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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]

23 Interventions ofRenal Vessels
285
23.5.2.8 Embolic Protection Device’s (EPD) Role
inPTRA andStenting
Atherosclerotic embolism can occur during renal artery
angioplasty and stenting procedure secondary to manipulation of the aorta and renal arteries with resultant variable
degree of renal function impairment [28]. The true incidence
of these phenomena is not unknown. EPD can be used to
prevent this atheroembolism. EPD includes lters (Fiber Net
EP system), which are made up of densely woven bers and
can catch particles as tiny as 40 microns without interfering
with ow [29]. Prior to performing the interventional procedure (angioplasty and/or stenting), the lter is positioned distal to the target lesion. During the interventional process, the
lter is opened by the actuator, which subsequently catches
and recovers emboli while maintaining physiological ow to
the kidneys. With the syringe and connected stopcock assembly, the collected embolic material (thrombus/debris) is
sucked into the retrieval catheter at the end of the process.
While the capture wire lter is closed and pulled into the
retrieval catheter [30], aspiration continues. EPDs are discovered to be an effective and safe way to stop atheroembolization brought on by angioplasty and stenting of ostial
lesions [29].
23.5.2.9 Post-Procedural Care
Renal function and BP monitoring should be done for
24hours after the procedure. Intravenous administration of
normal saline should be done if there is a signicant drop in
BP.Clopidogrel 75mg for 6weeks and aspirin 75mg for life
are recommended after renal artery stenting.
23.5.2.10 Complications
Access site complications are the most common complications with a complication rate approaching 2% after renal
angioplasty which include AV stula, pseudoaneurysm,
hematoma at the femoral access site, atheroembolism, retroperitoneal hematoma (RPH), renal artery rupture, aortic and
renal artery dissection, contrast-induced nephropathy, renal
infarction, and, very rarely, mortality too. Radial artery vascular access, usage of embolic protection devices, catheterin- catheter approach, no-touch technique, stent sizing with
IVUS, and adequate hydration before and after angiography
are some of the procedural considerations to minimize these
procedure-related complications [9].
sympathetic nerve bers to heat, catheter-based renal sympathetic denervation via radiofrequency ablation has been
developed in humans for resistant hypertension [30]. It has
been shown to reduce renal sympathetic nervous system
activity and improve BP in patients with resistant hypertension. It has been reported in growing data from many uncontrolled clinical studies using several types of ablation
catheters that RDN can be used safely and is successful in
decreasing BP in patients with drug-resistant hypertension.
Up to three years of sustained blood pressure reduction have
been reported in several trials [31].
However, renal artery denervation is deferred in pathological conditions like severe RAS, a stent in situ, diffuse
atherosclerotic aortorenal lesions, and abdominal aortic
aneurysms. These coexisting pathological do not rule out the
possibility of renal denervation but require extra care and a
more precise clinical assessment of the risk-to-benet ratio
[32].
23.6.1 Procedure
In catheter-based renal sympathetic denervation, arterial
access is achieved using a 6F access sheath through the femoral route, and angiography is performed to determine the
location of the origin of all renal arteries (including accessory renal arteries). Analgesics are given to provide effective
pain management because the RDN typically results in
severe backache and abdominal discomfort. Thereafter, a
guide catheter (usually a renal double curve catheter) is used
to specically engage the renal artery, and selective renal
angiography is done. A radiofrequency catheter with an electrode at its distal end is used for RDN.The catheter’s tip may
be bent and twisted using a hand control. It is carefully
inserted into the renal artery’s mid to distal portion, where
wall contact is achieved. Radiofrequency energy (8 W) is
delivered for 2minutes at a time. After ablation in one region,
the RFA catheter is gradually withdrawn, with radiofrequency energy applied in a spiral-circumferential pattern.
Generally, 4–8 ablations are conducted at least 5mm apart in
each artery. To avoid harm to surrounding soft tissue, RFA
energy delivery is controlled by temperature and impedance
feedback from the catheter tip [30].
23.6 Renal Denervation inResistant
Hypertension
Overactivity of the renal sympathetic nervous system has
been observed to commonly accompany essential hypertension. Because of the kidney’s proven role in blood pressure
control, location, and exquisite high sensitivity of the renal
23.7 Renal Artery Aneurysms (RAAs)
Although the exact prevalence of RAAs is unknown, it has
been reported that it occurs in around 0.1% of the population
and accounts for 20% of visceral aneurysms [33]. RAAs are
being more commonly detected with increased use of crosssectional imaging done for other diagnostic purposes. They
can be both true and false aneurysms. True renal aneurysms

286
P. Jagia et al.
occur secondary to atherosclerosis or FMD, whereas false
aneurysm/pseudoaneurysms occur secondary to iatrogenic
causes, trauma, and infections.
Most patients with RAAs are asymptomatic and are diagnosed as incidental ndings on imaging and symptoms, if
present, include hypertension (~90% of patients) [34] gross
hematuria, pain abdomen, and rarely hemodynamic shock
secondary to rupture.
Angiographically, RAA can be classied into three types
[35]:
A: Saccular aneurysm from main RA or proximal segmental
RA.
B: Fusiform aneurysms from main RA or proximal segmen-
tal RA.
C: Intraparenchymal aneurysms involving small segmental
or accessory RA.
Management Asymptomatic renal artery aneurysms <3cm
are managed conservatively and imaged annually until two
consecutive imaging results are stable; beyond that, imaging
Fig. 23.4 A 32-year-old male
patient, known hypertensive
on medication, presented with
right ank pain for
3–4weeks. CTA showed two
fusiform aneurysms from an
anterior inferior segmental
branch of the right renal
artery after its bifurcation
measuring 3.0×2.5cm and
1×0.8cm, respectively.
Accessory renal arteries are
seen on both sides supplying
the upper poles (a and b). In
DSA, a selective run of
anterior inferior segmental
artery conrmed these
ndings (c). AVP IV: 4mm
and 6mm were deployed in
an anterior inferior segmental
artery proximally (yellow
asterisk) and postdeployment; complete
occlusion with no distal lling
of segmental arteries and
aneurysms was seen (d)
a
c
is done every 2 to 3years. Aspirin 75mg is also given to
prevent thromboembolism in patients with RAAs [36].
23.7.1 Denitive Treatment
It is indicated in the following:
• Uncomplicated RAA with a size >3cm.
• Patients of childbearing potential with refractory hypertension and hemodynamically signicant RAS regardless
of their sizes.
• Emergent intervention is done in symptomatic RAAs or
ruptured RAAs regardless of size [36].
23.7.2 Endovascular Management inRAAs
Endovascular management is preferred over surgery for
RAAs treatment wherever possible (Fig.23.4). The type of
endovascular method depends on the aneurysms’ location
b
d

23 Interventions ofRenal Vessels
287
Table 23.1 Management in RAA
Type of renal aneurysm/site of
involvement Treatment of choice
Saccular aneurysm from main RA or
proximal segmental RA
Fusiform aneurysm from main RA or
proximal segmental RA
Intraparenchymal involving small
segmental or accessory RA
Stent/balloon-assisted
coiling or plug
Surgical method
Coiling [38]
and morphology. Types A and C are usually amenable to
endovascular intervention and type B is usually treated surgically [37]. The main aim of the intervention is to preserve the
MRA or proximal segmental artery by putting a stent or coiling or both. Stent-assisted coiling is done in a saccular aneurysm with a wide neck. Alternatively, if the neck is narrow,
aneurysmal sac embolization is done with coils/plugs to preserve the main or proximal segmental artery. In case of aneurysms from small segmental arteries, embolization of the
feeding artery is done using detachable coils proximal to the
sac. Non-detachable coils and liquid embolic agents can be
used where segmental arteries are sacriced, but it can result
in non-target embolization [35]. Management in RAAs is
summarized in Table23.1 [37].
biopsy), trauma, or associated with neoplasm. Congenital
AVMs represent a cirsoid tangle of vessels and constitute
~20% of all renal AV shunt, whereas idiopathic AVMs are
cavernous connections between arteries and veins with
aneurysmal changes and are seen in ~5% of all renal
AVMs [39].
23.8.2 Clinical Presentation
Symptoms include ank pain, gross hematuria, and highoutput cardiac failure.
23.8.3 Endovascular Management
Endovascular mode of intervention is preferred over surgery
whenever possible (Fig.23.5). The main aim of treatment in
renal AV shunts is to embolize the nidus/communication
while at the same time preserving the renal function and preventing non-target systemic embolization. So, a particulate
embolism agent such as PVA particles is not recommended
in renal AV shunts because of the higher risk of pulmonary
embolization with high-ow renal shunts [40].
23.8 Renal Arteriovenous Shunts
(Malformations andFistulas)
Renal arteriovenous malformations (AVMs) and arteriovenous stulas (AVFs) are abnormal pathological communication between renal arteries and veins. Renal AVFs are
characterized by direct communication between an arterial
branch and a venous channel, whereas AVMs are characterized by intervening nidus or tangle of vessels between the
arterial branch and venous channel.
23.8.1 Etiology
Arteriovenous shunts can be both acquired and congenital
or idiopathic. Acquired shunts constitute 75% of all renal
AV shunts and are mostly due to iatrogenic causes (post-
AV F Small post-traumatic AVFs may heal spontaneously
and no intervention is needed. But large and symptomatic
AVFs need active intervention. Different endovascular management methods in AVF include embolization with coils,
detachable balloons, vascular plugs, and liquid embolic
agents or exclusion of the stulous communication by using
a covered stent. Vascular plugs are advantageous in AVFs
with large feeding arteries and a precise deployment is
required [39].
AV M Renal AVMs do not show spontaneous regression.
The target of AVM embolization should be focused on the
nidus to decrease the future incidence of recurrence. For this,
liquid embolic agents such as ethanol or glue are useful. It
has been found that the success of treating AVMs is lower
compared to AVFs with high recurrence rates requiring reinterventions [40].

288
P. Jagia et al.
Fig. 23.5 A 73-year-old male
patient who presented with
right ank pain and frank
hematuria for the last
2–3weeks; CT volumerendered images showed a
dilated main renal artery (red
asterisk) with stulous
communication (black
asterisk) and early
opacication of renal veins
(blue asterisk) and IVC (a and
b). Selective cannulation of
the right renal artery
conrmed dilated renal artery
in the proximal and mid part
with stulous communication
with renal vein and early
lling of IVC s/o AVF (c).
Amplatzer vascular plug
(AVP2) of 18mm (blue
arrow) was deployed under
uoroscopic guidance in the
mid part of the right renal
artery. A check angiogram
with the catheter in a
proximal position showed
non-opacication of the
stula and draining veins as
compared to pre-embolization
state (d)
a
c
b
d
23.9 Endovascular Intervention forRenal
Neoplasms
23.9.1 Angiomyolipoma
Renal angiomyolipomas (AMLs) are benign tumors consisting of variable proportions of smooth muscles, adipose tissue, and blood vessels. They can be sporadic and syndromic
(tuberous sclerosis, etc.). Syndromic AMLs are usually bilateral and larger at presentation. Renal AMLs are usually
asymptomatic if small in size. Larger AML can present with
ank pain, frank hematuria, and rarely hemodynamic collapse secondary to rupture.
Endovascular Intervention Selective renal artery embolization (RAE) is considered in AMLs for both prophylactic
and therapeutic purposes. Prophylactic selective renal artery
embolization is a safe, efcacious, and parenchymal preserving method for renal angiomyolipomas (>4cm in size) for
reducing tumor volume and preventing future risk of hemorrhagic complications [41]. In symptomatic AMLs, RAE can
be termed as the rst line of treatment for individuals with
symptomatic and often large syndromic renal AMLs as it
prevents active bleeding from the tumor [42].
The different embolic agents which can be used for embolization in AMLs include gelatin particles, metallic coils
[41], ethanol, polyvinyl alcohol particles, and a mixture of
96% ethanol and polyvinyl alcohol particles [43]. The procedure is well tolerated and is associated with minimal adverse
reactions [43]. Minor complications include access site complication, post-embolization syndrome (~ 24% of patients),
and rare complications like non-target embolization.
The advantage of selective renal artery embolization in
AML is there is the preservation of signicant residual
renal parenchyma with normal renal function. Despite renal
preservation following RAE, higher reintervention rates are
seen compared to other management options. Thus, there
should be continued disease surveillance post-RAE in
AML and there are no clear-cut guidelines for follow-up
post-RAE, and usually yearly follow-up is done in previous
studies [44].

23 Interventions ofRenal Vessels
289
23.9.2 Renal Cell Carcinoma (RCC)
Renal cell carcinoma is the most common malignant renal
tumor and usually patients present with hematuria, abdominal pain, and palpable renal lump. The denitive treatment in
RCC remains nephrectomy (surgery), and therefore the role
of endovascular intervention in RCC is limited.
Endovascular Intervention The main indication of endovascular intervention in RCC is preoperative embolization of
feeding arteries to decrease intraoperative blood loss and
perform easier surgical resection [45]. Preoperative RAE has
been shown to increase tissue edema between the normal tissue and tumor, which promotes better delineation of tumor
margins and thus dissection of the tumor [46]. The ideal time
to perform preoperative embolization is uncertain and mostly
depends on the surgical objectives. It is suggested that surgery should be performed between 24 and 72 hours after
embolization. But owing to the heterogeneity in benecial
results, preoperative RAE has not been established as routine
practice prior to surgery [47].
RAE may also be utilized for palliative purposes in
patients with unresectable renal cell carcinoma to reduce
tumor mass and provide symptomatic alleviation of hematuria and/or ank discomfort [45] with a 75% success rate of
symptomatic relief [47].
Agents that can be used for tumor embolization include
ethanol, coils, PVA particles, and microspheres. Ethanol
injection may require simultaneous balloon occlusion to prevent systemic side effects.
Recently, trans-arterial chemoembolization of RCCs with
doxorubicin has been evaluated, and it has been found that
trans-arterial chemoembolization is safe for treating localized RCC and has a considerably greater cytoreductive
impact with less systemic adverse effects than TAE [48].
23.10 Venous Interventions
Renal vein interventions include stenting for nutcracker syndrome (NCS) and catheter-directed thrombectomy (CDT)
with or without thrombolysis for renal vein thrombosis
(RVT).
23.10.1 Nutcracker Syndrome (NCS)
NCS is a rare vascular compression syndrome, and it constitutes a diagnosis of exclusion. Patients with NCS are clinically present in third and the fourth decades and have clinical
features of venous hypertension in the left kidney (LK) secondary to anatomic compression of the left renal vein. NCS
can be divided into two types: anterior (more common) and
posterior NCS.In anterior NCS, the compression of the LRV
occurs between the superior mesenteric artery (SMA) and
aorta, whereas it occurs between the aorta and spine in posterior NCS.Drainage of the left gonadal vein occurs through
LRV which results in varicocele or pelvic congestion in men
and women respectively. The symptoms of NCS include
ank pain, gross hematuria, and secondary varicocele.
23.10.1.1 Diagnosis
The diagnosis of NCS requires a higher degree of clinical
suspicion. Compression of LRV is considered clinically signicant if the AP diameter of the renal vein is >5 times than
at the stenosis site or if the peak systolic velocity (PSV) at
the site of stenosis is >5 times than at the renal hilum on
Doppler [49], SMA branching angle of <35 degree [50],
venous collaterals in the retroperitoneum and renal hilum,
and >3mmHg pressure gradient between left renal vein and
the IVC [51]. With these constellations of ndings, the sensitivity, specicity, and accuracy to diagnose NCS have been
reported to be more than 80% in the literature [52].
23.10.1.2 Management
Patients with mild symptoms and younger age are managed
conservatively.
This conservative approach is maintained in young
patients under the age of 18 for 24months [53] because of
physical development, adipose tissue growth at SMA ostium,
and collateralization of veins in retroperitoneum which can
relieve LRV compression resulting in spontaneous symptom
resolution [54].
Intervention is considered when there are persistent clinical symptoms after a sufciently long period of conservative
treatment. Both surgery and endovascular stenting are treatments available for NCS.Open repair for NCS is associated
with better long-term outcomes and includes LRV transposition into IVC 3–5cm below the previous LRV drainage site,
renal auto transplantation, and LRV bypass [55].
23.10.1.3 Endovascular Management
Endovascular procedure has been a popular alternative to
surgery considering its minimally invasive nature which has
offered good short-term results in the past. Endovascular
therapy with renal venous stenting is a technically possible,
clinically effective procedure with a good safety prole in
carefully selected adolescents.
23.10.1.4 Procedure
Left renal vein stenting can be performed via the femoral,
internal jugular, or brachial vein approaches. A direct renal
venogram should be done to demonstrate the site of compression and its extent after crossing the stenosed segment
with a 0.035″ guidewire and catheter combination. As there

290
P. Jagia et al.
is no primary stenosis within the vein (external compression), venoplasty prior to stenting is not recommended.
However, there is no consensus regarding the oversizing of
the stents with respect to the renal vein diameter. Studies
have shown that 20% of oversizing results in minimum stent
migration. Balloon-expandable stents are preferred over selfexpandable stents which offer the advantage of precise
placement and high radial strength, thus minimizing the risk
of migration. After selective catheterization and conrmation of the position, the balloon-expandable stent is deployed
across the stenosed segment and a check venogram is
obtained to conrm the precise placement [56].
23.10.1.5 Complications
The complications of post-endovascular stenting in NCS
include in-stent thrombosis and in-stent stenosis which are
far more common than stent migration. But the most serious
complication of LRV stenting is stent migration: It can get
dislodged and migrate into the right atrium, pulmonary arteries, IVC, or peripheral LRV.Stent migration may be fatal and
usually necessitates open surgical removal; however, endovascular stent retrieval has been reported in the literature
[55].
23.10.2 Renal Vein Thrombosis
Renal vein thrombosis (RVT) is an extremely uncommon
condition, and the frequency of both acute and chronic renal
vein thrombosis is unknown [57]. RVT occurs in nephrotic
syndrome, hypercoagulable states, an extension of thrombus
from iliocaval veins or IVC, recent surgery and malignancy,
and post-renal transplant.
with acute kidney injury (AKI) and poor collateral runoff.
Contraindications for CDT include previous stroke, ongoing
bleeding, a known bleeding condition, trauma, or recent
surgery.
23.10.2.4 Procedure
Selective cannulation of the renal vein should be done using
a 7F guide catheter. A 0.035″ guidewire and catheter combination should be used to cross the acute thrombus followed
by venography to show the extent and relation of the thrombus with the catheter tip.
Subsequently, mechanical thrombectomy should be done
using 6F AngioJet hemolytic thrombectomy catheter or
Helix Clot buster thrombectomy device. Residual thrombosis if any should be treated with thrombolysis.
For thrombolysis, recombinant tissue plasminogen (rtPA)
infusion should be given at a rate of between 0.5 and 1.0mg/
hr. using a multiple-side hole infusion catheter placed into
the renal vein. Simultaneously i.v. heparin may be given.
However, heparin should be given at a sub-therapeutic dose
when being used along with a thrombolytic agent. Daily
venography may be done to monitor response and thrombolysis should be discontinued after complete dissolution of
the clot [59].
CDT for acute renal vein thrombosis has been found to be
effective and appears to be efcacious in both native and
allograft renal veins. Kim etal. demonstrated a 30-day survival rate of 100% and improvements in renal function in all
patients treated with CDT for acute renal vein thrombosis
with no severe complications [59].
References
23.10.2.1 Clinical Presentation
It depends on the time of presentation and severity. Symptoms
include ank pain, hematuria, and non-specic symptoms
such as fever, nausea, and vomiting [58].
23.10.2.2 Management
Anticoagulation is the standard treatment in RVT.The rstline therapy for partial venous obstruction which does not
appear to affect renal function remains systemic anticoagulation only [57].
23.10.2.3 Role ofCatheter-Directed
Thrombectomy (CDT)
andThrombolysis
In patients with acute RVT, CDT with or without thrombolysis is useful to obtain prompt relief from symptoms secondary to acute RVT and improve deteriorating renal function
[57]. It is recommended in certain situations where quick
clot removal is essential owing to total renal vein obstruction
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Interventions oftheMesenteric Arterial
Circulation
NarenHemachandran andShivanandGamanagatti
24
Key Messages
1. The celiac trunk, superior mesenteric artery, and inferior
mesenteric artery form an intricate system of vessels supplying the gastrointestinal tract (from the lower esophagus to the proximal rectum), the liver, spleen, and
pancreas and exhibit signicant inter-territorial collateralization with a rich network of anastomotic vessels.
2. Revascularization procedures (mechanical thrombectomy in patients with embolic mesenteric ischemia,
thrombectomy with or without catheter-directed thrombolysis, and treatment of underlying stenosis with balloon angioplasty or stenting in patients with thrombotic
acute mesenteric ischemia) are best performed within the
rst 12hours for the best results in patients with acute
mesenteric ischemia.
3. Balloon angioplasty with stenting of one of the affected
mesenteric arteries is commonly done in patients with
chronic mesenteric ischemia.
4. Endovascular embolization is useful in the management
of gastrointestinal hemorrhage not amenable to treatment
by endoscopy or not responding to medical
management.
5. Coils and n-butyl cyanoacrylate glue are the most commonly used embolizing agents in the management of gastrointestinal hemorrhage.
6. Left gastric artery embolization is a relatively new and
safe technique for inducing modest weight loss in morbidly obese individuals.
N. Hemachandran
Diagnostic and Interventional Radiology, MGM Healthcare,
Chennai, Tamil Nadu, India
S. Gamanagatti (
Department of Radiodiagnosis and Interventional Radiology,
JPNA Trauma Centre, All India Institute of Medical Sciences,
Delhi, India
*)
24.1 Introduction
The three arteries of the mesenteric arterial circulation,
namely the celiac trunk, superior mesenteric artery (SMA),
and inferior mesenteric artery (IMA), form an intricate system of vessels supplying the gastrointestinal tract (from the
lower esophagus to the proximal rectum), the liver, spleen,
and pancreas. These arteries are known for exhibiting signicant inter-territorial collateralization with a rich network of
anastomotic vessels. These arteries can be affected by a wide
range of disorders in which endovascular management can
play a signicant role. Thrombolysis with recanalization
using balloon angioplasty or stent placement can be used in
the management of mesenteric arterial ischemia. Similarly, a
few causes of acute as well as chronic gastrointestinal bleeding can also be effectively managed by endovascular embolization using a variety of agents depending on the anatomy
and technical feasibility. Left gastric artery embolization is a
relatively new technique used in the management of obesity
with promising results.
24.2 Relevant Anatomy
The mesenteric vessels are the three anterior branches of the
abdominal aorta. These arteries have relatively constant levels of origin. The celiac trunk arises from the abdominal
aorta just below the diaphragm behind the median arcuate
ligament, commonly at the level of D12 or upper border of
L1 vertebra. It is relatively short and divides into three arteries: left gastric artery, common hepatic artery, and splenic
artery. The left gastric artery is the smallest branch and supplies the lower esophagus and proximal stomach along the
lesser curvature. The common hepatic artery divides into the
proper hepatic artery, which supplies the liver and the gall
bladder, and the gastroduodenal artery. The gastroduodenal
artery gives rise to supraduodenal artery, superior pancreaticoduodenal branches (supplies the duodenum, head of pancreas), and right gastroepiploic artery (supplies the greater
© 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_24
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294
N. Hemachandran and S. Gamanagatti
curvature of the stomach). The splenic artery predominantly
supplies the spleen. Its branches include short gastric
branches (supplying the fundus of stomach), left gastroepiploic artery (supplies the greater curvature of the stomach),
and pancreatic branches (supplying the pancreas).
SMA arises from the abdominal aorta below the celiac
of renal arteries, at the level of L1 vertebra. It is the major
artery of the mesenteric circulation and supplies blood to the
jejunum, ileum, ascending colon, and most of the transverse
colon. The major branches are the inferior pancreaticoduodenal artery, middle colic artery, right colic artery, ileocolic
artery, and multiple jejunal and ileal arteries (4–6 arteries).
The jejunal and ileal arteries typically rise along the right
side of the superior mesenteric artery while the colonic
branches arise from the left side. The jejunal and ileal
branches pass between the layers of the mesentery and form
multiple anastomotic arcades from which smaller numerous
straight arteries (vasa recta) arise and supply the bowel loops.
The jejunal branches have a relatively smaller number of
arterial arcades with longer vasa recta, while the ileal
branches have more arterial arcades with shorter vasa recta.
IMA, typically the smallest of the three mesenteric arteries, arises from the abdominal aorta below the origin of SMA
(typically ~6–7cm), at the level of L3 vertebra. It supplies
the splenic exure of the colon, descending colon, sigmoid
colon, and the proximal portion of the rectum. Its branches
include the left colic artery, rectosigmoid artery, and superior
rectal arteries. The left colic artery is usually the rst branch
of IMA and divides into ascending and descending branches.
The ascending branch supplies the upper half of the descending colon and the splenic exure region while the descending
branch supplies the lower part of the descending colon.
Unlike the arterial arcades of the small bowel loops, the marginal artery of Drummond forms a continuous arterial circle
along the mesenteric border of the colon with anastomosis
between the colonic branches of the superior and inferior
mesenteric arteries. The vasa recta supplying the colon is
from the marginal artery.
Numerous collateral pathways and anastomosis exist
between the three mesenteric arteries and help in preservation of arterial ow in case of occlusion of one of the arteries.
The primary collateral pathway between the celiac trunk and
SMA is the gastroduodenal artery forming the pancreaticoduodenal arcade and anastomosing with the inferior pancreaticoduodenal branch of the SMA. Other less commonly
seen collateral pathways include arc of Buhler (a direct communication between the celiac and SMA seen in 1–4% of
individuals), arc of Barkow (anastomosis between the left
gastroepiploic artery and superior mesenteric artery in the
omentum), and the dorsal pancreatic artery which can also
anastomose with the pancreaticoduodenal arcades. The mar-
ginal artery of Drummond and the arc of Riolan (a direct
anastomosis between the middle colic and left colic arteries)
form the primary collateral pathway between the SMA and
IMA.These collateral pathways, though present in normal
individuals, are hypertrophied and better visualized in
patients with chronic mesenteric ischemia. The watershed
areas that lie at the level of anastomosis between the arterial
territories include the splenic exure of the colon and the
rectosigmoid junction. These areas are commonly affected in
patients with ischemic colitis and nonocclusive mesenteric
ischemia [1].
24.3 Mesenteric Ischemia
24.3.1 Clinical Features
Mesenteric ischemia refers to a state where there is signicant reduction in the blood ow or circulation in the mesenteric vessels beyond the level required for routine tissue
metabolism in the bowel loops. It can occur due to a wide
range of causes leading to arterial or venous occlusion or
nonocclusive causes (like low ow states and bowel obstruction). The clinical presentation is usually nonspecic, leading to a delay in the diagnosis of mesenteric ischemia and
high mortality rate. Based on the clinical presentation it can
be classied into acute and chronic mesenteric ischemia.
Acute mesenteric ischemia usually presents with sudden
onset abdominal pain and acute abdomen while chronic mesenteric ischemia has a very indolent course with postprandial
abdominal pain and weight loss being the major presenting
complaints. Severe acute abdominal pain out of proportion to
physical examination ndings should be assumed to be
related to mesenteric ischemia and imaging to be done
accordingly at the earliest.
Acute mesenteric ischemia is due to abrupt cessation of
blood supply due to either occlusive or nonocclusive causes.
Acute arterial obstruction is secondary to thromboembolism
(40–50%) or thrombosis (~20–30% of cases) or dissection
(<5% of cases), resulting in complete occlusion of an artery.
The superior mesenteric artery is commonly affected in
thromboembolism due to its oblique angle of origin from the
aorta. Existing cardiac disorders like arrhythmia, valvular
pathology, or recent myocardial infarction are commonly
associated factors in patients with acute embolic mesenteric
ischemia. Nonocclusive eccentric ischemia is due to insufcient blood ow through patent arteries (secondary to hypovolemic shock/cardiac failure/vasoconstrictor drugs). This
leads to reduced ow predominantly affecting the watershed
areas.
Chronic mesenteric ischemia is usually seen in the elderly
population due to advanced atherosclerotic changes. The
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