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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3591_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Acknowledgments
- •Contents
- •About the Editor
- •1.6 Acute Gastrointestinal Bleeding
- •1.7 Transjugular Intrahepatic Portosystemic Shunt
- •1.8 Conclusion
- •References
- •2.1 Introduction
- •2.2 History-Taking
- •2.4 Pre-procedure Imaging
- •2.5 Pre-procedure Investigations
- •2.8 Informed Consent
- •2.10 Part Preparation
- •2.11 Antibiotic Prophylaxis
- •References
- •3.1 Introduction
- •3.2 Ultrasonography
- •3.2.1 Advantages
- •1.1 Introduction
- •1.2 Early Beginnings
- •1.3 Catheter-Directed Thrombolysis
- •1.4 Stents
- •1.5 Coronary Angiography
- •3.2.3 Limitations
- •3.3 Fluoroscopy
- •3.3.1 Indications
- •3.3.2 Interventional Fluoroscopy
- •3.3.2.1 Digital Subtraction Angiography
- •3.4 Computed Tomography
- •3.4.2 Indications
- •3.4.3 Limitations
- •3.5 Magnetic Resonance Imaging
- •3.5.3 Limitations
- •3.6.3 Remove Anti-scatter Grid
- •3.6.4 Pulsed Fluoroscopy
- •3.6.5 Checklist
- •3.9 Conclusion
- •References
- •4.1 Introduction
- •4.2 Pharmaceutical Agents
- •4.2.1 Contrast Agents
- •4.2.2 Iodinated Contrast Media (ICM)
- •Pathogenesis
- •Risk Factors
- •Diagnosis
- •Risk Threshold
- •4.5 Conclusion
- •References
- •4.3 Carbon Dioxide
- •4.3.1 Indication
- •4.3.2 Contraindications
- •4.3.3 Equipment
- •4.3.4 Preparation
- •4.3.5 Technique
- •4.3.6 Complications
- •4.3.7 Advantages
- •4.3.8 Disadvantages
- •4.4.1 Thrombolytics
- •First-Generation Thrombolytic Agents
- •Second-Generation Thrombolytic Agents
- •Third-Generation Thrombolytic Agents
- •4.4.1.2 Contraindications
- •4.4.2 Anticoagulants
- •4.4.2.1 Unfractionated Heparin (UFH)
- •Mechanism
- •Indications
- •4.4.2.2 Low-Molecular-Weight Heparin (LMWH)
- •Mechanism
- •Indications
- •Special Considerations
- •4.4.2.3 Warfarin
- •Mechanism
- •Indications
- •Special Considerations
- •4.4.3 Antiplatelet Drugs
- •4.4.3.1 Aspirin
- •Mechanism
- •Recommendations
- •4.4.3.2 Clopidogrel
- •Mechanism
- •Recommendations
- •4.4.3.3 Glycoprotein IIb/IIIa Inhibitors (GPI)
- •Mechanism
- •Recommendations
- •4.4.4 Vasodilators
- •4.4.4.1 Nitroglycerine
- •Mechanism
- •Indications
- •4.4.4.2 Verapamil
- •Mechanism
- •Indications
- •Contraindications
- •Complications
- •4.4.5 Vasoconstrictors
- •4.4.5.1 Mechanism
- •4.4.5.3 Indication
- •4.4.6 Prothrombotics
- •4.4.6.1 Mechanism
- •4.4.6.3 Indications
- •4.4.6.5 Special Considerations
- •5.1 Introduction
- •5.2 Pre-procedure Tasks
- •5.2.4 Pre-anesthetic Evaluation
- •5.3 Anesthesia Techniques
- •5.3.1 Local Anesthesia
- •5.4 Pediatric IR Procedures
- •5.5 Anesthesia Considerations
- •5.11 Conclusion
- •References
- •6.1 Introduction
- •6.3 Pre-procedural Workup
- •6.3.1 Prothrombin Time (PT-INR)
- •6.3.3 Viscoelastic Tests
- •6.4.1 Procedure-Related Bleeding Risk
- •6.5.1 Chronic Liver Disease
- •6.5.2 Chronic Kidney Disease
- •6.5.3 Thrombocytopenia
- •6.5.4 Disseminated Intravascular Coagulation (DIC)
- •6.5.5 Malignancy
- •6.6 Bridge Therapy
- •6.7 Deep Vein Thrombosis (DVT)
- •6.8 Atrial Fibrillation (AF)
- •6.9 Coronary Stents
- •6.10 Conclusion
- •References
- •7.1 Introduction
- •7.4 Embolic Agent Selection
- •7.5.1 Gelfoam Embolization
- •7.5.2 Coil Embolization
- •7.5.3 Amplatzer Vascular Plug Embolization
- •7.5.4 Glue Embolization
- •7.6 Clinical Applications
- •7.6.1.1 Endovascular Approach
- •Parent Artery Preservation [16, 17]
- •Stent or Balloon-Assisted Coiling [20, 21]
- •Multi-Layered Flow-Diverting Stents [22]
- •7.6.1.2 Parent Artery Occlusion
- •Sandwich Technique [19–22]
- •7.6.1.3 Percutaneous Approach [16, 17, 24, 25]
- •7.6.2 Tumoral Embolization
- •7.6.3 AVM Embolization
- •7.6.5 Special Scenario
- •7.6.5.1 Provocative Angiography
- •7.6.5.2 Lower GI Bleeding
- •7.6.5.3 Hepatic Artery Aneurysm
- •7.6.5.4 Renal Artery Aneurysm (RAA)
- •7.7 Newer Embolizations
- •7.7.1 Genicular Artery Embolization
- •7.8 Conclusion
- •References
- •8.1 Introduction
- •8.2 Puncture Needles
- •8.3 Guidewires
- •8.4 Sheath System
- •8.5 Catheters
- •8.6 Microcatheters
- •8.7 Embolizing Agents
- •8.7.1 Gelatin Foam
- •8.7.2 Autologous Blood Clot
- •8.7.3 Thrombin
- •8.7.4 Coils
- •8.7.5 Vascular Plugs
- •8.7.6 Particulate Agents
- •8.7.7 Liquid Embolic Agents
- •8.8 Detachable Balloons
- •References
- •9.1 Introduction
- •9.2 Balloons
- •9.2.1 Basics
- •9.2.7 Balloon Ratings
- •9.2.11 Balloon Catheter Design
- •9.2.13 Complications
- •9.2.14 Occlusion Balloons
- •9.2.15 Angioplasty–Pearls
- •9.3 Stents
- •9.3.4 Raw Material Form
- •9.3.5 Fabrication
- •9.3.6 Geometry
- •9.3.7 Additions
- •9.3.8 Drug-Eluting Stents
- •9.3.10.1 Arterial Indications
- •9.3.10.2 Venous Indications
- •9.3.10.3 Non-vascular Indications
- •9.3.11 Uncovered vs. Covered (PTFE) SEMS
- •9.3.12 Stent Grafts
- •References
- •10: Vascular Access
- •10.1 Introduction
- •10.2 Indications
- •10.3 Hardware
- •10.3.1 Intravenous Cannula
- •10.3.2 Puncture Needle
- •10.3.3 Arterial Access Sheath
- •10.4 Local Anesthesia
- •10.6 General Considerations Before Procedure
- •10.7 Arterial Access
- •10.7.2 Arterial Access Sites
- •10.7.2.1 Common Femoral Artery
- •10.7.2.2 High Brachial or Axillary Artery
- •10.7.2.3 Radial Artery
- •10.7.2.4 Pedal Access [3]
- •10.7.2.5 Others
- •10.8 Post-procedure Care
- •10.8.1 Manual Compression
- •10.8.2 Vascular Closure Devices (VCD)
- •10.9 Complications [5–8]
- •10.10 Venous Access
- •10.10.1 Common Femoral Vein
- •10.10.2 Internal Jugular Vein
- •10.10.3 Subclavian Vein Access
- •10.10.4 Upper Extremity Vein Access
- •10.11 Conclusion
- •References
- •11: Neurointerventions Including Aneurysm Interventions
- •11.1 Introduction
- •11.2 Neurovascular Interventions
- •11.3.1 Introduction
- •11.3.3 Clinical Presentation
- •11.3.8 Endovascular Techniques
- •11.3.9 General Technical Guidelines
- •11.3.10 Simple Coiling
- •11.3.11 Balloon-Assisted Coiling
- •11.3.12 Stent-Assisted Coiling
- •11.3.13 Flow Diverter/Braided Stents
- •11.3.14 Stent Graft
- •11.3.15 Parent Artery Occlusion
- •11.3.16 Endosaccular Devices
- •11.4.1 Pathophysiology
- •References
- •12.1 Introduction
- •12.4 Thrombectomy Techniques
- •12.5 Aspiration Technique
- •12.5.1 Stentriever Technique
- •12.6 Combination Technique
- •12.7 Balloon Guide Catheters (BGC)
- •12.8 Special Situations
- •12.8.1 Posterior Circulation Stroke
- •12.8.2 Tandem Occlusions
- •12.8.3 Intracranial Atherosclerotic Disease (ICAD)
- •12.8.4 Medium Vessel Occlusions (MeVO)
- •12.9 Complications
- •12.10 Immediate Post-procedure Care
- •References
- •13.1 Introduction
- •13.2 Brain AVMs
- •13.2.1 Introduction
- •13.2.2 Epidemiology
- •Embolic Agents
- •Embolization Techniques
- •Embolization by Copolymers: Technical Aspects
- •13.3 Intracranial Dural Arterio-Venous Fistulas (DAVFs)
- •13.4 VGAM
- •13.5 Spinal Vascular Malformations
- •13.5.1 Introduction
- •13.5.2 Anatomy
- •13.5.4.3 Spinal Epidural AVMs
- •13.5.4.4 Metameric AVMs
- •References
- •14: Other Neurointerventions
- •14.1 Introduction
- •14.2 Direct CCF
- •14.2.2 Treatment
- •14.3 Epistaxis
- •14.4 Neck Vessel Pathologies
- •14.4.2 Etiopathogenesis
- •14.4.3 Clinical Presentation
- •14.4.4 Management
- •References
- •15.1 Introduction
- •15.4.2 Embolization Agents
- •15.5 Conclusion
- •References
- •16: Carotid Artery Interventions
- •16.1 Introduction
- •16.2.1 Imaging
- •16.2.2.1 Symptomatic Carotid Artery Stenosis
- •16.2.2.2 Asymptomatic Carotid Artery Stenosis
- •16.2.3 Best Medical Therapy
- •16.3 Carotid Artery Stenting
- •16.3.1 Preprocedure
- •16.3.2 Hardware
- •16.3.2.1 Procedure
- •16.5 Complications
- •16.5.1 Early Complications
- •16.5.2 Late Complications
- •16.6 Internal Carotid Artery Stenting
- •16.7 Conclusion
- •References
- •18.1 Introduction
- •18.2 Anatomical Considerations
- •18.3 Aortic Dissection
- •18.3.1 Introduction
- •18.3.2.3 Natural History
- •18.3.2.4 Imaging Options
- •18.3.2.6 Conventional Management Plan
- •18.4 Aortic Aneurysms
- •18.4.1 Overview
- •18.4.4 Thoraco-Abdominal Aortic Aneurysm
- •18.4.5 Abdominal Aortic Aneurysm (AAA)
- •18.4.5.3 Endovascular Intervention
- •18.4.6.1 Epidemiology
- •18.4.6.3 Pathophysiology
- •18.4.7 PAU
- •18.4.7.1 Imaging
- •18.4.7.2 Prognosis
- •18.4.7.3 Management
- •18.4.8 PAU
- •18.5.1 Access Site
- •18.5.2 Procedure
- •18.5.3 Post-Procedure Care
- •18.5.4 Follow-Up Imaging
- •18.6.1 Device-Related Complications
- •18.6.2 Systemic Complications
- •18.7 Endoleaks
- •References
- •19: Vascular Thoracic Interventions
- •19.1 Introduction
- •19.2 Bronchial Artery Embolization (BAE)
- •19.2.1.3 Pre-Procedure Evaluation
- •19.2.2 Bronchoscopy
- •19.2.2.1 Technique
- •19.2.2.2 Post-Procedure Care
- •19.2.2.3 Complications
- •19.3 Pulmonary Artery Pseudoaneurysm (PAPA)/Pulmonary AVM (PAVM) Embolization
- •19.3.1 Pre-Procedure Evaluation
- •19.3.1.2 Technique
- •19.3.2 Post-Procedure Care
- •19.3.3 Complications
- •19.4.1 Pre-Procedure Evaluation
- •19.4.2 Technique
- •19.4.3 Complications
- •19.4.4 Post-Procedure Follow-Up
- •19.5 Thoracic Duct Interventions
- •19.5.1 Pre-Procedure Evaluation
- •19.5.2 Lymphangiography Technique
- •19.5.3 Thoracic Duct Embolization Technique
- •19.5.4 Complications
- •19.5.4.2 Central Lymphatic Access Complications
- •References
- •20.1 Introduction
- •20.2 Pulmonary Embolism
- •20.2.3 Pulmonary Angiography
- •20.2.3.1 Technique
- •20.2.3.2 Post-Procedure Care
- •20.2.3.3 Complications
- •20.2.4.1 Intravenous Thrombolysis
- •20.2.4.2 Catheter-Directed Thrombolysis
- •20.2.4.3 Mechanical Thrombectomy
- •Rheolytic Thrombectomy Devices
- •Aspiration Thrombectomy Devices
- •20.3.1 Clinical Manifestations [16, 17]
- •20.3.3 Radiological Findings
- •20.3.4 Endovascular Management
- •20.3.4.1 Pre-Procedure Evaluation
- •20.3.4.2 Technique
- •20.3.4.3 Post-Procedure Care
- •20.3.4.5 Current Evidence
- •20.4 Pulmonary Artery Aneurysm
- •20.4.1 Endovascular Management
- •20.4.1.1 Technique
- •References
- •21: Hepatic Arterial Interventions
- •21.1 Introduction
- •21.2 Hepatic Arterial Anatomy
- •21.2.1 Normal Celiac Anatomy
- •21.2.2 Normal Hepatic Artery Anatomy
- •21.2.3 Variant Anatomies
- •21.3.1.2 Contraindications
- •21.3.1.3 Patient Selection
- •21.3.1.4 Patient Preparation
- •21.3.1.6 Response Evaluation
- •21.3.1.7 TACE Failure
- •21.3.1.8 TACE Discontinuation
- •21.3.1.9 Complications
- •21.3.2 Transarterial Radioembolization (TARE)
- •21.3.2.2 Contraindications [24]
- •21.3.2.3 Agents Used
- •21.3.2.4 First Visit (Planning)
- •21.3.2.5 Second Visit (Microsphere Injection)
- •21.3.2.6 Complications
- •21.3.3 Transarterial Bland Embolization (TAE)
- •21.3.4 Hepatic Artery Infusion Chemotherapy (HAIC)
- •21.4.1 Neuroendocrine Liver Metastasis (NELM)
- •21.4.2 Other Liver Metastases
- •21.4.3 Intrahepatic Cholangiocarcinoma (IHCC)
- •21.4.4 Benign Liver Tumors
- •21.4.4.1 Hemangiomas
- •21.4.4.2 Focal Nodular Hyperplasia
- •21.4.4.3 Hepatocellular Adenoma
- •21.4.4.4 Polycystic Liver Disease
- •21.8 Hepatic Parenchyma Repopulation
- •References
- •22.1 Introduction
- •22.2 Transjugular Liver Biopsy (TJLB)
- •22.2.1 Patient Preparation
- •22.2.2 Procedure
- •22.2.3 Post-Procedural Care
- •22.2.4 Complications
- •22.3 Transjugular Intrahepatic Portosystemic Shunt (TIPS)
- •22.3.3 Pre-Procedural Evaluation [12–14]
- •22.3.4 Technique
- •22.3.5 Post-Procedural Care
- •22.3.6.1 Extrahepatic Portal Vein Puncture [18, 19]
- •22.3.6.2 Hepatic Artery Injury [18–20]
- •22.3.7 Discussion
- •22.4 Balloon-Occluded Retrograde Transvenous Obliteration (BRTO)
- •22.4.1 Indications and Contraindications of BRTO
- •22.4.2 Pre-Procedural Evaluation
- •22.4.3 Requirements
- •22.4.4 Sclerosants
- •22.4.5 Relevant Anatomy
- •22.4.6 Techniques
- •22.4.8 Discussion
- •22.5 Portal Vein Thrombosis (PVT)
- •22.6.2 HV/IVC Stenting
- •22.6.3 Tips/Dips
- •22.6.4 HV/IVC Thrombolysis
- •22.6.5 Discussion
- •22.7 Portal Vein Embolization
- •22.7.5 Pre-Procedural Evaluation
- •22.7.6 Techniques
- •22.7.7 Embolizing Materials
- •22.7.8 Hypertrophy Response
- •22.7.11 Discussion
- •22.8 Transjugular Kidney Biopsy (TJKB)
- •22.8.1 Indications
- •22.8.2 Rationale
- •22.8.3 Pre-Procedural Workup
- •22.8.4 Techniques
- •22.9 IVC Filter
- •22.9.2 Patient Preparation
- •22.9.4 Procedure
- •22.9.5 Complications [98, 102]
- •References
- •23.1 Introduction
- •23.2 Anatomy
- •23.2.1 Arterial Anatomy
- •23.2.2 Venous Anatomy
- •23.3 Arterial Interventions
- •23.3.1 Renovascular Hypertension
- •23.3.2 Atherosclerotic Renal Artery Stenosis
- •23.3.3 Non-atherosclerotic RAS
- •23.3.4 Takayasu Arteritis (TA)
- •23.3.5 Fibromuscular Dysplasia (FMD)
- •23.5.2.1 Preprocedural Evaluation
- •23.5.2.2 Preprocedural Instructions
- •23.5.2.3 Procedure
- •23.5.2.4 Angiography
- •23.5.2.5 Balloon Angioplasty
- •23.5.2.6 Cutting Balloon Angioplasty
- •23.5.2.7 Stenting
- •23.5.2.9 Post-Procedural Care
- •23.5.2.10 Complications
- •23.6.1 Procedure
- •23.7 Renal Artery Aneurysms (RAAs)
- •23.8.1 Etiology
- •23.8.2 Clinical Presentation
- •23.8.3 Endovascular Management
- •23.9.1 Angiomyolipoma
- •23.9.2 Renal Cell Carcinoma (RCC)
- •23.10 Venous Interventions
- •23.10.1 Nutcracker Syndrome (NCS)
- •23.10.1.1 Diagnosis
- •23.10.1.2 Management
- •23.10.1.3 Endovascular Management
- •23.10.1.4 Procedure
- •23.10.1.5 Complications
- •23.10.2 Renal Vein Thrombosis
- •23.10.2.1 Clinical Presentation
- •23.10.2.2 Management
- •23.10.2.4 Procedure
- •References
- •24.1 Introduction
- •24.2 Relevant Anatomy
- •24.3 Mesenteric Ischemia
- •24.3.1 Clinical Features
- •24.3.2 Imaging
- •24.3.3 Treatment
- •24.3.3.2 Intra-Arterial Thrombolysis
- •24.3.3.3 Mechanical Thrombectomy
- •24.4 Gastrointestinal Hemorrhage
- •24.4.1 Clinical Features
- •24.4.2 Endoscopy
- •24.4.3 Imaging
- •24.4.4.2 Complications
- •24.5 Bariatric Embolization
- •24.5.1 Technique
- •References
- •25.1 Introduction
- •25.2 Uterine Artery Embolization (UAE)
- •25.2.1 Indications [1, 2]
- •25.2.2 Contraindications [1, 2]
- •25.2.3 Relevant Vascular Anatomy [2]
- •25.2.4 Preprocedural Evaluation
- •25.2.5 Technique
- •25.2.6 Post-Procedural Care
- •25.2.7 Complications
- •25.2.8 Outcome
- •25.3 Prostatic Artery Embolization (PAE)
- •25.3.1 Rationale Behind PAE
- •25.3.2 Indications [17, 18]
- •25.3.3 Contraindications [18]
- •25.3.4 Preprocedural Evaluation [17]
- •25.3.5 Clinical Assessment
- •25.3.7 Imaging
- •25.3.7.1 Ultrasonography (USG)
- •25.3.7.2 Computed Tomography (CT)
- •25.3.7.3 Magnetic Resonance Imaging (MRI)
- •25.3.9 Relevant Vascular Anatomy
- •25.3.10 Technique
- •25.3.11 Complications
- •25.3.12 Post-Procedural Follow-Up
- •25.3.13 Outcome
- •25.4 Varicocele Embolization
- •25.4.1 Indications [22, 26]
- •25.4.4 Relevant Vascular Anatomy
- •25.4.5 Preprocedural Evaluation [23, 25]
- •25.4.6 Technique
- •25.4.6.2 Venous Access [25, 27, 28]
- •25.4.6.3 Venography [25, 27]
- •25.4.6.4 Embolization [25, 27, 29–31]
- •25.4.7 Post-Procedural Care
- •25.4.8 Complications
- •25.4.9 Outcome
- •25.5 Pelvic Congestion Syndrome
- •25.5.1 Indication [38]
- •25.5.2 Contraindications [38]
- •25.5.3 Preprocedural Evaluation
- •25.5.4 Relevant Vascular Anatomy
- •25.5.5 Technique
- •25.5.6 Post-Procedural Care
- •25.5.7 Complications
- •25.5.8 Outcome
- •25.6 Penile Angiography
- •25.6.1 Penile Vascular Anatomy
- •25.6.2 Technique
- •25.6.3 Complications
- •25.6.4 Outcome
- •References
- •26.2 Peripheral Arterial Disease (PAD)
- •26.2.1 Introduction
- •26.2.5.1 Non-imaging/Functional Modalities
- •26.2.5.2 Imaging Evaluation
- •26.2.6 Management Strategies
- •26.2.6.3 Revascularization Strategies
- •26.3.2 Preprocedural Evaluation
- •26.3.5 Complications
- •26.3.6 Stenting
- •26.3.7 Post-Procedure
- •26.5 Recent Advances
- •26.5.2 Drug-Eluting Technology
- •26.5.3 Bioresorbable Stents
- •26.5.6 Pedal Arch Revascularization
- •26.5.7 Percutaneous Deep Vein Arterialization (DVA)
- •26.6 Acute Limb Ischemia
- •26.7 Popliteal Artery Entrapment Syndrome (PAES)
- •26.8 Genicular Artery Embolization (GAE)
- •References
- •27.1 Introduction
- •27.2 Relevant Anatomy
- •27.3 Varicose Veins
- •27.3.1 Clinical Evaluation
- •27.3.2 Physical Examination
- •27.3.3 Sonological Evaluation
- •27.3.3.1 Duplex Sonographical Evaluation
- •27.3.5.1 Thermal Ablation
- •Endovenous Laser Ablation
- •Radiofrequency Ablation
- •Endovenous Steam Ablation
- •27.3.5.2 Non-thermal Ablative Methods
- •Foam Sclerotherapy
- •Cyanoacrylate Closure (CAC)
- •Mechanochemical Ablation (MOCA)
- •Cryosclerosis
- •27.4 Deep Vein Thrombosis
- •27.4.1 Diagnosis
- •27.4.1.1 Pre-Test Probability
- •27.4.1.2 D-Dimer Assessment
- •27.4.1.3 Radiological Evaluation
- •27.4.5.1 Catheter-Directed Thrombolysis
- •Single-Session (Second-Generation) Pharmacomechanical Catheter-Directed Thrombolysis
- •27.5.1 Pulmonary Embolism (PE)
- •27.5.2 Clinical Features
- •27.5.3 Imaging Evaluation
- •27.5.4 Management
- •27.5.5 Endovascular Techniques
- •References
- •28.1 Introduction
- •28.3.2 Imaging Evaluation
- •28.4 Endovascular Management
- •28.4.1 Nonmature Fistulas
- •28.4.3 Acute Thrombosis
- •28.5 Central Venous Stenosis
- •28.7 Pseudoaneurysm
- •References
- •29.1 Introduction
- •29.2 Low-Flow Vascular Malformations
- •29.2.1.1 Pre-procedural Requirements
- •29.2.1.2 Procedure
- •29.2.1.3 Post-procedure Care
- •Ethanol
- •Detergent Sclerosant
- •Bleomycin
- •Doxycycline
- •OK-432 (Picibanil)
- •29.2.1.5 Complications
- •29.3 High-Flow Vascular Malformations
- •29.3.1.1 Pre-procedure Evaluation
- •29.3.1.2 Technique
- •29.3.1.3 Complications
- •29.4 Fibro-Adipose Vascular Anomaly (FAVA)
- •29.5 Conclusion
- •References
- •30.1 Introduction
- •30.2 Splenic Injuries
- •30.2.2 Technique
- •30.2.3 Patient Preparation
- •30.2.4 Procedure
- •30.2.5 Embolizing Agent
- •30.2.6 Post-procedural Care
- •30.2.7 Complication
- •30.3 Hepatic Injury
- •30.3.1 Background
- •30.3.2 Indication
- •30.3.3 Technique
- •30.3.4 Patient Preparation
- •30.3.6 Embolization Agent
- •30.3.7 Post-procedural Care
- •30.3.8 Complications
- •30.4 Peripheral Vascular Injuries (PVI)
- •30.4.1 Background
- •30.4.2 Indication
- •30.4.3 Patient Preparation
- •30.4.5 Embolization Agent
- •30.4.6 Post-procedural Care
- •30.4.7 Complications
- •30.5 Pelvic Trauma
- •30.5.1 Background
- •30.5.2 Indication
- •30.5.3 Technique
- •30.5.4 Patient Preparation
- •30.5.6 Embolization Agent
- •30.5.7 Complications
- •30.6 Maxillofacial Injury (MFI)
- •30.6.1 Background
- •30.6.2 Indication
- •30.6.3 Technique
- •30.6.4 Patient Preparation
- •30.6.6 Embolization Agent
- •30.6.7 Complications
- •30.7 Conclusion
- •References
- •31.1 Introduction
- •31.2 Inferior Petrosal Sinus Sampling
- •31.2.2 Cushing Syndrome (CS)
- •31.2.4 Pre-Procedure Instructions
- •31.2.5 Minimum Hardware Required
- •31.2.7 Result Interpretation
- •31.3 Adrenal Venous Sampling
- •31.3.1 Adrenal Gland Anatomy
- •31.3.2 Vascular Anatomy
- •31.3.3 Primary Hyperaldosteronism
- •31.3.5 Pre-Procedure Instructions
- •31.3.6 Minimum Hardware Required
- •31.3.8 Result Interpretation
- •31.4 Pancreatic Venous Sampling
- •31.4.1 Pancreatic Venous Anatomy
- •31.4.3 Pancreatic Neuroendocrine Tumors
- •31.4.4 Pre-Procedure Instructions
- •31.4.5 Minimum Hardware Required
- •31.4.7 Result Interpretation
- •31.5 Ovarian Venous Sampling
- •31.5.1 Anatomy
- •31.5.2 Hyperandrogenism
- •31.5.3 Pre-Procedure Instructions
- •31.5.4 Minimum Hardware Required
- •31.5.6 Result Interpretation
- •31.6.1 Anatomy
- •31.6.2 Pre-Procedure Instructions
- •31.6.3 Minimum Hardware Required
- •31.6.4 Procedure
- •31.6.5 Result Interpretation
- •31.7.1 Pre-Procedure Instructions
- •31.7.2 Minimum Hardware Required
- •31.7.3 Procedure
- •31.7.4 Result Interpretation
- •31.8 Conclusion
- •References
- •32.1 Introduction
- •32.2 Priapism
- •32.3 Erectile Dysfunction
- •32.3.2 Epidemiology
- •32.3.3 Aetiology
- •32.3.4 Pathophysiology
- •32.3.6 Imaging
- •32.3.7 Relevant Anatomy
- •32.3.7.2 Venous Anatomy
- •32.3.8 Penile Doppler
- •32.4.1 Indications
- •32.4.2 Contraindications
- •32.4.3 Equipment
- •32.4.4 Technical Aspects
- •32.4.5 Procedure Timing
- •32.4.6 Outcomes
- •32.4.7 Complications
- •32.4.8 Post-Procedural Care
- •32.5.1 Indications
- •32.5.2 Contraindications
- •32.5.3 Equipment
- •32.5.4 Technical Aspects
- •32.5.5 Outcomes
- •32.5.6 Complications
- •32.6.1 Indications
- •32.6.2 Contraindications
- •32.6.3 Equipment
- •32.6.4 Procedural Planning
- •32.6.5 Technical Aspects
- •32.6.6 Outcomes
- •32.6.7 Complications
- •32.7 Conclusion
- •References
- •33: Image-Guided Biopsy
- •33.1 Introduction
- •33.2 Biopsy Devices
- •33.3 Pre-Procedural Evaluation
- •33.4 Ultrasound-Guided Biopsy
- •33.5 CT-Guided Biopsy
- •33.6 MRI-Guided Biopsy
- •33.7.2 Breast
- •33.7.3 Lung
- •33.7.4 Mediastinum
- •33.7.5 Liver
- •33.7.6 Gallbladder
- •33.7.7 Spleen
- •33.7.8 Bowel
- •33.7.9 Retroperitoneum
- •33.7.11 Pelvis
- •33.7.12 Spine
- •33.7.13 Extremities
- •33.8 Conclusion
- •References
- •34: Image-Guided Drainage Procedures
- •34.1 Introduction
- •34.2 Etiology
- •34.4 Contraindications
- •34.5 Imaging Modalities
- •34.6 Pre-Procedure Evaluation
- •34.8 Post-Procedure Care
- •34.9 Complications
- •34.10.1 Postoperative Fluid Collection
- •34.10.2 Ascites
- •34.10.3 Liver Abscess
- •34.10.4 Peripancreatic Fluid Collection
- •34.10.5 Splenic Abscess
- •34.10.6 Appendicitis
- •34.10.8 Renal Abscess
- •34.10.9 Pelvic Abscess
- •34.10.10 Prostatic Abscess
- •34.11 Summary
- •References
- •35: Ablation Techniques
- •35.1 Introduction
- •35.2 Chemical Ablation
- •35.3 Thermal Ablation Techniques
- •35.3.1 Radiofrequency Ablation
- •35.3.2 Microwave Ablation
- •35.3.3 Cryoablation
- •35.3.4 High-Intensity Focused Ultrasound
- •35.3.5 Laser Ablation
- •35.4 Non-thermal Ablation Techniques
- •35.4.1 Irreversible Electroporation
- •35.6.1 Liver
- •35.6.2 Kidney
- •35.6.3 Lung
- •35.6.4 Breast
- •35.6.5 Thyroid
- •35.6.6 Musculoskeletal System
- •35.6.7 Nerve Ablation
- •35.7 Conclusion
- •References
- •36.1 Introduction
- •36.3 CT-Guided Biopsy
- •36.3.2 Complications
- •36.3.3 Technical Approaches
- •36.3.4.3 Paramaxillary Approach
- •36.3.4.4 Submastoid Approach
- •36.3.4.5 Transoral Approach
- •36.3.5.1 Anterolateral Approach
- •36.3.5.2 Posterolateral Approach
- •36.3.5.3 Posterior Approach
- •36.4 Ultrasound-Guided Biopsy/FNAC
- •36.4.2.5 Carotid Space
- •36.7 Conclusion
- •References
- •37: Nonvascular Thoracic Interventions
- •37.1 Introduction
- •37.2 Thoracic Drainage Procedures
- •37.2.1 Pre-Procedure Evaluation
- •37.2.2 Imaging
- •37.3 Thoracocentesis
- •37.3.1 Indications
- •37.3.2 Relative Contraindications
- •37.3.4 Technique
- •37.4.1 Indications
- •37.4.2 Contraindications
- •37.4.3 Drain Size
- •37.4.5 Post-Insertion Care
- •37.5 Intrapleural Fibrinolytic Therapy
- •37.5.1 Catheter Removal
- •37.6 Practice Points
- •37.7 Indwelling Pleural Catheter Insertion
- •37.7.1 Duration
- •37.8.1 Procedure
- •37.8.2 Trocar Drainage
- •37.8.3 Seldinger Technique
- •37.8.4 Post-Procedure Follow-Up
- •37.8.5 Removal
- •37.9 Complications
- •37.9.1 Thoracentesis Related
- •37.9.2 Drainage Chest Tube Related
- •37.9.3 IPC Related
- •37.11.1 Pre-Procedure Evaluation
- •37.11.3 Technique
- •37.11.4 Post-Procedure Care
- •37.11.5 Complications [11, 14, 15]
- •37.12.1 Indications [11, 19]
- •37.12.2 Contraindications [11, 19]
- •37.12.3 Technique
- •37.12.4 Post-Procedure Care
- •37.12.5 Complications
- •References
- •38.1 Introduction
- •38.2 Biliary Anatomy
- •38.3 Biliary Obstruction
- •38.4 Percutaneous Transhepatic Biliary Drainage
- •38.4.2 Indications
- •38.4.3 Contraindications
- •38.4.4 Technique
- •38.4.5 Post-Procedure Care
- •38.4.6 Complications
- •38.5 Biliary Stenting
- •38.5.1 Indications
- •38.5.2 Technique
- •38.7 Intraluminal Procedures Through Percutaneous Biliary Access
- •38.7.1 Endobiliary Biopsy
- •38.7.2 Intraluminal Brachytherapy
- •38.7.3 Gallstone Extraction
- •38.8 Percutaneous Cholecystostomy
- •38.8.1 Indications
- •38.8.2 Technique
- •References
- •39.1 Introduction
- •39.2 Percutaneous Gastrostomy
- •39.2.1 Indications
- •39.2.2 Contraindications
- •39.2.3 Pre-procedural Work-Up
- •39.2.4 Technique
- •39.2.6 Pull-Type PRG
- •39.3 Percutaneous Jejunostomy
- •39.3.1 Indications
- •39.3.2 Technique
- •39.4 Percutaneous Cecostomy
- •39.4.1 Indications
- •39.4.2 Technique
- •39.4.3 Post-procedure Care
- •39.5.1 Technique
- •39.6.1 Technique
- •39.6.3 Malignant Tracheoesophageal Fistula Stenting
- •39.6.5 Complications
- •References
- •40.1 Introduction
- •40.2 Percutaneous Nephrostomy (PCN)
- •40.2.5 Post-procedure Care
- •40.4.3 Ureteroarterial Fistula
- •References
- •41.1 Introduction
- •41.2 Fallopian Tube Recanalization (FTR)
- •41.2.1 Technique
- •41.2.2 Complications
- •41.2.3 Results
- •41.3 Amniocentesis
- •41.3.1 Indications
- •41.3.2 Contraindications [7]
- •41.3.4 Technique
- •41.3.5 Complications
- •41.4 Chorionic Villous Sampling (CVS)
- •41.4.1 Indications
- •41.4.2 Contraindications
- •41.4.4 Technique
- •41.4.5 Complications
- •41.5.1 Indications [15–19]
- •41.5.2 Contraindications [20–23]
- •41.5.3 Technique [15, 23]
- •41.5.4 Complications [15, 23, 24]
- •41.5.5 Outcome [23]
- •41.6.1 Technique
- •41.6.2 Complications
- •41.7.1 Contraindications
- •41.7.2 Technique
- •41.7.3 Complications
- •41.8.1 Technique
- •41.8.2 Complications
- •41.9.1 Technique
- •41.9.2 Complications [28, 44, 45]
- •References
- •42.1 Introduction
- •42.2 Breast Biopsy
- •42.2.2 USG-Guided Biopsy [1, 2]
- •42.2.3 MG-Guided Biopsy [3, 4]
- •42.2.4 MRI-Guided Biopsy [1, 11–13]
- •42.2.5 Vacuum-Assisted Biopsy [1, 4, 14, 15, 16]

26 Interventions oftheExtremity Arteries
327
26.5 Recent Advances
26.5.1 Advances inAngioplasty Balloons
Cutting balloons are noncompliant balloons provided with
3–4 atherotomes which “score” the plaque and increase target lesion compliance especially in severe calcication and
recurrent stenosis. However, their superiority over plain balloon angioplasty is yet to be established [30]. Cryotherapy
balloons use a temperature of −10 °C caused by nitrous
oxide that reduces plaque inammation and proliferation of
smooth muscle cells.
26.5.2 Drug-Eluting Technology
Drug-eluting agents inhibit post-intervention inammation
and neointimal hyperplasia. The drugs used can be cytotoxic agents like paclitaxel (M phase inhibitors) or cytostatic agents like sirolimus and its analogs (G1-phase
inhibitors). Drug-coated balloons use standard balloon
angioplasty and antiproliferative agent. In a meta-analysis
of drug-eluting balloons versus plain balloon in peripheral
arterial disease, there was advantage of drug-eluting balloons in anatomic endpoints like primary patency and target
lesion revascularization. However, no advantage was demonstrated in terms of clinical endpoints like amputation,
mortality or change in ABI [31]. Stent-based drug delivery
systems are composed of a metallic platform, drug carrier
vehicle, and a therapeutic agent that reduces neointimal
growth. Zilver PTX randomized controlled trial evaluated
the durability of paclitaxel- coated drug-eluting stents for
femoropopliteal arterial lesions [32]. SIROCCO trial demonstrated no signicant difference between sirolimus-eluting and bare metal stents in femoropopliteal disease,
whereas everolimus-eluting stents had favorable outcomes
and clinical improvement [33, 34]. Drug-eluting stents have
been shown to decrease reintervention risk and amputation
in focal disease of infrapopliteal arteries with no effect on
mortality as compared to plain balloon angioplasty or bare
metal stent implantation [35].
26.5.4 Techniques forChronic Total Occlusion
(CTO)
CTOs are characterized by atherosclerotic plaque causing
complete occlusion of artery for more than three months. A
rigid brous cap is seen at both ends with core consisting of
lipid, thrombus, and extracellular matrix. Antegrade, retrograde, or combined intimal/subintimal approach can be used
for traversing a CTO.A variety of crossing devices have
been developed that cause microdissection
(FRONTRUNNER), mechanical vibration (CROSSER catheter), or mechanical rotation (WILDCAT) and aid in intimal
crossing. Subintimal angioplasty can circumvent the diseased portion of the vessel and provide a plaque-free space.
The disadvantage is difcult re-entry into true lumen which
can be achieved by various re-entry devices like outback
catheter, pioneer catheter, or enteer catheter. Various combined approaches of subintimal crossing include CART
(controlled antegrade and retrograde subintimal tracking),
reverse CART, and SAFARI (subintimal arterial ossing
with antegrade-retrograde intervention. Nowadays, classic
CART is rarely performed due to risk of delivering the balloon across fragile collaterals. Hence, reverse CART is a
more safe method.
26.5.5 Advances inDebulking andPlaque
Removal
Atherectomy devices obliterate atheromatous plaque and
increase luminal diameter without placing a foreign body.
Atherectomy can be of four types: directional, rotational,
orbital, and laser atherectomy [37]. Intravascular lithotripsy
results in plaque modication in lesions with severe calcication. In a recent meta-analysis, lithotripsy is a safe and
effective method for calcied plaques with diameter reduction up to 59%; however, high-quality evidence is required to
prove its efcacy in terms of clinical characteristics and
comparison with other modalities [38].
26.5.6 Pedal Arch Revascularization
26.5.3 Bioresorbable Stents
These stents dissolve and disappear from the vessel after a
period of 2–4years. This avoids potential complications
like in-stent restenosis and long-term antiplatelet therapy.
Most of the bioresorbable stents tested in human studies
are derived from synthetic polymers such as poly-L-lactic
acid (PLLA) [36]. The disadvantages include inferior tensile modulus, thicker struts, and increased crossing
prole.
The main pedal-plantar connection is the pedal-plantar loop
which is formed by the anastomosis between dorsalis pedis
artery with plantar arch and lateral plantar artery. Pedalplantar loop technique consists of recanalization of both
pedal and plantar arteries with their anastomosis. In a systematic review and meta-analysis, no statistically signicant
difference was observed when tibial and pedal artery interventions were performed as compared to tibial interventions
alone. However, wound healing was better when both tibial
and pedal artery interventions were combined [39].

328
M. Verma and N. N. Pandey
26.5.7 Percutaneous Deep Vein Arterialization (DVA)
DVA is performed in no-option chronic limb-threatening
ischemia and occlusion of pedal arteries with the rationale of
providing nutritional support by reversal of ow through
venules and stimulation of angiogenesis. A nitinol stent is
used to create an arteriovenous stula [40].
26.5.8 Therapeutic Angiogenesis andStem
Cell Therapy
Cell-based therapies are newer approaches in no-option
chronic limb-threatening ischemia and therapeutic angiogenesis with bone marrow-derived stem cells (BM-SC) or
progenitor cells have been used in various clinical studies.
The stem cells are stimulated by the surrounding hypoxic
environment, and due to the paracrine effects of various factors, neo-angiogenesis is initiated [41]. A meta-analysis has
demonstrated the efcacy of cell-based therapy in terms of
ulcer healing, reduced amputation rate, and improvement in
pain-free walking distance [42].
26.6 Acute Limb Ischemia
In patients with possible diagnosis of acute limb ischemia,
Rutherford classication is recommended for clinical evaluation (Table26.1) and computed tomography angiography is
the rst-line modality for anatomical imaging [43].
Initial medical management includes analgesia and intravenous administration of unfractionated heparin—initially
70–100IU/kg followed by infusion and monitoring by activated clotting time or activated partial thromboplastin time
(APTT). Threatened limbs require revascularization which
can be performed by open surgical or endovascular tech-
niques. Open revascularization techniques include thromboembolectomy and surgical bypass. For patients with ALI,
intravenous thrombolysis is not recommended. The various
endovascular methods for treatment of ALI include catheterdirected thrombolysis (CDT), thrombus aspiration, mechanical thrombectomy, and ultrasound accelerated thrombolysis.
In patients with Rutherford class IIa, CDT can be considered
as an alternative to surgery (IA), whereas in IIb class, CDT
may be considered if initiated promptly and can be combined
with thromboaspiration or thrombectomy (IIb B) [43].
Patients with Rutherford class I have signicant morbidity
and mortality when thrombolysis is performed for condition
that does not threaten their limbs. Hence, these patients are
treated conservatively with best medical treatment and
supervised walking therapy.
Anterior wall puncture is recommended ideally under
ultrasound guidance. Urokinase and recombinant tissue
plasminogen activator (rtPA) are the most commonly used
thrombolytic agents. Society of Interventional Radiology
recommends weight-based dose to be 0.02–0.1mg/kg/hour
[44]. The non-weight related dose is between 0.25 and
1 mg/hour with the maximum recommended dose being
40 mg. For patients undergoing thrombolysis systemic
therapeutic, heparinization is not recommended. Patients
should be monitored for vital signs, access site complications, and limb condition. Mechanical thrombectomy can
be performed using rheolytic catheters or microfragmentation. Ultrasound accelerated thrombolysis can be performed using high frequency low intensity ultrasound that
hastens enzymatic clot lysis by loosening brin strands and
exposing more plasminogen receptors for binding. In a
Cochrane review comparing open surgery versus thrombolysis in ALI, there were no signicant differences in limb
survival or mortality after 30days, 6 months, or 1 year.
However, after 1month the thrombolysis group had more
hemorrhagic strokes, major bleeding, and distal embolization [45].
Table 26.1 Rutherford classication for acute limb ischemia [6]
Category
I.Viable – – Audible Audible
II.Threatened
(a) Marginally Minimal (toes) – Inaudible Audible
(b) Immediately More than toes Mild to moderate Inaudible Audible
III.Irreversible Profound Profound Inaudible Inaudible
Findings
Sensory loss Muscle weakness Arterial Venous
Doppler signals

ab
26 Interventions oftheExtremity Arteries
329
26.7 Popliteal Artery Entrapment Syndrome (PAES)
It is characterized by abnormal compression of popliteal
artery due to its abnormal relationship with surrounding
myofascial structures. There are six types according to
anatomy- based classication: medial course of artery (type
1), lateral insertion of medial head of gastrocnemius muscle
(type 2), accessory muscle slip (type 3), brous band or popliteus muscle (type 4), abnormality with entrapment of popliteal vein and artery (type 5), and hypertrophy of
gastrocnemius muscle (type 6).Repeated trauma to the artery
during plantar or dorsal exion results in premature atherosclerosis and thrombosis or distal thromboembolism [46].
Imaging modalities depict stenosis of popliteal artery during
dynamic compression. The denitive treatment for PAES
types 1–5 is the surgical release of gastrocnemius muscle /
brous band. In acute arterial thrombosis, catheter-mediated
thrombolysis can be performed.
Fig. 26.9 A 50-year-old man
with moderate osteoarthritis.
Digital angiogram revealed
signicant synovial blush
from descending genicular
artery in medial knee joint (a)
which was embolized using
imipenam/cilastin with
reduction in synovial blush
(b)
26.8 Genicular Artery Embolization (GAE)
Osteoarthritis (OA) is a degenerative joint disease characterized by wear and tear of joint, cartilage, and bone.
Mechanical forces result in degenerative changes and
inammation which stimulates angiogenesis. Kallgren and
Lawrence (KL) classication denotes the grading system
based on OA severity. GAE is the selective intra-arterial
embolization of geniculate arteries supplying the hypervascular segments related to pain (Fig.26.9). The reduction in
the blood supply of synovium results in decreased neovascularity and pain. The various embolic agents that can be
used include imipenam/cilastin, embozene, or PVA particles
[47]. In a meta-analysis, GAE resulted in signicant
improvement in VAS (Visual Analogue Scale) and WOMAC
score. Pain with better functional status and decreased need
for pain medication [48].

330
M. Verma and N. N. Pandey
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Interventions oftheExtremity Veins
ReshamSingh andVineetaOjha
27
Key Messages
1. Chronic venous insufciency (CVI) results from venous
valve dysfunction, leading to leg swelling, varicose
veins, leg pain, and skin changes.
2. CVI carries a considerable burden on the healthcare system while also deteriorating patients and quality of life.
3. Endovascular management of varicose veins is a minimally invasive treatment option which provides faster
recovery and improved cosmetic outcomes compared to
surgery.
4. Different endovascular interventions for varicose veins
include thermal ablative methods and non-thermal ablative methods.
5. Thermal ablative methods use thermal energy under
perivenous tumescent anaesthesia and include endovenous laser ablation (EVLA), radiofrequency ablation
(RFA) and endovenous steam ablation (EVSA).
6. Non-thermal ablative methods include foam sclerotherapy, cyanoacrylate glue, mechanochemical ablation and
cryosclerosis, which involve inciting endothelial damage to venous wall leading to venous thrombosis and
brosis.
7. In deep venous thrombosis (DVT), endovascular management is mainly done in patients with severe symptoms of extensive iliofemoral DVT who have a
reasonable life expectancy.
8. Different endovascular interventions in DVT include
catheter-directed thrombectomy, catheter-directed
thrombolysis, or pharmacomechanical catheter-directed
thrombolysis.
9. Different endovascular interventions in pulmonary
embolism (PE) also include catheter-directed thrombolysis or catheter-directed thrombectomy (if thrombolysis
is contraindicated).
R. Singh · V. Ojha (*)
Department of Cardiovascular Radiology and Endovascular
Interventions, All India Institute of Medical Sciences, Delhi, India
10. Endovascular intervention in PE is done in acute massive PE or submissive PE with RV strain pattern if systemic thrombolysis is contraindicated.
27.1 Introduction
The individual, mental and societal burden caused by venous
disorders is considerable, and the beginning of different
interventions in veins of extremities for varicose veins dates
back to 1500BC [1]. There has been a continuous evolution
in endovascular intervention from performing the rst
attempts of venous thrombectomy in DVT (in the early
1920s) to venous stents and mechanical thrombectomy in the
previous two to three decades to treat a complicated disorder
of the lower limb venous system. The surgical method of
treatment in chronic venous insufciency has been associated with high recurrence rates (up to 60%), neurovascular
injuries and more postoperative complications [2]. Success
rates after endovenous techniques, for example, radiofrequency ablation (RFA) and endovenous laser ablation
(EVLA) are excellent in chronic venous insufciency. So in
this chapter, we will be discussing the diseases affecting the
extremities of peripheral veins and different interventions in
detail.
27.2 Relevant Anatomy
Classical venous vascular anatomy elaborated in the literature is present in less than 16% of individuals [3]. There are
marked embryological variations and developmental anomalies in the lower limb. The lower limb venous system consists
of deep veins, supercial veins and perforating veins
which are described by their relationships and proximity to
muscular fascia. The deep veins primarily drain muscles
and travel in close vicinity of arteries of the lower limb. The
supercial veins run in subcutaneous space and drain primarily the cutaneous and subcutaneous microcirculation.
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
S. H. Chandrashekhara (ed.), Textbook of Interventional Radiology, https://doi.org/10.1007/978-981-97-9601-4_27
333

334
b
R. Singh and V. Ojha
The supercial venous system consists of a small saphenous
vein (SSV), a great saphenous vein (GSV) and various
venous tributaries. Perforating veins connect the supercial
veins to deep veins after traversing the muscular fascia.
27.3 Varicose Veins
Varicose veins are dilated, tortuous supercial venous channels and represent venous dysfunction which occurs due to
venous valvular incompetence. This incompetence of valves
can occur in supercial, perforating and/or deep veins which
leads to the ow reversal and resultant venous hypertension
in the lower limb venous system. The cause of valvular
incompetence is multifactorial, which mostly occurs because
of
• Pathological dilatation of supercial vein.
• Post-thrombotic syndrome occurring as a result of recanalization of deep venous thrombosis (DVT).
• Congenital absence/hypoplastic valves.
Varicose veins include spider veins, reticular veins and
true varicosities. The signicantly high prevalence of chronic
venous insufciency in the general population, high patient
morbidity and the cost of treating its complications contribute to a signicant burden on healthcare resources and patient
nancial status [4].
27.3.2 Physical Examination
Physical examination includes signs of CVI, size, location of
varicosities and venous ulcer if present and lastly status of the
arterial system. There are many clinical classications/scoring systems available in the literature which are used to elaborate these varicose veins. CEAP classication is the most
commonly used classication to narrate the varicose veins
(Fig.27.1). In general, the CEAP clinical classes stand for:
C0: none.
C1: telangiectasia.
C2: varicosity.
C3: oedema.
C4: skin changes.
C4a: pigmentation or eczema.
C4b: lipodermatosclerosis or atrophie blanche.
C5: healed ulcer.
C6: active ulcer.
Recently, there have been certain additions in the above
classication like corona phlebectasia as the C4c subclass,
and “r” was added for recurrent ulcers or varicose veins and
the numeric descriptions of the venous segments were
replaced with their common abbreviations.
27.3.3 Sonological Evaluation
27.3.3.1 Duplex Sonographical Evaluation
27.3.1 Clinical Evaluation
A detailed history of patient with chronic venous insufciency is must, and it includes the nature and duration of
clinical symptoms, previous history of deep venous thrombosis and prior treatments for varicose veins.
a
Fig. 27.1 Varicose vein CEAP classication. (a) Varicose Vein—C2, (b) Oedema—C3, (c) skin changes—lipodermatosclerosis—C4, (d) active
ulcer—C6, (e) healed ulcer—C6
c
Duplex sonographical evaluation is the investigation of choice
and primary diagnostic modality for chronic venous insufciency. A number of patient positioning have been described
for duplex sonography in the literature which include
Standing on an examination bed.
Combination of standing and sitting/supine position.
de

27 Interventions oftheExtremity Veins
335
Lying position 0-degree tilt.
Lying on a tilt table in reverse-Trendelenburg position at
≥30° or ≥60° incline.
Sonographical evaluation of varicose veins includes
assessment of
• The saphenofemoral (SFJ) or saphenopopliteal (SPJ)
junctional incompetence.
• Truncal veins (GSV) diameter at proximal thigh ~2cm
below saphenofemoral junction, mid-thigh level and just
above the knee.
• Supercial telangiectasia/reticular vein/varicosities/ in
the lower limb.
• Location and diameter of incompetent perforators (location described as a distance from xed bony landmarks).
• Deep venous reux.
• Presence of DVT: It is of utmost importance to preclude
DVT before taking the patient for endovascular ablative
procedure as it can be extremely catastrophic to perform
ablation in signicantly occluded deep veins.
27.3.4 Current Consensus among Dierent
Vascular Societies
The current consensus among different vascular societies
recommends the cut-off time for valvular incompetence
with the reux duration of
• 1 second in common femoral vein, supercial femoral
vein (SFV) and popliteal vein (PV)
• 0.5s for great saphenous veins (GSV) and short saphenous veins (SSV), deep femoral and calf veins
• 0.35s for lower limb perforators.
27.3.5 Endovascular Interventions forVaricose
Veins
27.3.5.1 Thermal Ablation
Endothermal ablative techniques are highly efcacious
methods of treatment of chronic venous insufciency as
compared to surgery [5]. Thermal ablation techniques
include endovenous laser ablation (EVLA), endovenous
steam ablation (EVSA) and radiofrequency ablation (RFA).
All these endothermal ablation techniques use thermal
energy and involve the administration of perivenous tumescent anaesthesia. The perivenous administration of tumescent anaesthesia acts as a sink to the heat generated during
thermal ablation in addition to the anaesthesia [6]. It also
collapses the venous lumen and increases the area of contact
between the endovenous laser/catheter and the venous wall.
Endovenous Laser Ablation
This procedure involves the administration of endoluminal
laser energy (Fig. 27.3). In the past two decades, signicant
evolution in EVLA’s laser bres has happened with higher
wavelength lasers making ablation of signicantly dilated
veins (5–15mm) possible. The mechanism of action includes
damage and perforations in the venous wall caused by the
laser energy due to direct contact as well as due to superheated steam bubbles resulting in injury to the endothelium
of the wall resulting in the thickening, contraction and brosis of the venous wall [7].
Procedure GSV is punctured at the knee with a needle of
16–18G in the Trendelenburg position, followed by the introduction of vascular sheath. Laser bre is introduced through
vascular sheath and is advanced up to 2cm caudal to the
saphenofemoral junction and is conrmed with sonography
followed by tumescent anaesthesia administration (Fig. 27.3).
Laser is then red and supercial vein is ablated with slow
withdrawal of the laser bre. The withdrawal rate of laser
bres in continuous mode is 2–4mm/sec and is stepwise at
10–15W power if red in pulsed mode. It has been found that
the pulsed mode leads to more complications than the continuous mode, so the continuous mode is usually preferred
over the pulsed mode [8]. There are laser bres of different
wavelengths available ranging from 810 to 1920 nm. Laser
bres of lower wavelength use haemoglobin as chromophore,
and water is used as chromophore in higher wavelength laser
bres. 1470nm wavelength laser bres are most commonly
used nowadays. It has been found that higher wavelength
laser bres are more efcient in energy transmission and
result in high occlusion rate. Higher wavelength laser bres
lead to less post-operative complications like pain and skin
discolouration [9]. After the procedure, patients are told to
use compression bandages and advised to do their daily activities immediately. A follow-up sonogram is done 24h after
the procedure to assess and conrm the ablation of the supercial vein and rule out deep vein thrombosis(Fig. 27.4).
C/I to this procedure includes targeted supercial vein
thrombosis, deep vein thrombosis, pregnancy and critical
limb ischaemia secondary to arterial disease.
Procedural success of this intervention ranges between
96% and 100% with a success rate of up to 90–94% at 3years
and 85–88% at 5years [10]. But recurrence rates are very
similar to the surgical methods (33.3%) at 5years after the
EVLA (36.6%) [11].
Complications Most common side effects include ecchy-
moses and pain. Rare complications include burns, DVT,
nerve injury and pulmonary embolism [12]. Other rare complications of EVLA include endovenous heat-induced thrombosis (EHIT) in which there occur thrombus extension into
deep veins with an incidence of 0–5.6%.

336
Fig. 27.2 Ultrasound-guided
foam sclerotherapy (UGFS)
procedure: Under aseptic
precautions and USG
guidance, varicosities are
punctured with buttery
cannula (a, b). Venogram of
varicosities is obtained to
assess any communication
with deep veins and the
amount of contrast injected
(c). Foam sclerosant is
prepared with the Tessari
method and the same amount
of foam sclerosant by
buttery cannula (d)
R. Singh and V. Ojha
a
b
cd
Radiofrequency Ablation
RFA is a thermal ablative technique used to obliterate reuxing supercial veins and was approved by the FDA in 1999.
In RFA, high-frequency alternating current of temperature 80–120°C is passed to the supercial vein by RFA catheter which results in heating, loss of vascular architecture
and disintegration of the vessel.
Procedure The initial step of the RFA procedure is similar
to EVLA.The catheter is advanced to 2–3cm caudal to the
saphenofemoral junction. Temperature, impedance and generator output should be monitored, and the rate of withdrawal
adjusted accordingly during the procedure. The procedural
success, recurrence and occlusion rates for RFA are largely
similar to EVLA [13]..
Complications of RFA Post-procedural pain and ecchymosis are less frequent than that with EVLA [13]. The DVT
incidence after RFA is slightly higher than EVLA with a
reported incidence of 0.2–1.4%, which is slightly higher in
patients with RFA compared to EVLA [14]. The rest of the
procedural complications of RFA are very similar to the
EVLA.
Endovenous Steam Ablation
The procedural steps of EVSA are similar to endovenous
laser ablation. But once the tumescent anaesthesia is administered, pulses of steam at ~120°C as 3–4 puffs are delivered
each at 1cm intervals in the supercial vein to be ablated.
The procedural success is similar to EVLA at 1year. But it
has been found that EVSA is associated with lesser pain and
time to recovery and more satisfaction rates compared to
EVLA [15].
27.3.5.2 Non-thermal Ablative Methods
Foam Sclerotherapy
Venosclerotherapy under USG guidance is based on the
usage of the physical and biochemical properties of a sclerosant (Fig.27.2). Selective intravenous delivery of a sclerosant causes endothelial damage and resultant brosis and
thrombosis. The most commonly used sclerosant in venosclerotherapy are polidocanol and sodium tetradocyl sulphate. Sclerotherapy also produces other effects like
denaturation of proteins, protein extraction from lipids, cell
dehydration by osmosis and luminal obstruction by polymerization of sclerosant.

27 Interventions oftheExtremity Veins
Fig. 27.3 EVLA procedure.
Under aseptic precaution,
EVLA is done after taking
venous access with 6 French
vascular sheath (a) and laser
bre (b) advanced in GSV/
SSV 2cm below SFJ/SPJ (c).
Perivenous tumescent
anaesthesia is administered
under USG guidance (d)
337
a
c
abc
b
d
Fig. 27.4 Laser bre is red (a) with continuous withdrawal (b) and the amount of energy used is noted (c)
Technique Percutaneous introduction of buttery needle is
done in supercial varicosity till retrograde ow of blood is
observed in buttery cannula followed by venogram.
Sclerosant foam is injected slowly into the vein (amount varies from case to case). The Tessari method is the most commonly used method of foam preparation (Fig.27.2). Local
compression is applied after injection for 5–10min. If patent
venous channels remain after sclerotherapy on follow-up
USG, second- stage venosclerotherapy can be planned after
6–8 weeks. Some contraindications to venosclerotherapy
include hypersensitivity to the sclerosant, skin infection and
deep venous thrombosis.
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