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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5760_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface to the Third English and Fourth German Edition
- •Preface to the Second English and Third German Edition
- •Preface to the First English Edition
- •Preface to the Second German Edition
- •Preface to the First German Edition
- •Contents
- •1: Fundamental Principles
- •1.1.1.2 Sound Waves
- •1.1.1.3 Generating Ultrasound Waves
- •1.1.1.4.3 Interference
- •1.1.1.5.1 Pulse-Echo Technique
- •1.1.1.5.2 Time Gain Compensation
- •1.1.1.5.3 A-Mode
- •1.1.1.5.4 B-Mode
- •1.1.1.5.5 M-Mode
- •1.1.1.6 Resolution
- •1.1.1.7 Beam Focusing
- •1.1.1.8.2 Linear Arrays
- •1.1.1.8.3 Curved or Convex Arrays
- •1.1.1.8.4 Sector Scanners
- •1.1.1.8.5 Phased Arrays
- •1.1.1.8.6 Mechanical Sector Scanners
- •1.1.1.8.7 Annular Phased Arrays
- •1.1.1.9 Ultrasound Artifacts
- •1.1.1.9.1 Posterior Shadowing
- •1.1.1.9.2 Acoustic Enhancement
- •1.1.1 Gray-Scale Ultrasonography (B-Mode)
- •1.1.1.1 Historical Milestones
- •1.1.1.9.4 Side Lobes
- •1.1.1.9.5 Reverberation Artifact
- •1.1.1.9.6 Geometric Distortion
- •1.1.2.1 Continuous Wave Doppler Ultrasound
- •1.1.2.3 Frequency Processing
- •1.1.2.4 Blood Flow Measurement
- •1.1.3.1 Velocity Mode
- •1.1.3.2 Power Doppler Mode
- •1.1.3.3 B-Flow Mode (Brightness Flow)
- •1.1.3.4 Intravascular Ultrasound
- •1.1.4.2 Mirror Artifact
- •1.1.4.6 Doppler Angle
- •1.1.5 Ultrasound Contrast Agents
- •1.1.5.3.1 Contrast-Enhanced Duplex Ultrasound
- •1.1.5.3.2 Contrast Harmonic Imaging
- •1.1.5.3.3 Stimulated Acoustic Emission Imaging
- •1.1.6.3.1 B-Mode
- •1.1.6.3.2 M-Mode
- •1.1.6.3.3 CW Doppler
- •1.1.6.3.4 PW Doppler
- •1.1.6.3.5 Color Doppler
- •1.1.6.4 Conclusion
- •1.2 Hemodynamic Principles
- •1.2.1 Laminar Flow
- •1.2.2.1 Low-Resistance Flow
- •1.2.2.2 High-Resistance Flow
- •1.2.2.3 Perfusion Regulation
- •1.2.3.1 Poststenotic Parameters
- •1.3 Machine Settings
- •2: Extremity Arteries
- •2.1.1 Vascular Anatomy
- •2.1.1.1 Pelvic Arteries
- •2.1.1.2 Leg Arteries
- •2.1.2.1 Pelvic Arteries
- •2.1.2.2 Leg Arteries
- •2.1.6 Abnormal Findings
- •2.1.6.1 Atherosclerotic Occlusive Disease
- •2.1.6.1.1 Pelvic Arteries
- •2.1.6.1.3 Stenosis Grading
- •2.1.6.1.4 Leg Arteries
- •2.1.6.1.9 Profunda Femoris Artery
- •2.1.6.1.13 Multilevel Obstruction
- •2.1.6.1.14 Arterial Occlusion
- •2.1.6.2 Arterial Embolism
- •2.1.6.3 Aneurysm
- •2.1.6.3.1 True Aneurysm
- •2.1.6.3.2 Pseudoaneurysm
- •2.1.6.4.1 Adventitial Cystic Disease
- •2.1.6.4.2 Popliteal Artery Entrapment Syndrome
- •2.1.6.4.3 Raynaud’s Disease
- •2.1.6.4.5 Buerger’s Disease
- •2.1.6.4.7 Dissection
- •2.1.6.4.8 Arteriovenous Fistulas
- •2.1.7.1 Thromboendarterectomy
- •2.1.7.3 Bypass Graft Surveillance
- •2.2 Arm Arteries
- •2.2.1 Vascular Anatomy
- •2.2.3.1 Atherosclerosis
- •2.2.3.2 Vascular Compression Syndromes
- •2.2.4 Documentation
- •2.2.5 Normal Findings
- •2.2.6.1 Atherosclerosis
- •2.2.6.2 Vascular Compression Syndromes
- •2.2.6.4 Buerger’s Disease
- •2.2.6.5 Raynaud’s Disease
- •2.3 Atlas: Extremity Arteries
- •3.1.2.1.2 Patient Positioning
- •3.1.2.1.3 Examination Technique
- •3: Extremity Veins
- •3.1.1 Vascular Anatomy
- •3.1.2 Examination Protocol
- •3.1.2.1 Thrombosis
- •3.1.2.1.1 Equipment
- •3.1.3 Normal Findings
- •3.1.4 Documentation
- •3.1.5.1.1 Leg Vein Thrombosis
- •3.1.5.2 Varicosis
- •3.1.6.1 Thrombosis
- •3.1.6.1.3 Pulmonary Embolism
- •3.1.6.1.5 Thrombus Age
- •3.1.6.1.6 Recurrent Thrombosis
- •3.1.6.3 Varicosis
- •3.1.6.3.1 Treatment Options
- •3.1.6.4 Varicophlebitis
- •3.1.7 Rare Venous Disorders
- •3.1.7.1 Venous Aneurysm
- •3.1.7.1.1 Sonographic Workup
- •3.1.7.3 Venous Compression
- •3.1.7.4 Venous Adventitial Cystic Disease
- •3.1.8 Vein Mapping
- •3.1.9.1 Deep Vein Thrombosis
- •3.1.9.1.1 Ultrasound Versus Venography
- •3.1.9.3 Varicosis
- •3.2.1 Vascular Anatomy
- •3.2.3 Normal Findings
- •3.2.4 Documentation
- •3.2.5 Clinical Role
- •3.3 Atlas: Extremity Veins
- •4: Arteriovenous Fistulas
- •4.1.1 Background
- •4.2.2 Hemodialysis AV Fistula
- •4.5 Documentation
- •4.7 Hemodialysis Access Complications
- •4.7.1 Hemodialysis Access Stenosis
- •4.7.1.3 Proximal Feeding Artery Stenosis
- •4.7.2.1 Peripheral Ischemia
- •4.7.2.2 Hemodialysis Access Aneurysm
- •4.7.2.3 Inadequate or Excessive Fistula Flow
- •4.7.2.4 Arm Swelling
- •4.8.1 Therapeutic Decision-Making
- •4.8.2 Surveillance Programs?
- •4.9 Atlas: Arteriovenous Fistulas
- •5: Extracranial Cerebral Arteries
- •5.1.1 Carotid Arteries
- •5.1.2 Vertebral Arteries
- •5.2.1 Carotid Arteries
- •5.2.2 Vertebral Arteries
- •5.3 Documentation
- •5.4 Normal Findings
- •5.4.1 Carotid Arteries
- •5.4.2 Vertebral Arteries
- •5.5.1 Carotid Arteries
- •5.5.1.1 Stenosis Grading
- •5.5.1.2 Plaque Morphology
- •5.5.2 Vertebral Arteries
- •5.6.1 Carotid Arteries
- •5.6.1.1.1 Intima-Media Thickness
- •5.6.1.1.2 Plaque Features
- •5.6.1.1.4 Plaque Thickness
- •5.6.1.1.5 Plaque Morphology: Plaque Surface
- •5.6.1.3 Occlusion
- •5.6.1.3.1 Persistent Primitive Hypoglossal Artery
- •5.6.1.4 Postoperative Follow-Up
- •5.6.1.4.1 Carotid Endarterectomy (CEA)
- •5.6.1.4.2 Carotid Artery Stenting (CAS)
- •5.6.1.4.5 Stent Dislocation
- •5.6.2 Vertebral Arteries
- •5.6.2.1 Stenosis
- •5.6.2.2 Occlusion
- •5.6.2.3 Dissection
- •5.6.2.4 Subclavian Steal Syndrome
- •5.8.1 Dissection
- •5.8.2 Vasculitis
- •5.8.3 Fibromuscular Dysplasia
- •5.8.4 Aneurysm
- •5.8.5 Arteriovenous Fistula
- •5.8.6 Idiopathic Carotidynia
- •5.8.7 Vasospasm
- •5.10 Atlas: Extracranial Cerebral Arteries
- •6.1.1 Vascular Anatomy
- •6.1.1.1 Aorta
- •6.1.1.2 Visceral Arteries
- •6.1.1.3 Renal Arteries
- •6.1.2.1 Aorta
- •6.1.2.2 Visceral Arteries
- •6.1.2.3 Renal Arteries
- •6.1.2.3.1 Ultrasound Technique
- •6.1.3 Normal Findings
- •6.1.3.1 Aorta
- •6.1.3.2 Visceral Arteries
- •6.1.3.3 Renal Arteries
- •6.1.5.1 Aorta
- •6.1.5.1.1 Abdominal Aortic Aneurysm
- •6.1.5.2 Visceral Arteries
- •6.1.5.3 Renal Arteries
- •6.1.6.1 Renal Arteries
- •6.1.6.1.2 Therapy-Oriented Stenosis Grading
- •6.1.6.1.3 Contrast-Enhanced Ultrasound (CEUS)
- •6.1.6.1.5 Diagnostic Algorithm
- •6.1.6.1.6 Renal Artery Occlusion
- •6.1.6.1.7 Transplant Kidney
- •6.1.6.2 Visceral Arteries
- •6.1.6.2.1 Celiac Trunk
- •6.1.6.2.2 Visceral Artery Aneurysm
- •6.1.6.2.3 Dissection
- •6.1.6.2.4 Superior Mesenteric Artery
- •6.1.6.2.5 Acute Mesenteric Artery Occlusion
- •6.1.6.3 Aorta
- •6.1.6.3.2 Abdominal Aortic Aneurysm
- •6.1.6.3.6 Aortic Dissection
- •6.2.1 Vascular Anatomy
- •6.2.1.1 Vena Cava
- •6.2.1.2 Renal Veins
- •6.2.2 Examination Technique
- •6.2.2.1 Vena Cava
- •6.2.2.2 Renal Veins
- •6.2.3.1 Renal Veins
- •6.2.3.2 Portal Venous System
- •6.2.4 Normal Findings
- •6.2.4.2 Portal Venous System
- •6.2.5 Documentation
- •6.2.6.1 Vena Cava
- •6.2.6.1.1 Membranous Vena Cava Obstruction
- •6.2.6.2 Renal Veins
- •6.2.6.3.1 Splenic Vein Thrombosis
- •6.2.6.4.1 Portal Vein Thrombosis
- •6.2.6.4.2 Portal Hypertension
- •6.2.6.4.3 Hepatic Veins

224
Chapter 3 · Extremity Veins
3.3 Atlas: Extremity Veins
. Table3.8 lists the gures presented in the Atlas. e gures illustrate normal ndings, methodology, and vascular diseases
of the extremity veins.
3
. Table 3.8 Extremity veins– gures
Entity/pathology Figure
Pelvic veins– normal ultrasound ndings
Venous Doppler waveform
Normal valve function– gray-scale imaging
Pelvic vein thrombosis
Pelvic vein thrombosis– beginning recanalization
Pelvic vein thrombus surrounded by owing blood
Loss of respiratory phasicity due to obstructed venous drainage
Collateral circulation in pelvic vein thrombosis
External pelvic vein compression by lymphoma
Criteria for estimating thrombus age
Older femoral vein thrombosis
Calf vein thrombosis
Older calf vein thrombosis
Recurrent thrombosis after recanalization
Recurrent calf vein thrombosis after partial recanalization
Diagnosis of calf vein thrombosis– ultrasound versus venography
Isolated bular vein thrombosis– venography
Diagnosis of thrombosis– ultrasound versus venography
Duplicated femoral vein
Free-oating thrombus of femoral vein
Asymptomatic venous thrombosis developing in valve pockets
Pelvic vein thrombosis secondary to ascending deep femoral vein thrombosis
Calf muscle vein thrombosis with thrombus extension into popliteal vein
Thrombophlebitis of great saphenous vein with thrombus extension into femoral vein (natural history)
Thrombophlebitis of small saphenous vein
Femoropopliteal vein
Thrombosis arising from thrombophlebitis extending through perforator
Monitoring of thrombolytic therapy
Postthrombotic syndrome– valve function
Postthrombotic syndrome– recanalized lumen
Postthrombotic syndrome– paradoxical ow during Valsalva’s maneuver
Postthrombotic recanalization with arteriovenous stula
Chronic venous insuciency
Valve incompetence of calf veins
Dilated muscle veins
Fig.3.41 (Atlas), page 226
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Fig.3.42 (Atlas), page 226
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Fig.3.43 (Atlas), page 226
Fig.3.44 (Atlas), page 227
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Fig.3.45 (Atlas), page 227
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Fig.3.46 (Atlas), page 228
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Fig.3.47 (Atlas), page 228
Fig.3.48 (Atlas), page 229
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Fig.3.49 (Atlas), page 229
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Fig.3.50 (Atlas), page 229
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Fig.3.51 (Atlas), page 230
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Fig.3.52 (Atlas), page 230
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Fig.3.53 (Atlas), page 230
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Fig.3.54 (Atlas), page 231
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Fig.3.54 (Atlas), page 231
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Fig.3.55 (Atlas), page 231
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Fig.3.56 (Atlas), page 232
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Fig.3.57 (Atlas), page 232
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Fig.3.58 (Atlas), page 233
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Fig.3.59 (Atlas), page 233
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. Fig.3.60 (Atlas), page 234
Fig.3.61 (Atlas), page 235
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Fig.3.62 (Atlas), page 236
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Fig.3.63 (Atlas), page 237
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Fig.3.64 (Atlas), page 238
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Fig.3.65 (Atlas), page 238
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Fig.3.66 (Atlas), page 239
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Fig.3.67 (Atlas), page 239
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Fig.3.68 (Atlas), page 240
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Fig.3.69 (Atlas), page 240
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Fig.3.69 (Atlas), page 240
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Fig.3.70 (Atlas), page 241
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Fig.3.71 (Atlas), page 242
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Fig.3.71 (Atlas), page 242
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Fig.3.72 (Atlas), page 242
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3.3 · Atlas: Ex tremity Veins
. Table 3.8 (continued)
Entity/pathology Figure
225
3
Postthrombotic syndrome– residual lesions/synechia
Postthrombotic residues– wall sclerosis
Degrees of valve incompetence
Respiratory phasicity and cardiac pulsatility of reux in severe valve incompetence
Truncal varicosis of great saphenous vein (distal extent)
Incomplete truncal varicosis of great saphenous vein
Truncal varicosis of small saphenous vein
Valve incompetence of perforating vein
Thromboembolism from great saphenous vein and Dodd perforator incompetence
Recanalized great saphenous vein after thrombophlebitis
VNUS closure of great saphenous vein
Follow-up of VNUS closure
Follow-up after endovenous varicose treatment
Recurrent varicosis
Venous aneurysm
Venous aneurysm with thrombus
Venous aneurysm and deep vein thrombosis of leg
Saccular popliteal vein aneurysm
Venous ectasia of the calf
Dierential diagnosis of venous thrombosis– Baker’s cyst
Dierential diagnosis of calf vein thrombosis– hematoma
Calf swelling due to torn muscle
Calf swelling due to popliteal fossa tumor
Calf swelling due to subfascial abscess
Edema of various etiologies, lymphoma, lymphedema, lipedema
Calf swelling caused by edema
Vein compression by Baker’s cyst
Adventitial cystic disease of the popliteal vein
Venous wall tumor
Entrapment syndrome
Axillary vein– normal ndings
Thoracic outlet obstruction
Jugular vein aneurysm
Jugular vein thrombosis– central venous catheter
Axillary vein thrombosis– thrombolytic therapy
Recanalization
Costoclavicular compression syndrome with thrombosis
Costoclavicular compression syndrome
Follow-up of subclavian vein thrombosis after pacemaker implantation
Thrombophlebitis of arm veins
Fig.3.73 (Atlas), page 243
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Fig.3.73 (Atlas), page 243
Fig.3.74 (Atlas), page 244
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Fig.3.75 (Atlas), page 245
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Fig.3.76 (Atlas), page 245
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Fig.3.77 (Atlas), page 246
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Fig.3.78 (Atlas), page 246
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Fig.3.79 (Atlas), page 247
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Fig.3.80 (Atlas), page 247
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Fig.3.81 (Atlas), page 248
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Fig.3.82 (Atlas), page 248
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Fig.3.83 (Atlas), page 248
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Fig.3.83 (Atlas), page 248
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Fig.3.84 (Atlas), page 249
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Fig.3.85 (Atlas), page 249
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Fig.3.86 (Atlas), page 250
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Fig.3.87 (Atlas), page 250
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Fig.3.88 (Atlas), page 251
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Fig.3.89 (Atlas), page 251
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Fig.3.90 (Atlas), page 252
Fig.3.91 (Atlas), page 252
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Fig.3.91 (Atlas), page 252
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Fig.3.92 (Atlas), page 253
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Fig.3.93 (Atlas), page 253
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Fig.3.94 (Atlas), page 254
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Fig.3.94 (Atlas), page 254
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Fig.3.95 (Atlas), page 255
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Fig.3.96 (Atlas), page 255
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Fig.3.97 (Atlas), page 256
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Fig.3.98 (Atlas), page 256
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Fig.3.99 (Atlas), page 257
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Fig.3.100 (Atlas), page 257
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Fig.3.101 (Atlas), page 257
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Fig.3.102 (Atlas), page 258
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Fig.3.103 (Atlas), page 259
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Fig.3.104 (Atlas), page 259
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Fig.3.105 (Atlas), page 260
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Fig.3.106 (Atlas), page 261
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Fig.3.107 (Atlas), page 262
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Fig.3.108 (Atlas), page 262

226
Chapter 3 · Extremity Veins
3
. Fig. 3.41a–c (Atlas) Pelvic veins– normal ultrasound ndings (see . Fig. 2.2).
a Like in the vena cava (VC), blood ow in the iliac veins is subject to respiratory phasicity. The resulting variation in diameter is apparent in the
time-motion mode (right part of a). In slender individuals, the iliac vein is also compressible (KOMP).
b Compression ultrasound of pelvic veins is reliable only in slender patients. Therefore, incompressibility is not a reliable indicator of thrombosis in
this territory, while compressibility rules out thrombosis. The example illustrates compressibility in the time- motion mode (arrow).
c The pelvic veins (common iliac vein/V.I.C and external iliac vein/V.I.E) take an arched course through the true pelvis posterior to the arteries of
the same name (A). The internal iliac vein (V.I.I) enters the common iliac vein on its posterior aspect at its lowest point (ow toward transducer,
coded in red). There is respiratory phasicity of venous ow, and younger individuals (as in this case) sometimes also show cardiac pulsatility. In
addition, a second pelvic vein (red) enters the common iliac vein (blue) slightly above the internal iliac vein
. Fig. 3.42 (Atlas) Venous Doppler waveform.
Just below the inguinal ligament, the common femoral vein (V.F.C)
divides into the deep femoral vein (V.P.F) and the supercial femoral
vein (V.F.S). Flow in the veins is characterized by respiratory uctuation
when no proximal obstruction (thrombus, compression) is present. The
Doppler waveform illustrates the respiratory variation in ow velocity
in the deep femoral vein. Venous ow velocity decreases with increasing intra-abdominal pressure during inspiration. In this young woman,
there is additional cardiac modulation of venous ow, which even
perists during expiration. With the PRF adjusted to venous ow, the
femoral artery close to the transducer shows aliasing (A) and reversed
ow in diastole (arrows)
. Fig. 3.43 (Atlas) Normal valve function– gray-scale imaging.
a Under good insonation conditions, normal valve function is apparent on gray-scale imaging. The valve (VK) depicted in the supercial femoral
vein (V.F.S) just before it receives the deep femoral vein (V.P.F) is shown during expiration (valve open) in the left gray-scale image and during
inspiration (valve closed) in the right image. The cusps prevent backward ow toward the periphery during the inspiration-induced increase
in intra-abdominal pressure. The respiratory variation in blood ow is documented in the Doppler waveform. Flow toward the transducer is
increased in expiration and decreased in inspiration. Flow may even drop to zero, and the short transient reux until valve closure may be absent
if the sample volume is placed near a valve

3.3 · Atlas: Ex tremity Veins
227
. Fig. 3.44a–e (Atlas) Pelvic vein thrombosis.
a The left iliac vein coursing posterior to the iliac artery (red) has low echogenicity and is markedly dilated. These ndings, along with the absence
of ow signals, indicate acute thrombosis.
b The thrombus protrudes into the vena cava (V.C), and there is marginal blood ow along the thrombus entering from the right iliac vein
(A.I.C=common iliac artery).
c Proximal venous stenosis leads to reduced ow and loss of respiratory phasicity in the left supercial femoral vein (VFS) (. Fig.3.24).
d With thrombosis extending into the common femoral vein, collateral ow occurs through the deep femoral vein (VPF), where ow is retrograde
(blue, away from transducer), and through pelvic collaterals.
e Beginning recanalization with blood ow toward the heart (red) along the thrombus (T) in the common iliac vein (V.I.C)
3
. Fig. 3.45a, b (Atlas) Pelvic vein thrombosis– beginning recanalization.
a Follow-up ultrasound after acute thrombosis shows a shrunken lumen of the common iliac vein as well as ow signals, indicating beginning recanalization (smaller diameter compared with recent thrombosis). Flow in the vena cava (V.C) is displayed in blue (due to transducer position) (A=aorta).
b Retrograde ow in the deep femoral vein (V.P.F; blue, away from transducer; below the baseline in the Doppler waveform) indicates inadequate
or absent drainage at the pelvic level, which is due to descending pelvic thrombosis in the case presented here

228
Chapter 3 · Extremity Veins
3
. Fig. 3.46a, b (Atlas) Pelvic vein thrombus surrounded by owing blood.
a In this young woman with scintigraphically proven pulmonary embolism, ultrasound showed patent deep leg veins, while there were thrombi
in the iliac vein. Unlike recanalization with central ow signals (as shown in . Fig.3.45 (Atlas)), the fresh thrombus (TH) in the external iliac vein
(V.I.E) is attached to the wall and surrounded by owing blood.
b More proximally, close to the junction with the internal iliac vein, the thrombus is surrounded by owing blood posteriorly. The ow obstruction
produces a high-frequency, continuous signal (with loss of respiratory phasicity) typical of venous stenosis. The peak ow velocity is 50cm/s. With
the PRF adjusted to venous ow, there is aliasing in the artery anterior to the vein. The thrombus is indicated by arrows. The Doppler waveform
from the uninvolved common femoral vein distal to the thrombus is not shown. The patent lumen of the common femoral vein is relatively wide,
and respiratory phasicity is only slightly reduced. A thrombus in an otherwise patent lumen as in this case may be overlooked if only the waveform from the common femoral vein is analyzed, even if it is compared with the contralateral waveform and valve function is evaluated. Routine
venography may likewise fail to identify such mural thrombi in an otherwise patent iliac vein or to dierentiate them from ow phenomena
. Fig. 3.47 (Atlas) Loss of respiratory phasicity due to obstructed venous drainage.
a Flow obstruction in a partially thrombosed vein eliminates or reduces respiratory phasicity and results in a higher- frequency ow signal in the
Doppler waveform, unless the blood is drained through collaterals (similar to the situation in arterial stenosis).
b Since some residual respiratory variation may still be present, the waveform should be compared with the other side. In the example, respiratory
phasicity is markedly reduced on the aected side compared with the contralateral side. The common femoral vein (V.FEM.COM, blue) receives
the great saphenous vein (V.S.M, blue) and a deep femoral vein (V.PRF.F) displayed in red (ow toward transducer)

3.3 · Atlas: Ex tremity Veins
229
. Fig. 3.48 (Atlas) Collateral circulation in pelvic vein thrombosis (see . Fig.3.49 (Atlas)).
The degree of recanalization is not always easy to estimate in older thrombosis of the external iliac vein. The shrunken vein is more dicult to
evaluate along its course into the true pelvis and must be dierentiated from collaterals such as the epigastric veins, which arise at the level of the
inguinal ligament and, when dilated, may be of similar size as the shrunken external iliac vein (left color ow image). Retrograde ow in the saphenofemoral junction (right image, V.S.M) indicates outow obstruction of the pelvic veins; the course of the abdominal wall collaterals can be followed using color duplex ultrasound. The Doppler waveform (right) also shows retrograde ow toward the transducer in the great saphenous vein
3
. Fig. 3.49 (Atlas) External pelvic vein compression by lymphoma.
Leg swelling and widening of major veins secondary to obstructed
venous drainage at the pelvic level due to external compression of the
external iliac vein (V.I.E) by lymphoma (L). (V.I.I=internal iliac vein). The
Doppler waveform shows high ow velocity of 170cm/s in the external
iliac vein and loss of respiratory phasicity
. Fig. 3.50 (Atlas) Criteria for estimating thrombus age.
The major signs of acute deep vein thrombosis (DVT) of the legs are
marked dilatation of the vein and good delineation of the homogeneous, often hypoechoic, thrombosed venous lumen from perivascular
connective tissue. The two images obtained in the same patient show
acute DVT with the venous lumen dilated to well over twice that of the
accompanying artery in the right leg (right image) and an old thrombosis of the common femoral vein already partially recanalized in the
area of the femoral bifurcation at the same level on the left (V.F.C, ow
displayed in blue). (A.F.C=common femoral artery; A.P.F=deep femoral artery; A.F.S=supercial femoral artery)

230
Chapter 3 · Extremity Veins
3
. Fig. 3.51 (Atlas) Older femoral vein thrombosis.
Older thrombosis is associated with shrinkage of the lumen (relative to the corresponding artery). The image on the left shows the thrombotically
occluded supercial femoral vein (V) posterior to the supercial femoral artery (A.F.S, red). Demarcation is much poorer than in acute thrombosis. The
image obtained with application of pressure (middle section) shows incompressibility of the vein depicted posterior to the artery. The longitudinal
image (right section) of the occluded supercial femoral vein (V.F.S) shows absence of ow in the vein posterior to the artery shortly before receiving the deep femoral vein (V.P.F). The deep femoral vein is recanalized with ow toward the transducer coded in red. However, marginal hypoechoic
thrombosis still persists along the patent venous lumen
. Fig. 3.52 (Atlas) Calf vein thrombosis.
With a satisfactory acoustic window, fresh venous thrombosis below the
knee is easily identied as a hypoechoic tubular structure within the soft
tissue in the typical anatomic location of the vein. The lumen is wider
than that of the corresponding artery. The bular artery and vein course
along the medial aspect of the bula. Compression ultrasound and color
duplex imaging are highly accurate in dierentiating between patent
and thrombotic segments. The image on the right shows one patent
vein and one thrombosed vein, and the left image shows thrombosis of
both bular veins, while both adjacent posterior tibial veins are patent
(blue-coded ow)
. Fig. 3.53 (Atlas) Older calf vein thrombosis.
Following acute thrombosis, recanalization may set in early as indicated in the example by partial recanalization (blue) of the left posterior tibial
vein (left section; diameter of the vein indicated by calipers). On the other hand, recanalization may occur late or not at all, which is indicated by
a shrunken lumen without ow signals, shown here for the bular vein (V.FIB) on longitudinal and transverse views (middle and right sections).
Older thrombosis is characterized by more echogenic thrombus and shrinkage of the venous lumen, which is more dicult to distinguish from
surrounding muscle and fatty connective tissue. The examples illustrate the diculties encountered in diagnosing older thrombosis both in partial recanalization and in completely occluded postthrombotic veins with shrunken lumina

3.3 · Atlas: Ex tremity Veins
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3
. Fig. 3.54a–c (Atlas) Recurrent thrombosis after recanalization.
a The posterior tibial vein to the right of the artery (A, red) is markedly dilated (6.1mm) and shows no ow, suggesting acute thrombosis. The vein
to the left exhibits ow coded in blue with a surrounding hypoechoic margin corresponding to wall thickening as a sign of recanalized thrombosis. Compression ultrasound (right) shows only little compressibility of the thrombosed vein. No venous ow signals are depicted to the left of the
artery during compression. However, the vein is not fully compressed. There is a hypoechoic area in the connective tissue corresponding to the
postthrombotically thickened walls. The vein is surrounded by hyperechoic connective tissue of the deep crural fascia, and the tibia is depicted
farther away from the transducer.
b,c Recurrent calf vein thrombosis after partial recanalization.
b Partial recanalization and recurrent thrombosis in the paired veins coursing to the right and left of the artery of the same name (A). Ultrasound
images obtained without compression (left) and with compression (right) show residual thrombosis with partial recanalization in the bular vein
(indicated by “V.F>”) to the left of the artery, close to the bula, while there is acute recurrent thrombosis of the bular vein (V) to the right of
the artery. Residual thrombosis results in poor demarcation of the lumen from the wall and incomplete compressibility (with reduction of the
lumen from 3.7 to 2.7mm in the compression image (calipers). The bular vein with acute thrombosis (V) shows some deformability although it is
occluded and the lumen is widened by the thrombus (F.C.P=deep crural fascia).
c Color duplex imaging shows blood ow (blue) lling approx. half the lumen of the older, partially recanalized bular vein (“V>”), while there is
no ow in the other, markedly dilated and acutely thrombosed bular vein (indicated by “V” in the transverse image (left) and “V.FIV” in the longitudinal image (right). Aliasing in the artery is due to the low PRF chosen to depict slow venous ow (. Fig.3.54b, c adapted from Schäberle 2014)
. Fig. 3.55a, b (Atlas) Diagnosis of calf vein thrombosis– ultrasound versus venography.
a Isolated calf vein thrombosis of a single vein group may be overlooked or misinterpreted on venography. Moreover, small lling defects may be
dicult to assign to a muscle vein or a major vein. B-mode ultrasound identies acute thrombosis of a calf vein as a hypoechoic tubular structure
along the artery of the same name, which can serve as a landmark. Color duplex imaging corroborates the diagnosis by the failure to demonstrate
ow when performed with a low PRF.When only little residual ow is present, augmentation by manual compression distal to the transducer may be
necessary to obtain a ow signal. The left image shows a patent posterior tibial vein (V) with blue-coded ow to the right of the red artery (A), while
the second vein (V) to the left of the artery is thrombosed. The marked dilatation of the vein (to more than twice the width of the arterial lumen) and
the low-level echo of the thrombus suggest acute thrombosis. The longitudinal image (right) shows the bular vein to be thrombosed as well. The
lumen is much wider than that of the corresponding artery (A) with ow depicted in red. The thrombosed vein is hypoechoic and homogeneous,
clearly demarcating it from the surrounding soft tissue.
b Venogram: Filling defect in the posterior tibial vein. The bular vein is not depicted

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Chapter 3 · Extremity Veins
3
. Fig. 3.56a–c (Atlas) Isolated bular vein thrombosis– venography.
Venography is limited in the evaluation of the bular veins. A lling defect in this vein may be due to a technical limitation or thrombosis.
a Sonographic examination identies one thrombosed and one patent bular vein. The transverse view (left section) depicts round, tubular structures
to the left and right of the artery and the bula (FIB) to the left. The veins are indicated by calipers: the thrombosed vein (right) is markedly dilated
compared with the patent bular vein (7.7mm versus 3.5mm). The image obtained while compression is being applied (middle section) no longer
shows the bular vein to the left of the artery (A), indicating complete compressibility. The vein to the right shows only little compressibility (diameter
reduced from 7.7 to 5.8mm), consistent with acute thrombus. The color duplex image (right section) depicts the patent vein in blue to the left of the
artery (red), the thrombosed vein (V ) to the right (marked with calipers). The thrombosed vein is hypoechoic, markedly dilated, and shows no ow.
b Longitudinal duplex image of the markedly dilated vein with the Doppler waveform conrming absence of blood ow. The clot immobilizes a
valve in the center of the image.
c The venogram fails to depict the bular veins. Based on the duplex sonographic demonstration of one patent and one thrombosed bular
branch, this example nicely illustrates that absence of contrast lling may be due to thrombosis or technical limitations of the method
a b
. Fig. 3.57a, b (Atlas) Diagnosis of thrombosis– ultrasound versus venography.
a Transverse image (left) and longitudinal images (middle and right) of a duplicated popliteal vein with one patent and one thrombosed branch.
Flow in the patent branch is coded blue. The rst of the two longitudinal views shows the junction where the two branches (V) unite to form a
single vein (V.POP).
b Venogram showing normal appearance of the common popliteal vein segment and the patent branch of the paired segment. As there is a
smooth transition from the doubled popliteal segment to the single branch, there is no chance of identifying the thrombosed, second popliteal
vein by venography

3.3 · Atlas: Ex tremity Veins
. Fig. 3.58 (Atlas) Duplicated femoral vein.
A duplicated femoral vein with one patent branch and one completely
occluded branch is a pitfall in venography. Color duplex imaging shows
a perfused vein (V ) to the left of the artery (A) and a markedly dilated
vein (V) without ow to the right. The image obtained with compression (right) demonstrates complete compressibility of the vein to the
left of the artery with only little compression of the vein to the right,
which is still apparent as a hypoechoic tubular structure
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3
. Fig. 3.59a, b (Atlas) Free-oating thrombus of femoral vein.
a Free-oating thrombus in the supercial femoral vein (V.FEM.S); transverse view on the left and longitudinal view on the right. A circular ow
signal around a thrombus in a color ow image is diagnostic of free-oating thrombus (TH) and enables determination of the extent of the oating component. The slow ow around the oating tail proximal to the occlusion may be dicult to depict despite adequate instrument settings
(high gain, low PRF). The problem may be overcome by having the patient perform a Valsalva maneuver to augment ow. Instrument adjustment
to slow venous ow leads to aliasing in the supercial femoral artery (A, anterior to the vein). Collaterals with ow in blue (KOL) are depicted
anterolaterally and the deep femoral vein (V.P.F) posteriorly.
b Venogram: The femoral vein is thrombosed; a second plane is necessary to estimate the length of the oating tail
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