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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5790_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Acknowledgements
- •Contents
- •1: Theory and Basics
- •1.1.2.3 Reflection
- •1.1.2.4 Absorption
- •1.1.2.5 Deflection
- •1.1.2.6 Focus
- •1.1.2.7 Resolution
- •1.2 Practical Application in US Device
- •1.2.1 Emission, Transmission, Reception and Amplification
- •1.2.1.1 Emission
- •1.2.1.2 Transmission
- •1.2.1.3 Reception
- •1.2.1.4 Amplification
- •1.2.2 Signal Processing
- •1.2.2.1 Preprocessing
- •1.2.2.2 Post-processing
- •1.2.2.3 Time Gain Compensation (TGC)
- •1.2.2.4 Sound Energy = Output
- •1.2.2.5 Gain
- •1.2.2.6 Frame Rate/Persistence
- •1.2.3 Components of US Device
- •1.2.3.1 Transducers
- •Sector Transducers
- •Linear Array Transducers
- •Curved Linear Array
- •Other Transducers
- •1.2.3.2 Other Parts of US Device
- •1.3 US Methods
- •1.3.1 A (Amplitude)-Mode
- •1.3.2 (T)M-Mode (Time-Motion-Mode)
- •1.3.3 B (Brightness)-Mode
- •1.3.4 Doppler Sonography
- •1.4 Artefacts
- •1.4.1 General Remarks
- •1.1 Ultrasound (US) Physics
- •1.1.1 US Waves
- •1.1.2 Propagation and Modulation of US
- •1.1.2.1 Acoustic Impedance
- •1.1.2.2 Impedance Change
- •1.4.2 Common Artefacts
- •1.4.2.1 Side Loop Artefact
- •1.4.2.2 Bowing Artefact
- •1.4.2.3 Noise
- •1.4.2.4 Marginal Shadowing
- •1.4.2.5 Posterior Enhancement – Increased Through Transmission
- •1.4.2.6 Reverberation Artefact
- •1.4.2.7 Increment or Slice Thickness/Beam Width Artefact
- •1.4.2.8 Mirror Image Artefact
- •1.4.2.9 Shadowing
- •1.4.2.10 Refraction Artefact
- •1.4.2.11 Anisotropy
- •1.5 Biologic Effects
- •1.5.1 General Remarks
- •1.5.2 Thermal Effects
- •1.5.2.1 Tissue Heating
- •1.5.2.2 Biological Effects, Tissue Heating
- •1.5.3 Mechanical Effects and Resonance
- •1.5.3.1 Cavitation
- •Acoustic Cavitation
- •Negative Peak Pressure
- •1.5.4 Potential Risks of Diagnostic US
- •1.5.4.1 Specific Risks
- •1.5.4.2 Guidelines and Recommendations
- •1.5.5.1 Mechanical Index (MI)
- •1.5.5.2 Thermal Index (TI)
- •1.5.5.3 Display of Actual Indices
- •1.6 How to Perform Paediatric US
- •1.6.1 Requisites
- •1.6.1.1 Indications
- •1.6.1.2 Environmental Requisites
- •1.6.1.3 Specific Needs in Children
- •1.6.1.4 Specific Needs in Infants and Newborns
- •1.6.2 Positioning
- •1.6.3 Device Handling
- •1.6.4 Transducer Selection
- •1.6.4.1 General Remarks
- •1.6.4.2 Neurosonography
- •1.6.4.3 Small Part US
- •1.6.4.4 Chest US
- •1.6.4.5 Abdominal US
- •1.6.5 Course of Investigation and Measurements
- •1.6.5.1 General Remarks
- •1.6.5.2 Transducer Handling
- •1.6.5.3 Measurements
- •1.7 Documentation and Interpretation
- •1.7.1 Image Documentation
- •1.7.2 Report
- •1.7.2.1 How to Issue a Report
- •1.7.2.2 Diagnosis
- •1.7.2.3 Predefined Reports
- •1.7.2.4 Nomenclature
- •1.8 Doppler Sonography
- •1.8.1 The Doppler Phenomenon
- •1.8.2.1 Continuous Wave Doppler (CW)
- •1.8.2.2 Pulsed Wave Doppler (PW)
- •1.8.2.3 Duplex-Doppler Sonography
- •1.8.2.5 Amplitude-Coded Colour Doppler Sonography (aCDS)
- •1.8.2.6 Other Flow-Sensitive US Techniques
- •1.8.2.7 Important Parameters and Measurements (Fig. 1.16)
- •1.8.3 Artefacts in (Colour) Doppler Sonography
- •1.8.3.1 Aliasing
- •1.8.3.2 Spectral Broadening
- •1.8.3.3 Sample Volume Artefact
- •1.8.3.4 Filtering Artefacts
- •1.8.3.5 Scaling Problems
- •1.8.3.6 Gain-Induced Errors
- •1.8.3.7 Angle Correction
- •1.8.3.8 Motion Artefact
- •1.8.3.9 Twinkling Artefact
- •1.8.3.10 Others
- •1.8.4 How to Perform (Colour) Doppler Investigations
- •1.8.5 Limitations
- •1.8.6 Interpretation
- •1.9 Modern and Future US Methods and Techniques
- •1.9.1 High-Resolution US (HR-US)
- •1.9.2 Image Compounding
- •1.9.3 Harmonic Imaging (HI)
- •1.9.4 Extended Field of View US
- •1.9.5 US Texture Analysis
- •1.9.6 Sonoelastography
- •1.9.7.1 Basics
- •1.9.7.2 Applications
- •Contrast-Enhanced Voiding Urosonography (ce-VUS)
- •Other Intracavitary Use of ce-US: Sono-Genitography, Sonographic Pyelography, Etc.
- •Intravenous ce-US (CEUS)
- •Future ce-US Potential
- •1.9.8 Three- and Four-Dimensional US (3D-/4DUS)
- •1.9.8.1 Physics and Techniques
- •1.9.8.2 Typical Paediatric 3DUS Applications
- •Neonatal Neurosonography
- •3DUS of the Kidney
- •Urinary Bladder 3DUS
- •3DUS of the Paediatric (Female) Genitalia
- •Musculoskeletal 3DUS Applications
- •Small Part 3DUS Applications
- •Other Potential 3D-/4DUS Applications
- •1.9.8.3 Benefits of 3D-/4DUS
- •1.9.8.4 Restrictions of 3D-/4DUS
- •2: Ultrasound-Guided Interventions
- •2.1 General Aspects
- •2.1.1 Requisites
- •2.1.1.1 Other Important Needs
- •2.1.2 Precautions and Preparations
- •2.2 US-Guided Filling of Structures for Diagnostic or Therapeutic Purpose
- •2.2.2 Diagnostic Sonographic Enema
- •2.2.3 Therapeutic Sonographic Enema
- •2.2.4 US Genitography
- •2.2.5 Contrast-Enhanced Voiding Urosonography (ce-VUS)
- •2.2.6 Other Intracavitary Contrast Applications
- •2.2.7 Intravenous ce-US
- •2.3 Biopsies and Punctures
- •2.4 Drainage
- •2.5 Vascular Access
- •2.6 Lumbar Puncture
- •2.7 Foreign Body Removal
- •3: Neurosonography in Neonates, Infants and Children
- •3.1 Requisites
- •3.1.1 Equipment and Transducer Needs
- •3.1.2 Indications for Brain US
- •3.1.3 How to Investigate
- •3.2 Normal Findings
- •3.2.1 Transfontanellar Access
- •3.2.2 Alternate Access Findings
- •3.2.3 Colour Doppler Sonography (CDS)
- •3.2.4 Normal Variances in Preterm Babies
- •3.2.4.1 Periventricular Echogenicities
- •3.2.4.2 Ventricular Asymmetry
- •3.2.4.3 Ventriculomegaly
- •3.2.4.4 Cisterna Magna
- •3.2.4.5 Vascular Variations
- •3.3 Pathologic Findings
- •3.3.1 Neural Tube Defects
- •3.3.1.1 Anencephaly
- •3.3.1.2 Meningomyelocele and Encephalocele
- •3.3.1.3 Arnold Chiari Malformation
- •3.3.1.4 Dandy-Walker Malformations
- •3.3.1.5 Corpus Callosum Malformations
- •3.3.1.6 Lipoma
- •3.3.2 Migration and Gyration Alterations and Disturbances
- •3.3.2.2 Megalencephaly
- •3.3.2.3 Schizencephaly
- •3.3.2.4 Holoprosencephaly
- •3.3.2.5 Hydranencephaly
- •3.3.3 Phakomatoses
- •3.3.4 Cerebral Cysts
- •3.3.5 Ischemic Encephalopathy
- •3.3.5.1 Preterm Infant
- •3.3.5.2 Global or Diffuse Brain Oedema
- •3.3.5.3 Focal Hypoxemia and Ischemia
- •3.3.5.4 (C)DS in Brain Hypoxia
- •3.3.6 Inflammation
- •3.3.6.1 Prenatal Intrauterine Infections and Residuals
- •3.3.6.2 Postnatal Inflammation
- •3.3.7 Dilatation of CSF Spaces: Hydrocephalus
- •3.3.8 Cerebral Haemorrhage
- •3.3.8.2 Haemorrhage in Term Infants
- •3.3.8.3 Role of CDS in Neonatal Haemorrhage
- •3.3.8.4 Haemorrhage in Infants and Older Children
- •3.3.9 Tumours and Space-Occupying Lesions
- •3.3.9.1 Vascular Malformations
- •3.3.10 Cerebral Calcifications
- •3.4 Ultrasound of the Skull
- •3.4.1 Introduction
- •3.4.2 Haematoma
- •3.4.3 Space-Occupying Lesions and Tumours
- •3.4.4 Skull Fracture
- •3.5 Additional Imaging
- •3.5.1 Plain Film
- •3.5.2 CT
- •3.5.3 MRI
- •3.5.4 Catheter Angiography
- •3.5.5 Additional Supporting Procedures
- •3.6 Ultrasound of the Eye and the Orbit
- •3.6.1 Introduction
- •3.6.2 Normal Findings
- •3.6.3 Sonographically Depictable Pathology
- •3.7 Ultrasound of the Spinal Canal
- •3.7.1 Requisites
- •3.7.2 Transducers and Technique
- •3.7.3 Indications
- •3.7.4 Normal Findings
- •3.7.5 Pathologic Findings of the Spinal Cord
- •3.7.5.1 Dysraphism
- •3.7.5.2 Other Associated Pathology
- •3.7.5.3 Other “Occult” Dysraphisms
- •3.7.6 Trauma
- •3.7.7 Tumours
- •3.7.8 Other Spinal and Vertebral Pathology
- •3.7.9 Additional Imaging
- •3.7.10 Value of US
- •4: Ultrasound of the Neck
- •4.1 Indications, Requisites and Techniques
- •4.1.1 Transducers
- •4.1.2 Positioning and Handling
- •4.1.3 Typical Examinations
- •4.1.3.1 Cervical Lymph Nodes
- •4.1.3.2 Glands
- •4.1.3.3 Cervical Arteries
- •4.1.3.4 Cervical Veins
- •4.1.3.5 Intervention
- •4.2 Normal Findings
- •4.2.1 Lymph Nodes
- •4.2.2 Cervical Glands
- •4.2.2.1 Thyroid Gland
- •4.2.2.2 Parotid, Submandibular and Sublingual Glands
- •4.2.3 Other Cervical Soft Tissues
- •4.2.3.1 Muscles
- •4.2.3.2 Tonsils
- •4.2.3.3 Tongue
- •4.2.3.4 Para- and Retropharyngeal Spaces
- •4.2.3.5 Larynx
- •4.2.4 Cervical Vessels
- •4.3 Pathologic Findings
- •4.3.1 Lymph Nodes
- •4.3.2 Pathology of Cervical Soft Tissue
- •4.3.2.1 Malformations
- •Cervical Cyst
- •Dermoid Cyst
- •Duplication Cysts
- •Thymic Cyst
- •Cervical Ectopic Thymus
- •4.3.2.2 Tumours
- •Haemangioma
- •Lymphatic Malformation
- •Other Mesenchymal Tumours
- •Neuroblastoma, (Ganglio-)Neuroma, Neurofibroma and Other Nerve (Sheath) Tumours
- •Teratoma
- •Other Malignant Tumours
- •Role of US
- •4.3.2.3 Abscess Formations
- •4.3.2.4 Traumatic Changes
- •Haematoma (Including Sternocleidomastoid Muscle “Haematoma”)
- •4.3.3 Thyroid Gland
- •4.3.3.1 Cystic Changes
- •4.3.3.2 Malformations
- •4.3.3.3 Inflammation
- •4.3.3.4 Other Conditions
- •Hypothyroidism/Struma Diffusa/Colloides (Fig. 4.17)
- •Nodular Goitre
- •Amyloid Goitre
- •Adenoma/Carcinoma
- •4.3.4.1 Inflammation
- •4.3.4.2 Cysts
- •4.3.4.3 Calcifications/Sialolithiasis
- •4.3.4.4 Tumours
- •4.3.5 Cervical Vessels
- •4.3.5.1 Arteriosclerosis
- •4.3.5.2 Dissection
- •4.3.5.3 Stenosis
- •4.3.5.4 Other Vascular Anomalies
- •4.3.5.5 Thrombosis and Occlusion
- •5: Basics of Paediatric Echocardiography
- •5.1 Introduction
- •5.2 Equipment Needs and Specific Considerations
- •5.2.1 Transducers
- •5.2.2 Standard US Techniques
- •5.2.3 Patient Position
- •5.2.4 Sedation
- •5.3 Standard Planes and Standardised Course of Examination
- •5.4 Normal 2D Echocardiogram Findings
- •5.4.1 Parasternal Views
- •5.4.1.1 Parasternal Long Axis View (Fig. 5.2)
- •5.4.1.2 Parasternal Short Axis Views (Figs. 5.3 and 5.4)
- •5.4.2 Apical Views
- •5.4.3 Subcostal Views
- •5.4.3.1 Sagittal Subcostal View
- •5.4.3.2 Subcostal Four-Chamber View (Fig. 5.6)
- •5.4.4 Suprasternal View (Fig. 5.7)
- •5.5 Other Techniques
- •5.5.1 M (Motion)-Mode Echocardiography
- •5.5.2 Doppler Sonography
- •5.5.2.1 CDS with 2DUS
- •5.5.2.2 PW- and CW-Doppler
- •5.5.2.3 Calculation of Pressure ( P) Gradients ( P 1 Minus P 2)
- •5.5.3 Other Calculations and Functional Parameters
- •5.6 Special Echocardiographic Techniques
- •5.6.1 Transoesophageal Echocardiography (TEE)
- •5.6.2 Three-Dimensional (3D) Echocardiography
- •5.6.3 Tissue Doppler Imaging (TDI)
- •5.6.4 Contrast-Enhanced US
- •5.7 Normal Values
- •5.8 Pathologic Findings
- •5.8.1 Congenital Heart Defects with Left-to-Right Shunt
- •5.8.1.1 Atrial Septal Defect (ASD)
- •5.8.1.2 Atrioventricular Septal Defects (AVSD)
- •5.8.1.3 Ventricular Septal Defects (VSD)
- •5.8.1.4 Patent Ductus Arteriosus of Botalli (PDA)
- •5.8.1.5 Persistent Truncus Arteriosus (Truncus Arteriosus Communis)
- •5.8.2 Obstructions of Left Ventricular Outflow
- •5.8.2.1 Aortic Valve Stenosis (AS)
- •5.8.2.2 Subaortic Stenosis (Sub AS)
- •5.8.2.3 Supravalvular Aortic Stenosis
- •5.8.2.4 Aortic Coarctation (CoA)
- •5.8.2.5 Interrupted Aortic Arch
- •5.8.3 Obstructions of the Right Ventricular Outflow
- •5.8.3.1 Isolated Pulmonary Valve Stenosis (PS)
- •5.8.3.2 Subvalvular Pulmonary Stenosis
- •5.8.3.3 Supravalvular Pulmonary Stenosis
- •5.8.4 Miscellaneous Congenital Heart Defects
- •5.8.4.1 Transposition of Great Arteries (TGA)
- •5.8.4.2 Total Anomalous Pulmonary Venous Return (TAPVR)
- •5.8.4.3 Univentricular Heart (UVH)
- •5.8.4.4 Double Outlet Right Ventricle (DORV)
- •5.8.4.5 Ebstein Anomaly
- •5.8.4.6 Cor Triatriatum
- •5.9 Acquired Paediatric Heart Diseases
- •5.9.1 Cardiomyopathies (CMP)
- •5.9.1.1 Hypertrophic CMP
- •5.9.1.2 Hypertrophic Obstructive CMP (HOCMP)
- •5.9.1.3 Dilated (Congestive) CMP
- •5.9.1.4 Restrictive CMP
- •5.9.2 Acute Myocarditis
- •5.9.3 Acute (Infective) Endocarditis
- •5.9.4 Pericarditis/Pericardial Effusion
- •5.9.5 Kawasaki Disease
- •5.9.6 Intracardiac Thrombi
- •5.9.7 Cardiac Tumours
- •5.10 Complementing Investigations
- •5.10.1 Cardiac Catherisation and Angiography
- •5.10.2 Cardiac MRI and CT
- •5.11 When to Do What
- •5.11.1 Imaging in Typical Clinical Scenarios
- •5.11.1.1 Typical Orientating Examination
- •5.11.1.2 Typical Clinical Queries
- •5.11.2 Trauma and Emergency
- •6: Ultrasound of the Chest
- •6.1 Requisites
- •6.1.1 Transducers
- •6.1.2 Positioning
- •6.1.3 Indications
- •6.1.4 How to Perform Chest US
- •6.2 Normal Findings
- •6.2.1 Chest Wall
- •6.2.2 Breast
- •6.2.3 Pleural Space
- •6.2.4 Diaphragm
- •6.2.5 Lung
- •6.2.6 Mediastinum
- •6.2.6.1 Anterior Mediastinum/Thymus
- •6.2.6.2 Middle Mediastinum
- •6.2.6.3 Posterior Mediastinum
- •6.2.7 CDS
- •6.3 Pathology of Chest Wall
- •6.3.1 Aplasia, Variations of Ribs
- •6.3.2 Congenital Malformations
- •6.3.3 Traumatic Changes
- •6.3.4 Chest Wall Tumours
- •6.3.4.1 Lymphangioma (veno-lymphatic vascular malformation)
- •6.3.4.2 Lipoma
- •6.3.4.3 Fibroma/Neurofibroma
- •6.3.4.4 Other Tumours
- •6.3.5 Breast
- •6.3.6 Role of US and Additional Imaging
- •6.4 Pathology of Pleural Space
- •6.4.1 Pleural Effusion
- •6.4.2 Empyema
- •6.4.3 Other Pleural Pathology
- •6.4.4 Role of Imaging
- •6.5 Pathology of Diaphragm
- •6.5.1 Diaphragmatic Hernia
- •6.5.2 Diaphragmatic Motion Disturbance
- •6.5.3 Role and Potential of Imaging
- •6.6 Lung Pathology
- •6.6.1 Pneumonia
- •6.6.2 Lung Abscess
- •6.6.3 Atelectasis
- •6.6.5 Sequestration
- •6.6.6 Congenital Cystic Adenomatoid Malformation (CCAM)
- •6.6.7 Cysts
- •6.6.8 Infarction
- •6.6.9 Tumours and Space-Occupying Lesions
- •6.7 Other Miscellaneous and Rare Applications
- •Many More Partially Rare Applications Reported: Most Relevant Ones
- •6.7.1 US for Interstitial Lung Disease
- •6.7.2 US for Pneumothorax
- •6.8 Additional Imaging
- •7: Liver and Bile System
- •7.1 Requisites and Investigation
- •7.1.1 Preparation
- •7.1.2 Positioning
- •7.1.3 Transducers
- •7.1.4 Course of Investigation
- •7.1.5 Standard Planes
- •7.2 Normal Findings
- •7.2.1 Structure
- •7.2.2 Ligaments
- •7.2.3 Hepatic Veins (HV)
- •7.2.4 Portal Vein (PV)
- •7.2.5 Hepatic Artery (HA)
- •7.2.6 Gall Bladder
- •7.2.8 Intrahepatic Bile Ducts
- •7.2.9 Doppler Findings
- •7.2.9.1 Hepatic Veins (HV)
- •7.2.9.2 Portal Vein (PV)
- •7.2.9.3 Hepatic Artery (HA)
- •7.2.10 Special Aspects of Newborns and Infants
- •7.3 Pathology of the Liver
- •7.3.1 Congenital Changes and Normal Variance
- •7.3.1.1 Situs Inversus (Abdominalis)
- •7.3.1.2 Butterfly or Midline Liver
- •7.3.1.3 Hypoplasia/Atrophy of Left Liver Lobe and Other Variations
- •7.3.2 Inflammatory Conditions
- •7.3.2.1 Hepatitis
- •7.3.2.2 Liver Abscess
- •7.3.2.3 Granulomatous Disease
- •7.3.2.4 Role of US
- •7.3.3 Other Parenchymal Liver Disease
- •7.3.3.1 Hepatopathy
- •Fatty Liver/Steatosis
- •Liver Congestion
- •7.3.3.2 Liver Fibrosis
- •7.3.3.3 Cirrhotic Liver
- •7.3.3.4 Liver Involvement in Systemic Disease
- •Cystic fibrosis
- •Glycogen storage disease
- •Tyrosinaemia
- •Wilson disease
- •α1-antitrypsin deficiency
- •Haemosiderosis
- •7.3.3.5 Role of US
- •7.3.4 Portal Hypertension and Vascular Problems
- •7.3.4.1 Portal Hypertension
- •7.3.4.2 Vascular Malformations
- •7.3.4.3 Portal vein and hepatic artery stenosis
- •7.3.4.5 Hepatic vein thrombosis/occlusion/stenosis
- •Budd-Chiari syndrome
- •Veno-occlusive disease (VOD)
- •Increased right atrial/intrathoracic pressure
- •7.3.4.6 Portosystemic Shunts
- •7.3.5 Liver Trauma
- •7.3.5.1 Liver Haematoma
- •7.3.5.2 Contusion
- •7.3.5.3 Laceration
- •7.3.5.4 Haemobilia
- •7.3.5.5 Associated Diaphragmatic Injury
- •7.3.5.6 Liver Infarction
- •7.3.5.7 Role of US in Liver Trauma
- •7.3.5.8 Additional Imaging
- •7.3.6 Space-Occupying Liver Lesions
- •7.3.6.1 Simple Cysts
- •7.3.6.2 Complicated Cysts
- •7.3.6.3 Liver Calcifications
- •7.3.6.4 Intrahepatic Gas
- •7.3.6.5 Haemangioma
- •7.3.6.6 Mesenchymal Hamartoma
- •7.3.6.7 Focal Nodular Hyperplasia (FNH)
- •7.3.6.8 Hepatic Adenoma
- •7.3.6.9 Fatty Tumours
- •7.3.6.10 Hepatoblastoma
- •7.3.6.11 Hepatocellular Carcinoma
- •7.3.6.12 Hepatic Sarcomas
- •Embryonal Cell Sarcoma
- •Rhabdomyosarcoma
- •Angiosarcoma
- •Hepatic Leiomyosarcoma
- •7.3.6.13 Metastasis
- •7.3.6.14 Proliferative Disorders
- •7.3.6.15 Role of US
- •7.3.6.16 Additional Imaging
- •7.4 Biliary Tract and Gall Bladder
- •7.4.1 General Findings
- •7.4.2 Congenital Conditions and Normal Variants of Biliary Tract
- •7.4.2.1 Intrahepatic Gall Bladder
- •7.4.2.3 Choledochal cyst
- •7.4.3 Biliary Tract Diseases
- •7.4.3.1 Aerobilia
- •7.4.3.2 Cholestatic Changes/Inspissated Bile/Gall \stone
- •7.4.3.3 Sclerosing cholangitis
- •7.4.3.4 Other Forms of Cholangitis and Cholecystitis
- •7.4.4 Tumour-Like Conditions
- •7.4.4.1 Polyps
- •7.4.4.2 Tumours
- •Cholangiocellular Tumours
- •Granular Cell Tumour
- •7.4.5 Role of US
- •7.4.5.1 Cholestasis and Jaundice
- •7.4.5.2 Malformations
- •7.4.5.3 Trauma
- •7.4.5.4 Postoperative Conditions
- •7.4.5.5 Metabolic Disease
- •7.4.7 Additional Imaging
- •7.5 US in Liver Transplantation
- •7.5.1 Pretransplant US
- •7.5.1.1 Recipient Evaluation
- •7.5.2 Intraoperative US
- •7.5.3 Postoperative Assessment
- •7.5.4 Typical Complications
- •8: Spleen and Pancreas
- •8.1 Spleen
- •8.1.1 Requisites
- •8.1.2 Positioning
- •8.1.3 Indications
- •8.1.4 Course of Investigation
- •8.1.5 Normal Anatomy
- •8.1.6 Normal Variants
- •8.1.6.1 Splenunculus (Accessory Spleen)
- •8.1.6.2 Splenic Lobulations and Clefts
- •8.1.7 Malformations
- •8.1.7.1 Asplenia
- •8.1.7.2 Polysplenia Syndrome
- •8.1.7.3 Wandering Spleen
- •8.1.8 Splenomegaly
- •8.1.9 Trauma
- •8.1.10 Splenic Infarction
- •8.1.11 Space-Occupying Lesions of the Spleen
- •8.1.11.1 Cysts
- •8.1.11.2 Abscess
- •8.1.11.3 Tumours and Space-Occupying Lesions
- •8.1.11.4 Role of US
- •8.2 Pancreas
- •8.2.1 Requisites
- •8.2.2 Indication
- •8.2.3 Course of Investigation
- •8.2.4 Normal Findings
- •8.2.5 Variations and Malformations
- •8.2.5.1 Annular Pancreas
- •8.2.5.2 Pancreas Divisum
- •8.2.6 Inflammation: Pancreatitis
- •8.2.6.1 Oedematous or Reactive Pancreatitis
- •8.2.6.2 Haemorrhagic or Necrotising Pancreatitis
- •8.2.6.3 Chronic Pancreatitis
- •8.2.7 Trauma
- •8.2.8 Space-Occupying Lesions
- •8.2.8.1 Cysts/Pseudocysts
- •8.2.8.2 Tumours
- •8.2.9 Role of US
- •8.2.10 Additional Imaging
- •8.3.1 Abdominal Vessels
- •8.3.1.1 Positioning
- •8.3.1.2 Transducers
- •8.3.1.3 How to Investigate
- •8.3.1.4 US Findings
- •8.3.1.5 Important Variants and Malformations
- •8.3.2 Vascular Pathology
- •8.3.2.1 Thrombosis/Occlusion
- •8.3.2.2 Pelvic Congestion Syndrome
- •8.3.2.3 Mid-aortic Syndrome
- •8.3.2.4 Retroaortic Left Renal Vein: Nutcracker Syndrome (see Chap. 10)
- •8.3.2.6 Arteriosclerotic Changes and Aneurysms
- •8.3.2.7 Embolic Thrombus to Abdominal Aorta
- •8.3.2.8 Role of US
- •8.3.2.9 Complementing Imaging
- •8.3.3 Mesentery
- •8.3.3.1 Mesenteric (Peritoneal) Masses
- •Cyst
- •Lymphatic Vascular Malformation and Other Tumours
- •8.3.3.2 Abscesses
- •8.3.3.3 Twisted Appendices Epiploica
- •8.3.4 Mesenteric Lymph Nodes
- •8.3.5 Free Intraperitoneal Air
- •8.3.6 Free Intraperitoneal Fluid: Ascites
- •8.3.7 Retroperitoneal Soft Tissues
- •8.3.7.1 Lymph Nodes
- •8.3.7.2 Retroperitoneal Tumours
- •8.3.8 Abdominal Wall
- •9: US of the Gastrointestinal (GI) Tract
- •9.1 Stomach
- •9.1.1 Requisites
- •9.1.2 How to Investigate
- •9.1.2.1 Access
- •9.1.2.2 Functional Assessment of Bowel and Stomach
- •9.1.3 Normal Findings
- •9.1.4 Normal Variants
- •9.1.5 Malformations
- •9.1.5.1 Microgastria
- •9.1.5.2 Pyloric Atresia
- •9.1.5.3 Congenital Hiatal Hernia
- •9.1.6 Pathologic Findings
- •9.1.6.1 Gastro-Oesophageal Reflux (GOER)
- •9.1.6.2 Hypertrophic Pyloric Stenosis (HPS)
- •9.1.6.3 Other Stomach Conditions
- •Gastritis/Ulcers
- •Bezoars and Foreign Bodies
- •Hyperplastic Gastric Mucosa
- •Menetrier’s Disease: Giant Hypertrophy of Gastric Mucosa
- •Eosinophilic Gastr(oenter)itis
- •Gastric Perforation
- •Granulomatous Disease
- •Duplication Cysts
- •Teratoma
- •Focal Foveolar Hyperplasia
- •Inflammatory Pseudotumour
- •Other Benign Tumours
- •Malignant Masses
- •9.1.7 Role of US
- •9.2 Bowel
- •9.2.1 Preparation and Requisites
- •9.2.2 Course of Investigation
- •9.2.3 Normal US Findings
- •9.2.4 Pathology
- •9.2.4.1 Congenital Anomalies
- •Atresia
- •Malrotation
- •Volvulus
- •Hirschsprung Disease/Neuronal Intestinal Dysplasia (NID)
- •Duplication/Diverticula
- •Meckel’s Diverticulum
- •9.2.5 Acquired Obstructive Pathology
- •9.2.5.1 Meconium Ileus
- •9.2.5.2 Midgut Volvulus
- •9.2.5.3 Sigma Volvulus
- •9.2.5.4 Hernia
- •9.2.5.5 Intussusception
- •9.2.5.6 Tumours
- •9.2.6 Inflammatory Conditions
- •9.2.6.1 Necrotising Enterocolitis (NEC)
- •9.2.6.2 Gastroenteritis
- •9.2.6.3 Henoch-Schönlein Purpura
- •9.2.6.4 Appendicitis
- •9.2.6.5 Crohn’s Disease
- •9.2.6.6 Colitis
- •9.2.6.7 Other Inflammatory Bowel Conditions
- •9.2.6.8 Bowel Trauma
- •10: Ultrasound of the Urogenital Tract
- •10.1 Requisites
- •10.1.1 Indications
- •10.1.2 Preparation
- •10.1.3 Transducers
- •10.1.4 Positioning
- •10.1.5 How to Investigate
- •10.1.5.1 Diuretic US
- •10.2 Normal Findings
- •10.2.1 Bladder
- •10.2.2 Kidney
- •10.2.2.1 Normal Variants
- •Duplex Kidney
- •Ectopic Kidneys
- •Renal Agenesis
- •Fusion Anomalies and Other Rare Findings
- •10.3 Pathology of the Kidney
- •10.3.1 Congenital Conditions
- •10.3.1.1 Dysplasia/Hypoplasia
- •10.3.1.2 Cystic Renal Disease
- •Inherited/Congenital Cystic Disease
- •Acquired Cystic Kidney Disease
- •10.3.1.3 Alteration of Urinary Drainage
- •Hydronephrosis (HN)
- •Ureteropelvic Junction Obstruction (UPJO)
- •Uretero-Vesical Junction Obstruction (UVJO)/Obstructive Megaureter (POM/MU)
- •Posterior Urethral Valve (PUV)
- •Vesico-Ureteric Reflux (VUR)
- •Secondary Obstruction
- •10.3.2 Inflammatory Renal Parenchymal Conditions
- •10.3.2.1 Pyelitis
- •10.3.2.2 Acute Pyelonephritis (aPN)/Interstitial Nephritis
- •10.3.2.3 Necrosis and Abscess Formation
- •10.3.2.4 Scarring
- •10.3.2.5 Tuberculosis
- •10.3.2.6 Xanthogranulomatous Pyelonephritis
- •10.3.2.7 Glomerulonephritis/Nephrotic Syndrome
- •10.3.3 Vascular Conditions
- •10.3.3.1 Renal Artery Stenosis
- •10.3.3.2 Arteriovenous Fistula (AVF)
- •10.3.3.3 Infarction
- •10.3.3.4 Renal Vein Thrombosis
- •10.3.4 Nephrocalcinosis
- •10.3.5 Urolithiasis
- •10.3.6 Other Important Renal Parenchymal Disease
- •10.3.6.1 Haemolytic Uremic Syndrome (HUS)
- •10.3.6.2 Glomerulonephritis/Nephrotic Syndrome
- •10.3.6.3 Scars, Cirrhotic Kidney
- •10.3.7 Renal Failure (RF)
- •10.3.8 Renal/Urinary Tract Trauma
- •10.3.9 Renal Tumours
- •10.3.9.1 Benign Tumours
- •10.3.9.2 Pre- or Semimalignant Tumours
- •10.3.9.3 Malignant Tumours
- •10.4 Renal Biopsy and Interventions
- •10.4.1 Renal Biopsy
- •10.4.2 Drainage/Nephrostomy
- •10.4.3 Postoperative Imaging
- •10.4.3.1 After VUR Treatment
- •Cystoscopic Treatment
- •Antireflux Surgery
- •10.4.3.2 Findings After Pyeloplasty
- •10.4.3.3 After Various Interventions
- •10.5 Renal Transplant
- •10.5.1 Normal US Findings in Renal Transplant
- •10.5.2 Pathologic US Findings
- •10.6 Adrenal Glands and Pararenal Space
- •10.6.1 General Remarks
- •10.6.2 Typical Normal US Finding
- •10.6.3 Pathologic Findings
- •10.6.3.1 Adrenal Gland Haemorrhage
- •10.6.3.2 Inflammatory Condition
- •10.6.3.3 Tumours
- •Adrenal Cysts
- •Adrenal Adenoma
- •Neuroblastoma
- •Ganglioneuroma
- •Phaeochromocytoma
- •Adrenal Carcinoma
- •Role of US
- •10.7 US of Urinary Bladder
- •10.7.1 Requisites
- •10.7.2 Pathologic Findings
- •10.7.2.1 Atypical Shape (Neurogenic Bladder, “Valve Bladder”)
- •10.7.2.2 Polyps
- •10.7.2.3 Bladder Tumours
- •10.7.2.4 Calcification in/of Bladder
- •10.7.2.5 Ureterocele
- •10.7.2.6 Persisting Urachus
- •10.7.2.7 Megaureter
- •10.7.2.8 Infravesical Obstruction
- •10.7.2.9 Inflammation
- •10.7.2.10 Traumatic Changes
- •10.7.2.11 Vesico-ureteric Reflux
- •10.7.3 Paravesical Changes
- •10.7.3.1 Abscess Formations
- •10.7.3.2 Tumours of Paravesical Region
- •10.7.3.3 Cystic Perivesical Structures
- •10.7.4 Role of US
- •10.8 US of Male Genitals
- •10.8.1 US Technique
- •10.8.2 Normal Findings
- •10.8.3 Common Pathologic Findings
- •10.8.3.1 Hydrocele
- •10.8.3.2 Undescended Testes
- •10.8.3.3 Varicocele
- •10.8.3.4 Cystic Dysplasia of Rete Testis and Seminal Vesicles
- •10.8.3.6 Microlithiasis
- •10.8.4 Inflammation – Orchitis, Ependymitis
- •10.8.5 Scrotal Trauma
- •10.8.6 Torsion
- •10.8.6.1 Torsion of Appendages
- •10.8.6.2 Inguinal Hernia
- •10.8.7 Testicular Tumours
- •10.8.8 Role of US and Additional Imaging
- •10.9 Female Genitals
- •10.9.1 Indications
- •10.9.2 Requisites
- •10.9.3 Transducers
- •10.9.4 How to Perform Investigation
- •10.9.5 Normal Findings
- •10.9.5.1 Sonogenitography
- •10.9.6 Pathologic Findings
- •10.9.6.1 Congenital Malformations
- •Vaginal Septum and Duplications
- •Vaginal Atresia
- •Vaginal Fistula
- •Other Vaginal Malformations
- •Vaginal Aplasia
- •Uterine Malformations
- •Ovarian Malformations
- •10.9.6.2 Inflammatory Conditions of Female Genitalia
- •10.9.6.3 Genital Tumours and Space-Occupying Lesions
- •Cysts
- •Teratoma
- •Other Genital Tumours
- •Rhabdomyosarcoma
- •10.9.6.4 Traumatic Changes
- •Ovarian Torsion
- •Pregnancy
- •10.9.6.6 Role of US/Additional Investigations
- •11: Small Part and Hip Ultrasound
- •11.1 Hip US
- •11.1.1 General Remarks
- •11.1.2 Examination Technique
- •11.1.2.1 Hip US According to Graf
- •11.1.2.2 Modified Graf Classification (Rosendahl)
- •11.1.2.3 Hip US According to Harcke
- •11.1.3 Normal Anatomy
- •11.1.3.1 US Criteria in Graf
- •11.1.3.2 Rosendahl Modification
- •11.1.3.3 Normal Findings During Harcke Investigation
- •11.1.3.5 Hip US in Older Children
- •11.1.4 Pathologic Findings
- •11.1.4.1 Developmental Dysplasia of the Hip (DDH)
- •11.2 Other Conditions of Hip Joint
- •11.2.1 Arthritis and Inflammation of Hip Joint
- •11.2.1.1 Capsular Thickening
- •11.2.1.2 Joint Fluid/Effusion
- •11.2.1.3 Hip Osteoarthritis
- •11.2.3 Perthes Disease
- •11.3 Investigation of Bones, Joints, Tendons
- •11.3.1 Requisites and Technique
- •11.3.2 Typical Normal Findings
- •11.3.3 Pathologic Findings
- •11.3.3.1 Fracture
- •11.3.3.2 Joint Effusion
- •Simple Effusion
- •Complicated Effusion
- •11.3.3.3 Arthritis
- •11.3.3.4 Trauma
- •Haematoma
- •Rupture of Tendon
- •11.3.3.5 Cysts
- •11.3.3.6 Inflammation
- •Myositis
- •Cellulitis
- •Fasciitis
- •Tendinitis – Tendovaginitis/Synovitis
- •Osteomyelitis, Soft Tissue Abscess
- •11.3.3.7 Neoplasia
- •11.3.3.8 Foreign Bodies
- •11.3.3.9 Peripheral Nerves
- •11.4 US for Peripheral Vessels
- •11.5 US-Guided Interventions
- •Index

306
abc
Fig. 9.14 Dynamic US after drinking tea for fi lling a duplication cyst. ( a ) Some fl uid within a
typical duplication cyst that could easily be mistaken for a fl uid-fi lled atypical bowel loop or stomach. ( b ) After drinking tea cyst starts to fi ll and enlarge. ( c ) Increasing dilatation some time after
drinking tea, proving connection oft cyst with bowel lumen and also explaining the intermittent
nature of the patients’ obstructive symptoms
9 US of the Gastrointestinal (GI) Tract
Fig. 9.15 Meckel’s diverticulum. Axial section, right lower quadrant – typical US image of
Meckel’s diverticulum: thick wall, some complex fl uid content, adjacent to coecum
NOTE : US not always 100 % decisive. If necessary for treatment decision –
Meckel’s scintigraphy/laparoscopy. If equivocal and no surgery planned – additional imaging (sectional? fl uoroscopic?).
9.2.5 Acquired Obstructive Pathology
9.2.5.1 Meconium Ileus
Defi nition
• Obstruction by inspissated meconium, commonly seen in preterm infants, after
dehydration, or associated with cystic fi brosis.
US Findings
• Dilated small bowel loops with very echogenic content, typical for meconium
(Fig. 9.16 ).

9.2 Bowel
a b
Fig. 9.16 Meconium ileus. ( a ) Dilated small bowel loop with echogenic content and some ascites
in preterm with meconium transport problems; note collapsed bowel loop more distal. ( b ) Same
baby as in ( b ), during saline enema for DDx (e.g. atresia) and reduction of meconium ileus: fl uid-
fi lled narrow colon (“small left colon”), tip of thin feeding tube for enema positioned in descending
colon seen at right upper corner, dilated small bowel loop fi lled with echogenic meconium and
some ascites
• Abrupt calibre change from dilated to very narrow bowel.
• Improved: depiction of transition zone to nonused bowel by saline enema.
• Secondary perforation with formation of complicated ascites/meconium peritonitis (typically develop calcifi cations along peritoneum, even descending into
calcifi cation in cyst wall).
NOTE : Repeated bedside saline enema under US guidance may be used for relief
of meconium ileus (see also Fig. 2.1 ). Acetylcysteine or isotonic radiopaque con-
trast material may be added to improve results + enable post-procedure plain fi lm for
documentation.
307
9.2.5.2 Midgut Volvulus
See above.
9.2.5.3 Sigma Volvulus
May occur in children, no indication for US.
No specifi c fi ndings, except for demonstration of course of sigmoid after thera-
peutic saline enema.
9.2.5.4 Hernia
Defi nition
Herniation of abdominal content to atypical location causing transport problems,
kinks, vascular compromise and mechanic obstruction.
Causes
Adhesions of various origin, atypical peritoneal bands (related to internal hernias)
or remnant/reoccurrence of pathologic openings of peritoneal cavity to other locations (inguinal, diaphragmatic, Ladd’s bands, abdominal wall, etc.).
US Findings (and Role)
To depict and assess herniation if area accessible for US.

308
a
9 US of the Gastrointestinal (GI) Tract
b
cd
Fig. 9.17 Inguinal hernia. ( a ) Seen in longitudinal section of inguinal canal and scrotum. ( b )
Slight gapping of inner opening of inguinal canal (+ +), bowel just starts to enter into hernia (longitudinal section paramedian at inguinal area). ( c ) Inguinal hernia, longitudinal section: course of
canal seen with some mesentery entering into hernia. No typical testis seen. ( d ) Inguinal hernia
with unusual content in infant girl: obviously ovary entrapped in inguinal canal. CDS activated
(low-velocity scale settings used, accepting aliasing) to prove existing ovarian perfusion
NOTE: Internal hernias usually not depicted, but indirect signs hint towards
mechanical obstruction (e.g. dilated bowel loops, thickening of bowel wall, marked
difference of bowel lumen size between proximal and distal loops and yo-yo
hyperperistalsis).
Inguinal hernia : demonstration of abdominal content within inguinal canal/scro-
tum/labia, enlarged entrance to inguinal canal (Fig. 9.17 ):
• Content varies (mesentery, ascites, bowel – rarely also bladder or ovary).
• Provocation manoeuvres help depicting intermittent herniation.
Diaphragmatic hernia : see chest chapter.
Abdominal wall hernia : same rules apply as for inguinal hernia, may also occur
postoperatively in scars.
DDx :
• Clinically any other cause of obstruction causing mechanical obstruction or
mimicking herniation.
• In boys consider funiculocele, in preterms physiological weakness of inguinal
canal with physiologically persisting continuity that resolves spontaneously.
NOTE : US may not rule out all defects, only demonstrates herniation of (intraperi-
toneal) content.
9.2.5.5 Intussusception
Parts of more proximal bowel (intussusceptum) slip into more distal parts
(intussuscipiens):

9.2 Bowel
Fig. 9.18 Transient small bowel intussusception. Target sign in left upper quadrant, diameter
1.5 cm, spontaneously resolved during US investigation, in child with hyperperistalsis and
gastroenteritis – typical appearance of transient small bowel intussusception
• Small bowel intussusception: commonly happens in many conditions in the jejunum/ileum (gastroenteritis, hyperperistalsis, hyperreactive bowel, etc.) – spontaneously resolve unless there is a pathologic lead point (diverticula, large lymph
node, etc.). Diameter usually <2 cm (Fig. 9.18 ).
• Ileo-colic intussusception/invagination: less common, but most important (emergency condition!) – associated with gastroenteritis, mesenteric adenopathy and
mobile coecum. Long-standing intussusception causes venous congestion, eventually ischemic damage and bowel necrosis with perforation. Compromised vascular supply in the mesentery also pulled into intussusception and compressed,
rarely resolves spontaneously.
• Colo-colonic intussusception: much rarer, usually happens only with underlying
pathologic conditions (e.g. polyps).
US and CDS Findings
• US – mainstay of diagnosis, can reliably diagnose (and most often exclude)
intussusception in skilled hands; also used for follow-up after reduction/to see
alternate fi ndings (DDx, atypical lead points, etc.).
• “Bowel in bowel” appearance; if ileocolonic – additionally entrapped hyperechoic mesentery with respective vessels, often lymph nodes. Bowel wall may be
thick and oedematous. “Pseudo-kidney sign” (longitudinal section) or “doughnut
sign” (axial section) (Fig. 9.19 ).
• Reactive changes – ascites, mesenteric oedema and mesenteric nodes.
• Entrapped fl uid at head of intussusceptum, restricted/absent perfusion – sign for
poor reducibility and higher complication risk, potentially pathologic lead structures (Meckel’s diverticula, lymphoma, bowel wall tumour, polyp etc.).
NOTE : Always follow entire colon to coecum; intussusception usually encoun-
tered in right upper quadrant (coecum mobile); intussusceptum can extend to
rectum, or even prolapse.
• If equivocal US fi ndings: use sonographic saline enema or conventional fl uoroscopic technique.
• Same technique with higher fi lling pressure used for US-guided hydrostatic
reduction (Fig. 9.19d, e , also see Fig. 2.3 ).
309

310
a
bc
9 US of the Gastrointestinal (GI) Tract
de
Fig. 9.19 Ileo-colic intussusception. ( a ) Axial section: typical doughnut sign in ileo-coecal intus-
susception, with centrally some echogenic mesentery supplying inner small bowel loop (intussusceptum). ( b ) Longitudinal view: pseudo-kidney sign created by inner and outer loop. Some
entrapped fl uid. ( c ) Some adjacent fl uid in this intussusception which already has reached into
descending colon – visible from left fl ank. ( d ) Hydrostatic reduction of intussusception: fl uid from
enema in intussuscipiens starts to surround and mobilise intussusceptum. ( e ) Axial section lower
right quadrant: after hydrostatic reduction coecum fi lled with fl uid, intussusception has been
reduced, ileo-coecal (Bauhin’s) valve leafs still swollen
9.2.5.6 Tumours
Rare. May originate from polyps (familial). Rhabdomyosarcoma and adenocarcinoma (in familial conditions) extremely rare.
US and CDS Findings
• No difference from any other tumour.
• Do not exhibit any specifi c features (Fig. 9.20 ).
Depending on involvement/stage: local mesenteric nodes, ascites, stenosis, peri-
toneal/mesenteric nodes and liver metastasis.
Diagnosis by histology, staging by standard sectional imaging mandatory in
malignant conditions.
9.2.6 Inflammatory Conditions
9.2.6.1 Necrotising Enterocolitis (NEC)
Defi nition
• Severe infl ammatory bowel disease of preterm and newborn babies, potentially lethal due to necrosis and peritonitis, in late stages only surgically
manageable.

9.2 Bowel
ab c
Fig. 9.20 Gatrointestinal tumours. ( a ) Large bowel tumour causing intussusception – proven to be a
nodular type lymphoma. ( b ) Infi ltrated and thickened bowel wall with destroyed stratifi cation in Burkitt
lymphoma. ( c ) (Complex) ascites and peritoneal metastasis (+ +) – in this case from rare familiar child-
hood adenocarcinoma of the sigmoid: stenosis better depictable after saline enema.
US Findings
• Initially nonspecifi c thickened, hazy structured bowel wall, often echogenic content, hypervascularisation, ascites (Fig. 9.21a, b ).
• In later stages intramural air bubbles – seen as echogenic foci within wall (“pneumatosis”), secondarily gas bubbles passing through portal vein into liver, accumulating in liver periphery (see chapter liver) (Figs. 9.21c, d and 9.22 , see also
Fig. 7.17 ). Enlarged nodes rare; abscess formations may occur.
• Calcifi ed peritoneal content indicates old (fetal) perforation with meconium
peritonitis.
• In perforation free air detectable by meticulous scanning – see respective entry.
CDS Findings
• Initially hyperaemia of mesenteric arteries (increased fl ow velocities, decreased
RI – seen in superior mesenteric artery and celiac trunk). The longer the disease,
the higher the resistance/RI values. Eventually in necrosis completely unstructured segments of devascularised bowel (Fig. 9.21e ).
• Portal venous gas bubbles seen as typical spikes on spectral fl ow pattern – diffi cult to visualise in main portal vein on CDS, but reverberation echoes and twinkling like artefacts seen within liver periphery (Fig. 7.22 , see also Fig. 7.17 ).
• Systolic velocity >100 cm/s and RI < .80 (coeliac trunk/mesenteric artery) highly
suspicious for infl ammatory condition – provided patient is fasted.
Role of US
• Increasingly important.
• Very sensitive to early changes before plain fi lm shows typical pathology.
• However, specifi city of fi ndings low, unless intramural air/portal venous gas
seen.
NOTE : Intramural air/portal venous gas rarely also seen with other conditions (e.g.
idiopathic, severely dilating bowel obstruction).
• DDx of intrahepatic portal venous gas – peripheral intrabiliary air/gas.
Additional Imaging
Abdominal plain fi lm, laboratory.
311

312
a
bc
9 US of the Gastrointestinal (GI) Tract
de
Fig. 9.21 NEC. ( a ) Early phase of NEC: atypical bowel wall, dilatation (similar to plain fi rm fi nd-
ings in the early stage) and some ascites. ( b ) CDS reveals infl ammatory hypervascularisation in
now thickened bowel wall. ( c ) Small echogenic foci ( arrow ) in thickened bowel wall consistent
with pneumatosis. ( d ) CDS shows reverberations (like “twinkling sign”) from intramural gas bub-
bles in NEC with pneumatosis. ( e ) Thickened bowel wall with destroyed stratifi cation, no depict-
able vasculature – necrotic segment
abcd
Fig. 9.22 Portal venous/liver gas. ( a ) CDS with spectral trace of portal vein: on CDS normal fl ow
direction displayed, whereas spectral analysis additionally demonstrates short fl ow spikes typical
for passing gas bubbles. ( b , c ) Echogenic intrahepatic foci – portal venous or intrabiliary gas
bubbles in minor and more central distribution ( b , more likely to represent biliary gas) and severe
extent ( c , more likely to be portal venous gas, particularly as it accumulates in periphery). ( d )
Spectral analysis mandatory to prove intravascular nature of gas bubbles – enabling differentiating
of intravascular from intrabiliary gas by depicting typical gas spikes in portal venous fl o w
9.2.6.2 Gastroenteritis
Not an indication for US – however, fi ndings often encountered during US for
unclear abdominal complaints, appendicitis, etc.
US and CDS Findings
• Atypical bowel content, often complex fl uid.
• Hyperperistalsis, mesenteric changes (increased echogenicity, mesenteric lymph
nodes) and some ascites.
• Nonspecifi c bowel wall changes, no specifi c features.

9.2 Bowel
313
• If toxic paralytic component: bowel may get dilated/lose peristalsis.
NOTE : Often self-limiting, spontaneously resolving ileo-ileal/jejunal intussuscep-
tions can be observed.
• Hyperperfusion of mesenteric artery with hypervascular bowel wall.
9.2.6.3 Henoch-Schönlein Purpura
Defi nition
Systemic vasculopathy that may affect intestines (as well as kidney and other organs).
US and CDS Findings
• Nonspecifi c image with echogenic, thickened bowel wall (particularly mucosa).
• Lumen may have echogenic content due to haemorrhage, hypervascularisation.
• Reactive mesenteric hyperechogenicity/thickening, some ascites. Adenopathy rare.
NOTE : Bowel wall thickening due to intramural haematoma (typically at duode-
num/proximal jejunum) rarely associated with bloody stools (more likely in bleeding diathesis) very uncommon, only after trauma or with NAI.
Role of US
• Diagnosis usually made by laboratory and clinical fi ndings.
• Helpful for depiction of similar changes in bowel segments other than appendix –
helps to reduce rate of unnecessary surgery, improves DDx.
• Follow up possible but usually not necessary.
• US used in protracted/complicated course with higher rate of complications
(such as intussusception) or with worsening of symptoms.
9.2.6.4 Appendicitis
Defi nition
Infl ammation of appendix with risk of perforation, abscess formation, peritonitis
and fi stulae:
• Reactive changes often seen in many other abdominal conditions (Crohn’s disease, cystic fi brosis, gastroenteritis, Henoch-Schönlein purpura, etc.) - may
mimic appendicitis.
US Findings
Typically located in right lower quadrant, can commonly be found when actively
searching area around coecal pole (remember abnormal position such as retrocoecally, also look to lower margin of liver, behind/in front of ascending colon, mediocranially, etc.).
• Normal appearance of appendix: blind ending tubular structure with typical gut
wall appearance, commonly without content, compressible and painless on US
palpation Diameter in children: 3–6 mm.
• In infl ammation: appendix enlarged, enhanced wall structure, may show mural
follicles (follicular appendicitis) and may show content in lumen – particularly
appendicolith (with distal shadowing), stiff/uncompressible (Fig. 9.23 ).
• Painful on graded compression/sono-palpation.
• Surrounding mesentery usually hyperechoic, commonly some ascites, regional
nodes.
• With ongoing disease there is necrosis – wall structures get hazy, differentiation
lost, increasingly enlarged.

314
9 US of the Gastrointestinal (GI) Tract
a
d
g
Fig. 9.23 Appendicitis. ( a ) Normal appendix in right lower quadrant, nicely depictable due to
ascites. ( b ) Thick incompressible appendix (+ +) in typical position adjacent to pelvic vessels. ( c )
CDS exhibits vivid hypervascularisation in acute appendicitis (same patient as in b ). ( d ) Typical
target sign of enlarged, incompressible appendix (+ +) with thickened wall and perifocal mesenteric reaction. ( e ) Cross section of enlarged and infl amed incompressible appendix with echogenic
adjacent mesentery; wall stratifi cation nearly lost – intraoperatively found to be phlegmonous,
almost necrotic. ( f ) Enlarged thick infl amed appendix with mesenteric reaction and appendicolith
( shadow ). ( g ) Thickened echogenic mucosa of swollen enlarged appendix in Henoch-Schönlein
purpura. ( h ) Retrocoecal appendicitis – typical target sign of thickened, stiff and infl amed appen-
dix deep behind bowel loops
bc
fe
h
• With perforation peri-appendiceal fl uid, complex collections and abscess formation (pericoecal, cul-de-sac, infl ammatory intestinal pseudotumour) (Fig. 9.24 ) –
may be distributed to other parts of peritoneal cavity and thus missed.
• Floating appendicolith may enable diagnosis of abscess origin.
• After perforation appendix may be normal sized as content evacuated.
• Chronic appendicitis usually exhibits enlarged appendix with rather thin, but
structured wall, only little pain on sono-palpation, may not be very
compressible:
• Potentially only little perifocal mesenteric reaction.
• Typically in chronic diseases (e.g. Yersinia, cystic fi brosis and intestinal obstruction syndromes).

9.2 Bowel
ab c
Fig. 9.24 Perforation in appendicitis. ( a ) Pericoecal abscess after ruptured appendicitis. ( b )
Postoperative collection with fl oating, intraoperatively lost appendicolith – consistent with peritoneal abscess. ( c ) Complex cystic mass with echogenic thickened mesentery – mesenteric abscess
(originating from mesenteric lymphadenopathy)
CDS
Acute appendicitis: initially hypervascularisation of appendiceal wall with diastolic
hyperaemia on spectral analysis:
• However, may also be reactive in other infl ammatory bowel conditions, tachycardia, systemic conditions and therefore not specifi c.
• In late/gangraenous stages vascularity reduced, even lacking.
• Chronic appendicitis: usually no hyperaemia.
NOTE : In appendicitis changes often restricted to/focused on appendix. If several
changes observed in other bowel segments – consider other entities (e.g. HenochSchönlein purpura and Crohn’s disease).
Role of US
Increasingly promoted, used in initial assessment of clinically unclear abdomen,
particularly in girls, to different tubarian/ovarian pathology, urinary tract causes for
underlying symptoms:
• However, early stages of acute appendicitis may appear sonographically normal,
perforated old/subacute appendicitis may even be missed and reactive appendiceal changes observed in other conditions (e.g. severe gastroenteritis).
Additional Imaging
Sometimes helpful – increasingly questioned in the majority of cases for radiation
protection, as US + laboratory + clinical inspection often suffi ce:
• Abdominal plain fi lm: for depiction of appendicoliths/free peritoneal air in
perforation.
• Emergency CT (if MRI not available) – unclear cases with pending decision on
surgery (e.g. obesity hindering US assessment).
• Elective MR (if available), particularly for DDx (e.g. infl amed Meckel’s diverticulum, appendiceal tumour/appendiceal carcinoid).
315
9.2.6.5 Crohn’s Disease
Defi nition
Typical autoimmune condition – may manifest during (late) childhood, usually
effects small bowel, may also affect colon and can be multi-segmental:
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