Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
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

148
M. Riccabona
• Calcications—after infection and ischemia, particularly in basal ganglia.
• Residual choroid plexus or parenchymal lesions—posthaemorrhagic, postischemic, posttraumatic, etc.
Signs for increased intraventricular and/or intracranial pressure:
• Inhomogenous structure around ventricles, potentially some small hyperechoic
cystic lesions—sign for either focal hypoxia or posthaemorrhagic or venous
infarction (e.g. due to obstruction of draining periventricular veins during ventricular dilatation).
• Ballooning of temporal horn.
• Narrowing of external CSF spaces.
• Ventricles can be very narrow or slit like (e.g. in brain oedema after
hypoxia).
• Extra-axial cause for increased brain pressure due to focal pathology (arachnoid
cyst, subdural/epidural haemorrhage/effusion)—locally compressed parenchyma, attened brain surface and potentially midline shift.
Differentiation epidural/subdural from subarachnoid space:
• Subarachnoid space—reaches into sulci, has network of crossing vessels and
mildly echoic lines.
• Subdural space—does not reach into sulci, usually anechoic and only a few
major bridging veins ⇨ use aCDS.
Note In chronic and recurrent subdural effusion, multiple septae and layers of dif-
ferent echogenicity may occur.
Role of CDS in Increased Intracranial Pressure
Early phase, only slight increase in intracranial pressure—normal or slightly
reduced resistive index (RI) (reactive diastolic hyperaemia), generally increased
ow velocities.
Things change when pressure gets higher:
• Diastolic ow velocity decreasing—elevated RI:
– There may be tent-shaped antegrade diastoly in early phases—similar to
severe hypoxia.
• Systolic velocities decreasing—transient “pseudo-normal” RI.
• Diastole more affected ⇨ reversed diastolic ow, RI>100%:
– Sometimes difcult to differentiate from other systemic reasons
such as PDA.
– Severely increased brain pressure—eventually leads to signicant reduction
of systolic ow velocity and signicant arterial perfusion decit (see also:
brain oedema and brain death).

8 Neurosonography inNeonates, Infants andChildren
149
Other Techniques to Depict Increased Brain Pressure
Fontanellar pressure: apply gentle pressure on fontanel with nger while performing DS of one of the major basal vessels (commonly MCA)—in case of signicantly increased brain pressure rst diastolic and then systolic ow velocities
reduced during manoeuvre (Fig.8.9).
DS of ICA at extra- and intracranial portion from transfontanellar access (Fig.8.31):
fontanellar DS visualises ICA siphon cursing into head (both in coronal and parasagittal view)—place duplex gate for spectral trace in extracranial and intracranial ICA
portion (Fig.8.32), calculate ratio between systolic intra- and extracranial velocities
and RIs (equation=V
intracranially divided by V
syst max
extracranially):
syst max
• Normal—ow spectra do not differ, velocity ratio=1 (0.8–1.2).
• Slightly increased brain pressure (<10mmHg)—slight elevation of systolic ow
velocity intracranially and only mild variation of diastolic ow, velocity
ratio=>1.2.
• Signicantly elevated brain pressure (>10mmHg)=altered systolic+diastolic
ow, velocity ratio<0.8.
US for Following Up Hydrocephalus With/Without Shunts
• All basic US criteria apply.
• Additionally try to visualise shunt drain: course, tip of drain and look for drain
discontinuity.
Note Can be difcult, often transtemporal or transmastoid access necessary
(Fig. 8.33). Tip of shunt may be less echogenic than more peripheral part and
missed, depending on US beam angle and access:
Fig. 8.32 Doppler in hydrocephalus. (a) Slightly elevated brain pressure, indicated by change of
ow prole in intra-/extracranial ICA portion measured from fontanellar access in a coronal section. (b) TCI-Doppler for measuring ow response during fontanellar pressure (“druck”): no signicant change in MCA ow pattern in this preterm baby with posthaemorrhagic hydrocephalus

150
Fig. 8.33 US/TCI in shunted hydrocephalus—mostly used in slightly older infants with (nearly)
closed fontanel. (a) TCI: two drains, one in each lateral ventricle, with different ventricular distension. Note a slight subdural effusion on the side with the smaller ventricle as a sign of overshunting.
(b) TCI, axial view, 9month old infant: shunted hydrocephalus (shunt=arrow), still large ventricles
M. Riccabona
Fig. 8.34 US for assessing complications in shunted hydrocephalus. (a) Linear transducer, neck:
disruption (++) of subcutaneous portion of shunt. (b) Fluid pouch in supercial subcutaneous soft
tissue next to the drain (arrow) that is disconnected
• Always assess valve (effusion?).
• Try to follow extracranial partition of drain (subcutaneous track in skull, neck
and chest easily seen)—disruption—focal uid effusions along drain path due to
leakage/rupture (Figs.8.33a, b and 8.34).
• CDS: only useful if cellular components in CSF (if sound can penetrate—
depending on material of shunt).
• Assess abdominal part of shunt: pseudocyst around intraabdominal tip may
cause obstruction, free peritoneal/pleural uid helps to indicate drain function
(but not a proof of proper drain function!), evaluate for peritonitis in children
with pain, etc. (see respective chapter).
Note US may nd causes of obstruction or dysfunction and can depict size increase
of CSF space or perfusion deterioration due to increased brain pressure. However,
US does not depict/rule out all causes of potential shunt complications, chronically
or moderately increased brain pressure, stiff ventricle syndrome, etc.:
• CDS may show CSF flow in foramina of Monro, Magendie and Luschka and
aqueduct—provided that there are reflectors in CSF (e.g. posthaemorrhagic
particles, increased CSF protein levels and inflammatory cells) (Fig.8.35a, b).

ab
8 Neurosonography inNeonates, Infants andChildren
c
151
Fig. 8.35 Special applications of modern US in hydrocephalus. (a) Magnied fontanellar sagittal
midline view: CDS demonstrates CSF ow in aqueduct. (b) Duplex Doppler trace conrms bidirectional undulating CSF ow. (c) 3DUS in hydrocephalus: three orthogonal views and rendered
lateral ventricles (right lower box)
• Unusual access to extracerebral CSF spaces—use eye/orbit as US window. In
increased intracranial pressure—optic nerve sheet dilatation and protrusion of
papilla (see section/entry: US of eye).
• In CSF fistula: US may demonstrate fistula (if large enough and accessible)
and show flow through fistula by aCDS if particles in CSF or relatively high
flow velocities (cause some jet phenomenon, where one may find intermittent undulating jets that vary with respiration or with other forms of

152
M. Riccabona
increased thoracic pressure, such as, crying, breath hold and ventilation
manoeuvres).
Note For any measurements of CSF spaces, standardised approach with reproduc-
ible measurements should be applied; CSF overdrainage can cause ventricular collapse and secondary subdural haemorrhage/effusion which may clinically mimic
shunt dysfunction and increased brain pressure.
• 3DUS particularly valuable: complete documentation, reproducible measurement at comparable section and comparison to other sectional imaging (any
desired section may be reconstructed from 3DUS data set) (Figs. 8.35c and
respective chapter).
8.3.9 Cerebral Haemorrhage
Various forms of haemorrhage need to be differentiated in terms of location and
aetiology: intra- and extracranial, intra- or extraventricular, parenchymal, extracerebral (sub-galeal haematoma, subcutaneous haematoma, subdural, epidural, subarachnoid, etc.). etc. (Fig.8.36). Type of haemorrhage varies with age: preterms
have different haemorrhages than term neonates or infants.
8.3.9.1 Haemorrhage inPreterm Babies: IVH Grades I–III, PVH
(Fig.8.37)
Typically occur in germinal matrix near head of caudate nucleus, where immature
vessels tend to rupture with only mild trauma, unstable blood pressure and intravascular volume changes, etc.
IVH I: on US echogenic round or oval-shaped area below plexus and head of
caudate nucleus (intraventricular haemorrhage grade I = IVH I)—to be
Fig. 8.36 Scheme: cranial haemorrhages. Typical extra- (a) and intracranial (b) haemorrhages—
site and respective appearance. Abbreviations: SEB/SEH subependymal bleed/haemorrhage, EDH
epidural haematoma, SDH subdural haematoma, ICH intracerebral haemorrhage, IVH intraventricular haemorrhage, SAH subarachnoid haemorrhage and PVH periventricular haemorrhage
(adapted from C. Roll / Datteln Germany)

de
8 Neurosonography inNeonates, Infants andChildren
153
a
b
c
fg
Fig. 8.37 Images and schematic drawings demonstrating classication and image appearance of
brain (intraventricular) haemorrhage in preterms. (a) Scheme plexus bleed and IVH grade I° (subependymal bleed/haemorrhage=SEB/SEH), IVH intraventricular haemorrhage. (b) Scheme IVH
grade II°, III° and IVH+periventricular haemorrhage (=PVH, older term IHV IV°). (c) Parasagittal
view: IVH I°/SEB, clot seen as somewhat echogenic nodular structure (may be difcult to differentiate from plexus haemorrhage). (d) Parasagittal view: IVH II°, huge clot in the plexus, a little
bit of blood in the posterior horn. (e) Coronal view: fresh haemorrhage with blood lling the entire
ventricle lumen=IVH grade III°. (f, g) Coronal view: haemorrhage with periventricular haemorrhagic infarction/PVH on right (f) or left (g) (++) side
differentiated from swollen choroid plexus (also echogenic, but usually entire plexus
affected) or choroid plexus bleeds (occur at any location of plexus, but commonly
close to frontal attachment, located within plexus). For differentiation—axial section or axial 3DUS reconstruction helpful.

154
M. Riccabona
IVH II: if grade I haemorrhage increases, it ruptures into ventricle—some blood
seen in ventricle (grade II haemorrhage). Initially ventricles not dilated, only little
blood or some clotting in ventricle.
IVH III: with progression of haemorrhage ventricles get dilated, increasingly
lled with blood (grade III haemorrhage). Blood also seen in third and fourth
ventricle due to physiological CSF drainage pathways. Due to dilatation of ventricle paraventricular draining veins get compressed/obstructed/congested—
cause venous infarction of periventricular respective areas ⇨ haemorrhagic
infarction.
IVH III + PVH: combination of periventricular haemorrhagic infarction with
grade III haemorrhage (initially called type IV haemorrhage, now classied as
haemorrhage grade III + periventricular haemorrhage = PVH)—attributing new
insight into aetiology and pathophysiology.
8.3.9.2 Haemorrhage inTerm Infants
Much rarer, usually do not occur as IVH but as intraparenchymal haemorrhages
(intracerebral haemorrhage—ICH).
Typical locations: basal ganglia and locations of haemorrhagic venous infarc-
tions (Fig.8.38).
Rare other causes that dene locations—secondary haemorrhage into hypoxic
areas or trauma:
• Epidural haemorrhages—EDH (e.g. after forceps delivery or skull fractures), use
TCI (Fig.8.39).
• Subdural haemorrhages—SDH (consider shaken baby syndrome), linear transducer and TCI helpful (Figs.8.30 and 8.20d).
• Subarachnoid haemorrhages—difcult to see on US unless large; cause increased
echogenicity between the sulci.
• Tentorial bleeds (e.g. after complicated foetal repositioning manoeuvres or
breach delivery) (Fig.8.40).
• Direct impact (trauma), by caesarean section (e.g. cutting too deep, thus injuring
brain through fontanel).
Unexplained haemorrhages in neonates and young infants raise suspicion of
Note
nonaccidental injury (NAI)—thorough workup.
US Appearance
All haemorrhages have similar US appearance and development:
• Hyperacute state: blood has similar echogenicity as surrounding tissue—not seen.
• (Sub)acute state: bright echogenic spot.
• Further course—sedimentation and resorption: inhomogenous with some hyperechoic areas and clot formation—usually inhomogenously echogenic, tumourlike areas (Fig.8.41).

8 Neurosonography inNeonates, Infants andChildren
Fig. 8.38 Examples for other cerebral haemorrhages and DDx. (a, b) Basal ganglia haemorrhage
(echogenic mass) in term infant (a) coronal and (b) (para-)sagittal section. (c, d) DDx in haemorrhage: Echogenic swollen plexus (b, sagittal section) with hypervascularity on CDS (c, coronal
view) in a plexus papilloma
155
Fig. 8.39 Epidural haemorrhage (++). Axial
view—TCI, magnied section: subcalvarian
complex ovaloid uid space-occupying lesion in
terms of a subacute EDH
• Eventually resorbed—cystic remnants, hyperechoic ventricular wall and parenchymal defects (Fig.8.20).
• Impairment of CSF circulation may cause hydrocephalus—careful monitoring
and assess need for CSF drainage:
– Early phase: drainage sometimes achievable by repeated lumbar punctures.
– Later phases: external drainage and shunt placement necessary.

156
M. Riccabona
ab
Fig. 8.40 Tentorial and cerebellar haemorrhage. (a) Coronal section, linear transducer: tentorial
and cerebellar haemorrhage. (b) Same patient as in (a) tilted mastoid-axial view: superior demonstration of bleed
Fig. 8.41 Clot and hydrocephalus after IVH III. (a) Coronal section demonstrating inhomoge-
nously echogenic masses within lateral ventricles obstructing foramen of Monro. (b) Parasagittal
view: demonstrates clots in dilated lateral ventricle after IVH III
Note Every term neonate and young infants with haemorrhage may suffer from
rare underlying disease, e.g. coagulopathies, venous thrombosis, vascular anomalies, underlying tumours, hyperviscosity, hypoxia, ischemia, dehydration, septicaemia and meningoencephalitis. Differentiation by US often difcult or impossible
(e.g. haemorrhagic infarction difcult to differentiate from haemorrhage without
underlying infarction).
8.3.9.3 Role ofCDS inNeonatal Haemorrhage
Doppler and CDS does not help in dening aetiology or predicting haemorrhage,
however, reduced ow velocities and large uctuation of ow spectra with repeated
examinations (due to lack of autoregulation) associated with higher risk of
haemorrhage:
• Only in severe active bleeding increased particularly diastolic ow with reduced
RI seen in feeding vessel.
• Sometimes CDS depicts vascular anomaly that caused haemorrhage.

8 Neurosonography inNeonates, Infants andChildren
157
• CDS helpful for depiction of thrombosis of large venous pathways.
• aCDS is helpful to differentiate swollen choroid plexus (with existing perfusion)
from choroid plexus bleed or clot.
8.3.9.4 Haemorrhage inInfants andOlder Children
After fontanel closure and increasing skull ossication, US possibilities decrease;
particularly detailed assessment of small changes or exclusion of haemorrhage
becomes increasingly difcult and eventually impossible. However, TCI can used
as a rst orientation - but often CT and MRI are mandatory.
US Findings
• Haemorrhage as in transfontanellar view—initially echogenic, relatively sharp
margins.
• As long as US access and penetration possible, large parenchymal bleeds and
large SDH/EDH can be depicted, particularly if it causes some mass effect and
distorts ventricles or midline structures.
Note Do not mistake repeating echoes from (contralateral) skull on transtemporal
images for haemorrhage.
• SDH may be recurrent—thus septae develop, with different echogenicity in various compartments. If chronic—hygroma.
Note Usually brain surface attened and sulci narrow in area of haematoma—in
atrophy sulci enlarged without attening of brain surface. If SDH of different age,
always think of NAI, then try to assess near-eld cortex for depiction of typical
teardrop lesion (resorbed focal venous infarctions) in (sub)cortical area—may be
missed if only sector array used (Fig.8.20).
• Cerebellar and tentorial haemorrhages rare, also bleeds of brain stem and other
posterior fossa structures. Difcult for US once skull ossied. Usually have poor
prognosis.
• Transmastoid, -occipital and -temporal access mandatory when evaluating these
potential pathologies.
In older children with appropriate history or symptoms, emergency imaging
Note
by CT and/or MRI indicated.
• Helpful application: assessment of skull and galea by high-resolution linear
transducers. Haematoma seen, formation of seroma can be documented and
measured, skull fractures—even if only subtle—usually nicely depicted by
showing disruption of skull surface echo (Fig.8.42).
• Skull US also helpful for assessment of other skull or skin lesions; e.g. epithelial
cysts, histiocytosis, eosinophilic granuloma, metastases, and in some places also
applied for assessment of craniosynostosis.
Соседние файлы в папке Библиотека им академика М.И. Перельмана
