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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]

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Interventions ofRenal Vessels
PriyaJagia, ReshamSingh, andSravanNagulkonda
23
Key Messages
1. Percutaneous renal vascular interventions are minimally
invasive techniques, which offer faster recovery at low
complication rates.
2. Different renal arterial interventions include PTRA and
stenting, embolization, and renal denervation
procedures.
3. Indications for renal arterial interventions include arterial pathologies like renal artery stenosis, renal AVM,
and renal aneurysms.
4. In carefully selected patients of RAS, PTRA offers
immediate improvement in blood ow and long-term
benets for blood pressure control and kidney function.
5. Endovascular intervention has a high technical success
rate in excluding renal artery aneurysms by plug, or
stent-assisted coiling.
6. In renal AVM, endovascular embolization with glue is
highly effective for nidus exclusion to alleviate
symptoms.
7. Selective renal artery embolization in angiomyolipoma
is effective for reducing tumor volume and preventing
future risk of hemorrhagic complications.
8. Renal vein interventions include stenting for nutcracker
syndrome and catheter-directed thrombectomy (CDT)
with or without thrombolysis for renal vein thrombosis.
9. In nutcracker syndrome, endovascular management with
renal vein stenting offer good results comparable to
surgery.
10. CDT in acute renal vein thrombosis is reserved for cases
with deteriorating renal function tests.
P. Jagia (*) · R. Singh · S. Nagulkonda
Department of Cardiovascular Radiology and Endovascular
Interventions, All India Institute of Medical Sciences, Delhi, India
23.1 Introduction
The role of interventional radiology in disease management is
expanding rapidly and is already established in the management
of different renovascular diseases. Renal interventions can be
broadly classied into vascular and non-vascular subtypes. The
array of endovascular procedures performed by interventional
radiologists includes different techniques like renal artery stenting, percutaneous transluminal renal angioplasty (PTRA), renal
artery embolization, thrombolysis, and thrombectomy, and
some new emerging modalities like renal denervation for resistant hypertension. This chapter includes a brief discussion of
different renal vascular interventions with an emphasis on their
indications, procedural details, and complications.
23.2 Anatomy
23.2.1 Arterial Anatomy
In normal individuals, there is a single main renal artery
(RA) on each side which originates from the abdominal aorta
(AA) at L1-L2 lumbar vertebral level. The right renal artery
(RRA) arises from the anterolateral aspect of AA, having a
long downward course, whereas the left renal artery (LRA)
originates from the lateral aspect and has a relatively short
and horizontal course.
Main RA divides into a larger anterior division (~75%
blood) and a smaller posterior division (~25% blood) before
entering the renal hilum and further divides into segmental
and lobar arteries [1]. Single renal artery is seen in ~65% of
the population, and multiple renal arteries are seen in 35% of
individuals which usually arise from the aorta or iliac arteries [2]. These vessels can reach the renal parenchyma either
by the renal hilum (accessory renal artery) or through extra
hilar penetration of the renal capsule (aberrant renal artery).
Accessory renal arteries are very common and found in
~30% of individuals unilaterally and in 10% of individuals
bilaterally [2].
© 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_23
279

280
P. Jagia et al.
23.2.2 Venous Anatomy
Each kidney drains the deoxygenated blood into the inferior
vena cava (IVC) via the renal vein (RV). Renal veins are situated anterior to the ipsilateral renal artery. Left RV is longer
and receives tributaries such as the left adrenal vein, gonadal
vein, and phrenic vein. Right RV, on the contrary, is shorter
and receives no tributary veins [2].
23.3 Arterial Interventions
Different renal arterial interventions include procedures that
augment the renal blood ow like percutaneous renal angioplasty and stenting in renal artery stenosis (RAS) or procedures that occlude/embolize the renal artery with various
embolization agents. The indication of renal artery embolization includes the presence of an aneurysm, AV shunts, neoplasms, and traumatic injury to the kidney.
23.3.1 Renovascular Hypertension
Renovascular hypertension (RVH) is a potentially treatable
cause of secondary hypertension. It refers to clinical sequelae
(i.e., hypertension and nephropathy) of hemodynamically
signicant renal artery stenosis (RAS) owing to atherosclerotic and non-atherosclerotic causes. The exact prevalence of
RAS is unknown in normal population. RVH is known to
occur in 1–5% of individuals those who have hypertension
[3].
23.3.2 Atherosclerotic Renal Artery Stenosis
Atherosclerosis is the most common cause of RAS [4] and is
reported to account for ~90% of the renovascular cause of
RAS [5]. Age, diabetes mellitus (DM), peripheral arterial
disease (PAD), coronary artery disease (CAD), hypertension
(HTN), and dyslipidemia all raise the likelihood of atherosclerotic RAS (ARAS) [6]. According to epidemiological
data, atherosclerotic RAS is a relatively common clinical
nding, affecting more than 6.8% of patients over the age of
65years [7]. The treatment of ARAS remains somewhat contentious, owing to the apparent inconsistency in outcomes
between observational cohorts indicating a treatment advantage and randomized trials failing to discover such differences in treatment outcome [8].
Since ARAS is typically caused by thick aorta-ostial
plaques, balloon angioplasty alone is generally ineffectual
due to the accompanying recoil, making renal artery stenting
the preferred therapy [9]. Stenting has higher primary and
secondary patency rates than angioplasty alone [10] and is
associated with signicantly lower restenosis rates and a signicant drop in blood pressure [11].
23.3.3 Non-atherosclerotic RAS
Non-atherosclerotic cause of RAS accounts for a wide spectrum of etiologies. This includes Takayasu arteritis (most
common in India) and bromuscular dysplasia (FMD) (most
common in the West), vasculitis, neurobromatosis, trauma,
congenital bands, post-radiative therapies, tumor dissection,
and compression [5]. The two most common causes of nonatherosclerotic RAS, viz. Takayasu arteritis and FMD, are
discussed in details here.
23.3.4 Takayasu Arteritis (TA)
Takayasu arteritis is a chronic, nonspecic, inammatory
vasculitis that primarily affects young females [12], and
involves the aorta and its major branches. The frequency of
renal artery involvement and subsequent hypertension in TA
is reported to range from 34% to 85% [13]. PTRA (Fig.23.1)
is a well-established endovascular intervention for hemodynamically signicant non-atherosclerotic RAS [14]. Before
performing PTRA, adequate anti-inammatory treatment
and disease activity control are crucial since active disease is
linked to an increased risk of procedure-related complications and a higher risk of restenosis if revascularization is
performed in an active disease state [15]. Balloon angioplasty has demonstrated greater long-term patency and an
equivalent clinical outcome compared with the surgery and
stenting in hemodynamically signicant RAS caused by
Takayasu’s arteritis [16]. It has been found that the results of
PTRA are heavily impacted by the lesions length and residual stenosis rate. Restenosis rates reported in literature are up
to 9% by angioplasty and 62.5% in the setting of a stent [16].
Hence, stenting is avoided in TA unless there is a vessel
recoil with signicant residual stenosis or a ow-limiting
dissection ap following balloon dilation.
23.3.5 Fibromuscular Dysplasia (FMD)
FMD is a rare non-atherosclerotic and non-inammatory
vascular condition that affects the renal, carotid, and vertebral arteries in young girls and is most commonly associated

23 Interventions ofRenal Vessels
281
Fig. 23.1 An 18-year-old
female, who was a known
case of non-specic
aortoarteritis presented with
uncontrolled hypertension. A
ush angiogram of the
abdominal aorta revealed
complete occlusion of the
right renal artery and
signicant stenosis (70–80%)
in the most proximal segment
of the left main renal artery
(*) with post-stenotic
dilatation (a). 0.014″ guide
wire was placed across the
stenosis (b) followed by
balloon angioplasty with
3.5×15mm and 5×20mm
balloons (Sterling, BS) (c).
Post-angioplasty angiogram
showed mild residual stenosis
(~30%) with a good left
nephrogram (d). Note:
suboptimal angioplasty was
done in view of active disease
a
c
b
d
with hypertension or cerebrovascular episodes [17]. In FMD,
the renal arteries are the most commonly affected vessel
(60–70% of all FMD cases), with bilateral renal involvement
found in 35% of cases [18]. The most common symptom of
renal artery FMD is hypertension, which varies in severity
and onset [19]. The majority of FMD patients (66%) have a
characteristic angiographic appearance of a “string of beads,”
typically in the distal 2/3 of the renal artery, although a
minority may have a more localized stenosis (“atypical
FMD”).
PTRA is the most commonly used revascularization technique in FMD (Fig.23.2), and stenting should be considered
if ow-limiting dissection occurs or balloon angioplasty fails
[20]. PTRA has a higher rate of technical success, signicantly greater BP rate reductions [21], and less complications
as compared to surgical method of revascularization. This
makes it the preferred method of treatment for RAS secondary to FMD [22].

282
P. Jagia et al.
Fig. 23.2 A 33-year-old
female presented with
uncontrolled hypertension and
Doppler nding of signicant
renal artery stenosis on the
left side. Abdominal
angiogram showed distal tight
stenosis of LRA with
alternative stenosis and
dilation (black asterisk) s/o
bromuscular dysplasia (a
and b). The lower pole
segmental artery showed
40–50% stenosis (blue
asterisk). RRA shows no
signicant disease.
Angioplasty was done using a
4×20 balloon (Sterling,
Bostin Scientic) at a
maximum of 6atm pressure
(c). Mild residual stenosis
(<20%) is seen post-balloon
dilation (d)
a
c
b
d
23.4 Imaging inRAS
Renal Doppler sonography is the rst-line imaging modality
done in patients with suspected RAS.If Doppler ndings are
equivocal or suggestive of RAS, subsequently CTA/MRI
should be done to conrm RAS and plan revascularization.
Non-contrast MR angiography may be useful for evaluating
RAs in patients with renal dysfunction. In case the Doppler
is negative and clinical suspicion is high, catheter angiography should be considered for the diagnosis of RAS which is
the gold standard investigation to diagnose RAS, especially
involving peripheral renal arteries.
23.5 Revascularization inRAS
The endovascular method of revascularization is preferred
over surgery in RAS (Fig.23.3). It is signicantly less costly,
minimally invasive, has lower morbidity, may frequently be
done without an inpatient stay, and has a shorter recovery
period. Consequently, PTRA is the procedure of choice for
RAS in an appropriately selected cohort of patients meeting
the criteria for an endovascular method of revascularization
in hemodynamically signicant RAS [23]. Surgical method
of revascularization is indicated if the endovascular intervention fails or if there is early primary branching of the main
renal artery or if simultaneous reconstruction of the perirenal
aorta is necessary. As discussed earlier, in the case of ostialatherosclerotic RAS, primary renal artery stenting is indicated (Class I Recommendation, LOE-B). If the lesion is
non-ostial—either atherosclerotic or non-atherosclerotic,
balloon angioplasty with bailout stenting is indicated (Class
I Recommendation, LOE-B) [24].
23.5.1 Indications andGuidelines
forEndovascular Revascularization
inRAS
Percutaneous revascularization is indicated in patients with
hemodynamically signicant RAS, unexplained congestive
heart failure (CHF), or abrupt unexplained pulmonary

cd
23 Interventions ofRenal Vessels
283
Fig. 23.3 Case of a
65-year-old with uncontrolled
hypertension due to
atherosclerotic left renal
artery stenosis. (a) Selective
left renal artery angiogram
showing signicant
ostioproximal stenosis; (b)
balloon angioplasty using
4×25mm monorail balloon
(Sterling, Boston Scientic),
across the stenotic segment;
(c) check angiogram showing
no signicant residual
stenosis; (d) angiogram post
stent (balloon mounted stent
5×15mm) deployment
a
b
edema (Class I Recommendation, LOE-B) and should be
considered in patients with hemodynamically signicant
23.5.2 Percutaneous Transluminal
Angioplasty (PTRA) andStenting
RAS and accelerated hypertension, resistant hypertension,
unexplained unilateral small kidney, medication-intolerant
hypertension, or unstable angina (Class IIa, Evidence level
B). The endovascular method of revascularization should
be considered in patients with hemodynamically signicant
bilateral RAS or RAS of single functioning kidney and progressive chronic kidney disease (CKD) (Class IIa, Evidence
level B).
Percutaneous revascularization may be considered in
symptomatic B/L or single-functioning kidneys with hemodynamically signicant RAS and in patients with u/l RAS
and CKD (Class IIb, Evidence level C) [24].
23.5.2.1 Preprocedural Evaluation
Thorough preprocedural workup should be done before taking the patient for endovascular intervention, which includes
biochemical evaluation (Hb, platelet count, renal function
test (RFT), and coagulation proles), and CTA/MRA should
be reviewed for evaluation of access vessels (caliber and
course) and renal artery for number, origin, caliber, stenosis
site, severity, and length.
Usual hardware needed for PTRA includes puncture needle, arterial access sheath, guidewires (0.014″ balanced middle weight (BMW) wire, 0.035″ hydrophilic wire with J tip,

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catheters (Pigtail, Cobra, Renal guiding catheter), balloons
(0.014″ monorail balloons), balloon-expandable stents, and
drugs (heparin and nitroglycerin).
23.5.2.2 Preprocedural Instructions
The patient is advised to start aspirin and clopidogrel 75mg
OD for 5days prior to the procedure. Antihypertensive medication can be continued on the day of the procedure. If the
patient is diabetic and is on oral hypoglycemics (OHAs), he
is advised not to take the morning dose of the OHAs.
23.5.2.3 Procedure
Almost all renal interventions can be performed through
femoral access. Ipsilateral femoral arterial access allows
the guidewire-catheter combination to rest against the contralateral wall of the neighboring aorta. This makes selective cannulation of the renal artery, easier advancement of
balloon catheters, and stent delivery devices. Brachial
access can be used to achieve selective cannulation, particularly when there is acute angulation of the ostioproximal
renal artery. Left brachial access is preferred over right brachial as this avoids crossing across the undersurface of the
arch.
23.5.2.4 Angiography
A ush angiogram of the aorta should be done by placing the
pigtail catheter’s side holes at L1/L2 vertebral disc level.
Ostia of both renal arteries can be proled by a single run by
placing the imaging tube in shallow LAO (~15-degrees) in
most cases. In the case of bilateral RAS, angioplasty on the
side with a larger kidney should be attempted rst. Selective
catheterization of the renal arteries should be done with a
0.035″ wire. Once the ostium of the renal artery is hooked, a
0.035″ guidewire should be exchanged for a 0.014″ BMW
wire. Subsequently, the diagnostic catheter should be
replaced with a guide catheter, the tip of which should be
positioned near the ostium of the renal artery. Selective angiography of the renal artery is done in I/L anterior oblique
view to prole the entire renal artery better.
If the severity of the stenosis is not evaluated previously,
the length and severity of the stenosis are assessed from the
angiogram, and stenosis is considered signicant if the luminal diameter is reduced by 70% (~90% CSA reduction).
However, when diameter reduction is between 50 and 75%,
the pressure gradient is assessed across the stenosis to determine hemodynamic signicance. The pressure difference
across the lesion equal to 10% peak systolic pressure and an
absolute gradient of 10–20mm of Hg is considered hemodynamically signicant [25].
23.5.2.5 Balloon Angioplasty
The tip of the 0.014″ BMW guidewire is advanced across the
lesion and parked preferentially in the inferior segmental
artery. This provides greater support for the balloon catheter
during angioplasty. Pre-dilatation with a 3-mm monorail balloon may be done in case of tight stenosis. A balloon catheter
with a diameter equivalent to the size of the normal artery
adjacent to the lesion should be used for primary balloon
angioplasty. The length of the balloon should be selected
such that it covers the entire length of the stenosis from normal to normal segment. The 0.014″ compatible monorail
balloon catheters are advanced through the guide catheters.
Once balloon markers are placed across the lesion, the balloon should be inated fully or until it reaches nominal pressure for 1min. The balloon should be deated if the patient
experiences severe pain. After deation, a check angiogram
should be obtained to look for any residual stenosis. In case,
there is residual stenosis, angioplasty should be done using a
balloon of a diameter 1mm smaller than the previous one. If
there is still persistent waist or recoil, stenting should be
considered.
23.5.2.6 Cutting Balloon Angioplasty
In conventional PTRA, even a suitably sized balloon may not
be enough to overcome the degree of stenosis, particularly in
non-atherosclerotic RAS with severe stenosis [26]. While a
typical balloon rips the stenotic artery wall, a cutting balloon
features 3–4 microsurgical blades positioned longitudinally
on the outer balloon surface, causing sharp longitudinal incisions which are directed radially into the media and lead to
dilation of refractory stenosis. As a result, a cutting balloon
can cause a controlled and safe dilatation of the vessel wall.
The use of a cutting balloon to overcome tight stenosis that is
recalcitrant to standard angioplasty is widely established in
non-atherosclerotic RAS, particularly in bromuscular
dysplasia.
23.5.2.7 Stenting
Balloon-mounted stents are preferred over self-expandable
stents for ostial atherosclerotic lesions due to their greater
radial force and precise deployment. The stent should be
oversized by 10% or 1mm above the diameter of the reference normal artery. The length of the stent should be selected
such that it covers the length of the lesion and ostium of the
renal artery. The stent’s proximal end must protrude out into
the aorta by at least 2mm. Instant balloon angioplasty should
be done after deployment of the stent if a check angiogram
shows incomplete expansion.
Despite the result of CORAL and ASTRAL trials showing no signicant difference between medical management
and renal artery stenting in terms of BP reduction and renal
and cardiovascular outcomes, the persistent benet of renal
artery stenting in BP reduction has been found on long-term
follow-up in a properly chosen cohort of patient with signicant stenosis >70% and uncontrolled hypertension which is
not responding to multiple drugs [27].
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