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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]

160
bc
L. J. D. Sebastian et al.
a
e
fd
Fig. 14.4 Endovascular management of PSA of the neck. MRA (a)
showing giant pseudoaneurysm from right cervical ICA.DSA (b, c, d)
showing giant pseudoaneurysm with minimal antegrade ow into distal
good landing zone and small size of the rent that can be
covered easily.
• The main challenges in the management of stent grafts are
the need for relatively large bore access for deployment of
stent graft, the need for antiplatelets, and determining their
ICA.DSA (e) showing stent graft balloon angioplasty. Angiography (f)
shows no ow into aneurysm with a good distal ow into ICA
dosage, especially in younger kids. From the technical point
of view, for the deployment of a stent graft, the aneurysm
should be crossed with a microguidewire initially. Hence
complex aneurysms that are difcult to cross are best managed with parent vessel sacrice with proximal occlusion.

14 Other Neurointer ventions
161
14.5 Intra-Arterial Chemotherapy
forRetinoblastoma
Intra-arterial chemotherapy is used as salvage therapy in
children with retinoblastoma after systemic chemotherapy
and intravitreous treatments fail (Fig.14.5). Selective cannulation of ophthalmic artery origin using the microcatheter
is done. Melphalan, carboplatin, and topotecan are
administered directly into the ophthalmic artery.
As these children are usually below 5years of age, 4F or
5F transfemoral arterial access is used, and a guiding cathe-
Fig. 14.5 (a, b) Intra-arterial
chemotherapy for
retinoblastoma
a
ter is placed in a petrous ICA. ICA is frequently tortuous
with loops. Cannulating ophthalmic arteries can be difcult.
The shape of the carotid siphon and ophthalmic artery origin
in relation to the anterior genu are some of the factors to be
considered. Intelligent steam shaping of the microcatheter
tip depending on individual anatomy will be of great help.
Selective ophthalmic artery cannulation as seen in the gure
is ideal. However, in difcult cases, hooking the ophthalmic
artery origin (ostium) can sufce, provided antegrade ow is
conrmed by microcatheter angiogram.
b

162
L. J. D. Sebastian et al.
14.6 Preoperative Embolization
forVascular Tumors
Meningioma, hemangioblastoma, nasopharyngeal angiobroma, glomus jugulare, and paragangliomas are highly
vascular tumors where surgical resection is restricted by
blood loss. Pre-op embolization is frequently requested for
such tumors. Particle or liquid embolic agents are commonly used in any part of the body. However, few precautions are mandatory while dealing with head and neck
tumors.
• Nontarget embolization should be strictly avoided given
the functional eloquence of the structures involved. This
requires super-selective cannulation of the feeding pedicle and avoiding reux.
• Thorough knowledge of the intra- and extracranial anastomosis is required, to avoid inadvertent intracranial
embolization/cranial nerve palsies while treating tumors
supplied by ECA and other neck arteries.
• PVA particles are commonly used; the particle sizes
(100–250microns) are chosen based on the vascular bed,
presence of AV shunting, and size of the feeding
pedicles.
• Liquid adhesive (N-butyl cyanoacrylate) and nonadhesives (onyx (ethyl vinyl alcohol)) liquid embolic agents
can also be used. However, utmost care should be taken to
avoid reux, especially in the case of liquid embolic
agents.
References
1. Ellis JA, Goldstein H, Connolly ES, Meyers PM.Carotid-cavernous
stulas. FOC. 2012;32(5):E9. https://doi.org/10.3171/2012.2.FO
CUS1223.
2. Chun GFH, Tomsick TA. Transvenous embolization of a direct
carotid cavernous stula through the pterygoid plexus. AJNR Am J
Neuroradiol. 2002;23(7):1156–9.
3. Malan J, Lefeuvre D, Mngomezulu V, Taylor A.Angioarchitecture
and treatment modalities in posttraumatic carotid cavernous
stulae. Interv Neuroradiol. 2012;18(2):178–86. https://doi.
org/10.1177/159101991201800209.
4. Da Silva PSL, Waisberg DR. Internal carotid artery pseudoaneurysm with life-threatening epistaxis as a complication of deep neck
space infection. Pediatr Emerg Care. 2011;27(5):422–4. https://doi.
org/10.1097/PEC.0b013e3182187539.
5. Maldonado-Naranjo A, Kshettry VR, Toth G, Bain M. Nontraumatic superior hypophyseal aneurysm with associated pseudoaneurysm presenting with massive epistaxis. Clin Neurol
Neurosurg. 2013;115(10):2251–3. https://doi.org/10.1016/j.
clineuro.2013.07.003.
6. Mortimer A. Endovascular management of cavernous internal carotid artery pseudoaneurysms following transsphenoidal surgery: a report of two cases and review of the literature.
Clin Neuroradiol. 2014;20. Accessed March 30, 2024 https://
www.academia.edu/97789597/Endovascular_Management_
of_Cavernous_Internal_Carotid_Artery_Pseudoaneurysms_
Following_Transsphenoidal_Surgery_A_Report_of_Two_Cases_
and_Review_of_the_Literature.
7. Coldwell DM, Novak Z, Ryu RK, et al. Treatment of posttraumatic internal carotid arterial pseudoaneurysms with endovascular stents. J Trauma. 2000;48(3):470–2. https://doi.
org/10.1097/00005373- 200003000- 00016.
8. Patel JV, Rossbach MM, Cleveland TJ, Gaines PA, Beard
JD. Endovascular stent-graft repair of traumatic carotid artery
Pseudoaneurysm. Clin Radiol. 2002;57(4):308–11. https://doi.
org/10.1053/crad.2001.0808.
9. Ko JK, Lee TH, Lee JI, Choi CH.Endovascular treatment using
graft-stent for Pseudoaneurysm of the cavernous internal carotid
artery. J Korean Neurosurg Soc. 2011;50(1):48–50. https://doi.
org/10.3340/jkns.2011.50.1.48.
10. Wolfe SQ, Mueller-Kronast N, Aziz-Sultan MA, Zauner A,
Bhatia S. Extracranial carotid artery pseudoaneurysm presenting with embolic stroke in a pediatric patient: case report. PED.
2008;1(3):240–3. https://doi.org/10.3171/PED/2008/1/3/240.
11. Tan MA, Armstrong D, MacGregor DL, Kirton A.Late complications
of vertebral artery dissection in children: Pseudoaneurysm, thrombosis, and recurrent stroke. J Child Neurol. 2009;24(3):354–60.
https://doi.org/10.1177/0883073808324775.
12. Wang A, Santarelli JG, Stiefel MF. Traumatic cervical internal carotid artery pseudoaneurysm in a child refractory to initial
endovascular treatment: case report and technical considerations.
Childs Nerv Syst. 2016;32(12):2459–64. https://doi.org/10.1007/
s00381- 016- 3171- 6.
13. Steinberg J, Cheung V, Goel G, Pannell JS, Nation J, Khalessi
A.Vessel-preserving stent-assisted coil embolization of an extracranial internal carotid artery pseudoaneurysm that developed
after tonsillectomy in a pediatric patient: initial case report. PED.
2017;19(1):8–12. https://doi.org/10.3171/2016.7.PEDS14457.
14. Gralla J, Brekenfeld C, Schmidli J, Caversaccio M, Do DD,
Schroth G. Internal carotid artery aneurysm with life- threatening
hemorrhages in a pediatric patient: endovascular treatment
options. J Endovasc Ther. 2004;11(6):734–8. https://doi.
org/10.1583/1308R.1.

Vascular Interventions inHead
andNeck
ShwaitSharma, AshuSeithBhalla, PriyankaNaranje,
AnthoniBalaSubashree, andSmitaManchanda
15
Key Messages
1. Pre-operative endovascular embolization in cases of head
and neck tumours can be used as an adjunctive to surgery
or as a palliative procedure in inoperable cases. It reduces
intraoperative blood loss, improves the visualization of
the surgical eld with less injury to adjacent normal tissue, and reduces the procedure time.
2. Endovascular embolization is also key in reducing the
vascular supply to the high-ow vascular malformations
with a reduction in size and other clinical symptoms like
bleeding and functional impairment.
3. Various anastomotic pathways exist between extracranial
and intracranial arteries of the head and neck. Most common anastomoses are around the orbit (ophthalmic artery
with ECA branches) and around the calvarium and base
of the skull (ICA and vertebral artery branches with middle meningeal, supercial temporal, and facial artery
branches). Care must be taken to demonstrate any anastomosis around these sites, especially after a session of
embolization.
4. Embolization is started with small-size embolization
material to occlude the distal vessels followed by gradually increasing particle size to occlude more proximal
vessels.
5. Endovascular particulate embolization of the internal
maxillary artery is now the treatment of choice for intractable posterior nasal epistaxis not controlled by posterior
nasal packing.
6. Radiofrequency ablation is a promising alternative for the
palliative treatment of advanced head and neck tumours
with minimal complications. The procedure is performed
under GA, and the patient can be discharged the next day.
15.1 Introduction
Endovascular interventions in the head and neck region
include angioembolization in head and neck bleeding, embolization of tumours, and arteriovenous malformations.
Nonvascular interventions of the head and neck region are
covered in Chap. 36.
15.2 Vascular Malformations oftheHead
andNeck
Interventional radiology plays a key role in the management
of vascular malformations and vascular tumours. Detailed
knowledge of head and neck anatomy, potential site involved,
and associated specic complications is required before treating any vascular malformation. The malformations are
broadly classied into low ow and high ow depending on
the presence of arterial feeders. Understanding International
Society for the Study of Vascular Anomalies (ISSVA) classication and its management implications is imperative before
treating any vascular malformation. The classication is covered in detail in the chapter on vascular malformations.
Pre-treatment dynamic MRI is essential to understand the
nature of vascular malformation and vascular feeders if any.
Low-ow malformations are treated with percutaneous
sclerotherapy while the high-ow ones are treated with
endovascular embolization.
15.3 Percutaneous Sclerotherapy ofHead
andNeck Low-Flow Vascular
Malformations andCystic Lesions
Image-guided sclerotherapy is a minimally invasive and relatively safe percutaneous technique for the treatment of low-
S. Sharma · A. S. Bhalla (*) · P. Naranje · A. B. Subashree ·
S. Manchanda
Department of Radiodiagnosis and Interventional Radiology, All
India Institute of Medical Sciences, Delhi, India
© 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_15
ow vascular malformations and cystic lesions of the head
and neck (Fig.15.1). This technique is particularly useful for
poorly dened trans-spatial vascular malformations close to
163

164
S. Sharma et al.
Fig. 15.1 USG-guided
sclerotherapy of slow ow
malformation. (a) USG
reveals a well-dened
multiseptated cystic lesion
(arrow) in the right
submandibular space deep
into subcutaneous plane. (b)
Under USG guidance, a 22G
needle was inserted with its
tip (arrow) in the cystic space,
and 15UmL of bleomycin
reconstituted in 5ml normal
saline was injected. (c) Post
sclerotherapy injection, USG
shows multiple internal
echoes (asterisk) within the
cyst
a
c
vital structures where complete surgical resection is technically challenging and the risk of injury to adjacent structures
is high. Sclerotherapy in cystic lesions like thyroglossal duct
cyst, branchial cleft cyst, ranulas, and benign thyroid cysts is
less frequently done, and surgery remains the rst line of
treatment as epithelium-lined cystic lesions are pathologically distinct from endothelium-lined vascular malformations. Reports on the use of sclerotherapy for the treatment of
such cystic lesions are limited and need further validation.
15.3.1 Sclerosing Agents andProcedure
Technique
b
d
tially thrombosed echogenic areas of the malformation
(Fig.15.1).
The choice of sclerosant also depends on the anatomic
area of malformation. Use of STS is avoided in areas like the
face, joints, and neck due to the increased risk of postprocedure swelling.
The procedure is done under aseptic conditions with
ultrasound and uoroscopy guidance. For the rst injection,
a 22G needle is placed within the cystic space, and an angiogram is obtained to rule out any deep vein communication of
the malformation. Sclerosant foam is injected into the spaces
and compression is applied to the lesion for 5–10min. Antiinammatory drugs are prescribed after the procedure.
Various sclerosants used for the treatment of vascular malformations include polidocanol, sodium tetradecyl sulphate
(STS), and bleomycin. Polidocanol and STS are non-ionic
surfactants, and both act on the endothelium of cystic spaces
of malformations leading to inammation and thrombosis of
the vascular spaces. Three percent solution of polidocanol or
STS is mixed with air in a ratio of 1:1 to 1:4 and made into
foam by the Tessari technique. The foam is then injected into
cystic spaces of low-ow vascular malformation.
Bleomycin was originally developed as an anti-cancer
drug, and its side effect of pulmonary brosis is well known.
It directly acts on the endothelium to cause damage and
brosis of the vessel wall. Bleomycin is used as a liquid sclerosant predominantly in solid-appearing areas of the malformation. 5–15 IU of bleomycin diluted in an appropriate
amount of normal saline (5–10ml) is injected into the par-
15.3.2 Treatment Response andFollow-Up
Treatment of vascular malformations aims to achieve a
reduction in clinical symptoms like pain, swelling, bleeding,
functional impairment, and cosmetic disgurement. The
patient is called for follow-up after 4–6weeks during which
the clinical response is evaluated. Screening USG is done to
see for residual cystic spaces. The sclerosant is injected into
the residual spaces and the response is evaluated during the
follow-up visit. Treatment is stopped once the patient shows
good clinical improvement with resolution of functional
impairment and bleeding.
To conclude, sclerotherapy of low-ow vascular malformations of the head and neck is a less invasive and relatively
safe procedure with good clinical outcomes.

15 Vascular Interventions inHead andNeck
165
15.4 Endovascular Embolization ofHead
andNeck Tumours andArteriovenous
Malformations
Head and neck cancers account for ~30% of all the cancer
cases in India. Angiographic study provides details about the
vascular supply of tumours as well as relation of tumour with
surrounding vessels. Also, distinctive angiographic features
of various tumours have diagnostic implications. Diagnostic
angiography also helps to delineate the vascular supply and
shunting, if any.
Pre-operative endovascular embolization can be done as
an adjunct to surgery or as a palliative procedure in inoperable cases. It reduces intraoperative blood loss, improves the
visualization of the surgical eld with less injury to adjacent
normal tissue and reduces the procedure time. Morbidity
associated with complex surgeries is thus signicantly
reduced.
Endovascular therapy has expanded its role to include targeted delivery of chemotherapeutic agents to the tumours
with fewer systemic side effects.
a
b
The two most common tumours referred for pre-operative
embolization include juvenile nasopharyngeal angiobroma
(Fig.15.2) and head and neck paragangliomas (Fig. 15.3).
Other head and neck tumours where pre-operative embolization is done include extracranial meningiomas, endolymphatic sac tumours, schwannomas, solitary hypervascular
metastasis and hemangiopericytomas. Demonstrating crosscirculation becomes imperative in cases where the internal
carotid artery of one side may need to be sacriced during
tumour surgery. Table15.1 shows the predominant arterial
supply to the most commonly embolized head and neck
tumours.
Another clinical condition where endovascular embolization plays a signicant role is high-ow vascular malformations. They are less frequently encountered as compared to
low-ow malformations. Nonetheless, they have variable
clinical presentations from being asymptomatic to lifethreatening cardiovascular failure. Endovascular embolization is key in reducing the vascular supply to the
malformations with reduction in size and other clinical
symptoms like bleeding and functional impairment.
c
d
Fig. 15.2 Embolization of juvenile nasopharyngeal angiobroma
(JNA) by polyvinyl alcohol (PVA) particles. (a). CECT shows an illdened hyper-enhancing lesion (asterisk in a) causing widening of left
sphenopalatine foramen, pterygopalatine foramen and pterygomaxillary ssure with erosion of pterygoid plates. (b). Left internal maxillary
artery (IMA) DSA selective run taken using 5F Picard catheter showing
abnormal tumour blush (arrow in b). (c). Superselective run of one of
e
f
the branches of left IMA using microcatheter showing abnormal tumour
blush (arrow in c). (d). Superselective run of inferior alveolar artery, a
branch of left IMA using microcatheter showing abnormal tumour
blush (asterisk in d). (e). Post-embolization superselective run of inferior alveolar artery using microcatheter showing no blush in the region
of tumour (asterisk in e). Post-embolization DSA run of left ECA showing no tumour blush

166
ab
Fig. 15.3 DSA diagnostic
run in carotid body tumour.
Lateral run of left CCA shows
splaying (asterisk in a) of
ECA and ICA with intense
vascularity within the lesion
(asterisk in b). Lateral (c) and
frontal (d) run of left ECA
show predominant supply of
the tumour from branches of
ECA
S. Sharma et al.
c
Table 15.1 Arterial supply of common head and neck tumours
Tumour Location Predominant arterial supply Accessory arterial supply
1. Paraganglioma Jugular fossa Ascending pharyngeal artery Occipital
2. Paraganglioma Tympanic Ascending pharyngeal artery Occipital, middle meningeal, extracranial
3. Juvenile nasopharyngeal
angiobroma
4. Meningioma Intracranial Anterior cerebral, middle cerebral and
5. Endolymphatic sac tumour Skull base Ascending pharyngeal artery Stylomastoid, extracranial branches of
Nasopharynx Sphenopalatine artery Ascending pharyngeal artery, vidian artery
posterior cerebral branches
d
branches of vertebral
(ICA branch)
Middle meningeal, occipital, ophthalmic
artery, ethmoidal arteries
vertebro-basilar system
15.4.1 Principles andTechnique
ofEmbolization
The head and neck region is principally supplied by branches
of the external carotid artery (ECA). The lower neck region
receives supply from costocervical and thyrocervical trunks
of subclavian arteries. Hence, tumours and malformations of
the head and neck invariably draw their arterial supply from
external carotid branches. Arterial feeders from surrounding
arteries including common carotid, vertebral, and internal
carotid arteries (ICA) are not uncommon. Demonstration of
all the arterial feeders and venous drainage pathways is
imperative for chalking out an effective treatment.
Various anastomotic pathways exist between extracranial
and intracranial arteries. Most common anastomoses are
around the orbit (ophthalmic artery with ECA branches) and
around the calvarium and base of the skull (ICA and vertebral artery branches with middle meningeal, supercial tem-

15 Vascular Interventions inHead andNeck
167
poral and facial artery branches). Care must be taken to
demonstrate any anastomosis around these sites, especially
after a session of embolization.
Pre-operative tumour embolization is aimed to selectively
reduce the vascular supply of malformation/tumour and preserve the normal arterial supply of the head and neck. It is
aimed to block the arterial feeders and capillary bed of
tumour without any spillage of the embolizing agent into the
venous side of the circulation. Arteriovenous shunting within
the tumour should be looked for in check angiograms to aid
in selecting the type of embolic agent.
Embolization starts with obtaining arterial access.
Femoral artery access is the one that is most commonly
taken. Selective angiograms of the subclavian, common
carotid artery, ECA, ICA and vertebral arteries of both sides
are taken to demonstrate the feeder arteries and any collateral vascular anastomosis. Superselective microcatheterization is also done to demonstrate vascular anatomy
and shunting if any.
Selective embolization of the feeder arteries to the
tumours is carried out after demonstrating the vascular anatomy. Ideally, superselective embolization is done by placing
the microcatheter as close to the tumour as possible to prevent inadvertent embolization of normal tissues. Embolization
is started with small-size embolization agents to occlude the
distal vessels followed by gradually increasing particle size
to occlude more proximal vessels. Various embolic materials
used for tumour embolization are briey described in
Table15.2. Post-embolization angiograms are taken to demonstrate the adequacy of embolization.
Pre-operative embolization is ideally planned 2–3 days
before the intended surgery to thrombose the feeder arteries
maximally and decrease the chances of collateral revascularization of tumour [1–4].
15.4.2 Embolization Agents
Various agents, each with its own merits and demerits, are
available for use during embolization. The choice of material
depends on the intended outcome of the procedure. For vascular tumours, embolization is primarily aimed to reduce the
tumour vascularity prior to surgery with reduced blood loss
and peri-operative morbidity.
Malformations on the other hand are usually large and
trans-spatial which precludes surgical resection.
Embolization is aimed to reduce clinical symptoms like
bleeding, functional impairment, and cosmetic
disgurement.
Endovascular embolization is the key treatment technique
for high-ow vascular malformations and is adjunctive to
surgery for vascular tumours. With the continuous advancements in hardware and embolic agents and with technical
expertise more selective and safe embolization is possible.
15.4.3 Embolization forIntractable Epistaxis
Epistaxis is a common condition which rarely requires acute
medical attention. Most cases of epistaxis arise from the vascularized anterior septal area, also known as the Little’s area,
and are usually managed by methods like applying pressure
to the nostrils or anterior nasal packing. Other treatment
methods like chemical or electrocautery, topical haemostatic
or vasoconstricting agents and cryotherapy can also be used
to control bleeding.
In a few cases, the bleeding is from the posterior nasal
area and is not controlled by these conventional methods.
Historically, this posterior nasal bleed was treated by posterior nasal packing and sometimes surgical ligation of the
Table 15.2 Various embolization agents used for embolization of tumours and vascular malformations of the head and neck
Embolic agent Advantages Limitations
Polyvinyl alcohol (PVA) Cheap, good distal tumour bed embolization Variable size, catheter blockage
Trisacryl microspheres Uniform size of particles, improved distal penetration and
tumour embolization, reduced in-catheter aggregation of
particles
Gelfoam Inexpensive, easily available Temporary occlusion
Glue Can ow distally into complex tortuous vessels,
polymerization independent of patient’s coagulation prole
Onyx Slow solidication, more controlled embolization of tumour
bed, polymerization independent of patient’s coagulation
prole
Coils Easy and explicit deployment, useful in high-ow vessels Dislodgement and non-target embolization
Vascular plugs Useful in larger vascular shunts Costly
Costly
Catheter blockage, insignicant tumour bed
embolization, less control while embolization
Costly, separate hardware for injection
(DMSO compatible)

168
S. Sharma et al.
internal maxillary artery. Endovascular particle embolization
of the internal maxillary artery is now the treatment of choice
for intractable posterior nasal epistaxis not controlled by
posterior nasal packing.
15.4.4 Principles andTechnique
ofEmbolization
Pre-embolization diagnostic angiograms of the ICA and
ECA are vital to reveal the cause and location of the haemorrhage. It may also reveal vascular anomalies, variants or
anastomoses between the ECA and ICA that could increase
the risk of complications, such as stroke or blindness during
embolization. The goal of management in intractable epistaxis is to control bleeding by reducing the ow to the
bleeding mucosa but allowing sufcient collateral ow to
avoid necrosis. For intractable posterior epistaxis, the internal maxillary artery is the most common culprit, and it can
be safely embolized. Embolization of the ipsilateral facial
artery, contralateral IMA, and even the contralateral facial
artery can also be done. Particulate materials most commonly used for embolization include gelatin sponge,
polyvinyl alcohol (PVA) particles, ranging in size from 50
to 700 μm, platinum coils, or a combination of these
materials.
Complications following embolization can be minor and
transient, like headache, facial pain, jaw pain, trismus, facial
oedema, facial numbness, paraesthesias, mild palate ulceration, altered mental status, groin haematoma, groin pain and
fever, or major, like skin or mucosal necrosis, temporary
hemiparesis and monocular visual eld loss. Rarely, persistent complications like facial scarring following ischaemia,
monocular blindness, peripheral facial nerve paralysis, cerebral infarction and ischaemic sialadenitis requiring surgery
can be seen.
Transarterial particle embolization is now the treatment of
choice for intractable epistaxis and is safe and well tolerated
when performed by experienced hands [5–10].
15.5 Conclusion
Percutaneous sclerotherapy under USG guidance is used
widely for low-ow vascular malformations. Endovascular
embolization is the treatment of choice for high-ow vascular malformations and intractable posterior epistaxis and is
essential prior to surgery for vascular tumours.
References
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2. Lazzaro MA, Badruddin A, Zaidat OO, Darkhabani Z, Pandya DJ,
Lynch JR.Endovascular embolization of head and neck tumors.
Front Neur. 2011;2:64.
3. Gemmete JJ, Ansari SA, McHugh J, Gandhi D.Embolization of
vascular tumors of the head and neck. Neuroimaging Clin N Am.
2009;19(2):181–98.
4. Singla A, Singh N, Singh S, Kumar M, Srivastava R.Embolization
of vascular tumors of the head and neck: a review of literature. Int J
Contemp Med Surg Radiol. 2020;5(1):A47–A5.
5. Small M, Murray JA, Maran AG.A study of patients with epistaxis
requiring admission to hospital. Health Bull (Edinb). 1982;40:20–9.
6. Lasjaunias P, Marsot-Dupuch K, Doyon D. The radio- anatomical
basis of arterial embolisation for epistaxis. J Neuroradiol.
1979;6:45–53.
7. Elden L, Montanera W, Terbrugge K, etal. Angiographic embolization for the treatment of epistaxis: a review of 108 cases.
Otolaryngol Head Neck Surg. 1994;111:44–50.
8. Tseng EY, Narducci CA, Willing SJ, et al. Angiographic embolization for epistaxis: a review of 114 cases. Laryngoscope.
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9. Gurney TA, Dowd CF, Murr AH.Embolization for the treatment of
idiopathic posterior epistaxis. Am J Rhinol. 2004;18:335–9.
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J. 2004;94:373–8.

Carotid Artery Interventions
NeerajKumar, TejPal, andS.H.Chandrashekhara
16
Key Messages
1. For carotid artery stenosis patients who are being considered for surgical/endovascular intervention, duplex
ultrasound should be followed by either CT angiography
or MR angiography.
2. Even for asymptomatic carotid artery stenosis (>50%)
patients, lower dose aspirin (75–325 mg) should be
considered.
3. Carotid endarterectomy/carotid artery stenting is recommended for asymptomatic patients having carotid artery
stenosis 70–99% and symptomatic patients having
carotid artery stenosis 50–99%.
4. Complete occlusion of carotid artery and carotid artery
stenosis <50% in symptomatic and <70% in asymptomatic can be managed with best medical therapy
alone.
5. For patients undergoing carotid artery stenting, combination antiplatelet therapy with aspirin (75–325mg) and
clopidogrel is recommended. Clopidogrel (75 mg)
should be started at least three days prior to stenting or
300mg loading dose in urgent cases.
6. Stent design (open cell/closed cell, tapered/non-tapered)
should be considered at the discretion of the operator.
7. If pre-dilatation is required for stenting, balloon diameters <5 mm should be used to reduce periprocedural
stroke risk.
8. Post-stenting dilation is not recommended if residual
stenosis is <30%.
N. Kumar
Department of Cardiovascular Radiology and Endovascular
Interventions, All India Institute of Medical Sciences, Delhi, India
T. Pal (
*)
Department of Radiology, National Cancer Institute, Jhajjar, All
India Institute of Medical Sciences, Delhi, India
All India Institute of Medical Sciences, Delhi, India
S. H. Chandrashekhara
Department of Radiodiagnosis and Interventional Radiology,
IRCH, All India Institute of Medical Sciences, Delhi, India
9. Cerebral protection systems should be considered during carotid artery stenting.
10. Routine population screening for asymptomatic carotid
stenosis is not recommended.
16.1 Introduction
Ischaemic stroke accounts for 85% of cases of stroke, and
25% of ischaemic strokes are caused due to thromboembolism from internal carotid artery (ICA) or middle cerebral
artery (MCA) [1]. The prevalence of carotid artery stenosis
>50% in acute ischaemic stroke is between 15% and 20%.
Major risk factors for carotid artery stenosis are male sex,
age, hypertension, and smoking [2].
16.2 Measurement ofCarotid Artery
Stenosis
The two most common methods employed for carotid artery
stenosis quantication are ECST (European Carotid Artery
Surgery Trial) and NASCET (North American Symptomatic
Carotid Endarterectomy Trial) which are depicted in
Fig.16.1.
ECST method uses the maximum expected diameter at
the level of stenosis as the denominator, and NASCET
method uses the diameter of normal cervical ICA as denominators. Since these methods use different denominators for
calculating stenosis; therefore, they provide different measurements. It can be inferred from Fig.16.1 that the ECST
method overestimates stenosis as compared to the NASCET
method. Fifty percent stenosis in NASCET is equivalent to
75% stenosis in ECST, and 70% stenosis in NASCET is
equivalent to 85% stenosis in ECST [3]. The NASCET
method is more widely accepted.
© 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_16
169
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