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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]

150
L. J. D. Sebastian et al.
a
c
d
Fig. 13.21 Spinal dural AVF embolization. A 56-year-old male presented with insidious onset, gradually progressive, weakness, and tingling sensation in both lower limbs (power 4/5) with straining during
micturition for last 3years. (a) Sagittal T2W MRI spine shows a long
segment, T2 hyperintensity involving the cord from D9-D12 vertebral
body levels, with ow voids over cord surface (D10–D12 vertebral
body levels), without any contrast enhancement or hematomyelia. (b)
e
Diagnostic angiogram shows a dural AVF feeding from the radicular
branch of right D8 segmental artery, draining into the perimedullary
venous plexus. (c) Microcatheter angiogram into the radicular vessel
conrmed the ndings. (d & e) 20% NBCA glue was injected to completely obliterate the stula, which was conrmed on a check angiogram. (f) Follow-up MRI after 2months revealed reduction in spinal
cord signal changes with reduction in ow voids
fb
3. Dilute glue—15–25%, depending on the microcatheter
position and ow—is the embolic agent of choice. Glue
should reach the footplate and proximal segment (1–2cm)
of the draining vein. Falling short of the venous footplate
or excessive glue into the coronal plexus can leave persistent stula or precipitate excessive venous thrombosis,
respectively.
13.5.4.2 SCAVS (Figs.13.22 and13.23)
Treatment is essentially endovascular. In SCAVF, treatment
intent is curative (stula elimination and venous decongestion). For SCAVM, intent is stabilization and elimination of
weak points. All feeder pedicles are identied, after which
the larger and shorter one is used for superselective microcatheter navigation and embolization. Glue is embolic agent
of choice. Non-adhesive liquid embolics (like Onyx) are better avoided for spinal vascular embolizations.
13.5.4.3 Spinal Epidural AVMs
Treatment goal is inducing thrombosis and causing size
reduction of large venous sacs in epidural/osteodural AVM/
AVFs. The most appropriate vessel, among the leash of vessels applying epidural AVM, is selected based on proximity
to the venous sac, and the absence of radiculo-medullary
supply from the same vascular pedicle is ensured. Dilute
glue is injected such that it reaches the venous sacs. Even
minimal amount of glue has the capacity to cause progressive thrombosis of the sac.
13.5.4.4 Metameric AVMs
They are difcult to treat. Among the intradural and osteodural components, epidural component is easier to treat.
Cord component is better not touched, unless there are denitive indications like hematomyelia.

13 Interventions inIntracranial andSpinal Arteriovenous Malformations
151
a
b
d
e
f
c
Fig. 13.22 Glomerular AVM.A 14-year-old boy presented with severe
backache and sudden onset quadriparesis. (a) Sagittal T2W MRI reveals
hematomyelia (arrow) with multiple intradural vascular ow voids
along the anterior aspect of the spinal cord (arrowhead). (b) Diagnostic
angiogram shows a glomerular type AVM in cervical region (black
arrow), feeding from a branch (white arrow) of left vertebral artery and
draining into the anterior spinal vein (arrowhead). (c) Selective micro-
catheter angiogram reveals the origin of anterior spinal artery from
feeding branch. The AVM was embolized using NBCA, and control
angiogram post-embolization (d) revealed no residual AVM. (e) The
anterior spinal artery was seen reconstituted from radiculomedullary
arteries at other cervico-dorsal levels. (f) Resolution of ow voids was
seen in MRI after 3months

152
L. J. D. Sebastian et al.
a
b
ce
f
d
Fig. 13.23 Spinal cord AVF.A 1-year-old male child presented with
spastic paraparesis. (a) Sagittal T2W MRI shows a large venous pouch
(arrow), anterior-lateral to the spinal cord at lower dorsal level, possibly
feeding from a branch of the segmental artery arising from the aorta and
draining into a dilated anterior spinal vein superiorly (arrowhead). (b)
Diagnostic angiogram reveals a spinal cord macro-stula (AVF) (black
arrow) at the lower dorsal level, feeding from radiculomedullary artery
References
1. Valavanis A, Pangalu A, Tanaka M.Endovascular treatment of cerebral arteriovenous malformations with emphasis on the curative
role of embolisation. Interv Neuroradiol. 2005;11(Suppl 1):37–43.
2. Krings T, Geibprasert S, terBrugge K.Classication and endovascular Management of Pediatric Cerebral Vascular Malformations.
Neurosurg Clin N Am. 2010;21(3):463–82. https://doi.
org/10.1016/j.nec.2010.03.010.
3. Müller-Forell W, Valavanis A.How angioarchitecture of cerebral
arteriovenous malformations should inuence the therapeutic
considerations. Minim Invasive Neurosurg. 1995;38(01):32–40.
https://doi.org/10.1055/s- 2008- 1053458.
4. Mast H, Young WL, Koennecke HC, et al. Risk of spontaneous
haemorrhage after diagnosis of cerebral arteriovenous malformation. Lancet. 1997;350:1065.
5. Lasjaunias P. A revised concept of the congenital nature of
cerebral arteriovenous malformations. Interv Neuroradiol.
1997;3(4):275–81. https://doi.org/10.1177/159101999700300401.
6. Valavanis A, Yasargil MG. The endovascular treatment of brain
arteriovenous malformations. In: Cohadon F, Dolenc VV, Antunes
JL, et al., editors. Advances and technical standards in neurosurgery, vol. 24. Vienna: Springer; 1998. p. 131–214. https://doi.
org/10.1007/978- 3- 7091- 6504- 1_4.
(white arrow) (from D9 segmental artery) and draining into the dilated
anterior spinal vein superiorly (arrowhead). (c & d) Microcatheter was
navigated into the radiculomedullary artery close to stula, wedged
along the vessel wall and concentrated NBCA glue (90%) was injected
to obliterate the stula site and proximal venous pouch. (e) Control
angiogram revealed the full occlusion of the macrostula. (f) MRI after
15days revealed thrombosis within the venous pouch
7. Hak JF, Boulouis G, Kerleroux B, et al. Noninvasive follow-up
imaging of ruptured pediatric brain AVMs using arterial spinlabeling. AJNR Am J Neuroradiol. 2022;43(9):1363–8. https://doi.
org/10.3174/ajnr.A7612.
8. Heit JJ, Thakur NH, Iv M, etal. Arterial-spin labeling MRI identies residual cerebral arteriovenous malformation following stereotactic radiosurgery treatment. J Neuroradiol. 2020;47(1):13–9.
https://doi.org/10.1016/j.neurad.2018.12.004.
9. Spetzler RF, Martin NA.A proposed grading system for arteriovenous malformations. J Neurosurg. 1986;65(4):476–83. https://doi.
org/10.3171/jns.1986.65.4.0476.
10. Lawton MT, Kim H, McCulloch CE, Mikhak B, Young WL.A supplementary grading scale for selecting patients with brain arteriovenous malformations for surgery. Neurosurgery. 2010;66(4):702–13.
https://doi.org/10.1227/01.NEU.0000367555.16733.E1.
11. Dumont TM, Kan P, Snyder KV, Hopkins LN, Siddiqui AH, Levy
EI.A proposed grading system for endovascular treatment of cerebral arteriovenous malformations: Buffalo score. Surg Neurol Int.
2015;6:3. https://doi.org/10.4103/2152- 7806.148847.
12. Mohr JP, Parides MK, Stapf C, etal. Medical management with or
without interventional therapy for unruptured brain arteriovenous
malformations (ARUBA): a multicentre, non-blinded, randomised
trial. Lancet. 2014;383(9917):614–21. https://doi.org/10.1016/
S0140- 6736(13)62302- 8.

13 Interventions inIntracranial andSpinal Arteriovenous Malformations
153
13. Al-Shahi Salman R, White PM, Counsell CE, etal. Outcome after
conservative management or intervention for Unruptured brain
arteriovenous malformations. JAMA. 2014;311(16):1661. https://
doi.org/10.1001/jama.2014.3200.
14. van Rooij WJ, Jacobs S, Sluzewski M, van der Pol B, Beute GN,
Sprengers ME.Curative embolization of brain arteriovenous malformations with onyx: patient selection, embolization technique,
and results. AJNR Am J Neuroradiol. 2012;33(7):1299–304.
https://doi.org/10.3174/ajnr.A2947.
15. Fournier D, TerBrugge KG, Willinsky R, Lasjaunias P, Montanera
W. Endovascular treatment of intracerebral arteriovenous malformations: experience in 49 cases. J Neurosurg. 1991;75(2):228–33.
https://doi.org/10.3171/jns.1991.75.2.0228.
16. Lasjaunias P, Manelfe C, Terbrugge K. Endovascular treatment of cerebral arteriovenous malformations. Neurosurg Rev.
1986;9(4):265–75.
17. Mounayer C, Hammami N, Piotin M, etal. Nidal embolization of
brain arteriovenous malformations using onyx in 94 patients. AJNR
Am J Neuroradiol. 2007;28(3):518–23.
18. Saatci I, Geyik S, Yavuz K, Cekirge HS. Endovascular treatment
of brain arteriovenous malformations with prolonged intranidal
Onyx injection technique: long-term results in 350 consecutive
patients with completed endovascular treatment course: clinical
article. JNS. 2011;115(1):78–88. https://doi.org/10.3171/2011.2.
JNS09830.
19. Mosimann PJ, Chapot R. Contemporary endovascular techniques
for the curative treatment of cerebral arteriovenous malformations
and review of neurointerventional outcomes. J Neurosurg Sci.
2018;62(4):505. https://doi.org/10.23736/S0390- 5616.18.04421- 1.
20. Vollherbst DF, Chapot R, Bendszus M, Möhlenbruch MA.Glue,
onyx, squid or PHIL? Liquid embolic agents for the embolization of
cerebral arteriovenous malformations and Dural arteriovenous stulas. Clin Neuroradiol. 2022;32(1):25–38. https://doi.org/10.1007/
s00062- 021- 01066- 6.
21. Weber W, Kis B, Siekmann R, Kuehne D.Endovascular treatment
of intracranial arteriovenous malformations with onyx: technical
aspects. AJNR Am J Neuroradiol. 2007;28(2):371–7.
22. Murayama Y, Viñuela F, Ulhoa A, et al. Nonadhesive liquid embolic agent for cerebral arteriovenous malformations: preliminary histopathological studies in swine rete
mirabile. Neurosurgery. 1998;43(5):1164–72. https://doi.
org/10.1097/00006123- 199811000- 00081.
23. Wang J, Wu HC, Wang WW, etal. Trigeminal cardiac reex caused
by Onyx embolization of intracranial dural arteriovenous stula.
Turk Neurosurg. 2016;26(3):325–30.
24. Flores BC, See AP, Weiner GM, Jankowitz BT, Ducruet AF,
Albuquerque FC.Use of the Apollo detachable-tip microcatheter
for endovascular embolization of arteriovenous malformations and
arteriovenous stulas. J Neurosurg. 2019;130(3):963–71. https://
doi.org/10.3171/2017.9.JNS17397.
25. Chapot R, Stracke P, Velasco A, etal. The pressure cooker technique
for the treatment of brain AVMs. J Neuroradiol. 2014;41(1):87–91.
https://doi.org/10.1016/j.neurad.2013.10.001.
26. Waldeck S, Chapot R, Von Falck C, Froelich MF, Brockmann M,
Overhoff D.First experience in the control of the venous side of
the brain AVM. JCM. 2021;10(24):5771. https://doi.org/10.3390/
jcm10245771.
27. He Y, Bai W, Xu B, et al. Perioperative complications of
Transvenous embolization of ruptured intracranial arteriovenous malformations. Front Neurol. 2022;13:873186. https://doi.
org/10.3389/fneur.2022.873186.
28. Koyanagi M, Mosimann PJ, Nordmeyer H, et al. The transvenous retrograde pressure cooker technique for the curative
embolization of high-grade brain arteriovenous malformations. J
NeuroIntervent Surg. 2021;13(7):637–41. https://doi.org/10.1136/
neurintsurg- 2020- 016566.
29. Lv X, Jiang C, Wang J.Pediatric intracranial arteriovenous shunts:
advances in diagnosis and treatment. Eur J Paediatr Neurol.
2020;25:29–39. https://doi.org/10.1016/j.ejpn.2019.12.025.
30. Kuiper L, Sánchez Van Kammen M, Coert BA, etal. Association
between Dural AVFs and cerebral venous thrombosis. AJNR Am
J Neuroradiol. 2022;43(12):1722–9. https://doi.org/10.3174/ajnr.
A7652.
31. Kondo R, Kumabe T, Yamamoto D, Koizumi H, Kuroda H,
Miyasaka K. Visual disorders caused by cranial arteriovenous stula with venous drainage into the superior ophthalmic vein. Interv Neuroradiol. 2019;25(4):460–8. https://doi.
org/10.1177/1591019919829626.
32. Borden JA, Wu JK, Shucart WA. A proposed classication for
spinal and cranial dural arteriovenous stulous malformations
and implications for treatment. J Neurosurg. 1995;82(2):166–79.
https://doi.org/10.3171/jns.1995.82.2.0166.
33. D’Aliberti G, Talamonti G, Boeris D, etal. Intracranial Dural arteriovenous stulas: the sinus and non-sinus concept. In: Esposito
G, Regli L, Cenzato M, Kaku Y, Tanaka M, Tsukahara T, editors.
Trends in cerebrovascular surgery and interventions. Springer;
2021. Accessed March 27, 2024. http://www.ncbi.nlm.nih.gov/
books/NBK573772/.
34. Xu K, Yang X, Li C, Yu J.Current status of endovascular treatment
for dural arteriovenous stula of the transverse-sigmoid sinus: a
literature review. Int J Med Sci. 2018;15(14):1600–10. https://doi.
org/10.7150/ijms.27683.
35. Kortman H, Boukrab I, Sluzewski M, Van Rooij WJ, Peluso
JP, Majoie C. Endovascular treatment of dural arteriovenous
stulas with sinus drainage: do we really need to protect the
sinus? Interv Neuroradiol. 2019;25(3):315–21. https://doi.
org/10.1177/1591019918819187.
36. Rabinov JD, Yoo AJ, Ogilvy CS, Carter BS, Hirsch JA.ONYX versus n-BCA for embolization of cranial dural arteriovenous stulas.
J NeuroIntervent Surg. 2013;5(4):306–10. https://doi.org/10.1136/
neurintsurg- 2011- 010237.
37. Renieri L, Michelozzi C, Brinjikji W, et al. PTA stent of Dural
sinuses in brain DAVF: a report of 4 cases. Clin Neuroradiol.
2019;29(2):331–9. https://doi.org/10.1007/s00062- 017- 0652- 2.
38. Raybaud CA, Strother CM, Hald JK. Aneurysms of the vein of
Galen: embryonic considerations and anatomical features relating to the pathogenesis of the malformation. Neuroradiology.
1989;31(2):109–28. https://doi.org/10.1007/BF00698838.
39. Lasjaunias PL, Chng SM, Sachet M, Alvarez H, Rodesch G, GarciaMonaco R.The Management of Vein of Galen aneurysmal malformations. Neurosurgery. 2006;59(suppl_5):S3-184–94. https://doi.
org/10.1227/01.NEU.0000237445.39514.16.
40. Agarwal H, Sebastian LJD, Gaikwad SB, Garg A, Mishra NK.Vein
of Galen aneurysmal malformation—clinical and angiographic
spectrum with management perspective: an institutional experience.
J NeuroIntervent Surg. 2017;9(2):159–64. https://doi.org/10.1136/
neurintsurg- 2015- 012137.
41. Alvarez H, Garcia Monaco R, Rodesch G, Sachet M, Krings
T, Lasjaunias P. Vein of Galen aneurysmal malformations.
Neuroimaging Clin N Am. 2007;17(2):189–206. https://doi.
org/10.1016/j.nic.2007.02.005.
42. Arko L, Lambrych M, Montaser A, Zurakowski D, Orbach
DB.Fetal and neonatal MRI predictors of aggressive early clinical
course in vein of Galen malformation. AJNR Am J Neuroradiol.
2020;41(6):1105–11. https://doi.org/10.3174/ajnr.A6585.
43. Miyasaka K, Asano T, Ushikoshi S, Hida K, Koyanagi I.Vascular
anatomy of the spinal cord and classication of spinal arteriovenous malformations. Interv Neuroradiol. 2000;6(Suppl 1):
195–8.
44. Takai K. Spinal arteriovenous shunts: angioarchitecture and
historical changes in classication. Neurol Med Chir (Tokyo).
2017;57(7):356–65. https://doi.org/10.2176/nmc.ra.2016- 0316.

154
L. J. D. Sebastian et al.
45. Rodesch G, Lasjaunias P. Spinal cord arteriovenous shunts: from
imaging to management. Eur J Radiol. 2003;46(3):221–32. https://
doi.org/10.1016/S0720- 048X(03)00093- 7.
46. Kona MP, Buch K, Singh J, Rohatgi S. Spinal vascular shunts: a
patterned approach. Am J Neuroradiol. 2021;14:2110. https://doi.
org/10.3174/ajnr.A7312.
47. Krings T, Geibprasert S. Spinal dural arteriovenous stulas. Am
J Neuroradiol. 2009;30(4):639–48. https://doi.org/10.3174/ajnr.
A1485.

Other Neurointerventions
LeveJosephDevarajanSebastian, NikhilaGunnaReddy,
andSavyasachiJain
14
Key Messages
1. Apart from intracranial aneurysms, Arterio-Venous malformations (AVMs), and stroke, a neurointerventionist
has to tackle a wide range of vascular and sometimes nonvascular problems of the head, neck, and spine.
2. Endovascular coiling is the technique of choice for
carotico-cavernous stula (CCF).
3. Massive epistaxis caused by cavernous internal carotid
artery (cICA) pathologies can be managed by endovascular means.
4. Intra-arterial chemotherapy is used as salvage therapy in
retinoblastoma when systemic chemotherapy and intravitreous treatments fail.
5. Preoperative embolization is performed in many tumors
such as meningioma, hemangioblastoma, nasopharyngeal angiobroma, glomus jugulare, and paragangliomas
to reduce blood loss.
14.1 Introduction
Apart from aneurysms, AVMs, and stroke, a neurointerventionist is called to tackle a wide range of vascular and sometimes nonvascular problems involving the head, neck, and
spine. Here we shall briey review some of these conditions.
This will be largely a pictorial essay based on illustrative
cases.
14.2 Direct CCF
Penetrating injuries by sharp objects can lead to CCF,
especially in children. Injury to cavernous ICA during skull
base or trans-sphenoidal surgeries can also cause CCF.
14.2.1 Relevant Anatomy andPathogenesis
Cavernous ICA (C4 segment) is surrounded by the venous
plexus (cavernous sinus) and is partially xed by the dura
distally at the dural ring just before the ICA enters subarachnoid space and proximally to the petrous bone. This relative
xity of the ICA in the region makes it vulnerable to
injuries.
Since cavernous sinus has extensive connections, ow
from the stula can be in multiple directions. Clinical symptoms and severity depend on the direction and severity of
venous ow, as listed below. In many cases, symptoms are
predominantly due to venous hypertension [1]. Symptoms
due to arterial steal can also occur.
Anterior: drainage into the ophthalmic venous system pro-
duces proptosis, chemosis, raised ocular pressure (glau-
coma), and loss of vision.
Posterior: drains into the inferior/superior petrosal sinus or
the occipital transverse sinus. Patients complain of tinni-
tus or cranial nerve dysfunction.
Contralateral: both cavernous sinuses anastomose anteri-
orly and posteriorly. Both eyes may be involved with vari-
able severity.
Direct CCFs are mostly traumatic in nature and are common
in the Indian subcontinent mostly due to road trafc accidents, especially motorbike accidents. It is more common in
young males.
L. J. D. Sebastian (*) · N. G. Reddy · S. Jain
Department of Neuro-radiology and Neurointerventions, 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_14
14.2.2 Treatment
It is essentially endovascular (Figs. 14.1 and 14.2). DSA
helps determine the exact location of stula and adequacy of
the cross-ow. Previously available options include embolization with detachable balloons, an elegant way of treatment.
It requires 8F or 9F access and the meticulous process of
loading of a suitable gold valve balloon of suitable size in the
155

156
L. J. D. Sebastian et al.
a
e
b
f
c
d
g
Fig. 14.1 Endovascular treatment of direct CCF by simple coiling. A
young man presented with right proptosis 3months after a road trafc
accident. Right ICA angiogram in anteroposterior (a) and lateral (b)
projections demonstrates the direct CCF with near complete steal.
Cross-compression study reveal the exact location of the stula. Here
specially designed delivery microcatheter. This technique is
almost obsolete as the balloons are no more available in
many parts of the world.
Coiling Currently endovascular coiling is the technique of
choice. We can take transarterial, transvenous, or both. One
or two microcatheters may be used. A balloon microcatheter
can also be used to prevent coil prolapse into the parent
artery. Strategic coiling aimed at reducing gradient across
the stula and increasing antegrade laminar ow helps early
obliteration of the stula with a minimum number of coils
[2, 3].
vertebral angiogram in lateral projection (c) with right carotid manual
compression shows the rent close to the anterior genu of right cavernous ICA.A microcatheter is navigated across the stula (d) and progressive coiling is done (e and f). Control angiogram (g) shows complete
occlusion of the stula with restoration of antegrade ow
Onyx (high density) can also be used along with coils
where protection of the neck by a balloon microcatheter is
essential.
Parent artery occlusion can also be done in severely lacerated arteries if there is adequate cross-ow.
Outcomes Generally immediate improvement in proptosis
and chemosis is seen with good long-term outcomes.
However, decits due to direct injury, e.g., loss of vision due
to optic nerve injury, may not be reversed. Hence thorough
pre-op examination and prognostication are essential.

bc
14 Other Neurointer ventions
a
157
d
Fig. 14.2 Endovascular treatment of direct CCF by detachable balloons.
Right ICA angiogram (a, b) shows direct CCF with rent in the horizontal
segment of cavernous ICA. A detachable balloon mounted on a delivery
microcatheter is navigated across the stula (c) and inated and detached
e
14.3 Epistaxis
Massive epistaxis due to cavernous internal carotid artery
(cICA) pathology is a life-threatening condition. Most common causes are craniofacial trauma, mishaps during skull
base surgeries, and rarely spontaneous rupture of giant, dissecting, or mycotic cICA aneurysms. Immediate post nasal
packing can provide temporary cessation of nasal bleeding,
but denitive management of cICA aneurysm is a must, otherwise recurrence will be there. Surgical management of
cICA aneurysm is often cumbersome and difcult, whereas
endovascular methods can offer better solutions.
• The diagnosis of clinically suspected cICA pathology causing nasal bleeding should be conrmed using CT imaging,
CT angiography, or magnetic resonance imaging. Catheter
angiography (DSA—digital subtraction angiography) is
the gold standard and offers the opportunity to perform
endovascular treatment simultaneously [4, 5].
• Management options are endovascular embolization,
clipping of aneurysm neck, or ligation of the internal
f
close to the rent by gently pulling the microcatheter. Native image
(d)shows two such balloons deployed sequentially. The inated balloons
on the venous side of the rent shut the stula. Control angiogram shows
(e, f) complete sealing of the stula with good antegrade ow
carotid artery. Endovascular treatment is often superior to
surgical management.
• Being relatively rare conditions, there are no well-set
guidelines evolved for the treatment of cICA pseudoaneurysms. Both vessel preserving (reconstructive procedure)
and parent artery occlusion (deconstructive) techniques
have been proposed in the literature for the management
of cICA pathology depending upon several factors like
the etiology, anatomy of rent, involved segment length,
site, diseased or dissected segment of ICA proximal or
distal to lesion, age of the patient, and the status of cross
circulation.
• Trapping of the pseudoaneurysm by parent artery occlusion (PAO) by coils is a safe and effective treatment strategy in patients with patent circle of Willis and good
collateral circulation. Deploying some coils in the aneurysmal sac, i.e., endosaccular coiling along with PAO provides additional safety by eliminating the chance of
recanalization. This method of treatment is especially
preferred if a long segment of the arterial segment is diseased or dissected. As implied, prior balloon occlusion

158
L. J. D. Sebastian et al.
test is preferable before proceeding with permanent
occlusion.
• Treatment decisions become difcult when collateral circulation is proven inadequate on balloon occlusion test in
a given patient. An emergency external carotid-middle
cerebral artery (ECA–MCA) bypass followed by PAO as
described above is an option, though it is logistically challenging in many centers. Use of ow diverter or stent graft
may be useful in such cases.
• Reconstruct techniques include endosaccular coiling,
stent-assisted coiling, stent graft, or ow diverter placement [6]. Endosaccular coiling can be challenging as it
involves careful selective coiling of the pseudoaneurysm
which invariably projects into the sphenoid sinus. If the
aneurysmal neck is broad or of dissecting type, it will be
difcult to safeguard the parent arterial lumen. Stentassisted coiling is of help in these situations. Though bare
stents are technically easy to deploy, there are multiple
reports related to recanalization of the PSAs after using
such stents as the blood can ow through the interstices in
the stent into the pseudoaneurysm [7, 8].
• Covered stents or stent grafts, when deployed optimally,
are the fool-proof means of immediate and complete
obliteration of PSAs. But they are relatively stiffer, and
their negotiability and deployment are challenging, especially in intracranial ICA [9]. Various reported complications such as embolic strokes, dissection, thrombosis,
rupture, and stent kinks are the potential drawbacks.
14.4 Neck Vessel Pathologies
14.4.1 Pediatric Pseudoaneurysms oftheNeck
14.4.2 Etiopathogenesis
• Most common causes are infection and trauma. A few
rare cases of congenital aneurysms and spontaneous dissecting aneurysms in the setting of weakened vessel wall
such as collagen vascular disorders and neurobromatosis- I are also reported [10]. Infections of the deep neck
space including retropharyngeal/parapharyngeal/peritonsilar abscesses and cervical lymphadenitis can involve the
arterial wall contiguously, resulting in pseudoaneurysm.
• Traumatic pseudoaneurysms are common as the child
ages, especially in teenage children, probably due to the
increased outdoor activities. Traumatic pseudoaneurysms
are reported after a fall from trampoline and paintball
injuries.
• These aneurysms are also seen after iatrogenic trauma in
the setting of tonsillectomy or abscess drainage of neck
space infections. Pseudoaneurysms arising after partial
healing of either traumatic or spontaneous dissection,
especially of vertebral arteries, are usually small with or
without coexisting stenosis of the involved vessel [11].
14.4.3 Clinical Presentation
The etiology and location of the aneurysm dictate the clinical
presentation in a given case. Large pulsatile neck swelling,
difculty in breathing or stridor due to airway compression,
and difculty in swallowing due to pharyngeal compression
are some of the common presentations. Stroke or transient
ischemic attacks due to emboli and life-threatening bleeding
are other presentations.
Infectious or posttraumatic pseudoaneurysms involving
major arteries of the neck are not uncommon in pediatric
population. They are often associated with or mimic lymph
nodal or other inammatory masses of the neck such that an
unsuspecting physician may tend to biopsy or drain them
with disastrous consequences. High index of suspicion and a
good quality ultrasonogram and Doppler examination will
help make the correct diagnosis in most of the cases. CT
angiogram is useful for treatment planning and for clarifying
the diagnosis in doubtful cases.
These lesions carry the potential for massive bleeding or
airway compression due to sudden enlargement. Hence
timely evaluation and treatment are warranted. Surgical
treatment is often difcult and cumbersome while endovascular techniques can offer simpler solutions in most of the
cases (Figs. 14.3 and 14.4). Parent vessel occlusion is the
commonly adopted strategy, while in selected cases reconstructive approaches are also possible as illustrated here.
14.4.4 Management
• In acute presentations attention should be paid to basic
resuscitation steps before venturing into denitive
treatment.
• Securing airway with elective intubation or tracheostomy
will be useful in most of the patients.
• In cases of mycotic aneurysms, appropriate antibiotics in
adequate dosage is the rst and essential step in the
management.
• Emergent endovascular treatment is indicated in children
presenting with life-threatening oral/ear bleeding or rapidly
enlarging neck swelling with a fall in hemoglobin. These
patients are best treated with parent vessel sacrice after
ensuring adequacy of collateral ow to the affected vascular territories. Deconstructive procedures can be surgical
ligation of the parent vessel, endovascular parent vessel
sacrice, or endovascular trapping of the aneurysm.

a
c
14 Other Neurointer ventions
b
159
d
e
Fig. 14.3 Endovascular management of PSA of neck. CT (a, b) showing
large extracranial pseudoaneurysm. Right CCA (c, d) run showing giant
distal cervical ICA aneurysm with tortuous cervical ICA.Left vertebral
f
run (e, f) showing good cross-ow across PCOM into the right MCA territory. Native unsubtracted right CCA angiogram (g) showing patent
artery occlusion (PAO) with coils in cervical ICA proximal to the loop
g
• Parent vessel reconstructive procedure can also be successfully employed in suitable cases, especially in nonemergent situations. Surgical resection of the aneurysmal
segment with end-to-end anastomosis or vessel grafting
can prove a demanding procedure with high rate of complications. Endovascular options like stent-assisted coiling or stent graft (covered stent) deployment across the
aneurysm offer elegant solutions.
• Use of bare metal stent alone or with coils has a high
chance of recurrence. Coils can also erode into the pharyngeal mucosa over time and can protrude into the oral
or pharyngeal cavity [12, 13].
• Stent graft can provide immediate sealing off of the aneurysm [14]. Favorable factors for using the stent graft
include relatively straight segment of the involved vessel,
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