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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

2.2 · Arm Arteries
123
2
a
b
. Fig. 2.49 a 65-year-old woman presenting with a 5-day history of progressive hand ischemia. The waveform from the brachial artery shows
monophasic ow with a reduced peak systolic velocity (PSV) and delayed upstroke, consistent with poststenotic ow. b Poststenotic ow in the
brachial artery is due to concentric wall thickening of a long segment of the axillary artery (and also of the subclavian artery), causing high-grade
stenosis (transverse and longitudinal color ow images). Because of the length of the aected segment, the intrastenotic PSV is only 78cm/s
despite high-grade luminal narrowing. c After one month of cortisone treatment, there is only residual circumferential wall thickening without
relevant hemodynamic eects
c

124
Chapter 2 · Extremity Arteries
2.3 Atlas: Extremity Arteries
. Table2.23 lists the gures presented in the Atlas. e gures illustrate normal ndings, methodology, and vascular diseases
2
of the extremity arteries.
. Table 2.23 Extremity arteries– gures
Entity/Pathology Figure
Vascular anatomy
Femoral bifurcation– normal blood ow
Pelvic artery stenosis
Iliac artery stenosis with good collateralization– Doppler waveform analysis
Iliac artery– stenosis/occlusion and collateral pathways
Common iliac artery stenosis
Iliac artery aneurysm– stenting
Floating plaque in common femoral artery in a patient with blue toe
High-grade stenosis/occlusion of common femoral artery
Common femoral artery occlusion– collateralization
Stenosis at origin of profunda femoris artery– TEA
Stenosis at origin of profunda femoris artery (recurrence)
Distal profunda femoris stenosis
Profunda femoris artery– variable origin and branching pattern
Stenosis at origin of profunda femoris artery in diabetes mellitus
Femoral artery occlusion and sequential popliteal artery stenosis
Artifact due to acoustic shadowing
Embolizing popliteal artery plaque before and after PTA
Grading of stenosis caused by eccentric plaque
Bypass planning– mapping for suitable vein, target vessel
Selection of recipient vessel for distal bypass procedure
Stage IV PAOD with arterial occlusion below the knee
Contrast-enhanced ultrasound (CEUS)– bypass recipient vessel in popliteal artery occlusion
Recipient vessel for pedal bypass
Bypass complications: graft infection, graft occlusion
Graft occlusion
Interpretation of Doppler waveforms from within bypass grafts
Low-ow bypass– failing bypass
Low-ow bypass and new stenosis of proximal anastomosis
Saphenous vein bypass graft– stenosis at valve site
Aneurysmal dilatation of vein graft
In situ vein graft– AV stula and stenosis
Bypass graft– inow stenosis
Fig.2.50 (Atlas), page 126
.
Fig.2.51 (Atlas), page 127
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Fig.2.52 (Atlas), page 128
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Fig.2.53 (Atlas), page 129
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Fig.2.54 (Atlas), page 130
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Fig.2.55 (Atlas), page 130
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Fig.2.56 (Atlas), page 131
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Fig.2.57 (Atlas), page 131
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Fig.2.58 (Atlas), page 132
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Fig.2.58 (Atlas), page 132
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Fig.2.59 (Atlas), page 133
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Fig.2.60 (Atlas), page 134
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Fig.2.60 (Atlas), page 134
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Fig.2.61 (Atlas), page 135
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Fig.2.62 (Atlas), page 135
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Fig.2.63 (Atlas), page 136
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Fig.2.64 (Atlas), page 137
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Fig.2.65 (Atlas), page 137
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Fig.2.66 (Atlas), page 137
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Fig.2.67 (Atlas), page 138
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Fig.2.68 (Atlas), page 138
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Fig.2.69 (Atlas), page 139
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Fig.2.70 (Atlas), page 140
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Fig.2.71 (Atlas), page 141
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Fig.2.72 (Atlas), page 142
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Fig.2.72 (Atlas), page 142
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Fig.2.73 (Atlas), page 143
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Fig.2.74 (Atlas), page 143
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Fig.2.75 (Atlas), page 144
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Fig.2.76 (Atlas), page 144
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Fig.2.76 (Atlas), page 144
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Fig.2.77 (Atlas), page 145
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Fig.2.78 (Atlas), page 145
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2.3 · Atlas: Extremity Arteries
. Table 2.23 (continued)
Entity/Pathology Figure
125
2
Pseudoaneurysm– thrombin injection treatment
Pseudoaneurysm– challenges for thrombin injection treatment
Pseudoaneurysm– dierentiation from hematoma
Suture aneurysm
Pseudoaneurysm– compression therapy/thrombin injection
Large pseudoaneurysm with multiple perforation– thrombin injection
Internal iliac artery– pseudoaneurysm, thrombin injection
Arteriovenous stula
Popliteal artery occlusion– atherosclerosis versus embolism
Embolic occlusion
Arterial occlusion in deep leg vein thrombosis and patent foramen ovale
Bilateral popliteal artery aneurysm
Small popliteal artery aneurysm with arterioarterial embolism
Pseudoaneurysm following arthroscopy
Aneurysm of posterior tibial artery
Adventitial cystic disease
Adventitial cystic disease– treatment by ultrasound-guided aspiration
Adventitial cystic disease– dierentiation from dissection
Entrapment syndrome
Entrapment syndrome
Entrapment constellation
Dissection
Progressive ischemia due to venous outow obstruction (extensive venous thrombosis)
Cardiac causes of abnormal spectral Doppler ndings
Vasculitis
Inammatory vascular disease
Subclavian artery stenosis due to atherosclerosis
Axillary artery stenosis due to atherosclerosis
Distal axillary artery stenosis in arteritis
Cervical rib syndrome
Subclavian artery compression by cervical rib
Aneurysm of subclavian/axillary artery
Thoracic outlet syndrome with poststenotic dilatation
Pectoralis minor syndrome
Takayasu’s arteritis with subclavian artery occlusion
Aneurysm of the ulnar artery (hypothenar syndrome)
Interdigital artery occlusion– Raynaud’s disease
Radial artery occlusion with peripheral ischemia
Fig.2.79 (Atlas), page 146
.
Fig.2.79 (Atlas), page 146
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Fig.2.79 (Atlas), page 146
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Fig.2.80 (Atlas), page 146
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Fig.2.81 (Atlas), page 147
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Fig.2.81 (Atlas), page 147
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Fig.2.82 (Atlas), page 148
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Fig.2.83 (Atlas), page 148
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Fig.2.84 (Atlas), page 149
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Fig.2.85 (Atlas), page 149
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Fig.2.86 (Atlas), page 150
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Fig.2.87 (Atlas), page 150
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Fig.2.88 (Atlas), page 151
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Fig.2.89 (Atlas), page 152
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Fig.2.90 (Atlas), page 152
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Fig.2.91 (Atlas), page 153
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Fig.2.92 (Atlas), page 154
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Fig.2.93 (Atlas), page 154
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Fig.2.94 (Atlas), page 155
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Fig.2.95 (Atlas), page 156
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Fig.2.96 (Atlas), page 156
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Fig.2.97 (Atlas), page 157
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Fig.2.98 (Atlas), page 157
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Fig.2.99 (Atlas), page 158
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Fig.2.100 (Atlas), page 158
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Fig.2.101 (Atlas), page 159
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Fig.2.102 (Atlas), page 159
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Fig.2.103 (Atlas), page 160
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Fig.2.103 (Atlas), page 160
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Fig.2.104 (Atlas), page 161
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Fig.2.104 (Atlas), page 161
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Fig.2.105 (Atlas), page 162
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Fig.2.106 (Atlas), page 163
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Fig.2.107 (Atlas), page 163
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Fig.2.108 (Atlas), page 164
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Fig.2.109 (Atlas), page 164
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Fig.2.110 (Atlas), page 165
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Fig.2.111 (Atlas), page 165
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126
femoral circumflex artery
Chapter 2 · Extremity Arteries
2
a
1 Middle sacral artery
2 Common iliac artery
3 External iliac artery
4 Inferior epigastric artery
5 Deep circumflex iliac artery
6 Internal iliac artery
7 lliolumbar artery
8 Lateral sacral artery
9 Superior gluteal artery
10 Inferior gluteal artery
11 Internal pudendal artery
12 Middle rectal artery
13 Obturator artery
14 Uterine artery
15 Inferior vesical artery
16 Superficial epigastric artery
17 (Common) femoral artery
18 External pudendal artery
19 Profunda femoris artery
20 (Superficial) femoral artery
21 Perforating arteries
22 Superficial circumflex iliac artery
23 Medial femoral circumflex artery
24 Lateral femoral circumflex artery
25 Ascending branch of lateral femoral
circumflex artery
26 Descending branch of lateral
27 Transverse branch of lateral femoral circumflex artery
28 Muscular branches of femoral and profunda femoris arteries
29 Descending genicular artery
30 Popliteal artery
31 Articular branch of descending genicular artery
32 Saphenous branch of descending genicular artery
33 Lateral superior genicular artery
34 Medial superior genicular artery
35 Lateral inferior genicular artery
36 Medial inferior genicular artery
37 Sural artery
38 Anterior tibial artery
39 Posterior tibial artery
40 Fibular (peroneal) artery
41 Anterior tibial recurrent artery
42 Dorsalis pedis artery
43 Perforating branch of fibular artery
44 Medial tarsal artery
45 Lateral plantar artery
46 Lateral tarsal artery
47 Medial plantar artery
48 Arcuate artery
49 Deep branch of dorsalis pedis artery
50 Dorsal and plantar metatarsal arteries,
dorsal and plantar digital arteries
51 Medial malleolar branch
52 Lateral malleolar branch
b
. Fig. 2.50 (Atlas) Vascular anatomy.
a Pelvic arteries.
b Leg arteries (courtesy of Eastman Kodak Company)

c
2.3 · Atlas: Extremity Arteries
a
127
2
b
. Fig. 2.51 (Atlas) Femoral bifurcation– normal blood ow.
a Gray-scale and color duplex imaging supplement each other: along the course of an artery, some segments may be better appreciated in
the B-mode image, others in the color ow mode. In the example, the supercial femoral artery (A.F.S) and profunda femoris artery (A.P.F) are
insonated with a smaller angle, improving their visualization in the color mode, whereas wall structures perpendicular to the ultrasound beam
(here: common femoral artery, A.F.C, left part of image) are seen more clearly in the B-mode image. Ultrasound pulses striking the vessel wall at a
perpendicular angle produce a detailed image of the wall, which is a strong reector. In contrast, a smaller angle between the direction of owing
blood and the beam is necessary to ensure accurate spectral Doppler measurement and reliable evaluation of blood ow. Although all extremity arteries have a triphasic pulsatile ow prole under normal conditions, resulting from the high peripheral resistance at rest, dierent spectral
waveforms may be obtained, depending on the territory supplied by the artery interrogated. High-resistance ow as in the supercial femoral
artery, which mostly supplies skin and subcutaneous tissue and only some muscle tissue, gives rise to a pulsatile, triphasic waveform with zero
ow in end diastole. The example shows the femoral bifurcation with the Doppler sample volume placed in the supercial femoral artery (A.F.S).
Blue indicates arterial ow away from the transducer, red the ow in the supercial femoral vein toward the transducer. The corresponding Doppler tracings illustrate the hemodynamic situation at rest (left waveform) and after exercise (right waveform). Peak systolic velocity (PSV) increases
from 90cm/s at rest to 141cm/s after exercise (ten tiptoe movements). The increased muscular blood demand during exercise is met by a decrease
in peripheral resistance and is reected in the Doppler waveform by an increase in end-diastolic velocity (EDV) from 0 (left waveform) to 16cm/s
(right waveform).
b Femoral bifurcation: The profunda femoris (A.P.F) supplying more muscle tissue has a slightly less pulsatile ow but the prole is still triphasic. At
rest (left waveform), PSV is 77cm/s and EDV is 7cm/s. After exercise (right waveform), PSV increases to 90cm/s with EDV doubling to 15cm/s. The
color change from red, to black, to blue reects the change in ow direction relative to the ultrasound beam (toward transducer: red; away from
transducer: blue) (A.F.S=supercial femoral artery; A.F.C=common femoral artery).
c In patients with occlusion of the supercial femoral artery (A.F.S), the profunda femoris is the main collateral to bridge the occluded segment
and supply the supercial femoral territory. When the profunda femoris artery is recruited as a collateral, the higher ow volume in the profunda
femoris circulation may result in a 40–60% increase in blood ow velocity without this indicating stenosis at its origin. In the example shown, a PSV
of 145cm/s and an EDV of 18cm/s are measured in the profunda femoris artery (A.P.F) bridging the occluded supercial femoral artery. Reversed
ow due to eddy currents at the origin of the occluded supercial femoral artery is displayed in red (knocking waveform)

128
bc
Chapter 2 · Extremity Arteries
2
a
d
. Fig. 2.52a–d (Atlas) Pelvic artery stenosis.
a In evaluating a patient with suspected ow obstruction at the pelvic level, the examiner rst obtains Doppler tracings from both common femoral arteries to compare these with regard to triphasic ow, steep systolic upslope, and peak systolic velocity (PSV). Reliable Doppler shift analysis
requires an insonation angle below 60°. In this example, the angle is 50° on the right and 54° on the left. The Doppler waveform from the right
groin shows triphasic ow with a systolic upslope and a PSV>80cm/s.
b The waveform from the left common femoral artery illustrates postocclusive ow with a monophasic prole, reduced PSV (57cm/s), and delayed
systolic rise.
c The monophasic ow prole is due to high-grade stenosis of the common iliac artery (A.I.C) caused by plaque, mainly of the posterior wall.
Sonographic signs of stenosis in this case are aliasing in the color duplex image and a Doppler-derived PSV of over 4m/s. Due to aliasing, the
velocity peaks are cut o, and PSV must be interpolated (approx. 4.5m/s). The simplied Bernoulli equation, P=4 x (PSV x PSV), yields a maximum
pressure gradient of 81mmHg across the stenosis, resulting in a poststenotic decrease in systolic velocity.
d Angiogram demonstrates the high-grade iliac artery stenosis as a lling defect in the lumen

2.3 · Atlas: Extremity Arteries
abc
de f
129
2
gh
Epigastric circulation
Lumbar circulation
Mesenteric circulation
Iliofemoral circulation
Profunda femoris
circulation
Collateral recipient
R
segment of popliteal
artery
i
. Fig. 2.53a–i (Atlas) Iliac artery stenosis with good collateralization– Doppler waveform analysis.
a–i Ultrasound protocol based on segmental spectral Doppler evaluation illustrated in a 58-year-old patient with stage IIa peripheral arterial occlusive disease (PAOD) and a walking distance of >1km. The patient has high-grade common iliac artery stenosis with very good collateralization and
an ankle-brachial index (ABI) of 0.9 (versus 1.1 on the left).
a The Doppler waveform from the right groin is triphasic. The peak systolic velocity (PSV) is 154cm/s with an acceleration time of 75ms.
b A triphasic Doppler waveform is also obtained from the left groin; however, the PSV is 85cm/s and systolic rise is delayed with a prolonged accel-
eration time of 143ms.
c Triphasic Doppler waveform and PSV of 60cm/s in the right popliteal artery.
d Triphasic Doppler waveform with a lower PSV of 50cm/s in the left popliteal artery. Overall, the velocity peaks are slightly damped compared with
the waveform from the contraleral popliteal artery (c). To ensure reliable acoustic and visual spectral analysis as illustrated here, it is important to
perform spectral Doppler imaging with small angles of insonation (<50°).
e On the left side, blood ow begins to return to normal 1min after activity, as shown by the triphasic waveform. Only PSV (170cm/s) is still slightly
higher compared with the situation at rest (compare waveform obtained 5min after activity in a).
f The Doppler waveform obtained from the right proximal common femoral artery 1min after rapidly walking a distance of 50m shows monophasic
ow and a delayed systolic rise. These ndings indicate that ow has not yet returned to normal, and a longer period of rest is necessary before a
triphasic waveform is obtained (b).
g High-grade common iliac artery stenosis with a PSV of 6m/s. The pressure gradient across the stenosis, calculated using the simplied Bernoulli
equation, is 4 x (PSV x PSV)=4 x (6 x 6)=144mmHg.
h In the common iliac artery just upstream of the stenosis, a PSV of 40cm/s is measured, corresponding to a 15-fold PSV increase in the stenosis,
consistent with subtotal occlusion.
i Diagram of collateral pathways that can be recruited to bridge arterial obstruction at the pelvic and thigh levels. The better the collateral circulation, the less marked the changes in the postocclusive Doppler waveform

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d ef
bc
ab
Chapter 2 · Extremity Arteries
2
a
g
. Fig. 2.54a–g (Atlas) Iliac artery– stenosis/occlusion and collateral pathways.
a The iliac bifurcation with the origin of the internal iliac artery (A.I.I) is situated at the deepest point of the true pelvis. The internal iliac artery
courses posteriorly (blue, away from transducer, toward periphery). The waveform shows a pulsatile prole but with diastolic ow because the
internal iliac artery empties into the pelvic vessels. The color change from red to blue in the bifurcation is due to the changed ow direction relative to the ultrasound beam. With the high PRF selected to depict fast arterial ow, no ow signals are obtained from the iliac vein (V) posterior to
the artery (A.I.E=external iliac artery; A.I.C=common iliac artery).
b, c 54-year-old patient with intermittent claudication with a short walking distance and erectile dysfunction (see 7 Chap. 7) due to external iliac
artery occlusion (Doppler waveform with wall pulsation but no ow signals) and concomitant high-grade internal iliac stenosis (aliasing and peak
systolic velocity (PSV) of 4m/s).
d Oblique angiographic projection showing right-sided external iliac artery occlusion and internal iliac artery stenosis. The internal iliac artery
stenosis on the left is obscured by superimposed structures.
e In common iliac artery occlusion, the internal iliac artery supplies the external iliac artery and shows retrograde ow (red, toward transducer).
No ow signal in the common iliac artery (A.I.C).
f The relled external iliac artery (A.I.E) is depicted with normal ow toward the periphery (red). The waveform is monophasic, consistent with
postocclusive ow.
g Angiogram showing common iliac artery occlusion
. Fig. 2.55a, b (Atlas) Common iliac artery stenosis.
a Stenosis of the iliac and common femoral arteries is typically caused by eccentric plaque on the posterior wall, and angiographic grading is difcult when only an anteroposterior view is obtained. In the example, ultrasound demonstrates high-grade stenosis at the origin of the common
iliac artery with aliasing and a Doppler-derived PSV of 6m/s.
b The angiogram suggests a stenosis with 50–60% diameter reduction at the origin of the common iliac artery. The angiographic underestimation
of stenosis in this territory underlines the importance of obtaining dierent angiographic projections for adequate diagnostic evaluation– even
if a segment appears fairly normal or shows only mild to moderate stenosis. This is also important to ensure comparability of angiography and
ultrasound

2.3 · Atlas: Extremity Arteries
. Fig. 2.56a–d (Atlas) Iliac
artery aneurysm– stenting.
a Partially thrombosed common
iliac artery aneurysm. The left
image shows the origin of the
common iliac artery from the
aorta (AO) and the aneurysm
(AN). The right image shows the
partially thrombosed aneurysm
(AN) and the iliac bifurcation
(A.I.E.= external iliac artery).
b CT scan showing the partially
thrombosed iliac artery aneurysm.
c Color duplex imaging after
endovascular repair with a covered stent demonstrates normal
ow in the stent. No signs of
endoleak or stenosis. The waveform shown is from the distal
stent end.
d CT angiography (3D reconstruction) conrms elimination of the
iliac artery aneurysm (arrow) after
stent placement
131
2
a
b
c
. Fig. 2.57 (Atlas) Floating plaque in common femoral artery in a
patient with blue toe.
Multiple plaques in the common femoral artery in a 72-year-old patient
with blue toe. The peripheral arteries, unlike the carotid arteries, rarely
harbor embolizing plaques that give rise to thromboembolic complications. Therefore, the presence of plaque alone does not prove that it is
the cause of embolism, and the examiner has to look for other possible
sources (cardiac thrombus, partially thrombosed aneurysm). In unclear
cases, as in the example shown here, the time-motion mode can
demonstrate plaque motion (arrow). Demonstration of plaque oating
in the bloodstream is an indication for local TEA even if the stenosis
caused by the plaque is of little hemodynamic relevance
d

132
Chapter 2 · Extremity Arteries
2
a
bcd
. Fig. 2.58 (Atlas) High-grade stenosis/occlusion of common femoral artery.
a High-grade stenosis of the common femoral artery caused by eccentric posterior plaque just upstream of the origin of the profunda femoris
artery. The ratio of intrastenotic to prestenotic peak systolic velocity (PSV ratio) is 10.
b Intraoperative site showing the characteristic “cauliower” appearance of eccentric posterior wall plaque. A segment from the common femoral
artery to the profunda femoris artery has been incised longitudinally. The lumen of the supercial femoral artery is also narrowed and the artery is
clamped o at its origin. A curved clamp is in place around the proximal end of the common femoral artery. Eccentric posterior wall plaque typically occurs in the common femoral and external iliac arteries and may be dicult to appreciate on anteroposterior angiograms (see . Fig.2.17).
Common femoral artery occlusion– collateralization.
c, d Occlusion (absence of ow signals) of the common femoral artery with relling of the supercial femoral artery (A.F.S; forward ow coded in
blue, away from transducer) via the profunda femoris artery (A.P.F), which shows ow reversal at its origin (red, toward transducer). These ndings
indicate good collateralization (PSV of 53cm/s). The profunda femoris artery is supplied by the femoral circumex artery (A.C). The Doppler waveform shows postocclusive ow (monophasic, delayed systolic rise). In addition, there is plaque with posterior acoustic shadowing in the common
femoral artery (see . Fig.2.11)
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