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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

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cba
Fig. 16.7 Common pitfall in Hips US = wrong angulation with respective implication on angle
measurements in the Graf and modied Rosendahl method: As demonstrated in schematic drawing
of a table corner, the angle will appear different depending on the viewing angle and perspective
(a), inuencing angle measurements on US (b) – where the correct angle measurement is only
lower Hip US image, whereas the upper image exhibits wrong angle measurements; the malposition is recognisable by missing femoral structures on the US image. Note that the measurement
lines do not have to cross in one point to be correct! (c) Shows a technical device (arrow) that may
help to avoid accidental tilting of transducer
16.6 Other Conditions ofHip Joint
16.6.1 Arthritis andInflammation ofHip Joint
As in all joints, examination of contralateral (not affected side) helpful for comparison (TIP: start there—less painful, know individual normal anatomy).
Most common cause: transient synovitis of hip.
US ndings and Staging
• Joint effusion, thickening of joint capsule (Fig.16.5b).
Note Differentiation (viral, bacterial, septic, rheumatoid) impossible by
US.Usually achieved by clinical data (possibly US-guided arthrocentesis).
16.6.1.1 Capsular Thickening
Can be measured, does not need to be present, no cut-off value, can have varying
echogenicity:
• Appearance not specic—depends on kind of inammation, age, duration, transducer used.
• Sometimes CDS shows hypervascularisation of capsule (Fig.16.5c).
• If increased vascularity depicted: spectral analysis may show diastolic hyperemia:
• Unless increased joint pressure, then diastolic perfusion impaired.

16 Neonatal andPaediatric Hip US
483
16.6.1.2 Joint Fluid/Effusion
Widening of joint space due to uid, forces capsule to convex shape:
• Simple/uncomplicated: clear uid, up to 10 mm (intraindividual difference
>3mm) (Fig.16.5b).
• Complicated: larger, echogenic particles within, potentially signicantly thickened
synovial layer; may reect also haematoma / haemarthros (e.g. haemophilia)
• Suspect septic/bacterial arthritis (Fig.16.5c).
Note In osteoarthritis of infants, there may be distention and consecutive luxation
and osseous defects. Luxation can be identied by applying DDH US techniques
(e.g. Graf’s criteria)—search for it!
And Simple effusion does not rule out bacterial / septic arthritis, and complicated
effusion does not proof septic arthritis = if any doubt do (US-guided) sampling.
16.6.2 Hip Osteoarthritis
US ndings similar to any other joint.
Usually unilateral, whereas transient synovitis may occur on both sides, as well
as Perthes disease (rarer).
Particularly after long-standing and bacterial arthritis, defects may remain—with
poor ossication of femoral neck and defects in convexity of femoral head. Important
to assess and monitor development of disease—persisting effusion always hints
towards underlying condition or Perthes, where osseous defects can also/additionally be seen.
16.6.3 (Femoral Head) Epiphysiolysis/Slipped
(Capital Femoral) Epiphysis
US superior to plain lm in infants due to poor ossication of femoral head—
improved assessment, same approach accounts for all other joints with cartilaginous
epiphysis (e.g. shoulder, elbow—birth trauma) (Fig.16.8):
• Displacement in any direction—US access from different directions and positions recommended.
US Findings
Typically anechoic cartilage of femoral head with or without ossication centre
slipped:
• Continuity of bone margin disrupted at level of physis—step-off phenomenon.
• One millimetre displacement equals approximately 5° displacement on plain lm.

484
Fig. 16.8 Epiphysiolysis in a newborn after
birth trauma. Note discontinuity between ossied
bone and hypoechoic cartilaginous epiphysis
indicating dislocation of epiphysis
G. Schweintzger et al.
Complex joint uid representing haemorrhagic components—particularly in
acute phase.
Periosteal reaction—late stage.
Secondary changes of surrounding soft tissues.
US-guided reposition feasible.
Note If tolerated, dynamic assessment may reveal pathologic motion at physis.
Same criteria apply to epiphysiolysis of any other joint in neonates and infants.
16.6.4 Perthes Disease
Definition
Avascular necrosis of femoral head of unclear aetiology and unknown origin, 20%
of affected children have history of transient synovitis of hip.
US Findings and Staging
Grade I:
• Potentially only joint effusion.
• Slight asymmetric reduction in height of epiphysis as well as femoral head on
affected side.
• Contour of femoral head is maintained.
Grade II (Fig.16.9):
• Fragmentation; irregular disruption of outer contour of bony femoral head—
sonographically irregular.
• There may be secondary effusion.

16 Neonatal andPaediatric Hip US
Fig. 16.9 Perthes disease. (a) Scattered epiphysis of femoral head in early Perthes disease (stage
II). (b) Both hips imaged for comparison (split image technique): note reduced height of affected
right (R) femoral head (Grade IV—US appearance varies with stage); additional imaging compulsory (plain lm+MRI)
485
Grade III and IV:
• Reparative mechanisms—femoral head increasingly homogeneous.
• Signicantly reduced femoral head height.
• Joint effusion diminishing.
• However, lateralisation and atypical contour of remodeled femoral head persists.
Note In suspicion of Perthes always perform plain lms and (dynamic contrast-
enhanced) MRI

Musculoskeletal andOther Small Part US
inChildhood
MichaelRiccabona, GerolfSchweintzger, andBrianColey
17.1 Investigation ofBones, Joints, Tendons
17.1.1 Requisites andTechnique
Transducers and Techniques
• Linear transducers with high resolution (18/12–5MHz). Features such as trapezoid mode, image compounding and harmonic imaging helpful.
• In very supercial structures stand-off pad helpful, however, using highresolution transducers stand off-pads not routinely needed, particularly if US gel
used liberally.
• For deeper structures, curved linear arrays and lower frequencies helpful—as
trapezoid mode of linear transducers usually lacks same penetration (or try to get
out of trapezoid mode).
• For long structures such as tendons, extended view techniques helpful, alternatively split/dual image technique.
• In tumours or inammatory conditions (abscess, arthritis, etc.): (a) CDS (and
potentially ce-US) helpful.
17
M. Riccabona (*)
Department of Radiology, Division of Pediatric Radiology, Medical University Graz
and University Hospital Graz, Graz, Austria
e-mail: michael.riccabona@medunigraz.at
G. Schweintzger
Abteilung fur Kinder und Jugendliche Neonatologische und padiatrische Intensivstation,
LKH Leoben/Eisenerz, Leoben, Austria
e-mail: Gerolf.Schweintzger@lkh-leoben.at
B. Coley
Department of Radiology, ML5031, Cincinnati Children’s Hospital Medical Center,
Cincinnati, OH, USA
e-mail: brian.coley@cchmc.org
© Springer Nature Switzerland AG 2020
M. Riccabona (ed.), Pediatric Ultrasound,
https://doi.org/10.1007/978-3-030-47910-7_17
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• Elastography—promising future method for assessment of tendons and tumours,
but not yet validated in children.
Positioning and Handling
• Varies depending on affected area, therefore no standard planes.
• Important to choose comfortable position that minimises pain.
• Start investigation at non-painful area, work to area of disease—in young children consider applying analgesic ointment before investigation.
Tip Very often initial evaluation of contralateral normal side proves valuable—
serves as intraindividual normal reference, helps optimise equipment settings and
enables child to get used to scanning (reducing anxiousness and fear).
• All joints and pathologies usually assessed in two orthogonal sections.
• Surface alterations better visualised and documented by 3DUS using surface
rendering.
Indications
Applicable to acute and chronic conditions:
• Joint pain or effusions (most commonly used in large joints but also feasible in
small joints).
• Skin, soft tissue, muscular and tendon disease (e.g., achilles tendon, shoulder
capsule, wrist and foot tendons).
• Evaluation of unclear swelling, e.g., suspected haematoma or node or cyst versus
other causes for bumps.
• Suspected tumorous conditions with lumps.
• Search for and detection of foreign bodies.
• Assessment of all accessible osseous structures (e.g., continuity or focal disruption, callus).
• Evaluation of periosteal reaction—exquisitely visualised by US, particularly
periosteal thickening and abscess.
• Assessment of all accessible peripheral muscles (e.g., follow structures from origin to insertion, show transition zone to tendon or bone).
Advantage: US allows comprehensive assessment of all surrounding structures
(bones, joints, etc.) and perfusion (CDS).
Disadvantage: If very painful or if diagnostic benet restricted in some areas—
US not justify; imaging then performed by plain lm, CT or MRI.
Restrictions: Deeper joint spaces and bony structures beyond surface not visual-
ised by US—commonly need MRI.
Note In osseous structures, usually only surface component (cortex) assessable for
continuity or disruption, e.g., fracture or tumour. If US can penetrate cortical layer (e.g.,
due to disruption or reduced ossication/calcication by tumour inltration, osteomy-

17 Musculoskeletal andOther Small Part US inChildhood
489
elitis and decalcifying disease), visualisation of processes in deeper bone compartments
achievable. Detailed demonstration of all major joints and their US appearance beyond
scope here—refer to extended literature and textbooks. Different for non-ossied parts
of skeleton in younger age: US ideal for showing cartilaginous structures= primary
imaging approach. US shows continuity of cartilaginous parts with ossied bone and/
or other surrounding structures—particularly useful for assessing children with nonaccidental injuries (corner fractures, etc.) or even in diagnosing epiphysiolysis.
17.1.2 Typical Normal Findings
Bone
If US beam perpendicular, and cortical layer of normally ossied bone intact: only
surface echo seen as an echogenic border with complete shadowing behind. Subtle
layer seen in front represents periosteum.
Note Pseudo-periosteal layer may occur if gain too high producing strong
reections.
Cartilaginous Structures
• Hyaline cartilage: usually anechoic/hypoechoic with more or less echoes within,
depending on maturity (and setting of US system) (Fig.17.1a).
• Collagenous (bro-)cartilage: US appearance becomes more echogenic in areas
of more brous components (e.g., brous annulus of vertebral disc, acetabular
labrum of newborn and infant hip).
• Ossication centres become centrally echogenic, with increasing shadowing
(Fig.17.1b).
Remark: Cartilaginous echostructure and contour usually show slight irregularity
at transition zone to ossied bone (may represent physis). However, even with this
short disruption, surface usually remains continuous.
Fig. 17.1 Cartilaginous epiphysis in infants. Hypoechoic cartilaginous epiphysis with some stippled physiologic echoes representing the venous sinusoids—without (a) and with (b) central echogenic ossication centres causing shadowing

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M. Riccabona et al.
Joint Capsule and Tendons
Depending on angle of insonation, these structures change echogenicity and appearance (anisotropy) (see Fig in respective chapter and Fig).
Capsules usually have just one visible layer except for insertion (varies with
transducer frequency and resolution).
Tendons have several parallel echogenic layers.
17.1.3 Pathologic Findings
17.1.3.1 Fracture
• Interruption of cortical contour (high sensitivity).
• Additional ndings: periosteal reaction, haematoma, later callus formation can
be seen, depending on phase/age of fracture (Fig.17.2):
• If dual/split image/extended view techniques or 3DUS used: angle measurements can be performed to dene deviation of displaced fracture, provided longitudinal axis of respective bone clearly identied.
• In all fractures: periosteal reaction, calcication and callus formation seen as
(pseudo-)tumorous, more or less ossied, formation at site of fracture.
• In reparative phases: CDS can show hypervascularity and hyperaemia as sign of
reparative processes; difcult to distinguish from tumorous or inammatory
conditions.
a
Fig. 17.2 Subperiosteal haematoma. (a) Typical early image appearance of traumatic haematoma
due to fracture with dislocation. (b) DDx: osteomyelitis versus subperiosteal abscess: may appear
similar on US as subperiosteal haematoma in this forearm fracture (c, markers)—not always
hypoechoic as in the shown skull fracture, (d) depending on age, etc.
b

a b
17 Musculoskeletal andOther Small Part US inChildhood
491
• Growing fractures and pseudo-arthrosis can be visualised—particularly when
performing dynamic study showing not only disruption and distraction of fracture ends but also painless mobility towards each other.
Note US cannot always replace plain radiographs. Plain lm simpler and
allows clearer denition of dislocation angles, also avoiding possible pain during examination. US demonstration and documentation of entire bone may be
cumbersome.
But specic applications exist where US is very helpful due to restrictions of
plain lm: e.g., skull fractures (where plain lm is usually not indicated any longer
except for nonaccidental injury queries), corner fractures and toddler’s fractures,
non-dislocated and ungapping fractures and recently even proposed for assessing
forearm fractures (WRIST safe protocol; Ackermann O.Eckert K “Fraktursonograe”,
Elsevier, 2019)—but particularly for the latter the bones must be assessed from all
directions! (Fig.17.3)
Note Fractures and dislocation of cartilaginous bone=US domain—much better
than plain lm, US also used for image-(US-)-guided reduction, e.g., after epiphysiolysis (see Fig. 16.8 in hip US chapter).
d
g
Fig. 17.3 US in fractures. (a) Fracture without destruction of periosteum and slight bending. (b)
Subtle skull fracture poorly depictable by plain lm; note regional haematoma; (c–f) US of different forearm fractures, also demonstrating possibility of angle (e) and dislocation (f) measurements.
(g) Impressive callus formation after femur fracture)
c
e
f

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Remark: In long bones, usually only the part of a fracture close to transducers
can be visualised and assessed, as US cannot penetrate healthy ossied bone. If one
needs to see entire circumference, scan from every direction.
Therapeutic insonation can increase callus formation and bone healing (by caus-
ing hyperaemia)—requires specialised equipment.
17.1.3.2 Joint Effusion
US highly sensitive in detection. Extremely helpful also in management of rheumatologic and haemostatic disorders.
Simple Effusion
Sonographically dened by usually anechoic uid (uncomplicated effusion) within
joint space, causing widening of joint and enlargement of joint space.
Commonly capsule appears normal, may be slightly thickened (see Fig.17.5).
Complicated Effusion
Echoes within uid, potentially sedimentation (see Figs.17.4 and 17.5).
Fig. 17.4 Joint effusion with septations (knee arthritis). Relatively clear uid, some thickening of
joint capsule in rheumatoid arthritis, some nodular components indicating pannus formation in
longitudinal (a) and axial (b) sections
Fig. 17.5 Thickened joint capsule (a) and hyperaemia on CDS (b). (a) Septic knee arthritis—with
marked thickening of capsule and complex uid. (b) Thickened elbow joint capsule with effusion
(osteoarthritis). (c) CDS depicts hypervascularisation (same joint as b)
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