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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]

6 Periprocedural Bleeding andThrombotic Considerations inInterventional Radiology
Table 6.2 (continued)
S no. Drug Withholding before the procedure Restarting after the procedure
1. Cyclooxygenase inhibitors
Aspirin Do not with hold in low risk procedures. May
withhold for 3–5 days for high-risk procedures
after multidisciplinary discussion.
2. P2Y12 receptor inhibitors
Ticlopidine 10–14 days 1 day
Clopidogrel 5–7days 6h if 75mg dose used; 24h if 300–600mg
Prasugrel 5–7days 2–3days
Ticagrelor 2–3days 2–3days
Cangrelor 1h Patients receiving Cangrelor are undergoing
3. GpIIbIIIa inhibitors
Abciximab 24h Patients receiving GpIIbIIIa inhibitors are
Eftibatide, tiroban 4–8h
4. Phosphodiesterase inhibitors
Cilostazol Do not withhold NA
aPTT activated partial thromboplastin time, CrCl creatinine clearance
1day
loading dose used
PCI or are within immediate periprocedural
period from cardiac intervention - need
multidisciplinary discussion for shared
decision making
undergoing PCI or are within immediate
periprocedural period from cardiac
intervention - need multidisciplinary
discussion for shared decision making
45
Table 6.3 Reversal agents for various antiplatelet and anticoagulant
agents
Drug Reversal agent
Unfractionated
heparin
Low molecular weight
heparin
Fondaparinux Recombinant factor VIII, prothrombin
Warfarin Vitamin K, prothrombin complex
Factor Xa inhibitors Andexanet alpha, ciraparantag
Dabigatran Idarucizumab, prothrombin complex
Antiplatelet agents Platelet transfusion, desmopressin
Protamine
Protamine (reverses 60% of the effect)
complex concentrate
concentrate, fresh frozen plasma
concentrate, cryoprecipitate
during procedures with high risk of bleeding, except cangrelor and GpIIb-IIIa inhibitors which need to be withheld for
low-bleeding risk procedures as well. If the procedure is to
be done on an emergency basis and cannot be postponed till
the therapeutic effect of the drug weans off, reversal agents
can be used (Table6.3).
6.5 Specic Disease Considerations
While each patient has a unique set of clinical issues, certain
conditions are known predisposing factors for bleeding complications. Chronic liver disease, chronic kidney disease,
thrombocytopenia, and intake of anti-thrombotic medications are some of the commonly encountered situations
where the patient is at an increased risk of bleeding due to
the derangement of the primary or secondary hemostatic
mechanisms.
6.5.1 Chronic Liver Disease
Coagulopathy is a common manifestation of liver disease.
However, a patient with liver disease is not just at an increased
risk for bleeding, but the risk of thrombosis is also higher
than the general population [9]. Both primary and secondary
hemostatic mechanisms are rebalanced in liver disease.
Thrombocytopenia is compensated by an increase in the
level of vWF.
There is a deciency of all procoagulants other than factor
VIII and vWF and all-natural anticoagulants including protein C and S and antithrombin III [10]. Therefore, overcorrection of deranged INR or platelet count in these patients
may lead to thrombotic complications [11]. Therefore, it is
recommended that the threshold for transfusing FFP or platelets be higher in patients with liver disease.
6.5.2 Chronic Kidney Disease
Impaired function of vWF and platelet-endothelial interaction, along with erythrocytopenia leading to reduced ADP
for platelet activation, increases the risk of bleeding in
patients with renal disease. Reduced renal clearance of

46
N. Baijal et al.
drugs causes the longer duration of action of drugs such as
low- molecular weight heparin, fondaparinux, and some oral
anticoagulants. Platelet dysfunction and altered pharmacokinetics are exacerbated in uremia. While these patients will
often be referred to the interventional radiologist for lowrisk procedures such as the placement of venous catheters
for dialysis access, their laboratory parameters must be
evaluated before the procedure to avoid hemorrhagic
complications.
6.5.3 Thrombocytopenia
Non-immune conditions causing a low platelet count such as
dengue fever are easily managed by platelet transfusion.
Immune thrombocytopenia is characterized by autoantibodies against platelets, and patients with this condition do not
benet from platelet transfusions until the autoimmune
response is suppressed using steroids or intravenous immunoglobulins. Inherited disorders of bleeding and coagulation,
such as hemophilia and von Willebrand disease, require
appropriate management.
6.5.6 Patients withProsthetic Heart Valves
There are two kinds of prosthetic heart valves: mechanical
and bioprosthetic. Mechanical heart valves are at increased
risk of thrombosis. As per the study by Roudaut etal., the
risk for thrombosis in mechanical heart valves is maximum
during the rst year after the procedure and then plateaus till
the fourth year after surgery, followed by a gradual decline
over the following years. On the other hand, bioprosthetic
valves are at lower risk of thrombosis, and the risk becomes
negligible 3months after the implantation once the endothelialization occurs at the suture site.
According to American Heart Association (AHA) guidelines, a patient with a prosthetic heart valve might be receiving vitamin K antagonist (VKA) or single/dual antiplatelet
therapy, or both. Irrespective of the anticoagulant/ antiplate-
let drug or whether the procedure is elective/emergency,
there is no need to discontinue any drug in low-risk
procedures.
On the other hand, if a patient is undergoing a high-risk
procedure, the management depends on whether the procedure is elective or emergent.
Elective high-risk procedures:
6.5.4 Disseminated Intravascular Coagulation (DIC)
Commonly associated with sepsis or underlying malignancy,
DIC is a consumptive coagulopathy in which the formation
of microthrombi leads to a deciency of platelets and coagulation factors and bleeding diathesis. Management of such
patients is complex as replacement of the decient factors
leads to further thrombotic complications and may not necessarily control bleeding. However, such patients would
require emergency endovascular interventions, and a multidisciplinary approach is necessary along with the treatment
of the underlying disease to correct the deranged coagulation
prole.
6.5.5 Malignancy
Interventions in patients with malignancy are usually palliative or adjunctive to the primary therapy. Such patients have
a lower tolerance for bleeding complications due to the overall clinical condition and commonly associated
DIC.Multidisciplinary discussion with the medical and surgical oncologists is essential to decide upon the appropriate
management of such patients.
1. Bi-leaet mechanical heart valve: Temporary cessation of
VKA is recommended.
(a) Stopped 3–4days before the procedure to allow INR
to fall below 1.5.
(b) Re-started once the bleeding risk subsides, typically
12–24h after the procedure.
(c) Bridging anticoagulant therapy with heparin is not
required.
2. Patient with other mechanical heart valves/other risk factor for thrombosis:
(a) Bridging therapy is recommended in addition to the
above.
6.6 Bridge Therapy
Bridge therapy means replacing a long-acting anticoagulant
with a short-acting one so that the time period with subtherapeutic INR can be minimized during a procedure.
Intravenous unfractionated heparin or subcutaneous low
molecular weight heparin (LMWH) is the commonly used
short-acting anticoagulants used for bridging. The patient’s
INR is regularly monitored. When it falls below 2.0–2.5,
based on the clinical scenario, these drugs are started usually
36–48h before the procedure and stopped as follows:

6 Periprocedural Bleeding andThrombotic Considerations inInterventional Radiology
47
(a) UFH: 4–6h before the procedure
(b) LMWH: 12h before the procedure
UFH can be restarted in 6–8 h, and LMWH can be
restarted 12h after surgery. This way, we can minimize the
time period with subtherapeutic INR. However, before
restarting anticoagulants, every patient should be assessed
for potential risk of bleeding.
Current Role of Bridging: Multiple randomized controlled trials have proven the futility of bridging therapy.
Studies have shown that while there was no signicant difference in the incidence of periprocedural thrombotic events,
the periprocedural bleeding events were more in patients
started on bridge therapy with UFH/LMWH, as compared to
those who were continued on VKA therapy. The AHA guidelines advise that the decision for bridging should be individualized based on the patient’s prole.
Emergency high-risk procedure: For a patient who is to
undergo an invasive procedure with a high risk of bleeding
and is on anticoagulants for a mechanical heart valve, the
clotting factors can be restored by transfusing fresh frozen
plasma or prothrombin complex concentrate.
Table 6.4 Wells criteria for assessment of DVT
Criteria points
Active cancer (treatment ongoing, within previous 6months
or palliative)
Paralysis, paresis, or recent plaster immobilization of lower
extremities
Recently bedridden >3days or major surgery within
12weeks requiring general or regional anesthesia
Localized tenderness along distribution of deep venous
system
Entire leg swollen 1
Calf swelling 3cm larger than asymptomatic side measured
10cm below tibial tuberosity
Pitting oedema conned to symptomatic leg 1
Collateral supercial veins (non-varicose) 1
Alternative diagnosis at least as likely as deep vein
thrombosis
1
1
1
1
1
−2
3months after the initial episode of acute DVT.However, in
case of an emergency, oral anticoagulants can be discontinued 3–4 days before surgery and restarted as discussed
above. There is no data available on the need for bridge therapy in such situations. However, based on clinical prole, or
a high Wells score, bridging may be done. DVT prophylaxis
may be given to patients with a high risk of developing DVT.
6.7 Deep Vein Thrombosis (DVT)
DVT can occur due to multiple factors like obesity, immobility, trauma, cancer, use of oral contraceptive pills, or in case
of congenital or acquired thrombophilia. The most common
site of DVT is the muscular calf veins.
A patient with acute DVT is usually managed on parenteral anticoagulant till the symptoms improve, followed by
oral anticoagulant (OAC) for at least 3months. This is based
on the fact that the risk of recurrence of DVT is maximum in
the rst 30 days of the initial episode after which it starts
decreasing and plateaus at 3months from the initial episode.
The risk of recurrence is higher for proximal compared to
distal vein thrombosis.
Wells criteria can be used to assess for recurrence of DVT,
and a score<1 is associated with a low probability of DVT
(<3%), while a score of ≥3 is associated with a very high
probability of DVT (~75%) (Table6.4).
IR procedures in patients with DVT: Low-risk procedures
can be performed without interrupting OACs. Ideally, a highrisk elective procedure should be postponed for at least
6.8 Atrial Fibrillation (AF)
When the patient’s heart is contracting ineffectively and at a
high rate, there is a relative stasis of blood in the heart chambers, which predisposes the patient to thrombus formation
and associated embolic phenomenon. It is for this reason that
patients with AF are not only started on rate/rhythm control
drugs but also on anticoagulants. As every patient doesn’t
need anticoagulation, European Society of Cardiology and
National Institute for Health and Care Excellence (NICE)
recommend the use of the CHA2DS2VASc score for stratication of patients with AF to start anticoagulants (Table6.5).
Management
1. Low-risk patients (Score 0 for males and 1 for females)—
No anticoagulant therapy is recommended.
2. Moderate-risk patients, i.e., males with a score 1—Oral
anticoagulation therapy should be considered.
3. High-risk patient (score 2 or above)—it is recommended
to start anticoagulation, usually on VKA or DOACs.

48
N. Baijal et al.
Table 6.5 CHA2DS2VASc score for risk stratication in patients with
atrial brillation
Condition Points
C Congestive heart failure (or left ventricular systolic
dysfunction)
H Hypertension: BP consistently >140/90mmHg 1
A2
Age≥75years
D Diabetes mellitus 1
S2 Prior stroke or TIA or thromboembolism 2
V Vascular disease (e.g., peripheral artery disease) 1
A Age 65–76years 1
Sc Sex category (i.e., female sex) 1
1
2
6.9 Coronary Stents
There are different types of coronary stents—bare metal
stents, drug-eluting stents, bioresorbable stents, and dual
therapy stents. Each of these is managed with a combination
of antiplatelet drugs and anticoagulants for different periods.
Stent thrombosis is associated with a high risk of myocardial infarction and high mortality. Multiple studies have shown
that the incidence of stent thrombosis is maximum during the
rst 2 years after the intervention (~2%). The Academic
Research Consortium denes stent thrombosis as acute
(<24h), early (1–30days), late (30days–1year), and very late
thrombosis. The risk of early and late thrombosis is high in
both bare metal stents and drug eluting stents; however, very
late thrombosis is highly associated with DES. It is for this
reason that dual antiplatelet therapy is continued for a longer
period in DES for ~1year (vs 4–6weeks in bare metal stents).
An important factor associated with stent thrombosis,
besides the type of stent, number, and length of stents, presence of comorbidities like diabetes and chronic renal failure,
and extent of coronary artery disease is early discontinuation
of dual antiplatelet therapy, especially during the rst
30 days after the intervention. As per AHA recommenda-
tions, an elective high-risk procedure should be discontinued
for at least 30days in case of bare metal stents and 365days
in case of drug eluting stents.
There are no clear guidelines for the management of antiplatelet therapy in patients with coronary stents when it
comes to IR procedures. However, the practice based on
multiple studies done on patients with coronary stents undergoing cardiac surgeries is as follows:
I. Bare metal stent placed >12 weeks ago for ACS
and>6weeks ago for non-ACS indication:
(a) If the patient has a high bleeding risk, antiplatelet
therapy is discontinued 5–7days before surgery.
(b) If the patient has a low bleeding risk, aspirin is con-
tinued at a low dose of 81mg.
II. DES placed <1year ago: based on patient bleeding risk,
aspirin is reduced to a low dose of 81mg, or stopped,
and bridge therapy is started.
III. DES placed >1year ago: based on patient bleeding risk,
aspirin can be discontinued 5–7days before procedure,
or it can be reduced to 81mg minimal dose (for low risk).
6.10 Conclusion
Periprocedural bleeding and thrombotic risk depends on several patient- and procedure-related factors. A thorough preprocedure workup includes clinical history and laboratory
investigations to identify and optimize abnormalities of
hemostasis. In case an emergency procedure is required in a
patient with a bleeding tendency, platelets or coagulation factors may be transfused to reduce the bleeding risk. Antithrombotic medications may be withheld for a short duration
prior to elective procedures as per SIR guidelines, with bridge
therapy in selected patients who have a high risk of thrombosis. Multidisciplinary discussion and shared decision-making
is necessary in complicated cases with multiple comorbidities
in order to minimize bleeding risk from the procedure and
thrombotic risk from the underlying disease condition.
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Embolization inInterventional
Radiology
RanjanKumarPatel, TaraprasadTripathy,
M.MaivizhiShruthi, andTejPal
7
Key Messages
1. Adequate knowledge about hardwires and embolic
agents is essential for therapeutic embolization without
non-target embolization.
2. Pre-procedural imaging (most commonly CT angiography) aids in procedural planning and decreasing procedural time and radiation exposure.
3. Coagulopathy may limit the effectiveness of solid
embolic agents, such as coils and vascular plugs. In such
a situation, liquid embolic may be required as they do
not depend on the patient’s coagulation status.
4. NBCA or glue is difcult to control and requires adequate technical expertise to avoid complications.
5. Due to superior exibility, trackability, and control,
hardwires used in neurointervention may be used in
complex peripheral vascular embolization cases.
6. Due to the lack of a denite adventitia, sac packing
should be avoided in pseudoaneurysms owing to the risk
of sac rupture and rebleeding.
7. Aneurysm with a wide neck requires balloon or stentassisted remodeling techniques for sac packing.
8. Embolization should be performed super-selectively in
organs with end-arteries (e.g., kidney) to prevent the risk
of larger ischemia or necrosis.
9. A detailed knowledge of ICA-ECA anastomosis is very
crucial to avoid life-threatening complications following
embolization of head and neck pathologies.
10. To avoid recurrence, nidus and outow veins must be
embolized in case of AVM.
R. K. Patel (*) · T. Tripathy · M. MaivizhiShruthi
Department of Radiodiagnosis, All India Institute of Medical
Sciences, Bhubaneswar, India
e-mail: radiol_tara@aiimsbhubaneswar.edu.in
T. Pal
Department of Radiology, National Cancer Institute, Jhajjar, All
India Institute of Medical Sciences, Delhi, India
7.1 Introduction
Embolization or embolotherapy refers to an intentional vascular occlusion at any level, from large arteries or veins to
capillary beds, using the deployment of a device or embolic
agent. Embolization per se encompasses a wide range of
clinical situations, from control of hemorrhage to tumor
devascularization. In many situations, embolization provides
treatment of several clinical conditions in a minimally invasive manner but with a lower morbidity and mortality rate
than surgery [1]. With newer embolic agents and hardwires,
many complex vascular pathologies are increasingly managed through percutaneous transcatheter embolization.
However, inadvertent non-target embolization may lead to
various complications. Hence, a comprehensive understanding and adequate knowledge of the various embolization
techniques are essential for optimal and safe use [2].
Various broad categories of vascular embolization include:
1. Occlusion of aneurysm, pseudoaneurysm, or vascular
anomalies (e.g., intracranial berry aneurysm, pancreatitisrelated visceral artery pseudoaneurysm, arteriovenous
malformation, etc.)
2. Control of hemorrhage by occluding placing a covered
stent to occlude the ow in a pathologic segment of a vessel or to slow the ow in a branch feeding the site of a
hemorrhage or stula.
3. Tumoral devascularization for palliation or to reduce
operative blood loss (TACE for hepatocellular carcinoma,
preoperative embolization of juvenile nasopharyngeal
angiobroma).
4. Devascularization of benign/nonneoplastic tissue producing adverse health effects (partial splenic embolization
for hypersplenism, uterine broid embolization).
5. Flow diversion to protect normal tissue (collateral embolization before radioembolization for hepatic tumors, portal vein embolization for hepatic hypertrophy).
6. Endoleak management (direct sac puncture or collateral
vessel embolization in type II endoleak).
© 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_7
51

52
R. K. Patel et al.
7.2 Role ofPre-embolotherapy Imaging
Prior imaging is crucial to successful embolization and to
avoid complications. Ultrasonography (USG), CT, and MRI
are commonly performed imaging modalities. Invasive digital subtraction angiography (DSA) is reserved for specic
situations. USG helps evaluate pseudoaneurysms or vascular
abnormalities in supercial locations. USG also helps in vascular access required for embolization procedures. Of note,
poor visualization in case of obesity, bowel gas, and deep
location, and operator dependency are disadvantages of USG
[1, 3].
CT angiography (CTA) is the most commonly used imaging modality for pre-embolization work-up. It provides a
detailed vascular road map and helps choose an appropriate
embolization approach, resulting in shorter procedure time
and lower radiation dose. MRI is uncommonly used except
for a few clinical scenarios, such as patients with vascular
anomalies [4]. With technical advancements in CT, DSA is
less commonly used as pre-embolization vascular mapping,
and now its role is preferentially therapeutic rather than diagnostic. However, when exact ow dynamics, sizing of vessels and pathologies, and deciding expendability of target
artery are required for successful embolization, preembolization DSA is performed for procedural planning,
e.g., embolization of intracranial arteriovenous malformation [1, 3, 4].
7.3 Vascular Access andHardwires
Generally, an access site that will provide the safest, shortest,
and most anatomically feasible route to the target vasculature is chosen, given the limitation of the available sheath
and catheters. Overall, transfemoral access (TFA) is the most
commonly used for vascular access. However, there is an
increasing shift from TFA to trans-radial access (TRA)
because TRA results in a faster time to ambulate and less
discomfort at the access site (Fig.7.1). TRA has an advantage for morbidly obese patients and patients with severe
peripheral vascular disease. Nevertheless, TRA requires longer hardwires, is less adaptable to larger sheaths and devices,
and may provide inferior guide support than TFA in certain
situations. Thus, both the TFA and TRA are necessary for the
expert interventionalist to master [5, 6].
A myriad of sheaths, catheters, and guidewires are available in the market, and choosing the best possible combination depends not only on the operators but also on their
availability and cost of the hardwires. For embolotherapy, a
coaxial or often a triaxial system is preferred. The targeted
proximal conduit vessel is selected using an angiographic
catheter or a specialty sheath. Further, an angiographic catheter may be advanced through a specialty sheath more distally toward the target point. Once the target point is reached,
a microcatheter is advanced within the angiographic catheter
to administer super-selective catheterization of the target
a
Fig. 7.1 Transradial partial splenic embolization for hypersplenism.
(a) Coronal CECT showing a huge spleen with dilated splenic vein; (b)
splenic artery was accessed through left trans-radial approach (black
b
c
arrow b), followed by 60–70% of splenic parenchymal embolization
(dotted white encircled area c) using 20% glue-lipiodol mixture. CECT
contrast-enhanced CT

7 Embolization inInterventional Radiology
Fig. 7.2 Summary of different embolic agents and their use
53
vessel and embolic agent [7]. As a general rule, catheters
should not be advanced into vessels with diameters less than
twice the catheter’s diameter to avoid focal occlusion of the
vessel or diminished antegrade ow [1, 3, 7].
Due to their superior exibility and trackability, hardwires used in neurointervention are increasingly used in
peripheral interventions, particularly in complex and/or tortuous vascular anatomy (e.g., balloon-assisted coiling of
renal artery pseudoaneurysm at the bifurcation) [8, 9].
However, usage of these hardwires increases the procedural
cost.
7.4 Embolic Agent Selection
One of the critical steps in the embolization procedure is to
choose the best embolic agent. A detailed discussion about
embolic agents is beyond the scope of this chapter and is
discussed elsewhere. A brief summary of the different
embolic agents and their use is summarized in Fig.7.2 [10,
11].
Deciding whether or not the vessel can be safely sacriced without signicant ischemic risk to the downstream
organ(s) is the rst and foremost step for the operator to
decide before embolization. After that, the following three
factors must be considered to determine the best embolic
agent to use: (1) target vessel diameter (small/large), (2)
length of the vessel to be occluded, and (3) downstream
organ(s) viability is maintained or not after embolization.
In general, the smaller the agent, the greater the likelihood of ischemia of the organ supplied by the embolized
vessel. Smaller agents embolize the vascular bed distal to the
level of collateralization, thereby occluding the blood supply
from primary and collateral vessels, resulting in much greater
ischemia than larger agents [10, 11].
In addition, the presence of coagulopathy may affect the
efcacy of embolic agents. In particular, coils and plugs
depend on the patient’s coagulation status; hence, they are
less effective in coagulopathy. However, liquid embolic
agents, such as glue and polymers, work well even in coagulopathy [12].
Permanent Large Vessel Occlusion [10, 11]
Permanent large vessel occlusion using endovascular embolization is equivalent to surgical ligation of the vessel. It is
considered when the following points are met: (1) angiographically visible vascular abnormality arising from the
large vessel and (2) expendable vessel with adequate collateral supply to the end organ to prevent end-organ damage.
Examples of clinical scenarios include splenic artery pseudoaneurysm, pulmonary arteriovenous malformation
(PAVM), carotid or vertebral artery sacrice, etc. Coils or
vascular plugs are usually used for permanent large vessel
occlusion.
Temporary Large Vessel Occlusion [10, 11]
Temporary occlusion of large vessels is desired when temporary arrest of bleeding is necessary with subsequent recana-

54
R. K. Patel et al.
lization and vessel healing. A typical example is bleeding
from pelvic trauma. In such a situation, gelfoam slurry or
torpedoes are used.
Permanent Small Vessel Occlusion [10, 11]
Before permanently embolizing the small vessel, the most
important factor to consider is whether the tissue viability
will be maintained or not. In general, the larger the particle
size, the lesser the likelihood of risk of organ ischemia.
Where tissue viability must be maintained, particles of larger
size >300μm should be used (e.g., bronchial artery embolization, uterine broid embolization, selective tumor embolization, and in gastrointestinal bleeding from small vessels).
In clinical scenarios where the desired endpoint is tissue
death or end-organ ischemia, such as super selective tumor
embolization, renal ablation, peripheral AVM, glue (cyanoacrylate and Onyx), or liquid sclerosing agents (sodium tetradecyl sulfate, absolute alcohol) or particle of size <300μm
are used.
Temporary Small Vessel Occlusion [10, 11]
Temporary occlusion of small vessels is considered when
there is an expectation of repeat procedures in case of tumor
embolization. Agents used are gelfoam and starch microspheres. These agents cause tissue ischemia but allow the
vessel to recanalize, resulting in temporary occlusion.
7.5 Technical Pearls forUsing Dierent
Embolic Agents [10–13]
7.5.1 Gelfoam Embolization
• For distal embolization, gelfoam slurry must be thin,
while a thick slurry or torpedoes is used for proximal ves-
sel embolization.
• Gelfoam can be used with coils in patients with coagu-
lopathy, where coils provide a scaffold and gelfoam aids
in mechanical occlusion.
• Gelfoam traps air bubbles, so post-embolization imaging
shows air foci, which should not be confused with
infection.
• Gelfoam is a temporary embolic agent, and vessels recan-
alize within 3weeks to 3 months. However, the degree
and timing of recanalization is unpredictable.
7.5.2 Coil Embolization
1. Scaffolding:
• Initial deployment of larger coils, followed by smaller
ones, provides a better scaffold.
• Stiffer coils are generally deployed rst to use as a
“backstop.” Softer and pliable coils with unpredictable
coil shapes conforming to vascular anatomy should be
deployed following stiffer coil placement.
• Steel coils are generally stiffer than platinum coils.
2. Choosing the appropriate catheter:
• Microcoils (<0.018 inches) must be used with a
microcatheter.
• Small coils within a larger lumen catheter often form
partially, leading to catheter blockage. Similarly, a
larger coil will not t within a smaller caliber catheter.
Hence, choosing an appropriate delivery catheter is
important while performing coil embolization.
3. Coil sizing:
• To attain a proper coil shape, the coil should be 20%
larger than the vessel diameter.
• Undersizing may lead to distal embolization and must
be avoided, especially in PAVM.On the contrary, too
much oversizing will prevent the coil from attending
proper shape, leading to inadequate occlusion. A
markedly longer coil in such a situation may cause
proximal coil malposition.
4. Deployment:
• Retrievable/ detachable coils are used when an exact
deployment is required. These coils can be repositioned until they detach from the delivery system (e.g.,
intracranial vascular procedure). Pushable coils are
used when the precision of deployment is not a
concern.
• In the case of a pushable coil, a pushing coil using a
saline bolus can be used when the deployment precision is not required, while a relatively precise deployment is needed; pushable coils are deployed using the
oppy end of a pusher wire.
Additional embolic agents, such as gelfoam or glue, may
be required along with coils for effective vascular occlusion
in patients with coagulopathy.
7.5.3 Amplatzer Vascular Plug Embolization
• Usually used for larger vessel occlusion, the largest size
plug available is 22mm.
• The vascular plug is generally deployed through the
sheath; hence, advancing the sheath to the target emboli-
zation site is crucial and is a rate-limiting step.
• AVP type IV plug (Amplatzer vascular plug, Abbott)
comes in smaller sizes and can be delivered through a 5F
catheter.
• Microplugs, which are compatible with microcatheters,
are also available.

7 Embolization inInterventional Radiology
Table 7.1 Differences between NBCA and Onyx [14, 15]
NBCA Onyx
Chemical composition N-butyl cyanoacrylate Ethylene vinyl alcohol copolymer (EVOH)
Mechanism Instant polymerization upon contact with an
Catheter compatibility Can be used with any catheter DMSO compatible catheter
Preparation time Requires at least 20min shaking in a mixer
Agent required for catheter priming before
delivery
Visibility during embolization Lipiodol is added for radio-opacity Tantalum powder provides radio-opacity
Non-target embolization risk Lesser More
Catheter stuck risk Lesser More
Cost Costly Cheaper
ionic environment, adhesive
to obtain a homogenous solution with
tantalum powder
Dextrose DMSO
Precipitation, non-adhesive
short preparation time
55
• A plug should be 30–50% oversized relative to the vessel
to prevent distal migration.
• Two platinum bands serve as radiopaque markers, and a
simple unscrewing mechanism allows precise device
deployment.
7.5.4 Glue Embolization
• N-butyl cyanoacrylate (NBCA) is called as glue. The use
of glue requires technical expertise because it polymerizes instantly upon contact with body uid and may lead
to proximal and non-target embolization.
• NBCA is radiolucent and must be used with lipiodol to
visualize under uoroscopy. Glue embolization should be
performed strictly under direct uoroscopic visualization
to prevent non-target embolization.
• The higher the glue percentage, the faster the polymerization rate and the more proximal the embolization. On the
contrary, a lower percentage of glue leads to delayed
polymerization and more distal embolization. Notably, a
higher glue percentage means a lower lipiodol proportion,
decreasing the radio-opacity under uoroscopy.
• Prior contrast injection through a properly placed catheter should be performed to evaluate the target vessels’
ow dynamics, diameter, and volume. Accordingly, the
optimal volume, injection speed, and ratio of the NBCAlipiodol mixture should be determined for
embolization.
• Before the glue injection, the catheter is thoroughly
ushed with 5% dextrose solution to remove any ionic
solution from its lumen.
• A small aliquot of glue-lipiodol mixture within the catheter, followed by pushing of glue with a bolus of dextrose,
is a frequently used approach for glue embolization (sandwich technique). Alternatively, a continuous column technique can be used.
• The catheter should be retracted immediately after the
NBCA injection to avoid unintentional adherence of the
catheter to the vessel.
Ethylene vinyl alcohol copolymer (Onyx) is another liq-
uid embolic that provides better control than NBCA.The differences between NBCA and Onyx are summarized in
Table7.1 [14, 15].
7.6 Clinical Applications
7.6.1 Aneurysm andPseudoaneurysm
A key consideration when selecting an endovascular technique is whether a particular embolization technique can
protect vital branches and avoid inadvertent end-organ ischemia or visceral damage. Various essential factors required
in formulating a management strategy include selecting
embolic agents, accurately evaluating the size and length of
a stent-graft, the size and length of coils/coil packing density
or embolic plugs, and estimating the amount of liquid
embolic agents [16]. Detailed vascular anatomy should be
assessed for the take-off angle of the native artery, ostial stenosis, and vessel tortuosity to decide the optimal arterial
access (femoral, brachial, axillary, or radial). Intracranial
aneurysms often arise from an inexpendable artery, and
embolization should be performed accordingly to preserve
ow in the parent artery [16, 17].
7.6.1.1 Endovascular Approach
Different endovascular transarterial embolization techniques
are discussed below in detail.
Parent Artery Preservation [16, 17]
Filling the aneurysmal sac with the embolic agent(s) is
used to exclude the aneurysm from the parent artery. This is
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