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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

15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
Fig. 15.51 Microlithiasis. (a) Diffuse microlithiasis. (b) Bicolour mode conspicuously enhances
testicular calcications
Fig. 15.52 (Epididymo-)orchitis. Asymmetrically
enlarged swollen testis with vivid hypervascularity
of testis
(and epididymis) on CDS
451
US/CDS Finding
Orchitis: unilateral increase of size of affected scrotum, may be hyperechoic.
• Reactive hydrocele, scrotal wall thickening. Secondary abscess/necrosis possible.
• Hypervascularisation with hyperemic diastolic ow on spectral analysis (low RI)
(Fig.15.52).
Epididymitis: Epididymis enlarged, more or less echogenic, potentially
inhomogeneous.
Exhibits signicant hypervascularisation without hyperperfusion of testis itself.
Often associated complex hydrocele:
• May also manifest combined with orchitis (epididymo-orchitis).
Rarer in children, always think of associated urological problems/ascending
Note
infections from prostatic ducts, particularly in urethral obstruction.
Paratesticular inammation may arise from descending infection from peritoneal
cavity (peritonitis) or septicemic involvement. Similar ndings seen after inguinal
surgery with haemorrhage/secondary infection:

452
M. Riccabona
• Typical paediatric entity: echogenic complex material in scrotum around testis—
potentially with calcication after meconium peritonitis in newborn.
Complications
Particularly in orchitis: abscess, necrosis, segmental infarction—can be
depicted on US.
Note Differentiation of necrosis versus abscess may be difcult, particularly in
early phases.
15.8.5 Scrotal Trauma
US used to assess contusion versus haematoma versus rupture.
• Contusion: focal inhomogeneous parenchyma seen with swelling of testis, but no
parenchymal disruption; continuity of the outer border maintained.
• Haematoma: (intra- or extratesticular) easily depicted—CDS allows assessment
of viable testicular parenchyma (Fig.15.53).
• Testicular rupture: dened by discontinuity of tunica and intrascrotal haema-
toma. Viability of different testicular components assessed by CDS, helping to
decide on surgery.
– Penis fracture not addressed, as not a query in childhood (sometimes in ado-
lescents)—but well suited for assessment by US (visualisation of haematoma
and disruption of tunica).
15.8.6 Torsion
Clinically typical acute onset of pain, swelling.
Two different types: neonatal extra-/supravaginal torsion; intravaginal torsion
common during puberty—usually no impact on therapy except for delayed diagnosis in neonates (often has happened much earlier, e.g. during birth/fetally—then no
emergency surgery!).
Fig. 15.53 Scrotal trauma. Testicular
trauma with haemorrhage into
scrotal sack and injured, partially
destroyed testis—obviously
with disrupted tunica and
irregular contour

bc
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
453
a
d
Fig. 15.54 Testicular and hydatid torsion. (a) Enlarged testis with hypoechoic (necrotic) paren-
chyma—no perfusion on CDS in older testicular torsion. (b, c) Echogenic testicular appendix (b)
without ow on CDS (c), consistent with hydatid torsion. (d) Whirlpool sign in testicular torsion—
note that CDS visibility of vessels is only granted if there is some residual perfusion
Note Often adolescent presents delayed because of shyness about seeking care.
Thus “missed torsion” with completely necrotic testis not uncommon.
US Finding
Superiorly positioned, swollen, homogeneously hyperechoic testis—in peracute
phase. Some accompanying hydrocele, swelling of scrotal wall (Fig.15.54).
Whirlpool sign/spiral like twisting of spermatic vessels in inguinal canal at entry
into scrotum.
In longer duration/late torsion echogenicity of testis decreases, may become
more inhomogeneous—eventually anechoic when necrotic; secondary abscess formation possible. More complex appearance of associated hydrocele uid.
CDS
Asymmetric ow or lack of intratesticular vessels.
Twist of vascular pedicle when following it into inguinal canal (“whirl pool”
appearance as in volvulus):
• Partial torsion may exhibit residual but asymmetric perfusion—rstly affecting
veins (haemorrhagic infarction).
• After (spontaneous) detorsion, transient hyperaemia may be seen.

454
M. Riccabona
Note Mandatory to depict intratesticular ow and prove symmetry with spectral
Doppler analysis—torsion can only be excluded when symmetric intraparenchymal
ow prole in arterial and venous compartment is depictable. In every suspicion of
torsion on US, emergent surgical exploration mandatory.
US-guided detorsion/manual relief of torsion: detwisting testis by rotation in
steps of 180°, checking for reappearance of perfusion—does not obviate surgery as
partial detorsion may still exist (reactive hyperaemia will always show some asymmetric perfusion—thus residual partial torsion cannot be ruled out).
15.8.6.1 Torsion ofAppendages
Quite common. Important DDx for testicular torsion/inammation (clinical ndings may be similar) or inguinal hernia.
US Finding
Enlarged appendage (hydatid) with lack of perfusion, hyperaemia of adjacent structures, but always symmetric intratesticular perfusion. Often some hydrocele, scrotal
swelling, epididymitis-like changes observed (Fig.15.54b, c).
After appendiceal torsion extratesticular calcications often present.
DDx Criteria
Scrotal oedema, normal testis, hydrocele, increased vascularisation. No inguinal hernia.
15.8.6.2 Inguinal Hernia
If inguinal hernia detected, try to follow through inguinal canal, assess inner ring
and describe content (mesentery, uid, intestines—potentially with peristalsis, perfused bowel wall?) Other rare hernia contents: parts of bladder, in girls ovaries/uterus.
Particularly if incarcerated—confusing images seen; sometimes spermatic cord
vessels compromised, thus endangering testis.
May sometimes only be seen with increased intra-abdominal pressure—consider
provocative manoeuvres (imaging while crying/straining, Valsalva, image with
patient standing).
A “soft”/open inguinal canal physiologic in preterm newborns; movement of
Note
mobile testis or entrance of bowel commonly observed—no worry if transient.
15.8.7 Testicular Tumours
Rather rare in childhood, most commonly germ cell tumours or teratoma.

15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
a bc
+
+
455
+
de
Fig. 15.55 Testicular tumours and DDx: (a) Small tumour (+…+) slightly resembling a cystic
dysplasia of the rete testis. (b) Larger testicular tumour x … x), nicely outlined by hypervascularisation on CDS (c). (d) Testicular teratoma with a solid component (…) on CDS. (e) Huge haemorrhagic spermatocele only entirely imageable by a curved array
US Findings
Typically appearance of ovoid space occupying lesion. May be cystic, particularly
in teratoma/epidermoids, or completely solid. May have more complex cystic
appearance with septae (Fig.15.55)
• Often mild associated hydrocele. Denition of underlying entity rarely
achievable.
• Always assess pelvic/retroperitoneal lymph nodes, and perform abdomi-
nal survey.
+
Secondary involvement in systemic diseases (e.g. leukaemia/lymphoma, neuroblastoma) where testis can even serve as host region for recurrence, involvement
may be uni- or bilateral.
DDx
Intratesticular cysts, dermoids, septated hydroceles, epithelial cysts, cystic dysplasia of rete testis, intratesticular ectopic adrenal tissue, infection/abscesses/necrosis,
posttraumatic alteration.
Note Rhabdomyosarcoma in male pelvis mostly from pelvic oor muscles, pros-
tate, seminal vesicles, or bladder, rarer in scrotum.

456
No other sonographically important aspects of prostate need to be addressed in
childhood; only sometimes after infection prostate calcication may be seen, as
well as an atypical appearance of enlarged seminal vesicles in cystic dysplasia and
then often combined with other urogenital malformations.
M. Riccabona
15.8.8 Role ofUS andAdditional Imaging
US—ideal initial imaging tool with high reliability, when performed skillfully.
Supplementing Investigations
• Scintigraphy and MRI have been performed for torsion—but potential time delay
usually demands early surgery in unclear cases.
• In tumours: staging by CT/MR.
• Assessment of ectopic testis/cryptorchidism: may benet from MRI, although
small dysplastic testis in abdominal cavity may be difcult to depict—many
centres perform laparoscopy if testis not found in pelvis/inguinal region
directly.
• Assessment of complex genital (cloacal)/intersex states: may benet from MRI/
ce-CT and uoroscopy/genitography.
• Angiography of spermatic vein only performed in complex/recurrent varicocele
for therapeutic reasons (embolisation in the same session).
15.9 Female Genitals
15.9.1 Indications
Suspected genital malformation/disease by clinical ndings on inspection, ambiguous gender, associated urogenital malformation, hormonal abnormality (e.g. precocious puberty, adrenogenital syndrome).
15.9.2 Requisites
Sufciently lled bladder mandatory for detailed assessment.
Perineal approach very helpful—looking at vagina/pelvic oor/rectum (cloacal
malformation):
• In unclear ndings/obvious pathology, lling of the bladder and vagina with
saline helpful (“Sonogenitography”) (see respective chapter).
• For depiction of stulae, optional/additional UCA instillation.

15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
457
15.9.3 Transducers
Particularly in neonates, high-resolution linear/micro-curved arrays applied.
Otherwise use curved linear areas with highest applicable frequency.
Transvaginal investigations usually only performed after puberty:
• Some centres perform transrectal investigations.
15.9.4 How toPerform Investigation
Consecutive longitudinal and axial sections through region of genital organs behind
bladder by rotating transducer into respective organ axis of fallopian tube, ovaries, uterus.
Take size measurements, document ndings:
• Always include entire US of all other pelvic structures/urinary tract, include
adrenal glands.
Measurements particularly important in suspected hypodysplasia or early onset
of puberty:
• Compare results to tables with normal values.
Always try to assess detailed structure of ovary (size? follicles present?) and
uterus (size, shape, horns, wall structure/endometrium?):
• In older girls additional assessment of breast valuable for complete work-up in
hormonal imbalance.
15.9.5 Normal Findings
Uterus Changes during growth/development (Fig.15.56):
• In neonate (stimulated by maternal hormones): rather large, with long cervix,
endometrium nicely differentiated.
• In infancy/early childhood: small, difcult to assess.
• With onset of peri-/prepuberty/hormonal activity: uterus grows again. Eventually
becomes shape of typical adult uterus—pear shaped= relatively short cervix,
large body, exhibits well-differential wall/endometrium (varies throughout cycle).
Uterus muscle rather hypoechoic, with clear contour. Thickness of endometrium
depends on hormonal situation. Often positioned not strictly sagittal/in midline—
some deviation physiological:

458
Fig. 15.56 Different stages of uterine development. (a–c) Longitudinal section: (a) neonatal
shape, (b) infantile appearance, (c) prepubertal conguration. (d, e) Axial section: (d) pubertal
uterus with prominent ovarian follicles, (e) adult uterus with prominent endometrium
M. Riccabona
• Useful measurement for assessing maturity: index made from corpus to cervix
length. Cervix longer in neonates, corpus longer in mature girls.
Vagina Tubular muscular structure with central lumen, reaching from cervix to
external orice/vulva
• For assessing patency/duplications, lling of vagina with saline infusion
necessary.
• Distal portion only visible by perineal US, once symphysis ossied. This
approach also useful for distal vaginal atresia—imperforated hymen.
Adnexae Fallopian tube/adnexa often poorly visualised unless ascites or
hydrosalpinx.
Ovaries Undergo stepwise development, being relatively prominent in neonate
(maternal hormones) with multiple follicles that create cyst-like appearance:
• Remember: ovary= “cystic organ”; ovarian “cysts” usually represent normal
follicles.
• In neonates ovaries positioned throughout abdominal cavity, sometimes at unsus-
pected high location, may have large cysts (Fig.15.57).

ab
cd
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
Fig. 15.57 Normal neonatal “cystic” ovary. (a) Typical large “multicystic” neonatal ovary
(
+ …+) that may be positioned relatively high and ventrally. (b) Ovary during childhood—
1
smaller, more difcult to nd (full bladder mandatory), in this case exhibiting physiologic follicles
that may not be depictable in many cases. (c) Pubertal/adult ovaries with multiple follicles (physiologically a “multicystic organ”), observe large paravaginal/retro-uterine cyst and some ascites.
(d) Ovarian “functional” cyst (not always able to be differentiated from a cystic teratoma on a
single US exam)
459
• In infancy/childhood during “silent” phase—ovaries small, often difcult
to depict.
• With onset of hormonal activity/(pre−/peri-) puberty—ovaries grow, manifest as
typical “multicystic” retrovesical organs lateral to uterus—more peripheral follicles, some central tissue. Follicles vary in size, neonatally far more than 1cm, in
infants usually less than 5mm, in puberty—depending on phase of cycle—up
to 4cm.
15.9.5.1 Sonogenitography
Assessment of internal genitalia after vaginal lling via small exible catheter with
saline infusion (for further details see respective chapter):
• Bladder also needs to be full/lled.
• Sometimes simultaneous rectal saline enema may be helpful (prove absence of
uterus/vagina, depict stulae).
Tip Rinse catheter before inserting to avoid introducing obscuring air
into vagina.

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M. Riccabona
15.9.6 Pathologic Findings
15.9.6.1 Congenital Malformations
Vaginal Septum andDuplications
Midline anomalies—most commonly only recognised if outow occluded: cystic
formation manifests. Alternatively lling by saline infusion after careful catheterisation may support diagnosis, additionally may help detect potential connections,
particularly when supported by ce-US and perineal US:
• Echogenic septum dividing vagina will become visible.
• Echogenic ultrasound contrast agents (UCA) may pass from one to another cavity through potential opening.
Vaginal Atresia
Atretic (single/duplex) vagina—usually thick membrane, leads to hydro−/
haematocolpos:
• To be differentiated from hymenal atresia by thickness of septum (hymen—thin
membrane).
US Findings
Difcult to evaluate without lling of obstructed vagina.
Obstruction manifests as more or less prominent tubular-ovoid space occupying
lesion in midline below bladder in anatomic area of the vagina (Fig.15.58):
• Sonomorphologic aspect depends on content (uid, haemorrhage, sedimentation, etc.).
• Can become huge, may also include cervix/uterus—then uterus seen by meticulous assessment as (often small) pear-shaped end of “cyst,” connecting uidlled cavity to salpinx (hydrosalpinx) (Fig.15.58).
• Secondary ascites. Associated with uterine duplication if duplex vagina.
Vaginal Fistula
Remnant of disturbed foetal development. Often associated with urogenital/cloacal
malformations:
• Also after trauma, infection, surgery.
Commonly connect to distal urethra (urogenital sinus) or (additionally) rectum
(cloacal malformation):
• This combination only seen in phenotypic female babies.
Fistula to more proximal parts of the vagina/bladder usually have acquired origin:
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