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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]

368
A. Gupta et al.
29.3.1.2 Technique
Diagnostic angiography is performed as the rst step before
endovascular embolization. It is required to assess ow characteristics and to identify arterial feeders, draining veins and
nidus. Distinct AVM nidal architectures have been described
on angiography [12, 13] (Table29.3)—Type I AVMs have
three or less arterial feeders with single draining vein. Type
II AVMs have multiple arterial feeders with a single draining
vein. According to the morphology of the draining vein, type
II is subclassied into types IIa, IIb and IIc. Type III AVMs
have multiple arterial inows and draining veins which are
either non-dilated (type IIIa) or dilated (type IIIb). Type III
AVMs are the most common variety; however, type I and
Table 29.3 Yakes angiographic classication of AVMs and treatment strategy
Angiographic
type of AVM Description Endovascular treatment strategy
Type I Three or less feeding arteries and a single draining vein Trans-arterial embolization of stula with coils or plugs
Type II Multiple arterioles shunt into a single draining vein Coil packing of venous segment followed by ethanol injection
Type IIa Multiple arterioles shunt to a focal segment of draining
vein
Type IIb Multiple arterioles shunt into a venous sac with
multiple draining veins
Type IIc Multiple arterioles shunt along a long segment of
draining vein
Type III Multiple arterial inows and draining veins Trans-arterial super-selective catheterization of feeding arteries
Type IIIa Multiple arterioles shunt to multiple draining veins via
multiple ne stulae
Type IIIb Multiple arterioles shunt to multiple draining veins via
multiple enlarged stulae
type II AVMs respond better to embolization. The embolization technique depends on the type of AVM architecture and
anatomical location [14].
Flow reduction is of paramount importance to ensure sufcient contact time of the sclerosant with the nidus. Manual/
tourniquet compression or blood pressure cuff ination
should be used to compress draining vein wherever possible.
Temporary balloon occlusion or coil embolization of the
inow or outow can also be used.
In type I AVMs, the goal is blockage of the direct stula
between artery and vein using coils, vascular plugs or EVOH
via trans-arterial route (Fig.29.7). For type II AVMs, blood
ow in AVM is rst limited either by manual compression or
Trans-venous or direct puncture approach
Direct puncture of the venous sac is preferable
Trans-venous or direct puncture approach
followed by ethanol/NBCA glue/EVOH injection
Dilute ethanol (50–60%) or NBCA glue/EVOH is preferred
NBCA glue/EVOH embolization may be used rst for ow
reduction; direct puncturing of dilated stulae may also be done
Fig. 29.7 Type I AVM. (a)
Angiogram shows AVM
(black arrow) with a single
feeding artery from supercial
temporal artery (dotted white
arrow) and a single draining
vein (white arrow). There is
direct arteriovenous stula
(asterisk). (b) The AVM
shows the absence of contrast
opacication (arrow)
following trans-arterial
embolization
with onyx. c—catheter
ab
*
c
c

ab
29 IR Management ofVascular Malformations
Fig. 29.8 Type II AVM. (a)
Angiogram shows AVM
(black arrow) in the forearm
with multiple feeding
arterioles (white arrows) and
a single dominant outow
vein (dotted arrows). c—
catheter. (b) Digital
subtraction angiography
(DSA) image showing
multiple coils (black arrows)
deployed in the venous sac of
AVM by direct puncture
(dotted arrows)
369
c
coils in the venous segment commonly by transvenous or
direct puncture approach followed by high-concentration
ethanol (80–100%) injection transarterially (Fig.29.8). For
type III AVMs, a trans-arterial approach is preferred. For
type IIIa lesions, diluted ethanol (50–60%) is used especially
for supercial lesions to prevent skin necrosis. For type IIIb
AVMs, direct puncture of the dilated stulae may also be
done, but care has to be taken to avoid any extravascular
extension of glue (Fig.29.9). A combination approach can
also be taken.
Ethanol is the most widely used liquid sclerosing agent
for AVM treatment because of its high efcacy owing to
endothelial damage, protein denaturation and rapid thrombosis [15]. It is highly cost-effective as well but carries signicant risk of complications including signicant local-site
pain and oedema after injection. Thus, general anaesthesia is
usually required during the procedure. Skin necrosis is
another potential complication, and thus, ethanol should be
avoided in AVMs with signicant cutaneous involvement.
Pulmonary hypertension is a dreaded complication which
occurs if high dose of ethanol is used. The maximum volume
of ethanol that can be used is 1 mL/kg body weight, and
while planning for high volume of ethanol injection
(>0.5mL/kg body weight), a pulmonary artery Swan-Ganz
line and arterial line monitoring is recommended. Use of
nitroglycerin infusion is recommended if mean pulmonary
artery pressure rises above 25mm Hg. Without pulmonary
artery monitoring, max volumes of 15–20ml alcohol can be
used (not more than 5ml in a single arterial branch).
Other embolizing agents have also been used for the
treatment of AVMs. NBCA glue (mixed with ethiodized
oil) is preferred in AVMs with large draining veins or in the
setting of coagulopathy, as it quickly polymerizes into a
cast when exposed to anions. Ethylene vinyl alcohol copolymer (EVOH) is another cast-forming agent that has been
used especially in central nervous system AVMs. EVOH
injection can be better controlled by the operator because
of its longer casting time as compared to glue. However, the
clinical results with cast-forming agents are not long-lasting. Polyvinyl alcohol (PVA) particles carry a high risk of
non- target embolization in cases of AVMs and are thus
avoided.
Overall cure rate of peripheral AVMs with endovascular
therapy has been reported to be 40% and clinical success rate
(cure or marked symptomatic improvement) of 60% [14]. In
larger lesions, some practitioners advocate treating individual compartments serially, eventually resulting in complete
treatment over time. Post-procedure follow-up of the patient
can be done after 4weeks, before planning a re-embolization
if the desired symptomatic relief is not achieved. Time interval between sessions is generally 3–6months, depending on
the patient’s symptoms and extent of lesion.

370
ab
A. Gupta et al.
Fig. 29.9 Type III AVM. (a)
Angiogram shows AVM in the
arm with multiple feeding
arterioles and multiple
draining veins (arrows). (b)
The AVM shows the absence
of contrast opacication
(arrow) following transarterial embolization with
glue. c—catheter
c
c
29.3.1.3 Complications
The most common minor complications (20% cases)
reported with ethanol embolotherapy are focal skin necrosis,
bullae formation and transient nerve injuries. Major complications, occurring in around 3% cases, include signicant
skin necrosis requiring grafts, tissue necrosis requiring
amputation, permanent nerve injury, pulmonary hypertension, acute pancreatitis and acute renal failure [14]. Nontarget embolization and occlusion of the parent arteries are
other potential complications.
cent subcutaneous phlebectasia. Their diagnosis is often
delayed due to overlapping clinical and imaging features
with the more common venous malformation. On MRI, three
morphological types have been described: focal mass-like
(limited to one anatomical region with >75% perceptible
margins), focal inltrative (ill-dened margins) and diffuse
inltrative (involving more than one compartment with
imperceptible margins) [1].
In the limited available literature regarding the management of FAVA, cryoablation has been described as an effective
modality [16]. It is more benecial in cases with focal lesions
and before contracture sets in. In our experience, radiofre-
29.4 Fibro-Adipose Vascular Anomaly (FAVA)
quency ablation has also reaped good results for palliation of
pain. For diffuse inltrative lesions with contractures not
responding to conservative measures, surgical excision of the
FAVA is a recently described distinct vascular anomaly
categorized under ‘provisionally unclassied vascular anomalies’ in ISSVA 2018 classication. It classically occurs in
young or adolescent patients and presents with swelling,
pain, functional impairment and contracture involving the
calf and forearm muscles. Imaging usually demonstrates a
solid-looking enhancing mass with interspersed dilated
venous channels, brofatty inltration and associated adja-
lesion is a viable option along with nerve decompression, tendon lengthening or osteotomy as required for deformity correction. Systemic treatment with sirolimus, a mediator of
phosphoinositol 3-kinase signalling pathway, has also been
described in the management of diffuse FAVA.No signicant
role for sclerotherapy has been shown for the management of
FAVA, and lack of response to sclerotherapy in a suspected
venous malformation may suggest a diagnosis of FAVA [16].

29 IR Management ofVascular Malformations
371
29.5 Conclusion
Vascular malformations are complex diseases requiring multidisciplinary management. They are classied based on their
ow characteristics depending on the presence of an arterial
component. Interventional radiology plays a major role in the
management of such patients since many of them are not
amenable to a denitive surgery. For low-ow vascular malformations (venous and lymphatic malformations), percutaneous imaging-guided sclerosant injection into cystic spaces
is the preferred management. For high-ow arteriovenous
malformations, endovascular therapy including embolization
for ow occlusion and glue/ethanol injection is the preferred
treatment, approach based on the type of AVM architecture
on angiography. Recently described solid- appearing lesions
like bro-adipose vascular anomaly can be treated with ablation for pain relief. The role of radiologist is pivotal in both
the diagnosis and management of vascular anomalies.
References
1. Das A, Goyal A, Sangwan A, Kumar A, Bhalla AS,
Kandasamy D, et al. Vascular anomalies: diagnostic features and step-wise approach. Acta Radiol Stockh Swed 1987.
2022;18:2841851221085379.
2. Burrows PE.Endovascular treatment of slow-ow vascular malformations. Tech Vasc Interv Radiol. 2013;16(1):12–21.
3. Mazoyer E, Enjolras O, Laurian C, Houdart E, Drouet
L. Coagulation abnormalities associated with extensive venous
malformations of the limbs: differentiation from Kasabach-Merritt
syndrome. Clin Lab Haematol. 2002;24(4):243–51.
4. Burrows PE, Mason KP.Percutaneous treatment of low ow vascular malformations. J Vasc Interv Radiol JVIR. 2004;15(5):431–45.
5. de Lorimier AA.Sclerotherapy for venous malformations. J Pediatr
Surg. 1995;30(2):188–93. discussion 194
6. Bagga B, Goyal A, Das A, Bhalla AS, Kandasamy D, Singhal M,
etal. Clinicoradiologic predictors of sclerotherapy response in lowow vascular malformations. J Vasc Surg Venous Lymphat Disord.
2021;9(1):209–219.e2.
7. McCafferty I. Management of low-ow vascular malformations:
clinical presentation, classication, patient selection, imaging and
treatment. Cardiovasc Intervent Radiol. 2015;38(5):1082–104.
8. Suh JS, Shin KH, Na JB, Won JY, Hahn SB.Venous malformations:
sclerotherapy with a mixture of ethanol and lipiodol. Cardiovasc
Intervent Radiol. 1997;20(4):268–73.
9. Cabrera J, Cabrera J, Garcia-Olmedo MA. Sclerosants in microfoam. A new approach in angiology. Int Angiol J Int Union Angiol.
2001;20(4):322–9.
10. Yang Y, Sun M, Ma Q, Cheng X, Ao J, Tian L, etal. Bleomycin
A5 sclerotherapy for cervicofacial lymphatic malformations. J Vasc
Surg. 2011;53(1):150–5.
11. Das A, Goyal A, Sangwan A, Bhalla AS, Kumar A, Kandasamy
D, et al. Vascular anomalies: nomenclature, classication,
and imaging algorithms. Acta Radiol Stockh Swed 1987.
2022;12:2841851221082241.
12. Cho SK, Do YS, Shin SW, Kim DI, Kim YW, Park KB, et al.
Arteriovenous malformations of the body and extremities: analysis of therapeutic outcomes and approaches according to a modied angiographic classication. J Endovasc Ther Off J Int Soc
Endovasc Spec. 2006;13(4):527–38.
13. Ko SE, Do YS, Park KB, Kim DI, Heo SH, Bae SH, et al.
Subclassication and treatment results of ethanol embolotherapy
of type II arteriovenous malformations of the extremity and body. J
Vasc Interv Radiol JVIR. 2019;30(9):1443–51.
14. Kim R, Do YS, Park KB. How to treat peripheral arteriovenous
malformations. Korean J Radiol. 2021;22(4):568–76.
15. Yakes WF, Rossi P, Odink H.How I do it. Arteriovenous malformation management. Cardiovasc Intervent Radiol. 1996;19(2):65–71.
16. Lipede C, Nikkhah D, Ashton R, Murphy G, Barnacle AM, Patel
PA, et al. Management of Fibro-adipose Vascular Anomalies
(FAVA) in paediatric practice. JPRAS Open. 2021;29:71–81.

Vascular Interventions inTrauma
RichaYadav, ShivanandGamanagatti, andAtinKumar
30
Key Messages
1. Hemodynamically stable patients with high-grade liver
and splenic injuries are candidates for nonoperative
management.
2. Splenic artery and hepatic artery embolization can be performed with curative intent, i.e., to treat active bleeding,
or as a preventive measure in high-grade injury with no
active bleeding to reduce the risk of secondary bleeding.
3. Proximal splenic artery embolization is done in case of
extensive injury to the spleen, while distal embolization is
done in case of focal vascular injury.
4. Vascular injuries of the extremities are managed by
embolization if the injured artery can be sacriced and by
stent graft placement if the injury is in a major artery that
cannot be sacriced.
5. Pelvic vascular injury is associated with high risk of mortality and endovascular embolization is the primary
modality for treatment.
6. Nonselective embolization of bilateral internal iliac arteries can be done using gelfoam in hemodynamically
unstable patients to achieve rapid hemostasis.
7. Heparin and heparin saline may be withheld during the
procedure in the acute setting of trauma.
30.1 Introduction
Interventional radiology has emerged as an integral adjunct to
nonoperative management of traumatic solid organ and vascular injuries, which can mitigate life-threatening hemorrhage
and the need for surgical interventions1. The primary aim is to
secure the hemostasis on time either by operative or nonoperative management, depending on the hemodynamic status of
the patient; hence patient selection and timing of the proce-
R. Yadav (*) · S. Gamanagatti · A. Kumar
Department of Radiodiagnosis and Interventional Radiology,
JPNA Trauma Centre, All India Institute of Medical Sciences,
Delhi, India
dure are crucial factors in determining the success of the interventional procedure. The imaging protocols and management
decisions strictly adhere to American Association for the
Surgery of Trauma (AAST) guidelines for acute trauma.
Computed tomography (CT), coupled with an enhanced
understanding of patient selection criteria for embolization
procedures, holds tremendous promise for further rening
the pivotal role of interventional radiologists in trauma care.
In this chapter, we tried to emphasize the clinical indication,
techniques, and complications of vascular intervention in
traumatic solid organ injuries like splenic, liver, and arterial
injury of the extremity and head and neck region.
30.2 Splenic Injuries
Though the spleen is the most common organ to be injured
after blunt trauma, the management strategy depends upon
the hemodynamic status and imaging ndings. In the last few
decades, the management paradigm has considerably shifted
from operative (OM) to nonoperative management (NOM).
NOM is dened as close observation, monitoring, or angioembolization to preserve the immune functions of the spleen
to prevent overwhelming infection from encapsulating
organisms [1]. A successful treatment relies on the ability to
quickly assess the hemodynamic stability and categorize the
injury severity. Angioembolization is an important addition
to NOM and is a safe, effective, and rational way to improve
the success rate of NOM and can be used as curative as well
as preventive purposes. It is said curative when done to treat
active bleeding and preventive when done in high-grade
injury with no active bleeding where the aim is to reduce the
secondary bleeding and to secure the hemostasis.
According to Advanced Trauma Life Support (ATLS)
guidelines for trauma, a hemodynamically unstable patient is
a surgical candidate while hemodynamic stable patients and
transient responders are ideal candidates for splenic artery
embolization (SAE) [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_30
373

374
R. Yadav et al.
30.2.1 Indications ofSAE
According to ATLS guidelines, the evaluation starts with a
computed tomography (CT) scan in a stable patient, which
helps to shortlist the candidates for embolization, reveals
additional injuries, and serves as baseline mapping [3]. The
ideal candidates for angioembolization are:
1. Moderate to severe splenic injury (AAST grade IV-V)
with hemoperitoneum.
2. Vascular injury (active contrast extravasation, pseudoaneurysm, AV stula formation).
30.2.2 Technique
Includes patient preparation, procedure, approaches, the
embolic agent used, and post-procedural care. The planning
is based on ndings on CECT ndings.
30.2.3 Patient Preparation
Includes ongoing resuscitation, securing the airway, breathing, and circulation. Ensuring adequate IV access with a
large bore IV line. The basic laboratory parameters are not
prerequisites for trauma patients where the main aim is to
achieve a rapid hemostasis [4].
30.2.4 Procedure
The arterial access is obtained by puncturing the common
femoral artery under uoroscopic or USG guidance with the
placement of an appropriate-sized vascular sheath. USG
guidance when available is preferable, especially in cases
with poor or nonpalpable common femoral pulse. Heparin
and heparin saline may be withheld in the setting of trauma.
A selective celiac artery angiogram is performed using appropriately shaped diagnostic catheters like RC (Rosch) or SIM
(Simmons) reverse curve. Superselective catheterization of
the splenic artery is usually done with a coaxial microcatheter. Depending upon the angiographic injury pattern, proximal, distal, or combined embolization is done using various
embolizing agents [4]. Proximal embolization is done in the
main splenic artery segment between dorsal pancreatic artery
and pancreatic artery magna with preservation of collateral
vascularity, with the aim of reduction in perfusion pressure in
cases with diffuse high-grade injury (Fig.30.1) [5]. Distal
embolization is performed close to the site of focal vascular
Fig. 30.1 Splenic artery
embolization (proximal
technique) in a young patient
following blunt trauma
Axial (a) and coronal reformatted
(b) contrast- enhanced CT images
display a grade IV splenic injury
(AAST grade) and intraparenchymal extravasation. The selective
celiac angiogram (c) reveals
multifocal areas of active
extravasation with abnormal
parenchymal blush. Postembolization images (d)
demonstrate coil occlusion of the
main splenic artery between the
dorsal pancreatic and pancreatic
magna branch with no further
contrast extravasation
a
c
b
d

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30 Vascular Interventions inTrauma
375
abnormalities like pseudoaneurysm, arteriovenous stula,
and focal extravasation (Fig.30.2). A combination of both
proximal and distal embolization can be done, however is not
preferable due to higher complication rates [6]. In the context
of splenic artery embolization (SAE) for splenic injury, the
Fig. 30.2 Splenic artery
embolization (distal
technique) in a young patient
following a road trafc
accident
Axial (a) and coronal reformatted
(b) contrast- enhanced CT images
demonstrate a grade IV splenic
injury and an intraparenchymal
pseudoaneurysm at the upper
pole (arrow). The selective celiac
angiogram (c) reveals a focal
well- dened contrast blob at the
upper pole, suggesting a
pseudoaneurysm. The splenic
artery angiogram after embolization (d) shows complete coil
occlusion of the upper pole
segmental splenic artery, as close
as possible to the site of arterial
injury, with no residual pseudoaneurysm and preserved perfusion
in the mid-lower pole
a
decision to perform proximal or distal coil embolization or
combined depends on the specic characteristics of the injury,
the location of the bleeding, and the anatomy of the splenic
artery. Both proximal and distal coil embolization techniques
have their advantages and considerations (Table30.1).
b
Table 30.1 The merits and demerits of proximal versus distal splenic artery angioembolization (SAE)
Proximal SAE (P) Distal SPE (D)
Aim of procedure Decreases the overall perfusion pressure in the spleen with
Site of
embolization
Advantages Preferred for high-grade trauma without any focal arterial
Disadvantages Higher risk of complications related to the potential
maintained viability of the spleen via the collateral pathway
Coils are placed closer to the origin of the splenic artery, near
the celiac axis (b/w dorsal pancreatic and pancreatic magna
artery), or the main splenic artery at the hilum
abnormality.
More secure and complete occlusion of the main blood
supply to the spleen can be advantageous for controlling
signicant or diffuse bleeding from the spleen.
Effective for managing high-grade splenic injuries and cases
where there is a need for extensive hemostasis on time.
Less time-consuming especially in cases where the time main
bounding factor to secure hemostasis.
compromise of collateral circulation, such as ischemia to the
stomach, pancreas, or liver.
Careful consideration of the patient’s overall vascular
anatomy is essential to minimize the risk of unintended
ischemic complications.
Segmental arterial embolization of the source focal
bleed within splenic parenchyma
Coils are placed further downstream in the smaller
segmental branches of the splenic artery, closer to the
site of the bleeding within the spleen
It is more selective and spares some of the healthy
splenic tissue, potentially reducing the risk of postembolization syndrome and preserving some immune
function of the spleen.
Particularly suitable for focal or localized bleeding
within the spleen, allowing targeted occlusion of the
bleeding vessels.
Potential risk of incomplete embolization, leading to the
need for additional interventions or ongoing bleeding.
In signicant or diffuse bleeding cases, distal
embolization may not provide as robust hemostasis as
proximal embolization.

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R. Yadav et al.
30.2.5 Embolizing Agent
The most commonly used embolization agents are coils, vascular plugs, and gelatin foam, glue. Coils are preferred and
most commonly used [7].
Sizing of the coil: Coil diameter should be approximately
20% size more than the diameter of the embolizing vessel.
30.2.6 Post-procedural Care
The immediate post-procedural care includes close observation of vitals and access site care at least for 24hours to prevent complications. A routine post-procedural
ultrasonography (USG) is recommended on the next day to
look for residual pseudoaneurysm and to assess the puncture
site complication.
30.2.7 Complication
SAE is a part of NOM and post-procedural complications are
rare compared to OM.The main predictors for the success of
NOM include grading of injury and associated preexisting
splenic disease. The higher the grade, the more failure rates
will be. The minor complications include post-embolization
syndrome and contrast-induced nephrotoxicity which is
managed conservatively [8]. The major complications that
may require surgery are splenic infection or abscess formation. Others are large splenic and pancreatic infractions [9].
Late complications are pseudoaneurysms or delayed splenic
rupture [9].
candidate, and a stable patient undergoes single phase or
multiphasic CECT torso depending upon FAST status [11].
Single-phase CECT is done in FAST-negative while
multiphasic in FAST-positive patients. Indications for hepatic
artery embolization (HAE) in liver injury include:
1. High-grade liver injury (AAST IV-V) with an active
source of bleeding in a hemodynamically stable patient.
2. High-grade injury (AAST grade IV/V) with massive
hemoperitoneum, without any focal source of bleeding.
3. As an adjunct treatment for patients with damage control
laparotomy, persistent tachycardia, or drop in hemoglobin or transient responders.
30.3.3 Technique
Includes patient preparation, procedure, approaches, the
embolic agent used, and post-procedural care. The planning
is based on ndings on CECT ndings, which provide not
only the characteristics of injury but also a roadmap to localize the bleeder site and associate common anatomical variations of the origin of the hepatic artery to avoid undue time
wasted in hooking or localizing the origin of vessels.
30.3.4 Patient Preparation
Includes ongoing resuscitation, securing the airway, breathing, and circulation. Ensuring adequate IV access with a
large bore IV line. The basic laboratory parameters are not
prerequisites for trauma patients where the main aim is to
achieve a rapid hemostasis [12].
30.3 Hepatic Injury
30.3.1 Background
Interventional radiology (IR) angiographic embolization is a
minimally invasive procedure used in the management of
liver injury and can be indicated in certain clinical scenarios.
The procedure involves using imaging guidance to locate
and treat bleeding vessels within the liver [10].
30.3.2 Indication
As per institutional guidelines, the evaluation started with
the status of FAST and the hemodynamic status of the
patient. A hemodynamically unstable patient is a surgical
30.3.5 Procedure (Figs.30.3 and30.4)
After obtaining the arterial access and withholding heparin,
a selective celiac artery angiogram is performed using appropriately shaped diagnostic catheters like RC (Rosch) or SIM
(Simmons) reverse curve. Superselective catheterization of
the hepatic artery is usually done with a coaxial microcatheter. Depending upon the imaging and angiographic injury
pattern of injury, embolization or vascular reconstruction is
done. In case of focal active bleeding or pseudoaneurysm or
large AV stula, with an appropriate landing zone in the sacricable artery, embolization is done using permanent embolizing agents like coils or coils with glue or plug, aimed to
complete blockage of the forward ow of the targeted artery.
In case of focal active bleeding or pseudoaneurysm or AV

cd
30 Vascular Interventions inTrauma
377
Fig. 30.3 Hepatic artery
gelfoam embolization in a
young patient with high-grade
injury (AAST grade IV/V)
presenting with massive
hemoperitoneum, without any
focal source of bleeding
Axial (a) contrast-enhanced CT
images depict a large intraparenchymal hematoma with
lacerations, involving the entire
right lobe of the liver. The
selective celiac angiogram (b)
reveals a large area of abnormal
blush in the right lobe of the liver
with no active contrast extravasation or pseudoaneurysm
formation. The hepatic artery
angiogram after gelfoam
embolization (d) demonstrates
complete occlusion of the
forward ow of the right hepatic
artery, with no abnormal
parenchymal blush
a
b
a
Fig. 30.4 Hepatic artery embolization in a patient with high-grade
injury (AAST grade IV) with a pseudoaneurysm following a road trafc accident
Axial (a) contrast-enhanced CT images show a grade IV liver injury
with an intraparenchymal pseudoaneurysm in the right lobe of the liver
(arrow). Selective celiac angiogram (b) reveals a large, focal, well-
b
dened contrast blob arising from the anterior division of the right
hepatic artery. The hepatic artery angiogram after embolization (c)
demonstrates complete coil occlusion of the anterior division of the
right hepatic artery, as close as possible to the site of arterial injury, with
no residual pseudoaneurysm
c

378
R. Yadav et al.
stula, with an appropriate landing zone in the main artery or
non-sacricable artery, vascular reconstruction is done using
a stent graft, aimed to salvage the main feeding artery. In
case of high-grade injury without a denitive active bleed or
pseudoaneurysm, a temporary embolizing agent like gelfoam injection is done in the segmental/lobar artery of the
injured part of the liver, aimed to temporarily block the forward ow in a targeted artery to achieve hemostasis.
30.3.6 Embolization Agent
The choice of embolic material is tailored to the specic
needs of each individual case, the imaging characteristics of
the injury (size and location of bleeding vessels), and the
preferences of the interventional radiologist [13]. Commonly
used embolizing materials are coils (preferably micro coils),
gelfoam, and occasionally glue [14]. Coils are the most
commonly used embolizing agent in liver injury when aimed
to complete permanent blocking of the targeted bleeder
artery, and gelfoam is the next commonly used temporary
biodegradable embolizing agent when aimed to achieve
immediate temporary hemostasis in grade IV/V liver injuries
with no active source of bleeder is identied. Other rarely
used embolizing agents are glue, particles, and Onyx [15].
30.3.7 Post-procedural Care
The immediate post-procedural care is the same as splenic
artery angioembolization.
either hemorrhagic or ischemic and are listed in Table30.2.
The hemorrhagic types of arterial injury on imaging include
pseudoaneurysm, AV stula, and active contrast extravasation either from large arteries or small- to medium-sized
arteries. The imaging patterns of ischemic injury include
thrombus, transection, and dissecting ap with intramural
hematoma. Imaging plays an integral role in characterizing
both types. Endovascular management plays an important
role in the hemorrhagic form of PVI and very limited or no
role in the ischemic form [21].
Management of hemorrhagic form of PVI depends on the
amount and speed of bleeding from PVI and the hemodynamic status of the patient, as per ATLS protocols.
30.4.2 Indication
According to ATLS guidelines, the evaluation starts with a
computed tomography angiography (CTA) in a stable patient,
which helps to assess the type and extent of the injury and
shortlist the candidates for embolization, reveals additional
injuries, and serves as baseline mapping [22]. The ideal candidates for angioembolization are:
1. The presence of hard signs on clinical examination and
CT angiographic signs of a hemorrhagic pattern of
peripheral arterial injury in hemodynamically stable
patients following blunt trauma.
2. Unrecognized or delayed-onset peripheral vascular injury
in follow-up cases of extremity fractures, managed nonoperatively, and subsequently developed a hemorrhagic
type of arterial injury.
30.3.8 Complications
Complications are rare and can be local site complications or
rebleeding after embolization. Others are bilioma formation,
hepatic necrosis/ischemia, liver abscess, gallbladder necrosis, abdominal compartment syndrome, and peritonitis [16].
30.4 Peripheral Vascular Injuries (PVI)
30.4.1 Background
Vascular trauma (VT) accounts for 1% of all traumatic injuries to extremities [17]. Three types of traumatic mechanisms
can lead to PVI blunt, penetrating, and a combination of
both. Peripheral vascular injury manifests either in hemorrhagic form or ischemic form; hence, early recognition and
prompt treatment are important for good outcomes [18–20].
The clinical manifestations of arterial injuries are divided
into hard and soft signs depending on the pattern of injury
Technique Includes patient preparation, procedure,
approaches, the embolic agent used, and post-procedural
care. The planning is based on CT angiography ndings,
which provide not only the characteristics of injury but also
a roadmap to localize the bleeder site.
30.4.3 Patient Preparation
In an acute trauma setting patient preparation is the same for
all the IR procedures.
30.4.4 Procedure (Figs.30.5 and30.6)
The contralateral (retrograde) or ipsilateral (antegrade) common femoral approach for arterial access is chosen based on
the site of injury. For example, the contralateral transfemoral
retrograde approach is used for proximal supercial femoral
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