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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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M. Riccabona
• With increasing ossication of dorsal processes: try parasagittal, slightly tilted
sections for longitudinal views:
– High-contrast post-processing helpful.
– Use high-resolution techniques (image compounding), harmonic imaging,
and extended eld of view.
• CDS helps to depict major vessels.
• M-Mode: assessment and documentation of cord movement and motion of
nerve roots.
Ventral transabdominal approach: possible in slim patients and neonates, use
sector/(curved) linear arrays with age appropriate frequency:
• Depiction of continuity and pathology of vertebral bodies.
• Assessment of pre−/paravertebral extension of spinal pathology (e.g. ventral
meningocele and teratoma).
Focus of US Imaging: Assessment of spinal canal and content
• Vertebral bodies outlined by (echogenic) surface even if ossied ⇨ pathology
depictable (e.g. hemivertebra).
• Discs not target of US in neonates and infants, except for rare query spondylodiscitis with abscess formation or tumerous invasion.
9.4 Indications
• Spinal dysraphisms, other pathology of cord and conus (e.g. tethered cord and
dermal sinus)—possibly based on external clinical ndings such as a dorsal lumbar hairy patch.
• Suspicion of spinal trauma—bedside investigation before additional imaging
• Spinal tumours in rst months of life:
– Particularly neuroblastoma growing into spinal canal through
neuroforamina.
Normal sacral dimple—no indication for spinal US, general US screening of
Note
neonatal spinal canal not considered effective.
9.5 Normal Findings
Cervical and Thoracic Spinal Canal
• Cervical cord shows widening (intumescentia cervicalis)—normal physiologic
thickening, do not mistake for pathology.
• Cord itself: central echogenicity caused by border between anterior commissure
and median anterior ssure—not central canal (not seen unless dilated).

fissure
e
9 US oftheNeonatal Spinal Canal andCord
a
169
b
de f
c
spinal cord spinous
border anterior
commissure and
median anterior
ConusFilum
process
vertebral body
with central
ossification center
terminale
nerve
roots
subarachnoid spac
cord
central
echo complex
nerve roots
spinal canal
vertebral body
Fig. 9.1 Normal spinal US. (a) Extended eld of view showing long portion of spine and canal
(sacral to thoracic segments). (b) Axial section at level of lumbar intumescence. (c) Sagittal section, split dual image technique: superior assessment of position of conus, lum terminale, and
nerve roots of cauda equina. (d) Nuchal dorsal sagittal section tilted cranially: visualisation of
cranio-cervical junction.(e, f) Schematic drawing indicating the relevant, sonographically depictable structures for spinal US (a=sagittal, b=axial)
• Cord surrounded by more or less hypoechoic subarachnoid space, limited by
echogenic dura (Fig.9.1):
• Modern high-resolution transducers may enable differentiation of gray and
white matter
– Following cervical cord upwards: visualise cranio-cervical junction with its
extension into medulla oblongata and cisterna magna as well as foramen magnum (by transoccipital/nuchal approach).
• Visualise (dentate) ligaments and nerve roots (axial access), assess motion of
nerve roots
– Spine image varies with ossication; usually ossication centres of spinous
process, posterior arches and vertebral bodies seen. Anechoic gap between
echogenic vertebral body surface—discs, allowing vertebral body counting.
• For counting vertebral bodies, extended eld of view/panorama imaging helpful
and provides conspicuous overview and reliable level assignment.

170
M. Riccabona
Tip Cervical and thoracic cord more easily visualised in exed position.
– Axial section: used to identify cord, central echo complex, duplicated cord
(diastematomyelia), paracordal structures (dentate ligaments, nerve roots,
vessels), and paravertebral structures (muscles and adjacent osseous structures,
such as transverse processes or ribs).
Lumbar Spine
• Physiologic thickening (distal thoracic and lumbar cord)—intumescencia
lumbalis.
• Position of conus medullaris: depends on age, should be at L2 from 40week of
gestation and gradually increasing in height with age.
• Always include axial sections: assess lum terminale (thickened?), identify cord
(single, duplicated, diastematomyelia), central echo, paracordal structures (dentate ligaments, nerve roots, vessels), and paravertebral structures (muscles and
adjacent osseous structures, such as transverse processes or ribs).
• Nerve roots of cauda equina with central lum terminale (should not measure
>2mm axial diameter) usually identiable as slightly thicker echogenic band
cursing sacrally:
– Motion of nerve roots and lum—some respiratory as well as pulse synchro-
nous movement.
Normal variant: little cyst in conus or lum terminale (e.g. ventriculus terminalis
or lum cyst) (Fig.9.2a).
For reliable assignment of level of conus:
(a) Extended eld of view, starting from coccyx, going up to thoracolumbar
spine—count vertebrae.
(b) Wide view (“phased”/trapezoid/convex mode) linear transducer, view includes
sacral promontory to level of lower thoracic spine; count vertebrae form lowest
lumbar vertebral body (identied by direction change of lumbar spine towards
sacrum—promontory—L5/S1)—additional dual image helpful.
(c) Identication of highest level of posterior pelvic crest—usually at level of L4
(axial section).
(d) Identication of lowest rib insertion at level T12 (axial view).
Additional vertebral bodies or sacralisation of a lumbar vertebral body may
Note
cause errors—in these cases an extended view of entire spine or plain lm of entire
spin mandatory.
Sacrum and Coccyx
• Usually not much content in spinal canal, thecal sac ends at S2, may be echogenic due to physiological fat.
• Sacral centres ossify earlier than in coccyx.
• Sometimes lowest coccygeal body bent dorsally, ending in “dorsal dimple”—tail
remnant, a normal variant (Fig.9.2b).

9 US oftheNeonatal Spinal Canal andCord
171
a
bc
Fig. 9.2 Physiologic ndings on spine US. (a) Filum cyst (+ +) in conus or at origin of lum
terminale—also called terminal ventricle or fth ventricle. (b) Dorsally bent distal end of nonossied coccyx—a normal variant. A small sacral skin dimple seen. (c) US in normal sacral dimple
(+ +), with narrow tract leading from skin to distal end of coccyx and anechoic small air bubble at
the deepest part of the sacral dimple tract (arrow)
• If cystic-tubular or band-like structure connects from lowest coccygeal body
upwards dorsally to skin—“sacral porus”, “pilonidal sinus”, may get infected,
sometimes excised, but not to be mistaken for dorsal dermal sinus tract (Fig.9.2c).
9.6 Pathologic Findings oftheSpinal Cord
9.6.1 Dysraphism
Definition
Caused by disruption of development of osseous and neural structures, commonly
combined ndings of meningeal and/or cord pathology and vertebral body anomalies—plain lm of spine helpful.
Pathology may be:
• Obvious/visible (palpable mass with/without cutaneous defect).
• Occult (covered by skin without any visible or palpable mass).
Note Open and visible dysraphic pathology with skin defect very susceptible to
infection, no initial US assessment routinely performed prior to early surgery;
potentially examine higher parts of cord+brain for depiction of associated malformations, add abdominal US (e.g. kidneys and VACTERL malformation).

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M. Riccabona
Myelocele/Myelomeningocele (MMC)
Meninges and/or cord herniated dorsally through defect of posterior arches and
form typical terminal placode (band-like dorsal insertion of conus).
Associated with syringomyelia, diastematomyelia, cerebral ndings (e.g.
Arnold–Chiari malformation):
• Syringomyelia and hydrocephalus may only develop after closure of defect.
US performed only for additional assessment of associated malformations and
postoperatively:
• Follow-up, neurological symptoms with suspicion of tethering, increasing
hydrocephalus, etc.
Lipomyelocele/Myelocystocele/Meningocele
Covered by skin, constitute defect of dorsal containment with herniation of meninges with/without cord through dysraphic defect and potentially associated
with lipoma.
As defects usually covered by skin, initial US possible to dene content (Fig.9.3):
• Lipomeningocele—echogenic tumorous lesion, may be connected to subcutaneous fat and may cause tethering of cord—conus medullaris commonly positioned
caudal to L2.
• Myelocystocele—hydromyelia (dilatation of central canal), often ends in baglike cyst herniated into subcutaneous space. Associated with (partial) sacral
agenesis ⇨ carefully assess lower spine/sacrum and/or perform plain lm.
• Simple meningocele—anechoic CSF-lled cystic structure, caused by herniation
of meninges through posterior defect, usual in lumbosacral region. Can be
through ventral defect—“ventral meningocele”.
Usually not associated with a “simple sacral dimple”, but have other cutane-
Note
ous stigmata: externally visual hyperpigmentation, hairy naevus, mass, etc.—these
ndings as well as posterior cutaneous haemangioma in midline indicate US.
9.6.2 Other Associated Pathology
Dural Lipoma
Positioned sub- or intradural, may be attached to cord dorsally, may completely ll
spinal canal, may reach into central canal and may grow exophytically and cause
mass effect of cord surface.
Symptoms depend on size, position, and affected tissue.
US Findings
More or less echogenic mass (Fig.9.3b). Cord tethering, potentially hydromyelia.

9 US oftheNeonatal Spinal Canal andCord
173
ab
c
Fig. 9.3 US in spinal dysraphism. (a) MMC covered by skin. (b) Tethering of deep-reaching cord
(+ +) attached to intraspinal sacral lipoma. (c) NEW Dermal sinus tract (+ … +), imaged
from dorsal
Fig. 9.4 Spine US pathology. (a) Lipomatous, thickened, and somewhat irregularly shaped lum
(+ +). (b) Deep ending conus with obvious hydro−/syringomyelia (+ +)
Filum Terminale
Thickened lum (either lipomatous or brous) usually attached sacrally, measuring
>2mm diameter (Fig.9.4a) ⇨ cord tethering increases during growth—eventually
conus ends inferior than level of L2. Clinical symptoms comparable to any form of
tethered cord syndrome.

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M. Riccabona
Hydromyelia—dilatation of central canal, in extreme forms called syringomyelia
(Fig.9.4b):
• Primary malformation, or secondary by CSF-drainage/secretion problems.
• Secondary to parenchymal damage and atrophy of cord tissue.
9.6.3 Other “Occult” Dysraphisms
Diastematomyelia
Denition
Complete/partial splitting of cord for one to several segments, varying coverage of
individual hemicord by single or separate meninges, sometimes with central dividing cartilaginous/osseous spur.
US Findings
Best seen in axial views—any spinal cord US always must include axial assessment
(Fig.9.5). At level of diastematomyelia two adjacent cords, usually some hydromyelia cranially; caudally intradural lipoma may be present.
Fig. 9.5 Diastematomyelia. Axial dorsal view in
lower thoracic level: two cords slightly differing in
size adjacent to each other, consistent with
diastematomyelia
Dermal Sinus Tract
Denition
Connection between spinal canal and midline skin surface dimple. Commonly
located lumbosacral, but also cervical or thoracic. Associated epidermoid cysts may
compress cord.
Fistula track facilitates extension of infection from skin into CSF space ⇨ men-
ingitis, subdural abscess.
US Findings
Usually very tiny anechoic lumen of echoic band connecting skin with spinal canal
and may be difcult to visualise lumen if very narrow (Fig.9.3c and 9.6)
Differentiation against pilonidal sinus (no connection to spinal canal)—assess
course of connection:
• Dermal sinus tract usually travels from dorsal cutaneous opening to cranial insertion into spinal canal.
• Sinus pilonidalis typically travels from more cranially from cutaneous dimple to
end of (cartilaginous) coccyx.

9 US oftheNeonatal Spinal Canal andCord
Fig. 9.6 Large dermal sinus tract (from skin into
spinal canal). Sagittal dorsal section at lumbosacral
level: hypoechoic tract disrupting normal (echoic)
skin, coursing from skin at lumbosacral junction
level upwards to eventually enter lumbar spinal
canal, consistent with a large dermal sinus tract
175
Tip Use plenty US gel or Standoff pad.
Caudal Regression Syndrome
Complex malformation, US reveals spinal/cord contribution/involvement, conus
often appears squared or blunted as opposed to normal tapered shape.
• Associated malformations common—perform perineal US, complete abdominal
US and sometimes MRI.
Others
Anterior sacral, lateral, or thoracic and ventral meningoceles—very rare.
9.7 Trauma
Introduction
US only in neonatal period (rst orienting bedside study)—decide on urgency and
necessity of additional imaging.
US Findings
• Extramedullary lesions—usually haemorrhages—typically present as echogenic
extrameningeal space-occupying lesion (e.g. after lumbar puncture) (Fig.9.7a).
Position/size vary as well as potential mass effect on cord. In chronic stages—
similar to chronic subdural hygroma, become anechoic.
• Nerve root pathology: visualisation difcult, depicted by indirect signs/on paravertebral views (e.g. haematoma and swelling).
• Oedema, haemorrhage, necrosis, or disruption of cord: initially hyperechoic,
disruption of normal cord contour and echotexture with oedematous swelling+mass effect of haematoma, disruption of continuity of external borders in
case of rupture (Fig.9.7b).
Usually further assessed by MRI (some by CT).

176
M. Riccabona
Fig. 9.7 Traumatic spinal canal changes visible on US. (a) Sagittal US at lumbar level: extradural
haematoma after lumbar puncture. (b) Sagittal section, thoraco-cervical cord level: birth trauma
with cord disruption and haematoma
9.8 Tumours and Miscellaneous Others
Rare, except for congenital tumours listed above (lipoma, dermoid, epidermoid,
haemangioma, cystic teratoma) (Fig.9.8).
Others: Extraspinal tumours that invade spinal canal—neuroblastoma or metas-
tases of cerebral tumours (see respective chapters, Fig.9.8b). Cause compression of
cord with corresponding symptoms by intraluminal growth. On follow-up one may
observe atrophic cord (Fig.9.8c).
Spinal vascular malformations—rare, difcult to visualise on US, and may dem-
onstrate increased vascularity on CDS.
Other spinal pathology (meningitis, focal lesions in demyelinating disease, pri-
mary nerve tumours): nonspecic changes.
Value of US
• May depict conditions incidentally and may be useful for bedside follow-up after
surgery.
• Restricted potential, not regularly performed—other sectional imaging preferred
(CT/MRI).
Intraspinal Haematoma
Usually traumatic, after lumbar puncture or sedimented from brain CSF space as
seen, e.g. in non-accidental injury (NAI)/inicted trauma.
• Consider additional spinal US in young infants presented with a suspicion of
NAI—not only for a more complete overall picture, but also particularly in
equivocal brain US ndings.
Other Spinal Cord Anomalies
Hydromyelia (see above—of different origin)
Hypoplastic cord, usually the end is higher and rounded—typically in caudal
regression syndrome,

9 US oftheNeonatal Spinal Canal andCord
177
a
b
c
Fig. 9.8 (a) Sacral cystic teratoma. Huge congenital sacral teratoma, with large external as well
as internal portion—reaching up to prelumbar levels. Dual/split image technique used to try to
demonstrate entire extent, dorsal acquisition (note sacral vertebral bodies with beginning ossication in upper left image corner). (b) Paravertebral neuroblastoma (*) inltrating through neuroforamen (arrow) into spinal canal and compressing spinal cord dotted circle), imaged from dorsal in
an axial section. (c) Remnants after spinal cord compression—atrophic cord (arrow), beautifully
visible even in older infant due to surgical removal of posterior arches when decompressing the
spinal cord initially; arrowhead=postoperative clip. Longitudinal paramedian section from dorsal
• Commonly associated with neurologic impairment, particularly concerning
evacuation functions, anomalies of the pelvis, the lower urogenital tract, or anorectal malformations.
Pathology of Paravertebral Structures
Haematoma, lipoma, and abscess formation: see small-part applications.
Disc Pathology
Very rare in childhood.
Discitis may occur—usually manifest in ventral parts and in older child—poorly
accessible by US.
US Findings
Disc looks abnormal and swollen, adjacent tissue oedema (see also above):
• Normal disc: periphery=− anechoic, homogeneous, and ovoid. Centrally more
echogenic nucleus.
• If disc herniates into spinal canal sometimes visible by bulging of contour, however, MRI preferred.
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