Diagnostic Ultrasound, 2-Volume Set [2-Volume Set, 6 ed.] 0323877958, 9780323877954

Table of contents :
Cover
Front Matter
Copyright
About the Editors
Contributors
Dedication
Preface
Acknowledgments
Our Cover
Video Contents
ONE - Ultrasound Physics, Bioeffects, and Contrast
1. Physics of Ultrasound
BASIC ACOUSTICS
Wavelength and Frequency
Propagation of Sound
Distance Measurement
Acoustic Impedance
Reflection
Refraction
Attenuation
INSTRUMENTATION
Transmitter
Transducer
Receiver
Image Display
Mechanical Sector Scanners
Arrays
Linear Arrays
Curved Arrays
Phased Arrays
Transducer Selection
IMAGE DISPLAY AND STORAGE
SPECIAL IMAGING MODES
Tissue Harmonic Imaging
Spatial Compounding
Three-Dimensional Ultrasound
Ultrasound Elastography
Strain Elastography
Shear Wave Elastography
IMAGE QUALITY
Spatial Resolution
DOPPLER SONOGRAPHY
Doppler Signal Processing and Display
Doppler Instrumentation
Power Doppler
Interpretation of the Doppler Spectrum
Interpretation of Color Doppler
Other Technical Considerations
Doppler Frequency
Wall Filters
Spectral Broadening
Doppler Angle
Sample Volume Size
Doppler Gain
ULTRASOUND ARTIFACTS
Assumptions in Gray-Scale Imaging
Speed of Sound Artifacts
Attenuation of Sound Artifacts
Shadowing
Increased Through-Transmission
Path of Sound-Related Artifacts
Mirror Image Artifact
Reverberation Artifact
Comet-Tail Artifact
Refraction Artifact
Anisotropy
Gas-Related Artifacts
Ring-Down Artifact
Dirty Shadowing Artifact
Beam Profile-Related Artifacts
Side Lobe and Grating Lobe Artifacts
Partial Volume Averaging
Doppler Imaging Artifacts
Loss or Distortion of Doppler Information
Artifactual Vascular Flow
Tissue Vibration Artifact
Aliasing and Velocity Scale Errors
Artifactual Spectral Broadening
Blooming Artifact
Twinkle Artifact
THERAPEUTIC APPLICATIONS: HIGH-INTENSITY FOCUSED ULTRASOUND
ACKNOWLEDGMENT
REFERENCES
2 Biologic Effects and Safety
2. Biologic Effects and Safety
Regulation of Ultrasound Output
Physical Effects of Sound
Effects of Acoustic Cavitation
Potential Sources for Bioeffects
Sonochemistry
Mechanical Index
Evidence of Cavitation From Lithotripters
Bioeffects in Lung and Intestine
Ultrasound Contrast Agents
Considerations for Increasing Acoustic Output
Summary Statement on Gas Body Bioeffects
Thermal Effects
Ultrasound Produces Heat
Factors Controlling Tissue Heating
Spatial Focusing
Temporal Considerations
Tissue Type
Bone Heating
Soft Tissue Heating
Hyperthermia and Ultrasound Safety
Thermal Index
Homogeneous Tissue Model (Soft Tissue)
Tissue Model With Bone at the Focus (Fetal Applications)
Tissue Model With Bone at the Surface (Transcranial Applications)
Estimate of Thermal Effects
Summary Statement on Thermal Effects
Output Display Standard
General AIUM Safety Statements
Epidemiology
Controlling Ultrasound Output
Impact on Image Quality
Ocular Imaging Safety
Obstetric Ultrasound Safety
Ultrasound Entertainment Videos
Conclusion
References
3 Contrast Agents for Ultrasound
3. Contrast Agents for Ultrasound: From Principles to Practice
INTRODUCTION
CONTRAST AGENTS FOR ULTRASOUND
Contrast Agent Types
Blood Pool Agents
Free Gas Bubbles
Encapsulated Air Bubbles
``Second-Generation'' Agents
Selective Uptake Agents
THE NEED FOR BUBBLE-SPECIFIC IMAGING
Bubble Behavior and Incident Pressure
The Mechanical Index
NONLINEAR ECHOES AND HARMONIC IMAGING
Harmonic B-mode Imaging
Harmonic Spectral and Power Doppler Imaging
Tissue Harmonic Imaging
Pulse Inversion Imaging
Pulse Inversion Doppler Imaging
Plane-Wave Contrast Imaging
Amplitude and Phase Modulation Imaging
Temporal Maximum Intensity Projection Imaging
DISRUPTING BUBBLES: INTERMITTENT IMAGING
Triggered Imaging
Intermittent Harmonic Power Doppler for Bubble Detection
Disruption-Replenishment Imaging: Measuring Perfusion
SUMMARY OF MICROBUBBLE CONTRAST PRINCIPLES
SAFETY CONSIDERATIONS AND REGULATORY STATUS
HOW TO START A CONTRAST-ENHANCED ULTRASONOGRAPHY PRACTICE
Clinical Applications
Practical Considerations
Initially, Focus on 1-2 Key Areas/Organs
Renal
Liver
US Guided Interventions
Endovascular Aortic Repair Endoleak Detection
Vesicoureteral Reflux
US/PACS Equipment Requirements
Ultrasound Contrast Agent Selection/Patient Safety Requirements
Training (Radiologist/Sonographer)
Contrast-Enhanced Ultrasonography Workflow
Ordering/Scheduling/Billing
Patient History Evaluation
Who Will Start the Intravenous, Prepare and Inject the Contrast
Day of Study
Contrast-Enhanced Ultrasonography Study
Market Your Contrast-Enhanced Ultrasonography Capabilities
Limitations
CONCLUSION
THE FUTURE
REFERENCES
4 The Liver
TWO - Abdominal Sonography
4. The Liver
SONOGRAPHIC TECHNIQUE
NORMAL ANATOMY
Couinaud Anatomy
Ligaments
Hepatic Circulation
Portal Veins
Arterial Circulation
Hepatic Venous System
Normal Liver Size and Echogenicity
DEVELOPMENTAL ANOMALIES
Agenesis
Anomalies of Position
Accessory Fissures
Vascular Anomalies
CONGENITAL ABNORMALITIES
Liver Cyst
Peribiliary Cysts
Autosomal Dominant Polycystic Disease
Biliary Hamartomas (von Meyenburg Complexes)
INFECTIOUS DISEASES
Viral Hepatitis
Clinical Manifestations
Bacterial Diseases
Fungal Diseases: Candidiasis
Parasitic Diseases
Amebiasis
Hydatid Disease
Schistosomiasis
Other infections
DISORDERS OF METABOLISM
Fatty Liver
Glycogen Storage Disease (Glycogenosis)
Cirrhosis
Doppler Ultrasound Characteristics
Elastography
VASCULAR ABNORMALITIES
Portal Hypertension
Portal Vein Thrombosis
Budd-Chiari Syndrome
Portal Vein Aneurysm
Intrahepatic Portosystemic Venous Shunts
Aneurysm, Pseudoaneurysm, and Dissection
Hereditary Hemorrhagic Telangiectasia
Peliosis Hepatis
HEPATIC MASSES
Liver Mass Characterization With Gray-Scale and Doppler Sonography
Liver Mass Evaluation With Contrast-Enhanced Ultrasound
Advantages Unique to Contrast-Enhanced Ultrasound
Lesional Enhancement
Liver Mass Detection
PRIMARY BENIGN HEPATIC NEOPLASMS
Cavernous Hemangioma
Focal Nodular Hyperplasia
Hepatic Adenoma
Fatty Tumors: Hepatic Lipomas and Angiomyolipomas
PRIMARY MALIGNANT HEPATIC NEOPLASMS
Hepatocellular Carcinoma
CEUS LI-RADS
LI-RADS Malignant Categories
Fibrolamellar Carcinoma
Hemangiosarcoma (Angiosarcoma)
Hepatic Epithelioid Hemangioendothelioma
METASTATIC LIVER DISEASE
Peripheral Cholangiocarcinoma
Kaposi Sarcoma
HEPATIC TRAUMA
Portosystemic Shunts
Transjugular Intrahepatic Portosystemic Shunts
PERCUTANEOUS LIVER BIOPSY
INTRAOPERATIVE ULTRASOUND
CONCLUSION
ACKNOWLEDGMENTS
References
5 The Spleen
5. The Spleen
EMBRYOLOGY, ANATOMY, AND FUNCTION
SONOGRAPHIC TECHNIQUE
SONOGRAPHIC APPEARANCE
Elastography
PATHOLOGIC CONDITIONS
Splenomegaly
Focal Abnormalities
Splenic Cysts
Nodular Splenic Lesions
Focal Solid Splenic Lesions
Malignancies
Benign Lesions
Other Abnormalities
Sickle Cell Disease
Gaucher Disease
Gamna-Gandy Bodies
Splenic Trauma
CONGENITAL ANOMALIES
INTERVENTIONAL PROCEDURES
PITFALLS IN INTERPRETATION
CONCLUSION
ACKNOWLEDGMENT
REFERENCES
6 The Biliary Tree and Gallbladder
6. The Biliary Tree and Gallbladder
THE BILIARY TREE
Anatomy and Normal Variants
Sonographic Technique
Choledochal Cysts (Congenital Biliary Dilatation)
Caroli Disease
Overview of Biliary Tree Obstruction
Choledocholithiasis
Intrahepatic Stones
Common Bile Duct Stones
Mirizzi Syndrome
Hemobilia
Pneumobilia
Biliary Tree Infection
Acute (Bacterial, Ascending) Cholangitis
Low Phospholipid-Associated Cholelithiasis Syndrome
Liver Flukes
Recurrent Pyogenic Cholangitis
Ascariasis
HIV Cholangiopathy
Immune-Related Diseases of the Biliary Tree
Primary Biliary Cirrhosis and Autoimmune Cholangitis
Sclerosing Cholangitis
Primary Sclerosing Cholangitis
IgG4-Related Cholangitis
Cholangiocarcinoma
Intrahepatic Cholangiocarcinoma
Hilar Cholangiocarcinoma
Assessment by Contrast-Enhanced Sonography
Distal Cholangiocarcinoma
Metastases to Biliary Tree
THE GALLBLADDER
Anatomy and Normal Variants
Sonographic Technique
Gallstone Disease
Biliary Sludge
Acute Cholecystitis
Coexisting Common Bile Duct Stones
Gangrenous Cholecystitis
Perforated Gallbladder
Emphysematous Cholecystitis
Acalculous Cholecystitis
Hemorrhagic Cholecystitis
Torsion (Volvulus) of Gallbladder
Xanthogranulomatous Cholecystitis
Porcelain Gallbladder
Adenomyomatosis (Adenomatous Hyperplasia)
Polypoid Masses of Gallbladder
Management of Gallbladder Polyps
Cholesterol Polyps
Adenomas, Adenomyomas, Inflammatory, and Fibromyoglandular Polyps
Gallbladder Malignancies
Gallbladder Carcinoma
Patterns of Tumor Spread
Sonographic Appearance
Metastases to the Gallbladder
REFERENCES
7 Pancreatic Sonography
7. Pancreatic Sonography
INTRODUCTION
ANATOMY AND SONOGRAPHIC TECHNIQUE
Pancreatic Body
Pancreatic Head
Pancreatic Tail
Pancreatic Parenchyma
Fatty Pancreas
Embryology and Pancreatic Duct
Imaging Anatomic Variants
Peripancreatic Structures
ACUTE PANCREATITIS
Approach to Imaging
Ultrasound Findings
Complications
Acute Fluid Collections
Pseudocysts
Necrosis and Abscess
Treatment
Vascular Complications
CHRONIC PANCREATITIS
Approach to Imaging
Ultrasound Findings
Pseudocysts
Portal and Splenic Vein Thrombosis
Masses Associated With Chronic Pancreatitis
PANCREATIC NEOPLASMS
Periampullary Neoplasm
Pancreatic Carcinoma
Detection of Pancreatic Cancer
Ultrasound Findings
Resectability Imaging
Color Doppler Ultrasound
Biopsy
CYSTIC PANCREATIC LESIONS
Simple Pancreatic Cysts
Cystic Neoplasms
Serous Cystic Neoplasm
Intraductal Papillary Mucinous Neoplasm
Mucinous Cystic Neoplasm
Solid-Pseudopapillary Tumor
Rare Cystic Tumors
OTHER PANCREATIC MASSES
Endocrine Tumors
Unusual and Rare Neoplasms
Lipoma
Metastatic Tumors
CONTRAST-ENHANCED ULTRASOUND
CONCLUSION
ACKNOWLEDGMENT
REFERENCES
8 The Gastrointestinal Tract
8. The Gastrointestinal Tract
ANATOMY AND SONOGRAPHIC TECHNIQUE
The Gut Signature
Gut Wall Pathology
Imaging Technique
Gray-Scale Imaging
Doppler Evaluation of Gut Wall
Contrast-Enhanced Ultrasound and Elastography of the Bowel
GASTROINTESTINAL TRACT NEOPLASMS
Adenocarcinoma
Gastrointestinal Stromal Tumors
Lymphoma
Metastases
Benign Bowel Lesions
INFLAMMATORY BOWEL DISEASE: CROHN DISEASE
Classic Features
Gut Wall Thickening
Inflammatory Fat
Lymphadenopathy
Hyperemia
Mucosal Abnormalities
Conglomerate Masses
Complications
Strictures
Incomplete Mechanical Bowel Obstruction
Localized Perforation
Inflammatory Masses
Fistula Formation
Perianal Inflammatory Disease
ACUTE ABDOMEN
Right Lower Quadrant Pain
Acute Appendicitis
Granulomatous Appendicitis
Right-Sided Diverticulitis
Acute Typhlitis
Mesenteric Adenitis With Terminal Ileitis
Segmental Omental Infarction
Left Lower Quadrant Pain
Acute Diverticulitis
Epiploic Appendagitis
OTHER ABNORMALITIES
Mechanical Bowel Obstruction
Paralytic Ileus
Gut Edema
Gastrointestinal Tract Infections
AIDS Patients
Pseudomembranous Colitis
Congenital Cysts
Ischemic Bowel Disease
Pneumatosis Intestinalis
Mucocele of Appendix
Gastrointestinal Tract Hematoma
Peptic Ulcer
Bezoars
Intraluminal Foreign Bodies
Celiac Disease
Cystic Fibrosis
ENDOSONOGRAPHY
Upper Gastrointestinal Tract
Gastric Lymphoma
Rectum: Tumor Staging of Rectal Carcinoma
Anal Canal
Fecal Incontinence
Perianal Inflammatory Disease
CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
9 The Kidney and Urinary Tract
9. The Kidney and Urinary Tract
EMBRYOLOGY
Development of the Kidneys and Ureter
Development of the Bladder
Development of the Urethra
ANATOMY
Kidney
Ureter
Bladder
SONOGRAPHIC TECHNIQUE
Kidney
Ureter
Bladder and Urethra
HYDRONEPHROSIS
PITFALLS IN ASSESSMENT OF OBSTRUCTION
CONGENITAL ANOMALIES
Anomalies Related to Renal Growth
Hypoplasia
Fetal Lobation
Compensatory Hypertrophy
Anomalies Related to Ascent of Kidney
Ectopia
Crossed Renal Ectopia
Horseshoe Kidney
Anomalies Related to Ureteral Bud
Renal Agenesis
Supernumerary Kidney
Duplex Collecting System and Ureterocele
Ureteropelvic Junction Obstruction
Congenital Megacalyces
Congenital Megaureter
Anomalies Related to Vascular Development
Aberrant Vessels
Retrocaval Ureter
Anomalies Related to Bladder Development
Bladder Agenesis
Bladder Duplication
Bladder Exstrophy
Urachal Anomalies
Anomalies Related to Urethral Development: Diverticula
GENITOURINARY INFECTIONS
Pyelonephritis
Acute Pyelonephritis
Renal and Perinephric Abscess
Pyonephrosis
Emphysematous Pyelonephritis
Emphysematous Pyelitis
Chronic Pyelonephritis
Xanthogranulomatous Pyelonephritis
Papillary Necrosis
Tuberculosis
Fungal Infections
Candida Albicans
Parasitic Infections
Schistosomiasis
Echinococcal (Hydatid) Disease
Acquired Immunodeficiency Syndrome
Cystitis
Infectious Cystitis
Malacoplakia
Emphysematous Cystitis
Chronic Cystitis
FISTULAS, STONES (CALCULI), AND CALCIFICATION
Bladder Fistulas
Renal Calculi
Staghorn Calculus
Ureteral Calculi
Bladder Calculi
Nephrocalcinosis
GENITOURINARY TUMORS
Renal Cell Carcinoma
Imaging and Treatment Approaches
Sonographic Appearance
Biopsy and Prognosis
Pitfalls in Interpretation
Urothelial Carcinoma
Renal Tumors
Ureteral Tumors
Bladder Tumors
Squamous Cell Carcinoma
Adenocarcinoma
Oncocytoma
Angiomyolipoma
Lymphoma
Leukemia
Metastases
Urachal Adenocarcinoma
Rare Neoplasms
Kidney
Bladder
RENAL CYSTIC DISEASE
Cortical Cysts
Parapelvic Cysts
Medullary Cysts
Medullary Sponge Kidney
Medullary Cystic Disease
Polycystic Kidney Disease
Multicystic Dysplastic Kidney
Lithium Nephropathy
Multilocular Cystic Nephroma
Localized Cystic Disease
Neoplasm-Associated Renal Cystic Disease
Acquired Cystic Kidney Disease
Von Hippel-Lindau Disease
Tuberous Sclerosis
TRAUMA
Renal Injuries
Ureteral Injuries
Bladder Injuries
VASCULAR ABNORMALITIES
Renal Vascular Doppler Sonography
Renal Artery Occlusion and Infarction
Arteriovenous Fistula and Malformation
Renal Artery Stenosis
Renal Artery Aneurysm
Renal Vein Thrombosis
Ovarian Vein Thrombosis
MEDICAL GENITOURINARY DISEASES
Acute Tubular Necrosis
Acute Cortical Necrosis
Glomerulonephritis
Acute Interstitial Nephritis
Diabetes Mellitus
Amyloidosis
Endometriosis
BLADDER OUTLET OBSTRUCTION
Interstitial Cystitis
NEUROGENIC BLADDER
BLADDER DIVERTICULA
POSTSURGICAL EVALUATION
Nephrectomy
Urinary Diversion
CONTRAST ENHANCED ULTRASOUND
CONCLUSION
ACKNOWLEDGMENT
REFERENCES
10 The Prostate and Transrectal Ultrasound
10. The Prostate and Transrectal Ultrasound
INTRODUCTION
ANATOMY
Zonal Anatomy
Vascular and Neural Structures
SONOGRAPHIC APPEARANCE
EQUIPMENT AND TECHNIQUES
BENIGN CONDITIONS
Normal Variants
Benign Prostatic Hyperplasia
Chronic Prostatitis/Chronic Pelvic Pain Syndrome
Prostate Cysts
Seminal Vesicles and Vas Deferens
INFERTILITY AND TRANSRECTAL ULTRASOUND
HEMATOSPERMIA
PROSTATE CANCER
Epidemiology
Prostate-Specific Antigen and Variants
Alternate Prostate Cancer Biomarkers
Multiparametric Magnetic Resonance Imaging
Screening
Clinical Staging and Histological Grading
Therapy
Sonographic Appearance of Prostate Cancer
Gray-Scale Ultrasound
Color and Power Doppler Imaging
Multiparametric Ultrasound
Contrast-Enhanced Ultrasound
Three-Dimensional Ultrasound and TRUS/MR fusion
Elastography
MICRO-ULTRASOUND
ULTRASOUND GUIDED BIOPSY
Indications
Preparation for Biopsy
Antibiotic Prophylaxis
Bowel Preparation
Analgesia
Anticoagulation
Technique
Side Effects and Complications
Sampling
MpMRI-TRUS Fusion Biopsy
Transperineal and Template Biopsy
Biopsy After Radical Prostatectomy
Biopsy in Men With Absent Anus
OTHER APPLICATIONS OF TRUS AND BIOPSY IN MEN AND WOMEN
CONCLUSION
REFERENCES
11 The Adrenal Glands
11. The Adrenal Glands
ANATOMY AND PHYSIOLOGY
SONOGRAPHIC IMAGING AND SCANNING TECHNIQUE
BENIGN ADRENAL MASSES
Adrenal Adenomas
Myelolipomas
Pheochromocytomas
Adrenal Cysts
Adrenal Hemorrhage
Infectious and Inflammatory Masses
MALIGNANT ADRENAL MASSES
Adrenocortical Carcinomas
Metastases
Lymphoma
RARE ADRENAL MASSES
MANAGEMENT OF ADRENAL LESIONS
INTERVENTIONS
Ultrasound-Guided Biopsy and Interventions
Endoscopic Ultrasound
Intraoperative Ultrasound
CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
12 Retroperitoneal Sonography
12. Retroperitoneal Sonography
INTRODUCTION
ATHEROSCLEROSIS
Association of Atherosclerosis and Abdominal Aortic Aneurysm
ABDOMINAL AORTIC ANEURYSM
Normal Anatomy
Definition
Mortality
Pathophysiology
Natural History and Medical Therapy
Screening
Recent Studies
Ultrasound Approach
Surveillance
Sonographic Technique
Computed Tomography
False-Positive/False-Negative Results
Ultrasound Versus Computed Tomography for Evaluation of Rupture
Treatment Planning
Postoperative Ultrasound Assessment
OTHER ENTITIES CAUSING ABDOMINAL AORTIC DILATION
Inflammatory Abdominal Aortic Aneurysm
Arteriomegaly and Aortic Ectasia
Penetrating Ulcer and Acute Aortic Syndromes
Pseudoaneurysm
STENOTIC DISEASE OF THE ABDOMINAL AORTA
DISEASES OF ABDOMINAL AORTA BRANCHES
Renal Arteries
Anatomy
Renal Artery Stenosis and Renovascular Hypertension
Causes of Renal Artery Stenosis
Renal Artery Duplex Doppler Sonography
Doppler Interpretation
False-Positive/False-Negative Results
Renal Artery Aneurysm
Mesenteric Arteries
Anatomy
Mesenteric Ischemia
Acute Ischemia
Chronic Ischemia
Median Arcuate Ligament Syndrome
Mesenteric Artery Duplex Doppler Sonography
Mesenteric Duplex Interpretation
Iliac Veins and Inferior Vena Cava
Anatomy
Anatomic Variants
Thrombosis
Nutcracker Syndrome
Pelvic Congestion Syndrome/Pelvic Venous Insufficiency
Budd-Chiari Syndrome
Inferior Vena Cava Neoplasms
Other Inferior Vena Cava Findings
NONVASCULAR DISEASES OF THE RETROPERITONEUM
Solid Masses
Retroperitoneal Fibrosis
CONCLUSION
REFERENCES
13 Hernias of the Groin and Anterior Abdominal Wall
13. Dynamic Ultrasound of Hernias of the Groin and Anterior Abdominal Wall
TECHNICAL REQUIREMENTS
THE REPORT FOR DYNAMIC ULTRASOUND OF GROIN HERNIAS
HERNIA CONTENTS
DYNAMIC MANEUVERS
KEY SONOGRAPHIC LANDMARKS
INGUINAL AND INGUINAL REGION HERNIAS
Indirect Inguinal Hernias
Direct Inguinal Hernias
Femoral Hernias
Spigelian Hernias
Sports Hernias
ABDOMINAL WALL OR VENTRAL HERNIAS
Linea Alba Hernias
Umbilical Hernias
Paraumbilical or Periumbilical Hernias
Incisional Hernias
Multiple Hernias
ADDITIONAL ISSUES REGARDING HERNIAS
Recurrent Groin Hernias
Hernia Complications
Entities That Simulate Groin Hernias
Entities That Simulate Anterior Abdominal Wall Hernias
CONCLUSION
References
14 The Peritoneum
14. The Peritoneum
PERITONEUM, OMENTUM, AND MESENTERY
SONOGRAPHIC TECHNIQUE
ASCITES
PERITONEAL INCLUSION CYSTS
MESENTERIC CYSTS
PERITONEAL TUMORS
Peritoneal Carcinomatosis
Primary Tumors of Peritoneum
Pseudomyxoma Peritonei
PERITONITIS
Infectious Peritonitis
Abscess
Tuberculous Peritonitis
Noninfectious Peritonitis
Chemical Peritonitis
Noninfectious Granulomatous Peritonitis
Sclerosing Peritonitis
SEGMENTAL OMENTAL INFARCTION
EPIPLOIC APPENDAGITIS
MESENTERIC PANNICULITIS
PSEUDOLIPOMA OF THE GLISSON CAPSULE
ENDOMETRIOSIS
LEIOMYOMATOSIS PERITONEALIS DISSEMINATA
PNEUMOPERITONEUM
CONCLUSION
Acknowledgment
References
15 Biopsy of Chest, Abdomen, and Pelvis
15. Ultrasound-Guided Biopsy of Chest, Abdomen, and Pelvis
INTRODUCTION
Periprocedural Antithrombotic Management
Imaging Methods
Ultrasound
Computed Tomography
Pre-Procedure Considerations and Time-Out
PERCUTANEOUS NEEDLE BIOPSY
Indications and Contraindications
Imaging Methods
Needle Selection
Biopsy Procedure
Needle Visualization
Specific Anatomic Applications
Liver
Pancreas
Kidney
Adrenal Gland
Spleen
Lung
Complications
ULTRASOUND-GUIDED DRAINAGE
Indications and Contraindications
Catheter Selection
Patient Preparation
Diagnostic Aspiration
Catheter Placement
Drainage Procedure
Follow-Up Care
Catheter Removal
Abdominal and Pelvic Abscesses: General
Specific Anatomic Applications
Liver
Biliary Tract
Pancreas
Spleen
Kidney
PERCUTANEOUS CYST MANAGEMENT
Renal Cyst
Liver Cyst
Ovarian Cyst
CONCLUSION
REFERENCES
16 Solid-Organ Transplantation
16. Solid-Organ Transplantation
LIVER TRANSPLANTATION
Surgical Technique
Normal Liver Transplant Ultrasound
Arterial Complications
Hepatic Artery Thrombosis
Hepatic Artery Stenosis
Hepatic Artery Pseudoaneurysms
Arteriovenous Fistulas
Portal Vein Complications
Portal Vein Thrombosis
Portal Vein Stenosis
Portal Vein Steal
Venous Outflow (Inferior Vena Cava/Hepatic Vein) Complications
Biliary Complications
Biliary Strictures
Biliary Leaks
Recurrent Sclerosing Cholangitis
Biliary Sludge and Stones
Dysfunction of the Sphincter of Oddi
Parenchymal Abnormalities
Rejection
Infarction
Intrahepatic Abscess
Intrahepatic Solid Masses
Extrahepatic Fluid Collections
KIDNEY TRANSPLANTATION
Surgical Technique
Normal Kidney Transplant Ultrasound
Grayscale Assessment
Doppler Assessment
Arterial Complications
Renal Artery Thrombosis
Renal Artery Stenosis
Arteriovenous Fistula
Pseudoaneurysm
Venous Complications
Venous Stenosis
Urinary Obstruction
Parenchymal Abnormalities
Rejection
Interstitial Fibrosis and Tubular Atrophy
Acute Tubular Injury
Infection
Cortical Necrosis
Solid Renal Masses
Extrarenal Fluid Collections
Hematoma
Urinoma
Lymphocele
Abscess
PANCREAS TRANSPLANTATION
Surgical Technique
Normal Pancreas Transplant Ultrasound
Vascular Complications
Thrombosis
Arteriovenous Fistula
Pseudoaneurysm
Parenchymal Abnormalities
Fluid Collections
REFERENCES
17 Thyroid Gland and Cervical Lymph Node Sonography
III - THREE Small Parts, Carotid Artery, and Peripheral Vessel Sonography
17. Thyroid Gland and Cervical Lymph Node Sonography
INTRODUCTION
ULTRASOUND TECHNIQUE AND INSTRUMENTATION
Transducer Selection and Technique
Patient Positioning and Other Practical Considerations
Newer Ultrasound Techniques
Role of Other Imaging Modalities
THYROID EMBRYOLOGY, PHYSIOLOGY, AND ANATOMY
Embryology
Thyroid Physiology
Normal Thyroid Gland Anatomy, Ultrasound Appearance, and Size
CONGENITAL ABNORMALITIES
Pyramidal Lobe
Tubercle of Zuckerkandl and Other Developmental Abnormalities
Thyroglossal Duct Cysts
DIFFUSE THYROID DISEASE
Infectious and Inflammatory Conditions
Autoimmune Conditions
Infiltrative Disease in Systemic Conditions
BENIGN FOCAL THYROID DISEASE
Hyperplasia
Adenoma and Variants
Abscess
Intrathyroidal Parathyroid Adenoma
Ectopic Thymus
MALIGNANT FOCAL THYROID DISEASE
Papillary Carcinoma of the Thyroid
Classical Variant Papillary Carcinoma of the Thyroid
Follicular Variant Papillary Carcinoma of the Thyroid
Other Unusual Papillary Carcinoma of the Thyroid Variants
Noninvasive Follicular Thyroid Neoplasms With Papillary-Like Features
Follicular Carcinoma
Medullary Thyroid Carcinoma
Anaplastic Thyroid Carcinoma
Primary Thyroid Lymphoma
Thyroid Metastases
CASTLE Tumors
ULTRASOUND ASSESSMENT OF THYROID NODULES
Does a Nodule Correspond to a Palpable Abnormality or a Lesion on Another Imaging Modality?
What Is a Nodule's Malignancy Risk Based on Its Ultrasound Appearance?
Ultrasound-Based Risk Stratification: Signs of Malignancy
Composition
Echogenicity
Shape
Margin
Echogenic Foci
Size, Measurement, and Growth
Classic Benign Appearances
RISK STRATIFICATION SYSTEMS
ATA Guidelines and ACR TI-RADS: Similarities and Differences
Lymph Node Evaluation
Reporting Considerations
Other Factors Related to Malignancy Risk
Doppler Imaging and Contrast-Enhanced Ultrasound
Future of Thyroid Nodule Risk Stratification
THYROID NODULE BIOPSY
Fine-Needle Aspiration
Core-Needle Biopsy
Bethesda Classification
Mutations in Thyroid Cancer and Molecular Testing
ULTRASOUND EVALUATION OF CERVICAL LYMPH NODES
Technique and Anatomic Classification
Normal and Abnormal Lymph Nodes
Predictive Value of Nodal Assessment in Thyroid Cancer
Lymphadenopathy From Other Cancers
Other Ultrasound Techniques
ROLE OF ULTRASOUND FOLLOWING THYROID SURGERY
Indications and Technique
The Thyroid Bed
ROLE OF ULTRASOUND IN TREATING THYROID NODULES
Ethanol Ablation
Thermal Ablation
CONCLUSION
ACKNOWLEDGMENT
REFERENCES
18 Other Glands in the Head and Neck
18. Other Glands in the Head and Neck
PARATHYROID EMBRYOLOGY AND ANATOMY
Primary Hyperparathyroidism
Prevalence
Diagnosis
Pathology
Treatment
Sonographic Appearance
Shape
Echogenicity and Internal Architecture
Vascularity
Size
Multiple Gland Disease
Carcinoma
Adenoma Localization
Sonographic Examination and Typical Locations
Ectopic Locations
Retrotracheal/Retroesophageal Adenoma
Mediastinal Adenoma
Intrathyroid Parathyroid Adenoma
Carotid Sheath/Undescended Adenoma
Persistent or Recurrent Hyperparathyroidism
Secondary Hyperparathyroidism
Pitfalls in Interpretation
False-Positive Examination
False-Negative Examination
Accuracy in Imaging
Ultrasound
Other Modalities
Importance of Imaging in Primary Hyperparathyroidism
Intraoperative Sonography
Percutaneous Biopsy
SALIVARY GLANDS
Salivary Gland Embryology and Anatomy
Sonographic Examination and Sonographic Appearance
Obstructive Disease
Sialadenitis
Sialolithiasis
Ranula
Acute and Chronic Sialadenitis
Infectious Sialadenitis
Noninfectious Causes of Sialadenitis
Sjögren Disease
IgG4-related Salivary Disease
Juvenile Recurrent Parotitis
Salivary Gland Tumors
Primary Tumors of the Salivary Glands
Salivary Lymphoma
Parotid Metastases
CONCLUSION
ACKNOWLEDGMENT
REFERENCES
19 The Breast
19. The Breast
APPLICATIONS OF BREAST ULTRASOUND
BREAST ANATOMY AND PHYSIOLOGY
SONOGRAPHIC EQUIPMENT
SONOGRAPHIC TECHNIQUE
Patient Position
Annotation
Documentation of Lesions
Split-Screen Imaging
Special Sonographic Techniques
Doppler Sonography
Harmonic Imaging and Spatial Compounding
Elastography
Three-Dimensional Ultrasound
Contrast-Enhanced Ultrasound
Artificial Intelligence and Ultrasound
REPORTING
SONOGRAPHIC FINDINGS
Normal Tissues and Variations
Cysts and Cystic Masses
Simple Cysts
Complicated Cysts
Complex Cystic and Solid Masses
Papillary Lesions
Inflammation and Infection
Malignant Solid Masses
Morphologic Features of Cancer
Suspicious for Invasive Malignancy
Suspicious for Ductal Carcinoma In Situ
Either Invasive or Ductal Carcinoma In Situ
Features Associated With Ductal Carcinoma In Situ
Indistinct Margins
Spiculation or Thick Echogenic Rim
Angular Margins
Microlobulations
Not Parallel (Not Taller-Than-Wide) Orientation
Duct Extension
Acoustic Shadowing
Hypoechogenicity
Calcifications
Associated Features
Benign Solid Masses
Hyperechoic Tissue
Parallel (Wider-Than-Tall) Orientation
Thin Echogenic Capsule
DIAGNOSTIC ULTRASOUND INDICATIONS
Symptomatic Breast
Breast Pain
Palpable Abnormality
Nipple Discharge
Sonographic Assessment After Mammography
Size Correlation
Shape Correlation
Location or Position Correlation
Surrounding Tissue Density Correlation
Sonographic-Mammographic Confirmation
NICHE APPLICATIONS FOR BREAST ULTRASOUND
Infection
Implants
Breast Cancer Staging
Sonographic-Magnetic Resonance Imaging Correlation
ULTRASOUND-GUIDED INTERVENTION
CONCLUSION
Acknowledgment
REFERENCES
20 The Scrotum
20. The Scrotum
INTRODUCTION
SONOGRAPHIC TECHNIQUE
NORMAL ANATOMY
INTRATESTICULAR SCROTAL MASSES
MALIGNANT TUMORS
Germ Cell Tumors
Seminoma
Nonseminomatous Germ Cell Tumors
Regressed Germ Cell Tumor
Non-Germ Cell Tumors
Sex Cord-Stromal Tumors
Testicular Metastases
Lymphoma and Leukemia
Extramedullary Myeloma
Metastatic Disease
Benign Intratesticular Lesions
Cysts
Tubular Ectasia of Rete Testis
Cystic Dysplasia
Epidermoid Cysts
Abscess
Segmental Infarction
Adrenal Rests
Splenogonadal Fusion
Calcifications
EXTRATESTICULAR PATHOLOGIC LESIONS
Tunica Vaginalis
Hydrocele, Hematocele, and Pyocele
Paratesticular Masses
Hernia
Calculi
Varicocele
Fibrous Pseudotumor
Polyorchidism
Epididymal Lesions
Cystic Lesions
Tumors
Sperm Granuloma
Postvasectomy Changes in the Epididymis
Chronic Epididymitis
Sarcoidosis
ACUTE SCROTAL PAIN
Torsion
Epididymitis and Epididymo-Orchitis
Fournier Gangrene
TRAUMA
CRYPTORCHIDISM
CONCLUSION
REFERENCES
21 Overview of Musculoskeletal Sonography
21. Overview of Musculoskeletal Sonography-Techniques and Applications
INTRODUCTION
Doppler Imaging
Elastography
Extended Field-of-View Imaging
MUSCLES
TENDONS
LIGAMENTS
NERVES
JOINT ASSESSMENT
SOFT TISSUE MASSES
FOREIGN BODIES
SOFT TISSUE INFECTION
CONCLUSION
References
22 The Shoulder
22. The Shoulder
CLINICAL PERSPECTIVE
SHOULDER ANATOMY
SCAN TECHNIQUE
Biceps Tendon Evaluation
Subscapularis Tendon Evaluation
Supraspinatus Evaluation
Infraspinatus, Teres Minor, and Posterior Shoulder Evaluation
Rotator Cuff Musculature Evaluation
ROTATOR CUFF DEGENERATION AND TEARS
Background
Tendinosis
Full-Thickness Rotator Cuff Tears
Partial-Thickness Rotator Cuff Tears
Postsurgical Rotator Cuff
Muscle Atrophy
Subacromial-Subdeltoid Bursa
Calcific Tendinitis
LONG HEAD BICEPS TENDON PATHOLOGY
ARTHROPATHY
Degenerative
Inflammatory
PITFALLS IN SHOULDER ULTRASOUND
CONCLUSION
REFERENCES
23 Musculoskeletal Interventions
23. Musculoskeletal Interventions
TECHNICAL CONSIDERATIONS
INJECTION TECHNIQUE
INJECTION MATERIALS
INJECTION OF JOINTS
SUPERFICIAL PERITENDINOUS AND PERIARTICULAR INJECTIONS
Foot and Ankle
Hand and Wrist
INJECTION OF DEEP TENDONS
Biceps Tendon
Iliopsoas Tendon
Abductor and Hamstring Tendons
BURSAL, GANGLION CYST, AND PARALABRAL INJECTIONS
Calcific Tendinitis
INTRATENDINOUS INJECTIONS: PERCUTANEOUS TENOTOMY
PERINEURAL INJECTIONS
CONCLUSION
REFERENCES
24 The Extracranial Cerebral Vessels
24. The Extracranial Cerebral Vessels
INTRODUCTION: INDICATIONS FOR CAROTID ULTRASOUND EXAMINATION
CAROTID ARTERY ANATOMY
CAROTID ULTRASOUND EXAMINATION
CAROTID ULTRASOUND INTERPRETATION
Visual Inspection of Gray-Scale Images
Vessel Wall Thickness and Intima-Media Thickening
Plaque Characterization
Ultrasound Plaque Classification System
Plaque Ulceration
Gray-Scale Evaluation of Stenosis
Doppler Spectral Analysis
Standard Examination
Spectral Broadening
Pitfalls in Interpretation
High-Velocity Blood Flow Patterns
Color and Power Doppler Ultrasound
Optimal Settings for Low-Flow Vessel Evaluation
Pitfalls and Adjustments
Internal Carotid Artery Occlusion
Follow-Up of Stenosis
Preoperative Strategies for Patients With Carotid Artery Disease
Postoperative Ultrasound
Carotid Artery Stents and Revascularization
Grading Carotid Intrastent Restenosis
NONATHEROSCLEROTIC CAROTID DISEASE
Pulsatile Neck Masses in the Carotid Region
TRANSCRANIAL DOPPLER SONOGRAPHY
VERTEBRAL ARTERY
Anatomy
Sonographic Technique and Normal Examination
Subclavian Steal
Stenosis and Occlusion
INTERNAL JUGULAR VEINS
Sonographic Technique
Thrombosis
CONCLUSION
ACKNOWLEDGMENT
REFERENCES
25 Peripheral Arteries
25. Peripheral Arteries
SONOGRAPHIC EXAMINATION TECHNIQUE
SPECTRAL DOPPLER WAVEFORM EVALUATION
Focal Abnormality
Diffuse Abnormality
LOWER EXTREMITY ARTERIES
Normal Anatomy
Ultrasound Examination and Imaging Protocol
Peripheral Arterial Occlusion
Peripheral Arterial Stenosis
Functional Popliteal Artery Entrapment Syndrome
Aneurysm
Pseudoaneurysm
Arteriovenous Fistula
Lower Extremity Vein Bypass Grafts
UPPER EXTREMITY ARTERIES
Normal Anatomy
Ultrasound Examination and Imaging Protocol
Arterial Occlusion, Aneurysm, and Pseudoaneurysm
Arterial Stenosis
Subclavian Stenosis
Thoracic Outlet Syndrome
Radial Artery Evaluation for Coronary Bypass Graft
CONCLUSION
REFERENCES
26 Peripheral Veins
26. Peripheral Veins
INTRODUCTION
PERIPHERAL VEINS
Sonographic Examination Technique
Lower Extremity Veins
Normal Anatomy
Deep Venous System
Superficial Venous System
Ultrasound Examination
Lower Extremity Imaging Protocol
Acute Deep Venous Thrombosis
Chronic Postthrombotic Change and Acute Deep Venous Thrombosis on Chronic Postthrombotic Change
Potential Pitfalls
Complete Venous Doppler Versus More Limited Examinations
Recommendations for Deep Venous Thrombosis Follow-Up
Venous Insufficiency
Venous Mapping
Upper Extremity Veins
Normal Anatomy
Ultrasound Examination
Upper Extremity Imaging Protocol
Upper Extremity Acute Deep Venous Thrombosis
Differentiation of Acute From Chronic Post-thrombotic Change
Potential Pitfalls
CONCLUSION
REFERENCES
27 Hemodialysis
27. Hemodialysis
INTRODUCTION
SONOGRAPHIC EXAMINATION TECHNIQUE FOR HEMODIALYSIS ACCESS EVALUATION
Vascular Mapping Imaging Protocol Before Hemodialysis Access
Upper Extremity Imaging Protocol
Arterial Evaluation
Venous Evaluation
Additional Examination for pAVF Planning
Lower Extremity
Thigh Imaging Protocol
Vascular Imaging After Hemodialysis Access Placement
AVF Imaging Protocol
Arteriovenous Fistula Maturation Evaluation
Arteriovenous Graft Imaging Protocol
ARTERIOVENOUS FISTULA AND GRAFT COMPLICATIONS
Arteriovenous Fistula and Graft Stenosis
Arterial Steal
Arm and Leg Swelling With Arteriovenous Fistula or Graft
Palpable Focal Masses Near Arteriovenous Fistula and Graft
Arteriovenous Fistula and Graft Thrombosis
Hematoma, Abscess, and Infected Graft
Aneurysm and Pseudoaneurysm
CONCLUSION
References
28 The Uterus
FOUR - Gynecologic Sonography
28. The Uterus
INTRODUCTION, ANATOMY, AND SCANNING TECHNIQUES
NORMAL UTERINE FINDINGS
MÜLLERIAN DUCT ANOMALIES
Embryology
ABNORMALITIES OF THE MYOMETRIUM
Leiomyomas
Leiomyosarcoma
Adenomyosis
ABNORMALITIES OF THE CERVIX
ABNORMALITIES OF THE ENDOMETRIUM
Premenopausal Bleeding
Postmenopausal Endometrium
Hormone Use
Postmenopausal Bleeding
The Obstructed Uterus-Hydrometrocolpos and Hematometrocolpos
Endometrial Hyperplasia
Endometrial Polyps
Endometrial Carcinoma
Endometrial Sarcoma
Endometrial Adhesions
Endometrial Ablation
INFERTILITY AND RECURRENT MISCARRIAGE
SONOGRAPHY OF CONTRACEPTIVE DEVICES
Intrauterine Contraceptive Devices
Tubal Occlusion Devices
POSTPARTUM FINDINGS
Normal Findings
Bleeding Postpartum
Retained Products of Conception
Endometritis
Subinvolution of the Placental Site
Findings After Cesarean Section
CONCLUSION
Acknowledgment
REFERENCES
29 Adnexal Sonography
29. Adnexal Sonography
BACKGROUND
Normal Anatomy
Ultrasound Technique
Sonographic Appearance
NON-NEOPLASTIC CONDITIONS
Punctate Echogenic Foci
Polycystic Ovarian Syndrome
Endometriosis
Ovarian Remnant Syndrome
Adnexal Torsion
Pelvic Inflammatory Disease
Postpartum Ovarian Vein Thrombosis
Pelvic Venous Congestion Syndrome
NON-NEOPLASTIC MASSES
Physiologic Cyst
Hemorrhagic Ovarian Cyst
Endometrioma
Postmenopausal Non-Neoplastic Adnexal Cyst
Paraovarian and Paratubal Cysts
Peritoneal Inclusion Cyst
Hydrosalpinx
Pregnancy-Associated Ovarian Abnormalities
Postoperative Collections
NEOPLASMS
Overview
Epithelial Cell Neoplasms
Serous Cystadenoma and Cystadenofibromas
Serous Borderline Tumor and Low-Grade Serous Cystadenocarcinoma
High-Grade Serous Cystadenocarcinoma
Mucinous Cystadenoma and Cystadenocarcinoma
Endometrioid Carcinoma and Clear Cell Carcinoma
Brenner Tumor
Germ Cell Neoplasms
Cystic Teratoma
Dysgerminoma
Yolk Sac Tumor
Sex Cord Stromal Neoplasms
Granulosa Cell Tumor
Fibroma, Fibrothecoma, and Thecoma
Sertoli-Leydig Cell Tumor
Metastatic Neoplasms
Non-Ovarian Adnexal Neoplasms
DIAGNOSTIC APPROACH TO THE ADNEXAL MASS
REFERENCES
30 Overview of Obstetric Imaging
FIVE - Obstetric Sonography
30. Overview of Obstetric Imaging
INTRODUCTION
TRAINING, PERSONNEL, AND EQUIPMENT
ULTRASOUND PRACTICE PARAMETERS
First Trimester
Second and Third Trimesters
ROUTINE ULTRASOUND SCREENING
Estimation of Gestational Age
Identification of Twin/Multiple Pregnancies
Maternal Anatomy: Ovaries
Maternal Anatomy: Uterus
Fibroids
Post-Cesarean Section Uterus
Entrapped Uterus
Uterine Synechia
Congenital Uterine Anomalies
Screening and Perinatal Outcomes
Fetal Malformations: Diagnostic Accuracy
Three-Dimensional Ultrasound
Prudent Use of Ultrasound
MAGNETIC RESONANCE IMAGING
CONCLUSION
REFERENCES
31 The First Trimester
31. The First Trimester
INTRODUCTION
MATERNAL PHYSIOLOGY AND EMBRYOLOGY
ULTRASOUND OF THE NORMAL EARLY FIRST TRIMESTER
Gestational Sac
Yolk Sac
Embryo and Amnion
Gestational Age by Measurements and Embryo Morphology
Corpus Luteum and hCG Levels
Twin Gestation
PREGNANCY FAILURE
Diagnostic of Early Pregnancy Loss
Concerning for Early Pregnancy Loss
Cardiac Activity
Gestational Sac Size
Gestational Sac Appearance and Location
Amnion-Enlarged or Empty
Yolk Sac Size and Appearance
Subchorionic Hematoma
INCOMPLETE EARLY PREGNANCY LOSS/RETAINED PRODUCTS OF CONCEPTION
ECTOPIC PREGNANCY
Clinical Findings
Sonographic Findings
Hemoperitoneum
Heterotopic Pregnancy
Other Implantation Sites
Pregnancy of Unknown Location
Treatment of Ectopic Pregnancy
First-Trimester Anomalies
GESTATIONAL TROPHOBLASTIC DISEASE
Complete Molar Pregnancy
Partial Molar Pregnancy
Coexistent Hydatidiform Mole and Normal Embryo
Persistent Trophoblastic Neoplasia
CONCLUSION
References
32 Chromosomal Abnormality
32. Chromosomal Abnormality
INTRODUCTION
PRENATAL SCREENING FOR ANEUPLOIDY
Screening Test in Any Trimester of Pregnancy
Cell-Free Deoxyribonucleic Acid Screening
First Trimester Screening
Ultrasound Only With Nuchal Translucency
Ultrasound and Serum Biochemical Markers
Second Trimester Screening
Combined Screening
Combined First Trimester Screening
Integrated and Serum Integrated Screening
Sequential and Contingent Screening
FIRST TRIMESTER ULTRASOUND
Standardization of Nuchal Translucency Measurement Technique
Nuchal Translucency and Other Aneuploidies
Cystic Hygroma
Nasal Bone
Other Markers of Aneuploidy
Reversed Flow in Ductus Venosus
Tricuspid Regurgitation
Thickened Nuchal Translucency With Normal Karyotype
SECOND TRIMESTER ULTRASOUND
Nuchal Fold
Facial Profile (Nasal Bone)
Femur Length
Humerus Length
Urinary Tract Dilation
Echogenic Bowel
Echogenic Intracardiac Focus
Structural Anomalies
Adjunct Features of Trisomy 21
Combined Ultrasound Markers
ULTRASOUND FETAURES IN OTHER ANEUPLOIDIES
Trisomy 18 (Edwards Syndrome)
Choroid Plexus Cyst
Trisomy 13 (Patau Syndrome)
Triploidy
Monosomy X (Turner Syndrome)
PRENATAL DIAGNOSTIC TESTING FOR ANEUPLOIDY
First Trimester Diagnostic Testing-Chorionic Villus Sampling
Second and Third Trimester Diagnostic Testing-Amniocentesis
CONCLUSION
REFERENCES
33 Multifetal Pregnancy
33. Multifetal Pregnancy
ZYGOSITY/CHORIONICITY
DETERMINATION OF CHORIONICITY
GENERAL ISSUES
LOSS OF A TWIN
COMPLICATIONS OF MONOCHORIONICITY
Twin-Twin Transfusion Syndrome
Twin Anemia Polycythemia Sequence
Twin Reversed Arterial Perfusion Sequence
MONOAMNIOTIC TWINS
CONJOINED TWINS
CONCLUSION
REFERENCES
34 Fetal Face and Neck Sonography
34. Fetal Face and Neck Sonography
EMBRYOLOGY AND DEVELOPMENT
Face
Neck
SONOGRAPHY OF THE NORMAL FETAL FACE
ABNORMALITIES OF THE HEAD
Abnormal Size
Abnormal Shape
Craniosynostosis
Wormian Bones
Forehead Abnormalities
Encephaloceles
ORBIT ABNORMALITIES
Hypotelorism
Hypertelorism
Microphthalmia and Anophthalmia
Coloboma
Dacryocystocele
Congenital Cataracts
EAR ABNORMALITIES
MIDFACE ABNORMALITIES
Hypoplasia
Absent Nasal Bone
Other Nasal Abnormalities
Cleft Lip and Palate
Unilateral Cleft Lip/Palate
Bilateral Cleft Lip/Palate
Median Cleft Lip/Palate
Unusual Facial (Tessier) Clefts
Isolated Cleft of Secondary Palate
LOWER FACE ABNORMALITIES
Macroglossia and Oral Masses
Micrognathia and Retrognathia
SOFT TISSUE TUMORS
NECK ABNORMALITIES
Nuchal Translucency and Thickening
Lymphatic Malformation
Cervical Teratoma
Thyromegaly and Goiter
CONCLUSION
REFERENCES
35 The Fetal Brain
35. The Fetal Brain
DEVELOPMENTAL ANATOMY
Embryology
Sonographic Anatomy
Incremental Benefit of MRI
Variants (Usually Normal)
Choroid Plexus Cysts
Blake Pouch ``Cyst''
Cavum Veli Interpositi
VENTRICULOMEGALY AND HYDROCEPHALUS
Pathogenesis of Ventriculomegaly
Ultrasound Evaluation of Ventriculomegaly
Additional Studies and Prognosis
SPECIFIC ABNORMALITIES
ERRORS OF DORSAL INDUCTION
Anencephaly and Exencephaly
Cephalocele and Encephalocele
Ciliopathies
Joubert Syndrome
Meckel-Gruber Syndrome
Amniotic Band Sequence and Limb-Body Wall Complex
Cranial Changes in Spina Bifida
ERRORS OF VENTRAL INDUCTION
Holoprosencephaly
Posterior Fossa and Cerebellum
Dandy-Walker Malformation
Vermis Hypoplasia or Dysplasia
Mega-Cisterna Magna
Rhombencephalosynapsis
Other Posterior Fossa Abnormalities
Arachnoid Cysts
Malformations of Cortical Development
Microcephaly
Macrocephaly and Megalencephaly
Hemimegalencephaly
Lissencephaly
Focal Cortical Changes
Tuberous sclerosis
Agenesis of Corpus Callosum and Dysgenesis of Corpus Callosum
Absence of Septi Pellucidi and Septo-optic Dysplasia
INTRACRANIAL CALCIFICATIONS
INFECTIONS
VASCULAR MALFORMATIONS
Thrombosis of Dural Sinuses
Hemorrhagic Lesions
Ischemic Lesions
Hydranencephaly
TUMORS
CONCLUSION
REFERENCES
36 The Fetal Spine
36. The Fetal Spine
INTRODUCTION
DEVELOPMENT OF THE FETAL SPINE
Spinal Embryogenesis
Ossification of the Fetal Spine
Spinal Cord Position
SCANNING TECHNIQUES
Three-Dimensional Ultrasound
SPINA BIFIDA
Pathogenesis and Pathology
Role of Nutrition in Neural Tube Defects
Folic Acid in Neural Tube Defects
Additional Environmental and Nutritional Risk Factors
Maternal Serum Alpha-Fetoprotein
Sonographic Findings in the Spine
Associated Cranial Findings
Additional Supratentorial Findings of Neural Tube Defects
Associated Noncranial Abnormalities
Prognosis
Fetal Surgery for Open Spina Bifida
CLOSED NEURAL TUBE DEFECTS
Lipomyelomeningocele and Lipomyeloschisis
Myelocystocele
Split Cord Malformation
SCOLIOSIS AND KYPHOSIS
SACRAL AGENESIS AND CAUDAL REGRESSION
SIRENOMELIA
SACROCOCCYGEAL TERATOMA
PRESACRAL FETAL MASSES
ACKNOWLEDGMENTS
REFERENCES
37 The Fetal Chest
37. The Fetal Chest
DEVELOPMENT OF STRUCTURES IN THE CHEST
Pulmonary Development
Normal Sonographic Features of the Fetal Chest
Normal Diaphragm
Normal Thymus
PULMONARY HYPOPLASIA, APLASIA, AND AGENESIS
CONGENITAL PULMONARY AIRWAY MALFORMATION SPECTRUM
Congenital Pulmonary Airway Malformation
Bronchopulmonary Sequestration
Congenital Lobar Overinflation
PLEUROPULMONARY BLASTOMA
CONGENITAL HIGH AIRWAY OBSTRUCTION
BRONCHOGENIC CYST
NEURENTERIC CYST
PLEURAL EFFUSION
PERICARDIAL EFFUSION
PULMONARY LYMPHANGIECTASIA
CONGENITAL DIAPHRAGMATIC HERNIA
Other Hernias and Eventration
Associated Anomalies
Morbidity and Mortality
In Utero Therapy
Conclusion
References
38 Fetal Echocardiography
38. Fetal Echocardiography
INTRODUCTION
NORMAL FETAL CARDIAC ANATOMY AND SCANNING TECHNIQUES
STRUCTURAL ANOMALIES
Atrial Septal Defect
Ventricular Septal Defect
Atrioventricular Septal Defect
Ebstein Anomaly
Hypoplastic Right Ventricle
Hypoplastic Left Heart Syndrome
Univentricular Heart
Tetralogy of Fallot
Persistent Truncus Arteriosus
Double-Outlet Right Ventricle
Transposition of Great Arteries
Anomalous Pulmonary Venous Return
Coarctation of Aorta
Aortic Stenosis
Pulmonic Stenosis
Cardiosplenic Syndromes (Heterotaxy)
Cardiac Tumors
Cardiomyopathy
Ectopia Cordis
ARRHYTHMIAS
Premature Atrial and Ventricular Contractions
Tachycardia
Bradycardia
Congenital Heart Block
CONCLUSION
REFERENCES
39 The Fetal Gastrointestinal Tract and Abdominal Wall
39. The Fetal Gastrointestinal Tract and Abdominal Wall
THE GASTROINTESTINAL TRACT
Embryology of the Digestive Tube
Esophagus
Esophageal Atresia
Stomach
Small or Absent Fetal Stomach
Dilated Fetal Stomach
Midline or Right-Sided Stomach
Intraluminal Gastric Masses
Small Bowel and Colon
Duodenal Obstruction
Jejunal and Ileal Obstruction
Meconium Ileus
Anorectal Malformations
Cloacal Malformation
Hirschsprung Disease
Megacystis Microcolon Intestinal Hypoperistalsis Syndrome
Abdominopelvic Cysts
Enteric Duplication Cysts
Meconium Peritonitis and Pseudocyst
Echogenic Bowel
Liver
Hepatomegaly
Hepatic Calcifications
Hepatic Cysts and Masses
Gallbladder and Biliary System
Nonvisualization of the Gallbladder
Fetal Gallstones
Choledochal Cyst
Pancreas
Annular Pancreas
Pancreatic Cysts
Spleen
Splenomegaly
Splenic Cysts
ABDOMINAL WALL
Embryology
Gastroschisis
Omphalocele
Bladder Exstrophy
Cloacal Exstrophy
Other Complex Body Wall Defects
Pentalogy of Cantrell
Body Stalk Anomaly
Amniotic Band Syndrome
CONCLUSION
REFERENCES
40 The Fetal Urogenital Tract
40. The Fetal Urogenital Tract
NORMAL URINARY TRACT
Embryology
Sonographic Appearance
Amniotic Fluid Assessment
URINARY TRACT ABNORMALITIES
Renal Agenesis
Bilateral Renal Agenesis
Unilateral Renal Agenesis
Renal Ectopia
Horseshoe Kidney
Renal Cystic Disease
Multicystic Dysplastic Kidney
Obstructive Cystic Renal Dysplasia
Autosomal Recessive Polycystic Kidney Disease
Autosomal Dominant Polycystic Kidney Disease
Syndromes Associated With Renal Cystic Disease
Hyperechogenic Kidneys
Renal Neoplasms
Adrenal Mass
Upper Urinary Tract Dilation
Hydronephrosis, Pelviectasis, and Renal Pelvic Diameter
Ureteropelvic Junction Obstruction
Ureterovesical Junction Obstruction and Primary Megaureter
Duplication Anomalies
Vesicoureteral Reflux
LOWER URINARY TRACT OBSTRUCTION
Megacystis
In Utero Intervention: Fetal Vesicoamniotic Shunting and Cystoscopy
Non-Visualized Bladder
Bladder Exstrophy
Cloacal Anomalies
THE GENITAL TRACT
Normal Genitalia
Abnormal Genitalia
Hydrocolpos
Ovarian Cysts
CONCLUSION
REFERENCES
41 The Fetal Musculoskeletal System
41. The Fetal Musculoskeletal System
INTRODUCTION
NORMAL FETAL SKELETON
Development
Extremity Measurements
SONOGRAPHIC EVALUATION OF A FETUS WITH SKELETAL DYSPLASIA
Positive Family History
Abnormal Bone Length or Appearance
Additional Diagnostic Techniques
Three-Dimensional Ultrasound
Radiography
Three-Dimensional Computed Tomography
Magnetic Resonance Imaging
Molecular Diagnosis
LETHAL OR LIFE-LIMITING SKELETAL DYSPLASIAS
Thanatophoric Dysplasia
Achondrogenesis
Osteogenesis Imperfecta
Hypophosphatasia
Campomelic Dysplasia
Skeletal Ciliopathies
Short-Rib Polydactyly Syndromes
Other Dysplasias
NONLETHAL OR VARIABLE-PROGNOSIS SKELETAL DYSPLASIAS
Heterozygous Achondroplasia
Diastrophic Dysplasia
Asphyxiating Thoracic Dysplasia
Ellis-van Creveld Syndrome
Chondrodysplasia Punctata
Dyssegmental Dysplasia
Osteogenesis Imperfecta Types I, III, IV-Nonlethal Types
LIMB REDUCTION DEFECTS AND ASSOCIATED CONDITIONS
Proximal Focal Femoral Deficiency
Radial Ray Defects
Amniotic Band Sequence
Caudal Regression Syndrome and Sirenomelia
Arthrogryposis Multiplex Congenita
Hand and Foot Malformations
Skeletal Findings Associated with Aneuploidy
SUMMARY
Acknowledgments
References
42 Sonography of Fetal Hydrops
42. Sonography of Fetal Hydrops
SONOGRAPHIC FEATURES
Ascites
Pleural Effusions
Pericardial Effusion
Subcutaneous Edema
Placentomegaly
Polyhydramnios
ETIOLOGY
IMMUNE HYDROPS
Noninvasive Assessment of Alloimmunization
NONIMMUNE HYDROPS
Pathophysiology
Causes and Associations
Cardiovascular Abnormalities
Cardiac Tumors
Arrhythmias
Heart Block
Decreased Myocardial Function
Neck Abnormalities
Thoracic Anomalies
Pleural Effusion
Thoracic Mass
Chest Drainage Procedures
Gastrointestinal Anomalies
Urinary Tract Anomalies
Lymphatic Dysplasia
Twins
Chromosomal Anomalies
Genetic Disorders
Tumors
Anemia
Decreased Red Blood Cell Production
Hemolysis
Hemorrhage
Infection
Parvovirus B19
Toxoplasmosis
Other Infections
Metabolic Disorders
Skeletal Disorders
Endocrine Disorders
Drugs
DIAGNOSTIC APPROACH TO HYDROPS
History
Maternal Investigations
Complete Obstetric Ultrasound
Fetal Investigations Beyond the Anatomic Survey
Performing Percutaneous Umbilical Cord Blood Sampling
Fetal Transfusion
Cavity Aspiration
Postnatal Investigations
FETAL WELFARE ASSESSMENT IN NONIMMUNE HYDROPS
OBSTETRIC PROGNOSIS
Maternal Complications (Mirror Syndrome)
Delivery
Postnatal Outcome
CONCLUSION
REFERENCES
43 Fetal Measurements- Normal and Abnormal Fetal Growth
43. Fetal Measurements: Normal and Abnormal Fetal Growth and Assessment of Fetal Well-Being
GESTATIONAL AGE DETERMINATION
First Trimester
Second and Third Trimesters
Fetal Head Measurements
Femur Length
Abdominal Circumference
Composite Formulas
Gestational Age Estimation by Ultrasound: Most Accurate Approach at Each Stage of Pregnancy
WEIGHT ESTIMATION AND ASSESSMENT
Estimation of Fetal Weight
Recommended Approach
Weight Assessment in Relation to Gestational Age
FETAL GROWTH ABNORMALITIES
The Large Fetus: Large-for-Gestational Age and Macrosomia
General Population
Diabetic Mothers
The Small Fetus: Small-for-Gestational-Age Fetus and Fetal Growth Restriction
ASSESSMENT OF FETAL WELL-BEING
Biophysical Profile
Fetal Doppler
Umbilical Artery Doppler
Uterine Artery Doppler
Ductus Venosus Doppler
Middle Cerebral Artery Doppler
Fetal Doppler in Clinical Practice: Societal Recommendations
CONCLUSION
REFERENCES
44 Sonographic Evaluation of the Placenta
44. Sonographic Evaluation of the Placenta
PLACENTAL DEVELOPMENT
Placental Appearance
Placental Size
Placental Vascularity and Doppler Ultrasound
Amnion-Chorion Separation
PLACENTAL POSITION
PLACENTA PREVIA
PLACENTA ACCRETA SPECTRUM
PLACENTAL ABRUPTION
PLACENTAL INFARCTION
PLACENTAL MASSES
MESENCHYMAL DYSPLASIA OF THE PLACENTA
MOLAR GESTATION
MORPHOLOGIC PLACENTAL ABNORMALITIES
Circumvallate Placenta
Succenturiate Lobe
Bilobed Placenta
Membranous Placenta
PLACENTAL INFECTIONS
NOVEL AND INNOVATIVE USES OF PLACENTAL ULTRASOUND
Elastography
Slow Flow Imaging
UMBILICAL CORD
Size and Appearance
Cord Insertion Into the Placenta
Velamentous and Marginal Cord Insertions
Furcate Cord Insertion
Vasa Previa
PLACENTA DURING LABOR AND POSTPARTUM
Third Stage of Labor
Retained Products of Conception
CONCLUSION
Acknowledgment
References
45 Cervical Ultrasound and Preterm Birth
45. Cervical Ultrasound and Preterm Birth
PRETERM BIRTH
SONOGRAPHY OF THE UTERINE CERVIX
Transabdominal Approach
Transperineal/Translabial Approach
Transvaginal Sonography
Technical Limitations and Pitfalls
Normal Cervix
``Short'' Cervix
PREDICTION OF SPONTANEOUS PRETERM BIRTH
Obstetric Factors
Cervical Funneling
Rate of Cervical Change
Dynamic Cervical Change
Other Sonographic Features
CERVICAL ASSESSMENT IN SPECIFIC CLINICAL SCENARIOS
Asymptomatic Patients
General Obstetric Population Screening
High-Risk Obstetric Population Screening
Prior Preterm Birth
Multiple Gestations
Uterocervical Anomalies and Cervical Surgery
Preterm Premature Rupture of Membranes
Polyhydramnios
Fetal Therapy
Symptomatic Patients
Cervical Incompetence and Cervical Cerclage
Post-cerclage Follow-up
Who Should Not Get a Cerclage?
Cervical Incompetence and Vaginal Pessary
Vaginal Progesterone and 17-α Hydroxyprogesterone Caproate
MANAGEMENT PROTOCOLS FOR THE ABNORMAL CERVIX
CONCLUSION
AKNOWLEDGMENT
References
46 Neonatal and Infant Brain Imaging
SIX - Pediatric Sonography
46. Neonatal and Infant Brain Imaging
EQUIPMENT
SONOGRAPHIC TECHNIQUE
Coronal Imaging
Sagittal Imaging
Posterior Fontanelle Imaging
Mastoid Fontanelle Imaging
Three-Dimensional Ultrasound
STANDARDIZED REPORTS
Standardized Views for Display
DEVELOPMENTAL ANATOMY
Brain Sulcal Development and Subarachnoid Spaces
Cavum Septi Pellucidi and Cavum Vergae
Cavum Velum Interpositum
Frontal Horn Variants (Connatal Cysts)
Choroid Plexus and Variants
Germinal Matrix
Calcar Avis
Cerebellar Vermis
Cisterna Magna
CONGENITAL BRAIN MALFORMATIONS
DISORDERS OF NEURAL TUBE CLOSURE
Chiari Malformations
Agenesis of Corpus Callosum
Corpus Callosum Lipoma
Dandy-Walker Spectrum
DISORDERS OF DIVERTICULATION AND CLEAVAGE: HOLOPROSENCEPHALY
Septo-Optic Dysplasia
Alobar Holoprosencephaly
Semilobar Holoprosencephaly
Lobar Holoprosencephaly
Middle Interhemispheric Form of Holoprosencephaly
DISORDERS OF SULCATION AND CELLULAR MIGRATION
Schizencephaly
Lissencephaly
DESTRUCTIVE LESIONS
Porencephalic Cyst
Hydranencephaly
Cystic Encephalomalacia
Metabolic Disorders
HYDROCEPHALUS
Normal Cerebrospinal Fluid Production and Circulation
Diagnosis
Level of Obstruction
HYPOXIC-ISCHEMIC EVENTS
Arterial Watershed Determines Regional Pattern of Brain Damage
Germinal Matrix Hemorrhage
Subependymal Hemorrhage (Grade I Hemorrhage)
Intraventricular Hemorrhage (Grade II IVH)
Intraventricular Hemorrhage With Hydrocephalus (Grade III Hemorrhage)
Intraparenchymal Hemorrhage (Grade IV Hemorrhage or PVHI)
Cerebellar Hemorrhage
Subarachnoid Hemorrhage
Cerebral Edema and Infarction
White Matter Injury of Prematurity/Periventricular Leukomalacia
Term Infants With Hypoxic Ischemic Injury
Focal Infarction
Lenticulostriate Vasculopathy
Hyperechoic Caudate Nuclei
POSTTRAUMATIC INJURY
Subdural and Epidural Hematomas
INFECTION
Congenital Infections
Cytomegalovirus and Toxoplasmosis
Zika
Herpes Simplex Virus
Rubella
Neonatal Acquired Infections
Meningitis and Ventriculitis
INTRACRANIAL MASSES
Brain Tumors
Cystic Intracranial Lesions
Arachnoid Cysts
Porencephalic Cysts
Choroid Plexus Cysts
Supratentorial Periventricular Cystic Lesions
Frontal Horn Cysts (Connatal Cysts)
Subependymal Cysts
Periventricular Leukomalacia
Galenic Venous Malformations
REFERENCES
47 Neonatal Brain Doppler and Advanced Ultrasound Imaging Techniques
47. Neonatal Brain Doppler and Advanced Ultrasound Imaging Techniques
SONOGRAPHIC TECHNIQUE
Transducer Selection and Imaging Approaches
Color Doppler, Power Doppler, and Microvascular Imaging
Doppler Imaging and Optimization
Doppler Measurements and Factors That Change Resistive Index
Shear Wave Elastography Principles
Doppler and Shear Wave Elastography Safety Considerations
Contrast-Enhanced Ultrasound Principles
Technique
Interpretation
Contrast-Enhanced Ultrasound Safety Considerations
NORMAL HEMODYNAMICS
Normal Arterial Blood Flow Patterns
Normal Venous Blood Flow Patterns
INTENSIVE CARE THERAPIES AND CEREBRAL HEMODYNAMICS
Mechanical Ventilation
Extracorporeal Membrane Oxygenation
Therapeutic Hypothermia and Brain Cooling
DIFFUSE NEURONAL INJURY
Hypoxic Ischemic Injury and Asphyxia
Cerebral Edema
Brain Death
INTRACRANIAL HEMORRHAGE AND STROKE
Focal Arterial Ischemic Stroke
HYDROCEPHALUS
Advanced Microvessel Ultrasound Imaging Techniques
VASCULAR MALFORMATIONS
INTRACRANIAL TUMORS
NEAR-FIELD STRUCTURES
Differentiation of Subarachnoid From Subdural Fluid Collections
Dural Venous Sinus Thrombosis
UNCOMMON VASCULAR APPLICATIONS
PITFALLS OF ADVANCED SONOGRAPHY
References
48 Doppler Sonography of the Brain in Children
48. Doppler Sonography of the Brain in Children
SONOGRAPHIC TECHNIQUE
ULTRASOUND POWER SETTINGS
LIMITATIONS AND PITFALLS IN TRANSCRANIAL DOPPLER
CONTRAST ENHANCEMENT
INDICATIONS FOR TRANSCRANIAL DOPPLER IMAGING
Sickle Cell Disease
Other Conditions With Increased Risk of Stroke
Evaluation of Collateral Flow
Headaches
Sleep Apnea
Vasospasm
Hydrocephalus
Central Nervous System Infections
Vascular Malformations
Traumatic Brain Injury
Evaluation of Right-to-Left Shunt
Hypoxic-Ischemic Brain Injury Events
Brain Death
Neuromonitoring and Intraoperative Neuroradiologic Procedures
Transcranial Doppler and Tissue Plasminogen Activator
Functional Transcranial Doppler
Other Potential Uses
REFERENCES
49 The Pediatric Head and Neck
49. The Pediatric Head and Neck
NORMAL CERVICAL ANATOMY
SUPRAHYOID SPACE
Salivary Glands
Normal Anatomy
Congenital Salivary Lesions
Inflammatory Salivary Lesions
Acute Salivary Gland Inflammation
Chronic Inflammatory Disease
Masses
Vascular Masses
Neoplasms
Other Suprahyoid Solid Lesions
Suprahyoid Cystic Lesions
Masticator Space
INFRAHYOID SPACE
Thyroid Gland
Normal Anatomy
Congenital Thyroid Lesions
Inflammatory Thyroid Disease
Thyroid Masses
Pseudonodules Mimicking a Thyroid Nodule
Benign Thyroid Masses
Malignant Thyroid Lesions
Factors Increasing Thyroid Cancer Risk
Types of Thyroid Cancer
Potential Sonographic Markers of Thyroid Malignancy
Parathyroid Glands
Other Cystic Lesions
LACKING DEFINITION BY THE HYOID
Congenital Lesions
Branchial Anomalies
Ectopic Thymus
Dermoid and Epidermoid Lesions
Teratomas
Vascular Lesions
Vascular Anomalies
Vascular Tumors
Vascular Malformations
Other Congenital Lesions
Iatrogenic Lesions
Inflammatory Lesions
Lymph Nodes
Benign Soft Tissue Masses
Fibromatosis Colli
Neoplastic Soft Tissue Masses in the Head and Neck
Adipocytic Tumors
Infantile Myofibromatosis
Rhabdomyosarcoma
Langerhans Cell Histiocytosis
Pilomatricoma
Lymphoma
Neuroblastoma
Other Neoplasms
Metastatic Disease
REFERENCES
50 The Pediatric Spinal Canal Sonography
50. The Pediatric Spinal Canal Sonography
EMBRYOLOGY
SONOGRAPHIC TECHNIQUE AND NORMAL ANATOMY
SPINAL ANOMALIES
Tethered Spinal Cord
SPINAL DYSRAPHISM
Open Spinal Dysraphism
Closed Spinal Dysraphism With a Subcutaneous Mass
Closed Spinal Defects Without a Subcutaneous Mass
Complex Dysraphic States (Disorders of Gastrulation)
Disorders of Midline Notochordal Integration
Disorders of Midline Notochordal Formation
Tumors
HEMORRHAGE AND INFECTION
ARACHNOID CYSTS
INTRAOPERATIVE AND OTHER USES OF SPINAL SONOGRAPHY
REFERENCES
51 The Pediatric Chest
51. The Pediatric Chest
ULTRASOUND TECHNIQUE
PLEURAL EFFUSION AND EMPYEMA
Sonographic Signs of Pleural Fluid
Free Fluid Movement With Respiration
Fluid Color Flow Doppler Signal
Diaphragm Sign
Displaced-Crus Sign
Bare-Area Sign
Sonography Versus Computed Tomography Scan
Mass Versus Fluid
Parapneumonic Collections and Empyema
Lung Abscess Versus Empyema
LUNG PARENCHYMAL DISORDERS
Pneumonia
Round Pneumonia
Chest Radiograph or Ultrasound?
Atelectasis
Congenital Pulmonary Airway Malformation
Bronchopulmonary Foregut Malformation
DIAPHRAGM DISORDERS
VASCULAR DISORDERS
Vascular Thrombosis
Lymphovascular Malformation
MEDIASTINAL MASSES
Thymic Index
Abnormal Location of Thymus Mimicking Mass Lesion
Anterior Mediastinal Masses
Lymphadenopathy
Posterior Mediastinal Masses
ULTRASOUND-GUIDED INTERVENTIONAL PROCEDURES
OTHER LESS ESTABLISHED INDICATIONS
REFERENCES
52 The Pediatric Liver and Spleen
52. The Pediatric Liver and Spleen
ANATOMY
Portal Vein Anatomy
Left Lobe of Liver
Right Lobe of Liver
Hepatic Vein Anatomy
NEONATAL JAUNDICE
Choledochal Cyst
Spontaneous Rupture of Bile Duct
Paucity of Interlobular Bile Ducts and Alagille Syndrome
Biliary Atresia
Neonatal Hepatitis
Neonatal Jaundice and Urinary Tract Infection or Sepsis
Inborn Errors of Metabolism
STEATOSIS
CIRRHOSIS
CHOLELITHIASIS
LIVER TUMORS
Identification
Benign Liver Tumors
Hemangiomas
Hemangioendotheliomas
Mesenchymal Hamartomas
Adenomas
Focal Nodular Hyperplasia
Malignant Liver Tumors
Hepatoblastoma
Hepatocellular Carcinoma
Undifferentiated Embryonal Sarcoma
Biliary Rhabdomyosarcoma
Metastases
Detection of Tumor Angiogenesis
Pyogenic Abscess
Parasitic Abscesses
Amebiasis
Echinococcosis
Schistosomiasis
Granulomas of the Liver
DOPPLER ASSESSMENT OF LIVER DISEASE AND PORTAL HYPERTENSION IN CHILDREN
Basic Principles
Physics of Doppler
Normal Flow Patterns in Splanchnic Vessels
Possibilities and Pitfalls
Sonographic Technique
Child With Liver Disease: Doppler Examination for Portal Hypertension
Abnormal Flow Patterns Within the Portal System
Absent Doppler Signal
Arterialized Portal Venous Flow
Reversed or To-and-Fro Flow
Abnormal Hepatic Arterial Doppler Patterns
Portal Venous Hypertension
Prehepatic Portal Hypertension
Intrahepatic Portal Hypertension
Suprahepatic (Posthepatic) Portal Hypertension
Surgical Portosystemic Shunts
Hepatic Shear Wave Elastography
DOPPLER SONOGRAPHY IN CHILDREN RECEIVING LIVER TRANSPLANT
Pretransplantation Evaluation
Posttransplantation Evaluation
Multiorgan Transplants
THE SPLEEN
ACKNOWLEDGMENT
REFERENCES
53 Pediatric Kidney, Urinary Tract, and Adrenal Sonography
53. Pediatric Kidney, Urinary Tract, and Adrenal Sonography
PEDIATRIC RENAL SONOGRAPHY
Technique
Normal Renal Anatomy
Normal Bladder Anatomy
CONGENITAL RENAL ANOMALIES
Renal Duplication
Other Renal Anomalies
CAUSES OF RENAL COLLECTING SYSTEM DILATION
Ureteropelvic Junction Obstruction
Ureteral Obstruction
Bladder Outlet Obstruction
Vesicoureteral Reflux
Prune-Belly Syndrome
Megacystis-Microcolon-Intestinal Hypoperistalsis Syndrome
Bladder Exstrophy
Urachal Anomalies
URINARY TRACT INFECTION
Acute Pyelonephritis
Chronic Pyelonephritis
Fungal Infection
Cystitis
MEDICAL RENAL DISEASE
Acute Kidney Injury
Chronic Kidney Disease
URINARY TRACT CALCIFICATION
Renal Cortical Calcification
Medullary Nephrocalcinosis
Urinary Stasis
Renal Vein Thrombosis Calcifications
Dystrophic Calcification
Urolithiasis
RENAL TRAUMA
RENAL VASCULAR DISEASE
Doppler Sonographic Examination Technique
Normal Vascular Anatomy and Flow Patterns
Causes of Increased Resistance to Intrarenal Arterial Flow
Clinical Applications
Vessel Patency
Acute Renal Vein Thrombosis
Renal Artery Stenosis
Intrarenal Arterial Disease
RENAL TRANSPLANTATION
Vascular Complications
Perinephric Fluid Collections
Parenchymal Abnormalities
Urologic Complications
Tumors
RENAL CYSTIC DISEASE
Autosomal Recessive Polycystic Kidney Disease
Autosomal Dominant Polycystic Kidney Disease
Multicystic Renal Dysplasia
Nephronophthisis and Medullary Cystic Disease
Autosomal Dominant Tubulointerstitial Kidney Disease
Congenital Renal Cysts
Tuberous Sclerosis and Von Hippel-Lindau Disease
Congenital Obstruction
Acquired Cysts
RENAL TUMORS
Wilms Tumor
Mesoblastic Nephroma
Renal Cell Carcinoma
Angiomyolipoma
Multilocular Cystic Nephroma
Renal Lymphoma
Bladder Tumors
PEDIATRIC ADRENAL SONOGRAPHY
Normal Anatomy
Congenital Adrenal Hyperplasia
Neonatal Adrenal Hemorrhage
Neuroblastoma
Pheochromocytoma
Adrenocortical Neoplasm
REFERENCES
54 Pediatric Gastrointestinal Tract Sonography
54. Pediatric Gastrointestinal Tract Sonography
ESOPHAGUS AND STOMACH
Normal Anatomy and Technique
Esophagus
Stomach
Hypertrophic Pyloric Stenosis
Pylorospasm and Minimal Muscular Hypertrophy
Pitfalls in Sonographic Diagnosis
Gastric Diaphragm
Gastritis and Ulcer Disease
Bezoar
DUODENUM AND SMALL BOWEL
Normal Anatomy and Technique
Congenital Duodenal Obstruction
Midgut Malrotation and Midgut Volvulus
Duodenal Hematoma
Small Bowel Obstruction
Intussusception
COLON
Normal Anatomy and Technique
Ectopic or Imperforate Anus
INTESTINAL INFLAMMATORY OR INFECTIOUS DISEASE
Necrotizing Enterocolitis
Appendicitis
Gastrointestinal Neoplasms and Cysts
PANCREAS
Normal Anatomy and Technique
Annular Pancreas
Pancreatitis
Pancreatic Masses
REFERENCES
55 Pediatric Pelvic Sonography
55. Pediatric Pelvic Sonography
SONOGRAPHIC TECHNIQUE
GENITOURINARY EMBRYOLOGY
NORMAL FEMALE ANATOMY
The Uterus
The Vagina
The Ovary
OVARIAN ABNORMALITIES
Ovarian Cysts
Complications: Torsion, Hemorrhage, Rupture
Polycystic Ovarian Disease (Stein-Leventhal)
Massive Ovarian Edema
Ovarian Neoplasms
UTERINE AND VAGINAL ABNORMALITIES
Congenital Anomalies
Neoplasm
Pregnancy
Infection
Pelvic Inflammatory Disease
Foreign Bodies
ENDOCRINE ABNORMALITIES
Causes of Primary Amenorrhea
Precocious Puberty
NORMAL MALE ANATOMY
The Prostate
The Scrotum
The Testes
CONGENITAL MALE ABNORMALITIES
ACUTE SCROTAL PAIN OR SWELLING
Color Doppler Sonography in Testicular Torsion
SCROTAL MASSES
Intratesticular Causes
Extratesticular Causes
Paratesticular Tumors
LOWER URINARY TRACT
Congenital Anomalies
The Ureter
Neurogenic or Dysfunctional Bladder
Infection
Neoplasm
Trauma
Postoperative Bladder
PRESACRAL MASSES
REFERENCES
56 Pediatric Musculoskeletal Ultrasound
56. Pediatric Musculoskeletal Ultrasound
INTRODUCTION
BASICS OF PEDIATRIC MUSCULOSKELETAL ULTRASOUND
Developmental Dysplasia of the Hip
Sonographic Technique
Coronal or Longitudinal Plane
Transverse Plane
Treatment
The Painful Hip
Hip Effusion
Transient or Toxic Synovitis
Septic Arthritis
Slipped Capital Femoral Head Epiphysis
Legg-Calve-Perthes Disease
Apophyseal Avulsion Injuries Around the Hip
Snapping Hip Syndrome
ROLE OF ULTRASOUND IN TRAUMA
Sports-Related Soft Tissue Injuries
Fractures
Neonatal Brachial Plexus Palsy
INFECTION AND INFLAMMATORY CONDITIONS
Osteomyelitis
Juvenile Idiopathic Arthritis
Soft Tissue Masses
Hemangioma
Lymphatic Malformation
Pilomatricoma
Fibrosarcoma
CONGENITAL ANOMALIES
Congenital Vertical Talus
Tibial Hemimelia
CONCLUSION
REFERENCES
57 Pediatric Interventional Sonography
57. Pediatric Interventional Sonography
GENERAL PRINCIPLES
SEDATION
Equipment and Transducers
Biopsy
Drainage of Fluid Collections
Lumbar Puncture
Sclerotherapy of Vascular Malformations
Neonatal Central Venous Access
Botox of Salivary Glands
Musculoskeletal Interventions
Contrast-Enhanced Ultrasound
Intravascular Ultrasound
REFERENCES

Citation preview

DIAGNOSTIC ULTRASOUND 6th Edition

Carol M. Rumack, MD, FACR Distinguished Professor of Radiology and Pediatrics University of Colorado School of Medicine Denver, Colorado

Deborah Levine, MD, FACR Professor Emerita of Radiology Harvard Medical School Boston, Massachusetts

Elsevier 1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899 DIAGNOSTIC ULTRASOUND, SIXTH EDITION Copyright © 2024 by Elsevier Inc. All rights reserved.

ISBN: 978-0-323-87795-4

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/ permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notice Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds or experiments described herein. Because of rapid advances in the medical sciences, in particular, independent verification of diagnoses and drug dosages should be made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or contributors for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Previous editions copyrighted 2018, 2011, 2005, 1998, and 1993.

Senior Content Strategist: Melanie Tucker Senior Content Development Specialist: Lisa Barnes Publishing Services Manager: Julie Eddy Senior Project Manager: Cindy Thoms Printed in Canada Last digit is the print number: 9 8 7 6 5 4 3 2 1

ABOUT THE EDITORS

Deborah Levine, MD, FACR, is Professor Emerita of Radiology at Harvard Medical School. Her clinical practice was based at Beth Israel Deaconess Medical Center in Boston. Her research focused on two main areas. The first was imaging of adnexal cysts, particularly to decrease follow-up and interventions for benign adnexal cysts. The second area was obstetric magnetic resonance imaging, particularly for care of the pregnant patient and assessment of fetal anomalies when ultrasound was insufficient to provide a specific and complete diagnosis. She has published extensively and lectured widely. She is a Fellow, previous Chair of the Ultrasound Commission, and past Vice President of the American College of Radiology. She is also a Fellow and past President of the Society of Radiologists in Ultrasound. She has also been a Fellow of the American Association for Women Radiologists and the American Institute of Ultrasound in Medicine. She and her husband, Alex, have two children, Becky and Julie.

Carol M. Rumack, MD, FACR, is Distinguished Professor of Radiology and Pediatrics at the University of Colorado School of Medicine in Denver, Colorado. Her clinical practice is based at the University of Colorado Hospital. Her primary research has been in neonatal sonography of high-risk infants, particularly the brain, on which she has published and lectured widely. She is a Fellow, previous Chair of the Ultrasound Commission, past President of the American College of Radiology and the American Association for Women Radiologists, and a Fellow of both the American Institute of Ultrasound in Medicine and the Society of Radiologists in Ultrasound. She and her husband, Barry, have two children, Becky and Marc, and five grandchildren.

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CONTRIBUTORS Patricia T. Acharya, MD, FAAP Director of Musculoskeletal Radiology Associate Program Director Pediatric Radiology Fellowship Department of Radiology Children’s Hospital Los Angeles Los Angeles, California Assistant Professor Department of Radiology Keck School of Medicine University of Southern California, Los Angeles Clinical Adjunct Assistant Professor Department of Radiology Loma Linda University School of Medicine Loma Linda, California United States Ronald S. Adler, MD, PhD Professor of Radiology Department of Radiology New York University School of Medicine New York, New York United States Allison Aguado, MD Associate Professor Department of Radiology Nemours Children’s Hospital Wilmington, Delaware United States Lauren Freeman Alexander, MD Associate Professor Department of Radiology Mayo Clinic Jacksonville, Florida United States Elizabeth Asch, MD Instructor in Radiology Department of Radiology Brigham and Women’s Hospital Boston, Massachusetts United States Thomas D. Atwell, MD Professor Department of Radiology Mayo Clinic Rochester, Minnesota United States

Amanda K. Auckland, BS, RT(R), RDMS, RDCS, RVT, RMSKS Lead Diagnostic Medical Sonographer Division of Ultrasound University of Colorado Hospital Aurora, Colorado United States Muhammad U. Aziz, MD Assistant Professor Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States Carol B. Benson, MD Professor of Radiology Department of Radiology Harvard Medical School Radiologist Department of Radiology Brigham and Women’s Hospital Boston, Massachusetts United States Edward I. Bluth, MD, FACR, FSRU, FAIUM Chairman Emeritus Department of Radiology Ochsner Health United States Professor Ochsner Clinical School University of Queensland, School of Medicine New Orleans, Louisiana United States Dorothy Bulas, MD Professor of Pediatrics and Radiology Diagnostic Imaging and Radiology Children’s National Hospital Washington, District of Columbia United States Constantine M. Burgan, MD Associate Professor, Chief of Ultrasound and Body Procedures Department of Radiology Abdominal Imaging Section The University of Alabama at Birmingham Birmingham, Alabama United States

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CONTRIBUTORS

Peter N. Burns, PhD Professor Medical Biophysics and Radiology University of Toronto Senior Scientist Imaging Research Sunnybrook Research Institute Toronto, Ontario Canada Christopher M. Buros, MD Assistant Professor Department of Radiology University of Pittsburgh Pittsburgh, Pennsylvania United States

Beverly G. Coleman, MD, FAAWR, FACR, FAIUM, FSRU Professor Department of Radiology Children’s Hospital of Philadelphia Philadelphia, Pennsylvania United States Mary E. Cunnane, MD Staff Radiologist Department of Radiology Massachusetts Eye and Ear Infirmary Boston, Massachusetts United States

Molly B. Carnahan, MD Radiology Fellow Department of Radiology Mayo Clinic in Arizona Phoenix, Arizona United States

Peter M. Doubilet, MD, PhD Professor Department of Radiology Harvard Medical School Senior Vice Chair Department of Radiology Brigham and Women’s Hospital Boston, Massachusetts United States

Ilse Castro-Aragon, MD Section Head Pediatric Radiology Department of Radiology Boston Medical Center Boston, Massachusetts United States

Julia A. Drose, BA, RDMS, RDCS, RVT Associate Professor Department of Radiology University of Colorado School of Medicine Aurora, Colorado United States

J. William Charboneau, MD Emeritus Professor of Radiology Department of Radiology Mayo Clinic Rochester, Minnesota United States

Lisa R. Dunn-Albanese, MD Assistant Professor Harvard Medical School Maternal Fetal Medicine Brigham and Women’s Hospital Boston, Massachusetts United States

David Chitayat, MD, FACMG, FCCMG, FRCPC Head, The Prenatal Diagnosis and Medical Genetics Program Department of Obstetrics and Gynecology Mount Sinai Hospital University of Toronto Staff, Division of Clinical and Metabolics Genetics Department of Pediatrics The SickKids Hospital Toronto, Ontario Canada William Choi, MD, PhD Clinical Fellow Maternal-Fetal Medicine Beth Israel Deaconess Medical Center Boston, Massachusetts United States

Alexia M. Egloff, MD Radiology Consultant Department of Radiology Guys and St. Thomas Northwood, London United Kingdom Staff Radiologist Department of Perinatal Imaging and Health King’s College London London, United Kingdom Judy A. Estroff, MD Section Chief, Fetal-Neonatal Imaging Department of Radiology Boston Children’s Hospital Boston, Massachusetts United States

CONTRIBUTORS Ghaneh Fananapazir, MD Associate Professor Department of Radiology University of California Medical Center Sacramento, California United States J. Brian Fowlkes, PhD Professor Department of Radiology Department of Biomedical Engineering University of Michigan Ann Arbor, Michigan United States Mary C. Frates, MD Professor Harvard Medical School Vice Chair, Department of Radiology Brigham and Women’s Hospital Boston, Massachusetts United States Helena Gabriel, MD Professor of Radiology Department of Radiology Northwestern University Chicago, Illinois United States Kara Gaetke-Udager, MD Associate Professor Department of Radiology University of Michigan Ann Arbor, Michigan United States Sangeet Ghai, MD Professor JT Department of Medical Imaging University Health Network Mount Sinai Hospital Women’s College Hospital University of Toronto Toronto, Ontario Canada Hournaz Ghandehari, MD, FRCPC Medical Imaging, Abdominal Division University of Toronto Sunnybrook Hospital Toronto, Ontario Canada Phyllis Glanc, MD Professor, University of Toronto Department Medical Imaging Toronto, Ontario Canada

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Christy K. Holland, PhD Professor Department of Internal Medicine Division of Cardiovascular Health and Disease Department of Biomedical Engineering University of Cincinnati Cincinnati, Ohio United States Mindy M. Horrow, MD Emerita Vice Chair Department of Radiology Einstein Healthcare Network Professor (Retired) Department of Radiology Sidney Kimmel Medical School of Thomas Jefferson University Philadelphia, Pennsylvania United States Misun Hwang, MD, MS Director of the Section of Neonatal Imaging Attending Radiologist Department of Radiology Children’s Hospital of Philadelphia Philadelphia, Pennsylvania Susan D. John, MD Professor and Chair Department of Diagnostic and Interventional Imaging University of Texas McGovern Medical School Houston Houston, Texas United States Stephen I. Johnson, MD Section Head of Abdominal Imaging Department of Radiology Ochsner Clinic Foundation Jefferson, Louisiana United States Dilkash Kajal, MD, FRCPC Joint Department of Medical Imaging Abdominal Division University Health Network Mount Sinai Health Women’s College Hospital University of Toronto Toronto, Ontario Canada Ashley N. Kalor, MD Assistant Professor Department of Radiology University of Pittsburgh Medical Center Pittsburgh, Pennsylvania United States

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CONTRIBUTORS

Johannes Keunen, MD, PhD Associate Professor Director, Continuing Professional Development Department of Obstetrics and Gynecology University of Toronto Toronto, Ontario Canada Korosh Khalili, MD, FRCPC, MHSc Professor of Radiology Department of Medical Imaging University of Toronto Director of Ultrasound Joint Department of Medical Imaging University Health Network Toronto General Hospital Toronto, Ontario Canada Beth M. Kline-Fath, MD, FAIUM, FACR, FAAP Professor Department of Radiology Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio United States Boris Bulat Kumaev, DO, MD, MD/DO Department of Radiology Mass Eye and Ear Boston, Massachusetts United States Jessica Leschied, MD Department of Radiology Henry Ford Hospital Detroit, Michigan United States Deborah Levine, MD Professor Emerita of Radiology Department of Radiology Harvard Medical School Boston, Massachusetts United States Yi Li, MD Assistant Professor Radiology and Biomedical Imaging University of CaliforniaeSan Francisco San Francisco, California United States Mark E. Lockhart, MD, MPH Professor, Tenured Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States

Alexandra Medellin, MD Department of Radiology University of Calgary Calgary, Alberta Canada HaiThuy N. Nguyen, MD Associate Professor Department of Radiology Keck School of Medicine Staff Radiologist Department of Pediatric Radiology Children’s Hospital Los Angeles Los Angeles, California United States Barbara O’Brien, MD Beth Israel Deaconess Hospital Department of Obstetrics and Gynecology Harvard Medical School Boston, Massachusetts United States Sara M. O’Hara, MD, FACR, FAIUM Professor Department of Radiology Cincinnati Children’s Hospital Cincinnati, Ohio United States Edward R. Oliver, MD, PhD Associate Clinical Professor Department of Radiology Children’s Hospital of Philadelphia Philadelphia, Pennsylvania United States Harriet J. Paltiel, MDCM Radiologist Department of Radiology Boston Children’s Hospital Associate Professor of Radiology Harvard Medical School Director, Ultrasound Division Department of Radiology Boston Children’s Hospital Boston, Massachusetts United States Maitray D. Patel, MD Professor Department of Radiology Mayo Clinic Arizona Phoenix, Arizona United States

CONTRIBUTORS Catherine H. Phillips, MD Medical Director of Ultrasound Assistant Professor Department of Radiology and Radiological Sciences Vanderbilt University Medical Center Nashville, Tennessee United States Jordana Phillips, MD Breast Imager Department of Radiology Boston Medical Center, Breast Imaging Section Chief Associate Professor of Radiology Boston University School of Medicine Boston, Massachusetts United States Theodora A. Potretzke, MD Associate Professor Department of Radiology Mayo Clinic Rochester, Minnesota United States Deborah Rabinowitz, MD Division Chief Department of Interventional Radiology Nemours Children’s Health Wilmington, Delaware Clinical Associate Professor Department of Pediatrics and Radiology Sidney Kimmel Medical College at Thomas Jefferson University Philadelphia, Pennsylvania United States Rupa Radhakrishnan, MBBS, MS, DABR Associate Division Chief of Neuroradiology Department of Radiology and Imaging Sciences Indiana University School of Medicine Pediatric Neuroradiologist Riley Hospital for Children at Indiana University Health Indianapolis, Indiana United States Michelle LaVonne Robbin, MD, MSME Professor of Radiology and Biomedical Engineering Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States Carol M. Rumack, MD, FACR Distinguished Professor of Radiology and Pediatrics University of Colorado School of Medicine Denver, Colorado United States

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Ramon Sanchez-Jacob, MD Associate Professor Department of Radiology and Pediatrics Childrens National Hospital Washington, District of Columbia United States Alison M. Savicke, BS, RDMS, RVT Sonographer Practitioner Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States Chetan Chandulal Shah, MD, MBA Chair Department of Pediatric Radiology Nemours Children’s Health Faculty, Department of Radiology Mayo Clinic Chairman Department of Pediatric Radiology Wolfson Children’s Hospital Jacksonville, Florida United States Kedar Gopal Sharbidre, MD Assistant Professor Department of Abdominal Imaging University of Alabama at Birmingham Birmingham, Alabama United States Thomas D. Shipp, MD Associate Professor of Obstetrics, Gynecology & Reproductive Biology Harvard Medical School Department of Obstetrics & Gynecology Brigham & Women’s Hospital Boston, Massachusetts United States Judy H. Squires, MD Associate Professor of Radiology Department of Pediatric Radiology University of Pittsburgh Medical Center, Children’s Hospital of Pittsburgh Pittsburgh, Pennsylvania United States Franklin N. Tessler, MD CM, FSRU, FAIUM Emeritus Professor Department of Radiology Marnix E. Heersink School of Medicine University of Alabama at Birmingham Birmingham, Alabama United States

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CONTRIBUTORS

Ants Toi, MD, FRCPC, FAIUM Professor of Radiology Department of Medical Imaging University of Toronto Princess Margaret Hospital Toronto, Ontario Canada Laurie Troxclair, BS, RDMS, RVT Ochsner Clinic Foundation New Orleans, Louisiana United States Mitchell E. Tublin, MD Professor and Executive Vice Chair Department of Radiology University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania United States Heidi R. Umphrey, MD MidSouth Imaging Germantown, Tennessee United States Darci J. Wall, MD Assistant Professor Department of Radiology Mayo Clinic Rochester, Minnesota United States Therese M. Weber, MD, MS Professor of Radiology Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States Pei-Kang Wei, MD Instructor in Radiology Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States Stephanie R. Wilson, MD Clinical Professor Department of Radiology Department of Gastroenterology University of Calgary Calgary, Canada

Thomas Winter, III, MD Emeritus Professor Department of Radiology University of Utah Salt Lake City, Utah United States Christine L. Xue, MD Radiology Resident Department of Diagnostic Radiology Loma Linda University Medical Center Loma Linda, California United States Corrie M. Yablon, MD Assistant Professor Department of Radiology University of Michigan Ann Arbor, Michigan United States Hojun Yu Master Radiologist Department of Diagnostic Imaging Grande Prairie Regional Hospital Grande Prairie, Alberta Canada Mohd Zahid, MBBS, MD Assistant Professor Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States Da Zhang, PhD Program Director, Diagnostic Medical Physics Department of Radiology Boston Children’s Hospital Assistant Professor of Radiology Harvard Medical School Boston, Massachusetts United States

To Alex, Becky, and Juliedyour love and support made this work, and the work of my career, possible. Debbie Levine In memory of my parents, Drs. Ruth and Raymond Masters, who encouraged me to enjoy the intellectual challenge of medicine and the love of making a difference in patients’ lives. To Amanda K. Auckland, RDMS, who captured images and videos that greatly enhance the Neonatal Brain Imaging chapter. To Barry Rumack, for his outstanding support through all six editions of this textbook. To our wonderful children, Becky and Marc, and our marvelous grandchildren, Cody, Alex, Kimberly, Gavin, and Natalie, who add so much joy to our lives. Carol M. Rumack

PREFACE It is an honor to present to you the sixth edition of Diagnostic Ultrasound. As in previous editions, we have included experts in the field to share their authoritative experience. Given the nature of ultrasound practice, which in radiology departments is moving toward a more body imaging/organ-based approach, this edition has been expanded to include more correlative imaging, and thus is a substantial update from the previous versions. We have also greatly expanded our video library to enable real-time examples of anatomy and pathology. Previous editions have been very well accepted as reference textbooks and have been the commonly used reference in ultrasound education and practices worldwide. The text and references have all been updated and are available online. We are pleased to provide over 2,300 images, with 657 videos of ultrasound anatomy and pathology that complement the static images in the book. The display of real-time ultrasound has helped to capture those areas of anatomy that are difficult to depict on a still image. The video sweeps also allow a more complete depiction of pathology, and the relationship of pathology to surrounding anatomy. Another new feature of this book is incorporating artifacts into the physics chapter, which allows the reader to better appreciate the relationship between the creation of images and the artifacts that help define intrinsic details of tissue. 41 outstanding new and 43 continuing authors have contributed to this edition, and all are recognized experts in the field of ultrasound. As in previous editions, we have emphasized the use of collages to show many examples of similar anatomy and pathology. These images reflect the spectrum of sonographic changes that may occur in a given disease, instead of only the most common manifestation.

We have again used colored boxes to highlight the important or critical features of sonographic diagnoses. Key terms and concepts are emphasized in boldface type. To direct the readers to other research and literature of interest, comprehensive updated reference lists are provided. Diagnostic Ultrasound is again divided into two volumes. Volume I consists of Parts I to III. Part I contains chapters on physics (including artifacts and elastography) and biologic effects of ultrasound. It also includes description of ultrasound contrast technique and images, with an entirely new section on starting an ultrasound contrast practice in your laboratory. Part II covers abdominal, pelvic, retroperitoneal, interventional, and hernia sonography. Part III covers vascular sonography and small parts imaging, including testicular, breast, thyroid, and a newly expanded chapter on parathyroid and other glands in the head and neck. Volume 2 comprises Part IV (gynecology), Part V (obstetrics), and Part VI (pediatrics). Each of these sections has been expanded to include correlative imaging and description of the value of elastography and ultrasound contrast when appropriate. Diagnostic Ultrasound is for practicing physicians, residents, medical students, sonographers, and others interested in understanding the vast applications of diagnostic and interventional sonography in patient care. Our goal is for Diagnostic Ultrasound to continue to be the most comprehensive reference book available in the sonographic literature, with a highly readable style and superb images and video clips. Deborah Levine, MD, FACR Carol M. Rumack, MD, FACR

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ACKNOWLEDGMENTS We wish to express our deepest appreciation and sincerest gratitude: We owe sincere thanks to all our outstanding authors. Writing a revision during the COVID pandemic has brought strain to many of our authors, and we gratefully thank them for their dedication to education at this difficult time in our medical careers. This time has been taxing for all of us, as individuals and professionals, and we sincerely appreciate our authors’ contributions of newly updated and authoritative text, beautiful imaging examples with correlative imaging as a more predominant feature in this edition, and high-quality educational supplemental videos. To Alexander Jesurum, PhD, whose outstanding support allowed completion of this text in a timely fashion. To Alison M. Savicke, RDMS, who spent hours finding, cropping, and annotating videos to supplement our online content. To Beth Post, who greatly assisted with the Pediatric Ultrasound chapters. To the editorial team at Elsevier, who kept us on track for the process of updating and copyediting the entire manuscript. It has been an intense few years for everyone, and we are very proud to share this superb sixth edition of Diagnostic Ultrasound.

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OUR COVER When you look at the images on the cover of this book, you will notice the use of gray-scale, color Doppler, elastography, contrast, three-dimensional, and cross-sectional correlative imaging. These images span chapters on ultrasound in pediatric, obstetrics, spleen, liver, gastrointestinal, small parts, and vascular ultrasounddall very representative of the many aspects of ultrasound that we discuss in detail in the book. To be chosen for the cover, the images had to be new to this edition and had to represent diagnoses you could reasonably suggest after seeing just one image (and in one case, two), as long as you know the portion of anatomy being scanned. We also thought it would be nice to acknowledge all our authors in the front matter because it was a difficult choice to narrow new images down to the 9 images you see on the cover and spine of the book. Thank you again to all our authors. Thank you as well to our readers, who make this edition and future updates of this textbook possible. Chapter 17, Thyroid Gland and Cervical Lymph Node Sonography, written by Drs. Kedar Gopal Sharbidre and Franklin N. Tessler. Figure 17.18b “Thyroid Inferno.” Exuberant flow in the right lobe on sagittal color Doppler in a patient with Graves’ disease.

Chapter 5, The Spleen, written by Dr. Darci J. Wall. Figures 5.20E and F are of a patient with B-cell lymphoma. Gray-scale ultrasound and correlative PET scan demonstrate multiple lesions in the spleen that are hypoechoic on ultrasound and metabolically active on PET scan.

Chapter 36, The Fetal Spine, written by Drs. Edward R. Oliver and Beverly G. Coleman. Figure 36.33A Sagittal image of Type II Sacrococcygeal teratoma at 22 weeks’ gestation. There is a mixed cystic and solid mass beginning at the lower sacrum (arrow) and extending distally. The mass is predominantly external (arrowheads) but has a cystic presacral component (*) that displaces the rectum anteriorly (open arrowheads).

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OUR COVER

Chapter 4, The Liver, written by Drs. Stephanie R. Wilson and Alexandra Medellin. Figure 4.61B isa hemangioma in an at-risk patient for hepatocellular carcinoma, LiRADs-1. A grayscale image of the liver (shown in the chapter) illustrates a deep large echogenic mass. Intravenous ultrasound contrast was given with this image taken at the peak of arterial phase enhancement. The image shows multiple discontinuous pools of contrast enhancement around the periphery of the mass with no linear vascularity. In the portal venous phase and in the late phase imaging (shown in the chapter) the enhancement was also classic for a hemangioma.

Chapter 47, Neonatal Brain Doppler and Advanced Ultrasound Imaging Techniques, written by Drs. Judy H. Squires and Misun Hwang. Figure 47.14 Term Infant With Left Middle Cerebral Artery (MCA) Stroke and Luxury Hyperperfusion. (A) Coronal gray-scale ultrasound demonstrates illdefined hyperechogenicity of the left MCA territory with mild local mass effect and left-to-right midline shift.

Chapter 8, The Gastrointestinal Tract, written by Drs. Stephanie R. Wilson and Alexandra Medellin. Figure 8.7F. Shear wave elastography of the bowel in axial view. The stiffness display shows blue, indicating soft bowel. Chapter 12, Retroperitoneal Sonography, written by Drs. Helena Gabriel and Constantine M. Burgan. Figure 44A, Azygos Continuation of the Inferior Vena Cava (IVC). This transverse color Doppler image shows the hepatic veins but no intrahepatic IVC.

VIDEO CONTENTS 1 Physics of Ultrasound Da Zhang, Korosh Kahlili, Hojun Yu, and Deborah Levine Video 1.1 Speed of Sound Artifact Explained Video 1.2 Attenuation Artifacts Explained Video 1.3 Clinical Example of Dilated Ureter From Ureteral Stone With Shadowing Video 1.4 Shadowing From Behind Ovarian Fibroma Video 1.5 Through Transmission Explained in a Patient With a Hepatic Cyst Video 1.6 Mirror Image Artifact Explained Video 1.7 Comet Tail Artifact Explained Video 1.8 Clinical Example of Comet Tail Artifact in a Patient With Adenomyomatosis Video 1.9 Refraction Artifact Explained Video 1.10 Anisotropy Explained Video 1.11 Anisotropy in Biceps Tendon Video 1.12 Ring-Down Artifact Illustrated Video 1.13 Ring-Down and Reverberation Artifacts Video 1.14 Reverberation Artifact Video 1.15 Dirty Shadowing From a Combination of Relfection, Reverberation, and Ring-Down Artifacts Originating From Multiple Layers of Gas Bubbles Video 1.16 Side Lobe Artifact Explained Video 1.17 Partial Volume Artifact Explained Video 1.18 Tissue Vibration Artifact in Patient With Left Renal Artery Stenosis With Color Bruit Video 1.19 Aliasing in Pseudoaneurysm Video 1.20 Aliasing in Femoral Artery to Femoral Vein Dialysis Graft Video 1.21 Twinkle Artifact Explained Video 1.22 Twinkle Artifact in Patient With Chronic Pancreatitis

4 The Liver Stephanie R. Wilson and Alexandra Medellin Video 4.1 Normal Liver, Sagittal Sweep Video 4.2 Normal Liver, Subcostal Sweep Video 4.3 Focal Fat in the Liver Video 4.4 Geographic Fatty Infiltration of the Liver Video 4.5 Contrast-Enhanced Ultrasound of Focal Nodular Hyperplasia With Classic Enhancement Features Video 4.6 Contrast-Enhanced Ultrasound of the Flash-Filling Hemangioma Video 4.7 Contrast-Enhanced Ultrasound of Focal Nodular Hyperplasia Video 4.8 Contrast-Enhanced Ultrasound of Focal Nodular Hyperplasia Video 4.9 Contrast-Enhanced Ultrasound of Hepatic Adenoma in a Young Woman Video 4.10 Contrast-Enhanced Ultrasound of Small Hepatocellular Carcinoma Video 4.11 Contrast-Enhanced Ultrasound of Hepatocellular Carcinoma Video 4.12 Classic Colorectal Metastasis Video 4.13 Contrast-Enhanced Ultrasound of Liver Metastasis Video 4.14 Contrast-Enhanced Ultrasound of Liver Metastasis Video 4.15 A Large Hepatocellular Carcinoma With Classical Enhancement Features

Video Video Video Video

4.16 4.17 4.18 4.19

A Precursor Nodule in a Cirrhotic Liver, LR-3 Hemangioma Wash-in in an at Risk Patient for HCC, LR.1 LI-RADS LR-M in a Patient With a New Hypoechoic Nodule Portal Vein Thrombosis in an At-Risk Patient for HCC, LR-TIV

5 The Spleen Darci J. Wall Video 5.1 Normal Spleen in Sagittal Plane Video 5.2 Normal Spleen in Transverse Plane Video 5.3 Contrast Study of Lymphoma Manifesting as a Hypoechoic Solitary Splenic Lesion Video 5.4 Massive Splenomegaly Video 5.5 Splenic Varices Grayscale Video 5.6 Splenic Varices Color Doppler Video 5.7 Granulomas Video 5.8 Littoral Cell Angiomas

6 The Biliary Tree and Gallbladder Korosh Khalili and Stephanie R. Wilson Video 6.1 Distal Common Bile Duct and Ampulla of Vater Video 6.2 Intrahepatic Bile Duct Stones Video 6.3 Intrahepatic Microlithiasis Video 6.4 Distal Common Bile Duct Stone Video 6.5 Mirizzi Syndrome Video 6.6 Pneumobilia in Nondilated Bile Ducts Video 6.7 Choledochoduodenal Fistula Video 6.8 Fasciola hepatica Infection, Acute Phase Video 6.9 Fasciola hepatica Infection, Live Parasite Video 6.10 Primary Sclerosing Cholangitis Video 6.11 Primary Sclerosing Cholangitis Video 6.12 Cholangiocarcinoma Complicating Primary Sclerosing Cholangitis Video 6.13 Cholangiocarcinoma Complicating Primary Sclerosing Cholangitis Video 6.14 Duplication of the Gallbladder Video 6.15 Contracted Gallbladder Video 6.16 Acute Cholecystitis Video 6.17 Gangrenous Cholecystitis With Focal Perforation Video 6.18 Perforated Cholecystitis With Liver Abscess Video 6.19 Gallbladder Wall Edema Video 6.20 Cholesterol Polyps Video 6.21 Gallbladder Metastases

7 Pancreatic Sonography Thomas Winter, III Video Video Video Video Video Video Video Video Video

7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 7.9

Normal Pancreas Acute Pancreatitis Acute Pancreatitis Chronic Pancreatitis Chronic Pancreatitis Pancreatic Pseudocyst Infiltrating Pancreatic Cancer Pancreatic Carcinoma Pancreatic Carcinoma

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VIDEO CONTENTS

Video 7.10 Ultrasound-Guided Core Biopsy of a Pancreatic Adenocarcinoma Video 7.11 Intraductal Papillary Mucinous Neoplasm Video 7.12 Main Duct Intraductal Papillary Mucinous Neoplasm (IPMN) on CT Video 7.13 Contrast-Enhanced Ultrasound of Pancreatic Adenocarcinoma Video 7.14 Contrast-Enhanced Ultrasound of a Mucinous Cystic Neoplasm of the Pancreas

8 The Gastrointestinal Tract Stephanie R. Wilson and Alexandra Medellin Video 8.1 Incidentally Detected Neuroendocrine Tumor (Carcinoid) of the Small Bowel Video 8.2 Classic Features of Crohn disease on a Sweep Through the Terminal Ileum Video 8.3 Loss of Stratification of the Bowel Wall Layers in Severe Subacute Inflammation of the Sigmoid Colon in a Patient With Crohn Disease Video 8.4 Stricture in Crohn Disease Video 8.5 Color Doppler Shows Hyperemia in Thickened Bowel Wall in Crohn Disease, Indicating Active Disease. Video 8.6 Contrast-Enhanced Longitudinal Image of Crohn Disease Video 8.7 Contrast-Enhanced Axial Image of Bowel in Crohn Disease Video 8.8 Severe Fixation and Acute Angulation of the Ileum With Stricture and Enteroenteric Fistula. Video 8.9 Incomplete Small Bowel Obstruction in Patient With Crohn Disease Video 8.10 Dysfunctional and Excess Peristalsis Video 8.11 Localized Perforation With a Phlegmonous Inflammatory Mass Video 8.12 Enteroenteric Fistula Video 8.3 Normal Appendix Video 8.14 Perforated Appendix Video 8.15 Acute Diverticulitis in Second Trimester of Pregnancy Video 8.16 Paralytic Ileus Video 8.17 Incomplete Bowel Obstruction Due to an Inflammatory Stricture From Crohn Disease

9 The Kidney and Urinary Tract Christopher M. Buros, Ashley N. Kalor, and Mitchell E. Tublin Video Video Video Video Video Video Video Video Video Video Video Video Video Video Video Video Video Video Video Video Video Video

9.1 Hypertrophied Column of Bertin 9.2 Crossed Fused Renal Ectopia 9.3 Horseshoe Kidney 9.4 Acute Pyelonephritis 9.5 Renal Abscess 9.6 HIV Nephropathy 9.7 Emphysematous Cystitis 9.8 Renal Calculus 9.9 Ureteral Calculus 9.10 Doppler Jet 9.11 Hypercalcemic Nephrocalcinosis 9.12 Renal Cell Carcinoma 9.13 Urothelial Carcinoma of the Bladder 9.14 Exophytic Enhancing Renal Lesion 9.15 Renal Metastasis 9.16 Renal Cyst With Non-Enhancing Debris 9.17 Hemorrhagic Renal Cyst 9.18 Lithium Nephropathy 9.19 Renal Hematoma in a Transplant Kidney 9.20 Bladder Diverticula 9.21 Clear Cell Renal Cell Carcinoma 9.22 Pseudotumor

10 The Prostate and Transrectal Ultrasound Ants Toi and Sangeet Ghai Video Video Video Video Video Video Video Video Video

10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 10.9

Normal Prostrate in Axial Cine Sweep Normal Prostrate in Sagittal Cine Sweep Normal Prostate Vascularity Bacterial Prostatitis Abscess Aspiration Prostate Cancer Power Doppler Imaging of Prostate Cancer Micro-Ultrasound Micro-Ultrasound Biopsy

11 The Adrenal Glands Ashley N. Kalor and Mitchell E. Tublin Video Video Video Video Video

11.1 11.2 11.3 11.4 11.5

Normal Adrenal Gland Adrenal Adenoma Adrenal Adenoma Hemorrhage Within an Adrenal Adenoma Adrenal Gland With Calcification

12 Retroperitoneal Sonography Constantine M. Burgan and Helena Gabriel Video 12.1 Saccular Aneurysm of the Aorta Video 12.2 Type II Video 12.3 Type II Endoleak Video 12.4 Type III Endoleak Video 12.5 Type III Endoleak Video 12.6 Contained Rupture Video 12.7 Aortic Pseudoaneurysm (Contained Rupture) Transverse Video 12.8 Aortic Pseudoaneurysm (Contained Rupture) Long Axis Video 12.9 Left Renal Artery Stenosis With Color Bruit and Aliasing Throughout Cardiac Cycle Video 12.10 Angiogram of Stented Accessory Left Renal Artery Restenosis Video 12.11 Angiogram of Stented Accessory Left Renal Artery Restenosis Video 12.12 Sonogram After Stent Was Placed in the Accessory Left Renal Artery Restenosis Post Re-stenting Video 12.13 Inferior Vena Cava Longitudinal Images Video 12.14 Nutcracker Syndrome Video 12.15 Nutcracker Syndrome Post Stent Placement Video 12.16 Longitudinal Images of Mildly Prominent Ovarian Veins Crossing From One Side of Uterus to the Other Video 12.17 Transverse Images of Mildly Prominent Ovarian Veins Crossing From One Side of Uterus to the Other Video 12.18 Angiogram of Left Ovarian Vein During Coil Placement Video 12.19 Leiomyosarcoma Video 12.20 Leiomyosarcoma Video 12.21 Normal Transverse Clip Through the Retroperitoneum Video 12.22 Lymphoma Video 12.23 Schwannoma

13 Dynamic Ultrasound of Hernias of the Groin and Anterior Abdominal Wall Alison M. Savicke and Deborah Levine Video 13.1 Direct Inguinal Hernia With Intraperitoneal and Preperitoneal Fat Video 13.2 Fat-Containing Indirect Inguinal Hernia Video 13.3 Bowel-Containing Inguinal Hernia

VIDEO CONTENTS Video 13.4 Large Fat-Containing Direct Inguinal Hernia Which Slides Obliquely During Compression Maneuver Video 13.5 Change in Hernia Contents During Valsalva Maneuver Video 13.6 Completely Reducible Large Wide-Necked Fat-Containing Ventral Hernia Video 13.7 Partially Reducible Indirect Inguinal Hernia Containing Fat and Bowel Video 13.8 Nonreducible Fat-Containing Epigastric Linea Alba Hernia Video 13.9 Large Bowel-Containing Indirect Inguinal Hernia Extending into Scrotum. Video 13.10 Fat-Containing Femoral Hernia Video 13.11 Nonreducible Femoral Hernia Video 13.12 Moderate-Sized Fat-Containing Nonreducible Left Spigelian Hernia Video 13.13 Large Fat- and Bowel-Containing Incompletely Reducible Spigelian Hernia Video 13.14 Adjacent Spigelian Hernias Video 13.15 Diastasis Recti Without Hernia Video 13.16 Fat-Containing Linea Alba Hernia Video 13.17 Small Fat-Containing Nonreducible Epigastric Linea Alba Hernia Video 13.18 Two Adjacent Moderate-Sized Fat-Containing Incompletely Reducible Epigastric Linea Alba Hernias Video 13.19 Umbilical Hernia Video 13.20 Moderate-Sized Fat-Containing Reducible Incisional Hernia Video 13.21 Two Adjacent Moderate-Sized Fat-Containing Incisional Hernias in Patient After Transverse Rectus Abdominis Myocutaneous (TRAM) Flap Breast Reconstruction Video 13.22 Pantaloon Hernias Video 13.23 Mesh With Strong Shadow Makes Evaluation for Recurrent Hernia Difficult Video 13.24 Moderate-Sized Fat-Containing Reducible Recurrent Inguinal Hernia at the Superior Edge of Mesh Video 13.25 Strangulated Right Femoral Hernia Video 13.26 Canal of Nuck Cyst Video 13.27 Canal of Nuck Cyst Video 13.28 Desmoid Tumor

14 The Peritoneum Dilkash Kajal and Deborah Levine Video 14.1 Normal Visceral Peritoneum Video 14.2 Normal Mesentery Video 14.3 Normal Mesentery Video 14.4 Normal Mesentery Video 14.5 Normal Greater Omentum Video 14.6 Normal Omentum Without Ascites Video 14.7 Tumor Infiltration of the Greater Omentum Video 14.8 Tumor Infiltration of the Omentum Video 14.9 Tumor Implant in the Pouch of Douglas Video 14.10 Tumor Implant in the Pouch of Douglas With Manipulation at Real-Time Imaging Video 14.11 Pelvic Hematoma Video 14.12 Peritoneal Inclusion Cyst Video 14.13 Peritoneal Carcinomatosis Parietal Peritoneum Video 14.14 Visceral Peritoneal Metastasis on Dome of Liver From Ovarian Granulosa Cell Tumor Video 14.15 Visceral Peritoneal Metastasis on Dome of Liver From Ovarian Granulosa Cell Tumor Video 14.16 Peritoneal Carcinomatosis Visceral Peritoneum Video 14.17 Peritoneal Carcinomatosis Visceral Peritoneum Video 14.18 Endometrioma in the Pouch of Douglas

Video Video Video Video Video Video Video Video Video

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14.19 Peritoneal Mesothelioma 14.20 Inflamed Fat 14.21 Left-Sided Segmental Omental Infarction 14.22 Left-Sided Segmental Omental Infarction 14.23 Normal Epiploic Appendage 14.24 Epiploica Appendagitis 14.25 Mesenteric Panniculitis 14.26 Endometriotic Plaque 14.27 Endometriotic Plaque

15 Ultrasound-Guided Biopsy of Chest, Abdomen, and Pelvis Theodora A. Potretzke, Thomas D. Atwell, and J. William Charboneau Video 15.1 Ultrasound-Guided Omental Core Biopsy Video 15.2 Ultrasound-Guided Liver Core Biopsy Video 15.3 Ultrasound-Guided Liver Mass Biopsy Using “Freehand” Technique Video 15.4 Ultrasound-Guided Liver Mass Biopsy Using “Freehand” Technique Video 15.5 Power Doppler Imaging Improving Drain Conspicuity Video 15.6 Transvaginal Adnexal Cyst Local Anesthesia Video 15.7 Transvaginal Adnexal Cyst Aspiration

16 Solid-Organ Transplantation Molly B. Carnahan and Ghaneh Fananapazir Video Video Video Video Video Video Video

16.1 16.2 16.3 16.4 16.5 16.6 16.7

Normal Liver Parenchyma Liver Transplant Torsion Acute Renal Arterial Thrombosis Chronic Renal Arterial Thrombosis Renal Transplant Pseudoaneurysm After Biopsy Renal Vein Thrombosis Pancreatic Transplant Pseudoaneurysm

17 Thyroid Gland and Cervical Lymph Node Sonography Kedar Gopal Sharbidre and Franklin N. Tessler Video 17.1 Transverse Clip of a Normal Right Thyroid Lobe Video 17.2 Sagittal Clip of a Normal Right Lobe Video 17.3 Transverse Sweep Through the Right Lobe and Isthmus Shows Multiple Nodules Video 17.4 Sagittal Clip of the Right Lobe Demonstrates Two Degenerating Mixed Cystic and Solid Nodules Video 17.5 Clip Shows a Papillary Thyroid Carcinoma Containing Multiple Punctate Echogenic Foci/Microcalcifications Video 17.6 Spongiform Nodule Contains Innumerable Small Cystic Spaces, a Classic Benign Appearance Video 17.7 Transverse Sonogram of the Right Lobe Shows a Solid (2 Points), Hypoechoic (2 Points) Nodule With No Other Suspicious Features Video 17.8 Transverse Clip During a Fine-Needle Aspiration Shows Needle Excursions Inside the Target Nodule Video 17.9 Fine-Needle Aspiration of a Nodule at the Junction of the Left Lobe and Isthmus Using a Shallow Approach Video 17.10 Clip Demonstrates Multiple Lymph Nodes With Echogenic and Cystic Areas Due to Metastases From Papillary Thyroid Cancer Video 17.11 Transverse Scan of the Upper Left Neck Demonstrates an Abnormal, Hypoechoic Level I Lymph Node Adjacent to the Echogenic Submandibular Gland Video 17.12 Transverse Sweep Through a Normal Echogenic Thyroid Bed With No Masses

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VIDEO CONTENTS

18 Other Glands in the Head and Neck

21 Overview of Musculoskeletal SonographydTechniques and

Mary E. Cunnane and Boris Bulat Kumaev Video 18.1 Cystic and Solid Parathyroid Adenoma Video 18.2 Small Parathyroid Adenoma Video 18.3 Multiple-Gland Parathyroid Hyperplasia Video 18.4 Multiple-Gland Parathyroid Hyperplasia Video 18.5 Superior Parathyroid Adenoma Video 18.6 Superior Parathyroid Adenoma Video 18.7 Inferior Parathyroid Adenoma Video 18.8 Inferior Parathyroid Adenoma Video 18.9 Ectopic Superior Parathyroid Adenoma Video 18.10 Intrathyroid Parathyroid Adenoma Video 18.11 Intrathyroid Parathyroid Adenoma Video 18.12 Ectopic Parathyroid Adenoma Video 18.13 Parathyromatosis in the Postoperative Neck Video 18.14 Parathyroid Adenoma Video 18.15 Small Inferior Parathyroid Adenoma and Multinodular Goiter Video 18.16 Ectopic Intrathyroid Parathyroid Adenoma Biopsy Video 18.17 Ectopic Parathyroid Adenoma in the Carotid Sheath Biopsy Video 18.18 Ethanol Ablation of Recurrent Graft-Dependent Hyperparathyroidism

19 The Breast Jordana Phillips Video 19.1 Importance of Light Pressure for Color Doppler Examination Video 19.2 Importance of Light Pressure for Color Doppler Examination Video 19.3 Normal Cyst Video 19.4 Intraductal Papilloma Video 19.5 Ductal Debris Video 19.6 Percutaneous Biopsy Using Spring-Loaded Biopsy Device Video 19.7 Percutaneous Biopsy Using a Non-Throw Video

20 The Scrotum Thomas Winter, III Video 20.1 Atrophic Testis With Seminoma Video 20.2 Teratoma Video 20.3 Mixed Germ Cell Tumor Video 20.4 Carney Complex and Presumed Benign Large-Cell Calcifying Sertoli Cell Tumor Video 20.5 Epidermoid Cyst Video 20.6 Epidermoid Cyst Video 20.7 Varicocele in Patient Performing a Valsalva Maneuver Video 20.8 Varicocele Shown on Color Doppler Imaging Video 20.9 Pseudotesticular Appearance of Epidermoid Cyst Mimicking Polyorchidism Video 20.10 Postvasectomy Appearance of Epididymis and Vas Deferens Video 20.11 Dancing Sperm Postvasectomy Appearance Video 20.12 Torsion With Infarct Video 20.13 Whirlpool Sign in Testicular Torsion Video 20.14 Acute Orchitis Video 20.15 Inferior Traumatic Tunica Albuginea Rupture, Hematoma in Testis, and Extrusion of Seminiferous Tubules Video 20.16 Mixed Germ Cell Tumor in an Undescended Testicle

Applications Kara Gaetke-Udager and Corrie M. Yablon Video Video Video Video Video

21.1 21.2 21.3 21.4 21.5

Normal Biceps Muscle and Distal Tendon Normal Achilles Tendon Normal Finger Flexor Tendons Dynamic Imaging Dynamic Ulnar Nerve Subluxation Short-axis Imaging of a Baker Cyst

22 The Shoulder Kara Gaetke-Udager and Corrie M. Yablon Video 22.1 Dynamic Assessment for Subcoracoid Impingement Video 22.2 Imaging the Supraspinatus in Long Axis Then Transitioning to Infraspinatus Posteriorly Video 22.3 Dynamic Assessment for Subacromial Impingement Video 22.4 Dynamic Imaging Showing Increased Prominence of Glenohumeral Effusion on External Rotation Video 22.5 Short-Axis Imaging of the Supraspinatus Tendon

23 Musculoskeletal Interventions Ronald S. Adler Video 23.1 Intraarticular Injection of a Hip Under Ultrasound Guidance Video 23.2 Biceps Tendon Sheath Injection Using a Rotator Interval Approach Video 23.3 Aspiration of a Spinoglenoid Notch Cyst Video 23.4 Injection of Calcific Tendinosis Video 23.5 Knee Platelet-Rich Plasma Injection Video 23.6 Depiction of Tenex Procedure Video 23.7 Lateral Femoral Cutaneous Nerve Post Injection

24 The Extracranial Cerebral Vessels Edward I. Bluth, Stephen I. Johnson, and Laurie Troxclair Video 24.1 Minimal Homogeneous Plaque at Carotid Bulb (Gray-Scale) Video 24.2 Considerable Homogeneous Plaque at Internal Carotid Artery (Gray-Scale) Video 24.3 Type 3 Homogeneous Plaque With Less Than 50% Sonolucency (Gray-Scale) Video 24.4 Type 3 Homogeneous Plaque With Low-Grade Stenosis of the Internal Carotid Artery (Gray-Scale) Video 24.5 Calcified Plaque in the Internal Carotid Artery (Gray-Scale) Video 24.6 Heterogeneous Plaque in the Internal Carotid Artery (Type 1) (Gray-Scale) Video 24.7 Heterogeneous Plaque (Type 1) With Greater Than 50% Sonolucency Within the Plaque of the Left Internal Carotid Artery (Gray-Scale) Video 24.8 Heterogeneous Plaque (Type 2) in the Internal Carotid Artery (Gray-Scale) Video 24.9 High-Grade Stenosis in the Proximal Internal Carotid Artery (Color Doppler) Video 24.10 Heterogeneous Plaque in the Internal Carotid Artery (Color Doppler) Video 24.11 Heterogeneous Plaque in Left Internal Carotid Artery (Power Doppler) Video 24.12 High-Grade Stenosis in the Internal Carotid Artery (Transverse Power Doppler) Video 24.13 High-Grade Stenosis of the Internal Carotid Artery (Transverse Power Doppler) Video 24.14 Low-Grade Stenosis in the Internal Carotid Artery (Transverse Color Doppler)

VIDEO CONTENTS Video 24.15 Normal Spectral Waveform of the Proximal Internal Carotid Artery Video 24.16 Normal Spectral Waveform of the Mid Internal Carotid Artery Video 24.17 Normal Spectral Waveform of the Distal Internal Carotid Artery Video 24.18 Normal Spectral Waveform of the Distal Common Carotid Artery Video 24.19 High-Grade Stenosis in the Internal Carotid Artery (Power Doppler) Video 24.20 High-Grade Stenosis in the Internal Carotid Artery (Color Doppler) Video 24.21 High-Grade Stenosis With Markedly Elevated Peak Systolic Velocity as Well as Spectral Broadening (Color and Spectral Doppler) Video 24.22 Color and Spectral Doppler of Low-Grade Stenosis in the Internal Carotid Artery

25 Peripheral Arteries Mohd Zahid, Mark E. Lockhart, and Michelle LaVonne Robbin Video 25.1 Acute Thrombus in the Superficial Femoral Artery Video 25.2 Occlusion of the Superficial Femoral Artery With a Large Collateral Exiting Proximal to the Occlusion Video 25.3 Severe Calcification of the Superficial Femoral Artery Video 25.4 Common Femoral Artery Pseudoaneurysm Video 25.5 Common Femoral Artery to Common Femoral Vein Arteriovenous Fistula (AVF) Video 25.6 Visible Narrowing is Present on Gray-scale Video 25.7 Large Radial Artery Pseudoaneurysm With Rent in Arterial Wall Video 25.8 Large Radial Artery Pseudoaneurysm Video 25.9 Subclavian Steal

26 Peripheral Veins Muhammad U. Aziz, Mohd Zahid, Therese M. Weber, and Michelle LaVonne Robbin Video 26.1 Normal Femoral Vein Compression During Study to Assess for Deep Venous Thrombosis Video 26.2 Acute Common Femoral Vein (CFV) Thrombus Video 26.3 Nonocclusive Slightly Mobile Thrombus Within the Great Saphenous Vein (GSV) With Extension Into the Common FemoralVein (CFV) Video 26.4 Acute Deep Venous Thrombosis in Right Lower Extremity Video 26.5 Chronic Vein Occlusion With Collaterals Video 26.6 Chronic Common Femoral Vein (CFV) Occlusion With Normal Antegrade Flow in the Femoral Vein, and Flow Reversal in the Profunda Femoral Vein Video 26.7 Slow Flow in Patent, Compressible Vein Without Deep Venous Thrombosis, Longitudinal Cine Clip Video 26.8 Slow Flow in Patent, Compressible Vein Without Deep Venous Thrombosis, Transverse Cine Clip Video 26.9 Thrombus in One of Paired Femoral Veins Video 26.10 Normal Femoral Vein Valve Video 26.11 Normal Internal Jugular Vein (IJV) on Gray-Scale Compression Cine Clip Video 26.12 Acute Internal Jugular Thrombus Video 26.13 Nonocclusive Thrombus in One Brachial Vein in the Paired Brachial Veins Video 26.14 Acute Thrombus Around Peripherally Inserted Central Catheter (PICC) Line in the Basilic Vein

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Video 26.15 Acute Thrombus Around Peripherally Inserted Central Catheter (PICC) Line in the Basilic Vein

27 Hemodialysis Kedar Gopal Sharbidre, Lauren Freeman Alexander, Heidi R. Umphrey, and Michelle LaVonne Robbin Video 27.1 Thick-Walled Cephalic Vein With Chronic Thrombus Video 27.2 Normal Compression of the Right Internal Jugular Vein (IJV) Suggests the Absence of Thrombosis Video 27.3 Narrowing and Color Flow Aliasing at the Graft Venous Anastomosis Suggesting Anastomotic Stenosis Video 27.4 Moderate-sized Hematoma Adjacent to the Arteriovenous Fistula (AVF) Video 27.5 Small Basilic Vein Pseudoaneurysm Video 27.6 Graft Wall Irregularity and Degeneration From Repeated Punctures

28 The Uterus Pei-Kang Wei, Alison M. Savicke, and Deborah Levine Video 28.1 Complete Septate Uterus Video 28.2 Bicornuate Uterus Video 28.3 Uterus Didelphys Video 28.4 Unicornuate Uterus Video 28.5 Necrotic Fibroid Video 28.6 Adenomyosis Video 28.7 Prolapsing Polyp Video 28.8 Endometrial Polyp Video 28.9 Endometrial Polyp Video 28.10 Endometrial Carcinoma Video 28.11 Endometrial Carcinoma With Hematometra Video 28.12 Synechiae Video 28.13 Circular Intrauterine Device (IUD) Video 28.14 Low Position of Intrauterine Device (IUD) Video 28.15 Bladder Flap Hematoma and Sutures After Cesarean Section Video 28.16 Vascularized Retained Products of Conception Video 28.17 Endometritis Video 28.18 Hematometra Postpartum

29 Adnexal Sonography Maitray D. Patel Video 29.1 Corpus Albicans Video 29.2 Punctate Echogenic Foci Video 29.3 Polycystic Ovarian Morphology Video 29.4 Normal Slide Sign Video 29.5 Abnormal Slide Sign Video 29.6 Deep Infiltrating Endometriosis Video 29.7 Ovarian Torsion Video 29.8 Twist/Whirlpool Sign of Ovarian Torsion Video 29.9 Ovarian Torsion on CT Video 29.10 Flipped Ovary Schematic Video 29.11 Pelvic Inflammatory Disease Video 29.12 Hemorrhagic Ovarian Cyst Video 29.13 Endometrioma Video 29.14 Endometrioma, With Fluid/Fluid Layer, With Echogenic Blood Product and Debris Settling in the Dependent Portion of the Cyst Video 29.15 Postmenopausal Cyst Video 29.16 Hydrosalpinx

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VIDEO CONTENTS 29.17 Hydrosalpinx on CT 29.18 Theca Lutein Cysts 29.19 Borderline Ovarian Tumor 29.20 Mucinous Cystadenoma 29.21 Grade IIIa Endometrioid Ovarian Carcinoma 29.22 Clear Cell Carcinoma Arising in an Endometrioma 29.23 Dermoid 29.24 Subtle Large Dermoid 29.25 Mixed Germ Cell Tumor

30 Overview of Obstetric Imaging Deborah Levine and Alison M. Savicke Video 30.1 Early First Trimester Cine When M-Mode Cannot Capture an Accurate Heart Rate Video 30.2 Normal Midline View of Uterus, Anterior Placenta, and Fetus in Sagittal Plane in Cephalic Position Video 30.3 Normal Intracranial Anatomy Video 30.4 Transverse Fetal Chest and Four-Chamber Heart View Video 30.5 Transvaginal Imaging to Better Demonstrate Anatomy of Distal Spine and Kidneys Video 30.6 Transverse Spine and Assessing Situs Video 30.7 Assessing Umbilical Arteries Adjacent to the Bladder, Indicating a Three-Vessel Umbilical Cord. Video 30.8 Fibroid Uterus After Prior C-Section Video 30.9 Uterine Synechia Video 30.10 Septate Uterus With Pregnancy in Left Side Video 30.11 Uterus Didelphis With Pregnancy in the Left Uterine Horn

31 The First Trimester Mindy M. Horrow Video 31.1 Cardiac Activity in Same Embryo was Observed in Real Time and Recorded on a Cine Clip Because the Embryo Was Too Small to Obtain an M-Mode Tracing Video 31.2 Cine of Embryo Demonstrating Motion of Trunk and Extremities Video 31.3 Cine Through Embryo Demonstrating Motion in Legs Through Hands and Head Video 31.4 Monoamniotic Monochorionic Twins Video 31.5 Live 2mm CRL With Mobile Sac Went on to Spontaneous Abortion Video 31.6 Tubal Ectopic Pregnancy With Gentle Motion of the Probe to Assess Separate Movement of the Ectopic Pregnancy and the Adjacent Ovary

32 Chromosomal Abnormality Barbara O’Brien and William Choi Video 32.1 Nuchal Translucency Video 32.2 Cystic Hygroma Video 32.3 Nasal Bone in First Trimester Video 32.4 Absent Nasal Bone in Second-Trimester Fetus With Trisomy 21 Video 32.5 Echogenic Bowel Video 32.6 Amniocentesis Needle Being Withdrawn from Amniotic Fluid Cavity

33 Multifetal Pregnancy Catherine H. Phillips and Mary C. Frates Video 33.1 Quadrachorionic Quadraamniotic Gestation at 6 Weeks, 6 Days Video 33.2 Conjoined Embryos, 9 Weeks Gestational Age

Video 33.3 Monochorionic Monoamniotic Twins, 26 Weeks Gestational Age Video 33.4 Three Separate Placentas in a Trichorionic Triamniotic Triplet Pregnancy at 13 Weeks Gestational Age Video 33.5 Velamentous Cord Insertion in a Twin at 34 Weeks Gestational Age Video 33.6 Growth and Fluid Discrepancies in Dichorionic Twins, 24 Weeks Gestational Age Video 33.7 TwineTwin Transfusion Syndrome, 12 Weeks 4 Days Gestational Age Video 33.8 Monochorionic Diamniotic Twins With TwineTwin Transfusion Syndrome Video 33.9 Monochorionic Diamniotic Twins With TwineTwin Transfusion Syndrome Video 33.10 Twin Reversed Arterial Perfusion Syndrome, 16 Weeks Gestational Age Video 33.11 Monochorionic Monoamniotic Twins, 12 Weeks Gestational Age Video 33.12 Monochorionic Monoamniotic Entangled Cords at 29 Weeks Gestational Age Video 33.13 Monochorionic Monoamniotic Twins, 28 Weeks Gestational Age Video 33.14 Monochorionic Monoamniotic Conjoined Twins, 35 Weeks Gestational Age

34 The Fetal Face and Neck Sonography Deborah Levine and Judy A. Estroff Video 34.1 Computed Tomography (CT) Scan in Neonate With Zika Virus Video 34.2 Left Unilateral Complete Cleft Lip, Cleft Alveolus, and Cleft Palate in Sagittal Plane in 20-Week Gestational Age Fetus Video 34.3 Left Unilateral Complete Cleft Lip, Cleft Alveolus, and Cleft Palate in Coronal Plane in 20-Week Gestational Age Fetus Video 34.4 Left Unilateral Complete Cleft Lip, Cleft Alveolus, and Cleft Palate in Axial Plane in 20-Week Gestational Age Fetus Video 34.5 Micrognathia at 20 Weeks Gestational Age

35 The Fetal Brain Yi Li and Deborah Levine Video 35.1 Normal Brain, Axial Video 35.2 Normal Brain, Coronal Transvaginal Video 35.3 Normal Brain Sagittal Transvaginal, Using a Suture as an Imaging Window, Focusing on Normal Corpus Callosum Above Cavum Septum Pellucidum Video 35.4 Choroid Plexus Cysts Video 35.5 Bilateral Moderate Ventriculomegaly Video 35.6 Anencephaly at 15 weeks Video 35.7 Amniotic Band Sequence Masquerading as Anencephaly Video 35.8 Chiari Malformation in Fetus With Spinal Neural Tube Defect Video 35.9 Holoprosencephaly in Axial Plane Video 35.10 Same Fetus as Video 35.10 in Sagittal Plane Video 35.11 Syntelencephaly Video 35.12 Agenesis of Corpus Callosum in Second Trimester in Axial Plane Video 35.13 Agenesis of Corpus Callosum in Coronal Plane Video 35.14 Agenesis of Corpus Callosum in Sagittal Plane in Third Trimester Video 35.15 Agenesis of Corpus Callosum in Axial Plane With Midline Cyst Video 35.16 Transvaginal Cine of Absence of the Cavum of the Septum Pellucidum in Fetus With Septo-Optic Dysplasia

VIDEO CONTENTS 36 The Fetal Spine Edward R. Oliver and Beverly G. Coleman Video 36.1 Normal Transverse Spine at 19 Weeks’ Gestation Video 36.2 Normal Sagittal Thoracic and Cervical Spine at 19 Weeks’ Gestation Video 36.3 Normal Sagittal Lumbosacral Spine at 19 Weeks’ Gestation Video 36.4 Normal Coronal Thoracolumbar Spine at 19 Weeks’ Gestation Video 36.5 Normal Transverse Lower Thoracic and Upper Lumbar Spine to Localize Vertebral Level at 21 Weeks’ Gestation Video 36.6 Normal Sagittal Lower Thoracic and Upper Lumbar Spine to Localize Vertebral Level at 21 Weeks’ Gestation Video 36.7 Transverse Lumbosacral Myelomeningocele at 21 Weeks’ Gestation Video 36.8 Sagittal Lumbosacral Myelomeningocele at 21 Weeks’ Gestation (same case as Video 36.7) Video 36.9 Transverse Lumbosacral Myelomeningocele at 22 Weeks’ Gestation to Localize Defect Level (same case as Video 36.7) Video 36.10 Sagittal Lumbosacral Lipomyelomeningocele at 21 Weeks’ Gestation Video 36.11 Coronal Thoracolumbar Spine in Fetus With Hemivertebra and Associated Scoliosis at 21 Weeks’ Gestation Video 36.12 Sagittal Type II Sacrococcygeal Teratoma at 22 Weeks’ Gestational Age

37 The Fetal Chest Dorothy Bulas Video 37.1 Congenital Pulmonary Adenomatoid Malformation (Macrocystic) Video 37.2 Congenital Pulmonary Adenomatoid Malformation (Microcystic) With Moderate Mediastinal Shift Video 37.3 Bronchopulmonary Sequestration Video 37.4 Small Pleural Effusion at 16 Weeks’ Gestational Age Video 37.5 Left-Sided Congenital Diaphragmatic Hernia at 32 Weeks’ Gestational Age (Transverse View) Video 37.6 Left-Sided Congenital Diaphragmatic Hernia at 32 Weeks’ Gestational Age (Sagittal View) Video 37.7 Large Left-Sided Congenital Diaphragmatic Hernia With Large Amount of Liver in Chest Video 37.8 Right-Sided Congenital Diaphragmatic Hernia

38 Fetal Echocardiography Julia A. Drose Video 38.1 Angling the Transducer from a Subcostal Four-Chamber View into a Long-Axis View of the Aorta, Long-Axis View of the Pulmonary Artery, a Short-axis View of the Ventricles, and a ShortAxis View of the Great Arteries Video 38.2 Moving the Transducer Cephalad from an Apical Four-Chamber View into a Three-Vessel-Trachea View Video 38.3 Placing the M-mode Cursor through an Apical Wall and Ventricular Wall at the Same Time to Assess for an Arrhythmia Video 38.4 Using Spectral Doppler to Assess an Arrhythmia by Placing the Sample Volume in the Left Ventricle to Visualize Inflow Though the Mitral Valve and Outflow Through the Aortic Valve Simultaneously

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Video 38.5 Color Compare Image Showing a Ventricular Septal Defect (VSD) With Color on the Color Image that is not Visualized on the Gray-Scale Image Video 38.6 Complete Atrioventricular Septal Defect (AVSD) with an Atrial Septal Defect (ASD), Ventricular Septal Defects (VSD) and Single Multileaflet Atrioventricular Valve Video 38.7 Partial Atrioventricular Septal Defect (AVSD) with an Atrial Septal Defect (ASD), Ventricular Septal Defects (VSD) and Two Separate Atrioventicular Valves Video 38.8 Ebstein Anomaly Showing the Tricuspid Valve Displaced Too Low in the Right Ventricle Video 38.9 Hypoplastic Right Ventricle Secondary to Tricuspid Atresia Showing a Very Small Right Ventricle Video 38.10 Another Example of Hypoplastic Right Heart Video 38.11 Hypoplastic Left Heart Syndrome Video 38.12 Multiple Rhabdomyomas

39 The Fetal Gastrointestinal Tract and Abdominal Wall Elizabeth Asch and Deborah Levine Video Video Video Video Video Video Video Video Video Video Video Video Video Video Video Video

39.1 Esophageal Atresia 39.2 Gastric Debris 39.3 Gastric Debris 39.4 Duodenal Atresia 39.5 Jejunal Atresia 39.6 Cloacal Malformation 39.7 Duplication Cyst 39.8 Meconium Peritonitis 39.9 Echogenic Bowel 39.10 Normal Gallbladder 39.11 Annular Pancreas 39.12 Splenic Cyst 39.13 Gastroschisis 39.14 Giant Omphalocele 39.15 Bladder Exstrophy 39.16 Cloacal Exstrophy

40 The Fetal Urogenital Tract Dilkash Kajal and Deborah Levine Video 40.1 “Lying Down” Adrenal Sign Due to Unilateral Renal Agenesis Video 40.2 Bilateral Renal Agenesis Video 40.3 Cross-Fused Renal Ectopia Video 40.4 Horseshoe Kidney Video 40.5 Right Multicystic Dysplastic Kidney (MCDK) and Left Vesico-Ureteric Reflux Video 40.6 Right Multicystic Dysplastic Kidney (MCDK) and Left Vesico-Ureteric Reflux Video 40.7 Postnatal Left Vesico-Ureteric Reflux Video 40.8 Autosomal Recessive Polycystic Kidney Disease Video 40.9 Autosomal Recessive Polycystic Kidney Disease With Atypical Large Cysts at 25 Weeks Video 40.10 Perinephric Urinoma at 22 Weeks Video 40.11 Duplex left Kidney With Hydroureteronephrosis Video 40.12 Prune Belly Syndrome at 15 Weeks Video 40.13 Prune Belly Syndrome at 35 Weeks Video 40.14 Megalourethra (in Association With Posterior Urethral Valves)

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VIDEO CONTENTS

Video 40.15 Cloacal Dysgenesis and Meconium Peritonitis at 17 Weeks Video 40.16 Fetal Ovarian Cysts

41 The Fetal Musculoskeletal System Phyllis Glanc, Johannes Keunen, and David Chitayat Video Video Video Video Video Video

41.1 41.2 41.3 41.4 41.5 41.6

Thanatophoric Dysplasia Achondrogenesis Type 1 Achondrogenenesis Type 1 Chondrodysplasia Punctata Acheiropodia Bilateral Clubfeet at 21 Weeks

42 Sonography of Fetal Hydrops Lisa R. Dunn-Albanese and Deborah Levine Video 42.1 Trace Ascites Video 42.2 Moderate Ascites Video 42.3 Small Left Pleural Effusion Video 42.4 The Diagnosis of Kabuki Syndrome Was Made With Whole Exome Sequencing After Birth Video 42.5 Hydrops From Cardiomyopathy With Poorly Contractile Heart, Moderate Bilateral Pleural Effusions, and Anasarca Video 42.6 Sagittal View Shows a Large Unilateral Pleural Effusion That Everts the Hemidiaphragm and Is Associated With Ascites Video 42.7 Small Pericardial Effusion in a Fetus With Poorly Contractile and Echogenic Heart Video 42.8 Fetus With Hydrops and Placentomegaly Video 42.9 Severe Mediastinal Shift and Hydrops Due to Large Macrocystic Congenital Pulmonary Adenomatoid Malformation (CPAM) Video 42.10 Bronchopulmonary Sequestration With Mild Mediastinal Shift and Secondary Cardiac Involvement Video 42.11 Mild Mediastinal Shift in Patient With Bronchopulmonary Sequestration With Hydrops Video 42.12 Ultrasound-Guided Fetal Thoracentesis of Pleural Effusion Around Bronchopulmonary Sequestration

43 Fetal Measurements: Normal and Abnormal Fetal Growth and Assessment of Fetal Well-Being Carol B. Benson and Peter M. Doubilet Video 43.1 Video Clip of Early Embryonic Heartbeat, Visible in Small Embryo Adjacent to Yolk Sac Video 43.2 Video Clip of Fetal Breathing Movements Video 43.3 Video Clip of Fetal Movement

44 Sonographic Evaluation of the Placenta Thomas D. Shipp Video Video Video Video Video Video Video Video Video Video Video Video Video Video

44.1 Placental Lake 44.2 Thick Placenta in Fetus With Villitis 44.3 Placenta Accrete 44.4 Placenta Increta 44.5 Placenta Percreta 44.6 Cesarean Scar Pregnancy With Placenta Accreta 44.7 Abruption 44.8 Abruption 44.9 Preplacental Hematoma 44.10 Preplacental Hematoma 44.11 Placental Infarction 44.12 Placental Infarction 44.13 Partial Molar Pregnancy 44.14 Circumvallate Placenta

Video 44.15 Circumvallate Placenta Video 44.16 Bilobed Placenta Video 44.17 Uncoiled Umbilical Cord With Color Doppler Video 44.18 Umbilical Cord Pseudocyst Video 44.19 Umbilical Cord Insertions Into Placenta of a Pair of Monoamniotic Twins Video 44.20 Velamentous Cord Insertion and Two-Vessel Cord Video 44.21 Vasa Previa

45 Cervical Ultrasound and Preterm Birth Hournaz Ghandehari and Phyllis Glanc Video 45.1 Cervical Polyp With Vascular Stalk Video 45.2 Cervical “Mucus Plug” With Surrounding Vascularity, Mimicking a Polyp Video 45.3 Short Cervix With Funnel and Bulging Membranes Video 45.4 Short Cervix With Fetal Foot Extending Into Large Funnel Video 45.5 Open Cervix With Floating Debris Video 45.6 Debris Mimicking Placental Tissue at the Internal Os Video 45.7 Cerclage Stitch Encircling the Cervix

46 Neonatal and Infant Brain Imaging Carol M. Rumack and Amanda K. Auckland Video 46.1 Normal Coronal Sweep Video 46.2 Normal Sagittal Sweep Video 46.3 Normal Mastoid Fontanelle Sweep Through the Posterior Fossa Video 46.4 Chiari II Malformation Video 46.5 Ventriculomegaly in Association With Chiari II Malformation (Seen in Video 46.4) Video 46.6 Chiari II Malformation (Same Neonate as in Videos 46.4 and 46.5) Video 46.7 Tethered Cord in Patient With Chiari II Malformation, Sagittal Scan Video 46.8 Absence of Septum Pellucidum, Coronal Scan Video 46.9 Right Subacute Subependymal, Intraventricular, and Right Frontal Intraparenchymal Hemorrhage, Coronal Scan Video 46.10 Right Subependymal, Caudothalamic Groove Hemorrhage Which Extends Into Posterior Caudate Nucleus, Often Seen in Extremely Premature Infants Video 46.11 Intraventricular Hemorrhage With Echogenic Clot in the Fourth Ventricle Extends Posteriorly Into the Cisterna Magna Video 46.12 Acute Intraventricular Echogenic Blood in Third and Fourth Ventricle and Cisterna Magna Sagittal View (Same Neonate as Video 46.11). Video 46.13 Bilateral Intraventricular HemorrhageeFormed Casts in Both Dilated Ventricles and Intraparenchymal Hemorrhage in Right Parieto-Occipital Region Are Shown on a Sweep Through a Coronal View Video 46.14 Acute highly echogenic hemorrhage formed a cast in lateral ventricle and obscures ventricular walls on this sagittal view Video 46.15 Intraventricular hemorrhage is a cast of echogenic material in the lateral ventricle in sagittal view Video 46.16 Cystic periventricular leukomalacia is extensive in frontal, parietal, and occipital parenchyma Video 46.17 Cytomegalovirus With Punctate Calcifications in the Posterior Parietal Region on This Right Sagittal Sweep Video 46.18 Multiple Focal Calcifications Caused by Cytomegalovirus and a Subependymal Cyst Video 46.19 Ventricular Septation Caused by Cytomegalovirus, Shown on This Posterior Fontanelle View

VIDEO CONTENTS 47 Neonatal Brain Doppler and Advanced Ultrasound Imaging Techniques Judy H. Squires and Misun Hwang Video 47.1 Normal Power Doppler of the Deep Anterior and Posterior Circulation Video 47.2 Normal Enhancement (Wash-In) of the Brain of a Term Female at Contrast-Enhanced Ultrasound Video 47.3 Term Infant With Left Middle Cerebral Artery (MCA) Stroke and Luxury Hyperperfusion Video 47.4 High-Grade Glioma in a 1-Day-Old Term Female

48 Doppler Sonography of the Brain in Children Dorothy Bulas and Alexia M. Egloff Video 48.1 Normal Color Doppler of Circle of Willis in 6-Year-Old Video 48.2 Spectral Wave Form of the Right Middle Cerebral Artery Video 48.3 Normal Spectral Doppler of Right Bifurcation Video 48.4 Four-Year-Old Pending Brain Death After Fall From Second Story Video 48.5 Eight-Year-Old Pending Brain Death After Motor Vehicle Accident Postcraniectomy for Hematoma

49 The Pediatric Head and Neck Rupa Radhakrishnan and Beth M. Kline-Fath Video Video Video Video Video Video Video

49.1 49.2 49.3 49.4 49.5 49.6 49.7

Wharton Duct Stone Multinodular Goiter Thyroid Cancer, Papillary Type Cervical Teratoma in Utero Infantile Hemangioma Lymphatic Malformation Jugular Vein Thrombosis

50 The Pediatric Spinal Canal Sonography Ilse Castro-Aragon and Ramon Sanchez-Jacob Video 50.1 Normal Sagittal Spine Anatomy Video 50.2 Normal Sagittal Filum Terminale and Cauda Equina Video 50.3 Skin Dimple and Hypoechoic Tract in Subcutaneous Tissues Extending to Normal Coccyx Video 50.4 Lipomyelocele in Sagittal View Video 50.5 Lipomyelocele in Sagittal View Video 50.6 Lipomyelocele in Transverse View Video 50.7 Lipomyelomeningocele Video 50.8 Filar Lipoma in Sagittal View Video 50.9 Filar Lipoma in Transverse View Video 50.10 Segmental Spinal Dysgenesis in Sagittal View Video 50.11 Segmental Spinal Dysgenesis Patient With Fatty Filum

51 The Pediatric Chest Chetan Chandulal Shah Video 51.1 Moving Septations Within Pleural Fluid are Seen in a Longitudinal Sonogram of a 14-Year-Old Girl With Cystic Fibrosis Video 51.2 Normal, Equal Bilateral Hemidiaphragmatic Movement in a Healthy 9-Month-Old Infant are Seen on Transverse Sonogram Performed Just Below the Sternum Using the Liver as an Acoustic Window Video 51.3 Normal Right Hemidiaphragmatic Movement on Longitudinal Sonogram in Healthy 31-Month-Old Child Video 51.4 Unilateral Diaphragmatic Paralysis in an Infant After Cardiac Surgery: Minimal Right Diaphragmatic Movement in a 1-YearOld Child With History of Mediastinitis After Orthotopic Heart Transplant

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52 The Pediatric Liver and Spleen Sara M. O’Hara Video 52.1 Normal Porta Hepatis Showing Portal Vein, Hepatic Artery, and Common Bile Duct Video 52.2 Neonatal Hepatitis Video 52.3 Steatosis from obesity Video 52.4 Multiple Cutaneous Hemangiomas in a 1-Month-Old Infant Video 52.5 Focal Liver Lesion Video 52.6 Hepatocellular Carcinoma Biopsy Video 52.7 Normal Flow in the Main Portal Vein Video 52.8 Normal Branching Vessels in the Liver Video 52.9 Normal Third and Fourth-Order Branches in the Liver Video 52.10 Cavernous Transformation of the Portal Vein Color Doppler Images Video 52.11 Pneumobilia, an Expected Finding Following Portoenterostomy Video 52.12 Splenic Laceration

53 Pediatric Kidney, Urinary Tract, and Adrenal Sonography Harriet J. Paltiel Video 53.1 Crossed Renal Ectopia Video 53.2 Contrast-Enhanced Urosonography Depicts a Normal Bladder Video 53.3 Contrast-Enhanced Urosonography Demonstrates Vesicoureteral Reflux Video 53.4 Contrast-Enhanced Urosonography Shows a Normal Male Urethra Video 53.5 Acute Pyelonephritis With Thickening of Renal Pelvic and Proximal Ureteral Walls Video 53.6 Pyonephrosis Video 53.7 Renal Candidiasis With Echogenic Microabscesses Video 53.8 Hemorrhagic Cystitis With Blood Clot Surrounding Foley Catheter Balloon Video 53.9 Inflammatory Pseudotumor Video 53.10 Laceration of the Mid-Lateral Aspect of the Left Kidney and Perirenal Hematoma Video 53.11 Multicystic Dysplastic Kidney Video 53.12 Burkitt Lymphoma Involving Kidney Video 53.13 Neuroblastoma

54 Pediatric Gastrointestinal Tract Sonography Susan D. John and HaiThuy N. Nguyen Video 54.1 Transverse Planes of the Gastroesophageal Junction Show Prominent Muscularis Mucosa in the Distal Esophagus With Fluid Passing Through the Lumen Video 54.2 Fluid Passes Freely Through the Normal Pylorus Video 54.3 Hypertrophic Pyloric Stenosis Video 54.4 Same Infant in Fig. 54.16C Showing the Dilated Stomach and Proximal Duodenum with to and fro Movement of Intraluminal Contents Video 54.5 Shows to-and-fro Motion of the Echogenic Enteric Contents Video 54.6 Six-Day-Old Male With Bilious Emesis With Small Bowel Obstruction Video 54.7 No Whirlpool Sign on the Transverse Cine Clip to Suggest Complicating Volvulus Video 54.8 Video Shows Blind-Ending Intraluminal Tubular Structure Within the Small Bowel in the Right Lower Quadrant, Presumed to Represent Ascariasis (tapeworm) Video 54.9 Ultrasound Supplemental Video of the Child in C

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VIDEO CONTENTS

55 Pediatric Pelvic Sonography Christine L. Xue and Patricia T. Acharya Video Video Video Video Video

55.1 55.2 55.3 55.4 55.5

Hydrosonovaginography Normal Ovary in a Child Polycystic Ovarian Disease Postpubertal Testes Legend Testicular Microlithiasis

56 Pediatric Musculoskeletal Ultrasound Ramon Sanchez-Jacob and Jessica Leschied Video 56.1 Posteriorly Dislocated Femoral Head That Can Be Manually Reduced With Hip Abduction Video 56.2 Longitudinal Cine Loop of the Medial Elbow With a Full-Thickness Ulnar Collateral Ligament Tear Video 56.3 Full-Thickness Disruption of the Ulnar Collateral Ligament of the Thumb Without Retraction or a So-Called Stener Lesion

PART ONE Ultrasound Physics, Bioeffects, and Contrast CHAPTER

1

Physics of Ultrasound Da Zhang, Korosh Kahlili, Hojun Yu, and Deborah Levine

CHAPTER OUTLINE BASIC ACOUSTICS, 1 Wavelength and Frequency, 1 Propagation of Sound, 2 Distance Measurement, 3 Acoustic Impedance, 3 Reflection, 4 Refraction, 5 Attenuation, 5 INSTRUMENTATION, 5 Transmitter, 5 Transducer, 6 Receiver, 7 Image Display, 8 Mechanical Sector Scanners, 9 Arrays, 9 Transducer Selection, 11 IMAGE DISPLAY AND STORAGE, 11

A

SPECIAL IMAGING MODES, 12 Tissue Harmonic Imaging, 12 Spatial Compounding, 12 Three-Dimensional Ultrasound, 13 Ultrasound Elastography, 13 IMAGE QUALITY, 15 Spatial Resolution, 15 DOPPLER SONOGRAPHY, 16 Doppler Signal Processing and Display, 19 Doppler Instrumentation, 20 Power Doppler, 21 Interpretation of the Doppler Spectrum, 21 Interpretation of Color Doppler, 24 Other Technical Considerations, 25 ULTRASOUND ARTIFACTS, 26

ll diagnostic ultrasound applications are based on the detection and display of acoustic energy reflected from interfaces within the body. These interactions provide the information needed to generate high-resolution gray-scale images of the body, as well as display information related to blood flow. Its unique imaging attributes have made ultrasound an important and versatile medical imaging tool. However, expensive state-of-the-art instrumentation does not guarantee the production of high-quality studies of diagnostic value. Gaining maximum benefit from this complex technology requires a combination of skills, including knowledge of the physical principles that empower ultrasound with its unique diagnostic capabilities. The user must understand the fundamentals of the interactions of acoustic waves with tissues and the methods and instruments used to produce and optimize ultrasound display. With this knowledge the user can collect the maximum information from each examination, avoiding pitfalls and errors in diagnosis that may result from the omission of information or the misinterpretation of artifacts.1 Ultrasound imaging and Doppler ultrasound are based on the reflection of sound energy by interfaces of materials with different properties through interactions governed by acoustic physics. The amplitude of reflected energy is used to generate ultrasound images, and frequency shifts in the backscattered ultrasound provide information relating to moving targets

Assumptions in Gray-Scale Imaging, 27 Speed of Sound Artifacts, 27 Attenuation of Sound Artifacts, 27 Shadowing, 27 Increased Through-Transmission, 29 Path of Sound-Related Artifacts, 29 Gas-Related Artifacts, 30 Beam ProfileeRelated Artifacts, 32 Doppler Imaging Artifacts, 35 THERAPEUTIC APPLICATIONS: HIGH-INTENSITY FOCUSED ULTRASOUND, 42 ACKNOWLEDGMENT, 45 REFERENCES, 45

such as blood. To produce, detect, and process ultrasound data, users must manage numerous variables, many under their direct control. To do this, operators must understand the methods used to generate ultrasound data and the theory and operation of the instruments that detect, display, and store the acoustic information generated in clinical examinations. This chapter provides an overview of the fundamentals of acoustics, the physics of ultrasound imaging and flow detection, and ultrasound instrumentation with emphasis on points most relevant to clinical practice. With a review of ultrasound image formation and assumptions employed, a section is dedicated to various types of artifacts in gray-scale and Doppler imaging. A discussion of the therapeutic application of high-intensity focused ultrasound concludes the chapter.

BASIC ACOUSTICS Wavelength and Frequency Sound is the result of mechanical energy traveling through matter as a wave producing alternating compression and rarefaction. Pressure waves are propagated by limited physical displacement of the material through which the sound is being

1

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transmitted. A plot of these changes in pressure is a sinusoidal waveform (Fig. 1.1), in which the Y axis indicates the pressure at a given point and the X axis indicates time. Change in pressure with time defines the basic unit of measurement for sound. The maximum pressure change relative to the background (ambient conditions in absence of the sound wave) is called the pressure amplitude (P). For audible sound, the pressure amplitude is associated with its “loudness.” The distance between corresponding points on the time-pressure curve is defined as the wavelength (l), and the time (T) to complete a single cycle is called the period. The number of complete cycles in a unit of time is the frequency (f) of the sound. Frequency and period are inversely related. If the period (T) is expressed in seconds, f ¼ 1/T. The unit of acoustic frequency is the hertz (Hz); 1 Hz ¼ 1 cycle per second (or second1). High frequencies are expressed in kilohertz (kHz; 1 kHz ¼ 1000 Hz) or megahertz (MHz; 1 MHz ¼ 1,000,000 Hz). In nature, acoustic frequencies span a range from less than 1 Hz to more than 100,000 Hz (100 kHz). Human hearing is limited to the lower part of this range, extending from 20 to 20,000 Hz. Ultrasound differs from audible sound only in that its frequencies are higher than the upper audible limit of human hearing. Sound frequencies used for diagnostic applications typically range from 2 to 15 MHz, although frequencies as high as 50 to 60 MHz are under investigation for certain specialized imaging applications, such as imaging the eye and skin as well as small animal imaging.2 In general, the frequencies used for ultrasound imaging are higher than those used for Doppler.

λ compression

Pressure

+

P

0

–

rarefaction

T Time

FIGURE 1.1 Sound Waves. Sound is transmitted mechanically at the molecular level. In the resting state, the pressure is uniform throughout the medium. Sound is propagated as a series of alternating pressure waves producing compression and rarefaction of the conducting medium. The time for a pressure wave to pass a given point is the period, T. The frequency of the wave is 1/T. The wavelength, l, is the distance between consecutive corresponding points of the same phase on the time-pressure curve, such as two neighboring crests or troughs. The maximum pressure change relative to the background (ambient conditions in absence of the sound wave) is called the pressure amplitude (P).

Regardless of the frequency, the same basic principles of acoustics apply.

Propagation of Sound In most clinical applications of ultrasound, brief pulses of energy are transmitted into the body which then propagate through tissue. Acoustic pressure waves can travel in a direction perpendicular to the direction of the particles being displaced (transverse waves), but in tissue and fluids, sound propagation is primarily along the direction of particle movement (longitudinal waves). Longitudinal waves are important in conventional ultrasound imaging and Doppler, while transverse waves are measured in shear wave elastography. The speed at which pressure waves move through tissue varies greatly and is affected by the physical properties of the tissue. Propagation velocity is largely determined by the resistance of the medium to compression, which in turn is influenced by the density of the medium and its stiffness or elasticity. Propagation velocity is increased by increasing stiffness and reduced by decreasing density. In the body, propagation velocity of longitudinal waves may be regarded as constant for a given tissue and is not affected by the frequency or wavelength of the sound. This is in contrast to transverse (shear) waves for which the velocity is determined by Young’s modulus, a measure of tissue stiffness or elasticity. Fig. 1.2 shows typical longitudinal propagation velocities for a variety of materials. In the body the propagation velocity of sound is assumed to be 1540 m/s. This value is the average of measurements obtained from normal soft tissue.3,4 Although

Air

330

Fat

1450

Water

1480

Soft tissue (average)

1540

Liver

1550

Kidney

1560

Blood

1570

Muscle

1580

Bone

4080

1400

1500

1600

1700

1800

Propagation velocity (meters/second) FIGURE 1.2 Propagation Velocity in Various Tissues. In the body, propagation velocity of sound is determined by the physical properties of tissue, which varies considerably. Medical ultrasound devices base their measurements on an assumed average propagation velocity of soft tissue of 1540 m/s.

CHAPTER 1 Physics of Ultrasound this value represents most soft tissues, some tissues, such as aerated lung and fat, have propagation velocities substantially less than 1540 m/s, whereas tissues such as bone have greater velocities. The propagation velocity of sound (c) is related to frequency and wavelength by the following simple equation: c ¼ fl Thus, a frequency of 5 MHz can be shown to have a wavelength of 0.308 mm in tissue: l ¼ c=f ¼ 1540 m=sec=5; 000; 000 sec1 ¼ 0:000308 m ¼ 0:308 mm Wavelength is an important determinant of spatial resolution in ultrasound imaging; the smaller the wavelength, the finer the ability to separate two points. Therefore, the selection of transducer frequency for a given application is a key user decision. Careless selection of transducer frequency and lack of attention to the focal characteristics of the beam will cause loss of clinically valuable information from deep, low-amplitude reflectors and small targets.

Distance Measurement Propagation velocity is a particularly important value in clinical ultrasound and is critical in determining the distance of a reflecting interface from the transducer. Much of the information used to generate an ultrasound scan is based on the precise measurement of time and employs the principle of echoranging (Fig. 1.3). If an ultrasound pulse is transmitted into the body and the time until an echo returns is measured, it is simple to calculate the depth of the interface that generated the echo, provided the propagation velocity of sound for the tissue

is known. For example, if the time from the transmission of a pulse until the return of an echo is 0.000145 seconds and the velocity of sound is 1540 m/s, the distance that the sound has traveled must be 22.33 cm (1540 m=sec  100 cm=m  0:000145 sec ¼ 22:33 cm). Because the time measured includes the time for sound to travel to the interface and then return along the same path to the transducer, the distance from the transducer to the reflecting interface is 22.33 cm/2 ¼ 11.165 cm. By rapidly repeating this process, a two-dimensional (2-D) map of reflecting interfaces is created to form the ultrasound image. The accuracy of this measurement is therefore dependent on how closely the presumed velocity of sound corresponds to the true velocity in the tissue being observed, as well as by the important assumption that the sound pulse travels in a straight path to and from the reflecting interface.

Acoustic Impedance Diagnostic ultrasound scanners rely on the detection and display of reflected sound or echoes. Imaging based on transmission of ultrasound is also possible, but this is not used clinically at present. To produce an echo, a reflecting interface must be present. Sound passing through a homogeneous medium like clear liquid encounters no interfaces to reflect sound, and the medium appears anechoic or cystic. The junction of tissues or materials with different physical properties produces an acoustic interface. These interfaces are responsible for the reflection of variable amounts of the incident sound energy. Thus, when ultrasound passes from one tissue to another or encounters a vessel wall or circulating blood cells, some of the incident sound energy is reflected.

0.00 ms 0.145 ms

FIGURE 1.3 Ultrasound Echo Ranging. The information used to position an echo for display is based on the precise measurement of time. In this image, time for an echo to travel from the transducer to the target and return to the transducer is 0.145 ms (0.000145 seconds). Multiplying the velocity of sound in tissue (1540 m/s) by time shows that the sound returning from the target has traveled 22.33 cm. Therefore, the target lies half this distance, or 11.165 cm, from the transducer. By rapidly repeating this process, a two-dimensional map of reflecting interfaces is created to form the ultrasound image.

D = 11.165 cm

0.0725 ms

3

1540 m/sec × 0.145 ms/2 = 154,000 cm/sec × 0.000145 sec/2 = 22.33 cm / 2 = 11.165 cm

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Ultrasound Physics, Bioeffects, and Contrast

PART ONE

The amount of reflection or backscatter is determined by the difference in the acoustic impedances of the materials forming the interface. Acoustic impedance (Z) is determined by product of the density (r) of the medium propagating the sound and the propagation velocity (c) of sound in that medium, such that Z ¼ rc Interfaces with large acoustic impedance differences, such as interfaces of tissue with air or bone, reflect almost all the incident energy. Interfaces composed of substances with smaller differences in acoustic impedance, such as a muscle and fat interface, reflect only part of the incident energy, permitting the remainder to continue onward. As with propagation velocity, acoustic impedance is determined by the properties of the tissues involved and is independent of frequency.

Reflection The way ultrasound is reflected when it strikes an acoustic interface is determined by the size and surface features of the interface (Fig. 1.4). If large and relatively smooth, the interface reflects sound much as a mirror reflects light. Such interfaces are called specular reflectors because they behave as “mirrors for sound.” The amount of energy reflected by an acoustic interface can be expressed as a fraction of the incident energy; this is termed the reflection coefficient (R). If a specular reflector is perpendicular to the incident sound beam, the amount of energy reflected is determined by the following relationship: 2

R ¼ ðZ2  Z1 Þ =ðZ2 þ Z1 Þ

2

where Z1 and Z2 are the acoustic impedances of the media forming the interface.

A

Because ultrasound scanners only detect reflections that return to the transducer, display of specular interfaces is highly dependent on the angle of insonation (exposure to ultrasound waves). Specular reflectors will return echoes to the transducer only if the sound beam is perpendicular to the interface. If the interface is not at or near a 90-degree angle to the sound beam, it will be reflected away from the transducer, and the echo will not be detected. Most echoes in the body do not arise from specular reflectors but rather from much smaller interfaces within solid organs. In this case the acoustic interfaces involve structures with dimensions much smaller than the wavelength of the incident sound. The echoes from these interfaces are scattered in all directions. Such reflectors are called diffuse reflectors and account for the echoes that form the characteristic echo patterns seen in solid organs and tissues. The constructive and destructive interference of sound scattered by diffuse reflectors results in the production of ultrasound speckle, a feature of tissue texture of sonograms of solid organs (Fig. 1.5). For some diagnostic applications, the nature of the reflecting structures creates important conflicts. For example, most vessel walls behave as specular reflectors that require insonation at a 90degree angle for best imaging, whereas spectral Doppler imaging requires an angle to be best kept at less than 60 degrees between the sound beam and the vessel.5

Examples of Specular Reflectors Diaphragm Vessel wall Wall of urine-filled bladder Endometrial stripe

B

FIGURE 1.4 Specular and Diffuse Reflectors. (A) Specular reflector. The diaphragm is a large and relatively smooth surface that reflects sound like a mirror reflects light. Thus, sound striking the diaphragm at nearly a 90-degree angle is reflected directly back to the transducer, resulting in a strong echo. Sound striking the diaphragm obliquely is reflected away from the transducer, and an echo is not displayed (yellow arrow). (B) Diffuse reflector. In contrast to the diaphragm, the liver parenchyma consists of acoustic interfaces that are small compared to the wavelength of sound used for imaging. These interfaces scatter sound in all directions, and only a portion of the energy returns to the transducer to produce the image, resulting in a weaker echo.

CHAPTER 1 Physics of Ultrasound

5

The attenuation of sound as it passes through tissue is of great clinical importance because it influences the depth of tissue from which useful information can be obtained. This in turn affects transducer selection and a number of operatorcontrolled instrument settings, including time (or depth) gain compensation, power output attenuation, and system gain levels. Attenuation of sound beam is measured in relative units instead of absolute units. The decibel (dB) notation is generally used to compare different levels of ultrasound power or intensity. This value is 10 times the log10 of the ratio of the power or intensity values being compared. For example, if the intensity measured at one point in tissues is 10 mW/cm2 and at a deeper point is 0.01 mW/cm2, the difference in intensity is as follows:


ð10Þ log10 0:01=10 ¼ ð10Þ log10 0:001 ¼ ð10Þ  log10 1000 FIGURE 1.5 Ultrasound Speckle. Close inspection of an ultrasound image of the breast containing a small cyst reveals it to be composed of numerous areas of varying intensity (speckle). Speckle results from the constructive (red) and destructive (green) interaction of the acoustic fields (yellow rings) generated by the scattering of ultrasound from small tissue reflectors. This interference pattern gives ultrasound images their characteristic grainy appearance and may reduce contrast. Ultrasound speckle is the basis of the texture displayed in ultrasound images of solid tissues.

Refraction When sound passes from a tissue with one speed of sound to a tissue with a different speed of sound, there is a change in the direction of the sound wave. This change in direction of propagation is called refraction and is governed by Snell law: sin q1 =sin q2 ¼ c1 =c2 where q1 is the angle of incidence of the sound approaching the interface, q2 is the angle of refraction, and c1 and c2 are the speed of sound in the media forming the interface (Fig. 1.6).

Attenuation As a sound beam travels through tissue, its amplitude is reduced with increasing distance traveleddthe general term for this reduction over distance traveled is attenuation. Contributing to the attenuation of sound are the transfer of energy to tissue, resulting in heating (absorption), and the removal of energy by reflection and scattering. Attenuation is therefore the result of the combined effects of absorption, scattering, and reflection. Acoustic power, expressed in watts (W) or milliwatts (mW), describes the rate of acoustic energy transmitted into the medium, that is, amount of energy transmitted per unit of time. Although measurement of power provides an indication of the energy as it relates to time, it does not take into account the spatial distribution of the energy. Intensity (I) is used to describe the spatial distribution of power.

¼ ð10Þð 3Þ ¼ 30 dB Attenuation depends on the insonating frequency as well as the nature of the attenuating medium. Sound waves of high frequencies are attenuated more rapidly than those of lower frequencies, and transducer frequency is thus a major determinant of the useful depth from which information can be obtained with ultrasound. Attenuation determines the efficiency with which ultrasound penetrates a specific tissue and varies considerably in normal tissues (Fig. 1.7).

INSTRUMENTATION Ultrasound scanners are complex and sophisticated imaging devices, but all consist of the following basic components to perform key functions: • Transmitter or pulser to energize the transducer • Ultrasound transducer • Receiver and processor to detect and amplify the backscattered energy and manipulate the reflected signals for display • Display that presents the ultrasound image or data in a form suitable for analysis and interpretation • Method to record or store the ultrasound image

Transmitter Most clinical applications use pulsed ultrasound, in which brief bursts of acoustic energy are transmitted into the body. The source of these pulses, the ultrasound transmitter, is energized by application of precisely timed, high-amplitude voltage. The maximum voltage that may be applied to the transducer is limited by federal regulations that restrict the acoustic output of diagnostic scanners. Most scanners provide a control that permits attenuation of the output voltage. Because the use of maximum output results in higher exposure of the patient to ultrasound energy, ALARA (as low as reasonably achievable) principle dictates use of the output attenuation controls to reduce power levels to the lowest levels consistent with the diagnostic problem.6

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Transducer

T1 = 20°

Tissue A c1 = 1540 m/sec Tissue B c2 = 1450 m/sec

18.8° 8 T2 = 18

FIGURE 1.6 Refraction. When sound passes from soft tissue with propagation velocity (c1) of 1540 m/s to fat with a propagation velocity (c2) of 1450 m/s, there is a change in the direction of the sound wave because of refraction. The degree of change is related to the ratio of the propagating velocities of the media forming the interface (sin q1/sin q2 ¼ c1/c2). Note that when the incident angle is changed to zero degreesdthat is, the incident beam is perpendicular to the interface (q1 ¼ 0 )dthe artifact disappears.

The transmitter also controls the rate of pulses emitted by the transducer, or the pulse repetition frequency (PRF). The PRF determines the time interval between ultrasound pulses and is important in determining the depth from which data can be obtained both in imaging and Doppler modes. The ultrasound pulses must be spaced with enough time between the pulses to permit the sound to travel to the depth of interest and return before the next pulse is sent. For imaging, PRFs from 1 to 10 kHz are used, resulting in an interval of 0.1 to 1 ms between pulses. Thus, a PRF of 5 kHz permits an echo to travel and return from a depth of 15.4 cm before the next pulse is sent: 1/5(kHz) ¼ 0.0002 (seconds) ¼ 2*0.154 m/1540 (m/s).

A transducer is any device that converts one form of energy to another. In ultrasound the transducer converts electric energy to mechanical energy, and vice versa. In diagnostic ultrasound systems the transducer serves two functions: (1) converting the electric energy provided by the transmitter to the acoustic pulses directed into the patient and (2) serving as the receiver of reflected echoes, converting weak pressure changes into electric signals for processing. Ultrasound transducers use piezoelectricity, a principle discovered by Pierre and Jacques Curie in 1880. Piezoelectric materials have the unique ability to respond to the action of an electric field by changing shape. They also have the property of generating electric potentials when compressed. Changing the polarity of a voltage applied to the transducer changes the thickness of the transducer, which expands and contracts as the polarity changes. This results in the generation of mechanical pressure waves that can be transmitted into the body. The piezoelectric effect also results in the generation of small potentials across the transducer when the transducer is struck by returning echoes. Positive pressures during the compression part of the acoustic wave cause a small polarity to develop across the transducer; negative pressure during the rarefaction portion of the acoustic wave produces the opposite polarity across the transducer. These tiny polarity changes and the associated voltages are the source of all the information processed to generate an ultrasound image or Doppler display. When stimulated by the application of an alternating voltage difference across its thickness, the transducer vibrates. The frequency of vibration is determined by the transducer material. When the transducer is electrically stimulated, a range or band of frequencies results. The preferential frequency produced by a transducer is determined by the propagation speed of the transducer material and its thickness. In the pulsed wave operating modes used for most clinical ultrasound applications, the ultrasound pulses contain additional frequencies that are either higher or lower than the preferential frequency. The range of frequencies produced by a given transducer is termed its bandwidth. Generally, the shorter the pulse of ultrasound produced by the transducer, the greater is the bandwidth. Most modern digital ultrasound systems employ broadbandwidth technology. Ultrasound bandwidth refers to the range of frequencies produced and detected by the ultrasound system. This is important because each tissue in the body has a characteristic response to ultrasound of a given frequency, and different tissues respond variably to different frequencies. The range of frequencies arising from a tissue exposed to ultrasound is referred to as the frequency spectrum bandwidth of the tissue, or tissue signature. Broad-bandwidth technology provides a means to capture the frequency spectrum of insonated tissues, preserving acoustic information and tissue signature. Broad-bandwidth beam formers reduce speckle artifact by a process of frequency compounding. This is possible because

CHAPTER 1 Physics of Ultrasound

Water

0.00 0.18

Blood Fat

0.63

Soft tissue (average)

0.70

Liver

0.94

Kidney

1.00

Muscle (parallel) Muscle (transverse)

1.30 3.30

Bone

5.00

Air

10.00 0

2

4

6

8

10

Attenuation (dB/cm/MHz) FIGURE 1.7 Attenuation. As sound passes through tissue, it loses energy through the transfer of energy to tissue by absorption, reflection, and scattering. Attenuation is determined by the insonating frequency and the nature of the attenuating medium. Attenuation values for normal tissues show considerable variation. Attenuation also increases in proportion to insonating frequency, resulting in less penetration at higher frequencies.

speckle patterns at different frequencies are independent of one another, and combining data from multiple frequency bands (i.e., compounding) results in a reduction of speckle in the final image, leading to improved contrast resolution. The length of an ultrasound pulse is determined by the number of alternating voltage changes applied to the transducer. For continuous wave (CW) ultrasound devices, a constant alternating current is applied to the transducer, and the alternating polarity produces a continuous ultrasound wave. For imaging, a single, brief voltage change is applied to the transducer, causing it to vibrate at its preferential frequency. Because the transducer continues to vibrate or “ring” for a brief time after it is stimulated by the voltage change, the ultrasound pulse will be several cycles long. The number of cycles of sound in each pulse determines the pulse length. For imaging, short pulse lengths are desirable because longer pulses result in poorer axial resolution. To reduce the pulse length, damping materials are used in the construction of the transducer. In clinical imaging applications, very short pulses are applied to the transducer, and the transducers have highly efficient damping. This results in very short pulses of ultrasound, generally consisting of only two or three cycles of sound. The ultrasound pulse generated by a transducer must be propagated in tissue to provide clinical information. Special transducer coatings and ultrasound coupling gels are necessary to allow efficient transfer of energy from the transducer to the body. Once in the body, the ultrasound pulses are propagated, reflected, refracted, and absorbed, in accordance with the basic acoustic principles summarized earlier.

7

The ultrasound pulses produced by the transducer result in a series of wavefronts that form a three-dimensional (3-D) beam of ultrasound. The features of this beam are influenced by constructive and destructive interference of the pressure waves, the curvature of the transducer, and acoustic lenses used to shape the beam. Interference of pressure waves results in an area near the transducer where the pressure amplitude varies greatly. This region is termed the near field, or Fresnel zone. Farther from the transducer, at a distance determined by the radius of the transducer and the frequency, the sound field begins to diverge, and the pressure amplitude decreases at a steady rate with increasing distance from the transducer. This region is called the far field, or Fraunhofer zone. In modern multielement transducer arrays, precise timing of the firing of elements allows correction of this divergence of the ultrasound beam and focusing at selected depths.7 Reflected ultrasound waves (echoes) that return to the transducer are capable of stimulating the transducer with small pressure changes, which are converted into the voltage changes that are detected, amplified, and processed to build an image based on the echo information.

Receiver When returning echoes strike the transducer face, minute voltages are produced across the piezoelectric elements. The receiver detects and amplifies these weak signals. The receiver also provides a means for compensating for the differences in echo strength, which result from attenuation by different tissue thickness by use of time gain control (TGC), also called time gain compensation. Sound is attenuated as it passes into the body, and energy is further removed as echoes return through tissue to the transducer. The attenuation of sound is proportional to the frequency and is constant for specific tissues. Because echoes returning from deeper tissues are weaker than those returning from more superficial structures, they must be amplified more by the receiver to produce a uniform tissue echo appearance. This adjustment is accomplished by TGC controls that permit the user to selectively amplify the signals from deeper structures or to suppress the signals from superficial tissues, compensating for tissue attenuation (Fig. 1.8). Although many machines offer some means of automatic TGC, the manual adjustment of this control is one of the most important user controls and may have a profound effect on the quality of the ultrasound image provided for interpretation. Improper adjustment of system gain and TGC can cause loss of image information. Another important function of the receiver is the compression of the wide range of amplitudes returning to the transducer into a range that can be displayed to the user. The ratio of the highest to the lowest amplitudes that can be displayed may be expressed in decibels and is referred to as the dynamic range. In a typical clinical application, the range of reflected signals may vary by a factor of as much as 1:1012, resulting in a dynamic range of up to 120 dB. Although the amplifiers used in ultrasound machines are capable of

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FIGURE 1.8 Time Gain Compensation (TGC). Without TGC, tissue attenuation causes gradual loss of display of deeper tissues (A). In this example, tissue attenuation of 1 dB/cm/MHz is simulated for a transducer of 10 MHz. At a depth of 2 cm, the intensity is 20 dB (1%) of initial value. By applying increasing amplification (gain) to the backscattered signal to compensate for this attenuation, a uniform intensity is restored to the tissue at all depths (B).

FIGURE 1.9 Dynamic Range. The ultrasound receiver must compress the wide range of amplitudes returning to the transducer into a range that can be displayed to the user. Here, compression and remapping of the data to display dynamic ranges of 35, 40, 50, and 60 dB are shown. The widest dynamic range shown (60 dB) permits the best differentiation of subtle differences in echo intensity and is preferred for most imaging applications. The narrower ranges increase conspicuity of larger echo differences.

handling this range of voltages, gray-scale displays are limited to display a signal intensity range of only 35 to 40 dB. Compression and remapping of the data are required to adapt the dynamic range of the returning signal intensity to the dynamic range of the display (Fig. 1.9). Compression is performed in the receiver by selective amplification of weaker signals. Additional manual postprocessing controls permit the user to map selectively the returning signal to the display. These controls affect the brightness of different echo levels in the image and therefore determine the image contrast.

Image Display Ultrasound signals may be displayed in several ways. Over the years, imaging has evolved from simple A-mode (amplitudemode) and bistable display to high-resolution, real-time, grayscale imaging. Another simple form of imaging, M-mode (motion-mode) ultrasound, displays echo amplitude and shows the position of moving reflectors (Fig. 1.10). M-mode imaging uses the brightness of the display to indicate the intensity of the reflected

signal. The time base of the display can be adjusted to allow for varying degrees of temporal resolution, as dictated by clinical application. M-mode ultrasound is interpreted by assessing motion patterns of specific reflectors and determining anatomic relationships from characteristic patterns of motion. Application of M-mode display include: (1) evaluation of embryonic and fetal heart rates; (2) echocardiography, to assess the rapid motion of cardiac valves and of cardiac chamber and vessel walls; and (3) assessment of cardiac arrhythmias. M-mode imaging may play a future role in measurement of subtle changes in vessel wall elasticity accompanying atherogenesis. The mainstay of imaging with ultrasound is provided by real-time, gray-scale, B-mode (brightness mode) display, in which variations in display intensity or brightness are used to indicate reflected signals of different amplitude. To generate a 2-D image, multiple ultrasound pulses are sent down a series of successive scan lines, sweeping through the object (Fig. 1.11). The positions and amplitudes of the reflected signals are stored, building a 2-D representation of echoes arising from the object being scanned. When an ultrasound image is displayed on a

CHAPTER 1 Physics of Ultrasound

A

C

B

A

C

B

FIGURE 1.10 M-Mode (Motion-Mode) Display. M-mode ultrasound displays changes of echo amplitude and position with time. Display of changes in echo position is useful in the evaluation of rapidly moving structures such as cardiac valves and chamber walls. Here, the three major moving structures in the upper gray-scale image of the fetus are recorded in the corresponding M-mode image and include the near ventricular wall (A), the far ventricular wall (B), and the interventricular septum (C). The baseline is a time scale that permits the calculation of heart rate from the M-mode data.

black background, signals of greatest amplitude appear as white; absence of signal is shown as black; and signals of intermediate amplitudes appear as shades of gray. The brighter portions of the resulting 2-D image indicate structures reflecting more of the transmitted sound energy back to the transducer. In most modern instruments, digital memory is used to store values that correspond to the echo amplitudes originating from corresponding positions in the patient. At least 28, or 256, shades of gray are possible for each pixel, in accord with the amplitude of the echo being represented. The image stored in memory in this manner can then be sent to a monitor for display. Because B-mode display relates the strength of a returning signal to a brightness level on the display device, it is important that the operator understand how the amplitude information in the ultrasound signal is translated into a brightness scale in the image display. Each ultrasound manufacturer offers several options for the way the dynamic range of the target is compressed for display, as well as the transfer function that assigns a given signal amplitude to a shade of gray. Although these technical details vary among machines, the way the operator uses them may greatly affect the clinical value of the final image. In general, it is desirable to display as wide a dynamic range as possible, to identify subtle differences in tissue echogenicity. Real-time, 2-D, B-mode ultrasound is the major method for ultrasound imaging throughout the body and is the most common form of B-mode display. Real-time ultrasound can produce a series of individual 2-D images at rates of 15 to 60 frames per second and permits assessment of both anatomy and

9

motion. When images are acquired and displayed at rates of several times per second, the effect is dynamic, and because the image reflects the state and motion of the organ at the time it is examined, the information is regarded as being shown in real time. In cardiac applications the terms 2-D echocardiography and 2-D echo are used to describe real-time, B-mode imaging; in most other applications the term real-time ultrasound is used. Transducers used for real-time imaging may be classified by the way the ultrasound beam is steered to rapidly generate each individual image. Beam steering may be done through mechanical rotation or oscillation of the transducer or by electronic means. Electronic beam steering is used in linear array and phased array transducers and permits a variety of image display formats. Most electronically steered transducers currently in use also provide electronic focusing that is adjustable for depth. Mechanical beam steering may use singleelement transducers with a fixed focus or may use annular arrays of elements with electronically controlled focusing. For real-time imaging, transducers using mechanical or electronic beam steering generate displays in a rectangular or sector format. Sector scanners with either mechanical or electronic steering require only a small surface area for contact and are better suited for examinations in which access is limited.

Mechanical Sector Scanners Early ultrasound scanners used transducers consisting of a single piezoelectric element. To generate real-time images with these transducers, mechanical devices were required to move the transducer in a linear or circular motion. Mechanical sector scanners using one or more single-element transducers do not allow variable focusing. This problem is overcome by using annular array transducers, which have a series of concentric elements nested within one another in a circular piece of piezoelectric material which allows for mechanical steering. Although important in the early days of real-time imaging, mechanical sector scanners with fixed-focus, single-element transducers are not presently in common use.

Arrays Current technology uses a high-density 2-D transducer composed of multiple elements, usually produced by precise slicing of a piece of piezoelectric material perpendicular to the transducer long axis to produce numerous small rectangular units, each with its own electrodes. By precise timing of the firing of elements in these arrays, interference of the wavefronts generated by the individual elements can be exploited to change the direction of the ultrasound beam, and this can be used to provide a steerable beam for the generation of real-time images in a linear or sector format. An advantage of 2-D array construction is that the beam can be focused in both the elevation plane and the lateral plane, and a uniform and highly focused beam can be produced (Figs. 1.12 and 1.13). These arrays

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Ultrasound Physics, Bioeffects, and Contrast

FIGURE 1.11 B-Mode (Brightness-Mode) Imaging. A two-dimensional (2-D), real-time image is built by ultrasound pulses sent down a series of successive scan lines. Each scan line adds to the image, building a 2-D representation of echoes from the object being scanned. In real-time imaging, an entire image is created 15 to 60 times per second.

improve spatial resolution and contrast, reduce clutter, and are well suited for the collection of data from volumes of tissue for 3-D processing and display.

Linear Arrays Linear array transducers are used for small parts, vascular, and obstetric applications because the rectangular image format produced by these transducers is well suited for these applications. In these transducers, individual elements are arranged in a linear fashion. By firing the transducer elements in sequence, either individually or in groups, a series of parallel pulses are generated, each forming a line of sight perpendicular to the transducer face. These individual lines of sight combine to form the image field of view. Depending on the number of transducer elements and the sequence in which they are fired, focusing at selected depths from the surface can be achieved. The resultant rectangular image display has the advantage of a larger field of view near the surface, allowing more precise imaging of superficial structures. The downside is that it requires a large surface area for transducer contact, and the field of view is limited compared to transducers that have a sector display.

Curved Arrays Linear arrays that have been shaped into convex curves produce an image that combines a relatively large surface field of view with a sector display format. Curved array transducers are used for a variety of applications, the larger versions serving for general abdominal, obstetric, and transabdominal pelvic scanning. Small, high-frequency, curved array scanners are often used in transvaginal and transrectal probes and for pediatric imaging. Phased Arrays Phased array transducers also produce sector field of views. By controlling the time and sequence at which multiple individual transducer elements are fired, the resulting ultrasound wave can be steered in different directions as well as focused at different depths. By rapidly steering the beam to generate a series of lines of sight at varying angles from one side of the transducer to the other, a sector image is produced. This allows the fabrication of transducers of relatively small size but with large fields of view at depth. These transducers have a small footprint and are particularly useful for neonatal head ultrasound, as well as for

CHAPTER 1 Physics of Ultrasound intercostal scanning, to evaluate the heart, liver, or spleen, and for examinations in other areas where access is limited. However, because of their narrow aperture, phased array transducers typically have a narrow field of view at superficial depths and are not well suited to assessment of superficial structures.

Elevation focus (Slice thickness)

Lateral focus

11

Transducer Selection Practical considerations in the selection of the optimal transducer for a given application include not only the requirements for spatial resolution, but also the distance of the target object from the transducer because penetration of ultrasound diminishes as frequency increases. In general, the highest ultrasound frequency permitting penetration to the depth of interest should be selected. For superficial vessels and organs, such as the thyroid, breast, or testicle, lying within 1 to 3 cm of the surface, imaging frequencies of 7.5 to 15 MHz are typically used. These high frequencies are also ideal for intraoperative applications. If the region to be scanned is very superficial, such that the probe does not allow for focusing at the area of interest, a standoff pad can be utilized. For evaluation of deeper structures in the abdomen or pelvis more than 12 to 15 cm from the surface, frequencies as low as 2.25 to 3.5 MHz may be required. When maximal resolution is needed, a high-frequency transducer with excellent lateral and axial resolution at the depth of interest is required.

IMAGE DISPLAY AND STORAGE FIGURE 1.12 Two-Dimensional Array. High-density, two-dimensional (2-D) arrays consist of a 2-D matrix of transducer elements, permitting acquisition of data from a volume rather than a single plane of tissue. Precise electronic control of individual elements permits adjustable focusing on both lateral and elevation planes.

A

B

With real-time ultrasound, feedback to user is immediately provided by video display. The brightness and contrast of the image on this display are determined by the ambient lighting in the examination room, the brightness and contrast settings of the video monitor, the system gain setting, and the TGC adjustment. The factor most affecting image quality in many

C

FIGURE 1.13 Transducers. (A) Linear array. In a linear array transducer, individual elements or groups of elements are fired in sequence. This generates a series of parallel ultrasound beams, each perpendicular to the transducer face. As these beams move across the transducer face, they generate the lines of sight that combine to form the final image. Depending on the number of transducer elements and the sequence in which they are fired, focusing at selected depths from the surface can be achieved. (B) Curved array. A variant of the linear array, the curved array uses transducer elements arranged in an arc, producing a pie-shaped image. (C) Phased array. A phased array transducer produces a sector field of view by firing multiple transducer elements in precise sequence to generate interference of acoustic wavefronts that steer the beam. The resultant ultrasound beam generates a series of lines of sight at varying angles from one side of the transducer to the other, producing a sector image format. They are useful for scanning in areas where access is limited.

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ultrasound departments is probably improper adjustment of the video display, with a lack of appreciation of the relationship between the video display settings and the appearance of hard copy or images viewed on a workstation. Because of the importance of the real-time video display in providing feedback to the user, it is essential that the display and the lighting conditions under which it is viewed are standardized and matched to the display used for interpretation. Interpretation of images and archival storage of images may be in the form of transparencies printed on film by optical or laser cameras and printers, videotape, or digital picture archiving and communications system (PACS).

Tissue harmonic imaging takes advantage of the generation, at depth, of these harmonics. Because the generation of harmonics requires interaction of the transmitted field with the propagating tissue, harmonic generation is not present near the transducer/skin interface, and it only becomes important some distance from the transducer. In most cases the near and far fields of the image are affected less by harmonics than by intermediate locations. Using broad-bandwidth transducers and signal filtration or coded pulses, the harmonic signals reflected from tissue interfaces can be selectively displayed. Because most imaging artifacts are caused by the interaction of the ultrasound beam with superficial structures or by aberrations at the edges of the beam profile, these artifacts are eliminated using harmonic imaging because the artifact-producing signals do not consist of sufficient energy to generate harmonic frequencies and therefore are filtered out during image formation. Images generated using tissue harmonics often exhibit reduced noise and clutter (Fig. 1.15).11 Because harmonic beams are narrower than the originally transmitted beams, spatial resolution is improved, and side lobes are reduced.

SPECIAL IMAGING MODES Tissue Harmonic Imaging Variation of the propagation velocity of sound in fat and other tissues near the transducer results in a phase aberration that distorts the converging ultrasound wavefront, producing noise and clutter in the ultrasound image, and deteriorating resolution for deeper tissues.8,9 Tissue harmonic imaging provides an approach for reducing the effects of phase aberrations.10 Nonlinear propagation of ultrasound through tissue is associated with the more rapid propagation of the compressional component of the high-pressure ultrasound wave than its negative (rarefactional) component. This results in increasing distortion of the acoustic pulse as it travels within the tissue and causes the generation of multiples, or harmonics, of the transmitted frequency (Fig. 1.14).

FIGURE 1.14 Tissue Harmonics. As high-pressure ultrasound waves propagate through tissue, the compressional component of the waves travel more rapidly than the rarefactional component, producing distortion of the wave and generating higher-frequency components (harmonics). (A) The acoustic field of the primary frequency is represented in blue. (B) The second harmonic (twice the primary frequency) is represented in red. (C) Using a broadbandwidth transducer, the receiver can be tuned to generate an image from the harmonic frequency rather than the primary frequency. As a result, near-field clutter is reduced, since the harmonic only develops at depth in the tissue and the beam profile is improved, leading to better spatial resolution.

Spatial Compounding An important source of image degradation and loss of contrast is ultrasound speckle. Speckle results from the constructive and destructive interaction of the acoustic fields generated by the scattering of ultrasound from small tissue reflectors. This interference pattern gives ultrasound images their characteristic grainy appearance, reducing contrast (Fig. 1.16)11 and making the identification of subtle features more difficult. By summing images from different scanning angles through spatial

A

B

C

CHAPTER 1 Physics of Ultrasound

FIGURE 1.15 Tissue Harmonic Imaging. (A) Conventional image and (B) tissue harmonic image of gallbladder in a patient with acute cholecystitis. Note the reduction of noise and clutter in the tissue harmonic image. Because harmonic beams do not interact with superficial structures and are narrower than the originally transmitted beam, spatial resolution is improved, and clutter and side lobes are reduced. (With permission from Merritt CR. Technology update. Radiol Clin North Am. 2001;39:385 e397.11)

FIGURE 1.16 Effect of Speckle on Contrast. (A) Speckle noise partially obscures the simulated lesion. (B) The speckle has been reduced, increasing contrast resolution between the lesion and the background. (With permission from Merritt CR. Technology update. Radiol Clin North Am. 2001;39:385e397.11)

A

A

compounding (Fig. 1.17), significant improvement in the contrast-to-noise ratio can be achieved. This is because speckle is random, and the generation of an image by compounding will reduce speckle noise because only the signal is reinforced. In addition, spatial compounding may reduce artifacts that result when an ultrasound beam strikes a specular reflector at an angle other than 90 degrees. In conventional real-time imaging, each scan line used to generate the image strikes the target at a constant, fixed angle. As a result, strong reflectors that are not perpendicular to the ultrasound beam scatter sound in directions that prevent their clear detection and display. This in turn results in poor margin definition and less distinct boundaries for cysts and other masses. Compounding reduces these artifacts. Limitations of compounding are diminished visibility of shadowing and decreased through transmission; however, these are offset by the ability to evaluate lesions, both

13

B

B

with and without compounding, preserving shadowing and through transmission when these features are important for establishing a diagnosis.11

Three-Dimensional Ultrasound Dedicated 3-D scanners used for fetal (Fig. 1.18), gynecologic, and cardiac scanning may employ hardware-based image registration, high-density 2-D arrays, or software registration of scan planes as a tissue volume is acquired. 3-D imaging permits volume data to be viewed in multiple imaging planes and allows accurate measurement of lesion volume.

Ultrasound Elastography Palpation is an effective method for detection of tissue abnormality by detecting changes in tissue stiffness or elasticity and may provide the earliest indication of disease, even when

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A

B

FIGURE 1.17 Spatial Compounding. (A) Conventional imaging is limited to a fixed angle of incidence of ultrasound scan lines to tissue interfaces, resulting in poor definition of specular reflectors that are not perpendicular to the beam as shown in this image overlay of a thyroid. (B) Spatial compounding combines images obtained by insonating the target from multiple angles. In addition to improving detection of interfaces, compounding reduces speckle noise because only the signal is reinforced; speckle is random and not reinforced. This improves contrast, as shown in the reduced speckle as well as better definition of regions (arrows) such as superficial tissue as well as small cysts and calcifications.

conventional imaging studies are normal. Ultrasound elastography provides a noninvasive method for evaluation of tissue stiffness.12 Bulk modulus is a measure of compressibility when compressive forces are applied to an object in all directions equally. Tissue contrast in conventional ultrasound imaging is based on the bulk modulus, which is determined by the molecular composition of tissue. Elastography reflects shear properties that are determined by a higher level of tissue organization, and the strain modulus, which is a measure of distortion when force is applied unequally and/or not in all directions. This higher level of tissue organization is most likely to be altered by disease. Elastography therefore offers the

potential for a high degree of both sensitivity and specificity in differentiating normal and abnormal tissues.12,14,15 Tissue stiffness or elasticity is expressed by Young’s modulusdthe ratio of compression pressure (stress) and the resulting deformation (strain) E ¼ s=ε where E is Young’s modulus expressed in Pa (pascals), s is the stress expressed in Newtons, and ε is displacement expressed in m2. Ultrasound-based elastography permits study of the elastic behavior of tissue through two general approaches (Fig. 1.19): strain elastography and shear wave elastography.

CHAPTER 1 Physics of Ultrasound

15

proportional to Young’s modulus and provides a quantitative estimate of tissue stiffness.18,19

Key Points of Ultrasound Elastography Ultrasound imaging is based on tissue bulk modulus, reflecting interactions at the molecular level. Changes in tissue stiffness based on the tissue shear modulus are important indications of disease. Ultrasound elastography provides relative and quantitative assessment of tissue stiffness. Ultrasound elastography is based on tissue organization (strain modulus). Strain elastography provides an indication of relative tissue stiffness. Shear wave elastography provides a quantitative estimate of the tissue stiffness (Young’s modulus).

IMAGE QUALITY The key determinants of the quality of an ultrasound image are its spatial, contrast, and temporal resolution, as well as freedom from certain artifacts. FIGURE 1.18 Three-Dimensional Ultrasound Image, 24-Week Fetus. Three-dimensional ultrasound permits collection and review of data obtained from a volume of tissue in multiple imaging planes, as well as a rendering of surface features.

Strain Elastography Strain elastography involves measurement of longitudinal tissue displacement before and after compression, usually by manual manipulation of the ultrasound transducer (Fig. 1.20). Speckle tracking using radiofrequency backscatter or Doppler is then used to evaluate tissue motion. Strain elastography cannot determine Young’s modulus because the compression pressure (stress) cannot be measured directly. Instead, strain ratios are estimated by comparing lesion strain to surrounding normal tissues and displayed in the image in different shades of gray or through color maps. Strain elastography provides an indication of relative stiffness of an area of interest compared to its surroundings. Shear Wave Elastography Longitudinal tissue compression results in the generation of transverse shear waves16,17 (Fig. 1.21). In shear wave elastography, shear waves are generated by repetitive compression produced by high-intensity pulses from the ultrasound transducer. In contrast to longitudinal compressional waves that propagate very quickly in the human body (z1540 m/s), shear waves propagate slowly (z1 to 50 m/s). Shear waves are tracked with high frame rate images to determine their velocity. The propagation velocity of shear waves is directly

Spatial Resolution The ability to differentiate two closely situated objects as distinct structures is determined by the spatial resolution of the ultrasound device. Spatial resolution must be considered in three planes, with different determinants of resolution for each. Simplest is the resolution along the axis of the ultrasound beam, or axial resolution. With pulsed wave ultrasound, the transducer introduces a series of brief bursts of sound into the body. Each ultrasound pulse typically consists of two or three cycles of sound. The pulse length is the product of the wavelength and the number of cycles in the pulse. Axial resolution, the maximum resolution along the beam axis, is determined by the pulse length (Fig. 1.22). Because ultrasound frequency and wavelength are inversely related, the pulse length decreases as the imaging frequency increases. Because the pulse length determines the maximum resolution along the axis of the ultrasound beam, higher transducer frequencies provide higher image resolution. For example, a transducer operating at 5 MHz produces sound with a wavelength of 0.308 mm. If each pulse consists of three cycles of sound, the pulse length is slightly less than 1 mm, and this becomes the maximum resolution along the beam axis. If the transducer frequency is increased by a factor of three to 15 MHz, the pulse length becomes one-third as long, that is less than 0.4 mm, permitting resolution of smaller details. In addition to axial resolution, resolution in the planes perpendicular to the beam axis must also be considered. Lateral resolution refers to resolution in the plane perpendicular to the beam and parallel to the transducer and is

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FIGURE 1.19 Elastography. (A) Strain elastography qualitatively depicts tissue stiffness generated by analysis of speckle displacements before and after mechanical compression of tissue. The precompression frame is compared to a frame obtained after compression. In this example, the lesion is compressed much less than the surrounding tissue, indicating relative stiffness. (B) In Shear wave elastography (SWE) high-intensity compression pulses from the transducer are focused on an area of interest, resulting in the generation of low-frequency shear waves. Speckle displacement resulting from shear (transverse) waves is tracked with multiple imaging frames in order to estimate shear wave velocity. Shear wave velocity is directly related to Young’s modulus, permitting a quantitative estimate of tissue stiffness.

x

x’

y x=y precompression

A

A

y’ x’ < y’ compression

shear waves

B

B

FIGURE 1.20 Strain elastography qualitatively depicts tissue stiffness generated by analysis of speckle displacements before and after mechanical compression of tissue. The precompression frame is compared to a frame obtained after compression. In this example of breast masses, (A) is benign and (B) is malignant. (A) A benign-appearing hypoechoic macrolobulated mass has a strain value, which is similar to the strain value of the surrounding tissue. The ratio is therefore close to 1. (B) An irregular, spiculated, not parallel mass has a lower strain value as compared with surrounding tissue, consistent with malignancy. (Courtesy Sughra Raza, MD.)

determined by the width of the ultrasound beam. Elevation resolution refers to the slice thickness in the plane perpendicular to the beam and to the transducer (Fig. 1.23). The width and thickness of the ultrasound beam are important determinants of image quality. Excessive beam width and thickness limit the ability to delineate small features and may obscure shadowing and through transmission from small structures, such as breast microcalcifications and small thyroid cysts. The width and thickness of the ultrasound beam determine lateral resolution and elevation resolution, respectively. Lateral and elevation resolutions are significantly poorer than the axial resolution of the beam. Lateral resolution is controlled by focusing the beam, usually

by electronic phasing, to alter the beam width at a selected depth of interest. Elevation resolution is determined by the construction of the transducer and generally cannot be controlled by the user. Because of the relative lack of divergence of the beam, linear transducers have higher lateral resolution than curved and phased array transducers.

DOPPLER SONOGRAPHY Conventional B-mode ultrasound imaging uses pulse-echo transmission, detection, and display techniques. Brief pulses of ultrasound energy emitted by the transducer are reflected from acoustic interfaces within the body. Precise timing allows

CHAPTER 1 Physics of Ultrasound

Liver EQI 8 EQI Avg Vel 1.37 m/s EQI Med Vel 1.37 m/s

17

A

B Liver Site 1 1 Vs Median=3.03 m/s E Median=27.6 kPa Depth=4.04 cm Diam=1.00 cm

1

C FIGURE 1.21 Shear Wave Elastography (SWE) in Normal and Cirrhotic Liver. High-intensity compression pulses from the transducer are focused on an area of interest, resulting in the generation of low-frequency shear waves. Speckle displacement resulting from shear (transverse) waves is tracked with multiple imaging frames in order to estimate shear wave velocity. Shear wave velocity is directly related to Young’s modulus, permitting a quantitative estimate of tissue stiffness. (A) Normal liver with good quality of the measurement and liver stiffness value of 1.37 m/s, in the range of normal. (B and C) Cirrhotic liver with good quality of the measurement and liver stiffness value of 3.03 m/s, in the range of cirrhosis with clinically significant portal hypertension. The color-coded confidence map is an evaluation of the quality of the acquired signals. The confidence threshold (CT) is set at 60% in A. In C a color scale is used where yellow/green is good quality and red is low quality. (Images courtesy of Richard G. Barr, MD, PhD.)

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E A L

A 5.0 MHz 0.0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 mm

A

B

0.3 mm (300µ) wavelength

B0.9 mm (900µ) pulse length FIGURE 1.22 Axial Resolution. (A) Axial resolution (A) is the resolution along the beam axis and is determined by the pulse length. (B) The pulse length is the product of the wavelength (which is inversely proportional to frequency) and the number of waves (usually two to three). Because the pulse length determines axial resolution, higher transducer frequencies provide higher image resolution. In this example, a transducer operating at 5 MHz produces sound with a wavelength of 0.31 mm. If each pulse consists of three cycles of sound, the pulse length is slightly less than 1 mm, and objects A and B, which are 0.5 mm apart, cannot be resolved as separate structures. If the transducer frequency is increased to 15 MHz, the pulse length is less than 0.3 mm, permitting A and B to be identified as separate structures.

determination of the depth from which the echo originates. When pulsed wave ultrasound is reflected from an interface, the reflected (backscattered) signal contains amplitude, phase, and frequency information (Fig. 1.24). This information permits inference of the position, nature, and motion of the interface that reflects the pulse. B-mode ultrasound imaging uses only the amplitude information in the reflected signal to generate the image, with differences in the strength of reflections displayed in the image in varying shades of gray. Rapidly moving targets, such as red cells in the bloodstream, produce echoes of low

FIGURE 1.23 Lateral and Elevation Resolution. Resolution in the planes perpendicular to the beam axis is an important determinant of image quality. Lateral resolution (L) is the resolution in the plane perpendicular to the beam and parallel to the transducer and is determined by the width of the ultrasound beam. Lateral resolution is controlled by focusing the beam, usually by electronic phasing to alter the beam width at a selected depth of interest. Elevation resolution (E) is determined by the slice thickness in the plane perpendicular to the beam and the transducer. Elevation resolution is controlled by the construction of the transducer. Both lateral resolution and elevation resolution are lower than the axial resolution.

amplitude that are not usually displayed, resulting in a relatively anechoic pattern within the lumens of large vessels. Although gray-scale display relies on the amplitude of the reflected ultrasound signal, additional information is present in the returning echoes that can be used to evaluate the motion of moving targets.20 When high-frequency sound impinges on a stationary interface, the reflected ultrasound has essentially the same frequency or wavelength as the transmitted sound. If the reflecting interface is moving with respect to the sound beam emitted from the transducer, however, there is a change in the frequency of the sound scattered by the moving object (Fig. 1.25). This change in frequency is directly proportional to the velocity of the reflecting interface relative to the transducer and is a result of the Doppler effect. The relationship of the returning ultrasound frequency to the velocity of the reflector is described by the Doppler equation, as follows: DF ¼ ðFR  FT Þ ¼ 2 , FT , v=c The Doppler frequency shift is DF; FR is the frequency of sound reflected from the moving target; FT is the frequency of

CHAPTER 1 Physics of Ultrasound

FIGURE 1.24 Amplitude, Frequency, and Phase Information. The reflected ultrasound signal contains amplitude, phase, and frequency information. Signals B and C differ in amplitude but have the same frequency. Amplitude differences are used to generate B-mode images. Signals A and B differ in frequency but have similar amplitudes. Such frequency differences are the basis of Doppler ultrasound.

sound emitted from the transducer; v is the velocity of the target toward the transducer; and c is the velocity of sound in the medium. The Doppler frequency shift (DF) applies only if the target is moving directly toward or away from the transducer (Fig. 1.26). In most clinical settings the direction of the ultrasound beam is seldom directly toward or away from the direction of flow, and the ultrasound beam usually approaches the moving target at an angle designated as the Doppler angle. In this case, DF is reduced in proportion to the cosine of this angle, as follows: DF ¼ ðFR  FT Þ ¼ 2 , FT , v=c,cos q where q is the angle between the axis of flow and the incident ultrasound beam. If the Doppler angle can be measured, estimation of flow velocity is possible. Accurate estimation of target velocity requires precise measurement of both the Doppler frequency shift and the angle of insonation to the direction of target movement. As the Doppler angle (q) approaches 90 degrees, the cosine of q approaches 0. At an angle of 90 degrees, there is no relative movement of the target toward or away from the transducer, and no Doppler frequency shift is detected (Fig. 1.27). Because the cosine of the Doppler angle changes rapidly for angles more than 60 degrees, accurate angle correction requires that Doppler measurements be made at angles less than 60 degrees. Above 60 degrees, small changes in the Doppler angle q are associated with substantial changes in cosq, and therefore a small error in estimation of the Doppler angle may result in a large error in the estimation of velocity. These considerations are important in using both duplex and color Doppler instruments. Optimal imaging of the vessel wall is obtained when the axis of the transducer is perpendicular to the wall, whereas maximal Doppler frequency differences are obtained when the transducer axis and the direction of flow are at a relatively small angle.

A

Stationary target: (FR  FT)

B

Target motion toward transducer: (FR  FT) > 0

C

Target motion away from transducer: (FR  FT) < 0

19

0

FIGURE 1.25 Doppler Effect. (A) Stationary target. If the reflecting interface is stationary, the reflected ultrasound has the same frequency or wavelength as the transmitted sound, and there is no difference in the transmitted frequency (FT) and the reflected frequency (FR). (B and C) Moving targets. If the reflecting interface is moving with respect to the sound beam emitted from the transducer, there is a change in the frequency of the sound reflected by the moving object. When the interface moves toward the transducer (B), the difference in reflected and transmitted frequencies is greater than zero. When the target is moving away from the transducer (C), this difference is less than zero. The Doppler equation is used to relate this change in frequency to the velocity of the moving object.

Doppler Signal Processing and Display Several options exist for the processing and representation of DF, the Doppler frequency shift, to provide useful information regarding the direction and velocity of blood. Doppler frequency shifts encountered clinically are in the audible range. This audible signal may be analyzed by ear, and, with training, the operator can identify many flow characteristics. More often, the Doppler shift data are displayed in graphic form as a timevarying plot of the frequency spectrum of the returning signal. A Fast Fourier Transform is used to perform the frequency analysis. The resulting Doppler frequency spectrum displays the following (Fig. 1.28): • Variation with time of the Doppler frequencies present in the volume sampled • The envelope of the spectrum, representing the maximum frequencies present at any given point in time • The width of the spectrum at any point, indicating the range of frequencies present The amplitude of the Doppler signal is related to the number of targets moving at a given velocity. In many instruments the amplitude of each frequency component is displayed in gray scale as part of the spectrum. The presence of a large number of different frequencies at a given point in the cardiac cycle results in spectral broadening. In color Doppler imaging systems, a representation of the Doppler frequency shift is displayed as a feature of the image itself. When pulsed wave Doppler is combined with a 2-D, real-

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decreases error in interpretation of frequency data obtained at different Doppler angles.

Doppler Instrumentation FR FT

V

'F = FR – FT = 2 · FT · Q /c

A

FT

FR

T

V

B 'F = FR – FT = 2 · FT · Q /c · cosT FIGURE 1.26 Doppler Equation. The Doppler equation describes the relationship of the Doppler frequency shift to target velocity. (A) In its simplest form, it is assumed that the direction of the ultrasound beam is parallel to the direction of movement of the target. This situation is unusual in clinical practice. More often, the ultrasound impinges on the vessel at angle q. (B) In this case the Doppler frequency shift detected is reduced in proportion to the cosine of q. DF, Frequency shift; FR, reflected frequency; FT, transmitted frequency; v, velocity of the target; c, velocity of sound.

time, B-mode imager in the form of a duplex scanner, the position of the Doppler sample can be precisely controlled and monitored (see Fig. 1.28). In addition to the detection of Doppler frequency shift data from each pixel in the image, these systems also provide range-gated pulsed wave Doppler with spectral analysis for display of Doppler data. In vascular applications, it is necessary that measured Doppler frequencies are corrected for the Doppler angle to provide accurate velocity measurement. This allows comparison of data from systems using different Doppler frequencies and

In contrast to A-mode, M-mode, and B-mode gray-scale ultrasonography, which display the structural information from tissue interfaces, Doppler ultrasound instruments are optimized to display flow information. The simplest Doppler devices use continuous wave (CW) Doppler rather than pulsed wave ultrasound, using two transducers that transmit and receive ultrasound continuously. The transmit and receive beams overlap in a sensitive volume at some distance from the transducer face (Fig. 1.29). Although direction of flow can be determined with CW Doppler, these devices do not allow discrimination of motion coming from various depths, and it is difficult, if not impossible, to ascertain the source of the signal being detected. Inexpensive and portable, CW Doppler instruments are used primarily at the bedside or intraoperatively to confirm the presence of flow in superficial vessels. Because of the limitations of CW systems, most imaging applications use range-gated, pulsed wave Doppler. Rather than using a continuous wave of ultrasound, pulsed wave Doppler devices emit brief pulses of ultrasound waves. With pulses of sound, the time interval between the transmission of a pulse and the return of the echo is used to determine the depth from which the Doppler shift arises. In color Doppler imaging (Fig. 1.30), frequency shift information determined from Doppler measurements is displayed as a feature of the image itself. Stationary or slowly moving targets provide the basis for the B-mode image, based on amplitudes of returned echoes. Phase of Doppler signal provides information about the presence and direction of motion, and changes in echo signal frequency relate to the velocity of the target.21 Backscattered signals from red blood cells are displayed in color as a function of their motion toward or away from the transducer, and the degree of saturation of the color is used to indicate the relative frequency shift produced by the moving red cells. Color Doppler imaging expands conventional duplex sonography by providing additional capabilities. The use of color saturation to display variations in Doppler shift frequency allows an estimation of relative velocity from the image alone, provided that variations in the Doppler angle are noted. The display of flow throughout the image field allows the position and orientation of the vessel of interest to be observed at all times. The display of spatial information with respect to velocity is ideal for display of small, localized areas of turbulence within a vessel, which provide clues to stenosis or irregularity of the vessel wall caused by atheroma, trauma, or other disease. Flow within the vessel is observed at all points, and stenotic jets and focal areas of turbulence are displayed that might be overlooked with duplex instrumentation. The contrast of flow within the vessel lumen permits visualization of small vessels that are not visible when using conventional imagers and enhances the visibility of wall irregularity. Color Doppler aids in determination of the direction of flow and measurement of the Doppler angle.

CHAPTER 1 Physics of Ultrasound

T 60q cos T 0.5 'F 0.5

21

T 90q cos T 0.0 'F 0.0

T 0q cos T 1.0 'F 1.0

FIGURE 1.27 Effect of Doppler Angle on Frequency Shift. (A) At an angle of 60 degrees, the detected frequency shift (DF) detected by the transducer is only 50% of the shift detected at an angle of 0 degrees. At 90 degrees, there is no relative movement of the target toward or away from the transducer, and no frequency shift is detected. The detected Doppler frequency shift is reduced in proportion to the cosine of the Doppler angle. Because the cosine of the angle changes rapidly at angles above 60 degrees (thus small changes in angle correction can lead to large differences in calculated velocity), the use of Doppler angles of less than 60 degrees is recommended in making velocity estimates. (B) Each color pixel in a color Doppler image represents the Doppler frequency shift at that point, and it cannot be used to estimate velocity. Even though the points A and B have similar color values and therefore similar Doppler frequencies, the velocity at A is much higher than at B because of the large Doppler angle at A compared to B. The velocity represented by a given Doppler frequency increases in proportion to the Doppler angle.

A

A

B

B

Power Doppler Key Points of Ultrasound Elastography COLOR DOPPLER Shows direction of flow Saturation of color gives qualitative representation of velocity Less sensitive for small vessels and areas of severe stenosis Aliasing Noise appears across the entire frequency spectrum and limits sensitivity

POWER DOPPLER No data on flow direction No data on velocity Increased sensitivity for flow detection No aliasing Noise is a homogeneous background color, allowing for use of higher gain settings for improved flow detection

An alternative to the display of frequency information with color Doppler imaging is to use a color map that displays the integrated power of the Doppler signal instead of its mean frequency shift. Because frequency shift data are not displayed, there is no aliasing. The image does not provide information related to flow direction or velocity, and power Doppler imaging is much less angle dependent than frequency-based color Doppler display. In contrast to color Doppler, where noise may appear in the image as any color, power Doppler permits noise to be assigned to a homogeneous background color that does not greatly interfere with the image. This results in a significant increase in the usable dynamic range of the scanner, permitting higher effective gain settings and increased sensitivity for flow detection.

Interpretation of the Doppler Spectrum Doppler data components that must be evaluated both in spectral display and in color Doppler imaging include the

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FIGURE 1.28 Duplex Doppler Display. At the top of the image in color is an image of the carotid artery that is being interrogated. The phase of Doppler signals provides information about the presence and direction of motion, and changes in frequency relate to the velocity of the target. Backscattered signals from red blood cells are displayed in color as a function of their motion toward or away from the transducer, and the degree of the saturation of the color is used to indicate the frequency shift from moving red cells. Note that the operator makes the choice of direction (towards or away from the transducer) so “red” does not always indicate flow toward the transducer. In this image of the left mid common carotid artery, the flow is actually away from the transducer, but the scale has been flipped as shown in the color scale to the right of the image. At the lower portion of the image, a Doppler spectral waveform shows changes in flow velocity and direction by vertical deflections of the waveform above and below the baseline. The width of the spectral waveform (spectral broadening) is determined by the range of frequencies present at any instant in time. A brightness (gray) scale is used to indicate the amplitude of each frequency component.

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FIGURE 1.29 Continuous Wave and Pulsed Wave Doppler. (A) Continuous wave (CW) Doppler uses separate transmit and receive crystals that continuously transmit and receive ultrasound. Although able to detect the presence and direction of flow, CW devices are unable to distinguish signals arising from vessels at different depths (green-shaded area). (B) Pulsed wave Doppler uses the principle of ultrasound ranging (see Fig. 1.3) and permits the sampling of flow data from selected depths by processing only the signals that return to the transducer after precisely timed intervals. The operator is able to control the position of the sample volume and, in duplex systems, to view the location from which the Doppler data are obtained.

Doppler shift frequency and amplitude, the Doppler angle, the spatial distribution of frequencies across the vessel, and the temporal variation of the signal. Because the Doppler signal itself has no anatomic significance, the examiner must interpret the Doppler signal and then determine its relevance in the context of the image. The detection of a Doppler frequency shift indicates movement of the target, which in most applications is related to the presence of flow. The sign of the frequency shift (positive or negative) indicates the direction of flow relative to the transducer. Vessel stenosis is typically associated with large Doppler frequency shifts in both systole and diastole at

the site of greatest narrowing, with turbulent flow in poststenotic regions. In peripheral vessels, analysis of the Doppler changes allows accurate prediction of the degree of vessel narrowing. Information related to the resistance to flow in the distal vascular tree can be obtained by analysis of changes of blood velocity with time, as shown in the Doppler spectral display. Doppler imaging can provide information about blood flow in both large and small vessels. Small vessel impedance is reflected in the Doppler spectral waveform of afferent vessels. Fig. 1.31 provides a graphic example of the changes in the Doppler spectral waveform resulting from physiologic changes

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FIGURE 1.30 Color Doppler, Power Doppler, and noise. Color Doppler (A) uses a color map to display information on the detection of frequency shifts for moving targets. Power Doppler (B) uses a color map to show the distribution of the power or amplitude of the power signal. Flow direction and velocity information are not provided. (C) Color Doppler Noise. Noise appears over the entire spectrum, thus, the scan levels are limited to settings that do not not introduce, excessive noise. (D) Power Doppler noise. Noise is of low amplitude: that is, it’s possible to map this to the colors near the background. This permits the use of high gain settings that offer substantial improvement over conventional color Doppler in flow detection.

FIGURE 1.31 Impedance. (A) Highresistance waveform in brachial artery, produced by inflating forearm blood pressure cuff to a pressure above the systolic blood pressure. As a result of high peripheral resistance, there is low systolic amplitude and reversed diastolic flow. (B) Low-resistance waveform in peripheral vascular bed, caused by vasodilation stimulated by the prior ischemia. Immediately after release of 3 minutes of occluding pressure, the Doppler waveform shows increased amplitude and rapid antegrade flow throughout diastole.

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in the resistance of the vascular bed supplied by a normal brachial artery. A blood pressure cuff has been inflated to be above systolic pressure to occlude the distal branches supplied by the brachial artery. This occlusion causes reduced systolic amplitude and cessation of diastolic flow, and results in a waveform different than that found in the normal resting state. During the period of ischemia induced by pressure cuff occlusion of the forearm vessels, vasodilation has occurred. Immediately after release of the occluding pressure the Doppler waveform reflects a low-resistance peripheral vascular bed with increased systolic amplitude and rapid flow throughout diastole, typical for vasodilation. Doppler indices include the systolic-to-diastolic ratio (S/D ratio), resistive index (RI), and pulsatility index (PI) (Fig. 1.32). These compare blood flow in systole and diastole, show resistance to flow in the peripheral vascular bed, and help evaluate the perfusion of tumors, renal transplants, the placenta, and other organs. With Doppler ultrasound, it is therefore possible to identify vessels, determine the direction of blood flow, evaluate narrowing or occlusion, and characterize blood flow to organs and tumors. Analysis of the Doppler shift frequency with time can be used to infer both proximal stenosis and changes in distal vascular impedance. Most work using pulsed wave Doppler imaging has emphasized the detection of stenosis, thrombosis, and flow disturbances in major peripheral arteries and veins. In these applications, measurement of peak systolic and end diastolic frequency or velocity, analysis of the Doppler spectrum, and calculation of certain frequency or velocity ratios have been the basis of analysis. Changes in the spectral waveform measured by indices comparing flow in systole and diastole indicate the resistance of the vascular bed

FIGURE 1.32 Doppler Indices. Doppler flow indices used to characterize peripheral resistance are based on the peak systolic frequency or velocity (A), the minimum or end diastolic frequency or velocity (B), and the mean frequency or velocity (M). The most frequently used indices are the systolic-to-diastolic ratio (A/B); resistive index [(AB)/A]; and pulsatility index [(AB)/M]. In calculation of the pulsatility index, the minimum diastolic velocity or frequency is used; calculation of the systolic-to-diastolic ratio and resistive index use the end diastolic value.

supplied by the vessel and the changes resulting from a variety of pathologic conditions. Changes in Doppler indices from normal may help in the early identification of rejection of transplanted organs, parenchymal dysfunction, and malignancy. Although useful, these measurements are influenced not only by the resistance to flow in peripheral vessels, but also by heart rate, blood pressure, vessel wall length and elasticity, extrinsic organ compression, and other factors.

Interpretation of Color Doppler Although the graphic presentation of color Doppler imaging suggests that interpretation is relatively easy, the color Doppler image is actually quite complex. To be confident that a conventional Doppler study has achieved reasonable sensitivity and specificity in detection of flow disturbances, a methodical search and sampling of multiple sites within the field of interest must be performed. In contrast, color Doppler imaging devices permit simultaneous sampling of multiple sites and are less susceptible to this error. Although color Doppler can indicate the presence of blood flow, misinterpretation of color Doppler images may result in important errors. Each color pixel displays a representation of the Doppler frequency shift detected at that point. The frequency shift displayed is not the peak frequency present at sampling but a weighted mean frequency that attempts to account for the range of frequencies and their relative amplitudes at sampling. Manufacturers use different methods to derive the weighted mean frequency displayed in their systems. In addition, the PRF and the color map selected to display the detected range of frequencies affect the color displayed. The color assigned to each Doppler pixel is determined by the Doppler frequency shift (which in turn is determined by target velocity and Doppler angle), the PRF, and the color map selected for display; therefore, the interpretation of a color Doppler image must consider each of these variables. Although most manufacturers provide on-screen indications suggesting a relationship between the color displayed and flow velocity, this is misleading because color Doppler does not show velocity and only indicates the weighted mean frequency shift measured in the vessel; without correction for the effect of the Doppler angle, velocity cannot be estimated. Because the frequency shift at a given point is a function of velocity, Doppler angle, and PRF, any velocity may be represented by any color, and under certain circumstances, low-velocity flow may not be shown at all. As with spectral Doppler, aliasing is determined by PRF. With color Doppler, aliasing causes frequencies greater than half of the PRF to “wrap around” and to be displayed in the opposite colors of the color map. Inexperienced users tend to associate color Doppler aliasing with elevated velocity, but even low velocities may show marked aliasing if PRF is sufficiently low. As PRF is increased, aliasing of high Doppler frequency shifts is reduced; however, low-frequency shifts may be eliminated from the display, resulting in diagnostic error.

CHAPTER 1 Physics of Ultrasound

Other Technical Considerations Although many problems and artifacts associated with B-mode imaging (e.g., shadowing) are encountered with Doppler sonography, the detection and display of frequency information related to moving targets present additional technical considerations. It is important to understand their influence on the interpretation of the flow measurements obtained in clinical practice.

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pass filters, or wall filters, which remove signals that fall below an operator-selected frequency limit. Although effective in eliminating low-frequency noise, these filters may also remove signals from low-velocity blood flow (Fig. 1.33). In certain clinical situations the measurement of these slower flow velocities is of clinical importance, and the improper selection of the wall filter may result in serious errors of interpretation. For example, low-velocity venous flow may not be detected if an improper filter is used, and low-velocity diastolic flow in certain arteries may also be eliminated from the display, resulting in errors in the calculation of Doppler indices, such as the S/D ratio or RI. In general, the filter should be kept at the lowest practical level, usually 50 to 100 Hz.

Doppler Frequency A primary objective of the Doppler examination is the accurate measurement of characteristics of flow within a vascular structure. The moving red blood cells that serve as the primary source of the Doppler signal act as point scatterers of ultrasound rather than specular reflectors. This interaction results in the intensity of the scattered sound varying in proportion to the fourth power of the frequency, which is important in selecting the Doppler frequency for a given examination. As the transducer frequency increases, Doppler sensitivity improves, but attenuation by tissue also increases, resulting in diminished penetration. Careful balancing of the requirements for sensitivity and penetration is an important responsibility of the operator during a Doppler examination. Because many abdominal vessels lie several centimeters beneath the skin surface, Doppler frequencies in the range of 3 to 3.5 MHz are usually required to permit adequate penetration.

Spectral Broadening Spectral broadening occurs when there are multiple different velocities of flow within a vessel, which is one of the signs of stenosis. As a target moves through the sample volume at a fixed speed the Doppler angle varies, which generates a slightly different Doppler frequency shift for each position of the target. These variations in the Doppler frequency shift broaden the spectrum.5 Spectral broadening refers to the presence of a broad range of flow velocities at a given point in the pulse cycle and, by indicating turbulence, is an important criterion of high-grade vessel narrowing (Fig 1.34).

Wall Filters Doppler instruments detect motion not only from blood flow but also from adjacent structures. To eliminate these lowfrequency signals from the display, most instruments use high

Doppler Angle When making Doppler measurement of velocity, it is necessary to correct for the Doppler angle. The accuracy of a velocity estimate obtained with Doppler is only as great as the accuracy of the

FIGURE 1.33 Wall Filters. Wall filters are high-pass filters employed to eliminate lowfrequency noise from the Doppler display, but high wall filter settings may result in interpretation errors. Here the effect on the display of lowvelocity flow is shown with wall filter settings of (A) 100 Hz and (B) 400 Hz. In general, wall filters should be kept at the lowest practical level, usually in the range of 50 to 100 Hz.

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FIGURE 1.34 Spectral Broadening. The range of velocities detected at a given time in the pulse cycle is reflected in the Doppler spectrum as spectral broadening, and is a sign of vessel stenosis, as can be seen in this image of the external carotid artery.

measurement of the Doppler angle. This is particularly true when the Doppler angle exceeds 60 degrees, because small changes in the Doppler angle above 60 degrees result in substantial changes in the calculated velocity. Therefore, measurement inaccuracies result in much greater errors in velocity estimates than do similar errors at lower Doppler angles. Angle correction is not required for the measurement of Doppler indices such as the resistive index, because these measurements are based only on the relationship of the systolic and diastolic amplitudes.

Sample Volume Size With pulsed wave Doppler systems, the length of the Doppler sample volume is controlled by the operator, and the width is determined by the beam profile. Analysis of Doppler signals requires that the sample volume be adjusted to exclude as much of the unwanted clutter as possible from near the vessel walls. Doppler Gain As with imaging, proper gain settings are essential to achieving accurate and reproducible Doppler measurements. Excessive Doppler gain results in noise appearing at all frequencies and may result in overestimation of velocity. Conversely, insufficient gain may result in underestimation of peak velocity (Fig. 1.35). A consistent approach to setting Doppler gain should be used. After placing the sample volume in the vessel, the Doppler gain should be increased to a level where noise is visible in the image, then gradually reduced to the point at which the noise first disappears completely.

ULTRASOUND ARTIFACTS Almost all ultrasound images contain artifacts. Although many artifacts go unnoticed because they are buried in and

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FIGURE 1.35 Doppler Gain. Accurate estimation of velocity requires proper Doppler gain adjustment. Excessive gain will cause an overestimation of peak velocity (A), and insufficient gain will result in underestimation of velocity (C). To adjust gain properly, the sample volume and Doppler angle are first set at the sample site. The gain is turned up until noise appears in the background (A), then is gradually reduced just to the point where the background noise disappears from the image (B). PSV, Peak systolic velocity.

contribute to the background noise, when artifacts substantially alter the signal within a region of an image, they become recognizable. Some artifacts distort the images and must be identified in order to prevent a false diagnosis or to improve image quality. Other artifacts add useful information and thus are important for understanding the composition, anatomy, and pathology of the region being imaged. Understanding artifacts is essential for correct interpretation of ultrasound examinations.

CHAPTER 1 Physics of Ultrasound

Assumptions in Gray-Scale Imaging

ultrasound beam encounters a focal lesion that attenuates the sound to a greater or lesser degree than the surrounding tissues, the intensity of the beam deep to the lesion will be either weaker (shadowing) or stronger (increased through transmission) than in the surrounding tissues (Video 1.2). Because attenuation increases with frequency, the effects of shadowing and throughtransmission are greater at higher than at lower frequencies. The conspicuity of shadowing and through-transmission is reduced by excessive beam width, improper focal zone placement, and use of spatial compounding.

In gray-scale B-mode imaging, multiple ultrasound pulses are sent down a series of scans lines, sweeping through the object. The positions and amplitudes of the returned echoes are stored, building a 2-D representation of the object. Several assumptions about the propagation of sound waves are made when ultrasound equipment maps detected echoes onto the image.8 When one or more of these assumptions prove invalid, artifacts result.

Speed of Sound Artifacts

Shadowing

Ultrasound processing assumes that the speed of sound in tissue is a constant 1540 m/s. This speed, together with the delay between transmitting a pulse and detecting an echo, are used to calculate the distance between the transducer and the target. Speed of sound artifacts occur when a large enough structure composed of a tissue with substantially different speed of sound than 1540 m/s is encountered.7,8 In the case of a fatty lesion, where sound waves propagate at slower speed (approximately 1450 m/s, Fig 1.36, Video 1.1), it takes longer for an echo to return to the transducer, and the lesion is thus displayed deeper in the image than its true location.

Shadowing (Fig. 1.37) results when there is a notable reduction in the intensity of the ultrasound deep to a strong attenuator, reflector, or refractor. It causes partial or complete loss of information due to attenuation of the sound by superficial structures. Shadowing can be thought of as a failure of TGC or other algorithms to adequately compensate for the reduction in ultrasound intensity9 (Videos 1.3 and 1.4). A clean dark shadow will be seen behind calcified objects when the focal zone is at or just below the structure. Shadowing is decreased when there is inappropriate placement of the focal zone, when there is an excessive beam width (such that the stone is too small with respect to the beam width), and when spatial compounding is utilized.9 More irregular shadowing can be seen behind dense masses, such as an ovarian fibroma (see Video 1.5). Edge shadowing is caused by excessive refraction and commonly occurs from the edges of vessels, cystic structures, and bones such as the example of edge shadowing from the fetal skull, shown in Fig. 1.38.

Attenuation of Sound Artifacts The intensities of sound waves decrease as they travel through tissues. Ultrasound equipment assumes that this decreasing of intensity (attenuation) occurs at a uniform rate (e.g., 0.7 dB/cm/ MHz), and that the attenuation is adequately compensated by first-order correction schemes such as TGC.9 However, attenuation varies considerably in normal tissues. When the

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FIGURE 1.36 Speed of Sound Artifact. (A) Transverse image of liver and right kidney. When sound passes through a fatty mass, in this case a myelolipoma, its speed slows down to 1450 m/s. Because the ultrasound scanner assumes that sound propagates at the average velocity of 1540 m/s, the delay in echo return is interpreted as indicating a deeper target. Therefore, the final image shows a misregistration error in which the diaphragm (arrow) and other structures deep to the fatty lesion are shown in a deeper position than expected. (B) Correlative CT image showing the fatty nature of the mass, and normal position of the diaphragm. See also Video 1.1.

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FIGURE 1.37 Shadowing. (A) Gallstone With Shadowing. Note the hypoechoic, well-defined shadow directly behind the gallstone, and increased through transmission behind the gallbladder sludge. (B) Shadowing From Hernia Repair Mesh. (C) Shadowing From Ovarian Fibroma. This is a slightly less “clean” shadow, since the fibroma is not as dense as a calcified stone. (D) Shadowing From an Intrauterine Device. (E) Coned down view of distal neonatal spine with tethered cord shows shadowing from vertebral bodies that interrupt the linear appearance of the nerve roots. (F) Shadowing from dense plaque prevents assessment of color flow in that region. Note that there must be flow present because similar color is visualized before and after the shadow. See also Videos 1.2e1.5.

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is falsely mapped mirror image of the second reflector beyond the specular reflector. The image is displayed deeper because of the longer path of the reflected sound. Mirror image artifact can be reduced or eliminated by moving the transducer to center it on the region of interest and/or placing the focal zone at the level of interest in the real structure.

FIGURE 1.38 Edge Shadowing. Note the edge shadowing artifact behind the posterior aspect of the fetal skull. The beam bends at curved surface and loses intensity, producing a shadow (arrow).

Increased Through-Transmission Increased through-transmission occurs when an object, such as a cyst, attenuates the ultrasound less than the surrounding tissues. It can be thought as an over correction of ultrasound signal based on the assumed uniform attenuation, with distal tissues appearing echogenic9 (Fig. 1.39, Video 1.6). However, not all through-transmission is due to fluid, as some homogeneous solid lesions can have through transmission (Fig. 1.40). Therefore, when a homogenous solid breast mass is in the differential diagnosis for a lesion with through transmission, care should be taken to assess with power and color Doppler to better characterize the lesions as a complex cyst with layering debris or a homogeneous solid mass.

Path of Sound-Related Artifacts When creating an image, the ultrasound equipment assumes that the generated pulse of ultrasound waves travels from the surface of the probe in a straight line, then is reflected off a reflector only once, and returns back directly to the probe at the same angle to the exact point where it left the probe. If the ultrasound waves undergo more than one reflection, artifacts such as mirror image, reverberation, or comet-tail occur. If the direction of the beam or its echo is altered, refraction or anisotropy artifacts may result. These artifacts may suggest the presence of structures that are not actually existent.

Mirror Image Artifact A mirror image artifact (Fig. 1.41, Video 1.7) is generated when the primary beam encounters a specular reflector that acts like a mirror, and the reflected echoes encounter a second reflector and bounce back onto the mirror before being directed to the transducer. As only a straight beam path is assumed, the result

Reverberation Artifact Reverberation artifact occurs in the presence of two parallel reflective interfaces, such as the skin surface and another strong reflector close to the skin.8,24 The sound waves may get partially trapped between the two reflective surfaces, reverberating back and forth before returning to the transducer for detection. When this happens, multiple echoes are detected and displayed, causing the appearance of multiple regular lines (Video 1.8). Often the reflectors are the skin and subcutaneous fascia (Fig. 1.42). Reverberation can be helpful during biopsies, to see a needle. Reverberation artifacts can usually be reduced or eliminated by changing the scanning angle or transducer placement to avoid the parallel interfaces that contribute to the artifact. Using a different window or decreasing the gain can also reduce the artifact. Comet-Tail Artifact Comet-tail artifact is a subtype of reverberation artifact.9,24 The repetitive reflections occur within closely spaced interfaces (Fig. 1.43), such as tiny cysts in the case of von Meyenburg complexes and tiny crypts in the wall of the gallbladder in the case of adenomyomatosis (Videos 1.8 and 1.9), and the reverberated echoes may not be individually discernable. The tapered, comet-tail appearance is due to the decreasing amplitude of each reverberation as a result of attenuation. Refraction Artifact As sound passes through the interface between two tissues that propagate sound at different speeds, such as from muscle to fat, its direction changes at the interface. This phenomenon is known as refraction and can cause misregistration of a structure in an ultrasound image. When an ultrasound scanner detects an echo, it assumes that the source of the echo is along a fixed line of sight from the transducer. If the sound has been refracted, the echo detected may be coming from a different depth or location than the image shown in the display (Fig. 1.44, Video 1.10).25 If this is suspected, this artifact can be minimized by increasing the scan angle so that it is perpendicular to the interface. Anisotropy Anisotropy is an artifact caused by structures that are composed of bundles of highly reflective fibers running parallel to each other, such as tendons and ligaments. If the sound beam hits the tendon or ligament fibers perpendicular to their length, it is reflected directly back, resulting in an echogenic appearance. If the angle of insonation is not perpendicular to the tendon

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FIGURE 1.39 Increased Through-Transmission. (A and B) Increased through-transmission in a breast cyst with layering debris. Note how the debris (*) changes with patient position with patient in (A) supine and (B) upright position. The through-transmission is seen regardless of patient position, due to the cystic nature of mass. (C) Hepatic cyst. The hepatic parenchyma distal to the cysts is display as increased in echogenicity (arrows) secondary to increased through-transmission. See also Video 1.6. (D) Transvaginal sagittal image of cervix shows multiple Nabothian cysts with through-transmission and edge shadowing.

fibers, the beam is reflected away from the transducer, leaving the image with artifactual hypoechogenicity within the tendon (Fig. 1.45, Videos 1.11 and 1.12).

Gas-Related Artifacts Several physical properties of gases lead to unique artifacts in ultrasound that help identify gas but may also hinder visualization of other organs. These properties include large

difference in acoustic impedance between gas and soft tissue, which results in high reflectivity at their interfaces. The varied and ever-changing shape of gas in the body, including foam, leads to variability of its appearance even in the same field. The low density of gases makes them quite compressible, and they can undergo resonant oscillation in response to sound waves, leading to amplification of echoes. These properties result in ring-down and dirty shadowing artifacts.26

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FIGURE 1.40 Increased Through-Transmission in a Homogeneous Solid Breast Mass. Color Doppler ultrasound is helpful in distinguishing between complex cysts and solid nodules when the distinction is uncertain based on the gray-scale image alone. (A) Metastatic leiomyosarcoma of the breast shows a homogenous hypoechoic mass with posterior increased through-transmission, simulating a complex cyst. (B) Color Doppler sonography shows abundant internal flow, indicating that the lesion is solid.

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FIGURE 1.41 Mirror Image Artifact. (A and B) Soft tissueegas interfaces, such as the diaphragm, are excellent reflectors of the sound beam owing to the large difference in the acoustic impedance between the two materials. Therefore, hepatic structures are frequently seen mirrored beyond the diaphragm onto the lungs. These two figures show liver parenchyma, hepatic veins in part A, and a hepatic hemangioma in part B all inversely projected onto lung. See also Video 1.7.

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Reverberation artifact Free intraperitoneal gas

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C FIGURE 1.42 Reverberation Artifact. Reverberation artifacts arise when the ultrasound signal reflects repeatedly between highly reflective interfaces near the transducer, resulting in delayed echo return to the transducer. This appears in the image as a series of regularly spaced echoes at increasing depth. (A) Reverberation artifact due to free intraperitoneal gas (thin arrow). Note the parallel linear echoes (large arrows) behind this. (B) Mirror Image and Reverberation Artifacts Behind a Pacemaker. The highly reflective and mirrorlike surface of the pacemaker (arrow) results in repeated bouncing of sound wave among the probe surface, pacemaker, and skin. (C) A small amount of gas within the bladder is recognizable by the reverberation artifact (arrow). See also Video 1.8.

Ring-Down Artifact Ring-down artifact (Fig. 1.46, Video 1.13) appears as a series of parallel bands or a solid streak extending away from gas collections, and it arises from resonant vibrations within fluid trapped between a tetrahedron of gas bubble.27 These vibrations produce a continuous sound wave transmitted back to the transducer. Signal processing by the ultrasound machine converts this continuous sound wave into the streak or series of bands seen in the ring-down artifact, which has the similar appearance of comet-tail artifact. However, the underlying mechanisms of these two types of artifacts are different.

Dirty Shadowing Artifact Dirty shadowing (Fig. 1.47, Videos 1.14-1.16) results from a combination of reflection, reverberation, and ring-down artifacts originated from multiple layers of bubbles in foam. The individual artifacts superimpose on each other and produce a chaotic set of bright streaks.26

Beam ProfileeRelated Artifacts The sound beam generated by a transducer is assumed to be a single narrow line. When the beam is not sufficiently narrow in the imaging plane or in the elevation plane,

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FIGURE 1.43 Comet-Tail Artifact. (AeD) Adenomyomatosis. (A and B) Gray-scale images show comet-tail artifact that is felt to be due to cholesterol crystals within the prominent Rokitansky-Aschoff sinuses. (C and D) On color and spectral Doppler this can look like a twinkle artifact, but it is a color representation of the comet-tail. (E and F) von Meyenburg Complexes in two patients. Note the multiple comet-tail artifacts. (G) Colloid Cyst in Thyroid Gland with characteristic comet-tail artifact (Arrow). (H) Comet-Tail Artifact Due to Fiducial Marker in patient with prostate cancer (note position of the probe at the bottom of the screen, such that the bladder is the hypoechoic region superiorly). See also Videos 1.8 and 1.9.

beam-width artifacts or partial volume averaging may occur. These artifacts can create echoes within otherwise anechoic structures.

Side Lobe and Grating Lobe Artifacts Though assumed to be a narrow straight line, ultrasound beam has a complex profile that varies depending on the construction of the transducer (Fig. 1.48, Video 1.7). Although most of

the energy generated by a transducer is emitted in a beam along the central axis of the transducer, a small amount of energy (approximately 1%) is also emitted at the periphery of the primary beam.9 These are called secondary lobes (side lobes and grating lobes) and are lower in intensity than the primary beam. When these side lobes encounter a highly reflective interface, they can be reflected back and detected by the transducer. Because ultrasound machine assumes that all

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FIGURE 1.44 Refraction Artifact Caused by the Rectus Abdominis Muscle. (A) The direct sound path properly depicts the location of the object. (B) A “ghost image” (red) produced by refraction at the edge of the rectus abdominis muscle. The transmitted and reflected sound waves travel along the path of the black arrows. The scanner assumes the returning signal is from a straight line (red arrow) and displays the structure at the incorrect location. (C) Transverse transabdominal image of the uterus showing a small gestational sac (A) and what appears to be a second sac (B) due to refraction artifact. See also Video 1.10. (D) In another patient, refraction artifact shows what appears to be 2 aortas. (D, Reproduced with permission from Hertzberg BS, Middleton WD. Ultrasound: The Requisites. 3rd ed. Philadelphia, PA: Elsevier.25)

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C FIGURE 1.45 Anisotropy. (A and B) Anisotropy in the Achilles tendon. (A) In this long-axis scan of the Achilles insertion on the calcaneus, the proximal portion of the imaged tendon demonstrates a normal fibrillar appearance (arrow), whereas the distal tendon insertion is hypoechoic (arrowhead). (B) When the transducer is angled 90 degrees to the distal tendon insertion, the tendon then becomes fibrillar and is normal in appearance (arrowhead). C, Calcaneus. (C) Neonatal head ultrasound. The peritrigonal region of the white matter (ellipse) appears relatively echogenic, also called “peritrigonal blush.” This anisotropic effect artifact occurs because in the trigone region, the parallel white matter fibers run perpendicular to the incident sound beam, causing increased reflection. The artifact is visible only in the region of the trigone when the anterior fontanelle is used as a scanning window. See also Videos 1.11 and 1.12.

returned echoes originate from the primary beam, the echoes are misregistered and falsely displayed in the primary beam, not at their true location. They are often not detectable when superimposed on soft tissues but are more evident when the misplaced echoes overlap an expected anechoic structure. These artifacts are of clinical importance because they may create the impression of structures or debris in fluid-filled structures (see Fig. 1.48, Video 1.17). Secondary lobes may also result in errors of measurement by reducing lateral resolution. Repositioning the transducer and its focal zone or using a different transducer will usually allow the differentiation of artifactual from true echoes.

Partial Volume Averaging The ultrasound beam has not only a complex shape in the imaging plane but also a profile in the third dimension (i.e., the

elevation plane or “Z plane”). The ultrasound image appears as a flat 2-D image, but the brightness of each pixel represents the average of all the echoes received within the thickness of the beam in the elevation plane. This results in the echoes being displayed in structures that are expected to be anechoic (Fig. 1.49, Video 1.18).

Doppler Imaging Artifacts Artifacts in color Doppler imaging can be confusing and lead to misinterpretation of flow information. These artifacts can originate from physical limitations of the modality or inappropriate equipment settings such as color-write priority, gain setting, and PRF. For example, if the gain setting is too low, flow might not be visualized (Fig. 1.50). If the gain setting is too high, artifactual flow may be seen in adjacent soft tissues, and thrombus within the vessel might be missed.5

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C FIGURE 1.46 Ring-Down Artifact. (A and B) Pneumobilia causing ring-down artifact in the biliary tree (A) and gallbladder (B). (C) Iatrogenic air in the bladder introduced at cystoscopy appears as a nondependent bright region with ring-down artifact. See also Videos 1.13.

Major Sources of Doppler Imaging Artifacts DOPPLER FREQUENCY Higher frequencies lead to more tissue attenuation Wall filters remove signals from low-velocity blood flow

INCREASE IN SPECTRAL BROADENING Excessive system gain or changes in dynamic range of the grayscale display Excessively large sample volume Sample volume too near to the vessel wall

INCREASE IN ALIASING Decrease in pulse repetition frequency Decrease in Doppler angle Higher frequency transducer

DOPPLER ANGLE Relatively inaccurate above 60 degrees

SAMPLE VOLUME SIZE Large sample volumes increase vessel wall noise

Loss or Distortion of Doppler Information Incorrect gain, wall-filter, and velocity scale all can lead to loss or distortion of Doppler signal (Fig. 1.51). A rule of thumb for gain setting in Doppler imaging is to turn up the Doppler gain until noise is encountered and then back off until the noise just clears from the image. When estimating frequency, the rule of thumb is to use a Doppler angle less than 60 degrees. Wall filters eliminate unwanted low-frequency signals from slowly moving soft-tissue reflectors, and the cut-off frequency is operator selectable. A filtration setting that is too high can lead to loss of diagnostically significant velocity information. In general, wall filters should be kept at the lowest practical level, typically in the range of 50 to 100 Hz. Artifactual Vascular Flow Doppler effect is not specific to vascular flow and can occur with movement of any reflectors toward or away from the ultrasound beam (Fig. 1.52). Fluid or solid tissue motion can thus mimic vascular flow. Transmitted pulsations, especially close to the heart or major arteries, can therefore result in artifactual

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FIGURE 1.47 Dirty Shadowing. (A) Diagram showing the ultrasound beam and illustrating the gas bubbles that are the basis for dirty shadowing. See also Videos 1.14-1.16. (B) Image of small amount of intraperitoneal air with dirty shadowing. (C and D) Dirty shadowing in liver mass. (C) Transverse view of the left lobe of the liver shows gas in a mass with reverberation artifact filling the cavity. (D) Comparison CT scan. (EFG) Dirty Shadowing Posterior to Emphysematous Cholecystitis. (E) Sagittal sonogram of the gallbladder with intraluminal air appearing as bright echogenicities with dirty shadowing. (F) The pancreas also shows dirty shadowing due to gas that has refluxed into the pancreatic duct. (G) Corresponding CT scan shows air in the gallbladder wall and lumen as well as in the pancreas.

appearance of flow within thrombosed veins or avascular areas. Artifactual vascular flow can also be visualized if the Doppler gain is too high or the color-write priority is too high.

Tissue Vibration Artifact Tissue vibration artifact (Fig. 1.53, Video 1.19) consists of color pixels erroneously placed in the adjacent soft tissue by the ultrasound scanner because of the transmitted vibration from a region of marked turbulence. It is commonly seen with shunts, tight stenoses of large arteries, and especially arteriovenous fistulas. If tissue vibration artifact is seen, a search should be made for an arteriovenous fistula. Aliasing and Velocity Scale Errors Aliasing is an artifact due to under sampling of Doppler signal, which results in incorrect estimation of flow velocity (Fig. 1.54, Video 1.20). To ensure that samples originate from only a selected depth when using a pulsed wave Doppler system, it is necessary to wait for the echo from the area of interest before transmitting the next pulse. This limits the rate with which pulses can be generated, a lower PRF being required for greater

depth. The PRF also determines the maximum depth from which unambiguous data can be obtained. PRF is the sampling frequency of Doppler signals. If PRF is less than twice the maximum frequency shift produced by movement of the target, or in other words, the maximum frequency shift is larger than half of the sampling frequency PRF (Nyquist limit), aliasing results. When PRF is less than twice the frequency shift being detected, lower frequency shifts than those actually present are displayed. Because of the need for lower PRFs to reach deep vessels, signals from deep abdominal arteries are prone to aliasing if high velocities are present. In practice, aliasing is usually readily recognized. This error is manifested by a wraparound of the higher frequencies to display below the baseline in spectral Doppler. In color Doppler, aliasing is manifested by wraparound of the frequency color map, from the top to the bottom of the color scale bar, without showing the color indicating the wall filter between the reversed colors. The most common methods for correcting for aliasing are5: (1) shift the baseline down or up; (2) increase velocity scale (which also increases PRF); (3) use a lower ultrasound frequency or a lower-frequency transducer; (4) increase the

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FIGURE 1.48 Complex Beam Profile of Ultrasound Beam. (A) The ultrasound beam is not a narrow straight line but has a complex profile that varies depending on the type and shape of the transducer. Although most of the energy generated by a transducer is emitted in a beam along the central axis of the transducer (A), some energy is also emitted at the periphery of the primary beam (B and C). These are called “side lobes” (B) or “grating lobes” (C) and are lower in intensity than the primary beam. Side lobes or grating lobes may interact with strong reflectors that lie outside of the scan plane and produce artifacts that are displayed in the ultrasound image. They are more evident when the misplaced echoes overlap an expected anechoic structure. (B) Side or Grating Lobe. Transverse image of the gallbladder reveals an intermediate intensity linear internal echo (arrow A) that suggests a band or septum within the gallbladder. This is a side lobe artifact related to the presence of a strong out-of-plane reflector (arrow B) medial to the gallbladder. The low-level echoes in the dependent portion of the gallbladder (C) are also artifactual and are caused by the same phenomenon. Side lobe and slice thickness artifacts are of clinical importance because they may create the impression of debris in fluid-filled structures. (C) In this patient with a ureterovesical junction stone there are echoes seen in the nondependent portion of the bladder. These are due to grating lobe artifact, wherein off-axis signal projects into the field of view. Note also the shadowing behind the bladder stone. See also Video 1.17.

A

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Doppler angle (thereby decreasing the frequency shift). However, as angulation approaches 90 degrees, directional ambiguity can occur, suggesting bidirectional flow. Errors in Doppler angle correction can also lead to misleading assessments of flow velocity.

Artifactual Spectral Broadening Improper positioning of the sample volume near the vessel wall, use of an excessively large sample volume, excessive system gain, changes in the dynamic range of the gray-scale display of the Doppler spectrum, or angle of insonation closer to 90 degrees can cause artifactual spectral broadening (Fig. 1.55). FIGURE 1.49 Partial Volume Averaging. The bladder wall is indistinct in region of this image. It is unclear if there are masses or if this is due to grating lobe artifact or partial volume artifact or both. Moving the patient or transducer to avoid bowel gas and putting the focal zone in the region in question should aid in evaluation. For the area closer to the patient’s anterior abdominal wall, a higher-frequency transducer might be helpful. See also Video 1.18.

Blooming Artifact Blooming artifact (Fig. 1.56) occurs when color reaches beyond the vessel wall, making the vessels look larger than expected. It is gain dependent in that lowering the gain will decrease

CHAPTER 1 Physics of Ultrasound

FIGURE 1.50 Artifactual Lack of Flow in color Doppler image of a carotid artery and jugular vein. In (A), the pulse repetition frequency (PRF) is 700 Hz and there is aliasing in the carotid artery, but slow flow in the jugular vein is seen. In (B), the PRF is 4500 Hz, eliminating aliasing in the artery but also suppressing the display of the low Doppler frequencies in the internal jugular vein. Depending on the color map selected, velocity of the target, Doppler angle, and PRF, a given velocity may appear as any color with color Doppler.

A (PRF = 700 Hz)

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39

B (PRF = 4500 Hz)

C

FIGURE 1.51 Color Direction. (A) Shown in color is a portion of the portal venous system. Note how the flow direction appears to change in the region of branching, but this is merely a result of the orientation of flow with respect to the midpoint of transducer. Note the aliasing in the posterior branch of the right portal vein. This is due to the curve of the vein and change in Doppler angle. (B and C) Color Direction in Recanalized Umbilical Vein. Gray-scale (B) and color Doppler (C) sonograms show left lobe of liver in a child with cirrhosis, portal hypertension, and recanalized umbilical vein. The recanalized umbilical vein is always flowing in relatively the same direction out of the liver, but at times, due to tortuosity, appears to change flow direction. Note that the flow changes from red (toward the transducer) to blue (away from the midpoint of the transducer), but at each interface there is a black region where the Doppler angle is 90 degrees.

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FIGURE 1.52 Artifactual Vascular Flow. (A) Color Doppler jets in the bladder use color motion to indicate that there is flow from each ureteral orifice. (B and C) Color flow Doppler signal in pleural fluid with debris. (B) Gray-scale sonogram shows left pleural fluid with much debris. (C) Color flow Doppler signal.

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FIGURE 1.53 Tissue Vibration Artifacts. (A) Gray-scale and (B) Power Doppler ultrasound demonstrate how vocal fremitus can be used to distinguish a mural nodule from a fat-fluid level. The lipid layer is not attached to the cyst wall, so the fremitus will not pass through it. On the other hand, true papillary lesions that are attached to the cyst wall will vibrate and transmit the fremitus artifact on power Doppler; having the patient hum in a deep voice creates a color artifact on power Doppler ultrasound. (C and D) Color streaking artifact. (C) This complicated cyst contains floating punctate echoes that move posteriorly while being scanned, creating a scintillating appearance on gray-scale sonography. (D) Power Doppler ultrasound pushes the echoes posteriorly faster and with more energy than does the gray-scale beam. The echoes move fast enough that color persistence creates the appearance of “color streaking” artifact. (E) Flash artifact from pulsation. In this image of the left portal vein, note how transmitted pulsation from the heart causes artifactual flow in the adjacent liver owing to motion. (F and G) Posterenal biopsy arteriovenous fistula (AVF). Color Doppler image (F) shows markedly increased lower-pole blood flow (arrows) with adjacent soft tissue color artifact related to tissue vibration (arrowheads). Tissue vibration artifact may be the first clue that an AVF is present, confirmed on spectral Doppler (G). (H) Color bruit. Spectral waveform at site of superior mesenteric artery stenosis shows very high systolic velocity, and diastolic velocities of greater than 290 cm/s. Color portion of the image shows color bruit consisting of color outside the vessel near the stenosis site. See also Video 1.19.

CHAPTER 1 Physics of Ultrasound

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FIGURE 1.54 Aliasing. Pulse repetition frequency (PRF) determines the sampling frequency of a given Doppler signal. (A) If PRF (dashed lines) is sufficient, the sampled waveform (the lower curve) will accurately estimate the frequency of the real signal (the upper curve). Solid circles along the dashed lines indicate the sample points. (B) If PRF is less than two times the frequency of the real signal, undersampling will produce a lower-frequency “alias” of the original signal (the lower curve), and result in lower frequency being displayed. (C) In a clinical setting, aliasing appears in the spectral display as a “wraparound” of the higher frequencies to display below the baseline. (D) In color Doppler display, aliasing results in a wraparound of the frequency color map from one flow direction to the opposite direction, passing through a transition of unsaturated color. The velocity throughout the vessel is constant, but aliasing appears only in portions of the vessel because of the effect of the Doppler angle on the Doppler frequency shift. As the angle increases, the Doppler frequency shift decreases, and aliasing is no longer seen. (E) Color and Spectral Doppler of right internal carotid artery. Note that aliasing prevents precise calculation of the maximum systolic velocity. However, because it is greater than 500 cm/s, the precise number is not needed. The aliasing in the image allows for easier identification of the region of highest velocity for placement of the spectral Doppler gate. (F and G) Aliasing due to Doppler angle changes. (B) Velocity obtained in the distal internal carotid artery with Doppler angle of 60 degrees is higher than that obtained at 44 degrees (arrow). (C) However, the sample angle does not parallel the vessel wall at 60 degrees. Note central color aliasing in the region of highest velocity (curved arrow). (H) Aliasing in pseudoaneurysm. Note the swirling flow in a pseudoaneurysm, resulting in a yin-yang appearance. At the midline border of red and blue, there is a black line where the Doppler angle is 90 degrees. Here the flow is perpendicular to the sound beam, and so it is not detected. At 3 and 9 o’clock positions, there is aliasing within the blue and red areas. Here the Doppler angle is zero degrees with the flow directly toward and away from the transducer, thus appearing with maximal velocity. As the velocity exceeds the selected 35 cm/s Doppler velocity range, aliasing results with artifactual opposite direction color signal. See also Video 1.20.

blooming. It is also wall filter and color-overwrite dependent, in that increasing the wall filter will decrease the artifact.

Twinkle Artifact Twinkle artifact is a color Doppler artifact that appears as discrete foci of alternating colors with or without an associated color comet-tail artifact (Fig. 1.57, Videos 1.21 and 1.22). The appearance of twinkle artifact is highly dependent on machine settings and is likely resulted from a type of

intrinsic machine noise called “phase (or clock) jitter” within the Doppler circuitry of the ultrasound machine.28,29 This, along with a strongly reflecting, rough surface such as a renal stone interrogated with color Doppler, results in a high-amplitude, broadband signal that appears as random motion on color Doppler sonography. The twinkle artifact is useful clinically because it can aid in the detection of small stones, calcifications, and other crystalline material within the body.

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THERAPEUTIC APPLICATIONS: HIGHINTENSITY FOCUSED ULTRASOUND Although the primary medical application of ultrasound has been for diagnosis, therapeutic applications are developing rapidly, particularly the use of high-intensity focused ultrasound (HIFU). HIFU is based on three important capabilities of ultrasound: (1) focusing the ultrasound beam to produce highly localized energy deposition, (2) controlling the location and size of the focal zone, and (3) using intensities sufficient to destroy tissue at the focal zone. This has led to an interest in HIFU as a means of destroying noninvasive tumor and controlling bleeding and cardiac conduction anomalies. HIFU exploits thermal (heating of tissues) and mechanical (cavitation) bioeffect mechanisms. As ultrasound passes through tissue, attenuation occurs through scattering and absorption. Scattering of ultrasound results in the return of some of the transmitted energy to the transducer, where it is detected and used to produce an image, or Doppler display. The remaining energy is transmitted to the molecules in the acoustic

A

field and produces heating. At the spatial peak temporal average intensities (ISPTA) of 50 to 500 mW/cm2 used for imaging and Doppler, heating is minimal, and no observable bioeffects related to tissue heating in humans have yet been documented with clinical devices. With higher intensities, however, tissue heating sufficient to destroy tissue may be achieved. Using HIFU at 1 to 3 MHz, focal peak intensities of 5000 to 20,000 W/cm2 may be achieved. This energy can be delivered to a small point several millimeters in size, producing rapid temperature elevation and resulting in tissue coagulation, with little damage to adjacent tissues (Fig. 1.58). The destruction of tissue is a function of the temperature reached and the duration of the temperature elevation. In general, elevation of tissue to a temperature of 60 C for 1 second is sufficient to produce coagulation necrosis. Because of its ability to produce highly localized tissue destruction, HIFU has been investigated as a tool for noninvasive or minimally invasive treatment of bleeding sites, uterine fibroids, and tumors in the prostate, liver, and breast.30,31 As with diagnostic ultrasound, HIFU is limited by the presence of gas or bone interposed between the transducer and the target

B

C FIGURE 1.55 Artifactual Spectral Broadening. Artifactual spectral broadening can be produced by improper positioning of the sample volume near the vessel wall, use of an excessively large sample volume or by excessive system gain. (AeC) Images of a volunteer’s carotid artery. (A) Sample gate is well positioned in the middle of the vessel. The waveform is normal. (B) Doppler gate is placed just outside the vessel walls. Note how the spectral waveform is “filled in” by many different velocities. (C) Doppler gate is wider than appropriate and the Doppler gain has been increased excessively. Note that not only is the spectral waveform “filled in,” but there is noise visible throughout the spectral Doppler display.

CHAPTER 1 Physics of Ultrasound

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FIGURE 1.56 Blooming Artifact. (A and B) Two images of the carotid artery. In (A) the gain and wall filter are appropriate to show the flow centrally in the vessel. In (B) the gain and wall filter have been changed (in a manner beyond what would be used in clinical imaging) to demonstrate how these can make the vessel “bloom” and appear larger. (CeF) Blooming artifact due to use of contrast and tissue motion in a patient with hepatocellular carcinoma. (C) Grayscale image of the liver shows large solid mass. (D) Color Doppler creates artifacts due to blooming and tissue motion. (E and F) Contrast-specific imaging shows blood vessels not seen with Doppler.

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FIGURE 1.57 Twinkle Artifact (A) Chronic Pancreatitis. Twinkle artifact makes the extensive pancreatic calcification much more conspicuous. (B and C) Ureterovesical junction stone. Note how the twinkle can be utilized to confirm the presence of a small stone. (DeF) Kidney stones with twinkle artifact as seen on (D) color Doppler, (E) power Doppler, and (F) spectral Doppler. Note how the spectral Doppler tracing of a twinkle artifact shows lines going through the tracing, which allow distinction from true blood flow. (G and H) Power Doppler image of twinkle behind prostatic calcifications. (G) Axial view shows extensive echogenic material, both calcifications and corpora amylacea (arrows), along the surgical capsule and peripheral zone. This has no clinical importance but hinders ultrasonic visibility. (H) Doppler examination of same patient shows the extensive Doppler noise artifact caused by the calcifications. Virtually all the visible color is artifactual. See also Videos 1.21 and 1.22.

tissue. The reflection of high-energy ultrasound from strong interfaces produced by bowel gas, aerated lung, or bone may result in tissue heating along the reflected path of the sound, producing unintended tissue damage. Major challenges with HIFU include image guidance and accurate monitoring of therapy as it is being delivered.

Magnetic resonance imaging (MRI) provides a means of monitoring temperature elevation during treatment, which is not possible with ultrasound. Guidance of therapy may be done with ultrasound or MRI, with ultrasound guidance having the advantage of verification of the acoustic window and sound path for the delivery of HIFU.

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Thomas Winter, MaryEllen R.M. Sun (Pancreas) William L. Simpson, Jr, Humaira Chaudry, Henrietta K. Rosenberg (Pediatric pelvis) Derek Muradali and Tanya P. Chawla (Organ transplantation) REFERENCES

FIGURE 1.58 High-Intensity Focused Ultrasound (HIFU). Local tissue destruction by heating may be achieved using HIFU delivered with focal peak intensities of several thousand W/cm2. Tissue destruction can be confined to a small area a few millimeters in size without injury to adjacent tissues. HIFU is a promising tool for minimally invasive treatment of bleeding sites, uterine fibroids, and tumors in the prostate, liver, and breast.

ACKNOWLEDGMENT The content of this chapter was modified from 5th edition of Diagnostic Ultrasound, chapter on Ultrasound Physics as well as the Virtual Chapter on Artifacts. We are deeply grateful to Christopher Merritt, the author of the physics chapter, for the use of his work from prior editions of the text. Ultrasound images are rich in artifacts. To demonstrate the diversity of artifacts and where they occur, we reused many of the images from chapters in the 5th edition of Diagnostic Ultrasound, Carol Rumack and Deborah Levine, editors. Elsevier Publisher. 2016. We thank the following chapter authors and content experts for the use of their work: Korosh Khalili and Stephanie Wilson (Biliary tree and gallbladder) Douglas Brown (Uterus) Ants Toi (Prostate and Fetal Brain) Stephanie Wilson and Cynthia Withers (Liver) Luigi Solbiati, J. William Charboneau, Vito Cantisani, C Reading, Giovani Mauri (Thyroid). Colm McMahon, Corrie Yablon (Shoulder and Overview of MSK US techniques) Mitchell Tublin, Wendy Thurston, Stephanie Wilson (Kidney and urinary tract) Sara M. O’Hara (Pediatric liver and spleen) Chetan C. Shah and S. Bruce Greenberg (Pediatric chest) Jordana Phillips and Rashmi Mehta (Breast Ultrasound) Barbara Hertzberg and Bill Middleton (Reverberation artifact) Richard Barr (Elastography) Ilse Castro Aragon (Pediatric spine) Harriet Paltiel, Diane Babcock (Pediatric kidney and adrenal glands) Raymond Bertina and Elton Mustafaraj (Retroperitoneum) Mark E. Lockhart, Heidi R. Umphrey, Therese M. Weber, Michele L. Robbin (Peripheral vessels) Peter Burns (Contrast agents)

1. Medical Diagnostic Ultrasound Instrumentation and Clinical Interpretation: Report of the Ultrasonography Task Force. JAMA. 1991;265(9):1155e1159. 2. Shung KK. High frequency ultrasonic imaging. J Med Ultrasound. 2009;17(1):25e30. 3. Chivers RC, Parry RJ. Ultrasonic velocity and attenuation in mammalian tissues. J Acoust Soc Am. 1978;63(3):940e953. 4. Goss SA, Johnston RL, Dunn F. Comprehensive compilation of empirical ultrasonic properties of mammalian tissues. J Acoust Soc Am. 1978;64(2):423e457. 5. Pozniak MA, Zagzebski JA, Scanlan KA. Spectral and color Doppler artifacts. Radiographics. 1992;12(1):35e44. 6. Nelson TR, Fowlkes JB, Abramowicz JS, Church CC. Ultrasound biosafety considerations for the practicing sonographer and sonologist. J Ultrasound Med. Published online 2009. 7. Zagzebski JA. Essentials of Ultrasound Physics. Mosby; 1996. 8. Hoskins PR, Martin K, Thrush A. Diagnostic Ultrasound: Physics and Equipment. CRC Press; 2019. 9. Baad M, Lu ZF, Reiser I, Paushter D. Clinical significance of US artifacts. Radiographics. 2017;37(5):1408e1423. 10. Krishnan S, Li P-C, O’Donnell M. Adaptive compensation of phase and magnitude aberrations. IEEE Trans Ultrason Ferroelectr Freq Control. 1996;43(1):44e55. 11. Merritt CRB. Technology update. Radiol Clin North Am. 2001;39(3):385e397. 12. Wells PNT, Liang H-D. Medical ultrasound: imaging of soft tissue strain and elasticity. J R Soc Interface. 2011;8(64):1521e1549. 13. Krouskop TA, Wheeler TM, Kallel F, Garra BS, Hall T. Elastic moduli of breast and prostate tissues under compression. Ultrason Imaging. 1998;20(4):260e274. 14. Ophir J, Cespedes I, Ponnekanti H, Yazdi Y, Li X. Elastography: a quantitative method for imaging the elasticity of biological tissues. Ultrason Imaging. 1991;13(2):111e134. 15. Shiina T, Nightingale KR, Palmeri ML, et al. WFUMB guidelines and recommendations for clinical use of ultrasound elastography: Part 1: basic principles and terminology. Ultrasound Med & Biol. 2015;41(5):1126e1147. 16. Madsen EL, Sathoff HJ, Zagzebski JA. Ultrasonic shear wave properties of soft tissues and tissuelike materials. J Acoust Soc Am. 1983;74(5): 1346e1355. 17. Sarvazyan AP, Rudenko OV, Swanson SD, Fowlkes JB, Emelianov SY. Shear wave elasticity imaging: a new ultrasonic technology of medical diagnostics. Ultrasound Med & Biol. 1998;24(9):1419e1435. 18. Ferraioli G, Parekh P, Levitov AB, Filice C. Shear wave elastography for evaluation of liver fibrosis. J Ultrasound Med. 2014;33(2):197e203. 19. Yoneda M, Suzuki K, Kato S, et al. Nonalcoholic fatty liver disease: USbased acoustic radiation force impulse elastography. Radiology. 2010;256(2):640e647. 20. Merritt CR. Doppler US: the basics. Radiographics. 1991;11(1):109e119. 21. Boote EJ. AAPM/RSNA Physics Tutorial for Residents: Topics in US, Doppler US techniques: concepts of blood flow detection and flow dynamics. Radiographics. 2003;23(5):1315e1327. https://doi.org/10.1148/rg.235035080. 22. Rubin JM, Bude RO, Carson PL, Bree RL, Adler RS. Power Doppler US: a potentially useful alternative to mean frequency-based color Doppler US. Radiology. 1994;190(3):853e856. 23. Kasai C, Namekawa K, Koyano A, Omoto R. Real-time two-dimensional blood flow imaging using an autocorrelation technique. IEEE Trans Sonics Ultrason. 1985;32(3):458e464. 24. Feldman MK, Katyal S, Blackwood MS. US Artifacts. Radiographics. 2009;29(4):1179e1189. https://doi.org/10.1148/rg.294085199. 25. Hertzberg BS, Middleton WD. Ultrasound: The Requisites. 3rd ed. Philadelphia, PA: Elsevier.

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26. Wilson SR, Burns PN, Wilkinson LM, Simpson DH, Muradali D. Gas at abdominal US: appearance, relevance, and analysis of artifacts. Radiology. 1999;210(1):113e123. 27. Avruch L, Cooperberg PL. The ring-down artifact. J Ultrasound Med. 1985;4(1):21e28. 28. Dillman JR, Kappil M, Weadock WJ, et al. Sonographic twinkling artifact for renal calculus detection: correlation with CT. Radiology. 2011;259(3):911e916.

29. Hindi A, Peterson C, Barr RG. Artifacts in diagnostic ultrasound. Reports Med Imaging. 2013;6:29e48. 30. Dubinsky TJ, Cuevas C, Dighe MK, Kolokythas O, Hwang JH. Highintensity focused ultrasound: current potential and oncologic applications. Am J Roentgenol. 2008;190(1):191e199. 31. Kennedy JE, Ter Haar GR, Cranston D. High intensity focused ultrasound: surgery of the future? Br J Radiol. 2003;76(909):590e599.

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Biologic Effects and Safety Christy K. Holland and J. Brian Fowlkes

CHAPTER OUTLINE REGULATION OF ULTRASOUND OUTPUT, 47 PHYSICAL EFFECTS OF SOUND, 48 EFFECTS OF ACOUSTIC CAVITATION, 48 Potential Sources for Bioeffects, 48 Sonochemistry, 49 Mechanical Index, 49 Evidence of Cavitation From Lithotripters, 50 Bioeffects in Lung and Intestine, 50 Ultrasound Contrast Agents, 51 Considerations for Increasing Acoustic Output, 52

Summary Statement on Gas Body Bioeffects, 52 THERMAL EFFECTS, 53 Ultrasound Produces Heat, 53 Factors Controlling Tissue Heating, 53 Bone Heating, 54 Soft Tissue Heating, 54 Hyperthermia and Ultrasound Safety, 55 Thermal Index, 56 Summary Statement on Thermal Effects, 57 OUTPUT DISPLAY STANDARD, 60

U

ltrasound has provided a wealth of knowledge in diagnostic medicine and has greatly impacted medical practice, particularly obstetrics. Millions of sonographic examinations are performed each year, and ultrasound remains one of the fastest-growing imaging modalities because of its low cost, realtime interactions, portability, and apparent lack of biologic effects (bioeffects). No causal relationship has been established between clinical applications of diagnostic ultrasound and bioeffects on the patient or operator.

REGULATION OF ULTRASOUND OUTPUT The US Food and Drug Administration (FDA) regulates the maximum output of ultrasound devices to an established level. The marketing approval process requires devices to be equivalent in efficacy and output to those produced before 1976. This historic regulation of sonography has provided a safety margin for diagnostic ultrasound while allowing clinically useful performance. The process has restricted ultrasound exposure to levels that apparently produce few, if any, obvious bioeffects based on epidemiologic evidence, although animal studies have shown some evidence for biologic effects.

GENERAL AIUM SAFETY STATEMENTS, 60 EPIDEMIOLOGY, 63 CONTROLLING ULTRASOUND OUTPUT, 63 Impact on Image Quality, 65 OCULAR IMAGING SAFETY, 65 OBSTETRIC ULTRASOUND SAFETY, 65 ULTRASOUND ENTERTAINMENT VIDEOS, 66 CONCLUSION, 66 REFERENCES, 66

To increase the efficacy of diagnostic ultrasound, the maximum acoustic output for some applications has increased through an additional FDA market approval process termed “510K Track 3.” The vast majority of ultrasound systems currently in use were approved through this process. The Track 3 process provides the potential for better imaging performance and requires that additional information be reported to the operator regarding the relative potential for bioeffects (see section on Considerations for Increasing Acoustic Output). Therefore informed decision making is important concerning the possible adverse effects of ultrasound in relation to the desired diagnostic information. Current FDA regulations that limit the maximum output are still in place, but in the future, systems might allow sonographers and physicians the discretion to increase acoustic output beyond a level that might induce a biologic response. Although the choices made during sonographic examinations may not be equivalent to the risk-versus-benefit decisions associated with imaging modalities using ionizing radiation, the operator will be increasingly responsible for determining the diagnostically required amount of ultrasound exposure. Thus the operator should know the potential bioeffects associated with ultrasound exposure. Patients also need to be reassured about the safety of a diagnostic ultrasound scan. The scientific community has

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identified some potential bioeffects from sonography, and although no causal relation has been established, it does not mean that no effects exist. Therefore it is important to understand the interaction of ultrasound with biologic systems.

PHYSICAL EFFECTS OF SOUND The physical effects of sound can be divided into two principal groups: mechanical and thermal. Most medical professionals recognize the thermal effects of elevated temperature on tissue, and the effects caused by ultrasound are similar to those of any localized heat source. With ultrasound, the heating mainly results from the absorption of the sound field as it propagates through tissue. However, “nonthermal” sources can generate heat as well. Many mechanical mechanisms for bioeffects exist. Acoustic fields can apply radiation forces (not ionizing radiation) on the structures within the body both at the macroscopic and the microscopic level, resulting in exerted pressure and torque. The temporal average pressure in an acoustic field is different than the hydrostatic pressure of the fluid, and any object in the field is subject to this change in pressure. The effect is typically considered smaller than other effects because it relies on less significant factors in the formulation of the acoustic field. Radiation force is used in specific ultrasound imaging modes to “push” on tissue to determine stiffness. For example, acoustic radiation force impulse (ARFI) imaging1-7 transmits acoustic pulses to induce tissue motion and then monitors the propagation of shear waves with high frame rate imaging sequences. These shear waves are transverse waves and differ from the compressional waves associated with the ultrasound “push” pulses. Tissue elasticity, or stiffness, can be calculated from the shear wave speed. Radiation force has been shown to induce biologic effects on cells,8 produce an auditory response, or modulate neurosensory receptors.9 ARFI imaging allows “remote palpation” of the tissue, which induces a desired mechanical effect to gather clinically useful diagnostic information with clear benefits to the patient.1 Acoustic fields can also cause motion of fluids, termed acoustic streaming.10 The fluid motion is a secondary effect of the acoustic field, whereby acoustic absorption results in a net force that induces fluid flow. The flow is typically in the direction of sound propagation but can result in rotational flow (vortices) forming as well. Acoustic streaming builds up with distance away from the transducer, so physical boundaries such as tissue layers can disrupt and minimize streaming. However, within small pockets of fluid, streaming can been observed and has been examined as a diagnostic tool for identifying cystic lesions in the breast11,12 and uterus.13 Although the exact mechanism of interaction is not understood, mechanical bioeffects of ultrasound are likely the source of neurostimulation,14 which is increasingly studied as a means of neuromodulation.15 Although the ultrasound parameters used to elicit neurostimulation extend beyond those used in ultrasound imaging, understanding how pulses of ultrasound interact with neural tissue is important. Acoustic cavitation is the action of acoustic fields within a fluid to generate bubbles and cause volume pulsation or even

collapse in response to the acoustic field. The result can be heat generation and associated free radical formation, microstreaming of fluid around the bubble, radiation forces generated by the scattered acoustic field from the bubble, and mechanical actions from bubble collapse. The interaction of acoustic fields with bubbles or “gas bodies” (as they are generally called) has been an important area of bioeffects research for many years. The potential for cavitation was also the impetus for one of the safety indices employed on ultrasound imaging systems, and as such we will address this particular mechanical bioeffect in more detail.

EFFECTS OF ACOUSTIC CAVITATION Potential Sources for Bioeffects Knowledge concerning the interaction of ultrasound with gas bodies (which many term “cavitation”) has substantially increased over time, although it is not as extensive as that for ultrasound thermal effects and other sources of hyperthermia. Acoustic cavitation inception is demarcated by a specific threshold value: the minimum acoustic pressure necessary to initiate the growth of a cavity in a fluid during the rarefaction phase of the cycle. Several parameters affect this threshold, including initial bubble or cavitation nucleus size, acoustic pulse characteristics (e.g., center frequency, pulse repetition frequency [PRF], pulse duration), ambient hydrostatic pressure, and host fluid parameters (e.g., density, viscosity, compressibility, heat conductivity, surface tension). Inertial cavitation refers to bubbles that undergo large variations from their equilibrium sizes in a few acoustic cycles. Specifically, during contraction, the surrounding fluid inertia controls the bubble motion.16 Large acoustic pressures are necessary to generate inertial cavitation, and the collapse of these cavities is often violent. The effect of preexisting cavitation nuclei may be one of the principle controlling factors in mechanical effects that result in biologic effects. The body is such an excellent filter that these nucleation sites may be found only in small numbers and at selected sites. For example, if water is filtered down to 2 mm, the cavitation threshold doubles.17 Theoretically, the tensile strength of water that is devoid of cavitation nuclei is about 100 megapascals (MPa).18 Various models have been suggested to explain bubble formation in animals,19,20 and these models have been used extensively in cavitation threshold determination. One model is used in the prediction of SCUBA diving tables and may also have applicability to patients.21 It remains to be seen how well such models will predict the nucleation of bubbles from diagnostic ultrasound in the body. Fig. 2.1 shows a 1-MHz therapeutic ultrasound unit generating bubbles in gas-saturated water. The medium and ultrasound parameters were chosen to optimize the conditions for cavitation. Using continuous wave ultrasound and many preexisting gas pockets in the water set the stage for the production of cavitation. Even though these acoustic pulses are longer than those typically used in diagnostic ultrasound, cavitation effects

CHAPTER 2

FIGURE 2.1 Acoustic Cavitation Bubbles. This figure shows a 1-MHz therapeutic ultrasound unit generating bubbles in gas-saturated water. The medium and ultrasound parameters were chosen to optimize the conditions for cavitation. Using continuous wave ultrasound and many preexisting gas pockets in the water set the stage for the production of cavitation. (Courtesy J. Brian Fowlkes.)

have also been observed with diagnostic pulses in fluids.22 Ultrasound contrast agents composed of stabilized gas bubbles should provide a source of cavitation nuclei, as discussed later in the section on ultrasound contrast agents.

Sonochemistry Free radical generation and detection provide a means to observe cavitation and to gauge its strength and potential for damage. The sonochemistry of free radicals is the result of very high temperatures and pressures within the rapidly collapsing bubble. These conditions can even generate light, or sonoluminescence.23 With the addition of the correct compounds, chemical luminescence can also be used for free radical detection and can be generated with short pulses similar to that used in diagnostic ultrasound.24 Fig. 2.2 shows chemiluminescence generated by a therapeutic ultrasound device; the setup is backlit (in red) to show the bubbles and experimental apparatus. The chemiluminescence emissions are the blue bands seen through the middle of the liquid sample holder. The light emitted is sufficient to be seen by simply adapting one’s eyes to darkness. Electron spin resonance can also be used with molecules that trap free radicals to detect cavitation activity capable of free radical production.25 A number of other chemical detection schemes are presently employed to detect cavitation from diagnostic devices in vitro.

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FIGURE 2.2 Chemical Reaction Induced by Cavitation Producing Visible Light. This figure shows chemiluminescence generated by a therapeutic ultrasound device. The setup is backlit (in red) to show the bubbles and experimental apparatus. The chemiluminescence emissions are the blue bands seen through the middle of the liquid sample holder. The light emitted is sufficient to be seen by simply adapting one’s eyes to darkness. The reaction is the result of free radical production. (Courtesy J. Brian Fowlkes.)

The collapse temperature for inertial cavitation is very high. For the derivation of the MI, a collapse temperature of 5000 kelvins (K) was chosen as the threshold based on the potential for free radical generation.

The Mechanical Index To gauge the potential for inertial cavitation, the mechanical index (MI) is defined as Pr MI ¼ pffi f where Pr is the rarefactional acoustic pressure in MPa, which is derated to account for attenuation, and f is the center frequency in MHz.26-29 The frequency dependence of the pressure required to generate inertial cavitation takes a relatively simple form. The MI is a type of “mechanical energy index” because the square of the MI is about proportional to mechanical work that can be performed on a bubble in the acoustic rarefaction phase.

Mechanical Index Calculations for inertial cavitation prediction have yielded a trade-off between peak rarefactional pressure and frequency.26 This predicted trade-off assumes short-pulse (a few acoustic cycles) and low-duty cycle ultrasound ( 5 for hind limb paralysis in the mouse neonate.43 4. For mammalian biologic effects research relating to diagnostic ultrasound, including experiments with pulsed ultrasound,66,117,118 no adverse nonthermal bioeffects have been observed for MI values less than the FDA maximum recommended level for diagnostic ultrasound, MI ¼ 1.9, in tissues without gas bodies. THE AIUM STATEMENT ON BIOLOGIC EFFECTS IN TISSUES WITH NATURALLY OCCURRING GAS BODIES Biologically significant adverse nonthermal effects have been identified in organs containing stable bodies of gas for diagnostically relevant exposure conditions. Gas bodies occur naturally in postnatal lungs and in the folds of the intestinal mucosa. This section concerns naturally occurring gas bodies encountered in pulmonary and abdominal ultrasound, whereas a separate statement deals with the use of gas body contrast agents as would be used for contrast-enhanced diagnostic ultrasound. (See AIUM Statement on Biological Effects in Tissues with Ultrasound Contrast Agents.75) 1. Currently available diagnostic ultrasound devices have been shown to produce capillary hemorrhage in the lungs53,119 and intestines43 of some mammals under certain experimental conditions. 2. The minimum threshold value of the MI for pulmonary capillary hemorrhage in laboratory mammals is approximately 0.4.54 The corresponding threshold for intestines is 1.4. No adverse nonthermal effects have been observed in these organs below these levels. For pulmonary and intestinal imaging, the ALARA (as low as reasonably achievable) principle should be practiced.120 3. The mechanism for pulmonary capillary hemorrhage by ultrasound is presently uncertain.12 4. In experimental mammalian models of ultrasound, induced pulmonary hemorrhage was shown by the presence of BLines (comet tails artifacts).53 5. The translation of laboratory bioeffects findings to human clinical conditions is problematic, but the risk to human patients should be less than that for laboratory animal studies due to differences in body size and biophysical conditions. The health implications of these bioeffects observations for humans, should they occur during thoracic or abdominal ultrasound examinations, are yet to be determined.

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The AIUM Statement on Biologic Effects of Ultrasound in Vivo114dcont’d BIOLOGIC EFFECTS OF HEAT Diagnostic ultrasound scanners can produce significant thermal effects under certain conditions. This section concerns the conditions under which significant thermal effects can occur when using diagnostic ultrasound parameters. 1. An excessive temperature increase can produce adverse effects in mammals. Temperature increases of several degrees Celsius above the normal core range can occur naturally (i.e., even in the absence of ultrasound). The probability of an adverse biologic effect increases with both the magnitude and the duration of the temperature rise. 2. Calculations are used to obtain safety indices for clinical exposures in which direct temperature measurements are not feasible. Experimental evidence shows that thermal index (TI) resulting from ultrasound exposure is generally capable of predicting measured values of maximum temperature increase (DTmax in  C) within a factor of 2.121 (For instance, a TI value of 2 could correspond to a DTmax between 1 C and 4 C.) Temperature increases also depend on dwell time. These thermal indices provide a real-time display of the relative probability that a diagnostic system could induce thermal injury in the exposed subject. Under most clinically relevant conditions, the soft tissue thermal index (TIS) either overestimates or closely approximates the maximum temperature increase (DTmax). However, in some applications, such as fetal examinations in which the ultrasound beam passes through a layer of relatively low attenuating liquid (e.g., urine or amniotic fluid), the TI can underestimate DTmax by up to a factor of 2.121,122 3. Maximum combinations of temperature rise and exposure duration without adverse effects based on empirical evidence103,104,122 are shown in Table 1. For guidance on limiting TI values in clinical applications, see AIUM Statement on Recommended Maximum Scanning Times for Displayed Thermal Index (TI) Values.123 In that statement, recommended TI values are lower than DT values because a safety margin is included. TABLE 1 Maximum combinations of temperature rise and exposure duration without adverse effects.

Temperature Increase DT (8C) 9.6 6.0 5.0 4.0 3.0 2.0 1.5

MAXIMUM EXPOSURE DURATION WITHOUT ADVERSE EFFECTS Fetal

9.6 C) and B ¼ 0.6 (DT < 6 C) or 0.3 (DT > 6 C).103,104,124 4. In general, adult tissues are more tolerant of temperature increases than fetal and neonatal tissues. Therefore higher temperatures and/or longer exposure durations would be required for thermal damage. General considerations applicable to fetal and postnatal subjects are as follows: a. A diagnostic exposure that produces a maximum in situ temperature rise of no more than 1.5 C above normal physiological levels (37 C) may be used clinically without reservation on thermal grounds.125 b. In general, temperature elevations become progressively greater from B-mode to color Doppler to M-mode to spectral Doppler / Acoustic Radiation Force Impulse (ARFI) applications due to differences in the temporal average ultrasound intensity. c. Transducer self-heating can be a significant component of the temperature rise of tissues close to the transducer. This may be of significance in transvaginal scanning, but no data for the fetal temperature rise are available. 5. Although less data are available for fetal tissues than for adult tissues, the following conclusions are justified103,125,126: a. Current FDA-cleared ultrasound scanners may be capable of increasing the temperature of the conceptus by more than 1.5 C. b. For identical exposure conditions, the temperature rise near bone is significantly greater than in soft tissues, and it increases with ossification development throughout gestation. For this reason, conditions in which an acoustic beam impinges on ossifying fetal bone deserve special attention due to its proximity to other developing tissues. For obstetric exams, monitoring the TIS is recommended up to 10 weeks from the last menstrual period and TIB (TI with bone near focus) thereafter. c. Although an adverse fetal outcome is possible at any time during gestation, most severe and detectable effects of thermal exposure in mammals have been observed during the period of organogenesis. For this reason, exposures during the first trimester should be restricted to the lowest outputs and dwell times consistent with the ALARA principle to obtain the necessary diagnostic information. This is particularly relevant for spectral Doppler exposure. d. Ultrasound exposures that elevate fetal temperature by 4 C above normal for 5 minutes or more have the potential to induce severe developmental defects. Thermally induced congenital anomalies have been observed in a large variety of animal species. In current clinical practice, using commercially available equipment, it is unlikely that such thermal exposure would occur at a specific fetal anatomic site provided that the thermal index (TI) is at or below 2.5 and the dwell time on that site does not exceed 4 minutes. There is no time limit for scans in which TI always remains below 0.7.

Reproduced with permission of American Institute of Ultrasound in Medicine (AIUM). Statement on Biological Effects of Ultrasound in Vivo114 Laurel MD, AIUM: 2021. Available from: https://www.aium.org/officialStatements/82.

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Ultrasound Physics, Bioeffects, and Contrast

OUTPUT DISPLAY STANDARD Several groups, including the FDA, AIUM, and NEMA, developed the “Standard for real-time display of thermal and mechanical acoustical output indices on diagnostic ultrasound equipment”,27 which introduced a method to provide the user with information concerning the TI and MI. Real-time display of the MI and TI allow a more informed decision on the potential for bioeffects during ultrasound examinations (Fig. 2.10). The standard requires dynamic updates of the indices as instrument output is modified and allows the operator to learn how controls will affect these indices. This standard has been superseded by documents published by the IEC.29,127-129 Important points to remember about the display standard include the following: • The MI and TI should be clearly visible on the screen (or alert the operator by some other means) and should begin to appear when the instrument exceeds a value of 0.4. An exception is made for instruments incapable of exceeding index values of 1; these are not required to display the bioeffects indices. • When the indices are required to be displayed, both indices are to be displayed at all times. • Appropriate default output settings need to be in effect at power-up, new patient entry, or when changing pre-sets. After that time the operator can adjust the instrument output as necessary to acquire clinically useful information while attempting to minimize the index values. • As indicated previously, the bioeffects indices do not include any factors associated with the time taken to perform the scan. Efficient scanning is still an important component in limiting potential bioeffects.

Sonographers and physicians are being presented with realtime data on acoustic output of diagnostic scanners and are being asked not only to understand how ultrasound propagates through and interacts with tissue but also to gauge the potential for adverse bioeffects. The output display is a tool that can be used to guide an ultrasound examination and control for potential adverse effects. The TI and MI provide the user with more information and more responsibility in limiting output.

Education on MI and TI In the document “Medical Ultrasound Safety,” the AIUM suggests that the operator ask the following four questions to use the output display effectively130: 1. Which index should be used for the examination being performed? 2. Are there factors present that might cause the reading to be too high or low? 3. Can the index value be reduced further even when it is already low? 4. How can the ultrasound exposure be minimized without compromising the scan’s diagnostic quality?

GENERAL AIUM SAFETY STATEMENTS It is important to consider some official positions concerning the status of bioeffects resulting from ultrasound. Most important is the high level of confidence in the safety of ultrasound in official statements. For example, in 2019 the AIUM reiterated its earlier statement concerning the clinical use of diagnostic ultrasound,131 which indicated that no independently confirmed adverse effects

FIGURE 2.10 Display of Bioeffects Indices. Typical appearance of an ultrasound scanner display showing (right upper corner) the thermal index in soft tissue (TIS) and mechanical index (MI) for an endocavitary broadband curved array transducer. (Courtesy Man Zhang.)

CHAPTER 2 are caused by exposure from current diagnostic equipment, and the patient benefits from prudent use that outweigh the risks, if any. The AIUM also strongly discourages the nonmedical use of ultrasound during pregnancy for entertainment purposes. In commenting on the use of diagnostic ultrasound in research, the AIUM recommends that in the case of ultrasound exposure for other than direct medical benefit, the person should be informed concerning the exposure conditions and how these relate to normal exposures. For the most part, even examinations for research purposes are comparable to normal diagnostic exams

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and pose no additional risk. Many research exams can be performed in conjunction with routine exams. The effects based on in vivo animal models are summarized by the AIUM Statement on Biological Effects of Ultrasound in Vivo.114 No independently confirmed experimental evidence indicates damage in animal models below certain prescribed levels (temperature rises 125 cm/s) on angle-corrected spectral Doppler with a ratio of stenotic velocity to prestenotic velocity of greater than 3:1. Additional complementary findings include distal turbulence on color Doppler, hepatofugal portal flow, and arterial parvus-tardus waveforms likely owing to the hepatic arterial buffer response (Fig. 16.12). Additionally, lack of flow within the portal vein on Doppler ultrasound has been described as a sign for a stenosis, which can be due to low amplitude flow after a critical venous stenosis is reached.19

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FIG. 16.10 Arteriovenous Fistula. (A) Color Doppler shows tissue vibration within the left hepatic lobe. (B) Spectral Doppler interrogation of this area shows high-velocity, low-resistance waveform with turbulent pattern, consistent with arteriovenous fistula. (C) Spectral Doppler of the left hepatic artery supplying the fistula also shows high-velocity, low-resistance waveform. (D) Comparison normal resistance is seen within the right hepatic artery on spectral Doppler. (E and F) Axial CT angiogram shows decreased enhancement of the right hepatic lobe with early filling of the left portal vein (arrows), compatible with arteriovenous fistula.

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Portal Vein Steal Given that a large number of liver transplant recipients had cirrhosis and portal hypertension that led to their transplantation, the presence of venous shunts bypassing the portal vein are common in this population. After liver transplantation, smaller shunts usually collapse after normalization of the portal venous flow. However, if the shunts are large, vascular flow through the transplant liver portal vein can be diminished from vascular steal through these varices, and this can lead to graft function impairment and graft loss.20 Ultrasound findings include slow or even reversal of flow within the portal vein. The splenic vein can be assessed to evaluate for reversal of flow. Intraoperative ligation of the large shunts can normalize blood flow through the portal vein (Fig. 16.13).

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Venous Outflow (Inferior Vena Cava/ Hepatic Vein) Complications Venous outflow issues occur in 2% to 11% of liver transplants.18 In the conventional IVC anastomosis, stenosis can occur at the suprahepatic or infrahepatic portions, while in those employing the piggyback technique, stenosis can occur at the anastomosis or rarely due to torsion of the liver allograft. In partial liver donations, stenosis can occur at the level of the hepatic veins. Stenosis typically occurs around 1 year after liver transplantation. Clinical presentation includes acute Budd-Chiaritype symptoms with the development of hepatomegaly and ascites. Grayscale images can depict dilation of the hepatic veins in the presence of a suprahepatic or piggyback-related stenosis as well as the actual area of luminal narrowing. Doppler findings

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C Fig. 16.11 Acute Portal Vein Thrombosis. (A) Color Doppler shows no flow within the portal vein (arrow). (B) Spectral Doppler shows elevated hepatic artery velocity, possibly due to compensatory blood flow through the hepatic arterial system due to portal vein thrombosis. (C) Coronal CT venogram confirms thrombus in the main portal vein (arrow).

can include aliasing on color Doppler at the area of outflow stenosis. On spectral Doppler, the waveform of the hepatic veins and IVC can change from the normal multiphasic waveform, which is due to pressures from the right atrium to a monophasic waveform. Monophasic waveforms, although supportive of an outflow stenosis, can also be seen in nonobstructed hepatic veins. However, a normal waveform essentially rules out an outflow venous stenosis. It is also possible to see elevated velocities at the site of stenosis, with a greater than 3:1 ratio of the stenotic region to prestenotic segment supportive of the diagnosis (Fig. 16.14). In the case of allograft torsion, altered positioning of the liver on grayscale imaging may also serve as a clue of twisting (Video 16.2). Outflow thrombosis is a rare complication that can be caused by hypercoagulable states or compression from an adjacent fluid collection. Grayscale ultrasound shows echogenic thrombus within the IVC that may continue into the hepatic

veins. In cases of recurrent HCC, tumor thrombus may extend from the hepatic veins into the IVC.

Biliary Complications Biliary tract complications are an important cause of morbidity and mortality in 15% to 30% of patients with liver grafts. Complications related to biliary-enteric anastomoses usually manifest within the first month of surgery and include anastomotic breakdown, bleeding, and an increased risk of ascending cholangitis from bacterial overgrowth. Choledochocholedochostomy-related complications most frequently manifest after the first month and are often managed by endoscopic retrograde cholangiopancreatography (ERCP). Regardless of the type of anastomoses used, biliary tract complications can be broadly classified as those related to leaks, strictures, intraluminal sludge or stones, dysfunction of the sphincter of Oddi, and recurrent disease.

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C Fig. 16.12 Portal Vein Stenosis. (A) Color Doppler shows aliasing of the extrahepatic portal vein, which on spectral Doppler had borderline elevated velocities. (B) The more proximal portion of the main portal vein on spectral Doppler shows a lower velocity rendering a ratio of >3:1, concerning for portal vein stenosis. (C) Confirmation of the stenosis was seen on conventional angiography.

Biliary Strictures The early diagnosis of biliary tree complications may be difficult since transplant recipients do not typically experience colic, owing to the severing of the existing nerves during the process of transplantation. Therefore, patients with biliary strictures may be asymptomatic or may have painless jaundice or abnormal liver function test results. Biliary strictures can broadly be categorized as anastomotic and nonanastomotic. Anastomotic strictures are the most common cause of biliary obstruction after transplantation and arise from postsurgical scarring, resulting in retraction of the duct wall and narrowing of the luminal diameter (Fig. 16.15). These strictures are more common in patients with a Roux-en-Y hepatico/ choledochojejunostomy than in patients with choledochocholedochal anastomosis. On ultrasound, a focal narrowing can sometimes be observed at the anastomosis, associated with dilation of the intrahepatic bile ducts with a normal- or near-normal-sized distal CBD. Nonanastomotic strictures occur proximal to the anastomosis and can be unifocal or multifocal (Fig. 16.16). The arterial supply of the recipient duct in cases of choledochocholedochal anastomosis is rich given the presence of prominent collateral flow; however, the proximal CBD and intrahepatic bile ducts

are initially solely reliant on the hepatic arterial supply. Therefore, hepatic arterial occlusion or severe stenosis can lead to biliary strictures related to ischemia/infarction. Ultrasound findings include focal areas of narrowing in the intrahepatic or proximal BD and segmental dilation of the intrahepatic bile ducts, without evidence of an obstructing mass. The presence of echogenic intraluminal material within a dilated biliary tree is an ominous sign, sometimes caused by severe biliary ischemia, resulting in sloughing of the entire biliary epithelium. In this scenario, the intraluminal echogenic material represents a combination of biliary sludge or stones, sloughed biliary epithelium, and intraluminal hemorrhage.

Biliary Leaks Bile leaks are a fairly common complication in liver transplant recipients, with an incidence of 5% to 23%. Biliary leaks can be anastomotic, at the T-tube exit site, as a result of bile duct necrosis, at the cut-surface of the liver in case of split liver or living donor liver, or rarely as a result of percutaneous liver biopsies. Anastomotic leaks and T-tube exit site leaks occur within the first postsurgical month. Anastomotic leaks may be related to surgical technique or may result from ischemia caused by

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Fig. 16.13 Vascular Steal of the Portal Vein. (A) Color Doppler failed to show convincing portal venous flow. (B) Magnetic resonance angiogram with ferumoxytol shows presence of portal vein flow in the setting of very large splenorenal varices. (C) Intraoperative spectral Doppler shows low velocity in the main portal vein. (D) After ligation of splenorenal shunt, intraoperative spectral Doppler shows improved velocity in the main portal vein.

hepatic artery compromise. Clinically, anastomotic leaks are associated with bile peritonitis or intraabdominal sepsis and may manifest on ultrasound as a large periportal collection, a subhepatic collection, or ascites. Leaks from bile duct necrosis usually occur after the first postsurgical month and are a result of severe hepatic artery stenosis or thrombosis. This condition is often associated with progressive hepatic dysfunction and a poor clinical course, eventually necessitating retransplantation. On ultrasound, the biliary tree may be dilated and thick-walled and may communicate with surrounding bilomas (Fig. 16.17). Small leaks may be managed conservatively while larger persistent bilomas may require drainage and stent placement.

Recurrent Sclerosing Cholangitis Recurrent sclerosing cholangitis occurs in up to 20% of recipients undergoing orthotopic transplantation for sclerosing cholangitis, with a mean interval of 350 days. Ultrasound findings include diffuse mural thickening of the intrahepatic bile duct and CBD and diverticulum-like outpouchings of the CBD. Recurrent disease should be suspected in patients who have undergone transplantation for end-stage primary

sclerosing cholangitis and who have biliary dilatation and mural thickening in the presence of normal hepatic arterial waveform. Occasionally, patients with ascending cholangitis show a similar ultrasound appearance. Infectious causes include both enteric flora and opportunistic infections (e.g., CMV, Cryptosporidium).

Biliary Sludge and Stones Biliary sludge in liver transplant patients is a nonspecific finding and can be seen in ischemia, infection, rejection, mechanical obstruction, and biliary leaks. It is more commonly seen in patients with hepaticojejunostomy. Bile sludge can case biliary obstruction and lead to cholangitis. The detection of biliary sludge is an ominous sign and should prompt meticulous evaluation of the CBD to rule out an obstructing lesion or leak and patency of the hepatic artery. Intraductal stones are uncommon and may result from cyclosporine-induced changes in bile composition inciting crystal formation in the CBD, with subsequent stone formation. Other causes include retained donor stones and stones secondary to biliary stasis. These appear echogenic

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Abdominal Sonography

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C Fig. 16.14 Venous Outflow Obstruction Due to Torsion of Liver Transplant. (A) Spectral Doppler shows elevated hepatic artery resistive indices with reversal of diastolic flow, suggestive of outflow obstruction. (B) Color Doppler shows focal area of aliasing at the piggyback anastomosis. (C) Spectral Doppler of the hepatic vein more proximally shows a more flattened waveform than expected. In combination, these findings are suggestive of outflow obstruction which was confirmed with torsion at the piggyback anastomosis intraoperatively. See also Video 16.2.

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Fig. 16.15 Biliary Anastomotic Stricture. (A) Color Doppler image of the common bile duct shows an echogenic band in the mid portion (arrowhead) with mild dilation both proximal and distally. (B) Magnetic resonance cholangiopancreatography shows severe narrowing at the biliary anastomosis, consistent with anastomotic stricture. (C) Subsequent fluoroscopic endoscopic retrograde cholangiopancreatography image again shows a short stricture in the mid common bile duct, confirming anastomotic stricture.

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Fig. 16.16 Biliary Nonanastomotic Stricture From Hepatic Arterial Stenosis. (A) Color Doppler of the left hepatic lobe shows mild thickening and dilation of the intrahepatic ducts. (B) Gray-scale image of the common bile duct also shows wall thickening without dilation. (C) Spectral Doppler of the main hepatic artery shows elevated velocity (317 cm/s). (D) Spectral Doppler of the right intrahepatic arteries shows parvus-tardus waveforms and borderline low resistive indices (0.44). (E) Magnetic resonance cholangiopancreatography shows diffuse multifocal intrahepatic dilation and ductal irregularity narrowing of intrahepatic bile ducts. (F) Coronal maximum-intensity projection of CT angiogram shows a sharp kink in the main hepatic artery (arrow). The arteries distal to this are patent. Overall, findings are consistent with ischemic cholangiopathy due to hepatic artery prominent kink/stenosis.

with posterior clean acoustic shadowing and should be distinguished from biliary gas which usually has dirty acoustic shadowing.

Dysfunction of the Sphincter of Oddi In patients with biliary end-to-end anastomoses, biliary obstruction can be caused by sphincter of Oddi dysfunction, which will lead to diffuse CBD and intrahepatic biliary ductal dilatation, as opposed to anastomotic strictures, which will not

involve the entire length of the extrahepatic bile duct. The cause of this dysfunction is unclear but may relate to the devascularization and denervation during the transplant process.

Parenchymal Abnormalities Rejection Despite improvements in immunosuppressive mediation, rejection of the liver graft is common, affecting 15% to 25% of

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FIG. 16.17 Biloma. (A) Color Doppler shows a heterogeneous hypoechoic avascular area in the right hepatic lobe. (B) Spectral Doppler of the main hepatic artery shows elevated velocity (226 cm/s). (C) Spectral Doppler of the right intrahepatic arteries shows parvus-tardus waveforms, although the resistive indices are only borderline low (0.52). Axial postgadolinium contrast T1 subtraction image shows (D) circumferential common bile duct thickening and enhancement (arrowhead); (E) multiple fluid collections in the right hepatic lobe with thick peripheral enhancement (arrowhead). (F) Axial arterial phase postgadolinium contrast T1 fat saturation image shows focal stenosis of the main hepatic artery (arrow). (G) Percutaneous transhepatic cholangiogram shows contrast pooling in the right hepatic lobe, consistent with biliary leak (B). Overall, these imaging findings are consistent with ischemic cholangiopathy and multiple bilomas due to main hepatic artery stenosis.

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grafts.21 The sonographic findings of rejection are consistent with an enlarged inflamed liver, with heterogeneous parenchyma, increased blood flow to the liver (increased hepatic artery and portal vein velocity), and monophasic hepatic venous waveforms. These findings, however, are nonspecific and can be seen in patients with hepatitis, ischemia, and cholangitis.22 Shear-wave elastography has shown some promise in distinguishing between rejection and other etiologies of liver graft dysfunction, with higher stiffness values noted in patients with rejection.23,24 However, given that there are no reliable imaging findings of liver graft rejection, the diagnosis is made based on core liver biopsy.

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Infarction Infarctions can initially appear as subtle wedge-shaped subcapsular hypoechoic regions (Fig. 16.18). Infarctions may subsequently organize into avascular round or wedge-shaped lesions, which can eventually develop areas reflecting liquefaction and necrosis. A focal liver infarct should be diagnosed with accompanying Doppler evidence of hepatic arterial compromise.

Intrahepatic Abscess Liver abscesses early on can mimic findings of liver infarction with subtle hypoechoic regions associated with a localized

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Fig. 16.18 Liver Infarction. (A) Wedge-shaped area of hypoattenuation in the right hepatic lobe. Color Doppler was normal (not shown). (B) Maximum intensity projection of venous phase of IV contrast on coronal CT shows a focal kink in the vascular conduit (arrow). Heterogeneous hypoattenuating area in the right hepatic lobe again noted (arrowhead). Findings consistent with hepatic infarction, possibly related to arterial conduit kink/stenosis.

coarsening of the parenchymal echotexture. Like infarcts, abscesses also vary with their maturation. The classic sonographic appearance of a mature transplant liver abscess is a complex, cystic structure with thick, irregular walls and particulate internal fluid with or without associated septations. Abscesses may also contain bubbles of air, visualized as bright echogenic foci with or without posterior acoustic shadowing (Fig. 16.19). Occasionally, bubbles of air within the lumen of an intraparenchymal abscess can be confused with benign pneumobilia or may be mistaken for air outside the liver within the gastrointestinal tract. A high index of suspicion is critical in patients at risk for either abscess to avoid misinterpretation.

Intrahepatic Solid Masses The differential diagnosis of a solitary mass in the transplanted liver is similar to that in the native liver, with benign lesions such as hemangiomas and cysts being relatively common findings in the transplanted liver with the same imaging appearances. As in the general population, transplant recipients can develop any type of primary or secondary neoplasm of the liver. However, the liver transplant has a greater likelihood of developing pseudolesions that can complicate the diagnosis, such as is seen with hepatic infarction and abscesses. In addition, recurrence of HCC as well as PTLD are observations that are especially important in the liver transplant. Recurrent HCC is a serious complication that can develop after transplantation in patients with a preoperative history of end-stage cirrhosis with known or occult HCC. The most common site of recurrent HCC is the lung, presumably caused by embolization with tumor cells through the hepatic veins before or during transplantation. The second most common location is within the allograft, followed by regional or distant

lymph nodes. Early detection in the transplant liver is essential to facilitate resection, ablation, or chemotherapy. PTLD represents a group of lymphoid disorders ranging from polyclonal lymphoid proliferation to monoclonal lymphoid proliferations that meet the criteria for lymphoma. PTLD is a rare but serious complication in liver transplant patients, occurring in 1% to 4% of patients, and is strongly associated with Epstein-Barr seropositivity.25,26 The ultrasound features of PTLD are nonspecific, typically appearing as hypoechoic hypovascular masses or without lymphadenopathy. The presence of a new mass in a patient with a liver transplant should elicit concern for PTLD development (Fig. 16.20). The diagnosis is typically made by image-guided biopsy.

Extrahepatic Fluid Collections Perihepatic fluid collections and ascites are frequently observed after transplantation. In the early postoperative period, a small amount of free fluid or a right pleural effusion may be observed, but these usually resolve in a few weeks. Fluid collections and hematomas are common in the areas of vascular anastomosis (hepatic hilum and adjacent to the IVC) and biliary anastomosis, in the lesser sac, and in the perihepatic and subhepatic spaces. Because the peritoneal reflections surrounding the liver are ligated at transplantation, fluid collections can occur around the bare area of the liver, a location for fluid that is not encountered in the preoperative liver. Hematomas tend to demonstrate heterogeneous echogenicity, which can evolve into simple-appearing fluid collections over time (Fig. 16.21). The absolute and change in size of the peritransplant hematoma as well as mass effect on the liver graft are important to note to determine whether these need surgical exploration or can be monitored.

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Fig. 16.19 Liver Abscess. (A) Gray-scale ultrasound of the right hepatic lobe shows a heterogeneous area including multiple echogenic foci with shadowing, consistent with air. (B) Spectral Doppler of the main hepatic artery shows decreased velocity (20 cm/s) with minimally delayed upstroke suggestive of arterial inflow restriction. (C) Coronal CT with IV contrast (venous phase) shows an air and fluid collection in the right hepatic lobe, correlating with the US findings. (D) Conventional hepatic angiogram shows a high-grade narrowing at the hepatic artery anastomosis (arrow).

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Fig. 16.20 Posttransplant Lymphoproliferative Disorder (PTLD). (A) Color Doppler image near the porta hepatis shows an echogenic common bile duct stent (arrow) with a surrounding avascular hypoechoic mass (arrowhead). The liver transplant appears markedly heterogeneous. (B) Axial FDG F-18 PET CT shows a ringlike hypermetabolic lesion centered at the porta hepatis with central necrosis. This lesion was biopsy proven PTLD.

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Fig. 16.21 Hematoma With Mass Effect. (A) Gray-scale shows large retrohepatic heterogenous fluid collection in the immediate postoperative period, consistent with a hematoma. (B) Color and spectral Doppler of the main portal vein shows bidirectional flow, possibly due to compressive hematoma. Axial CT images during arterial (C) and venous (D) phases shows active extravasation of contrast in the intrahepatic inferior vena cava (arrow) with an associated retroperitoneal hematoma. Decreased enhancement of the right hepatic lobe, consistent with compression from the hematoma.

Ultrasound is highly sensitive in detecting these fluid collections, although it lacks specificity regarding its etiology because bile, blood, pus, and lymphatic fluid can all have a similar sonographic appearance. The presence of internal echoes in a fluid collection suggests blood or infection. Particulate ascites may also be observed in peritoneal carcinomatosis, although this would seem less likely in the transplant recipient.

KIDNEY TRANSPLANTATION Kidneys are the most commonly transplanted organ. In the United States in 2020, there were 22,817 kidney transplant cases.5 Transplantation is the treatment of choice for many patients with end-stage renal disease. Contraindications include active infection or malignancy, severe respiratory conditions, severe heart disease, severe peripheral vascular disease, and psychosocial factors. Living donor kidneys confer longer graft survival, often approaching 15 to 20 years, when compared to deceased donor

kidneys, with an average life expectancy of 7 to 10 years. The greater number of deceased donors and limited living donors has made deceased donor transplantation to be the more common graft option. The rise in patients with end-stage renal disease has led to a shortage of suitable donor kidneys, and as such the boundaries have been pushed in transplantation with use of marginal kidney grafts. With the increasing use of marginal kidneys and innovative surgical techniques, increased complications can arise, and therefore familiarity with the surgical technique as well as identifying complications is critical in ultrasound assessment of the kidney graft.

Surgical Technique The preferred placement of kidney grafts is extraperitoneal in the right iliac fossa, with the left iliac fossa being utilized in the setting of simultaneous pancreas kidney transplants, severe atherosclerotic disease in the right iliac vessels, or previously failed right-sided graft. On occasion, kidney grafts may be too large for the iliac fossa and may need to be placed in an

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intraperitoneal location. Rarely, in cases where severe bilateral iliac or aortic atherosclerotic disease is present, kidney grafts will be placed orthotopically. Deceased donor kidney grafts are more common than living donor grafts and may sometimes be transplanted together “en bloc” in donors that are either too marginal to expect a single graft to function adequately or in very small pediatric donors in which the anatomical anastomosis of the artery and vein may be too technically challenging. Arterial anastomosis most commonly occurs in an end-toside fashion with the external iliac artery, though the common iliac artery and even the aorta can be utilized. In deceased donor grafts, the renal artery may also contain an ovoid patch of the donor aorta, termed a Carrel patch, which can facilitate anastomosis (Fig. 16.22). In patients with severe disease of the external iliac artery, an end-to-end anastomosis with the internal iliac artery can be performed. Donors with multiple renal arteries can either be anastomosed separately or undergo backbench preparation with various surgical techniques to allow for fewer anastomoses with the recipient. In patients with pediatric en bloc grafts, the donor aorta is typically attached to the iliac artery.

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The venous anastomosis is almost always anastomosed in an end-to-side technique with the external iliac vein. In patients with pediatric en bloc grafts, the donor IVC is used for anastomosis. The ureteral anastomosis is most commonly performed via a ureteroneocystostomy to the ipsilateral bladder dome. In cases where the ureter may be too short, a ureteroureterostomy can be performed to the native ureter. Rarely, the ureter can be anastomosed to a loop of bowel (ureteroileostomy), which can be performed in cases where the ureter is shortened or in patients with a challenging bladder. In en bloc kidneys, the ureters are usually anastomosed to the bladder separately or through a common tunnel.

Normal Kidney Transplant Ultrasound Grayscale Assessment Sonography of the renal transplant is usually easily visible because of the superficial location of the kidney in either the right or left lower quadrant. Because the allograft is held in place by its pedicles, a variety of orientations may be

Native external iliac artery

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Fig. 16.22 Diagram of Anastomoses. (A and B) Types of arterial anastomoses: (A) Carrel patch. (B) End-to-end anastomosis with the native internal iliac artery. (C) Venous anastomosis. (D-F) Types of ureteral anastomoses: (D) Ureteroneocystostomy. (E) Ureteroneocystostomy to native ureter. (F) Ureteroileostomy.

CHAPTER 16 Solid-Organ Transplantation encountered. Most often the kidney is aligned with its long axis parallel to the surgical incision, with the hilum oriented medially. The kidney allograft appears morphologically similar to the native kidney. The normal renal cortex is well-defined, hypoechoic, and easily differentiated from the highly reflective, central echogenic renal sinus fat. The renal pyramids usually appear mildly hypoechoic relative to the cortex and may seem more prominent when compared to the native kidney; however, this difference is likely due to the improved resolution of typically more superficial renal allograft. The collecting system should be assessed for the presence of hydronephrosis. If a stent is present, its proximal and distal positions should be documented and can be visualized as two parallel linear echogenic bands. The urothelium is normally thin enough to not be visualized by ultrasound. Transverse and sagittal images of the bladder should be recorded. The perinephric space needs to be assessed for the presence of fluid collections or free fluid.

Doppler Assessment Perfusional assessment of the kidney allograft is typically performed with color Doppler; however, B flow, a non-Doppler method to look at perfusion, has gained popularity. In assessing for allograft perfusion, flow should normally be seen all the way to the edge of the cortex (Fig. 16.23). Screening of the graft should be performed to assess for global or focal areas of hypoperfusion. Spectral interrogation of the intraparenchymal arteries of the superior, mid, and inferior portions of the renal allograft are a part of the routine assessment. Optimally, the interlobar arteries should be interrogated; however, in hypoperfused states, more centrally located segmental vessels may need to be assessed in lieu of the interlobar arteries to provide greater signal and less noise on the spectral images. The normal intraparenchymal waveform is low impedance with a brisk upstroke and continuous diastolic flow, with a resistive index of 0.6-0.8 considered normal (Fig. 16.24).

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The number of main renal arteries should be documented and correlated with the transplant operative note. Each renal artery anastomosis should be assessed and interrogated separately, both on color Doppler and via spectral evaluation of the proximal, mid, and distal renal portions of the renal arteries as well as anywhere aliasing may be appreciated on the color Doppler portion (Fig. 16.25). Normal renal artery velocities are less than 300 cm/s; however, in the immediate posttransplant period, velocities over 300 cm/s can also be considered normal and usually normalize in the first few weeks after transplantation. Color and spectral Doppler assessment of the iliac artery, both pre and post anastomosis, are also typically performed. The intraparenchymal and extraparenchymal renal veins normally show either monophasic continuous flow or phasicity with the cardiac cycle (Fig. 16.26). There are no accepted normal peak velocity values for these vessels. Documentation of the presence or absence of flow with the transplant and main renal vein is of prime importance especially in the first few weeks after transplantation. Contrast-enhanced ultrasound is a useful tool to assess patients who have concerns of perfusion based on color Doppler images. Normal contrast-enhanced perfusion will show prompt continuous delivery of contrast out to the cortex. In patients receiving ultrasound contrast, software can be used to derive the arrival time and time to peak and provide quantitative assessment of perfusion (Fig. 16.27).

Arterial Complications Renal Artery Thrombosis Transplant renal artery thrombosis is uncommon (0.1 s), elevated ratio of peak velocity in the renal artery to iliac artery (>2:1), tissue vibration at the site of narrowing, and lower resistive indices.29 It is possible that patients with transplant renal artery stenosis will have normal or elevated resistive indices as the lower resistive index may be

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Fig. 16.29 Chronic Renal Artery Thrombosis. (A) Color Doppler shows normal perfusion in the upper pole but no perfusion in the lower pole. (B) Gray-scale image shows thinning and slightly hypoechoic parenchyma in the lower pole, consistent with chronic arterial thrombosis. See also Video 16.4.

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C Fig. 16.30 Renal Artery Stenosis. (A) Intraparenchymal spectral Doppler shows delayed systolic upstroke (tardus-parvus waveform) with low resistive index (0.41). (B) Spectral Doppler shows elevated velocities at the renal artery anastomosis (over 300 cm/s). (C) Conventional angiogram showed a moderate stenosis at the anastomosis partly due to tortuosity (arrow). This was successfully treated with angioplasty.

CHAPTER 16 Solid-Organ Transplantation hidden by a baseline higher resistive index, or prolonged ischemia from the stenosis can lead to fibrosis and elevated resistive indices. Confirmation with CT or MR angiography may be prudent before invasive angiography in order to decrease false-positive ultrasound results as well as to provide a vascular roadmap. Stenoses are typically treated with angioplasty or stent placement.

Arteriovenous Fistula Arteriovenous fistulas are abnormal connections between an artery and a vein that bypass the higher-resistance arterioles. In kidney grafts, arteriovenous fistulas usually occur within the parenchyma at the level of the arcuate, interlobar, or segmental vessels and are typically the result of biopsies or percutaneous nephrostomy tube placement. Although post-biopsy arteriovenous fistulas are quite common, most are small and resolve spontaneously and if noticed may be followed up to ensure resolution. Arteriovenous fistulas can present as an audible bruit on auscultation or cause hematuria. In very rare cases, an arteriovenous fistula is large enough that it can lead to significant ischemic change in the involved segment of the renal parenchyma or to high-output cardiac failure. Large arteriovenous fistulas may need to be embolized endovascularly. Grayscale ultrasound may not reveal arteriovenous fistulas. Color Doppler may be the best method to depict arteriovenous fistulas owing to the tissue vibration caused by the turbulent flow, which manifests as an area of increased Doppler signal. When further interrogated by spectral Doppler, an arteriovenous fistula will show high velocities and low resistance patterns with a turbulent waveform (Fig. 16.31). Arterial flow feeding the involved arteriovenous fistula may show a lower resistance waveform than those supplying the unaffected portion. Additionally, the venous drainage, if the fistula is large enough, may show an arterialization of the venous waveform on spectral Doppler.

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Pseudoaneurysm Pseudoaneurysms are contained arterial injuries that typically result from three processes: anastomotic breakdown, infectious breakdown of the arterial wall, or biopsy/percutaneous nephrostomy-related. Anastomotic breakdowns typically occur within the immediate posttransplant setting, whereas infectious-related pseudoaneurysms can occur at any time. Biopsy- or nephrostomy-related pseudoaneurysms usually occur incident with the procedure and are usually intraparenchymal. On ultrasound, the pseudoaneurysmal sac is anechoic, though peripheral clot can appear hyperechoic. At the site of arterial insult, blood enters into the sac, swirls around, and exits during a cardiac cycle, leading to a “Yin-Yang” or swirling pattern of flow on color Doppler. Spectral interrogation at the site of arterial insult will show a “to-and-fro” waveform pattern (Fig. 16.32; Video 16.5). On B-flow images, one can usually see the swirling of blood well on cine clips. Any anechoic collection within or around the kidney graft should be assessed with color Doppler so as not to mistake a pseudoaneurysm for a simple fluid collection. Extrarenal pseudoaneurysms in particular can be catastrophic. Any hematoma medial to a kidney graft should be closely inspected for an anastomotic or main arterial pseudoaneurysm.31 Arteriovenous fistulas can sometimes mimic pseudoaneurysms, as the venous outflow can sometimes become dilated owing to the increased pressure on the vein from the arteriovenous fistulas. Interrogation of the spectral Doppler waveform is important to differentiate the two, with arteriovenous fistulas demonstrating high-velocity, low-resistance waveform patterns, whereas pseudoaneurysms will show to-and-from flow.

Venous Complications Venous thrombosis is rare but more common than arterial thrombosis, occurring in up to 8% of renal transplants.32 Clinically, venous thrombosis can present as acute pain and swelling of the allograft and an abrupt cessation of renal

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Fig. 16.31 Arteriovenous Fistula (AVF). (A) Color Doppler shows AVF in the upper pole with tissue vibration artifact (arrowhead) and feeding vessel (arrow). (B) Spectral Doppler of AVF shows high-velocity, low-resistance waveform.

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C Fig. 16.32 Pseudoaneurysm After Biopsy. (A) Gray-scale image shows a hypoechoic circumscribed area in the lower pole (arrow) in a patient with recent renal transplant biopsy. (B) Color Doppler shows swirl sign within this area (arrow), consistent with a pseudoaneurysm due to recent biopsy. (C) Bflow shows a small vessel (arrowhead) extending from the edge of the pseudoaneurysm.

function. Venous thrombosis almost always occurs within the first few weeks after transplantation. Risk factors include surgical technical factors, hypovolemia, propagation of iliac vein thrombosis, and compression by fluid collections. Venous thrombosis by ultrasound can be more challenging to diagnose than arterial thrombosis, since perfusion can still be present in venous thrombosis. However, the perfusion is markedly decreased in cases of occlusive venous thrombosis. Spectral Doppler interrogation of the arterial flow will show reversal of diastolic flow (Fig. 16.33; Video 16.6). It may be difficult to assess the flow in the parenchymal arteries owing to the decreased perfusion, but reversal of diastolic flow can be assessed easier in the main renal artery. Both decreased perfusion and reversal of diastolic flow can be seen in other processes, however, such as severe acute tubular injury. Differentiating between these two entities can be challenging and often relies on whether or not the renal vein can be visualized on color Doppler. Failure to depict renal venous flow on Doppler in the setting of decreased perfusion and reversal of diastolic flow in the artery usually necessitates surgical exploration, as prompt diagnosis and treatment of venous thrombosis is critical to salvage the kidney allograft.

Venous Stenosis Transplant renal vein stenosis is a rare complication that can be caused by venous stricture or mass effect from peritransplant collections or even the graft itself. By ultrasound, venous stenosis usually manifests on color Doppler as an area of aliasing, with a focal area of increased velocity on spectral Doppler. A ratio of 3:1 or 4:1 of stenotic-to-prestenotic velocity is necessary to suggest the diagnosis, which, in the setting of renal dysfunction without an alternative etiology, may need to be confirmed with venography with pressure measurements.

Urinary Obstruction Less than 5% of kidney grafts experience collecting system obstruction.33 Clinical presentation can include increasing serum creatinine and decreased urinary outflow; however, many are clinically silent, since the graft and ureter are denervated. Ureteral obstruction can occur from ureteral strictures, compression by adjacent fluid collections, or stone disease. Ureteral strictures have a similar time frame to transplant renal artery stenosis, with most cases occurring within 1 month to 1 year after transplantation. The degree of collecting system obstruction needs to be assessed in the light of denervation of the ureter and the less competent ureteroneocystostomy, in which a mild degree of

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Fig. 16.33 Venous Thrombosis. (A) Color Doppler shows decreased cortical perfusion. (B) Spectral Doppler shows reversed diastolic flow in the renal artery. The renal vein was not visualized (not shown). Findings are consistent with renal vein thrombosis. See also Video 16.6.

pelvicaliectasis is considered normal. However, increasing degrees of obstruction on serial ultrasound as well as moderate to severe grades of hydronephrosis should raise concern for urinary obstruction (Fig. 16.34). If obstruction is suspected, a careful look at the course of the ureter to assess for the presence of obstructing intraluminal calculi or surrounding fluid collection should be performed. Ureteral obstruction from stricture disease can be treated with ureteroplasty or surgical revision.

Parenchymal Abnormalities Rejection Hyperacute rejection occurs from preformed antibody or ABO incompatibility and occurs so acutely that imaging is never performed. This type of rejection is very rare in the modern era. Acute rejection typically occurs within the first 6 months after transplantation and causes inflammation of the glomeruli, tubules, arteries, and interstitium. Rejection takes the form of antibody-mediated rejection (graded on a scale of borderline, types 1A, 1B, 2A, 2B, and 3 with increasing levels of severity) and T-cell-mediated rejection. Rejection can often be asymptomatic, being incidentally discovered on routine biopsies. More severe cases of rejection can manifest with increased serum creatinine, proteinuria, fever, malaise, oliguria, and graft pain. Rejection is associated with a reduction in longterm graft survival. Treatment is guided by the type and grade of rejection, with immunosuppressive medication adjustments and corticosteroids playing important roles. Chronic rejection manifests as interstitial fibrosis and tubular atrophy. The imaging features of rejection are nonspecific. The most sensitive sonographic clue for rejection is urothelial thickening seen on grayscale imaging (Fig. 16.35). The presence of urothelial thickening is, however, nonspecific, and can be seen in infection, inflammation related to ureteral stent placement, and acute tubular injury. More classic sonographic features (decreased perfusion, increased resistive index, corticomedullary differentiation, graft swelling) have not proven to be

a discriminating factor in assessing for rejection in the modern era and are often absent/normal. Diagnosis ultimately relies on the core biopsy samples.

Interstitial Fibrosis and Tubular Atrophy Interstitial fibrosis and tubular atrophy (which includes the previous terms, chronic rejection and chronic allograft nephropathy) represent the common pathway for chronic injury to the renal graft. It can be seen from chronic episodes of rejection, hypertension, recurrent primary disease, and drug toxicity. There are various degrees of interstitial fibrosis and tubular atrophy with progression correlating with decreased renal function. Imaging features of interstitial fibrosis and tubular atrophy can include diminished size and cortical thickness of the graft on grayscale imaging, decreased perfusion, and higher resistive indices (Fig. 16.36). These changes are more likely to be present in kidney grafts greater than 1 year after transplantation, with a rate approaching 50%, with near universal involvement of kidney grafts 10 years after transplantation.34 Acute Tubular Injury Acute tubular injury results from donor organ ischemia and is most encountered in the immediate posttransplant period either as a result of prolonged cold ischemic time or from intraoperative hypotension. Because of its association with prolonged graft ischemic time, acute tubular injury is more commonly seen in patients with deceased donor kidney grafts. Acute tubular injury is a common contributor to delayed graft function, which is usually defined as need for dialysis within the first week of transplantation. Recovery of function from acute tubular injury may take weeks to months. Imaging features of acute tubular injury include decreased cortical perfusion and increased intraparenchymal resistive indices (sometimes with reversed diastolic flow). The imaging features and timing of acute tubular injury can overlap with

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C Fig. 16.34 Urinary Obstruction From Stricture. (A) Initial postoperative gray-scale image shows normal renal transplant without hydronephrosis. (B) Two months later the patient presented with acute kidney injury, and gray-scale imaging shows new hydronephrosis despite a foley catheter in place. (C) Antegrade nephrostogram obtained during percutaneous nephrostomy tube placement shows narrowing in the mid ureter (arrow).

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Fig. 16.35 Rejection. (A) Gray-scale and color Doppler image shows urothelial thickening (arrowheads). (B) Spectral Doppler shows normal intraparenchymal waveforms and resistive index (0.70). Subsequent biopsy showed acute 1A rejection.

those of renal vein thrombosis. In cases of acute tubular injury, the renal vein should be able to be visualized on color Doppler, with confirmation of venous flow on spectral Doppler (Fig. 16.37). Diagnosis of acute kidney injury is made by biopsy.

Infection Infection involving the kidney graft is a common complication following transplantation, with an estimated 70% of kidney transplant recipients experiencing an infectious episode within

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Fig. 16.36 Interstitial Fibrosis and Tubular Atrophy. (A) Gray-scale sonogram shows diffuse cortical atrophy and increased echogenicity. There is renal replacement lipomatosis (arrowhead). (B) Color Doppler shows visible but not robust cortical flow. Overall, findings are consistent with chronic parenchymal disease. This patient was 19 years status post living unrelated kidney transplant.

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C Fig. 16.37 Acute Tubular Injury. (A) Color Doppler shows decreased cortical perfusion on postoperative day 1 renal transplant. (B) Spectral Doppler shows absent diastolic flow and resistive indices of 1.0. (C) Color Doppler shows patent renal vein and artery. In the immediate postoperative setting, these findings are consistent with acute tubular injury. This patient had delayed graft function and a biopsy performed several weeks later showed severe tubular injury and no rejection.

the first three years after transplantation.35 Patients undergoing transplantation are immunosuppressed and therefore may be clinically silent. Infections within the first month tend to be related to surgical complications or donor-derived pathogens, while those in the one to sixth month period tend to be opportunistic infections owing to the higher degree of immunosuppression

during this time period. Reactivation of existing viruses such as the Polyoma BK virus may be more likely to occur during this time frame. After 6 months, the risk for infection decreases but still remains. Ascending infections may be more likely given the decreased competency of the ureteroneocystostomy compared with the native ureterovesicular junction.

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The ultrasound features of infections related to kidney grafts are varied and can often be sonographically occult. Imaging features that suggest infection include low-level echoes in the bladder or collecting system and urothelial thickening in cases of cystitis and pyelitis. Pyelonephritis may manifest as a wedgeshaped area of increased or decreased echogenicity involving the kidney parenchyma with associated decreased perfusion. Abscesses can develop and may appear as complex cystic structures and may be associated with fluid-fluid levels and sometimes gas, manifesting as areas of increased echogenicity with associated dirty shadowing. Abscesses can sometimes appear solid and may mimic renal masses (Fig. 16.38).

Cortical Necrosis Acute cortical necrosis is a rare cause of kidney graft dysfunction. Precipitating events include hypovolemia, septic shock, and microangiopathic hemolysis. Acute cortical necrosis can involve the kidney globally or be in a patchy distribution, with

the greater the degree of involvement correlating with greater renal dysfunction. Acute cortical necrosis is irreversible, and retransplantation in patients with extensive necrosis may be required. Initial grayscale appearance of the kidney graft can be normal. However, with developing infarction in the cortex, a more hypoechoic rim becomes apparent. On color Doppler imaging, perfusion is often maintained to the central portions of the kidney and medulla, with lack of perfusion to the outer two-thirds of the renal cortex. On spectral Doppler, resistive indices can appear elevated, but normal resistive indices can be encountered in the interlobar arteries owing to shunting of blood away from the infarcted cortex (Trueta phenomenon). Contrast-enhanced ultrasound can play a role in demonstrating lack of perfusion to the cortex (Fig. 16.39) and can help distinguish acute cortical necrosis from acute tubular injury, in which cortical perfusion is decreased but maintained.

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Fig. 16.38 Intraparenchymal Abscess. (A) Gray-scale image shows an ovoid cystic appearing intraparenchymal lesion within the lateral moiety (arrows) in this patient with a dual renal transplant. (B) Axial T1 fat sat post with contrast (venous phase) MRI shows nonenhancing fluid collection within the lateral moiety (arrow), corresponding with the US findings. This lesion showed restricted diffusion, consistent with an intraparenchymal abscess in this patient with klebsiella bacteremia. (C) Whole body dual tracer (Tc99m sulfur colloid and indium-111 WBC) planar imaging shows discrepancy between the two tracers with increased indium-111 uptake within the right pelvis projecting over the right iliac bone. (D) Axial SPECT/CT of indium-111 WBC shows diffuse uptake in the medial moiety (arrowhead), but greatest in the lateral transplant moiety (arrow). Findings are again consistent with inflammation/infection.

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Fig. 16.39 Acute Cortical Necrosis. (A) Color Doppler shows diminished cortical flow in this postoperative day 1 renal transplant. (B) Split-screen contrast-enhanced ultrasound was performed, which shows diffuse lack of cortical enhancement.

Solid Renal Masses Masses commonly seen in native kidneys can also be present in kidney grafts, either imported from the donor or more commonly developing after transplantation. The most common solid renal mass is renal cell carcinoma, with clear cell and papillary subtypes being the most common, with oncocytomas and angiomyolipomas also being reported.36 The imaging features of these masses are indistinct from their imaging features in the native kidney (Fig. 16.40). PTLD can be seen rarely in patients with kidney grafts. It can present as a solid or infiltrating renal mass, as nodal disease, or with other organ involvement, including the liver. PTLD is typically hypoechoic and hypovascular on grayscale and Doppler ultrasound (Fig. 16.41). Biopsy is ultimately required to differentiate this disease from other solid renal masses.

Extrarenal Fluid Collections Peritransplant fluid collections are commonly encountered and include hematomas, urinomas, lymphoceles, and abscesses. The ultrasound appearances of these collections are nonspecific; however, the timing of the appearance of these collections as well as their sonographic features can play a role in determining which collection may be more likely.

Hematoma Hematomas usually are seen in the immediate postoperative period as well as any time an intervention such as a biopsy or percutaneous nephrostomy tube placement is performed. Hematomas have a variety of grayscale appearances depending on their chronicity, with acute hematomas often appearing echogenic, subacute as complex fluid collections, and chronic hematomas as simple fluid collections. Hematomas can be difficult to assess by ultrasound, both in their presence and size, as echogenic hematomas can blend into the background tissues.37 Small hematomas typically spontaneously resolve within a few weeks. Larger hematomas can evolve into abscesses, and surgical washout of these may therefore be important. Hematomas should be classified into superficial incisional, lateral, subcapsular, and medial collections, as their etiology and prognosis are

different. Incisional collections are the least concerning, as they are limited to the superficial tissues. Hematomas lateral to the kidney graft are usually the result of venous oozing. If large enough, these can exert some mass effect on the kidney graft, leading to local elevation of the resistive indices on spectral Doppler, but are usually of limited concern. Subcapsular collections will develop mass effect on the kidney graft leading to decreased cortical perfusion and increased resistive indices (Fig. 16.42). The subcapsular collection may be difficult to distinguish from parenchyma, and use of contrast-enhanced ultrasound, color Doppler imaging to depict the edge of the parenchyma, as well as demonstration of increased resistive index (with some showing reversal in flow) are useful imaging clues. Medial collections imply the source of the hematoma as being from the anastomoses or main renal vessels. Careful inspection of this region by color Doppler and contrast-enhanced ultrasound is important to evaluate for extrarenal pseudoaneurysms (Fig. 16.43). In cases in which the visualization of this type of hematoma is challenging by ultrasound, use of contrastenhanced CT or MRI may be advisable.

Urinoma Urinomas are typically apparent within the first couple of weeks after transplantation and can be caused by urothelial injury owing to technical error or from ureteral necrosis. Urinomas are most encountered by ultrasound as a simple-appearing fluid collection between the bladder and the kidney graft, since the urine leak usually arises from the pelvis, ureter, or ureteroneocystostomy site (Fig. 16.44). Diagnosis can be made noninvasively either during an excretory phase of a CT, MRI, or nuclear medicine study, or invasively by fluid sampling (high fluid creatinine and potassium) or percutaneous nephrostogram or retrograde urogram. Lymphocele Lymphoceles after transplantation present typically between 2 weeks and 6 months after transplantation and are caused by disruption of the lymphatics during the transplantation process. Lymphoceles may be small or large and may encircle the kidney

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FIG. 16.40 Papillary Renal Cell Carcinoma. (A) Gray-scale ultrasound shows a heterogenous mass in the lower pole (arrow). (B) Spectral Doppler shows vascular flow internally. (C) Coronal and (D) axial postgadolinium contrast subtraction MR image shows areas of nodular enhancement (arrows).

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graft. Rarely, lymphoceles can be symptomatic, causing increased serum creatinine, pain, and lower extremity swelling.38 By ultrasound, these collections usually show simple fluid characteristics. Diagnosis is made utilizing fluid sampling with fluid creatinine and potassium levels similar to serum levels, but with higher triglycerides and chylomicrons.

Abscess Any of the above collections can become infected. Patients may present with fever, pain, and chills; however, the symptoms may be muted owing to their immunosuppression. Abscesses may show, by ultrasound, a thicker rim, more complex fluid, and sometimes echogenic foci of gas. Fluid sampling is ultimately required to make the diagnosis.

PANCREAS TRANSPLANTATION Pancreas transplantation aims to restore glycemic control in diabetic patients, ultimately leading to a reduction in its complications and an improvement in long-term survival. Pancreas transplants are usually indicated in patients with type 1 diabetes, but it can also be used in some cases of type 2 diabetes, or rarely in patients with pancreatic or biliary malignancies. Pancreas grafts are commonly transplanted simultaneously with a kidney graft (termed “simultaneous pancreas-kidney transplant”), owing to the improved outcome compared with pancreas transplantation alone. The number of pancreas transplants performed in the United States has stabilized to around 1000 cases per year, after noting a decline in the early 2000s.39

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C Fig. 16.41 Posttransplant Lymphoproliferative Disorder. (A) Gray-scale ultrasound of the medial renal transplant in a patient status post en bloc transplant 5 months ago shows enlarged cortex with new hydronephrosis. There is a vague ovoid mass in the inferior pole (arrow). (B) On color Doppler there is minimal internal vascularity within the mass (arrow). (C) Coronal CT with IV contrast shows diffuse enlargement and hypoenhancement of the medial transplant with an ill-defined mass in the lower pole (arrow).

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Fig. 16.42 Subcapsular Hematoma Secondary to Nephrostomy Tube Placement. (A) Gray-scale sonogram shows acute hematoma appearing as a heterogeneous collection along the cortex (arrows), displacing the kidney. (B) Spectral Doppler shows increased resistive index (1.0) with reversal of diastolic flow.

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Fig. 16.43 Extraparenchymal Pseudoaneurysm With Medial Hematoma. (A) Gray-scale image of left lower quadrant transplant shows hydronephrosis and large heterogeneous collection of fluid (F) medial and deep to the transplant in this patient who presented to the ED 1 month after renal transplant. (B) Color Doppler of the external iliac artery anastomosis shows a small outpouching with swirl sign, characteristic of pseudoaneurysms. (C) Axial CT with IV contrast (venous phase) shows a heterogeneous fluid collection (arrowhead) medial to the transplant, corresponding with the US findings and consistent with a hematoma. (D) Conventional angiogram performed after transplant nephrectomy shows a large pseudoaneurysm arising from the mid left external iliac artery. This was treated with a covered vascular stent.

Surgical Technique Almost all pancreas grafts come from deceased donors. Very rarely, a partial living donor pancreas transplant can be performed, in which the body/tail of the donor is transplanted. For deceased donor pancreas transplants, the arterial supply and venous and exocrine drainage require anastomoses. The arterial supply to the pancreas is usually dual, arising from the superior

mesenteric artery (with the key branch being the inferior pancreaticoduodenal artery) and the splenic artery. Commonly, a y-graft is created using the donor iliac arteries (common, internal, and external) which is connected to the donor superior mesenteric artery and splenic artery, allowing a single anastomosis in the recipient. On the venous side, the drainage consists of the superior mesenteric vein and the splenic vein. As these

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FIG. 16.44 Urinoma. (A) Gray-scale image shows a complex fluid collection adjacent to the left renal transplant lower pole. Differential includes a hematoma, seroma, lymphocele, or urinoma. The fluid was aspirated and found to have high creatine levels. (B) Tc99m MAG 3 study shows a urine leak (arrow), collecting between the bladder (B) and the transplant, but also extending laterally (arrowhead). (C) Percutaneous nephrostomy tube was placed. Nephrostogram shows a large urine leak in the distal ureter with fluid collecting (arrow) between the transplant and the bladder (B).

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naturally drain into the portal vein, this can serve as the venous anastomosis. The donor duodenum is inextricably attached to the pancreatic head. Therefore, a portion of the duodenum is explanted and serves as the reservoir for exocrine drainage. The pancreas graft is placed intraperitoneally with the pancreatic head positioned cranially or caudally, depending on the orientation of the anastomoses of the arterial y-graft, donor portal vein, and donor duodenum with the recipient. There are many options and combinations regarding these anastomoses. The arterial y-graft is typically anastomosed end-to-side with the common or external iliac artery, although aortic anastomosis can be performed. When an internal iliac artery anastomosis is chosen, this is in an end-to-end fashion. Venous drainage is usually systemic, involving the iliac veins or IVC, in which case the pancreatic head will be oriented caudally. Portal drainage can be performed through anastomosis with the superior mesenteric vein, which will orient the pancreatic head cephalad. Finally, the duodenum is most commonly anastomosed to small bowel in a side-to-side fashion or end-to-side as a Roux-en-Y anastomosis (Fig. 16.45).

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Normal Pancreas Transplant Ultrasound The usually superficial location of the pancreas graft allows for high-resolution imaging by ultrasound. However, because of its intraperitoneal location, overlying bowel gas can provide a serious limitation in assessing the pancreas graft, especially for those oriented cranially. On grayscale imaging, a pancreas graft has similar features to the native pancreas and demonstrates homogeneous, uniform, low-level echoes. The normal pancreatic duct is nondilated and may be difficult to appreciate. By ultrasound, the pancreatic head has a fuller appearance than the tail, and knowledge of the surgical report may be useful to guide sonographic findings (Fig. 16.46). An attempt should be made to visualize the donor Y graft on color Doppler imaging, ensuring the perfusion of both the superior mesenteric artery supplying the pancreatic head and the splenic artery extending to the pancreatic tail. Both the donor superior mesenteric vein and splenic vein as well as the donor portal vein anastomosis should be attempted. The donor venous drainage is oversized compared to the size of the

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SV SA Fig. 16.45 Anastomoses for Pancreas Transplant. Schematics of the (A) transplanted pancreas with donor Y graft and (B) systemic vascular connection with duodenal cystoplasty, (C) systemic venous drainage, and (D) portal venous drainage. Ao, native aorta; IPDA, inferior pancreaticoduodenal artery; IVC, native inferior vena cava; PV, donor portal vein; SA donor splenic artery; SMA, donor superior mesenteric artery; SMV, donor superior mesenteric vein, SV, donor splenic vein; Y, donor Y graft.

pancreas graft, and slow flow and even a small amount of thrombus within the distal splenic vein can be normally expected. Spectral evaluation of the arteries supplying the pancreas graft should show a sharp arterial upstroke and continuous diastolic flow, with resistive indices normally in the 0.5-0.7 range. The lack of a capsule around the pancreas prevents interstitial edema from having as much of an effect on the resistive index as is seen in the kidney graft.

Vascular Complications Thrombosis Vascular thrombosis, which includes both arterial and venous thrombosis, is the most common cause of pancreas graft failure, seen in 2% to 19% of patients, and typically occurs within the first few weeks after transplantation.40 The clinical symptoms are nonspecific and include lack of glycemic control. Therefore, imaging features are important in diagnosing thrombosis. Venous thrombosis is far more common than arterial

thrombosis. Venous thrombosis can be caused by pancreatitis, stasis from compression from a perigraft collection, surgical error, or prothrombotic states. The relatively lower flow state of the pancreas graft compared with the kidney or liver grafts contributes to thrombosis being more common in pancreas grafts. Venous thrombosis can be partial or complete, involving one or both venous drainages (from the donor splenic vein or donor superior mesenteric vein) or extending all the way to the donor portal vein and into the recipient vein (usually the recipient iliac vein, IVC, or superior mesenteric vein). Partial thrombosis of the distal portion of the donor splenic vein can be expected, especially given the oversized vein diameter relative to the smaller venous drainage of the pancreas and may not affect graft perfusion or function. However, propagation of thrombus can occur, and treatment with anticoagulation, endovascular thrombectomy, or surgical thrombectomy may need to be considered. The venous thrombosis may be difficult to visualize by ultrasound, especially when partial, and meticulous documentation of the entire venous drainage is important. An acute

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head tail

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E Fig. 16.46 Normal Pancreas Graft Anatomy. (A) Gray-scale ultrasound of pancreas transplant shows normal echogenicity and echotexture. (B) Color Doppler image shows normal perfusion of the pancreatic transplant. (C) Color Doppler of normal donor arterial Y graft with anastomosis to the recipient right common iliac artery. The donor SMA supplies the pancreatic head, and the donor splenic artery supplies the tail. (D) Normal spectral waveform in the donor SMV supplying the pancreatic head. The donor splenic vein supplies the tail. (E) Normal intraparenchymal spectral waveform in the pancreatic head. SMA, Superior mesenteric artery; SMV, superior mesenteric vein.

thrombosis may lead to expansion of the draining vein (Fig. 16.47). Thrombosis of the vein can lead to venous hypertension with subsequent graft edema. On color Doppler, the perfusion can appear decreased, though this can be difficult to appreciate given that the pancreas is not normally as perfused as

the kidney or liver grafts. Spectral Doppler of the arterial flow may show highly elevated resistive indices with reversal of diastolic flow. Of visualization of the thrombus, graft edema, or reversal of arterial diastolic flow, the latter is most strongly associated with graft failure.41

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Parenchymal Abnormalities

Fig. 16.47 Venous Thrombosis of Splenic Vein in Pancreatic Transplant. Right lower quadrant image shows the pancreatic treansplant deep to the thrombosed donor splenic vein (arrow).

Arterial thrombosis may affect the splenic artery, superior mesenteric artery, or y-graft, therefore affecting a portion or the whole pancreas graft. Lack of arterial flow is helpful in assessing for thrombosis; however, collateral vessels may provide perfusion to the affected portion of the graft. Ultimately, if sonographic features are either suggestive or inconclusive for an arterial or venous thrombosis, a CT or MR angiogram should be considered.

Arteriovenous Fistula Arteriovenous fistula is a rare complication of pancreatic transplantation, occurring in less than 1% of grafts, and is typically an iatrogenic complication, either incurred during back-bench preparation, transplantation, or as the result of posttransplant biopsy. Arteriovenous fistulas may be clinically silent, incidentally discovered on imaging, or may be symptomatic from rupture leading to abdominal hemorrhage or gastrointestinal hemorrhage, or cause vascular steal which can affect graft function.42 Fistulas can be treated endovascularly or surgically. On ultrasound, the arteriovenous fistula can often best be initially screened for and identified on color Doppler imaging due to the tissue vibration caused by the fistula. On spectral Doppler, the arterial portion will show a high-velocity, low-resistance waveform, while the venous drainage can show an arterialization of venous flow (Fig. 16.48).

Pseudoaneurysm Arterial pseudoaneurysm can be seen at the anastomotic sites due to technical issues or secondary to infections, pancreatitis, or biopsy. These contained vascular injuries should be suspected in the setting of perigraft hematomas, and careful assessment should be performed for a fluid collection on grayscale imaging that demonstrates swirling flow on color Doppler and to-and-fro waveforms on spectral Doppler at the neck of the pseudoaneurysm (Fig. 16.49, Video 16.7).

Both transplant rejection and pancreatitis can have similar clinical and imaging features. Rejection is a common cause of pancreatic graft loss after transplantation. Early recognition of rejection can be challenging because the clinical and laboratory parameters have low sensitivity and specificity in diagnosing rejection. Imaging also lacks the sensitivity and specificity in diagnosing rejection or distinguishing it from pancreatitis. On ultrasound, both can show graft enlargement and interstitial edema. In addition, PTLD can present as diffuse pancreas graft enlargement. PTLD can be distinguished from rejection based on a failure to respond to immunosuppression as well as the presence of masses outside of the graft.43 Acute rejection usually occurs within 1 week to 3 months after transplantation. Small vessel occlusion can result in diminished perfusion and long-term infarction if not recognized and treated early. Chronic effects of rejection can eventually cause graft atrophy and gradual decline in exocrine and then endocrine function. Pancreatitis is very common, especially immediately after allograft implantation, presumably caused by ischemic times and reperfusion injury. However, in patients with pancreatic graft dysfunction undergoing biopsy, rejection seems to be a far more common reason for dysfunction than pancreatitis.44 Pancreatitis can also lead to the development of vascular thrombosis and can be a cause of later development of venous thrombosis. On ultrasound, gray-scale appearances of both rejection and pancreatitis include a more hypoechoic and heterogeneousappearing pancreas. The graft itself may appear enlarged and edematous (Fig. 16.50). On color Doppler images, the perfusion may appear decreased. Arterial resistive indices do not appear to be significantly elevated in patients with rejection or pancreatitis; however, in patients who secondarily develop thrombosis, the resistive indices may be elevated or show reversal of diastolic flow. Patients with pancreatitis can develop peripancreatic fluid collections, which, when aspirated, will show high levels of amylase. Image-guided biopsy is needed to diagnose rejection of the pancreas graft. However, in patients with SPK grafts, rejection of the pancreas graft can often be determined based on the often technically less challenging biopsy of the kidney graft.

Fluid Collections Peritransplant collections may indicate hematomas, pseudocysts from pancreatitis, or duodenal leaks. Duodenal leaks occur from dehiscence of the blind end of the donor duodenum or from the anastomosis with the recipient Roux-en-Y loop. On ultrasound, gross ascites, duodenal thickening, or free intraperitoneal air may be observed with breakdown of the duodenal anastomosis. Any of these collections may form into abscesses. By ultrasound, abscesses may show a thicker echogenic rim and, when they contain air, will show areas of increased echogenicity with dirty shadowing. Although these signs may be suggestive of an abscess, definitive diagnosis will often require fluid aspiration.

RLQ PANC TX VN

B

A

RLQ PANC TX ART

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D

E Fig. 16.48 Arteriovenous Fistula. (A) Color Doppler shows tissue vibration artifact in the head of the pancreatic transplant. (B) Spectral Doppler shows aneurysmal dilation and arterialization of one of the portal venous outflow limbs. (C) Spectral Doppler of the arterial Y graft shows elevated systolic velocity (533 cm/s) and low-resistance waveform. Both the venous and arterial Doppler findings are consistent with an AV fistula. (D) MR angiogram with ferumoxytol shows a large arteriovenous fistula arising from the Y graft donor SMA (arrowhead) with rapid filling of the donor SMV and splenic veins (arrow). (E) Conventional angiogram shows a large AV fistula arising from the Y graft donor SMA (arrowhead) with rapid filling of the donor SMV and splenic veins (arrow). SMA, Superior mesenteric artery; SMV, superior mesenteric vein.

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T

A

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Fig. 16.49 Pseudoaneurysm. (A) Color Doppler of the right lower quadrant adjacent to a pancreatic transplant (not shown) shows swirling to and fro flow, indicating a pseudoaneurysm. This patient was 4 months status post combined kidney-pancreas transplant, complicated by infected postoperative hematoma requiring multiple abdominal drains. (B) Oblique coronal reformat maximum intensity projection CT angiogram shows a large pseudoaneurysm (P) adjacent to the pancreas transplant (T), likely arising from a tiny proximal Y graft (arrow). (C) Conventional angiogram of the right common iliac artery y graft (arrow) shows narrowing of the proximal superior mesenteric artery (SMA) (arrowhead) with brisk bleeding into a large pseudoaneurysm (P) arising from the SMA. (D) Repeat angiogram after coil embolization of the pseudoaneurysm and placement of a covered stent from the Y graft anastomosis extending into the splenic artery (arrow), covering the donor SMA branch. No residual bleeding noted. Nonocclusive thrombus noted in the distal splenic artery (arrowhead). See also Video 16.7.

A

B

Fig. 16.50 Pancreatitis (Edematous Pancreas). (A) Gray-scale image shows mild enlargement and heterogeneity. The patient’s lipase was elevated (586). Findings are consistent with pancreatitis. (B) Follow-up gray-scale ultrasound 2 months later shows interval resolution of edema, corresponding with normalization of lipase.

CHAPTER 16 Solid-Organ Transplantation

REFERENCES 1. Misra AC, Eckhoff D. The development of artificial livers. Curr Opin Organ Transplant. 2021;26(5):468e473. 2. Kwong AJ, Kim WR, Lake JR, et al. OPTN/SRTR 2019 annual data report: liver. Am J Transplant. 2021;21 suppl 2(S2):208e315. 3. Hart A, Lentine KL, Smith JM, et al. OPTN/SRTR 2019 annual data report: kidney. Am J Transplant. 2021;21 suppl 2(S2):21e137. 4. Kandaswamy R, Stock PG, Miller J, et al. OPTN/SRTR 2019 annual data report: pancreas. Am J Transplant. 2021;21 suppl 2(S2):138e207. https:// doi.org/10.1111/ajt.16496. 5. National Data. Organ Procurement and Transplantation Network; Published February 3, 2022. https://optn.transplant.hrsa.gov/data/view-data-reports/ national-data/#. Accessed February 8, 2022. 6. Bekker J, Ploem S, de Jong KP. Early hepatic artery thrombosis after liver transplantation: a systematic review of the incidence, outcome and risk factors. Am J Transplant. 2009;9(4):746e757. 7. García Bernardo CM, Argüelles García B, Redondo Buil P, et al. Collateral development in thrombosis of the hepatic artery after transplantation. Transplant Proc. 2016;48(9):3006e3009. 8. Pulitano C, Joseph D, Sandroussi C, et al. Hepatic artery stenosis after liver transplantation: is endovascular treatment always necessary? Liver Transpl. 2015;21(2):162e168. 9. Park YS, Kim KW, Lee SJ, et al. Hepatic arterial stenosis assessed with Doppler US after liver transplantation: frequent false-positive diagnoses with tardus parvus waveform and value of adding optimal peak systolic velocity cutoff. Radiology. 2011;260(3):884e891. 10. Mohamed Afif A, Anthony APM, Jamaruddin S, et al. Diagnostic accuracy of Doppler ultrasound for detecting hepatic artery stenosis after liver transplantation. Clin Radiol. 2021;76(9):708.e19e708.e25. 11. Zheng BW, Tan YY, Fu BS, et al. Tardus parvus waveforms in Doppler ultrasonography for hepatic artery stenosis after liver transplantation: can a new cut-off value guide the next step? Abdom Radiol (NY). 2018;43(7): 1634e1641. 12. Zheng RQ, Mao R, Ren J, et al. Contrast-enhanced ultrasound for the evaluation of hepatic artery stenosis after liver transplantation: potential role in changing the clinical algorithm. Liver Transpl. 2010;16(6):729e735. 13. Fistouris J, Herlenius G, Bäckman L, et al. Pseudoaneurysm of the hepatic artery following liver transplantation. Transplant Proc. 2006;38(8):2679e2682. 14. Saad WEA. Arterioportal fistulas in liver transplant recipients. Semin Intervent Radiol. 2012;29(2):105e110. 15. Li W, Liu B, Zhu R, Qu W, Wei L, Feng H. Percutaneous transhepatic AngioJet-assisted mechanical thrombectomy for the treatment of posttransplant portal vein thrombosis: a case report. Ann Vasc Surg. 2022;79:443.e1e443.e6. 16. Xue Z, Zhang X, Li Z, Deng R, Wu L, Ma Y. Analysis of portal vein thrombosis after liver transplantation. ANZ J Surg. 2019;89(9):1075e1079. 17. Como G, Montaldo L, Baccarani U, Lorenzin D, Zuiani C, Girometti R. Contrast-enhanced ultrasound applications in liver transplant imaging. Abdom Radiol (NY). 2021;46(1):84e95. 18. Craig EV, Heller MT. Complications of liver transplant. Abdom Radiol (NY). 2021;46(1):43e67. https://doi.org/10.1007/s00261-019-02340-5. 19. Byun J, Kim KW, Choi SH, et al. Indirect Doppler ultrasound abnormalities of significant portal vein stenosis after liver transplantation. J Med Ultrason. 2001;46(1):89e98, 2019. 20. Horrow MM, Phares MA, Viswanadhan N, Zaki R, Araya V, Ortiz J. Vascular steal of the portal vein after orthotopic liver transplant. J Ultrasound Med. 2010;29(1):125e128. 21. Choudhary NS, Saigal S, Bansal RK, Saraf N, Gautam D, Soin AS. Acute and chronic rejection after liver transplantation: what A clinician needs to know. J Clin Exp Hepatol. 2017;7(4):358e366. 22. Jamieson LH, Arys B, Low G, Bhargava R, Kumbla S, Jaremko JL. Doppler ultrasound velocities and resistive indexes immediately after pediatric liver transplantation: normal ranges and predictors of failure. Am J Roentgenol. 2014;203(1):W110eW116. 23. Yoon JH, Lee JY, Woo HS, et al. Shear wave elastography in the evaluation of rejection or recurrent hepatitis after liver transplantation. Eur Radiol. 2013;23(6):1729e1737.

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24. Monti L, Salsano M, Candusso M, et al. Diagnosis of acute rejection of liver grafts in young children using acoustic radiation force impulse imaging. AJR Am J Roentgenol. 2020;215(5):1229e1237. 25. Lucey MR, Terrault N, Ojo L, et al. Long-term management of the successful adult liver transplant: 2012 practice guideline by the American Association for the Study of Liver Diseases and the American Society of Transplantation. Liver Transpl. 2013;19(1):3e26. 26. Haider MZ, Zamani Z, Shahid H, et al. Post-transplant lymphoproliferative disorder after liver transplant: a systematic review. Blood. 2020;136(supplement 1):34e35. 27. Sugi MD, Albadawi H, Knuttinen G, et al. Transplant artery thrombosis and outcomes. Cardiovasc Diagn Ther. 2017;7(suppl 3):S219eS227. 28. Fananapazir G, Tse G, Corwin MT, et al. Pediatric en bloc kidney transplants: clinical and immediate postoperative US factors associated with vascular thrombosis. Radiology. 2016;279(3):935e942. 29. Fananapazir G, LaRoy JR, Navarro SM, Corwin MT, Carney B, Troppmann C. Ultrasound screening for transplant renal artery stenosis risk stratification using standardized criteria in structured reporting: a validation study. J Ultrasound Med. Published online. September 18, 2021. 30. Willicombe M, Sandhu B, Brookes P, et al. Postanastomotic transplant renal artery stenosis: association with de novo class II donor-specific antibodies. Am J Transplant. 2014;14(1):133e143. 31. Fananapazir G, Hannsun G, Wright LA, Corwin MT, Troppmann C. Diagnosis and management of transplanted kidney extrarenal pseudoaneurysms: a series of four cases and a review of the literature. Cardiovasc Radiol. 2016;39(11):1649e1653. 32. Keller AK, Jorgensen TM, Jespersen B. Identification of risk factors for vascular thrombosis may reduce early renal graft loss: a review of recent literature. J Transplant. 2012;2012:793461. 33. Karam G, Hétet JF, Maillet F, et al. Late ureteral stenosis following renal transplantation: risk factors and impact on patient and graft survival. Am J Transplant. 2006;6(2):352e356. 34. Nakorchevsky A, Hewel JA, Kurian SM, et al. Molecular mechanisms of chronic kidney transplant rejection via large-scale proteogenomic analysis of tissue biopsies. J Am Soc Nephrol. 2010;21(2):362e373. 35. Dharnidharka VR, Agodoa LY, Abbott KC. Risk factors for hospitalization for bacterial or viral infection in renal transplant recipients–an analysis of USRDS data. Am J Transplant. 2007;7(3):653e661. 36. Griffith JJ, Amin KA, Waingankar N, et al. Solid renal masses in transplanted allograft kidneys: a closer look at the epidemiology and management. Am J Transplant. 2017;17(11):2775e2781. 37. Fananapazir G, Rao R, Corwin MT, Naderi S, Santhanakrishnan C, Troppmann C. Sonographic evaluation of clinically significant perigraft hematomas in kidney transplant recipients. AJR Am J Roentgenol. 2015;205(4):802e806. 38. Zargar-Shoshtari MA, Soleimani M, Salimi H, Mehravaran K. Symptomatic lymphocele after kidney transplantation: a single-center experience. Urol J. 2008;5(1):34e36. 39. Kandaswamy R, Stock PG, Gustafson SK, et al. OPTN/SRTR 2018 annual data report: pancreas. Am J Transplant. 2020;20 suppl s1(s1): 131e192. 40. Dickey K, Anderson S. Sonographic detection and evaluation of thrombosis in a patient with recent pancreas transplant. J Diagn Med Sonogr. 2019;35(3):212e218. 41. Morgan TA, Smith-Bindman R, Harbell J, Kornak J, Stock PG, Feldstein VA. US findings in patients at risk for pancreas transplant failure. Radiology. 2016;280(1):281e289. 42. Bratton CF, Hamid A, Selby JB, Baliga PK. Case report: gastrointestinal hemorrhage caused by a pancreas transplant arteriovenous fistula with large psuedoanuerysm 9 years after transplantation. Transplant Proc. 2011;43(10): 4039e4043. 43. Meador TL, Krebs TL, Cheong JJ, Daly B, Keay S, Bartlett S. Imaging features of posttransplantation lymphoproliferative disorder in pancreas transplant recipients. Am J Roentgenol. 2000;174(1):121e124. 44. Redfield RR, Kaufman DB, Odorico JS. Diagnosis and treatment of pancreas rejection. Curr Transplant Rep. 2015;2(2):169e175.

PART THREE Small Parts, Carotid Artery, and Peripheral Vessel Sonography CHAPTER

17

Thyroid Gland and Cervical Lymph Node Sonography Kedar Gopal Sharbidre and Franklin N. Tessler

CHAPTER OUTLINE INTRODUCTION, 686 ULTRASOUND TECHNIQUE AND INSTRUMENTATION, 687 Transducer Selection and Technique, 687 Patient Positioning and Other Practical Considerations, 687 Newer Ultrasound Techniques, 687 Role of Other Imaging Modalities, 687 THYROID EMBRYOLOGY, PHYSIOLOGY, AND ANATOMY, 688 Embryology, 688 Thyroid Physiology, 688 Normal Thyroid Gland Anatomy, Ultrasound Appearance, and Size, 689 CONGENITAL ABNORMALITIES, 691 Pyramidal Lobe, 691 Tubercle of Zuckerkandl and Other Developmental Abnormalities, 691 Thyroglossal Duct Cysts, 692 DIFFUSE THYROID DISEASE, 692 Infectious and Inflammatory Conditions, 692 Autoimmune Conditions, 693 Infiltrative Disease in Systemic Conditions, 695 BENIGN FOCAL THYROID DISEASE, 695 Hyperplasia, 695 Adenoma and Variants, 697 Abscess, 698 Intrathyroidal Parathyroid Adenoma, 699

Ectopic Thymus, 699 MALIGNANT FOCAL THYROID DISEASE, 700 Papillary Carcinoma of the Thyroid, 700 Noninvasive Follicular Thyroid Neoplasms With Papillary-Like Features, 702 Follicular Carcinoma, 702 Medullary Thyroid Carcinoma, 702 Anaplastic Thyroid Carcinoma, 703 Primary Thyroid Lymphoma, 704 Thyroid Metastases, 705 CASTLE Tumors, 705 ULTRASOUND ASSESSMENT OF THYROID NODULES, 705 Does a Nodule Correspond to a Palpable Abnormality or a Lesion on Another Imaging Modality?, 706 What Is a Nodule’s Malignancy Risk Based on Its Ultrasound Appearance?, 706 Ultrasound-Based Risk Stratification: Signs of Malignancy, 706 Size, Measurement, and Growth, 710 Classic Benign Appearances, 711 RISK STRATIFICATION SYSTEMS, 711 ATA Guidelines and ACR TI-RADS: Similarities and Differences, 713 Lymph Node Evaluation, 713 Reporting Considerations, 713 Other Factors Related to Malignancy Risk, 715

INTRODUCTION Because of its widespread availability, relatively low cost, high resolution for scanning superficial structures, and absence of ionizing radiation, sonography is the ideal procedure for imaging the thyroid gland. Most nonfocal (diffuse) thyroid conditions have a nonspecific ultrasound appearance. Similarly,

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Doppler Imaging and ContrastEnhanced Ultrasound, 715 Future of Thyroid Nodule Risk Stratification, 715 THYROID NODULE BIOPSY, 717 Fine-Needle Aspiration, 717 Core-Needle Biopsy, 719 Bethesda Classification, 719 Mutations in Thyroid Cancer and Molecular Testing, 719 ULTRASOUND EVALUATION OF CERVICAL LYMPH NODES, 720 Technique and Anatomic Classification, 720 Normal and Abnormal Lymph Nodes, 721 Predictive Value of Nodal Assessment in Thyroid Cancer, 722 Lymphadenopathy From Other Cancers, 723 Other Ultrasound Techniques, 723 ROLE OF ULTRASOUND FOLLOWING THYROID SURGERY, 723 Indications and Technique, 723 The Thyroid Bed, 723 ROLE OF ULTRASOUND IN TREATING THYROID NODULES, 724 Ethanol Ablation, 725 Thermal Ablation, 725 CONCLUSION, 725 ACKNOWLEDGMENT, 725 REFERENCES, 725

although focal nodules exhibit a broad range of ultrasound features, it is important to evaluate them for signs of malignancy, since most are benign. These findings have been incorporated into risk stratification systems (RSSs) that estimate cancer risk and guide management. Ultrasound is also routinely used to assess cervical lymph nodes, look for recurrent disease

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Thyroid Gland and Cervical Lymph Node Sonography

after thyroidectomy, and guide percutaneous biopsy or therapy. This chapter will review all these applications, beginning with technical considerations.

ULTRASOUND TECHNIQUE AND INSTRUMENTATION Transducer Selection and Technique For imaging the neck, small footprint linear array transducers with either a rectangular or trapezoidal scan format are preferred to sector transducers because of their wider near field of view. However, a tightly curved array transducer facilitates imaging in patients in whom the thyroid gland extends inferiorly toward the superior mediastinum, and transducers typically used for imaging the abdomen may be needed to encompass enlarged glands. The thyroid gland is highly vascular, and Doppler interrogation may provide useful diagnostic information in patients with focal or diffuse thyroid pathology. Absence of detectable flow suggests that the area being scanned is either fluidcontaining or represents nonviable tissue or debris. For most applications, either color or power Doppler are sufficient to display vessels and patterns qualitatively, although measurement of flow velocities and related indices may be helpful in some situations. More recently, so-called microvascular imaging has been shown to further increase sensitivity for detecting tissue perfusion. This may improve the diagnostic ability to differentiate malignant from benign solid lesions, potentially reducing the need for intravascular ultrasound contrast.1,2

Patient Positioning and Other Practical Considerations The patient is typically examined in the supine position, with the neck extended. A pad or rolled towel should be placed under the neck to provide better neck exposure and increase comfort. The thyroid gland is examined thoroughly following a

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standard protocol.3 Images include sagittal and axial scans through both lobes and the isthmus (Fig. 17.1). In patients with elongated lobes, visualization of the lower poles may be improved by asking the patient to swallow, which momentarily lifts the thyroid gland in the neck. The examination should also be extended laterally, superiorly, and inferiorly to encompass cervical lymph node bearing areas. Capture of real-time clips is often helpful to document normal or abnormal findings (Videos 17.1e17.3).

Newer Ultrasound Techniques Contrast-enhanced ultrasound (CEUS) using microbubble agents can provide useful information about tissue perfusion, which may be of value for the diagnosis of nodular thyroid disease. CEUS can also help guide ultrasound-guided diagnostic and therapeutic procedures by improving visualization of vascularity within a target lesion and distinguishing viable from nonviable tissue. Quantitative assessment includes time intensity curves, which are obtained by placing a region of interest (ROI) over an enhancing soft tissue abnormality, as well as generation of parameters such as contrast arrival time, area under the curve, wash-in and wash-out slope, peak enhancement intensity, and time-to-peak. As with gray-scale scanning, imaging settings must be optimized, and particular attention should be paid to parameters like depth, focus, gain, and mechanical index.4,5 Ultrasound elastography uses various sonographic methods to measure the stiffness of tissues noninvasively. Techniques include strain imaging, shear wave elastography (SWE), and acoustic radiation force impulse imaging (ARFI).6,7 Because malignant tissues tend to be stiffer, qualitative or quantitative elastography may be used to assess thyroid nodules and cervical lymph nodes, although they have not yet been widely adopted.

Role of Other Imaging Modalities CT and MRI are not used for the initial evaluation of thyroid disease but may be helpful for assessment of large thyroid masses and for evaluation of cervical lymph nodes for surgical planning. Contrast-enhanced CT and MRI are particularly

M

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FIGURE 17.1 Normal Thyroid. (A) Transverse sonogram of thyroid and (B) sagittal scan though right lobe. C, Common carotid artery; M, muscle; Tr, trachea. See also Videos 17.1 and 17.2.

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THYROID EMBRYOLOGY, PHYSIOLOGY, AND ANATOMY Embryology The thyroid gland arises as a small midline anlage in the floor of the primitive pharynx between the first and second pharyngeal pouches, late in the fourth week of development. The primitive thyroid proliferates and descends inferiorly along the anterior neck at the caudal end of an elongated tubular structure called the thyroglossal duct. It then descends further, anterior to the hyoid bone and laryngeal cartilages, reaching its final pretracheal location by the end of the seventh week. The thyroglossal duct maintains its pharyngeal attachment to the ventral floor of the pharynx at the foramen cecum, where it contributes to development of the tongue. Some portions of the thyroid gland originate from the fourth and fifth pharyngeal pouches forming the neural crest cells (ultimobranchial bodies), eventually developing into parafollicular C cells that produce calcitonin.11

Thyroid Physiology FIGURE 17.2 Cervical Adenopathy on CT. Axial neck CT showing multiple enlarged lymph nodes in a patient with lymphoma.

sensitive for assessment of cervical nodal metastases (Fig. 17.2). The American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer (ATA Guidelines) recommend preoperative contrast enhanced CT or MRI as an adjunct to ultrasound for patients with advanced or invasive disease or with multiple or bulky lymph node involvement.8 MRI has some advantages over CT, including excellent soft tissue contrast and lack of ionizing radiation. It can provide accurate evaluation of tumor extent and infiltration of surrounding vessels and skeletal structures.9 The radioactive isotope iodine-123 (123I) is routinely used to quantify uptake by the thyroid gland (Fig. 17.3). 123I is harmless to thyroid cells. As such, 123I scans are sometimes used to work up indeterminate or suspicious thyroid nodules by assessing if the lesion is “hot” (increased uptake) or “cold” (decreased uptake), since the former are rarely malignant. Scanning is also used to detect residual or recurrent malignancy after treatment. Another isotope, iodine-131 (131I), is used as a therapeutic agent for treatment of residual disease after thyroidectomy since it is toxic to thyroid cells. As many as 34.8% of incidental nodules detected on 18FDGPET/CT are malignant (Fig. 17.4).10 The ATA Guidelines recommend PET/CT for initial staging in poorly differentiated thyroid cancers and invasive Hürthle cell carcinomas, to identify lesions and patients at the greatest risk for rapid disease progression, and to evaluate post-treatment response following systemic or local therapy for metastatic or locally invasive disease.8

The thyroid gland secretes thyroxine (T4), which is the major product of the gland, triiodothyronine (T3), and calcitonin, which is secreted by the C cells. After conversion to iodide in the stomach, dietary iodine is absorbed from the gastrointestinal tract and actively transported from the bloodstream across the follicular cell basement membrane of the thyroid gland. Within the follicular cells, iodide is enzymatically oxidized by thyroid peroxidase, and further iodination of the tyrosine residues leads to formation of monoiodotyrosine and

FIGURE 17.3 123I Scan. Anterior view shows diffusely increased thyroid uptake in a patient with Graves disease.

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FIGURE 17.4 PET/CT With Focal Uptake. (A) Axial PET/CT of the neck shows FDG uptake in the right thyroid lobe. (B) Corresponding transverse ultrasound shows a hypoechoic nodule proven to be a metastatic melanoma (calipers).

diiodotyrosine and further their coupling to T3 and T4. Thyroid-stimulating hormone (TSH) secreted by pituitary gland stimulates T4 synthesis and release, which in turn has a negative feedback control on secretion of TSH and thyrotropin-releasing hormone (TRH) by the pituitary and hypothalamus, respectively. Thyroglobulin is the precursor for the synthesis of thyroxine and triiodothyronine. Measurement of the serum thyroglobulin levels is often done for follow-up of patients with thyroid cancer after thyroidectomy and 131I therapy, with elevated levels suggesting recurrence. Thyroglobulin assays of aspirates from lesions in the thyroid bed or elsewhere in the neck may also be helpful to diagnose postoperative recurrence.

Normal Thyroid Gland Anatomy, Ultrasound Appearance, and Size The thyroid gland lies in the anteroinferior neck in a region outlined by muscles, the trachea, the esophagus, the carotid arteries, and the internal jugular veins (Fig. 17.5). It consists of two lobes that are connected across the midline by the isthmus, which lies anterior to the airway. The configuration of the gland varies, with the lobes having a more elongated configuration in tall individuals. Muscular landmarks include the sternohyoid and sternothyroid muscles (known as strap muscles because of their belt-like shape), which lie anterior to the thyroid, the sternocleidomastoid muscles anterolaterally, and the longus colli muscle posteriorly, in close contact with the prevertebral space (Fig. 17.6).12 The muscles are hypoechoic compared to the normal thyroid parenchyma and serve as a reference for assessing the echogenicity of thyroid nodules.

A Strap muscles

Trachea

Sternocleidomastoid muscle

VII Cervical vertebrae Common carotid artery Esophagus

Thyroid gland Internal jugular vein

Longus colli muscle

B FIGURE 17.5 Normal Thyroid Gland. (A) Midline transverse ultrasound image of the thyroid gland. C, Carotid artery; J, internal jugular vein; Tr, Trachea. (B) Schematic diagram of the normal thyroid gland and adjacent structures in the transverse plane.

Normal thyroid parenchyma has a homogeneous, medium- to high-level echogenicity that facilitates detection of hypoechoic thyroid nodules and other lesions. The thin connective tissue that surrounds the gland, usually termed the capsule, is incomplete.13 On sonography, it is often visible as an echogenic line that is best appreciated anteriorly, where it is orthogonal to the ultrasound beam (Fig. 17.7). The superior

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FIGURE 17.6 Strap Muscles. Transverse midline image of the thyroid shows the strap muscles (M) in cross section. C, Common carotid arteries; Tr, trachea.

thyroid artery and vein are located at the upper pole of each lobe. The inferior thyroid vein is found at the lower pole, and the inferior thyroid artery enters the lower third of each lobe (Fig. 17.8).14 The mean peak systolic velocities in healthy adults are 25.9 cm/s and 21.5 cm/s for the superior and inferior thyroid arteries, respectively, with women exhibiting higher velocities than men.15 The esophagus is often visualized along the posterior aspect of the left thyroid lobe, though it may lie slightly further laterally. It is easily identified by its characteristic bowel-like appearance on transverse images (Fig. 17.9). The tracheoesophageal groove, which refers to the sulcus where the trachea meets the esophagus, is an important landmark because it houses the recurrent laryngeal nerve on both sides. The size of the thyroid gland is typically assessed with three orthogonal linear measurementsdthe maximum anteroposterior (AP), transverse (TR), and longitudinal (L) dimensions of each lobedand the AP measurement of the isthmus (Fig. 17.10). Of these dimensions, the AP diameter provides the best indication of enlargement because it is relatively independent of asymmetry

FIGURE 17.8 Inferior Thyroid Artery. Oblique color Doppler image showing a segment of the right inferior thyroid artery.

between the two lobes. In newborns, the thyroid lobes measure 1.8e2.0 cm sagittally and 0.8e0.9 cm AP, increasing to 2.5 cm and 1.2e1.5 cm AP, respectively, at 1 year. In adults, each thyroid lobe measures approximately 5
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FIGURE 17.7 Thyroid Capsule. Transverse sonogram of right lobe and isthmus shows a thin white line representing the capsule (arrowheads), which is best seen anteriorly.

FIGURE 17.9 Esophagus. Transverse image of a heterogeneous left lobe showing the normal esophagus (E) with its characteristic layered appearance. C, Common carotid artery.

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carotid arteries are also signs of thyroid gland enlargement. The thyroid gland may be considered enlarged when the AP lobar measurement is greater than approximately 2.0 cm.12 In neonates, the thyroid volume ranges from 0.40 to 1.40 mL, increasing by 1.0e1.3 mL for each 10 kg of body weight, up to a normal volume in adults of 10 to 11  3 mL.18 In general, the thyroid volume is larger in people in regions with iodine deficiency and in patients who have acute hepatitis or chronic renal failure.19-21 Volume estimates may be useful to assess the need for surgical resection of large glands or assist with calculation of the dose of 131I needed to treat thyrotoxicosis and evaluate response to suppression.22 The most common method for calculating thyroid volume using ultrasound is based on the prolate ellipsoid formula: volume ¼ length
width
thickness
0.524 for each lobe, although the appropriate value for the correction factor has been debated.23 With this method, which is incorporated into many ultrasound scanners, the error is approximately 15%.24 Threedimensional sonography enables estimation of thyroid volume that more closely corresponds to measurements of thyroidectomy specimens.25

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FIGURE 17.10 Thyroid Measurements in Three Planes. (A) Transverse image of the left lobe (calipers). Tr, Trachea; C, common carotid artery; E, esophagus. (B) Sagittal sonogram of the right lobe with anteroposterior (AP) (x calipers) and longitudinal (þ calipers) measurements. (C) Transverse image showing AP measurement of the isthmus (calipers).

CONGENITAL ABNORMALITIES Pyramidal Lobe The distal portion of the thyroglossal duct persists as the pyramidal lobe (Fig. 17.11). approximately half the time.26 It is cylindrical or conical and usually arises from the isthmus, but it may project from either lobe in the absence of the isthmus.27 On ultrasound, it is similar in echogenicity to the rest of the gland. Because it consists of thyroid tissue, it may be affected by diffuse or focal disease. Preoperative identification is essential to ensure its resection during total thyroidectomy, particularly when minimally invasive surgery is performed.28

Tubercle of Zuckerkandl and Other Developmental Abnormalities Extension of normal thyroid tissue from the posterior aspect of the right or left lobe inferomedially is characterized as the tubercle of Zuckerkandl, more often visible on the right (Fig. 17.12). Meticulous dissection of this region is needed to avoid inadvertent injury to the recurrent laryngeal nerve or

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FIGURE 17.11 Pyramidal Lobe. Longitudinal scan above isthmus shows an enlarged pyramidal lobe (calipers).

FIGURE 17.13 Congenital Thyroid Hypoplasia. Axial image shows a hypoplastic right thyroid lobe. C, Carotid artery; Tr, trachea.

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FIGURE 17.12 Tubercle of Zuckerkandl. Sagittal image of right lobe demonstrates the tubercle of Zuckerkandl (calipers), which should not be confused for a nodule or an enlarged parathyroid gland.

inferior parathyroid gland during thyroidectomy.29 On ultrasound, the tubercle of Zuckerkandl may mimic a thyroid nodule or enlarged parathyroid, but its continuity with the thyroid parenchyma should be appreciated on sagittal images.12 Congenital conditions of the thyroid gland include aplasia of one lobe or the whole gland, varying degrees of hypoplasia (Fig. 17.13), and ectopia. Sonography helps establish the diagnosis by demonstrating a diminutive gland in hypoplasia or absence of gland or part of it in aplasia. In patients with an absent thyroid gland, it is important to identify any ectopic thyroid tissue along the embryonic migration pathway in the midline. The base of the tongue is the most common location for the so-called lingual thyroid. Radionuclide scans are particularly sensitive in this regard.30

Thyroglossal Duct Cysts Thyroglossal duct cysts (TDCs) are the most common congenital abnormalities of the neck and result from failure of involution of the thyroglossal duct, usually in an infrahyoid location. They are anechoic, thin-walled, unilocular cysts in the midline, deep to the strap muscles (Fig. 17.14). Suprahyoid TDCs are always located centrally, but they may be paramedian when located below the hyoid. The presence of echogenic

FIGURE 17.14 Thyroglossal Duct Cyst. Sagittal midline image of the upper neck shows an anechoic cyst (C). H, Hyoid bone.

intraluminal debris suggests secondary infection or hemorrhage, and a fistula to the skin may form if a TDC ruptures. Solid neoplasms develop within TDCs in fewer than 1% of patients, with the majority being papillary carcinomas. A thick wall, nodular soft tissue components, and calcifications suggest carcinoma, and biopsy should be performed for confirmation.31 Any suspicious lymph nodes should also be sampled when a nonanechoic TDC is discovered.

DIFFUSE THYROID DISEASE This category includes conditions that affect the entire gland, although involvement may be asymmetrical.

Infectious and Inflammatory Conditions Thyroiditis encompasses a variety of diseases with distinctive clinical and laboratory features.32 Acute suppurative thyroiditis

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FIGURE 17.15 Subacute Thyroiditis. Transverse scan shows an enlarged right lobe (calipers) with heterogeneous echotexture.

is a rare inflammatory disease usually caused by bacterial infection, particularly in immunocompromised patients and children. Infection typically begins in the perithyroidal soft tissues. The gland has a nonspecific ultrasound appearance with normal or increased vascularity. Sonography may be useful to detect the development of a frank abscess. Subacute granulomatous thyroiditis, or de Quervain disease, is a spontaneously remitting inflammatory disease following viral infection such as hepatitis B, hepatitis C, mumps, or cytomegalovirus. Clinical findings include fever, enlargement of the gland, and pain on palpation. Sonographically, the gland may appear enlarged and hypoechoic (Fig. 17.15), with normal or decreased vascularity caused by diffuse edema, or the process may manifest as focal hypoechoic regions or heterogeneity.33

Autoimmune Conditions Autoimmune lymphocytic thyroiditis, or Hashimoto thyroiditis, is the most common type of thyroiditis. It typically manifests as painless, diffuse enlargement of the thyroid gland in young or middle-aged women and is the most common cause of hypothyroidism in North America. Patients develop antibodies to thyroglobulin, thyroid peroxidase (the major enzyme of thyroid hormonogenesis), and to TSH receptors. Histologically, the thyroid parenchyma is infiltrated by lymphocytes, with progressive fibrosis and atrophy over time. The typical ultrasound appearance of Hashimoto thyroiditis (Fig. 17.16A) is a diffuse, coarsened, parenchymal echotexture, generally more hypoechoic than the normal thyroid.34 The gland is usually enlarged initially. Multiple, discrete hypoechoic micronodules from 1 to 6 mm in diameter are strongly suggestive of chronic Hashimoto thyroiditis, an appearance known as micronodulation (Fig. 17.16B). It is a highly sensitive sign of Hashimoto thyroiditis, with a positive predictive value of 94.7%.35

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C FIGURE 17.16 Hashimoto Thyroiditis. (A) Sagittal sonogram demonstrates a hypoechoic right lobe. (B) Micronodular hashimoto thyroiditis. Longitudinal sonogram of right lobe demonstrates heterogenous echotexture with multiple, small, hypoechoic nodules. (C) Hashimoto thyroiditis “Giraffe” appearance. Sagittal image of the right lobe in a patient with Hashimoto thyroiditis demonstrates a variegated pattern.

Histologically, the micronodules represent lobules of thyroid parenchyma that have been infiltrated by lymphocytes and plasma cells. They are surrounded by multiple linear echogenic fibrous septations, sometimes giving the parenchyma a giraffelike appearance (Fig. 17.16C).36 On color Doppler imaging, flow is normal or decreased. Cervical lymphadenopathy also may be present, most evident near the lower pole of the thyroid gland. In the end stage, the gland is small, with poorly defined margins and a heterogeneous echotexture caused by progressive fibrosis. Both benign and malignant thyroid nodules may coexist with chronic lymphocytic thyroiditis, and biopsy is often necessary to establish the final diagnosis. As with other autoimmune disorders, there is an increased risk of malignancy,

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FIGURE 17.17 Multinodular Goiter. (A) Transverse image shows enlargement of the right lobe and isthmus by multiple confluent hypoechoic and hyperechoic nodules. Tr, Trachea. (B) and (C) Longitudinal images show multiple confluent nodules (arrows). (D) Longitudinal image shows enlargement of a lobe by multiple nodules.

particularly B-cell malignant lymphoma. This should be suspected when there is rapid enlargement of the atrophic gland and development of hypoechoic masses. Diffuse parenchymal inhomogeneity also may be seen in other conditions, notably multinodular or adenomatous goiter (Fig. 17.17). Adenomatous goiter affects women three times as frequently as men. Most patients have multiple discrete nodules separated by otherwise normal-appearing thyroid parenchyma, but others show enlargement of the gland, with rounding of the poles, diffuse parenchymal heterogeneity, and no recognizable normal tissue. Painless (silent) thyroiditis has the typical histologic and sonographic patterns of Hashimoto thyroiditis, including hypoechogenicity, micronodulation, and fibrosis. The clinical findings resemble those of classic subacute thyroiditis, but tenderness is absent. Moderate hyperthyroidism and thyroid enlargement usually occur in the early phase. In most cases the disease spontaneously remits in 3e6 months, and the gland returns to a normal appearance. Postpartum thyroiditis is a similar condition that occurs within one year of pregnancy. Graves disease is another autoimmune disease that more commonly occurs in young females and is characterized by thyroid hyperfunction (thyrotoxicosis). There is diffuse glandular enlargement or hyperplasia, and the echotexture may be more heterogeneous than in diffuse goiter (Fig. 17.18A), mainly because of numerous large intraparenchymal vessels and arteriovenous shunting. As well, the parenchyma may be diffusely

hypoechoic because of extensive lymphocytic infiltration or predominant cellularity with little colloid. Color Doppler sonography often demonstrates a hypervascular pattern sometimes referred to as the thyroid inferno (Fig. 17.18B).37 In patients with thyrotoxicosis, spectral Doppler interrogation of the superior thyroidal artery may enable differentiation of Graves disease from thyroiditis.38 Although there is no correlation between the degree of thyroid hyperfunction assessed by laboratory studies and the extent of hypervascularity or blood flow velocities, Doppler analysis is sometimes helpful to monitor therapeutic response.39,40 Invasive fibrous thyroiditis, also called Riedel struma or Riedel thyroiditis, is a rare fibrosing form of immune-mediated chronic thyroiditis that is now considered as a part of the IgG4related sclerosing disease spectrum.41 This condition primarily affects women and progresses to complete destruction of the gland with irreversible hypothyroidism requiring life-long thyroid hormone replacement. There is dense lymphocytic infiltration of the thyroid parenchyma with development of a firm goiter and elevated serum IgG4 levels. Multiorgan involvement, including mediastinal or retroperitoneal fibrosis, sclerosing cholangitis, or other fibrotic diseases, is frequent. In the few cases of invasive fibrous thyroiditis examined sonographically, the gland was diffusely enlarged and had a heterogeneous parenchymal echotexture. Extensive fibrosis can infiltrate adjacent soft tissues, leading to recurrent laryngeal nerve paralysis or Horner syndrome. The primary indication for

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C B FIGURE 17.18 Graves Disease. (A) Transverse sonogram of the right lobe demonstrates enlargement and heterogeneous echotexture. Calipers show measurement of the right lobe in the artery. C, Common carotid artery Tr, trachea. (B) “Thyroid Inferno.” Exuberant flow in the right lobe on sagittal color Doppler in a patient with Graves disease.

sonography is to check for extrathyroidal extension (ETE) and encasement of adjacent vessels (Fig. 17.19). Anaplastic thyroid cancer or lymphoma cannot be reliably differentiated from this entity based on imaging and biopsy is generally required.42

Infiltrative Disease in Systemic Conditions Amyloid deposition within the thyroid gland leading to amyloid goiter is rarely associated with systemic amyloidosis and should be differentiated from conditions like fibrotic variant of Hashimoto thyroiditis, lymphoplasmacytic neoplasm, and medullary thyroid carcinoma (MTC). No specific imaging features of these entities have been reported.43 Diffuse thyroid lipomatosis is an unusual benign condition with diffuse infiltration of thyroid parenchyma with mature adipose tissue, leading to progressive enlargement.44 On ultrasound, the thyroid gland appears markedly hyperechoic. Differential diagnoses include amyloid goiter, anaplastic carcinoma, and lymphoma. Fat also may be present in focal thyrolipomas.

FIGURE 17.19 Riedel Struma (Invasive Fibrous Thyroiditis). (A) Transverse and (B) sagittal ultrasound images of the thyroid show a diffuse hypoechoic process in the right lobe enveloping the common carotid artery (arrows). (C) Contrast-enhanced CT scan shows mild enlargement of the right thyroid lobe and soft tissue thickening (arrows) around the right common carotid artery. Incidentally noted is dilation of the air-filled esophagus (E). Tr, Trachea.

BENIGN FOCAL THYROID DISEASE Focal thyroid disease typically manifests as nodules, which the American Thyroid Association defines as “discrete (lesions) within the thyroid gland that (are) radiologically distinct from the surrounding thyroid parenchyma,” noting that a palpable abnormality may not meet this definition.8 Goiter refers to enlargement of the gland from any cause, while nontoxic goiter applies when this condition is not associated with inflammation, neoplasm, or overt hypo- or hyperthyroidism.

Hyperplasia Thyroid gland hyperplasia results from anything that lessens intrathyroidal iodine levels, such as endemic iodine deficiency, disorders of hormonogenesis (hereditary familial forms), and poor utilization of iodine because of medication. Other genetic, demographic, and environmental factors may also play a role. The peak age is 35e50 years, and women

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are affected three times more often than men. Although most patients are euthyroid, some may develop hyperthyroidism, which is known as toxic multinodular goiter or Plummer disease. A large multinodular goiter also may cause symptoms due to compression of the trachea, esophagus, or neck vessels. Histologically, the initial stage is characterized by cellular hyperplasia of the thyroid acini, followed by micronodule and macronodule formation that is often indistinguishable from normal thyroid parenchyma, even at histology. Pathologically, these nodules may be referred to as nodular hyperplasia, or hyperplastic, adenomatous, or colloid nodules. Sonographically, most hyperplastic or adenomatous nodules are isoechoic compared with normal thyroid tissue, but they may become hyperechoic because of numerous interfaces between the cells and colloid45 (Fig. 17.20). When the nodule is isoechoic or hyperechoic, a thin peripheral hypoechoic halo, most likely caused by perinodular blood vessels and edema or compression of the adjacent normal parenchyma, may be visualized (Fig. 17.21). Perinodular blood vessels are often detected with color Doppler sonography, and intranodular flow may be present. Hyperfunctioning (autonomous) nodules may

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FIGURE 17.20 Hyperplastic (Adenomatous) Nodules. Longitudinal ultrasound images. (A) Oval homogeneous nodule (arrows) with thin, uniform halo. (B) Three hyperechoic nodules, typical of hyperplasia. (C) Solitary hyperechoic nodule, which was benign on fine-needle aspiration biopsy.

FIGURE 17.21 Halo. Transverse ultrasound of the left lobe shows a nodule with a hypoechoic halo (arrowheads).

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FIGURE 17.22 Degenerating Nodules. (A) Transverse image demonstrates a heterogeneous nodule (calipers) with a few cystic spaces. (B) Sonogram in another patient shows a nodule with solid and cystic components.

also exhibit abundant perinodular and intranodular vascularity, but this feature is not discriminatory. Degenerative changes lead to a variety of sonographic appearances (Video 17.4). Anechoic areas are caused by serous fluid or colloid (Fig. 17.22). Bright echogenic foci with comettail artifacts are caused by microcrystals or aggregates of colloid (Fig. 17.23).46 Thin, intracystic septations probably correspond to attenuated strands of thyroid tissue and are

avascular on color Doppler ultrasound. Degeneration also may lead to calcification, which is also seen in malignant nodules. Peripheral (rim) calcifications follow the nodule’s margin and may obscure its contents (Fig. 17.24). Coarse macrocalcifications are located within the substance of the nodule and typically cause acoustic shadowing (Fig. 17.25). Most thyroid cysts are hyperplastic nodules that have undergone extensive liquefactive degeneration. True epithelial-lined cysts of the thyroid gland are rare.

Adenoma and Variants

FIGURE 17.23 Comet-Tails. Colloid cyst containing multiple echogenic foci with V-shaped comet-tail artifacts (arrowhead), which are thought to result from multipath echoes in colloid.

Adenomas represent 5% to 10% of all nodules and are seven times more common in women than men. The majority do not lead to thyroid dysfunction, but less than 10% of the time they become autonomously hyperfunctioning and cause thyrotoxicosis. Most are solitary. Benign follicular adenomas are encapsulated neoplasms with thyroid follicular cell differentiation. Their growth pattern is distinct from the surrounding thyroid parenchyma and is characterized by compression of adjacent tissues and fibrous encapsulation.47 Sonographically, they are difficult to differentiate from hyperplastic nodules. Importantly, the cytologic features of follicular adenomas are generally indistinguishable from those of their malignant counterpart, follicular carcinomas. Subtypes of follicular adenoma include follicular tumors of uncertain malignant potential, which were included in the World Health Organization (WHO) 2017 classification along with many other variants. They are neoplasms with an irregular interface and questionable capsular or vascular invasion.48 Hyalinizing trabecular tumors are another well-circumscribed type of follicular adenoma with a low malignant potential.49

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FIGURE 17.24 Peripheral Calcifications. (A) Coarse peripheral calcification (arrows) casts a large acoustic shadow. (B) Peripheral calcification and an adjacent colloid cyst on the right side in another patient. (C) Area of rim calcification partially engulfed by a papillary thyroid cancer. (D) Peripheral calcification (calipers).

Sonographically, follicular adenomas are usually solid masses that may be hyperechoic, isoechoic, or hypoechoic (Fig. 17.26). They often have a hypoechoic halo resulting from the fibrous capsule and blood vessels, which can be readily seen on color Doppler imaging (Fig. 17.26C). Vessels may pass from the periphery to the central regions of the nodule creating a “spoke and wheel” appearance that is also seen on gray-scale imaging.50,51 This vascular pattern is seen in both hyperfunctioning and poorly functioning adenomas and thus does not allow detection of hyperfunctioning nodules. A spiculated margin and calcifications suggest malignancy.51

Abscess

FIGURE 17.25 Macrocalcifications. Papillary thyroid cancer (calipers) containing dense calcifications with acoustic shadowing.

Isolated thyroid abscesses are rare and usually seen in patients with acute suppurative thyroiditis who complain of painful neck swelling, tenderness, and overlying skin erythema. They can also develop following trauma, as well by hematogenous or lymphatogenous infection. Patients with recurrent suppurative thyroiditis, particularly in the pediatric age group, should be investigated for a pyriform sinus fistula, a branchial pouch abnormality connecting the pyriform sinus to perithyroidal soft tissues anteriorly, traversing the thyroid parenchyma.52 At

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ultrasound, abscesses are complex fluid collections with surrounding parenchymal hypervascularity (Fig. 17.27). Guided aspiration may be diagnostic as well as therapeutic, with surgical drainage reserved for large collections.

Intrathyroidal Parathyroid Adenoma Parathyroid adenomas occurring within the thyroid gland are uncommon, with a prevalence of up to 2.4%.53 They may be complete, where the adenoma is completely encased by the thyroid parenchyma, or partial, where the adenoma is only partly embedded. At ultrasound, intrathyroidal parathyroid adenomas are round to oval, well-circumscribed, hypoechoic to markedly hypoechoic solid lesions similar to typical extrathyroidal adenomas.53 A thin, linear hyperechoic line representing a capsule may be seen at the interface between the thyroid gland and adenoma.54 They are hypervascular and

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FIGURE 17.26 Benign Follicular Adenomas: Transverse images of (A) right lobe and (B) left lobe of the thyroid gland in two patients show homogeneous, hypoechoic, round to oval masses with surrounding thin halos. C, Carotid artery; Tr, trachea. (C) Peri-nodular flow. Transverse color Doppler sonogram shows abundant flow in and around a follicular adenoma.

marginal vessels are usually present (Fig. 17.28). Ultrasound has a higher accuracy than technetium-99m sestamibi scintigraphy in diagnosing intrathyroidal parathyroid adenomas.55 However, biopsy with an assay of parathyroid hormone may be needed to distinguish them from thyroid nodules.

Ectopic Thymus Ectopic thymic tissue is an uncommon entity that may be seen incidentally in children.56,57 Embryologically, this entity arises due to migration arrest, sequestration, or failure. At ultrasound, ectopic thymus (Fig. 17.29) appears as a well-defined, irregular lesion in or immediately caudal to the thyroid containing multiple linear and punctate bright internal echoes, a so-called dot-dash pattern56,58 This condition should be distinguished from carcinoma showing thymus-like differentiation, described below.

FIGURE 17.27 Thyroid Abscess. Sonogram of an abscess containing echogenic debris.

FIGURE 17.29 Ectopic Thymus. Sagittal image caudal to the left thyroid lobe (not shown) demonstrates the “dot-dash” appearance of thymic tissue, which may lie within or below the thyroid. Calipers delineate the ectopic thymus.

MALIGNANT FOCAL THYROID DISEASE

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Thyroid cancer is the most common endocrine malignancy. As will be discussed below, its incidence has increased markedly in recent decades, largely secondary to incidental detection of nodules on ultrasound and other imaging modalities. Most tumors are differentiated cancers of epithelial origin. They include papillary thyroid cancer (PTC) (approximately 80% to 85%), follicular cancer (approximately 5% to 10%), and Hürthle cell carcinoma (approximately 3%).8,59,60 The remainder include anaplastic cancer and medullary carcinoma, the latter arising from the parafollicular C cells. Nonepithelial tumors include malignant lymphoma, which most often occurs secondarily in the setting of systemic disease, rare mesenchymal tumors such as sarcoma and hemangioendothelioma, and metastases to the thyroid. The classification of thyroid cancer has undergone multiple changes over the last few decades, paralleling improved understanding of its molecular basis. A new category for encapsulated well differentiated borderline follicular tumors with a very low (approximately 1%) risk of recurrence or metastasis was added to the WHO 2017 classification.48,61 This category includes noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP). Well-differentiated tumors that maintain follicular architecture and lack nuclear atypia, capsular invasion, and vascular involvement are low risk.

Papillary Carcinoma of the Thyroid

B FIGURE 17.28 Intrathyroidal Parathyroid Adenoma. (A) Sagittal sonogram of left lobe demonstrates a small hypoechoic nodule (arrowheads) in the upper pole. (B) Corresponding color Doppler image shows marginal vascularity.

Papillary carcinoma of the thyroid (PTC) accounts for most of the increase in the incidence of thyroid cancer noted previously. Risk factors include a history of exposure to ionizing radiation during childhood and a family history of thyroid cancer.62 They are typically seen in the third to fifth decade of life and are more common in females. Studies have also shown a connection between thyroid cancer and obesity.63 Approximately 5% of thyroid cancers have a hereditary component and are associated

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FIGURE 17.30 Papillary Carcinoma: Small Cancer With Microscopic Correlation. (A) Longitudinal image shows a 7 mm, hypoechoic solid nodule containing punctate echogenic foci. They usually do not shadow individually but may do so if clumped, as in this case. (B) Microscopic histology image shows psammoma bodies (arrow). See also Video 17.5.

with syndromes such as Gardner syndrome, Cowden disease, familial adenomatous polyposis, and Werner syndrome.64 Histologically, PTCs are epithelial tumors with follicular differentiation, and they demonstrate specific nuclear characteristics with the presence of papillae and/or invasion. Multiple variants have been described. Classical PTC and the follicular variant of PTC (FVPTC) have very favorable outcomes, while subtypes such as the tall cell, columnar and hobnail variants present at a more advanced stage and have a worse prognosis.65,66

Classical Variant Papillary Carcinoma of the Thyroid Genotypically, PTCs are classified as “BRAF-like” tumors that exhibit either the BRAFV600E mutation or its variants, and “RAS-like” tumors with RAS mutations.67 The BRAF-like PTCs are classical tumors with papillary architecture and florid nuclear atypia, often showing infiltrative growth. They demonstrate characteristic nuclear and cytomorphologic features. Grossly, PTCs are encapsulated, firm solid tumors that may contain small cystic foci containing calcified material. Fibrosis is commonly present. Cytologically, PTCs contain enlarged cuboidal or low columnar cells with distinct large irregular nuclei, nuclear overlapping, and crowding. Nucleoli may be eccentrically placed, giving an appearance of a “ground glass nucleus.”68 Delicate nuclear chromatin condensation and clearing (“Orphan Annie” nuclei) may be present.59 Papillae are characteristic of PTCs. Infarction at their tips leads to formation of laminated spherules called psammoma bodies that sometimes manifest as punctate echogenic foci (PEF) or microcalcifications on ultrasound (Fig. 17.30, Video 17.5). They may be present in both the primary tumor and cervical lymph node metastases (Fig. 17.31).69 Multifocal tumors are seen in about 50% of cases, and irregular, invasive borders, and capsular and lymphovascular invasion are also common. The major route of spread of papillary carcinoma is through the lymphatics to nearby cervical lymph nodes.

Patients with PTC may present with enlarged cervical nodes and a palpably normal thyroid gland.70,71 Distant metastases are unusual (2% to 3%) and are mostly to the mediastinum and lung. Sonographic characteristics of papillary carcinoma usually include hypoechogenicity (90% of cases) resulting from closely packed cellular content with minimal colloid. Flow at color Doppler sonography is variable.

Follicular Variant Papillary Carcinoma of the Thyroid Follicular variant PTC demonstrates the characteristic nuclear features of PTC as well as an exclusively follicular growth pattern. These tumors are encapsulated or unencapsulated, with

FIGURE 17.31 Metastatic Cervical Lymph Node. Axial image shows a very enlarged lymph node containing multiple punctate echogenic foci.

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the former further classified into invasive and noninvasive types. RAS gene mutations are the dominant genetic alteration. They are well-circumscribed on imaging without any necrosis but cannot be reliably differentiated from classic PTC. Cytologically, the infiltrative forms are invasive and sclerotic, while the encapsulated types show capsular or lymphovascular invasion.59 Their clinical course and treatment are similar to typical PTC.

Other Unusual Papillary Carcinoma of the Thyroid Variants Tall cell variant PTCs occur in an older age group and at a more advanced stage than other PTCs. They are more aggressive, even without any ETE.72 At sonography, tall cell variants are markedly hypoechoic solid lesions with microcalcifications and ETE.73 Diffuse sclerosing variant PTCs are typically seen in younger patients and are characterized by generalized involvement of both lobes. Patients usually have cervical lymph node metastases at presentation. Histologically, there is extensive fibrosis, intravascular invasion, dense lymphocytic infiltration, and ETE.74 On ultrasound, diffuse sclerosing variant tumors are solid, heterogeneous ill-defined nodules with scattered PEF (Fig. 17.32).75 Despite their aggressive presentation, long-term survival following thyroidectomy and radioiodine ablation therapy is excellent.59 Cribriform-morular variant PTCs are seen exclusively in patients with familial adenomatous polyposis, commonly in females. They present as multiple encapsulated thyroid nodules without any calcifications and with a low frequency of nodal or distant metastases.61,76

Noninvasive Follicular Thyroid Neoplasms With Papillary-Like Features Tumors previously categorized as noninvasive encapsulated variants of PTC have been reclassified as noninvasive follicular thyroid neoplasms with papillary-like features (NIFTP). They show no invasion at pathology, are genetically distinct from invasive tumors, and are indolent.77 Key histologic features include a follicular growth pattern, lack of invasion, and

absence of psammoma bodies.48 On immunohistochemistry, they do not show BRAFV600E mutations but can exhibit the RAS gene mutations that are usually associated with follicularpattern thyroid tumors. No specific sonographic features are present, but some studies have shown NIFTPs to be solid, hypoechoic nodules with a smooth margin, perinodular vascularity, and no echogenic foci or perinodular halo.78,79 This reclassification is more than just of academic interestdit also has practical benefits for healthcare delivery. In a recent analysis, resultant changes in management were shown to significantly reduce costs and improve quality of life for patients.80

Follicular Carcinoma Follicular carcinoma (FC) is the second subtype of welldifferentiated thyroid cancer. It affects women more often than men and is predominant in the fifth and sixth decades of life. It lacks the characteristic nuclear features of PTC and differs from follicular adenoma because of its invasive nature. Radiation exposure, iodine deficiency, and preexisting thyroid disease are risk factors, and it may occur in hereditary syndromes such as Cowden disease, Werner syndrome, and the Carney complex.59 Capsular and/or lymphovascular penetration are diagnostic pathologic features. The three variants of FC differ in histology and clinical course. Minimally invasive FCs demonstrate limited capsular and/or lymphovascular invasion, encapsulated angioinvasive FCs show limited vascular invasion, and the uncommon aggressive widely invasive FCs have extensive invasion of the capsule, vessels, and the adjacent thyroid parenchyma.48 The dominant molecular alterations in FCs are RAS family mutations. All the variants of FC tend to spread through the bloodstream rather than the lymphatics, and distant metastases to bone, lung, brain, and liver are more likely than metastases to cervical lymph nodes. The widely invasive FC variant metastasizes in about 20% to 40% of cases, and the minimally invasive type metastasizes in 5% to 10%. No unique sonographic features allow differentiation of FC from adenoma, which is not surprising given the cytologic and histologic similarities of these tumors (Fig. 17.33). Similarly, fine-needle aspiration (FNA) is not reliable in differentiating benign from malignant follicular neoplasms because the pathologic diagnosis is not based on cellular appearance but rather on capsular and vascular invasion. Genomic testing may obviate the need for diagnostic lobectomy, however.

Medullary Thyroid Carcinoma

FIGURE 17.32 Diffuse Sclerosing Variant of Papillary Thyroid Cancer. Transverse image of the right lobe demonstrates innumerable punctate echogenic foci throughout the parenchyma.

Medullary thyroid carcinomas (MTCs) are the third most common thyroid neoplasms and account for approximately 5% of all malignant thyroid nodules. They are derived from the parafollicular C cells, which secrete the hormone calcitonin. The C cells arise from the ultimobranchial bodies derived from the fourth branchial pouches and tend to settle in the upper and mid portions of both thyroid lobes rather than the isthmus. No gender predilection is seen with these tumors, nor are any environmental risk factors known. MTCs are malignant, and most are sporadic and occur between the fourth and sixth decades of life. They have a

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FIGURE 17.33 Follicular Carcinomas. (A) and (B) Longitudinal images of two patients with oval homogeneous hypoechoic masses. (C) and (D) Transverse images of two other patients with round homogeneous masses. These four tumors are similar in appearance to follicular adenomas. Genomic testing or lobectomy may be needed for a diagnosis.

strong hereditary association, most commonly with multiple endocrine neoplasia (MEN) and other inherited syndromes with mutations of the RET oncogene. MEN2A syndrome is associated with MTCs, parathyroid hyperplasia, pheochromocytoma, and pancreatic neuroendocrine neoplasm, while MEN2B includes features of MEN2A and mucosal neuromas.81 Familial-associated MTCs may be incidentally detected during workup of MEN syndromes and are usually seen in younger age groups. When associated with MEN syndromes, MTCs are multicentric and/or bilateral in approximately 90% of cases (Fig. 17.34A).82 They are variable in size and are encapsulated. On histology, they contain round to oval, spindled to plasmacytoid cells with intranuclear cytoplasmic inclusions and stippled nuclei. Amyloid deposition is seen in up to 90% of cases.59 Cervical lymph node metastases commonly occur with MTCs, but distant metastases to lungs, liver, and bone are rare. Elevated calcitonin levels at presentation, ETE, distant metastasis, age greater than 50 years, and MEN2B-associated MTCs have an unfavorable prognosis.83 Other MTCs have high cure rates, however. The ultrasound features of MTCs are not specific. Reported findings include irregular solid nodules, hypoechogenicity, heterogeneous echotexture, coarse calcifications that

correspond to calcified nests of amyloid, and increased vascularity (Fig. 17.34).84-86

Anaplastic Thyroid Carcinoma Anaplastic thyroid carcinomas (ATC) are rare, highly aggressive cancers composed of undifferentiated follicular cells with epithelioid and/or spindle cell features. They are typically seen in patients greater than 60 years of age and account for approximately 2% to 3% cases of thyroid cancer.59 They carry a considerably worse prognosis than other thyroid malignancies, with a 5-year mortality rate of more than 95%, although newer therapies have shown promise.87 ATCs typically manifest as rapidly enlarging firm masses that extend beyond the thyroid gland and invade adjacent structures, limiting surgical options. Histologically, ATCs include various morphological subtypes, including sarcomatoid/ spindle cells and epithelioid cells with lymphovascular invasion and ETE. Microscopic foci of papillary or FC may be present, suggesting de-differentiation of these neoplasms. There is substantial overlap with other malignancies such as metastatic lung and renal carcinomas, and immunohistochemistry is often required for diagnosis. Sonographically, ATCs present as large, ill-defined masses with heterogeneous, often markedly hypoechoic, echogenicity,

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FIGURE 17.34 Medullary Thyroid Carcinoma. (A) Transverse image of multicentric medullary thyroid carcinoma in a patient with multiple endocrine neoplasia type II (MEN II) shows bilateral hypoechoic masses (arrows) that contain macrocalcification. C, Carotid arteries; E, esophagus; Tr, trachea. (B) and (C) Medullary thyroid carcinoma. Ultrasound images of two patients with medullary cancer (B) with and (C) without calcifications.

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and calcifications.88 There is extensive invasion of perithyroidal soft tissues (Fig. 17.35A). Locally invasive disease is more common than lymph node metastases. These tumors may be too large to adequately encompass on ultrasound, and CT or MRI may be needed for adequate assessment (Fig. 17.35B). Primary thyroid lymphoma (PTL) may have a similar appearance.

Primary Thyroid Lymphoma Primary thyroid lymphoma accounts for approximately 1% to 5% of all thyroid malignancies and about 3% to 7% of all extranodal lymphomas.89 It is most often seen in females older than 60 years. The typical clinical presentation is a rapidly growing, painless mass that causes obstructive symptoms such as dyspnea and dysphagia. Types of PTL include diffuse large B-cell lymphoma (DLBCL) and marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT) lymphoma.90 DLBCL is more common in the western hemisphere and is more aggressive than MALT lymphoma. In 70% to 80% of patients, lymphoma arises from preexisting Hashimoto thyroiditis in patients with subclinical or overt hypothyroidism. The prognosis is variable and depends on the stage of the disease. Five-year survival ranges from almost 90% in early-stage cases to less than 5% in advanced, disseminated disease. PTL has a variable appearance on ultrasound, including a nodular pattern with well-circumscribed, homogeneously hypoechoic lesions, a diffuse pattern with bilateral, ill-defined hypoechoic masses, and a mixed pattern.91,92 In one recent study, DLBCL presented diffusely with involvement of both the lobes and the isthmus, mimicking ATC, while MALT lymphoma exhibited multifocal nodular masses mimicking

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B FIGURE 17.35 Anaplastic Thyroid Cancer. (A) Transverse sonogram shows a bulky, lobulated hypoechoic mass (calipers) centered in the midline. Tr, Trachea. (B) Axial CT scan in another patient demonstrates a bulky mass (M) engulfing the carotid artery (arrowhead).

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appear hypovascular or show blood vessels with chaotic distribution and arteriovenous shunts.

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Metastases to the thyroid gland are uncommon, with the most common primary sites being lung and kidney.94 On ultrasound, they have similar features to benign and other malignant thyroid lesions. Usually, patients have a known primary tumor and thyroid metastases are incidentally detected on FDG PET/ CT. On sonography, they are solid, homogeneously hypoechoic masses that sometimes contain micro- or macrocalcifications depending on the primary tumor95 (Fig. 17.37). Metastatic cervical lymph nodes may be present as well, necessitating biopsy to establish the diagnosis.

CASTLE Tumors

FIGURE 17.36 Thyroid Lymphoma With Vessel Encasement. Sagittal scan shows encasement of the right common carotid artery (C) by lymphomatous masses (L).

multinodular goiter.92 PTL lesions are typically markedly hypoechoic with internal echogenic strands, posterior acoustic enhancement, and absence of calcification. Background changes of Hashimoto thyroiditis may be present.88 Rarely, necrosis or cystic degeneration occurs in the DLBCL type, as does encasement of adjacent neck vessels (Fig. 17.36). It may not be possible to distinguish PTL from nodular Hashimoto thyroiditis, which has a variable sonographic appearance that depends on the degree of lymphocytic infiltration. The diffuse sclerosing variant of PTC also exhibits lymphocytic thyroid infiltration, and it can be difficult to differentiate it from PTL based on imaging.93 On color Doppler ultrasound, both nodular and diffuse thyroid lymphomas may

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Carcinoma showing thymus-like differentiation (CASTLE) tumors are rare neoplasms with features similar to thymic carcinoma, possibly because of their embryologic origin.96,97 They tend to occur in the fifth or sixth decades of life and are indolent, with a good prognosis after resection. Their sonographic appearance is nonspecific.

ULTRASOUND ASSESSMENT OF THYROID NODULES Although the value of ultrasound in characterizing thyroid nodules was recognized more than forty years ago, for several decades ultrasound was mostly used to characterize so-called cold nodules as solid or cystic.98 Since then, it has become the procedure of choice for evaluating known, suspected, or incidental nodules because of its exquisite ability to assess their internal architecture and other relevant findings in and adjacent to the thyroid gland. Ultrasound has four primary goals in this regard: 1. Is there a nodule that corresponds to a lesion suspected on physical exam?

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FIGURE 17.37 Thyroid Metastasis From Renal Cell Carcinoma. (A) Longitudinal gray scale and (B) power Doppler images show a 1 cm solid, vascular mass.

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2. Is a nodule that was detected on another imaging modality visible sonographically? 3. What is a nodule’s malignancy risk based on its ultrasound appearance? 4. Are there ancillary findings such as nonfocal thyroid disease or cervical lymphadenopathy that influence the probability of cancer?

Does a Nodule Correspond to a Palpable Abnormality or a Lesion on Another Imaging Modality? Requests for thyroid sonography to assess a palpable focal abnormality usually are not accompanied by a detailed description of the location of the suspected nodule, but it is important to correlate sonographic and physical exam findings as much as possible. The ultrasound report should indicate whether any correlate was identified. Other imaging exams should be reviewed prior to scanning, if available. Calcifications should be noted and sought with ultrasound, as they may distinguish two nodules that lie immediately adjacent to one another. Not all nodules detected on CT, MRI, or nuclear medicine studies warrant further evaluation with ultrasound. In 2015, the American College of Radiology’s Incidental Thyroid Findings Committee published recommendations for managing incidental thyroid nodules, or ITNs.99 These guidelines take into account factors such as the presence of suspicious findings on CT or MRI, as well as the patient’s life expectancy, comorbidities, and age, and the diameter of the nodule.99 ITNs are frequently found incidentally on sonograms performed for other indications. Occasionally, it may be possible to determine whether additional imaging is warranted based on the limited images obtained. However, if a complete thyroid ultrasound is needed, it may be done contemporaneously or at a later date after obtaining a formal request from the referring practitioner.

What Is a Nodule’s Malignancy Risk Based on Its Ultrasound Appearance? Estimating cancer risk is the primary aim of assessing thyroid nodules. In large part, this is because they are so common, being detected on up to 68% of adults using high-resolution ultrasound.100 It is estimated that only 9% of nonpalpable nodules are malignant, therefore it is vital to determine which ones require further investigation with biopsy or genomic testing, or, for those that remain indeterminate, diagnostic lobectomy.101 Moreover, many thyroid cancers are not aggressive, and some may not need any intervention or treatment at all; as many as 11% of individuals harbor a clinically silent thyroid cancer at autopsy.102 This possibility was recognized more than 40 years ago by Dr. George Leopold, who suggested that some of these cancers might have been visible on ultrasound.98

The danger of detecting and treating small cancers drawn from a large reservoir of subclinical thyroid malignancies is underscored by the experience in South Korea, where inexpensive thyroid cancer screening was offered beginning in 1999.103 During subsequent years, the prevalence of thyroid cancer rose quickly, but the mortality rate remained extremely low. A similar increase in incidence without a concomitant rise in mortality has been seen in the United States and elsewhere.104-106 Although some of this growth represents a true change due to environmental exposures and other factors, there is broad consensus that the surge has mostly resulted from increased use of imaging. This has led to detection of cancers that would not have caused symptoms or death, characterized as overdiagnosis.103,107 While percutaneous biopsy and thyroid surgery are safe, it is costly to work up nodules that turn out to be benign. Over the past two decades, this has spurred interest in identifying ultrasound findings that, alone or in combination, can reliably and reproducibly estimate the likelihood that a thyroid nodule is malignant, with the expectation that nodules above a certain threshold will require further investigation, while others may be ignored or undergo surveillance. The process has been incorporated into a multitude of schemata that are termed risk stratification systems (RSSs). Although they vary in structure, ease-of-use, accuracy, and adoption rate, they are largely founded on similar sonographic signs. Importantly, recent research suggests that changes in practice patterns due to application of RSSs has led to a decline in the diagnosis of small, indolent cancers.108

Ultrasound-Based Risk Stratification: Signs of Malignancy Sonographic signs, also called descriptors, are typically grouped into five categoriesdcomposition, echogenicity, shape, margin, and echogenic focidfor the purpose of risk stratification. This classification provides a useful construct to consider ultrasound features, whether a particular RSS uses it or not.

Composition Composition refers to the nature of a nodule’s content on a spectrum that ranges from cystic to solid (Fig. 17.38). While distinguishing solid from fluid components is usually straightforward, this may be challenging. For example, solid tissue that is markedly hypoechoic may mimic fluid, particularly if gain and other machine settings are not set appropriately. If there is any doubt, color flow or power Doppler imaging can help, as fluid should never contain vessels. Conversely, fluid containing hemorrhagic or other nontissue content may appear solid if the gain is too high. If there is any doubt, turning the patient from side to side or balloting the nodule with the transducer will cause internal echoes to change position or move, allowing confident characterization. Although many nodules are readily classified as completely solid (Fig. 17.38A), it is common to see fluid as well. Most RSSs require sonologists to estimate the percentage of a nodule’s solid

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FIGURE 17.38 Nodule Composition. (A) Solid nodule. Nodule (calipers) contains no appreciable cystic components. (B) Almost completely solid nodule. Transverse image shows a nodule that is mostly solid with fluid-containing spaces (arrowheads). (C) cystic or almost completely cystic nodule. Transverse sonogram shows a fluid-filled nodule. (D) mixed cystic and solid nodule. Note that this nodule contains an eccentric mural component. Most mixed composition nodules are benign, but eccentric solid components that are lobulated or form an acute angle with the cyst wall (arrowhead) are suspicious. (E) Spongiform nodule. Nodule (arrowheads) contains multiple small cystic spaces. This appearance is highly specific for a benign nodule. See also Video 17.6.

versus cystic components, as their risk levels may be different. This can be difficult in nodules in which the fluid-containing spaces are not confluent. The terms predominantly or almost completely solid (Fig. 17.38B) and predominantly or almost completely cystic (Fig. 17.38C) are applied to nodules that only contain a small amount of the nondominant component based on the principle that such nodules have a similar cancer risk to completely solid or completely cystic nodules. Mixed composition nodules in which the solid components protrude into the lumen of a cyst comprise a special subset, as the geometric

conformation of the mural tissue is significant. Notably, if the solid components form an acute angle with the cyst wall, or if they have a lobulated configuration, the likelihood of malignancy is slightly higher (Fig. 17.38D). Notwithstanding, mixed cystic and solid nodules are overall less concerning than nodules that are completely solid or nearly so.109 One category of mixed cystic and solid nodules has received considerable attention in the literature because of its high negative predictive value for malignancy.36,110 They are often termed spongiform because, in cross section, they resemble the

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E FIGURE 17.38 cont'd (E) Spongiform nodule. Nodule (arrowheads) contains multiple small cystic spaces. This appearance is highly specific for a benign nodule. See also Video 17.6.

cut surface of a sponge (Fig. 17.38E, Video 17.6). This definition typically requires the cystic spaces that comprise them to be small and evenly distributed throughout the nodule’s volume, but some practitioners also include nodules in which the individual fluid components are larger and/or do not occupy the entire nodule.

Echogenicity This category encompasses the nodule’s ultrasound backscatter, with isoechoic or hyperechoic nodules being considerably less suspicious.111-113 Although fluid-containing areas may reflect sound if they contain hemorrhagic debris, echogenicity applies to a nodule’s solid components (Fig. 17.39). The intensity of echoes depends on their intrinsic properties, scan settings, and the characteristics of overlying structures that affect their appearance. For example, fluid in a nodule influences the apparent echogenicity of its solid components. This effect may be mitigated by changing the angle of insonation to produce a more direct path to the solid tissue. Echogenicity is graded in comparison to normal parenchyma in the ipsilateral or contralateral lobe. Nodules that are less echogenic than the strap muscles are considered markedly or very hypoechoic, a concerning sign (Fig. 17.39E). The uniformity of a nodule’s solid tissue, characterized as homogeneous or heterogeneous, adds to the challenge of assigning overall echogenicity. For heterogeneous nodules in which components of differing reflectivity are sharply demarcated from one another, it is usually relatively simple to determine predominant echogenicity. However, if areas of lower and higher reflectivity are interspersed throughout the nodule, assignment of predominant echogenicity may be difficult. In such cases, a gestalt impression suffices. Fortunately, in most RSSs, the distinction between nodules that are only mildly

Shape Shape refers to a nodule’s orientation with respect to the portion of the thyroid in which they reside. Nodules that exhibit growth in the AP direction have a higher likelihood of malignancy because they have violated natural tissue planes that favor the cranio-caudal direction.115-117 This is usually evaluated on transverse images by measuring the nodule’s AP and transverse diameters perpendicular to the skin surface (Fig. 17.40). Shape is classified as taller-than-wide or widerthan-tall, with the former conferring a greater likelihood of malignancy. The term “tall” is sometimes a source of confusion. It refers to the AP dimension of a nodule obtained perpendicular to the skin surface on a transverse image. Importantly, this may be different than the measurements used for nodule size and/or volume. Occasionally, nodules may be oriented obliquely such that their growth in the AP dimension is more apparent on sagittal images. Some RSSs account for this by adopting alternative terminology, using parallel for nodules that grow along tissue planes and anti-parallel for those that grow perpendicular to them. Nodules with identical AP and transverse dimensions fall into neither category. Some RSSs consider such nodules suspicious, but others do not.114,118 Because minimal measurement differences have an effect on estimated malignancy risk, a height-to-width ratio of 1.2 may be more appropriate, especially in nodules that are small or poorly defined.119 While this recommendation has yet to be formally adopted by any RSS, it is helpful to keep in mind to avoid overcalling nodules as tallerthan-wide. Margin Margin (Fig. 17.41) denotes the characteristics of the interface between a nodule and its surroundings. The margin may be smooth (Fig. 17.41A) or uneven, where the interface nodule protrudes into the adjacent parenchyma (Fig. 17.41B). Some RSSs distinguish between a lobulated margin with rounded projections, and an irregular or jagged margin, with smaller protrusions that create a sawtooth appearance. However, both increase the nodule’s suspicion level, since they represent the uneven growth that is more characteristic of malignant nodules.113,115,120 Marginal conspicuity is influenced by the nature of adjacent tissue. The more heterogenous, the more difficult it may be to determine if a nodule’s margin is smooth. This applies in situations where the thyroid parenchyma is coarse or heterogeneous and when adjacent nodules abut the index nodule.

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FIGURE 17.39 Nodule Echogenicity. (A) Anechoic nodule. This descriptor applies to cystic nodules. (B) Hyperechoic nodule. Transverse image shows a hyperechoic nodule (calipers) in the isthmus (I). (C) Isoechoic nodule. Nodule (calipers) is similar in echogenicity to adjacent parenchyma. Its hypoechoic halo does not contribute to its echogenicity. Note that the measurement of the nodule includes the hypoechoic halo. (D) Hypoechoic nodule. Nodule in the isthmus (calipers) is less echogenic than normal thyroid tissue but more than anterior strap muscles (M). Tr, Trachea.

Even if the surrounding thyroid is normal, a nodule’s margin may be too inconspicuous to characterize. Some RSSs account for this by including an ill-defined descriptor in this category (Fig. 17.41C). Absence of marginal conspicuity has not been shown to confer higher or lower cancer risk, however.121 A nodule’s margin should not be confused with its halo, which refers to a discrete layer of tissue, different in echogenicity than the nodule or adjacent parenchyma, that surrounds it (see Fig. 17.21). Halos are more common in benign nodules, but they are not a reliable sign and so are not incorporated into

most RSSs.117,121 However, some studies suggest that the microscopic environment immediately adjacent to a nodule may be related to its aggressiveness, suggesting that the halo may need to be considered in estimating cancer likelihood at some point.122 In some RSSs, the margin category also encompasses the appearance of the interface between a nodule and the capsule.114,115 Determining whether a nodule has breached the capsuledtermed extracapsular extension (ECE) or extrathyroidal extension (ETE)dhas prognostic and therapeutic implications. ECE is classified as microscopic/minimal or

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E FIGURE 17.39 cont'd (E) Very hypoechoic nodule. Nodule (calipers) is less echogenic than the anterior strap muscles (M). Color Doppler shows vascularity, consistent with viable tissue.

gross.123 Nodules that are entirely encompassed within thyroid tissue have no ECE. Nodules that abut or bulge the capsule but do not extend beyond it (Fig. 17.41D) are less concerning than those that clearly invade adjacent soft tissues.123,124 In equivocal cases, careful inspection of the interface and use of microflow scanning to look for small vessels that traverse it may be helpful. Even considerable bulging may not indicate gross invasion, but definite extension into the adjacent tissues is essentially pathognomonic for malignancy (Fig. 17.41E). The degree of invasion and the structures involved are important for surgical planning, so it is important to report them in detail. Meticulous technique is important when evaluating nodules in patients who are candidates for active monitoring in which small suspected or proven cancers measuring 1 cm or less, so called microcarcinomas, are subjected to a program of periodic surveillance for growth.125-127 Capsular abutment and proximity to structures such as the trachealesophageal groove should be reported (Fig. 17.42).

Echogenic Foci This category (Fig. 17.43) encompasses a variety of ultrasound features that range from benign to suspicious for malignancy (SM). Unlike descriptors in the other categories, they are not mutually exclusive, and more than one may be present simultaneously. Historically, microcalcifications or punctate echogenic foci (PEF) have been considered a strong indication of malignancy because of their association with the psammomatous calcifications in papillary thyroid cancers (Fig. 17.43A, Video 17.5).120 While the positive predictive value of PEF for psammoma bodies is variable, most RSSs treat them as a highly suspicious feature, and so it is critical not to overcall them.69,128 Concerning PEF are discrete, small (1 mm or less), and do not produce acoustic shadows.129,130 As noted above, the diffuse

sclerosing variant of papillary cancer is a notable exception, as PEF are widely scattered without a discrete nodule (see Fig. 17.32).93,131 This entity is an example of a malignant process that affects the entire thyroid gland, as also may be seen with other conditions such as ATC and lymphoma. PEF should not be confused with minute foci that are embedded within the speckle ultrasound pattern in the normal thyroid gland. When PEF are suspected, the ROI should be carefully compared to adjacent tissues. In addition, the tiny echoes that represent the walls of minute cysts should not be confused for PEF. Unlike PEF, which tend to be rounded or nearly so, back wall echoes tend to be more linear (Fig 17.44).118 Other types of echogenic foci include macrocalcifications, which are larger than PEF and are embedded within a nodule (Fig. 17.43B), and peripheral or rim calcifications (Fig. 17.43C), which lie along a nodule’s border. Both are often large enough to cause shadowing. Most RSSs consider peripheral calcifications as suspicious, with some calling attention to interruption with protruding soft tissue as a suspicious sign.8 The significance of embedded macrocalcifications is controversial.132 Additionally, macrocalcifications may be present as isolated findings in small cancers without a discernible nodule. The final two descriptors in the echogenic foci category are artifacts. Comet-tails are V-shaped echo trains deep to small reflectors in colloid.46,133 Some RSSs distinguish large and small comet-tails, with the former measuring more than 1 mm in length (Fig 17.43D).114 Making this distinction may be difficult in practice, however, and so it is best to treat comet-tails as a reliable sign of benignity only when they are found within a nodule’s fluid components.115

Size, Measurement, and Growth In addition to classifying nodules from their ultrasound appearance, all RSSs base management, particularly

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small nodules, as slight errors in caliper placement will have a proportionally greater effect on measurement accuracy. The importance of changes in a nodule’s size over time remains unclear.134,135 However, nodules that remain unchanged over long periods are more likely to be benign, or, if malignant, not aggressive. Size may be reported via linear measurements, as above, or as a volume. Some RSSs define significant growth as a 20% increase in at least two nodule dimensions and a minimal increase of 2 mm, or a 50% or greater increase in volume.8 When performing follow-up scans, the current measurements should be compared to those on the earliest prior sonogram, not just the most recent one.

Classic Benign Appearances Some nodules have a characteristic ultrasound appearance that enables them to be classified as benign with a high degree of certainty. These include the previously mentioned spongiform nodules, which have a negligible malignancy risk.110 Also included in this category are highly echogenic nodules, socalled white knights, found in patients with a background of Hashimoto thyroiditis.36,136 They are considerably more echogenic than other hyperechoic nodules (Fig. 17.46). Finally, nodules that have undergone biopsy or other intervention may have a mummified appearance that includes calcification, highlighting the need to always obtain an accurate history (Fig. 17.47).

RISK STRATIFICATION SYSTEMS

B FIGURE 17.40 Nodule Shape. Transverse scans. (A) Showing a wider-than-tall nodule (calipers). (B) A taller-than-wide nodule (calipers) with an anteroposterior dimension larger than its transverse measurement. Note the nodule’s hypoechogenicity and lobulated margin, which are other suspicious findings.

recommendations for FNA biopsy, on size. Therefore, it is critical to measure nodules consistently. Measurement calipers should extend to the nodule’s border and should include the halo, if present. Nodules should always be measured in three axes: the longest dimension on an axial image, the longest perpendicular measurement in the same plane, and the greatest dimension on a sagittal plane image of the thyroid (Fig. 17.45). The longest of these measurements, which should be reported to the nearest mm, determines management. Special care should be taken when measuring nodules that are obliquely oriented. To increase confidence, it is useful to boost the contrast of the image via pre- or post-processing on the ultrasound scanner or in viewing software. As well, the image should be adjusted to make the nodule fill as much of the screen as possible while still encompassing adjacent tissue. This is particularly important for

The association between many of the above signs and thyroid nodule cancer risk has been known for many decades, but only since the early 2000s have they been codified into RSSs. A 2002 study highlighted four suspicious descriptors in nonpalpable nodulesdmicrocalcification, irregular or microlobulated margin, marked hypoechogenicity, and more tall than wided recommending that the presence of any one feature should prompt FNA biopsy, regardless of size.120 Two years later, the Society of Radiologists in Ultrasound (SRU) convened a multidisciplinary panel of experts, who produced a consensus statement that expanded on this work, adding recommendations based on size and addressing mixed cystic/solid nodules and growth.137 In 2009, Horvath and co-workers published the first comprehensive RSS, which they characterized as TIRADS, for Thyroid Imaging, Reporting, And Data System, styled after BI-RADS, which had achieved widespread adoption for evaluation and reporting of breast lesions.138 Their system comprised 10 ultrasound patterns that spanned six suspicion categories ranging from TIRADS 1, for a normal thyroid, to TIRADS 6, for confirmed cancers. Since then, many additional RSSs have been proposed. As of this writing, no fewer than seven RSSs have adopted the TIRADS acronym. Unfortunately, they often differ in management recommendations for a given nodule, leading to confusion for practitioners and patients. Table 17.1 shows some of the leading RSSs in use worldwide.

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E FIGURE 17.41 Nodule Margin. A nodule’s margin is easiest to assess anteriorly, where the ultrasound beam is perpendicular to its interface with surrounding tissues. (A) Smooth margin. Note the smooth anterior aspect (arrowheads) of the nodule (calipers). (B) Lobulated or irregular margin. Image of a right lobe malignant nodule shows rounded protrusions into the surrounding tissues (arrowheads). (C) Ill-defined margin. The border of this nodule (calipers) is nearly imperceptible. (D) Capsular abutment. Transverse ultrasound of a right lobe nodule shows the nodule touching the anterior thyroid capsule (arrowheads). This should be mentioned in the ultrasound report. However, in this case, the margin is smooth. (E) Extrathyroidal extension. Longitudinal image of papillary carcinoma shows a bulky mass extending into the soft tissues posteriorly (arrowheads).

The varied RSSs take different approaches to how ultrasound descriptors translate to cancer risk. Some, such as the ATA Guidelines, use a pattern method.8 In contrast, the American

College of Radiology (ACR) TI-RADS uses a scoring system that assigns points to each descriptor, with the sum determining management.114 Others, including K-TIRADS and EU-

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FIGURE 17.42 Nodule Adjacent to Trachealesophageal Groove. Hypoechoic nodule (calipers) lies immediately adjacent to the trachealesophageal groove. This should be reported, as it is critical for surgical planning and/or decision-making regarding active monitoring. E, Esophagus; Tr, trachea.

TIRADS, use an intermediate approach based on key findings.115,118 The newest RSS, C-TIRADS, is similar to ACR TIRADS in its use of points.139 Many studies over the past decade have evaluated RSS performance, with mixed results, partly because of differences in the populations studied and other methodological distinctions. However, all share the same goal. Given the low overall malignancy rate for thyroid nodules and the lack of aggressiveness of many thyroid cancers, the aim should be to identify the cancers that are likely to cause harm to patients while avoiding biopsy and additional workup for nodules that turn out to be benign.114,140,141 Importantly, however, RSSs developed for adult populations are not meant to be applied to children, even though pediatric thyroid cancers tend to exhibit the same features as those in adults.142

ATA Guidelines and ACR TI-RADS: Similarities and Differences In the ATA Guidelines, nodules are matched to one of 15 constellations of findings. Although they have been extensively validated in clinical practice, a limitation is their inability to classify nodules that do not fit any of the patterns.143 The number of uncategorized nodules is as high as 13.9%, with as many of 9.4% of them ultimately being shown to be malignant.144 In ACR TI-RADS, ultrasound features are assigned zero to three points, with one chosen from each of the first four categories and as many as are present from the fifth.114 Points from all the categories are then summed to give a final score that, in combination with the nodule’s maximum dimension, governs management (Table 17.2). Unlike some other RSSs, ACR TI-RADS provides explicit guidance for all nodules. The two lowest classifications, termed

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TR1 and TR2, have no recommended follow-up, while the other threedTR3, TR4, and TR5dhave recommendations for follow-up sonography or biopsy at diminishing maximum size thresholds for higher suspicion levels (Video 17.7). The recommendation for ultrasound follow-up for some nodules that would be biopsied under other RSSs mitigates the likelihood that cancers will be missed over the long term.145 Each TR level also specifies a dimension below which no further action is recommended. The chart from the 2017 ACR TIRADS white paper also includes explanatory notes, as well as a suggestion to give two points if a nodule’s composition cannot be ascertained, and one point if its echogenicity cannot be determined.114 As for all RSSs, the recommendations in ACR TI-RADS are not standards, but always should be applied taking clinical circumstances into account in shared decision-making with the patient and their physician. For example, a 1.5 cm TR5 nodule may not warrant FNA in a patient with known metastatic malignancy, whereas a nodule that otherwise falls below the threshold for biopsy may need FNA because of a history of neck irradiation or if the patient or their physician is highly concerned. Although much attention has been focused on studying differences between RSSs, closer scrutiny shows that their nodule risk assignments and management recommendations are more similar than not. Table 17.3 illustrates how this applies to the ATA Guidelines and ACR TI-RADS, which shows each of the 15 ATA patterns, the corresponding TR category, and the FNA thresholds under both systems. The two RSSs are fully concordant in seven of the 15 ATA patterns. In another three, ACR TI-RADS recommends biopsy at a threshold only 0.5 cm greater than ATA, with the major differences only affecting low and very low suspicion nodules. The importance of size cutoffs applies to other RSSs as well, and has already been incorporated into one RSS revision.115,146

Lymph Node Evaluation Ultrasound of the neck in patients with suspected or known thyroid cancer should always include assessment of regional cervical lymph nodes. This may be performed at the same time as the initial diagnostic sonogram, before malignancy has been tentatively or definitively diagnosed, or after cancer has been established by biopsy. Unlike other RSSs, ACR TI-RADS does not formally include pretreatment nodal evaluation, although the finding of a suspicious cervical node may prompt FNA and/ or biopsy of an ipsilateral nodule that would otherwise not warrant percutaneous sampling.

Reporting Considerations Regardless of which RSS is used, consistency in reporting thyroid sonograms and nodules is critical. Every reportable nodule should have its location, ultrasound characteristics, size, and management recommendations provided in a uniform manner. Numbering of nodules should persist over time. For example, a nodule reported as number 1 on an initial sonogram should retain its numbering on subsequent scans, even if the nodule is no longer present or confidently visualized, or if other

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A

B

C

D

FIGURE 17.43 Echogenic Foci. (A) Punctate echogenic foci/microcalcifications in papillary carcinoma. Sonogram of a papillary thyroid cancer (calipers) containing scattered tiny, nonshadowing echogenic foci (arrowheads). (B) Macrocalcifications. Nodule (calipers) containing shadowing calcification (arrowhead). (C) Peripheral (rim) calcifications. Dense rim calcification casts an acoustic shadow that obscures the nodule’s architecture. (D) Large comettails. Two small colloid cysts with comet-tale artifacts (arrowheads). See also Video 17.5.

nodules appear in the interim. For management, ACR TI-RADS recommends targeting no more than two nodules with the highest scores for biopsy and suggests that up to four nodules with the highest point totals that fall below the size cutoff for FNA should be followed. Some practitioners have questioned whether nodules should be characterized as benign, not suspicious, mildly suspicious, moderately suspicious, or highly suspicious. This is understandable, as patients may be concerned if, for example, a TR5 nodule that was described as highly

suspicious is not recommended for FNA. Accordingly, these qualifiers may be omitted from ultrasound reports depending on referring physician preferences. Like other RSSs, ACR TI-RADS lends itself to the use of templates and macros in voice recognition systems. Their use has been shown to improve consistency of reporting in practices.147,148 In addition, templated reporting facilitates collection of data for registries for quality assurance and research.

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A

FIGURE 17.44 Microcysts. The back walls of tiny cysts in a nodule may be mistaken for punctate echogenic foci but are usually linear in configuration (arrowheads).

Other Factors Related to Malignancy Risk In addition to intrinsic characteristics, such as composition and echogenicity, some investigators have found that a nodule’s location within the thyroid gland independently influences its malignancy risk. Other than showing lower lobe nodules to be less concerning, results to date have been inconsistent. Some studies have shown that risk is highest in upper pole nodules, while others demonstrated mid-lobe nodules had the greatest cancer likelihood.149,150 More recently, isthmus nodules were found to have a higher malignancy rate.151 While the mechanism for this remains unclear, isthmus nodules exhibit more capsular invasion and regional nodal metastases.152,153 Therefore, they warrant special scrutiny when ultrasound is performed. A definitive role for ultrasound elastography in assessing malignancy risk has yet to be established. There is consensus that increased stiffness is suspicious (Fig. 17.48). However, recent RSSs and revisions have noted that elastography has not shown a discriminatory capability beyond gray-scale ultrasound alone, and so its potential contribution remains unclear.115,139

Doppler Imaging and Contrast-Enhanced Ultrasound Like elastography, the role of spectral, color, and power Doppler imaging is uncertain. Classification systems for flow patterns are available, but results in applying them to estimating cancer risk have been inconsistent.154 Therefore, they are not incorporated into any of the major RSSs. Still, color Doppler is helpful to distinguish viable from necrotic tissue or debris. As

B FIGURE 17.45 Tri-Dimensional Measurement. (A) Sagittal image of a nodule showing measurement of its longest axis (calipers). (B) Orthogonal measurements (calipers) on a transverse image. These measurements may be angled and therefore different from the ones used to assess shape.

well, color Doppler is helpful to avoid vessels within or adjacent to a nodule during biopsy. Several studies have suggested that CEUS may be helpful to distinguish benign from malignant nodules, with nodules that exhibit slow or heterogeneous enhancement being more suspicious for cancer.155,156 As with elastography, the inclusion of CEUS in RSSs will have to await further, prospective confirmation of its value, although widespread application will no doubt be influenced by the added cost and time to perform.

Future of Thyroid Nodule Risk Stratification Artificial Intelligence (AI) and its related techniques, machine learning and deep learning, show great promise in evaluating thyroid nodules, either by suggesting modifications to existing RSSs, selecting nodules that warrant special attention, or assigning risk levels to nodules.157 Deep learning has performed similarly to expert radiologists who used ACR

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TABLE 17.1 Risk Stratification Systems for Thyroid Nodules

SYSTEM ATA Guidelines8 ACR TI-RADS114 K-TIRADS115

EU-TIRADS118 C-TIRADS139

FIGURE 17.46 White Knight. Transverse scan of a patient with autoimmune thyroiditis shows an echogenic pseudo-nodule, which is a classic benign finding.

AACE/ACE/AME Medical Guidelines209

BTA Guidelines211 TIRADS (Horvath et al.)138

FIGURE 17.47 Mummified Nodule. Transverse sonogram of left lobe shows a nodule (arrowhead) with dense calcification from prior biopsy.

TI-RADS to evaluate nodules for biopsy.158 Even if computational techniques only perform on par with seasoned observers, they may turn out to be immensely valuable in

SPONSORING ORGANIZATIONS American Thyroid Association American College of Radiology Korean Society of Thyroid Radiology, Korean Thyroid Association European Thyroid Association Chinese Medical Association American Association of Clinical Endocrinologists, American College of Endocrinology, Associazione Medici Endocrinologi British Thyroid Association N/A

YEAR OF MOST RECENT REVISION 2016 2017 2021

2017 2020 2016

2014 2009

settings where practitioners lack such experience, or they may improve the efficiency and consistency of ultrasound interpretation. Of all the limitations of existing RSSs, perhaps the greatest one is their multiplicity, with many systems in use around the globe. Indeed, more than one RSS may be used in a single practice because of physician preferences. To address this issue, in 2018, the International Thyroid Nodule Ultrasound Working Group embarked on a grassroots effort that includes endocrinologists, radiologists, and surgeons with an interest in thyroid nodule evaluation with ultrasound and treatment. This project comprises two phases: phase 1, in which a universal lexicon of descriptors is being developed; and phase 2, yet to be initiated as of this writing, in which the lexicon will be used to generate a malignancy risk level for any thyroid nodule. Recognizing that ultrasound practitioners prefer different approaches to applying ultrasound findings to cancer risk, it is hoped that workflows will accommodate these preferences while ensuring that the system will lead to the same estimate for any nodule regardless of the algorithm employed. Ultimately, the aspirational goal is

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TABLE 17.2 ACR TI-RADS Categories, Features, and Points114 CATEGORY Composition

a

Echogenicityb

Shape Margin Echogenic foci (choose all that apply)

FEATURE

POINTS

Cystic or almost completely cystic Spongiform Mixed cystic and solid Solid or almost completely solid Anechoic Hyperechoic or isoechoic Hypoechoic Very hypoechoic Wider-than-tall Taller-than-wide Smooth or ill-defined Lobulated or irregular Extrathyroidal extension None or large comet-tail artifacts Macrocalcifications Peripheral (rim) calcifications Punctate echogenic foci

0

POINT TOTAL

LEVEL

0 2 3

TR1 TR2 TR3

4-6

TR4

7 or more

TR5

0 1 2 0 1 2 3 0 3 0 2 3 0 1 2 3 RECOMMENDED MANAGEMENT No FNA or follow-up No FNA or follow-up FNA if  2.5 cm, follow if  1.5 cm FNA if  1.5 cm, follow if  1.0 cm FNA if  1.0 cm, follow if  0.5 cm

a

Assign 2 points if composition cannot be determined because of calcification. Assign 1 point if echogenicity cannot be determined. FNA, Fine-needle aspiration. b

to produce a harmonized RSS that is easy to use regardless of experience and that considers geographical differences in malignancy rates.

THYROID NODULE BIOPSY Fine-Needle Aspiration Because it is rapid, effective, and safe, fine-needle aspiration (FNA) is the most frequently performed procedure to sample thyroid nodules. It has had a substantial impact on the management of thyroid nodules because it provides more specific diagnostic information than noninvasive imaging techniques. The successful use of FNA in clinical practice, however, depends heavily on the availability of experienced proceduralists and expert cytopathologists. Below we describe procedures that are representative of our practice and experience.

Although some practitioners perform FNA by palpation, sensitivity is less than achieved with US guidance.159 As well, small nodules that are located deep within the gland are unlikely to be successfully sampled without imaging. Routine laboratory testing (prothrombin time/INR, platelet count, hemoglobin) is not recommended but may be considered in selected patients.160 Patient positioning is similar to diagnostic thyroid sonography. After preparation with chlorhexidine or another suitable antiseptic agent, the ROI is draped. The target nodule is identified using a high-frequency probe and the needle trajectory is planned. Depending on its location, a medial or lateral approach is chosen. The needle path should avoid vital structures, particularly vessels and the trachea. With ultrasound guidance, the needle should be placed in the most suspicious components of the target, whether, for example, solid mural tissue in a mixed solid-cystic nodule or a region that contains PEF. The skin and the needle path may be

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Small Parts, Carotid Artery, and Peripheral Vessel Sonography

Comparison Between ATA Guidelines8 and ACR TI-RADS114

ATA PATTERN Cyst Spongiform Partially cystic, no suspicious features Hyperechoic, solid regular margin Isoechoic, solid regular margin Partially cystic, eccentric solid area Hypoechoic, solid regular margin Hypoechoic, irregular margin, microcalcifications Hypoechoic, irregular margin Hypoechoic, taller-thanwide Hypoechoic, irregular margin, extrathyroidal extension Hypoechoic, Interrupted rim calcification with soft tissue extension

ATA SUSPICION LEVEL

ACR TR LEVEL

ATA FNA THRESHOLD

ACR FNA THRESHOLD

Benign Very low Very low

TR1 TR1 TR2

No FNA Consider if  2 cm Consider if  2 cm

No FNA or follow-up No FNA or follow-up No FNA or follow-up

Low

TR3

1.5 cm

2.5 cm

Low

TR3

1.5 cm

2.5 cm

Low

TR4

1.5 cm

1.5 cm

Intermediate

TR4

1 cm

1.5 cm

High

TR5

1 cm

1 cm

High

TR4

1 cm

1.5 cm

High

TR5

1 cm

1 cm

High

TR5

1 cm

1 cm

High

TR5

1 cm

1 cm

FNA, Fine-needle aspiration biopsy.

A

B

FIGURE 17.48 Ultrasound Strain Elastography of Papillary Carcinoma. (A) Conventional longitudinal sonogram demonstrates a hypoechoic papillary carcinoma with irregular, poorly defined margin (arrow). (B) Ultrasound elastography shows a predominantly blue appearance, consistent with stiffer malignant tissue.

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anesthetized using 1% to 2% lidocaine, and the patient should be instructed to remain still and not swallow during the FNA. The FNA is then performed by inserting a 23G to 27G needle into the target nodule. Larger-gauge needles increase the likelihood of a hemorrhagic smear, while smaller needles are difficult to direct and may not retrieve adequate material. When the tip is confirmed to lie within the target, the needle is moved back and forth, which shears and loosens cells (Videos 17.8 and 17.9). Material passes into the needle shaft by capillary action or by syringe suction. With the aspiration technique, motion is accompanied by syringe suction, which is released prior to removal of the needle. In the capillary technique, no syringe is needed. When available, contemporaneous review by a cytotechnologist or cytopathologist is helpful to confirm adequacy of the specimen and allows for fewer needle passes. Pain is the most common complication and is easily managed by application of cold compresses and administration of analgesics. Hemorrhage in cystic nodules may cause pain and swelling, but is usually self-limited.161 Significant hemorrhage into the adjacent soft tissues is unusual and should prompt observation and re-examination with ultrasound until it stabilizes. Acute transient swelling of the thyroid is a rare, self-limiting complication that is characterized by multiple linear areas of decreased echogenicity in an enlarged gland.162

Core-Needle Biopsy Core-needle biopsy (CNB) is performed less often than FNA, but it may be considered if there is a high concern for malignancy and FNA has been suboptimal or inadequate. It is particularly helpful if lymphoma is suspected. CNB may be superior to repeat FNA in reducing the need for diagnostic surgery for indeterminate nodules.163 Unlike FNA, coagulation parameters and related lab measures should be checked prior to the procedure because of the risk of hemorrhage. The procedure is typically performed using 18G or 20G needles under ultrasound guidance, and the specimens are processed as with core samples from other organs.

Bethesda Classification In most institutions, FNA samples are reported using the Bethesda System for Reporting Thyroid Cytopathology (BSRTC).164 This system defines six categories: I. Nondiagnostic/unsatisfactory (ND/UNS) II. Benign III. Atypia of undetermined significance/follicular lesion of underdetermined significance (AUS/FLUS) IV. Follicular neoplasm/suspicious for follicular neoplasm (FN/SFN) V. Suspicious for malignancy (SM) VI. Malignant Nondiagnostic or unsatisfactory specimens are more frequent with inexperienced proceduralists and poor specimen preparation.165 This may be mitigated by on-site slide review. Most thyroid nodules can be classified as benign (up to 70% in

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adults) or malignant (approximately 5% to 15%).8 The remaining 20% to 25% in Bethesda categories III, IV, and V are considered indeterminate and carry a malignancy risk of approximately 5% to 47%, 20% to 40%, and 50% to 75% respectively.164,166 Management of indeterminate nodules is controversial, and recommendations include repeat FNA, surveillance, molecular testing, and diagnostic surgery. The ATA Guidelines recommend molecular testing for repeat FNA or molecular testing instead of surveillance or diagnostic lobectomy for AUS/FLUS nodules.8 Molecular testing is also recommended for FN/SFN and SM nodules after taking clinical and sonographic features into consideration.

Mutations in Thyroid Cancer and Molecular Testing Extensive research on the molecular pathogenesis of thyroid cancer has been conducted in the past decade. In 2014, the Cancer Genome Atlas demonstrated that 97% of PTCs are associated with molecular alterations, including the BRAF and RAS mutations noted previously.167 It has also been shown that the mitogen-activated protein kinase (MAPK) signaling pathway plays a key role in thyroid carcinogenesis, as do other uncommon pathways, including the phosphatidylinositol-3kinase (PI3K)/Akt and the mammalian target of rapamycin (mTOR) signaling pathways.168 The cascade of events in these pathways leads to altered cell proliferation, differentiation, and survival, resulting in different subtypes of thyroid carcinoma.169 Some of the common molecular alterations in thyroid cancer are shown in Table 17.4. Notably, however, approximately 5% to 10% of thyroid cancers may not show any genetic mutation, and there is overlap in the mutational profiles between benign and malignant lesions. For example, both follicular adenomas and carcinomas may show RAS gene mutations.170 Research into the genetics of thyroid cancer has led to the development of molecular diagnostic techniques that are applied to cytologically indeterminate nodules. If the test has a low probability of malignancy, ultrasound surveillance may be

TABLE 17.4 Molecular Alterations in Thyroid Cancer TUMOR SUBTYPE Papillary thyroid cancer

Follicular thyroid cancer Anaplastic thyroid cancer Medullary thyroid cancer

COMMON GENETIC ALTERATIONS BRAF V600E (most common), RAS, RET-PTC, TERT promoter mutation RAS (most common), PAX8-PPARg, TERT promoter mutation BRAF, RAS, TERT promoter mutation, TP53 mutation RET (most common), RAS

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TABLE 17.5 Molecular Tests for Thyroid Cancer in the United States171,212,213 TEST TYPE Next-generation RNA sequencing and expression

Next-generation DNA and RNA sequencing

Next-generation DNA and RNA sequencing; microRNA expression

COMMERCIAL TEST Afirma Gene Sequencing Classifier (GSC) and Xpression Atlas (Veracyte, South San Francisco, CA) ThyroSeq genomic classifier v3 (Sonic Healthcare USA, Rye Brook, NY) ThyGeNEXT/ ThyraMIR (Interpace Diagnostics, Parsippany, NJ)

PERFORMANCE NPV 96%, PPV 47% (“rule out” test)

Posterior boundary of submandibular gland IIA

IB IA

IIB Jugular vein

Lower border of hyoid bone

Carotid artery III

VA

Cricoid cartilage

NPV 97%, PPV 66% (“rule in” and “rule out” test)

VI

VB IV Top of manubrium VII

NPV 94%, PPV 74% (“rule in” and “rule out” test)

FIGURE 17.49 Cervical Node Levels. Levels I through VI lie in the neck. Level VII nodes (not shown) are located in the superior mediastinum and may not be visible on ultrasound.

NPV, Negative predicted value; PPV, positive predicted value.

undertaken as an alternative to surgery. Nodules with an intermediate probability may be subjected to lobectomy, while total thyroidectomy may be considered for those with a high cancer probability.171 Recent studies have validated the ability of these tests to reduce the need for diagnostic lobectomy, particularly for nodules with indeterminate cytology.172 The cost for these tests is offset by the even greater expense and risks of diagnostic lobectomy.173 Currently available molecular tests used in the United States are shown in Table 17.5.

ULTRASOUND EVALUATION OF CERVICAL LYMPH NODES Technique and Anatomic Classification Evaluation of cervical lymph nodes, whether performed in conjunction with thyroid ultrasound, to evaluate for locoregional recurrence after resection for thyroid cancer, or for non-thyroid-related conditions, follows a similar protocol. Lymph nodes in the neck number in the hundreds and are often small, so it is impossible to confidently visualize them all, particularly if they are normal.174 A practical approach includes scanning known lymph node-bearing areas in a systematic fashion to detect nodes that are indeterminate or suspicious. Cervical nodes are usually classified by their location in one of seven regions, or levels, that are bounded by anatomic landmarks (Fig. 17.49).175,176

Cervical Lymph Node Levels Level I (submental and submandibular): Superior to the hyoid bone and below the mylohyoid muscle and mandible, anterior to the posterior border of the submandibular gland. Level II (upper jugular): Between the skull base and the hyoid bone, behind the posterior border of the submandibular gland, anterior to the posterior border of the sternocleidomastoid muscle. Level III (middle jugular): Between the hyoid bone and the lower border of the cricoid cartilage, lateral to the medial border of the common and internal carotid arteries, in front of the posterior border of the sternocleidomastoid muscle. Level IV (lower jugular): From the lower margin of the cricoid cartilage to the clavicle, anterior to the posterior margin of the sternocleidomastoid muscle, lateral to the medial margin of the common and internal carotid arteries. Level V (posterior triangle): From the skull base to the clavicle, behind the posterior border of the sternocleidomastoid muscle. Level VI (central): Between the hyoid and suprasternal notch, medial to the medial border of the common and internal carotid arteries. Level VII: Superior mediastinum.

Levels I, II, and V are further subdivided into areas A and B that are demarcated by additional landmarks. Level VI and VII

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constitute the central compartment, while levels I-V correspond to the lateral compartment, which is important surgically and prognostically.176 This classification scheme was originally based on crosssectional CT and MR imaging, and so some of the anatomic structures and the planes that delineate them may not be identifiable on ultrasound. However, the key landmarksdthe mandible, submandibular gland, hyoid bone, cricoid cartilage, sternocleidomastoid muscle, carotid arteries, and clavicled should be visible on most neck sonograms and guide labeling of lymph nodes and other normal and abnormal findings. As well, level VII nodes, which lie in the superior mediastinum and are

A

C

721

therefore usually not accessible to ultrasound, are sometimes visualized with tightly curved array transducers angled caudally.

Normal and Abnormal Lymph Nodes Normal nodes are typically ovoid in shape, with a smooth margin, an echogenic hilum with vascularity on color or power Doppler imaging, and a uniform, hypoechoic parenchyma (Fig. 17.50). Their size varies depending on location, but benign nodes are typically less than or equal to 8 mm in short axis at level II and 5 mm at levels III, IV, and VI.177 However, size alone is not a reliable indicator of malignancy, as benign reactive nodes may be enlarged.178

B

FIGURE 17.50 Normal Lymph Nodes (A, B, C). Cervical nodes in three different patients have an elongated shape and normal echogenic hilum. Calipers in A delineate the node’s long and short axes (+ and x, respectively). Calipers in C measure the node’s short axis.

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Nodes in patients with thyroid cancer are categorized as indeterminate or suspicious based on their ultrasound appearance. Indeterminate nodes have a rounded shape and increased central flow. Because of this, the ratio between a node’s axes has been proposed as a proxy for shape to distinguish benign from malignant nodes.179 This measure should not be confused with the so-called lymph node ratio, which refers to the number of metastatic nodes divided by the number of nodes evaluated at surgery.180 However, the axis ratio for indeterminate nodes may not be significantly different than for nodes ultimately shown to be benign.181 Suspicious nodes exhibit one or more of the following findings: PEF, cystic change, peripheral or diffusely increased

A

C

flow, or hyperechoic cortical areas (Fig. 17.51, Video 17.10). These nodes, particularly those with echogenic foci or hyperechoic areas, are highly predictive of metastasis from PTC.182,183 Indeterminate nodes are more likely to be malignant than benign nodes, but their cancer risk is considerably less than for nodes deemed suspicious.181

Predictive Value of Nodal Assessment in Thyroid Cancer Overall, cervical lymph node metastases in young patients with PTC are associated with lower survival, spurring the need to detect them preoperatively and potentially influence the extent

B

FIGURE 17.51 Thyroid Cancer Nodal Metastases. Metastatic lymph nodes in patients with thyroid cancer show (A) echogenic foci, (B) cystic change, and (C) an ill-defined area of increased echogenicity (arrowheads). See Video 17.10. Calipers in B and C delineate the long axis of the node.

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of surgery.184 However, the performance of ultrasound in detecting metastatic nodes in the central compartment is poor, with a pooled sensitivity of only 0.33, compared to 0.70 for lateral compartment adenopathy.185 This may be due to the presence of nodes that harbor micro-metastases that escape detection because of their size.115 Nevertheless, preoperative sonography should include evaluation of both compartments and call attention to suspicious nodes, which may be biopsied percutaneously if needed.

Lymphadenopathy From Other Cancers Metastases and nodal involvement from other head and neck cancers, distant malignancies, or lymphoma exhibit a wide range of appearances. In patients with head and neck cancers, the presence of lymph node metastases is an important prognostic indicator, and so their detection is critical (Fig. 17.52).186 In addition to the architectural changes and size thresholds described above for metastatic nodes from thyroid malignancies, findings include border irregularity due to uneven cortical enlargement and matting of nodes. A markedly hypoechoic appearance and a micronodular echotexture are associated with lymphomatous enlargement.178,187,188 Lymph nodes that are clearly abnormal may be biopsied percutaneously, but the need for sampling or imaging follow-up for enlarged nodes in the absence of other suspicious findings depends on the clinical history. Notably, some suspicious features are not diagnostic of malignancy, as they may be seen in inflammatory and infectious conditions such as tuberculosis.189 As well, in selected patients with cervical adenopathy on ultrasound, CT or MRI are often helpful for a more global assessment of lymph nodes and other structures.

IJV

723

Other Ultrasound Techniques As with evaluation of thyroid nodules, newer methods, including elastography and CEUS, have shown promise for assessing cervical nodes.190 Heterogeneous enhancement and centripetal or hybrid enhancement on CEUS may be useful to distinguish benign from malignant nodes in thyroid cancer patients.191,192 Given the added time and cost, however, it is unclear whether CEUS will play a part in the routine evaluation of patients with suspected or known thyroid cancer, although it may turn out to be helpful in selecting nodes for FNA pre- or postoperatively. Radiomics, which refers to the computational technique of extracting qualitative and quantitative features from clinical images to enable diagnosis, has shown promise in evaluating cervical lymph nodes in patients with thyroid cancer.193,194 In some cases, so-called radiomics signatures have been incorporated into nomograms that include demographic and laboratory data to predict the likelihood of cervical nodal metastases.195 Wide adoption of this and other computerbased methods will require them to be made available in diagnostic workstations or ultrasound machines, as well as demonstration that they can be used without adding appreciably to cost or time.

ROLE OF ULTRASOUND FOLLOWING THYROID SURGERY Indications and Technique The 2015 ATA Guidelines recommend ultrasound to detect signs of malignancy in the surgical bed and regional lymph node chains, collectively termed locoregional recurrence, at 6e12 months, and then periodically.8 However, while some centers still perform surveillance at yearly intervals, recent research has called this into question. Patients who have undergone total thyroidectomy and radioactive iodine ablation have low or undetectable thyroglobulin levels, and neck ultrasound is more likely to be false positive than false negative.196,197 This suggests that serum thyroglobulin levels may be used to select patients for imaging. The scanning protocol is similar to that used for preoperative assessment of the thyroid gland and regional lymph nodes. Meticulous comparison with prior sonograms, if available, is mandatory, especially when following indeterminate lesions and lymph nodes. To facilitate follow-up, the level of any abnormalities detected on the initial postoperative scan should be labeled using nodal levels. Documentation may be further refined by indicating a lesion’s distance from reproducible anatomic landmarks (e.g., “level III lymph node 1.5 cm lateral to common carotid artery.”) Additionally, real-time clips that encompass the lesion and its surroundings are useful for followup (Video 17.11).

The Thyroid Bed FIGURE 17.52 Head and Neck Cancer Metastasis. Transverse ultrasound of a left level III node (calipers) in a patient with squamous cell carcinoma shows a rounded shape and cystic change centrally (arrowhead). IJV, Internal jugular vein.

The normal thyroid bed, which refers to the space left after surgical resection of the thyroid gland or a part of it, is typically echogenic on transverse images (Fig. 17.53, Video

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C Tr

FIGURE 17.53 Normal Thyroid Bed. After thyroidectomy, the surgical bed (arrowheads) is often echogenic in the transverse plane. See Video 17.12. C, Common carotid artery; Tr, trachea.

17.12).198 Occasionally, surgical clips are evident as bright reflectors.199 Close approximation of the common carotid artery and the trachea confidently excludes recurrence at this site, but it is more common to see structures that have a variable sonographic appearance. A small amount of thyroid tissue left behind to preserve the recurrent laryngeal nerve may appear isoechoic or hypoechoic, but this is unusual in patients who have received radioiodine therapy.198,200 Other

nonpathologic findings include the thyroid and cricoid cartilages, cervical extension of the thymus, ganglia, nerve roots, and spinal transverse processes, which may be distinguished by their configuration or continuity with adjacent structures.198 Some ultrasound findings that mimic recurrent malignancy are related to the surgical procedure, and therefore appear early in the postoperative course. Echogenic material bordered by a thin, hypoechoic rim may represent Gelfoam.201 Similarly, perioperative hematomas that simulate a thyroid bed recurrence should be followed to resolution. Diverticula arising from the proximal esophagus sometimes simulate masses, but should be recognized by their gaseous content and motion.198 Finally, enlarged parathyroid glands may be mistaken for thyroid bed recurrence, but they should show characteristic peripheral vascularity on color Doppler imaging and be associated with clinical or laboratory abnormalities. Commonly, however, nonspecific nodules of varying echogenicity are present. The majority are clinically insignificant and remain stable over time. In a study of postoperative thyroid cancer patients, only the presence of minute calcifications was a significant predictor of malignancy. As well, only 0.2% of lesions that measured less than 6 mm were malignant, strongly suggesting that they can be safely ignored unless they contain PEF. Larger lesions may be followed with ultrasound or biopsied (Fig. 17.54).

ROLE OF ULTRASOUND IN TREATING THYROID NODULES Its superficial location makes the thyroid gland a primary candidate for treatment of nodules using percutaneous techniques. While these techniques were initially used to treat

C C

Tr Tr

A

B

FIGURE 17.54 Thyroid Bed Recurrence. Transverse ultrasounds of the left thyroid bed (A) at baseline and (B) 1 year later, showing recurrent thyroid carcinoma (calipers). C, Common carotid artery; Tr, trachea.

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A

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B

FIGURE 17.55 Ethanol Treatment of Large Colloid Cyst. (A) Transverse image shows a large colloid cyst with a needle in place. Injected ethanol appears as low-level echoes (E). Tr, Trachea. (B) Follow-up image 1 month later shows that the large cystic component has mostly resolved, leaving a residual nodule (arrows).

clinically significant benign nodules, there has been growing interest in applying them to thyroid cancers in patients who desire a nonsurgical alternative, as well as in treating metastatic cervical lymph nodes.202-204 Although a detailed consideration of indications and techniques is beyond the scope of this chapter, an understanding of basic principles, advantages, and disadvantages is helpful for radiologists, endocrinologists, surgeons, and others who deal with thyroid nodules.

Ethanol Ablation Ethanol ablation, which was initially developed to treat hepatocellular carcinoma, has since been used in a wide variety of clinical settings.203 A primary benefit is the lack of need for the specialized equipment required for other ablation techniques, potentially making it more widely available. Ethanol ablation is chiefly used for benign cystic or mostly cystic nodules that cause compressive symptoms or are cosmetically undesirable (Fig. 17.55).205,206 While relief may also be achieved by aspirating without injecting ethanol, the fluid tends to reaccumulate over time.207 In contrast, administration of ethanol into the cyst after aspiration leads to necrosis, inflammation, and fibrosis, preventing recurrence.207,208 Clinical results with ethanol ablation have been good, with an acceptable decrease in volume of the treated nodule and little or no periprocedural pain.205,206 This suggests that ethanol ablation should be recommended as a first-line therapy for selected benign cysts.209

Thermal Ablation This category, so named because of its reliance on heating of tissues, includes radiofrequency ablation (RFA), laser thermal ablation (LTA), and microwave ablation (MWA), as well as high-intensity focused ultrasound (HIFU).203,210 All four techniques require specialized equipment and training, and are therefore less cost-effective than ethanol ablation, but unlike ethanol ablation are applicable to solid thyroid nodules. The

efficacy of RFA for benign, nonfunctional nodules has been well established, with less evidence for LTA and MWA, and the least for HIFU.203 The role of thermal ablation for treating functional nodules is less clear but will likely be elucidated in the coming years. With the increasing recognition of the indolent nature of many PTCs and interest in offering active monitoring as an alternative to surgery, the potential role of thermal ablation in treating selected cancers has garnered interest.204 However, even if LTA turns out to be effective, careful preprocedural examination with ultrasound will be needed to search for multifocality and/or metastatic nodes. Currently, it is recommended that thermal ablation be considered for patients with papillary microcarcinoma who are unfit for or decline surgery or active monitoring.203

CONCLUSION Ultrasound is indispensable for evaluating the thyroid gland and cervical lymph nodes, and it serves as the foundation for RSSs for thyroid nodules. Sonography is also valuable to assess for thyroid cancer recurrence and to guide percutaneous biopsies and ablation procedures. In the coming years, application of newer techniques such as elastography and CEUS will ensure its continued preeminent role.

ACKNOWLEDGMENT The authors thank Drs. Luigi Solbiati, J. William Charboneau, Vito Cantisani, Carl Reading, and Giovanni Mauri for use of material from the previous edition of this chapter and Dr. Deborah Levine for use of ultrasound clips.

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Thyroid Gland and Cervical Lymph Node Sonography

143. Yoon JH, Lee HS, Kim EK, et al. Malignancy risk stratification of thyroid nodules: comparison between the Thyroid Imaging Reporting and Data System and the 2014 American Thyroid Association management guidelines. Radiology. 2016;278(3):917e924. 144. Middleton WD, Teefey SA, Reading CC, et al. Comparison of performance characteristics of American College of Radiology TI-RADS, Korean Society of Thyroid Radiology TIRADS, and American Thyroid Association guidelines. AJR Am J Roentgenol. 2018;210(5):1148e1154. 145. Middleton WD, Teefey SA. Reply to “Nonclassifiable nodules in Korean Society of thyroid Radiology TIRADS and size threshold of fine-needle aspiration”. AJR Am J Roentgenol. 2018;211(6):W304. 146. Ha SM, Baek JH, Na DG, et al. Diagnostic performance of practice guidelines for thyroid nodules: thyroid nodule size versus biopsy rates. Radiology. 2019;291(1):92e99. 147. Hoang JK, Middleton WD, Farjat AE, et al. Interobserver variability of sonographic features used in the American College of Radiology Thyroid Imaging Reporting and Data System. AJR Am J Roentgenol. 2018;211(1):162e167. 148. Griffin AS, Mitsky J, Rawal U, et al. Improved quality of thyroid ultrasound reports after implementation of the ACR Thyroid Imaging Reporting and Data System nodule lexicon and risk stratification system. J Am Coll Radiol. 2018;15(5):743e748. 149. Zhang F, Oluwo O, Castillo FB, et al. Thyroid nodule location on ultrasonography as a predictor of malignancy. Endocr Pract. 2019;25(2):131e137. 150. Ramundo V, Lamartina L, Falcone R, et al. Is thyroid nodule location associated with malignancy risk? Ultrasonography. 2019;38(3):231e235. 151. Jasim S, Baranski TJ, Teefey SA, Middleton WD. Investigating the effect of thyroid nodule location on the risk of thyroid cancer. Thyroid. 2020;30(3):401e407. 152. Lee YS, Jeong JJ, Nam KH, et al. Papillary carcinoma located in the thyroid isthmus. World J Surg. 2010;34(1):36e39. 153. Li G, Lei J, Peng Q, et al. Lymph node metastasis characteristics of papillary thyroid carcinoma located in the isthmus: a single-center analysis. Medicine (Baltim). 2017;96(24):e7143. 154. Chung J, Lee YJ, Choi YJ, et al. Clinical applications of Doppler ultrasonography for thyroid disease: consensus statement by the Korean Society of Thyroid Radiology. Ultrasonography. 2020;39(4):315e330. 155. Fang F, Gong Y, Liao L, et al. Value of contrast-enhanced ultrasound in partially cystic papillary thyroid carcinomas. Front Endocrinol. 2021;12:783670. 156. Xu Y, Qi X, Zhao X, et al. Clinical diagnostic value of contrast-enhanced ultrasound and TI-RADS classification for benign and malignant thyroid tumors: one comparative cohort study. Medicine (Baltim). 2019;98(4):e14051. 157. Wildman-Tobriner B, Buda M, Hoang JK, et al. Using artificial intelligence to revise ACR TI-RADS risk stratification of thyroid nodules: diagnostic accuracy and utility. Radiology. 2019;292(1):112e119. 158. Buda M, Wildman-Tobriner B, Hoang JK, et al. Management of thyroid nodules seen on US images: deep learning may match performance of radiologists. Radiology. 2019;292(3):695e701. 159. Taha I, Al-Thani H, El-Menyar A, et al. Diagnostic accuracy of preoperative palpation-versus ultrasound-guided thyroid fine needle aspiration cytology: an observational study. Postgrad Med. 2020;132(5):465e472. 160. Patel IJ, Rahim S, Davidson JC, et al. Society of Interventional Radiology consensus guidelines for the periprocedural management of thrombotic and bleeding risk in patients undergoing percutaneous image-guided interventions-Part II: recommendations: endorsed by the Canadian Association for Interventional Radiology and the Cardiovascular and Interventional Radiological Society of Europe. J Vasc Interv Radiol. 2019;30(8):1168e1184.e1161. 161. Crockett JC. The thyroid nodule: fine-needle aspiration biopsy technique. J Ultrasound Med. 2011;30(5):685e694. 162. Zheng BW, Wu T, Xu SC, et al. Acute transient swelling of the thyroid following fine-needle aspiration: a case series. J Clin Ultrasound. 2021. 163. Joo L, Na DG, Kim JH, Seo H. Comparison of core needle biopsy and repeat fine-needle aspiration in avoiding diagnostic surgery for thyroid nodules initially diagnosed as atypia/follicular lesion of undetermined significance. Korean J Radiol. 2022;23(2):280e288.

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164. Cibas ES, Ali SZ. The 2017 Bethesda system for reporting thyroid cytopathology. Thyroid. 2017;27(11):1341e1346. 165. Baloch ZW, Tam D, Langer J, et al. Ultrasound-guided fine-needle aspiration biopsy of the thyroid: role of on-site assessment and multiple cytologic preparations. Diagn Cytopathol. 2000;23(6):425e429. 166. Eloy C, Russ G, Suciu V, et al. Preoperative Diagnosis of Thyroid Nodules: An Integrated Multidisciplinary Approach. Cancer Cytopathol; 2022. 167. Killock D. Genetics: the Cancer Genome Atlas maps papillary thyroid cancer. Nat Rev Clin Oncol. 2014;11(12):681. 168. Hsiao SJ, Nikiforov YE. Molecular approaches to thyroid cancer diagnosis. Endocr Relat Cancer. 2014;21(5):T301eT313. 169. Haroon Al Rasheed MR, Xu B. Molecular alterations in thyroid carcinoma. Surg Pathol Clin. 2019;12(4):921e930. 170. Poller DN, Glaysher S. Molecular pathology and thyroid FNA. Cytopathology. 2017;28(6):475e481. 171. Nishino M, Bellevicine C, Baloch Z. Molecular tests for risk-stratifying cytologically indeterminate thyroid nodules: an overview of commercially available testing platforms in the United States. J Mol Pathol. 2021;2:135e146. 172. Livhits MJ, Zhu CY, Kuo EJ, et al. Effectiveness of molecular testing techniques for diagnosis of indeterminate thyroid nodules: a randomized clinical trial. JAMA Oncol. 2021;7(1):70e77. 173. Nicholson KJ, Roberts MS, McCoy KL, et al. Molecular testing versus diagnostic lobectomy in Bethesda III/IV thyroid nodules: a costeffectiveness analysis. Thyroid. 2019;29(9):1237e1243. 174. Ying M, Ahuja A. Sonography of neck lymph nodes. Part I: normal lymph nodes. Clin Radiol. 2003;58(5):351e358. 175. Som PM, Curtin HD, Mancuso AA. Imaging-based nodal classification for evaluation of neck metastatic adenopathy. AJR Am J Roentgenol. 2000;174(3):837e844. 176. Chasen NN, Wang JR, Gan Q, Ahmed S. Imaging of cervical lymph nodes in thyroid cancer ultrasound and computed tomography. Neuroimag Clin N Am. 2021;31:313e326. 177. Leenhardt L, Erdogan MF, Hegedus L, et al. 2013 European Thyroid Association guidelines for cervical ultrasound scan and ultrasound-guided techniques in the postoperative management of patients with thyroid cancer. Eur Thyroid J. 2013;2(3):147e159. 178. Prativadi R, Dahiya N, Kamaya A, Bhatt S. Chapter 5 Ultrasound characteristics of benign vs malignant cervical lymph nodes. Semin Ultrasound CT MR. 2017;38(5):506e515. 179. Steinkamp HJ, Cornehl M, Hosten N, et al. Cervical lymphadenopathy: ratio of long- to short-axis diameter as a predictor of malignancy. Br J Radiol. 1995;68(807):266e270. 180. Kim J, Park J, Park H, et al. Metastatic lymph node ratio for predicting recurrence in medullary thyroid cancer. Cancers. 2021;13(22). 181. Yoo RE, Kim JH, Bae JM, et al. Ultrasonographic indeterminate lymph nodes in preoperative thyroid cancer patients: malignancy risk and ultrasonographic findings predictive of malignancy. Korean J Radiol. 2020;21(5):598e604. 182. Hwang HS, Orloff LA. Efficacy of preoperative neck ultrasound in the detection of cervical lymph node metastasis from thyroid cancer. Laryngoscope. 2011;121(3):487e491. 183. Hu M, Xia C, Zhou Y, et al. Ultrasound surveillance of abnormal cervical lymph nodes in patients with papillary thyroid carcinoma after surgery. J Ultrasound Med. 2021;40(1):29e37. 184. Adam MA, Pura J, Goffredo P, et al. Presence and number of lymph node metastases are associated with compromised survival for patients younger than age 45 Years with papillary thyroid cancer. J Clin Oncol. 2015;33(21):2370e2375. 185. Zhao H, Li H. Meta-analysis of ultrasound for cervical lymph nodes in papillary thyroid cancer: diagnosis of central and lateral compartment nodal metastases. Eur J Radiol. 2019;112:14e21. 186. Stuckensen T, Kovacs AF, Adams S, Baum RP. Staging of the neck in patients with oral cavity squamous cell carcinomas: a prospective comparison of PET, ultrasound, CT and MRI. J Craniomaxillofac Surg. 2000;28(6):319e324. 187. Ahuja AT, Ying M, Ho SY, et al. Ultrasound of malignant cervical lymph nodes. Cancer Imag. 2008;8:48e56.

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188. Ahuja AT, Ying M, Yuen HY, Metreweli C. ‘Pseudocystic’ appearance of non-Hodgkin’s lymphomatous nodes: an infrequent finding with highresolution transducers. Clin Radiol. 2001;56(2):111e115. 189. Moon IS, Kim DW, Baek HJ. Ultrasound-based diagnosis for the cervical lymph nodes in a tuberculosis-endemic area. Laryngoscope. 2015;125(5):1113e1117. 190. Kanagaraju V, Rakshith AVB, Devanand B, Rajakumar R. Utility of ultrasound elastography to differentiate benign from malignant cervical lymph nodes. J Med Ultrasound. 2020;28(2):92e98. 191. Xiang D, Hong Y, Zhang B, et al. Contrast-enhanced ultrasound (CEUS) facilitated US in detecting lateral neck lymph node metastasis of thyroid cancer patients: diagnosis value and enhancement patterns of malignant lymph nodes. Eur Radiol. 2014;24(10):2513e2519. 192. Li QL, Ma T, Wang ZJ, et al. The value of contrast-enhanced ultrasound for the diagnosis of metastatic cervical lymph nodes of papillary thyroid carcinoma: a systematic review and meta-analysis. J Clin Ultrasound. 2022;50(1):60e69. 193. Rizzo S, Botta F, Raimondi S, et al. Radiomics: the facts and the challenges of image analysis. Eur Radiol Exp. 2018;2(1):36. 194. Yu J, Deng Y, Liu T, et al. Lymph node metastasis prediction of papillary thyroid carcinoma based on transfer learning radiomics. Nat Commun. 2020;11(1):4807. 195. Zhou SC, Liu TT, Zhou J, et al. An ultrasound radiomics nomogram for preoperative prediction of central neck lymph node metastasis in papillary thyroid carcinoma. Front Oncol. 2020;10:1591. 196. Verburg FA, Mader U, Giovanella L, et al. Low or undetectable basal thyroglobulin levels obviate the need for neck ultrasound in differentiated thyroid cancer patients after total thyroidectomy and (131)I ablation. Thyroid. 2018;28(6):722e728. 197. Epstein S, McEachern R, Khot R, et al. Papillary thyroid carcinoma recurrence: low yield of neck ultrasound with an undetectable serum thyroglobulin level. J Ultrasound Med. 2018;37(10):2325e2331. 198. Chua WY, Langer JE, Jones LP. Surveillance neck sonography after thyroidectomy for papillary thyroid carcinoma: pitfalls in the diagnosis of locally recurrent and metastatic disease. J Ultrasound Med. 2017;36(7):1511e1530. 199. Grant EG, Malhi H. The post-thyroidectomy US examination: less may be more. Radiology. 2021;299(2):381e382. 200. Shin JH, Han BK, Ko EY, Kang SS. Sonographic findings in the surgical bed after thyroidectomy: comparison of recurrent tumors and nonrecurrent lesions. J Ultrasound Med. 2007;26(10):1359e1366. 201. Tublin ME, Alexander JM, Ogilvie JB. Appearance of absorbable gelatin compressed sponge on early post-thyroidectomy neck sonography: a mimic of locally recurrent or residual thyroid carcinoma. J Ultrasound Med. 2010;29(1):117e120.

202. Frich PS, Sigstad E, Berstad AE, et al. Long-term efficacy of ethanol ablation as treatment of metastatic lymph nodes from papillary thyroid carcinoma. J Clin Endocrinol Metab. 2021. 203. Orloff LA, Noel JE, Stack Jr BC, et al. Radiofrequency ablation and related ultrasound-guided ablation technologies for treatment of benign and malignant thyroid disease: an international multidisciplinary consensus statement of the American Head and Neck Society Endocrine Surgery Section with the Asia Pacific Society of Thyroid Surgery, Associazione Medici Endocrinologi, British Association of Endocrine and Thyroid Surgeons, European Thyroid Association, Italian Society of Endocrine Surgery Units, Korean Society of Thyroid Radiology, Latin American Thyroid Society, and Thyroid Nodules Therapies Association. Head Neck. 2022;44(3):633e660. 204. Kim HJ, Chung SM, Kim H, et al. Long-term efficacy of ultrasound-guided laser ablation for papillary thyroid microcarcinoma: results of a 10-year Retrospective study. Thyroid. 2021;31(11):1723e1729. 205. Reverter JL, Vazquez F, Puig-Jove C, et al. Long-term efficacy evaluation of a protocol for the management of symptomatic thyroid cysts with ultrasound-guided percutaneous ethanol injection. Endocrinol Diabetes Nutr (Engl Ed). 2021;68(4):236e242. 206. Merchante Alfaro AA, Garzon Pastor S, Perez Naranjo S, et al. Percutaneous ethanol injection therapy as the first line of treatment of symptomatic thyroid cysts. Endocrinol Diabetes Nutr (Engl Ed). 2021;68(7):458e464. 207. Papini E, Pacella CM, Hegedus L. Diagnosis of endocrine disease: thyroid ultrasound (US) and US-assisted procedures: from the shadows into an array of applications. Eur J Endocrinol. 2014;170(4):R133eR146. 208. Monzani F, Caraccio N, Basolo F, et al. Surgical and pathological changes after percutaneous ethanol injection therapy of thyroid nodules. Thyroid. 2000;10(12):1087e1092. 209. Gharib H, Papini E, Garber JR, et al. American Association of Clinical Endocrinologists, American College of Endocrinology, and Associazione Medici Endocrinologi medical guidelines for clinical practice for the diagnosis and management of thyroid nodulesd2016 update. Endocr Pract. 2016;22(5):622e639. 210. Papini E, Monpeyssen H, Frasoldati A, Hegedus L. 2020 European Thyroid Association clinical practice guideline for the use of image-guided ablation in benign thyroid nodules. Eur Thyroid J. 2020;9(4):172e185. 211. Perros P, Boelaert K, Colley S, et al. Guidelines for the management of thyroid cancer. Clin Endocrinol (Oxf). 2014;81(suppl 1):1e122. 212. Patel SG, Carty SE, Lee AJ. Molecular testing for thyroid nodules including its interpretation and Use in clinical practice. Ann Surg Oncol. 2021;28(13):8884e8891. 213. Nylen C, Mechera R, Marechal-Ross I, et al. Molecular markers guiding thyroid cancer management. Cancers (Basel). 2020;12(8).

CHAPTER

18

Other Glands in the Head and Neck Mary E. Cunnane and Boris Bulat Kumaev

CHAPTER OUTLINE PARATHYROID EMBRYOLOGY AND ANATOMY, 731 Primary Hyperparathyroidism, 732 Sonographic Appearance, 734 Adenoma Localization, 736 Persistent or Recurrent Hyperparathyroidism, 740 Secondary Hyperparathyroidism, 742 Pitfalls in Interpretation, 743

Accuracy in Imaging, 745 Intraoperative Sonography, 749 Percutaneous Biopsy, 750 SALIVARY GLANDS, 752 Salivary Gland Embryology and Anatomy, 752 Sonographic Examination and Sonographic Appearance, 753 Obstructive Disease, 753

H

igh-frequency sonography is a well-established, noninvasive imaging method used in the evaluation and treatment of patients with parathyroid disease. Sonography is often used for the preoperative localization of enlarged parathyroid glands or adenomas in patients with hyperparathyroidism. Ultrasound is also used to guide the percutaneous biopsy of suspected parathyroid adenomas or enlarged glands, particularly in patients with persistent or recurrent hyperparathyroidism, as well as in some patients with suspected ectopic glands. This chapter also discusses ultrasound in assessment of the salivary glands.

PARATHYROID EMBRYOLOGY AND ANATOMY The paired superior and inferior parathyroid glands have different embryologic origins, and knowledge of their development aids in understanding their ultimate anatomic locations.1-3 The superior parathyroid glands arise from the paired fourth branchial pouches (clefts), along with the lateral lobes of the thyroid gland. Minimal migration occurs during fetal development, and the superior parathyroids usually remain associated with the posterior aspect of the middle to upper portion of the thyroid gland. The majority of superior

Acute and Chronic Sialadenitis, 754 Noninfectious Causes of Sialadenitis, 755 Salivary Gland Tumors, 756 CONCLUSION, 761 ACKNOWLEDGMENT, 761 REFERENCES, 761

parathyroid glands (>80%) are found at autopsy within a 2-cm area located just superior to the crossing of the recurrent laryngeal nerve and the inferior thyroid artery.4 The inferior parathyroid glands arise from the paired third branchial pouches, along with the thymus.2 During fetal development, these “parathymus glands” migrate caudally along with the thymus in a more anterior plane than their superior counterparts, bypassing the superior glands to become the inferior parathyroid glands.3 Because of their greater caudal migration, the inferior parathyroid glands are more variable in location than the superior glands and can be found anywhere from the angle of the mandible to the pericardium. The majority of inferior parathyroid glands (>60%) come to rest at or just inferior to the posterior aspect of the lower pole of the thyroid1,4,5 (Fig. 18.1). A substantial percentage of parathyroid glands lie in relatively or frankly ectopic locations in the neck or mediastinum. The ectopic superior parathyroid gland usually lies posterior to the esophagus or in the tracheoesophageal groove, in the retropharyngeal space, or has continued its descent from the posterior neck into the posterosuperior mediastinum.6-8 Superior glands are less often found higher in the neck, near the superior extent of the thyroid, or, in rare cases, surrounded by thyroid tissue within the thyroid capsule.4 The inferior parathyroid gland is more frequently ectopic than its superior

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PART THREE

counterpart.4,7,8 About 25% of the inferior glands fail to completely dissociate from the thymus and continue to migrate in an anterocaudal direction and are found in the low neck along the thyrothymic ligament or embedded within or adjacent to the thymus in the low neck and anterosuperior mediastinum. Less common ectopic positions of the inferior parathyroid glands include an undescended position high in the neck anterior to the carotid bifurcation associated with a remnant of thymus, and lower in the neck along or within the carotid sheath.6,8 In other rare cases, ectopic glands have also been reported in the mediastinum posterior to the esophagus or carina, in the aortopulmonic window, within the pericardium, or even far laterally within the posterior triangle of the neck. Most adults have four parathyroid glands, two superior and two inferior, each measuring about 5  3  1 mm and weighing on average 35-40 mg (range, 10-78 mg).3,9 Supernumerary glands (>4) may be present and result from the separation of

Superior Parathyroids

Inferior Parathyroids

9%

2%

74 %

7%

6% 6%

1%

5%

2%

7%

54 %

2%

13% 7% 1% 1%

T

T

cm below lower pole

parathyroid anlage when the glands pull away from the pouch structures during the embryologic branchial complex phase.10,11 These supernumerary glands are often associated with the thymus in the anterior mediastinum, suggesting a relationship in their development with the inferior parathyroid glands.12 Supernumerary glands have been reported in 13% of the population at autopsy studies3,4; however, many of these are small, rudimentary or split glands. “Proper” supernumerary glands (>5 mg and located well away from the other four glands) are found in 5% of patients. The presence of fewer than four parathyroid glands is rare clinically but has been reported in 3% at autopsy. Normal parathyroid glands vary from a yellow to a redbrown color, depending on the degree of vascularity and the relative content of yellow parenchymal fat and chief cells.9 The chief cells are the primary source for the production of parathyroid hormone (PTH, parathormone). The percentage of glandular fat typically increases with age or with disuse atrophy. Hyperfunctioning glands resulting from adenomas or hyperplasia contain relatively little fat and are vascular, thus more reddish. The glands are generally ovoid or bean shaped but may be spherical, lobular, elongated, or flattened. Until recently, it has been difficult to identify normal parathyroid glands, because of their small size, deep location, and poor conspicuity related to increased glandular fat. However, as higher-frequency transducers become more available, it has become possible to appreciate normal parathyroids in some patients, particularly using intraoperative ultrasound. On ultrasound, normal parathyroid glands are hyperechoic and bean shaped with smooth margins13,14 (Fig. 18.2). Eutopic parathyroid glands typically derive their major blood supply from branches of the inferior thyroid artery, with a lesser and variable contribution to the superior glands from the superior thyroid artery.3,6

Not over:

Primary Hyperparathyroidism

0.5 cm

Prevalence Primary hyperparathyroidism is a common endocrine disease, with prevalence in the United States of 1-2 per 1000 population.15 Women are affected two to three times more frequently than men, particularly after menopause. Incidence increases with increasing age and hyperparathyroidism is more common in non-whites.16 More than half of patients with primary hyperparathyroidism are older than 50 years, and cases are rare in those younger than age 20.

1.0 cm 2.0 cm 3.0 cm 4.0 cm

MAYO 1987

FIGURE 18.1 Location of Parathyroid Glands. Frequency of the location of normal superior and inferior parathyroid glands. Anatomic drawing from 527 autopsies. T, Thymus. (Modified from Gilmour J. The gross anatomy of the parathyroid glands. J Pathol. 1938;46:133e148.1)

Diagnosis Primary hyperparathyroidism is usually suspected because an increased serum calcium level is detected on routine biochemical screening. Elevated ionized serum calcium level,

CHAPTER 18 Other Glands in the Head and Neck

A

733

B

FIGURE 18.2 Normal Parathyroid Gland. (A) Longitudinal and (B) transverse images demonstrate a hyperechoic oval nodule inferior to the lower pole of the left thyroid lobe in the expected location of an inferior parathyroid gland in this patient without hyperparathyroidism.

hypophosphatasia, and hypercalciuria are further biochemical clues to the disease. A serum PTH level that is “inappropriately high” for the corresponding serum calcium level confirms the diagnosis. Even when the PTH level is within the upper limits of the normal range in a hypercalcemic patient, the diagnosis of primary hyperparathyroidism should still be suspected, since hypercalcemia from a non-parathyroid cause (including malignancy) can suppress the glandular function and decrease the serum PTH level. Because of earlier detection by increasingly routine laboratory tests, the later “classic” signs of hyperparathyroidism, such as “painful bones, renal stones, abdominal groans, and psychic moans,” are often not present. Many patients are diagnosed before severe manifestations of hyperparathyroidism, such as nephrolithiasis, osteopenia, subperiosteal resorption, and osteitis fibrosis cystica. In general, patients rarely have obvious symptoms unless their serum calcium level exceeds 12 mg/dL. However, subtle nonspecific symptoms, such as muscle weakness, malaise, constipation, dyspepsia, polydipsia, and polyuria, may be elicited from these otherwise asymptomatic patients by more specific questioning.

Pathology Primary hyperparathyroidism is caused by a single adenoma in 80% to 90% of cases, by multiple gland enlargement in 10% to 20%, and by carcinoma in less than 1%.7,17,18 A solitary adenoma may involve any one of the four glands. Multi-gland enlargement most often results from primary parathyroid hyperplasia and less often from multiple adenomas. Hyperplasia usually involves all four glands asymmetrically, whereas multiple adenomas may involve two or possibly three glands. An adenoma and hyperplasia cannot always be reliably distinguished histologically, and the sample may be referred to as “hypercellular parathyroid” tissue. Because of this inconsistent pattern of gland involvement, and because distinguishing hyperplasia from multiple adenomas is difficult histologically,

these two entities are often histologically considered together as “multiple gland disease.”19

Causes of Primary Hyperparathyroidism Type of Disease

Percentage

Single adenoma Multiple gland disease Carcinoma

80% to 90% 10% to 20% 14 mg/dL). The diagnosis is often made at operation when the surgeon discovers an enlarged, firm gland that is adherent to the surrounding tissues due to local invasion. A thick, fibrotic capsule is often present. Treatment consists of en bloc resection without entering the capsule, to prevent tumor seeding. In many cases, cure is not possible because of the invasive and metastatic nature of the disease. Generally, death occurs not from tumor spread but from complications associated with unrelenting hyperparathyroidism.

Treatment No effective definitive medical therapies are available for the treatment of primary hyperparathyroidism. Medications used include short-term hypocalcemic agents such as calcitonin and calcimimetics (calcium-sensing receptor agonists) such as cinacalcet. The bisphosphonates aid in preventing bone mass loss. Synthetic vitamin D analogs such as paricalcitol are mainly used in the treatment of secondary hyperparathyroidism. Surgery is the only definitive treatment for primary hyperparathyroidism. Studies demonstrate that surgical cure rates by an experienced surgeon are greater than 95%, and the morbidity and mortality rates are extremely low.25,26 Therefore, in symptomatic patients with primary hyperparathyroidism, the treatment of choice is surgical excision of the involved parathyroid gland(s). However, since in current practice most cases of primary hyperparathyroidism are discovered in the early stages of the disease, some controversy exists as to whether asymptomatic patients with minimal hypercalcemia should be treated surgically or followed medically with frequent measurements of bone density, serum calcium levels, and urinary calcium excretion and monitoring for nephrolithiasis.27 Recommendations for the management of asymptomatic primary hyperparathyroidism have been outlined in various articles, many of which are based

T

Tr

on International Workshop and National Institutes of Health Consensus Conference statements and subsequent updates. This area continues to evolve, and approaches to treatment may differ slightly among clinical practices.25-32

Sonographic Appearance Shape Parathyroid adenomas are typically ovoid or bean shaped (Fig. 18.3). As parathyroid glands enlarge, they dissect between longitudinally oriented tissue planes in the neck and acquire a characteristic oblong shape. If this process is exaggerated, they can become tubular or flattened (Fig. 18.4). There is often asymmetry in the enlargement, and the cephalic and/or caudal end can be more bulbous, producing a triangular, tapering, teardrop, or bilobed shape.21,33-35 Echogenicity and Internal Architecture The echogenicity of most parathyroid adenomas is substantially less than that of normal thyroid tissue (Fig. 18.5). The characteristic hypoechoic appearance of parathyroid adenomas is caused by the uniform hypercellularity of the gland with little fat content, which leaves few interfaces for reflecting sound. Occasionally, adenomas have a heterogeneous appearance, with

FIGURE 18.4 Elongated Parathyroid Adenoma. A hypoechoic parathyroid adenoma (arrows) has grown longitudinally in the tissue planes, to acquire a tubular appearance posterior to the thyroid gland. An inferior pole thyroid nodule is incidentally noted.

T

T

T

C

J C

A

B

FIGURE 18.3 Typical Parathyroid Adenoma. (A) Transverse and (B) longitudinal sonograms of a typical adenoma (arrows) located adjacent to the posterior aspect of the thyroid (T). C, Common carotid artery; J, internal jugular vein; Tr, trachea.

CHAPTER 18 Other Glands in the Head and Neck

A

B

735

C

T T J

D

E

F

T

T

T

G

H

I

FIGURE 18.5 Spectrum of Echogenicity and Internal Architecture of Parathyroid Adenomas and Enlarged Hyperplastic Glands. Longitudinal sonograms. (A) Typical homogeneous hypoechoic appearance of a parathyroid adenoma (arrows) with respect to the overlying thyroid tissue. (B) Highly hypoechoic solid adenoma. (C) Mixed-geographic echogenicity. The adenoma is hyperechoic in its cranial portion and hypoechoic in its caudal portion. (D) An adenoma with diffusely heterogeneous echogenicity. (E) Partial cystic change. An ectopic adenoma posterior to the jugular vein (J) has both solid and cystic components. (F) Completely cystic 2-cm adenoma (calipers) near the lower pole of the thyroid (T). See also Video 18.1. (G) A lipoadenoma is more echogenic than the adjacent lower pole thyroid tissue. (H) Enlarged parathyroid gland with small, non-shadowing calcifications in the setting of secondary hyperparathyroidism related to chronic renal failure. (I) Enlarged parathyroid gland with densely shadowing peripheral calcifications in the setting of secondary hyperparathyroidism.

areas of increased and decreased echogenicity. The rare, functioning parathyroid lipoadenomas are more echogenic than the adjacent thyroid gland because of their high fat content36 (see Fig.18.5G). A great majority of parathyroid adenomas are homogeneously solid. About 2% have cystic degeneration (most often) or true simple cysts (less often)37-39 (see Fig. 18.5E and F,

Video 18.1). Adenomas may rarely contain internal calcification (see Fig. 18.5H and I).

Vascularity Color flow, spectral, and power Doppler sonography of an enlarged parathyroid gland may demonstrate a hypervascular

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pattern with prominent diastolic flow. An enlarged extrathyroidal artery, often originating from branches of the inferior thyroidal artery, may be visualized supplying the adenoma with its insertion along the long-axis pole.39-44 A finding described in parathyroid adenomas is a vascular arc, which envelops 90-270 degrees of the mass (Fig. 18.6). This vascular flow pattern may increase the sensitivity of initial detection of parathyroid adenomas and aid in confirming the diagnosis by allowing for differentiation from lymph nodes, which have a central hilar flow pattern. Asymmetric increased vascular flow may also be present in the thyroid gland adjacent to a parathyroid adenoma.

Size Most parathyroid adenomas are 0.8-1.5 cm long and weigh 5001000 mg. The smallest adenomas can be minimally enlarged glands that appear virtually normal during surgery but are found to be hypercellular on histologic examination (Fig. 18.7, Video 18.2). Large adenomas can be 5 cm or more in length and

weigh more than 10 g. Preoperative serum calcium levels are usually higher in patients with larger adenomas.33,45,46

Multiple Gland Disease Multiple gland disease (MGD) may be caused by diffuse hyperplasia or multiple adenomas. Individually, these enlarged glands may have the same sonographic and gross appearance as other parathyroid adenomas (Fig. 18.8, Videos 18.3 and 18.4). However, the glands may be inconsistently and asymmetrically enlarged, and the diagnosis of multi-gland disease can be difficult to make sonographically. For example, if one gland is much larger than the others, the appearance may be misinterpreted as a solitary adenoma. Alternatively, if multiple glands are only minimally enlarged, the diagnosis could be missed altogether. On four-dimensional computed tomography (4DCT), size of the largest parathyroid candidate can be used, in combination with lab values, to suggest the possibility of single versus MGD, using the 4D-CT MGD score.45,46 However, no similar validated scoring system exists for ultrasound at this time. Carcinoma Parathyroid carcinomas are usually larger than adenomas,47-49 often measuring more than 2 cm compared with about 1 cm for adenomas (Fig. 18.9). On ultrasound, carcinomas also frequently have a lobular contour, heterogeneous internal architecture, and internal cystic components. However, large adenomas can also have these features. In many instances, carcinomas are indistinguishable sonographically from large, benign adenomas.48 Some authors report that a depth-to-width ratio of 1 or greater is a sonographic feature more associated with carcinoma than with adenoma, with sensitivity and specificity of 94% and 95%, respectively.49 Gross evidence of invasion of adjacent structures, such as vessels or muscles, is a reliable preoperative sonographic criterion for the diagnosis of malignancy, but this is an uncommon finding.

Adenoma Localization FIGURE 18.6 Typical Hypervascularity of Parathyroid Adenoma. Longitudinal color Doppler ultrasound images show hypervascularity of a parathyroid adenoma with polar feeding vessel and prominent peripheral vascular arc.

A

B

Sonographic Examination and Typical Locations The sonographic examination of the neck for parathyroid adenoma localization is performed with the patient supine. The patient’s neck is hyperextended by a pad centered under the

C

FIGURE 18.7 Spectrum of Size of Parathyroid Adenomas. Longitudinal sonograms. (A) Minimally enlarged, 0.5  0.2ecm parathyroid adenoma (calipers). See also Video 18.2. (B) Typical midsized, 1.5  0.6ecm, 400-mg adenoma (arrow). (C) Large, 3.5  2ecm, greater than 4000-mg adenoma (calipers).

CHAPTER 18 Other Glands in the Head and Neck

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FIGURE 18.8 Multiple Gland Disease. (A) Longitudinal sonogram of the right neck shows superior and inferior parathyroid gland enlargement (arrows) in the setting of secondary hyperparathyroidism, which can be difficult to distinguish from multiple adenomas. T, Thyroid. (B) Transverse sonogram in another patient shows enlargement of bilateral superior parathyroid glands in the setting of secondary hyperparathyroidism. C, Common carotid artery; Tr, trachea. See also Videos 18.3 and 18.4.

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FIGURE 18.9 Parathyroid Carcinoma. (A) Longitudinal sonogram shows heterogeneous 4-cm parathyroid carcinoma (arrow) located near tip of lower pole of the left thyroid lobe (T). (B) Transverse sonogram with color Doppler flow imaging shows prominent internal vascularity of the carcinoma. C, Common carotid artery. (C) Longitudinal sonogram in another patient shows lobulated, solid and cystic, 4-cm parathyroid carcinoma (arrows) adjacent to the lower pole of the thyroid. (D) Longitudinal sonogram in another patient shows a 3-cm heterogeneous solid low-grade parathyroid carcinoma (calipers) with irregular lobulated margins (arrows) posterior to the thyroid.

T

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scapulae, and the examiner usually sits at the patient’s head. High-frequency transducers (6-15 MHz and 8-18 MHz) are used to provide optimal spatial resolution and visualization in most patients; the highest frequency possible should be used that still allows for tissue penetration to visualize the deeper structures, such as the longus colli muscles. In obese patients with thick necks or with large multinodular thyroid glands, use of a 5- to 8-MHz transducer may be necessary to obtain adequate depth of penetration.

D

The pattern of the sonographic survey of the neck for adenoma localization can be considered in terms of the pattern of dissection and visualization that the surgeon uses in a thorough neck exploration. The typical superior parathyroid adenoma is usually adjacent to the posterior aspect of the midportion of the thyroid (Fig. 18.10, Videos 18.5 and 18.6). The location of the typical inferior parathyroid adenoma is more variable but usually lies close to the lower pole of the thyroid (Fig. 18.11, Videos 18.7 and 18.8). Most of these inferior adenomas are

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FIGURE 18.10 Superior Parathyroid Adenoma. (A) Longitudinal and (B) transverse sonograms show an adenoma (arrows) adjacent to the posterior aspect of the midportion of the left lobe of the thyroid (T). C, Common carotid artery; E, esophagus; Tr, trachea. See also Videos 18.5 and 18.6.

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FIGURE 18.11 Inferior Parathyroid Adenoma. (A) Longitudinal and (B) transverse sonograms show an adenoma (arrows) adjacent to lower pole of right lobe of the thyroid (T). C, Common carotid artery; Tr, trachea. See also Videos18.7 and 18.8.

A

adjacent to the posterior aspect of the lower pole of the thyroid, and the rest are in the soft tissues 1-2 cm inferior to the thyroid. Therefore, the examination is initiated on one side of the neck, centered in the thyroid gland, with the focal zone placed deep to the thyroid. High-resolution gray-scale images are obtained in the transverse and longitudinal planes. Any potential parathyroid adenomas detected in the transverse scan plane must be confirmed by longitudinal imaging to prevent mistaking other structures for an adenoma. Some authors recommend the use of compression of the superficial soft tissues to aid in adenoma detection.43,50,51 This has been described as “graded” compression with the transducer to effect minimal deformity of the overlying subcutaneous tissues and strap muscles and increase the conspicuity of deeper, smaller adenomas (2%e10% >10%e50% >50%e50% sonolucent) Type 3: Predominantly echogenic with small areas of echolucency (95%),

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FIGURE 24.19 Internal Carotid Artery (ICA) Stenosis. (A) ICA stenosis of 50% to 69% diameter shows a peak systolic velocity (PSV) of 187 cm/s. (B) Left ICA demonstrates a visible high-grade stenosis on color Doppler with end diastolic velocities (EDVs) of greater than 180 cm/s and PSVs that alias at greater than 350 cm/s. This is consistent with a very high-grade stenosis. (C) Right carotid bulb seen in longitudinal projection with color Doppler demonstrates a high-grade narrowing and spectral broadening with an approximately 500 cm/s velocity in peak systole and 250 cm/s in end diastole, consistent with an 80% to 95% stenosis. (D) and (E) Power transverse and long images demonstrate high-grade stenosis of the ICA.

the velocity measurements may actually decrease, and the waveform becomes dampened.99,108 In these cases, correlation with color or power Doppler imaging is essential to diagnose correctly the severity of the stenoses. Velocity increases are focal and most pronounced in and immediately distal to a stenosis, emphasizing the importance of sampling directly in these regions. Moving further distal from a stenosis, flow begins to reconstitute and assume a more normal pattern, provided a tandem lesion does not exist distal to the initial site of stenosis. Spectral broadening results in the jets of high-velocity flow associated with carotid stenosis; however, correlation with gray-scale and color Doppler images can define other causes of spectral broadening. An awareness of normal flow spectra combined with appropriate Doppler techniques can obviate many potential diagnostic pitfalls. The degree of carotid stenosis that is considered clinically significant in the symptomatic or asymptomatic patient is in evolution. Initially, it was thought that lesions causing 50% diameter stenosis were significant; this perception changed as more information was gathered from two large clinical trials. As noted earlier, NASCET demonstrated that CEA was more beneficial than medical therapy in symptomatic patients with 70% to 99% ICA stenosis.7 ECST demonstrated a CEA benefit when the degree of stenosis was greater than 60%.8

Interestingly, the method used to grade stenoses in the ECST study was substantially different than that used in the NASCET trials. The NASCET trials compared the severity of the ICA stenosis on arteriogram with the residual lumen of a presumably more normal distal ICA. The ECST methodology entailed an assessment of the severity of stenosis with a “guesstimation” of the lumen of the carotid artery at the level of the stenosis. The ECST assessment is more comparable to ultrasound’s visible assessment of the degree of narrowing, whereas velocity tables currently in use have been derived to correspond to the NASCET angiographic determinations for stenosis. The ECST method for grading carotid artery stenosis tends to give a more severe assessment of narrowing than the NASCET technique (Fig. 24.20). The initial NASCET trials retrospectively compared velocity data obtained on the Doppler examination with angiographic measurements of stenosis. No standardized ultrasound protocol was employed by the numerous centers involved in the trials. Despite the lack of uniformity, moderate sensitivity and specificity ranging from 65% to 77% were obtained for grading ICA stenoses using Doppler velocities. If the ultrasound technique is standardized and criteria are validated in a given laboratory, peak systolic velocity (PSV) and peak systolic ratios have proved to be an accurate method for determining carotid stenosis.109 The ECST group compared three

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CCA FIGURE 24.20 Comparative Measurement Methodology. Different methodologies for grading internal carotid artery stenoses, from the North American Symptomatic Carotid Endarterectomy Trial (NASCET),7 Asymptomatic Carotid Atherosclerosis Study (ACAS),4 and European Carotid Surgery Trial (ECST).8 CCA, Common carotid artery; ECA, external carotid artery; ICA, internal carotid artery.

different angiographic measurement techniques: the NASCET, the ECST, and a technique comparing distal CCA measurements with those of ICA stenosis. Researchers concluded that the ECST and NASCET techniques were similar in their prognostic value, whereas the CCA/stenosis measurement was the most reproducible of the three techniques. They also concluded that the CCA method, although reproducible, would be invalidated by the presence of CCA disease.110 Virtually all investigators advocate using the NASCET angiographic measurement technique. The results of these trials, as well as the ACAS and moderate NASCET studies, generated reappraisals of the Doppler velocity criteria that most accurately define 70% or greater stenosis and, more recently, greater than 50% diameter stenoses.111 Attempts have been made to determine the Doppler parameters or combination of parameters that most reliably identify a certaindiameter stenosis. Most sources agree that the best parameter is the PSV of the ICA in the region of a stenosis.108 Using multiple parameters can improve diagnostic confidence, particularly when combined with color and power Doppler imaging (see Video 24.19). The degree of stenosis is best assessed using the gray-scale and pulsed Doppler parameters, including ICA PSV, ICA end diastolic velocity (EDV), CCA PSV, CCA EDV, peak systolic ICA/CCA ratio, and peak end diastolic ICA/CCA ratio (EDR)108,109,112 (Videos 24.21 and 24.22). PSV has proved accurate for quantifying high-grade stenoses.98,109 The relationship of PSV to the degree of luminal narrowing is welldefined and easily measured.113,114 Although Doppler velocities have proved reliable for defining 70% or greater stenosis, Grant et al.109 showed less favorable results for sub-stenosis classification between 50% and 69% using PSV and ICA/

CCA PSV ratios. In our experience, however, using all four parameters and determining a correct category for the degree of stenosis is the most efficacious way to ensure accuracy. Agreement for all four parameters for a clinical situation is most common. When there is an outlying parameter, further assessment and careful attention to technique and detail are required. EDV and EDR are particularly useful in distinguishing between high grades of stenosis. Additionally, correlating the visual estimation of the degree of stenosis and the velocity numbers will help in correctly grading stenosis, particularly when the degree of stenosis is “near occlusion” (Figs. 24.21 and 24.22; see also Fig. 24.19CDE). On rare occasions, alternate imaging methodologies (e.g., MRA, CTA) may need to be recommended. No criteria for grading external carotid artery stenoses have been established. A good general rule is that if the ECA velocities do not exceed 200 cm/s, no significant stenosis is present. However, we usually rely on a visible assessment of the degree of narrowing associated with velocity changes. Occlusive plaque involving the ECA is less common than in the ICA and is rarely clinically significant. Similarly, velocity criteria used to grade common carotid artery stenoses have not been well established.115,116 However, if one is able to visualize 2 cm proximal and 2 cm distal to a visible CCA stenosis, a PSV ratio obtained 2 cm proximal to the stenosis (vs. in region of greatest visible stenosis) can be used to grade the “percent diameter stenosis” in a manner similar to that used in peripheral artery studies. A doubling of the PSV across a lesion would correspond to at least a 50% diameter stenosis, and a velocity ratio in excess of 3.5 corresponds to a greater than 75% stenosis. One persistent problem with duplex Doppler with gray-scale ultrasound evaluation of the carotid arteries is that different institutions use PSVs ranging from 130 cm/s117 to 325 cm/s111 to diagnose greater than 70% ICA stenosis.118,119 Factors adding to these discrepancies include technique and equipment.120 While there is a strong level of correlation between techniques and criteria, the choice of criteria has a significant impact on which patients go to surgery.119 This wide range of PSVs reinforces the need for individual ultrasound laboratories to determine which Doppler parameters are most reliable in their own institution.120 Correlation of the velocity ranges obtained by ultrasound with angiographic and surgical results is necessary to achieve accurate, reproducible examinations in a particular ultrasound laboratory.121 The Society of Radiologists in Ultrasound, representing multiple medical and surgical specialties, held a consensus conference in 2002 to consider carotid Doppler ultrasound.122 In addition to guidelines for performing and interpreting carotid ultrasound examinations, panelists devised a set of criteria widely applicable among vascular laboratories (Table 24.1).122 Although the conference did not recommend all established laboratories with internally validated velocity charts alter their practices, they suggested physicians establishing new laboratories consider using the consensus criteria; those with preexisting charts might consider comparing in-house criteria with those provided by the consensus conference. Velocity criteria

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FIGURE 24.21 Abnormal High-Resistance Waveforms. High-resistance waveforms: (A) CCA, (B) proximal ICA, and (C) distal ICA. Color-flow Doppler imaging of the carotid bulb in (D) transverse and (E) sagittal projections demonstrates a significantly narrowed ICA. These findings are consistent with a greater than 95% stenosis of the ICA and a distal tandem stenosis of the intracranial carotid artery. CCA, Common carotid artery; ICA, internal carotid artery.

corresponding to specific degrees of vascular stenosis are listed in the tables. Our institution uses Table 24.2, which has a category for 80% to 95% stenoses; our surgeons are more inclined to consider surgery for patients with asymptomatic stenoses greater than 80% than for those with less severe stenoses.45,123 The ICA values should be obtained at or just distal to the point of maximum visible stenosis and at the point of greatest color Doppler spectral abnormality. Values from the CCA should be obtained 2 cm proximal to the widening in the region of the carotid bulb. Because velocities normally decrease from proximal to distal in the CCA and increase from proximal to distal in the ICA, it is important that standardized levels be used routinely for obtaining the ICA/ CCA velocity ratio.

Color and Power Doppler Ultrasound Color Doppler ultrasound displays blood flow information in real time over the entire image or a selected area. Stationary soft tissue structures, which lack a detectable phase or frequency shift, are assigned an amplitude value and displayed in a grayscale format with flowing blood in vessels superimposed in color. Color assignments depend on the direction of blood flow relative to the Doppler transducer. Blood flow toward the transducer appears in one color and blood flow away from the transducer is in another. These color assignments are arbitrary. Color saturation displays indicate the variable velocity of blood

flow. Deeper shades usually indicate low velocities centered around the zero-velocity color-flow baseline. As velocity increases, the shades become lighter or are assigned a different color hue. Some systems allow selected frequency shifts to be displayed in a contrasting color, such as green. This green-tag feature provides a real-time estimation of the presence of high-velocity flow. Setting the color Doppler scale can also be used to create an aliasing artifact corresponding to the highest-velocity flow within a vessel (see Figs. 24.15B and 24.17). These high-velocity jets pinpoint areas for spectral analysis. Color assignments are a function of both the mean frequency shift produced by moving RBC ensembles and the Doppler angle theta. If the vessel is tortuous or diving, the angle theta between the transducer and vessel will change along the course of the vessel, resulting in changing color assignments that are unrelated to the change in RBC velocity. The color assignments will reverse in tortuous vessels as their course changes relative to the Doppler transducer, even though the absolute direction of flow is unchanged. Portions of a vessel that parallel the Doppler beam when the angle theta is 90 degrees will have little or no frequency shift detected, and no color will be seen.

Optimal Settings for Low-Flow Vessel Evaluation Color Doppler flow studies should be performed with optimal flow sensitivity and gain settings. Color flow should fill the entire vessel lumen but not spill over into adjacent soft tissues.

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E FIGURE 24.22 Near Occlusion (95% to 99% Stenosis) With Homogeneous Plaque. (A) Transverse and (B) sagittal gray-scale images of the left internal carotid artery (ICA) demonstrate homogeneous (type 3) plaque. (C) Transverse and (D) sagittal power Doppler images demonstrate extremely narrowed residual lumen. (E) Velocity measurements for the ICA were peak systolic velocity, 51 cm/s; acoustic Doppler velocity, 19 cm/s; systolic velocity ratio, 51/64 ¼ 0.8; diastolic velocity ratio, 19/12 ¼ 1.5. The combination of visual images and Doppler spectral analysis findings indicates a 95% to 99% stenosis.

The pulse repetition frequency (PRF) and frame rates should be set to allow visualization of flow phenomena anticipated in a vessel. Frame rates will vary as a function of the width of the area chosen for color Doppler display and for the depth of the region of interest. The greater the color image area is, the slower the frame rate will be. The deeper the posterior

boundary of the color image is, the slower the PRF will be. Color Doppler sensitivity should be adjusted to detect anticipated velocities, such that if slow flow in a pre-occlusive carotid lesion is sought, low-flow settings with decreased sampling rates are employed. However, the system will then alias at lower velocities because of the decrease in PRF. In

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TABLE 24.1 Diagnostic Criteria for Carotid Ultrasound Examinations ICA PSV

PLAQUE

Normal 2.15 2.7 4.15 >2 >125 2.45 4.3

3.8 >4

>4

CCA, Common carotid artery; EDV, end diastolic velocity; ICA, internal carotid artery; PSV, peak systolic velocity. Modified from Chahwan S, Miller MT, Pigott JP, et al. Carotid artery velocity characteristics after carotid artery angioplasty and stenting. J Vasc Surg. 2007;45(3):523-526206; Fleming SE, Bluth EI, Milburn J. Role of sonography in the evaluation of carotid artery stents. J Clin Ultrasound. 2005;33(7):321328.198

or no obvious abnormalities on ultrasound; however, some patients may demonstrate redundancy of the mid to distal ICA causing an S-shaped curve.215 Fibromuscular dysplasia may be asymptomatic or can result in carotid dissection or subsequent thromboembolic events (Fig. 24.35). Arteritis resulting from autoimmune processes (e.g., Takayasu arteritis, temporal arteritis) or radiation changes can produce diffuse concentric thickening of carotid walls, which most frequently involves the CCA23,216,217 (Fig. 24.36). Carotid artery webs are thin non-atheromatous tissue that protrudes into the lumen of the artery.218 Webs are most commonly observed distal to the origin of the internal carotid artery originating from the posterior wall of the vessel.218 Carotid artery webs are increasingly recognized as a cause of stroke in patients who lack an alternative cause, particularly in young patients and African American women.219 Carotid webs on ultrasound may be seen as a low echo that protrudes into the arterial lumen and does not flutter with blood flow.220 Carotid webs may be difficult to observe with ultrasound and are better evaluated with CTA of the neck.221 Cervical trauma can produce carotid dissections or aneurysms. Carotid artery dissection results from a tear in the intima, allowing blood to dissect into the wall of the artery, which produces a false lumen. The false lumen may be blind-ended or may reenter the true lumen. The false lumen may occlude or narrow the true lumen, producing symptoms similar to carotid plaque disease. Dissections may arise spontaneously or secondary to trauma or to intrinsic disease with elastic tissue degeneration (e.g., Marfan syndrome) or may be related to atherosclerotic plaque disease.20 The ultrasound examination of a carotid dissection may reveal a mobile or fixed echogenic intimal flap, with or without thrombus formation.222 Frequently, there is a striking image/Doppler mismatch with a paucity of gray-scale abnormalities seen in association with marked flow abnormalities (Fig. 24.37).

Color or power Doppler ultrasound can readily clarify the source of this mismatch by demonstrating abrupt tapering of the patent, filled lumen to the point of an ICA occlusion. When the ICA is occluded, the proximal ipsilateral CCA will demonstrate a high-resistance waveform. When the ICA is severely narrowed (secondary to hemorrhage and a thrombus in the area of the false lumen), flow in the ICA may demonstrate high velocities. In these nonoccluded ICA cases, flow velocity waveforms in the CCA may be normal. Although conventional angiography, MRA, or CTA can be used initially to diagnose a dissection, ultrasound can be used to follow patients to assess the therapeutic response to anticoagulation. Repeat sonographic evaluation of patients with ICA dissection after anticoagulation therapy reveals recanalization of the artery in as many as 70% of cases.223-225 It is important to consider the diagnosis of dissection as a cause of neurologic symptoms, particularly when the clinical presentation, age, and patient history are atypical for that of atherosclerotic disease or hemorrhagic stroke.

Internal Carotid Artery Dissection: Spectrum of Findings INTERNAL CAROTID ARTERY Absent flow or occlusion Echogenic intimal flap, with or without thrombus Hypoechoic thrombus, with or without luminal narrowing Normal appearance

COMMON CAROTID ARTERY High-resistance waveform Dampened flow Normal appearance

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Pulsatile Neck Masses in the Carotid Region 2The most common CCA aneurysm occurs in the region of the carotid bifurcation. These aneurysms may result from atherosclerosis, infection, trauma, surgery, or contagious disease, such as syphilis. The normal CCA usually measures no more than 1 cm in diameter. Carotid body tumors, one of several paragangliomas that involve the head and neck, are usually benign, well-encapsulated masses located at the carotid bifurcation.29 These tumors may be bilateral, particularly in the familial variant, and are very vascular, often producing an audible

FIGURE 24.35 Fibromuscular Dysplasia. (A) Longitudinal color Doppler image of the middle to distal portion of the ICA shows velocity elevation and significant stenosis. (B) Same patient’s proximal portion of the ICA shows no stenosis. (C) Angiogram demonstrates typical appearance of fibromuscular dysplasia in the mid and distal ICA. Note the beaded appearance resulting from focal bands (arrow) of thickened tissue that narrow the lumen. ICA, Internal carotid artery.

bruit.29 Some of these tumors produce catecholamines, leading to sudden changes in blood pressure during or after surgery. Color Doppler ultrasound demonstrates an extremely vascular soft tissue mass at the carotid bifurcation29 (Fig. 24.38). Color Doppler ultrasound can also be used to monitor embolization or surgical resection of carotid body tumors. A classic nonmass is the ectatic innominate/proximal CCA, frequently occurring as a pulsatile supraclavicular mass in older women. The request to rule out a carotid aneurysm almost invariably shows the classic normal features of these tortuous vessels (Fig. 24.39).

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Extravascular masses (e.g., lymph node masses [Fig. 24.40], hematomas, abscesses) that compress or displace the carotid arteries can be readily distinguished from primary vascular masses, such as aneurysms or pseudoaneurysms. Posttraumatic pseudoaneurysms can usually be distinguished from true carotid aneurysms by the characteristic to-and-fro waveforms in the neck of the pseudoaneurysm, as well as the internal variability (yin-yang) characteristic of a pseudoaneurysm (Fig. 24.41).

TRANSCRANIAL DOPPLER SONOGRAPHY In transcranial Doppler (TCD) ultrasound, a low-frequency 2-MHz transducer is used to evaluate blood flow within the intracranial carotid and vertebrobasilar system and the circle of Willis. Access is achieved through the orbits, foramen magnum, or, most often, the region of temporal calvarial thinning (transtemporal window).226,227 However, many patients (up to

FIGURE 24.36 Long-Segment Stenosis of Common Carotid Artery (CCA) Caused by Takayasu Arteritis. Power Doppler images of (A) left and (B) right CCA shows long-segment concentric narrowing caused by greatly thickened walls of the artery (arrows). (C) Spectral Doppler waveform shows a mildly tardus-parvus waveform.

55% in one series228) may not have access to an interpretable TCD examination. Women, particularly African American women, have a thick temporal bone through which it is difficult to insonate the basal cerebral arteries.228,229 This difficulty limits the feasibility of TCD imaging as a routine part of the noninvasive cerebrovascular workup.227,228 By using spectral analysis, various parameters are determined, including mean velocity, PSV, EDV, and the pulsatility and resistive indices of the blood vessels. Color or power Doppler ultrasound can improve velocity determination by providing better-angle theta determination and localizing the course of vessels.226 TCD applications include (1) evaluation of intracranial stenoses and collateral circulation, (2) detection and follow-up of vasoconstriction from subarachnoid hemorrhage, (3) determination of brain death, (4) evaluation of patients with sickle cell disease, and (5) identification of arteriovenous malformation.223-227,230,231 TCD is most reliable in diagnosing stenoses of the middle cerebral artery, with sensitivities as high as 91% reported. TCD is less reliable for detecting stenoses of the intracranial vertebrobasilar system,

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FIGURE 24.37 Carotid Artery Dissection. (A) Abnormal high-resistance waveforms (arrow) at the origin of the right internal carotid artery (ICA) with no evidence of flow distal to this point (curved arrow). (B) Gray-scale evaluation of the vessel in the area of the occlusion demonstrates only a small, linear echogenic structure (arrow) without evidence of significant atherosclerotic narrowing. (C) Subsequent angiogram demonstrates the characteristic tapering to the point of occlusion (arrow) associated with carotid artery dissection and thrombotic occlusion. (D) Transverse and (E) longitudinal images of another patient show an intimal flap (arrow) in an external carotid artery (ECA). I, Internal carotid artery.

ECA

ICA

A

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FIGURE 24.38 Carotid Body Tumor. (A) Transverse image of the carotid bifurcation shows a mass (arrows) splaying the internal carotid artery (ICA) and external carotid artery (ECA). (B) Pulsed Doppler traces of the carotid body tumor show typical arteriovenous shunt (low-resistance) waveform.

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FIGURE 24.41 Pseudoaneurysm of the Common Carotid Artery (CCA). Transverse image of the right CCA demonstrates a jet of flow into a pseudoaneurysm, which resulted from an attempted central venous line placement.

FIGURE 24.39 Ectatic Common Carotid Artery. Color Doppler image shows ectatic proximal common carotid artery (CCA) arising from the innominate artery (I) and responsible for a pulsatile right supraclavicular mass.

E

I

FIGURE 24.40 Pathologic Lymph Node Near Carotid Bifurcation. Power Doppler image shows a malignant lymph node (arrow) lateral to the carotid bifurcation. E, External carotid artery; I, internal carotid artery.

anterior and posterior cerebral arteries, and terminal ICA. However, TCD is helpful in assessing vertebral artery patency and flow direction when no flow is detected in the extracranial vertebral artery (Fig. 24.42). Diagnosis of an intracranial stenosis is based on an increase in the mean velocity of blood flow in the affected vessel compared to that of the contralateral vessel at the same location.227-229 The advantages of TCD ultrasound also include its availability for monitoring patients in the operating room or angiographic suite for potential cerebrovascular complications.229 Intraoperative TCD monitoring can be performed with the transducer strapped over the transtemporal window, allowing evaluation of blood flow in the middle cerebral artery during CEA. The adequacy of cerebral perfusion can be assessed while the carotid artery is clamped.229,232 TCD is also capable of detecting intraoperative microembolization, which produces high-amplitude spikes (high-intensity transient signals [“HITS”]) on the Doppler spectrum.227,228,231,233-235 The technique can be used for the serial evaluation of vasospasms. This diagnosis is usually based on serial examinations of the relative increase in blood flow velocity and resistive index changes resulting from a decrease in the lumen of the vessel caused by vasospasms.229 More description of transcranial Doppler is in Chapter 47.

VERTEBRAL ARTERY The vertebral arteries supply the majority of the posterior brain circulation. Through the circle of Willis, the vertebral arteries also provide collateral circulation to other portions of the brain in patients with carotid occlusive disease. Evaluation of the extracranial vertebral artery seems a natural extension of carotid duplex and color Doppler imaging.236,237 Historically, however,

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FIGURE 24.42 Transcranial Doppler Imaging. (A) Transcranial duplex scan of the posterior fossa in a patient with an incomplete left subclavian steal syndrome demonstrates retrograde systolic flow (arrow) and antegrade diastolic flow (curved arrow). The scan is obtained in a transverse projection from the region of the foramen magnum (open arrowhead). (B) Color Doppler image obtained in the same patient demonstrates that there is retrograde flow not only within the left vertebral artery but also within the basilar artery (arrow).

these arteries have not been studied as intensively as the carotids. Symptoms of vertebrobasilar insufficiency also tend to be rather vague and poorly defined compared with symptoms referable to the carotid circulation. It is often difficult to make an association confidently between a lesion and symptoms. Furthermore, interest in surgical correction of vertebral lesions has been limited. The anatomic variability, small size, deep course, and limited visualization resulting from overlying transverse processes make the vertebral artery more difficult to examine accurately with ultrasound.236,238-240 The clinical utility of vertebral artery duplex scanning in diagnosing subclavian steal and presteal phenomena is well established.241-243 Less clear-cut is the use of vertebral duplex scanning in evaluating vertebral artery stenosis, dissection, or aneurysm.244

Anatomy The vertebral artery is usually the first branch off the subclavian artery (Fig. 24.43). However, variation in the origin of the vertebral arteries is common. In 6% to 8% of people, the left vertebral artery arises directly from the aortic arch proximal to the left subclavian artery.238,245 In 90%, the proximal vertebral artery ascends superomedially, passing anterior to the transverse process of the seventh cervical vertebra (C7), and enters the transverse foramen at the C6 level. The rest of the vertebral arteries enter into the transverse foramen at the C5 or C7 level and, rarely, at the C4 level. The size of vertebral arteries is variable, with the left larger than the right in 42%, the two vertebral arteries equal in size in 26%, and the right larger than the left in 32% of cases.246 One vertebral artery may even be congenitally absent. Usually, the vertebral arteries join at their confluence to form the basilar artery. Rarely, the vertebral artery may terminate in a posterior inferior cerebellar artery.

Sonographic Technique and Normal Examination Vertebral artery visualization with Doppler flow analysis can be obtained in 92% to 98% of vessels.236,247 Vertebral artery duplex examinations are performed by first locating the CCA in the longitudinal plane. The direction of flow in the CCA and jugular vein is determined. A gradual sweep of the transducer laterally demonstrates the vertebral artery and vein running between the transverse processes of C2 to C6, which are identified by their periodic acoustic shadowing. Angling the transducer caudad allows visualization of the vertebral artery origin in 60% to 70% of the arteries, in 80% on the right side, and in 50% on the left. This discrepancy may relate to the left vertebral artery origin being deeper and arising directly from the aortic arch in 6% to 8% of cases.238,245 The presence and direction of flow should be established. Visible plaque should be assessed. The vertebral artery usually has a low-resistance flow pattern similar to that of the CCA, with continuous flow in systole and diastole; however, wide variability in waveform shape has been noted in angiographically normal vessels.248 Because the vessel is small, the flow tends to demonstrate a broader spectrum. The clear spectral window seen in the normal carotid system is often filled in the vertebral artery.102 The vertebral vein (often a plexus of veins) runs parallel and adjacent to the vertebral artery. Care must be taken not to mistake its flow for that of the adjacent artery, particularly if the venous flow is pulsatile. Comparison with jugular venous flow during respiration should readily distinguish between vertebral artery and vein. At times, the ascending cervical branch of the thyrocervical trunk can be mistaken for the vertebral artery. This can be avoided by looking for landmark transverse processes that accompany the vertebral artery and by paying careful attention to the waveform of the visualized vessel. The

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FIGURE 24.43 Vertebral Artery. (A) Lateral diagram of vertebral artery (arrows) shows its course through the cervical spine transverse foramina en route to joining the contralateral vertebral artery to form the basilar artery (B). C, Carotid artery; S, subclavian artery. (B) MRA of posterior circulation shows course of bilateral vertebral arteries. Note how they connect in the circle of Willis. This is important for understanding the basis of reversal of flow in the vertebral artery. (C) Normal vertebral artery and vein. Longitudinal color Doppler image shows a normal vertebral artery (A) and vein (V) running between the transverse processes of the second to sixth cervical vertebrae (C2-C6), which are identified by their periodic acoustic shadowing (S). (D) Normal vertebral artery waveform. Normal low-resistance waveform of the vertebral artery with filling of the spectral window.

ascending cervical branch has a high-impedance waveform pattern similar to that of the ECA.241 TCD sonographic examination of the vertebrobasilar artery system can be performed as an adjunct to the extracranial evaluation. The examination is conducted with a 2-MHz transducer with the patient sitting, using a suboccipital midline nuchal approach, or with the patient supine, using a

retro-mastoidal approach. Color or power Doppler facilitates TCD imaging of the vertebrobasilar system.249

Subclavian Steal The subclavian steal phenomenon occurs when there is highgrade stenosis or occlusion of the proximal subclavian or innominate arteries with patent vertebral arteries bilaterally.

CHAPTER 24 The artery of the ischemic limb “steals” blood from the vertebrobasilar circulation through retrograde vertebral artery flow, which may result in symptoms of vertebrobasilar insufficiency (Figs. 24.44 and 24.45). Symptoms are usually most pronounced during the exercise of the upper extremity but can be produced by changes in head position. However, there is often a poor correlation between vertebrobasilar symptoms and the subclavian steal phenomenon. In most cases, flow within the basilar artery is unaffected unless severe stenosis of the vertebral artery supplying the steal exists.249 Also, surgical or angioplastic restoration of blood flow may not result in relief of symptoms.250 The subclavian steal phenomenon is most often caused by atherosclerotic disease, although traumatic, embolic, surgical, congenital, and neoplastic factors have also been implicated. Although the proximal subclavian stenosis or occlusion may be difficult to image, particularly on the left, the vertebral artery waveform abnormalities correlate with the severity of the subclavian disease.

W

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Doppler evaluation of the vertebral artery reveals four distinct abnormal waveforms that correlate with subclavian or vertebral artery pathology on angiography. These include the complete subclavian steal, partial or incomplete steal, pre-steal phenomenon, and tardus-parvus vertebral artery waveforms.243,248 In a complete subclavian steal, flow within the vertebral artery is completely reversed (see Fig. 24.45). Incomplete steal or partial steal demonstrates transient reversal of vertebral flow during systole243,249 (Fig. 24.46). Incomplete steal suggests high-grade stenosis of the subclavian or innominate artery rather than occlusion. Provocative maneuvers, such as exercising the arm for 5 minutes or 5-minute inflation of a sphygmomanometer on the arm to induce rebound hyperemia on the side of the subclavian or innominate lesion, can enhance the sonographic findings and convert an incomplete steal to a complete steal.155,185 The pre-steal (“bunny”) waveform shows antegrade flow but with a striking deceleration of velocity in peak systole to a level less than EDV. This is seen in patients with proximal subclavian stenosis, which is usually less severe than in those with partial steal waveform.243 The bunny waveform can be converted into a partial steal or complete steal waveform by provocative maneuvers (Fig. 24.47). A tardus-parvus waveform (also called a dampened waveform) can be seen in patients with high-grade proximal vertebral stenosis.242,243

Abnormal Vertebral Artery Waveforms COMPLETE SUBCLAVIAN STEAL Reversal of flow within vertebral artery ipsilateral to stenotic or occluded subclavian or innominate artery R

INCOMPLETE OR PARTIAL SUBCLAVIAN STEAL

L

Transient reversal of vertebral artery flow during systole May be converted into a complete steal using provocative maneuvers Suggests stenotic, not occlusive, lesion

PRESTEAL PHENOMENON S

“Bunny” waveform: systolic deceleration less than diastolic flow May be converted into partial steal by provocative maneuvers Seen with proximal subclavian stenosis

TARDUS-PARVUS (DAMPENED) WAVEFORM Seen with vertebral artery stenosis

FIGURE 24.44 Hemodynamic Pattern in Subclavian Steal Syndrome. Proximal left subclavian artery occlusive lesion (arrowhead) decreases flow to the distal subclavian artery (S). This produces retrograde flow (large arrows) down the left vertebral artery (L) and stealing from the right vertebral artery (R) and other intracranial vessels through the circle of Willis (W).

With a subclavian steal, color Doppler may show two similarly color-encoded vessels between the transverse processes, representing the vertebral artery and vein.129 Transverse images of the vertebral artery with color Doppler show reversed flow compared with those of the CCA. A Doppler spectral waveform must be produced in all such cases to avoid mistaking flow reversal within an artery for flow in a pulsatile vertebral vein.129,241

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FIGURE 24.45 Reversal of Vertebral Artery Flow in Subclavian Steal. Subclavian steal causes reversed flow in vertebral artery. Spectral Doppler (A) demonstrates complete vertebral artery flow reversal due to right subclavian artery occlusion. Color-flow Doppler (B) demonstrates flow toward the transducer.

FIGURE 24.46 Incomplete Subclavian Steal. Flow in early systole is antegrade, flow in peak systole is retrograde, and flow in late systole and diastole (arrow) is again antegrade.

Stenosis and Occlusion Diagnosis of vertebral artery stenosis is more difficult than diagnosis of flow reversal. Most hemodynamically significant stenoses occur at the vertebral artery origin, situated deep in the upper thorax, and seen in only 60% to 70% of patients.238,247,244 Even if the vertebral artery origin is visualized, optimal adjustments of the Doppler angle for accurate velocity measurements may be difficult because of the deep location and vessel tortuosity. No accurate reproducible criteria for evaluating vertebral artery stenosis exist. Because flow is

normally turbulent within the vertebral artery, spectral broadening cannot be used as an indicator of stenosis. Velocity measurements are not reliable as criteria for stenosis because of the wide normal variation in vertebral artery diameter. Although velocities greater than 100 cm/s often indicate stenosis, they can occur in angiographically normal vessels. For example, high-flow velocity may be present in a vertebral artery that is serving as a major collateral pathway for cerebral circulation in cases of carotid occlusion34,188,251 (Fig. 24.48). Thus, only a focal increase in velocity of at least 50%, visible stenosis on gray-scale or color Doppler, or a striking tardus-parvus vertebral artery waveform is likely to indicate significant vertebral stenosis. The variability of resistive indices in normal and abnormal vertebral arteries precludes the use of this parameter as an indicator of vertebral disease.248 Diagnosis of vertebral artery occlusion is also difficult. Often, the inability to detect arterial flow results from a small or congenitally absent vertebral artery or a technically difficult examination. The differentiation of severe stenosis from occlusion is difficult for the same reasons. Extremely dampened blood flow velocity in high-grade stenoses may result in a Doppler signal with an amplitude too low to be detected.239 Power Doppler imaging may prove useful in this situation. Visualization of only a vertebral vein may indicate vertebral artery occlusion or congenital absence.

INTERNAL JUGULAR VEINS The internal jugular veins are the major vessels responsible for the return of venous blood from the brain. The most common clinical indication for duplex and color Doppler flow ultrasound

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FIGURE 24.47 Incomplete Subclavian Steal and Provocative Maneuver. (A) Pre-steal left vertebral artery waveform. Flow decelerates in peak systole but does not reverse. (B) After provocative maneuver, there is reversal of flow in peak systole in response to a decrease in peripheral arterial pressure.

internal jugular or subclavian vein cannulation,263-269 particularly in difficult situations where vascular anatomy is distorted.

Sonographic Technique

FIGURE 24.48 Increased Flow Velocity in Vertebral Artery. Pulsed Doppler spectral trace from a left vertebral artery demonstrates strikingly high velocities and disturbed flow (arrow). Although this degree of velocity elevation and flow disturbance could be associated with a focal stenosis, in this case there was increased velocity throughout the vertebral artery from bilateral internal carotid artery occlusion and increased collateral flow into the vertebral artery.

of the internal jugular vein is the evaluation of suspected jugular venous thrombosis.252-260 Thrombus formation may be related to central venous catheter placement. Other indications include a diagnosis of jugular venous ectasia258,259,261,262 and guidance for

The normal internal jugular vein is easily visualized. The vein is scanned with the neck extended and the head turned to the contralateral side. Longitudinal and transverse scans are obtained with light transducer pressure on the neck to avoid collapsing the vein. A coronal view from the supraclavicular fossa is used to image the lower segment of the internal jugular vein and the medial segment of the subclavian vein as they join to form the brachiocephalic vein. The jugular vein lies lateral and anterior to the CCA, lateral to the thyroid gland, and deep to the sternocleidomastoid muscle. The vessel has sharply echogenic walls and a hypoechoic or anechoic lumen. Normally, a valve can be visualized in its distal portion.255,264,270 The right internal jugular vein is usually larger than the left.263 Real-time ultrasound demonstrates venous pulsations related to right heart contractions, as well as changes in venous diameter that vary with changes in intrathoracic pressure. Doppler examination graphically depicts these flow patterns (Fig. 24.49). On inspiration, negative intrathoracic pressure causes flow toward the heart and the jugular veins to decrease in diameter. During expiration and during the Valsalva maneuver, increased intrathoracic pressure causes a decrease in the blood return, and the veins enlarge, with minimal or no flow noted. The walls of the normal jugular vein collapse completely when moderate transducer pressure is applied. Sudden patient

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Thrombosis

J

FIGURE 24.49 Normal Jugular Vein. Complex venous pulsations in a normal jugular vein (J) reflect the cycle of events in the right atrium. IJV, Internal jugular vein.

sniffing reduces intrathoracic pressure, causing a momentary collapse of the vein on real-time ultrasound, accompanied by a brief increase in venous flow toward the heart as shown by Doppler.254,256,258

Clinical features of jugular venous thrombosis include a tender, poorly defined, nonspecific neck mass or swelling. The correct diagnosis may not be immediately obvious.255 Thrombosis of the internal jugular vein can be completely asymptomatic because of the deep position of the vein and the presence of abundant collateral circulation.258 Internal jugular thrombosis most often results from complications of central venous catheterization.253,257,258 Other causes include intravenous drug abuse, mediastinal tumor, hypercoagulable states, neck surgery, and local inflammation or adenopathy.255 Some cases are idiopathic or spontaneous.255 Possible complications of jugular venous thrombosis include suppurative thrombophlebitis, clot propagation, and pulmonary embolism.255,259 Real-time examination reveals an enlarged, noncompressible vein, which may contain a visible echogenic intraluminal thrombus. An acute thrombus may be anechoic and indistinguishable from flowing blood; however, the characteristic lack of compressibility and absent Doppler or color Doppler flow in the region of a thrombus quickly lead to the correct diagnosis. In addition, there is a visible loss of vein response to respiratory maneuvers and venous pulsation. Spectral and color Doppler interrogations reveal absent flow (Fig. 24.50). Collateral veins may be identified, particularly in cases of

C C

A

B

C

D

E

F

FIGURE 24.50 Internal Jugular Vein (IJV) Thrombosis: Spectrum of Appearances. (A) Transverse image of an acute left internal jugular vein thrombus (arrow). The vein is distended and noncompressible. C, Common carotid artery. (B) Longitudinal image of a different patient demonstrates a hypoechoic thrombus and no Doppler signal. (C) Longitudinal color Doppler image shows a small amount of thrombus arising from the posterior wall of the IJV. (D) Transverse image shows an echogenic thrombus, indicating chronic thrombus in IJV. (E) Longitudinal image demonstrates a thrombus (arrow) around jugular vein catheter. (F) Longitudinal images show a thrombus arising from anterior wall. This thrombus probably results from previous catheter placement in this region.

CHAPTER 24 chronic internal jugular vein thrombosis. Central liquefaction or other heterogeneity of the thrombus also suggests chronicity. Chronic thrombi may be difficult to visualize because they tend to organize and are difficult to separate from echogenic perivascular fatty tissue.264 The absence of cardiorespiratory plasticity in a patent jugular or subclavian vein can indicate a more central, nonocclusive thrombus (Fig. 24.51). The confirmation of bilateral loss of venous pulsations strongly supports a more central thrombus, which can be documented by angiographic or magnetic resonance venography. A thrombus that is related to catheter insertion is often demonstrated at the tip of the catheter, although it may be seen anywhere along the course of the vein. The catheter can be

A

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visualized as two parallel echogenic lines separated by an anechoic region. Flow is not usually demonstrated in the catheter, even if the catheter itself is patent. Sonography is a reliable means of diagnosing jugular and subclavian vein thrombosis. Sonography has limited access and cannot image all portions of the jugular and subclavian veins, especially those located behind the mandible or below the clavicle, although knowledge of the full extent of a thrombus is not typically a critical factor in treatment planning.255,259 Serial sonographic examination to evaluate response to therapy after the initial assessment can be performed safely and inexpensively. Sonography can also document venous patency before vascular line placement, facilitating safer and more successful catheter insertion.

B

FIGURE 24.51 Normal and Abnormal Venous Waveforms in Three Patients. (A) Brachiocephalic vein has normal cardiorespiratory change in the venous waveforms, implying a patent superior vena cava. (B) Near-occlusive left central brachiocephalic vein stenosis caused by a prior central venous catheter. Pulsed Doppler waveform shows reversed nonpulsatile flow in the internal jugular vein (IJV). (C) Left subclavian vein shows monophasic flow with respiratory phasicity upon sniffing.

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CONCLUSION The combination of gray-scale, color-flow Doppler, and Doppler spectral analysis is highly accurate in determining plaque characterization and degree of carotid stenosis, which are findings critical for patients for patient management. The assessment of the vertebral arteries is an integral component of the carotid ultrasound examination. However, the degree of stenosis of the vertebral arteries cannot be accurately assessed. Standard reporting should be used in the interpretation of these examinations.

ACKNOWLEDGMENT Thanks to Kathleen McFadden and Barbara Siede for their assistance with manuscript preparation and to Andrew Steven, MD for MRA cases.

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250. Thomassen L, Aarli JA. Subclavian steal phenomenon. Clinical and hemodynamic aspects. Acta Neurol Scand. 1994;90(4):241e244. 251. Nicolau C, Gilabert R, Garcia A, et al. Effect of internal carotid artery occlusion on vertebral artery blood flow: a duplex ultrasonographic evaluation. J Ultrasound Med. 2001;20(2):105e111. 252. Williams CE, Lamb GH, Roberts D, Davies J. Venous thrombosis in the neck. The role of real time ultrasound. Eur J Radiol. 1989;9(1):32e36. 253. Hubsch PJ, Stiglbauer RL, Schwaighofer BW, et al. Internal jugular and subclavian vein thrombosis caused by central venous catheters. Evaluation using Doppler blood flow imaging. J Ultrasound Med. 1988;7(11): 629e636. 254. Gaitini D, Kaftori JK, Pery M, Engel A. High-resolution real-time ultrasonography. Diagnosis and follow-up of jugular and subclavian vein thrombosis. J Ultrasound Med. 1988;7(11):621e627. 255. Albertyn LE, Alcock MK. Diagnosis of internal jugular vein thrombosis. Radiology. 1987;162(2):505e508. 256. Falk RL, Smith DF. Thrombosis of upper extremity thoracic inlet veins: diagnosis with duplex Doppler sonography. Am J Roentgenol. 1987;149(4):677e682. 257. Weissleder R, Elizondo G, Stark DD. Sonographic diagnosis of subclavian and internal jugular vein thrombosis. J Ultrasound Med. 1987;6(10): 577e587. 258. de Witte BR, Lameris JS. Real-time ultrasound diagnosis of internal jugular vein thrombosis. J Clin Ultrasound. 1986;14(9):712e717. 259. Wing V, Scheible W. Sonography of jugular vein thrombosis. Am J Roentgenol. 1983;140(2):333e336. 260. Chin EE, Zimmerman PT, Grant EG. Sonographic evaluation of upper extremity deep venous thrombosis. J Ultrasound Med. 2005;24(6):829e838. 261. Gribbin C, Raghavendra BN, Ginsburg HB. Ultrasound diagnosis of jugular venous ectasia. N Y State J Med. 1989;89(9):532e533. 262. Hughes PL, Qureshi SA, Galloway RW. Jugular venous aneurysm in children. Br J Radiol. 1988;61(731):1082e1084. 263. Jasinski RW, Rubin JM. CT and ultrasonographic findings in jugular vein ectasia. J Ultrasound Med. 1984;3(9):417e420. 264. Stevens RK, Fried AM, Hood Jr TR. Ultrasonic diagnosis of jugular venous aneurysm. J Clin Ultrasound. 1982;10(2):85e87. 265. Lee W, Leduc L, Cotton DB. Ultrasonographic guidance for central venous access during pregnancy. Am J Obstet Gynecol. 1989;161(4):1012e1013. 266. Bond DM, Champion LK, Nolan R. Real-time ultrasound imaging aids jugular venipuncture. Anesth Analg. 1989;68(5):700e701. 267. Machi J, Takeda J, Kakegawa T. Safe jugular and subclavian venipuncture under ultrasonographic guidance. Am J Surg. 1987;153(3):321e323. 268. Oh C, Lee S, Seo JM, Lee SK. Ultrasound guided percutaneous internal jugular vein access in neonatal intensive care unit patients. J Pediatr Surg. 2016;51(4):570e572. 269. Vezzani A, Manca T, Vercelli A, et al. Ultrasonography as a guide during vascular access procedures and in the diagnosis of complications. J Ultrasound. 2013;16(4):161e170. 270. Dresser LP, McKinney WM. Anatomic and pathophysiologic studies of the human internal jugular valve. Am J Surg. 1987;154(2):220e224.

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Peripheral Arteries Mohd Zahid, Mark E. Lockhart, and Michelle LaVonne Robbin

CHAPTER OUTLINE SONOGRAPHIC EXAMINATION TECHNIQUE, 995 SPECTRAL DOPPLER WAVEFORM EVALUATION, 995 Focal Abnormality, 995 Diffuse Abnormality, 996 LOWER EXTREMITY ARTERIES, 996 Normal Anatomy, 996 Ultrasound Examination and Imaging Protocol, 996 Peripheral Arterial Occlusion, 998

P

Peripheral Arterial Stenosis, 999 Functional Popliteal Artery Entrapment Syndrome, 1003 Aneurysm, 1004 Pseudoaneurysm, 1004 Arteriovenous Fistula, 1005 Lower Extremity Vein Bypass Grafts, 1006 UPPER EXTREMITY ARTERIES, 1008 Normal Anatomy, 1008

rior chapters have described details of the physics underlying Doppler analysis and the use of ultrasound in the assessment of the vasculature supplying the head and neck. In this chapter, we describe the sonographic assessment of the peripheral arteries, excluding the head and neck. In general, these structures are readily evaluated by Doppler ultrasound. Because they are usually located at depths of 6 cm or less, the extremity vessels are more consistently imaged than those in the abdomen or thorax. In the extremities, availability of sufficient imaging windows consistently allows the transducer to be placed over the vascular area of interest without being obscured by overlying bone or gas. Due to shallow depths, transducers with frequencies of 5 to 12 MHz can typically be used. Gray-scale sonography is useful for evaluating the presence of atherosclerotic plaque or confirming extravascular masses. Color Doppler imaging allows for a rapid survey of the area of interest, followed by spectral Doppler to characterize blood flow waveforms. Standardized protocols, such as those provided by the American College of Radiology (ACR), the American Institute of Ultrasound in Medicine (AIUM), and the Society of Radiologists in Ultrasound, should be followed.1 It is recommended that ultrasound examinations be performed in a laboratory accredited by one of the vascular accreditation programs, such as the ACR or the Intersocietal Accreditation Commission, in order to achieve a national standard of excellence and to improve the likelihood of successful peripheral arterial and venous ultrasound examinations.2 In the setting of a dedicated staff and with physician support, ultrasound can diagnose many peripheral vascular

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Ultrasound Examination and Imaging Protocol, 1009 Arterial Occlusion, Aneurysm, and Pseudoaneurysm, 1009 Arterial Stenosis, 1009 Subclavian Stenosis, 1010 Thoracic Outlet Syndrome, 1011 Radial Artery Evaluation for Coronary Bypass Graft, 1012 CONCLUSION, 1014 REFERENCES, 1014

abnormalities definitively and avoid the need for ionizing radiation or contrasted CT/MRI. A variety of symptoms and signs can be evaluated by arterial ultrasound. Sonographic examination has benefits over other modalities, such as real-time technique, lack of ionizing radiation, and relatively low expense. In the last few decades, the number of indications for peripheral artery ultrasound has expanded. Indications for peripheral arterial sonography is detailed in the most recent AIUM (with input from the ACR and Society of Radiologists in Ultrasound) practice parameter on the topic.1 In patients with claudication and/or rest pain in the lower extremities, ultrasound is indicated to evaluate for arterial stenosis or occlusion.1 Patients with pain, discoloration, or ulcer formation in the extremities (most commonly lower) should be imaged, since they may have tissue ischemia or necrosis from arterial stenosis or occlusion. Additional symptoms of numbness or cold extremity may be noted. However, symptomatology may vary among patients depending on the rapidity of onset and whether collaterals have developed to mitigate the effects of stenosis on the tissues. In some patients, vascular abnormalities may even be subclinical and found incidentally at imaging for other indications. Once an abnormality has been identified, ultrasound can monitor progression of disease, determine success or failure after intervention, and identify acceptable vessels for bypass graft creation. Other extremity abnormalities can also be evaluated sonographically. Focal masses can be assessed to exclude vascular abnormalities such as aneurysm or fistula with venous or arterial enlargement as the underlying cause. When chronic

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Indications for Peripheral Arterial Sonography 1. The detection of stenoses or occlusions in segment(s) of the peripheral arteries in symptomatic patients with suspected arterial occlusive disease 2. The monitoring of sites of previous surgical interventions, including sites of previous bypass surgery with either synthetic or autologous vein grafts 3. The monitoring of sites of various percutaneous interventions, including angioplasty, thrombolysis/thrombectomy, atherectomy, and stent placement 4. Follow-up for progression of previously identified disease, such as documented stenosis in an artery that has not undergone intervention, aneurysms, atherosclerosis, or other occlusive diseases 5. The evaluation of suspected vascular and perivascular abnormalities, including such entities as arteritis, fibromuscular dysplasia, masses, aneurysms, pseudoaneurysms, arterial dissections, vascular injuries, arteriovenous fistulae, thromboses, emboli, and vascular malformations 6. Mapping of arteries before surgical interventions 7. Clarifying or confirming the presence of significant arterial abnormalities identified by other imaging modalities 8. Evaluation of arterial integrity in the setting of trauma 9. Evaluation of patients suspected of thoracic outlet syndrome, such as those with positional numbness, pain, tingling, or a cold hand 10. Allen’s test to establish patency of the palmar arch 11. Temporal artery evaluation for temporal arteritis and/or to localize temporal arterial biopsy for suspected diagnosis of temporal arteritis a

Used with permission from AIUM practice parameter for the performance of peripheral arterial ultrasound examinations using color and spectral doppler imaging. J Med Ultrasound. 2021;40:E17eE24.1

positional upper extremity symptoms are present, ultrasound can evaluate for thoracic outlet syndrome. More peripherally in the upper extremity, Doppler can document patency of the palmar arch in surgical planning for bypass graft harvesting, and it can assess the radial artery before and after vascular access. In the acute setting, traumatic injuries can be evaluated to determine adjacent arterial involvement. Pseudoaneurysms and dissections are visible by ultrasound in these patients. Specific levels of occlusion or embolic disease can also be depicted.

SONOGRAPHIC EXAMINATION TECHNIQUE Gray-scale evaluation of the peripheral arteries is important to localize the structures, determine the amount of atherosclerotic disease or thrombus present, and to detect nonvascular abnormalities that may affect flow. The imager should use the highest frequency transducer that allows good penetration and visualization, typically a 5- to 12-MHz linear array transducer; a higher-frequency transducer can be used in areas where the

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arteries are more superficial. Occasionally, a 3- to 5-MHz sector or curved array probe may be necessary in large patients or those with severe extremity edema. Occasionally, atherosclerotic plaque or intraluminal thrombus is hypoechoic or nearly anechoic, and color Doppler is extremely useful to evaluate the residual lumen. The gain is initially increased to where color begins to “bleed” into the adjacent tissues, and then the gain is turned down so that the color just fills the lumen of a normal segment of the artery. Next, the spectral Doppler gate is adjusted within the lumen of the artery to allow adequate signal. The scale and gain should be optimized to show strong flow signals that use most of the scale to better display the morphology of the waveform. Normally, a medium- or high-wall filter is used in arterial evaluation, but a low-wall filter may be used to improve detection if there is slow flow. In general, for detection of small channels of slow flow in areas of near-occlusion, power Doppler is more sensitive than color Doppler,3 with newer more sensitive low-flow techniques becoming more widely available. The components of the sonographic evaluation differ based on the specific clinical indication for the exam. For example, imaging for suspected arterial stenosis or occlusion of the thigh vessels is very different from evaluation of a focal mass or aneurysm. The technical components of the examination have been previously described in the practice parameter.1

SPECTRAL DOPPLER WAVEFORM EVALUATION Focal Abnormality Color and spectral Doppler imaging are key components for evaluation of extremity stenosis and occlusion, using a combination of waveform morphology and velocity characteristics. On gray-scale imaging, a focal stenosis or occlusion may be suggested, but this should always be confirmed by color or power Doppler. Collaterals should also prompt additional attention with Doppler to evaluate for associated stenosis or occlusion of the vessels in this region. Any areas of visible narrowing or turbulent color Doppler signal should be further characterized with spectral Doppler. A change in spectral waveform morphology from one arterial segment to the next should also be insonated with color and spectral Doppler to locate a point of transition (Fig. 25.1). Spectral Doppler images should be obtained in the longitudinal plane and should be angle-corrected 60% or less from the center beam. If a jet is identified at the level of a stenosis, angle correction parallel to the orientation of the jet should be performed to more accurately measure peak systolic velocity (PSV). In general, waveform morphology and peak velocity should be evaluated at any suspected area of stenosis, as well as at the feeding vessel within 4 cm upstream, and the draining artery within 4 cm downstream. The inflow velocity is used as a reference baseline to assess for increased peak velocity at the stenosis, and the downstream location is evaluated for any decreased peak velocity, decreased resistance, or tardus-parvus morphology.4,5

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Triphasic Normal Biphasic, low velocity, high resistance Distal obstruction

Inflow obstruction

Monophasic, low velocity, lower resistance

Monophasic, high velocity, lower resistance

capillary perfusion from cardiac or other etiologies. If the extremity waveforms have a high-resistance morphology with a low PSV, but with a relatively normal upstroke (time to peak is not delayed), a significant distal obstruction should be considered. Importantly, this obstruction could be caused by extensive venous extremity thrombosis, as seen in phlegmasia cerulean dolens, which can be seen in multiple clinical settings such as malignancy, hypercoagulable syndrome, and May-Thurner syndrome, where the left iliac vein is compressed by the right iliac artery6e8 (Fig. 25.2). The same concepts apply to bypass grafts when searching for stenosis and occlusion, but additional attention is given to the anastomoses, which are common sites of abnormality. Ultrasound is the primary screening modality for bypass abnormalities but can be a time-consuming study if used to cover all areas of concern in a patient with diffuse atherosclerotic disease. If diffuse multi-segmental atherosclerotic disease is suspected, other imaging techniques such as computed tomography angiography (CTA) or magnetic resonance angiography (MRA) may be able to survey large areas more effectively.

Arteriovenous fistula

LOWER EXTREMITY ARTERIES Normal Anatomy Biphasic, reciprocating Pseudoaneurysm FIGURE 25.1 Diagrams of Doppler Flow Patterns in Normal and Abnormal Scenarios. The normal Doppler spectrum of flowing blood in the lower extremity arteries typically has a triphasic pattern: (1) forward flow during systole, (2) a short period of flow reversal in early diastole, and (3) low-velocity flow during the remainder of diastole. Arterial Doppler signals are altered depending on the pathologic change. The four other patterns are examples of common arterial pathologies: distal obstruction, inflow obstruction, arteriovenous fistula, and pseudoaneurysm.

Diffuse Abnormality Careful evaluation of the spectral Doppler waveform can be the key to determining the etiology of a diffusely abnormal extremity waveform. Additional areas may need to be evaluated, either upstream to the extremity or by assessing the contralateral extremity for comparison. In the case of a diffusely low PSV, low-resistance monophasic waveform with a tardusparvus pattern throughout the extremity, the upstream artery(s) from the extremity should be evaluated for significant stenosis or obstruction. In the case of an upstream obstruction, a tardus-parvus pattern can be seen in a downstream vessel that is reconstituted by collaterals. In a diffusely low-resistance (monophasic) extremity waveform with a relatively normal PSV throughout the extremity, clinical correlation should include the possibility of diffuse infection, or other etiology that would cause increased capillary perfusion in the extremity. Conversely, a diffusely high-resistance waveform (biphasic or monophasic) with a relatively normal PSV and normal upstroke (time to peak is not delayed) throughout the extremity could be the result of decreased

Each lower extremity arterial system is primarily supplied from the common femoral artery, which originates from the external iliac artery at the level of the inguinal ligament and extends caudally a few centimeters until it divides into the superficial femoral artery (SFA) and profunda femoris artery. The profunda femoris artery supplies the femoral head and the deep muscles of the thigh through perforators, as well as the medial circumflex artery and the lateral circumflex artery. The SFA continues along the medial thigh to the adductor canal in parallel with the femoral vein (FV). Below the adductor canal, it becomes the popliteal artery, coursing posterior to the knee and supplying branches of the calf. The popliteal artery branches into the anterior tibial artery and the tibioperoneal trunk. The anterior tibial artery courses laterally, perforating through the interosseous membrane between the tibia and fibula into the anterior compartment of the lower leg. The anterior tibial artery becomes the dorsalis pedis artery in the dorsum of the ankle and along the first intertarsal space of the foot, coursing between the first and second metatarsals. The tibioperoneal trunk divides after approximately 3 to 4 cm into the posterior tibial artery and the peroneal artery. The posterior tibial artery courses posterior to the medial malleolus of the ankle. The peroneal artery courses through the interosseous membrane above the ankle, and it then supplies branches of the lateral ankle and foot.

Ultrasound Examination and Imaging Protocol Lower extremity arterial inflow from the external iliac artery is assessed by groin insonation while the patient is in supine position, and then each major vessel in the leg is directly

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L Dist PTA PSV 10.9 cm/s

A

C

B L Dor Pedis PSV 12.6 cm/s

F

E

D

G

H

FIGURE 25.2 Phlegmasia Cerulean Dolens. A 42-year-old female with May-Thurner syndrome had extensive deep venous thrombosis (DVT) in the left common femoral vein (A) and popliteal vein (B) and significantly decreased peak systolic velocity and high resistance monophasic flow in the posterior tibial artery (C) and dorsalis pedis artery (D). CT angiogram axial (E) and coronal (F) images show compression of left common iliac vein with occlusive thrombus (large white arrow) by the right common iliac artery (small white arrow). The patient had mechanical thrombectomy and stent placement in the left common iliac vein (G); the vein and stent patency were confirmed with angiogram (H).

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evaluated throughout its entire course. Normal arteries have thin smooth walls with anechoic lumens and lack of atherosclerotic plaques or stenosis on gray-scale imaging (Fig. 25.3). After gray-scale evaluation, long arterial segments can be screened rapidly with color Doppler to find areas of suspected stenosis. Color Doppler settings should be adjusted to barely fill the lumen in a normal segment of the artery. Color aliasing can alert the sonographer to areas of luminal narrowing that need to be evaluated further with spectral Doppler to determine severity of the narrowing. For evaluation of focal abnormalities other than stenosis, the ultrasound examination can be limited to the region of concern. The AIUM practice parameter for the performance of peripheral arterial ultrasound suggests that a lower extremity arterial ultrasound should examine the common femoral artery; the proximal, mid, and distal SFA; and the popliteal artery above and below the knee.1 Other arteries are examined as deemed clinically appropriate. The practice parameter states that these may include “iliac, deep femoral, tibioperoneal trunk, anterior tibial, posterior tibial, peroneal, and dorsalis pedis arteries.” The practice parameter further suggests that anglecorrected longitudinal Doppler and/or gray-scale imaging should be documented in each normal vessel and at any abnormal segment. Angle-corrected spectral Doppler is recommended proximal to, at, and beyond any suspected stenosis. Supine position of the patient is acceptable for the thigh vessels, but a decubitus position may aid evaluation of the popliteal artery. Depending on the symptoms and sonographic findings of these arteries, imaging of the iliac arterial system may look for inflow disease, or imaging of the calf arteries may be indicated. Normal outer diameters of the common femoral artery, SFA, popliteal artery, posterior tibial artery, and anterior tibial artery are 8.1 mm, 6.1 mm, 6.0 mm, 2.1 mm, and 2.0 mm, respectively, and these vessels are slightly larger in males. The common femoral artery, SFA, and popliteal artery become slightly larger

A

with age, whereas the calf arteries become smaller. Laminar flow is present without turbulence or aliasing on color Doppler. A high-resistance triphasic waveform with sharp upstroke and transient flow reversal is typically present in the normal lower extremity arteries on spectral Doppler.9 Although a monophasic waveform morphology that does not return to baseline can occur after exercise in normal patients, this finding can be also seen in lower extremity atherosclerotic disease. For differentiation, the PSV will decrease in the ischemic limb of a patient with peripheral artery disease after exercise, whereas it will increase in a patient with a healthy arterial system. For calf assessment, a posterior medial approach is used for the posterior tibial artery in the mid calf with longitudinal Doppler, and then the artery can be followed proximally and distally. Alternatively, it can be found at the medial malleolus at the ankle and followed cranially. For the anterior tibial artery, an anterior transducer placement is applied with the patient lying supine. The anterior tibial artery is well seen along the interosseous membrane near the fibula. The peroneal artery can also be seen from this anterior probe placement; it is more deeply located posterior to the interosseous membrane. A posterior lateral approach may also be used to locate the peroneal artery.

Peripheral Arterial Occlusion Acute arterial occlusion is an emergent situation that can generate severe symptomatology and requires immediate attention. It is usually identified in the setting of atherosclerotic disease, although traumatic dissection or embolic disease can occur (Fig. 25.4). Use of Doppler allows for sensitive and specific demonstration of absent flow, and it can differentiate occlusion from stenosis in the lower extremity with 98% accuracy.10 In another study, sensitivities of Doppler for occlusion of the SFA and popliteal artery were 97% and 83%, respectively.11 In the lower leg, Doppler performs better in the anterior and posterior tibial arteries than in the peroneal artery.

B

FIGURE 25.3 Normal Common Femoral Artery Bifurcation. (A) Gray-scale imaging shows the normal appearance of arterial wall with lack of plaque. (B) Color and spectral Doppler normal triphasic spectral waveform in the profunda femoris artery.

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SFA

PF

A

B

C

FIGURE 25.4 Acute Thrombus in the Superficial Femoral Artery. Note the echogenic material within the arterial lumen; (A) color doppler image shows patent CFA and PF and an echogenic thrombus occluding the cranial segment of SFA, (B) color and spectral doppler image demonstrates high resistance low PSV flow and (C) no flow in the middle segment of SFA. See also video 25.1 of a different patient which shows slightly mobile thrombus.

Doppler sensitivity for patency of the anterior tibial artery was 93%, posterior tibial artery was 97%, and only 71% in the peroneal artery.12 On gray-scale imaging, the anechoic lumen is typically filled with medium-echogenicity thrombus. Using a similar technique as generally performed for detection of deep venous thrombus, the artery can be externally compressed by the transducer to show focal thrombus that is noncompressible. However, if the artery walls completely coapt, then the findings are likely artifactual. During color and spectral Doppler of an occluded artery, no flow signal should be detectable (Fig. 25.5). Collaterals suggest chronic occlusion, but there may be a superimposed acute-on-chronic thrombotic component (Fig. 25.6, Video 25.2). The waveform upstream to the occlusion should be high resistance, low PSV, unless well-developed collaterals are present.

Peripheral Arterial Stenosis Detection of stenosis in the setting of atherosclerotic disease is important owing to its role as a precursor to occlusion. Ultrasound is the primary screening tool for detection of stenosis,

using a combination of gray-scale, color, and spectral Doppler.13 A study of systemic reviews of duplex ultrasonography, MRA, and CTA for diagnosis and assessment of symptomatic, lower limb peripheral arterial disease reported 80% to 98% sensitivity and 89% to 99% specificity of duplex ultrasound in detection of 50% or greater stenosis.14 The sensitivity of the ankle-brachial index (ABI) in detecting angiographically significant stenoses has been reported as 94% to 97%.15 Spectral broadening can be seen in non-flow-limiting stenoses less than 50%, with an otherwise normal waveform (Fig. 25.7). As regional measurements are made in the arteries of the lower extremity, there may be a change noted from normal triphasic arterial morphology to a pulsatile but monophasic waveform that does not return to baseline or demonstrate transient reversal (Fig. 25.8). When this transition is encountered, the artery between these two measurements should be more closely evaluated by color and spectral Doppler to locate a focal velocity elevation associated with visible narrowing of the artery. Grayscale can characterize overall plaque burden, but calcifications can limit sonographic penetration into the artery lumen (Fig. 25.9, Video 25.3). As previously noted, color Doppler

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A

C

improves the examination by rapidly depicting areas of turbulent or high-velocity flow that can be further sampled by spectral Doppler for velocity characterization. However, in a patient with diffuse atherosclerotic disease and generalized atherosclerotic calcifications, there may be numerous mild stenoses that have a combined effect to reduce flow pressures to the lower leg without a dominant stenosis. The main criteria for characterizing arterial stenosis involve waveform morphology, PSV, and end-diastolic velocity (EDV). For velocity criteria, the absolute peak systolic values and the peak velocity ratio (defined as peak velocity at the stenosis or in the downstream jet divided by peak velocity of the artery 2 cm

B

FIGURE 25.5 Occluded Popliteal Artery. (A) Spectral Doppler shows high-resistance flow pattern upstream to the occlusion. (B) Occluded portion of the popliteal artery without flow on spectral Doppler. (C) Tardus-parvus pattern in the dorsalis pedis distal to the occluded popliteal artery indicates reconstitution of the artery by collaterals.

upstream) have both been applied effectively. In a study of 338 arterial segments, a focal PSV ratio greater than 2:1 at the stenosis relative to the adjacent nonstenotic inflow artery is consistent with at least 50% diameter stenosis when this elevated ratio is combined with findings of spectral broadening and loss of transient flow reversal in the artery (Fig. 25.10).16,17 The distal artery waveform will be abnormal with tardus-parvus waveforms in the setting of stenosis greater than 50% (Fig. 25.11), but the morphology commonly remains normal if a lesser degree of stenosis is present.16 For the femoral-popliteal region of native vessels, a combination of thresholds, including PSV greater than 200 cm/s and PSV ratio above 2:1,

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FIGURE 25.6 Occlusion of the Superficial Femoral Artery With a Large Collateral Exiting Proximal to the Occlusion (Arrow). The presence of a collateral suggests chronic occlusion. See also Video 25.2.

FIGURE 25.7 Common Femoral Artery Stenosis. Color and spectral Doppler shows normal biphasic waveform, with fill-in of the waveform spectral envelope, indicating some degree of stenosis but less than 50%.

have been suggested as criteria for diagnosing greater than 70% stenosis with sensitivity of 79% and specificity of 99% (Fig. 25.12).18 In addition to diagnosis, ultrasound can also direct intervention. Patients with nonacute conditions can benefit from ultrasound to characterize subacute occlusion or embolic disease versus chronic ischemic disease to help the surgeon decide among therapies such as thrombectomy or bypass procedure.19,20 Mapping with Doppler before arterial bypass graft surgery is very useful. Lesions are characterized by severity using the Trans-Atlantic Inter-Society Consensus (TASC) guidelines.21 Isolated and short lesions (categories A and B) typically are directed to endovascular repair, whereas more

complex or longer lesions (categories C and D) commonly require bypass. In one study of 622 TASC category C or D lesions, Doppler mapping successfully identified lesions for intervention with sensitivity of 97% and specificity of 99%.22 Doppler can also successfully predict which lesions are suitable for percutaneous transluminal angioplasty.23,24 The lesions treated by angioplasty are generally short and isolated and have a diameter reduction of greater than 50%. However, duplex assessment may underestimate the length of stenosis. For evaluation of stenosis within a stented artery, the best Doppler criteria to characterize SFA in-stent stenosis of 80% or greater include a combination of (1) PSV above 275 cm/s and (2) PSV ratio greater than 3.5 (the ratio of the highest PSV

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B

FIGURE 25.8 Focal High-Grade Stenosis in the Proximal Superficial Femoral Artery (SFA). (A) Elevated peak systolic velocity at a focal highgrade stenosis in the proximal SFA. (B) Tardus-parvus pattern downstream.

A

B

FIGURE 25.9 Calcification of the Superficial Femoral Artery (SFA). (A) Severe calcification of the SFA limits ability to see within the artery lumen with gray-scale imaging. Color Doppler is useful to locate a place where spectral Doppler can be sampled. (B) Spectral Doppler of the artery has mild spectral broadening but otherwise normal triphasic waveform, without significant stenosis in this location. See also Video 25.3.

within the stent to the PSV in a disease-free arterial segment 3 cm above the stented area).25 Patients who meet the 80% stenosis criteria should undergo angiography to further evaluate and possibly treat the stenosis in order to optimize stent patency.25 In patients with stent repair of SFA stenosis, Doppler and CT angiography have strong agreement regarding detection of re-stenosis.26 A retrospective study of patients with SFA occlusion treated with a stent compared those having routine ABI follow-up with those having duplex Doppler exams. They demonstrated an advantage of follow-up arterial duplex stent

imaging reflected as improved assisted primary patency, secondary patency, fewer major limb events, and more use of endovascular procedures rather than amputation.27 Thus, in patients with endovascular intervention and stenting, Doppler can monitor success of the procedure and survey for recurrent stenosis at follow-up. In asymptomatic patients, after a revascularization procedure (such as angioplasty, stent or bypass grafting) it is recommended to perform an initial scan at 1 month, then at 6 to 8 months, and then yearly. Patients with new symptoms after a vascularization

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Time 2 to 4 cm proximal

A

Velocity

FIGURE 25.10 Blood Flow Velocity Alterations Occur With Stenosis of at Least 50%. Proximal to the lesion, the flow pattern is normal. At the stenosis, the peak systolic velocity increases in proportion to the degree of stenosis. Alterations in the diastolic portion of the Doppler waveform sampled at the lesion depend on the state of the distal arteries and the severity and geometry of the lesion; diastolic flow may increase dramatically or may be almost absent.

Time At the stenosis

B

FIGURE 25.11 Iliac Artery Stenosis With Tardus-Parvus Waveform. (A) Tardus-parvus waveform in the right common femoral artery indicates severe upstream stenosis or occlusion. (B) Normal velocity biphasic waveform of the contralateral left common femoral artery indicates atherosclerotic disease is in right common or external iliac artery, and not in the aorta (unilateral abnormal waveform).

procedure should be rescanned regardless of when those symptoms occur.

Functional Popliteal Artery Entrapment Syndrome Functional popliteal artery entrapment syndrome (FPAES) is a rare condition found in young athletes that results in claudication symptoms that resolve with rest. Hypertrophy of gastrocnemius, soleus, and plantaris muscles causes impingement/stenosis of the popliteal artery secondary to exercise. A

recent provocative study conducted by Browne et al. measured ABI and popliteal artery diameter using duplex ultrasound in symptomatic and asymptomatic patients after 1 minute of treadmill exercise. The study found a greater reduction in popliteal artery diameter and ABI in symptomatic patients.28 Another study conducted by Hislop et al. used provocative duplex ultrasound during graded compression at rest, during 25% of full plantar-flexion, and at 50% to 100% of full plantarflexion to assess arterial waveforms, velocities of peripheral arteries, and areas of intimal thickening or fixed arterial disease. Those patients whose arteries occluded either during rest or

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A

B

FIGURE 25.12 Superficial Femoral Artery (SFA) With Greater Than 70% Stenosis. (A) Moderately severe stenosis in the SFA with a peak systolic velocity (PSV) of 269 cm/s. (B) At 4 cm upstream from the stenosis the PSV is 85.0 cm/s, for a ratio exceeding 3:1, indicative of greater than 70% stenosis.

25% of full plantar-flexion were considered severe cases of FPAES. The waveform also changed from triphasic to monophasic morphology in symptomatic patients.29 Sinha et al. showed a sensitivity of 90% with provocative duplex ultrasound coupled with ABI and sensitivity of 94% with provocative MRI/ MRA.30 Based upon these studies, provocative ABI and duplex ultrasound have been shown as reliable first-line tools to detect this condition with further characterization using MRI/MRA when necessary.

Aneurysm An aneurysm occurs when weakness of the arterial layers allows expansion of the arterial caliber beyond normal limits. Aneurysms of the peripheral arteries are uncommon, but when present, most are found in the popliteal regions.31 Less commonly, aneurysms occur in the SFA. In more than half of patients with popliteal artery aneurysm, they are bilateral. The association that more than 50% of patients with bilateral popliteal artery aneurysms have abdominal aortic aneurysm is well known. Thus, if a popliteal artery aneurysm is found, the abdominal aorta should be evaluated.32 There is also an association among peripheral artery aneurysm, tobacco use, and hypertension.33 Peripheral artery aneurysms may contain clot, which may result in distal emboli with or without soft tissue ischemia and infarction. In these cases, intervention is necessary regardless of aneurysm size.34 The walls of an aneurysm may calcify, and the presence of calcifications may increase the risk of being symptomatic or rupture.35 On gray-scale ultrasound, an aneurysm may appear as a fusiform anechoic or hypoechoic mass along the course of an artery. The Doppler signal depends on the amount of thrombus, the size of the neck of the aneurysm, and the presence of calcification. Aneurysms may be saccular, and they commonly occur at branch points. Enlargement can be compared to normal proximal artery; the normal popliteal artery measures 4

to 6 mm in diameter.36 A bulge or focal enlargement of 20% of the vessel diameter constitutes a simple functional definition of an aneurysm (Fig. 25.13). Empirically, a 2-cm cutoff has been used to determine need for intervention.37 For popliteal artery aneurysm, surgical exclusion (ligation of the aneurysm) is the traditional treatment, and this therapy has a high rate of success.38 However, a 2015 meta-analysis showed that endovascular repair has similar successful outcomes.39 Doppler ultrasound can be used to monitor the patency of the stent and confirm the exclusion of the aneurysm from the circulation.40,41

Pseudoaneurysm Pseudoaneurysm describes disruption of an artery with flow in a space beyond the vessel wall. It may arise from any arterial structure and occur with direct trauma, tumor, or inflammatory erosion. Pseudoaneurysms are found in less than 1% of diagnostic angiography examinations but occur more commonly after coronary angiography.42,43 Pathologically, the arterial wall has been at least partially breached. Outer arterial layers, perivascular tissues, clot, or reactive fibrosis contain the pseudoaneurysm sac.44 The mechanism of pseudoaneurysm formation has been well characterized; a hematoma initially forms adjacent to the artery at the point of injury. Eventual lysis of the clot leads to an unobstructed opening in the vessel wall, and when the exiting blood flow returns to the vessel, this results in a pseudoaneurysm. A pseudoaneurysm is different from an aneurysm in that at least one layer of wall is disrupted in a pseudoaneurysm, whereas all three layers are expanded (but not disrupted) in an aneurysm. Unlike active extravasation, the blood within the pseudoaneurysm flows back into the feeding artery through a narrowed opening rather than into adjacent tissues. Detection of pseudoaneurysm begins with gray-scale ultrasound to identify the abnormality. A pseudoaneurysm can appear as a round or oval anechoic structure with or without associated thrombus. When present, thrombus appears

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FIGURE 25.13 Popliteal Artery Aneurysms. (A) Popliteal artery aneurysm measures 1.2 cm diameter (arrows). (B) In a different patient, a 3.7 cm popliteal artery aneurysm contains low-level echoes and is partially thrombosed (cursors).

isoechoic or hypoechoic; it may fill the lumen or only involve the edge of the pseudoaneurysm lumen. Attention should be directed to any areas of extraluminal hematoma or any anechoic collections to determine if there are areas of flow with color Doppler. If flow is detected, spectral Doppler is next performed to characterize arterial versus venous flow and to exclude a superimposed arteriovenous fistula (AVF). In the patent portion of a pseudoaneurysm, there may be turbulent or disorganized intra-aneurysmal flow with a traditionally described “yin-yang” appearance. Communication of the sac with the adjacent artery occurs through a neck with a typical “to-and-fro” biphasic flow on spectral Doppler (Fig. 25.14, Video 25.4).45,46 The neck length and diameter of the neck off the artery are measured. If the sac is thrombosed, the neck may represent the only patent portion of the pseudoaneurysm. At least one-third of pseudoaneurysms require repair, but spontaneous closure is common for pseudoaneurysms smaller than 1.8 cm in diameter.47,48 Treatment with sonographically guided direct compression was used in the past but was less successful (up to 85% pseudoaneurysm thrombosis and 81% in a more recent study).49 If the sac is patent, ultrasound-guided thrombin injection into the sac to thrombose the pseudoaneurysm is commonly performed, with a success rate of 91% to 100%.49e52 A recent study by Yang et al. suggested the use of thrombin injection in the treatment of all pseudoaneurysms irrespective of their dimension including pseudoaneurysm with short neck.53 Most institutions use a thrombin concentration of 1000 IU/mL and 0.5 mL to 1.0 mL volume.54e56 However, some institutions have advocated the use of lower concentration of 100 IU/mL.56 The success rate of the treatment of a pseudoaneurysm with thrombin injection is 94% to 100%.57 A second injection of thrombin is required in 10% of cases of pseudoaneurysm.57 The procedure has few reported complications, with the significant complication of downstream distal arterial embolization reported in only 1% to 2% of cases.57 Allergic reactions to bovine thrombin injection are rare. However, severe anaphylactic reactions have been

reported.58,59 It is important to inquire about any previous exposure or allergy to thrombin. There is a recommendation to do skin prick testing of 1000 IU/mL thrombin concentration before intravascular injection in patients with a history of exposure. If no local swelling or redness occurs within 15 minutes, patients can safely receive thrombin injection.59,60 Human thrombin should be considered as an alternative to bovine thrombin, as it may have a lower risk of allergic reactions.61 Importantly, if there is an arteriovenous communication (arteriovenous fistula, AVF), thrombin repair is contraindicated owing to the potential for embolization of the thrombin into the venous system with resultant unintended potential venous thrombosis.62

Arteriovenous Fistula The term “fistula” describes an abnormal communication between the arterial and venous circulations. There is disruption through all layers of the arterial wall as well as a focal disruption of a nearby venous structure, allowing communication from high-arterial pressure to low-pressure veins and bypassing the capillary bed. AVFs are classified into two groups: acquired and congenital. Acquired fistulas can be further subclassified into surgically created, as in for hemodialysis, or secondary to trauma, whether accidental or procedure-related. Fistulas may be seen after autologous vein bypass grafting63 and do not appear to affect patency of the graft.64 In the absence of bypass graft, most fistulas are acquired and usually associated with a history of trauma.65 A traumatic arteriovenous fistula may course from normal artery to normal vein in the setting of trauma, but congenital arteriovenous malformations (AVMs) frequently occur with associated abnormal vascular structures. Many are asymptomatic. However, symptomatic AVFs do not typically spontaneously resolve (due to a continuous patent pathway for blood flow from high to low pressure) and often require surgery.66 A rare cause of acquired AVF is deep vein thrombosis. The exact pathogenesis is not clear, but venous hypertension is considered a main cause of AVF.67 It is also

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FIGURE 25.14 Common Femoral Artery Pseudoaneurysm. (A) Common femoral artery pseudoaneurysm with “yin-yang” color flow pattern in the pseudoaneurysm (arrows). (B) Spectral Doppler of the pseudoaneurysm neck shows a high-velocity “to-and-fro” pattern. (C) Measurement of the length of the neck from the common femoral artery to the pseudoaneurysm (calipers). (D) Measurement of the diameter of the neck (calipers) off of the common femoral artery indicates size of hole in artery; a “rent” in the artery is less amenable to thrombin injection. It is preferable to measure the diameter in gray-scale because color may overestimate the diameter, but sometimes the neck cannot be seen without color (as in this case). See also Video 25.4.

hypothesized that DVT induces inflammation and angiogenesis that result in AVF formation. A retrospective study by Yuan H et al. found AVF in 24 patients with DVT, and all the patients had venous hypertension.68 Gray-scale imaging may show very little arterial abnormality in a traumatic fistula, but the cluster of dilated vessels of an AVM can be identified. In either abnormality, there may be venous dilation. Color Doppler ultrasound is the best noninvasive imaging modality to evaluate AVF or AVM and may show a large cluster of tortuous vessels with abnormal hyperemic flow. Spectral Doppler waveforms of the inflow arteries feeding the AVF may show low-resistance flow because they bypass the capillary bed. Doppler can show arterialized waveforms in the venous structures near the AVF. Tissue vibration

artifact is commonly seen with AVFs, consisting of color pixels placed in the adjacent soft tissue by the ultrasound scanner because of vibrations induced by the marked turbulence of the AVF. If tissue vibration artifact is seen, a search should be made for an AVF. The arterialized waveform may be better seen during the Valsalva maneuver because normal antegrade venous flow is decreased due to the increased thoracic pressure from Valsalva (Fig. 25.15, Video 25.5).

Lower Extremity Vein Bypass Grafts Bypass grafts may use arterial segments or veins for arterial revascularization. Like bypass conduits in other portions of the body, these have potential complications that can limit their functionality. Failures soon after surgery may result from poor

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FIGURE 25.15 Common Femoral Artery to Common Femoral Vein Arteriovenous Fistula (AVF). (A) Color Doppler shows common femoral artery to common femoral vein AVF. Note the adjacent tissue vibration artifact (arrowheads). (B) Arterialized turbulent flow is seen within the vein just downstream to the AVF. See also Video 25.5.

bypass conduit selection or surgical technical factors such as poor selection of the sites for anastomosis. In addition, the valves of an autologous vein may not be fully lysed during surgical preparation. Although completion imaging is commonly performed at the time of surgery, a recent study showed no improvement in graft survival in patients with intraoperative completion angiography or ultrasound.69,70 In the longer term, fibrosis may occur at the site of a vein valve, or there may be intimal hyperplasia at an anastomotic region. If the bypass survives long enough, the underlying atherosclerotic disease may affect the bypass and inflow vessels to limit function. For synthetic grafts, the characterization of occlusion is similar to that of native vessels, with the absence of flow on color or spectral Doppler. Echogenic thrombus may be identified within the graft using the gray-scale technique. Cadaveric vein allografts have been used in selected patients for whom autologous veins were not available and who were not candidates for synthetic graft. These grafts are at high risk for thrombosis, and the risk is further enhanced by tissue rejection, immune-related intimal hyperplasia, and fibrosis.71 A study done by O’Banion et al. in 70 patients who underwent infrainguinal bypass with cadaveric vein found an overall estimated 1-year patency rate of 35%.72 Recently, a retrospective study of cadaveric vein lower extremity bypass on 25 patients reported even lower 1-year primary patency rate of 28%.73 Ultrasound is a good technique to identify lesions that are likely to result in native vein bypass graft failure. Once the arterial bypass graft has been created, ultrasound is the primary screening modality; Doppler surveillance with revisions when needed is cost-effective.74 The diagnosis depends on visible identification of stenosis on gray-scale imaging in combination

with characterization by color and spectral Doppler. Normal triphasic or biphasic waveforms in the ankle arteries distal to the bypass are consistent with patency of the bypass. Generalized reduced or monophasic flow velocities in a graft are concerning for disease, and further search for a focal abnormality should be performed. Color Doppler sonography can be used to search for areas of aliasing, and subsequent spectral Doppler evaluation for velocity changes is then performed in regions of concern. When a stenosis is detected in a nonbranching vessel, a velocity ratio can be applied to evaluate its significance. Similar to native arteries, the PSV ratio is calculated by dividing the PSV at the stenotic site in the graft by peak velocity 2 cm upstream. A PSV ratio of at least 2.0 corresponds to at least 50% diameter stenosis.75e77 Likewise, a PSV above 180 cm/s has been associated with stenosis of greater than 50% diameter in lower extremity bypass vein grafts (Fig. 25.16, Video 25.6).78,79 Several ultrasound parameters, including PSV ratio, are associated with future bypass graft dysfunction. Once the PSV ratio measures at least 3.5 to 4.0 at any location in the graft, showing severe stenosis, treatment should be considered if it has not been performed at less severe degrees of stenosis, even in less symptomatic patients.75,76 A study of Doppler and CT showed that patients with PSV ratio above 3.5 were at high risk for graft failure, whereas high-grade stenosis on CT did not correlate as well with subsequent graft failure.78 Velocity criteria for severe stenosis used by Wixon and colleagues suggest that PSV above 300 cm/s and PSV ratio above 3.5 should direct the patient to intervention of a vein graft stenosis.74 In patients who meet these criteria, the intervention should be immediate if flow velocity within the graft falls below 45 cm/s.74,78 Decreased PSV relative to a prior study is also a worrisome finding on spectral Doppler.

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In surveillance of vein grafts by Doppler with intervention on stenotic lesions, there is increased survival of the surveillance group. In patients with greater than 70% stenosis, 100% of grafts failed without revision, but only 10% failed with ultrasound detection and a subsequent revision pathway.79 A prospective study carried out by Lundell et al. reported that duplex ultrasound graft surveillance of vein grafts improved the longterm patency by about 15% compared to no surveillance,80 and appropriately conducted graft surveillance should result in graft failure rate less than 3% per year.78 Patients with venous bypass grafts may develop pseudoaneurysms or true aneurysms, but these are rare. When present, they occur most frequently in the anastomotic regions. In a study of saphenous vein grafts, only 10 of 260 (4%) developed true arterial aneurysm,81 with higher incidence in patients with preexisting aneurysm and in males. Nonanastomotic

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FIGURE 25.16 Superficial Femoral Artery Bypass Graft. (A) Color and spectral Doppler shows normal biphasic flow in the proximal bypass graft, with a peak systolic velocity of 83.5 cm/s. (B) Gray-scale imaging in the midcalf shows a focal area of narrowing or thrombosis (arrow). (C) Spectral Doppler at the stenosis with aliasing and a peak velocity of 253 cm/s, consistent with at least 50% stenosis. See also Video 25.6.

aneurysmal degeneration of a saphenous vein graft is a rare complication that can lead to thrombosis, distal embolization, acute rupture, or skin ulceration. Atherosclerotic changes in the graft are considered to be the main reason for the aneurysm formation. The mean time from graft implantation to clinical manifestation of the aneurysm is 7 years.82e84

UPPER EXTREMITY ARTERIES Normal Anatomy Each upper extremity arterial system is supplied from either the brachiocephalic artery (right) or the subclavian artery (left) in patients without anatomic variations. The artery is located anterior to the vein when insonated from the supraclavicular fossa. The subclavian artery courses laterally and

CHAPTER 25 becomes the axillary artery once it is beyond the lateral margin of the first rib. The axillary artery courses medially over the proximal humeral head to the inferior margin of the pectoralis muscle, where it becomes the brachial artery. The brachial artery typically courses along the medial upper arm to the antecubital fossa and divides into the radial, ulnar, and smaller interosseous arteries. Occasionally, there is high brachial artery bifurcation above the antecubital fossa (Fig. 25.17).85 Regardless of the level of origin, the radial and ulnar branches extend to the wrist. Occasionally, a prominent brachial artery branch courses to the region of the elbow; this branch artery can be differentiated from high brachial artery bifurcation by tracing the path to the elbow rather than the wrist. On gray-scale imaging, normal upper extremity arteries have smooth walls with anechoic lumens and lack of atherosclerotic plaques or stenosis, similar to lower extremity arteries. Laminar flow is present without turbulence or aliasing on color Doppler. A high-resistance triphasic waveform with sharp upstroke and transient flow reversal is typically present in the upper extremity arteries on spectral Doppler.

Ultrasound Examination and Imaging Protocol Higher-frequency imaging is usually possible owing to smaller size of the arm relative to the leg. The subclavian artery, axillary artery, and brachial artery are evaluated to the level of the elbow. Both upper extremities should usually be insonated so that the symptomatic side can be compared with the asymptomatic. The ipsilateral innominate (brachiocephalic) artery should be evaluated to detect an inflow abnormality when the right subclavian artery waveform is abnormal. In the forearm, imaging of the radial and ulnar arteries is the key to most diagnoses. The ACR-AIUM-SRU practice parameter for the performance of peripheral arterial ultrasound suggests that upper extremity ultrasound should examine the subclavian artery, axillary artery, and brachial artery.1 Other arteries are examined as deemed clinically appropriate. It states that these may include

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“innominate, radial, and ulnar arteries, and the palmar arch.” The practice parameter further suggests that angle-corrected longitudinal Doppler and/or gray-scale imaging should be documented in each normal and at any abnormal segment. Angle-corrected spectral Doppler is also recommended proximal to, at, and beyond any suspected stenosis.1

Arterial Occlusion, Aneurysm, and Pseudoaneurysm Upper arm arterial occlusion is usually the result of trauma, often iatrogenic. The rate of radial artery occlusion after the artery access for coronary angiography has been reported in up to 3.3% in a recent study.86 For surgical bypass harvest planning, documentation of patency of the palmar arch is an additional component that should be considered, discussed later. For detection and characterization of arterial aneurysm, the maximal outer diameters of the aneurysm should be measured in transverse (short axis) by grayscale. Doppler can differentiate the patent component from mural thrombus. In pseudoaneurysm characterization, the size and Doppler components are similarly measured, but the pseudoaneurysm neck is also evaluated with spectral Doppler, as detailed earlier in the section regarding lower extremity arteries (Fig. 25.18, Videos 25.7 and 25.8). If there is concern for AVF, both the arterial inflow portion and venous outflow should be characterized by duplex Doppler within several centimeters of the pseudoaneurysm, because the characteristic arterialization of the downstream venous waveform may be dampened farther away from the fistula. Turbulent flow through the fistula may affect surrounding tissues, causing a tissue reverberation artifact, which may be the first clue that an AVF is present.

Arterial Stenosis Atherosclerotic disease can cause upper extremity stenosis, but it is a less common problem in the arm than encountered in the lower extremities. Gray-scale findings are similar to the lower extremities and include intimal plaque and/or visible irregularity of the vessel lumen. Color Doppler may show aliasing with turbulent flow similar to those findings seen in lower

FIGURE 25.17 High Brachial Artery Bifurcation. High brachial artery bifurcation, with two arteries (A) (radial and ulnar) and their paired accompanying veins (V), above the antecubital fossa.

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extremity arterial stenosis. A PSV ratio greater than 2:1 of the stenosis relative to the upstream artery within 2 to 4 cm in most nonbranching arteries is consistent with at least 50% diameter stenosis.17 Depending on the timing and whether collaterals have formed, this degree of stenosis may or may not be symptomatic or clinically significant (Fig. 25.19).

Subclavian Stenosis Subclavian stenosis most commonly occurs proximal to the origin of the left vertebral artery. The prevalence of significant subclavian artery stenosis is 2.5% to 5.4% in patients with coronary and extracranial artery disease and approximately up to 30% in patients with severe peripheral artery disease.87 In a subset of patients, flow to the arm is provided by filling through the vertebral artery via retrograde flow. If this reversed flow is substantial, there can be a steal phenomenon (“subclavian steal”) from the brain, leading to dizziness with certain arm movements as additional flow is diverted to the arm, resulting

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FIGURE 25.18 Radial Artery Pseudoaneurysm. (A) Large radial artery (*) pseudoaneurysm with rent in arterial wall (arrows). (B) Color Doppler shows typical “yin-yang” flow in pseudoaneurysm. (C) “To-and-fro” flow in pseudoaneurysm neck. See also Videos 25.7 and 25.8.

in subclavian steal syndrome. Most patients are asymptomatic, and only less than 10% develop arm ischemia or posterior circulation transient ischemic attack (TIA).87 In patients with suggestive symptoms, the vertebral artery waveform should be insonated (Figs. 25.20 and 25.21, Video 25.9). The steal phenomenon, as per duplex scanning, is classified into three grades: grade I, or occult steal, refers to a decreased antegrade vertebral arterial blood flow with midsystolic deceleration and can be reversed in the late systolic phase when performing arm exercise; grade 2, or partial steal, demonstrates a partially reversed flow pattern in the midsystolic and diastolic phases; and grade III, or complete subclavian steal, represents a complete and permanent reversal of blood flow in the vertebral artery throughout the cardiac cycle.88 This is explained in detail in Chapter 24, extracranial arteries under section vertebral artery. In a seminal study, transient early systolic deceleration with resultant transient cessation of antegrade flow or transient reversal of flow (see Fig. 25.21) correlated with subclavian artery

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mean diameter stenosis of 72% and 78%, respectively.89 Similar stenosis can occur in the right subclavian artery, but less frequently. If these abnormal vertebral artery waveforms are seen, an attempt should be made to directly visualize a stenosis by gray-scale and duplex Doppler in the subclavian artery itself. A study by Paivansalo with ultrasound and angiographic correlation showed that more than 90% stenosis of the subclavian artery is associated with a complete steal in the vertebral artery, while a 75% to 90% stenosis corresponds to partial steal. Furthermore, compensatory increased flow in the contralateral carotid and vertebral arteries is associated with retrograde blood flow in the vertebral artery in order to compensate for the central nervous system ischemia.90 Moreover, more than 90% of patients have at least intermittent flow reversal in the vertebral artery if there is more than 50% stenosis in the proximal portion

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FIGURE 25.19 Subclavian Artery Stenosis Due to Atherosclerotic Disease. (A) Focal hypoechoic approximately 50% stenosis (arrow) in the proximal subclavian artery, outlined by color Doppler. (B) Peak systolic velocity (PSV) elevation at 208 cm/s at stenosis. (C) PSV 2 cm upstream (proximal) to stenosis is 89.1 cm/s for a PSV ratio of greater than 2:1.

of the subclavian artery.91 The 2017 European Society of Cardiology guidelines on the diagnosis and treatment of peripheral arterial diseases stressed the importance of cross-sectional imaging in patients with abnormal or indeterminate sonographic findings with regards to subclavian steal syndrome; these patients should have either CTA or MRA for detection of underlying pathology and characterization of anatomic abnormalities.92

Thoracic Outlet Syndrome In distal upper extremity ischemic symptoms, embolic or traumatic injury (commonly iatrogenic) to the artery should also be considered. If embolic phenomena are seen, evaluation for thoracic outlet syndrome should be performed. In patients with symptoms elicited by specific positioning of the arm,

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FIGURE 25.20 Subclavian Steal Phenomenon. (A) Reversed flow in the right vertebral artery. Note that artery and vein are the same color, indicating abnormal flow direction in one of the vessels. (B) MRI confirms significant stenosis in the subclavian artery just distal to the vertebral artery (arrow). See also Video 25.9.

thoracic outlet syndrome is a form of arterial stenosis that should be excluded. It occurs by external compression of the artery by adjacent muscles during abduction of the arm, and this narrowing can affect the waveform morphology of the downstream arteries.93 Bone and rib anomalies frequently contribute to the pathology.94 Ultrasound is the initial imaging study preferred for the evaluation of vascular forms of thoracic outlet syndrome, since it is noninvasive and easily accessible.95 The duplex scan has high sensitivity and specificity in detecting venous stenoses or occlusions.96 The velocities in the artery should be evaluated during adduction or neutral position then compared with velocities and waveforms in abduction. Over time, the artery may become injured, and this can lead to occlusion and formation of emboli, which may also be visible sonographically. These emboli can then migrate distally within the upper extremity to cause pain in regions such as the hand. For sonographic evaluation of thoracic outlet syndrome in the proper clinical presentation, it is important to initially insonate the subclavian and axillary arteries with the arm in neutral position for baseline waveform characterization. Waveforms are acquired from the distal radial and ulnar arteries with the patient sitting comfortably in an upright, seated position. Once the baseline morphology is clearly defined, the arm is moved into the inciting position, usually with abduction and elevation of the arm with external rotation. A combination of inspiration, breath holding, neck extension, and neck turn to the affected side, known as the Adson maneuver, may elicit a positive finding on Doppler.97 The waveform is monitored as the arm is moved into a variety of positions from neutral position to 90, 120, and 180 degrees of abduction to elicit symptoms (Fig. 25.22). If positive, a diminished PSV and

prolongation of acceleration time waveform should be apparent in the radial and ulnar arteries of the forearm.98 Once this has been identified, it is helpful to repeat the baseline and positive results to show reproducibility of the findings. Further support of the diagnosis includes visible narrowing identified in the subclavian artery or the presence of an aneurysm in this region.98,99 Pseudoaneurysms are frequently present in the setting of thoracic outlet syndrome and can lead to embolic events. Care must be taken in the diagnosis because hyperextension can produce arterial flow abnormality in up to 20% of normal volunteers.100

Radial Artery Evaluation for Coronary Bypass Graft Another use of Doppler in bypass patients is to determine suitability of the radial artery for coronary artery grafting. The ulnar artery typically provides the dominant source of blood flow to the hand. The ulnar artery supplies the superficial palmar arch, which is often incomplete. The radial artery supplies the deep palmar arch, which is more commonly complete, in communication with the ulnar artery. If the superficial palmar arch in the hand is patent, allowing flow to the entire hand through the ulnar artery, then the radial artery can be harvested. Thus, evaluation of palmar arch patency is necessary before harvest. Doppler evaluation of patency is more accurate than the modified Allen test on physical examination, because only about 12% of patients with an abnormal modified Allen test result have abnormal Doppler findings.101 A small linear array 12- to 15-MHz “hockey stick” transducer is initially used to determine antegrade flow of the

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FIGURE 25.21 Left Subclavian Steal Syndrome. (A) High-grade left subclavian stenosis of 90% or more based upon very elevated Doppler velocity and (B) Type 4 waveform, with reversal during systole in the left vertebral artery. See also Video 25.9. (C) CT angiography of the neck shows mixed calcified atheromatous plaque causing severe stenosis (arrow), and (D) digital subtraction angiography (DSA) of left upper extremity confirms above findings.

ulnar artery and radial artery at the wrist. With duplex Doppler, arterial flow to the hand in the superficial palmar arch at the thenar eminence near the crease of the base of the thumb is characterized first with normal distal radial artery inflow. Subsequently, the radial artery is transiently occluded by direct compression of the radial artery at the wrist, and the resultant spectral Doppler waveform is evaluated. Care should be taken during examination not to hyperextend the hand with regard to the wrist, because a false-negative examination finding may incorrectly suggest

lack of patency of the arch. In patients with a patent superficial palmar arch, there should be reversed flow of the radial artery in the hand, measured at the thenar eminence or in the region of the snuff box between the first metacarpal and second carpal bone.102e104 If there is no flow or absent reversed flow during radial artery occlusion, then the radial artery of that upper extremity is not suitable for harvest owing to an incomplete arch (Fig. 25.23).104 Increased flow in the ulnar artery may also occur during radial artery compression if the arch is patent.105

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FIGURE 25.22 Thoracic Outlet Syndrome. (A) Normal baseline subclavian artery waveform. (B) Altered waveform during hyperextension, with compression against the clavicle causing stenosis.

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FIGURE 25.23 Radial Artery Evaluation for Coronary Bypass Graft. (A) Patent palmar arch, with reversal of flow in the superficial palmar arch on radial artery compression at the wrist. (B) Incomplete palmar arch, with lack of flow in the superficial palmar arch on radial artery compression at the wrist.

CONCLUSION Ultrasound plays an important role in evaluating the peripheral vasculature. Although peripheral artery ultrasound is commonly considered for its uses in atherosclerotic disease, the technique can be applied in numerous clinical scenarios. For evaluation of stenosis in native or bypassed vessels, the concepts are similar, although some of the threshold values differ. For evaluation of aneurysm, pseudoaneurysm, or AVF, the examination can be more localized in scope to determine the size of the abnormality by grayscale and the use of Doppler to focus on the inflow and outflow characteristics.

REFERENCES 1. AIUM practice parameter for the performance of peripheral arterial ultrasound examinations using color and spectral Doppler imaging. J Ultrasound Med. 2021;40:E17eE24. 2. Sanyal R, Kraft B, Alexander LF, Ismail A, Lockhart ME, Robbin ML. Scanner-based protocol-driven ultrasound: an effective method to improve efficiency in an ultrasound department. Am J Roentgenol. 2016;206:792e796. 3. AbuRahma AF, Jarrett K, Hayes DJ. Clinical implications of power Doppler three-dimensional ultrasonography. Vascular. 2004;12:293e300. 4. Kohler TR, Nance DR, Cramer MM, Vandenburghe N, Strandness Jr DE. Duplex scanning for diagnosis of aortoiliac and femoropopliteal disease: a prospective study. Circulation. 1987;76:1074e1080.

CHAPTER 25 5. Gerhard-Herman M, Gardin JM, Jaff M, Mohler E, Roman M, Naqvi TZ. Guidelines for noninvasive vascular laboratory testing: a report from the American Society of Echocardiography and the Society for vascular Medicine and Biology. Vasc Med. 2006;11:183e200. 6. Llerena S, Piezny D, Ríos F, Arias C, Sagardía J. [Phlegmasia cerulea dolens. Treatment with systemic fibrinolysis]. Medicina (B Aires). 2021;81:454e457. 7. Gutierrez JR, Volteas P, Skripochnik E, Tassiopoulos AK, Bannazadeh M. A Case of phlegmasia cerulea dolens in a patient with COVID-19, effectively treated with fasciotomy and mechanical thrombectomy. Ann Vasc Surg. 2022;79:122e126. 8. AS EL, AlQattan AS, Elashaal E, AlSadery H, AlGhanmi I, Aldhafery BF. The ugly face of deep vein thrombosis: phlegmasia Cerulea Dolens-Case report. Int J Surg Case Rep. 2019;59:107e110. 9. Hwang JY. Doppler ultrasonography of the lower extremity arteries: anatomy and scanning guidelines. Ultrasonography. 2017;36:111e119. 10. Moneta GL, Yeager RA, Antonovic R, et al. Accuracy of lower extremity arterial duplex mapping. J Vasc Surg. 1992;15:275e283. 11. Hatsukami TS, Primozich JF, Zierler RE, Harley JD, Strandness Jr DE. Color Doppler imaging of infrainguinal arterial occlusive disease. J Vasc Surg. 1992;16:527e531. 12. Moneta GL. Tibial artery velocities in the diagnosis and follow-up of peripheral arterial disease. Semin Vasc Surg. 2020;33:65e68. 13. Mohler 3rd ER, Gornik HL, Gerhard-Herman M, Misra S, Olin JW, Zierler E. ACCF/ACR/AIUM/ASE/ASN/ICAVL/SCAI/SCCT/SIR/SVM/ SVS 2012 appropriate use criteria for peripheral vascular ultrasound and physiological testing part I: arterial ultrasound and physiological testing: a report of the American College of Cardiology Foundation Appropriate Use criteria Task Force, American College of Radiology, American Institute of ultrasound in Medicine, American Society of Echocardiography, American Society of Nephrology, Intersocietal Commission for the Accreditation of Vascular Laboratories, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, Society for Interventional Radiology, Society for Vascular Medicine, and Society for Vascular Surgery. J Vasc Surg. 2012;56:e17ee51. 14. Collins R, Cranny G, Burch J, et al. A systematic review of duplex ultrasound, magnetic resonance angiography and computed tomography angiography for the diagnosis and assessment of symptomatic, lower limb peripheral arterial disease. Health Technol Assess. 2007;11:iiieiv, xiexiii, 1e184. 15. Foley TR, Armstrong EJ, Waldo SW. Contemporary evaluation and management of lower extremity peripheral artery disease. Heart. 2016;102:1436e1441. 16. Jager KA, Phillips DJ, Martin RL, et al. Noninvasive mapping of lower limb arterial lesions. Ultrasound Med Biol. 1985;11:515e521. 17. Mazzariol F, Ascher E, Hingorani A, Gunduz Y, Yorkovich W, SallesCunha S. Lower-extremity revascularisation without preoperative contrast arteriography in 185 cases: lessons learned with duplex ultrasound arterial mapping. Eur J Vasc Endovasc Surg. 2000;19:509e515. 18. Khan SZ, Khan MA, Bradley B, Dayal R, McKinsey JF, Morrissey NJ. Utility of duplex ultrasound in detecting and grading de novo femoropopliteal lesions. J Vasc Surg. 2011;54:1067e1073. 19. Elbadawy A, Aly H, Ibrahim M, Bakr H. Impact of Duplex arterial mapping on decision making in non-acute ischemic limb patients. Int Angiol. 2015;34:538e544. 20. Fontcuberta J, Flores A, Orgaz A, et al. Reliability of preoperative duplex scanning in designing a therapeutic strategy for chronic lower limb ischemia. Ann Vasc Surg. 2009;23:577e582. 21. Norgren L, Hiatt WR, Dormandy JA, Nehler MR, Harris KA, Fowkes FGR. Inter-society Consensus for the management of peripheral arterial disease (TASC II). J Vasc Surg. 2007;45:S5eS67. 22. Sultan S, Tawfick W, Hynes N. Ten-year technical and clinical outcomes in TransAtlantic Inter-Society Consensus II infrainguinal C/D lesions using duplex ultrasound arterial mapping as the sole imaging modality for critical lower limb ischemia. J Vasc Surg. 2013;57:1038e1045. 23. Edwards JM, Coldwell DM, Goldman ML, Strandness Jr DE. The role of duplex scanning in the selection of patients for transluminal angioplasty. J Vasc Surg. 1991;13:69e74.

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24. Lai DT, Huber D, Glasson R, et al. Colour-coded duplex ultrasonography in selection of patients for transluminal angioplasty. Australas Radiol. 1995;39:243e245. 25. Baril DT, Rhee RY, Kim J, Makaroun MS, Chaer RA, Marone LK. Duplex criteria for determination of in-stent stenosis after angioplasty and stenting of the superficial femoral artery. J Vasc Surg. 2009;49:133e138. 26. Langenberger H, Schillinger M, Plank C, et al. Agreement of duplex ultrasonography vs. computed tomography angiography for evaluation of native and in-stent SFA re-stenosis–findings from a randomized controlled trial. Eur J Radiol. 2012;81:2265e2269. 27. Draxler MS, Al-Adas Z, Abbas D, et al. Outcome benefit of arterial duplex stent imaging after superficial femoral artery stent implantation. J Vasc Surg. 2021;73:179e188. 28. Brown CD, Muniz M, Kauvar DS. Response of the popliteal artery to treadmill exercise and stress positioning in patients with and without exertional lower extremity symptoms. J Vasc Surg. 2019;69:1545e1551. 29. Hislop M, Kennedy D, Cramp B, Dhupelia S. Functional popliteal artery entrapment syndrome: poorly understood and frequently missed? A review of clinical features, appropriate Investigations, and treatment Options. J Sports Med. 2014;2014, 105953. 30. Sinha S, Houghton J, Holt PJ, Thompson MM, Loftus IM, Hinchliffe RJ. Popliteal entrapment syndrome. J Vasc Surg. 2012;55:252e262.e230. 31. Hamper UM, DeJong MR, Scoutt LM. Ultrasound evaluation of the lower extremity veins. Radiol Clin. 2007;45:525e547, ix. 32. Tuveson V, Löfdahl HE, Hultgren R. Patients with abdominal aortic aneurysm have a high prevalence of popliteal artery aneurysms. Vasc Med. 2016;21:369e375. 33. Ravn H, Pansell-Fawcett K, Björck M. Popliteal artery aneurysm in Women. Eur J Vasc Endovasc Surg. 2017;54:738e743. 34. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American association for vascular surgery/Society for vascular surgery, Society for Cardiovascular angiography and interventions, Society for vascular Medicine and Biology, Society of interventional Radiology, and the ACC/AHA Task Force on practice guidelines (Writing Committee to develop guidelines for the management of patients with peripheral arterial disease). TransAtlantic Inter-Society Consensus; and vascular disease Foundation. Circulation. 2006;113:e463ee654. 35. Buijs RV, Willems TP, Tio RA, et al. Calcification as a risk factor for rupture of abdominal aortic aneurysm. Eur J Vasc Endovasc Surg. 2013;46:542e548. 36. Stiegler H, Brandl R. Importance of ultrasound for diagnosing periphereal arterial disease. Ultraschall der Med. 2009;30:334e374. 37. Shortell CK, DeWeese JA, Ouriel K, Green RM. Popliteal artery aneurysms: a 25-year surgical experience. J Vasc Surg. 1991;14:771e776. 38. Dorigo W, Pulli R, Alessi Innocenti A, et al. A 33-year experience with surgical management of popliteal artery aneurysms. J Vasc Surg. 2015;62:1176e1182. 39. von Stumm M, Teufelsbauer H, Reichenspurner H, Debus ES. Two decades of endovascular repair of popliteal artery aneurysm–A meta-analysis. Eur J Vasc Endovasc Surg. 2015;50:351e359. 40. Rajasinghe HA, Tzilinis A, Keller T, Schafer J, Urrea S. Endovascular exclusion of popliteal artery aneurysms with expanded polytetrafluoroethylene stent-grafts: early results. Vasc Endovascular Surg. 2006;40: 460e466. 41. Antonello M, Frigatti P, Battocchio P, et al. Endovascular treatment of asymptomatic popliteal aneurysms: 8-year concurrent comparison with open repair. J Cardiovasc Surg. 2007;48:267e274. 42. Lumsden AB, Miller JM, Kosinski AS, et al. A prospective evaluation of surgically treated groin complications following percutaneous cardiac procedures. Am Surg. 1994;60:132e137. 43. Erol F, Arslan S, Yuksel IO, et al. Determinants of iatrogenic femoral pseudoaneurysm after cardiac catheterization or percutaneous coronary intervention via the femoral artery. Turk Kardiyol Dern Ars. 2015;43: 513e519. 44. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. 10th ed. Elsevier; 2020.

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45. Middleton WD, Dasyam A, Teefey SA. Diagnosis and treatment of iatrogenic femoral artery pseudoaneurysms. Ultrasound Q. 2005;21:3e17. 46. Middleton WD, Robinson KA. Analysis and Classification of postcatheterization femoral arteriovenous fistulas based on color Doppler examinations. J Ultrasound Med. 2021. 47. Kent KC, McArdle CR, Kennedy B, Baim DS, Anninos E, Skillman JJ. A prospective study of the clinical outcome of femoral pseudoaneurysms and arteriovenous fistulas induced by arterial puncture. J Vasc Surg. 1993;17:125e131. 48. Toursarkissian B, Allen BT, Petrinec D, et al. Spontaneous closure of selected iatrogenic pseudoaneurysms and arteriovenous fistulae. J Vasc Surg. 1997;25:803e808. 49. Altuwaijri T, Alsalman M, Altoijry A, Iqbal K, AlGhofili H. Ultrasoundguided thrombin injection versus ultrasound-guided compression repair in the treatment of post-catheterization femoral artery pseudoaneurysm: King Saud University Medical Center Experience. Turk Gogus Kalp Damar Cerrahisi Derg. 2020;28:114e119. 50. Franklin JA, Brigham D, Bogey WM, Powell CS. Treatment of iatrogenic false aneurysms. J Am Coll Surg. 2003;197:293e301. 51. Shah KJ, Halaharvi DR, Franz RW, Jenkins Ii J. Treatment of iatrogenic pseudoaneurysms using ultrasound-guided thrombin injection over a 5year period. Int J Angiol. 2011;20:235e242. 52. La Perna L, Olin JW, Goines D, Childs MB, Ouriel K. Ultrasound-guided thrombin injection for the treatment of postcatheterization pseudoaneurysms. Circulation. 2000;102:2391e2395. 53. Yang EY, Tabbara MM, Sanchez PG, et al. Comparison of ultrasoundguided thrombin injection of iatrogenic pseudoaneurysms based on neck dimension. Ann Vasc Surg. 2018;47:121e127. 54. Gale SS, Scissons RP, Jones L, Salles-Cunha SX. Femoral pseudoaneurysm thrombinjection. Am J Surg. 2001;181:379e383. 55. Morgan R, Belli AM. Current treatment methods for postcatheterization pseudoaneurysms. J Vasc Interv Radiol. 2003;14:697e710. 56. Sadiq S, Ibrahim W. Thromboembolism complicating thrombin injection of femoral artery pseudoaneurysm: management with intraarterial thrombolysis. J Vasc Interv Radiol. 2001;12:633e636. 57. Paulson EK, Nelson RC, Mayes CE, Sheafor DH, Sketch Jr MH, Kliewer MA. Sonographically guided thrombin injection of iatrogenic femoral pseudoaneurysms: further experience of a single institution. Am J Roentgenol. 2001;177:309e316. 58. Ha L, Yiu SW, Wang FF, Han JL. A possible allergic reaction case to thrombin injected into pseudoaneurysm after radiofrequency ablation. Am J Case Rep. 2019;20:1497e1499. 59. Jalaeian H, Misselt A. Anaphylactic reaction to bovine thrombin in ultrasound-guided treatment of femoral pseudoaneurysm. J Vasc Interv Radiol. 2015;26:915e916. 60. Pope M, Johnston KW. Anaphylaxis after thrombin injection of a femoral pseudoaneurysm: recommendations for prevention. J Vasc Surg. 2000;32:190e191. 61. Elford J, Burrell C, Freeman S, Roobottom C. Human thrombin injection for the percutaneous treatment of iatrogenic pseudoaneurysms. Cardiovasc Intervent Radiol. 2002;25:115e118. 62. Shetty R, Lotun K. Treatment of an iatrogenic femoral artery pseudoaneurysm with concomitant arteriovenous fistula with percutaneous implantation of an Amplatzer vascular plug. Catheter Cardiovasc Interv. 2013;81:E53eE57. 63. Wolodiger F, Dardik H, Johnson F, Ibrahim IM. Rupture of arteriovenous fistula after in situ saphenous vein bypass. J Vasc Surg. 1991;13:503e505. 64. Lundell A, Nyborg K. Do residual arteriovenous fistulae after in situ saphenous vein bypass grafting influence patency? J Vasc Surg. 1999;30, 9910. 65. Davidovic L, Lotina S, Vojnovic B, et al. Post-traumatic AV fistulas and pseudoaneurysms. J Cardiovasc Surg. 1997;38:645e651. 66. Straton CS, Tisnado J. Spontaneous arteriovenous fistulas of the lower extremities: angiographic demonstration in five patients with peripheral vascular disease. Cardiovasc Intervent Radiol. 2000;23:318e321. 67. Link DP, Granchi PJ. Chronic iliac vein occlusion and painful nonhealing ulcer induced by high venous pressures from an arteriovenous malformation. Case Rep Radiol. 2011;2011:514721.

68. Yuan H, Sun J, Zhou Z, et al. Diagnosis and treatment of acquired arteriovenous fistula after lower extremity deep vein thrombosis. Int Angiol. 2019;38:10e16. 69. Woo K, Palmer OP, Weaver FA, Rowe VL. Outcomes of completion imaging for lower extremity bypass in the Vascular Quality Initiative. J Vasc Surg. 2015;62:412e416. 70. Tan TW, Rybin D, Kalish JA, et al. Routine use of completion imaging after infrainguinal bypass is not associated with higher bypass graft patency. J Vasc Surg. 2014;60:678e685.e672. 71. Buckley CJ, Abernathy S, Lee SD, Arko FR, Patterson DE, Manning LG. Suggested treatment protocol for improving patency of femoralinfrapopliteal cryopreserved saphenous vein allografts. J Vasc Surg. 2000;32:731e738. 72. O’Banion LA, Wu B, Eichler CM, Reilly LM, Conte MS, Hiramoto JS. Cryopreserved saphenous vein as a last-ditch conduit for limb salvage. J Vasc Surg. 2017;66:844e849. 73. Singh K, Juneja A, Bajaj T, et al. Single Tertiary Care center outcomes after lower extremity cadaveric vein bypass for limb salvage. Vasc Endovascular Surg. 2020;54:430e435. 74. Wixon CL, Mills JL, Westerband A, Hughes JD, Ihnat DM. An economic appraisal of lower extremity bypass graft maintenance. J Vasc Surg. 2000;32:1e12. 75. Mills Sr JL, Wixon CL, James DC, Devine J, Westerband A, Hughes JD. The natural history of intermediate and critical vein graft stenosis: recommendations for continued surveillance or repair. J Vasc Surg. 2001;33:273e278. 76. Gonsalves C, Bandyk DF, Avino AJ, Johnson BL. Duplex features of vein graft stenosis and the success of percutaneous transluminal angioplasty. J Endovasc Surg. 1999;6:66e72. 77. Rehfuss J, Scali S, He Y, et al. The correlation between computed tomography and duplex evaluation of autogenous vein bypass grafts and their relationship to failure. J Vasc Surg. 2015;62:1546e1554.e1541. 78. Tinder CN, Bandyk DF. Detection of imminent vein graft occlusion: what is the optimal surveillance program? Semin Vasc Surg. 2009;22:252e260. 79. Idu MM, Blankenstein JD, de Gier P, Truyen E, Buth J. Impact of a colorflow duplex surveillance program on infrainguinal vein graft patency: a five-year experience. J Vasc Surg. 1993;17:42e52. 80. Lundell A, Lindblad B, Bergqvist D, Hansen F. Femoropopliteal-crural graft patency is improved by an intensive surveillance program: a prospective randomized study. J Vasc Surg. 1995;21:26e33. 81. Szilagyi DE, Elliott JP, Hageman JH, Smith RF, Dall’olmo CA. Biologic fate of autogenous vein implants as arterial substitutes: clinical, angiographic and histopathologic observations in femoro-popliteal operations for atherosclerosis. Ann Surg. 1973;178:232e246. 82. Bikk A, Rosenthal MD, Wellons ED, Hancock SM, Rosenthal D. Atherosclerotic aneurysm formation in a lower extremity saphenous vein graft. Vascular. 2006;14:173e176. 83. López MT, Dorgham AS, Rosas FC, de Loma JG. Aneurysmal degeneration of a saphenous vein graft following the repair of a popliteal aneurysm: case report and literature review. Vascular. 2012;20:294e298. 84. Tamellini P, Recchia A, Garriboli L, Miccoli T, Pruner G, Jannello AM. Non-anastomotic aneurysmal degeneration of great saphenous vein graft A case report and review of the literature. Ann Ital Chir. 2019;90:83e87. 85. McCormack LJ, Cauldwell EW, Anson BJ. Brachial and antebrachial arterial patterns; a study of 750 extremities. Surg Gynecol Obstet. 1953;96:43e54. 86. Steinmetz M, Radecke T, Boss T, et al. Radial artery occlusion after cardiac catheterization and impact of medical treatment. Vasa. 2020;49:463e466. 87. Saha T, Naqvi SY, Ayah OA, McCormick D, Goldberg S. Subclavian artery disease: diagnosis and therapy. Am J Med. 2017;130:409e416. 88. Tahmasebpour HR, Buckley AR, Cooperberg PL, Fix CH. Sonographic examination of the carotid arteries. Radiographics. 2005;25:1561e1575. 89. Kliewer MA, Hertzberg BS, Kim DH, Bowie JD, Courneya DL, Carroll BA. Vertebral artery Doppler waveform changes indicating subclavian steal physiology. Am J Roentgenol. 2000;174:815e819. 90. Päivänsalo M, Heikkilä O, Tikkakoski T, Leinonen S, Merikanto J, Suramo I. Duplex ultrasound in the subclavian steal syndrome. Acta Radiol. 1998;39:183e188.

CHAPTER 25 91. Potter BJ, Pinto DS. Subclavian steal syndrome. Circulation. 2014;129:2320e2323. 92. Aboyans V, Ricco JB, Bartelink MEL, et al. 2017 ESC guidelines on the diagnosis and treatment of peripheral arterial diseases, in collaboration with the European Society for Vascular Surgery (ESVS): document covering atherosclerotic disease of extracranial carotid and vertebral, mesenteric, renal, upper and lower extremity arteries Endorsed by: the European Stroke Organization (ESO) the Task Force for the diagnosis and treatment of peripheral arterial diseases of the European Society of Cardiology (ESC) and of the European Society for Vascular Surgery (ESVS). Eur Heart J. 2018;39:763e816. 93. Longley DG, Yedlicka JW, Molina EJ, Schwabacher S, Hunter DW, Letourneau JG. Thoracic outlet syndrome: evaluation of the subclavian vessels by color duplex sonography. Am J Roentgenol. 1992;158:623e630. 94. Wadhwani R, Chaubal N, Sukthankar R, Shroff M, Agarwala S. Color Doppler and duplex sonography in 5 patients with thoracic outlet syndrome. J Ultrasound Med. 2001;20:795e801. 95. Grunebach H, Arnold MW, Lum YW. Thoracic outlet syndrome. Vasc Med. 2015;20:493e495. 96. Moore R, Wei Lum Y. Venous thoracic outlet syndrome. Vasc Med. 2015;20:182e189. 97. Lee AD, Agarwal S, Sadhu D. Doppler Adson’s test: predictor of outcome of surgery in non-specific thoracic outlet syndrome. World J Surg. 2006;30:291e292.

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98. Baz AA. An overview of the findings of dynamic upper limbs’ arterial and venous duplex in cases of vascular thoracic outlet syndrome. Egyptian J of Radiol and Nuc Med. 2019;50. 99. Criado E, Berguer R, Greenfield L. The spectrum of arterial compression at the thoracic outlet. J Vasc Surg. 2010;52:406e411. 100. Chen H, Doornbos N, Williams K, Criado E. Physiologic variations in venous and arterial hemodynamics in response to postural changes at the thoracic outlet in normal volunteers. Ann Vasc Surg. 2014;28:1583e1588. 101. Abu-Omar Y, Mussa S, Anastasiadis K, Steel S, Hands L, Taggart DP. Duplex ultrasonography predicts safety of radial artery harvest in the presence of an abnormal Allen test. Ann Thorac Surg. 2004;77:116e119. 102. Habib J, Baetz L, Satiani B. Assessment of collateral circulation to the hand prior to radial artery harvest. Vasc Med. 2012;17:352e361. 103. Kochi K, Sueda T, Orihashi K, Matsuura Y. New noninvasive test alternative to Allen’s test: snuff-box technique. J Thorac Cardiovasc Surg. 1999;118:756e758. 104. Zimmerman P, Chin E, Laifer-Narin S, Ragavendra N, Grant EG. Radial artery mapping for coronary artery bypass graft placement. Radiology. 2001;220:299e302. 105. Pola P, Serricchio M, Flore R, Manasse E, Favuzzi A, Possati GF. Safe removal of the radial artery for myocardial revascularization: a Doppler study to prevent ischemic complications to the hand. J Thorac Cardiovasc Surg. 1996;112:737e744.

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26

Peripheral Veins Muhammad U. Aziz, Mohd Zahid, Therese M. Weber, and Michelle LaVonne Robbin

CHAPTER OUTLINE INTRODUCTION, 1018 PERIPHERAL VEINS, 1018

Sonographic Examination Technique, 1019 Lower Extremity Veins, 1019

INTRODUCTION In this chapter we describe ultrasound assessment of the peripheral veins. In general, being more superficial in anatomic location, these structures are well seen by gray-scale, color, and spectral Doppler ultrasound. In comparison to the thoracoabdominal veins, the extremity vessels are more robustly evaluated due to the availability of adequate imaging windows for the transducer to be placed over the vascular area of interest without overlying tissue containing bone or gas. Linear transducers with frequencies greater than 5 MHz are usually used. Gray-scale sonography is useful for evaluating the presence of thrombus/occlusion or confirming extravascular masses. Color Doppler imaging allows for a rapid survey of the area of interest, and then spectral Doppler can be used to characterize blood flow patterns. Standardized protocols, such as those provided by the American College of Radiology (ACR), American Institute of Ultrasound in Medicine, and Society of Radiologists in Ultrasound, should be followed.1,2 It is recommended that examinations be performed in an accredited laboratory with participation in one of the vascular accreditation programs, such as the ACR or the Intersocietal Accreditation Commission, in order to achieve a national standard of excellence and to improve the quality of peripheral arterial and venous ultrasound examinations.3 In the setting of a dedicated staff and with physician support, ultrasound can be used to diagnose many peripheral vascular abnormalities definitively and avoid the need for ionizing radiation or intravenous contrasted crosssectional studies.

PERIPHERAL VEINS Evaluations of lower extremity (LE) and upper extremity (UE) venous systems are primarily performed with sonography. Useful

1018

Upper Extremity Veins, 1029 CONCLUSION, 1036 REFERENCES, 1036

applications include evaluation for thrombus, localization for venous access procedures, and preoperative venous mapping for hemodialysis AVF and graft placement. Key aspects of venous gray-scale, color, and spectral Doppler imaging include knowledge of anatomy, scanning technique, and attention to detail. The most common indication for venous Doppler ultrasound is to identify deep venous thrombosis (DVT). Undiagnosed and untreated DVT can result in fatal pulmonary embolism (PE). Sudden death is the first symptom in about 25% of people who have PE4 (Fig. 26.1). There is also a substantial risk of cardiac arrest due to PE, reported to be close to 5%.5 The incidence of recurrent PE in patients with provoking risk factors (i.e., recent immobility, surgery, bone fracture, active cancer, estrogen use, pregnancy, puerperium, or long-term travel) is similar to patients with DVT of the lower extremities. Clinical evaluation of the peripheral venous system is frequently difficult, nonspecific, and often inaccurate. Clinical decision rules to improve pretest probability are recommended by the American College of Physicians and the American Academy of Family Physicians.6-8 The Wells criteria generate a score for certain physical examination findings and pertinent clinical history.9 Clinical factors associated with increased probability of DVT include active cancer, immobilization, localized tenderness along the distribution of the deep venous system, swollen extremity, pitting edema localized to the symptomatic extremity, collateral superficial veins, and previously documented DVT. A modification of the Wells score creates two groups: DVT unlikely or DVT likely as detailed below in Table 26.1.10 Current guidelines recommend a D-dimer test for those with low risk.11,12 The D-dimer test measures a degradation product of fibrin and has a high negative predictive value that is sensitive, but not specific for DVT.13 If the D-dimer test result is positive, the patient should be evaluated with venous Doppler. As with patients without cancer, the combination of low probability and negative D-dimer result can exclude DVT in

CHAPTER 26

A

Peripheral Veins

1019

B

FIGURE 26.1 Pulmonary Emboli. (A) Axial CT with contrast shows a large saddle pulmonary embolus extending into the left and right pulmonary arteries (arrows). (B) Maximum-intensity projection coronal CT with contrast in the same patient shows extent of bilateral pulmonary emboli (arrows).

cancer patients.14,15 In practice, many patients do not undergo this workup.16 Going directly to sonography is frequently faster than waiting for workup results and may offer an alternative musculoskeletal diagnosis such as popliteal fossa cyst. In cases of technically limited sonographic evaluation of the more central deep venous system (iliac veins and inferior vena cava [IVC]), magnetic resonance venography may be more sensitive if positive results would affect patient management.17,18

Sonographic Examination Technique The superficial location of the upper and lower venous system allows the use of linear, higher-frequency transducers. The highest-frequency linear transducer that still gives adequate penetration should be used to optimize spatial resolution. Typically, the examination is best performed using a 5- to 10-MHz linear array transducer, with application of the higherfrequency range in upper arm, forearm, calf, and more superficial veins. A curved array or sector probe in the 3- to 5-MHz range may be necessary in very large patients or those with substantial extremity edema. Gray-scale imaging should include compression and should be performed in the transverse plane. Color flow and spectral analysis are the most common applications of Doppler sonography, with occasional use of power Doppler. These Doppler techniques evaluate the disease process in the peripheral veins and give additional information regarding altered venous hemodynamics. Anatomic and functional detail make sonography a valuable tool. Color Doppler sonography can be used to evaluate venous segments that cannot be directly assessed by compression, such as the subclavian veins. Power Doppler and perfusion techniques19

provide improved detection of very slow flow, especially in small veins.

Lower Extremity Veins Normal Anatomy Deep Venous System. The venous anatomy of the leg is illustrated in Fig. 26.2. The common femoral vein (CFV) begins at the level of the inguinal ligament as the continuation of the external iliac vein and extends caudally to the bifurcation into the femoral vein (FV) and the profunda femoris vein, which lie medial to the adjacent artery. The FV courses medially to the adjacent artery through the adductor canal in the caudal thigh. The term “femoral vein,” previously called the “superficial femoral vein,” should be used to avoid clinical confusion regarding the deep versus superficial venous system.20 The popliteal vein (PV) represents the continuation of the FV after its exit from the adductor canal in the posterior caudal thigh. The PV is located superficial to the artery and courses through the popliteal space into the proximal calf. Duplication of the FV is seen in about 30% of patients.21 Duplication of the FV can also be segmental. These variants are associated with increased incidence of DVT.22-24 About 40% of patients with multiple vessels within the popliteal fossa arise from a high confluence of the posterior tibial and peroneal veins, rather than true PV duplication.21 Description of these anatomic variants assists in avoiding a missed diagnosis on follow-up examinations. The paired anterior tibial veins arise from the PV and course laterally along the anterior calf to the dorsum of the foot. The tibioperoneal trunk originates from the PV slightly

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PART THREE

Small Parts, Carotid Artery, and Peripheral Vessel Sonography

TABLE 26.1 Dichotomized Wells Score for the Diagnosis of Deep Venous Thrombosis CLINICAL CHARACTERISTICS

POINTS

Active cancer (patient receiving treatment for cancer within the previous 6 months or currently receiving palliative treatment) Paralysis, paresis, or recent plaster immobilization of the lower extremities Recently bedridden for 3 days or more, or major surgery within the previous 12 weeks requiring general or regional anesthesia Localized tenderness along the distribution of the deep venous system Entire leg swollen Calf swelling at least 3 cm larger than that on the asymptomatic side (measured 10 cm below tibial tuberosity) Pitting edema confined to the symptomatic leg Collateral superficial veins (nonvaricose) Previously documented deep-vein thrombosis Alternative diagnosis at least as likely as deep-vein thrombosis

þ1

Common femoral vein

A þ1

A Profunda femoris vein

þ1

Femoral vein Adductor magnus muscle

þ1 þ1 þ1

Great saphenous vein

Adductor canal

C

Popliteal vein

þ1 þ1 þ1 2

B

B

C

D

E

Anterior tibial veins Small saphenous vein

D TOTAL SCORE

CLINICAL PREVALENCE PROBABILITY OF DVT

1 cm

BICORNUATE UTERUS

BICORNUATE UTERUS WITH R/L COMMUNICATING TRACT

UTERUS BICORNUATE BICOLLIS

COMBINED BICORNUATE SEPTATE UTERUS

Fig. 28.8 2021 American Society for Reproductive Medicine (ASRM) Classification System for Diagnosis of Müllerian Anomalies. (Reproduced with permission from Pfeifer SM, Attaran M, Goldstein J, et al. ASRM Müllerian anomalies classification 2021. Fertil Steril. 2021;116:1238e1252.62)

with a rudimentary horn, but the categorization scheme deems this unicornuate. The rudimentary horn may or may not have an endometrium and may or may not communicate with the

endometrial cavity of the main uterine horn. A unicornuate uterus develops when one paramesonephric duct fails to normally develop; this, in the absence of a rudimentary horn,

CHAPTER 28 The Uterus

SEPTATE UTERUS Septum length >1 cm Septum angle 90°

NORMAL/ARCUATE UTERUS

COMPLETE SEPTATE UTERUS WITH SEPTATE CERVIX AND LONGITUDINAL VAGINAL SEPTUM

ROBERT’S UTERUS

COMPLETE SEPTATE UTERUS, DUPLICATED CERVICES, AND OBSTRUCTED R/L HEMIVAGINA

LONGITUDINAL VAGINAL SEPTUM

MID VAGINAL SEPTUM

DISTAL VAGINAL AGENESIS

COMPLEX ANOMALIES

LONGITUDINAL VAGINAL SEPTUM OF VARIABLE LENGTH

LONGITUDINAL VAGINAL SEPTUM OF VARIABLE LENGTH AND UTERUS DIDELPHYS

BICORNUATE UTERUS WITH BILATERAL OBSTRUCTED ENDOMETRIAL CAVITIES

OBSTRUCTED R/L HEMIVAGINA AND UTERUS DIDELPHYS

LONGITUDINAL VAGINAL SEPTUM OF VARIABLE LENGTH AND COMPLETE SEPTATE UTERUS WITH DUPLICATED CERVIX

OBSTRUCTED R/L HEMIVAGINA, HEMIUTERUS AND SINGLE CERVIX WITH SEPARATE CONTRALATERAL R/L PATENT HEMIUTERUS, CERVIX AND VAGINA

OBSTRUCTED R/L HEMIVAGINA AND COMPLETE SEPTATE UTERUS WITH DUPLICATED CERVICES

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Scan QR code to view the ASRM MAC 2021 tool (page 2 of 2) © 2021 American Society for Reproductive Medicine Fig. 28.8 cont'd

UTERUS DIDELPHYS WITH COMMUNICATING HEMIUTERI AND UNILATERAL R/L CERVICO-VAGINAL ATRESIA

BICORNUATE UTERUS WITH R/L COMMUNICATING TRACT AND TRANSVERSE VAGINAL SEPTUM

UTERUS ISTHMUS AGENESIS

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results in a uterus with one fallopian tube.60 When the median septum formed by the medial walls of the müllerian ducts fails to resorb, a septate uterus is present. The 2021 definition of a septate uterus has an endometrial septum length of greater than 1 cm measured from the bicornual line with the leading edge of the septum having an angle of less than 90 degrees.62 Other anomalies can be seen in patients exposed to diethylstilbestrol (DES) in utero, though this is seen less frequently now since its use was stopped in the early 1970s. In DES exposure, sonography can demonstrate a diffuse decrease in the size of the uterus and an irregular T-shaped uterine cavity.64,65 However, the diagnosis of a T-shaped uterus is subjective, and agreement among one expert group was only moderate (k of 0.43)66; the authors suggest instead use of a combination of lateral internal indentation depth 7 mm, lateral indentation angle 130 degrees and T-angle 40 degrees, and otherwise if only one criterion is present, and no other abnormalities are seen, calling a uterus normal.66 The coronal view of the uterus is important for many of the MDAs (Fig. 28.9, Video 28.1e28.4), particularly when trying to diagnose the more common anomalies such as septate uterus. One cannot usually obtain a view of the uterus in its coronal plane with two-dimensional (2D) TVS, though occasionally one can obtain a coronal view of the uterus with TAS when there is little fluid in the urinary bladder, and the uterus is anteverted and anteflexed. Thus, 3D ultrasound is generally needed for determining the type of MDA.67,68 In a 2013 study by Ludwin et al. SHG and 3D TVS had similar diagnostic capability as hysteroscopy in the differentiation between normal uterus, arcuate, septate, and bicornuate uteri.69 The most common distinction to be made in clinical practice is when the endometrium appears slightly divided on 2D ultrasound and one needs to determine whether this is an arcuate, septate, or bicornuate uterus. This is an important distinction to make, particularly for infertility patients, since MDAs have reproductive consequences. A septate uterus in a patient with multiple miscarriages will generally be treated surgically (since the septum may have a poor blood supply and can contain fibrous and/or myometrial tissue70,71 and is associated with recurrent miscarriage), whereas a bicornuate uterus will generally not be treated surgically, but is associated with incompetent cervix (thus will have additional imaging during the second trimester of pregnancy). Using the 3D TVS reconstructed coronal view of the uterus, one should evaluate the contour of the fundal myometrium. If the fundal myometrium is outwardly convex or has an inwardly concave indentation of less than 1 cm (from a reference line across the superior aspect of the myometrial edge in the two cornual regions), the distinction narrows to a septate (or subseptate) versus arcuate uterus. The term “subseptate” or “partial septate” is sometimes used when the septum does not extend all the way from the fundus to cervix. There is also a measurement transversely.62 Arcuate uterus now has a definition that will be new to most of our readers. The arcuate uterus has an endometrial indentation length (from side to side of the fundal endometrium) of greater

than 1.0 cm, with a normal external uterine contour. Another needed category has now been included, which is the combined bicornuate and septate uterus, where a fundal indentation of greater than 1 cm is present but a uterine septum is also present.62 If there is an indentation of greater than 1 cm in the fundal myometrium, one generally then needs to distinguish between a bicornuate uterus and uterus didelphys. In bicornuate uterus, the two endometrial cavities join at some point, usually just above the cervix. There can be either one cervix (bicornis unicollis) or two cervices (bicornis bicollis). In uterus didelphys, there are two separate uterine horns and two cervices, and the endometrial cavities never communicate. Arrested development of one müllerian duct results in variable forms of a unicornuate uterus. Unicornuate uterus is generally easily recognized on 3D ultrasound, since the “banana-shaped” unicornuate uterus will be deviated to one side of the pelvis, but this uterine deviation can be overlooked on 2D ultrasound. When a unicornuate uterus is seen, it is important to determine if there is a rudimentary horn and if that rudimentary horn contains endometrium, as such determination will generally affect management of the patient.72,73 About a third of patients with unicornuate uterus will not have a rudimentary horn. For the approximate two-thirds of patients with a unicornuate uterus that have a rudimentary horn, about half will have endometrium in the rudimentary horn.72,73 In most patients with a rudimentary horn that has endometrium, the rudimentary horn does not communicate with the other horn. These latter patients are at increased risk for endometriosis and rudimentary horn pregnancy, which has a high likelihood of uterine rupture. Hydrometra in the rudimentary horn can be mistaken for a uterine or adnexal mass. Surgical resection of a rudimentary horn that contains endometrium, especially if noncommunicating, is often recommended.73 It is not clear how reliably ultrasound, whether 2D or 3D, can exclude the presence of a rudimentary horn as they are sometimes small and may be obscured by bowel gas. If a rudimentary horn is not seen on ultrasound, one should consider MRI to be more confident there is truly no rudimentary horn. There are variable and often complex forms of uterine hypoplasia or agenesis. It may not be possible to perform TVS in such patients and MRI may be needed to fully define the anatomy as small uterine remnants can be present and difficult to identify sonographically. The most common form is MayerRokitansky-Küster-Hauser syndrome, with most patients having uterine and vaginal agenesis.74 Vaginal septa may be transverse or longitudinal in orientation and are most commonly seen with uterus didelphys though can occur with other MDAs. A transverse septum may cause obstruction and result in hematocolpos or hematometrocolpos. A duplicated cervix is a component of uterus didelphys but can occur with other anomalies. Other than clearly separated cervices, it can be difficult to distinguish true cervical duplication from a cervix divided by a septum. With

CHAPTER 28 The Uterus

B

A

D

C

F

E

R

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L

G

H

I

Fig. 28.9 Müllerian Anomalies. (AeD) and (H) are reconstructed 3D coronal images. (E) and (G) are oblique coronal images obtained directly from 2D imaging. (A) Arcuate uterus. Note the minimal indentation of the fundal endometrium. (B) Subseptate uterus. (C) Complete septate uterus. Note how the septum extends to the cervix. See Video 28.1 (D) Septate uterus with pregnancy in left horn. (E) Bicornuate uterus. Note how the two horns diverge on the image. Other images showed a single cervix (not shown) and two separate uterine horns. See Video 28.2. (F) Hysterosalpingogram of uterine duplication abnormality. From this image one cannot tell if this is a septate or bicornuate uterus. Further imaging to obtain a view of the uterine fundus is needed to distinguish between these entities. (G) Uterus didelphys. Note two separate uterine cavities (R, L) and two cervices (arrows). The endometrial cavities were always separate. See Video 28.3. (H) Unicornuate uterus. See Video 28.4. (I) Right unicornuate uterus with noncommunicating left horn. This 3D image was taken to demonstrate the endometrial cavities. Other views (not shown) demonstrated normal-appearing myometrium in the right horn, and thinned myometrium on the left.

this in mind, in women with a double cervix it is important to evaluate the full uterine anatomy as a complete septate uterus is at least as common as uterus didelphys.75

The kidneys should be evaluated in patients with MDAs as renal anomalies occur with increased frequency in such patients compared to the general population.73 The most common renal

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anomalies are absent or ectopic kidney. The most common types of MDAs to have associated renal anomalies are uterus didelphys (often with renal agenesis ipsilateral to an obstructed horn) and unicornuate uterus (usually renal agenesis ipsilateral to the side of the absent or rudimentary horn).

ABNORMALITIES OF THE MYOMETRIUM Assessment of the myometrium and endometrium are important in patients with symptoms of pelvic mass, pelvic pain, and abnormal bleeding. Bleeding in the premenopausal population has a different differential diagnosis since disorders of menstruation and pregnancy can cause abnormal bleeding. The acronym PALM-COIEN has been introduced to etiologies of premenopausal bleeding such as Polyp, Adenomyosis, Leiomyoma, and Malignancy/hyperplasia. The COIEN are etiologies of bleeding that are not image based. This classification system also includes a system for classification of fibroids (Fig. 28.10). In the postmenopausal population with abnormal uterine bleeding, endometrial carcinoma is of most concern, given its increased likelihood in the older population (discussed later in this chapter).

Leiomyomas Uterine leiomyomas, commonly referred to as fibroids, are the most common neoplasm of the uterus. They are benign and are composed of varying amounts of smooth muscle and fibrous tissue. The lifetime prevalence of uterine leiomyomas is greater than 80% among black women and approaches 70% in white women.76 Fibroids are more common, tend to present at a younger age, are greater in number, and larger in size in women of African ancestry versus white or Asian women.77 A combination of genetic alterations and endocrine, autocrine, environmental, and other factors such as race, older age, nulliparity, and increased body mass index all play a role in fibroid development.78 Some women with leiomyomas are asymptomatic, but leiomyomas, depending on location and size, can cause symptoms. Fibroid-associated symptoms peak in the perimenopausal years and decline after menopause, likely due to change in size. Menorrhagia is the most frequent symptom and often results in iron deficiency anemia.78 The mechanisms of heavy bleeding include increase in endometrial surface, fragile and engorged blood vessels, impaired platelet action, impaired myometrial contractility, uterine venous ectasia, impaired vasoconstriction of spiral arterioles, increase in transforming growth factor (TGF)-b3, and molecular changes

Coagulopathy

Polyp

Ovulatory dysfunction

Adenomyosis

Submucosal Endometrial

Leiomyoma

Other

Iatrogenic

Malignancy and hyperplasia

Not yet classified

Leiomyoma subclassification system

SM - Submucosal

O - Other

3

2-5

4 1

0 6

2 5 7 Hybrid leiomyomas (impact both endometrium and serosa)

0

Pedunculated intracavitary

1

4 mm, recommend biopsy >4 mm, recommend biopsy Follow-up early in the cycle after normal bleeding cycle is complete. Sonohysterography (SHG) to assess if endometrial abnormality is present

Recommendations for biopsy are assumed in a homogeneous endometrium. A heterogeneous endometrium should always lead to a recommendation for biopsy unless taking tamoxifen, when SHG may be used to avoid biopsy of reactivation of adenomyosis.

Tamoxifen and other hormonal treatments for breast cancer can have estrogenic effects in the uterus. An increased risk of endometrial carcinoma has been reported in patients receiving tamoxifen therapy,131 as well as an increased risk of endometrial hyperplasia and polyps.132,133 A correlation exists between increased endometrial thickness and cumulative dose of tamoxifen.134 On sonography, tamoxifen-related endometrial changes are nonspecific and similar to those described in hyperplasia, polyps, and carcinoma.133,135,136 Cystic changes within the thickened endometrium are frequently seen (Fig. 28.15). Polyps are frequently present, have a higher

incidence in women receiving tamoxifen than in untreated women, and can be quite large.134,137 However, since cancer occurs in polyps in a higher percentage of women taking tamoxifen than in the general population, focal lesions in these women should be removed and examined histologically.138 As mentioned previously, in some women taking tamoxifen, the cystic changes are subendometrial in location and represent reactivation of adenomyosis in the inner layer of myometrium.139 Because it is difficult to distinguish the endometrialmyometrial border in many of these patients, SHG can aid in determining whether an abnormality is endometrial or subendometrial.11,140 It is also important to recognize that this adenomyosis-like change is a diagnosis of exclusion. When a cystic endometrial appearance is seen in a woman taking tamoxifen, while tamoxifen effect should be mentioned as part of the differential diagnosis, polyps, hyperplasia, and cancer also need to be considered, and in constructing the report impression, tamoxifen should be listed last to emphasize the importance of assessment for the other entities in the differential diagnosis.

Postmenopausal Bleeding Postmenopausal bleeding is considered to be any vaginal bleeding that occurs in a postmenopausal woman other than the expected cyclic bleeding with sequential HRT. Because the prevalence of endometrial cancer is low, and endometrial atrophy accounts for a large proportion of cases of postmenopausal bleeding, the negative predictive value of a thin endometrium is high; therefore, a thin endometrium can be reliably used to exclude cancer. Several studies have shown that in patients with postmenopausal bleeding who have had endometrial sampling, an endometrial measurement of up to 3 mm,141 up to 4 mm,142,143,144 or up to 5 mm145,146,147 can be considered normal. The bleeding in these patients is often related to an atrophic endometrium. The ACR appropriateness criteria document for abnormal uterine bleeding states that an endometrial thickness of 4 mm has a negative predictive value of almost 100%.122 The majority of women with postmenopausal uterine bleeding have endometrial atrophy.143-148 On TVS, an atrophic endometrium is thin and homogeneous. Histologically, the endometrial glands may be dilated, but the cells are cuboidal or flat, and the stroma is fibrotic. A thin endometrium with cystic changes on TVS is consistent with a diagnosis of cystic atrophy, but when the endometrium is thick, the appearance is indistinguishable from that of cystic hyperplasia or cysts within polyps.149 A meta-analysis of 35 published studies that included 5892 women showed that an endometrial thickness greater than 5 mm detected 96% of endometrial cancer and 92% of any endometrial disease.150 For a postmenopausal woman with vaginal bleeding with a 10% pretest probability of cancer, her probability of cancer is 1% following a normal TVS result. However, many of the studies used in the meta-analysis were

CHAPTER 28 The Uterus

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Fig. 28.15 Tamoxifen-Related Changes on Transvaginal (TVS). (A) Thick, cystic endometrium caused by endometrial hyperplasia in patient taking tamoxifen. (B) Thick, cystic endometrium caused by a large polyp in patient receiving tamoxifen. The so-called “tamoxifen effect” on the endometrium is felt to be due to reactivation of adenomyosis but since tamoxifen acts as an estrogen agonist in the endometrium, there is increased risk for polyps, hyperplasia, and cancer. Thus, the cystic endometrial appearance in these two patients show why “tamoxifen effect” should be a diagnosis of exclusion.

biased by only including those patients who underwent biopsy. In a recent study by Wong et al. of 4383 women who all underwent an ultrasound and biopsy after presenting with postmenopausal bleeding, 3 mm was found to be the optimal threshold. The sensitivity for the detection of endometrial cancer at 3-, 4-, and 5-mm cut-offs were 97.0%, 94.1%, and 93.5%, respectively. The corresponding estimates of specificity at these thresholds were 45.3%, 66.8%, and 74.0%.151 However, it should be noted that the incidence of endometrial cancer was low in this population (3.8%, which is much lower than the expected rate of 10% in postmenopausal women with bleeding), so results might not be reproducible in other populations. Local practice will likely dictate the threshold that is acceptable to patients and their physicians. It may also be that in the future, individualized risk ratios will be used, assessing risk factors such as increasing age, older age at menopause, body mass index, nulliparity, and diabetes.152 Regardless, if a woman has continued postmenopausal bleeding after a normal sonogram, then biopsy is typically recommended. TVS assessment of endometrial thickness has been shown to be highly reproducible, with excellent intraobserver and good interobserver agreement.153 If the endometrium cannot be visualized in its entirety or its margins are indistinct, the examination should be considered “nondiagnostic” and lead to further investigation (e.g., SHG, hysteroscopy).154 Some recommend that all women with postmenopausal bleeding should undergo SHG, even if the TVS is normal155,156; however, if the endometrium is well seen by TVS and is thin with no morphologic abnormality, we feel this is usually adequate. Dubinsky et al. found that of 81 postmenopausal women with bleeding and thickness greater than 4 mm within 1 month after aspiration biopsy, endoluminal masses were present in 45 (56%) and that 41 of these were false-negative biopsies.157 The important question is whether finding and treating these benign conditions (such as small polyps or fibroids) improves the

patient’s quality of life, morbidity, and survival; further investigation is warranted.154 Other studies have assessed the endometrium in asymptomatic postmenopausal patients and concluded that an endometrium of 8 mm or less can be considered normal.43-47 Most of these reports include a mixed group of patients, with some using HRT and some not. In a theoretical cohort of postmenopausal women age 50 years or older who were not bleeding or receiving HRT, Smith-Bindman et al.48 recommended that biopsy should be considered if the endometrium measures greater than 11 mm, because the risk of cancer is 6.7% (similar to that of a postmenopausal woman with bleeding and endometrial thickness >5 mm). If the endometrium measures 11 mm or less, biopsy is not needed because the risk of cancer is extremely low.48 Using this cutoff provides an acceptable tradeoff between cancer detection and unnecessary biopsies prompted by an incidental finding. In a study by Jokubkiene et al. it was confirmed that even if endometrial focal lesions are present, there is likely no malignancy. In that study of 510 asymptomatic postmenopausal women 11% had workup for endometrium greater than 5 mm and 34 (7%) underwent hysteroscopic surgery or ultrasound surveillance. There were 14.5 surgical procedures per premalignant lesion (endometrial complex hyperplasia with atypia) diagnosed, and two women suffered severe complications from hysteroscopy.158 At our institution we currently use the more sensitive but less specific threshold of 8 mm.

The Obstructed UterusdHydrometrocolpos and Hematometrocolpos Obstruction of the genital tract results in the accumulation of secretions and blood in the uterus (metro) and/or vagina (colpos), with the location depending on the amount and level of obstruction. Before puberty, the accumulation of secretions in

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the vagina and uterus is referred to as hydrometrocolpos. After menstruation, hematometrocolpos results from the presence of retained menstrual blood. The obstruction may be congenital and is usually caused by an imperforate hymen. Other congenital causes include a vaginal septum, vaginal atresia, or a rudimentary uterine horn.159 Hydrometra and hematometra can also be acquired as a result of cervical stenosis from endometrial or cervical tumors or from postradiation fibrosis.160,161

Causes of Endometrial Fluid Congenital (imperforate hymen, vaginal septum, müllerian anomaly) Current menstruation Pregnancy Recent instrumentation/trauma Prior radiation Infection Cervical stenosis Obstructing lesion (endometrial or cervical cancer, rarely a fibroid)

Sonographically, if the obstruction is at the vaginal level, there is marked distention of the vagina and endometrial cavity with fluid. If seen before puberty, the accumulation of secretions is often anechoic. After menstruation, the presence of old blood results in echogenic material in the fluid (Fig. 28.16). There may also be layering of the echogenic material, resulting in a fluidfluid level. Infrequently, blood can distend only the cervix, which has been termed hematotrachelos.162 Acquired hydrometra or hematometra usually shows a distended, fluid-filled endometrial cavity that may contain echogenic material (Fig. 28.17). Superimposed infection (pyometra) is difficult to distinguish from hydrometra on sonography, and this diagnosis is usually made clinically in the presence of hydrometra.161 In postmenopausal women endometrial fluid is of particular concern given their increased risk of endometrial cancer due to age. However, even in this population the accumulation of

endometrial fluid is more likely to be from a benign than from a malignant etiology. A small amount of fluid (83 cm/s) suggesting the need for embolization and lower velocities allowing for more conservative management.231 However in most published studies the reported velocities are not true velocities, since angle correction was not used, confounding the utility of such measurements. In a series of 18 women with RPOC and increased myometrial vascularity, Van Den Bosch et al. assessed if PSV greater than 60 cm/s was associated with blood loss and procedure-related complications, and found poor correlation.229 Thus, when performing a sonographic examination for postpartum bleeding, and a lesion that resembles an AVM is seen, it is important to document the location, any intraendometrial contents, and the peak systolic velocity of the spectral waveform. While contrast-enhanced MR can be utilized to assess for an early draining vein, these can be present both in subinvolution of the placental site as well as an AVM. Thus, in stable patients, one should try for conservative management, as many of these seeming vascular anomalies will resolve spontaneously. A uterotonic medication can be utilized to aid in resolution of the abnormal myometrial flow. A negative serum hCG may be helpful, since hCG is typically elevated

in patients with gestational trophoblastic disease, which can show a similar pattern in the myometrium.13 Serum hCG level may not be as helpful for RPOC as about half of patients with RPOC are reported to have a negative or only minimally positive hCG level.232 Placental site trophoblastic tumor (PSTT), a type of gestational trophoblastic disease is an uncommon cause of postpartum bleeding, but should be considered when there are persistently low serum levels of hCG and/or elevated levels of human placental lactogen.233 The hCG levels tend to be low, sometimes only minimally elevated, compared to the more common forms of gestational trophoblastic neoplasia. The sonographic appearance of PSTT is most commonly a heterogeneous, predominately solid mass involving the endometrium and/or myometrium; occasionally it can be predominately cystic with marked vascularity simulating an AVM.234 This is discussed in more depth in Chapter 31.

Findings After Cesarean Section Most patients undergoing a cesarean delivery will have a transverse incision in the lower uterine segment. In the initial postpartum period after a cesarean section, one typically will see

CHAPTER 28 The Uterus small echogenic foci, due to sutures and/or gas, in the anterior myometrium of the lower uterine segment (see Fig. 28.27E, Video 28.15). It is uncertain how long these can normally be seen but likely for several weeks or months. One may also see heterogeneity in this region of the myometrium, probably due to small areas of hemorrhage. For the minority of cesarean section patients who have a classical hysterotomy with a longitudinal incision higher in the uterus, one may see similar heterogeneity and/or echogenic foci in that region of the myometrium in the postpartum period. Bladder flap hematomas, due to bleeding at the incision site, occur in or between the lower uterine segment of the uterus and the urinary bladder. Sonographically, they appear as a mass of variable echogenicity (see Fig. 28.27F, Video 28.15). Small hematomas ( or ¼5-year) follow-up. Am J Surg Pathol. 2005;29:707e723. 153. Peres LC, Cushing-Haugen KL, Köbel M, et al. Invasive epithelial ovarian cancer survival by Histotype and disease stage. J Natl Cancer Inst. 2019;111:60e68. 154. Alfuhaid TR, Rosen BP, Wilson SR. Low-malignant-potential tumor of the ovary: sonographic features with clinicopathologic correlation in 41 patients. Ultrasound Q. 2003;19:13e26. 155. Yazbek J, Raju KS, Ben-Nagi J, Holland T, Hillaby K, Jurkovic D. Accuracy of ultrasound subjective ’pattern recognition’ for the diagnosis of borderline ovarian tumors. Ultrasound Obstet Gynecol. 2007;29:489e495. 156. Engelen MJ, Kos HE, Willemse PH, et al. Surgery by consultant gynecologic oncologists improves survival in patients with ovarian carcinoma. Cancer. 2006;106:589e598. 157. Marko J, Marko KI, Pachigolla SL, Crothers BA, Mattu R, Wolfman DJ. Mucinous neoplasms of the ovary: Radiologic-pathologic correlation. Radiographics. 2019;39:982e997. 158. Mills AM, Shanes ED. Mucinous ovarian tumors. Surg Pathol Clin. 2019;12:565e585.

159. Fadare O, Parkash V. Pathology of endometrioid and clear cell carcinoma of the ovary. Surg Pathol Clin. 2019;12:529e564. 160. Sainz de la Cuesta R, Eichhorn JH, Rice LW, Fuller Jr AF, Nikrui N, Goff BA. Histologic transformation of benign endometriosis to early epithelial ovarian cancer. Gynecol Oncol. 1996;60:238e244. 161. Matsuura Y, Robertson G, Marsden DE, Kim SN, Gebski V, Hacker NF. Thromboembolic complications in patients with clear cell carcinoma of the ovary. Gynecol Oncol. 2007;104:406e410. 162. Weinberger V, Minár L, Felsinger M, et al. Brenner tumor of the ovary ultrasound features and clinical management of a rare ovarian tumor mimicking ovarian cancer. Ginekol Pol. 2018;89:357e363. 163. Green GE, Mortele KJ, Glickman JN, Benson CB. Brenner tumors of the ovary: sonographic and computed tomographic imaging features. J Ultrasound Med. 2006;25:1245e1251; quiz 1252-1244. 164. Euscher ED. Germ cell tumors of the female genital tract. Surg Pathol Clin. 2019;12:621e649. 165. Rabinovich I, Pekar-Zlotin M, Bliman-Tal Y, Melcer Y, Vaknin Z, Smorgick N. Dermoid cysts causing adnexal torsion: what are the risk factors? Eur J Obstet Gynecol Reprod Biol. 2020;251:20e22. 166. Park CH, Jung MH, Ji YI. Risk factors for malignant transformation of mature cystic teratoma. Obstet Gynecol Sci. 2015;58:475e480. 167. Chiang AJ, Chen MY, Weng CS, et al. Malignant transformation of ovarian mature cystic teratoma into squamous cell carcinoma: a Taiwanese Gynecologic Oncology Group (TGOG) study. J Gynecol Oncol. 2017;28:e69. 168. Savelli L, Testa AC, Timmerman D, Paladini D, Ljungberg O, Valentin L. Imaging of gynecological disease (4): clinical and ultrasound characteristics of struma ovarii. Ultrasound Obstet Gynecol. 2008;32:210e219. 169. Kawamoto S, Sato K, Matsumoto H, et al. Multiple mobile spherules in mature cystic teratoma of the ovary. Am J Roentgenol. 2001;176: 1455e1457. 170. Tongsong T, Wanapirak C, Khunamornpong S, Sukpan K. Numerous intracystic floating balls as a sonographic feature of benign cystic teratoma: report of 5 cases. J Ultrasound Med. 2006;25:1587e1591. 171. Quinn SF, Erickson S, Black WC. Cystic ovarian teratomas: the sonographic appearance of the dermoid plug. Radiology. 1985;155:477e478. 172. Guttman Jr PH. In search of the elusive benign cystic ovarian teratoma: application of the ultrasound "tip of the iceberg" sign. J Clin Ultrasound. 1977;5:403e406. 173. Smith HO, Berwick M, Verschraegen CF, et al. Incidence and survival rates for female malignant germ cell tumors. Obstet Gynecol. 2006;107: 1075e1085. 174. Vicus D, Beiner ME, Klachook S, Le LW, Laframboise S, Mackay H. Pure dysgerminoma of the ovary 35 years on: a single institutional experience. Gynecol Oncol. 2010;117:23e26. 175. Guerriero S, Testa AC, Timmerman D, et al. Imaging of gynecological disease (6): clinical and ultrasound characteristics of ovarian dysgerminoma. Ultrasound Obstet Gynecol. 2011;37:596e602. 176. Shaaban AM, Rezvani M, Elsayes KM, et al. Ovarian malignant germ cell tumors: cellular classification and clinical and imaging features. Radiographics. 2014;34:777e801. 177. Anfelter P, Testa A, Chiappa V, et al. Imaging in gynecological disease (17): ultrasound features of malignant ovarian yolk sac tumors (endodermal sinus tumors). Ultrasound Obstet Gynecol. 2020;56:276e284. 178. Kawai M, Kano T, Kikkawa F, et al. Seven tumor markers in benign and malignant germ cell tumors of the ovary. Gynecol Oncol. 1992;45:248e253. 179. Javadi S, Ganeshan DM, Jensen CT, Iyer RB, Bhosale PR. Comprehensive review of imaging features of sex cord-stromal tumors of the ovary. Abdom Radiol (NY). 2021;46:1519e1529. 180. Tanaka Y, Sasaki Y, Nishihira H, Izawa T, Nishi T. Ovarian juvenile granulosa cell tumor associated with Maffucci’s syndrome. Am J Clin Pathol. 1992;97:523e527. 181. Tamimi HK, Bolen JW. Enchondromatosis (Ollier’s disease) and ovarian juvenile granulosa cell tumor. Cancer. 1984;53:1605e1608. 182. Van Holsbeke C, Domali E, Holland TK, et al. Imaging of gynecological disease (3): clinical and ultrasound characteristics of granulosa cell tumors of the ovary. Ultrasound Obstet Gynecol. 2008;31:450e456.

CHAPTER 29 Adnexal Sonography 183. Young RH. Ovarian sex cord-stromal tumors: reflections on a 40-year experience with a Fascinating group of tumors, including comments on the seminal observations of Robert E. Scully, MD. Arch Pathol Lab Med. 2018;142:1459e1484. 184. Kimonis VE, Goldstein AM, Pastakia B, et al. Clinical manifestations in 105 persons with nevoid basal cell carcinoma syndrome. Am J Med Genet. 1997;69:299e308. 185. Shinagare AB, Meylaerts LJ, Laury AR, Mortele KJ. MRI features of ovarian fibroma and fibrothecoma with histopathologic correlation. Am J Roentgenol. 2012;198:W296eW303. 186. Li Z, Hu Q, Luo Z, Deng Z, Zhou W, Xie L. Analysis of magnetic resonance imaging features of ovarian thecoma. Medicine (Baltim). 2020;99, e20358. 187. Durmus¸ Y, Kılıç Ç, Çakır C, et al. Sertoli-Leydig cell tumor of the ovary: analysis of a single institution database and review of the literature. J Obstet Gynaecol Res. 2019;45:1311e1318. 188. Guo Y, Wang J, Li Y, Wang Y. Ovarian Sertoli-Leydig cell tumors: an analysis of 13 cases. Arch Gynecol Obstet. 2020;302:203e208. 189. Young RH, Scully RE. Ovarian Sertoli-Leydig cell tumors. A clinicopathological analysis of 207 cases. Am J Surg Pathol. 1985;9:543e569. 190. Testa AC, Ferrandina G, Timmerman D, et al. Imaging in gynecological disease (1): ultrasound features of metastases in the ovaries differ depending on the origin of the primary tumor. Ultrasound Obstet Gynecol. 2007;29:505e511. 191. Kolin DL, Nucci MR. Fallopian tube neoplasia and mimics. Surg Pathol Clin. 2019;12:457e479. 192. Huang CC, Chang DY, Chen CK, Chou YY, Huang SC. Adenomatoid tumor of the female genital tract. Int J Gynaecol Obstet. 1995;50:275e280. 193. Tao K, Zeng X, Liu W, et al. Primary gastrointestinal stromal tumor mimicking as gynecologic mass: characteristics, management, and prognosis. J Surg Res. 2020;246:584e590. 194. Chan JK, Kapp DS, Shin JY, et al. Influence of the gynecologic oncologist on the survival of ovarian cancer patients. Obstet Gynecol. 2007;109:1342e1350. 195. Patel MD. Invited Commentary: Categorizing adnexal masses at US, CT, and MRI-the Radiologist’s not-impossible mission. Radiographics. 2022:210196. 196. Timmerman D, Schwärzler P, Collins WP, et al. Subjective assessment of adnexal masses with the use of ultrasonography: an analysis of

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interobserver variability and experience. Ultrasound Obstet Gynecol. 1999;13:11e16. Valentin L. Prospective cross-validation of Doppler ultrasound examination and gray-scale ultrasound imaging for discrimination of benign and malignant pelvic masses. Ultrasound Obstet Gynecol. 1999;14:273e283. Valentin L, Ameye L, Jurkovic D, et al. Which extrauterine pelvic masses are difficult to correctly classify as benign or malignant on the basis of ultrasound findings and is there a way of making a correct diagnosis? Ultrasound Obstet Gynecol. 2006;27:438e444. Kaijser J, Sayasneh A, Van Hoorde K, et al. Presurgical diagnosis of adnexal tumours using mathematical models and scoring systems: a systematic review and meta-analysis. Hum Reprod Update. 2014;20:449e462. Timmerman D, Van Calster B, Testa A, et al. Predicting the risk of malignancy in adnexal masses based on the simple rules from the international ovarian tumor analysis group. Am J Obstet Gynecol. 2016;214:424e437. Timmerman D, Testa AC, Bourne T, et al. Simple ultrasound-based rules for the diagnosis of ovarian cancer. Ultrasound Obstet Gynecol. 2008;31:681e690. Ameye L, Timmerman D, Valentin L, et al. Clinically oriented three-step strategy for assessment of adnexal pathology. Ultrasound Obstet Gynecol. 2012;40:582e591. Andreotti RF, Timmerman D, Benacerraf BR, et al. Ovarian-adnexal reporting lexicon for ultrasound: a white paper of the ACR ovarianadnexal reporting and data system committee. J Am Coll Radiol. 2018;15:1415e1429. Andreotti RF, Timmerman D, Strachowski LM, et al. O-RADS US risk stratification and management system: a consensus guideline from the ACR ovarian-adnexal reporting and data system committee. Radiology. 2020;294:168e185. Cao L, Wei M, Liu Y, et al. Validation of American College of Radiology Ovarian-Adnexal Reporting and Data System Ultrasound (O-RADS US): analysis on 1054 adnexal masses. Gynecol Oncol. 2021;162:107e112. Strachowski LM, Jha P, Chawla TP, et al. O-RADS for ultrasound: a user’s guide, from the AJR special series on radiology reporting and data systems. Am J Roentgenol. 2021;216:1150e1165.

PART FIVE Obstetric Sonography CHAPTER

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Overview of Obstetric Imaging Deborah Levine and Alison M. Savicke

CHAPTER OUTLINE INTRODUCTION, 1156 TRAINING, PERSONNEL, AND EQUIPMENT, 1156 ULTRASOUND PRACTICE PARAMETERS, 1157 First Trimester, 1158 Second and Third Trimesters, 1161 ROUTINE ULTRASOUND SCREENING, 1164

Estimation of Gestational Age, 1164 Identification of Twin/Multiple Pregnancies, 1167 Maternal Anatomy: Ovaries, 1168 Maternal Anatomy: Uterus, 1168 Screening and Perinatal Outcomes, 1174 Fetal Malformations: Diagnostic Accuracy, 1175

INTRODUCTION There were an estimated 3.66 million births in the United States in 2021.1 Ultrasound is the most frequently used imaging modality for assessment of pregnancy. With care being taken to keep exposure to ultrasound limited to medically needed information, and with imaging performed at the appropriate power settings, ultrasound is safe for use in pregnancy. Indications for ultrasound during the first trimester include pregnancy dating, assessment of women with bleeding or pain, and assessment of nuchal translucency. In the second trimester, ultrasound is routinely used for pregnancy dating, assessment of interval growth, assessment of patients with abnormal pain or bleeding, assessment of size-to-dates discrepancy, and routine survey of fetal anatomy. High-risk anatomic surveys are performed for assessment of maternal complications due to conditions such as age, drug exposure, history of abnormalities in prior pregnancy, and assessment of the current pregnancy after an earlier scan shows an anomaly, or in the case of monochorionic multiple gestations. In cases of multiple gestations, ultrasound is used to assess growth and complications of twinning (see Chapter 33). In women with a history of cervical incompetence, transvaginal ultrasound is used to screen for cervical changes that put a patient at risk for preterm delivery (see Chapter 44). In the third trimester, ultrasound is predominantly used to assess fetal presentation, growth, and well-being (see Chapter 43). Ultrasound is also used for fetal procedures such as testing for aneuploidy, drainage of abnormal fetal fluid collections, and guidance for fetal surgery. Ultrasound is well recognized as the

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Three-Dimensional Ultrasound, 1176 Prudent Use of Ultrasound, 1176 MAGNETIC RESONANCE IMAGING, 1176 CONCLUSION, 1179 REFERENCES, 1179

screening modality of choice in pregnancy, but additional information may be needed beyond that available with ultrasound. In many of these cases, especially those with fetal central nervous system abnormalities or those who are potentially undergoing fetal surgery, fetal magnetic resonance imaging (MRI) can help clarify the diagnosis, and assess for synchronous abnormalities. Part IV of this textbook focuses on obstetric ultrasound and reviews specific fetal organ system anatomy and pathology. Fetal magnetic resonance (MR) and three-dimensional (3D) ultrasound images and postnatal follow-up are added throughout to illustrate the benefit of these techniques in select cases. Elastography in pregnancy is investigational only at this time, and should not be routinely utilized.

TRAINING, PERSONNEL, AND EQUIPMENT Obstetric ultrasound diagnosis is critically dependent on examiner training and experience.2,3 As with all medical examinations, ultrasounds should only be performed by trained professionals when they are medically necessary. Thus, physicians and sonographers performing obstetric ultrasound examinations should have completed appropriate training and should be appropriately credentialed and/or boarded. While there are no known ultrasound bioeffects when used in medical settings, adherence to the as low as reasonably achievable (ALARA) principle decreases the time and intensity of the exposure to ultrasound.

CHAPTER 30 Overview of Obstetric Imaging When performing an obstetrical ultrasound, the performing examiner should be conscious of the output power emitted from the scan and ways to regulate it (see Chapter 2). In Doppler scanning, adjusting the sample volume and velocity range will affect the overall output power. Additionally, an experienced performing examiner will have extensive knowledge of fetal anatomy and operate the ultrasound machine efficiently, limiting dwell time (actual scanning time) as much as possible. Accreditation of ultrasound laboratories improves compliance with published minimum standards and practice parameters.4 Ultrasound practitioners should be knowledgeable regarding the basic physical principles of ultrasound, equipment, record-keeping requirements, indications, and safety of using ultrasound in pregnancy. Studies should be conducted with real-time scanners using a transabdominal and/or transvaginal approach, depending on the gestational age and the region of interest. The choice of transducer frequency is a trade-off between beam penetration and resolution. In general, a 3 to 5 MHz transducer frequency provides sufficient resolution with adequate depth penetration in all but the extremely obese patient. In obese patients, scanning transvaginally in early pregnancy, using windows such as the umbilicus with a small footprint probe, scanning with the patient in lateral decubitus position, or scanning at the pelvic crease with the pannus being held up to aid in extending the window are helpful. During early pregnancy, a 4 to 7 MHz abdominal transducer or a 5 to 10 MHz vaginal transducer can provide superior resolution while still allowing adequate penetration. Higher-frequency transducers are most useful in achieving high-resolution scans of anatomy close to the probe, and lowerfrequency transducers are useful when increased penetration of the sound beam is necessary and when a wider field of view is needed. Use of Doppler ultrasound and 3D imaging depends on the specific indication. Care should be taken to use the least amount of power while providing images of diagnostic clarity. Use of pulsed Doppler is the sonographic technique with the most power deposition in a concentrated area when compared to other types of scanning (such as routine grayscale imaging, or M-mode). Therefore, care should be taken to avoid scanning in the same fetal region of interest for prolonged periods of time, as this is how power deposition from the ultrasound can occur. This is particularly important when performing spectral Doppler studies near a bony surface (e.g., when performing Doppler of the middle cerebral artery). As in all imaging studies, complete documentation of the images and a formal written interpretation are essential for quality assurance, accreditation, and medicolegal issues.

ULTRASOUND PRACTICE PARAMETERS A collaborative guideline from the American College of Radiology (ACR), American College of Obstetricians and Gynecologists (ACOG), American Institute of Ultrasound in Medicine (AIUM), Society of Radiologists in Ultrasound (SRU), and

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Society of Maternal-Fetal Medicine (SMFM)5 list standard indications for obstetric sonograms, shown in the boxes.

Indications for Standard First-Trimester Ultrasound Confirmation of the presence of an intrauterine pregnancy Confirmation of cardiac activity Estimation of gestational age Diagnosis or evaluation of multiple gestations including determination of chorionicity Suspected ectopic pregnancy Vaginal bleeding Pelvic pain Suspected gestational trophoblastic disease Adjunct to chorionic villus sampling, embryo transfer, localization, and removal of an Intrauterine device Assessment for certain fetal anomalies, such as anencephaly Measurement of nuchal translucency when part of a screening program Maternal pelvic masses and/or uterine abnormalities Modified from Collaborative Subcommittee. AIUM-ACR-ACOG-SMFM-SRU Practice Parameter for the Performance of Standard Diagnostic Obstetrical Ultrasound. J Ultrasound Med. 2018;37(11):E13-E24.5

Indications for Standard Second- and ThirdTrimester Ultrasound Screening for fetal anomalies Evaluation of fetal anatomy Estimation of gestational (menstrual) age Evaluation of suspected multiple gestation Evaluation of cervical length Evaluation of fetal growth and fetal well-being Evaluation of discrepancy between uterine size (as measured by fundal height) and clinical dates Determination of fetal presentation Suspected amniotic fluid abnormalities Premature rupture of membranes and/or premature labor Vaginal bleeding Abdominal or pelvic pain Suspected placental abruption Evaluation/follow-up of placental appearance and location. Includes suspected placenta previa, vasa previa, and abnormally adherent placenta Suspected fetal death Follow-up of fetal anomalies Adjunct to amniocentesis or other procedure Adjunct to cervical cerclage placement Pelvic mass or uterine anomaly Adjunct to external cephalic version Suspected gestational trophoblastic disease Suspected ectopic pregnancy Modified from Collaborative Subcommittee. AIUM-ACR-ACOG-SMFM-SRU Practice Parameter for the Performance of Standard Diagnostic Obstetrical Ultrasound. J Ultrasound Med. 2018;37(11):E13-E24.5

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First Trimester The practice parameter from the collaborative committee of the AIUM-ACR-ACOG-SMFM-SRU for the performance of standard first-trimester obstetric ultrasound examination include documentation of the location of the pregnancy (intrauterine vs. extrauterine), documentation of the appearance of the maternal uterus and ovaries and assessment of gestational age, either by measurement of mean sac diameter (before visualization of embryonic pole; Fig. 30.1) or by embryonic/fetal pole crown-rump length5 (Fig. 30.2A and B). Another important structure to assess is the yolk sac (Video 30.1). An image of the heart rate is taken using M-mode ultrasound (see Fig. 30.2C). When heart rate is difficult to document, a cine clip may be helpful (see Video 30.1). It is important to use M-mode rather than spectral Doppler ultrasound on the embryo to limit power deposition. Late in the first trimester, dating can be performed with measurement of the biparietal diameter and head circumference rather than crown-rump length.

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General Survey Guidelines for First-Trimester Ultrasound Gestational sac Location of pregnancy: intrauterine vs. extrauterine Gestational age (as appropriate) Mean sac diameter (until there is a measurable embryo) Embryonic pole length or crown rump length Yolk sac Heart rate on M-mode ultrasound Embryo/fetal number (amnionicity/chorionicity) Maternal anatomy: uterus (including the cervix) and adnexa Appropriate fetal anatomy for the first trimester should be assessed and include the calvarium, fetal abdominal cord insertion, and presence of limbs when fetus is of sufficient size, and nuchal region Modified from Collaborative Committee. AIUM-ACR-ACOG-SMFM-SRU Practice Parameter for the Performance of Standard Diagnostic Obstetric Ultrasound Examinations 2018. J Ultrasound Med. 2018:37(11):E13eE24.5

Sac Diam1 0.31 cm Sac Diam2 0.25 cm Mean Sac Diam 0.30 cm

D

FIGURE 30.1 Normal Early First-Trimester Ultrasound Images: Intrauterine Gestational Sac and Yolk Sac. (A) Intradecidual sac sign. Note the 2 mm gestational sac with echogenic rim (arrow) eccentrically located within the endometrium. This is a normal finding at about 4.5 weeks, but due to variable specificity, this is not a definitive sign of an intrauterine pregnancy and must be followed-up in symptomatic patients (those with pain and/or bleeding). (B and C) Mean sac diameter measurements in a different pregnancy. Transvaginal sagittal (B) and transverse (C) images show an intrauterine gestational sac, with calipers showing the orthogonal measurements. The measurements are taken inside the echogenic rim of the gestational sac. Measurements in three orthogonal planes are averaged to calculate the mean sac diameter. (D) Gestational sac with yolk sac.

CHAPTER 30 Overview of Obstetric Imaging

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FIGURE 30.2 First-Trimester Ultrasound Images: Embryo and Fetus. (A) Normal embryo at 6.5 weeks’ gestation. Note embryonic pole (calipers) adjacent to yolk sac. (B) Normal embryo at 8 weeks’ gestation. Note embryo (calipers) and adjacent yolk sac (arrow). (C) Normal M-mode. Note normal heart rate of 157 beats/min. (D) Normal embryo at 9 weeks’ gestation. Note embryo within amnion (arrow) and umbilical cord (arrowhead). (E) Just lateral to image in D, note yolk sac (arrowhead) is located outside the amnion (arrow). (F) Sagittal ultrasound at 10.5 weeks’ gestation. (G) Sagittal ultrasound at 11.5 weeks’ gestation. (H) Coronal view of face at 13 weeks’ gestation. (I) Sagittal ultrasound of nuchal translucency (calipers) at 13 weeks’ gestation. See also Videos 30.1 and 30.2.

In the first trimester, it is important to not only establish the location of the pregnancy (intrauterine versus extrauterine) but, when intrauterine, to carefully determine if it is a potentially viable pregnancy or if it is a nonviable pregnancy.6-9 Due to the variety of medical professionals performing and interpreting ultrasound in a variety of clinical settings, thresholds for the diagnosis of a failed pregnancy have been increased in order to not misdiagnose a potentially viable pregnancy. For example, although we typically see embryonic cardiac activity by the time an embryonic pole is visualized, we allow the crown-rump

length (CRL) to be 7 mm before diagnosing a failed pregnancy. These generous thresholds may mean an additional sonogram for the patient, but they also ensure that a potentially viable pregnancy is not diagnosed as a miscarriage. These issues are discussed in detail in Chapter 31. In cases of multiple gestation, first-trimester scans should document the fetal number as well as the amnionicity and chorionicity (Fig. 30.3). In addition, the ACOG recommends that prenatal testing for aneuploidy be offered to all pregnant women.10 Clinicians must understand current screening options

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FIGURE 30.3 Multiple Gestations. The entire gestational sac should be examined to identify multiple gestations. (A) Diamniotic dichorionic twins at 8 weeks’ gestation. Transverse transvaginal image of the uterus shows the thick, dividing membrane that separates twin A (A) from twin B (B). (B) Diamniotic monochorionic twins at 8 weeks’ gestational age (calipers denote crown rump length [CRL]) with two thin membranes (arrows, amnion) close to embryonic poles due to early gestational age.

(and the trade-offs between them), including cell-free deoxyribonucleic acid (DNA) and serum analysis (with or without nuchal translucency ultrasonography). Cell-free DNA testing uses maternal serum to obtain circulating DNA from the placenta to assess the risk of the fetus having a chromosomal abnormality; it does not assess risk for fetal anomalies such as neural tube defects or ventral wall defects. Management decisions, including termination of the pregnancy, should not be based on the results of the cell-free DNA screening alone.10 This is an important concept, since if the cell-free DNA test results indicate that the fetus has an increased risk of a chromosomal abnormality, an ultrasound showing typical anomalies associated with the karyotype abnormality, amniocentesis or CVS will be needed to confirm the diagnosis. In addition, patients should be counseled that a negative cell-free DNA test result does not ensure an unaffected pregnancy, as it only screens for specific abnormalities such as trisomy 13, 18, and 21. According to a 2015 ACOG committee opinion, “Given the performance of conventional screening methods, the limitations of cell-free DNA screening performance, and the limited data on cost-effectiveness in the low-risk obstetric population, conventional screening methods remain the most appropriate choice for first-line screening for most women in the general obstetric population.”10 Thus, despite the increased use of cell-free DNA testing, ultrasound screening is still being performed by measuring nuchal translucency between 11 and 14 weeks of gestation (see

Fig. 30.2I) and anatomic surveys. The nuchal translucency measurement, in conjunction with maternal age and serology, is used to determine an individualized risk of fetal aneuploidy (see Chapter 32). Increased use of maternal serum screening, as well as first- and second-trimester ultrasound have reduced the number of interventional procedures to detect aneuploidy while increasing the number of prenatal diagnoses of aneuploidy.11 Given the increased scanning late in the first trimester, it is also increasingly common for a limited or detailed anatomic survey to be conducted in the late first trimester. Anomalies that should be detected by the end of the first trimester, even in the low-risk setting, include anencephaly, omphalocele, and megacystis. Although substantial information can be obtained at this time, the first-trimester anatomic survey is unlikely to replace the second-trimester anatomic survey, since many structures are difficult to visualize completely early in pregnancy (e.g., posterior fossa and distal spine). For high-risk patients, there is a 2021 publication describing the detailed first-trimester diagnostic ultrasound exam, which is performed between 12 weeks 0 days and 13 weeks 6 days.12 The detailed obstetric ultrasound examination in the late first trimester is an indication-driven examination for women at increased risk for fetal or placental abnormalities that are potentially detectable between 12 and 14 weeks’ gestation. It is performed and interpreted by personnel with advanced training and skill. This is discussed in more detail in Chapter 31.

CHAPTER 30 Overview of Obstetric Imaging

Examples of detailed first trimester diagnostic ultrasound indications Previous fetus or child with a congenital, genetic, or chromosomal anomaly Known or suspected fetal abnormality detected by ultrasound in the current pregnancy Fetus at increased risk for a congenital anomaly based on the following: 35 years or older at delivery Maternal pregestational diabetes Pregnancy conceived via in vitro fertilization Multiple gestation Teratogen exposure Enlarged nuchal translucency Positive screening test results for aneuploidy Other conditions possibly affecting the pregnancy/fetus, including: Maternal body mass index of 30 kg/m2 or higher Placental implantation covering the internal cervical os Pregnancy in region of cesarean scar Modified from: AIUM practice parameter for the performance of detailed diagnostic obstetric ultrasound examinations between 12 weeks 0 days and 13 weeks 6 days. J Ultrasound Med, 2021;40(5):E1eE16. doi:10.1002/jum.15477.12

Second and Third Trimesters The current AIUM-ACR-ACOG-SMFM-SRU practice parameter for the performance of the obstetric ultrasound examinations describe the standard second- and third-trimester sonographic examinations.5 It is important to understand that the guidelines were written to maximize detection of many fetal abnormalities but are not expected to allow for detection of all structural abnormalities. The terminology level I and level II examinations refer to “standard” or “routine” (level I) and “high risk,” “specialized,” or “detailed” (level II) obstetric ultrasound. The concept of these two levels of scanning is that the standard, basic, routine, or level I examination is performed routinely on pregnant patients (see Figs 30.4e30.12, Videos 30.2e30.7). The methods to obtain the required images are described in detail in subsequent chapters. This chapter provides a collage of figures as a guide for the anatomic survey and common additional views obtained during a standard fetal survey. This chapter also describes important maternal structures to assess in pregnancy, including ovarian and uterine normal and abnormal findings (see Videos 30.8e30.11). In general, the “standard fetal anatomic survey” refers to the second-trimester scan, typically performed between 16 and 22 weeks of gestation. When anatomic surveys are performed at 20 to 22 weeks’ gestational age, there is less need for repeat scans to document normal anatomy compared to studies performed earlier in pregnancy.13 However, there are practical considerations when determining the optimal timing of studies. In well-dated pregnancies in women who are unlikely to want amniocentesis, a survey at 20 to 22 weeks’ gestation is optimal. However, if a pregnancy is not well dated, an earlier scan may be needed both to establish accurate dates for the pregnancy and to assess the anatomy. Some centers offer the scan at 16 weeks’ gestation to coincide with performance of genetic amniocentesis and/or midtrimester quadruple serum screening.

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The level I examination consists of investigation of the maternal uterus and ovaries, the cervix, amniotic fluid, and placenta (Fig. 30.4), as well as a systematic assessment of fetal anatomy. It is helpful to begin the examination with a sagittal midline view to assess the cervix. If the cervix appears abnormally short or if placenta previa is suspected, a vaginal scan can then be performed.

Survey Guidelines for Second- and ThirdTrimester Ultrasound GENERAL SURVEY Cardiac activity: document with M-mode Presentation: cephalic, breech, transverse, variable Fetal number: for multiples, amnionicity/chorionicity, concordance with size, amniotic fluid Maternal anatomy: uterus, adnexa, and cervix Gestational age and fetal weight assessment Biparietal diameter Head circumference Abdominal circumference Femur length Amniotic fluid Estimate as normal If abnormal, quantify if high or low Placenta Location Relationship to internal os Placental cord insertion site: normal, marginal, velamentous

ANATOMIC SURVEY Head, Face, and Neck Cerebellum Choroid plexus Cisterna magna Lateral cerebral ventricles Midline falx Cavum septi pellucidi Upper lip

Chest Four-chamber view Outflow tracts Thoracic three-vessel view (if technically feasible) Three-vessel trachea view (if technically feasible) Abdomen Stomach (presence, size, and situs) Kidneys, bladder Umbilical cord insertion site into fetal abdomen Umbilical cord vessel number

Spine Cervical, thoracic, lumbar, and sacral

Extremities Legs and arms Hands and feet Genitalia (sex)dIn multiple gestations and when medically indicated Modified from Collaborative Committee. AIUM-ACR-ACOG-SMFM-SRU Practice Parameter for the Performance of Standard Diagnostic Obstetric Ultrasound Examinations 2018. J Ultrasound Med. 2018:37(11):E13eE24.5

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FIGURE 30.4 Overview of Uterus, Cervix, and Fetal Position. (A) Sagittal sonogram of uterus shows a normal-appearing cervix (C) and an anterior placenta (P), with the placental tip far away from the internal cervical os. B, Bladder. (B) Transverse sonogram of posterior placenta (P). (C) Normal cervix, sagittal transabdominal (arrow on internal os). Note bladder (B) and fetal head (H). With the head as the presenting part, the fetus is in cephalic position. (D) Normal cervix (calipers), sagittal transvaginal image.

Transverse and longitudinal scans of the entire uterine cavity are then performed for assessment of fetal cardiac activity, amniotic fluid volume, localization of the placenta, and determination of fetal presentation and situs (Fig. 30.5). Knowledge of the plane of section across the maternal abdomen, combined with the position of the fetal spine and right-sided and left-sided structures within the fetal body, allows accurate determination of fetal position and identification of normal and pathologic anatomy. Some congenital anomalies, such as dextrocardia, will be recognized only if a structure is

identified as “abnormal” by virtue of its atypical position related to the position of the fetus. Biometry is performed to estimate gestational age and fetal weight (Fig. 30.6). Assessment of gestational age in the second and third trimesters is discussed in more detail in Chapter 43. Additional views in routine obstetric sonography include fetal and placental position (Video 30.2), the head and face (Fig. 30.7, Video 30.3), heart and outflow tracts (Fig. 30.8, Video 30.4), abdomen and pelvis (Fig. 30.9, Video 30.5), spine (Fig. 30.10, Video 30.6), extremities (Fig. 30.11), and umbilical

CHAPTER 30 Overview of Obstetric Imaging

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FIGURE 30.5 Determination of Situs. (A) Scan plane and (B) transverse scan diagram. With fetus in cephalic position and spine on the maternal right side, the left-sided stomach is “up” on the side closest to the transducer. (C) Scan plane and (D) scan diagram with the fetus in breech position and spine on the maternal right side, the left-sided stomach is “down” on the side farthest away from the transducer. See also Video 30.6.

cord and its three vessels (Fig. 30.12, Video 30.7). Imagers can take advantage of the reproducible succession of epiphyseal ossification to aid in assessment of gestational age in late pregnancy when earlier scans are not available: The distal femoral epiphysis (see Fig. 30.11I) ossifies first at approximately 32 weeks; the proximal tibial epiphysis ossifies at approximately 35 weeks; and the proximal humeral epiphysis ossifies starting as early as 36 weeks. Other specialized sonographic examinations include fetal Doppler sonography, biophysical profile, and fetal echocardiography. The high-risk, targeted, detailed, or level II scan should have a specific indication that requires a detailed fetal sonogram, performed by a clinician with expertise in obstetric imaging.14,15 This high-risk scan is performed when an anomaly is suspected because of maternal medical or family history, or if abnormal results are suspected on a routine scan. These high-risk scans may include detailed views of fetal anatomy, biometry, and placental assessment beyond those obtained in the routine exam. Wax et al.15 provide a more complete description of these high-risk examinations.

Indications for Detailed Fetal Anatomic Survey Previous fetus or child with a congenital, genetic, or chromosomal abnormality Known or suspected fetal anomaly or known growth disorder Fetus at increased risk for a congenital anomaly, such as maternal diabetes, pregnancy conceived via assisted reproductive technology, high maternal body mass index (35 kg/m2), multiple gestation, abnormal screening results, teratogen exposure Fetus at increased risk for a genetic or chromosomal abnormality, such as parental carrier of a chromosomal or genetic abnormality, maternal age 35 years or older at delivery, abnormal screening results Other conditions affecting the fetus, including congenital infections, maternal drug dependence, isoimmunization, abnormalities of amniotic fluid Modified from Wax J, Minkoff H, Johnson A, et al. Consensus report on the detailed fetal anatomic ultrasound examination: indications, components, and qualifications. J Ultrasound Med. 2014;33(2):189e195.15

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FIGURE 30.6 Second-Trimester Biometry. (A) Biparietal diameter. Note the level of this ultrasound image at the thalamus and third ventricle. The calipers are placed from the outer skull in the near field to the inner skull in the far field. (B) Head circumference. Note how circumference is measured around the outside of the skull. Arrow, cavum of the septum pellucidum. (C) Abdominal circumference (AC). Note the curve of the portal vein and stomach on this transverse image, with circumference drawn around the outside of the skin. (D) Femur length (FL). Note that the “upside” femur should be measured, with the shaft of the bone as near to perpendicular to the scan plane as possible, excluding the distal femoral epiphysis.

ROUTINE ULTRASOUND SCREENING Estimation of Gestational Age Determination of the expected date of delivery (EDD) is especially important in obstetric practice because it is used to intervene in pregnancies considered to be growth restricted and in post-term pregnancies. Multiple studies have demonstrated that routine use of ultrasound results in more accurate assessment of the EDD than does last menstrual period (LMP) dating or physical examination, even in women with regular and

certain menstrual dates.16-19 Pregnancy dating is most accurately performed in the first half of pregnancy. Fetal growth should be assessed by comparison to the earliest study of the current pregnancy, as long as that exam showed a heartbeat. In a Cochrane review of nine trials of routine ultrasound in early pregnancy, routine use of early ultrasound and the subsequent adjustment of the EDD led to a significant reduction in the number of post-term pregnancies.20 A rule of thumb is that in the first trimester, LMP dating should be maintained unless ultrasound yields an EDD more

CHAPTER 30 Overview of Obstetric Imaging

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FIGURE 30.7 Sonographic Views of Fetal Head and Face. In addition to the biparietal diameter and head circumference, required views of the head include images of the cerebral ventricles, cerebellum, cavum of the septum pellucidum, midline falx, and nose and lips. Additional views that can be obtained are angled views to demonstrate both sides of the choroid plexus and views through the anterior fontanelle or midline sutures to demonstrate the corpus callosum as well as views of the orbits and profile. (A) Axial and (B) oblique axial images show cerebral ventricles filled with choroid plexus. (C) Cerebellum (arrow) and cavum of the septum pellucidum (arrowhead). (D) Corpus callosum (arrows). Required view of the face is of the nose and lips. Additional views include orbits and profile. (E) Nose and lips, coronal view. (F) Orbits, coronal view. (G) facial profile. (H and I) Fetal face, 3D images. See also Video 30.3.

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Heart Rate 151 bpm

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FIGURE 30.8 Views of Fetal Heart, Outflow Tracts, and Three Vessel Thoracic view. Required views include demonstration of normal situs, with heart and stomach on left side, four-chamber view of the heart, documentation of normal heart rate, outflow tracts, and three vessel thoracic view, if possible. (A) Four-chamber view of fetal heart. Note the normal axis of the heart, at about 60 degrees from midline. (B) M-mode ultrasound. Note normal heart rate (151 beats/min). (C) Left ventricular outflow tract (arrow). (D and E) Right ventricular outflow tract in oblique axial and oblique sagittal views with ductus arteriosus (arrow) extending posteriorly to aorta. (F) Three vessel thoracic view. Ao, Aorta; PA, pulmonary artery; SVC, superior vena cava. See also Video 30.4.

CHAPTER 30 Overview of Obstetric Imaging

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FIGURE 30.9 Views of Fetal Abdomen and Pelvis. Required views in the abdomen/pelvis are stomach, kidneys, bladder, and cord insertion site into the anterior abdominal wall. (A) Transverse view of the stomach. (B) Cord insertion site in the anterior abdominal wall. (C and D) Transverse views of kidneys (LK, left kidney; RK, right kidney) at 18 and 30 weeks’ gestation. A small amount of central renal pelvic dilation (2 mm in this fetus) is a normal finding. (E) Bladder. Note symmetric umbilical arteries on either side of bladder. Additional views, not required in a routine anatomy scan: (F) Diaphragm. Sagittal view. Note how the liver (Li) is of lower echogenicity than the lungs (Lu), with the hypoechoic curvilinear diaphragm (arrowheads) in between. (G) Male genitalia (arrow). (H) Female genitalia (arrow).

than 7 days off (although some obstetricians use 5 or 6 days in the early first trimester); in the second trimester, ultrasound should be used to change EDD if it is off by more than 2 weeks (and follow-up is then needed to ensure appropriate interval growth); and in the third trimester, a 3-week discrepancy between LMP and ultrasound dating is allowed but needs to be taken into the clinical context, with assessment for growth restriction or macrosomia if appropriate. It is important to

recognize that pregnancies are infrequently “re-dated” after the first trimester, and if this is done, it is important to obtain follow-up to assess for appropriate interval growth.

Identification of Twin/Multiple Pregnancies A major benefit of routine ultrasound screening is early identification of multiple gestations.3,17,21-23 Randomized clinical trials comparing routine second-trimester ultrasound

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FIGURE 30.10 Views of Fetal Spine. (A) Transverse image of cervical spine. (B) Transverse image of the thoracic spine, in conjunction with fourchamber view of the heart. Note transverse images of lumbar spine between the kidneys (see Fig. 30.9C and D). (C) Transverse view of lumbosacral spine. Note how the posterior elements point toward each other and the skin covers the distal spine. (D) Oblique sagittal image of cervical and thoracic spine. (E) Oblique sagittal view of entire spine. (F) Sagittal view focused on the distal spine. Note how the spinal canal narrows and the sacral spine has a gentle upturn distally. See also Videos 30.5 and 30.6.

examination with sonography performed for clinical indications have shown that a substantial number of twin pregnancies are not recognized until the third trimester or delivery in women who do not undergo routine ultrasound. The improved diagnosis of twins leads to improved perinatal outcome because of a reduced incidence of low birth weight, smallness for gestational age, prematurity, low Apgar scores, and stillbirths.21

Maternal Anatomy: Ovaries Adnexal cysts are common in pregnant women. In early pregnancy, a cyst is most likely the corpus luteum (Fig. 30.13). The corpus luteum can become quite large (up to 10 cm), so if a large cyst is seen at around 16 weeks gestational age, it is worth reviewing old studies or getting a follow-up before determining if this is most likely a corpus luteum or if a neoplasm is suspected. If a cyst appears atypical or enlarges beyond the middle second trimester, it should be further assessed, either with sonography (transvaginal if in the range of the transducer) or if that does not clearly lead to a diagnosis, then with MRI (without contrast) if this would change management in pregnancy (surgical removal in the second trimester, for example). Pregnancy is often the first time young women have an ultrasound examination, thus benign ovarian tumors, such as dermoids, are

often found on their initial scan. However, about .05% of pregnancies are affected by ovarian malignancy,24 so complex cysts without a classic ovarian appearance for benign neoplasm should be followed. Decidualization of an endometrioma can be a difficult diagnosis to make if a patient does not have a prior diagnosis of endometriosis. The soft tissue in the decidualized endometrioma has blood flow and can be mistaken for an ovarian cancer. If not surgically removed, these can be followed closely by ultrasound to assess change in morphology and growth, and at times MRI to assess for signs of endometriosis.25 Surgical removal is frequently needed, and is best performed in the second trimester when there is less risk of miscarriage compared to first-trimester surgery.

Maternal Anatomy: Uterus Fibroids Fibroids are frequently seen in pregnancy. The practice parameter for standard obstetric ultrasound calls for leiomyoma position and size to be documented5 (Fig. 30.14). Fibroids typically increase in size in early pregnancy and then typically decrease in size in the third trimester. Most fibroids are

CHAPTER 30 Overview of Obstetric Imaging

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FIGURE 30.11 View of Fetal Extremities. Required views include documentation of all four extremities. Additional views include measurements of all the long bones and demonstration of the fingers and toes. (A and B) Lower extremities. (CeE) Upper extremities. (F) Hand. Note four fingers with thumb partially out of the field of view. (G) Feet. This is the “hang ten” view, which means that the feet are in the same plane of imaging, so club foot is not possible. (H) Three-dimensional view of upper extremity. (See also Fig. 30.7H for 3D view of hands.) (I) Distal femoral ossification center. Ossification centers of the proximal and distal femur, proximal tibia, and proximal humerus can all be used to aid in dating a pregnancy in the third trimester.

relatively asymptomatic in pregnancy. However, fibroids may lead to complications.26,27 A 2020 study from the Danish National Birth Cohort, the Danish National Patient Registry, and the Danish National Birth Registry showed that clinically significant fibroids are associated with preterm birth and need for cesarean section.27 If the endometrium is severely distorted by fibroids, it may lead to multiple miscarriages. If a fibroid is in the lower uterine segment (LUS), it can be associated with fetal malpresentation and/or preclude vaginal delivery (Video 30.8). When fibroids grow in pregnancy, they can necrose and cause

pain. When this is in the right side of the uterus, it may mimic the pain from appendicitis. The size and location of fibroids may make it difficult for the clinician to estimate growth by the fundal height measurement. Finally, fibroids are associated with increased risk of abruption.28

PosteCesarean Section Uterus In patients with a history of prior cesarean section, the uterus may have an atypical contour (see Video 30.8). Adhesions between the uterus and bladder may cause the uterus to change

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FIGURE 30.12 Views of Umbilical Cord. Required views include cord insertion site into the anterior abdominal wall (see Fig. 30.9B), cord insertion site into the placenta, and documentation of number of vessels in the umbilical cord. Additional views Doppler examination of the cord. (A) Transverse image of three-vessel umbilical cord. Note two arteries (long thin arrows) that are smaller than the single vein (short fat arrow). See also Video 30.7 and Fig. 30.9E. (B) Color Doppler longitudinal image of three-vessel cord. (C) Cord insertion site (arrow) into the placenta. (D) Spectral Doppler image documents normal umbilical arterial systolic-to-diastolic ratio in third-trimester fetus.

position as the bladder fills, with a stretched appearance to the anterior myometrium, causing an angular deformity in the mid uterus as it is stretched out of the pelvis. These adhesions are an expected finding after cesarean section, and should not be confused with the LUS adhesions, discussed subsequently. When assessment of the LUS is the indication for the examination, or when the myometrium of the LUS appear thin (180 beats per minute) Persistent fetal bradycardia (heart rate 3.5 mm or 99th percentile for gestational age Chromosomal abnormality by invasive genetic testing or with cell-free fetal deoxyribonucleic acid (DNA) screening Monochorionic twinning Systemic venous anomaly (e.g., a persistent right umbilical vein, left superior vena cava [SVC], or absent ductus venosus)

MATERNAL FACTORS

Combined data published during two decades from European and North American populations.4,249

TABLE 38.3 Suggested Offspring Recurrence Risk (%) for Congenital Heart Defects Given One Affected Parent

Pre-gestational diabetes regardless of hemoglobin A1C level Gestational diabetes diagnosed in the first or early second trimester IVF, including intracytoplasmic sperm injection Phenylketonuria (unknown status or a periconceptional phenylalanine level >10mg/dL) Autoimmune disease with anti-Sjogren syndrome-related antigen A antibodies First-degree relative of a fetus with CHD (parents, siblings, or prior pregnancy) First- or second-degree relative with disease of Mendelian inheritance and a history of childhood cardiac manifestations Retinoid exposure First-trimester rubella infection

AFFECTED PARENT DEFECT

FATHER

MOTHER

Aortic stenosis Atrial septal defect Atrioventricular septal defect Coarctation of aorta Pulmonary stenosis Tetralogy of Fallot Ventricular septal defect

5 1-2 1

15-20 6 14

2-3 2 1-2 2-3

4 6-7 2-3 9-10

Combined data published during two decades from European and North American populations.4,249

NORMAL FETAL CARDIAC ANATOMY AND SCANNING TECHNIQUES The fetal heart is similar to that of the adult, with several anatomic and physiologic differences. The long axis of the fetal heart is perpendicular to the long axis of the body, such that a transverse section through the fetal thorax demonstrates the four cardiac chambers in a single view. The adult heart, in contrast, is obliquely oriented with its long axis along a line between the left hip and the right shoulder. The four-chamber view is important because, depending on the operator, equipment, and population, 10% to 96% of structural anomalies are detectable on this view.25-30

CHAPTER 38 Fetal Echocardiography Cardiac axis and position are normally such that the apex of the heart points to the left and the bulk of the heart is in the left side of the chest (Fig. 38.1A). This is levocardia. In mesocardia the heart is central with the apex pointing anteriorly (see Fig 38.1B). In dextrocardia, the apex is directed rightward, and the heart is primarily in the right side of the chest (see Fig. 38.1C). This abnormality must be distinguished from dextroposition (see Fig. 38.1D), in which the heart maintains a normal axis but is displaced to the right by an external process, such as a left chest mass or pleural effusion. Abnormal cardiac axis is associated with a 50% mortality and abnormal cardiac position with an 81% mortality.31 The fetal cardiovascular system contains several unique shunts: the ductus venosus, foramen ovale, and ductus

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arteriosus (Fig. 38.2). Antenatally, the placenta rather than the lungs is the fetal sole source of oxygen. Oxygenated blood leaves the placenta through the umbilical vein and travels through the hepatic vasculature and ductus venosus to the inferior vena cava (IVC) and then into the fetal right atrium (RA). As a result of increased velocity, blood entering the IVC via the ductus venosus is shunted across the foramen ovale to the left atrium (LA) and then into the left ventricle (LV), the aorta, and the fetal brain. Poorly oxygenated blood from the superior vena cava (SVC) also enters the RA, and mixes with the blood entering from the IVC, but continues to the right ventricle (RV) and pulmonary artery. Most of this blood is directed through the ductus arteriosus into the descending aorta. Thus, these shunts function so that the majority of output from both

LT LT LV LV

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FIGURE 38.1 Heart Position and Axis. (A) Normal position and axis of the heart. The heart is predominantly in the left side of the chest, with the apex of the heart pointing leftward at an angle of 45  20 degrees from the spine. (B) Mesocardia with the apex of the heart pointing midline (arrow). (C) Dextrocardia showing the apex pointing abnormally to the right side of the fetal chest (arrow). (D) Dextroposition of fetal heart caused by a large, congenital pulmonary airway malformation (M). Transverse image through the fetal chest shows the heart displaced to the right, but the apex (arrow) remaining leftward. LA, Left atrium; LT, left side of fetal chest; LV, left ventricle; RA, right atrium; RV, right ventricle. RT, right side of fetal chest.

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Placenta FIGURE 38.2 Diagram of Fetal Shunts. Blood from the umbilical vein is shunted through the ductus venosus to the right atrium and then across the foramen ovale to the left atrium. Fetal cardiac output from the right side of the heart is shunted to the descending aorta through the ductus arteriosus.

ventricles enters the systemic circulation, rather than a substantial portion entering the pulmonary circulation, as in the adult. Blood that enters the pulmonary vasculature via the pulmonary artery is returned to the LA by the four pulmonary veins. From the LA it enters the LV and ultimately the descending aorta, returning to the placenta via the iliac and umbilical arteries. Normal values for measurements of the fetal heart and great vessels are shown in Figs. 38.3 and 38.4. Fetal echocardiography is best accomplished at 18-22 weeks of gestation.19 Before 18 weeks, image resolution is frequently limited by the small size of the fetal heart and fetal movement. After 22 weeks, the examination may be compromised by progressive ossification of the fetal skull, spine, and long bones; the relatively smaller amniotic fluid volume; and an unaccommodating fetal position. Importantly, some congenital cardiac abnormalities progress in utero and may be subtle or unrecognizable at or before 22 weeks but more obvious closer to term.32-33 Tachyarrhythmias may not occur until the third trimester.34-35 In some cases, late first-trimester/early second-trimester evaluation of the fetal heart may be feasible. This may be accomplished with transvaginal ultrasound as early as 1114 weeks.36-38 With continuing advances in image resolution, diagnostic results are also sometimes possible with a transabdominal approach at 13-14 weeks.38 However, first-trimester fetal echocardiography is often limited and should be considered an adjunct to second-trimester evaluation, not a replacement.

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G FIGURE 38.3 Cardiac Dimensions. (A) Left atrial internal dimension versus gestational age. (B) Right atrial internal dimension versus gestational age. (C) Left ventricular internal dimension in diastole versus gestational age. (D) Right ventricular internal dimension in diastole versus gestational age. (E) Left ventricular heart wall thickness. (F) Right ventricular heart wall thickness. (G) Interventricular septal thickness versus gestational. (Graphs generated from the original data of Tedesco GD. Reference ranges of fetal cardiac biometric parameters using three-dimensional ultrasound with spatiotemporal image correlation m mode and their applicability in congenital heart diseases. Pediatr Cardiol. 2017;38:271-279.)

CHAPTER 38 Fetal Echocardiography

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FIGURE 38.4 Diameter of Aortic Root and Pulmonary Artery. (A) Diameter of aortic root versus gestational age. (B) Diameter of pulmonary artery (PA) versus gestational age. (Graphs generated from the original data of Shapiro I. Fetal cardiac measurements derived by transvaginal and transabdominal cross-sectional echocardiography from 14 weeks of gestation to term. Ultrasound Obstet Gynecol. 1998;12:404-418.46)

LV RV

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FIGURE 38.5 Four-Chamber View of Heart. (A) Apical four-chamber view shows the interatrial and interventricular septa parallel to the angle of insonation. (B) Subcostal four-chamber view shows the interatrial and interventricular septa perpendicular to the angle of insonation. LA, Left ventricle; LV, left ventricle; RA, right atrium; RV, right ventricle; PV, pulmonary vein; LAA, left atrial appendage.

Scanning the fetal heart requires a systematic approach, beginning with the determination of the position of the fetus within the uterus and the heart within the fetal chest. A transverse view through the fetal thorax above the level of the diaphragm demonstrates four cardiac chambers. Four-chamber views can be obtained with the angle of insonation parallel to the interventricular septum (apical four-chamber view; Fig. 38.5A) or perpendicular to the septum (subcostal fourchamber view; see Fig. 38.5B). In a normal four-chamber view the echogenic foraminal flaps of the foramen ovale can be observed moving into the LA. The pulmonary veins should be seen entering the spherical LA. The appendages of the atria may also be appreciated in the four-chamber views, with the right atrial appendage described as having a triangular shape and the left atria appendage appearing as more of a finger-like structure. The atrioventricular valves (mitral and tricuspid) are visible in the fourchamber view. The septal leaflet of the tricuspid valve inserts slightly more apically on the interventricular septum than the anterior leaflet of the mitral valve. The LV has a relatively

smooth inner wall, and a more elongated shape than the RV. In the normal heart, the LV is the apex forming ventricle. The internal surface of the RV is coarse, particularly near the apex, where the moderator band of the trabecula septomarginalis is frequently recognized as a thicker, more echogenic structure. This helps identify the morphologic RV. From the subcostal four-chamber view, angling the transducer toward the fetus’s right shoulder permits evaluation of the continuity of the LV with the ascending aorta (Fig. 38.6, Video 38.1). Further angulation in the same direction shows the RV in continuity with the pulmonary artery (Fig. 38.7). The diameter of the pulmonary artery is approximately 9% larger than that of the aorta between 14 and 42 weeks. The measured differences in these vessels and with M-mode versus 2D imaging are negligible (2% to 5%) for both the pulmonary artery and the aorta.39-40 Importantly, measurements of the pulmonary artery and the aorta should be performed at the level of the valves. Further rightward rotation produces a sagittal view of the fetal thorax and a short-axis view of the ventricles (Fig. 38.8). Angulation toward the left fetal shoulder from this view shows the aorta as a

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FIGURE 38.6 Continuity of aorta (AO) with left ventricle (LV). LA, Left atrium; RV, right ventricle.

RV RPA PA DA

FIGURE 38.7 Continuity of main pulmonary artery (PA) with right ventricle (RV), bifurcating into the right pulmonary artery (RPA) and the ductus arteriosus (DA).

central circle, with the pulmonary artery draping anteriorly and to the left (Fig. 38.9). The apical four-chamber view may also be used as a starting point when evaluating normal cardiac anatomy. Yagel and colleagues32 described a series of planes arising from the apical four-chamber view, all accomplished by moving the transducer in a cephalad direction (Video 38.2). A slight cephalad advancement will show an apical five-chamber view, which is useful in assessing continuity of the ascending aorta with the LV (Fig. 38.10A). Continued cephalad movement should result in visualization of the bifurcating pulmonary artery and its relationship to the RV (see Fig. 38.10B). A three-vessel view and just slightly higher a three-vessel trachea view (3VT) should be

visualized next (Fig. 38.11A). These views allow evaluation of the main pulmonary arteryeductus arteriosus confluence, the transverse aortic arch, and the SVC. Confirmation of vessel presence, comparison of vessel size, and determination of blood flow direction with color Doppler can all be accomplished at this level. In addition, appropriate location of both great vessels to the left of the trachea should be confirmed.41 Moving the transducer just slightly above the 3VT will allow evaluation of the left brachiocephalic vein. Confirming the presence, size, and location of this structure can aid in suggesting or ruling out several types of CHD (see Fig. 38.11B). In addition, a 2022 meta-analysis found that in fetuses 11-14 weeks, the fourchamber view alone could detect over half of cardiac anomalies, and that this value increased when adding color or a three-vessel view.42 Returning to a sagittal plane of the fetus and directing the transducer from the fetal left shoulder to the right hemithorax demonstrates the distinctive candy-cane shape of the aortic arch (Fig. 38.12). The three major vessels to the head and neck (innominate artery, left carotid artery, left subclavian artery) should be identified arising from the arch. An abnormal number or abnormal spacing of the head and neck vessels may imply CHD. The aortic arch should not be confused with the ductal arch (Fig. 38.13), which is formed by the right ventricular outflow tract, pulmonary artery, and ductus arteriosus. The ductal arch is broader and flatter than the aortic arch. The ductal arch is often visualized by sliding the transducer slightly to the left of the aortic arch. Lastly, sliding the transducer to the right of the aortic arch while maintaining a sagittal plane on the fetus should allow visualization of the IVC and SVC (bicaval view) entering the RA (Fig. 38.14). M-mode echocardiography provides a 2-D image of motion over time. It is useful in evaluating heart rate, chamber size, wall thickness, and wall motion (Fig. 38.15A). Simultaneous Mmode imaging through an atrial and ventricular wall is helpful in analyzing arrhythmias (see Fig. 38.15B, Video 38.3). Chamber size, ventricular wall, and interventricular septal thickness should be measured just inferior to the level of the atrioventricular (A-V) valves.43 Measurements may be performed on either the 2D images or M-mode. Spectral Doppler ultrasound evaluation of the fetal heart can be used to determine the presence, velocity, and direction of flow through the vessels or valves (Fig. 38.16) and to evaluate valvular regurgitation or insufficiency (Fig. 38.17). Variation in flow velocity reflects structural or functional cardiac abnormalities. In the setting of valvular stenosis, an increased velocity will be appreciated distal to the affected valve. If regurgitant flow is present, retrograde flow is visualized proximal to the affected valve during the portion of the cardiac cycle that the valve should be closed. If a valve is atretic, no blood flow should be appreciated though the valve. Spectral Doppler ultrasound is also useful in assessing fetal arrhythmias. The ideal placement of the spectral Doppler cursor in this setting is within the LV, with the sample gate size wide enough to appreciate both ventricular inflow though the mitral valve and ventricular outflow though the aortic valve simultaneously (see Fig. 38.16, Video 38.4).

CHAPTER 38 Fetal Echocardiography

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RV IVS LV

FIGURE 38.8 Short-Axis View of Ventricles With and Without Color Doppler. Anterior right ventricle (RV) is normally slightly larger than the left ventricle (LV). IVS, Interventricular septum.

ultrasound often reduces the amount of time required for spectral Doppler ultrasound interrogation of the heart, particularly in the setting of complex cardiac anomalies.43-45 Subtle lesions such as small VSDs are more reliably and easily identified with the use of color flow Doppler ultrasound, particularly in the muscular portion of the septum. The utility of several advanced technologies has been reported in the evaluation of the fetal heart, including threedimensional (3-D) and four-dimensional (4-D) ultrasound, tissue Doppler imaging, strain and strain rate imaging, as well as fetal magnetocardiography and cardiovascular magnetic resonance imaging (MRI).46-48 However, many of these require specialized transducers or other equipment, sophisticated algorithms, and specialized technical expertise. Additionally, limited resolution and cardiac motion are still considered major disadvantages in some settings.20

PV PA RVOT AO RA

LA

SP FF

STRUCTURAL ANOMALIES FIGURE 38.9 Short-Axis View of Great Vessels. Aorta (AO) in center with pulmonary artery (PA) draping anteriorly. FF, Foraminal flap; LA, left atrium; PV, pulmonic valve; RA, right atrium; RVOT, right ventricular outflow tract; SP, spine.

Color Doppler ultrasound permits a rapid interrogation of flow patterns within the heart and great vessels (Fig. 38.18A and B), allowing functional and structural abnormalities to be more rapidly characterized. For example, valvular stenosis is clearly demonstrated with color Doppler ultrasound, as is reversed flow through insufficient valves or in the great vessels. Color Doppler

Atrial Septal Defect An atrial septal defect (ASD) results from an error in the amount of tissue resorbed or deposited in the interatrial septum. ASDs occur in 1 per 1500 live births49-52 and comprise 6.7% of CHD in live-born infants.49 ASDs occur twice as often in females as males.53,54 ASDs are associated with a variety of cardiac, extracardiac, and chromosomal abnormalities. ASDs are classified by embryogenesis, size, or relationship to the fossa ovalis. Embryologically, between the fourth and sixth weeks of gestation, the primitive atrium is divided into right and left halves. The septum primum, a crescent-shaped membrane, develops along the cephalad portion of the atrium and grows

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PA LV

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DA RPA

A LA

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FIGURE 38.10 (A) Apical five-chamber view shows continuity of the aorta (A) with the left ventricle (LV). LA, Left atrium; RA, right atrium; RV, right ventricle; SP, spine. (B) Main pulmonary artery bifurcating into the ductus arteriosus (DA) and right pulmonary artery (RPA).

S T

S T

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LBCV

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P

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FIGURE 38.11 (A) Three-vessel and trachea view shows the correct orientation of the main pulmonary arteryeductus arteriosus confluence (P), the transverse aortic arch (A), and the superior vena cava (S). This view also shows the two great vessels correctly positioned on the left side of the trachea (T). Color Doppler confirms blood flow through both great vessels in moving in the correct direction towards the descending aorta. (B) Moving the transducer slightly above the three-vessel trachea view allows visualization of the left brachiocephalic vein (LBCV)

PA

AO

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LC D

I AO

FIGURE 38.12 Normal Aortic Arch. Sagittal view shows the rounded, “candy-cane” appearance of aortic arch and the head and neck vessels arising from it. AO, Descending aorta; I, innominate artery; LC, left carotid artery; LS, left subclavian artery.

FIGURE 38.13 Normal Ductal Arch. Sagittal view shows pulmonary artery (PA) draping over the aorta (A) and joining the ductus arteriosus (D), which then joins the descending aorta (AO). LA, Left atrium.

CHAPTER 38 Fetal Echocardiography caudally toward the endocardial cushions. The space between these two structures, termed the ostium primum, disappears when the septum primum fuses with the endocardial cushion. Before complete fusion, however, multiple small fenestrations develop in the septum primum, coalescing to form the ostium secundum. A second crescent-shaped membrane subsequently develops just to the right of the septum primum. As this membrane grows toward the endocardial cushion, it partially covers the ostium secundum. Its crescent-shaped lower border never entirely fuses with the endocardial cushion, leaving an opening, the foramen ovale (Fig. 38.19). Ostium secundum ASDs make up more than 80% of all ASDs and generally occur in isolation. This ASD is caused by excessive resorption of the septum primum (foraminal flap) or by inadequate growth of the septum secundum (Fig. 38.20A).

IVC

SVC RA

FIGURE 38.14 Bicaval view of the inferior vena cava (IVC) and superior vena cava (SVC) entering the right atrium (RA).

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The ostium primum ASD is the second most common type and is located low in the atrial septum, near the A-V valves. Although the ostium primum ASD may occur alone, it is more frequently associated with a more complex congenital cardiac anomaly, the atrioventricular septal defect (AVSD) (see Fig. 38.20B). Sinus venosus ASDs are a rare defect that can be divided into two types: (1) sinus venosus ASD of the SVC, with the defect adjacent to the orifice of the SVC into the RA; and (2) sinus venosus ASD of the IVC, with the defect adjacent to the IVCs right atrial entrance. The first type is often associated with anomalous pulmonary venous return (APVR) (see Fig. 38.20C). Coronary sinus ASDs, located at the ostium of the coronary sinus in the RA, are exceedingly rare. The prenatal sonographic diagnosis of ASD is difficult because the normal patent foramen ovale, which allows blood to flow from the right to the LA in utero, itself represents an ASD. It can be difficult to distinguish a small, pathologic ASD from the normal patent foramen ovale. The foraminal flap, or septum primum, is clearly visualized in the four-chamber view. It has a “loose pocket” configuration, appearing either circular or linear in shape as it opens into the LA55,56 (Fig. 38.21). The septum secundum, which is thick and relatively stationary, makes up the majority of the atrial septum. The foramen ovale is an opening in the septum secundum. The septum secundum and foramen ovale are well visualized in the fourchamber views. The maximal size of the normal foramen ovale differs by 1 mm or less from the aortic root diameter at all gestational ages.55-57 Sonographically, an ostium secundum ASD appears as a larger-than-expected defect in the central portion of the atrial septum near the foramen ovale

RA LV

LA

IVS

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LV

V

A

A

FHR

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PA–

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A

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FIGURE 38.15 M-Mode Echocardiography. (A) Simultaneous m-mode tracing through the right atrium (RA) and the left ventricle (LV) showing normal atrial contractions followed by normal ventricular contractions. (B) Simultaneous m-mode tracing through the left ventricle (LV) and the right atrium (RA) shows normal atrial beats (A) followed by a premature atrial contraction (PA) which is conducted to the ventricles triggering a premature ventricular response (PV). IVS, Interventricular septum; LA, left atrium; RV, right ventricle; V, normal ventricular contractions. See Video 38.3.

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A E

FIGURE 38.16 Spectral Doppler Ultrasound Used to Interrogate a Normal Mitral Valve. Spectral Doppler sample volume is placed distal to the mitral valve in the left ventricle (LV). A normal mitral valve waveform is appreciated above the baseline, showing the normal early diastolic (E) and atrial contraction (A) wave points. LA, Left atrium; RA, right atrium; RV, right ventricle. See Video 38.4.

MV AO

A large right-to-left shunt is physiologic in utero, and thus an ASD usually does not compromise the fetus hemodynamically. After birth, the shunt may cause right ventricular overload and pulmonary hypertension. Spontaneous closure of an ASD occurs in approximately two-thirds of patients.60 Patients with small ASDs can remain asymptomatic into their 50s.61

RA RV

Vel 519 cm/s PG 108 mmHg

R

R

T

R

T

R

T

R

T

FIGURE 38.17 Tricuspid Insufficiency. Spectral Doppler sample volume is placed proximal to the tricuspid valve in the right atrium (RA). Significant regurgitant flow (R) can be seen above the baseline. This implies that the valve has not closed during systole, and therefore blood flow is retrograde into the right atrium. RV, Right ventricle; T, tricuspid valve.

(Fig. 38.22A). Alternatively, it can appear as a deficient foraminal flap. If the lowest portion of the atrial septum (just adjacent to the A-V valves) is deficient, an ostium primum defect should be suspected (see Fig. 38.22B). Sinus venosus and coronary sinus ASDs are rarely appreciated by fetal echocardiography. Color Doppler is helpful in the diagnosis of larger ASDs. However, small ASDs are commonly obscured by the normal flow through the patent foramen ovale.58,59

Ventricular Septal Defect Isolated VSD is the most common cardiac anomaly, accounting for 30% of heart defects diagnosed in live-born infants and 9.7% diagnosed in utero.49,50,62 VSDs are associated with other cardiac anomalies in 50% of cases.63 Of the structural cardiac defects, VSDs have the highest recurrence rate and the highest association with teratogen exposure. They are classified according to their position in the interventricular septum (Fig. 38.23) as membranous or muscular VSD (inlet, outlet, mid-muscular or trabecular, apical).63 About 80% of VSDs occur in the membranous portion of the septum.64 However, because most membranous defects also involve a portion of the muscular septum, they are commonly referred to as perimembranous defects. The subcostal fourchamber view provides optimal evaluation of the interventricular septum. At sonography, a VSD appears as an area of discontinuity in the interventricular septum (Fig. 38.24A). When the defect is small, this diagnosis is problematic, and at least one-third of VSDs are missed on the four-chamber view.20,25,65,66 Small VSDs not detectable on gray-scale echocardiography may be documented with color Doppler ultrasound.39 Thus, use of color Doppler imaging improves the diagnostic accuracy for VSD. However, most are missed on fetal echocardiography.59,66,67 Color is particularly helpful in identifying small VSDs within the muscular portion of the septum (see Fig. 38.24B, Video 38.5). In the setting of an isolated VSD, color Doppler ultrasound imaging typically shows bidirectional

CHAPTER 38 Fetal Echocardiography

RA

LA

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RV

RA

LV

LV LA

A Vel -107 cm/s

AA

FIGURE 38.18 Using Color Doppler Ultrasound to Assess Normal Blood Flow. (A) Dual subcostal four-chamber image with color Doppler ultrasound shows normal flow through the foramen ovale (arrow) from the right atrium (RA) to the left atrium (LA). (B) Color and spectral Doppler showing normal blood flow through the aortic arch (AA). LV, Left ventricle; RV, right ventricle.

B

interventricular shunting, with a systolic right-to-left shunt and a late diastolic left-to-right shunt. The prognosis for an infant with an isolated VSD is excellent, and many such defects go undetected. The rate of spontaneous closure of isolated muscular VSDs by 5 years of life is much higher (65%) than that for isolated perimembranous VSDs (20%).68 Overall about 40% of VSDs spontaneously close in the first year of life.63-69,70 However, large defects detected in the fetus are associated with an 84% mortality.71 Concurrent cardiac, extracardiac, and chromosomal anomalies (trisomy 13, 18, 21, and 22q11 micro-deletion) are associated with a worse prognosis. VSDs may be extremely difficult to diagnose in utero, particularly when small in size. In addition, many small VSDs will close in utero or shortly after birth. A “pseudo” VSD in the

membranous portion of the septum may be appreciated when evaluating the interventricular septum from an apical fourchamber view (see Fig. 38.24C). This occurs when the angle of insonation is parallel to the septum, causing an artifactual dropout of the thin, membranous septum. The short-axis view of the ventricles is useful in confirming the presence of a VSD, as is a long-axis view of the aorta, looking for a loss of continuity between the interventricular septum and the anterior wall of the aorta.

Atrioventricular Septal Defect AVSD refers to a spectrum of cardiac abnormalities involving various degrees of deficiency of the interatrial and interventricular septa and of the mitral and tricuspid valves. These defects arise when the endocardial cushions fail to properly

4 wk

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41/2 – 5 wk

Septum primum Ostium primum

RT LT Atrium

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Developing ostium secundum

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FIGURE 38.19 Development of Interatrial Septum (Viewed Facing Patient). (A) At 4 weeks’ gestation the septum primum is small. A large ostium primum is present. (B) At 4½ weeks, enlargement of the septum primum results in reduction in size of the ostium primum. Perforations in the septum primum develop. (C) Perforations in the septum primum coalesce to form the ostium secundum. (D) At 5 weeks the septum primum has fused to the endocardial cushions, and the septum secundum begins to develop to the right of the septum primum. (E) At 8 weeks the septum secundum has enlarged, now covering the ostium secundum. Blood flows from the right atrium through the valve mechanism (foraminal flap) of the foramen ovale. LA, Left atrium; LT, left; RA, right atrium; RT, right.

SVC SVC

SVC

RA

RA RA RV

IVC

A

RV RV IVC

IVC Ostium secundum ASD

B

Ostium primum ASD

C

Sinous venosus ASD

FIGURE 38.20 Types of Atrial Septal Defect (ASD). Schema of the atrial septum viewed from the right atrium (RA). (A) Ostium secundum ASD. (B) Ostium primum ASD. (C) Sinus venosus ASD. IVC, Inferior vena cava; RV, right ventricle; SVC, superior vena cava.

RV

RA

LV

RV LA

LA

A

RA

LV

B

FIGURE 38.21 Foraminal Flap and Foramen Ovale. (A) Linear appearance of the foraminal flap (arrow) as it enters the left atrium (LA). (B) Circular appearance of the foraminal flap (arrow) entering the LA. LV, Left ventricle; RV, right ventricle; RA, right atrium.

CHAPTER 38 Fetal Echocardiography

1471

LV RV

RV

RA RA

LA

LA LV

A

B

FIGURE 38.22 (A) Four-chamber view shows an ostium secundum atrial septal defect (arrow) appearing as a larger than expected opening between the left atrium (LA), and the right atrium (RA). (B) Ostium primum atrial septal defect (arrow) directly above the atrioventricular (A-V) valves. LV, Left ventricle; RV, right ventricle.

Pulmonary valve

Outlet Tricuspid valve Membranous

Inlet

Trabecular

FIGURE 38.23 Interventricular Septum Viewed From Right Ventricle. The membranous septum and the three portions of the muscular septum (inlet, outlet, and trabecular) are demonstrated. Ventricular septal defects may occur in any of these locations.

fuse. AVSDs are also referred to as endocardial cushion defects or A-V canal defects. Almost two-thirds of fetuses with AVSD have additional cardiac anomalies.72-74 About one-third are associated with left atrial isomerism (both atria anatomically resemble the left), and of these the majority of affected fetuses have complete heart block.71,72 Chromosomal (especially trisomy 21) or extracardiac anomalies are associated in 78% of AVSDs.75 Embryologically, in the primitive heart, the common atrium and ventricle communicate through the A-V canal. Development of the endocardial cushions results in division of the single, large A-V canal into two separate orifices, separating the atria from the ventricles (Fig. 38.25). The interatrial and interventricular septa develop concurrently, eventually dividing the single atrium and ventricle into right and left portions. When the endocardial cushions fail to fuse properly, normal development of the mitral and tricuspid valves cannot occur, and an AVSD results (Fig. 38.26).

AVSDs are divided into complete, partial or intermediate forms. Since it is often difficult to distinguish between an intermediate or partial AVSD, both are more commonly referred to as incomplete.75-76 In both types, the A-V valves are abnormal. In a complete AVSD a single, multi-leaflet valve is present, whereas in an incomplete AVSD leaflets from each AV valve are fused, resulting in the appearance of two valve orifices. Complete AVSD has variable amounts of deficient tissue in the atrial and ventricular septa. The incomplete form is associated with an ostium primum ASD. A small inlet VSD may or may not be present. At fetal echocardiography, 97% of AVSDs are complete, although after birth only 69% are complete.71-75 The fetal incidence of AVSD is four times greater than that in the liveborn population, indicating a high incidence of in utero demise.20,49,50 AVSDs are considered balanced when the A-V junction is connected to both the right and the LV, such that blood flow is relatively evenly distributed. If this connection exists with primarily one ventricle, such as in the setting of a hypoplastic LV, it is termed an unbalanced AVSD. Sonographically, a defect in the atrial and ventricular septa with an associated single abnormal A-V valve is visible in a four-chamber view with a complete AVSD (Fig. 38.27A, Video 38.6). The single, abnormal valve can be confirmed in a shortaxis view. An incomplete AVSD should be suspected when the normal offset of the mitral and tricuspid valves is not visualized, instead appearing as a straight line across the AV canal (see Fig. 38.27B, Video 38.7). Demonstration of two A-V valve orifices in the short-axis view allows for differentiation between complete and incomplete forms of AVSD.77-78 Color Doppler demonstrates an open area of flow across the AVSD and the abnormal A-V valve (see Fig. 38.27C). Color Doppler imaging is particularly useful in the detection of

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LV

LV LV RV

LA

RV

RV

RA

RA

B

A

RV

LV

RA

FIGURE 38.24 Ventricular Septal Defect (VSD). (A) Subcostal four-chamber view shows a VSD (arrow) across the interventricular septum. (B) Color Doppler showing a VSD (arrow) in the muscular portion of the septum that is not well visualized on the gray-scale image. (C) Apical four-chamber view with a “pseudo” defect (arrow) in the upper portion of the interventricular septum, which reflects an artifact caused by angle of insonation. LA, Left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. See Video 38.5.

LA

C

4 wk

5 wk

Septum primum

Septum secundum

Atrioventricular canal

Ostium secundum Septum primum fused to endocardial cushions

Endocardial cushion Common ventricle

Fused endocardial cushions

Interventricular septum

A

B 8 wk

FIGURE 38.25 Normal Development of Endocardial Cushions. (A) In the fourth week the endocardial cushions divide the atrioventricular canal into two orifices. (B) By the fifth week the communication between the atria, the ostium secundum, is smaller. The ventricular septum has grown, almost obliterating the communication between the ventricles. (C) At 8 weeks, complete development of the endocardial cushions and atrioventricular valves results in four distinct cardiac chambers.

Septum secundum Ostium secundum Septum primum Mitral valve

C

Tricuspid valve

Interventricular septum

CHAPTER 38 Fetal Echocardiography

Normal tricuspid and mitral valves

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Partial atrioventricular septal defect

Anterosuperior leaflet

Aortic leaflet

Inferior leaflet

Mural leaflet

RT

LT

Septal leaflet “Cleft”

Tricuspid Mitral valve valve

A

B

Complete atrioventricular septal defect Anterosuperior leaflet

FIGURE 38.26 Valve Leaflet Morphology. (A) Normal heart. (B) Partial atrioventricular septal defect (AVSD). (C) Complete AVSD. LT, Left abnormal valve; RT, right abnormal valve.

Anterior bridging leaflet RT

Right mural leaflet

LT

Left mural leaflet Posterior bridging leaflet

C

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RA RV

RV

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LA

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FIGURE 38.27 Atrioventricular Septal Defect (AVSD). (A) Subcostal four-chamber view shows an ostium primum atrial septal defect (ASD) between the right atrium (RA) and left atrium (LA), an inlet ventricular septal defect (VSD) between the right ventricle (RV) and left ventricle (LV) and a single, multi-leaflet atrioventricular valve (arrow), consistent with a complete AVSD See Video 38.6. (B) Apical four-chamber view shows an ostium primum ASD, an inlet VSD and fused AV Valves (circled) consistent with an incomplete AVSD. See Video 38.7. (C) Color Doppler confirms blood flow through a single AV valve (arrow).

valvular insufficiency, which is commonly present.78-79 Holosystolic valvular insufficiency is closely associated with fetal hydrops and a worse prognosis.78 Frequently, a left ventricularetoeright atrial jet can be identified across the ostium primum defect before the onset of holosystolic valvular insufficiency42 Cardiac malformations associated with AVSD include septum secundum ASD, hypoplastic left heart syndrome (HLHS), valvular pulmonary stenosis, coarctation of the aorta, and tetralogy of Fallot (TOF). A meta-analysis of prenatal diagnosis of AVSD confirmed that chromosomal anomalies are common, occurring in 25% to 58% of affected fetuses.80 Therefore genetic counseling and discussion of obtaining the karyotype is indicated. Associated extracardiac anomalies are common, including omphalocele, duodenal atresia, tracheoesophageal atresia, facial clefts, cystic hygroma, neural tube defects, and multicystic kidneys.75 Heterotaxy is also associated with AVSD. It occurs in 90% of fetuses with asplenia and 40% to 50% of fetuses with

polysplenia. AVSD with heart block is also common with polysplenia.72 The fetus with an AVSD and associated defects has a poor prognosis. When hydrops is present, few survive the neonatal period.80 Despite advances in pediatric cardiothoracic surgery, the overall outcome for antenatally diagnosed AVSD remains variable, with many studies reporting 5% to 15 year survival rates below 50%.75,78 Others have reported excellent long-term results with newer surgical techniques such as the two-patch technique with early complete cleft closure for complete AVSD repair.81,82

Ebstein Anomaly Ebstein anomaly is characterized by inferior displacement of the tricuspid valve, frequently with tethered attachments of the leaflets, tricuspid dysplasia, and right ventricular dysplasia83-87 (Fig. 38.28A, Video 38.8). Ebstein anomaly makes up approximately 7% of cardiac anomalies in the fetal population and has

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Ebstein anomaly

RV RA

LA LV RA

Mitral valve LA Tricuspid valve

Anterior

A

B

FIGURE 38.28 Ebstein Anomaly. (A) Diagram showing the tricuspid valve apically displaced, resulting in an enlarged right atrium (RA) and a small, functional right ventricle (RV). See Video 38.8 (B) Gray-scale image shows tricuspid valve (arrow) displaced inferiorly, resulting in an “atrialized” RV and enlarged R(A). LA, Left atrium; LV, left ventricle.

an incidence of 0.5% to 1% in high-risk populations.20,88,89 It occurs in approximately 1 per 20,000 live births.90 Early data from biased retrospective studies suggested that lithium use during pregnancy was associated with an estimated 500-fold increase in the incidence of Ebstein anomaly in exposed fetuses.90-95 It is now clear that the increased risk is less than 2%.20,96 Ebstein anomaly may be associated with a variety of structural cardiovascular defects, particularly pulmonary atresia or stenosis,97 arrhythmias, and chromosomal anomalies.85,98-101 Ebstein anomaly is readily detected in utero.89,102 The sonographic diagnosis rests on recognition of apical displacement of the tricuspid valve into the RV, resulting in an enlarged RA containing a portion of the “atrialized” right ventricle, and a reduction in size of the functional RV (see Fig. 38.28B, Video 38.8). Differential diagnosis includes tricuspid valvular dysplasia, Uhl anomaly, and idiopathic right atrial enlargement, but none of these has an inferiorly displaced tricuspid valve, the most reliable sign of Ebstein anomaly.89,103 Ebstein anomaly is one of the few structural defects that may cause substantial cardiac dysfunction in utero, frequently with cardiomegaly, hydrops, and tachyarrhythmias.85,100 Examination with spectral and color Doppler ultrasound is helpful in visualizing tricuspid valve regurgitation, which causes further enlargement of the RA and ventricle.104 Tethered distal attachments of the tricuspid valve, marked right atrial enlargement, and left ventricular compression with narrowing of the pulmonary outflow tract are all associated with a poor prognosis.85 Fetuses diagnosed with Ebstein anomaly and tricuspid dysplasia have a poor prognosis, with an overall perinatal mortality (fetal demise or death before neonatal discharge) of 45%.105

Arrhythmias, particularly supraventricular tachycardias (SVTs), are common with Ebstein anomaly and can further compromise the fetus. Overall, the 3-month mortality rate for patients diagnosed in utero is 80%.85,100,102 Surgical correction of Ebstein anomaly in young children is associated with a low mortality rate and an excellent quality of life.106-108 Because clinical presentation, treatment options, and prognosis are inconsistent, case-by-case management is variable.109

Hypoplastic Right Ventricle In general, hypoplastic RV occurs secondary to pulmonary atresia with intact interventricular septum. It has an incidence of 1.1% among stillbirths.49,110 Tricuspid atresia may also be associated with a hypoplastic RV, but this is not as common.111 Pathophysiologically, hypoplasia of the RV develops because of a reduction in blood flow secondary to inflow impedance from tricuspid atresia or outflow impedance from pulmonary arterial atresia. Typical sonographic findings include a small, hypertrophic RV and a small or absent pulmonary artery112 (Fig. 38.29, Video 38.9). Spectral and/or color Doppler ultrasound may be helpful in confirming decreased (or absent in the setting of tricuspid atresia) flow through the tricuspid valve or pulmonary artery. Congestive heart failure and hydrops may develop from tricuspid regurgitation. Other sonographic characteristics of hypoplastic RV may include retrograde blood flow through the ductus arteriosus and pulmonary artery often readily apparent on the 3VT view, or the presence of abnormal sinusoids within the myocardium of the RV. These sinusoids are referred to as ventriculocoronary arterial communications and can be appreciated with color Doppler.113 After birth, closure of the ductus arteriosus frequently results in neonatal

CHAPTER 38 Fetal Echocardiography

decreased blood flow into and/or out of the LV. The primary abnormalities present include aortic atresia, aortic stenosis, and mitral valve atresia. It is associated with other cardiac malformations, such as coarctation of the aorta in 20% of cases.117 The primary sonographic feature of HLHS is a small LV (Fig. 38.30A, Video 38.10). The mitral valve is typically hypoplastic or atretic, as is the aorta.118 Spectral and Color Doppler are extremely helpful in the setting of HLHS, usually showing the absence of flow through the mitral and aortic valves.44 Retrograde blood flow from the ductus arteriosus back though the aortic arch and ascending aorta is not unusual and can be appreciated on the 3VT view. It should be borne in mind that HLHS can be a progressive abnormality that may not be appreciated in early pregnancy. Identifying the RV as the primary apex-forming chamber may be the first sign that HLHS is present (see Fig. 38.30B). Four decades ago this syndrome had an extremely poor prognosis, with 25% mortality in the first week of life and most untreated infants dying within 6 weeks.119 Comfort care was provided, but little could be done to prolong survival. Currently, it is expected that up to 70% of newborns with HLHS may reach adulthood owing to advancements in surgical techniques, perioperative management, and postoperative care.120 Prenatal diagnosis of HLHS is beneficial for preventing ductal shock and keeping affected infants stable in the preoperative stage.121-122 Monophasic blood flow across the mitral valve, restricted or absent flow through the foramen ovale, and retrograde flow through the aorta are all considered poor prognostic signs in utero. Despite significant advancements in medical and surgical management over the past 30 years, follow-up studies indicate that children with HLHS often experience major developmental delays123 and decreased exercise performance, even after heart

death. Prognosis improves with preoperative prostaglandin infusion to maintain the patency of the ductus.114

Hypoplastic Left Heart Syndrome In HLHS, the left ventricular cavity is pathologically reduced in size. HLHS constitutes approximately 7% to 9% of all congenital cardiac lesions.115 It has a 2:1 male predominance and a recurrence risk of 0.5%.115,116 The small LV results from

RV

RA

LV

LA

SP

FIGURE 38.29 Hypoplastic Right Ventricle. Apical four-chamber view shows small, right ventricular chamber (RV). See Video 38.9. LA, Left atrium; LV, left ventricle; RA, right atrium; SP, spine.

RV

RV

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FIGURE 38.30 Hypoplastic Left Heart Syndrome (HLHS). (A) Subcostal four-chamber view showing a small left atrium (LA) and left ventricle (LV), and an enlarged right atrium (RA) and right ventricle (RV) diagnostic of HLHS. (B) Apical four-chamber view in another fetus with HLHS showing the right ventricle becoming the apex-forming ventricle (arrow) due to the small left heart. See Video 38.10. SP, Spine.

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transplantation.124 One published meta-analysis found that although deficits remain, substantial improvement in neurodevelopment has occurred over the past 20 years in patients with surgically corrected HLHS.125

Univentricular Heart There are a variety of descriptions in the literature regarding what constitutes a univentricular heart. The most common form consists of two atria empty into a single ventricle, via two A-V valves. Univentricular heart is rare, accounting for approximately 2% of CHD.50 The single chamber has a left ventricular morphology in 85% of cases.126 Associated cardiac anomalies are common,127 as is heterotaxy, which is found in 13%.127-128 Sonographically, a single ventricle with absence of the interventricular septum is seen (Fig. 38.31, Video 38.11). Doppler ultrasound examination is helpful in determining if normal outflow tracts are present, as well as assessing for valvular insufficiency. A nonfunctioning, rudimentary accessory ventricle and interventricular septum may be present in some cases. Patients with unrepaired univentricular hearts have a poor prognosis, with 70% dying before age 16. A variety of surgical interventions have reported survival rates of 78% to 91% at 12 years.129,130,131

49%. TOF in conjunction with AVSD is often seen with Trisomy 21. The first-trimester nuchal translucency was above the 95th percentile in 47% of these fetuses.132 TOF occurs when the conus septum is located too far anteriorly, thus dividing the conus into a smaller, anterior right ventricular portion and a larger posterior part. Closure of the interventricular septum is incomplete, causing the aorta to override both ventricles. Sonographically, a perimembranous VSD is typically seen, with the aorta overriding the ventricular septum. Right ventricular hypertrophy rarely occurs in utero133 (Fig. 38.32A). Pulmonary atresia or stenosis, or less commonly a dilated pulmonary artery and branch PAs secondary to absence of the valve, may be appreciated. The long-axis view of the aorta is helpful in identifying the VSD and overriding aorta. Additionally, the 3VT view provides a simple method of visualizing the small (see Fig. 38.32B) or, less commonly, dilated pulmonary artery. The diagnosis of TOF has been made before 15 weeks’ gestation using transvaginal ultrasound.37 Color Doppler imaging is helpful in making the diagnosis of TOF.134

Tetralogy of Fallot

RV

TOF consists of: (1) VSD; (2) overriding aorta; (3) hypertrophy of the RV; and (4) stenosis/atresia of the right ventricular outflow tract. It accounts for 5% to 10% of CHD in live births49 and is associated with a variety of cardiac, extracardiac, and chromosomal anomalies.71 A study of 129 fetuses diagnosed in utero with TOF reported additional cardiac anomalies in 57%, extracardiac anomalies in 50%, and chromosomal anomalies in

AO IVS LV

A

P

V A

LA

S

RA

B

FIGURE 38.31 Univentricular Heart with the right atrium (RA) and left atrium (LA) connected to the single ventricle (V). See Video 38.11.

FIGURE 38.32 Tetralogy of Fallot. (A) The aorta (AO) overrides both the right ventricle (RV) and the left ventricle (LV). A ventricular septal defect (arrows) is also appreciated. IVS, Interventricular septum. (B) Three-vessel view showing a small pulmonary artery (P) and enlarged aorta (A). S, Superior vena cava.

CHAPTER 38 Fetal Echocardiography

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The newborn with the classic form of TOF who has pulmonary stenosis rather than pulmonary atresia is typically asymptomatic at birth but develops cyanosis and a murmur in the first weeks of life. Early primary repair of TOF is routinely performed with a low surgical mortality and postoperative morbidity.135 Typical cases of TOF are repaired at 4-6 months of age, with close to 90% survival at 1 year.136 Patients surviving early surgery (before 5 years old) have a 32-year survival of 90%.137 The presence of congestive heart failure in the fetus or newborn with TOF is associated with 17% to 41% mortality.138,139

Persistent Truncus Arteriosus

RV TA

Persistent truncus arteriosus, also referred to as a common arterial trunk, arteriosus communis, or aorticopulmonary trunk accounts for 1.3% of fetal cardiac anomalies and is characterized by a single large vessel arising from the base of the heart. This vessel supplies the coronary arteries and the pulmonary and systemic circulations. This abnormality results when the single truncal artery present in early embryology fails to divide. Aortic anomalies occur in 20% and noncardiac anomalies in 48% of patients with truncus arteriosus.140 In almost all patients a VSD is present. The truncal valve may have two to six cusps and, in general, overrides the ventricular septum. Four types of truncus arteriosus have been identified by Collett and Edwards,141 as follows: • Type I has a pulmonary artery that bifurcates into right and left branches after it arises from the ascending portion of the truncal vessel. • Type II has right and left pulmonary arteries arising separately from the posterior truncus. • Type III has pulmonary arteries that arise from the sides of the proximal truncus. • Type IV has systemic collateral vessels from the descending aorta as the source of flow. The single, large truncal artery overriding the ventricular septum and an associated VSD is identified on four-chamber and outflow tract views (Fig. 38.33A). It is also readily visualized as a single large vessel at the level of the 3VT view. This anomaly has been diagnosed as early as 13 weeks.34 Color Doppler imaging is particularly helpful in the setting of truncus arteriosus because it facilitates accurate localization of the pulmonary arteries arising from the single truncal artery and rapidly detects truncal valvular insufficiency. In the 1980s, prognosis was poor, with an overall mortality of 70%.140 More recent studies have indicated that 10-year to 20-year survival is excellent for infants undergoing complete repair of truncus arteriosus.142,143 However, these patients continue to experience significant comorbidities throughout childhood, with significant deficits in exercise tolerance and overall functional status.144 Persistent truncus arteriosus, as with other conotruncal abnormalities, carries an increased association with maternal diabetes and 22q11 micro-deletion.143

and the pulmonary artery arise from the RV.145,146 DORV is classified into the following three types: • Aorta posterior and to the right of the pulmonary artery • Aorta and pulmonary artery parallel, with the aorta to the right (Taussig-Bing type) • Aorta and pulmonary artery parallel, with the aorta anterior and to the left Sonographically, the aorta and pulmonary artery both arise predominantly from the RV (Fig. 38.34). In both the short- and long-axis views of the great arteries, the aorta and pulmonary often appear to run parallel to each other. The differential diagnosis for DORV often includes transposition of the great arteries and tetralogy of Fallot. DORV is associated with a variety of other cardiac defects, particularly pulmonary stenosis which occurs in about 70% of cases.147 Extracardiac defects are also very common, as are chromosomal anomalies.7,146,148 With surgical intervention, 10-year survival as high as 97% has been reported.144 A more recent study reported nearly 94% overall 5-year survival after surgical correction.147 When extracardiac or chromosomal anomalies are present, prognosis is poor, with 69% mortality when the diagnosis of DORV is made in utero.147,148

Double-Outlet Right Ventricle

Transposition of Great Arteries

Double-outlet right ventricle (DORV) represents less than 1% of all CHD and occurs when more than 50% of both the aorta

Transposition of great arteries (TGA) is subdivided into two types: (1) complete or dextrotransposition (D-TGA or simply

LV

SP

FIGURE 38.33 Truncus Arteriosus. The single truncal artery (TA) overrides both the right ventricle (RV) and left ventricle (LV). A ventricular septal defect (arrow) is present. No pulmonary artery was seen, helping to differentiate from tetralogy of Fallot. SP, Spine.

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RV

RV

AO

PA

LV

PA

AO

FIGURE 38.34 Double-Outlet Right Ventricle. The aorta (AO) and pulmonary artery (PA) both arise from the right ventricle (RV) in a parallel fashion.

TGA) in 80% and (2) congenitally corrected or levotransposition (L-TGA or cc-TGA) in 20% of fetuses with transposition. In both types, ventriculoarterial discordance is present. (The aorta arises from the RV, and the pulmonary artery arises from the LV.) Complete transposition (D-TGA) is defined as atrioventricular concordance (atria and ventricles are correctly paired) with ventriculoarterial (VA) discordance (great arteries are transposed). It comprises 5% to 7% of heart disease in the fetal population. D-TGA is also classified into two types, depending on the absence (70%) or presence of a VSD. A variety of cardiac anomalies are associated with D-TGA, including obstruction of the outflow tracts, right-sided aortic arch, and anomalous venous connections. Chromosomal anomalies are not commonly associated with TGA.149 In D-TGA, the aorta arises from the RV, receives systemic blood, and returns it to the systemic circulation. The pulmonary artery arises from the LV, receives pulmonary venous blood, and returns it to the lungs. In general, the aortic root lies anterior and slightly to the right of the pulmonary outflow tract. With the closure of the ductus arteriosus and foramen ovale after birth, this condition is incompatible with life unless an associated shunt allows mixing of the separate right and left circulations. D-TGA occurs during embryologic development when the single truncal vessel is separated into an aortic and pulmonic artery, but the rotating that occurs simultaneously during this process is abnormal, resulting in the great arteries being transposed. Sonographic diagnosis depends on demonstrating that the great vessels exit the heart in parallel, rather than crossing in the normal fashion (Fig. 38.35). This is optimally seen in a long-axis or short-axis view of the great vessels. A three-vessel view is also

FIGURE 38.35 Complete Transposition of Great Arteries. The aorta (AO) is anterior to the pulmonary artery (PA). This abnormal arrangement results in both vessels running parallel to each other in this long-axis view.

useful because only one great vessel (aorta) is usually visualized at this level, due to the parallel path of the arteries. Most neonates with D-TGA require immediate treatment. Initially, a temporizing shunt may be created before definitive treatment, frequently with the arterial switch procedure. With surgical intervention, 12-month survival is 80%. Early intervention (within 3 days of life) when using the arterial switch operation is optimal and is associated with an operative mortality below 2%.150 Corrected transposition (L-TGA or cc-TGA) is characterized by A-V discordance with VA discordance. It comprises less than 1% of CHD.151 The aorta, which arises from the left-sided, morphologic RV, is anterior and to the left of the pulmonary artery. The pulmonary artery arises from the right-sided, morphologic LV. A VSD is present in most cases, and pulmonic stenosis is reported in approximately 35%.126,151 Malformation of the tricuspid valve may also be present. Fetal A-V block is common with TGA.152 Pathophysiologically, the flow of blood through the heart to the pulmonic and systemic circulations is normal, even though the morphologic RV is on the left and the morphologic LV is on the right. Abnormal cardiac looping during embryologic development of the heart is responsible for cc-TGA. It occurs when the primitive heart tube bends leftward, instead of to the right, resulting in the ventricles being transposed. The antenatal sonographic diagnosis of cc-TGA rests on identification of the morphologic right and LVs. The moderator band will be seen on the anatomic left side. In addition, the tricuspid valve will be situated on the anatomic left side, so its more apical septal leaflet should be identified (Fig. 38.36A). A parallel arrangement to the great vessels, similar to D-TGA, may also be appreciated in both the long- or short-axis views of the great arteries (Fig. 38.36B). At the level of the three-vessel view, the great arteries

CHAPTER 38 Fetal Echocardiography

RV

LA

LV RA

A

B FIGURE 38.36 Congenitally Corrected Transposition of Great Arteries. (A) An apical four-chamber view shows the morphologic right ventricle (RV) and morphologic left ventricle (LV) located on the incorrect sides of the heart. This is evidenced by identifying the atrioventricular valve leaflets inserting (arrow) on the left side of the heart in a more apical location than the right-sided atrioventricular valve leaflet insertion. (B) Parallel orientation of the great arteries can be appreciated. LA, Left atrium; RA, right atrium.

often take on a more parallel orientation as well, losing the normal “V” configuration normally seen. In the absence of associated cardiac anomalies, patients with corrected TGA may remain asymptomatic throughout their lives.

Anomalous Pulmonary Venous Return APVR can be divided into two subgroups: total anomalous pulmonary venous return (TAPVR), in which none of the pulmonary veins drain into the LA; and partial anomalous pulmonary venous return (PAPVR), in which at least one of the pulmonary veins has an anomalous connection. TAPVR constitutes 2.3% of cases of CHD.153 The four types of anomalous pathways are as follows: (1) All or some of the pulmonary veins drain into a vertical vein that empties into the innominate vein and then into the SVC; (2) All or some of pulmonary veins drain into the coronary sinus and then into the RA; (3) All or

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some of the pulmonary veins drain directly into the RA; (4) All or some of the pulmonary veins drain into the portal vein and into the IVC via the ductus venosus. Embryologically, TAPVR is thought to result from failure of obliteration of the normal connections between the primitive pulmonary vein and the splanchnic, umbilical, vitelline, and cardinal veins. TAPVR is associated with AVSDs and polysplenia and asplenia syndromes. The antenatal sonographic diagnosis of TAPVR is difficult because the anomalous veins are generally extremely small and variable in their course. Often the first sign of APVR is mild right ventricular and pulmonary artery prominence, in which case a careful search for the four normal pulmonary veins should be undertaken.154,155 This can be difficult because the two superior pulmonary veins are usually more difficult to visualize than the two inferior veins, even in a normal fetal heart. Color and spectral Doppler ultrasound are helpful in documenting the normal pulmonary venous anatomy and in detecting and following the anomalous connections (Fig. 38.37). The diagnosis of TAPVR is suspected when no pulmonary veins are seen entering the LA (Fig. 38.38). A small LA resulting from decreased blood return and lack of normal incorporation of the common pulmonary vein complex into the LA is also suggestive of TAPVR. Sonographically this may result in a greater distance between the wall of the LA and the descending aorta being appreciated in a four-chamber view.156 Secondary sonographic signs of APVR include dilatation of the left brachiocephalic vein when scanning above the 3VT view and absence of the normal tissue with the LA (often referred to as the Coumadin ridge), which normally separates the pulmonary veins from the left atrial appendage.154 Approximately onethird of patients with TAPVR have associated cardiac anomalies.157 Right atrial isomerism is common. Associated extracardiac anomalies include gut malrotation and midline liver and stomach.157,158 TAPVR causes minimal hemodynamic disturbance in utero, although hydrops occasionally results. Left untreated, the majority of infants die before 1 year of age.158 TAPVR is associated with high morbidity and mortality, largely because of the high incidence of additional cardiac anomalies.156,158 Surgical correction of TAPVR is associated with an operative mortality of nearly 20%.159 Although PAPVR has also been diagnosed in utero, the diagnosis is much more difficult and can be made only when pulmonary veins are seen entering the LA as well as the RA or an accessory pathway to the RA.158 PAPVR is also classified by the location of the abnormal connections160: (1) left pulmonary veins connect to the LA and the right pulmonary veins connect to the superior vena cava; (2) left pulmonary veins connect to the LA and the right pulmonary veins connect to the inferior vena cava; (3) right pulmonary veins connect correctly to the LA and the left pulmonary veins connect via a vertical vein to the left brachiocephalic vein, which connects to the superior vena cava; and (4) right pulmonary veins connect correctly to the LA and the left pulmonary veins connect to the RA via the coronary sinus. PAPVR may go unrecognized in the pediatric and adult populations unless the patient becomes symptomatic.

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LA

40 30 20

FIGURE 38.37 Normal Pulmonary Venous Anatomy. Color Doppler ultrasound shows a pulmonary vein (arrow) entering the left atrium (LA). The spectral Doppler waveform shows the direction of pulmonary venous flow into the LA, with antegrade systolic (S) and diastolic (D) components with normal reversal of the A wave.

LV

10

S

cm/s

A -10

RV P

LA

RA

D

P P P

FIGURE 38.38 Total Anomalous Pulmonary Venous Return. Apical four-chamber view shows anomalous insertion of all four pulmonary veins (P) into the right atrium (RA). LA, Left atrium; LV, left ventricle; RV, right ventricle.

Coarctation of Aorta Aortic coarctation is a narrowing of the aortic lumen, usually occurring between the insertion of the ductus arteriosus and the left subclavian artery (aortic arch isthmus). Its severity ranges from a slight narrowing at the distal end of the arch to severe

hypoplasia of the entire arch. Coarctation occurs in 6% to 8% of live births with CHD.161 Almost 80% of the cases are associated with other cardiac anomalies, including abnormal aortic valve (bicuspid or stenotic), VSD, DORV, cc-TGA, PLSVC, and AVSD. Chromosomal abnormalities occur in 5%, and almost 5% of coarctations are associated with maternal diabetes.62,161,162 Coarctations are present in approximately 20% of individuals with Turner syndrome (45X).7 A variety of embryologic theories have been proposed to explain the origin of coarctation of the aorta, including: (1) a primary developmental defect with failure of connection of the fourth and sixth aortic arches with the descending aorta163; (2) aberrant ductal tissue at the level of the aortic arch163-165; and (3) decreased blood flow through the aortic isthmus.166 Sonographic detection of coarctation is difficult because the presence of the ductus arteriosus usually prevents significant narrowing of the isthmus.29,167,168 Ventricular size discrepancy with a prominent RV and relatively small LV,58,167 with a rightto-left ventricle diameter ratio greater than two standard deviations (SDs) above the norm,168,169 may suggest coarctation of the aorta. However, this is not a reliable sign of coarctation later in pregnancy when the RV is generally larger than the LV. More recent literature suggests measurements of isthmal z-scores and isthmal-to-ductal ratios may be more sensitive indicators.161,170 Color Doppler ultrasound is useful in identifying the area of isthmal narrowing (Fig. 38.39A). Spectral Doppler ultrasound may detect increased velocity distal to the narrowed segment (see Fig. 38.39B) or early diastolic reversal of flow, although this is uncommon in the fetus. Other sonographic signs that have

CHAPTER 38 Fetal Echocardiography

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A

Vel 186 cm/s 180 120

FIGURE 38.39 Coarctation of Aorta. (A) Gray-scale and color Doppler images showing narrowing of the aortic arch (arrow) at the level of the isthmus, with turbulent flow. (B) Spectral Doppler tracing shows increased velocity through the aortic arch.

60

cm/s

B

been reported include abnormal spacing of the head and neck vessels on an aortic arch view or disproportion of the great vessels on the 3VT view.170 Many coarctations do not become evident until the closure of the ductus arteriosus at birth. In addition, infants with coarctation of the aorta may not develop clinical or echocardiographic signs of coarctation until 612 weeks after the closure of the ductus arteriosus. If coarctation of the aorta is suspected on fetal echocardiogram, the infant should be followed to at least 1 year of age.171 Although isolated coarctation has a good prognosis, 39% mortality is reported when associated anomalies are present.161,172 Treatment is usually accomplished with angioplasty or stenting with good results.161,173

Aortic Stenosis Congenital aortic stenosis is a stricture or obstruction of the ventricular outflow tract occurring in 0.2-0.5 per 1000 live births.174 Aortic stenosis is classified as supravalvular, valvular, or subvalvular according to location of the obstruction. Valvular aortic stenosis is most commonly seen in utero. It

AORTIC ARCH

3.6sec

occurs more frequent in males and is associated with a bicuspid or unicuspid aortic valve.175 Associated extracardiac abnormalities are rare, as are chromosome anomalies. Subvalvular and supravalvular aortic stenosis are rarely seen in the fetus. Thickening or doming of the aortic valve, poststenotic dilation of the aorta, and ventricular hypertrophy are clues to valvular aortic stenosis on fetal echocardiography. In addition, real-time evaluation of the aortic valve may show it persisting, as opposed to moving normally in and out of the field of view, implying the valve is not opening and closing as it should. Increased peak systolic velocity through the aortic valve may be identified on spectral Doppler, while turbulent flow across the valve is seen with color (Fig. 38.40). Critical aortic stenosis can result in a hypoplastic LV. Aortic stenosis progresses in utero and may not be apparent on early (