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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

258
bc
M. Riccabona
a
de
Fig. 12.19 PAE and pulmonary perfusion decit: (a) Axial view, infant after Glen procedure—
with peripheral pneumonia-like oedematous lung. (b) Same child as in (a): note severe postoperative perfusion decit of one lung. (c) Axial view through liver: Large infarction, no air
sonobronchogram as would be seen with infection. (d) Dorsal scan through intercostals space:
triangular subpleural pneumonia-like lung area, typical for infarction induced pneumonia. (e) CDS
demonstrates lack of perfusion in the peripheral triangular subpleural consolidation
Fig. 12.20 Lung tumour. Axial view: chest lled
with partially cystic tumour that turned out to be
a pulmonary blastoma
• Pneumonia, atelectasis: CDS helpful for showing normal vascular supply allow-
ing differentiation from infarction or depiction of necrotic area before typical
abscess formations manifest.
• Supercial/pleural/soft tissue arteriovenous malformation: CDS irreplaceable for diagnosis.
DDx Any other cause of non-aerated lung, particularly CCAM, sequestration,
pneumonia, abscess, complicated cysts and hernia:
• In medial/mediastinal aspect: thymus versus lymphoma, etc.
• Extremely rare intrathoracic kidney (normal kidney in atypical location):
– Typical renal vascularisation pattern—undisputable diagnosis.

12 Ultrasound oftheChest
259
12.7 Other Miscellaneous andRare Applications
Many more partially rare applications reported: Most relevant ones listed.
12.7.1 US forInterstitial Lung Disease/
Alveolar-Interstitial Syndrome
Increased extravascular lung water, but also thickened interstitium creates
“B-line” on lung US; however, a few B-lines can be found in a healthy population—particularly in newborn and infants (due to physiologic immature lung
histology):
• B-lines are vertical, sharply dened hyperechoic lines and structures without
decrease in brightness with depth (ring-down artefact) (Fig.12.21).
• Low-frequency convex transducer detects more B-lines than high-frequency lin-
ear transducers; other settings such as compounding or harmonic imaging also
affect appearance of B-lines.
• Multiple B-lines suggest (alveolo-)interstitial lung syndrome (Fig.12.21a).
• Non-specic in terms of aetiology—wide variety of conditions (pulmonary
oedema, ARDS, pulmonary contusion, pneumonia, pulmonary brosis, etc.)
(Fig.12.21b–d).
• B-lines correlate with CT abnormalities (e.g. thickened interlobular septa and
ground-glass opacities—closely packed B-lines).
Note Differentiate those appearances from other pathology such as pneumonia,
atelectasis or effusion/empyema (Fig.12.21f, g), and search for possible transition
zones with a (double) lung point (Fig.12.21e). Remember that those ndings may
be unspecic, but often very valuable in conjunction with clinical information and
symptoms.
12.8 Additional Imaging
Plain lm, CT, sometimes (and increasingly) MRI:
• Rarely angiography (vascular malformations) or uoroscopy.
• Role/value of US exquisite for follow-up of effusions or diaphragmatic palsy:
– Image-guided interventions: diagnostic or therapeutic puncture (in effusions,
abscess, chylothorax, haematothorax, tumour biopsy, etc.).
Note US has limitations in the chest—complementary imaging tool. Plain lm
often initially compulsory or more easily available and reliable. But for some situations and queries US has become the primary imaging tool and has reduced number

260
M. Riccabona
a
c
d
b
gef
Fig. 12.21 Different B-line appearance in different scenarios: (a) Grouped B-lines in dystelecta-
sis/alveolo-interstitial syndrome. (b) More bulky appearance in a child after aspiration. (c) Diffuse
and inhomogeneous B-lines in a baby with RSV bronchiolitis—with some mild effusion. (d)
Homogenous packed B-lines in secondary RDS (“white lung”). Note the difference to other
pathology, e.g. to A-lines with a stratosphere (or barcode) sign on M-mode in pneumothorax—
with an obvious lung point at transition to ventilated lung (arrow) (e), an atelectatic consolidation
with airsonobronchogram (f), or a neonatal pneumonia with complicated effusion (g)
of lms in follow-up helping to reduce overall radiation burden to paediatric
population.
US often used for work-up of in equivocal ndings and may help tailor further
imaging, decide on method or modify protocol (e.g. white hemithorax) (Fig.12.22).
Include assessment of lung base in upper abdominal US and FAST
examinations.

12 Ultrasound oftheChest
261
Fig. 12.22 Case examples where US was helpful to further dene the cause of equivocal chest
lm ndings: White hemithorax on chest lm (a). US reveals a partially atelectatic, partially pneumonic lung with elevated position of the diaphragm (b). The pulmonary vessels are well perfused
on CDS, no sign of tumour, only slight effusion. (c) Atypical opacication of right lower lung on
plain lm: (d) US demonstrates collapsed lung with secondary pneumonic changes in a child after
aspiration

Upper Abdominal US inNeonates,
Infants andChildren: (Excluding the
13
Kidneys)
MichaelRiccabona
13.1 Introduction
Liver, bile system, spleen and pancreas are common queries in paediatric US.Agedependent differences in appearance and size need to be noticed, also different
queries than encountered in adults.
13.2 Requisites andInvestigation
13.2.1 Preparation
Fasting helpful for sufcient lling of gall bladder and bile duct assessment, as well
as for assessing splanchnic perfusion in a standardised fashion.
Additional provocation by feeding during investigation helpful to enhance visualisation of intrahepatic and extrahepatic bile ducts and allows for assessment of
gall bladder emptying.
For quantitative assessment of liver perfusion (portal vein velocity and hepatic
artery ow—e.g. query portal hypertension) child must be fasted to avoid ow alterations from increased splanchnic activity and ow mimicking pathology or masking
disease.
Tip Fasted means no food, no drink, no chewing gum, no sweets, no smoking, etc.
M. Riccabona (*)
Department of Radiology, Division of Pediatric Radiology, Medical University Graz
and University Hospital Graz, Graz, Austria
e-mail: michael.riccabona@medunigraz.at
© Springer Nature Switzerland AG 2020
M. Riccabona (ed.), Pediatric Ultrasound,
https://doi.org/10.1007/978-3-030-47910-7_13
263

264
M. Riccabona
13.2.2 Positioning
Conventionally supine position.
• In small children positioning manoeuvres difcult.
• Potentially intercostal access necessary.
• Manoeuvres can be attempted, instructing child “to show a big tummy” or “take
a deep breath and hold it like you were diving” or similar child-adapted wording,
sometimes mandatory to depict or differentiate ndings (e.g. gallstones, etc.).
13.2.3 Transducers
Usually curved arrays of age-adapted frequencies used, but may not work well for intercostal access (children do not like pressure on ribs)—for these applications and sometimes assessing deeper compartments or subdiaphragmatic areas, sector array helpful.
Linear transducers recommended for assessing liver surface and details of parenchymal structure as well as common bile duct and gall bladder wall; furthermore, in
small children or infants these can be used as primary transducers. High-resolution
linear arrays (potentially using trapezoid format) recommended in neonates and infants.
Frequency range depends on age and size (18–2MHz).
Harmonic imaging, image compounding, speckle reduction and other sophisticated post-processing options helpful. Thorough study always includes colour and
spectral Doppler analysis; aCDS less useful in liver or pancreas.
Note For improving lesion detection and characterisation, intravenous US
particularly helpful—although currently no UCA registered for paediatric
use in Europe (only in USA approved for paediatric liver applications).
13.3 Liver
13.3.1 Course ofInvestigation
Liver usually assessed from ventral and lateral, rarely dorsal approach necessary or
helpful. Systematically sweep through entire liver in sagittal, axial and oblique sections. Follow course of major structures (portal vein, liver veins), assess gall bladder
and eventually add Doppler if indicated.
Small children do not respond to positioning commands—use respiration or asking
them to “take deep breath” may enable assessment, particularly of subdiaphragmatic areas.
13.3.2 Standard Planes
• Sagittal section in sternal line (STL), left and right in middle clavicular line (MCL)
and right ventral (= anterior), middle and posterior axillary line (V/M/PAL).

13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
265
• Axial sections particularly focused on portal vein and hilar structures—from
ventral and lateral approach.
• Oblique sections tilted cranially for meticulously scanning entire liver, particu-
larly for documentation of portal vein branching, hepatic veins and gall bladder.
• Standardised documentation (VAL—dened by upper pole of right kidney,
MCL—commonly dened by gall bladder, STL—dened by abdominal aorta),
section through hepatic veins, portal vein branching, main portal vein (if not
included gall bladder view) (Fig.13.1) (www.oegum.at).
Note Due to complexity of the liver, documentation and measurements in stan-
dardised sections are essential. For identication of section—include other key
structures on image, particularly important for comparison during follow-up.
Fig. 13.1 Standard liver measurements and liver segments: (a) Liver anatomy with liver segments
(I–VIII), relevant liver vessels for anatomical classication (portal vein, hepatic vein, inferior vena
cava) and standard planes for US measurements, particularly right anterior axillar line (AL), right
and left middle clavicular line (r/lMCL) and medially positioned sterna line (STL). Two respective
normal sagittal views with important reference structure (upper pole of right kidney for AL,
abdominal aorta for STL) given. (b) Standard image appearance of typical liver sections: the transducer position and orientation given in the schematic drawing, with respective US images

266
Table 13.1 Normal liver size in relation to age/height
Measurements of body height related (cm) to normal liver size (cm) during childhood
M. Riccabona
13.3.3 Normal Findings
13.3.3.1 Structure
Liver has larger right and smaller left lobe, internal architecture classied by liver
segments (Fig.13.1).
Parenchyma—homogenous echo of medium echogenicity, contour and borders
as well as sharp and smooth margins. Size varies with age, particularly height—
measurements correlated with normograms (Table13.1).
Note Physiologically left liver lobe much larger in neonates than in older ages; it
gradually shows relative decrease in size after closure of ductus venosus.
13.3.3.2 Ligaments
Ligamentum falciforme hepatis, ligamentum teres hepatis and ligamentum triangulare hepatis x liver within abdomen, usually only seen with ascites.
13.3.3.3 Hepatic Veins (HV)
Converge cranially to drain into subdiaphragmatic inferior cava vein (ICV) or into
right atrium. Usually three main liver veins (+ caudate vein); additional veins or
varied insertion at different levels of intrahepatic ICV exist as normal variants. Size
may vary with respiration and intravascular volume—usually exhibit smooth border
and straight course, with relatively thin low echogenicity wall.
13.3.3.4 Portal Vein (PV)
Enters at hepatic hilus, should not show tapering (would be a sign of portal hypertension). Branches between left and right PV in liver centrally, left PV shows focal
ectasia (Rex recessus, sinus venosus) at area of former insertion of umbilical vein
draining via venous duct of Arantii (ductus venosus) to right atrium during foetal
circulation. Wall slightly more echogenic, partially increased by periportal structures (bile ducts, accompanying arteries). Periportal region gets enlarged and more

abc
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
Fig. 13.2 Neonatal liver: (a) Physiologic persistent ductus venosus (++). (b) Flow and patency
of neonatally persistent ductus venosus depicted by CDS—ow direction documented by Doppler
trace. (c) Still visible umbilical vein with catheter (arrow)
267
echogenic in various conditions or may appear prominent with decreased echogenicity of liver parenchyma.
Note In neonates (during rst weeks of life), communication may persist between
sinus venous and ICV/right atrium (“physiologically persistent ductus venous”
Fig. 13.2a)—should obliterate spontaneously. Persistent ductus venosus usually
indicates underlying liver disease with increased peripheral liver resistance.
Umbilical vein may be visible in neonates physiologically, but shows no ow—
consequently thromboses and vanishes; persisting (inverted) ow in umbilical
vein—sign for portal hypertension and consequent portosystemic shunt. A nonfunctioning umbilical vein catheter may end in this vein—actively search for it
(Fig.13.2b).
13.3.3.5 Hepatic Artery (HA)
Can be followed from its origin at coeliac trunk parallel to PV to branching into left
and right HA.
Usually CDS enables easy identication and differentiation from other tubular
structures, particularly in liver periphery, where differentiation of HA from (dilated)
intrahepatic bile ducts is otherwise difcult.
Numerous normal variants in HA anatomy, e.g. accessory left HA from coe-
Note
liac trunk or gastric artery, separate origin of right HA from superior mesenteric
artery. CDS particularly valuable for assessing these anatomic variants.
13.3.3.6 Gall Bladder
Positioned on lower surface of liver, centrally close to hilus on right side. Usually
shows thin wall, contents unechoic. Size can vary with time since feeding. Best seen
in subcostal oblique view in MCL.
Note
An empty or poorly lled gall bladder, particularly if relatively large when
lled, may show a pseudothickened wall (Fig.13.3a) and can be difcult to depict
(e.g. in a gaseous abdomen of a crying neonate).

268
M. Riccabona
Fig. 13.3 Bile system: (a) Normal, nearly empty gall bladder (+…+) with pseudothickening of
wall. (b) Normal common hepatic duct (
tion shows pancreatic portion of prominent common bile duct
3, 2
++), conuence with cystic duct (1++). (c) Axial sec-
13.3.3.7 Common Bile Duct
Commonly Addressed asHepato-Choledochal Duct
Usually crosses main PV and runs through head of pancreas to papilla/ampulla
of Vater.
Note Duct (even ductus cysticus) often visible using high-resolution linear trans-
ducers (Fig.13.3b, c).
13.3.3.8 Intrahepatic Bile Ducts
Course parallel to PVs—usually only depicted centrally or if dilated.
13.3.3.9 Doppler Findings
Hepatic Veins (HV)
Show bi- or triphasic undulating ow pattern, bidirectional ow direction.
Undulation caused by respiration and heart cycle (Fig.13.4a). Absence of typical
pattern usually indicates either increased liver resistance or increased right atrial
pressure/volume overload.
Note Flow proles may vary within the three main veins, also depends on point of
insertion and manoeuvres used for visualisation (such as breath holding). Undulation
must always persist; bidirectional or triphasic pattern may physiologically be absent.
Portal Vein (PV)
Usually shows constant ow into liver with some mild respiratory modulation
(Fig.13.4b–d).
Flow velocities vary with age (Table13.2a) and fasting status.
Note Also main intrahepatic PV branches should be assessed to show patency of at
least main right and main left PV. Flow velocity measurements strongly rely on
proper angle correction and good insonation angle (<60°).
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