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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5795_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Preface for the Second Edition
- •Acknowledgements
- •Contents
- •1: US Physics
- •1.1 US Waves
- •1.2.5 Deflection
- •1.2.6 Focus
- •1.2.7 Resolution
- •1.3.1 Emission
- •1.3.2 Transmission
- •1.3.3 Reception
- •1.3.4 Amplification
- •1.4 Signal Processing
- •1.4.1 Preprocessing
- •1.4.2 Post-Processing
- •1.4.3 Time Gain Compensation (TGC)
- •1.4.5 Gain
- •1.4.6 Frame Rate/Persistence
- •1.5.1 Transducers
- •1.6 Modern US Techniques
- •1.6.1 High-Resolution US (HR-US)
- •1.6.2 Image Compounding
- •1.2.1 Acoustic Impedance
- •1.2.2 Impedance Change
- •1.2.3 Reflection
- •1.2.4 Absorption
- •1.6.3 Harmonic Imaging (HI)
- •1.6.5 US Texture Analysis
- •2: US Methods, Artefacts, Biologic Effects, Practice
- •2.1 A (Amplitude)-Mode
- •2.2 (T)M-Mode (Time-Motion-Mode)
- •2.3 B (Brightness)-Mode
- •2.4 Doppler Sonography
- •2.5 Artefacts
- •2.5.1 General Remarks
- •2.5.2 Common Artefacts
- •2.5.2.1 Side Loop Artefact
- •2.5.2.2 Bowing Artefact
- •2.5.2.3 Noise
- •2.5.2.4 Marginal Shadowing
- •2.5.2.5 Posterior Enhancement—Increased through Transmission
- •2.5.2.6 Reverberation Artefact
- •2.5.2.7 Increment or Slice Thickness/Beam Width Artefact
- •2.5.2.8 Mirror Image Artefact
- •2.5.2.9 Shadowing
- •2.5.2.10 Refraction Artefact
- •2.5.2.11 Anisotropy
- •2.6 Biologic Effects
- •2.6.1 General Remarks
- •2.6.2 Thermal Effects
- •2.6.2.1 Tissue Heating
- •2.6.2.2 Biological Effects, Tissue Heating
- •2.6.3.1 Cavitation
- •2.6.4.1 Specific Risks
- •2.6.5.1 Mechanical Index (MI)
- •2.6.5.2 Thermal Index (TI)
- •2.7.1 Requisites
- •2.7.1.1 Indications
- •2.7.1.2 Environmental Requisites
- •2.7.2 Positioning
- •2.7.3 Device Handling
- •2.7.3.1 General Remarks
- •2.7.4 Transducer Selection
- •2.7.4.1 General Remarks
- •2.7.4.2 Neurosonography (See Chap. 8)
- •2.7.4.4 Chest US (See Chap. 12)
- •2.7.4.5 Abdominal US (See Respective Chapters)
- •2.7.5.1 General Remarks
- •2.7.5.2 Transducer Handling
- •2.7.5.3 Measurements
- •2.8.1 Image Documentation
- •2.8.2 Report
- •2.8.2.2 Diagnosis
- •2.8.2.3 Predefined Reports
- •2.8.2.4 Nomenclature
- •3.1 Doppler Sonography
- •3.1.1 The Doppler Phenomenon
- •3.1.2.1 Continuous Wave Doppler (CW)
- •3.1.2.2 Pulsed Wave Doppler (PW)
- •3.1.2.3 Duplex-Doppler Sonography/Spectral Flow Analysis
- •3.1.2.5 Amplitude-Coded Colour Doppler Sonography (aCDS)
- •3.1.2.6 Other Flow-Sensitive US Techniques
- •3.2.1 Aliasing
- •3.2.2 Spectral Broadening
- •3.2.3 Sample Volume Artefact
- •3.2.4 Filtering Artefacts
- •3.2.5 Scaling Problems
- •3.2.6 Gain-Induced Errors
- •3.2.7 Angle Correction
- •3.2.8 Motion Artefact
- •3.2.9 Twinkling Artefact
- •3.2.10 Others
- •3.3.1 Limitations
- •3.3.2 Interpretation
- •3.4.2 Typical Paediatric 3DUS Applications
- •3.4.2.1 Neonatal Neurosonography
- •3.4.2.7 Other Potential 3D-/4DUS Applications
- •3.4.5 Potential Future Paediatric 3DUS Applications
- •4.1 Contrast-Enhanced Ultrasound (ce-US)
- •4.1.1 Basics
- •4.1.2 ce-US Applications-General Remarks
- •4.1.3 Contrast-Enhanced Voiding Urosonography (ce-VUS)
- •3.4.2.3 Urinary Bladder 3DUS
- •3.4.2.5 Musculoskeletal 3DUS Applications
- •3.4.2.6 Small Part 3DUS Applications
- •4.1.5 Intravenous ce-US (CEUS)
- •4.1.5.2 Dose Recommendations
- •4.1.6 Future ce-US Potential
- •4.2 Ultrasound-/Sonoelastography
- •4.2.1 Methods
- •4.2.1.1 Strain Elastography
- •4.2.1.2 Transient Elastography (TE)
- •4.2.1.3 Shear Wave Elastography (SWE)
- •4.2.2 Applications
- •4.2.2.1 Focal Lesions
- •4.2.2.2 Diffuse Changes
- •4.2.2.3 Possible Indications—Summary
- •5.1 Requirements
- •5.2 Typical Applications
- •6.1 Introduction
- •6.2.1 Urinary Tract Infection (UTI)
- •6.2.3.1 Pelvi-Ureteric Junction Obstruction (PUJO)
- •6.2.3.3 Gross Vesico-Ureteric Reflux (VUR)
- •6.2.4 Urolithiasis (and Nephrocalcinosis)
- •6.2.5 Cystic Kidney Disease (CKD)
- •6.2.6 Torsion (Ovary, Testis)
- •6.2.7 Genital Malformations
- •6.2.8 Renal Hypertension
- •6.3.1 Necrotizing Enterocolitis (NEC)
- •6.3.3 Acute Abdomen
- •6.3.4 Acute Appendicitis
- •6.3.5 Splenomegaly
- •6.3.6 Cholestasis
- •6.3.7 Pancreatitis
- •6.3.8 Biliary Atresia
- •6.3.9 Abdominal Trauma
- •6.3.10 Abdominal Tumours
- •6.4.1 Pneumonia, Pleural Effusion
- •6.4.2 Enlarged Mediastinum
- •6.4.3 Painful Hip/Limping Child: Osteomyelitis
- •7.1 General Considerations
- •7.3.1 Miscellaneous Other Considerations
- •8.1 Requisites
- •8.2 Normal Findings
- •8.2.1 Transfontanellar Access
- •8.2.2 Alternate Access Findings
- •8.2.3 Colour Doppler Sonography (CDS)
- •8.2.4.1 Periventricular Echogenicities
- •8.2.4.2 Ventricular Asymmetry
- •8.2.4.3 Ventriculomegaly
- •8.2.4.4 Cisterna Magna
- •8.2.4.5 Vascular Variations
- •8.3 Pathologic Findings
- •8.3.1 Neural Tube Defects
- •8.3.1.1 Anencephaly
- •8.3.1.3 Arnold Chiari Malformation
- •8.3.1.4 Dandy–Walker Malformations/Spectrum
- •8.3.1.5 Corpus Callosum Malformations
- •8.3.1.6 Lipoma
- •8.3.2.2 Megalencephaly
- •8.3.2.3 Schizencephaly
- •8.3.2.4 Holoprosencephaly
- •Alobar Holoprosencephaly
- •Semilobar Holoprosencephaly
- •Lobar Holoprosencephaly
- •De Morsier Syndrome: Septo-Optic Dysplasia
- •8.3.2.5 Hydranencephaly
- •8.3.3 Phakomatoses
- •8.3.4 Cerebral Cysts
- •8.3.5 Ischemic Encephalopathy
- •8.3.5.1 Preterm Infant
- •8.3.5.2 Global or Diffuse Brain Oedema
- •8.3.6 Other applications of (C)DS:
- •8.3.7 Inflammation
- •8.3.7.2 Postnatal Inflammation
- •8.3.9 Cerebral Haemorrhage
- •8.3.10.1 Vascular Malformations
- •8.3.11 Cerebral Calcifications
- •8.4.1 Introduction
- •8.4.2 Haematoma
- •8.4.4 Skull Fracture
- •8.5 Additional Imaging
- •8.5.1 Plain Film
- •8.5.2 CT
- •8.5.3 MRI
- •8.5.4 Catheter Angiography
- •8.5.5 Additional Supporting Procedures
- •8.6.1 Introduction
- •8.6.2 Normal Findings
- •8.6.3 Sonographically Depictable Pathology
- •9.1 Introduction
- •9.2 Requisites
- •9.4 Indications
- •9.5 Normal Findings
- •9.6.1 Dysraphism
- •9.6.2 Other Associated Pathology
- •9.6.3 Other “Occult” Dysraphisms
- •9.7 Trauma
- •9.8 Tumours and Miscellaneous Others
- •9.10 Additional Imaging
- •10.1.1 Transducers
- •10.1.3 Typical Examinations
- •10.1.3.1 Cervical Lymph Nodes
- •10.1.3.2 Glands
- •10.1.3.3 Cervical Arteries
- •10.1.3.4 Cervical Veins
- •10.1.3.5 Intervention
- •10.2 Normal Findings
- •10.2.1 Lymph Nodes
- •10.2.2 Cervical Glands
- •10.2.2.1 Thyroid Gland
- •10.2.3 Other Cervical Soft Tissues
- •10.2.3.1 Muscles
- •10.2.3.2 Tonsils
- •10.2.3.3 Tongue
- •10.2.3.5 Larynx
- •10.2.4 Cervical Vessels
- •10.3 Pathologic Findings
- •10.3.1 Lymph Nodes
- •10.3.2.1 Malformations
- •Cervical Cyst
- •Dermoid Cyst
- •Duplication Cysts
- •Thymic Cyst
- •Cervical Ectopic Thymus
- •10.3.2.2 Tumours
- •Haemangioma
- •Lymphatic Malformation
- •Other Mesenchymal Tumours
- •Teratoma
- •Other Malignant Tumours
- •10.3.2.3 Abscess Formations
- •10.3.2.4 Traumatic Changes
- •Haematoma (Including Sternocleidomastoid Muscle “Haematoma”)
- •10.3.3 Thyroid Gland
- •10.3.3.1 Cystic Changes
- •10.3.3.2 Malformations
- •10.3.3.3 Inflammation
- •10.3.3.4 Other Conditions
- •Nodular Goitre
- •Amyloid Goitre
- •Adenoma/Carcinoma
- •10.3.4 Salivary Glands (Parotid, Sublingual, Submandibular Gland)
- •10.3.4.1 Inflammation
- •10.3.4.2 Cysts
- •10.3.4.3 Calcifications/Sialolithiasis
- •10.3.4.4 Tumours
- •10.3.5 Cervical Vessels
- •10.3.5.1 Arteriosclerosis
- •10.3.5.2 Dissection
- •10.3.5.3 Stenosis
- •10.3.5.4 Other Vascular Anomalies
- •11.1 Introduction
- •11.2.1 Transducers
- •11.2.2 Standard US Techniques
- •11.2.3 Patient Position
- •11.2.4 Sedation
- •11.4 Normal 2D Echocardiogram Findings
- •11.4.1 Parasternal Views
- •11.4.1.3 Apical Views
- •11.4.2 Subcostal Views
- •11.4.2.1 Sagittal Subcostal View
- •11.5 Other Techniques
- •11.5.1 M (Motion)-Mode Echocardiography
- •11.6 Special Echocardiographic Techniques
- •11.6.1 Transoesophageal Echocardiography (TEE)
- •11.6.2 Three-/Four-Dimensional (3D/4D) Echocardiography
- •11.6.3 Tissue Doppler Imaging (TDI)
- •11.6.4 Contrast-Enhanced US (ce-US/CEUS)
- •11.7 Normal Values
- •11.8 Pathologic Findings
- •11.8.1.1 Atrial Septal Defect (ASD)
- •11.8.1.2 Atrioventricular Septal Defects (AVSD)
- •11.8.1.3 Ventricular Septal Defects (VSD)
- •11.8.2.1 Aortic Valve Stenosis (AS)
- •11.8.2.2 Subaortic Stenosis (Sub-AS)
- •11.8.2.3 Supravalvular Aortic Stenosis
- •11.8.2.4 Aortic Coarctation (CoA)
- •11.8.2.5 Interrupted Aortic Arch
- •11.8.3.1 Isolated Pulmonary Valve Stenosis (PS)
- •11.8.3.2 Subvalvular Pulmonary Stenosis
- •11.8.3.3 Supravalvular Pulmonary Stenosis
- •11.8.4 Miscellaneous Congenital Heart Defects
- •11.8.4.2 Total Anomalous Pulmonary Venous Return (TAPVR)
- •11.8.4.3 Univentricular Heart (UVH)
- •11.8.4.4 Double Outlet Right Ventricle (DORV)
- •11.8.4.5 Ebstein Anomaly
- •11.8.4.6 Cor Triatriatum
- •11.9 Acquired Paediatric Heart Diseases
- •11.9.1 Cardiomyopathies (CMP)
- •11.9.1.1 Hypertrophic CMP
- •11.9.1.2 Hypertrophic Obstructive CMP (HOCMP)
- •11.9.1.3 Dilated (Congestive) CMP
- •11.9.1.4 Restrictive CMP
- •11.9.2 Acute Myocarditis
- •11.9.3 Acute (Infective) Endocarditis
- •11.9.4 Pericarditis/Pericardial Effusion
- •11.9.5 Kawasaki Disease
- •11.9.6 Intracardiac Thrombi
- •11.9.7 Cardiac Tumours
- •11.11 Complementing Investigations
- •11.12.1.1 Typical Orientating Examination
- •11.12.1.2 Typical Clinical Queries
- •12.1 Requisites
- •12.1.1 Transducers
- •12.1.2 Positioning
- •12.1.3 Indications
- •12.2 Normal Findings
- •12.2.1 Chest Wall
- •12.2.2 Breast
- •12.2.3 Pleural Space
- •12.2.4 Diaphragm
- •12.2.5 Lung
- •12.2.6 Mediastinum
- •12.2.6.1 Anterior Mediastinum/Thymus
- •12.2.6.2 Middle Mediastinum
- •12.2.6.3 Posterior Mediastinum
- •12.2.7 (Colour) Doppler Sonography
- •12.2.8 Contrast Enhanced US (ce-US)
- •12.3.2 Congenital Malformations
- •12.3.3 Traumatic Changes
- •12.3.4 Chest Wall Tumours
- •12.3.4.1 Lymphangioma (Venolymphatic Vascular Malformation)
- •12.3.4.2 Lipoma
- •12.3.4.3 Fibroma/Neurofibroma
- •12.3.4.4 Other Tumours
- •12.3.5 Breast
- •12.3.6 Miscellaneous Other Applications
- •12.4.1 Pneumothorax
- •12.4.2 Pleural Effusion
- •12.4.2.1 Empyema
- •12.4.3 Other Pleural Pathology
- •12.5.1 Diaphragmatic Hernia
- •12.5.2 Diaphragmatic Motion Disturbance
- •12.6 Lung Pathology
- •12.6.1 Pneumonia
- •12.6.2 Lung Abscess
- •12.6.3 Atelectasis
- •12.6.5 Sequestration
- •12.6.6 Congenital Cystic Adenomatoid Malformation (CCAM)
- •12.6.7 Cysts
- •12.6.8 Infarction
- •12.8 Additional Imaging
- •13.1 Introduction
- •13.2.1 Preparation
- •13.2.2 Positioning
- •13.2.3 Transducers
- •13.3 Liver
- •13.3.2 Standard Planes
- •13.3.3 Normal Findings
- •13.3.3.1 Structure
- •13.3.3.2 Ligaments
- •13.3.3.3 Hepatic Veins (HV)
- •13.3.3.4 Portal Vein (PV)
- •13.3.3.5 Hepatic Artery (HA)
- •13.3.3.6 Gall Bladder
- •13.3.3.7 Common Bile Duct
- •13.3.3.8 Intrahepatic Bile Ducts
- •13.3.3.9 Doppler Findings
- •Situs Inversus (Abdominalis)
- •Butterfly or Midline Liver
- •13.3.4.2 Inflammatory Conditions
- •Hepatitis
- •Liver Abscess
- •Granulomatous Disease
- •13.3.4.3 Other Parenchymal Liver Disease
- •Fatty Liver/Steatosis
- •Liver Congestion
- •Liver Fibrosis
- •Cirrhotic Liver
- •Portal Hypertension
- •Vascular Malformations
- •Hepatic Vein Thrombosis/Occlusion/Stenosis
- •Portosystemic Shunts
- •13.3.4.5 Liver Trauma
- •Liver Haematoma
- •Contusion
- •Laceration
- •Haemobilia
- •Associated Diaphragmatic Injury
- •Liver Infarction
- •Additional Imaging
- •13.3.4.6 Space-Occupying Liver Lesions
- •Simple Cysts
- •Complicated Cysts
- •Liver Calcifications
- •Intrahepatic Gas
- •Haemangioma
- •Mesenchymal Hamartoma
- •Focal Nodular Hyperplasia (FNH)
- •Hepatic Adenoma
- •Fatty Tumours
- •Hepatoblastoma
- •Hepatocellular Carcinoma
- •Hepatic Sarcomas
- •Metastasis
- •Proliferative Disorders
- •Additional Imaging
- •13.4.1 General Findings
- •13.4.2.1 Intrahepatic Gall Bladder
- •13.4.2.3 Choledochal Cyst
- •13.4.3 Biliary Tract Diseases
- •13.4.3.1 Aerobilia
- •13.4.3.2 Cholestatic Changes/Inspissated Bile/Gallstone
- •13.4.3.3 Sclerosing Cholangitis
- •13.4.3.5 Tumour-like Conditions
- •Polyps
- •Tumours
- •13.4.3.7 Additional Imaging
- •13.5.1 Pretransplant US
- •13.5.1.1 Recipient Evaluation
- •13.5.2 Intraoperative US
- •13.5.3 Postoperative Assessment
- •13.5.4 Typical Complications
- •13.6 Spleen
- •13.6.1 Requisites
- •13.6.2 Positioning
- •13.6.3 Indications
- •13.6.5 Normal Anatomy
- •13.6.6 Normal Variants
- •13.6.6.1 Splenunculus (Accessory Spleen)
- •13.6.7 Malformations
- •13.6.7.1 Asplenia
- •13.6.7.2 Polysplenia Syndrome
- •13.6.7.3 Wandering Spleen
- •13.6.8 Splenomegaly
- •13.6.9 Trauma
- •13.6.10 Splenic Infarction
- •13.6.11.1 Cysts
- •13.7 Pancreas
- •13.7.1 Requisites
- •13.7.2 Indication
- •13.7.4 Normal Findings
- •13.7.5.1 Annular Pancreas
- •13.7.5.2 Pancreas Divisum
- •13.7.6 Inflammation: Pancreatitis
- •13.7.6.1 Oedematous or Reactive Pancreatitis
- •13.7.6.2 Haemorrhagic or Necrotising Pancreatitis
- •13.7.6.3 Chronic Pancreatitis
- •13.7.7 Trauma
- •13.7.8 Space-Occupying Lesions
- •13.7.8.1 Cysts/Pseudocysts
- •13.7.8.2 Tumours
- •13.7.10 Additional Imaging
- •13.8.1 Abdominal Vessels
- •13.8.1.1 Positioning
- •13.8.1.2 Transducers
- •13.8.1.4 US Findings
- •13.8.2 Vascular Pathology
- •13.8.2.1 Thrombosis/Occlusion
- •13.8.2.2 Pelvic Congestion Syndrome
- •13.8.2.3 Mid-Aortic Syndrome
- •13.8.2.4 Retroaortic Left Renal Vein: Nutcracker Syndrome
- •13.8.2.9 Complementing Imaging
- •13.8.3 Retroperitoneal Soft Tissues
- •13.8.3.1 Lymph Nodes
- •13.8.3.2 Retroperitoneal Tumours
- •13.8.3.3 Abdominal Wall
- •14.1 Stomach
- •14.1.1 Requisites
- •14.1.2.1 Access
- •14.1.3 Normal Findings
- •14.1.4 Normal Variants
- •14.1.5 Malformations
- •14.1.5.1 Microgastria
- •14.1.5.2 Pyloric Atresia
- •14.1.5.3 Congenital Hiatal Hernia
- •14.1.6 Pathologic Findings
- •14.1.6.1 Gastro-Oesophageal Reflux (GOER)
- •14.1.6.2 Hypertrophic Pyloric Stenosis (HPSt)
- •14.1.6.3 Other Stomach Conditions
- •14.2 Bowel
- •14.2.3 Normal US Findings
- •14.2.4 Pathology
- •14.2.4.1 Congenital Anomalies
- •14.2.5 Acquired Obstructive Pathology
- •14.2.5.1 Meconium Ileus
- •14.2.5.2 Midgut Volvulus
- •14.2.5.3 Sigma Volvulus
- •14.2.5.4 Hernia
- •14.2.5.5 Intussusception
- •14.2.6 Inflammatory Conditions
- •14.2.6.1 Necrotising Enterocolitis (NEC)
- •14.2.6.2 Gastroenteritis
- •14.2.6.3 Henoch–Schönlein Purpura
- •14.2.6.4 Appendicitis
- •14.2.6.5 Crohn’s Disease
- •14.2.6.6 Colitis
- •14.2.6.7 Other Inflammatory Bowel Conditions
- •14.2.6.8 Bowel Trauma
- •14.2.7 Mesentery
- •14.2.7.1 Mesenteric (Peritoneal) Masses
- •14.2.7.2 Abscesses
- •14.2.7.3 Twisted Appendices Epiploica
- •14.2.8 Mesenteric Lymph Nodes
- •14.2.9 Free Intraperitoneal Air
- •14.2.10 Free Intraperitoneal Fluid: Ascites
- •14.2.11 Mesenteric Vessels
- •15.1 Requisites
- •15.1.1 Indications
- •15.1.2 Preparation
- •15.1.3 Transducers
- •15.1.4 Positioning
- •15.1.5.1 Diuretic US
- •15.1.6 Contrast-Enhanced Voiding Urosonography (ce-VUS)
- •15.2 Normal Findings
- •15.2.1 Bladder
- •15.2.2 Kidney
- •15.2.2.1 Normal Variants
- •Duplex Kidney
- •Ectopic Kidneys
- •Renal Agenesis
- •15.3.1 Congenital Conditions
- •15.3.1.1 Dysplasia/Hypoplasia
- •15.3.1.2 Cystic Renal Disease
- •Inherited/Congenital Cystic Disease
- •Acquired Cystic Kidney Disease
- •Urinary Tract Dilatation (UTD) or Pelvicalyceal Dilatation/Distention (PCD)
- •Pelvi-ureteric Junction Obstruction (PUJO)
- •Uretero-Vesical Junction Obstruction (UVJO)/Obstructive Megaureter (POM/MU)
- •Posterior Urethral Valve (PUV)
- •Vesico-Ureteric Reflux (VUR)
- •Secondary Obstruction
- •15.3.2 Inflammatory Renal Parenchymal Conditions
- •15.3.2.1 Pyelitis
- •15.3.2.2 Acute Pyelonephritis (aPN)/Interstitial Nephritis
- •15.3.2.4 Scarring
- •15.3.2.5 Tuberculosis
- •15.3.2.6 Xanthogranulomatous Pyelonephritis
- •15.3.2.7 Glomerulonephritis/Nephrotic Syndrome
- •15.3.3 Vascular Conditions
- •15.3.3.1 Renal Artery Stenosis
- •15.3.3.2 Arteriovenous Fistula (AVF)
- •15.3.3.3 Infarction
- •15.3.3.4 Renal Vein Thrombosis
- •15.3.4 Nephrocalcinosis
- •15.3.5 Urolithiasis
- •15.3.6 Other Important Renal Parenchymal Disease
- •15.3.6.1 Haemolytic Uremic Syndrome (HUS)
- •15.3.6.2 Glomerulonephritis/Nephrotic Syndrome
- •15.3.6.3 Scars, Cirrhotic Kidney
- •15.3.7 Renal Failure (RF)
- •15.3.8 Renal/Urinary Tract Trauma
- •15.3.9 Renal Tumours
- •15.3.9.1 Benign Tumours
- •15.3.9.2 Pre- or Semi-Malignant Tumours
- •15.3.9.3 Malignant Tumours
- •15.4.1 Renal Biopsy
- •15.4.2 Drainage/Nephrostomy
- •15.4.3 Postoperative Imaging
- •15.4.3.1 After VUR Treatment
- •Cystoscopic Treatment
- •Antireflux Surgery
- •15.4.3.2 Findings after Pyeloplasty
- •15.4.3.3 After Various Interventions
- •15.5 Renal Transplant
- •15.5.2 Pathologic US Findings
- •15.6.1 General Remarks
- •15.6.2 Typical Normal US Finding
- •15.6.3 Pathologic Findings
- •15.6.3.1 Adrenal Gland Haemorrhage
- •15.6.3.2 Inflammatory Condition
- •15.6.3.3 Tumours
- •Adrenal Cysts
- •Adrenal Adenoma
- •Neuroblastoma
- •Ganglioneuroma
- •Phaeochromocytoma
- •Adrenal Carcinoma
- •15.7.1 Requisites
- •15.7.2 Pathologic Findings
- •15.7.2.1 Atypical Shape (Neurogenic Bladder, “Valve Bladder”)
- •15.7.2.2 Polyps
- •15.7.2.3 Bladder Tumours
- •15.7.2.4 Calcification in/of Bladder
- •15.7.2.5 Ureterocele
- •15.7.2.6 Persisting Urachus
- •15.7.2.7 Megaureter
- •15.7.2.9 Inflammation
- •15.7.2.10 Traumatic Changes
- •15.7.2.11 Vesico-Ureteric Reflux
- •15.7.3 Paravesical Changes
- •15.7.3.1 Abscess Formations
- •15.7.3.3 Cystic Perivesical Structures
- •15.8.1 US Technique
- •15.8.2 Normal Findings
- •15.8.3 Common Pathologic Findings
- •15.8.3.1 Hydrocele
- •15.8.3.2 Undescended Testes
- •15.8.3.3 Varicocele
- •15.8.3.6 Microlithiasis
- •15.8.4 Inflammation—Orchitis, Ependymitis
- •15.8.5 Scrotal Trauma
- •15.8.6 Torsion
- •15.8.6.2 Inguinal Hernia
- •15.8.7 Testicular Tumours
- •15.9 Female Genitals
- •15.9.1 Indications
- •15.9.2 Requisites
- •15.9.3 Transducers
- •15.9.5 Normal Findings
- •15.9.5.1 Sonogenitography
- •15.9.6 Pathologic Findings
- •15.9.6.1 Congenital Malformations
- •Vaginal Atresia
- •Vaginal Fistula
- •Other Vaginal Malformations
- •Vaginal Aplasia
- •Uterine Malformations
- •Ovarian Malformations
- •Cysts
- •Teratoma
- •Other Genital Tumours
- •Rhabdomyosarcoma
- •15.9.6.4 Traumatic Changes
- •Ovarian Torsion
- •Pregnancy
- •16.1 General Remarks
- •16.2 Examination Technique
- •16.2.2 Modified Graf Classification (Rosendahl)
- •16.3 Normal Anatomy
- •16.3.2 Rosendahl Modification
- •16.3.3 Normal Findings During Harcke Investigation
- •16.5 Pathologic Findings
- •16.6.1.1 Capsular Thickening
- •16.6.1.2 Joint Fluid/Effusion
- •16.6.2 Hip Osteoarthritis
- •16.6.4 Perthes Disease
- •17.1.2 Typical Normal Findings
- •17.1.3 Pathologic Findings
- •17.1.3.1 Fracture
- •17.1.3.2 Joint Effusion
- •17.1.3.3 Arthritis
- •17.1.3.4 Trauma
- •17.1.3.5 Cysts
- •17.1.3.6 Inflammation
- •17.1.3.7 Neoplasia
- •17.2 Other Small Part Applications
- •17.2.1 General Remarks
- •17.2.2 Foreign Bodies

17 Musculoskeletal andOther Small Part US inChildhood
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Note US not specic to aetiology or content of effusion (haemorrhagic, proteinous,
infectious, etc.). Diagnosis of underlying disease only in combination with clinical
context (trauma, inammation, aseptic necrosis) and laboratory evaluation.
Only those parts of joint assessable where US can access. Therefore—to properly
assess joint for potential effusion—scan all around joint accessing joint space from
different directions not to miss focal effusion in specic compartment, recess or bursa.
• US used for guided diagnostic arthrocentesis and drainage (see chapter on interventional US).
17.1.3.3 Arthritis
Effusion commonly seen; small amounts detectable by careful examination (see
also Sect. 17.1.3.2. Joint Effusion).
Typical US feature (high sensitivity, low specicity): thickening of joint capsule
with more or less hyperaemia on CDS (Fig.17.5a).
Note Etiological correlation by US not possible (needs history, physical exam,
laboratory ndings, etc.).
• In rheumatoid conditions capsular thickening can become irregular and nodular,
with varying amount of hypervascularisation—US used to guide therapy and assess
therapeutic response, also for drug instillation (see chapter on interventional US).
17.1.3.4 Trauma
Most commonly, US used to assess disruption of tendons, muscles, bony structures
(see above) and apophyseal avulsions in adolescents (Fig.17.6).
Note In these conditions, do not only assess tendon or joint but also surrounding
structures and muscles which may show haematoma or disruption (see respective
chapter) (Fig.17.2a, b).
Haematoma
• More or less ovoid-shaped mass, with varying echogenicity (Fig.17.2a, b).
• Appearance varies with age, site and kind of haematoma (diffuse bleed into preserved structures, haematoma without preserved structures) and insonation angle.
• Old haematoma either resorbs completely, leaves some brous scarred tissue or
forms seroma (more or less complicated uid collection with some capsule-like
wall), may calcify or even ossify (myositis ossicans), then show complete or
punctuated internal echogenicities with posterior shadowing (see below).
Rupture of Tendon
Extremely rare in paediatric population; dynamic investigation very helpful for ligamentous queries and function assessment, as well as dening compartment and origin/connections.

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a
d
f
e
Fig. 17.6 US in musculoskeletal trauma. (a) Most important in US of musculoskeletal trauma—
observe anisotropy effect; tendens (as well as muscles) appear different depending on the insonation
angle: Longitudinal image of a forearm exor tendon—(a) shows echogenic brillar architecture.
Transverse image performed at 90°(b) shows bright echogenic reectors from the tendon (arrow).
(c) Transverse image performed off-perpendicular shows the same tendon to now appearing
hypoechoic (arrow). (d–f) Apophyseal avulsion on right side (left part of image)—comparison to
contralateral normal left anterior inferior iliac spine using split image technique: (d) cross section,
(e) longitudinal scan in a different patient with same pathology. (f) Partial rupture of achilles tendon: tendon swollen, hypoechoic, disruption of continuity clearly depictable
Complete tear: continuity of tendon disrupted, often signicant distance between
lower and upper part (measure distance for treatment decisions)—ends difcult to
nd and assess.
Partial tear: persisting continuity of some parts of tendon, though potentially
swollen and altered, whereas other parts are disrupted with some sort of haematoma
formation (Fig.17.6c).
Chronic tear/chronic microtrauma—different image appearance: organisation
and reparative processes = inhomogeneous small spots with some calcications
appear in somewhat unusually and inhomogeneously structured tendon. Tendon
may be thickened and edematous—altered echotexture. If tendon sheath intact,
there may be thickening and effusion due to chronic alteration with variable hyperaemia and hypervascularisation (CDS).
• Elastography promises to become a useful tool for detecting areas of chronic damage.
Note Observe anisotropy effects and potential risk of misreading.

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Fig. 17.7 Baker cyst and DDx of soft tissue cysts. (a, b) Baker cyst (+ +2) longitudinal (b) and
cross section (a), the latter showing the connection to joint space (+ +
masses: “cystic lymphangioma”—cystic lymphatic/vascular malformation. (d) Abscess formation
in breast with reactive changes in surrounding soft tissue
1
). (c) DDx in complex cystic
17.1.3.5 Cysts
Number of situations with soft tissue cysts—potentially connected with joints
space—e.g.:
• Posttraumatic and chronic stress, seroma remnants; effusion-lled recesses
and bursae.
• Physiological variations/uid-lled recesses.
• Cystic tumours.
• DDx: even in uncomplicated cysts—evaluate if connected to joint space (e.g.,
Baker cyst), tendon sheath (e.g., ganglion), muscle (e.g., posttraumatic seroma)
or vessel (ectasia or aneurysm) (Fig.17.7).
Note An irregular, thickened and hypervascular wall or complicated echoic content
(with potential sedimentations) usually indicates complications—such as inammation or tumorous origin.
17.1.3.6 Inflammation
US extremely helpful for differentiating supercial versus deep soft tissue infection
(e.g., fasciitis). Used for depiction of necrosis or abscess and differentiation of
other causes.
Note Increases index of suspicion in early phase of osteomyelitis (see below).

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Cellulitis
Usually diagnosis made clinically; US used to assess extent of involvement, complications (abscess) and differentiate from fasciitis:
• US ndings: enlarged echogenic subcutaneous tissue with irregular ovoid uid
collections; reticular hypoechoic striations occur (but US ndings nonspecic—
insect bites, etc. may appear similar).
• CDS: hypervascularity and hyperaemia.
Fasciitis
Often induced by minor supercial skin lesion and in immunocompromised patients:
• US ndings: perifascial uid, swollen and echogenic subcutaneous layer (phlegmonous), poor fascial border, muscle usually spared (Fig.17.8).
In necrotising fasciitis, air/gas seen—no further US access to deeper structures
achievable (as in subcutaneous emphysema—see Fig.17.22).
Tendinitis: Tendovaginitis/Synovitis
Not so common in children, however increasingly observed with excessive sports
and training with non-physiological strain (“overuse injury”):
• Characterised by swelling and thickening of tendon sheath with some effusion,
tendon inhomogeneous and thickened, surrounding soft tissues can be edematous and swollen (Figs.17.8 and 17.9).
• CDS: often hypervascularity and hyperaemia.
ab
Fig. 17.8 Subcutaneous tissue pathology. (a) Oedematous subcutis and thickened, multilayered
fascia that is accompanied by some uid. (b) Phlegmonous fasciitis with huge swelling and uidlled septae
Fig. 17.9 Tenosynovitis. Echogenic swollen
tendon with uid within the tendon sheath; note
echogenic adjacent soft tissue as a sign for
oedematous-inammatory reaction. Plenty of US
gel used causing the supercial dark area in front
of the skin with some echoic spots

c
17 Musculoskeletal andOther Small Part US inChildhood
497
Osteomyelitis
Specic pathophysiology in early childhood: predominantly starting at physis
involving also joint as septic arthritis always affecting growing plate. US very helpful in early phase.
• US ndings (Fig.17.10).
– Thickening of joint capsule.
– Periosteal thickening.
– Subperiosteal collections—subperiosteal abscess, DDx haematoma
(Fig.17.10, see also Fig.17.2c).
– Osseous surface disruption (when extending into spongiosa in later phase),
increased sound penetration into bone when already demineralised.
– Adjacent inammatory reaction and soft tissue oedema, (secondary) soft tis-
sue/periosteal abscesses.
– CDS: hypervascularisation and hyperaemia.
Note US = rst-line exam, MRI mandatory for early detection, complementary
plain lm shows soft tissue swelling and only in later stage osseous changes.
a
b
d
e
Fig. 17.10 Abscess and osteomyelitis. (a) Subcutaneous abscess after injection. (b) 3DUS of a
parosteal abscess after IV line-induced thrombophlebitis in a newborn. (c) Subperiosteal abscess
(axial section) with more complex appearance and enormous surrounding inammatory changes.
(d) Subperiosteal abscess—longitudinal view (+ +). (e) Osteomyelitis (split/dual image technique): normal knee of an infant on left image. The image of left knee (L) shows the abscess formation with a more prominent sound penetration into the less ossied distal femoral metaphysis. Note
irregularities of the cortical border close to the physis

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17.1.3.7 Neoplasia
Bone tumours: US ndings in all bone tumours with extraosseous components or
bone erosion are very sensitive but nonspecic.
Childhood-specic bone tumours: osteosarcoma and Ewing sarcoma:
• Added value to mandatory plain lm: assessment of soft tissue components,
periosteum, vascularisation.
Other soft tissue tumours: US ndings nonspecic, show tumour and relation to
surrounding structures (osseous, joint and vascular), give information on components (solid, cystic, necrotic, vascular, etc.).
• Common benign childhood entities: Lipo(-bro-)ma, haemangioma, neurobroma, lymphatic malformation, vascular malformations, bromatosis of sternocleidomastoid muscle (neonates—see neck chapter).
• Malignant tumours: Practically only rhabdomyosarcoma, rare other sarcomatous
tumours exist.
• Cutaneous metastasis: except for neuroblastoma extremely rare.
US Appearance
All features known from other imaging modalities (Fig.17.11):
• Codman triangle and spicules—echogenic disruption of more or less homogeneously anechoic tumour bursting from cartilaginous or bony surface.
• Periosteal inltration.
• Inltration of soft tissues.
Also assess:
• Relation to joint, physis or muscles, tendons and vessels.
• Depict solid or cystic component of soft tissue tumours.
• Use CDS to demonstrate vascularity, particularly valuable for haemangioma/
vascular malformations.
Some typical features that may help suggesting specic entities:
Cartilaginous tumours—anechoic structure:
• Particularly in cartilaginous exostosis, US ideal for depiction and assessing
extent as well as judging cartilaginous component of exostosis and DDx from
enchondroma; difcult without plain lm.
• US useless in chondroma and osteochondroma when positioned within bone.
Osteosarcoma—irregular structure with bony cortical defects.
Ewing sarcoma—dominant periosteal reaction with paralleled echogenic struc-
ture; large soft tissue component may be present, with matric calcication and

17 Musculoskeletal andOther Small Part US inChildhood
a
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b
c
de f
g
hi
j
Fig. 17.11 Bone and soft tissue tumours. (a) Osteosarcoma: soft tissue component of a bone
tumour with destruction of the cortical layer. (b, c) Pathologic fracture with neurobroma: longitudinal (b) and (c) axial section of affected hand. (d) Eosinophilic granuloma of the skull: note
bony spiculae in the soft tissue bony defect. (e) (Cartilaginous) Exostosis (+ +) with only narrow
cartilaginous layer. (f) Inhomogeneous hypoechoic soft tissue tumour of deep gluteal muscle
which proved to be a soft tissue sarcoma. (g, h) Septated, relatively clearly demarked tumour (g),
with vivid colour signals on CDS (h), consistent with a high-ow haemangioma. (i) US appearance of osteochondroma—thick cartilaginous layer, irregular cortical margin. (j) Osteosarcoma
with typical spiculae in exophytic soft tissue part of bone tumour, Codman triangle, perifocal
reaction

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spiculation as well as radial vessels. Note that intraosseous or, e.g., intracranial
extension not well depictable by US unless bone is destructed (Fig.17.12).
Other bone tumours (lymphoma) and metastasis only seen by US if outer ossi-
ed cortex disrupted, or with large extraosseous soft tissue component (Fig.17.12).
Muscular and cutaneous metastasis more easily detectable, difcult to classify—
same approach as in any other body region (see neck chapter).
Pilomatrixoma—hypoechoic, cyst-like, well-dened tumour with typical central
spot like echo.
“Lymphangioma” [= (veno-)lymphatic vascular malformation—the old term
lymphangioma should be avoided!] multiple cystic components with thin walls,
b
c
Fig. 17.12 Metastasis of Ewing sarcoma in occipital skull: US visualises extracranial soft tissue
component with spiculae, matrix mineralisation (a) and radiating vessels (b), but cannot access
intracranial portion as shown on MRI (c)

17 Musculoskeletal andOther Small Part US inChildhood
may contain echoes from haemorrhage (with sedimentation), some vessels in septae
depictable (see Fig.17.7c, see also chapter neck/chest/mesentery).
Haemangioma and vascular malformation—more or less echogenic and homog-
enous tissue with varying sharpness of margins (“capillary haemangioma”); large
tubular-cystiform hypoechoic structures (vessels), which may dominate picture in
venous malformations; ow seen on aCDS—can be classied by spectral analysis
(shunt ow? High-ow haemangioma? Low-ow angioma? Only venous ow?—
potentially only reliable assessable sonographically with contrast enhanced US)
(Fig.17.11 h; see also chapter neck).
Additional Imaging
US may be rst-line examination. Plain lm+MRI (and sometimes CT) mandatory
according to specic oncology protocols (extent, characterisation, staging, etc. ).
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17.2 Other Small Part Applications
17.2.1 General Remarks
Basically, similar rules apply as detailed above. Particularly for muscle US anisotropy phenomena have to be observed—oblique angling and tilting of the transducer
may obscure the normal structure—as does to a lesser extend image compounding.
For detailed analysis of muscle and soft tissue echostructure a relatively high
dynamic range setting helpful.
Labelling/body markers are of particular importance, also indicating transducer
position—to allow for a proper interpretation particularly on follow-up or second
opinion.
17.2.2 Foreign Bodies
US most effective in detecting supercial or tiny foreign bodies using highresolution transducers, with US stand-off pads or copious US gel. Helpful to compare rst unaffected and then affected side.
US Findings
Depends on physical characteristics:
• Metal, glass—produce reverberation echoes (comet-tail artefact) (Fig.17.13a).
• Wood—acoustic shadowing (Fig.17.13b).
Note US also used successfully to guide foreign body removal (Fig.17.13c)—see
chapter on interventional US.
US also useful to judge size of foreign body, relation to other structures, or assess
complications such as granuloma formation or abscesses (Fig. 17.14).

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Fig. 17.13 Foreign body. (a) Reverberation caused by a metallic foreign body (similar to needles
for punctures). (b) Echogenic foreign body (wooden splinter causing acoustic shadowing) in the
wrist. Note inammatory reaction of the edematous and swollen surrounding soft tissue. (c)
Subcutaneous echogenic foreign body (+ +) without shadowing, but reverberations, consistent
with glass splinter (foot)
M. Riccabona et al.
b
Fig. 17.14 US convincingly displays size/length (a) and location as well as relation to surround-
ing structures (e.g., reaching to muscle or a compromising a vessel/nerve?) (b) of foreign body and
also allows visualisation of complications such as abscess formation (c)
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