viscosity, and these factors improve muscle blood flow. Capecchi and colleagues demonstrated that patients with claudication who perform short-term exercise of

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moderate intensity before a maximal exercise test can induce a reduction in blood viscosity and improved blood filterability even after a short-term exercise protocol.

Walking Economy Patients with claudication, compared to healthy subjects, have lower maximal oxygen consumption and higher oxygen utilization when they are walking. Walking economy during ambulation represents the metabolic cost of exercise. Patients with PAD adapt to claudication symptoms by favoring greater gait stability at the expense of walking speed. This change in biomechanics increases oxygen consumption during walking. Thus, at any level of walking, the associated energy requirement is achieved at a higher oxygen consumption. In normal persons, oxygen consumption begins to rise at the lactate threshold. In patients with claudication, this rise starts at a lower walking threshold before lactate production increases. This abnormal walking economy translates to higher heart rate, oxygen uptake, respiratory exchange ratio, and lactate concentration at a fixed exercise level. Exercise-trained patients with claudication significantly improve oxygen consumption during walking while they increase the time and distance of walking. In summary, exercise training leads to a reduction in the oxygen cost of exercise, higher peak oxygen utilization, and a reduction in heart rate. This provides a major improvement in the cardiorespiratory status for the trained patient with PAD.

CLAUDICATION TRAINING TREATMENT PROTOCOL All patients with PAD experience increased risk of fatal and nonfatal myocardial infarction and stroke, yet there is no evidence that therapeutic exercise is associated with increasing this risk. Other forms of revascularization for claudication, including endovascular and open surgical therapies, are invariably associated with minor or major increases in these ischemic risks. A baseline graded exercise treadmill is obtained for each PAD claudication exercise training candidate for many reasons. First, monitoring of the 12-lead electrocardiogram (ECG) during active treadmill exercise establishes the patient’s candidacy and the safety of the intervention. It also objectively establishes the severity of the limb ischemic symptoms (claudication onset and peak walking times), establishes the site (laterality and muscle group) of the leg symptoms, and defines any other contraindications (comorbidities) to a successful and safe exercise program (whether a result of gait instability, osteoarthritis, chronic obstructive pulmonary disease [COPD], etc.), and it permits heart rate, blood pressure, and ST–T wave changes to be monitored during exercise. Upon completion of an initial maximal exercise test, further routine ECG monitoring during subsequent exercise sessions is usually not required unless new chest symptoms arise (a rare event). Supervision of exercise is a key determinant of an exercise program’s success. Supervision ensures that exercise modalities are correctly selected, workloads are sequentially applied, and long-term adherence is sustained. Patients with claudication can have low initial confidence in their ability to achieve exercise success, might have concerns that the ischemic pain is a harmful effect of walking, and without aid are often unable to measure ongoing success (achieving positive behavioral feedback). Without supervision, home exercise (casual office advice without a prescription) is usually ineffective. The potential benefit of casual exercise advice alone (no supervision) on quality of life was assessed in an observational study using the SF-36 questionnaire. Patients with claudication (n = 202) undergoing leg revascularization or given casual exercise advice were studied, and little benefit was demonstrated in those given exercise advice only. New data comparing supervised versus unsupervised exercise training programs have suggested that unsupervised exercise may be

able to provide some functional benefit, albeit not as effectively as supervised therapy. The robust data supporting supervised interventions is why the American College of Cardiology/American Heart Association (ACC/AHA) PAD care guidelines provided a IA recommendation in favor of a primary role for supervised training and noted that the role of unsupervised training is not clear. Important elements of a therapeutic PAD exercise program are relatively well defined (Box 1). The exercise program is based on walking or resistance training. Data defining the efficacy of walking or isotonic exercise is more robust when compared to resistance training. A study of 156 patients randomized to three arms (control, supervised treadmill exercise, and lower extremity resistance training program) BOX 1:  Key Elements of a Therapeutic Claudication Exercise Training Program

Primary Clinician Role

• Establish the PAD diagnosis using the ABI measurement or other objective vascular laboratory evaluations. • Determine that claudication is the major symptom limiting exercise. • Discuss risks and benefits of claudication therapeutic alternatives, including pharmacologic, percutaneous, and surgical interventions. • Initiate systemic atherosclerosis risk modification. • Perform treadmill stress testing. • Provide formal referral to a claudication exercise rehabilitation program.

Exercise Guidelines for Claudication

• Warm-up and cool-down period is 5 to 10 minutes for each type of exercise. • Treadmill and track walking are the most effective exercise for claudication. • Resistance training has conferred benefit to patients with other forms of cardiovascular disease, and its use, as tolerated, for general fitness is complementary to but not a substitute for walking.

Intensity

• The initial workload of the treadmill is set to a speed and grade that elicit claudication symptoms within 3 to 5 minutes. • Patients walk at this workload until they achieve claudication of moderate severity, which is then followed by a brief period of standing or sitting rest to permit symptoms to resolve.

Duration

• The exercise–rest–exercise pattern should be repeated throughout the exercise session. • The initial duration usually includes 35 minutes of intermittent walking and should be increased by 5 minutes each session until 50 minutes of intermittent walking can be accomplished.

Frequency

• Treadmill or track walking three to five times per week

Role of Direct Supervision

• As patients improve their walking ability, the exercise workload should be increased by modifying the treadmill grade or speed (or both) to ensure that there is always the stimulus of claudication pain during the workout. • As patients increase their walking ability, there is the possibility that cardiac signs and symptoms may appear (e.g., dysrhythmia, angina, or ST-segment depression). These events should prompt physician reevaluation.   ABI, Ankle-to-brachial index; PAD, peripheral arterial disease. From Stewart KJ, Hiatt WR, Regensteiner JG, et al: Exercise training for claudication, N Engl J Med 347:1941–1951, 2002, with permission.



Exercise in Peripheral Arterial Disease

demonstrated superiority of the supervised treadmill training program. Lower extremity resistance training was also effective compared to the control group. Training intensity should produce moderate claudication in the first 5 minutes of treadmill walking. Each training session should consist of short periods of treadmill walking that is interrupted by rest and followed by repeated claudication-limited exercise bouts for a total 50-minute exercise session and should be performed three times weekly. For patients with reduced muscle mass or reduced muscle strength and endurance, resistance training may be used to supplement the treadmill walking exercise training. Contraindications to these exercise programs are well known to the exercise physiology community and include symptomatic unstable coronary heart disease, decompensated heart failure, severe pulmonary hypertension (mean pulmonary artery pressure >55 mm Hg), uncontrolled hypertension (blood pressure >180/110 mm Hg), severe aortic stenosis, and Marfan’s syndrome. The comparative effectiveness of a PAD-supervised exercise program compared to endovascular or pharmacologic claudication treatment has been objectively defined by the Claudication: Exercise Vs. Endoluminal Revascularization (CLEVER) study. This trial was designed by an independent interdisciplinary academic leadership group and funded by the National Heart, Lung, and Blood Institute of the National Institutes of Health. This prospective multicenter randomized, controlled clinical trial has evaluated the relative efficacy, safety, and health economic impact of three treatment strategies for patients with aortoiliac PAD and claudication. The treatment arms included optimal medical care (OMC), defined as a home walking program plus cilostazol as an effective claudication pharmacotherapy); primary proximal stent placement with OMC; and supervised exercise training with OMC. All treatments were effectively delivered, dropouts and crossovers were nearly nonexistent, cilostazol was used in more than 90% without adverse event, and patients were compliant with all treatments. The CLEVER study demonstrated that the primary endpoint of improvement in maximal walking distance on a graded treadmill test was achieved within 6 months, with superiority of the exercise intervention compared to successful stenting or pharmacotherapy. The key secondary endpoints (claudication onset time, health-related quality of life, and free-living daily activity levels assessed by pedometer) were similar across the exercise and stent treatments, with improved subjective quality of life often reported as superior in the stent group. High-density lipoprotein cholesterol (HDL) and inflammatory markers were also superior in the exercise cohort. A key CLEVER finding was that this functional superiority and quality-of-life benefit of exercise was durable, persisting for the full 18 months of follow-up. The health economic impact was also prospectively demonstrated to favor the supervised exercise intervention. The dissociation between the functional status primary outcome superiority and differential secondary outcome health-related quality of life responses in the exercise and stent groups cannot be interpreted to diminish the benefit of exercise. Whenever invasive therapies are studied in the absence of a sham cohort (e.g., lumbar laminectomy, arthroscopy, Parkinson’s and other diseases), quality of life is invariably reported to improve out of proportion to, or in the absence of, physiologic benefit. The ACC/AHA guideline has thus established a class IA as an initial treatment modality for patients with intermittent claudication. The supervised exercise training should be performed for a minimum of 30 to 45 minutes, in sessions performed at least three times per week for a minimum of 12 weeks (class IA). The ACC/AHA guideline has established the use of unsupervised exercise programs as class IIb-B.

EFFECT OF EXERCISE ON ATHEROSCLEROSIS RISK FACTORS Sedentary behavior is one of the leading preventable causes of death, and an inverse relationship exists between the amount of physical

605

activity and all-cause mortality. Regular physical activity decreases the risk of cardiovascular disease, as it does for type 2 diabetes, osteoporosis, depression, obesity, breast cancer, colon cancer, and falls in older adults. A graded relationship of decreasing cardiovascular event rates with increasing levels of activity is noted in the general population and in patients with established CAD. In a preliminary report from Japan, supervised exercise training was reported to improve survival in patients with PAD. After a mean follow-up of 5.4 years, event-free survival was higher in PAD patients who completed supervised exercise training than in those who did not (80.5% vs. 56.7%, p < .01). Physical activity improves many established atherosclerotic risk factors including elevated blood pressure, insulin resistance and glucose intolerance, elevated triglyceride concentrations, low levels of HDL, and obesity. The prevalence and severity of the metabolic syndrome (a constellation of obesity, glucose intolerance, reduced HDL, elevated triglycerides, and hypertension), which is associated with a marked increase in cardiovascular risk, can be dramatically reduced following exercise training. Comprehensive programs of exercise training provide a framework for successful achievement of other behavioral interventions that are known to assist the patient toward achieving better health, including nutritional counseling with dietary recommendations, smoking cessation, stress management, and PAD care.

ALL CLAUDICATION THERAPIES ARE EFFECTIVE AND CAN BE USED TOGETHER Claudication is rarely cured, and all treatments require vigilance to achieve sustained efficacy. During a patient’s lifetime, exercise training, cilostazol pharmacotherapy, and endovascular and open surgical treatments may be needed to sustain health. An ideal strategy of care uses every effective modality without bias. Revascularization, with an endovascular or open approach, cannot be performed on a population scale risk free. Patients undergoing open vascular approaches continue to face a minimum 3% in-hospital mortality and 4% to 10% 30-day cardiovascular morbidity. Percutaneous revascularization is associated with measurable local arterial site complication rates, renal toxicity, radiation exposure, and relatively high long-term costs. Thus, current evidence-based standards of care—beyond fad—always rely on the use of all claudication modalities, prescribed without bias, and with the least invasive and most cost-effective strategies employed as first-line approaches. Patients are capable of assisting in the selection of each therapy if they are fairly informed.

POTENTIAL OBSTACLES TO THERAPEUTIC SUCCESS All effective therapies are associated with contraindications and limitations. Yet the underutilization of supervised exercise training is not caused by the science base or by government policy or to patient choice. Underutilization is more likely caused by a lack of support for the exercise modality by a practice community that has not received adequate specialty-based training and experience. At this time, the choice of claudication therapy within every health system is not appropriately incentivized, and thus advocacy for the use of exercise is absent in many clinical environments. Payers consistently provide coverage when health professionals, and their societies, support evidence-based medical practice. Supervised exercise training is not consistently reimbursed, though many payers now recognize the benefit and cost-efficacy. Wizened clinicians increasingly use practice- and hospital-based resources to ensure that supervised exercise is available in their practice environment, with the same degree of advocacy for capital investment as might occur for a hybrid operating room or new venous procedure room.

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LOWER EXTREMITY OCCLUSIVE DISEASE

Vascular professionals now know that the high response rate to exercise is also sustained over the long term, with a major disease-modifying impact on risk factors. Perceived barriers to patients’ participation in a supervised exercise program (transportation and time dedication) can be consistently lowered when physicians’ prescriptions (not mere casual advice) are linked to standard physicians’ letters of support to work places and payers. Transportation to supervised exercise sites can be improved when medical vans are used (as for any other condition requiring rehabilitative techniques). Motivation for reluctant patients can be improved when spouses, family and friends, and nursing personnel are asked to create a supportive environment. Vascular specialists have always been successful in lowering therapeutic barriers, and they can do so for this most effective claudication treatment.

CONCLUSIONS Supervised exercise training for PAD patients with claudication remains the most proven, safest, and cost-effective approach to improve maximal walking distance and pain-free walking distance, with associated benefits to atherosclerosis risk factors and quality of life. Exercise is effective based on the proven interplay of many mechanisms, including complex cellular pathways and modification of muscle metabolism. To date, the exercise benefit is likely not caused by increased collateralization of the lower extremity. It is likely, but not proved, that exercise would blunt the progression of PAD and lower cardiovascular ischemic events. Other claudication therapies are also effective and can be used with supervised exercise training. It seems wise and patient-focused for all vascular professionals to work to ensure that their patients have easy access to this treatment strategy.

Pharmacologic Management of Intermittent Claudication James B. Froehlich and John D. Bisognano

Many pharmacologic agents have been studied for the medical management of intermittent claudication, there has been little success in identifying drugs that significantly alter the natural history of peripheral artery disease (PAD), and so far none has proved superior to exercise therapy. Critically important to the medical management of patients with claudication is the significant cardiac comorbidity in these patients and the need for treatment with pharmacologic agents that lessen cardiac risk. Several drugs have been shown to lessen the risk of these events and possibly improve peripheral vascular symptoms. The American College of Cardiology/American Hearth Association (ACC/AHA) Guidelines for the Management of Patients with Peripheral Arterial Disease, published in 2005, is the most comprehensive review of the epidemiology, diagnosis, and management of PAD.

Selected References Bronas UG, Hirsch AT, Murphy T, et al: CLEVER Research GroupDesign of the multicenter standardized supervised exercise training intervention for the Claudication: Exercise Vs Endoluminal Revascularization (CLEVER) study, Vasc Med 14:313–321, 2009. Hirsch AT, Haskal ZA, Hertzer NR, et al: ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic), Circulation 113:e463–e654, 2006. Mazari FA, Gulati S, Rahman MN, et al: Early outcomes from a randomized, controlled trial of supervised exercise, angioplasty, and combined therapy in intermittent claudication, Ann Vasc Surg 24:69–79, 2010. Murphy TP, Cutlip D, Regensteiner JG, et al: Stenting vs. Supervised Exercise for Claudication Due to Aortoiliac Peripheral Artery Disease: 6-Month Outcomes from the CLEVER Study, Circulation 125:130–139, 2012. Murphy TP, Hirsch AT, Ricotta JJ, et al: CLEVER Steering Committee. The Claudication: Exercise Vs. Endoluminal Revascularization (CLEVER) study: Rationale and methods, J Vasc Surg 47:1356–1363, 2008. Nordanstig J, Gelin J, Hensater M, et al: Walking performance and healthrelated quality of life after surgical or endovascular invasive versus non-invasive treatment for intermittent claudication: A prospective randomised trial, Eur J Vasc Endovasc Surg 42:220–227, 2011. Perkins JM, Collin J, Creasy TS, et al: Exercise training versus angioplasty for stable claudication: Long and medium term results of a prospective, randomised trial, Eur J Vasc Endovasc Surg 11:409–413, 1996. Spronk S, Bosch JL, den Hoed PT, et al: Intermittent claudication: Clinical effectiveness of endovascular revascularization versus supervised hospital-based exercise training—randomized controlled trial, Radiology 250:586–595, 2009. Stewart KJ, Hiatt WR, Regensteiner JG, et al: Exercise training for claudication, N Engl J Med 347:1941–1951, 2002. Watson L, Ellis B, Leng GC: Exercise for intermittent claudication, Cochrane Database Syst Rev(4): CD000990, 2008, doi: 10.1002/14651858.CD000990.pub2.

NATURE OF THE PROBLEM Ischemic intermittent claudication becomes asymptomatic when metabolic demands in exercising muscles exceed the oxygen and nutrient supply. The relative ischemia presumably elicits a maximal endogenous vasodilator response. Theoretically, numerous pharmacologic avenues can benefit patients in this setting, including augmenting vasodilation with exogenous vasodilators, altering skeletal muscle metabolic demands, enhancing blood flow by altering flow characteristics of the blood itself, and improving the endothelial dysfunction in atherosclerotic vessels. Pharmacologic therapies addressing each of these physiologic avenues have been proposed.

CONCOMITANT CORONARY ARTERY DISEASE The most important aspect of pharmacologic treatment for this disease is the recognition that coronary artery disease (CAD) accompanies peripheral artery disease in the majority of patients. CAD represents the greatest cause of morbidity and mortality for these patients; estimated to be as high as 25% to 30% over 5 years in symptomatic PAD. Measures to prevent myocardial infarction (MI) are strongly indicated. In fact, it is generally agreed that patients with PAD, even without documented or known CAD, should be treated as if they had known CAD, with the same appropriate secondary prevention measures. These include routine use of antiplatelet agents, smoking cessation, aggressive treatment of diabetes, appropriate control of hypertension, and, most importantly, aggressive lipid lowering.

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Vascular professionals now know that the high response rate to exercise is also sustained over the long term, with a major disease-modifying impact on risk factors. Perceived barriers to patients’ participation in a supervised exercise program (transportation and time dedication) can be consistently lowered when physicians’ prescriptions (not mere casual advice) are linked to standard physicians’ letters of support to work places and payers. Transportation to supervised exercise sites can be improved when medical vans are used (as for any other condition requiring rehabilitative techniques). Motivation for reluctant patients can be improved when spouses, family and friends, and nursing personnel are asked to create a supportive environment. Vascular specialists have always been successful in lowering therapeutic barriers, and they can do so for this most effective claudication treatment.

CONCLUSIONS Supervised exercise training for PAD patients with claudication remains the most proven, safest, and cost-effective approach to improve maximal walking distance and pain-free walking distance, with associated benefits to atherosclerosis risk factors and quality of life. Exercise is effective based on the proven interplay of many mechanisms, including complex cellular pathways and modification of muscle metabolism. To date, the exercise benefit is likely not caused by increased collateralization of the lower extremity. It is likely, but not proved, that exercise would blunt the progression of PAD and lower cardiovascular ischemic events. Other claudication therapies are also effective and can be used with supervised exercise training. It seems wise and patient-focused for all vascular professionals to work to ensure that their patients have easy access to this treatment strategy.

Pharmacologic Management of Intermittent Claudication James B. Froehlich and John D. Bisognano

Many pharmacologic agents have been studied for the medical management of intermittent claudication, there has been little success in identifying drugs that significantly alter the natural history of peripheral artery disease (PAD), and so far none has proved superior to exercise therapy. Critically important to the medical management of patients with claudication is the significant cardiac comorbidity in these patients and the need for treatment with pharmacologic agents that lessen cardiac risk. Several drugs have been shown to lessen the risk of these events and possibly improve peripheral vascular symptoms. The American College of Cardiology/American Hearth Association (ACC/AHA) Guidelines for the Management of Patients with Peripheral Arterial Disease, published in 2005, is the most comprehensive review of the epidemiology, diagnosis, and management of PAD.

Selected References Bronas UG, Hirsch AT, Murphy T, et al: CLEVER Research GroupDesign of the multicenter standardized supervised exercise training intervention for the Claudication: Exercise Vs Endoluminal Revascularization (CLEVER) study, Vasc Med 14:313–321, 2009. Hirsch AT, Haskal ZA, Hertzer NR, et al: ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic), Circulation 113:e463–e654, 2006. Mazari FA, Gulati S, Rahman MN, et al: Early outcomes from a randomized, controlled trial of supervised exercise, angioplasty, and combined therapy in intermittent claudication, Ann Vasc Surg 24:69–79, 2010. Murphy TP, Cutlip D, Regensteiner JG, et al: Stenting vs. Supervised Exercise for Claudication Due to Aortoiliac Peripheral Artery Disease: 6-Month Outcomes from the CLEVER Study, Circulation 125:130–139, 2012. Murphy TP, Hirsch AT, Ricotta JJ, et al: CLEVER Steering Committee. The Claudication: Exercise Vs. Endoluminal Revascularization (CLEVER) study: Rationale and methods, J Vasc Surg 47:1356–1363, 2008. Nordanstig J, Gelin J, Hensater M, et al: Walking performance and healthrelated quality of life after surgical or endovascular invasive versus non-invasive treatment for intermittent claudication: A prospective randomised trial, Eur J Vasc Endovasc Surg 42:220–227, 2011. Perkins JM, Collin J, Creasy TS, et al: Exercise training versus angioplasty for stable claudication: Long and medium term results of a prospective, randomised trial, Eur J Vasc Endovasc Surg 11:409–413, 1996. Spronk S, Bosch JL, den Hoed PT, et al: Intermittent claudication: Clinical effectiveness of endovascular revascularization versus supervised hospital-based exercise training—randomized controlled trial, Radiology 250:586–595, 2009. Stewart KJ, Hiatt WR, Regensteiner JG, et al: Exercise training for claudication, N Engl J Med 347:1941–1951, 2002. Watson L, Ellis B, Leng GC: Exercise for intermittent claudication, Cochrane Database Syst Rev(4): CD000990, 2008, doi: 10.1002/14651858.CD000990.pub2.

NATURE OF THE PROBLEM Ischemic intermittent claudication becomes asymptomatic when metabolic demands in exercising muscles exceed the oxygen and nutrient supply. The relative ischemia presumably elicits a maximal endogenous vasodilator response. Theoretically, numerous pharmacologic avenues can benefit patients in this setting, including augmenting vasodilation with exogenous vasodilators, altering skeletal muscle metabolic demands, enhancing blood flow by altering flow characteristics of the blood itself, and improving the endothelial dysfunction in atherosclerotic vessels. Pharmacologic therapies addressing each of these physiologic avenues have been proposed.

CONCOMITANT CORONARY ARTERY DISEASE The most important aspect of pharmacologic treatment for this disease is the recognition that coronary artery disease (CAD) accompanies peripheral artery disease in the majority of patients. CAD represents the greatest cause of morbidity and mortality for these patients; estimated to be as high as 25% to 30% over 5 years in symptomatic PAD. Measures to prevent myocardial infarction (MI) are strongly indicated. In fact, it is generally agreed that patients with PAD, even without documented or known CAD, should be treated as if they had known CAD, with the same appropriate secondary prevention measures. These include routine use of antiplatelet agents, smoking cessation, aggressive treatment of diabetes, appropriate control of hypertension, and, most importantly, aggressive lipid lowering.

Pharmacologic Management of Intermittent Claudication

Antiplatelet agents have specifically been shown to improve outcomes in patients with cardiovascular disease and also to improve patency of peripheral bypass grafts. However, more recent studies have called the efficacy of antiplatelet agents in the PAD population specifically into question. A meta-analysis of aspirin use in controlled trials specifically looking at PAD treatment failed to find significant reductions in cardiovascular events. However, in studies that evaluated aspirin use alone (versus in combination with dipyridamole), there was a strong trend toward reduction in total cardiovascular events (relative risk [RR], 0.75; 95% confidence interval [CI], 0.48–1.18), as well as a statistically significant reduction in stroke risk (RR, 0.64; 95% CI, 0.42–0.99). Likely, such meta-analyses suffer from being underpowered, because there are not many randomized trials of aspirin use specifically in PAD. Similarly, smoking cessation is associated with improved outcomes in peripheral vascular disease, although for obvious reasons, randomized, controlled trials do not exist. Observational studies have clearly shown an improvement in outcomes for patients with PAD and other forms of vascular disease who quit smoking over those who do not quit. Every patient seen in a vascular clinic, or by vascular specialists, should be asked about smoking status, and smokers should be offered smoking cessation therapy. Lipid-lowering therapy has been shown to decrease the incidence of MI and cardiovascular death, as well as stroke, in patients with hyperlipidemia, PAD, and CAD. More specifically, the Heart Protection Study demonstrated a 24% reduction in the endpoint of MI, MIrelated death, stroke, or revascularization in all these patient groups. This was particularly evident in patients with PAD and no known CAD. Two studies even demonstrated that lipid-lowering with statin therapy lessened claudication symptoms as well.

RHEOLOGIC AGENTS For many years the only FDA-approved medication for the treatment of claudication was pentoxifylline. This agent is thought to increase red blood cell pliability and thereby decrease blood viscosity. Data also suggest that it can increase smooth muscle cell relaxation and inhibit platelet aggregation. All of these effects would be of theoretical advantage in the setting of PAD-related claudication. A meta-analysis of all pentoxifylline studies showed an improvement in pain-free walking distance and total walking distance with pentoxifylline compared with placebo; the improvement achieved statistical significance, but the difference was very small. This finding was of unclear clinical significance and was much smaller than that seen with exercise therapy. Furthermore, the minimal increase in claudication distance is inconsequential in most patients. For these reasons, pentoxifylline is not usually recommended for the treatment of claudication.

VASODILATOR THERAPY From a physiologic perspective, vasodilators would also appear to provide a potential advantage in patients with claudication. Numerous vasodilators, including calcium channel blockers, α-receptor blockers, and prostaglandin analogues, have been evaluated in the treatment of PAD. Although this is theoretically an appealing treatment avenue, the clinical results have been disappointing. It may be that the majority of vasodilating agents do not augment the blood flow in a physiologically relevant or timely fashion. Also, the endogenous vasodilators might have already maximally increased blood flow within the ischemic bed. In any event, previous evaluations of vasodilator therapy failed to document any benefit. Prostaglandin analogues may be an exception. These are the only group of vasodilators that have shown clinical efficacy in improving claudication symptoms. These agents can inhibit platelet function, which might contribute to their effectiveness. Specifically, European trials of intravenous prostacyclin analogues might have suggested efficacy for the treatment of claudication. Trials of oral prostacyclin

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analogues have been disappointing, and there is no FDA-approved prostanoid for use in treating PAD. Several studies have suggested that cilostazol is effective in the symptomatic treatment of claudication, both versus placebo and versus pentoxifylline. Cilostazol inhibits cyclic adenosine monophosphate (AMP) phosphodiesterase, which leads to vascular smooth muscle relaxation and inhibition of platelet aggregation. Trials have documented improved walking distance, symptomatic improvement by formal questionnaire, and some beneficial effect on lipid levels. In a randomized study, the onset of action of cilostazol occurred within a month in many patients. Patients with claudication were given cilostazol 100 mg or 50 mg twice daily, and a third group was given placebo twice daily. At the end of the study, walking distance increased 100% in the group taking 100 mg of cilostazol twice daily, and increased 50% in the group taking 50 mg of cilostazol twice daily. Because of an adverse event, (usually headaches, abnormal stool, dizziness, and palpitations) 14% of the patients withdrew. There was no difference in the withdrawal rate among the three treatment groups. Of particular note, there were no differences in overall mortality or cardiovascular mortality in the three treatment arms. Currently, the authors recommend cilostazol 100 mg twice daily, along with a prescribed (preferably supervised) walking exercise regimen for 6 months. After such a trial, clinical reassessment is indicated, with continuation if there is improvement in walking and discontinuation if there is not. Other oral phosphodiesterase inhibitors have been used for symptomatic relief in patients with heart failure, but mortality is increased. Because cilostazol is chemically similar to these medications, its use is contraindicated in patients with heart failure, and care should be taken to ensure that a patient has normal cardiac function before instituting therapy with cilostazol.

ADDRESSING ENDOTHELIAL DYSFUNCTION Numerous investigations have identified endothelial dysfunction, with impaired vasodilation or paradoxical vasoconstriction, increased cellular adhesion to vascular walls, and increased platelet aggregation, as playing a major role in the pathogenesis of atherosclerotic disease. Endothelial dysfunction is associated with hypertension, hyperlipidemia, diabetes, and hyperhomocysteinemia. It appears to be mediated either by down-regulation of nitride oxide (NO) synthesis or increased oxidant stress. Treatment of the underlying causes, including blood pressure control, lowering low-density lipoprotein (LDL) cholesterol, and controlling diabetes, has been shown to improve endothelial dysfunction, even in the absence of any known atherosclerotic disease. Most of the beneficial functions of vascular endothelial cells, including antithrombosis, vasodilation, inhibition of platelet adhesion, inhibition of smooth muscle cell proliferation, and a general inhibition of the atherogenetic process itself, are mediated by NO. l-Arginine, an amino acid byproduct of the urea cycle, is the precursor of NO synthesis. Dietary supplementation with l-arginine has been shown to retard atherogenesis in animal models and improve endothelial function in humans. In spite of this promising biologic plausibility in improving claudication symptoms and outcomes in patients with PAD, the largest randomized trial of dietary supplementation with l-arginine was negative. Likewise, studies of oral prostaglandins such as beraprost and iloprost have been disappointing, and none are currently approved for this indication.

CONCLUSION Pharmacologic management of claudication has been limited in the past. The most important tenet of medical treatment for claudication is aggressive treatment of modifiable cardiovascular risk factors,

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LOWER EXTREMITY OCCLUSIVE DISEASE

TABLE 1:  Class I Therapy in Peripheral Artery ­Disease Treatment

Agents

Selected References

Therapy for Risk Reduction

Lipid lowering to LDL 6 hours) ischemia. In all instances, the administration of mannitol is undertaken with reperfusion, to sustain a diuresis and lessen the risk of myoglobin-induced renal injury.

OUTCOMES The reported operative mortality following thromboembolectomy for acute macroembolic limb ischemia varies widely, ranging from 7.5% to 34%. Limb salvage rates range from 86% to 95%. Patients should remain anticoagulated postoperatively given the 6% to 45% incidence of recurrent embolism.

Selected References Blaisdell FW, Steele M, Allen RE: Management of acute lower extremity arterial ischemia due to embolism and thrombosis, Surgery 84:822–834, 1978. Eliason JL, Wainess RM, Proctor MC, et al: A national and single institutional experience in the contemporary treatment of acute lower extremity ischemia, Ann Surg 238:382–389, 2003. discussion, 389–390.

Noninvasive Methods of Diagnosing Cardiac and Noncardiac Sources of Macroemboli Shipra Arya and John E. Rectenwald

Peripheral arterial macroembolism is an important cause of acute limb ischemia. Identification of the underlying source is imperative in managing the threatened extremity and preventing recurrence. Many noninvasive studies are readily available that can aid in identifying the cardiac and noncardiac sources of arterial macroemboli.

ECHOCARDIOGRAPHY Echocardiography has emerged as the primary diagnostic tool for detecting cardiogenic and proximal aortic sources of peripheral arterial emboli. Two forms of echocardiograms are available: transthoracic (TTE) and transesophageal (TEE). The standard TTE has a diagnostic yield of 10% to 25% for identifying cardiac emboli in patients because it cannot visualize all heart chambers. It does evaluate the left ventricle more completely than a TEE, but it does not image the left atrial appendage, which is the most common site of thrombus in patients with atrial fibrillation. TTE is also limited by body habitus, young age, the presence of prosthetic heart valves, and overinflation of the lung as occurs in chronic obstructive pulmonary disease. Nevertheless, TEE can pick up greater than 50% of sources of cardiac emboli in patients with no clinically apparent heart disease. TTE is a useful first-line screening test because it can easily be done at the bedside without sedating the patient, as is required for TEE. TTE can detect most cardiac anomalies that predispose to arterial embolism (Figure 1), including prosthetic valves, vegetations, left ventricular aneurysms, dilated cardiomyopathy, mitral valve prolapse,

Fogarty TJ, Cranley JJ, Krause RJ, et al: A method for extraction of arterial emboli and thrombi, Surg Gyn Obstet 116:241–244, 1963. Kalinowski M, Wagner HJ: Adjunctive techniques in percutaneous mechanical thrombectomy, Tech Vasc Intervent Radio l6:6–13, 2003. O'Connell JB, Quinones-Baldrich WJ: Proper evaluation and management of acute embolic versus thrombotic limb ischemia, Sem Vasc Surg 22:10–16, 2009. Ouriel K, Shortell CK, DeWeese JA, et al: A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia, J Vasc Surg 19:1021–1030, 1994. Panetta T, Thompson JE, Talkington CM, et al: Arterial embolectomy: A 34year experience with 400 cases, Surg Clin North Am 66:339–353, 1986. Rutherford RB: Clinical staging of acute limb ischemia as the basis for choice of revascularization method: When and how to intervene, Sem Vasc Surg 22:5–9, 2009. Tawes Jr RL, Harris EJ, Brown WH, et al: Acute limb ischemia: Thromboembolism, J Vasc Surg 5:901–903, 1987. Zaraca F, Stringari C, Ebner JA, et al: Routine versus selective use of intraoperative angiography during thromboembolectomy for acute lower limb ischemia: Analysis of outcomes, Ann Vasc Surg 24:621–627, 2010.

and left ventricular thrombus. It also can evaluate for left ventricular dysfunction as well as delayed left atrial appendage emptying, both being risk factors for systemic emboli in patients with atrial fibrillation. Atrial septal defects can also be seen on TTE. Primary cardiac tumors, the majority of which are myxomas and sarcomas, can also be detected on TTE. TEE evaluates the entire heart from the esophagus behind the left atrium. The left atrial appendage may be the source of thrombus in up to 40% of patients with valvular heart disease and peripheral emboli. In addition, TEE is highly sensitive in recognizing a patent foramen ovale and valvular strands and vegetations, especially in a patient with high clinical suspicion of infective endocarditis and a negative TTE. TEE is also a great adjunct to guide therapy for patients in atrial fibrillation in terms of short-term anticoagulation and subsequent cardioversion. TEE carries the distinct advantage of being able to image the thoracic aorta and aortic arch. Complex aortic atheromas in the descending thoracic aorta can be evaluated, and the dynamic nature of TTE is sometimes better at identifying the embolizing aortic thrombi and mobile thrombus compared to the static contrast imaging of computed tomography (CT) or magnetic resonance imaging (MRI). A grading system is used to classify aortic atherosclerosis from lowest to highest embolic potential: grade I: normal or intimal thickening less than 4 mm; grade II: diffuse intimal thickening 4 mm or more; grade III: atheroma less than 5 mm; grade IV: atheromas greater than 5 mm; and grade V: any mobile atheroma. The use of intravenously injected agitated saline for a bubble study can detect a right-to-left shunt by both TTE and TEE. Direct visualization of bubbles passing from the right atrium into the left atrium within three beats, either spontaneously or after valsalva maneuver, is diagnostic of a patent foramen ovale. Late appearance of bubbles may be a result of passage through lungs and then entry into the left atrium. The bubble load can define the size of the defect.

DIAGNOSTIC VASCULAR LABORATORY STUDIES Peripheral arterial and venous duplex studies are often helpful to detect the source of emboli when the clinical picture is relevant or other central sources of arterial emboli are eliminated. Distal tibial embolism is often seen as the first presentation of popliteal artery

Noninvasive Methods of Diagnosing Cardiac and Noncardiac Sources of Macroemboli

FIGURE 1  A, Thickened prosthetic tricuspid valve with mobile vegetation (circled area) as shown on transthoracic echocardiography. B, Peripheral embolus in the brachial artery of the same patient diagnosed on computed tomography angiography of the upper extremity for acute ischemia.

A

641

B

DIAGNOSTIC APPROACH TO A PATIENT WITH PERIPHERAL ARTERIAL EMBOLI

FIGURE 2  Aortic arch thrombus detected on computed tomography

angiography.

aneurysms in half of the cases. Upper extremity embolic sources can also be detected by arterial duplex in the setting of arterial thoracic outlet syndrome (TOS). Poststenotic dilatations of the subclavian artery and their subsequent development into aneurysms can lead to presentation of acute limb ischemia in as many as one third of arterial TOS patients. Venous duplex is useful in establishing an embolic source when a right-to-left shunt is suspected in the workup of a patient in whom peripheral arterial emboli has occurred and no other arterial source is identified.

COMPUTED TOMOGRAPHY AND MAGNETIC RESONANCE IMAGING Multidetector CT (MDCT) scanning and cardiac-gated CT angiography (CTA), allow imaging of the heart, the entire length of the aorta, and branch vessels (including extremity runoffs) and can identify potential sources of, as well as location of, emboli (Figure 2). MDCT is complementary to TTE in diagnosing cardiogenic sources of emboli. In comparison to TEE, spiral CTA has been found to be equally effective in identifying aortic atheromas, although CTA was better in identifying smaller atheromas and defining plaque morphology and is less invasive than TEE. The abdominal aorta and iliac vessels are well imaged using CTA. CTA easily demonstrates the presence of ulcerated plaques, heavy calcifications, or mural thrombi as potential sources of embolism. Direct MRI of the thrombus can be used to evaluate complicated arterial plaques in the aortic arch and thoracic aortic. MRI offers the advantage of better soft tissue characterization. The noninvasive nature of MRI makes it an attractive alternative to TEE. However, the need for a long image acquisition time and inability of patients to lie still in an enclosed space limit the use of this imaging modality.

Patients with acute peripheral ischemia (thrombotic or embolic) need a complete history and physical examination to identify risk factors for arterial embolization, the degree of ischemia, and the time of onset and possible sources of emboli. At our institution, all patients are anticoagulated using unfractionated intravenous heparin unless there is suspicion of heparin-induced thrombocytopenia. A TTE is obtained without delay. If there is no immediate threat to the extremity, a CTA of the chest, abdomen, and pelvis with extremity runoffs is obtained in patients with normal renal function. Alternatively, MRA may be used to evaluate the aorta and runoff if feasible. If the CTA shows no source and the TTE is negative, a TEE is performed. The TEE may be done after revascularization has been accomplished. Patients with abnormal kidney function might have to go to the operating room based on noninvasive vascular studies (ankle-to-brachial index and extremity arterial duplex). Occasionally, the cause of limb ischemia is thrombotic rather than embolic, especially in patients with prior history of peripheral arterial disease. This may be identified by the noninvasive CT, MR, or duplex studies. In a few cases, the etiology might not become apparent till angiography or surgical exploration.

Selected References Abbott WM, Maloney RD, McCabe CC, et al: Arterial embolism: A 44 year perspective, Am J Surg 143:460–464, 1982. Bitar R, Moody AR, Leung G, et al: In vivo identification of complicated upper thoracic aorta and arch vessel plaque by MR direct thrombus imaging in patients investigated for cerebrovascular disease, AJR Am J Roentgenol 187:228–234, 2006. Criado E, Berguer R, Greenfield L: The spectrum of arterial compression at the thoracic outlet, J Vasc Surg 52:406–411, 2010. Elliott JP: Arterial embolization: Problems of source, multiplicity, recurrence, and delayed treatment, Surgery 88:833–845, 1980. Hussain SI, Gilkeson RC, Suarez JI, et al: Comparing multislice electrocardiogram-gated spiral computerized tomography and transesophageal echocardiography in evaluating aortic atheroma in patients with acute ischemic stroke, J Stroke CerebrovascDis 17:134–140, 2008. Kim SJ, Choe YH, Park SJ, et al: Routine cardiac evaluation in patients with ischaemic stroke and absence of known atrial fibrillation or coronary heart disease: Transthoracic echocardiography vs. multidetector cardiac computed tomography, Eur J Neurol 19:317–323, 2012. O'Connell JB, Quiñones-Baldrich WJ: Proper evaluation and management of acute embolic versus thrombotic limb ischemia, Semin Vasc Surg 22:10–16, 2009. Pepi M, Evangelista A, Nihoyannopoulos P, et al: Recommendations for echocardiography use in the diagnosis and management of cardiac sources of embolism, Eur J Echocard 11:461–476, 2010. Reber PU, Patel AG, Stauffer E, et al: Mural aortic thrombi: An important cause of peripheral embolization, J Vasc Surg 30:1084–1089, 1999. Robinson WP, Belkin M: Acute limb ischemia due to popliteal artery aneurysm: A continuing surgical challenge, Semin Vasc Surg 22:17–24, 2009.

Amputation

Minor Amputations Malachi G. Sheahan, Claudie M. Sheahan, and Frank B. Pomposelli

The first use of limb amputation was as an implement of punishment or torture. Hippocrates is credited with performing the first amputation for therapeutic purposes. Well into the 20th century, toe or forefoot gangrene was associated with limb loss. Leland McKittrick’s publication of his technique for transmetatarsal amputation (TMA) in 1949 led to thousands of spared limbs. For decades, however, a TMA was much more likely to succeed when infection was the indication rather than ischemia. As recently as the 1970s, up to 70% of patients who underwent minor amputation progressed to limb loss within 3 years. Better understanding of microbiology, risk modification of risk factors, and the ability to perform femoral-to-popliteal and more distal arterial bypass grafts and, more recently, catheter-based interventions, have led to contemporary limb-salvage rates approximating 80% at 5 years. In the United States, hospital admissions for foot ulceration increase yearly. One of the most important and overlooked aspects of successful limb salvage in these patients is a properly timed and executed minor amputation. Currently, minor amputations are performed twice as frequently as major amputations. Avoidance of major amputation is critical for a myriad of reasons. Transtibial and transfemoral amputations result in inefficient ambulation. The increase in metabolic cost after these procedures is proportional to the number of functional joints that are lost. Increased oxygen consumption leads to reduced metabolic reserve and a dramatically altered exercise capacity. Adverse consequences of major amputation are decline in quality of life, difficulty maintaining independence, and high medical costs. Body image issues, depression, and shortened life expectancy are other sequelae. The risk of amputation is approximately three times higher after age 80 years, which is precisely the population most at risk for loss of independence. Patients with diabetes mellitus are especially prone to foot ulcers due the presence of polyneuropathy. Their predisposition for both ischemia and multimicrobial infection can result in extensive tissue loss and/or osteomyelitis and result in major limb amputation when ulcers are left unhealed. A properly performed toe, ray, or transmetarsal amputation results in closure of the skin envelope and salvage of a walking foot. When a débridement, drainage procedure, or open amputation is required to control infection, considerable ingenuity may be needed to fashion an amputation that both closes the wound and preserves a walking foot. Recognizing the presence of ischemia and correcting it by either bypass or catheter-based intervention is critical to achieving success with partial foot amputation. In general, any patient without palpable foot pulses should undergo evaluation for ischemia. When

limb-threatening ischemia of the foot is identified, the goal of treatment should be the restoration of a palpable foot pulse when possible. In our experience, a palpable foot pulse is the most reliable clinical indicator of adequate arterial perfusion for successful healing of an amputation in the foot. If an incision and drainage procedure or open amputation is necessary to control infection in an ischemic patient, vascular evaluation should occur soon after and revascularization should be performed with 2 to 4 days in most patients to prevent further necrosis or tissue loss.

INDICATIONS The goals of minor amputation surgery are to remove anatomic pressure points and prevent recurrent ulceration, control osteomyelitis and infection, preserve and restore the foot to optimum ambulatory function, and control and relieve pain. A simple toe amputation is indicated in the case of irreversible tissue loss or osteomyelitis of one toe distal to the proximal interphalangeal joint. The more extensive ray amputation is performed when gangrene or osteomyelitis extends to the web space, metatarsophalangeal joint, or metatarsal head. Other indications for ray amputation include the need to decompress one deep fascial compartment or extension of skin necrosis past margins acceptable for a simple amputation. The basic indication for transmetatarsal foot amputation is irreversible tissue loss or infection extending beyond the boundaries of a single-ray amputation but still allowing the creation of a viable plantar flap. Many patients undergoing TMA have had previous ipsilateral foot procedures such as ray amputations and incision and drainage. Common scenarios include failure of a previous toe amputation, the need for multiple ray amputations, forefoot infection involving multiple deep fascial compartments, forefoot deformity causing severe disability, and intractable pain. Because a TMA spares the tibialis anterior, peroneus longus, and peroneus brevis tendon insertions, it is a much more functional amputation than the Lisfranc, Chopart, or Syme amputations. These latter three, in our opinion, provide little to no advantage over a below-knee amputation, especially in diabetic patients. Relative contraindications to a minor forefoot amputation include extensive tissue loss especially on the plantar aspect of the foot or the heel, untreatable foot ischemia, knee contractures, and immobility without chance for rehabilitation. These conditions usually necessitate a major amputation.

SURGICAL TECHNIQUE Transphalangeal Toe Amputation The foot and leg are prepped and draped to the knee using sterile technique. The incision is made at the level of the mid-proximal 643

644 AMPUTATION phalanx down to the level of the bone. The incision should be circumferential rather than fish-mouth when possible to avoid compromising blood supply to the flap. Trimming the phalynx back to allow tension-free closure is an important principle. In the case of the first toe, the approach may be altered to include a plantar flap if possible (Figure 1). The periosteum is stripped with an elevator. The bone is then transected with an oscillating saw at the proximal phalangeal level, approximately 1 cm proximal to the level of the skin incision. In firsttoe amputations, the metatarsophalangeal joint should be spared if possible to improve gait stability. The tendons are pulled down, sharply divided, and allowed to retract. After hemostasis is obtained and the wound is irrigated, the skin is closed without tension in an anteroposterior orientation. Interrupted monofilament sutures are preferred. Dry gauze dressing is applied and full weight bearing is avoided until the wound has healed.

Transmetatarsal (Ray) Toe Amputation The foot and leg are prepped to the thigh and draped using sterile technique. A racquet-type longitudinal incision is made on the dorsum of the foot parallel to the metatarsal bone extending on each side of the toe as a semielliptical incision converging on the plantar surface of the foot (Figure 2). A circular incision should be avoided if primary closure is to be attempted, because there is less tension in the closure of an elliptical incision and therefore greater chance of wound healing. A ratio of incision length to width of at least 3:1 will aid primary closure. If ulceration is present on the plantar surface at the level of the metatarsal head, this may be included in the excision as well. Preoperative assurance of adequate circulation is critical to the healing of this amputation type. The initial incision is carried down to bone, and the toe is disarticulated at the metatarsophalangeal joint. The periosteum is elevated circumferentially down the shaft of the metatarsal bone as far proximally as necessary. This is determined based on preoperative imaging of bony involvement of infection as well as intraoperative inspection of the quality of the viable tissue and extent of infection. It is only rarely necessary to extend this to the level of the metatarsal–cuneiform joint. In the case of the second, third, or fourth toe, removal of the entire metatarsal disrupts the Lisfranc joint, leading to foot instability.

The bone is then transected at the proximal diaphysis or the diaphyseal–metatarsal junction. This is best accomplished using an oscillating saw rather than a rongeur because splintering is sure to occur with a rongeur. The bone is passed off and, if wound-healing parameters are found to be adequate, primary closure may be performed after irrigation. Interrupted monofilament sutures are placed in the skin. There is no role for staples or subcuticular sutures in these wounds. Dry gauze dressing with adequate padding is applied, taking care to avoid contact of tape with the skin. Full weight bearing should be avoided until the wound has healed. We usually wait 4 weeks. Amputation for Forefoot Sepsis If the amputation is being performed for control of forefoot sepsis, the wound is left open. Special considerations should be made in this setting when making the initial incision to protect the future plantar flap for transmetatarsal amputation closure. If ischemic eschar is present that is not part of the immediate infectious process, it should not be débrided at the initial drainage procedure because this can ultimately hurt the chances of creating a functional foot. After removing the head of the metatarsal, the foot is now assessed for ascending infection. In compressing the foot, if pus is noted along the extensor or flexor tendons, these compartments are opened for more aggressive drainage. After draining all purulence and débridement of all involved tissue, aggressive irrigation is undertaken. We use a power-irrigation and suction system with 3 L of antibiotic mixture. The wound is then left open to either heal by secondary intention or delayed primary closure. Postoperative care of the open wound should include moist saline gauze dressings changed twice daily. Vacuum-assisted dressing devices are a useful alternative in some patients. Cultures are obtained during the débridement, and appropriate antibiotics are administered until all objective parameters of infection have resolved. If osteomyelitis was present, intravenous antibiotics are continued for a total of 6 weeks after débridement. Amputation of the First Ray In the case of a first-ray amputation, the incision is made as two curvilinear lines on both the dorsum and plantar surfaces of the foot, extending down to the level of the bone, exposing the metatarsal

FIGURE 1  Digital amputation of the first toe demonstrating an alter-

native skin incision yielding a plantar flap.

FIGURE 2  Ray amputation of the third toe with a racquet incision.



Minor Amputations

head. The flexor hallucis tendon is visible and usually is sacrificed to prevent recurrence of infection. The sesamoids should now be apparent and are resected as well. When transecting the first metatarsal head, as much of the metatarsal should be left behind as possible to maintain function without leaving infected bone. The shaft is cut obliquely to prevent medial prominence of the bone, which could lead to pressure ulceration. The skin is closed with interrupted nonabsorbable monofilament sutures. Deep sutures are avoided as a result of the risk of retained infection. Often, first-ray amputations do not allow primary closure given the extensive tissue loss. Again, these may be left to heal by secondary intention or delayed primary closure with skin grafting in some cases. Amputation of the Fifth Ray For a fifth-ray amputation, an incision is made directly over the metatarsal shaft and extended down to encircle the fifth toe. Again, as in the first-ray amputation, the cut in the metatarsal shaft is made obliquely to avoid protrusion of bone.

Transmetatarsal Foot Amputation The entire lower leg and foot are prepped and draped using sterile technique. If the blood supply to the foot is normal, exanguination and a tourniquet can be used. This is ill advised in patients with bypass grafts. First, a transverse incision is made on the dorsum of the foot at the mid metatarsal level. A right-angle turn is performed at the medial aspect, and the incision is extended around the foot to the plantar surface at the level of the metatarsophalangeal joints (Figure 3). The incision is sharply carried through the tendons and neurovascular structures to the bone. Large vessels, such as branches of the dorsalis pedis artery, should be ligated. The extensor tendons are pulled out slightly, sharply divided, and allowed to retract. Examine the tendon sheaths for pockets of infection. The plantar fascia and fat pad are included in the flap. As Dr. Sanders demonstrated in 1997, the plantar incision line can be modified to include excision of an ulcer (Figure 4). The periosteum of the metatarsal shafts are elevated circumferentially to the level of the intended transection. The skin flaps are carefully retracted and the bones are transected with an oscillating or Gigli saw at the mid-metatarsal level, approximately 2 cm proximal to the skin incision, thereby preserving the insertions of the peroneus longus,

645

peroneus brevis, and tibialis anterior tendons. Manual bone cutters are to be avoided because they cause bone splintering and can also lead to unwanted bone regrowth, which can precipitate late ulceration. The first and fifth metatarsal bones are transected in an oblique fashion to avoid bone protrusion, the first in a medial and plantar direction, the fifth laterally and plantar. Any sesamoids should be resected. The second through fourth metatarsals should be divided in a parabolic manner, with a longer cut on the dorsal aspect, beveling in the plantar direction. Care must be taken to divide all of the metatarsals at the same length. The divided bones are reflected upward proximally to distally, and the amputation is completed at the level of the plantar flap. All neurovascular structures are ligated. All nonviable tissue is carefully removed. The flexor tendons are resected in a similar manner to the extensors, again inspecting the sheaths for residual infection. The key to success in this procedure is a thick, well-vascularized plantar flap that can be closed without tension. The tourniquet is released if one was placed. The site is irrigated copiously with normal saline solution. At least 2 to 3 minutes after tourniquet release should be allowed to ensure hemostasis. A drain can be placed if prolonged bleeding is encountered, but this is not our usual practice. The skin is closed with interrupted vertical mattress monofilament sutures. Just enough tension is applied to barely approximate the skin edges because postoperative edema will occur. Skin trauma should be avoided and great care should be used in its handling. We avoid grasping the ends of the skin flaps with forceps. Potentially ischemic wounds are closed once infection is controlled because the limited circulation does not lend itself to effective granulation and closure of the wound by secondary intention. The foot is dressed with a soft, circumferential padded dressing from the stump to the mid shin. If the incision was not left open, we splint the foot in neutral position to prevent equinus contracture. Several commercially available splints are available, or one can be constructed from plaster or fiberglass casting materials.

POSTOPERATIVE MANAGEMENT Deep vein thrombosis prophylaxis should be given to every patient while confined to bed. In the case of a simple toe or ray amputation, cane- or walker-assisted ambulation in an open-toe healing sandal

FIGURE 4  An alternative incision for transmetatarsal amputation FIGURE 3  Transmetatarsal amputation with a long plantar flap.

allowing the excision of a plantar ulcer.

646 AMPUTATION can begin early, usually within 24 hours. If the wound was left open, dressing changes should be provided twice a day with normal saline and sterile gauze. If packing was required, this should be reduced on a daily basis to allow wound contraction. Full weight bearing should be delayed until the wound is completely healed. Culture-directed antibiotics are administered as indicated and the sutures are left for approximately 14 days. After a transmetatarsal foot amputation, the patient remains strictly non–weight bearing until the incision is completely healed. The foot and ankle are elevated as often as possible, especially in the early postoperative period. Sutures are left in place for 4 weeks or occasionally longer. If the incision was not left open, we prefer to splint the foot in neutral position until ambulation. In preparation for ambulation, a prosthetist should evaluate the patient for appropriate footwear. Some patients require a functional brace or molded footwear, but most need only a laced shoe with insert. Running shoes are a good choice as a first shoe, and cotton wool or lambswool makes an excellent filler of the forefoot compartment of the shoe in the early postoperative period. We prefer a graduated partial weight-bearing regimen under the guidance of a physical therapist when resuming walking after a TMA. After ambulation, the patient should be monitored for transfer ulcers.

COMPLICATIONS Failure to heal suggests vascular insufficiency, persistent infection, or malnutrition. Premature weight bearing is another culprit. Most simple toe amputations are tolerated well, with few gait disturbances. Resection of a lesser toe rarely results in long-term disability, with the exception of the second toe, which can precipitate a hallux valgus deformity (Figure 5). A spacer can prevent this medial deviation of the first toe. The first toe is important for propulsion, and even a simple amputation can cause problems in this regard. Additionally, abnormal pressure may be placed on the plantar aspect of the second or even first metatarsal head after first-toe amputation. These issues can be prevented or corrected with orthotics. A ray amputation of the first toe is even more likely to cause a transfer lesion to the second metatarsal head or occasionally the tip of the second toe. This can be severe enough to require conversion to TMA. Other mechanical complications of first-ray amputation include increased pronation during ambulation and mid-tarsal Charcot deformity. Persistent infection indicates inadequate débridement, possibly in other deep metatarsal tissue planes. Ray amputations of the other toes are usually well tolerated. The fewest complications occur when the third metatarsal is amputated. Again, occult sources of deep space infection should always be suspected when poor wound healing is displayed. Soft tissue contracture after transmetatarsal foot amputation often leads to an abnormal plantar flexion or equinus deformity. Achilles tendon lengthening procedures are a reasonable option to correct this condition. Some surgeons perform it routinely after every TMA. Improper bone resection can cause pressure points in the stump, leading to skin breakdown and ulceration. Treatment is usually reoperation with resection of the involved metatarsal. Intractable pain requires conversion to a major amputation. Because of the prolonged non–weight-bearing status after a TMA, these patients are at increased risk for deep vein thrombosis and pulmonary embolus.

OUTCOMES There are surprisingly few studies in the literature addressing longterm outcomes after lower extremity minor amputation. In our mainly diabetic series of 670 patients, limb salvage was 89.8% at 1 year

FIGURE 5  Hallux valgus deformity of the first toe after second toe

amputation.

and 82.3% at 5 years. Limb loss was associated with end-stage kidney disease and the need for an initial amputation at the transmetatarsal level. The need to perform a bypass subsequent to the amputation was an independent predictor of limb loss. Overall patient survival was 83.9% at 1 year and 43.5% at 5 years. Renal insufficiency and conversion to major amputation were associated with adverse longterm survival.

Selected References Berceli S, Brown JE, Irwin P, et al: Clinical outcomes after closed, staged, and open forefoot amputations, J Vasc Surg 44:347–351, 2006. Boulton AJ, Armstrong DG, Albert SF, et al: Comprehensive foot examination and risk assessment. A report of the Task Force of the Foot Care Interest Group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists, Diabetes Care 31:1679–1685, 2008. Brem H, Sheehan P, Boulton AJ, et al: Protocol for treatment of diabetic foot ulcers, Am J Surg 187:1S–10S, 2004. Clayton W, Elasy T: A review of the pathophysiology, classification, and treatment of foot ulcers in diabetic patients, Clin Diabetes 27:52–58, 2009. LoGerfo FW, Coffman JD: Current concepts. Vascular and microvascular disease of the foot in diabetes. Implications for foot care, N Engl J Med 311:1615–1619, 1984. Pomposelli FB, Kansal N, Hamdan AD, et al: A decade of experience with dorsalis pedis artery bypass: Analysis of outcome in more than 1000 cases, J Vasc Surg 37:307–315, 2003. Rogers L, Andros G, Caporusso J, et al: Toe and flow: Essential components and structure of the amputation prevention team, J Podiat Med Assoc 100:342–348, 2010. Sheahan M, Hamdan A, Veraldi J, et al: Lower extremity minor amputations: The roles of diabetes mellitus and timing of revascularization, J Vasc Surg 42:476–480, 2005. Veves A, Giurini JM, LoGerfo FW, (eds): The Diabetic Foot, ed 2, Totowa, NJ, 2006, Humana Press.



647

Below-Knee Amputation

Below-Knee Amputation Kenneth E. McIntyre, Jr.

Amputation Statistics by Cause, United States, 1988 to 1996 58.5

Congenital

41.5 23.9

Cancer

76.1 68.6

Trauma

Amputation is one of the oldest surgical procedures known to humans. The earliest forms of below-knee amputation (BKA) occurred on or near battlefields, where wounded warriors had few alternatives other than to face the surgeon’s knife. Amputations for lower extremity trauma are still performed when the leg is so mangled that salvage is precluded. However, the most common indications for limb amputation today is not trauma, but rather critical limb ischemia (CLI) and diabetes with infectious gangrene. In the United States, between 1988 and 1996, an average of 133,735 hospital discharges/year were for amputations, and the predominant cause was vascular disease in 82% (Figure 1). The rate of amputations occurring in dysvascular patients increased from 38.3/100,000 people in 1988 to 46.19/100,000 people in 1996. With the numerous techniques available to the vascular surgeon to accomplish limb salvage, it is surprising that any patient would ever eventually require a major lower extremity amputation for irreversible lower extremity ischemia. However, some patients with chronic lower extremity ischemia simply do not offer a suitable anatomic alternative for limb-salvage procedures, either open or endovascular. Furthermore, some patients who come to the hospital with acute lower extremity ischemia, despite aggressive mechanical thrombectomy and/or intraarterial thrombolysis, sustain irreversible tissue loss. After repeated failures of infrainguinal arterial reconstructions for limb salvage, a BKA may be the only reasonable alternative left.

DETERMINING AMPUTATION LEVEL It is very important to have some idea of the healing potential of the skin at the level of amputation that is selected before surgery. Because the ability of an amputation stump to heal depends on skin blood flow, if the skin at a particular level will heal, then an amputation at that level will also heal. In general, a longer lever arm offers an improved mechanical advantage that will be of benefit to the patient during rehabilitation. Therefore, it requires significantly more energy to ambulate with an above-knee prosthesis (50%–70%) than it does with a below-knee prosthesis (10%–40%). This fact can help to explain the lower percentage of prosthetic use in above-knee (10%–30%) amputees compared to below-knee amputees (50%–100%). However, if a patient is unable to walk before the amputation or has another disability apart from a leg with infection and/or critical ischemia, such as a neuromuscular disorder, stroke, or hip osteoarthritis, then amputation at the transfemoral (above-knee) level should be considered. Before amputation, the longer the interval between a patient’s most recent independent ambulation and operation, the less likely rehabilitation will result in autonomous locomotion even after successful healing of the amputation stump. Initially, a thorough physical examination with palpation of the pulses must be performed. If the femoral pulse is absent, a BKA stump is unlikely to heal primarily. O’Dwyer found that less than 25% of BKAs healed when a femoral pulse was not present. If the femoral pulse is not normal, an ipsilateral iliac endovascular intervention or even an open groin arterial reconstruction should be considered to ensure that the planned BKA will have enough perfusion to heal primarily. Special attention should be directed to the skin where the proposed skin incision is planned. The skin must be healthy, without signs of infection, breakdown, or ischemia.

31 3

Dysvascular

97

0

20

40

60

80

100

per 100,000 limb-loss related hospital discharges lower limb

upper limb

FIGURE 1  Amputation statistics by cause.

Finally, both hip and knee joints should be examined for range of motion. Patients who have been at bed rest for some time develop joint stiffness and/or flexion contractures. These joint abnormalities are very serious and pose a significant threat to successful rehabilitation even if the amputation heals uneventfully. If amputation is planned electively, it is beneficial to begin physical therapy exercises well in advance of the intended procedure to improve knee and hip joint mobility and enhance upper body strength. Unfortunately, no known objective test can perfectly predict BKA stump healing. However, some standard testing metrics deserve mention. Absolute pressure at the ankle of greater than 60 mm Hg as determined by Doppler insonation has predicted healing BKAs 50% to 90% of the time. Inability to compress calcified vessels with a blood pressure cuff, however, can be problematic and is one reason this objective test is not always reliable. The transcutaneous partial pressure of oxygen (tcPo2) diffusing through the skin can be determined directly over the proposed surgical incision site. A value of greater than 40 mm Hg correlates very well with primary amputation site healing, and values less than 20 mm Hg correlate well with failure to heal. The accuracy of transcutaneous oximetry has been reported to be between 87% and 100% in predicting amputation healing. The examination should be performed in a room with constant warm temperature, and the technician must avoid testing skin areas that are involved with edema and/ or infection. These latter technical pitfalls can produce false-positive and false-negative results. Unfortunately, there is no absolute threshold of tcPo2 that accurately predicts healing 100% of the time.

SURGICAL TECHNIQUE Although a BKA involves excision of ischemic and/or infected tissue, the procedure should be viewed as a reconstructive technique, not simply as an ablative operation. If the indication for a BKA is irreversible loss of foot architecture secondary to infection with or without overt systemic sepsis, then the best approach is to perform the BKA procedure in two stages. The first step is to perform open guillotine leg amputation just above the ankle. This procedure can be performed in 10 minutes or less and can be performed under general or regional anesthesia. The initial step is simply making a circumferential incision just proximal to the malleoli. Any patent named vessels are suture ligated. The ligamentous attachments of the ankle are incised, exposing the periosteum of the tibia and fibula. The periosteum is elevated and a saw is used to divide the bones. There generally is little if any significant bleeding, but electrocautery can be used to ensure hemostasis. A moist sterile dressing is applied. Cultures are taken to help refine specific adjunctive antibiotic therapy. This initial step allows the infected

648 AMPUTATION

Outline of skin flap 3½ - 5”

Venous thromboembolism prophylaxis using low-molecularweight heparin should be employed in all patients during the entire hospitalization owing to the recognized high risk of this complication following amputation. Yeager and colleagues prospectively studied amputees to document the incidence of deep vein thrombosis in the perioperative period. They recorded an incidence of deep vein thrombosis in 12.5%.

RESULTS AND COMPLICATIONS ½ - 3 8”

5 - 6”

FIGURE 2  Construction of the posterior flap.

lymphatics to drain, and adjunct antibiotics can be administered. Any significant medical comorbidities can be improved upon before the next stage of therapy. The second step is the definitive BKA revision, which should take place after another 5 to 7 days. Several key elements help ensure primary healing of the BKA stump. Of utmost importance is careful, meticulous surgical technique. No proximal leg tourniquet is ever used. The skin flaps are constructed sharply with a long, thick posterior myocutaneous flap as described by Burgess. Although skew flaps, equal anterior and posterior flaps, sagittal flaps, and medial-based flaps have all been used successfully to close the amputated stump, the long posterior flap is easy to construct and offers excellent coverage and padding of the stump. The anterior skin incision is placed approximately five finger breadths below the tibial tuberosity and extended medially and laterally until approximately one half of the circumference of the calf has been reached. A long posterior myocutaneous flap consisting of skin, subcutaneous tissue, gastrocnemius, and a portion of soleus is then constructed. The length of this posterior flap measures 5 to 6 inches, but it should be long enough to avoid any undue tension on the closure over the end of the tibia (Figure 2). Electrocautery is used to divide the muscles to ensure scrupulous hemostasis. Large nerves are grasped, advanced, tied, transected, and allowed to retract into the depths of the wound. Major vessels are all suture ligated. The tibia is divided perpendicular to its axis, and the anterior portion of the bone is beveled smoothly to alleviate any subsequent potential pressure on the overlying skin. The fibula is divided approximately 1 cm more proximally than the tibia. The stump is closed in two layers, with an interrupted layer of absorbable suture for the fascia and interrupted nylon sutures loosely approximating the skin. No tissue forceps are ever used during closure to avoid trauma to the skin. Tying the skin sutures too snugly predisposes the skin to develop ischemic necrosis. No drains are ever used. The stump is placed in a well-padded plaster dressing extending well above the knee. This rigid dressing helps to protect the stump from trauma and reduces swelling and postoperative pain. It is important to cast the knee in neutral position without extension or flexion.

POSTOPERATIVE CARE Every patient who undergoes a BKA experiences some edema in the stump. The rigid plaster dressing helps to reduce this edema, but the amputated leg should be elevated on two pillows for 24 to 48 hours postoperatively. If an IPOP (immediate postoperative prosthesis) is used, then the amputee can begin with partial weight bearing on the amputated leg with supervision on the second postoperative day. The plaster dressing is usually changed at weekly intervals. The cast change is necessary in these circumstances because of the rapid shrinkage of the amputation stump. When the cast is removed, the stump is carefully inspected. Skin sutures are not removed for a minimum of 6 weeks.

Performing single-stage BKA in the presence of a necrotic foot infection risks infecting the below-knee stump and often results in the need for amputation revision at a higher level. McIntyre’s group retrospectively reviewed their results of two-stage versus one-stage BKAs that were performed for infectious gangrene. In the two-stage group (guillotine amputation followed by definitive BKA) there was a significantly lower incidence of stump infection, breakdown, and revision to a higher level. In the two-stage group, primary healing occurred in 97% compared to only 78% following a single-stage lower extremity amputation. A few years later, Fisher and colleagues performed a prospective randomized trial comparing BKAs performed in one stage versus two stages in patients with infectious gangrene of the lower extremity and found strikingly similar results. Lack of primary healing can also lead to the need for revision to the above-knee level in 11% to 25% of below-knee amputees. When a two-stage BKA was performed for infectious gangrene, no patient required revision to a higher level. Although the operation itself is usually not complicated and generally does not involve significant blood loss, there remains an alarmingly high perioperative mortality rate of 7% to 15%. This high perioperative mortality rate compared to lower extremity revascularization clearly reflects a selection bias. Patients who have severe comorbidities or who do not walk are selected for amputation rather than revascularization. There is also a known association between critical limb ischemia requiring major lower extremity amputation and ischemic heart disease. This group of patients is poorly mobile and is prone to venous thromboembolism in the perioperative period as well. Both ischemic heart disease and pulmonary embolism contribute to this high perioperative mortality rate. Even after successful healing of the amputation stump, a few patients are plagued with symptoms of chronic pain that can be very difficult to treat. Phantom pain refers to a chronic condition of neurogenic origin. The precise etiology is not known. The definition of phantom pain can differ among investigators, and therefore the true incidence is unknown. However, Malone’s group repots an incidence of significant phantom pain in less than 5% of lower extremity amputees. The natural history of the dysvascular amputee is grim. Of those surviving the amputation procedure, 15% to 28% undergo amputation on the contralateral leg within 3 years, and only half are alive in 3 years. In the large Veterans Administration Surgical Quality Improvement Program (VASQUIP) database, the anticipated 3-year mortality rate of patients who underwent BKAs was 43%.

Selected References Burgess EM, Romano RL, Zettl JH, et al: Amputations of the leg for peripheral vascular insufficiency, J Bone Joint Surg Am 53:874–890, 1971. DeFrang RD, Taylor LM, Porter JM: Basic data related to amputations, Ann Vasc Surg 5:202–207, 1991. Dillingham TR, Pezzin LE, MacKenzie EJ: Limb amputation and limb deficiency: Epidemiology and recent trends in the United States, South Med J 95:875–883, 2002. Feinglass J, Pearce WH, Martin GJ, et al: Postoperative and late survival outcomes after major amputation: Findings from the Department of Veterans Affairs National Surgical Quality Improvement Program, Surgery 130:21–29, 2001.



Above-Knee Amputation and Hip Disarticulation

Fisher Jr DF, Clagett GP, Fry RE, et al: One-stage versus two-stage amputation for wet gangrene of the lower extremity: A randomized study, J Vasc Surg 8:428–433, 1988. Malone JM, Anderson GG, Lalka SG, et al: Prospective comparison of noninvasive techniques for amputation level selection, Am J Surg 154:179–184, 1987. Malone JM, Moore WS, Leal JM, et al: Rehabilitation for lower extremity amputation, Arch Surg 116:93–98, 1981.

Above-Knee Amputation and Hip Disarticulation Robert J. Feezor and Thomas S. Huber

The incidence of major above-knee amputation (AKA) and belowknee amputation (BKA) has been relatively stable over the past few decades, with approximately 60,000 procedures per year performed in the United States. It is not clear that the widespread implementation of the endovascular therapies has favorably affected these rates, and this apparent paradox has been attributed to the aging population, the increasing incidence of diabetes and peripheral arterial occlusive disease (PAOD), the limited durability of the endovascular therapies, and the delays in presentation, among other factors. Most chapters on amputation highlight the fact that major amputations are among the most important procedures performed by vascular surgeons and therefore should not be relegated to the most junior members of the team; they are an important step in the rehabilitation process for patients with chronic limb ischemia, associated with the highest mortality rates of the elective vascular procedures; they are a treatment option rather than a failure of revascularization; and they have a major psychological impact on the patient. Although somewhat cliché, these common sentiments all merit consideration.

ABOVE-KNEE AMPUTATION Indications The indications for AKA include acute limb ischemia, chronic limb ischemia, infection, trauma, and malignancy. The first three indications account for the overwhelming majority in most vascular practices. These indications are somewhat interrelated and often are complications of peripheral vascular disease and diabetes. Acute limb ischemia can lead to AKA in the presence of irreversible ischemia or severe tissue loss and/or for patients with no revascularization options or those with failed revascularization attempts. Chronic limb ischemia can lead to AKA for essentially the same indications, with the notable additions of patients with severe ischemic rest pain, patients whose BKA does not heal, patients who would not benefit from a BKA (i.e., no likelihood of ambulating with a prosthesis), or those with a nonuseable leg that would not benefit from attempts at revascularization and limb salvage (e.g., nonambulatory nursing home patient with a knee contracture). AKA can also be indicated for patients with extensive soft tissue infections or osteomyelitis not responsive to antibiotics. The choice between revascularization and major amputation can be difficult. The data suggest that the mortality rate associated with major amputation exceeds that for revascularization. Although

649

McIntyre KE, Bailey SA, Malone JM, et al: Guillotine amputation in the treatment of nonsalvageable lower-extremity infections, Arch Surg 119:450–453, 1984. O’Dwyer KJ, Edwards MH: The association between the lowest palpable pulse and wound healing in below knee amputations, Ann R Coll Surg Engl 67:232–234, 1985. Yeager RA, Moneta GL, Edwards JM, et al: Deep vein thrombosis associated with lower extremity amputation, J Vasc Surg 22:612–615, 1995.

somewhat counterintuitive based upon the magnitude of the respective procedures, this observation likely reflects the inherent selection bias and the underlying comorbidities of the patients relegated to amputation. Nehler and colleagues provided a thoughtful, qualitative approach based upon the extent of tissue loss, the patient’s comorbidities, and the complexity of the revascularization, recommending amputation over revascularization if two of the three categories were extensive or severe (e.g., amputation for a patient with extensive tissue loss and severe comorbidities). It is important to emphasize that primary amputation is a better option for many patients and is clearly superior to multiple repeated attempts at limb salvage. Notably, delays in presentation, diabetes, end-stage kidney diseases, extensive tissue loss, and poor functional status have repeatedly been identified as predictors of primary amputation. It is worthwhile to consider the potential amputation incisions in this subset of high-risk patients at the time of attempted revascularization so that it does not compromise a later amputation should that become necessary. The selection of the most appropriate major amputation level merits comment, similar to the decision about the choice of revascularization versus amputation. The common choice between an AKA and a BKA reflects an inverse relationship between wound healing and the rehabilitation potential or the likelihood of walking on a prosthesis. Although a variety of factors can affect wound healing, including blood flow, infection, and soft tissue injury, approximately 80% of all BKAs heal and 95% of AKAs heal. It has been estimated that it takes approximately 40% more energy expenditure to walk on a BKA prosthesis and 70% more energy to walk on an AKA prosthesis. From a practical standpoint, this translates into the fact that less than 10% will walk on an AKA prosthesis. Not surprisingly, advanced age, multiple comorbidities, dementia, end-stage kidney disease, advanced coronary artery disease, and nonambulatory status preoperatively have all been negatively associated with rehabilitation potential. Worldwide, the BKA-to-AKA ratio is approximately 1:1, although many patients who undergo BKA for complications of peripheral vascular disease or diabetes do not take advantage of walking on a prosthesis. A variety of tests and techniques have been used to help predict whether an amputation can heal at a specific level, including simple pulse examination, hemodynamic measurements (e.g., blood pressure), anatomic assessment (e.g., arteriographic findings), and physiologic assessments (e.g., skin and muscle perfusion). Unfortunately, their overall predictive values are only fair, and they universally suffer from their inability to identify the lowest possible threshold value that predicts healing. The best predictor is likely an experienced clinician. Outside of an experienced clinician, a palpable pulse above the anatomic level of the amputation usually predicts healing (e.g., palpable femoral pulses predict AKA healing). Among the other assessment tools, the transcutaneous partial pressure of oxygen (tcPo2) is likely the most useful, with a value of greater than 30 mm Hg associated with healing. Although the usual clinical decision is between a BKA and an AKA, a through-knee amputation is worth considering in younger patients with good rehabilitation potential. The longer limb length can provide some advantages in terms of walking speed and energy expenditure when compared to an AKA. The published experience



Above-Knee Amputation and Hip Disarticulation

Fisher Jr DF, Clagett GP, Fry RE, et al: One-stage versus two-stage amputation for wet gangrene of the lower extremity: A randomized study, J Vasc Surg 8:428–433, 1988. Malone JM, Anderson GG, Lalka SG, et al: Prospective comparison of noninvasive techniques for amputation level selection, Am J Surg 154:179–184, 1987. Malone JM, Moore WS, Leal JM, et al: Rehabilitation for lower extremity amputation, Arch Surg 116:93–98, 1981.

Above-Knee Amputation and Hip Disarticulation Robert J. Feezor and Thomas S. Huber

The incidence of major above-knee amputation (AKA) and belowknee amputation (BKA) has been relatively stable over the past few decades, with approximately 60,000 procedures per year performed in the United States. It is not clear that the widespread implementation of the endovascular therapies has favorably affected these rates, and this apparent paradox has been attributed to the aging population, the increasing incidence of diabetes and peripheral arterial occlusive disease (PAOD), the limited durability of the endovascular therapies, and the delays in presentation, among other factors. Most chapters on amputation highlight the fact that major amputations are among the most important procedures performed by vascular surgeons and therefore should not be relegated to the most junior members of the team; they are an important step in the rehabilitation process for patients with chronic limb ischemia, associated with the highest mortality rates of the elective vascular procedures; they are a treatment option rather than a failure of revascularization; and they have a major psychological impact on the patient. Although somewhat cliché, these common sentiments all merit consideration.

ABOVE-KNEE AMPUTATION Indications The indications for AKA include acute limb ischemia, chronic limb ischemia, infection, trauma, and malignancy. The first three indications account for the overwhelming majority in most vascular practices. These indications are somewhat interrelated and often are complications of peripheral vascular disease and diabetes. Acute limb ischemia can lead to AKA in the presence of irreversible ischemia or severe tissue loss and/or for patients with no revascularization options or those with failed revascularization attempts. Chronic limb ischemia can lead to AKA for essentially the same indications, with the notable additions of patients with severe ischemic rest pain, patients whose BKA does not heal, patients who would not benefit from a BKA (i.e., no likelihood of ambulating with a prosthesis), or those with a nonuseable leg that would not benefit from attempts at revascularization and limb salvage (e.g., nonambulatory nursing home patient with a knee contracture). AKA can also be indicated for patients with extensive soft tissue infections or osteomyelitis not responsive to antibiotics. The choice between revascularization and major amputation can be difficult. The data suggest that the mortality rate associated with major amputation exceeds that for revascularization. Although

649

McIntyre KE, Bailey SA, Malone JM, et al: Guillotine amputation in the treatment of nonsalvageable lower-extremity infections, Arch Surg 119:450–453, 1984. O’Dwyer KJ, Edwards MH: The association between the lowest palpable pulse and wound healing in below knee amputations, Ann R Coll Surg Engl 67:232–234, 1985. Yeager RA, Moneta GL, Edwards JM, et al: Deep vein thrombosis associated with lower extremity amputation, J Vasc Surg 22:612–615, 1995.

somewhat counterintuitive based upon the magnitude of the respective procedures, this observation likely reflects the inherent selection bias and the underlying comorbidities of the patients relegated to amputation. Nehler and colleagues provided a thoughtful, qualitative approach based upon the extent of tissue loss, the patient’s comorbidities, and the complexity of the revascularization, recommending amputation over revascularization if two of the three categories were extensive or severe (e.g., amputation for a patient with extensive tissue loss and severe comorbidities). It is important to emphasize that primary amputation is a better option for many patients and is clearly superior to multiple repeated attempts at limb salvage. Notably, delays in presentation, diabetes, end-stage kidney diseases, extensive tissue loss, and poor functional status have repeatedly been identified as predictors of primary amputation. It is worthwhile to consider the potential amputation incisions in this subset of high-risk patients at the time of attempted revascularization so that it does not compromise a later amputation should that become necessary. The selection of the most appropriate major amputation level merits comment, similar to the decision about the choice of revascularization versus amputation. The common choice between an AKA and a BKA reflects an inverse relationship between wound healing and the rehabilitation potential or the likelihood of walking on a prosthesis. Although a variety of factors can affect wound healing, including blood flow, infection, and soft tissue injury, approximately 80% of all BKAs heal and 95% of AKAs heal. It has been estimated that it takes approximately 40% more energy expenditure to walk on a BKA prosthesis and 70% more energy to walk on an AKA prosthesis. From a practical standpoint, this translates into the fact that less than 10% will walk on an AKA prosthesis. Not surprisingly, advanced age, multiple comorbidities, dementia, end-stage kidney disease, advanced coronary artery disease, and nonambulatory status preoperatively have all been negatively associated with rehabilitation potential. Worldwide, the BKA-to-AKA ratio is approximately 1:1, although many patients who undergo BKA for complications of peripheral vascular disease or diabetes do not take advantage of walking on a prosthesis. A variety of tests and techniques have been used to help predict whether an amputation can heal at a specific level, including simple pulse examination, hemodynamic measurements (e.g., blood pressure), anatomic assessment (e.g., arteriographic findings), and physiologic assessments (e.g., skin and muscle perfusion). Unfortunately, their overall predictive values are only fair, and they universally suffer from their inability to identify the lowest possible threshold value that predicts healing. The best predictor is likely an experienced clinician. Outside of an experienced clinician, a palpable pulse above the anatomic level of the amputation usually predicts healing (e.g., palpable femoral pulses predict AKA healing). Among the other assessment tools, the transcutaneous partial pressure of oxygen (tcPo2) is likely the most useful, with a value of greater than 30 mm Hg associated with healing. Although the usual clinical decision is between a BKA and an AKA, a through-knee amputation is worth considering in younger patients with good rehabilitation potential. The longer limb length can provide some advantages in terms of walking speed and energy expenditure when compared to an AKA. The published experience

650 AMPUTATION

Greater trochanter

Site of transection

Skin incision

FIGURE 1  The skin incision for an above-knee amputation using the

equal length anterior and posterior fish-mouth technique is illustrated. The distal aspect of the incision on the anterior aspect of the thigh is a site approximately two fingerbreadths above the patella. The flaps are approximately 3 to 4 cm in length, and the femur is transected proximal to the angle of the fish mouth.

with through-knee amputations is somewhat limited, although there is some suggestion that the wound complication rate may be higher. The earlier limitations of fitting a prosthesis at this level have been largely overcome.

Operative Technique The operative technique for an AKA is fairly straightforward and has been well established. However, proper surgical technique with gentle handling of the tissues is paramount given the compromised state of the patient and tissue and the significant potential for wound complications. Both general and regional or spinal anesthesia techniques are appropriate, with the choice dictated by surgeon’s and anesthesiologist’s preference. Although the regional or spinal approach has been touted as safer from a cardiovascular standpoint in this highrisk patient population, the data supporting this contention has been somewhat equivocal. However, we have found these techniques beneficial in terms of postoperative pain control. The choice of incision is dictated by the surgeon’s preference. We prefer a fish-mouth incision with equal-length anterior and posterior flaps because of the early cosmetic appearance (Figure 1). However, the circumferential incision and the fish-mouth incision with sagittal flaps are both acceptable. Notably, the muscle and other soft tissues atrophy and remodel during the early postoperative period so that the residual extremity looks essentially the same at 6 months regardless of the initial incision. The incision is usually made over the distal

two thirds of the thigh in an attempt to preserve as much of the femur length as possible if there is any chance that the patient will walk on a prosthesis. The distal aspect of the anterior and posterior flap of the fish-mouth incision is commonly cited two finger breadths proximal to the patella, with the angle of the incision in the mid portion of the thigh, roughly 3 to 4 cm proximal to the most distal extent. The planned incision is marked on the skin, and then the anterior skin and soft tissues are incised along the planes of the skin mark. Electrocautery is used to incise the muscle and soft tissues despite the concerns about local tissue injury, because we believe that the hemostatic benefit outweighs this potential disadvantage. The soft tissue is incised down to the femur, and the major vessels are suture ligated. The periosteum over the femur is elevated for a limited distance, and the bone is transected perpendicular to its long axis and proximal to the angle of the fish mouth. The power saw is preferred because it is precise and because the bone above the incision has smooth, nonjagged edges. The muscle and soft tissue of the posterior flap are likewise incised along the planes of the skin marks, and the specimen is removed from the operative field. The sciatic nerve is transected under mild tension, suture ligated, and allowed to retract. Hemostasis is confirmed, and the fascia immediately below the skin and subcutaneous tissue is reapproximated with interrupted absorbable sutures. The deep dermis is likewise reapproximated with interrupted absorbable sutures, and the final layer of skin is closed with staples. A dressing is applied, and the residual extremity is wrapped with an elastic bandage to help control the swelling. Several important technical points merit discussion. It is important to cut the bone short enough so there is no tension on the overlying soft tissue because excess tension can lead to wound breakdown and/or erosion of the bone through the skin. If there is any concern about the length of the bone after the initial transection, the overlying periosteum should be elevated and the bone should be transected more proximal. We do not use bone wax, to prevent having a foreign body in the wound. All prosthetic graft material should be removed from the wound to prevent future infections and/or wound complications if possible. Making a separate inguinal incision and dissembling the proximal anastomosis (in the case of a common femoral artery– based graft) is not recommended, but the graft material should be dissected as proximal as possible from the open thigh wound and transected. We do not reapproximate the antagonistic muscle groups (myoplasty) or suture the musculotendinous unit to the bone (myodesis) as recommended by some. No special wound dressings or adjuncts (e.g., rigid removal dressing, posterior splint) are applied to an AKA other than a gauze dressing and an elastic wrap. Given the short length of the residual extremity after AKA, it is difficult to keep a dressing on the wound, even an elastic wrap.

Postoperative Care and Perioperative Outcome The postoperative care of patients after AKA is comparable to that after any vascular surgical procedure as would be predicted based upon the severity of their underlying comorbidities. The medical management of the various organ systems should be optimized, particularly the cardiac and respiratory systems, given the high incidence of cardiac events and pneumonia. Several specific concerns relative to patients undergoing amputation merit discussion given the associated morbidity and mortality. The incidence of wound complications after AKA can range as high as 40%, with frank nonhealing secondary to ongoing ischemia in 5% to 10% of cases. An aggressive approach to wound care should be implemented including liberal débridement, systemic antibiotics (as appropriate for evidence of cellulitis), and optimization of nutrition. Although a nonhealing AKA can be catastrophic, we have found that this to be quite rare and less than the rates reported. Vacuum-assisted dressings are quite helpful in this setting although the overall duration of the wound care (and open wound) may be quite prolonged.

651

Above-Knee Amputation and Hip Disarticulation

In the truly rare patient in whom local wound care is ineffective secondary to ongoing ischemia, an aggressive attempt should be made to revascularize the ischemic residual extremity because a more proximal amputation is rarely effective: If a high AKA does not heal, a hip disarticulation will not heal, either. The potential revascularization options include femorofemoral bypass, iliofemoral bypass, or hypogastric bypass, with the choice dictated by the patent vessels, commonly the profunda femoris. Indeed, we occasionally explore the profunda femoris in this setting even if it is not visualized on preoperative imaging. Importantly, the goal of revascularization in this setting is to facilitate wound healing, with any concerns about long-term patency being secondary. Deep vein thrombosis and pulmonary embolus have been reported in up to 50% of patients after major lower extremity amputation. All patients should be on some type of venous thromboembolic prophylaxis, and screening for deep vein thrombosis may be justified given the high incidence. Postoperative pain can be debilitating and difficult to control. Indeed, some type of chronic pain complaints have been reported in 95% of patients after major lower extremity amputation. The potential sources of pain include the incision, ongoing ischemia, the peripheral nerves (i.e., neuropathy, nerve injury, neuroma), infection, and phantom pain. Regional or spinal anesthesia can be helpful in the perioperative period, and we have found pain specialists to be helpful in the outpatient setting for chronic complaints. The importance of perioperative pain control cannot be overemphasized. The normal tendency for amputees with uncontrolled pain is to withdraw the extremity. Unfortunately, this compromises their physical therapy and can lead to a contracture at the hip (or knee in the case of a BKA) that can preclude ambulation on a prosthesis. Lastly, it is very common for patients undergoing a major amputation to become depressed given their new limitations and altered body image. Medical treatment for depression and early initiation of a rehabilitation program may be beneficial. Perioperative mortality after AKA ranges from 11% to 18% and exceeds those reported for most other elective major vascular surgical procedures. This reflects the patient’s underlying comorbidities. The leading causes of death include cardiac causes, sepsis, and pneumonia. Not surprisingly, advanced systemic disease (e.g., cardiac, pulmonary, renal), malnutrition, and the need for an emergent staged amputation (e.g., guillotine amputation, ankle disarticulation) have all been associated with increased mortality.

Long-Term Outcome Not surprisingly, the long-term outcome after AKA is fairly dismal. The survival rate at 1 year is approximately 50% (Figure 2), and less than 10% of elderly patients can walk on a prosthesis. Indeed, Taylor and colleagues reported from of a large series of patients undergoing major amputation (BKA and AKA) that the largest predictors of not ambulating on a prosthesis were nonambulatory status before amputation (odds ratio [OR], 0.5) and AKA (OR, 4.4). Despite not being able to ambulate, a large percentage of patients undergoing AKA can remain independent by modifying their home environment, and thus the need for a major amputation no longer mandates a longterm care facility. Patients undergoing a major amputation are at a particularly high risk for requiring a contralateral amputation, with values ranging from 15% to 35% reported for diabetics. This possibility is predictably very distressing for the patient and underscores the importance of vigilant care for the contralateral limb.

HIP DISARTICULATION Amputation at the level of the hip or a hip disarticulation is a rare event and accounts for less than 1% of all amputations. The indications are essentially the same as those for an AKA and include

100

1y

80 Survival (%)



5y

BKA (n = 704) AKA (n = 255)

74.5%

60

50.6% 37.8%

40

22.5%

20 0 0

1000

2000 3000 Time (d)

4000

5000

FIGURE 2  Long-term survival after above-knee and below-knee

amputations are shown. Note that the 1-year mortality rate after above-knee amputation is 51%.

ischemia, infection, trauma, and malignancy. The role of a hip disarticulation in patients with peripheral vascular disease and ischemia is not clear because in patients with a high AKA that does not heal, usually a hip disarticulation will not heal. Notably, Endean and coworkers reported their experience with 53 patients undergoing hip disarticulation, including 10 procedures performed for ischemia and 14 for ischemia and infection. Their overall wound complication and mortality rates were 63% and 21%, respectively, with a mortality rate of 50% for patients with ischemia and 33% for those with ischemia and infection. Given these prohibitive morbidity and mortality rates, aggressive wound care and potential revascularization are likely better alternatives for patients with proximal extremity ischemia or a nonhealing AKA. The operative technique for hip disarticulation has been well described, and the appropriate citations are provided among the references. Given the procedure’s rarity and the equivocal indications for patients with peripheral occlusive disease, most vascular surgeons’ experience with the procedure is limited. At our institution, patients in need of a hip disarticulation are usually referred to the orthopedic oncologists, who have a more extensive experience with the procedure.

Selected References Eidt JF, Kalapatapu VR: Lower extremity amputation: Techniques and results. In Cronenwett JL, Johnston KW, (eds): Rutherford's Vascular Surgery, ed 7, Philadelphia, 2010, Saunders Elsevier, pp 1772–1790. Endean ED, Schwarcz TH, Barkey DE, et al: Hip disarticulation: Factors affecting outcome, J Vasc Surg 14:398–404, 1991. Morse BC, Cull DL, Kalbaugh C, et al: Through-knee amputation in patients with peripheral arterial disease: A review of 50 cases, J Vasc Surg 48:638–643, 2009. Nehler MR, Hiatt WR, Taylor LM: Is revascularization and limb salvage always the best treatment for critical limb ischemia? J Vasc Surg 37:704–708, 2003. Taylor SM, Kalbaugh CA, Blackhurst DW, et al: Preoperative clinical factors predict postoperative functional outcomes after major lower limb amputation: An analysis of 553 consecutive patients, J Vasc Surg 42, 2005 277–235. Wakelin SJ, Oliver CW, Kaufman MH: Hip disarticulation—the evolution of a surgical technique, Injury 35:299–308, 2004. Zhang WW, Abou-Zamzam AM: Lower extremity amputation: General considerations. In Cronenwett JL, Johnston KW, (eds): Rutherford's Vascular Surgery, ed 7, Philadelphia, 2010, Saunders Elsevier, pp 1761–1771.

652 AMPUTATION

Upper Extremity Amputations Paul J. Dougherty and James E. Carpenter

Upper extremity amputations are less common than lower extremity amputations in both wartime and civilian settings. During wartime, the incidence of upper extremity amputees is between 13% and 25% of all extremity amputations. A survey of the U.S. National Trauma Databank found 8910 amputations reported from 2000 to 2004, of which 41.1% of those with single-limb amputation were of the upper extremity. Indications for surgery for the upper extremity differ from those for the lower extremity. The function of a hand is still far more complex than the best prosthetic hand, so care should be taken to preserve the upper extremity with extensive limb salvage techniques, if feasible. The most common indication for upper extremity amputation surgery in the United States is trauma, with a smaller number indicated as the result of tumor or vascular disease. Major amputations of the upper extremity follow the same principles of management as for the lower extremity. The ultimate objective is to provide a functional limb for the patient, with a well-padded, pain-free residual limb that is without prominences. For all types of amputation, a myodesis (where muscle tendon is attached to bone via suture and bone tunnels) should be done to provide residual limb soft tissue coverage and to anchor the muscle for residual limb function. There is high rate of prosthetic use for patients with transradial amputations, but prosthetic use for shoulder disarticulation and for forequarter and transhumeral amputations remains below 50%. Efforts of targeted muscle reinnervation, in which remaining arm nerves are transferred to muscles in the chest or shoulder, has shown promise to improve function in patients using a myoelectric prosthesis. The implanted nerves allow a greater, more specific signal to help the myoelectric arm. Whether this will improve the long-term outcome for transhumeral or more proximal amputations remains to be seen. Early fitting (within 30 days after the amputation) has been shown to increase acceptance rates of prosthesis use by upper extremity amputees. Because of this, a prosthesis should be fitted early, fitting either a temporary or permanent prosthesis, depending on the residual limb.

SHOULDER DISARTICULATION Burkhalter reported that nine of 96 upper extremity amputees had a shoulder disarticulation at Fitzimmons Army Hospital after the Vietnam war. The majority of patients in the series had amputations as a result of war wounds. This procedure is for nonsalvageable proximal arm injuries or for severe brachial plexopathies. The surgical technique most often cited for shoulder disarticulation was reported by Slocum after caring for amputees during World War II. The patient is placed on the operating room table at a 45-degree angle. An anterior incision is made from the coracoid just medial to the deltoid muscle. As the incision is carried distally, it is then brought circumferentially around the arm and proximally into the axilla. Once the site is opened through the skin, the cephalic vein is identified and ligated. The deltoid is retracted laterally, and the pectoralis major is incised near its insertion and retracted medially. The axillary artery and vein and the thoracoacromial artery are then isolated and

ligated before transection. The radial, musculocutaneous, ulnar, and median nerves are isolated, drawn into the field, ligated, and transected as proximally as possible. Next, the insertions of the coracobrachialis, teres minor and teres major, the deltoid, and the origin of the triceps are incised, followed by the subscapularis and the anterior joint capsule. Once the humerus is dissected free, the limb may be removed. The deltoid is then sutured inferior to the glenoid to cover the open wound, and the skin is closed (Figure 1). Postoperative care should include close monitoring of the patient for the first 24 hours. There is relatively little fluctuation in the shape of the amputation site after wound healing; therefore the patient may be fitted initially with a permanent prosthesis. In one series, three of nine patients with shoulder disarticulations became successful prosthetic wearers.

TRANSHUMERAL AMPUTATION Transhumeral amputation is performed for severe elbow or arm injuries or for nonsalvageable forearm injuries (Figure 2). Other reported indications are infection and brachial plexopathies. The amputation is done by constructing flaps at the lowest viable level of soft tissue to allow the best fitting of a prosthetic limb. Very proximal amputations, especially those proximal to the deltoid tuberosity, should be fitted with a prosthesis similar to that for a shoulder disarticulation. Flaps should be made to utilize the available soft tissues and may be irregular in shape. In general, anterior and posterior flaps are made, followed by transection of the muscle more proximally. The brachial artery and vein are isolated and doubly ligated before transection. Nerves (radial, ulnar, median, musculocutaneous) are isolated, put on traction, and ligated. They are then transected and allowed to retract into the soft tissues to avoid a symptomatic neuroma. Enough muscle should be left to cover the distal end of the bone. The muscle should be sutured to the bone, and antagonist muscle groups should be sutured to each other. Skin should be closed with interrupted sutures. A rigid dressing is placed over the residual limb to reduce swelling. Postoperatively, the patient should begin activities of daily living training. For patients with brachial plexopathies, no advantage has been found in performing a shoulder arthrodesis to stabilize the limb in addition to the amputation. Additional length may be obtained by reflecting a portion of the pectoralis muscle. Patients should be fitted with a temporary or practice prosthesis to obtain the best function. In selected cases, distal replantation of an acute traumatic transhumeral amputation can be done. One report on the functional results of seven patients with transhumeral amputation and subsequent early limb replantation have found that only two of seven had regained useful hand function. The authors felt that transhumeral replantation might be useful in preserving the elbow, with the patient becoming a transradial amputee rather than a transhumeral amputee. The patients in this study all had a discrete transhumeral transection, and the distal limb was available for replantation. Unfortunately, some wounds are so destructive that they do not allow this procedure.

TRANSRADIAL AMPUTATION Transradial amputation is most often the direct result of trauma. Because function of the transradial amputee is better than that of a transhumeral amputee, every effort should be made to preserve the elbow joint. A formal transradial amputation is done by creating flaps at the lowest viable level of soft tissue. Because of injury, irregular flaps may be used for soft tissue coverage. The major nerves should be isolated (median, ulnar, radial, lateral antebrachial cutaneous), put under



Upper Extremity Amputations

A

B

C

D

E

F

FIGURE 1  Shoulder disarticulation.  A, Skin incision; B, Pectoralis major muscle detached, vessels ligated;

C, Deltoid, Biceps and Coracobrachialis detached; D,  Triceps and rotator cuff detached; E, Muscular closure (myodesis); F, Skin closure.

A

B

C

FIGURE 2  Transhumeral amputation. A, Skin incision; B, Muscle transection at shorter level; C, Skin closure after myodesis over bone.

653

654 AMPUTATION tension, ligated, and then transected and allowed to retract. Major vessels (radial, ulnar) should be isolated and ligated. Muscle groups are then trimmed to provide coverage over the distal bone ends. Myodesis or myoplasty are done to provide muscle coverage over the bone ends and stability. The skin is then closed with interrupted sutures. A rigid dressing is applied to reduce swelling. A patient should be fitted with a preparatory prosthesis, and rehabilitation should begin as soon as possible. Limb length may be added through the use of an Ilizarov fixator. Limited data for this procedure exists, making careful application advisable for those using this procedure. Partial-thickness skin grafts may be used to cover muscle. A problem with partial-thickness skin grafts, however, is that they are less durable than sensate, full-­ thickness skin. One report lists a reoperation rate of 29% when using them.

KRUKENBERG AMPUTATION A Krukenberg procedure is a surgical procedure having very unusual surgical indications. With this procedure, the forearm bones are separated and made into active, sensate pinchers. This procedure is useful for a patient who is blind and has bilateral upper extremity amputations or who has a severe contralateral hand injury. It is also useful in developing nations where prosthetic fitting is limited or not available.

WRIST DISARTICULATION A wrist disarticulation may be indicated for a nonsalvageable hand injury. The disadvantage to this procedure (when compared to a transradial amputation) is that it provides limited space for the terminal device of the artificial limb, and use of a myoelectric prosthesis may be limited by the available space. Advantages are that it preserves forearm rotation and provides an improved area for prosthesis suspension.

Rehabilitation of the Amputee Brian M. Kelly and James A. Leonard, Jr.

Approximately 100,000 to 150,000 persons experience some level of major lower limb amputation in the United States each year. The majority of these patients have diabetes and/or peripheral vascular disease (approximately 90%). A rehabilitation medicine physician (physiatrist) has much to offer the patient who is going to require an amputation. The physiatrist can provide counsel to the patient and family about rehabilitation and the possibility of future prosthetic function, comment on the advantages or disadvantages of the proposed level of amputation for future prosthetic fitting and function, determine and direct the patient’s rehabilitation needs during the acute hospital stay, determine the need for and oversee any additional inpatient rehabilitation care before discharge home, and manage the patient’s ongoing prosthetic restoration and rehabilitation once the amputation incision has healed. The earlier rehabilitation professionals are involved in the care of patients who are to have or who have had an amputation, the more they can contribute.

The skin flaps created depend on the extent of injury. Enough skin should be available to form a well-contoured residual limb. Myodesis is done to stabilize muscles and provide function. The triangular fibrocartilage complex and distal radioulnar joint ligaments must be preserved to allow stable pronation and supination. Care should be taken to identify the superficial branch of the radial nerve, the dorsal sensory branch of the ulnar nerve, and possibly the medial and lateral antebrachial cutaneous nerves. These should be pulled distally and transected and then allowed to retract away from any bone prominence. As with other upper extremity amputees, prosthetic fitting and training should begin as soon as possible. Wright and colleagues found that eight of fourteen patients with a wrist disarticulation were successfully fitted with a prosthesis.

Selected References Burkhalter WE, Mayfield G, Carmona LS: The upper-extremity amputee, J Bone Joint Surg Am 58:46–51, 1976. Cleveland KB: Amputations of the upper extremity. In Canale ST, Beaty JH, (eds): Campbell’s Operative Orthopaedics, ed 11, Philadelphia, 2007, Saunders Elsevier, pp 625–637. Garst RJ: The Krukenberg hand, J Bone Joint Surg Br 73:385–388, 1991. McAuliffe JA: Elbow disarticulation and transhumeral amputation. In Bowker JH, Michael JW, (eds): Atlas in Limb Prosthetics, Chicago, 1992, American Academy of Orthopaedic Surgeons, pp 251–253. McAuliffe JA: Shoulder disarticulation and forequarter amputation. In Bowker JH, Michael JW, (eds): Atlas in Limb Prosthetics, Chicago, 1992, American Academy of Orthopaedic Surgeons, pp 265–275. Ouellette EA: Wrist disarticulation and transradial amputation. In Bowker JH, Michael JW, (eds): Atlas in Limb Prosthetics, Chicago, 1992, American Academy of Orthopaedic Surgeons, pp 429–452. Pinzur MS, Angelats J, Light TR, et al: Functional outcome following traumatic upper limb amputation and prosthetic limb fitting, J Hand Surg Am 19:836–839, 1994. Slocum DB: An Atlas of Amputations, St. Louis, 1949, C.V. Mosby. Wright TW, Hagen AD, Wood MB: Prosthetic usage in major upper extremity amputations, J Hand Surg Am 20:619–622, 1995. Zelle BA, Pape HC, Gerich TG, et al: Functional outcome following scapulothoracic dissociation, J Bone Joint Surg Am 86:2–8, 2004.

The rehabilitation care of an amputee is best organized temporally in relation to the amputation surgery because specific rehabilitation activities are appropriate for the different time periods. The time periods are best identified as preoperative, postoperative, preprosthetic, and prosthetic rehabilitation. This care is a team effort and can require the contributions of many individuals including physical and occupational therapists, prosthetists, social workers, psychologists, vocational specialists, and peer counselors.

BEFORE AMPUTATION The focus of the preamputation evaluation is counseling. The goal is to provide the patient and family with information and answer questions to help the patient to make an informed decision about whether to proceed with an amputation or not, and it will also help prepare the patient for what will occur following amputation. Most patients facing a major limb amputation are frightened, anxious, depressed, and uncertain of their future. They may be reluctant to proceed with their surgeon’s recommendation of amputation either as a treatment from among one of a number of treatment options or as the final treatment option after all other treatments for limb salvage have been explored and exhausted. The rehabilitation team provides patients and family with information about life after amputation, which can help to allay their fears and allow them to make an informed decision on treatment course, if they

654 AMPUTATION tension, ligated, and then transected and allowed to retract. Major vessels (radial, ulnar) should be isolated and ligated. Muscle groups are then trimmed to provide coverage over the distal bone ends. Myodesis or myoplasty are done to provide muscle coverage over the bone ends and stability. The skin is then closed with interrupted sutures. A rigid dressing is applied to reduce swelling. A patient should be fitted with a preparatory prosthesis, and rehabilitation should begin as soon as possible. Limb length may be added through the use of an Ilizarov fixator. Limited data for this procedure exists, making careful application advisable for those using this procedure. Partial-thickness skin grafts may be used to cover muscle. A problem with partial-thickness skin grafts, however, is that they are less durable than sensate, full-­ thickness skin. One report lists a reoperation rate of 29% when using them.

KRUKENBERG AMPUTATION A Krukenberg procedure is a surgical procedure having very unusual surgical indications. With this procedure, the forearm bones are separated and made into active, sensate pinchers. This procedure is useful for a patient who is blind and has bilateral upper extremity amputations or who has a severe contralateral hand injury. It is also useful in developing nations where prosthetic fitting is limited or not available.

WRIST DISARTICULATION A wrist disarticulation may be indicated for a nonsalvageable hand injury. The disadvantage to this procedure (when compared to a transradial amputation) is that it provides limited space for the terminal device of the artificial limb, and use of a myoelectric prosthesis may be limited by the available space. Advantages are that it preserves forearm rotation and provides an improved area for prosthesis suspension.

Rehabilitation of the Amputee Brian M. Kelly and James A. Leonard, Jr.

Approximately 100,000 to 150,000 persons experience some level of major lower limb amputation in the United States each year. The majority of these patients have diabetes and/or peripheral vascular disease (approximately 90%). A rehabilitation medicine physician (physiatrist) has much to offer the patient who is going to require an amputation. The physiatrist can provide counsel to the patient and family about rehabilitation and the possibility of future prosthetic function, comment on the advantages or disadvantages of the proposed level of amputation for future prosthetic fitting and function, determine and direct the patient’s rehabilitation needs during the acute hospital stay, determine the need for and oversee any additional inpatient rehabilitation care before discharge home, and manage the patient’s ongoing prosthetic restoration and rehabilitation once the amputation incision has healed. The earlier rehabilitation professionals are involved in the care of patients who are to have or who have had an amputation, the more they can contribute.

The skin flaps created depend on the extent of injury. Enough skin should be available to form a well-contoured residual limb. Myodesis is done to stabilize muscles and provide function. The triangular fibrocartilage complex and distal radioulnar joint ligaments must be preserved to allow stable pronation and supination. Care should be taken to identify the superficial branch of the radial nerve, the dorsal sensory branch of the ulnar nerve, and possibly the medial and lateral antebrachial cutaneous nerves. These should be pulled distally and transected and then allowed to retract away from any bone prominence. As with other upper extremity amputees, prosthetic fitting and training should begin as soon as possible. Wright and colleagues found that eight of fourteen patients with a wrist disarticulation were successfully fitted with a prosthesis.

Selected References Burkhalter WE, Mayfield G, Carmona LS: The upper-extremity amputee, J Bone Joint Surg Am 58:46–51, 1976. Cleveland KB: Amputations of the upper extremity. In Canale ST, Beaty JH, (eds): Campbell’s Operative Orthopaedics, ed 11, Philadelphia, 2007, Saunders Elsevier, pp 625–637. Garst RJ: The Krukenberg hand, J Bone Joint Surg Br 73:385–388, 1991. McAuliffe JA: Elbow disarticulation and transhumeral amputation. In Bowker JH, Michael JW, (eds): Atlas in Limb Prosthetics, Chicago, 1992, American Academy of Orthopaedic Surgeons, pp 251–253. McAuliffe JA: Shoulder disarticulation and forequarter amputation. In Bowker JH, Michael JW, (eds): Atlas in Limb Prosthetics, Chicago, 1992, American Academy of Orthopaedic Surgeons, pp 265–275. Ouellette EA: Wrist disarticulation and transradial amputation. In Bowker JH, Michael JW, (eds): Atlas in Limb Prosthetics, Chicago, 1992, American Academy of Orthopaedic Surgeons, pp 429–452. Pinzur MS, Angelats J, Light TR, et al: Functional outcome following traumatic upper limb amputation and prosthetic limb fitting, J Hand Surg Am 19:836–839, 1994. Slocum DB: An Atlas of Amputations, St. Louis, 1949, C.V. Mosby. Wright TW, Hagen AD, Wood MB: Prosthetic usage in major upper extremity amputations, J Hand Surg Am 20:619–622, 1995. Zelle BA, Pape HC, Gerich TG, et al: Functional outcome following scapulothoracic dissociation, J Bone Joint Surg Am 86:2–8, 2004.

The rehabilitation care of an amputee is best organized temporally in relation to the amputation surgery because specific rehabilitation activities are appropriate for the different time periods. The time periods are best identified as preoperative, postoperative, preprosthetic, and prosthetic rehabilitation. This care is a team effort and can require the contributions of many individuals including physical and occupational therapists, prosthetists, social workers, psychologists, vocational specialists, and peer counselors.

BEFORE AMPUTATION The focus of the preamputation evaluation is counseling. The goal is to provide the patient and family with information and answer questions to help the patient to make an informed decision about whether to proceed with an amputation or not, and it will also help prepare the patient for what will occur following amputation. Most patients facing a major limb amputation are frightened, anxious, depressed, and uncertain of their future. They may be reluctant to proceed with their surgeon’s recommendation of amputation either as a treatment from among one of a number of treatment options or as the final treatment option after all other treatments for limb salvage have been explored and exhausted. The rehabilitation team provides patients and family with information about life after amputation, which can help to allay their fears and allow them to make an informed decision on treatment course, if they

Rehabilitation of the Amputee

have that option, or to move forward with their surgery. The rehabilitation team counseling should include discussion of several topics, including phantom limb sensation, phantom limb pain, residual limb pain, management of the residual limb after amputation, physical and occupational therapy to occur while on the acute surgical service, the possibility of additional rehabilitation care before discharge to home (whether in an acute or subacute facility), the anticipated timing of initial prosthetic fitting (typically 6 to 8 weeks after amputation for the dysvascular population), the processes of prosthetic fitting, expected prosthetic function (if the patient is deemed a candidate for prosthetic restoration) and the therapy necessary to learn to successfully use a prosthesis. Assessment of the patients’ physical status and prior level of function is another key part of the physiatrist’s initial evaluation. In addition to the history of the patient’s chief complaint leading to amputation and any other acute or chronic medical conditions, the rehabilitation team must know the patient’s prior level of function, living situation, and family support. When did the patient last walk? Was the patient using a cane or walker to walk? Was the patient living at home or in a nursing home? If the patient lives at home, what is the home like? Is the home accessible, or are there stairs to be managed to get in or out of the home? Are there other environmental barriers that might prevent a return to home? Does the patient live alone, or is there a spouse or family available to assist with care upon return to home? Is the spouse’s or family’s health or time commitments such they can actually provide assistance if needed? The physical examination must assess the patient’s general physical condition, strength of all extremities, endurance, joint range of motion, the status of the other lower extremity in the case of lower limb amputation, and the patient’s cognitive abilities. Being nonambulatory or having significant joint contractures, weakness, and/or significant cognitive impairments limiting the ability to learn new skills can preclude patients from ever being considered candidates for prosthetic restoration. This initial evaluation helps to define the patient’s rehabilitation goals, direct the therapies, and determine if the patient is likely to require continuing inpatient rehabilitation services after acute surgical care.

AMPUTATION LEVEL The goal when selecting an amputation level for a particular dysvascular patient is to choose the level that will most likely heal while preserving the most function for the patient. In general, the more joints that are preserved and the longer the residual limb is, the more function and the lower the energy expenditure the amputee is likely to experience when using a prosthesis. In addition to this general guideline to preserve length and joints, there are some considerations that will result in better prosthetic outcomes for the amputee patient. It is important that all amputations have a secure myoplasty or myodesis, with a minimum of redundant soft tissue to maximize the efficiency of force transfer from the bone of the residual to the prosthesis. The more the major long bone of the residual limb (femur and tibia for lower limb amputations and humerus and ulna for upper limb amputations) has to move through soft tissues before contacting and initiating movement of the prosthetic socket, the greater the loss in efficiency and the greater the decrease in prosthetic function. Sometimes, as a result of posttraumatic swelling, complications of cellulitis, associated compartment syndrome, or other morbidity, the soft tissues cannot be closed as ideally as desired, resulting in significant soft tissue redundancy. It is better to have the outcome of redundant distal soft tissue with a preserved knee than an ideal closure at a transfemoral amputation level. If the resulting prosthetic function is less than optimal or problematic as a result of redundant soft tissue, a plastic and reconstructive revision of the residual limb to remove redundant tissue can be considered at a later date. Toe amputations and most transmetatarsal amputations are very functional levels of amputation that can be accommodated quite easily with shoe modifications for walking on level surfaces in most

655

cases. Very proximal transmetatarsal amputations, Lisfranc amputations, Chopart amputations, and amputations through the hind foot have the advantage of preserving some or all of the weight-bearing surface of the foot together with maintaining normal limb length. These amputation levels, however, can result in significant functional difficulty if special care is not taken to balance the opposing plantar and dorsiflexion forces about the ankle by relocating the attachment of the ankle dorsiflexors. When this is not done properly the patient develops an equinus deformity of the ankle, making it difficult or impossible to walk. Amputations through the mid and hindfoot while preserving length can also be quite challenging to impossible to provide a good functional prosthetic option. A more proximal level amputation can often be a better option for improved function. A Syme amputation or ankle disarticulation can be a very acceptable and functional amputation level with reasonable prosthetic options. Because the limb length difference is relatively small, the patient is capable of walking without a prosthesis by flexing the contralateral knee and hip to accommodate for the limb length difference. These same advantages also present some disadvantages when considering prosthetic restoration, which may be unexpected or unacceptable to patients if they are not aware of them when discussing options for amputation level. The long length of the residual limb significantly limits the options for prosthetic foot choice because of the limited space between the end of the residual limb and the floor (about 2 ½ to 3 inches) and precludes the use of specialized components such as shock pylons and rotators commonly used in prostheses for a more proximal transtibial amputation. The bulbous distal limb must be accommodated for in the design of the prosthesis and requires a socket that may be much larger in circumference than the contralateral limb, resulting in a prosthesis that might be either esthetically unpleasing or unacceptable to the patient. Similar advantages and disadvantages are associated with knee disarticulation amputations. The advantages of a knee disarticulation are a good end-bearing residual limb able to tolerate distal residual limb weight bearing in a prosthesis, long residual limb or lever arm to reduce energy expenditure, and a bulbous shape to the distal residual limb allowing anatomic suspension of the socket. The bulbous shape of the distal femur from the retained condyles can also be one of its disadvantages, necessitating a less-than-cosmetically acceptable shape to the socket for some patients. The greatest disadvantage of the knee disarticulation has always been the long length of the residual limb because the entire femur remains, leading to a knee axis center in the prosthesis that is longer than that on the nonamputated lower extremity. The resulting longer thigh length (full femur, prosthetic socket, and prosthetic knee) can result in functional problems for the amputee where seating space may be limited as in theater, airplane, and automobile seats. Fortunately this is somewhat less of a problem than it used to be with the availability of prosthetic knee units designed to minimize this difference. Disarticulation level amputations have a unique advantage in children requiring an extremity amputation because this minimizes the risk of bony overgrowth that occurs in approximately 15% of trans– long bone amputations in children. This bony overgrowth often results in a prosthetic misfit and use problems, necessitating revision of the bone to eliminate the spurring. Maintaining the distal cartilage with disarticulation-level amputations prevents this overgrowth. Saving a functional knee, even if it results in a short transtibial residual limb, conveys advantage to the amputee for prosthetic function over that of a transfemoral amputation.

POSTOPERATIVE RESIDUAL LIMB MANAGEMENT AND THERAPY The goal of postoperative residual limb management is to facilitate wound healing, diminish pain, eliminate edema from the residual limb in anticipation of prosthetic restoration (if that is a goal), and maintain or improve extremity strength and range of motion. There are a number of dressing options for the residual limb. These include

656 AMPUTATION soft postoperative dressings of gauze with or without an overlying elastic bandage, elastic shrinker socks, nonremovable rigid dressings, removable rigid dressings (RRD), and immediate postoperative prosthetic fitting (IPOP). Reduction of edema in the residual limb has been demonstrated to enhance healing, reduce pain, and speed time to eventual prosthetic fitting. Even though there are systems designed to be used in the early postoperative period, most of these tend not to be considered for the dysvascular population until primary wound healing has occurred, if at all. Rigid removable dressings (RRDs) are typically fabricated by a prosthetist of plaster or synthetic casting materials over the distal portion of the residual limb and are made to be easily removed and replaced to allow inspection and dressing changes of the residual limb. The RRD helps to control limb edema and also provides protection for the residual limb from trauma to the residual limb, such as a fall, which might result in wound dehiscence. The RRD must be applied by trained professionals and monitored closely. If applied or donned improperly, the RRD can lead to incision breakdown or pressure sores on the residual limb and could require a revision to a more proximal level of amputation. Elastic bandages, when applied with proper technique, can also be very successful at controlling edema, minimizing pain, and stabilizing limb volume in anticipation of prosthetic fitting. Because they loosen quickly, elastic bandages must be reapplied every 4 hours, or more frequently as needed, to maintain their maximum effectiveness, making this approach to residual limb management less convenient for staff and patient. Shrinker or compression socks have replaced elastic wraps for most patients who do not use an RRD. Shrinker socks are easier for the patient to place independently than having to rewrap the limb with elastic bandages every few hours. During the postoperative period, physical and occupation therapy play an important role in management. The goal of therapy is to reduce or eliminate joint contractures and improve and restore strength. For lower extremities, it is particularly important to avoid development of hip and knee flexion contractures, which can occur quickly with patients who now spend most of their time sitting with hips and knees flexed. It is easier to prevent contractures with proper positioning and regular range-of-motion exercises than it is to eliminate them once they develop. Hip abduction contractures must also be avoided, especially for the transfemoral amputee. In addition to working on range of motion and strength, the therapists also assess the patient’s safety; current level of ability with bed mobility, transfers, wheelchair mobility, and ambulation; and activities of daily living. The goal is to determine the level of strength, mobility, and function the patient will require to be safely discharged from the surgical service to the previous living situation. If the patient does not possess sufficient skills for a safe discharge to home, the therapists work with the patient to reach the required level of function. Many patients undergoing amputation achieve the required level of functional mobility and self-care skills to be discharged safely to home by the time they are able to be discharged from the acute surgical service. A number of patients will not be at this level of function when deemed ready for discharge by the surgeon. This population of patients requires some level of ongoing postacute care rehabilitation to achieve the level of function for safe discharge to home. This could be in an acute inpatient rehabilitation setting, where the current requirements are that the patient be able and want to participate in 3 or more hours of physical and occupational therapy, as well as psychological help if needed, 5 or more days per week. The typical length of stay is 2 to 4 weeks to achieve the level of strength and function to permit a discharge to home.

PROSTHETIC RESTORATION The cost of a prosthesis can be significant, depending on the components chosen to be part of the prosthesis. For this reason, it is important to try to determine if an amputee is likely to be capable of using and wearing a prosthesis. As a general rule, an amputee who demonstrates sufficient balance and strength to be able to ambulate with a walker or crutches will likely be a successful prosthetic user. Some patients do not demonstrate this ability and require having two feet on the ground, and would benefit from a prosthesis to provide the balance to be able to master walking with a walker. Typically the patient’s initial prosthesis is a preparatory prosthesis. A preparatory prosthesis is designed to be worn for a limited time, usually no more than 6 months. Following delivery of the initial prosthesis, lower limb amputees should begin a program of outpatient physical therapy. The therapist reinforces the instructions provided to the patient by the prosthetist and works with the patient on donning and doffing the prosthesis correctly and checking skin for irritation or potential breakdown. The therapist develops a schedule of progressing wearing time, with a goal of eventually wearing the prosthesis all day long, and a prosthetic gait-training program emphasizing balance, coordination, and weight shift onto the prosthesis, as well as walking with the prosthesis. The goal of therapy is independent ambulation without gait aids (walker, crutches, or cane). As the patient progresses with prosthetic gait skills, the therapist then begins working with household and community barriers: curbs, steps, stairs, inclines, uneven terrain, and escalators, among others. The patient should be instructed in how to fall safely and how to get up from having fallen. At some point, all lower limb amputees may not be able to wear their prostheses for some period. In these circumstances, patients need to have available the use of a wheelchair, walker, or crutches for their mobility. The prosthesis should be looked at as a tool to be provided to the amputee to accomplish the task at hand. The goal is to get the right tool to the right patient for the right job. The definitive prosthesis has a socket made of lighter and more durable material, which is a bit more limited in its ability for the fit to be adjusted to compensate for limb volume change. A definitive prosthesis can be expected to last from 3 to 5 years with moderate day-to-day use. Significant change in residual limb volume, growth, or heavy use can require earlier replacement. Prosthetic wearers are advised to keep their weight stable because a weight change of 10 pounds results in a noticeable change in socket fit. It is easier to adapt to weight loss with the addition of socks or pads in the socket than it is to manage weight gain. Significant weight gain requires fabrication of a new socket.

Selected References Aulivola B, Hile CN, Hamdan AD, et al: Major lower extremity amputation: Outcome of a modern series, Arch Surg 139:395–399, 2004. Deutsch A, English RD, Vermeer TC, et al: Removable rigid dressings versus soft dressings: A randomized, controlled study with dysvascular, transtibial amputees, Prosthet Orthotics Internat 29:193–200, 2005. Dillingham TR, Pezzin LE, Mackenzie EJ: Discharge destination after dysvascular lower-limb amputations, Arch Phys Med Rehabil 84:1662–1668, 2003. Mayfield JA, Reiber GE, Maynard C, et al: Trends in lower limb amputation in the Veterans Health Administration, 1989–1998, J Rehabil Res Dev 37:23–30, 2000. Soldado F, Kozin SH: Bony overgrowth in children after amputation, J Pediatr Rehabil Med 2:235–239, 2009. Taylor SM, Kalbaugh CA, Cass AL, et al: “Successful outcome” after belowknee amputation: An objective definition and influence of clinical variables, Am Surg 74:607–612, 2008.

Vascular Trauma

Conventional and Computed Tomographic Arteriography in Penetrating Vascular Injuries Jonathan L. Eliason

The mid-20th century saw the emergence of contrast angiography to clarify and define the extent of vascular wounds. Percutaneous catheter-based angiography began to replace surgical cutdown and needle injection of contrast in the 1950s and 1960s, and became the gold standard for the diagnostic evaluation of penetrating vascular injury over subsequent decades. However, as the quality of computed tomography (CT) imaging using spiral multidetector techniques has improved, diagnostic imaging for penetrating vascular injury has migrated away from invasive catheter-based angiography. The exception to this trend is the patient in whom a combined diagnostic and therapeutic endovascular intervention is planned. Nevertheless, CT angiography (CTA) is often used as a guide for planning minimally invasive procedures.

IMAGING FOR PENETRATING VASCULAR INJURIES OF THE NECK CT angiography can be used in place of catheter-based angiography for penetrating vascular injuries in the neck, excluding patients who should typically undergo immediate surgical exploration. In the absence of hard signs of vascular injury, the physical examination alone is unreliable for excluding an arterial injury. Numerous reports have described delayed neurologic deficits from pseudoaneurysms or other arterial wounding patterns that were not initially identified following penetrating injury. Imaging, therefore, is an important component of the thorough evaluation of patients with penetrating trauma to the neck. Catheter-based angiography has proved sensitive and specific for arterial injury in the neck. Despite this, stab wounds in asymptomatic patients do not seem to warrant routine arteriography owing to a very low rate of detection of significant vascular injury; gunshot wounds are more likely to result in positive findings leading to surgical intervention. Symptoms (e.g., hematoma, swelling, altered mental status) result in higher rates of detection of arterial injury with angiography.

The cost-effectiveness of catheter-based angiography was evaluated in 111 patients with penetrating neck trauma. The cost was $3 million per central nervous system (CNS) event prevented, leading some to believe that angiography in the neck should be largely abandoned in favor of less expensive and less invasive imaging such as ultrasound or CT. CT has emerged as a very important imaging modality for penetrating neck trauma. Its utility lies in part in the evaluation of aerodigestive tract injury, although these injuries have a higher falsepositive rate than vascular injuries, in which the sensitivity and specificity for arterial injuries are both greater than 95%. Metal artifacts from ballistic injury limit the utility of CT in some patients. CT has been demonstrated to accompany decreased rates of unnecessary neck exploration and limits the need for oesophagogram or catheterbased arteriogram. If CT demonstrates ballistic trajectories that are remote from important structures then additional invasive imaging can be avoided. CTA is also a useful for preoperative planning when the patient’s stability permits and there is need for clarification of the best surgical approach (Figures 1 and 2).

IMAGING FOR PENETRATING VASCULAR INJURIES OF THE THORAX CTA has clearly emerged as the screening modality of choice with blunt injury to the aorta. In contrast, the benefit of CTA is less clear with penetrating vascular injuries to the chest. The majority of penetrating injuries to the chest occur from knife wounds or projectiles from handguns. Injuries from nail guns and other atypical injuries have also been reported. Penetrating wounds that traverse the mediastinum are often lethal as a result of involvement of the heart and great vessels, whereas those that are outside the mediastinum typically do not result in vascular injury, but rather cause pulmonary, chest wall, and diaphragm wounds. Nevertheless, CTA is useful in patients in whom the missile trajectory crosses the midline and can involve the mediastinum. If these patients are hemodynamically stable, CTA can aid with determining patients in whom expeditious operation is warranted, patients who warrant aerodigestive tract evaluation, and those patients in whom diagnostic angiography may be of benefit (Figure 3).

IMAGING FOR PENETRATING VASCULAR INJURIES OF THE ABDOMEN Penetrating vascular injuries within the abdomen rarely occur in isolation. They are usually accompanied with solid organ or hollow viscus injuries. Therefore, imaging of the abdomen either with CTA or conventional angiography is predicated on the patient’s hemodynamic status and whether a laparotomy is required. The high 657

A

C

B FIGURE 1  A, Axial computed tomography (CT) image showing hemodialysis (HD) catheter placement entering the left subclavian artery adjacent to the left vertebral artery origin. B, Axial CT image showing HD catheter traversing the aortic arch. C, Reconstructed CT image revealing the course of the HD catheter from the left subclavian artery extending down into the mid-descending thoracic aorta. D, CT angiogram of the neck revealing codominant vertebral arteries (white arrows) ordered to determine risk of potential endovascular coverage of the left vertebral artery.

D

A

B

C

D

FIGURE 2  A, Arch aortogram with a faint outline of the hemodialysis (HD) catheter seen within the left subclavian artery on the subtracted image. B, Selective left subclavian artery angiogram via sheath injection revealing the outline of the HD catheter entering the left subclavian artery adjacent to the left vertebral artery (black arrow). C, Fluoroscopic image revealing stent graft placement within the left subclavian artery deployed across the site of iatrogenic penetration simultaneous with removal of the HD catheter. D, Completion arch aortogram revealing the widely patent left subclavian artery following stent graft placement, but notably absent visualization of the left vertebral artery, internal mammary artery, and thyrocervical trunk.



Conventional and Computed Tomographic Arteriography in Penetrating Vascular Injuries

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demonstrates extravasation from the liver or kidney, angiography with embolization has been employed with good success in controlling hemorrhage and provides a less invasive surgical strategy for such patients. Diagnostic angiography is not as effective as CT for initial imaging because of the risk of missed bowel injury, and it should be used in circumstances in which more detailed imaging is required or when an endovascular therapy is planned.

IMAGING FOR PENETRATING VASCULAR INJURIES OF THE EXTREMITIES

FIGURE 3  Computed tomography angiography (CTA) of the chest

demonstrates a large proximal subclavian artery pseudoaneurysm in a hemodynamically stable patient with a zone 1 penetrating neck injury. CTA facilitated operative planning and guided surgical incision.

mortality associated with missed bowel injury can affect the methodology of CT imaging to include either rectal or oral contrast, or both, when imaging is required. Patients with significant diffuse abdominal tenderness or hemodynamic instability in the setting of penetrating abdominal injuries require emergent laparotomy, and imaging is not indicated. In the hemodynamically stable patient with an unreliable physical examination, imaging should be considered to determine peritoneal violation. Alternatively, such patients may be considered for laparotomy. When imaging is required, CT is the modality of choice. This diagnostic tool can aid greatly in surgical decision making. Stab wounds have accumulated the preponderance of useful data in this regard. These studies make an important distinction between stab wounds to the back or flank versus those to the abdomen. CT with IV and oral contrast is associated with nearly 90% sensitivity and 98% specificity in evaluating stab wounds to the back. These data have been reproduced in several single-institution studies. One study suggested that if rectal contrast is added to CT, giving the triple-contrast CT, the sensitivity for major injury can be improved to 100%. The majority of these injuries are not to major vessels. CT has also been evaluated in anterior abdominal stab wounds in a patient cohort with 156 stable patients without peritonitis or evisceration of the omentum; 28% had a positive CT finding, and 10 of these patients underwent laparotomy. The remaining patients with negative CT scans were observed. Three had laparoscopy and two had laparotomy for either diaphragm assessment or clinical deterioration. The negative predictive value of CT was found to be 100%. Triple-contrast CT is useful in evaluating gunshot wounds to the abdomen in hemodynamically stable patients without peritonitis. In a prospective study of 47 patients with this injury pattern, 20 had negative CT scans and no major vascular injury was missed. This study concluded that stable patients with gunshot wounds to the abdomen can be safely observed without immediate surgery. These findings were confirmed by a second prospective study in 200 patients with penetrating torso trauma. Patients with negative CT scans were observed, with two patients ultimately undergoing therapeutic laparotomy. One patient had active bleeding from a mesenteric hematoma, and the other had a diaphragm injury. CT had 98% accuracy for peritoneal violation. Conventional angiography has been reserved for patients in whom a nonoperative strategy is employed. When CT imaging

The management of penetrating vascular injures of the extremities depends heavily upon whether there are hard signs of vascular injury, including active hemorrhage, rapidly expanding hematoma, pulse deficit, or palpable thrill or audible bruit. Patients exhibiting these signs generally require surgical intervention without delay, and imaging is not indicated. One exception occurs in the hybrid trauma operating room in which diagnostic or therapeutic angiography may be employed without delay. However, diagnostic imaging even within a hybrid trauma operating room in patients with hard signs of vascular injury should be the exception rather than the rule. Some patients have soft signs of vascular injury such as stable hematoma, proximity of the wound to a major artery, neurologic deficit, or history of arterial bleeding. These patients may be considered for imaging. Catheter-based angiography has been shown to be highly sensitive for arterial injury, but it is not risk free and is very resource intensive. Its major advantage is the opportunity for therapeutic intervention. The incidence of major vascular injury is low in the patients with soft signs of vascular injury, and the number of those requiring therapeutic intervention in conjunction with conventional angiography would be anticipated to be low. More recent studies have focused on CTA for patients with penetrating wounds to the extremities. One prospective study included more than 500 patients. Patients with hard signs of vascular injury underwent emergent operation. Those with no signs of vascular injury were observed. Patients underwent CTA for soft signs of vascular injury (n = 62) or at the preference of the surgeon (n = 11). The sensitivity and specificity of CTA in detecting clinically significant arterial injuries was 100%. CTA was also directly compared to conventional angiography in another prospective study. Patients with potential vascular injuries to an extremity were enrolled. In this study, ankle-to-brachial index (ABI) was used to assess patients without hard signs of vascular injury, with imaging reserved for patients with an ABI less than 0.9. All patients underwent CTA and conventional angiography, except for two patients who had evidence of severe injuries on CTA, who underwent operative exploration rather than angiography. CTA had 100% sensitivity and specificity for detecting clinically significant arterial injuries. These data suggest that patients with soft signs of vascular injury following penetrating trauma may be safely evaluated with CTA as the initial diagnostic study. Limitations to CT efficacy include scatter from metallic artifact and resolution or detail at the tibial or pedal level. Within the realm of penetrating trauma, CTA appears to be supplanting conventional angiography as the initial diagnostic study of choice in most cases and within most vascular territories. Catheterbased angiography remains useful in that it provides both a diagnostic and a therapeutic tool, albeit with some risk because of its invasive nature and the requirement for intensive resources (imaging suite, inventory, support personnel, and qualified interventionalist). CTA and conventional angiography can be successfully used in conjunction with penetrating vascular injury (Figures 1 and 2), with CTA facilitating planning for open, hybrid open–endovascular, and total endovascular treatment. The drawbacks to CTA followed by conventional angiography include greater cost and use of larger volumes of contrast.

660 VASCULAR TRAUMA

Selected References Hanpeter DE, Demetriades D, Asensio JA, et al: Helical computed tomographic scan in the evaluation of mediastinal gunshot wounds, J Trauma 49:689–694, 2000. Himmelman RG, Martin M, Gilkey S, et al: Triple-contrast CT scans in penetrating back and flank trauma, J Trauma 31:852–855, 1991. Inaba K, Munera F, McKenney M, et al: Prospective evaluation of screening multislice helical computed tomographic angiography in the initial evaluation of penetrating neck injuries, J Trauma 61:144–149, 2006. Inaba K, Munera F, Rivas L, et al: Computed tomographic angiography in the initial assessment of penetrating extremity injuries, J Trauma 62:520–522, 2007. Inaba K, Potzman J, Munera F, et al: Multi-slice CT angiography for arterial evaluation in the injured lower extremity, J Trauma 60:502–506, 2006.

Nonarteriographic Diagnosis of Penetrating Vascular Trauma Kaj H. Johansen Massive bleeding, acute limb ischemia, or a pulsatile hematoma can make the diagnosis of penetrating vascular trauma straightforward, and the first diagnostic procedure is often an appropriate operative exploration. However, the vast majority of vascular injuries arising from penetrating trauma are not so clinically obvious, manifesting signs that are subtle, evanescent, and minimal. Even more vexing are clinical scenarios in which there is no evidence for an underlying arterial injury at all, but the nature of the wounding mechanism obliges concern about a silent arterial or venous disruption. Basic initial noninvasive vascular diagnostic methods to assess the extent of injury in victims of penetrating trauma are an essential element of current best practice.

HISTORICAL BACKGROUND Deliberate efforts to repair arterial injuries arose during the Korean conflict in the early 1950s, and the pioneering work of Rich and colleagues during the Vietnam war catalogued the predictability of successful outcomes for major vascular trauma, particularly in the extremities, presuming that an accurate diagnosis was made early and that operative management was timely and effective. Routine operative exploration was initially promoted for occult vascular trauma but was found to have a very low yield. Physical examination was thought, except when the diagnosis was obvious, to be inadequately sensitive for identifying many occult arterial injuries. Accordingly, the introduction of routine exclusion arteriography in settings where signs of vascular injury were minimal, or where clinical suspicions were high, was advocated in the 1970s in numerous urban trauma centers, particularly by Perry, Thal, and colleagues at Parkland Hospital in Dallas. These workers were particularly concerned that early identification of silent or minimal arterial injuries be accomplished owing to concerns for subsequent delayed hemorrhage, dissection, or acute arterial occlusion. Indeed, contrast arteriography proved to be quite highly accurate, with several studies demonstrating false positive and false negative rates of

Jarvik JG, Philips 3rd GR, Schwab CW, et al: Penetrating neck trauma: Sensitivity of clinical examination and cost-effectiveness of angiography, AJNR Am J Neuroradiol 16:647–654, 1995. Munera F, Morales C, Soto JA, et al: Gunshot wounds of abdomen: Evaluation of stable patients with triple-contrast helical CT, Radiology 231:399–405, 2004. Munera F, Soto JA, Palacio D, et al: Diagnosis of arterial injuries caused by penetrating trauma to the neck: Comparison of helical CT angiography and conventional angiography, Radiology 216:356–362, 2000. Salim A, Sangthong B, Martin M, et al: Use of computed tomography in anterior abdominal stab wounds: Results of a prospective study, Arch Surg 141:745–750, 2006. Seamon MJ, Smoger D, Torres DM, et al: A prospective validation of a current practice: The detection of extremity vascular injury with ct angiography, J Trauma 67:238–243, 2009.

less than 2% for such studies performed to detect or rule out occult arterial injuries. However, routine use of contrast arteriography in this setting is invasive, expensive, and time consuming, and it requires transfer of the patient, who often needs ongoing evaluation, surveillance, and resuscitation, to an angiography suite that is outside of, and often remote from, the emergency department. Most importantly, several studies demonstrated that when contrast arteriography was performed for exclusion indications, in only a very few of these trauma victims—less than 5%—were arterial injuries identified that were so serious they required operative intervention. For this reason, alternative diagnostic measures were investigated in this patient population.

ARTERIAL PRESSURE MEASUREMENTS The 1970s saw the introduction and development of ultrasonographic means of assessing arterial pressure measurement in patients with chronic arterial occlusive disease, usually of the lower extremities. Over the next 20 years we and others evaluated the use of Doppler pressure measurement and the calculation of ankle-to-brachial indices (ABIs) as means of carrying out noninvasive determination of the patency and vessel integrity of patients with penetrating trauma, predominantly to the extremities. Some groups used an ankle pressure index (ratio of highest ankle arterial pressure to arm arterial pressure; ABI) of 0.90 as a threshold value below which the presence of an arterial disruption was possible and above which such an injury was unlikely (Figure 1). Others promoted the even greater sensitivity of an ABI of 1.0, accepting that such an approach resulted in the performance of many more negative arteriograms. Most importantly, whichever ABI threshold was chosen, these studies validated the use of a simple bedside diagnostic test, using a blood pressure cuff and a hand-held Doppler, to assess patients with potential occult penetrating arterial trauma of the extremities. Limitations of the ABI diagnostic algorithm quickly became clear. While excellent in the assessment of major vessel disruptions, acute thromboses or large intimal flaps, Doppler arterial pressure measurement and ABI calculation fails to diagnose branch artery (e.g., profunda femoris artery) disruptions, cannot detect small intimal lesions (pseudoaneurysms, small intimal flaps, or arteriovenous fistulas), is a good deal less accurate for arterial injuries proximal to the inguinal or axillary crease, can overread the effect of arterial spasm, does not detect arterial wall lacerations, and does not enable any assessment of the venous system. Fortunately, the vascular ultrasound revolution provided a further useful tool in this clinical scenario.

660 VASCULAR TRAUMA

Selected References Hanpeter DE, Demetriades D, Asensio JA, et al: Helical computed tomographic scan in the evaluation of mediastinal gunshot wounds, J Trauma 49:689–694, 2000. Himmelman RG, Martin M, Gilkey S, et al: Triple-contrast CT scans in penetrating back and flank trauma, J Trauma 31:852–855, 1991. Inaba K, Munera F, McKenney M, et al: Prospective evaluation of screening multislice helical computed tomographic angiography in the initial evaluation of penetrating neck injuries, J Trauma 61:144–149, 2006. Inaba K, Munera F, Rivas L, et al: Computed tomographic angiography in the initial assessment of penetrating extremity injuries, J Trauma 62:520–522, 2007. Inaba K, Potzman J, Munera F, et al: Multi-slice CT angiography for arterial evaluation in the injured lower extremity, J Trauma 60:502–506, 2006.

Nonarteriographic Diagnosis of Penetrating Vascular Trauma Kaj H. Johansen Massive bleeding, acute limb ischemia, or a pulsatile hematoma can make the diagnosis of penetrating vascular trauma straightforward, and the first diagnostic procedure is often an appropriate operative exploration. However, the vast majority of vascular injuries arising from penetrating trauma are not so clinically obvious, manifesting signs that are subtle, evanescent, and minimal. Even more vexing are clinical scenarios in which there is no evidence for an underlying arterial injury at all, but the nature of the wounding mechanism obliges concern about a silent arterial or venous disruption. Basic initial noninvasive vascular diagnostic methods to assess the extent of injury in victims of penetrating trauma are an essential element of current best practice.

HISTORICAL BACKGROUND Deliberate efforts to repair arterial injuries arose during the Korean conflict in the early 1950s, and the pioneering work of Rich and colleagues during the Vietnam war catalogued the predictability of successful outcomes for major vascular trauma, particularly in the extremities, presuming that an accurate diagnosis was made early and that operative management was timely and effective. Routine operative exploration was initially promoted for occult vascular trauma but was found to have a very low yield. Physical examination was thought, except when the diagnosis was obvious, to be inadequately sensitive for identifying many occult arterial injuries. Accordingly, the introduction of routine exclusion arteriography in settings where signs of vascular injury were minimal, or where clinical suspicions were high, was advocated in the 1970s in numerous urban trauma centers, particularly by Perry, Thal, and colleagues at Parkland Hospital in Dallas. These workers were particularly concerned that early identification of silent or minimal arterial injuries be accomplished owing to concerns for subsequent delayed hemorrhage, dissection, or acute arterial occlusion. Indeed, contrast arteriography proved to be quite highly accurate, with several studies demonstrating false positive and false negative rates of

Jarvik JG, Philips 3rd GR, Schwab CW, et al: Penetrating neck trauma: Sensitivity of clinical examination and cost-effectiveness of angiography, AJNR Am J Neuroradiol 16:647–654, 1995. Munera F, Morales C, Soto JA, et al: Gunshot wounds of abdomen: Evaluation of stable patients with triple-contrast helical CT, Radiology 231:399–405, 2004. Munera F, Soto JA, Palacio D, et al: Diagnosis of arterial injuries caused by penetrating trauma to the neck: Comparison of helical CT angiography and conventional angiography, Radiology 216:356–362, 2000. Salim A, Sangthong B, Martin M, et al: Use of computed tomography in anterior abdominal stab wounds: Results of a prospective study, Arch Surg 141:745–750, 2006. Seamon MJ, Smoger D, Torres DM, et al: A prospective validation of a current practice: The detection of extremity vascular injury with ct angiography, J Trauma 67:238–243, 2009.

less than 2% for such studies performed to detect or rule out occult arterial injuries. However, routine use of contrast arteriography in this setting is invasive, expensive, and time consuming, and it requires transfer of the patient, who often needs ongoing evaluation, surveillance, and resuscitation, to an angiography suite that is outside of, and often remote from, the emergency department. Most importantly, several studies demonstrated that when contrast arteriography was performed for exclusion indications, in only a very few of these trauma victims—less than 5%—were arterial injuries identified that were so serious they required operative intervention. For this reason, alternative diagnostic measures were investigated in this patient population.

ARTERIAL PRESSURE MEASUREMENTS The 1970s saw the introduction and development of ultrasonographic means of assessing arterial pressure measurement in patients with chronic arterial occlusive disease, usually of the lower extremities. Over the next 20 years we and others evaluated the use of Doppler pressure measurement and the calculation of ankle-to-brachial indices (ABIs) as means of carrying out noninvasive determination of the patency and vessel integrity of patients with penetrating trauma, predominantly to the extremities. Some groups used an ankle pressure index (ratio of highest ankle arterial pressure to arm arterial pressure; ABI) of 0.90 as a threshold value below which the presence of an arterial disruption was possible and above which such an injury was unlikely (Figure 1). Others promoted the even greater sensitivity of an ABI of 1.0, accepting that such an approach resulted in the performance of many more negative arteriograms. Most importantly, whichever ABI threshold was chosen, these studies validated the use of a simple bedside diagnostic test, using a blood pressure cuff and a hand-held Doppler, to assess patients with potential occult penetrating arterial trauma of the extremities. Limitations of the ABI diagnostic algorithm quickly became clear. While excellent in the assessment of major vessel disruptions, acute thromboses or large intimal flaps, Doppler arterial pressure measurement and ABI calculation fails to diagnose branch artery (e.g., profunda femoris artery) disruptions, cannot detect small intimal lesions (pseudoaneurysms, small intimal flaps, or arteriovenous fistulas), is a good deal less accurate for arterial injuries proximal to the inguinal or axillary crease, can overread the effect of arterial spasm, does not detect arterial wall lacerations, and does not enable any assessment of the venous system. Fortunately, the vascular ultrasound revolution provided a further useful tool in this clinical scenario.

Nonarteriographic Diagnosis of Penetrating Vascular Trauma

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FIGURE 1  A diagnostic algorithm for potential extremity arterial

injury based on Doppler-derived arterial pressure indices (API).  (From Lynch K, Johansen KH: Can Doppler pressure measurements replaces “exclusion” arteriography in extremity trauma? Ann Surg 214:737–741, 1991, with permission.)

DUPLEX ULTRASONOGRAPHY Duplex ultrasonography—pulsed-wave Doppler ultrasound—was introduced in the early 1980s, initially to assess carotid arterial occlusive disease but soon after to assess disease in other arterial beds, particularly for chronic arterial disease of the lower extremities. Once again, the rapidity, portability, and noninvasive nature of this normal ultrasound technique was exploited to assess trauma victims, primarily for occult arterial injuries in the extremities. An algorithm for the use of duplex sonography in extremities potentially harboring occult arterial trauma, screened by Doppler ABI determination, is shown in Figure 2. Initial animal studies by Panetta and coworkers comparing duplex scanning and contrast arteriography in the assessment of various experimental arterial injuries showed that the ultrasonographic technique was more accurate than the catheter-directed approach both for arterial disruption and particularly for arterial laceration. In studies in trauma patients the sensitivity and specificity of duplex ultrasound for an identifiable extremity arterial injury exceeded 95% and approached 100%, and studies by Fry and colleagues comparing the use of duplex ultrasound and contrast arteriography for penetrating extremity trauma suggested virtual equivalency of the two techniques’ diagnostic accuracy. Of particular note was the identification by duplex ultrasonography of a number of significant venous injuries that had no way, of course, of being defined by contrast arteriography. Limitations of duplex ultrasonography to assess penetrating arterial trauma are several. Access to the artery may be limited by wound or wound dressings or various types of orthopedic hardware and, like Doppler ABI measurement, may be less accurate in assessing more proximal (e.g., truncal) arterial injuries. Duplex scanning technique and interpretation depends quite heavily on the operator. Perhaps most importantly, at a time of chronic economic retrenchment by urban trauma hospitals, night and weekend vascular laboratory coverage is less and less commonly available.

FIGURE 2  A current diagnostic algorithm for potential extremity

arterial injury based on Doppler-derived arterial pressure indices and duplex sonography.

injuries risked delayed hemorrhage, embolization, or acute arterial occlusion. However, the endovascular revolution of the late 20th and early 21st centuries has demonstrated that the small pseudoaneurysms, arteriovenous (AV) fistulas, and intimal flaps that are ubiquitous in patients undergoing various catheter-directed arterial interventions almost never cause later problems. This observation reflects that of earlier longitudinal studies of patients with minimal arterial injuries following penetrating trauma: Weaver’s group at the University of Southern California demonstrated that no more than 5% of such patients require a later operative intervention. In penetrating trauma, minimal arterial injuries seem to be of minimal clinical significance.

ROLE OF THE SERIAL PHYSICAL EXAMINATION The simplest, least expensive, and most noninvasive diagnostic test is a careful physical examination. However, a major stimulus for introducing routine contrast arteriography in that large portion of patients who have penetrating arterial injuries and minimal or no signs of arterial disruption was the contention by several authorities in trauma, particularly at Parkland Hospital in Dallas, that physical examination is inaccurate, or at least inadequate, for assessing penetrating vascular injuries. However, if it is accepted that Doppler ABI measurement is a simple extension of pulse palpation and other aspects of the vascular examination, it can be argued that physical examination is in fact highly sensitive in assessing patients who potentially harbor an arterial injury, particularly of the extremities. A similar conclusion can be drawn from studies of trauma victims with penetrating extracranial arterial trauma: Demetriades and colleagues demonstrated the equivalency of serial physical examination to duplex sonography and contrast arteriography in such a setting. Coming full circle, authors from Parkland conceded that serial physical examination by an experienced surgeon is an accurate means of screening victims of penetrating trauma for occult arterial trauma.

Selected References

MINIMAL ARTERIAL INJURY Inherent in prior diagnostic approaches mandating routine wound exploration, or routine contrast arteriography, in patients with actual or presumed occult arterial injury was the concern that missing such

Bynoe RP, Miles WS, Bell RM, et al: Noninvasive diagnosis of vascular trauma by duplex ultrasonography, J Vasc Surg 14:346–350, 1991. Demetriades D, Theodorou D, Cornwell E, et al: Penetrating injuries of the neck in patients in stable condition: Physical examination, angiography or color flow Doppler imaging, Arch 130:971–975, 1995.

662 VASCULAR TRAUMA Francis III H, Thal ER, Weigelt JA, et al: Vascular proximity: Is it a valid indication for arteriography in asymptomatic patients? J Trauma 1991(31):512–514, 1991. Fry WR, Smith RS, Sayers DV, et al: The success of duplex ultrasonographic scanning in the diagnosis of extremity vascular proximity trauma, Arch Surg 128:1368–1372, 1993. Meissner M, Paun M, Johansen K: Duplex scanning for arterial trauma, Am J Surg 161:552–555, 1991. Panetta TF, Hunt JP, Buechter KJ, et al: Duplex ultrasonography versus arteriography in the diagnosis of arterial injury: An experimental study, J Trauma 33:627–635, 1992.

Penetrating and Blunt Injuries of the Carotid Artery Jihad Abbas and Gerald B. Zelenock

Injuries to the carotid arteries are relatively uncommon, but not rare. Despite some variability in reported data from center to center, certain principles have evolved. Injuries to the carotid artery are traditionally considered blunt or penetrating (Box 1).

PENETRATING CAROTID ARTERY INJURIES Management algorithms for penetrating neck trauma have been well established for more than 4 decades. Treatment of penetrating vascular injuries in the neck takes into consideration the type of injury, the location (zone I, II or III) (Figure 1), and potential associated injuries to the aerodigestive tracks as well as the neurologic and overall status

BOX 1:  Selected Perspectives on Carotid Artery Trauma • Penetrating neck injuries have a 20% incidence of major vascular injury. • Routine exploration of penetrating neck wounds produces a 40% to 60% negative exploration rate. • Physical examination signs of carotid artery injuries are often unreliable; they are absent in 30% of patients with carotid injury established at exploration. • Penetrating carotid artery injuries are usually from stab wounds; usually involve young men, who are often intoxicated (drugs and/or alcohol); and are more common on the left side (right-handed assailants). • Penetrating carotid artery injuries usually involve the common carotid artery; blunt injuries usually involve the internal carotid artery. • Blunt carotid artery injuries represent approximately 3% to 10% of total carotid artery injuries. • Blunt carotid artery injuries are bilateral in up to 20% of cases. • Blunt carotid artery injuries have a 20% to 40% mortality, and 25% to 80% of survivors have a neurologic deficit.

Patterson BO, Holt PS, Cleanthis M, et al: Imaging vascular trauma, Br J Surg 99:494–505, 2012. Schwartz MR, Weaver FA, Yellin AE, et al: Refining the indications for arteriography in penetrating extremity trauma: A prospective analysis, J Vasc Surg 17:166–170, 1993. Stain SC, Yellin AE, Weaver FA, et al: Selective management of non occlusive arterial injuries, Arch Surg 124:1136–1140, 1989.

of the patient. Zone II injuries are usually handled through conventional surgical exposures. Zone I penetrating injuries require careful consideration of intrathoracic bleeding and/or the need for intrathoracic vascular control. Zone III injuries involving the distal internal carotid artery at the base of the skull require exposures commonly used in conventional carotid artery surgery. The exact approach to a given injury, especially zone I and zone III, can be precisely tailored depending upon the results of the imaging studies. In the presence of a hard sign of vascular injury (Box 2), either direct exploration or conventional angiography, if endovascular repair is being contemplated, is appropriate. Zone I and zone III injuries require serious consideration of a dedicated imaging study even when hard signs of vascular injury are lacking. Treatment strategies for zone II injuries remain somewhat controversial. Some advocate routine exploration; others advocate selective exploration based upon the clinical scenario. When circumstances allow, one should always prep a leg for saphenous vein harvest in the event that a vascular patch or interposition graft could be needed. Endovascular repair of carotid injuries can be considered when a lesion is favorable and all requisite equipment and clinical expertise is readily available. Carotid artery injuries cause morbidity by three principle mechanisms: exsanguinating hemorrhage, a high-pressure hematoma that compresses adjacent soft tissue structures (airway compromise), or significant brain ischemia. Brain ischemia occurs as a result of embolization or thrombosis. Brain ischemia can be exacerbated by systemic hypotension, shock, spasm, hypoxia, and inadequate resuscitation. Some surgeons favor mandatory exploration for virtually all penetrating neck injuries. We favor immediate exploration for zone II injuries with hard signs of vascular injury and/or hemodynamic instability. Some suggest that stable patients with low-velocity penetrating injuries and no hard signs of vascular or aerodigestive injury can simply be observed. For stable zone II patients, we greatly prefer the advantages offered by urgent imaging. The diagnosis can be readily made, and if an injury is detected its precise nature is defined. Zone 1 and zone 3 injuries virtually all require imaging for diagnosis and determining the extent of injury. While some have suggested that repeated physical examination and a plain chest x-ray suffice for zone I injury, we believe the widespread availability of sophisticated imaging and the consequences of a missed injury favor liberal use of advanced imaging. Computed tomography angiography (CTA) and magnetic resonance imaging (MRI) provide excellent quality of images, but we prefer conventional angiography when endovascular treatment is being considered.

Operative Approach General anesthesia with endotracheal intubation, elevation of the head of the bed to 30 degrees, avoidance of glucose, and prepping a wider field than used for standard carotid surgery is advised

662 VASCULAR TRAUMA Francis III H, Thal ER, Weigelt JA, et al: Vascular proximity: Is it a valid indication for arteriography in asymptomatic patients? J Trauma 1991(31):512–514, 1991. Fry WR, Smith RS, Sayers DV, et al: The success of duplex ultrasonographic scanning in the diagnosis of extremity vascular proximity trauma, Arch Surg 128:1368–1372, 1993. Meissner M, Paun M, Johansen K: Duplex scanning for arterial trauma, Am J Surg 161:552–555, 1991. Panetta TF, Hunt JP, Buechter KJ, et al: Duplex ultrasonography versus arteriography in the diagnosis of arterial injury: An experimental study, J Trauma 33:627–635, 1992.

Penetrating and Blunt Injuries of the Carotid Artery Jihad Abbas and Gerald B. Zelenock

Injuries to the carotid arteries are relatively uncommon, but not rare. Despite some variability in reported data from center to center, certain principles have evolved. Injuries to the carotid artery are traditionally considered blunt or penetrating (Box 1).

PENETRATING CAROTID ARTERY INJURIES Management algorithms for penetrating neck trauma have been well established for more than 4 decades. Treatment of penetrating vascular injuries in the neck takes into consideration the type of injury, the location (zone I, II or III) (Figure 1), and potential associated injuries to the aerodigestive tracks as well as the neurologic and overall status

BOX 1:  Selected Perspectives on Carotid Artery Trauma • Penetrating neck injuries have a 20% incidence of major vascular injury. • Routine exploration of penetrating neck wounds produces a 40% to 60% negative exploration rate. • Physical examination signs of carotid artery injuries are often unreliable; they are absent in 30% of patients with carotid injury established at exploration. • Penetrating carotid artery injuries are usually from stab wounds; usually involve young men, who are often intoxicated (drugs and/or alcohol); and are more common on the left side (right-handed assailants). • Penetrating carotid artery injuries usually involve the common carotid artery; blunt injuries usually involve the internal carotid artery. • Blunt carotid artery injuries represent approximately 3% to 10% of total carotid artery injuries. • Blunt carotid artery injuries are bilateral in up to 20% of cases. • Blunt carotid artery injuries have a 20% to 40% mortality, and 25% to 80% of survivors have a neurologic deficit.

Patterson BO, Holt PS, Cleanthis M, et al: Imaging vascular trauma, Br J Surg 99:494–505, 2012. Schwartz MR, Weaver FA, Yellin AE, et al: Refining the indications for arteriography in penetrating extremity trauma: A prospective analysis, J Vasc Surg 17:166–170, 1993. Stain SC, Yellin AE, Weaver FA, et al: Selective management of non occlusive arterial injuries, Arch Surg 124:1136–1140, 1989.

of the patient. Zone II injuries are usually handled through conventional surgical exposures. Zone I penetrating injuries require careful consideration of intrathoracic bleeding and/or the need for intrathoracic vascular control. Zone III injuries involving the distal internal carotid artery at the base of the skull require exposures commonly used in conventional carotid artery surgery. The exact approach to a given injury, especially zone I and zone III, can be precisely tailored depending upon the results of the imaging studies. In the presence of a hard sign of vascular injury (Box 2), either direct exploration or conventional angiography, if endovascular repair is being contemplated, is appropriate. Zone I and zone III injuries require serious consideration of a dedicated imaging study even when hard signs of vascular injury are lacking. Treatment strategies for zone II injuries remain somewhat controversial. Some advocate routine exploration; others advocate selective exploration based upon the clinical scenario. When circumstances allow, one should always prep a leg for saphenous vein harvest in the event that a vascular patch or interposition graft could be needed. Endovascular repair of carotid injuries can be considered when a lesion is favorable and all requisite equipment and clinical expertise is readily available. Carotid artery injuries cause morbidity by three principle mechanisms: exsanguinating hemorrhage, a high-pressure hematoma that compresses adjacent soft tissue structures (airway compromise), or significant brain ischemia. Brain ischemia occurs as a result of embolization or thrombosis. Brain ischemia can be exacerbated by systemic hypotension, shock, spasm, hypoxia, and inadequate resuscitation. Some surgeons favor mandatory exploration for virtually all penetrating neck injuries. We favor immediate exploration for zone II injuries with hard signs of vascular injury and/or hemodynamic instability. Some suggest that stable patients with low-velocity penetrating injuries and no hard signs of vascular or aerodigestive injury can simply be observed. For stable zone II patients, we greatly prefer the advantages offered by urgent imaging. The diagnosis can be readily made, and if an injury is detected its precise nature is defined. Zone 1 and zone 3 injuries virtually all require imaging for diagnosis and determining the extent of injury. While some have suggested that repeated physical examination and a plain chest x-ray suffice for zone I injury, we believe the widespread availability of sophisticated imaging and the consequences of a missed injury favor liberal use of advanced imaging. Computed tomography angiography (CTA) and magnetic resonance imaging (MRI) provide excellent quality of images, but we prefer conventional angiography when endovascular treatment is being considered.

Operative Approach General anesthesia with endotracheal intubation, elevation of the head of the bed to 30 degrees, avoidance of glucose, and prepping a wider field than used for standard carotid surgery is advised

Penetrating and Blunt Injuries of the Carotid Artery

(i.e., prep the entire chest in case sternotomy is required). If direct exploration of the wound reveals that the platysma has not been violated, no further intervention is needed. A simple puncture wound can be treated with lateral arteriorrhaphy, taking care not to compromise the lumen of the injured artery. Occasionally, interposition grafting rather than patch angioplasty is necessary. If the patient is comatose, we still, in most instances, revascularize. The totally occluded carotid should be repaired when technically feasible, and imaging studies have shown retrograde blood flow into the distal internal carotid artery. Establishing backflow with a Fogarty catheter thrombectomy must be limited to passing the catheter to the base of the skull to avoid arterial rupture and development of a carotid–cavernous fistula. Finally, ligation may be required when the patient is critically unstable and the injury is irreparable. If a decision to sacrifice the carotid artery has been made, either direct ligation or endovascular occlusion may be used. Endovascular repair of zone I and zone III injuries has been successful using covered stents.

Outcomes A mortality rate of at least 10% and stroke rate of 25% are aggregate anticipated outcomes in penetrating carotid trauma. However, an individual patient’s outcome is determined by the severity and duration of hemorrhagic shock and the patient’s neurologic status at the time of arrival at the hospital. Prolonged cerebral ischemia from shock or carotid occlusion, massive blood loss, severe associated injuries, zone I and zone III carotid trauma, and coma all portend a high mortality (≥50%) and neurologic morbidity (>80%).

BLUNT CAROTID ARTERY INJURIES Blunt injuries affecting the carotid artery can be difficult to diagnose. They represent only 3% to 10% of total carotid artery injuries. Patients who come to the hospital with blunt trauma carotid injuries are rare (0.1%–0.05%). In contrast to penetrating injuries, which typically involve the common carotid artery, blunt carotid trauma usually (90%) involves the internal carotid artery. Blunt carotid injuries are bilateral in 20% of cases. Diagnosis requires clinical suspicion; however, the widespread availability of sophisticated imaging technologies such as duplex ultrasonography, CTA, MRI or MR angiography (MRA), and conventional angiography means that diagnosis should be relatively straightforward. Half of blunt injuries to the

FIGURE 1  Classic zones for penetrating neck injury.

These zones have been variably described in clinical reports. Zone I is easily remembered as periclavicular or low neck (from the sternal notch to 1 cm above the clavicular head); zone II is the midneck from 1 cm above the clavicular head to either the angle of the jaw or the hyoid bone; zone III is the high neck (anything above zone II). Zone II injuries are most familiar and typically require less in the way of sophisticated imaging or complex surgical approaches. Zone I injuries can require a sternotomy or thoracotomy for proximal control. Zone III injuries require high carotid exposures infrequently used in daily practice.

663

carotid artery manifest when, or are diagnosed after, a fixed neurologic deficit occurs. Because patients with blunt carotid injury can have other severe injuries, treatment priorities must be established and interventions tailored to the patient’s overall status. Clearly a patient with a serious head injury or massive bleeding from chest, abdominal, or extremity injuries is not a candidate for thrombolytics, anticoagulants, or antiplatelet agents, at least in the initial stages of treatment. Each of these pharmacologic modalities can have utility with isolated blunt injury to the carotid artery such as a direct blow to the neck (karate chop), intraoral trauma (typically a child falling with a pencil in the mouth), or a basilar skull fracture. Carotid dissection is increasingly recognized following blunt trauma, and the stretch–traction–rotation and directcompression mechanisms of carotid dissection following blunt trauma have been well defined.

Treatment In contrast to penetrating injuries, blunt carotid artery injury is rarely treated with operative interventions. When circumstances allow, antiplatelet or anticoagulation therapy is begun. There does not appear to be a significant difference between antiplatelet or anticoagulant therapy. Newer anticoagulants including direct thrombin inhibitors have yet to be evaluated. Late-presenting pseudoaneurysms, typically at the skull base, can be controlled with a covered stent or can be

BOX 2:  Signs of Carotid Injury

Hard Signs

• Active bleeding • Large or enlarging neck hematoma • Pulsatile hematoma • Ongoing shock • Neurologic deficit

Soft Signs

• History of bleeding • Small stable hematoma • Cranial nerve injury • Proximity    • Worrisome mechanism (shotgun blast) Any suggestion of aerodigestive injury should also be considered an indication for neck exploration.

664 VASCULAR TRAUMA embolized, or the carotid can be occluded if the risk-to-benefit ratio is favorable. A trial occlusion of the carotid is warranted if permanent occlusion is required.

Outcomes Clinical outcomes for blunt carotid trauma are generally poor. Mortality is typically reported as 20% to 40%, and permanent neurologic morbidity occurs among 50% of survivors. Such statistics are to be anticipated given that half of patients come to the hospital with a fixed neurologic deficit and fully a third have a Glasgow Coma Scale score of less than 8. It seems likely that detection at an earlier, presymptomatic state would improve outcomes, and in this regard heightened awareness and liberal screening might produce better overall results.

Penetrating and Blunt Injuries of the Vertebral Artery Ramon Berguer

ETIOLOGY The most common vertebral artery injuries fall within one of two categories: blunt trauma of the neck, usually related to motor vehicle accidents, or iatrogenic injuries. A minority are secondary to firearms (Figure 1).

FIGURE 1  Aneurysm of a vertebral artery at C1–C0 following a

shotgun injury.

Selected References Ballard J, Teruya T: Carotid and vertebral artery injuries. In Rutherford RB, (ed): Vascular Surgery, ed 6, Philadelphia, 2005, Saunders Elsevier, pp 1006–1015. Fabian TC, Patton Jr JH, Croce MH, et al: Blunt carotid injury: Importance of early diagnosis and anticoagulant therapy, Ann Surg 223:513–525, 1996. Feliciano DV: Management of penetrating injuries to carotid artery, World J Surg 25:1028–1035, 2001. Martin MJ, Mullenix PS, Steele SR, et al: Functional outcome after blunt and penetrating carotid artery injuries: Analysis of the National Trauma Data Bank, J Trauma 59:860–864, 2005. Zelenock GB, Kazmers A, Whitehouse Jr WM, et al: Extracranial internal carotid artery dissections: Noniatrogenic traumatic lesions, Arch Surg 117:425–430, 1982.

Systematic screening of patients with blunt neck injuries with magnetic resonance imaging (MRI) or computed tomography (CT) shows a high incidence of vertebral artery injury, with a majority of patients not experiencing clinical symptoms, but with a potentially high morbidity for those who develop signs of a stroke involving the vertebrobasilar territory. From a practical standpoint, CT angiography (CTA) with multidetector machines is now considered a good screening modality for patients with acute cervical spine trauma. Angiography is still the most sensitive imaging technique to define vertebral artery injuries, but its invasiveness and risk in patients with severe head and neck injuries makes it an unlikely choice as a screening measure. MRI has been used in most prospective studies, but it is not universally available in areas that receive acute trauma patients. In addition, the fixation and life support devices in these patients interfere with MRI protocols. Nevertheless, MRI remains the best modality to detect early parenchymatous changes in the vertebrobasilar territory. Patients undergoing systematic MRI studies following acute cervical spine trauma have a high incidence (20%–25%) of abnormalities in their vertebral artery, mostly occlusion and dissection, and 3% to 5% will develop a cerebellar or brain infarct, which is often lethal. The mechanism of injury in cervical spine trauma patients is usually distraction or compression of the artery, resulting in intimal flaps, dissections (Figures 2 and 3), pseudoaneurysms, or arteriovenous fistulas (Figure 4) of the vertebral artery. In a review of 1941patients with blunt trauma, the incidence of carotid or vertebral injury was 1.1%. Another extensive literature review reported that most patients with a vertebral artery injury have no clinical symptoms, but the few who develop a sudden deterioration after a brief normal neurologic interval have a morbid course. In acute cervical spine trauma, the vertebral artery is injured along its transforaminal course, from C6 to C1. Vertebral artery injury occurs in 25% of patients with a fracture of the transverse process and in 35% of those with a facet dislocation. However, 20% of patients with acute cervical spine trauma sustain a vertebral artery injury in the absence of any identifiable bony fracture or dislocation. In these patients, the vertebral artery is injured by distraction–flexion and distraction–extension forces. A particularly worrisome course in patients with a history of cervical trauma is the development of stroke symptoms after several days, or even weeks, of neurologic clinical normality. This morbid course is the result of the progression to occlusion of the injured vertebral artery or its embolization into the basilar artery. Vertebral artery injury associated with chiropractic manipulation of the neck falls into both blunt and iatrogenic categories of

664 VASCULAR TRAUMA embolized, or the carotid can be occluded if the risk-to-benefit ratio is favorable. A trial occlusion of the carotid is warranted if permanent occlusion is required.

Outcomes Clinical outcomes for blunt carotid trauma are generally poor. Mortality is typically reported as 20% to 40%, and permanent neurologic morbidity occurs among 50% of survivors. Such statistics are to be anticipated given that half of patients come to the hospital with a fixed neurologic deficit and fully a third have a Glasgow Coma Scale score of less than 8. It seems likely that detection at an earlier, presymptomatic state would improve outcomes, and in this regard heightened awareness and liberal screening might produce better overall results.

Penetrating and Blunt Injuries of the Vertebral Artery Ramon Berguer

ETIOLOGY The most common vertebral artery injuries fall within one of two categories: blunt trauma of the neck, usually related to motor vehicle accidents, or iatrogenic injuries. A minority are secondary to firearms (Figure 1).

FIGURE 1  Aneurysm of a vertebral artery at C1–C0 following a

shotgun injury.

Selected References Ballard J, Teruya T: Carotid and vertebral artery injuries. In Rutherford RB, (ed): Vascular Surgery, ed 6, Philadelphia, 2005, Saunders Elsevier, pp 1006–1015. Fabian TC, Patton Jr JH, Croce MH, et al: Blunt carotid injury: Importance of early diagnosis and anticoagulant therapy, Ann Surg 223:513–525, 1996. Feliciano DV: Management of penetrating injuries to carotid artery, World J Surg 25:1028–1035, 2001. Martin MJ, Mullenix PS, Steele SR, et al: Functional outcome after blunt and penetrating carotid artery injuries: Analysis of the National Trauma Data Bank, J Trauma 59:860–864, 2005. Zelenock GB, Kazmers A, Whitehouse Jr WM, et al: Extracranial internal carotid artery dissections: Noniatrogenic traumatic lesions, Arch Surg 117:425–430, 1982.

Systematic screening of patients with blunt neck injuries with magnetic resonance imaging (MRI) or computed tomography (CT) shows a high incidence of vertebral artery injury, with a majority of patients not experiencing clinical symptoms, but with a potentially high morbidity for those who develop signs of a stroke involving the vertebrobasilar territory. From a practical standpoint, CT angiography (CTA) with multidetector machines is now considered a good screening modality for patients with acute cervical spine trauma. Angiography is still the most sensitive imaging technique to define vertebral artery injuries, but its invasiveness and risk in patients with severe head and neck injuries makes it an unlikely choice as a screening measure. MRI has been used in most prospective studies, but it is not universally available in areas that receive acute trauma patients. In addition, the fixation and life support devices in these patients interfere with MRI protocols. Nevertheless, MRI remains the best modality to detect early parenchymatous changes in the vertebrobasilar territory. Patients undergoing systematic MRI studies following acute cervical spine trauma have a high incidence (20%–25%) of abnormalities in their vertebral artery, mostly occlusion and dissection, and 3% to 5% will develop a cerebellar or brain infarct, which is often lethal. The mechanism of injury in cervical spine trauma patients is usually distraction or compression of the artery, resulting in intimal flaps, dissections (Figures 2 and 3), pseudoaneurysms, or arteriovenous fistulas (Figure 4) of the vertebral artery. In a review of 1941patients with blunt trauma, the incidence of carotid or vertebral injury was 1.1%. Another extensive literature review reported that most patients with a vertebral artery injury have no clinical symptoms, but the few who develop a sudden deterioration after a brief normal neurologic interval have a morbid course. In acute cervical spine trauma, the vertebral artery is injured along its transforaminal course, from C6 to C1. Vertebral artery injury occurs in 25% of patients with a fracture of the transverse process and in 35% of those with a facet dislocation. However, 20% of patients with acute cervical spine trauma sustain a vertebral artery injury in the absence of any identifiable bony fracture or dislocation. In these patients, the vertebral artery is injured by distraction–flexion and distraction–extension forces. A particularly worrisome course in patients with a history of cervical trauma is the development of stroke symptoms after several days, or even weeks, of neurologic clinical normality. This morbid course is the result of the progression to occlusion of the injured vertebral artery or its embolization into the basilar artery. Vertebral artery injury associated with chiropractic manipulation of the neck falls into both blunt and iatrogenic categories of

Penetrating and Blunt Injuries of the Vertebral Artery

trauma. The attribution of vertebrobasilar stroke to the manipulation of the cervical spine has long been a subject of controversy. Although the incidence of vertebrobasilar stroke after chiropractic manipulation is low, its outcome is most serious: 52% develop a permanent neurologic deficit, and 5% to 18% die. The chiropractic literature states, on the basis of self-reporting, that the incidence of stroke following chiropractor manipulation is very small: between 1 per 1.3 million and 1 per 400,000 treatment sessions. However, a population-based study, using data from hospital admission codes for vertebrobasilar stroke and billing data for cervical spine manipulation, showed that the incidence was 1.3 per 100,000 cases of neck manipulation. Patients admitted with

665

symptomatic vertebrobasilar occlusion or dissection were five times more likely than matched controls to have visited a chiropractor for cervical pain in the previous week. In ascribing the vertebrobasilar stroke of a patient to a chiropractic manipulation one must also consider the fact that most patients go to a chiropractor because of neck pain, and the neck pain could have been the initial symptom of a spontaneous vertebral artery dissection. In that case the manipulation could have extended what was, till then, a limited dissection. Given the propensity for spontaneous dissection in patients with connective tissue disease, it seems sensible to advise them to avoid chiropractic manipulations. Iatrogenic injuries of the V1 segment usually follow the placement of a central venous catheter. The most common lesion resulting from accidental puncture of a vertebral artery is a fistula either between the vertebral artery and the jugular vein or the vertebral artery and the vertebral vein. This injury is common because the vertebral vein

FIGURE 4  Arteriovenous fistula of the vertebral artery in a young FIGURE 2  Dissection involving the transforamen of the vertebral

artery following an equestrian fall.

FIGURE 3  Dissection of the V3 segment of

the vertebral artery after a skiing accident. The washout phase of the injection shows the contrast (arrow) lingering on the surface of the dissection flap.

boy who was playing “hangman,” suspending his neck on a rope. The vertebral artery ruptured its the surrounding venous plexus.

666 VASCULAR TRAUMA

TREATMENT

FIGURE 5  The lateral screw was placed through the transverse fora-

men, thrombosing the vertebral artery within.

is anatomically adjacent to the vertebral artery. The same mechanism just as often could result in an arteriovenous aneurysm. Anterior diskectomy seldom (0.3%–0.5%) results in vertebral artery injury in its intraspinal segment. When injury occurs it usually follows a lateral exploration or the drilling of an uncovertebral joint (Figure 5). It is easy to understand how this complication can occur when we observe in some patients the tortuosity and redundancy of their vertebral artery between the transverse processes. The vertebral artery is more likely to be injured during anterior cervical corpectomy. The favored technique for atlantoaxial fixation involves inserting a screw into the C1–C2 facet joint, and this maneuver carries a risk of 8% of lacerating the vertebral artery. In posterior cervical spine surgery, a rare vertebral artery injury is the perforation of the artery by the screw used for a plate fixation. Although spine surgeons have precisely defined the anatomic landmarks for safe drilling, variations in the course of the vertebral artery, including its extraforaminal excursions, are responsible for some of these infrequent injuries. Iatrogenic injuries secondary to angiography were more common in the 1960s and early 1970s, when the vertebral artery was punctured directly for vertebrobasilar arteriography. Today the vertebral artery may be dissected during arteriography by advancing the catheter into the vertebral artery proper and pressure-injecting into it. Because of this, most angiographers place the catheter tip in the subclavian artery proximal to the ostium of the vertebral artery when performing a selective vertebrobasilar arteriogram.

There is consensus but no proof that an acute dissection should be treated with anticoagulation, first with heparin and, after a few days, with warfarin. The basis for this recommendation is that the infarction that follows a dissection is almost always secondary to embolization and not a result of low-flow. If a vertebral artery is injured during spinal surgery, tamponade with procoagulants and pressure can provide a temporal solution to the hemorrhage, although this is not always effective. Recurrent bleeding, pseudoaneurysm, or arteriovenous fistula can follow. Ligation of the proximal vertebral artery does not control the hemorrhage because the distal vertebral artery bleeds retrograde when the contralateral vertebral artery is normal. But even effective ligation is not without risks: In cases with a contralateral hypoplastic vertebral artery, the ligation can cause ascending thrombosis and involve the basilar artery. A neurosurgical literature review recorded a death incidence of 12% following simple ligation. This is probably an overestimation because the authors included cases published a century ago with unacceptable indications, such as treatment of epilepsy. Deaths after ligation are presumed to be secondary to distal extension of the thrombus into the basilar artery. A competent contralateral vertebral artery substantially diminishes this risk of distal thrombosis. Once the bleeding has been temporarily controlled, an arteriogram permits a better assessment of the injury and, if indicated, initiation of a plan for reestablishing continuity of the vertebral artery by transposition or bypass.

Selected References Burke JP, Gerszten PC, Welch WC: Iatrogenic vertebral artery injury during anterior cervical spine surgery, Spine J 5:508–514, 2005: discussion 514. Friedman D, Flanders A, Thomas C, et al: Vertebral artery injury after acute cervical spine trauma: Rate of occurrence as detected by MR angiography and assessment of clinical consequences, AJR Am J Roentgenol 164:443– 447, 1995: discussion 448–449. Giacobetti FB, Vaccaro AR, Bos-Giacobetti MA, et al: Vertebral artery occlusion associated with cervical spine trauma. A prospective analysis, Spine (Phila Pa 1976) 22:188–192, 1997. Inamasu J, Guiot BH: Iatrogenic vertebral artery injury, Acta Neurol Scand 112:349–357, 2005. Kerwin AJ, Bynoe RP, Murray J, et al: Liberalized screening for blunt carotid and vertebral artery injuries is justified, J Trauma 51:308–314, 2001. Frisoni GB, Anzola GP: Vertebrobasilar ischemia after neck motion, Stroke 22:1452–1460, 1991. Reuter U, Hamling M, Kavuk I, et al: Vertebral artery dissections after chiropractic neck manipulation in Germany over three years, J Neurol 253:724–730, 2006. Rothwell DM, Bondy SJ, Williams JI: Chiropractic manipulation and stroke: A population-based case-control study, Stroke 32:1054–1060, 2001. Shintani A, Zervas NT: Consequence of ligation of the vertebral artery, J Neurosurg 36:447–450, 1972.



Blunt Arterial Injuries of the Shoulder: Open and Endovascular Therapy

Blunt Arterial Injuries of the Shoulder: Open and Endovascular Therapy Robert R. Carter and Eric D. Endean

The major vessels injured with shoulder girdle trauma are the axillary and subclavian arteries. The muscles and bones of the shoulder girdle, which surround these vessels, provide considerable protection against injury. Thus, blunt injuries to the axillary and subclavian arteries are relatively unusual, and most series of upper extremity arterial injuries report that a majority are caused by penetrating injury and involve the brachial artery and its branches. Blunt arterial injury to the axillary or subclavian artery accounts for only 7% to 10% of all arterial injuries to the upper extremity. The types of blunt trauma that result in axillary and subclavian artery injury include hyperabduction of the arm, shoulder dislocation, scapulothoracic dissociation, and fracture of the first rib or clavicle. Hyperabduction of the arm can result in avulsion of arterial branches of the axillary and subclavian arteries, transection of the arteries, or disruption of intima by stretch injury. Intimal injury or disruption of the vessel wall can in turn result in vessel thrombosis, embolism, or pseudoaneurysm formation. Shoulder dislocations typically do not result in arterial injury. When arterial injury does occur, it is most often associated with anterior dislocations in elderly persons. Such patients likely lack elasticity of the vessel. Consequently, the artery cannot accommodate the stretch caused by the dislocation. Axillary artery injury can also occur during reduction of chronic shoulder dislocations. Under these circumstances, scarring and atherosclerosis act to fix the vessel, and the axillary artery cannot accommodate the additional stretch needed during the traction required to reduce the dislocation. Scapulothoracic dissociation occurs after severe crush or traction injury to the shoulder and is associated with subclavian and/or axillary artery injury. Fractures of the first rib and the clavicle occasionally impinge on the underlying subclavian artery. The branches of the subclavian and axillary arteries provide an extensive arterial collateral network around the shoulder. As a result, signs and symptoms of ischemia might not be evident even if the axillary or subclavian arteries are occluded or transected. Because the brachial plexus is in close proximity to the distal subclavian and the axillary arteries, blunt shoulder trauma often results in injury to these nerves. The axillary vessels and the brachial plexus are surrounded by an extension of the prevertebral layer of the deep cervical fascia in the arm. Bleeding into this sheath can cause significant compression of the brachial plexus, which can result in brachial plexus damage.

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extremity ischemia; they can even have palpable wrist pulses. Signs of hemorrhage can be difficult to appreciate, especially in muscular or obese patients. Therefore, one must have a high index of suspicion to make an early diagnosis of a vascular injury. Blunt arterial trauma is less likely to result in hemodynamic instability. Patients who come to the hospital with hard signs of vascular injury such as pulsatile bleeding, expanding hematoma, palpable thrill, or evidence of peripheral ischemia should be taken to the operating room without delay. At operation, either an intraoperative angiogram or exploration of the injury is done depending on the hemodynamic stability of the patient and the surgeon’s expertise and preference. In patients without obvious signs of arterial injury, the presence of associated shoulder injuries often provides a clue regarding the presence of an underlying vascular injury. Clavicular fracture, shoulder dislocation, first rib fracture, brachial plexus injury, scapular fracture, or proximal humeral fracture increase the likelihood of an associated major arterial injury. Often, nerve root avulsion causes a devastating brachial plexus injury when the arm is forcibly hyperabducted. Additionally, compression of the brachial plexus by hematoma within the neurovascular sheath can also cause substantial neurologic impairment. In all cases, prompt exploration is indicated. Arteriography has been the cornerstone for diagnosis of arterial injury associated with blunt shoulder trauma (Figure 1). Computed tomography (CT) angiography has largely replaced conventional arteriography for initial evaluation of arterial injuries. All patients who are hemodynamically stable and come to the hospital with signs of upper extremity arterial insufficiency should undergo an imaging study. Such is useful to plan the best operative approach, especially when a proximal subclavian artery injury is identified. A potential advantage of conventional arteriography is that after vascular access has been obtained, the surgeon may consider endovascular options to treat the identified injury. Patients with axillary or subclavian artery injuries commonly have other concomitant injuries. Treatment priorities for the other injuries need to be established. Because of the excellent arterial collateral circulation around the shoulder, the upper extremity is often at less risk for severe ischemic sequelae. Therefore, treatment of other

PRESENTATION AND DIAGNOSIS Patients with shoulder trauma can come to the hospital with signs and symptoms of arterial insufficiency of the upper extremity, an expanding hematoma, a pulsatile mass, signs of ongoing hemorrhage, or hemothorax. However, because of the rich collateral circulation around the shoulder joint, some patients with significant arterial injuries come to the hospital with minimal or no signs of upper

FIGURE 1  Intraoperative arteriogram in a patient with a crush injury

to his right arm and torso. An intimal tear within the distal axillary artery (white arrow) is demonstrated.

668 VASCULAR TRAUMA life-threatening injuries can and should be given priority over arterial repair. However, vascular reconstruction should not be excessively delayed.

OPEN OPERATIVE MANAGEMENT The type of incision and exposure needed for control of the subclavian or axillary arteries must be individualized and depends on the location, severity, and extent of the injury. In general, patients should be positioned and prepped so that, if needed, the proximal subclavian artery can be quickly exposed for control. Injuries to the distal two thirds of the subclavian artery can be successfully approached with a supraclavicular incision. A portion of the clavicle can be resected to improve exposure. If the proximal third of the subclavian artery is injured, obtaining control of the artery is more difficult. If the injury involves the right subclavian artery, exposure of the brachiocephalic trunk is usually required. A median sternotomy, with supraclavicular extension, offers the best exposure. Because the left subclavian artery arises posteriorly from the aortic arch, an anterolateral thoracotomy, through the third or fourth intercostal space, provides the best access to the proximal left subclavian artery. Additional exposure can be obtained with a supraclavicular incision on the left. The supraclavicular incision and the thoracotomy can be joined medially by incising the sternum, creating a trap door that provides exposure of the entire left subclavian artery. The axillary artery is exposed through an infraclavicular incision extended into the deltopectoral groove. The fibers of the pectoralis major and minor muscles may be split or the tendons may be transected if additional exposure of the injured portion of the vessel is needed. The pectoralis major muscle tendon should be reapproximated at the completion of the operation. In some patients, proximal exposure of the subclavian artery through a separate supraclavicular incision may be useful. Care should be taken to preserve the major branches of these axial vessels because they serve as important collateral pathways. When the vascular injury is localized to a short segment of the artery, a resection and end-to-end primary repair is preferred. This is often not possible because blunt trauma more often affects a long segment of the artery, and the numerous branches do not allow sufficient mobilization of the artery to create a tension-free anastomosis. In such cases, resection of the injured segment of artery and an interposition graft are often needed (Figure 2). Autogenous tissue is the conduit of choice, the most accessible conduit being the saphenous vein. Because the subclavian and axillary arteries are large vessels, a size mismatch between these vessels and saphenous vein can make the use of this conduit less than ideal. A spiral graft or a panel graft created from the saphenous vein or the deep femoral vein can be used, or a prosthetic graft can be used. Both Dacron and polytetrafluoroethylene have been implanted successfully in these situations. Systemic heparin anticoagulation should be used cautiously in patients with concomitant injuries. Local or regional anticoagulation to impede arterial thrombus formation can be achieved by injecting saline containing heparin sodium (10 IU/mL) into the artery locally after proximal and distal control have been obtained. During operative exploration, the brachial plexus should be evaluated. Unless a severed nerve is sharply and cleanly transected, which is unusual in blunt trauma, the nerve ends should be tagged with nonabsorbable suture for future repair. Venous injuries are commonly associated with the arterial injury. Such injuries can be difficult to control because of the large size of the vessel, the thin wall, and the rapid bleeding. An attempt to repair injured veins is appropriate in otherwise stable patients. However, in some situations, injured veins can require ligation, recognizing that upper extremity edema and venous hypertension can occur as a result. The long-term outcome for repair of axillary and subclavian injuries secondary to blunt trauma has not been well defined because

A

B FIGURE 2  Intraoperative photos of the same patient. A, An intimal

injury within the axillary artery. B, After resection and replacement of the axillary artery with an interposition greater saphenous vein graft.

these vessels are so rarely injured and most series do not distinguish between blunt and penetrating trauma. Patency of repair for blunt and penetrating injuries has been reported as high as 95% in some series. Mortality is usually related to associated injuries, especially those that involve the heart or origin of the great vessels. Significant morbidity results from associated brachial plexus injuries. Patients with avulsion injuries of the brachial plexus have a poor prognosis for recovery of upper extremity function, regardless of a patent vascular repair. Arm amputation is indicated in some patients to control intractable pain.

ENDOVASCULAR MANAGEMENT Endovascular techniques have increasingly been used to treat penetrating and blunt vascular injuries. The experience using endovascular techniques to treat atherosclerotic lesions has been good but might not be replicated in the younger trauma patient with undiseased arteries. The incidence of long-term complications resulting from intimal hyperplasia and restenosis in this population is unknown. Proponents of using endovascular techniques in trauma patients point out that diagnostic angiography is often the first step in the management of these patients. They advocate attempting endovascular repair of injuries identified on angiography and proceeding with operative repair only if the endovascular approach is unsuccessful. Traversing the injury with a wire should not result in further injury. If acute hemorrhage is encountered, the arterial access allows rapid placement of a balloon occlusion catheter to obtain proximal control until an emergent open repair of the injury can be performed. In cases of traumatic arterial injury, the open exposure of the traumatized tissues may be difficult because of hematoma or ongoing hemorrhage, making endovascular repair an attractive alternative, with the access point chosen remote from the acute arterial injury. Short-term patency rates have been reported as high as 100% in some series.

Penetrating Injuries to the Aortic Arch and Intrathoracic Great Vessels

Endovascular techniques have been used to treat pseudoaneurysms, arteriovenous fistulas, and intimal disruptions within the upper extremity. Angioplasty may be used to treat dissections by attempting to glue the injured intima to the vessel wall. Endovascular stents can be placed to tack down the dissection flap or cover an arteriotomy to control bleeding, arteriovenous fistula, and pseudoaneurysm. Stents have even been used to bridge arterial transection. The use of stents to repair injuries to the subclavian and axillary arteries has been described with reportedly good short-term results. Embolization of avulsed branches of major vessels has also been described, but its role in blunt trauma is limited. Thrombolytics are generally contraindicated in trauma patients. There are potential disadvantages with an endovascular repair. The location of the arterial injury can preclude endovascular repair. Stents placed in the axillary artery are subjected to stress from shoulder joint movement, and with the passage of time this movement can result in compression or fracture of the stent, necessitating future open arterial repair or bypass. In patients with hematoma causing nerve compression, endovascular repair does not address nerve compression by hematoma within the sheath, and open evacuation might still be required to prevent permanent nerve injury. Similarly, concomitant venous injury is not addressed with arterial angioplasty and stenting. Finally, endovascular reestablishment of flow through an occluded vessel can result in distal embolization of thrombus, requiring further intervention to restore distal flow. These factors currently limit the application of endovascular techniques in the treatment of blunt traumatic injuries to the shoulder. Endoluminal placement of covered stents to treat axillosubclavian blunt arterial injury has been reported. The authors described their technique for crossing a focal area of transection and/or occlusion with a guidewire, allowing placement of a covered stent graft. The advantage of such an approach is that extensive exposure and dissection is not required in patients who often have other serious injuries. The authors acknowledge that associated hematomas that can compress the brachial plexus are not addressed with endovascular repair, but they argue that stretch injury to the brachial plexus is more likely the cause of any nerve injury, and evacuation of an associated hematoma would likely not improve the neurologic outcome in these patients.

Penetrating Injuries to the Aortic Arch and Intrathoracic Great Vessels Nickolay P. Markov and Todd E. Rasmussen

This chapter provides an overview of penetrating injures to the aortic arch and intrathoracic great vessels. Because these short-segment vascular structures are clustered in the confined space of the mediastium, the first portion of this chapter reviews the overall epidemiology, presentation, diagnosis, and management of all arterial injuries in this location. The second part of this chapter addresses penetrating injury to each of the innominate, subclavian, and common carotid arteries individually.

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An open approach may be the procedure of choice in patients with large tissue defects and exposed artery or with long segment or multiple arterial injuries to a single segment of artery. Direct exposure and repair of the injured artery provide adequate coverage and achieve a secure repair of the injured vessel. Patients with intracranial hemorrhage, solid organ injury, or other contraindications to anticoagulation also may be best served with an open approach given that anticoagulation or antiplatelet therapy is often needed with endovascular repairs. On the other hand, the endovascular approach may be useful in the hemodynamically unstable patient where inflation of a proximal occlusion balloon can control hemorrhage. At the time that the artery is cannulated, an angiogram can further define the location and extent of the injury. Depending on a variety of factors including the location of the injury, extent of injury, and patient factors, subsequent repair of the artery can be accomplished using an open, endovascular, or combined approach.

Selected References Brandt M, Kazanjian S, Wahl W: The utility of endovascular stents in the treatment of blunt arterial injuries, J Trauma 51:901–905, 2001. Diamond S, Gaspard D, Katz S: Vascular injuries to the extremities in a suburban trauma center, Am Surg 69:848–851, 2003. Franz RW, Goodwin RB, Hartman JF, et al: Management of upper extremity arterial injuries at an urban level I trauma center, Ann Vasc Surg 23:8–16, 2009. Graham JM, Mattox KL, Feliciano DV, et al: Vascular injuries of the axilla, Ann Surg 195:232–238, 1982. Lönn L, Delle M, Karlström, et al: Should blunt arterial trauma to the extremities be treated with endovascular techniques? J Trauma 59:1224–1227, 2005. Marin ML, Veith FJ, Panetta TF, et al: Transluminally placed endovascular stented graft repair for arterial trauma, J Vasc Surg 20:466–473, 1994. McCready RA, Procter CD, Hyde GL: Subclavian–axillary vascular trauma, J Vasc Surg 3:24–31, 1986. Papaconstantinou HT, Fry DM, Giglia J, et al: Endovascular repair of a blunt traumatic axillary artery injury presenting with limb-threatening ischemia, J Trauma 57:180–183, 2004. Raskin KB: Acute vascular injuries of the upper extremity, Hand Clin 9:115–130, 1993. Shalhub S, Starnes BW, Tran NT: Endovascular treatment of axillosubclavian arterial transection in patients with blunt traumatic injury, J Vasc Surg 53:1141–1144, 2011.

ARTERIAL INJURIES IN THE MEDIASTINUM Epidemiology Penetrating trauma to the aortic arch and its major branch vessels is rare and associated with high mortality. Penetrating aortic arch injuries constitute 1% of all thoracic vascular injuries and 13% of all penetrating thoracic aortic injuries in the civilian setting. In an epidemiologic study by White and Rasmussen, brachiocephalic and subclavian injuries accounted for only 3% of all vascular injuries during a decade of war in Afghanistan and Iraq. In a separate comparison of arterial injury between military and civilian trauma registries, including blunt and penetrating mechanisms, these authors found the rate of innominate and subclavian injury to be higher in the civilian (6.4%) than in the military (3.7%) cohort. We speculate that this difference is likely a result of the higher incidence of motor vehicle crashes in the civilian population and the use of protective body armor in the military cohort. In military and civilian studies, 95% of persons with penetrating injuries to the arch and great vessels are male, and single-projectile

Penetrating Injuries to the Aortic Arch and Intrathoracic Great Vessels

Endovascular techniques have been used to treat pseudoaneurysms, arteriovenous fistulas, and intimal disruptions within the upper extremity. Angioplasty may be used to treat dissections by attempting to glue the injured intima to the vessel wall. Endovascular stents can be placed to tack down the dissection flap or cover an arteriotomy to control bleeding, arteriovenous fistula, and pseudoaneurysm. Stents have even been used to bridge arterial transection. The use of stents to repair injuries to the subclavian and axillary arteries has been described with reportedly good short-term results. Embolization of avulsed branches of major vessels has also been described, but its role in blunt trauma is limited. Thrombolytics are generally contraindicated in trauma patients. There are potential disadvantages with an endovascular repair. The location of the arterial injury can preclude endovascular repair. Stents placed in the axillary artery are subjected to stress from shoulder joint movement, and with the passage of time this movement can result in compression or fracture of the stent, necessitating future open arterial repair or bypass. In patients with hematoma causing nerve compression, endovascular repair does not address nerve compression by hematoma within the sheath, and open evacuation might still be required to prevent permanent nerve injury. Similarly, concomitant venous injury is not addressed with arterial angioplasty and stenting. Finally, endovascular reestablishment of flow through an occluded vessel can result in distal embolization of thrombus, requiring further intervention to restore distal flow. These factors currently limit the application of endovascular techniques in the treatment of blunt traumatic injuries to the shoulder. Endoluminal placement of covered stents to treat axillosubclavian blunt arterial injury has been reported. The authors described their technique for crossing a focal area of transection and/or occlusion with a guidewire, allowing placement of a covered stent graft. The advantage of such an approach is that extensive exposure and dissection is not required in patients who often have other serious injuries. The authors acknowledge that associated hematomas that can compress the brachial plexus are not addressed with endovascular repair, but they argue that stretch injury to the brachial plexus is more likely the cause of any nerve injury, and evacuation of an associated hematoma would likely not improve the neurologic outcome in these patients.

Penetrating Injuries to the Aortic Arch and Intrathoracic Great Vessels Nickolay P. Markov and Todd E. Rasmussen

This chapter provides an overview of penetrating injures to the aortic arch and intrathoracic great vessels. Because these short-segment vascular structures are clustered in the confined space of the mediastium, the first portion of this chapter reviews the overall epidemiology, presentation, diagnosis, and management of all arterial injuries in this location. The second part of this chapter addresses penetrating injury to each of the innominate, subclavian, and common carotid arteries individually.

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An open approach may be the procedure of choice in patients with large tissue defects and exposed artery or with long segment or multiple arterial injuries to a single segment of artery. Direct exposure and repair of the injured artery provide adequate coverage and achieve a secure repair of the injured vessel. Patients with intracranial hemorrhage, solid organ injury, or other contraindications to anticoagulation also may be best served with an open approach given that anticoagulation or antiplatelet therapy is often needed with endovascular repairs. On the other hand, the endovascular approach may be useful in the hemodynamically unstable patient where inflation of a proximal occlusion balloon can control hemorrhage. At the time that the artery is cannulated, an angiogram can further define the location and extent of the injury. Depending on a variety of factors including the location of the injury, extent of injury, and patient factors, subsequent repair of the artery can be accomplished using an open, endovascular, or combined approach.

Selected References Brandt M, Kazanjian S, Wahl W: The utility of endovascular stents in the treatment of blunt arterial injuries, J Trauma 51:901–905, 2001. Diamond S, Gaspard D, Katz S: Vascular injuries to the extremities in a suburban trauma center, Am Surg 69:848–851, 2003. Franz RW, Goodwin RB, Hartman JF, et al: Management of upper extremity arterial injuries at an urban level I trauma center, Ann Vasc Surg 23:8–16, 2009. Graham JM, Mattox KL, Feliciano DV, et al: Vascular injuries of the axilla, Ann Surg 195:232–238, 1982. Lönn L, Delle M, Karlström, et al: Should blunt arterial trauma to the extremities be treated with endovascular techniques? J Trauma 59:1224–1227, 2005. Marin ML, Veith FJ, Panetta TF, et al: Transluminally placed endovascular stented graft repair for arterial trauma, J Vasc Surg 20:466–473, 1994. McCready RA, Procter CD, Hyde GL: Subclavian–axillary vascular trauma, J Vasc Surg 3:24–31, 1986. Papaconstantinou HT, Fry DM, Giglia J, et al: Endovascular repair of a blunt traumatic axillary artery injury presenting with limb-threatening ischemia, J Trauma 57:180–183, 2004. Raskin KB: Acute vascular injuries of the upper extremity, Hand Clin 9:115–130, 1993. Shalhub S, Starnes BW, Tran NT: Endovascular treatment of axillosubclavian arterial transection in patients with blunt traumatic injury, J Vasc Surg 53:1141–1144, 2011.

ARTERIAL INJURIES IN THE MEDIASTINUM Epidemiology Penetrating trauma to the aortic arch and its major branch vessels is rare and associated with high mortality. Penetrating aortic arch injuries constitute 1% of all thoracic vascular injuries and 13% of all penetrating thoracic aortic injuries in the civilian setting. In an epidemiologic study by White and Rasmussen, brachiocephalic and subclavian injuries accounted for only 3% of all vascular injuries during a decade of war in Afghanistan and Iraq. In a separate comparison of arterial injury between military and civilian trauma registries, including blunt and penetrating mechanisms, these authors found the rate of innominate and subclavian injury to be higher in the civilian (6.4%) than in the military (3.7%) cohort. We speculate that this difference is likely a result of the higher incidence of motor vehicle crashes in the civilian population and the use of protective body armor in the military cohort. In military and civilian studies, 95% of persons with penetrating injuries to the arch and great vessels are male, and single-projectile

670 VASCULAR TRAUMA firearms are the leading cause of injury (69%) followed by stab (18%) and shotgun (12%) wounds. Despite developments in the diagnosis and management of vascular trauma leading to improved survival for persons sustaining blunt descending thoracic aortic injury, the lethality of penetrating aortic arch injury remains unchanged. Similar to that for blunt aortic injury, survival following penetrating arch and great vessel trauma depends upon the propensity for the vascular disruption to be contained by the adventitia of the vessel and surrounding soft tissue. In most instances of arch and great vessel trauma this favorable interval of vascular disruption does not occur and patients do not survive to be transferred to a medical treatment facility. Even if patients do survive to a treatment facility, only 12% survive to be discharged from the hospital. As described, pseudoaneurysm formation following arch and great vessel injury is the only chance for survival, which emphasizes the importance of avoiding overresuscitation and hypertension in the immediate postinjury period because either could precipitate rupture of an otherwise contained injury. The mortality for patients with this injury pattern and an unrecordable blood pressure on admission or for patients who require a resuscitative thoracotomy with aortic clamping is nearly 100%.

Clinical Presentation The majority of patients with penetrating aortic arch and great vessel injuries present in shock (82%), requiring immediate surgical intervention in the form of tube thoracostomy, resuscitative thoracotomy, or median sternotomy. Demetriades and colleagues reported that only 8% of patients with this injury pattern arrived at their facility with a systolic blood pressure of greater than 90 mm Hg, and nearly half (41%) were in extremis without a recordable pressure. Most patients with this injury pattern come to the hospital with hypovolemic shock, and a smaller percentage come to the hospital with cardiac tamponade, neurologic deficits, hemothorax, and/or a precordial bruit. Aortic arch injuries are often associated with multiple other vascular injuries, including vena cava, innominate vein, and pulmonary artery injuries. Injury to the innominate vein with an arteriovenous fistula has been reported in some cases of this injury pattern. Pulmonary injuries constitute 54% of concomitant noncardiovascular injuries with aortic arch trauma.

Diagnosis Given the propensity of this injury pattern for hemorrhage, many arch injuries are first diagnosed during resuscitative anterolateral thoracotomy because patients are too unstable to undergo radiographic or angiographic evaluation. For patients who are able to undergo imaging, the most common appearance is a widened mediastinum on chest x-ray. Previously, angiography was the gold standard for the diagnosis and preoperative evaluation of this injury pattern, but contrast-enhanced computed tomography (CT) scanning is now the favored modality. To a large degree, contrast arteriography is now only performed in selected cases following a CT scan that diagnoses the injury. In these instances, subsequent arteriography may be used as a necessary step in consideration of endovascular treatment of the injury (e.g., placement of a covered stent) and not for diagnosis. Although either CT scan or arteriography is preferable before surgery, less than half of patients are stable enough to undergo such preoperative imaging.

Management Open Operative Management Operative management of penetrating arch and great vessel injuries depends on the named vessel or vessels that are injured. The aortic

FIGURE 1  Illustration of operative exposure of the aortic arch

and proximal great vessels provided through a median sternotomy approach. Note the crossing innominate vein, which must be carefully divided to allow full exposure of the innominate artery, proximal common carotid arteries, and proximal right subclavian artery. Note how the origin of the left subclavian artery is not seen in this illustration because it lies more posterior in the mediastinum.

arch can be divided into three segments: ascending, transverse aorta with the origins of the proximal great vessels (innominate, carotid, and subclavian arteries) and descending distal to the left subclavian artery and proximal to the main thoracic aorta. For instances of diagnosed or suspected injury to the first and second sections, a median sternotomy is the operative exposure of choice. (Figure 1). Care must be taken in these cases to avoid injury to the innominate vein, which crosses superficial to the aorta and proximal great vessels in the superior aspect of this exposure. Sternotomy followed by division of the innominate vein allows the pericardium to be opened for release of any associated cardiac tamponade. Once these maneuvers have been accomplished, a sternotomy provides visualization and control of the ascending aorta as well as the innominate and proximal right carotid and subclavian arteries (see Figure 1). Exposure of these vessels can be facilitated by extending the sternotomy incision proximally on the right as a longitudinal cervical or supraclavicular incision with division of the sternocleidomastoid muscle. The aortic arch traverses in an anteroposterior direction in the mediastinum, making exposure of the distal transverse arch and proximal left common carotid challenging through a median sternotomy. However, these vessels can be controlled using this approach alone or in conjunction with an extension to a left cervical or supraclavicular incision, including division of the sternocleidomastoid. Injuries of the arch distal to the left common carotid, including those to the left subclavian artery origin, typically require a high left anteromedial thoracotomy. At the time of operative exposure, one often encounters a hematoma surrounding the vessel that must be entered to control and repair the injury. Blood loss notwithstanding, this task is necessary and often results in identification of an arterial disruption that can be controlled with a finger or a Kittner dissecting sponge. Before entering such a hematoma, the surgeon can take heart in knowing that

Penetrating Injuries to the Aortic Arch and Intrathoracic Great Vessels

patients with large or complete vessel disruptions with free hemorrhage would not have survived to undergo the operation. Small lacerations of the transverse aortic arch or proximal great vessels can be primarily repaired often using full-thickness polypropylene sutures with pledgets. When possible, use of a strong partial-occlusion (side-biting) clamp such as a Wiley J-clamp allows isolation of the injured segment of the ascending aorta, innominate, or even proximal carotid artery. If it can be applied and secured proximal to the injury site, the partial-occlusion clamp greatly facilitates full-thickness primary repair with pledgets in some cases. Injuries to the proximal innominate and origin of the common carotid arteries at or just distal to the aortic arch can be managed with a synthetic bypass graft (single or bifurcated). In these instances the proximal portion of the graft originates from an area of the ascending aorta proximal to the zone of injury. The distal anastamosis or bypass limbs are sewn distal to the subclavian and or the carotid artery as the intervening segment of injured vessel is oversewn. More extensive injuries to the transverse arch and origins of the great vessels require a synthetic patch, vessel replacement, or interposition or graft. Although median sternotomy provides access for cardiopulmonary bypass, this maneuver is exceedingly rare in the setting of trauma. Even if the appropriate surgical and perfusion teams are readily available, the hypothermia and coagulopathy associated with bypass make the use of this adjunct very uncommon. A technical note to be mindful of pertains to selection of the suture needle. In many instances the surgeon is more effective using a needle that is large enough (e.g., small half [SH] or CT needle) to be seen and steered in considerable amounts of blood. Although it seems intuitive to select a smaller, atraumatic needle, this often leads to frustration because the needle is difficult to see and manipulate to achieve full thickness purchase in arterial wall. Endovascular Management The difficult nature of exposure and repair of aortic arch and proximal great vessel injuries makes endovascular management appealing. The use of covered stent grafts to manage proximal common carotid and even innominate artery injuries has been reported. However, because of the complex anatomic relationships involving the origins of the carotid and vertebral arteries, endovascular repair is not as straightforward as it can be in the longer, more distal branch vessels or the descending thoracic aorta. Furthermore, motion from the beating heart and the need to image vessels in the thorax make placement of endovascular devices in this region less precise than in other locations. Unlike stent grafts in the management of descending thoracic aortic and selected side-branch injuries, use of this technique to repair transverse aortic arch injuries has not been established. Growing experience with staged debranching procedures originating from the ascending aorta to perfuse the great vessels beyond the zone of injury makes it possible that hybrid, open, and endovascular procedures may be used more in the future to treat selected cases of transverse arch injury.

Outcomes There is a paucity of data regarding the outcome of patients who survive penetrating injury to the aortic arch and great vessels. Extrapolating from the experience with patients undergoing repair of descending thoracic aortic injury, complications can be expected to arise secondary to hemorrhage and/or ischemia. Risk of neurologic sequelae such as stroke and paraplegia can be expected to be as high as 15% to 20%, and multisystem organ failure has been reported in 30% to 40% of patients. Concomitant pulmonary injury has been reported in 50% of patients with penetrating arch and great vessel injury and is a source of postoperative morbidity.

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SPECIFIC ARTERIAL INJURIES The following sections present aspects of injury as they pertain to individual segments of the aortic arch and great vessels. Some of the information in these sections was covered in the overview, but some aspects of managing this difficult location of vascular trauma are specific to the individual arterial segments or vessels.

Innominate Injury Incidence, Etiology, and Presentation Penetrating innominate injuries are rare, and the incidence is unknown because 50% to 75% of patients succumb to injury before reaching a hospital. According to civilian series, innominate injuries account for 0% to 3% of arterial trauma, with the majority occurring secondary to gunshot wounds. The high mortality relates to the relative inaccessibility of the innominate, the propensity for hemorrhage, and the vessel’s proximity to the carotid and vertebral arteries. Concomitant pulmonary injuries increase the morbidity and mortality associated with this injury pattern. In patients who survive to be treated, in-hospital mortality has been reported in the range of 10% to 43%. Patients with penetrating innominate injuries usually present in shock with hard signs of arterial injury. If the vascular disruption has been contained by the adventitia and/or mediastinum, other findings can include hematoma, hemothorax, pulseless extremity, and neurologic deficit. The majority of innominate injuries occur with or are categorized as zone I neck injuries. One should be cognizant that a seemingly routine zone II neck wound can harbor an innominate artery injury at its inferior extent. Numerous nonvascular injuries can occur in conjunction with innominate artery trauma, of which pulmonary hemopneumothorax is the most common. Diagnosis Patients who are hemodynamically normal should undergo an initial plain chest x-ray understanding that a widened mediastium has been reported in up to 70% of patients with penetrating innominate injury. Although contrast CT imaging has replaced aortography as the study of choice for innominate artery injuries, the proximity of this vessel to the lungs and beating heart mean that motion artifact can obscure subtle injuries. The sensitivity of CT imaging can be as low as 50% to 75% in excluding aortic arch and proximal branch vessel injuries. In instances in which hematoma surrounds the innominate without a luminal defect or in cases in which metal fragments scatter the CT beam, digital subtraction arteriography may be useful to better demonstrate the injury to allow potential endovascular intervention to be planned. Open Operative Management Patients who have penetrating upper chest or zone I neck wounds and have hemorrhage and hemodynamic compromise should be taken to the operating room for exploration through a median sternotomy. The median sternotomy can be extended to a longitudinal cervical incision or a supraclavicular incision, depending on the injury. After the hematoma has been entered and the injury has been identified, the innominate should be controlled. Often this is initially accomplished with a finger or a low-profile Kittner dissection sponge. Subsequently, the injury can be isolated using strong vascular clamps including the Wylie-J, Statinsky, or angled DeBakey. If the innominate injury is partial, it may be amenable to primary repair using polypropylene suture with pledgets. If the injury is more significant it can require oversewing after a bypass is made originating from the ascending aorta to the mid right common carotid and/or right subclavian arteries.

672 VASCULAR TRAUMA Endovascular Management The innominate artery is short and has a variable bifurcation, which is difficult to image. Stent graft repair of this segment therefore is not straightforward and should only be attempted in centers with endovascular experience including inventory and imaging capability. When one is considering endovascular repair, it is important to be able to assess the diameter of the artery and also to identify landing or seal zones proximal and distal to the injury. In this location, repair is best performed with balloon-expandable covered stents, which allow more accurate placement to avoid imposing on or covering the origin of the right common carotid artery. Endovascular repair of this injury pattern has been performed but is generally reserved for hemodynamically normal patients with pseudoaneurysm or arteriovenous fistula. Relative contraindications to endovascular repair include vessel transection, luminal thrombus, compressive symptoms from a large hematoma, and concomitant injuries requiring exploration, including aerodigestive injuries.

Subclavian Injury Epidemiology, Presentation, and Diagnosis Penetrating subclavian artery injuries account for 1% to 2% of vascular trauma and have mortality rates ranging from 5% to 35%. Three quarters of injuries are the result of penetrating wounds (e.g., gunshot), and 25% are from blunt mechanisms. Patients with subclavian artery injuries commonly have at least one other associated injury, most commonly the vein or brachial plexus. Penetrating subclavian injuries that result in vessel disruption or occlusion manifest with hard signs such as hemorrhage, expanding hematoma, bruit, or distal ischemia. Less severe injuries can manifest with soft signs such as nonexpanding hematoma, transient hypotension, or an injury tract that is next to the subclavian artery. Collateral circulation to the arm might allow a palpable pulse on examination despite a subclavian artery injury. If there are signs or suspicion of injury, the simplest method of diagnosis is blood pressure measurements in both arms. Using this maneuver, the injured extremity index (i.e., systolic pressure of the injured arm divided by the systolic pressure of the uninjured arm) should be greater than 0.9. Repeated measurements of less than 0.9 indicate a flow-limiting arterial injury to the arm. With or without signs of injury, contrast CT is the favored mode of evaluating patients with penetrating trauma to the torso and cervical region. CT or arteriography is especially indicated if there are signs of arterial injury. Standard arteriography may be useful as a first diagnostic step if there is suspicion for an injury that may be amenable to endovascular treatment.

larger defects, interposition grafts with saphenous vein or, more commonly, synthetic conduit are necessary. The subclavian artery can be ligated as a damage-control maneuver and may be tolerated because of the extensive collateral flow around the shoulder girdle to the arm. Endovascular Management Catheter-based treatment of subclavian artery injuries has become increasingly common. This technique uses covered stents to bridge the arterial disruption and can require a combination of transfemoral and retrograde transbrachial arterial access. To date, endovascular techniques have been applied mostly in patients who are hemodynamically normal and able to undergo angiography for diagnostic purposes and then placement of the covered stent. These patients most often have an injury that manifests as pseudoaneurysm, arteriovenous fistula, or partial transection. For endovascular treatment to be considered there must be adequate proximal and distal landing zones remote from the injury itself. When considering endovascular management of subclavian injury, one must also be aware of the origin of the vertebral and internal mammary arteries. As long as the mammary artery has not been used as inflow for coronary artery bypass grafting, its origin may be covered without significant morbidity. However, the origin of the vertebral artery should not be covered during endovascular repair of subclavian injuries unless the vertebral artery is small and nondominant and there are no other options. Outcomes Morbidity and mortality of subclavian artery injury depend on mechanism of injury, hemodynamics on presentation, and concomitant injuries. Hypotension on arrival is associated with 57% mortality, and patients with three or more injuries have a fivefold increase in mortality. Shock and intraoperative exsanguination account for the majority of early deaths, followed by multiple organ failure in the postoperative period. In patients who survive, brachial plexus injury (20%–43%) resulting from the original trauma or the operative repair is the main source of morbidity. Early complications after endovascular repair include access site hematoma, pseudoaneurysm formation, graft thrombosis, and cerebral embolization. One study examining outcomes 48 months after stent-graft repair of subclavian injury found restenosis and occlusion to be the two most common. In this study, in-stent restenosis was successfully managed with endovascular intervention, and occlusions were treated without reoperation with no adverse outcome.

Common Carotid Injury

Open Operative Management

Epidemiology, Presentation, and Diagnosis

The approach to subclavian artery injury depends upon the patient’s hemodynamic status. Patients in shock or extremis require an emergent operation, whereas those who are hemodynamically normal have time for CT imaging and consideration of open versus endovascular operation. Complete exposure of the right subclavian artery requires a median sternotomy with or without extension to the supraclavicular space (see Figure 1). The proximal left subclavian artery is exposed and controlled through a left anterior lateral thoracotomy. The middle segment of the artery lies behind the anterior scalene muscle and can be approached via a supraclavicular incision on the right and the left side. The clavicle can be removed to help expose the injury. However, this carries significant morbidity and is often not necessary if one uses a combination of supra- and infraclavicular incisions to control the mid- and distal subclavian artery, respectively. The specific method of repair depends on the appearance of the vessel and surrounding injuries. Primary end-to-end repair is uncommon but may be undertaken after débridement of the damaged segments as long as the vessel is long enough. For injuries with

Penetrating injury to the common carotid in the thorax is rare, because this segment of artery is short. Most studies group injury to this arterial segment with those to the cervical carotid or those to the aortic arch and great vessels. Unlike the innominate and subclavian arteries, which are more fixed or adjacent to the clavicle, the common carotids are relatively mobile and therefore less prone to blunt injury. Thus, more than 90% of injuries are a result of penetrating causes. Hard signs of common carotid injury include hemorrhage, expanding hematoma, bruit, or stroke. Less severe injuries may be present with soft signs such as nonexpanding hematoma, transient hypotension, or proximal injury tract. Open Operative Management Operative approach to intrathoracic common carotid injury is through a median sternotomy. The right carotid originates from the innominate artery in most cases, and approach to this segment is the same as described for the innominate artery. In the setting of normal

Open and Endovascular Management of Blunt and Penetrating Nonaortic Abdominal Vascular Injury

arch anatomy, the left common carotid is the last arch branch vessel that can be exposed through a median sternotomy. In the case of common carotid injuries, the median sternotomy needs to be extended to a longitudinal cervical incision along the border of the sternocleidomastoid muscle (see Figure 1). Similar to other arterial segments, the method of common carotid repair depends on the appearance of the vessel. Primary or end-toend repair is uncommon but may be undertaken after débridement of the segment as long as vessel length is sufficient and full-thickness closure can be achieved. For injuries with larger defects interposition grafts with saphenous vein, or more commonly, synthetic conduit are necessary. Synthetic grafts such as expanded polytetrafluoroethylene (ePTFE) or Dacron are better suited for common carotid artery repair than saphenous vein because of their cylindrical construct with memory and size matching. Temporary vascular shunts should be considered in repair of common carotid injuries to limit cerebral ischemia. However, for the most proximal injuries, shunts might not be practical because there is a risk of losing control of the vessel at the aortic arch during shunt placement. In these instances it may be best to clamp the carotid at the origin of the aortic arch and sew quickly rather than risk losing control of the artery at the aortic arch. Unlike in repair of the subclavian, systemic anticoagulation should be used during repair of carotid artery lesions if at all possible. Endovascular Management The challenging nature of open common carotid exposure in the chest makes endovascular treatment appealing. This is particularly true because the common carotid is relatively long and has no branches, a fact that increases the likelihood of acceptable seal or landing zones for the covered stent. Endovascular treatment of common carotid injuries can also result in less cerebral ischemic time

Open and Endovascular Management of Blunt and Penetrating Nonaortic Abdominal Vascular Injury Jonathan L. Eliason

Abdominal vascular trauma is quite infrequent within the broader context of all traumatic injuries. However, these injuries can have high morbidity and mortality. Their significant heterogeneity in acuity of presentation, associated morbidity, and recommended management styles make an algorithmic approach to their treatment more challenging. Several arbitrary distinctions facilitate the review of abdominal vascular trauma, such as whether it is primarily arterial or venous, if it has a blunt or penetrating mechanism, and whether the management strategy is open or endovascular.

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than reconstruction using interposition graft. However, similar to the innominate, the proximal portions of the common carotid arteries can be difficult to image with precision, and endovascular repair of this segment should only be attempted by institutions with experience, good imaging capability, and good inventory.

Selected References Carrick MM, Morrison CA, Pham HQ, et al: Modern management of traumatic subclavian artery injuries: A single institution’s experience in the evolution of endovascular repair, Am J Surg 199:28–34, 2010. DuBose JJ, Rajani R, Gilani R, et al: The Endovascular Skills for Trauma and Resuscitative Surgery (ESTARS) Working Group. Endovascular management of axillo-subclavian arterial injury: A review of published experience, Injury 43:1785–1792, 2012. Du Toit DF, Lambrechts A, Stark H, et al: Long-term results of stent graft treatment of subclavian artery injuries: Management of choice for stable patients? J Vasc Surg 47:739–743, 2008. Du Toit DF, Odendaal W, Lambrechts A, et al: Surgical and endovascular management of penetrating innominate artery injuries, Eur J Vasc Endovasc Surg 36:56–62, 2008. Hoffberger JD, Rossi H, Keen R, et al: Penetrating trauma to the aortic arch: A case report, J Trauma 58:381–383, 2005. Hoffer EK: Endovascular intervention in thoracic arterial trauma, Injury 39:1257–1274, 2008. Johnston Jr RH, Wall MJ, Mattox KL: Innominate artery trauma, a thirty year experience, J Vasc Surg 17:134–139, 1993. Markov NP, DuBose JJ, Scott D, et al: Anatomic distribution and mortality of arterial injury in the wars in Afghanistan and Iraq with comparison to a civilian standard, J Vasc Surg 56:728–736, 2012. Mattox KL, Feliciano DV, Burek J, et al: Five thousand seven hundred sixty cardiovascular injuries in 4459 patients, Ann Surg 209:698–707, 1989. Pate JW, Cole Jr FH, Walker WA, et al: Penetrating injuries of the aortic arch and its branches, Ann Thoracic Surg 55:586–592, 1993.

ZONES OF INJURY Most major vascular structures within the abdomen are retroperitoneal, and therefore the retroperitoneal zone that contains them can also aid in understanding basic management paradigms. There are three retroperitoneal zones (Figure 1). Zone I extends from the aortic hiatus to the sacral promontory and includes the midline vascular structures (aorta and vena cava). Zone II includes the retroperitoneal structures within the paracolic gutters (kidneys, renal artery, renal vein), and zone III includes the pelvic retroperitoneum (iliac arteries and veins). If major vascular injury occurs within zone I, as evidenced by active bleeding or large hematoma, the injury should be explored and repaired regardless of whether it resulted from a blunt or penetrating mechanism. For retroperitoneal hematomas in zones II and III, typical management includes operative exploration if the mechanism is penetrating and nonexploratory management if the mechanism is blunt, including observation, urologic evaluation, or angioembolization. Pelvic fixation for unstable fractures is a critical component for safe management of zone III trauma to limit hematoma expansion or a worsening of the vascular injury.

VENA CAVA INJURIES Major injury to the inferior vena cava (IVC) is a highly lethal event, especially when involving the retrohepatic region. Surgical treatment has primarily involved open techniques. Compression of the vena

Open and Endovascular Management of Blunt and Penetrating Nonaortic Abdominal Vascular Injury

arch anatomy, the left common carotid is the last arch branch vessel that can be exposed through a median sternotomy. In the case of common carotid injuries, the median sternotomy needs to be extended to a longitudinal cervical incision along the border of the sternocleidomastoid muscle (see Figure 1). Similar to other arterial segments, the method of common carotid repair depends on the appearance of the vessel. Primary or end-toend repair is uncommon but may be undertaken after débridement of the segment as long as vessel length is sufficient and full-thickness closure can be achieved. For injuries with larger defects interposition grafts with saphenous vein, or more commonly, synthetic conduit are necessary. Synthetic grafts such as expanded polytetrafluoroethylene (ePTFE) or Dacron are better suited for common carotid artery repair than saphenous vein because of their cylindrical construct with memory and size matching. Temporary vascular shunts should be considered in repair of common carotid injuries to limit cerebral ischemia. However, for the most proximal injuries, shunts might not be practical because there is a risk of losing control of the vessel at the aortic arch during shunt placement. In these instances it may be best to clamp the carotid at the origin of the aortic arch and sew quickly rather than risk losing control of the artery at the aortic arch. Unlike in repair of the subclavian, systemic anticoagulation should be used during repair of carotid artery lesions if at all possible. Endovascular Management The challenging nature of open common carotid exposure in the chest makes endovascular treatment appealing. This is particularly true because the common carotid is relatively long and has no branches, a fact that increases the likelihood of acceptable seal or landing zones for the covered stent. Endovascular treatment of common carotid injuries can also result in less cerebral ischemic time

Open and Endovascular Management of Blunt and Penetrating Nonaortic Abdominal Vascular Injury Jonathan L. Eliason

Abdominal vascular trauma is quite infrequent within the broader context of all traumatic injuries. However, these injuries can have high morbidity and mortality. Their significant heterogeneity in acuity of presentation, associated morbidity, and recommended management styles make an algorithmic approach to their treatment more challenging. Several arbitrary distinctions facilitate the review of abdominal vascular trauma, such as whether it is primarily arterial or venous, if it has a blunt or penetrating mechanism, and whether the management strategy is open or endovascular.

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than reconstruction using interposition graft. However, similar to the innominate, the proximal portions of the common carotid arteries can be difficult to image with precision, and endovascular repair of this segment should only be attempted by institutions with experience, good imaging capability, and good inventory.

Selected References Carrick MM, Morrison CA, Pham HQ, et al: Modern management of traumatic subclavian artery injuries: A single institution’s experience in the evolution of endovascular repair, Am J Surg 199:28–34, 2010. DuBose JJ, Rajani R, Gilani R, et al: The Endovascular Skills for Trauma and Resuscitative Surgery (ESTARS) Working Group. Endovascular management of axillo-subclavian arterial injury: A review of published experience, Injury 43:1785–1792, 2012. Du Toit DF, Lambrechts A, Stark H, et al: Long-term results of stent graft treatment of subclavian artery injuries: Management of choice for stable patients? J Vasc Surg 47:739–743, 2008. Du Toit DF, Odendaal W, Lambrechts A, et al: Surgical and endovascular management of penetrating innominate artery injuries, Eur J Vasc Endovasc Surg 36:56–62, 2008. Hoffberger JD, Rossi H, Keen R, et al: Penetrating trauma to the aortic arch: A case report, J Trauma 58:381–383, 2005. Hoffer EK: Endovascular intervention in thoracic arterial trauma, Injury 39:1257–1274, 2008. Johnston Jr RH, Wall MJ, Mattox KL: Innominate artery trauma, a thirty year experience, J Vasc Surg 17:134–139, 1993. Markov NP, DuBose JJ, Scott D, et al: Anatomic distribution and mortality of arterial injury in the wars in Afghanistan and Iraq with comparison to a civilian standard, J Vasc Surg 56:728–736, 2012. Mattox KL, Feliciano DV, Burek J, et al: Five thousand seven hundred sixty cardiovascular injuries in 4459 patients, Ann Surg 209:698–707, 1989. Pate JW, Cole Jr FH, Walker WA, et al: Penetrating injuries of the aortic arch and its branches, Ann Thoracic Surg 55:586–592, 1993.

ZONES OF INJURY Most major vascular structures within the abdomen are retroperitoneal, and therefore the retroperitoneal zone that contains them can also aid in understanding basic management paradigms. There are three retroperitoneal zones (Figure 1). Zone I extends from the aortic hiatus to the sacral promontory and includes the midline vascular structures (aorta and vena cava). Zone II includes the retroperitoneal structures within the paracolic gutters (kidneys, renal artery, renal vein), and zone III includes the pelvic retroperitoneum (iliac arteries and veins). If major vascular injury occurs within zone I, as evidenced by active bleeding or large hematoma, the injury should be explored and repaired regardless of whether it resulted from a blunt or penetrating mechanism. For retroperitoneal hematomas in zones II and III, typical management includes operative exploration if the mechanism is penetrating and nonexploratory management if the mechanism is blunt, including observation, urologic evaluation, or angioembolization. Pelvic fixation for unstable fractures is a critical component for safe management of zone III trauma to limit hematoma expansion or a worsening of the vascular injury.

VENA CAVA INJURIES Major injury to the inferior vena cava (IVC) is a highly lethal event, especially when involving the retrohepatic region. Surgical treatment has primarily involved open techniques. Compression of the vena

674 VASCULAR TRAUMA

1

2

2

3

FIGURE 2  Laceration of the inferior vena cava with proximal and

distal compression using sponge sticks. 

FIGURE 1  Retroperitoneal zones and their associated vascular

structures.  (From Selivanov V, Chi HS, Alverdy JC, et al: Mortality in retroperitoneal hematoma, J Trauma 24:1022–1027, 1984, with permission.)

cava proximally and distally is an important part of hemorrhage control, with sponge-sticks being a useful adjunct in this regard (Figure 2). Even with adequate compression, hemorrhage can be significant as a result of renal and lumbar venous bleeding. The surgeon must be ready to make the initial repair the definitive repair, because suture laceration of the vein can easily convert a manageable injury to one that is complex or stellate. Allis clamps can aid in the repair of linear caval injuries and facilitate suture placement in a relatively bloodless field (Figure 3). Lacerations and puncture wounds should be sutured using permanent monofilament suture. The author recommends 4–0 nonabsorbably polypropylene monofilament (Prolene) suture on an SH needle, which may be manually straightened to lengthen the throw on the needle and enhance control. Using Teflon felt or skeletal muscle pledgets can aid in hemostasis if the vein wall is friable or if initial suture attempts pull through the vein wall. Retrohepatic injury presents a unique clinical problem that is one of the most lethal encountered by vascular and trauma surgeons. Total vascular isolation in this setting was described by Heaney and colleagues and is specifically designed for this injury pattern. The steps in this strategy for controlling retrohepatic IVC injuries consist of clamping the aorta just below the diaphragmatic hiatus; encircling the hepatic artery, portal vein, and common bile duct with an umbilical tape for en-mass clamping; encircling the IVC just above the renal veins with an umbilical tape; and controlling the suprahepatic IVC, just above the diaphragm in children and intrapericardially in adults. Endovascular control of IVC injuries has been relegated to case reports. Nevertheless, in the setting of major venous bleeding from the IVC, transfemoral venous sheath placement with subsequent inflation of a large vessel-occlusion balloon such as the CODA (Cook Medical, Bloomington, IN) or Reliant (Medtronic, Fridley, MN)

FIGURE 3  Multiple Allis clamp placement on a linear inferior vena cava

laceration facilitates suture repair. 

below or across the region of IVC injury can aid in hemorrhage control. Adequate accessible endovascular inventory, radiolucent surgical table, and imaging capabilities with either a fixed system or C-arm are essential for using these adjuncts.

CELIAC ARTERY INJURIES Direct injuries to the celiac artery are exceptionally infrequent. Limited series and single case reports that do exist suggest this is

Open and Endovascular Management of Blunt and Penetrating Nonaortic Abdominal Vascular Injury

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an injury associated with a high mortality rate. This is likely due in large part to patients who come to the hospital in extremis, rather than the actual difficulty of the surgical exposure and management of such injuries. Ligation is recommended for the patient in extremis to avoid time-consuming repairs. This is often tolerated because of the collateral circulation from the superior mesenteric artery (SMA) through the gastroduodenal and pancreaticoduodenal arterial collaterals. In spite of these often rich arterial collaterals, gallbladder necrosis has been reported following celiac artery ligation, so a low threshold for cholecystectomy should exist in the post-ligation period if a clinical suspicion of gallbladder ischemia and acalculous cholecystitis exists.

HEPATIC ARTERY INJURIES Isolated hepatic artery ligation for perihepatic hemorrhage has been a safe and effective method for controlling bleeding when concomitant major hepatic vein and vena cava injuries are excluded. Angiographic embolization can accomplish the same results in many cases with potential avoidance of a laparotomy. In some instances, embolization is most effective following an exploratory laparotomy during which perihepatic packing has been the initial treatment. Complications of hepatic artery ligation or embolization are infrequent but have been well described. In a retrospective review, 79 patients had a 16% mortality and 20% hepatic-related morbid complication rate after undergoing hepatic artery angiography and/or embolization for traumatic injuries, when they had a blush seen on computed tomography (CT), had a high-grade liver injury, or exhibited hemodynamic instability. The spectrum of complications following hepatic artery ligation can include hepatic necrosis, acalculous cholecystitis, or even acute or chronic liver failure.

PORTAL VEIN INJURIES Portal vein injuries are uncommon, but they are accompanied by mortality rates ranging from 39% to 71%. Penetrating mechanisms account for 90% of portal vein injuries. Affecting these high mortality rates are concomitant major vascular injuries in 70% to 90% of cases, including those of the inferior vena cava, aorta, SMA, and renal vessels. A complete vascular exploration is therefore indicated when a portal vein injury is identified. When exploring portal vein injuries, life-threatening hemorrhage can ensue. Techniques for decreasing portal venous blood flow and obtaining vascular control include simultaneous aortic clamping above the celiac axis and below the renal arteries, and balloon occlusion catheters when inadequate exposure of the injury limits formal vascular clamp placement. When the patient’s stability and adequate exposure are obtained, lateral venorrhaphy or interposition vein grafting may be pursued. In more severe wounding patterns and in patients with profound hemodynamic impairment, ligation of the portal vein may be a lifesaving maneuver. In a retrospective analysis using this strategy, authors stated that “whenever lateral repair was impossible or impractical [ligation] was successful.”

SUPERIOR MESENTERIC ARTERY INJURIES More than 55% of patients with traumatic SMA injury survive. Management of more distal injuries may be explored through the mesentery, and proximal injuries are typically exposed using left medial visceral rotation (Figure 4). Surgical management occurs primarily

FIGURE 4  Left medial visceral rotation for exposure of the proxi-

mal superior mesenteric artery. 

for exsanguinating hemorrhage. Bowel necrosis may be present at the time of exploration, and it can occur following reconstruction. Open surgical management has been the mainstay, although endovascular management of SMA injury has been reported. This most commonly includes covered stent graft placement for traumatic arteriovenous fistulas involving the SMA, and it appears effective in fistula closure.

RENAL ARTERY INJURIES Perhaps the nonaortic abdominal vascular injury most likely to undergo an endovascular intervention is blunt injury to the renal artery. Unfortunately, interpretation of these reports is limited by the lack of prospective cohort studies in the literature. Blunt renal artery injuries are more common than penetrating injuries and often result in renal malperfusion, and they can progress to kidney loss or, in some cases, can induce a flow-limiting stenosis that can cause renovascular hypertension. Open repair is difficult and often fraught with incomplete or failed revascularization and prolonged renal ischemia. Nonoperative management is therefore typical. Angiographic evaluation provides an excellent diagnostic tool, and in cases where the injury results in a dissection or focal occlusion, it can provide the platform for stent expansion of the renal artery and restoration of renal artery flow. Although such therapy has been widely reported, the prevalence of endovascular treatment resulting in incomplete revascularization or failure is unknown, and some express doubts regarding the overall efficacy of this therapy. Penetrating injuries to the renal artery most commonly result in exploration to control hemorrhage. Renal artery ligation with or without nephrectomy or attempted immediate arterial repair are the typical management strategies. The stability of the patient is the most important factor in whether arterial repair is attempted. A more aggressive approach toward kidney salvage is prudent in patients with solitary kidneys or bilateral renal artery injuries.

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Selected References Accola KD, Feliciano DV, Mattox KL, et al: Management of injuries to the superior mesenteric artery, J Trauma 26:313–319, 1986. Buckman RF, Pathak AS, Badellino MM, et al: Portal vein injuries, Surg Clin North Am 81:1449–1462, 2001. Feliciano DV: Approach to major abdominal vascular injury, J Vasc Surg 7:730–736, 1988. Graham JM, Mattox KL, Beall Jr AC, et al: Injuries to the visceral arteries, Surgery 84:835–839, 1978. Heaney JP, Jacobson A: Simplified control of upper abdominal hemorrhage from the vena cava, Surgery 78:138–141, 1975.

Aortic Injury Thomas J. Percival and Todd E. Rasmussen

Aortic trauma is typically fatal, with 80% of mortality occurring at the scene of injury. Recent improvements in prehospital care, decreases in transport times, and improvement in diagnosis have increased the opportunity for patients to undergo operative intervention. The management of patients with aortic trauma has undergone a paradigm shift. Historically, recommendations were that all aortic trauma should be repaired immediately upon diagnosis, but this doctrine is changing to allow observation or delayed repair in selected cases. A shift in the operative management of this injury pattern has also occurred, and less invasive endovascular options are available for some patients in lieu of open repair.

Lee JT, White RA: Endovascular management of blunt traumatic renal artery dissection, J Endovasc Ther 9:354–358, 2002. Misselbeck TS, Teicher EJ, Cipolle MD, et al: Hepatic angioembolization in trauma patients: Indications and complications, J Trauma 67:769–773, 2009. Rubin BE, Katzen BT: Selective hepatic artery embolization to control massive hepatic hemorrhage after trauma, AJR Am J Roentgenol 129:253–256, 1977. Selivanov V, Chi HS, Alverdy JC, et al: Mortality in retroperitoneal hematoma, J Trauma 24:1022–1027, 1984. Simeone A, Demlow T, Karmy-Jones R: Endovascular repair of a traumatic renal artery injury, J Trauma 70:1300, 2011.

the direct, indirect, deceleration, compression, and blast forces that produce aortic rupture. Direct forces include displacement of the vertebrae that cause rupture of the aorta by shearing forces. Indirect forces act through a sudden and significant increase of pressure within the aorta. Experiments have been performed, and the pressure to burst the aorta by this mechanism has been shown to be as high as 2500 mm Hg. Deceleration forces such as those often sustained in automobile crashes are the most common cause of blunt aortic rupture as a result of the stress and strain placed on the aorta at the ligamentum arteriosum. At this location, it is likely a combination of these forces that causes first aortic wall tear and then rupture. Of victims who suffer aortic rupture, approximately 70% have been shown to be involved in a broadside or head-on collision, suggesting that rupture involves lateral oblique compression of the chest, causing numerous different force vectors.

INCIDENCE Aortic trauma is most common in men between the ages of 20 and 40 years. In 1989, Mattox and colleagues reported that 90% of cardiovascular trauma was caused by penetrating mechanisms and only 7% was caused by blunt injury. The descending thoracic aorta is the one anatomic location where blunt mechanism is nearly as common (44%) as penetrating trauma (56%). The higher incidence of injury in the descending thoracic aorta is as a result of its relatively fixed nature at the ligamentum arteriosum, which, as the remnant of the ductus arteriosus, connects the pulmonary artery to the inferior surface of the aortic arch. In cases of thoracic trauma with significant deceleration, this anatomic relationship predisposes the proximal portion of the descending thoracic aorta to tears in the wall of the vessel (Figure 1). Overall, blunt aortic trauma only accounts for 0.3% of all trauma. Automobile accidents account for the majority of those causes, followed by pedestrian–versus–motor vehicle accidents. In the abdominal aorta, the leading cause of injury is penetrating mechanism, which represents 88% to 95% of the injury pattern. In the conflicts in Iraq and Afghanistan, aortic trauma accounted for 2.9% of all vascular injuries, and the primary mechanism was explosions or gunshot wounds. FIGURE 1  Arteriographic image of a blunt thoracic aortic injury just

PATHOPHYSIOLOGY The majority of blunt aortic injuries occur at the aortic isthmus, which is an area of slight constriction immediately distal to the left subclavian artery origin at the point of attachment of the ligamentum arteriosum (see Figure 1). In a classic 1958 report, Parmley described

beyond the origin of the left subclavian artery. This is an example of a type III or pseudoaneurysm as described per the Starnes classification system. Note the disruption in the external aortic contour.  (From Propper BW, Alley JB, Gifford SM, et al: Endovascular treatment of a blunt aortic injury in Iraq: Extension of innovative endovascular capabilities to the modern battlefield, Ann Vasc Surg 23:687.e19–e22, 2009.)

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Selected References Accola KD, Feliciano DV, Mattox KL, et al: Management of injuries to the superior mesenteric artery, J Trauma 26:313–319, 1986. Buckman RF, Pathak AS, Badellino MM, et al: Portal vein injuries, Surg Clin North Am 81:1449–1462, 2001. Feliciano DV: Approach to major abdominal vascular injury, J Vasc Surg 7:730–736, 1988. Graham JM, Mattox KL, Beall Jr AC, et al: Injuries to the visceral arteries, Surgery 84:835–839, 1978. Heaney JP, Jacobson A: Simplified control of upper abdominal hemorrhage from the vena cava, Surgery 78:138–141, 1975.

Aortic Injury Thomas J. Percival and Todd E. Rasmussen

Aortic trauma is typically fatal, with 80% of mortality occurring at the scene of injury. Recent improvements in prehospital care, decreases in transport times, and improvement in diagnosis have increased the opportunity for patients to undergo operative intervention. The management of patients with aortic trauma has undergone a paradigm shift. Historically, recommendations were that all aortic trauma should be repaired immediately upon diagnosis, but this doctrine is changing to allow observation or delayed repair in selected cases. A shift in the operative management of this injury pattern has also occurred, and less invasive endovascular options are available for some patients in lieu of open repair.

Lee JT, White RA: Endovascular management of blunt traumatic renal artery dissection, J Endovasc Ther 9:354–358, 2002. Misselbeck TS, Teicher EJ, Cipolle MD, et al: Hepatic angioembolization in trauma patients: Indications and complications, J Trauma 67:769–773, 2009. Rubin BE, Katzen BT: Selective hepatic artery embolization to control massive hepatic hemorrhage after trauma, AJR Am J Roentgenol 129:253–256, 1977. Selivanov V, Chi HS, Alverdy JC, et al: Mortality in retroperitoneal hematoma, J Trauma 24:1022–1027, 1984. Simeone A, Demlow T, Karmy-Jones R: Endovascular repair of a traumatic renal artery injury, J Trauma 70:1300, 2011.

the direct, indirect, deceleration, compression, and blast forces that produce aortic rupture. Direct forces include displacement of the vertebrae that cause rupture of the aorta by shearing forces. Indirect forces act through a sudden and significant increase of pressure within the aorta. Experiments have been performed, and the pressure to burst the aorta by this mechanism has been shown to be as high as 2500 mm Hg. Deceleration forces such as those often sustained in automobile crashes are the most common cause of blunt aortic rupture as a result of the stress and strain placed on the aorta at the ligamentum arteriosum. At this location, it is likely a combination of these forces that causes first aortic wall tear and then rupture. Of victims who suffer aortic rupture, approximately 70% have been shown to be involved in a broadside or head-on collision, suggesting that rupture involves lateral oblique compression of the chest, causing numerous different force vectors.

INCIDENCE Aortic trauma is most common in men between the ages of 20 and 40 years. In 1989, Mattox and colleagues reported that 90% of cardiovascular trauma was caused by penetrating mechanisms and only 7% was caused by blunt injury. The descending thoracic aorta is the one anatomic location where blunt mechanism is nearly as common (44%) as penetrating trauma (56%). The higher incidence of injury in the descending thoracic aorta is as a result of its relatively fixed nature at the ligamentum arteriosum, which, as the remnant of the ductus arteriosus, connects the pulmonary artery to the inferior surface of the aortic arch. In cases of thoracic trauma with significant deceleration, this anatomic relationship predisposes the proximal portion of the descending thoracic aorta to tears in the wall of the vessel (Figure 1). Overall, blunt aortic trauma only accounts for 0.3% of all trauma. Automobile accidents account for the majority of those causes, followed by pedestrian–versus–motor vehicle accidents. In the abdominal aorta, the leading cause of injury is penetrating mechanism, which represents 88% to 95% of the injury pattern. In the conflicts in Iraq and Afghanistan, aortic trauma accounted for 2.9% of all vascular injuries, and the primary mechanism was explosions or gunshot wounds. FIGURE 1  Arteriographic image of a blunt thoracic aortic injury just

PATHOPHYSIOLOGY The majority of blunt aortic injuries occur at the aortic isthmus, which is an area of slight constriction immediately distal to the left subclavian artery origin at the point of attachment of the ligamentum arteriosum (see Figure 1). In a classic 1958 report, Parmley described

beyond the origin of the left subclavian artery. This is an example of a type III or pseudoaneurysm as described per the Starnes classification system. Note the disruption in the external aortic contour.  (From Propper BW, Alley JB, Gifford SM, et al: Endovascular treatment of a blunt aortic injury in Iraq: Extension of innovative endovascular capabilities to the modern battlefield, Ann Vasc Surg 23:687.e19–e22, 2009.)

Aortic Injury

PRESENTATION AND DIAGNOSIS The majority of those who suffer blunt aortic injury die at the scene; approximately 60% die within 30 minutes and only 6% to 8% live longer than 4 hours. In studies of this injury pattern, of patients who survived to arrival at the hospital, 76% lived past the triage phase of care. Patients who suffer abdominal aortic injuries also have a high mortality rate. To improve survival following this injury pattern, consistent and rapid prehospital care and retrieval from point of injury is required, as are early injury detection methods. Patients who have sustained penetrating torso trauma and who are hemodynamically unstable should receive measured hypotensive resuscitation and undergo immediate surgical control of the bleeding. Such patients need to be recognized early and treated in an expeditious fashion to maximize chance of survival. For patients who arrive to the emergency department hemodynamically normal, the classic treatment algorithm includes radiographic evaluation. After primary and secondary survey, evaluation of trauma patients with significant mechanism of injury should include a chest radiograph. Signs indicating the need for further aortic imaging include a widened mediastinum (>8 cm); fractured sternum, first rib, or multiple ribs; obscured aortic knob; deviation of the left main stem bronchus or nasogastric tube; and opacification of the aortopulmonary window and widened paraspinal line. If an upright chest x-ray is negative, it has a negative predictive value of 95%. In cases of significant trauma, patients who remain hemodynamically normal undergo contrast-enhanced computed tomography (CT) of the aorta. In most studies, aortic CT has been shown to have near 100% sensitivity and negative predictive value (Figure 2). If the CT scan raises question of an aortic injury, traditional contrast aortography is indicated (see Figure 1). Recognizing that not all blunt aortic injuries are the same, Starnes and colleagues have performed multiple studies to advance understanding of the natural history based on CT imaging. Specifically, this group created a novel classification system based on the presence or absence of aortic external contour abnormality, defined as an alteration in the symmetric, round shape of the aorta (Box 1). The grades of aortic injury are intimal tear without an external contour abnormality

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and an intimal defect and or thrombus of less than 10 mm of length or width; large intimal flap without an external contour abnormality and intimal defect and/or thrombus of greater than 10 mm of length or width; pseudoaneurysm with an external contour abnormality and contained rupture; and rupture with an aortic external contour abnormality and contrast extravasation. This grading allows one to characterize mortality and make recommendations regarding the timing of appropriate management strategies for patients with blunt aortic injury. Other imaging modalities that have been used to diagnose aortic injury include magnetic resonance angiography (MRA) and transesophageal echocardiography. MRA is useful for patients with contrast allergies as well as repeat scans in a short period for surveillance. Transesophageal echocardiography has fallen out of favor as a diagnostic tool owing to lack of availability and user variability associated with its performance.

TIMING OF REPAIR Penetrating aortic trauma requires immediate surgical repair in nearly all circumstances. In contrast, blunt aortic injury does not have a clearly defined time to operation. As published by Nagy and colleagues, the Eastern Association for the Surgery of Trauma (EAST) management guidelines of blunt aortic injury state “prompt repair of the blunt aortic injury is preferred. If the patient has more immediately life-threatening injuries that require intervention such as emergent laparotomy or craniotomy, or if the patient is a poor operative candidate because of age or co-morbidities, the aortic repair may be delayed. Medical control of blood pressure is advised until surgical repair can be accomplished.” Delayed aortic repair beyond 24 hours is now an acceptable treatment plan because of observations of improved mortality. In fact, Demetriades and the American Association for the Surgery of Trauma (AAST) study group reported that the mean time to aorta repair in a contemporary cohort of patients with blunt injury was more than 50 hours. In nearly all cases in which a patient is determined to have a blunt aortic injury, it is recommended that antihypertensive medications be initiated. The first-line medication is a β-blocker (esmolol), with a target systolic blood pressure of 90 to 100 mm Hg and a heart rate of less than 100 beats/min. If these targets are unattainable with a single-agent β-blocker, then a vasodilator should be added, which is commonly nitroprusside or a calciumchannel blocker. Judicious use of hypotensive resuscitation and careful initiation of antihypertensive medication in patients with the diagnosis

BOX 1:  Computed Tomography Classification of Blunt Aortic Injury

Intimal Tear

Normal external aortic contour Intimal tear or thrombus 10 mm FIGURE 2  Contrast computed tomography image of the same blunt

thoracic aortic injury shown in Figure 1. Note again the loss in normal external aortic contour and contained pseudoaneurysm. Also note that there is no free extravasation of contrast in the left thorax.  (From Propper BW, Alley JB, Gifford SM, et al: Endovascular treatment of a blunt aortic injury in Iraq: Extension of innovative endovascular capabilities to the modern battlefield, Ann Vasc Surg 23:687.e19–e22, 2009.)

Pseudoaneurysm

Disrupted external aortic contour with contained pseudoaneurysm

Rupture

Disrupted external aortic contour with contrast extravasation From Starnes BW, Lundgren RS, Gunn M, et al: A new classification scheme for treating blunt aortic injury, J Vasc Surg 55:47–54, 2012.

678 VASCULAR TRAUMA of blunt aortic injury has reduced the rate of early in-hospital rupture. Demetriades and colleagues reported that the delayed repair of blunt aortic injury in patients with multiple concomitant injuries was associated with improved survival. In contrast, the rate of complications was higher in patients with no associated injuries (isolated blunt aortic injury) who underwent delayed repair. The same study demonstrated greater lengths of intensive care unit (ICU) and hospital stays in the cohort undergoing delayed repair of blunt aortic injury. Findings from this and similar studies confirm that delayed repair of blunt aortic injury is safe and effective in a select group of patients. As more is learned about the natural history of the spectrum of blunt aortic injury, a set of patients with minimal injury on CT has been identified in whom nonoperative management is the preferred option.

OPERATIVE REPAIR The basic principles of open operative and endovascular surgery apply to repair of aortic injury. For open operative techniques, this includes exposure of the aorta and control of the vessel proximal and distal to the damaged artery and major branch vessels. For endovascular repair, these principles include adequate arterial access and positioning of the delivery sheath to allow deployment of a covered stent graft across the area of injury without causing significant side branch occlusion and ischemia. The options for open reconstruction of aortic injury include primary repair, patch angioplasty, and repair with an interposition graft. Endovascular aortic repair is typically accomplished with placement of a covered stent graft.

Open Thoracic Technique The open approach is taken through the left fourth intercostal space with an anteriolateral thoracotomy. Once the chest is exposed and one-lung ventilation is instituted, proximal control is obtained between the left common carotid artery and the left subclavian artery, with a separate clamp for the left subclavian artery. Special care should be taken to identify the phrenic and vagus nerves because their location may be distorted by hematoma. The ligamentum arteriosum should be divided sharply, and surrounding structures should be bluntly dissected to improve proximal exposure. Care should be taken not to clamp the esophagus or damage bronchial structures. Once proximal control is obtained, distal control should be obtained as proximal as possible to the injury to maximize spinal cord perfusion. A shift in standard of care has occurred: The majority of thoracic repairs are performed while patients have some mechanism of distal aortic perfusion or even cardiopulmonary bypass, as opposed to the clamp-and-sew technique. Previously, clamp-andsew was the common method, but several series indicated a higher risk of paraplegia with this technique if clamp times were greater than 30 minutes. The most common form of distal aortic perfusion is the left atrium to femoral or distal aortic bypass using an active roller pump. Full anticoagulation is not necessary for this form of distal aortic perfusion, but it is necessary if full cardiopulmonary bypass is chosen. Other options to mitigate paraplegia include lumbar drain placement and/or hypothermia. Unlike the elective open repair of thoracic or thoracoabdominal aortic aneurysms, many of these adjuncts are not feasible or available in the setting of trauma. Repair of the aorta can then be completed primarily using 3–0 nonabsorbable polypropylene (Prolene) suture, as long as the method does not narrow the aorta. For most injuries, placement of an interposition graft (Dacron or expanded polytetrafluoroethylene [ePTFE]) is necessary for more extensive aortic injuries.

Open Abdominal Technique Traditionally, abdominal aortic trauma is divided into two groups based on anatomic location above and below the mesenteric vessels: supramesocolic and inframesocolic. Starnes and colleagues further differentiated blunt abdominal aortic trauma into three zones based on possible surgical approaches (Table 1): zone I, diaphragmatic hiatus to superior mesenteric artery; zone II, superior mesenteric and renal arteries; and zone III, lowest renal artery to aortic bifurcation. Differentiating among these aortic zones is critical because the open operative exposure for each is different. Regardless of the anatomic location of the aortic injury, control of the aorta in patients who are unstable or hemorrhaging should be at the aortic hiatus. This maneuver can be accomplished with either direct manual pressure or direct compression of the aorta with a retractor device. More precise operative exposure of the supraceliac aorta is obtained at the hiatus by retracting the stomach and esophagus down and to the patient’s left. Identification of the esophagus and performance of this maneuver can be aided by ensuring a very proximal extent of the laparotomy incision along the xyphoid, placement of a nasogastric tube to allow palpation of the esophagus, and reverse Trendelenburg positioning of the patient. After the esophagus has been retracted to the patient’s left, the diaphragmatic crus is divided and the aorta is exposed and clamped. The supramesocolic aorta is best exposed through a left medial visceral rotation. This exposure is achieved through division of the white line of Toldt along the lateral border of the left colon extending proximally to the spleen. The plane of dissection is then on the muscles of the posterior abdominal wall. In most cases, the retroperitoneal hematoma resulting from the aortic injury has done much of the dissection. Exposure should be taken lateral to medial to the aortic hiatus of the diaphragm. Often the left crus needs to be incised and blunt dissection of the aorta must be performed to achieve additional proximal length for control. The colon, spleen, distal pancreas, and stomach should be rotated medially and the abdominal aorta should be exposed. Inframesocolic hematomas from aortic trauma are approached by elevating the transverse colon and mesocolon cephalad. The small bowel is then eviscerated to the patient’s right, and the ligament of ­Treitz is transected. The tissue to the left of the aorta, including the inferior mesenteric vein, should be divided to expose the aorta. To expose the suprarenal aorta or inferior vena cava from this approach, the line of Toldt of the right colon should be divided and the right colon and duodenum should be elevated with an extended Kocher maneuver. Based on their categorization of and report on abdominal aortic injuries, Starnes and colleagues suggested that zone I injuries require extensive open exposure but may also be amenable to an endovascular approach. This group also suggested that zone II lesions, those in the paravisceral aortic segment, are not amenable to endovascular repair but are best approached with open operation. Finally, this study demonstrated that zone III aortic injuries are amenable to open or endovascular repair, although in cases of concomitant visceral injury with enteric spillage, endovascular repair provides an attractive option (see Table 1).

TABLE 1:  Classification of Abdominal Aortic Injury Zones and Options for Operative Approach Zone of Injury

Definition

Operative Approach

Zone I

Celiac artery to lowest renal artery

Extensive open approach or endovascular

Zone II

Perivisceral aorta

Extensive open approach

Zone III

Lowest renal artery to bifurcation

Basic open or endovascular approach

From Shalhub S, Starnes BW, Tran NT, et al: Blunt abdominal aortic injury, J Vasc Surg 55:1277–1285, 2012.

Aortic Injury

Endovascular Technique In nearly all cases, contrast-enhanced CT is performed before endovascular repair, but selected cases may be performed using contrast arteriography and endovascular ultrasound (IVUS) at the time of the initial operation. A classification system has been proposed for blunt aortic injury based on CT findings to enable the provider make decisions as to the urgency or need for repair (see Box 1). Once endovascular repair has been identified as the option of choice, evaluation of the aortic CT is critical to ensure adequate seal zones 2 cm on either side of the injured segment (see Figures 1 and 2). Without sufficient seal or landing zones, the patient is at risk for endoleak and inadequate repair of the injury. The diameter of the aorta at these seal zones is also an important measurement, with most endografts oversized 10% to 15% greater than the aorta segment itself. A greater number of commercially available thoracic endografts are now available, with sizes amenable to the smaller aortas encountered in the setting of trauma. Examples of grafts used to treat this condition are Zenith TX2 (Cook Medical, Bloomington, IN), Conformable TAG or C-TAG (W.L. Gore and Associates, Inc., Flagstaff, AZ), and Valiant Thoracic Stentgraft (Medtronic, Inc., Minneapolis, MN), although none of these thoracic endoprostheses are expressly indicated for traumatic aortic repair. Access to the femoral to artery is obtained by an open surgical exposure in most cases. The recommended diameter of the femoral artery is 8 mm for placement of the femoral sheaths. Once the femoral sheath is placed, a contrast aortogram is performed to visualize the injury and its position in relation to major branch arteries (see Figure 1). Endovascular ultrasound or IVUS may also be used to size the aortic diameter and examine the proximal and distal seal zones. Once the injury and stent graft landing zone are well visualized and marked, the imaging arm should be locked in place, and in most cases systemic anticoagulation should be administered. The renal and mesenteric arteries should never be covered by the endografts device. In some instances in which the aortic injury is within 1 to 2 cm of the origin of the left subclavian, this artery may be covered to achieve adequate endograft seal. If the left subclavian artery is covered, the surgeon must ensure the patient does not have a thrombosed right vertebral artery or a dominant left vertebral artery because the patient would then be at high risk to develop vertebrobasilar syndrome or stroke. Some centers have advocated prophylactic or preemptive carotid–to–left subclavian artery bypass before endovascular repair of thoracic aortic trauma to reduce the risk of posterior circulation complications as well as paralysis. Routine drainage of the spinal cord to reduce the incidence of cord ischemia and paralysis is not indicated in endovascular repair of most thoracic aortic injuries. Typically, patients are monitored closely in the postoperative period for this uncommon complication and a drain is placed if cord symptoms manifest. Once the stent graft is deployed and adequate coverage of the injury is obtained, the sheaths are removed and the

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femoral artery is closed primarily or with a commercially available percutaneous closure device.

CHANGE IN PARADIGM Endovascular repair of aortic injuries has become common because it has been found equivalent, if not superior, to open aortic repair. A study sponsored by the AAST examined a cohort of patients who had traumatic aortic repair between 1994 and 1996. During that time, no endovascular repairs were performed. However, a similar study by the same organization 10 years later found that 65% of aortic injuries were repaired using endovascular techniques. Additionally, mortality improved in this modern cohort (13% from 22%), as did rates of spinal cord ischemia and paralysis (1.6% from 7%). The time to traumatic aortic repair also increased in the later cohort to 55 hours from the time of injury. The shift in the use of endovascular stent grafts to treat aortic injury parallels the endovascular advances that have affected nontraumatic aortic aneurysm disease. Numerous other studies have been published confirming the benefits of endovascular over open aortic repair in the setting of trauma.

Selected References Asensio JA, Chahwan S, Hanpeter D, et al: Operative management and outcome of 302 abdominal vascular injuries, Am J Surg 180:528–533, 2000. Dake MD, White RA, Diethrich EB, et al: Society for Vascular Surgery Outcomes Committee. Report on endograft management of traumatic thoracic aortic transections at 30 days and 1 year from a multidisciplinary subcommittee of the Society for Vascular Surgery Outcomes Committee, J Vasc Surg 53:1091–1096, 2011. Demetriades D, Velmahos GC, Scalea TM, et al: Operative repair or endovascular stent graft in blunt traumatic thoracic aortic injuries: Results of an American Association for the Surgery of Trauma Multicenter Study, J Trauma 64:561–570, 2008. Nagy K, Fabian T, Rodman G, et al: Guidelines for the diagnosis and management of blunt aortic injury: An EAST Practice Management Guidelines Work Group, J Trauma 48:1128–1143, 2000. Parmley LF, Mattingly TW, Manion WC, et al: Nonpenetrating traumatic injury of the aorta, Circulation 17:1086–1101, 1958. Patel HJ, Hemmila MR, Williams DM, et al: Late outcomes following open and endovascular repair of blunt thoracic aortic injury, J Vasc Surg 53:615–620, 2011. Propper BW, Alley JB, Gifford SM, et al: Endovascular treatment of a blunt aortic injury in Iraq: Extension of innovative endovascular capabilities to the modern battlefield, Ann Vasc Surg 23, 2009 687.e19–e22. Shalhub S, Starnes BW, Tran NT, et al: Blunt abdominal aortic injury, J Vasc Surg 55:1277–1285, 2012. Starnes BW, Lundgren RS, Gunn M, et al: A new classification scheme for treating blunt aortic injury, J Vasc Surg 55:47–54, 2012. White JM, Stannard A, Burkhardt GE, et al: The epidemiology of vascular injury in the wars in Iraq and Afghanistan, Ann Surg 253:1184–1189, 2011.

680 VASCULAR TRAUMA

Complications of Upper and Lower Extremity Percutaneous Arterial Puncture and Catheterization Rachael Nicholson and Timothy F. Kresowik

Although there is appeal in the less invasive nature of percutaneous procedures, access-related complications can be a source of significant morbidity and even mortality. Bleeding, arterial injury, ischemia, and nerve injury are common problems encountered in an environment where high volumes of percutaneous procedures are performed.

COMPLICATIONS OF LOWER EXTREMITY ARTERIAL PUNCTURES Risk factors for complications associated with lower extremity arterial punctures include increasing sheath size, increasing age, cannulation of arteries other than the common femoral artery, increasing body mass index (BMI), female gender, post-procedure anticoagulation, and combined arterial and venous puncture. Measures taken to minimize access-related problems include using the smallest sheath possible, locating the puncture over the femoral head with fluoroscopy, and employing ultrasound guidance to ensure puncture of the common femoral artery.

for control while a repair suture is placed. This technique allows repair of the puncture site with minimal dissection of the artery. Usually one or two transversely placed repair stitches are sufficient. It is important to make sure that one has actually dissected to the level of the artery and is not just repairing an opening superficial to the artery in an overlying tissue plane. The minimal dissection technique can also result in missed secondary punctures or back-wall bleeding sites from a catheterization employing the double-wall puncture technique. A more conservative technique involves an initial dissection cephalad to obtain proximal control. Classic vascular teaching would even include a suprainguinal retroperitoneal incision to obtain control of the external iliac artery, although in our experience, this is rarely required. It is preferable to use a balloon catheter directed from a distal site or the puncture site itself for proximal control. Obtaining proximal and distal control allows complete dissection of the artery at the site of the puncture and identification of any additional puncture site complications. Retroperitoneal hematomas usually result from punctures of the external iliac artery above the level of the inguinal ligament. The retroperitoneal areolar tissue is much less dense than that of the thigh and is less likely to tamponade major hemorrhage. The severity of this complication ranges from a self-limited process to an unstable patient who might need an emergent operation to stop the bleeding and repair the artery. If unrecognized, this is a potentially lethal complication. Retroperitoneal hematoma should be considered in a patient who has unexplained hypotension or a drop in hematocrit after an arterial puncture. The hematoma may be associated with back or lower abdominal pain, but significant hemorrhage can occur without localizing symptoms. Computed tomography or ultrasound examination can confirm the diagnosis. The puncture site can often be repaired from a groin approach by incising or mobilizing the inguinal ligament, with proximal control achieved with a balloon catheter. If available, fluoroscopy can be very useful for angiographydirected placement of a proximal balloon catheter or even repair of the puncture site with a stent graft.

Bleeding Bleeding after arterial puncture can be external, can form a localized hematoma, or can extend into the thigh or the retroperitoneal space (Figure 1). External bleeding can initially be controlled with direct pressure using one or two fingers over the arterial puncture site. The temptation to place a sandbag or large dressing over the entire groin should be resisted because this results in nonspecific compression of the artery and interferes with visualization of the groin. If a large hematoma develops after initial hemostasis, surgical intervention should be considered if the hematoma continues to expand or if the overlying skin becomes ischemic as a result of pressure from the underlying hematoma. Even when bleeding has stopped, a hematoma can accumulate more volume as the clot lyses and extracellular fluid is absorbed. It is preferable to have drained a hematoma unnecessarily than to have to deal with the morbidity of extensive groin skin necrosis. Bleeding puncture sites can be approached directly through a standard longitudinal groin incision. An alternative in obese patients is a transverse suprainguinal incision, which facilitates better skin healing and is more than adequate exposure for a simple repair or thromboembolectomy. Repairs can be carried out using local anesthesia. However, in the presence of a large hematoma, it may be difficult to obtain adequate pain control, and general or regional anesthesia provides a more controlled setting for an exploration. It is often easiest to approach the puncture site directly and use finger pressure initially for control. An appropriately sized metal dilator may be placed into the puncture site

FIGURE 1  Ruptured false femoral artery aneurysm. Computed

tomography (CT) scan of a patient who experienced sudden groin swelling and pain after a cough while at home 2 days after cardiac catheterization through a right femoral approach. Hemostasis was initially achieved with Angioseal. Gross extravasation and a large hematoma was not considered typical of a false aneurysm. Surgical repair revealed the Angioseal device to be floating free in the tract. The closure device masked visible bleeding from the tract without really achieving closure of the arteriotomy site.

C omplications of Upper and Lower Extremity Percutaneous Arterial Puncture and Catheterization

Pseudoaneurysm Pseudoaneurysms occur in up to 5% of diagnostic femoral arterial punctures. The diagnosis should be considered in any patient with a mass or significant pain following a percutaneous procedure. Color flow duplex scanning usually readily confirms or excludes the diagnosis of a pseudoaneurysm, but occasionally contrast CT imaging is necessary in very obese patients and proximal punctures. Treatment options for pseudoaneurysms following catheterization include observation, ultrasound-guided compression, ultrasound-guided thrombin injection of the pseudoaneurysm, and surgical repair. A prospective study of 144 cardiac catheterizations followed by routine postprocedure color-flow duplex scanning that asymptomatic pseudoaneurysms were discovered in approximately 5% of patients (size ranging from 1.3 to 3.5 cm). The majority (77%) of these spontaneously thrombosed during a 4-week observation period, which suggests that observation alone for small pseudo­ aneurysms in patients without evidence of ongoing hemorrhage is reasonable. Duplex-guided compression can be used to achieve pseudoaneurysm thrombosis in the majority of patients in whom it is attempted. An ultrasound probe is used to apply pressure with enough force to occlude flow to the pseudoaneurysm without occluding flow within the native artery. The procedure is hampered by significant pain for the patient and long compression times, and it is labor intensive for the practitioner performing the guided compression. Ultrasound-guided thrombin injection has emerged as the standard treatment for pseudoaneurysms following percutaneous access. It has replaced duplex-guided compression in our practice. A 1-mL syringe is attached to a 21-gauge needle, which is inserted into the pseudoaneurysm cavity away from the neck of the pseudoaneurysm under ultrasound guidance. Thrombin (1000 U/mL) is slowly injected into the pseudoaneurysm using ultrasound visualization until complete thrombosis occurs. Typically, the amount of thrombin required is only 300 to 700 units. Initial success rates have been reported as high as 100%, with only a small number of patients demonstrating recurrent flow at 1 month follow-up. Complications are rare but can include thrombosis, embolization, infection, and allergic reactions. Injection should be avoided where there is femoral vein compression, arteriovenous fistula, or infection. Very small false aneurysms (70%) was 90% of the surgical group versus 80% in the endovascular group. Although this was a small study and its design was subject to criticism, it appears that open renal revascularization in experienced hands is a safe procedure and provides benefits that are longer lasting. Restenosis after renal angioplasty and stenting is not benign. A large retrospective review from West Virginia on the outcomes of 122 renal artery stents associated with symptomatic restenosis found that independent of any treatment of the recurrent stenosis, 23% progressed to renal failure and 28% had no benefit or a worsening of their hypertension. This was particularly problematic in patients with a single functional kidney and a previously thrombosed renal artery stent.

CONDITIONS IN FAVOR OF ENDOVASCULAR RENAL ARTERY REVASCULARIZATION In current practice, most patients who have an established diagnosis of renovascular hypertension or ischemic nephropathy have undergone an endovascular intervention because of its lower procedure-related mortality. This is certainly appropriate in patients with a hostile abdomen or severely diseased arterial bed that makes an open procedure more risky and less likely to succeed. However, this also assumes that there are no anatomic or physiologic issues that will prevent a successful outcome of the endovascular procedure and that the long-term results of endovascular therapy are equal to that of an open surgical procedure. The assumption of equivalent results has not been validated in any study to date. Nevertheless, patients who have a relatively large renal artery (≥6 mm) who prefer the least invasive approach should be considered for an endovascular intervention as long as they are adequately informed of the lower long-term patency rate. Any medical contraindication to an open renal revascularization requiring a lengthy anesthetic and extensive abdominal operation is an indication for angioplasty with stenting. Because the primary renal artery patency following angioplasty with stenting is estimated to be at least 60% at 5 years, patients whose expected life span at the time of the proposed intervention is less than 5 years might be best managed with an endovascular intervention. The majority of patients in this setting are older than 70 years.

CONCLUSION The most important issue facing clinicians when evaluating patients with a known renal artery stenosis is whether such a lesion is of any relevance to the patient’s elevated blood pressure or, in some patients, their impaired kidney function. It is predictable that little or no benefit will accompany open surgery or angioplasty with stenting if one fails to document the presence of a critical renal artery stenosis

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of hemodynamic and functional relevance. Selection errors have clouded the value of open therapy in the past and more recently have cast doubt on the value of an endovascular intervention. Ignorance of proper patient selection has led some to categorize both therapies as useless and too costly, thus denying therapy to many who might appropriately benefit from these treatments. It is illogical to believe that in carefully selected patients, a technically successful renal angioplasty with stenting should have a less salutary early outcome than that of open surgery. However, inconsistent techniques and the absence of rigorous entrance criteria in most studies comparing angioplasty to medical therapy have clearly resulted in unconvincing data regarding the efficacy of this therapy. That is most unfortunate. Poorly selected patients undergoing treatment of arteriosclerotic renal artery stenoses continue to bear a real risk of morbidity and mortality. It is unacceptable if flawed clinical studies become the basis of current practice and lessen the opportunity to offer an open surgical procedure or renal angioplasty with stenting to properly selected patients who have critical arteriosclerotic renal artery stenotic disease. Conversely, ignoring the mistakes made in published trials having disappointing outcomes, and performing renal artery procedures using ill-defined criteria for the interventions will undoubtedly yield equally disappointing results.

Selected References Balzer KM, Pfeiffer T, Rossbach S, et al: Prospective randomized trial of operative versus interventional treatment for renal artery ostial disease (RAOOD), J Vasc Surg 49:667–675, 2009. Bax L, Wolttiez A-JJ, Kouwenberg HJ, et al: Stent placement in patients with atherosclerotic renal artery stenosis and impaired renal function, Ann Intern Med 150:840–848, 2009. Cooper CJ, Murphy TP, Cutlip DE, et al: Stenting and medical therapy for atherosclerotic renal-artery stenosis, N Engl J Med 370:13–22, 2014. Plouin P-F, Chatellier G, Darne B, et al: Essai Multicentrique Medicaments vs Angioiplastie (EMMA) Study Group. Blood pressure outcome of angioplasty in atherosclerotic renal artery stenosis, Hypertension 31:823–829, 1998. Stone PA, Campbell JE, Aburahma AF, et al: Ten-year experience with renal artery in-stent stenosis, J Vasc Surg 53:1026–1031, 2011. Textor SC, Lerman L, McKusick M: The uncertain value of renal artery interventions, JACC Cardiovasc Interv 2:175–182, 2009. van Jaarsveld BC, Krijnen P, Pieterman H, et al: For the Dutch Renal Artery Stenosis Intervention Cooperative Study Group. The effect of balloon angioplasty on hypertension in atherosclerotic renal artery stenosis, N Engl J Med 342:1007–1014, 2000. Webster J, Marshall F, Abdalla M, et al: Randomised comparison of percutaneous angioplasty vs continued medical therapy for hypertensive patients with atheromatous renal artery stenosis. Scottish and Newcastle Renal Artery Stenosis Collaborative Group, J Hum Hypertens 12:329–335, 1998. Wheatly K, Ives N, Gray R, et al: For The Astral Investigators. Revascularization versus medical therapy for renal-artery stenosis, N Engl J Med 361:1953–1962, 2009.

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RENOVASCULAR DISEASE

Percutaneous Arterial Dilation and Stenting for Arteriosclerotic Renovascular Hypertension and Ischemic Nephropathy

criteria to identify patients in whom hemodynamically and physiologically significant anatomic renal artery stenosis is the cause of the clinical manifestations of potentially reversible ischemic nephropathy and renal vascular hypertension. A summary of the author's selection criteria are shown in Boxes 1 and 2 and Table 1. In the CORAL, ASTRAL and STAR trials, most of these selection criteria were not met by the patients who were included, and there were also serious problems associated with the interventional treatment in the ASTRAL and STAR trials; these flaws are critical in understanding the failure of stenting to show superiority to medical therapy, as is discussed in detail later.

TECHNIQUES OF RENAL ARTERY STENTING

Thomas A. Sos

Anecdotal experience and many retrospective studies support the utility of renal artery stenting in carefully selected patients, yet Level 1 evidence has been lacking. Several multicenter prospective randomized studies have been conducted to determine whether renal artery stenting was superior to medical therapy for treatment of ischemic nephropathy. The negative conclusions of the widely quoted Angioplasty and STenting for Renal Artery Lesions (ASTRAL) trial, a large European trial, the Stent Placement in Patients with Atherosclerotic Renal Artery Stenosis and Impaired Renal Function (STAR) trial, a much smaller Dutch trial, and the Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL), a large, primarily US-based trial have all been reported, who results were published in January 2014. Based on the conclusions of these studies, many clinicians no longer consider renal artery stenting a reasonable option for their patients with renal artery stenosis, renal dysfunction, and hypertension.

PATIENT SELECTION Hypertension, renal dysfunction, and atheromatous renal artery stenosis can occur independently or can be causally linked (Figure 1). There are unfortunately no foolproof and universally agreed upon

RENAL ARTERY STENOSIS

RENAL VASCULAR HYPERTENSION

Almost all atheromatous renal artery stenoses occur at the aortic ostium. Extreme care must be taken during all catheter and wire manipulations in the juxtarenal abdominal aorta to minimize manipulations and iodinated contrast use to decrease the chances of microcholesterol embolization or contrast-induced nephropathy. As suggested by logarithmic glomerular filtration rate (GFR) curves (Figure 2), the likelihood of deterioration of kidney function following an equal insult during renal artery stenting is related to the preprocedure kidney function. The author advocates performing the procedure in the obliquity where the lesion is best seen on prior imaging and where the catheter tip is en face to the stenosis (Figures 3 to 5). The Sos flick technique (Figure 6) is used with the Sos Omni Selective (AngioDynamics, Queensbury, NY) recurve-type catheter and a soft-tipped Bentson-type wire for approaching and crossing renal artery stenoses. The Sos flick usually results in renal artery entry on one pass and almost never requires contrast injection. The author only 10 mL of half or third dilution of full-strength low-osmolar iodinated contrast by saline for aortography (Figures 6 and 7) and prehydrate patients before renal artery stenting, especially those with preexisting renal insufficiency or those at high risk for it. The evidence for using renal artery protection devices is lacking. They all are potentially dangerous and, most importantly, most cholesterol embolization has already occurred by extended fishing in the diseased juxtarenal aorta.

HYPERTENSION

RENAL VASCULAR HYPERTENSION and ISCHEMIC NEPHROPATHY ISCHEMIC NEPHROPATHY

HYPERTENSIVE NEPHROPATHY

RENAL INSUFFICIENCY FIGURE 1  The complex relationship of renal artery

stenosis, hypertension, and renal insufficiency and their clinical presentation.



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RENAL ARTERY STENTING FOR ATHEROMA

After the stenosis is crossed, pressure measurements are obtained through a long 5-Fr vascular sheath in the aorta and at the tip of the selective catheter to measure the gradient. A 0.014-in. or 0.018in. stiff shaft and very floppy tipped guidewire is advanced into a proximal renal artery branch for good purchase. In some cases the stent can be advanced bareback into the stenosis; however, in very severely stenotic and or heavily calcified stenoses it is preferred to first advance the 5-Fr sheath with its introducer through the stenosis over the 0.014-in. or 0.018-in. guidewire, which prevents heaving to deal with a stent that will not cross the lesion and is then difficult to retract back into the sheath. This technique is preferred to balloon predilation, which is another option in these types of cases. The stent should be deployed extending a few millimeters into the aorta and

SCr

NORMAL

HIGH RISK

INT. RISK

LOW RISK

% RENAL FUNCTIONAL RESERVE (GFR)

{

25 50 75 100 FIGURE 2  Renal functional reserve (GFR) and serum creatinine

BOX 1:  Clinical Criteria for Renal Vascular Hypertension and Ischemic Nephropathy

(SCr) concentration. Note: SCr increases logarithmically only after 50% or more of renal parenchyma is lost. Int, Intermediate.

Clinical Criteria for Diagnosis of Renal Vascular H ­ ypertension

Recent onset Resistant to drug treatment (difficult to control) Retinopathy and end organ damage greater than for equivalent essential hypertension Kidney dysfunction Recurrent flash pulmonary edema Continuous abdominal bruit History of smoking Other vascular disease

RRA 30° ± 19°

LRA –7° ± 15° 0°

Clinical Criteria for Diagnosis of Ischemic Nephropathy No intrinsic kidney disease Recent-onset azotemia Progressive azotemia Hypertension Other vascular disease Smoking Unequal kidney size

BOX 2:  Anatomic Criteria for Diagnosis of Hemodynamically Significant Renal Artery Stenosis Stenosis ≥70% diameter (∼85% cross-sectional area) Post-stenotic dilatation Collateral circulation Reduced kidney size • Absolute length discrepancy ≥1.5 cm • Documented length decrease ≥1cm

FIGURE 3  The right renal artery (RRA) origin is 30 degrees ventral

and the left renal artery (LRA) is 7 degrees dorsal to the mid coronal plain of the aorta (0 degrees).  (From Kim PA, Khilnani NM, Trost DW, et al: Fluoroscopic landmarks for optimal visualization of the proximal renal arteries, J Vasc Interv Radiol 10:37–39, 1999.)

TABLE 1:  Physiologic Screening and Criteria for Diagnosis of Hemodynamically Significant Renal Artery Stenosis Method

Unreliable in Bilateral Disease and Elevated SCr

Radionuclide scan

X

Renal vein renin assay

X

Duplex ultrasound Pressure gradient ≥10% mean arterial pressure SCr, Serum creatinine.

Technically Difficult and Operator Dependent

Invasive

X X X

780

RENOVASCULAR DISEASE [H]

RIGHT

8.8 cm

LEFT

7.1 cm

FIGURE 4  Magnetic resonance arteriography

(MRA) with gadolinium. There is a severe focal ostial right renal artery stenosis (arrows) and a viable 8.8 cm right kidney, a very severe left renal artery stenosis with an atrophic 7.1 cm left kidney, and severe aortic atheroma.

A

B FIGURE 5  A, Intraarterial digital subtraction aortogram (DSA). B, Selective right renal arteriogram. Each DSA sequence was obtained at 7.5 frames per second using 1⁄3 dilution of low-osmolar contrast medium. The aortogram was made with 10 mL injected at 10 mL/second, and the selective renal arteriogram was made with 4 mL injected at 4 mL/second. DSA confirms the severe right ostial renal artery stenosis (black arrow) and severe left renal artery stenosis and also shows severe and extensive aortic atheroma and heavy wall calcification seen as subtraction artifacts.

a few millimeters beyond the distal margin of the lesion; attempts to deploy a shorter stent more accurately often results in having to deploy additional overlapping stents to cover the lesion adequately, with a greater likelihood of restenosis.

Illustrative Case In contrast to the STAR and ASTRAL trials, Patient A presented with clinically, anatomically, and hemodynamically (physiologically) significant renal artery stenosis and the serious clinical sequelae of chronic renal insufficiency as a result of ischemic nephropathy and renovascular hypertension. This patient was 84 years old and had an at least 10-year history of hypertension that had recently become uncontrolled (239/99 mm Hg) on three medications. On five

antihypertensive medications BP was 160–180/60–70 mm Hg. She had a 10-year history of Sjögren’s syndrome and progressive chronic renal insufficiency (serum creatinine [SCr] increased from 1.5 mg/dL to 2.7 mg/dL over the previous 6 months). Magnetic resonance angiography (MRA) with gadolinium (see Figure 5) was performed, recognizing that there was a slight risk of nephrogenic systemic fibrosis. MRA demonstrated severe bilateral ostial renal artery stenosis, left renal atrophy, and severe aortic atheroma in the region of the renal arteries. Aortography, selective right renal arteriography, and pressure gradient measurement confirmed these findings and the hemodynamic significance of the right renal artery stenosis. We do not routinely perform a selective renal arteriogram prior to stenting. In this case, following the Sos flick, which successfully engaged the renal artery ostium, the wire could not be advanced through the stenosis into the distal renal artery. An ostial

Percutaneous Arterial Dilation and Stenting for Arteriosclerotic Renovascular Hypertension

781

FIGURE 6  The Sos flick technique of

selective renal artery catheterization for ostial renal artery stenosis using the Sos Omni Selective (AngioDynam Queensbury, NY) recurve-type catheter. A, The catheter in the aorta. B to D, As the catheter and wire are advanced cephalad, the wire tip (arrow) flicks laterally (D) when it reaches the nubbin of the stenotic or occluded renal artery. E, The wire enters the artery.

BOX 3:  Criteria for Intervention

Clinical Criteria for Ischemic Nephropathy and Renal Vascular Hypertension

Chronic progressive renal insufficiency: SCr ≥2.7 mg/dL Drug resistance (five medications) and accelerated hypertension

Anatomic Criteria (by MRA and DSA) for Hemodynamically Significant Renal Artery Stenosis ≥80% right renal artery stenosis ≥90% left renal artery stenosis Atrophic left kidney

Physiologic Criterion (Selective Right Renal Artery and Aortic Pressure Measurements) for Hemodynamically Significant Renal Artery Stenosis ≥25% mean arterial right renal artery pressure gradient

DSA, Digital subtraction angiography; MRA, magnetic resonance arteriography; SCr, serum creatinine.

FIGURE 7  Digital subtraction aortogram (DSA) obtained using 5 mL

of 1⁄3 dilute contrast after successful stenting (black arrow). Note the branch stenosis (white arrow), which was not treated.

arteriogram was performed with a nontraumatic technique using 4 mL of 1⁄3 dilute contrast injected at 4 mL/sec to guide further wire manipulation. The patient in this case had many of the most important criteria for intervention outlined in Box 3. Several treatment options are available including medical therapy, surgical revascularization, and percutaneous stenting. In this case, she had already clearly failed medical therapy. For surgical revascularization, hepatorenal bypass is an extra-anatomic reconstruction that has little risk of cholesterol embolization, but the patient had a moderately high anesthesia and surgical risk as a result of her age, diffuse vascular disease, and Sjögren’s syndrome. For percutaneous stenting, the irregular atheroma of the aortic wall and the intraluminal atheroma increased the chances of cholesterol embolization to 3% to 5%, but there was a low technical procedural and sedation risk.

Following thorough discussions with the patient, her family, and all the physicians taking care of her about the risks and benefits of each of the previous three therapies, the patient chose renal artery stenting. If stenting failed, she would undergo hepatorenal bypass. Renal artery stenting was quick and uneventful. Kidney function improved immediately and returned to almost normal within a few weeks, and blood pressure became easily controlled. One and a half years following stenting the patient’s SCr is stable at 1.65 mg/dL and her blood pressure is easily controlled at 140–160/40–60 mm Hg. This case demonstrates that in carefully selected patients who have ischemic nephropathy and renovascular hypertension caused by physiologically and hemodynamically significant renal artery stenosis, revascularization by renal artery stenting is an effective treatment.

ASTRAL AND STAR TRIALS Neither ASTRAL nor STAR enrolled many patients who met the clinical, anatomic, and hemodynamic criteria, which are the most accurate predictors of a favorable response to revascularization. Further,

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RENOVASCULAR DISEASE

TABLE 2:  Endovascular Renal Artery Revascularization with Angioplasty and Stenting* KIDNEY FUNCTION RESPONSE (%)

HYPERTENSION RESPONSE (%)

Preop. Bilateral Kidney No. of Treatment Dysfunction Patients (%) (%) Improved Unchanged Worsened Cured Improved Failed

First Author

Year

Burket

2000

127

NR

29

43

57

Lederman

2001

300

41

37

9

78

14

70

Bush

2001

73

16

68

23

51

26

NR

RochaSingh

2002

51

55

100

77

18

5

91

Kennedy 2003

261

NR

36

61

39

NR

Gill

2003

100

26

75

31

38

31

4

Zeller

2003

215

23

52

52

48

Henry

2003

56

14

32

14

66

0

18

Zeller

2004

456

NR

52

34

39

27

46

Nolan

2005

82

NR

59

23

53

24

NR

Kayshap 2007

125

36

100

42

23

25

NR

2006

63

32

100

97

Corriere 2008

99

11

75

28

30

55

31

Holden

Mean %†

NR

4