AIIMS MAMC - PGI's Comprehensive Textbook of Diagnostic Radioloigy 935250187X, 9789352501878

Table of contents :
Cover
Contents
Neuroradiology including Head and Neck
E v aluation of Plain X-ray Skull: A Systematic Approach
Niranjan Khandelwal, Sudha Suri
LATERAL VIEW OF SKULL
FRONTAL VIEW (FIG. 2)
W A TERS VIEW
T O WNE’S VIEW
B ASAL VIEW
CALDWELL’S VIEW
A bnormal Contour of the Skull
A bnormal Density
A bnormal Intracranial Volume
Single Radiolucent Defect
Sclerotic Areas of the Skull
Intracranial Calcification
Normal Anatomy of Brain on CT and MRI
P aramjeet Singh
TECHNIQUES AND NORMAL APPEARANCE
General Considerations
Normal Anatomy of Brain
CEREBRAL HEMISPHERES
Lateral Surface of the Cerebral Hemisphere (Fig. 2A)
Medial Surface of the Cerebral Hemisphere (Fig. 2B)
Inferior Surface of the Cerebral Hemisphere (Fig. 2C)
BRAINSTEM AND CRANIAL NERVES
CEREBELLUM
WHITE MATTER OF THE CEREBRUM
VENTRICLES AND CISTERNS
GRAY MATTER NUCLEI AND ADJACENT STRUCTURES
SUGGESTED READING
Normal Cerebral Angiography
Shailesh B Gaikwad, Ajay Kumar
P ART 1: CEREBRAL ANGIOGRAPHY TECHNIQUE
INTRODUCTION
Historical Background
Definition
Six Vessel Angiography
P a tient Preparation
Requirement
C a theterization Equipment
Indications
Site of the Puncture
P r eparation
L ocal Anesthesia
A rtery Puncture
P uncture Technique
T ypes of Angiographic Catheters
P ART 2: CEREBRAL ANGIOGRAPHIC ANATOMY
A rterial Anatomy
Seldinger Needle
Important Points to Remember
P ostprocedural Management
V enous Anatomy (Fig. 14)
Dural Sinuses
C erebral Veins
A dvances in Computed T omography Technology
Niranjan Khandelwal, Paramjeet Singh, Sameer Vyas
MULTIDETECTOR C OMPUTED TOMOGRAPHY
DUAL SOURCE COMPUTED TOMOGRAPHY
FLAT-PANEL VOLUME COMPUTED T OMOGRAPHY
D Y NAMIC C OMPUTED TOMOGRAPHY ANGIOGRAPHY
C OMPUTED TOMOGRAPHY IN NEUROIMAGING
NONCONTRAST COMPUTED T OMOGRAPHY OF HEAD
C omputed Tomography A ngiography
T echnique
Image Processing
APPLICATIONS
Extracranial Vasculature
C arotid Artery Stenosis
Dissections
Intracranial Vasculature
Aneurysms
Arteriovenous Malformations
T umors
C omputed Tomography P erfusion
T umors
T echnique
CLINICAL APPLICATIONS
A cute Stroke
C omputed Tomography Imaging of Acute Ischemic Stroke
C omputed Tomography Venography
T echnique
MULTIDETECTOR COMPUTED T OMOGRAPHY OF SPINE
CLINICAL APPLICATIONS
RADIATION CONCERNS
C ONCLUSION
REFERENCES
A dvances in Neuroimaging T echniques: Magnetic Resonance Imaging
P aramjeet Singh, Niranjan Khandelwal
IMPROVEMENTS IN MR HARDWARE AND SOFTWARE TECHNOLOGY (GRADIENTS, C OILS AND
LARGE FIELD OF VIEW IMAGING
HIGH FIELD STRENGTH MR IMAGING (3T AND BEYOND)
IMPROVEMENTS IN PULSE SEQUENCES
SHORT REVIEW OF PRINCIPLES BEHIND NEW MR PULSE TECHNIQUES
EFFICIENT DATA PROCESSING TECHNIQUES
CLASSIFICATION OF THE PULSE SEQUENCES (FLOW CHART 1)
F AST SPIN ECHO
Characteristics of FSE
FLUID ATTENUATED INVERSION RECOVERY
CLINICAL APPLICATION
Single Shot Techniques of FSE (HASTE, SSFSE)
Magnetic Resonance Myelography
Gradient Echo Imaging and its Variants
Cranial and Extracranial MR Angiography
Susceptibility Weighted Imaging
Steady State Variants of Gradient Echo Sequences
MR Cisternography Using CISS/SPACE
Special MR Techniques in Medial T emporal Sclerosis
Echo Planar Imaging
Clinical Applications of EPI
Diffusion Studies
Diffusion Tensor Imaging (DTI, T r actography or Fiber Tracking)
Clinical Applications
P erfusion Weighted Imaging
Neuronal Activation Studies (fMRI)
PWI in Stroke
PWI of Cerebral Tumors
Disadvantages
REFERENCES
Magnetization Transfer
Magnetic Resonance Spectroscopy
Niranjan Khandelwal, Paramjeet Singh
PRINCIPLE
Spectrum
Spectrum and Echo Time
Observable Biochemicals on MRS
Hydrogen 1 ( 1 H-MRS)
P hosphorus 31 ( 31 P -MRS)
B 0 Field Gradient Methods
Static Field Gradient
Slice-selective B 0 -gradient
L OCALIZATION TECHNIQUES
B 1 Field Gradient Methods
Surface Coils
Quantitative Spectroscopy
Data Acquisition and Analysis
CLINICAL APPLICATIONS OF MRS OF BRAIN
Brain Tumors
Differentiation of I n tracranial Ring Enhancing L esions
MRS IN PEDIATRICS
P r ematurity and Birth Asphyxia
Metabolic Disorders and Leukodystrophies
MRS IN EPILEPSY
Lateralization in T emporal L obe E pilepsy
MRS in N eurodegenerative D iseases
Alzheimer’s Disease
Amyotrophic Lateral Sclerosis (ALS)
Idiopathic Parkinson’s Disease (IPD) versus Other P arkinsonian Syndromes
Huntington’s Disease (HD)
MRS IN DEMYELINATING DISEASES
Multiple Sclerosis
MRS IN STROKE
MRS IN HEAD TRAUMA
MRS IN PSYCHIATRIC DISEASES
MRS IN HIV/AIDS
CLINICAL SUCCESS
F uture Developments
REFERENCES
F unctional Magnetic Resonance Imaging
Ajay Garg
PRINCIPLE OF f MRI AND BOLD CONTRAST
LIMITATIONS OF BOLD TECHNIQUE
IMAGING ACQUISITION
FUNCTIONAL MRI EXAMINATION DESIGN
CURRENT CLINICAL APPLICATIONS OF FUNCTIONAL MRI
Neurosurgical Planning
FUNCTIONAL MRI EXAMINATION T ASK PARADIGM
POSTPROCESSING AND DATA ANALYSIS
Dementia
Defining Disease Based on Patterns of Brain Function
P sychiatric Disorders
FUTURE DIRECTIONS
Imaging and Interventions in C erebral Ischemia
P A THOPHYSIOLOGICAL CONSIDERATIONS
Significance of a Penumbra
ROLE OF IMAGING IN ACUTE ISCHEMIC STROKE
Imaging of Ischemic Infarct
C omputed Tomography
Magnetic Resonance Imaging
C OMBINATION OF DIFFUSION AND PERFUSION MRI IN EVALUATION OF A CUTE STROKE
V ascular Imaging in Ischemic Stroke
C arotid Ultrasound (US)
Magnetic Resonance Angiography
CT Angiography
IMAGING IN DIFFERENT STROKE SUBGROUPS
Ischemic Stroke
A therosclerotic Vascular Disease (ASVD)
Arterial Dissection
Other Vasculopathies
Hemorrhagic Stroke
A ortoarteritis
F ibromuscular Dysplasia
RECANALIZATION STRATEGIES
Intravenous TPA
E u r o pean Cooperative Acute Stroke Study (ECASS) Trials I and II 70
INTRA-ARTERIAL THERAPY
T echnique
Intra-arterial Abciximab
C OMBINED IA + I/V
MECHANICAL THROMBOLYSIS
A cute Stroke Imaging Protocol (Flow chart 1)
Imaging of Subarachnoid Hemorrhage
INCIDENCE
CLINICAL FEATURES
GRADING SYSTEM OF SUBARACHNOID HEMORRHAGE
DIAGNOSIS
L umbar Puncture (LP)
Magnetic Resonance Imaging
C omputed Tomography
C erebral Angiography
CT Angiography (CTA)
Magnetic Resonance Angiography (MRA)
T r anscranial Doppler Ultrasound
ANEURYSMS
Clinical Presentation
L ocation
Multiple Aneurysms
Unruptured Aneurysms
T hrombosed Aneurysms
Giant Aneurysms
Mycotic Aneurysms
F low-related Aneurysms
V ASCULAR MALFORMATIONS
P arenchymal AVMs
Dural AVMs
CAVERNOUS ANGIOMAS
Mixed Pial and Dural AVMs
CAPILLARY TELANGIECTASIAS
VENOUS ANGIOMAS
Nonaneurysmal SAH
TRAUMATIC SUBARACHNOID HEMORRHAGE
Subarachnoid Hemorrhage of Unknown Etiology
SUMMARY
Endovascular Management of Intracranial Aneurysms
NK Mishra
EPIDEMIOLOGY AND NATURAL HISTORY
P A THOPHYSIOLOGY
Diagnosis
Initial Assessment, Management and Grading
TIMING OF ANEURYSM OBLITERATION
POOR GRADE PATIENT
INTRACEREBRAL HEMORRHAGE
A CUTE INTRAVENTRICULAR HEMORRHAGE AND HYDROCEPHALUS
PREOPERATIVE CARE AND DIAGNOSTIC STUDIES
PHARMACOLOGIC THERAPY
ANEURYSM REPAIR SURGERY OR ENDOVASCULAR COILING
POSTPROCEDURAL MANAGEMENT
MONITORING CEREBRAL VASOSPASM AND IMPLEMENTING TREATMENT
SUMMARY
REFERENCES
Endovascular Management of Arteriovenous Malformations
Shailesh B Gaikwad, NK Mishra
THERAPEUTIC OPTIONS
T echnique of Endovascular Intervention
Heparin Regimen
F low-dependent Catheters
Guidewire Dependent Catheters
Guidewires
Embolic Agents
Liquid Agents: Acrylic Glue
P articulate Agents
P r eoperative Embolization
Intraoperative Embolization
P r eradiosurgery Embolization
C urative Embolization
P alliative (Partial) Embolization
Staging Embolization
C OMPLICATIONS OF AVM EMBOLIZATION
DURAL ARTERIOVENOUS FISTULAE (DAVFs)
Classification
Radiological Evaluation
T herapeutic Options
C ompression Therapy
T r ansarterial Embolization
Brain AVM Embolization with Onyx
INDICATION FOR TREATMENT
T r ansvenous Embolization
P r eoperative Embolization
Onyx Liquid Embolic Agent
C ONCLUSION
REFERENCES
Endovascular Management of C arotid-cavernous Fistulas
SEGMENTS OF INTRACAVERNOUS INTERNAL CAROTID ARTERY
Angiogram
Radiological Evaluation
CT Scan
T echniques of Embolization
Endovascular Management
Embolic Materials
Embolization Procedure
T r ansarterial Embolization
T r ansvenous Embolization
Results of Endovascular Therapy
DISCUSSION
C entral Nervous System Infections
NORMAL CRANIAL MENINGES AND EXTRA A XIAL SPACES
BACTERIAL/PYOGENIC INFECTIONS
P Y OGENIC MENINGITIS
Clinical and Pathophysiologic Features
Imaging in Meningitis
MENINGITIS
C OMPLICATIONS OR ALTERNATIVE MANIFESTATIONS OF BACTERIAL MENINGITIS
Hydrocephalus
Extra-axial Fluid and Pus Collections
Subdural Effusion and Hygroma
Subdural Abscess (Empyema)
Epidural Abscess (Empyema)
C erebritis and Abscess
Imaging of Brain Abscess
Diffusion Tensor Imaging (DTI)
Distinction between Cerebral Abscesses and High Grade Neoplasms by Dynamic S
Multiple Brain Abscesses Secondary to Septic Emboli
C entral Nervous System Infarction
V entriculitis
RECURRENT MENINGITIS
GRANULOMATOUS INFECTION
TUBERCULOSIS
P a thophysiology
TUBERCULOUS MENINGITIS
Clinical Manifestations
C omputed Tomography
Magnetic Resonance
C OMPLICATIONS
Hydrocephalus
V asculitis
Cranial Neuropathies
GRANULOMATOUS TUBERCULOUS MENINGITIS
P A CHYMENINGITIS
P ARENCHYMAL TUBERCULOMAS
Noncaseating Granuloma
C aseating Solid Granuloma
Granulomas with Central Liquefaction
DISSEMINATED TUBERCULOMA
P aradoxic Expansion
TUBERCULOUS ABSCESSES
TUBERCULOSIS ENCEPHALOPATHY
FOCAL TUBERCULOUS CEREBRITIS
CENTRAL NERVOUS SYSTEM TUBERCULOSIS AND ACQUIRED IMMUNE DEFICIENCY SYNDROME
NEUROSARCOIDOSIS
FUNGAL INFECTIONS OF THE CENTRAL NERVOUS SYSTEM
ASPERGILLOSIS
CRYPTOCOCCAL INFECTION
MR Spectroscopy in Cryptococcomas 62
MUCORMYCOSIS
Imaging Findings
CANDIDIASIS
C OCCIDIOIDOMYCOSIS
HISTOPLASMOSIS
NOCARDIOSIS
P arenchymal Cysts
P ARASITIC INFECTIONS
NEUROCYSTICERCOSIS
Hosts
Clinical Features
Intraventricular Cysticercosis
Subarachnoid Cysticercosis
SPINAL CYSTICERCOSIS
ORBITAL DISEASE
CENTRAL NERVOUS SYSTEM T O X OPLASMOSIS
Imaging Findings
Differentiation of Toxoplasmosis from CNS Lymphoma
H Y D A TID DISEASE
C ONGENITAL INFECTIONS
C ONGENITAL TOXOPLASMOSIS
SYPHILIS
RUBELLA
CYTOMEGALOVIRUS
HERPES SIMPLEX VIRUS
HUMAN IMMUNODEFICIENCY VIRUS (HIV)
VIRAL INFECTIONS
ENCEPHALITIS
A CUTE INFECTIVE ENCEPHALITIS/HERPES SIMPLEX ENCEPHALITIS
Imaging Findings
Magnetic Resonance Spectroscopy
HERPES VARICELLA ZOSTER ENCEPHALITIS
JAPANESE ENCEPHALITIS
Imaging Findings
MEASLES ENCEPHALITIS
A cute Measles Encephalitis
Subacute Sclerosing Panencephalitis
Imaging Findings
Subacute Measles Encephalitis
A CUTE DISSEMINATED ENCEPHALOMYELITIS
RASMUSSEN’S ENCEPHALITIS
A C QUIRED IMMUNODEFICIENCY SYNDROME (AIDS) AND ITS RELATED CNS INFECTIONS
HUMAN IMMUNODEFICIENCY VIRUS ENCEPHALITIS
PRION INFECTIONS—CREUTZFELDT–JAKOB DISEASE
P r ogressive Multifocal Leukoencephalopathy
Imaging Findings
CYTOMEGALOVIRUS (CMV) ENCEPHALITIS
REFERENCES
Immune Reconstitution Inflammatory S yndrome (IRIS) 89
White Matter Diseases and Metabolic Brain Disorders
Sumedha Pawa, Anjali Prakash
MYELIN AND WHITE MATTER
DEMYELINATING DISEASES: CLASSIFICATION
Associated with Physical/Chemical Agents or Therapeutic Procedures
IMAGING OF WHITE MATTER DISEASES
NEWER MAGNETIC RESONANCE TECHNIQUES
P r oton Magnetic Resonance Spectroscopy
P rimary Demyelinating Diseases
Multiple Sclerosis
Disorders with Secondary Demyelination and Destruction of White Matter
Associated with Infectious Agents and/or Vaccination
Associated with Nutritional/Vitamin Deficiency
Magnetization Transfer Magnetic Resonance Imaging
PRIMARY DEMYELINATING DISORDERS
Multiple Sclerosis
Diffusion Magnetic Resonance
Diagnosis
Magnetic Resonance Findings
Distribution and Characteristics of L esion in the Brain
A cute or Chronic Multiple Sclerosis?
T1 Black Holes: Chronic T1 Hypointense Lesions 22,23
Characteristics and Distribution of L esions in Spinal Cord
NORMAL APPEARING WHITE AND GRAY MATTER
Magnetization Transfer Imaging
Diffusion Tensor Imaging in Multiple Sclerosis
P r oton Magnetic Resonance Spectroscopy in Multiple Sclerosis
Imaging of Basal Ganglia in Multiple Sclerosis
P erfusion Imaging
F unctional Magnetic Resonance Imaging
High-Field Magnetic Resonance Imaging and Multiple Sclerosis
Monitoring Patients by Magnetic Resonance Imaging
V ariants of Multiple Sclerosis
A cute Multiple Sclerosis (Marburg Type)
Schilder Type or Diffuse Sclerosis
C oncentric Sclerosis (Balo Type)
Devic’s Neuromyelitis Optica
TREATMENT
DIFFERENTIAL DIAGNOSIS OF MULTIPLE SCLEROSIS LESION ON MAGNETIC RESONANCE
Ischemic White Matter Lesions/Small Vessel Ischemic Changes/Leukoaraiosis
V asculitis
Migraine
A cute Disseminated Encephalomyelitis
T r auma
Space-occupying Lesions
DISORDERS WITH SECONDARY DEMYELINATION AND/OR DESTRUCTION OF WHITE MATTER
W hite Matter Diseases Associated with V iral Agents Viral Encephalitides
A cute Disseminated Encephalomyelitis
A cute Hemorrhagic Leukoencephalitis
Subacute Sclerosing Panencephalitis
P r ogressive Rubella Panencephalitis
P r ogressive Multifocal Leukoencephalopathy
L yme Disease of the Central Nervous System
Human Immunodeficiency Virus Encephalopathy
METABOLIC CAUSES: WHITE MATTER DISEASES ASSOCIATED WITH NUTRITIONAL AND VITA
C entral Pontine and Extrapontine Myelinolysis ( Osmotic Demyelination)
Chronic Alcoholism
W ernicke Encephalopathy
Marchiafava–Bignami Disease
Subacute Combined Degeneration of the Spinal Cord
V ASCULAR CAUSES
Reversible Posterior Leukoencephalopathy
Eclampsia
Ischemia and Arteritis
Binswanger’s Disease (Subcortical Arteriosclerotic Encephalopathy) 70
C erebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and L eu
Global Hypoperfusion Syndromes
C entral Nervous System Vasculitis
Hypoxic–Ischemic Leukoencephalopathies
WHITE MATTER DISEASES ASSOCIATED WITH PHYSICAL/CHEMICAL AGENTS OR THERAPEUTI
Radiation and Chemotherapy
Solvent Vapor Abuse Leukoencephalopathy
C ONCLUSION
REFERENCES
C urrent Trends in Imaging of Epilepsy
Shailesh B Gaikwad
INDICATIONS FOR IMAGING 1
IMAGING OF REFRACTORY SEIZURES
MRI Protocols
S tructural Lesions in Chronic Epilepsy
Mesial Temporal Sclerosis
Disorders of Neuronal Migration and C ortical Organization
T umors
V ascular Malformations
Other MR Features Associated with Epilepsy
NEWER ADVANCES IN IMAGING IN EPILEPSY
Reformatted Images
Quantitative MRI
Magnetic Resonance Spectroscopy
T2 Relaxometry (Mapping)
Diffusion Tensor Imaging
T r actography
F unctional MR
Magnetoencephalography
W ada’s Test
P ositron Emission Tomography
Single-photon Emission Computed T omography
REFERENCES
Imaging of Supratentorial Brain Tumors
CLASSIFICATION OF SUPRATENTORIAL BRAIN TUMORS
P rimary Brain Tumors
GLIAL TUMORS
Astrocytoma
— Chordoma Metastatic Tumors
C alvarial/Meningeal/Masses
L o w -grade Astrocytoma
V ariants: Protoplasmic, Gemistocytic, F ibrillary, Mixed
L ocation
Imaging Features
Glioblastoma Multiforme (GBM) (WHO Grade IV )
V ariants: Giant Cell Glioblastoma, Gliosarcoma
L ocation
Imaging Features (CT/MRI)
Anaplastic Astrocytoma (Malignant) (WHO Grade III)
A dvanced MR Imaging: Techniques in Glioma Grading and Apparent Diffusion C
Pleomorphic Xanthoastrocytoma (Noninvasive, WHO Grade I)
Subependymal Giant Cell Astrocytoma
Imaging Features
Gliomatosis Cerebri
Gliosarcoma
Imaging Features
Oligodendroglioma
Imaging Features
Ependymoma
Imaging Features
Subependymoma
Choroid Plexus Papilloma
Imaging Features
C entral Neurocytoma
Imaging Features
Dysembryoplastic Neuroepithelial Tumor
Imaging Features
Ganglioglioma
TUMORS OF THE MENINGES
Meningioma
Imaging Features
P ineal Region Tumors
Germ Cell Tumors
P ineal Germinoma and Teratoma
P ineal Cell Tumors
Imaging Features
E pendymoblastoma Supratentorial Primitive Neuroectodermal Tumors
P rimary Cerebral Neuroblastoma
Cranial Nerve Tumors
Imaging Features
P rimary Central Nervous System Lymphoma
P ituitary Adenoma and Craniopharyngioma
Imaging of Metastatic Tumors
P a r enchymal Metastases
Imaging Features
L eptomeningeal Metastases
Imaging Features
Dural Metastases
C alvarial Metastases
Recent Advances in Brain Tumors
MAGNETIC RESONANCE SPECTROSCOPY IN BRAIN
T umor Imaging
Magnetic Resonance Perfusion Imaging
MAGNETIC RESONANCE SPECTROSCOPY
P ositron-emission Tomography in Neuro-oncology
Radiologic Pitfalls Encountered in Imaging of Brain Tumor
Late Diagnosis of Gliomatosis Cerebri
Differentiation between Peripherally Located Glioma (Gliosarcomas) and Meningi
L ocalized Enhanced Meninges (Meningeal Tail) or Meningioma
Differentiation of Radiation Effect from Recurrent or Residual Neoplasm
Radiation Necrosis versus Glioma Recurrence
C onventional MR Imaging Clues to Diagnosis
Differentiation of Hemorrhagic Metastasis or Gliomas from Hematoma
MR Features of Tumoral Hemorrhage
Differentiation of Infarcts from Glioma
Differentiating Multicentric Glioma/Multifocal Gliomas from Metastasis
Differentiating Inflammatory Meningitis from L eptomeningeal Carcinomatosis 32,
C erebrospinal Fluid Examination
Imaging Features of Normal Meningeal Enhancement
C ONCLUSION
REFERENCES
Imaging of Infratentorial Tumors
Ajay Garg
CLASSIFICATION OF INFRATENTORIAL TUMORS BASED ON TOPOGRAPHY 1
C erebellar Hemispheres and Vermis
Medulloblastoma
Ependymoma
P ilocytic Astrocytoma
Atypical Teratoid/Rhabdoid Tumor
Hemangioblastoma
Metastases
Dysplastic Cerebellar Gangliocytoma
Brainstem and Cervicomedullary Junction
Brainstem Gliomas
C erebellopontine Angle and Internal Auditory Canal
V estibular Schwannomas
Meningiomas
Epidermoid and Dermoid
Arachnoid Cyst
F acial Nerve Schwannomas
C erebellopontine Angle/Internal A uditory Canal Lipomas
Metastatic Disease
P rimary Parenchymal Neoplasms
Endolymphatic Sac Tumor
P araganglioma
F ourth Ventricle
Choroid Plexus Papillomas
Subependymoma
C ONCLUSION
REFERENCES
Sellar and Parasellar Lesions
P aramjeet Singh, Niranjan Khandelwal
NORMAL ANATOMY AND APPLIED PHYSIOLOGY
IMAGING MODALITIES
C OMPUTED TOMOGRAPHY
MAGNETIC RESONANCE IMAGING
P A THOLOGY OF THE SELLAR AND P ARASELLAR REGION
TUMORS
P ituitary Adenoma
T ypes of Adenomas
Imaging of Adenomas
A typical Presentations of Adenomas
P ostoperative Sella
Craniopharyngioma
P ituicytoma
Meningioma
Germinoma and Teratoma
Dermoid and Epidermoid Tumors
Chiasmatic/Hypothalamic Glioma
Schwannoma
SKULL BASE LESIONS
Chordoma
Metastasis
C ongenital and Metabolic Abnormalities of P ituitary Gland
Developmental Anomalies of Pituitary Gland
P ituitary Hypoplasia and Congenital P ituitary Deficiency Disorders
Empty Sella
Diabetes Insipidus
Hemochromatosis
TUMOR LIKE LESIONS
P ituitary Hyperplasia
Arachnoid Cysts
Rathke’s Cleft Cysts
T uber Cinereum Hamartoma
INFECTIVE CONDITIONS
F ungal Infection
INFLAMMATORY/GRANULOMATOUS C ONDITIONS
Langerhans Cell Histiocytosis
L ymphocytic Hypophysitis
Sarcoidosis
T olosa-Hunt Syndrome
V ASCULAR LESIONS
Aneurysms and Vascular Loops
C arotid Cavernous Fistula and Cavernous Malformations
Sheehan’s Syndrome
REFERENCES
Intraventricular Lesions
Niranjan Khandelwal, Paramjeet Singh
IMAGING MODALITIES
Lateral Ventricular Masses
Choroid Plexus Papilloma (CPP)
Astrocytoma
Subependymal Giant Cell Astrocytoma (SGCA)
Ependymoma
Meningioma
Metastases
P rimary CNS Lymphoma
C entral Neurocytoma
Subependymoma
V ascular Malformations
Choroid Plexus Cysts and Xanthogranulomas
T hird Ventricular Masses
Anterior Third Ventricular Masses
C olloid Cyst
Astrocytoma
Ependymoma
Germinoma
Metastases
Craniopharyngioma
Epidermoid and Dermoids
C ysticercosis
P ituitary Tumor
P osterior Third Ventricular Masses
Glial Tumors
Germinoma
T eratoma
P ineoblastoma
P ineocytoma
V ascular Masses
F ourth Ventricular Masses
C e r e bellar Astrocytoma
Medulloblastoma
Ependymoma
Brainstem Gliomas
REFERENCES
Imaging of the Temporal Bone
V ivek Gupta, Niranjan Khandelwal
C OMPUTED TOMOGRAPHY TECHNIQUE
MAGNETIC RESONANCE IMAGING
C ONGENITAL ANOMALIES OF THE TEMPORAL BONE
Anomalies of the External and Middle Ear
Inner Ear Abnormalities
C omplete Labyrinthine Aplasia or Michele Aplasia
C ommon Cavity
C ochlear Aplasia
C ochlear Hypoplasia
Incomplete Partition or Dilatational Defects
C ongenital Dilatation of the Vestibular Aqueduct
V estibular Anomalies
V ascular Anomalies
T emporal Bone Fractures
Inflammatory Diseases of the Temporal Bone
Inflammatory Conditions of the External Ear
Inflammatory Condition of the Middle Ear
C OMPLICATIONS
A c quired Cholesteatomas
O THER COMPLICATIONS
Inflammatory Conditions of the Inner Ear
RADIOLOGICAL EVALUATION OF VASCULAR TINNITUS AND VASCULAR TYMPANIC MEMBRANE
C auses of Pulsatile Tinnitus 33
Normal Vascular Variants
P a thological Vascular Causes
Arterial Causes
Arteriovenous Causes
V enous Tinnitus
Otosclerosis
D Y SPLASTIC CONDITIONS OF THE TEMPORAL BONE
T umors of the Temporal Bone
Imaging of the Globe and Orbit
Sanjay Sharma, Smriti Hari, Deep N Srivastava
Radiographic Views
Ultrasound
NORMAL ANATOMY
C omputed Tomography
Magnetic Resonance Imaging
P A THOLOGICAL CONDITIONS
OCULAR LESIONS
Ocular Detachments
V itreous Hemorrhage
Retinoblastoma
P ersistent Hyperplastic Primary Vitreous
C oats’ Disease
U v eal Malignant Melanoma
C horoidal Metastases
F oreign Body
C ongenital Anomalies
P arasitic Infestation
ORBITAL LESIONS
ORBITAL TUMORS
Hemangioma
C apillary Hemangioma
C avernous Hemangioma
L ymphangioma
Lacrimal Gland Tumors
Optic Nerve Glioma
Meningioma
Sphenoid Wing Meningioma
Optic Nerve Sheath Meningioma
Rhabdomyosarcoma
Meningioma Arising from Arachnoid Cells Rests W ithin the Orbit
L ymphoma
Schwannoma/Neurofibroma
Orbital Metastases
Developmental Cysts
INFLAMMATORY LESIONS
P seudotumor
Endocrine Orbitopathy
P arasitic Cysts
V ASCULAR LESIONS
C arotico-cavernous Fistula
Orbital Varices
Osseous Lesions
T r auma
REFERENCES
Imaging of the Paranasal Sinuses
V ivek Gupta, Niranjan Khandelwal
P ARANASAL SINUS EMBRYOLOGY
IMAGING MODALITIES AND TECHNIQUE OF EVALUATION
C onventional Radiography
MAGNETIC RESONANCE IMAGING
NORMAL ANATOMY AND ANATOMIC V ARIATIONS 1 2-14
Normal Anatomy
Nasal Structures
Draining Pathways
Anatomic Variations
C oncha Bullosa
Nasal Septum Deviation
P aradoxical Middle Turbinate
V ariations in the Uncinate Process
INFLAMMATORY SINUS DISEASE
A cute Sinusitis
Chronic Sinusitis
P ost-FESS Scanning
Mucocele
F ungal Sinusitis
Allergic Fungal Rhinosinusitis (AFRS)
GRANULOMATOUS DISEASES
Invasive Fungal Sinusitis
Noninvasive Chronic Fungal Sinusitis
P olyps and Cysts
NEOPLASTIC LESIONS OF THE PARANASAL SINUSES
Epithelial Tumors of the PNS
Epithelial Tumors of Glandular Origin
NONEPITHELIAL TUMOR OF PARANASAL SINUSES
Angiofibroma
L ymphomas
Plasmacytoma
Olfactory Neuroblastoma (Olfactory Neuroepithelioma/Esthesioneuroblastoma)
Neurofibromas
FIBROSSEOUS LESIONS OF CRANIOFACIAL BONES 45,46
Ossifying Fibroma
P aget’s Disease
REFERENCES
Imaging of the Neck Spaces
NORMAL RADIOLOGICAL ANATOMY OF SUPRAHYOID AND INFRAHYOID NECK
Superficial or Investing Layer
Masticator Space
P arotid Space
Submandibular Space
V isceral or Pretracheal Layer
Pharyngeal Mucosal Space
P arapharyngeal Space
Buccal Space
Retropharyngeal Space
Deep Layer of Deep Cervical Fascia or P r evertebral Fascia
C arotid Space
P r evertebral Space
IMAGING TECHNIQUES
P erfusion Computed Tomography
Magnetic Resonance Imaging
Diffusion-weighted MRI of Nodes
P erfusion MR Imaging
L ymph Node Specific MR-contrast Agents
T umor Recurrence versus Treatment Changes: P ositron-emission Tomography
Dynamic Contrast-enhanced CT and MRI of the Nodes
P r oton MR Spectroscopy
NODAL NECK MASSES
Staging
Imaging Characteristics: Cross-sectional Imaging
L ymph Node Size and Contour
Nodal Necrosis
Nodal Calcification
Extracapsular Neoplastic Spread
Skull Base and Vertebral Invasion
NON-NODAL NECK MASSES
MASSES OF DEVELOPMENTAL ORIGIN
Branchial Cleft Cysts
Ranula
L ymphangioma
T h yroglossal Duct Cyst
T ornwaldt’s Cyst
Imaging Features
MASSES OF INFLAMMATORY ORIGIN
Dermoid and Epidermoid Cysts
T onsillitis and Peritonsillar Abscess
Imaging Features
A cute and Chronic Parotitis
A cute Parotitis
Chronic Parotitis
Sialolithiasis
L udwig’s Angina
Ranula
Inflammatory Pathology of the Carotid Space
Inflammatory Disease of the Retropharyngeal Space
Imaging Features
Inflammatory Lesions of the Prevertebral Space
MASSES OF NEOPLASTIC ORIGIN
Benign Tumors
Juvenile Nasopharyngeal Angiofibroma
W arthin’s Tumor
Neurogenic Tumors
Benign Tumors of the Parotid
Hemangiomas and Lymphangiomas
Malignant Tumors
Nasopharyngeal Carcinoma
Oropharyngeal Carcinoma
Non-Hodgkin’s Lymphoma
Nasopharyngeal Rhabdomyosarcoma
Malignant Tumors of the Salivary Glands
Imaging Patterns on CT and MR
P rimary Malignant Lesions in the P r evertebral Space
MASSES OF NEURAL ORIGIN
Neurofibromas
Imaging Features
Imaging Features
MASSES OF VASCULAR ORIGIN
Aneurysm
P aragangliomas
Diffusion-weighted Imaging in Paragangliomas 51
MASSES OF MESENCHYMAL ORIGIN
REFERENCES
Thyroid Imaging
Alpana Manchanda
THYROID GLAND
Embryology
Anatomy
Endocrinology
CLINICAL MANIFESTATIONS OF THYROID DISEASE
THYROID IMAGING
Plain Radiographs
Nuclear Scintigraphy
Ultrasonography
Cross-sectional Imaging
P A THOLOGY OF THE THYROID GLAND DEVELOPMENTAL ANOMALIES
Lingual Thyroid
T h yroglossal Duct Cyst
DIFFUSE THYROID DISEASE
Diffuse Nontoxic Goiter
Imaging Features
Graves’ Disease (Diffuse Toxic Goiter)
Chronic Autoimmune Lymphocytic (Hashimoto’s) Thyroiditis
Silent Painless Thyroiditis and P ostpartum Thyroiditis
A cute Suppurative Thyroiditis
Imaging Features
Subacute Granulomatous Thyroiditis (de Quervain’s Disease)
Imaging Features
Invasive Fibrous Thyroiditis (Riedel’s Struma)
MISCELLANEOUS THYROID C ONDITIONS
Nodular Thyroid Disease
Imaging Features
DIFFERENTIATION OF BENIGN AND MALIGNANT THYROID NODULES
Ultrasound-elastography
C ontrast-enhanced Ultrasound for Evaluation of Thyroid Nodules
Diffusion-weighted MRI (DW-MRI)
T h yroid Incidentalomas
MANAGEMENT OF THYROID NODULES DETECTED AT ULTRASOUND
P ercutaneous Aspiration and Biopsy
ULTRASOUND-GUIDED THYROID NODULE ALCOHOL ABLATION
BENIGN NEOPLASMS
T h yroid Adenoma
Imaging Features
MALIGNANT NEOPLASMS
P apillary Carcinoma
Imaging Features
F ollicular Carcinoma
Imaging Features
Hurthle Cell Neoplasms of the Thyroid
Medullary Carcinoma
Anaplastic Carcinoma
Imaging Features
P rimary Lymphoma
Metastatic Disease
REFERENCES
Malignancies of Upper A erodigestive Tract
Sanjay Thulkar, Ashu Seith Bhalla, Sanjay Sharma
ORAL CAVITY
F loor of Mouth
Oral Tongue
Lip
Gingivoalveolus
Retromolar Trigone
Buccal Mucosa
Hard Palate
S taging of Oral Cavity Cancers
Imaging Strategies in Oral Cavity Cancer
T r eatment of Oral Cavity Cancers
NASOPHARYNX
Nasopharyngeal Carcinoma
S taging of Nasopharyngeal Carcinoma
Imaging Strategies in Nasopharyngeal C arcinoma
T r eatment of Nasopharyngeal Carcinoma
OROPHARYNX
C arcinoma of Tonsil
C arcinoma of Soft Palate
C arcinoma of Base of Tongue
T r eatment of Carcinoma of Oropharynx
H Y POPHARYNX
C arcinoma of Posterior Wall of Hypopharynx
C arcinoma of the Pyriform Sinus
C arcinoma of the Postcricoid
T r eatment of Carcinomas of Hypopharynx
LARYNX
Supraglottic Carcinoma
Glottic Carcinoma
Subglottic Carcinoma
Imaging Strategies in Carcinoma of Larynx
C artilage Invasion by Carcinoma of Larynx
T r eatment of Carcinoma of Larynx
CERVICAL LYMPH NODES
Imaging of Cervical Lymph Nodes
Management of Cervical Lymph Nodes
C ervical Lymphadenopathy with Carcinoma of Unknown Primary Site (CUPS)
Distant Metastases and Second Primary Tumors
MISCELLANEOUS TUMORS
Minor Salivary Gland Tumors
Rhabdomyosarcoma
L ymphoma
POST-TREATMENT IMAGING
P ostradiotherapy Neck
Late Effects of Radiotherapy
P ostoperative Neck
REFERENCES
Imaging of Skull Base Lesions
Atin Kumar, Ashu Seith Bhalla
ANATOMICAL DIVISION
IMAGING TECHNIQUES AND THEIR ROLE
ANTERIOR SKULL BASE
Anatomy
P a thology
L esions Arising from Below
Sinonasal Lesions
Orbital Lesions
Lacrimal Gland Tumors
L esions Arising from Above
Olfactory Groove Meningioma
L esions of the Proper Skull Base
T r auma and CSF Leak
MIDDLE SKULL BASE
Anatomy
P a thology
Midline Sagittal Central Skull Base Lesions
Sphenoid Mucocele
Clival Chordoma
P ituitary Macroadenoma
Craniopharyngioma
Meningiomas
Encephaloceles
Other Miscellaneous Lesions
P arasagittal, Central Skull Base Lesions
P eripheral Nerve Sheath Tumors
P erineural Spread
Juvenile Nasopharyngeal Angiofibroma
C avernous Sinus Lesions
Chondroid Tumors
Lateral Central Skull Base Lesions
Meningioma
T emporomandibular Joint Lesions
POSTERIOR SKULL BASE
Anatomy
P a thology
Jugular Foramen Lesions
Glomus Jugulare Paraganglioma
Nerve Sheath Tumors
L esions Extending into the Jugular Foramen
Jugular Bulb Pseudolesion
Large or High Riding Jugular Bulb
P etrous Apex Lesions
Nonaggressive Cystic Expansile Lesions
A g gressive Appearing Solid Lesions
F oramen Magnum Lesions
DIFFUSE/NONSITE-SPECIFIC SKULL BASE LESIONS
Metastases
F ibrous Dysplasia
C ONCLUSION
REFERENCES
P aget’s Disease
Miscellaneous Conditions
Maxillofacial Imaging: Imaging of Cysts, Tumors and Tumor-like C onditions o
Ashu Seith Bhalla, Atin Kumar, Sanjay Thulkar
IMAGING MODALITIES
Plain Radiography
Intraoral Radiographs
Extraoral Radiographs
Computed Tomography
Dental Computed Tomography Reformatting Programs
Cone-Beam Computed Tomography
CLASSIFICATION
CLINICAL FEATURES
RADIOLOGICAL FEATURES/APPROACH
Anatomical Location/Site
Radiodensity and Internal Architecture of Lesion
Relation to Dentition
Relation to Mandibular Canal
Size
Shape
OUTLINE/DEFINITION/MARGINATION
Surrounding Bone
Surrounding Soft Tissues
WELL-DEFINED RADIOLUCENT LESIONS
Jaw Cysts
Odontogenic Cysts
Effect on Surrounding Structures
Teeth
Nonodontogenic Cysts
TUMORS OR TUMOR-LIKE CONDITIONS
Odontogenic Tumors
Ameloblastoma
Nonodontogenic Lesions
Central Giant Cell Granuloma
Ameloblastic Fibroma
Eosinophilic Granuloma
Central Hemangioma
Arteriovenous Malformation
Radiolucent Lesions with Ill-defined Margins
Malignant Tumors
Primary Tumors
Mixed-Density Lesions
Odontogenic Lesions
Nonodontogenic Lesions
Radiopaque Lesions
Odontogenic Lesions
CONCLUSION
REFERENCES
Craniovertebral Junction Anomalies
ANATOMY AND EMBRYOLOGY
Skeletal Anatomy (Figs 1A to D)
F oramen Magnum and the Occiput
Atlas
Ligamentous Anatomy (Figs 2A and B)
Embryology
BIOMECHANICS
CLINICAL PRESENTATION
CRANIOMETRY
CLASSIFICATION OF CVJ ANOMALIES 12
C ongenital Anomalies and Malformations of the Craniovertebral Junction
— Segmentation failure of C2-C3 Developmental and Acquired Abnormalities
NEURORADIOLOGIC INVESTIGATIONS
INCIDENCE
SPECIFIC CONDITIONS
Basilar Invagination
Assimilation of Atlas
A tlas Arch Anomalies
Dens Dysplasias
Os Terminale
Os Odontoideum
A tlantoaxial Instability
Classification of AAI
Inflammatory, Arthritic and Infectious Disorders
TRAUMA
SYNDROMES INVOLVING THE CVJ 35
Klippel-Feil Syndrome
Down Syndrome
Arnold-Chiari Malformation
Chiari I Malformation
Chiari II Malformation
Chiari III Malformation
A chondroplasia
Mucopolysaccharidoses
Osteogenesis Imperfecta
SUMMARY
REFERENCES
Endovascular Management of Craniofacial Vascular Lesions
Ajay Kumar, Niranjan Khandelwal
EMBOLIC AGENTS
PRETHERAPEUTIC EVALUATION
IMPORTANT ANATOMIC CONSIDERATION
POSTEMBOLIZATION CARE
NASOPHARYNGEAL ANGIOFIBROMAS
P ARAGANGLIOMA
CRANIOFACIAL VASCULAR LESIONS
V ascular Tumor
Hemangiomas
V ascular Malformations
Aneurysms
MISCELLANEOUS LESIONS
Epistaxis
SUMMARY
Imaging of Head Trauma
Shivanand Gamanagatti, Atin Kumar, Arun Kumar Gupta
A c c ording to Clinical Severity [ Glasgow Coma Scale (GCS)] 3
Marshall CT Classification of Head Injury 4
C ategories
TBI CLASSIFICATION
Broad Classification
A c c ording to Location of Lesions
A c c o r ding to Mechanism
GOALS OF NEUROIMAGING
IMAGING TECHNIQUES
Plain Radiographs
E vidence Based Guidelines for Imaging Patients with Head Injury
IMAGING FINDINGS
Scalp Injury
T y pes of Scalp Injury
Skull Fractures
T y pes of Skull Fractures
Recommendations
TEMPORAL BONE FRACTURES
W hen to Suspect Temporal Bone Fractures?
T ypes of Temporal Bone Fractures 23 (Figs 8A and B)
PRIMARY HEAD INJURY LESIONS
EXTRA-AXIAL INJURY 9,22
Epidural Hematoma
Imaging Features
Ominous Sign
Management 25
Subdural Hematomas
Imaging Features
Challenges during Interpretation 9,22
Subdural Hematoma Evolution on MRI
Subarachnoid Hemorrhage
Magnetic Resonance Imaging of SAH
Intraventricular Hemorrhage
INTRA-AXIAL INJURY
Diffuse Axonal Injury
V ASCULAR INJURY
CAROTID CAVERNOUS FISTULA
T r eatment of Carotid Cavernous Fistula 31
T ypes of Carotid Cavernous Fistula 31
SECONDARY HEAD INJURY
A CUTE SECONDARY CHANGES
Diffuse Cerebral Swelling
Imaging Features of Cerebral Edema
Brain Herniation
Subfalcine Herniation
Uncal Herniation
T r anstentorial Herniation
Infarction or Ischemia
CHRONIC SECONDARY CHANGES
T r aumatic Hydrocephalus
C erebrospinal Fluid
Imaging 32,33
Encephalomalacia
CT Imaging
Magnetic Resonance Imaging
C omputed Tomography Cisternography
L eptomeningeal Cyst or “Growing Fracture”
Imaging of Facial Trauma
Ajay Kumar, Vivek Gupta
IMAGING TECHNIQUES
F A CIAL BUTTRESSES AND REGIONAL CLASSIFICATION OF INJURIES 5,6
Importance of Facial Buttresses 14
Regional Facial Fractures
F r ontal Sinus Fractures
CLASSIFICATION OF MAXILLOFACIAL FRACTURES
Nasal Fractures
C entral Midface Fractures
L e Fort Fractures
L ateral Midface Fractures
Blowout Fractures of the Orbit
Mandibular Fractures
Sphenoid Sinus Fractures
PEDIATRIC FACIAL FRACTURES
CLINICAL ASPECTS OF MAXILLOFACIAL IMAGING
Imaging of Acute Spinal Trauma
Sameer Vyas, Niranjan Khandelwal, Paramjeet Singh
IMAGING INDICATIONS
IMAGING MODALITIES
P lain Radiography
C omputed Tomography
Magnetic Resonance Imaging
CLASSIFICATION OF SPINAL TRAUMA
L e v el of Injury
Severity of Injury
Mechanism of Injury
CERVICAL SPINE INJURY
Upper Cervical Spine Injuries
S table versus Unstable Fracture
A tlanto-occipital Dislocation
A tlantoaxial Injuries
RADIOLOGICAL INTERPRETATION OF SPINAL TRAUMA (ABCS)
F r actures of the Atlas (C1)
F r actures of the Axis (C2)
L o w er Cervical Spine Injury (C3-C7)
THORACOLUMBAR SPINE INJURY
C ompression or Wedge Fracture
Burst Fracture
F r acture Dislocation
Lap Seat-belt Type Fracture or Chance Fracture
NONOSSEOUS INJURY
Spinal Cord Injuries
Subacute and Chronic Injuries
SCIWORA
W hiplash Injury
V ascular Injury
SUMMARY
REFERENCES
Imaging of Spinal Neoplasms
Ajay Garg
INTRAMEDULLARY TUMORS
Solitary Lesions
Ependymomas
CLASSIFICATION OF LESIONS
Subependymoma
Myxopapillary Ependymoma
Astrocytomas
Gangliogliomas
Hemangioblastomas
P araganglioma
Multiple Lesions
Intramedullary Lymphoma
Intramedullary Metastases
Nerve Sheath Tumors
INTRADURAL-EXTRAMEDULLARY TUMORS
Solitary Lesions
Meningiomas
Intradural Metastases
EXTRADURAL TUMORS
Multiple Lesions
Metastatic Disease
Multiple Myeloma
L ymphoma
Hemangioma
Solitary Lesions
Aneurysmal Bone Cyst
Giant Cell Tumor
Osteoid Osteoma
Osteoblastoma
Osteosarcoma
Osteochondromas
Chordoma
Chondrosarcoma
Chondroblastoma
EPIDURAL LESIONS
A ngiolipoma
Epidural Lipomatosis
Spinal Vascular Malformations
SPINAL DURAL ARTERIOVENOUS FISTULA
SPINAL CORD PERIMEDULLARY ARTERIOVENOUS FISTULA
SPINAL CORD AVMS
SPINAL VASCULAR MALFORMATIONS
Imaging of Low Backache
Raju Sharma, Shivanand Gamanagatti, Arun Kumar Gupta
IMAGING OF LOW BACK PAIN
W hen to Image
C onditions Causing Back Pain
IMAGING MODALITIES
Radiographs
Magnetic Resonance Imaging, Computed T omography, Myelography, Myelography/CT
Magnetic Resonance Imaging
Myelography/CT
Discography, CT Discography
Isotope Bone Scan
TRANSITION VERTEBRA
C omputed Tomography
SPONDYLOLYSIS AND SPONDYLOLISTHESIS
Imaging
DEGENERATIVE DISEASES OF LUMBAR SPINE
Degenerative Changes in the Anterior Elements
SCHEUERMANN’S DISEASE
Clinical Presentation
Imaging and Diagnosis
Degenerative Changes in the P osterior Elements
DEGENERATIVE CHANGE OF THE NUCLEUS PULPOSUS
Normal Disk
C omplications of Degenerative Spinal Disease
P r esentation
MR Appearance of Normal Disk
MR Appearance
Abnormal Nucleus
Disk Herniation (Abnormalities in Disk Morphology)
P oints to Remember
Sequestered disk. 25-27 P oints to Remember
Annular Tears
Method of Quantifying the Severity of Disk Disease
L ocation of Focal Disk Abnormalities
Significance of Disk Contour Abnormalities
Intraosseous Disk Herniations
P r esentation
P oints to Remember
OSSEOUS DEGENERATIVE CHANGES
V e rtebral Bodies
Osteophytes
Endplates
C auses
F acet Joints
Normal Facet Joints
F a c et Joint Arthropathy
P osterior Spinous Processes
Spinal Stenosis
T y pes of Involvement
F ailed Back Syndrome
Seronegative Spondyloarthropathy
INFECTIONS
T ubercular Infection
CT Features
MR Features
Uncommon Patterns
Differential Diagnosis
Pyogenic Infection
TUMORS
Benign Tumors
Hemangioma
Osteoid Osteoma
Osteoblastoma
Aneurysmal Bone Cyst
Giant Cell Tumor
Malignant Tumors
Chordoma
Metastases
Multiple Myeloma (Figs 28A to D)
C ONCLUSION
REFERENCES
L ymphoma
L ocalization in Clinical Neurology
Manish Modi, Sudesh Prabhakar
L OCALIZATION IN CLINICAL NEUROLOGY
C linical Diagnosis and Lesion Localization
DISORDERS OF CRANIAL NERVES
OLFACTORY NERVE (CRANIAL NERVE I)
A nosmia
APPROACH TO NEUROLOGICAL DISORDER
OPTIC NERVE (CRANIAL NERVE II)
V isual Pathway Localization (Fig. 2)
OCULOMOTOR SYSTEM
(CRANIAL NERVE III, IV, VI) (TABLE 1)
Supranuclear Lesions
Nuclear Lesions
Internuclear Ophthalmoplegia
Infranuclear Lesions
Other Disorders of Oculomotor System
TRIGEMINAL NERVE (CRANIAL NERVE V)
F A CIAL NERVE (CRANIAL NERVE VII)
L ocalization of Facial Nerve Lesions (Fig. 3)
Supranuclear Palsy
Infranuclear Facial Nerve Palsy
VESTIBULOCOCHLEAR NERVE (CRANIAL NERVE VIII)
GLOSSOPHARYNGEAL AND VAGUS NERVE (CRANIAL NERVE IX, X)
P alatal Myoclonus
SPINAL ACCESSORY NERVE (CRANIAL NERVE XI)
Muscle Bulk
P o w er Testing
Muscle Tone
H Y POGLOSSAL NERVE (CRANIAL NERVE XII)
DISORDERS OF MOTOR SYSTEM
Spasticity
Extrapyramidal Rigidity
Reflexes
Biceps Jerk
Supinator Jerk
T riceps Jerk
Knee Jerk
Ankle Jerk
Hoffman Reflex
A bnormalities of Tendon Reflexes
Superficial Reflexes
Abdominal Reflexes
Cremasteric Reflex
Anal Reflex
P lantar Reflex
Other Important Reflexes
Grasp Reflex
F orced Grasping Reflex
Sucking Reflex
Glabellar Tap
C oordination
F inger Nose Test
Heel-Knee Test
Dysdiadochokinesis
P ast Pointing Test
Sensory System
Gait
Dysphasia
DISORDERS OF HIGHER MENTAL FUNCTION
DISORDERS OF SPEECH
Dysarthria
APRAXIA
P ARIETAL LOBE DYSFUNCTIONS
A GNOSIA
V isual Agnosia
T actile Agnosia
A uditory Agnosia
C ONCLUSION
SUGGESTED READING
Basic Neuropathology
Kirti Gupta, Rakesh Kumar Vasishta
REMOVAL OF THE BRAIN FROM SKULL
REMOVAL OF VENOUS SINUS, CAVERNOUS SINUS AND MIDDLE EAR EXAMINATION
EXAMINATION OF THE BRAIN
Gross Features to be Noted
Slicing of Brain
Choice of Blocks for Histology
P ediatric Brain Examination
Appearance of the Ventricles
INFECTIONS
C onsequences of Infection
L eptomeningitis
A cute Meningitis
Routes of Infection
T ubercular Meningitis (Figs 3B to 6)
Chronic Meningitis
F ungal Meningitis/Encephalitis
Subdural Empyema
Brain Abscess
P urulent Encephalitis Associated with Subacute Bacterial Endocarditis
V iral Encephalitis (Fig. 10)
P ostmortem Examination in Cases of Suspected V iral Encephalitis
Macroscopic Examination of the CNS and the Choice of Blocks for Microscopy
P athological Features Common to Most Forms of V iral Encephalitis
NEUROVASCULAR DISEASES
Arterial Infarcts or Territorial Infarcts
Embolic Infarcts
C erebral Venous Infarcts (Fig. 13)
Lacunar Infarcts
P r actical Considerations
Intracranial Hemorrhage
Aneurysm
Arteriovenous Malformations
Demyelinating Disease and Multiple Sclerosis
Gross Features
Inherited Metabolic Diseases
TUMORS
P ostmortem Examination of Cases of CNS Tumor
T umors of Neuroepithelial Tissue
General Guidelines
Recent Advances and Applied P h y sics in Imaging
Ultrasound Instrumentation: P r actical Applications
K ushaljit Singh Sodhi, Akshay Kumar Saxena, Mukesh Kumar Yadav
High-frequency Transducer
Medium-frequency Transducer
L o w -frequency Transducer
M A CHINE CONTROLS
FREQUENCY OF TRANSDUCERS
TYPES OF TRANSDUCERS
Linear-array Transducer
C urvilinear-array Transducer
P hased-array Transducer
Doppler
T issue-harmonic Imaging
Spatial-compound Imaging
EXTENDED FIELD OF VIEW
Elastography
3D and 4D Ultrasound
Gynecology
Obstetrics
Limitations
F usion Imaging
CLINICAL APPLICATIONS OF FUSION IMAGING
T herapeutic Applications of Ultrasound
Limitations
Ultrasound-based Molecular Imaging and Oncotherapy
Ultrasound-image Artifacts
Image Optimization in Ultrasound
GRAYSCALE IMAGING
Basic Guidelines 2-5
Factory Presets
Transducer Selection
Overall Gain
Time-gain Compensation
Depth Setting
Focal-zone Setting
Zoom
Dynamic Range
ARTIFACTS IN B MODE IMAGING 3 ,
Beam-width Artifact
Slice-thickness Artifact
Side-lobe and Grating-lobe Artifacts
Artifacts Associated with Multiple Echoes
Reverberation Bands
Mirror-image Artifact
Artifacts Associated with Velocity Errors
Refractory Errors
Attenuation Errors
Acoustic Shadowing
Edge Shadowing
Increased through Transmission or Distal Bright-up’
Noise
SPECTRAL AND COLOR DOPPLER EXAMINATION
Basic Guidelines 7
Optimizing Color Doppler and Spectral Doppler Settings 7-11
Color Box or Color Doppler Sampling Window
Doppler or Color Gain
Velocity Scale
Gate Size or Sample Volume Box
Sample Volume or Gate Position
Angle Correction
Color-write Priority
Directional Ambiguity
Baseline
Wall Filters
Inversion of Flow
Slow Flow
Anatomically Related Artifacts
Artifacts Unrelated to Blood Flow
Perivascular or Color-bruit Artifact
SPECIAL IMAGING MODES 1-3,10,13-16
Tissue-harmonic Imaging
COMPOUND IMAGING
Spatial-compound Imaging
Coded-pulse Excitation
Adaptive-image Processing
Photopic-ultrasound Imaging
Extended Field of View Imaging
B-Mode Flow Imaging
3D–4D Ultrasound
CONCLUSION
REFERENCES
Ultrasound Elastography: P rinciples and Application
V eenu Singla, Tulika Singh, Anindita Sinha
B ASIC PHYSICS
S tress
S train
Elasticity
V iscosity
V iscoelasticity
P oroelasticity
DEPICTION OF ELASTOGRAMS
DIFFERENT ELASTOGRAPHY TECHNIQUES
C ompression Elastography
Limitations
A c oustic Radiation Force Impulse
P rinciple and Technique
Measurement
Quantitative versus Qualitative
A dvantages
Disadvantages
Safety
Shear-wave Imaging
Principle and Technique
Measurement
Qualitative versus Quantitative
Advantages
Disadvantages
Advances in Shear-wave Imaging
Harmonic-motion Imaging
Technique
Application
Shear-dispersion Ultrasound Vibrometry
T echnique
Measurement
Mechanical Imaging
Measurement
Application
ELASTOGRAPHY APPLICATIONS
Breast
Elastosonographic Score (Fig. 3)
Elastographic Appearances of the Breast Masses
Liver
Diffuse Liver Diseases: Fibrosis, Cirrhosis, Acute Hepatitis, Nonalcoholic Fat
F actors Influencing Liver Stiffness
Ultrasound Elastography
C omparison Between ARFI, Real-time Elastography and Transient Elastography f
F ocal Liver Lesions
P r ostate
L ymph Nodes
T h yroid
G ynecology
C ervical Elastography
C ervical Cancer
F ibroids
F ibroids vs Adenomyosis
Endometrial Pathologies
Musculoskeletal
Appearance of Normal Tendons
V enous Thrombosis
O THER APPLICATIONS
Renal Transplant A ssessment
S kin and Soft Tissue
Endoscopic Ultrasonography
C ardiovascular Applications
Limitations of EUS Elastography
P itfalls
C ONCLUSION
C omputed Tomography Hardware: An Update
Ashu Seith Bhalla, Arun Deep Arora
B ASIC WORKFLOW OF CT SCANNER
DETERMINANTS OF AN OPTIMAL IMAGE
Spatial Resolution
T emporal Resolution
C ontrast Resolution
ADVANCES IN HARDWARE
A dvances in CT Tube
A dvances in Detectors
A dvances in Reconstruction
Rebinning Algorithms
SPECIAL C OMPUTED TOMOGRAPHY
C one-beam CT/Volume CT
C one-beam Geometry
F lat-panel Detector
Reconstruction
R adiation Dose
Applications
C-arm Based CBCT
Navigation Systems
C ONCLUSION
Dual-energy Computed Tomography
Arun Kumar Gupta, Manisha Jana
HISTORICAL PERSPECTIVE
PRINCIPLE
DUAL-ENERGY RATIO
Spectral Separation and Selective-photon Shield
Dual-source DEC T
P r ocessing of Data and Image Reconstruction in Dual-energy Imaging
Single-source DECT
Dual-energy CT with Layered Detectors
Image Display in DECT
APPLICATIONS OF DECT
Applications in Abdomen
Renal Applications
Applications in Adrenal
A drenal Adenoma
Hepatic Mass Characterization
Application in Pancreas
P ulmonary Applications
Musculoskeletal Applications
Applications in Head and Neck
V ascular Applications
C ardiac Applications
Applications in Neuroimaging
DOSE CONSIDERATIONS
REFERENCES
Limitation
C ONCLUSION
A CKNOWLEDGMENTS
C omputed Tomography P erfusion Imaging
PERFUSION COMPUTED TOMOGRAPHY TECHNIQUE BASIC PRINCIPLE
Unenhanced CT Acquisition
Dynamic CT Acquisition
PERFUSION COMPUTED TOMOGRAPHY PROTOCOLS
T echnique of CT Perfusion
C OMPUTED TOMOGRAPHY PERFUSION IN A CUTE ISCHEMIC STROKE
C ontrast Medium
A c quisition Parameters
C OMPUTED TOMOGRAPHY PERFUSION IN ONCOLOGY
HEPATIC COMPUTED TOMOGRAPHY PERFUSION 3 5-39
P erfusion Parameters of Normal Liver
CT Perfusion in Hepatocellular Carcinoma
CT Perfusion in Metastatic Disease
CT Perfusion in Focal Liver Lesions
C OMPUTED TOMOGRAPHY PERFUSION IN P ANCREATIC NEOPLASMS
C OMPUTED TOMOGRAPHY PERFUSION IN COLORECTAL CARCINOMA
C OMPUTED TOMOGRAPHY PERFUSION IN PROSTATE CANCER
C OMPUTED TOMOGRAPHY PERFUSION IN LYMPHOMA
C OMPUTED TOMOGRAPHY PERFUSION IN BRAIN TUMORS
C OMPUTED TOMOGRAPHY PERFUSION IN HEAD AND NECK TUMORS
C OMPUTED TOMOGRAPHY PERFUSION IN L UNG CANCER
O THER APPLICATIONS
Nephrology
Chronic Liver Diseases
CT Perfusion in Liver Transplantation
A cute Pancreatitis
RADIATION ISSUES
C ONCLUSION
REFERENCES
Magnetic Resonance Instrumentation: An Update
Anjali Prakash
THE MAGNET
PREPOLARIZED MRI
Superconducting Magnet
Quench
M A GNET GEOMETRY
S him Coils
3 TESLA AND HIGHER-MAGNET STRENGTHS
Gradient System
Radiofrequency System
MULTICHANNEL RF COILS AND P ARALLEL IMAGING
C omputer
Data Processing and Image Reconstruction
ADVANCED MR APPLICATIONS AND HARDWARE
Magnetic Resonance-High-Density Focussed Ultrasound (or MRgFUS)
Magnetic Resonance Elastogram
MR Surgical S uite: Interventional MRI
Magnetic Resonance–Positron Emission Tomography
REFERENCES
Image Optimization in Magnetic Resonance Imaging
P r oton Density
C oil Type and Position
SIGNAL-TO-NOISE RATIO
F ield Strength
Repetition Time
F lip Angle
Number of Signal Averages
S lice Thickness
Receiver Bandwidth
E cho Time
C ONTRAST-TO-NOISE RATIO
A dministration of a Contrast Agent
Magnetization Transfer C onstant
C hemical Suppression
E cho-train Length
T ime from Inversion
SPATIAL RESOLUTION
V o x el Volume, FOV, Matrix
SCAN TIME
Scan time = TR × number of excitations × number of phase encodings
Number of Excitations
ARTIFACTS
P hase Matrix
Number of Slice Encodings in 3D Sequences
Scan time = TR × number of excitations × number of phase encodings × sl
Motion Artifacts (Phase Mismapping)
Ghosting and Smearing
Distance = TR × phase encoding steps × NEX × motion frequency
P ulsatile Flow-related Artifacts
Remedy
A rtifacts Due to Measurement T echnique/Parameters
Aliasing
Moiré /Fringe Artifact
Remedy
Chemical-shift Artifacts
A dvantage
Chemical Shift in Echoplanar Imaging
P hase-cancellation Artifact
A dvantage
T runcation Artifacts
Magnetic Susceptibility Difference Artifacts
A dvantage
Section Cross Talk
P arallel-imaging Artifact
External Artifacts
Artifacts Caused by Field Distortions
A dvantage
Zipper Artifact
Spike (Herringbone) Artifact
C ONCLUSION
BIBLIOGRAPHY
Diffusion Weighted Magnetic Resonance Imaging
Devasenathipathy Kandasamy, Raju Sharma
B ASIC PRINCIPLE
B VALUE
ADC AND EXPONENTIAL IMAGE
D WI SEQUENCES AND OPTIMIZATION
E cho Planar Imaging
T urbo Spin Echo Sequences or
Half-Fourier-acquisition Single-shot T urbo-spin Echo
S t eady-state Free-precession
ARTIFACTS AND PITFALLS
Susceptibility Artifacts
C hemical-shift Artifacts
Motion Artifacts
E ff ect of Contrast Media
T2 S hine Through
T2 Washout
T2 Blackout
E ddy Current Artifacts
ADVANCED D W TECHNIQUES
Diffusion Tensor Imaging
W hole Body Diffusion-weighted Imaging
DIFFUSION KURTOSIS IMAGING
Intravoxel Incoherent Motion
Histogram Analysis of ADC
CLINICAL APPLICATIONS OF DWI
Brain
Head and Neck
P ediatric Applications
T horax
Breast
Liver
Gallbladder and Biliary Ducts
P ancreas
Kidneys and Adrenal
P r ostate
F emale Pelvis
C ONCLUSION
F unctional Magnetic Resonance: P erfusion and Dynamic Contrast enhanced Mag
Niranjan Khandelwal, Sameer Vyas
PERFUSION MAGNETIC RESONANCE IMAGING
Magnetic-contrast Agents in Neural Tissues
Imaging Techniques and Methods
Dynamic-susceptibility Contrast-enhanced MR Perfusion
MRI Sequence Type
Dynamic Contrast-enhanced MR Perfusion
Arterial-spin Labeling MR Imaging
D Y NAMIC CONTRAST-ENHANCED MRI
Magnetic Resonance Angiography
Ajay Kumar, Sameer Vyas, Naveen Kalra
HISTORY AND INTRODUCTION
FLOW PHENOMENA
Outflow-related Signal Loss (Washout Effect, T2 Flow Void)
Inflow-related Signal Enhancement (Inflow Effect)
P hase Effects
TIME-OF-FLIGHT ANGIOGRAPHY: TECHNIQUES
P itfalls with TOF MRA
Important Points for Optimization of TOF A ngiography 5-7
PHASE-CONTRAST ANGIOGRAPHY
Magnitude-contrast Technique
P hase-contrast Technique
Optimization
C ONTRAST-ENHANCED MR ANGIOGRAPHY
CE-MRA Advantages 14
P arallel Imaging 12
T ime Resolved/4D CE-MRA
A dvantages of Time-resolved MRA
Limitation
F uture Perspectives
REFERENCES
Magnetic Resonance Imaging Pulse Sequences: An Evolution
V ivek Gupta, Niranjan Khandelwal
B ASIC TERMINOLOGIES
TYPES OF SEQUENCES
C onventional Spin-echo Sequences
F ast-spin-echo Sequences
Half-fourier Acquisition Single-shot T urbo Spin Echo
Inversion Recovery Sequence
Gradient-echo Sequences
Steady State Sequences
C oherent-gradient-echo Sequence
CISS/FIESTA-C
Ultrafast Sequences
T2*-Weighted Ultrafast Sequences
Ultrafast-gradient-echo Sequence
3D Ultrafast-gradient-echo Sequence
Hybrid Sequences
Gradient/Spin-echo Hybrid
BIBLIOGRAPHY
Digital Radiography: An Update
Alpana Manchanda
LIMITATIONS OF FILM SCREEN RADIOGRAPHY
EVOLUTION OF DIGITAL RADIOGRAPHY
ADVANTAGES OF DIGITAL RADIOGRAPHY 2,3
PRINCIPLE OF DIGITAL RADIOGRAPHY
DIGITAL-RADIOGRAPHY SYSTEMS
Computed Radiography
PHYSICS BEHIND DIGITAL RADIOGRAPHY
A dvantages of Storage Phosphor Systems
Drawbacks of CR/Storage Phosphor Systems
Direct-digital Radiography
Direct Conversion
Selenium Drum-based System of Direct Conversion
T hin-film Transistor—Direct Conversion
T hin-film Transistor—Indirect Conversion
TYPES OF SCINTILLATORS
C harged-coupled Devices
P hoton-counting Type DR System
IMAGE PROCESSING
ASPECTS OF IMAGE QUALITY
P ixels
Detector Size
Grayscale
Spatial Resolution
C ontrast Resolution and Dynamic Range
Modular Transfer F unction
Detective-quantum Efficiency
Radiation Exposure
Newer Applications in CR
Newer Applications in DR
Exposure Indicator for Digital Radiography
A CR Practice Guideline for Digital Radiography
C ONCLUSION
REFERENCES
Digital Mammography
Smriti Hari, Chandrashekhara SH, Surabhi Vyas
DIGITAL MAMMOGRAPHY
B ASIC PHYSICS OF DIGITAL MAMMOGRAPHY
Detectors
Spatial Resolution
A nalog to Digital Units
P r ocessing Algorithms
Dynamic Range
C omparison between Digital Mammograms and Film/Screen Mammograms
S t orage of Digital Images
Display of Digital Images
A rtifacts
APPLICATIONS OF DIGITAL MAMMOGRAPHY
C omputer-aided Detection and Diagnosis
Dual-energy Subtraction Mammography
Digital Breast Tomosynthesis
T echnique
C ontrast-enhanced Digital Mammography
R adiation Dose
P otential Benefits of Clinical Breast Imaging with Tomosynthesis
Clinical Tomosynthesis Evaluations
T eleradiology Applications
S t ereotactic Breast Biopsy
S t ereo Mammography
C ONCLUSION
REFERENCES
F luoroscopy and Digital Subtraction Angiography
Deep N Srivastava, Madhusudhan KS
O VERVIEW
FLUOROSCOPY
C omponents of Fluoroscopic System
Image Intensifier
Input S creen
Electrostatic L ens
Output P hosphor and A node
P r operties of Image Intensifier
Limitations of Image-intensifier System
Optical Coupling and Video System
Optical Distributor System
V ideo S ystem
Digital F luoroscopy
P ostprocessing Techniques
DIGITAL SUBTRACTION ANGIOGRAPHY
T ypes of S ubtraction
T echniques used in DSA
P ostprocessing in DSA
F lat-panel Detector
A dvantages and L imitations of FPD S ystems
A utomatic Exposure Control
Recording M otion
T ypes of Fluoroscopic E quipment
Recording Fluoroscopic Images
Direct-film Recording
Indirect R ecording
R adiography – Fluoroscopy Unit with Under-couch Tube
R adiography – Fluoroscopy Unit with Over-couch Tube
F ixed C-arm Fluoroscopic System
Mobile C-arm System
F actors Affecting Image Quality
Radiation S afety in F luoroscopy
P atient Dose Monitoring Methods
Dose-reduction Techniques
SUMMARY
T ools in Interventional Radiology
A tin Kumar, Chandan Jyoti Das
PUNCTURE NEEDLES
DILATORS
SHEATHS
CATHETERS
P arts of C a theter
Materials
Sizes
S hapes and H oles
Balloon C a theters
GUIDEWIRE
Selection of Guidewires
FINE NEEDLE ASPIRATION CYTOLOGY AND BIOPSY NEEDLE
STENT
V ascular S tent
Biliary S tent
Ureteral S t ents
P ermanent Proximal Occluders
EMBOLIZING AGENTS
P ermanent Distal Occluders
T emporary Distal Occluders
BIBLIOGRAPHY
T emporary Proximal Occluders
Magnetic Resonance Contrast Media
B ASIC PRINCIPLES OF MR CONTRAST AGENTS
CLASSIFICATION OF MR CONTRAST AGENTS
Magnetic Properties
P aramagnetic Contrast Agents
Superparamagnetic Contrast Agents
Intravascular Agents
Image Enhancement
Biodistribution
Extracellular-fluid Agents
T issue-specific Agents
GADOLINIUM-BASED CONTRAST AGENTS
Interaction between Extracellular MRI C ontrast Agents with Clinical Tests
A dverse Effects of GBCAs
C ontrast-induced Nephropathy
Extravasation
Nephrogenic Systemic Fibrosis
Risk F actors for NSF
Guidelines on GBCA Usage
GBCA Administration in Children 20
GBCAs during Pregnancy and Lactation 20
M ANGANESE-BASED CONTRAST AGENTS
IRON OXIDE-BASED CONTRAST AGENTS
L o w -low I n t ensity (Dark Lumen)
High-high or Bright L umen
ORAL-CONTRAST AGENTS
High-low Intensity
L o w -high Intensity
ONGOING RESEARCH AND FUTURE TRENDS
C ONCLUSION
REFERENCES
Ultrasound Contrast Agents
Shashi Bala Paul, Manisha Jana
EVOLUTION OF UCAS
TECHNIQUE OF CEUS
SAFETY OF UCA s
DIAGNOSTIC APPLICATIONS OF UCA s
A pplications in Hepatic Imaging
Detection of Focal Liver Lesions by CEUS
Characterization of FLL
CEUS Patterns of Benign Focal Liver Lesions ( T able 3)
CEUS Patterns of Malignant Focal L iver L esions ( T able 4)
Guidance for Interventional Procedures
Assessment of Treatment Response of Malignant T umors and Plan Additional T
Hepatic Vein Transit Time Estimation
Liver Transplant
A pplications in Pancreatic Imaging
Detection of Focal Pancreatic Lesions
Differentiation of Cystic Pancreatic Tumors from Pancreatic Pseudocyst
Detection of Pancreatic Necrosis in Acute Pancreatitis
C ontrast-enhanced Endoscopic Ultrasound
A pplications in Renal Imaging
Characterization of Renal Masses
Differentiation of Renal Tumors from Pseudotumors
Renal Vascular Lesions
Renal Tumor Ablation under CEUS Guidance
A pplication in Abdominal Trauma
A pplications in Breast Imaging
Characterization of Breast Masses
Assessment of Tumor Response after Chemotherapy in Breast Cancer
A pplication in Prostatic Imaging
Miscellaneous Intravascular Applications
Intracavitary Applications
Upcoming Applications
A CKNOWLEDGMENTS
Iodinated Contrast Media: An Update
Chandrashekhara SH, Sanjay Thulkar
HISTORY OF DEVELOPMENT OF ICM
B ASIC CHEMISTRY OF ICM
T ypes of ICM
ICM PHARMACOKINETICS
Basic Properties
P ulmonary Effects of ICM
Effects of ICM on Blood and Endothelium
General Policies for ICM Administration
Guidelines for Intravenous A dministration of ICM
Dosage of Iodinated Contrast Media Administration
A dverse Reactions
ICM Interaction with Other Drugs and C linical Tests
Guidelines for Selective Use of LOCM
Iso-osmolar Dimeric Contrast Media
FUTURE OF ICM
C ONCLUSION
C ontrast Reactions and Its Management
Gaurav S Pradhan, Rajat Jain
TYPES OF ADVERSE REACTION
IDIOSYNCRATIC ANAPHYLACTOID REACTIONS
Mechanism of Idiosyncratic Anaphylactoid Reactions 1,3-7
Risk Factors for Acute Idiosyncratic Drug Reactions 8
P r e v ention of Acute Idiosyncratic Reactions 9-11
T ypes and Management of A cute Idiosyncratic Reactions 1
C linical Features
NONIDIOSYNCRATIC REACTIONS 22-25
C ontrast-extravasation Treatment
Extravasation of Contrast 26-30
C ontrast-induced Nephropathy
Diagnosis
A cute Kidney Injury Network: Definition of Acute Kidney Injury 28,31
Risk Factors for CIN
P a thogenesis
Renal Dialysis Patients and the Use of Iodinated Contrast Medium 1
C ontrast Administration and Lactation 1
C ontrast Administration in Patients on Metformin 1
Recommendation of C ontrast Agents Based on Serum Creatinine Level
C ontrast Administration and Pregnancy 1
C ontrast Administration and T h yroid Dysfunction 11
P r ophylaxis of Contrast Induced Thyrotoxicosis
C ontrast Administration in Pheochromocytoma and Paraganglioma 11
C ontrast and Drug Interaction 47
C omorbidities for Lactic Acidosis with Use of Metformin
C ontrast Administration and Interleukin-2 Therapy 47,11
Delayed Adverse Events to Iodinated Contrast Media
Recommendations for the Departments P erforming Contrast-related Investigatio
P icture Archiving and C ommunication System and R adiology Information Sys
Shivanand Gamanagatti, Devasenathipathy Kandasamy, Arun Kumar Gupta
PICTURE ARCHIVING AND C OMMUNICATION SYSTEM
C omponents and Architecture of PACS
W orkflow
Mini-PACS
T eleradiology
A c quisition
Image Compression
T ypes of Image Compression
Bits and Bytes
Database Server
Storage
Storage Hardware
N AS stands for N etwork Attached Storage
S AN stands for S t orage Area Network.
W orkstation
Display Monitors
R adiologist Reading Stations
P h ysician Review Stations
S ystem Architecture
Network
Client/Server-based Systems
Distributed Systems
W eb-based Systems
Related Applications
Industry Standards
RADIOLOGY INFORMATION SYSTEM
REFERENCES
E vidence-based Radiology
Sanjay Sharma, Manisha Jana
B A CKGROUND
WHY EVIDENCE-BASED PRACTICE?
F orms of Evidence-based Practice
‘Bottom-up’ Evidence-based Practice
z I mpact assessment:
How does Evidence-based Radiology Differ from Evidence-based Medicine?
Limitations of Evidence-based Practice
REFERENCES
R adiation Hazards and Radiation Units
P r atik Kumar, Anil K Pandey
RADIATION HAZARDS
D AMAGE TO DNA BY THE RADIATION
THE EFFECT OF RADIATION
S t ochastic and Nonstochastic (Deterministic) Effects
Radiation Doses and Expected Effect
Radiation Effect on Embryo
T en-day Rule
P r otection of Patient, Staff and P ublic from Radiation
R adiation Risk
R adiation Protection Guidelines and LNT Model
Justification
C ardinal principle of radiation protection is distance,
Radiation Units
F luence
Flux
Energy Fluence
Exposure
Absorbed Dose
K erma
E quivalent Dose
Effective Dose
R adiation Dose Measurement in CT
C omputed-Tomography Dose Index
R adiation Dose Measurement in Fluoroscopy
BIBLIOGRAPHY
R adiation Protection
Sapna Singh
HISTORICAL PERSPECTIVE
RADIATION UNITS
C onventional Units
SI Units
Dose Equivalent
SPECIFIC QUANTITIES AND THEIR ASSOCIATED UNITS EXPOSURE
A bsorbed Dose
Units
BIOLOGICAL IMPACT
E ff ective Dose Equivalent (Effective Dose)
INTERACTION OF RADIATION WITH M A TTER RADIATION TYPES AND SOURCES
BIOLOGICAL EFFECT OF RADIATION
CLASSIFICATION OF RADIATION INJURY
Malignancies Associated with Radiation Exposure
Genetic Effects of Radiation
DETERMINISTIC EFFECTS AS DOCUMENTED FROM RADIATION ACCIDENTS
A cute Total-body Irradiation
THE REGULATORY BODIES
C hronic Radiation Effects
Role of AERB
Radiation Protection Survey and Program (Flow chart 1)
PROTECTION AGAINST RADIATION HAZARD PRINCIPLES OF RADIATION PROTECTION
S hielding
CARDINAL PRINCIPLE OF RADIATION PROTECTION
T ime
Distance
X -ray Tube Shielding (Source Shielding)
Room Shielding (Structural Shielding)
Exposure Calculations
Shielding of the X-ray Control Room
P ersonnel Shielding
P atient Shielding
E quipment
SAFETY OF RADIOGRAPHIC IMAGING DURING PREGNANCY
RECOMMENDED DOSE LIMITS TO PREGNANT WOMEN 18,19
RADIATION DETECTION AND MEASUREMENT
Methods of Detection
Ionization
P hotographic Effect
L uminescence
Scintillation
PERSONNEL DOSIMETRY
P ocket Dosimeter
F ilm Badge Monitoring
Electronic Dosimeters
W earing the Dosimeter
During Radiography
During Fluoroscopy
C OMPUTED TOMOGRAPHY (RADIATION EXPOSURE AND DOSE MODULATIONS)
Radiation Dose Measures: CT Specific
C onventional Radiographic Projections
CT Radiation Projections
TYPICAL DOSE MEASUREMENTS
CTDI W
CTDI vol
Dose-length Product (DLP)
T echniques for Controlling Radiation Dose at CT
Multiple Scan Average Dose
C omputed Tomography Dose Index (CTDI)
CTDI 100
USING AUTOMATED EXPOSURE CONTROL
MODIFYING THE ACQUISITION PARAMETERS
Increasing Pitch
V arying the Milliampere-seconds Value b y Patient Size
Optimum Tube P otential 47
ITERATIVE RECONSTRUCTION
Reducing the Milliampere-seconds Value
C ONCLUSION
P lanning a Modern Imaging Department
S C Bansal, Niranjan Khandelwal, Ajay Gulati
PLANNING AND ORGANIZATION
Divisions of the Radiology Department
LAYOUT
EQUIPMENT
C onventional Radiography
Darkroom
L OCATION
Storage Phosphor Radiography ( C omputed Radiography)
Dual-reading CR systems
Digital Radiography
P arallel Reading (Line Scanning)
Needle-crystalline CR Detectors
F lat-panel Direct Detector Systems
C CD Detector Technology
Slot-scanning CCD Technology
C omputer-aided Diagnosis
Dual-energy Subtraction
T emporal Subtraction
Digital Tomosynthesis
Mobile Image Intensifiers Units
M AMMOGRAPHY
Dual-energy X-ray Absorptiometry
C OMPUTED TOMOGRAPHY
ULTRASOUND
Magnetic Resonance Imaging
Digital Subtraction Angiography
Nuclear Imaging Systems
PICTURE ARCHIVING AND C OMMUNICATION SYSTEMS
SAFETY STANDARDS AND QUALITY ASSURANCE
TELERADIOLOGY
REFERENCES
C ommon Drugs Used in an Imaging Department
Anupam Lal, Vivek Gupta, Manphool Singhal
DRUGS FOR PATIENT PREPARATION: SEDATIVES
L ocal Anesthetics
A dverse Effects
Sting Free LA
Methods of Administration
DRUGS USED FOR OPTIMIZING IMAGING EVALUATION: DIURETICS
Infiltration Anesthesia
U ses
V asodilators
P apaverine
Nimodipine
Milrinone
P a tient Preparation in Suspected P heochromocytoma
Drugs for Cardiac Imaging
C ardiac CT
β-blockers
Ivabradine
C ardiac Stress MRI
Dobutamine
A denosine
DRUGS AFFECTING COAGULATION: PROCOAGULANTS
T hrombin
A n ticoagulants
T hrombolytics
Classification of Thrombolytics
Heparin
Antiplatelets
C ontraindications
C y clooxygenase-1 Inhibitor
T hienopyridines
F or thrombosis associated with Aneurysmal coiling:
P hosphodiesterase Inhibitors
SCLEROSANTS AND EMBOLIC AGENTS
GELATIN FOAM
POLYVINYL ALCOHOL
TRIS-ACRYL GELATIN MICROSPHERES
N-BUTYL-2 CYANOACRYLATE
ETHYLENE VINYL ALCOHOL COPOLYMER
ABSOLUTE ALCOHOL
SODIUM TETRADECYL SULFATE
T r ansarterial Chemoembolization
REFERENCES
Molecular Imaging
Anish Bhattacharya, BR Mittal
MOLECULAR IMAGING PROBES IN NUCLEAR MEDICINE
CLINICAL APPLICATIONS OF NUCLEAR MOLECULAR IMAGING
Oncology
Diagnosis and Staging
Assessment of Response to Treatment
Role in Drug Development
CENTRAL NERVOUS SYSTEM DISORDERS
Epilepsy
Dementia
Movement Disorders
C oronary Flow Reserve
A therosclerosis
INFECTIOUS AND INFLAMMATORY PROCESSES
CARDIOVASCULAR DISORDERS
Myocardial Viability
Newer Agents for Imaging Infection/Inflammation
C ONCLUSION
E thical and Legal Issues in Radiology
Mandeep Kang, Manavjit Singh Sandhu
ETHICAL ISSUES
DOCTOR-PATIENT RELATIONSHIP
RADIATION ISSUES
P a tient Protection
S taff Protection
P ublic Protection
P r otection During Interventions
LEGAL ISSUES
Image Interpretation and Reporting
F irst Study the Images
Know How the Examination was Performed
How to Look (Detect the Abnormalities)
When an Abnormality is Found
Reach a Conclusion
When to Make the Report
Giving the Report a Title
P r oofread the Report
General Format
L ength of the Report
Negative Reporting
Internal Architecture
LAWS/LEGAL ACTS APPLICABLE T O MEDICINE
PCPNDT Act
C onsumer Protection Act (1986)
Archiving and Ownership of Diagnostic Imaging Data
P atient Referral
Radiologist as a Witness
As Expert Witness
Radiologist as a Defendant
In a Malpractice Claim
Duty of Care
C onsent
W riting a Radiological Opinion
C omments on Other Radiological Reports
Appearing in Court
P ersonal Communication by the Radiologists
Issue of Self-referral
TELERADIOLOGY: WHO IS RESPONSIBLE?
REFERENCES
Gastrointestinal and Hepatobiliary Imaging
C urrent Status of Conventional T echniques and Advances in Gastrointestinal
Arun Kumar Gupta, Atin Kumar, Chandan Jyoti Das
DEVELOPMENT OF GASTROINTESTINAL RADIOLOGY
C ONVENTIONAL TECHNIQUES: PRESENT SCENARIO
ADVANCES IN GASTROINTESTINAL TRACT IMAGING
Ultrasonography (US) in GIT
CT Enteroclysis (Fig. 2)
T echnique of CT Enteroclysis
Indications
CT Enterography
MRI and MR Enteroclysis (MRE)
PET-CT Enteroclysis and PET-CT Colonography
Nuclear Scintigraphy
CHARACTERISTIC
T uberculosis
C r ohn’s Disease
Imaging in Small Bowel Obstruction
Mesenteric Ischemia
Neoplasms Malignant
C ONCLUSION
REFERENCES
Nontraumatic Acute Abdomen
Mandeep Kang, Veenu Singla
DIAGNOSTIC WORK-UP
CT Technique
P lain Radiographs in Evaluation of the Acute Abdomen
P erforation
Miscellaneous Conditions
Role of Cross-sectional Imaging in Specific Disease Entities
A cute Appendicitis
A cute Cholecystitis
A cute Pancreatitis
Intra-abdominal Abscess
Bowel Perforation
Mesenteric Ischemia
V ascular Causes
MISCELLANEOUS
Diverticulitis
T o xic Megacolon
P elvic Disease
A cute Pyelonephritis
A cute Urinary Colic
A cute Epiploic Appendagitis, Omental Infarction
REFERENCES
Imaging in Abdominal Trauma
A tin Kumar, Sanjay Thulkar
DIAGNOSTIC IMAGING
P lain Radiography
Ultrasonography
Radionuclide Scanning
Magnetic Resonance Imaging
A ngiography
C omputed Tomography
C omputed Tomography Technique
CT Signs in Blunt Abdominal Trauma 10
ORGAN TRAUMA
P eritoneal Cavity
P neumoperitoneum
Hemoperitoneum
SPLEEN
LIVER AND BILIARY TRACT
A AST Liver Injury Grading System
P ANCREAS
URINARY TRACT
ADRENAL
HOLLOW VISCUS, OMENTAL AND MESENTERIC INJURY
DIAPHRAGM
PENETRATING ABDOMINAL TRAUMA
RETROPERITONEUM
ABDOMINAL WALL INJURY
C ONCLUSION
REFERENCES
Imaging of the Esophagus
Sumedha Pawa, Anjali Prakash
P haryngeal and Esophageal Anatomy
P h y siology of Swallowing
Examination Technique
CLINICAL PERSPECTIVE
Investigation of Dysphagia
Barium Studies
C r oss-sectional Studies
P harynx
Esophagus
Endoscopic Ultrasound
Others Techniques for Evaluation of Esophagus
V ideoendoscopic Swallowing Study
Esophageal Scintigraphy
Esophageal Manometry
Ambulatory pH Monitoring
Oropharyngeal Lesions
Neuromuscular Disease
Cricopharyngeal Prominence
Cricopharyngeal Webs
P haryngeal Diverticula and Pouches
P haryngeal Tumors
P haryngeal Foreign Bodies
Esophageal Motility Disorders
P rimary
Nonspecific Esophageal Motility Disorder
Diffuse Esophageal Spasm
A chalasia
Nutcracker Esophagus
Secondary Motility Disorders
ESOPHAGITIS
Gastroesophageal Reflux Disease and Barrett’s Esophagus
Infectious Esophagitis
C andida Esophagitis
V iral Esophagitis
T uberculosis
C austic Esophagitis
Drug-induced Esophagitis
Radiation-induced Esophagitis
Miscellaneous Causes
ESOPHAGEAL DIVERTICULA
Intramural Pseudodiverticulosis
ESOPHAGEAL VARICES
TRAUMATIC LESIONS
F oreign Bodies
MISCELLANEOUS LESIONS
ESOPHAGEAL TUMORS
Benign Tumors
Malignant Tumors
C arcinoma
Metastases
INDENTATIONS AND DISPLACEMENT
RECENT ADVANCES AND FUTURE DIRECTIONS
REFERENCES
Benign Lesions of Stomach and Small Intestine
Gaurav S Pradhan
T echniques of Examination
Hypotonic Duodenography
MDCT and 3D Imaging Techniques
Erosive and Ulcerative Lesions of Stomach and Duodenum
NARROWING OF STOMACH
THICKENED GASTRIC FOLDS AND FILLING DEFECTS
REDUCED OR ABSENT RUGAL FOLDS
GAS IN WALL OF STOMACH
GASTRIC OUTLET OBSTRUCTION
GASTRIC DILATATION WITHOUT OBSTRUCTION
POSITIONAL ABNORMALITIES
THICKENING OF DUODENAL FOLDS
DUODENAL FILLING DEFECTS
DUODENAL NARROWING OR OBSTRUCTION
EXTRINSIC IMPRESSION ON BULB
WIDENING OF DUODENAL SWEEP
REFERENCES
MISCELLANEOUS ABNORMALITIES
C ONCLUSION
Malignant Lesions of the Stomach and Small Intestine
Sanjay Thulkar, Arun Kumar Gupta
CARCINOMA OF THE STOMACH
Risk Factors for Gastric Cancer
Clinical Features
P a thology
Diagnosis
Barium UGI Series Features of Gastric Cancer
Staging
CT Features of Gastric Cancer
Other Investigations for Preoperative Staging of Gastric Cancer
Limitations of CT
T r eatment and Prognosis
CARCINOMA OF THE SMALL BOWEL
A denocarcinoma of the Small Bowel
Clinical Features
Barium Studies of the Small Bowel
Barium Study Features of Carcinoma of the Small Bowel
CT of the Small Bowel
CT Features of Adenocarcinoma of the Small Bowel
MRI of the Small Bowel
Staging
T r eatment and Prognosis
F ollow-up
C arcinoid
C arcinoids of the Stomach and Duodenum
Imaging Features of Gastric and Duodenal Carcinoids
Small Bowel Carcinoids
Imaging Features of Small Bowel Carcinoids
Differential Diagnosis of Carcinoids
T r eatment and Prognosis
GASTROINTESTINAL STROMAL TUMORS
Imaging Features of GIST
T r eatment of GIST
METASTASES TO THE STOMACH AND SMALL BOWEL
MISCELLANEOUS MALIGNANT TUMORS OF STOMACH AND SMALL BOWEL
REFERENCES
Abdominal Tuberculosis
P a thological Findings
Clinical Spectrum
TUBERCULOUS PERITONITIS
P eritoneum
Omentum
Small Bowel Mesentery
TUBERCULAR LYMPHADENITIS
GASTROINTESTINAL TUBERCULOSIS
ESOPHAGEAL TUBERCULOSIS
GASTRIC TUBERCULOSIS
DUODENAL TUBERCULOSIS
TUBERCULOSIS ENTERITIS
F irst Stage
Second Stage
Third Stage
ILEOCECAL TUBERCULOSIS
Group 1
Group 2
Group 3
Group 4
APPENDICEAL TUBERCULOSIS 41
C OLONIC TUBERCULOSIS
ANORECTAL TUBERCULOSIS 29
Enterolithiasis
VISCERAL TUBERCULOSIS
Liver and Spleen
P ancreas
V ascular Involvement in Gastrointestinal T uberculosis
AIDS AND TUBERCULOSIS
P ercutaneous Biopsy in the Diagnosis of Abdominal Tuberculosis
NUCLEAR IMAGING
REFERENCES
Nontubercular Inflammatory Bowel Diseases
Birinder Nagi, Anupam Lal, Manphool Singhal
INFLAMMATORY BOWEL DISEASES
RADIOLOGY
ULCERATIVE COLITIS
CROHN’S DISEASE
A ctive Inflammatory Subtype
F ibrostenotic Subtype
F istulizing/Perforating Subtype
Reparative or Regenerative Subtype
C omplications of IBD
Extraintestinal Complications
Ulcerative Colitis versus Crohn’s Disease
Crohn’s Disease versus Tuberculosis
Distribution of Disease
O THER INFLAMMATORY BOWEL DISEASES
Ischemic Bowel Disease
Appendicitis
Epiploic Appendagitis
Diverticulitis
Radiation Colitis
P seudomembranous Colitis
Amebic Colitis
T yphilitis
C eliac Disease
Eosinophilic Enteritis
Amyloidosis
REFERENCES
C olorectal Malignancies
Naveen Kalra, Mandeep Kang
EPIDEMIOLOGY
RISK FACTORS
P A THOGENESIS
CLINICAL FEATURES
P A THOLOGY
R OUTE OF SPREAD
STAGING
R OLE OF RADIOLOGY
P rimary Tumor (T )
Regional Lymph Node (N)
Distant Metastasis (M)
S tage Grouping 24
Screening for Colorectal Cancer
DIAGNOSTIC METHODS
Plain Radiographs
Barium Enema
Problem Areas in Barium Studies
Ultrasound
Computed Tomography
CT Colonography
MR Imaging
Arteriography
MR Colonography
Immunoscintigraphy
Positron Emission Tomography
Recent Advances
Other Malignant Tumors of Colon
CONCLUSION
REFERENCES
L ymphoma of the Gastrointestinal Tract
Anupam Lal, Mahesh Prakash
P A THOLOGY
STAGING
CLINICAL PRESENTATION AND INVESTIGATION
Imaging Modalities
Barium Studies and Computed T omography
CT Enteroclysis
Magnetic Resonance Imaging
Radionuclide Imaging
Radiological Findings
Esophagus
Stomach
Small Intestine
Appendix
C olon and Rectum
L ymphoma Variants
Burkitt’s Lymphoma
Mediterranean Lymphoma
Multiple Lymphomatous Polyposis
Imaging of Appendix
NORMAL IMAGING APPEARANCE
A CUTE APPENDICITIS
P a thophysiology
C linical Picture
IMAGING
C onventional Radiography
Ultrasonography
U S Technique
Sonographic Findings
Doppler Imaging
P itfalls in Sonographic Diagnosis
CT Technique
CT Findings in Acute Appendicitis
Magnetic Resonance Imaging
WHICH MODALITY AND WHEN
MUCOCELE OF APPENDIX
PRIMARY APPENDICEAL INTUSSUSCEPTION
POSTOPERATIVE APPENDICEAL DEFECTS
TUMORS OF THE APPENDIX
Liver Anatomy and T echniques of Imaging
Smriti Hari
NORMAL ANATOMY
BISMUTH AND COUINAUD’S SEGMENTAL NOMENCLATURE
ULTRASONOGRAPHY
T echnique
Ultrasound Contrast Agents
Sonographic Anatomy
Intraoperative Ultrasonography
C omputed Tomography
CT Anatomy
Magnetic Resonance Imaging
T echnique
Magnetic Resonance Imaging Contrast Agents
Magnetic Resonance Anatomy
ANGIOGRAPHY
T echnique
Anatomy
POSITRON EMISSION TOMOGRAPHY
REFERENCES
Benign Focal Lesions of the Liver
Sapna Singh, Veena Chowdhury
CLASSIFICATION
HEPATIC CYSTS
Ultrasonography
Nuclear Scintigrams
Angiogram
MRI
C ONGENITAL HEPATIC FIBROSIS AND POLYCYSTIC LIVER DISEASE
BILIARY CYSTADENOMA
U S G and CT
MR Imaging
BILE DUCT HAMARTOMA
HEMANGIOMA
P a thology
Imaging Features of Cavernous Hemangiomas
Plain Film Findings
USG and CT
Microbubble-enhanced USG
Multiple Phase Imaging
MRI
Red Blood Cell Scintigraphy
MR Imaging Characteristics in Giant Hemangioma of the Liver
Angiographic Findings
HEPATOCELLULAR ADENOMA
USG
T riphasic Study
Radionuclide Scintigraphy
MRI
Angiograms
FOCAL NODULAR HYPERPLASIA
F ocal Nodular Hyperplasia and Hepatic Adenoma: Differentiation with Low Index
P a thology
Imaging Features
USG
C olor Doppler
C ontrast-enhanced USG
Hemodynamic Characterization of F ocal Nodular Hyperplasia
Nuclear Scintigraphy
Hepatic Adenoma and Focal Nodular Hyperplasia: MR Findings with Super parama
NODULAR REGENERATIVE HYPERPLASIA
ADENOMATOUS HYPERPLASTIC NODULE
MRI
PEDIATRIC LIVER TUMORS
Mesenchymal Hamartoma
LIPOMATOUS TUMORS
MRI
Infantile Hemangioendothelioma
USG
MRI
Hepatic Arteriograph
FOCAL INFLAMMATORY LESIONS OF LIVER
Bacterial (Pyogenic) Liver Abscess
P athology
Plain Film Findings
USG
ERCP
CT and MR Imaging
Amebic Abscess
P athology
Plain Film Findings
Nuclear Scintigrams
USG
MRI
C omplications
F ungal Hepatic Abscesses
Imaging Features
H Y D A TID DISEASE
Hydatid Cyst Structure
Hepatic Hydatid Disease
Imaging Features
Plain Film Findings
Nuclear Scintigraphy
MRI
L ocal Complications
Intrahepatic Complications
Exophytic Growth
T r ansdiaphragmatic Thoracic Involvement
P erforation into Hollow Viscera
P ortal Vein Involvement
P eritoneal Seeding
Biliary Communication
Abdominal Wall Invasion
HEPATIC TUBERCULOSIS
P a thology
Imaging Features
Plain Film Findings
Nuclear Scintigraphy
USG
HEPATIC SCHISTOSOMIASIS
Plain Film Findings
USG
MRI
HEPATIC PNEUMOCYSTIS CARINII INFECTION
Miscellaneous Lesions
F atty Infiltration
Hematoma
Biloma
REFERENCES
Malignant Focal Lesions of the Liver
Raju Sharma, Madhusudhan KS
PRIMARY MALIGNANT FOCAL LESIONS
Hepatocellular Carcinoma
Clinical Presentation
Imaging in HCC
Ultrasonography
C omputed Tomography
Magnetic Resonance Imaging
Angiography
Interventional Techniques
Intrahepatic Cholangiocarcinoma
Imaging
F ibrolamellar Hepatocellular Carcinoma
Hepatoblastoma
Imaging
Epithelioid Hemangioendothelioma
Imaging
Angiosarcoma
SECONDARY MALIGNANCIES
Metastatic Disease
Ultrasonography
C omputed Tomography
Magnetic Resonance Imaging
Image-guided Biopsy
L ymphoma
REFERENCES
Diffuse Liver Diseases
Ashu Seith Bhalla, Harsh Kandpal, Sanjay Thulkar
F A TTY LIVER (HEPATIC STEATOSIS)
Ultrasonography
C omputed Tomography
Magnetic Resonance Imaging
C omputed Tomography
Magnetic Resonance Imaging
A lcoholic Hepatitis
Radiation Hepatitis
HEPATITIS
V iral Hepatitis
Ultrasonography
HEMOCHROMATOSIS AND HEMOSIDEROSIS
C omputed Tomography
Magnetic Resonance Imaging
AMYLOIDOSIS
WILSON’S DISEASE
GRANULOMATOUS DISEASES
T uberculosis
Sarcoidosis
Schistosomiasis
Liver Fluke or Fasciola Hepatica
CIRRHOSIS
Ultrasonography
C omputed Tomography
Magnetic Resonance Imaging
M ALIGNANT DIFFUSE LIVER DISEASES
Imaging of Obstructive Biliopathy
R aju Sharma, Harsh Kandpal
Ultrasonography
Endoscopic Ultrasonography
C omputed Tomography
Hepatobiliary Scintigraphy
Magnetic Resonance Imaging
Endoscopic Retrograde C holangiopancreatography
BENIGN LESIONS CAUSING OBSTRUCTIVE BILIOPATHY
C holedocholithiasis
Ultrasonography
C omputed Tomography
Magnetic Resonance Cholangiopancreatography
Benign Strictures
P ostoperative Biliary Strictures
P ostinflammatory Strictures
Bile Duct Fistula
Mirizzi Syndrome
C holedochal Cysts
P rimary Sclerosing Cholangitis
P rimary Biliary Cirrhosis
Recurrent Pyogenic Cholangitis
P arasitic Diseases
Bacterial Cholangitis and Aids-related Biliary Abnormalities
Rare Infections
A mpullary Stenosis
P ortal Biliopathy
Hemobilia
Benign Tumors of the Bile Duct
M ALIGNANT LESIONS CAUSING OBSTRUCTIVE BILIOPATHY
C arcinoma Gallbladder
C holangiocarcinoma
Intrahepatic (Peripheral) Cholangiocarcinoma
Hilar Cholangiocarcinoma (Klatskin Tumor)
Extrahepatic Cholangiocarcinoma
C arcinoma Head of the Pancreas
Other Malignant Tumors of Biliary Tract
REFERENCES
Clinical Aspects of Liver Cirrhosis: A Perspective for the Radiologists
Shashi Bala Paul, Shivanand Gamanagatti, Arun Kumar Gupta, Subrat Kumar Achary
EPIDEMIOLOGY
P A THOLOGY
CAUSES AND RISK FACTORS OF CIRRHOSIS
NATURAL HISTORY AND PROGNOSIS
SEVERITY OF CIRRHOSIS
TYPES OF CIRRHOSIS
DIAGNOSIS OF CIRRHOSIS
Endoscopy
Liver Biopsy
Imaging in Cirrhosis
C OMPLICATIONS OF CIRRHOSIS
C irrhosis and Hepatocellular Carcinoma
Screening Tests
Surveillance Intervals
P r otocol for HCC Surveillance
C ost Effectiveness
TREATMENT OF CIRRHOSIS
T r eatment of Complications
C ONCLUSION
REFERENCES
Imaging and Interventions in Pancreatitis
Ashu Seith Bhalla, Chandan Jyoti Das
A CUTE PANCREATITIS
Classification
Assessment of Severity
Role of Imaging in Patient Management
C omputed Tomography
CT Protocol
CT Findings in Acute Pancreatitis
MILD ACUTE PANCREATITIS OR EDEMATOUS PANCREATITIS
SEVERE ACUTE PANCREATITIS
A cute Fluid Collections
A cute Pseudocyst
P ancreatic Abscess
P ancreatic Necrosis
V ascular Complications
Extrapancreatic Adjacent Organ Involvement
Staging of Acute Pancreatitis
Magnetic Resonance Imaging
P ercutaneous Cross-sectional Image-guided Interventions
CHRONIC PANCREATITIS
Etiology and Pathophysiology
Plain Films
Imaging in Chronic Pancreatitis
Endoscopic Ultrasonography
Endoscopic Retrograde Pancreatography
MR Cholangiopancreatography
Magnetic Resonance Imaging
A dvantages of MRP over ERP
A dvantages of ERP over MRP
P ositron-emission Tomography
Imaging in Special Situations and Variants
SUMMARY
REFERENCES
T umors of Pancreas
ANATOMY
T opography
Histology
Physiology
MACROANATOMY
Ductal System
V ascular System
P A THOLOGY
Classification of Tumors (Based on Predominant C ell Type and Radiological App
Epithelial Exocrine
Other Pancreatic Neoplasms
P ANCREATIC ADENOCARCINOMA
P A THOLOGICAL ANATOMY AND BIOLOGICAL BEHAVIOR
Endocrine Islets Cell Tumors
Ultrasonography
C olor Doppler Flow Imaging
Endoscopic US
C omputed Tomography
Dual Phase Helical CT
Magnetic Resonance Imaging
MRCP
ERCP
PET
DSA
T umor Markers in Pancreatic Carcinoma
Laparoscopy
F ine Needle Aspiration
STAGING OF PANCREATIC TUMORS
CYSTIC TUMORS
Mucinous Cystic Neoplasms
Microcystic Adenoma (Serous Cystadenoma)
Intraductal Papillary Mucinous T umors/Neoplasms
Solid and Papillary Epithelial T umors/ Neoplasms
UNCOMMON CYSTIC PANCREATIC TUMORS
C y stic Endocrine Tumors
Glucagonoma
V ipoma
Insulinoma
Gastrinoma
Somatostatinoma
Nonfunctioning ICTs
Arteriography and Venous Sampling
Arterial Stimulation and Venous Sampling
Endoscopic US
UNCOMMON SOLID PANCREATIC TUMORS
P ancreatoblastoma
A cinar Cell Carcinomas
T umors of Neural Origin
Metastasis
L ymphoma
REFERENCES
Imaging in Portal Hypertension
V eena Chowdhury, Rashmi Dixit
ANATOMY AND COLLATERAL CIRCULATION
T ributary Collaterals (Hepatofugal)
Developed Collaterals (Hepatofugal)
Bridging Collaterals (Hepatopedal)
ETIOLOGY OF PORTAL HYPERTENSION
NONINVASIVE RADIOLOGICAL EVALUATION
Barium Contrast Examinations
Sonography and CDFI
C omputed Tomographic Imaging
Magnetic Resonance Imaging
MR Portography
P itfalls 22
INTRAHEPATIC PORTAL HYPERTENSION
Organ Parameters
Splenomegaly
Ascites
V ascular Evaluation
P ortal Vein, Superior Mesenteric Vein and Splenic Vein Diameter
P itfalls of Portal Flow Assessment
P ortosystemic Venous Collaterals 12
Assessment of Hepatic Veins
Arterial Evaluation
Extrahepatic Portal Hypertension: Prehepatic
P ortal Vein Occlusion
Spleinic Vein Occlusion
SMV Occlusion
Extrahepatic Portal Hypertension: Posthepatic
Hyperkinetic Portal Hypertension 6
MEDICAL TREATMENT FOLLOW-UP
E v aluation of Surgical Portosystemic Shunts and Tips
T r ansjugular Intrahepatic Portosystemic Shunt
REFERENCES
Hepatic Venous Outflow Tract Obstruction
DIAGNOSTIC TECHNIQUES
EVALUATION OF HEPATIC VEINS IN BCS
EVALUATION OF IVC IN BCS
ASSESSMENT OF LIVER PARENCHYMA IN BCS
C ollateral Pathways
M ANAGEMENT OF BCS
REFERENCES
Gastrointestinal Hemorrhage
Deep N Srivastava, Shivanand Gamanagatti
Angiography
T echnical Considerations
Radionuclide Studies
Angiographic Findings in GIH
C omputed Tomography
Barium Studies
C ONTROL OF GASTROINTESTINAL HEMORRHAGE
T r anscatheter Embolization
SPECIFIC SITUATIONS IN GI HEMORRHAGES
Upper Gastrointestinal Hemorrhage
Hemobilia
L o w er Gastrointestinal Hemorrhage
C olonic Diverticula
P ancreatitis and UGIH
Meckel’s Diverticulum
Angiodysplasia
Hemangioma and Arteriovenous Malformation
T umors
Inflammatory Bowel Diseases and Small Bowel or Colonic Ulcers
Others
REFERENCES
Interventions in Obstructive Biliopathy
Mandeep Kang, Naveen Kalra
INDICATIONS FOR BILIARY DRAINAGE
P ercutaneous Transhepatic C holangiography
P r eprocedure Evaluation and Preparation
P ercutaneous Transhepatic Biliary Drainage
F luoroscopic Guidance
T echnique
Internal and External Drainage
C omplications of Biliary Drainage
F ollow-up of Biliary Catheters
Biliary Stenting
Intraluminal Brachytherapy with PTBD
P ercutaneous Cholecystostomy
T echnique
Dilatation of Benign Biliary Structures
C omplications
Gallbladder Biopsy
BIBLIOGRAPHY
Interventional Treatment of Liver Tumors
Deep N Srivastava, Shivanand Gamanagatti
TREATMENT OF LIVER TUMORS
Hepatocellular Carcinoma
Chemical Ablation
Radiofrequency Ablation
T r anscatheter Arterial Chemoembolization
T r anscatheter Arterial Embolization
T r ansarterial Radionuclide Therapy
Right Portal Vein Embolization
Hepatic Vein Stenting
METASTATIC TUMORS OF LIVER
BENIGN TUMORS OF LIVER
C ONCLUSION
REFERENCES
P ercutaneous Nonvascular Gastrointestinal Tract Interventions
Shivanand Gamanagatti, Deep N Srivastava
PERCUTANEOUS GASTROSTOMY
Indications
Other Indications
C ontraindications
T echnique
C omplications
PERCUTANEOUS JEJUNOSTOMY
Indications
T echnical Difficulty
T echnique (Figs 1A to D)
C omplications
ESOPHAGEAL STENTING
S t ent Designs
C ommercially Available Stents (Fig. 2) 18
S t ent Selection
Indications
T echnique (Figs 3 and 4)
P ostprocedure Care
C omplications
E arly Complications
L ate Complications
GASTRODUODENAL STENTING
Indications
C ontraindications
A v ailable Devices
Endoscopic versus Fluoroscopic Placement
T echnique (Figs 5A to D)
P ostprocedure Care
C omplications
C OLORECTAL STENTING
Indications
P ostprocedure Follow-up
C omplications
PERCUTANEOUS ENTEROCUTANEOUS FISTULA CLOSURE WITH
N-BUTYL-2-CYANOACRYLATE
T echnical Considerations
F luoroscopic Guidance
Mechanism of Action of the Glue (N-butyl-2-cyanoacrylate)
P r erequisites
T echnical Consideration
P r eparation
T echnique (Figs 6A to D)
REFERENCES
Interventional Radiology in Portal Hypertension
TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT
Indications of TIPS 2
C ontraindications of TIPS 2
C omplications of TIPS 2
REVISION OF OCCLUDED SURGICAL SHUNT
ARTERIOPORTAL FISTULAS
RECANALIZATION OF OCCLUDED PORTAL VEIN AND ITS TRIBUTARIES
P ARTIAL SPLENIC EMBOLIZATION
PERCUTANEOUS TRANSHEPATIC VARICEAL EMBOLIZATION
A ngiographic Vasopressin Infusion
B ALLOON-OCCLUDED RETROGRADE TRANSVENOUS OBLITERATION OF GASTRIC VARICES
BUDD–CHIARI SYNDROME
RECENT ADVANCES
REFERENCES
Genitourinary Imaging
C urrent Status of Conventional T echniques in Urogenital Imaging
Naveen Kalra, Manavjit Singh Sandhu
B A CKGROUND
Ultrasound of Urogenital Tract: T echniques and Normal Appearances
Anju Garg
KIDNEYS AND URETERS
T echnique
Normal Sonographic Appearance
Normal Variations
Doppler Evaluation
T echnique
Normal Doppler Pattern
Ureters
URINARY BLADDER AND URETHRA
T echnique
Indications
Urethra
Normal Sonographic Appearance
PROSTATE AND SEMINAL VESICLES
T echnique
Normal Sonographic Appearance
Normal Variants
SCROTUM
T echnique
Normal Appearances
Doppler Evaluation
Indications
PENIS
T echnique and Normal Appearance
UTERUS AND ADNEXA
T echnique
Normal Appearances
CERVIX AND VAGINA
ADNEXA
Indications for Evaluation of Uterus and Adnexa
Doppler Evaluation
Indications
T hree-dimensional Sonography
Indications
Extended Field of View (EFOV) Imaging 33
Elastography 34
C ontrast-enhanced Ultrasonography (CEUS)
C ONCLUSION
REFERENCES
C omputed Tomography of Urogenital Tract: Techniques and Normal Appearances
NORMAL RENAL STRUCTURE AND CT ANATOMY OF KIDNEYS
NORMAL CT ANATOMY OF THE PELVIS
MULTIDETECTOR CT
Advantages of Renal Multidetector Row CT
Increased Diagnostic Images
Increased Temporal Resolution
Isotropic Data Acquisition and Increased Spatial Resolution
EXAMINATION TECHNIQUE AND IMAGING PROTOCOLS OF MULTI DETECTOR ROW CT OF THE
Noncontrast CT
Contrast-enhanced CT Oral Contrast Medium
Administration of Intravenous Contrast Medium
PHASES OF RENAL ENHANCEMENT/ MULTIPHASIC HELICAL CT
Normal CT Nephrogram
Corticomedullary Phase (CMP)
Nephrographic Phase (NP)
Pathological CT Nephrogram
Excretory Phase (EP)
IMAGE PROCESSING AND POSTPROCESSING TECHNIQUES
Multiplanar Reformation (MPR)
Maximum Intensity Projection (MIP)
Shaded Surface Displays (SSD)
V olume Rendered Technique (VRT )
MULTIDETECTOR CT UROGRAPHY
C alculi
Renal Tumors
Urothelial Tumors
PUJ Obstruction
C ongenital Anomalies
MDCTU Protocol
Split Bolus MDCT Urography with Synchronus Nephrographic and Exceretory Phase
C ompression
Saline Infusion
Diuretic Administration
P atient Positioning
Image Interpretation
MULTIDETECTOR CT IN RENAL MASSES
MDCT IN BLUNT RENAL TRAUMA
MDCT IN EVALUATION OF FLANK PAIN AND URINARY CALCULI
MDCT IN RENAL INFECTIONS
HELICAL CT FOR LOWER URINARY TRACT AND PELVIS
CT ANGIOGRAPHY (CTA) OF RENAL ARTERIES
VIRTUAL CYSTOSCOPY/ENDOSCOPY
REFERENCES
MRI of Urogenital Tract: Techniques and Normal Appearances
P aramjeet Singh, Sameer Vyas
KIDNEY
T echniques and Recommended Imaging Sequences
MR Urography
Renal Angiography and Venography
Normal Appearances
URINARY BLADDER
Normal Appearance
T echnique and Recommended Sequences
PROSTATE GLAND
Normal Appearance of Prostate on MRI
UTERUS AND OVARIES
T echnique and Recommended Sequences
Normal MR Appearance
PELVIC LYMPH NODES
C urrent Status of Nuclear Medicine in Urinary Tract Imaging
Rakesh Kumar, Shamim Ahmed Shamim, Rama Mohan Reddy
99m T c-MAG-3
99m T c-LLEC
RADIOPHARMACEUTICALS
99m T c-DTPA
123 I-OIH
99m T c-GHA
99m T c-DMSA
IMAGING TECHNIQUES
Renal Dynamic Scintigraphy
Dynamic Renography
Normal Dynamic Renal Study
Diuretic Renography
C aptopril Renography
C ortical Scintigraphy/Static Renal Scintigraphy
Imaging Techniques
Radionuclide Cystography
Clinical Applications
Measurement of Renal Function
P ositron Emission Tomography—Computed T omography (PET-CT )
Renal Cancer
Urinary Bladder Cancer
REFERENCES
C urrent Status of Urographic C ontrast Media
Sumedha Pawa, Gaurav S Pradhan
DEVELOPMENT OF CONTRAST MEDIA
TYPES OF RADIOGRAPHIC CONTRAST MEDIA
PHARMACOKINETICS OF EXTRACELLULAR IODINATED CONTRAST AGENTS
PHYSICOCHEMICAL PROPERTIES OF C ONTRAST MEDIA
W a t er Solubility, Hydrophilicity and Osmolality
V iscosity
P harmaceutical Characteristics: T he Role of Formulation
ADVERSE REACTIONS TO CONTRAST MEDIA
Guidelines on Prevention and Management of Acute Reactions
Guidelines on Late Adverse Reactions
Guidelines on Renal Adverse Reactions
Guidelines on Prevention and Management of Extravasation of Contrast Media
EVALUATING THE PATIENT BEFORE C ONTRAST MEDIA INJECTION AND IDENTIFYING GROU
A GGRAVATION OF DISEASES B Y CONTRAST MEDIA
Guidelines on the Use of Iodinated Contrast Media in Patients with Thyroid Di
Guidelines on the Use of Contrast Media in P a tients with Catecholamine-prod
Guidelines on Interaction between Contrast Media with Other Drugs and Clinica
Guidelines on the Use of Iodinated Contrast Media during Pregnancy or Lactati
SELECTIVE VERSUS UNIVERSAL USE OF NONIONIC CONTRAST MATERIAL
STRATEGIES FOR CLINICAL USE: C OST CONTAINMENT
T u bercular Infection of the Urinary Tract
Ashu Seith Bhalla, Arun Kumar Gupta, Raju Sharma
P A THOGENESIS
CLINICAL PICTURE
LABORATORY INVESTIGATIONS
CYSTOSCOPY
RADIOLOGICAL EXAMINATION
Plain Films
Intravenous Urography (IVU)
Kidney
Ureter
Urinary Bladder
Urethral TB
Retrograde Pyelography
Ultrasonography
Kidney
Ureter
C omputed Tomography
Kidney
Ureter
MRI
C OMPLICATIONS
Differential Diagnosis
Genitourinary Tuberculosis in HIV
REFERENCES
Nontubercular Infections of the Urinary Tract
Naveen Kalra, Ajay Kumar
A CUTE PYELONEPHRITIS
P a thology
Radiology
A CUTE FOCAL BACTERIAL NEPHRITIS
RENAL AND PERIRENAL ABSCESS
EMPHYSEMATOUS PYELONEPHRITIS
P Y ONEPHROSIS
CHRONIC PYELONEPHRITIS
REFLUX NEPHROPATHY
X ANTHOGRANULOMATOUS P Y ELONEPHRITIS
HIV-ASSOCIATED NEPHROPATHY
F A T PROLIFERATION IN THE KIDNEY
RENAL PAPILLARY NECROSIS
M ALACOPLAKIA
SQUAMOUS METAPLASIA
P ARASITIC INFECTION
P athology of Renal Tumors
K usum Joshi
ADULT RENAL TUMORS
Renal Cell Tumors
Clear Cell
(or Nonpapillary or C onventional) RCC
Multilocular Cystic Renal Cell Carcinoma
P apillary (or Chromophilic) Renal Cell Carcinoma
Chromophobe Renal Cell Carcinoma
C ollecting Duct (Duct Bellini) RCC (CDC)
Renal Medullary Carcinoma
Renal Carcinomas Associated with XP11.2 T r anslocations/TFE3 Gene Fusions
Mucinous Tubular and Spindle Cell C arcinoma
Renal Cell Carcinoma—Unclassified
P apillary Adenoma
Renal Oncocytoma
MOLECULAR/GENETIC FEATURES OF RENAL CELL CARCINOMA
Clear Cell Renal Cell Carcinoma
P apillary Renal Adenomas and Carcinomas
Renal Oncocytoma
Chromophobe Renal Carcinomas
C ollecting Duct Carcinomas
Sarcomatoid Transformation in RCC
NUCLEAR GRADING
P a thological Staging
AJCC Staging
METANEPHRIC TUMORS
MESENCHYMAL RENAL TUMORS OCCURRING IN ADULTS
Angiomyolipoma (AML)
Epithelioid Angiomyolipoma
Juxtaglomerular Cell Tumor
Renomedullary Interstitial Cell Tumor
Nephroblastoma [Wilms’ Tumor (WT)]
PEDIATRIC RENAL TUMORS
Gross Features
Microscopic Features
Anaplasia
Nephrogenic Rests
C y stic Partially Differentiated Nephroblastoma (CPDN)
C ongenital Mesoblastic Nephroma (CMN)
Clear Cell Sarcoma of Kidney (CCSK)
Rhabdoid Tumor
BIBLIOGRAPHY
P athology of Gynecological Malignancies
Radhika Srinivasan
NEOPLASMS OF THE OVARY
Ovarian Surface Epithelial Tumors
Serous Tumors
Mucinous Tumors
Endometrioid Tumors
Clear Cell Adenocarcinoma of the Ovary
Brenner’s Tumor
Malignant Mixed Müllerian Tumor (MMMT)
Germ Cell Tumors
Dysgerminoma
Yolk Sac Tumor (Endodermal Sinus Tumor)
Immature Teratoma
Mature Cystic Teratoma
Carcinoid Tumor and Strumal Carcinoid
Sex Cord Stromal Tumors
Granulosa Cell Tumor
Juvenile Granulosa Cell Tumor (JGCT)
Thecoma, Fibroma and Other Tumors
Sertoli-Leydig Cell Tumor
Metastatic Tumors
CARCINOMA OF THE FALLOPIAN TUBE
MALIGNANT TUMORS OF THE UTERUS
Type I: Endometrioid Adenocarcinoma
Type II: Carcinoma
Endometrial Stromal Tumors
MMMT Carcinosarcoma
Müllerian Adenosarcoma
Leiomyosarcoma
CARCINOMA OF THE UTERINE CERVIX
Invasive Cervical Carcinoma
MALIGNANT TUMORS OF THE VULVA
Squamous Cell Carcinoma
Vulvar Paget’s Disease
BIBLIOGRAPHY
Imaging in Renal Tumors
BALLS VERSUS BEANS
Imaging Modalities
Plain Films
Intravenous Urograms
Magnetic Resonance Imaging
Angiography
Retrograde and Antegrade Pyelography
RENAL CELL CARCINOMA 23
Ultrasound
Doppler
Magnetic Resonance Imaging
Angiography
Nuclear Scintigraphy
Staging of Renal Cell Carcinoma 7-11
F ollow-up
UROTHELIAL TUMOR
T r ansitional Cell Carcinoma
Ultrasonography
C omputed Tomography and Magnetic Resonance Imaging 13-15
Staging
Squamous Cell Carcinoma
C ollecting Duct Carcinoma (Bellini Duct C a r cinoma/Renal Medullary Carcino
Renal Sarcoma 3
L ymphoma
Renal Metastasis 23
Oncocytoma
Renal Adenomas
MIXED EPITHELIAL AND STROMAL TUMORS (MESTs) 3,26
CYSTIC NEPHROMA
ANGIOMYOLIPOMA
PNET OF THE KIDNEY
Biopsy 2,3,35
Incidental Solid Renal Mass
Imaging of Urinary Bladder and Urethra
Anupam Lal, Paramjeet Singh
ANATOMY
Urinary Bladder
Urethra
Male Urethra
F emale Urethra
P lain Films
Retrograde Urethrography
V oiding Cystourethrography (VCUG)
C y stography
Urodynamic Studies of the L o w er Urinary Tract
Ultrasonography
Magnetic Resonance Imaging
Radionuclide Imaging
SPECIFIC DISEASES OF THE URINARY BLADDER
Bladder Diverticulae
Urachal Anomalies
Exstrophy
Other Anomalies
Neurogenic Bladder
Infections
A cute Cystitis
Chronic Cystitis
C ystitis Cystica
Malakoplakia
Schistosomiasis
Extravesical Processes
Bladder Tumors
SPECIFIC DISEASES OF URETHRA
Gonococcal and Nongonococcal Urethritis
C ondyloma Acuminata (Venereal Warts)
T uberculosis
Urethral Strictures
Urethral Calculi
Urethral Diverticulum
T umors of the Male Urethra
T umors of the Female Urethra
Metastatic Tumors of Urethra
Imaging of the Prostate Gland
P aramjeet Singh, Anupam Lal
ANATOMY
IMAGING MODALITIES 3
Ultrasonography
C omputed Tomography
BENIGN PROSTATIC HYPERPLASIA
Ultrasonography
Magnetic Resonance Imaging
Other Imaging Modalities
PROSTATE CANCER
T r ansrectal Ultrasonography
C omputed Tomography
Magnetic Resonance Imaging
P ositron Emission Tomography
EVALUATION OF THE METASTASES
PROSTATITIS AND PROSTATIC ABSCESS
PROSTATIC CYSTS
REFERENCES
Renal Cystic Diseases
V eena Chowdhury
EMBRYOLOGY
CLASSIFICATION
Bosniak Classification System
IMAGING MODALITIES
Conventional Radiography
Ultrasonography
Computed Tomography
Magnetic Resonance Imaging
Angiography
Cyst Puncture/Cystography
SIMPLE RENAL CYST
Pathology
Clinical Features
Complicated Simple Renal Cyst
Hemorrhagic Cyst
Infected Cyst
Cyst Rupture
Carcinoma in Wall of a Preexisting Cyst
ATYPICAL SIMPLE CYSTS
Calcified Cyst
Hyperdense Cyst
Septated Cysts
Multiple Simple Cysts
Localized Cystic Disease
POLYCYSTIC KIDNEY DISEASE
Autosomal Dominant Polycystic Kidney Disease (ADPKD) (Potter Type III)
Pathology
Clinical Features
Autosomal Recessive Polycystic Kidney Disease (ARPKD) (Potter Type I)
Imaging Features
Clinicopathologic Features
Imaging Features
MEDULLARY SPONGE KIDNEY
Imaging Features
MEDULLARY CYSTIC DISEASE
Clinical Features
Clinicopathologic Features
Imaging Features
MULTICYSTIC DYSPLASTIC KIDNEY (MCDK) (POTTER TYPE II)
Pathology
Imaging Features
CYSTIC DISEASE ASSOCIATED WITH RENAL NEOPLASM
Acquired Cystic Kidney Disease (ACKD)
Clinical Features
Imaging Features
von Hippel–Lindau Disease (VHL)
Pathology
Imaging Features
TUBEROUS SCLEROSIS (TSC)
CYSTS OF RENAL SINUS
MISCELLANEOUS CYSTIC DISEASE
Inflammatory
Hydatid Cysts
Pyogenic Cyst
Tuberculous Cysts
Pleuricystic Kidney Disease
Glomerulocystic Disease
Microcystic Disease
CYSTIC RENAL CELL CARCINOMAS
Renovascular Hypertension
Niranjan Khandelwal, Anupam Lal, Manphool Singhal
P A THOPHYSIOLOGY
ETIOLOGY OF RENAL ARTERY STENOSIS
A therosclerosis
F ibromuscular Dysplasia
Nonspecific Aortoarteritis/Takayasu’s A rteritis 22-24
Middle Aortic Syndrome 25-27
SCREENING FOR RENOVASCULAR H Y PERTENSION
C linical
C linical and Biochemical Tests
IMAGING MODALITIES FOR ASSESSMENT OF RAS
Radionuclide Renal Scintigraphy
P rinciples of Angiotensin-converting Enzyme Inhibitor (Captopril) Scintigrap
P r otocol
Results
Ultrasound
C olor Doppler Flow Imaging (CDFI)
Direct Approach
Indirect Approach
CT Angiography (CTA)
Magnetic Resonance Angiography
C ontrast-enhanced MRA (CE-MRA)
Noncontrast-enhanced MR Imaging of the Renal Arteries
T OF MRA
P hase-contrast (PC) MRA
Steady-state Free Precession Magnetic Resonance Angiography
Arterial Spin Labeling
Renal Angiography
F eatures of RAS on Arteriography
P ercutaneous Transluminal Renal Angioplasty (PTRA) and Stenting
TREATMENT
A therosclerotic Disease
Renal Artery Stenting
F uture Management of RAS
T akayasu’s Arteritis/Nonspecific Aortoarteritis
Surgical Therapy
Renal Artery Stenosis in Children 27,90
C auses
Renal Parenchymal Disease and Renal Failure
Anupam Lal, Hina Arif Mumtaz
DEFINITION AND CLASSIFICATION OF RENAL FAILURE
A cute Renal Failure
Radiological Approach to Renal P arenchymal Disease
C hronic Renal Failure (CRF)
R OLE OF IMAGING IN RENAL FAILURE
Imaging Techniques
P lain Radiography and Urography
C olor Doppler
Magnetic Resonance Imaging
Renal Angiography
R adionulceotide Imaging
C ontrast Medium-associated Nephropathy
IMAGING IN RENAL PARENCHYMAL DISEASE
A cute Renal Parenchymal Disease
A cute Tubular Necrosis
Imaging Features
A cute Cortical Necrosis
Imaging Features
L eukemia
Imaging Features
A cute Interstitial Nephritis
Imaging Features
A m yloidosis
Imaging Features
A m yloidosis of Renal Pelvis
Multiple Myeloma
Imaging Features
P aroxysmal Nocturnal Hemoglobinuria (PNH)
C hronic Renal Parenchymal Disease
Renal Papillary Necrosis
A lport’s Syndrome
Imaging Features
Benign and Malignant Nephrosclerosis
Imaging Features
Renal Osteodystrophy
C ONCLUSION
REFERENCES
Renal Transplant
Ajay Gulati, Manavjit Singh Sandhu
TECHNIQUE
C OMPLICATIONS
A cute Tubular Necrosis
Rejection
Renal Artery Thrombosis
Renal Artery Stenosis
P seudoaneurysm
Renal Vein Thrombosis
Arteriovenous Fistula
P eritransplant Fluid Collections
Urinary Complications
Malignancy
IMAGING TECHNIQUES
Radiography
Plain Radiography
Intravenous Urography
C ystography
Radionuclide Imaging
Ultrasonography (US)
C omputed Tomography
Magnetic Resonance Imaging
Angiography
P ercutaneous Interventional Techniques
REFERENCES
A CKNOWLEDGMENTS
Imaging of Obstructive Uropathy and Diseases of Ureter
Mahesh Prakash, Mandeep Kang
IMAGING OF ACUTE OBSTRUCTION
Plain X-ray
Intravenous Urography
PATHOPHYSIOLOGY
Sonography
Duplex and Color Doppler Sonography
Computed Tomography
Radionuclide Renography
Magnetic Resonance Imaging
IMAGING OF CHRONIC OBSTRUCTION
Sonography
Intravenous Urography
Computed Tomography
Magnetic Resonance Imaging
INVASIVE TECHNIQUES IN URINARY OBSTRUCTION
Antegrade Pyelography
Retrograde Pyelography
CAUSES OF OBSTRUCTION AND DISEASES OF URETER
Congenital Ureteric Obstruction
Ureteropelvic Junction Obstruction
Ureterocele
Primary Megaureter
Circumcaval Ureter
Acquired Ureteric Obstruction
Intraluminal Causes
Ureteric Calculus
Intramural Causes
Ureteral Tumors
Transitional Cell Carcinoma
Benign Tumors
Nonepithelial Tumors
Secondary Tumors and Contiguous Infiltration
Inflammatory Lesions of Ureter
Retroperitoneal Fibrosis
Inflammatory Bowel Disease
Extrinsic Causes of Ureteral Obstruction
Retroperitoneal Neoplasms
Pelvic Lipomatosis
Gynecological Causes
Gastrointestinal Diseases
P regnancy-related Dilatation of Ureter
Miscellaneous Diseases of Ureter
Ureteral Injury
Ureteral Herniation
Ureteral Fistula
REFERENCES
Urinary Tract Trauma
Atin Kumar, Shivanand Gamanagatti
Role of Radiography (Plain Radiographs)
Role of Ultrasound
RENAL TRAUMA
Imaging Work-up in a Patient with Suspected Renal Trauma
Role of Intravenous Urography
Role of CT
Role of Angiography
Role of Retrograde Pyelography
Role of Radionuclide Renal Scintigraphy
Role of MRI
Radiological Findings
Grade 1
Grade 4
Grade 2
Grade 3
Grade 5
Vascular Contrast Extravasation
Renal Trauma with Pre-existing Abnormality
Management of Renal Trauma
URETERAL TRAUMA
Imaging Work-up
Role of IVU
Classification
Role of CT
Role of Antegrade and Retrograde Ureterograms
Management
BLADDER TRAUMA
Cystography
Conventional Cystography
CT Cystography
Classification
Blunt Trauma
Iatrogenic Bladder Trauma
Management of Bladder Trauma
Penetrating Bladder Trauma
URETHRAL TRAUMA
Radiology
Technique of Urethrography
Blunt Urethral Trauma
Posterior Urethral Injuries Associated with Pelvic Fracture
Anterior Urethral Injury
Classification
Evaluation before Delayed Urethroplasty
Management of Urethral Trauma
Penetrating Injury
Iatrogenic Injury
Female Urethra
Imaging the Adrenal Gland
Raju Sharma, Ashu Seith Bhalla, Arun Kumar Gupta
ANATOMY AND PHYSIOLOGY
IMAGING MODALITIES
Ultrasound
Computed Tomography
Magnetic Resonance Imaging
Radionuclide Imaging
Positron Emission Tomography
ADRENAL DISEASES
Group I: Adrenal Hyperfunctional Diseases
Cushing’s Syndrome
ACTH-independent Cushing’s Syndrome
Aldosteronism
Androgenital Syndrome
Pheochromocytoma
Group II : Adrenal Insufficiency
Group III: Adrenal Diseases with Normal Function
Incidentaloma
Adenoma versus Metastasis
Adrenal Carcinoma
Adrenal Lymphoma
Adrenal Collision Tumor
Adrenal Cyst
Myelolipoma
Neuroblastoma
SUMMARY
REFERENCES
Retroperitoneum
Smriti Hari, Atin Kumar
NORMAL ANATOMY
IMAGING MODALITIES
RETROPERITONEAL COLLECTIONS
A ORTA
A ortic Aneurysm
A o rtic Dissection
C ongenital Anomalies
V enous Thrombosis
INFERIOR VENA CAVA
P rimary Tumors of the IVC
L Y MPH NODES
Benign Lymphadenopathy
L ymphoma
HIV Lymphadenopathy
Metastatic Lymphadenopathy
PRIMARY NEOPLASMS
Malignant Neoplasms
Liposarcomas
L eiomyosarcomas
Hemangiopericytomas
Malignant Fibrous Histiocytomas
Other Malignancies
Benign Neoplasms
P aragangliomas
Neurogenic Tumors
T eratomas
Lipoma
RETROPERITONEAL FIBROSIS
Iliopsoas Muscle Compartment
REFERENCES
Nonvascular Interventions in the Urinary Tract
Mandeep Kang, Anupam Lal, Naveen Kalra
PERCUTANEOUS NEPHROSTOMY
Indications
A natomy Relevant to Percutaneous Renal Entry
T echnique
Results
C omplications
S ystemic Complications
P ostprocedure Care
L ocal Complications
Extended Applications of Percutaneous Nephrostomy
Antegrade Ureteric Stenting
L arge Bore Track Creation
SCLEROTHERAPY FOR RENAL CYSTS
PERCUTANEOUS CATHETER DRAINAGE
BIOPSIES
C OMPLICATED RENAL TRANSPLANT
RADIOFREQUENCY ABLATION OF RENAL TUMORS
A blation Process
E quipment
P a tient Selection and Preprocedure Evaluation
Guidance
P r ocedure
P ostprocedure and Follow-up
C omplications
Other Applications of RFA
REFERENCES
V ascular Interventions in the Genitourinary Tract
Shivanand Gamanagatti, Deep N Srivastava
RENAL ARTERY ANGIOPLASTY
Imaging the Renal Arteries
Renal Artery Angioplasty
RENAL ARTERY STENTING
Outcome
Renal Artery Intervention in Renal Transplants
C omplications
RENAL ARTERIAL EMBOLIZATION
T echnique
TRANSCATHETER EMBOLIZATION OF RENAL NEOPLASMS
T r anscatheter Embolization of Renal P seudoaneurysms
Incidence
C auses
Risks Posed by the Aneurysm
Anatomic/Physiologic Considerations
T echnique
Results of Embolization
C omplications
Embolization of End-stage Kidney
T echnique
UTERINE ARTERY EMBOLIZATION
Indications
Uterine Leiomyoma
Uterine Arteriovenous Malformations
P ostsurgical and Postpartum Hemorrhage
T echnique
Results
C omplications
V ARICOCELE EMBOLIZATION
V A GINAL AVM EMBOLIZATION
C ONCLUSION
SCROTAL AVM AND TESTICULAR TUMOR EMBOLIZATION
REFERENCES
Imaging in Female Infertility
Rashmi Dixit
CAUSES OF INFERTILITY
Imaging Modalities
Hysterosalpingography 8,9
T r ansvaginal Sonography
Sonohysterosalpingography
Normal Menstrual Cycle 1
C ervical Factor
L eiomyoma
Endometrial–Uterine Factor
Endometrial Adhesions or Synechiae
Endometrial Polyps 9
Mullerian Duct Abnormalities 1,9,21,22
A denomyosis
Nontubercular Chronic Endometritis
T ubal Factor
P eritoneal Factor
Endometriosis
Genital Tuberculosis
Ovarian Factor
P olycystic Ovarian Syndrome
F ollicular Monitoring
Spontaneous Cycles 15,52
Induced Cycles 2,15
P r ediction of Ovulation 1,15,52
L uteinized Unruptured Follicle (LUF) 3,15
Ovarian Hyperstimulation Syndrome
F ollicle Aspiration 15,64,65
TREATING INFERTILITY
REFERENCES
Benign Diseases of the Female Pelvis
Alpana Manchanda, Veena Chowdhury
BENIGN UTERINE LESIONS
C ongenital Uterine Anomalies
Classification
Class I: Müllerian Agenesis or Hypoplasia
Class II: Unicornuate Uterus
Class III: Uterus Didelphys
Class IV: Bicornuate Uterus
Class V: Septate Uterus
Class VI: Arcuate Uterus
Class VII: Diethylstilbestrol Exposed Uterus
L eiomyomas
T r eatment of Uterine Leiomyomas
O THER BENIGN MESENCHYMAL TUMORS
A denomyosis
Endometrial Polyps
Endometrial Hyperplasia
Endometrial Synechiae
UTERINE ARTERIOVENOUS MALFORMATION
BENIGN OVARIAN MASSES
BENIGN CYSTIC MASSES OF PELVIS
FUNCTIONAL CYSTS
F ollicular Cysts
C orpus Luteum Cyst
Hemorrhagic Cyst
P eritoneal Inclusion Cyst
T heca Lutein Cysts
P olycystic Ovarian Disease
Hydrosalpinx
P araovarian Cysts
CYSTADENOMAS
C OMPLEX MASSES
T ubo-ovarian Abscess
Endometriosis
Dermoid Cyst/Mature Cystic Teratoma
Ovarian Torsion
Ectopic Pregnancy
BENIGN SOLID OVARIAN MASSES
C ONCLUSION
Imaging in Gynecological Malignancies
Sanjay Thulkar, Smriti Hari
GYNECOLOGICAL MALIGNANCIES IN INDIA
CARCINOMA OF CERVIX
Imaging Modalities
Conventional Radiography
Ultrasonography
Computed Tomography
Magnetic Resonance Imaging
Imaging Strategies in Cervical Cancer
Positron Emission Tomography
Treatment and Follow-up
CARCINOMA OF ENDOMETRIUM
Spread and Staging
Imaging Modalities
Conventional Radiography
Ultrasonography
Computed Tomography
Magnetic Resonance Imaging
Imaging Strategies in Endometrial Cancer
Treatment and Follow-up
OVARIAN MALIGNANCIES
Epithelial Ovarian Carcinoma
Ultrasonography
Screening for Ovarian Cancer
Computed Tomography
Magnetic Resonance Imaging
Positron Emission Tomography
Staging and Treatment
Imaging Strategies in Carcinoma of Ovary
Primary Papillary Serous Carcinoma of the Peritoneum
Borderline Epithelial Carcinoma
Pseudomyxoma Peritonei
Follow-up Imaging
Germ Cell Tumors of the Ovary
Stromal Sex Cord Tumors
Metastatic Ovarian Tumors
Rare Ovarian Tumors
MISCELLANEOUS GYNECOLOGICAL MALIGNANCIES
Carcinoma of Vagina and Vulva
Sarcoma of the Uterus
Fallopian Tube Carcinoma
Gestational Trophoblastic Neoplasms
Lymphoma of the Female Genital Tract
REFERENCES
Imaging of Scrotum
Anupam Lal, Manphool Singhal
ANATOMY
IMAGING MODALITIES
T echnique of Sonography
MRI of Scrotum
C ONGENITAL ANOMALIES OF THE TESTIS
C ryptorchidism
Miscellaneous Congenital Anomalies
A CUTE SCROTUM
Epididymitis and Orchitis
T orsion
Scrotal Trauma
TESTICULAR TUMORS
Germ-cell Tumors
Seminomas
Nonseminomatous Germ-cell Tumors
Nongerm C ell Testicular Tumors
S taging or Testicular Cancer
P rimary Tumor ( T )
Regional Lymph Nodes (N)
Distant Metastasis (M)
Imaging in Evaluation of Testicular Cancer
MRI
PET
C alcifications
BENIGN INTRATESTICULAR LESIONS
C y sts
A drenal Rests
EXTRATESTICULAR PATHOLOGIES
F luid Collections
Epididymal Cysts
P ostorchidectomy Scrotum
Extratesticular Tumors
V aricocele
REFERENCES
Male Infertility and Erectile Dysfunction
Deep N Srivastava, Sanjay Thulkar
M ALE INFERTILITY
E tiology
Imaging Approach in Male Infertility
V aricocele
T estis
Epididymis
TRUS Evaluation of Distal Genital Ductal System
Seminal Vesicles and Vas Deferens
P r ostate
Ejaculatory Ducts
MRI in Infertility
Imaging in Assisted Fertilization
ERECTILE DYSFUNCTION
A natomy and Physiology of Penile Erection
E v aluation of Erectile Dysfunction
P harmacopenile Duplex Ultrasonography
P eyronie’s Disease
C avernosometry
C avernosography
P enile Angiography
P riapism
P ediatric Imaging
T echnical Considerations in P ediatric Imaging
Ashu Seith Bhalla, Arun Kumar Gupta, Amar Mukund
MINIMIZING HEAT LOSS
SEDATION
IMMOBILIZATION
NIL PER ORALLY STATUS
P harmacological Agents
REDUCTION OF RADIATION DOSAGE
Radiography and Fluoroscopy
R adiographic Equipment Factors
Operator-dependent Techniques
C omputed Tomography
USE OF CONTRAST MEDIA
High Osmolality Contrast Media
L o w Osmolality Contrast Agents
Iso-osmolar Contrast Agents
MR Contrast Agents
Recent Advances in Pediatric R adiology
RADIATION PROTECTION
NEURORADIOLOGY
THORACIC IMAGING
GASTROINTESTINAL IMAGING
URORADIOLOGY
MUSCULOSKELETAL IMAGING
SUMMARY
REFERENCES
Interventions in Children
P ART A: VASCULAR INTERVENTIONS
Gurpreet Singh Gulati, Sanjiv Sharma
INTRODUCTION
P A TIENT PREPARATION
History and Physical Examination
Informed Consent
C oagulation
SPECIAL CONSIDERATIONS FOR THE PEDIATRIC PATIENT
A nesthesia
P a tient Immobilization
T emperature Control
Diet and Medications
Dose of Radiation and Fluids
TECHNIQUES
Access
PROCEDURES
Hemangioma
EMBOLIZATION
Embolization Materials and Substances
V ascular Anomalies
Arteriovenous Malformation
C ervicofacial AVMs
Extremity AVMs
P ulmonary AVMs
Arteriovenous Fistula
V ascular Malformation
L ymphatic Malformation
Hemorrhage
Gastrointestinal Hemorrhage
P elvic Hemorrhage
Hemoptysis
Epistaxis
P ost-traumatic Hemorrhage
P seudoaneurysm
Malignant Tumors
Chemoembolization
Organ Ablation
ANGIOPLASTY
C omplications of Angioplasty Procedures
THROMBOLYSIS
FOREIGN BODY REMOVAL
C ONCLUSION
P ART B: NONVASCULAR INTERVENTIONS
Amar Mukund, Ashu Seith Bhalla, Shivanand Gamanagatti
P A TIENT EVALUATION
SEDATION AND ANESTHESIA
B ASIC PROCEDURES
F ine Needle Aspiration/Biopsy
Sampling Technique
A bscess Drainage
THORACIC INTERVENTIONS
GASTROINTESTINAL INTERVENTIONS
Salivary Gland Interventions
Esophageal Interventions
Gastric Interventions
Hepatic Interventions
Biliary Intervention
P ancreatic Interventions
GENITOURINARY INTERVENTIONS
Renal Biopsy
P ercutaneous Nephrostomy
Ureteric Dilatation and Stenting
Imaging of Pediatric Trauma
Shivanand Gamanagatti, Atin Kumar
IMAGING METHODS 6
P otential Uses of the FAST Examination 8
Abdominal Trauma 11-13
Spleen and Liver
P ancreas
Kidney
Bowel and Mesentery
Pleura
Chest Trauma
Blunt Trauma Chest 9
P enetrating Chest Trauma
Musculoskeletal Injuries 7,10
Imaging 15
T y pes of Pediatric Fractures
Physeal Fractures
Salter-Harris Classification
Head Trauma 16
Broad Classification
A c c ording to Location of Lesions
Skull Fractures 17
Extra-axial Injury
Secondary Head Injury
T r aumatic Ischemia–infarction
Spinal Injuries
Thoracic and Lumbar Spine Trauma
C ONCLUSION
REFERENCES
Neonatal Respiratory Distress
MEDICAL CAUSES OF NEONATAL RESPIRATORY DISTRESS
Hyaline Membrane Disease
T r ansient Tachypnea of Newborn
Neonatal Pneumonia
Meconium Aspiration Syndrome
P neumothorax
SURGICAL CAUSES OF NEONATAL RESPIRATORY DISTRESS
C ongenital Lobar Emphysema
C ongenital Cystic Adenomatoid Malformation
C ongenital Diaphragmatic Hernia
Esophageal Atresia with T r acheoesophageal Fistula
MISCELLANEOUS CAUSES
REFERENCES
Childhood Pulmonary Infections
Jyoti Kumar
PNEUMONIA
Epidemiology
Imaging
V iral Pneumonia
Bacterial Pneumonia
Exclusion of Other Pathologies
Nonresolving Pneumonia
EVALUATION OF ASSOCIATED C OMPLICATIONS
Pleural Complications
L ung Parenchymal Complications
P urulent Pericarditis
Chronic Effects of Pneumonia
TUBERCULOSIS
P rimary Pulmonary Tuberculosis
P ostprimary Tuberculosis
FUNGAL INFECTIONS
A ctinomyces
Aspergillosis
Histoplasmosis
C occidioidomycosis
P ARASITIC INFESTATIONS
Hydatid Disease of the Lung
Others
PULMONARY INFECTIONS IN HIV-POSITIVE CHILDREN
Bacterial Pneumonias
Mycobacterial Pneumonias
F ungal Pneumonias
V iral Pneumonias
L ymphocytic Interstitial Pneumonitis
C ONCLUSION
REFERENCES
Chest Masses
Sanjay Thulkar, Arun Kumar Gupta
L UNG MASSES
C ongenital Cystic Adenomatoid Malformation
P ulmonary Sequestration
Bronchogenic Cyst
V ascular Lesions
L ung Abscess
Hydatid Cysts
P ulmonary Metastasis
P rimary L ung Tumors
MEDIASTINAL MASSES
A n t erior Mediastinal Masses
Germ C ell Tumors
L ymphoma
T h ymic Masses
L ymphangioma
P ericardial Cysts
Middle and Posterior Mediastinal Masses
Neurogenic Tumors
Neuroblastoma and Other Ganglion Tumors
Neurofibroma and Schwannoma
A n t erior Thoracic Meningocele
Extramedullary Hematopoiesis
P araganglioma
CHEST WALL MASSES
C hest Wall Infections
Duplication Cysts
L ymphangioma
Hemangioma
Neurofibroma
Benign Osseous Masses
P rimitive Neuroectodermal Tumor
Rhabdomyosarcoma
Miscellaneous Malignant Chest Wall Masses
P ediatric Airway
Ashu Seith Bhalla
IMAGING MODALITIES
Plain Radiographs
F luoroscopy
Barium Swallow
MDCT
MRI
UPPER AIRWAY OBSTRUCTION
Normal Anatomy (Plain Radiographs) (Figs 1A and B)
A CUTE OBSTRUCTION
Croup (Acute Laryngotracheobronchitis)
Epiglottitis
Retropharyngeal Cellulitis and Abscess
Exudative Tracheitis
F o r eign Body
CHRONIC OBSTRUCTION
Obstructive Sleep Apnea (OSA)
Enlarged Tonsils/Adenoids
Glossoptosis
Hypopharyngeal Collapse
Subglottic Obstruction
Subglottic Stenosis
P ostintubation Stenosis
Subglottic Hemangioma
L O WER AIRWAY OBSTRUCTION
C entral Airways
Extrinsic Causes
V ascular Causes
V a scular Rings
Intrinsic Causes
W all Abnormalities
V ascular Malformations
Intraluminal Causes
P eripheral Airways
Bronchiolitis/Small Airway Disease
L ung Disease of Prematurity
Bronchiectasis
Asthma
REFERENCES
Developmental Anomalies of Gastrointestinal Tract
Alpana Manchanda, Sumedha Pawa
FUNCTIONAL
ANATOMICAL
C OMBINED ANATOMICAL: FUNCTIONAL
P lain Film Radiography
C ontrast Studies
Ultrasonography
ESOPHAGUS
Esophageal Atresia and Tracheoesophageal F istula
Embryology
Clinical Features
Classification
Radiological Evaluation of Postoperative C omplications
STOMACH
Microgastria
DEVELOPMENTAL OBSTRUCTIVE DEFECTS
Gastric Atresia
Pyloric Stenosis or Prepyloric Membrane or Antral Web
E ctopic Pancreas
Hypertrophic Pyloric Stenosis
Ultrasonography
Barium Study
A dult Idiopathic Hypertrophic Pyloric S t enosis (AIHPS)
DUODENUM
Duodenal Atresia and Stenosis
Duodenal Web
A nnular Pancreas
P r eduodenal Portal Vein
SMALL BOWEL
A nomalies of Rotation and Fixation
Embryology
Imaging Features
Jejunoileal Atresia and Stenosis
Embryology
Classification
Meconium Ileus
Megacystis-microcolon-intestinal Hypoperistalsis Syndrome (Berdon’s Syndrome)
Meckel’s Diverticulum
Enteric Duplication
Clinical Features
Imaging Features
LARGE BOWEL
C olonic Obstruction
C olonic Atresia
Embryology
Clinical Features
Imaging Features
Hirschsprung’s Disease (Aganglionosis of the Colon)
Clinical Features
Imaging Features
F unctional Immaturity of the Colon/Neonatal F unctional Colonic Obstruction
Clinical Features
Meconium Plug Syndrome
Small Left Colon Syndrome
C ONCLUSION
REFERENCES
Imaging of Anorectal Anomalies
Arun Kumar Gupta
EMBRYOLOGY OF THE CLOACA RELATED TO ARA
Internal Cloaca
External Cloaca
CLASSIFICATION
INFORMATION REQUIRED IN A PATIENT OF ARA
CLINICAL CLUES
Males
F emales
IMAGING WORK-UP
Invertography
C ontrast Studies
C ontrast Studies in Males
ANORECTAL ANOMALIES IN MALES
High Anomalies
Anorectal Agenesis without Fistula
Anorectal Agenesis with Rectoprostatic Urethral Fistula
H or N Type of Rectoprostatic Urethral Fistula
Rectovesical Fistula
Rectal Atresia
Intermediate Anomalies
Anal Agenesis without Fistula
Anal Agenesis with Rectobulbar Urethral Fistula
Anorectal Stenosis
L o w Anomalies
Anocutaneous Fistula
Anterior Perineal Anus
ANORECTAL ANOMALIES IN FEMALES
High Anomalies
Anorectal Agenesis without Fistula
Anorectal Agenesis with High Rectovaginal F istula ( W ithout a Urogenital S
Cloacal Anomalies
Rectovesical Fistula
Rectal Atresia
Intermediate Anomalies
Anal Agenesis without Fistula
Rectovestibular Fistula
L o w Rectovaginal Fistula
L o w Anomalies
Anovestibular Fistula
Anocutaneous Fistula/Anterior Perineal Anus
Anal Stenosis
INVESTIGATIONS
O THER INVESTIGATIONS
Ultrasound
CT Scan
MRI Scan
Relationship of Sacral Development and Levator Muscle Development
A ssociated Anomalies
Diagnostic Algorithm
REFERENCES
BIBLIOGRAPHY
Gastrointestinal Masses in Children
PLAIN RADIOGRAPHS
C ONTRAST STUDIES
ULTRASONOGRAPHY
C OMPUTED TOMOGRAPHY
M A GNETIC RESONANCE IMAGING
ESOPHAGEAL MASSES IN CHILDREN
z N eoplastic C ongenital Masses
Clinical Presentation
Imaging Features
Neoplasms
GASTRIC MASSES IN CHILDREN
C ongenital
A c quired Outlet Obstruction of Stomach
E tiology
Clinical Presentation
F indings on US
Imaging Features
Ultrasound 6-12
Barium Study 4
Neoplastic Masses
Benign Masses 4,13
Gastric Teratoma 1,4,14,15
Gastric Leiomyoma 4,16-19
Malignant Gastric Tumors
A denocarcinoma of Stomach
Gastric Lymphoma
Gastric Leiomyosarcoma
Gastrointestinal Stromal Tumors
BEZOARS 4,28
SMALL BOWEL MASSES IN CHILDREN
Clinical Presentation
Imaging Features
C ongenital
Enteric Duplication Cyst 4,29-32
Infection
Neoplastic Masses
Benign
Malignant Small Bowel Masses
Small Bowel Lymphoma 4,17,23,38
L eiomyosarcomas 36
Gastrointestinal Stromal Tumor (GIST ) 27
A denocarcinoma
Intussusception
Clinical Presentation
Imaging Features
Clinical Presentation
Imaging Features
MESENTERIC MASSES IN CHILDREN
Differential Diagnosis
Mesenteric and Omental Tumors
C OLONIC MASSES IN CHILDREN
Neoplastic Mass
Benign Colonic Neoplasms
z N eoplastic C ongenital Mass
Duplication Cysts 50
Inflammatory Mass
Appendicular Lump 51
Malignant Colonic Neoplasm 52,53
C ONCLUSION
Hepatic and Pancreatic Masses in Children
Akshay Kumar Saxena, Kushaljit Singh Sodhi, Naveen Kalra
IMAGING
HEPATIC MASSES
Malignant Hepatic Tumors
HEPATOBLASTOMA
HEPATOCELLULAR CARCINOMA (HCC)
F ibrolamellar HCC
RHABDOMYOSARCOMA
HEPATIC METASTASES
Benign Hepatic Neoplasms
HEMANGIOMA
MESENCHYMAL HAMARTOMA
INFANTILE HEMANGIOENDOTHELIOMA
FOCAL NODULAR HYPERPLASIA (FNH) AND HEPATIC ADENOMA
PELIOSIS HEPATIS
INFLAMMATORY LESIONS
Pyogenic Hepatic Abscess
Amebic Hepatic Abscess
F ungal Abscess
Granulomatous Lesions
Echinococcal Disease (Hydatid Cyst)
SIMPLE HEPATIC CYST
POLYCYSTIC LIVER DISEASE
CAROLI’S DISEASE
P ANCREATIC MASSES
P ancreatoblastoma
ISLET CELL TUMORS
SOLID AND PAPILLARY EPITHELIAL NEOPLASM (SPEN) (FRANTZ TUMOR)
MESENCHYMAL TUMORS
P ANCREATIC ADENOCARCINOMA
PSEUDOCYSTS
P ANCREATIC TUBERCULOSIS
SUMMARY
REFERENCES
Childhood Biliopathies
V eena Chowdhury
DEFINITION AND PATHOPHYSIOLOGY OF CHOLESTASIS
PHYSIOLOGICAL NEONATAL JAUNDICE
ETIOLOGY OF JAUNDICE IN THE NEONATE AND INFANT
T r ansient Causes
P ersistent Causes
C ommon
Uncommon
Other Causes of Cholestasis
DIAGNOSIS OF JAUNDICE IN INFANCY AND CHILDHOOD
H e patobiliary scintigraphy (99mTc HIDA scan) is usually required to dif
NEONATAL HEPATITIS
P a thology
Imaging Features
BILIARY ATRESIA
P a thology
Ultrasonography
Gallbladder Length and Gallbladder Contraction
Biliary Atresia Splenic Malformation Syndrome
T riangular Cord Sign
Objective Criteria of Triangular Cord Sign in Biliary Atresia on US
C olor Doppler US in Biliary Atresia
C ontrast Enhanced MR Cholangiography for E v aluation of Biliary Atresia
HEPATOBILIARY CYSTIC MALFORMATIONS
Choledochal Cyst
Kasai Operation
Etiopathogenesis
Anomalous Junction of the P ancreaticobiliary Duct
Imaging Features
CAROLI’S DISEASE
P a thology
Imaging Features
C ongenital Hepatic Fibrosis
PRIMARY SCLEROSING CHOLANGITIS
P a thology
Imaging Features
CYSTIC FIBROSIS
DESTRUCTIVE CHOLANGITIS ASSOCIATED WITH LANGERHANS’ CELL HISTIOCYTOSIS
P a thology
Imaging Features
BILE DUCT PAUCITY
SPONTANEOUS PERFORATION OF CBD
INSPISSATED BILE SYNDROME
JAUNDICE IN OLDER CHILDREN
Hepatocellular Causes
HEPATITIS
Imaging Features
CHRONIC ACTIVE HEPATITIS
METABOLIC
CIRRHOSIS
P o rtal Hypertensive Biliopathy
BILIARY TRACT NEOPLASMS
Embryonal Rhabdomyosarcoma (Sarcoma Botryoides)
P a thology
Imaging Features
DISEASES OF THE GALLBLADDER
Cholelithiasis
P athogenesis of Gallstones in Infancy and Childhood
Imaging Features
A cute Acalculus Cholecystitis and A cute Hydrops of the Gallbladder
C ongenital Anomalies of the Urinary Tract
Smriti Hari, Arun Kumar Gupta
IMAGING MODALITIES
A n t enatal Sonography
Magnetic Resonance Urography
Static MRU (Precontrast Imaging)
Dynamic MR Urography (Postcontrast Imaging)
Limitations
V oiding Urosonography
CT Angiography (CTA) and CT Urography (CTU)
Neonatal Kidney
Embryologic Development of the Urinary Tract
ABNORMALITIES OF KIDNEY
Renal Agenesis
Imaging Features
Rotational Anomalies
A nomalies of Renal Position
Ipsilateral/Uncrossed Ectopia
Imaging Features
C r ossed Renal Ectopia
Horseshoe Kidney
Imaging Features
Ureteropelvic Duplication (Duplex Kidney)
Imaging Features
Renal Hypoplasia
C y stic Renal Dysplasia
A utosomal Recessive Polycystic Kidney Disease
Imaging Features
Multicystic Dysplastic Kidney
A utosomal Dominant (Adult Type) Polycystic Kidney Disease (ADPKD)
Imaging Features
PUJ Obstruction
Imaging Features
T he Prominent Normal Extrarenal Pelvis
P ostoperative Evaluation
ANOMALIES OF THE URETER
E ctopic Ureter
Imaging Features
Ureterocele
Simple Ureterocele
Imaging Features
E ctopic Ureterocele
Imaging Features
P rimary Megaureter
ANOMALIES OF THE URINARY BLADDER
A genesis
C omplete Duplication
Bladder Exstrophy
Bladder Diverticulae
Neurogenic Bladder
T ypes of Anomalies
Megacystis
P rune Belly Syndrome
Urachal Anomalies
Imaging Features
ABNORMALITIES OF THE URETHRA
P osterior Urethral Valve
P osterior Urethral Polyp
P r ostatic Utricle and Mullerian Duct Cyst
C o wper’s Duct Cyst
Male Hypospadias/Epispadias
A n t erior Urethral Diverticulum and Anterior Urethral Valve
Urethral Duplication
Megalourethra
C ongenital Meatal Stenosis
Urinary Tract Infections (Including VUR and Neurogenic Bladder)
RADIOLOGICAL MODALITIES FOR IMAGING OF UTI
R OLE OF ULTRASOUND IN FIRST TIME UTI
INCIDENCE
V esicoureteral Reflux
P A THOPHYSIOLOGY OF VUR AND P Y ELONEPHRITIS
IMAGING FINDINGS IN ACUTE P Y ELONEPHRITIS
A CUTE FOCAL BACTERIAL NEPHRITIS
Grading of VUR
Imaging of VUR
MICTURATING CYSTOURETHROGRAM
PRACTICE AND CONCEPT OF CYCLICAL VOIDING
RADIONUCLIDE CYSTOGRAPHY
ULTRASOUND IN VUR
R OLE OF MRI IN UTI IMAGING
MICTURATING CYSTOURETHROGRAM VERSUS VOIDING UROSONOGRAPHY
GUIDELINES FOR IMAGING IN UTI:
FROM HISTORY TO CURRENT PERSPECTIVE
DMSA for Renal Scar:
W hen is the Best Time to Scan?
TREATMENT GUIDELINES FOR REFLUX
NEUROGENIC BLADDER
A CKNOWLEDGMENTS
REFERENCES
Renal and Retroperitoneal Masses
IMAGING
RENAL MASSES
WILMS’ TUMOR (NEPHROBLASTOMA)
E tiopathogenesis
C linical Features
P a thology
S taging
Imaging
Differential Diagnosis
F ollow-up and Screening
T r eatment and Prognosis
NEPHROBLASTOMATOSIS
P a thology
Imaging Features
P a thology
MESOBLASTIC NEPHROMA (BOLANDE’S TUMOR)
C linical Presentation
Imaging
CLEAR CELL SARCOMA
P a thology
Imaging
RHABDOID TUMOR
C linical Presentation
Differential Diagnosis
T r eatment and Prognosis
P a thology
Imaging
C linical Presentation
P a thology
Imaging
T r eatment and Prognosis
RENAL CELL CARCINOMA
MULTILOCULAR CYSTIC RENAL TUMOR
P a thology
Imaging
Differential Diagnosis
T r eatment and Follow-up
ANGIOMYOLIPOMA
C linical Presentation
P a thology
Screening, Follow-up and Treatment
OSSIFYING RENAL TUMOR OF INFANCY
Imaging
METANEPHRIC ADENOMA (NEPHROGENIC ADENOFIBROMA, EMBRYONAL ADENOMA)
L ymphoma
C linical Presentation
LEUKEMIA
PRIMARY NEUROGENIC TUMORS OF THE KIDNEY
P rimitive Neuroectodermal Tumor
Neuroblastoma
CYSTIC DISEASES OF THE KIDNEY
ADRENAL MASSES
NEUROBLASTOMA
Site
C linical Features
P a thology
S taging
Imaging
Differential Diagnosis
Management and Follow-up
GANGLIONEUROBLASTOMA
GANGLIONEUROMA
PHEOCHROMOCYTOMA
C linical Presentation
Imaging
ADRENAL C ORTICAL TUMORS
C linical Features
ADRENAL HEMORRHAGE
C linical Features
ADRENAL CYSTS
PRIMARY RETROPERITONEAL TUMORS
NEUROGENIC TUMORS
GERM CELL TUMORS
MESENCHYMAL TUMORS
Lipomatous Tumors
Rhabdomyosarcoma and Undifferentiated Sarcomas
RETROPERITONEAL LYMPHANGIOMA
L Y MPH NODE MASSES
C ONCLUSION
RETROPERITONEAL ABSCESS AND HEMATOMA
REFERENCES
E v aluation of Female Pelvis and T esticular Abnormalities
K ushaljit Singh Sodhi, Akshay Kumar Saxena
NORMAL US ANATOMY OF GENITAL ORGANS IN INFANTS AND CHILDREN
UTERUS
O V ARIES
O V ARIAN CYSTS
ANOMALIES OF THE FEMALE PELVIS
Müllerian Anomalies
Obstructive Müllerian Anomalies
Nonobstructive Müllerian Anomalies
P rimary Amenorrhea
P olycystic Ovary Syndrome (PCOS)
PELVIC MASSES IN CHILDREN
Benign Ovarian Neoplasms
Malignant Neoplasms
Malignant Ovarian Neoplasm
Ovarian Torsion
C olor Doppler Imaging in Ovarian Torsion
T ubo-ovarian Abscess
Ectopic Pregnancy
NONGYNECOLOGIC PELVIC MASSES
Role of MRI in Imaging of Female Pelvis
C ongenital Uterine Anomalies
Role of MRI in Characterization of Adnexal Lesions
C ONCLUSION
IMAGING OF TESTICULAR ABNORMALITIES
Undescended Testes
Inguinal-Scrotal Hernia
V aricoceles
Hydrocele
C y stic Dysplasia of the Testis
T esticular Calcification (Microcalcification)
A cute Scrotum
Epididymo-orchitis
T orsion of the Testicular Appendages
T esticular Torsion
A cute Idiopathic Scrotal Edema
Scrotal Tumors
T esticular Tumors
Nonseminomatous Germ Cell Tumors
Other Testicular Tumors
EXTRATESTICULAR TUMORS
P aratesticular Rhabdomyosarcoma
Lipoma
F ibrous Pseudotumor
ADRENAL RESTS
A denomatoid Tumor
Epididymal Cystadenoma
Scrotal Involvement in Systemic Diseases
Scrotal Trauma
Role of MRI in Testicular Abnormalities
C ONCLUSION
REFERENCES
Imaging of Intersex Disorders
Sanjay Sharma, Arun Kumar Gupta
NORMAL SEXUAL DIFFERENTIATION 1
IMAGING OF AN INTERSEX CHILD 2-6
Genitography 2,7
Other Imaging Modalities
MR Appearance of Genital Structures
CLASSIFICATION OF INTERSEX
F emale Pseudohermaphroditism (FPH) 1,2,7,14,15
E tiology
T ypes
Male Pseudohermaphroditism (MPH) 1,2,7
C ause
T rue Hermaphroditism (TH) 1,7
Mixed Gonadal Dysgenesis (MGD) and Dysgenetic Male Pseudohermaphroditism (DM
CLUES TO THE DIAGNOSIS
C ONCLUSION
Skeletal Dysplasias
Gaurav S Pradhan
TERMINOLOGY
Newer Imaging Modalities
OSTEOCHONDRODYSPLASIAS
Defects of Growth of Tubular Bones, Spine or Both
Dysplasias Manifested at Birth
Dysplasias Manifested in Later Life
Disorganized Development of Cartilage and F ibrous Components of the Skeleton
Dysplasia Epiphysealis Hemimelica
Multiple Cartilaginous Exostoses
Enchondromatosis (Ollier’s Disease)
Enchondromatosis with Hemangiomas (Maffucci’s Syndrome)
F ibrous Dysplasia
A bnormalities of the Density of Cortical Diaphyseal Structure or Metaphyseal
Dysplasias with Decreased Bone Density
Increased Bone Density without Modification of Bone Shape
Increased Bone Density with Diaphyseal Involvement
Increased Bone Density with Metaphyseal Involvement
D Y SOSTOSES
Dysostoses with Cranial and Facial Involvement
Craniosynostosis
Craniofacial Synostosis
Dysostoses with Predominant Axial Involvement
Osteo-onychodysostosis
Dysostosis with Predominant Involvement of Extremities
IDIOPATHIC MULTICENTRIC OSTEOLYSIS
PRIMARY DISTURBANCE OF GROWTH
C ornelia de Lange Syndrome
P r ogeria
C ONSTITUTIONAL DISEASES OF BONE WITH KNOWN PATHOGENESIS
C hromosomal Aberrations
P rimary Metabolic Abnormalities
C alcium Phosphorus Metabolism (Hypophosphatasia)
Mucopolysaccharidoses and Mucolipidoses
Bone Abnormalities Secondary to Disturbances of Extraskeleton Systems
REFERENCES
Skeletal Maturity Assessment
MEASUREMENT OF MATURITY
S k eletal Maturity Assessment: W h y is it Necessary?
Methods to Assess Skeletal Maturity
A ppearance and Fusion of Ossification Centers
Greulich and Pyle (G–P) Method
T anner and Whitehouse Method
C omparison of G–P and TW2 Methods
T echnique
C omputer-assisted Skeletal Age Scores
Ultrasound-based Bone Age Calculation
Indian Scene
REFERENCES
Spinal Dysraphism
Raju Sharma, Ankur Gadodia
EMBRYOLOGY
CLASSIFICATION
IMAGING MODALITIES
OPEN SPINAL DYSRAPHISM
Myelocele and Myelomeningocele
Chiari II Malformation
Hemimyelocele/Hemimyelomeningocele
CLOSED SPINAL DYSRAPHISM
CSD with Subcutaneous Mass
Lipoma with Dural Defect (Lipomyelocele and Lipomyelomeningocele)
Meningocele
Anterior Sacral Meningocele
Myelocystocele
CLOSED SPINAL DYSRAPHISM WITHOUT SUBCUTANEOUS MASS
P osterior Bony Spina Bifida
F ilum Terminale Lipoma
Lipoma (Intradural and Intramedullary)
T ight Filum Terminale Syndrome
P ersistent Terminal Ventricle
Neurenteric Cyst
SPLIT CORD MALFORMATION
DORSAL DERMAL SINUS
CAUDAL AGENESIS (CAUDAL REGRESSION SYNDROME, CRS)
SEGMENTAL SPINAL DYSGENESIS
C ONCLUSION
REFERENCES
Imaging of Pediatric Hip
Normal Anatomy
METHODS OF INVESTIGATION
C onventional Radiography
Normal Sonoanatomy of the Hip
Scintigraphy
Arthrography
C omputed Tomography ( CT )
Magnetic Resonance Imaging (MRI)
PEDIATRIC HIP DISORDERS
DEVELOPMENTAL DYSPLASIA OF THE HIP
Natural History and Pathology
Clinical Examination
Radiological Diagnosis and Screening of DDH
IMAGING IN DEVELOPMENTAL DYSPLASIA OF THE HIP
C onventional Radiography
Ultrasonography in DDH
C OMPUTED TOMOGRAPHY
MAGNETIC RESONANCE
Differential Diagnosis of DDH
T he Painful Hip
Septic Arthritis
P athology
Imaging
T uberculosis of the Hip Joint
P a thology and Imaging
Stage I—Tubercular Synovitis
Stage II—Tubercular Arthritis with Damage to Articular Cartilage
Stage III—Advanced Arthritis
TRANSIENT SYNOVITIS OF HIP
LEGG-CALVE-PERTHES’ DISEASE
Imaging
CT and MRI in Perthes’ Disease
P r o ximal Femoral Focal Deficiency (PFFD)
Imaging
Slipped Capital Femoral Epiphysis
Imaging
Differential Diagnosis
Traumatic SCFE Developmental Coxa Vara
P ediatric Hip Trauma
Neuromuscular Hip Dysplasia
Childhood Idiopathic Chondrolysis of the Hip
C alcification of Cartilage and Joints
F emoroacetabular Impingement
REFERENCES
Benign Bone and Soft Tissue T umors and Conditions
Mahesh Prakash, Kushaljit Singh Sodhi
CARTILAGINOUS TUMORS
Osteochondroma
Enchondroma
C hondroblastoma
C hondromyxoid Fibroma
OSSEOUS TUMORS
Osteoid Osteoma
Osteoblastoma
FIBROUS TUMORS
Nonossifying Fibroma
F ibrous Dysplasia
Osteofibrous Dysplasia
HISTIOCYTOSIS X (LANGERHANS CELL HISTIOCYTOSIS)
GIANT CELL TUMOR
TUMOR-LIKE LESIONS
Simple Bone Cyst
A neurysmal Bone Cyst
P seudotumor of Hemophilia
SOFT TISSUE TUMORS
V ascular Lesions
Hemangioma
V ascular Malformations
FIBROBLASTIC/MYOFIBROBLASTIC TUMORS
Nodular Fasciitis
Myositis Ossificans
Myofibroma/Myofibromatosis
F ibromatosis
Neurogenic Tumor
A dipocytic Tumor
Lipoma
Lipoblastoma
P seudotumors
F a t Necrosis
Hematoma
Inflammatory Lesions
P eriarticular Cysts
C ONCLUSION
P ediatric Malignant Bone and Soft Tissue Tumors
Manisha Jana, Ashu Seith Bhalla, Deep N Srivastava
IMAGING MODALITIES
P lain Radiographs
Sonography
Magnetic Resonance Imaging
MRI Techniques for Bone and Soft Tissue Tumors
Role of Contrast-enhanced MRI
Newer MR Imaging Techniques
S taging of Malignant Bone and Soft Tissue Tumors
M ALIGNANT BONE TUMORS
Osteosarcoma
E wing’s Sarcoma
C hondrosarcoma
L ymphoma
Metastases
Malignant Fibrous Histiocytoma
SOFT TISSUE TUMORS
Rhabdomyosarcoma
S ynovial Sarcoma
Other Non-rhabdomyosarcomatous Tumors
C ONCLUSION
REFERENCES
C ongenital Brain Anomalies
Niranjan Khandelwal
DISORDERS OF ORGANIZATION
Supratentorial Malformations
Migrational Disorders
Holoprosencephaly
Septo-optic Dysplasia
Dysgenesis of Corpus Callosum
Hydranencephaly
Infratentorial Malformations
C hiari Malformations
Supra- and Infratentorial Malformations
DISORDERS OF HISTOGENESIS
Neurofibromatosis
T uberous Sclerosis
S turge–Weber Syndrome
Hypoxic–Ischemic Encephalopathy
A tin Kumar, Arun Kumar Gupta
NEUROIMAGING IN INFANTS WITH HIE
BELOW 34 WEEKS GROUP: THE PREMATURE NEONATE
Severe, Total Hypoxia
Mild-to-moderate Hypoxia
Hemorrhage
Germinal Matrix Hemorrhage (GMH)
Intraventricular Hemorrhage (IVH)
P arenchymal Hemorrhage (Periventricular Hemorrhagic Infarction)
Grading of Intracranial Hemorrhage
Imaging of Intracranial Hemorrhage
W hite M a tter I njury of P r ematurity/ P eriventricular Leukomalacia
Imaging of Early PVL
Imaging of End-stage PVL
ABOVE 34 WEEKS GROUP: THE TERM NEONATE
Severe, Total Hypoxia
P r olonged Partial Hypoxia
H Y POXIC–ISCHEMIC INJURY IN POSTNATAL AGE GROUP
Severe, Total Hypoxia
Mild-to-moderate Hypoxia
IMAGING CHOICE FOR EVALUATION OF H Y POXIC–ISCHEMIC INJURY
PREDICTION OF CLINICAL OUTCOME
Ultrasound
E chogenic Thalamus
C erebral Artery Doppler
MR Imaging
C onventional Sequences
Reversal Sign
Diffuse Decreased Density
MR Spectroscopy
Cranial Sonography
Rashmi Dixit, Veena Chowdhury
TECHNIQUE AND NORMAL ANATOMY
Cranial Doppler US
C ONGENITAL BRAIN ANOMALIES
F ailure of Neural Tube Closure
Chiari II Malformation
Sonographic Appearance
A genesis of the Corpus Callosum
Dandy–Walker (DW) Complex
Disorders of Diverticulation
Holoprosencephaly
Schizencephaly
Lissencephaly
P ellucidal Agenesis and Dysgenesis
T uberous Sclerosis
Sturge–Weber Syndrome
V ascular Malformations
DESTRUCTIVE BRAIN LESIONS
P orencephalic Cyst
Hydranencephaly
H Y DROCEPHALUS
INTRACRANIAL HEMORRHAGE
Grade I
Grade II
Grade III
Grade IV
H Y POXIC OR ISCHEMIC ENCEPHALOPATHY
Mild-to-moderate Hypotension in the P r eterm Neonate
Severe Hypotension in the Preterm Neonate
Diffuse Cerebral Edema
Extracorporeal Membrane Oxygenation (ECMO)
P ost-traumatic Injury
Intracranial Infection
NEONATAL AND ACQUIRED INFECTIONS
Pyogenic Meningitis
T ubercular Meningitis
Neoplasms and Cysts
C y sts
REFERENCES
Inflammatory Diseases of the Brain
V ivek Gupta, Niranjan Khandelwal, Paramjeet Singh
INVESTIGATIVE MODALITIES
BACTERIAL INFECTIONS
Brain Abscess
Abscesses Evolve in Four Stages
CRANIAL TUBERCULOSIS
T uberculous Meningitis
Basal Exudates
Hydrocephalus
Infarction
P a r enchymal Tuberculous Granulomas
C ompound Parenchymal and Me ningeal T uberculosis
Clinical Features and Pathology
NEUROCYSTICERCOSIS
L eptomeningitic Form
Intraventricular Form
Racemose Cysts (Subarachnoid Form)
H Y D A TID DISEASE
VIRAL ENCEPHALITIS
Herpes Simplex Encephalitis
Japanese Encephalitis
DWI in Encephalitis
C ONGENITAL INFECTIONS
C ytomegalovirus
T o x oplasmosis
Neonatal Herpes Simplex Encephalitis
Rubella
C ongenital HIV Infection
FUNGAL INFECTIONS
Aspergillosis
Mucormycosis
C ONCLUSION
REFERENCES
P ediatric Brain Tumors
Shailesh B Gaikwad, Ajay Garg
CLASSIFICATION OF CHILDHOOD TUMORS BASED ON TOPOGRAPHY 3
POSTERIOR FOSSA TUMORS
Medulloblastoma
P athology
P ilocytic Astrocytoma
P athology
Ependymoma
P athology
Imaging
Brainstem Gliomas
P athology
Imaging
A typical Teratoid/Rhabdoid Tumor
P athology
Imaging
Hemangioblastoma
P athology
Imaging
Epidermoid and Dermoid
SUPRATENTORIAL TUMORS
C erebral Astrocytoma
P athology
Imaging
Subependymal Giant Cell Astrocytoma
Ganglioglioma
Imaging
Supratentorial Ependymoma
P athology
P rimitive Neuroectodermal Tumor
P athology
Imaging
Oligodendroglioma
Dysembryoplastic Neuroepithelial Tumors
Desmoplastic Infantile Ganglioglioma
C r aniopharyngioma
SELLAR AND SUPRASELLAR TUMORS
C hiasmatic/Hypothalamic Gliomas
Imaging
Hypothalamic Hamartoma
Imaging
P ituitary Adenomas
A r achnoid Cyst
PINEAL REGION MASSES
Germinomas
Imaging
T eratomas
P athology
Imaging
Other Germ Cell Tumors
P ineal P arenchymal Tumors
P ineal Cysts
EXTRAPARENCHYMAL TUMORS
C horoid P lexus Tumors
P athology
Imaging
Meningiomas and Related Tumors
P athology
L eukemia and Lymphoma
TUMORS OF THE ORBIT AND NECK
OCULAR TUMORS
Retinoblastoma
RETROBULBAR ORBITAL TUMORS
V ascular Tumors
Orbital Varices
P lexiform Neurofibroma
Rhabdomyosarcoma
Neuroblastoma
Juvenile Angiofibroma
MR SPECTROSCOPY IN BRAIN
T umor Imaging
P ositron-emission Tomography (PET ) in Neuro-oncology
U ses in Glioma Evaluation
NANOTECHNOLOGY
Imaging and Nanomedicine for Diagnosis and Therapy of CNS Tumors
Diffusion-weighted Imaging
N ewly codified glial neoplasms of the 2007 WHO classification of tumors of th
C ONCLUSION
REFERENCES
Metabolic Disorders of the Brain
Normal Myelination of the Brain
MR Imaging at 1.5 T (Tables 1A and B)
Graywhite Matter Differentiation
METABOLIC DISORDERS
Classification According to C ellular Organelle Dysfunction
Classification of Metabolic Disorders on the Basis of Organelle Disorder 9,10
L ysosomal Storage Diseases with White Matter Involvement
Mitochondrial Dysfunction with L eukoencephalopathy
P eroxisomal Disorders
K e arns–Sayre syndrome Disorders of Amino Acid and Organic Acid Metaboli
White Matter Disorders with Unknown Metabolic Defect
Classification of Metabolic Disorders A c c ording to Brain Substance Involvem
L eukodystrophies
P oliodystrophies
P andystrophies
L Y SOSOMAL STORAGE DISORDERS
Metachromatic Leukodystrophy
Clinical Features
P athologic Findings
Krabbe Disease/Globoid Cell L eukodystrophy (GLD)
Clinical Features
P athologic Findings
Sphingolipidosis
Clinical Features
Imaging Features
P athologic Findings
Imaging Features
Gaucher’s Disease
F abry Disease
Clinical Features
PEROXISOMAL DISORDERS
Clinical Features
Imaging
Mucopolysaccharidoses
X -linked Adrenoleukodystrophy
Clinical Features
P athologic Findings
A drenomyeloneuropathy
Z ellweger Syndrome
MR imaging reveals diffuse demyelination with abnormal gyration that is most
Refsum Disease
P athologic Findings
C erebrotendinous Xanthomatosis
Rhizomelic Chondrodysplasia C alcificans Punctata
UNCLASSIFIED LEUKODYSTROPHIES
C anavan Disease
Clinical Features
Imaging Features
Alexander Disease
P athologic Findings
Clinical Features
Imaging Features
V an der Knaap Disease/Megaloencephalic L eukodystrophy with Subcortical Cyst
V anishing White Matter Disease/Childhood A taxia with CNS Hypomyelination
P athologic Findings
Clinical Features
Imaging Features
Aicardi–Goutieres Syndrome
P elizaeus–Merzbacher Disease
Mitochondrial Encephalomyopathy: Lactic A cidosis and Stroke-like Symptoms
Clinical Features
P athologic Findings
C ockayne Syndrome
MR Spectroscopy
MITOCHONDRIAL DISORDERS/
DEFECTS OF THE RESPIRATORY CHAIN
Imaging Features
Myoclonic Epilepsy with Ragged Red Fibers (MERRF)
P athologic Findings
K earns–Sayre Syndrome
Clinical Features
Imaging Features
Subacute Necrotizing Encephalomyopathy (Leigh Disease)
P athologic Features
Imaging Features
LEBER’S HEREDITARY OPTIC NEUROPATHY
DISORDERS OF AMINO ACID METABOLISM/AMINOACIDOPATHIES
Urea Cycle Defects
Phenylketonuria
Clinical Features
Imaging Findings
Malignant Form of Phenylketonuria
Maple Syrup Urine Disease
Imaging Findings
Classic Homocystinuria
Clinical Features
Imaging
Nonketotic Hyperglycinemia
Imaging
5, 10 Methylene-tetrahydrofolate Reductase Deficiency
ORGANIC ACIDEMIAS
Methylmalonic Acidemia
Imaging Findings during Metabolic Crisis
Imaging Findings after Metabolic Crisis
P r opionic Acidemia
Imaging Findings
Ethylmalonic Acidemia
Methylglutaconic Aciduria
Imaging Finding
3-Hydroxy-3-methylglutaryl (HMG)- C oenzyme a Lyase Deficiency
Glutaric Aciduria Type 1
METABOLIC DISORDERS PRIMARILY AFFECTING GRAY MATTER
Hallervorden–Spatz Disease
Neuronal Ceroid Lipofuscinosis (NCL)
Rett Syndrome
DISORDERS OF METAL METABOLISM
W ilson’s Disease (Hepatolenticular Degeneration)
Imaging Findings
Imaging
Menkes’ Disease
C ONCLUSION
REFERENCES
C hest and Cardiovascular Imaging
Chest X-ray: Techniques and Anatomy
Mahesh Prakash, Manavjit Singh Sandhu
TECHNICAL ADVANCES
High kV Technique
C ONVENTIONAL CHEST RADIOGRAPHY
New Screen Film Combinations
Beam Equalization Radiography
Digital Radiography
Digital Radiography and Chest
RADIOGRAPHIC PROJECTIONS
P osteroanterior View
P atient Positioning
P atient Respiration
F ilm Exposure
Kilovoltage
Grids and Filters
Lateral View
A n t eroposterior View
Decubitus View
L ordotic View
Oblique View
SPECIAL RADIOGRAPHIC TECHNIQUES
Inspiratory–Expiratory Radiography
V alsalva and Müller Maneuvers
Bedside/Portable Radiography
NORMAL ANATOMY ON CHEST X-RAY
T r achea
T r acheobronchial Divisions
L ungs
Bronchopulmonary Segments
Hilum and Pulmonary Vasculature
P leura
Mediastinum
Mediastinal Lines and Interfaces
REFERENCES
Heart
Diaphragm
C ONCLUSION
Multidetector Computed T omography of Chest: T echniques and Anatomy
Deep N Srivastava, Atin Kumar, Shivanand Gamanagatti
C OMPUTED TOMOGRAPHY
Indications for CT of the Chest
Definition of Spiral Pitch
Dose Considerations
Intravenous Contrast Medium Enhancement
W indow Settings
HIGH-RESOLUTION COMPUTED T OMOGRAPHY
Sequential HRCT Protocol
V olumetric HRCT Protocol
V olumetric Standard CT Protocol
V olumetric Low-dose CT Protocol
P ediatric MDCT Chest
ANATOMY
T r acheobronchial Tree
L ungs
Mediastinum
Esophagus
L ymph Nodes
Mediastinal Spaces
Basic Patterns of Lung Diseases
Sumedha Pawa, Sapna Singh
P A TTERN RECOGNITION
High-resolution CT Patterns of Disease
L UNG DISEASES THAT INCREASE RADIOGRAPHIC DENSITY
P r edominantly Airspace Disease
P arenchymal Consolidation
Radiographic Criteria of Airspace Disease
Airspace Nodule
C oalescence
Distribution Characteristics
Margination
Air Bronchogram
T ime Factor
P arenchymal Atelectasis
Maintenance of Lung Volume
Resorption Atelectasis
RADIOGRAPHIC SIGNS OF ATELECTASIS
Direct Signs
Indirect Signs
L ocal Increase in Density
Elevation of the Hemidiaphragm
Mediastinal Displacement
P assive Atelectasis
A dhesive Atelectasis
C ompensatory Overinflation
Displacement of the Hila
Changes in the Chest Wall
P r edominantly Interstitial Disease
Radiographic Patterns of Diffuse Interstitial Disease
Reticular Pattern
Nodular Pattern
Reticulonodular Pattern
Linear Pattern
C ombined Airspace and Interstitial Disease
General Signs in Diseases that Increase Radiographic Density
Characteristics of the Border of a Pulmonary Lesion
C avitation
C alcification and Ossification
Changes in Position of Interlobar Fissures
Bullae and Cysts
Distribution of Disease within the Lungs ( A natomic Basis)
Radiologic Localization of Pulmonary Disease (The Silhouette’s Sign)
Line Shadows
T ubular Shadows (Bronchial Wall Shadows)
Horizontal or Obliquely Oriented Linear Opacities of Unknown Nature
HIGH-RESOLUTION CT SCAN FINDINGS MANIFESTING AS INCREASED LUNG OPACITY
P arenchymal Scarring
Line Shadow of Pleural Origin
Nodules
Linear Abnormalities
Interlobular Septal Thickening
P arenchymal Bands
Subpleural Lines
Reticular Abnormalities
Ground-glass Opacity
C onsolidation
L UNG DISEASES THAT DECREASE RADIOGRAPHIC DENSITY
Increased Air with Unchanged Blood and Tissue
Increased Air with Decreased Blood and Tissue
Normal Amount of Air but Decreased Blood and Tissue
Reduction in All Three Components
RADIOGRAPHIC SIGNS
Alteration in Lung Volume
General Excess of Air in the Lungs
L ocal Excess of Air
Static Signs
Dynamic Signs
L ocal Reduction in Vasculature
P ulmonary Air Cysts
Alteration in Vasculature
General Reduction in Vasculature
HIGH-RESOLUTION CT SCAN FINDINGS MANIFESTING AS DECREASED OPACITY
Areas of Decreased Attenuation with Walls
Bronchiectasis
Honeycomb Pattern
C ystic Pattern
Areas of Decreased Attenuation without Walls
Emphysema
Mosaic Perfusion and Inhomogeneous L ung Opacity
Normal Inspiratory Scans with Air Trapping on Expiratory Imaging
Multidetector CT in Assessment of Diffuse Lung Disease
C ONCLUSION
REFERENCES
R adiographic Manifestations of P ulmonary Tuberculosis
Mandeep Kumar Garg, Naveen Kalra
NEW CONCEPT OF RADIOLOGIC M ANIFESTATIONS OF PULMONARY TUBERCULOSIS
RADIOLOGICAL PATTERNS OF PULMONARY TUBERCULOSIS
T ypical Radiological Patterns of P rimary Tuberculosis
P ostprimary TB or Phthisis
Radiological Patterns Encountered in Both P rimary and/or Postprimary TB
Miliary TB
Exudative Pleuritis
T r acheobronchial TB
T uberculoma
C omplications and Sequelae of Pulmonary TB
A typical Patterns
PET/CT IN TUBERCULOSIS
Nontubercular Pulmonary Infections
Anju Garg
IMAGING MODALITIES
RADIOGRAPHIC PATTERN
ETIOPATHOGENESIS OF PULMONARY INFECTIONS
SPECIFIC PNEUMONIAS
Bacterial Pneumonias
P neumococcal P neumonia
Staphylococcal Pneumonia
Gram-negative Pneumonias
Chlamydia pneumoniae
Anaerobic Pneumonias
A ctinomycosis
Mycoplasma Pneumonia
V iral Pneumonia
Influenza Virus
Respiratory Syncytial Virus
V aricella
A denovirus
FUNGAL INFECTIONS
Opportunistic Invaders
Aspergillosis
P rimary Pathogens
Histoplasmosis
Cryptococcosis
C occidioidomycosis
P ARASITIC INFECTIONS
P r otozoal Infections
Metazoal Infestations
Roundworm, Hookworm and Strongyloides Infections
F ilariasis
E chinococcus Infection/Hydatid Disease
C OMPLICATIONS OF PNEUMONIA
P leural Effusion and Empyema
Hydropneumothorax
P neumatoceles
A bscess
Bronchiectasis
Miscellaneous Complications
Delayed Resolution of Pneumonia
INTERVENTIONAL PROCEDURES IN THE P A TIENTS WITH PNEUMONIA
C ONCLUSION
REFERENCES
Imaging of the Tracheobronchial Tree
Ashu Seith Bhalla, Raju Sharma
IMAGING MODALITIES
Chest Radiograph
Computed Tomography
Acquisition
Axial CT Images
Advanced Reconstruction Techniques
NORMAL AIRWAY ANATOMY
Anatomic Variants
TRACHEOBRONCHIAL LESIONS
Central Airways
Strictures
Inflammatory Tracheal Stenosis due to Tuberculosis
Tracheobronchomalacia
Fungal Infections
Postintubation Stenosis
Neoplasms of Tracheobronchial Tree
Malignant Tumors
Miscellaneous
Mucous Plug/Mucoid Pseudotumor
Benign Tumors
Broncholithiasis
T r acheopathia Osteoplastica
T r acheoesophageal Fistulas
Diffuse Diseases Involving T r acheobronchial Tree
Amyloidosis
Relapsing Polychondritis
Sarcoidosis
W egener Granulomatosis
Saber Sheath Trachea
P eripheral Airways
Bronchiectasis
C ongenital Airway Wall Abnormality
T r acheobronchomegaly (Mounier–Kuhn Disease)
W illiams–Campbell Syndrome
C ongenital Bronchial Atresia
A c quired Wall Abnormalities
Mucociliary Clearance Abnormalities
Hyperimmune Response
Small Airway Disease/Bronchiolitis
C ellular Bronchiolitis
Bronchiolitis Obliterans with Intraluminal Polyps
Obliterative or Constrictive Bronchiolitis
Asthma
Chronic Obstructive Pulmonary Disease
C ONCLUSION
Imaging of Interstitial Lung Disease
Smriti Hari, Sanjay Sharma, Deep N Srivastava
PLAIN RADIOGRAPHY
High-resolution CT
A natomy of the Secondary Pulmonary Lobule
SARCOIDOSIS
C ONNECTIVE TISSUE DISEASE ASSOCIATED INTERSTITIAL LUNG DISEASE
RHEUMATOID ARTHRITIS-ASSOCIATED INTERSTITIAL LUNG DISEASE
SYSTEMIC LUPUS ERYTHEMATOSUS
PROGRESSIVE SYSTEMIC SCLEROSIS
H Y PERSENSITIVITY PNEUMONITIS
SILICOSIS AND COAL-WORKER PNEUMOCONIOSIS
ASBESTOSIS
L Y MPHANGIOLEIOMYOMATOSIS
LANGERHANS CELL HISTIOCYTOSIS
PULMONARY ALVEOLAR PROTEINOSIS
IDIOPATHIC INTERSTITIAL PNEUMONIAS
IDIOPATHIC PULMONARY FIBROSIS
NONSPECIFIC INTERSTITIAL PNEUMONITIS
CRYPTOGENIC ORGANIZING PNEUMONIA
RESPIRATORY BRONCHIOLITIS-ASSOCIATED INTERSTITIAL LUNG DISEASE
DESQUAMATIVE INTERSTITIAL PNEUMONIA
L Y MPHOID INTERSTITIAL PNEUMONIA
A CUTE INTERSTITIAL PNEUMONIA
P ulmonary Manifestations in Immunocompromised Host (HIV and Solid Organ Tra
Mandeep Kang
HIV/AIDS
S y stematic Approach to Imaging Diagnosis
Imaging Methods
Radiological Pattern Approach to Diagnosis
Normal C hest R adiograph
Ground-glass O pacities
C onsolidation
Multiple P ulmonary N odules
L ymphadenopathy
P leural E ffusion
NON-HIV IMMUNOCOMPROMISED HOSTS
Imaging Approach
B A CTERIAL INFECTIONS
PNEUMOCYSTIS JIROVECI PNEUMONIA
MYCOBACTERIAL INFECTIONS
HIV/AIDS Patients
HIV Negative Immunocompromised Patients
VIRAL INFECTIONS
FUNGAL INFECTIONS
L ymphoma
L ymphocystic Interstitial Pneumonitis
P ost-transplant Lymphoproliferative Disorder
NONINFECTIOUS MANIFESTATIONS OF AIDS
Kaposi’s Sarcoma
Chest in Immunocompromised Host (Hematological Infections and Bone Marrow
Sanjay Sharma, Sanjay Thulkar
C OMPLICATIONS NOT SPECIFIC TO HSCT
Infections
Bacterial Pneumonia
P neumocystis jirovecii Pneumonia
F ungal Infections
T uberculosis
Drug Toxicity
P ulmonary Hemorrhage
C OMPLICATIONS SPECIFIC TO HSCT
Infections
C ytomegalovirus Pneumonia
P ulmonary Edema
Idiopathic Pneumonia Syndrome
Bronchiolitis Obliterans
Bronchiolitis Obliterans Organizing Pneumonia
R adiation Injury
Spontaneous Pneumothorax
REFERENCES
Imaging the Mediastinum
Raju Sharma, Ashu Seith Bhalla, Arun Kumar Gupta
IMAGING MODALITIES
Chest Radiograph
C omputed Tomography
Magnetic Resonance Imaging
DIFFERENTIAL DIAGNOSIS OF MEDIASTINAL MASSES
ANTERIOR MEDIASTINUM
L esions of Thymus
Thymic Rebound
Thymoma
Thymic Hyperplasia
Germ Cell Tumors
Thyroid Mass
P arathyroid Adenoma
L ymphangioma (Cystic Hygroma)
P ericardial Cyst
Other Vascular Tumors
MIDDLE MEDIASTINUM
Bronchogenic Cyst
Esophageal Duplication Cyst
Esophageal Lesions
POSTERIOR MEDIASTINUM
Neurenteric Cyst
P eripheral Nerve Tumors
Lateral Thoracic Meningocele
T umors from Sympathetic Ganglia
P araganglioma
P a r aspinal Infection
Extramedullary Hemopoiesis
Mediastinal Varices
MULTICOMPARTMENT MEDIASTINAL MASSES/LESIONS
Mediastinal Lymphadenopathy
T u berculosis
Sarcoidosis
L ymphoma
Metastasis
V ascular Lesions
A ortic Aneurysm
A o rtic Dissection
Superior Vena Cava Obstruction
A bnormalities of the Mediastinal Fat
Mediastinal Lipomatosis
Herniation of Abdominal Fat
MISCELLANEOUS LESIONS OF THE MEDIASTINUM
Mediastinal Hemorrhage
P neumomediastinum
A cute Mediastinitis
F ibrosing Mediastinitis
C ONCLUSION
REFERENCES
Imaging of Solitary and Multiple Pulmonary Nodules
MORPHOLOGICAL CHARACTERISTICS OF SPN
Size
Shape
L ocation
Edge Characteristics
INTERNAL CHARACTERISTICS OF SPN
C alcification
C alcification in a Benign Nodule
Indeterminate Calcification
Fat
Nodule Attenuation
C alcification in Tumor
C a vitation
Air Bronchograms and Pseudocavitation
Air Crescent Sign
AIR FLUID LEVEL
Satellite Nodules
F eeding Vessel Sign
P ositive Bronchus Sign
INDETERMINATE SOLITARY PULMONARY NODULE
C ontrast-enhancement/Hemodynamic Characteristics on Dynamic Helical CT
F or Benign Nodules
Growth Rate Assessment
V OLUME QUANTIFICATION ON CT/THREE– DIMENSIONAL EVALUATION
C OMPUTER-AIDED DIAGNOSIS
IMAGE REGISTRATION
Bayesian Analysis
Decision Analysis
FDG Positron Emission Tomography
Biopsy
T r ansthoracic Needle Aspiration Biopsy (TNAB)
F iberoptic Bronchoscopy (FOB)
V ideo Assisted Thoracic Surgery
NEWER TECHNIQUES FOR THE EVALUATION OF SPN
Dynamic MR Imgaing
Diffusion Weighted MRI Imaging
Infective Causes
Inflammatory (Noninfectious)
Airway and Inhalational Disease
Dual Energy CT in the Evaluation of SPN
DIFFERENTIAL DIAGNOSIS OF SOLITARY PULMONARY NODULE 72
Malignant Neoplasm
Septic embolism C ongenital Lesions
Sequestration Idiopathic/Miscellaneous
Benign Neoplasm and Neoplasm Like C ondition
MORPHOLOGICAL CHARACTERISTICS IN SPECIFIC LESIONS
Malignant Lesions
L ung Malignancies
L ymphoma
Metastatic Neoplasm
C arcinoid Tumor
Benign Neoplasms
P ulmonary Hamartoma
Other Benign Tumors
Infective Causes
Granuloma
Mycetoma
Hydatid Cyst
Round Pneumonia
L ung Abscess
Inflammatory (Noninfectious)
Rheumatoid Nodules
Airway or Inhalational Disease
Lipoid Pneumonia
V ascular Lesions
P ulmonary Artery Aneurysm
P ulmonary Vein Varix
Arteriovenous Malformation (AVM)
P ulmonary Infarction
C ongenital Lesions
P ulmonary Bronchogenic Cyst
Sequestration
Miscellaneous
Round Atelectasis
MULTIPLE PULMONARY NODULES
MORPHOLOGICAL CHARACTERISTICS IN SPECIFIC CAUSES
Metastatic Lung Nodules
Kaposi’s Sarcoma
Rheumatoid Nodules and Caplan Syndrome
P r ogressive Massive Fibrosis
W egener’s Granulomatosis
Sarcoidosis
Septic Emboli with Infarction
Arteriovenous Malformation
Amyloidosis
Bronchiolitis Obliterans Organizing Pneumonia (BOOP)
C ONCLUSION
L ung Malignancies
Sanjay Thulkar, Smriti Hari, Arun Kumar Gupta
P A THOLOGY
CLINICAL FEATURES
IMAGING FEATURES
P eripheral Tumors
C entral Tumors
Methods to Establish Tissue Diagnosis
Imaging Work-up for the Staging of NSCLC
Mediastinal Invasion
STAGING OF NSCLC
CHEST WALL INVASION
P ancoast Tumor
L ymph Node Staging
A dditional Lung Nodules
Pleural Effusion
Distant Metastases
PET in Management of Lung Cancer
Bronchoalveolar Carcinoma
TREATMENT OF NSCLC
F ollow-up Imaging
Recurrent Lung Cancer
SCREENING FOR LUNG CANCER
NEUROENDOCRINE TUMORS OF THE L UNG
Bronchial Carcinoid
Small-cell Lung Cancer
T r eatment of Neuroendocrine Tumors
RARE LUNG MALIGNANCIES
L UNG METASTASES
L ymphangitis Carcinomatois
Detection of Lung Metastases
T r eatment of Lung Metastases
L Y MPHOMA OF THE LUNG
REFERENCES
Intensive Care Chest Radiology
Akshay Kumar Saxena, Kushaljit Singh Sodhi, Madhu Gulati
A t electasis
CHEST X-RAY IN IMAGING OF ICU PATIENTS
A spiration Pneumonitis
P neumonia
Hydrostatic Pulmonary Edema
CT in Hydrostatic Pulmonary Edema
Noncardiogenic Pulmonary Edema
P ulmonary Embolism
Barotrauma
P ulmonary Interstitial Emphysema
P neumomediastinum
P neumothorax
Subcutaneous Emphysema
Support and Monitoring Apparatus
Respiratory Support
Endotracheal and Tracheostomy Tube
Intravascular Catheters
C entral Venous Line
S w an-Ganz Catheter
ULTRASOUND IN IMAGING OF ICU PATIENTS
CT SCAN IN IMAGING OF ICU PATIENTS
Imaging in Pulmonary T hromboembolism
PLAIN RADIOGRAPHS
PULMONARY ANGIOGRAPHY
E chocardiography
D-dimer
Scintigraphy
Duplex Ultrasound and Compression Ultrasound of Lower Limbs
C OMPUTED TOMOGRAPHY
Spiral CT
V ASCULAR FINDINGS
T echnique
P ARENCHYMAL FINDINGS
A cute Thromboembolism
C hronic Thromboembolism
A cute Versus Chronic Thromboembolism
PITFALLS IN DIAGNOSIS OF PULMONARY EMBOLISM
EFFICACY AND ACCURACY OF MULTIDECTOR C OMPUTED TOMOGRAPHY
ISOLATED SUBSEGMENTAL PULMONARY EMBOLISM
C OMPUTED TOMOGRAPHY VENOGRAPHY
M A GNETIC RESONANCE IMAGING
MR Venography
IMAGING-GUIDED INTERVENTION IN THE MANAGEMENT OF PULMONARY THROMBOEMBOLISM
P ulmonary Embolism in Pregnancy
A CKNOWLEDGMENTS
Imaging in Thoracic Trauma
Atin Kumar, Shivanand Gamanagatti
PULMONARY PARENCHYMAL INJURIES
P ulmonary Contusion
P ulmonary Laceration
Aspiration Pneumonitis
A t electasis
T r aumatic Lung Herniation
PLEURAL INJURIES
P neumothorax
Hemothorax
INJURIES OF THE MEDIASTINUM
T r acheobronchial Injury
Esophageal Injury
P neumomediastinum
V ascular Injury
INJURY OF DIAPHRAGM
C ardiac and Pericardial Injury
Injury of Chest Wall
C ONCLUSION
REFERENCES
Imaging of Pleura
IMAGING MODALITIES
Layers of Pleura
PLEURAL EFFUSION
T ypes of Effusion: Exudates and Transudates
Exudates
T r ansudate
F ibrin Body
IMAGING IN PLEURAL EFFUSION
Plain Radiographs
ULTRASONOGRAPHY OF PLEURAL EFFUSION
C OMPUTED TOMOGRAPHY
PLEURAL EFFUSION OR ASCITIS
L oculated Pleural Fluid (Encysted/
Encapsulated)
MAGNETIC RESONANCE IMAGING OF PLEURAL EFFUSION
Specific Causes of Pleural Effusion
P arapneumonic Effusion with Empyema 9-14
Organization Stage (Pleural Peel)
Empyema Necessitans
T ube Drainage of Empyema
BRONCHOPLEURAL FISTULA
P ostsurgical BPF
Infective BPF
PLEURAL THICKENING
V isceral Pleural Thickening
Pleural Apical Cap and Fibrous Thickening
Pleural Thickening
Mimics
PLEURA AND ASBESTOSIS 1 8-19
ASBESTOSIS PSEUDOTUMOR (ROUND ATELECTASIS)
PLEURAL CALCIFICATION
PNEUMOTHORAX
Spontaneous Pneumothorax
P rimary Spontaneous Pneumothorax
Secondary Spontaneous Pneumothorax
P neumothorax Ex Vacuo
T r aumatic Pneumothorax
C a tamenial Pneumothorax
IMAGING FINDINGS
X-ray
Upright Patient
Supine Patients
Ultrasonography
C omputed Tomography
T ension Pneumothorax
SIZE OF PNEUMOTHORAX 21
PLEURAL NEOPLASM
Pleural Thickening
MESOTHELIOMA (MALIGNANT PLEURAL MESOTHELIOMA) 2 3-24
Pleural or Extrapleural Masses
Pleural Effusion
Radiographic Findings
Ultrasonography
C omputed Tomography
Magnetic Resonance Imaging
P ositron Emission Tomography
L ocalized Fibrous Tumor
Pleural Metastasis
REFERENCES
Pleural Lymphoma
Imaging of the Diaphragm and Chest Wall
Sameer Vyas, Anupam Lal
DIAPHRAGM
Anatomy
Imaging Modalities
P lain Radiograph
Ultrasonography (USG)
C omputed Tomography (CT )
Magnetic Resonance Imaging (MRI)
R adionuclide Scan
Normal Variants
A c c essory Diaphragm
Elevated Hemidiaphragm
Unilateral Elevation
Bilateral Elevation
L o w Lying Diaphragm
Inversion of the Diaphragm
P eridiaphragmatic Collections
DIAPHRAGMATIC MOVEMENTS
Diaphragmatic Hernias
Bochdalek Hernia
Morgagni Hernia
Intrapericardial Hernia
Diaphragmatic Injury
T umors of the Diaphragm
CHEST WALL
C ongenital and Developmental Anomalies
Inflammatory and Infectious Diseases
T umors of the Chest Wall
Malignant C hest Wall Tumors
REFERENCES
Bronchial Artery Embolization
Shivanand Gamanagatti, Ashu Seith Bhalla
P A THOPHYSIOLOGY AND ETIOLOGY
C auses of Hemoptysis (Figs 1A to D)
DIAGNOSTIC WORK-UP
Idiopathic pulmonary hemosiderosis
C onventional Radiography (Figs 2A to C)
C omputed Tomography (CT) (Figs 1 and 3)
F iberoptic Bronchoscopy (FB)
BRONCHIAL ARTERY ANATOMY
NONBRONCHIAL SYSTEMIC ARTERY ANATOMY
TECHNIQUE OF BRONCHIAL ARTERY EMBOLIZATION
Embolic Agents (Figs 9A to D)
RESULTS
C OMPLICATIONS
C ONCLUSION
Diagnostic and Therapeutic Interventions in Chest
Naveen Kalra, Mandeep Kang, Anupam Lal
IMAGE GUIDANCE MODALITIES
Nonvascular Interventions
T r ansthoracic Needle Biopsy of P ulmonary Lesions
Indications
P atient Evaluation
C ontraindications
Image Guidance
Biopsy Technique
Results
C omplications
T r ansthoracic Needle Biopsy from Other Sites
P ercutaneous Needle Biopsy of the Pleura
L ocalization of a Nodule for T horacoscopic Resection
Diagnostic Thoracocentesis
PERCUTANEOUS DRAINAGE OF PLEURAL SPACE FLUID COLLECTIONS
Pleural Sclerotherapy or Pleurodesis
P neumothorax Drainage
L ung Abscess Drainage
SECONDARY PULMONARY ASPERGILLOMA
Endoluminal Tracheobronchial S t enting
Mediastinal Abscess Drainage
P ericardial Effusion Drainage
P neumatocele and Bulla Drainage
RADIOFREQUENCY ABLATION OF LUNG LESIONS
V ASCULAR INTERVENTIONS
P ulmonary Artery Embolization
Endovascular Therapy of SVC Obstruction
P ercutaneous Vascular Foreign Body Retrieval
C ONCLUSION
REFERENCES
Chest X-ray Evaluation in C ardiac Disease
Sanjiv Sharma, Gurpreet Singh Gulati, Priya Jagia
CARDIAC SILHOUETTE
C ardiac Shape
C ardiac Contour
P osteroanterior (PA) View
C ardiac Size
C ardiac Volume
Right Anterior Oblique View
L eft Anterior Oblique View
L ateral View
A ssessment of Chamber Enlargement
Right Atrium
L eft Ventricle
Right Ventricle
L eft Atrium
A orta
N ormal Radiographic Anatomy
PULMONARY VASCULATURE
Increased Pulmonary Blood Flow (Pulmonary Plethora)
Decreased Pulmonary Blood Flow (Pulmonary Oligemia)
R adiological Signs (Fig. 7)
R adiological Signs of Plethora (Fig. 6)
P ulmonary Arterial Hypertension (Fig. 8)
P ulmonary Venous Hypertension
Stage 1: Redistribution/Cephalization of the Blood Flow (Fig. 9)
Stage 2: Interstitial Edema (Fig. 10)
Stage 3: Alveolar Edema (Fig. 11)
A symmetrical Pulmonary Blood Flow (Fig. 12)
Orientation of Pulmonary Outflow Tract
Imaging in Ischemic Heart Disease
Gurpreet Singh Gulati, Sanjiv Sharma, Priya Jagia
P A THOPHYSIOLOGY OF ISCHEMIC HEART DISEASE
Myocardial Ischemia
Myocardial Viability and Myocardial Infarction (MI)
Rationale for Ischemia and Viability Imaging
Imaging Modalities
E chocardiography
Nuclear Imaging
C ardiac Magnetic Resonance
Imaging Sequences
Stress Cardiac Magnetic Resonance
C ardiac Magnetic Resonance for Viability
CMR for Myocardial Mass and Function
Other Useful Sequences
Multidetector Computed Tomography
Limitations of MDCT
E v aluation of Various Components of IHD
C oronary Artery Imaging
P laque Imaging
Detection of Myocardial Ischemia
Myocardial Viability
Myocardial Function
FUTURE DIRECTIONS
A ppropriateness Criteria for use of Cardiac MDCT and CMR in the Investigatio
C ONCLUSION
REFERENCES
Imaging Approach in Children with C ongenital Heart Disease
P riya Jagia, Sanjiv Sharma, Gurpreet Singh Gulati
PHYSICAL EXAMINATION
RADIOLOGICAL APPROACH
C hest Radiograph
L eft-to-Right (L–R) Shunt
P r etricuspid Shunt
L arge Aorta
Normal Aorta
P ost-tricuspid L–R Shunt
Right-to-Left (R–L) Shunt
Large Aorta with Decreased Lung Vascularity
Small Aorta with Increased Vascularity
L arge Pedicle with Increased Vascularity
Normal Aorta with Decreased L ung Vascularity
Other Conditions
MULTISLICE CARDIAC CT
CARDIAC MRI
A nalyzing CT or MRI Images
Anatomy
CARDIAC CATHETERIZATION
REFERENCES
Normal Connections
C ardiac Tumors
F ollow-up after Surgery or after Endovascular Intervention
Imaging in Cardiomyopathies
P riya Jagia, Gurpreet Singh Gulati, Sanjiv Sharma
CLASSIFICATION
DIAGNOSTIC TECHNIQUES
DILATED CARDIOMYOPATHY
Hypertrophic Cardiomyopathy
Restrictive Cardiomyopathy
Amyloidosis
Sarcoidosis
Siderotic (or Iron Overload) Cardiomyopathy
Endomyocardial Fibrosis
Anderson–Fabry Disease
T uberculosis
Miscellaneous Myocardial Diseases
BIBLIOGRAPHY
C ONCLUSION
Imaging Evaluation of Cardiac Masses
Gurpreet Singh Gulati, Priya Jagia, Sanjiv Sharma
CLINICAL FEATURES
Imaging Techniques
Angiocardiography
ECHO
MDCT
MRI
MR Imaging Sequences for Evaluation of Cardiac Masses
Spin Echo (SE) Sequences
Gradient Echo (GRE) and Steady-state Free P r ecession Sequences
C ontrast-enhanced Imaging
Other Techniques
C lassification (Table 1)
NEOPLASTIC LESIONS OF THE HEART
P rimary
Benign Tumors
Malignant Tumors
Sarcoma
Secondary Neoplasms
P aracardiac and Extracardiac Tumors
NON-NEOPLASTIC LESIONS
T hrombus
A neurysm of Sinus of Valsalva (SOV )
A trial Septal Aneurysm
P leuropericardial Cyst
Infective Lesions
V alvular Vegetation
Hydatid Cyst
T uberculoma
V ARIANT AND NORMAL ANATOMICAL STRUCTURES SIMULATING A CARDIAC MASS
P ericardium
L eft Atrium
L eft Ventricle
Right Atrium
Right Ventricle
C ONCLUSION
REFERENCES
Imaging Diagnosis of V alvular Heart Disease
P riya Jagia, Sanjiv Sharma, Gurpreet Singh Gulati
INTRODUCTION
A ORTIC VALVULAR DISEASE
MITRAL VALVULAR DISEASE
TRICUSPID VALVULAR DISEASE
HEMODYNAMIC EFFECTS ON PULMONARY VASCULATURE
A ssociated Pulmonary Pathologies
E ff ects of Treatment during Follow-up
Heart Size
L eft Atrial Size
Other Changes
ECHOCARDIOGRAPHY
V alvular Stenosis
V alvular Regurgitation
Infective Endocarditis
P r osthetic Valves
CARDIAC MAGNETIC RESONANCE IMAGING
V alve Leaflet Morphology
V alvular Stenosis
V alvular Regurgitation
V alve Endocarditis and Tumors
P r osthetic Valve
C OMPUTED TOMOGRAPHY
ANGIOCARDIOGRAPHY
C ONCLUSION
BIBLIOGRAPHY
Imaging of the Pericardium
ANATOMY
T r ansverse Sinus
Superior Aortic Recess
Inferior Aortic Recess
Right and Left Pulmonic Recesses
Oblique Sinus
Recesses of the Pericardial Cavity Proper
Right and Left Pulmonary Venous Recesses
P ostcaval Recess
PHYSIOLOGY
C ONGENITAL PERICARDIAL ANOMALIES
P ericardial Cysts
C ONGENITAL ABSENCE OF THE PERICARDIUM
PERICARDIAL EFFUSION
C ardiac Tamponade
P ericarditis
Nonconstrictive Pericarditis
C onstrictive Pericarditis
P neumopericardium
PERICARDIAL TUMORS
Metastases
P rimary P ericardial Tumors
C ONCLUSION
Nuclear Medicine in CVS and Chest
Chetan D Patel, Madhavi Chawla
MYOCARDIAL PERFUSION IMAGING
Radiopharmaceuticals
Rationale of Myocardial Perfusion Imaging
S tudy Protocol for Stress MPI
C linical Indications of Myocardial P erfusion Imaging
Detection of Coronary Artery Disease
Assessment of Prognosis and Risk Stratification
E v aluation of Myocardial Perfusion after Revascularization
Detection of Myocardial Viability
RADIONUCLIDE VENTRICULOGRAPHY
P a tient Preparation
Data Acquisition
Interpretation
C linical Application
Chemotherapy Toxicity
C oronary Artery Disease
C ardiomyopathy
CARDIAC POSITRON EMISSION T OMOGRAPHY
C linical Application of Cardiac PET
Diagnosis of CAD
Assessment of Myocardial Viability
NEW DIRECTIONS IN NUCLEAR CARDIOLOGY
L UNG VENTILATION: PERFUSION IMAGING
L ung Perfusion Scan
V entilation Scan
Interpretation of V-Q Scan for P ulmonary Embolism
C urrent Status and Future Developments in V-Q Imaging
POSITRON EMISSION TOMOGRAPHY IN L UNG CANCER
P a tient Preparation for F-18 FDG Study
PET-CT in Solitary Pulmonary Nodules (SPN)
PET-CT in Staging Lung Cancer
Restaging and Assessment of Response t o Therapy
PET in Radiotherapy Planning
Imaging of Aorta
ANGIOGRAPHIC ANATOMY
Abdominal Aorta
Measurement (Diameter) of Aorta
Normal Anatomic Variations
Indications for Imaging the Aorta
IMAGING MODALITIES
Intravascular Ultrasound (IV US)
C omputed Tomography ( CT )
C onventional Technique
Spiral/Helical Technique
Ultrasound (US)
T r ansesophageal Echocardiography (TEE)
Limitations
Magnetic Resonance Imaging (MRI) and MR Angiography
Black-blood Imaging
White-Blood Imaging
C ontrast MR Angiography
C a theter Angiography
T echnique
C omplications of Angiography
Radiological Findings
C onventional X-ray Chest
C ONGENITAL AORTIC ANOMALIES
A ortic Arch Anomalies
C oarctation of Aorta
Associated Anomalies
Hemodynamics in Adults
Noninvasive Imaging
A C QUIRED AORTIC DISEASES
A ortic Aneurysms
Incidence
Classification
Objectives of Imaging
Plain Radiography
Growth Rates of Aneurysm and Risk of Rupture
Ultrasound (US)
C omputed Tomography and Magnetic Resonance Imaging
C a theter Angiography
A ORTIC DISSECTION
Classification
A o rtography
Imaging
C omputed Tomography
P r econtrast Images
T AKAYASU’S ARTERITIS
P ostcontrast Images
T ypes 31
Magnetic Resonance Imaging
Imaging Findings
A ORTIC TRAUMA
Grading of Aortic Injuries 37
Imaging
C omputed Tomography
Magnetic Resonance Imaging
A THEROSCLEROSIS
P a thology
Imaging
C ONCLUSION
REFERENCES
P ostoperative Aorta
Imaging of Peripheral V ascular Disease
EVALUATION OF THE PERIPHERAL ARTERIAL SYSTEM
Imaging Modalities
Ultrasound and Doppler Scanning
Arterial Flow Patterns on Spectral Doppler
CT Angiography
MR Angiography
C o n v entional Angiography/DSA 9,10
PERIPHERAL ARTERIAL OCCLUSIVE DISEASE
Clinical Features
Radiological Evaluation
Angiography
L O WER LIMB ARTERIOGRAPHY 9
Arteritis 9,10
Upper Extremities 20,21
E v aluation of Bypass Grafts 10,22-24
T r eatment
Etiology
Clinical Features
Imaging
A cute Limb Ischemia 9,10,20,25
Angiography
Clinical Features
T horacic Outlet Syndrome 20,22,24
Imaging
Aneurysms
P seudoaneurysms
V enous Malformations
V ascular Malformations 9,20,26,29
C apillary Malformations
Arteriovenous Malformations
Arteriovenous Fistulae 23,24
Dialysis Fistulae
EVALUATION OF THE PERIPHERAL VEINS
L o w er Extremity
A cute Deep Venous Thrombosis
Sonography and Color Doppler Flow Imaging
C olor Doppler Flow Imaging
Upper Extremity DVT 20,24,32,33
A cute Versus Chronic DVT
CT Venography 33,34
MR and MR Venography 33-36
V enography 30,31,35
Chronic Venous Disease 30,37,38
Imaging
Sonography
P erforating Veins
V enography
V enous Mapping
O THER DISORDERS
V enous Aneurysms 30,31
C ONCLUSION
Basic Principles and Current C oncepts of Musculoskeletal Magnetic Resonan
R aju Sharma, Shivanand Gamanagatti
HARDWARE ISSUES
3 T IMAGING
SEQUENCES
F ast Spin-echo Sequences
Gradient-recalled Echo Sequences
F a t Suppressed Sequences
Role of Contrast
Reduction of Metallic Artifact from Orthopedic Hardware
NORMAL APPEARANCE OF MUSCULOSKELETAL TISSUES
IMAGING OF ARTICULAR CARTILAGE
MORPHOLOGICAL ASSESSMENT OF CARTILAGE
C OMPOSITIONAL ANALYSIS OF CARTILAGE
T1ρ Mapping
T2 Mapping
MUSCULOSKELETAL TUMORS
d-GEMRIC
USE OF ADVANCED MR TECHNIQUES IN TUMOR EVALUATION
P r oton Spectroscopy
Diffusion-weighted Imaging
Dynamic Perfusion Imaging
M ARROW IMAGING
MUSCULOSKELETAL INFECTIONS
INFLAMMATORY ARTHRITIS
INTERVENTIONAL MR IMAGING
Nuclear Medicine Imaging for Musculoskeletal Disorders
BONE SCINTIGRAPHY
SPECT AND SPECT-CT
PET AND PET-CT
MUSCULOSKELETAL TUMOR IMAGING
Metastasis
P rimary Malignant Tumors
Benign Tumors
INFECTION IMAGING
A cute and Chronic Osteomyelitis
Diabetic Foot
P r osthetic Infection
FDG PET-CT for Musculoskeletal Infection
MUSCULOSKELETAL TRAUMA
S tress Fractures
S hin Splints
F r actures in Childhood
Sport Injuries
METABOLIC BONE DISEASE IMAGING
P aget’s Disease
Hyperparathyroidism
Renal Osteodystrophy
Osteoporosis and Osteomalacia
Bone Dysplasias
A v ascular Necrosis
C omplex Regional Pain Syndrome (Reflex Sympathetic Dystrophy)
JOINT IMAGING
FUTURE DIRECTION
REFERENCES
Angiography and Interventions in Musculoskeletal Lesions
Deep N Srivastava
TECHNIQUE
Diagnostic Angiography
Angioembolization
ANGIOGRAPHY IN BONE TUMORS
Osteochondroma
Osteoid Osteoma
Osteosarcoma
Giant Cell Tumor
Aneurysmal Bone Cyst
ANGIOGRAPHY IN BONE AND SOFT TISSUE LESIONS OF VASCULAR ORIGIN
Hemangioma
Hemangiopericytoma
Angiosarcoma
ANGIOGRAPHY IN METASTATIC TUMORS IN BONE AND SOFT TISSUES
ANGIOGRAPHY IN PERIPHERAL TRAUMA
IMAGE-GUIDED INTERVENTIONS IN BONE AND SOFT TISSUE LESIONS
Aspiration Cytology and Biopsy
Embolization
P r eprocedural Preparations
Indications
Embolizing Materials
C omplications
P ercutaneous Vertebroplasty
T echnique
C ontraindications
Intra-arterial Chemotherapy
Results
C omplications
P ercutaneous Treatment of Disk Herniation
F uture Directions
PERCUTANEOUS ABLATION OF BONE TUMORS
T uberculosis of Bones and Joints
Gaurav S Pradhan, Veena Chowdhury
ETIOPATHOGENESIS
C linical Features
Radiological Features
TUBERCULOSIS OF JOINTS
T ubercular Arthritis
Hip
Knee
Ankle and Foot
Shoulder
Elbow
W rist and Carpus
Sacroiliac Joints
TUBERCULOSIS OF LONG AND FLAT BONES
T ubercular Osteomyelitis
T uberculosis of Long Bones
F lat Bones
Ribs
P athology
Scapula
Sternum
Skull
P elvis
Sternoclavicular Joint
T uberculosis of Tendon Sheaths and Bursae
A cromioclavicular Joint
TUBERCULOSIS OF SHORT BONES
T ubercular Infection of Prosthetic Joint
C ONCLUSION
REFERENCES
A typical Mycobacterial Infection
Nontubercular Bone and Joint Infections
Manphool Singhal, Niranjan Khandelwal
IMAGING MODALITIES
A CUTE OSTEOMYELITIS
C linical Features
Radiologic Features
L OCALIZED OSTEOMYELITIS (BRODIE’S ABSCESS)
CHRONIC OSTEOMYELITIS
SCLEROSING OSTEOMYELITIS OF GARRE
SYPHILIS OF BONE
C ongenital (Infantile) Syphilis
Late Congenital Syphilis
A c quired Syphilis
R UBELLA OSTEOMYELITIS
A CTINOMYCOSIS OF BONE
M ADURAMYCOSIS
LEPROSY OF BONE
DIABETIC FOOT
H Y D A TID DISEASE
SEPTIC ARTHRITIS
T uberculosis of the Spine
R ashmi Dixit
PATHOPHYSIOLOGY
CLINICAL FEATURES
LABORATORY INVESTIGATIONS 21-24
IMAGING MODALITIES
Conventional Radiographs
Nuclear Medicine Scintigraphy
Computed Tomography
Magnetic Resonance Imaging
Central
Anterior Subperiosteal
IMAGING APPEARANCES
CONVENTIONAL RADIOGRAPHS
Paradiskal
Appendiceal or Neural Arch Tuberculosis
Computed Tomography
Cord Changes
ATYPICAL SPINAL TUBERCULOSIS 21
Post-treatment Follow-up
Conventional Radiographs
PET/CT 65
Computed Tomography
Magnetic Resonance Imaging 40,48,57
DIFFERENTIAL DIAGNOSIS
Noninfective Inflammatory Arthritis
Mandeep Kang, Mahesh Prakesh
RHEUMATOID ARTHRITIS
Pathophysiology
Radiographic Features
Late Changes
Axial Skeleton Involvement
OTHER IMAGING MODALITIES
Ultrasonography
Computed Tomography
Radionuclide Scanning
Magnetic Resonance Imaging
Synovial Imaging
Bone Marrow Edema
Erosions
Large Joints
SCORING SYSTEMS FOR RA
Tendons and Ligaments
JUVENILE IDIOPATHIC ARTHRITIDES
Juvenile-onset Adult Type (Seropositive) Rheumatoid Arthritis
Seronegative Chronic Arthritis
Radiologic Features
SERONEGATIVE SPONDYLOARTHROPATHIES
ANKYLOSING SPONDYLITIS
Pathophysiology
Radiologic Features
Sacroiliac Joints
Spine
Peripheral Joints
PSORIATIC ARTHROPATHY
REITER’S SYNDROME
ENTEROPATHIC SPONDYLOARTHROPATHY
CRYSTAL DEPOSITION ARTHROPATHY
Gout
CALCIUM PYROPHOSPHATE DIHYDRATE CRYSTAL DEPOSITION DISEASE
Nontubercular Infections of the Spine
Sameer Vyas, Manavjit Singh Sandhu
P A THOGENESIS OF SPINAL INFECTIONS
IMAGING OF SPINAL INFECTIONS
P lain Radiography
Radioisotope Scanning
C omputed Tomography
TYPES OF INFECTIONS
Myelography/CT Myelography
Pyogenic Bacterial Infections
Pyogenic Disc Space Infections
Spinal Infections in Children
Childhood Disc Infection or Discitis
Differential Diagnosis of Spinal Infection
P ostoperative Spondylodiscitis
Epidural Space Infections
Nonpyogenic Bacterial Infections
Brucellosis
A ctinomycosis
Nocardiosis
V iral Infections
Spinal Infections in AIDS
C occidioidomycosis
Cryptococcosis ( T orulosis)
F ungal Infections
Aspergillosis
Blastomycosis
C andidiasis (Moniliasis)
P arasitic Infections
E chinococcosis or Hydatid
C ysticercosis
REFERENCES
Degenerative Disease of the Spine and Joints
Jyoti Kumar, Sumedha Pawa
DEGENERATIVE DISORDERS OF THE SPINE
Imaging Modalities
Pathophysiology
Anatomy of Intervertebral Disk
Degenerative Disk Changes
Disk Herniation
Endplate Changes
Disease of Facets, Uncovertebral Joints and Ligaments
Spondylosis Deformans and Intervertebral Osteochondrosis
Complications of Degenerative Spinal Disease
Spinal and Foraminal Stenosis
Scoliosis and Kyphosis
Segmental Instability
Clinical Implications
DEGENERATIVE DISEASE OF JOINTS
Prevalence and Incidence of Osteoarthritis
Imaging Modalities
Pathogenesis
Systemic Risk Factors
Local Joint Vulnerabilities
Extrinsic Factors Acting on the Joint
Joint Overuse from Occupations and Athletics
Radiographic–Pathologic Correlation
HIP OSTEOARTHRITIS
Radiographic Views
Radiographic Appearance
Superior Migration Pattern
Medial Migration Pattern
Axial Migration Pattern
Rapid Destructive Osteoarthritis
KNEE OSTEOARTHRITIS
Radiographic Views
Cartilage Space
Osteophytes
Subchondral Sclerosis
Radiographic Findings
Malalignment
Differential Diagnosis
Radiographic Grading of Osteoarthritis
SHOULDER OSTEOARTHRITIS
ROTATOR CUFF TEAR ARTHROPATHY
HAND AND WRIST OSTEOARTHRITIS
Interphalangeal Joints
Thumb Base
Metacarpophalangeal Joints
Erosive (Inflammatory) Osteoarthritis
FOOT AND ANKLE OSTEOARTHRITIS
SECONDARY OSTEOARTHRITIS
CONCLUSION
REFERENCES
Skeletal Disorders of Metabolic and Endocrine Origin
Alpana Manchanda, Arun Kumar Gupta
DISORDERS OF METABOLIC ORIGIN
RICKETS AND OSTEOMALACIA
C auses
Biochemical Findings
P a thology of Rickets and Osteomalacia
Clinical Features
Radiological Features
RICKETS
Signs of Healing Rickets
Sequelae
Etiologic Considerations of Rickets
ABNORMALITIES OF VITAMIN D METABOLISM
Renal Osteodystrophy
Hereditary Vitamin D-dependent Rickets
X -linked Hypophosphatemia
T y pe I VDDR
Biochemical Findings
Radiological Features
T y pe II VDDR
RICKETS AND OSTEOMALACIA SECONDARY TO PHOSPHATE LOSS
Renal Tubular A cidosis
T y pe I (Distal) RTA
T y pe II (Proximal) RTA
T umor-associated Rickets and Osteomalacia
Chemotherapeutic Drug-induced Rickets
SYNDROMES WITH THE RADIOGRAPHIC APPEARANCE OF RICKETS OR OSTEOMALACIA BUT W
Hypophosphatasia
Metaphyseal Chondrodysplasia (Schmid Type)
A typical Axial Osteomalacia
OSTEOMALACIA
Radiological Changes
H Y PERPARATHYROIDISM
P rimary HPT
Secondary HPT
T ertiary HPT
P a thophysiology
Clinical Features
Biochemical Findings
Radiological Approach
Radiological Findings
BONE RESORPTION
Subperiosteal Resorption
Intracortical Bone Resorption
Endosteal Bone Resorption
Subchondral Bone Resorption
Subphyseal Bone Resorption
Subligamentous and Subtendinous Bone Resorption
T r abecular Bone Resorption
BROWN TUMORS
RENAL OSTEODYSTROPHY
JOINT DISORDERS
OSTEOSCLEROSIS
RENAL LESIONS
NEPHROCALCINOSIS
P ARATHYROID LOCALIZATION
Surgical Treatment
P arathyroid Imaging
PREOPERATIVE LOCALIZATION TECHNIQUES
ANATOMICAL AND PATHOLOGICAL C ONSIDERATION IMPORTANT
FOR LOCALIZATION
Embryology and Anatomy
Sonographic Evaluation
P itfalls in Interpretation
P ercutaneous Aspiration/Biopsy
C ontrast-enhanced Computed Tomography
Magnetic Resonance Imaging
P arathyroid Scintigraphy
Clinical Presentation
Biochemical Findings
RADIOLOGICAL FINDINGS
Single Photon Emission Computed T omography
H Y POPARATHYROIDISM
PSEUDOHYPOPARATHYROIDISM
Clinical Findings
Biochemical Findings
Radiological Findings
PSEUDOPSEUDOHYPOPARATHYROIDISM
DISORDERS OF ENDOCRINE ORIGIN
⁄ ) ZQFSHPOBEJTN H Y PERCORTISOLISM
Clinical Findings
Radiological Findings
H Y POPITUITARISM
H Y POTHYROIDISM
H Y PERTHYROIDISM
Clinical Findings
Biochemical Findings
Radiological Findings
H Y PERGONADISM
H Y POGONADISM
T urner’s Syndrome
GROWTH HORMONE DISORDERS
A CROMEGALY
Clinical Findings
Definitive Diagnosis
Radiological Findings
GIGANTISM
SCURVY
Clinical Findings
Biochemical Findings
P a thophysiology
Radiological Findings
FLUOROSIS
Clinical Findings
Radiographical Findings
REFERENCES
Osteoporosis
Mukesh Kumar Yadav, Vivek Gupta, Niranjan Khandelwal
DEFINITION
P A THOGENESIS
CLASSIFICATION
P rimary Osteoporosis
Juvenile Osteoporosis
Endocrine Causes
Malignant Diseases
Immobilization
Drugs
Genetic Abnormalities in Bone Collagen Synthesis
Gastrointestinal Diseases
Organ Transplantation
CLINICAL FEATURES
INVESTIGATIONS
Bone Mineral Analysis
S tandard Radiography
Radiogrammetry
P hotodensitometry
Neutron Activation Analysis
C ompton Scattering
Single Energy Photon Absorptiometry
Dual Energy Photon Absorptiometry
Dual Energy X-ray Absorptiometry
Quantitative C omputed Tomography
Quantitative Ultrasound
High-resolution Bone Imaging
T r abecular Bone Assessment Using
C ortical Bone Assessment Using MRI
C linical Applications
High-resolution Peripheral Quantitative C omputed Tomography (HR-pQCT )
Multidetector CT (MDCT )
M ANAGEMENT OF OSTEOPOROTIC C OMPRESSION FRACTURES: PERCUTANEOUS VERTEBROPL
Indications
P r ocedure
P ostprocedure Care
C omplications
Benign Bone Tumors and T umor-like Conditions
Mahesh Prakash, Niranjan Khandelwal
IMAGING MODALITIES
Radiography
C omputed Tomography
Magnetic Resonance Imaging
BONE-FORMING TUMORS
Enostosis
Osteoma
Osteoid Osteoma
Osteoblastoma
CARTILAGE-FORMING TUMORS
Osteochondroma
Enchondroma
C hondroblastoma
C hondromyxoid Fibroma
FIBROUS TUMORS/LESIONS
F ibrous Cortical Defects and Nonossifying Fibroma
F ibrous Dysplasia
Osteofibrous Dysplasia
Desmoplastic Fibroma
V ASCULAR AND CONNECTIVE TISSUE TUMORS
Hemangioma
Lipoma
O THER TUMORS
Giant C ell Tumor
A neurysmal Bone Cyst
TUMOR-LIKE LESIONS
Simple Bone Cyst
E osinophilic Granuloma
P seudotumor of Hemophilia
Brown Tumor of Hyperparathyroidism
C ONCLUSION
Malignant Bone Tumors
CLASSIFICATION OF PRIMARY M ALIGNANT BONE TUMORS
General Principles of Diagnosis
S taging of Bone Tumors
IMAGING MODALITIES
C onventional Radiography
Magnetic Resonance Imaging
C omputed Tomography
A ngiography
Ultrasonography
Nuclear Medicine
OSTEOSARCOMA
Intraosseous Osteosarcoma
C linical Presentation
Surface Osteosarcomas
P eriosteal Osteosarcoma 20
Juxtacortical/Parosteal Osteosarcoma
High-grade Surface Osteosarcoma
Extraosseous Osteosarcoma
P rimary Multifocal Osteosarcoma 24
CHONDROSARCOMA
Secondary Osteosarcoma
Imaging Features 27,28
Other Varieties of Chondrosarcoma
FIBROSARCOMA
C linical Presentation
Imaging Features 32
M ALIGNANT FIBROUS HISTIOCYTOMA 12
C linical Presentation
M ALIGNANT ROUND CELL TUMORS (MRCT)
EWING’S SARCOMA 33
C linical Presentation
Imaging Features 34
P rimitive Neuroectodermal T umor of Bone (PNET ) 12
Non-Hodgkin’s Lymphoma of Bone 38 (Lymphosarcoma, Reticulum Cell Sarcoma)
C linical Presentation
Hodgkin’s Lymphoma of Bone
Imaging Features
LIPOSARCOMA
V ASCULAR TUMORS OF THE BONE
A ngiosarcoma
CHORDOMA
C linical Presentation
Imaging Features
ADAMANTINOMA OF LONG BONES 41
C linical Presentation
Hemangioendothelioma
M ALIGNANT GIANT CELL TUMOR
Imaging Features
MULTIPLE MYELOMA
C linical Presentation
Imaging Features
POEMS Syndrome
PLASMACYTOMA (SOLITARY MYELOMA)
C linical Presentation
METASTATIC BONE DISEASE
Imaging Features
Differential Diagnosis
C ONCLUSION
REFERENCES
Magnetic Resonance Imaging of the Knee
Sapna Singh
IMAGING PROTOCOLS/TECHNICAL FACTORS
P a tient Positioning
Slice Thickness
Imaging Planes and Pulse Sequences
Microanatomy of the Menisci
MENISCI
Normal Anatomy
Macroanatomy and MRI Appearance
Lateral Meniscus
Anatomic Variants
Discoid Meniscus
Medial Meniscus
Meniscus Flounce (Buckled Meniscus)
Meniscal Ossicle
ABNORMAL MENISCUS
Meniscal Degenerations and Tears
MR Grading of Meniscal Tears
Abnormal Morphology
CLASSIFICATION OF MENISCAL TEARS
Horizontal Tears
Radial/Free Edge Tears
L ongitudinal Tears
P eripheral Tear
Meniscocapsular Separation
IMAGING CHALLENGES
P otential Pitfalls
T r ansverse Intrameniscal Ligament
Meniscofemoral Ligaments
P opliteus Tendon
Magic Angle Effect
P ulsation Artifact from the Popliteal Artery
Surgical Considerations in Meniscal Tear
T ear Location
T ear Morphology and Length
A c curacy of MR in the Diagnosis of Meniscal Tears
LIGAMENTS AND TENDONS OF THE KNEE
CENTRAL STRUCTURES OF THE KNEE
Anatomy of Anterior Cruciate Ligament
MR Appearance of ACL
A CL Tears
Indirect Signs of ACL Tear
A c curacy of MR in ACL Tears
P osterior Cruciate Ligament
Anatomy of the PCL
MR Appearance of PCL
MEDIAL STRUCTURES OF THE KNEE
Anatomy
Magnetic Resonance Imaging
MCL Injury
POSTEROMEDIAL STRUCTURES OF THE KNEE
Anatomy
POSTEROLATERAL CORNER OF THE KNEE
Anatomy
Magnetic Resonance Imaging
POSTERIOR STRUCTURES OF THE KNEE
Anatomy
KNEE DISLOCATIONS
ANTEROLATERAL CORNER OF THE KNEE
Normal Anatomy
Iliotibial Band Injury
Segond Fracture
Iliotibial Band Friction Syndrome
ANTERIOR STRUCTURES OF THE KNEE OR THE EXTENSOR MECHANISM OF THE KNEE
Anatomy
P a t ellar Tendinosis (Jumper’s Knee)
A cute Patellar Tendon Disruption
F emoral Trochlear Groove
P a t ellar Tendon–Lateral F emoral C ondyle Friction Syndrome
P a t ella Alta and Patella Baja
KINEMATIC MR IMAGING
T echniques
Incremental, Passive Positioning Technique
P A TELLOFEMORAL JOINT
P a t ellofemoral Joint Anatomy
A ctive Movement or Dynamic Technique
Motion Triggered Cine Technique
A ctive Movement, Loaded Technique
MR IMAGING OF THE ARTICULAR CARTILAGE
Articular Cartilage Structure and Damage
MRI of Articular Cartilage
MRI Assessment of Articular Cartilage Injury
QUANTITATIVE CARTILAGE MR IMAGING
Chondromalacia Patellae
Osteoarthritis
EVALUATION OF THE SYNOVIUM
Rheumatoid Arthritis
T uberculosis of the Knee
Juvenile Rheumatoid Arthritis
P igmented Villonodular Synovitis
Hemophilia
S ynovial Chondromatosis of the Knee
Deferiprone-induced Arthropathy
MR IMAGING OF BONE MARROW ABNORMALITIES OF THE KNEE
T r auma
A cute and Chronic Avulsive Injuries
F a tigue and Insufficiency Fractures
Stress Fractures
Spontaneous Osteonecrosis
Medullary Infarction
Osteochondritis Dissecans
T r ansient Bone Marrow Edema S yndrome (Transient Osteoporosis)
Reflex Sympathetic Dystrophy
Infection
Bone Neoplasms
MR ARTHROGRAPHY
T echnique
Meniscal Lesions
C artilage Lesions
Osteochondritis Dissecans
Intra-articular Bodies
Plica Synovialis
POSTOPERATIVE EVALUATION OF THE KNEE
Imaging of the ACL Graft
Graft Rupture
Graft Impingement
Arthrofibrosis
P ostoperative Meniscus
P ostoperative Articular Cartilage
C ONCLUSION
REFERENCES
Magnetic Resonance Imaging of Hip and Pelvis
NORMAL ANATOMY
TECHNIQUE
HIP AND PELVIS: EVALUATION OF STRUCTURES
C oronal (Figs 7A and B)
Osseous Structures
Nonosseous Structures
Axial (Figs 8A to C)
Osseous Structures
Nonosseous Structures
Sagittal
A V ASCULAR NECROSIS
C ause and Pathogenesis
P r esentation
MRI OF AVN
Magnetic Resonance Imaging and P r ognostic Indicators
P itfalls in Diagnosis 20
Study Choice and Work-up
Staging
BONE MARROW EDEMA SYNDROME
P r ognosis
MONITORING OF TREATMENT
MINIMAL AVN
Insufficiency or Stress Fractures of the Femoral Head
F emoral Head Osteonecrosis and BMEs
FEMOROACETABULAR IMPINGEMENT
C am Impingement
P incer Impingement
HERNIATION PITS
FRACTURE
Magnetic Resonance Imaging
STRESS FRACTURES
OSTEOCHONDRAL INJURY 41,42
Muscle Contusions
Muscle Strain—Myotendinous Strain
TRAUMATIC MUSCULOTENDINOUS INJURIES 43,44
A vulsion Injury
Gluteus Medius Tendon Tear—Greater T r ochanteric Pain Syndrome
LABRUM
BURSAE
PIRIFORMIS SYNDROME
MAGNETIC RESONANCE IN POSTARTHROPLASTY
ARTHRITIS
INFECTION
P igmented Villonodular Synovitis (PVNS)
Magnetic Resonance Imaging
P rimary Synovial Chondromatosis
Magnetic Resonance Imaging
Amyloid Arthropathy
NERVES
MARROW REPLACEMENT PROCESSES
Chondroblastoma
Magnetic Resonance Imaging
Chondrosarcoma
TUMORS
Osteoid Osteoma
Magnetic Resonance Imaging
Chordomas
Magnetic Resonance Imaging
C ONCLUSION
REFERENCES
Magnetic Resonance Imaging of Shoulder and T emporomandibular Joints
Mahesh Prakash, Paramjeet Singh
SHOULDER JOINT
MR IMAGING PROTOCOLS
MR ARTHROGRAPHY
NORMAL ANATOMY
OSSEOUS STRUCTURES
LIGAMENTS
MUSCULOTENDINOUS ANATOMY
BURSAE
NORMAL MR APPEARANCE
Axial Sections (Figs 1 and 4)
C oronal Sections (Figs 2 and 4)
Sagittal Sections (Figs 3 and 4)
SHOULDER IMPINGEMENT SYNDROME
P rimary Extrinsic Impingement
Secondary Extrinsic Impingement
Internal Impingement
ROTATOR CUFF TENDINOPATHY AND TEARS
MR Appearance
INSTABILITY
Imaging Techniques for Labral Tears
MR Findings in Patients with Instability
P itfalls
ABNORMALITIES OF BICEPS TENDON
Bicipital Tendinopathy/Rupture
Bicipital Tendon Dislocations
NERVE ENTRAPMENT SYNDROMES
Quadrilateral Space Compression Syndrome
Suprascapular Nerve Entrapment
ADHESIVE CAPSULITIS
CALCIFIC TENDINITIS
ARTHRITIS
OSTEOARTHRITIS
INFECTIVE ARTHRITIS
RHEUMATOID ARTHRITIS
A V ASCULAR NECROSIS
TEMPOROMANDIBULAR JOINT
MR Imaging Technique
NEOPLASMS
NORMAL ANATOMY AND MR APPEARANCE (FIGS 34 TO 37)
Normal MR Appearance
Movements
DISEASES OF TEMPOROMANDIBULAR JOINT
INTERNAL DERANGEMENT
DISK DISPLACEMENTS
DISK DEFORMITY AND OSTEOARTHRITIS
STUCK DISK
OPEN LOCK JAW
OSTEONECROSIS AND OSTEOCHONDRITIS DISSECANS
POSTOPERATIVE IMAGING
EVALUATION OF MANDIBULAR ASYMMETRY
INFECTIONS AND ARTHRITIDES
TUMORS AND TUMOR-LIKE CONDITIONS
REFERENCES
Magnetic Resonance Imaging in Bone Marrow Disorders
DISTRIBUTION OF NORMAL BONE MARROW AND NORMAL CONVERSION
MR IMAGING TECHNIQUES FOR EVALUATION OF NORMAL BONE MARROW
RECENT ADVANCES IN MR IMAGING OF BONE MARROW
Dynamic Contrast-enhanced MR Imaging and Bone Marrow Perfusion
C ONTRAST-ENHANCED MR IMAGING OF THE BONE MARROW USING IRON OXIDE P ARTICLES
MR SPECTROSCOPY
WHOLE BODY MRI
3T MRI
C OMBINED PET AND MR IMAGING
NORMAL MR APPEARANCES OF BONE MARROW
IMAGING OF BONE MARROW DISORDERS
Reconversion of Fatty Marrow to Hematopoietic Marrow
Marrow Replacement or Infiltration
Myeloid Depletion
Depletion of Myeloid Elements with Fibrosis
Differential Diagnosis of Gaucher’s Disease and Hemosiderosis
Deposition of Metabolic Products
MR IMAGING OF THERAPY-INDUCED CHANGES OF BONE MARROW
CHANGES IN MARROW SIGNAL DUE TO CHEMOTHERAPY
NEW THERAPY REGIMENS
BONE MARROW TRANSPLANTATION
FOCAL DISORDERS OF THE BONE MARROW
C ONCLUSION
REFERENCES
R adiological Evaluation of Appendicular Trauma
A tin Kumar, Arun Kumar Gupta
CLINICAL EVALUATION
RADIOLOGICAL EVALUATION
Definitions and Classification
Osseous Evaluation
P r esence or Absence of Bony Injury
Anatomic Location and Extent of the Fracture
T ypes of Fracture
Direction of Fracture Line
Spatial Relationship of the Fragments
P r esence of Special Features
P r esence of Associated Abnormalities of the Adjacent Joints
Involvement of Growth Plate/Physis: Seen in Children
Soft-tissue Evaluation
FRACTURE HEALING
P r esence of Special Types of Fractures
C OMPLICATIONS OF FRACTURE
Immediate Complications
Intermediate Complications
Delayed Complications
Imaging Modalities
UPPER LIMB TRAUMA
Dislocation of the Shoulder
F r acture of Neck of Humerus
F r acture of Shaft of Humerus
F r acture of Distal Humerus
Dislocation of the Elbow
F r acture of the Head and Neck of Radius
F r acture of Upper End of Ulna
F r actures of the Shaft of the Radius and Ulna
F r actures of Distal End of Radius
F r actures of the Carpal Bones
Dislocation of the Wrist
Single Carpal Dislocations
Multiple Carpal Dislocations
F r actures and Dislocations of the Hand
L O WER LIMB TRAUMA
Dislocations of the Hip
P osterior Dislocation
Anterior Dislocation
F r actures of the Proximal Femur
Intracapsular Fractures
Extracapsular Fractures
F r actures of the Shaft of Femur
F r actures of the Proximal Tibia
F r actures of the Patella
Dislocation of the Patella
F r actures of the Calcaneum
F r actures of Shaft of Tibia and Fibula
F r actures of the Distal Tibia and Fibula
F r actures of the Talus
Dislocations of the Foot
C ONCLUSION
Imaging of Soft Tissue Lesions
Ashu Seith Bhalla, Sanjay Thulkar
Ultrasonography
Magnetic Resonance Imaging
Plain Radiography
MR Spectroscopy
Staging
Location
Computed Tomography
PET-CT
SOFT TISSUE LESIONS
ARTIFACTS
CALCIFICATION AND OSSIFICATION IN SOFT TISSUES
Metastatic Calcification
Parasitic Infestations
Vascular Calcification
Dystrophic Calcification
Metabolic Diseases
Collagen Vascular Diseases
Dermatomyositis
Idiopathic Calcification
Idiopathic Calcinosis Universalis
Calcinosis Circumscripta
Tumoral Calcinosis
OSSIFICATION
Myositis Ossificans
Myositis Ossificans Progressiva (Fibrodysplasia Ossificans Progressiva)
Soft Tissue Masses with Calcification/Ossification
AREAS OF DECREASED DENSITY
Air in the Soft Tissues
Air Leaks (Surgical Emphysema)
Air Formed within the Soft Tissues
Air Introduced from Outside
FAT IN THE SOFT TISSUES
SOFT TISSUE MASSES
Cystic Soft Tissue Lesions
Bursae
Cystic Masses around the Knee
Inflammatory Lesions
Soft Tissue Tumors
Adipocytic Tumors
Hemangioma
Vascular Lesions
Soft Tissue Angiosarcoma
Vascular Malformations
High-flow Vascular Malformations
Low-flow Vascular Malformations
Fibroblastic/Myofibroblastic Tumors
Fibrohistiocytic Tumors
Dermatofibrosarcoma Protuberans
Malignant Fibrous Histiocytoma
Smooth Muscle Tumors
Leiomyoma
Leiomyosarcoma
Skeletal Muscle Tumors
Rhabdomyosarcoma
Pericytic Tumors
Chondro-osseous Tumors
Mesenchymal Chondrosarcoma
Extraskeletal Osteosarcoma
Tumors of Uncertain Origin
Synovial Sarcoma
Miscellaneous
Neurogenic Tumors
EXTRASKELETAL EWIN G’S SARCOMA AND PRIMITIVE NEUROECTODERMAL TUMOR
SUMMARY
ACKNOWLEDGMENT
REFERENCES
A Systematic Approach to Imaging of Breast Lesions
Smriti Hari, Sanjay Thulkar, Arun Kumar Gupta
IMAGING TECHNIQUES
Mammography (Basic Physics, Equipment and Technique)
RADIATION DOSE
Mammography Projections
Supplementary Views
NORMAL MAMMOGRAPHIC ANATOMY
Interpretation and Reporting of Mammograms
Mass
C alcification
ARCHITECTURAL DISTORTION
FOCAL ASYMMETRY
BREAST EDEMA
Abnormal Axillary Lymph Nodes
AMERICAN COLLEGE OF RADIOLOGY BI-RADS ASSESSMENT CATEGORIES
C ategory 3
Mammographic Assessment is Incomplete
C ategory 0
Mammographic Assessment is Complete: F inal Categories
C ategory 1
C ategory 2
Management of Probably Benign Lesions
C ategory 4
C ategory 5
C ategory 6
Indications for Mammography
DIGITAL MAMMOGRAPHY
FULL FIELD DIGITAL IMAGING
A dvantages and Applications of the Digital Mammography
C omputer-aided Detection
Digital Breast Tomosynthesis
C ONTRAST-ENHANCED DIGITAL MAMMOGRAPHY
BREAST ULTRASOUND
Normal Anatomy
Indications for Breast Ultrasound
A CR BI-RADS Ultrasound Lexicon Descriptors
Challenges in Assigning Final Assessment C a t egories and the Influence of Cl
C ontrast-enhanced Ultrasound
Ultrasound Elastography
C oils and Patient Positioning
MR Field Strength
D Y NAMIC CONTRAST-ENHANCED BREAST MRI
Basic MR Technique for Breast Cancer Imaging
Imaging Protocols
Plane of Imaging
F at Suppression
Nongadolinium-enhanced Sequences
Kinetic Analysis
Normal MRI Appearances
Interpretation of Breast MRI
Mass
Nonmass like Enhancement
Internal Enhancement Pattern
FOCUS
ASSOCIATED FINDINGS
Distribution
Kinetic Curve Assessment
Sensitivity and Specificity of MRI
Indications for MRI
PROTON MR SPECTROSCOPY
DIFFUSION-WEIGHTED IMAGING
NUCLEAR MEDICINE IN BREAST IMAGING
Breast-specific Gamma Imaging
P ositron Emission Tomography
Limitations
P ositron Emission Mammography
Benign and Malignant Lesions of the Breast
Smriti Hari, Ashu Seith Bhalla, Sanjay Thulkar
PROLIFERATIVE BENIGN LESIONS OF THE BREAST
A denosis
F ibroadenoma
F ibrocystic Disease
C y sts
Intraductal Papilloma
Duct Ectasia
Ductal Epithelial Hyperplasia
MISCELLANEOUS BENIGN BREAST C ONDITIONS
Lipoma
F a t Necrosis
Galactocele
Radial Scar
Hamartoma
P seudoangiomatous Stromal Hyperplasia
Breast Tuberculosis
Desmoid Tumor
Diabetic Mastopathy
Superficial Thrombophlebitis (Mondor’s Disease)
Breast Infections
Breast Implants
M ALIGNANT LESIONS OF THE BREAST
Risk Factors for Breast Cancer
Diagnosis of the Breast Cancer
BREAST CANCER SCREENING
Mammography Screening
MRI Screening
Ultrasound Screening
Breast Cancer Screening in Developing Countries
IMAGING FEATURES OF BREAST CANCER
P r einvasive Breast Lesions
Ductal Carcinoma in Situ
L obular Carcinoma in Situ
Invasive Ductal Carcinoma
Invasive Lobular Carcinoma
Invasive Breast Cancer
Medullary Carcinoma
T ubular Carcinoma
P apillary Carcinoma
Mucinous Carcinoma
T riple Negative Breast Cancer
STAGING AND TREATMENT OF BREAST CANCER
P r eoperative Breast Imaging
Breast C onservation Therapy
Mastectomy
Management of Axilla
P erioperative Breast Imaging
A djuvant Treatment
ADVANCED BREAST CANCER
L ocally Advanced Breast Cancer
Inflammatory Breast Cancer
Neoadjuvant Chemotherapy
Metastatic Breast Cancer
POST-TREATMENT BREAST IMAGING AND FOLLOW-UP
Occult Primary Breast Cancer
MISCELLANEOUS MALIGNANT LESIONS OF THE BREAST
P aget’s Disease
P h yllodes Tumor
Sarcoma
Metastases to Breast
Male Breast Cancer
REFERENCES
Breast Interventions
Smriti Hari, Sanjay Thulkar
BREAST BIOPSY
BREAST BIOPSY TECHNIQUES
Surgical Biopsy
F ine Needle Aspiration Cytology
C ore Needle Biopsy
V acuum-assisted Biopsy
A dvantages of VAB
Marker Clip Placement with VAB
Disadvantages of VAB
C omplete Lesion Removal with VAB
L esion Selection for Breast Biopsy
Selection of Guiding Modality
P r ebiopsy Assessment
Ultrasound-guided Breast Biopsy
T echnique
Stereotactic Breast Biopsy
Equipment
T echnique
Specimen Radiography
P ostbiopsy Care
C OMPLICATIONS OF BREAST BIOPSY
Histopathological Correlation
MRI-guided Breast Biopsy
PREOPERATIVE HOOKWIRE LOCALIZATION
Equipment
T echnique
Specimen Radiography
C omplications
Special Techniques of Localization
MISCELLANEOUS BREAST INTERVENTIONS
Ductography
C y st Aspiration
Ultrasound-guided Axillary Lymph Node FNAC
ABLATIVE PROCEDURES FOR BREAST CANCER
REFERENCES
PET-CT in Management of Breast Cancer
PRIMARY MALIGNANCY
POSITRON EMISSION MAMMOGRAPHY
LOCOREGIONAL STAGING
FDG-PET-CT for Axillary Disease
FDG-PET-CT for Other Regional Lymph Nodes
SYSTEMIC STAGING
Distant Metastasis
Bone Metastasis
18 F-Fluoride PET-CT for Bone Metastasis
RESPONSE TO CHEMOTHERAPY
Neoadjuvant Chemotherapy
Adjuvant Chemotherapy in Metastatic Disease
RESTAGING
Prognostication
RECEPTOR IMAGING
FUTURE DIRECTIONS
CONCLUSION
REFERENCES

Citation preview

1

SECTION

Neuroradiology including Head and Neck Evaluation of Plain X-ray Skull: A Systematic Approach

„„

Normal Anatomy of Brain on CT and MRI

„„

Normal Cerebral Angiography

„„

Advances in Computed Tomography Technology

„„

Advances in Neuroimaging Techniques: Magnetic Resonance Imaging

„„

Magnetic Resonance Spectroscopy

„„

Functional Magnetic Resonance Imaging

„„

Imaging and Interventions in Cerebral Ischemia

„„

Imaging of Subarachnoid Hemorrhage

„„

Endovascular Management of Intracranial Aneurysms

„„

Endovascular Management of Arteriovenous Malformations

„„

Endovascular Management of Carotid-cavernous Fistulas

„„

Central Nervous System Infections

„„

White Matter Diseases and Metabolic Brain Disorders

„„

Current Trends in Imaging of Epilepsy

„„

Imaging of Supratentorial Brain Tumors

„„

Imaging of Infratentorial Tumors

„„

Sellar and Parasellar Lesions

„„

Intraventricular Lesions

„„

Imaging of the Temporal Bone

„„

Imaging of the Globe and Orbit

„„

Imaging of the Paranasal Sinuses

„„

Imaging of the Neck Spaces

„„

Thyroid Imaging

„„

Malignancies of Upper Aerodigestive Tract

„„

Imaging of Skull Base Lesions

„„

Maxillofacial Imaging: Imaging of Cysts, Tumors and Tumor-like Conditions of the Jaw

„„

Craniovertebral Junction Anomalies

„„

Endovascular Management of Craniofacial Vascular Lesions

„„

Imaging of Head Trauma

„„

Imaging of Facial Trauma

„„

Imaging of Acute Spinal Trauma

„„

Imaging of Spinal Neoplasms

„„

Spinal Vascular Malformations

„„

Imaging of Low Backache

„„

Localization in Clinical Neurology

„„

Basic Neuropathology

„„

Evaluation of Plain X-ray Skull: A Systematic Approach

1

CHAPTER

Niranjan Khandelwal, Sudha Suri

INTRODUCTION In the past, skull radiograph was considered an essential step in the investigative protocol of a patient suspected to have a neurological disease. With the introduction of computed tomography (CT) and magnetic resonance imaging (MRI), there has been a tremendous decline in the usage of plain films and the indications for skull radiographs have been redefined.1,2 The major indication for skull radiographs is in the evaluation of skeletal dysplasia, diagnostic survey in abuse, abnormal head shapes, infections and tumors affecting the skull bones, metabolic bone disease, leukemia and multiple myeloma. Abnormalities in skull radiographs may be seen in the form of change in the size, density and shape of the skull, as well as the other defects of the skull. In patients presenting with stroke, epilepsy, dementia or in postoperative cases, skull X-rays generally provide no useful information and MRI or CT is the investigation of choice.3 In patients of trauma, CT should be the first line of investigation except in patients who suffer from facial and orbital fractures where plain films are helpful in orientation and in medicolegal cases.4-6 Occasionally, skull X-rays may reveal linear fractures with more certainty than a CT scan.4 In patients suspected to have intracerebral tumors, posteroanterior (PA) and lateral view of skull may provide additional information like detection of hyperostosis in case of meningiomas, presence of lytic and sclerotic metastasis in neuroblastomas and tram-track calcification in Sturge-Weber syndrome which may compliment the diagnosis on CT. The present chapter will describe the normal roentgen anatomy as seen in the basic views of skull followed by systematic approach to the analysis of the abnormal skull X-rays.7-9

LATERAL VIEW OF SKULL A single lateral view of the skull (Fig. 1A) is the most common radiographic X-ray examination to be performed. A systematic approach to the examination consists of evaluation of the size and shape of the cranium, the thickness and density of the bones, the sutures, the vascular markings, the base of skull and the cranial cavity.

Size and shape of the skull is determined by examining the relative size of face and cranium. When the skull is longer and has a relatively shorter vertical diameter, it is referred to as dolichocephalic. On the other hand, when the vertical diameter is greater, it is termed as brachycephalic. The outer table, the inner table and the diploic space of the bones should be carefully examined for presence of any erosion, sclerosis or widening. The normal sutures in adults are surrounded by a narrow area of increased density, a fact that helps in distinguishing fracture lines from sutures. Sutures are difficult to visualize in newborns but in children older than 3 years, the width of the suture should not be more than 2 mm. Width of the sutures can be best assessed at the top of the coronal suture in the lateral view. To see the sagittal and the lambdoid sutures, PA and Towne’s views are performed. Vascular markings are seen along the coronal suture due to middle meningeal vessels. Arterial grooves become narrower as they go distally. They may be confused with fracture lines but the latter are more radiolucent whereas vascular markings have a halo of increased density around them. Posterior branch of middle meningeal artery as it ascends upward and posteriorly sometimes causes a shadow over the temporal bone that should not be mistaken for a fracture. Enlargement of the arterial grooves may occur in meningioma and arteriovenous malformations (Fig. 1B). Diploic venous channels are extremely variable in position but are generally seen in the frontal and parietal bones. Venous lakes may be seen as round or oval radiolucent areas and should not be confused with destructive lesions of the bone. Besides the arterial and diploic venous channels, the dural sinuses also produce grooves on the inner table of the skull. The structures along the base of the skull should be carefully examined, in particular the three lines which represent the floor of the anterior cranial fossa. The upper two lines are formed by the roofs of the orbits, which end posteriorly at the anterior clinoid processes. The lower line is formed anteriorly by the cribriform plate of the ethmoid bone and posteriorly by planum sphenoidale ending at the

4

Section 1 Neuroradiology including Head and Neck

A

B

Figs 1A and B:  (A) Normal lateral view of skull demonstrates the normal coronal sutures, lambdoid sutures and the vascular grooves due to

middle meningeal vessels posterior to coronal sutures. Note the two lines formed by the roof of the orbits ending posteriorly at the anterior clinoid processes. Arrow head marks the tuberculum sellae. Vertical arrows (anterior) show the cribriform plate and the (posterior) planum sphenoidale. Open arrow shows the greater wing of sphenoid bone forming anterior borders of middle cranial fossa. The dorsum sellae (horizontal arrow) with posterior clinoid processes above and the clivus posteriorly are well seen; (B) Lateral view of skull shows multiple dilated vascular markings in the parieto-occipital region in a case of parasagittal meningioma

tuberculum sellae, which marks the superior limit of the anterior wall of the sella turcica. A depression just anterior to the tuberculum sellae is called sulcus chiasmaticus. The roof of the sella posteriorly is formed by the dorsum sellae, which ends in the posterior clinoid processes. Sphenoid sinus is seen below the floor of the sella turcica. The pneumatization of this sinus shows considerable variation. Floor of the middle cranial fossa is formed by the greater wings of the sphenoid on each side, which appear as curvilinear shadows concave outward. These lines serve as a point of reference for locating the temporal lobe of the brain. The dorsum sellae continues as the clivus, which is followed by the occipital bone ending at the anterior margin of the foramen magnum. Clivus is seen to terminate just above the top of the odontoid process of the axis. The normal calcification may be seen in the falx cerebri, petroclinoid ligaments, tentorium, pineal body, habenular commissure and choroid plexus.

FRONTAL VIEW (FIG. 2) Posteroanterior projection with 15-20° craniocaudal angulation is preferred to straight PA projection as the petrous pyramids are projected below the orbits and the superior orbital fissure as well as greater and lesser wings of the sphenoid are clearly visualized. PA view is also examined for shape of the skull, with special attention to the symmetry of the two sides. The bony landmarks, which require to be carefully examined for any erosions, sclerosis or lack of continuity include crista galli in the midline, planum sphenoidale, floor of the sella, lesser and greater wings of the sphenoid and the three lines of the orbit formed by the

Fig. 2:  Posteroanterior (PA) view with 15° caudal angulation

demonstrates the dense vertical bony projection in the midline due to crista galli, lesser wings of the sphenoid on both sides joining to form the planum sphenoidale (arrow heads). Floor of sella is faintly visualized in the midline (vertical arrows). Oblique line of the orbit is formed by the greater wing of sphenoid in its lower two-thirds and by the frontal bone in its upper one-third

palpable superior border of orbit, highest point of roof of the orbit and the sphenoid ridge which represents the floor of the anterior cranial fossa. The floor of the posterior cranial fossa can also be seen inferiorly. Pacchionian depressions due to arachnoid granulations can be seen in both PA and lateral views as tiny radiolucent areas usually within 2.5–3 cm from the midline. Their margins are well defined superiorly,

Chapter 1 Evaluation of Plain X-ray Skull: A Systematic Approach

Fig. 3:  Towne’s view shows foramen magnum in the center with dorsum sellae projecting through it. The parallel lucencies (short arrows) on either side represent the internal auditory canals. Further, laterally pneumatized mastoids air cells can also be seen

whereas inferiorly the margins fade away—a feature helpful in distinguishing these from destructive lesions.

TOWNE’S VIEW Towne’s view (Fig. 3) is performed by angling the tube 35° caudally from the orbitomeatal line. It is generally performed when pathology is suspected in the petrous pyramids. This projection also shows the occipital bone, foramen magnum, dorsum sellae, the internal acoustic canals, mastoids and the condyles of mandible.

BASAL VIEW Basal view (Fig. 4) of the skull or the submentovertical view is an infrequent examination and is generally performed in specific situations such as looking for the skull base lesions, middle ear or inner ear lesions, nasopharyngeal masses or oropharyngeal lesions and sinus pathologies. The bony landmarks that should always be identified and carefully examined include three lines, constituted by the lateral wall of the maxillary antrum (S-shaped), the posterolateral wall of the orbit, and the anterior wall of the middle cranial fossa which is arched with concavity pointing posteriorly. The lesser wing of the sphenoid is seen just behind the anterior wall of middle cranial fossa. A transverse dense line in the center represents the anterior margin of sella. The medial and lateral pterygoid processes are projected over the sphenoid ridge. Sphenoid sinuses should be carefully seen as early bone destruction in patients of nasopharyngeal carcinoma or sphenoid sinus carcinoma is well demonstrated in this view. There are three important foramina seen in the basal view. Foramen ovale lying behind the pterygoid processes gives passage to the third division of the trigeminal nerve, an

Fig. 4:  Basal view of skull shows the nasopharynx, sphenoid sinus

and ethmoid sinuses in the midline. Posteriorly odontoid process is seen to project into the foramen magnum posterior to the arch of atlas. Laterally, the foramen ovale (open arrow), foramen spinosum, (long arrow), eustachian tube posterior to foramen spinosum and the carotid canal are well visualized. Anterolaterally, the three lines formed by the posterior wall of orbit (arrow head), maxillary sinus (S-shaped) (curved arrow) and the anterior wall of middle cranial fossa (thick arrow) (arched shadow with concavity posteriorly) should be looked for in each case. Medial and lateral pterygoid plates are well seen

accessory meningeal artery and superficial petrosal nerve. Foramen spinosum lying behind and lateral to foramen ovale transmits the middle meningeal artery. Foramen lacerum is seen anterolateral to the petrous apex and has a well-defined medial margin produced by the internal carotid artery. The eustachian canal is seen behind the foramen spinosum. The external auditory canal is seen behind the condyle of the mandible. Internal auditory canals and inner ear structures including semicircular canals should be carefully looked for. The clivus and foramen magnum are well seen through which the anterior arch of atlas and odontoid process of axis are seen to project. Jugular fossa and jugular foramen are seen laterally on each side of the junction of petrous portion of the temporal bone and occipital bone.

WATERS VIEW It is one of the standard views to study the maxillary and anterior ethmoidal sinuses. Waters view (Fig. 5) is generally performed with the patient in sitting position to facilitate demonstration of any fluid level in the sinuses. Patient is instructed to keep the mouth open with nose and chin touching the cassette in order to visualize the sphenoid sinuses. It is performed by placing the orbitomeatal line at an angle of 35° with the plane of film by either raising the chin or by tilting the tube. It also gives clear picture of the roof of the orbits, destruction of which may be seen in mucocele of frontal sinus and in carcinoma of lacrimal gland.

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Section 1 Neuroradiology including Head and Neck

Fig. 5:  Waters view of skull shows bilateral maxillary antrum (lower

horizontal arrows), frontal sinuses (vertical arrows), ethmoid sinuses (upper horizontal arrows) and lower margin of sphenoid sinuses (arrowheads)

CALDWELL’S VIEW Caldwell’s view is the best projection for examining the frontal and ethmoid sinuses. Patient is positioned directly facing the cassette in either sitting or prone position with midsagittal plane and orbitomeatal line perpendicular to the film with nose and forehead touching the cassette. Central ray is directed 15° caudally to the nasion. The various abnormalities that can be detected on the plain skull X-rays can be categorized in the following groups: zz Abnormal density zz Abnormal contour of the skull zz Abnormal intracranial volume zz Intracranial calcification zz Increased thickness of the skull zz Single lucent defect zz Multiple lucent defects zz Sclerotic areas.

Abnormal Density Generalized reduced density: Thinning of the skull bones with decreased done density is seen in osteogenesis imperfecta, hypophosphatasia and achondrogenesis. In hypophosphatasia, there is decreased ossification of the skull and vertebrae or as isolated areas of unusually thin calvarial bone. Osteogenesis imperfecta shows increased osseous fragility leading to multiple fractures in addition to decreased density. Focal reduced density: Focal areas of defective ossification can occur in the lacunar skull where in well-defined lucent areas

Fig. 6:  Craniosynostosis. Anteroposterior (AP) view of skull shows

silver beaten appearance due to exaggerated convolutional markings all over the skull vault. None of the sutures is seen

are seen corresponding to nonossified fibrous bone and the lacunae are bounded by normally ossified bone. Generalized increased density: It is seen in sclerosing bone dysplasias such as osteopetrosis, and pyknodysostosis. In osteopetrosis increased density is seen in the basal bones initially and later the calvaria becomes dense and thick. The density of facial bones is relatively less dense. Localized increased density: It may be seen in fibrous dysplasia, osteoma, craniometaphyseal dysplasia, etc.

Abnormal Contour of the Skull Normal contour of the skull is maintained by sutures, the intracranial contents and normal bone formation. Abnormality in any of these may result in abnormal contour of the skull. Premature fusion of the sutures, craniosynostosis, is the most common cause of abnormal contour in children. If the suture closes early, the calvarium expands to accommodate the growing brain in the axis of the fused suture. Sagittal synostosis (scaphocephaly) is the most common form of isolated synostosis with M:F = 4:1.10 It leads to an elongated narrow boat-shaped skull. The closure of both coronal sutures and lambdoid sutures (turricephaly) produces a short wide skull with towering head, with bulging temporal areas and shallow orbits (Fig. 6). The recessed supraorbital rims and hypoplasia of the basal frontal bone, gives cloverleaf-like skull appearance. Plagiocephaly means skewed or oblique head. It results when there is unilateral such as coronal or lambdoid

Chapter 1 Evaluation of Plain X-ray Skull: A Systematic Approach

synostosis. Unicoronal synostosis is the second most common form of craniosynostosis, after sagittal synostosis. Two-thirds cases occur in female patients and 10% are familial in nature. In this condition, there is elongation of the orbit, elevation of the lateral portion of ipsilateral orbital rim (the harlequin eye appearance) and tilting of the nasal septum and crista galli toward the affected side. Margins of the affected sutures develop sclerosis. Any decrease or increase in the cerebral volume may result in abnormal contour. Premature fusion of multiple sutures on one side is associated with signs of raised intracranial tension in the form of increased convolutional markings. The hemicalvarium on the ipsilateral side is smaller than the opposite side. The tables of bones of the skull are thickened and there may be elevation of the petrous pyramid on the same side. Expansion of the bony calvarium due to the presence of slow growing intracerebral or subarachnoid space occupying lesions such as arachnoid cysts may also result in abnormal contour (Figs 7A and B). The bony vault bulges outward with thinning of the inner table. Chronic subdural hematomas may also cause expansion of the adjacent calvarium and may even erode the inner table. Calcifications when present facilitate the diagnosis. Abnormal bone formation such as that occurs in achondroplasia characterized by defective endochondral ossification, results in shortening of the bones of the skull base as these bones develop from cartilage. Since the bones of the vault develop from membranous bones, these remain unaffected. The result is a small foramen magnum and enlarged cranium with frontal bossing and large jaws.

Abnormal Intracranial Volume Size of the calvarium is dependent on the size of the intracranial contents. The most accurate way to determine abnormal cranial volume is to measure the skull directly and

A

compare the measurements to standard for age and body size. A simple method of assessing the size of the skull is to compare the skull vault to the size of the face. At birth, the volume of skull is approximately four times that of face. This ratio decreases to 3:1 by age 2 and 1.5:1 by adulthood.8 Enlarged head size may result from hydrocephalus, macrocephaly, hydranencephaly and in pituitary dwarfism. The most common cause of hydrocephalus in children is congenital obstruction of the ventricular system and is associated with raised intracranial tension. Sutures become wide due to expansion of the intracranial contents. Small skull but otherwise normal contour is characteristically seen in microcephaly associated with mental retardation. Cranial sutures fuse early but this is a result of microcephaly and not the cause. The sinuses are large and the digital or convolutional markings are absent or decreased. It is important to differentiate premature closure of all the sutures from microcephaly with fused sutures. When multiple sutures fuse prematurely, the fusion does not occur simultaneously and the result is an irregular skull due to expansion of the skull in unusual directions to accommodate the brain. Clinically, signs of raised intracranial tension are present. Convolutional markings are exaggerated. Increased thickness of the skull may result due to early cessation of brain growth or due to cerebral atrophy. Increased width of diploic space due to increased hematopoiesis is seen in hemolytic anemia. Progressive hydrocephalus leads to large bony calvarium and a decreased diploic space. However, if a ventricular shunt is performed and abnormal expansion ceases resulting in arrested hydrocephalus, the cranial sutures close and the inner table of bones of the skull become thicker and the diploic space becomes larger. A history of hydrocephalus and the presence of a ventricular shunt facilitate the diagnosis. Among the hemolytic anemia producing hyperplasia of the bone marrow, thalassemia causes most marked changes.

B

Figs 7A and B:  Arachnoid cyst. (A) Basal view of skull shows thinning and ballooning of anterior and lateral walls of the left middle cranial fossa (arrow); (B) Axial CT scan of the same patient shows a large left temporoparietal arachnoid cyst

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Section 1 Neuroradiology including Head and Neck

Fig. 8:  Thalassemia. Lateral skull radiograph shows widened diploic

space with coarsened trabeculae giving “hair-on-end” appearance typical of hemolytic anemia

Fig. 9:  Craniolacunia. Lateral skull radiograph in an infant

shows multiple lucencies with intervening dense areas typical of craniolacunia. Note the associated occipital encephalocele and absence of sutural widening

The diploic space is widened with striking radial striations, the “hair-on-end” appearance (Fig. 8). The paranasal sinuses may also be completely obliterated due to widening of the diploic space of facial bones. Such changes may also be seen in other forms of anemia, such as sickle cell disease, hereditary spherocytosis, but the changes are much less marked.

Single Radiolucent Defect When there is a single lucent lesion, the important considerations that help in deciding its nature are its location, associated soft tissue swelling, table of the bone involved and margins of the lytic lesion, whether sharp, ill-defined or sclerotic. Radiolucent defects in the skull bone may be due to variety of causes, which may be congenital or acquired. Congenital causes may be parietal foramina, anomalous apertures, meningoencephalocele or dermal sinus. The acquired causes include trauma, infections, tumors and histiocytosis. Bilaterally symmetrical rounded lytic defects located in the posterior parietal bone are characteristic of parietal foramina and are of no clinical significance. Lytic defects due to meningoencephalocele are located in the midline in the frontal or occipital regions and have sharp margins. Associated soft tissue mass clinches the diagnosis. In the first 3  months of life, meningoencephalocele is generally associated with lacunar skull (craniolacunia) (Fig. 9). A dermal sinus also occurs in the midline of the skull and may present as a radiolucent defect with a sharp slightly sclerotic border. It is generally associated with a lipoma or a nevus in the overlying soft tissues. These lesions may have an intracranial components which may require a CT scan for demonstration. Fractures generally occur at the site of injury and may be associated with soft tissue swelling. Linear nondepressed

Fig. 10:  Depressed fracture. Frontal radiograph shows the parallel

dense lines due to depressed bone fragments and associated lucency due to absence of bone

fractures may be seen as radiolucent lines and should not be confused with sutures or vascular grooves. Fracture lines are nontapering, nonbranching and have sharp borders whereas vascular grooves have ill-defined borders and an undulating course. Sutures are seen in known anatomical positions and have saw tooth edges. Depressed fractures generally occur after severe trauma and are considered more serious than linear fractures. Radiologically, the depressed fragment presents as area of increased radiodensity surrounded by a radiolucent zone (Fig. 10). In children, when the dura beneath the suture is torn, the arachnoid membrane herniates through the dura into the bony defect. The pulsations of the brain lead to progressive enlargement of the arachnoid collection resulting in expansion of the fracture line termed as growing skull

Chapter 1 Evaluation of Plain X-ray Skull: A Systematic Approach

fracture. The bulging membranes result in the formation of leptomeningeal cyst (Fig. 11). Infections of the skull are uncommon and generally follow trauma or arise secondary to infection elsewhere in the body. The radiographic appearance consists of mottled irregular lucencies, which have ill-defined borders and are associated with soft tissue swelling of the scalp. Epidermoid tumors develop from a congenital inclusion of epithelial cells within the calvarium. Radiologically, these lesions present as well-defined lytic lesions, which have sclerotic border and are not necessarily located in the midline such as dermoid (Fig. 12). Intracranial epidermoids may also produce a radiolucent shadow, which may mimick a lytic lesion (Figs 13A and B).

Malignant lesions such as primary osteosarcoma or metastasis can also produce lytic defects. Osteosarcoma causes gross destruction of the bone with ill-defined margins  and soft tissue swelling (Figs 14A and B). Neuro­ fibromatosis is a rare cause of a lytic defect seen along the suture. This defect is not due to the presence of neurofibroma but is a manifestation of mesenchymal defect. Intracranial mass lesions can also rarely present as lytic areas of the skull. Eosinophilic granulomas, Hand-Schüller-Christian disease and Letterer-Siwe disease all form part of a complex comprising histiocytosis. The severity ranges from mild in eosinophilic granuloma to very malignant course in LettererSiwe disease. A single lytic lesion having sharp nonsclerotic

Fig. 11:  Growing fracture. Posteroanterior (PA) skull radiographs in a

Fig. 12:  Dermoid scalp. Skull radiograph shows a well-circumscribed

child demonstrate fracture of the right frontal bone with thickening, sclerosis and wide separation of the fracture ends. Note the soft tissue swelling overlying this area

A

lucency overlying the coronal suture

B

Figs 13A and B:  Single lucent lesion. (A) Skull radiograph shows a well-circumscribed lucency overlying the coronal suture mimicking a lytic lesion; (B) Coronal computed tomography (CT) scan in the same patient shows a large hypodense lesion due to epidermoid in the temporoparietal region. No lytic lesion of skull vault is seen

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Section 1 Neuroradiology including Head and Neck

A

B

Figs 14A and B:  Osteosarcoma. (A) Large lytic area with irregular margin is seen affecting the left parietal bone; (B) Computed tomography (CT) scan of the same patient shows the soft tissue swelling, destruction of the bone and extradural extension of the tumor

Fig. 15:  Eosinophilic granuloma. Lateral skull radiograph shows

Fig. 16:  Histiocytosis (Hand-Schüller-Christian disease). Lateral

border and bevelled edges is characteristic of eosinophilic granulomas (Fig. 15). Occasionally, a small bone is seen in the center representing button sequestrum. Lytic lesions in the other two variants are larger, multiple and punched out (Fig. 16). Multiple radiolucent defects in the skull in children may be due to craniolacunia, presence of wormian bones, increased convolutional makings due to raised intracranial tension, histiocytosis and metastasis from neuroblastoma (Figs 17A and B), leukemia or Ewing’s sarcoma. In adults, multiple myeloma (Fig. 18), metastasis and hyperparathyroidism (Fig. 19) are the usual causes. Craniolacunia is due to a defect in ossification of the bones, which develop from membranous tissue. There are multiple radiolucent defects seen all over the cranial

vault interspersed with strips of normal bone, which appear dense. Craniolacunia (lacunar skull) by itself is not of much significance, but it is generally associated with myelomeningocele or encephalocele (Fig. 9). Appearance must not be confused with increased convolutional markings that result from raised intracranial tension and are seen as multiple radiolucent areas not exceeding the diameter of a finger. Convolutional marking may also be seen in normal children in the frontal and occipital region. Presence of increased convolutional markings in the parietal region should generally be considered abnormal. Wormian bones are seen along the sutures and results due to defective mineralization. Multiple wormian bones are seen in cleidocranial dysostosis, osteogenesis imperfecta, hypothyroidism and pyknodysostosis.

a single lytic lesion having sharp nonsclerotic border and bevelled edges

radiograph of skull shows multiple well-defined lytic lesions of the vault with bevelled edges characteristic of histiocytosis

Chapter 1 Evaluation of Plain X-ray Skull: A Systematic Approach

A

B

Figs 17A and B:  Metastatic lesions of the skull in a child with abdominal neuroblastoma. (A) Sutural metastasis: Frontal skull radiograph shows

widening of the sagittal suture with an overlying soft tissue swelling; (B) Diffuse metastasis of skull vault: Lateral skull radiograph shows multiple lytic areas involving both tables of skull and diploic space. Note widening of coronal suture also

Fig. 18:  Multiple myeloma. Lateral skull radiographs shows multiple well-defined punched out lytic lesions affecting the skull vault as well as mandible typical of myeloma

Lytic lesions seen in multiple myeloma are punched out, usually associated with osteoporosis and involve the mandible more frequently compared to metastasis. However, many times differentiation from metastasis may not be possible on radiological appearance alone. The sclerosis or sclerotic rim is very rare seen in 3% of cases in multiple myeloma and usually occur after therapy.11 Hyperparathyroidism generally results in mottled demineralization (Fig. 19) but may sometimes cause multiple well-defined lytic areas (Fig. 20).

Fig. 19:  Hyperparathyroidism. Lateral skull radiograph shows multiple lytic lesions with mottled appearance

Sclerotic Areas of the Skull Areas of increased density in the skull may be seen in both normal as well as pathological conditions. Osteopetrosis is a rare condition, which is characterized by diffuse thickening of the skull and face (Fig. 21). Fibrous dysplasia may involve the vault or base of skull. There may be a single lesion or it may be part of syndrome (McCune-Albright syndrome) seen in females when it affects multiple bones and is associated

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Section 1 Neuroradiology including Head and Neck

Fig. 20:  Hyperparathyroidism. Lateral skull radiograph shows multiple well-circumscribed rounded lytic lesions involving skull vault with bone within bone appearance—an unusual feature of hyperparathyroidism

A

B

Fig. 21:  Osteopetrosis. Frontal radiograph shows diffuse increased density affecting all bones of the skull vault as well as base

C

Figs 22A to C:  Fibrous dysplasia. (A) Frontal and (B) lateral views of skull reveal sclerotic lesion involving the frontal bone. The frontal sinus is opaque; (C) Axial computed tomography (CT) scan in the same patient shows expanded sclerotic frontal bone

Fig. 23:  Paget disease. Lateral view of skull reveals focal areas of

opacities in previous areas of osteoporosis giving “cotton wool” appearance

with precocious puberty. The lesions are sclerotic with loss of normal trabecular pattern. Mixed types of lesions with sclerotic and lytic areas are also known to occur (Figs 22A to C). Paget disease in the mixed phase shows marked thickening of the diploic space, particularly the inner calvarial table, causing marked enlargement. The areas of sclerosis may be circular and occur in previous areas of osteoporosis. This pattern often creates focal areas of opacity giving “cotton wool” appearance at radiography (Fig. 23). Multiple hyperostotic lesions affecting the calvarium measuring 5–10 mm in size may be seen in tuberous sclerosis in association with calcified lesion in periventricular region. Thickening of the frontal and parietal bones may occur in rickets due to presence of poorly mineralized bone, which on healing becomes dense. An osteoma affecting the skull bones is a benign tumor, which appears as a dense lesion projecting extracranially from the outer table of skull. Osteoma is also the most common benign tumor affecting the sinuses (Fig. 24). Focal areas of

Chapter 1 Evaluation of Plain X-ray Skull: A Systematic Approach

hyperostosis are characteristic of meningioma (Figs 25A and B). When the hyperostosis affects the frontal bone, in a case of convexity meningioma, it must be differentiated from hyperostosis frontalis interna (Fig. 26), the later is generally seen in elderly females and affects the inner table with sparing of diploic space and does not cross the midline.

Intracranial Calcification

Fig. 24:  Osteoma. Waters view of skull shows osteoma of the frontal sinus

A

Presence of calcification can provide important clue to the diagnosis in several conditions. Although causes are numerous (Box 1), some of these conditions have specific appearance, which can be diagnostic. The most common physiological calcification occurs in the pineal gland. It is seen in the midline approximately 3 cm above and behind the posterior clinoids in the lateral view (Fig. 27). Size of the pineal calcification is most important as

B

Figs 25A and B:  Sphenoid wing meningioma. (A) Posteroanterior (PA) view of skull shows hyperostosis of the left lesser and greater wings of the sphenoid bone typical of meningioma; (B) Contrast enhanced computed tomography (CT) scan in the same patient shows proptosis and hyperostosis of sphenoid wings with enhancing extradural mass due to meningioma on the left side

Box 1:  Abnormal intracranial calcification

Fig. 26:  Hyperostosis frontalis interna. Lateral skull radiograph shows

irregular thickening of the frontal bone in an elderly female. The inner table is involved more than the outer table with sparing of diploic spaces

Familial conditions: •  Tuberous sclerosis •  Sturge-Weber syndrome •  Idiopathic familial cerebrovascular calcinosis (Fahr’s disease) Metabolic causes: •  Hypoparathyroidism •  Pseudohypoparathyroidism Inflammatory diseases: •  Cytomegalic inclusion disease •  Toxoplasmosis •  Rubella •  Abscess Vascular causes: •  Arteriovenous malformation •  Intracerebral hematoma •  Subdural hematoma Neoplasms: •  Craniopharyngioma •  Astrocytomas •  Oligodendrogliomas •  Pinealoma

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Section 1 Neuroradiology including Head and Neck

Fig. 27:  Lateral view skull shows pineal gland calcification (arrow)

A

B

Figs 28A and B:  Sturge-Weber syndrome. (A) Posteroanterior (PA) and (B) lateral view of the skull shows gyriform calcification on the left side

any increase in size more than 10 mm is abnormal and raises the possibility of pinealoma. Habenular commissure calcification has a characteristic appearance and is seen as a C-shaped structure open posteriorly. It lies above and anterior to pineal gland. Choroid plexus calcification is generally bilateral and may be unequal on the two sides. Other normal sites of calcification are the falx and anterior petroclinoid ligaments above the sella. Tuberous sclerosis is a syndrome comprised of epilepsy, mental retardation and adenoma sebaceum. Multiple hamartomas occur in the brain as well as at other sites such as kidneys. Tumors consist of glial tissue and ganglion cells. In the brain they are usually multiple and are seen in the subcortical, subependymal and basal ganglia regions. Calcification is seen in 50% of the lesions. Sturge-Weber syndrome is another important cause of intracranial calcification. Patients present with epilepsy and mental retardation and often have cutaneous hemangioma in the distribution of trigeminal nerve on the same side as calcification. Calcification has a typical tram-track appearance and is seen in the cerebral cortex (Figs 28A and B). Basal ganglia calcification is an important feature of hypoparathyroidism and pseudohypoparathyroidism. Widespread irregular and punctate areas of calcification, which are diffusely scattered, are characteristic of Fahr’s disease. In this condition, patients present with severe growth and mental retardation. The disease is hereditary and is characterized by microscopic deposits of iron and calcium in the basal ganglia, cerebellum and subcortical region. Infections due to toxoplasma and cytomegalovirus are important causes of intracranial calcification in the newborn. Calcifications are multiple and diffusely scattered in the brain parenchyma or paraventricular region. Bacterial infections may progress to cerebral abscess, which may get calcified. Arteriovenous malformations calcify in 2–25% of all affected patients. Typically, calcification is in the form of an incomplete ring but may be nodular or amorphous. A large arc like calcification seen in the region of pineal gland in a newborn presenting with congestive heart failure and hydrocephalus is characteristic of vein of Galen aneurysm. Intracerebral or chronic subdural hematomas may reveal curvilinear calcification. A variety of tumors may show calcification. In children, suprasellar craniopharyngioma is the most common tumor, which reveals calcification whereas in adults oligodendrogliomas and meningiomas are the common tumors to calcify.

REFERENCES 1. Tress BM. The need for skull radiography in patients presenting for CT. Radiology. 1983;146(1):87-9.

Chapter 1 Evaluation of Plain X-ray Skull: A Systematic Approach 2. Moseley I. Long-term effects of the introduction of noninvasive investigations in neuroradiology. Neuroradiology. 1988;30(3):193-200. 3. Rastogi SC, Barraclough BM. Skull radiography in patients with psychiatric illness. Br Med J. 1983;287(6401):1259. 4. Taveras JM. Anatomy and examination of skull. In: Interactive Review of Radiology. Lippincotts Williams and Wilkins, 1999. 5. Sanders R, MacEwen CJ, McCulloch AS. The value of skull radiography in ophthalmology. Acta Radiol. 1994;35(5):429-33. 6. Baker HL Jr. The impact of computed tomography on neuroradiologic practice. Radiology. 1975;116(3):637-40. 7. Taveras JM. The skull. In: Taveras JM, Wood EH (Eds). Diagnostic Neuroradiology, 2nd edition. The Williams and Wilkins Company. 1986.pp.1-65.

8. Gerald B. Systematic radiographic evaluation of the abnormal skull. In: Rabinowitz JG (Ed). Pediatric Radiology. Philadelphia: JB Lippincott Company. 1978.pp.285-313. 9. Butler P, Jeffiree MA. The skull and brain. In: Butler P, Mitchell AWM, Ellis H (Eds). Applied Radiological Anatomy, 1st edition. Cambridge University Press. 2001.pp.17-60. 10. Kirmi O, J Lo S, Johnson D, et al. Craniosynostosis: a radiological and surgical perspective. Seminars in ULTRASOUND CT and MRI. 2009;30(6):492-512. 11. Baur-Melnyk A, Reiser M. Oncohaematologic disorders affecting the skeleton in the elderly. Radiol Clin North Am. 2008;46(4):785-98.

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Normal Anatomy of Brain on CT and MRI

2 CHAPTER

Paramjeet Singh

INTRODUCTION An understanding of basic anatomy of the brain is vital to the planning and interpretation of neuroradiologic studies. Modern imaging techniques provide cross sections of the brain similar to the dissected brain. Computerized tomography (CT) provides cross-sectional anatomy of the brain in axial plane. Magnetic resonance imaging (MRI) due to its multiplanar capabilities also allows direct coronal and sagittal sections. Better tissue differentiation on MRI allows not only morphological but also histological information to some extent. Recent advances in functional imaging and diffusion tensor imaging makes understanding of brain anatomy even more important. Current MRI scanners and multidetector computerized tomography (MDCT) have further expanded the scope of three-dimensional conceptualization of complex brain structures through true volumetric data sets. This chapter reviews the essentials of surface and cross-sectional anatomy of the brain as seen on CT and MRI.

TECHNIQUES AND NORMAL APPEARANCE General Considerations Noncontiguous axial CT sections are usually obtained at 15–20° angulation to the orbitomeatal line, while axial MRI sections are generally obtained parallel to it (along bicommissural plane). MRI, owing to its multiplanar capability allows direct coronal and sagittal sections. However, MDCT scanners and newer MR techniques allow volumetric data acquisitions. T1- and T2-weighted (T1W and T2W) images are routinely obtained on MRI. The T1WI are excellent for showing anatomy while T2WI are highly sensitive in detecting brain pathology. The white matter is hypodense to gray matter on CT. The cerebral white matter appears bright while the gray matter is relatively dark on T1WI. The relationship reverses as white matter becomes progressively darker on increasing the T2-weighting; the crossover occurring in the proton density

images. The basal ganglia, red nucleus and putamen appear hypointense on T2WI due to their mineral contents. The cerebrospinal fluid (CSF) shows low density on CT (0-15HU) depending on its protein content. The CSF is hypointense on T1WI and extremely bright on T2WI due to its long T1 and T2 relaxation times. The CSF is in constant motion which may occasionally result in flow-related artifacts and loss of signal (flow void), classically seen in the region of cerebral aqueduct. The glomera of the choroid plexus within the lateral ventricles are seen as soft tissue density on CT and show homogeneous enhancement on CECT. On T2WI the choroid plexus appears heterogeneous due to the presence of calcification and cysts. Visualization of blood vessels needs administration of iodinated contrast in CT. On MRI, major blood vessels are visualized without contrast administration and appear as flow voids on spin echo imaging or show flow-related enhancement on gradient echo imaging. Flow-related artifacts are often seen in phase encoding direction especially in long TR sequences and should not be mistaken for pathology. Familiarity with normal variations like dilated perivascular spaces is important. Modern MR imaging also provides a good understanding of white matter tracts through diffusion tensor imaging and functional areas of the brain through BOLD imaging. Except for the intraorbital segment of the optic nerves, the remaining cranial nerves are usually not visualized on CT. On MR, using thin sections and fluid sensitive techniques like SPACE and CISS, the cisternal segments of most of the cranial nerves can be identified. The inner meningeal layers are not normally visualized on noncontrast MRI and may show no or fine linear enhancement following contrast administration. Major dural folds like falx and tentorium appear hypointense on MRI and enhance after contrast administration along with the venous sinuses within them. Contrast-enhanced MR angiograms are increasingly used for demonstrating vascular anatomy. The diploic space appears bright on T1WI due to its fat content and is outlined by the low signal intensity compact

Chapter 2 Normal Anatomy of Brain on CT and MRI

bones of the inner and outer tables of skull. CT better demonstrates the bony outlines. Similarly, it is superior to MR for visualization of intracranial calcification.

Normal Anatomy of Brain Figure 1 shows the major subdivisions of brain. Brain consists of three major components. 1. Forebrain (prosencephalon) comprised of two cerebral hemispheres (telencephalon) and fiber tracts connecting the cerebral hemisphere with the midbrain (diencephalon). 2. The midbrain (mesencephalon). 3. The hindbrain (rhombencephalon) comprised of cerebellum and pons (metencephalon), and medulla oblongata (myelen-cephalon).

CEREBRAL HEMISPHERES Cerebrum consists of two hemispheres which are partially connected with each other through corpus callosum. Each cerebral hemisphere has three borders superomedial, inferomedial and inferolateral. The superomedial border separates the superolateral and medial surfaces, the inferolateral border separates the superolateral and inferior surfaces, and the inferomedial border separates medial surface and inferior surface.

Lateral Surface of the Cerebral Hemisphere (Fig. 2A) The two cerebral hemispheres are incompletely divided by the interhemispheric fissure. The sylvian fissure (lateral fissure)

separates the temporal lobe from the frontal and parietal lobes. Its anterior horizontal and anterior ascending rami extend into the inferior frontal gyrus. The posterior ramus passes backward and upward terminating into ascending and descending rami. The central sulcus separates the frontal from the parietal lobe (Fig. 3E). It originates slightly behind the mid-point between the frontal and occipital poles on the superomedial border and continues obliquely inferolaterally on the lateral surface. The frontal lobe is bounded posteriorly by the precentral gyrus, which lies between the central and precentral sulci (Fig. 4E). The precentral gyrus contains the primary motor area with inverse topographic representation of contralateral body parts. The superior frontal sulcus and inferior frontal sulcus divide the frontal lobe anterior to precentral gyrus into superior, middle and inferior gyri (Figs 3E, F, 5A, B and 6H, J, K). In front of the precentral gyrus is the premotor area, consisting of posterior part of the superior, middle and inferior frontal gyri. The Broca’s area which is concerned with the motor mechanisms of speech also lies at the posterior part of the inferior frontal gyrus in the dominant lobe usually seen at the level of frontal horns on axial sections. The convexity of the parietal lobe consists of the postcentral gyrus and the superior and inferior parietal lobules separated by the horizontally running intraparietal sulcus (Figs 3E and F). The postcentral gyrus is located between the central and postcentral sulcus and contains the primary (somesthetic, tactile, thermal and kinesthetic) areas, with body representation corresponding to that in precentral gyrus. The inferior parietal lobule is further subdivided into the supramarginal and angular gyri, which are located around the terminal ascending ramus of the sylvian fissure and the superior temporal sulcus, respectively (Fig. 3E). The temporal

Fig. 1: Midline sagittal image of brain showing embryonal divisions

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lobe is divided into superior, middle and inferior temporal gyri by two horizontally running sulci—the superior and middle temporal sulcus (Fig. 3F). In the dominant cerebral hemisphere at the posterior portion of the superior temporal gyrus lies the Wernicke’s area, linked with comprehension

of language. A lesion of this area causes sensory aphasia. Another important area is the area for hearing — acoustic area, which is also located in the temporal lobe. It lies in that part of the superior temporal gyrus which forms the inferior wall of posterior ramus of lateral sulcus and is defined as the

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Figs 2A to C: Diagrammatic representation showing anatomy of cerebral hemispheres on the (A) Lateral; (B) Medial; and (C) Inferior surface

Fig. 2D: Line diagram and corresponding coronal inversion recovery image of right hippocampus Abbreviations: AC, ambient cistern; BS, brainstem; C, cornu ammonis; CHF, choroid fissure; CS, collateral sulcus; D, dentate gyrus; FG, fusiform gyrus; F, fimbria; TH, temporal horn; TG, inferior temporal gyrus; PHG, parahippocampal gyrus

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Figs 3A to F: (A) Mid-sagittal MR section shows the entire length of the corpus callosum bordered above by the pericallosal sulcus. Cingulate gyrus and sulcus lie above it. The brainstem divisions, cerebellar vermis and the sellar/suprasellar anatomy are exquisitely shown on this section. The vein of Galen and straight sinus are seen behind the splenium leading to the torcula. A large rounded mass of gray matter within the 3rd ventricle represents interthalamic adhesion. The fornix is seen beneath the corpus callosum. The 3rd and 4th ventricles with the interconnecting aqueduct are well shown in this section. The tectal plate lies posterior to the aqueduct. The suprasellar cistern interpeduncular fossa, quadrigeminal plate cistern and cisterna magna are important cerebrospinal fluid (CSF) spaces identified in this section; (B to D) Parasagittal MR sections. The parieto-occipital fissure marks the boundary between parietal (precuneus) and occipital (cuneus) lobes. The calcarine fissure separates lingual gyrus from cuneus. The central, pre- and postcentral sulci and the related gyri can be followed. The parahippocampal gyrus can be seen following the temporal horn closely. The frontal lobe consists of superior and middle frontal gyri on these sections; (E and F) Sagittal MR sections at and lateral to sylvian fissure. The sylvian fissure can be traced anteriorly where its anterior ascending and horizontal rami form a V or Y configuration. These divide the inferior frontal gyrus into pars orbitalis, pars triangularis and pars opercularis giving it a characteristic M shape. Posteriorly the fissure ends in ascending and descending rami. The horse-shoe shaped supramarginal gyrus sits atop the ascending ramus. The middle frontal gyrus extends posteriorly to meet the precentral gyrus and the inferior frontal sulcus meets the obliquely coursing precentral sulcus. The central sulcus can be traced inferiorly to the subcentral gyrus. The superior and inferior temporal gyri are identified in the extreme lateral sections

Chapter 2 Normal Anatomy of Brain on CT and MRI

transverse temporal gyrus. This is best seen in the coronal sections. The lateral surface of the occipital lobe consists of the lateral occipital gyri (Fig. 5I) (visual associative functions). The preoccipital notch indents the inferolateral border of the hemisphere about 4 cm from the occipital pole. An imaginary line drawn from the superior end of the parieto-occipital fissure to the preoccipital notch marks the boundary between the occipital lobe and the parietal and temporal lobes. Insula (central lobe) is the part of cerebral cortex which lies in the depth of the lateral sulcus. It is formed by portions of the frontal, parietal and temporal lobes (Figs 5C and 6H).

Medial Surface of the Cerebral Hemisphere (Fig. 2B) The corpus callosum is a large mass of nerve fibers which connect the cerebral hemispheres and forms most of the roof of the lateral ventricles. It is arbitrarily divided from front to back into rostrum, genu, body, and splenium (Fig. 3A). The small anterior commissure ventral to the rostrum of the corpus callosum connects portions of the middle and inferior temporal gyri. The two lateral ventricles are separated by septum pellucidum (Fig. 4D) which extends from the inferior aspect of the body and genu of the corpus callosum to the superior aspect of the columns of the fornix (Figs 5C and D). The callosal sulcus separates the corpus callosum from the cingulate gyrus. The cingulate sulcus separates the cingulate gyrus from the superior frontal gyrus anteriorly and the paracentral lobule posteriorly (Figs 3A and B). The central sulcus is deficient on medial surface and continuations of the precentral and postcentral gyri form the paracentral lobule on medial surface which is limited posteriorly by the marginal branch of the cingulate sulcus and anteriorly by the paracentral sulcus, a direct continuation of the precentral sulcus from the lateral surface. On the medial surface the parietal lobe (precuneus) is separated from the occipital lobe by parieto-occipital fissure (Figs 3B, C and 6J, K). The calcarine fissure divides the medial surface of occipital lobe into the cuneus above and the lingual gyrus below (Figs 6H and I). The calcarine (primary visual) cortex, consisting of portions of the cuneate and lingual gyri lies along the banks of the calcarine fissure deep within the occipital lobe. At the inferolateral aspect of the occipital and temporal lobes lies the fusiform (lateral occipitotemporal) gyrus. The cingulate gyrus continues posteriorly behind the corpus callosum through the isthmus into the parahippocampal gyrus which is separated from the fusiform gyrus by the collateral sulcus. The uncus is the most anterior part of the parahippocampal gyrus which points medially (Fig. 4B). Understanding of anatomy of medial temporal lobe is important to interpret the MR findings in hippocampal sclerosis in epilepsy. Hippocampus is located on the medial aspect of temporal lobe, superior to the parahippocampal

gyrus bounded superolaterally by the floor of the temporal horn of lateral ventricle. It is composed of two interlocking U-shaped lamina of gray matter called cornu ammonis and dentate gyrus. White matter tracts extend form cornu ammonis to alveus, which converge medially to form fimbria. Cornu ammonis is connected with gray matter of parahippocampal gyrus through subiculum. Choroid fissure lies superomedial to hippocampus and medially lies the ambient cistern (Fig. 2D). Anteroposteriorly hippocampus is divided into head, body and tail.

Inferior Surface of the Cerebral Hemisphere (Fig. 2C) The lingual and fusiform gyri course through this areas separated by collateral sulcus. The inferior temporal sulcus separates the inferior temporal gyrus from the fusiform gyrus (Figs 5I and J). The inferior aspects of the occipital lobe and the temporal lobe sit over the tentorium of the cerebellum. On the inferior (orbital) surface of frontal lobe the olfactory bulb and the olfactory tract over lie the olfactory sulcus which runs in the anteroposterior direction. Area medial to this is called gyrus rectus. Area lateral to olfactory sulcus is divided into four parts by a H-shaped sulcus into anterior, posterior, medial and lateral orbital gyri (Figs 5A and B).

BRAINSTEM AND CRANIAL NERVES The brainstem comprises of midbrain, pons and medulla (Fig. 3A). The diencephalon connects the cerebral hemispheres to the mid brain and is made of thalamus, hypothalamus, subthalamus and epithalamus. The hypothalamus lies within the floor and lateral walls of the third ventricle. It extends from the lamina terminalis anteriorly to the caudal aspect of the mamillary bodies and includes the tuber cinereum which gives rise to the pituitary stalk (Fig. 6F). Each thalamus is a large mass of gray matter in the lateral wall of the 3rd ventricle. It is bounded laterally by the posterior limb of the internal capsule and ventrally by the hypothalamic sulcus (Fig. 6G). The interthalamic adhesion projecting through the 3rd ventricle forms a medial connection with the opposite thalamus. The dorsolateral margin of the thalamus forms part of the floor of the lateral ventricle. The posterolaterally bulging portion of the thalamus is called the pulvinar (Fig. 5F). It overhangs medial and lateral geniculate bodies. Ventral to the pulvinar lie the medial and lateral geniculate bodies on each side of midbrain, together called the metathalamus. They relay auditory and visual information to their respective receptor areas of cortex. The subthalamus is bounded by the hypothalamus anteriorly, the internal capsule laterally, and the thalamus above. The subthalamic nucleus integrates and relays connections from the globus pallidus and the thalamus.

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Figs 4A to E: Axial CT sections: The middle cerebellar peduncles are large fiber bundler that extend dorsally connecting the pons to the cerebellum (A); The uncus is the most interior part of the parahippocampal gyrus which points medially (B); The frontal horns are bounded medially by the septum pellucidum (C); Lateral ventricles are separated by septum pellucidum(D); Midbrain (E)

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The most dorsal division of the diencephalon, the epithalamus, includes the habenular nuclei, posterior commissure and pineal body. The structure is a part of limbic system. The midbrain consists of a smaller dorsal portion the tectum and larger ventral portion, the cerebral peduncles

Abbreviations: C, cerebellum; CN, caudate nucleus; CS, central sulcus; CSO, centrum semiovale; FH, frontal horn; FX, falx cerebri; GR, gyrus rectus; IHF, interhemispheric fissure; LN, lentiform nucleus; LV, lateral ventricle; MB, midbrain; MCP, middle cerebellar peduncle; OL, occipital lobe; P, pons; PCS, postcentral sulcus; PCG, precentral gyrus; PoCG, postcentral gyrus; PG, pineal gland; SF, sylvian fissure; SFG, superior frontal gyrus; SFS, superior frontal sulcus; SP, septum pellucidum; SSC, suprasellar cistern; TH, thalamus; TL, temporal lobe; TmH, temporal horn; TV, third ventricle; U, uncus; V, vermis

(Fig. 6F). Aqueduct connecting the 3rd and 4th ventricles runs in the center of the junction of the tectum and cerebral peduncles (Fig. 3A). Each cerebral peduncle has a ventral part–the crus and a dorsal part—the tegmentum, separated by substantia nigra. The red nucleus, another pigmented nucleus is located posterior and medial to the substantia nigra

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Fig. 5J: Figs 5A to J: (A and B) Coronal MR sections anterior to the frontal horn. The entire slice contains frontal lobe. The olfactory nerve nestles between the gyrus rectus and medial orbital gyrus on the cribriform plate. (A) The more anterior section shows a continuous interhemispheric fissure which is; (B) Interrupted by corpus callosum on a more posterior section. The optic strut separates the optic nerve from superior orbital fissure; (C and D) Coronal MR sections through the frontal horn. The frontal horns are outlined by corpus callosum and caudate nucleus. The internal capsule, putamen, external capsule, claustrum and insula can be seen from medial to lateral. The two columns of fornix outline the foramen of Monro with septum pellucidum above it separating the two frontal horns. Optic chiasma can be identified above the pituitary gland and its infundibulum. In the parasellar area, the cavernous sinuses containing third, fourth, fifth and sixth nerves are outlined by low intensity dura; (E) Coronal MR sections at the third ventricle level. Mid third of the lateral convexity is parietal lobe and lower third is temporal lobe. Corpus callosum lies at the bottom of the interhemispheric fissure. The lateral ventricles (with crus fornix on its superior medial part) and third ventricle are seen more inferiorly. The interpeduncular fossa is seen as a CSF space below third ventricle. The tail of caudate nucleus lies on the lateral aspect of lateral ventricle. The medial temporal lobe consists of hippocampus with overlying choroid fissure; (F) Coronal MR sections through the body of lateral ventricle. This section cut through the splenium of corpus callosum with the cingulate gyrus lying just above it. Below it lie the quadrigeminal plate (tectum) and its cistern. The sections pass through the mid brain, pons and medulla. The lateral convexity consists entirely of parietal and temporal lobes; (G and H) Coronal MR sections through the trigone and occipital horns. Superior two-thirds of the lateral convexity of brain at this level consists of superior and inferior parietal lobules. The lower third belongs to the temporal lobe. The inferior surface of temporal lobe consists of parahippocampal, fusiform and inferior temporal gyri; (G) The section through trigones cuts the cerebellar peduncles while; (H) A more posterior section shows the cerebellar hemispheres, vermis and the tonsils; (I and J) Coronal MR sections posterior to the occipital horn. The interhemispheric fissure completely divides the two cerebral hemispheres. The lingual, fusiform and inferior temporal gyri are clearly identified. The precuneus and cuneus are separated by parieto-occipital fissure and between the cuneus and lingual gyrus lies the calcarine fissure

on each side. Pars compacta separates the substantia nigra and red nucleus (Fig. 6L). The tectum consists of four rounded prominences – the two superior colliculi and two inferior colliculi or corpora quadrigemina. Each superior colliculus is connected to the ipsilateral lateral geniculate body through the superior brachium, where the optic tract ends. Similarly, the inferior colliculi are connected to the medial geniculate bodies through the inferior brachium thereby connecting it to the auditory cortex (Fig. 6F). The oculomotor nerves (CN III) exit from the caudal aspect of the interpeduncular fossa (Fig. 7A). The paired trochlear nerves (CN IV) emerge from the dorsal surface of the brainstem caudal to the inferior colliculi, and wrap around the lateral aspects of the midbrain. The ventral and dorsal aspects of the cerebral peduncles are separated by

semilunar substantia nigra with red nuclei on its dorsomedial aspect (Fig. 6L). The pons has a bulging ventral surface with a shallow midline basal sulcus. The middle cerebellar peduncles are large fiber bundles that extend dorsally connecting the pons to the cerebellum (Fig. 4A). Emerging from the lateral aspect of the pons are the trigeminal nerves (CN V) (Fig. 7B), while the paired paramedian abducens nerves (CN VI) exit ventrally from the pontomedullary junction. The facial nerves (CN VII) and the vestibulocochlear nerves (V III) emerge from the lateral aspect of the pontomedullary junction and pass through the cerebellopontine angle cistern (Fig. 7C). The medulla oblongata connects the midbrain and the spinal cord. It measures 3 cm in length and 2 cm in width. On the ventral aspect of the medulla the paramedian pyramids

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Figs 6A to M: (A) T1-weighted axial MR section at the level of medulla shows the midline ventral sulcus, pyramids and olives separated by ventromedial sulcus. Dorsolateral sulcus is seen posterior to olives. Cerebellar tonsils are seen posterolateral to the medulla. Vallecula is seen posteriorly. Fourth ventricle with foramen of Luschka is seen posterior to medulla; (B) T1-weighted axial MR section at slightly higher level than Figure 6A shows the IX, X and XI cranial nerves seen as a common bundle exiting from the dorsolateral sulcus; (C) T1-weighted axial MR section through the pons. Pons is seen in front of the fourth ventricles. The CP angle cisterns lie lateral to the pons. Seventh and eight cranial nerves course through the cistern anterior to flocculus towards internal auditory canals. The inferior vermis and its various divisions are well seen; (D) T1-weighted axial MR section through middle part of fourth ventricle. Middle cerebellar peduncles connecting the pons with cerebellar hemispheres are well seen. Fifth nerves are seen emerging from the lateral surface of pons on both sides. Also seen are globes with optic nerve and lower part of temporal lobes; (E) T1-weighted axial MR section through the midbrain shows the superior cerebellar peduncles, and the parts of superior vermis. Anteriorly the olfactory nerve and gyrus rectus on each side of inter-hemispheric fissure are seen clearly. The structures of the middle cranial fossa-cavernous sinus, both temporal lobes with superior, middle and inferior temporal gyri, are also seen; (F) T1-weighted axial MR section at the level of midbrain. Inferiorly frontal and temporal lobes are seen separated by sylvian fissure. V shaped tentorium outlining the superior vermis is seen with quadrigeminal plate and cistern located anterior to it. Parahippocampal gyrus and fusiform gyrus course forward from occipital pole to midbrain. Anterior to midbrain, mammillary bodies, optic radiations and hypothalamus are seen; (G) T1-weighted axial MR section at the level of lower third ventricle shows the basal ganglia, internal capsule, thalami and retrothalamic cistern. Peripherally superior temporal and middle temporal gyri are seen posterior to sylvian fissure. Frontal horns of lateral ventricles are seen anteriorly and occipital horns posteriorly. Pineal gland is seen posterior to the third ventricle. Optic radiations are seen ending in the occipital cortex. Also seen is the Y-shaped parietooccipital fissure and calcarine fissure, the later forming the lateral boundary of lingual gyrus; (H) T1-weighted axial MR section at the level of mid-3rd ventricle showing various parts of frontal lobe, anteriorly and occipital lobes posteriorly. In the mid line genu of the corpus callosum is seen anteriorly connecting the frontal lobes. Septum pellucidum is seen separating the frontal horns of lateral ventricles. Posteriorly in the mid line splenium of the corpus callosum is seen forming posterior wall of 3rd ventricle and medial wall of atria of lateral ventricle. Peripherally the central sulcus is seen separating the frontal (precentral) and parietal (postcentral) lobes. The sylvian fissure separates the parietal lobe (post central gyrus) from the temporal lobe (superior temporal gyrus). In the depth of the sylvian fissure, portions of frontal, parietal and temporal lobe form the insula; (I) T1-weighted axial MR section at the superior part of 3rd ventricle shows the superior frontal gyrus and middle frontal gyrus separated by superior frontal sulcus. Body of fornix is seen anterior to 3rd ventricles which separate the lateral ventricles. The other structures seen in Figure 6H are also seen; (J and K) T1-weighted axial MR section at supraventricular level show the deep white matter of cerebral hemispheres, the centrum semiovale. The central sulcus characteristically dips posteriorly and leads to paracentral lobule. Posterior to it the precuneus and cuneus are separately seen. Only superior and middle frontal gyri are seen at this level; (L) T2-weighted axial MR section at midbrain level. Semilunar band of pigmented gray matter anteriorly—the substantia nigra, appears hypointense. Another area of hypointensity is seen dorsomedial to substantia nigra called the red nucleus. The substantia nigra and red nuclei are separated by pars compacta; (M) T2weighted axial MR section at the level of basal ganglia. Slit like third ventricle in midline is flanked by thalamus on each side. The interhemispheric fissure anteriorly separates the two frontal lobes. Medial to the sylvian fissure, lie the insular cortex and external capsule. The caudate and lentiform nuclei with intervening internal capsule lie medially. Globus pallidus appears hypointense in comparison to putamen on T2-weighted images. Claustrum—a strip of gray matter lies between the external and extreme capsule

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Fig D: Figs 7A to D: Axial MR cisternography sections using SPACE technique through (A) Midbrain; (B and C) Pons; and (D) Medulla show III, V, VI, VII, VIII, IX and X cranial nerves in relation to brainstem as labeled

form longitudinal protrusions on each side of the ventral median fissure. The paired ventrolateral sulci separate the medullary pyramids and the inferior olives (Fig. 6A). The hypoglossal nerves (CN XII) emerge from the ventrolateral sulci. The rootlets of the glossopharyngeal (CN IX), vagus (CN X) and spinal accessory (CN XI) nerves exit from the dorsolateral sulcus which is located further laterally (Fig. 7D). The paired cuneate and gracilis tubercles form longitudinal ridges on the dorsal aspect of the medulla oblongata just caudal to the fourth ventricles separated by posterior median sulcus.

CEREBELLUM The cerebellum lies posterior to the pons and medulla. The superior, middle, and inferior cerebellar peduncles connect the cerebellum to midbrain, pons and medulla respectively. The narrowest leaf-like subdivisions of the cerebellar cortex are termed folia. The cerebellum consists of the midline cerebellar vermis connecting the paired lateral hemispheres. The hemisphere is divided into anterior lobe, middle lobe and flocculonodular lobe by deep fissures named primary fissure and posterolateral fissure (Figs 3D and 5H). A deep horizontal fissure divides it into superior and inferior halves. Caudal to the inferior vermis and between the cerebellar tonsils is the vallecula (Fig. 6A) which communicates with the fourth ventricle through the foramen of magendie. The superior divisions of the vermis are lingula, centrum, culmen, declive and folium (Fig. 6E). The inferior divisions are tuber, pyramid, uvula and nodule (Fig. 6C). Immediately caudal to the inferior medullary velum is the nodulus of the vermis. The flocculus projects into the cerebellopontine angle cistern ventral to the inferior cerebellar peduncle (Fig. 6B). The deep cerebral

nuclei are laterally placed dentate and medially placed paired emboliform, globose and fastigial nuclei.

WHITE MATTER OF THE CEREBRUM The fiber connections of the cerebral cortex are divisible into three major groups (Figs 8A to E). Projection fibers are corticospinal, corticobulbar, corticopontine and corticothalamic tracts. Association fibers consist of subcortical U fibers, long projection fibers of cingulum, superior/inferior longitudinal fasciculi, uncinate fasciculus and superior/ inferior occipitofrontal fasciculi. The commissural fibers interconnecting the two hemispheres are corpus callosum, anterior and posterior commissure, hippocampal/habenular commissures and the hypothalamic commissure. The common central mass of white matter is known as the centrum semiovale (Fig. 4D). Projection fibers passing through the corona radiata converge to form the internal capsule consisting of anterior and posterior limbs and the genu (Figs 6M and 4C). The columns of fornix which lie on either side of the foramen of Monro continue posteriorly as body of fornix. It is a C-shaped bundle of white matter forming the roof of III ventricle. Posteriorly it divides into the two crura which continue into the fimbria and alveus of hippocampal formation (Fig. 2B). This is part of limbic system concerned with emotional and sexual behavior and recent memory.

VENTRICLES AND CISTERNS The ventricular system consists of lateral, third, fourth ventricles and the cerebral aqueduct. The lateral ventricles communicate with the third ventricle by the foramen of

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Figs 8G to J: Figs 8A to J: Fractional anisotropy maps superimposed on T1 weighted images of brain showing the white matter tracts Abbreviations: ALIC, anterior limb of internal capsule; CBT, corticobulbar tract; Cng, cingulum; CR, corona radiate; CST, corticospinal tract; CTT, corticothalamic tract; FMj, forceps major; FMn, forceps minor; Fx, fornix; ILF, inferior longitudinal fasciculus; IOFF, inferior occipitofrontal fasciculus; MCP, middle cerebellar peduncles; ML, medial lemniscus; OR, optic radiation; PLIC, posterior limb of internal capsule; SCP, superior cerebellar peduncle; SLF, superior longitudinal (arcuate) fasciculus; SOFF, superior occipitofrontal fasciculus; St, stria terminalis; TPF, transverse pontine fibers; Tpt, tapetum; UF, uncinate fasciculus

Monro while the third ventricle communicates with the fourth ventricle via the aqueduct of Sylvius. The lateral ventricles consist of frontal horns, body, trigone, occipital and temporal horns. Foramen of Monro defines the junction between frontal horns and body of lateral ventricles and the splenium of corpus callosum arbitrarily separates the body from the trigone. The frontal horns are bounded medially by the septum pellucidum (Fig. 4C), inferiorly and laterally by the head of the caudate nucleus, and superiorly and anteriorly by the corpus callosum. The body is bounded superiorly by the corpus callosum, inferiorly by caudate nucleus and the thalamus, medially by the fornix and laterally by the body of the caudate nucleus (Fig. 5E). The

trigone contains large tuft of choroid plexus called glomus (Fig. 5H). The third ventricle is bounded laterally by the thalami, inferiorly by the hypothalamus (Figs 5D and E), anteriorly by the anterior commissure and lamina terminalis, posteriorly by the epithalamus and posterior commissure, and superiorly by the cistern of the velum interpositum and body of the fornix. The inferior aspect of third ventricle has downward invaginations called optic, infundibular recesses anteriorly and, suprapineal and pineal recesses posteriorly. The fourth ventricle is rhomboid in shape and lies between the pons and cerebellum. It communicates above with the third ventricle via the aqueduct and with subarachnoid

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space through posterior midline foramen of magendie and posterolateral foramina of Luschka (Fig. 6A). The major cisterns at the base of the brain are suprasellar cistern, perime-sencephalic cistern, prepontine and perimedullary cisterns and the cerebellopontine angle cistern. The suprasellar cistern is a five pointed CSF space, communicating anteriorly with interhemispheric fissure, laterally with sylvian fissure and posteriorly with perimesencephalic cistern. It contains optic chiasma, internal carotid artery and circle of Willis and pituitary stalk (Fig. 4B). The perimesencephalic cistern consists of interpeduncular, crural, ambient and quadrigeminal plate cisterns lying along the anterior, anterolateral, posterolateral and posterior aspects of the midbrain respectively. The upper end of basilar artery and the III cranial nerve lie within the interpeduncular cistern. Intimately related to the quadrigeminal plate cistern (Fig. 5G) are the pineal gland and the vein of galen. The fourth cranial nerves course in the ambient cisterns around the midbrain. The cerebellopontine angle cistern (Figs 5C, 7B and C) is bounded medially by the middle cerebellar peduncle and the anteroinferior surface of the cerebellum and laterally by the temporal bone. It contains VII/VIII cranial nerves and anterior inferior cerebellar arteries. Prepontine cistern (Fig. 7B and C) lies anterior to the pons and contains basilar artery. The perimedullary cisterns surround the medulla and contain lower cranial nerves (CN IX, X and XI) and vertebral arteries (Fig. 7D). Superior cerebellar cistern lies superior to the cerebellum and contains vein of Galen. The cisterna magna is a CSF space at the posteroinferior aspect of cerebellum and may be sometimes very large in normal people.

GRAY MATTER NUCLEI AND ADJACENT STRUCTURES Basal ganglia represent central gray matter consisting of corpus striatum (caudate nucleus and lentiform nucleus)

and claustrum a strip of gray matter lateral to the lentiform nucleus and amygdala at the roof of temporal horn. The caudate nucleus has a larger head anteriorly and a narrow posterior part the tail, which follows the superolateral border of thalamus and the temporal horn into the amygdala. The lentiform nucleus is wedge shaped and comprised of globus pallidus medially and putamen laterally. External capsule, claustrum, extreme capsule and insular cortex lie lateral to the putamen in that order (Fig. 5C). The internal capsule is bounded anteromedially by caudate head, laterally by lentiform nucleus and posteromedially by thalamus (Figs 6G and M).

SUGGESTED READING 1. Atlas S (Ed). Magnetic Resonance Imaging of the Brain and Spine, 4th edition. Philadelphia: Lippincott Williams & Wilkins. 2009. 2. Berry M, Standring SM, Bannister LH. Nervous system. In: Susan Standring (Ed): Gray’s Anatomy, 40th edition—The Anatomical Basis of Clinical Practice, New York: Elsevier, Churchill Livingstone. 2008. 3. Butler P, Jeffiree MA. The skull and brain. In: Butler P, Mitchell AWM, Ellis H (Eds). Applied Radiological Anatomy, 1st edition. Cambridge University Press. 2001. pp. 17-60. 4. Lee SH, Rao KCVG, Zimmerman RA (Eds). Normal Anatomy in Cranial MRI and CT, 4th edition. New York: McGraw Hill Inc. 1999. pp.105-37. 5. Patel VH, Friedman L. MRI of the brain: Normal Anatomy and Normal Variants, 1st edition, Philadelphia: WB Saunders Company. 1997. 6. Scott WR, Hanaway J. Correlative anatomy of the brain. In: Radiology-diagnosis-imaging-intervention Vol 3, Philadelphia: JB Lippincott Co. 1986. 7. Snell RS (Ed). Snell’s Textbook of Clinical Anatomy, 7th edition. Boston: Little Brown and Company. 2004. pp. 790-830.

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Normal Cerebral Angiography

CHAPTER

Shailesh B Gaikwad, Ajay Kumar

PART 1: CEREBRAL ANGIOGRAPHY TECHNIQUE

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INTRODUCTION

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This is an important albeit invasive procedure wherein most cases of suspected vascular pathologies baring few exceptions are diagnosed. It is a direct examination of the blood vessels that provide not only the information of the vascular anatomy but also the flow dynamics.

Contraindications zz zz zz

Historical Background Within months of Karl Roentgen’s discovery of X-rays, an angiographic study of an amputated arm was conducted successfully in Vienna using the Teichmann mixture of lime, mercuric sulfide, and petroleum.

Definition It is the demonstration of the vascular anatomy by direct injection of the iodinated contrast medium into the vessel.

Six Vessel Angiography It includes the study of the following vessels: 1. Right internal carotid artery 2. Left internal carotid artery 3. Right external carotid artery 4. Left external carotid artery 5. Right vertebral artery 6. Left vertebral artery.

Indications zz

Primary vascular diseases —— Vaso-occlusive diseases —— Aneurysms

Ateriovenous malformations Ateriovenous fistula Vascular assessment of tumors Source of hemorrhage Congenital vascular condition Interventional procedure ——

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Bleeding disorders Thrombogenic condition Skin infection Abnormal renal function Cardiac condition (CCF) Allergy to iodinated contrast agents Pregnancy Nonpalpable pulse.

Patient Preparation Careful history taking is very important part before most of the procedure. It is advisable to take informed consent from the patient in case of elective procedure and from relatives in case of emergency. Patient should be well hydrated along with four hour fasting before the procedure. Part preparation includes shaving of both the groins. It is recommended to obtain the xylocaine sensitivity test. Patient must have passed urine before the procedure.

Requirement zz zz zz

DSA machine (Figs 1A and B) Catheterization equipment (Fig. 2) Disposables.

Catheterization Equipment Cleaning agents, blade no. 11, puncture needle, vascular sheath, mini-guidewire, various catheters, Terumo guidewire, syringes.

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Section 1 Neuroradiology including Head and Neck

A

B

Figs 1A and B:  DSA biplane machine with monitors

Fig. 2:  Instruments required: (left to right) Sheath, dilator, puncture needle, syringes, terumo wire, short guidewire, single puncture needle, catheter

Site of the Puncture

Fig. 3:  Marking the site of puncture on fluoroscopy

Local Anesthesia

If the femoral pulsations are good in the groins, then access is usually through the right femoral artery. Palpate the site of the puncture and feel the inguinal ligament along the ASIS and pubic symphysis. Inguinal ligament is 1–2 cm below the site of the palpation. Puncture over middle of medial 3rd of femoral head (Figs 3 and 4).

For local anesthesia, give subcutaneous injection of 2% xylocaine without adrenaline. Palpate the artery with index, mid and ring finger of the left hand. Infiltrate 2–3 mL each on the either side of the artery. Care must be taken to not to inject LA into the vessel, before giving injection always check by withdrawing to rule out arterial puncture. Give injection slowly for the patient comfort (Fig. 5).

Preparation

Artery Puncture

Sterilize the site first with savalon, then with betadine and with spirit in the last. Wipe with sterilized gauze piece.

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Give 3 mm wide and 3 mm deep, superficial skin incision at the puncture site by using 11 no. blade. It is ideal to check the site under fluoroscopy before arterial puncture.

Chapter 3 Normal Cerebral Angiography

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B

Figs 4A and B:  Localization and palpation of femoral artery

Fig. 5:  Infiltrating local anesthetic at the site of puncture

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Seldinger technique: Palpate femoral artery by the index, middle and ring finger, of the left hand. Take Medicut (puncture needle with needle inside and plastic canula outside) in the right hand and advance towards the artery at about 45 degree angle. Feel the pulse of the artery through the needle in the right hand and as one feel it over femoral artery, enter artery with a jab (Fig. 6). Remove the needle and slowly withdraw the canula till the jet of the blood is obtained. Rule out venous puncture (blood will not come out in jets). After confirming arterial access introduce mini-guidewire, and remove the canula. Then introduce arterial sheath over the short guidewire. Again check the position of the sheath by withdrawing blood using syringe. Arterial blood will come into syringe in pulsatile manner and with thrust.

Fig. 6:  Arterial puncture

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zz

Inject 2500 unit of heparin (0.5 mL) and flush sheath with saline to flush in remaining part of heparin in the sheath lumen. Take the desired catheter and start angiography (Fig. 7).

Puncture Technique It is of two types: 1. Single wall puncture 2. Double wall puncture. In single wall puncture technique, only the anterior wall of artery get punctured and in double wall both anterior as well as posterior wall get punctured. Single wall is safe in experienced hand and double wall is safe in inexperienced hand as chances of dissection of artery are high in single

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Section 1 Neuroradiology including Head and Neck

extended legs for next 8 hours, (patient may be allowed for leg roll). Check groin for hematoma formation. Monitor BP, pulse and neurological status of the patient. If patient is unable to pass urine then catheterize the patient until the patient is able to ambulate.

Types of Angiographic Catheters zz zz zz zz zz zz zz

Pigtail catheter Head hunter catheter Cobra catheter Renal double curve catheter Multipurpose catheter Sims/Sidewinder Roberts uterine catheter.

Fig. 7:  Placement of arterial sheath

wall technique. In double wall technique, posterior wall hematoma is high, but can be affordable as compared to the dissection of the artery. Improper technique can lead to trauma of the vessel regardless of the type of needle used.

Seldinger Needle This needle is comprised of three parts. Outer one is 16 G cannula. Middle one is a needle with a lumen inside. Stillete is inner most. The length of the needle is 7 cm. This is no longer used now. Recent needles consists of two parts; outer one is a cannula and inner one is thin needle.

Important Points to Remember Check for free backflow of the blood in the catheter. Inject test amount 2–3 mL of contrast before taking run to check the exact position of the catheter and to check vascular spasm. Instruct the patient before every injection and inform the effect of the contrast like flushing and warm sensation or alteration in the taste, etc.

Postprocedural Management Before removing the sheath, aspirate few mL of the blood to aspirate out any thrombus that could have formed during the procedure. If there is free backflow and if no clots are visible in the aspirate, the sheath can be safely removed. Compress the artery which is about 0.5 cm above the puncture site (for about 20 min). Compress the actual puncture site with middle finger, compress above it with index finger and below it with ring finger. Puncture site should be clearly visible during compression so that hematoma formation can be avoided. Do not obliterate the pulse, distal pulse should be faintly palpable. Apply steady moderate pressure for 15 minutes, reduce the pressure in next 5 min. Never remove compression abruptly. After compression feel all distal pulses. Bed rest with

PART 2: CEREBRAL ANGIOGRAPHIC ANATOMY Arterial Anatomy The brain is supplied by the two internal cerebral arteries, and two vertebral arteries which join to form the basilar artery. The basilar artery divides into two posterior cerebral arteries which along with posterior communicating arteries form the posterior part of circle of Willis. The anterior part of circle of Willis is constituted by both anterior cerebral arteries, anterior communicating artery and internal cerebral arteries. The internal carotid artery (ICA) on each side enters the cranium by passing through the carotid canal in the petrous temporal bone (petrous segment). Petrous ICA give rise to tympanic branches as Vidian artery (artery of pterygoid canal) and caroticotympanic artery which supplies middle and internal ear and persistent stapedial artery. At times, the ICA courses posterolaterally than anteromedial (normal course) and present as pulsatile retrotympanic mass called as aberrant ICA. Knowledge of this variant is necessary to differentiate it from glomus tympanicum so that hazardous biopsy can be avoided. The ICA exits from the carotid canal at the apex of the petrous bone and runs within the cavernous sinus to pierce the dura to enter the subarachnoid space adjacent to the anterior clinoid process. The cavernous ICA can be subdivided into ascending cavernous (C5). It starts from carotid canal to first posterior genu (C4). This segment can give rise to meningohypophyseal artery near junction of C5 and C4. Meningohypophyseal artery branches supply the posterior pituitary, cavernous sinus, clival dura and sometimes III to VI cranial nerves. The horizontal part (C3) extends between first posterior (C4) and second anterior genu (C2). After second genu (C2), rest of the cavernous ICA is called as C1 segment (Fig. 8). The inferolateral trunk arises from C4 segment and supplies the dura of the cavernous sinus and cranial nerves

Chapter 3 Normal Cerebral Angiography

Fig. 8:  ICA cavernous segments. C5 segment extends from carotid canal opening to first posterior genu (C4), horizontal segment (C3) extends between first posterior genu (C4) and second anterior genu (C2). Rest of cavernous ICA is called (C1)

III, IV, V and VI. The superior hypophyseal trunk arises from supraclinoid ICA and supplies anterior pituitary. The ophthalmic artery arise from paraclinoid ICA (Fig. 9). The anterior choroidal artery arises from ICA just above PCom origin which arises posteromedially from supraclinoid ICA. The anterior choroidal artery supplies the choroid plexus of the lateral ventricles, medial temporal lobe and some striate branches to deep ganglionic structures (Fig. 10). The PCom runs posteriorly to join the posterior cerebral arteries (branches of basilar artery) to complete the circle of Willis. PCom supplies the deep ganglionic structures including the thalamus. The anterior cerebral arteries proceed medially within the interhemispheric fissure separated by the falx. Both anterior cerebral arteries are connected by the anterior communicating artery in the midline completing the anterior part of circle of Willis (located in the suprasellar cistern). Anterior cerebral artery (ACA) is thus divided into three segments. Horizontal (A1) segment which extends from the ACA origin to its junction with the anterior communicating artery (ACoA). The medial lenticulostriate arteries arise from A1 segment. A2 segment which extends from the junction of ACoA to its bifurcation into pericallosal and callosomarginal arteries. The orbitofrontal and frontopolar arteries arise from A2 segment. The recurrent artery of Heubner which is a lenticulostriate branch may arise from proximal A2 segment and less commonly from A1 segment. A3 segment refers to the cortical branches that supply the anterior two-thirds of medial hemispheric surface and a small superior area over the convexities. Middle cerebral artery (MCA) is also divided into three major segments. Horizontal (M1) segment: Extends from the origin of MCA to its bifurcation or trifurcation at sylvian

Fig. 9:  Anterior circulation lateral view. Selective ICA angiogram

lateral view showing different important branches (as annotated) Abbreviations: ICA, internal carotid artery; OA, ophthalmic artery; CRA, central retinal artery; PCom, posterior communicating artery; MCA, middle cerebral artery; ACA, anterior cerebral artery; OF, orbitofrontal artery; FP, frontopolar artery; CM, callosomarginal artery; PC, pericallosal artery; RICA, right internal carotid artery

Fig. 10:  Lateral ICA angiogram showing fetal PCA (1), anterior

choroidal artery (2), and the plexal point (3), the point where artery enters the choroidal fissure Abbreviations: RICA, right internal carotid artery; LAT, lateral

fissure. The lateral lenticulostriate arteries arise from M1 segment and supply the lentiform nucleus, parts of internal capsule and caudate nucleus. Insular (M2) segment: At its genu, the MCA divides into its insular (M2) branches, which loop over the insula and pass laterally to exit from sylvian fissure. Opercular (M3) segment: Which gives off branches that emerge from the sylvian fissure and ramify over the hemispheric surface. The insular and the opercular branches supply the temporal, parietal and variable parts of frontal and occipital lobes (Figs 11 and 12).

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Section 1 Neuroradiology including Head and Neck

Fig. 11:  Right internal carotid artery angiogram PA view. 1 = Cervical

segment of ICA, 2 = Petrous segment of ICA, 3 = Cavernous segment of ICA, 4 = Anterior cerebral artery (A1), 5 = Middle cerebral artery (M1), 6 = Anterior cerebral artery (A2), 7 = Anterior cerebral artery (A3), 8 = Middle cerebral artery (M2), 9 = Middle cerebral artery (M3), 10 = Lenticulostriate arteries

The two vertebral arteries (VA) arise from the respective subclavian arteries, course cephalad and enter the cranium through the foramen magnum. These unite in the posterior fossa, usually anterior to the medulla to form the basilar artery. Most of the time vertebral arteries are asymmetrical. In about 60% left vertebral artery is dominant, in 25% right can be dominant and in about 25% both vertebral artery can be symmetrical in size. Left vertebral artery can arise directly from aorta in small percentage. The intracranial VA gives two major branches: Anterior spinal artery supplying the spinal cord and posterior inferior cerebellar artery (PICA) on each side which supplies choroid plexus of fourth ventricle, medulla, cerebellar tonsils, inferior vermis and parts of cerebellar hemispheres. Basilar artery (BA) runs anterior to pons in the prepontine cistern and terminates in the interpeduncular cistern by dividing into posterior cerebral arteries (PCA). In prepontine cistern, it lies within the space marginated by lateral margin of clivus. Any further deviation from these boundaries are considered as dolichoectasia. In addition, the basilar artery gives off anterior inferior cerebellar artery (AICA) and superior cerebellar artery (SCA) on each side, just before bifurcation into posterior cerebral arteries. The anterior inferior cerebellar artery is the first major branch of basilar artery and most of the time (about 70%) arises as single vessel. AICA courses posterolaterally within the CP angle cistern, whereas SCA curves around the pons and the midbrain just below the tentorial hiatus (Figs 13 and 14). The AICA supplies the VII, VIII CN, inferorlateral pons, middle cerebellar peduncle and anterolateral surface of cerebellum. The SCA supplies the entire superior surface of cerebellum, vermis,

Fig. 12:  Left ICA angiogram frontal view revealing ICA bifurcation, MCA, ACA segments and ACom (as annotated)

deep cerebellar white matter and dentate nuclei. In addition, BA also gives off multiple short and long segment circumflex perforating branches which supply the ventral pons and rostral brainstem. The PCAs are usually terminal branches of basilar artery but they can arise directly from supraclinoid ICA with hypertrophy of PCom and hypoplasia of ipsilateral P1 segment of PCA called as fetal PCA (Fig. 10). Posterior cerebral artery (PCA) on each side is divided into three major segments. Precommunicating (P1 or peduncular) segment: It extends from the origin of PCA to its junction with the posterior communicating artery (PCoA). The posterior thalamoperforating arteries and medial posterior choroidal artery usually arise from P1 segment. Ambient (P2) segment: It courses around the midbrain above the trochlear nerve and tentorial incisura. The lateral posterior choroidal artery and thalamogeniculate arteries arise from the P2 segment. Quadrigeminal (P3) segment: It runs behind the midbrain in the quadrigeminal plate cistern. The major branches of P3 segment are inferior temporal arteries, parieto-occipital artery, calcarine artery and posterior pericallosal arteries which supply the occipital lobe and posterior part of parietal lobe (Figs 13A and B).

Venous Anatomy (Fig. 14) The cerebral venous system is composed of two components, the dural venous sinuses and the cerebral veins.

Dural Sinuses Superior sagittal sinus (SSS): It is situated in the midline and typically originates near the crista galli anteriorly and extends posteriorly to its confluence with the straight and lateral sinuses at the torcula.

Chapter 3 Normal Cerebral Angiography

A

B

Figs 13A and B:  Posterior circulation frontal and lateral view showing the major arteries and their branches. Abbreviations: VA, vertebral artery; BA, basilar artery; PICA, posterior inferior cerebellar artery; AICA, anterior inferior cerebellar artery; SCA, superior cerebellar artery; PCA, posterior cerebral artery; PCom, posterior communicating artery; PA, pulmonary artery; LVA, left ventricular artery; LAT, lateral

Cavernous sinuses: The cavernous sinuses are the largest venous sinuses located in the parasellar region. Its major tributaries are superior and inferior ophthalmic veins. The ICA and 3rd, 4th, 6th, ophthalmic and maxillary divisions of 5th cranial nerves course within each sinus. Both cavernous sinuses communicate with each other, preclival venous plexus, sigmoid sinuses, and jugular bulb (through superior and inferior petrosal sinuses).

Cerebral Veins These are divided into superficial (cortical) veins and deep veins.

Fig. 14:  Right internal carotid angiogram venous phase (lateral view). 1 = Superior sagittal sinus, 2 = Superior cerebral veins, 3 = Vein of Trolard, 4 = Basal vein of Rosenthal, 5 = Vein of Galen, 6 = Straight sinus, 7 = Transverse sinus, 8 = Torcular herophili, 9 = Sigmoid sinus, 10 = Internal jugular vein, 11 = Internal cerebral vein

Inferior sagittal sinus is situated in the inferior free margin of the falx cerebri and joins the vein of Galen to form the straight sinus. Straight sinus courses backwards to unite with the SSS at the torcular herophili. Transverse and occipital sinuses: The torcular herophili divides into the transverse (lateral) and occipital sinuses. The transverse sinuses course laterally around the tentorial attachment to form the sigmoid sinuses and drain into the internal jugular veins on either side. The occipital sinus is rudimentary.

Superficial cortical veins: These are variable in number and enter the SSS near the vertex. The larger veins which may be identified are superficial middle cerebral vein which runs along the sylvian fissure, vein of Trolard which courses from sylvian fissure to SSS and vein of Labbe which courses from sylvian fissure to the transverse sinus. Deep cerebral veins: The medullary veins originate 1–2 cm below the cortex and course centrally towards subependymal veins which surround the lateral ventricles. The thalamostriate vein and septal vein join near the foramen of Monro to form the internal cerebral vein (ICV). The two ICVs and basal veins of Rosenthal (BVR) join to form the vein of Galen which runs under the splenium of corpus callosum and unites with the inferior sagittal sinus to form the straight sinus which join the SSS at the torcula. The major veins draining the posterior fossa are anterior pontomesencephalic vein, precentral cerebellar vein, superior and inferior vermian veins and hemispheric veins.

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Advances in Computed Tomography Technology

4

CHAPTER

Niranjan Khandelwal, Paramjeet Singh, Sameer Vyas

INTRODUCTION Computed tomography (CT) technology has evolved from first generation scanners with a single detector to multidetector computed tomography (MDCT), dual source CT, flat panel CT and dynamic CT.1-8 Better collimation of the X-ray beams, higher heat capacity of the newer X-ray tubes and increased sensitivity of detector assembly have significantly upgraded the technology. Introduction of spiral (helical) CT scans in 1990 which use slip ring technology allows continuous data acquisition of a volume by 360° gantry rotation during continuous table movement during the scan. The technique reduced slice thickness to submillimeter levels, allowed faster scanning and acquisition of a large volumetric data which can be used to generate thin slices and high resolution reformations of images in any desired plane from very thin isotropic voxels.

MULTIDETECTOR COMPUTED TOMOGRAPHY The introduction of multidetector computed tomography (MDCT) system into clinical radiology has brought a revolution in the field of medical imaging. MDCT are the latest techniques where multiple rows of detectors are used to acquire multiple slices per rotation through interweaving helices (2, 4, 16 up to 320 slices). 1 mm × 20 mm detectors are replaced with arrays of 1 mm × 1.25 mm channels in MDCT which can be arranged in a symmetrical, adaptive or hybrid fashion. MDCT uses high gantry speed (0.5–0.8 seconds) allowing faster imaging and larger volume coverage particularly for CT angiography.2,3 This technology allowed the maturing of traditional CT from plain axial cross-section imaging to a modern reallike three-dimensional (3D) tool with identical spatial resolution along all directions allowing excellent multiplanar reformations and high quality 3D reconstructions. The scan parameters can be manipulated by changing the collimation, detector configuration and reconstruction algorithm. 3 Retrospective data analysis allows flexibility of examination.

Simultaneous development of efficient computer systems made possible postprocessing and analysis of enormous data sets. The two chief benefits of helical or multislice CT are an increase in the speed and defined ability of performance of volume acquisitions. 1. Increased speed: Multislice CT allows high-speed scanning, thinner sections or longer scan ranges. Increased scanning speed leads to less motion artifacts, especially in the cases of children and patients who are critically ill or are in trauma. Since scanning 0 is rapid, more volume can be covered and more data of higher resolution can be acquired for better 3D reconstructions. The contrast requirement is also less compared with standard CT or better images can be obtained with the same amounts of contrast material. 2. Volume acquisition: A continuous volume acquisition in a helical CT makes sure that none of the lesions go as miss when a patient respirates or makes a movement. These improved 3D capabilities of multiplanar reformations and exhaustive 3D representations are the prime benefits for volume acquisition. This technology provides best result if the thickness of the chosen section is reduced to the minimum. The utility of volume rendering techniques has risen so much that interpretation of images has progressed from observation of aerial sections to evaluation of real 3D data sets.

DUAL SOURCE COMPUTED TOMOGRAPHY Dual source CT uses two separate X-ray sources of different energies to enhance the contrast between adjacent structures and their respective detector sets which are placed orthogonal to one another.4,5 It provides high temporal resolution and enables bone removed CT neuroangiographic images of diagnostic quality. In addition, calcified plaques and surgical clips can be removed by processing the data. Recent studies have reported contrast-enhanced dualenergy CT angiography had high diagnostic accuracy for

Chapter 4 Advances in Computed Tomography Technology

the detection of intracranial aneurysm as compared with 3D digital subtraction angiography (DSA) at a lower radiation dose.5

FLAT-PANEL VOLUME COMPUTED TOMOGRAPHY Flat-panel volume computed tomography is recent development in the CT technology that allows coverage of a large volume per rotation, fluoroscopic and dynamic imaging, and high spatial resolution.6 It represents combining of different modalities like radiography, fluoroscopy, X-ray angiography, and volumetric CT into one system. Area detectors have replaced the detector rows in this new technology. The flat-panel detector with its wide Z-axis coverage makes the imaging of entire organs possible in a single axial acquisition. Its fluoroscopic and angiographic capabilities permit intraoperative and vascular applications. The flat-panel volume CT is advantageous in comparison to multidetector CT as it allows ultra-high spatial resolution, real-time fluoroscopy, dynamic imaging capabilities, and whole-organ coverage in one rotation.6 The main limitations of flat-panel volume CT is that it requires a higher radiation dose [needed to achieve a comparable signal-to-noise ratio (SNR)], lower contrast resolution, and a slower scintillator that slows down the scanning process.

DYNAMIC COMPUTED TOMOGRAPHY ANGIOGRAPHY Inability to provide any dynamic (i.e. temporal resolved) information was a major limitation of MDCT compared to the gold standard of angiographic, digital subtraction angiography. But this limitation seems to be resolved with the recent introduction of a 320-detector row CT scanner that provides the possibility of dynamic volume scanning (four-dimensional scanning with the fourth dimension being the time).7,8 Volumetric CT using 320 detector rows enables full brain coverage in a single rotation that allows for combined time-resolved whole-brain perfusion and fourdimensional computed tomography angiography (CTA). Its potential applications in neuroradiology are in stroke, steno-occlusive disease, arteriovenous malformations and dural shunts. The broad coverage enabled by it offers Z-axis coverage allowing for whole-brain perfusion and subtracted dynamic angiography of the entire intracranial circulation. It has the potential of scanning entire organs such as the heart and brain in a single rotation as it provides large maximum detector area that can be used for this scanner, therefore allowing the visualization of dynamic flow and perfusion, as well as motion of an entire volume at very short time interval.

COMPUTED TOMOGRAPHY IN NEUROIMAGING Computed tomography scan has been the workhorse of neuroimaging. It is a cost-effective and quick screening test with established role in cross-sectional imaging of craniospinal trauma, subarachnoid hemorrhage, stroke, evaluation of postoperative patients as well as of bone and detection of calcifications in brain lesions. In addition, it has a role in those patients in which MRI is contraindicated. The concept of CT imaging was challenged with the advent of MRI; however, with multislice the modality has seen a new resurgence. Many of these CT applications are current standards in clinical practice. Computed tomography angiography now plays an expanded role in evaluation of subarachnoid hemorrhage by detecting vascular lesions like aneurysms and arteriovenous malformations. These patients are already on the CT table and it only requires a few more minutes to obtain detailed information about possible causes of the hemorrhage. By now, there are an increasing number of surgeons who are willing to operate solely on the basis of a CTA exam. With MDCT, spatial resolution is excellent and the results are similar or even superior to angiography. There is an increasing use of the modality in imaging of stroke through CTA of intracranial and neck vessels, venography and CT perfusion imaging. The excellent reconstructions of CT data have also enhanced the utility of CT in neuroimaging, i.e. in spinal trauma and evaluation of craniovertebral junction.

NONCONTRAST COMPUTED TOMOGRAPHY OF HEAD Helical CT has not caught on for routine imaging of the neurocranium and axial mode is still used for routine imaging; however, thin-sections obtained on multichannel scans have distinct advantage. Thin sections of the middle cranial and posterior fossa reduce the beam hardening artifacts and improve delineation of the brain stem and temporal lobe. A usual spiral protocol is 5 mm acquisition with a table speed of 15–30 mm/s for brain. Thin sections (i.e. 1.5 mm) can be merged into thicker (2.5 mm or more) thus reducing noise and radiation dose. The data may be split back for high resolution reconstructions. Thus, there is now the option of not only axial but also coronal or sagittal images of the brain. The clinical usefulness of this technique, however, has not yet been tested. The technology has affected pediatric neuro applications in many ways. Increased speed has eliminated the need for sedation and a reconstruction of data obtained in least provocative position allows multiplanar depiction of anatomy.

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Section 1 Neuroradiology including Head and Neck

Computed Tomography Angiography Catheter angiography; the gold standard for diagnostic neuroangiography, is an expensive and invasive procedure with a morbidity and mortality of 1.5–2%. Accurate imaging of vascular anatomy of head and neck requires excellent spatial resolution for visualization of small and tortuous vessels. In addition speed is needed to avoid venous enhancement. CTA of the intracranial or cervical vessels thus has strikingly benefits from the technology of MDCT. At submillimeter collimation (0.5–0.75), the entire length of the carotids or the cerebral arteries is scanned in a few seconds in pure arterial phase. Finest anatomic detail can be achieved by this isotropic data set providing high quality 2D and 3D renderings of vascular anatomy through different reconstruction techniques, such as multiplanar reconstruction (MPR), surface-shaded display (SSD) or volume-rendering technique (VRT).9-12 Magnetic resonance angiography (MRA) and color Doppler ultrasound (DUS) are some noninvasive alternatives. The limitations of MRA include motion artifacts, long examination times, loss of signal due to turbulence and in plane saturation leading to exaggeration of stenosis, poor demonstration of calcium and bony landmarks and limitations in evaluating postoperative patients with metallic clips and stents. With recent advances in MR technology [contrast enhanced magnetic resonance angiography (CE MRA)], some of these have been overcome. Color Doppler (CD) is operator-dependent and limited in evaluating the intracranial vasculature. Computed tomography angiography the current noninvasive modality of choice for neuroangiography, overcomes many of the disadvantages of MRA. It is faster, available in smaller centers, cheaper, sensitive to presence of calcium, displays bony landmarks and can be used in patients with aneurysm clips and other MR incompatible metallic hardware. CTA depends on volume expansion and opacification of blood in the vessel and hence more accurate. Drawbacks of CTA are the use of intravenous contrast and radiation exposure.

study at C5 level can be used. An arbitrary delay of 15–20 seconds is also adequate for CTA of brain. A rapid intravenous injection of nonionic contrast, preferably from right hand, via pressure injector with flow rate of at least 3 mL/s achieves a luminal density of 150 HU which is considered to give best results. Higher rates do not offer any significant advantage.13 The images are reformatted with section thickness of 1.25 mm and overlap of 1 mm at a narrow field of view (120 mm).

Image Processing The display technique consists of multiplanar reconstructions (MPR), maximum intensity projection (MIP), shaded-surface display (SSD) and volume-rendering technique (VRT). MPR allows for viewing of the raw data in any desired plane along the course of the vessel and is good for relatively straight vessels such as the carotid arteries but is not very effective for vascular anatomies which are complex like circle of Willis. MIP images are obtained by projection of imaginary rays through the image data and mapping the maximum attenuation values. The attenuation value, i.e. vessel lumen, calcium and thrombus are well delineated but depth information is totally lost. The degree of stenosis is calculated accurately but there may be overlapping of vessels with bone. Surface shaded display computes all surface connecting neighboring pixels above a particular threshold. Unlike MIP it preserves depth information (displays complex anatomic relationship in region of vessel overlap) but loses attenuation information. It does not show interiors of the vessels, thrombus and wall calcification and as underestimates stenosis. Volume rendering allows integration of all available information through most advanced 3D rendering algorithm. An opacity as well as color is assigned to all the voxels available and VR incorporates all the relevant data into the final resulting image. It overcomes many of the problems seen with MIP and SSD. Since some data loss is inherent with all postprocessing techniques, raw images should be analyzed in all cases.

APPLICATIONS

Technique

Extracranial Vasculature

Computed tomography angiography evaluates the area from arch of aorta to vertex for cervicocerebral study in one sitting or from C1 to vertex for cerebral angiogram in 15–20 seconds. Typical parameters can be as follows: 120–140 kVp, 200–350 mAs, 1.25 mm cuts with 1 mm overlap, a pitch of 3 for head (1.25 mm/3.75 mm/rev) and 6 (1.25 mm/7.5 mm/rev) for neck and 0.5 second rotation time. 100 mL of contrast is injected at a rate of 4 mL/s by a power injector which can be chased by bolus tracking. When a threshold attenuation of 100 HU is reached as detected by the ROI placed in one of the common carotids, the scan starts automatically. Alternatively, a test bolus method (20 mL), using a single axial section dynamic

Carotid Artery Stenosis The detection and accurate quantification of carotid artery stenosis is important for appropriate treatment since carotid endarterectomy has a clear benefit in symptomatic patients with high grade stenosis (70–99%) [North American Symptomatic Carotid Endarterectomy Trial (NASCET)].14 The gold standard of carotid evaluation has been conventional angiography but the risks associated with it, interobserver variability in interpreting stenosis (up to 7%), a tendency to overestimate stenosis (6%) and limited number of views are some of the limitations.15 CTA can provide infinite views

Chapter 4 Advances in Computed Tomography Technology

for accurate estimation of eccentric or irregular stenosis, delineates mural calcium from luminal contrast and prevents inaccuracy in grading stenosis. Magnified axial images with a window setting half way between luminal contrast and wall are considered best to evaluate stenosis followed by MIP and SSD.16 Length of thickness, thickness of slices presence of calcification and direction of vessel in the imaged volume also affect measurements.17-19 It is difficult to assess exact accuracy of CTA in carotid stenosis due to different criteria and parameters used on different machines; however, reported sensitivity for severe stenosis and occlusion has ranged from 88–100%, which correlates well with conventional angiography (Figs 1A to D). Lee et al. reported 100% accuracy for occlusion, 90% for critical stenosis (90–99%), greater than 95% for severe stenosis (70– 89%), greater than 85% for moderate stenosis (50–69%) and 95% for minimal stenosis.17-19 CTA also has a good correlation of plaque morphology (calcified, soft or ulcerated). Computed tomography angiography has a higher accuracy compared to DUS and is comparable or slightly better than CE MRA (100% vs 93%) for assessing high-grade stenosis and distinguishing it from complete occlusion.18 This is crucial, as high-grade stenosis is an indication for carotid endarterectomy whereas complete occlusion is a contraindication to surgery. CTA also provides assessment of the brain parenchyma at the same time.

Dissections Dissection of carotid or vertebral artery is an increasingly recognized cause of stroke in young is adequately evaluated with CTA and results are comparable to other noninvasive techniques like MRA and CD.20 Subadventitial dissections,

A

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C

D

Figs 1A to D:  Left common and internal carotid artery stenosis. (A) MIP; (B) SSD; (C) VR and (D) DSA images showing moderate stenosis of distal common carotid and proximal internal carotid artery. The stenosis is not complete

presence of intramural hematoma, stenosis, occlusions and pseudoaneurysms can be picked up. Computed tomography angiography is not successful for hemodynamic of blood flow. MDCT can simultaneously evaluate the intracranial vasculature for tandem stenosis in same sitting. Polytrauma patients with a high index of vascular injury can also be evaluated by CTA. Helical CT provides simultaneous assessment of vascular, soft tissue and vertebral injury in this setting.

Intracranial Vasculature Aneurysms Digital subtraction angiography is the gold standard for the evaluation of patients with subarachnoid hemorrhage secondary to suspected aneurysmal rupture, but it is time consuming, invasive and carries a less than 0.1% complication rate of permanent neurological deficit.13 There is an associated increased risk of rebleed. As shown by some clinical studies, CTA seems suitable in the acute stage after subarachnoid hemorrhage (SAH) as it does not require intra-arterial catheterization, uses short scan times and can immediately follow the initial unenhanced CT examination.21 A recent study found CTA to detect 90% of all aneurysms associated with acute SAH and neurosurgeons assessed CTA as equal or superior to DSA in 83% of cases. In 74% of patients, surgery might have been based on CTA findings alone.21 The reported sensitivity of CT angiography lies in the range of 80–97% depending on the size and location of an aneurysm.22 Sensitivity is highest for aneurysms more than 5 mm in size, however, those less than 5 mm in size can be detected with a sensitivity of only about 20%.23 For diagnosed aneurysms, CTA provides a more detailed analysis of the sack morphology, neck, parent vessel caliber and its spatial relationship with aneurysm, additional vascular relationships and surrounding anatomy (bony and soft tissue landmarks) which helps in finding the appropriate options for treatment (surgical or minimally invasive endovascular) (Figs 2 to 4). Computed tomography angiography is also a problemsolving modality in poorly defined aneurysms on DSA and particularly useful for evaluation of paraclinoid aneurysms for their anatomically complex relationships with bony and vascular structures (Figs 2A to D). CTA is significant in the characterization of giant aneurysms preceding surgical or endovascular treatment and helps in the detection of pseudoaneurysms. CTA is also indicated in the assessment of postoperative/postintervention status of aneurysm. Though conventional angiography is more sensitive for small aneurysms, CTA may show small thrombosed aneurysms not shown on DSA.24 CTA can be very efficient for screening of vasospasm following SAH. It can be a screening technique to detect aneurysms in high-risk group patients

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Figs 2A to D:  A giant carotico-ophthalmic aneurysm. Maximum

intensity projection (A), volume-rendering (B and C) images; and digital subtraction angiography (D). The carotid artery is incorporated into the aneurysm. Post processing shows vascular relationship better than DSA

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Figs 3A to D:  Posterior inferior cerebellar artery (PICA) aneurysm: volume-rendering images (A and B) posterior view showing the aneurysm arising from the left PICA. The relationship with C1 posterior arch was clearly shown (C and D) helping the decision for surgical approach

such as those with strong family histories, though MRA is currently the modality of choice. Computed tomography angiography and MRA have been found to be generally equivalent in their ability to detect and characterize aneurysms (>5 mm).25 CTA however, is superior to MRA, as turbulent flow or slow flow may cause artifactual loss of signal in MRA. CE MRA may circumvent some of these disadvantages. MRI and MRA are currently the noninvasive modality of choice for screening patients in the high-risk group for aneurysms and following up incidentally detected aneurysms being managed conservatively. Some drawbacks of CT angiography include bleak visibility of small arteries, difficulty in distinguishing the infundibular dilatation at the origin of an artery from an aneurysm, the kissing vessel artifact, display of venous structures that can simulate aneurysms, inability to identify thrombosis and calcification on three-dimensional images, and beam-hardening artifacts produced by aneurysm clips.

Arteriovenous Malformations Computed tomography angiography though has limited role in intracranial arteriovenous malformations (AVMs), it can visualize the feeding arteries, nidus and draining veins but

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Figs 4A to D:  Left vertebral artery aneurysm: Volume-rendering (A and C) and digital subtraction angiography (B and D) showing left vertebral artery aneurysm with complex configuration better shown on computed tomography volume-rendering images

Chapter 4 Advances in Computed Tomography Technology

optimal temporal information regarding arterial and venous phases may not be adequate as compared to DSA.26 CTA does not possess a high spatial resolution which is required for detecting associated aneurysm, stenosis and small feeding vessels provided by conventional angiography. The major use of CTA today is in the evaluation of the AVM nidus during radiosurgery planning and post-treatment follow-up.27 Though any study has not yet compared the roles of CTA and MRA in AVMs yet each modality appears to have its own advantages and disadvantages but flow encoded MR may provide more information in AVM. Embolization material can interfere with delineation of vasculature on MRA but usually is not a problem with CTA.

Tumors Computed tomography angiography can demonstrate vascular encasement by skull-base tumors. It also provides preoperative assessment of the 3D bony and vascular anatomy prior to tumor excision. Computed tomography venography (CTV) is also useful for showing venous invasion by meningioma.

Computed Tomography Perfusion It has been shown that cerebral blood volume when falls below 20 mL/100 g/min synaptic transmission in neurons fails and below 10 mL irreversible cell death occurs. Therefore tissue salvage is possible in areas with lesser degrees of compromise of blood flow. Computed tomography perfusion (CTP) is a rapid means to evaluate cerebral perfusion as there is a linear relationship between the contrast agent concentration and attenuation.28-34 CTP is based on the central volume principle as per the equation: CBF = CBV/MTT [cerebral blood flow (CBF), cerebral blood volume (CBV), mean transit time (MTT)]. During the first pass of a bolus of contrast, there is a transient increase in attenuation proportional to the concentration of the agent in a given region. Contrast agenttime concentration curves are generated in an arterial and venous region of interest (ROI) (i.e. middle cerebral artery and superior sagittal sinus) and in the area of perfusion abnormality. Deconvolution of this data gives the MTT. Cerebral blood volume (CBV) is calculated as the area under the curve of parenchymal pixel and the arterial ROI. From this CBF can be calculated.28

Technique Four adjacent 5 mm slices are selected starting at the level of basal ganglia. About 50 mL of a nonionic contrast is injected at a rate of 3 mL/s. Five seconds later a continuous scan is initiated using 80 kVp, 190–200 mA at one second rotation for 50 seconds. The perfusion data is analyzed at a work station to generate color coded CBF, CBV and MTT maps.

With the advent of 256 and 320 MDCT, whole brain perfusion CT can be performed which provides access to the entire brain with the administration of one contrast medium bolus so that ischemic region can be identified. I can improve the diagnostic utility in neuroimaging.33-34

CLINICAL APPLICATIONS Acute Stroke The goal is to identify potentially salvageable tissue for thrombolytic therapy. In a retrospective study, Eastwood et al. found significant difference in CBV, CBF and MTT in symptomatic hemisphere of which MTT was the best indicator for stroke.30 A 35% decrease in CBF had a good correlation with ischemic penumbra in another study.30 Early studies do indicate that CTP may enable predication of patients who would benefit from therapy and determine final infarct size. Cerebrovascular reserve: In patients with chronic ischemia related to underlying stenotic lesions, the involved territory is maximally vasodilated due to autoregulation and cannot respond to acetazolamide challenge. An increase of 5% in CBF indicates insufficiency and a decrease in CBF indicates higher risk of stroke. CTP has been used to show low CBV and CBF in patients of SAH with moderate-to-severe vasospasm.31,32

Tumors Many studies has shown that modified CTP technique has high permeability surface product (a measure of microvascular permeability) in tumors and may prove advantageous over MR in tumor perfusion studies. CTP can be used for preoperative grading of gliomas and can provide additional information about tumor hemodynamics. 33,34 In addition, perfusion computed tomography (PCT) maps are also useful for surgical biopsy and/or radiosurgery guidance to target the areas of increased CBV which can yield better histology and better response to treatment.

Computed Tomography Imaging of Acute Ischemic Stroke Several studies have shown better neurological outcome in patients with acute stroke with thrombolytic therapy which were based on the imaging criteria. Multimodal CT (noncontrast CT, CT Angiography and perfusion CT) allows the assessment of the four Ps (parenchyma, pipes perfusion, and penumbra).35-40 MDCT provides a ‘one-stopshop’ approach for comprehensive noninvasive assessment of acute stroke patients by demonstrating the site of arterial occlusion and hemodynamic status of the brain parenchyma. A non-contrast scan is done to diagnose infarct, determine its extension and rule out hemorrhage. A CTA is an accurate

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Fig. 5A:  Noncontrast CT within 2 hours of stroke showing ill-defined hypodensity in the right parietotemporal region

Fig. 5C:  Cerebral blood flow, cerebral blood volume and mean transit

time maps showing perfusion defect and a large ischemic penumbra. MTT maps shows delayed transit of contrast. Time attenuation curve of penumbra region showing less attenuation compared to normal side

choices. MRI imaging with DWI and PWI is equally powerful alternative and both CT and MR techniques are comparable in evaluating the tissue at risk in acute stroke according to a recent study.40 However, widespread availability of CT in smaller centers is a big advantage.

Computed Tomography Venography Fig. 5B:  Computed tomography angiography in posterosuperior view showing complete occlusion of the inferior division of the right middle cerebral artery (MCA) (arrow)

technique for evaluation of vascular patency in acute stroke by allowing comprehensive evaluation of the intra- and extracranial vasculature. A CTA from the aortic arch to the intracerebral vessels helps to detect carotid plaques as possible causes of the event, distinguishes between proximal and distal occlusions of an intracranial artery, differentiates arterial from venous infarct and provides information about hypoperfusion and collateralization of blood flow. Finally, a CT perfusion scan distinguishes between penumbra of hypoperfused and umbra of nonperfused tissue in order to select patients who would benefit from thrombolytic therapy. The above information provides a rational basis on which to choose the optimal treatment for patients with acute stroke39 (Figs 5A to C). Due to limited availability of PET, SPECT and Xenon CT, CT and MR perfusion are the two practical

Computed tomography venography allows visualization of the cerebral venous structures and has high sensitivity for depicting the cerebral veins and sinus compared to DSA.41-43 MDCT venography is a fast, widely accessible, and cost-effective method for evaluating cerebral sinuses in emergency setting. Dural sinus thrombosis is difficult to diagnose clinically due to varied clinical presentation. The most commonly affected sinuses are the superior sagittal sinus, the transverse sinus and the sigmoid sinus. On CTV, a thrombosed dural sinus is seen as a filling defect and is often associated with contrast enhancement of the walls of the dural sinus as well as abnormal collateral venous drainage and tentorial enhancement (Figs 6A to E). MR venography (MRV) is currently the technique of choice for diagnostic evaluation and follow-up for patient with cerebral sinovenous thrombosis. Studies have shown CTV as comparable to accuracy of MRV in the diagnosis of dural sinovenous thrombosis.41-43 CT venography overcomes flowrelated artifacts (differentiates slow flow from thrombosis) seen on time-of-flight (TOF) MR, takes less time and also

Chapter 4 Advances in Computed Tomography Technology

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Figs 6A to E:  Magnetic resonance angiography (A) and venous phase of DSA (B) show thrombosis of superior sagittal sinus and left transverse sinuses. Base image of CTV (C) shows thrombus in the left transverse sinus (double arrows). CTV (D and E) superior and anteroposterior views showing thrombus within the sinus

helps in distinction of tumors that compress dural sinuses, from those which occlude them. However, CT needs contrast administration and lacks sensitivity of MR in showing venous infarction of brain. Overall, CTV is a reliable alternative to MRV in case MR is contraindicated in such patients or is not diagnostic.

Technique Computed tomography venography is performed using 100 mL of intravenous contrast injected at the rate of 3 mL/s with power injector. After a scan delay of 40 seconds, 1 mm collimated sections with a pitch of 2:1 are done covering the skull.

MULTIDETECTOR COMPUTED TOMOGRAPHY OF SPINE Multidetector CT has been a major advancement in imaging of trauma patients to facilitate rapid diagnosis before the patient can be shifted to operation theater. Bony abnormalities are

depicted better with MDCT when compared to single slice CT. Current scanners with 16 or more detectors are used to scan from head to below hips using whole body single pass technique. Imaging metallic hardware, which was impossible due to streak artifacts in the single slice helical CT scanning can now be assessed easily with MDCT due to increase in the of detector rows.44 With improvement of isotropic resolutions, multi-planer reformations now enable diagnosis that are not so apparent on axial images, i.e. transverse fractures and fusions. Understanding of complex spatial relationships of bone becomes easier which translates into increased confidence level of the radiologist. While 3D-CT may not add to diagnostic information achieved by use of 2D reformatted image but it does aid the surgeons to plan reconstructive surgery.

CLINICAL APPLICATIONS zz

Trauma: —— Cervical trauma: CT is cost effective in patients with closed head injury with high risk of associated

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Figs 7A to C:  Sagittal reconstructed (A) helical CT images of cervical spine showing malalignment on CT. Parasagittal reconstructed image of CT (B) better shows the fracture and the locked facet. Axial image (C) shows fracture of lateral mass on left side

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cervical spine injury, i.e. in confirming and better depicting the extent of the injuries. MDCT gives excellent reformatted images to identify fractures in horizontal plane that may not be apparent otherwise (Figs 7A to C). Craniovertebral junction is one area well suited for reformatted images. Any associated vascular injury can also be simultaneously evaluated with CTA. —— Thoracolumbar trauma: Combination of 5–10 mm routine abdominal sections for visceral injuries and plain radiography for lumbar spine fracture is inadequate. In such situations, MDCT due to thinner sections and better reformations is 97% sensitive for detection of unstable fractures as compared to 33% sensitivity of plain radiography.45 In degenerative diseases of spine, CT is inferior to MRI for evaluating soft tissue detail. Main advantage of MDCT is to show bony canal, i.e. oblique reformations for foraminal stenosis. MDCT depicts trabecular anatomy in the bone marrow with remarkable clarity and early trabecular destruction by tumors is readily apparent. MDCT complements MR and plain radiographic assessment for marrow infiltrative disorders like multiple myeloma, detects vertebrae at risk for fracture and differentiate benign from neoplastic fractures.46,47 Multidetector CT is also useful in evaluation of postoperative patients for hardware and in assessing progression of healing. The artifacts due to metallic hardware implants can be reduced by various advanced CT techniques. Maximizing the peak voltage and tube current, minimizing the detector collimation and pitch during acquisition can help in reducing the artifacts.

Using thin slice reconstruction, thicker slice reformats and 3D-VR techniques are also helpful in reducing the artifacts.47 zz Miscellaneous: Numerous vascular conditions like aortic dissection, aortic aneurysm and aneurysm of artery of Adamkewicz and post-intervention procedures like aortic stent graft placement can endanger the vascular integrity of artery of Adamkeiwicz. In these conditions, MDCT angiography of spinal vasculature with adapted brain reconstruction algorithm may provide the details of perfusion and anatomy of artery of Adamkeiwicz.48 With multiplanar and 3D reformations, spinal deformities can be assessed in all planes allowing identification of previously unrecognized malformations and better characterization of previously identified deformities. MDCT has a role in depiction of postoperative bony fusions and in patients with indwelling hardware. However, MR still remains the modality of choice to evaluate disc abnormalities and post disc surgery scanning.46

RADIATION CONCERNS Radiation hazard is a major issue as there is a manifold increase in the number of CT examinations performed currently. Helical CT provides a reduction in patient dose over “step and shoot” scans due to short scan times (higher pitch). However, it is known that increasing the pitch does not necessarily decrease the dose as there is an automatic increase in the tube current.49 Further advancement in X-ray tube technology can accomplish decreased dose by modulating the X-ray tube current. The penumbra of the CT beam is a source of wasted radiation. Efforts are on to harvest

Chapter 4 Advances in Computed Tomography Technology

these for diagnostic information. The organ-specific and shape-specific beam profiles are also being developed like tilted gantries which may reduce radiation to lens.

CONCLUSION Recent introduction of MDCT have revolutionized the neuroimaging with extensive anatomic coverage and thinner sections. Dynamic 320-section CT, dual source CT and flatpanel detector are noninvasively demonstrating entire cranial and extracranial vasculature with high spatial and temporal resolution. Fusion imaging, i.e. metabolic images of PET superimposed on anatomical images of CT is already changing the way cancers are treated. With the recent MDCT scanners, visualization of dynamic flow and perfusion as well as motion of an entire volume at a very short time interval is possible.

REFERENCES 1. Fox SH, Tanenbaum LN, Ackelsberg S, et al. Future directions in CT technology. Neuroimag Clin North Am. 1998;8:497-513. 2. Wintersperger BJ, Herzog P, Jakobs T, et al. Initial experience with the clinical use of a 16 detector row CT system. Crit Rev Comput Tomogr. 2002;43:283-316. 3. Hu H. Multi-slice helical CT: Scan and reconstruction. Med Phys. 1999;26:5-18. 4. Hegde A, Chan LL, Tan L, et al. Dural Energy CT and its Use in Neuroangiography. Ann Acad Med Singapore. 2009;38:817-20. 5. Zhang LJ, Wu SY, Niu JB, et al. Dual energy CT angiography in the evaluation of intracranial aneurysms: Image quality, radiation dose, and comparison with 3D rotational digital subtraction angiography. AJR. 2010;194:23-30. 6. Gupta R, Cheung AC, Bartling SH, et al. Flat-Panel Volume CT: Fundamental Principles, Technology, and Applications. Radiographics. 2008;28:2009-22. 7. Salomon EJ, Barfett J, Willems PW, et al. Dynamic CT Angiography and CT Perfusion Employing a 320-detector Row CT. Klin Neuroradiol. 2009;19:187-96. 8. Brouwer PA, Bosman T, Van Walderveen MA, et al. Dynamic 320 slice CT angiography in cranial arteriovenous shunting lesions. AJNR. 2010;31:767-70. 9. Blank M, Kalender WA. Medical volume exploration: Gaining insights virtually. Eur J Radiol. 2000;33:161-9. 10. Westerlaan HE. Gravendeel J, Fiore D, et al. Multislice CT angiography in the selection of patients with ruptured intracranial aneurysms suitable for clipping or coiling. Neuroradiology. 2007;49:997-1007. 11. Lovbald K-O, Baird AE. Computed tomography in acute ischemic stroke. Neuroradiology. 2010;52:175-87. 12. Saini M, Butcher K. Advanced imaging in acute stroke management-Part 1: Computed tomographic. Neurol India. 2009;57:541-9.

13. Kuszyk BS, Beauchamp NJ Jr, Fishman EK. Neurovascular applications of CT angiography. In CT angiography. Semin Ultrasound CT MR. 1998;19:394-404. 14. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Eng J Med. 1991;325:445-53. 15. Eliaziw M, Fox AJ, Shaupe BL, et al. Carotid artery stenosis. External Validity of the North American Symptomatic Carotid Enarterectomy Trial Measurement Method. Radiology. 1997;204:229-33. 16. Anderson GB, Ashforth R, Steinke DE, et al. CT angiography for the detection and characterization carotid artery bifurcation disease. Stroke. 2000;31:2168-74. 17. Dillon EH, Van Leeuwen MS, Fernandes MA, et al. CT angiography: Application to the evaluation of carotid artery stenosis. Radiology. 1993;189:211-9. 18. Wise SW, Hopper KD, Have TT, et al. Measuring carotid artery stenosis using CT angiography: The Dilemma of Artifactual Lumen Eccentricity. AJR. 1998;170:919-3. 19. Lee A, Boss J, Ngyuyen T, et al. Application of helical computed tomographic angiography in evaluation of carotid artery stenosis. Applied Radiology. 1998;26-30. 20. Link J, Brossman J, Pensclen V, et al. Common carotid artery bifurcation: Preliminary results of CT angiography and color coded duplex sonography compared with digital subtraction angiography. AJR. 1997;168:361-5. 21. Leclerc X, Godefroy O, Salhi A, et al. Helical CT for the diagnosis of extracranial carotid artery dissection. Stroke. 1996;27:461-6. 22. Zouaori A, Sahil M, Mairo B, et al. Three-dimensional computed tomographic angiography in detection of cerebral aneurysms in acute subarachanoid hemorrhage. Neurosurgery. 1997;41:125-30. 23. Korogi Y, Takahashi M, Katada K, et al. Intracranial aneurysms: Detection with three-dimensional CT angiography with volume rendering-comparison with conventional angiographic and surgical findings. Radiology. 1999;211:497-506. 24. Hope JK, Wilson JL, Thomson FJ. Three-dimensional angiography in the dectection and characterization of intracranial berry aneurysms. AJNR. 1996;17:439-45. 25. Brown JH, Lustrin ES, Lev MH, et al. Characterization of intracranial aneurysms using CT angiography. AJR. 1997;169: 889-93. 26. Barboriak DP, Provenzale JM. MR arteriography of intracranial circulation. AJR. 1998;171:1469-78. 27. Reiger J, Hoston N, Neuman, K et al. Initial clinical experience with spiral CT and 3D arterial reconstruction in intracranial aneurysm and arteriovenous malformations. Neuroradiology. 1996;36:245-51. 28. Wintermark M, Reichhart M, Cuisenaire O, et al. Comparison of admission perfusion computed tomography and qualitative diffusion and perfusion weighted magnetic resonance imaging in acute stroke patients. Stroke. 2002;33:2025-31.

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Section 1 Neuroradiology including Head and Neck 29. Nabavi DG, Cenic A, Craen RA, et al. Assessment of cerebral perfusion: Experimental validation and the initial clinical experience. Radiology. 1999;213:141-9. 30. Eastwood JD, Lev MH, Azhari T, et al. Perfusion scanning with deconvolution analysis: Pilot study in patients with acute middle cerebral artery stroke. Radiology. 2002;222:227-36. 31. Wintermark M, Reichhart M, Thiran JP, et al. Prognostic accuracy of cerebral blood flow measurement by perfusion computed tomography, at the time of emergency room admission, in acute stroke patients. Ann Neurol. 2002;51:417-32. 32. Nabavi DG, LeBlanc LM, Baxter B, et al. Monitoring cerebral perfusion after subarachnoid hemorrhage using CT. Neuroradiology. 2001;43:7-16. 33. Murayama K, Katada K, Nakane M, et.al. Whole-Brain Perfusion CT Performed with a Prototype 256–Detector Row CT System: Initial Experience. Radiology. 2009; 250:202-11. 34. Ellika SK, Jain R, Patel SC, et.al. Role of Perfusion CT in Glioma Grading and Comparison with Conventional MR Imaging Features AJNR. 2007;28:1981-7. 35. Srinivasan A, Goyal M, Azri FA, Lum C. State-of-the-Art Imaging of Acute Stroke. Radiographics. 2006;26:75-95. 36. Ledezma CJ, Wintermark M. Multi-modal CT in Stroke Imaging: New Concepts. Radiol Clin North Am. 2009;47(1):109-16. 37. Tomandl BF, Klotz E, Handschu R, et al. Comprehensive Imaging of Ischemic Stroke with Multisection CT. Radiographics. 2003;23:565-92. 38. Schwartz RB. Helical (spiral) CT in nueroradiologic diagnosis in Helical (spiral) computed tomography. Radiologic Clinics of North America 1995;33:981-95.

39. Wardlaw JM. Overview of Cochrane thrombolysis metaanalysis. Neurology. 2001;57:S69-76. 40. Sunshine J. CT, MR and MR angiography in evaluation of patients with acute stroke. J Vasc Interv Radiol. 2004;15:S47-55. 41. Khandelwal N, Agarwal A, Kochhar R, et al. Comparison of CT Venography with MR Venography in cerebral sinovenous thrombosis. AJR. 2006;187:1637-43. 42. Linn J, Erlt-Wagner B, Seelos KC, et al. Diagnostic value of multidetector-row CT angiography in the evaluation of thrombosis of the cerebral venous thrombosis. AJNR. 2007;28: 946-52. 43. Ozsvath RR, Casey SO, Lustrin ES, et al. Cerebral venography: Comparison of CT and MR projection venography. AJR. 1997;169:1699-707. 44. Buchwalter KA, Rydberg J, Kopecky KK, et al. Musculoskeletal imaging with multislice CT. AJR. 2001;176:979-86. 45. Rhee PM, Bridgeman A, Acosta JA, et al. Lumbar fractures in adult blunt trauma: Axial and single slice helical abdominal and pelvic computed tomographic scans versus portable plain X ray. J Trauma. 2002;53:663-7. 46. Crim JR, Tripp D. Multidetector CT of the spine. Semin in US, CT and MRI. 2004;25:55-66. 47. Ohashi K, El-Khoury GY. Musculoskeletal CT: Recent advances and current clinical applications. Radiol Clinc N Am. 2009;47: 387-409. 48. Boll DT, Bulow H, Blackam KA, et al. MDCT Angiography of the spinal vasculature and the artery of the Adamkiewicz. AJR. 2006;187:1054-60. 49. Mahesh M, Scatarige JC, Cooper J, et al. Dose and pitch relationship for a particular multislice CT scanner. AJR. 2001;177:1273-75.

Advances in Neuroimaging Techniques: Magnetic Resonance Imaging

5 CHAPTER

Paramjeet Singh, Niranjan Khandelwal

Due to technological advances, application of MRI in neuroimaging has expanded significantly in last decade yielding new approaches to diagnosis and management of the neurological diseases. Improvements have been directed towards reducing scan times and improving image quality through developing new pulse sequences, improved receiver coil technology, enhanced gradient performance, use of higher field strength magnets and application of more efficient data processing. Modern ultrafast sub-second sequences virtually freeze the physiological motion. Thus, MRI has established itself as a powerful tool not only for fast routine scanning but also expanded its applications into studying organ function, metabolism and physiology leading to and an integrative approach.

IMPROVEMENTS IN MR HARDWARE AND SOFTWARE TECHNOLOGY (GRADIENTS, COILS AND PARALLEL IMAGING) During the last decade, advances in field strength, MR hardware and pulse sequences brought tremendous improvements in imaging speed.1 More efficient shielded rapidly switching gradients of amplitudes up to 50 mT/m, rise time of 0.1 ms with slew rates of 200 T/m/s and beyond allowed rapid acquisition of data facilitating EPI, short TE imaging like MRA and spiral imaging. Improvements in coil technology, i.e. use of phased array coils (combination of multiple surface coils) significantly improved the image quality through a higher SNR and parallel data generation. Newer high density coils with up to 16 RF receiver elements and 32 receiver channels are supported by efficient and fast data processing and image reconstruction algorithms. At the same time, it became obvious that further increases in speed along these lines would be progressively difficult to achieve because of physiological limitations. Excessive RF pulse trains can lead to unacceptable levels of RF energy deposition and tissue heating.

Parallel acquisition techniques (PAT) use the spatial information inherent in local coil arrays to partially replace time-consuming phase encoding steps performed by gradients. Simultaneous data acquisition and image reconstruction through a set of decoupled receiver coils and separate channels are used in the method. Each channel covers a sub-FOV in a parallel fashion, and the acquired data is combined in the K space to form an entire image using a sophisticated reconstruction algorithm. This dramatically reduces the scan time proportional to the number of coils (called PAT factor) with gain in resolution. PAT reduces artifacts and helps scanning larger field of view. There is some inherent loss of SNR which can be made up through reduction in scanning time and higher coil sensitivity (Figs 1A and B). Parallel imaging uses one of two image reconstruction techniques; namely image based SENSE (sensitivity encoding) and k space based SMASH (Simultaneous Acquisition of Spatial Harmonics).2,3 ASSET and SPEEDER are other acronyms for the technique. GRAPPA (Generalized Autocalibrating Partial Parallel Acquisition) is a variation of SMASH. Applications such as single-shot EPI, diffusion, perfusion, and fMRI are better suited to PAT and it is a valuable tool for high field imaging.

LARGE FIELD OF VIEW IMAGING Development of sliding or rolling table platform or a multi-coil technique using a combination of surface coils in position allows unlimited field of view (FOV) for whole body imaging. Total Imaging Matrix (TIMS-SIEMENS) uses 102 seamlessly integrated matrix coil elements and up to 32 RF channels. Fat saturated 3D gradient echo sequences with isotropic resolution have been successfully employed for whole body angiography or metastasis survey4 (Figs 2 and 3). In neuroimaging large FOV imaging is a distinct advantage in evaluation of entire neuraxis at one go and in angiography covering the area from arch of the aorta to circle of Willis using a neurovascular coil in patients with stroke.

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Figs 1A and B: Parallel imaging: (A) T2TSE axial

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section with 2 signal averaging and PAT factor-0, time-2 minutes 30 seconds; (B) Same section with PAT factor-2, time-45 seconds. Image quality is same with reduction in the acquisition time

Fig. 2: T2-weighted sagittal section of spine with excellent artifact

Fig. 3: Large FOV imaging. Inversion recovery image of the whole

free depiction of spinal cord, thecal sac and nerve roots. Note hyperintense foci within the marrow due to metastatic deposits

body using multiple coils showing multiple metastasis in the liver, spine and right hip regions

Chapter 5 Advances in Neuroimaging Techniques: Magnetic Resonance Imaging

HIGH FIELD STRENGTH MR IMAGING (3T AND BEYOND) There are several advantages of high field imaging. A large number of MR systems operating at a field strength of 3 Tesla (and higher) have been installed worldwide and are gaining acceptance for clinical and research purpose particularly for neuroimaging.5 A major advantage is improved signal to noise ratio (SNR) which increases linearly with field strength, thus increasing signal. Speed and resolution can be traded judiciously, i.e. imaging time can be reduced for a similar SNR as 1.5 T or spatial resolution increased for an equal imaging time on both.6 Chemical shift increases in proportion to the magnetic field and resultant increase in the spectral separation of resonance frequencies is used to advantage in spectroscopy, fat suppression and opposed phase imaging. It can also lead to disturbing chemical shift artifacts at fat-tissue interface. Ferromagnetic elements cause high local field disturbances resulting in loss of signal on 3T (susceptibility effect) which may provide a desirable contrast or disturbing artifacts. These translate into a higher sensitivity for picking up blood products and mineralization in brain as well as robust BOLD (blood oxygen level dependent) contrast and perfusion imaging.7 RF deposition scales with square of field strength and can be a limiting factor for SAR intensive sequences like FSE. Many of above disadvantages can be offset by increasing the bandwidth, use of parallel imaging (at the cost of lower SNR), flip angle modulation, low TE, higher matrix, higher order shimming, spiral imaging, etc. Parallel imaging and 3T are particularly synergistic in terms of improving the lower SNR of former and reducing susceptibility artifacts and high RF deposition of latter. VERSE (variable rate selective excitation), hyperechoes and SPACE are also novel means of reducing SAR.8 There is T1 prolongation and T2 shortening on 3T, which reduces gray white matter contrast. These can be partially compensated by using longer TR for T1 and shorter TR/TE for T2 or simply using alternative sequences. However, T1 of fluids and blood are less affected thus improving the vessel conspicuity in MR angiograms.9 Constant relaxivity of gadolinium compared to T1 times of background tissue leads to stronger enhancement thus reducing the dose of contrast media.7,8 Greatest technical superiority of 3T over 1.5 T by virtue of speed, SNR and resolution gains is in volumetric structural brain imaging, small lesion detection, i.e. multiple sclerosis, evaluation of epilepsy, diffusion tensor imaging, MR angiography, fast spectroscopic imaging and techniques exploiting susceptibility effects, i.e. BOLD and perfusion imaging.10

IMPROVEMENTS IN PULSE SEQUENCES Concepts like single shot imaging conceived several years back have now crystallized into robust techniques. They provide fast imaging, artifact free high resolution images, enhanced tissue contrast and increased patient throughput. Following is a discussion on some of the important new techniques and pulse sequences with an impact on neurological imaging.

SHORT REVIEW OF PRINCIPLES BEHIND NEW MR PULSE TECHNIQUES Spin echo sequence uses 180° rephasing pulses typically filing one line of K space for each phase encoding step during each TR interval; thus inherently slow. The scan time for any multislice two dimensional technique is given by ‘Scan time = TR × number of phase encode steps × signal averages’. To achieve high SNR, good spatial resolution and short acquisition time, the above parameters need to be manipulated. These objectives are rarely met as improving one factor invariably leads to compromise of the others. Thus, the time cannot be reduced indefinitely or the image cannot be improved to a great extent without certain trade-off. Development of newer pulse sequences was directed towards overcoming these problems. Low flip angle imaging (Gradient echo) was the first major development towards reducing scan time. Reduction in flip angle and use of gradient recall of echo instead of 180º rephasing pulse allowed shorter TR and significant reduction in acquisition time. Gradient echo and its variants allowed applications like dynamic scanning, angiographies, cine studies, high resolution scanning and functional brain mapping.10

EFFICIENT DATA PROCESSING TECHNIQUES Along with MR hardware, more efficient methods of data processing were also developed simultaneously. The unprocessed 2D data set prior to Fourier transformation referred to as K space map is a stacked plot of horizontally oriented phase encoded views (Ky), the vertical arm (Kx) being the frequency axis. Each time the phase encode moves the trajectory to a given location vertically, the frequency encode moves across the K space horizontally. More efficient ways of filling up the K space are closely linked to some of the new pulse sequences. Multiple lines of K space in the same TR can be acquired by using differently phase encoded echoes as in fast spin echo (FSE) and/or by use of oscillating gradients as in single shot techniques like EPI.11 The emergence of FSE and subsequently EPI imaging have revolutionized the field of MRI.

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Figs 4A and B: (A) Axial T2 FSE section in an uncooperative child.

Figs 5A and B: T2TSE (A) without and (B) with BLADE; sharper

HASTE imaging allows diagnostic good quality images in spite of movements (B)

image with 40% reduction in time

The two halves of the K space data (top to bottom and left to right) are symmetrical. Thus, less than full data can be acquired and the remaining part interpolated from it as is used in HASTE sequence (half acquisition single shot turbo spin echo). It shortens the scan time at the cost of SNR but not the spatial resolution (Figs 4A and B).12 The K space also being symmetrical along the vertical axis, TE can be moved to a shorter value ignoring second half of the spin echo (Fractional echo). This allows for more slices and maximum T1 and proton density weighting for a given TR. This is the basis of fast gradient echo method of Turbo FLASH. Unlike EPI and segmented scanning, the data acquisition can be in a spiral or radial trajectory through K space, starting at the center and ending at the periphery. The technique is fast and artifact free and holds a lot of promise for breath hold and high field strength imaging. Dynamic studies where contrast changes rapidly are done by ‘keyhole technique’. Only central K space acquisition would give very low resolution images but one has to choose between temporal and spatial resolution. Key hole concept first acquires a single high resolution image by scanning full range of K space before beginning dynamic study. This data is later used to fill in missing values. Since data of first set is static, dynamic changes are not shown in smaller structures but often end results are better.13 PROPELLER (periodically rotated overlapping parallel lines with enhanced reconstruction) and BLADE reduce motion artifact and improve image quality particularly at high field. The data is collected in strips rotated about the center of K space thus oversampling it and correcting in-plane motion (Figs 5A and B).14

Techniques that read only one Fourier encoded echo are called single echo and those utilizing multiple echoes with different Fourier encoding are referred to as multiecho techniques. The techniques that use only one excitation for filling the K space with multiple phase encoded echoes are called single shot techniques. Sequences which utilize previous preparation of the longitudinal magnetization to improve contrast are labeled as magnetization prepared sequences. Lastly some of the gradient family sequences refocus the magnetization of the previously measured Fourier lines (steady state free precession) while others spoil away the residual magnetization (spoiled GRASS). Hybrid sequences use more than one of the above techniques.

CLASSIFICATION OF THE PULSE SEQUENCES (FLOW CHART 1) MR pulse sequences can be categorized into two main groups built around spin echo and gradient recalled echo. 5

FAST SPIN ECHO Originally called rapid acquisition with relaxation enhancement (RARE) by Henning in 1986;15 fast spin echo (FSE) was one of the most important advances in MRI. In FSE a train of multiple spin echoes with different phase encoding steps are generated from multiple closely applied 180° RF pulses to fill up the K space. The number of echoes (ETL) utilized are directly proportional to the reduction of time. As the number of echoes is increased the SNR falls, however larger matrix size and more signal averaging compensate to improve the SNR even at small FOV.

Characteristics of FSE The sequence is less sensitive to magnetic susceptibility effects, thus less prone for artifacts. However, this is a disadvantage in imaging intracranial hemorrhage and calcification. The signal intensity of the FSE is more than expected because of contribution by stimulated echoes and some element of magnetization transfer between slices. There is a tendency for loss of small details in the phase encoding axis with use of long

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Flow chart 1: Useful MR pulse sequences for neuroimaging

effective TE or ETL. FSE has totally replaced the conventional SE for T2 weighted images and gives exquisite images of brain and spine16 (Fig. 2). Variations in FSE include 3D FSE, incorporation of fat saturation as well as magnetization preparation for IR and water saturation (fast FLAIR). HASTE and RARE sequences are single shot variations of FSE. 3D FSE: Various methods have been tried for 3D FSE volume imaging. Recently, isotropic full volume coverage by 3D FSE has become feasible within a reasonable time using strong gradients, long ETLs and short echo spacings. One method is to manipulate T2 decay by variable flip angle nonselective short refocusing pulses replacing 180° pulses, thus allowing ultra long echo time and high reduction factor in scan time.17 (SPACE-Sampling perfection with application optimized contrasts). A half Fourier method can also be incorporated. The technique allows one time volume acquisition of T1, T2, Proton and even FLAIR contrast. From this free slice generation through MPR with sub-millimeter resolution can be done (Fig. 6). This can be of help in evaluating multiple sclerosis plaques, ear structures, sialography, etc. SAR reduction is significant and PAT is a useful adjunct.

FLUID ATTENUATED INVERSION RECOVERY First described in 1992, 18 fluid attenuated inversion recovery (FLAIR) has proved to be an extremely useful sequence for neuroimaging. FLAIR uses a long TR and TE and

Fig. 6: 3D FLAIR using SPACE. Temporal lobe granuloma (arrows). Isotropic voxels allow multiplanar free slicing using neuro 3D task card with submillimeter resolution

an inversion pulse designed to null the signal of CSF using modulus reconstruction of images. Since a long inversion pulse of the order of 2000 ms is required to null the CSF such a sequence is practically possible only with a multi-echo sequence like FSE (fast FLAIR including 3D version using

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SPACE) where a sequential inversion of a group of slices is followed by sampling (Fig. 7).

CLINICAL APPLICATION Brain pathologies with intermediate T2 times are poorly visualized if they are located near the CSF interface. FLAIR being heavily T2 weighted improves conspicuity of such lesions after suppressing the CSF. Major indication of FLAIR imaging is in evaluation of multiple sclerosis plaques particularly those situated near CSF interface, i.e. ventricles. 18 Sagittal sections are particularly good to demonstrate inner callosal lesions. Superficial small infarcts are detected better and chronic infarcts with hyperintense periphery can be differentiated from Virchow Robin spaces. FLAIR images are also useful in imaging neonatal hypoxic brain injury, epidermoid cysts,

Fig. 7: 3D FLAIR using SPACE. ADEM. Multiplanar reconstruction shows corpus callosum (arrow) and brainstem lesions

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(differentiates them from arachnoid cysts), dysplasias, subcortical diffuse axonal injuries (superior to GRE for nonhemorrhagic lesions), encephalitis and brain tumors (Figs 8A to C). Subarachnoid space disease is also well shown on FLAIR imaging. An additive T1 and T2 effect facilitates detection of blood in CSF space18 (Figs 9A and B). Subarachnoid infections and tumors due to increase in protein contents also appear bright. However, artifactual increased signal in and around CSF spaces on FLAIR images is a disadvantage. This limits the use of the sequence in posterior fossa lesions. Volume FLAIR acquisitions are excellent for showing small MS plaques/ demyelination and follow-up for lesion activity19 (Fig. 7).

Single Shot Techniques of FSE (HASTE, SSFSE) It is a single shot FSE technique which during one excitation uses multiple echoes to fill slightly more than half the K space (half Fourier) to obtain T2 weighted images.20 There is image blurring in phase direction particularly for tissues with short T2 resulting in poor gray white matter distinction. This decreases RF power deposition at high field images. More commonly used for body imaging, the sequence allows rapid multiple heavily T2 weighted images of the brain in the same TR generating individual slices within 2 seconds. The artifacts due to susceptibility effects are minimum (poor visualization of blood products). Addition of an EPI gradient sequence to HASTE can overcome this disadvantage. Segmented HASTE uses two excitation pulses to separately acquire two halves of the K space with greater T2 weighting and sharper images. HASTE is ideal for imaging claustrophobic/uncooperative patients, inadequately sedated children (Figs 4A and B) and for imaging postoperative spine with metal hardware to show cord anatomy.20 An important role of HASTE is in evaluating fetus. Fetal mobility and magnetic inhomogeneity of abdominal structures makes EPI and gradient based

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Figs 8A to C: T2 FLAIR axial (A) and coronal (B) sections show an impaction injury on the right aspect of the brainstem not well shown on FSE (C) axial section

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Figs 9A and B: T2 coronal FLAIR section. (A) Hyperintense signal in the sylvian fissures on both sides due to unsuspected subarachnoid hemorrhage in a patient with anterior communicating artery aneurysm. T1 SE axial section (B) does not give any clue to the hemorrhage

Fig. 10: Excellent depiction of fetal anatomy in a full term fetus with meningomyelocele and Arnold-Chiari malformation II. The spinal defect and the posterior fossa anomaly is well shown

sequences less fruitful. Further HASTE is fluid sensitive and normal fetal brain contains abundant water, thus normal anatomy, development and anomalies of brain are well shown (Fig. 10). HASTE imaging confirms and often adds information to ultrasonographic findings. FISP sequence has also been used for fetal imaging but it suffers from three-fold higher RF deposition as well as artifacts.20

Magnetic Resonance Myelography Magnetic resonance myelography (MRM) uses fat suppressed heavily T2 weighted images to demonstrate thecal sac and nerve roots. After the initial description of RARE sequence21 various techniques like 3D FSE, 3D FISP, T2 * GRE, single shot FSE (EPI) and 3D CISS have been used successfully with comparable results. Strong T2 contrast, rapid acquisition and suppression of background generated by hybrid RARE sequences make them the preferred technique over gradient echo based steady state sequences. Single slice projection images (RARE) are preferred over multislice protocols with MIP (HASTE). Slabs in coronal, sagittal and both oblique orientations are applied in MRM. This fast noninvasive technique can be incorporated into MR imaging of spine without much time penalty. The results of MRM are as accurate as radiographic myelography. According to various studies MRM shows nerve roots and dorsal root ganglia better and thecal stenosis as accurately21 (Figs 11A and B). It also demonstrates conjoined nerve roots, arachnoid adhesions, syringomyelia, pseudomeningoceles, root avulsions, perineural and arachnoid cysts. In future, evaluation of CSF leaks and flow dynamics will eventually be possible using low doses of intrathecal gadolinium, a technique already successfully tried but yet to be approved in many countries.

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Figs 11A and B: Sagittal T2 FSE (A) shows extensive degenerative changes in the lumbar spine causing multilevel thecal sac compressions; (B) Sagittal and coronal myelography images using a RARE hybrid sequence shows the thecal constrictions and nerve root cut-off at corresponding levels

Gradient Echo Imaging and its Variants A major gain in speed came with the introduction of Fast Low Angle Shot (FLASH) in 1986.22 Instead of using a 180° refocusing pulse, a gradient echo is formed by reversing the polarity of the frequency encoded gradient. This prototype fast sequence using short TR and TE, yielded images at less than one second per slice. In situations where contrast based on T1 or proton density is sufficient, FLASH has proven a reliable alternative to spin echo. Short flip angle used in gradient echo imaging (GRE) leads to build up of longitudinal relaxation and persistence of transverse relaxation (steady state) in subsequent

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echoes. Depending on whether this residual transverse magnetization is spoiled or refocused, GRE sequences can be coherent (spoiled GRE) or incoherent (steady state GRE). The spoiled GRE images provide accentuated T1 contrast (spoiled GRASS, spoiled FLASH) particularly when prepared with an inversion pulse (turbo FLASH).22 A 3D version of the same, called MPRAGE is used for volume acquisition of brain and provides better gray white matter contrast which is generally helpful for evaluating brain anatomy, brain segmentation for fMRI studies and volumetry of hippocampus. The improved T1 contrast is also helpful on 3T where longitudinal relaxation is long. Hardware permitting, the FLASH method may be extended to the domain of extremely short TR, if sufficiently small flip angles are used (‘snapshot’ methods).23 Modern scanners allow TR of well under 10 msecs and have incorporated ‘RF spoiling’ to provide more precise control of image contrast in FLASH scans. This has resulted in a highly expanded range of functions, i.e. examination of the details of mental processes through in vivo study of brain physiology and pathophysiology. FLASH images are more susceptible to the effects of iron containing substances, an advantage for evaluation of hemorrhage and calcification. The relatively high sensitivity of FLASH and other gradient echo imaging techniques to magnetic field distortions has also helped the development of functional brain imaging (See functional imaging). The reduction in acquisition time for a given number of slices with GRE makes 3D volume studies to be completed within a reasonably short time. This sequence is used for time of flight and dynamic contrast enhanced MR angiography (CE MRA) of brain.

Susceptibility Weighted Imaging Susceptibility weighted imaging (SWI) further exploits the magnetic inhomogeneity where tissues of higher susceptibility distort the magnetic field and become out

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of phase from their neighbors at long echo times.24 Thus, there is signal loss on magnitude images. It is fully velocity compensated high resolution 3D gradient echo sequence that uses magnitude and filtered phase information, separately and in combination to create a new source of contrast. Unlike initial experience with Spoiled GRE, with advent of 3T and parallel imaging, it is now possible to image the entire brain with SWI in a short time. Delineation of small vessels particularly veins is exquisite on SWI, due to high T2* of deoxygenated blood. The technique provides additional clinical information in evaluation of traumatic brain injuries, coagulopathic and other hemorrhagic disorders (Figs 12A and B), vascular malformations, cerebral infarctions, neoplasms (Figs 13A and B), and neurodegenerative disorders associated with calcifications or iron depositions.25

Cranial and Extracranial MR Angiography Magnetic resonance angiography (MRA) uses inflow effects of blood in 2D and 3D TOF angiography or phase contrast technique in PC MRA. TOF MRA provides satisfactory images of extra and intracranial vasculature and is recommended for screening of aneurysms in asymptomatic patients. TOF MRA suffers from limitations like saturation effects and turbulence related signal loss. An ultra fast 3D gradient echo version is used for CE MRA which overcomes many of these drawbacks.26 The short TR nulls fat signal. Being fast, the sequence freezes motion and provides temporal (arterial and venous phases) and spatial resolution. This leads to better visualization of vascular bifurcations, distal vessels and quantification of stenosis and correlates better with other diagnostic modalities. CE MRA needs timing of the sequence with contrast bolus arrival so that data acquisition is in the center of the K space. This is achieved by rapid contrast infusion with power injector and sequence triggering with test bolus. PAT enabled neurovascular MR coils allow imaging of neck and intracranial vessels at one sitting (Figs 14A and B) and can be used in stroke protocols along with diffusion and

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Figs 12A and B: T2 TSE (A) and SWI (B); Patient of coagulopathy. The

Figs 13A and B: T2 TSE (A) and SWI (B); Glioblastoma multiforme.

left parietal hemorrhage shows significant blooming on SWI along with detection of multiple microbleeds compared to TSE

SWI image shows multiple tumor related vessels

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Figs 14A (AP) and B (oblique view): Contrast enhanced MR angiography showing a stenotic lesion of the right carotid artery, shown to advantage in anteroposterior view (arrow) (A)

Fig. 15: Time of flight MRA; Excellent angiogram due to background suppression and better flow related signal leading to better distal smaller vessel visibility

perfusion imaging. CE MRA also better evaluates intracranial aneurysms (particularly giant aneurysms) and post coiling follow-up of aneurysms. Improved vessel to background signal, higher visibility of gadolinium, higher resolution, larger FOV, K space reordering and keyhole techniques on 3T produces superior quality diagnostic angiograms with improved visualization of smaller vessels (Fig. 15).8 Time resolved CE MRA with sub-second temporal resolution and digital substraction has become feasible and initial results are exciting (Time resolved imaging of contrast kinetics, or TRICKS).27 Using parallel imaging, key hole acquisition and CENTRA K space sampling yields nearly isotropic volume acquisition. This allows direct observation of the fast hemodynamic changes associated with abnormal vasculature of AVM’s and directionality of flow in unilateral carotid occlusion syndromes.28 Generated MIP’s show the angioarchitexture of AVM in any spatial orientation with enough temporal resolution to differentiate between early arterial, arterial, parenchymal and venous phases (Figs 16A to G). When the technique fails to show smaller vessels, it can be combined with high spatial resolution MRA. Degree of stenosis and plaque morphology is important predictors of stroke. High resolution MR imaging is a developing technique. It can characterize atherosclerotic plaques for instability (irregularity and ulceration) with 81% sensitivity and 90% specificity thus facilitating prognosis and decision making of plaque stabilizing therapy.29

MR Cisternography Using CISS/SPACE

Steady State Variants of Gradient Echo Sequences The steady state GRE sequences being heavily T2 weighted (FISP, GRASS) are useful for myelography, cisternography and fetal imaging.

The steady state GRE sequences like FISP can suffer from destructive interference due to dephasing and rephasing pulses. To overcome this, the two sequences can be executed together with alternating RF pulses resulting in constructive interference in steady state (CISS). The 3D FSE (SPACE) and 3D CISS sequence are useful for MR cisternography, i.e. for evaluation of cerebellopontine angle lesions30 (Figs 17A to C), cranial nerve tumors and neurovascular compression, intraventricular tumors/cysts and neural/ inner ear anatomy for cochlear implants (Figs 18A and B). Thin sections, high resolution and 3D reconstructions offer additional information on these sequences.

Special MR Techniques in Medial Temporal Sclerosis MRI has been extensively used to depict various brain lesions causing epilepsy. T2 FSE, FLAIR and contrast enhanced T1 sequences adequately show the underlying structural lesion. Lesions of developmental origin like heterotopias can be shown to advantage by using accentuated T1 contrast images like inversion recovery. Hippocampal sclerosis (HS) is the most common cause of medial temporal lobe epilepsy (MTLE). Being refractory; often a surgical resection of hippocampus is contemplated for MTLE for which a proper diagnosis and correct lateralization is needed. Qualitative and quantitative assessment of hippocampus in MTLE has received a lot of attention in MR literature.31 Visual analysis of high resolution inversion recovery T1 or a 3D set of MP RAGE gradient echo are useful in showing atrophy of hippocampus (90–95% sensitivity). 32 These images provide good SNR, gray white matter contrast

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Figs 16A to G: 18-year-male with left thalamic AVM. (A to D) sequential arterial, nidus and venous enhancement (white arrows) on time resolved MRA. (E) High spatial resolution MRA – lateral MIP projection with corresponding DSA (F). On DSA left PCA run showing feeders (black arrow), nidus and draining veins (white arrowhead) similar to MRA (E). (G) T2 TSE axial section

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Figs 17A to C: Axial T2 FSE. (A) A small right acoustic schwannoma is barely made out from surrounding CSF. The lesion is much better shown with bright fluid CISS sequence on coronal and axial sections (B and C) (arrows)

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Figs 18A and B: One mm axial section (A) and reconstructed image (B) showing excellent anatomy of CP angle and inner ear

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Figs 19A and B: Coronal MP RAGE images showing left hippocampal volume loss (A) and increased signal intensity on T2 FSE coronal sections (B)

and are reproducible in multiple planes. Morphological assessment of abnormal increased signal on T2 FLAIR and FSE coronal sections (80–85% accuracy) can also be done along with other analysis of other features of HS. Special techniques: Hippocampal volume is calculated by summing cross-sectional area multiplied by section thickness and number of sections.32 Such measurements increase the accuracy however it has been reported that a good visual analysis correctly lateralizes atrophy in 94% identified with volumetry (Figs 19A and B). T2 relaxometry measures hippocampal T2 relaxation time (HRT) using a dual echo protocol using SE or FSE sequence. T2 value equals {TE(2) – TE(1)} divided by {lnS(1) – lnS(2)} where T(1) and T(2) are echo times at first and second echo and S(1) and S(2) are corresponding signal intensities. The sequence takes a long time (4–12 minutes). As the method

needs no external reference, it increases sensitivity and objectivity of T2 signal change interpretation and is a precise and reliable measurement as shown on surgical series. False negative and positive results have however been reported in nonsurgical series.33 Diffusion imaging has been tried in HS and an increase in ADC of water around 10% and decrease in anisotropy index has been described in HS.31

Echo Planar Imaging The ultrafast imaging technique EPI was originally described by Mansfield.33 The EPI technique involves very rapid gradient reversal (instead of the 180° pulse used in FSE) to acquire multiple phase encoding echoes that form a complete image in one TR during a single T2* decay (approximately 20–100 ms in brain). The frequency encoding is done by rapid movement

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of the gradients between positive and negative values. The phase encoding can be done by applying a constant low phase encoding gradient, by blipping the encode (blipped EPI) or spiraling the data acquisition path through K space (spiral EPI). EPI can be performed as a single shot technique or as a combination of multiple interleaved acquisitions (multishot EPI). Depending on data acquisition method, the EPI is labelled ‘spin echo’ EPI (90–180° pulse) or gradient echo EPI (90° pulse without refocusing). It can be variously prepared with inversion pulse, diffusion sensitized pulse, fat saturated and even as a 3D sequence. The EPI technique requires more efficient eddy current free gradient systems with short rise times and data acquisition software like fast ADC’s.

Clinical Applications of EPI EPI sequences being extremely fast allow study of dynamic processes and motion free images, i.e. brain scan of uncooperative patients, breath hold imaging of the abdomen and heart. The speed of the sequence practically freezes the physiological motion and allows newer applications like diffusion imaging, perfusion imaging, bolus tracking and functional task activation in real time.

Diffusion Studies Diffusion contrast depends on molecular motion of water. As initially described by Stejskal and Tanner in 1965, spin echo T2 EPI sequences can be sensitized to random diffusion of water molecules using bipolar gradients of equal magnitude and opposite polarity. The directional nature of net water movement of water in the white matter tracts (anisotropy) is depicted as signal loss on images by application of gradients in three orthogonal directions. This signal loss or diffusion weighting is determined by sequence specific parameter named ‘b value’ (depending on strength, duration and interval of DW gradient) and tissue specific diffusivity factor called ‘ADC coefficient’. Usually a ‘b value’ of 1000 sec/mm2 allows good diffusion weighting but it is used in tandem with a nonzero (20 sec/mm2) value for calculations. Anisotropic images can be combined to yield isotropic mean diffusivity TRACE images (Diffusion Weighted Imaging-DWI) which are used for evaluating stroke and other routine purposes. Alternately ADC maps can be calculated to yield true magnitude images. These remove the inherent T2 contrast in these images which cause interpretative problems.34 The primary use of DWI has been in brain imaging due to its exquisitely unique sensitivity for ischemic stroke. This noninvasive test for cerebral tissue viability came at a vital time when thrombolytic and neuroprotective agents were entering clinical practice. It is a FDI-approved sequence for routine stroke protocol in neuroimaging now. Diffusion changes are detectable within minutes of cerebral ischemia (as early as 20 minutes in humans). This is due to cytotoxic

edema (Na+/K– ATP pump failure) and squeezed extracellular compartment. DWI picks up infarcts with a sensitivity and specificity of 88–100% within 6 hours compared to conventional CT and MRI images which are abnormal only in less than 50% of cases (Figs 20A to G). Diagnosis of hyperacute infarction within this window period is vital for initiation of therapy. Infarcts appear bright on DWI (dark on ADC maps). The reduced ADC persists variably (usually ten days), returns to baseline and then remains elevated subsequently due to ensuing brain softening and gliosis. However, DWI changes may pseudonormalize after natural reperfusion or neuroprotective therapy within 1–2 days. DWI when assessed along with perfusion imaging is a better guide to treatment decisions and clinical outcome. DWI also has a role in the setting of acute on chronic ischemia, neonatal hypoxic injuries and venous thrombosis. More importantly DWI helps excluding stroke in an equivocal clinical setting, i.e. differentiating stroke from multiple sclerosis plaques and from other stroke mimics like vasogenic edema syndromes (hypertensive encephalopathy, eclampsia, meningioma cyclosporine toxicity, etc.) which are not associated with restriction of diffusion.34 The other uses of DWI are in diagnosing abscesses (Figs 21A and B), encephalitides and diffuse axonal injuries. All these conditions show high signal on DWI. It also help in characterizing tumors, i.e. differentiating epidermoids from cysts, by showing restricted diffusion in hypercellular tumors, i.e. lymphoma, malignant meningioma, differentiating necrotic from solid enhancing components, radiation necrosis from recurrent tumor (higher diffusion in necrosis) and postoperative cavity/cystic neoplasms from abscess in operated tumors.35

Diffusion Tensor Imaging (DTI, Tractography or Fiber Tracking) Dependency of molecular diffusion on the orientation of white matter fiber tracts (anisotropy) can be mapped spatially by acquiring relatively high-resolution DWI.35 Computer algorithms allow the generation of white matter fiber tract maps from the tensor data. Tensor is a map of directional vectors in 3D space and it is a mathematic construct that describes the properties of an ellipsoid. The data for tensor must be measured along six or more collinear directions by gradients (multidirectional diffusion weighting – MDDW6–256 directions). From this data, diffusion coefficients or eigen values along the three principle directions, eigen vectors defining the orientation of fibers and fractional anisotropy (FA) can be calculated (Fig. 22A). Thus, TRACE image (isotropic diffusion), ADC image (pure diffusion contrast from diffusion coefficients), FA maps with and without color codes (directional diffusion) and tensor image (calculated diffusion data with direction and velocity) are the data sets available for analysis from which fiber tracks can be constructed (Fig. 22B).

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Figs 20A to G: 42-year-female with acute onset left hemiparesis. (A) T2W image-subtle signal changes along the right insula (B) DWI–restriction in right MCA territory at the level of basal ganglia. Perfusion maps above the level of basal ganglia show normal color maps of CBV (C) decreased CBF (D) and raised MTT (E) in the right MCA territory. (F) DWI showed no concordant extent of restriction at the corresponding level (G) suggestive of DWI-PWI mismatch – evolving ischemic penumbra

Quantitative brain maps can be generated co-registering the 3D white matter fiber tracts on the anatomic images using Automated Image Registration Software. 3T due to its high SNR and reduced scan times allows sampling of high number of directions for DTI within an acceptable time. Higher b values enhance anisotropy effects helping more complex evaluations like fiber tracking and tensor imaging more so for trajectory of crossing fiber. Susceptibility effects can be overcome using PAT, radial imaging or PROPELLER.8

Clinical Applications DTI is valuable in assessment of white matter structural integrity and connectivity. Use of DTI has been incorporated by various groups into imaging protocols of stroke, trauma (to study DAI and its long-term effects) and multiple sclerosis (loss of anisotropy in damaged white matter) (Fig. 23). The disruption of fibers can be shown in all the above conditions.34,35 It has been used to study brain development

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Figs 21A and B: DW (A) and ADC (B) images show diffusion

Figs 22A and B: Directionally color coded FA map (A) and fiber

restriction in the abscess cavity in left temporal lobe (bright on DWI and dark on ADC)

tracking (B) showing corticospinal tracts

Fig. 23: Patient of multiple sclerosis with white matter subtle lesions on T2. FA data shows severe disruption of white matter anisotropy due to destruction of myelin

and included in a number of psychiatric protocols. The most advanced application is that of fiber tracking along with functional MRI to trace the connectivity of various areas of brain. Studies in schizophrenia have revealed disturbances of anisotropy which reflects possible functional disconnectivity. It can help surgical planning of tumors and when used along with cortical mapping technique, the entire functional unit can be shown. Some studies have also suggested that DTI can differentiate white matter tracts infiltrated with tumors (e.g. in high grade glioma) from those merely displaced (low grade tumor)35,36(Figs 24A and B).

Perfusion Weighted Imaging Perfusion weighted imaging (PWI) measures signal reduction induced in the brain during passage of injected paramagnetic

contrast agents which induce magnetic susceptibility effects (T2*).37 Intravascular compartmentalized contrast produces large magnetic field gradients across the vascular boundaries leading to reduction in T2* and loss of signal which relates to proportion of vascularity. Best results are achieved with gradient based EPI with 2 second sampling rate over a minute. This can be plotted as a time intensity curve or concentration time curve. Integration of area under this curve yields regional cerebral blood volume (rCBV). Similarly mean transit time (MTT), total blood flow (rCBF), time to arrival (TTA) or time to peak (TPP) can also be calculated. High field MR provides better results due to higher SNR, longer T2*, faster scans, parallel imaging and requirement of lower optimal contrast volumes.8 Brain perfusion can also be measured by spin labelling of arterial water by EPI signal tagging with alternating frequency (EPISTAR, ASL) or other techniques.38

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Figs 24A and B: (A) The tensor and anatomy fusion image showing displacement of intact white matter in perirolandic area by the lesion in right high frontal cortex – DNET; (B) Tensor+ anatomy fusion image – white matter infiltration by glioblastoma multiforme leading to loss of anisotropy

PWI in Stroke Ischemic brain after acute vascular occlusion shows reduced rCBV and elevated MTT and TTP as lack of signal drop after contrast arrival. The ischemic penumbra, i.e. ‘functionally impaired but not irreversibly damaged’ area around an established infarction is identified when areas of PWI and DWI defect are compared. A mismatch; perfusion defect being larger than diffusion abnormality as seen in large arterial occlusion, denotes viable tissue at risk. The neurological deficit will likely increase in such a situation and needs aggressive treatment. When there is a match between the two (PWI = DWI or PWI < DWI) infarct is presumed stable or already reperfused (Fig. 20). Thus, an MRI stroke protocol should include T2 FSE and FLAIR sections of brain followed by MRA, DWI, PWI and a GRE sequence for hemorrhage. This comprehensive protocol should take less than 15 minutes on a modern state of the art MR scans.37

PWI of Cerebral Tumors Tumor angiogenesis and vascularity determines biological aggressiveness of the cerebral neoplasms. These can be predicted by MR perfusion imaging. The technique is particularly useful for differentiating tumor necrosis from recurrent tumors (the former being avascular) and assesses response to treatment by antiangiogenetic chemotherapeutic agents (in terms of reduced rCBV post treatment). The rCBV correlates well with histological neovascularity and grades of gliomas. It progresses from lower values in low grade gliomas to high values in glioblastoma multiforme. PWI also acts as a guide in heterogenous tumors for biopsy from more aggressive areas for appropriate staging. These areas may not necessarily

show maximum enhancement on contrast enhanced MR or CT sections. Lymphomas show low vascularity and solitary metastases reduced perilesional contrast activity as compared to gliomas. Another possible role can be in atypical infections and demyelinating lesions mimicking neoplasms. Thus, PWI helps in diagnosing, characterizing and follow-up of brain neoplasms.37

Neuronal Activation Studies (fMRI) Ultra-high speed imaging decouples gross motion from BOLD contrast (blood oxygen dependant contrast) which is the result of local changes in blood flow in response to a variety of neuronal stimulation tasks. The oxygenated blood has longer T2*, thus appearing bright. Data is acquired using gradient based single shot EPI during an activation paradigm (e.g. 20 T2* images every 2–3 seconds for several minutes).39 Due to higher spatial and temporal resolution, noninvasive nature and being repeatable, it can replace other more invasive tests; for example, to decide laterality and localization of motor and sensory centers before corticectomy and other brain surgeries (see Functional Imaging) (Fig. 25).

Disadvantages Misregistration artifacts and ghosting of the fat due to low bandwidth used in EPI, image distortions and signal loss in areas like base of the brain due to susceptibility effects, noise and excess radiofrequency deposition are some disadvantages. However, these are reduced on modern scanners due to better coils, gradients and pulse designs, parallel imaging, spiral scanning and fat suppression.39 Prescans with field maps define areas of susceptibility and compensate for distortions.

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Section 1 Neuroradiology including Head and Neck

has been applied in multiple sclerosis to characterize plaques, determining total lesion load/response to treatment and predict clinical course.41 It has also been applied for studying myelination in developing brain, SLE, multisystem atrophy, amyotropic lateral sclerosis, schizophrenia, Alzheimer’s disease, etc. It is reliable in differentiating tuberculoma (low MTR) from pyogenic abscess and tumors.42 MT suffers from an increased imaging time (longer minimum TR) and significant inter-center variation of values as parameters vary under different experimental conditions. The technique avoids multiple contrast injections and coil positioning, thus reducing cost and examination time.

REFERENCES

Fig. 25: 35 years female with epilepsy; fMRI with hand motor paradigm shows BOLD activation in right precentral gyrus which is displaced anterolaterally by the parasagittal DNET. Neuro 3D automated image fusion of anatomy and functional data

Magnetization Transfer The contrast depending on exchange of magnetization between different tissues (i.e. water pool and macromolecular pool) is called magnetization transfer (MT) contrast. The macromolecules transfer magnetization to water protons leading to a decrease in their relaxation time and loss of signal. Off resonance pulses are added to the routine MR pulse sequences to suppress the macromolecular pool (around 1000–2000 Hz) with subsequent reduction in signal intensity of background tissue in brain.40 The effect can be used qualitatively in clinical imaging, i.e. suppression of the background tissue in cerebral MRA for better contrast and small vessel detection, achieve better conspicuity of contrast enhancing lesions and to increase the cord CSF contrast on T2* images of spine. The MT effect can be quantitatively measured from images acquired with and without MT pulse saturation and expressed in form of MT ratio (MTR): Mo – Ms/Mo × 100% where Mo and Ms are signal intensities without and with MT pulse. MTR can be measured at the region of interest or for the entire brain with pixel to pixel co-registration. Disorders of neural tissue often manifest as reduced MT ratios due to destruction of macromolecules (i.e. myelin). MT

1. Schenck JF, Kelley DAC, Marinelli L. Instrumentation: Magnets, coils, and hardware. In: Atlas SW (Ed): Magnetic Resonance Imaging of the Brain and Spine. Lippincott Williams & Wilkins: Philadelphia. 2009. pp. 2-24. 2. Pruessmann KP, Weiger M, Scheidegger MB, Boesiger P. “SENSE: Sensitivity encoding for fast MRI”. Magn Reson Med. 1999;42:952-62. 3. Sodickson DK, Manning WJ. “Simultaneous acquisition of spatial harmonics (SMASH): Fast imaging with radiofrequency coil arrays”. Magn Reson Med. 1997;38:591-603. 4. Lauenstein TC, Goehde MD, Herborn CU, et al. Whole body MR imaging: Evaluation of patients for metastasis. Radiology. 2004;233:139-48. 5. Runge VM, Case RS, Sonnier HL. Advances in clinical 3-tesla neuroimaging. Invest Radiol. 2006;41:63-7. 6. ScarabinoT, Nemore F, Giannatempo GM, et al. 3.0 T magnetic resonance in neuroradiology. Eur J Radiol. 2003;48:154-64. 7. Salvolini U, Scarabino T (Eds). Text book of ‘High field brain MR’, Springer-Verlag, Berlin, Hiedelberg. 2006. 8. Kuhl CK, Träber F, Schild HH. Whole-body high-fieldstrength (3.0-T) MR imaging in clinical practice. I Technical considerations and clinical applications. Radiology. 2008;246: 675-96. 9. Lin W, An H, Chen Y, et al. Practical considerations for 3T imaging. Magn Reson Imaging. Clin N Am. 2003;11:615-39. 10. Frayne R, Goodyear BG, Dickhoff P, et al. Magnetic resonance imaging at 3.0 Tesla: Challenges and advantages in clinical neurological imaging. Invest Radiol. 2003;38:385-402. 11. Bradley WG, Chen DY, Atkinson DJ, et al. Fast spin echo and echo planar imaging. In: Stark DD, Bradley WG (Eds): Magnetic resonance imaging. St Louis, Mosby. 1999. 12. Kieffer B, Grassner J, Hausmann R. Image acquisition in a second with half Fourier acquired single shot turbo spin echo. J Magn Reson Imaging. 1994;4:86. 13. Gao JH, Xiong J, Lai S, et al. Improving the temporal resolution of functional MR imaging using key hole technique. Magn Reson Med. 1996;35:854-60. 14. Forbes KP, Pipe JG, Bird CR, et al. PROPELLER MRI: Clinical testing of a novel technique for quantification and

Chapter 5 Advances in Neuroimaging Techniques: Magnetic Resonance Imaging

15. 16.

17.

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20.

21.

22.

23. 24.

25.

26.

27.

28.

compensation of head motion. J Magn Reson Imaging. 2001;14:215-22. Hennig J, Nauerth A, Friedburg H. Rare imaging a fast imaging method for clinical MR. J Magn Reson Med. 1986;3:823-33. Jones KM, Mulken RV, Schwartz RB, et al. Fast spin echo MR imaging of the brain and spine: Current concepts. Am J Roentgenol. 1992;158:1313-20. Mugler JP III, Bao S, Mulkern RV, et al. Optimized singleslab three-dimensional-spin-echo MR imaging of the brain. Radiology. 2000;216:891-9. De Coene B, Hajnal JV, Gatehouse P, et al. MR of the brain using fluid-attenuated inversion recovery (FLAIR) pulse sequence. Am J Neuroradiol. 1992;13:1555-64. Okuada T, Korogi Y, Shigematsu Y, Sugahara T, et al. Brain lesion: When should fluid attenation inversion recovery sequence be used in MR evaluation? Radiology. 1999;212:793-8. Rumboldt Z, Marotti M. Magnetization transfer, HASTE and FLAIR imaging. Magn Reson Imaging Clin N Am. 2003;11: 471-92. Eberhardt KEW, Hollenbach HP, Tomandl B, Huk WJ. Three dimensional MR myelography of the lumbar spine: Comparative case study to X-ray myelography. Eur Radiol. 1997;7:737-42. Haase A, Frahm J, Matthaei D, et al. FLASH imaging – rapid imaging using low flip angle pulses. J Magn Reson. 1986;67:1256-66. Haase A. “Snapshot FLASH MRI. Applications to T1, T2 and chemical shift imaging.” Mag Reson Med. 1990;13:77-89. Haacke EM, Mittal S, Wu Z, et al. Susceptibility-WeightedImaging: Technical aspects and clinical applications, Part I. 2009;30:19-30. Mittal S, Wu J, Neelavalli EM, Haacke EM. SusceptibilityWeighted-Imaging: Technical Aspects and Clinical Applications, Part II. Am J Neuroradiol. 2009;30:232-52. Sohn CH, Sevick RJ, Frayne R. Contrast-enhanced MR angiography of the intracranial circulation. Neuroimag Clin N Am. 2003;11:599-14. Korosec FR, Frayne R, Grist TM, et al. Time-resolved contrast-enhanced 3D MR angiography. Magn Reson Med. 1996;36:345–51. Taschner CA, Gieseke J, Thuc VL, et al. Intracranial Arteriovenous Malformation: Time–Resolved Contrast-Enhanced

29.

30.

31.

32. 33. 34. 35.

36. 37. 38.

39.

40. 41.

42.

MR Angiography with combination of parallel imaging, keyhole acquisition and k-space sampling techniques at 1.5 T. Radiology. 2008;246; 871-9. Hatsukami TS, Ross R, Polissar NL, Yuan C. Visualization of fibrous cap thickness and rupture in human atherosclerotic plaques in vivo with high resolution magnetic resonance imaging. Circulation. 2000;102:959-64. Stuckey SL, Harris AJ, Mannolini SM. Detection of acoustic schwannoma: Use of constructive interference in steady state three dimensional MR. Am J Neuroradiol. 1996;17:1219-25. Paesschen WV. Quantitative and qualitative imaging of the hippocampus in mesial temporal lobe epilepsy with hippocampal sclerosis. Neuroimag Clin N Am. 2004;14: 373-400. Roberts N, Puddephat MJ, McNulty V. The benefit of stereology for quantitative radiology. Br J Radiol. 2000;73:679-97. Mansfield P, Pykett IL. Biological and medical imaging by NMR. J Magn Reson. 1978;29:355-73. Schaefer PW, Grant PE, Gonzalez RG. Diffusion-weighted imaging of the brain. Radiology. 2000;217:331-45. Sundgren PC, Dong Q, Go’mez-Hassan D, Mukherji SK, et al. Diffusion tensor imaging of the brain: Review of clinical applications. Neuroradiology. 2004;46:339-50. Bammer R, Acar B, Moseley ME. In vivo MR tractography using diffusion imaging. Eur J Radiol. 2003;45:223-34. Cha S. Perfusion MR imaging: Basic principles and clinical applications. Magn Reson Imaging Clin N Am. 2003;11:403-13. Wang J, Alsop DC, Li L, et al. Comparison of quantitative perfusion imaging using arterial spin labeling at 1.5 and 4.0 Tesla. Magn Reson Med. 2002;48:242-54. Thulborn KR. Clinical fMRI. In: Atlas SW (Ed): Magnetic Resonance Imaging of the Brain and Spine. Lippincott Williams and Wilkins: Philadelphia. 2009. pp. 1786-804. McGowan JC. The physical basis of magnetization transfer imaging. Neurology. 1999;53(5 suppl 3):S3-7. Santos AC, Narayanan S, de Stefano N, et al. Magnetization transfer can predict clinical evolution in patients with multiple sclerosis. J Neurol. 2002;249:662-8. Gupta RK, Hussain M, Vatsal DK, Kumar R, Chawla S, Hussain N. Comparative evaluation of magnetization transfer imaging and in vivo proton MR spectroscopy in brain tuberculomas. Magn Reson Imaging. 2002;20:375-81.

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CHAPTER

Magnetic Resonance Spectroscopy Niranjan Khandelwal, Paramjeet Singh

INTRODUCTION

PRINCIPLE

Nuclear magnetic resonance (NMR) and spectroscopy were introduced as experimental techniques as a method of delineating structure and composition of various physical and chemical materials. Subsequently, it was found to have many applications in medicine and in vivo magnetic resonance spectroscopy (MRS) evolved as a noninvasive technique to determine the molecular metabolites in any given living tissue. The metabolites are measured due to their slightly different magnetic frequencies or chemical shifts.1 The MR spectroscopy can be considered as a method of molecular imaging. Since in many pathologic processes, metabolic changes precede anatomic changes during disease progression and treatment, MRS offers a method for early detection of new disease and can influence the therapeutic success or failure.2 In simple words, when electromagnetic energy of a certain wavelength or frequency is allowed to impinge on a tissue sample, it either absorbs or emits the energy. Through the distribution and intensities of this measurable energy, information about the physical and chemical properties of the tissue sample is obtained in the form of the spectrum called MRS. The nuclei with an odd number of protons and neutrons, such as hydrogen-1 (1 proton), phosphorus-31 (15 protons and 16 neutrons), carbon-13 (6 protons and 7 neutrons), fluorine-19 (9 protons and 10 neutrons), have a magnetic moment and interact with the external magnetic field and are commonly observed in MR spectroscopic studies. 3 Unfortunately, MRS can detect metabolites or chemicals in concentration more than 0.1 mM and hence is limited in term of metabolites it can monitor. This is one of the major reasons that hindered the growth of MRS in clinical setting in spite of its many promises. With the introduction of improved localization techniques, many facets of the origin of the metabolites and their role in the normal function and pathologic process are opening up.

Magnetic resonance imaging (MRI) and MRS are based on same fundamental principles inspite of many differences.4 MRI provides anatomic information as a visual image whereas MRS obtains chemical information as a “spectrum” or numerical values. The simple MRI sequence block contains slice excitation by RF pulse followed by application of slice encoding, phase encoding, and frequency encoding gradients in mutually orthogonal planes. Whereas, in a classical spectroscopic imaging sequence, the MRS signal is acquired without a frequency-encoding gradient. Consequently, in contrast to MRI, the acquired MRS signal contains different frequencies that correspond to the chemical shift and not to the spatial origin of the signal. The amplitude of chemical shifts of various metabolites depends on the gyromagnetic ratio of the nuclei and intensity of external magnetic field (Table 1). So, at a given external magnetic field, every chemically distinct nucleus resonates at a slightly different frequency—the chemical shift—giving rise to separate peaks in the MR spectrum. By the same principle, in a given

Table 1:  MRS: Properties of nuclei Nucleus

Spin quantum number

1

H

Natural abdudance (%)

Gyromagnetic ratio (MHz/T)

Resonance frequency (MHz) at 1.5T

1/2

100

42.6

63.9

31

1/2

100

17.2

25.9

19

1/2

100

40.1

60.1

23

3/4

100

11.3

16.9

14

3/2

99.6

3.1

4.6

39

K

3/2

93.1

2.0

3.0

7

Li

3/2

92.6

16.5

24.8

1/2

1.1

10.7

16.1

P F Na N

13

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Chapter 6 Magnetic Resonance Spectroscopy

standard chemical environment increasing the external magnetic field strength transforms into better separation of signal frequencies of various metabolites in MR spectrum. J coupling or spinspin coupling is due to interactions with a neighbouring nuclear spin and provides additional information.

a known chemical like NAA at 2.0 ppm is used as chemical shift reference. The ppm scale describes the shifts in hertz from a reference peak divided by frequency of excitation. For example, 31P-MRS acquired at 1.5 T shows resonance frequency at 25.86 MHz and 25.86 Hz is 1 ppm. The ppm scales provides easy comparison of data obtained in different fields.

Spectrum

Spectrum and Echo Time

An MRS provides in vivo biochemical information represented as spectrum with the peaks in the spectra obtained correspond with various metabolites. The horizontal axis (abscissa) represents resonance frequency as parts per millions to the total resonance frequency. The vertical axis plots the relative signal amplitude or concentrations for various metabolites. The sharpness of the peak and line width is affected by (a) homogeneity of the external magnetic field, (b) magnetic field inhomogeneity due to susceptibility gradient and (c) T2 time of the sample (long T2 causes narrowing of the line). The MR spectra are analyzed in the following format (Fig. 1). 1. Center of the resonance frequency in ppm 2. Peak height 3. Line width at half-height 4. Peak area and shape 5. Composition of the peaks, e.g. single, doublet, triplet. The standard conventions to display MR spectra include: a. Up-field is to the right represents lower frequencies and are shielded b. Down-field is to the left represents higher frequencies and are deshielded. c. Chemical shifts (in ppm) is positive going to the left and is negative towards the right. Zero setting is done by RF of a particular compound, e.g. phosphocreatine for 31P-MRS and tetramethylsilane (TMS) for 1H and 13C MRs (at 4.8 ppm). Since TMS is not seen in vivo

The metabolites and their spectral pattern that can be identified with proton MRS are dependent on the echo time (TE). At 1.5T, metabolites visualized utilizing intermediate to long TE (144–288 ms) include N-acetylaspartate (NAA), choline (Cho), creatine (Cr), possibly alanine (Ala), and lactate. Short echo-time acquisitions (TE 70% stenosis and asymptomatic patients with >60% stenosis according to NASCET technique of stenosis measurement.43-45 The initial screening is done by a noninvasive technique, i.e. either ultrasound or MRA. Both the techniques have shown similar sensitivity in identifying critical stenosis at the carotid bifurcation. In view of its operator dependence, we feel that MRA should be the initial screening modalities; most patients would undergo catheter angiography for confirmation of stenosis and for ruling out any tandem lesions. Recent literature shows that in case

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Chapter 8 Imaging and Interventions in Cerebral Ischemia

the results of Doppler and MRA are concordant, catheter angiography can be avoided.40-42,47 However, one should be clear about the reliability of Doppler studies and MRA in one’s center before such approach is followed. In addition, MRA in such a situation must be extended to include the entire cervical ICA and circle of Willis to look for associated lesions. Some reports have indicated that noninvasive imaging alone, in spite of its lack of 100% accuracy in identifying critical stenosis, may be the best approach for preoperative carotid artery evaluation in asymptomatic patients.61

Arterial Dissection Dissection of the internal carotid artery is an important cause of stroke in young patients, responsible for up to 20% of all cases of stroke in young.62 As a whole, arterial dissection is the cause of stroke in about 3% of all cases. It may be spontaneous or may occur secondary to blunt or penetrating trauma to the vessel. Catheter angiography has been traditionally used for the diagnosis of carotid dissection (Figs 18 to 20). Typical findings on angiogram include long segment tapering/ narrowing of the cervical ICA extending from just beyond the carotid bulb to the base of skull. With the development of MRI and MRA, it is now possible to diagnose arterial dissection noninvasively.63 Apart from demonstrating luminal changes; wall hematoma can also be directly visualized. Associated pseudoaneurysms, if present, can also be visualized. Catheter angiography is needed only if any additional information is required.

Aortoarteritis Aortoarteritis is an important cause of stroke in young and middle-aged female patients in India. Clue to the diagnosis is usually evident in the form of differential limb pulses/blood pressures or hypertension due to renal artery involvement. Catheter angiography is invariably required for complete assessment in these patients as multiple vascular systems are usually involved. By virtue of its ability to visualize arterial wall, ultrasound serves as an excellent modality to document carotid arterial wall thickness and monitor response to medical therapy.

Fibromuscular Dysplasia Catheter angiography (Fig. 21) remains the investigation of choice for diagnosis of FMD for two reasons. One is that due to irregular areas of stenosis and dilatation seen in most cases of FMD, the flow pattern in the vessels is complex and, therefore, liable for misinterpretation by Doppler or MRA.62 Secondly, FMD is known to be associated with intracranial aneurysms in up to 21–51% of cases. 62 Therefore, these patients merit a pan-cerebral angiography to detect incidental aneurysms.

Other Vasculopathies This is an important, though uncommon, heterogeneous group of conditions, which can present with ischemic or hemorrhagic stroke. The diagnosis may be suggested by the related clinical features, e.g. stroke in young, stroke in the setting of disorders known to cause vasculitis or features suggestive of involvement of other organ systems, e.g. skin, kidneys, etc. Vascular imaging in these patients is needed to reach the diagnosis, to suggest areas suitable for biopsy, and to monitor response to treatment. Catheter angiography is almost invariably required to assess the intracranial circulation. Sometimes, however, MRI and MRA may provide sufficient information needed for diagnosis, e.g. in Moya Moya disease (Figs 22A to D), particularly in the very young.

Hemorrhagic Stroke Intracranial hemorrhage in hypertensive, elderly patients at typical sites, e.g. putamen, thalamus or posterior fossa is invariably assumed to be secondary to rupture of micro- aneurysms (Bouchard aneurysms) produced by hypertension. In majority of other patients presenting with intracranial bleed, DSA is the modality of choice to visualize indolent vascular malformation or aneurysm as the cause of bleed, particularly when surgical intervention is warranted as a life-saving measure. Other causes of spontaneous intracranial hemorrhage, including bleeding diathesis, cerebral amyloid angiopathy, granulomatous angitis, CNS SLE, tumor bleed, vasculitides, cavernomas, venous angiomas and its associations, venous sinus thrombosis, antiphospholipid syndrome, drug abuse, etc. should be kept in mind and appropriate investigations such as DSA, MRI, biochemical/hematological or immunological studies should be done to ascertain the underlying cause of bleed. In a recent study from Taiwan, up to 16% of cases otherwise thought to be spontaneous and not necessitating an imaging study were found to be harboring a vascular lesion. It must be remembered that the imaging has to be of the highest quality and on occasions done with hyperselectivity to pickup microangiomas64 or else one could easily overlook many of the above-listed pathologies. Spontaneous bleed simultaneously to two sites or at same site at two different times is also reported.64 There are even some lesions, such as old infarcts and lacunas with hemosiderin (picked up on SWI sequences) which are the evidence of past hemorrhages and indicators of possible sites of future hemorrhages.65

RECANALIZATION STRATEGIES New thrombolytic and neuroprotective therapies are being developed to treat acute ischemic infarction. Although these therapies may salvage ischemic but viable tissue, they are associated with risks such as intracranial hemorrhage. It is

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3 hours of acute ischemic stroke onset.66 In this study there was a trend towards improved outcome despite the presence of early CT hypodensity. The beneficial effects occurred in all subtypes of stroke including suspected lacunar infarction and were sustained at 1 year. There were 12% absolute (30% relative) differences in 2 groups in patients having minimal or no disability at 3 months (32% vs. 44%). Mortality rate of 17% vs. 25% was insignificant and symptomatic intracerebral hemorrhage within 36 hours was reported as 6.4% vs. 0.6%. In both the PROACT II and NINDS trial, the rate of intracerebral hemorrhage was greater in the drug versus placebo group; yet clinical outcomes were significantly improved in those patients receiving fibrinolytic therapy.67

In this trial, higher TPA dose of 1.1 mg/kg (maximum 100 mg) was used, of which 10% of the total dose was used as bolus. This study showed an increased risk of fatal parenchymal hemorrhage (30% vs. 6.5%) after IV thrombolysis administered within 6 hours (median time of 4 hours) of stroke onset, in patients with initial CT findings of a greater than one-third MCA territory hypodensity or sulcal effacement. Because of this, many still consider these findings to be a contraindication to thrombolytic therapy. Unacceptable increased risk of ICH may be attributed to various reasons, such as (i) increased dose, (ii) increased therapeutic window and (iii) inclusion of large number (17%) of patients with protocol violations—unrecognized abnormality on pretreatment CT. This, however, did not statistically affect significant outcome. However, the results of subsequent studies with use of the one-third rule showed poor interobserver correlation.19 The Alberta Stroke Program Early CT Score (ASPECTS) was proposed in 2001 to quantitatively assess acute ischemia on CT images by using a 10-point topographic scoring system.71 Tested NINDS dose of 0.95 mg/kg, administered within 6 hours of stroke onset was still as safe as within 3 hours, although no statistical benefit could be confirmed as compared with a placebo. This study confirmed the

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Chapter 8 Imaging and Interventions in Cerebral Ischemia

importance of the extent of hypodensity as a major risk factor for severe hemorrhagic transformation. Intravenous TPA therapy requires careful patient selection. Fresh blood is needed for rapid effective fibrinolysis even with TPA. I/V thrombolysis remains a very beneficial effective therapy. But it is not completely adequate in many cases. The ultimate role of I/V thrombolysis may be an initial therapy. Emergency DSA would then be performed and patients with demonstrable thrombus would then undergo local I/A thrombolysis.

INTRA-ARTERIAL THERAPY The safety and benefits of intraarterial cerebral fibrinolytic therapy (Figs 23A and B) has  been supported by various multiple anecdotal reports and small nonrandomized or controlled series in acute ischemic stroke.67-69 Proact I: Results of the first Prolyse in Acute Cerebral Thromboembolism (PROACT I) trial was published in 1998.68 The trial tested the recanalization efficacy and safety of IA recombinant pro-urokinase (r-proUK) in patients with acute ischemic stroke of less than 6 hours duration caused by middle cerebral artery occlusion. Patients with TIMI grade 0 or 1 with occlusion of M1/M2 were included in the trial. The dosage of r-proUK (6 mg) or placebo over 120 minutes was administered into proximal thrombus face along with IV heparin. Recanalization efficacy assessed at the end of 2 hours infusion and ICH causing neurological deterioration assessed at 24 hours. Recanalization rates were 58% (partial or complete) versus 14% for placebo and this difference was significant. Hemorrhagic transformation causing neurological deterioration within 24 hours of treatment was 15.4% in r-proUK and 7.1% of placebo. Both recanalization and hemorrhage frequencies were influenced by heparin dose. However, neurological outcome was not significant.

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CSBODIFT

PROACT II: First randomised controlled trial published in 1999.69 One hundred eighty patients with proximal middle cerebral artery (MCA) occlusions were enrolled and treated within 6 hours of the onset of stroke. Patients were randomised in a 2:1 ratio to receive 9 mg recombinant prourokinase infused into MCA over 2 hours with heparin low dose (2000 U bolus followed by 500 U/hours infusion) × 4 hours (n = 121) or placebo and low dose heparin (n = 59) alone. Arterial recanalization was achieved in 66% of patients who received recombinant prourokinase and 18% of controlled group. Despite an increased risk of early intracerebral hemorrhage in the patients who received recombinant prourokinase (27.8% vs. 5.5% within 24 hours), 90 days mortality rates were not significantly different between the two groups (24% r-proUK vs. 27% control). This is the first randomised acute stroke trial to show a benefit of therapy as long as 6 hours after the onset of stroke. The PROACT II trial has, however, validated intraarterial fibrinolytic therapy for treatment of selected acute nonhemorrhagic stroke within 6 hours time to treatment (TTT) window. The median time for recanalization after start of thrombolytic therapy was about 2 hours. The results of this trial are convincing evidence that intra-arterial thrombolytic therapy can now be considered an acceptable and appropriate therapy for acute stroke. This will help pave the way for FDA approval for what has been to this time an experimental approach to stroke care.

Technique No glucose-containing fluids are given. Oxygen is continuously given by facemask (2–4 L/min). Routine blood tests including complete blood count, urea, creatinine, electrolytes, glucose, platelets and PTT are performed. Access is made through a 6-F neurosheath. An initial angiogram is performed to assess exact location of occlusion and to assess hemodynamics of cerebral perfusion. The target vessel is catheterized last to allow adequate assessment of collateral supply. This information is useful in planning the strategy of rescue, knowing how much time is available and also to determine the risk of the procedure. Heparin is given in a bolus dose of 5,000 U followed by 1,000 U/hour for 2 hours or until the end of the procedure. This provides an effective heparin level of 2 cm in diameter). Osteoblastomas occur in young adults, with 90% of cases diagnosed in the 2nd and 3rd decades of life. There is a male predominance (2:1). Clinical symptoms often differ from those of osteoid osteoma, with osteoblastoma producing dull localized pain and neurologic symptoms, including paresthesias, paraparesis and paraplegia. Scoliosis occurs less frequently with osteoblastoma than with osteoid osteoma and may be convex toward the side of the tumor.

Osteoblastoma of the spine accounts for 30–40% of all osteoblastomas and the lesions are equally distributed in the cervical, thoracic and lumbar segments.52 Osteoblastoma most frequently involves the posterior vertebral elements (55% of cases), although extension into the vertebral body is also common (42%).45,49 Osteoblastoma confined to only the vertebral body is rare. Pathologically, the typical osteoblastoma is larger than 1.5–2.0 cm in diameter. Histological examination may reveal features very similar to those of osteoid osteoma (interconnecting trabecular bone and fibrovascular stroma), but overall the microscopic pattern is not as well organized as that seen in osteoid osteomas. Three radiographic patterns have been described with osteoblastoma.52 The first, which consists of a central radiolucent area (with or without calcification) and surrounding osseous sclerosis, is similar to the radiographic appearance of osteoid osteoma, but the lesion is larger than 1.5 cm in diameter. The second, an expansile lesion with multiple small calcifications and a peripheral sclerotic rim, is the most common appearance of spinal osteoblastomas (Fig. 13).53 The third pattern has a more aggressive appearance, consisting of osseous expansion, bone destruction, infiltration of surrounding soft tissue and intermixed matrix calcification. Mineralization within an osteoblastoma may have the radiological appearance (rings and arcs) of chondroid matrix. At CT, the lesion shows areas of mineralization, expansile bone remodeling and sclerosis or a thin osseous shell about its margins. MRI appearance of osteoblastoma is generally

Chapter 33 Imaging of Spinal Neoplasms

Fluid-fluid levels have been described in association with telangiectatic osteosarcoma. 42,56,58 As opposed to ABCs, telangiectatic osteosarcomas with prominent fluid-filled hemorrhagic spaces are characterized by thick, solid nodular tissue surrounding the cystic spaces, matrix mineralization and a more aggressive growth pattern.58 Patients with osteosarcoma of the spine should be treated with a combination of chemotherapy and at least marginal excision (assuming the tumors are surgically accessible).59 Postoperative radiation therapy may be of benefit in selected patients.58

Osteochondromas Fig. 13:  Osteoblastoma. Axial computed tomography (CT) of the

dorsal spine reveals expansile lesion of left pedicle and lamina of D6 vertebra with small foci of mineralized matrix

nonspecific, with low-to-intermediate signal intensity seen on T1WI and intermediate-to-high signal intensity seen on T2WI.52 MRI optimally depicts the effects of the tumor on the spinal canal and surrounding soft tissues and extensive peritumoral edema has been reported.54 At bone scintigraphy, osteoblastoma demonstrates marked radionuclide uptake. Treatment of spinal osteoblastoma is surgical resection and the recurrence rate for conventional lesions is 10–15%.52,55 The diagnosis of aggressive osteoblastomas is important because they have a far greater recurrence rate (approaching 50%), which is probably related to their larger size and the resultant inability to perform complete resection.55

Osteosarcoma Only 4% of all osteosarcoma involve the spine. 56 Peak prevalence occurs during the 4th decade of life.56 Patients may present with pain, signs of neurologic compression and a palpable mass.57 The thoracic and lumbar segments are equally involved, followed by the sacrum and the cervical vertebral column.56 In most cases, the posterior elements are primarily involved, but secondary extension into the vertebral body is also common.56 Pathologically, conventional osteosarcoma is a highgrade malignant osteoblastic lesion with varying amount of osteoid production, cartilage or fibrous tissue.56 Radiographs of spinal osteosarcoma usually reveal densely mineralized matrix and an ivory vertebral body may be recognized.56,57 Purely lytic lesions have also been encountered, although infrequently and are difficult to distinguish from other solitary lesions of the spine.56 Lesions with large amounts of matrix mineralization may remain lowsignal intensity on all MR images, regardless of pulse sequence.

Spinal osteochondromas are uncommon, representing only 1–4% of solitary exostoses and constituting 4% of all solitary spinal tumors.60 In patients with hereditary multiple exostoses, only 7–9% of patients have a spinal lesion and usually there is only one spinal osteochondroma despite the multiplicity of lesions throughout the remainder of the skeleton.61 Spinal osteochondromas are usually discovered during the 3rd and 4th decades of life when solitary and 1 decade earlier in patients with hereditary multiple exostoses.60,61 There is a male predominance, which is more striking, in solitary osteochondroma than in hereditary multiple exostoses. Osteochondromas have been encountered at all levels of the spine, but they have a predilection for the cervical spine, particularly C2. Lesions most commonly arise from the posterior elements, although some originate from the vertebral body as well. Osteochondromas are composed of normal bone (cortex and marrow space) with a cartilage cap from which growth occurs. The pathologic and radiologic hallmark of osteochondroma is continuity of the lesion with the marrow and cortex of the underlying bone. Spinal osteochondromas may be sessile or pedunculated. The diagnosis of spinal osteochondroma can be definitively made from radiographic findings in only a minority of cases (21%), usually in large lesions protruding posteriorly from the spinous process where cortical and marrow continuity is easily assessed.60 Thin-section CT is the radiological examination of choice for detecting the osseous characteristics of the exostosis and the pathognomonic marrow and cortical continuity of the lesion to the underlying bone. MRI often reveals yellow marrow centrally (which has high-signal intensity on T1WI and intermediate-signal intensity on T2WI) with a lowsignal-intensity cortex. The hyaline cartilage cap is often small and thin, with low-to-intermediate signal intensity on T1WI and high-signal intensity on T2WI. In adults, spinal osteochondromas with marked thickening (> 1.5 cm) of the cartilage cap should be viewed with suspicion of malignant transformation to chondrosarcoma. Surgical excision of osteochondroma is usually curative.

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Chordoma Chordoma is the most common non-lymphoproliferative primary malignant tumor of the spine and accounts for 2–4% of malignant osseous neoplasms.35 These arise from notochordal rests, and therefore, almost always occur in a midline or paramedian location in relation to the spine. Nearly, 50% of all chordomas originate in the sacrococcygeal region, particularly in the 4th and 5th sacral segments.35 Another 35% are in the spheno-occipital region; only 15% of chordomas occur in the spine above the sacrum. Men are affected twice as frequently as women; the mean age of patients is 50 years.35 Chordomas are slow-growing tumors that are commonly discovered as large masses. As they enlarge, they tend to involve adjacent vertebral bodies and extend into the adjacent paraspinal tissues and epidural space; they may even grow into and expand neural foramina, potentially mimicking nerve sheath tumors.62 Uncommonly, they can arise solely in the musculature of the perivertebral space, presumably from extraosseous notochordal nests.62 Pathologically, typical chordomas contain clear cells with intracytoplasmic vacuoles (physaliphorous cells) and abundant mucin, both intracellular and extracellular. In atypical or dedifferentiated chordomas, the mucinous matrix is replaced by chondroid or osteoid elements.35 The most suggestive manifestation is a destructive lesion of a vertebral body associated with a soft-tissue mass with a “collar button” or “mushroom” appearance and a “dumb-bell” shape, spanning several segments and sparing the disks.63 Areas of amorphous calcifications are noted in 40% of chordomas of the mobile spine and in up to 90% of sacrococcygeal lesions. 41 Most chordomas are iso-/ hypointense relative to muscle on T1WI. The focal areas of hemorrhage and high-protein content of the myxoid and mucinous collections may account for the high-signal intensity on T1WI. 41 On T2WI, most chordomas have a high-signal intensity due to the presence of their signature physaliphorous cells (clear cells with intracytoplasmic vacuoles and abundant mucin).35 The fibrous septa that divide the gelatinous components of the tumor are seen as areas of low-signal intensity on T2WI. The presence of hemosiderin also accounts for the low-signal intensity seen on T2WI. This MRI feature has been reported in 72% of sacrococcygeal chordomas but is rare in spinal chordomas.64 After the injection of gadolinium-based contrast material, most tumors demonstrate moderate heterogeneous enhancement, but ring and arc enhancement and peripheral enhancement have also been described.63 Chordomas generally have a poor prognosis due to local recurrence following resection.

Chondrosarcoma Chondrosarcoma is a malignant cartilage-producing neoplasm. It is the second most common non-lymphoproliferative

primary malignant tumor of the spine following chordoma. The patient may present with pain, neurological symptoms and a palpable mass. The peak incidence is in the 5th decade, with men affected 2–4 times more frequently than women. The spine is affected in 3–12% of cases.45 Chondrosarcomas are seen at all levels of the spine, although the thoracic spine is the most common site. Chondrosarcoma originates in the vertebral body (15% of cases), posterior element (40%), or both (45%) at presentation.41 Chondrosarcoma of the spine is usually a relatively lowgrade lesion (either grade I or grade II), which likely accounts for the long-term survival of many patients. Most lesions represent primary chondrosarcoma; however, secondary chondrosarcoma may also occur when osteochondroma (solitary or multiple with hereditary multiple exostoses) undergoes malignant transformation. Chondrosarcomas of the spine usually manifest as a large, calcified mass with bone destruction.41 The characteristic chondroid matrix mineralization (rings and arcs) may be evident on radiographs, but better evaluated with CT. Calcified matrix is detected as areas of signal void at MRI. The nonmineralized portion of the tumor has low attenuation on CT scans, low-to-intermediate signal intensity on T1WI and very-high-signal intensity on T2WI due to the high-water content of hyaline cartilage.65 An enhancement pattern of rings and arcs at gadolinium-enhanced MRI reflects the lobulated growth pattern of these cartilaginous tumors. Extension through the intervertebral disk has been reported in 35% of cases.66 Chondrosarcoma arising from osteochondroma is seen as thickening at the peripheral cartilaginous cap and large masses may also develop at this site. Treatment of spinal chondrosarcoma is surgical resection and vertebral corpectomy with strut bone grafting may be necessary. Radiation therapy is also used as adjunct treatment, but its effectiveness is controversial.

Chondroblastoma Chondroblastoma is a benign cartilaginous neoplasm with a predilection for the growing skeleton. Chondroblastoma of the vertebral column presents in the 3rd decade of life, a decade later than its appendicular counterpart. There is a male predominance (2–3:1, male-to-female ratio). Back pain is the most common symptom.67 However, neurologic symptoms may occur when the spinal canal or foramina are invaded. The tumor involves the vertebral body and posterior elements.68 The tumor shows aggressive features at imaging, with bone destruction and a soft-tissue mass but no surrounding bone edema. In other cases, CT may demonstrate a geographic lesion with sclerotic borders.67 Most lesions have hypointense areas on T2WI. Low-signal intensity on T2WI is associated with immature chondroid matrix, hypercellularity, calcifications and hemosiderin at histologic analysis.69

Chapter 33 Imaging of Spinal Neoplasms

EPIDURAL LESIONS Angiolipoma Spinal angiolipomas are rare lesions usually found in the epidural space of the thoracic spine.70,71 Mean age of occurrence is 42.9 years (range 10 days to 85 years) with most patients presenting with slowly progressive symptoms of spinal cord compression. Most of these lesions are found in adults and in the thoracic region. Spinal angiolipomas are typically located in the posterior and lateral aspects of the epidural space. However, infiltrating forms of tumor are generally in the anterior epidural space.70 On MRI, angiolipomas are predominantly hyperintense on T1WI and inhomogeneous owing to interspersed vascular elements (Figs 14A to D). A high-vascular content is correlated with the presence of large-hypointense regions on T1WI. These masses are hyperintense on T2WI.70 The larger tumors may result in compression of the spinal cord. Intramedullary angiolipomas have been rarely described (Figs 15A to C).70

A

B

C

D

Epidural Lipomatosis This entity, although not a tumor, may behave as one and result in compression of neural elements and thus is discussed here. The most common cause of epidural lipomatosis is prolonged therapy with glucocorticoids, only a very few cases are related to endogenous Cushing’s syndrome.72 Epidural lipomatosis may also be seen in morbidly obese patients. In this rare entity, there is hypertrophy of normal epidural fat, particularly in the dorsal aspects of the thoracic spine and less commonly in the lumbar region. The most common symptom

A

B

Figs 14A to D:  Extradural angiolipoma. Axial T1-weighted images (T1WIs) (A) and T 2-weighted images (T2WIs) (B) show extradural hyperintense mass displacing the spinal cord anteriorly and left side. Axial T1W fat-saturated image (C) showing diffuse, nearly homogeneous decrease in the signal intensity of mass suggestive of fatty tissue. Axial T1W postgadolinium fat-saturation image (D) showing enhancement of extradural lesion

C

Figs 15A to C:  Intramedullary angiolipoma. Sagittal T1-weighted images (T1WIs) (A) and T2-weighted images (T2WIs) (B) showing the intramedullary angiolipoma. The dorsal component of mass shows homogeneous high-signal intensity, while the ventral component is heterogeneously hyperintense. No vascular flow voids are seen. Sagittal T1W-fat-saturated image (C) shows suppression of signal in the dorsal component

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is back pain, but compression of the spinal cord may occur. If the fat grows at the level of neural foramina, radiculopathies also occur. The typical MRI appearance of epidural lipomatosis is that of excessive bright T1W-fat-saturated (> 5–6 mm) in the posterior aspect of the canal on sagittal images. The subarachnoid spaces are narrowed and the thoracic spinal cord appears thin. The superior and inferior aspects of the lipomatosis taper smoothly and usually extend at least 6 vertebral segments in length. On axial images, excessive fat is noted in the posterior aspect of the canal and extending laterally. This normal fat does not enhance after contrast administration. On sagittal MRI, the width of the normal posterior epidural fat is less than 3–5 mm. On CT, the abnormal fat is of low density and on myelography the fat may compress the canal and result in complete blockage of the passage of contrast. Similar findings are noted when epidural lipomatosis develops in the lumbar region.

CONCLUSION It is important for the radiologist to familiar with imaging characteristics of spinal neoplasms. A reasonable differential diagnosis can be developed for most spinal neoplasms on the basis of patient’s age, lesion location and radiological appearance. A multimodality approach can be used to fully characterize the lesion and the combination of information obtained from different modalities usually narrows down the diagnostic possibilities significantly. MRI is a particularly useful tool for evaluation of intramedullary neoplasms.

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Chapter 33 Imaging of Spinal Neoplasms 27. Angtuaco EJ, Fassas AB, Walker R, et al. Multiple myeloma: Clinical review and diagnostic imaging. Radiology. 2004;231(1):11-23. 28. Guermazi A, Brice P, de Kerviler EE, et al. Extranodal Hodgkin disease: spectrum of disease. Radiographics. 2001;21(1): 161-79. 29. Laredo JD, Reizine D, Bard M, et al. Vertebral hemangiomas: Radiologic evaluation. Radiology. 1986;161(1):183-9. 30. Baudrez V, Galant C, Vande Berg BC. Benign vertebral hemangioma: MR-histological correlation. Skeletal Radiol. 2001;30(8):442-6. 31. Ross JS, Masaryk TJ, Modic MT, et al. Vertebral hemangiomas: MR imaging. Radiology. 1987;165(1):165-9. 32. Laredo JD, Assouline E, Gelbert F, et al. Vertebral hemangiomas: Fat content as a sign of aggressiveness. Radiology. 1990;177(2):467-72. 33. Cross JJ, Antoun NM, Laing RJ, et al. Imaging of compressive vertebral haemangiomas. Eur Radiol. 2000;10(6):997-1002. 34. Capanna R, Van Horn JR, Biagini R, et al. Aneurysmal bone cyst of the sacrum. Skeletal Radiol. 1989;18(2):109-13. 35. Llauger J, Palmer J, Amores S, et al. Primary tumors of the sacrum: diagnostic imaging. AJR Am. 2000;174(2):417-24. 36. Sanerkin NG, Mott MG, Roylance J. An unusual intraosseous lesion with fibroblastic, osteoclastic, osteoblastic, aneurysmal and fibromyxoid elements: Solid variant of aneurysmal bone cyst. Cancer. 1983;51(12):2278-86. 37. Koci TM, Mehringer CM, Yamagata N, et al. Aneurysmal bone cyst of the thoracic spine: Evolution after particulate embolization. AJNR. 1995;16(4 Suppl):857-60. 38. Kransdorf MJ, Sweet DE. Aneurysmal bone cyst: Concept, controversy, clinical presentation, and imaging. AJR. 1995;164(3):573-80. 39. Diel J, Ortiz O, Losada RA, et al. The sacrum: Pathologic spectrum, multimodality imaging, and subspecialty approach. Radiographics. 2001;21(1):83-104. 40. Wang K, Allen L, Fung E, et al. Bone scintigraphy in common tumors with osteolytic components. Clin Nucl Med. 2005;30(10):655-71. 41. Murphey MD, Andrews CL, Flemming DJ, et al. From the archives of the AFIP, Primary tumors of the spine: Radiologic pathologic correlation. Radiographics. 1996;16(5):1131-58. 42. Tsai JC, Dalinka MK, Fallon MD, et al. Fluid-fluid level: A nonspecific finding in tumors of bone and soft tissue. Radiology. 1990;175(3):779-82. 43. Suzuki M, Satoh T, Nishida J, et al. Solid variant of aneurysmal bone cyst of the cervical spine. Spine (Phila Pa 1976). 2004;29(17):E376-81. 44. Dahlin DC. Caldwell Lecture. Giant cell tumor of bone: Highlights of 407 cases. AJR. 1985;144(5):955-60. 45. Drevelegas A, Chourmouzi D, Boulogianni G, et al. Imaging of primary bone tumors of the spine. Eur Radiol. 2003;13(8):1859-71.

46. Schwimer SR, Bassett LW, Mancuso AA, et al. Giant cell tumor of the cervicothoracic spine. AJR. 1981;136(1):63-7. 47. Aoki J, Tanikawa H, Ishii K, et al. MR findings indicative of hemosiderin in giant-cell tumor of bone: Frequency, cause, and diagnostic significance. AJR. 1996;166(1):145-8. 48. Kransdorf MJ, Stull MA, Gilkey FW, et al. Osteoid osteoma. Radiographics. 1991;11(4):671-96. 49. Flemming DJ, Murphey MD, Carmichael BB, et al. Primary tumors of the spine. Semin Musculoskelet Radiol. 2000;4(3):299-320. 50. Tourniaire J, Bossard D, Gleize B, et al. Case report 801: Osteoid osteoma of the coccyx. Skeletal Radiol. 1993;22(6):457-9. 51. Houang B, Grenier N, Gréselle JF, et al. Osteoid osteoma of the cervical spine. Misleading MR features about a case involving the uncinate process. Neuroradiology. 1990;31(6): 549-51. 52. Kroon HM, Schurmans J. Osteoblastoma: clinical and radiologic findings in 98 new cases. Radiology. 1990;175(3):783-90. 53. Kumar R, Guinto FC, Madewell JE, et al. Expansile bone lesions of the vertebra. Radiographics. 1988;8(4):749-69. 54. Crim JR, Mirra JM, Eckardt JJ, et al. Widespread inflammatory response to osteoblastoma: The flare phenomenon. Radiology. 1990;177(3):835-36. 55. Lucas DR, Unni KK, McLeod RA, et al. Osteoblastoma: Clinicopathologic study of 306 cases. Hum Pathol. 1994; 25(2):117-34. 56. Ilaslan H, Sundaram M, Unni KK, et al. Primary vertebral osteosarcoma: Imaging findings. Radiology. 2004;230(3): 697-702. 57. Barwick KW, Huvos AG, Smith J. Primary osteogenic sarcoma of the vertebral column: A clinicopathologic correlation of ten patients. Cancer. 1980;46(3):595-604. 58. Murphey MD, wan Jaovisidha S, Temple HT, et al. Telangiectatic osteosarcoma: Radiologic-pathologic comparison. Radiology. 2003;229(2):545-53. 59. Ozaki T, Flege S, Liljenqvist U, et al. Osteosarcoma of the spine: experience of the Cooperative Osteosarcoma Study Group. Cancer. 2002;94(4):1069-77. 60. Albrecht S, Crutchfield JS, SeGall GK. On spinal osteochondromas. J Neurosurg. 1992;77(2):247-52. 61. Barros Filho TE, Oliveira RP, Taricco MA, et al. Hereditary multiple exostoses and cervical ventral protuberance causing dysphagia: A case report. Spine (Phila Pa 1976). 1995;20(14):1640-2. 62. Wippold FJ, Koeller KK, Smirniotopoulos JG. Clinical and imaging features of cervical chordoma. AJR. 1999;172(5):1423-6. 63. Smolders D, Wang X, Drevelengas A, et al. Value of MRI in the diagnosis of non-clival, non-sacral chordoma. Skeletal Radiol. 2003;32(6):343-50. 64. Sung MS, Lee GK, Kang HS, et al. Sacrococcygeal chordoma: MR imaging in 30 patients. Skeletal Radiol. 2005;34(2):87-94.

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Section 1 Neuroradiology including Head and Neck 65. Mummaneni PV, Rosenberg WS. Spinal chondrosarcoma following adenocarcinoma of the breast: Case report. Surg Neurol. 2000;53(6):580-2. 66. Shives TC, McLeod RA, Unni KK, et al. Chondrosarcoma of the spine. J Bone Joint Surg Am. 1989;71(8):1158-65. 67. Vialle R, Feydy A, Rillardon L, et al. Chondroblastoma of the lumbar spine. Report of two cases and review of the literature. J Neurosurg Spine. 2005;2(5):596-600. 68. Leone A, Costantini A, Guglielmi G, et al. Primary bone tumors and pseudotumors of the lumbosacral spine. Rays. 2000;25(1):89-103.

69. Jee WH, Park YK, McCauley TR, et al. Chondro-blastoma: MR characteristics with pathologic correlation. J Comput Assist Tomogr. 1999;23(5):721-6. 70. Samdani AF, Garonzik IM, Jallo G, et al. Spinal angiolipoma: Case report and review of the literature. Acta Neurochir (Wien). 2004;146(3):299-302. 71. Garg A, Gupta V, Gaikwad S, et al. Spinal angiolipoma: Report of three cases and review of MRI features. Australas Radiol. 2002;46(1):84-90. 72. Bodelier AG, Groeneveld W, van der Linden AN, et al. Symptomatic epidural lipomatosis in ectopic Cushing’s syndrome. Eur J Endocrinol. 2004;151(6):765-9.

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CHAPTER

Spinal Vascular Malformations NK Mishra

INTRODUCTION Vascular lesions of the spinal cord are a heterogeneous group of conditions that require careful analysis for instituting appropriate management. They produce considerable morbidity and severely affect the patient’s life, family and society. Credit for first recognizing that spinal vascular malformations can cause subarachnoid hemorrhage (SAH) must be given to Heboldt in 1885 and Gaupp in 1888, who referred to these lesions as “hemorrhoids of the pia mater”.1 The introduction of selective spinal angiography in the late 1960s and early 1970s and the studies of large series of patients by Houdart, Di Chiro, Baker, Djindjian, and their colleagues further improved our anatomical and hemodynamic understanding of these rare lesions. Prior to development of selective spinal angiography, our understanding of the conditions was quite limited. With demonstration of the abnormal vascular anatomy, however, a clearer localization of nidus or arteriovenous shunt has been made possible. Finally along with the development of selective spinal catheterization techniques by neuroradiologists, a new treatment has developed—embolization. Thus began the era of endovascular therapy, which along with microneurosurgery is the mainstay of modern treatment. In recent times, magnetic resonance angiography (MRA) is being experimented for evaluation of spinal vascular anatomy. However, the high volume of contrast required for spinal MRA raises concerns regarding systemic sclerosis particularly in patients who have renal insufficiency. Also the true utility of such studies in the present era of high resolution selective angiography is unknown. The recognition and proper categorization of spinal arteriovenous malformations (AVMs) are both crucial for treatment planning. Among modern imaging techniques, selective spinal angiography plays a decisive role in diagnosis and classification of the spinal vascular malformations 2,3 (Tables 1 and 2). It is likely that spinal vascular malformations are the result of a range of underlying biologic defects that result in a susceptibility to form a pathologic condition, such as an AV shunt, but that require one or two triggering events after

Table 1:  Morphologic classification (Anson and Spetzler 1993) Type I

SDAVF IA-single pedicle IB-multiple pedicle

Type II

SCAVM (Intramedullary glomus)

Type III

SCAVM (Intramedullary juvenile with extramedullary component)

Type IV

SCAVG (Intradural extramedullary AVF)

Abbreviations: SCAVMs, spinal cord arteriovenous malformations; SDAVF, spinal dural arteriovenous fistula

Table 2:  Primary classification (Lasjaunias) Spinal dural AVFs

•

Isolated (Type I)

•

Multiple (Type II)

Spinal extradural AVFs Spinal cord vascular lesions •

Isolated (AVM, AVF)

•

Multiple-metameric (Cobb’s and other Assoc.)

•

Non-metameric (Rendu-OslerWeber and Klippel-Trenaunay and other)

Abbreviations: AVF, arteriovenous fistula; AVM, arteriovenous malformations

embryogenesis to achieve complete phenotypic expression, as has been proposed for other central nervous system (CNS) vascular lesions.4-6 In fact, there is evidence that a biologic defect is responsible for a large number of malformations, particularly those that present in the pediatric population. More recently in 2002, Rodesch et al. proposed a reappraisal of this classification based on their experience at Bicetre, Paris, which is more comprehensive and relates to pathogenesis.5 Further, in a series of SAVSs presenting in children younger than 2 years of age, for example, found that nearly two-thirds of patients (62%) had evidence of a heritable genetic defect [hereditary hemorrhagic telangiectasia (HHT)] or a somatic nonheritable mutation [spinal arteriovenous

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8. Branchial AVF 9. Vertebrovertebral arteriovenous formation (VVAVF) 10. Paraspinal arteriovenous formation (PSAVF) Kim and Spetzler recently proposed a new classification system based on the anatomical description of SVMs: zz Extradural zz Intradural dorsal/ventral zz Intradural intramedullary zz Extradural-intradural, and conus medullaris vascular malformations.

SPINAL DURAL ARTERIOVENOUS FISTULA A

B

Figs 1A and B:  Spinal AVM with pial afferent and epidural efferent

(arrows in A and B) Abbreviation: AVM, arteriovenous malformation

metameric syndrome (SAMS)]7 (Figs 1A and B). They even proposed a more comprehensive classification: Classifications of pediatric spinal cord arteriovenous shunts (intradural) by Cullen, Rodesch et al. A. According to biologic abnormality: 1. Heritable genetic defect: • HHT type 1 [endoglin (ENG)] 9q33-34 • HHT type 2 [activin receptor-like kinase (ALK1)] 12q11-14 • HHT type 3 (Smad 4) 5q31-32 2. Nonheritable defect (somatic genetic) often segmental SAMS • Klippel-Trenaunay syndrome with limb venolymphatic-associated lesions • Parkes-Weber syndrome 3. Sporadic-isolated arteriovenous lesion (forme fruste of 1 and 2) 4. Acquired lesion (?) B. According to morphology of AVS: 1. Nidus [spinal cord arteriovenous malformation (SCAVM)] 2. Fistula [spinal cord arteriovenous fistula formation (SCAVF)] • Macrofistula • Microfistula 3. Multifocal intradural lesions C. According to location of SAVS: 1. Intradural 2. Intramedullary 3. Extramedullary 4. Radicular 5. Filum 6. Epidural AVS (intraspinal) 7. Parachordal arteriovenous formation (AVF)

Spinal dural arteriovenous fistulas (SDAVFs) are slow-flow extramedullary lesions that generally consist of a small, single arteriovenous communication in the surface of dura adjacent to the origin of dural root sleeve.7 This fistula is fed by dural branch of the dorsospinal artery in the region of the intervertebral foramen and from the shunt a highly tortuous single draining vein emerges which pierces the dura some millimeters from the accompanying nerve root to reach perimedullary venous system and produces venous hypertension in the medullary veins.8 Patients with both posterior and anterior drainage tend to have more severe symptoms than those with exclusively posterior drainage.2 In most cases, drainage is mainly upwards to thoracic and cervical levels. In general, arteriovenous (AV) shunt is microscopic and not visualized from extradural aspect.8 The large draining vein is always single and shows thickening limited to a cushion-like plaque circumferentially. Thickening involves intima and/or media, in addition atherosclerotic changes and calcification can be sometimes found in the veins.3 Extensive pathological changes may be present within cord particularly involving lateral corticospinal tracts. More advanced changes progressively involve the anterior gray matter and the posterior columns but consistently sparing anterior median segment.9 Atypical feature in long-standing advanced lesions is the appearance of “neocapillaries” within the cord, which could be confused with an “AV nidus.” These “neocapillaries” represent primarily the congested, intrinsic, venous network of spinal cord.3 SDAVFs are the most common lesions among all types of vascular malformations affecting the spinal cord. 3 They usually present after the fourth or fifth decade of life and there is an 85% male predominance.3 Most SDAVFs occur at or near the thoracolumbar junction and do not occur in cervical cord because of divergent and favorable venous drainage. Occasionally, dural fistulas located at the foramen magnum, in the posterior fossa, or in the pelvis may drain into spinal veins and cause myelopathy. The main clinical features consist of a combination of upper and lower motor neuron dysfunction associated with sensory and sphincter disturbances. The principal site of

Chapter 34 Spinal Vascular Malformations

cord dysfunction is at the level of lumbar enlargement, which probably represents the effect of venous hypertension below the level of heart and back flow to the residual veins that drain the spinal cord. Symptoms are usually gradual in onset, but there may be a steadily progressive or stepwise course. The initial presenting symptoms in patients with SDAVFs are leg weakness (40%), root and/or pain in the back (28%), bowel (4%) and bladder (5%) disturbances.3 Hemorrhage is remarkable for its absence. The progressive myelopathy may be confused with other, more common neurologic conditions such as motor neuron or degenerative disease (e.g. amyotrophic lateral sclerosis, multiple sclerosis, syringomyelia), prolapsed disk, lumbar canal stenosis and spinal cord tumor. Approximately 10–20% of patients experience acute exacerbation of myelopathy with or without pain but without hemorrhage as a result of thrombosis or other additional hemodynamic changes. SDAVFs are considered as an acquired disease predisposed by spinal venous thrombosis. The development of SDAVFs causes venous hypertension, leading to hypoperfusion of spinal cord and clinical symptoms. The mixed clinical

A

B

C

features of an intramedullary and conal lesion especially in a male (rarely female) in the fifth or sixth decade of life, should prompt consideration and evaluation for SDAVF.10 Magnetic resonance imaging without and with intravenous injection of contrast material is currently the first step of diagnostic evaluation. Symptomatic SDAVFs show abnormal increased signal intensity in the spinal cord on T2WI and intradural flow-voids on T1 and T2WI. 11-13 Acute presentation is invariably associated with cord swelling and chronic cases show atrophy of the spinal cord. Angiography is necessary for confirmation of diagnosis and for pretherapeutic evaluation. Angiographically, the feeding vessel of SDAVFs is almost invariably a single pedicle often not dilated; a small microfistula that can be observed with a single, coiled, draining vein (Figs 2A to E). We have encountered a few epidural fistulae in the lower dorsal spine, which are AV shunts between osteodural branches of intercostal arteries and the epidural veins (anterior internal vertebral veins), which drain into paraspinal (azygos and hemiazygos) system of veins. These large shunts produce epidural compression of the cord with attendant paraparesis in mostly young adults. Embolization

D

E

Figs 2A to E:  (A) Sagittal T2WI showing hyperintensity in the conus and dorsal flow voids; (B and C) DSA images reveal a SDAVF on the right

side arising from the right 2nd lumbar artery communicating with the radicular vein which drains into the perimedullary venous plexus. Note the correspondence of the flow voids in MR with the maximally dilated venous plexus at D12 level; (D and E) Unsubtracted angiographic AP and lateral view images show the relationship of the fistula to the right pedicle of L2 and the dilated perimedullary plexus at D12 Abbreviations: DSA, digital subtraction angiography; SDAVF, spinal dural arteriovenous fistula

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A

B

C

E

F

D

G

H

Figs 3A to H:  (A and B) Sagittal T1, and T2 and (C and D) Axial T1 MRIs of a young adult presenting with paraparesis shows anterior epidural vascular lesion with epidural cord compression. (E and F) Spinal DSA AP, and (G and H) Lateral view show the large epidural fistulae from left D8 intercostal artery and draining into hemiazygos vein Abbreviations: AP, anteroposterior; DSA, digital subtraction angiography

of these fistulae is difficult, since there usually are myriad of micro-fistulae in the wall of the epidural veins, often from segmental intercostal arteries from both sides as well as multiple contiguous segments (Figs 3A to H). The presence of SDAVF is an indication for treatment in all patients as risks of endovascular or open surgery are minimal and possible benefits are multiple. Most neuroradiologists use n-butyl cyanoacrylate (NBCA) as the primary embolic agent. The goal of embolization is to penetrate a column of NBCA to the proximal portion of draining vein through the fistula without mixture with blood, because a portion of a vessel occluded with thrombus can recanalize later (Figs 4A to C). The only significant contraindications for endovascular interventions are: 1. Anterior spinal artery (ASA) arising from the same pedicle as SDAVF where risk of compromising of the ASA is likely. 2. Technically difficult catheterization (very small radicular artery). 3. If extraspinal longitudinal anastomosis cannot be cleared safely to prevent accidental embolization to ASA or posterior spinal artery (PSA). Only if endovascular treatment is not possible or contraindicated, surgery can be performed.3 Coagulation of abnormal vascular structures on the dural layer or excision

A

B

C

Figs 4A to C:  (A) SDAVF arising at D12 level on the right side shows

conus swelling and flow voids dorsal to the cord; (B) Frontal DSA image shows enlarged right D12 radicular arterial network draining into coronary venous plexus; (C) Postembolization radiograph demonstrates glue cast in the radicular arterial network and the descending limb of the radicular vein and proximal coronary plexus

Chapter 34 Spinal Vascular Malformations

of the whole area of abnormality is the correct surgical treatment of the dural fistula. Berenstein and Lasjaunias have shown improvement or stabilization of clinical status after embolization in 83% of their 63 patients of SDAVF (27 operated 36 embolized).9 Results published by Merland et al. also achieve 50% significant improvement in symptoms, 20% minor improvement, 16% progressive myopathy stabilized, 4% aggravation or continued deterioration, 8% technical failure and 2.7% paraplegia secondary to distal migration of isobutyl-2-cyanoacrylate (IBCA).14 In our study done in 2000, 9 patients of SDAVF underwent surgery while 4 had embolizations and all these patients had anatomical cure. The same distribution of cases between endovascular and surgical treatment is prevalent at our institute. Often the dural feeder pedicle is extremely thin precluding selective catheterization to obliterate the fistula and the efferent vein, whereupon surgical treatment is carried out. However, precise localization of the fistula and its topography by imaging is essential for successful surgery. Follow-up MRI in successfully treated spinal dural AVFS, shows progressive regression/disappearance of signal voids and abnormal high signal intensity in the spinal cord on T2WI concurrent with clinical improvement. The degree of clinical and radiological improvement depends on the severity and duration of venous hypertension preceding definitive treatment.

SPINAL CORD PERIMEDULLARY ARTERIOVENOUS FISTULA The perimedullary AVFs are direct arteriovenous shunts without a nidus of abnormal vessels between the spinal arteries and medullary veins. In contrast to SDAVF, perimedullary AVFs are located in subpial space,15,16 usually opacified by multiple sources, although the fistula is most often a single hole. These fistulae were described for the first time by Djindjian and associates in 1977.17 The presentation of perimedullary AVFs is characterized by rapidly progressive ascending sensory and motor disturbances accompanied by disorders of the sphincter. Because it is situated intradurally, spinal subarachnoid hemorrhage is also one of the occasional presenting symptoms. The age at onset of symptoms ranges from 2 to 24 years with a predominance in the second decade of life.9 They are usually thoracolumbar, occasionally thoracic, and rarely cervical in location. According to size, quantity of flow and venous drainage, Gueguen and his group distinguish three types of perimedullary fistulae.15 Type I: A small low-flow, single-hole fistula without obvious dilation of the feeding artery and draining vein. Type II: A high-flow, single-hole fistula with apparent dilatation of the feeding artery and draining vein.

There is an arterialized venous pouch near the fistula (Figs 5A to G). Type III: A giant high-flow fistula with multiple feeders and an extremely dilated and varicose vein often occupying the entire spinal canal at the fistula level and the fistula site is hard to localize (Figs 6A and B).16 Similar pial fistulae may also arise in the subpial surface of spinal root, often in sacral area. These may be isolated radicular pial fistulae or occur in conjunction with metameric syndromes (Figs 7A to C). Such pial AVFs may be associated with malformations in other systems, such as seen in one of or cases, where a young boy had renal aneurysms along with hypermobile joints (Figs 8A to H). They can also be encountered on the filum teminale (Fig. 9A to D). The presentation of perimedullary AVFs is characterized by acute onset, devastating neurological deficits and poor prognosis, if left untreated, similar to what is seen in patients with SCAVMs. Ling F et al. have reported overlooked history of meningitis during childhood in one-third of the cases.18 Surgical elimination is the therapy of choice in type I perimedullary AVFs, as it is difficult for endovascular navigation through long and minimally dilated artery to reach the fistula site. Only in cases of ventrally situated type I perimedullary fistulae should embolization with particles be tried. Type II and type III AVFs are suitable for embolization with glue or balloon.

SPINAL CORD AVMS Spinal cord AVMs (SCAVMs) are lesions in which the “nidus” is within the parenchyma of the spinal cord or pia and recruits its blood supply from medullary arteries which run on the surface of the spinal cord. These are further subclassified into “glomus” and “juvenile” types. The glomus AVM is composed of tightly packed localized nidus of abnormal blood vessels confined to a segment of spinal cord. The juvenile AVMs consist of a much looser tangle of abnormal vessels that occupy almost the entire spinal canal at the involved levels. Intramedullary AVMs are frequently encountered in adolescence or young adults. There is slight male predominance in most large series of SCAVMs.2 SCAVMs are located in the cervical area in 30% and in the thoracolumbar area in 70%, which is grossly proportional to the volume of the spinal cord in each segment. Syndromes known to be associated with SCAVM are the Osler-RenduWeber syndrome, neurofibromatosis and Klippel-Trenaunay and Parkes-Weber syndromes.2 Metameric AVMs involving the skin, vertebrae and spinal cord are part of the Cobb syndrome.2 Subarachnoid hemorrhage or hematomyelia is the most significant clinical presentation of SCAVMs.14 This occurs in approximately 30% of the patients as the initial symptom and in more than 50% by the time of diagnosis—less frequently,

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Section 1 Neuroradiology including Head and Neck

A

E

B

C

F

D

G

Figs 5A to G:  Spinal AVF from a posterior spinal contributor: (A) Distending the spinal veins (B) with additional contribution from a pial branch from left costocervical trunk embolized with one shot glue injection (E and F). Sagittal T1 and T2 MRIs (D and E) before and after embolization (G and H) show regression of venous engorgement

a patient can present with acute or progressive neurologic deterioration without evidence of hemorrhage. Hemorrhage is seen most frequently in cervical lesions.14 Magnetic resonance imaging is currently the best modality for first step pre-therapeutic evaluation and for a follow-up of SCAVMs. MRI has almost 100% sensitivity for detection of SCAVMs, which are demonstrated as intradural signal voids of dilated arteries or veins that can be within or on the surface of the spinal cord. MR imaging is also very helpful to evaluate associated findings with SCAVMs such as spinal cord edema, hematomyelia, thrombosis, cavitation, atrophy and venous drainage. MR imaging can also assist in demonstrating extraspinal extension of metameric or extraspinal AVMs.

Angiography remains the gold standard for precise evaluation of SCAVMs and determines the feasibility and type of treatment to be considered. Practically, all SCAVMs can be considered as monocompartmental lesions: even if each feeder fills different portion of the network, the venous outlet remains the same. Co-existence of AVF and nidus within a single SCAVM is possible. All patients with SCAVMs are indicated for treatment considering their high predilection for hemorrhage and poor prognosis, if untreated. The primary objective of any therapeutic modality should be to obtain a complete cure. In those patients in whom complete cure is not possible, partial cure is accepted as the rationale to arrest or improve

Chapter 34 Spinal Vascular Malformations

a

b

c

d

Figs 6A (a to d) Fig. 6A:  Sagittal T1, T2 (a and b) and coronal T1, T2 (c and d) images of a 3-year-old girl presenting with quadriparesis and poor respiratory effort, shows a giant spinal pial AVF in cervicodorsal spinal canal expanding the canal

e

l

f

m

g

h

n

clinical problem or to favorably modify natural history of disease. SCAVM should only be treated by embolization or as a front part of combined approach (Figs 10A to E). All patients with symptomatic lesions that can be cured are suited for endovascular embolization. Young symptomatic individuals should be treated aggressively and in those with associated aneurysms, treatment should be expedited, as there is high potential for bleeding. In patients with fixed deficits or clinically diagnosed cord transection in which it is unlikely that any functional benefit will ensue, nonetheless treatment is indicated as repeated life-threatening hemorrhages can be prevented. In these cases, complete obliteration is also easier as it will not aggravate a fixed deficit or cord transection. Lesions at thoracic or cervical level should be aggressively treated since progression can affect upper extremity function, sphincter control or affect respiratory muscles (Figs 11A to F). In a series by Berenstein and Lasjaunias, 3 55% of embolized SCAVMs/SCAVFs (perimedullary fistulae) had anatomical cure, while 40% of our cases of SCAVMs.

i

o

p

j

k

q

Figs 6B (e to q) Fig. 6B:  Vertebral angiogram right (e), left (f and g) and superior intercostal angiogram (h) show a spinal pial AVF fed by pial contributors from

all three arteries. Microcatheter introduced through the supreme intercostals artery (i) enters the venous sac (j) and could be navigated into the proximal ASA (k). Vertebral angiogram after fistula closure by glue embolization (l, m, n, o) shows restitution of the ASA (p and q)

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Section 1 Neuroradiology including Head and Neck

A

B

A

C

Figs 7A to C:  (A and B) Sagittal T2 MRI showing flow voids in lumbar

canal in a young adult with spinal deformities; (C) DSA shows a sacral root pial fistula (arrow) draining into spinal venous plexus seen in the magnetic resonance Abbreviation: DSA, digital subtraction angiography

C

A

B

G

B

C

D

Figs 9A to D:  Sagittal T2 MRI of (A) lumbar and (B) dorsal spine

show extensive flow voids on the cord surface with hyperintense cord parenchyma. Spinal DSA shows the ASA descending up to L3 vertebral level with a fistulous communication with the spinal vein (arrows in C and D) which ascends by the side of the enlarged terminal ASA, (C) AP view and (D) lateral. This fistula is situated over the filum terminale Abbreviations:  ASA, anterior spinal artery; DSA, digital subtraction angiography

D

E

F

H

Figs 8A to H:  Sagittal T1 and T2 (A and B): MRI show extensive flow voids in lumbar canal in a young boy, due to major spinal pial AVF (C to F). He also had renal arterial and venous aneurysms (G and H) with hypermobile joints

Chapter 34 Spinal Vascular Malformations

Flow chart 1:  Classification of spinal arteriovenous fistula (AVFs)

A

Source: Rodesch et al. 2002 B

C

D

E

Figs 10A to E:  (A and B) Spinal intramedullary arteriovenous

malformation at D12 fed by anterior spinal artery; (C) Glue cast in the nidus after withdrawal of the microcatheter and; (D) postembolization angiogram shows near complete obliteration of the intramedullary nidus; (E) Postembolization radiograph showing glue cast in the nidus in the lower dorsal cord

Table 3:  Spinal cord arteriovenous malformation and spinal cord arteriovenous fistula formation management (Results) Embo

Surgery

Cure

Rosenblum20

-

43/57 (80%)

?

Berenstein/Lasjaunias

47/50 (94%)

AIIMS

15/36 (42%)

25/47 (55%) 10/36 (27%)

11/25 (44%)

SPINAL VASCULAR MALFORMATIONS The classification of spinal AVFs is given in Flow chart 1. SCAVFs, which were embolized, showed complete cure. The overall result of management at our institution as of 2002 is summarized in Table 3.

REFERENCES A

D

C

B

E

F

Figs 11A to F:  Sagittal T1 and T2 MR images of 45-year-old man (A and B) before, (D and E) after and (C and F) DSA AP view before and after embolization of cervical intramedullary glomus type AVM. Patient made uneventful recovery from the embolization and regained power in all four limbs in subsequent months

1. Gaupp J. Casvistische Beitrage zur pamologischen Anatomie des Ruckenmarks und seiner Haute. Beitr Pathol Anat. 1888;2:510-924. 2. Anson JA, Spetzler RF. Classification of spinal arteriovenous malformatioms for treatment. Barrow Neurological Institute Quarterly. 1992;8:2-8. 3. Berenstein A, Lasjaunias P. Spine and spinal cord vascular lesions. In: Endovascular Treatment of Spine and Spinal Cord Lesions (Surgical Neuroangiography, Vol. 5). Berlin: SpringerVerlag; 1992. pp.1-109. 4. Lasjaunias P. A revised concept of the congenital nature of cerebral arteriovenous malformations. Intervent Neuroradiol. 1997;3:275-81. 5. Rodesch G, Hurth M, Alvarez H, et al. Classification of Spinal Cord Arteriovenous Shunts: Proposal for a reappraisal—the Bicetre experience with 155 consecutive patients treated between 1981 and 1999. Neurosurgery. 2002;51:374-80. 6. Lasjaunias P, terBrugge K, Berenstein A. Spinal arteriovenous shunts. In: Surgical neuroangiography, vol. 3. Clinical and interventional aspects in children, 2nd edition. New York: Springer Verlag; 2006. pp. 721-66.

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Section 1 Neuroradiology including Head and Neck 7. Rodesch G, Hurth M, Alvarez H, et al. Angio-architecture of spinal cord arteriovenous shunts at presentation. Clinical correlations in adults and children. The Bicêtre experience on 155 consecutive patients seen between 1981 and 1999. Acta Neurochir (Wien). 2004;146(3):217-26; discussion 226-7. 8. Cullen S, Alvarez H, Rodesch G, et al. Spinal arteriovenous shunts presenting before 2 years of age: Analysis of 13 cases. Childs Nerv Syst. 2006. 9. Merland JJ, Riche MC, Chiras J. Intraspinal extramedullary arteriovenous fistulae draining into medullary veins. J Neuroradiolol. 1980;7:271-320. 10. Benhain N, Piorier J, Hurth M. Arteriovenous fistulae of the meninges draining into spinal veins: A histological study of 28 cases. Acta Neuropath (Berl). 1983;62:103-11. 11. Gillilian LA. Veins of the spinal cord. Anatomic details: Suggested clinical applications. Neurology. 1970;20:860-68. 12. Yasargil MG, Symon L, Teddy PG. Arteriovenous malformations of the spinal cord. In: Symon L (Ed) Advances and technical standards in neurosurgery, Springer, Wein 1984;11:61-102. 13. Mesaryk TJ, Ross JS, Modic MT, et al. Radiculomeningeal vascular malformations of the spine: MR imaging. Radiology. 1987;164:845-9.

14. Merland JJ, Reizine D. Treatment of arteriovenous spinal cord malformations. Semin Interven Radiolol. 1987;4:281-90. 15. Guegen B, Merland JJ, Riche MC, et al. Vascular malformations of the spinal cord: Intrathecal perimedullary arteriovenous fistulas fed by medullary arteries. Neurology. 1987;37:969-79. 16. Heros RC, Debrun GM, Ojemann RG, et al. Direct spinal arteriovenous fistulas: A new type of spinal AVM. J Neurosurg. 1986;64:134-9. 17. Djindjian M, Djindjian R, Rey A, et al. Intradural extramedullary spinal arteriovenous malformation fed by the anterior spinal artery. Surg Neurol. 1977;8:85. 18. Ling F, Li TL, Bao Y, et al. Chinese experience in endovascular management of spinal cord vascular malformations. Interventional Neuroradiology. 1999;5:109-26. 19. Gaikwad SB, Mishra NK, Goyal M, et al. Spinal cord arteriovenous fistula associated with a giant venous pouch in a three-year-old child. Interventional Neuroradiology. 1997;3:247-53. 20. Rosenblum B, Oldfield EH, Doppmann JL, et al. Spinal arteriovenous malformations: A comparison of dural arteriovenous fistulas and intradural AVMs in 81 patients. J Neurosurg. 1987;67:795-802.

35 CHAPTER

Imaging of Low Backache Raju Sharma, Shivanand Gamanagatti, Arun Kumar Gupta

IMAGING OF LOW BACK PAIN

z z

Nearly half the adult population in India suffers from back pain, lasting at least 24 hour at sometimes every year. 1 The impact of back pain on society is considerable and is associated with an enormous economic burden. Low back pain (LBP) most commonly affects the 30–50 year age-group, with the prevalence peaking during the 6th decade. Young people are more likely to have brief, acute episodes of back pain, whilst chronic pain tends to occur in older people. There is an equal sex distribution. This chapter summarizes the etiology, clinical presentation and radiological investigation of LBP.

When to Image There are many causes of back pain with a complex interrelationship between anatomical, pathological and psychological factors leading to the eventual clinical presentation. A careful history and physical examination remains the mainstay of initial assessment of back pain. Imaging is not necessary in most cases of back pain because of the high rate of spontaneous remission within 6–8 weeks.2 Furthermore, the use of early imaging does not appear to alter management in most patients. There are, however, certain features or “red flags” that should suggest serious pathology and prompt early imaging.3 It is increasingly recognized that plain radiographic evaluation of back pain in the absence of trauma is of limited value, as degenerative changes are very common and sinister pathology may easily be missed. Signs of a more complicated status, often termed “red flags”, consist of the following:3 z Recent significant trauma, or milder trauma, age more than 50 years z Unexplained weight loss z Unexplained fever z Immunosuppression z History of cancer

z z

z

Intravenous (IV) drug use Prolonged use of corticosteroids, osteoporosis Age more than 70 years Focal neurologic deficit with progressive or disabling symptoms Duration longer than 6 weeks.

Four main clinical scenarios are following:4 1. Acute nonspecific back pain, which usually resolves spontaneously within 6–8 weeks. 2. Chronic back pain without sinister features. This is a very common situation that is usually related to degenerative disease. 3. Back pain with sciatica: A condition usually caused by disk prolapse. 4. Possible serious pathology or cauda equina syndrome; this group encompasses various conditions, such as tumor, infection and inflammatory disorders. Of these conditions, the first two do not usually warrant imaging. In patients suffering from sciatica, the cause is usually a prolapsed disk, and those who have had a failed period of conservative therapy may require imaging. In patients with possible serious pathology, urgent imaging is indicated.

Conditions Causing Back Pain The physical causes of back pain can be divided into mechanical conditions, such as disk disease, and nonmechanical conditions, such as infection, inflammation or neoplasm (Table 1).4-6 There are also conditions which do not involve the spine, such as abdominal aortic aneurysms and urological conditions that may present with back pain. Due to the complexity of the bony, ligamentous, muscular and neural elements of the back, a specific anatomical diagnosis often cannot be made. Even when radiological investigations show an abnormality, the positive findings may not necessarily relate directly to the back pain. Close clinicoradiological correlation is therefore required.4-6

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Section 1 Neuroradiology including Head and Neck

Table 1: Conditions causing back pain Mechanical (95%)

Specific cause

Acquired

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IMAGING MODALITIES The purpose of diagnostic imaging is twofold: First is to provide accurate anatomic information and the second perhaps more important purpose is to affect the therapeutic decisionmaking process.

Radiographs Radiographs are recommended when a patient is diagnosed with any of the above red flags. Lumbar radiographs may prove to be sufficient for the initial evaluation of the following red flags, but further imaging is suggested for treatment planning if findings are abnormal or inconclusive.3,7 z Recent significant trauma (at any age) z Osteoporosis z Age more than 70 years. The initial evaluation of the LBP patient may also require further imaging if other red flags, such as suspicion of cancer or infection, are present. Plain and contrast-enhanced magnetic resonance imaging (MRI) can demonstrate inflammatory, neoplastic, and most traumatic lesions as well as show anatomic details which are not available on isotope studies. Gadoliniumenhanced MRI is reliable and shows the presence and extent of spinal infection, and is valuable in assessing therapy.7,8 MRI has therefore taken over the role of the isotope scan in many cases where the location of the lesion is known. The isotope scan becomes important when a survey of the entire skeleton is indicated (e.g. for metastatic disease).

Magnetic Resonance Imaging, Computed Tomography, Myelography, Myelography/CT Uncomplicated acute LBP and/or radiculopathy (no red flags) do not warrant the use of any of these imaging studies. The early and indiscriminate use of expensive imaging procedures should be averted. It is crucial to know the appropriate usage of these imaging procedures, e.g. LBP complicated by “red flags” suggesting infection or tumor may justify early use of computed tomography (CT) or MRI even if radiographs are negative. The most common indication for the use of these imaging procedures, however, is the clinical setting of LBP complicated by radiating pain (radiculopathy, sciatica) or cauda equina syndrome (bilateral leg weakness, urinary retention, saddle anesthesia), usually due to herniated disk and/or canal stenosis.3

Magnetic Resonance Imaging Magnetic resonance imaging of the lumbar spine (LS) has become the initial imaging modality of choice in complicated LBP, replacing myelography and CT in recent years. Although abnormalities of disk are not uncommon on MRI in asymptomatic people, acute back pain with radiculopathy indicates the presence of demonstrable nerve root compression on MRI. However, verifying the cause of back pain is problematic as it is often multifactorial and anatomical abnormalities are common in the spine and may not necessarily transform into clinical symptoms. Thus, in nonspecific LBP, the use of MRI should be avoided and it should be reserved for the investigation of severe or progressive neurological deficits or for those cases in which suspicion of serious underlying pathology. However, its role is vital in planning surgical management in cases of radiculopathy and spinal stenosis.3,7,8 Magnetic resonance imaging is very efficient in detection of “red flag” diagnoses, chiefly using the short tau inversion recovery (STIR) and fat-saturated T2-weighted (T2W) fastspin-echo (FSE) sequences. MR with contrast is useful for suspected infection and neoplasia. In postoperative patients, enhanced MRI allows for distinction between disk and scar when tissue extends beyond the disk space. MR protocol for imaging patients with backache:9 z Coils and patient position: — Phased array spine coils should be used for all spine imaging. Patients are positioned supine in the magnet. z Image orientation: — Sagittal and axial images are acquired in the lumbar region. In the axial imaging plane, stacked cuts are acquired that cover an entire block of the spine. Acquiring images angled only through the disks is

Chapter 35 Imaging of Low Backache

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considered inadequate because portions of the spinal canal are not imaged in the axial plane, and sequestered disk fragments and spondylolysis defects are often missed. — Sagittal images alone are sometimes inadequate to detect a disk fragment that has migrated from the parent disk. Because sequestered disks are a cause of failed back surgery and persistent symptoms, it is important to identify them on MRI by obtaining stacked axial images in addition to sagittal images through the canal. — In the unoperated LS, stacked axial images should be obtained from the middle of the L3 vertebral body to the middle of the S1 vertebral body. — In the postoperative spine, stacked axial images (matched images before and after contrast administration) are obtained by centering at the level of the previous surgery. — Axial images are often better than sagittal for detection of lesions in the neural foramina. Generally, axial and sagittal planes of imaging are complementary to each other. — Coronal images may be useful for a better definition of the anatomy in patients with scoliosis. Pulse sequences and regions of interest: — T -weighted (T1W) and fast T2W images are the 1 standard for sagittal imaging in any segment of the spine. — Gradient echo sagittal sequences are used when looking for blood in the cord after trauma to take advantage of the blooming effect. — A fast STIR sagittal sequence also is useful in trauma patients when looking for ligamentous injury with changes of hemorrhage and edema. — Gradient echo axial images are used to detect disk disease in the cervical spine, whereas fast T2W axial images are used in the thoracic and LS for the same indications. — T1W and FSE T2W images are selected in the sagittal and axial planes for most indications. Slice thickness generally is 3 mm or 4 mm. — The fields of view are as small as possible; larger ones are required for sagittal than for the axial imaging planes. — Phase and frequency encoding gradients should be reversed for imaging the spine in the sagittal plane so that chemical shift artifacts at the diskovertebral interfaces do not obscure pathology in the vertebral body endplates or disks. Contrast: — Contrast medium is always used for postoperative spine imaging, suspected infection, tumor, intradural or nontraumatic cord lesions. — If any abnormality is identified in the epidural space when evaluating for osseous metastases or cord

compression, gadolinium is given to show these lesions better.

Computed Tomography Computed tomography scans have the advantage of providing superior bone detail but are not as efficient in depicting disk protrusions as the multiplanar MRI. With the added value associated with high-quality reformatted sagittal and coronal plane images, CT is useful for depicting spondylolysis, pseudoarthrosis, scoliosis, and for postsurgical evaluation of bone-graft integrity, surgical fusion and instrumentation.3

Myelography/CT “Plain” myelography had been the mainstay of lumbarherniated disk diagnosis for decades. Now, it is usually combined with postmyelography CT in problematic cases. The combined study is complementary to plain CT or MRI and occasionally more accurate in diagnosing disk herniation, but the only disadvantage is that it requires lumbar puncture and contrast injection.

Discography, CT Discography When other studies are unsuccessful in localizing the cause of pain, discography may occasionally be helpful. Although the images often depict nonspecific aging or degenerative changes, the injection itself may reproduce the pain of patient, which may have diagnostic value.10,11

Isotope Bone Scan The role of isotope bone scan in patients with acute LBP has undergone a change in the recent years due to the wide availability of MRI, especially the contrast-enhanced MRI. The bone scan is a moderately sensitive test for detecting the presence of tumor, infection, or occult fractures of the vertebrae but is nonspecific. For spondylolysis or stress fracture in athletes, bone scintigraphy with single photon emission CT (SPECT), followed by limited CT if scintigraphy is positive, is more sensitive than MRI. High-resolution isotope imaging, including SPECT, may localize the source of pain in patients with articular facet osteoarthritis prior to therapeutic facet injection.12 Similar scans may be helpful in detecting and localizing the site of painful pseudoarthrosis in patients following lumbar spinal fusion.

TRANSITION VERTEBRA In 1917, Mario Bertolotti, an Italian surgeon, was the first to put forward a possible relationship between LBP and congenital anatomical abnormalities in the last lumbar vertebra, described as “sacral assimilation of the lumbar vertebrae”.13

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The presence of a transverse mega-apophysis in a lumbar vertebra with transitional characteristics may be associated with LBP. 4–7% of patients with LBP have transitional vertebra. Motion between the transitional vertebra and the sacrum is reduced and asymmetrical, resulting in early degenerative changes within the “neoarticulation” or in the normal contralateral facet joint, which gives rise to facet pain. Biomechanical stress transferred to the upper mobile vertebral segment can accelerate the disk degeneration, another mechanism responsible for pain. Lumbosacral transitional disk has reduced height compared with normal lumbosacral intervertebral disks. If a lumbosacral transitional vertebra (LSTV) is suspected on MRI, it has to be decided whether it represents a sacralized L5 or lumbarized S1. Many complimentary imaging findings have been described to identify the transition vertebra. The true nature of the lower vertebral segmentation can be established only on conventional radiographs, which include the thoracolumbar junction, so that hypoplastic true ribs may be differentiated from large transverse processes, thus allowing correct identification of the L1 vertebral body. It has been recommended to use a whole spine localizer to count the number of vertebra from C2 with the assumption that there are 7 cervical and 12 thoracic segments that helps in assigning the LSTV.14 It has been proposed that the position of the right renal artery may be used to identify lumbar levels on sagittal MRI, because it usually lies closest to the L 1-2 disk space and the aortic bifurcation lies at L4. The iliolumbar ligament can be clearly identified on axial MRI as a single or double hypointense band extending from the transverse process of L5 to the posteromedial iliac crest that also helps in localization of L5 vertebra. The identification of vertebral level and transitional vertebra is also important in communicating the correct level of disk abnormalities to the operating surgeon.14

Imaging In spondylolysis, the aim of imaging is to detect lysis, distinguish acute and active lesions from chronic inactive nonunion, assess bony healing in follow-up of acute lesions, detect listhesis and grade it, and identify spinal and neural foramina stenosis.17,18 Conventional radiography is often the first-line imaging modality (Figs 1A and B). Its techniques include routine anteroposterior (AP) lateral views and oblique views. Although chronic nonunion may be demonstrated, radiography is not reliable for detection of early and acute lesions. Oblique radiographs of the lumbosacral spine are more sensitive than frontal and lateral radiographs, which may miss 20% of unilateral pars defects.19 Computed tomography is probably the best method for demonstrating spondylolytic defects and may also be helpful in assessment of healing. Three-dimensional (3D) reconstruction along the pars has been utilized successfully for identifying defects, by demonstrating discontinuity in the bony ring of the posterior elements of the vertebra. However, CT has limited scope in detection of other pathological processes, and it cannot reliable in distinguishing between active and inactive lesions.17,18 Magnetic resonance imaging may not depict the bony pars defects; however, it gives accurate evaluation of the degree of slippage (Figs 2A to D), spinal stenosis, nerve roots, and the associated pathologic disk changes. A morphological grading system of pars defects has been described on MRI.19 A new grading system has been described that utilizes both the morphological information of MRI combined with the presence or absence of marrow edema on fat-suppressed

SPONDYLOLYSIS AND SPONDYLOLISTHESIS Spondylolysis refers to a defect in the pars interarticularis, which appears to be secondary to a stress fracture. A bilateral defect would result in spondylolisthesis (forward slippage of a vertebra on the one below it) of varying degrees. Most common levels are L4-5 and L5-S1. The prevalence of spondylolysis is low in young children and increases with age. There is a high incidence in adolescent athletes. There is a genetic predisposition to spondylolisthesis, with 30–70% prevalence in other family members. Spondylolisthesis may be secondary to stress fracture of bilateral pars in young or may be due to degenerative disease in elders.15,16 Spondylolisthesis has been graded as follows, according to forward slippage of a vertebra on the one below it: grade I (0–25%), grade II (25–50%), grade III (50–75%) and grade IV (75–100%).

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Chapter 35 Imaging of Low Backache

study suggests that the presence of a gene defect in the COL9A3 gene is associated with Scheuermann’s disease and intervertebral disk degeneration.

Clinical Presentation Adolescents typically present to medical attention because of cosmetic deformity; adults more commonly present because of increased pain.

Imaging and Diagnosis

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T2W images. This distinguishes between stress reaction and active and inactive spondylolysis.19,20 Indications for surgery include worsening pain and progressive listhesis, significant neurologic findings and slippage of more than 50%. Healing is not a feature of developmental spondylolysis, and patients with chronic inactive lysis can usually return to normal physical activities.

SCHEUERMANN’S DISEASE 21

Scheuermann’s disease, also known as juvenile kyphosis, is a disorder that presents with a rigid thoracic or thoracolumbar kyphosis. Its incidence is estimated at 1–8%. Lumbar localization of Scheuermann’s disease is more painful than the thoracic counterpart. It was first described in 1920 by Scheuermann,21 who believed that the endplate irregularity and vertebral wedging was caused by avascular necrosis of the cartilage ring apophysis. Although the etiology is still unknown, it is thought to be related to stress and repeated trauma. A recent

The diagnosis of classical Scheuermann’s disease is based on involvement of three contiguous thoracic vertebrae with 5° of wedging associated with endplate irregularity, and a thoracic kyphosis greater than 40°. The diagnosis of lumbar Scheuermann’s disease is based on varying degrees of endplate irregularities and disk narrowing in the LS or thoracolumbar junction, but with no abnormal kyphosis.21,22 Radiographs may show vertebral endplate irregularities, anterior vertebral body wedging, Schmorl’s nodes (Figs 3A and B), and relative narrowing of the disk spaces. The diagnostic role of MRI (Figs 3C and D) is very crucial, particularly in cases of severe and painful kyphosis. It demonstrates, with great detail, endplate irregularities, Schmorl’s nodes, disk degeneration, disk space narrowing and anterior wedging of the vertebral bodies. Assessment of vertebral canal is imperative, especially in case of severe kyphosis.23 When reporting on radiographs of the LS with a combination of features, such as endplate irregularity, disk narrowing and Schmorl’s nodes, particularly at the thoracolumbar junction, which would usually be recorded as being indicative of Scheuermann’s disease, radiologists should avoid the use of this term and report only the anatomical and pathological features seen. The radiological diagnosis of Scheuermann’s disease should be restricted to those patients who demonstrate the above features associated with an increased kyphosis of the thoracic spine.23

DEGENERATIVE DISEASES OF LUMBAR SPINE Degenerative Changes in the Anterior Elements z z z z z

Degenerative change of the nucleus pulposus Annular tears Disk herniation Degenerative endplate changes Spondylosis deformans.

Degenerative Changes in the Posterior Elements Degenerative changes of the facet joints.

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Degenerative change may present with local back pain, radiculopathy, or myelopathy. Degenerative facet arthropathy, degenerative disk disease, degenerative endplate changes and ligamentous injury are all possible pain generators in the setting of axial back pain. Narrowing of the spinal canal or neural foramina can result in myelopathy and radiculopathy, respectively. Segmental instability, kyphosis and scoliosis malalignment that may occur secondary to degenerative disease. Imaging of patients who have suspected spine pathology characterizes the level and extent of degenerative changes that may be a source of symptoms. Significant morphological changes on imaging are often found in asymptomatic patients without any significant clinical symptomatology, which does not require further evaluation in terms of acquiring electrophysiologic data to determine the significance of anatomic findings seen on imaging studies.

DEGENERATIVE CHANGE OF THE NUCLEUS PULPOSUS Normal Disk Intervertebral disks consist of a central gelatinous nucleus pulposus composed of water and proteoglycans. The nucleus pulposus is surrounded by the annulus fibrosus. The inner portion of the annulus is composed of fibrocartilage, whereas the outer fibers are made of concentrically oriented lamellae of collagen fibers. The annulus is anchored to the adjacent vertebral bodies by Sharpey’s fibers.

MR Appearance of Normal Disk On MRI, the ideal normal disk is low-signal intensity on T1W images, slightly lower signal than adjacent normal red marrow and very similar to muscle. T2W images show diffuse highsignal intensity (Figs 4A and B) throughout the disk except for the outer fibers of the annulus, which are homogeneously lowsignal intensity. Distinction between the nucleus pulposus and the inner annulus fibrosus is impossible by MRI. Normal disks typically do not extend beyond the margins of the adjacent vertebral bodies; however, diffuse extension beyond the margins by 1–2 mm may occur in some histologically normal disks. The posterior margins

Chapter 35 Imaging of Low Backache

Annular Tears

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Annular tears represent a biomechanical failure of the annulus fibrosis and are usually associated with degenerative changes in the nucleus pulposus. The three basic types of annular tears are: (1) vertical, (2) radial and (3) peripheral rim tears, of these radial tear is of practical interest.25-27 Radial tears involve either part or the entire thickness of the annulus from the nucleus to the outer annular fibers. Radial tears run perpendicular to the long-axis of the annulus and occur more commonly in the posterior half of the disk, usually at L4-5 and L5-S1.25-27 Radial tears may lead to pain either because the vascularized granulation tissue grows into the tear and causes painful stimulation of nerve endings or the chemical and mechanical irritation to the nociceptive fibers that normally exist in the annulus.

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of disks tend to be mildly concave in the upper LS, straight at the L4-5 level, and slightly convex at the lumbosacral junction.24

Abnormal Nucleus With aging and degeneration, the intervertebral disks lose hydration, lose proteoglycans, and gain collagen as they become more fibrous. A horizontally oriented fibrous intranuclear cleft develops in the nucleus. MRI shows the intranuclear cleft as a horizontal, low-signal intensity line that divides the disk into upper and lower halves on T2W sagittal images. Eventually, there is diffuse decreased signal intensity on T2W images (Figs 4A and B) from the increased collagen content in the nucleus. Gradually, the disk starts losing height against the increasing degrees of degeneration.24

Points to Remember z

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The term “early degenerative changes” refers to accelerated age-related changes in the disk without evidence of structural failure. A degenerated disk is a term reserved for those with structural failure combined with accelerated or advanced signs of aging. Degenerative disk disease is best defined as symptomatic degenerative disk changes. Many patients exhibit degenerative changes on MR without associated symptoms. Intervertebral disk height at the lumbosacral junction is variable because of segmentation differences and a decreased disk height at this interspace is not necessarily pathologic.24

z

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Show focal areas of high-signal intensity on T2W images or on contrast-enhanced T1W images. Radial tears may be seen on T2W sagittal images within the posterior annulus as globular or horizontal lines of high-signal intensity. On axial images, radial tears may be seen as focal areas of high-signal intensity that parallel the outer disk margin for a short distance. Radial tears or fissures on MRI are termed as highintensity zones.

Disk Herniation (Abnormalities in Disk Morphology) It is a nonspecific term used to indicate disk that extends in some abnormal manner beyond the margin of vertebral body. Most surgeons dealing with spine disorders use a more standardized nomenclature that helps to distinguish what are likely to be clinically relevant lesions from lesions that probably are not. Standard nomenclatures used by the orthopedic surgeons include: z Diffuse disk bulge z Broad-based protrusion z Focal disk protrusion z Disk extrusion 25-27 z Sequestered disk.

Points to Remember z

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A herniation is “focal” if it involves less than 25% of the disk circumference. A “broad-based” disk herniation involves between 25% and 50% of the disk circumference. Involvement of more than 50% of the circumference of the disk is defined as a “disk bulge”.

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Mild if the anterior epidural fat is not obliterated Moderate if the epidural fat is obliterated and the thecal sac is being displaced Severe if the cord is being effaced or nerve roots displaced.

Diffusely bulging disk: It extends symmetrically and circumferentially by more than 2 mm beyond the margins of the adjacent vertebral bodies. This diagnosis is based on axial and sagittal images by comparing the size of the disk with the size of the adjacent vertebral bodies. A segment of disk tissue that projects beyond the margin of the vertebral body but that does not involve the entire circumference of the disk can be called either a focal bulge or a broad-based protrusion.

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A “disk protrusion” (Figs 5A to D) is defined as a herniation that demonstrates continuity with the adjacent disk. Herniated disk shows AP more than mediolateral diameter. If the size of the disk fragment (in any plane) is greater than the width of the base (AP > mediolateral diameter), it is termed a “disk extrusion” (Figs 6A and B). A “sequestered disk” refers to a disk fragment that has lost all continuity with the parent disk (Figs 7A to D).

Disk protrusion: It is a focal, asymmetric extension of disk tissue beyond the vertebral body margin, usually into the spinal canal or neural foramen. The base (the mediolateral dimension along the posterior margin of the disk) is broader than any other dimension (Figs 5A to D). Some of the outer annular fibers remain intact, and hence it is referred to as a contained disk. The protruded disk does not extend in a cranial or caudal direction from the parent disk. Extruded disk: It is a more pronounced version of a protrusion and often is responsible for symptoms. There is disruption of the outer fibers of the annulus, and the disk abnormality usually is greater in its AP dimension than it is at its base (mediolateral dimension). The extruded disk may migrate up or down behind the adjacent vertebral bodies (Figs 6A and B) but maintains continuity with the parent disk. These also

Chapter 35 Imaging of Low Backache

may be referred to as noncontained disks. MRI shows the described contour abnormalities, and because of a significant inflammatory reaction that may occur in response to the extruded disk material, there may be high-signal intensity on T2W and contrast-enhanced T1W images in or surrounding the disk. Lumbar disk extrusions that cause radiculopathy but are managed nonoperatively have been shown to do well about 90% of the time. Spontaneous reduction in size of disk extrusions and protrusions that were managed conservatively has been well documented with imaging. The regression in disk size may not be the reason for reduction in pain. Much of the pain from extruded disks is probably from the inflammatory response to them rather than from compression of neural elements from the mass effect. Sequestered disk: When extruded disk material loses its attachment to the parent disk, it is called a sequestered fragment (Figs 7A to D). These fragments may migrate in a cranial or caudal direction with equal frequency and generally remain within about 5 mm of the parent disk. They may be located between the posterior longitudinal ligament and the osseous spine or extend through the posterior ligament into the epidural space. They almost always remain in the anterior epidural space, but occasionally the fragment may migrate into the posterior epidural space. It is extremely important to recognize these fragments because they may be overlooked at surgery. The fragment of disk material that migrates from the parent disk often shows peripheral or diffuse high-signal intensity on T2W and contrast-enhanced T1W images, caused by the inflammatory reaction within or surrounding it. Otherwise, a low-signal intensity mass resembling the signal of the parent disk is seen. Sequestrations are a contraindication to chymopapain, percutaneous diskectomy, and other limited disk procedures.

Location of Focal Disk Abnormalities While reporting a focal disk abnormality the size, contour, location and relationship to nerves or other important structures should be described. The location of a focal disk abnormality needs to be conveyed accurately so that the surgical approach can be planned properly and so that it can be determined whether symptoms correlate to the anatomic abnormality seen on MRI. Focal disk abnormalities that remain at the level of the parent disk should be described as being central, left or right paracentral, left or right foraminal, or left or right extraforaminal (also called lateral or far lateral).25-27

Significance of Disk Contour Abnormalities Degenerative disk disease can cause following consequences: Neural compression z Chemical irritation of nerves z

z z z z

Osseous abnormalities Segmental instability Spinal stenosis Disk-related compressive myelopathy.

Intraosseous Disk Herniations Disk material not only projects into the spinal canal, but also may directly herniate into the adjacent vertebral bodies through the endplates which are known as a Schmorl’s or cartilaginous nodes.

Presentation These are usually asymptomatic; however traumatic Schmorl’s nodes resulting from axial loading forces may be acutely painful. Multiple thoracic Schmorl’s nodes can occur in very active teens from axial stresses and result in irregularity of several endplates, loss of disk height, and narrowing of the height of the affected anterior vertebral bodies from fractures, with a resultant kyphosis (Scheuermann’s disease).21,22 An inflammatory, foreign body-type response to intraosseous disk herniation may occur, with vascularization around the disk material and surrounding marrow edema, which may cause severe pain.

Points to Remember Vascularized Schmorl’s nodes on MRI tend to have large, dome-shaped regions of marrow edema surrounding them; marrow edema is low signal on T1W and high signal on T2W and contrast-enhanced T1W images. A rim of contrast enhancement around the periphery of the Schmorl’s node is seen in addition to the surrounding marrow edema. These can have an aggressive look, similar to infection or tumor, and careful evaluation is necessary to make the proper diagnosis.25-27

OSSEOUS DEGENERATIVE CHANGES Vertebral Bodies The vertebral bodies respond to degenerative changes in the adjacent intervertebral disks in two major ways: 1. Formation of osteophytes 2. Marrow changes paralleling the endplates.

Osteophytes Osteophytes are the excrescences of bone that occur on the upper or lower margins of vertebral bodies. They occur as disks degenerate and bulge, placing traction stresses on Sharpey’s fibers, which attach the disks to the vertebral bodies. They usually are located anteriorly in the lumbar and thoracic spine, but are commonly anterior or posterior in the

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cervical spine. MRI of most osteophytes shows low-signal intensity cortical margins with fatty marrow centers that follow the signal of fat on all pulse sequences.

Endplates The marrow in vertebral bodies adjacent to degenerated disks may change in response to the disk disease. Parallel bands of abnormal signal in the endplates have been divided into three types and are called Modic type I, II, or III changes. These marrow changes may be focal or diffuse along the endplate but tend to be linear and always parallel to the endplates.26-28 z Type I: Decreased signal T , increased signal T 1 2 (inflammatory tissue) z Type II: Increased signal T , follows fat on T (focal 1 2 conversion to fat) z Type III: Decreased signal T and T (sclerosis). 1 2

Posterior Spinous Processes Degenerative changes of the spinous processes and intervening interspinous soft tissues are called as kissing spine or Baastrup’s disease. The main appearance to be aware of on MRI is the high-signal intensity bursal fluid collections between spinous processes on T2W images.

Spinal Stenosis Spinal stenosis is narrowing of the central spinal canal, neural foramen, lateral recess, or any combination of these anatomic regions, by soft tissue or osseous structures that impinge on neural elements and may result in symptoms.28,29

Causes Degenerative: — Disk contour abnormalities (bulges, herniations) — Vertebral body osteophytes — Degenerative spondylolisthesis — Facet joint degeneration, osteophytes, synovial cysts — Ligamentum flavum buckling z Congenital short pedicles: — Usually requires superimposed degeneration to be symptomatic z Any mass arising from bone, disk, or within canal: — Osseous tumor, fracture fragments — Spondylolysis, spondylolisthesis — Ossification of posterior longitudinal ligament — Epidural lipomatosis, hematoma, abscess, tumor, scarring. Symptoms from spinal stenosis are often nonspecific and include back pain, intermittent neurogenic claudication, extremity radiculopathy, pain with hyperextension relieved by flexion, and pain on standing relieved by lying down. The presence of imaging findings of spinal stenosis does not indicate that a patient has symptoms from the stenosis. z

Facet Joints Normal Facet Joints They are formed by the inferior articular process of the vertebra above articulating with the superior articular process of the lower vertebra. The articular surfaces are covered with hyaline cartilage. The osseous structures are enveloped in a joint capsule lined by synovium; these are true synovial joints. The anterior aspects of the facet joints and the laminae are covered by the ligamentum flavum.

Facet Joint Arthropathy Degenerative changes of the facet joints manifest as cartilage fibrillation with joint space narrowing, subchondral sclerosis, subchondral cysts, and osteophyte formation that result in overgrowth or hypertrophy of the osseous portions of the joints. Synovial cysts may develop from degenerated spinal facet joints and project either anteriorly (through the ligamentum flavum) or posteriorly from the joints.26,27 Symptoms from degenerative changes of the facet joints may result from compression of adjacent neural structures (spinal stenosis) by overgrowth of the bone, inward buckling of the ligamentum flavum, protrusion of synovial cysts into the spinal canal, or the joints themselves being painful.

Types of Involvement z z z

Imaging findings: MRI of degenerative facet joint disease is typical of degenerative changes in any joint (subchondral sclerosis is low-signal intensity on all pulse sequences; synovial cysts are low-signal intensity on T1W and high-signal intensity on T2W images). The osteophytes and hypertrophic osseous changes create a rounded and enlarged appearance of the articular processes of the facets on axial images that may cause narrowing of the adjacent spinal canal, lateral recesses, or neural foramina.

Central canal stenosis Neural foramina stenosis Lateral recesses stenosis.

Central canal stenosis: It usually is the result of facet joint osteophytes and inward buckling of the ligamentum flavum posteriorly, with disk bulging anteriorly in the canal. Normally, the central canal and thecal sac are round or nearly round (a plump oval) structures on axial images; if they become flattened ovals or triangular in shape, it indicates central stenosis. Central stenosis can cause edema in the affected nerve roots, or in the cervical spine, there may be abnormalities of the cord, probably myelomalacia from

Chapter 35 Imaging of Low Backache

ischemia at the site of stenosis, which shows high-signal intensity on T2W images.28,29 Lateral recess stenosis: It usually is caused by hypertrophic degenerative changes of the facet joints, or less commonly by a disk fragment or postoperative fibrosis. Lateral recesses are located on the medial aspects of pedicles. Nerve roots lie in these recesses after leaving the thecal sac, but before entering the exiting neural foramina. There is a neural foramen bordering the upper and the lower margins of a lateral recess. If there is deformity in the shape of the recess, and the descending nerve is displaced or compressed, there is lateral recess stenosis. This space is best evaluated in the axial plane of imaging. Neural foramen stenosis: It occurs as a result of degenerative osteophytes of the facet joints or a foraminal disk protrusion (Fig. 5D), extrusion, or sequestered fragment; a diffuse disk bulge; or postoperative fibrosis. Narrowing of the neural foramina can be evaluated on sagittal and axial images. On sagittal images, the normal neural foramen has the appearance of a vertical oval. If disk material extends into the foramen, the oval narrows inferiorly, creating a keyhole shape. Axial images may be more accurate for diagnosis because they show more of the extent of each foramen.28,29

Failed Back Syndrome Patients may have persistent, recurrent, or new and different symptoms after surgery of the spine. The reasons for these problems are many and varied. The most common reasons are recurrent or persistent disk extrusions, postoperative scarring, spondylodiskitis, arachnoiditis, nerve root damage (neuritis) and inadequate surgery.30,31 Distinguishing postoperative scarring (epidural fibrosis) from extruded disk material is one of the most important tasks for radiologists in evaluating postoperative MRI studies. All postoperative spine MRI studies should be done with contrast enhancement to distinguish between these two common causes of symptoms in postoperative patients. Scar tissue that is more than 6 months old enhances diffusely (Figs 8A to F) and early after the IV administration of gadolinium (high-signal intensity on T1W images). Disk material does not enhance until late, if at all, and usually enhances only peripherally. These rules do not work as well during the first 6 months after surgery, when asymptomatic fibrosis may show peripheral rather than diffuse contrast enhancement that is indistinguishable from an extruded disk. Extruded disk material may be an indication for another operation, whereas there is no benefit from reoperating on a patient with postoperative scarring.30,31 Other signs that may help distinguish postoperative scarring from a disk abnormality are that postoperative scarring often has irregular margins; it may not be contiguous

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with the adjacent disk; and, instead of producing a mass effect on the dural sac, it may cause retraction. Recurrent disk herniations, conversely, usually are contiguous with the disk, have sharp margins, and cause mass effect on the dural sac.30,31

Seronegative Spondyloarthropathy This group of disorders includes ankylosing spondylitis, Reiter’s or reactive arthropathy, psoriatic arthropathy and spondyloarthropathy associated with inflammatory disease. They are characterized by rheumatoid factor negative inflammatory arthritis and enthesopathy affecting the spine and sacroiliac (SI) joints. It presents in early-to-mid adulthood, more commonly in males with symptoms of low backache and stiffness which is worse in the morning. It has a strong association with human leukocyte antigen B27 (HLAB27) haplotype. A detailed discussion of this entity is beyond the scope of this chapter and only the salient features are presented. The disease first affects bilateral SI joints followed by the thoracolumbar junction and may eventually involve the entire spine. The erosive sacroiliitis is best appreciated on a posteroanterior (PA) view of the pelvis and affects the lower third of the joint. The earliest sign is loss of definition

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of subchondral bone, and other features are small erosions, widening of joint space, sclerosis and eventually fusion of the joint.32,33 Early manifestations of sacroiliitis may be better evaluated by CT and MRI. Small erosions are well seen on CT and MRI in the early stage of disease shows T2 and STIR hyperintensity (Figs 9A to C).34 The vertebral bodies show squaring, corner erosions which undergo sclerotic repair. This leads to shiny corner sign or Romanus lesion (Fig. 9C). Multilevel syndesmophytes give rise to a bamboo spine appearance. Facet joints are commonly involved and erosions progress to fusion. Fractures and pseudoarthrosis may occur through the disk or endplate, and are referred to as Anderson lesion (Figs 10A and B). This can mimic infectious spondylodiskitis and the differentiating feature is extension across the posterior elements.34

INFECTIONS Infections of the spine are a common cause of back pain in India. It should be suspected in patients with severe back pain that does not improve with rest; that wakes them at night; and that is associated with a fever. Tuberculosis (TB) of the spine is common in India and needs to be kept in the list of differential diagnosis for a wide variety of spinal abnormalities. Conventional radiographs are the initial screening modality when infectious spondylitis is suspected. Compared to MRI and radionuclide scans, radiographs are relatively insensitive early in the course of infection. It takes weeks for destructive changes to become evident.32,35 This initial imaging study, however, guides the next diagnostic step.

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Tubercular Infection The spine is the most common site of osseous tuberculous involvement, comprising in most series about 50% of cases. Patients present with long-standing and insidious onset of stiffness and local tenderness, with or without constitutional symptoms. The lower dorsal and upper lumbar vertebrae are most frequently affected; cervical and sacral involvement occurs uncommonly. The spread of TB to the spine is usually

Chapter 35 Imaging of Low Backache

by hematogenous route, by perivertebral arterial or venous plexi, or rarely by extension from a paraspinal infection. It is often difficult to differentiate tubercular from pyogenic spondylitis both clinically and on imaging. There are four different patterns of involvement: (1) paradiskal, (2) central, (3) subligamentous and (4) posterior.35 Plain film evaluation of the tuberculous spondylodiskitis may demonstrate loss of vertebral height or disk interval, erosions, indistinct margins of endplates (Figs 11A and B) paravertebral masses, and sequestrae. The infection usually begins in the anterior aspect of the vertebral body, adjacent to the vertebral endplate. Focal areas of erosion and osseous destruction in the anterior corners of the vertebral body are typical plain film findings. Involvement of the adjacent intervertebral disk or vertebral body results from penetration of the disk itself or spread of infection beneath the anterior or posterior longitudinal ligament. Contiguous vertebral involvement, destruction of the intervertebral disk and progressive vertebral body collapse result in the characteristic gibbus deformity of the spine commonly associated with spinal TB.32,35 Paraspinal abscess formation may be detected on radiographs as fusiform paravertebral soft-tissue masses. Disk space narrowing may be quite subtle. Over 50% of the trabecular bone is lost before a lesion is conspicuous on plain film; this process may take up to 6 month. In the thoracic spine visualization of a paravertebral abscess requires an adequately penetrated view. In the LS asymmetry or bulging of the psoas shadow may be detected. Scalloping of the anterior vertebral contour (aneurysmal appearance) is more commonly seen with children. Plain film is limited in evaluation of the posterior arch, particularly in the thoracic spine. No specific or pathognomonic plain film signs distinguish tuberculous from pyogenic spinal infection, and correlation with the clinical picture is important.

CT Features Features of spinal TB that are well delineated on CT include anterior vertebral body destruction, vertebral body collapse and large paraspinal abscesses. The extension of these abscesses including extradural, intraspinal extension can be well evaluated. Paraspinal and intraosseous abscesses show thick and irregular peripheral enhancement. When they are deep seated CT can provide guidance to drain them percutaneously. In the early stage of disease, bone destruction may be subtle and is better shown on sagittal and coronal reformatted images.

MR Features Multiplanar capability and optimal tissue contrast make MRI the optimal modality for evaluation of spondylodiskitis.36-38 The entire spine and canal can be visualized, including the posterior elements. MRI has higher sensitivity for early infiltrative disease including endplate changes and marrow infiltration than bone scan and plain films. MRI affords excellent definition of epidural, paravertebral, intraosseous abscesses and extent of cord compromise. Paravertebral abscesses may be large, and discharge through tracts well seen on multiple planes. The involved vertebrae show hypointense signal on T1W images and heterogeneous increased signal on T2W images. The IV administration of contrast improves definition of epidural abscesses and masses, and cord and nerve root compromise (Figs 12A to D).

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The abscesses show peripheral enhancement with central necrosis. Acute stage shows inhomogeneous enhancement in areas of marrow infiltration, and enhancing lesion borders. With tuberculous spondylodiskitis, the disk shows signal characteristics seen with pyogenic diskitis in at least three quarters of cases, of bright signal on T2W images, decreased signal on T1W images, and enhancement of disk after contrast administration. Disk space preservation, normal signal intensity and lack of enhancement have been reported in approximately 25% of cases. In paradiskal variety MRI shows hypointense signal on T1W and high signal on T2W images in the endplate, narrowing of the disk, and large paraspinal and epidural abscesses. In the central type of lesion, signal intensity abnormality is confined to the vertebral body and the disk space is preserved. The appearance can be indistinguishable from metastases or lymphoma.36-40

Differential Diagnosis Uncommon infections: Brucellosis is a zoonotic infection, and the most common site of bone brucellosis is the spine. The imaging manifestations closely resemble tubercular spondylitis. Brucellar spondylitis has a predilection for the lower LS. Features reported in the literature include intact vertebral architecture in spite of diffuse vertebral osteomyelitis, marked T2-hyperintensity and enhancement of the intervertebral disk and facet joint involvement.

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Chapter 35 Imaging of Low Backache

Gibbus deformities are rare and paraspinal abscesses are smaller than those in tubercular spondylitis. This possibility should be kept in mind when apparent tubercular spondylitis does not respond to treatment.37 Fungal spondylitis caused by organisms like Aspergillus may be seen in immunocompromised hosts and very rarely in immunocompetent patients. The imaging findings mimic pyogenic or tubercular spondylitis and diagnosis is made usually after tissue sampling. T2-hyperintensity in disks is typically lacking in this entity, a fact attribute to the para- and ferromagnetic elements in fungi.40 Noninfectious diseases that mimic spondylodiskitis: Noninfectious inflammatory diseases and degenerative disease may simulate spinal infection. Discogenic vertebral body degeneration (Modic type I) may resemble infectious spondylitis because of the presence of bone marrow edema which has high-signal intensity on T2W images. These marrow changes and the associated disk may also enhance on contrast-enhanced images. The lack of increased signal intensity of associated disk on T2W images and the absence of soft-tissue abnormality distinguish degenerative changes from infectious spondylitis.38,39 Pseudoarthrosis secondary to spinal fracture (Anderson lesion) are not an uncommon complication of advanced ankylosing spondylitis. They commonly involve the disk space or juxta-articular endplate. In pseudoarthrosis subchondral sclerosis and endplate erosion may be seen on radiographs that mimic infectious spondylitis. MRI can help in the differentiation by showing the extension of fracture line across the posterior elements.38 Occasionally Schmorl’s nodes can also mimic infectious spondylodiskitis. The herniation of the disk into the vertebral endplate can incite marrow edema and vascularization which can result in vertebral endplate hyperintensity and enhancement. However, if the bone defect involves only one endplate and the disk does not show diffuse signal abnormality, Schmorl’s node rather than spondylodiskitis should be suspected. Neuropathic spine is seen in patients of diabetes, syringomyelia, syphilis, etc. It most often involves the thoracolumbar junction and LS. Destructive changes in the vertebral bodies lead to fracture, bone sclerosis, large osteophytes and decreased disk space. The disk space and surrounding marrow show lower T2 signal than in infectious spondylitis. Other distinguishing findings of this entity include facet involvement, osseous joint debris and joint disorganization. In neoplastic lesions, the disk is usually preserved and disk height reduction is rare. The endplates are usually distinct. If posterior elements are involved, neoplastic lesions should be included in the differential. Other infiltrative granulomatous lesions like sarcoidosis may show signal intensity abnormalities similar to TB, but diskitis is usually not seen.

Pyogenic Infection The vertebral infection generally begins adjacent to the endplate; it invades the subchondral bone and extends to the disk. The common causative organism is Staphylococcus aureus. This pattern of hematogenous infection gives rise to the classic radiographic picture of infectious spondylitis: destructive changes of two adjacent vertebral bodies and the intervening disk. This is manifested on the radiograph as loss of height of the vertebral bodies and a narrowed disk space. Because of endplate destruction, the disk space may have an apparent increase in height, rather than narrowing. The destructive changes of metastatic tumor have a different pattern. Tumor tends to respect the endplates, extending into the surrounding soft tissues by cortical invasion. The initial radiographs may be completely normal and the findings typically lag behind symptoms by 2–3 weeks. The earliest signs include blurring of endplates and decrease in the height of disk space followed by bone destruction in the adjacent vertebrae. Eventually sclerosis supervenes and is a manifestation of a reparative response. Radionuclide scan using technetium-99m (99mTc) has an accuracy as high as 90% in patients with more than 2 days of symptoms.40-42

TUMORS A wide spectrum of tumors can affect the bony spine. Some of them like hemangiomas are common and discovered incidentally. The most common malignant lesions in the spine are metastases and myeloma. Primary tumors are rare and radiographic and MR features can help to narrow the differential diagnosis.43

Benign Tumors Hemangioma They are benign vascular lesions, majority of which are asymptomatic and discovered incidentally. They have been reported in up to 10% of all individuals undergoing spinal imaging. Most spinal hemangiomas occur in thoracic spine and are usually confined to the vertebral bodies. They are usually asymptomatic and do not require clinical attention. However, rarely, they are aggressive and can grow beyond the vertebral body and may compress the spinal cord or nerve roots.32,43 They show characteristic imaging findings. The radiographic appearance is of prominent vertical striations giving a corduroy cloth or honeycomb appearance. This translates into the polka-dot appearance on CT. Thickened trabeculae are surrounded by hypodense fatty tissue. Typical hemangiomas appear hyperintense on both T1W and T2W sequences (Figs 15A and B) and may enhance after contrast administration. The aggressive hemangiomas are hypointense

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Section 1 Neuroradiology including Head and Neck

on T1W and bright in T2W scans, may be associated with a paravertebral soft tissue (Figs 16A to F) and resemble metastases or myeloma.43,44

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Osteoid Osteoma It is a relatively common benign osseous lesion. The peak incidence is in the 2nd decade. It has a tendency to involve the posterior elements and occurs commonly in the pedicle. The LS is most commonly affected (59%) followed by cervical and thoracic spine.45,46 The histological hallmark is a nidus, which is smaller than 1.5 cm. Clinically, the spinal osteoid osteoma presents with a painful scoliosis. The pain is worse at night, and is relieved with aspirin. The LS radiographs may show scoliosis, concave to the side of lesion. The central lucent nidus may be obscured by the reactive sclerosis. CT is the modality of choice for a careful search of a nidus (Figs 17A to C). The nidus is usually a subcentimeter lytic area with a sclerotic center surrounded by periosteal thickening. Occasionally, vascular channels leading to this lesion may be seen adjacent to the nidus. As with other nonaggressive osteoid lesions, MRI is not indicated. In fact, MR may be misleading, as the nidus is commonly not evident. If visible, it appears as a lowsignal focus with extensive adjacent marrow and soft-tissue edema. The nidus is hypointense on T1W images and hypoto hyperintense on T2W images. Surrounding hyperintensity is reactive host response and involves a much larger area than the tumor. Severe reactive response may lead to a

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Chapter 35 Imaging of Low Backache

misdiagnosis of malignancy or infection. The lesion is positive on all three phases of a 99mTc methylene diphosphonate (MDP) bone scan. The differential diagnosis of osteoid osteoma in the spine includes osteoblastoma which is larger, unilateral absent pedicle, osteoblastic metastases and stress fracture of pedicle. CT plays a valuable role in distinguishing these entities.45,46 The treatment is surgical or image-guided percutaneous excision or radiofrequency (RF) ablation. The entire nidus has to be removed to prevent recurrence.

Osteoblastoma Osteoblastomas are related to osteoid osteomas and by definition are larger than 1.5 cm in diameter. They are seen in patients in the 1st to 3rd decades. Up to 40% osteoblastomas are found in the spine. They also have a tendency to involve the posterior elements.43 Radiographs show a lytic, expansile lesion (Fig. 18A) in the posterior elements. CT is ideal to show the expansile lesion (Fig. 18B) with sclerotic border, which may have foci of calcification representing an osteoid matrix. MRI is usually not required except to show the relationship with the cord and nerve roots. It is T1-hypointense and shows intermediate-to-high signal on T2W images. 46 Secondary aneurysmal bone cyst may be seen within the lesion and they are T2-hyperintense (Fig. 18C) with fluid-fluid levels. Extensive peritumoral edema is common and may involve adjacent bones and soft tissues. The differential diagnosis includes osteoid osteoma, aneurysmal bone cyst, infection and metastases.

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Aneurysmal Bone Cyst They are benign lesions with blood-filled cavities. They occur in the younger age-group within the first 20 years of age. The spine is a common location with the LS ranking second to the thoracic spine. Radiograph shows expansile lesion in the posterior elements (Figs 19A and B) which often extends to involve the vertebral body. CT shows a lesion with balloon-like expansion and thinned out cortex, with a nonsclerotic narrow zone of transition. Fluid-fluid levels with sedimentation of blood products are a typical finding. It commonly extends into the epidural space and causes cord compression. MRI is ideal for showing the cystic spaces (Figs 19C and D) within the lesion separated by septae. Fluid levels of varying signal intensities due to different stages of hemorrhage (Fig. 19D) are well seen on MRI.43,45 On contrast administration only the periphery of the lesion and septae enhance.

Giant Cell Tumor It is an aggressive but benign bone tumor composed of osteoclastic giant cells. It occurs in mature skeleton commonly in the age group of 20–40 years. Spine is the fourth most common location for this lesion and majority of spinal giant cell tumors (GCTs) occur in the sacrum. Radiographs show an ill-defined expansile lytic lesion (Figs 20A and B) with a narrow zone of transition and without a sclerotic border. Sacral lesions can be occult on radiography and may only be picked up on cross-sectional imaging. MRI is ideal for showing the extension into the spinal canal and

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cord compression. It shows a lesion which is hypointense on T 1 and intermediate-to-high signal on T2W images (Figs 20C to F). Secondary aneurysmal bone cysts are seen as T2-hyperintense foci within the lesion.32,43 The differential diagnosis includes aneurysmal bone cyst, metastases, plasmacytoma and chordoma.

Malignant Tumors Chordoma Chordomas are relatively rare slow-growing low-grade malignant tumors. They arise from notochord remnants in

Chapter 35 Imaging of Low Backache

the centers of the vertebral bodies. They are more common at the cranial and caudal ends of the spine, i.e. clivus and sacrum, respectively, but may occur at any level, with 35% arising in the lumbosacral spine. Chordoma is always kept in the differential diagnosis when a midline lesion is seen involving the sacrum.47 The clinical presentation depends on the location of the tumor. The tumors may present with nonspecific back pain, which may be accompanied with neurological symptoms. It commonly affects patients in the 3rd to 6th decades of life, with no sex predominance. It appears as a lytic lesion on radiography and CT scanning with some amorphous calcification. MRI is the modality of choice for defining the extent of the tumor and its intraspinal extension. This tumor is hypointense on T1W and hyperintense on T2W sequence (Figs 21A to D) with low-signal septations.45,47 Postcontrast images show mild-to-intense enhancements. These characteristics along with its midline location in an older patient are suggestive of this diagnosis. En bloc resection is the treatment of choice and radiotherapy may play a useful role.

sources of vertebral metastases are the breast, lungs, thyroid, kidney and prostate.32,43 As the metastatic lesions grow, they destroy the vertebral body, penetrate through cortical bone, invade the spinal canal, and compromise the neural elements. Cord compression and neurological deficits may also occur when vertebral bodies collapse due to bone destruction. Radiographs have poor sensitivity for spinal metastases detection. Vertebral bodies can lose upwards of 50% of their density before it becomes detectable in plain films. The vertebral bodies may appear heterogeneous on plain films. This appearance is not specific and can be found in osteoporosis as well. The vertebral bodies’ shape, texture and cortices should be critically observed. Special attention should be paid to the posterior vertebral body wall. The metastatic deposit may be seen as a presence of a lytic or blastic vertebral lesion (Figs 22A to D). In some patients with metastatic prostate cancer, the vertebral bodies may

Metastases Skeletal metastases are significantly more common than primary bone tumors. Spinal metastases are common because they occur in hematopoietic active bone marrow, which is predominantly located in the adult spine. Most spinal metastases are found in the thoracic and lumbar regions. They are frequently disseminated via the hematogenous route. Both venous and arterial disseminations may occur. Batson’s plexus of veins is a major source of spinal metastases, and it connects with venous plexuses inside the spinal canal. Pressure difference in these veins directs tumor cells from the pelvis (prostate) into the lumbar or thoracic vertebral bodies. They frequently invade the vertebral bodies or the pedicles. Metastases can also grow along nervous tissue and thus enter the epidural space inside the spinal canal. The most common

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seem completely white. The pedicles should be inspected carefully. They are well seen in PA views and can be screened rather quickly. Absence, erosion, or sclerosis of a pedicle may indicate the presence of a bone metastasis at that location. Bone scan is an efficient and inexpensive tool for detecting skeletal metastases which is sensitive, but not specific. Multiplicity of lesions is well-evaluated. False-positive scans may be seen in degenerative disease, fracture and infection. Areas of increased activity that may correspond to facet joints or disk spaces are more likely to be due to degenerative changes. Computed tomography can also detect bony metastases and associated soft-tissue mass in patients undergoing CT as a part of imaging work-up to look for tumor or for staging of known malignancy. Multidetector-row computed tomography (MDCT) allows excellent sagittal and coronal multiplanar reconstructions (MPRs) (Figs 23A and B) which when viewed on bone window can pick up vertebral metastases. However, MRI is the most sensitive modality for picking up early vertebral metastases.43,48 T1W and STIR sagittal sequences of the whole spine (Figs 24 to 26) can be performed and are very sensitive for vertebral deposits and their impact on the spinal canal and the spinal cord. MRI is also very useful to differentiate osteoporotic vertebral collapse from neoplastic collapse. The features are summarized in Table 2.

edema gives rise to hypointense signal on T1W images and hyperintense signal on T2W and STIR sequences. Majority of the times some fatty marrow signal is preserved, the posterior cortex remains concave and the pedicles are normal. The spectrum of findings are related to the age of the collapse and within 3 months of injury there is always some restoration of fatty marrow and a linear hypointense band may persist. In chronic fractures return to the fatty marrow signal occurs and at this stage there is no difficulty in distinguishing it from

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Chapter 35 Imaging of Low Backache

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malignant collapse. Multiple lesions of different ages may occur confounding the problem further.43,49 Malignant collapse also shows T1-hypointensity and T2-hyperintensity and contrast enhancement.50 Considering that up to one-third of vertebral collapse in patients with

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Multiple Myeloma (Figs 28A to D) It is a plasma cell neoplasm of bone marrow and commonly involves the spine. The imaging appearance in spine is nonspecific and mimics metastatic disease. The differential diagnosis is better made on radiographs which in myeloma show osteopenia and typical punched out lytic lesions in the skull vault (Fig. 28A). Occasionally sclerotic

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Section 1 Neuroradiology including Head and Neck

The radiographs show a nonspecific lytic lesion, but it may also be sclerotic. Bone scan shows increased uptake and gallium-67 scintigraphy has been shown to have a high sensitivity and specificity.32,48 MRI shows a lesion which is T1-hypointense and T2-iso- to hyperintense, which enhances on contrast administration. The soft-tissue mass may show T2-hypointensity due to hypercellularity. A

CONCLUSION Low backache is a very common clinical problem. Majority of patients do not require imaging. It is important to triage patients into chronic nonspecific pain versus those with more ominous pathology who would benefit with imaging. Plain radiographs and MRI play the most useful role and CT and scintigraphy are used as problem solving tools.

REFERENCES B

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lesions may be seen, especially in the setting of POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, myeloma, sclerosis). Myeloma lesions are usually cold on bone scan. MRI is a sensitive screening tool but may be normal even in the presence of proven marrow infiltration. Focal T1-hypo- and T2-hyperintense lesions of variable sizes (Figs 28B and C) may be seen or there may homogeneously decreased signal may be seen on T1W images which can easily be overlooked. T2W images in the latter group will show hyperintense signal and enhancement will be seen on contrast administration.43,51

Lymphoma Primary lymphoma of bone is a rare entity and spine is the fourth most common location for it. It is usually a nonHodgkin lymphoma with a peak incidence in 5th to 7th decade. Secondary lymphomas are far more common and up to 30% of systemic lymphomas have osseous involvement. Lymphoma in the spine can present as an epidural mass, osseous involvement, leptomeningitis and as an intramedullary mass. In this discussion, we will confine ourselves to osseous lymphoma which is frequently associated with epidural soft-tissue masses.

1. Sharma SC, Singh R, Sharma AK, et al. Incidence of low back pain in workage adults in rural North India. Indian J Med Sci. 2003;57(4):145-7. 2. Gilbert FJ, Grant AM, Gillan MG, et al. Low back pain: influence of early MR imaging or CT on treatment and outcome— multicenter randomized trial. Radiology. 2004;231(2): 343-51. 3. Davis PC, Wippold FJ, Brunberg JA, et al. ACR Appropriateness Criteria on low back pain. J Am Coll Radiol. 2009;6(6):401-7. 4. Teh J, Imam A, Watts C. Imaging of back pain. Imaging. 2005;17:171-207. 5. Deyo RA, Weinstein JN. Low back pain. N Engl J Med. 2001;344(5):363-70. 6. Borenstein D. Epidemiology, etiology, diagnostic evaluation, and treatment of low back pain. Curr Opin Rheumatol. 1996;8(2):124-9. 7. Jarvik JG, Hollingworth W, Martin B, et al. Rapid magnetic resonance imaging vs radiographs for patients with low back pain: a randomized controlled trial. JAMA. 2003;289(21):2810-8. 8. McNally EG, Wilson DJ, Ostlere SJ. Limited magnetic resonance imaging in low back pain instead of plain radiographs: experience with first 1000 cases. Clin Radiol. 2001;56(11): 922-5. 9. Singh K, Helms CA, Fiorella D, et al. Disk space-targeted angled axial MR images of the lumbar spine: a potential source of diagnostic error. Skeletal Radiol. 2007;36(12):1147-53. 10. Kim HG, Shin DA, Kim HI, et al. Clinical and radiological findings of discogenic low back pain confirmed by automated pressure-controlled discography. J Korean Neurosurg Soc. 2009;46(4):333-9. 11. Carragee EJ, Lincoln T, Parmar VS, et al. A gold standard evaluation of the “discogenic pain” diagnosis as determined by provocative discography. Spine. 2006;31(18):2115-23. 12. Dolan AL, Ryan PJ, Arden NK, et al. The value of SPECT scans in identifying back pain likely to benefit from facet joint injection. Br J Rheumatol. 1996;35(12):1269-73.

Chapter 35 Imaging of Low Backache 13. Elster AD. Bertolotti’s syndrome revisited. Transitional vertebrae of the lumbar spine. Spine (Phila Pa 1976). 1989; 14(12):1373-7. 14. Konin GP, Walz DM. Lumbosacral transitional vertebrae: classification, imaging findings, and clinical relevance. AJNR Am J Neuroradiol. 2010;31(10):1778-86. 15. Beutler WJ, Fredrickson BE, Murtland A, et al. The natural history of spondylolysis and spondylolisthesis: 45-year follow-up evaluation. Spine (Phila Pa 1976). 2003;28(10):1027-35. 16. Fredrickson BE, Baker D, McHolick WJ, et al. The natural history of spondylolysis and spondylolisthesis. J Bone Joint Surg Am. 1984;66(5):699-707. 17. Campbell RS, Grainger AJ, Hide IG, et al. Juvenile spondylolysis: a comparative analysis of CT, SPECT and MRI. Skeletal Radiol. 2005;34(2):63-73. 18. Harvey CJ, Richenberg JL, Saifuddin A, et al. The radiological investigation of lumbar spondylolysis. Clin Radiol. 1998;53(10):723-8. 19. Paajanen H, Tertti M. Association of incipient disk degeneration and instability in spondylolisthesis. A magnetic resonance and flexion-extension radiographic study of 20-year-old low back pain patients. Arch Orthop Trauma Surg. 1991;111(1):16-9. 20. Collier BD, Johnson RP, Carrera GF, et al. Painful spondylolysis or spondylolisthesis studied by radiography and single-photon emission computed tomography. Radiology. 1985;154(1): 207-11. 21. Scheuermann HW. Kyfosis dorsalis juvenilis. Ugeskr Laeger. 1920;82:385-93. 22. Blumenthal SL, Roach J, Herring JA. Lumbar Scheuermann’s, a clinical series and classification. Spine (Phila Pa 1976). 1987;12(9):929-32. 23. Summers BN, Singh JP, Manns RA. The radiological reporting of lumbar Scheuermann’s disease: an unnecessary source of confusion amongst clinicians and patients. Br J Radiol. 2008;81(965):383-5. 24. Yu S, Haughton VM, Sether LA, et al. Criteria for classifying normal and degenerated intervertebral disks. Radiology. 1989;170(2):523-6. 25. Fardon DF. Nomenclature and classification of lumbar disc pathology. Spine (Phila Pa 1976). 2001;26(5):461-2. 26. Modic MT. Degenerative disc disease and back pain. Magn Reson Imaging Clin N Am. 1999;7(3):481-91. 27. Lee SH, Coleman PE, Hahn FJ. Magnetic resonance imaging of degenerative disk disease of the spine. Radiol Clin North Am. 1988;26(5):949-64. 28. Modic MT. Degenerative disorders of the spine. In: Modic MT, Masaryk TJ, Ross JS (Eds). Magnetic Resonance Imaging of the Spine, 2nd illustrated edition. Chicago, IL, USA: Mosby Year Book; 1994. 29. Modic MT, Masaryk TJ, Boumphrey F, et al. Lumbar herniated disk disease and canal stenosis: prospective evaluation by surface coil MR, CT, and myelography. AJR Am J Roentgenol. 1986;147(4):757-65. 30. Ross TS, Masaryk TJ, Schrader M, et al. MR imaging of the postoperative lumbar spine: assessment with gadopentetate dimeglumine. AJR Am J Roentgenol. 1990;155(4):867-72.

31. Ross JS. Magnetic resonance assessment of the postoperative spine. Degenerative disk disease. Radiol Clin North Am. 1991;29(4):793-808. 32. Ross JS, Brant-Zawadski M, Moore KR, et al (Eds). Neuroblastic tumor. In: Diagnostic Imaging: Spine. Salt Lake City, UT, USA: Amirsys/Elsevier Saunders; 2005. pp. 70-3. 33. Braun JM, Bollow M, Sieper J. Radiologic diagnosis and pathology of the spondyloarthropathies. Rheum Dis Clin North Am. 1998;24(4):697-735. 34. Vinson EL, Major NM. MR imaging of ankylosing spondylitis. Semin Musculoskeletal Radiol. 2003;7(2):103-13. 35. Shanley DJ. Tuberculosis of the spine: imaging features. Am J Roentgenol. 1995;164(3):659-64. 36. Moorthy S, Prabhu NK. Spectrum of MR imaging findings in spinal tuberculosis. Am J Roentgenol. 2002;179(4):979-83. 37. Moore SL, Rafii M. Imaging of musculoskeletal and spinal tuberculosis. Radiol Clin North Am. 2001;39(2):329-42. 38. Forrester DM. Infectious spondylitis. Semin Ultrasound CT MR. 2004;25(6):461-73. 39. Ledermann HP, Schweitzer ME, Morrison WB, et al. MR imaging findings in spinal infections: rules or myths. Radiology. 2003;228(2):506-14. 40. Thrush A, Enzmann D. MR imaging of infectious spondylitis. AJNR Am J Neuroradiol. 1990;11(6):1171-80. 41. Varma R, Lander P, Assaf A. Imaging of pyogenic infectious spondylodiskitis. Radiol Clin North Am. 2001;39(2):203-13. 42. Carragee EJ. The clinical use of magnetic resonance imaging in pyogenic vertebral osteomyelitis. Spine (Phila Pa 1976). 1997;22(7):780-5. 43. Motamedi K, Ilaslan H, Seeger LL. Imaging of the lumbar spine neoplasms. Semin Ultrasound CT MR. 2004;25(6): 474-89. 44. Baudrez V, Galant C, Vande Berg BC. Benign vertebral hemangioma: MR-histological correlation. Skeletal Radiol. 2001;30(8):442-6. 45. Flemming DJ, Murphey MD, Carmichael BB, et al. Primary tumors of the spine. Semin Musculoskeletal Radiol. 2000;4(3):299-320. 46. Ozaki T, Liljenqvist U, Hillman A, et al. Osteoid osteoma and osteoblastoma of the spine: experiences with 22 patients. Clin Orthop Relat Res. 2002;(397):394-402. 47. Diel J, Oritz O, Losada RA, et al. The sacrum: pathologic spectrum, multimodality imaging, and subspecialty approach. Radiographics. 2001;21(1):83-104. 48. Nöbauer I, Uffmann M. Differential diagnosis of focal and diffuse neoplastic diseases of bone marrow in MRI. Eur J Radiol. 2005;55(1):2-32. 49. Uetani M, Hashmi R, Hayashi K. Malignant and benign compression fractures: differentiation and diagnostic pitfalls of MRI. Clin Radiol. 2004;59(2):124-31. 50. Tehranzadeh J, Tao C. Advances in MR imaging of vertebral collapse. Semin Ultrasound CT MR. 2004;25(6): 440-60. 51. Angtuaco EJ, Fassas AB, Walker R, et al. Multiple myeloma: clinical review and diagnostic imaging. Radiology. 2004; 231(1):11-23.

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Localization in Clinical Neurology

CHAPTER

Manish Modi, Sudesh Prabhakar

LOCALIZATION IN CLINICAL NEUROLOGY Localization, derived from Latin term locus, is the diagnostic exercise of determining from the signs or symptoms of the patient, what site of the nervous system has been affected by the disease process. Clinical localization has particular relevance to the adequate use of ancillary diagnostic procedures. Current techniques of imaging, electrodiagnosis and other laboratory studies have revolutionized the practice of neurology. However, their use must be integrated with findings of history and neurological examination.

Clinical Diagnosis and Lesion Localization Clinical diagnosis in neurology requires several steps: zz Recognition of impaired function zz Identification of site of central nervous system (CNS) affected zz Definition of most likely etiology zz Use of ancillary procedures. Recognition of impaired function depends on a good history and neurological examination. Abnormal neurological findings come in the form of abnormal behavior or cognition, impaired posture or gait, difficulty in movement of face or extremities, and finally the sensory disturbances, including pain. Neuroanatomy is the key to localization. Neuroanatomy has two broad based aspects: (1) the morphology of the structure, and (2) its “functional representation”. Functional representation refers to the function mediated by a given structure of the nervous system. Damage to a structure results in dysfunction in the realm mediated by this structure.

APPROACH TO NEUROLOGICAL DISORDER Neurological localization and diagnosis is approached in each patient with the following six questions in mind: 1. Is there a disease in the nervous system? 2. At what level(s)? 3. What longitudinal system(s) is (are) involved? 4. Is the process—focal/multifocal/diffuse? 5. What is the lateralization right/left or bilateral?

6. What is the course acute/subacute/chronic? Then further queries like: a. Static versus progressive b. Relapsing/remitting or monophasic c. Onset sudden or insidious Based on the anatomic-temporal profile, the neurological disorders are broadly grouped into: zz Degenerative: Progressive and tend to be chronic and diffuse. zz Neoplastic: Progressive, may be subacute or chronic, and tend to be focal or multifocal but may be diffuse (e.g. carcinomatous meningitis). zz Vascular: Acute and usually focal but may be diffuse (e.g. subarachnoid hemorrhage). zz Inflammatory: Subacute or chronic and tend to be progressive. They may be focal (e.g. abscess), diffuse (e.g. meningitis, encephalitis), or multifocal (e.g. autoimmune disease). zz Demyelination: Acute, focal, may be relapsing and remitting. zz Toxic metabolic: Diffuse and may have any time course. zz Traumatic: Processes are always acute, may be static and improving or progressive, and may be diffuse, focal, or multifocal. zz Congenital: Developmental diseases are chronic and typically diffuse, and may be static or progressive. The present chapter will focus on few important symptoms and signs, which refer to a particular area of the neuraxis and help in clinical localization. The chapter is subdivided into disorders of cranial nerves, motor system, including gait and coordination, sensory system, and finally disorders of higher mental function.

DISORDERS OF CRANIAL NERVES OLFACTORY NERVE (CRANIAL NERVE I) Anosmia Significant olfactory dysfunction has been described with Alzheimer’s disease, Lewy body disease, Huntington’s chorea,

Chapter 36 Localization in Clinical Neurology

Parkinson’s disease, spinocerebellar ataxia, multiple sclerosis. Tumors of sphenoid or frontal bone, pituitary tumors with suprasellar extension, nasopharyngeal carcinoma or giant anterior communicating artery aneurysm can also present with anosmia. Foster Kennedy syndrome noted with olfactory groove or sphenoid ridge mass and space occupying lesion of frontal lobe is characterized by: zz Ipsilateral anosmia zz Ipsilateral optic atrophy zz Contralateral papilledema. Pseudo Foster Kennedy syndrome is noted when increased intracranial pressure of any cause occurs in patient who has previous unilateral optic atrophy. However, mostly pseudo Foster Kennedy syndrome is due to sequential anterior optic neuropathy or optic neuritis in which optic disk atrophies on the other side.

OPTIC NERVE (CRANIAL NERVE II) Papilledema: Optic disk swelling, manifested by disk hyperemia, blurring of disk margin, loss of venous pulsations (Fig. 1) are usually secondary to raised intracranial pressure and can be manifestation of large number of pathological conditions (Box 1).

tumor, suprasellar meningiomas, craniopharyngiomas and gliomas. Binasal hemianopias are usually due to bilateral intraocular disease of retina or optic nerve. Rarely bilateral compression of lateral chiasma may result in binasal defect. Homonymous hemianopia appears with lesions in the retrochiasmatic pathways, i.e. optic tract, lateral geniculate body, optic radiations or occipital lobe. A host of diseases like tumors, demyelination, trauma arteriovenous malformation (AVM), infections, surgery, etc. can lead to homonymous hemianopia. Superior homonymous quadrantic defects (“pie in the sky” field defects) result from lesion of temporal loop (Meyer’s loop) of optic radiation like space occupying lesion (tumor, abscess, hemorrhage), arteriovenous malformation, infections, infarctions, demyelinating disease, trauma, etc. Inferior quadrantic defects (“pie on the floor” field defects) occur due to involvement of optic radiations in the depth of parietal lobe.

Box 1:  Syndromes causing increased intracranial pressure and papilledema

Monocular visual loss is usually caused by lesions affecting retina or optic nerve. Binocular visual loss is seen in lesions localized to or beyond optic chiasm. Bitemporal field defects are most often due to a compressive mass lesion affecting the optic chiasm, such as pituitary

Primary causes •  Hydrocephalus •  Mass lesions: Tumor, hemorrhage, large infarction, abscess •  Meningitis/encephalitis •  Subarachnoid hemorrhage •  Trauma •  High flow arteriovenous malformations with overloading venous return •  Intracranial or extracranial venous obstruction •  Pseudotumor cerebri syndrome

Fig. 1:  Fundus photograph showing papilledema

Fig. 2:  Visual pathways and field defects

Visual Pathway Localization (Fig. 2)

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OCULOMOTOR SYSTEM (CRANIAL NERVE III, IV, VI) (TABLE 1)

commissure and is found in tumor of pineal glands, encephalitis, multiple sclerosis vascular and other lesions.

Supranuclear Lesions

Nuclear Lesions

Disturbance of conjugate gaze may be found in association with midbrain, pontine or cerebral lesions. Destructive lesion of the motor eye field of the frontal lobe (area 8) causes paresis of the gaze to the opposite side, with deviation of eyes towards the side of the lesion, while an irritative lesion (or an epileptic focus) in this region causes strong, rapid involuntary conjugate deviation of the eye to the opposite side. Parinaud’s syndrome is characterized by paralysis of conjugate upward gaze, impairment of convergence. It is seen in lesions at the level of superior colliculi (anterior quadrigeminal bodies), the foretectal region, or the posterior

Nuclear involvement of ocular nerves may result from vascular lesions (infarct or hemorrhage), inflammatory lesions, neoplasms, trauma, metabolic disorders, multiple sclerosis, and syringobulbia. There is usually associated involvement of medial longitudinal fasciculus, corticospinal tract, sensory pathways, cerebellar connections, other cranial nerve nuclei, sympathetic pathways, etc. Weber’s syndrome: Caused by involvement of oculomotor nerve as it passes through the cerebral peduncles and produce ipsilateral third nerve paralysis with contralateral paresis of lower face, tongue and extremities.

Table 1:  Localization of lesions of ocular motor nerves Location

Symptoms

Signs

Extraocular muscle/ orbit

Eye swelling Monocular vision loss Dry eyes

Periorbital edema Conjunctival injection and chemosis Proptosis Eyelid retraction Lagophthalmos (inability to close the eye completely) Lid lag (higher than normal lid position in downgaze) Von Graefe’s sign (dynamic slowing of lid descent during eye movement from upgaze into downgaze) Optic neuropathy (from optic nerve compression)

Neuromuscular junction

Fluctuating symptoms Proximal muscle Weakness Shortness of breath Swallowing difficulty Worsening at night or with exercise

Moment-to-moment or visit-to-visit variability Fatigue of lids or eye elevation with prolonged upgaze Cogan’s lid twitch Peek sign Orbicularis oculi weakness Ptosis and enhanced ptosis

Cranial nerve

Arm and leg weakness

Contralateral hemiparesis: pyramidal tract

Brainstem

Clumsiness or imbalance Facial numbness or tingling Facial weakness

Ataxia: cerebellar peduncle Ipsilateral facial sensory loss: trigeminal tracts and nuclei Upper and lower facial weakness: facial nerve fasciculus and nucleus

Cranial nerve Subarachnoid space

Stiff neck Vision loss Headache

Kernig’s and Brudzinski’s signs Papilledema

Cranial nerve

Facial numbness and tingling

Ipsilateral facial sensory loss in the first (V1) and second (V2) trigeminal distributions

Cavernous sinus Cranial nerve

Facial numbness and tingling

Ipsilateral Horner’s syndrome: sympathetic fibers Ipsilateral facial sensory loss in the first (V1) trigeminal distribution

Orbital apex

Eye prominence

Proptosis

Supranuclear

Arm and leg weakness Clumsiness or imbalance Facial numbness or tingling Facial weakness

Contralateral hemiparesis: pyramidal tract Ataxia: cerebellar peduncle Ipsilateral facial sensory loss: trigeminal tracts and nuclei Upper and lower facial weakness: facial nerve fasciculus Ocular motility: saccades affected greater than smooth pursuit; vestibulo-ocular reflexes spared

Chapter 36 Localization in Clinical Neurology

Benedict’s syndrome: Caused by lesion of midbrain involving third nerve as it passes through the red nucleus. It is characterized by an ipsilateral oculomotor paralysis with contralateral ataxia, tremor and hyperkinesias of upper extremity. Nothnagel’s syndrome: There is unilateral oculomotor paralysis combined with ipsilateral ataxia due to involvement of third nerve and brachium conjunctivum. Millard-Gubler syndrome: There is ipsilateral lateral rectus paralysis, ipsilateral facial paralysis with contralateral hemiplegia. Raymond’s syndrome: Consists of an ipsilateral sixth nerve paralysis and contralateral hemiplegia. Foville’s syndrome: Ipsilateral gaze paralysis, facial paralysis with contralateral hemiplegia. There is contralateral deviation of eyes and head.

Internuclear Ophthalmoplegia Paralysis of adduction of the contralateral eye, together with variable paresis and monocular nystagmus of the abducting eye. Internuclear ophthalmoplegia (INO) is found in brain stem lesions and is seen with multiple sclerosis, vascular, neoplastic, inflammatory or degenerative lesions of the brain stem or compression of latter by neoplasms of the posterior fossa. There are usually symptoms and signs indicating involvement of neighboring centers and pathways.

Infranuclear Lesions These may be caused by lesions within skull, middle cranial fossa, cavernous sinus, superior orbital fissure or orbit. Involvement in the skull may be produced by meningitis, trauma, subarachnoid hemorrhage, etc. Cavernous sinus thrombosis consists of ipsilateral ptosis, chemosis, edema of eyelids and orbital tissue, paralysis of third, fourth, sixth cranial nerves, involvement of upper division of trigeminal nerve, and at times papilledema. In superior orbital fissure syndrome, including TolosaHunt syndrome, there is usually painful ophthalmoplegia with or without vision loss. It may also result from sphenoid sinusitis, skull fractures, etc.

Other Disorders of Oculomotor System Nystagmus: Involuntary oscillation or trembling of the eyeball. It can be congenital or acquired. Vestibular nystagmus is caused by either irritation or destruction of semicircular canals, vestibular nerve or

vestibular nuclei. It is a fine nystagmus, usually associated with vertigo. Cerebellar nystagmus indicates that vestibulocerebellar pathways are affected, i.e. either the vermis or the inferior cerebellar peduncle, though can be seen in cerebellar hemispheric lesions. It is usually a coarse type of nystagmus. Other central nystagmus is produced mainly by lesions affecting structures in the region of fourth ventricle or brain stem principally zone between oculomotor nuclei and vestibular nuclei. Downbeat nystagmus is seen in brainstem lesions, especially in craniovertebral junction anomalies. Upbeat nystagmus is usually caused by lesions of anterior vermis of the cerebellum though can be seen in any brain stem lesion. See-saw nystagmus, in which one eye moves upward while the other moves down, is seen in patients with tumors of suprasellar region or anterior third ventricle. Opsoclonus: Coarse, irregular, nonrhythmic, agitated oscillations of eyes in both horizontal and vertical planes. These have been observed in encephalitis, cerebellar or brain stem disorders, comatose states, metabolic encephalopathies or as part of “paraneoplastic syndromes”. Ocular bobbing: Coarse, synchronous, downward “bobbing” movements of eyes are observed in coma with pontine lesions and is of grave significance.

TRIGEMINAL NERVE (CRANIAL NERVE V) The fifth nerve may be affected by lesions of brainstem or outside it at different level, by tumor of the cerebellopontine angle, tumors of base of skull, lesions within cavernous sinus, infections of petrous bone, orbital cellulitis, etc. Trigeminal neuralgia (tic douloureux), characterized by sudden attacks of excruciating, lancinating pain, is usually caused by vascular pressure on the nerve outside the brain stem but can also be a presenting symptom of multiple sclerosis, syringobulbia, herpes zoster and cerebellopontine angle tumor.

FACIAL NERVE (CRANIAL NERVE VII) Localization of Facial Nerve Lesions (Fig. 3) Supranuclear Palsy Supranuclear palsy is the paresis of lower part of the face with relative sparing of upper part. There are two varieties of central facial palsy: (1) Volitional and (2) emotional type. In volitional palsy, the involvement is most marked on voluntary contraction (like baring teeth, etc.) while on

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more apt to be continuous, less clearly defined and may not be accompanied by nystagmus and there may be evidence of other CNS changes. Deafness, tinnitus, and vertigo are important presenting symptoms of cerebellopontine angle neoplasms, usually a neurinoma or a neurofibroma. Partial deafness may be an early symptom of a tumor of glomus jugulare (chemodectoma), later there may be tinnitus, vertigo, and involvement of other cranial nerves (facial, vagus and others).

Fig. 3:  Facial nerve course in pons

involuntary contractions such as smiling, crying, etc. There is preservation of function with no evidence of paresis. This variety of volitional palsy is seen in lesions of cortical center in the lower-third of precentral convolution or pathways between this center and nucleus of facial nerve. In emotional or mimetic type of facial palsy, the impairment is most marked on smiling or weeping, though the patient can voluntarily retract his mouth. This type of palsy is considered to be result of deep seated lesion in extrapyramidal, basal ganglia, thalamus, or hypothalamus or frontal lobe lesions anterior to precentral convolution. Masked facies are seen in Parkinson’s disease and other Parkinsonian syndromes. There is loss of associated movements like infrequent blinking and smiling.

Infranuclear Facial Nerve Palsy It can occur in variety of conditions but the most common is Bell’s palsy. In this condition, both upper and lower part of face is involved and patient is unable to close the eyes on the affected side. Bell’s phenomenon, i.e. eyeball turns upward and cornea is hidden, when the patient attempts to close eyes on involved side.

GLOSSOPHARYNGEAL AND VAGUS NERVE (CRANIAL NERVE IX, X) Lesions of these nerves lead to dysarthria and dysphagia, with associated nasal regurgitation of fluids and nasal intonation of voice. Examination reveals asymmetrical movement of uvula and impaired or absent gag reflex and palatal reflex. Supranuclear involvement leads to pseudobulbar palsy with associated dysphagia and dysarthria. In this condition, the gag, palatal and jaw jerk reflexes are brisk. Nuclear involvement occurs in a variety of vascular, demyelinating, neoplastic, degenerative conditions. Wallenberg’s syndrome (lateral medullary syndrome), caused by occlusion of posterior inferior cerebellar artery (PICA) or vertebral artery, leads to acute dysphagia, dysarthria, ipsilateral anesthesia of face, ipsilateral Horner’s syndrome, ipsilateral cerebellar hypotonia and asynergy, with contralateral loss of pain and temperature sensation on limbs and trunk (Fig. 4). Infranuclear involvement may follow lesions at the base of skull, jugular foramen or along the course of vagus nerve. Syndrome of Vernet, caused by lesion at the jugular foramen, is characterized by ipsilateral paralysis of ninth,

VESTIBULOCOCHLEAR NERVE (CRANIAL NERVE VIII) Vertigo is a sensation of movement and is often accompanied by feelings of unsteadiness and loss of balance. True organic or vestibular vertigo is usually rotator in type and has been described as Objective, if the external objects seem to be rotating around the individual, and as Subjective, if the individual himself is rotating. The presence of associated symptoms, like nausea, vomiting, staggering, deviation of eyes, disturbance of balance, tinnitus, hearing loss, effect of change of posture are important clues to localization. In general, vertigo of peripheral origin is usually episodic in character, aggravated by change in posture, and accompanied by nystagmus, which that of central origin is

Fig. 4:  Magnetic resonance imaging of the brain (T2WI) showing left lateral medullary syndrome

Chapter 36 Localization in Clinical Neurology

tenth and eleventh nerves. It is usually of traumatic origin and follows basilar skull fracture; however, vascular or neoplastic lesions may also cause this syndrome. Syndrome of Villaret is the result of lesion in the retropharyngeal space and results in paralysis of ninth-tenth, eleventh and twelfth nerve and Horner’s syndrome.

Palatal Myoclonus Palatal myoclonus is a rhythmic movement of palate and associated muscles, in frequency of 50–240/min. It probably results from brainstem lesion with interruption of connections between the inferior olivary body, dentate nucleus and red nucleus (The triangle of Guillain and Mollaret).

Table 2:  Upper motor neuron versus lower motor neuron signs Clinical test

Upper motor neuron

Lower motor neuron

Reflexes Muscle tone Fasciculation Atrophy Babinski sign

Hyper-reflexia Increased/spastic None None Present

Hyporeflexia Decreased/flaccid Present Severe Absent

zz zz zz zz zz zz

SPINAL ACCESSORY NERVE (CRANIAL NERVE XI) The lesion of this nerve causes paralysis of sternocleidomastoid and trapezius muscles. More commonly hyperkinetic manifestation with tonic or clonic spasm of the muscles is encountered. The muscle contraction of sternomastoid pulls head and occiput to one side and face to opposite side (Torticollis). There are many causes of torticollis: congenital, structural, traumatic and myogenic factors; Klippel-Feil syndrome, rickets, cervical arthritis, spina bifida, trauma, etc. Reflex torticollis may be secondary to vascular lesions, tumor, cervical lymph node metastasis, retrotonsillar abscess, etc. Disorders of extrapyramidal system, especially of the basal ganglia, are probably the most common causes of neurologic torticollis.

HYPOGLOSSAL NERVE (CRANIAL NERVE XII) This nerve supplies the muscles of tongue. Lesions cause weakness and atrophy of the tongue muscles and may be seen in a variety of lesions in brainstem (neoplasm, vascular, granuloma, multiple sclerosis); within the skull (like meningitis, neoplasm), basilar invagination, Arnold-Chiari malformation; in the hypoglossal canal or in neck (trauma, tumor, vascular lesions).

DISORDERS OF MOTOR SYSTEM Motor function is a complex process and involves many areas of the CNS, like cerebral cortex, basal ganglia, cerebellum, and reticular activating system in addition to the final common spinomuscular pathway. Lesions of any of the constituent portions of motor system lead to walking difficulty/weakness. The classical features of upper motor neuron lesion versus lower motor neuron are tabulated in Table 2.

The examination of motor system involves: Inspection for muscle bulk, wasting, fasciculation Power for objective weakness Tone for any increase or decrease in tone Tendon reflexes for any attenuated or exaggerated reflexes Coordination Gait per se can give important clue to the localization and diagnosis.

Muscle Bulk Localized wasting or fasciculation in the weak limb indicates either radicular or anterior horn cell involvement, as well as plexus or nerve involvement. Focal wasting has great localizing value and can be seen in syringomyelia, cord tumors, spondylosis, motor neuron disease, etc.

Power Testing It is done in individual group of muscles and is graded from Grade 0 (no contraction) to Grade V (normal power), as per Medical Research Council (MRC) grading.

Muscle Tone It is the resistance to passive movement, when the patient is asked to relax. Tone is a reflex phenomenon and involves alpha motor and gamma efferent fibers. The tone is usually tested by supination-pronation of the forearm; flexion and extension of elbow and dorsiflexion and plantar flexion of wrist joint. In lower limbs, passive flexion and extension of hip, knee and ankle joint is done to assess the tone. Other soft signs of documenting abnormal tone are: zz Pronator sign: In the presence of hypotonia with cerebellar lesions, there is tendency of the hands to assume a position of pronation, when the arms are outstretched horizontally. zz Pronator drift sign: With eyes closed, the patient holds both arms outstretched in front of him. The elbows should be fully extended, the wrist extended and the hands open with palms up. In the presence of mild hemiparesis (there is mild increase in tone), there may be slow pronation of wrist, slight flexion of elbows and fingers, downward and lateral drift of the hand.

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Various pathological conditions can cause either decrease (hypotonia) or increase in tone (hypertonia). Hypotonia is usually seen in lesions involving spinomuscular level, proprioceptive pathways, cerebellar lesions and choreas. Hypertonia is caused by interruption of impulses from supraspinal regions. Two types of hypertonia are observed clinically: (1) spasticity, and (2) rigidity.

Spasticity This is seen with corticospinal lesions. There is clasp knife type of resistance, where there is elastic, spring like resistance to stretching at beginning of movement, which continues till certain point and then suddenly the muscle relaxes. Occasionally, spasticity is so marked that the examiner cannot passively move the extremity. The level of corticospinal tract affliction is generally based on associated symptoms and signs.

Extrapyramidal Rigidity Lesions of extrapyramidal system produces either lead pipe or cog wheel rigidity. In this type of hypertonia, there is same degree of resistance in entire range of movement and is seen in both flexor and extensor groups. Often there is intermittent yielding of muscles to stretching. Rigidity of this kind is seen in Parkinson’s disease and other Parkinsonian syndromes. Parkinsonism is characterized by bradykinesia, tremor and rigidity. A large variety of Parkinsonian syndrome produce these symptoms and can be distinguished from Parkinson’s disease by a variety of clinical and other diagnostic tests. zz Idiopathic Parkinson’s disease is characterized by asymmetric onset rigidity, tremor and bradykinesia. Cognition is preserved till late stage and no gross dysautonomia is observed. Usually magnetic resonance imaging (MRI) of brain reveals age-related atrophic change. zz Multisystem atrophy is characterized by associated severe dysautonomia, affecting bowel, bladder and postural hypotension. MRI reveals cruciform hyperintensity in pons (“Hot Cross Bun” sign) (Fig. 5). zz Progressive supranuclear palsy is characterized by recurrent falls (usually backward), with predominant axial rigidity. There is severe upgaze and downgaze restriction and in later stages lateral gaze restriction is seen. MRI reveals atrophy of the rostral midbrain tegmentum, the pontine base, giving hummingbird appearance on midsagittal view.

Fig. 5:  Magnetic resonance imaging of the brain showing “Hot Cross Bun” sign in multiple-system atrophy (MSA)

other effector element. Any breach in this arc results in an absent reflex. Commonly used tendon reflexes are discussed below.

Biceps Jerk Press forefinger gently on biceps tendon in antecubital fossa and then strike the finger with the hammer. Normal result: Flexion of elbow with visible contraction of biceps muscle. S egmental inner vations : C5; Peripheral ner ve: Musculocutaneous.

Supinator Jerk Strike lower end of radius 5 cm above the wrist. Normal result: Contraction of brachioradialis and flexion of elbow. Segmental innervations: C5, C6; Peripheral nerve: Radial.

Triceps Jerk Strike the triceps 5 cm above elbow, held in midflexed position. Normal result: Extension of elbow and visible contraction of triceps. Segmental innervations: C6, C7; Peripheral nerve: Radial.

Reflexes Reflex action requires a stimulus, a sensory pathway, a link with motor unit, motor neuron and finally, a contractile or

Knee Jerk Tap the patellar tendon in midflexed position of knee.

Chapter 36 Localization in Clinical Neurology

Normal result: Extension of knee and contraction of quadriceps.

The abdominal reflexes are usually absent in pyramidal tract lesions, though they may normally be absent in obese individuals and multiparous women.

Segmental innervations: L 3-4; Peripheral nerve: Femoral.

Ankle Jerk

Cremasteric Reflex

Achilles tendon is struck after dorsiflexing the ankle.

Inner part of thigh is stroked in downward and inward direction.

Normal result: Plantar flexion of the foot and contraction of gastrocnemius.

Normal result: The contraction of cremasteric muscle pulls up the scrotum and testicle on the side examined.

Segmental innervations: S1; Peripheral nerve: Medial popliteal.

Segmental innervations: L1-2.

Anal Reflex

Hoffman Reflex

Lightly scratch the perianal skin.

The terminal phalanx of the patient’s middle finger is flicked downwards between examiner’s finger and thumb. In hyperreflexia, the tips of other fingers flex and the thumb flexes and adduct.

Normal result: Contraction of external anal sphincter.

Abnormalities of Tendon Reflexes zz

zz

zz

zz

Hyper-reflexia is usually seen in pyramidal tract lesions but can also be seen in agitation, anxiety and fear. Clonus indicates marked degree of reflex excitability and usually means pyramidal system disease. Absent reflex indicates breach in a part of reflex arc either in sensory nerve, root or anterior horn cell, anterior root, peripheral nerve, etc. The other differences in upper versus lower motor neuron lesions are summarized in Table 2. Inverted supinator reflex: When supinator jerk is tested, there is no contraction of brachioradialis or biceps and only exaggerated finger flexion is seen. It indicates cord lesion at fourth or fifth cervical level, as in disk disease, syringomyelia, cervical neoplasm, etc.

Superficial Reflexes

Segmental innervations: S4-5.

Plantar Reflex Babinski sign: Extension of great toe with fanning of other toes on striking the outer aspects of foot with blunt key.

Other Important Reflexes Grasp Reflex Place first and second finger between the thumb and forefingers of patient’s hand and try to draw them lightly away. If grasp reflex is present, the fingers will be held tightly by the patient’s hand. It is due to bilateral corticospinal tract involvement, usually seen in neurodegenerative diseases like Alzheimer’s disease, multi-infarct state, tumor or vascular accidents in the premotor cortex.

Forced Grasping Reflex

Lightly stroking the abdomen from without inwards in all four quadrants of abdomen.

Lightly and repeatedly touching the side of palm results in hand following the stimulus and attempting to grasp it and is usually seen in widespread cerebral lesions. In advanced cases, patient may try to follow the movement of hand (Groping reflex).

Normal result: The muscles of the quadrant stimulated contract and umbilicus moves in that direction.

Sucking Reflex

Segmental innervations: Upper abdominal, T9-10; midabdominal, T10-11; lower abdominal, T11-12.

Touching the corner of mouth produces a sucking movement of the lips and is seen in widespread hemispheric lesions.

Abdominal Reflexes

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Glabellar Tap Tapping at root of nose is accompanied by synchronous blinking and is commonly seen in Parkinson’s disease.

Coordination For proper coordination, both sensory and motor system should be intact. Various tests used to test coordination are:

Finger Nose Test Each arm is drawn out to full abduction, with forefinger pointed. Patient is asked to alternatively touch the nose tip with his finger and the examiner’s finger. In cerebellar disease, the finger moves to the nose in a wavering side to side or up and down fashion.

Heel-Knee Test The patient is told to run heel down the front of shin to the top of the foot. In cerebellar disease, the heel overshoots the knee sideways and develops rotating oscillation as it approaches it.

Dysdiadochokinesis There is failure to efficiently perform rapid alternating movements. Patient is asked to rotate hands rapidly at wrists, holding the forearms vertically, with elbows flexed. In cerebellar disease, the movements will be coarse, irregular and slow.

Past Pointing Test Patient sits holding his arm forward, so that his fingers touch fingers of the examiner. Then he is asked to lower or raise the arm above head and bring it back to original position. In cerebellar disease, the arm on the side of lesion will deviate outwards towards the side of lesion.

Sensory System The various modalities of sensation tested in clinical neurology are: zz Pain, light touch and temperature. These are exteroceptive sensations derived from sources outside the body. zz Sense of position, passive movement, vibration and deep pain. These are the proprioceptive sensation derived from the body itself. zz Stereognosis and graphesthesia are two point of discrimination. These are the cortical sensations. It is wise to move from area of impaired sensation to normal sensation, for the change is easier to detect.

The common patterns of sensory loss with localizing value are: zz Total unilateral loss of all forms of sensation is seen in extensive lesion of thalamus or internal capsule. zz Unilateral hyperalgesia and hyperesthesia follows partial lesions of thalamus. zz Crossed hemisensory loss, on face on one side and body on opposite side, is seen in lesions of medulla (lateral medullary syndrome). zz Bilateral loss of all sensations below a definite level is seen in gross lesion of spinal cord. zz Suspended sensory loss: Impairment of pain and temperature sensation over several segments with normal sensation above and below are seen in intrinsic lesion of the cord, like syringomyelia and intrinsic cord tumor. zz Saddle anesthesia: Impairment of sensation over the lowest sacral segments is seen in cauda equina/conus medullaris lesion. zz Unilateral loss of pain and temperature below a definite level is seen in Brown-Sèquard syndrome of hemisection of cord, as in compression or demyelination. zz Glove and stocking anesthesia is seen in peripheral neuropathy. zz Patchy areas of sensory loss can be seen in a nerve or radicular distribution. zz Romberg’s sign: The patient sways from the heels, when the eyes are closed, after making the patient stand with feet opposed. This is characteristic of proprioceptive deficiency (large fiber neuropathy or affliction of dorsal columns).

Gait At the end of the clinical examination, the patient should be made to walk for few meters. Note the posture of the body while walking, the position and movements of the arms, legs, the distance between feet, the regularity of movement, the ability to maintain a straight course, the ease of turning and stopping. The various gaits of clinical significance are: zz Dragging of feet: The patient who drags one foot usually has an upper motor neuron lesion of that leg. In the presence of marked hemiparesis, he will throw the whole leg outwards from the hip, producing the movement called “circumduction”. This is usually seen following hemiplegia of any cause. zz Scissoring gait: In bilateral upper motor neuron lesions, both feet drag, steps are slow and short, the gait is stiff legged. The feet tend to cross in “scissor” fashion, most commonly seen in spastic diplegia of childhood. zz High stepping gait: The patient raises the foot high to overcome a foot drop; the toe hits the ground first. This gait occurs in lumbosacral root, cauda equina lesions or

Chapter 36 Localization in Clinical Neurology

zz

zz

zz

zz

zz

zz

peripheral nerve lesions causing anterior tibial muscle paralysis. Stamping gait: The heels tend to strike the floor first and result from loss of position sense, when the patient does not know where his foot is. The abnormality is increased in dark. This is seen in sensory neuropathies or disorders of posterior columns. Shuffling gait: Movement is a series of small, flat footed shuffles is commonly seen in extrapyramidal syndromes, particularly Parkinson’s disease. The steps become quicker as the movement progresses (festination). Gait apraxia: The gait is irregular and hesitant with small stepped shuffling. The patient may lean backwards rather than forwards. This type of gait is seen in syndrome of normal pressure hydrocephalus (NPH) and can also be seen in multi-infarct states. Ataxic gait: The patient tends to reel and sway as if drunk and is seen in cerebellar diseases. Waddling gait: The pelvis is rotated through an abnormally large arc, accompanied by compensatory movements of upper trunk and associated with marked lordosis. This is usually seen in myopathies. Hysterical gaits: Bizarre gait, which varies from moment to moment and can be altered by suggestion.

DISORDERS OF HIGHER MENTAL FUNCTION DISORDERS OF SPEECH Two main types of speech defects are encountered in neurological disorders: (1) Dysarthria and (2) dysphasia (aphasia).

Dysarthria When the articulation and enunciation of individual words and phrases is distorted, this is dysarthria. Articulation requires coordination of tongue, lips, palate, larynx and muscles of respiration and may be affected by lesions of upper and lower motor neuron, extrapyramidal and cerebellar systems. Various types of dysarthria are: zz Spastic dysarthria: This is caused by lesions of bilateral upper motor neuron. The tongue is small and spastic. The speech is slurred, as if the patient is talking from the back of the throat. zz Rigid dysarthria: Speech is monotonous, all inflections and accents disappear, and words run into one another. This is a result of extrapyramidal lesion. zz Ataxic dysarthria: Speech is irregular, slurred and drunken. The rhythm is jerky, sometimes explosive, staccato or scanning. This is a result of cerebellar disease.

zz

Weakness of facial, palatal, tongue muscles can also produce dysarthria. There is nasal intonation of speech in bulbar palsy.

Dysphasia When the patient is failing to put into properly constructed words or phrases the thoughts he wishes to express, even if articulation is adequate, then it is called dysphasia (or aphasia). Evaluation of dysphasia includes assessment of spontaneous speech, comprehension, naming objects, repetition, reading, writing and calculation. Various types of dysphasias are: zz Broca’s aphasia: Speech is nonfluent with preserved comprehension, poor repetition and naming ability. Usually seen in an infarct in the territory of anterior part of the left middle cerebral artery. zz Wernicke’s aphasia: Speech is fluent with profoundly affected comprehension, impaired repetition. Naming is poor. The patient produces jumbled string of meaningless words and neologisms. Posterior left middle cerebral artery territory infarction is the most common cause with damage to the posterior third of superior temporal gyrus. zz Transcortical aphasia: There is retained repetition with fluent or nonfluent aphasia. zz Echolalia: Involuntary repetition of words and phrases spoken by someone else. The lesion lies in the temporoparietal region. zz Pure word deafness: Patient cannot recognize the spoken word. This is due to a lesion in the middle of first temporal gyrus. zz Pure word dumbness: This is an apraxic speech defect with inability to articulate. The lesion may be widespread in the left hemisphere. Usually reading, writing, and copying are preserved. zz Alexia: Inability to understand written material. There is lesion in left occipital cortex and splenium of corpus callosum. There is associated right homonymous hemianopia and is seen in infarction of posterior cerebral artery. zz Alexia with agraphia: The patient cannot read or write spontaneously. The lesion lies in the left angular gyrus and is usually accompanied by nominal aphasia, acalculia, hemianopia and visual agnosia. zz Agraphia: Pure writing defect may occur in lesion that lies between angular gyrus and motor area. zz Acalculia: Inability to calculate may be seen in lesions of left angular gyrus.

APRAXIA Inability to carry out well organized voluntary movement correctly despite the fact that motor, sensory, coordinative

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functions are not significantly impaired. Four types of apraxia are commonly recognized. 1. Ideomotor apraxia: Inability to imitate or mime an act involving use of objects. There is lesion between dominant parietal lobe and motor area. 2. Ideational apraxia: Carrying out a whole of complex act is defective though execution of different parts of complete act may be normal. 3. Constructional apraxia: Inability to make or copy simple designs. The lesion is in the angular gyrus of either hemisphere but when isolated, is usually from nondominant parietal lesions. 4. Dressing apraxia: The patient is unable to dress or undress himself in the absence of motor or sensory deficit. The lesion is usually in nondominant posterior parietal lobe lesions.

PARIETAL LOBE DYSFUNCTIONS zz

zz

zz

zz

zz

zz

AGNOSIA Failure to recognize some object or sound, when the sense by which it is normally recognized remains intact.

Visual Agnosia The patient is unable to name or describe the use of the objects shown but is able to identify them, when he touches them. The site of lesion lies in second and third occipital gyri and the adjacent subcortical white matter in the dominant hemisphere. The patient may be unable to find his way around an obstruction or find his way to a given point. This type of visual disorientation is seen in bilateral posteroinferior parietal lesions or in the nondominant hemispheric affliction.

Tactile Agnosia The patient may be unable to recognize an object, by touching but is able to give its name on seeing. The patient with true tactile agnosia is able to describe its shape, size, texture. The site of lesion is in contralateral supramarginal gyrus or in corpus callosum.

Auditory Agnosia The patient who is unable to recognize the sound, but can recognize the object on sight or touch, has auditory agnosia. The site of the lesion is in the posterior part of the temporal convolutions of the dominant hemisphere.

Right left disorientation: Patient is unable to correctly point towards the right or left side of the body in parietal lobe lesion. Autotopagnosia: Patient is unable to identify any part of the body. Finger agnosia: Inability to pick out individual digit is termed finger agnosia. Gerstmann syndrome: It consists of finger agnosia, acalculia, right-left disorientation and agraphia without alexia and is found in lesions of the dominant hemisphere in the region of angular gyrus. Anosognosia: Complete lack of awareness of opposite half of the body is seen in lesions of parietal lobe of nondominant hemisphere. Sensory inattention: Bilateral stimulation by visual, auditory or tactile stimuli may result in inattention in one of the fields, though can be appreciated when stimuli are given in individual fields. This phenomenon of inattention is commonly seen in parietal lobe lesion, usually after vascular accidents, or tumor of the contralateral hemisphere.

CONCLUSION The importance of neurologic examination in the diagnosis of diseases of the nervous system cannot be overemphasized. Neurological examination is a time consuming and tiring exercise for both patient as well as physicians. However, a good history and proper examination can localize the disease process accurately and based on the temporal course of the disease a likely etiology can be postulated. This exercise helps in judicious use of ancillary investigations including radiology.

SUGGESTED READING 1. Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology, 5th edition. Philadelphia, USA: Lippincott Williams & Wilkins. 2007. 2. Haerer AF. DeJong’s The Neurologic Examination, 6th edition. Philadelphia, USA: Lippincott-Raven. 2005. 3. Hauser SL. Harrison’s Neurology in Clinical Medicine. USA: McGraw Hill Professional. 2006. 4. Patten J. Neurological Differential Diagnosis, 2nd edition. New York, USA: Springer-Verlag. 2000. 5. Spillane J. Bickerstaff’s Neurological Examination in Clinical Practice, 6th edition. USA: Wiley-Blackwell. 1996.

37 CHAPTER

Basic Neuropathology Kirti Gupta, Rakesh Kumar Vasishta

REMOVAL OF THE BRAIN FROM SKULL The most common method of removal of brain from the skull involves a reflection of the scalp followed by the removal of a generous cap of bone using a circumferential saw-cut. The left covering of the brain is called dura. This is the stage at which the superior longitudinal sinus can be tested in two ways: either by opening it or by simply running a fingertip along it and examining any motion of the surrounding blood. When the brain is suspended by the basilar artery, each side of the dura is incised and reflected medially, piercing through the bridging veins with knife or scissors. After dividing the anterior attachment of the falx, the dura is reflected backwards. The frontal lobes are lifted very gently from the base of the anterior cranial fossa, while trying to ensure that the olfactory bulbs remain attached to the brain. The optic nerves, internal carotid arteries (ICA), oculomotor nerves and pituitary stalk are cut neatly across close to the base, when they become visible. The tentorium is uncovered, first on one side then on other, by delicately lifting the temporal lobes; and the attachments of the tentorium to the petrous temporal bones are cut with a sharp knife. As a result of the piercing of the dura, the same cut will separate the roots of the trigeminal, facial and the auditory nerves. In the gap which shows up between the clivus and the pons, the visible abducents nerves are cut. The lower cranial nerves and the vertebral arteries, which are still holding the brainstem down are cut, either with a knife or with long-bladed scissors, without causing any damage to the lower brainstem. This can usually be carried out blind, but cutting as far as possible to each side. After the cutting of vertebral arteries, the lower brainstem and upper cervical cord become visible, thus making it possible to cut across with the knife. After this, a number of bridging veins remain to be, including the great vein of Galen, which performs the function of draining blood from the deeper cerebral gray matter into the straight sinus. Throughout the whole procedure, the brain should be held by the left hand very carefully, so that the tension and distortion remain at a minimum level. Once its free, the brain should only be placed with its base upwards in a bowl of a suitable size instead of a flat surface.

REMOVAL OF VENOUS SINUS, CAVERNOUS SINUS AND MIDDLE EAR EXAMINATION After removal of the brain all abnormalities in the dura at the base of the cranial cavity is noted and the patency of the principal venous sinuses (straight, lateral, sigmoid, superior longitudinal) is examined. A hammer and chisel are used for checking the ICA, the ear drums and middle ears. The chisel is applied to the base of the middle cranial fossa and a sharp hit with the hammer then displays the middle ear drum and the internal carotid artery lying within the carotid canal, which can lead to the wall of the cavernous sinus. In the similar way, after removing the pituitary and the sphenoid sinus the frontal and ethmoidal sinuses are opened and demonstrated. A vibrating saw is used for removing a square piece of sphenoid block for the cavernous sinus. The portion includes the area around the pituitary fossa containing the parts of ICA, optic tracts, cranial nerves—III, V, VI.

EXAMINATION OF THE BRAIN After its removal, the brain is fixed in 20% buffered, neutral formalin for the duration of 10–14 days. The fixed brain is then weighed (usually the weight of brain is slightly higher than when unfixed). The normal brain weight ranges from 1,100 g to 1,600 g for males and 1,050–1,500 g for females.

Gross Features to be Noted z

z

z

Meninges — For exudates Gyri and sulci — For flattening and narrowing of sulci-cerebral edema — Narrowing and thinning of gyri—atrophy Convexities/surface — For exudates  Pyogenic meningitis — Enlargement  Unilateral (space occupying lesion)  Bilateral (bilateral lesions, cerebral edema) — Atrophy of frontal lobes—senile atrophy

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Base of brain — Exudate  Tubercular meningitis  Mucoid—both at base and at convexities (cryptococcal meningitis) — Circle of Willis  For aneurysm  For emboli—in case of stroke the most common sites being the bifurcation of an ICA and the origin of a branch of a middle cerebral artery (MCA)  Sites of atheromatous narrowing should be noted — Mammillary bodies and optic chiasm-atrophy (alcohol induced) — Uncal notching and tonsillar herniation — Atrophy of brainstem — Cerebellum—cerebellar atrophy  Ataxia, chronic debilitating illness.

Slicing of Brain Coronal slicing: Normally, the first incision separates the hindbrain (brainstem and cerebellum) from the cerebral hemispheres. This should be done with a clean transverse cut across the midbrain, just in front of the third nerve, at right angles to the long axis of the brainstem. The first cut passes through the optic chiasm or mammillary bodies, going through the anterior margin of the thalamus. The anterior part of the cerebrum is then placed to be cut surface down, between a pair of centimeter (or less) guides, and successive slices taken at centimeter intervals or less and laid out, posterior surface upward, with the right side on the right. The same procedure is repeated on the posterior part. z In the cases which have undergone computerized tomography (CT) scans during their life are preferably sliced at the alternative-horizontal plane because that clearly shows the contrast between the actual and radiographic slices. Usually, the initial cut for horizontal slicing is at level of the upward end of the Sylvian fissure. The slices are spread out, upper surface upward, with right side facing right. z Hindbrain dissection: After serving the midbrain, a clear observation of the occurreance of the transtentorial herniation becomes possible or not. It is visible in the following signs: — Excessive grooving of the parahippocampal gyrus, on one side or both, and — Lateral compression of the upper brainstem. There are two commonly used practiced routines for slicing the hindbrain. The first, which is also the most commonly followed, involves cutting through the upper medulla at the level of the lateral apertures (foramina of Luschka) in a plane vertical to the long axis of the medulla, and continuing the cut through the cerebellum. This displays an extremely broad view of the fourth ventricle, the dentate z

nuclei, and the flocculi, uvula and nodulus of the cerebellum. Further cuts are made through the lower part of the specimen, using 5 mm guides or free-hand slices 3–4 mm apart, until it ends. On the other hand, if the interest is intended for the regional differences between areas of cerebellum, the alternate method can be applied. Oblique cuts are made to separate the cerebellum from the brainstem. These cuts pass through the cerebral peduncles ending in the fourth ventricle. These oblique cuts can then be made at right angles to the folia on the upper surface, and a midline cut will display the whole of cerebral vermis. The brainstem is sliced at 3–4 mm intervals as before.

Appearance of the Ventricles The lateral ventricles may be larger or smaller than normal, or unequal. Various points to note: Whether the ventricles contain blood z Whether the capaciousness of the subarachnoid spaces between the cerebral sulci and in the basal cisterns is normal or abnormal. If it is more than normal, there is a presumption of cerebral atrophy; but if it is less, a block in the cerebrospinal fluid (CSF) pathway must be looked for z Whether the dilation of the ventricles affects the ventricular system wholly or partially; and if it is partially affected, whether the difference can be accounted for by local atrophy or tissue destruction. z

Choice of Blocks for Histology There are no strict rules regarding the choice of blocks for embedding, except that at least some should be relevant to the probable diagnosis. Five standards for brain: 1. The left frontal lobe to include the border zone between anterior and middle cerebral arteries 2. Hippocampus to include the Ammon’s nucleus 3. Basal ganglia including globus pallidus, putamen, internal capsule, insular cortex 4. Pons 5. Cerebellum to include the dentate nucleus.

Pediatric Brain Examination Special and intensive care is required for extracting infants’ brains. The tissues of an infant’s brain are not only softer and more friable, but the leptomeninges are also fragile. The risk involved in manipulating a soft brain can also be reduced by taking the brain out under water. The brain of an infant can easily be removed by cutting the sutures and reflecting the parietal and frontal bones outwards.

Chapter 37 Basic Neuropathology

The maturity of the infant brain can be evaluated by weighing it, and by examining the state of development of the cerebral gyri and the extent and distribution of myelination. The same method is followed for slicing of pediatric brain as well as an adult brain. —

Points to be noted: Hemorrhages: Subdural and subarachnoid hemorrhage (Fig. 1D). z Congenital malformations: Common — Anencephaly—failure of brain formation — Spina bifida occulta — Meningocele/meningomyelocele/encephalocele — Porencephaly z Hydrocephalus (HC) characterized by dilated ventricular system (Figs 1A to D). — Obstructive HC—secondary to obstruction within the ventricular system. — Communicating HC—secondary to extraventricular obstruction or due to impaired absorption or overproduction of CSF. — HC ex vacuo—secondary to primary cortical disease with cerebral atrophy z Acquired perinatal lesions — Germinal matrix hemorrhage: This is encountered in premature infants. These begin as hemorrhagic z

—

—

infarcts in the involuting subependymal matrix layer of the lateral ventricle. When extensive they produced massive—intraventricular hemorrhagic lesions (Fig. 1C). Smaller lesions are resolved leaving subependymal matrix cysts. Periventricular leukomalacia: This is encountered more often in the premature infants and consists of focal areas of necrosis in the periventricular white matter. These necrotic foci may undergo mineralization. Kernicterus: It refers to heavy bilirubin staining of deep gray nuclei with selective damage to some parts of brain in deeply jaundiced infants (Fig. 1C). Hypoxia: Dusky discoloration of central white matter (Fig. 2).

INFECTIONS While examining a neuropathological case with possibility of a central nervous system (CNS) infection the main aims to be established are: z The root cause of the infection z The route taken by the organism to reach nervous system z The effects of the infection on the nervous system.

A

B

C

D

Figs 1A to D: (A) Hydrocephalus: Dilated lateral ventricular system; (B) Superior view of the neonatal brain with hydrocephalus; (C) Intraventricular hemorrhage (left) with kernicterus (bilirubin staining of the thalamus); (D) Patch of subarachnoid hemorrhage over the left temporal lobe

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At autopsy, the following samples are taken: CSF samples for — Microscopic examination — Culture and sensitivity z Brain tissue for culture and sensitivity z Crush smears for organisms, fungal hyphae z Fresh tissue for PCR especially in case of — Viral infections (1 cm square of tissue) — Cerebellum, hippocampus—Rabies.

Consequences of Infection

z

Routes of Infection Hematogenous from established infection (e.g. osteomyelitis, septic arthritis, endocarditis, bronchiectasis) z Spread from a nearby focus of infection (paranasal air sinuses, middle ears and bones of skull and spine) z Penetrating injury. The outcome is influenced by a number of factors including the virulence of the invading organism, the effectiveness of number of the defenses of the host and the pace of initiating the suitable antibiotic therapy. The CSF provides an excellent culture medium for many organisms to multiply at a rapid speed, it is because it is moderately removed from immune defenses. The low vascularity of the dura makes it difficult to remove organisms in the subdural space. Even antibiotics fail here due to poor penetration unless these are directly instilled. Less virulent organisms, such as cryptococci and other fungi, and toxoplasmosis, are generally found in very young or elderly and debilitated patients because they have weak immunity, and may evoke little in the way of an inflammatory response. z

z z z

Edema, acute possibly fatal Sagittal sinus thrombosis with venous infarction Cerebral arterial infarction due to arteritis and HC.

Leptomeningitis Acute Meningitis A purulent exudate is readily evident in the subarachnoid space and it may be more marked over the vertex or at the base (Figs 3A and B). Acute inflammatory cells which are found in the superficial perivascular spaces surround the tiny penetrating vessels present on the walls of the cortex and the brainstem. Cortical and hippocampal neurons also show signs of acute hypoxic (homogenizing) changes. The subarachnoid space and leptomeninges contain a neutrophil-rich infiltrate. Fibrin strands can also be frequently seen. Organisms may be demonstrated with the appropriate stains (Gram’s PAS), unless treatment with antibiotics during life has largely eradicated them. There may be adrenal or skin hemorrhages outside the CNS, along with evidence of more prevalent intravascular coagulation.

Tubercular Meningitis (Figs 3B to 6) Thick exudates more at the base of the brain with opacity of meninges at the convexities. Microscopically, presence of epithelioid cell granulomas with Langhans’ giant cells within the subarachnoid space. Meningeal vessels may be entrapped producing arteritis leading to infarcts. Tuberculomas may be single or multiple. Sites of predilection— cerebellum, pontine tegmentum and paracentral lobule (Fig. 5). Round oval masses composed of necrotic, caseous center. Become cystic, fibrous and get calcified.

Chronic Meningitis

Fig. 2: Coronal slice of a neonatal brain showing marked hypoxic changes with dusky discoloration of the central white matter

Various organisms are responsible for causing chronic meningitis, which may be accompanied by granulomas or brain abscesses as well. When the inflammatory process in the subarachnoid space persists for duration more than a week or two, secondary effects also start developing in the brain. z Hydrocephalus z Multiple cerebral infarcts due to narrowing of, and thrombosis in, arteries affected by endarteritis obliterans, particularly common in fungal infections z Collagenous thickening of leptomeninges, chiefly at the base

Chapter 37 Basic Neuropathology

B

A

B

Figs 3A and B: (A) Thick exudates over the surface of the convexities in a case of acute pyogenic meningitis; (B) Organized exudate at the base of the brain in a case of tubercular meningitis

A

C

Figs 6A to C: In a case of tubercular meningitis: (A) Ventriculitis with hydrocephalus; (B) Thick exudates at the base of the brain around the optic chiasm; (C) Epithelioid cell granuloma with acid fast tubercular bacilli (ZN stain, inset)

Cryptococcus is liable to produce widened perivascular spaces, particularly in the basal ganglia z Granular ependymitis is invariably present in cases of chronic meningitis. The organisms can themselves be identified with appropriate stains (Gram for bacteria, Ziehl-Neelsen (ZN) for Mycobacteria), periodic acid-Schiff (PAS) and methenamine silver stains for fungi, Giemsa for protozoa). z

Fungal Meningitis/Encephalitis The more common fungi to involve the brain are: Aspergillus—commonly in diabetics and produce large areas of hemorrhagic necrosis (Fig. 7). z Zygomyces—commonly in diabetics and produce large areas of hemorrhagic necrosis (Figs 8A and B). z Candida—usually in neonates produce large areas of hemorrhagic necrosis (Fig. 9A). z Cryptococcus—produces meningitis with basal exudates and because of mucoid capsule gives a “slippery” feel to the brain (Fig. 9B). z

Fig. 4: Thick, organized exudates at the base of the brain with destruction of the bilateral basal ganglia, hippocampus, and optic chiasm in a case of tubercular meningitis

Subdural Empyema It is from a focus of local osteomyelitis or paranasal sinus infection that the pus spreads in the subdural space. There may also be associated acute meningitis.

Brain Abscess Fig. 5: Tuberculoma at the gray-white junction in the middle frontal gyrus. Microscopically shows a central necrotic focus with minimal inflammatory infiltrate

Despite the probability of abscesses cropping up anywhere in the brain, these are most common in the white matter. Those with a local cause have particular sites of predilection. There may also be multiple, in which case they may be small

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and easily overlooked, especially when the organisms are blood-borne. At beginning, they consist of a small focus of liquefaction necrosis, or purulent encephalitis. Its expansion leads to the collection of pus in the center which forms a wall around it which composes of glial fibrils. If the abscess is situated near the ependymal surface, it may be incapable of to barring it from penetrating into the ventricle. Bacteria are the organisms most commonly responsible for the brain abscess are bacteria, but there can be involvement of other organisms as well, and these should be considered, particularly if bacterial cultures are not positive.

Purulent Encephalitis Associated with Subacute Bacterial Endocarditis Fig. 7: In a case of fungal meningoencephalitis: Large areas of hemorrhagic necrosis involving the basal ganglia region, corpus callosum and central white matter

Septic emboli which arise from the infected heart valves occasionally become the cause of solitary or multiple brain abscesses. They may also block an artery and cause cerebral infarction, which eventually becomes an extension from the septic embolus. If numerous neutrophil polymorphs are found present in and around the edge of an infarct, it should raise the suspicion of the diagnosis, and immediately a Gram stain should be performed to find organisms. A mycotic aneurysm is also another likely consequence of the presence of septic embolus in the cerebral artery. It is caused by a local infection and weakening of the arterial wall. This in turn may crack, thus producing brain hemorrhage of the subarachnoid space.

Viral Encephalitis (Fig. 10)

A

B

Figs 8A and B: (A) Broad, aseptate hyphae of zygomycetes; (B) Fungal hyphae infiltrating the vessel wall with fibrinoid necrosis (Grocott’s stain)

A

Unlike bacteria and fungi, viruses depend for reproduction on the existence of suitable host cells. Aseptic meningitis due to viral infection is well recognized and relatively common, but generally self-limiting. Enterovirus infection is the most common cause of viral meningitis. Viral encephalitis and myelitis, due to infection of cells of the brain and spinal cord, tend to produce more severe disease, though the extent of

B

Figs 9A and B: (A) Yeast and pseudohyphae of Candida in a neonatal case of fungal meningoencephalitis; (B) Cryptococci around the perivascular spaces

Chapter 37 Basic Neuropathology

Fig. 10: A case of viral (Japanese B) encephalitis with softening and petechial hemorrhages in the thalami and the midbrain

the harm incurred is highly variable. The range of viruses pathogenic to nervous system is very wide. Some enter into the blood through bloodstream (e.g. arboviruses), whereas others take a neural route to the CNS after initial replication in extraneural tissues and uptake into peripheral nerves (e.g. rabies). HIV and arboviruses are the most widespread brain infections in the world so far.

lobes. If the patient survives until months or years later there is destruction and collapse of same regions. In chronic forms of encephalitis there is likely to be some degree of cerebral atrophy, granular discoloration of the white matter and fibrous thickening of the leptomeninges. When preparing blocks for microscopy from cases of postmortem, samples should be taken both from areas which appear normal as well as from those which are obviously abnormal, and from transition zones in between. Samples from each major cerebral lobe, hippocampus, basal ganglia, thalamus and several levels of brainstem and cerebellum should be taken. It is necessary to have a wide sampling of the CNS because, although the type of damage caused by viral infections tends to be stereotyped, the location and distribution of the damage is often characteristic of particular viruses. The most reliable evidence about the cause of encephalitis appears from culture of a specific organism or detection of specific viral nucleic acid sequences by PCR, and from the use of immune-histological studies or in situ hybridization used to detect the presence of specific viral antigens or nucleic acid.

Pathological Features Common to Most Forms of Viral Encephalitis z z

Postmortem Examination in Cases of Suspected Viral Encephalitis Cerebrospinal fluid and samples of serum should be collected for estimating the viral antibody titers. A rise in the serum antibody titer to a particular virus is not a sufficient evidence to declare a virus as the reason for encephalitis. However, with the comparison of antibody titers in CSF with those in serum it is possible to know if intrathecal synthesis of antibody to a specific virus has occurred or not. If it has, this is an indication of the existence of the virus within the CNS, despite the attempts to culture the virus being unsuccessful. In viral encephalitis there is usually also evidence of oligoclonal immunoglobulin in the CSF. Due to its characteristic of being sensitive and specific, the use of polymerase chain reaction (PCR) to detect specific viral nucleic acid in CSF or brain has become the chosen method for verifying the viral etiology of encephalitis.

Macroscopic Examination of the CNS and the Choice of Blocks for Microscopy There is a possibility of some generalized swelling and congestion, perhaps with a few petechial hemorrhages on the pial surface. The meninges may be slightly blurred in the acute phase of herpes simplex encephalitis, there is swelling, hemorrhage and softening centered on one or both temporal

z z

Death of cell with neuronophagia Perivascular lymphocytic collections Microglial nodules Inclusion bodies—which contain virus-coded material. Most characteristic are the RNA inclusions that form Negri bodies, cytoplasmic inclusions found in neurons in rabies. Round or oval, intranuclear, eosinophilic inclusion bodies, larger than nucleoli, and usually surrounded by a halo of clear nucleoplasm, are found in neurons and oligodendrocyte nuclei in subacute sclerosing panencephalitis (SSPE) and “immunosuppressive” measles encephalitis (Cowdry type A inclusions). They can sometimes be spotted in neurons in herpes simplex encephalitis.

NEUROVASCULAR DISEASES These are those disorders attributable to pathologic structural and functional modifications of the blood vessels in the central, peripheral and autonomic nervous systems. This term is more encompassing and better than stroke, or cerebrovascular disease. Enormous importance should be imparted to the neurovascular diseases as these are the major cause of morbidity and are the third most common cause of death in this country. Numerous causes can be attributed to the occurrence of a stroke and the following discussion is divided into hemorrhagic and ischemic. The arterial infarcts are generally ischemic and are characterized by the involvement of an area

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corresponding to a territory supplied by a major cerebral artery. The venous infarcts are hemorrhagic.

Arterial Infarcts or Territorial Infarcts The arterial infarcts may be caused by thrombotic or embolic occlusion. The thrombotic infarcts are pale whereas embolic infarcts are hemorrhagic. The pale infarcts may also transform into hemorrhagic infarcts due to re-establishment of circulation. The three major branches coming of the circle of Willis (Fig. 11), the anterior, middle and the posterior cerebral arteries, provide the vast majority of the arterial blood supply of the cerebral hemispheres. Territorial infarcts in the distribution of the anterior cerebral artery are extremely uncommon due to the adequacy of collateral flow through the circle of Willis. Most often these are the result of vasospasm related to rupture of a berry aneurysm on its proximal portion. Infarcts which involve the territory of the posterior cerebral artery are either embolic in nature, or are related to the effects of severe transtentorial herniation. Infarcts created by the MCA occlusion by embolic or thrombotic episodes manifest as massive strokes (Fig. 12).

Fig. 11: Circle of Willis at the base of the brain

Embolic Infarcts Since the total cerebral blood flow represents about 20% of the cardiac output, emboli are a relatively common cause of infarction. In several clinic-pathological studies, embolic infarcts are said to be the most common cause of stroke. Such embolic infarcts may occur in virtually any location in the nervous system, but some locations are more typical. The embolic material rises up the cerebral vessels which bifurcate multiple times leading to the gradual narrowing of the lumina. The embolus finally settles in a vessel that is too small to enable its further travel. In situations with thromboembolism, the clot will rapidly break up into smaller fragments. Attempts to find the embolus by inspection or histologic investigation are mostly unsuccessful. Characteristically, thromboembolic infarcts are multiple and have the tendency of being peripheral in location and have a hemorrhagic appearance to some extent. Since emboli producing such lesions typically originate from either cardiac or carotid sources, they have a tendency of favoring the involvement of the cerebral hemispheres. There are innumerable possible sources for such emboli. In cases of chronic arterial fibrillation, mural thrombi in the auricular appendage of the left atrium may dislodge leading to the embolic infarction in the brain. Another common source of multiple cerebral emboli is from thrombi adherent to the endocardium following myocardial infarction with the formation of a left ventricular aneurysm. Carotid arteries are also a source of cerebral embolization. The carotid arteries, particularly in the region of the carotid bifurcation, are common sites for ulcerative atherosclerosis. Thrombi

Fig. 12: Ischemic infarct in the region of MCA with softening and breaking down of the left cortical white matter (thalamus and hippocampus) Abbreviation: MCA, middle cerebral artery

can form in the region of such lesions, and can embolize, as can fragments of atherosclerotic plaque. The cerebral artery at the center and its branches is the most common vessel to suffer embolic occlusion from an origin in the internal carotid artery. When emboli travel up the vertebrobasilar system, they can readily reach both posterior cerebral arteries, giving rise to bilateral infarcts in this distribution as a consequence of going either to the right or the left as they reach the top of the basilar artery. Paradoxical embolization of the brain may occur in the situations in which natural filtering capacity of the capillary bed of the lungs has been bypassed, that is, in situations with

Chapter 37 Basic Neuropathology

right to left shunting of blood. Therefore, patients with patent foramen ovale, ventricular septal defects or pulmonary arteriovenous (AV) fistulae are at increased risk for cerebral embolization.

in the lenticulostriate arteries arising from the proximal MCA. By definition, lacunes should not exceed 1 cm in their greatest dimension.

Practical Considerations Cerebral Venous Infarcts (Fig. 13) Thrombosis of one, or more, of major dural sinuses can give rise to the entity of cerebral venous infarcts. Within the system of venous drainage of the cerebral hemispheres, there are numerous interconnecting collateral channels, so one must achieve fairly extensive occlusion of a sinus and its associated major cortical veins, to cause a sufficient degree of interference in cerebral blood flow necessary to induce infarction of the tissues being drained. These causes include women who are taking oral contraceptives or who are postpartum, postoperative patients, hypercoagulable states associated with certain cancers, sickle cell disease, various forms of polycythemia, severe dehydration and cachexia. Local infection can also give rise to such occlusions with the formation of local thrombophlebitis. The resultant occlusion causes a hemorrhagic usually bilateral infarction within the area of drainage of the thrombosed veins.

Lacunar Infarcts When the brain of elderly patients is being sliced, one commonly comes across small elongated, often multiple, cystic infarcts involving the thalamus, basal ganglia (especially the putamen and globus pallidus) and intervening internal capsule. These are called lacunes or lacunar infarcts and are usually bilateral and multiple. Advanced age, hypertension and diabetes influence the growth of such lesions. Lacunes stand for infarcts that are related to arteriosclerotic pathology

While evaluating a brain specimen suspected of having an ischemic lesion, the circle of Willis should be examined most carefully, along with its feeding and exiting vessels. Determine the extent and distribution of artherosclerotic lesions, possible occlusion, and for portions that are either incomplete or atretic. Understanding of ischemic stroke in the brain mostly involves a knowledge of the status of the carotid arteries, in particular, the relative patency. The practice of removing the carotid arteries has gone out of favor, leaving the prosector to guess as to what might or might not be present in these extremely important vessels. Broad guidelines for autopsy on stroke patients: Look for extradural or subdural hemorrhage. If present, search for skull fractures. z In case of SAH, examine circle of Willis and look for aneurysm, AVM, etc. in fresh state. z Look at carotid siphon, cavernous sinus and dural venous sinuses and remove them if involved. z Remove carotid arteries and vertebral arteries. z Look for stenosis, atheroma, thrombosis (serial transverse sections), arterial dissection, etc. Gentle perfusion with water after removal and before cutting gives an idea of blockage. z Size, site, anatomical location and nature of lesion whether arterial or venous infarct (usually hemorrhagic); single or multiple lesions. Infarcts-central or peripheral. Lesions—single or multiple. z Observe edema, midline shift, ventricular size, herniation, secondary hemorrhages in pons, secondary infarction and whether hemorrhagic transformation of ischemic infarcts has occurred due to thrombolysis. z For venous infarct sample the involved venous sinuses, infarcts with overlying thrombosed cortical veins, areas adjacent to look for vascular fibrin thrombi and their age etc. z

Intracranial Hemorrhage Intracranial hemorrhage may occur as a result of head trauma or it may be spontaneous (Flow chart 1). The major causes of nontraumatic ICH are as follows: Hypertension—common sites are putamen, thalamus, lobar, cerebellum, pons (Fig. 14) z AVM and aneurysms z Cerebral amyloid angiopathy (CAA) z Anticoagulant therapy z

Fig. 13: Venous infarcts: Thrombosed superior sagittal sinus with hemorrhagic infarct involving the right frontal lobe with midline shift, edema and herniation of cingulated gyrus

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Flow chart 1: Causes of intracranial hemorrhage

Abbreviations: AVM, arteriovenous malformation; EDH, extradural hemorrhage; ICH, intracerebral hemorrhage; SDH, subdural hemorrhage; SAH, subarachnoid hemorrhage

Arteriovenous Malformations

Fig. 14: Hypertensive bleed involving the right basal ganglia region z z

Tumors Abuse of illicit with licit drugs.

Arteriovenous malformations may also be the underlying lesion leading to an intracerebral hemorrhage. Usually these represent developmental abnormalities in which arteries have direct communication with veins, without any intervention of a capillary bed. This subjects the veins associated with the malformation of arterial blood pressure directly. Greatly enlarged draining veins may be observed on the vertex lying over such a lesion. After cutting the brain, one can often see with the naked eye many irregular large vascular channel profiles within the hemorrhage. In some cases the arteriovenous malformation is so small that it can be completely eradicated by the hemorrhage. In such cases, identifying the underlying lesion may be quite difficult and require extensive histological sampling. The use of an elastic stain is helpful in visualizing the arterial vascular walls within the pool of blood clot.

Demyelinating Disease and Multiple Sclerosis

Aneurysm

Gross Features

Subarachnoid hemorrhage is most commonly caused due to rupturing of berry aneurysm. With large aneurysm, a layered thrombus may be found partially filling the inner cavity. Berry aneurysms arise in a very particular geographic pattern of predilection, with approximately 70% of such lesions occurring within 1 cm of the anterior portion of the circle of Willis. Most common sites are the anterior communicating artery, the proximal anterior cerebral artery, the most distal extent of the internal carotid artery, the proximal MCA and the most rostral extent of the posterior extent of the posterior communicating artery.

z

z

z

Irregular gray patches on the normally whitish surface of the pons or on the cut surfaces of the upper cervical cord and optic nerves. When the brain is freshly incised, sharply demarcated gray or pinkish-gray firm patches (called plaques) can be found on the cut surfaces of cerebral hemispheres (especially subependymal region, angles of lateral ventricles, optic nerves) and spinal cord (mostly at cervical level). Chronic plaques are sharply demarcated with smooth edge.

Chapter 37 Basic Neuropathology

Inherited Metabolic Diseases

—

In examining cases of inherited metabolic disease it is very important to reserve some fresh tissue for biochemical and genetic study before fixing the remainder of the tissue. Fresh tissue should be taken for electron microscopy.

—

TUMORS

—

Tumors of Neuroepithelial Tissue z

Postmortem Examination of Cases of CNS Tumor When examining the CNS in cases with tumors at the postmortem, the presence of midline shift, herniations, are the consequences of intracranial space occupation and other associated CNS disease should be noted. If the tumor caused epilepsy, the brain may show pathological changes associated with this condition, it is very crucial to examine the intracranial viscera very carefully, searching particularly for sources of metastatic deposits. There may also, rarely, be evidence of extracranial spread of primary CNS or pituitary tumor to other sites.

z

z z z

z

z

General Guidelines z

z

z

z

z

Fresh tissue is snap frozen for rapid intraoperative diagnosis. Crush smears may also be prepared from fresh tissue for rapid diagnosis. Sampling of adjacent brain is essential to assess the margins and pattern of infiltration. Grading the proposed WHO classification is followed which grades the tumor according to their malignant potential on a scale ranging from I for benign to IV for highly malignant tumors. Common immunohistochemical stains: — GFAP—Glial fibrillary acidic protein-astrocytic differentiation. — NSE (neuron specific enolase), synaptophysin for neuronal differentiation. — N F P — N e u r o f i l a m e n t protein-neuronal differentiation.

EMA (epithelial membrane antigen), cytokeratinepithelial differentiation—positive in meningiomas. Vimentin-mesenchymal marker—positive in meningiomas. S-100—positive in choroid plexus tumors.

z

z

z

z z

Astrocytic tumors—pilocytic astrocytoma, low grade astrocytoma, anaplastic astrocytoma, glioblastoma Oligodendroglial tumors—oligodendroglioma, anaplastic oligodendroglioma, oligoastrocytoma Ependymal tumors—ependymoma and its variants Mixed gliomas Tumors of choroid plexus—choroid plexus papilloma, atypical papilloma, choroid plexus carcinoma Neuronal and neuroglial cell tumors — Gangliocytomas, dysplastic gangliocytomas of cerebellum — Central neurocytomas Mixed neuroglial tumors — Gangliogliomas, desmoplastic infantile gangliogliomas — Desmoplastic cerebral astrocytomas of infancy, ganglioneuromas Tumors of pineal region — Pineocytomas, pineoblastomas Embryonal tumors — Ependymoblastomas — Neuroblastomas — Olfactory neuroblastomas — PNET — Medulloblastomas — Atypical teratoid-rhabdoid tumors Tumors of meninges — Meningiomas and its types — Mesenchymal nonmeningeal tumors — Hemangiopericytomas — Tumors of uncertain histogenesis — Hemangioblastomas Germ cell tumors Lymphomas.

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SECTION

Recent Advances and Applied Physics in Imaging Ultrasound Instrumentation: Practical Applications

„„

Image Optimization in Ultrasound

„„

Ultrasound Elastography: Principles and Application

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Computed Tomography Hardware: An Update

„„

Dual-energy Computed Tomography

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Computed Tomography Perfusion Imaging

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Magnetic Resonance Instrumentation: An Update

„„

Image Optimization in Magnetic Resonance Imaging

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Diffusion Weighted Magnetic Resonance Imaging

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Functional Magnetic Resonance: Perfusion and Dynamic Contrast-enhanced Magnetic Resonance Imaging

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Magnetic Resonance Angiography

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Magnetic Resonance Imaging Pulse Sequences: An Evolution

„„

Digital Radiography: An Update

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Digital Mammography

„„

Fluoroscopy and Digital Subtraction Angiography

„„

Tools in Interventional Radiology

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Magnetic Resonance Contrast Media

„„

Ultrasound Contrast Agents

„„

Iodinated Contrast Media: An Update

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Contrast Reactions and Its Management

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Picture Archiving and Communication System and Radiology Information System

„„

Evidence-based Radiology

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Radiation Hazards and Radiation Units

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Radiation Protection

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Planning a Modern Imaging Department

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Recent Advances in Positron Emission Tomography/Computed Tomography and Positron Emission Tomography/Magnetic Resonance

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Common Drugs Used in an Imaging Department

„„

Molecular Imaging

„„

Ethical and Legal Issues in Radiology

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Ultrasound Instrumentation: Practical Applications

38

CHAPTER

Kushaljit Singh Sodhi, Akshay Kumar Saxena, Mukesh Kumar Yadav

INTRODUCTION Ultrasonography (USG) in the last few decades has undergone massive transformation and today occupies a crucial role in practice of most of the domains of medicine. Advances in ultrasound technology include enhanced spatial, vascular and contrast resolution, besides encompassing various therapeutic options. New transducers and emerging imaging paradigms allow real-time acquisition of large field of views and even three-dimensional volumetric data. In sonography, transducer, is the central component, which is responsible for both, generation of ultrasound beam and detection of returning echoes.1 It is the changes in the generation of echo signals, it’s reception, analysis and display that helps differentiate one scanner from another.1 Its safety, portability, low cost and real-time application makes it one of the most widely used imaging modalities. This section provides a brief overview of practical aspects of ultrasound instrumentation.

High-frequency Transducer zz zz

zz

zz

Medium-frequency Transducer zz zz zz

In this section we shall briefly talk about some of the functions of the ultrasound machine which are most frequently put to use (Figs 1A and B). It is of course recommended that all sonologists must learn the various capabilities of their own equipment to optimize the quality of the image as well as the diagnosis. zz Keyboard: Various capabilities as provided by manufacturer zz Transducer select: To chose one of the many transducer probes attached to the transducer ports on the ultrasound machine

FREQUENCY OF TRANSDUCERS Transducer frequency can vary from 2.0 MHz to 16.0 MHz and its selection is primarily based upon patient’s body habitus and the region to be scanned.2

Frequency range of 3.0–5.0 MHz Curvilinear or sector transducers Most commonly used probe for adult abdominal imaging.

Low-frequency Transducer zz zz

MACHINE CONTROLS

Frequency range of 7.0–14.0 MHz Linear transducer mostly, sector transducer more suited for children Provides increased resolution of images, however, with reduced penetration Linear probes best for evaluation of superficial structures like, thyroid, scrotum, etc.

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Frequency of 2.0 MHz Transducer is sector type Provides increased depth of penetration but also results in loss of resolution More suited for ultrasound studies of obese patients2 Overall gain control: This is used for equal amplification of all signals received. Time-gain compensation: This is used to balance for attenuation of the ultrasound beam in the scanned tissue.2 With time-gain compensation, a depth-dependent gain is applied to the echoes; with echoes that originate deeper in tissue (which are attenuated to a larger degree) have larger gain factors compared to those echoes which originate close to the transducer.2,3 The signals from shallow structures are not amplified as much as those from deep structures. This process thus results in producing equally reflective structures to be displayed in B-mode image with the same brightness, regardless of their age. Time-gain compensation is controlled in most machines with a set of 6–10 gain knobs, each of which adjusts the receiver gain at a different depth.

Section 2 Recent Advances and Applied Physics in Imaging

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Figs 1A and B:  Modern ultrasound scanning unit with LCD screen zz

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Near and far gains: These controls help in equalizing the differences in echoes received from various depths as they are displayed on the screen. When compensating for sound attenuation, the near to far gain controls (usually slide pods) should gradually be increased.2,3 Compression: This is used to vary the amplitude range (dynamic range) of echoes which appear as shades of gray on the image. Most of the ultrasound machines apply logarithmic compression to the echo signals which emerge from the receiver; amount of compression is under the control of the operator.2 Dynamic range is the ratio of the largest to smallest echo signals. It decreases as signals pass through imaging system as rejection and TGC remove many large and small signals.3 Depth: This control is useful in adjusting the size of image so that the organs and adjacent structures or regions of interest can be equally clearly visible. Focal point(s): This is a control which has one or more toggle buttons. This allows the operator to choose the level at which the ultrasound beam is focussed so as to enhance the resolution at a specific point or points. The placement of this control should be at the most posterior aspect of the organ or structure to be imaged.2,3 Postprocessing: This can be used to change the appearance of echo signals, already stored in memory, on the image. Various postprocessing applications are available; each emphasizes different portions of the echo amplitudes stored in the image memory.

zz

Failure to properly adjust the gain control and/or improper placement of focal point during scanning might result in suboptimal image quality and misdiagnosis.

TYPES OF TRANSDUCERS Ultrasound scanners automatically scan the ultrasound beam through transducers which consist of an array of many narrow piezoelectric elements.3 Array may be made up of as many as 128–196 elements.4 Ultrasound transducers convert mechanical energy into electrical energy and produce images that can be displayed subsequently in a variety of formats. These can be of following types as shown in Figures 2A to C.

A

B

C

Figs 2A to C:  Photograph showing various types of transducers: linear (A), curvilinear (B) and sector (C) array transducer

Chapter 38 Ultrasound Instrumentation: Practical Applications

Linear-array Transducer Linear-array transducers are optimal for superficially placed structures, such as vessels, neck, testes. In this, final image is displayed as a rectangle. In a linear array, each time only a group of elements work together to transmit or receive.2,5 The ultrasound beam is perpendicular to the transducer surface, centered over element subset and scans a rectangular area. Size of the field of view is equal in both the far field (area of penetration farthest away from transducer) and near field (area of penetration closest to transducer).2

Curvilinear-array Transducer These are commonly used for routine abdominal and pelvic imaging. In curvilinear-array transducer, array of elements instead of a straight line (linear array) are arranged across a convex arc.2,5 This fan like arrangement of elements result in a sector shaped imaging field. Compared to linear-array, curved array provides a wider image at large depths (field of view is wide in far field than near field) from a narrow scanning window.

Phased-array Transducer In contrast to linear- and curved-arrays, all the elements work together in phased-array (all elements are used for each beam line).5 Phase-array steer the beam by applying different delay on each element and it requires small acoustic window. Its main advantage is in providing a very broad imaged field at larger depths that too with a narrow transducer footprint. It is widely used in cardiac scanning as the transducer fits easily between the ribs (rib gap is a small acoustic window).

Doppler The Doppler effect was first proposed by Christian Doppler, an Austrian physicist, in 1843.6 According to this effect, if there is relative motion between an object and an observer (receiver), the frequency of sound wave perceived by the observer (receiver) is different from that emitted/reflected by the object.5,6 In diagnostic radiology, Doppler effect is utilized to detect blood flow in peripheral vessels (e.g. lower limb) as well as those supplying different organs (renal artery, portal vein, etc.). The information provided by a Doppler examination includes presence or absence of blood flow, direction of blood flow, type of blood flow (arterial high resistance/ venous, presence and quantification of arterial stenosis, etc.2 The difference in emitted frequency and received frequency is called the Doppler shift and is given by the equation:6 ∆ν = 2 νS cosθ/V where ∆ν = frequency change (Doppler shift) ν = frequency of original beam



S = velocity of blood V = velocity of sound (1540 m/sec) θ = angle between the direction of blood flow and sound beam In clinical practice, three different Doppler techniques are utilized. Continuous wave Doppler is used for evaluation of peripheral vessels and the fetal heart. It provides information regarding the blood flow but lacks information regarding the depth from which the Doppler signal is coming from. Pulsed Doppler provides information regarding the presence, direction and depth from which the Doppler signal is coming from. Power Doppler is useful for the evaluation of slow flow. The basic transducer for continuous wave Doppler contains an oscillator, two piezoelectric crystals and a demodulator (Fig. 3A).6 One of these crystals acts as the transmitter while the other acts as the receiver. Both of these crystals work continuously. The two crystals are inclined at an angle to each other. The purpose of inclining the crystals is to cause overlap between the beam regions of the transmitter and receiver which in turn increases the sensitivity for detecting the returning signal (beam). The oscillator provides electrical voltage at the resonant frequency of the transducer which is converted into the transmitted ultrasound beam by the transmitter. The beam, after reflection, is received by the receiver piezoelectric crystal. The frequency of received beam is different from the transmitted frequency because of Doppler shift. The received signal is amplified and fed into the demodulator which also receives signal from the oscillator. The comparison of signals from the oscillator and received beam provides Doppler shift signal. The demodulator can also detect whether the received beam has frequency higher or lower than the transmitted frequency which provides information regarding the flow of blood towards or away from the transducer. It is important to note that apart from the moving blood, the moving vessel wall also generates Doppler shift. However, it has low frequency. The machines are equipped with circuits which filter off such low level frequencies and ensure that the signal from moving vessel wall does not hamper the evaluation of blood flow.7-10 The problem with continuous wave Doppler is that all the moving objects within the sonographic beam contribute to frequency shift. Thus, the observer cannot ascertain the depth from which the signal originates. This problem can be overcome by the use of pulsed Doppler. In this technique, very short bursts of the sound wave are repetitively emitted by the transducer. However, a new pulse is not emitted till such time the returning signal from the previous pulse is detected by the transducer. The receiver is designed to be turned on for a short period on at a specific moment. The time at which receiver is turned on (or gated on) provides the information regarding the depth at which the signal originated. The duration for which the receiver (or the gate) is turned on determines the axial length of the beam over which the signal

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is received. A combination of real-time imaging and pulsed Doppler is known as Duplex Doppler. Although pulsed Doppler and duplex scanners provide information regarding the depth from which Doppler signal originates, it is limited to a very small region of the image. As a result, the sonologist needs to sample large number of areas to evaluate the entire vessel. This limitation is overcome in the color flow Doppler imaging. Recall that in pulsed (and duplex) Doppler, the depth from which Doppler signal is recorded is determined by the time lag (after emission of sound beam) after which the gate is opened to receive the signal.8,9 Use of multiple gates, which open after different time lags, allows detection of depths of multiple Doppler signals. A modification of this principle is utilized in color flow imaging wherein electronically steered (phased array) transducers are used to detect signals at different depths of a real-time image. Thus, the signal can be detected from the vessels as well as surrounding tissues. The Doppler signal is assigned color proportionate to the strength of the Doppler signal. The superimposition of such colored information on the gray scale image generates the color flow image. Pulsed Doppler does not provide information regarding the intensity (or power) of the Doppler signal. This information can be obtained in the power Doppler mode which displays the power (or intensity) of the Doppler signal, as it changes with time in every region within the chosen area. Higher intensity Doppler signals are imparted lighter hue of color. However, there is no information available regarding the velocity. The power Doppler has superior flow sensitivity as compared to conventional color Doppler and is used to evaluate the presence and characteristics of the flow in blood vessels that are poorly imaged with conventional color Doppler (Figs 3B and C).10,11

Tissue-harmonic Imaging Tissue-harmonic imaging (THI) is a grayscale ultrasound mode  that provides higher quality images than those of conventional sonography by using information from harmonics (which are generated by nonlinear wave propagation of ultrasound in tissue).12-15 Harmonics are produced by the vibration of the tissues and are usually integral multiples of the

A

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transmitted frequency. In conventional grayscale sonography, the same frequency spectrum that is transmitted into the patient is subsequently received to produce the sonographic image. However, in THI, higher harmonic frequencies (multiples) generated by the propagation of the ultrasound beam through tissues are used in producing the image. Conventionally, only the second harmonic, or twice the fundamental frequency, is used for imaging. Tissue-harmonic imaging holds a great potential for improving the quality of image since it provides improved lateral resolution and signal to noise ratio and reduces the side lobe artifacts..12,16 The higher harmonic can also be used but it requires transducers with extremely wide bandwidth.14 In THI, it is the reduced width of the ultrasound beam that improves lateral resolution (more harmonics are produced at the centre of a pulse than at the periphery). Increased lateral resolution improves the ability to resolve small anatomic structures and detail. Harmonic imaging is chiefly useful in obese patients because it reduces the deleterious effects of body wall. Intensity of harmonic waves generated is dependent upon the nonlinearity coefficient of the tissue insonated. Body tissues with a higher amount of fat have the highest nonlinearity coefficients, which increase the intensity of harmonic waves generated, thus improving the visibility of lesion in obese patients, whose body walls typically contain a high proportion of fat.12,16,17 Side lobe artifacts occur when the ultrasound beam hits an interface and is reflected back to the transducer, thus producing artifactual echoes. Reduction in side lobe artifacts improves the signal-to-noise ratio which results in an image which shows tissues as brighter whereas the cavities appear as darker. Harmonics are generated deep in relation to the body wall and because they are produced in tissues, they pass only once through the body wall, resulting in decreased artifacts from the body wall.18-20 Although better demonstration of cystic structures by THI has been emphasized, authors have now observed that THI provides additional information in both solid and cystic lesions12,18 (Figs 4 and 5). Harmonic imaging increases diagnostic confidence in differentiating cystic from solid hepatic lesions, improves detection of the gallbladder and biliary calculi, improves the pancreatic definition

C

Figs 3A to C:  Components of a typical Doppler ultrasound transducer (A), color Doppler scan of common carotid artery (B) and power Doppler image showing normal Doppler signals in kidney (C)

Chapter 38 Ultrasound Instrumentation: Practical Applications

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Figs 4A and B:  Comparison of conventional grayscale imaging (A) with THI (B) Tissue-harmonic imaging clearly demonstrates target lesions (indeterminate on conventional) in a metastatic liver disease. Also note that additional lesions are also detected with THI

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Figs 5A and B:  Tissue-harmonic imaging (A) demonstrates much better delineation of both cystic and solid lesions in this patient of renal angiomyolipomas, when compared to conventional grayscale imaging (B)

and allows distinction between simple and complex renal cysts. Another harmonic technique, known as 1.5 harmonic imaging has also been described. 21 This detects and visualizes signals that are a factor of 1.5 times higher than the fundamental center frequency of the transducer and are intermediate between the fundamental and the second harmonic frequency spectrum.21,22 Obvious advantage is that this frequency range is nearly free of tissue echoes and only contains microbubbles echoes. Hence, it is featured with contrast improvement between tissue and microbubbles of 20dB or more compared to the second harmonic technique.

Spatial-compound Imaging Spatial-compound imaging is a speckle reducing ultrasound technique, which uses electronic steering of ultrasound beams

from a transducer array to obtain overlapping scans of a target object from different angles (same tissue is imaged many times by using parallel beams directed along different directions).3,23 Resulting echoes from these multiple acquisitions are then averaged to produce a single compound image of improved quality due to reduction in image speckle. When compared to conventional B-mode imaging, in compound imaging, more time is required for acquisition of data (as here multiple ultrasound beams are used to evaluate same tissue) and frame rate is also reduced. Spatial-compound imaging demonstrates reduced level of speckle, noise, refraction, reduced shadowing and enhancement artifacts and improved contrast and margin definition3,23,24 (Figs 6 and 7). Application of spatial-compound imaging has been described in imaging of breast, peripheral vessels and musculoskeletal system. It can also be combined with other ultrasound applications, e.g. harmonic imaging.

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Figs 6A and B:  Spatial-compound imaging in a patient with nephrocalcinosis. Note medullary hyperechogenicity is not well appreciated on conventional grayscale mode (A), but is clearly demonstrated on compound imaging (B)

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Figs 7A and B:  Spatial-compound imaging in carotid vessels helps clear depiction of intima-media thickness for accurate measurements. (A) refers to conventional grayscale while (B) refers to compound imaging

EXTENDED FIELD OF VIEW This technique available in most of the new scanners allows sonologists to visualize large anatomic regions in a single image. It can be performed on superficial structures with a linear array transducer or abdominal structures using a curvilinear probe, although most of its applications are in superficial structures.3,23 Extended field of view imaging, also called panoramic imaging in some machines allows easy measurements of large lesions/structures and exact delineation of anatomical relationships in a single image (Figs 8A to C). Transducer is initially moved laterally across the anatomic area of interest and multiple images are acquired from many transducer positions.3 Images are

registered with respect to each other. This registered data is subsequently combined to form one complete large field of view image.

Elastography Imaging of tissue stiffness or elasticity is one of the rapidly evolving ultrasound based application. It is based on the fact that stiffness of tissue tends to alter with disease and can be imaged by measuring the tissue’s distortion (strain) under an applied stress (compression from ultrasound transducer).23 Images produced may be in grayscale, color or both. Although most of its initial application has been carried out in the breast, it is now increasingly being evaluated in diagnosis

Chapter 38 Ultrasound Instrumentation: Practical Applications

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Figs 8A to C:  Extended field of view. Routine grayscale mode (A) is able to demonstrate only limited part of thyroid in a single image, while

extended field of view mode (B) clearly demonstrates the composite image showing both lobes of thyroid, isthmus besides cervical vessels in a single image. Extended field of view (C) demonstrates quadriceps tendon, patella and patellar tendon in a single image

of complex cysts, liver cirrhosis, characterization of thyroid nodules and metastatic lymph nodes.25

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3D and 4D Ultrasound Three-dimensional USG or volume sonography is the imaging technology which involves acquiring a large number of data sets of 2D images from patient. After acquisition, this volumetric data can be qualitatively and quantitatively assessed with the use of many analysis tools, such as surface and volume rendering, multiplanar imaging and volume calculation techniques, etc. Hence similar to other cross-sectional imaging like computer tomography (CT) and magnetic resonance imaging (MRI), the volumetric data of this 3D ultrasound can also be ‘postprocessed’. Because of volume imaging it is possible to display information in any orientation and any of the planes. If the 3D ultrasound is acquired and displayed over time, it is termed as 4D ultrasound, live 3D ultrasound or real-time 3D ultrasound.26 Currently there are two commonly used techniques to acquire 3D volumetric data - free hand technique and automated technique. In the free hand technique the examiner requires to manually move the probe within the region of interest. In the automated technique dedicated 3D probes (also called volume probes) have to be used. In this method probe is held stationary and on activation the transducer elements within the probes automatically sweep through the ‘volume box’ which has been selected by the operator. The resultant images are digitally stored and can be ‘processed’ later in various display modes for analysis.27 It is perceived that the potential of 3D and 4D ultrasound has not been fully utilized till now. It is still being used as problem solving tool although it can be incorporated in routine day-to-day practice. There are numerous areas in which the use of 3D and 4D can be very useful (Figs 9A and B). Few of these are as follows:26

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For assessment of congenital anomalies of uterus28,29 For evaluation of endometrial and uterine cavity (can also be done with saline infusion sonohysterography) For preprocedure localization of fibroids for planning myomectomy For evaluation of possible cornual ectopic pregnancies For exact delineation of intrauterine device location and type For imaging of adnexal lesions for better differentiation of ovarian lesions from tubal or uterine lesions Three-dimensional guidance for interventional procedures Evaluation and follow-up of patients of polycystic ovaries and tubal occlusion for infertility workup.

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For evaluation of facial anomalies like cleft palate and cleft lip Evaluation of nasal bone, ears and cranial sutures Detection of central nervous system anomalies like corpus callosal agenesis and Dandy-Walker cyst For evaluation of ribs and intrathoracic masses For evaluation of spine, e.g. vertebral abnormalities, neural, tube defect,30,31 diastematomyelia (Figs 9A and B), etc. For evaluation of extremities like club feet and skeletal dysplasia, etc. For evaluation of heart, placenta and umbilical cord For evaluation of multiple gestations for mapping of vasculature for twin transfusion syndrome Telemedicine and education Storing volumetric data for subsequent interpretation and review For quality control by way of central monitoring, e.g. procedures done at different peripheral sites and in multicenter research studies

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Figs 9A and B:  (A) Transabdominal sonographic coronal 2D image showing bony spur in a case of diastemeomyelia; (B) Corresponding 3D image showing the bony spur

Teaching postprocessing techniques and standardized views to residents. Studies have suggested that the mothers who are viewing the 3D images of the babies feel enhanced bonding with their fetus.32 With the use of 4D ultrasound many facial expressions, such as yawning, tongue protrusion, mouth opening, eye opening and blinking, etc. can also be studied in greater details.33-35 Four-dimensional ultrasound has also been used in the evaluation of fetal heart.36-38 Three-dimensional images are very useful for demons­ trating the abnormality to the referring physician as these images are better comprehended by those who are not tuned to understand grayscale format of 2D images. Similarly storage of ‘volume’ data allows us to reprocess the data in future for subsequent interpretation or reviews. These volume data can be sent to remote workstations for telemedicine and teaching purposes. It has also been shown in a few studies that acquisition of 3D data needs less time which can potentially increase patient through put and increase efficiency of the imaging department.39 zz

Limitations As 3D ultrasound information is dependent on reformation of acquired 2D ultrasound data, it is expected that the problems which affect the 2D ultrasound like motion, unfavorable body habitus, shadowing artifacts and suboptimal scanning techniques also result in poor quality 3D images.27

Fusion Imaging Fusion imaging or hybrid imaging means combination of two imaging techniques. This can be in the form of fusion of two anatomical techniques like ultrasound with MRI or CT; or it can be fusion of anatomical technique (ultrasound, CT or

MRI) with molecular imaging technique like SPECT or PET (Fig. 10). One example of fusion imaging is real-time virtual sonography (RVS). To obtain virtual fusion images, an initial step is to transfer the previously acquired CT or MRI data to the ultrasound machine.40 A point like magnetic positioning sensor unit is attached to the ultrasound probe to detect any change in position of probe during investigation. The transmitter of this sensor unit is placed onto the surface of patient. During examination ultrasound screen is seen as split images with virtual reconstructed CT/MR image on one side and currently acquired USG image on other side of the screen. An attempt is made to match these two images with each other. This is usually done by freezing the CT or MR section with some clearly visible anatomic landmark (e.g. portal vein bifurcation, superior most margin of kidney or the lesion itself, etc.) and identifying the same landmark by freehand USG.41 Then these two images are matched. The real-time USG image can also be superimposed on the virtual reconstructed CT image with adjustable difference in the grayness (Figs 10A to D).

CLINICAL APPLICATIONS OF FUSION IMAGING It has been observed that there are few lesions/tumors in liver which are isoechoic and hence not well appreciable on gray scale ultrasound. Similarly there are subgroups of patients who have been treated with either TACE or RFA and now there is recurrence in the vicinity of the primary tumor site. These lesions are also poorly localized on grayscale USG. Hence detection by USG or further biopsy/treatment by the local ablative therapies were difficult for such lesions. These lesions are usually clearly visible on contrast enhanced CT/ MR. However, interventional treatment is usually easier to perform with USG guidance which also avoids radiation to the operator. The RVS combines the advantages of both

Chapter 38 Ultrasound Instrumentation: Practical Applications

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Figs 10A to D:  Figure shows application of fusion imaging on a patient with well visualized lesion on both CT as well as on USG. Four split images

seen on the screen. (A) Overlay image showing good matching of the lesions from sonographic and CT images; (B) Current sonographic image; (C) Previously acquired CT images feeded in ultrasound machine. On moving the ultrasound transducer, there will be automatic reformation of these feeded images corresponding to the axis of ultrasound transducer so that the same imaging plane is matched to the ultrasound image. (D) 3D view which is being displayed during the fusion work flow

imaging techniques.42 In one way this technique provides real-time visualization of the needles in preprocedural CT scan images. The feasibility of RVS module has been proven in many studies.43-45 The RVS module has been shown to be compatible with B mode, color Doppler mode as well as with harmonic imaging mode.46 However, the data on accuracy and efficacy of this technique are still emerging.47

Limitations Real-time virtual sonography cannot be used in those patients in whom CT/MRI are contraindicated (e.g. contrast allergy, renal failure, metallic implants, etc). Another limitation is that sometimes the best synchronization is not achievable hence limiting the utility.46 It definitely prolongs the examination time and it is more expensive as it adds the cost of CT/MRI also.

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Ultrasound guided aspirations, drainages and biopsies form the backbone of any interventional radiology unit. With the help of ultrasound, one can easily track the needle path and perform any such interventional procedure easily. Not only it is noninvasive, radiation free, portable modality, it also offers a real-time navigation facility to the interventionists. High-intensity focused ultrasound (HIFU): High intensity focused ultrasound is rapidly emerging as a noninvasive method for tumor ablation. In this, high intensity ultrasonic waves are focused at a focal lesion with high accuracy, resulting in a lethal rise in the temperature at the desired target site, with resultant damage of the tumoral cells.48 Simply put, tranducers help thermally ablate tumors without introducing needles or wires

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into the tumor.49 High intensity energy is absorbed and converted into heat at the focal lesion. This heat raises the temperature causing coagulative necrosis at the site.50 It is guided by real-time ultrasound imaging and can be run by one of several transducers with focal lengths varying from 90 to 160 mm. Although choice of transducer would depend upon depth of the target lesion, the most commonly used transducer is the one with a focal length of 135 mm and operating frequency of 0.8 MHz.48,49 Presently, HIFU is being widely used for ablation of both benign and malignant tumors. It’s most common applications worldwide are in the treatment of uterine fibroids, liver tumors and prostate cancer. Apart from these, it has also been used in the ablation of breast, bone, pancreas and soft tissue tumors.

Ultrasound-based Molecular Imaging and Oncotherapy Ultrasound molecular imaging, which is based on the use of molecularly targeted contrast agents, combines the advantages of contrast enhanced ultrasound with the ability to characterize neoplastic processes at a molecular level. 51 Ultrasound molecular imaging has enormous potential applications, which can range from early cancer detection and tumor characterization to monitoring treatment response and guiding cancer therapies.51,52 There is also potential role for ultrasound contrast agents in improved delivery of chemotherapeutic drugs and gene therapies across existing biological barriers. Most of the preclinical studies have used contrast micro bubbles, which are emulsions (gas-liquid) of several micrometer in size, confined to intravascular space. Much smaller newer nanoparticles are currently being investigated for future application.

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Ultrasound-image Artifacts Image artifacts on ultrasound are commonly seen in day to day clinical ultrasound practice. Some artifacts are generated by the physical limitations of the modality while some arise secondary to improper scanning technique. Artifacts can interfere with image interpretation. Ultrasound artifacts can be understood with a basic appreciation of the physical properties of the  ultrasound  beam, the propagation of sound in matter and the assumptions of image processing.53 Ultrasound artifacts often arise secondary to errors inherent to the ultrasound beam characteristics, the presence of multiple echo paths, velocity errors and attenuation errors. The beam width, side lobe, reverberation, comet tail, ring-down, mirror image, speed displacement, refraction, attenuation, shadowing and increased through-transmission artifacts are encountered on a routine basis in clinical practice.53 An ability to recognize and then correct potentially correctable ultrasound artifacts  is significant for  patient care and improvement in the image quality.

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Ultrasound artifacts can be grouped under the following: Resolution-related artifacts includes: Speckle in con­ ven­tional ultrasound imaging results from the use of phase-sensitive transducer and occurs when structure in the object is on a scale too small to be resolved by the imaging system.54 ‘It is an interference phenomenon— small scatterers cause constructive and destructive phase interference at the receiving array. The ability of a speckle to mask small but perhaps diagnostically important image features makes it an undesirable property’.55 Speckle pattern does not alter with time, so repeat imaging if obtained through same plane with same trans­ducer position and orientation, will show the same speckle pattern. However, if we change the transducer orientation and position, the speckle pattern shall also change. Attenuation-related artifacts include attenuation, shadowing and enhancement attenuation. It occurs due to lack of transmission of sound through a mass lesion. It points to solid internal consistency of the lesion.2 When an ultrasound beam encounters a focal object that attenuates the sound to a lesser or greater extent than in the surrounding tissue, the strength of the beam distal to this given structure will be either stronger or weaker than in the adjoining field. Thus, when the ultrasound beam encounters a strongly attenuating or highly reflective structure, the amplitude of the beam distal to this structure is diminished. The echoes returning from structures beyond the highly attenuating structure will also be diminished. In clinical practice, this is seen as a dark band known as a “shadow” deep to a highly attenuating structure (calculi) (Fig. 11A). Similarly, when the ultrasound beam traverses a focal weakly attenuating structure within the imaging field, the amplitude of the beam beyond this structure is greater than the beam amplitude at the same depth in the rest of the field and thus echoes returning from structures deep to the focal weak attenuator will have a higher amplitude and will be falsely displayed as increase in echogenicity or “enhancement’’, typically seen posterior to a cystic lesion (low attenuation lesion)53-55 (Fig. 11B). Propagation-related (artifacts associated with multiple echoes) (Fig. 12)56 includes reverberation, comet tail, ring down, sidelobe and mirror image artifacts. Reverberation: In the presence of two parallel highly reflective surfaces, the echoes produced from a primary ultrasound beam may be repeatedly reflected back and forth before returning to the transducer for detection. When this happens, multiple echoes are recorded and displayed. At imaging, this is seen as multiple equidistantly spaced linear reflections and is referred to as reverberation artifact.53,56 Typically, it occurs when sound beam travels with minimal or no attenuation through a cystic (fluid) structure. These become weak as sound travels into the tissue deeper and can mimic solid

Chapter 38 Ultrasound Instrumentation: Practical Applications

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Figs 11A and B:  Ultrasound image artifact shadowing (A) and enhancement (B) in two different patients. (A) Demonstrates shadowing with gallbladder calculi; (B) Demonstrates enhancement from a large abdominal cystic lesion

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Fig. 12:  Reverberation artifact (arrow) at anterior part of grossly hydronephritic kidney





component in a cystic structure (urinary bladder). This artifact can be resolved by simply changing the scanning angle. Comet tail artifact is also a form of reverberation. In this artifact, the two reflective interfaces and thus sequential echoes are closely spaced. The sequential echoes may be so close together on the display that individual signals remain unperceivable. It appears as a dense, tapering echoes distal to a structure which reflects strongly.2 Classic examples include metallic objects which may produce such artifacts. Mirror image artifacts: are generated when a highly reflective interface is encountered by the primary beam. The reflected echoes then encounter the “back side” of a structure and are reflected back toward the reflective

interface before being reflected to the transducer for detection.53 The display shows a duplicated structure which is equidistant from but deep to the strongly reflective interface. In clinical imaging, this duplicated structure is commonly identified at the level of the diaphragm, where the pleural-air interface acts as the strong reflector. Ultrasound beam characteristics related artifacts Beam width artifact: A highly reflective object located within the widened beam beyond transducer’s margin may generate detectable echoes. Ultrasound display presumes echoes to be originating from within narrow imaging plane and displays them as such.53 Its clinical application can be manifested as when anechoic structure (urinary bladder) shows peripheral echoes. This can be corrected and removed during scanning by adjusting the focal zone to the level of interest and by placing transducer at the center of the object. Side lobes are multiple beams of low amplitude ultrasound energy that project radially from the main beam axis and artifacts seen mainly with linear array transducers.53 Similar to beam width artifact, this phenomenon is most likely to be recognized as extraneous echoes present within an expected anechoic structure, such as the bladder.57

REFERENCES 1. Rizzatto G. Ultrasound  transducers. Eur J Radiol. 1998;27 (Suppl 2):S188-95. 2. Silkowski C. Ultrasound Nomenclature, Image Orientation and Basic Instrumentation. In: Abraham D, Silkowski C, Odwin C. Emergency Medicine Sonography. Jones and Bartlett Publishers; 2010. pp. 1-24. 3. Hangiandreou NJ. Radiographics AAPM/RSNA physics tutorial for residents. Topics in US: B-mode US: basic concepts and new technology. 2003;23(4):1019-33.

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Section 2 Recent Advances and Applied Physics in Imaging 4. Thomenius KE. Instrumentation for B-mode imaging. In: Goldman LW, Fowlkes JB (Eds). Categorical course in diagnostic radiology physics: CT and US cross-sectional imaging. Oak Brook, Ill: Radiological society of North America; 2000. pp. 9-20. 5. Zagzebski JA. Physics and Instrumentation in Doppler and B-mode ultrasonography. In: Zwiebel & Pellerito. Introduction to Vascular Ultrasonography, 5th edition. Elsevier Saunders; Philadelphia: Chapter 2. 2005. pp. 19-60. 6. Curry ST, Dowdey JE, Murry RC. Ultrasound. In: Christensen’s Physics of Diagnostic Radiology, 4th edition. Lea & Febiger; 1990.pp. 323-70. 7. Kremkau F. Diagnostic ultrasound principles, Instrumentation and Exercises, 5th Edn. Orlando FL: Grune & Startton;1993. 8. Taylor KJW, Wells PNT, Burns PN. Clinical applications of doppler ultrasound. New York: Raven Press;1995. 9. Evans D. Doppler ultrasound physics instrumentation and clinical applications. New York: John Wiley and Sons;1989. 10. Rubin JM, Bude RO,Carson PL, et al. Power Doppler US: A potentially useful alternative to mean frequency-based color doppler US. Radiology. 1994;190:853-6. 11. Martinoli C, Derchi LE, Rizzatto G, Solbiati L. Power Doppler sonography: general principles, clinical applications, and future prospects. Eur Radiol. 1998;8:1224-35. 12. Sodhi KS, Sidhu R, Gulati M, Saxena A, Suri S, Chawla Y. Role of tissue harmonic imaging in focal hepatic lesions: comparison with conventional sonography. J Gastroenterol Hepatol. 2005;20(10):1488-93. 13. Shapiro RS, Wagreich J, Parsons RB, Pasik AS, Yeh HC, Lao R. Tissue harmonic imaging sonography: evaluation of image quality compared with conventional sonography. AJR. 1998;171:1203-6. 14. Yucel C, Ozdemir H, Asik E, Oner Y, Isik S. Benefits of tissue harmonic imaging in the evaluation of abdominal and pelvic lesions. Abdom. Imaging. 2003;28:103-9. 15. Ward B, Baker AC, Humphrey VF. Nonlinear propagation applied to the improvement of resolution in diagnostic medical ultrasound. J Acoust Soc Am. 1997;101:143-54. 16. Rosenthal SJ, Jones PH, Wetzel LH. Phase inversion tissue harmonic sonographic imaging: a clinical utility study. AJR. 2001;176:1393-8. 17. Choudhry S, Gorman B, Charbonear JW, et al. Comparison of tissue harmonic imaging with conventional US in abdominal disease. Radiographics. 2000;20:1127-35. 18. Hann LE, Bach AM, Cramer LD, Siegel D, Yoo HH, Gaxia R. Hepatic sonography: comparison of tissue harmonic and standard sonography techniques. AJR. 1999;173:201-6. 19. Desser TS, Jeffrey RB. Tissue harmonic imaging techniques: physical principles and clinical applications. Semin. Ultrasound CT MR. 2001;22:1-10. 20. Lencioni R, Cioni D, Bartolozzi C. Tissue harmonic and contrast specific imaging: back to gray scale in ultrasound. Eur. Radiol. 2002;12:151-65.

21. Kollmann C. New sonographic techniques for harmonic imaging--underlying physical principles. Eur J Radiol. 2007;64(2):164-72. Epub 2007 Sep 17. Review. 22. Kawagishi T. Technical description of 1.5 harmonic imaging, an effective technique for contrast–enhanced ultrasound diagnosis. Medical review 2003-Cardiology special Issue. Cardiac imaging & Networking. Toshiba Medical systems. 23. Harvey CJ, Pilcher JM, Eckersley RJ, Blomley MJK, Cosgrove DO. Advances in Ultrasound. Clin Radiol. 2002;57;157-77. 24. Jespersen SK, Wilhjelm JE, Sillesen H. Multiangle compound imaging. Ultrason Imaging. 1998;20:81-102. 25. Garra BS. Elastography Current status, future prospects and making it work for you. Ultrasound Quarterly. 2011;27:177-86. 26. Benacerraf BR, Benson CB, Abuhamad AZ, et al. Three- and 4-dimensional ultrasound in obstetrics and gynecology: proceedings of the American Institute of Ultrasound in Medicine Consensus Conference. J Ultrasound Med. 2005; 24(12):1587-97. 27. Bega G, Lev-Toaff AS, O’Kane P, et al. Three-dimensional Ultrasonography in Gynecology Technical Aspects and Clinical Applications. J Ultrasound Med. 2003;22(11):1249-69. 28. Raga F, Bonilla-Musoles F, Blanes J, et al. Congenital mullerian anomalies: diagnostic accuracy of three-dimensional ultrasound. Fertil Steril. 1996;65(3):523-8. 29. Wu MH, Hsu CC, Huang KE. Detection of congenital mullerian duct anomalies using three-dimensional ultrasound. J Clin Ultrasound. 1997;25(9):487-92. 30. Dyson RL, Pretorius DH, Budorick NE, et al. Three dimensional ultrasound in the evaluation of fetal anomalies. Ultrasound Obstet Gynecol. 2000;16(4):321-8. 31. Lee W, Chaiworapongsa T, Romero R, et al. A diagnostic approach for the evaluation of spina bifida by three-dimensional ultrasonography. J Ultrasound Med. 2002;21(6):619-26. 32. Ji E, Pretorius D, Newton R, et al. Effects of ultrasound on maternal-fetal bonding: a comparison of two- and threedimensional imaging. Ultrasound Obstet Gynecol. 2005; 25(5):473-7. 33. Kurjak A, Azumendi G, Vecek N, et al. Fetal hand movements and facial expression in normal pregnancy studied by fourdimensional sonography. J Perinat Med. 2003;31(6):496-508. 34. Kurjak A, Stanojevic M, Andonotopo W, et al. Behavioral pattern continuity from prenatal to postnatal life: a study by four-dimensional (4D) ultrasonography. J Perinat Med. 2004;32(4):346-53. 35. Kurjak A, Stanojevic M, Azumendi G, et al. The potential of four-dimensional (4D) Ultrasonography in the assessment of fetal awareness. J Perinat Med. 2005;33(1):46-53. 36. DeVore GR, Falkensammer P, Sklansky MS, et al. Spatiotemporal image correlation (STIC): new technology for evaluation of the fetal heart. Ultrasound Obstet Gynecol. 2003;22(4):380-7. 37. Viñals F, Poblete P, Giuliano A. Spatio-temporal image correlation (STIC): a new tool for the prenatal screening of

Chapter 38 Ultrasound Instrumentation: Practical Applications congenital heart defects. Ultrasound Obstet Gynecol. 2003; 22(4):388-94. 38. Gonçalves LF, Lee W, Chaiworapongsa T, et al. Four dimensional ultrasonography of the fetal heart with spatiotemporal image correlation. Am J Obstet Gynecol. 2003;189(6):1792-802. 39. Benacerraf BR, Shipp TD, Bromley B. How sonographic tomography will change the face of obstetric sonography: a pilot study. J Ultrasound Med. 2005;24(3):371-8. 40. Real-time Virtual Sonography Unit. Instruction Manual. Hitachi Medical Corporation. 2004-2006. 41. Sandulescu L, Saftoiu A, Dumitrescu D, Ciurea T. The role of real-time contrast-enhanced and real-time virtual sonography in the assessment of malignant liver lesions. J Gastrointestin Liver Dis. 2009;18(1):103-8. 42. Sandulescu L, Dumitrescu D, Rogoveanu I, Saftoiu A. Hybrid ultrasound imaging techniques (fusion imaging). World J Gastroenterol. 2011;17(1):49-52. 43. Minami Y, Kudo M, Chung H, et al. Percutaneous radiofrequency ablation of sonographically unidentifiable liver tumors. Feasibility and usefulness of a novel guiding technique with an integrated system of computed tomography and sonographic images. Oncology. 2007;72(Suppl 1):111-6. 44. Minami Y, Chung H, Kudo M, et al. Radiofrequency ablation of hepatocellular carcinoma: value of virtual CT sonography with magnetic navigation. AJR Am J Roentgenol. 2008;190(6): W335-41. 45. Kitada T, Murakami T, Kuzushita N, et al. Effectiveness of real-time virtual sonography guided radiofrequency ablation treatment for patients with hepatocellular carcinomas. Hepatol Res. 2008;38(6):565-71. 46. Sandulescu L, Saftoiu A, Dumitrescu D, Ciurea T. Real-time contrast-enhanced and real-time virtual sonography in the

assessment of benign liver lesions. J Gastrointestin Liver Dis. 2008;17(4):475-8. 47. Krücker J, Xu S, Venkatesan A, et al. Clinical Utility of Real-time Fusion Guidance for Biopsy and Ablation. J Vasc Interv Radiol. 2011;22(4):515-24. 48. Shehata IA. Treatment with high intensity focused ultrasound: secrets revealed. Eur J Radiol. 2012;81(3):534-41. 49. Wu F, Wang ZB, Chen WZ, Zhu H, Bai J, Zou JZ, et al. Extracorporeal high intensity focused ultrasound ablation in the treatment of patients with large hepatocellular carcinoma. Ann Surg Oncol. 2004;11(12):1061-9. 50. Dubinsky TJ, Cuevas C, Dighe MK, Kolokythas O, Hwang JH. High-intensity focused ultrasound: current potential and oncologic applications. AJR Am J Roentgenol. 2008;190(1):191-9. 51. Kaneko OF, Willmann JK. Ultrasound for molecular imaging and therapy in cancer. Quant Imaging Med Surg. 2012;2(2):87-97. 52. Kircher MF, Willmann JK. Molecular body imaging: MR imaging, CT, and US. Part II. Applications. Radiology. 2012;264(2):349-68. 53. Feldman MK, Katyal S, Blackwood MS. US  artifacts. Radio­ graphics. 2009;29(4):1179-89. 54. Burckhardt CB. Speckle in ultrasound B-Mode scans, IEEE Trans. Sonics Ultrasonics. 1978;SU-25:1-6. 55. Chen Y, Broschat SL , Flynn PJ. Phase Insensitive Homomorphic Image Processing for Speckle Reduction. Ultrasonic Imaging. 1996;18:122-39. 56. Bushberg JT, Seibert JA, Leidholdt EM, Boone JM. The essential physics of medical imaging, 2nd edition. Philadelphia, PA: Lippincott Williams & Wilkins; 2002. pp. 469-553. 57. Laing FC, Kurtz AB. The importance of ultrasonic side-lobe artifacts. Radiology. 1982;145(3):763-8.

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39 Image Optimization in Ultrasound

CHAPTER

Rashmi Dixit

INTRODUCTION Ultrasound imaging with its inherent flexibility, low cost and real time physiologic measurement capability with no known bioeffects, at intensities used in medical imaging, plays a vital role in diagnostics. Image formation in ultrasound depends on the physical properties of ultrasound pulse formation, transmission and interaction with tissues. Acoustic energy undergoes essentially three different types of interactions in the tissuesreflection (specular and diffuse), refraction, and attenuation. Diagnostic applications of ultrasound are based on detection and display of acoustic energy reflected from interfaces within the body. The amplitude of the reflected energy is used to generate ultrasound images while frequency shifts in backscattered ultrasound provide information relating to moving targets such as blood. Real-time, grayscale, B-mode display, in which variations in display intensity or brightness are used to show signals of differing amplitude, is the mainstay of ultrasound imaging. Real-time ultrasound produces an impression of motion by generating a series of 2D images several times per second or frames per second. The quality of an ultrasound image1-3 depends on its spatial resolution, temporal resolution, contrast resolution and freedom from certain artifacts. Spatial resolution has three components: axial, lateral and elevational or azimuthal resolution. Axial resolution is the resolution along the axis of the ultrasound beam. It is also called longitudinal or depth resolution and depends on spatial pulse length, which is the product of wavelength and number of pulses, being equal to half the spatial pulse length. As frequency is increases the pulse length decreases permitting resolution of smaller details. Hence, axial resolution improves with increasing frequency (which reduces wavelength). Axial resolution at a frequency of 3.5 MHz is 0.5–1.0 mm. It does not change significantly with depth. Lateral resolution refers to the ability to distinguish two structures lying side by side. The width of the main beam defines the lateral resolution of the ultrasound image because objects can be resolved separately only if the beam is narrower than the distance

between them. Hence in modern systems-transducers are focused to reduce beam width. Focal zone is the area where the beam is 3–4 wavelengths wide and the area where lateral resolution is highest, deteriorating rapidly beyond it. Lateral resolution with frequency of 3.5 MHz is approximately 2 mm. Focusing in the elevation plane is also possible with current technology. Temporal resolution refers to the ability to locate the position of a particular moving structure in time. This increases as the frame rate increases. Contrast resolution is the ability to show very subtle difference in echo strength. Contrast resolution improves when a system can recognize and store a wide range of echo amplitudes. New technical developments and remarkable improvement in image quality have marked several new applications for diagnostic ultrasound. The rise of state of the art, expensive equipment has greatly eased the sonologist’s job. Nonetheless, it does not by itself guarantee, high-quality ultrasound images. Variables, many of which are under direct user control, must be managed to guarantee the production of quality studies. An accurate ultrasound diagnosis relies heavily on the experience and skill of the examiner and requires adjustment of the equipment settings from patient to patient and organ to organ. Hence, the image optimization is an essential prerequisite for diagnostic ultrasound imaging.

GRAYSCALE IMAGING Basic Guidelines2-5 Patient should be positioned in such a way that the area of interest can be easily accessed and the patient is comfortable during the examination. Changing the patient position to better elucidate pathology is also important, e.g. an extended neck for thyroid examination, left lateral decubitus position for gallbladder calculi, etc. A good acoustic window improves scanning accuracy and image quality. Solid organs like the liver or spleen or fluid filled structures, which do not attenuate the sound

Chapter 39 Image Optimization in Ultrasound

beam, e.g. full bladder or fluid filled stomach provide a good acoustic window to see deeper structures. Use of adequate amount of coupling gel is essential as air has high-acoustic impedance.

Factory Presets The more complicated machine settings are saved as presets. Presets provide a useful starting point; however, these are settings which are optimized for patients of average body habitus and further optimization of the image by manual adjustments is invariably required in order to increase diagnostic confidence and avoid artifacts. A single touch image optimization is also available on some systems; however this only resets the parameters to the chosen preset.

Transducer Selection Choosing the appropriate transducer both in terms of frequency as well as footprint is extremely important for a good examination. Higher frequencies provide a better resolution but are attenuated much more as attenuation is proportional to the fourth power of frequency. A trade off thus has to be made between the need for penetration and resolution. While performing superficial scans as for the thyroid, musculoskeletal system or testicular examination a linear transducer with a high frequency (7–10 mHz or even 15–17 MHz) is suitable but for deeper structures a lower frequency, such as 2.5–3 MHz is used. Currently, many multifrequency and broad band width transducers are available. For intercostal scanning or scanning the neonatal brain transducers with a smaller footprint which fit into the small acoustic window are appropriate (Figs 1A and B). Sector transducers are thus useful to evaluate deeper structures through a small acoustic window, e.g. echocardiography. In sector scanning, however, resolution becomes poorer with increasing depth as

A

the same echo lines are spread out over a wider area deeper in the tissue.

Overall Gain Overall gain amplifies all the returning echoes/signals uniformly. An excessively high gain can result in a washed out image and can obscure many details.

Time-gain Compensation Time-gain compensation (TGC) is also referred to as distancegain-compensation (DGC) or spatial-time compensation (STC). Signals that arrive later, i.e. from greater depths are amplified more than earlier signals to compensate for the attenuating effect of tissues. TGC controls permit the user to selectively amplify the signals from deeper structures or suppress signals from superficial tissues so that a smooth grayscale picture can be obtained (Figs 2A and B). Although most newer machines provide for some automatic TGC, manual adjustment by the user is one of the most important factors that may have a profound effect on image quality.

Depth Setting This parameter selects the depth of the imaging field. If too much depth is selected the image will be small and the area of interest difficult to visualize, measurements may also be inaccurate. On the other hand of the depth setting is too shallow the complete region or organ is not visualized and pathology at a deeper levels may be completely missed (Figs 3A and B). Practically depth can be adjusted by starting at a higher depth, subsequently depths should be decreased so that the area of interest in at about three-fourth the depth of the screen. A small area should be available behind the area of interest of observe useful artifacts.

B

Figs 1A and B: Cranial sonogram performed with a curvilinear array abdominal probe (A) shows shadowing obscuring the cerebral convexities on both sides due to mismatch between the large transducer footprint, acoustic window. The second scan (B) performed with a small foot print transducer shows good visualization of cerebral convexities. Arrow, Sylvian fissure; T, tentorium; C, cerebellum

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A

B

Figs 2A and B: (A) Improper TGC setting resulting in a dark band over the deep aspect of the liver; (B) With the correct TGC setting the whole liver shows a uniform echopattern

A

B

Figs 3A and B: Improper depth setting in (A) results in nonvisualization of posterior most portion of liver with consequently missed metastatic focus, which is easily appreciated (arrow) with proper depth setting in (B)

Focal-zone Setting To improve resolution diagnostic transducers are focused electronically . As already discussed, the resolution of ultrasound is best in the focal zone. The focal zone should thus be set over the area of interest. A significant difference in image resolution depending on the focal-zone setting is the hallmark of a well-focused beam (Figs 4A and B). Modern scanners allow the use of multiple focal zones; however, this may result in decreased frame rate and hence decreased temporal resolution.

Zoom Zoom is used to magnify the area of interest. There are two types of zoom available. Read zoom is used to enlarge a frozen image whereas write zoom is used to enlarge the display magnification, when scanning is taking place.

In read-zoom-gray level values are read only from a small part of the computer memory and the pixels are enlarged while displaying, something like a magnifying glass. If the magnification factor is too large image matrix becomes obvious and renders the image to grainy. In write zoom use is made of the fact that the echo samples are received fast enough for several samples to occur in each pixel. In this situation, the image scale can be enlarged to a point where only one sample occurs in each pixel. Each pixel, whose size remains unchanged, displays less tissue. Thus, there is magnification without loss of definition. If the scale is increased further, there is a larger space between scan lines so that further interpolation and smoothening may be required to maintain an acceptable image. More real-scan lines can be introduced using sophisticated signal processing so that definition is improved. One such option is referred to as high-density (HD) zoom. This magnifies the region of interest while increasing line density by redistributing

Chapter 39 Image Optimization in Ultrasound

A

B

Figs 4A and B: Effect of focal zone: In (A) the focal zone (denoted by the small arrowhead) is placed anteriorly resulting in a blurred appearance of the posteriorly placed hepatic cyst and diaphragm. These become more sharply defined with proper focal zone positioning over the area of interest (B)

A

B

Figs 5A and B: Images of the liver displayed at dynamic ranges of 70 and 36 dB are shown. The wide dynamic range (A) permits appreciation of subtle differences in echointensity between the diffusely fatty liver and a focal area of sparing. The narrow range (B) increases the conspicuity of larger echo differences with the area of focal sparing appearing darker and the diaphragm brighter than the wide dynamic range image

and reformatting all scan lines for the defined region of interest. Hence, one should always try to use the write zoom. Zoom is extremely useful for accurate measurement of small structures as the CBD.

Dynamic Range Dynamic range is the ratio of the highest to the lowest amplitudes that can be displayed, expressed in decibels. Dynamic range adjustment changes the contrast. The widest dynamic range that permits best differentiation of subtle differences in echo intensity is preferred for the most applications. The narrower ranges increase the conspicuity of larger echo differences (Figs 5A and B).

ARTIFACTS IN B MODE IMAGING3,5-7 Artifact is a term used to describe any unwanted information generated in the process of image formation. Most artifacts interfere with image interpretation while some artifacts which contain diagnostic information are referred to as friendly artifacts. A number of artifacts may occur during scanning. Understanding how and why a particular artifact occurs is imperative to eliminate it and avoid errors in diagnosis. The ultrasound equipment relies on physical assump tions to assign location and intensity of each received echo. The assumptions are: r
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Beam-width Artifact The real ultrasound beam is not of a uniformly narrow, laser-like configuration which would be optimal for image resolution. A typical ultrasound focused ultrasound beam exits the transducer at the same width as transducer and progressively narrows to a focus after which it spreads rapidly in the far field, where it may widen beyond the actual width of the transducer. A highly reflective object located within the widened beam beyond the edges of the transducer may generate detectable echoes. The system assumes that these echoes arose from within the imaging plane and displays them accordingly (Fig. 6). The more intense the reflection the further off axis its echoes will be received. During clinical scanning the artifact is recognized when a structure which should be anechoic has peripheral echoes. It is generally most obvious when a bony or gaseous structure lies adjacent to a fluid space (Fig. 7). This also means that a strong reflector will continue to give detectable echoes further from the central axis than a weak reflector. Hence, the resolution is better for weak reflectors than strong reflectors which tend to blur laterally and are therefore seen as cigar-shaped smears or streaks so that the width is exaggerated. It also results a general tendency to fill in small echo free regions, such as ducts producing slightly reduced measurements. This can be rectified and image quality improved by adjusting the focal zone to the area of interest and placing the transducer over the center of the object of interest.

Slice-thickness Artifact Beam-width artifacts also occur in the orthogonal plane, i.e. in the slice thickness or elevation plane. With circular transducers either simple disc or annular array types the beam is symmetrical in all planes but for linear and phased array transducers the beam wider in the orthogonal plane resulting in information from adjacent planes being depicted in te image. The beam width may be wider than a fluid collection. Some of the sound energy may hit structures outside the plane of intersection and may be projected into it to simulate a layer of sludge causing a simple fluid collection to appear complicated (Fig. 8). Since the reflector which has caused the artifact is not visualized in the image it is more difficult to recognize them than the same artifact occuring in the scanned

Fig. 7: Beam-width artifact: Strong echoes arising from a gas-filled bowel loop in the pelvis smear across the bladder

Fig. 6: Mechanism of beam-width artifact. Dotted lines represent the imaging plane. Echoes from the circle are assumed to arise from within the imaging plane in A and displayed within the square. This is rectified with proper focal-zone setting in B

Fig. 8: Low-level echoes are seen in the bladder not from debris but due to slice-thickness artifact arising from gas present in the bowel in the adjacent planes

Chapter 39 Image Optimization in Ultrasound

plane. However, with the latest 2D and X-matrix transducers, It is possible to focus the beam in the elevation plane a wellproviding, a uniformly focused ultrasound beam.

Side-lobe and Grating-lobe Artifacts These are low energy beams directed at angles away from the central line due to vibration of the edges of the transducer called side lobes and grating lobes. The latter occurs only in array transducers (Fig. 9). Strong reflectors present in the path of these low energy off-axis beams may generate echoes detectable by the transducer. These are displayed as having originated from within the main beam usually within an anechoic structure. They often have a convex shape and are also referred to as Chinese hat artifacts.

Fig. 10: Mechanism of reverberation artifact: T, transducer, R1 R2, reflecting surfaces

Artifacts Associated with Multiple Echoes Reverberation Bands A very important assumption in pulse-echo ultrasound imaging is that an echo returns to the transducer after a single reflection and that the depth is related to the time taken for the echo to return. If two highly reflective surfaces lie parallel to each other, the echoes generated may be reflected back and forth before they reach the transducer. The first echo returning after a single reflection is displayed in its proper position. The later echoes returning after multiple reflections are presumed to be arising deeper to the original structure (due to the delay) and are displayed as equally spaced linear reflections in a striped pattern called reverberation artifact (Figs 10 and 11). The deeper echoes are weaker than the superficial ones due to loss of sound energy due to attenuation by intervening tissues and incomplete reflection so that the bands become narrower and less intense with depth. Since the distance between the reverberation bands depends on the distance between the reflectors if the reflectors are very closely spaced the sequential echoes may be so close

Fig. 9: Off-axis beams: Side lobes (a) and grating lobes (b)

Fig. 11: Multiple equally spaced lines are seen within the gallbladder due to multiple reflections originating in the anterior abdominal wall

that individual bands cannot be seen. The resulting artifact is triangular with a tapered shape resembling a comet with its bright tail hence referred to as a comet-tail artifact. This artifact is commonly seen deep to calcifications, surgical clips, IUCD and in adenomyosis of gallbladder. It is presumed that many small fluid spaces like the Aschoff–Rokitansky sinuses in the wall of the gallbladder in this condition cause repeated reflections from the walls of the fluid space producing reverberation or the comet tail artifact. The artifact is diagnostic of adenomyosis (Fig. 12). Another artifact the ring-down artifact was previously thought to be a variant of comet-tail artifact because of the similar appearance of the two; however, this has a separate mechanism. The ultrasound energy is believed to cause vibrations within fluid trapped between air bubbles. These vibrations create a continuous sound wave that is transmitted back to the receiver. This is displayed as a line or series of parallel bands extending posterior to a gas collection.

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In some situations, this artifact can be confusing for example in the pelvis a repeat echo of the bladder or structures just behind it may appear as a deeper line apparently marking back of an echo poor mass. This in reality is a mirror image of the bladder. The clues that help to distinguish this pseudomass from the true mass are: the typical position, the back wall of the mass often lies behind the sacrum and hence is anatomically not possible, and the poorly discerned or weak superior and inferior walls compared to strong anterior and posterior walls.

Artifacts Associated with Velocity Errors

Fig. 12: Adenomyosis of the anterior wall of gallbladder producing a typical comet-tail artifact

Fig. 13: Mirror reflection of the liver is seen above the diaphragm in this patient (asterix)

Mirror-image Artifact This artifact is also generated by a repeat echo. It is sometimes also referred to as a multipath artifact. The ultrasound beam encounters a highly reflective surface. The reflected echoes then encounter another reflective structure on their way back and are reflected back towards the reflective interface before being reflected to the transducer, where they are detected. The display shows a duplicated structure equidistant but deep to the strongly reflective interface. This artifact is commonly seen at the diaphragm with the air–pleural interface acting as a strong reflector. It is recognized as hepatic parenchyma seen in the expected position of the lung (Fig. 13). At this level, it does not cause any diagnostic problem, in fact may be useful, e.g. increased through transmission behind a peripheral cyst may be seen in the mirror image which would otherwise be obscured by the hyperechoeic reflection of air in the lung.

An important assumption in ultrasound imaging is that the velocity of US in soft tissues is constant (1540 m/s). This is not absolutely true in clinical sonography; fat, for example, conducts sound about 15% slower than most other soft tissues do (Table 1). When sound travels through a tissue with a velocity significantly lower than the assumed constant of 1540 m/sec the returning echo takes longer to return to the transducer. Scanners use the amount of delay to calculate the depth of the echo (0.13 μs delay corresponding to ~1 cm depth on final image). The processor assumes that the delay is due to the increased distance traveled by the echo. The echoes are thus displayed deeper on the image than they actually are. This is called speed-displacement artifact or propagationvelocity artifact. This geometric distortion does not affect the lateral dimension of the image as this is determined by the scanning action of the transducer rather than by the speed of sound. In clinical practice, this artifact is most commonly seen when an area of focal fat is encountered, e.g. areas of focal fat in the subdiaphragmatic region of the liver can result in a discontinuous appearance of the diaphragm because of fallacious posterior displacement of diaphragmatic segments behind the fatty change. In most cases, velocity errors are too small to be clinically significant and may in fact provide diagnostic clues to the presence of fat within lesions. However, in ophthalmic measurement where great precision is required the distortion

Table 1: Velocity of ultrasound in biologically important materials3 Tissue type

Velocity (m/s)

Air

330

Fat

1450

Water

1480

Brain

1565

Muscle

1580

Liver

1600

Lens of eye

1650

Soft tissue average

1540

Chapter 39 Image Optimization in Ultrasound

caused by the significantly higher velocity in the lens can be important. The speed of sound in the lens of the eye is 1620 m/s (vs 1540 of average soft tissues) so regions of the retina imaged through the lens appear closer than the parts imaged through the sclera producing a shelf-like anterior distortion called Baum’s bumps after sonologist who first described them.

Refractory Errors Changes in velocity also produces refractory errors. When a nonperpendicular incident ultrasound beam encounters an interface between two materials with different speeds of sound, it changes direction. The degree of this change and the direction is dependent both on the angle of incidence and the difference in velocity between the two media. The scanner working on the assumption that the US beam travels in a straight line misplaces the echoes to the side of their true location. This situation may become important clinically during transabdominal pelvic scans due to refraction occurring deep to the junction of rectus abdominis muscle and midline fat. This can cause lateral stretching of pelvic structures and obstetric measurements made under these conditions may be erroneous. In more extreme cases, it may cause apparent duplication of structures Repositioning the transducer eliminates this artifact.

Attenuation Errors As an ultrasound beam travels through the tissues, its energy gets attenuated due to combined effect of absorption, scattering and reflection. The greater distance the ultrasound beam travels through the body, the more the attenuation for a beam of similar energy. To compensate for this attenuation, ultrasound processing incorporates a compensatory amplification of echoes that take longer to return, i.e. arising in the deeper tissues. Attenuation also varies with different tissues depending on the attenuation coefficient which expresses the loss of ultrasound intensity per distance traveled (Table 2).

tissue in the beam shadowing occurs. This is because the gain compensation is only set to an average value; hence, an inadequate correction will be applied to this region. Both it and tissues deeper to it are depicted as less reflective than they actually are. This is visible as a dark band called an acoustic or distal shadow (Fig. 14). Shadowing can also be caused by an extremely efficient reflector such as gas bubble or calcification where 99% and 80% of the incident sound beam, respectively is reflected back. This is because very little of the sound energy penetrates to insonate deeper tissues and in addition any echoes from them would probably not cross the reflective layer on the return journey since they would be rereflected distally.

Edge Shadowing Shadowing is also sometime seen deep to the edges of strongly curved surfaces, such as cyst walls, fetal skull and vessels. Fine dark lines can be seen extending distal to such edges and become even more striking in the case of a cyst due to the increased through transmission behind the cyst itself. Two explanations have been offered for this: refraction of the ultrasound beam as it strikes a curved surface and increased attenuation at the edges because the ultrasound beam passing through the edge travels a larger distance through the cyst wall than that passing through the diameter of the cyst. Since the cyst wall is presumed to be more attenuating than the surrounding tissues, the beam is attenuated more resulting in shadowing. Although acoustic shadows have diagnostic significance and are useful for diagnosis of calcification or calculi, edge shadows do not have this diagnostic significance (Figs 15A and B). Edge shadows commonly occur in situations where shadowing erroneously suggests calcification, e.g. vessel walls in renal

Acoustic Shadowing When the ultrasound beam encounters a tissue that attenuates sound to a greater extent than the majority of the Table 2: Attenuation coefficients for selected tissues6 Material

Attenuation coefficient (dB/cm)

Water

0.000

Soft tissue

0.3–0.8

Fat

0.5–1.8

Bone

13–26

Air

40

Fig. 14: Acoustic shadows: Seen as dark bands posterior to multiple gallbladder calculi

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Figs 15A and B: (A) Refractive and attenuation model to explain mechanism of edge shadowing; (B) Subtle edge shadowing seen along the edges of fibroadenoma breast

sinus or malignancy, Coopers ligaments in the breast. It is important to recognize them as artifactual and dismiss them.

Increased through Transmission or Distal Bright-up’ Attenuation errors also occur if a tissue attenuates less than its surrounding tissues (e.g. a full bladder or a simple cyst). In this situation the echoes from it and the tissues posterior to it are overcorrected appearing as a bright band often termed ‘distal enhancement’ but in view of the enhancing effect of ultrasound contrast agents it is better termed increased through transmission or distal bright up (Fig. 16).

Noise

Fig. 16: A bright band is seen posterior to this hepatic cyst— Increased through transmission or distal bright-up

All imaging systems are prone to two types of noise random and structured. Electrical components produce random lowlevel voltages which, when amplified, are seen as fluctuating moving grey spots on the image producing a snow storm appearance. There are various other sources of‘noise’ within ultrasound images. Perhaps the most important is speckle. Speckle is an important source of image degradation and loss of contrast in ultrasound image. Small tissue reflectors approximately the size of wavelength of sound cause scattering of sound waves which are sent out almost uniformly in all directions. Constructive and destructive interference of these acoustic fields result in speckle. Most biologic tissues appear in US images as though they are filled with tiny scattering structures. Most of the visible signal in US images results from speckle interactions. The interference pattern also gives ultrasound images a characteristic grainy appearance reducing contrast and making identification of subtle features and abnormal tissue patterns more difficult.

Another problem is clutter, which arises from electrical interference or beamforming artifacts, reverberations, and other acoustic phenomena. Clutter consists of spurious echoes which can often be seen within structures of low echogenicity, such as a cysts, or within amniotic fluid, and which may be confused with ‘real’ targets as already discussed. Finally, another potential source of noise, especially in deeplying regions, is thermal noise arising in the electronics of the transducer or beamformer. All these sources of noise affect the ability of the radiologist to recognize tissue anomalies by interfering with the pattern recognition process in the observer’s brain. Various techniques, such as temporal smoothening (i.e. frame averaging or persistence) are used to reduce noise. The real information is reinforced while noise cancels out. In addition a number of special imaging modes are available on high end scanners to deal with these problems which are discussed later.

Chapter 39 Image Optimization in Ultrasound

SPECTRAL AND COLOR DOPPLER EXAMINATION Basic Guidelines7 Gray-scale settings should always be optimized before color Doppler flow mapping is applied. Fine details, such as small plaques or intimal thickening may be washed over by color if the grayscale image is not evaluated first. Of the various technical parameters that can be controlled the choice of the correct transducer or the correct transducer frequency is the most important like grayscale imaging. A trial of different transducer frequencies till the best compromise between penetration and signal strength is reached is usually required. Knowledge of anatomic variants is very important while scanning for vascular especially venous disease; for example, failure to recognize duplication of common femoral vein can result in missing the diagnosis of deep venous thrombosis. It is important to scan the entire length of vessel from its origin to termination when possible. If the ostium of a vessel is not evaluated, lesions at the ostia may be missed, e.g. atherosclerotic plaque commonly involve the origin of carotid and vertebral arteries. In such a situation, the elevated velocities may render evaluation of more distal stenotic lesions by velocity criteria alone difficult. Each vessel must also be examined in two planes, i.e. longitudinal and transverse to avoid missing partially occlusive eccentric thrombi, which may not be centered in the imaging plane in a longitudinal scan alone. While scanning peripheral vessels, it is important not to mistake a collateral that runs parallel and close to the occluded vessels for the main vessel. Identification of the vein that accompanies the artery and familiarity with the normal orientation of the vessels can help in distinguishing a parallel collateral from the main vessel as the collateral usually runs quite separate from the vein. Use of a lower frequency transducer with a wide field of view which enables visualization of both the patent segments of the native vessel and the collateral is also useful. Another useful technique is to follow the vessel from its origin to be certain of its source.

Optimizing Color Doppler and Spectral Doppler Settings7-11 Color Box or Color Doppler Sampling Window The color box is a user adjustable area within the ultrasound image in which all color Doppler information is displayed. The angle of incidence of the color box can changed by angling the color box to the ‘right’ or ‘left’ so called ‘steering’ or by angling the transducer. As the size width and depth of color box increases frame rate decreases, image resolution and quality are affected. Thus, the box should be as small

and superficial as possible while still providing the necessary information. This will maximize the frame rate. The frame rate refers to the rate at which complete images are produced. Frame rate affects the temporal resolution. With grayscale imaging alone the frame rate can exceed 50 fps but the time required to produce color images is much longer. The frame rate in color imaging is dependent on several factors. The wider the color box more the scan lines required and longer it will take to acquire data to produce the image. Increasing the depth (or height) of the box alone will not produce any major change in the frame rate, increasing the imaging depth however will require a lower PRF (due to more time for the echo to travel to and fro) hence decreasing the frame rate.

Doppler or Color Gain Gain refers to amplification of sampled information for purposes of improving the depiction of acquired data. It controls the amplitude of color display in color or power mode and the spectral display in pulsed Doppler mode. If flow is present and the gain is set too low it is possible that no flow will be depicted on the monitor; however, an excessively high gain setting produces noise obscuring true Doppler signal and filling in the spectral waveform resulting in falsely increased flow with little meaningful quantitative flow data. For spectral Doppler the gain should be adjusted so that the tracing should be continuous and easy to visualize without any low level noise band above and below baseline. For color imaging the color gain should be set as high as possible without displaying random color speckles. This is set by turning it up until noise (i.e. scattered isolated color pixels overwriting grayscale pixels) is encountered and then backing off until the noise just clears. The color should just reach the intimal surface of the vessel. A high color gain setting may cause bleeding of color or blooming into the wall or even outside the vessel lumen. This impairs visualization of plaques and partial thrombi (Figs 17A and B).

Velocity Scale This is one of the most important parameters under user control during a Doppler examination. It determines the range of velocities that are depicted with either the color or spectral component. It is not synonymous with pulse repetition frequency (PRF) but PRF is related to the velocity scale setting so that increasing the velocity scale increases the PRF and vice versa. If the velocity setting is too low for the velocities being examined, the high velocity signals will not be displayed accurately and aliasing results. Aliasing is an incorrect and paradoxical display of the colors or spectral Doppler velocity. This is related to the fact Doppler and color flow utilize pulsed beams which are transmitted and received by the transducer. The number of such pulses sent

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determines the pulse repetition frequency. If the Doppler shift is higher than PRF/2 or the Nyquist limit then the display wraps around the scale and appears to change direction. For spectral Doppler the velocity peak is cutoff at the top of the scale and written from the lowest portion of the scale back toward the top. On the color Doppler image aliasing is seen

A

as color change from red to yellow to light blue to dark blue. Color aliasing projects the color of reversed flow within central areas of higher laminar velocity. With aliasing no black stripe is seen from the low velocity filter between the reversed colors unlike flow reversal (Figs 18A to D). Higher velocities require a higher PRF for accurate sampling

B

Figs 17A and B: (A) Color Doppler images of the carotid with very-low-color gain showing incomplete color fill in the carotid; (B) Excessively high-color gain resulting in bleeding of color into the wall of the carotid and some noise in the surrounding tissues

A

B

C

D

Figs 18A to D: (A) At high PRF settings of 12000 Hz only minimal flow is seen in the carotid artery; (B) When the velocity scale is lowered to 4000 Hz complete wall-to-wall color fill is seen with an area of aliasing seen where the artery dips away from the transducer; (C) A very low PRF results in aliasing throughout the vessel; (D) Aliasing in spectral Doppler with the top of the peak being cut off and written at the bottom

Chapter 39 Image Optimization in Ultrasound

Aliasing is one of the most important artifacts in Doppler and can be advantageously used to demonstrate high- or low-flow turbulence. It can be useful to quickly identify the higher velocity region within the vessel and readily place the sample volume for velocity measurement. However, if the color velocity scale is set much lower than the mean velocity of blood flow, aliasing occurs throughout the vessel lumen making it difficult to identify the high velocity turbulent jet associated with a significant stenosis. Tortuosity of a vessel can cause erroneously produce the appearance of aliasing. The options available to reduce spectral aliasing are increasing the Doppler angle with resultant decrease Doppler shift, increasing velocity scale, changing the baseline setting or using a lower ultrasound frequency. Aliasing is not seen in power Doppler because it has no directional or velocity component.

Gate Size or Sample Volume Box It is the user defined area from where the spectral Doppler information is obtained depicted as a pair of cross hairs within the 2D image. Although on the image it looks like a flat box, sample volume has a third dimension in and out of the plane of the image which may be up to a centimeter at times. Hence, signals may be displayed from unwanted areas of vessels or even unwanted vessels. Normally, the gate should cover approximately two thirds of the vessel lumen (Figs 19A and B). If the sample volume encompasses the entire vessel slower velocities from the vessel margins are included resulting in spectral broadening. However, if the gate is too small the Doppler signal may be missed. In addition, if the vessel is mobile as well the Doppler signal may be discontinuous with loss of diastolic signal in each cycle. Increasing the Doppler gate is helpful when searching for trickle flow or trying to obtain a Doppler signal from behind a calcified plaque.

A

Sample Volume or Gate Position The optimal position of a sample volume in a normal vessel is in the midposition parallel to the wall whereas in a diseased vessel there is some controversy whether the cursor should be angled parallel to the flow or parallel to the vessel wall. Whichever method is used the same technique must be used every time to allow reproducibility and standardization. If the sample volume is placed eccentrically too close to the vessel wall it will be degraded by signal from vessel wall motion and will also show artificial spectral broadening.

Angle Correction In vascular applications optimal imaging of the vessel wall is obtained when the transducer is perpendicular to the vessel wall. However, this selection is not suitable for Doppler examination. In diagnostic Doppler imaging the Doppler equation is used to calculate the blood flow velocity, i.e. 'f = (2f v/c) Cos q where 'f = Change in frequency f = Original transmitted frequency v = Velocity of blood flow c = Speed of sound in tissue T = Angle of insonation. Thus, the angle q which is the angle between the direction of Doppler pulses and the direction of blood flow affects the frequency shift. At a Doppler angle of 0 the maximum Doppler shift is achieved as cosine of 0° equals is 1, conversely no Doppler shift will be recorded if the angle is 90° because cosine of 90° is 0. Ideally a small Doppler angle, i.e. less than 60° should be used approximately between 45° and 60° because within this range a linear relationship exists between Doppler shifts and velocity. The cosine of Doppler angle changes rapidly for angles more than 60°; hence, a small

B

Figs 19A and B: (A) A properly positioned sample volume in the center of the vessel covering almost 2/3rds of vessel lumen results in a spectral trace with a clear window; (B) An excessively large sample volume covering the entire vessel lumen results in inclusion of lower flow from the edges with consequent spectral widening

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change in the angle is associated with a large change in the value of cos q. Hence, a small error in estimation of Doppler angle will result in a large change in the estimated velocity producing unreliable results.

Color-write Priority Color write priority is a setting closely related to color gain. This selects a grayscale value above which all color information is suppressed. While larger vessels require a low setting of color-write priority, in small vessels that do no have resolvable anechoic lumen on grayscale color information can be suppressed by inappropriate color-write priority. In such a situation, color is not seen in the image even when the system has detected it. This is of particular importance in areas like the testis where the intratesticular vessels are small and Doppler is an important means of diagnosing torsion.

result in red-blue color inversion on the color Doppler image and inversion of spectral waveform with spectral Doppler. Hence, flow direction in a vessel should never be presumed but carefully determined after comparing with the color bar. Misinterpretation of flow direction may erroneously suggest a malfunctioning TIPS or result in a missed flow reversal in an artery.

Directional Ambiguity

The baseline is depicted on both the color bar and spectral waveform. It divides the color bar into positive and negative Doppler shifts. Baseline can be adjusted to emphasize certain aspects of flow, although the overall range of depicted velocities does not change, the depicted flow that is emphasized changes. Adjustment of baseline is one method to prevent aliasing.

Directional ambiguity or indeterminate flow direction refers to a spectral Doppler tracing in which the waveform is displayed with nearly equal amplitude above and below the baseline in a mirror image pattern. Directional ambiguity can result when the interrogating beam intercepts the vessel at 90° (or close to 90°). If a Doppler signal is detected it is seen as a tracing both above and below the baseline. At higher gain settings directional ambiguity is worse. This can be corrected by changing the angle of interrogation. This should be distinguished from true-bidirectional flow. In this case blood actually flows in two directions such as in the neck of a pseudoaneurysm. The clue here is that flow here is first in one direction and then in the other in the same cardiac cycle. It is never simultaneously symmetric above and below the baseline. Bidirectional flow can also be seen in the setting of high resistance organ flow such a torsion, venous thrombosis, etc. and is seen as diastolic reversal.

Wall Filters

Slow Flow

Wall filters selectively filter out all information below a defined frequency threshold. It eliminates the typically lowfrequency–high-intensity noise that may arise from vessel wall motion. There are usually preset by the manufacturer as high, medium or low which can be applied separately to spectral, color and power imaging. The aim is to eliminate low frequency noise, but if it is set too high, it can result in the loss of signal from slow flow. In some arteries diastolic flow may be eliminated resulting in errors in calculation of Doppler indices, hence it should be kept as low as possible (typically in the range of 50–100 Hz). Filters can be applied separately to the color Doppler image or spectral Doppler depending on which scanning mode is active. On the color bar, the filter setting is indicated by a black band on both sides of the baseline. Increase in filter settings show up as widening of the black band. On spectral waveform a high wall filter wall results in loss of depicted spectral information immediately above baseline. Reducing the wall filter setting results in filling of spectral data towards the baseline.

If one is unable to visualize color flow in a vessel despite optimization of all Doppler parameters, the flow may be too slow for the color flow image to visualize. In such a situation use of power Doppler or spectral Doppler which are more sensitive to slow flow may help to detect flow. The power Doppler technique uses the intensity or power of the Doppler signal rather than the frequency shift. Strength of a Doppler signal that exceeds a particular threshold level is displayed, hence it is less angle dependent. It is also more sensitive as more extensive dynamic range can be used than with standard color Doppler imaging because noise that would overwhelm the color Doppler image can be assigned a uniform background color. The spectral wave form makes use of 256 pulse cycles per scan line and contains qualitative and quantitative diagnostic information for interpretation. The color map on the other hand contains only about 8 pulse cycles per scan line there by providing considerably less information than spectral Doppler. Also the color Doppler images display the mean frequency shift rather than the peak frequency shift. Appropriate settings of the above mentioned Doppler parameters eliminate or greatly reduce Doppler artifacts related to machine settings. There are certain other artifacts, such as those due to anatomical factors or those

Baseline

Inversion of Flow It is possible to electronically invert the direction of flow as depicted on both color flow and spectral waveform. This can

Chapter 39 Image Optimization in Ultrasound

unrelated to blood flow which one must be aware of to avoid misinterpreting the artifact as true flow.7-12

Anatomically Related Artifacts Mirror-image artifacts As already discussed in the section on grayscale imaging, reflection of ultrasound by an interface between zones of high and low acoustic impedance produces an image of an object on both sides, although it is located only on one side. A similar artifact can occur with color Doppler imaging most often in the supraclavicular region where mirror images of the subclavian artery or vein are caused by reflection from the pleura/lung causing apparent duplication of the vessel with the phantom vessel being projected deeper in the image. Carotid and brachial arteries may also show mirror images. Changing the scanning angle will cause the mirror artifact to disappear.

Artifacts Unrelated to Blood Flow Pseudo flow Pseudo-flow artifact is related to motion of fluid rather than blood flow within a vessel. The signal will appear as long as fluid motion continues. Pseudo flow may be caused by motion of ascites, amniotic fluid and urine from the ureteric orifice. It can mimic real blood flow on color or power Doppler. Spectral analysis reveals the presence of a Doppler signal but that which is atypical for a normal vessel. Some pseudoflow artifacts, such as those seen at ureteral orifice are useful to identify the ureteric orifice and can be useful to exclude complete obstruction. Twinkling artifact This occurs behind a strongly reflecting granular interfaces such as urinary tract stones or parenchymal calcification.

A

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Although primarily seen posterior to urinary calculi and parenchymal calcification it can also be seen behind any irregular highly reflective surface, biliary calculi, gallbladder adenomyosis and cholestrolosis Twinkling artifact is believed to be caused by a narrow band of intrinsic machine noise called phase (or clock) jitter. On a flat surface, system noise generates a narrow band of Doppler shift as a result of tiny clock errors. This is generally excluded by wall filters and not displayed. Rough surfaces increase the delays in measuring the signal and amplify the errors which increases the spectral bandwidth of this noise above the level of wall filter. It is seen as rapidly fluctuating mixture of Doppler signals, i.e. red and blue pixels which imitate turbulent flow. On spectral Doppler analysis the tracing is absolutely flat suggestive of noise. The artifact is dependent on the color write priority and grayscale gain. As the color write priority decreases the twinkling artifact decreases. The key to the identification of twinkling artifact is that color is produced behind the calcification and concomitant Doppler spectral trace shows noise thus a calcified carotid plaque with twinkling can be differentiated from a potentially ulcerated plaque with flow in ulcer cavities. Also increasing the velocity scale eliminates flow signal but not twinkling (Figs 20A to C). It is important to recognize this signal as artifactual in the gallbladder because it may simulate high velocity blood flow within a gallbladder mass suggesting the diagnosis of gallbladder carcinoma. On the other hand, the presence of twinkling artifact can be very useful for diagnosis of small stones that do not generate a strong echo. However, twinkling is not invariable. Authors suggest that calcium oxalate dihydrate and calcium phosphate calculi always produce twinkling artifact while calcium oxalate monohydrate and urate stones may lack a twinkling artifact.

C

Figs 20A to C: (C) The gray-scale image shows a large renal calculus with distal acoustic shadowing; (B) On application of color a mosaic of color is seen behind the calculus due to the twinkling artifact. Note the presence of flow in the intrarenal vessels as well; (C) On increasing the velocity scale the intrarenal flow disappears but the twinkling artifact persists

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Edge artifact This is related to strong specular reflectors and is seen as steady color along the rim of calcified structures such as gallstones or cortical bone. It is more commonly seen with power Doppler than color Doppler. The spectral Doppler tracing is characteristic being a straight line pattern equal above and below the baseline representing noise not true flow (Figs 21A and B). Flash artifact Flash artifact is a sudden burst of random color that fills the frame obscuring the grayscale image. It can be caused by tissue motion or transducer motion. It is most commonly seen in hypoechoic areas, such as cysts or fluids collection and in the left lobe of liver (due to cardiac pulsation). Power Doppler is more susceptible to flash artifact than color-flow Doppler because of the longer time required to build the image as more frames are averaged to create a power Doppler image than with standard color Doppler. Flash artifact occurs due to a system setting that suppresses color pixels which would otherwise overwrite grayscale echoes or the color write priority. In the absence of grayscale echoes, color pixels take priority so that flow is seen in nearly stationary fluid. The artifact is transitory coinciding with transducer or patient motion such as respiration or cardiac pulsation and hence can be easily interpreted. In fact the flash artifact may at times be used to denote fluid nature of solid appearing material.

Perivascular or Color-bruit Artifact This is a tissue motion artifact in which movement is generated within an organ rather than involving an entire organ or image. It is seen as a color mosaic in soft tissue (rather than a single homogeneous color) adjacent to vessels with turbulent

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flow and is thought to be caused by actual vascular tissue vibration. These artifacts are more common with low PRF as a result of increased sensitivity of the system but may also be caused by low wall filter setting. This artifact is the imaging equivalent of an auditory bruit or palpable thrill. It varies with the cardiac cycle being most prominent in systole and least in diastole. It is commonly seen in association with anastamotic sites, stenotic arteries or arteriovenous fistulae and can be useful to detect their presence.

SPECIAL IMAGING MODES1-3,10,13-16 The modern imaging systems incorporate a number of special imaging modes involving advances in beamforming, ultrasound signal acquisition, and postprocessing to deal with inherent artifacts in ultrasound and improve image quality.

Tissue-harmonic Imaging Difference in propagation velocity of ultrasound between tissues such as fat and other soft tissues, near the transducer results in phase aberrations that distort the ultrasound field producing noise and clutter. In addition, the focusing of the ultrasound beam depends on phase coherence of the sound waves at the focal zone and at the transducer surface during receive focusing. If the intervening tissue has heterogeneous velocities defocusing will occur because the waves no longer coincide precisely, degrading lateral resolution. Tissue harmonic imaging provides a means to reduce the effects of phase aberrations. The term harmonic refers to frequencies that are integral multiples of true frequency of the transmitted pulse which is called the fundamental frequency or first harmonic. The second harmonic has a frequency twice the fundamental.

B

Figs 21A and B: (A) Edge artifact: Power Doppler image showing steady color along the rim of a gallbladder calculus; (B) The spectral trace is characteristic of noise being a straight-line pattern above and below the baseline

Chapter 39 Image Optimization in Ultrasound

Harmonics are generated due to the non-linear propagation of sound waves in the tissues. The wave velocity is higher for high pressure waves, i.e. compression than low pressure component, i.e. rarefaction. This causes increasing distortion of the ultrasound pulse as it travels through the tissue changing the wave pattern from a perfect sinusoidal shape to a sharper saw tooth shape. This generates waves of higher frequencies which are multiple of the fundamental frequency (2nd, 3rd, 4th, etc.) which are referred to as harmonics (Fig. 22). The intensity decreases as the order of the harmonics increases. In addition, the higher-frequency harmonics are also attenuated more. Hence, current harmonic imaging is mostly performed using the second harmonic component (Work is in progress in order to utilize higher-order harmonics or the so called superharmonic imaging and frequencies lower than the transmitted frequency or subharmonic imaging for use with ultrasound contrast media). The final image is formed by the harmonic frequency bandwidth in the received signal after eliminating the transmitted frequency by frequency filtering, pulse inversion/phase cancellation or coded harmonics. The generation of harmonics requires interaction of transmitted pulse with the propagating tissues; hence, harmonic generation is not important near the transducer or

skin surface and becomes important only some distance away from the transducer. Harmonic images therefore show good rejection of artifacts and clutter arising from the body wall and also reduce the defocusing effect of the body wall. Artifacts are also reduced in harmonic imaging as the amplitude of the harmonic waves is relatively small reducing detection of echoes from multiple scatters. In addition artifacts produced by the fundamental frequency and side lobes do not have sufficient energy to generate harmonic frequencies and are therefore filtered out during image formation. Penetration can be improved by using a low-fundamental transmitted pulse and imaging at the higher-harmonic frequency. Other advantages include improved axial resolution due to shorter wavelength and better lateral resolution due to improved focusing with higher frequencies. Also because harmonics originate in regions of the ultrasound pulse with the greatest pressure amplitude, i.e. near the pulse center (as the amplitude at the periphery is too weak to generate harmonics) it results in a narrower beam producing images with superior lateral and elevational resolution. Harmonic images thus show less haze, noise, clutter and better cyst clearance (Figs 23A and B). The technique is most useful in patients with thick complicated body wall structure or the so-called difficult patients for mid field imaging. At greater depths harmonic signals begin to decrease substantially relative to fundamental signal due to increased attenuation.

COMPOUND IMAGING Fig. 22: Generation of harmonics: As the path length through the tissue increases the sinusoidal waveform (A). Changes to a more saw tooth pattern with higher frequency due to the compression wave traveling faster than the rarefaction wave (D)

A

Compound imaging is the ability to aquire multiple frames from different frequencies, i.e. frequency-compound imaging or from different angles, i.e. spatial-compound imaging. Frequency compounding is the combination of multiple images detected from different frequency bands

B

Figs 23A and B: (A) A transverse scan of the liver in a relatively obese patient with a large-right-lobe abscess. Although the abscess is visualized in the image without harmonics; (B) The margins of the abscess, its internal echopattern and the diaphragm are much better appreciated in the harmonic-imaging mode

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into a single image. This reduces noise and speckle as the appearance of speckle varies with frequency. This is possible with the use of broad band width transducers.

Spatial-compound Imaging In spatial-compound imaging electronic steering of ultrasound beams from an array transducer is used to image the same tissue multiple times by using parallel beams oriented in different directions. Data from many such beam lines is acquired and averaged together into a single image. The appearance of speckle varies according to the beam line direction, averaging echoes from different directions tends to average and smooth speckle making the images look less grainy. Since speckle noise is random it cancels out during compounding while signal is reinforced. Spatial compounding is also useful to image specular reflectors. Relatively large smooth surfaces reflect sound like a mirror with angle of incidence being equal to angle of reflection. Such specular reflectors include diaphragm, wall of urinary bladder, endometrial stripe, etc. Since the ultrasound beam is not dispersed like scatters, the signals are much stronger but are highly directional. Display of specular interfaces is therefore highly dependent on angle of insonation and specular reflectors return echoes to the transducer only if the sound beam is perpendicular to the interface. As the surface is titled away from 90° the signal intensity falls rapidly (as the sound beam is reflected away from the transducer). This results in poor margin definition and less distinct boundaries for cysts and other masses in conventional imaging where each scan line used to generate the image. It is of particular importance in sonography of the musculoskeletal system because of the anisotropic nature of muscles and tendons. The fibrillar pattern of a tendon is best appreciated when the ultrasound beam is perpendicular to the tendon and appears relatively echo-poor at oblique

A

angles simulating tears or tendinosis. In spatial compound imaging since the image is generated from more than one angle of insonation the chances that at at least one of these is perpendicular to the specular reflector is greater, reducing anisotropic effects improving tissue plane definition and display of curved structures. Spatial-compound images show reduced levels of speckle, noise, clutter and refractive shadows and improve contrast and margin definition. Enhancement and shadowing artifacts may be reduced which may be an advantage or potential drawback depending on the clinical situation (Figs 24A and B). Another drawback is that because multiple US beams are used to image one tissue region instead of just one beam as in conventional B-mode imaging more time is required for data acquisition and processing so the compound frame rate is reduced compared to conventional B-mode imaging depending on the processing capabilities of the imaging system. Spatial compounding can also be achieved by using a single transmit pulse and varying the crystals that receive. This typically maintains higher frame rates as less transmit pulses are used.

Coded-pulse Excitation Higher frequency US pulses produce images with better spatial resolution, however, increased attenuation with increasing frequency limits evaluation of deep structures with high frequencies. Coded-pulse excitation is a means of overcoming this limitation providing good penetration at higher frequencies necessary for high-spatial resolution. This technique uses longer ultrasound pulses instead of the routinely used short ultrasound pulses. These longer pulses carry greater ultrasound energy, which increases the energy of echoes that return from the deeper tissues allowing use

B

Figs 24A and B: Fibroadenoma of the breast imaged without (A) and with spatial-compound imaging (B). The margins of the lesion, internal architecture and calcifications are better visualized. Note the reduced edge shadows

Chapter 39 Image Optimization in Ultrasound

Fig. 25: (A) Normal pulse; (B) A chirp pulse; (C) A coded pulse

of higher frequencies. The coded pulses are produced with a very characteristic shape and the returning echoes also have a similar shape, which makes their identification from background noise easier (Fig. 25). The returning echoes are then processed using a pulse-compression technique in which the location of the long characteristic pulse shapes are identified. These pulse shape locations may be determined with a tight-spatial tolerance and correspond to the location of structures from where they are reflected. Hence, the location of reflectors is identified with good spatial resolution. This produces an image with good echo signal and good spatial resolution at greater depths.

Adaptive-image Processing An adaptive-image processing algorithm is one that able to recognize the difference between real targets and artifacts, and to modify its processing accordingly. Multiresolution adaptive image processing algorithms to smooth speckle and enhance structural edges are now available (e.g. XRES Philips). It involves an analysis phase (in which artifacts and targets are identified) and an enhancement phase (in which artifacts are suppressed and targets enhanced). The analysis phase takes into account multiple characteristics of the target, such as local statistical properties, textural and structural properties. The textural and structural information in particular is vital for identifying the strength and orientation of interfaces and thus allowing directional filtering of these targets in the enhancement phase. For example, smoothing is applied along an interface to improve continuity, while edge enhancement is applied in the perpendicular direction. In regions identified by the analysis phase as being homogeneous, smoothing is applied equally in all directions.

Photopic-ultrasound Imaging This technique can be use to optimize image contrast. Gray levels are converted to monochromatic color value, allowing very subtle structural differences to be appreciated.

Extended Field of View Imaging Early static B-mode scanners had a large field of view (FOV) which was lost with the introduction of real-time scanning.

Extended-FOV imaging restores the capability of visualizing large anatomic regions in a single image. The transducer is translated across the region of interest, during which multiple images are acquired from multiple transducer positions. Image features in regions of overlap between successive images are used to determine the exact position of the multiple images relative to each other by the scanner. The images are thus registered with respect to each other accounting for both translation and in plane rotation of the transducer. The registered image data is processed in a large image buffer and combined to form the large FOV image. It is a useful image presentation format

B-Mode Flow Imaging B-mode flow imaging is a new method for flow imaging available in ultrasound. This technique shows blood flow with grayscale or B-mode imaging and is not a Doppler method. For B flow imaging digitally encoded wide band pulses are transmitted and reflected from moving blood cells. The returning echoes are decoded and filtered to increase sensitivity of moving scatterers and distinguish blood from tissue. Both the surrounding stationary tissue and flowing blood are shown in shades of gray. As this is not a Doppler technique no velocity or frequency information is provided. It is a purely visual nonquantitative method. The major advantage is that it allows precise definition of the boundary between flowing blood and vessel wall. There is no problem of blooming or over amplification of flow signals as this is a non-Doppler technique. The technique does not degrade the spatial or temporal resolution of the grayscale image unlike color Doppler and is more accurate in showing the extent of plaque and surface irregularity of the plaque as compared to color Doppler or grayscale imaging alone in superficial vessels. The technique is, however, most useful in superficial vessels as it relies on amplification of very weak echoes from red blood cells.

3D–4D Ultrasound Although 3D–4D technology has been available in ultrasound for years it is mainly used in cardiology, obstetrics and gynecology. Uses in other areas are being gradually explored. Among the primary approaches used for 3D data acquisition are the free hand scanning, mechanical devices integrated into the transducer and matrix array technology. The 4D refers to real-time acquisition of 3D data set. Volume data is generally displayed using three primary methods, multiplanar images (3 slices orthogonal to each other) and rendered images that show entire structures throughout volume. The 3D/4D ultrasound, provides the ability to acquire the entire volume at one time so that there is no risk of missing

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out details which were not included in the original scan. Organ volumes, especially of irregularly shaped organs may be more accurately measured using volume data, 3D data results in more reproducible measurements can thereby assist in monitoring therapy and allow better definition of fetal facial features, uterine congenital anomalies, etc.

CONCLUSION With increasing technological advances, applications of ultrasound and Doppler have grown tremendously both for detection of pathology and physiology. Gaining maximum benefit from this complex technology requires a combination of skills, including knowledge of physical principles that empower ultrasound with its unique diagnostic unique capabilities. With this information the radiologist can gather maximum information from each examination while avoiding pitfalls and errors in diagnosis that may result from omission of information or misinterpretation of artifacts. Careful attention to technical parameters, appropriate use of special imaging features and diligence of examination technique will avoid day-to-day scanning pitfalls and result in studies with improved diagnostic accuracy.

REFERENCES 1. Hangiandreou NJ. B-mode US: basic concepts and new technology. Radiographics. 2003;23(4):1019-33. Review. 2. Merrit Christopher RB. Physics of ultrasound in Diagnostic ultrasound vol 1, 3rd edn. Rheumack Wilson SR Charboneau JW (Eds). Elsevier. 2005.pp.3-34. 3. Cosgrove D. Artefacts in B mode imaging in Abdominal and general ultrasound vol 1, 2nd edn. Meire H, Cosgrove D, Dewbury K, Farrant P (Eds). Churchill Livingstone; 2001.pp. 47-65. 4. Rubens DJ, Bhatt S, Nedelka S, Cullinan J. Doppler artifacts and pitfalls. Radiol Clin North Am. 2006;44(6):805-35.

5. Farina Robrterto Saparano Amelia. Errors in ultrasonography in Errors in Radiology. Luigia Romano Antonio Pinto (Eds). Springer Verlag. 2012.pp.76-85. 6. Feldman MK, Katyal S, Blackwood MS. US artifacts. Radiographics. 2009;29(4):1179-89. 7. Acampara Ciro, Fabia Pinto, Magistris Giuseppe De Errors in color Doppler ultrasonography in Errors in Radiology. Springer Verlag; 2012.pp.86-103. 8. Tahmasebpour HR, Buckley AR, Cooperberg PL, Fix CH. Sono graphic examination of the carotid arteries. Radiographics. 2005;25(6):1561-75. 9. Kruskal JB, Newman PA, Sammons LG, Kane RA. Optimizing Doppler and color flow US: application to hepatic sonography. Radiographics. 2004;24(3):657-75. 10. Zagzebski James A. Physics in Doppler and B-mode ultrasound in Introduction to vascular sonography, 6th edn. Pellirito, Polak (Eds). Elsevier; 2012.pp.20-51. 11. Campbell SC, Cullinan JA, Rubens DJ. Slow flow or no flow? Color and power Doppler US pitfalls in the abdomen and pelvis. Radiographics. 2004;24(2):497-506. 12. Rahmouni A, Bargoin R, Herment A, Bargoin N, Vasile N. Color Doppler twinkling artifact in hyperechoic regions. Radiology. 1996;199(1):269-71. 13. Choudhry S, Gorman B, Charboneau JW, Tradup DJ, Beck RJ, Kofler JM, Groth DS. Comparison of tissue harmonic imaging with conventional US in abdominal disease. Radiographics. 2000;20(4):1127-35. 14. Rosenthal SJ, Jones PH, Wetzel LH. Phase inversion tissue harmonic sonographic imaging: a clinical utility study. AJR Am J Roentgenol. 2001;176(6):1393-8. 15. Desser TS, Jeffrey RB. Tissue harmonic imaging techniques: physical principles and clinical applications. Semin Ultrasound CT MR. 2001;22(1):1-10. 16. Lin DC, Nazarian LN, O’Kane PL, McShane JM, Parker L, Merritt CR. Advantages of real-time spatial compound sonography of the musculoskeletal system versus conventional sonography. AJR Am J Roentgenol. 2002;179(6):1629-31.

Ultrasound Elastography: Principles and Application

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Veenu Singla, Tulika Singh, Anindita Sinha

INTRODUCTION Elastography is a noninvasive technique of imaging stiffness or elasticity of tissues by measuring movement or deformation of tissue in response to a small applied pressure. It is a method of “virtual palpation” of tissue or lesions, which has the potential to overcome the subjectivity associated with clinical palpation. It can also provide objective and quantitative measures of tissue stiffness.

BASIC PHYSICS Some common terminologies like stress, strain, shear, elasticity, viscoelasticity and Hooke’s law and Young’s modulus are often used and a basic understanding of these is required to understand elastography.

Stress Stress is defined as force per unit area. Unit of stress is Pascal or pounds per square inch (psi) (Pascal = Newton/m2). Stress can be due to compression, which acts perpendicular to a surface and causes shortening of an object. Shear stress acts parallel to a surface and causes deformation. In elastography, stress can be applied exogenously by transducer compression, vibrators or acoustic radiation force. Endogenous motion of vessels, cardiac or respiratory motion can also be utilized. Although endogenous sources overcome the shortcomings of exogenous source like attenuation (e.g. due to obesity or ascities), endogenous stress is difficult to quantify.1

Strain When subjected to stress an object tends to undergo deformation of its original size and shape; the amount of deformation is known as strain. Longitudinal strain, like compression causes change in length of an object. Shear strain causes changes in angles of an object.

Strain is unitless, expressed as change in length per unit length of the object. So hard objects have lower strain values than softer objects. When compression is applied, lesions nearer the applied force undergo more displacement than objects lying in a deeper plane. This is similar to clinical difficulty in palpating deep seated lesions and is one of the factors which may influence efficacy of elastography.

Elasticity The property of materials to return back to its original form after stress is removed, is known as elasticity. Elastic materials strain immediately when stressed and also return quickly back to their original position.

Viscosity Viscosity is the measure of resistance of a fluid when it undergoes shear stress or tensile (compression or stretching) stress.

Viscoelasticity This is the property of materials to exhibit both viscous and elastic properties. In viscoelastic material like soft tissue, there is a time delay between application of force and displacement. When stress is applied, the strain increases rapidly as free fluid in soft tissues is exuded. Then, the relationship of stress over strain becomes linear for small changes.

Poroelasticity A material in which a solid matrix is permeated by an interconnecting network of fluid filled pores. Tissue may be viscoelastic, poroelastic, anisotropic (e.g. muscle fibers or nerve fibers oriented in a particular direction) or contractile or a combination of these and disease conditions may modify their character. Elastography techniques which can estimate visco/ poroelasticity, give a more accurate estimate of tissue

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conditions than techniques where simple stress, strain or Young’s modulus is measured, as here tissue is assumed to be a homogeneous and isotropic material. Hooke’s law states that stress is proportional to the strain within an object’s elastic limit. Young’s modulus (E) is the ratio of stress over strain and has the same unit as stress. Young’s modulus measures the tissue’s resistance to compression. Hooke’s law holds true for homogeneous isotropic solids. Softer tissues like fat undergo more deformation (strain) when stress (e.g. compression during palpation) is applied. Harder tissues like muscle and fibrous tissue resist strain and thus have a higher Young’s modulus.2-4 Poisson’s ratio: When exposed to stress, tissue may contract in one dimension (like width) while its length increases. Poisson’s ratio = lateral contraction per unit breadth/ longitudinal extension per unit length.5 Poisson’s ratio for normal soft tissue is 0.5. Shear modulus: Shear modulus or modulus of rigidity (G) is the ratio between shear stress and shear strain. Elasticity imaging can be based on imaging either strain, stress or Young’s modulus, shear modulus or shear wave velocity imaging.

DEPICTION OF ELASTOGRAMS Elastograms are generally viewed simultaneously with a sonogram to identify area of abnormality. This can be done with either grayscale depiction or a semitransparent color overlay of the elastogram over the sonogram. On grayscale elastograms, stiffer lesions are darker and appear to increase in size when compared to sonograms. On color overlay images, blue and green depicts stiff areas and red to yellow denotes soft areas.

DIFFERENT ELASTOGRAPHY TECHNIQUES

compression. 6 Compression causes deformation of the tissue that varies as a function of the elastic coefficient. This principle is expressed by Young’s modulus of elasticity.7 RF waveform before and after compression are windowed and the signals in the same segment are compared to calculate the displacement. Around 97% of transmitted ultrasound waves are absorbed, only 3% of energy is scattered. Scattering occurs at the tissue boundaries, especially collagenous and fat surfaces. Tracking of displacement of this scatter in real-time is the objective of strain imaging.8 A simple approach to extract elasticity information from soft tissue involves acquiring maps of the tissues before and after the compression (Fig. 1). Radiofrequency echo signals are typically the “map of tissue” used and tiny motion induces a change in the phase of radiofrequency echoes that can be tracked.9 The amount of shift in the signal equals the amount of tissue displacement at the point in the image frame. This rate of change values is known as strain. Specialized software is used to calculate the relative difference in the tissue movement from one frame to another and then to estimate the tissue deformation.10 Three methods have been introduced for measuring tissue strain at elastography are spatial correlation method, phase shift tracking method and combined autocorrelation method. The spatial correlation method is 2D pattern matching algorithm to search for the position that maximizes the cross correlation between ROIs selected from two images. The phase shift tracking method is based on autocorrelation method and can be used rapidly and precisely to determine longitudinal tissue motion because of phase domain processing. This method fails when used for large displacement and it poorly compensates for lateral movement known as lateral slip.11 To overcome this problem, a method known as combined autocorrelation method is employed, which enables rapid and accurate detection of longitudinal displacement by using phase domain processing without aliasing.12 Clinical implementation typically involves freehand scanning, which

Elastographic techniques vary depending upon: zz The method used for tissue excitement (either mechanical or ultrasonic force) zz By the response of tissue to compression, i.e. static or quasistatic, where a single compression is applied or dynamic system in which response to rapid compression or vibration is measured.

Compression Elastography Compression elastography is calculating a strain profile in a direction perpendicular to the tissue surface in response to an externally applied force. This technique is most widely used in different ultrasound systems to evaluate the elastic properties of the tissues by analyzing the radiofrequency pulses generated by a structure in response to external

Fig. 1:  The windowed segment of scattered RF waveform is crosscorrelated with the waveform obtained pre- and postcompression. The amount of shift between the matching segments is equal to tissue displacement (d)

Chapter 40 Ultrasound Elastography: Principles and Application

requires real-time implementation for instant feedback to the user to control the direction of deformation.13 Hard or stiff materials tend to move as a whole with all points displacing with the same amount on compression, which results in zero or small rate of change of displacement called as zero or no strain. Softer tissue shows larger change in rate of displacement versus depth giving large strain values. The deformation measurement is mapped on elastogram on which stiffer areas are depicted as dark and elastic area lighter. This actually allows the differentiation of the lesion, which otherwise isoechoic on grayscale ultrasound image.10 Free hand scanning is usually induced at a rate resulting in nearly completely elastic deformation making interpretation much easier than it otherwise. The most common clinical application is breast imaging. But any organ which can be clinically palpated has been scanned for elastography including breast, prostate, thyroid muscle and lymph node.

Limitations The amount of tissue displacement and the rate of change in displacement vary with the amount of compression applied. Hence, the tissue strain is dependent on the amount of the compression applied and it does not quantify the intrinsic elastic property of the given tissue. This makes it operator dependent. It is a qualitative imaging of relative stiffness, so the actual strain value cannot be compared with the next imaging.6 However, it can be used as semiquantitative elastography with evaluation of strain ratio, which is the ratio of strain between the lesion and adjoining normal tissue. Because it shows only changes in strain from one area to other in the same image, hence it is suitable for the detection and evaluation of the small focal lesion and not sensitive to the diffuse disease process that produces same stiffness all over in one image.

however, they are much longer in duration (200 cycles vs 10 cycles).

Measurement Ultrasound pulses track these displacements by locating change in the peak along multiple tracking lines. The excitation can be performed in a sequential fashion by translating the tracking line along the tissue to assess the response. Parallel acquisition of push pulses and tracking displacements can also be done. Peak displacement, time taken to reach peak displacement and recovery time are utilized to characterize tissue response. Tissue recoil also generates shear waves, which propagate away from the focal point of excitation. The speed of the shear waves is proportional to the tissue stiffness. Shear modulus can be calculated from the shear wave velocity (Fig. 2). Mapping shear-wave velocity (cm/sec or m/sec) at multiple lateral points from the region of excitation can generate quantitative measurements of tissue stiffness.

Quantitative versus Qualitative In lesion identification and monitoring ablation procedures, higher spatial resolution qualitative images are required. Quantitative analysis is required for diffuse stiffening associated with advanced liver fibrosis, differentiation of malignant and benign lesions based upon their absolute stiffness, and monitoring of disease progression and response to therapy.

Advantages The ARFI images are found to be more homogeneous and have better contrast than surface displacement (compression)

Acoustic Radiation Force Impulse Principle and Technique Acoustic radiation force impulse (ARFI) imaging is a technique where short duration acoustic forces known as pushing pulses are used to cause tissue displacements. No external or physiological (pulsation or respiration) compression is needed. The cessation of force causes tissue to return to its original position. Pushing pulses can be applied by the ultrasound transducer array (frequency of 2–7 MHz) to a volume of 2 mm3 for 1 ms per pulse resulting in a displacement of 10–20 m. Pushing frequency is in the lower end of the transducer bandwidth, and the transmit voltage is at the upper end of the system capability. The pushing pulses are similar to those for power Doppler imaging;

Fig. 2:  Schematic diagram for shear wave sonography. Longitudinal

acoustic pulse transmission causes tissue displacement. Shear waves propagate away perpendicular to transmitted pulse. Separate tracking pulses in the region of interest (ROI) track these shear waves. The stiffer the tissue, faster the shear-wave velocity

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elastography. Deeper tissue, not accessible by superficial external compression elastography can be evaluated.

Disadvantages Physiological (respiration, pulsation) and transducer motion can degrade image quality as 1–3 ms is required per tracking line pair. Lower ultrasound frequencies and motion compensation techniques like premonitory physiological motion and subtracting this expected motion have been applied to overcome these limitations.5,14 Tissues at a depth of more than 10 cm cannot be accurately assessed due to attenuation of the radiation force at greater depths.

Safety Peak temperature increase for one pushing pulse from a single excitation is largest near the focal point. The typical temperature rise associated with an individual excitation ranges from 0.02°C to 0.2°C, varying primarily as a function of transmit frequency and pulse duration. The duration of pushing pulses and the frame rate is limited to keep within the standard diagnostic limits of mechanical and thermal index.15

Shear-wave Imaging Principle and Technique Shear waves are induced remotely within tissue when an impulsive acoustic radiation force of a focused ultrasound beam produced by the transducer interacts with tissue. Shear waves propagate perpendicular to the axial displacement caused by the ultrasound pulse and attenuate about 10,000 times more rapidly than compression waves.5 The high attenuation of shear waves enables mechanical oscillations to be induced within a very limited area of tissue. Deformations by the focused ultrasound radiation are generally very small (at submicron level). Sophisticated signal processing is required to detect such motion differences. A shear wave is created and tracked at lateral, spatially offset positions from the radiation force excitation by a parallel tracking method (Fig. 2).5,9

Measurement Velocity of shear waves (in cms–1) can be measured and used to evaluate tissue stiffness by calculating the elastic Young’s modulus according to the formula: E=3V2 (E-Young’s modulus in kPa, V-shear wave velocity in cms–1).

Qualitative versus Quantitative This technique results in both qualitative color coded elastogram and also quantitative maps either of elasticity (in kPa) or of shear-wave velocity (in cms–1).

Advantages Lack of tissue compression makes it a more objective measurement, the direct assessment of elasticity and the quantitative measurements are provided.

Disadvantages Assessment of superficial structures may be difficult, as a certain depth of ultrasound penetration is needed for shear waves to be produced.

Advances in Shear-wave Imaging 1. Spatially modulated ultrasound radiation force (SMURF): In this technique, a linear array transducer is used to acquire a reference scan at a specified position. Two pushing pulses are then transmitted and focused at the same depth laterally from the original position. This is followed by a series of scan lines, from which the induced shear-wave peaks are estimated. This allows fast and accurate estimation of shear modulus with improved resolution.16 2. Supersonic shear-wave imaging: In supersonic shearwave imaging, the focus of the radiation force from one location is changed to different depths (typically five) along the beam axis. Shear waves are created at multiple locations and these interfere constructively to create a conical shear wave front like a Mach cone of an aircraft traveling at supersonic speed. Imaging the shear-wave propagation requires an ultrafast scanner capable of 5000 frames per second. This is achieved by elimination of focusing of the pulses used for motion detection. One plane wave or a set of plane waves is transmitted with different angular direction to track the shear wave. B-mode data is also acquired in real time at about 50 frames per second. Measurement: Shear-wave propagation is measured and wave speeds are assessed to give viscoelastic moduli.17 3. Axial shear-strain imaging: Malignant lesions tend to be more tightly bound to surrounding tissue than benign lesions. Axial shear strain images as how tightly the lesion is fixed to the surrounding tissue. Loosely bound lesions have a thin band of color at the boundary whereas malignant lesions have a much thicker band. This simple depiction is much easier to interpret than elastography images.18

Chapter 40 Ultrasound Elastography: Principles and Application

Harmonic-motion Imaging Technique Low frequency ultrasound (10–300 Hz) produces oscillations in tissue, which is measured at the center of vibration. Two separate focused ultrasound transducers are used. One transducer has a very large aperture, which is used to generate the radiation force. A small phased array transducer placed through a hole in the larger transducer detects motion.

Application The same transducer, which generates the radiation force, can be utilized for creating thermal lesions. This allows real-time and simultaneous generation and monitoring of high-intensity focused ultrasound (HIFU) therapy. Tissue stiffening signifying successful ablation can be monitored and the treatment procedure can be performed in a timeefficient manner. Real-time monitoring of RF ablation of arrhythmogenic foci in the heart may help spare the surrounding healthy myocardium from ablation.19

Shear-dispersion Ultrasound Vibrometry Technique This involves creating a shear-wave by an external actuator or by acoustic radiation force. Multiple pushing pulses or excitation pulses are transmitted at a particular frequency and motion stimulated at harmonic frequencies is detected by ultrasound.

Measurement Shear-wave speed dispersion is measured from the data generated at several frequencies. Dispersion of shearwave gives a measurement of the viscoelastic properties of tissue.

Mechanical Imaging Stress patterns of internal structures of tissue are measured by compressing the tissue by an ultrasound probe. Pressure sensors mounted on the contact surface of the probe detects the temporal and spatial changes in stress pattern, thus providing information about the different elastic properties (viscosity and porosity).

Measurement Surface stress data is recorded, allowing 2D and 3D reconstruction of tissues on the basis of elasticity. Nonlinear

elasticity imaging which is most sensitive to cancerous changes can be evaluated by mechanical imaging.20

Application Detection of cancer and differentiating benign from malignant lesions.

ELASTOGRAPHY APPLICATIONS Breast As the breast cancer tissue is harder than the adjoining normal breast parenchyma, because of its desmoplastic reaction, the evaluation of breast masses to differentiate benign lesion from malignant was one of the initial application of the ultrasound elastography.21 Initially elastograms were done by using a computer controlled device, which needed precise control of amount of compression which is typically very small (0.1–0.5 mm). It was slow and very few elastogram could be taken. It also needs postprocessing. Over a period of time, hand held compression with the ultrasound transducer was substituted with more recently developed real-time processing.22 The evaluation of hardness has the same principle of conventional clinical examination, i.e., palpation of any breast lump. Initial clinical work in this field appeared in 1997 and showed that cancer generally appeared stiffer (darker) than benign lesion and surrounding normal breast tissue. 23 Cancerous lesions almost invariably appeared larger on elastography. Other authors demonstrate the use of color maps to depict the tissue stiffness.11 A proposed scoring system for the lesions on color maps is based upon elastographic properties of the tissue.

Elastosonographic Score (Fig. 3) Score 1: Presence of even strain in the lesion (green) Score 2: Prevalence of green with few, if any blue spots with inconstant locations Score 3: Prevalently green but with central blue area Score 4: Almost completely blue, with few green points, most of all in periphery.

Fig. 3:  Colored diagrams representing the general appearance of elasticity score breast nodule in Tsukuba scoring of 1(a), 2(b), 3(c), 4(d) and 5(e)

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Score 5: Completely blue, also with a peripheral glow around the nodule. For elastography score when cut-off point is taken between 3 and 4 for the malignant lesion, it showed 86.5% sensitivity, 89.8% specificity and 88.3% accuracy in one study.11 This gives information about local strain estimated at a given location in tissues, but it depends on surrounding mechanical properties and it is not quantitative (Figs 4 to 7).24 Recently, the methods of semiquantitative assessment of the breast lesions with strain ratio between the nodule and the adjoining normal breast tissue is used for the differentiation of benign versus malignant nodule have been developed.25 With freehand compression, the influence of probe movement has certain limitation as the elasticity map obtained is highly dependent on the organ’s compressibility limits under pressure and on the extent of tissue compression applied. This makes it operator dependent. To overcome this problem, the quantitative methods are developed with assessment of the shear module, which is overall tissue stiffness like shear wave elastography and supersonic shear imaging. It combines two concepts. Instead of using mechanical external compression, the system itself remotely induces mechanical vibration by using acoustic radiation force created by a focused ultrasound beam. The displacement induced at the

focus, generates a shear wave that conveys information linked to the local viscoelastic properties of the tissue, thus enabling a quantitative approach to elasticity values.26 The interpretation and measurement of elasticity is done in terms of the Young’s modulus (in kilo Pascal, kPa). It is reported that mean elasticity values are significantly higher in malignant masses (153.3 kPa ± 58.1) than in benign masses (46.1 kPa ± 42.9) (Fig. 8).27

Elastographic Appearances of the Breast Masses Simple cyst versus complex cyst Simple cyst is the most common type of breast lesion. It usually appears on conventional ultrasound as anechoic round or oval well-defined lesion with posterior acoustic enhancement, with imperceptible posterior wall. On elastography, it gives a target or bulls-eye appearance, with central bright area surrounded by a dark concentric rim. 28 Complex cyst with debris because of its internal contents can appear as a solid lesion on B-mode conventional ultrasound, and can be subjected to biopsy. Ultrasound elastography can help in revealing the cystic nature of the lesion with the typical target appearance. Fibroadenoma: Represent most common type of solid breast lesion. Ultrasound typically shows fibroadenoma as well-

Fig. 4:  Elastography image of fibroadenoma showing elastographic

score 2 with few small blue areas of no strain in the periphery. B-mode image shows well-defined ovoid hypoechoic nodule with posterior acoustic enhancement

Fig. 6:  Electrographic image IDC breast shows elastographic score 4

with complete lesion appearing blue with no strain. The picture also shows the strain ratio 4.4 between the lesion and the adjoining normal breast

Fig. 5:  Elastographic image of another fibroadenoma showing elastographic score 3 with more central blue areas of no strain

Fig. 7:  Elastographic image of IDC breast shows elatsographic score 5 with blue area of no strain in the lesion and in the peripheral echogenic halo

Chapter 40 Ultrasound Elastography: Principles and Application

Fig. 8:  Shear wave elastography image of malignant breast lesion showing red color in hard tissue with values above 130 kPa

circumscribed hypoechoic masses, which are wider than tall with long axis parallel to the chest wall. Sometimes, fibroadenoma can present as atypical shape like taller than wide. In such cases, sonoelastography can help elucidate the benign nature of the lesion. Usually, it appears smaller than B-mode images in contrast to the malignant lesion, which show larger size on elastography because of its desmoplastic reaction in surrounding tissue. In one study as many as 73% of fibroadenoma could be differentiated from malignant on the basis of elastographic size and brightness criteria. Other methods to differentiate are quantitative and semiquantitative like calculating the strain ratio or assessment of overall stiffness as discussed earlier. Fibroadenoma larger than 2 cm and with calcification can give false positive for malignancy on elastography.29 Invasive ductal carcinomas: It is the most common invasive tumor of the breast. On B-mode ultrasound it appears as a hypoechoic spiculated or microlobulated mass, which is taller than wide with angular margins and a hyperechoic halo.

On sonoelastography, invasive ductal carcinoma typically appears darker than normal tissue or benign lesion and it is slightly larger on the elastogram as compare to the B-mode ultrasound images. Overall, ultrasound elastography is reported to have a sensitivity of greater than 95% and specificity of about 85% for differentiation between benign and malignant lesion using different qualitative and quantitative methods.30 False negative elastogram can be seen in few well-defined benign looking masses, masses with tumor necrosis with acoustic enhancement can mimic cysts.

Liver Diffuse Liver Diseases: Fibrosis, Cirrhosis, Acute Hepatitis, Nonalcoholic Fatty Liver Disease In diffuse liver diseases, imaging modalities like B-mode ultrasound, CT and MRI have limited role in diagnosing liver fibrosis and early cirrhosis.

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On ultrasound, hyperechoic nodular liver may be present with both liver fibrosis as well as fatty liver. A normal CT or MRI cannot rule out cirrhosis. Liver biopsy has been the reference method for diagnosing liver inflammation and fibrosis. However, it is an invasive procedure with accompanying risk and even life threatening complications and also prone to sampling errors as only a small volume of the liver is sampled. Interobserver variability is also high. Elastography (by ultrasound or magnetic resonance) is a noninvasive modality for assessment of fibrosis and degree of fibrosis. It is painless, reproducible and repeatable and easy to perform, allowing monitoring of disease. Although MRI elastography is sensitive for evaluation of fibrosis, it has limited availability; is time consuming and costly and not suitable for screening patients for presence or degree of fibrosis.

Factors Influencing Liver Stiffness 1. Chronic liver parenchymal pathology may cause changes in liver stiffness by inducing fibrotic changes. On liver biopsy, fibrosis can be divided into four stages:31 Stage 0 (normal): No fibrosis around portal triads Stage 1(portal fibrosis): Fibrosis surrounds the portal triads, but is limited to these areas Stage 2 (periportal fibrosis): Fibers begin to extend into the periportal space, but do not connect with other portal triads

B

A

Stage 3 (septal fibrosis): Fibrous connective tissue links neighboring portal triads and begins to extend to the central veins. Shape of lobule is distorted Stage 4 (cirrhosis): Most portal triads are connected by fibrous tissue. Some portal triads and central veins are also connected. 2. Necro-inflammatory activity in the setting of acute hepatitis which causes hepatocyte swelling, edema and inflammatory infiltration may also increase liver stiffness. Patients with acute hepatitis (viral, autoimmune and druginduced) may have a discrepancy between the liver stiffness measurement (LSM) and the fibrosis grade by biopsy. Liver stiffness may be in the cirrhotic range (above 12.5 kPa) whereas fibrosis staging by biopsy is not more than stage 2. Similar increase in stiffness measurement is found in patients with chronic viral hepatitis who have acute exacerbations associated with rise in alanine amino transferase.32 3. Congestive cardiac failure and extrahepatic cholestasis or congestive heart failure. Light meals also alter elasto­ graphy values.33-35

Ultrasound Elastography Techniques for liver stiffness measurement Transient elastography-FibroscanTM apparatus (Echosens, Paris, France)—is a nonimaging modality which has been widely used for liver stiffness measurement (Figs 9A and B).

Figs 9A and B:  Image of the Fibroscan device

(Echosens, Paris) for transient elastography. (A) The probe has a piston (arrow), which is placed in the right intercostal space. A single low frequency vibration is generated and shear wave elasticity in a cylinder of 1 cm × 4 cm of hepatic tissue is measured (inset). Measurements of 10 successful acquisitions in a normal liver (B) with a success rate of at least 60%, and with Interquartile Range (IQR-median of the middle 50% of the values) 6 mm Hg). However, it is an invasive procedure. Patients with cirrhosis and gastroesophageal varices have an HVPG of at least 10–12 mm Hg. Variceal hemorrhage, ascites or encephalopathy may develop when HVPG increases over a threshold value of 10–12 mm Hg. Splenic elasticity has a close linear relationship with HVPG and can help predict the presence of esophageal varices in patients with chronic liver disease. Values of splenic stiffness above 8.7 kPa correlates with HPVG above 6 mm Hg and values above 17.6–23 kPa correlate with severe portal hypertension (HVPG > 12 mm Hg). Splenic stiffness measurements show better and linear correlation with degree of portal hypertension than liver stiffness measurements. Combination of the liver stiffness with spleen

Table 1:  Comparison of different elastography techniques for liver diseases Fibroscan (Transient elastography)

ARFI

Shear wave elastography

Imaging

Not possible

Yes

Yes

Assessment of focal lesions

Possible for large (>5 cm) and superficial lesions. Requires prior localization with B-mode imaging. No real-time image guidance

Yes

Yes Different areas within focal lesion can also be measured

Maximum depth of tissue for assessment

2.5–6.5 cm from skin

10 cm from skin

8 cm from skin

Maximum region of interest

1 cm × 5 cm

0.6 × 0.5 cm – 0.6 × 10 mm

Variable

Technique

Static–no images generated

Static images

Real-time 2D evaluation

Obesity

Difficult(better with XL probe)

Less difficult

Less difficult

Ascites

Difficult to impossible

Difficult assessment

Difficult assessment

Quantification

Yes

Possible

Yes

Range of values

Large

Small

Large

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diameter and platelet count, however, better correlates with degree of portal hypertension.41 Assessment of TIPSS Splenic stiffness also decreases significantly with a functional TIPSS, whereas liver stiffness measurements do not show significant changes.42 Assessment of liver transplant Repeated liver stiffness measurements (LSM) following transplant can discriminate between slow and rapid fibroses (fibrosis stage F2-F4 at 1-year). Liver transplant recipients with hepatitis C virus infection undergo rapid fibrosis within the first year. Serial measurements of elastography within the first year shows much higher LSM than non-HCV infected recipients (9.9, 9.5, 12.1 kPa vs 6.9, 7.5, 6.6 kPa).43 Assessment of nonalcoholic fatty liver disease Nonalcoholic fatty liver disease (NAFLD) is a range of liver disorders with hepatic steatosis without alcohol consumption, viral, or drug-related etiologies. Histologically, it can be a simple accumulation of triglyceride droplets in hepatocytes or may progress to cellular injury and inflammation with resultant fibrosis and even cirrhosis and HCC. Fibrosis and cirrhosis due to NAFLD can be detected by transient elastography or other routine elastographic techniques. A newer technique of controlled attenuation parameter (CAP) gives an estimate of the attenuation of ultrasound at 3.5 MHz and is expressed in decibel per meters (dB/m). CAP is evaluated using the same radiofrequency data and in the same region of interest that is used for transient elastography and is a nonimaging based modality which shows promise in assessing the degree of steatosis noninvasively.44 Advantages Elastography is a noninvasive, painless and repeatable procedure. zz It can evaluate a much larger liver volume than liver biopsy zz It can be used for initial assessment, monitoring as well as diagnosis of complications (portal hypertension, esophageal varices) zz It can help in biopsy planning from stiffest regions to reduce sampling error zz Tumor ablation monitoring is also possible real-time with this procedure. Limitations Parenchymal thickness of less than 4 cm under the probe, presence of ascites, severe obesity, and the absence of an intercostal space sufficiently wide for probe, limit the usage of elastography. Male sex, body mass index more than 30, metabolic syndrome and acute viral hepatitis are all known to cause increased liver stiffness.45

Focal Liver Lesions ARFI Malignant and benign liver lesions appeared stiffer compared with the surrounding liver parenchyma on ARFI in a study by Shuang–Ming T et al. There were statistical differences between malignant and benign liver lesions. The median value of malignant and benign liver lesions were 3.14 m/sec (average value 3.16 ± 0.80 m/sec, range 1.17–4.45 m/sec) and 1.35 m/sec (average value 1.47 ± 0.53 m/sec, range 0.74–3.26 m/sec). A cut-off value of 2.22 m/sec resulted in sensitivity, specificity, and accuracy for malignancy of 89.7%, 95.0%, and 92.2%, respectively.46 Compression ultrasonography Onur MR et al. evaluated benign and malignant focal hepatic lesions, such as hemangiomas, focal nodular hyperplasia (FNH), nodular regenerative hyperplasia, adenomas, hepatocellular carcinomas (HCC), metastases, and cholangiocarcinomas. The strain ratio of liver parenchyma was compared with that of the focal lesion to give the strain index value. Mean strain index values of malignant liver lesions were significantly higher than that of benign lesions [The mean strain index value of malignant liver lesions ± SD (2.82 ± 1.82) was significantly higher than that of benign liver lesions (1.45 ± 1.28)]. Stiffness of hemangiomas vary depending on the amount of fibrotic septa dividing the vascular spaces. Strain index as well as mean values of hemangiomas on ARFI (1.5-2.3 m/sec) are significantly low.47,48 Shear wave Shear wave values (in kPa) can distinguish between FNH and adenoma. The FNH have a radial pattern of elasticity whereas adenomas and hemangiomas are homogeneous. Scars from radiofrequency ablation or healed abscesses have the highest stiffness values among benign lesions. A significant difference was also found between HCCs and cholangiocarcinoma elasticity. Cholangiocarcinomas were the stiffest among malignant lesions (56.9 ± 25.6 kPa). The HCC stiffness depends on the underlying liver, with lesions in cirrhotic livers appearing softer than lesions in normal or mildly cirrhotic livers. Metastasis stiffness also is highly variable and depends on the primary source. Carcinoid metastases are stiffer than colorectal metastases.49

Prostate Prostate gland is one of the earliest organs for which elastography was proposed. Endorectal ultrasound continues to be most commonly used imaging modality for assessing the prostate. On B-mode ultrasound, most carcinoma prostate show varying echogenicity mostly being hypoechoic to few isoechoic or hyperechoic also. So the overall sensitivity is approximately 50%.50

Chapter 40 Ultrasound Elastography: Principles and Application

Real-time endorectal elastography shows the sensitivity 68% with accuracy of about 76%.51 Prostate cancers have a higher elastic modulus than that of surrounding normal prostate tissue.13 Eventually, the prostate cancer appears dark on elastogram more in the peripheral lesion. Sometimes, the malignant lesions which are very small or invisible on B-mode ultrasound images are prominent on elastogram as dark area of low strain (Fig. 10). Elastographic imaging of the prostate gland can be performed with manual compression strain imaging (twodimensional) or with external vibration with Doppler imaging, which permits two- and three-dimensional imaging. Vibration elastography generates tissue displacement through the use of an independent external vibration source. Relative displacement is measured by using a variant of Doppler imaging that depicts differential motion of tissue types. This technique provides good correlation for tissues that have a large difference in stiffness.52 Another role is for sonoelastographic guided prostate biopsies which increase the detection rate about three times than the routine endorectal ultrasound guided biopsies.53 Benign prostatic hyperplasia appears as heterogeneous hypoechoic area on endorectal B-mode ultrasound. Area with benign hyperplasia also show higher stiffness than that of normal prostate tissue but less than that of carcinoma prostate. However, it is difficult to differentiate between two and sometime it can give a false positive findings for the cancer prostate.52 In a recent study, the ARFI was implemented to image excised human prostate.53 The ARFI imaging is an elasticity imaging technique, which uses remotely generated, focused acoustic beam to excite tissue and generate the images of tissue displacement response.54 Various prostatic zonal structures and pathologies were demonstrated on ARFI imaging. The ARFI images are produced by evaluation of displacement within the ROE from multiple excitation and formation of an image from all location. The central zone (CZ), Ca prostate and atrophy show

smaller displacement than the normal tissue in transitional zone (TZ) and peripheral zone (PZ). The stiffness ratio of Ca prostate to normal tissue calculated to be 2.2 with their shear moduli for Ca prostate, CZ and atrophy are from 8 to 10 kPa and for PZ and TZ/BPH are 4–5 kPa, respectively.53 More recently ARFI imaging is used for human prostate in vivo. Carcinoma prostate appears as bilaterally asymmetric stiff structures; benign prostatic hyperplasia (BPH) appears heterogeneous with a nodular texture, and the boundary of the transitional zone (TZ) forms a stiff rim separating the TZ from the peripheral zone (PZ). Compared with the matched B-mode images, ARFI images, in general portray prostate structures with higher contrast. The ARFI imaging holds promise for guidance of targeted prostate needle biopsies and therapy.55

Lymph Nodes Elastography is also useful in differentiating reactive and metastatic axillary lymph nodes in carcinoma breast. As axillary lymph nodes status is the most important prognostic factor in carcinoma breast. The B-mode ultrasonography criteria for metastasis have based on the size, shape, hilum and the cortical thickening of lymph nodes.56,57 For elastography, axillary lymph nodes also given on elasticity scoring system on the basis of color coding. Score 1: Absent or very small blue area Score 2: Small, scattered blue area, total blue area less than 45% Score 3: Large blue area, total blue area more than 45% Score 4: Blue area with or without a green rim. Reported elasticity score of metastatic axillary lymph nodes (3.1 ± 0.7) is significantly higher than the score for reactive lymph nodes (2.2 ± 0.7; p < 0.001),58 when the cut-off was taken between 2 and 3, the sensitivity and specificity was approximately 80%. Similar kind of scoring done for cervical lymph nodes by Deng ke Teng et al. in which they found most benign lymph nodes showing elasticity score 1 or 2 and most of malignant node showing elasticity score 3 or 4 with sensitivity and specificity of 88.4% and 35.1%, respectively. They also calculated the strain ratio which showed strain ratio cut-off for malignant higher than 1.78 and for benign lower than 1.78 with sensitivity and specificity of 98.1% and 64.9%, respectively.59

Thyroid

Fig. 10:  Elastography image is showing hard nodule in the prostate in the right peripheral zone in blue color. Same nodule appeared hyperechoic on B-mode ultrasound image

Another area of potential usefulness is the evaluation of thyroid nodule because the ultrasound and nuclear medicine criteria for differentiating between benign versus malignant nodules are not reliable. A number of articles have shown the potential utility of nodular stiffness for characterizing it as malignant.60,61 Similar to the breast and other nodular

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lesion, the malignant thyroid nodule is stiffer than the benign thyroid nodules. Mainly semiquantitative methods with compression elastography using strain index is utilized. It is calculated by dividing nodule strain value by the strain of adjacent normal thyroid tissue. Good quality elastography of thyroid is challenging because of the shape of neck with sloping contour, which can cause lateral movement of thyroid and the pulsation from the adjoining carotid artery. Even with these technical difficulties as more and more results are reported, it can be used to help in deciding which nodule to be biopsied when many nodules are present.62 For the diffuse diseases of the thyroid quantitative or semiquantitative elastography is used. One study with shear wave velocity analysis shows increase stiffness in case of Hashimoto’s thyroiditis.63

Gynecology Cervical Elastography Labor assessment Cervical consistency and dilatation of internal os is assessed by palpation before induction of labor by prostaglandin or oxytocin. Cervical length measurement is done by ultrasound. Ripening of the internal os, which is not routinely evaluated during pregnancy by vaginal examination, can be assessed by transvaginal elastography. A soft internal os and harder external parts of the cervix are predictors of a favorable reaction to oxytocin during induction of labor. This can also help in deciding whether prostaglandins are required. Failed induction rates were higher in patients with increased stiffness of the internal os in a study by M Swiatkowska–Freund.64 Role Elastography may play a role in predicting delivery, and in detecting patients with a high risk of preterm delivery.

Cervical Cancer Transvaginal elastography has been evaluated for the diagnosis of cervical lesions. Malignant lesions are stiffer (blue on color coded maps), whereas benign lesions are of intermediate stiffness (green). Significant differences in strain ratios have been noted between benign (polyp/fibroid/erosion/inflammation) and malignant lesions (Strain ratio was obtained by dividing the mean strain within the lesion by the mean strain from the parametrial tissue). A cutoff value of strain ratio of 4.53 or higher has been suggested for confident diagnosis of malignancy. Elastography helps in the detection of endophytic cancers, which are more common in elderly women and are difficult to diagnose clinically or colposcopically. Depth of invasion

of stroma can also be accurately assessed by elastography, helping in staging.65 However, elastography is not helpful in the diagnosis of cervical intraepithelial neoplasia.66 Pitfalls Transvaginal elastography of the cervix lacks a proper reference tissue where comparison studies are possible. Infiltration of parametrial tissue by tumor would give rise to errors in strain ratio measurement as parametrial tissue is taken as reference. Normal cervix itself has heterogeneous elasticity. Moreover, the portion of the cervix nearest the transducer tip is prone to compression and even the mildest movement or pressure may result in erroneous impression of softening.67

Fibroids Fibroids are often dense and the posterior acoustic shadowing poses difficulty in correct assessment of size and extent on ultrasound. Fibroids appear harder and have well demarcated borders on elastography. Color coded images in elastography can help in better delineation of fibroids and also in characterizing changes associated with treatments like embolization.68

Fibroids vs Adenomyosis In adenomyosis and adenomyomas, which is often difficult to diagnose on B-mode ultrasound, elastographic color maps show a typical pattern of a soft lesion (green) with a central core which is even less stiffer (red). This pattern persists in both diffuse as well as focal varieties, though the margins are irregular in diffuse and well demarcated in the focal variety. Fibroids in comparison are stiffer and are depicted in blue on color maps.69

Endometrial Pathologies Color-coded elastographic images and elasticity indices (where stiffer tissues are given lower scores) have shown that normal or atrophic endometrium has significantly lower scores than endometrial hyperplasia, cancer or polyps.70

Musculoskeletal Compression ultrasonography has been the most commonly used technique for musculoskeletal applications. Strain of the region of interest is compared with the remaining tissue (usually fat) within the elastogram. The semiquantitative measurement method includes the ratio of the relative strains between the area of interest and a reference area. The ARFI and shear wave elasticity imaging are being increasingly used for musculoskeletal applications.

Chapter 40 Ultrasound Elastography: Principles and Application

Appearance of Normal Tendons Compression elastography In healthy volunteers, the normal Achilles tendons were found to have two distinct elastography patterns. They were either homogeneously hard structures or in the majority they had considerable inhomogeneity with soft areas (longitudinal bands or spots), which did not correspond to any changes in B-mode or Doppler ultrasound.71 Shear wave Shear wave elastography has also been used to measure mean elasticity values of muscles. For the gastrocnemius and masseter muscles, supraspinatus tendon, and Achilles tendon in both the longitudinal and transverse planes, shear wave elastographic values ranged from 11.1 ± 4.1 kPa (range 2–28 kPa), 10.4 ± 3.7 kPa (range 2–23 kPa), 31.2 ± 13 kPa (range 6–90 kPa), 74.4 ± 45.7 kPa (range 6–242 kPa), and 51.5 ± 25.1 kPa (range 10–111 kPa). The mean elasticity values for the muscles and tendons in the longitudinal plane were greater in men than in women, but the Achilles tendon in the transverse plane did not exhibit a significant difference between sexes. There was no significant correlation between age and elasticity for the muscles.72 Tendinopathy Symptomatic tendons were found in compression elastography to contain marked softening in 57%, mild softening in 11% and no soft areas (hard structures) in 32% of cases.73 The alterations in asymptomatic tendons were seen in the tendon mid-portion and were not always found to correspond to alterations in conventional ultrasound. Mild softening was not correlated with conventional ultrasound abnormalities, whereas marked softening was found mainly in cases with ultrasound evidence of disease. This could signify either a false positive finding or the increased sensitivity of elastography in early diagnosis. Another study has found increasing stiffness in diseased tendons, probably reflecting the stage of the disease, with fibrosis being the predominant component. 74 Increased stiffness of extensor tendon has been noted in lateral epicondylitis, with elastography being more sensitive than conventional ultrasound.75 Normal muscle Elastographic appearance of normal muscle needs further detailed investigation. Relaxed muscle gives an inhomogeneous appearance of intermediate or increased stiffness (green/ yellow or blue color, respectively) with scattered softer and harder areas especially at the periphery near boundaries.71 Exercise Elastography has also shown increase in muscle hardness (changes in strain ratio) immediately after exercise which lasted from 30 minutes to 4 days.76,77

Rheumatological disorders Soft tissue nodules: Elastography helps in differentiation of rheumatoid nodules and tophi; rheumatoid nodules were significantly less elastic than tophi and suggesting a possible role of this method for the investigation of soft tissue nodules.78 Synovitis: Inflammatory synovitis due to rheumatoid arth­ ritis was shown to be of intermediate stiffness, infectious synovitis (due to tuberculosis) was softer, whereas fatty villous proliferations (lipoma abrorescens) and pigmented villonodular synovitis were predominantly soft, as opposed to synovial sarcoma, which was hard.79 Skin: Elasticity of skin over the forearm in scleroderma patients have been evaluated with compression elastography leading to predominant blue areas (hard) as compared to green (intermediate) stiffness in controls.80 Soft tissue masses Data on the elastographic appearance of soft tissue masses with histological confirmation is limited. A study revealed lipoma and low flow vascular malformations and thyroglossal cysts to be soft due to fat/liquid content. Neurogenic tumors and dermoid/sebaceous cysts were stiffer. Stiffness of abscesses varied from soft to intermediate, probably due to varying liquid and solid components. Considerable overlap in elastography measurement was present. Elastography may be beneficial in cases of equivocal B-mode findings and for guiding aspiration or biopsy in abscesses or mixed solid/cystic lesions.81 Myofascial pain Elastography has also been utilized in identifying active trigger points in myofascial pain, which is a major cause of nonarticular pain with motor and sensory symptoms. Measurements have shown increased hardness in trigger points as compared to normal areas. This helps in objective classification instead of the subjective clinical assessment of nodular hard areas in involved muscles.82 Inflammatory/Dystrophic Conditions In inflammatory myositis, increased stiffness due to fibrosis and decrease in fatty infiltration has been documented using compression strain imaging. Elastography has shown correlation with serum markers in inflammatory myopathies and could help in disease monitoring.83 Elastography may also be more sensitive in detecting dystrophic changes in muscle stiffness earlier than ultrasound and MRI.84 In spasticity due to cerebral palsy, elastography has helped to establish site of botulinum toxin injection.85 Hyaline cartilage: Evaluation of elasticity of hyaline cartilage may help in evaluation prior to arthroscopy and in monitoring treatment.86

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Standardization Standardization is required, especially in musculoskeletal imaging. Differences in applied transducer pressure and ROI size can affect the elastic modulus even on shear wave imaging significantly. The larger the ROIs size, the higher the chance to include the muscle fascia, dense collagen fiber and bone. This leads to increase in the maximum value of elastic modulus, although mean values over large areas may remain the same. Increase in acquisition time may also lead to slippage of transducer from intended position. Elastography on muscle and tendon should be performed with the lightest transducer pressure and a shorter acquisition time.87 For the Achilles tendon, the suggested standard size for longitudinal scans is a depth of three times the tendon and about three-quarters of the screen, and for transverse scans the para-Tenon should be included.88 Role in musculoskeletal imaging Elastography may be utilized for early diagnosis, staging and monitoring inflammatory, degenerative, myopathic or dystrophic conditions. It may also have a role in guiding interventions. However, clinical utility and validity of ultrasound elastography in musculoskeletal applications is still to be established by further studies involving larger number of patients.

OTHER APPLICATIONS

Venous Thrombosis The use of elasticity imaging for evaluation of venous thrombosis has also been reported. 92 This application is important because new thrombi are at a higher risk for embolization than are older more fibrotic thrombi. Because the stiffness of a thrombus increases with increasing age,93 elasticity imaging may offer a way of gauging the age of thrombi, which can be difficult using grayscale sonography alone.

Skin and Soft Tissue Elastography can visualize components of skin and soft tissue abscesses, including the abscess cavity and surrounding induration. A percentage of patients who fail therapy will progress to more invasive infections, either by local spread, such as deeper tissue infection or via systemic spread, such as bacteremia. While B-mode sonography can help differentiate the contents of an abscess cavity from the surrounding tissue, sonoelastography by measuring tissue stiffness can visualize the indurated tissue surrounding the abscess cavity. Asymmetry of the inflammatory changes surrounding abscess cavities has been reported to be associated with a higher rate of failure after standard therapy.94 Also the size of the tissue indurations may predict progression to bacteremia or the time to resolution.95

Renal Transplant Assessment

Endoscopic Ultrasonography

Supersonic shear-wave imaging, transient elastography and strain imaging have been utilized to diagnose chronic allograft injury. It can be used to monitor allograft stiffness, so that patients with serial increase can be subjected to a biopsy before renal function deteriorates, instead of all patients undergoing routine protocol biopsies. It can also monitor effect of treatment. However, subclinical rejection, infection or recurrence of underlying disease cannot be detected.89

Endoscopic ultrasonography (EUS) is one of the most recent advances in gastrointestinal endoscopy. The EUS with real time tissue elastography can be more useful than EUS with only a B-mode imaging ability. Real-time EUS elastography can be performed with the conventional EUS probes without any need for additional equipment that induces vibration or pressure. Elastographic imaging of the normal pancreas is characterized by a uniform, homogeneous green color distribution (representing intermediate stiffness) throughout the organ. A green-predominant pattern, either homogeneous or heterogeneous, excludes malignancy with a high accuracy. On the contrary, a blue-predominant pattern, either homogeneous or heterogeneous, favors the diagnosis of malignant tumor. On quantitative analysis, a healthy pancreas shows a mean elasticity value of 0.55%. A strain ratio higher than 15.41 or a mass elasticity value below 0.03% is 100% specific for malignancy.96

Cardiovascular Applications The two major areas of cardiovascular applications are strain imaging of the myocardium and of atheromatous plaque and the arterial wall.90 Myocardial evaluation focuses on evaluation of localized areas of ischemia, infarction, and scarring. Arterial elasticity evaluation has focused on detection of vulnerable plaque and estimation of arterial wall compliance, as vulnerable plaques are known to be much softer than stable plaques. Elasticity estimation in these organs makes use of the normal movement of myocardium and vessel walls during the cardiac cycle rather than externally applied vibrations or pressure. Early work focused on intravascular ultrasound imaging of plaque,91 but that method is invasive, and much of the current work is focused on external methods of plaque stiffness imaging.

Limitations of EUS Elastography The main pitfall of EUS elastography is the inability to control tissue compression by the EUS transducer. Use of EUS elastography is also hampered by the induction of motion artifacts due to respiratory or heart movements, which cannot be adequately eliminated or quantified. The presence of

Chapter 40 Ultrasound Elastography: Principles and Application

nearby structures with very low or high density and stiffness, such as the heart, major vessels or spine are also difficult to be excluded from the ROI analyzed. Selection of the ROI has to carefully include surrounding soft tissues only, since the methodology of elastography assumes computations relative to the average strain inside the ROI. An intrinsic limitation of qualitative elastography is the subjective interpretation of the elastographic pattern that may be associated with significant intra-and interobserver variability.

Pitfalls Large lesions can be under assessed, with portions of the lesion lying out of the field of view. Moreover, painful lesions may be under-represented because of the increased discomfort related to elastography. Performing ultrasound elastography can be technically challenging in organs like the salivary glands in terms of achieving only longitudinal transducer compression, i.e. avoiding lateral or out-of beam movements, and achieving the correct amount of compression. In this respect, even slight nonaxial transducer movements detrimentally affect elastogram quality, observed as background noise, due to mistracking artifacts.

CONCLUSION In conclusion, elastography has emerged as a useful adjunct tool for ultrasound diagnosis. Elastograms are images of tissue stiffness and may be in color, grayscale, or a combination of the two. In a typical elastogram, low strain areas denoting a stiff or hard material are given darker gray values, whereas high strain areas denoting very soft tissues are given lighter gray values. The rapidly advancing field of tissue elasticity imaging and estimation has already produced several applications. The goal in breast elastography is not necessarily to diagnose cancers but to confidently classify questionable lesions on the sonogram as definitely benign. This will help reduce the number of biopsies of a benign lesion. Recent advances in elastography include quantification using strain ratios, ARFI and shear wave velocity estimation. These are useful not only for characterizing focal masses but also for diagnosing diffuse organ diseases, such as liver cirrhosis. Beyond breast mass evaluation, elastography is showing a greatest potential in the liver. Other promising applications include prostate cancer detection, atheromatous plaque and arterial wall evaluation, venous thrombus evaluation, graft rejection, and monitoring of tumor ablation therapy. Other modalities may be used for elasticity imaging, the most powerful being magnetic resonance elastography. Ultrasound, being less expensive and easier to use, will likely become the most widely used modality for clinical elasticity estimation and imaging.

REFERENCES 1. Mark L Palmeri, Kathryn R Nightingale. What challenges must be overcome before ultrasound elasticity imaging is ready for the clinic? Imaging Med. 2011;3:433-44. 2. Duck F. Physical properties of tissue, A Comprehensive Reference Book. NY; Academic Press:1990. 3. Sarvazyan A, Skovaroda AR, Emelianov SY, et al. Biophysical bases of elasticity imaging. Acoust Imaging. 1995;21:223-40. 4. Sarvazyan A. Handbook of Elastic Properties of Solids, Liquids and Gases. Elastic properties of soft tissue. 2001. pp.107-27. 5. Peter NT Wells, Hai-Dong Liang. Medical ultrasound: imaging of soft tissue strain and elasticity. J. R. Soc. Interface published online 16 June 2011 doi: 10.1098/rsif.2011.0054. 6. Garra BS. Imaging and estimation of tissue elasticity by ultrasound. Ultrasound Q. 2007;23:255-68. 7. Fehrenbach J. Influence of Poisson’s ratio on elastographic direct and inverse problems. Phys Med Biol. 2007;52:707-16. 8. Insana MF, Pellot-Barakat C, Sridhar M, Lindfors KK. Viscoelastic imaging of breast tumor microenvironment with ultrasound. J Mammary Gland Biol Neoplasia. 2004;9: 393-404. 9. Sarvazyan A, Timothy J Hall, Matthew W Urban, et al. an overview of elastography-An emerging branch of medical imaging. Curr Med Imaging Rev. 2011;7:255-82. 10. Daniel T Ginat, Stamatia V Destounis, et al. US Elastography of breast and prostate lesion. Radiographics. 2009;29: 2007-16. 11. Itoh A, Ueno E, Tohno E, et al. Breast disease: clinical application of US elastography for diagnosis. Radiology. 2006;239(2):341-50. 12. Shiina T, Doyley MM, Bamber JC. Strain imaging using combined RF and envelope autocorrelation processing. In: Proceedings of the IEEE Ultrasonics Symposium. Savoy, Ill:Institute of Electrical and Electronics Engineers Ultrasonics, Ferroelectrics, and Frequency Control Digital Archive. 1996;2:1331-6. 13. Zhang M, Nigwekar P, Castaneda B, et al. Quantitative characterization of viscoelastic properties of human prostate correlated with histology. Ultrasound Med Biol. 2008;34:1033-42. 14. Kathy Nightingale. Acoustic Radiation Force Impulse (ARFI) Imaging: a Review. Curr Med Imaging Rev. 2011;7(4):328-39. doi:10.2174/157340511. 15. EE Drakonaki, GM Allen, DJ. Ultrasound elastography for musculoskeletal applications. Wilson. British Journal of Radiology. 2012;85:1435-45. 16. McAleavey SA, Menon M, Orszulak J. Shear-modulus estima­ tion by application of spatially-modulated impulsive acoustic radiation force. Ultrason. Imaging. 2007;29:87-104. 17. Bercoff J, Tanter M, Fink M. Supersonic shear imaging: a new technique for soft tissue elasticity mapping. IEEE Trans Ultrason Ferro electr Freq Control. 2004;51:396–409.

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does not correlate with the changes in HVPG (abstract). Hepatology. 2010;52:1074A. 36. Laurent Castera. Noninvasive assessment of liver fibrosis in chronic hepatitis C. HepatolInt. 2011;5:625-34. 37. Sporea I, Bota S, Peck-Radosavljevic M, et al. Acoustic radiation force impulse elastography for fibrosis evaluation in patients with chronic hepatitis C: an international multicenter study. Eur  J Radiol. 2012;81(12):4112-8. doi: 10.1016/j.ejrad. 2012.08.018. Epub 2012 Sep 20. 38. Rizzo L, Calvaruso V, Cacopardo B, Alessi N, Attanasio M, Petta S, et al. Comparison of transient elastography and acoustic radiation force impulse for noninvasive staging of liver fibrosis in patients with chronic hepatitis C. Am J Gastroenterol. 2011. Dec;106(12):2112-20. doi: 10.1038/ajg.2011.341. Epub 2011 Oct 4. 39. Son CY, Kim SU, Han WK, et al. Normal liver elasticity values using acoustic radiation force impulse imaging: a prospective study in healthy living liver and kidney donors. J Gastroenterol Hepatol. 2012;27(1):130-6. doi: 10.1111/j.14401746.2011.06814.x. 40. Martinez SM, Foucher J, Combis JM, et al. Longitudinal liver stiffness assessment in patients with chronic hepatitis C undergoing antiviral therapy PLoS One. 2012;7(10):e47715. doi: 10.1371/journal.pone.0047715. Epub 2012 Oct 17. 41. Laurent Castera, Massimo Pinzani, Jaime Bosch. Noninvasive evaluation of portal hypertension using transient elastography. J Hep. 2012;56 j:696-703. 42. Gao J, Ran HT, Ye XP, et al. The stiffness of the liver and spleen on ARFI Imaging pre- and post-TIPS placement: a preliminary observation. Clin Imaging. 2012;36(2):135-41. 43. Carrión JA, Torres F, Crespo G, et al. Liver stiffness identifies two different patterns of fibrosis progression in patients with hepatitis C virus recurrence after liver transplantation. Hepatology 2010;51(1):23-34. doi: 10.1002/hep.23240. 44. Sasso M, Beaugrand M, de Ledinghen V, et al. Controlled attenuation parameter (CAP): a novel VCTE™ guided ultrasonic attenuation measurement for the evaluation of hepatic steatosis: preliminary study and validation in a cohort of patients with chronic liver disease from various causes. Ultrasound Med Biol. 2010;36(11):1825-35. doi: 10.1016/j. ultrasmedbio. 2010. 07. 005. Epub 2010 Sep 27. 45. Roulot D, Czernichow S, Le Clésiau H, et al. Liver stiffness values in apparently healthy subjects: influence of gender and metabolic syndrome. J Hepatol. 2008;48:606-13. 46. Shuang-Ming T, Ping Z, Ying Q, et al. Usefulness of acoustic radiation force impulse imaging in the differential diagnosis of benign and malignant liver lesions. Acad Radiol. 2011;18(7):810-5. Epub 2011 Mar 21. 47. Onur MR, Poyraz AK, Ucak EE, et al. Semiquantitative strain elastography of liver masses. J Ultrasound Med. 2012;31(7):1061-7. 48. Gallotti A, D’Onofrio M, Romanini L, et al. Acoustic radiation force impulse (ARFI) ultrasound imaging of solid focal liver lesions. Eur J Radiol. 2012;81:451-5.

Chapter 40 Ultrasound Elastography: Principles and Application 49. Aymeric Guibal, Camille Boularan, Matthew Bruce, et al. Evaluation of shear wave elastography for the characterization of focal liver lesions on ultrasound. EurRadiol. DOI 10.1007/ s00330-012-2692-y. 50. Kamoi K, Okihara K, Ochiai A, et al. The utility of transrectal real-time elastography in the diagnosis of prostate cancer. Ultrasound Med Biol. 2008;34(7):1025-32. 51. Akin O, Hricak H. Imaging of prostate cancer. Radiol Clin North Am. 2007;45(1):207-22. 52. Daniel T, Ginat, Stamatia V Destounis, et al. US Elastography of breast and prostate lesion. Radiographics. 2009;29:2007-16. 53. Zhai, et al. Characterizing the stiffness of human prostates using acoustic radiation force, ultrasound imaging. 2010;32(4):201-13. 54. Nightingale K, Palmeri M, Nightingale R, et al. On the feasibility of remote palpation using acoustic radiation force. JASA. 2001; 110:625-34. 55. Zhai, et al. Acoustic radiation force impulse imaging of Human Prostate: Initial in vivo demonstrations. Ultrasound Med Biol. 2012;38(1):50-61. 56. Choi YJ, Ko EY, Han BK, et al. High-resolution ultrasonographic features of axillary lymph node metastasis in patients with breast cancer. Breast. 2009;18:119– 122. 57. Bedi DG, Krishnamurthy R, Krishnamurthy S, et al. Cortical morphologic features of axillary lymph nodes as a predictor of metastasis in breast cancer: in vitro sonographic study. AJR Am J Roentgenol. 2008;191:646-52. 58. Jae Jeong Choi, et al. Role sonographic elastography in the differential diagnosis of axillary lymph nodes in breast cancer. J Ultrasound Med. 2011;30:429-36. 59. Deng Ke Teng, et al. Value of US elastography in assessment of enlarged cervical lymph nodes. Asian Pacific J Cancer Prev. 13: 2081-5. 60. Hong Y, Liu X, Li Z, et al. Real-time ultrasound elastography in the differential diagnosis of benign and malignant thyroid nodules. J Ultrasound Med [serial online]. 2009;28(7):861-Y7. 61. Lyshchik A, Higashi T, Asato R, et al. Thyroid gland tumor diagnosis at US elastography. Radiology. 2005;237:202-11. 62. Dighe M, Kim J, Luo S, et al. Utility of the ultrasound elastographic systolic thyroid stiffness index in reducing fineneedle aspirations. J Ultrasound Med. 2010;29:565-74. 63. Bahn MM, Brennan MD, Bahn RS, et al. Development and application of magnetic resonance elastography of the normal and pathological thyroid gland in vivo. J Magn Reson Imaging. 2009;30:1151-4. 64. M Swiatkowska-Freund, K Preis. Elastography of the uterine cervix: implications for success of induction of labor. Ultrasound Obstet Gynecol. 2011;38:52-6. 65. Sun LT, Ning CP, Liu YJ, Wang ZZ, et al. Is transvaginal elastography useful in preoperative diagnosis of cervical cancer? Eur J Radiol. 2012 Aug;81(8):e888-92. doi: 10.1016/j. ejrad.2012.04.025. Epub 2012 Jun 18. 66. Thomas A, Kümmel S, Gemeinhardt O, et al. Real-time sonoelastography of the cervix: tissue elasticity of the

normal and abnormal cervix. AcadRadiol. 2007;14(2): 193-200. 67. FS Molina, LF Gómez, J Florido, et al. Quantification of cervical elastography: a reproducibility study. Ultrasound in Obstetrics & Gynecology. 2012;39(6):685-9. 68. O Ami, F Lamazou, M Mabille, et al. Real-time transvaginal elasto­sonography of uterine fibroids. Ultrasound Obstet Gynecol. 2009;34:486-8. 69. Marco Tessarolo, Luca Bonino, Marco Camanni, et al. Elastosonography: a possible new tool for diagnosis of adenomyosis? EurRadiol. 2011;21:1546-52 DOI 10.1007/ s00330-011-2064-z. 70. Preis Krzysztof, Zielinska Katarzyna, Swiatkowska-Freund Malgorzata, et al. The role of elastography in the differential diagnosis of endometrial pathologies– preliminary report. GInekol Pol. 2011;82:494-7. 71. EE Drakonaki, GM Allen, DJ Wilson. Elastography for musculoskeletal applications. BJR. 2012;85:1435-45. 72. Kemal Arda, NazanCiledag, ElifAktas, et al. Quantitative assessment of normal soft-tissue elasticity using shear-wave ultrasound elastography. AJR. 2011;197:532-6. 73. De Zordo T, Chem R, Smekal V, et al. Real-time sonoelastography: findings in patients with symptomatic Achilles tendons and comparison to healthy volunteers. Ultraschall Med. 2010;31:394-400. 74. De Sconfienza LM, Silvestri E, Cimmino MA. Sonoelastography in the evaluation of painful Achilles tendon in amateur athletes. ClinExpRheumatol. 2010;28:373-8. 75. De Zordo T, Lill SR, Fink C, et al. Real-time sonoelastography of lateral epicondylitis: comparison of findings between patients and healthy volunteers. Am J Roentgenol. 2009;193: 180-5. 76. Niitsu M, Michizaki A, Endo A, et al. Muscle hardness measurement by using ultrasound elastography: a feasibility study. Acta Radiol. 2011;52(1):99-105. 77. Yanagisawa O, Niitsu M, Kurihara T, et al. Evaluation of human muscle hardness after dynamic exercise with ultrasound real-time tissue elastography: a feasibility study. Clin Radiol. 2011;66(9):815-9. 78. Sconfienza LM, Silvestri E, Bartolini B, et al. Sonoelastography may help in the differential diagnosis between rheumatoid nodules and tophi. Clin Exp Rheumatol 2010;28:144-5. Epub 2011 May 6. 80. 79. Lalitha P, Reddy MCh, Reddy KJ. Musculoskeletal applications of elastography: a pictorial essay of our initial experience. Korean J Radiol. 2011;12:365-75. 80. J Iagnocco A, Kaloudi O, Perella C, et al. Ultrasound elastography assessment of skin involvement in systemic sclerosis: lights and shadows. Rheumatol. 2010;37(8):1688-91. doi: 10.3899/jrheum.090974. Epub 2010 Jun 15. 81. Bhatia KS, Rasalkar DD, Lee YP, et al. Real-time qualitative ultrasound elastography of miscellaneous non-nodal neck masses: applications and limitations. Ultrasound Med Biol. 2010;36:1644-52.

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89. Robert Arndt, Sven Schmidt, ChristophLoddenkemper, et al. Noninvasive evaluation of renal allograft fibrosis by transient elastography – a pilot study. Transplant International. 2010;23:871-7. 90. Brian Stephen Garra. Imaging and estimation of tissue elasticity by ultrasound. Ultrasound Quarterly, 2007;23(4). 91. de Korte CL, Cespedes EI, van der Steen AFW, et al. Intravascular ultrasound elastography: assessment and imaging of elastic properties of diseased arteries and vulnerable plaque. Eur J Ultrasound. 1998;7:219-24. 92. Rubin JM, Xie H, Kim K, et al. Sonographic elasticity imaging of acute and chronic deep venous thrombosis in humans. J Ultrasound Med. 2006;25:1179-86. 93. Geier B, Barbera L, Muth-Werthmann D, et al. Ultrasound elastography for the age determination of venous thrombi. Evaluation in an animal model of venous thrombosis. Thromb Haemost. 2005;93:368-74. 94. Gaspari R, Blehar D, Briones J, et al. Sonoelastographic characteristics of abscess in duration associated with therapy failure. J Ultrasound Med. 2012;31(9):1405-11. 95. Gaspari R, Blehar D, Mendoza M, et al. Use of ultrasound elastography for skin and subcutaneous abscesses. J Ultrasound Med. 2009;28(7):855-60. 96. Lee TH, Cha S, Cho YD. EUS Elastography: advances in diagnostic EUS of the pancreas. Korean J Radiol. 2012; 13(S1):S12-S16.

41

Computed Tomography Hardware: An Update

CHAPTER

Ashu Seith Bhalla, Arun Deep Arora

Since the first clinical use of computed tomography (CT) in 1972, its technology has made notable advances. The first CT scanner which was built by British engineer Hounsfield had a rotation time of about 300 seconds with a maximum image matrix of 80 × 80 pixels. It has been a long journey to the present day 256 to 320-slice scanners with rotation times of 0.33 seconds and an image matrix of 512 × 512 pixels. Several vendors today offer 256-slice spiral CT scanners and even 320 slice is now available. But the ever evolving technology has more in store: scanners with new detector materials for higher sensitivity, dual-source CT, dual-energy detectors and flatpanel detectors are further milestones of CT development.1 The subject will be discussed under the following headings: zz Basic workflow of a CT scanner zz Determinants of an optimal image zz Advances in hardware zz Special CT: Cone-beam CT (CBCT)/volume CT, navigation systems.

BASIC WORKFLOW OF CT SCANNER The CT scanner consists of three primary systems; including the gantry, the computer and the operating console. Each of these is made up of various subcomponents. The largest among these systems is the gantry assembly. It is made up of all the equipment related to the patient positioning, including patient support, the positioning couch, mechanical supports and the scanner housing. It also contains the heart of the CT scanner, the X-ray tube, as well as detectors arranged around the patient (Fig. 1). Earlier versions of CT employed a pencillike X-ray beam (with single detector) and the tube-detector movement was both linear and rotary, termed as the “rotatetranslate” motion. In an attempt to shorten the scan time, a fan shaped beam with multiple detectors was adopted. The approach then shifted to “rotate-rotate” where multiple detectors are aligned as an arc and both detector arc and X-ray tube rotate around the patient. The quantum leap took place with the next level where the detectors formed a complete ring around the patient and only the X-ray tube rotates inside the detector ring, described as “rotate-fixed” motion.2

Fig. 1:  Schematic diagram showing the basic components and workflow of a CT scanner

DETERMINANTS OF AN OPTIMAL IMAGE Determinants of an optimal image in CT as in any image acquisition system are: zz Spatial resolution zz Contrast resolution zz Temporal resolution.

Spatial Resolution The key factors determining the spatial resolution are the detector size in the z-axis direction, reconstruction algorithms and patient motion. Spatial resolution is specified in the axial as well as z-axis plane. Scan plane is also called x-y plane and z-axis plane is also called out of plane (Figs 2A and B). The axial or x-y plane spatial resolution is dependent on the pixel size, which is a ratio of scan field of view (SFOV) and image reconstruction matrix. On the other hand, the number of rows in multidetector CT (MDCT) scanner and the detector size determines the out of plane (z-axis) resolution. The detector row width defines the minimum thickness of the reconstructed CT image and is influenced by the z-axis

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B

A

Figs 2A and B:  (A) Diagram showing the orientation of x, y and z-axis; (B) Photograph of a CT scanner. The gantry* houses the CT tube and the detector rows

dimension of the individual detector element. For example, a detector row width of 0.6 mm allows a slice thickness of 0.6 mm. To achieve improved through-plane spatial resolution, some systems use an X-ray focal spot that alternates between two z-positions (i.e. z-flying focal spot) to acquire two overlapping slices for each detector row. This feature has been reported to improve z-plane spatial resolution to 0.4 mm3. Cone-beam CT uses a high-resolution two-dimensional (2D) detector and allows isotropic data acquisition and reconstruction leading to higher spatial resolution. These systems however, offer poor contrast resolution as shall be discussed subsequently in the chapter.

Temporal Resolution The temporal resolution is determined by the gantry rotation time, acquisition mode, type of image reconstruction, and pitch. Gantry rotation time refers to the amount of time taken to complete one full rotation (360°) of the X-ray tube and detector around the patient. The recent advances in technology have brought considerable decrease in the gantry rotation time, almost as low as 330–370 msec. The lesser the gantry rotation time, the greater the temporal resolution achieved. Acquisition mode becomes especially important in cardiac CT where the dataset need be acquired at a very rapid speed to overcome the cardiac motion. It may be done through prospective ECG triggering wherein the data is acquired for only part of the complete gantry rotation, at a desired distance from the R-R peak in the cardiac cycle. This partial scanning reduces the radiation dose to the patient and achieves a temporal resolution in the range of 200–250 msec. The other mode of retrospective ECG gating in which data is acquired throughout the cardiac cycle and segmented reconstruction done from different cardiac cycles to increase temporal resolution to 80–250 msec. Multiple segment

reconstruction, though increases the temporal resolution, but runs the risk of misregistration artifacts as the reconstruction data is selected from different heartbeat cycles. The pitch can be defined as the ratio of table increment per gantry rotation to the total X-ray beam width. The pitch factor plays a major role in improving both the temporal and spatial resolution but at the same time has a dramatic effect on the overall radiation dose delivered during a spiral CT examination. Because radiation dose is inversely proportional to the pitch, the low-pitch protocols substantially increase radiation dose to patients.3 Another approach to increase the temporal resolution is to increase the number of X-ray sources (tubes) generating the X-rays. For a single-source scanner, the time required to collect all data needed for reconstruction of images (i.e. the acquisition time) is approximately one-half the gantry rotation time. The fastest single-source scanner currently available spins at 270 msec per rotation, for a nominal acquisition time and temporal resolution of 135 msec. For a dual-source scanner, the acquisition time is approximately one-fourth the gantry rotation time, because the two X-ray source/detector systems collect data in half the time needed for a single X-ray source/detector array. The fastest dualsource scanner currently available spins at 280 msec per rotation, for a nominal acquisition time of 70 msec.3

Contrast Resolution Contrast resolution is the ability of a CT scanner to differentiate small attenuation differences on the CT image. It is crucial to remember that the linear attenuation coefficient is an absorption measurement and it is dependent on thickness of a material, density of a material, atomic number and photon energy. A change in kVp results in alteration of linear attenuation coefficient of the structure, even if the

Chapter 41 Computed Tomography Hardware: An Update

same structure is being imaged. Contrast resolution is limited by noise and with the increase of noise in an image, there is a decrease in the contrast resolution. Special filters called bowtie filters absorb weaker energy photons, which reduce the probablility of scattered photons being detected by the CT detectors. An X-ray beam consists of polychromatic photons or photons having different energies. The bow-tie filters serve to absorb lower-energy photons primarily to “lessen” the effects from the polychromatic nature of an X-ray beam. A soft tissue, standard or smooth algorithm is used during the reconstruction process for enhancement of soft tissue and contrast resolution.4

ADVANCES IN HARDWARE The newest technology offers significant advantages, but, current CT hardware releases are far from uniform across vendors, reflecting different approaches to image acquisition in the current era. No single CT scanner offers the full range of the newest features. This underscores the importance of understanding the properties and advancements of individual components of CT scanner.

Advances in CT Tube Most modern commercial scanners use a hot-cathode, high-vacuum X-ray tube which is built with a liquid-cooled, copper-backed tungsten target. Lead can be found in various parts of the CT scanner system, which reduces the amount of excess radiation. In conventional CT, the tube and detectors moves clockwise and anti-clockwise 360° while in spiral/helical CT the tube and detector arrays continuously move with the table. The early CT scanners used the stationary anode X-ray tubes because the long scan times indicated that the instantaneous power level was low. Long scan times also allowed dissipation of heat. Shorter scan times in later versions of CT scanners required high-power X-ray tubes and use of oil-cooled rotating anodes for efficient thermal dissipation. Several technical advances have been brought about in component design for achieving these power levels and dealing with the problems of target temperature, heat storage and heat dissipation. For example, the tube envelope, cathode assembly and anode assemblies including anode rotation and target design have been redesigned. A decrease in scan times has increased the anode heat capacity by as much as a factor of five, thus preventing the requirement for cooling delays during most clinical procedures, and tubes with capacities of 5–8 million heat units (MHU) are also available now. In addition, improvement in the rate of the heat dissipation (kilo–heat units per minute) has increased the heat storage capacity of modern X-ray tubes. The large heat capacities are achieved with thick graphite backing of target disks, anode diameters of 200 mm or more, improved high-temperature

rotor bearings and metal housings with ceramic insulators among other factors.5 The working life of tubes used today ranges from 10,000 to 40,000 hours, with a marked improvement over the 1,000 hours typical of conventional CT tubes. Since many of the robust engineering changes led to an increase in the mass of the tube, a significant effort was also made towards reducing the mass to better withstand the increasing gantry rotational rates which were required by faster scan times. With an increase in the gantry rotation speed, the stress on the gantry structure also increases, since rapid movement of heavy mechanical components inside the CT gantry makes it harder to achieve a further reduction in gantry rotation time. In fact, even a small incremental gain in the gantry rotation time requires great effort in the engineering design.5 A major landmark in development of CT tubes is the advent of directly cooled X-ray tube. It allows gantry rotation time below 0.4 seconds and allows virtually unlimited volume coverage at maximum scan speed without compromise on resolution and image quality. Direct anode cooling enables extremely high cooling rates and eliminates the need for anode heat storage capacity. The very compact design is robust. The anode and inner tube assembly are significantly smaller than in the conventional tubes. In conventional X-ray tubes, the entire anode including the bearings is encapsulated in a vacuum and the cooling fluid cannot reach it efficiently, which results in lower cooling rates. Robust X-ray tubes with higher heat storage capacity up to 8 MHU, allows scanning until the heat storage capacity is filled. Once overheated, even such state-of-the-art conventional X-ray tubes cool down to normal operation temperatures in 5–10 minutes. The new directly cooled X-ray tubes provide direct cooling of the anode with all bearings being located outside the vacuum. Similar to a miniature electron beam CT, the electron beam in the tube is shaped and controlled by an electromagnetic field. The direct anode cooling enables unprecedented cooling rates of 4.7 MHU/min and eliminates the requirement for large heat storage capacities. In fact, the heat storage capacity of the new anode is close to 0 MHU. Even at maximum load, these tubes cool down within just 20 seconds which is much less than the time needed to begin the next scan or to position the next patient. With substantially higher tube lifetime even at much higher G-forces this revolutionary design is the key to increased gantry rotation speed and reduced life-cycle cost at the same time. A novel example of such a tube is Straton tube.6 X-ray tube with flying focus has a magnet system for deflecting and focusing the electron beam, whereby the magnet system including a carrier that is constructed as an iron yoke and that has four pole projections that are arranged around the axis of the electron beam offset from one another by 90 degree., on which two pairs of coils (z-coils and .phi.coils) are arranged so as to be offset from one another by

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90 degree. The individual coils of each pair supplied with a common high-frequency alternating current that deflects the electron beam in the .phi.- and z-directions, respectively, in a pulsed manner.5

Advances in Detectors The detector array design in multiple-row detector CT varies with each manufacturer. The detectors are arranged in rows and columns. The number of active detector rows and the z-axis width of detectors in an array define the detector configuration. A detector design that is subdivided into equal elements, or portions, is called uniform, matrix, or mosaic. Nonuniform or Variable detectors use variable detector size in the orthogonal direction or along the z-axis (the longitudinal axis of the patient table). In combination with a physical postpatient collimator, signals from these detectors can be combined to form various values of image thickness in a manner that improves detector efficiency over that of uniform detectors. This improvement is a result of the smaller proportion of dead space due to the divisions (cell walls) between detector elements. Hybrid detectors has a number of narrow detector elements in the center of the detector and a different number of wider detectors (usually double the width of the narrow detectors) on both sides of the span of narrow detectors (Figs 3A to C). The

number of narrow and wider detectors can vary among different vendors.7 Following the presentation of the first 4-slice CT scanner in 1998, all other manufacturers also offered scanners enabling acquisition of four simultaneous slices per rotation. The next step was the development of 16-slice CT scanners parallel to slimmed-down versions for the simultaneous acquisition of 6, 8, or 10 slices. And as the slice counts keep going up (128, 256 and even 320) the costs and clinical capabilities go up too. In-plane spatial resolution is determined primarily by the number of X-ray projections available for reconstruction, the scan field of view and the image matrix. The highest in-plane spatial resolution of current MDCT scanners has been reported to be in the range of 0.23–0.4 mm. During helical scanning, some overscanning in the longitudinal direction (z-overscan) is required to ensure that sufficient data are available for reconstruction. Dynamic or adaptive collimation is a hardware-based solution for collimating the X-ray beam such that extraneous radiation exposure is blocked by retractable collimator blades. Dynamic collimation has the greatest effect in reducing dose for shorterscan lengths and higher-pitch values. Z-overscanning can also occur during axial scanning. In this case, the amount of z-overscan depends on the planned scan length P and the total beam collimation. Adaptive collimation is a hardware solution offered on certain

A

B

C

Figs 3A to C:  Diagram showing the basic design of matrix (A), variable (B) and the hybrid (C) detector design. The measurements indicated in the diagram are relative and not to scale

Chapter 41 Computed Tomography Hardware: An Update

wide-detector array MDCT scanners. With this technique the detector collimation is automatically selected from a set of beam collimations in increments of 10 mm that are based on the planned scan length so as to minimize extraneous exposure. Adaptive collimation for axial scanning has the greatest effect in reducing dose with wide-detector array MDCT scanners because the portion of the total X-ray exposure in the axial scan mode attributed to z-overscanning increases with z-axis detector coverage.1 Dual energy may be principally achieved either by radiating the object with two different energy spectra from a single source through fast voltage switching or from multiple sources operating at different voltages, or by analyzing the energy spectrum on the detector side. A simple but effective solution lies in a double-layer detector design. The upper layer predominantly receives photons with lower energy and the lower layer receives photons with higher energy. Summing the signal from both detector layers returns the full signal as in a single layer detector, but separate readouts from both layers allow for simple spectral analysis of the X-ray beam.1 Most scanners use ceramic (solid-state) scintillation detectors coupled to photodiodes, which have improved spatial resolution and decreased noise compared with older xenon gas detector systems. Another milestone in CT technology lies in the development of new detector materials that exhibit higher sensitivity to radiation and allow faster sampling rates. There is a new scintillator that features a negligible afterglow in conjunction with a 100-fold faster reaction time, allowing for recording of 7000 views per second. Implementation of the new scintillator may be one of the prerequisites for singlesource ultra-fast dual energy switching, promising almost simultaneous spatial and temporal registration and material decomposition without the limitation of a reduced FOV due to the second smaller detector in dual-source CT. They have very low afterglow, extremely low radiation damage and very good chemical durability, mechanical properties, uniformity and manufacturability. Approximately 50% fewer beam-hardening artifacts, metal artifact reduction and further improvements in contrast-to-noise ratio are some of the benefits resulting from the new scintillator. The new scintillator is configured to emit fluorescence when irradiated with X-rays and it has a primary decay time of only 30 nsec, making it 100 times faster than the conventional scintillator material. It has afterglow levels that reach only 25% of the levels of conventional scintillator material. The most advantageous feature of MDCT with garnet-based detectors is the improved spatial resolution (high-definition imaging at up to 230 mm resolution). An example of this is Gemstone, which is a newly developed transparent polycrystalline scintillator for CT from GE health care.8,9

Advances in Reconstruction Conventionally, Filtered back projection method has been used for image reconstruction in single section CT, which

involves processing of each ray sum immediately after it is obtained while the data acquisition continues for other ray sums. It attempts to project a uniform value of attenuation over the path of the ray such that the calculated attenuation over the path is proportional to the measured attenuation. The final image obtained is rather blurred as a result of the assumption that the beam attenuation occurs uniformly over the entire path of the ray. A technique to eliminate the blurring is the ‘convolution operation’ or ‘filtering’ which involves a ‘filter function’ or convolution ‘kernel’. The filter or kernel may be chosen by the radiologist or automatically selected for a particular procedure. The most commonly used single-section spiral interpolation schemes are the 360° and 180° linear interpolation methods.10 Spiral CT requires an interpolation of the acquired measurement data in the longitudinal (through-plane) direction to estimate a complete CT data set at the desired plane of reconstruction. The 360° and 180° linear interpolation single-section spiral reconstruction approaches can be extended to multidetector row spiral scanning in a straightforward way but the cone angle of the measurement rays is not taken into account (Fig. 4). Scanners that rely on 180° or 360° multidetector linear interpolation techniques and extensions thereof provide selected discrete pitch values to the user to provide optimized sampling schemes in the longitudinal direction and, hence, optimized image quality. Scanning at low pitch optimizes image quality and longitudinal resolution at a given collimation but at the expense of increased patient dose. To reduce patient dose, either milliampere settings should be reduced at low pitch values or high-pitch values should be chosen. A further refinement to spiral interpolation is the Z-filter approach, in which reconstruction is not restricted to the two rays closest to the image plane and is contributed by all rays within a selectable distance from the image plane. An example of z-filter technique is adaptive axial interpolation algorithm, which allows the system to trade off z-axis resolution with image noise. Unlike in single section spiral CT, patient dose is independent of spiral pitch.11 For CT scanners with 16 or more detector rows, modified reconstruction approaches that account for the cone-beam geometry of the measurement rays have been developed. In three-dimensional (3D) convolution backprojection technique for multisection spiral scanning, the reconstruction is based on sorting of raw data from individual detector channels. In the raw data space, which is typically four times as large as the image data space, the signals from the individual detector rows are computed in such a way that axial images in parallel orientation are directly obtained from the raw data.1,11 Sorting of the raw data requires considerable processor power and more powerful computers. Direct 3D filtered back projection of raw data is superior to rebinning algorithms (mentioned later) in homogeneous distribution of image noise and uniform slice thickness in particular for scanners with larger cone angles. Iterative reconstruction

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Fig. 4:  Multidetector CT reconstruction techniques

techniques, based on back and forward projection promising significant noise reduction, have been proposed since the early times of CT technology. In single-slice spiral CT, the pitch factor did not affect image noise but higher-pitch factors resulted in thicker slices and increasingly blurred anatomy. Typical pitch factors used in spiral CT ranged between 1 and 2. In multislice spiral CT, the pitch factor does not affect the slice sensitivity profile of the reconstructed section but faster table feed (higher-pitch value) increases image noise because fewer photons are available for image reconstruction. This effect is compensated for on all scanners by automatically increasing the tube current (mA value) when a higher-pitch factor is selected. It is thus no longer possible to reduce the radiation dose by simply choosing a higher-pitch factor (which was possible on earlier spiral CT scanners). The image quality achieved with all currently available implementations of reconstruction algorithms may vary with the pitch factor. On most current scanners, optimal image quality is obtained when using pitch values slightly less than one because computation of supplementary projections obtained by overlapping scanning generally results in higher image quality.1

Rebinning Algorithms Advanced single-slice rebinning (ASSR) and its variations are algorithms optimized for small cone angles. The algorithm reduces (3D) cone-beam data to tilted slices by minimizing the deviation of the reconstruction plane from the spiral. The image planes are no longer perpendicular to the patient axis; instead, they are tilted to match the spiral path of the focal spot generating pseudoaxial slices. In a final z-axis reformation step, the traditional transverse images are calculated by interpolating between the tilted original image planes. The ASSR algorithm operates efficiently and requires fairly little computing power to reconstruct images of clinically acceptable image quality. Representative examples for rebinning algorithms are the adaptive multiplanar

reconstruction algorithm (AMPR) and the conjugate ray reconstruction (weighted hyperplane reconstruction).1

SPECIAL COMPUTED TOMOGRAPHY Cone-beam CT/Volume CT Cone beam CT is an emerging CT variant which is designed to provide a compact, low-cost, low-radiation dose system that can be used to image high-contrast structures as in the head and neck. Cone-beam CT uses divergent X-rays forming a “cone” between the source and detector, unlike the “fanbeam” geometry in conventional CT (Figs 5A and B). In CBCT multiple images are acquired during a single rotation of the gantry around the patient head producing a volumetric data. On the other hand, conventional CT requires both rotation as well as z-axis translation of the gantry to be able to acquire 3D data. X-ray tubes of relatively low power requirements are employed. Recent versions of the system use flat panel detectors (FPDs) of the indirect-conversion type based on a cesium iodide (CsI) scintillator.12 These digital flat panel CBCT systems can also be mounted on a C-arm for applications in interventional radiology suites. Cone-beam CT thus produces an entire volumetric data set in a single gantry rotation as it utilizes a 2D detector system unlike the one-dimensional (1D) detector or series used in MDCT.13,14 Depending on the variants of the system devised for various applications, several terms been used in literature to describe these new volumetric imaging techniques, such as cone-beam CT, C-arm CT, cone-beam volume CT, volume CT, angiographic CT and flat-panel CT.13

Cone-beam Geometry Cone-beam CT uses a high-resolution 2D detector instead of a series of row of 1D detector elements as in MDCT.13 Images obtained by CBCT have high-isotropic spatial

Chapter 41 Computed Tomography Hardware: An Update

reconstructions.12 The most commonly used reconstruction algorithm in CBCT systems is a modification of the filtered back-projection method called the Feldkamp algorithm.15 Compared to MDCT, CBCT however takes longer times for acquisition as well as reconstruction of images despite the acquisition being done in a single rotation.

Radiation Dose

Figs 5A and B:  Schematic diagram showing basic design of a conventional CT (A) and a cone-beam (B) CT

resolution.14 This is due to the isotropic nature acquisition and reconstruction in CBCT systems.12 The volumetric data obtained in CBCT yield a dataset with isometric voxel size as small as 150 × 150 × 150 μm3 at the isocenter, thus allowing high-quality multiplanar reconstructions.12,15 Multidetector CT on the other hand produces individual sections which are subsequently stacked typically yielding spatial resolution of 500 × 500 μm2 in-plane and 500–1000-μm in the z-axis.12 Conebeam CT however, suffers from poor contrast resolution due to higher scatter in cone-beam acquisition, a lower DQE of CBCT systems and reduced temporal resolution and dynamic range of the FPDs.13 CBCT is thus suited for imaging of highcontrast structures. Higher scatter is a major limiting factor with the cone-beam vs conventional fan-beam geometry acquisition leading to image degradation. In order to counter this effect, several anti-scatter measures are employed, such as grids, software correction algorithms, beam-stop scatter mapping and alteration of object-to-detector distance (airgap).16 Cone-beam CT also suffers from limited anatomic coverage as it is based on acquisition of images during single gantry rotation.13

Flat-panel Detector Cone-beam CT scanners use CsI scintillator detectors unlike the ceramic detectors used in MDCT. These suffer from a greater lag (afterglow) and hence scan times are much longer with CBCT relative to MDCT, thus reducing the temporal resolution of CBCT scanners. For instance, the current C-arm CBCT acquisitions take about 5 seconds.13, 15 In addition, CsI detectors also have a lower quantum efficiency reducing the dynamic range of the scanner.13 The low-dynamic range also result in low-contrast resolution of these systems.

Reconstruction Volumetric data thus acquired in CBCT as in MDCT can subsequently be manipulated and reconstructed with software to allow multiplanar as well as panoramic

The other major advantage of CBCT is reduction of radiation dose relative to MDCT. Effective dose of commercial CBCT scanner has been estimated as 0.2 mSv Vs 1–2 mSv for MDCT head.17,18 However, assessment of radiation dose during CBCT affords many challenges due to the altered beam geometry and underestimation of dose when using conventional methodology, such as ion-chamber inserts. 12,19 Also, conventional dosimetry metrics, such as the CTDIw cannot be directly applied to CBCT imaging. It is hence suggested that the difference in absorbed dose measurements may be insignificant when FOVs and image quality parameters between CBCT and MDCT are adjusted.15,19

Applications Cone-beam CT provides a compact system wherein the scan can be performed with the patient sitting in an upright position. It has primarily found widespread applications in maxillofacial imaging including dental imaging, sinus and temporal bone imaging. It is most popular as an office based system for dental imaging. Cone-beam CT systems for maxillofacial imaging became available in 2001. 20 The compact design also makes the system significantly cheaper than MDCT. It also delivers a lower radiation dose than MDCT. Cone-beam CT has high spatial resolution but low-contrast resolution and limited anatomic coverage. It is not meant to be a substitute for MDCT which is distinctly superior in image quality but as a compact, inexpensive, low-dose system for applications. C-arm based CBCT systems are also used in interventional radiology suites.13

C-arm Based CBCT The CBCT system is compact enough to allow it to be mounted on a C-arm. These systems allow projection radiography fluoroscopy, digital subtraction angiography, and volumetric CT applications through a single system. This has significant utility as it eliminates the need for transporting the patient to the CT room for procedures requiring guidance of crosssectional imaging. Currently, all commercially available C-arm mounted CBCT systems employ digital flat-panel detectors.13 Also, unlike MDCT as there is no z-axis translation and all acquisition occurs in a single rotation of the tubedetectors, it allows patient to remain stationary during the procedure.

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A

B

Figs 6A and B  (A) Photograph showing sternal biopsy in a patient with the help of PIGA; (B) The planner image on the console projects the expected trajectory of the needle path

Cone-beam CT has been employed for radiation therapy planning.21 Cone-beam CT has also been used for surgical planning particularly in orthopedic, chest,abdominal, head and neck and neurosurgical procedures.13,22 Electron beam tomography (EBT) is a specific form of computed tomography (CAT or CT) in which the X-ray tube is not mechanically spun in order to rotate the source of X-ray photons. In EBT, however, the X-ray tube itself is stationary and large and surrounds the imaging circle partially. Rather than moving the tube itself, electron beam focal point (and hence the X-ray source point) is swept electronically along a tungsten anode in the tube, tracing a large circular arc on its inner surface. This motion can be very fast. The heart always remains in motion and some important structures, such as arteries, move several times their diameter during each heartbeat. Thus, Rapid imaging is very useful to avoid the blurring of moving structures during the scan. It increasingly appears that the spiral CT designs, especially those with (b) 64 detector rows, (b) 3 × 360°/sec rotation speeds and designed for cardiac imaging, are largely replacing the EBT design from a commercial and medical perspective.

Navigation Systems Several navigation systems have recently become available to aid in CT guided interventions. One of the methods used for this purpose is electromagnetic tracking. These systems involve interaction with previously acquired images to provide real time spatial navigation information. This method does not involve continuous imaging of the patient. Combining electromagnetic tracking with preacquired imaging can be beneficial in guiding interventions, for instance in allowing real time targeting of lesions using previously acquired sequences in desired phase of enhancement. 23 Electromagnetic tracking also allows utilization of data from other imaging

modalities. Similarly this technology is also being used to guide endoscopic and surgical procedures. Previously acquired CT images are loaded into proprietary software which reconstructs 3D images as desired. These are then used to mark target locations and plan path of intervention. Real time visualization of position of the endoscope is also then available in relation to these images. Navigation devices may also be based on optical tracking systems.24 Automated guiding systems for CT-guided biopsies are also available now. These typically involve the use of a robotic, electromechanical arm (Figs 6A and B). A computer interface receives the CT images and calculates coordinates on DICOM images and then guides needle placement through the arm.25

CONCLUSION Computed tomography hardware thus is a rapidly evolving field, constantly introducing newer technologies for the user as the vendors continue to innovate.

REFERENCES 1. Rogalla P, Kloeters C, Hein PA, et al. CT Technology Overview: 64 –Slice and Beyond. Radiol Clin N Am. 2009;47:1-11. 2. Curry TS, Dowdey JE, Murry RC. Computed Tomography in Christensen’s Physics of Diagnostic Radiology, 4th Edn. Philadelphia and London: Lea & Febiger; 1990.pp.289-322. 3. Mahesh M, Cody DD. Physics of cardiac imaging with multiplerow detector CT. Radiographics. 2007;27(5):1495-509. 4. Reddinger W. www.e-radiography.net, [Place unknown] Out Source, Inc., 1998[Updated 2013 January 1; cited 2013 March 08] Available from www.e-radiography.net/mrict/CT_IQ.pdf 5. www.kau.edu.sa [cited 2013March 08] Available from “X-Ray Tube in CT Scanner” www.kau.edu.sa/.

Chapter 41 Computed Tomography Hardware: An Update 6. www.medical.siemens.com [cited 2013March 08] Available from www.medical.siemens.com/.../S_64-69_Science_Speed 4D.pdf 7. Cody DD, Mahesh M. Technologic Advances in Multidetector CT with a Focus on Cardiac Imaging. Radio Graphics. 2007;27: 1829-37. 8. www.gehealthcare.com [cited 2013 March 08] 9. Yanagawa M, Tomiyama N, Honda O, et al. Multidetector CT of the lung: image quality with garnet-based detectors. Radiology. 2010;255(3):944-54. 10. Miraldi F, Sims MS, Wiesen EJ. Imaging Principles in Computed Tomography in CT and MR Imaging of the Whole Body, 4th Edn. In: Haaga JR, Lanzieri CF, Gilkeson RC (Eds). United States of America: Mosby; 2003.pp.2-36. 11. Flohr TG, Schaller S, Stierstorfer K, et al. Multidetector row CT systems and image-reconstruction techniques. Radiology. 2005;235(3):756-73. 12. Miracle AC, Mukherji SK. Cone beam CT of the Head and Neck, Part 1: Physical Principles. AJNR. 2009;30:1088-95. 13. Orth RC, Wallace MJ, Kuo MD. For the Technology Assessment Committee of the Society of Interventional Radiology. C-arm cone-beam CT: general principles and technical considerations for use in interventional radiology. J Vasc Interv Radiol. 2008; 19:814-20. 14. Jaffray DA, Siewerdsen JH. Cone beam computed tomography with a flat-panel imager: initial performance characterization. Medical Physics. 2000;27:1311-23. 15. Gupta R, Grasruck M, Suess C, et al. Ultra-high resolution flatpanel volume CT: fundamental principles, design architecture and system characterization. Eur Radiol. 2006;16:1191-205. Epub 2006 Mar 10.

16. Endo M, Mori S, Tsunoo T, Miyazaki H. Magnitude and effects of X-ray scatter in a 256-slice CT scanner. Med Phys. 2006; 33:3359-68. 17. Bauhs JA, Vrieze TJ, Primak AN, et al. CT dosimetry: comparison of measurement techniques and devices. Radiographics. 2008;28:245-53. 18. Alspaugh J, Christodoulou E, Goodsitt M, et al. Dose and image quality of flat-panel detector volume computed tomography for sinus imaging. Med Phys. 2007;34:2634. 19. Fahrig R, Dixon R, Payne T, et al. Dose and image quality for a cone-beam C-arm CT system. Med Phys. 2006;33:4541-50. 20. Scarfe WC, Farman AG, Sukovic P. Clinical applications of cone-beam computed tomography in dental practice. J Can Dent Assoc. 2006;72:75-80. 21. Moore CJ, Am A, Marchant T, et al. Developments in and experience of kilovoltage X-ray cone beam image-guided radiotherapy. 22. Daly MJ, Siewerdsen JH, Moseley DJ, Jaffray DA, Irish JC. Intraoperative cone-beam CT for guidance of head and neck surgery: Assessment of dose and image quality using a C-arm prototype. Med Phys. 2006;33:3767-80. 23. Appelbaum L, Sosna J, Nissenbaum Y, Benshtein A, Goldberg SN. Electromagnetic Navigation System for CT-Guided Biopsy of Small Lesions. AJR. 2011;196:1194-1200. 24. Meier-Meitinger M, Nagel M, Kalender W, Bautz WA, Baum U. Computer-assisted navigation system for interventional CT-guided procedures: results of phantom and clinical studies. Rofo. 2008;180(4):310-7. [Article in German] 25. Chellathurai A, Kanhirat S, Chokkappan K, Swaminathan TS, Kulasekaran N. Technical note: CT-guided biopsy of lung masses using an automated guiding apparatus. Indian J Radiol Imaging. 2009;19(3):206-7.

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42 Dual-energy Computed Tomography

CHAPTER

Arun Kumar Gupta, Manisha Jana

INTRODUCTION Beginning from the single-slice sequential CT scanner and advancing towards multislice spiral CT with ultrafast true isotropic volume imaging, computed tomographic imaging technology has undergone significant changes in the last few decades. Conventional CT scanners, operating at a single energy, provide morphologic imaging only, with little material-specific information in body imaging. On the other hand, dual-energy CT utilizes the principle that different materials show different attenuation at varying energy levels, and this difference in attenuation can be used for tissue characterization. Since its inception, dual-energy CT scanning has undergone several technical modifications. This chapter describes the development, principle and applications of dual-energy CT.

HISTORICAL PERSPECTIVE The concept of dual-energy CT existed from the very beginning of the history of computed tomographic imaging. In the early days, Sir Hounsfield proposed that “two pictures are taken of the same slice, one at 100 kV and the other at 140 kV... areas of high-atomic numbers can be enhanced... Tests carried out to date have shown that iodine (Z = 53) can be readily differentiated from calcium (Z = 20)”.1 Alvarez and Macovski2 and Kalender et al.3 also described the theoretical basis of dual-energy CT scanning in the late 1970s and early 1980s. The constraints in dual-energy imaging in early days were poor-spatial resolution, increased-radiation dose, slower-CT scanners leading to image misregistration, and significant noise in the lower-kilovoltage image.4-8 With the advent of newer-multislice CT scanners having improved temporal resolution, dual-energy CT has finally become a reality in clinical applications. First commercially available dual-energy CT scanner came into use in 20068 (Somatom Definition, Siemens, Erlangen, Germany). It was dual-source dual-energy CT scanner (DS-DECT) having two X-ray tubes and two detector systems. Over the time, there have been

newer modifications and advancements in the dual-energy scanners. In second generation of dual source dual-energy scanners, the dual-energy scan FOV was increased (from 26 to 33 cm); and the addition of a selective photon shield led to increased contrast to noise ratio and better and accurate material characterization. The DSDECT scanner was followed by the development of a single-detector, single-source DECT (SS-DECT) system with the capability for rapid alternation/ fast switching between two kVp settings (Gemstone Spectral Imaging; GE Healthcare, Piscataway, NJ). 9 A SS-DECT scanner has a single ultrafast detector system with very-short afterglow and dual-energy scanning is made possible by rapid switching of the kVp settings of the tube. Currently available dual-energy CT scanners employ different technologies to obtain high and low-energy datasets: z Dual-source dual-energy CT (DS-DECT) z Single-source dual-energy CT (SS-DECT); and z Single-source dual-energy scanner with dual-detector layers (under development with Philips, not commercially available).

PRINCIPLE In clinical imaging, compton scatter and photoelectric effect are the two predominant interactions of matter with X-ray photons. The photoelectric effect occurs when an incident photon, having sufficient energy to overcome the K-shell binding energy of the electron in an atom, interacts with the atom to release the K-shell electron. The energy generated is released in the form of a photoelectron. The likelihood of photoelectric effect depends on the atomic number of the substance as well as the energy of the incident beam.10 As the energy of the incident photon beam approaches the K-shell binding energy of an electron (which varies with the atomic number), the chances of photoelectric effect increases. K-edge refers to an increased photoelectric effect and a spike in attenuation at an incident energy level just greater than the K-shell binding energy.7 The K-edge values of different materials are given in Table 1.

Chapter 42 Dual-energy Computed Tomography

The principle of dual-energy CT imaging is based on the differential absorption of energy at variable kVp settings. For example, let us consider a substance (A) with K-edge at 60 kVp and another (B) at 130 kVp. If we image multiple combinations of A and/or B at 80 and 140 kVp, there will be differential attenuation at both these energy settings depending on the relative percentage of these substances. The object containing large amount of substance A will show higher attenuation at 80 kVp and lower attenuation at 140 kVp; whereas object containing larger amount of substance B will show higher attenuation at 140 kVp. In clinical applications, the constituents of soft tissues have a different K-edge (variable from 0.01 to 0.53), away from that of iodine (33.2) or calcium (4); hence iodine or calcium can be distinguished from soft tissues at dual energy imaging (Fig. 1). In diagnostic imaging, once the datasets at 80 kVp and 140 kVp are generated, the attenuation of the enhanced structures containing iodine (vessels, highly perfused organs) are more

on a 80 kVp image than on a 140 kVp image. This difference in attenuation varies between different organs; for example, highly vascular organs and vessels have higher difference than muscles (Figs 2A to H). Postprocessing softwares use this information to generate a virtual noncontrast image, or

A

B

C

D

E

F

G

H

Table 1: Atomic number and k-edges of different substances and radiographic contrast agents11 Substance

Atomic number

K-edge (keV)

Hydrogen

1

0.01

Carbon

6

0.28

Nitrogen

7

0.40

Calcium

20

4

Iodine

53

33.2

Barium

56

37.45

Figs 2A to H: Different CT attenuation of tissues at different energy Fig. 1: Principle of dual-energy CT. Change in CT attenuation of substances at different energy levels of incident beam. Iodine (k-edge 33.2 keV), shows a peak attenuation at lower energies and a rapid decrease in attenuation at higher energies. When attenuation at 50 and 80 kVp are compared; iodine shows a greater decrease (A) in attenuation at higher energy than calcium (B). Water shows very minimal change in attenuation with changes in kV. This forms the basis of material characterization in dual-energy CT

levels, based on their constituents. Highly vascular organs containing iodine on CECT shows higher attenuation at lower-energy images. For example, renal parenchyma shows an attenuation of 250.8 HU at 70 kV images and 144.4 HU on 140 kV images (A and B). Calcium shows very little variation in the attenuation values over a change of energy from 70 to 140 kV (C and D). Water also shows very little change in attenuation (E and F). Fat, to the contrary, shows a minimal increase in attenuation at higher energy images (G and H); –116.2 HU at 70 kV and –96.7 HU at 140 kV

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to calculate the material composition within a specific region of interest.

DUAL-ENERGY RATIO The material characterization on DECT largely depends on their dual-energy ratio. The dual-energy ratio is a materialspecific parameter. It depends on the atomic number, not on the material density or concentration. For experimental derivation of dual-energy ratio of a given material X, the CT attenuations at any given kVp (for example, 140 kV) at different material concentrations are assessed and arranged along a graph (A). Similar graph (B) is made for different material concentrations at another kVp (for example 80 kVp). The dual-energy ratio of material X can be described as a ratio of the slope of the graph B to the slope of graph A.12 The difference between dual-energy ratio of different materials depends on several factors, for example: 1. Difference in the atomic number of the materials and 2. Spectral separation between X-ray spectra at the two energies. If the two incident X-ray beams have mean energies very close to each other, the difference in dualenergy ratios among various component materials (for example, iodine and soft tissue) will be less, and it will be difficult to differentiate them on imaging.

Spectral Separation and Selective-photon Shield As a continuation of the previous discussion, for efficient dual-energy imaging the two incident X-ray beams should have sufficiently different energies. In reality, whenever X-ray is generated, it is emitted in the form of a continuous spectrum with photons having different energy levels (Bremsstrahlung) and a mean energy. The mean energy of an X-ray spectrum

A

varies with the bombarding energy (kV). When two tubes with different kV are used, two spectra are generated with significant overlap between them (spectral overlap) (Figs 3A and B). As described earlier, the spectral overlap makes material characterization more difficult. Spectral overlap also reduces the dose efficiency as the 140 kVp spectrum contains significant percentage of low-energy photons also, which add to the patient dose. Spectral separation indicates a situation when there is minimal overlap between the different energy spectra, i.e. less spectral overlap. Adequate spectral separation can be achieved by several methods: 1. Adding separate filtration to one or more tubes in DS-DECT.13 2. Adding split filtration to SS-DECT.14 3. Sandwich (dual) detectors. 4. Energy discriminating, photon counting detectors. In DS-DECT, either one or both the tubes can have additional filtration. However, adding filters to the low-energy tube will further cut off the resultant kVp making it impossible to image a larger patient; hence, it is not practiced. Adding filtration to the higher-energy tube in the second-generation scanners using tin filters, termed selective photon shield, has led to improved spectral separation (Figs 3A and B).12 Selective-photon shielding also improves the SNR efficiency and reduces dose to the patient. Tin is chosen as a filter component as it is inexpensive and easily available. The ideal thickness of filter varies between 0.5 and 0.8 mm.

Dual-source DECT In the first-generation dual-source DECT scanner, X-rays are generated by two X-ray tubes, which are kept at 90 degrees angle to each other in the same gantry and operating at

B

Figs 3A and B: Spectral separation. When high- (140 kV) and low-energy X-rays (80 kV) are used, there is a significant energy overlap between them (shaded area A). Hence, generation of a true monoenergetic beam becomes difficult. After the use of a selective tin filter with the higherenergy tube in second-generation DS-DECT scanners (B), the lower-energy X-rays from 140 kV tube are filtered, thereby, reducing the overlap (shaded area B). This leads to better spectral separation, proper monoenergetic imaging and better material characterization

Chapter 42 Dual-energy Computed Tomography

different kVp (Fig. 4A). The average kVp of the higher-energy tube is 120–140 and that of the lower-energy tube is 80–100. The tube with larger kVp (tube A) has a larger detector of FOV 50 cm, and the lower energy tube (B) has a smaller FOV detector (26 cm). In the second-generation DS-DECT (Fig. 4B) scanner, the lower-energy tube (tube A) is paired with a detector with FOV of 50 cm while the higher-energy tube (tube B) is paired with a smaller detector with FOV of 33 cm. Higher-energy tube has a selective-proton shield made of tin filter. Two separate detector arrays lead to generation of

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two image datasets. Since both the tube kVp can be modified independently and additional selective-photon shield can be used in DS-DECT scanners, it results in better spectral separation. The temporal resolution of a DS-DECT is onequarter of the rotation time (approximately 75 ms), as one X-ray tube acquires data during 90° of rotation. However, the drawback of DS-DECT lies in term of temporal mis-registration, since the scans are not acquired simultaneously, but at a small time gap (although in ms). Another drawback is the limited dual-energy FOV (33 cm),

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Figs 4A to C: Dual-energy scanners—the first-generation DS-DECT scanners (A), the second-generation DS-DECT scanner (B) and SS-DECT scanner (C). In a first-generation DS-DECT scanner, two tubes are placed in the gantry at an angle of 90° to each other. Tube A has a higher kVp (140) and had a larger detector array of FOV 50 cm. The smaller-detector array (26 cm FOV) is paired against the lower-energy tube (80 KV). In a second-generation DS-DECT scanner, the smaller detector (FOV 33 cm) is paired with a higher-energy tube with a selective-photon shield. The SS-DECT scanner has a single tube and a detector array with 50 cm FOV. There is rapid switching of kVp in the tube

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which makes it difficult to image patients with larger body habitus.

Processing of Data and Image Reconstruction in Dual-energy Imaging

Single-source DECT

The images generated from a DECT should have the combined morphologic data and material specific information. To obtain a material-specific image, the datasets can be processed in two ways: 1. Processing after the reconstruction of low- and highenergy images; which is also called ‘image domain decomposition’. This method is used in DS-DECT scanners and dual (sandwich)-layer detector DECT scanners. In DS-DECT, images are generated by linear or nonlinear sigmoidal blending of both (high and low energy) datasets.19 In linear blending, a specific ratio of both high and low energy data are used. In sigmoidal blending, the pixels with higher attenuation are selected from the low energy datasets and the pixels with low noise are selected from high energy datasets. Material-specific images are obtained by calculating the difference in attenuation of varying materials between the low and high energy image datasets. For abdominal DS-DECT, a three-material decomposition (soft tissue, fat and iodine) process is commonly used to generate virtual noncontrast images. A color-coded overlay image (usually iodine overlay in abdominal imaging) is generated by assigning a color to the voxels containing the material and overlapping them on monochromatic images.20,21 2. Processing before the images are reconstructed from high and low energy sinograms; also called ‘projection-space decomposition’. It is a more robust processing which is preferred because of greater flexibility in material decomposition, and minimizing beam-hardening artifact.9 In this method, after data acquisition, the 80 kVp images are not routinely reconstructed. The highand low-energy datasets are calibrated and aligned in projection space to generate material density image and monochromatic images (providing energy- selective information). Material density image reconstruction

Single-source DECT (SS-DECT) scanners use a single X-ray tube, which generates high- and low-energy X-ray spectra by rapid changing of the kVp settings (at an interval of 0.5 msec) in the same rotation (Fig. 4C). Since the tube current cannot be changed so rapidly, in order to maximize the contrast to noise ratio, the exposure time ratio is changed between two acquisitions. For example, 65% exposure time is given for the 80 kVp beam and 35% for the 140 kVp beam.15,16 The SS-DECT requires a very- fast detector and data-acquisition system with fast-sampling capability. The detector arrays used in SS-DECT are made of cerium-activated garnet (Gemstone Spectral Imaging; GE Healthcare, Piscataway, NJ). The advantage of SS-DECT over DS-DECT includes: 1. Better temporal registration between two datasets, as the images from high and low-energy acquisition are acquired almost simultaneously. 2. Larger FOV of imaging (50 cm) and easier quantification of material density. The disadvantage of SS-DECT includes a poorer spectral separation (hence less accurate material characterization compared to DS-DECT with selective photon shielding) as a selective-photon shield is not commercially available in such scanners (refer to previous paragraphs).

Dual-energy CT with Layered Detectors This scanner contains a single X-ray source with hybrid detector for high and low energy imaging. The top layer captures low energy data and the bottom layer captures highenergy data; which are then used to reconstruct two separate image datasets.17 Such scanners are under development with Philips, not yet commercially available. Table 2 summarizes the comparison of DS-DECT and SS-DECT scanners.18

Table 2: Comparison between single-source and dual-source dual-energy CT17 Single-source-DECT

Dual-source-DECT

Tubes

Single X-ray tube with rapid switching of kVp

Two tubes operating at different kVp

Field of view (FOV)

Larger, 50 cm

FOV of dual energy acquisition 33 cm

Temporal and spatial registration

Good

Limited, as two separate image datasets are acquired

Spectral separation

Limited

Good, further improved by selective-photon shield (tin filter)

Data processing

Projection space dual-energy decomposition Image domain decomposition (limited flexibility) (more flexible)

Noise on lower kVp images

Higher (as tube current can not be modulated Less (because of modulation of individual tube while kVp is being altered) current)

Calculation of HU value on virtual Not possible NCCT image

Possible

Prototype

Somatom Definition; Siemens

Discovery CT 750 HD; GE healthcare

Chapter 42 Dual-energy Computed Tomography

in based on the theory of basis material decomposition; which proposes that the attenuation coefficients of any material can be computed as a weighted sum of the attenuation coefficients of two basis materials as long as the k-edge of the material is not within the evaluated energy range.2,3 The two base materials should have highly different atomic number. The commonly selected dual energy basis material pairs are iodine and calcium, and iodine and water. Two separate sets of material density images are generated (iodine density and water density images, for example). The lesions containing iodine (for example, enhanced organs, vessels) will show higher attenuation on iodine-density images than on water density images. Monochromatic images are generated during the processing of material density images by calculating the linear attenuation coefficient (μ) of an object.22 Advantage of a monochromatic image generated from a DECT over a single-energy image at the same kVp includes the reduction of beam hardening artifacts and provides accurate CT numbers.

Image Display in DECT Images generated in DECT can have two types of display: 1. Material-density display (Figs 5A and B): In DECT, the material-density display can be iodine-density display or water density display. — In an iodine-density display, the enhanced organs containing iodine appear bright whereas unenhanced areas remain dark. In abdominal

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imaging, iodine-density display has important role in the evaluation of a hyperdense cyst on CECT. Hemorrhagic/complicated cysts and often pose an imaging dilemma whenever incidentally detected on a CECT. On CECT images, they appear hyperdense and require an additional NCCT scan to rule out enhancement. On iodine-density display, they appear dark. Also, in the renal cysts, it can help reduce the problem of misdiagnosis of a cyst as a solid lesion due to ‘pseudoenhancement’, which refers to artifactual increase in CT numbers within a simple cyst on a single-energy CECT.23 — The water-density display is equivalent to virtual unenhanced images. Water-density display can obviate the need of an additional NCCT image acquisition when a CT urographic image detects a calculus within the pelvicalyceal system; or for detection of calcification within an enhancing mass lesion. 2. Monoenergetic image display (Fig. 6): The monoenergetic or pseudomonochromatic display are energy-specific display. Images are processed at any given kVp from the dual energy datasets, which resemble images physically acquired after scanning at that given kVp. Virtual monogengetic/ pseudomonochromatic images at lower kVp show higher-image contrast and make smallenhancing lesions more conspicuous than routine display at 70 kVp. However, the images at lower kVp (for example 40 kV) have more noise and higher kVp images have less contrast. The optimum-image contrast to noise ratio is achieved at 70 kVp.

B

Figs 5A and B: Material-density display. Iodine overlay map (A), created by overlapping the iodine-density images over monoenergetic image, highlight the organs containing iodine (colored red). The gradient of color varies according to the degree of enhancement of the organ. The water density display (B) is equivalent to virtual unenhanced image. Note that both calcium and iodine appear dense on a routine single-energy CT, but they can be differentiated on iodine map images as calcium will not be highlighted on a iodine map image (for example, the calculus in this image)

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Fig. 6: Virtual monoenergetic images generated from a DS-DECT scanner. It is evident from the images that the attenuation of iodine and the image contrast are high at lower-energy images, although the images appear more noisy. As the kVp increases, the contrast difference between various tissues becomes negligible and the 160 keV image becomes identical to a noncontrast image

APPLICATIONS OF DECT Applications in Abdomen Renal Applications 1. Renal calculi characterization (Figs 7A and B): On the basis of the dominant chemical component, urinary calculi can be divided into either uric acid (UA) or nonuric acid calculi. Uric acid calculi are often associated with metabolic causes such as hyperuricemia or gout. These stones are lucent on radiograph but can be identified on CT. Nonuric acid calculi are further divided into calcium, cystine and struvite. Calcium calculi are the most common type and contains calcium oxalate monohydrate (COM), calcium oxalate dihydrate (COD), calcium phosphate and hydroxyapatite in a variable proportion. Struvite stones are composed of magnesium ammonium phosphate (triple phosphate) and are the major constituent of a stag horn calculus (calculus in pelvis with extension into at least two calyces). Cystine calculi are rare and associated with certain metabolic conditions, such as cystinuria. A calculus containing both uric acid as well as nonuric acid component is labeled as mixed calculus. Determining the composition of calculi has direct treatment implications. Uric acid stones can be treated medically whereas cystine and COM stones are resistant to extracorporeal shock-wave lithotripsy (ESWL) and percutaneous nephrolithotomy (PCNL) is preferred.24

Till now, single-energy NCCT has remained the usual standard investigation for evaluating urinary tract calculi. However, single-energy NCCT is unreliable for characterizing the type of calculi since calculi of different proportions of constituents can have overlapping CT attenuation values. When imaging is done on DECT scanners, the change in attenuation between high-and low-energy scans can be used to differentiate types of calculi.25 UA calculi are composed of light elements whereas non-UA calculi are composed of heavy elements; hence, these two groups can be differentiated on imaging. On SS-DECT, calcium and uric acid material density images are generated, uric acid calculi are depicted on uric acid material density images and calcium containing calculi on calcium density images. DS-DECT has an added advantage of selective photon shield (tin filtration) in the 140 kVp tube for better spectral separation and more accurate composition analysis. In a DS-DECT scanner, keeping the reference dual-energy ratio at 1.13, the uric acid calculi are seen to lie below the reference line and non-UA calculi above it (Figs 7A and B). Several ex vivo studies have demonstrated the efficacy of DECT in characterizing stones, and also the advantage of additional tin filtration.26-28 2. Renal cysts: Detecting a simple cyst with water density is not an imaging challenge. Differentiating a complex/ complicated renal cyst from a solid renal mass lesion is often difficult, and depends on the detection of

Chapter 42 Dual-energy Computed Tomography

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Figs 7A and B: Renal calculi characterization by DECT. Images acquired at 100 and 140 kV in a DS-DECT scanner. A reference dual-energy ratio of 1.13 is taken to differentiate uric acid from nonuric acid calculi. The uric acid calculus (A) shows a dual energy ratio less than 1.13 and are colored red (arrow). The nonuric acid calculi show a dual-energy ratio above the reference line and are colored blue (B)

enhancement in the lesion. Conventional single-energy CT will require two acquisitions, one NCCT and another CECT. Using dual energy CT, the additional acquisition of NCCT can be avoided as it is possible to generate virtual NCCT from the datasets. On iodine-density images, the enhancing solid mass will appear bright; whereas high density cysts will be dark, since they do not have any iodine in them.29 In SS-DECT, it is not possible to calculate the HU value of the lesion, which is possible with DS-DECT.30 Moreover, effective beam hardening reduction in DECT helps avoid the phenomenon of ‘pseudoenhancement’ (vide supra). 3. Renal mass characterization and follow-up after ablation: Calcification within an enhancing renal mass can be detected on a virtual NCCT image generated from a dual-energy dataset. After thermal ablation of solid renal masses, the imaging assessment should consist of multiphase scanning with and without contrast to detect enhancement in residual tumor tissue. While imaging on DECT scanners, one contrast-enhanced acquisition can generate virtual NCCT scans, thus reducing the total dose to the patient. Iodine overlay maps help detect the enhancement in such masses. Both DS-DECT and SS-DECT have a few technical limitations for the evaluation of re nal masses. Firstly, virtual NCCT images have more image noise than real NCCT images. Second, because of the material decomposition algorithms used, calcification in renal lesions is less conspicuous on virtual unenhanced images than on real unenhanced images. Third, smaller amounts of fat in renal masses are difficult to detect on virtual NCCT images and can be measured only on conventional thin-section unenhanced CT images. 4. CT urography: CT urography is a routine imaging procedure in the evaluation of hematuria and multiple phase acquisitions (NCCT and delayed images) are performed for CT urography. On DECT imaging, virtual NCCT generated from the dual energy datasets can obviate the need for an additional NCCT acquisition and

thus reduce the radiation dose. Takahashi et al.31 reported that on virtual NCCT from excretory-phase CT urography performed with a DS-DECT scanner, the rate of detection of urinary tract stones was 100% for stones larger than 7 mm but decreased significantly (29%) for stones of 1–2 mm size. Quality of the generated virtual NCCT images depends on iodine concentration within the pelvicalyceal systems, hence a highly concentrated iodinated contrast material within the PCS may lead to a ‘rim artifact’ at the margins and obscure small calculi. Incomplete subtraction of concentrated iodine can also be mistaken as calculi.31

Applications in Adrenal Adrenal Adenoma Adrenal adenomas are common imaging occurrences, and most of them are detected incidentally on abdominal CECT scans. Attenuation of less than 10 HU on NCCT image is virtually diagnostic of adrenal adenoma. When an incidental adrenal nodule is detected on single-energy CECT, it becomes essential to get a delayed scan or separate NCCT scan for characterization of the nodule. On a DE-CECT acquisition, virtual NCCT images generated from the dual energy datasets help eliminate the need of another NCCT scan. The attenuation of adrenal adenoma at low and high kVp image depends on their lipid content. On several studies, there have been mixed reports related to the attenuation of adrenal adenoma on 80 and 140 kVp scans.32,33

Hepatic Mass Characterization 1. Characterization of hepatic mass lesions: Solid hepatic mass lesions are typically evaluated using a multiphase CECT. Like other organs, NCCT acquisition in liver also can be avoided by generating a virtual NCCT image from DECT acquisition in any one of the phases of multiphase CECT protocol. Secondly, hypervascular liver lesions

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Figs 8A and B: Simple hepatic cysts, imaging performed on a second generation DS-DECT scanner. Simulated monoenergetic image display at 70 kV generated from a dual-energy dataset (A) shows hypodense focal lesions in segment III and V (arrows). Iodine overlay maps (B) show them to be dark (not taking up iodine)

are most conspicuous in arterial phase of examination, however detection of a hypervascular lesion on a delayed arterial phase becomes difficult. In such a scenario, on a DECT scan, the lesions can become more appreciable on a lower kVp image.34,35 Monochromatic low kVp images and iodine-density display make detection of small hyperenhancing liver lesions easier. Non-enhancing lesions or cysts appear dark on iodine density maps (Figs 8A and B). 2. Follow-up after hepatic tumor ablation or TACE: After tumor ablation or embolization, detection of recurrence/ viable tumor depends on the demonstration of tumor mass enhancement, which in turn needs acquisition of both NCCT and a CECT scan in proper phase. With DECT, single CT acquisition can generate virtual non-contrast scans and iodine maps to detect enhancement; thereby avoiding excess radiation exposure. A word of caution needs to be remembered while imaging hepatocellular carcinoma after chemoembolization with lipiodol. Since lipiodol contains high concentration of iodine, iodine density display images shows the lipiodol accumulation as bright spot/hyperenhancement; which should not be diagnosed as recurrent or residual tumor.36 3. Hepatic steatosis or iron deposition: Hepatic focal fat deposition is often a diagnostic dilemma as it mimics solid tumor. Though there are several pointers like typical distribution and geographic nature of lesion and lack of mass effect on adjacent vasculature; sometimes, the diagnosis may be difficult on a single phase single energy CT. DECT can differentiate focal fat deposition from other hepatic mass lesion in the absence of iron deposition, which is a confounding factor. 11,37,38 Studies have described that attenuation values that are 9–13 HU lower at 80 kVp than at 140 kVp are suggestive of fat infiltration

(Figs 9A to E).37,38 Iron deposition in liver parenchyma will have higher attenuation at lower energy images.11

Application in Pancreas Pancreatic neoplasms are usually hypovascular and their detection is based on the attenuation difference between the normally enhancing pancreatic parenchyma and hypoenhancing mass lesion. Pancreatic parenchymal enhancement is best assessed in the pancreatic phase, 40–70 sec after injection of contrast material. However, significant percentage of pancreatic carcinomas are difficult to detect even on pancreatic phase images.39 With DECT, the normally enhancing pancreatic parenchyma shows higher attenuation on monochromatic lower-energy display image and the iodine-density display. It has been seen that the attenuation difference between the lesion and normal pancreatic parenchyma (hence the lesion detection) increases with 80 kVp image than a single-energy routine 120 kVp scan.40 Another potential application of DECT in pancreatic imaging is the accurate identification of pancreatic necrosis; although the clinical importance is not yet established.11

Pulmonary Applications 1. Pulmonary thromboembolism: Pulmonary thromboembolism (PTE) imaging has undergone significant change in the past few years. Pulmonary CT angiography (CTA) has been accepted as the imaging modality of choice in case of suspected high-risk population. Pulmonary CTA can detect intraluminal thrombus in segmental arteries and smaller vessels also, but smaller clots/partial occlusion in subsegmental arteries can be missed on CTA. When

Chapter 42 Dual-energy Computed Tomography

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B

C

D

E

Figs 9A to E: Focal hepatic steatosis. The area of focal fat deposition is seen as a hypodensity in segment 4b adjacent to the falciform ligament (arrow in A). Monoenergetic display (B) derived from a DSDECT scanner (Somatom Definition Flash, Siemens) with tin filtration shows the increase in attenuation in higher kV images (attenuation of 23.8 at 70 kV, shown with a yellow line and 34.2 at 140 kV, shown with a red line) (C), which is suggestive of fatty change. In comparison, normal enhancing liver parenchyma shows a decrease in attenuation (D and E) in the higher energy images (attenuation of 82.1 at 70 kV and 64.1 at 140 kV images)

imaging is done on a DECT scanner, smaller clots can be detected on an iodine overlay map visible as a perfusion defect. Compared to CTA and scintigraphy, dual-energy CT has a high sensitivity and specificity for perfusion mapping for the assessment of pulmonary embolism.41,42 The perfusion defects in cases of pulmonary embolism are usually peripheral and wedge-shaped; although they can be absent in cases of very small nonoccluding thrombus in smaller vessels. For the generation of a proper iodine perfusion map of the lungs, the maximum and minimum value for material decomposition are usually kept at -600 and 960 HU. It excludes all the enhancing mediastinal structure and all central vessels in the lung parenchyma from the iodine perfusion map. Hence, the relatively less perfused area in case of thromboembolism can be easily

visualized as perfusion defect (Fig. 10). For obtaining proper parenchymal enhancement, iodinated contrast agent should be injected at a proper rate (4–4.5 mL/ sec), followed by 40 mL saline chase to reduce artifacts resulting from dense contrast in SVC/ brachiocephalic vein. Imaging should be done in both pulmonary and aortic phase. A threshold value of 20 HU mean iodine attenuation can be used to differentiate areas of lung parenchyma with negligible perfusion from those with demonstrable flow. Perfusion defects can also be seen from non-PTE causes; for example, in cases of aberrant pulmonary vascular supply,43 or artefactual perfusion defects as in the lingual or right middle lobe (from cardiac pulsations), bilateral lower lobes near the diaphragm (from respiratory motion), in bilateral upper lobes (from streak artifacts in SVC or subclavian artery). Perfusion defects are also observed in parenchymal abnormalities, such as consolidation, atelectasis or emphysema (Figs 10A to I).44,45 2. Xenon perfusion CT: Xenon is a radiopaque gas with atomic number 54 and has photoelectric absorption characteristics similar to iodine. 46 During xenon ventilation CT, the patient usually inhales 30% xenon through a xenon gas inhalation system (Zetron V; Anzai Medical, Tokyo, Japan). Overlay maps are generated similar to iodine perfusion CT. DE xenon ventilation CT can be used to generate a ventilation map with areas of bronchial obstruction or atresia showing reduced ventilation.47,48 3. Pulmonary nodule evaluation: The degree of contrast enhancement on CECT is an important factor in differentiating a benign pulmonary nodule from a malignant one. DECT can generate virtual NCCT images and thereby quantify the enhancement. The differentiation of calcification from contrast enhancement is also possible on a single DE- CECT acquisition, thereby saving the additional radiation exposure of NCCT.

Musculoskeletal Applications 1. Application in gout: Gout is a disease resulting from intra-articular or soft-tissue uric acid crystal deposition leading to severe deforming arthropathy and gouty tophi formation. The causes may be multifactorial. Most often the diagnosis can be made on clinical and biochemical basis; however, the definitive diagnosis of gout requires microscopic analysis of fluid aspirated from the joint with the finding of negatively birefringent monosodium urate (MSU) crystals.49 But few studies have described a rate of negative aspiration as high as 25% in acute attacks.50 Plain radiography can show the arthropathy and corticated bone erosions in case of gouty soft tissue tophi. On DECT, the dual-energy ratio (vide supra) of uric acid varies significantly from that of calcium; hence, they can

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be easily differentiated. DS-DECT scans can generate material specific images and keeping the reference dualenergy ratio at 1.36, the uric acid crystals lie below the line and are differently color-coded (green), whereas the calcium deposits lie above the line (Figs 11A to D). The utility of DECT in gout diagnosis is twofold. First, it can

diagnose gout in an easy, noninvasive and reproducible manner. Secondly, using automated volume software, the tophi volume can be quantitatively measured with less interobserver variability.51,52 2. Metal artifact reduction: Imaging of patients with metallic prosthesis remains a challenge. As the X-ray beam passes

A

B

C

D

E

F

G

H

I

Figs 10A to I: Dual-energy CT perfusion in chronic pulmonary thromboembolism. Coronal reformatted CTA image acquired at pulmonary phase (A) shows non-enhancement and attenuation in caliber of the lower lobe pulmonary arteries (arrows). Aortic phase image reveals hypertrophic bronchial arteries (small arrows in B). Iodine overlay maps generated from dual-energy CTA during pulmonary phase (C and D) reveal patchy areas of perfusion defect in the basal segments of both lower lobes (arrows in D). Iodine maps (E and F) generated from aortic phase images shows near complete perfusion (via bronchial collaterals) in the corresponding area. Volume-rendered images generated from iodine distribution maps in pulmonary phase (G) also shows the areas of perfusion defect (black arrow); whereas aortic phase image (H) shows near complete perfusion except a small area of non-perfusion (notched arrow) secondary to a large bulla. Lung window axial image (I) confirms the presence of the bulla (arrow)

Chapter 42 Dual-energy Computed Tomography

A

B

C

D

Figs 11A to D: DECT in gout imaging. Scanning was performed at 80 and 140 kV in a patient with chronic gouty arthritis. Keeping a reference dual energy line at 1.36, MSU crystals are color-coded green. Color-coded volume rendered imgaes of the ankle (A) and knee (B) reveal extensive MSU crystal deposition around the joints. Plain radiographs of the feet and knee reveals periarticular soft-tissue swellings and corticated erosions (arrows in C and D)

through metal prosthesis, the lower energy photons are absorbed and the character of the X-ray spectrum changes (it becomes ‘harder’, i.e. having higher energy photons only). This gives rise to the beam hardening artifacts around metallic prostheses which hamper the visualization of periprosthetic abnormalities. The usual modifications to reduce metal artifact in a single energy scanner include: — Increasing the kVp, — Increasing the mAs, — Reducing slice collimation, — Using a softer kernel for reconstruction, and — Thicker slice reconstruction. Using DECT, monoenergentic reconstruction at a higher kVp has been shown in several studies to be more effective than routine single energy CT images at 120 kVp.53,54 3. Other musculoskeletal applications: Although evaluation of gout has remained the most widely used

musculoskeletal application of DECT, there are several other applications, for example, detection of bone marrow edema55 and evaluation of ligaments and tendons.56-59 Bone marrow edema is ideally best evaluated by MRI. Pache et al.55 described high sensitivity and specificity of DECT imaging in the detection of post-traumatic bone marrow edema. Using a three material decomposition (water, fat and calcium), the virtual non-calcium subtracted images can be generated to detect marrow edema. Tendons and ligaments are made up of collagen fibrils, which have a specific dual-energy ratio. In DECT, for material specific image generation a three material decomposition algorithm is used (collagen, fat and soft tissue). Several studies56-59 have showed conflicting efficacy of DECT in the evaluation of tendons and ligaments. Thicker ligaments like anterior and posterior cruciate ligaments and patellar ligament can be adequately visualized, however visualization of thinner anatomical structures may not be appropriate.

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Applications in Head and Neck Like other parts of the body, DECT imaging in head and neck also has the advantage of generating a virtual NCCT image from the dual-energy dataset, without the need for an additional non-contrast scanning in order to quantify enhancement in a mass lesion. Iodine overlay maps can increase lesion conspicuity of head and neck masses. Recent study by Kuno et al.60 has also demonstrated improved diagnostic performance and interobserver reproducibility by DECT imaging in laryngeal cartilage invasion in head and neck squamous cell carcinoma.

Vascular Applications Dual-energy CT angiography has been most widely used in aortic imaging. The advantages of DECT in aortic stent-graft imaging are multiple. First, virtual monoenergetic high kVp images in DECT are more effective in metal artifact reduction.54 Secondly, the virtual monoenergetic low kVp images are more sensitive in detection of iodine (hence small endoleaks which are otherwise difficult to detect), though have a high image noise. An optimum monoenergetic image can be generated to balance the iodine density and the image noise. Third, the iodine overlay map can detect smaller endoleaks (differentiate between blood and contrast).61 Fourth, DECT acquisition can help generate a virtual NCCT image which can detect intramural hematoma and has comparable image noise as that of a true NCCT image.62 Fifth, the DE subtracted angiographic images are easier to generate and provide more complete bone removal. Finally, In endoleak detection, single-delayed DECT scanning followed by reconstruction of virtual NCCT and mono energetic low-kV images has very high sensitivity, specificity and positive predictive value (96–100%) compared with a conventional multiphase single energy CTA acquisition, thereby significantly reducing the patient dose (40–64%).63,64 In peripheral or neck angiography, the drawbacks of threshold based bone subtraction is that in cases of arteries lying close to bone, a part of the artery can be subtracted and may mimic stenosis or occlusion. Since the bone subtraction in DECT is based on material differentiation, it takes less time and yields more complete bone removal (Fig. 12), which can reduce such artifacts.65 Unlike single energy CTA with threshold-based bone subtraction, DECT CTA can remove calcified plaques also, with better visualization of vascular lumen. Compared to threshold based bone removal, DECT bone subtraction are easier, quicker and more accurate in detection of vessel stenosis.66

Cardiac Applications Coronary CT angiography in a multidetector row scanner has become an established imaging tool in the detection of

Fig. 12: Volume rendered CTA image of the head and neck in a 10-year-old male with proliferative hemangioma (arrow) on the right side of face. The bone removal in dual energy CTA depends on material differentiation and leads to complete and quick bone subtraction compared to threshold based bone subtraction

significant coronary artery disease (CAD) in low to intermediate risk population.67,68 However, the mere detection of an artery stenosis does not predict the hemodynamic significance of it, which can be predicted by myocardial perfusion imaging or wall motion abnormalities. Till now, myocardial perfusion studies have been performed using nuclear medicine studies (SPECT) and MRI. However, SPECT has poor spatial resolution and is not useful for coronary artery assessment. MRI can detect myocardial perfusion and cine-MRI can detect regional wall motion abnormality; but it is timeconsuming and not useful for morphologic assessment of coronary artery disease.69,70 With the use of DECT technology, material density (iodine) maps can be generated for the myocardium, reflecting the myocardial perfusion. Although termed ‘perfusion’, the map usually reflects the myocardial blood pool and is a static acquisition. A typical DECT cardiac perfusion study consists of the following phases- an initial calcium scoring followed by arterial phase scan, injection of IV adenosine and acquisition of stress images 3 minutes after IV adenosine (140 μg/min/kg) infusion, rest scanning 2 minutes after the stress scan when the heart rate returns to the baseline level. Finally, a delayed scan (5–10 min) is acquired. Monoenergetic low kV, high kV and iodine overlay maps are generated.71 Normally perfused myocardium show uniform iodine distribution (Figs 13A and B). Myocardial infarcts are visualized as perfusion defects both at rest and under stress, whereas reversible ischemia shows perfusion defect only in stress images. Nonviable myocardium will show hyperenhancement on delayed scans.72 DECT thus can combine the benefits of superior resolution morphologic imaging in CAD coupled with detection of its hemodynamic significance in the form of ischemia/infarction, which is unique to this modality.

Chapter 42 Dual-energy Computed Tomography

A

B

Figs 13A and B: Stress myocardial perfusion imaging using DECT. A 52-year-old lady with effort intolerance. Iodine overlay maps at rest (A) shows perfusion defect (arrow) in the territory of the left anterior descending coronary artery (LAD) which is exaggerated on adenosine stress images (B); LAD territory ischemia

Material differentiation based on dual-energy ratio has been tried in the characterization of plaques. Although differentiating a calcified from a noncalcified plaque is possible, but the differentiation of various types of noncalcified plaques have not been successful.73

Applications in Neuroimaging As discussed for CTA elsewhere in the body, dual-energy CTA of intracranial vessels also has the similar advantage of easy and quick bone removal, especially with complex bony anatomy at the base of skull.74 Other advantages of DECT scanning include avoidance of additional non-contrast scanning in certain circumstances. For example, In a patient with suspected subarachnoid hemorrhage, a preliminary NCCT scan can be avoided and direct dual-energy CTA can be performed to look for the etiology. The virtual NCCT images generated from the dual energy dataset helps detect hemorrhage and can save crucial time.75 Studies have described dual energy CTA to be the ideal tool for evaluating an acute intracranial hemorrhage. Apart from the ease of assessment of vascular cause of hemorrhage (vide supra); iodine overlay maps can be useful in differentiating tumor bleed from a simple hematoma.76 Hemorrhage within a tumor will show hyperdensity on NCCT images and detection of any enhancing mass lesion in the background of hemorrhage can be an imaging challenge. Iodine overlay maps can detect the enhancing tumor tissue in the background of hematoma with greater accuracy; and also saves the patient from an additional radiation of NCCT scan.

DOSE CONSIDERATIONS Although DECT scanning involves imaging with two different X-ray beams, the dose is not doubled in comparison to the

single-energy scan. This is because the mAs are divided in the two sources; the higher-energy tube operates at a lower mAs and the lower-energy tube utilizes a relatively higher mAs. Till date, several experimental studies have been performed regarding dose comparisons of DECT scanning and singleenergy scanning. Most of the experiments are based on DS-DECT scanners. Data are sparse regarding dose issues in SS-DECT. There has been various studies comparing dose of the single and dual energy scanners, but very few of them are performed with normalization of the contrast to noise ratio (CNR) or image quality.77 Schenzle et al.77 performed a study on anthropomorphic phantom equipped with TLDs, with scanning performed at 140 and 80 kVp, 14 × 1.2 collimation in a first-generation DS-DECT scanner and in a second-generation DS-DECT scanner at 140 and 100 kVp settings with selective-photon shielding at 128 × 0.6 mm collimation. Dose comparison was done with a single-energy scan at 120 kV and 64 × 0.6 mm collimation at an equivalent dose index of 5.4 mGy x cm. The respective doses were 2.61 mSv (first-generation DS-DECT in dual-energy mode), 2.69 mSv (second-generation DS-DECT in dual-energy mode), 2.70 mSv (second-generation DS-DECT in single-energy mode). The image noise were also similar in all these three imaging techniques. Hence, there was no significant dose difference between the imaging techniques. In coronary CTA, the dose received by DECT imaging has been assessed by Kerl et al.,78 who compared the dose levels between DECT, first-generation DS-DECT in singleenergy mode, and single-energy single source 16 slice MDCT. The investigators reported a lower dose, higher CNR and good diagnostic image quality in DECT than single-source MDCT. The increase in CNR was attributed to the low- kVp acquisition in DECT scanning by the investigators. Several other studies78,79 regarding CT pulmonary angiography or CTA have shown that there is no significant increase in dose

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Section 2 Recent Advances and Applied Physics in Imaging

Table 3: Advantages and drawbacks of DECT Advantages of DECT

Disadvantages of DECT

Material specific image can be generated. Characterization of renal Increased radiation dose ( which can be reduced using SPS) calculi composition made possible Obviates the need for additional acquisition of NCCT images in Storage needs large capacity many clinical indications, thereby reducing dose Direct CT angiography—saves tedious post-processing and manual Lower kVp image has inherent increased noise. Scanning may not be bone removal suitable in obese patients Wider applications based on material characterization

Second detector in DS-DECT has smaller FOV, hence may not be beneficial in obese patients

Increased temporal resolution (helpful in cardiac CT)

while scanning by DS-DECT scanning, compared to a single energy scanning. The added benefit of DECT scanning lies in the generation of virtual unenhanced scans, which can obviate the need of another NCCT scanning and reduce radiation dose. In renal imaging, the replacement of NCCT by virtual NCCT can result in a dose reduction of up to 35% in first-generation DECT and up to 50% in second-generation DECT.80 Addition of tin filter in second-generation DS-DECT reduces the dose by eliminating lower-energy X-ray photons from the higher-energy spectrum. Future trends in DECT imaging towards using a sandwich detector or an energy specific, photon counting detector can reduce the radiation dose further, retaining the benefits of material characterization on DECT.

Limitation In spite of having significant advantages over single-energy CT in several applications, there are a few limitations of DECT (Table 3). First, the FOV of the smaller detector is significantly less in DS-DECT (33 cm in second-generation DS-DECT) which leads to incomplete area coverage in obese patients. Second, the images generated from the lower-energy tube have inherently high noise. Finally, the large number of datasets generated leads to a problem in storage and archival. Pitfalls in organ-specific imaging have been discussed in their respective sections.

CONCLUSION To conclude, dual-energy CT imaging adds another new di mension to conventional CT. the material-specific information gained by DECT scanning can be translated either to func tional analysis of organs (for example, myocardial perfusion analysis), improvement in diagnostic confidence (noninvasive confirmation of clinical diagnosis in gout), aid in management decision-making (for example in renal calculi) or to easy image postprocessing and avoidance of unnecessary scanning.

ACKNOWLEDGMENTS The authors sincerely acknowledge the contribution of Dr Gurpreet S Gulati for Figure 13 and Dr Ashu Seith Bhalla for Figure 10. The authors also sincerely acknowledge the contribution of Dr Sudeep Acharya and Dr Zohra Ahmad for Figure 7 and 11, respectively, from their MD thesis work at the Department of Radiodiagnosis, AIIMS.

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53. Bamberg F, Dierks A, Nikolaou K, Reiser MF, Becker CR, Johnson TR. Metal artifact reduction by dual energy computed tomography using monoenergetic extrapolation. Eur Radiol. 2011;21:1424-9. 54. Zhou C, Zhao YE, Luo S, et al. Monoenergetic imaging of dualenergy CT reduces artifacts from implanted metal orthopedic devices in patients with fractures. Acad Radiol. 2011;18:1252-7. 55. Pache G, Krauss B, Strohm P, et al. Dual-energy CT virtual noncalcium technique: detecting post-traumatic bone marrow lesions—feasibility study. Radiology. 2010;256:617-24. 56. Lohan DG, Motamedi K, Chow K, et al. Does dual-energy CT of lower extremity tendons incur penalties in patient radiation exposure or reduced multiplanar reconstruction image quality? AJR. 2008;191:1386-90. 57. Persson A, Jackowski C, Engström E, Zachrisson H. Advances of dual source, dual-energy imaging in postmortem CT. Eur J Radiol. 2008;68:446-55. 58. Deng K, Sun C, Liu C, Ma R. Initial experience with visualizing hand and foot tendons by dual energy computed tomography. Clin Imaging. 2009;33:384-9. 59. Sun C, Miao F, Wang XM, et al. An initial qualitative study of dual-energy CT in the knee ligaments. Surg Radiol Anat. 2008; 30:443-7. 60. Hirofumi Kuno, Hiroaki Onaya, Ryoko Iwata, et al. Evaluation of Cartilage Invasion by Laryngeal and Hypopharyngeal Squamous Cell Carcinoma with Dual-Energy CT. Radiology. 2012;265:488-96.  61. Ascenti G, Mazziotti S, Lamberto S, et al. Dualenergy CT for detection of endoleaks after endovascular abdominal aneurysm repair: usefulness of colored iodine overlay. AJR. 2011;196:1408-14. 62. Numburi UD, Schoenhagen P, Flamm SD, et al. Feasibility of dual-energy CT in the arterial phase: imaging after endovascular aortic repair. AJR. 2010;195:486-93. 63. Stolzmann P, Frauenfelder T, Pfammatter T, et al. Endoleaks after endovascular abdominal aortic aneurysm repair: detection with dual-energy dual- source CT. Radiology. 2008; 249:682-91. 64. Maturen KE, Kleaveland PA, Kaza RK, et al. Aortic endograft surveillance: use of fast-switch kVp dual-energy computed tomography with virtual noncontrast imaging. J Comput Assist Tomogr. 2011;35:742-6. 65. Yamamoto S, McWilliams J, Arellano C, et al. Dual-energy CT angiography of pelvic and lower extremity arteries: dualenergy bone subtraction versus manual bone subtraction. Clin Radiol. 2009;64:1088-96. 66. Brockmann C, Jochum S, Sadick M, et al. Dual energy CT angiography in peripheral arterial occlusive disease. Cardiovasc Intervent Radiol. 2009;32:630-7. 67. Mowatt G, Cummins E, Waugh N, et al. Systematic review of the clinical effectiveness and cost-effectiveness of 64-slice or higher computed tomography angiography as an alternative to invasive coronary angiography in the investigation of coronary artery disease. Health Technol Assess. 2008;12:iii–iv,ix–143.

Chapter 42 Dual-energy Computed Tomography 68. Stolzmann P, Donati OF, Scheffel H. Low-dose CT coronary angiography for the prediction of myocardial ischaemia. Eur Radiol. 2010;20:56-64. 69. Gaemperli O, Schepis T, Valenta I, et al. Functionally relevant coronary artery disease: comparison of 64-section CT angiography with myocardial perfusion SPECT. Radiology. 2008;248:414-23. 70. Greenwood JP, Maredia N, Younger JF, et al. Cardiovascular magnetic resonance and single-photon emission computed tomography for diagnosis of coronary heart disease (CE-MARC): a prospective trial. Lancet. 2012;379:453-60. 71. Weininger M, Schoepf UJ, Ramachandra A, et al. Adenosinestress dynamic real-time myocardial perfusion and adenosinestress first-pass dual-energy myocardial perfusion CT for the assessment of acute chest pain: Initial results. Eur J Radiol. 2012;81(12):3703-10. 72. Arnoldi E, Lee YS, Ruzsics B, et al. CT detection of myocardial blood volume deficits: dual-energy CT compared with singleenergy CT spectra. J Cardiovasc Comput Tomogr. 2011;5:421-9. 73. Henzler T, Porubsky S, Kayed H, et al. Attenuation-based characterization of coronary atherosclerotic plaque: comparison of dual source and dual energy CT with singlesource CT and histopathology. Eur J Radiol. 2011;80:54-9. 74. Watanabe Y, Uotani K, Nakazawa T, et al. Dualenergy direct bone removal CT angiography for evaluation of intracranial aneurysm or stenosis: comparison with conventional

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779

Computed Tomography Perfusion Imaging

43 CHAPTER

Veena Chowdhury

INTRODUCTION Perfusion computed tomography (CT) allows functional evaluation of tissue vascularity. It measures the temporal changes in tissue density after intravenous injection of a contrast medium (CM) bolus using a series of dynamically acquired CT images. The greatest impact of perfusion CT has been on the assessment of patients who have had strokes, wherein the rapid scan timing and faster image processing have cemented its role as the modality of choice for evaluation of structural and functional status of cerebral vasculature.1 In the field of oncology, perfusion CT has found applications in diagnosis, staging, prognostic evaluation and monitoring of response to therapies. 2,3 Although the role of ultrasound and magnetic resonance imaging have been explored for perfusion, there is a linear relationship between iodine concentration and density changes seen on CT expressed as Hounsefield units (HU), hence CT may be regarded as a preferred technique for perfusion imaging in general. Perfusion CT also has the potential to become the preferred technique for the assessment of tumor response to antiangiogenic drugs.4,5

PERFUSION COMPUTED TOMOGRAPHY TECHNIQUE BASIC PRINCIPLE The fundamental principle of perfusion CT is based on the temporal changes in tissue attenuation after intravenous administration of iodinated contrast medium. This enhancement of tissue depends on the tissue iodine concentration and is an indirect reflection of tissue vascularity and vascular physiology. After intravenous injection of the iodinated CM, the ensuing tissue enhancement can be divided into two phases based on the distribution in the intravascular or extravascular compartment. In the initial phase, the enhancement is mainly attributable to the distribution of contrast within the intravascular space and this phase lasts for approximately 40–60 seconds from the time of contrast injection. In the second phase, contrast passes from the intravascular to the extravascular compartment across the capillary basement membrane and tissue enhancement results from contrast distribution between the two compartments.

In the first phase, the enhancement is determined to a great extent by the tissue blood flow (BF) and blood volume (BV) whereas in the second phase, it is influenced by the vascular permeability to the CM.6 By obtaining a series of CT images in quick succession in the region of interest during these two phases, the temporal changes in tissue attenuation after injection of CM can be recorded. By applying appropriate mathematic modeling, tissue perfusion can be quantified. The various analytical methods vary from scanner to scanner and among the commercial vendors. Two most commonly used analytical methods are as follows: z Compartmental analysis: In this kinetic modeling technique, analysis can be undertaken using the single compartment or double compartment method. 4,6 The single compartment method assumes that the intravascular and extravascular spaces are a single compartment and calculates tissue perfusion based on the conservation of the mass within the system. It estimates perfusion using the maximum slope of peak height of the tissue concentration curve normalized to the arterial input function.7 Conversely, the double compartment method assumes that the intravascular and extravascular spaces are separate compartments and estimates capillary permeability and BV using a technique called Patlak analysis, which quantifies the passage of contrast from intravascular space into the extravascular space. z Deconvolution analysis: This CM kinetic modeling is based on the use of arterial and tissue time concentration curves to calculate the impulse residue function (IRF) for the tissue. The IRF is a theoretic tissue curve that is obtained from the direct arterial input, assuming that the concentration of contrast material in the tissue is linearly dependent on the input arterial concentration when the BF is constant.6,7 After accounting for the flow correction, the height of this curve reflects the tissue perfusion and the area under the curve provides the relative BV estimation.7 For the estimation of capillary permeability, a distributed parameter model is used, which is essentially an extended deconvolution method. Compartmental and deconvolution modeling methods have been found to be generally comparable, with differences in their theoretic assumptions and their susceptibility to

Chapter 43 Computed Tomography Perfusion Imaging

noise and motion.8 Compartmental analysis is based on the assumption that bolus of CM has to be retained within the organ of interest at the time of measurement, which may result in underestimation of perfusion values in organs with rapid vascular transit or with a large bolus injection.7 Deconvolution analysis, however, assumes that the shape of the IRF is a plateau with a single exponential washout. Although this assumption is believed to work for most organs, it might not be suitable for assessing perfusion in such organs as the spleen and kidney, which have complex microcirculations. Hence, it is preferable to use compartmental analysis for organs with the complex circulatory pathways. Deconvolution method is appropriate for measuring lower levels of perfusion (20 mT/m) with a fast slew rate. Fast switching gradients can lead to induction of eddy currents due to the changing magnetic fields produced. These degrade imaging sequences by producing geometric distortion, blurred images and artifacts like ghosting (Fig. 13). To overcome this, shielding of gradient coils is done, where a second coil surrounds the primary gradient coil and carries current in the opposite direction. These cancel the eddy currents but also reduce the overall strength of the gradient fields. These actively shielded gradients are increasingly used as rapid scan imaging protocols based on gradient echoes gained prominence. Specialized gradient coils are being developed for a variety of clinical applications. In echoplanar imaging, the requirements of gradient strengths, rise times and duty cycle have been increased as all the space is to be traversed in a single excitation. This requires each phase encoding projection to

Fig. 13:  “Eddy current’ artifact—inhomogeneities in the gradient cause distortion in the image

be acquired in less than 0.8 ms. Gradient coils required would have a maximum amplitude of 20 mT/m, minimum rise time of 0.1 ms (slew rate 200 T/m/s) and a duty cycle of 50–60%. This requires matching of gradient to power supplies that are capable of responding to the resonant mode at maximum amplitude and holding it at that level for a short period of time. Dual gradients’ have been developed wherein there is a short, higher-performance central region provided by one of the segments of the gradient tube and another mode of operation with the standard full region gradient. Specifically, in head imaging a physically smaller gradient tube can be used which combines improved gradient performance with satisfactory physical stimulation.14 At time of switching interval, the resulting force on the gradient coils is longer, producing a loud bang. Acoustic noise is the signature complaint of most patients about MRI. As gradient strength is increasing, so is the noise. Improvements in mounting techniques, use of damping materials and advances in materials used, placing the gradient tube in a vacuum have all been used to decrease the acoustic noise. One drawback of powerful gradients is peripheral nerve stimulation. There are standards that limit stimulation based on duration of the stimulus and the rate at which the magnetic field changes (db/dt). The shorter the stimulus the faster the magnetic field has to change to cause the stimulus. To decrease db/dt, gradient can be made shorter. Powerful gradient amplifiers are sited in a room with restricted access adjacent to the magnet room.

Radiofrequency System Radiofrequency system is required to transmit and receive signals at or near the Larmor frequency of the precessing spins. The frequency of the RF coil is defined by the Larmor equation. The Larmor frequency of protons being 63.8 MHz at 1.5 Tesla. MRI uses a Fourier transformation technique. This utilizes a brief burst of RF energy (lasting a few milliseconds) from a RF transmitter to excite the spins, followed by detection of the FID (free induction decay) signal that lasts 10–1000 ms. RF field B1 is two vectors rotating in opposite directions in a plane transverse to B0. At the Larmor frequency the vector rotating in the same direction as the precessing spins will interact strongly with the spins. RF coils work efficiently when physically aligned to receive signal that originate perpendicular to the main magnetic field B0. The RF subsystem consists of a transmitter, a receiver coils. The RF transmission system consists of RF synthesizer; amplifier and transmitter coil (usually built into the body of the scanner). RF transmitter generates a temporally stable basic frequency for the RF, delivers an appropriate waveform to amplifier which delivers an RF pulse of shape and flip angle to the coil and time the deliver of the pulses. This can be achieved by analog or digital process. The transmitter must display linearity, i.e. the output of the power amplifier should

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be directly proportional to the input power. This is achieved by a process called as envelope feedback. RF amplifier converts a low-level RF demand signal to a high-power level. RF source is combination of independent input signal and amplifiers. RF coil is a combination of coil elements arranged to produce an advantageous B1 field distribution. RF channel denotes the number of connections to the RF coil. Coil element is an arrangement of electrical conductors for converting an electrical current into magnetic field. RF receiver subsystem: The RF receiver consists of the coil, preamplifier and signal processing system. The primary role of the receiver in an MRI scanner is to convert the analog coil signals into digital format. The design of a modern digital receiver is based on an analog-to-digital converter (ADC), which samples the analog MRI signal and converts it into digital format. Important characteristics of the ADC are its conversion bandwidth and resolution. The conversion bandwidth equals half the digitization rate. Stateof-the-art ADCs allow conversion bandwidth of over 50 MHz at 14 bit resolution. Since frequencies are generally well above 50 MHz, usually an alias of the MRI signal is detected. Prior to input into the ADC, the MRI scanners signal needs to be amplified and filtered. Amplification serves to match the voltage range of the MRI signal to the input range of the ADC, in order to engage its full dynamic range. Analog filtering serves to reduce noise and interference signals that alias into the ADC conversion band from outside the target band around the MRI scanner Larmor frequency. In addition, depending on Larmor frequency, down conversion might be required to bring the signal frequency to within the input band of the ADC. The choice of ADC digitization rate is to some extent dependent on the master clock of the MRI scanner exciter. To avoid phase errors between excitation and reception, the digitization clock of the ADC needs to be synchronized to the clock of the MRI scanner exciter frequency that is a multiple of the exciter clock. In addition, it is beneficial to avoid digitization frequencies that put the Larmor alias at around 0 Hz. After digitization, digital downsampling is performed to reduce the amount of data. The output bandwidth and center frequency can be adjusted to match those of the MRI scanner signal bandwidth and (aliased) center frequency. An added advantage of downsampling is the increase in dynamic range, which amounts to 1 bit for every factor of 4 of down-sampling. RF coils can be transmit and receive or transmit only/ receive only coils. Receive only and transmit only coils must be electronically isolated. This means that when the transmitter is on, the receiver is open circuited to prevent the transmitting power from entering the receiving chain. During signal reception, the transmitting coil is open circuited to prevent mutual coupling. When the power amplifier is not active, its output is disconnected to avoid the output noise from interfering with the sensitive signal that is being received.

A wide range of RF coil designs are available in MRI. Ongoing developments in the RF system are one of the most profound changes in MRI system development. There are many types and geometries of the coil. RF coils are classified into two types—volume and surface coils. Volume coils surround the imaged object and provide homogeneous transmission and reception over a large anatomic region. These are both transmit and receive coils (transcieve). Head and body coils are referred as volume coils (Fig. 14). As the noise is nonlinearly proportional to the volume of tissue being imaged; the SNR of these is lower than the surface coils. Body coils are constructed on cylindrical coil forms—diameter of 50–60 cm and a length of 70–80 cm. These are large enough to surround the patient’s chest and abdomen. Head coils are smaller, 40 cm long and 28 cm in diameter. Surface coils are usually receiving coils with a limited area of sensitivity from which they receive signal. Surface coils fit closely over specific anatomic region. The sensitivity of the coil is related to the radius of the coil. As the coil size is increased, noise will also increase. These include circular coil configuration for orbits and TM joints, rectangular coils for lumbar spine or irregular shapes for shoulder, cervical spine. Surface coils are advantageous as they increase the SNR; however, the sensitivity is not uniform over its field of view. These need to be positioned carefully. Surface coils can be rigid or flexible in design. Flexible coils can be closely applied to the contour of the body, are more comfortable and however, are less durable due to higher wear and tear (Fig. 15). A large coil (body coil) is used as a transmitter and a smaller surface coil as a receiver combining the advantage of uniform excitation of a large coil and increased SNR of a smaller coil. However, if two separate coils are used, they need to be tuned to the same frequency. Coil decoupling is

Fig. 14:  Circularly polarized head coil, volume coil—both transmit and receive

Chapter 44 Magnetic Resonance Instrumentation: An Update

necessary to prevent current in one coil to excite current in the other. For a solenoidal magnet the transmitter and receiver coils are saddle shaped and have the volume of the greatest B1 field homogeneity along the linear portion of the coil, the ends being inhomogeneous (Fig. 16). An alternate design called a bird cage coil or resonator has improved B1 homogeneity and has higher sensitivity. These are volume coils consisting of two circular or elliptical conducting end rings joined by conducting rings or legs (Fig. 17). A common version uses 16 loops to span the cylinder. These coils provide a uniform RF field. Quadrature reception is applied with volume coils to improve SNR. Two pairs of coils (phase sensitive detectors) are used to detect signal that are out of phase. The signal of the two is combined to form a final image. A coil operating

in this manner is called “circularly polarized” (Fig. 18). This increases SNR by a factor of √2. It requires only half the power to generate; therefore less power is deposited in tissues. A circularly polarized birdcage resonator is called a quadrature coil and is the most frequently used RF coils in MRI today. Whole body sized birdcage coils are available. A related form of multimode resonator, referred to as TEM (transverse electromagnetic) resonator is also useful for head and neck imaging at higher field strengths. These are fitted just inside the gradient coil set. RF transmitting coils are also shielded to minimize power losses.15-17 Phased array coils: Arrays of surface coil are used to extend the effective FOV of the receiver coil while maintaining the improved SNR characteristics of a limited FOV of a single coil (Fig. 19). The coils in array can be activated remotely as single

Fig. 15:  Surface loop coil—receive only

Fig. 17:  Bird cage resonator

Fig. 16:  Linearly polarized body coil comprising flat conductors

Fig. 18:  Design of a circularly polarized body coil showing 2 RF fields

configured in a hollow tube

with a phase shift

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Fig. 19:  Phased array coil—multiple coil elements, increasing SNR and FOV

receivers and cover a limited FOV in the region of interest. There is also another method where each coil in the phased array has a separate receiver channel. The signal is collected from all coils in the array simultaneously, data combined to give an image of a complete FOV, with a SNR equivalent to a single coil. As number of receiver channels increase, so does the cost. The coils are electromagnetically decoupled from one another by selecting the overlap between neighboring coils, so that mutual inductances disappear. This is achieved by the use of low-impedance preamplifiers on the output of each individual coil or by physically overlapping the coil receiver elements. The hexagonal arrangement of coils and extent of overlap are chosen to minimize mutual inductances between coil elements. Noise is proportional to sensitivity volume of the coil, which is smaller for surface coil than for a volume coil. Phased array coils have to be positioned perpendicular to the main magnetic field. Phased array coils require an individual hardware channel for each reception element demanding more computer processors. As the number of channels increase, the coil elements become smaller and penetration may be compromised. This may lead to inhomogeneous SNR, which would be maximum near the surface of the coil and less within the deeper parts. This has been overcome with the use of postprocessing algorithm to correct intensity variation.18 Transmit phased array coils: A current is produced on each element via special amplifiers. Precise control of the relative amplitude and phase of each element enables them to be mutually independent. With reduced pulse duration, higher SNR, improved field homogeneity and reduced SAR, parallel MRI can be used in the excitation phase as in transmit SENSE at higher field strengths.7

Hybrid coil: This is a transmit/receive coil. It consists of a localized dedicated transmitter coil whose size is just optimized for a target FOV and an independent set of receiver coils. As the transmitter coil is much smaller than the typical whole body transmitter coil, it requires less input power to generate the necessary B1 with a potentially reduced SAR. Hybrid coils are thus useful for higher static magnet fields. Most of the RF transmit and receive subsystem component, such as digital to analogue converters, analogue to digital converters, power amplifiers, frequency mixers are sited in the electronics/cabinet room. Careful shielding of the MR scan room is required to prevent contamination of the weak signal arising from the patient with extraneous signal at the same frequency. These can be from broadcasting stations or operation of electronic equipment. MRI rooms have a shield called as Faraday cage, consisting of a conductive metal lining of copper or aluminum through which RF electromagnetic radiation will not pass. It keeps external electrical noise out and the generated RF signal within the examination room. Electronic filters are used to prevent noise from entering the scan room via wiring cables. Screened rooms possess wave guides/tubes fixed into the wall of the room, through which nonconductive tubing, such as fiber optical coil passes. The examination room door should be shut while acquiring data to enable the shield to work effectively. Machine should be away from lifts/elevators and power cables, which may cause RF interference, distorts the image and produce linear artifacts. A hardware and software system is provided which provides protection for the patient against the heating effect of RF energy absorption and RF hardware from excess transmitted RF energy or hardware failure in the RF transmit path. This takes into account various coil types, amount of transmitted power allowed for the body coil is much higher than that of a transmit receive head coil as the body coil is larger and can handle more power. Correct calibration of the MR system is essential.

MULTICHANNEL RF COILS AND PARALLEL IMAGING Multichannel radiofrequency and parallel imaging technologies are hardware and software implementations, respectively, aimed at improving the coverage, signal resolution and speed of MRI examinations. With multichannel RF technology, the MRI signal used to form an image is collected by an array of separate detectors, or coil elements. Each element relays signal information along a separate channel to an image reconstruction computer. Such arrays of coil elements and receivers can improve imaging coverage and the ratio of signal-to-noise in the image. The connection to the system of a coil with more elements than the number of channels requires complex logic switches in the coil, number of elements in the array of detectors and receivers is an important factor in characterizing an MRI scanner. Parallel

Chapter 44 Magnetic Resonance Instrumentation: An Update

imaging technology uses complex software algorithms to reconstruct the signals from multiple channels in a way that can reduce imaging times and/or increase image resolution. The concept of “multielement phased arrays receive coils” started around 1990; as a result MRI systems typically had up to 4 receive channels. Towards the end of the 1990s, with the introduction of parallel imaging, the technology related to MRI receiving architecture made enormous progress: over a period of 10 years, the number of receiving channels increased from the original 2–32. In the last decade, the move towards higher channel counts in coils has been at the forefront of MR development. This trend towards higher number of channels has resulted in an increased complexity of the MRI system with increased initial costs. Also upgrades to a higher number of channels are costly because a substantial expansion of the RF chain is required. Acquisition time in MRI is proportional to the number of phase encoding steps. Increasing the distance between each phase encoding lines in k space by a factor of R, reduces the acquisition time by the same factor, while keeping the spatial resolution fixed. Acquisition time is reduced by a factor (R = acceleration factor), equivalent to the number of independent coil elements (4–32). In practice, only a time reduction of 2–3 is possible as SNR is inversely proportional to √R and at higher R, SNR becomes unacceptably low. Decreasing the phase encoding lines decreases the FOV, resulting in aliasing or wraparound. There are two techniques to remove or prevent aliasing: 1. Simultaneous acquisition of spatial harmo­ n ics (SMASH): The missing k space lines are restored prior to Fourier transformation.19 Generalized auto­calibrating partially parallel acquisition (GRAPPA) is a variant of SMASH in which a small number of additional lines of k space data are acquired during the acquisition, eliminating the need for a separate coil sensitivity. 2. SENSE: Sensitivity encoding 20—data is first Fourier transformed, resulting in an aliased image. This is then by “unwrapped” by using the spatial information from the coil sensitivity profile. SENSE is the most commonly used parallel imaging technique available with many vendors as ASSET (GE healthcare, Waukesha, Wis), SPEEDER (Toshiba medical systems, Tokyo, Japan), SENSE (Philips medical system, Cleveland, Ohio), Siemens (Erlangen, Germany) offers both SENSE and GRAPPA as a single package under the trade name iPAT. Parallel imaging is useful in conditions where scan speed outweighs the need for a high SNR, e.g. cardiac imaging. Multitransmit technology: Imaging in conventional MR scanners, uses a single source to transmit a signal to the patient. Multitransmit uses multiple RF sources, each source individually adapted to patients anatomy. This cancels out dielectric shading seen at 3.0 T. Multitransmit also reduces

local specific absorption rate SAR. Interleaved sequences and saline bags are not required. Another advantage, as claimed by the vendor, of using multiple RF sources is increase in scanning speed by 40%.21,22 Total imaging matrix: Provided by one vendor,23 the system contains up to 102 matrix coil elements integrated seamlessly with up to 32 independent RF channels. These provide high SNR associated with local coils for an FOV ranging from 5 to 196 cm. There is no requirement for patient/coil repositioning. This system provides a PAT factor up to 16. Tim46 ultrahigh density array up to 204 coil elements with 128 RF channels increase SNR considerably (Fig. 20).

Computer The computer is the command center of the MRI system. It shapes and times the RF pulses, turns the gradients on and off, controls the RF receiver to collect data. After data collection, it is required for manipulation, storage, retrieval. A processor is required for computation.

Data Processing and Image Reconstruction The two primary dedicated digital control systems are the pulse generator and the data acquisition system. The pulse generator synchronizes the gradients and RF pulses after selection at operator console. Digital synchronization is provided for the receive channel analog to digital convertor, such that the detected signal correlate with the applied gradient and RF frequency. The temporal positional accuracy and repeatability (TPAR) is an important specification of the system. Data is collected from one or more receiver channels. This may be in analog or preferable digital domain. Digital

Fig. 20:  Total Imaging Matrix®—102 coil elements with 32 channels providing whole body coverage of up to 205 cm

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broadband MR is a new technology that samples the MR signal directly in the coil on the patient. The fiberoptic transmission of digital broadband data from the coil to the image reconstruction removes potential noise that is associated with analog RF. In conventional MR system, multiple analog coaxial cables are required (one per element/channel as digitization is performed away from the RF coil). In digital broadband system digitization is inside the RF receive coil, the number of RF channels is now determined by the coils, rather than the system. There is a single broadband fiberoptic cable that is independent of number of elements/channels in an RF coil. A gain of 40% in SNR is claimed. System also is channel independent. In a conventional system, 8 channels can receive coils up to 8 channels; to support a 16 channel coil an upgrade would be required. Digitization in the coil makes number of channels required redundant. Data processing from multiple channels in the digital domain allows for correction of the inhomogeneous sensitivity of the coil and produces an acceptable image with a required FOV. The required data acquisition rate increases with the number of channels being sampled. The sampling frequency needs to be twice the receiver bandwidth to meet the Nyquist criteria and prevent aliasing. To account from phase errors that may occur, a sample frequency of four times the bandwidth is used. Analog to digital converter are used. Digital data processing speeds are critical in higher field magnets with larger matrix size. The complex MR signal is sampled and computer analyzed into a spectrum of component frequencies using a mathematical process called Fourier analysis. The data from every signal in a selected slice are stored in k space. This space is a spatial frequency domain in the computer where the signal spatial frequencies and their origin are stored. The number of lines filled in k space matches the number of encodings in the sequence.7 The central part of k space is filled with data from shallow encoding gradients, low spatial frequencies, less details, but stronger signals. The upper and lower parts are filled with data from the steeper gradients, high spatial frequencies, better detail but lowsignal intensity. k space has to be completely filled with the data from the imaging sequence before the signal is analyzed and processed into the image. The data once acquired, is stored in a large memory array after being filtered. The memory is very large and a cached disk system is used. Powerful reconstruction processors are used computer servers, are important components of MR hardware and have many forms, rackmount servers used in many systems. Image reconstruction algorithms are implemented to distribute computational load and save time. The sample frequency and the number of simultaneously acquired channels determine the maximum data rates through the system. After the image is reconstructed, may be displaced for instantaneous viewing or stored in a database for review.

ADVANCED MR APPLICATIONS AND HARDWARE Magnetic Resonance-High-Density Focussed Ultrasound (or MRgFUS) A noninvasive method using high-density focused ultrasound and using MR for planning and temperature monitoring was first used in 2008 as an alternative to surgery for treatment of uterine fibroids. The clinical applications of this are increasing to include management of bone metastasis, prostate, etc. A focusing transducer is used to transmit ultrasound energy into a small volume at the target locations inside the body. The ultrasound energy penetrates the intact skin and soft tissue to produce a well-defined region of coagulative necrosis by producing high temperature and only in the focused area. Three-dimensional MR provides the anatomical reference data for planning. MRI based temperature map acquired in real-time during ablation provides monitoring support. This is an outpatient procedure. Dedicated abdominopelvic coils designed for therapy applications are integrated within the table for positioning ease. The same system can be used for both therapy and diagnosis. This is exclusive to GE MR Systems10 in collaboration with Insightec’s Ex-ablate 2000 (Fig. 21).

Magnetic Resonance Elastogram This is an acquisition hardware and reconstruction application that produces images with contrast related to stiffness of soft tissue. Sound waves (40–200 Hz) are generated in the body

Fig. 21:  Magnetic resonance-guided focused ultrasound—depicts

the position of the patient, ultrasound transducer and the focused beam

Chapter 44 Magnetic Resonance Instrumentation: An Update

by using an MRI compatible acoustic driver. These are then imaged by a special phase contrast MRI sequence. Finally the data generated is processed to generate elastograms—color coded anatomic images that depict the relative stiffness of tissue in the cross section of interest. The hardware component is compromised of an active sound wave generator and a passive transducer that produces vibrations in the subject to be scanned. The data is reconstructed in both magnitude and phase formats and the latter is used to produce strain wave and relative stiffness images. This technique is used to assess liver fibrosis.

MR Surgical Suite: Interventional MRI Interventional MRI is the use of MR techniques for guidance of both diagnostic and minimally invasive therapeutic interventions. The magnet is of the ‘open’ type to allow access to the patient. There is video camera sensor array which detects the correct location and orientation of the hand held instrument. Use of new fast gradient echo pulse sequences allows continuous MR images (0.3–7 seconds per image). These are viewed through a high-resolution radiofrequency shielded monitor in the operating room. This modality is especially useful in areas of complex anatomy like skull base, retropharynx, etc.

Magnetic Resonance–Positron Emission Tomography Fully integrated magnetic resonance–positron emission tomography (MR–PET) suite has been introduced. This has integrated cooling feature with specialized shielding to eliminate magnetic field interference in PET data processing. The detectors used in PET are MR compatible. This is dealt with in detail elsewhere in the book. The MRI is now a widely used and well-developed modality. Intense technical development is continuing to increase its clinical applications including in the field of molecular imaging and to provide the necessary hardware for the same.

REFERENCES 1. Gorter CJ. Negative result of an attempt to detect nuclear spins. Physica. 1936;3:995-8. 2. Lauterbur PC. Image formation by induced local interactions: examples employing nuclear magnetic resonance. Nature. 1973;242:190-1.

3. Schneck JF, Kelley DAC, Marinelli L. Instrumentation: Magnets, coils and Hardware. In: Wolters Kluwer (Ed). Magnetic Resonance Imaging of the Brain and Spine Atlas SW, 4th Edn. Lippincott Williams & Wilkins; 2009.pp.2-24. 4. Vaughan T, DelaBarre L, Synder C, et al. 9.4 T human MRI: preliminary results. Magn Med. 2006;56:1274-82. 5. Sagawa M, Fujimura S, Togawa N, et al. New material for permanent magnets on a base of Nd and Fe. J Appl Phys. 1984; 55:2083-7. 6. Scott Greig, Chronik Blaine, et al. A prepolarized MRI scanner. Proc Intl Soc Mag Med. 2001;9:610. 7. Allisy-Roberts P, Williams J. Farr’s Physics For Medical Imaging, 2nd edn. Saunders Elsiever; Magnetic Resonance Imaging 189. 8. McRobbie DW, Moore EA, Graves MJ, Prince MR. MRI from picture to proton. Cambridge:Cambridge university Press. 2003. 9. Adam A, Dixon AK, Grainger RG, Allison DJ. Magnetic Resonance Imaging Basic Principles in Diagnostic Radiology. 2008;87-107. 10. www.gehealthcare. 11. Akisk FM, Sandrasegaran K, Aisen AM, et al. Abdominal MR imaging at 3.0 T. Radiographics. 2007;27:1443-4. 12. Merkle EM, Dale BM. Abdominal MRI at 3.0 T: the basics revisited. Am J Roentgenol. 2006;186:1524-32. 13. Jellúš V, et al. New Modification of the Homomorphic Filter for Bias Field Correction. Proc ISMRM. 2005. p. 2247. 14. Turner R. Gradient coil design: a review of methods. Magn Reson Imag. 1993;11:903-20. 15. Walker KM, Tsuruda JS, Hadley JR, et al. Radiofrequency coil selection for MR imaging of the brain and skull base. Radiology. 2001;221:11-25. 16. Fujita H. New Horizons in MR Technology: RF coil designs and trends. Magn Reson Med Sci. 2007;6(1):29-42. 17. Schenck JF. Radiofrequency coils: types and characteristics. In: Bronskill MJ, Sprawls P (eds). The Physics of MRI. Woodbury, NY: American Institute of Physics; 1993.pp.98-134. 18. Roemer PB, Edelstein WA, Hayes CE, et al. The NMR phased array. Magn Reson Med. 1990;16(2):192-225. 19. Sodickson DK, Manning WJ. Simultaneous aquistion of spatial harmonics (SMASH): fast imaging with radiofrequency coil arrays. Magn Reson Med. 1997;38:591-603. 20. Prussmann KP, Weiger M, Scheidegger MB, et al. SENSE: Sensitivity encoding for fast MRI. Magn Reson Med. 1999; 42:952-62. 21. www. heathcare.philips.com/main/products/mri. 22. Harvey PR, et al. SAR behavior during whole-body multitransmit RF shimming at 3.0 T. Proc. ISMRM. 2009;p. 4786. 23. www.siemens.com/medical solutions.

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Image Optimization in Magnetic Resonance Imaging

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Jyoti Kumar

INTRODUCTION Optimizing image quality means finding a balance between the different aspects of image quality and image speed. For an image to be optimal for diagnosis, the anatomic and pathologic features within the image must be distinguishable from each other. Ideally, an image should have a high signal-to-noise ratio (SNR), high-spatial resolution, excellent contrast, minimum artifacts and an acceptable scan time. Generally, there is a conflict amongst these criteria. Knowledge about various MR parameters within the user interface that can be modified by the radiologist helps find the most appropriate balance between image quality and scan time. In this chapter, we shall discuss image optimization under these major headings: zz Signal-to-noise ratio zz Contrast-to-noise ratio (CNR) zz Spatial resolution zz Scan time zz Artifacts and their remedial measures.

SIGNAL-TO-NOISE RATIO MR signal is the voltage received by the receiver coil from each voxel in a slice after it is stimulated by a radiofrequency pulse. This is recorded at time interval TE and at specific frequencies. Bright pixels in the image represent stronger signals, and darker pixels represent weaker signals in the image. Noise is an unwanted occurrence in the MR image. Noise appears as a grainy random pattern superimposed on the MR image. This represents statistical fluctuations in signal intensity that is superimposed on the image and compromises image quality. It usually occurs at almost all frequencies at random times. The source of this noise is Brownian motion of charged particles throughout the body of the patient whereas signal comes from just the selected slice. The electronic noise of the receiver technology and the environment also contribute to the noise.

The SNR refers to the ratio of the amplitude of the MR signal to the amplitude of the background noise. A high SNR improves image quality. To increase the SNR, we need to increase the signal relative to the noise. The parameters which affect SNR are field strength, proton density, coil type and position, TR, TE, flip angle, number of signal averages, slice thickness and receiver bandwidth.

Field Strength With higher field strength, more protons are aligned parallel to the main field (spin up nuclei) as fewer protons have energy which could be enough for opposing this increased field strength and lie antiparallel to the main field (spin down nuclei). The net magnetism of the patient (termed the net magnetization vector or NMV), displays the balance between the parallel and antiparallel magnetic moments. In high field strengths, NMV increases and therefore the signal increases.

Proton Density The signal strength depends on the quantity of signal generating protons in the voxel (proton density). For example, pelvis contains structures with a high proton density, such as fat, bone and muscle, giving a high signal. On the other hand, chest contains air filled lungs and vessels with low proton density, and hence imaging of chest requires measures to boost SNR.

Coil Type and Position Imaging of small anatomical regions, such as extremities (e.g. ankles, wrists), neck or the breasts require specialized surface coils to maximize both the SNR and spatial resolution. Large coverage is provided by the large coils, such as the body coil but it results in a lower SNR. A phased array coil combines the two advantages by using multiple small coils which provide good SNR and the data from these are combined to produce an image with good coverage.

Chapter 45 Image Optimization in Magnetic Resonance Imaging

Positioning of coils is also of great importance. To understand this, let us revise few basic principles of MR imaging. In an external magnetic field (B0), spin up and spin down nuclei are in a state of equilibrium. Excess spins generate constant magnetization in the longitudinal plane (Z-axis). Spins are also precesssing like a wobbling top and they are out of phase with each other. NMV is zero in the transverse plane. Application of RF pulse leads to two things: energy absorption and phase coherence. Hydrogen nuclei absorb energy. If the appropriate amount of energy is absorbed, the number of nuclei in the spin up position is equal to the number in the spin down position. Consequently, the longitudinal magnetization reduces to zero. Secondly, on application of an RF pulse, the spins move into phase with each other. When spin up and spin down nuclei are equal in number, the net effect is one of precession so that NMV now precesses in the transverse or XY plane. As the NMV has been moved through 90° from the direction of the main magnetic field or the Z-axis, it is called a 90° RF pulse. It is the magnetization in the transverse plane that is used to produce the signal. As the NMV rotates in the transverse plane, it passes across the receiver coil to induce a voltage in it. This voltage is the MR signal. The position of the coil is kept such that the transverse magnetization created in the XY plane remains perpendicular to the coil. In a superconduc­ting system, this means positioning the coil either over, under, or to the right or left of the area to be examined. A coil positioned perpendicular to the table results in zero-signal generation.

Repetition Time Repetition time (TR) is the time between the application of two RF pulses. It is measured in milliseconds (msec). When the RF pulse is removed, longitudinal magnetization recovers (T1 recovery) and transverse magnetization begins to decay (T2 decay). The T1 time of a tissue is inherent in nature and refers to the time it takes for the recovery of 63% of the longitudinal magnetization. The period of time in which this longitudinal recovery occurs is the time TR. The longer the TR, the greater is the recovery of longitudinal magnetization, which is now available to be flipped into the transverse plane on the application of the next excitation pulse. Hence, the SNR is improved with a long TR. A short TR reduces the SNR. Although a short TR is required for T1 weighting, reducing this parameter excessively may severely compromise the SNR.

Echo Time Echo time (TE) refers to the time between an RF excitation pulse and collection of the signal. It is also measured in milliseconds (msec). The T2 decay time of a particular tissue is also inherent to the tissue. It is the time it requires for 63% of the transverse magnetization to be lost. The time period over which it occurs is the time between the excitation pulse

and the MR signal or the TE. The TE determines the extent of T2 decay occurring in a particular tissue. At short TEs, very little transverse magnetization has dephased, so the signal amplitude and hence SNR is high. A long TE reduces the SNR. Although a long TE is required for T2 weighting, an excessive increase in this parameter may severely compromise the SNR.

Flip Angle It is the angle through which NMV is moved as a result of RF excitation pulse. When a large flip angle is used, longitudinal magnetization is entirely converted into transverse magneti­ zation resulting in maximum signal. On the other hand, small flip angles convert only a proportion of the longitudinal magnetization to transverse magnetization. A small flip angle is used in gradient echo imaging which results in a low SNR and hence measures may be needed to improve it.

Number of Signal Averages Number of signal averages (NSA) determines the number of times frequencies in the signal are sampled with the same slope of phase encoding gradient. Multiple measurements of one slice are obtained and the results are averaged in a single image. Increasing the number of excitation (NEX) increases the signal collected. We need to remember that noise is also being increasingly sampled. As noise occurs randomly and at all frequencies, doubling the number of signal averages does not double the SNR but only increases the SNR by a square root of two. Also, when NEX is doubled the time required to obtain the scan is also doubled (Figs 1A and B).

Slice Thickness When we obtain thicker slices, the voxel is enlarged and hence more proton spins contribute to the signal, thereby increasing the signal intensity. Noise remains the same because it is not just coming from the slice, but the patient’s entire body and MR environment. Hence, SNR is directly proportional to the slice thickness. The drawback is that, increasing the slice thickness reduces the spatial resolution resulting in partial volume effects (Figs 2A and B).

Receiver Bandwidth This is the range of frequencies sampled within the FOV during readout in the frequency encoding direction. It is measured in kilo Hertz (kHz). Reduction of the receiver bandwidth reduces the proportion of noise sampled relative to signal, hence effectively increasing the SNR. The drawback here is that to reduce the bandwidth, the sampling time has to be increased to satisfy Nyquist theorem. This theorem states that the sampling rate must be at least double the frequency of the highest frequency in the echo to

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Figs 1A and B:  Image comparison: T2-weighted axial images of the brain acquired with one signal average on the left (A) and four signal averages on the right (B). The SNR of the image B was double than that of A. Also, the scan time of B was four times than that of A

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Figs 2A and B:  Image comparison: T1-weighted sagittal images of the brain: The image on the right (B) was acquired with double the slice thickness on the left (A). The SNR of the image B was double that of A. However, this occurred at the expense of spatial resolution

accurately reflect all the frequencies in the signal. If receiver bandwidth is reduced keeping all parameters unchanged, then sampling time needs to be increased to be able to sample all frequencies accurately. As the echo is centered in the middle of the sampling window, TE need to be increased. Therefore, it is not suitable for T1 or proton density weighted imaging, where a low TE is used. Also, chemical shift artifact is increased when receiver bandwidth is decreased. Reduced receive bandwidths should be used when there is no requirement of a short TE (T2 weighting) and when fat is absent (example: brain, and any other examination when fat is suppressed).

CONTRAST-TO-NOISE RATIO MR images would have no clinical value without satisfactory image contrast which is defined as the difference in signal

strength between two tissues in the image. A high SNR does not guarantee easy differentiation of two structures in an image. The CNR is the most significant image quality factor because this allows for differentiation between anatomical tissues in the image and also in differentiation between pathological and normal tissue, hence aiding in final analysis of the image. Superior soft-tissue contrast is a major advantage of MR imaging versus alternative modalities, such as computed radiography. Contrast in MR is a complex function of intrinsic characteristics of the structure, i.e. proton density, T1- and T2-relaxation times, magnetic susceptibility of the nuclei as well as programmable pulse-sequence parameters, e.g. TR, TE, flip angle, slice thickness, etc. For example, a longer TR permits more time for T1 relaxation and produces more signal from tissues with long T1 values. Longer TE, on the other

Chapter 45 Image Optimization in Magnetic Resonance Imaging

hand, allows more time for T2 relaxation and produces more signal from tissues with long T2 values. The factors that increase CNR are administration of a contrast agent, magnetization transfer constant, chemical sup­pression techniques and T2 weighting, where difference between pathology and anatomy is increased.

Administration of a Contrast Agent A contrast agent like gadolinium shortens the T1 time of structures, especially of pathological lesions when they have a break in blood brain barrier. Enhancing tissue appears much brighter, hence boosting the CNR.

Magnetization Transfer Constant In biological systems, protons usually exist in two pools. The ‘free pool’ consists of relatively mobile protons in free bulk water and some fat containing tissues. With standard MRI, this pool provides the bulk of the signal. The second pool or ‘bound pool’ consists of restricted protons bound in proteins, other large macromolecules, and cellular membranes. With conventional MRI, this pool does not contribute to MR signal due to very short T2. Under normal MR conditions magnetization is exchan­ ged from the ‘free pool’ to the ‘bound pool’ and vice versa, that results in a situation of equilibrium situation which is characteristic for that type of tissue. When additional RF pulses are use to suppress bound protons, it results in no net magnetization of the ‘bound pool’. A difference in magnetization between the pools is thereby created. The cross relaxation processes transfers the magnetization from the ‘free pool’ to the ‘bound pool’. A new equilibrium is reached decreasing the SNR of a particular tissue. Hence the contrast with the surrounding tissue is accentuated. It is primarily used to suppress normal tissue.

Chemical Suppression Signal is suppressed either from fat or water. For example, fat suppression techniques null fat and hence CNR between lesions and the surrounding normal tissues that contain fat is increased.

Echo-train Length In fast-spin-echo sequence (FSE), a train of 180 o rephasing pulses are used. The number of these pulses and resultant echoes is called the echo train length or turbo factor. Since each echo has a different TE and data from each echo are used to produce one image, the contrast of FSE is unique. On T2 FSE, fat is hyperintense as this echo train reduces spin-spin interactions in fat, thereby increasing T2 decay time (J-coupling). Muscle appears darker because the echo

train increases magnetization transfer effects that produce saturation.

Time from Inversion The time from inversion (TI) is the primary factor that controls the contrast in Inversion Recovery (IR) sequences. These are spin-echo-sequences that begin with a 180° pulse which flips the NMV by 180°. At time TI after the 180° inverting pulse, a 90° pulse is applied which is then followed by 180° pulse for rephasing spins that produces echo at time TE. If TI is long enough to let NMV pass through the transverse plane before the 90° pulse is applied, the contrast will depend on how much saturation this 90° pulse produces. Saturation is when NMV is pushed beyond the transverse plane by the 90° pulse and results in T1 weighting. TIs of 300 to 700 ms result in heavy T1 weighting. Certain specific TI values result in suppression of signal from specific tissues. For example, TI of 100–180 ms is used in STIR sequence. 90° pulse is here applied after this TI when NMV of fat is passing exactly through transverse plane. At this null point, there is no longitudinal magnetization of fat and hence no transverse magnetization results on application of 90o pulse, therefore resulting in no signal from fat. Similarly, TIs of 1700–2200 ms are used to null the signal from CSF on FLAIR imaging.

SPATIAL RESOLUTION Spatial resolution is defined as the ability to distinguish between two points that are close to each other in the patient. The size of the voxel determines the spatial resolution. The imaging volume is divided into slices. Each slice displays an area of anatomy which is called the field of view (FOV). This FOV is divided into pixels. The size of the pixels is determined by the matrix. The FOV may be specified separately for the frequency encoding and phase encoding directions which may be the same in a square or isotropic FOV and different in an anisotropic or a rectangular FOV. Frequency and phase encoding gradients are applied to spatially locate the signal coming from each pixel in the FOV.

Voxel Volume, FOV, Matrix Voxel volume is a product of pixel size and slice thickness. Therefore, slice thickness, FOV and matrix size determine voxel volume. The greater the voxel volume, more are the number of spins that contribute to MR signal, resulting in a higher SNR per voxel. However, when the voxels are larger, spatial resolution falls as the likelihood of two points close to one another in the patient, being in separate voxels decreases. When FOV is decreased, pixel size and hence voxel volume decreases, thereby decreasing the SNR and increasing spatial resolution (Figs 3A and B). When small coils are used which boost local SNR, a small FOV may be used. However,

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Figs 3A and B:  Image comparison: T1-weighted sagittal images of the brain: The image on the right (B) was acquired with reduced FOV and reduced pixel size compared with left (A). The spatial resolution of B was increased at the expense of reduced SNR

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Figs 4A and B:  Image comparison: T2-weighted axial images of the brain: The image on the left (A) was acquired with increased matrix and

hence reduced pixel size compared with right (B). The spatial resolution of A was improved. As the phase matrix was increased, the scan time was also increased

a small FOV should be used with caution with a large coil as SNR will be severely compromised unless other measures like increasing NEX is used. When the matrix is changed, the number of pixels that must fit into the FOV also changes. As the matrix increases, the dimension of each pixel decreases. This reduces the SNR but improves spatial resolution. In addition as the phase matrix increases, the scan time also increases (Figs 4A and B). However, if we increase the frequency matrix only, it increases the resolution but the scan time does not increase as only the phase matrix determines scan time. A rectangular FOV where the FOV is reduced in the phase direction reduces the scan time keeping the resolution same as that of square FOV. This is especially useful when anatomy of the area examined fits into a rectangle, as in sagittal image of pelvis.

Increasing the slice thickness increases the voxel volume, hence increasing SNR at the expense of spatial resolution (Figs 2A and B).

SCAN TIME The longer the examination time, the greater the discomfort to the patient resulting in increased chances of a bad image. Good immobilization is also vital, since a few minutes spent in making the patient comfortable can save us many minutes of wasted sequences. The scan time is determined by the following factors. Scan time = TR × number of excitations × number of phase encodings

Chapter 45 Image Optimization in Magnetic Resonance Imaging

TR The greater is the time between the application of two RF pulses, the greater is the scan time. When we reduce the TR, we can reduce the scan time. However, reducing TR reduces SNR as already discussed. As less longitudinal magnetization recovers during each TR period, the next 90° pulse flips it to beyond the transverse plane. This is called saturation and increases T1 weighting. As there is less time to excite slices in this reduced TR, the number of slices that can be acquired in a single acquisition also decreases.

Number of Excitations When the NEX or signal averages is increased, more and more measurements of one slice are being obtained to average the results. This increases the scan time (Figs 1A and B). But when we reduce the NEX to reduce scan time, SNR falls because now, the number of times data is stored in k-space is reduced. Since averaging of noise is also less, there is also an accompanying increase in motion artifact.

Phase Matrix Increasing the phase matrix increases scan time (Figs 4A and B). To understand this, we shall first discuss the basic physics behind MR gradients. Gradients are coils of wire which change the magnetic field strength of the magnet in a controlled manner when current is passed through them. They change the precessional frequency and phase of the spins. These are employed along three orthogonal axes, XYZ, to enable us to select a slice (slice-selection gradient), and to spatially locate the signal along the two dimensions of the image within a slice (frequency encoding and phase encoding gradient). Frequency encoding gradient is switched on to locate signal along one axis of the image (usually the long axis) and produces a frequency shift. At a frequency matrix of 256, 256 different frequencies are mapped along the long axis of the image. Fourier transformation allows us to determine signal contribution of each frequency, enabling us to allocate this signal to the location of origin along one axis of the image. Fourier transformation is like a prism (which disperses white light into its spectra) that causes physical dispersion of the frequencies collected and assigns them to a structure in the image. Phase-encoding gradient alters the phase of the nucleus, causing a phase shift. When this gradient is switched off, phase shift of spins remains. This phase shift is used to locate the signal along one dimension of the image (usually the short axis). For a phase resolution of 256, we have to generate 256 signals with different phase encodings for 256 different locations. The pulse sequence has to be repeated 256 times for a phase matrix of 256. Hence, the phase matrix is an important determinant of scan time. If we reduce the phase

matrix to reduce scan time, the spatial resolution of the image falls.

Number of Slice Encodings in 3D Sequences In three dimensional fast scan sequences, scan time is depends upon the number of slice locations needed in the volume in addition to TR, NEX and number of phase encodings Scan time = TR × number of excitations × number of phase encodings × slice encodings

ARTIFACTS Artifacts are structures in the MR image that do not correspond to spatial distribution of tissue in the image plane. The cause of this signal misregistration is variable; artifacts are divided into three main types based on the cause. 1. Motion artifacts 2. Artifacts related to particular measurement technique or parameters used, e.g. chemical shift, wrap around and truncation artifacts. 3. External artifacts results from either a malfunction of the MR scanner or external interference.

Motion Artifacts (Phase Mismapping) These may result from accidental patient movement, respiration, heart beat, blood flow, eye movements or swallowing motion. These signal misregistartions occur in the phase encoding direction. The tissue is excited at one location but is mapped to a different location during readout due to its motion. This occurs in the phase encoding direction rather than the frequency encoding or readout direction because the encoding of phase by the phase encoding gradient occurs before signal detection, whereas frequency encoding gradient, also called the readout gradient, is applied concurrently with signal detection. For example, if the abdominal wall is at one position during the application of phase encoding gradient, its phase shift value is allocated to it in accordance with this position. During readout, the abdominal wall moves to another position, but the system still allocates it according to its first position resulting in ghosting artifact. Also, patient motion normally is much slower than the faster sampling process along the frequency encoding direction (in order of milliseconds). On the other hand, sampling along phase encoding direction needs all phase encoding steps and is in the order of seconds. This is another reason why motion artifacts are appreciable more along phase encoding direction.

Ghosting and Smearing While ghosting results from periodic motion, smearing is a result of aperiodic motion.

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Figs 5A and B:  Ghosting artifact: T2 weighted image of the pelvis (A) shows marked ghosting artifact (arrows) due to periodic respiratory

motion. This was reduced in (B) by increasing the number of signal averages and placing a spatial-presaturation pulse in the overlying subcutaneous fat. However, both these techniques contributed to an increase in scan time

The periodic rise and fall of thorax/abdomen during breathing produces an artifact called ghosting (Figs 5A and B). If the respiration rate is constant, then during inspiration, the abdomen is in several equidistant phase encoding steps during the inspiration phase and it is in the expiration phase in the intervening steps. This periodic motion is seen a locally offset double or multiple structures in the phase encoding direction. These ghosts are offset by the true image by an amount that is proportional to the respiration rate. Structures rich in signal, for example subcutaneous fat, further increase ghosting artifact. In a strictly periodic motion, the localization of the ghost can be predicted by a simple formula, describing the distance between the ghost image and the original structure. Distance = TR × phase encoding steps × NEX × motion frequency The higher the frequency of the motion, e.g. higher the breathing rate, the greater the distance between the original and the ghost artifact. We can increase the distance between the ghosts by increasing TR, phase matrix or NEX so that the first ghost lies outside the image,; however scan time is increased by all these methods. The brightness of the ghost depends upon the amplitude of motion; larger the pulsation, brighter the ghost. Another type of artifact that may result from aperiodic motion like that of eyes is smearing (Fig. 6). Peristalsis, which is a random movement, produces motion artifacts that result in generalized blurring of the image, which appears to be superimposed by a layer of noise. Blood flow is a very common cause of motion artifacts in the image. Fast continuous flow compared to TR produces a continuous artifact throughout the FOV, resulting in blurring, as in spin echo images. In-plane flow, parallel to the slice plane produces a diffuse artifact seen in coronal images. Flow in aorta and IVC affects the entire image acquired in coronal

Fig. 6:  Smearing artifact: T1 weighted coronal image of the brain shows smearing artifact (arrows) due to aperiodic motion of the eyes

plane as these great vessels extend through the entire image. CSF flow artifacts can also degrade the image of the spine on T2-weighted images. Periodic motion due to pulsatile through plane flow (flow perpendicular to the image plane) will be discussed later. Remedy: Various methods are tried to decrease the severity of motion artifacts in the final image, depending upon whether signal from moving tissue is desired in the image or not. While spatial-presaturation pulse may be used in the former case, other remedial measures are required when signal from moving tissue is desired in the image. Spatial-presaturation pulse: When signal from moving tissue is not desired, spatial presaturation pulse can be used to

Chapter 45 Image Optimization in Magnetic Resonance Imaging

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Figs 7A to C:  Motion artifact: T2-weighted sagittal images of the spine show marked motion artifacts degrading the image in (A) (arrows) when

the phase encoding direction was anterior to posterior. On changing the phase encoding direction to head to foot in (B), the motion artifacts from the heart do not degrade the image. There is further improvement in image quality when a spatial-presaturation band (arrows) is used to suppress motion artifacts from the great vessels in (C)

reduce these artifacts. These are used in spine examinations to suppress cardiac and abdominal motion artifacts (Figs 7A to C). These saturation pulses are applied at the beginning of the pulse sequence and hence reduce the number of imaging sections that can be obtained per TR in multislice acquisitions. They may also result in increased heat deposition when specific absorption rate (SAR) is already high. When signal from moving tissue is desired in the image, other methods may be used. These include use of faster sequences, modification of acquisition parameters, physiological triggering and flow compensation. Faster imaging: The most effective technique may be shortening of acquisition time to minimize motion arti­facts. This has been achieved through the improvements in MR imaging hardware, which include faster and stronger gradients, multichannel coils, and higher magnetic field strengths. There are various techniques to obtain faster sequences. Fast spin echo sequences use multiple 180° refocusing pulses and allow multiple echoes to be obtained within a given TR. The number of additional echoes obtained is called the echo train length (ETL). However, excessive ETLs may blur the image and increase some flow artifacts. Sequences such as half Fourier single-shot turbo spin echo (HASTE) allow rapid acquisition by filling only half of k-space. Parallel imaging technique also reduces the scan time and hence motion artifacts. This technique uses multichannel, multicoil technology, with each coil possessing a distinct known sensitivity profile over the field of view. At least 2 coil elements are aligned in the phase encoding direction. The phase encoding steps are reduced by a factor of X, known as the parallel imaging factor. Only one of every X lines of k space is filled up in the phase encoding direction. The other lines are inferred from

the signal amplitude and known sensitivity profile of the coils used. Several data extrapolation algorithms like generalized autocalibrating partially parallel acquisition (GRAPPA) and sensitivity encoding (SENSE) are used before and after Fourier transformation, respectively. The major disadvantage is a decreased SNR. However, overall increase in SNR at 3T makes higher parallel imaging factors possible in clinical practice. Radial k-space filling technique: Multi-shot radial acquisi­tion technique (e.g syngoBLADE, Siemens healthcare, Erlangen, Germany; PROPELLOR, GE healthcare. Milwaukee, Wis) fills the k-space radially instead of standard line by line rectilinear filling. With this technique, MR imaging datasets are acquired in multiple overlapping radial sections. A series of low resolution images is reconstructed from each radial section which is then combined to produce high resolution images. Because the phase encoding direction varies with each radial section, ghosting artifact from motion is not propagated in the phase encoding direction but dispersed through the radial sections. The main disadvantage it has is the low spatial resolution because the periphery of k space is less densely filled than its central region. Modification of parameters: Parameters may be modified to alter the appearance of motion artifacts. Frequency and phase encoding direction can be swapped, which alters the position of the artifact (Figs 7A to C). These may now be relocated to image areas that do not affect image interpretation. For example, motion artifacts due to eye movement may obscure brain parenchyma if phase encoding direction is anteroposterior for an axial image. This may be overcome when phase encoding direction is made right to left and the artifact now lies outside the brain.

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Increasing NEX is another method of reducing motion artifacts. Increasing the number of signal averages increases the signal from the tissue and the motion artifact signal is reduced relative to the tissue signal (Figs 5A and B). Physiological triggering/gating: Physiological triggering syn­ chronizes the data collection with a periodic signal produced by the patient, such as pulse or heartbeat allowing normal movement of tissue. Data collection may be synchronized with ECG signal using lead wires, pulse using pulse sensor on an extremity, respiration using pressure transducer on the patient or a navigator echo indicating diaphragmatic motion. ECG gating is used in cardiac evaluation where artifacts from cardiac motion need to be minimized. This may be prospective or retrospective gating. In the prospective method, the timing signal is first detected. The echo signal is collected at the same time following the time signal. Since the moving tissue is stable at this time, there is minimal misregistration of signal. This is typically used in static cardiac examinations. Prospective triggering also allows the rejection of arrhythmic beats, which can degrade MR image quality. In the retrospective method, the timing signal and the echo signal are first acquired together. The timing signal does not control data collection. These are analyzed only after the scan is complete and the data collection is gated to the timing signal. This method is commonly used in cine cardiac imaging where sequential images are produced according to their time point in the cardiac cycle to allow a dynamic evaluation of cardiac function. Further artifact suppression can be achieved while imaging the heart, if the acquisition is performed during breath holding. The disadvantages of a triggered study include a longer scan time and misregistration artifacts if the trigger signal is irregular, e.g. with an irregular heart rate. In contradistinction to cardiac gating, respiratory gating is not frequently used in clinical imaging. The method of breath holding is used to avoid respiration artifacts. In infants, children, and patients with respiratory and cognitive impairment, either short sequences are used or imaging examination is divided

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into multiple brief sequences if the patient can hold breath for a limited time. However, multiple breath holds require cooperation from the patient. In respiratory gating, bellows or a belt is encircled over the abdomen and the acquisition is timed to end expiration when there is minimum motion. The disadvantages include an increased acquisition time and an additional setup time. Respiratory compensation or phase reordering [respiratory ordered phase encoding (ROPE)] is another effective way to reduce respiratory artifacts. In this technique, phase encoding steps are ordered on the basis of the phase of the respiratory cycle. K-space lines are reordered such that the adjacent samples in the final data have minimal differences in the respiratory phase. This works well only with regular respiratory rate. Navigator echo is a commonly used method to suppress periodic motion artifacts from breathing; it uses an additional navigator pulse. This is most commonly used in abdominal imaging where a small one dimensional spatial encoding gradient is placed perpendicular to the diaphragm (Figs 8A to C). The imaging dataset is then corrected by the navigator echo so that only the data acquired at end expiration (when diaphragm is at peak) is used in reconstruction of final image. Gradient moment rephasing: GRE flow compensation uses additional gradient pulses to correct for phase shifts of the moving protons. It is also known as gradient motion rephasing (GMR) or motion artifact suppression technique (MAST). Additional gradient pulses are used to eliminate the phase shifts in moving protons, bringing them back into phase with no effect on static spins. In most instances, correction is needed only for spins flowing with constant velocity (first order motion compensation). As additional gradient pulses are used, there is a modest increase in TE. In pulse sequences in which short TEs are desired, short duration high amplitude gradient pulses need to be used. This limits the minimum FOV for the sequence. Higher-order compensation can also be done for spins with either constant or varying acceleration, but this further increases the echo time.

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Figs 8A to C:  Motion artifact: Axial T1-weighted gradient echo image of the abdomen shows marked respiratory motion artifact resulting in blurring of the image (A). There is marked reduction in motion artifact (B), using a navigator echo pulse (C)

Chapter 45 Image Optimization in Magnetic Resonance Imaging

Pulsatile Flow-related Artifacts Periodic motion due to pulsatile through plane flow (flow perpendicular to the image plane) results in ghost vessels at discrete points, frequently seen in axial abdomen gradient echo images (Fig. 9). The distance between the ghosts depends on the difference between the heart rate and TR. GRE images are more prone to these ghost artifacts than SE sequences. In spin-echo sequences, flowing blood usually appears dark. This is because after being exposed to the 90° excitation pulse in SE sequences, flowing blood moves out of the imaging section before the refocusing 180° pulse is applied, while the blood protons that move into the imaging section has not been exposed to the excitation pulse; hence, resulting in dark

signal. In contrast, bright blood phenomenon is seen on GRE sequences. Remedy Saturation pulse: A common way to reduce the motion artifact due to through-plane flow is to apply a saturation band adjacent to the imaging section. The protons in this slab are saturated with the use of 90° RF pulse and then spoiled by strong gradients before image acquisition, hence resulting in no signal when spins flow into the imaging volume. When applied superior to the acquisition slab in the abdomen, it eliminates arterial pulsation artifact. When placed inferiorly, it eliminates artifacts from venous inflow in the iliac veins. Advantage of pulsation artifacts: Pulsation artifacts from vascular lesions can help us reach the correct diagnosis, when in doubt. The vascular nature of the lesion is confirmed if we see associated pulsation artifacts.

Artifacts Due to Measurement Technique/Parameters Aliasing

Fig. 9:  Ghosting artifact from pulsatile aortic flow: Pulsatile through

plane flow in the aorta is seen as ghost vessels at discrete points (arrows) on this T1-weighted axial gradient image

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Aliasing (wraparound artifact) occurs when the imaging FOV is smaller than the anatomy being imaged. This occurs mostly in the phase encoding direction. The tissue stimulated outside the sensitive volume of the coil contains higher or lower phase and frequency information. These are misinterpreted during Fourier transformation. This tissue is misrepresented in the image on the opposite side (Figs 10A and B). To explain this, let us recapitulate that the phase of the signal originating from inside the FOV has a range from 0 to 360°. Due to the circular nature of phase, a signal from outside the FOV with a phase

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Figs 10A and B:  Aliasing artifact: T2-weighted axial images of the brain depict aliasing artifact when it was acquired with a reduced FOV smaller than the anatomy of the image. The tissue outside the FOV was misrepresented on the opposite side (A). This was overcome by oversampling in the phase encoding direction (B). However, there was no penalty in scan time as NEX was halved

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in spatial resolution. Oversampling increases the scan time. Hence the NEX is usually halved to compensate for doubling of phase matrix. Usually, there is no penalty in scan time, SNR and spatial resolution. This may not be possible in fast scan techniques like those in abdominal imaging, when NEX is already minimum. Saturation pulse/regional coils: Aliasing can also be minimized by suppressing signal from outside the region of interest using a presaturation pulse or with the use of regional coils to diminish the amount of signal received from outside the region of interest. In 3D sequences, aliasing can be minimized by exciting only a limited part of the volume in the Z-direction by applying a Z-gradient pulse during the RF excitation. Fig. 11:  Aliasing artifact in volume imaging: 3D constructive

interference in steady state (CISS) GRE sequence shows overlap of information of the first and last sections of the sequence due to aliasing

of 400° (=360°+40°) is not distinguishable from a phase of 40° from inside the FOV and hence is misinterpreted within the FOV during Fourier transformation. Thus, the part of the body that lies beyond the borders of the FOV is wrapped inside to the other side of the image. This can mask anatomical structures in the FOV. Wraparound is seldom encountered along the frequency encoding axis because the frequency encoding direction is typically oversampled within the system. In the new imaging systems, the digital receiver automatically filters out unwanted high frequencies or makes use of a high bandwidth in the frequency encoding direction. Aliasing can also be seen in the section direction in volume imaging. The sidelobes of the RF pulse that excites the entire volume of tissue can also produce a signal form outside this slab and information in the first section of the slab may be aliased in the last section of the 3D acquisition (Fig. 11).

Moiré /Fringe Artifact In heavy patients, a special artifact may be seen in coronal imaging when a large field of view which is still smaller than the object is used. This results in aliasing superimposed on phase differences between the two edges. Over large fields of view, homogeneity of the field degrades at the edges, causing phase differences between the edges. Aliasing along with mismatched phases over the edges produces the moiré or fringe artifact (Fig. 12). These are seen in gradient echo images. Use of spin-echo sequences eliminates these artifacts. Another measure that may be taken to reduce these artifacts is to ensure that the arms of the patient are by the side of his/her body while positioning so that they are within the FOV while imaging chest/abdomen.

Remedy Increase FOV: The wraparound can be eliminated by enlarging the phase FOV to accommodate the entire object. Increase in FOV increases the SNR but decreases the spatial resolution. Swapping the phase and frequency encoding direction: The phase encoding and frequency encoding directions may also be swapped if the phase encoding is not already along the shorter axis. Oversampling/no phasewrap: Oversampling may be done in the phase encoding direction. This is done by increasing the sampling points; however, these are not used for image creation (Fig. 10). The FOV is doubled in the phase direction along with doubling of the phase matrix to avoid any decrease

Fig. 12:  Moiré artifact: T1 gradient coronal image of the abdomen in

a heavy patient using a large FOV that is still smaller than the patient depicts the Moiré artifact. This is seen as stripes (arrows), and occurs as a result of a combination of aliasing and field inhomogeneities between the two edges. These are especially prominent at areas of susceptibility borders (e.g. air tissue interfaces)

Chapter 45 Image Optimization in Magnetic Resonance Imaging

Chemical-shift Artifacts The chemical-shift phenomenon can be defined as the signalintensity alterations that occur due to the inherent differences in the resonant frequencies of precessing protons. Clinically, the chemical-shift phenomenon is most evident between the signals of water and lipid. In water, hydrogen is linked to oxygen and in fat, it is linked to carbon. The protons hence have different chemical environments. When placed in an external magnetic field, these protons have slightly different precessional frequencies. Hydrogen in fat resonates at a lower frequency than water. Because fat and water protons have different precessional frequencies, these are allocated to different image pixels along the frequency encoding axis. Although this occurs throughout the image, this is most apparent at fat fluid interfaces, e.g. in imaging of fluid filled structures like bladder, orbits and kidneys which are surrounded by fat. When the chemical shift misregistration is greater than or equal to the size of an individual pixel, a dark or bright band of signal intensity will occur at the lipid-water interface in the frequency-encoding direction of the image. The dark bands appear because of the shifting of the lipid proton signals to a lower frequency, away from the actual lipid–water interface, which causes a signal void. The bright bands result from the overlapping of water signal with “shifted” lipid signal on the high-frequency side of the interface. Despite their presence, the bright bands may be more difficult to appreciate when an object with curved surface is being imaged. The approximate chemical shift between lipid and water is 3.5 parts per million. At field strength of 1.5 T, protons from fat resonate at a point approximately 220 Hz downfield from water protons. This difference is directly proportional to magnetic field strength. The number of pixels involved in this shift is directly proportional to the field strength and frequency matrix but inversely related to the receiver bandwidth. CSA = Dω. Nfreq/BWrec CSA = chemical sift artifact, Dω = frequency difference between fat and water dependent on field strength, Nfreq = frequency matrix, BWrec = receiver bandwidth In high-field-strength magnets, frequency difference between fat and water increases, resulting in greater CSA. However, higher SNR at this field strength allows higher bandwidth sampling rates, which diminishes these artifacts. Use of narrow receiver bandwidths and large matrix in the frequency encoding direction can accentuate these artifacts. These artifacts were commonly seen in T2-weighted images before the invention of TSE imaging as the former used low bandwidths to increase the low SNR inherent in T2-weighted sequences. Remedy: To reduce these artifacts, various measures may be taken. The phase and frequency-encoding direction may be swapped. The frequency-encoding direction may be used

along the axis where there is narrow fluid–fat interface or in a direction where this artifact does not hamper the primary area of interest. Suppression of fat or water signal by the use of STIR/chemical/spectral presaturation is another means of reducing this artifact. Receiver bandwidth is another parameter that may be altered to reduce this artifact. Receiver bandwidth is the range of frequencies sampled within the FOV during readout in the frequency encoding direction. When this is increased, more frequencies are mapped across the same number of pixels. Consequently, there is a reduction in the chemical shift. However, when we increase the receiver bandwidth, signal to noise ratio of the image drops.

Advantage Chemical shift along the frequency axis forms the basis of MR spectroscopic imaging.

Chemical Shift in Echoplanar Imaging These artifacts also occur with echoplanar imaging, but in the phase-encoding direction. These are fast sequences where images are acquired in 50–80 ms. The receiver bandwidth is normally very large in the frequency encoding direction (greater than 100 kHz), hence chemical shift is not appreciable in this direction. However, the phase encoding occurs in a continuous fashion with a low bandwidth, resulting in pronounced chemical shift artifacts in this direction. Fat suppression techniques are necessarily used to minimize the artifact (Figs 13A and B).

Phase-cancellation Artifact This is the second artifact induced by chemical-shift differences between fat and water protons. It can also be referred to as chemical-shift artifact of the second kind. These artifacts are observed in gradient-echo images and not in spin echo sequences which use a 180° refocusing pulse. This pulse redirects the fat and water proton spins back into phase with respect to one other by the time of readout (TE). The lack of a 180° refocusing radio-frequency pulse in gradient-echo sequences results in the cycling of fat and water proton signals in and out of phase with respect to each other over time. The time interval between fat and water being in phase is called the periodicity. This time, depends on the frequency shift and hence the field strength. At 1.5 T, the periodicity is 4.8 ms. This periodicity decreases at lower field strengths, hence the time at which fat and water protons are in phase with each other increases at low field strengths. At 1.5 T, fat and water signals precess in phase approximately every 4.8 msec; every 7.2 ms at 1.0 T; and every 36.7 msec at 0.2 T. This periodicity is used to obtain in-phase and opposedphase MR images. In in-phase images, fat and water have

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Figs 13A and B  Chemical-shift artifact: (A) Echoplanar imaging depicts chemical shift artifact in phase encoding direction which is anterior to posterior; (B) Fat-suppression technique can be used to minimize the artifact

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Figs 14A and B:  Phase-cancellation artifact: In (A) and opposed phase (B) gradient echo MR images of the abdomen at TE 4.8 msec and TE 2.4 msec, respectively in a 1.5 T MR system show a dark rim surrounding the structures at fat water interfaces on the opposed phase images

the same phase orientation. The signal contribution of fat and water protons therefore is additive in the final image. In opposed-phase images, the transverse magnetization of fat and water cancel each other. Hence, in voxels containing equal fat and water such as those at interfaces between fat and water based tissues, this signal cancellation results in a dark ring surrounding the tissue, also known as contour artifact (Figs 14A and B).

Advantage Opposed-phase images are used to detect intracellular fat and can be used in assessment of fatty infiltration of liver, adrenal masses and in assessment of marrow infiltration.

Truncation Artifacts Truncation or Gibbs artifacts are ripple like features that appear at regions of abrupt transition between high and low signal intensity structures, e.g. in T1 weighted images when high signal from fat at the edge of the region is still present at the end of data collection or in T2 weighted MR images of the spine at the interface of low signal intensity spinal cord with high signal intensity CSF. These are seen as stripes or rings in the image with alternating high and low signal intensity. These are also known as edge oscillations. These artifacts are a result of insufficient digital sampling of the echo. Since there is a limited window period available for measurement of signal, there is interruption of this

Chapter 45 Image Optimization in Magnetic Resonance Imaging

measurement at certain locations and data is truncated or omitted in k-space. Approximation errors in Fourier transformation of these signals lead to truncation artifacts. As Fourier transformation is better used for estimating gradual transitions, abrupt transitions at high contrast interfaces results in these artifacts. These sharp borders which exist between areas of high contrast are represented by high spatial frequency data. The highest sampled frequency is inversely proportional to the size of the pixels. When we use a lower matrix, i.e. a bigger pixel size in the phase encoding direction, the higher frequencies are cut off, which leads to incorrect imaging of sharp edge lines. These artifacts can be seen in both phase and frequency encoding direction. However, they are usually seen in the phase encoding direction because usually a smaller phase matrix is used as compared to frequency matrix in order to reduce the acquisition time. Remedy: These artifacts can be diminished by reducing the size of pixels, by increasing the acquisition matrix. However, this occurs at the expense of reduced SNR and increased acquisition time. Another method of reducing these artifacts is by applying various filters. Raw data filters may be used prior to Fourier transformation (e.g. Fermi, Gaussian, Hanning filters). These filters force the signal amplitude to zero at the end of data collection period. These improve the SNR of the image as high frequency noise is removed from the signal. However, excessive filtering may result in loss of sharpness of the image as this eliminates high frequencies responsible for edge definition, resulting in blurring. Image reconstruction of rectangular raw data matrices automatically uses a weak filter.

A

Magnetic Susceptibility Difference Artifacts Magnetic susceptibility is a measure of spin polarization or magnetization induced by external magnetic field. The magnetic field contribution from the tissue may add to or subtract from the main magnetic field, depending upon whether the structure is paramagnetic or diamagnetic respectively. Differences in tissue susceptibility hence lead to magnetic-field inhomogeneities. Tissues, such as cortical bone or air filled organs, such as lungs and bowel have small magnetic susceptibility. Soft tissues, on the other hand, have more polarisable material and greater tissue susceptibility. At the interface between these regions with high and low magnetic susceptibility, significant distortion artifacts result due to local magnetic field gradients or field inhomogeneities. These result from enhanced dephasing of protons located at the boundaries of structures with a very different magnetic susceptibility. These artifacts are seen as areas of signal void. The second effect is that of strong distortion of the main magnetic field resulting in geometric distortion of anatomy (Figs 15A and B). The paranasal sinuses, the orbits, the lungs, heart, stomach and intestinal loops are the problematic areas. These are also observed in kidneys and bladder after administration of paramagnetic contrast agent which concentrates in these organs leading to significant signal loss. These artifacts are more pronounced with gradient echo sequences (Fig. 15A) and EPI imaging (Fig. 16A). In gradient echo imaging, signal amplitude is a function of T2*, in which proton dephasing from magnetic field inhomogeneities is an important factor that affects image contrast. On the other hand, spin-echo sequences use a refocusing 180° pulse which

B

Figs 15A and B:  Magnetic-susceptibility artifact. Gradient-echo sagittal image of the spine shows magnetic susceptibility artifact due to a metal fixator, seen as areas of signal void and geometric distortion (arrows in A). Use of spin-echo sequence (B) minimizes the artifact

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Figs 16A and B:  Magnetic-susceptibility artifact. Echoplanar imaging shows marked distortion when the phase-encoding gradient is from

right to left (A). This is minimized by keeping the direction of the phase-encoding gradient from anterior to posterior, and hence along the susceptibility gradient in brain (B)

rephases the protons and hence minimizes these artifacts (Fig. 15B). With EPI imaging, the entirety of k-space is filled by data from one RF pulse. This single-shot readout using gradient refocusing over a long period is predisposed to these artifacts. Generally, high bandwidth of this sequence in frequency encoding direction protects it from these distortions in this direction. However, low bandwidth in EPI sequence in the phase encoding direction affects distortions in this direction. Therefore, the phase encoding gradient is oriented along the axis of the susceptibility gradient (anteroposterior direction while imaging the brain) to reduce the distortion in EPI imaging (Fig. 16B). The higher the field strength of the main magnetic field, the stronger are these artifacts. Also, these artifacts are more pronounced when sequences having long echo times are applied. The longer the TE, greater is the time available for dephasing of protons. Remedy: Following remedies may be done to eliminate or reduce these artifacts. Spin echo sequences may be used which use a rephasing 180° pulse. TE may be reduced as longer the TE, greater is the time available for dephasing of protons. The best combination of spin echo and short TE is found in fast spin echo techniques rather than the conventional spin echo sequences. The voxel size may be reduced to reduce the local magnetic field inhomogeneities. Larger bandwidth sequences also reduce these artifacts. Although these susceptibility artifacts are more pronounced at higher field strengths, inherent improvement in SNR in 3T systems allows the use of higher bandwidth and parallel imaging to reduce these artifacts. These artifacts can be reduced in multishot EPI acquisitions, with parallel imaging and with radial k-space sampling technique.

Advantage These artifacts can be of great advantage when hemorrhage is being investigated, as blood products become more apparent due to magnetic susceptibility or blooming artifacts. They are also used to our advantage as they form the basis of perfusion imaging, functional imaging of the brain, quantification of liver iron content and use of reticuloendothelial specific agents in liver imaging.

Section Cross Talk In multisection two dimensional sequences, crosstalk artifact can result if there is no interslice gap. This is a result of imperfect shape of the RF slice profiles which should ideally be rectangular but are actually more curved shaped. Side lobes of RF pulses can excite part of adjacent sections. Hence these are excited twice by an RF pulse in the same TR, resulting in saturation and low-signal intensity. This is seen in all sections except the first and last slices. This is not seen in three dimensional sequences as the whole volume of tissue is excited together and gradients are used to obtain sections within this volume. Remedy: This can be overcome by using RF pulses with sharper section profiles, increasing the gap between sections, and/or imaging multiple sections in separate batches (interleaving).

Parallel-imaging Artifact Parallel-imaging techniques such as GRAPPA and SENSE help us to reduce acquisition time by extrapolating data before and

Chapter 45 Image Optimization in Magnetic Resonance Imaging

A

B

Figs 17A and B:  Parallel-imaging artifact. Axial T1-weighted gradient image acquired without parallel imaging (A) and axial T1-gradient image

acquired with a parallel imaging factor of 2 (B) shows noise and reconstruction artifacts in the middle of the FOV in the latter image (arrows in B) which limit the diagnostic quality of the image

after Fourier transformation, respectively. However, we must take care to avoid very high acceleration factors as the noise level increases and SNR falls with use of high acceleration factor. This noise can be seen in the center of the image (Figs 17A and B). Also, if field of view is smaller than the object being imaged, increased noise can be seen in addition to aliasing artifact. This aliasing artifact may also be projected in the central portion of the image. This moves outwards as the parallel imaging factor is reduced.

External Artifacts External artifacts are generated from sources other than the patient. These could be classified into two categories—those that are hardware related and those that are not. Improper calibration of gradients, RF transmitter and receiver system can lead to various distortions and incorrect spatial localization. The gradient system and RF transmitter system can sometimes malfunction and work in an unstable manner. This can result in amplitude and phase modulations resulting in ghosting or smearing artifacts and occur throughout the image field in the phase encoding direction. These may be indistinguishable from motion artifacts. These system related artifacts could be transient effects generated within one or more of the subsystems or could be a sign of degradation of some of the electronic components in the subsystem.

Artifacts Caused by Field Distortions Distortions artifacts may be caused by main magnetic field inhomogeneities or nonlinearity of the gradient field or RF field inhomogeneities.

Main field inhomogeneities: Although most manufacturers very carefully construct MR systems with homogeneous magnetic fields, but some inhomo­g eneities still occur because of field falloff towards the magnet periphery. This is more pronounced in large bore or open MR systems. This is especially important in spectral-fat suppression sequences. If the magnetic field is not homogeneous, fat suppression pulse may not uniformly suppress the fat. This is mostly seen at the edges of an image with large FOV. To minimize the artifact, the anatomy should be centered within the magnet as much as possible and field homogeneity correction should be done just prior to the scan, with the patient inside the scanner. Distortions in the main magnetic field may also result from ferromagnetic substances like zippers, metal clips on the patient’s body/clothing (Figs 15A and B). These result in magnetic susceptibility artifacts as described above, but these are more severe as metals have much higher magnetic susceptibility than body tissues. These can be minimized by using fast SE sequences using a high bandwidth and decreased echo time. However, care should be taken in these cases as metallic objects can result in more energy absorption and heating as compared to normal body tissues. Gradient-field nonlinearity: Gradient-field nonlinearity is related to gradient falloff due to finite size of gradient coils. Gradient coil produces a varying magnetic field that is linear through the isocenter of the magnet but tapers towards the side of the magnet. This leads to distortion and loss in spatial resolution. In a large FOV image, gradient field distortion is seen as compression of the structures at the edge of the image (Fig. 18A). As this is a predictable artifact, MR imaging software can correct these distortions before the final image

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electrical connections that produce arcs or because of breakage of interconnections in an RF coil. These are more frequently encountered when gradients are applied at high-duty cycle, e.g. in echoplanar imaging. These produce bad data points or a spike of noise, in k-space. Fourier transformation of this spike of noise results in a specific ‘crisscross’ or ‘herringbone’ pattern seen as dark stripes overlaid on the image (Fig. 19). Spike noise is usually transient but can become chronic if not attended to.

Advantage This pattern of stripes produced by spiking can be utilized for tagging, which is a vital technique in cardiac imaging. A

B

Figs 18A and B:  Field distortion due to gradient-field nonlinearity:

Sagittal T2-weighted image of the thoracic spine shows geometric distortions resulting from gradient nonlinearity, with vertebral bodies appearing progressively smaller toward the inferior edge of the FOV (arrow in A). Distortion correction software was used to correct the distortion (arrow in B)

is reconstructed. Postprocessing techniques can also correct the distortions but not the accompanying loss in spatial resolution (Fig. 18B). RF-field inhomogeneities: Inhomogeneities in RF pulse are not the cause of geometric distortions but can lead to nonuniformity in signal. These may be due to problems in RF construction or from dielectric (standing wave) effects. Dielectric effect is especially prominent at 3T systems because high-frequency low-wavelength RF pulse is required to excite protons at this high-field strength because of increased Larmor frequency of protons. The wavelength of these RF pulses approximates the dimensions of the anatomic structure and standing waves may result. These waves manifest as bands of destructive and constructive interference, seen as dark and bright zones respectively. Dielectric pads may also be used to change the patient’s apparent girth to reduce the effect. RF field distortions can also lead to inhomogeneous fat suppression on STIR imaging. RF shimming can help reduce the artifact. Alternatively, spectral-fat saturation may be used instead of STIR sequence to suppress fat. STIR is a nonspecific technique of fat suppression, as signal is suppressed from all tissues with a T1 equal to that of fat. Spectral-fat saturation, in contradistinction, suppresses the fat signal only because it is based upon differentiation of resonant frequency of fat from water.

Spike (Herringbone) Artifact Spikes are noise bursts of short duration that can occur randomly during data collection. These are a result of loose

Zipper Artifact Zipper artifact is an artifact that is caused by external interference resulting from external RF fields, as those caused by open doors, radios, mobile telephones, electronic controls, etc. These emit interfering electromagnetic signals that hamper MR image quality. Zipper artifact appears as a region of increased noise with a width of 1 or 2 pixels that extends perpendicular to the frequency encoding direction, throughout the image series. Remedy: To prevent these artifacts, MR tomographs are installed in RF-sealed rooms, also known as Faraday cage. These sealed rooms not only protect the equipment from external RF interference but also shield the environment from RF fields generated by the tomograph. The door of the MR room should always be closed properly to prevent this interference. If any constructional changes take place after the installation of the MR tomograph, e.g. drilling holes for cables, it may lead to interference in RF shielding. In this

Fig. 19:  Spike or herringbone artifact. Loss of data points in the

process of acquisition due to a spike of noise can lead to a “crisscross” or “herringbone” pattern of artifact

Chapter 45 Image Optimization in Magnetic Resonance Imaging

case, the source of interference needs to be carefully looked for. Sometimes, electrical connections from any patient monitoring device which work on alternating current can also interfere with RF shielding. The persistence of the artifact even after the equipment is removed indicates compromise of the RF shield.

CONCLUSION Clinical MR imaging is becoming more and more versatile and complex, making it difficult for the radiologist to grasp the physical principles underlining the changing technology. Nevertheless, knowledge of basic MR physics plays a key role in clinical imaging as its understanding can help us modify imaging protocols to obtain optimum image quality within acceptable scan time. Good-quality images enable us to reach the correct clinical diagnosis with greater confidence.

BIBLIOGRAPHY 1. Brown MA, Semelka RC. Artifacts. In: MRI- Basic principles and applications, 3rd edn. New Jersey: Willey Liss Inc; 2003. pp.113-40.

2. Brown MA, Semelka RC. Measurement parameters and image contrast. In: MRI- Basic principles and applications, 3rd edn. New Jersey: Willey Liss Inc; 2003.pp.93-102. 3. Hood MN, Ho VB, Smirniotopoulas JG, Szumowski J. Chemical shift: the artifact and clinical tool revisited. Radiographics. 1999;19:357-71. 4. Mitchell DG, Cohen M. In: MRI principles, 2nd edn. Philadelphia, Pa: Saunders; 2004.p.416. 5. Morelli JN, Runge VM, Ai F, Attenberger U, Vu L, Schmeets SH, Nitz WR, Kirsch JE. An image based approach to understanding the physics of MR artifacts. Radiographics. 2011;31:849-66. 6. Stadler A, Schima W, Ba-Ssalamah A, Kettenbach J, Eisenhuber E. Artifacts in body MR imaging: their appearance and how to eliminate them. Eur Radiol. 2007;17(5):1242-55. 7. Westbrook C. Artifacts. In: MRI at a glance. 1st edn. Great Britain: Blackwell Science; 2002.pp.73-78. 8. Westbrook C. Image quality. In: MRI at a glance. 1st edn. Great Britain: Blackwell Science; 2002.pp.64-72. 9. Yang RK, Rith CG, Ward RJ, deJesus JO, Mitchell DG. Optimising abdominal MNR imaging: approaches to common problems. Radiographics. 2010;30:185-99. 10. Zhuo F, Gullapaali RP. MR artifacts, safety and quality control. Radiographics. 2006;26:275-97.

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Diffusion Weighted Magnetic Resonance Imaging

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CHAPTER

Devasenathipathy Kandasamy, Raju Sharma

INTRODUCTION Magnetic resonance imaging (MRI) imaging has become an important imaging tool in the current clinical practice mainly because of its excellent contrast resolution without the risk of any ionizing radiation. This has become even more relevant with the growing concern for radiation issues in computed tomography (CT) and other imaging modalities which utilize ionizing radiation. Diffusion-weighted imaging (DWI) is a promising technique which was originally described by Le  Bihan 30 years back and because of the recent developments in MR hardware this has found a place in routine clinical MR protocols. The basic principle of DWI is based on the Brownian motion of water molecules which takes place in the body and it utilizes motion sensitizing gradients to study this motion.1,2 It provides unique information at a microstructural and functional level which can be used to characterize cellular dense lesions and this has applications in oncology. Other reasons why this technique is appealing are that it can be performed rather quickly and does not require the use of exogenous contrast agents. Diffusion can be assessed both qualitatively and quantitatively. It is quantified by the parameter called apparent diffusion coefficient (ADC) which is derived from the diffusion images. The ADC is a scalar quantity which has only magnitude without any directional information.3 This chapter will focus on the basic principles of DWI and optimization of the technique and briefly review its clinical applications.

large nuclei and scanty cytoplasm which results in restriction of diffusion (Fig. 1). On the other hand, benign cells are loosely packed with small nucleus and abundant cytoplasm that facilitates diffusion.5 Because of the interaction of water molecule within biological tissues which can impede the actual diffusion the measured diffusion is termed as ADC which is expressed in mm2/s. When the diffusion is not restricted in any particular direction it is called isotropic diffusion as seen in CSF space and cystic lesions. When the diffusion occurs preferentially in a particular direction it is called anisotropic diffusion which is usually seen in white matter of brain.6 In white matter and peripheral nerves the water diffuses preferentially along the axon. Diffusion-weighted imaging can generate images in which the contrast between the structures is based on the diffusion characteristics. There are various types of sequences with

BASIC PRINCIPLE Water molecules in the body undergo a random motion called “Brownian motion” which is as a result of body heat.2 Theoretically, these constant random motions are uniform in all directions. But the diffusion in body tissues is restricted by various organelles, membranes and tissue planes. The intracellular diffusion is more hindered than the extracellular component because of the presence of cell membrane.4 In case of malignant tumors the cells are densely packed with

Fig. 1:  Schematic representation of signal intensities on T2W, DW sequence and ADC map for disease entities and artifacts which are commonly encountered in day-to-day practice

Chapter 46 Diffusion Weighted Magnetic Resonance Imaging

diffusion sensitising gradients incorporated within but the basis of all of them is the technique suggested by Stejskal and Tanner in 1965 and implemented by Le Bihan in 1986.7,8 Their technique essentially involves adding two diffusion sensitizing gradient, one on either side of 180° refocusing pulse. These gradient lobes have the same magnitude but are opposite in direction. The first gradient lobe is called dephasing gradient which will dephase the spins of water molecules and the second is called the rephasing gradient which will rephase the spins to their original state. The 180° pulse will eliminate the dephasing due to the inhomogeneity of external magnetic field. This principle has been adopted with or without slight variation even in modern day sequences.9 The idea behind this technique is that the water molecules whose diffusion is not restricted will get dephased by the first gradient lobe and during the process the molecules will move to another location in which the water molecules will be subjected to a different magnetic environment so that the rephasing pulse will not exactly rephase them to their original state. This will cause attenuation of signal from these water molecules as they are not exactly rephased to produce a strong echo. Whereas, water molecules whose diffusion is restricted will not move and they will be subjected to the same magnetic environment and the dephasing and rephasing gradients will exactly neutralize each other and their spins will be in phase to produce a strong echo. These diffusion gradients can be applied in any of the axis (x, y, z) or in any combination and it is called diffusion sensitizing direction. This diffusion gradient addition can be applied in spin echo or in steady state sequences as long as they have a long TE to accommodate them and this is the reason why the diffusion sequences are T2 weighted.

B VALUE The magnitude, duration of diffusion gradient applied and the duration between the dephasing and rephasing lobe determines the sensitivity of the sequence to water diffusion which is described by a factor called diffusion weighting factor or b factor (s/mm2). All the above factors are directly proportional to the b value. Usually, the magnitude is kept maximal and the other two are altered to get a desired b value. At least 2 b values are needed for the calculation of ADC and multiple b values are used for more accurate quantification.2 When multiple b values are used the TE time which is maximum for highest b value is usually kept constant for all b values for better quantification.6 The choice of b value is very important and depends on the hardware, region of study, type of sequence and the quantitative or qualitative nature of the study. The usual thumb rule is that b value is about inverse of the expected ADC value.9 For example if the expected ADC value of a tissue is 1.2 × 10-3 then the approximate b value is 800. The SNR of the sequence is grossly affected by the b value selection. When the b value is increased, the SNR of the sequence reduces and at very high values the SNR becomes

very low so as to make the quantification unreliable. At the same time low b value will not generate an image whose contrast characteristics are truly based on diffusivity of water molecules. So optimal b value is a balance between the SNR required for quantification and the diffusion contrast of the image. High b values (>1000) are used in imaging techniques like diffusion weighted whole body imaging with background body signal suppression (DWIBS) in which background signal suppression is important. Although multiple b values increase the accuracy of quantification of diffusion it also increase the acquisition time and associated artifacts. There are several approaches developed to circumvent these issues which are discussed later in the chapter.

ADC AND EXPONENTIAL IMAGE Apparent diffusion coefficient (ADC) image is a parametric map which is derived from the DW image and it is devoid of T2 shine through (vide infra). It needs images acquired at minimum of two b values to calculate ADC and in present day scanners the calculation of ADC map is automatic. The ADC value is dependent on the b value used where it is inversely proportional to the b values used even in the same patient. It is also dependent on the field strength of the scanner, gradient hardware and the type of image processing software used.2 Since ADC map is the Gray Scale representation of pixel by pixel ADC values calculated from diffusion images, the artifacts associated with the diffusion sequences will also get reflected. In addition poor SNR in high b value images also adds to the deterioration of image quality. This is the reason for ADC map having poor image quality when compared to the diffusion image and in isolation it is not very useful for diagnostic purposes. Apparent diffusion coefficient values are usually inversely proportional to the degree of restriction. Area of restricted diffusion is seen as hyperintense on diffusion weighted images and hypointense on ADC and vice versa. Another way to remove the T2 effect on the diffusion weighted image is generating an exponential image which is done by calculating the ratio of diffusion weighted image and b 0 image.10 Contrary to ADC map, hyperintensity on the exponential image corresponds to hypointensity on ADC map and suggests diffusion restriction and vice versa.

DWI SEQUENCES AND OPTIMIZATION Many sequences are altered to introduce the diffusion gradient pair for the development of DWI sequences. Some of the most commonly used sequences are discussed here.

Echo Planar Imaging Although echo planar imaging (EPI) was initially proposed by Mansfield in 1978, it is the recent advancements in MR hardware and reconstruction software that made this

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sequence useful for clinical studies. It is an extremely fast technique which can fill the entire k space in single shot. It is robust and insensitive to motion artifacts which made it useful in DWI. After the initial excitation pulse, diffusion gradient pair, a series of fast gradient oscillations is applied for readout and the entire k-space is filled with a long echo train (Fig. 2). This can be implemented as spin echo EPI or gradient echo EPI. Typically, separate acquisition is done for 3 orthogonal axes which are averaged into one final image. One of the disadvantages of EPI is significant phase shift gets accumulated between the water and fat protons and this leads to geometric distortion along the phase encoding direction.6 As a result the fat signals can be offset by many pixels which will deteriorate the image quality, more so in higher field strengths. So, it is of paramount importance that all EPI sequences are done with fat suppression. There are various methods of fat suppression, such as water only excitation, chemical fat suppression, short-tau inversion recovery (STIR) and spectral selection attenuated inversion recovery (SPAIR) of which the latter two are inversion recovery sequences. SPAIR is a very good method of fat suppression for small FOV in which the fat suppression is uniform along with good SNR. For larger FOV, STIR is the best method to provide uniform suppression but at the cost of reduced SNR. Another disadvantage of EPI is that in longer echo train the water protons tend to show phase shift especially in the air–soft tissue and bone–soft tissue interfaces resulting in geometric distortion in the phase encoding direction.9 This can be reduced by using parallel imaging and high-performance gradient coils which will shorten the echo train length, echo spacing and the readout time. Another problem with single shot EPI is limited spatial resolution in the order of 128 × 128 because of the rapid signal decay and limited SNR. These problems can also be reduced by splitting the acquisition into more than one excitation. This is a challenge if it has to be implemented in body imaging where motion is an important consideration. For body

diffusion several approaches are followed which are discussed here. First approach is to perform a single shot acquisition with breath hold in which the disadvantages are the poor spatial resolution, limited number of b values, less number of averages and less anatomical coverage. Poor SNR can lead to unreliable ADC values. Second approach is acquisition across multiple excitations with respiratory/cardiac trigger. This overcomes the problems with single shot breath hold technique. However, triggers cannot totally rule out motion artifacts and the imaging time gets prolonged. Third approach is free breathing technique with multiple averages and can use multiple b values.11 Regarding the choice of b values it is a balance between the accuracy of quantification and contrast resolution in the diffusion image (vide supra).

Turbo Spin Echo Sequences or Half-Fourier-acquisition Single-shot Turbo-spin Echo This is an alternative to DW-EPI sequence and it is also rela­ tively insensitive to motion and can perform a single shot readout and the entire k-space is filled in single excitation. An important difference from EPI is that 180° refocusing pulse is applied during each readout so that the phase shift accumulation, because of long echo train, is avoided (Fig. 3). This reduces the geometric distortion and susceptibility artifacts. Apart from this it has other disadvantages of single shot EPI sequence. Parallel imaging can improve the spatial resolution and reduction of geometric distortions. This sequence can also be segmented into multi-shot acquisition which has similar advantages as multi-shot EPI.

Steady-state Free-precession Steady-state free-precession (SSFP) is also a fast sequence so it is relatively insensitive to motion. It is an atypical diffusion

Fig. 3:  Schematic representation of single shot fast spin echo Fig. 2:  Schematic representation of DW spin echo EPI sequence

showing the motion probing gradients (arrows) used to detect the diffusion of water molecules and multiple gradient oscillations (outlined arrow) to generate echoes. In this single shot sequence, the entire k space is filled in single excitation

sequence showing motion probing gradients (arrow) to detect the water diffusion. Multiple 180° refocusing pulses (outlined arrow) rather than gradient oscillations are used to generate echoes. In contrast to SE-EPI sequence, the use of refocusing pulses avoid the accumulation of phase shifts thereby reducing artifacts. This is also a fast sequence which is capable of acquiring the entire image in single excitation

Chapter 46 Diffusion Weighted Magnetic Resonance Imaging

sequence in comparison to the above two with regard to the usage of diffusion sensitizing gradients. Here, both the dephasing and the rephasing gradients are not applied in the same repetition time (TR). They are applied in different TRs and not necessarily in the immediately following TRs. Consequently, it is almost impossible to quantitate the diffusion using this sequence. However, the contrast resolution is excellent so that it can be used for qualitative assessment of images. Recently, three-dimensional diffusion weighted sequences have also been developed.

ARTIFACTS AND PITFALLS There are many artifacts and pitfalls which are inherent to the technique itself, so it is very important for the radiologists and the technicians to be aware of those. In this chapter we will discuss few of the important ones which are relevant to clinical practice.

T2 Shine Through This is one of the well-known phenomenon which can potentially lead to a wrong diagnosis when diffusion weighted images are interpreted in isolation. It is because DW sequence is based on a T2 weighted sequence and its effects are shown in the final image. It is very prominent in low b value images where the T2 effects predominate. For example, simple cysts in which diffusion is not restricted are seen as hyperintense structure on DW images. The ADC map or exponential images can help overcome this pitfall since both of them eliminate the T2 effect in the image and represent diffusion characteristics only (Fig. 1). In the above example of simple cyst the ADC map will show hyperintensity because of unrestricted diffusion. At the same time when the lesion is hyperintense on T2 weighted images and hypointense on ADC, the hyperintensity in DW images will get accentuated.6 When multiple b value images are available then the hyperintensity which is due to T2 effect decreases with increase in b value whereas the hyperintensity due to diffusion is retained.

T2 Washout This phenomenon is seen when the T2 hyperintensity is balanced by the increase in ADC in the DW image.12 This is usually seen in vasogenic edema in which there is increase in ADC because of increased diffusivity and that effect is balanced by the T2 hyperintensity. Thus in the DW image the lesion appears isointense. Again this effect can be circumvented by interpreting DW images along with ADC map in which the lesion appears hyperintense (Fig. 1).

in hematoma which is seen as T2 hypointensity because of susceptibility effect.13,14

Eddy Current Artifacts Eddy current artifact is worth mentioning here because it is commonly associated with EPI sequences which is the most common sequence used for DWI. Eddy Currents are produced in the patient body and in the scanner hardware by rapidly changing magnetic gradients which are used in EPI sequence for sensing diffusion and readout. This can cause image distortion, spatial blurring and misregistration artifacts. This necessitates postprocessing of the data before ADC calculation to prevent quantification errors.15 This artifact can also be reduced by using proper shielding in the hardware.

Susceptibility Artifacts This is also commonly seen in EPI sequences at the bonesoft tissue or air–soft tissue interface like close to skull base, sinuses, mastoids, bowel and lung bases. This leads to accumulation of phase shifts which are more pronounced in the phase encoding direction. This gets even worse if the matrix size is increased because of prolonged readout time. This can be reduced by using DW-HASTE sequences in which the phase shifts are periodically corrected or by using multi-shot acquisition or by using parallel imaging so that the readout time is reduced.

Chemical-shift Artifacts Usually in conventional spin echo sequences the effect of difference in precession frequency of water and fat protons are seen along the frequency encoding direction. Whereas in EPI sequences the artifact is seen along the phase encoding direction and it is very prominent again because of accumulation of phase shifts during longer readouts. This can be prevented by using effective fat suppression techniques (vide supra).

Motion Artifacts Motion artifacts are due to gross patient movement or cardiac/respiratory/bowel motion. Although the currently available single shot techniques are fast enough to avoid motion artifacts, multi-shot techniques suffer from motion in body imaging. This can be reduced by using cardiac/ respiratory triggered sequences, parallel imaging, propeller or high-amplitude gradients.2

T2 Blackout

Effect of Contrast Media

This effect is noted when the T2 hypointensity is reflected on the DW image as hypointensity (Fig. 1). It is usually seen

The gadolinium-based contrast media used for MR imaging can have an effect on the diffusion parameters especially in

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kidneys where they are concentrated by causing paramagnetic effects locally. Recent evidence suggests that the ADC values of kidneys can be significantly lower in the postcontrast image than the precontrast image. Similar effects were not found in the liver, pancreas and spleen.16

ADVANCED DW TECHNIQUES Diffusion Tensor Imaging There are newer techniques, such as diffusion tensor imaging (DTI) which have both magnitude and the directional information of diffusion also. The DTI is extensively studied in brain where it is used to show the white matter tracts. It uses the property of anisotropy of diffusion of water molecules. Because of the myelinated axons in the brain white matter, the diffusion is unhindered along the direction of the fiber which is called diffusion anisotropy. Diffusion information given by the DWI is a scalar quantity which lacks the directional component. To obtain the directional component gradient lobes are used in multiple directions and the resulting data is processed. As a result each voxel has the effective direction of diffusion which is called as Eigen vector and the value of diffusion in that direction is called as Eigen value. This information is used to reconstruct fiber tract network in the brain which is called as tractography. Although this tensor model holds good in many situations, it can be limited if there are crossing fibers with different direction of diffusion in a voxel. So there are newer approaches to overcome this limitation, such as high angular resolution diffusion imaging (HARDI) which can be used to study the complex diffusion process.

Whole Body Diffusion-weighted Imaging There is evidence that whole body DWI along with anatomical images, such as T1 and T2 can be very useful for the evaluation of malignant tumors.2,17 The DWIBS is a whole body diffusion technique which is done typically using DW-EPI sequence and STIR for fat suppression. It is a free breathing technique in which the scans are usually taken from the skull base till the level of mid-thigh. Acquisition is done in multiple stations using multiple thin slices and a large number of signals are collected and averaged. Typically, b value in the range of 1000 is used which will provide good background suppression. But, more than one b value can be used if quantification is needed at the expense of time. These multiple slices are fused and usually displayed in inverted gray scale with white background similar to PET images. It can be visualized as radial projections of MIP in coronal plane. Because of the high b value, body fat muscle and most of the organs gets suppressed which highlights the abnormal areas. However, normal structures with restricted diffusion, such as spleen, lymph nodes, uterus, ovary and testis can be

seen. The MIP images should always be interpreted along with the source images because improper fat suppression can lead to pseudotumor appearance. One disadvantage of this technique is long acquisition time. It has been shown to perform as well as PET/CT in the evaluation of tumors, such as lymphoma and nonsmall cell lung cancer.18 The DWIBS is a noninvasive technique without the use of radiation and has a huge potential in oncologic imaging.

DIFFUSION KURTOSIS IMAGING Diffusion of water molecules in a homogeneous solution follows a Gaussian distribution whereas diffusion of water molecules in biological tissues actually follows a nonGaussian distribution. 19 This difference in distribution is because of cellular microstructure (cell membranes and organelles) which alter the water diffusion.14 It is especially true in the brain where diffusion is restricted by the myelinated axons. Quantification of non-Gaussian diffusion can be useful in characterization of intracellular structures. Kurtosis is a metric which quantifies the non-Gaussianity of any distribution. Generally, a large kurtosis signifies higher diffusional heterogeneity and tissue complexity. This principle has been studied in the brain imaging especially in ischemia with promising results.

Intravoxel Incoherent Motion Intravoxel incoherent motion (IVIM) was initially described by Le Bihan in 1980s.8,20 They described D* as pseudo-diffusion coefficient which is dependent on capillary perfusion. The IVIM is based on the fact that the diffusion imaging at low b values (b 0–100) will have the effect of both the tissue perfusion (pseudo-diffusion) and the true diffusion. In fact at low b values the pseudo-diffusion predominates. This effect gets reduced at high b values where the true diffusion predominates. This is one proposed reason for decrease in ADC values with increase in b value. In a normally perfused tissue at low b value the motion of water molecules because of blood perfusion in tortuous capillary network adds to the actual water diffusion. So acquiring images at increasing b values would enable us to quantify the perfusion in a tissue noninvasively. Since IVIM is very sensitive to motion and other sequence related artifacts it should be performed with single shot EPI sequence and high-performance hardware. The current model available in most of the commercial scanners for the calculation of ADC is based on monoexponential function, considering that the logarithm of relative signal intensity plotted against the b value is a straight line which is not true.21 So ADC calculated with the monoexponential fit would have a component of microcapillary perfusion in addition to true diffusion especially with low b values. The IVIM model suggests that the relationship between the signal intensity and b value is not monoexponential rather

Chapter 46 Diffusion Weighted Magnetic Resonance Imaging

biexponential. Based on the IVIM model there is evidence that shows that DWI is sensitive to tissue perfusion and this potential can be applied to obtain the tissue perfusion assessment in addition to diffusion measurement.21–24

and improvements in software have made this technique a robust tool for body imaging also.

Histogram Analysis of ADC

Diffusion weighted imaging has become a gold standard in imaging of stroke to identify the infarct core mainly because of its ability to detect the infarcted area within minutes after the onset of symptoms, much earlier than other MRI sequences and CT can show changes.26 Diffusion weighted imaging is highly sensitive (81–100%) and specific (86–100%) in detecting the ischemic area within 12 hours of symptom onset. 14 It is also superior to FLAIR and T2-weighted sequences in detecting small area of infarct and has the ability to differentiate acute infarct from old lesions and nonspecific white matter changes (Figs 4A to C). Those areas which show diffusion abnormality usually progress to infarction unless early thrombolysis therapy is started. The area of diffusion abnormality also correlates well with the final clinical outcome thereby directing appropriate management for patients. The DWI and ADC parameters are used for the prediction of hemorrhagic transformation of infarct.14 The diffusion imaging in brain is further enhanced by newer sophisticated techniques, such as DTI and diffusion kurtosis imaging (DKI) (vide supra). They give additional information regarding the microstructural status of the brain tissue which will help in better understanding of the disease process.27 It also has an important role in brain tumor imaging as well. It helps in characterization of tumors and their response assessment to treatment. Solid gliomas which show low ADC values are associated with higher grade. 28

Usually ADC value is calculated by drawing region of interest (ROI) which will typically provide mean or median ADC value of the region. Recently attempts have been made to use histogram based analysis of ADC values. In this, the ADC values across a region can be represented as histograms, i.e. frequency of voxels having the ADC values.25 This will provide better understanding of heterogeneity of the lesion. It generally, utilizes volumetric evaluation of the lesion so that all the voxels of the lesion from different slices are evaluated rather than a selected ROI. The ADC calculation by this method is reproducible because the entire lesion is analyzed and the errors in ROI placement are reduced. Histogram analysis can provide various useful metrics, such as percentiles, kurtosis and skewness of distribution of ADC values which will provide better insights into the pattern of distribution. Comparison of these metrics based on histogram analysis between the pre- and post-treatment imaging can evaluate the response to therapy.

CLINICAL APPLICATIONS OF DWI Although initially DWI was established and successfully used in neuroimaging, recent developments in the sequence protocols and their optimization, hardware enhancements

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Figs 4A to C:  T2W axial image (A) of brain shows mild gyral hyperintensity (arrow) and swelling seen in the left parieto-occipital cortex.

Multifocal areas of hyperintensities (*) seen in right cerebral hemisphere with associated volume loss suggestive of chronic infarct. DW-EPI sequence with b value of 1000 in axial plane (B) shows a brightly hyperintense area (arrow) which on ADC map (C) shows hypointensity (arrow). The above features are suggestive of acute infarct on the left side. Apparent diffusion coefficient map also shows multifocal hyperintensity in right cerebral hemisphere suggestive of facilitated diffusion. As depicted in this case, DWI along with ADC can be very useful for the chronological dating of infarcts

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Similarly, medulloblastoma and rhabdoid tumors have been shown to have low ADC values compared to ependymoma and astrocytoma in posterior fossa. 27 The DTI also has a proven role in the preoperative assessment of brain tumors. Response of brain tumors after chemoradiation is assessed by DWI. Changes in ADC values in the first few weeks after the therapy are found to be noninvasive biomarkers for response to therapy and it can be used for prognostication also.29,30

imaging is not possible because of deranged renal function. Experience of DWI in paediatric imaging is limited but promising. The ADC values can be used to detect malignant tumors, characterize them and assess the treatment response. Studies have been done in variety of pediatric tumors and they found that DWI performed better or similar to conventional MRI.37,38

Head and Neck

Diffusion weighted imaging in thorax needs faster sequences with high-performance gradients and parallel imaging techniques along with phased array coils. The low proton density in lung and magnetic field inhomogeneity makes quantitative DWI even more challenging. Usually, two b values are used and STIR is used for fat suppression especially if quantification is needed. It can be done in breath holding or free breathing with respiratory and cardiac triggers. Studies have used various methods, such as qualitative, semiquantitative and quantitative to differentiate malignant lesions from benign lesions.4 In qualitative method the intensity of the lesion is compared with the intensity of spinal cord or chest wall muscle and the malignant lesions are usually hyperintense to spinal cord or chest wall muscles. In semiquantitative analysis, the ratio of the signal intensity of the lesion and the signal intensity of the reference structure is used to characterize the lesion. The quantitative analysis depends on the ADC measurement of the lesion itself. Most of the work has been done in lung carcinoma. Studies have shown that the ADC of the malignant lesions is usually lower than the benign lesions and small cell carcinoma which has closely packed cells shows lower ADC when compared to nonsmall cell carcinoma although overlap may occur. At the same time small metastatic nodules, inflammatory nodules and fibrotic nodules cannot be reliably differentiated.39 In case of collapsed lung it is very difficult on routine imaging to delineate the tumor boundary. Diffusion weighted imaging has been used successfully to delineate the tumor from the collapsed lung. 40 Diffusion weighted imaging has also been used to characterize the mediastinal nodes in patients with carcinoma lung. 41,42 The ADC values of malignant nodes were significantly lower than that of benign nodes. Another potential application of DWI is in the evaluation of tumor response after therapy.

Diffusion weighted imaging has potential to differentiate pleomorphic adenoma from other benign and malignant lesions of parotid gland.31 Because of the presence of glandular component and fluid these tumors show significantly higher ADC value than Warthin tumors which have hypercellular stroma.31 It can differentiate sinonasal malignant lesions from benign lesions because in the former ADC is lower. The ADC values can also be used to characterize a tumor, for instance it can differentiate squamous cell carcinoma (SCC) from lymphoma. The lymphoma usually shows low ADC values compared to SCC because of the hypercellular nature.32,33 The limitation of its use is that some malignant lesions like chondrosarcoma can have high ADC values.31 Prediction of tumor grading can be done by ADC values as poorly differentiated solid lesions show low ADC values compared to well-differentiated lesions. By differentiating necrotic area from viable tumor it can also help identify areas from where biopsy can be performed.31,34 In the assessment of tumor response to therapy one of the major limitations of PET is that it is sensitive to inflammatory changes also. The DWI has the potential to overcome this difficulty because the inflammatory lesions show high ADC values whereas tumor tissue would show low ADC values. So it can be used as a surrogate marker to assess the tumor response very early during therapy. Apparent diffusion coefficient values in SCC have been shown to significantly change even after the first week of treatment and the complete responders show higher increase in ADC when compared to partial responders.35 There is a recent study which evaluated the role of DWI in the orbit and suggested that it may help differentiate pseudotumor from lymphoma and cellulitis which is again based on the fact that lymphoma shows low ADC compared to pseudotumor and cellulitis.36 The DWI can reliably differentiate necrosis within a tumor from abscess formation. Abscess shows very low ADC because of the presence of macromolecules and increased viscosity.

Pediatric Applications The use of ionizing radiation in children is a concern because of long-term effects, so DWI can be an alternate technique in this age group. The DWI does not involve the use of contrast media so it can be used whenever contrast-enhanced

Thorax

Breast Contrast-enhanced MRI of the breast is an established technique in the diagnosis of carcinoma breast with sensitivity of 89–100% and specificity of 72%.18 Several studies have attempted to use DWI to differentiate malignant lesions from benign. There are no uniform b values or calculation methods used by the investigators which have resulted in different ADC

Chapter 46 Diffusion Weighted Magnetic Resonance Imaging

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Figs 5A to D  Axial T2W sequence of bilateral breasts (A) shows a hypointense mass lesion (arrow) in the right breast. It also shows areas of

necrosis (outlined arrow) within. Diffusion weighted sequence with b value of 1000 (B) shows a markedly hyperintense lesion (arrow) with good background suppression of other structures making the lesion more conspicuous. Apparent diffusion coefficient map (C) shows hypointensity (narrow) suggesting marked restriction of diffusion consistent with a highly cellular mass. Few areas show facilitated diffusion (outlined arrow) consistent with necrosis. These findings are also confirmed on subtracted postcontrast T1 fat suppressed image (D). Histopathology showed infiltrating ductal carcinoma

cut-off values. Generally, the malignant lesions showed lower ADC values when compared with benign lesions (Figs 5A to D). But there is significant overlap between the two groups.4 Lesions with fibrotic components, such as fibroadenoma and fibrocystic disease can result in low ADC values leading to diagnostic difficulty. Many optimizations were proposed including normalization of ADC of the lesion to the ADC of ipsilateral glandular parenchyma which would eliminate the ADC variations because of scanning parameters and effects of menstrual cycle.43 This approach has been shown to improve the diagnostic accuracy. Efforts have been made to use DWI in addition to dynamic contrast-enhanced imaging and this has also been shown to improve diagnostic accuracy.18 Diffusion weighted imaging has been used to grade the tumor, predict

the histological type and to better evaluate the local extent of the tumor. Recently, many studies have been published regarding the role of DWI in the evaluation of response to treatment. Decrease in size of the lesion as response criteria is not an optimal parameter since it takes a long time to show a significant difference. Chemotherapeutic agents are toxic and they have various side effects which necessitates earlier assessment of response. Studies have shown that the increase in ADC value in comparison with the pretreatment value can be used as a noninvasive biomarker of disease response.44,45 Using the change in ADC values, response can be evaluated as early as after the first cycle of chemotherapy and it has been found that the increase in ADC values was significantly more in responders than in nonresponders.

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Figs 6A to F  Axial T1W GRE sequence (A) shows an exophytic mildly hyperintense lesion (*) arising from the right lobe of liver. Rest of the liver is showing features of chronic liver disease. Lesion is markedly hyperintense on T2W sequence (B). Diffusion weighted image with b value of 500 (C) shows the hyperintense lesion which on ADC map (D) shows marked diffusion restriction suggestive of hypercellular tumor. With these findings along with arterial enhancement in postcontrast T1W image (E) and capsule formation in delayed postcontrast image (F), diagnosis of hepatocellular carcinoma was made

Liver It is challenging to apply DWI in any abdominal organ mainly because of the respiratory motion and susceptibility. The Liver is one of the most studied organs in abdomen using DWI. The Liver parenchyma shows relatively short T2 relaxation times, so the b values and the TE of the sequence should be optimized accordingly. Too high b value might cause unacceptable signal suppression which is because of long T2 time rather than diffusion characteristics itself. Usually, the recommended b values are 0, 100 and 500.3 Presence of branching vessels within the liver parenchyma poses a difficulty in the detection of small focal lesions. In black blood DWI images, the vessels are suppressed so that the lesion detection is relatively easier especially on low b values. At the same time lesion characterization is better done on high b value images. To support this studies have shown that DWI is better than fat suppressed T2 weighted sequences.46,47 Diffusion weighted imaging can be applied as a useful adjunct or can be used as a reasonable alternative to contrast enhanced images for the evaluation of the

liver metastasis.48,49 Hemangioma and simple cysts show significantly high ADC values that they can be reliably differentiated from hepatocellular carcinoma (HCC) and metastasis which show low ADC values (Figs 6 and 7). However, benign solid lesions like hepatic adenoma and focal nodular hyperplasia can have overlapping values which cannot be reliably differentiated from malignant lesions.3,18 Similarly, malignant lesions which are necrotic and mucinous tumors can have high ADC values and can mimic benign lesions on DWI. Diagnosis and detection of HCC and dysplastic nodules in a cirrhotic liver is very difficult based on ADC values because the diffusion is as it is restricted in cirrhotic liver as a result of fibrosis. As in other tumors, DWI has a role in the evaluation of tumor response and it has been shown to demonstrate significantly more ADC changes in responders than in nonresponders. In addition, the pretreatment high ADC values have been correlated with poorer response to therapy. It is well known that ADC values are low in cirrhotic liver and a recent study showed that ADC values correlated well with US elastography and serum markers for moderate and severe fibrosis.50

Chapter 46 Diffusion Weighted Magnetic Resonance Imaging

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Figs 7A to D  Axial T2W sequence (A) shows a mass lesion involving the gallbladder (*) with adjacent liver infiltration. Calculi were also noted

in the gallbladder. Multiple subtle hyperintense lesions (arrow) in both lobes of liver are suggestive of metastases. Diffusion weighted sequence with b value of 500 (B) shows these focal lesions (arrows) much better than the T2W sequence. Apparent diffusion coefficient map (C) also shows multiple focal lesions (arrow) which are showing restricted diffusion in the periphery of the lesion. Most lesions on ADC map show central hyperintensity suggestive of necrosis. Diffusion weighted sequence with b value of 1000 displayed in inverted gray scale (D) shows multiple metastatic lesions (arrow) with very good background suppression which is comparable to positron emission tomography image

Gallbladder and Biliary Ducts

Pancreas

There is emerging evidence that DWI can be helpful in differentiating malignant gallbladder lesions from benign. Malignant lesions tend to show high signal intensity on DWI and low ADC values compared to benign lesions.51 It can distinguish adherent or tumefactive sludge from gallbladder malignancy. A recent study has shown that DWI performed better than conventional MRCP in the detection of extrahepatic cholangiocarcinoma.52

Apparent diffusion coefficient values of pancreas have been shown to vary with age of the patient and the location in pancreas. With increase in age pancreas undergoes atrophy, fatty replacement and fibrosis which is proposed to be a cause for change in ADC.53,54 The ADC values of head and body of the pancreas is shown to be significantly more than the tail of pancreas. 54 Carcinoma of pancreas shows low ADC values compared to the rest of normal pancreas and

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Figs 8A to E  Axial T1W sequence of bilateral kidneys (A) shows hypointense exophytic lesions (arrow) in both the kidneys and an isointense

lesion (outlined arrow) in the posterior cortex of left kidney. T2-weighted fat suppressed and DW sequence with b value of 0 (B and C) shows markedly hyperintense lesions (arrow) in both kidneys suggestive of simple cysts whereas the posterior cortex lesion in left kidney (outlined arrow) is isointense to kidney parenchyma. On DW sequence with b value of 500 (D) the simple cysts are loosing signal compared to b 0 image whereas the posterior cortex lesion is retaining signal suggestive of solid nature of the lesion. Apparent diffusion coefficient map (E) shows the cystic lesions as hyperintense to renal parenchyma which is consistent with simple cysts. The solid lesion in the left kidney (outlined arrow) is mildly hypointense to renal parenchyma which is consistent with a hypercellular solid tumor. Solid lesion in the left kidney was proven to be clear cell carcinoma

the ADC values depend on the histological characteristics as well. However, there is overlap of ADC values of carcinoma pancreas with focal pancreatitis because of which their distinction is difficult. Cystic lesions of pancreas, such as pseudocysts, simple cysts show a relatively high ADC values compared to pancreatic abscesses, hydatid cysts and cystic neoplasms.55

Kidneys and Adrenal Diffusion weighted imaging has been successfully used in differentiating malignant renal lesions from benign lesions. Renal cysts show high ADC values than the normal parenchyma and other solid lesions (Figs 8A to E). Among the cysts, those with T1 hyperintensity show lower ADC than those which are T1 hypointense.56 This has been attributed to the presence of blood or proteinaceous content which can alter diffusion and the same can be helpful in differentiating simple cysts from necrotic neoplasms. Recent studies have shown DWI can be helpful in characterization of renal malignant masses and ADC values can be used to predict the histological subtype of renal cell carcinoma. 57,58 Renal Abscesses and infected cysts show low ADC values than other

cystic lesions.59 According to recent studies, DWI is not useful in differentiating benign adrenal lesions from malignant lesions based on ADC values although cysts and to some extent pheochromocytoma showed higher ADC values.60,61

Prostate Prostate is rich in glandular structures which facilitates free diffusion of water. Recent usage of high field strength, advancements in hardware and sequences have made DWI possible in the prostate with good SNR. The usage of endorectal coils have been shown to improve the image quality. Several studies have shown that prostate cancer is seen as hyperintense area in DWI and show hypointensity on corresponding ADC maps.62 However, there is overlap of ADC values of prostate cancer with focal chronic prostatitis and benign prostatic hyperplasia.2 There is a significant negative correlation found between the ADC values and the Gleason score which would help in management decisions. It is also found to be useful in locoregional staging and lymph nodal detection.2 It can be used as a biomarker to assess response in patients who are treated with radiation. The ADC values have been shown to increase in response to therapy.63

Chapter 46 Diffusion Weighted Magnetic Resonance Imaging

Female Pelvis Conventional MRI has an important role in detection and staging of female pelvic malignancies. Diffusion weighted imaging can be used as an adjunct to it to increase its diagnostic accuracy. Normal endometrium shows varying diffusion characteristics and ADC values during different phases of menstrual cycle. Lowest ADC values are seen at the end of the cycle.4 This variation should be taken in to account while interpreting the DW images and ADC values. Endometrial carcinoma has been shown to have significantly low ADC value compared to the normal endometrium.4,18,64 It can show the extent of myometrial invasion which is important in the management especially if contrast media cannot be used. It can differentiate endometrial carcinoma from other benign endometrial lesions, such as hyperplasia and polyp. Diffusion weighted imaging can detect the malignant nodes even though they are normal according to size criteria. Cervical carcinoma is a hypercellular tumor whose ADC values are less than the normal cervical stroma. It can clearly show the depth of invasion in cervix and can also be used for detection of involved nodes allowing to stage the disease more accurately.65 Because of low ADC value of SCC, it can be differentiated from adenocarcinoma of cervix. However, there is no clear-cut cut-off value for ADC available in the literature mainly because of variations in the technique and hardware used. There are contradicting reports regarding the potential of DWI to differentiate malignant ovarian lesions from benign lesions.66,67 However, it improves the detection of peritoneal deposits when combined with a conventional MRI sequences than the latter alone.68

CONCLUSION Diffusion weighted imaging is an evolving technique that provides a new paradigm for tissue characterization. Its ability to provide both qualitative and quantitative insight in to complex diffusion mechanisms and changes at a cellular level with only a small time penalty have made this technique a valuable addition to clinical MR protocols. However, DW sequences must be interpreted in conjunction with other MR sequences to avoid the pitfalls of this technique.

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4. Türkbey B, Aras Ö, Karabulut N, Turgut AT, Akpınar E, Alibek S, Pang Y, Ertürk \cS M., El Khouli RH, Bluemke DA. Diffusionweighted MRI for detecting and monitoring cancer: a review of current applications in body imaging. Diagn Interv Radiol. 2012;18:46-59. 5. Herneth AM, Mayerhoefer M, Schernthaner R, Ba-Ssalamah A, Czerny C, Fruehwald-Pallamar J. Diffusion weighted imaging: lymph nodes. Eur J Radiol. 2010;76(3):398-406. 6. De Figueiredo EH, Borgonovi AFNG, Doring TM. Basic concepts of MR imaging, diffusion MR imaging and diffusion tensor imaging. Magn Reson Imaging Clin N Am. 2011;19(1):1. 7. Stejskal EO, Tanner JE. Spin diffusion measurements: Spin echoes in the presence of a time-dependent field gradient. The J Chem Phys. 1965;42:288. 8. Le Bihan D, Breton E, Lallemand D, Grenier P, Cabanis E, Laval-Jeantet M. MR imaging of intravoxel incoherent motions: application to diffusion and perfusion in neurologic disorders. Radiology. 1986;161(2):401. 9. Dietrich O, Biffar A, Baur-Melnyk A, Reiser MF. Technical aspects of MR diffusion imaging of the body. Europ journ Radiology. 2010;76(3):314-22. 10. Provenzale JM, Engelter ST, Petrella JR, Smith JS, MacFall JR. Use of MR exponential diffusion-weighted images to eradicate T2“ shine-through” effect. Amer Jour of Roentg. 1999;172(2): 537-9. 11. Koh DM, Thoeny HC. Diffusion-weighted MR Imaging: Applications in the Body. Springer. 2010. 12. Provenzale JM, Petrella JR, Jr LCHC, Wong JC, Engelter S, Barboriak DP. Quantitative Assessment of Diffusion Abnormalities in Posterior Reversible Encephalopathy Syndrome. AJNR. 2001;22(8):1455-61. 13. Hiwatashi A, Kinoshita T, Moritani T, Wang HZ, Shrier DA, Numaguchi Y, Ekholm SE, Westesson PL. Hypointensity on diffusion-weighted MRI of the brain related to T2 shortening and susceptibility effects. Amer Journ Roentg. 2003;181(6):1705-9. 14. Fung SH, Roccatagliata L, Gonzalez RG, Schaefer PW. MR diffusion imaging in ischemic stroke. Neuroimaging Clin N Am. 2011;21(2):345. 15. Haselgrove JC, Moore JR. Correction for distortion of echoplanar images used to calculate the apparent diffusion coefficient. Magn Resonan Med. 2005;36(6):960-4. 16. Wang CL, Chea YW, Boll DT, Samei E, Neville AM, Dale BM, Merkle EM. Effect of gadolinium chelate contrast agents on diffusion weighted MR imaging of the liver, spleen, pancreas and kidney at 3T. Europ journ radiol. 2011;80(2):e1-e7. 17. Takahara T, Imai Y, Yamashita T, Yasuda S, Nasu S, Van Cauteren M. Diffusion weighted whole body imaging with background body signal suppression (DWIBS): technical improvement using free breathing, STIR and high resolution 3D display. Matrix. 2004;160(160):160. 18. Bonekamp S, Corona-Villalobos CP, Kamel IR. Oncologic applications of diffusion-weighted MRI in the body. Journ Magn Resonan Imag. 2012;35(2):257-79.

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Section 2 Recent Advances and Applied Physics in Imaging 19. Jensen JH, Helpern JA, Ramani A, Lu H, Kaczynski K. Diffusional kurtosis imaging: the quantification of non-Gaussian water diffusion by means of magnetic resonance imaging. Magn Reson Med. 2005;53(6):1432-40. 20. Le Bihan D, Breton E, Lallemand D. Perfusion in intravoxel incoherent motion MR imaging. Radiology. 1988;168:497-505. 21. Koh DM, Collins DJ, Orton MR. Intravoxel incoherent motion in body diffusion-weighted MRI: reality and challenges. Amer Journ Roentg. 2011;196(6):1351-61. 22. Wang Z, Su MY, Najafi A, Nalcioglu O. Effect of vasodilator hydralazine on tumor microvascular random flow and blood volume as measured by intravoxel incoherent motion (IVIM) weighted MRI in conjunction with Gd-DTPA-Albumin enhanced MRI. Magn resonan imag. 2001;19(8):1063-72. 23. Pickens III DR, Jolgren DL, Lorenz CH, Creasy JL, Price RR. Magnetic resonance perfusion/diffusion imaging of the excised dog kidney. Investigative radiology. 1992;27(4):287-92. 24. Lemke A, Laun FB, Simon D, Stieltjes B, Schad LR. An in vivo verification of the intravoxel incoherent motion effect in diffusion-weighted imaging of the abdomen. Magn Resonan in Med. 2010;64(6):1580-5. 25. Downey K, Riches SF, Morgan VA, Giles SL, Attygalle AD, Ind TE, Barton DPJ, Shepherd JH, deSouza NM. Relationship Between Imaging Biomarkers of Stage I Cervical Cancer and Poor-Prognosis Histologic Features: Quantitative Histogram Analysis of Diffusion-Weighted MR Images. AJR. 2013;200(2):314-20. 26. Hjort N, Christensen S, Solling C, Ashkanian M, Wu O, Røhl L, Gyldensted C, Andersen G, Ostergaard L. Ischemic injury detected by diffusion imaging 11 minutes after stroke. Ann Neurol. 2005;58(3):462-5. 27. Heiss WD, Raab P, Lanfermann H. Multimodality assessment of brain tumors and tumor recurrence. Journ of Nucl Med. 2011;52(10):1585-600. 28. Arvinda HR, Kesavadas C, Sarma PS, Thomas B, Radhakrishnan VV, Gupta AK, Kapilamoorthy TR, Nair S. Glioma grading: sensitivity, specificity, positive and negative predictive values of diffusion and perfusion imaging. Journ Neuro-oncolo. 2009;94(1):87-96. 29. Hamstra DA, Chenevert TL, Moffat BA, Johnson TD, Meyer CR, Mukherji SK, Quint DJ, Gebarski SS, Fan X, Tsien CI. Evaluation of the functional diffusion map as an early biomarker of timeto-progression and overall survival in high-grade glioma. Proc Natl Acad Sci USA. 2005;102(46):16759-64. 30. Hamstra DA, Galbán CJ, Meyer CR, Johnson TD, Sundgren PC, Tsien C, Lawrence TS, Junck L, Ross DJ, Rehemtulla A. Functional diffusion map as an early imaging biomarker for high-grade glioma: correlation with conventional radiologic response and overall survival. Journ Clini Oncol. 2008;26(20): 3387-94. 31. Razek AAKA. Diffusion-weighted magnetic resonance imaging of head and neck. Journ Comp Assis Tomog. 2010;34(6):808. 32. Maeda M, Kato H, Sakuma H, Maier SE, Takeda K. Usefulness of the apparent diffusion coefficient in line scan

diffusion-weighted imaging for distinguishing between squamous cell carcinomas and malignant lymphomas of the head and neck. Amer journ of Neuroradiol. 2005;26(5):1186-92. 33. Sumi M, Ichikawa Y, Nakamura T. Diagnostic ability of apparent diffusion coefficients for lymphomas and carcinomas in the pharynx. Europ Radiol. 2007;17(10):2631-7. 34. Razek AAKA, Megahed AS, Denewer A, Motamed A, Tawfik A, Nada N. Role of diffusion-weighted magnetic resonance imaging in differentiation between the viable and necrotic parts of head and neck tumors. Acta Radiologica. 2008;49(3):364-70. 35. Kim S, Loevner L, Quon H, Sherman E, Weinstein G, Kilger A, Poptani H. Diffusion-weighted magnetic resonance imaging for predicting and detecting early response to chemoradiation therapy of squamous cell carcinomas of the head and neck. Clinic Canc Resear. 2009;15(3):986-94. 36. Kapur R, Sepahdari AR, Mafee MF, Putterman AM, Aakalu V, Wendel LJA, Setabutr P. MR imaging of orbital inflammatory syndrome, orbital cellulitis, and orbital lymphoid lesions: the role of diffusion-weighted imaging. Amer Journ Neuroradiol. 2009;30(1):64–70.[cited 2012 Dec 23]. 37. Uhl M, Altehoefer C, Kontny U, Il’yasov K, Büchert M, Langer M. MRI-diffusion imaging of neuroblastomas: first results and correlation to histology. Eur Radiol. 2002;12(9):2335-8. 38. Humphries PD, Sebire NJ, Siegel MJ, Olsen E. Tumors in pediatric patients at diffusion-weighted MR imaging: apparent diffusion coefficient and tumor cellularity. Radiology. 2007;245(3):848-54. 39. Satoh S, Kitazume Y, Ohdama S, Kimula Y, Taura S, Endo Y. Can malignant and benign pulmonary nodules be differentiated with diffusion-weighted MRI? Amer Journ Roentgenol. 2008;191(2):464-70. 40. Qi LP, Zhang XP, Tang L, Li J, Sun YS, Zhu GY. Using diffusionweighted MR imaging for tumor detection in the collapsed lung: a preliminary study. Europ radiol. 2009;19(2):333-41. 41. Kosucu P, Tekinbas C, Erol M, Sari A, Kavgaci H, Öztuna F, Ersöz S. Mediastinal lymph nodes: Assessment with diffusion-weighted MR imaging. Journ Magn Reson Imag. 2009;30(2):292-7. 42. Nomori H, Mori T, Ikeda K, Kawanaka K, Shiraishi S, Katahira K, Yamashita Y. Diffusion-weighted magnetic resonance imaging can be used in place of positron emission tomography for N staging of non-small cell lung cancer with fewer false-positive results. Journ Thorac Cardiovasc Surg. 2008;135(4):816-22. 43. Khouli RHEI, Jacobs MA, Mezban SD, Huang P, Kamel IR, Macura KJ, Bluemke DA. Diffusion-weighted Imaging Improves the Diagnostic Accuracy of Conventional 3.0-T Breast MR Imaging. Radiology. 2010;256(1):64-73. 44. Sharma U, Danishad KKA, Seenu V, Jagannathan NR. Longitudinal study of the assessment by MRI and diffusionweighted imaging of tumor response in patients with locally advanced breast cancer undergoing neoadjuvant chemotherapy. NMR in biomed. 2009;22(1):104-13. 45. Park SH, Moon WK, Cho N, Song IC, Chang JM, Park IA, Han W, Noh DY. Diffusion-weighted MR Imaging: Pretreatment

Chapter 46 Diffusion Weighted Magnetic Resonance Imaging Prediction of Response to Neoadjuvant Chemotherapy in Patients with Breast Cancer. Radiology. 2010;257(1):56-63. 46. Bruegel M, Gaa J, Waldt S, Woertler K, Holzapfel K, Kiefer B, Rummeny EJ. Diagnosis of hepatic metastasis: comparison of respiration-triggered diffusion-weighted echo-planar MRI and five T2-weighted turbo spin-echo sequences. Amer Journ Roent. 2008;191(5):1421-9. 47. Zech CJ, Herrmann KA, Dietrich O, Horger W, Reiser  MF, Schoenberg SO. Black-blood diffusion-weighted EPI acquisition of the liver with parallel imaging: comparison with a standard T2-weighted sequence for detection of focal liver lesions. Investig Radiol. 2008;43(4):261-6. 48. Koh DM, Brown G, Riddell AM, Scurr E, Collins DJ, Allen SD, Chau I, Cunningham D, Desouza NM, Leach MO. Detection of colorectal hepatic metastases using MnDPDP MR imaging and diffusion-weighted imaging (DWI) alone and in combination. Europ Radiol. 2008;18(5):903-10. 49. Hardie AD, Naik M, Hecht EM, Chandarana H, Mannelli L, Babb JS, Taouli B. Diagnosis of liver metastases: value of diffusion-weighted MRI compared with gadolinium-enhanced MRI. Europ Radiol. 2010;20(6):1431-41. 50. Lewin M, Poujol-Robert A, Boëlle P-Y, Wendum D, Lasnier E, Viallon M, Guéchot J, Hoeffel C, Arrivé L, Tubiana J-M, Poupon R. Diffusion-weighted magnetic resonance imaging for the assessment of fibrosis in chronic hepatitis C. Hepatology. 2007; 46(3):658-65. 51. Sugita R, Yamazaki T, Furuta A, Itoh K, Fujita N, Takahashi S. High b-value diffusion-weighted MRI for detecting gallbladder carcinoma: preliminary study and results. Europ Radiol. 2009;19(7):1794-8. 52. Cui XY, Chen HW. Role of diffusion-weighted magnetic resonance imaging in the diagnosis of extrahepatic cholan­ giocarcinoma. World Journ Gastroenterol: WJG. 2010;16(25): 3196. 53. Ichikawa T, Haradome H, Hachiya J, Nitatori T, Araki T. Diffusion-weighted MR imaging with single-shot echo-planar imaging in the upper abdomen: preliminary clinical experience in 61 patients. Abdomin imag. 1999;24(5):456-61. 54. Yoshikawa T, Kawamitsu H, Mitchell DG, Ohno Y, Ku Y, Seo Y, Fujii M, Sugimura K. ADC Measurement of Abdominal Organs and Lesions Using Parallel Imaging Technique. AJR. 2006;187(6):1521-30. 55. Inan N, Arslan A, Akansel G, Anik Y, Demirci A. Diffusionweighted imaging in the differential diagnosis of cystic lesions of the pancreas. Americ Journ Roentgenol. 2008;191(4):1115-21. 56. Zhang J, Tehrani YM, Wang L, Ishill NM, Schwartz LH, Hricak H. Renal Masses: Characterization with Diffusion-weighted MR Imaging—A Preliminary Experience. Radiology. 2008;247(2): 458-64.

57. Goyal A, Sharma R, Bhalla AS, Gamanagatti S, Seth A, Iyer VK, Das P. Diffusion-weighted MRI in renal cell carcinoma: a surrogate marker for predicting nuclear grade and histological subtype. Acta Radiol. 2012;53(3):349-58. 58. Paudyal B, Paudyal P, Tsushima Y, Oriuchi N, Amanuma M, Miyazaki M, Taketomi-Takahashi A, Nakazato Y, Endo K. The role of the ADC value in the characterisation of renal carcinoma by diffusion-weighted MRI. British Journ Radiol. 2010;83(988):336-43. 59. Goyal A, Sharma R, Bhalla AS, Gamanagatti S, Seth A. Diffusionweighted MRI in inflammatory renal lesions: all that glitters is not RCC. Eur Radiol. 2013;23(1):272-9. 60. Miller FH, Wang Y, McCarthy RJ, Yaghmai V, Merrick L, Larson A, Berggruen S, Casalino DD, Nikolaidis P. Utility of diffusionweighted MRI in characterization of adrenal lesions. Americ Journ of Roentg. 2010;194(2):W179-85. 61. Tsushima Y, Takahashi-Taketomi A, Endo K. Diagnostic utility of diffusion-weighted MR imaging and apparent diffusion coefficient value for the diagnosis of adrenal tumors. Journ Magnet Reson Imag. 2009;29(1):112-7. 62. Gibbs P, Pickles MD, Turnbull LW. Diffusion imaging of the prostate at 3.0 Tesla. Investig Radiol. 2006;41(2):185-8. 63. Song I, Kim CK, Park BK, Park W. Assessment of response to radiotherapy for prostate cancer: value of diffusion-weighted MRI at 3T. Americ Journ Roentg. 2010;194(6):W477-82. 64. Fujii S, Matsusue E, Kigawa J, Sato S, Kanasaki Y, Nakanishi J, Sugihara S, Kaminou T, Terakawa N, Ogawa T. Diagnostic accuracy of the apparent diffusion coefficient in differentiating benign from malignant uterine endometrial cavity lesions: initial results. Europ Radiol. 2008;18(2):384-9. 65. Lin G, Ho KC, Wang JJ, Ng KK, Wai YY, Chen YT, Chang CJ, Ng SH, Lai CH, Yen TC. Detection of lymph node metastasis in cervical and uterine cancers by diffusion-weighted magnetic resonance imaging at 3T. Journ Magnet Reson Imag. 2008;28(1):128-35. 66. Moteki T, Ishizaka H. Diffusion-weighted EPI of cystic ovarian lesions: Evaluation of cystic contents using apparent diffusion coefficients. Journ Magnet Reson Imag. 2000;12(6):1014-9. 67. Nakayama T, Yoshimitsu K, Irie H, Aibe H, Tajima T, Nishie A, Asayama Y, Matake K, Kakihara D, Matsuura S. Diffusionweighted echo-planar MR imaging and ADC mapping in the differential diagnosis of ovarian cystic masses: Usefulness of detecting keratinoid substances in mature cystic teratomas. J Magn Reson Imaging. 2005;22(2):271-8. 68. Low RN, Sebrechts CP, Barone RM, Muller W. Diffusionweighted MRI of peritoneal tumors: comparison with conventional MRI and surgical and histopathologic findings—a feasibility study. Amer Journ Roentg. 2009;193(2):461-70.

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CHAPTER

Niranjan Khandelwal, Sameer Vyas

PERFUSION MAGNETIC RESONANCE IMAGING Perfusion can provide valuable information for detection, characterization and monitoring therapies in various disease processes like neoplasm, inflammations and ischemia.1,2 It is also referred as capillary or tissue-specific blood flow, and is an established physiologic and pathophysiologic measure of the volume of blood flowing through the microvasculature of a mass of tissue in a certain period of time. It is a quantitative measure, which can be determined with many different experimental techniques and often expressed in mL/100 g/ minute.3 The values of perfusion should be comparable across measurement modalities and the theoretical equations are usually used for determining perfusion that can be translated from one measurement technique to another. The perfusion can be noninvasive measured by the use of a tracer. Depending on the characteristics of these tracers, the blood flow measures can be divided into mainly three types, viz. diffusible tracers, intravascular tracers and microsphere type tracers.4,5 The diffusible tracers can easily pass through blood vessel walls and include H2O, or H2O15 (used in positron emission tomography), and xenon (used in computed tomography-based perfusion measures). The intravascular tracers are those tracers which remain within the vessel walls and include iodinated contrast in CT and gadolinium and other contrast agents in magnetic resonance imaging (MRI). However, these agents are partially diffusible in most tissues of the body and separating perfusion from vessel permeability effects can be a challenge. The microsphere type tracers are slightly larger than capillaries, and hence, they get stuck within the microvasculature indefinitely. They are widely used for invasive animal studies and are considered too risky for human studies. Clinical agents, such as the single-photon emission computed tomography (SPECT) agent Tc-HMPAO mimic microspheres by remaining in the target tissue for a long time but they achieve this by diffusing into tissue and then undergoing a chemical transformation within the tissue that discourages diffusing back out.

As unusual nuclear species are readily detected in the body with MRI, perfusion imaging is possible with many different tracers, including fluorinated compounds, deuterated water, O 17 and hyperpolarized gas, xenon. 5-7 The normal concentration of these tracer agents (nuclei) in tissue is almost zero and the only signal observed in clinical MRI is because of perfusion effects as the signal from these can be well separated from the water proton signal. These techniques are interesting and potentially promising, however these agents generally produce weak signals to noise ratio, have low spatial resolution, and lack the sensitivity of the proton MRI techniques, which is usually employed for clinical studies. Proton-based perfusion techniques using the strong signal from water protons in tissue have been found to be useful in the clinical setting and clinical research. Perfusion imaging with the proton signal can be performed either by dynamic imaging following the bolus injection of an MR contrast agent or by labeling of the water in the inflowing arterial blood.8-12 Contrast agent-based methods are commonly used as the effects of contrast agents in the vessels or tissue are quite strong. The bolus tracking technique is most widely used and it involves the injection of a bolus of magnetic contrast agent while repeatedly imaging.13,14 It is usually performed using T2* (or T2) contrast where the signal change is due to the magnetic susceptibility of the contrast agent and is known as dynamic susceptibility contrast (DSC) MR perfusion or the T1 properties of the contrast agent, where the signal change is due to the T1-shortening effects of the contrast agent and is known as dynamic contrast enhancement (DCE) MR perfusion.13-17 The DSC imaging is mostly employed in the brain whereas DCE-MR perfusion is usually employed outside the brain. By selectively affecting the MRI signal from water in the inflowing arterial blood, imaging without contrast agent is possible and is known as arterial spin labeling (ASL) technique. It produces a smaller signal change than the contrast agent methods but the lack of an injection and the use of diffusible water as the tracer make this approach an interesting alternative option.11,15

Chapter 47 Functional Magnetic Resonance: Perfusion and Dynamic Contrast-enhanced Magnetic Resonance Imaging

Magnetic-contrast Agents in Neural Tissues MR-contrast agents (paramagnetic and superparamagnetic) are intravascular within normal brain tissue, as they are too large to cross the blood–brain barrier. The signal changes resulting from alterations to the intravascular signal are relatively small because the brain–blood volume is small (3–6%). However, the magnetic-contrast agents within the vasculature can have effects beyond the vessels as an intravascular-contrast agent and can affect tissue signal by altering the magnetic fields in the nearby tissue.18-21 In addition, spins can move between small blood vessels in the microvasculature and the tissue.

Imaging Techniques and Methods Three techniques are mainly used for performing MR perfusion imaging: dynamic susceptibility contrastenhanced perfusion, dynamic contrast-enhanced perfusion and arterial-spin labeling.1 All these techniques involve repetitive serial imaging during the passage of blood that has been labeled with either contrast material or with an endogenous magnetic tracer label. In clinical studies, dynamic-susceptibility contrast-enhanced (DSC) MR perfusion is currently the most commonly used technique and it is very simple to perform in a clinical environment.

Dynamic-susceptibility Contrast-enhanced MR Perfusion Principle: Dynamic-susceptibility contrast-enhanced MR perfusion (DSC-MRP) tech­nique utilizes the T2* susceptibility effects of gadolinium, rather than the T1-shortening effects which are mostly associated with contrast-enhancement on conventional imaging.22-26 It uses rapid measurements of MR signal change following the injection of a bolus of a paramagnetic MRI contrast agent.1 The susceptibility effect is the shortening of T2 and T2* relaxation times, which leads to lower signal on T2- or T2*-weighted images. The signal loss which results from the passage of the contrast agent bolus on T2* weighted images helps in calculating the change occurring in the contrast concentration of each pixel. Contrast agent is treated as an intravascular marker and leakage into the interstitial space is either ignored or eliminated if possible. This data can be utilized to derive calculated estimates of cerebral blood volume (CBV), mean transit time (MTT) and cerebral blood flow (CBF). Image acquisition: The patient should be positioned comfortably with sufficient cushioning to reduce movement and light restraining straps be used in the same manner as used for normal MRI. Data is acquired by applying a fast imaging technique, such as single or multishot echoplanar imaging

(EPI) to produce a temporal resolution of approximately 2 seconds. The imaging sequence may be gradient echo which will maximize T2* weighting. Alternatively, a spin echo approach can also be used which minimizes the signal contribution from the large vessels. A series of at least five precontrast images should be collected prior to the passage of the bolus and many centers will collect for up to 1 minute to provide a large number of precontrast images to improve the estimation of the signal intensity baseline during analysis. A standard contrast dose (0.1 mmol/kg) is usually adequate, but a double dose of gadolinium (0.2 mmol/kg) may be used to improve the signal to noise ratio. The contrast is usually injected through an 18- or 20-gauge IV catheter at a high rate (3–7 mL/sec) using a power injector, to allow for a tight bolus of contrast material. After the injection, a saline flush of at least 25 mL (20–30 mL) should be delivered at the same rate to make sure that the bolus, which enters the central circulation is as coherent as possible. Alternatively, a careful manual injection technique can also be used. However, for manual techniques the injection should be given through a large cannula (at least 18 G). It should preferably be introduced into a large antecubital vein so that the resistance of the injection system is reduced. The injection should be given at an even rate and should be immediately followed by a chaser of the same amount of normal saline given at the same rate. Successive images of the region of interest (ROI) are then acquired during the first pass of contrast material. Data analysis: The analysis of DSC-MRI is based on the assumption that the contrast agent remains within the vascular space throughout the examination acting as a blood pool marker.25,26 This assumption does not stand true except within the brain where there is absence of contrast leakage because of the blood–brain barrier. The drop in T2* signal caused by the susceptibility effects of gadolinium is computed on a voxel-by-voxel basis and used for constructing a time-versus intensity curve. The degree of signal drop is then assumed to be proportional to the tissue concentration of gadolinium, so that relative concentration-time curves can be obtained (delta R2 curves) (Figs 1A to C).26-31 Relative cerebral-blood volume (rCBV) can be obtained by calculating the area under the concentration-time curves, normalized to a contralateral, uninvolved region. “Relative” refers to the fact that an arterial input function is not used in the calculation of CBV, and therefore, precise quantification of cerebral blood volume is not performed. Repetition of this process on a voxel-by-voxel basis can be done to construct an rCBV map (Fig. 2). The MTT is then estimated as some form of standardized measurement of the width of the curve, such as the width at half the maximum height (full width at half maximum; FWHM). The blood flow can then be calculated using the central volume theorem CBF = CBV/MTT. The initial calculation of local-contrast concentration from the observed signal change a straightforward and contrast

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A

B

C

Figs 1A to C:  Figure shows data analysis in DSC perfusion: (A) Time-versus MR signal intensity curve where signal intensity decreases during

passage of contrast agent bolus and is measured through a series of MR images; (B) Tissue concentration versus time curve where change in the relaxation rate (ΔR2*) is calculated from signal intensity, and a baseline subtraction method is applied to measured data; (C) Corrected ΔR2* curve after leakage correction

modifications have been brought in the analysis approach as an attempt to produce more accurate quantitative estimates of blood flow.26-43 Three main problems with the technique include: zz Contrast recirculation zz Contrast leakage zz Bolus dispersion. zz

Fig. 2:  Contrast (tissue concentration) versus time curve showing

the different parameters. Area under curve represents cerebral blood volume, height of curve represents cerebral blood flow and area/ height of curve represents mean transit time. Cmax, peak height and, full width half maximum (FWHM), time-to-peak concentration (TTP)

concentration is linearly related to the T2 rate changes (ΔR2), which can be calculated for using the relationship: ΔR2 = – ln [S(t)/S(0)]/TE where, S(0) is the base line signal intensity S(t) is the pixel intensity at time t and TE is the echo time. This allows transformation of signal-intensity time course data to contrast concentration time course data (Fig. 1). In addition to these flow related parameters, maps can also be produced on the basis of time taken by the contrast to reach the voxel using the time of arrival or, more commonly the time-to-peak concentration (TTP). Problems with DSC MRI: There are several major problems/ errors with the DSC MRP, therefore, numerous major

zz

Contrast recirculation: Analysis of the contrast bolus passage assumes that the bolus passes through the voxel and that the concentration of contrast then returns to zero. However, the contrast recirculates through the body and a second recirculation peak follows the first (Fig. 3A). When the contrast continues to circulate, the bolus disperses and widens so that the second peak is lower and broader than the first and by the time of the third recirculation the intravascular contrast must have evenly mixed throughout the blood volume, thus causing a small constant baseline elevation in the contrast concentration. Errors in measurement of CBV are due to the presence of both first pass and recirculating contrast in the vessels during the latter part of the bolus passage. The error can be approached is by use of curve fitting technique, which also smoothes the data, effectively reducing noise and eliminates the contamination of the first pass bolus due to contrast agent recirculation. Contrast leakage and tissue enhancement: Leakage of contrast into the interstitial space causes signal changes, principally by relaxivity mechanisms. High permeability in regions of severe bloodbrain barrier breakdown (e.g. high-grade neoplasm) leads to extravasation of contrast material into the interstitium, which increases signal above baseline due to the T1-shortening effects of gadolinium (i.e. enhancement) (Fig. 3B). Since, the algorithm for calculation of rCBV assumes a constant baseline, the area above baseline is interpreted by the algorithm as negative blood volume, and subtracted from the area below

Chapter 47 Functional Magnetic Resonance: Perfusion and Dynamic Contrast-enhanced Magnetic Resonance Imaging

A

B

Figs 3A and B:  (A) Signal-intensity time curve showing marked signal-intensity decrease during arrival of the contrast agent, followed by partial recovery of the signal-intensity loss. A second decrease in signal intensity (arrow) is due to recirculation; (B) Signal-intensity time curve showing contrast leakage and signal above baseline due to the T1 shortening effects of gadolinium

zz

baseline caused by the drop in T2* signal. This leads to significant underestimation of rCBV. Imaging methods based on susceptibility allow the separation of these relaxivity and susceptibility based effects and produce images in which the effects of contrast leakage are either removed or reduced. The use of techniques with reduced T1 sensitivity, such as low flip angle gradient echo-based sequences and increase the repetition time (TR), or uses a dual echo technique or use pre-enhancement [preinject an additional small dose of gadolinium (0.05 mmol/kg) to presaturate the interstitium, effectively elevating the baseline before the dynamic acquisition], which effectively removes relaxivity effects. In addition, newer contrast materials, which can act as ‘blood pool’ agents (such as gadobenate dimeglumine and monocrystalline iron oxide nanoparticles) may ameliorate this problem. The change which occurs in signal intensity due to T1 shortening is biexponential so that for any given sequence, there is a plateaux phase during which signal intensity remains relatively constant. The effect of this response curve is that pre-enhancement of tumors will reduce the relaxivitybased signal intensity responses to subsequent contrast doses. However, each approach offers a perfect solution and the choice of method must be based on individual analysis task to be undertaken. Bolus dispersion and the measurement of absolute CBF: To measure the absolute CBF it is assumed that the technique can produce quantitative measurements of CBV and MTT. However, the use of the area under the curve to estimate CBV results in relative measurement that allows comparison of CBV between tissues rather than

producing an absolute measurement.44-48 In addition, the measurement of CBF also requires accurate estimation of MTT (calculated from the width of the contrast bolus). The width of the contrast bolus is affected by the arterial input function (AIF), changes in bolus width (due to regional alterations in flow) and physical bolus broadening (due to dispersive effects).

MRI Sequence Type Gradient-echo versus spin-echo: Both gradient-echo and spinecho acquisitions can be used, but rapid spin-echo imaging capable of dynamic perfusion measurements is only practical with echoplanar systems. Theoretically, spin-echo produces signal changes which predominantly reflect the passage of contrast through the capillary bed and reflect the tumor physiology at the capillary level; however several studies have shown that in comparison to the benefit of using spinecho images, there is more of compromise in terms of signal to noise ratio. Spin-echo techniques are selectively sensitive to small vessels that are less than 20 μ in diameter, whereas gradient-echo images incorporate signals from larger tumor vessels as well as the microvascularity. Gradient-echo techniques have shown a stronger correlation between tumor grade and blood volume. Spatial coverage versus time resolution: The selection of the spatial coverage and time resolution usually happens as a compromise, in accordance with the particular application and tissue under study. The time resolution is limited by the transit time of the bolus through the tissue as for accurate

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quantification of DSC MRP data, a proper characterization of the transient signal drop is required. Typically, a repetition time (TR) of 2 s or less is necessary for acquisition of the fast changes during the first pass. Therefore, the spatial coverage will be limited by the maximum number of slices that can be acquired within this TR. Echo planar imaging (EPI), segmented EPI, FLASH, etc. can be used. 2D versus 3D sequences: Both 2D and 3D sequences can be used. 2D sequences are usually preferable; however 3D sequence allows increased coverage, but typically, it occurs at the expense of an increased TR, or a decreased spatial resolution. Single-echo versus dual-echo sequences: Dual-echo sequences provide a simple way to remove the relaxivity effects and allows the quantification of changes in R2* without assumption regarding the T1 behavior.41,42 However, the sampling of two echoes increases sampling time and thus reducing the maximum number of slices that can be acquired (and therefore, coverage) in a given TR. when spatial coverage is important, single-echo sequences with a pre-dose of contrast may be used as the use of a pre-enhancement approach is proven effective.

Dynamic Contrast-enhanced MR Perfusion Dynamic contrast-enhanced MR perfusion (DCE MRP) provides insight into the nature of the tissue properties at the microvascular level by demonstrating the wash-in, plateau, and washout contrast kinetics of the tissue.49-55 The DCE MRP, which is also referred as ‘permeability’ MRI, is an entirely different approach to MR perfusion that mainly focuses at the evaluation of tumor permeability.48-65 The main advantage of T1-based techniques is that tumor leakiness (enhancement) is used for data analysis rather than considering it as an artifact as in DSC MRP. It has been established that quantification of contrast leakage can provide powerful indicators of the state of neovascular angiogenesis in pathologies, such as tumors and inflammatory tissue; and capillary leakage of contrast on MRI can provide an approach for monitoring the effects of the antiangiogenic drugs. Principle: The T1-weighted technique measures the ‘relaxivity effects’ of the paramagnetic contrast material. The relaxivity effect of paramagnetic contrast material refers to the shortening of T1 relaxation time, leading to higher signal on T1-weighted images. The DCE MRP is based on a two-compartmental (plasma space and extravascularextracellular space) pharmacokinetic model (Fig. 4). Image acquisition: The patient should be positioned as used for normal MRI. The general steps in acquisition of DCE MRP are perform baseline T1 mapping, acquire DCE MRP images,

Fig. 4:  Dynamic contrast-enhanced MR perfusion: Two-compartment model demonstrates the exchange of contrast between plasma and extravascular and extracellular space

convert signal intensity data to gadolinium concentration, determine the vascular input function, and perform pharmacokinetic modeling. 56,57 The dynamic-imaging sequence must include precontrast images for a sufficient period to allow accurate estimation of the extracellular space and of the contribution of renal excretion. The data is acquired by three-dimensional (3D) gradient echo sequence. A bolus injection technique as used for DSC-MRP is used. A lower dose of gadolinium is administered (typically a single dose of 0.1 mmol/kg) at a lower rate (2 mL/sec) and repetitive acquisitions are then made through the lesion at longer intervals, typically every 15–26 seconds. Imaging is carried out over a much longer period of time than with T2*based techniques, to allow for the contrast to leak out into the extravascular space and come into equilibrium over several passes of the contrast bolus through the tumor bed. Data analysis: Various techniques can be employed for quantification of the contrast-enhancement effect, which include simple measures of the rate of enhancement to complex pharmacokinetic analyses.59-65 Simple-analysis techniques : The quantification of enhancement can be done by directly comparing the signalintensity curves from ROI. There are many measurements that allow this type of analysis and are designed to minimize the variation, which will occur among patients due to variations in contrast dose, injection and scanning techniques and scanner type. The simplest of these is a measurement of the time taken for the tumor tissue to attain 90% of its subsequent maximal enhancement (T90). Another parameter measures the maxi­mum rate of change of enhancement [maximal intensity change per time interval ratio (MITR)]. Various curve shapes can also provide insight into the quantification and calculate a standardized slope of the enhancement curve. However, the enhancement curve is poorly reproducible and most of these methods which are based on signal intensity remain sensitive to variations between acquisition systems as the relationship between contrast concentration and signal intensity is non-linear. Pharmacokinetic-analysis techniques: With pharmacoki­netic modeling of DCE MRP data, several metrics are commonly

Chapter 47 Functional Magnetic Resonance: Perfusion and Dynamic Contrast-enhanced Magnetic Resonance Imaging

derived: the transfer constant (ktrans), the fractional volume of the extravascular extracellular space (ve), the rate constant (kep, kep = ktrans/ve), and the fractional volume of the plasma space (vp). These quantitative techniques are intended to calculate the biological features, such as endothelial permeability and the endothelial surface area, which are relatively independent of imaging approach (scanner type, scanning technique or individual patient variations). The most frequently used metric in DCE MRP is ktrans. It can have different interpretations depending on blood flow and permeability. In situations, in which there is very high permeability, the flux of gadolinium-based contrast agent is limited only by flow, and thus ktrans mainly reflects blood flow; whereas if there is very low permeability, the gadolinium-based contrast agent cannot leak easily into the extravascular–extracellular space, and thus ktrans mainly reflects permeability. The product of the endothelial permeability and endothelial surface area represents the transfer coefficient ktrans which controls the leakage of contrast from the vascular to the extravascular compartment. The leakage of contrast can be calculated by:

approached by excluding any voxel which produces values over a certain threshold (1.2/ min) as being vascular in origin or more complex pharmacokinetic models.

dc 1 ve _________ = ktrans (Cp – C1) dt

Flow dependency of ktrans : The measurements of ktrans will be markedly affected by flow to the voxel as well as the permeability and surface area of the vascular endothelium. For measurements of ktrans it is assumed that for any given combination of intravascular and extravascular contrast concentrations the rate of contrast leakage will be proportional to the permeability and surface area of the vascular endothelium; however, it is true only where the supply of contrast to the vascular space is sufficiently high that the intravascular concentration will not be affected by the contrast leakage. There is limitation, in areas where there is contrast leakage and the blood flow is not adequate to replenish the contrast at an adequate rate; as a result plasma contrast concentration decreases and ktrans will reflect local blood flow.

zz

zz zz zz

where, ve is the proportion of the voxel into which contrast can leak (contrast distribution space) Cl is the concentration of contrast in the space Cp is the concentration of contrast in the blood. ktrans can be calculated if we accurately estimate the change in concentration of contrast in the bloodstream and in the tissue over time. The calculation of contrast concentration also requires knowledge of the initial T1 value of the tissues before contrast arrival which must therefore be measured before the dynamic imaging is performed and is usually measured by the use of gradient echo images with variable flip angles.

Problems with quantitative measurement of DCE MRI: The measurement of ktrans with pharmacokinetic analysis techniques have few disadvantages, which includes partial volume averaging effects, long acquisition time and flow dependency of ktrans. Partial-volume averaging effects: The pharma­c okinetic analysis technique is based on the assumption that the samples derived from voxels in blood vessels will represent changes in the blood concentration whereas voxels within the target tissue will represent leakage in the extravascular contrast. However, this assumption is not correct and voxels within the target tissue are actually likely to represent a mixture, some of which will have significant intravascular contrast content. This will result in overestimation of ktrans in these voxels which can be seen as areas of apparently high permeability in areas of normal brain. This problem can be

Long acquisition time: Another major problem with permeability imaging is long acquisition time as the measurement takes a considerable period of time (at least 5 min). There is rarely any misregistration of data in brain perfusion and can be easily corrected by data coregistration. However, in other areas of the body which are affected by respiratory motion, there is significant misregistration and respiratory gating techniques distinctly limit the image acquisition strategy and the achievable temporal sampling rate. This can be approached by modifying the pharmacokinetic model and describing only the first passage of the contrast bolus. This technique also eliminates the problems with partial volume averaging described above and produces highly reproducible parametric maps of both ktrans and CBV.

Arterial-spin Labeling MR Imaging Arterial-spin labeling (ASL) is an alternative technique of performing MR perfusion without the use of an intravenous contrast agent.66-68 The ASL can be thought of as a natural extension of magnetic resonance angiography (MRA) and is also closely related to blood flow imaging with H2O15PET. Many recent studies show that ASL provides similar information to the DSC or DCE MRP, and even have more advantages as compared to these techniques, including better ASL flow maps in detecting regions of disturbed vascularity and being independent of tumor permeability, so that corrections are not required. Hitherto, limitations of ASL like long imaging times and decreased spatial resolution as compared with contrast-based techniques have excluded widespread clinical application of ASL, but with recent advancement the ASL may contribute significantly to the future of MR perfusion imaging.

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Principle: ASL uses magnetically labeled blood as an endogenous contrast agent. In this technique, spatially selective excitation pulses or flow encoding gradient pulses are applied to inflowing blood to differentiate between static tissue and flowing blood. Time is allowed for the blood to move out of the vessels and into the perfused tissue, and then the signal change in tissue caused by the selective labeling of the arterial blood is measured which is closely related to the blood flow into that tissue. The arterial-spin labeling methods measure CBF by taking the difference of two sets of images: tag images, in which the longitudinal magnetization of arterial blood is inverted or saturated, and control images in which the magnetization of arterial blood is fully relaxed.69,70 To remove the contribution of the static tissue to the tag image, a control image of the same slice is acquired in which inflowing blood is not tagged. The magnetization difference (ΔM = Mcontr – Mtag), i.e. difference of the control and tag images yields an image that is proportional to CBF. Tag and control images are typically acquired in a temporally interleaved fashion, and the running difference of the control and tag images is used to form a perfusion time series. Image acquisition and labeling techniques: Different labeling techniques of ASL, that have been described or used for in vivo studies, are very similar and differ only in subtle aspects of implementation. However, they are broadly divided into spatially selective ASL and velocity-selective ASL.71-79 In spatially selective ASL, a spatial separation between the imaged region and inflowing arterial blood is required to cause signal change in the image whereas in velocity-selective ASL, bipolar gradients are used to label flowing blood. Velocityselective ASL, resemble phase contrast angiography, and can be used to label blood within the slice or slab and thus may permit labeling even closer to the capillary bed than spatially selective ASL. In most of the ASL techniques, magnetization is labeled along the main magnetic-field direction (Mz). The

A

B

advantage of labeling Mz is that changes in Mz return back to the equilibrium on the time scale of T1. The magnetization can also be labeled along the transverse direction (Mx or My) but since the transverse magnetization decays with T2, typically 5–10 times faster than T1 decay, the signal produced would be much smaller. Spatially selective ASL is by far the well-developed technique and most studies have been performed using this technique. It is similar to time-of-flight angiography. Inflowing blood may be tagged continuously or intermittently and can be broadly divided into continuous ASL and pulsed ASL (Figs 5A to C). Different pulsed labeling strategies differ from each other in primarily two issues. First is what inversions are applied to other tissue, including the imaged region, and secondly what is done to insure that the differences between the two RF preparations do not cause direct effects on the image which are independent of perfusion. Pulsed ASL: In this technique, single perturbing pulse is applied to the spins outside the slice at a single-time point, and then time is given for the spins to enter the tissue (Figs 5B and C). Usually, an RF pulse is applied at a time approximately 1 second before imaging. An inversion RF pulse is usually used as it creates the largest change in the arterial magnetization and the time before imaging is referred to as TI, as in inversion recovery sequences. Two images are obtained, one with the region containing the inflowing artery inverted and one where it is not inverted. The signal change with pulsed techniques is smaller than with continuous techniques as the spins which enter the tissue later are perturbed earlier than in the continuous technique, there is additional T1 decay of the label and generally. However, this technique also have additional advantages including more traditional RF and gradient strategies, are less subject to certain types of systematic error, and can produce excellent images. Pulsed ASL methods include echo planar imaging and

C

Figs 5A to C:  ASL techniques, schematic diagram illustrating arterial spin labeling strategies. (A) Continuous ASL (CASL) labels arterial spins as they flow through a labeling plane; (B and C) Pulsed ASL (PASL) labels arterial spins using a spatially selective labeling pulse

Chapter 47 Functional Magnetic Resonance: Perfusion and Dynamic Contrast-enhanced Magnetic Resonance Imaging

signal targeting with alternating radiofrequency (EPISTAR), flow-sensitive alternating inversion recovery (FAIR), signal targeting with alternating radio frequency (STAR), transfer insensitive labeling technique (TILT) (Gobay 1999) and proximal inversion with a control for off-resonance effect (PICORE) (Wong 1997).80-84 The EPISTAR technique is the simplest pulsed inversion strategy and was first proposed by Edelman et al. In this technique, a slab-selective inversion pulse is applied inferior to the imaged brain region to label arterial spins and a superior inversion slab is applied during the control image preparation. The superior inversion insures equal magnetization transfer effects from the two preparation pulses. The FAIR is an alternative strategy to EPISTAR where a nonselective inversion pulse is applied for the labeling and a slab selective inversion containing the entire imaged region is applied for a control image. In this technique, the effect on inflowing spins inferior to the slice is the same as in EPISTAR, but the spins in the imaged slab are inverted in both cases, rather than left unaffected. Because any slight difference in the flip angle of the two pulses will have a big effect upon the measured signal, special RF pulses with low sensitivity to variations in RF amplitude and very sharp slice profiles must be employed. There are number of variations of these basic labeling techniques and most of them may provide small improvements to the results but variations in implementation and methods of assessment overshadow these small differences.

with pulsed ASL, the continuous ASL can achieve a signal approximately 2–3 times larger is generally more sensitive. The greatest disadvantage of the continuous labeling approach is the unusual RF requirements of the labeling. As in CASL (Flow-driven adiabatic inversion), weaker RF for an extended period of time is required, implementation may be difficult because many scanners are designed specifically for brief, widely spaced pulses of RF at high power.

Continuous ASL: In this technique, spins are continuously inverted at a specific location before they enter the tissue. Thus spins which enter the tissue first are labeled first and spins which enter later are labeled later. One can approximate continuous saturation of spins as they flow past a certain plane by applying a series of thin saturation pulses repeatedly, but trying the same strategy with inversion pulses is problematic; some spins may remain within the saturation slab for two or more inversions and get doubly inverted. Inversion pulse is considered highly desirable to use a continuous inversion technique as it provides a stronger signal change. Continuous ASL methods include Saturation, inversion (Williams 1992) with flow-driven adiabatic inversion pulse and labeling with 2nd coil. Continuous ASL (CASL) usually employs a special RF labeling scheme known as flow-driven adiabatic inversion. Flow-driven adiabatic inversion is a simple technique because it requires only turning on a constant gradient and RF (Fig. 5A). While the pulsed ASL experiment is essentially a decaying bolus experiment where the labeled blood transiently enters the tissue, the continuous ASL experiment can be operated as a steady-state experiment. If the labeling is left on for a long time, a balance between the inflow of newly labeled spins and the T1 decay of the labeled spins already in the tissue is reached. This makes quantification of perfusion relatively simple. As compared

Data analysis (calculating blood flow from arterial-spin labeling measurements): The control and tag images ASL are acquired in an interleaved fashion and a perfusion time series is then formed from the running subtraction of the control and tag images.87-90 Hence, the simple subtraction image obtained can be a good reflection of relative blood flow without any calculations. However, because differences in tissue T1 and other factors can lead to different sensitivity to blood flow across the image and quantitative measurements of blood flow can be useful for some purposes, it can be useful to convert the difference images into actual blood flow maps in physiologic units. This conversion requires some consideration of how inflow impacts tissue MR signal.

Vessel-selective labeling: A recent approach has been introduced in which arterial water is labeled selectively on the basis of the blood velocity, termed velocity-selective ASL. The main difference between velocity-selective ASL and the other ASL techniques is that the arterial water is labeled everywhere, including the volume of interest, therefore minimizing the time for the blood to reach any region of interest. Pseudo-continuous arterial spin labeling (psCASL): This is also known as pulsed continuous arterial spin labeling (pCASL). This is a newly proposed technique that has eased the technical restrictions of CASL and employs a train of discrete RF pulses that mimics continuous ASL.85,86 In pCASL, continuous labeling is achieved by a train of rapidly repeating low tip RF pulses and alternating sign (bipolar) magnetic field gradients which is also suitable for MR systems that do not have continuous RF capabilities. Moreover, it has been shown that pCASL can achieve better compensation of adverse MT effects than CASL.

Problems with ASL: Despite its advantages, ASL imaging is limited by a large background signal and the motion artifacts. In addition, the small signal level of ASL reduces the signalto-noise ratio of the ASL perfusion imaging. With recent advancement in MRI technology, good quality images can be obtained.

DYNAMIC CONTRAST-ENHANCED MRI Dynamic contrast-enhancement techniques are well established for characterizing the benign or malignant lesions

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by providing functional information to the anatomically detailed morphological images as the malignant lesions usually show faster and higher levels of enhancement than normal tissue.91 This enhancement pattern of the malignant lesions reflects increased vascularity (neoangiogenesis) and higher endothelial permeability to the contrast molecules than do normal or less aggressive malignant tissues. Nowadays, dynamic contrast-enhanced MRI (DCE-MRI) is modality of choice for the diagnosis and characterization of the tumors of the brain, breast, prostate, liver, cervix and musculoskeletal system.92-95 Principle: The DCE-MRI relies on fast MRI sequences obtained before, during and after the rapid intravenous (IV) administration of a gadolinium-based contrast agent.64 IV-injected contrast agents pass from the arteries to the tissue microvasculature and extravasate within seconds to the extravascular–extracellular space. Contrast agents in vessels and in the extracellular space shorten local relaxation times, leading to increased signal on T1-weighted sequences. The ability to measure vessel leakiness is related to blood flow (i.e. it is difficult to identify leakiness if the flow is too low). Thus, the signal measured on DCE-MRI represents a combination of perfusion and permeability. The DCE-MRI is sensitive to alterations in vascular permeability, extracellular space and blood flow. The DCE-MRI enables the depiction of physiologic alterations as well as morphologic changes. It is an emerging imaging method to assess tumor angiogenesis and the clinical application of DCE-MRI for cancer is based on data showing that malignant lesions usually shows rapid, intense enhancement followed by a relatively rapid washout compared to normal healthy tissue. Image acquisition: The acquisition of DCE-MRI is done by acquiring a minimum of three sections through the tumor and imaging volume that includes a region outside the tumor, such as an artery or muscle for normalization. Quantity of the injected contrast material is usually standardized according to the patient’s body weight and preferentially should be injected at a constant rate with a power injector typically using 3D T1-weighted acquisition (spoiled gradient-echo sequences) to repeatedly image a volume of interest after the administration of a bolus of IV contrast agent. T1-weighted spoiled gradient-echo sequences provide high sensitivity to T1 changes, high signal-to-noise ratios (SNRs), adequate anatomic coverage, and rapid data acquisition. Serial image sets are obtained sequentially every 5 seconds (ranging from 2–15 seconds) for up to 5–10 minutes. The rapidity with which MRI must be acquired necessitates that larger voxels (i.e. lower matrix sizes) must be obtained to maintain adequate SNRs. Data analysis: Signal intensity (SI) enhancement patterns on T1W images can be evaluated by different analysis techniques,

viz. qualitative, semiquantitative and quantitative. The complexity and standardization of analytic technique is needed to be adjusted. Qualitative: The qualitative or visual analysis is most readily accessible analytic but also the least standardized method. It is based on the general assumption that tumor vessels are leaky and more readily enhance after IV contrast material. It is expressed by a fast exchange of blood and contrast media between capillaries and tumor tissues. Thus, DCEMRI patterns for malignant tumors are expected to show early rapid high enhancement after injection followed by a relatively rapid decline compared with a slower and continuously increasing signal for normal tissues during the first few minutes after contrast injection. The qualitative analysis shows higher accuracy and less interobserver variability but there is overlap of malignant and benign tissues, which is limiting the capabilities of this approach. Moreover, the qualitative approach is inherently subjective and therefore difficult to standardize among institutions, making multicenter trials less reliable. Semiquantitative analysis: Semiquantitative analysis cal­ culates various curve parameters and is also referred as curveology. It is also based on the assumption of early and intense enhancement and washout as a predictor of malignancy. Parameters are obtained to characterize the shape of the time-intensity curve, such as the time of first contrast uptake, time to peak, maximum slope, peak enhancement, and wash-in and washout curve shapes. There are three common dynamic curve types after initial uptake: type 1, persistent increase; type 2, plateau; and type 3, decline after initial upslope. Type 3 is considered to be indicator of malignancy. The semiquantitative approach is widely used and has the advantage of being simple to perform. It has limitations in terms of generalization across acquisition protocols, sequences, and all other factors contributing to the MR signal intensity, which in turn affect curve metrics, such as maximum enhancement and washout percentage. Quantitative analysis: Quantitative analysis is most generaliz­ able but most complex method. It depends on contrast concentration curves over time and pharmacokinetic models are applied to calculate permeability constants. Dynamic imaging data obtained with DCE-MRI can generate curves which are mathematically fit to compartment pharmacokinetic models. For functional analysis of tissue microcirculation, two-compartment model is considered for the kinetic parameters which demonstrates the exchange of contrast between plasma and extravascular space as proposed by Tofts et al. To describe tumor and tissue permeability, various kinetic parameters include, Ktrans [transendothelial transport of contrast medium from vascular compartment to the tumor interstitium (washin)], kep [reverse transport

Chapter 47 Functional Magnetic Resonance: Perfusion and Dynamic Contrast-enhanced Magnetic Resonance Imaging

parameter of contrast medium back into the vascular space (washout)], fpV (plasma volume fraction compared to whole tissue volume) and Ve [extravascular, extracellular volume fraction of the tumor; the fraction of tumor volume occupied by extravascular extracellular space (EES)]. Physiologically, the value of ktrans is tissue dependent; ktrans will indicate the tissue perfusion per unit volume, if the contrast uptake of the tissue is flow limited; on the other hand, ktrans indicates the tissue permeability, if the uptake is permeability limited. In majority of tumors, ktrans indicates a combination of both flow and permeability properties of the tissue and high ktrans values usually reflect both high permeability and high perfusion. This is thus a fundamental limitation of DCE-MRI that the parameters it generates are inherently ambiguous with regard to their physiologic significance.

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47. Mouridsen K, Christensen S, Gydensted L, et al. Automatic selection of arterial input function using cluster analysis. Magn Reson Med. 2006;55:524-31. 48. Lorenz C, Benner T, Lopez CJ, et al. Effect of using local arterial input functions on cerebral blood flow estimation. J Magn Reson Imag. 2006;24:57-65. 49. Sourbron S, Ingrisch M, Siefert A, Reiser M, Herrmann K. Quantification of cerebral blood flow, cerebral blood volume, and blood-brain-barrier leakage with DCE-MRI. Magn Reson Med. 2009;62:205-17. 50. Tofts PS, Brix G, Buckley DL, et al. Estimating kinetic parameters from dynamic contrast-enhanced T1-weighted MRI of a diffusable tracer: standardized quantities and symbols. J Magn Reson Imaging. 1999;10:223-32. 51. Dean BL, Lee C, Kirsch JE, et al. Cerebral hemodynamics and cerebral blood volume: MR assessment using gadolinium contrast agents and T1-weighted turbo-FLASH imaging. AJNR. 1992;13:39-48. 52. Moody AR, Martel A, Kenton A, et al. Contrast-reduced imaging of tissue concentration and arterial level (CRITICAL) for assessment of cerebral hemodynamics in acute stroke by magnetic resonance. Invest Radiol. 2000;35:401-11. 53. Shin W, Cashen TA, Horowitz SW, et al. Quantitative CBV mea­surement from static T1 changes in tissue and correction for intravascular water exchange. Magn Reson Med. 2006;56:138-45. 54. Lu H, Law M, Johnson G, Ge Y, et al. Novel approach to the measurement of absolute cerebral blood volume using vascular-space-occupancy magnetic resonance imaging. Magn Reson Med. 2005;54:1403-11. 55. ME Raichle, JO Eichling, MG Straatmann, et al. Blood–brain barrier permeability of 11C-labeled alcohols and 15O-labeled water. Am J Physiol. 1976;230:543-52. 56. Edelman RR, Siewert B, Darby DG, et al. Qualitative mapping of cerebral blood flow and functional localization with echoplanar MR imaging and signal targeting with alternating radio frequency. Radiology. 1994;192:513-20. 57. Kwong KK, Chesler DA, Weisskoff RM, et al. MR perfusion studies with T1-weighted echo planar imaging. Magn Reson Med. 1995;34:878-87. 58. Paldino MJ, Barboriak DP. Fundamentals of quantitative dynamic contrast-enhanced MR imaging. Magn Reson Imaging Clin N Am. 2009;17:277-89. 59. Tofts PS, Brix G, Buckley DL, et al. Estimating kinetic parameters from dynamic contrast-enhanced T(1)-weighted MRI of a diffusable tracer: standardized quantities and symbols. J Magn Reson Imag. 1999;10:223-32. 60. Tofts PS, Kermode AG. Measurement of the blood-brain barrier permeability and leakage space using dynamic MR imaging. Fundamental concepts. Magn Reson Med. 1991;17:357-67. 61. Cron GO, Santyr G, Kelcz F. Accurate and rapid quantitative dynamic contrast-enhanced breast MR imaging using spoiled gradient-recalled echoes and bookend T(1) measurements. Magn Reson Med. 1999;42:746-53.

Chapter 47 Functional Magnetic Resonance: Perfusion and Dynamic Contrast-enhanced Magnetic Resonance Imaging 62. Cron GO, Kelcz F, Santyr GE. Improvement in breast lesion characterization with dynamic contrast-enhanced MRI using pharmacokinetic modeling and bookend T(1) measurements. Magn Reson Med. 2004;51:1066-70. 63. Nguyen TB, Cron GO, Mercier JF, et al. Diagnostic accuracy of dynamic contrast-enhanced MR imaging using a phasederived vascular input function in the preoperative grading of gliomas. Am J Neuroradiol. 2012;33:1539-45. 64. Jackson A. Analysis of dynamic contrast enhanced MRI. Br J Radiol. 2004;77:S154-S166. 65. Claussen C, Laniado M, Schorner W, et al. Gadolinium-DTPA in MR imaging of glioblastomas and intracranial metastases. AJNR. 1985;6:669-74. 66. Talagala SL, Ye FQ, Ledden PJ, Chesnick S. Whole-brain 3D perfusion MRI at 3.0 T using CASL with a separate labeling coil. Magn Reson Med. 2004;52:131-40. 67. Wang Z, Wang J, Connick TJ, Wetmore GS, Detre JA. Continuous ASL (CASL) perfusion MRI with an array coil and parallel imaging at 3T. Magn Reson Med. 2005;54:732-7. 68. van Laar PJ, van der Grond J, Hendrikse J. Brain perfusion territory imaging: methods and clinical applications of selective arterial spin-labeling MR imaging. Radiology. 2008;246:354-64. 69. Buxton RB, Frank LR, Wong EC, et al. A general kinetic model for quantitative perfusion imaging with arterial spin labeling. Magn Reson Med. 1998;40:383-96. 70. Frank LR, Wong EC, Buxton RB. Slice profile effects in adiabatic inversion: application to multislice perfusion imaging. Magn Reson Med. 1997;38:558-64. 71. Golay X, Stuber M, Pruessmann KP, et al. Transfer insensitive labeling technique (TILT): application to multislice functional perfusion imaging. J Magn Reson Imaging. 1999;9:454-61. 72. Edelman RR, Chen G. EPISTAR MRI: multislice mapping of cerebral blood flow. Magn Reson Med. 1998;40:800-5. 73. Kim SG. Quantification of relative cerebral blood flow change by flow-sensitive alternating inversion-recovery (FAIR) technique: application to functional mapping. Magn Reson Med. 1995;34:293-301. 74. Yongbi MN, Branch CA, Helpern JA. Perfusion imaging using FOCI RF pulses. Magn Reson Med. 1998;40:938-43. 75. Dixon WT, Du LN, Faul DD, et al. Projection angiograms of blood labeled by adiabatic fast passage. Magn Reson Med. 1986;3:454-62. 76. Wong EC, Buxton RB, Frank LR. A theoretical and experimental comparison of continuous and pulsed arterial spin labeling techniques for quantitative perfusion imaging. Magn Reson Med. 1998;40:348-55. 77. Wong EC, Buxton RB, Frank LR. Quantitative imaging of perfusion using a single subtraction (QUIPSS and QUIPSS II). Magn Reson Med. 1998;39:702-8. 78. Herscovitch P, Raichle ME. What is the correct value for the brain–blood partition coefficient for water. J Cereb Blood Flow Metab. 1985;5:65-9.

79. Maccotta L, Detre JA, Alsop DC. The efficiency of adiabatic inversion for perfusion imaging by arterial spin labeling. NMR Biomed. 1997;10:216-21. 80. Siewert B, Bly BM, Schlaug G, et al. Comparison of the BOLD and EPISTAR technique for functional brain imaging by using signal detection theory. Magn Reson Med. 1996;36:249-55. 81. Garcia DM, Duhamel G, Alsop DC. Efficiency of inversion pulses for background suppressed arterial spin labeling. Magn Reson Med. 2005;54:366-72. 82. Zaharchuk G, Ledden PJ, Kwong KK, et al. Multislice perfusion and perfusion territory imaging in humans with separate label and image coils. Magn Reson Med. 1999;41:1093-8. 83. Alsop DC, Detre JA. Multisection cerebral blood flow MR imaging with continuous arterial spin labeling. Radiology. 1998;208:410-6. 84. Deibler AR, Pollock JM, Kraft RA, Tan H, Burdette JH, Maldjian JA. Arterial spin-labeling in routine clinical practice, part 1: technique and artifacts. AJNR. 2008;29:1228-34. 85. Järnum H, Steffensen EG, Knutsson L, et al. Perfusion MRI of brain tumours: a comparative study of pseudo-continuous arterial spin labelling and dynamic susceptibility contrast imaging. Neuroradiology. 2010;52:307-17. 86. Nezamzadeh M, Matson GB, Young K, Weiner MW, Schuff N. Improved pseudo-continuous arterial spin labeling for mapping brain perfusion. J Magn Reson Imaging. 2010;31:1419-27. 87. Golay X, Petersen ET, Hui F. Pulsed star labeling of arterial regions (PULSAR): a robust regional perfusion technique for high field imaging. Magn Reson Med. 2005;53:15-21. 88. Werner R, Norris DG, Alfke K, et al. Continuous artery-selective spin labeling (CASSL). Magn Reson Med. 2005;53:1006-12. 89. Warmuth C, Gunther M, Zimmer C. Quantification of blood flow in brain tumors: comparison of arterial spin labeling and dynamic susceptibility-weighted contrast-enhanced MR imaging. Radiology. 2003;228:523-32. 90. Gonzalez-At JB, Alsop DC, Detre JA. Cerebral perfusion and arterial transit time changes during task activation determined with continuous arterial spin labeling. Magn Reson Med. 2000; 43:739-46. 91. Hayes C, Padhani AR, Leach MO. Assessing changes in tumour vascular function using dynamic contrast-enhanced magnetic resonance imaging. NMR Biomed. 2002:15;154-63. 92. El Khouli RH, Macura KJ, Jacobs MA, et al. Dynamic contrastenhanced MRI of the breast: quantitative method for kinetic curve type assessment. AJR. 2009;193:W295-300. 93. Overview of Dynamic Contrast- Enhanced MRI in Prostate Cancer. AJR. 2012;198:1277-88. 94. Jackson AS, Reinsberg SA, Sohaib SA, et al. Dynamic contrastenhanced MRI for prostate cancer localization. Br J Radiol. 2009;82:148-56. 95. The role of dynamic contrast-enhanced MRI in cancer diagnosis and treatment. Diagn Interv Radiol. 2010;16:186-92.

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48

Magnetic Resonance Angiography

CHAPTER

Ajay Kumar, Sameer Vyas, Naveen Kalra

HISTORY AND INTRODUCTION The term angiography stands for the imaging depiction of vas­cular structures, and there are many ways to evaluate the vascular structures like Doppler, computed tomographic, catheter and magnetic resonance angiography (MRA). In last decade, MRA has been increasing in demand because of its physiological nature on the contrary to CTA and catheter angiography which involves catheterization, radiation and nephrotoxic iodinated contrast agents. However, there are many limitations, such as availability, cost, time consuming and high sensitivity to motion and flow related artifacts. The first research meeting devoted to MRA was hosted by Roberto Passariello in L’Aquila, Italy in 1989. Those days three-dimensional phase-contrast MRA would take 19 hours from the time the patient entered the magnet until images could be seen; one hour to acquire the image and 18 hours of overnight image postprocessing. Computational capabilities of modern equipment have reduced the delay to a few seconds. Postprocessing now has taken a more central role in the communication of enormous amounts of data with less cumbersome two- or three-dimensional projections. Many variations on the MRA theme have been presented over the ensuing 15 years. Dennis Parker developed the 3D multislab time-of-flight (TOF) MRA technique which remains in routine clinical use to this day. Pulse sequence design plays a major role in the continuing advancements in the field, most notably as a consequence of more sophisticated and novel k-space filling strategies. The work of Kent Yucel and Martin Prince at the Massachusetts General Hospital in1992 brought gadolinium-enhanced MR angiography to clinical utility. The first-pass dynamic contrast-enhanced MRA method provides robust and reproducible imaging results that have propelled the adoption of MRA into wider clinical use. This advance reliably produced images of sufficient quality to replace invasive catheter-based X-ray contrast angiography for most diagnostic purposes.

The advent of very high field clinical scanners operating at 3.0 tesla is now reinvigorating the earlier used noncontrast methods. 3.0 T MRA benefits from two key phenomena: zz THe signal to noise of 3.0 T is twice that of the 1.5 T, offering the opportunity to either increase the spatial resolution or to shorten scan times by up to a factor of four zz THe longer T1 of tissues at 3.0 T, ~20 to 40% higher than 1.5 T, provides better background suppression, additio­nal inflow enhancement, and improved contrast-to-noise.

FLOW PHENOMENA Flow phenomena in blood or cerebrospinal fluid (CSF) also influence the MR image contrast, in addition to inherent tissue factors like T1, T2 and proton density. Blood flow is complex and variable inside the body, so it is important to understand the various types of flow that are as follows: zz Laminar flow is flow where the particles move along in concentric sheets and laminae, i.e. different but consistent velocities across the vessel. It is seen in normal vessels zz Plug flow is flow where all fluid particles move forward in parallel lines with the same speed and has a characteristic blunt profile. It is seen in the descending thoracic aorta zz Turbulent flow is flow at different velocities which varies, i.e. velocities across the vessel changes and is seen at vascular bifurcations zz Vortex flow is flow after narrowing and is seen after stricture or stenosis. In it, the high velocities are seen at the center zz Stagnant flow is flow that nearly behaves like stationary tissue and is seen in occluded vessels and large aneurysms. The moving spins (spins that move during acquisition of data) show different contrast characteristics from the stationary spins. The moving spins causes mismapping of the signal because of the flow phenomena and result in flow motion artifacts or phase ghosting. The flow phenomena is generally categorized into time of flight, entry slice phenomenon and intravoxel dephasing.

Chapter 48 Magnetic Resonance Angiography

Outflow-related Signal Loss (Washout Effect, T2 Flow Void)

Inflow-related Signal Enhancement (Inflow Effect)

When images are obtained with a spin-echo (SE)-pulse sequence, the blood flowing at a high velocity perpendicular to the imaging plane produces a weaker signal than the surrounding stationary tissue. This phenomenon is caused by the washout of flowing spins from the slice during the imaging process. Spin-echo techniques are characterized by a sequence of slice-selective 90° and 180° radiofrequency (RF) pulses. Only those tissue components that are affected by both pulses can provide an MR signal. Moving material, such as blood in the vessels, flowing through the excited slice at a sufficiently high velocity, is affected by only one of these pulses, and therefore does not contribute to the MR signal. This is the so-called “flow void” (Figs 1A and B). The intensity of the vascular signal declines with decreasing slice thickness, increasing echo time (TE), and increasing flow velocity. If the blood flow velocity is so high that all spins leave the slice between the 90° and 180° pulses (v ≥ s/ (TE/2), then there will be no signal and the vessel will appear dark. Spins flowing within the imaging plane are not affected by this phenomenon. The washout effect is observed only for SE sequences and is most pronounced on T2- weighted imaging because of the long echo times used. With gradient-echo (GRE) techniques, the echo is refocused without a 180° pulse simply by reversing the imaging gradients. Since only one RF pulse is needed to form an echo, the washout effect does not occur. With standard SE sequences, the washout effect provides valuable and reliable information about blood flow. The absence of a flow void on T2- weighted imaging should be considered as indicative of very slow flow or even occlusion of the vessel. On the other hand, occlusion of the vessel can be excluded if a flow void is present.

The signal of blood flowing rapidly out of the measured slice is reduced with SE sequences, under these circumstances the opposite effect may occur: spins flowing into the slice may generate a higher signal than the surrounding tissue. This effect is referred to as “inflow enhancement”. On T1-weighted imaging, contrast is generated by repeated RF pulses that are applied with a time interval (repetition time, TR) that is shorter than the T1 relaxation time of the tissue (typically TR < 700 msec). As a result, the tissue components are saturated unequally, depending on their individual T1 times. This is the basis of T1-weighted image contrast. Irrespective of flow effects, blood in the vessels would appear hypointense on a normal T1-weighted image due to its relatively long T1 time. The signal emitted by the tissue diminishes when the TR is reduced. With GRE sequences, repetition time shorter than 50 msec can be achieved. This allows the majority of nonmoving spins to become saturated, thus minimizing the background signal. Spins outside the excited slice (or volume) are not influenced by the RF pulses. Consequently, blood entering into the slice being imaged is fully relaxed, experiencing not more than a few excitations on its way through the slice. As a result, flowing blood gives rise to considerably higher signal intensity relative to that of the saturated spins in the stationary tissue. This effect is called “inflow enhancement” or “flowrelated enhancement”. The signal intensity of flowing blood increases with decreasing slice thickness, and increasing flow velocity.

Fig. 1A:  Spin-echo sequence depicting the “Flow void” phenomenon

(A and B) represents the tissue sample with shaded area as stationary tissue (spins) and central nonshaded area as vessel having moving spins. (A) At the time of 90o excitation and 180o rephasing RF pulse for that particular selected slice location. (B) Same tissue with same slice location at the time of receiving signal or TE, now only stationary spins are giving signal in the selected slice, however, the moving spins have migrated out of selected slice with new nonexcited spins in that place giving no signals

Fig. 1B:  T2W axial image of the patient with bilateral ICA aneurysms

shown to explain “Flow voids”–Normal arteries, i.e. left ACA and basilar arteries (black arrows) are seen hypointense due to flow void, left aneurysm (white elbow arrow) postcoiling shows heterogeneous hypointese signals due to partial thrombosis. Right patent aneurysm (white arrows) reveals flow voids at periphery due to high flow, however central part giving bright signals due to relative stasis of blood

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If the blood flow velocity is so high that all vessel spins are replaced by unsaturated spins in the time interval TR, flow enhancement is maximal and the vessel appears bright on a gray or black background. Although the inflow effect occurs both with SE and GRE sequences, SE sequences are not practical for the TOF method because the competing washout effect tends to overbalance the inflow effect at higher flow velocities, leading to decreased flow signal. Consequently, flow-related enhancement using GRE sequences to produce bright-blood images is the basis of time-of-flight angiography.

Phase Effects Phase effects concern the transverse component of the magnetization. They occur whenever spins are moving in the presence of magnetic field gradients, as are applied for spatial encoding of the MR signal. Magnetic field gradients provoke a change in the Larmor frequency depending on gradient strength and spin position. A gradient pulse of certain length and amplitude, therefore, induces a phase shift of the transverse magnetization, which can be compensated by a second gradient pulse with identical strength and duration but opposite sign. Thus for stationary spins the net phase shift is zero. In contrast, the same gradients applied on a flowing spin generate a non-zero phase shift. Since the spins change their position during the bipolar gradient application, the second gradient pulse is no longer able to completely compensate for the phase shifts induced by the first gradient. The remaining phase shift Φ is proportional to the velocity component v of the spins along the gradient direction. On standard MR imaging, this flow-induced phase shift causes a spatial misencoding of the signal leading to ghost artifacts that are typically found in the phase-encoding direction. Spins in a blood vessel are moving with different velocities. Often, a parabolic flow profile is found. Spins moving faster, experience a larger phase shift than those moving more slowly. If there is a velocity distribution inside a voxel, phase dispersion (intravoxel dephasing) occurs resulting in decreased signal in the blood vessel. The extent of spindephasing depends on the strength and time interval of the gradient pulses, as well as the distribution of spin velocities. When complex flow patterns are encountered, for example, in vessels with turbulent flow, there may be a very broad spectrum of velocities within a voxel, leading to total signal loss in the vessel. Using additional gradient pulses of appropriate amplitude and duration, flow-induced phase shifts can be compensated, thus eliminating any signal loss. This technique is called “gradient motion rephasing (GMR)” or just “flow compensation”.1 However, GMR is normally restricted to first-order movements, i.e. spins that move at a constant velocity. Turbulent flow and effects of acceleration cannot be completely compensated by GMR. Optimal reduction of

Fig. 2:  Diagrammatic representation of phase-contrast MRA pulse sequence, note the velocity encoding gradient are in slice direction

flow-induced phase effects can be achieved by combining GMR with as short a echo times (TE) as possible, in order to reduce the time available for spin dephasing. Short TE also diminish the impact of pulsatile blood flow and turbulence (Fig. 2).

TIME-OF-FLIGHT ANGIOGRAPHY: TECHNIQUES The contrast mechanism of time-of-flight (TOF) MRA is based on the inflow effect. Fully relaxed blood entering the measured volume behaves as an endogenous contrast agent, by producing a bright signal. The bright depiction of flowing blood, however, requires the use of flow rephasing techniques (GMR) in order to overcome the effects of spin-dephasing due to transverse magnetization. TOF MRA using GRE sequences has several advantages: Firstly, GRE sequences are not affected by the washout phenomenon that diminishes the signal of fast flowing blood when using SE techniques. Secondly, GRE techniques permit the use of short repetition times (TR 70% internal carotid artery stenosis. Am J Neuroradiol. 2009;30:761-8. 20. A TJ, Kaufmann J, Huston III HJ, Cloft J Mandrekar L. A prospective trial of 3T and 1.5T time-of-flightand contrastenhanced MR angiography in the follow-up of coiled intracranial aneurysms. Am J Neuroradiol. 2010;31:912-8. 21. Maurizio Papa, Francesco De Cobelli, Elena Baldissera. Takayasu Arthritis: Intravascular Contrast medium for MR Angiography in the evaluation of disease activity. AJR. 2012; 198:W279-W284. 22. Lubicz B, et al. Is digital substraction angiography still needed for the follow-up of intracranial aneurysms treated by embolization with detachable coils? Neuroradiology. 2008;50:841-8. 23. RI Farb R, Agid RA, Willinsky DM Johnstone. Cranial dural arteriovenous fistula: diagnosis and classification with timeresolved MR Angiography at 3T. Am J Neuroradiol. 2009; 30:1546-51. 24. Kristine A Blackham, Matthew A Passalacqua, Gurpreet S Sandhu. Applications of time-resolved MR Angiography. AJR. 2011;196:W613-20. 25. HK Lim, CG Choi, SM Kim. Detection of residual brain arteriovenous malformations after radio surgery: diagnostic accuracy of contrast-enhanced four-dimensional MR angiography at 3.0T. BJR. 2012;85:1064-9. 26. Umutlu L, Maderwald S, Kinner S. First- pass contrastenhanced renal MRA at 7 Telsa: initial result. Eur Radiol. 2012 Oct (Epub ahead of print). 27. Samuel RS. Barnes, Mark Haacke. Susceptibility Weighted Imaging: Clinical angiographic applications. Magn Reson Imaging Clin N Am. 2009;17(1):47-61.

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Magnetic Resonance Imaging Pulse Sequences: An Evolution

49

CHAPTER

Vivek Gupta, Niranjan Khandelwal

INTRODUCTION Magnetic resonance sequences are continuously evolving, from simple sequences like conventional spin echo they have increased in number as well as complexity. However, the ultimate aim of every sequence is bring about better tissue contrast in least amount of time. Therefore, different sequences

are designed to account for varied tissue characteristics. Also, with the tremendous improvement in computational powers now the sequences have become less time consuming and less prone to artifacts. It is a vast and complex topic but basic understanding of the sequences is essential to interpret the MR images they produced. Table 1 gives an overview of the present generation of pulse sequences by various vendors.

Table 1:  MR pulse sequences and their classification Technique

Sequences

Weighting

Features

Application

T1, T2 and proton density (PD) T1, T2 and proton density (PD)

Robust sequences. Less susceptible to T2* effects Faster Less susceptible to motion artifacts and T2* effects Faster High resolution imaging

Now replaced by fast SE sequences

To suppress fluid and make adjacent lesions more prominent To suppress fat signal

Spin-echo (SE) sequences 1.

ConventionaL SE

SE

2.

Fast SE (RARE)

TSE (Turbo SE) FSE (Fast SE)

3 4.

HASTE Inversion recovery

SS-FSE (single-shot fast-spin echo) IR, turbo IR, TIRM (turbo IR magnitude reconstruction), IR TSE FLAIR (fluid attenuated inversion recovery)

T- weighting T1-weighting

T2-weighting

Very useful in brain imaging

STIR (short T1 inversion recovery)

T1-and T2weighted

Insensitive to susceptibility artifacts

T1 and T2*

High SNR and T2* weighting, suitable to 3D imaging

Application in orthopedic imaging

T2-weighted

True T2 weighting achievable, lower SNR

CSF flow studies, inner ear imaging

High resolution neurological and orthopedic imaging. Single breath hold abdominal imaging Used in MRCP For good contrast between white and gray matter

Gradient-echo (GRE) sequences A. 1.

Coherent sequences Postexcitation steady state sequences

2.

Pre-excitation steadystate refocused sequences

FISP (fast imaging with steady-state precession), GRASS (gradient recalled acquisition in the steady state), FFE (fast field echo) PSIF (reversed FISP), SSFP (steady state free precession)

Contd…

Chapter 49 Magnetic Resonance Imaging Pulse Sequences: An Evolution

Contd… Technique 3.

4. 5

B 1a.

1b.

2. 3.

4

Sequences

Fully refocused steady True FISP, state sequences FIESTA (fast imaging employing steady state acquisition), Balanced FFE (fast field echo) Combination of A3 and DESS (dual echo steady state) A4 Combination of A3 and CISS (constructive interference in the A4 steady state), FIESTA-C

Incoherent/Spoiled sequences 2D-spoiled GRE FLASH (fast low angle shot), T1-FFE (T1 fast field echo), SPGR (spoiled gradient echo) 3D-spoiled GRE VIBE (volumetric interpolated breath hold examination), THRIVE (T1weighted high resolution isotropic volume examination) Ultrafast GRE Turbo FLASH, TFE (turbo field echo) 3D-ultrafast GRE MP-RAGE (magnetization prepared rapid acquisition GE), 3D-TFE Echo planner imaging EPI

Hybrid Sequences 1. Gradient/spin echo Turbo GSE (gradient spin echo), hybrid GRASE (gradient echo and spin echo)

Weighting

Features

Application

T1- and T2weighting

Less sensitive to motion

Cardiac, fetal imaging Abdominal imaging

T1- and T2weighting T2-weighting

Orthopedic imaging Less prone to banding artifacts in comparison the true FISP

Inner ear 3D imaging

T1-weighted imaging

Fast imaging

MR angiography, In-out phase imaging

T1-weighting

Isotropic imaging, high resolution, fast imaging

Body imaging

T1-weighted

Very fast imaging

T1-weighted

To get rapid images like to track contrast arrival High resolution 3D Cerebral T1 3D imaging sequence

T2* weighting

Ultrafast sequence

Diffusion, perfusion and functional MRI

T2/T2* weighting

Fast imaging with T2 weighting imaging of brain low SAR and orthopedic imaging

MR sequence is a series of different RF pulses, which are applied at a particular time and in a specified way to obtain an image. A pulse sequence diagram is a schematic diagram, which depicts various pulse or gradients that are applied over a period of time. There are minimum of four horizontal lines, which depict the excitatory RF pulse, and three representing each gradient, i.e. phase gradient, frequency gradient and slice encoding gradient (Fig. 1). Additional lines may be used to depict the generated echo and other pulse or gradients used.

BASIC TERMINOLOGIES Image contrast is generated by variation of repetition time (TR) and echo time (TE) in any given sequence. TR is the time interval between application of an RF excitation pulse and start of the next RF pulse. TE is time between the initial RF pulse and the peak of the echo, which is produced. Both are usually in milliseconds. T1- and T2-weighting are other terms, which need to be understood. T1-weighted images would mean that though, image show all types of contrast

Fig. 1:  Pulse sequence diagram of conventional spin echo sequence. Here a single180° RF pulse is applied after an initial 90° excitatory pulse. Since TR and TE are short, the image is T1-weighted

but the T1 effect is more pronounced. T1 effect would mean that the TR and TE are both short and the difference between relaxation of longitudinal magnetization of fat and water can be detected. In T1-weighted images fat, blood products, slow moving blood and MR contrast would all be bright and tissues

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with fluid, mineral rich content like bone and air would be dark. T2-weighting is opposite of this. Here the TR and TE are both prolonged and thus the difference in T2 signal decay of fat and water can be detected. At short TE, this difference is not apparent. This makes high free water containing tissues bright of T2-weighted images. Another type of images are proton density images where TR is long and TE is short, thus the images are neither T1-weighted and nor T2-weighted but the image contrast produced is due to difference in proton density of the tissues, those having higher density of protons giving higher signal.

The major constrain in this sequence is the long acquisition times.

TYPES OF SEQUENCES

Fast-spin-echo Sequences

Spin echo sequences were the first sequences to be used for MR imaging. These were closely followed by gradient echo imaging. As more and more limitations of these classic sequences became apparent, they were modified to bring about better tissue contrast in less time. This was followed by ultrafast sequences in both these groups. Finally, sequences with features of both of these were created to generate hybrid sequences.

This sequence was developed to overcome the limitation of conventional spin-echo sequence, it involves use of multiple 180° rephasing pulses after the initial 90° RF pulse (Fig. 3). This sequence reduces time by reducing the phase encoding steps (The scan time is dependent on TR, phase encoding steps and the number of signal averaging or the number of excitations). Here each 180° rephasing pulse fills k-space by doing a phase encoding. Thus for a single excitatory RF pulse (90°) multiple 180° rephasing pulse are applied which in turn fills multiple lines in k-space, thereby filling the k-space faster and reducing the scan time. Typically 2,4,8,16 rephasing pulse are used and the time reduction achieved is inversely proportionate to them. The number of 180° pulse and the resultant echo is called “echo train length (ETL)”. Rapid acquisition and relaxation enhancement (RARE) sequence employ this method (e.g. Turbo-SE and fast-SE sequences are examples of this technique).

Conventional Spin-echo Sequences In a typical spin echo sequence, an initial 90° radio-frequency excitation pulse is followed by a 180° rephasing pulse which is then followed by an echo (Fig. 1). If there is only one 180° rephasing pulse, a T1-weighted image is produced since the resultant TR and TE are short. When two 180° pulse are used of results in two images. First image is proton density weighted, since here TR is long and TE is short and the second image is T2-weighted, as TR and TE are both prolonged (Fig. 2). Conventional spin echo sequences can be used in any part of the body with predictable tissue contrast characteristics.

Fig. 2:  Dual-echo-pulse sequence. Here first echo is proton-weighted

as TE is short and second echo is T2-weighted as TE is prolonged. TR is prolonged

Parameters Usually following parameters are applied: zz Single echo T1-weighting —— TR: 300–500 ms —— TE: 10–30 ms zz Dual echo T2-weighting —— TR: 2000 ms —— TE1: 20 ms —— TE2: 80 ms.

Parameters Usually following parameters are applied: zz Single echo T1-weighting —— TR: 600 ms

Fig. 3:  Fast-spin-echo sequence. Here multiple 180° pulse are applied after an initial 90° pulse. The acquisition time is reduced as for a single 90° pulse multiple phase encoding steps take place

Chapter 49 Magnetic Resonance Imaging Pulse Sequences: An Evolution

TE: 17 ms ETL: 4 Single echo T2-weighting —— TR: 4000–8000 ms —— TE: 102 ms —— ETL: 16 Dual echo T2-weighting —— TR: 2500-4500 ms —— TE1 effective: 17 ms —— TE2 effective: 102 ms —— ETL: 8. —— ——

zz

zz

Half-fourier Acquisition Single-shot Turbo Spin Echo Half-fourier acquisition single-shot turbo spin echo (HASTE) is another modification of fast spin echo where only half the lines of k-space are filled in a single shot (Single shot filling of k-space can also be done in RARE but filling of entire k-space will result in long acquisition time thus prone to significant T2 decay). For example, SS-FSE, FSE-ADA, FASE. Since k-space is symmetrical, rest half of k-space can be filled with interpolation.

Inversion Recovery Sequence This is basically a spin echo sequence where an additional 180° inverting RF pulse is applied which inverts the net magnetizing vector (NMV) through 180°. After removal of pulse the NMV begins to recover, a 90° excitation pulse is applied at a time interval TI (inversion time) after the initial 180° inverting pulse. Following which, like in conventional spin echo sequences a 180° rephasing pulse is applied to produce an echo at a time TE (Fig. 4). This sequence can be both T1- and T2-weighted. If inversion time is sufficiently long to allow net magnetizing

vector to pass through the transverse plane and then the 90° excitation pulse is applied, then the contrast is predominantly T1-weighted. Here TE is to be kept short. For T2-weighting the TE is prolonged so that T2 decay can occur and the resultant image is T2-weighted. The TR, the interval between the two inverting 180° pulses should be kept long to allow for complete recovery of NMV to the longitudinal plane. • Short T1 inversion recovery (STIR): This sequence is predominantly used to suppress fat to delineate the structures surrounded by fatty tissues. Here inversion time is kept low and 90° excitation pulse is applied when NMV of fat is crossing the transverse plane. At this point the longitudinal component of fat is zero so it does not contribute to any signal thus is suppressed. • Fluid attenuated inversion recovery (FLAIR) sequence: This is commonly used sequence in brain to suppress the CSF signal. Here inversion time is kept long (as opposed to in STIR) and 90° excitation pulse is applied when NMV of water is crossing the transverse plane. This selectively suppresses the CSF/free fluid signal. Parameters zz STIR —— TI 100–180 ms
 —— TE 70 ms + (for T2 weighting) —— TR long —— ETL-16 zz FLAIR —— TI 1500: 2200 ms
 —— TE 70 ms + (for T2 weighting) —— TR long —— ETL: 12.

Gradient-echo Sequences This is fundamentally different sequence when compared to spin echo sequence. In this type, an initial excitation pulse is applied with certain strength that it flips the NMV into transverse plane at an angle less than 90°. The angle to which it flips the NMV is called flip angle. After the pulse is withdrawn, the magnetic moments start to dephase due to presence of magnetic field inhomogeneities, which is called as T2* decay. A gradient pulse is then applied which dephase and then rephases the magnetic moments in the transverse component. This is followed by generation of signal called gradient echo (Fig. 5). Since the rephasing by a gradient is not as effective as the RF pulse some nuclei, which are dephased (due to T2* effect) are not rephased and thus the resultant GRE image has some T2* effect.

Fig. 4:  A typical inversion recovery pulse diagram. A 180° inversion

pulse is applied before 90° excitatory pulse to flip NMV by 180°. Inversion time (TI) is the time interval between the inversion pulse and initial excitatory pulse

Parameters zz T1-weighting —— TR: 10

>100

Increased risk of childhood cancer

>50

>500

Severe mental retardation observe at 16–25 wk

Table 12:  Fetal absorbed dose Gestational age

150 mGy)

< 2 weeks

Recom­ mended

Recommended

Recommended

2–8 weeks

Recom­ mended

May consider termination (in presence of other risk factors)

May consider termination (in presence of other risk factors)

May consider termination (in presence of other risk factors)

Higher risk conditions, but termination is not necessarily recommended

Recommended

Recommended

8–15 weeks

15 weeks to term

Recom­ mended

Recom­ mended

RECOMMENDED DOSE LIMITS TO PREGNANT WOMEN18,19

The instruments used to detect radiation are referred to as radiation detection devices. Instruments used to measure radiation are called radiation dosimeters.

Methods of Detection There are several methods of detecting radiation, and they are based on physical and chemical effects produced by radiation exposure. These methods are:31 zz Ionization zz Photographic effect zz Luminescence zz Scintillation.

Ionization The ability of radiation to produce ionization in air is the basis for radiation detection by the ionization chamber. It consists of an electrode positioned in the middle of a cylinder that contains gas. When X-rays enter the chamber, they ionize the gas to form negative-ions (electrons) and positive-ions (positrons). The electrons are collected by the positively charged rod, while the positive-ions are attracted to the negatively-charged wall of the cylinder. The resulting small current from the chamber is subsequently amplified and measured. The strength of the current is proportional to the radiation intensity.

Photographic Effect The photographic effect, which refers to the ability of radiation to blacken photographic films, is the basis of detectors that use film (e.g. film badge).

Luminescence Luminescence describes the property by which certain materials emit light when stimulated by a physiological

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process, a chemical or electrical action, or by heat. When radiation strikes these materials, the electrons are raised to higher orbital levels. When they fall back to their original orbital level, light is emitted. The amount of light emitted is proportional to the radiation intensity. Lithium fluoride, for example, will emit light when stimulated by heat. This is the fundamental basis of thermo luminescence dosimeter (TLD), a method used to measure exposure to patients and personnel.

Scintillation Scintillation refers to a flash of light. It is a property of certain crystals­, such as sodium iodide and cesium iodide to absorb radiation and convert it to light. This light is then directed to a photomultiplier tube, which then converts the light into an electrical pulse. The size of the pulse is proportional to the light intensity, which is in turn proportional to the energy of the radiation.18

PERSONNEL DOSIMETRY Personnel dosimetry refers to the monitoring of individuals who are exposed to radiation during the course of their work. Personnel dosimetry policies need to be in place for all occupationally-exposed individuals. The data from the dosimeter are reliable only when the dosimeters are properly worn, receive proper care, and are returned on time. Proper care includes not irradiating the dosimeter except during occupational exposure and ensuring proper environmental conditions. Monitoring is accomplished through the use of personnel dosimeters, such as the pocket dosimeter, the film badge or the thermoluminescent dosimeter. The radiation measurement is a time-integrated dose, i.e. the dose summed over a period of time, usually about 3 months. The dose is subsequently stated as an estimate of the effective dose equivalent to the whole body in mSv for the reporting period. Dosimeters used for personnel monitoring have dose measurement limit of 0.1–0.2 mSv (10–20 mrem).18

Emulsion on one side is slow and that on the other side is fast. zz The film dosimeter is energy dependent, because silver and bromine have much higher atomic numbers than the tissue or air. To identify various components of incident radiation, film badge sandwiches the film between at least 6 pairs of filters (Fig. 5). Six type of windows are: —— Open window: Alpha rays —— Plastic: Gray- beta rays —— Cadmium: Yellow-slow neutrons —— Thin copper: Green-diagnostic X-rays —— Thick copper: Pink-gamma and therapeutic rays —— Lead: Black-fast neutrons and gamma rays zz Radiation of a given energy is attenuated to a different extent by various type of absorbers. Therefore, the same quantity of radiation incident on the badge will produce a different degree of darkening under each filter. 31 zz In India, film badges have been replaced by TLD badges. zz

Thermoluminescent Dosimetry Monitoring The limitations of the film badge are overcome by the thermoluminescent­dosimeter (TLD). Thermoluminescence is the property of certain materials to emit light when they are stimulated by heat. Materials, such as lithium fluoride (LiF), lithium borate (Li2B4O7), calcium fluoride (CaF2), and calcium sulfate (CaSO4) have been used to make TLDs. zz When a LiF crystal is exposed to radiation, a few electrons become trapped in higher energy levels. For these electrons to return to their normal energy levels, the LiF crystal must be heated. As the electrons return to their stable state, light is emitted because of the energy difference between two orbital levels. The amount of light

Pocket Dosimeter The pocket dosimeter monitors dose to personnel. It consists of an ionization chamber with an eyepiece and a transparent scale, as well as a hollow charging-rod and a fixed and a movable fiber. When X-rays enter the dosimeter, ionization causes the fibers to lose their charges and, as a result, the movable fiber moves closer to the fixed fiber. The movable fiber provides an estimate of gamma or X-ray dose rate.

Film Badge Monitoring zz

These badges use small double coated X-ray films sandwiched between several filters to help detect radiation.

Fig. 5:  A film badge

Chapter 61 Radiation Protection

emitted is measured (by a photomultiplier tube) and it is proportional to the radiation dose.28 zz The measurement of radiation from a TLD is a two-step procedure: —— In step 1, the TLD is exposed to the radiation —— In step 2, the LiF crystal is placed in a TLD analyzer, where it is exposed to heat. As the crystal is exposed to increasing temperatures, light is emitted. When the intensity of light is plotted as a function of the temperature, a glow curve results. The glow curve can be used to find out how much radiation energy is received by the crystal because the highest peak and the area under the curve are proportional to the energy of the radiation. These parameters can be measured and converted to dose.   Whereas the TLD can measure exposure to individuals as low as 1.3 μC/kg (5 mR) the pocket dosimeter can measure up to 50 μC/kg (200 mR). The film badge, however, cannot measure exposures less than 2.6 μC/ kg (10 mR). TLDs can withstand a certain degree of heat, humidity, and pressure; their crystals are reusable; and instantaneous readings are possible if the department has a TLD analyzer. The greatest disadvantage of a TLD is its cost.

Electronic Dosimeters zz

zz

zz zz

Direct reading electronic dosimeters based on GeigerMuller tubes or single silicon diodes It can provide immediate dose readings and effective alarms when dose limit is exceeded The sensitivity is 50–200 times that of TLD badges The advantages and disadvantages can be tabulated as in Table 13.11,28

Wearing the Dosimeter During Radiography During radiography (when no protective lead apron is worn), the personnel dosimeter is worn at one of two regions: 1. On the trunk of the body at the level of the waist. 2. On the upper chest region at the level of the collar area outside the lead apron. At these positions, the dosimeter readings represent an estimate of exposure at two different levels, i.e. the whole body exposure is estimated by the trunk level badge and exposures dose to internal organs like thyroid is measured by the collar level badge.

During Fluoroscopy During fluoroscopy, a protective apron should always be worn. It is further recommended that ideally, two dosimeters

Table 13:  Advantages and disadvantages of electronic dosimeters Advantages

Disadvantages

Film badges Relatively cheap Permanent record of exposure Wide dose ranges (0.2–2000 mSv) Identifies type and energy of exposure Easy to identify individual dosimeters

Requires darkroom and wet processing Lower threshold for hard gamma radiation is 0.15 mSv is affected by heat, humidity and chemicals

TLD badges Chips can be reused Wide dose range (0.1–2000 mSv) Direct reading of personal dose Energy independent within ± 10% Compact: suitable for finger dosimetry

Requires high capital initially No permanent record (other than glow curves cannot distinguish radioactive contamination)

Electronic personal dosimeter Direct reading and cumulative record storage (up to16Sv) Flat response (20 keV to 10 MeV) can be ‘zeroed’ by user without deleting cumulative record Measures personal dose at depth and at the skin directly to 1 micro Sv audible warning at high-dose rates

Requires a filtered badge to provide energy discrimination High cost Linear response to dose is quite heavy Battery should be renewed every year

should be worn by radiation personnel, one at the collar level outside the lead apron and the other at the level of trunk underneath the lead apron. The one at the collar level gives an accurate estimate of the radiation dose to the unprotected regions of head and neck. The dosimeter worn underneath the lead apron at the trunk level provides an accurate estimate of the radiation to the protected organs. If only one dosimeter is worn, it must be worn at the collar outside the lead apron, because, the neck receives 10–20 times more radiation than the trunk which is protected by lead.

COMPUTED TOMOGRAPHY (RADIATION EXPOSURE AND DOSE MODULATIONS) Radiation Dose Measures: CT Specific Because of its geometry and usage, CT is a unique modality and therefore, has its own set of specific parameters for radiation dose. This modality is unique because the exposure is essentially continuous around the patient, rather than a projectional modality in which the exposure is taken from one or two source locations.37 Projectional radiographic exposures are taken from one source position and the entrance skin dose is much larger

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than the exit skin dose, creating a large radiation dose gradient across the patient (Fig. 6).

Conventional Radiographic Projections In contrast, the tomographic exposure of CT scans with a full 360° rotation results in a radially symmetric radiation dose gradient within the patient.

To account for the effects from multiple scans, several dose descriptors were developed.37 These are as follows: zz Multiple scan average dose (MSAD) zz Computed tomography dose index (CTDI) zz CTDI 100 zz CTDI W zz CTDI vol zz Dose length product

CT Radiation Projections However, there is a radial dose gradient which exists in computed tomography scanning (Fig. 7).

TYPICAL DOSE MEASUREMENTS The radial dose gradient (the size of the difference from center to periphery) will be affected by several factors, including the size of the object, the X-ray beam spectrum, and the attenuation of the material or tissue (Fig. 8).37 In addition to the variations within the scan plane, there are variations along the length of the patient or phantom. These can be characterized by the z-axis dose distribution or radiation profile (Fig. 9). The radiation profile is not limited to the primary area being imaged, and there are tails to this distribution from the nonideal collimation of the X-ray source and from scatter of photons within the object being exposed. These contributions can add-up, creating additional absorbed dose in the primary area being imaged.

Fig. 7:  Dose gradient resulting from a full 360° exposure from a CT

scan. The thicker lines represent the entrance skin dose, which is much larger than the dose at the inner radius, represented by the thinner lines. This difference results in a radially symmetric radiation dose gradient within the patient37

Fig. 6:  Dose gradient resulting from a projectional radiographic

exposure in which the source is stationary at one position. The thicker lines represent the entrance skin dose, which is much larger than the exit skin dose, represented by the thinner lines. This difference creates a linear difference through the patient37

Fig. 8:  Typical dose measurements in a 32 cm diameter (body) phantom from a single detector CT scan37

Chapter 61 Radiation Protection 5 cm

CTDI100 = (1/NT)∫ D series(z)dz –5 cm

where ‘N’ is the number of acquired sections per scan (also referred to as the number of data channels used during acquisition) and ‘T’ is the nominal width of each acquired section.

CTDIW

Fig. 9:  Radiation profile of a full-rotation CT scan measured at

CTDIw was created to represent a dose index that provides a weighted average of the center and peripheral contributions to dose within the scan plane. This index is used to overcome the limitations of CTDI100 and its dependency on position within the scan plane. CTDIw = (1/3)(CTDI100)center + (2/3)(CTDI100)periphery

Multiple Scan Average Dose

CTDIvol

This is defined as the average dose resulting from a series of scans over an interval I in length.38

One final CTDI descriptor takes into account the parameters that are related to a specific imaging protocol, the helical pitch or axial scan spacing, and is defined as CTDIvol. CTDIvol = CTDIw × NT/I where N is the number of acquired sections per scan and and T is the nominal width of each acquired section. The product of N × T is meant to reflect. The total nominal width of the X-ray beam during acquisition and I is the table travel per rotation for a helical scan. Hence NT/I = 1/pitch and CTDIvol = CTDIw/pitch.

isocenter. This profile is the distribution of radiation dose along the axis of the patient (the z-axis) and is known as D(z)

π2

MSAD = (1/I)∫ D series(z)dz –π2

where ‘I’ is the interval of the scan length and ‘D series(z)’ is the dose at position z parallel to the z (rotational)-axis resulting from the series of CT scans.

Computed Tomography Dose Index (CTDI) It is defined as the radiation dose normalized to beam width measured from 14 contiguous sections.39 π

CTDI = (1/nT)∫ D single(z)dz –π

where n is the number of sections per scan, T is the width of the interval equal to the selected section thickness, and D single(z) is the dose at point z on any line parallel to the z (rotational) axis for a single axial scan. However, to be measured according to the definition, only 14 sections could be measured and one had to measure the radiation dose profile—typically done with thermoluminescent dosimeters (TLDs) or film, neither of which was very convenient. Measurement of exposure could be done with pencil ionization chamber but its fixed length of 100 mm meant that only 14 sections of 7 mm thickness could be measured with that chamber alone. To overcome the limitations of CTDI with 14 sections, another radiation dose index—CTDI100—was developed.

Dose-length Product (DLP) This value is simply the CTDIvol multiplied by the length of the scan (in centimeters) and is given in units of milligray-centimeters: DLP = CTDIvol × scan length41 This descriptor is used to obtain an estimate of effective dose. The DLP values are easily­converted to millisieverts by using conversion factors specific to the anatomic region imaged: the conversion factors listed by the American Association of Physicists in Medicine for the chest, abdomen, and pelvis are 0.014, 0.015, and 0.015.42 These conversion factors are periodically updated, so care should be taken to apply the most recent ones (Table 14).

CTDI100

Techniques for Controlling Radiation Dose at CT

This index relaxed the constraint on 14 sections and allowed calculation of the index for 100 mm along the length of an entire pencil ionization chamber. 38 This index can be measured and calculated for the center location as well as at least one of the peripheral positions.40

Multidetector CT protocols can be directly modified in a variety of ways. These include using an automated exposure control system or modifying­individual acquisition parameters, such as the number of phases, section thickness, peak voltage (kVp setting), tube current–time product, and pitch.

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Table 14:  Effective radiation doses calculated from DLP values in a routine oncologic CT examination of the abdomen and pelvis43 Region scanned

DLP (mGy·cm)

Conversion factor

Effective dose (mSv)

Abdomen and pelvis (portal venous phase)

681

0.015

10.2

Kidneys (delayed phase)

230

0.015

3.5

Bladder (delayed phase)

214

0.015

3.2

increase image noise by 1/√(mAs), which means that a 50% reduction in the milliampere-seconds value results in a noise increase of 41%. For example, detection of high-contrast objects in the lung may not require a low-noise imaging protocol and the reduction in milliampere-seconds may be well-tolerated. On the other hand, imaging low-contrast lesions in the liver does require a low-noise imaging protocol and the reduction in milliampere-seconds may limit the ability to detect these lesions.

USING AUTOMATED EXPOSURE CONTROL

Increasing Pitch

Automated exposure control (AEC) systems are designed­to reduce the radiation dose by dynami­cally altering the tube current as the X-ray tube rotates around the patient during multidetector CT scanning. The tube current is automatically modulated according to the attenuation level (i.e. the size) of the patient.44 For smaller patients, i.e. the pediatric patients, the tube current is automatically decreased to adapt to the lower attenuation level. Conversely, the tube current is appropriately increased for larger patients. Use of AEC is an efficient way to tailor radiation dose to achieve a target image quality.

The radiation dose is inversely proportional to pitch. Increasing the pitch decreases the dose, increases the image noise, increases the effective section thickness, and reduces the scanning time.46 The trade-off in increasing pitch is an increase in effective section thickness, which results in increased volume averaging, which in turn may reduce the image signal. The ability to use this type of dose reduction again depends on the clinical applications.

MODIFYING THE ACQUISITION PARAMETERS

Computed tomography is an example of a digital modality in which the image quality continues to improve as the exposure increases. This is contrasted with analog projectional film, in which too high of an exposure results in an overexposed (too dark). However, the radiation dose to the smaller patient is potentially higher than is necessary to obtain a diagnostic image. Therefore, significant effort has recently been put into developing size- and weight-based imaging protocols. This has typically been in the form of a reduced milliampereseconds value for reduced patient size and has led to the development of suggested technique charts for pediatric patients.

Acquisition parameters, such as the number of scanning phases and the section thickness may be modified to achieve deeper dose reductions even when an automated exposure control system is used. If CT angiography-venography protocol initially includes four scanning phases (precontrast),­postcontrast arterial phase, postcontrast portal venous phase, and postcontrast delayed scanning), by decreasing the number of scanning phases to two (postcontrast arterial phase and slightly later portal venous phase), the radiation dose can be reduced by 50%. The acquisition section thickness also has an important effect on image noise and, consequently,­on the amount of radiation needed to meet the preset noise value. With regard to section thickness­at 64-row multidetector CT, if the section thickness of 5 mm were decreased to 2.5 mm, Kanal et al. found, the noise index of 15.3 would have to be increased to 23.4 to keep the dose constant. Conversely, if the noise index were kept constant at 15.3, the relative dose with 2.5 mm thick sections would be approximately 2.3 times that with 5 mm thick sections.45

Reducing the Milliampere-seconds Value The radiation dose is linear with milliampere seconds value, when all other factors are held constant, so the milliampereseconds value is reduced by 50%, the radiation dose will be reduced by the same amount. However, this reduction will

Varying the Milliampere-seconds Value by Patient Size

Optimum Tube Potential47 Use of an optimum tube potential may help improve image quality or reduce radiation dose particularly in pediatric CT examination. The main benefit of a lower tube potential is that it provides improved contrast enhancement, a characteristic that may compensate for the increase in noise that often occurs at lower tube potential and may allow radiation dose to be substantially reduced. The use of a lower tube potential should be carefully evaluated for each type of examination to achieve an optimum trade-off among contrast, noise, artifacts and scanning time.47

ITERATIVE RECONSTRUCTION Computed tomography scanner vendors have been working to develop­various image reconstruction techniques as

Chapter 61 Radiation Protection

alternatives to traditional filtered back projection for reducing image noise. One such technique is iterative reconstruction, which is also known by the trade names iDose (Philips), iterative recon­struction in image space (IRIS; Siemens), adap­tive iterative dose reduction (AIDR; Toshiba, Tochigi, Japan), and adaptive statistical iterative reconstructions (ASIR GE health care).43 For example, the selection of “ASIR 30%” results in a combination of 70% filtered back projection data and 30% adaptive statistical iterative reconstruction data. Ongoing development­ of iterative reconstruction techniques holds promise for achieving even lower levels of image noise, which will allow further reductions in radiation dose.

CONCLUSION When used under properly controlled conditions, radiation is a safe and indispensable tool for medical diagnosis. Proper radiation safety management should ensure that radiologists and clinicians are knowledgeable about typical patient doses that are important in each type of radiologic examination and about the factors that affect these doses. This should ensure a judicious requisition for a radiological examination as well as help keep doses as low as possible while still creating optimum diagnostic quality images.

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Section 2 Recent Advances and Applied Physics in Imaging 29. Shymko MJ. Minimizing occupational exposure. Radiologic Technology. 1998;70(1):89-90. 30. Wagner LK, Hayman LA. Pregnancy and women radiologists. Radiology. 1982;145:559-62. 31. Grover SB, Kumar J, Gupta A, et al. Protection against radiation hazards: regulatory bodies, safety norms, dose limits and protection devices. Indian J Radiol Imaging. 2002;12: 157-67. 32. National Council on Radiation Protection and Measurements. Medical X-ray, electron beam and gamma X-ray protection for energies up to 50 meV (equipment design, performance and use). Bethesda: NCRP publications (NCRP report no 102); 1989. 33. Sprawl P Jr. Physical Principles of Medical Imaging, 2nd Edn. Gaitherberg Md: Aspen; 1993.pp.165-7. 34. Graham DT, Cloke P. Principles of Radiological Physics, 4th Edn. Edinburg:Churchill Livingstone; 2003. pp. 325-38. 35. Bushong SC. Radiological Science for Technologists, Physics Biology and Protection, 6th Edn. St Louis year book; 1997. pp.442-7. 36. Steenvoorde P, Pauwels EKJ, Harding LK, et al. Diagnostic nuclear medicine and risk for the fetus. Eur J Nucl Med. 1998; 25:193-9. 37. McNitt Gray. Radiation dose in CT. Radiographics. 2002;22: 1541-53. 38. Jucius RA, Kambic GX. Radiation dosimetry in computed tomography. Appl Opt Instrum Eng Med. 1977;127:286-95.

39. Shope TB, Gange RM, Johnson GC. A method for describing the doses delivered by transmission. X-ray Computed Tomography Med Phys. 1991;8:488-95. 40. McCollough CM, Schueler BA. Calculation of effective dose. Med Phys. 2000;27:838-44. 41. Shrimpton PC, Edyvean S. CT scanner dosimetry. Br J Radiol. 1998;71:1-3. 42. American Association of Physicists in Medicine. The measure­ ment, reporting and management of radiation dose in CT. Report no 96, College park Md: American Association of Physicists in Medicine, 2008. 43. Tamm EP, Rong XJ, Coly D, et al. CT radiation dose reduction: how to implement change without sacrificing diagnostic quality. Radiographics. 2011;31:1823-32. 44. Lee CH, Goo JM, Lee HJ, et al. Radiation dose modulation technique in multidetector CT era: from basics to practice. Radiographics. 2008;28:1451-9. 45. Kanal KM, Stewart BK, Kolokythas O, et al. Impact of operator selected image noise index and reconstruction slice thickness on patient radiation dose in 64 MDCT. AJR. 2007;189(1):219-25. 46. Primak AN, McCollough CH, Bruesewitz MR, et al. Relationship between noise, dose and pitch in cardiac multidetector row CT. Radiographics. 2006;26(6):1785-94. 47. Yu L, Bruesewitz M, Thomas KB, et al. Optimal tube potential for radiation dose reduction in Pediatric CT: principles, clinical implementations and pitfalls. Radiographics. 2011;31: 835-48.

Planning a Modern Imaging Department

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SC Bansal, Niranjan Khandelwal, Ajay Gulati

INTRODUCTION During recent years, there has been increasing recognition that diagnostic imaging is an integral part of modern health care. Perhaps more than any other clinical service diagnostic imaging has been transformed by developments in information technology­fueled by digital information technologies over the last thirty years. This has enabled earlier, more accurate diagnosis and more appropriate interventions for almost all major health conditions. It is important to recognize that diagnostic imaging is not a technical service, but a clinical service that interprets information and requires the clinical expertise of imaging clinicians, who are increasingly making decisions about the management of patient care. There is increasing recognition of the need to place imaging early in care pathways to reduce the time to diagnosis and treatment and to improve efficiency and effectiveness.1 Most diagnostic imaging is carried out in clinical radiology departments, which deliver a range of services either within a hospital or as a stand-alone center. Apart from providing routine and specialized diagnostic services with various imaging techniques for indoor, outpatients and walk-in patients, the modern departments also provides therapeutic services like interventional radiology (minimally invasive treatments performed with imaging guidance). This acts as a big source of revenue generation for a hospital or a standalone center with high profitability.2

to do a critical project analysis. Doing a cost-benefit analysis and determining if the return on the investment will be positive are important for a project’s success. Good planning and communication with key staff members of the healthcare institution and the members of the design and construction team will help ensure successful implementation of any project. Analyzing the requirements for imaging equipment, space and personnel are other necessary steps. These are followed by scheduling and designing various aspects of the project.3 There are three horizontal levels of workflow (strategic, managerial and operational) in any organization, whether it is a government hospital or multinational corporate running a hospital. Planning must focus on the strategic level of decision making. The second level is the managerial or administrative level which focuses on daily issues such as employee attendance and productivity, patient backlogs, staff scheduling and reassignments­. The operational level is where the work actually gets done in any organization (Fig. 1).4 The major objectives of a radiology department include the following: zz To provide comprehensive high quality imaging service zz Establishment and confirmation of clinical diagnosis

PLANNING AND ORGANIZATION With rapid advancements in investigative technology, there is a continuous changing demand in the field of radiodiagnosis and imaging service resulting in an advanced and detailed systematic planning and organization for launching a modern imaging department. An understanding of what has changed – and what has not – is essential to developing safe, productive and comfortable imaging departments. Launching a new diagnostic and therapeutic imaging center involves very specific requirements and roadmaps that have a direct impact on planning. The essential first step is

Fig. 1:  Levels of radiological workflow

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zz

Providing high quality therapeutic/interventional radiology Commitment to training and research.

zz zz zz

Film processing and handling Image interpretation and reporting Filing.

Divisions of the Radiology Department

LAYOUT

Radiology department generally has diagnostic as well as therapeutic sections. The major components of radiology/imaging services are as follows: zz Radiography (X-ray machines/CR and DR System) zz Mammography zz Dual-energy X-ray absorptiometry (DEXA) zz Computed tomography (CT scan) zz Ultrasound and color Doppler zz Magnetic resonance imaging (MRI) zz Digital substraction angiography (DSA) zz Nuclear imaging systems. To manage such large number of sophisticated machines whose rays/emissions are hazardous to healthcare calls for a critical planning taking in to consideration the safety aspect of patient, public and the department staff.5

The layout of the department depends on the great extent the way the processes in the department are aligned and take place. Layout shall be prepared as per the AERB guidelines for layout and shielding of X-ray equipment. Planning should be done to create a safe, pleasant and efficient staff work environment. For a safe radiation environment, there are certain principles and considerations like “separation” of different functional areas helps control access: zz Public areas (waiting room, changing rooms, etc.) zz Staff areas (offices, reporting rooms, etc.) 2 zz Work areas (radiation rooms, console rooms, labs, etc.). Corridors and doors leading to all patient areas and examina­tion­rooms should allow easy and safe movement of all patients, including handicapped or injured. Availability of toilet facilities is essential, particularly those suitable for handicapped patients. Also, the provision of safe storage facilities for patients’ clothing and valuables during imaging is necessary.6

LOCATION The location of the department and the relative positions of the examination rooms have a considerable bearing upon the protection requirements. Aspects for planning are accessibility, convenience, privacy and traffic flow considerations, etc. i.e. that should be well connected. Accessibility towards OPD and emergency is a major point of consideration for this department. Central location on the ground floor with some space for future expansion is essential to allow upgradation and augmentation of services.2 The location should be 10 meters away from the elevators due to their effect on the functioning of equipment in the department.5 The correct design of medical imaging facilities will reduce radiation and nonradiation hazards and contribute to the care and wellbeing of patients and staff. It is the general responsibility of the medical imaging service to ensure the optimum design of their facility and to ensure that there is no radiation risk to anyone working or waiting in any room adjoining the radiation zone. Therefore, strategic planning must be done to have a clear understanding of the operations in the department (staff movement, patient flow, material flow, technical procedures). Special attention to minor details related to operations can have significant impact on staff effectiveness and morale. Study of traffic patterns is the key to the efficiency of an imaging department. This study should be based on interactive discussions with the staff of the department and should consider the various activities like:6 zz Movement of patients in and out of procedure rooms zz Activity sequence within procedure rooms

EQUIPMENT The equipment used in this department are highly sophisticated and expensive. Major equipment are described below:

Conventional Radiography The most important and easily performed imaging service in the front line of medical care is plain radiography. The X-ray unit must be able to perform all essential general radiographic examinations like chest, abdomen and extremities. Information is represented in the analog or continuous form rather than a discrete fashion. In conventional radiography, majority of the radiographic examinations have been carried out by projecting the beam through the patient allowing the transmitted beam to strike X-ray film or Intensifying screen to produce the latent image. Thelatent image can be made visible and permanent by processing the film with suitable chemicals (Fig. 2).

Darkroom When designing a darkroom, beside the operational considerations­concerning the film development, the primary concern is the shielding of unexposed film from exposure to radiation (X-rays and daylight). The common location for a main darkroom is central in the imaging department. All construction provisions must be made to ensure that all potential openings to the outside are light tight (doors,

Chapter 62 Planning a Modern Imaging Department

signal from X-ray quanta. MTF is a measure of image quality of an imaging system with respect to structural contrast and spatial resolution. Optimizing MTF and DQE simultaneously is a challenge: thicker detector material, for example, will improve absorption (thus, DQE), but generally also will induce more blur (deteriorate MTF). The following sections discuss recent developments for the three main digital detector technologies: storage phosphors (computed radiography; CR), flat-panel detectors (digital radiography;­DR) and CCD detectors.

Storage Phosphor Radiography (Computed Radiography)

1. Examination table; 2. Spot film device; 3. Column stand; 4. X-ray tube head; 5,6. Unit electronics; 7. Chest stand; 8. Control unit; 9. MPB with lead glass viewing window of 1.7 mm lead equivalence Fig. 2:  Model Layout—X-ray installation

ventilation, pass through, windows). Dry and wet areas should be separate from each other and chemicals must be stored safely.6

Digital Radiography Digital radiography is a form of X-ray imaging where digital X-ray sensors are used instead of radiography film. Digital radiography systems are replacing films in the modern departments. It is a representation of continuous analog information into digital form by the use of computer which processes the digital data to form an image. It not only has revolutionized communication between radiologists and clinicians, but also has improved image quality and allowed for further reduction of patient exposure. However, digital radiography also poses risks, such as unnoticed increase in patient dose and suboptimum image processing that may lead to suppression of diagnostic information. Advanced processing techniques, such as temporal subtraction, dual energy subtraction and computer-aided detection (CAD) will play an increasing role in the future and are all targeted to decrease the influence of distracting anatomic background structures and to ease the detection of focal and subtle lesions.7 The two most important objective performance measures to describe digital radiography systems with respect to dose requirements and detail resolution are the modulation transfer function (MTF) and the detector quantum efficiency (DQE).8 DQE describes the efficiency of a detector to generate

Computed radiography (CR) systems use storage-phosphor image plates having a detective layer of photostimulable crystals and separate image readout process. 9 A major advantage of CR systems is that they are cost effective way to getting digital images since they allow reutilization of existing X-ray equipment. CR cassettes utilize storage phosphors where electrons are trapped during exposure and subsequently extracted through a laser scanner.10 Standard CR systems use a single laser beam and a detector screen covered with an amorphous (powder-based) detector material.

Dual-reading CR systems Dual-reading CR systems are based on transparent detector material and employ light collection optics in the front and the back side of the detector. It improves quantum detection (DQE) and has only a minimum deteriorating effect on spatial resolution (MTF).11

Parallel Reading (Line Scanning) Traditional CR scanners use principle of flying spot scanning for readout where a tightly focused laser beam stimulates the latent image in a moving storage phosphor plate one point at a time over the entire screen surface. Parallel reading employs a linear array of laser diodes (linear-line laser diode) that reads out all pixels in one line simultaneously, therefore speeding up the process tremendously. The dual side the reading and line scanning reading with columnar phosphors provide remarkable improvement compared to conventional CR systems and yield results comparable to most digital detectors for radiography.10

Needle-crystalline CR Detectors A new crystalline detector material (CsBr:Eu2+) for storage phosphor systems allows for creating a thicker detector layer (better DQE) without deteriorating spatial resolution (MTF). The principle is similar to that of indirect flat panel systems (CsI-photodiode/TFT detectors).

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Flat-panel Direct Detector Systems

CCD Detector Technology

Two different DR technologies are available, both of which are based on TFT matrix arrays. Indirect conversion systems or opto-direct systems use a scintillator (e.g. cesium iodide, CsI or gadolinium oxysulphide, GOS or Gadox) layered on top of an array with light-sensitive photodiodes with thinfilm transistors (TFTs). The scintillator converts radiation into light that is detected by the photodiode/TFT array. CsI-photodiode/TFT systems are widely used for chest radiography and provide better DQE than standard CR or Gadox-TFT systems (Figs 3 and 4).12,13 Direct conversion systems or electro-direct systems use a photo conducting layer (amorphous selenium, a-Se), in which the absorbed X-ray energy is directly converted into charge on top of a TFT array. These systems are excellent for the high spatial frequencies required for mammography, but because they absorb less X-ray energy, they suffer from a lower-dose efficiency (DQE), which makes them less suited for chest radiography.12,14

The light emitted by a scintillator screen has to be collimated to the CCD by optical coupling (demagnification), which can reduce dose efficiency and degrade image quality.15 Recent improvements in coupling mechanism and use of larger CCD sensors have made these systems more attractive for chest radiography.16

Slot-scanning CCD Technology No demagnification is required for slot-scanning CCD technology:­a CsI scintillator is coupled to a linear array of CCDs that covers the whole slot that is used to scan the chest. The increased signal to noise yielded by scatter reduction effectively compensates for the 2.5 times lower intrinsic DQE of CCD technology.17 The increased SNR can be used to improve image quality or to reduce patient dose. The most advanced processing algorithms aim at analyzing images (CAD), selectively enhancing bones and soft tissues (dual-energy subtraction), and at visualizing change at follow-up (temporal subtraction).

Computer-aided Diagnosis Computer-aided diagnosis (CAD) programs have the goal to aid the radiologist in detecting or differentiating various disease entities in the chest. Usually the system suggests a lesion or abnormal region that then has to be verified by the radiologist.

Dual-energy Subtraction

Fig. 3:  Dual-reading flat panel X-ray unit

Dual-energy subtraction radiography involves taking a chest exposure at two different X-ray energies. By exploiting the difference in energy dependence of attenuation between bone and soft tissue, either bone or soft tissues can be eliminated by locally weighted subtraction of the two images. Dual-energy subtraction allows for differentiation of calcified and noncalcified lesions, improved detection of nodules and masses, especially in critical areas, and improved detection of rib lesions.18,19

Temporal Subtraction Temporal subtraction is a processing technique based on the matching and subsequent subtraction of a follow-up radiograph and a baseline image.

Digital Tomosynthesis

Fig. 4:  Dual-reading and fluoroscopy unit (flat panel)

Digital tomosynthesis is a medical imaging technique using a flat panel detector and tube rotation producing a series of slices at different depths. These projection images are

Chapter 62 Planning a Modern Imaging Department

subsequently shifted and added to bring objects in a given plane into focus, while other structures are spread across the image and are rendered with varying amounts of blur.20 Most developments in tomosynthesis have been in breast imaging, but orthopedic, chest and urinary applications have also been used.21 X-ray equipment fall broadly into two groups portable/mobile and fixed. Portable radiography equipment means the X-ray unit is capable of being taken to the destination to be used. It is very simple to use and can be packed into carrying cases and so transported. Portable sets relatively have low mA setting, can be dismantled for transfer. The word “mobile” means that X-ray equipment is capable of being moved. It is mounted on the wheels and can be pushed by human power. It is larger and heavier than portable sets and need to be motorized or pushed between locations. It cannot be separated into smaller components and cannot be taken outside the hospital. Mobile sets have high MA value. The digital mobile units are the ultimate solution to mobile X-ray imaging for digitalization in emergency rooms (ER), traumatology, intensive care units (ICU), in patient wards and pediatrics. These systems represents an evolutionary move in mobile diagnostic imaging equipment and include unique features in terms of operability, mobility and image quality.22,23 Wireless FPDs: Wireless portable DR system is now a reality. After exposure, it wirelessly transfer image data to the DR system. Alternatively the image data can be transferred to DR console via an Ethernet cable. It has no cables and does not interfere with surrounding machines, so it is easy to handle as a CR cassettes.24 Typically a 17” × 14” image size is made available within 3 seconds (Fig. 5).

Fig. 5:  Mobile digital radiography unit

Mobile Image Intensifiers Units Mobile unit for fluoroscopy with an image intensifier is generally used in operating theater. This reduces the number of radiographs taken and saves the time during surgery.

MAMMOGRAPHY Mammography is a specific type of imaging using high precision X-ray machine which gives a reliable radiographic examination of the breast. The low dose X-ray study using mammography machine can aid in the early detection and diagnosis of breast diseases in women.5 The use of mammography in breast cancer screening and treatment has represented a critical advance in the management of this disease. Current guidelines in India and by the American College of Radiology (ACR) recommended annual screening in women above the age of 40 years. Screen film mammography SFM was traditionally considered the gold standard in mammography until recently, however full field digital mammography (FFDM) is now increasingly being recognized as an attractive alternative to SFM (Fig. 6). The recent advances in mammography include digital mammography, computer-aided detection, breast tomosynthesis and performing stereotactic biopsy from indeterminate lesions. Digital mammography, also called full-field digital mammography­(FFDM), is a mammography system in which the X-ray film is replaced by solid-state detectors that convert X-rays into electrical signals. The electrical signals are used to produce images of the breast that can be seen on a computer screen or printed on special film similar to conventional mammograms.25 FFDM has improved contrast resolution and greater ability to image dense breast tissue thereby increasing the diagnostic accuracy. Computer-aided detection (CAD) systems use a digitized mammographic image and computer software then searches for abnormal areas of density, mass, or calcification that may indicate the presence of cancer. The CAD system highlights these areas on the images, alerting the radiologist to the need for further analysis and therefore improve the diagnostic capabilities. Breast tomosynthesis, also called three-dimensional (3D) breast imaging, is a mammography system where the X-ray tube and imaging plate move in an arc during the exposure. It creates a series of thin slices through the breast that allow for improved detection of cancer and reduces the recall rates for additional imaging.26 Dual energy substraction mammography and contrastenhanced digital mammography are also newer advanced techniques which help in improved lesion detection in difficult and indeterminate lesions.

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1. BMD equipment; 2. Examination table; 3. Evaluation unit Fig. 7:  Model layout—BMD installation 1. Mammography equipment, 2. Control unit with protective barrier of 1.5 mm lead equivalence Fig. 6:  Model layout—mammography installation

Dual-energy X-ray Absorptiometry Dual-energy X-ray absorptiometry (DEXA) is an imaging technology that uses a very low amount of X-ray energy to measure bone mineral density (BMD). The technique relies on transmission measurements made at two photon energies to allow calcium and thereby bone mineral, be assessed. When soft-tissue absorption is subtracted out, the BMD can be determined from the absorption of each beam by bone. The first-generation of modern DEXA scanners used a pencil X-ray beam; later designs employ fan beams, cone beams and c-arm technology and thereby, allow more rapid and convenient scanning (Fig. 7).27,28 Dual-energy X-ray absorptiometry is the most widely used and most thoroughly studied bone-density measurement technology. The DEXA scan is the most accurate and reliable way to diagnose and follow osteoporosis and predicts the future risk of fracture. It contrasts to the nuclear bone scan, which is sensitive to certain metabolic diseases of bones in which bones are attempting to heal from infections, fractures, or tumors. DEXA scans can also be used to measure total body composition and fat content with a high degree of accuracy comparable to hydrostatic weighing with a few important caveats.29 However, it has been suggested that, while very accurately measuring minerals and lean soft tissue (LST), DEXA may provide skewed results as a result of its method of indirectly calculating fat mass by subtracting it from the LST and/or body cell mass (BCM) that DEXA actually measures. Sites central—lumbar spine, hip, whole body Peripheral—forearm, calcaneous.

Whole body DEXA includes assessment of total Body Bone Mineral Content (calibrated against hydroxyapatite and consisting­of about 80% cortical bone), total body lean mass (calibrated against saline and consisting of lean soft tissue), total body fat mass (calibrated against stearic acid and consisting of fatty soft tissue).30

COMPUTED TOMOGRAPHY CT scan is a medical imaging modality which has become one of the most powerful tool for various diagnostic and therapeutic purposes in virtually all medical disciplines. The modern day CT systems generate volume of data that can be acquired by various techniques and protocols based on the clinical concern. CT is the workhorse imaging tool for the evaluation of chest, abdomen and pelvis. In a time sensitive situation particularly trauma, CT is generally the initial approach. Innovations in image acquisition and reconstruction technologies have greatly expanded the range of CT applica­ tions available in the routine clinical setting. The modern day CT scanner (64 and 128 slice) can acquire sub-millimeter resolution­images of entire body regions in a few seconds, allowing depiction of fine anatomical detail uncompromised by motion artifact (Figs 8A and B). With sophisticated visualization software, image data can be processed into multi-planar, volume-rendered, cine and other formats to better display anatomical abnormalities and facilitate newer applications such as dynamic CT, CT angiography, enterography, urography, tracheobronchography and cardiac CT. Newer applications including dual-energy material decomposition CT are furthering the transition of CT from a purely morphological to a combined anatomical, functional and metabolic imaging technique.31 CT angiography (CTA) enables the display of entire vascular system aided by injections of contrast medium.

Chapter 62 Planning a Modern Imaging Department

A

B

Figs 8A and B:  128 slice dual source CT scanner

Several imaging post processing techniques are available enabling good display of the entire vascular system. The most widely used techniques are multiplanar reformation (MPR), thin-slab maximum intensity projection (MIP), shaded surface display (SSD) and volume rendering technique (VRT). Sophisticated segmentation algorithms, bone removal with thresh holding or subtraction algorithms and vessel analysis tools are also newer techniques which provide quality of vessel analysis comparable to DSA (conventional angiography). The clinical applications for these various image postprocessing methods include steno occlusive disease, aneurysms, vascular malformations.32 Virtual endoscopy (VE) is a recent development in postprocessing technique which is used to generate virtual endoscopic views. This technique is used to obtain a perspective view of the display region mainly for anatomical cavities. These include, for example, the bronchial tree, large vessels, the colon and paranasal sinuses. VE is also used for areas not directly accessible for conventional endoscopy. The perspective volume rendering technique allows real-time fly through at high resolution mimicking the true endoscopy. Installation of X-ray and CT scanner unit requires approval of AERB and need to conform to radiation protections measures (Fig. 9). However, CT examination involves radiation exposure with potential risks and should be performed judiciously particularly in children who are more radio sensitive than adults.

ULTRASOUND It is a noninvasive diagnostic medical modality that uses high frequency sound waves to visualize the internal structures of the body in real time. It has the important advantages of being widely available, low cost and does not use ionizing radiation. This modality has become one of the most preferred imaging for diagnostic, interventional, monitoring and follow-up of

1. CT gantry; 2. Examination table; 3. Control unit; 4. Electronics; 5. Viewing glass 100 cm × 80 cm of 2.0 mm lead equivalence Fig. 9:  Model layout CT-scan installation

patients. It has a vital role in obstetrical imaging and is used both for assessing the fetal development and early diagnosis of many fetal anomalies. Ultrasound is also useful for various guided interventions and can be performed on bed side in the triage of trauma patients. The quality of examination is however highly depen­ dent on the experience of the sonographer in addition to the patient body habitus. The advanced ultrasound system includes capable of harmonic imaging, color and power Doppler and 3D and 4D reconstructions (Fig. 10). Technical advances like elastography and computer aided diagnosis have expanded the clinical applications especially in breast sonography.33 Recently, therapeutic applications with high intensity focused ultrasound (HIFU) and micro-bubble assisted delivery of drugs and genes has shown great promise.34

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Fig. 10:  Advanced ultrasound system

Magnetic Resonance Imaging Magnetic resonance imaging (MRI) is a medical imaging technique used in radiology which makes use of the property of nuclear magnetic resonance (NMR) to image nuclei of atoms inside the body. Unlike CT scans or traditional X-rays, MRI does not use ionizing radiation. MRI uses strong magnetic field to align atomic nuclei (usually hydrogen protons or any other nuclei with odd number of protons) within body tissues and various radio frequency pulses are put on and off repeatedly. The signal from human tissues are received by coils placed near the area of interest and fed to computer, which converts these signals into an image. MRI provides excellent contrast between the different soft tissues of the body and can be used to image any part of the body. It is especially useful in musculoskeletal radiology and neuroradiology. It can detect or sometimes help in characterizing vital ‘lesions’ that might be missed or indeterminate on other imaging modalities.35 The MRI provides excellent white and gray matter differentiation of nervous tissues. An advantage of MRI is its ability to produce images in axial, coronal, sagittal and multiple oblique planes with equal ease. MRI scans give the best soft-tissue contrast of all the imaging modalities. The advanced MR imaging techniques like perfusion imaging, diffusion-weighted imaging, and MR spectroscopy can improve the accuracy in diagnosis especially in the field of neuroimaging. With advances in scanning speed and spatial resolution and improvements in computer 3D algorithms and hardware, MRI has become an indispensable medical imaging technique in the current medical practice. One disadvantage is the patient has to hold still for long periods of time in a noisy, cramped space while the imaging is performed. Claustrophobia severe enough to terminate the MRI exam is reported in up to 5% of patients.

Fig. 11:  3 tesla MRI system with coils

Recent improvements in magnet design, including stronger magnetic fields (3 tesla), shortening exam times, wider, shorter magnet bores and more open magnet designs, have brought some relief for claustrophobic patients (Fig. 11). The modality is however contraindicated for patients with pacemakers, cochlear implants, some indwelling medication pumps, certain types of cerebral aneurysm clips and metallic prosthesis.36

Digital Subtraction Angiography Digital subtraction angiography (DSA) is a type of fluoroscopy technique used in interventional radiology to clearly visualize blood vessels in a bony or dense soft tissue environment. Images are produced using contrast medium by subtracting a ‘precontrast­image’ or the mask from later images, once the contrast medium has been injected. Most cerebral angiography can be done with 3–5 frames per second (fps). Higher rates (e.g. 8–20 fps) are useful for imaging arteriovenous malformations and other high-flow lesions.37 Not only anatomy but also function of blood flow can be studied using DSA, as X-ray images can be produced at a frame rate of up to 50 frames per second.38 DSA is very successful in displaying the vascular system of the entire body and can be used both for diagnostic and therapeutic purposes. While offering excellent spatial and temporal resolution as well as good contrast, single plane DSA suffers from its incapability of representing and displaying three-dimensional relationships. Such information can be introduced, if biplane angiography is applied (Figs 12 and 13). In biplane angiography, two X-ray devices generate images, which rotate around a common centre (called isocenter). Planning and executing neuroradiological intervention is guided by biplane angiography because it provides fast

Chapter 62 Planning a Modern Imaging Department

1. C-arm; 2. Examination table; 3. Monitor trolly; 4. Over head rails; 5. Fixed radiation shield; 6. Control unit; 7. Electronics; 8. Additional electronics; 9. Lead glass viewing window 120 cm × 100 cm with 2.0 mm lead equivalence Fig. 12:  Model layout—interventional radiology installation

information on the vascular system with high quality with 3D reconstructions. There has also been considerable progress in the development of catheters and embolization material. Using special microcatheters, the interventional neuroradiologist is able to reach almost every point in the brain by endovascular approach. Three-dimensional (3D) reconstruction of the dataset acquired during rotational DSA represents the latest development in the neurovascular imaging armamentarium. This technique combines the anatomic resolution of DSA with the 3D visualization abilities previously offered only by CT or MR angiography, and hence provides more detailed information than does DSA alone. The adequate evaluation of 3D-DSA requires post processing by 3D reconstruction algorithms at an external workstation. 3D DSA has taken a prominent role in treatment planning by enabling exquisite detailed anatomic information of complex vascular lesions and also helps in choosing the most appropriate working projection for subsequent endovascular therapy. It provides

Fig. 13:  Biplane DSA laboratory

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precise vascular information in sophisticated tasks such as aneurysm volume measurement. Three-dimensional DSA is therefore essential for optimal diagnosis and endovascular management of cerebral aneurysms/arteriovenous malformations and can reduce the number of exposures.39 Digital flat-panel detector cone-beam computed tomography (CBCT) has recently been adapted for use with C-arm systems. This configuration provides projection radiography, fluoroscopy, digital subtraction angiography, and volumetric computed tomography (CT) capabilities in a single patient setup, within the interventional suite. Such capabilities allow the intervention list to perform intra procedural volumetric imaging without the need for patient transportation.40

Nuclear Imaging Systems Nuclear medicine imaging noninvasively provides functional information at the molecular and cellular level by measuring the uptake and turnover of target-specific radiotracers in tissue. These functional processes include tissue blood flow and metabolism and by providing information on these processes, nuclear medicine imaging offers a broad array of tools for probing normal and disease-related states of tissue. The principal imaging device is the gamma camera which detects the radiation emitted by the tracer in the body and displays it as an image. With computer processing, the information can be displayed as axial, coronal and sagittal images (SPECT images, single-photon emission computed tomography). SPECT has enabled the evaluation of disease processes based on functional and metabolic information. Positron emission tomography (PET) is also a nuclear medical imaging technique that produces a three-dimensional image or picture of functional processes in the body. The system detects pairs of gamma rays emitted indirectly by a positronemitting radionuclide (tracer), which is introduced into the body on a biologically active molecule. If the biologically active molecule chosen for PET is FDG (fluorodeoxy glucose), the concentrations of tracer imaged then give tissue metabolic activity, in terms of regional glucose uptake. Use of this tracer to explore the possibility of cancer metastasis (i.e. spreading to other sites) is the most common type of PET scan in standard medical care (90% of current scans). However, on a minority basis, many other radiotracers are used in PET to image the tissue concentration of many other types of molecules of interest. The addition of anatomic imaging provided by Integration of computed tomography (CT) to functional imaging of positron emission tomography (PET) and single photon emission computed­ tomography (SPECT) has further expanded the utility and accuracy of nuclear medicine imaging. By using combined-modality PET/CT and SPECT/ CT hybrid imaging, functional processes can be localized at anatomic sites or, in some instances, as yet unidentifiable

structural alteration. These modalities have enhanced the accuracy of detection, determination of the extent and severity, and improved the ability to monitor patient’s response to therapy in oncology patients.41

PICTURE ARCHIVING AND COMMUNICATION SYSTEMS The development of electronic (filmless) department depends on the technological advances pertain to imaging and those arising from generally available computer technology. Picture archiving and communication systems (PACS) are computer systems dedicated to the storage, retrieval, distribution­and communication of medical images from multiple modalities. Electronic images and reports are transmitted digitally via PACS; this eliminates the need to manually file, retrieve, or transport film jackets. The universal format for PACS image storage and transfer is digital imaging and communications in medicine (DICOM). Development of PACS has replaced the conventional analogue film, paper clinical request forms and reports with a format that has completely computerized electronic display. PACS offers several advantages to radiologists and radiology departments as they work to trim costs, improve patient care, increase throughput and efficiency and have a major added value is efficiency of data management. Access to electronic images helps foster collaboration and support seamless care for patients across the primary and secondary care sectors. A modern PACS has (or should have) excellent capabilities for displaying new examinations in a user-friendly manner, perfecting and displaying pertinent prior examinations for comparison and providing access to prior reports. One would consider these features to represent baseline or core functionality for any modern PACS.42 The PACS architecture comprises of: Centralized PACS-(hub and spoke, star topology)—single short-term storage unit to which every modality and every workstation is connected on a point to point basis. Distributed PACS-composed of number of linked clusters, each with its own short-term storage unit and one or more image acquisition modalities and several diagnostic/review workstations. Short-term storage is provided by one or more random array of inexpensive disks (RAIDs). RAID is composed of magnetic hard disks which is linked to a server which is connected directly to the PACS workstations. Connection can be made at various bandwidths, the highest generally being gigabit ethernet (Figs 14A and B). The major benefits of PACS result from digitization of data which allows easy comparison, simultaneous multilocation viewing, faster image retrieval, automatic chronological ordering and rapid database search. Some of the disadvantages include the inherent costs and technological complexity which requires adequate trained

Chapter 62 Planning a Modern Imaging Department

A

It stores information specific to the radiology department including radiological reports .Modern RIS will incorporate some DICOM features such as modality work list, modality performed procedure­step, interpretation work list, and structured reporting. Health level 7 is an internationally accepted standard for HIS and RIS systems. HIS-RIS-PACS integration should preferably be bidirectional. Input of demographic data is only once thereby minimizing human error. Any update to a patients demographic data or any scheduling is propagated to all systems HIS, RIS, or PACS automatically, hence providing advanced notice of events and allowing them to prepare.45

SAFETY STANDARDS AND QUALITY ASSURANCE Safety standards and guidelines are an important aspect in early planning stages of a project. It is essential from the radiological safety view point, to exercise strict regulatory control over the safe use of ionizing radiation used in various diagnostic equipment. Statutory requirements for the safe operation of medical diagnostic­equipment by hospitals, clinics and other medical institutions­in India are given by atomic energy regulatory board, government of India. Adopted safety guidelines should be referenced in planning standards or regulations. For ionizing radiation, shielding characteristics are based on the National Council B on Radiation Protection and Measurements (NCRP) Report 147: Structural shielding design for medical X-ray imaging Figs 14A and B:  PACS architecture (A) with workstation (B) with facilities. The information has been updated, including networking guidelines on new modalities. Further, radiation protection devices (Fig. 15A) like lead flaps, radiation shield, thyroid shield, lead apron, lead goggles hospital staff. A dedicated maintenance programme and a and lead gloves, etc. should have appropriate lead equivalent carefully devised plan to provide essential clinical services in as per AERB guidelines. Further radiation warning signs require in case of PACS failure.43,44 (Fig. 15B) should be prominently displayed in front of the There should be tight integration of the digital dictation doors of all the radiation rooms in the radiology department. stations to the PACS workstations. This eliminates keying Although the clinical use of X-rays is governed by errors on the part of the radiologists when logging in to read optimization,­justification and the as-low-as-reasonablya particular case. achievable (ALARA) principle, these are to supplemented by sound quality control (QC) practices. Imaging professionals Digital reporting rooms: Incorporating image interpreta­ should develop clearly defined guidelines that promote tion, PACS and radiology information systems are carefully quality assurance in accordance with the latest technical designed for physical space demands, lighting and ergo-­ knowledge of the equipment concerned. This professional nomics. Lighting must be placed to avoid glare on the monitor. approach will promote the due process of developing technical Individual work spaces must be designed to allow privacy and specifications, standards, and quality management.46 collaboration at the same time. Digital images are created and processed with different Hospital information system (HIS) stores demographic parameters that must be continually assessed, different data of all the patients, e.g. patient name, identification artifacts are possible from the digital processes, and complex number, date of birth and also records admission and computer systems can fail in subtle ways. Acceptance testing, discharge dates, outpatient appointments, clinicians regular calibration and proactive and consistent QC can responsible for patient care and so forth. prevent systematic errors that occur in digital acquisition Radiology information system (RIS) can be a stand- or processing equipment and can contribute to overall alone computer platform, or may be a module of the HIS. department quality.47

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Fig. 15A:  Radiation protection devices

Fig. 15B:  Radiation warning signs

TELERADIOLOGY Teleradiology is the transmission of radiographic images from one location to another for interpretation by a radiologist. It is most often used to allow rapid interpretation of emergency room, ICU and other emergent examinations after hours of usual operation, at night and on weekends. The major advantage of teleradiology is the ability to utilize different time zones to provide real-time emergency radiology services

around-the-clock. The disadvantages include higher costs, limited contact between the ordering physician and the radiologist, and the inability to cover for procedures requiring an onsite radiologist. Successful planning of a modern imaging department depends on many things, and one of the most important factors relates to the amount of time and the quality of effort spent on strategic planning at the outset. Neglecting or skimping at this stage may lead to unforeseen problems that could ultimately derail the project. Fortunately, there are lessons that can be learned and applied from other healthcare organizations and even from the corporate world. Effectively utilizing planning as described in this article may help to steer a team in the right direction and ensure that underlying issues and the concerns of all facilities have been adequately addressed. Putting a high priority on strategic planning will relieve many of the headaches that can occur before, during and after the planning of a modern imaging department.

REFERENCES 1. Edwina H. The Future Delivery of Diagnostic Imaging Services in Wales. 2009.

Chapter 62 Planning a Modern Imaging Department 2. Aggarwal R. Planning an Imaging Department—Express Healthcare. (http://www.expresshealthcare.in). 3. Woodford DA. Project planning in the diagnostic imaging department. Radiol Manage. 1997;19(3):35-9. 4. Evan Leepson. Strategic Planning for Radiology: Opening an Out-patient Diagnostic Imaging Center. Radiology management. 2003. 5. Singh H, Gayatri S. Radiology and Imaging Department. (http:// www.drharisingh.com) 6. Salem D. Standard Specifications for Basic Diagnostic Radiology Departments. 2011. (moh-gr.org/pdf/Standard%20 Specifications.pdf) 7. Cornelia schaefor- Prokop, Uirich Neitzal, Henk W. Venema, et al. Pigtail chest radiography: on and control of image quality update on modern technology dose containments. Eur Radio. 2008;18:1818-30. 8. Samei E. Performance of digital radiographic detectors: Quantification and assessment methods. Advances in digital radiography: RSNA: Categorical course in diagnostic Radiology Physics. 2003.pp.37-47. 9. Korner M, Weber CH, Wirth S, Pfeifer K, Reiser MF, Treitl M. Advances in digital radiography: physical principles and system overview. Radio Graphics. 2007;27:675-86. 10. Rivetti S, Lanconelli N, Bertolini M, Nitrosi A, Burani A, Acchiappati D. Comparison of different computed radiography systems: physical characterization and contrast detail analysis. Med Phys. 2010;37(2):440. 11. Arakawa S, Itoh W, Kohda K, et al. Novel computed radiography system with improved image quality by detection of emissions from both sides of an imaging plate. SPIE Medical Imaging, poster presentation. 1999. 12. Samei E, Flynn MJ. An experimental comparison of detector performance for direct and indirect digital radiography systems. Med Phys. 2003;30(4):608-22. 13. Metz S, Damoser P, Hollweck R, et al. Chest radiography with a digital flat-panel detector: experimental receiver operating characteristic analysis. Radiology. 2005;234(3): 776-84. 14. Bacher K, Smeets P, Vereecken L, et al. Image quality and radiation dose in digital chest imaging: Comparison of an amorphous silicon and an amorphous selenium flat-panel system. AJR. 2006;187(3):630-7. 15. Bath M, Sund P, Mansson LG. Evaluation of the imaging properties of two generations of a CCD based system for digital chest radiography. Med Phys. 2002;29:2286-97. 16. Lawinski C, Mackenzie A, Cole H, et al. Digital detectors for general radiography: A comparative technical report. National Health Service report 05078. 2005. K-CARE website.http/www. kcare.co.uk/publkications/abstracts/ report05078.htm 17. Samei E, Saunders RS, Lo JY, et al. Fundamental imaging characteristics of a slot scan digital chest radiographic system. Med Phys. 2004;31(9):2687-98. 18. MacMahon H. Improvement in detection of pulmonary nodu­ les: digital image processing and computer-aided diagnosis. Radiographics. 2000;20(4):1169-77.

19. Gilkeson RC, Sachs PB. Dual energy subtraction digital radio­ graphy: technical considerations, clinical applications, and imaging pitfalls (review). J Thorac Imag. 2006;21(4):303-13. 20. Dobbins JT, Godfrey DJ, McAdams HP. Chest tomosynthesis. Syllabus RSNA, Advances in digital radiography: RSNA categori­ cal course in diagnostic radiology physics. 2003.pp.211-7. 21. Brice J. Will new DR technologies offer alternative to CT? Part 2. http://www.auntminnie.com/index.aspx?Sec=sup&Sub=xr a&Pag=dis&ItemId=90041. Updated March 25, 2010. Accessed October 28, 2010. 22. Heber MacMahon, Nicholas J. Yasillo, Michael Carlin Laser Alignment System for High Quality Portable Radiography Radio Graphics. 1992;12:111-20. 23. www.e-radiography.com 24. Lehnert T, Naguib NN, Ackermann H, Schomerus C, Jacobi V, Balzer JO, Vogl TJ. Novel, portable, cassette-sized, and wireless flat-panel digital radiography system: initial workflow results versus computed radiography. Am J Roentgenol. 2011; 196(6):1368-71. 25. http://www.radiologyinfo.org/en/info.cfm?pg=mammo 26. Katherine A. Leslie. Digital Mammography: Planning, Implementation, and Integration (Available at http://www. eradimaging.com) 27. Larkin A, et al. Commissioning and Quality Assurance of Dual Energy X-ray Absorptiometry (DEXA) systems, Rad. Prot. Dosim. 2008 (in press). 28. Sheahan NF, Dowling A, O’reilly G, Malone JF. Commissioning and quality assurance protocol for dual energy X-ray absorptiometry systems, Rad Prot Dosim. 2005;117:288-90. 29. Lohman TG, Harris M, Teixeira PJ, Weiss L. Assessing body composition and changes in body composition. Another look at dual-energy X-ray absorptiometry. Ann N Y Acad Sci. 2000; 904:45-54. 30. Lorente Ramos, RM, Azpeitia Armán J, Arévalo Galeano N, Muñoz Hernández A, García Gómez JM, Gredilla Molinero J. Dual energy X-ray absorptimetry: Fundamentals, methodology, and clinical applications. Radiologia. 2012;54:410-23. 31. Guillerman RP. Newer CT applications and their alternatives: what is appropriate in children? Pediatr Radiol. 2011;41(Suppl 2):534-48. 32. Lell MM, et al. New Techniques in CT Angiography. Radio Graphics. 2006;26:S45-S62. 33. Weinstein SP, Conant EF, Sehgal C. Technical advances in breast ultrasound imaging. Semin Ultrasound CT MR. 2006;27(4):273-83. 34. Harvey CJ, Pilcher JM, Eckersley RJ, Blomley MJ, Cosgrove DO. Advances in ultrasound. Clin Radiol. 2002;57(3):157-77. 35. Elsayes KM, et al. MRI characterization of 124 CT-indeterminate focal hepatic lesions: evaluation of clinical utility. HPB (Oxford). 2007;9(3):208-15. 36. http://www.frankshospitalworkshop.com/equipment/docu­ ments/X-ray/wikipedia/Radiology.pdf 37. Biplanar DSA Diagnosti cc Cerebra ll Angiography - Springer (www. springer. com/cda/content/document/cda) loaddocu­ ment/9781588297556-c1.pd

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Section 2 Recent Advances and Applied Physics in Imaging 38. Toennies KD, Oishi S, Koster D, Schroth G. Accuracy of distance measurements in biplane angiography. Proceedings of Medical Imaging; Image Display: 1997;3031:19-30; SPIE San Diego: Yongmin K, editor. 39. JV Byrne, C Colominas, J Hipwell, et al. Assessment of a technique for 2D–3D registration of cerebral intra-arterial angiography. The British Journal of Radiology. 2004; 77:123-8. 40. Orth RC, Wallace MJ, Michael D, Kuo MD. C-arm Conebeam CT: General principles and technical considerations for use in interventional radiology. Vasc Interv Radiol. 2008; 19:814-21. 41. Nuclear Medicine Imaging in Diagnosis and Treatment. National Research Council (US) and Institute of Medicine (US) Committee on State of the Science of Nuclear Medicine. Advan­ cing Nuclear Medicine through Innovation. Washington (DC): National Academies Press (US). 2007. 42. Ralston, Coleman RM, Beaulieu DM, Scrutchfield K, Perkins T. Progress toward paperless radiology in the digital environment:

planning, implementation, and benefits. J Digit Imaging. 2004; 17(2):134-43. Epu2004 Apr 19. 43. Samei E, Seibert JA, Andriole K, Badano A, Crawford J, Reiner B, et al. AAPM/RSNA Tutorial on Equipment Selection: PACS Equipment Overview General Guidelines for Purchasing and Acceptance Testing of PACS Equipment. Radio Graphics. 2004; 24:313-34. 44. Bryan S, Weatherburn GC, Watkins JR, Buxton MJ. The benefits of hospital-wide picture archiving and communication systems: a survey of clinical users of radiology services. Br J Radiol. 1999;72(857):469-78. 45. Dundas DD. Installation of a PACS system. The British Journal of Radiology. 2005;78:480-2. 46. Korir GK, Wambani JS, Korir IK. Establishing a quality assurance baseline for radiological protection of patients undergoing diagnostic radiology. SA Journal of Radiology. 2011. 47. Herrmann TL, et al. Best Practices in Digital Radiography. White paper Published by the American Society of Radiologic Technologists.

64

Common Drugs Used in an Imaging Department

CHAPTER

Anupam Lal, Vivek Gupta, Manphool Singhal

INTRODUCTION The beneficial or toxic effects of many plant and animal materials were known to us since the prehistoric times. Advances in chemistry and the further development of physiology in present time laid the foundation needed for understanding how drugs work at the organ and tissue levels. The last few decades have seen an exponential growth of information and understanding of the molecular basis for drug action. Better understanding of drug receptors and pharmacokinetics have led to modifying existing drugs for selective action or synthesizing newer drugs previously unknown to mankind. The recent era has also witnessed a dramatic growth in the field of electronics and computerization, leading to development of faster and more precise medical imaging equipment that have made possible the minimally invasive image-guided interventional procedures. The interventional procedures continue to evolve and the list is ever increasing, that includes central venous catheter placements, tumor treatments (uterine fibroid therapy, radio- and chemoembolization of tumor, percutaneous radiofrequency and cryoablation), and procedures, such as angioplasty, abdominal aortic aneurysm stent-graft repair, vertebroplasty, kyphoplasty, and varicose vein therapies. There have also been advancements in standard biliary and urinary drainage procedures, percutaneous gastrointestinal feeding tube placement, and transjugular intrahepatic portosystemic shunts. These complicated procedures mandates use of drugs required for patient preparation, therapeutic applications and for preventing complications of the radiological interventions. The radiologists are no longer supervising only contrast administration and managing contrast reactions but also providing therapies for many diseases. The present imaging departments thus are equipped with modern anesthetic and life support machines and a large number of drugs that will be required in various interventional procedures. A thorough knowledge and understanding of these drugs is of paramount importance to the interventional radiologist for their judicious use and for preventing untoward reactions. A brief description of common drugs used in modern

radiology department follows. The readers are encouraged to refer to standard textbooks of pharmacology for dosing and drug interactions in specific clinical scenario. Medications commonly used in radiology department can be divided into the following broad categories: zz Drugs used for patient preparation zz Drugs used for optimizing imaging evaluation zz Drugs affecting coagulation and antiplatelets zz Sclerosants and embolizing agents zz Drugs for transarterial chemoembolization (TACE).

DRUGS FOR PATIENT PREPARATION: SEDATIVES Midazolam is the most commonly used short-acting benzodiazepine that possesses potent anxiolytic, amnestic, hypnotic, anticonvulsant, skeletal muscle relaxant, and sedative properties. Like all benzodiazepines it bind to specific GABAA receptor subunits at central nervous system (CNS) neuronal synapses facilitating GABA-mediated chloride ion channel opening and enhance membrane hyperpolarization. Midazolam is roughly 3–4 times more powerful and has twice the affinity for benzodiazepine receptors than diazepam and has more potent amnesic effects and also has a fast recovery time. Typical adult dose is 1–2.5 mg IV, and can be repeated every 5–10 minutes to a maximum dose of 10 mg. Midazolam has more potential than other benzodiazepines to cause respiratory depression and arrest hence should be administered slowly and extreme caution to be exercised in pediatic patients. Intravenous midazolam is indicated for procedural sedation (often in combination with an opioid, such as fentanyl), for preprocedural sedation and for the induction of general anesthesia. Flumazenil, a benzodiazepine antagonist drug, can be used to treat an overdose of midazolam, as well as to reverse sedation. However, flumazenil can trigger seizures in mixed overdoses and in benzodiazepine-dependent individuals, so is not used in most cases. Among the antihistaminics used for sedation, prom­ ethazine (Phenergan) 12.5–25 mg every 4 hourly or

Chapter 64 Common Drugs Used in an Imaging Department

diphenhydramine (Benadryl) 25–50 mg are the most commonly employed.

zz zz

Epidural anesthesia Intravenous regional anesthesia.

Local Anesthetics

Adverse Effects

Local anesthetics (LA) effectively and reversibly block impulse conduction along nerve axons and other excitable membranes that use sodium channels as the primary means of action potential generation. Clinically, local anesthetics are used to block pain sensation from or sympathetic vasoconstrictor impulses to specific areas of the body. Newer local anesthetics were introduced with the goal of reducing local tissue irritation, minimizing systemic cardiac and CNS toxicity, and achieving a faster onset and longer duration of action. They are broadly classified as follows: zz Aminoamides, e.g. lignocaine, bupivacaine, rapiva­-caine, etc. zz Aminoesters, e.g. procaine, benzocaine, cocaine, etc. Lidocaine, is still a widely used local anesthetic, was synthesized in 1943 by Löfgren.

CNS: Causes stimulation of CNS, producing restlessness and tremors that may proceed to clonic convulsions.

Methods of Administration The choice of local anesthetic for infiltration, peripheral nerve blocks, and central neuraxis (spinal/epidural) blockade is usually based on the duration of action required. Procaine and chloroprocaine are short-acting; lidocaine, mepivacaine, and prilocaine have an intermediate duration of action; and tetracaine, bupivacaine, levobupivacaine, and ropivacaine are long-acting local anesthetics. The anesthetic effect of the agents with short and intermediate durations of action can be prolonged by increasing the dose or adding a vasoconstrictor agent (e.g. epinephrine or phenylephrine). The vasoconstrictor slows the removal of the local anesthetic from the injection site. In addition, it decreases the blood level and the probability of cardiovascular and CNS toxicity. The onset of local anesthesia can be accelerated by the addition of sodium bicarbonate (1–2 mL) to the local anesthetic solution. This maximizes the amount of drug in the more lipid-soluble (unionized) form. Repeated injections of local anesthetics can result in loss of effectiveness (i.e. tachyphylaxis) due to extracellular acidosis.

Infiltration Anesthesia It is injecting the agent directly into the tissue without taking into consideration of course of cutaneous nerves. It is so superficial as to include only the skin. However deeper structures can also be included. Others zz Surface anesthesia zz Nerve block zz Spinal anesthesia

CVS: Usually due to inadvertent intravascular injection. Hypotension, due to arteriolar dilatation and cardiovascular collapse probably due to action on pacemaker or sudden onset ventricular fibrillation may occur. Hypersensitivity: It is very rare and slightly more common with aminoesters. It can manifest either as allergic dermatitis or a typical asthmatic attack.

Sting Free LA Addition of sodium bicarbonate reduced the stinging sensa­ tion related to the acidic nature of adrenaline containing LA. zz 2% lignocaine, 19 mL zz Adrenaline 1: 1000, 0.1 mL zz Normal saline, 20 mL zz Sodium bicarbonate (8.3%), 4 mL.

DRUGS USED FOR OPTIMIZING IMAGING EVALUATION: DIURETICS Loop diuretics selectively inhibit NaCl reabsorption in the thick ascending limb of loop of Henle. Because of the large NaCl absorptive capacity of this segment and the fact that the diuretic action of these drugs is not limited by development of acidosis, as is the case with the carbonic anhydrase inhibitors, loop diuretics are the most efficacious diuretic agents currently available. Furosemide is the prototype of this group and is often used for optimizing urologic diagnostic procedures. The duration of effect for furosemide is usually 2–3 hours. Halflife depends on renal function. Reduction in the secretion of loop diuretics may result from simultaneous administration of agents such as NSAIDs or probenecid, which compete for weak acid secretion in the proximal tubule.

Uses zz

zz

MRU: Intravenous injection of low-dose furosemide (5–10 mg) and gadolinium (Gd) chelate is used for achieving a uniform distribution of the contrast material inside the entire urinary tract. CTU: Supplemental intravenous furosemide (10 mg) a vasodilator (an “inodilator”) by selective inhibition of cAMP-may be used to optimize urinary collecting system opacification and distention.

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Section 2 Recent Advances and Applied Physics in Imaging zz

IVU: 10–20 mg lasix (1 mg/kg pediatric dose) is used to differentiate between complete or partial PUJO, PUJO and extrarenal pelvis at 4 hours of IVU study.

Contraindications Furosemide, bumetanide, and torsemide may exhibit allergic cross-reactivity in patients who are sensitive to other sulfonamides, but this appears to be very rare. Overzealous use of any diuretic is dangerous in hepatic cirrhosis, borderline renal failure, or heart failure.

Vasodilators They are used to treat angiographic and clinical vasospasm either alone or in combination with transluminal balloon angioplasty (TBA). Commonly used agents include papavarine, calcium channel blocker (nimodipine, verapamil, nicardipine) and milrinone.

Papaverine Papaverine has been the most commonly used vasodilator for intra-arterial infusion therapy, a benzyllisoquinoline alkaloid and a potent smooth muscle relaxant, is believed to act by the inhibition of phosphodiesterse activity in smooth muscle cells. It has been associated with seizures and elevations in intracranial pressure. Dosage: 300 mg of papavarine diluted in 100 mL of normal saline forming a concentration of 0.3%. Approximately 2–4  mL of 0.3% papavarine solution injected as pulse spray. Papaverine should not be mixed with contrast agents or heparin because it may cause precipitation of crystals. Infusion of highly concentrated papaverine may have fewer vasodilatory effects and a higher risk of temporary deterioration, possibly because of emboli formed from papaverine precipitates.

Nimodipine It is a dihydropyridine type of calcium channel blocker and specifically block L-type voltage-gated calcium channels. Dosage (intra-arterial) - Nimodipine diluted in a solution of NaCl 0.9% to obtain a 25% concentration. Typical dose administered is 1–4 mg (5–20 mL) per vessel with the maximum rate of 2 mL/min. Intensive blood pressure monitoring is required during therapy as it can lead to hypotension.

Milrinone Milrinone is a bypyridine methyl carbonitrile analog of amrinone. Its mechanism of action is similar to that

of papaverine, which is a nonselective inhibitor of phosphodiesterase. Milrinone works as an inotropic drug and specific phosphodiesterase III in both cardiac and vascular smooth muscle. Parenteral milrinone delivered in large doses can cause systemic hypotension. Unlike Papavarine no significant elevation in intracranial pressure is seen. Dosage: (Intra-arterial) Milrinone diluted in a solution of NaCl 0.9% to obtain a 25% concentration. Typical dose is infusion at a rate of 0.25 mg/min, with a total dose of 10–15 mg. Recurrence of cerebral vasospasm, however, is common after vasodilator infusion, as these drugs have relatively short half-lives, therefore requiring additional infusion or TBA. At authors institute, Intra-arterial nimodipine is used and is reserved for patients with symptomatic vasospasm who have vessel diameter reduction between 25% and 50% of the initial diameter angiographically and in patients with distal vessel vasospasm not amenable to balloon angioplasty.

Patient Preparation in Suspected Pheochromocytoma Older literature suggested premedication with oral alpha and beta-adrenergic blockade (phentolamine 5 mg and meto­ prolol 10 mg) for IV contrast medium usage in patients with pheochromocytoma, for preventing adrenergic crisis. It is to be remembered that beta blockade should never be used without alpha blockade in patients with pheochromocytoma. However recent studies indicate no need for routine prophylaxis when nonionic contrast media are employed.

Drugs for Cardiac Imaging Cardiac CT Cardiac CT (coronary angiography) is unique in that, the image quality is inversely proportional to motion artifacts and the best image quality is achieved at low heart rates 7 cm diameter) who presents with acute aortic syndrome has a high likelihood of aneurysm rupture. Also, a rate of enlargement of >10 mm per year warrants surgical repair. zz Thrombus-to-lumen ratio—decreases with increasing aneurysm size. A thick circumferential thrombus is protective against rupture. zz Focal discontinuity in intimal calcification. zz Hyperattenuating crescent sign—due to hemorrhage in either the peripheral thrombus or aneurysm wall. Acute abdominal hemorrhage may result due to ruptured aneurysm in a case of polyarteritis nodosa, ruptured tumor (usually renal cell carcinoma) or in a patient on anticoagulant

Fig. 23:  CT angiography. MIP image shows an irregular, sac-like

lobulated outpouching from the wall of the thoracoabdominal aorta due to a mycotic pseudoaneurysm in a case of infective endocarditis. There is associated thrombus as well as a peripheral rim of hyperdensity because of the surrounding hematoma

therapy. Noncontrast CT demonstrates a hyperdense collection at the site of hemorrhage. MDCT angiography can accurately delineate the site and cause of hemorrhage. Rare causes of acute abdomen include hepatic vein thrombosis (acute Budd–Chiari syndrome) and portal vein thrombosis. US in the acute phase may show liver enlargement, partial or complete inability to visualize hepatic veins, intraluminal hepatic vein echogenicity or thrombosis, marked narrowing of intrahepatic IVC and ascites. Color Doppler is the technique of choice for initial evaluation. Absence of flow or flow in an abnormal direction in all or part of the hepatic veins may be seen. CT and MR

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Section 3 Gastrointestinal and Hepatobiliary Imaging

are complimentary techniques for definitive diagnosis which provide a more complete evaluation of the hepatic parenchyma, hepatic veins and IVC.

Pelvic Disease The various entities that have to be addi­tionally thought of while evaluating a young female in the reproductive age group presenting with acute abdomen are ruptured ectopic pregnancy, PID, twisted ovarian cyst and complications of early pregnancy, etc. zz Signs of a ruptured ectopic pregnancy on ultrasound include an inhomogeneous adnexal mass, pelvic fluid or hematoma, decidual reaction without intrauterine gestation sac, in the presence of a positive pregnancy test. Visualization of an echogenic adnexal ring separate from the ovary that has prominent peri­pheral flow on color Doppler is highly suggestive of ectopic gestation. Corpus luteum is a useful guide while looking for an ectopic pregnancy and is usually seen in the ipsilateral ovary in 70–85% cases.44 Using transvaginal ultrasound, the live embryo can be detected in up to 17% of all ectopic pregnancies. zz Fibroids may present with acute pain if there is torsion or degeneration of a submucosal or subserosal fibroid. On imaging, uterine enlargement with a focal mass or contour deformity are seen. Degenerated fibroids may have a cystic appearance. zz Ovarian torsion usually occurs in children and is attributed to excessive mobility of the ovary. In adults, a cyst or mass, frequently a cystic teratoma, is present in the ovary undergoing torsion. Sonographic findings include an enlarged ovary with peripherally distributed follicles, an associated cyst or mass, with diminished or absent central venous flow on Doppler. On CT, deviation of the uterus to the twisted side, obliteration of fat planes and an enlarged ovary displaced from its adnexal location is seen. Contrast enhanced CT may show surrounding enhancing blood vessels due to congestion. zz Hemorrhage into a corpus luteal or follicular cyst may manifest with abrupt onset of pelvic pain. If the cyst ruptures, associated hemoperitoneum can be life threatening. On imaging, hemorrhagic ovarian cysts can mimic a variety of solid and mixed solid-cystic masses. A fluid–fluid level may be present. On CT, high attenuation components are usually seen due to hemorrhage. zz Pelvic inflammatory disease (PID) is among the common causes of acute pain in young women. In the early stage of PID, US may demonstrate a small amount of fluid in the cul-de-sac or endometrial canal. On CT, there may be stranding in the parapelvic fat, thickening of uterosacral ligament and ovarian enlargement with oophoritis. In advanced stages, there is development of pyosalpinx or tubo-ovarian abscess.

zz

Ovarian vein thrombosis (OVT) should be suspected as a cause of abdominal pain in the postpartum period, in women with PID, recent abdominal surgery, malignancy or known hypercoagulable state. Pregnancy increases the risk for venous thrombosis due to stasis, alteration in coagulation factors and by nearly tripling the diameter of the ovarian veins. In 90% of cases, the right ovarian vein is involved due to dextrotorsion of the uterus.45 OVT may be diagnosed by US, CT or MRI, however, CT is the modality of choice and demonstrates a low attenua­tion thrombus in lumen of ovarian vein.45

MISCELLANEOUS Diverticulitis The tetrad of left lower quadrant pain and tenderness, fever and leukocytosis is the classic presentation of diverticulitis. Diverticular disease of the colon affects 65% of the Western population by the age of 65 years, and diverticulitis eventually develops in up to 25% of individuals with diverticulosis. 46 Findings on barium enema include diverticulae, muscular wall hypertrophy, intramural or extramural mass effect on the barium column, colonic obstruction or peritoneal extravasation of contrast material, such as with fistula or sinus tract formation. The full extent of peritoneal involvement cannot be estimated on barium examination, hence it has largely been replaced by CT for imaging of suspected diverticulitis. Findings on CT include diverticulae, muscular wall hypertrophy, symmetrical mural thickening > 4 mm, pericolonic fat stranding, phlegmon, extraluminal gas bubbles, extravasation of contrast in case of perforation and paracolic abscess formation. Adequate distension and opacification of the colon by contrast material administered per-rectally is the cornerstone of an optimal CT evaluation and helps distinguish true inflammatory wall thickening from apparent wall thickening due to incomplete luminal distension. Differential diagnosis includes carcinoma. Presence of enlarged lymph nodes, mural thickening >1.5 cm and an abrupt change from normal to abnormal colon favors carcinoma over diverticulitis.47

Toxic Megacolon Toxic megacolon is an acute transmural fulminant colitis which can occur as a complication of any colitis but is most commonly seen with ulcerative colitis (1.6–13% of cases). Plain radiographs show marked colonic dilatation (>8 cm) particularly of the transverse colon as this is the least dependent part of the large bowel in the supine position. The wall has a shaggy appearance with mucosal islands or pseudopolyps with absence of haustra due to profound inflammation and ulceration (Fig. 24). There may be air–fluid levels and small bowel dilatation. CT shows the distended

Chapter 68 Nontraumatic Acute Abdomen

Fig. 24:  Toxic megacolon. Plain radiograph, supine film shows

Fig. 25:  Axial CT image shows multiple, irregular, linear, hypodense

colon filled with air, fluid and blood with a distorted or absent haustral pattern and irregular, nodular wall.48 There may be presence of intramural air or blood. The prognosis is poor in the presence of perforation and complications.

demonstrate absence of the normal urinary jet on the obstructed side. Unenhanced helical CT has emerged as an attractive modality in the diagnostic workup of urinary tract disease. NCCT KUB is performed rapidly, without patient preparation and without risk of contrast reaction. It can provide information about size, localization and chemical composition of the stone. In addition to direct stone visualization, secondary CT signs of urinary obstruction, including ureteral dilatation, perinephric or periureteric fat stranding, blurring of renal sinus fat and ureteral wall edema, are usually present to confirm the diagnosis even after recent stone passage.49

dilatation of the large bowel loops particularly the transverse colon which has thick, shaggy walls due to mucosal islands

Acute Pyelonephritis Acute pyelonephritis is the bacterial or fungal infection of the renal parenchyma and collecting system. Presenting features include flank pain, dysuria and high grade fever with rigors. On US, renal enlargement, decreased visualization of sinus fat secondary to compression, loss of corticomedullary differentiation, focal poorly marginated hypoechoic areas representing interstitial edema or complications like abscesses may be seen. CT is the imaging modality of choice and can reveal calculi, obstruction, renal enlargement, striated nephrogram, ill-defined wedge-shaped areas of dec­ reased attenuation radiating from the papillae to the cortical surface, abscess, thickening of Gerota’s fascia and perinephric stranding (Fig. 25). Emphysematous pyelonephritis usually occurs in patients with poorly controlled diabetes with the most common infecting organism being Escherichia coli. Presence of air in the renal parenchyma is pathognomonic of this condition.

Acute Urinary Colic Impacted ureteric stone is the most common cause of acute postrenal obstruction. US is useful for the detection of small/ radiolucent calculi missed on plain films. Secondly, direct visualization of the effects of these calculi on the urinary tract is also possible. However, because pelvicaliectasis may be mild to negligible in acute obstruction, US may miss up to one-third of acute obstructions. Color Doppler US helps

areas in the left kidney due to pyelonephritis. A hypodense area with an air–fluid level is seen in anterior cortex suggestive of renal abscess. In addition, perinephric collection with air is also visualized

Acute Epiploic Appendagitis, Omental Infarction Epiploic appendages are fat-containing peritoneal outpouchings that arise from cecum to rectosigmoid junction, along the serosal surface of the colon. These are 0.5–5.0 cm long and contain fat and small vessels. Epiploic appendagitis is due to torsion of an epiploic appendage leading to venous occlusion and ischemia. It is usually associated with obesity, hernia and unaccus­tomed exercise. The condition manifests as acute left lower quadrant pain, predominantly in males in the 4th–5th decades of life. On US, a hyperechoic, incompressible mass delineated by a hypoechoic ring is seen at the point of maximum tenderness. The lesions are hyperechoic due to their fat content or hemorrhagic necrosis. CT features include an oval, fat attenuation lesion less than 5 cm in diameter that abuts the anterior or anterolateral serosal aspect of the colonic wall, surrounded by inflammatory changes.50 A hyperattenuating rim corresponding to the hypoechoic ring on US is seen on CT due to swollen serosa covered by fibrino-leukocyte exudate.

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Omental infarction commonly involves the inferior aspect of right side of omentum. It is characteristically situated between the anterior abdominal wall and the transverse or ascending colon, corresponding in location to the greater omentum. Predisposing factors include obesity, strenuous activity, congestive heart failure, digitalis administration, recent abdominal surgery and abdominal trauma. Pain is localized to the right lower or upper quadrant and the presumptive diagnosis is usually appendicitis. Both US and CT show an ovoid, soft tissue mass just beneath the anterior abdominal wall. The infarcted omental fat is hyperechoic on ultrasound and appears heterogeneous with no enhancement on CT. Although omental infarction may resemble acute epiploic appendagitis on CT, it lacks the hyper­attenuating ring seen in the latter. Moreover, omental infarction is larger than epiploic appendagitis which is often less than 5 cm. Omental infarction is commonly located next to the cecum and ascending colon whereas acute epiloic appendagitis is usually located adjacent to sigmoid colon.50

REFERENCES 1. Silen W. Cope’s early diagnosis of the acute abdomen (19th edn) Oxford University Press: New York; 1996. 2. Field S. The plain abdominal radiograph—The acute abdomen. In Grainger RG, Allison DJ (Eds). Diagnostic Radiology (3rd edn). Churchill Livingstone: Edinburgh; 1997. 3. de Bombal FT. Introduction. In de Bombal FT (Eds). Diagnosis of acute abdominal pain (2nd edn). Churchill Livingstone: Edinburgh; 1991. 4. Balthazar EJ, Chako AC. Computerized tomography in acute gastrointestinal disorders. Am J Gastroenterol. 1990;85:1445-52. 5. Macari M, Balthazar EJ. The acute right lower quadrant: CT evaluation. Radiol Clin N Am. 2003;41:1117-36. 6. Kundra V, Silverman PM. Impact of mutlislice CT on imaging of acute abdominal disease. Radiol Clin N Am. 2003;41:1083-93. 7. Lomas DJ. Technical developments in bowel MRI. Eur Radiol. 2003;13:1058-71. 8. Mindelzun RE, McCort JJ. Acute abdomen. In Margulis AR, Burhenne HJ (Eds): Alimentary Tract Radiology (4th edn) CV Mosby Co.: St. Louis, Mo; 1983. 9. Mirvis SE, Young JWR, Keramati B, et al. Plain film evaluation of patients with abdominal pain: Are three radiographs necessary? AJR.1986;147:501-3. 10. Miller RE, Nelson SW. The roentgenological demons­tration of tiny amounts of free intra-peritoneal gas: Experimental and clinical studies. AJR. 1971;112:574-85. 11. Rubesin SE, Levine MS. Radiologic diagnosis of gastrointestinal perforation. Radiol Clin N Am. 2003;41:1095-115. 12. Messmer JM. Gas and soft tissue abnormalities. In Gore RM, Levine MS (Eds): Textbook of Gastrointestinal Radiology (2nd edn). WB Saunders company; 2000.

13. Bongard F, Landers DV, Lewis F. Differential diagnosis of appendicitis and pelvic inflammatory disease. Am J Surg. 1985;150:90-6. 14. Rao PM, Rhea JT, Novelline RA, et al. Helical CT technique for the diagnosis of appendicitis: Prospective evaluation of a focused appendix CT examination. Radiology. 1997;140:139-44. 15. Gaitini D, Beck-Razi N, Mor-Yosef D, et al. Diagnosing acute appendicitis in adults: Accuracy of color Doppler sonography and MDCT compared with surgery and clinical follow-up. AJR. 2008;190:1300-6. 16. Lee JH, Jeong YK, Park KB, et al. Operator dependent techniques for graded compression sonography to detect the appendix and diagnose acute appendicitis. AJR. 2005;184:91-7. 17. Poortman P, Lahle PNM, Schoemaker CMC, et al. Comparison of CT and sonography in the diagnosis of acute appendicitis: A blinded prospective study. AJR.2003;181: 1355-9. 18. Uggowitzer M, Kugler C, Schramayer G, et al. Sono­graphy of acute cholecystitis: Comparison of color and power Doppler sonography in detecting a hyper­vascularized gallbladder wall. AJR. 1997;168:707-12. 19. Blankenberg F, Wirth R, Jeffry BR Jr, et al. Computed tomography as an adjunct to ultrasound in the diagnosis of acute acalculous cholecystitis. Gastrointestinal Radiol. 1991;16:149-53. 20. Fidler J, Paulson EK, Layfield L. CT evaluation of acute cholecystitis: Findings and usefulness in diagnosis. AJR. 1996;166:1085-8. 21. Watanabe Y, Nagayama M, Okumura A, et al. MR imaging of acute biliary disorders. Radiographics. 2007;27:477-95. 22. Bennett GL, Rusinek H, Lisi V, et al. CT findings in acute gangrenous cholecystitis. AJR. 2002;178:275-81. 23. Morris BS, Balpande PR, Morani AC, et al. The CT appearances of gallbladder perforation. BJR. 2007;80:898-901. 24. Gore RM, Yaghmai V, Newmark GM, et al. Imaging benign and malignant disease of the gallbladder. Radiol Clin North Am. 2002;40:1307-23. 25. Balthazar EJ, Ranson JHC, Naidich DP, Megibow AJ, Caccavak R, Cooper MM. Acute pancreatitis: Prognostic value of CT. Radiology. 1985;156:767-72. 26. Balthazar EJ, Robinson DL, Megibow AJ, Ranson JHC. Acute pancreatitis: Value of CT in establishing prognosis. Radiology. 1990;174:331-6. 27. Mortele KJ, Wiesner W, Intreire L, et al. A modified CT severity index for evaluating acute pancreatitis: Improved correlation with patient outcome. AJR. 2004;183:1261-5. 28. Dorffel T, Wruck T, Ruckert R, Romanivk P, Dorffel Q. Vascular complications of acute pancreatitis assessed by color duplex ultrasonography. Pancreas. 2000;21:126-33. 29. Stimac D, Miletic D, Radic M. The role of NEMRI in early assessment of acute pancreatitis. Am J Gastroenterol. 2007; 102(5):997-1104. 30. Joseph AEA, MacVicar D. Ultrasound in the diagnosis of abdominal abscess. Clin Radiol. 1990;42:154-6.

Chapter 68 Nontraumatic Acute Abdomen 31. Go Hl, Baarslaq HJ, Vermeulen H, Laméris JS, Legemate DA. A comparative study to validate the use of ultrasono­graphy and computed tomography in patients with post-operative intraabdominal sepsis. Eur J Radiol. 2005;54(3):383-7. 32. Federle MP, Anne VS. Small bowel obstruction. In Federle MP (Ed): Diagnostic imaging—Abdomen (1st edn). Amirsys Inc, Utah; 2004. 33. Canon CL. Gastrointestinal Tract. In Lee JKT, Sagel SS, Stanley RJ, Heiken JP (Eds): Computed body tomography with MRI correlation (4th edn). Lippincott Williams and Wilkins, Philadelphia PA; 2006. 34. Bondiaf M, Jaff A, Soyer P, Bouhnik Y, Hamzi L, Rymer R. Small bowel diseases: Prospective evaluation of multi-detector row helical CT enteroclysis in 107 consecutive patients. Radiology. 2004;233:338-44. 35. Beall DP, Fortman BJ, Lawler BC, et al. Imaging bowel obstruction: A comparison between fast magnetic resonance imaging and helical computed tomography. Clin Radiol. 2002;57(8):719-24. 36. Chen SC, Wang HP, Chen WJ, et al. Selective use of ultrasonography for the detection of pneumoperitoneum. Acad Emerg Med. 2002;9:643-5. 37. Jones R. Recognition of pneumo-peritoneum using bedside ultrasound in critically ill patients presenting with acute abdominal pain. Am J Emerg Med. 2007;25:838-41. 38. Furukawa A, Sakoda M, Yamasaki M, et al. Gastro­intestinal tract perforation: CT diagnosis of presence, site and cause. Abdom Imaging. 2005;30:524-34. 39. Rha SE, Ha HK, Lee S, et al. CT and MR imaging findings of bowel ischemia from various primary causes. Radiographics. 2000;20:29-42.

40. Wiesner W, Khurana B, Ji H, Ros PR. CT of acute bowel ischaemia. Radiology. 2003;226:635-50. 41. Ha HK, Rha SE, Kim AY, et al. CT and MR diagnosis of intestinal ischaemia. Seminars in US, CT and MRI. 2000;21(1): 40-55. 42. Scott RA, Ashton HA, Kay DN. Abdominal aortic aneurysm in 4,237 screened patients: Prevalence, development and management over 6 years. Br J Surg. 1991;78:1122-5. 43. Rakita D, Newatia A, Hines JJ, et al. Spectrum of CT findings in rupture and impending rupture of abdominal aortic aneurysms. Radiographics. 2007;27:497-507. 44. Condous G, Okaro E, Khalid A, et al. The accuracy of transvaginal ultrasonography for the diagnosis of ectopic pregnancy prior to surgery. Hum Reprod. 2005;20:1404-9. 45. Heavrin BS, Wrenn K. Ovarian vein thrombosis: A rare cause of abdominal pain outside the peripartum period. J Emerg Med. 2007;34:67-9. 46. Rao PM, Rhea JT, Novelline RA, et al. Helical CT with only colonic contrast material for diagnosing diverti­c ulitis: Prospective evaluation of 150 patients. AJR. 1998;170:1445-9. 47. Chintapalli KN, Esola CC, Chopra S, et al. Pericolic mesenteric lymph nodes: An aid in distinguishing diverticulitis from cancer of the colon. AJR. 1997;169:1253-5. 48. Imbriaco M, Balthazar EJ. Toxic megacolon: Role of CT in evaluation and detection of complications. Clin Imaging. 2001;25:349-54. 49. Sourtzis S, Thibeau JF, Damry N, et al. Radiologic investigation of renal colic: Unenhanced helical CT compared with excretory urography. AJR. 1999;172:1491-4. 50. Singh AK, Gervais DA, Halin PF, et al. Acute epiploic appen­ dagitis and its mimics. Radiographics. 2005;25:1521-34.

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CHAPTER

Imaging in Abdominal Trauma Atin Kumar, Sanjay Thulkar

INTRODUCTION Blunt abdominal trauma in isolation represents 5% of trauma mortality and further contributes 15% to mortality as part of polytrauma.1 Excessive bleeding accounts for 80–90% of acute deaths from abdominal injury. In recent years advances in cross-sectional imaging coupled with image-guided interventional therapies have made significant contributions in enabling nonsurgical management of blunt abdominal trauma in hemodynamically stable patients. A radiologist must have a detailed understanding of the patterns of injury, image appearances of traumatic injuries, assessment of hemodynamic status and common image artifacts. The patient evaluation must take place within the context of systematic and orderly resuscitation of the patient. Abdominal trauma could be blunt or penetrating. Blunt trauma occurs in approxi­mately two-thirds of abdominal injury patients. Motor vehicle accidents account for up to 80% of blunt trauma with the remainder being caused by falls, assault and industrial accidents. Penetrating injuries commonly result due to gunshot injuries and stab wounds. The incidence of organ injury in both categories of trauma as observed by Anderson et al.2 is given in Table 1. Up to two-thirds of the abdominal trauma pati­ents have a significant injury to other systems as well and these injuries may take prece­dence in terms of diagnosis and treat­ment. Prompt and accurate clinical assessment is essential in the initial evaluation of an abdominal trauma patient. Unfortunately, the clinical evaluation is often unreliable. Neurological impairment due to traumatic event itself or to concomitant factors, such as intoxication or inebriation significantly limits the usefulness of clinical examination. The most reliable signs in conscious patients are pain and tenderness with guarding. About 12–16% of patients with abdominal trauma present in a state of shock.3 After initial evaluation and resuscitation, subsequent management depends on hemodynamic stability of the patient. As per the ACR guidelines/appropriateness criteria4 the patients are divided into following categories discussed further.

Table 1:  Incidence of organ injury in blunt and penetrating trauma Blunt

Penetrating

Spleen

25%

Liver

37%

Kidney

12%

Small bowel

26%

Intestine

15%

Stomach

19%

Liver

15%

Colon

16.5%

Retroperitoneum

13%

Vascular retroperitoneum

11.0%

Mesentery

5%

Mesentery

7.0%

Pancreas

3%

Diaphragm

5.5%

Diaphragm

2%

Kidney

5.0%

Vascular

2%

Pancreas

3.5%

Duodenum

2.5%

Biliary system

1.0%

Others

1.0%

Category A: This category includes hemodynamically unstable patients following clinically obvious major abdominal trauma and with unresponsive profound hypotension, need rapid clinical evaluation and imme­diate resuscitation with volume replacement. If such unstable patients do not respond to resuscitation (become hemodynamically stable) and if they have clear clinical evidence of abdominal injury, they should go imme­diately to the operating room without imaging. During resus­citative efforts if time and circumstances permit, conventional radiographs of the chest and abdomen are often obtained as part of trauma protocols. This may help identify a pneumothorax, pneumoperitoneum, or significant bone injury. Ultrasound performed by an experienced sonologist to check for intraperitoneal free fluid may quickly provide information that can support a decision to operate immediately, with the caveat that the false negative rate is at least 15%. More detailed ultrasound to check for organ injury takes too long in this setting and suffers from poor sensitivity. There is now general agreement that routine diagnostic

Chapter 69 Imaging in Abdominal Trauma

peritoneal lavage (DPL) is obsolete because of its invasive nature, lack of specificity and inability to predict the need for therapeutic surgery. Category B: This category includes hemodynamically stable patients, patients with mild to moderate respon­sive hypotension presenting to the emergency room after blunt abdominal trauma and unstable patients who stabilize after initial resuscitation. These patients typically have a history of significant trauma and have at least moderate suspicion of intra-abdominal injury based on clinical signs and symptoms. These patients should be evaluated by imaging. In patients with clinical evaluation suggesting a lesser index of suspicion for significant intra-abdominal injury, chest and abdominal radiographs, hematocrit with blood chemis­ tries and a urinalysis should be performed. If these tests are unremarkable in the setting of a reliable clinical abdominal exam, a period of clinical observation may all be that is needed. However, if a reliable abdominal exam cannot be performed (patient is unconscious or prolonged nonabdominal surgery is anticipated) or if a clinical evaluation suggests organ injury, hemo­peri­toneum, or peritonitis, further imaging is needed. The need for initial radiographs may be obviated if the clinical condition at initial evaluation merits a computed tomography (CT). Ultrasound is not a good modality for further imaging because it is relatively much less sensitive than computed tomography for liver and spleen injuries and highly insensitive for renal, pancreatic, mesenteric, gut, bladder and retroperitoneal injuries. If due to circumstances, a negative ultrasound is the sole imaging modality used to triage a patient, for safety reasons it must be followed by a 12–24 hours period of in-hospital observation. A negative ultrasound alone may be adequate to release the patient from observation only in a separate subcategory of stable patients with trivial trauma, a low clinical index of suspicion and no signs or symptoms of intraabdominal injury. Any positive findings on ultrasound would however, warrant computed tomo­graphy. In contrast, computed tomography is an excellent modality for detecting solid organ and gut injuries together with even small amount of hemoperitoneum. The findings of computed tomography in combination with clinical status of the patient plays an important role in deciding whether a patient needs urgent therapeutic surgery or therapeutic angiography or whether he can be managed conservatively. Identification of active hemorrhage, parenchymal blush or pseudoaneurysm in spleen, gut perforation, diaphragmatic injury and pancreatic injury tilt the scales towards surgical or angiographic manage­ment. Selected stable patients with negative computed tomography can be discharged without observation whereas patients with positive computed tomography findings in which surgical intervention is not required may be managed conser­vatively under observation with imaging follow-up.

Category C: This category includes patients with hematuria which require some modification to imaging workup. Patients with microscopic hematuria (less than 35 red blood cells per high power field) do not need specific urinary tract imaging. All patients with microscopic hematuria greater than 35 red blood cells per high power field, with macroscopic hematuria, or with fracture/diastasis of the symphysis pubis and its rami plus any hematuria need imaging of the urinary tract. If the urethral meatus has gross blood, if there is a floating prostate, or if a Foley catheter cannot be passed, a retrograde urethro­ gram should first be performed to rule out urethral injury. However, if clinical evaluation or the urethrogram indicates no urethral injury, a computed tomography cystogram should be added to the abdominal computed tomography.

DIAGNOSTIC IMAGING Plain Radiography Stable patients and those who respond to initial fluid therapy should undergo radio­graphic studies of the cervical spine, chest and pelvis because of the relatively high incidence and potentially devastating injuries to these areas. The plain radiographs may reveal fractures. The upright chest X-ray is a relatively sensitive means of detecting pneumoperitoneum. Small amount of air may not be initially seen on upright chest radio­graph as it may take up to 10 minutes to rise to the highest point in the peritoneal cavity. It is possible with optimal radiographic technique to demonstrate upto 1.0 cc of free air on upright chest radiograph. Plain radiographs of the abdomen are insensitive for the detection of hemo­peri­toneum. Intraperitoneal volume of greater than 800 cc is usually necessary for the demons­tration of classic plain radiographic signs, e.g. “dog ear” or “bladder ear” sign when there is accumu­lation of intraperitoneal blood in the pouch of Douglas. In the true abdomen, the most dependent intraperitoneal areas are paracolic gutters. Blood tracking from liver and spleen will collect in the respec­tive gutter appearing as a soft tissue haze. This collection of blood displaces the right or left colon medially.

Ultrasonography Sonography is commonly used for the initial assessment of abdominal trauma. Abdominal ultrasound in cases of major trauma is usually performed with a focused assessment with sonography in trauma (FAST) examination. It provides a fast overview of abdomen to detect free fluid which indicates hemoperitoneum and visceral organ injury in this setting. The FAST scan should be completed within few minutes with an aim to primarily search for free intraperitoneal fluid and screen organs for injury. While parenchymal organ injuries may be detected, search for such injuries should not delay the exami­ nation specially in the setting of suspicion of hemorrhage. The recommended standard views are listed further.

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Transverse view of epigastrium to detect pericardial fluid and injury to left lobe of liver. zz Longitudinal view of right upper quadrant for right lobe of liver, right kidney and Morrison’s pouch and perihepatic free fluid. zz Longitudinal view of left upper quadrant for spleen, left kidney and perisplenic free fluid. zz Longitudinal views of bilateral flanks to look for free fluid in paracolic gutters zz Transverse and longitudinal views of suprapubic region for urinary bladder and free fluid in pelvis and pouch of Douglas. zz Bilateral longitudinal thoracic views for pleural effusion. The reported sensitivity of FAST for detection of free intraperitoneal fluid ranges from 0.64–0.98 and specificity from 0.86–1.00.5 So false negative rate of FAST is average 15% for free fluid detection. Negative FAST should be interpreted as indicating the absence of hemo­peritoneum, not the absence of intra-abdominal injury. However, it should be remembered that the sensitivity of FAST for free fluid is less than that of CT. A negative FAST should be viewed with suspicion if the finding is not commensurate with patient’s clinical pre­sentation. On the other hand, a positive FAST does not necessarily mandate laparotomy. Hemodynamically stable patients with positive FAST should have their injuries staged with CT, giving them the benefit of nonoperative manage­ment whenever possi­ ble. Focused assessment with sonography in trauma is not reliable for assessment of retroperitoneum. The sensitivity of ultrasound for detection of liver injury ranges from 0.15 to 0.885 and it misses average 15% injuries to liver. The sensitivity for splenic injuries is reported to be between 0.37 and 0.855 with an average false negative rate of more than 50%. Sensitivity for renal and pancreatic injuries is less than that of liver and spleen and even lesser for bowel and mesenteric injuries. The sensitivity for pericardial effusion is high (0.97–1.00).5 In a technically successful examination, hemo­peritoneum (Fig. 1) is visualized as a lenticular collection in the subphrenic space, triangular in Morison’s pouch and ovoid in the pelvis. Solid organ injury can be recognized by sub­capsular or intra­ parenchymal hema­toma. Ultrasonography appearance of hematoma depends on multi­ple factors, especially on its duration. The early hematoma is echogenic but gradually progresses to sonolucency over 96 hours. Ultrasound has certain limitations as the technique is operator dependent and may be limited by excessive bowel gas (especially in post-traumatic paralytic ileus). It may also be limited by open wounds and bandages and by cutaneous emphysema. zz

Radionuclide Scanning Nuclear medicine studies are generally not used in the screening evaluation of abdominal trauma. Although (Tc99m)

Fig. 1:  Axial ultrasound image shows free fluid in hepatorenal pouch

sulfur colloid may detect liver and spleen injury but this technique does not assess the entire abdomen and pelvis and cannot differentiate the defects specific to traumatic injuries. Serial nuclear scans can be used to follow known liver or splenic injuries. In the setting of hepatic injury involving the biliary tree, the use of a biliary scanning agent, such as Tc99mHIDA can demonstrate a biloma or bilious fluid leakage or fistula. In certain circumstances, radio­nuclide angiography can demons­trate small vascular injuries and may exceed the sensitivity of conventional angiography. This technique uses either Tc99m sulfur colloid, or more sensitive Tc99m labeled RBC study, that may demonstrate bleeding as low as 1 mL/mt.6

Magnetic Resonance Imaging Currently, magnetic resonance imaging (MRI) does not play a role in the initial evaluation of the acutely injured patient. Magnetic resonance cholangiopanereatography (MRCP) may be specifically useful in detecting biliary leaks. Magnetic resonance imaging is useful only in doubt­ful cases and in hemodynamically stable patients.

Angiography With recent trends towards nonoperative management of abdominal trauma patients, angiography with embolization has been increasingly used in the manage­ment. Angiographic embolization is indicated when CT shows evidence of vascular injury (pseudoaneurysm, arteriovenous fistula) and in active contrast extravasation as an alternative to surgery. It has also been used in controlling bleeding in patients with high grade (IV and V) liver and spleen injuries specially in hemo­dynamically stable patients with known visceral injury of high grade (IV and V) but falling hematocrit to determine the presence of active bleeding requir­ing embolization or surgical intervention.

Chapter 69 Imaging in Abdominal Trauma

Computed Tomography Computed tomography (CT) is now firmly established as the principal imaging modality for diagnostic evaluation of abdominal trauma. It is useful in detecting otherwise occult injuries to both intra-abdominal and retroperi­toneal structures and grading seve­rity of specific parenchymal injury. Associated injuries of head and chest, etc. can also be evaluated. Computed tomography is as accurate as DPL in detect­ing blunt abdominal injuries. Computed tomography offers a number of advantages over DPL, including detailed anatomic evaluation of injuries, quan­ti­fication of associated hemorrhage and detection of active arterial extra­vasation. CT excels in detection of retroperitoneal injuries that are not picked up by DPL or ultrasound. With these advantages of CT, DPL has now almost become obsolete. Following a negative abdo­minal CT study using helical scanner, trauma patients could be safely discharged from the emergency department without a period of obser­vation.7

Computed Tomography Technique Attention to scanning technique is essential. Scans should be done expeditiously and care should be taken to avoid artifacts and repeat scanning. Helical CT is preferred over the conventional CT as it offers optimal intra­venous contrast enhancement, avoids respira­tory misregis­tration, is less prone to motion artifacts and reduces scan time. Multidetector CT is very useful in this setting as excellent quality reconstructions can be obtained in coronal and saggital planes. Adminis­tration of intravenous iodinated contrast material is mandatory as it makes detection and location of parenchymal contusions and hematoma more conspicuous, identifies great vessels and provides information regarding integrity of organs or extent of the injury. Multidetector CT protocols vary from institution to

A

institution but typically involve imaging at sub-mm slice thickness 60–70 seconds after initiating an injection of 100–120 mL of 300 mg/dL low osmolar IV contrast medium at 2.5–3.0 mL per second. Successful breath holding is often not possible and image acquisition during shallow and quiet breath­ing is often necessary. Use of oral contrast is highly desirable. It is helpful in defining pancreas, integrity of bowel and free intra­peritoneal fluid from fluid filled bowel. Administration of 500 mL of 2–5% iodinated water-soluble contrast is generally sufficient. It is given orally or through the nasogastric tube and allowed to travel as far as possible through the gastrointestinal tract. Rectal contrast is used occasionally to detect colorectal injuries in patients with perineal lacerations and penetrating flank or back wounds. Delayed scanning of kidneys during urographic phase is essential to detect collecting system injuries. Delayed imaging is also useful in specific situations for differentiating between active contrast extravasation from vascular injuries.8 Viewing with bone window for subtle fractures and upper sections with lung windows for unsuspected pneumothorax, lung contusion or free peritoneal gas should be done.9

CT Signs in Blunt Abdominal Trauma10 Sentinel clot sign: Clotted blood adjacent to the site of injury is of higher attenuation (45–70 HU) than unclotted blood which flows away (Figs 2A and B). When source of intraperitoneal bleed is not evident, the location of highest attenuating blood clot is a clue to the most likely source. Water density fluid collection: Fluid collections of near water attenuation originate from rupture of gallbladder, urinary bladder, small bowel and cisterna chyli. When fluid of this density is encountered in the peritoneal cavity without an identifiable source, the safest assumption is that bowel injury is present.

B

Figs 2A and B:  Axial contranst enhanced CT (CECT) scans show hemoperitoneum in perisplenic region. Note the presence of higher density clotted blood adjacent to the spleen (arrows)—‘Sentinel clot sign’

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Section 3 Gastrointestinal and Hepatobiliary Imaging

Interloop fluid: Triangular fluid collection(s) between the leaves of mesentery are important indicators of bowel or mesenteric injury. Hemoperi­toneum from liver or spleen injury typically does not form such collections, but instead tracks from the upper abdomen along the paracolic gutters into the pelvis. When inter­loop fluid is of low attenuation (30 HU), mesenteric hematoma is likely. Hemodynamic status: Size of the IVC in adults and size of aorta in children, give valuable morphological infor­mation that correlates with the intravascular volume and cardiac output. Active arterial contrast extravasation: It must be actively looked for as most oftenly it is an indicator for surgical/ angiographic intervention. It must be distinguished from extravasated oral contrast material and from a vascular injury (pseudoaneurysm or arteriovenous fistula) within an injured organ. Vascular extravasation is typically poorly marginated, high attenuating collection, surrounded by a large hema­toma. Extra­vasated gastrointestinal contrast is usually not surrounded by hematoma. Pseudo­aneurysm usually has a well-defined margin. Vascular injuries show attenuation values paralleling the attenuation of adjacent vessel on delayed phase images while active bleeding shows attenuation values either increasing or remaining same. CT staging of abdominal injuries: Majority of the injuries to the liver, spleen and kidneys can be managed nonoperatively. Computed tomography is required to evaluate the extent of injury and to exclude other intra and retroperitoneal injuries to determine the manage­ment approach. It is generally based on the premise that large and deep lacerations, large hema­tomas and devitalized tissues are signs of more severe injuries and are more likely to require surgical management. Nonoperative management is generally not appropriate in presence of active arterial hemorrhage, favoring urgent surgery or angiographic embolization.

ORGAN TRAUMA Peritoneal Cavity Pneumoperitoneum It is a sign of perforated hollow viscus, but may also occur following pneumothorax and mechanical ventilation. 11 Small amount of air is easily detectable under the right hemi­ diaphragm on erect chest radiograph. Computed tomography is the most sensitive investigation for detection of free peritoneal air. In order not to miss small amounts of free air the images should be viewed in the lung window settings. It may be detected on CT over the liver and anteriorly in the mid

Fig. 3:  Axial CECT scan through upper abdomen in lung window settings shows pneumoperitoneum anterior to liver

abdomen (Fig. 3). Bubbles of free air may be trapped between the leaves of the mesentery or in the peritoneal recesses.

Hemoperitoneum Blood collects in the peritoneum following injury to the liver, spleen, bowel or mesentery. Computed tomography is sensitive in detecting intra-abdominal or pelvic hemorrhage. ‘Sentinel clot’ may be seen near the site of bleeding with lower attenuation blood elsewhere in the peritoneal cavity. In the supine position blood from the liver collects in the hepatorenal recess and travels down the right paracolic gutter into the pelvis. From the spleen the blood passes along the phrenicocolic ligament to the left paracolic gutter and pelvis. Hemoperito­neum typically has an attenuation value of 45 HU or greater, but a quarter of patients may have HU value less than 20 HU. Therefore, hemoperitoneum may not be distinguishable from ascites, extravasated small intestinal fluid from bowel perforation or from intra­peri­toneal urine from ruptured urinary blad­der.12 In women of child-bearing age small amounts of intraperitoneal fluid may be a normal finding. Detection of fluid in each paracolic gutter indicates that atleast 200 mL of blood must be present in each gutter. Computed tomography visualization of blood in the abdomen and pelvis corresponds with the amounts of more than 500 mL.

SPLEEN Spleen is the most commonly injured organ following blunt abdominal trauma. The spleen is the most vascular organ of the body containing approximately 500–600 mL of blood. Although it may occur as an isolated injury, most patients with splenic trauma have associated intra-abdominal injuries.

Chapter 69 Imaging in Abdominal Trauma

Over the last decade, there is increasing trend towards non­ surgical conservative management of splenic injuries. Imaging with multislice CT has greatly aided in evaluation of splenic trauma and CECT is the modality of choice for imaging of splenic injuries. The most widely used splenic injury grading system is the American Asssociation for the Surgery of Trauma (AAST) splenic injury scale.13 Grade I: Hematoma: Subcapsular, 25% of spleen). Grade V: Laceration: Completely shattered spleen. Vascular: Hilar vascular injury that devas­cularizes spleen. However, this AAST injury grading score is based on appearance of spleen on surgery. The CT may not be able to correctly show all the above features and hence may be a limitation in accurately grading the splenic injuries. Recently Marmery et al.14 have proposed a modified splenic injury grading system taking into account the findings of active splenic hemorrhage and vascular injuries on CT. According to their modified grading system, active intraparenchymal and subcapsular splenic bleeding, splenic vascular injury (pseudoaneurysm or arterio­venous fistula) and shattered spleen should be classified as grade IVa and active intraperitoneal bleeding as grade IVb. There is no grade V in their classification. It has now been well established that the presence of active hemorrhage and vascular injuries is predictive of the need for splenic artery transcatheter embolization or splenic surgery. The authors compared their modified grading with the AAST splenic injury grading scale and found it to be a better predictor for surgical or angiographic intervention in patients of splenic trauma (grade IV patients). As already stated above, CECT is the preferred modality for imaging splenic trauma. The images should be obtained in portal venous phase as hetero­geneous enhancement of spleen in the arterial phase can simulate injury. In selective cases where there is dense contrast pooling seen within or around spleen, delayed CT images may be obtained to differentiate active bleeding from post-traumatic vascular injuries. In delayed phase, the active bleeding would retain the same density or even may increase in attenuation but

in case of vascular injuries including pseudoaneurysms and arteriovenous fistulas the attenuation would decrease in proportion to the attenuation of adjacent artery or aorta. Delayed phase may also be useful in differentiating a laceration from a splenic cleft.14 The various CT manifestations of splenic trauma are as follows: zz Hematomas: Subcapsular or parenchymal. Subcap­ sular hematomas are characterized by their lenticular configuration and flattening of the adjacent splenic parenchyma. The compression of underlying parenchyma helps to differentiate subcapsular location of hematoma from free intraperitoneal fluid or blood. Uncomplicated subcapsular hematomas tend to resolve within 4–6 weeks. Parenchymal contusions/hematomas appear as focal, poorly marginated areas of low attenuation at CECT representing edema, hemorrhage and necrotic tissue (Fig. 4). zz Laceration of the spleen appears as nonenhancing linear or branching areas usually at the periphery of the parenchyma (Fig. 5). Lacerations decrease in size and number with time. When delayed phase images are taken, the lacerations appear to ‘fill-in’ from the periphery and become less visible. In contrast, splenic clefts remain unchanged in appearance on delayed phase images besides having smooth or rounded margins. Multiple lacerations can lead to shattered splenic parenchyma (Fig. 6). zz Active extravasation of contrast appears as linear or irregular hyperdensity (Figs 7A andB). The attenuation values ranges from 85–350 HU compared to that of clotted blood which lies between 40–70 HU. As described above, delayed phase imaging can help differentiate active bleeding from vascular injuries. Demonstration of active extravasation of contrast is a strong indicator of surgical or angiographic intervention.

Fig. 4:  Axial CECT scan through upper abdomen shows a splenic parenchymal hematoma

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Section 3 Gastrointestinal and Hepatobiliary Imaging

Fig. 5:  Axial CECT scan at level of lower pole of spleen shows a splenic

Fig. 6:  Axial CECT scan through spleen shows shattered splenic

laceration. Note the presence of minimal fluid in perisplenic region and in hepatorenal pouch (arrows)

parenchyma

B

A

Figs 7A and B:  Axial CECT scans through upper abdomen show active contrast extravasation (arrows) within the splenic parenchyma

zz

zz

zz

Vascular injuries including pseudoaneurysms and arteriovenous fistula appear as well circumscribed focal hyperattenuating areas on CECT with their attenuation value paralleling that of adjacent artery even on delayed images. Angiography is required to differentiate between pseudoaneurysm and arteriovenous fistula and possible embolization. Depiction of vascular injuries is also a strong marker for failure of nonsurgical management. Infarct appears as a well demarcated wedge shaped area of low attenuation which remains unchanged on delayed images. May decrease in size or remain unchanged on follow-up scans. Splenic vascular pedicle injury leads to splenic devas­ cularization which appears as nonenhancing spleen (Fig. 8).

Some potential pitfalls in CT evaluation of splenic injury are as follows: Motion artifacts simulating a subcapsular hematoma, volume averaging, splenic clefts or lobulation and peri-splenic fluid collection caused by ascites mistaken as hemoperitoneum, streak artifacts, premature scanning before the portal venous phase resulting in heterogeneous splenic enhance­ment, etc. A sequel of splenic hematoma/laceration is the splenic pseudocyst, which appears as simple intrasplenic fluid collection of 20–30 HU and a fibrous capsule.

LIVER AND BILIARY TRACT The liver is the second most frequently injured solid abdominal organ after spleen. The right lobe is injured more frequently and severely than the left and posterior

Chapter 69 Imaging in Abdominal Trauma

segments are more frequently injured than anterior. As with spleen, CT is currently the diagnostic modality of choice for the evaluation of blunt liver trauma in hemodynamically stable patients. Computed tomography is the most accurate technique in detecting, defining and characterizing the hepatic injury, associated hemoperitoneum and other abdominal abnormalities. Computed tomography based liver injury grading system established by the AAST is the most widely used grading system.13

Laceration: 1–3 cm in parenchymal depth, 50% surface area or expanding or ruptured subcapsular hema­toma with active bleeding; intraparen­chymal, >10 cm or expanding or ruptured. Laceration: >3 cm in parenchymal depth. Grade IV: Hematoma : Ruptured intraparenchymal hematoma with active bleeding. Laceration: Parenchymal disruption invol­ving 25–75% of a hepatic lobe or one to three Couinaud segments within a single lobe. Grade V: Laceration: Parenchymal disruption invol­ ving >75% of a hepatic lobe or more than three Couinaud segments within a single lobe. Vascular: Juxtahepatic venous injuries (i.e. retro­ hepatic vena cava or central major hepatic veins). Grade VI: Vascular: Hepatic avulsion. Majority (80%) of liver injuries cause hemoperitoneum. The finding of integrity of the liver capsule is important because it correlates with amount of blood loss. The various CT manifestations of liver trauma are as follows: zz Subcap­sular hematomas: The appearance is same as that described above in splenic trauma. They are located most commonly in antero-lateral aspect of right lobe of the liver (Figs 9A and B). zz Parenchymal contusions and hematomas (Fig. 10) have same appearance as described above in splenic trauma. Acute hematomas show increased density (40–60 HU) relative to adjacent normal liver paren­chyma at unenhanced CT. zz Laceration is the most common type of liver injury. It appears as nonenhancing linear or branching areas usually at the periphery of the liver (Figs 11 and 12). Lacerations frequently travel along the vascular planes (portal vein branches and hepatic veins) and fissures

AAST Liver Injury Grading System Grade I: Hematoma: Subcapsular, 4 cm diameter. Plain abdominal radiography may show distinctive radiolucency, within a large soft tissue mass with lot of fat, in 10% of patients. Ultrasonography reveals highly, echogenic circumscribed mass (more echogenic than central fat). It may appear as echogenic fat within a tumor or isolated foci of echogenicity (Figs 27 and 28). If fat content is less or admixed with hemorrhage, the echogenicity of tumor is diminished and may appear as any other renal mass. Recent work has suggested that 32% of renal carcinomas are also highly reflective, although there are other pointers towards RCC, such as hyporeflective rim or focal small spotty areas of reduced central reflectivity. Another feature that helps in distinguishing an angiomyolipoma from a small RCC is posterior shadowing, seen in approximately 30% of AML, but is not seen in small hyper-reflective renal carcinomas. CT is the most accurate imaging technique for detection and characterization of angiomyolipomas.29,30 The lesions show low attenuation with fat measurements and presence of gross fat being typical for these. The ROIs are typically less than –10 HU. Thin slices are necessary to demonstrate fat in small AMLs because of volume averaging. Higher specificity may be obtained with threshold measurements of –15 to –30 HU. The fat may be interposed with solid components. A subset of lesions will not meet fat attenuation criteria due to volume averaging or hemorrhage, others are fat poor and rarely a well-differentiated RCC can mimic this appearance. CT pixel mapping,31 over a region of interest within the tumor may be useful to detect small quantities of fat. With pixel mapping, three to six contiguous pixels with negative HU averaging below –20 HU indicates intratumoral fat (Figs 29 31).

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The presence of typical AML in the contralateral kidney helps in the diagnosis. AMLs are usually well-marginated, but do not have a true capsule, the lesion is usually at the margin of the kidney and may expand beyond as a small hypodense wedge-shaped defect in the renal parenchyma. This wedgeshaped defect is diagnostic of angiomyolipoma. These lesions are vascular, large vessels may be identified. Intratumoral aneurysms may be present and AML’s exhibit moderate enhancement after IVC. Homogeneous and prolonged enhancement is a valuable predictor for differentiating AML with minimal fat from RCC. MRI will also demonstrate fat component of an angiomyolipoma. On MRI, AMLs have a characteristic high T1-signal and on fat saturated images exhibit a drop in signal. The use of in–phase and opposed phase imaging is also helpful in the diagnosis of angiomyolipoma. In AML,

a characteristic India ink artifact is seen at the interface between the mass and the normal renal parenchyma on opposed phase T1 images, whereas the central part of the lesion does not demonstrate changes in signal intensity compared with in phase images. This is useful in very small lesions in which direct comparison with T1 images with and without fat suppression may be difficult (Figs 32A to F). The appearance of AML on T2-weighted images is variable and depends on bulk fat present in the lesion. An AML composed of predominantly fat would demonstrate homogeneous highsignal at T2 single shot images. Lipid poor angiomyolipomas are frequently hypointense on T2-weighted images. This may help to differentiate from RCC which will be T2 hyperintense.32 Angiography may demonstrate multiple aneurysms and onion layer appearances. Approximately 58–75% of these lesions grow with time. Growth of an isolated AML without

Chapter 103 Imaging in Renal Tumors

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TS is less than those with TS and multiple lesions. Annual follow-up is recommended for asymptomatic lesions 3 cm solid mass is discovered, renal cell carcinoma (provided there is no fat on CT/MR protocols) is the most probable diagnosis and surgery is recommended. If the tumor is 1–3 cm in size, RCC is most likely though percutaneous biopsy may be required. Very small lesions

right) enlargement of the adrenal glands. Few ill-defined focal are seen in the liver and spleen also suggesting disseminated tuberculosis. Patient was put on ATT. CECT obtained 1 year later (B) reveals small, atrophic adrenal glands

A

C

B

Figs 18A to C: US (A), Axial CECT (B) and coronal MPRs (C) reveal an enlarged, heterogeneous right adrenal gland. Biopsy: Tuberculosis

Chapter 112 Imaging the Adrenal Gland

A

B

Figs 19A to C: Axial CECT (A) and coronal MPRs (B and C) of two different patients with Addisons’s disease reveal bilateral, calcified adrenal glands, suggesting granulomatous involvement

C

Fig. 20: Axial CT showing a low attenuating left adrenal mass with

Fig. 21: US of a preterm neonate showing bilateral enlarged adrenal

blood-fluid level suggestive of adrenal hemorrhage

glands, suggesting adrenal hemorrhage

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Section 4 Genitourinary Imaging

A

B

Figs 22A and B: Adrenal hemorrhage: CT shows asymmetrically enlarged adrenals with heterogeneous attenuation but no calcification. Follow-up CT after 5 years shows small right adrenal with dense calcification and atropic left adrenal

A

B

Figs 23A and B: Adrenal adenoma. (A) NCCT shows a low attenuating well-defined mass in the right adrenal (arrow). The attenuation value was 6 HU (B)

Adenoma versus Metastasis Adenomas are thought to represent non-neoplastic overgrowth of adrenocortical cells of zona fasciculata. They consist of cholesterol laden clear cells and contribute little to steroid production. The imaging features of functional and nonfunctional adenomas on CT or MRI are similar (Figs 23 to 26) except the functional ones are usually smaller at the time of presentation than nonfunctional tumors. They account for almost 90% of all incidentalomas.5 Tumors of the lung, kidney, breast, digestive tract, ovary and melanoma are the most common primary sites to metastasize to adrenals.4,5 Metastases are well-defined with heterogeneous density and a thin irregular enhancing rim

following intravenous contrast injection, commonly unilateral and usually larger than adenoma (Figs 27A to D). On MRI, they are hypointense on T1 weighted image and hyperintense on T2 weighted image, relative to liver intensity. It has been reported that 27% of patients with known malignancy have microscopic adrenal metastasis. However, the detection of an adrenal mass in a patient with known malignancy does not necessarily indicate metastatic disease and it may be a nonfunctional adenoma. CT features of adenoma include size less than 5.0 cm and well-defined margins with smooth contour (Figs 23 and 24). Adrenal metastasis may show large mass with heterogeneous density and irregular shape (Figs 27A to D). However, these features are not specific. It has been also reported that size

Chapter 112 Imaging the Adrenal Gland

A

B

C

Figs 24A to C: Adrenal adenoma. CECT (A) coronal MPR (B) and 15-minute delayed CT scan (C) show a mass in left adrenal gland (arrow) which showed 65% washout on the delayed scan

A

B

C

Figs 25A to C: Incidentally detected adrenal adenoma. Gradient echo T1W in-phase image (A) shows a hypointense nodule in right adrenal (arrow) which shows marked signal loss on the opposed phase image (B). The lesion is hypointense on T2W scan (C) also

A

B

Figs 26A and B: Adrenal adenoma. GRE T1W in-phase (A) and opposed phase image (B) showing drop in signal intensity of right adrenal lesion from 124 to 45 whereas spleen signal intensity changes from 83 to 80 only

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Section 4 Genitourinary Imaging

A

B

C

D

Figs 27A to D: Adrenal metastases. CECT abdomen (A) shows bilateral solid adrenal masses. CECT chest (B) and coronal MPRs (C and D) show mediastinal adenopathy in a patient of bronchogenic carcinoma

alone is a poor discriminator between benign adenoma and malignant mass.5,6 In recent years, several studies have reported two imaging criteria based on attenuation value and differences in vascular enhancement pattern to differentiate benign adenoma from adrenal metastasis.2,20 Adenomas have abundant intra cyto plasmic fat and therefore show low attenuation on non-contrast CT (Fig. 23). On the other hand, metastases have little intracytoplasmic fat and thus do not show low attenuation. A large region of interest covering the adrenal mass should be used but should not include periadrenal fat for measuring attenuation value. It has been reported that a threshold of 10 HU has 71% sensitivity and 98% specificity for characterizing adenoma versus meta stasis. 22 This specificity may be increa sed further if other features of size, shape and morphology are considered. Although 70% of adenomas have abundant lipid, the remaining are lipid poor and are difficult to characterize on a noncontrast scan.

If attenuation of the adrenal mass on noncontrast CT is 10 HU or less (Figs 9 to 23), the diagnosis is lipid rich adenoma and no further evaluation is required. If attenuation is more than 10 HU, the mass is indeterminate and requires further evaluation by contrast enhanced CT and 15 minutes delayed enhanced CT scan (Figs 24A to C).23 Adenomas enhance rapidly with intravenous contrast media and show rapid washout. Metastasis also enhance rapidly but the washout is delayed when compared to adenoma.18,20 It has been speculated that this difference in enhancement wash out in nonadenoma is possibly due to disturbed capillary permeability, with prolonged retention of contrast in the effective extracellular space. Adrenal masses with an attenuation value less than 30–40 HU on 15 minute delayed contrast enhanced CT are almost always adrenal adenomas.1,24 In addition to the delayed CT attenuation itself, it is also possible to calculate the percentage wash-out of initial enhancement. The patient is first scanned without contrast, then again at

Chapter 112 Imaging the Adrenal Gland

70 seconds, and then 15 minutes after contrast administration. Contrast wash-out can be quantified using Relative percentage wash out (RPW) and Absolute percentage wash out (APW) as follows: RPW= 100 × (Enhanced HU–Delayed HU)/Enhanced HU APW=100 × (Enhanced HU–Delayed HU)/Enhanced HU-Non-enhanced HU If the APW is greater than 60% and the RPW is greater than 40%20,23,24 lesion is labeled benign. This technique has a sensitivity of 88% and a specificity of 96% for the diagnosis of adenoma.1,20 On the other hand, metastases and adrenocortical carcinoma have relative contrast retention on delayed contrast-enhanced CT. It has been said that the relative washout percentage is more accurate for the differentiation of lipid poor adenomas from metastases than are the absolute attenuation values on delayed contrast enhanced scans.25 Dual energy CT: This is an emerging technique which has been used for determining bone mineral density and for evaluation of fatty liver. The difference in CT attenuation images acquired at 140 and 80 kVp is measured, and if the difference between the two kVp is more than 6 HU, it is suggestive of fat containing lesion.2 Magnetic resonance imaging: In recent years, MRI has become a problem solving modality for the characterization of indeterminate adrenal masses. When results on CT examination are equivocal, MRI is the next imaging modality for characterizing the lesion. Due to increased fluid content in adrenal cancer and metastases, these appear bright on T2 weighted MRI images. However, there is significant overlap between T1- and T2-weighted MRI images of adenoma and metastases. With the introduction of higher field strength magnets (1.5T), chemical shift imaging and dynamic gadolinium enhanced MR imaging has shown promising results with adrenal gland lesions characterization. Confident diagnosis of adenomas on MRI requires the addition of chemical shift imaging to the protocol. Chemical shift MR imaging has been used to differentiate adenoma from metastasis. This technique is based on the different resonance frequency rates of protons in fat and water molecules in a magnetic field. Two breath hold T1-weighted acquisitions are taken, first using a short echo time (TE 2.1 ms at 1.5 tesla) when the fat and water protons are out of phase and second in-phase acquisition using long echo time (TE 4.2 ms at 1.5 tesla). On most current MR scanners the in and opposed phase images can be obtained by one dual echo breath hold gradient echo sequence. The signal intensity on the in-phase image is derived from the signal of water plus fat protons while in the out of phase image, MR signal of water and lipid protons cancel each other out within a voxel. Therefore a mass containing intracellular lipid and water will show loss of signal in the out of phase images when compared

with in-phase image (Figs 25A to C). Thus, adenoma appears darker on out of phase image than on in-phase image, while metastasis will show no significant signal loss on out of phase image and the signal intensity remains unchanged.2,8,9 The sensitivity and specificity ranging from 81% to 100% and 94% to 100% respectively on chemical shift MR imaging for differentiating adenoma from metastasis have been reported.6,9,20 The loss of signal can be assessed visually using spleen as the internal control (Fig. 26). The liver should not be used as the internal reference as it may also show signal loss on opposed phase image when there is steatosis. The chemical shift change can also be detected by quantitative methods. Two ratios have been defined in CSI. 1 – [SI (in) – (opp)] SI Index = _____________________________ SI (in) and Adrenal to spleen ratio SI adrenal (opp)

__________________________

SI spleen (opp)

SI adrenal (in)

______________________

SI spleen (in)

SI index of >16.5% and adrenal to spleen ratio of 50 HU to near water density within several weeks. Bleeding may be intermittent resulting in a heterogeneous appearance. MRI is more useful in determining the content of retroperitoneal fluid collections as it is more sensitive and specific for detection of blood products. An acute hematoma is isointense on T1-weighted and hyperintense on T2-weighted images. Within several days the signal gradually becomes hyperintense on T1-weighted images and a hematoma is then hyperintense on both T1and T2-weighted images with a developing, hypointense hemosiderin rim (Figs 9A and B).

Chapter 113 Retroperitoneum

A

Fig. 8: Perirenal hemorrhage. Axial CT image shows right perirenal hemorrhage (arrow) that occurred spontaneously from rupture of underlying renal angiomyolipoma

Abnormal perirenal fluid may be in either of two locations: within the renal capsule (subcapsular) or outside the capsule in the perinephric fat. Subcapsular fluid collections usually produce distortion of the renal parenchyma whereas perinephric collections do not. Urinomas result from obstructive uropathy and less frequently from abdominal trauma and surgical or diagnostic instrumentation. Retroperitoneal abscesses are particularly difficult to diagnose, because they may not exhibit the classic clinical features, i.e. fever, chills and an elevated white blood cell count. When an abscess is mature, its wall is thick and generally hypervascular. On contrast-enhanced CT, there is enhancement of the wall and the fluid is usually homogeneous and does not enhance. Many abscesses contain multiple septations. There may be substantial reactive inflammation in the surrounding fat. Abnormalities in the posterior pararenal space are much less common than abnormalities in the anterior pararenal space or the perirenal space. When present, these are most commonly the result of spread of pathologic processes in the pelvis. Causes can include hematoma, infection and neoplasm.

AORTA The most important abdominal aortic abnormalities are aneurysm formation and aortic dissection. MDCTA and MRA have gradually replaced conventional angiography as the procedures of choice for detailed evaluation of the aorta.

Aortic Aneurysm Most abdominal aortic aneurysms result from atherosclerosis. Other causes include trauma, infection, Takayasu’s arteritis,

B

Figs 9A and B: Spontaneous retroperitoneal hemorrhage in a patient on anticoagulant therapy. (A) Axial T1-weighted MR image shows a well-defined hyperintense lesion anterior to the left psoas. It is partially decompressing into the parietes; (B) Coronal T2-weighted image shows heterogeneous, predominantly high signal intensity within the mass. There is a markedly hypointense peripheral rim (arrow) due to hemosiderin deposition. These T1 and T2 signal intensities are diagnostic of a subacute hematoma

cystic medial necrosis and syphilis. The infrarenal aorta is the most common site of abdominal aortic aneurysms accounting for 95% of cases. If untreated, these aneurysms may enlarge and rupture with a mortality of 50–90%.12 The abdominal aortic aneurysm may show curvilinear calcification on plain abdominal radiography. On ultrasonography (US), CT and MRI the aneurysm is identified as focal area of dilatation exceeding 3 cm in size. Spontaneous rupture is a frequent complication of aneurysms measuring 6 cm or more in diameter. Therefore, most aneurysms larger than 6 cm require surgery. Important diagnostic information needed for management includes location, diameter of aneurysm, its longitudinal length, its relationship to the renal, common iliac and femoral arteries and assessment of the periaortic tissues for perianeurysmal fibrosis.13 US is a good

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Section 4 Genitourinary Imaging

crescent-shaped area of hyperattenuation within an abdominal aortic aneurysm represents an acute intramural hemorrhage and is another CT sign of impending rupture. Draping of the posterior aspect of an aneurysmal aorta over the vertebrae is associated with a contained rupture.14 The preferred surgical treatment of abdominal aortic aneurysms is an end-to-end anastomosis with aortic graft repair. Complications of abdominal aortic surgery that can be detected on CT include graft infections, aorto-enteric fistulae, anastomotic aneurysms, graft leak or rupture.

Aortic Dissection

Fig. 10: Abdominal aortic aneurysm. Dynamic, contrast-enhanced axial CT image shows markedly dilated abdominal aorta with a large eccentric thrombus. A conventional angiogram on this patient would significantly underestimate the size of the aneurysm as only the patent part of the lumen containing flowing blood would be opacified

modality for initial evaluation of aortic aneurysm. It may also be used for follow-up of patients who do not undergo surgical repair. However, CT and MRI are preferred techniques for evaluating the size, extent and complications of aneurysms. At several centers, CT angiography has replaced conventional angiography because it is less invasive and can provide all the necessary information required for the management. Angiography frequently underestimates the dimensions of an aneurysm because it shows only the flowing blood in the lumen and does not show mural thrombus, which is detected on CT (Fig. 10). Contrast-enhanced 3D gradient echo MRA demonstrates the full extent of the aneurysm and its relationship to aortic branches. Aneurysm rupture or leak is indicative of high morbidity and mortality if it is not promptly treated. CT findings of ruptured abdominal aortic aneurysms are often straightforward. Most ruptures are manifested as a retroperitoneal hematoma accompanied by an abdominal aortic aneurysm. Periaortic blood may extend into the perirenal space, the pararenal space, or both. Intraperitoneal extravasation may be an immediate or a delayed finding. Discontinuity of the aortic wall or a focal gap in otherwise continuous circumferential wall calcifications may point to the location of a rupture. There usually is a delay of several hours between the initial intramural hemorrhage and frank extravasation into the periaortic soft tissues. It is difficult to identify contained or impending ruptures. A small amount of periaortic blood may be confused with the duodenum, peri-aneurysmal fibrosis, or adenopathy. Imaging features suggestive of instability or impending rupture include increased aneurysm size, a low thrombus-to-lumen ratio and hemorrhage into a mural thrombus. A peripheral

Aortic dissection usually originates in the thorax but sometimes extends into the abdomen. Mortality rate of untreated dissection is very high approaching 25% at 1 day, 50% at 1 week and 75% at 1 month.15 The strategy for therapy is dependent on factors like the type and extent of dissection, the site of entry, involvement of aortic branches, patency of the false lumen and the presence of thrombus in the false lumen. Currently, the noninvasive modalities that are most frequently used to detect aortic dissections are US, CT and MRI. US, including transthoracic echocardiography and transesophageal echocardiography, is widely available and can be performed quickly and easily at the bedside. Thus, US can be used in most patients with aortic dissections, even in relatively unstable patients. However, US has major shortcomings, namely, a limited field of view and a diagnostic accuracy that largely depends on the investigator’s experience. Furthermore, US does not provide images that can be used to plan therapy. Multidetector CT has the advantages of shorter scanning times, wide availability and high diagnostic accuracy and has, therefore, classically been the modality of choice for the evaluation of aortic dissection. In the past, emergency MR imaging evaluation of aortic dissection has been impossible owing to prolonged examination times, but the advent of 3D contrast-enhanced MRA has changed this paradigm. Contrast-enhanced MR angiography has largely replaced unenhanced MR angiographic techniques and has dramatically shortened the total examination time required for confident diagnosis of aortic dissections; however, it is more suitable for stable patients. In principle, contrastenhanced MR angiography is similar to CT angiography. Both modalities provide excellent evaluation of aortic dissections. In patients without contraindications for either modality, at most centers, the use of each modality is based on equipment availability, the personal preference of the radiologist or referring physician and patient acceptance. Confident diagnosis and correct classification of aortic dissection is based on the detection of an intimal flap in the aorta that separates the true and false lumina (Fig. 11). Such a flap manifests as a hypointense line with a linear, arc, or S shape in the axial plane. The true and false lumina can be differentiated on the basis of signal intensity, morphologic

Chapter 113 Retroperitoneum

Fig. 11: Thoracoabdominal aortic dissection. Axial CT angiogram easily demonstrates the linear intimal flap between the anterior true lumen and posterior false lumen. Active extravasation into the retroperitoneum is also seen

Fig. 12: Congenital polysplenia with IVC anomaly. CT scan shows

features, the relationship between the lumina and the appearance of thrombosis. z Signal intensity: Similar to CT angiography, contrastenhanced MRA shows the true lumen with higher signal intensity than the false lumen owing to a higher concentration of contrast material during the arterial phase. z Morphologic features: The true lumen is usually smaller than the false lumen and would be thin or flat from being pressed, appearing oval in the axial plane. The false lumen is expanded or very large, appearing crescentic or winding around the true lumen in the axial plane. z Relationship between the lumina: The lumina may be parallel to each other, the false lumen may wind around the true lumen, or the true lumen may look like a ribbon floating in the false lumen. z Appearance of thrombosis: The false lumen usually contains a thrombus, especially at the retrograde end of the initial entry site, whereas the true lumen contains no thrombus in most cases.

Congenital Anomalies

INFERIOR VENA CAVA Mostly a routine CT or an MR abdominal protocol employing pre- and postcontrast SGE images provides sufficient evaluation of the IVC for patient management. At least one MR sequence should be performed in the sagittal or coronal plane, because it permits direct visualization of the longitudinal extent of IVC. However, when detailed evaluation of retroperitoneal veins is required, it is prudent to obtain CT or MR venography.

multiple splenenculi and interrupted IVC with hemiazygos venous continuation. Linear density (arrow) seen lateral to the right crus is part of the right adrenal gland

Congenital abnormalities of the IVC and related veins are common. Preoperative knowledge of the presence of these anomalies is helpful, particularly in patients undergoing a portasystemic shunt procedure, aortic surgery or nephrectomy and reduces the risk of major venous hemorrhage associated with these anomalies.16 CT and MRI are well suited to determine whether rounded or tubular retroperitoneal structures are vascular in nature. Some of the developmental anomalies of inferior vena cava are: Interruption of inferior vena cava with azygos and hemiazygos vein continuation (Fig. 12), left-sided inferior vena cava, duplication of the inferior vena cava, and anomalies of the left renal vein, e.g. circumaortic or retroaortic left renal vein.17 Retrocaval ureter is thought to be due to persistence of right posterior cardinal vein with failure of development of the infrarenal right supracardinal vein. It occurs with a frequency of 0.2 per thousand population. In retrocaval ureter the proximal right ureter courses medially behind the inferior vena cava, usually at L3 vertebral level and then courses anteriorly around the cava to partially encircle it. The anomaly is characterised by hydronephrosis and medial deviation (fish hook deformity) of the middle ureteral segment.

Venous Thrombosis Inferior vena caval thrombus may result from proximal extension of thrombi from lower extremity, pelvis or renal veins. Intracaval tumor extension may occur via veins

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draining neoplasms, such as renal cell carcinoma, hepatoma or adrenal carcinoma. CT and MRI perform well in evaluating IVC thrombosis and distinguishing tumor from bland thrombus.18 Tumor thrombus shows anatomic contiguity and an enhancement pattern identical to that of primary tumor (Fig. 13). The bland thrombus does not enhance with contrast. Depiction of the supradiaphragmatic extent of the thrombus into the right atrium is important for surgical planning as it requires combined thoracoabdominal surgery, whereas thrombus that ends below the hepatic veins may require only an abdominal approach.19

In cases of chronic venous thrombosis, the affected vessel may not be identified if the thrombus is organized and contacted. In these cases, careful evaluation reveals the absence of a vein in the expected location in combination with the presence of collateral vessels.

Primary Tumors of the IVC Primary tumors of the inferior vena cava are rare. Leiomyoma, endothelioma or leiomyosarcoma may arise as a primary neoplasm of the caval wall.20 The tumor is usually seen as a filling defect, which may be associated with venous expansion and enhancement of the tumor wall on CT scan (Figs 14A and B). Signal intensity of these tumors is moderately low on T1-weighted images and mixed to high on T2-weighted images. Areas of intermixed tumor and blood products may show bright signal intensity on T1-weighted images. MPRs in the sagittal or coronal plane are useful for demonstrating the craniocaudal extent of the tumor. Collateral vessels such as azygous and hemiazygous veins may be enlarged.

LYMPH NODES

Fig. 13: IVC thrombus: Axial contrast-enhanced CT image in a 57-year-old man shows a large right renal cancer extending into the right renal vein and the IVC. The mass within the distended IVC is of the same attenuation as the primary tumor

A

Normal lymph nodes appear as small, rounded soft tissue masses adjacent to the great vessels. Retrocrural, paraceliac, gastrohepatic para-aortic, aortocaval, periportal, peripan creatic, external and internal iliac groups together constitute the retroperitoneal nodes. Presently, CT is the most frequently used imaging technique for evaluation of enlarged retroperitoneal nodes. The diagnosis of lymph node abnormalities on CT is based on size and image morphology. Size of a node is best determined by measuring its

B

Figs 14A and B: IVC leiomyosarcoma. (A) Contrast-enhanced CT scan of the upper abdomen shows a large, mildly enhancing mass within the hepatic portion of the IVC; (B) Coronal multiplanar image reconstructed from CT data better depicts the craniocaudal extent of the mass and the dilated venous collaterals (arrow)

Chapter 113 Retroperitoneum

short axis diameter. The retroperitoneal lymph nodes are considered abnormal if their size is more than 10 mm, except in the retrocrural space where the upper limit is 6 mm. A variety of retroperitoneal structures can be confused with enlarged lymph nodes, including unopacified loops of bowel, vascular collaterals, dilated lymphatics and retroperitoneal fibrosis. Careful evaluation of serial CT images after oral and intravenous contrast is helpful in distinguishing between these structures. MR sequences suited for detection of lymph nodes include precontrast T1-weighted spin-echo or SGE, fat-suppressed T2-weighted turbo spin-echo and contrast-enhanced fatsuppressed sequences. The enlarged lymph nodes appear low in signal on precontrast SGE in a background of high-signal fat and nodes are moderately high in signal on fat-suppressed T2-weighted and contrast-enhanced T1-weighted images. Fat-suppressed T2-weighted images are very sensitive for the detection of lymph nodes and perform better than CT, particularly in pediatric patients or other patients with paucity of retroperitoneal fat.

Benign Lymphadenopathy

Whipples disease, lymphomatous or metastatic nodes following radiotherapy and chemotherapy. Enlarged retroperitoneal nodes have also been observed in 30% of patients with sarcoidosis. 22 The periportal, paraceliac and para-aortic groups are most often involved. On CT, the nodes affected by sarcoidosis generally show homogeneous soft-tissue attenuation and remain discrete. Nodal calcification is unusual in sarcoidosis. Castleman disease is occasionally also associated with retroperitoneal lymph node enlargement. Mostly the CT or MR appearance of these enlarged lymph nodes is not specific. However, identification of intense and uniform contrast enhancement in lymph nodes can suggest the diagnosis (Fig. 16).23 Lymphangioleiomyomatosis is a rare cause of bulky retroperitoneal lymphadenopathy. This is a progressive disease involving the lung, lymphatic trunks and lymph nodes, typically affecting young women of child-bearing age. Sometimes, it can primarily involve retroperitoneum with or without subsequent development in the lungs.24 On CT scans, the enlarged lymph nodes may show cystic, low-attenuation components.

Benign lymphadenopathy may occur secondary to inflammatory or infectious disease. Lymphadenopathy is the most common manifestation of abdominal tuberculosis.21 The mesenteric, omental and peripancreatic lymph nodes are most commonly involved. The nodes commonly demonstrate peripheral enhancement with central areas of low attenuation after intravenous contrast administration (Fig. 15). Discrete homogeneous lymph nodes may also be seen in some cases. Calcification is frequently seen in tubercular lymph nodes. Enlarged lymph nodes with low density centers may also be seen in pyogenic infections,

Lymphoma

Fig. 15: Retroperitoneal tubercular lymphadenopathy. Axial CT

Fig. 16: Castleman disease. Contrast enhanced axial CT image shows

image shows enlarged periportal and portocaval lymph nodes with characteristic central necrosis and peripheral rim enhancement

large, well-defined, markedly enhancing para-aortic lymph nodes (arrows) compatible with the diagnosis of Castleman disease in an 8-year-old boy

Abdominal lymph nodes are involved in 50% of the non-Hodgkin’s lymphoma (NHL) patients as against 25% of those with Hodgkin’s disease (HD) at presentation.25 Mesenteric involvement is seen in more than half of the NHL patients (versus 5% of those with HD). The patterns of lymphadenopathy are also markedly different, slight enlargement of upper para-aortic nodes and contiguous spread being characteristic of HD. NHL on the other hand manifests with bulky lymph nodes in multiple locations.

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Fig. 17: Non-Hodgkin lymphoma. Contrast enhanced Axial CT image shows large, confluent lymph nodal mass in the preaortic location. The celiac axis branches are engulfed by the mass but their patency is preserved

The enlarged lymph nodes may appear as discrete masses or as confluent soft tissue mass obliterating the retroperitoneal fat (Fig. 17). Lymphomas are ‘soft’ tumors and frequently surround the adjacent vessels (floating aorta sign) and ureters without compressing their lumina. Lymphomas are homogeneous, with minimal contrast enhancement and relatively low signal intensity at T2-weighted images representing densely packed cellular components. Nodes are rarely calcified ( 10,000

IIC (S3)

hCG > 50,000

All IIIC

None (seminoma is never classified as poor outlook)

LDH > 10

homogeneous, whereas NSGCTs are heterogeneous on MRI. Lymphoma and leukemia show testicular enlargement with decreased T2 signal, in a homogeneous and diffuse pattern. MRI is also useful in staging work-up of testicular tumors when CT is inconclusive or contraindicated. It is also useful for follow-up after the treatment.

CT CT is most commonly used for evaluation of tumor spread, staging and follow-up. CT is useful for detection of enlarged retroperitoneal or mediastinal lymph nodes as well as extranodal metastases in lungs and liver. In testicular carcinoma, even subcentimetric nodes are suspicious especially when seen in the regional nodal drainage site (e.g. aortocaval location on right side or renal hilum on the left) (Fig. 14). 7 mm as a cutoff has been suggested as more useful for nodal involvement in testicular cancer. 29 The enlarged lymph nodes may demonstrate necrotic center or heterogeneous contrast enhancement, particularly in NSGCTs. After completion of the treatment, some lymph nodes may not decrease in size and instead, develop more necrosis and fibrotic strands. Majority of such lymph nodal masses do not contain viable tumor; however, it cannot be ruled out on the basis of CT alone.

PET The role of fluoro-D-deoxyglucose positron-emission tomography (FDG-PET) in testicular tumors include three specific settings:

Fig. 14:  Axial CECT image at the level of renal hilum showing a

large metastatic homogeneous lymph nodal mass (star) in a case of seminomas testis

1. After chemotherapy in distinguishing active disease from fibrosis/mature teratoma. 2. After orchidectomy in primary disease staging and assessment and when there is elevation of tumor markers; looking for recurrence. 3. Predicting response to treatment. PET is more sensitive and specific for disgnosing recurrent disease at local and remote sites especially in patients with residual tumor masses or increasing tumor marker following treatment.40 Further investigation is needed to determine its eventual place as an imaging modality for staging at diagnosis. The

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exact role of PET in determining the prognosis of disease is not clearly defined in testicular malignancy but the initial results appear promising.

BENIGN INTRATESTICULAR LESIONS Cysts Testicular cysts are incidentally detected on sonography. These need to be differentiated from cystic tumors. Symptomatic or palpable testicular cysts or those with suspicious solid component need further evaluation and/or exploration. Others can be followed-up. Two types of simple benign cysts can be identified—cysts of tunica albuginea and simple testicular cysts. Tunica albuginea cysts are typically small (70

≥140

≥170

and Donnelly et al. in phantom studies.30,31 Selection of the most appropriate mA is a compromise between image quality and radiation dose. Phantom experiments have shown that an increase in mAs will always result in a decrease in image noise and thus an improvement in image quality. But at high tube current settings the gain in image quality will not be significant. Tube current should be adjusted to provide the lowest dose consistent with adequate diagnostic quality. A technique chart that relates current to patient’s weight is appropriate. Scan time can be shortened by more rapid gantry rotation or by decreasing beam rotation to less than a full 360°. In general, the fastest scan time that uses full rotation should be used.31-33 Similarly, it has been seen that radiation dose in helical CT is inversely proportional to the pitch used. When pitch is doubled, radiation dose gets halved.31 The dose increase caused by increasing kilovoltage is not linear, and is greater than often appreciated. An increase from 120–140 kVp increase dose by approximately 40%. Pediatric patients are rarely large enough to warrant the use of increased kVp.33 Newer multidetector CT scanners are equipped with automatic exposure control system (AEC) under different names (Care dose 4D, Dose right, AutomA, etc.). These dose modulation systems work in various ways, so as to adjust the radiation dose according to the patient’s body size and attenuation. AEC reduces the patient’s dose without compromising image quality. 34,35 The radiation dose is essentially reduced by controlling the tube current which is performed by three methods. These methods are based on: (a) patient size, (b) z-axis, and (c) angular or rotational AEC. Most of the scanners use combination of all these methods.35 The scanner uses the projection radiograph data (topogram/ scanogram) to assess size and attenuation of patient and accordingly dose is modulated using patient size and z-axis. In angular AEC, the dose is modulated so as to equalize the photon flux to the detector while the tube is rotating. This is needed because the human body is noncircular, and hence

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A

B

Figs 3A and B:  CT head: (A) At 94 mA and (B) at 206 mA. No significant difference in overall image quality. Radiation dose in A is 50% of B

the attenuation of the beam varies at different projections. Generally, lateral projections are more attenuating than AP projections. By using AEC, there is considerable reduction in the magnitude exposure dose, in the range of 35–60%.36 AEC thus is helpful in reducing the patient’s dose, especially in pediatric cases. Despite these developments, following facts should always be taken into account while performing a CT in pediatric cases. In a neonate approximately 30% of the marrow is contained in the skull and the marrow absorbed dose for a CT brain examination in a 6 years old patient phantom has been reported to be even higher than that for a CT chest or abdomen examination. Therefore, high priority should be given to dose reduction measures for head scans in children. Results of a study in our department at AIIMS also showed that a reduction of mAs from 115 or 141 mAs to 77 or 94 mA, which represents a 53–65% reduction in dose did not result in any significant difference in diagnostic accuracy although there was a slight reduction in image quality which was also not statistically significant,37 (Figs 3A and B). Chest is a naturally high contrast area because of large attenuation differences that result from the presence of air in lungs and fat in mediastinum. Scans of objects with large differences in attenuation values such as lungs are less likely to be sensitive to image noise as image noise mainly affects low-contrast resolution. So, low doses may be used. Low radiation dose technique was used by Rogalla et al. in their study of chest CT. Rogalla et al. had found that although there is no consensus regarding which mA setting may be regarded as ideal low dose technique for spiral CT scanning of pediatric chest, 25–75 mAs is sufficient for lung window and 50–75 mAs for mediastinal window. A mA of 77 (57.5 mAs) time represents a nearly 67% reduction in dose as compared to mA of 240 (180 mAs) with no significant loss of diagnostic information.38 Our departmental study also

showed similar results37 (Figs 4A and B). Now-a-days, most of the modern scanners provide CT dose index (CTDI) which is the most commonly used dose indicator. It does not provide the precise dose, rather it is an index of dose measured using a phantom. However, CTDI may greatly help in comparing radiation dose at different scanning parameters.35 Various manufacturers provide multiple protocols for different examination and as per the age of patient. Hence when imaging for children, pediatric protocols should be followed. Ideally, all institutions must set their own scanning protocol, involving various parameters (tube voltage, tube current, slice thickness, collimation and pitch) optimized as per the use. The important point to remember is that different manufacturers use different techniques for dose modulation so the user should know about the system’s characteristics before trying to attempt any change in scanning parameters.39 Any changes should be performed using appropriate (weight range) phantoms. Recently dual energy CT scanners have been introduced which are faster and have ability to provide greater information about tissue composition than obtained by single energy scanners. Although not much is known about its use in pediatric cases, however, with dual energy scanners noncontrast CT scans are not needed as contrast media can be subtracted, and the patient is spared the radiation dose of a second scan.

USE OF CONTRAST MEDIA Contrast media available for intravenous (IV) use in radiography are categorized as high-osmolality contrast media (HOCM), low-osmolality contrast media (LOCM) and isosmolar contrast media (IOCM). Considerations in choice amongst these are the concentration of iodine achieved within plasma and urine, economic factors, and safety factors.

Chapter 121 Technical Considerations in Pediatric Imaging

A

B

Figs 4A and B:  Chest CT: (A) At 240 mA and (B) at 77 mA. Image quality is comparable while radiation dose in B is less than one-third of that in A

High Osmolality Contrast Media

Iso-osmolar Contrast Agents

High osmolality contrast media (HOCM) have an iodine content ranging from 280 to 480 mg/mL and an osmolality range from 1,400 to 2,500 mOsm/kg. Dosage of contrast material is based upon grams of iodine administered in relation to body mass. It is appropriate to use a dosage of approximately 300 mg of iodine per kilogram. This represents approximately 1.0 mL/kg in the most commonly used forms of diatrizoate or iothalamate. The total dose for excretory urography or for CT is usually 2.0 mL/kg in children or 3.0 mL/kg in the newborn. Speed of injection is important for the resultant plasma concentration of contrast material. After rapid injection, there is an increase in serum osmolality within 3 minutes, a decrease in serum sodium concentration, and an increase in heart rate. The osmotic effect is particularly significant in young infants. A mean increase of 3% in serum osmolality is observed in adults. Excretion occurs rapidly by renal glomerular filtration. Because of a high osmotic load, these contrast media also produce diuresis, opposing tubular resorption.38

Iso-osmolar contrast media (IOCM) has an iodine content ranging from 270–320 mg/mL and an osmolality of 290 mOsm/kg. Initial-reports showed that the IOCM reduces the risk of contrast-induced nephropathy (CIN) in patients with deranged renal parameters. However, recently various metaanalysis of randomized control trials have shown that there is no statistically significant reduction in CIN-associated with iodixanol as compared to LOCM. 39,40 Hence, with this equivocal kind of reports IOCM offers no significant advantage over LOCM. Unlike HOCM, LOCM and IOCM have little or no effect on serum osmolality, serum sodium, vasodilation, hemodilution, red blood cell morphology, or vascular permeability. There is little or no effect on the blood-brain barrier, fewer electrocardiographic changes, and fewer alterations in myocardial contractility, cardiac output, and left ventricular, pulmonary artery, and aortic pressures. There is less endothelial damage, and lower release or activation of vasoactive substances including complement activation, histamine release, and acetylcholinesterase inhibition. Diminished effects on coagulation pathways have been demonstrated. These effects are attributed to the lower osmolality and the reduced chemotactic effect of the molecules. Of importance is reduction in the nephrotoxic effect noted with HOCM. Hence, there are definite advantages to adoption of LOCM. A major consideration is degradation of the resulting examination resulting from pain, heat or vomiting with HOCM.38 Performing a multiphasic CT scans in neonate and infants may be challenging, as the IV cannula is of smaller gage limiting the injection rate of power injector, moreover only

Low Osmolality Contrast Agents Low osmolality contrast agents have an iodine content ranging from 128–320 mg/mL and an osmolality range from 290–702 mOsm/kg. Agents with low iodine content are most suitable for intra-arterial digital subtraction arteriography. Those with iodine content of 240–300 mg/mL are used for excretory urography, venography, venous injection digital subtraction arteriography, and bolus IV enhancement for CT scans. The contrast media with high iodine content, 320–370 mg/mL, are used for aortography and selective arteriography.

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small amount of IV contrast can be used depending on the weight of the child. These situations may be handled by: (1) Using bolus tracking and saline chasing technique and, (2) Large bore cannula.41,42 An injection rate of 2–3 mL/sec is safe and provides good results.40 Although there is no consensus, but contrast may be administered using central venous line with a maximum injection rate of 2 mL/sec.41

MR Contrast Agents The most commonly used contrast agents are paramagnetic substances and amongst these gadolinium diethylenetriamine penta-acetic acid (Gd-DTPA) dimeglumine is most frequently used. Gd-DTPA is excreted by glomerular filtration with 90% excreted within 24 hours. Rapid renal clearance, and low toxicity are important features of this contrast material. The clinical dose of Gd-DTPA is 0.1 mmol/kg. It has an osmolality of 1,900 mOsm/kg. However, the high osmolality is of little importance because of the small volume administered.38,43 Although, gadolinium-enhanced MRI was once considered one of the safer imaging procedures, but recently there has been a significant concern regarding nephrogenic systemic fibrosis (NSF) associated with gadolinium-based contrast agents. The identified risk factors associated with development of NSF include—administration of a high dose of gadolinium– based contrast agent, acute or chronic renal failure, venous thrombosis and coagulopathy and vascular surgery.44,45 Some additional guiding principles for use of contrast in the neonates are: zz Use warm contrast for maintenance of body temperature. zz Use iso-osmolar positive, non-ionic contrast in most instances. zz When giving oral or rectal contrast, use low-osmolar, nonionic agents instead of barium to avoid barium contamination of the peritoneal cavity. zz Do not give contrast blindly; oral contrast may be aspirated, and rectal contrast may get into peritoneal cavity via a perforation. Even in the intact bowel, the contrast may not progress distally as quickly as predicted and therefore may lead to unnecessary radiographs. zz Be judicious in the volume of contrast administered. Renal function in neonates is less than in babies over 1 month of age, therefore excretion of contrast may be delayed. zz Gadolinium is the preferred contrast agent for magnetic resonance imaging. However, it should be used with a caution.43-47 In conclusion the aim of all departments and radiologists dealing with pediatric imaging should be to achieve a diagnostically adequate radiograph or examination, with minimum radiation exposure and discomfort to the child. This goal can only be achieved, if the radiologists and technicians in charge are committed to quality control programs, and are aware of the necessity for radiation protection in children.

REFERENCES 1. Levick RK, Spriqq A. In: Whitehouse GH, Worthington BS (Eds): Pediatric Radiology in Techniques in Diagnostic Imaging, 3rd edition. 1996. pp. 389-404. 2. Tani S, Mizuno N, Abe S. Availability and improvement of a vacuum-type immobilization device in pediatric CT. Abstract in English on pubmed. Nippon Hoshasen Gijutsu Gakkai Zasshi 2002; 58(8):1073-79. 3. Bontrages KL. Pediatric Radiography in Textbook of Radiographic Positioning and Related Anatomy, 5th edition. St Louis: Mosby; 2001. pp. 629-64. 4. Frush DP, Bisset GS. Sedation of children for emergency imaging. RCNA. 1997;35(4):789-97. 5. Chudnofsky C, Krauss B, Brustowic Z (Eds). Sedation for Radiologic Imaging in Pediatric Procedural Sedation and Analgesia Maryland, USA: Lippincott Williams and Wilkins; 2001. pp. 169-78. 6. Lim-Dunham JE, Narra J, Benya EC, et al. Aspiration following oral contrast administration for pediatric trauma CT scans [abstract 46]. In 82nd Scientific Assembly and Annual Meeting, Radiological Society of North America. Chicago, Radiological Society of North America. 1996. p. 137. 7. Ziegler MA, Fricke BL, Donnelly LF. Is administration of enteric contrast matrial safe before abdominal CT in children who require sedation? Experience with chloral hydrate and pentobarbital. AJR. 2003;180(1):13-5. 8. Iwata S, Okumura A, Kato T, et al. Efficacy and adverse effects of rectal thiamylal with oral triclofos for children undergoing magnetic resonance imaging. Brain Dev. 2006;28(3):175-7. 9. Frush DP, Bisset GS, Hal SC. Pediatric sedation in radiology: The practice of safe sleep. AJR. 1996;167:1381. 10. Pierce DA, Preston DL. Radiation-related cancer risks at low doses among atomic bomb survivors. Radiat Res. 2000;154:178-86. 11. Slovis TL. Executive summary, ALARA Conference: Pediatr Radiol. 2002;32:221. 12. Schneider K. Radiation Protection in pediatric radiology: How important is what? In syllabus of 20th Postgraduate Course European Society of Pediatric Radiology. 1997; 95-101. 13. Protection of the patient in diagnostic radiology: Summary of the current ICRP principles, by Atomic Energy Regulatory Board: Mumbai. 1987;3-16. 14. Gonzalez L, Vano E, Ruiz MJ. Radiation dose to pediatric patients undergoing micturating cystourethography examinations and potential reduction by radiation protection optimization. Br J Radiol. 1993;68:291-5. 15. Martin CJ, Darragh CL, Mc Kenzie GA, et al. Implementation of a program for reduction of radiographic doses and result achieved through increase in tube potential. Br J Radiol. 1993;66:228-33. 16. Mooney R, Thomas PS. Dose reduction in a pediatric X-ray department following optimization of radiographic technique. Br J Radiol. 1998;71:852-60.

Chapter 121 Technical Considerations in Pediatric Imaging 17. Kohn MM, et al. Guidelines on Quality Criteria for Diagnostic Radiographic Images in Pediatrics. CEC Directorate General XII/D/3, Brussels, 1996. 18. Uffmann M, Schaefer-Prokop C. Digital radiography: The balance between image quality and required radiation dose. Eur J Radiol. 2009;72(2):202-8. 19. Willis CE. Optimizing digital radiography of children. Eur J Radiol. 2009;72(2):266-73. 20. Fearon T, Vucich J. Normalized pediatric organ absorbed doses from CT examinations. AJR. 1987;148:171-74. 21. Nicholson RA, Thornton A, Akpan M. Radiation dose reduction in pediatric fluoroscopy using added filtration. Br J Radiol. 1995;68(807):296-300. 22. Bogaert E, Bacher K, Lapere R, et al. Does digital flat detector technology tip the scale towards better image quality or reduced patient dose in interventional cardiology? Eur J Radiol. 2009;72(2):348-53. 23. Chida K, Inaba Y, Saito H, et al. Radiation dose of interventional radiology system using a flat-panel detector. AJR. 2009;193(6):1680-5. 24. Shah R, Gupta AK, Rehani M. Evaluation of radiation dose to children undergoing radiological examinations and reduction of dose by protective methods. (Unpublished data) Department of Radio-diagnosis, AIIMS, 2002. 25. Schneider K. Evolution of Quality assurance in pediatric radiology. Radiation Protection Dosimetry. 1995;57:119-23. 26. Fendel H, Schineider K, Bakowski C, et al. Specific principles for optimization of image quality and patient exposure in pediatric diagnostic imaging. BJR. 1990;20:91-110. 27. Fendel H. Die zehn Gebote des Strahlenshutzes bei der Rontgendiagnostikim Kindesalter. Pediatric Prax. 1976;17:339-46. 28. Fendel H, Schneider K, Schofer H, et al. Optimization in pediatric radiology: Are there specific problems for quality – assurance in pediatric radiology. Brit J Radiol. 1985;18:159-65. 29. Drury P, Robinson A. Fluoroscopy without the grid: A method of reducing the radiation dose. Br J Radiol. 1980;53(626):93-9. 30. Brenner DJ, Ellison CD. Estimated risks of radiation induced fatal cancer from pediatric CT. AJR. 2001;176:289-96. 31. Frush DP, Donnelly LF. Helical CT in children technical considerations and body applications: Radiology. 1998;209:37-48. 32. Fearon T, Vucich J. Normalized pediatric organ absorbed doses from CT examinations. AJR. 1987;148:171-4. 33. Kuhn JP, Brody AS. High resolution of CT pediatric lung disease. RCNA. 2002;40(1):89-110.

34. McCollough CH, Bruesewitz MR, Kofler JM. CT dose reduction and dose management tools: Overview of available options. Radiographics. 2006;26(2):503-12. 35. Lee CH, Goo JM, Ye HJ, et al. Radiation dose modulation techniques in the multidetector CT era: From basics to practice. Radiographics. 2008;28(5):1451-9. 36. Söderberg M, Gunnarsson M. Automatic exposure control in computed tomography: An evaluation of systems from different manufacturers. Acta Radiol. 2010;51(6):625-34. 37. Shah R, Gupta AK, Rehani MM, et al. Effect of reduction in tube current on reader confidence in pediatric computed tomography. Clinical Radiology. 2005;60(2):224-31. 38. Rogalla P, Stöver B, Scheer I, et al. Low dose spiral CT applicability to pediatric chest imaging. Pediatr Radiol. 1999;29:565-9. 39. Gudjónsdóttir J, Ween B, Olsen DR. Optimal use of AEC in CT: A literature review. Radiol Technol. 2010;81(4):309-17. 40. Currarino G, Wood B, Mayd. In: Silverman FN, Kuhn JP (Eds). Diagnostic Procedures: The Genitourinary Tract and Retroperitoneum in Caffey’s Pediatric X-Ray Diagnosis, 9th edition. St Louis: Mosby; 1993. pp. 1148-71. 41. From AM, Al Badarin FJ, McDonald FS, et al. Iodixanol versus low-osmolar contrast media for prevention of contrast-induced nephropathy: meta-analysis of randomized, controlled trials. Circ Cardiovasc Interv. 2010;3(4):351-8. 42. Heinrich MC, Häberle L, Müller V, et al. Nephrotoxicity of iso-osmolar iodixanol compared with nonionic low-osmolar contrast media: Meta-analysis of randomized controlled trials. Radiology. 2009;250(1):68-86. 43. Nievelstein RA, van Dam IM, van der Molen AJ. Multidetector CT in children: Current concepts and dose reduction strategies. Pediatr Radiol. 2010;40(8):1324-44. 44. Fleishmann D, Kamaya A. Optimal vascular and parenchymal contrast enhancement: The current state of the art. Radiol Clin North Am. 2009;47:13-26. 45. Slovin TL. In: Kuhn JP, Slovin TL, Halles JO (Eds). Neonatal Imaging: Overview in Caffey’s Paediatric Diagnostic Imaging, 10th edition. Penn Sylvania: Mosby; 2004. pp. 15-8. 46. Prince MR, Zhang HL, Prowda JC, et al. Nephrogenic systemic fibrosis and its impact on abdominal imaging. Radiographics. 2009;29(6):1565-74. 47. Juluru K, Vogel-Claussen J, Macura KJ, et al. MR imaging in patients at risk for developing nephrogenic systemic fibrosis: Protocols, practices, and imaging techniques to maximize patient safety. Radiographics. 2009;29(1):9-22.

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Recent Advances in Pediatric Radiology

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CHAPTER

Akshay Kumar Saxena, Kushaljit Singh Sodhi

INTRODUCTION The articles dwelling upon pediatric radiology are published not only in the radiology journals, but also in journals in the fields of allied specialties, like pediatrics and pediatric surgery. There is no strict definition of recent advances. For an avid reader, recent advances mean the literature published in last few months (say 1 year); for a research worker dedicated to a particular topic, only the articles published in that context would constitute recent advances while for a general radiologist, changing trends over last few years would qualify for recent advances. Given the vast plethora of articles available in medical literature and differing needs of radiologists, it is impossible to cater to the need of all. This chapter dwells upon some of the recent trends in speciality of pediatric radiology as applicable to Indian scenario. Readers are encouraged to update their knowledge by reading the recent journals.

RADIATION PROTECTION The children are known to be at high-risk for developing radiation-induced malignancies. This is because the growing tissues are more radiosensitive. In addition, children have long lifespan available to manifest the ill effects of radiation. Hence, there is a need to keep the radiation dose to the minimum possible level in children. An Alliance for Radiation Safety in Pediatric Imaging (Image Gently campaign) 1 has recently taken shape with the objective of making the imaging community aware of the need to adjust the dose of radiation when they are imaging the children. In late 2006, it was started as a Committee within the Society for Pediatric Radiology and currently encompasses 56 professional associations globally. This alliance aims at changing the practice. The initial focus of the alliance has been computed tomography (CT) scan as there has been dramatic global increase in number of CT scans being performed for children. The alliance website (www.imagegently.org) provides information for radiologists, parents, pediatricians, medical physicists and radiology technologists. The alliance has evoked widespread interest.

The website has already been visited over 300,000 times, the CT protocol has been downloaded more than 20,000 times and the pledge has been taken by 4,528 medical professionals. Recently, the alliance has started targeting radiation safety pediatric interventional radiology. It has been labeled “Image Gently, Step Lightly”. It encourages the radiologists to “Step Lightly” on the fluoroscopy pedal during the pediatric interventional procedures. It also encourages the radiologists to use ultrasound or magnetic resonance imaging (MRI) for guidance during interventional procedures. The image gently campaign has been named to the 2009 Associations Advance America Honor Roll. Sponsored by the American Society of Association Executives, this award recognizes the ways in which nonprofit associations contribute towards improving the quality of life in America. Detailed guidelines are now available for reducing radiation dose during fluoroscopy, CT scan and interventional procedures in children.2-4

NEURORADIOLOGY Computed tomography scan of head is commonly performed for head trauma in children. However, very few of these patients show CT evidence of intracranial injury. Since CT scan imparts high-radiation dose, it is desirable to minimize number of children who do not require CT scan after head trauma. Palchak and colleagues5 conducted a prospective observational study to derive a decision rule for identifying those children who were at low risk for traumatic brain injuries. They enrolled 2,043 children and evaluated clinical predictors of traumatic brain injury on CT scan and traumatic brain injury requiring acute intervention, defined by: (1) a neurosurgical procedure (2) antiepileptic medications for more than 1 week (3) persistent neurologic deficits or (4) hospitalization for at least two nights. CT scan was performed in 1,271 (62%) patients of which 98 (7.7%) had traumatic brain injuries on CT scan. 105 (5.1% of 2,043 enrolled patients) had traumatic brain injuries which requires acute intervention. Abnormal mental status, clinical signs of skull fracture, history of vomiting, scalp hematoma (in children ≤ 2 years of age), or headache identified 97/98 (99%) of those with traumatic

Chapter 122 Recent Advances in Pediatric Radiology

brain injuries on CT scan and 105/105 (100%) of those with traumatic brain injuries requiring acute intervention. Amongst the 304 (24%) children undergoing CT with none of these predictors, only 1 (0.3%) patient had traumatic brain injury on CT. This patient was discharged from the emergency department without complications. The authors concluded that absence of abnormal mental status, clinical signs of skull fracture, history of vomiting, scalp hematoma (in children ≤ 2 years of age), and headache were important factors for identifying children at low risk for traumatic brain injuries after blunt head trauma. Magnetic resonance imaging, diffusion tensor imaging (DTI) and MR spectroscopy are important constituents of evaluation of neonatal encephalopathy. Barkovich and colleagues6 performed serial MRI in 10 neonates to describe the time course of changes in various regions of the brain during the first 2 weeks of life. DTI and MR spectroscopy of most patients revealed a characteristic pattern of evolution during the first 2 weeks after birth. Although, the anatomic images were normal or nearly normal on the first 2 days after birth in most patients, some abnormalities were observed on DTI and spectroscopy. The parameters would worsen until about day 5 and then become normal, though there was persistence of abnormal metabolite ratios on spectroscopy in several cases. During the serial scans, the areas of reduced diffusion pseudonormalized in some parts, while new abnormal areas developed in other parts. Thus, the pattern of injury looked very different on serial scans. Liauw and colleagues7 evaluated the predictive value of diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) measurements for outcome in children with perinatal asphyxia. MRI was performed in term neonates within 10 days of life because of birth asphyxia. In survivors, developmental outcome until early school age was graded as: I (normal), II (mildly abnormal) and III (definitely abnormal). For analysis, category III and death (category IV) were labeled “adverse”, I and II were “favorable” and II-III and death were “abnormal” outcome. The study demonstrated that ADC values in normal-appearing basal ganglia and brainstem correlated with outcome independent of all MRI findings. However, ADC values in visibly abnormal brain tissue on DWI did not show a predictive value for outcome. Another study (by Vermeulen and colleagues), which evaluated DWI and conventional MRI in neonatal hypoxic ischemia reported DWI to be a useful additional MR tool to predict the motor outcome at 2 years. In this study, local ADC values had a limited value. Recognition of the patterns of brain damage with DWI and conventional MRI appeared useful as a diagnostic tool. Although, ultrasound and MRI are frequently utilized for evaluation of neonatal hypoxic ischemic injury, there is striking paucity of prospective studies comparing these two modalities. Epelman and colleagues8 prospectively performed

ultrasound and MRI of 76 neonates and young infants (age range: 1–44 days; means age 9.8 days). Both the studies were done within 2 hours of each other. The diagnostic accuracy of ultrasound was found to be 95.7%. The authors recommended the use of ultrasound as screening modality with emphasis on correct technique. They also recommended early MRI for mapping delineating extent of injury. Tovar-Moll and colleagues9 utilized magnetic resonance DTI and tractography in patients of callosal dysgenesis to reveal the aberrant circuit. The study group consisted of 11 patients 9 of which belonged to pediatric age-group. Four main findings were reported: 1. In the presence of a callosal remnant or a hypoplastic corpus callosum (CC), fibers therein largely connect the expected neocortical regions. 2. Callosal remnants and hypoplastic CC display a fiber topography similar to normal. 3. At least two long abnormal tracts are formed in patients with defective CC: Probst bundle (PB) and a sigmoid, asymmetrical aberrant bundle connecting the frontal lobe with the contralateral occipito-parietal cortex. 4. Whereas the PB is topographically organized and has an ipsilateral U-connectivity, the sigmoid bundle is a long, heterotopic commissural tract. These observations revealed that when the process of CC fibers to cross the midline is obstructed, some properties of the miswired fibers are maintained (such as side-by-side topography), whereas others change dramatically, leading to the formation of grossly abnormal white matter tracts. Magnetic resonance imaging is considered inferior to CT scan in detecting calcification. However, susceptibilityweighted imaging (SWI) technique can identify calcification by using phase images. Using this technique, Wu and colleagues 10 were able to detect a partially calcified oligodendroglioma, multiple calcified cysticercosis lesions and multiple physiologic calcifications in a single patient. The authors concluded that SWI-filtered phase images can identify calcifications as well as CT scan. Wang and colleagues11 evaluated serial MRI changes compared to clinical outcome and evaluated their impact on clinical outcome in the follow-up of pyogenic spinal infection in children. In this study, 17 patients (age 2 months to 16 years) underwent 51 follow-up MRI scans done 2 weeks to 4.75 years after baseline scan. Follow-up scans done at short-term revealed epidural and/or paraspinal soft-tissue changes which correlated with the clinical status and laboratory findings in all patients. However, in some cases progression of bone and disk abnormalities was noted in spite of clinical improvement. Long-term follow-up scans revealed soft tissue, bone and disk changes 1–3 years after initial scan in spite of these children being symptom free. The authors concluded that management should be based on the clinical response and that long-term or serial routine follow-ups are not necessary.

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THORACIC IMAGING Lung pathologies have traditionally been evaluated using radiography and CT scan. A few recent studies have explored utility of ultrasound and MRI in lung pathologies. Bober and Swietliñski12 investigated the possible role of chest ultrasound in the diagnosis of the respiratory distress syndrome in newborn. Using transabdominal approach, they performed ultrasound examination in 131 consecutive newborns (admitted to the neonatal intensive care unit) in their 1st day of life with symptoms of respiratory failure. Retrohepatic or retrosplenic hyperechogenicity was shown in 109/131 newborns examined and the diagnosis of respiratory distress syndrome was confirmed by radiography in 101 cases. Respiratory distress syndrome was diagnosed in any patient without retrohepatic or retrosplenic hyperechogenicity. In 8 patients with positive ultrasound images unconfirmed by chest X-ray (i.e. false-positive sonographic examination), congenital pneumonia was diagnosed in 4 cases and pneumothorax in 1 case while in 3 cases no pathology was found. The authors reported 100% sensitivity and 92% specificity of ultrasound in diagnosis of respiratory distress syndrome. Copetti and Cattarossi 13 evaluated sonographic appearance of transient tachypnea of newborn (TTN) and its clinical relevance. They performed sonographic examination of 32 neonates with clinical suspicion of TTN and compared the findings with 60 normal infants, 29 with respiratory distress syndrome, 6 with pneumonia and 5 each with pulmonary hemorrhage and atelectasis. They noted that in TTN the echogenicity of upper lung fields was different from lower lung fields. Specifically, the lower lung fields showed very compact comet tail artifacts while these were rare in superior lung fields. The authors labeled this as “double lung point” which had 100% sensitivity and specificity for diagnosis of TTN. In another study, Copetti and colleagues14 attempted to define the sonographic appearance of neonatal respiratory distress syndrome and evaluate its clinical relevance. They enrolled 40 neonates with respiratory distress syndrome and performed transthoracic ultrasound. In all the patients, sonography revealed echographic “white lung”, pleural line abnormalities (small subpleural consolidations, thickening, irregularity and coarse appearance) and an absence of areas with a normal pattern (i.e. spared areas). When presented simultaneously, these signs had 100% sensitivity and specificity for diagnosis of respiratory distress syndrome. Kurian and colleagues 15 compared the findings of sonography and CT in pediatric patients suffering from pneumonia complicated by parapneumonic effusion. In this retrospective study of 19 patients (age range: 8 months to 17 years), images were assessed for traces of effusion, loculation, fibrin strands, parenchymal consolidation, necrosis and

abscess. In this study, CT of the thorax could not provide any added clinically useful information that was unavailable on chest ultrasound. The authors suggested that the imaging workup of complicated pediatric pneumonia be done with chest radiography and chest ultrasound and CT be reserved for cases where the chest ultrasound is technically limited or discrepant with the clinical findings. Montella and colleagues16 compared the efficacy of high-field MRI and high-resolution CT (HRCT) in children and adults with non-cystic fibrosis (CF) chronic lung disease with the aims of assessing whether chest high-field MRI is as efficient as chest HRCT in identifying pulmonary abnormalities; and to investigate the relationships between the severity and extent of lung disease, and functional data in patients with nonCF chronic lung disease. There were 30 children and 11 adults in this study (age range: 5.9–29.3 years; median age 13.8 years). The 14 patients each had primary ciliary dyskinesia and primary immunodeficiency while another 13 had recurrent pneumonia. All the patients underwent pulmonary function tests, chest HRCT (120 kV, dose-modulated mAs) and high-field 3.0 Tesla MRI (HASTE; transversal orientation; repetition time/echo time/flip angle/ acquisition time, infinite/92 ms/150°/approximately 90 seconds). The images of both HRCT and MRI were scored in consensus by two observers using a modified version of the Helbich scoring system. The maximal score was 25. HRCT and high-field MRI total scores were 11 (range: 1–20) and 11 (range: 1–17), respectively. There was good agreement between the two techniques for all scores (r > 0.8). HRCT and MRI total scores, and extent of bronchiectasis scores were significantly related to pulmonary function tests (r = −0.4, p < 0.05). Similarly, the MRI mucus plugging score was also notably related to pulmonary function tests (r = −0.4, p < 0.05). The authors concluded that high-field 3.0 Tesla MRI of chest surfaces to be as efficient as HRCT in determining the extent and severity of lung abnormalities in nonCF chronic lung diseases, and it might be a more dependable radiationfree option as compared to HRCT. Bannier and colleagues 17 evaluated the sensitivity of hyperpolarized helium-3 (3He) MRI for the detection of peripheral airway obstruction in younger CF patients showing normal spirometric results and the immediate effects of a single chest physical therapy (CPT) session. The study involved 10 children with ages varying from 8 years to 16 years. Spirometry followed by proton and hyperpolarized 3 He three-dimensional lung imaging were performed on a 1.5 Tesla MRI unit before and after 20 minutes of CPT. The number of ventilation defects per image (VDI) and the ventilated lung fraction (VF) were quantified. Despite the normality of Spirometry in all the patients, ventilation defects were discovered in all the patients (mean VDI: 5.1 ± 1.9; mean global VF: 78.5% ± 12.3; and mean peripheral VF: 75.5% ± 17.1). This was well above the VDI in healthy subjects (1.6)

Chapter 122 Recent Advances in Pediatric Radiology

as reported in literature. Although disparate changes in the distribution of ventilation defects were observed after CPT there was no significant change in the average VDI and VF. Tracheomalacia is characterized by excessive collapsibility of trachea in expiration. Lee and colleagues18 evaluated air trapping in pediatric patients with and without tracheomalacia. In this retrospective study, the study group and comparison group had 15 patients each. Tracheomalacia was diagnosed if the cross-sectional luminal area of trachea decreased by more than or equal to 50% during expiration as seen on CT scan and confirmed by bronchoscopy. The authors graded the severity of air trapping visually on a 5-point score. All the patients with tracheomalacia and 10/15 children without tracheomalacia showed air trapping. The median air trapping score was significantly higher (p = 0.002) in the study group. However, the patterns of air trapping were not significantly different. These findings have potential implications for diagnosis and management of children with tracheomalacia. Chest radiography, catheter angiography and echocardiography (ECG) have remained the mainstay of evaluation of patients with heart disease. With the recent availability of advanced multidetector scanners, it has now become possible to evaluate congenital heart diseases using CT scan. Cheng and colleagues19 evaluated the clinical value of low-dose prospective ECG-triggered dual-source CT angiography (DSCT) in infants and children with complex congenital cardiac diseases. They compared DSCT findings with transthoracic echocardiography (TTE). The study includes 35 patients with the age range of 2 months to 6 years. They demonstrated high sensitivity (97.3%) and specificity (99.8%) with mean effective dose of 0.38 ± 0.09 mSv. In this study, the subjective mean image quality score was 4.3 ± 0.7 using a 5-point scale. Another study evaluated step-andshoot DSCT for evaluation of heart coronary artery and other thoracic structures in young children (age < 6 years) with congenital heart disease.20 They utilized prospective gating with end-systolic reconstruction. The image quality was evaluated using a 5-point scoring system. They reported mean image quality score of 4.7 ± 0.6 and mean effective radiation dose of 0.26 ± 1.6 mSv.

GASTROINTESTINAL IMAGING Necrotizing enterocolitis (NEC) refers almost exclusively to an idiopathic, often severe, enterocolitis that occurs in neonates with premature babies being more at risk.21 The radiological evaluation is traditionally dependent upon radiography. Although there are sporadic reports of use of ultrasound in NEC, the first comprehensive evaluation of NEC with abdominal sonography was reported by Faingold and colleagues.22 They enrolled 30 controlled and 32 neonate of proven or suspected NEC. They performed color Doppler of the bowel wall and described the normal and abnormal flow patterns. In this study, the sensitivity of absent flow in

bowel wall on color Doppler, as marker for severe NEC, was 100%. This was significantly superior to 40% sensitivity of abdominal radiography which relied upon free air as sign of severe NEC. A recent study23 reported the findings of ultrasonography in early NEC. The authors evaluated 40 neonates with clinically diagnosed NEC and 10 controls. They evaluated the echogenicity of the bowel wall, involved region, ascites, and portal venous gas at initial and follow-up examinations. Echogenic dots were seen in bowel wall in 16 patients (40%) and dense granular echogenicities in 24 patients (60%). Portal venous gas was not visualized in any of the patients. None of the neonates in control group had echogenic foci in bowel wall. Follow-up examinations revealed decrease in the echogenicity of the bowel wall and ascites in 37 patients (93%). Silva and colleagues,24 in a retrospective study, correlated the sonographic findings with clinical outcome in 40 neonates. They divided the patients into two groups based on outcome: group A included neonates who had been treated medically and had fully recovered, while group B included neonates who required surgery for perforation in the acute setting (laparotomy or placement of a peritoneal drain), surgery for late strictures or those who died as a result of NEC. They calculated the risk ratios and 95% confidence intervals (CI) for those features for different sonographic patterns. The reports showed an adverse outcome associated with the sonographic findings of free gas, focal fluid collections or three or more of the following: increased bowel wall echogenicity, absent bowel perfusion, portal venous gas, bowel wall thinning, bowel wall thickening, free fluid with echoes and intramural gas. Interestingly, in this study, two babies in group A revealed absent flow in bowel wall suggesting that absent flow in bowel wall need not always be associated with adverse outcome. Dilli and colleagues25 also reported sonographic findings in NEC. They stated that sonography had high specificity but low sensitivity for detection of portal venous gas. In addition, sonography provided valuable information regarding intraabdominal collections. Bora and colleagues26 evaluated the role of postnatal superior mesenteric artery (SMA) flow in predicting feed intolerance and NEC in the babies of mothers showing absent end-diastolic flow in umbilical arteries during antenatal sonography. There were three groups in this study: group 1 (n = 23) was small for gestational age with mothers having absent end-diastolic flow; group 2 was small-forgestational age (n = 20) while the group 3 was appropriate for gestational age (n = 19). Antenatal color Doppler revealed normal umbilical artery blood flow in group 2 and 3. In all the patients, postnatal SMA color Doppler was performed before test feed (0.5 mL) and repeated every 15 minutes till 1 hour after administration of test feed. The study revealed higher incidence of NEC and feed intolerance in group 1. The study also suggested that serial SMA flow evaluation, especially

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the 60 minutes postfeed study may help in identifying babies likely to develop feed intolerance. Extrahepatic biliary atresia (EHBA) and neonatal hepatitis are two important causes of neonatal conjugated hyperbilirubinemia. Together, they account for 60–90% of patients.27,28 It is essential to differentiate between these two entities as the treatment is completely different. Some of the recent articles have utilized ultrasound and/or color Doppler for evaluation of babies suspected of having EHBA. Humphrey and Stringer29 performed sonographic evaluation of 90 infants with conjugated hyperbilirubinemia for gallbladder morphology, triangular cord sign, presence of a common bile duct, liver size and echotexture, splenic appearance and vascular anatomy. Using all of the above mentioned features, they were able to correctly classify 88/90 infants as having or not having EHBA (98% accuracy). The features with the greatest individual sensitivity and specificity, respectively, in the diagnosis of biliary atresia (BA) were triangular cord sign had sensitivity of 73% and specificity of 100% for diagnosis of EHBA. Corresponding figures were 91% and 95% for abnormal gallbladder wall; 70% and 100% for gallbladder shape, and 93% and 92% for absent common bile duct. The hepatic artery had statistically significant (p < 0.001) larger diameter in infants with EHBA than in those without EHBA. However, portal vein diameters were not significantly different between the two groups. Kim and colleagues 30 prospectively evaluated the accuracy of hepatic artery diameter and hepatic artery diameter-to-portal vein diameter ratio for ultrasonographic diagnosis of BA. The diameter of right hepatic artery and the ratio of hepatic artery diameter-to-portal vein diameter were larger in the EHBA group. The authors suggested right hepatic arterial diameter of 1.5 mm and hepatic artery diameter-toportal vein diameter ratio of 0.45 as optimal cut-off values for diagnosis of EHBA. Lee and colleagues 31 described the color Doppler ultrasonographic findings in livers of neonates with EHBA and compared them with US findings in livers of neonates with nonBA and control subjects. The study included 64 patients of neonatal cholestasis of which 29 had EHBA. In additional, they enrolled 19 control subjects. The authors evaluated the triangular cord sign and hepatic subcapsular flow. The images were interpreted by three pediatric radiologists independently and discrepancies were resolved by consensus. The triangular cord sign had sensitivity of 62% and specificity of 100% for diagnosis of EHBA. Hepatic subcapsular flow on color Doppler had sensitivity and specificity of 100% and 86% respectively for diagnosis EHBA on the basis of consensus reading. The gold standard for diagnosis of EHBA is intraoperative cholangiogram.32 Unfortunately, some infants are found not to have EHBA on peroperative cholangiogram. In a retrospective study, Nwomeh and colleagues33 evaluated the contribution of percutaneous cholecystocholangiography in preventing

unnecessary laparotomy in infants with cholestatic jaundice. The study included 35 infants of which 9 had sonographically visible gallbladder. In these patients ultrasound-guided percutaneous cholecystocholangiography was performed and diagnosis of EHBA excluded. This obviated the need of laparotomy in these patients. Rectal bleeding is commonly evaluated using CT colonoscopy (CTC) in adult population. However, this modality has not been extensively used in pediatric population. Anupindi and colleagues34 evaluated eight (3–17 years of age) children with noncontrast CTC and reported it to be a well tolerated, safe and useful investigation. The estimated mean effective dose in this study for CTC was 2.17 mSv as compared to 5–6 mSv for a standard air-contrast barium enema in a small child. Capuñay and colleagues35 performed 100 CTC studies in children with rectal bleeding. No complications were encountered. They reported sensitivity and specificity of 89% and 80% of CTC in diagnosis of elevated colonic lesions. The authors concluded that virtual colonoscopy is an alternative method for the evaluating the children with elevated lesions. It has fast speed without complications, and uses a low dose of radiation. The postulated advantages of using CTC included diagnosis of the exact location of the polyp, faster and easier polypectomy by conventional colonoscopist, reduction in the time of anesthesia and less complications in relation to the conventional procedure of colonoscopy. Sugiyama and colleagues 36 evaluated the feasibility of single scan CTC using polyethylene glycol electrolytes solution with contrast medium (PEG-C) bowel preparation in children. Seven patients suspected of colorectal-elevated lesions were subjected to CTC. All patients underwent bowel preparation using PEG at a dose of 32 ± 3 mL/kg body weight (BW) during the evening before the day of CTC. The water-soluble contrast agent (Gastrografin, Nihon Schering, Osaka, Japan) was given to the patients orally or through a nasogastric tube at a dose of 0.6 ± 0.1 mL/kg BW, the next morning. The water-soluble contrast agent was diluted 1:9 with PEG. The contrast agent was used for residual fluid tagging. Air was insufflated into the colon in the left decubitus position. The patient was scanned axially with a single run from the colonic flexures to the pelvis in the supine position. CTCs were negative for polyps in 2 patients and positive in 5 patients. The endoscopic findings were similar to the CTC images. In two cases which did not reveal polyps on CTC, no symptoms were noticed on follow-up for a period of more than 6 months. The authors concluded that the single scan CTC using PEG-C preparation was safe and less invasive compared to conventional colonoscopy due to the shorter examination time and lower radiation dose. Radiation exposure in this study was between 6.5 mGy and 15.0 mGy (mean dose: 9.1 mGy). Intussusception is a common emergency in infants and young children. Ultrasound or fluoroscopy guided reduction is frequently attempted to avoid surgery. However, many a

Chapter 122 Recent Advances in Pediatric Radiology

times the reduction is incomplete. Curtis and colleagues37 retrospectively reviewed whether a failed reduction of ileocolic intussusception at a referring hospital is predictor of failure of repeat attempt at a children’s hospital. The children with pathological lead point, these with age more than 10 years, those having successful reduction at referring hospital and those who did not undergo an enema reduction at the authors’ institute were excluded. 152 patients met the enrollment criteria. The authors did not find any significant difference in the rate of successful reduction for the patients who initially presented to author’s institute (60.5% as compared to those who had failed reduction at a referring hospital 60.7%). They concluded that children referred to a children’s hospital after failed enema reduction at a referring hospital should undergo repeat enema reduction provided there are no other contraindications. In another retrospective study, Pazo and Losek 38 evaluated the demographic and clinical characteristics of children with intussusception and failed initial air enema reduction who were managed by delayed repeat enema attempts. They attempted to identify predictors associated with successful reduction. In this study, there were 21 intussusception events in 20 patients which were managed by delayed repeat air enemas. 9/21 repeat enemas were successful. 4 of the patients who had unsuccessful reduction at first repeat enema underwent a second repeat enema with successful reduction in 3 patients. Thus, 12/25 (48%) repeat enemas were successful. The success rate of delayed repeat enemas was found to be greatest when the intussusception was initially reduced to the ileocecal valve. Demographic characteristics, clinical characteristics, or time from initial enema to first repeat enema were not significant determinant of success at repeat enema. Cystic fibrosis frequently involves liver early in evolution. Liver steatosis is the most common manifestation while focal biliary cirrhosis is the pathognomonic manifestation. Menten and colleagues39 evaluated the role of transient elastography of liver in patients of CF. In this prospective study, the authors evaluated 134 patients of CF of which 75 were children. In addition, 31 children without CF were enrolled as controls. Liver morphology was classified on a scale of 1–5 representing increasingly severe liver disease. 10 measurements were recorded for tissue elastography for each subject and median value was considered the elastic modulus of liver. The authors found elasticity values of controls, pancreatic sufficient CF and pancreatic insufficient CF patients with ultrasound score less than 3 to be comparable and significantly lower than compared to CF patients with ultrasound score of more than or equal to 3. In addition, male patients with CF had significantly higher median elasticity (4.7 kilopascals) as compared to female patients with CF (3.9 kilopascals). This preliminary study suggests that transient elastography may be an attractive noninvasive technique to assess and follow-up hepatic disease in CF patients.

URORADIOLOGY Intravenous urography and micturating cystourethrography are important radiological investigations in pediatric uroradiology. However, both of these investigations impart ionizing radiation to the children. Magnetic resonance urography (MRU) and voiding ultrasonography are being evaluated as radiation-free alternatives. Hydronephrosis is common urological problem in pediatric population which is evaluated using a combination of several modalities. Perez-Brayfield and colleagues 40 conducted a prospective study to compare ultrasound, nuclear scintigraphy and dynamic contrast-enhanced MRI for the estimation of hydronephrosis. 96 children with mean age of 4 years (range: 1 month to 17 years) were enrolled in the study. Patient sedation, an important issue in pediatric MRI, was administered without complications. The split renal function as calculated by nuclear and MRI scans were comparable in 71 cases (r = 0.93) evaluated. In 50/64 (78%) cases, the final diagnosis at MRU was similar to that on a combination of ultrasound and nuclear scintigraphy. The authors concluded that dynamic contrast-enhanced MRI provided the same information about renal function but superior information regarding morphology in a single study without ionizing radiation. Akgun and colleagues41 conducted a retrospective study to assess whether diuretic agent administration in MRU affects the renal length and to clarify whether the increase in length can be useful in assessing renal function. The study group consisted of 20 children of age group 10 months to 13 years. All these children had ureteropelvic junction stenosis. All had technetium-99m (99mTc)-mercaptoacetyltriglycine (MAG-3) and 99mTc-diethylene triamine pentaacetic acid (DTPA) diuretic renography performed within 1 month of MRU. The authors reported that the mean renal lengths measured before and after diuretic administration were 79.02 ± 16.84 mm and 85.61 ± 18.49 mm, respectively. This increase in renal length after diuretic administration was found to be statistically significant (p < 0.001; t = 8.082). In addition, a positive correlation was observed between the increase in renal length after diuretic injection and functional status of kidneys (p < 0.001; r = 0.547). The better functioning kidneys had higher increase in renal length after diuretic administration. Availability of sonographic-contrast agents and harmonic imaging has contributed significantly to the sonographic evaluation of vesicoureteric reflux. In a recent study, Papadopoulo and colleagues 42 prospectively evaluated sensitivity of voiding urosonography harmonic imaging (VUS HI) using a second-generation contrast agent (sulfurhexafluoride gas microbubbles, SonoVue, Bracco, Italy) for the diagnosis of vesicoureteral reflux. The study group included 228 children with 463 kidney-ureter units (KUUs). The patients underwent two cycles of VUS HI and two cycles

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of voiding cystourethrography (VCUG) at the same session. The findings of two modalities were compared. Vesicoureteric reflux was demonstrated in 161/463 (34.7%) KUUs, 57 by both methods, 90 only by VUS HI, and 14 only by micturating cystourethrogram. There was (77.5%) (k = 0.40) concordance (359/463 KUUs) in findings regarding the presence or absence of vesicoureteric reflux. There was a significant difference in the detection rate of reflux between the two methods (p < 0.01). Apart from showing inferior sensitivity, micturating cystourethrography also missed reflux of higher grade (2 grade I, 65 grade II, 19 grade III, 4 grade IV) as compared to VUS HI (8 grade I, 5 grade II, 1 grade III). The authors suggested that VUS HI and a second-generation contrast agent can be used as an alternative radiation-free imaging method for evaluation of vesicoureteric reflux. Another radiation-free approach to evaluation of vesicoureteric reflux involves utilization of MR fluoroscopy. Vasanwala and colleagues43 have attempted to develop an MRI voiding cystography protocol with continuous realtime MR fluoroscopy and validate it against micturating cystourethrography. In this study, eight follow-up patients of vesicoureteric reflux were evaluated in a specially designed machine capable of performing MRI as well as fluoroscopic VCUG. In this study, MRI had sensitivity of 88% when the grade of reflux differed by less than 1 on two modalities. MRI detected reflux in one patient which was not detected by fluoroscopic VCUG.

MUSCULOSKELETAL IMAGING Magni-Manzoni and colleagues 44 conducted a study to compare clinical evaluation and ultrasound in the assessment of joint synovitis in children with juvenile idiopathic arthritis. 52 joints in 32 children were evaluated by two pediatric rheumatologists for swelling, tenderness/pain on motion, and restricted motion. The same joints were evaluated by an experienced sonographer for synovial hyperplasia, joint effusion and power Doppler signal. Overall, 1,664 joints were assessed both clinically and sonographically. On clinical examination joint swelling, tenderness and restricted motion were noticed in 98 (5.9%), 59 (3.5%) and 40 (2.4%) of joints, respectively. Sonographic evaluation revealed synovial hyperplasia in 125 (7.5%), joint effusion in 153 (9.2%) and power Doppler signal in 53 (3.2%) joints. A total of 104 (6.3%) and 167 (10%) joints had clinical and sonographic evidence of synovitis, respectively. 86 (5.5%) of the clinically “normal” joints had sonographic features of synovitis. 5 patients were classified as having polyarthritis who were classified as having oligoarthritis or no synovitis on clinical evaluation. In this study, sonographic features moderately correlated with clinical measures of joint swelling, but poorly correlated with those of joint tenderness/pain on motion and restricted motion. The authors concluded that subclinical synovitis

is common in juvenile idiopathic arthritis which may have important implications for patient classification and may affect the therapeutic strategy in individual patients. Rooney and colleagues45 prevalence of synovitis and tenosynovitis in children with juvenile idiopathic arthritis who were felt clinically to have active inflammatory disease of the ankle. Forty-nine clinically swollen ankle joints in 34 patients were included in this study. There were 19 patients with polyarticular disease and 13 with oligoarticular disease. One patient had systemic juvenile idiopathic arthritis. The authors found that 71% of ankles had tenosynovitis and 39% had tenosynovitis alone. Only 29% of clinically swollen ankles had tibiotalar joint effusion alone while 33% had both tenosynovitis and tibiotalar joint effusion. There was statistically significant difference between different subgroups for the frequency of occurrence of medial ankle tenosynovitis (p = 0.048) and lateral ankle tenosynovitis (p = 0.001).

SUMMARY Several good articles have been published in recent years contributing to improved patient care. The current trends stress on the need of keeping the radiation dose to the minimum possible level when investigating the pediatric patients. Readers are encouraged to stay in touch with recent developments. Use of electronic resources is recommended as quick and inexpensive means for maintaining up to date knowledge.

REFERENCES 1. Image Gently: The Alliance for Radiation Safety in Pediatric Imaging. (2014). Campaign Overview. [online] Available from www.imagegently.org/FAQsMore/CampaignOverview.aspx. [Accessed July, 2015]. 2. Strauss KJ, Kaste SC. The ALARA concept in pediatric interventional and fluoroscopic imaging: striving to keep radiation doses as low as possible during fluoroscopy of pediatric patients--a white paper executive summary. Am J Roentgenol. 2006;187(3):818-9. 3. Strauss KJ, Goske MJ, Kaste SC, et al. Image gently: Ten steps you can take to optimize image quality and lower CT dose for pediatric patients. Am J Roentgenol. 2010;194(4):868-73. 4. Sidhu M, Strauss KJ, Connolly B, et al. Radiation safety in pediatric interventional radiology. Tech Vasc Interv Radiol. 2010;13(3):158-66. 5. Palchak MJ, Holmes JF, Vance CW, et al. A decision rule for identifying children at low risk for brain injuries after blunt head trauma. Ann Emerg Med. 2003;42(4):492-506. 6. Barkovich AJ, Miller SP, Bartha A, et al. MR imaging, MR spectroscopy, and diffusion tensor imaging of sequential studies in neonates with encephalopathy. Am J Neuroradiol. 2006;27(3):533-47.

Chapter 122 Recent Advances in Pediatric Radiology 7. Liauw L, van Wezel-Meijler G, Veen S, et al. Do apparent diffusion coefficient measurements predict outcome in children with neonatal hypoxic-ischemic encephalopathy? Am J Neuroradiol. 2009;30(2):264-70. 8. Epelman M, Daneman A, Kellenberger CJ, et al. Neonatal encephalopathy: a prospective comparison of head US and MRI. Pediatr Radiol. 2010;40(10):1640-50. 9. Tovar-Moll F, Moll J, de Oliveira-Souza R, et al. Neuroplasticity in human callosal dysgenesis: a diffusion tensor imaging study. Cereb Cortex. 2007;17(3):531-41. 10. Wu Z, Mittal S, Kish K, et al. Identification of calcification with MRI using susceptibility-weighted imaging: a case study. J Magn Reson Imaging. 2009;29(1):177-82. 11. Wang Q, Babyn P, Branson H, et al. Utility of MRI in the follow-up of pyogenic spinal infection in children. Pediatr Radiol. 2010;40(1):118-30. 12. Bober K, Swietliñski J. Diagnostic utility of ultrasonography for respiratory distress syndrome in neonates. Med Sci Monit. 2006;12(10):CR440-6. 13. Copetti R, Cattarossi L. The ‘double lung point’: an ultrasound sign diagnostic of transient tachypnea of the newborn. Neonatology. 2007;91(3):203-9. 14. Copetti R, Cattarossi L, Macagno F, et al. Lung ultrasound in respiratory distress syndrome: a useful tool for early diagnosis. Neonatology. 2008;94(1):52-9. 15. Kurian J, Levin TL, Han BK, et al. Comparison of ultrasound and CT in the evaluation of pneumonia complicated by parapneumonic effusion in children. Am J Roentgenol. 2009;193(6):1648-54. 16. Montella S, Santamaria F, Salvatore M, et al. Assessment of chest high-field magnetic resonance imaging in children and young adults with noncystic fibrosis chronic lung disease: comparison to high-resolution computed tomography and correlation with pulmonary function. Invest Radiol. 2009;44(9):532-8. 17. Bannier E, Cieslar K, Mosbah K, et al. Hyperpolarized 3He MR for sensitive imaging of ventilation function and treatment efficiency in young cystic fibrosis patients with normal lung function. Radiology. 2010;255(1):225-32. 18. Lee EY, Tracy DA, Bastos M, et al. Expiratory volumetric MDCT evaluation of air trapping in pediatric patients with and without tracheomalacia. Am J Roentgenol. 2010;194(5):1210-5. 19. Cheng Z, Wang X, Duan Y, et al. Low-dose prospective ECGtriggering dual-source CT angiography in infants and children with complex congenital heart disease: first experience. Eur Radiol. 2010;20(10):2503-11. 20. Paul JF, Rohnean A, Elfassy E, et al. Radiation dose for thoracic and coronary step-and-shoot CT using a 128-slice dual-source machine in infants and small children with congenital heart disease. Pediatr Radiol. 2010;41(2):244-9. 21. Buonomo C. The radiology of necrotizing enterocolitis. Radiol Clin North Am. 1999;37(6):1187-98. 22. Faingold R, Daneman A, Tomlinson G, et al. Necrotizing enterocolitis: assessment of bowel viability with color Doppler US. Radiology. 2005;235(2):587-94.

23. Kim WY, Kim WS, Kim IO, et al. Sonographic evaluation of neonates with early-stage necrotizing enterocolitis. Pediatr Radiol. 2005;35(11):1056-61. 24. Silva CT, Daneman A, Navarro OM, et al. Correlation of sonographic findings and outcome in necrotizing enterocolitis. Pediatr Radiol. 2007;37(3):274-82. 25. Dilli D, Oguz SS, Ulu HO, et al. Sonographic findings in premature infants with necrotising enterocolitis. Arch Dis Child Fetal Neonatal Ed. 2009;94(3):F232-3. 26. Bora R, Mukhopadhyay K, Saxena AK, et al. Prediction of feed intolerance and necrotizing enterocolitis in neonates with absent end diastolic flow in umbilical artery and the correlation of feed intolerance with postnatal superior mesenteric artery flow. J Matern Fetal Neonatal Med. 2009;22(11):1092-6. 27. Jonas MM, Perez-Atayde AR. Liver disease in infancy and childhood. In: Schiff ER, Sorell MF, Maddrey WC (Eds). Schiff’s diseases of liver, 10th edition. Philadelphia, PA, USA: Lippincott Williams & Wilkins. 2007. pp. 1307-31. 28. Nicotra JJ, Kramer SS, Bellah RD, et al. Congenital and acquired biliary disorders in children. Semin Roentgenol. 1997;32(3):215-27. 29. Humphrey TM, Stringer MD. Biliary atresia: US diagnosis. Radiology. 2007;244(3):845-51. 30. Kim WS, Cheon JE, Youn BJ, et al. Hepatic arterial diameter measured with US: adjunct for US diagnosis of biliary atresia. Radiology. 2007;245(2):549-55. 31. Lee MS, Kim MJ, Lee MJ, et al. Biliary atresia: color Doppler US findings in neonates and infants. Radiology. 2009;252(1):282-9. 32. de Carvalho E, Ivantes CA, Bezerra JA. Extrahepatic biliary atresia: current concepts and future directions. J Pediatr (Rio J). 2007;83(2):105-20. 33. Nwomeh BC, Caniano DA, Hogan M. Definitive exclusion of biliary atresia in infants with cholestatic jaundice: the role of percutaneous cholecysto-cholangiography. Pediatr Surg Int. 2007;23(9):845-9. 34. Anupindi S, Perumpillichira J, Jaramillo D, et al. Low-dose CT colonography in children: initial experience, technical feasibility, and utility. Pediatr Radiol. 2005;35(5):518-24. 35. Capuñay CM, Carrascosa PM, Bou-Khair A, et al. Low radiation dose multislice CT colonography in children: Experience after 100 studies. Eur J Radiol. 2005;56(3):398-402. 36. Sugiyama A, Ohashi Y, Gomi A, et al. Colorectal screening with single scan CT colonography in children. Pediatr Sur Int. 2007;23(10):987-90. 37. Curtis JL, Gutierrez IM, Kirk SR, et al. Failure of enema reduction for ileocolic intussusception at a referring hospital does not preclude repeat attempts at a children’s hospital. J Pediatr Surg. 2010;45(6):1178-81. 38. Pazo A, Hill J, Losek JD. Delayed repeat enema in the management of intussusception. Pediatr Emerg Care. 2010;26(9):640-5. 39. Menten R, Leonard A, Clapuyt P, et al. Transient elastography in patients with cystic fibrosis. Pediatr Radiol. 2010;40(7): 1231-5. 40. Perez-Brayfield MR, Kirsch AJ, Jones RA, et al. A prospective study comparing ultrasound, nuclear scintigraphy and

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43. Vasanawala SS, Kennedy WA, Ganguly A, et al. MR voiding cystography for evaluation of vesicoureteral reflux. Am J Roentgenol. 2009;192(5):W206-11. 44. Magni-Manzoni S, Epis O, Ravelli A, et al. Comparison of clinical versus ultrasound-determined synovitis in juvenile idiopathic arthritis. Arthritis Rheum. 2009;61(11):1497-504. 45. Rooney ME, McAllister C, Burns JF. Ankle disease in juvenile idiopathic arthritis: ultrasound findings in clinically swollen ankles. J Rheumatol. 2009;36(8):1725-9.

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Interventions in Children PART A: VASCULAR INTERVENTIONS Gurpreet Singh Gulati, Sanjiv Sharma INTRODUCTION

Fluid balance Radiation safety zz Equipment selection. A dedicated team consisting of the operating radiologist, the radiation and hemodynamic technologists, and the nursing attendant are needed to prepare the catheterization laboratory, prepare and handle the patient, and assist during the procedure. A high-resolution digital angiography system is required to obtain reliable diagnostic images quickly and to monitor the interventional procedure. zz zz

Interventional procedures in the pediatric age group have a long history. Probably the first intervention performed in a pediatric patient was the reduction of intussusception. The earliest cardio-vascular intervention in children performed with angiographic guidance was balloon atrial septostomy. Over the years, although vascular interventional techniques as applied to the adult population have undergone dramatic and continuous innovation, their application to pediatric patients has been delayed, due to a conservative attitude of pediatric medicine practitioners, lack of adequately trained physicians and staff in this subspecialty, and need for special equipment appropriate for pediatric use. Children are not merely “little adults”, nor are the diseases to which they are particularly susceptible, variants of diseases in adult life. Excessive crying, unwillingness for examination, and their inability to describe complaints make a child the most difficult patient. However, it is a challenge to the pediatric interventionist to master the art of “talking” and achieve a successful examination. A friendly environment, affectionate attitude of the medical staff, and a carefully and rapidly performed study, go a long way in conducting a successful procedure.

SPECIAL CONSIDERATIONS FOR THE PEDIATRIC PATIENT The interventional radiologist and referring physician hold a detailed discussion to decide the appropriate procedure to be performed. The risks for the particular patient are appreciated, and the likely benefit to accrue to the patient is understood. It is particularly imperative to pay special attention to the following details while conducting a pediatric angiography or intervention. These are: zz Choice of sedation or anesthesia zz Maintenance of temperature control

PATIENT PREPARATION History and Physical Examination A detailed discussion on the patient’s history taking and examination relevant to general as well as specific angiographic interventional procedures is outside the scope of this chapter. Table 1 lists the several components that need to be assessed while evaluating the patient.

Informed Consent The parent or guardian of a minor child, and when possible, the patient himself, should understand the reasons for undergoing the procedure. The risks and benefits should be clarified along with the consequences of refusing the procedure, and the alternative therapies available should be discussed. He/she should then give consent for the procedure.

Coagulation Whenever there is a bleeding diathesis, risk of hemorrhage, or a plan to perform systemic thrombolysis, coagulation studies are obtained. Blood is sent for grouping and cross-matching whenever there is ongoing or expected blood loss. Heparin is administered for arterial catheterization procedures in

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a dose of 50 units/kg for diagnostic and 100 units/kg for revascularization procedures. Table 1:  Pre-procedure clinical evaluation of the patient 1. History of the current problem 2. Pertinent medical and surgical history 3. Review of the organ systems •  Cardiac •  Pulmonary •  Renal •  Hepatic •  Hematologic (e.g. coagulopathy, hyper-coagulable state) •  Endocrine (diabetes)

Diet and Medications Small children need not be kept fasting for more than 3–4 hours prior to the procedure. Routine antibiotics are not prescribed except for high-risk procedures, e.g. splenic embolization.

Dose of Radiation and Fluids Isky Gordon et al.1 calculated and published the ratio of radiation dose to the skin (in rads) for various procedures as follows: Age (years)

1

5

10

15

4. History of allergies

Angiography – 20 films

1.4

3.0

4.8

7.5

5. Current medications

Fluoroscopy – 4 minutes

3.2

4.8

6.8

8.8

6. Directed physical examination

Anesthesia Most diagnostic studies are carried out with intravenous sedation. Difficult interventions such as device implantation or particularly painful procedures are conducted under general anesthesia. In most children, conscious sedation is used, in which the child is conscious, drowsy, and may even close his eyes, but is responsive to verbal commands and able to protect his reflexes and airway. Midazolam is a commonly used, shortacting benzodiazepine that is metabolized by the liver. Its dose is 0.2–1 mg/KBW IV. The onset of action is 3–5 minutes and the duration of action is 60 minutes. The major side effects are respiratory depression and apnea. A combination of three drugs namely, demerol (50 mg), promethazine (12.5 mg) and triclofos (12.5 mg), known as DPT, is the other agent used for conscious sedation. A mixture of the three is made into a 2 mL solution, to be given in a dose of 0.06–0.1 mL/KBW IM. For deeper sedation, a combination of diazepam (0.1 mg/KBW) and morphine (0.1 mg/KBW) may be given IV. Respiratory depression may occur with higher doses.

One must try and minimize the radiation exposure to children who are believed to be more sensitive to the effects of radiation and likely to live for many years with these effects. Digital systems probably do not reduce radiation exposure. However, several precautions may be taken by the operator to reduce the dose. Fluoroscopy at the lowest dose possible (reduce the mAS), pulsed fluoroscopy, removing the scatter grids, and addition of rare earth filters in the X-ray tubes help to reduce radiation doses to the patient. All fluids and medication must be scaled to the patient size. One may easily administer excessive amounts of fluids and contrast without realizing it. Digital systems (more so with biplane angiography systems) help to bring down the volume of contrast material and speeding up procedures. Most infants can tolerate 4 mL/kg of contrast, whereas children over 6 months can tolerate 6 mL/kg, if it is delivered as several injections spread over a period of time. It is important to maintain patient hydration if such large doses are employed.

TECHNIQUES

Smaller children are immobilized on a restraining board. Older children will have hand and leg restraints but, if uncooperative, will need to be anesthetized.

The vascular procedures used in pediatric patients require a substantially different approach than that of the adult population. An account must be kept of a few considerations when treating the pediatric population, including the small size of the caliber vessel, anticipation of spasm, the risk for infection, the tendency of children to rapidly form collateral circulation, the inevitability of growth, and the strong tendency for restenosis and growth arrest to occur.

Temperature Control

Access

Neonates and especially premature babies may become hypothermic if a warm operating environment is not maintained. The room temperature should be increased, radiation heaters are required, and the child should be covered quickly while preparing the groin and draping.

Introducer sheaths should be used to preserve vascular access, since multiple catheter/guidewire insertions or exchanges may be needed. Special pediatric access sheaths are available in 4–6 F sizes. These are usually introduced by using a cannula (18–21 G) and a 0.021" guidewire. The angle

Patient Immobilization

Chapter 123 Interventions in Children

of entry of the needle should be less perpendicular to the skin, and a small nick in the skin with the blade should be given before introducing the sheath, to prevent pain and a possible vasovagal reaction. Care should be taken to prevent an inadvertent incision in the anterior vessel wall while using the blade.

PROCEDURES The major vascular interventional procedures performed in children can be grouped into: zz Embolization zz Angioplasty zz Thrombolysis zz Foreign body removal.

Vascular Anomalies Vascular anomalies can be grouped into two categories: Hemangiomas and vascular malformations. Vascular malformations are categorized further as high-flow lesions (AVM, AVF), low-flow lesions (capillary malformation, VM, LM), or combined vascular malformations. Embolotherapy with a variety of embolic materials is commonly used in the treatment of vascular anomalies.

Hemangioma

Percutaneous transcatheter embolization has replaced surgery for many pediatric vascular problems, and is a treatment alternative in patients where surgery has little to offer. Microcatheter systems, which were initially developed for adult neurovascular interventions, are ideal for pediatric applications. They permit access to small vessels and territories that were previously inaccessible. Hydrophilic coated steerable guidewires permit negotiation of complex vascular loops without provoking spasm or causing dissection. Embolization procedures should only be performed by experienced physicians familiar with the equipment and technical aspects of the procedure. Discussion with the pediatric physicians or surgeons, their support and backup is essential for a safe and successful procedure. The various pediatric vascular conditions treated by using embolotherapy can be grouped as follows: zz Vascular anomalies, e.g. arteriovenous malformation (AVM), arteriovenous fistula (AVF), venous malformation (VM), lymphatic malformation (LM), and hemangioma. zz Hemorrhage from bleeding vessels (due to pseudoaneurysms or vascular involvement in trauma, tumor or inflammation) in various organ systems. zz Other conditions, e.g. tumors and organ ablation. Goals of embolotherapy include: (1) an adjunctive goal, e.g. preoperative, adjunct to chemotherapy or radiation therapy; (2) a curative goal, e.g. definitive treatment such as that performed in cases of aneurysms, AVFs, AVMs, and traumatic bleeding; and (3) a palliative goal, e.g. relieving symptoms, such as of a large AVM, which cannot be cured by using embolotherapy alone.

Hemangiomas are very benign tumors which do not require treatment in most patients. In some of the rare cases, embolization may be essential (particularly in patients with urgent need of therapy) because of spontaneous hemorrhage or functional abnormality caused by the extreme size of the lesion or the particular anatomic location or because of significant congestive heart failure.2 Additionly, embolotherapy is deemed useful prior to surgical resection in select patients, and in patients in whom a hemangio-endothelioma causes Kasabach-Merritt phenomenon (platelet trapping). 2 Embolotherapy of a hemangioma or hemangioendothelioma can be performed with the use of PVA particles. Coils are not used frequently as they cause more proximal occlusion with potential for recruitment of supply from other arteries and they block future access to the lesion if the need arises. Embolotherapy aims at blocking a large percentage of the tumoral vessels, thus preventing further trapping and destruction of the platelets and hastening involution of the lesion. Several sessions of embolotherapy may be required for some tumors because of revascularization of the tumor or to prevent exceeding the limits of radiation and contrast burden in one session. Infantile hepatic hemangioendotheliomas, a variant of infantile hemangioma, usually are multiple and are frequently complicated by congestive heart failure. In the clinical setting, embolotherapy aims at reducing the hepatic arterial flow, which sufficiently relieves high-output cardiac failure. A variety of embolic materials have been used. In some patients, embolization of other nearby arteries (e.g. intercostals) may also be necessary.3 Arterial portography should be performed to exclude the possibility of feeders from the portal system. A rare entity called noninvoluting hemangioma, which is found in the adult population, may also respond to transcatheter embolization (usually with particles such as PVA or micro-spheres). This procedure is usually performed to improve the cosmetic appearance.

Embolization Materials and Substances

Arteriovenous Malformation

Materials required in embolization include coils, sodium tetradecyl sulfate, ethanol, n-butyl cyanoacrylate (NBCA) glue, polyvinyl alcohol (PVA) particles, gelatin sponge (Gelfoam) and microspheres.

Arteriovenous malformations are typically characterized by a nidus of abnormal vessels in which shunting of arterial blood to veins occurs. These vascular anomalies are usually present during childhood but often demonstrate a sudden

EMBOLIZATION

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increase in size in response to trauma, hormones or other stimuli. Although, a clinical grading system has been used among surgeons, no grading system has yet been developed for imaging. Most AVMs can be managed by transcatheter embolization and/or sclerotherapy. Surgical excision can treat some focal AVMs. Proximal embolization or ligation of the feeding arteries usually has adverse effects because of subsequent recruitment of collaterals, and transluminal embolization of the nidus which cannot be performed afterwards. The collaterals that develop are more problematic in terms of transcatheter treatment; however, proximal embolization of the feeding arteries may be performed if it is indicated prior to surgical excision. During primary embolotherapy, the nidus should be embolized when possible.2 Absolute alcohol is the most effective agent in the treatment of AVMs. If the nidus is not reachable through the feeding arteries, then an attempt can be made for direct percutaneous cannulation of the nidus. In selected patients with AVMs, another therapeutic approach is embolic occlusion of the venous outflow.

Cervicofacial AVMs For dental arcade AVMs, spontaneous or catastrophic hemorrhage during tooth extraction is a common presentation. Embolization of an AVM in this region requires superselective catheterization of the involved branches of external carotid artery and other regional arterial branches (e.g. thyrocervical trunk) using microcatheters and the coaxial technique.4 Embolotherapy can be performed with NBCA, alcohol, particles, and/or microcoils, depending on the nature and extent of the malformation. Gelfoam can also be used for preoperative embolization. In cases of patients with dental AVMs associated with acute bleeding and loose

A

teeth embolization should be performed immediately prior to tooth extraction. Some complications related to embolotherapy of cervicofacial AVMs include stroke, nerve paralysis, skin necrosis, infection, blindness, and pulmonary embolism.

Extremity AVMs In the extremities, AVMs can be diffuse and may involve the entire extremity (Parkes-Weber syndrome). Extremity AVMs typically present with extremity-length discrepancy, high cardiac output, pain, and ulceration. Extremity lesions can be treated with multiple embolizations5 and/or surgical resections or amputation of the extremity (Figs 1A and B). A detailed pre-embolization angiographic examination is important for mapping the feeders and draining veins. During the injection of contrast material, the injection rate and duration should be adjusted so that there is accurate identification of arteriovenous connections. A high injection rate in a short period is appropriate for AVMs. Selective catheterization with microcatheters is required to reach the nidus of the AVM. Some possible complications of embolotherapy include skin necrosis (blisters), nontarget embolization (which also includes pulmonary emboli), and systemic sclerosant toxicity if a liquid agent (e.g. alcohol) is used.

Pulmonary AVMs Pulmonary AVMs are also termed as pulmonary AVFs. They have a high association with Osler-Weber-Rendu syndrome (also called hereditary hemorrhagic telangiectasia syndrome). Symptoms of which may include dyspnea, cyanosis, and clubbing. Paradoxical embolization may cause stroke or brain abscess. This anomaly can be classified as

B

Figs 1A and B:  An arteriovenous malformation of the right arm, with feeders from the profunda brachii artery. (A) Pre-embolization; (B) Postembolization (polyvinyl alcohol particles) angiograms

Chapter 123 Interventions in Children

Arteriovenous Fistula

simple or complex on the basis of the number of feeders and draining veins. In simple lesions, a single artery and vein are involved; in complex lesions, 2 or more supplying arteries and 1 or more draining veins are involved. Most pulmonary AVMs (80%) are simple. Although a surgical approach (thoracotomy and resection) is the traditional mode of therapy, currently, transcatheter embolization is a preferred alternative.6 Transcatheter embolization offers significantly reduced morbidity and mortality rates, particularly in hereditary hemorrhagic telangiectasia syndrome. Embolotherapy for AVMs can be performed with coils, vascular plugs or detachable balloons. Possible complications of embolotherapy include nontarget embolization in the systemic circulation (through the AVM shunt) or in other noninvolved pulmonary arteries. Therefore, it is vital to properly measure the size of the coil to the feeding (afferent) artery. A preliminary detailed angiography is essential for mapping the feeders and draining veins, while paying particular attention to the size of the feeders. Basically, a successful embolization is achieved by nesting 1 or more coils in the feeding artery, which occludes flow through the AVM shunt (Figs 2A and B). Generally, feeding arteries larger than 3 mm should be embolized. Feeders smaller than 3 mm have low risk of paradoxic embolization and should be left alone unless they are simple and straightforward technically. A coil that is 2–3 mm larger than the feeding artery is usually selected. For vascular plug, a 30–50% oversizing is recommended. If the feeding artery is large in caliber (>12 mm), a balloon occlusion of the proximal artery via a second groin puncture can be used for a more controlled coil deployment. Postembolization syndrome can occur and is characterized by pleuritic chest pain, pleural fluid, atelectasis, fever and leukocytosis.

A

Arteriovenous fistulas are relatively large arteriovenous connections and may be congenital or secondary to trauma, surgery, or underlying vascular abnormality (e.g. neurofibromatosis). AVFs may be seen in any part of the body. A patient may present with cardiac failure, localized growth disturbances, neurologic deficits, and ischemic changes. Unlike AVMs, AVFs can be cured with embolotherapy. The embolotherapy technique used depends on the size, location, and hemodynamics of individual lesions. The goal of embolotherapy is to occlude the fistula and the immediate draining vein. Embolization can be achieved by using detachable coils or balloons, or tissue adhesives (glue or onyx). It is not appropriate to use Gelfoam or particles in AVF embolization. Detachable coils7 or balloons are ideal because these embolic materials can be positioned optimally before they are detached. Balloons also have the advantage of conforming to the size and shape of the abnormal vessels. Microcoils can be dislodged; however, this complication can be minimized by performing flow-control techniques (e.g. balloon occlusion, tourniquet, or blood pressure cuff control). The other disadvantage of coil embolization is that the clot that forms around the coil may dissolve, leading to recanalization. Appropriate nesting of several coils (packing) can minimize recanalization. Also, thrombosis can be augmented by soaking the coils in thrombin before deployment or by injecting sclerosants around the coils. If adequate coil packing cannot be accomplished, tissue adhesive can be effectively used in combination with coils. Covered stents can also be particularly useful for acquired AVFs (single communications). They have the advantage of maintaining patency of the parent artery. Often, combining strategies by using different techniques becomes necessary.

B

Figs 2A and B:  Right upper lobe pulmonary arteriovenous malformation. (A) Pre-embolization; (B) Postembolization (fibered platinum coils) angiograms. Coils elsewhere are from embolization carried out for other PAVMs in the right lung

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Vascular Malformation The most common type of vascular malformations are VMs and can have significant variations in size and clinical presentation. These lesions (usually distinguished by a bluish discoloration with swelling and pain) may also be associated with systemic syndromes such as blue rubber-bleb nevus syndrome or Maffucci syndrome. Sinus pericranii (communication between intracranial and extracranial venous drainage) is also commonly associated with craniofacial VMs. These lesions can be treated with embolotherapy (sclerotherapy) and/or surgical excision.8,9 The type of treatment used depends on the morphology, size, and location of the malformation. A preliminary venogram is usually obtained to evaluate the deep venous system and to determine if any communication exists between the VM and the extremity veins. In particular, a venogram is performed on extremity VMs. The lesion is localized by using ultrasonography, and the largest-appearing cystic portion of the lesion is selected. Then, the lesion is accessed by using real-time ultrasonographic guidance and a small Angiocath needle [typically, 20–22 gauge (G)]. The lesion is studied with contrast agent injections under fluoroscopy as well as digital subtraction angiography. Subsequently, sclerotherapy is performed by using ethanol (absolute alcohol) or sodium tetradecyl sulfate mixed with a contrast medium (Ethiodol or iodinated contrast) under realtime fluoroscopic control (Figs 3A and B). Foam sclerotherapy is a technique where a mixture of room air and sclerosant is injected and potentially results in greater agent-malformation contact and lowers volume of sclerosant required. If draining veins are present (as they commonly are), manual compression or a tourniquet should be used to reduce washout of the sclerosant material from the malformation. If

A

large draining veins are present, these veins can be embolized with coils via a percutaneous approach before sclerotherapy. For large head and neck VMs, airway involvement can be a challenging component of the condition in terms of treating the patients. Because alcohol and sodium tetradecyl cause significant edema after sclerotherapy, airway patency should be carefully monitored during and after the sclerotherapy procedure. In patients with large head and neck VMs requiring surgical debulking, presurgical sclerotherapy with NBCA glue can be performed because NBCA causes no significant edema. Two common problems associated with sclerotherapy include skin necrosis (blisters) and/or nerve damage or paralysis. Nerve damage or paralysis can result from the direct toxic effect of the sclerosant agent and/or compression of the nerve by focal compartmental tissue edema (compartment syndrome). In addition, hemoglobulinuria is a relatively common complication; this is treated by aggressive hydration and alkalinization. A less common but more severe complication is cardiac toxicity resulting from the systemic effect of absolute alcohol.

Lymphatic Malformation Lymphatic malformations (LM) can be grouped as microcystic, macrocystic, and mixed. The mixed form of anomaly is probably the most common form of LM. Lymphatic cysts contain lymphatic fluid. When a single cystic mass (previously termed cystic hygroma when found in the neck) or a conglomerate mass containing a few macrocysts is encountered, surgical excision is considered the most effective treatment. However, some lesions respond really well to sclerotherapy without any complications after 1 or several sclerotherapy sessions.

B

Figs 3A and B:  A diffuse venous malformation in the right thigh. (A) Direct puncture venogram showed minimal flow into deep veins. Sodium tetradecyl sulphate was slowly injected under fluoroscopic control; (B) Successful occlusion of the malformation was achieved

Chapter 123 Interventions in Children

When a mixed form of LM is encountered, the best therapeutic approach may be sclerotherapy for cystic masses, followed by surgical debulking. The microcystic LM, or the microcystic component of the mixed form, does not contain cystic spaces on radiologic studies (including MRI). It demonstrates a characteristic contrast-enhanced pattern of rings and arcs. The sclerosant agents most commonly used are antibiotics (doxycycline), ethanol, sodium tetradecyl sulfate and, most recently, OK-432 (a derivative of group A streptococci). For patients older than 8 years of age, doxycycline is the most commonly used sclerosant agent. But if the patient is younger than 8 years, the options are alcohol, sodium tetradecyl, or OK-432. The amount of alcohol used depends on the weight of the patient, which proves to be a limiting factor in most procedures which involve alcohol. The interventional therapeutic approach used for LMs is similar to the sclerotherapy technique used for VMs; however, an initial venogram is usually unnecessary.

Hemorrhage Embolization can treat several types of hemorrhage. Examples of these include hemoptysis; epistaxis; and gastrointestinal (GI) tract, post-traumatic, and iatrogenic hemorrhage (e.g. postbiopsy or nephrostomy tube insertion).

Gastrointestinal Hemorrhage Major causes of upper GI tract hemorrhage are ulcer disease, varices and gastritis. The most common causes of a lower GI tract hemorrhage are vascular malformations and bleeding after endoscopic biopsy. If the bleeding source is identified on arterial angiogram, the patient is treated by using either intra-arterial vasopressin infusion (Pitressin) or embolization of the bleeding mesenteric artery. Embolization is usually the first line of treatment in patients with upper GI tract bleeding and is used as the second line of treatment in patients with lower GI tract bleeding (usually used if vasopressin treatment fails).10 Embolization in the arcades proximal to the bleeding vasa recta is recommended to minimize the risk of bowel necrosis. The most commonly used embolic agents are coils (macrocoils or microcoils) and Gelfoam pieces (torpedoes). Coil embolization is particularly helpful if the bleeding is caused by focal vascular abnormalities such as a false aneurysm. Some interventional radiologists have also used PVA, although the use of PVA or other particles should be avoided because of the risk of bowel infarction. After embolization, control angiography is performed to determine if bleeding (contrast material extra-vasation) continues via any collaterals. The primary advantage of embolotherapy is the immediate cessation of bleeding without need for prolonged catheterization (unlike vasopressin infusion therapy).

Pelvic Hemorrhage Intractable pelvic hemorrhage, usually post-traumatic, should be approached in a similar interventional fashion. It is usually not favorable to employ a surgical approach to control active bleeding in acute trauma setting. It is mandatory to hold a detailed angiographic examination with super selective injections in the branches of the internal iliac artery. Embolization can be performed by using an autologous blood clot, Gelfoam torpedoes, PVA particles, NBCA, coils, or detachable balloons.11 At the capillary level, embolization with small particles or Gelfoam powder is contraindicated (because of the elimination of collateral flow, which results in massive tissue necrosis). A specific anatomic relationship between the fracture site and the affected vessel often allows embolization of the branch (frequently the obturator artery) even when no obvious bleeding site is detected.12 In particular, liquid or particle embolization of the inferior gluteal branch of the anterior division should be avoided to minimize the possibility of sciatic nerve injury (this branch supplies muscles of the thigh and buttocks and the sciatic nerve). In addition, embolization of the posterior division of the internal iliac artery should be avoided because of the risk of gluteal necrosis.

Hemoptysis Hemoptysis is considered massive when at least 300 mL of blood is lost in less than 24 hours, and it may be lifethreatening. Common causes of massive hemoptysis are cystic fibrosis, bronchiectasis, tuberculosis, and aspergillosis. Malignancy is rarely a cause. Surgical intervention is usually not feasible because of severe pulmonary disease; therefore, embolization of the bleeding bronchial arteries can be lifesaving.13 Bronchial arteries are variable. They usually arise from the descending thoracic aorta between thoracic vertebrae T4 and T7. The right bronchial artery arises from the intercostobronchial trunk in most patients (>90%). The left bronchial artery usually arises directly from the aorta and is multiple in most patients. Occasionally, the right and left bronchial arteries arise from a common trunk. Although some bronchial branches may supply the spinal cord, the most important of these branches is the artery of Adamkiewicz. This artery usually arises from an intercostal or lumbar artery on the left. Other spinal branches from the right intercostobronchial artery, thyrocervical, or costocervical arteries may be identified. A preliminary thoracic aortogram may be performed, which usually shows abnormal bronchial arteries. An aortogram helps in outlining the bronchial anatomy. Because of potential source of collaterals, a subclavian arteriogram also is obtained, particularly if the upper lung field is involved. Then, the bronchial arteries are catheterized

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and studied with selective injections. The most common appearance of the abnormal bronchial artery (the bleeding source) is increased caliber of the bronchial artery with some hypervascularity over the lung field. Contrast agent extravasation, shunting from bronchial to pulmonary arteries, or aneurysmal changes in the involved bronchial artery rarely are identified. Embolotherapy is usually performed with particles (PVA or embospheres) and Gelfoam pledgets (Figs 4A and B). When the decision is made to use particles, appropriately sized particles should be used. Sizes are usually 500–710 µm for PVA and 500–800 µm for embospheres. Use of coils is inappropriate, and absolute alcohol or cyanoacrylate is no longer used for bronchial artery embolization because of the risk of tissue necrosis (bronchial and/or esophageal). Embolization is performed as selectively as possible (when necessary, by using a microcatheter and coaxial technique) to minimize tissue necrosis and nontarget embolization (e.g. spinal artery). Special care should be taken to prevent reflux by injecting the embolic material slowly under continuous fluoroscopic control. Gelfoam pledgets/torpedoes usually are used to occlude the abnormal artery more proximally after particle embolization.

Internal carotid arteriograms are obtained to exclude aneurysms. Then, the external carotid artery is catheterized and control angiography is performed initially to map the vascular anatomy and to check for the presence of a collateral supply to the intracranial circulation. During catheterization of the external carotid artery and its branches, vasospasm is a common problem. Nitroglycerin can be used to treat this. The target branch is usually the pterygopalatine division of the internal maxillary artery, which is distal to the origin of the meningeal and temporal arteries. By using a microcatheter, the pterygopalatine division is catheterized and embolized with particles (most commonly PVA). If bleeding is not caused by a neoplastic entity, embolotherapy can be performed in the 250–500 µm range. If a neoplastic entity is the cause, the capillary bed needs to be embolized. This embolization can be accomplished by using smaller particles (150–250 µm). Although the procedure is considered safe if performed by an experienced physician, possible complications can occur. These include ischemia, pain, cranial nerve damage, blindness, and stroke.

Epistaxis

Post-traumatic hemorrhage can be due to either a blunt or penetrating injury to a vessel, typically arteries in the extremities with penetrating injuries or associated fractures or arteries to the organs (e.g. renal arteries, after blunt trauma). Some patients may present after an orthopedic procedure, such as total hip replacement. An angiographic study is mandatory, not only to aid selecting in the appropriate subsequent embolization procedure but also in planning for possible future surgical interventions.

Intractable epistaxis is a nosebleed that does not respond to conservative treatment (nasal spraying of vasoconstrictors, nasal packing, blood transfusion). Etiologies include uncontrolled hypertension with or without superficial mucosal abnormality (e.g. Osler-Weber-Rendu syndrome). Epistaxis can be treated by either surgical means (e.g. cautery, vascular ligation) or endovascular embolotherapy.

A

Post-traumatic Hemorrhage

B

Figs 4A and B:  A patient with hemoptysis due to bronchiectasis in the right upper and middle lobe. Selective injection of the hypertrophied

right intercostobronchial trunk: (A) Revealed multiple feeders with parenchymal blush; (B) After embolization with PVA particles and gelfoam, the culprit vessel is completely occluded

Chapter 123 Interventions in Children

Coil embolization is appropriate in extremity branch arteries responsible for the bleeding because it offers a fast and permanent occlusion of the vessel. The bleeding vessel should be embolized proximal and distal to the site of arterial injury. Avoid embolization of arteries that endangers limb viability. Hemorrhage or AVF formation after organ biopsy (particularly renal biopsy), or iatrogenic traumatic hemorrhage, is a common complication (i.e. iatrogenic traumatic hemorrhage) that can be treated with embolization (Figs 5A and B).

Pseudoaneurysm Pseudoaneurysms occur secondary to trauma or infection and consist of leakage of blood into the confined perivascular space at the site of a vessel wall disruption. Embolization is a good alternative to surgical repair, and is often the treatment of choice, especially when pseudoaneurysms are not accessible or when the patient is not a surgical candidate because of sepsis or other medical conditions.14,15 Embolic materials used for pseudoaneurysms include coils, detachable balloons, thrombin, gelfoam, and NBCA. In large-neck pseudoaneurysms, a stent placement combined with coil embolization has been described. If the involved vessel cannot be catheterized or if a pseudoaneurysm is close to the skin surface (typically a pseudoaneurysm in the groin after cardiac catheterization), the pseudoaneurysm can be directly punctured with a fine needle (e.g. 22 G), and thrombin or NBCA can be injected (Figs 6A to D). When the involved artery is embolized with coils, the artery also should be embolized distal to the origin of the pseudoaneurysm so that collaterals do not fill the aneurysm

A

Malignant Tumors Indications for embolotherapy in neoplastic conditions include preoperative embolization and palliative embolization. Embolization helps to alleviate symptoms, reduces further dissemination, and increases the response to other treatment modalities (e.g. radiation therapy). Embolotherapy can be used for many types of malignant tumors.16 Renal malignancy is the most common type of tumor treated with embolotherapy. In particular, tumors extending into the hilum or other adjacent structures for which surgical removal is difficult are treated by using embolotherapy. In these patients, prior embolization of the tumor shrinks the mass and minimizes blood loss during surgical removal. Unresectable tumors can be made operable by means of embolotherapy. If the entity is in its end-stage (disseminated metastatic deposits), the technique can be used for palliation to control pain and hematuria. Other reported malignancies in which embolotherapy has been used include pelvic malignancies and bone tumors. Hemorrhage resulting from malignancy or radiotherapy (e.g. due to radiation cystitis) can be controlled by using embolotherapy.

Chemoembolization Chemoembolization is commonly performed in hepatic malig-nancies.17 The technique is used in patients with unresectable liver tumors and metastatic liver disease. An essential prerequisite for chemoinfusion/chemoembolization is the presence of a patent portal vein with hepatopetal flow. The bilirubin level should be less than 3 mg/dL to perform chemoinfusion/chemoembolization safely.

B

Figs 5A and B:  A patient with postrenal biopsy hematuria. (A) Selective left renal angiogram shows an arteriovenous fistula from an interlobar artery in the midpole with early filling of the inferior vena cava; (B) Complete occlusion of the branch was achieved with coils

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A

B

C

D

Figs 6A to D:  A postcatheterization pseudoaneurysm in the right groin: (A) Selective injections into the right common femoral artery;

(B) A branch of the profunda femoris artery show the jet and the lesion; (C) The lesion was percutaneously punctured and 800 U thrombin was injected; (D) Though the pseudoaneurysm occluded immediately, it recanalized a few days later and needed surgical repair

Vigorous intravenous hydration is required before the procedure for at least 24 hours. Initially, a superior mesenteric arteriogram is usually obtained to demonstrate a variant origin of hepatic artery (accessory or replaced, originating from the superior mesenteric artery) and to demonstrate patency of the portal vein. Then, the celiac trunk and, subsequently, the common hepatic artery are catheterized and studied to outline the vascular anatomy. The involved lobar hepatic artery or, more commonly, the first- or second-order branches of this artery is subsequently catheterized by using a microcatheter and the chemoinfusion material is injected under fluoroscopic guidance. The tip of the catheter must be placed distal to the cystic and gastroduodenal arteries. The most commonly used chemoinfusion mixture consists of 10 mL of iopamidol (Isovue), 20 mL of Ethiodol, and 60 mg of doxorubicin. The chemoinfusion is usually followed by embolization with slurry of gelatin sponge powder (Gelfoam). Lidocaine is intra-arterially administered to reduce pain after the chemoinfusion/chemoembolization treatment.

Organ Ablation Splenic embolization can be used as a preoperative therapy or as an alternative to surgical removal of the spleen. Indications include post-traumatic bleeding, variceal bleeding secondary to portal hypertension or splenic vein thrombosis, hypersplenism, thalassemia major, thrombocytopenia, idiopathic thrombocytopenic purpura, Gaucher’s disease, and Hodgkin’s disease. Embolotherapy is performed with superselective catheterization/embolization of the splenic artery by using embolic particles while the tip of the catheter is beyond the caudal pancreatic artery. Careful fluoroscopic control of the splenic area is required to limit the total infarction to approximately 60% of the spleen.

Renal embolization is an alternative to surgical removal of the kidney, and indications include end-stage renal disease or renovascular hypertension requiring unilateral or bilateral nephrectomy and renal transplant with native kidneys in situ. The procedure requires selective catheterization of the renal artery with further advancement of the catheter so that the catheter is wedged or with the use of a balloon occlusion catheter to minimize the possibility of embolic material spillage into the aorta. The preferred embolic agents are particles (e.g. PVA) and/or liquid agents such as ethanol or NBCA. Postinfarction syndrome is relatively common and characterized by pain, which can be managed with narcotics. This pain usually subsides within 48–72 hours.

ANGIOPLASTY The techniques for balloon dilatation of vascular stenosis are the same for children as for adults. Balloon dilatation can be carried out safely even in small children and can permit access to peripheral stenoses. Small balloon catheters (2 mm) and small shaft catheters (3.8 F) can be used with 4 F delivery systems. Small steerable guidewires (e.g. 0.018" or 0.014" PTCA wires) can be used to cross small distal stenosis. For the renal arteries, low profile balloons in diameters of 3–4 mm are employed. Larger balloons up to 20 mm in size are used to treat recurrent coarctation or peripheral pulmonary stenosis. High pressure balloons (up to 17 atm burst pressure) are available with smaller sizes for fibrous stenosis or restenotic lesions. The major indications for angioplasty in children are: zz Renal artery stenosis (RAS) zz Aortic stenosis zz Coarctation of aorta zz Transplant renal artery stenosis zz Peripheral pulmonary stenosis

Chapter 123 Interventions in Children

Systemic-to-pulmonary artery shunt stenosis Budd-Chiari syndrome due to hepatic vein/inferior vena cava (IVC) stenosis. Percutaneous transluminal renal angioplasty (PTRA) is the treatment of choice for RAS. Nonspecific aortoarteritis (NSAA) is responsible for 61% of RAS in our country. Other causes include fibromuscular dysplasia (28%), atherosclerosis (8%), polyarteritis nodosa (2.5%) and renal artery aneurysm of indeterminate etiology (0.5%). NSAA is a chronic and progressive panarteritis of unknown cause that commonly affects the aorta, its major branches and the pulmonary arteries, and results in stenosis, occlusion, dilatation or formation of aneurysms in the involved blood vessels.18,19 Stenosis or obstruction is the most common angiographic abnormality, frequently involving the aorta and the renal arteries, and resulting in systemic hypertension. The complexity of pathological changes in the wall of the aorta and widespread nature of involvement make surgical revascularization a very difficult option. There is also a high prevalence of graft occlusion. Due to these reasons, nonsurgical revascularization techniques have been increasingly used in the treatment of this group of patients.20-22 The therapy in RVH aims at controlling the blood pressure (BP) and restoration of renal blood flow. We accept the patients for treatment by nonsurgical revascularization if they have hypertension uncontrolled by single-drug therapy, angiographic evidence of at least 70% stenosis in the renal artery or the aorta with a pressure gradient of more than 20 mm Hg and a normal erythtrocyte sedimentation rate (ESR). Patients with an elevated ESR and/or a positive C-reactive protein test are considered to have an active arteritis and are not generally accepted for this treatment except in certain situations (uncontrolled hypertension, severe ventricular dysfunction, flash pulmonary edema and deteriorating renal function). Antihypertensive medication is stopped 24 hours before angioplasty, except for sublingual administration of 5–10 mg zz zz

A

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nifedipine if the blood pressure is more than 170/110 mm Hg. The patients are treated with aspirin (175–330 mg) daily for 3 days before angioplasty, and this treatment is continued for 6 months after treatment. Heparin (100 IU/kg body weight) is given IV during the procedure and is not reversed afterwards. Blood pressure medication is withheld for 24 hours after the procedure, except for sublingual administration of nifedipine (5–10 mg) if the blood pressure is above 160/100 mm Hg. If there is severe, uncontrolled hypertension before renal angioplasty, the BP is controlled with nitroprusside drip infusion. For renal angioplasty (Figs 7A to C), a pigtail catheter is positioned in the abdominal aorta above the origin of renal arteries for continuous pressure measurement and diagnostic DSA. The diseased renal artery is selectively catheterized through another arterial sheath in the opposite groin and transstenotic pressure gradient is measured. The angiographic catheter is replaced by a commercially available, appropriate sized balloon catheter by using standard exchange technique. The diameter of the involved vessel is measured and a balloon catheter of same size is used for angioplasty. Three to five inflations, for up to 45 seconds each, are performed until the balloon “waist” is no longer present or has decreased substantially. We do not use oversized balloon catheters in patients with mild residual stenosis or transstenotic pressure gradients in order to avoid the risk of arterial rupture. Immediately after the procedure, transstenotic pressure is measured and an angiogram is obtained to assess the adequacy of angioplasty. Alternatively, the procedure can be completed through a single groin approach too. After crossing the stenosis with the angiographic catheter, an 0.014" or 0.018" exchange guidewire is placed in a distal intrarenal branch, and a 6F or 7F (depending upon the patient size) guiding (right coronary or renal double curve configuration) catheter is placed at the ostium of the diseased artery. The appropriately compatible balloon catheters (sometimes, PTCA balloons in monorail

C

Figs 7A to C:  A 12-year-old female with hypertension: (A) Tight bilateral ostial renal artery stenosis due to aortoarteritis; (B) The right stenosis was treated with balloon angioplasty with a mild residual waist; (C) The lesion opened up well with mild residual disease. The left stenosis was then subjected to angioplasty with a similar result

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configuration may also be used) are then used to dilate the lesion. The advantage of this approach is the avoidance of a second puncture, although the cost of hardware increases. If there is an obstructive dissection or a recurrent ostial stenosis, renal artery stent placement is considered. Pretreatment with ticlopidine (250 mg twice daily) beginning three days before angioplasty is then advisable. This should be continued for at least 6 weeks after the procedure. A preshaped renal guiding catheter is positioned at the ostium of the diseased renal artery over an exchange guidewire positioned in a secure distal location in the artery. The selection of the diameter and length of the stent is based on the angiographic morphology of the involved artery. It is advisable to give sublingual nifedipine (5–10 mg) or an intra-arterial bolus of trinitroglycerine (100–200 mg) in the renal artery before stent placement. The stent is positioned across the lesion and released by inflating the balloon at the desired inflation pressure for up to 30 seconds. Various stent designs are available for use in this location. Balloonmounted stents are generally preferred for an ostial stenosis. A check angiogram is obtained at the end of the procedure to assess the adequacy of stent release. Intravascular ultrasound is a useful technique to define the endpoint of intervention. Angioplasty or stent placement in the aorta is performed by a similar technique. Angioplasty is considered technically successful if: (1) the aortic or renal artery lumen after angioplasty has less than 30% residual stenosis (2) the arterial lumen is at least 50% larger than its pretreatment diameter, and (3) the pressure gradient is less than 20 mm Hg and has decreased at least 15 mm Hg from the pretreatment gradient. The clinical results of the angioplasty are judged as follows: (1) cure (normal BP after the procedure without antihypertensive drug therapy), (2) improved (at least 15% reduction in diastolic pressure or a diastolic pressure less than 90 mm Hg with the patient taking less antihypertensive medication than before the procedure), and (3) failed (no change in BP after the procedure). All patients cured or improved are considered to have benefited from angioplasty. Follow-up is performed by BP and medication evaluation 1 day, 1 week, and 4–6 weeks after treatment and then at 6-month intervals. Follow-up angiograms are performed in patients with recurrence of hypertension, in whom contralateral nephrectomy of poorly or nonfunctioning kidney for residual hypertension is planned and in those patients who consent for the procedure. Angioplasty is repeated if restenosis is detected. Percutaneous transluminal angioplasty (PTA) of the aortic stenosis in NSAA can also be carried out by a similar technique (Figs 8A and B). The angiographic features, including eccentricity of the stenosis and presence of diffuse adjacent disease, location of the stenosis in juxtadiaphragmatic segment of the aorta and presence of calcification adversely affect the outcome of PTA, most of whom develop large intimal flaps. Stents have been occasionally used as a “bail-out” measure in salvaging an obstructive dissection in

such situations and rarely electively in the treatment of native stenosis. Stents provide an immediate relief of symptomatic obstructive dissection and are also useful in the treatment of recurrent stenosis after successful angioplasty. We do not advocate elective use of stents due to young age of the patients, the cost involved and lack of knowledge about the long-term behavior of stents in the aorta at a growing age. Until recently, it was felt that this diesease is characterized by skip areas of involvement. The findings of recent studies, using cross-sectional imaging techniques, suggest that nonspecific aortitis involves a continuous length of the aorta, producing mural and luminal changes in some areas, and only mural changes in the intervening segments. This observation has therapeutic implications. The site of surgical reconstruction or balloon positioning in PTA is based on the demonstration of angiographically normal adjacent segments. The results of cross-sectional imaging suggest that there are extensive wall changes even in angiographically normal areas. The unpredictable outcome of PTA and surgical revascularization in nonspecific aortitis, in our opinion, is caused by the placement of a bypass graft or the balloon catheter within the diseased segments and not from normal to normal aortic segment. In this regard, intravascular ultrasound may be useful in guiding the interventional procedures. Overall, aortic PTA has specific technical problems but has a high technical and clinical success rate. The complication rate is low. Late remodeling occurs in most patients and is responsible for delayed clinical benefit despite poor technical success in some patients. Arterial stenosis associated with renal transplantation can often be improved. These obstructions may be at or beyond the suture line. It is important to evaluate the hemodynamic significance of proximal stenosis because in some of these

A

B

Figs 8A and B:  (A) Juxtadiaphgramatic aortic stenosis (due to

aortoarteritis) in an 18-year-old girl with resistant hypertension; (B) The stenosis responded well to balloon angioplasty alone with a small dissection flap. The systolic pressure gradient across the lesion was significantly reduced and the patient did well on clinical follow-up

Chapter 123 Interventions in Children

patients extensive peripheral disease due to rejection nullifies the benefit of dilating the proximal lesions. Peripheral pulmonary artery stenosis can sometimes be treated effectively but at moderate risk. Because of the elasticity of pulmonary arteries, these lesions require large balloons for small increases in artery size. Arterial rupture can occur, resulting in death. Because there are no surgical options to treat these lesions, balloon dilatation is the procedure of choice when treatment is clinically indicated. Stenting is a safer and more effective approach to these lesions. After the modified Blalock-Taussig (BT shunt) is placed, stenosis can develop in the subclavian artery, the proximal or distal anastomosis, the graft, or the pulmonary artery. All of these may be treated except the graft stenosis. The best results are obtained in those patients with a traditional BT shunt where the subclavian artery has been directly connected to the pulmonary artery, but this surgery is rarely performed nowadays. Most BT shunts are performed with Goretex grafts, which limit the amount of stretching of the stenosis. Narrowing within the graft is probably caused by kinking, thrombosis, or fibrointimal proliferation.

Complications of Angioplasty Procedures Vascular spasm can occur, particularly in PTRA, and may in turn provoke thrombosis and segmental infarction. 100 Units/kg of heparin is usually given to prevent this, and more may be required for prolonged procedures. Monitoring of heparinization with measurements of activated clotting time (ACT) should be done. Spasm may be treated with direct intraarterial injection of nitroglycerin (0.25–1.00 µg/kg/minute). Thrombosis may occur at the PTA site or at the groin. If it does, then thrombolytic therapy is indicated. Intimal dissection is part of any PTA procedure, and usually does not cause flow obstruction. If an obstructive dissection develops, stents may be used. Vascular rupture is always a concern but can be avoided by appropriate balloon selection.

THROMBOLYSIS Experience with thrombolysis in children is limited but has increased because of the need to treat complications of cardiac or peripheral angiography or intervention. Procedures requiring insertion of devices mounted on large shafts are more likely to result in femoral artery thrombosis. The other indications include thrombosis of BT shunts, dialysis fistula, pulmonary artery thrombosis, iliofemoral thrombophlebitis, aortic thrombosis in neonates, and brachial artery occlusion after supracondylar fracture. Contraindications for the procedure include recent surgery or trauma (within the past 6 weeks), any intracranial or gastrointestinal bleed within the past 3 months, renal failure, gangrene or significant pregangrenous changes in the affected organ system or extremity.

Thrombolytic agents include streptokinase, urokinase, or r-tpa. Urokinase is the most commonly employed agent. Local low-dose therapy is unlikely to produce systemic changes in coagulation, whereas systemic therapy may cause undesirable bleeding. The dose of urokinase for local low dose infusion is 300–500 IU/kg/hour. High-dose, short-duration treatment given locally often produces clearing of thrombus (Figs 9A to D). Treatment failures usually relate to delays in implementing therapy, resulting in maturation of thrombus. The fibrinogen level, thrombin time, prothrombin time, and activated partial thromboplastin time are monitored at regular intervals, and the children are observed in an intensive care unit or neonatal nursery. Complications of intra-arterial thrombolysis include systemic bleeding ( 60 per minute) 2. Retractions (intercostal, subcostal, sternal or suprasternal) 3. Noisy respiration (grunt, stridor or wheeze). Respiratory distress occurs in 11–14% of all live births.2 Gestational age has pronounced effect on incidence of neonatal respiratory distress with incidence of respiratory distress on first day of life being higher in babies born at lesser gestation. Kumar et al. reported 60% incidence of respiratory distress in babies less than 30 weeks of gestational age which reduced to 5–6% in babies with gestational age more than 34 weeks.2 There are several causes which can give rise to respiratory distress during the neonatal period. They can broadly be classified as follows:3 zz Causes affecting respiration at alveolar level: Hyaline membrane disease (HMD), pneumonia, meconium aspiration syndrome, pneumothorax, pulmonary hemorrhage, primary pulmonary hypertension, transient tachypnea of newborn (TTNB), etc. zz Structural anomalies of the respiratory tract: Congenital lobar emphysema (CLE), congenital caustic adenomatoid malformation (CCAM), congenital diaphragmatic hernia (CDH), choanal atresia, tracheoesophageal fistula (TEF), etc. zz Extrapulmonary causes: Chest wall abnormalities, congenital heart disease, metabolic acidosis, etc. The management of neonatal respiratory distress depends upon clinical history, examination, radiology and laboratory data. The radiology of important causes of respiratory distress in neonatal period is discussed in this chapter.

MEDICAL CAUSES OF NEONATAL RESPIRATORY DISTRESS Hyaline Membrane Disease Hyaline membrane disease, also known as respiratory distress syndrome (RDS), constitutes the most common cause of respiratory distress in the premature newborn infant accounting for up to 60% incidence in babies born at or before 29 weeks of gestation.4 It is a manifestation of pulmonary immaturity and results from impaired surfactant production by type 2 pneumocytes leading to formation of hyaline membranes within alveoli and terminal airways, hence the name. Oxygen therapy along with surfactant supplementation currently forms the cornerstone of treatment for HMD. Persistent barotraumas and oxygen toxicity in these neonates, due to intensive oxygen and ventilation therapy, can lead to bronchopulmonary dysplasia (BPD).5 The radiological evaluation of HMD has traditionally relied upon chest radiography. The radiographic findings in untreated HMD reflect the generalized acinar collapse that results from surfactant deficiency. Chest radiograph features in these neonates demonstrate decreased expansion of lungs, symmetric generalized consolidation of variable severity, effacement of normal pulmonary vessels and air bronchograms (Figs 1A and B).6 The commonly seen “reticulogranular” pattern of lung opacities in HMD represents the summation of collapsed alveoli, transudation of fluid into the interstitium from capillary leak and distension by air of innumerable bronchioles that are more compliant than surfactant deficient lung. This radiographic picture reaches maximum severity around 12–24 hours of life. In severe cases, there may be complete bilateral “whiteout” of lungs due to extensive consolidation.7 The radiographic findings of HMD also depend on the timing of the administration of surfactant. Early on, despite

Chapter 125 Neonatal Respiratory Distress

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Figs 1A and B:  (A) Chest X-ray AP view of a preterm neonate with respiratory distress soon after birth reveals low volume lungs with bilateral consolidation with “whiteout” of lungs suggestive of hyaline membrane disease (HMD); (B) In another preterm neonate with respiratory distress soon after birth, consolidation is less extensive

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Figs 2A and B:  (A) Chest X-ray AP view of a preterm neonate with respiratory distress soon after birth reveals low volume lungs with bilateral consolidation with “whiteout” of lungs suggestive of hyaline membrane disease (HMD); (B) 18 hours after surfactant administration, there is asymmetric clearing of upper zones

prevention with surfactant, the lungs are hypoaerated and have a reticulogranular pattern due to interstitial fluid and atelectatic alveoli. The administration of surfactant usually produces some clearing (Figs 2A and B), which may be symmetrical or asymmetrical; the asymmetry usually disappears in 2–5 days. Since the surfactant is not evenly distributed throughout the lungs, areas of improving lung alternating with areas of unchanged RDS are common findings.8 With positive-pressure ventilation usually given in these infants, the lung opacity decreases, and they appear radiographically improved. However, the positive pressure required to aerate the lungs can disrupt the epithelium, producing interstitial and alveolar edema. It can also cause

the dissection of air into the interlobar septae and their lymphatics, producing pulmonary interstitial emphysema (PIE) (Fig. 3). Radiographically, PIE appears as tortuous, 1–4 mm linear lucencies that are relatively uniform in size and radiate outwards from the pulmonary hilum. The lucencies do not empty on expiration and extend to the periphery of the lungs.9 PIE can be symmetrical, asymmetrical, or localized to one portion of a lung. Peripheral PIE can produce subpleural blebs which can rupture into pleural space to produce pneumothorax or can extend centrally to produce pneumomediastinum or pneumopericardium. Since, portable chest radiography imparts ionizing radiation and involves delay in availability of information to the clinician, alternative strategies in evaluation of HMD

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are desirable. A few studies have evaluated use of sonography in diagnosis of HMD.10,11 Using the transabdominal approach for visualization of lung bases, these studies reported a typical pattern of increased retrodiaphragmatic hyperechogenicity which has high sensitivity and specificity for diagnosis of HMD (Figs 4A and B). Another study by Copetti et al.,12 tried transthoracic approach for evaluation of HMD. They suggested that a combination of whiteout lung, absence of areas of sparing and pleural line abnormalities to be 100% sensitive and specific for diagnosis of RDS. Sonography has also been used for follow-up of HMD and early prediction of BPD in neonates suffering from HMD.13,14 In these studies, the incomplete clearance of retrodiaphragmatic hyperechogenicity was found to be

a good predictor of later development of BPD. Avni and colleagues13 suggested that day 18 was the earliest day where the persistence of the abnormal retrodiaphragmatic hyperechogenicity was observed in 100% of the patients developing BPD at day 28. At that time, 95.2% of the patients without abnormal hyperechogenicity showed uncomplicated evolution and no BPD. They concluded that sonography can be a useful diagnostic tool to determine the occurrence of BPD and to predict as early as day 18 the premature at risk for the disease. In another similar study, Pieper et al.14 reported that day 9 was the earliest day where persistence of abnormal retrodiaphragmatic hyperechogenicity was observed with the highest predictor values for the development of BPD. These preliminary studies suggest that sonography has a role in early identification of neonates who are at risk of developing BPD in future. However, there is some discrepancy regarding the exact postnatal age at which this can be achieved.

Transient Tachypnea of Newborn

Fig. 3:  Follow-up chest X-ray of a patient of hyaline membrane disease (HMD) reveals lucent lesions suggestive of pulmonary interstitial emphysema (PIE)

A

Whereas HMD is a disease of premature neonates, transient tachypnea of newborn (TTNB) affects term babies. In the fetal life, the lungs are distended with fluid. This fluid is cleared from the lungs during the squeeze through the birth canal while additional fluid is removed by pulmonary capillaries and lymphatics. The delay in clearance of pulmonary fluid leads to TTNB which is also known as “wet lung disease”. The risk factors include delivery by cesarean section; precipitous delivery; and very small, hypotonic or sedated babies. The babies present with mild or moderate respiratory distress soon after birth.15 Typically, the disease is self-limiting with resolution of symptoms in 6–24 hours. Uncommonly, the symptoms may last 2–5 days when it becomes necessary to exclude alternative causes of respiratory distress.3

B

Figs 4A and B:  (A) Chest X-ray AP view of a preterm neonate with respiratory distress soon after birth reveals low volume lungs with bilateral consolidation with “whiteout” of lungs suggestive of hyaline membrane disease (HMD); (B) Coronal transabdominal sonography reveals diffuse retrodiaphragmatic hyperechogenicity suggestive of HMD

Chapter 125 Neonatal Respiratory Distress

The radiographic features of TTNB include mild overaeration, mild cardiomegaly, small pulmonary effusion and prominent perihilar interstitial markings (Fig. 5). TTNB may mimic reticulogranular pattern of HMD but lacks the underaeration seen in HMD. The radiographic features may occasionally look similar to pulmonary edema or meconium aspiration syndrome.15 Copetti and Cattarossi16 have recently evaluated the lung sonographic findings in TTNB and its clinical relevance. They reported that in neonates with TTNB, lung sonography revealed difference in lung echogenicity between the upper and lower lung areas. There were very compact comet-tail artifacts in the inferior lung fields which were rare in the superior lung fields. They designated this finding the “double lung point”. In this study, “double lung point” was not seen in healthy infants, infants with RDS, atelectasis, pneumothorax, pneumonia, or pulmonary hemorrhage. Thus, the sensitivity and specificity of the “double lung point” was 100% for the diagnosis of TTNB. However, a recent report suggests that “double lung point” may be seen in pneumothorax as well.17

associated pneumonia is the second most common hospitalacquired infection among pediatric and neonatal ICU patients,19,20 and is responsible for a very high mortality in neonatal ICU patients. The majority of cases are of bacterial etiology. Radiographically, pneumonia is characterized by pulmonary opacities (Fig. 6). However, similar appearance may be seen in hyaline membrane disease, transient tachypnea of newborn and meconium aspiration syndrome. Presence of pleural effusion is a helpful pointer towards pneumonia. Furthermore, some of these conditions may coexist with pneumonia.15 The patients with positive radiograph who do not grow causative organism from blood culture are considered “probable pneumonia”.21 It is important to note that in some of the patients with pneumonia, chest X-ray may be normal and diagnosis is made on isolation of organism from blood culture.18 Rarely, pneumonia may mimic mass lesion (Figs 7A to D).

Neonatal Pneumonia Pneumonia is an important cause of neonatal respiratory distress in India with all cases of neonatal respiratory distress being treated as pneumonia at the first referral unit.18 In a recent study which evaluated the causes of respiratory distress in outborn neonates brought to a referral unit, Mathur et al.18 reported pneumonia to be the cause of respiratory distress in more than two-thirds of cases. However, this study did not include patients having surgical causes of respiratory distress. The pneumonia may set in due to transplacental spread, lack of asepsis during delivery, aspiration of amniotic fluid or be acquired during hospital stay for other ailments. Ventilator

Meconium aspiration is a disease predominantly affecting term and postmature neonates. While, 10–15% of neonates pass meconium in utero, it is rare before 37 weeks.21 Fetus manifests normal shallow regular respiratory movements during intrauterine life. Fetal hypoxia stimulates deep gasping respirations. In addition, it also leads to premature passage of meconium in utero. Meconium is sterile but locally irritant. It can cause obstruction of medium and small airways. In addition, it is a good medium for bacterial growth. The severity of meconium aspiration syndrome depends on several factors including consistency of meconium, adequacy of oropharyngeal suction, associated asphyxia, resuscitative measures, etc.

Fig. 5:  Transient tachypnea of newborn: Chest X-ray of a term

Fig. 6:  Chest X-ray AP view of a neonate on ventilator with respiratory

neonate born by cesarean section and respiratory distress soon after birth reveals normal volume lungs with perihilar infiltrates, prominent cardiac silhouette and pleural fluid in minor fissure (arrow)

Meconium Aspiration Syndrome

distress reveals patchy consolidation in right lung suggestive of pneumonia

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Figs 7A to D:  Pneumonia mimicking mass lesion—(A) Chest X-ray AP view of a 3-week-old male child with fever and respiratory distress reveals

mass like opacity in left upper zone; (B) Mediastinal; and (C) Lung window of contrast-enhanced computed tomography (CECT) scan confirm mass like consolidation in left upper lobe; (D) Lung window of repeat CECT scan after 4 weeks of antibiotics reveals resolution of opacity

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Figs 8A and B:  (A) Term neonate with meconium aspiration. Chest X-ray AP view reveals bilateral hyperinflation; (B) In another neonate with

respiratory distress and suspected meconium aspiration, chest X-ray AP view reveals bilateral pulmonary opacities. Pulmonary opacities in meconium aspiration may be due to atelectasis, chemical pneumonitis or super added pneumonia

Chapter 125 Neonatal Respiratory Distress

The radiographic appearance in meconium aspiration is variable (Figs 8A and B). Incomplete bronchial obstruction leads to generalized overaeration along with patchy areas of atelectasis secondary to complete bronchial obstruction. There may be subsequent development of pneumothorax and pneumomediastinum. The radiographic appearance may be further complicated by pulmonary edema (because of cerebral, myocardial or renal dysfunction secondary to ischemia), pulmonary hemorrhage, RDS or pneumonia. 15 Some of the babies with meconium aspiration may eventually develop persistent pulmonary hypertension of newborn.3

Pneumothorax Pneumothorax, defined as presence of air in the pleural cavity, is an uncommon but significant cause of neonatal respiratory distress.18,22 Timely identification can be lifesaving. It can occur spontaneously or be secondary to infection, meconium aspiration, ventilation barotraumas (Fig. 9) or lung deformity. The incidence of spontaneous pneumothorax is more in premature babies (about 6%) as compared to term babies (1–2%). The radiographic diagnosis of pneumothorax, although of great clinical significance, can be missed on the X-rays as apicolateral accumulation of air is rather uncommon in the supine films. In the supine position, air preferentially accumulates in anteromedial and subpulmonic recesses.23 The position of air collection is also modified by underlying lung disease. Subpulmonic pneumothorax presents as a relatively lucent region in the left or right upper abdominal quadrant. Sometimes, the only radiographic sign of subpulmonic pneumothorax is deep lateral costophrenic angle (deep sulcus sign).24

Fig. 9:  Neonate on ventilator developed respiratory distress. Chest X-ray AP view revealed gross right pneumothorax

SURGICAL CAUSES OF NEONATAL RESPIRATORY DISTRESS Several conditions of neonatal chest require surgical procedure for management. Although listed here as causes of neonatal respiratory distress, it is to be remembered that they may present beyond the neonatal period. In addition, even if discovered during neonatal period, they may be managed conservatively initially. Some of these conditions, like diaphragmatic hernia, can be diagnosed antenatally. Conversely, some of these pathologies may be discovered accidentally in later life and pose dilemma regarding the need for surgery.

Congenital Lobar Emphysema Congenital lobar emphysema or congenital lobar hyper­ inflation is a disease of multifactorial origin characterized by focal abnormality of a large airway. Unfortunately, the exact abnormality of large airway frequently remains a mystery as it is left inside the body of the patient proximal to the ligated bronchial stump. However, potential culprits include bronchomalacia, kinks, webs, mucosal webs and crossing vessels. Whatever the etiology may be, the result is impairment of bronchial function and hyperinflation of a pulmonary lobe.25 Left upper lobe is the most common site of involvement (40–50%) followed by right middle lobe (28–34%) and right upper lobe (20%).26 The hyperinflated lobe causes mediastinal shift and atelectasis of the adjacent lobes. Prenatal diagnosis is unusual in congenital lobar emphysema. Postnatally, the age of onset of symptoms and

Fig. 10:  Chest X-ray AP view of a neonate with respiratory distress

reveals emphysematous left upper lobe with contralateral mediastinal shift suggestive of congenital lobar emphysema. Presence of vascular markings differentiate congenital lobar emphysema from pneumothorax

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degree of respiratory distress may be variable. However, more than 50% become symptomatic within first week. Not all the symptomatic patients may require immediate surgery.25,27 The postnatal chest radiograph, if acquired early in life, may reveal overdistended fluid filled lobe. Later on, the radiograph shows characteristic hyperinflation of a lobe with splayed pulmonary vessels, atelectasis of adjacent lobes and contralateral mediastinal shift (Fig. 10). The differential diagnosis is pneumothorax wherein the hyperlucent region will be devoid of pulmonary vascular markings. If required, computed tomography (CT) scan can be performed to resolve the diagnosis. The findings seen on chest X-ray can all be seen on CT scan. CT scan can also reveal treatable extrinsic and intrinsic treatable cause of partial bronchial obstruction.26 Uncommonly, the lobar emphysema may affect two lobes. Either the lobes may be affected simultaneously or the second hyperinflated lobe may be detected after first thoracotomy.

The bilobectomy procedure may be performed as one stage or two stage procedure.27

Congenital Cystic Adenomatoid Malformation Congenital caustic adenomatoid malformation (CCAM), also called congenital pulmonary airway malformations (CPAM), is a hamartomatous lesion believed to occur because of the failure of pulmonary mesenchyme into normal bronchoalveolar tissue.15,26 On the basis of pathological findings, Stocker,28 classified the CCAM into five types. However, radiological classification consists of three types:26 zz Type I: It constitutes 50% of CCAM patients and shows multiple or single large cysts which communicate with the bronchial tree of the affected lobe. zz Type II: It constitutes 40% of CCAM and shows multiple cysts that rarely exceed 1.2 cm in diameter and

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Figs 11A to D:  A 3-day-old neonate with respiratory distress. Mediastinal window of contrast enhanced computed tomography (CT) scan— (A) Axial; (B) Coronal reconstruction; and (C) Right parasagittal reconstruction reveal a cystic mass lesion in right upper lobe; (D) Lung window additionally reveals bilateral pneumonia. This lesion can be congenital caustic adenomatoid malformation (CCAM) or bronchogenic cyst. The patient was managed conservatively and is awaiting surgery

Chapter 125 Neonatal Respiratory Distress

communicate with the bronchial tree of the affected lobe. About one-third of these patients have associated congenital anomalies. zz Type III: It is least common type (10% of patients). It consists of multiple small (2 cm) in the posterior nasopharyx narrowing or obliterating the nasopharyngeal air lucency. CT also demonstrates tonsillar adenoidal enlargements well (Figs 4A to C). Enlarged palatine tonsils appear as soft tissue mass projecting on the posterior aspect of soft palate.1 On T2W and STIR images adenoids and tonsils appear hyperintense.

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Figs 3A to C: Foreign body. Axial CT scan (A) of a 7-month-old infant with sudden onset stridor reveals a radiopaque foreign body lodged in the trachea. Coronal minIP (B) and sagittal MPR (C) demonstrate the object well

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Figs 4A to C: Enlarged adenoids and tonsils. CECT of a 9-yearC

old boy with history of snoring reveals enlarged adenoids (A) and palatine tonsils (B). Sagittal MPR (C) shows narrowing of the nasopharyngeal airway

Chapter 128 Pediatric Airway

Glossoptosis

Subglottic Obstruction

Glossoptosis means abnormal posterior motion of the tongue during sleep and is associated with underlying hypotonia, macroglossia or micrognathia. Macroglossia and micrognathia may be diagnosed on lateral radiograph. However, glossoptosis can be demonstrated on dynamic sleep fluoroscopy or cine MRI.

Subglottic Stenosis

Hypopharyngeal Collapse

Prolonged intubation can lead to either tracheomalacia or airway stenosis, particularly with oversized endotracheal tubes or balloon cuffs. Airway stenosis consequent to prolonged intubation usually occurs at the level of cricoid cartilage, which is the narrowest part of the upper airway7 (Figs 6A to C).

Hypopharyngeal collapse refers to cylindrical collapse of the hypopharynx; with its anterior, posterior and lateral walls all moving centrally. It is associated with disorders of decreased muscular tone. This can be diagnosed on cine fluoroscopy or MRI.

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Short segment subglottic stenosis is often congenital in origin (Figs 5A and B).

Postintubation Stenosis

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Figs 5A and B: Subglottic stenosis. CECT of a newborn with stridor. Axial (A), sagittal VRT (B) images show a short segment, smooth subglottic stenosis (arrow)

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Figs 6A to C: Postintubation stenosis. A short segment, smooth subglottic stenosis is seen on sagittal MPR (A), coronal minIP (B) and VB (C) CT images of a child with history of prolonged intubation

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Subglottic Hemangioma Hemangiomas located in the soft tissues of the neck may extend into the subglottic airway. Large hemangiomas or vascular malformations can cause obstruction at any level (Figs 7 and 8). These present in infancy, often at less than 6 months of age; and may be associated with hemangiomas of the face or trunk. Plain radiographs reveal asymmetric subglottic narrowing with associated soft tissue. On cross-sectional imaging, the lesions show intense contrast enhancement which may be nodular. These lesions are unilateral or bilateral, but often asymmetric and occasionally circumferential. On T2W images, as elsewhere hemangiomas appear hyperintense.2 Although a benign lesion with a natural history of proliferation and involution, complications of bleeding and airway obstruction can be life threatening. Spontaneous regression is typical. Endoscopy confirms the diagnosis. When the presentation demands active management, as in patients with symptomatic airway compromise, treatment options include systemic or intralesional corticosteroids, laser ablation, interferon therapy or surgical excision.4,8

aortic arch, mediastinal widening, asymmetric lung aeration, lung collapse or consolidation and radiopaque foreign body. The length of tracheal narrowing and involvement of anterior/posterior walls should be noted. If the radiographs are suggestive of an intrinsic cause of obstruction, then one can proceed with fiberoptic bronchoscopy. If the suspected cause is extrinsic then further cross-sectional imaging is indicated. The choice between CT and MRI is not clearly defined. While MRI has the advantage of being radiation free and not dependent on intravenous contrast, its main drawback is the long scanning times. The need for sedation especially in a child with airway compromise often negates the advantages of MRI, making CT the preferred modality. Both modalities offer good contrast between the central airway and surrounding structures, while the lungs are better visualized on CT.

LOWER AIRWAY OBSTRUCTION Central Airways Small airway diseases such as asthma and bronchiolitis are more common than central causes of obstruction. The central causes may be extrinisic or intrinsic (involving either the wall or lumen). Investigations include frontal and lateral radiographs of the airway and chest. The neck radiographs help to exclude upper airway obstruction. Chest radiographs should be evaluated for tracheal caliber, cardiac size, position of the

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Fig. 8: Lymphangioma. CECT neck of a neonate showing a large multiseptated, multicompartmental cystic lesion obliterating the oropharyngeal airway

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Figs 7A to C: Hemangioma. NCCT (A) and CECT (B, C) image reveal an enhancing, well-defined soft tissue mass significantly narrowing the oropharyngeal and subglottic airway

Chapter 128 Pediatric Airway

Extrinsic Causes

Vascular Causes

Any mass lesion of the mediastinum such as nodes and cysts include the nonvascular causes of airway compression. Chest wall deformities may similarly result in airway compromise. The classical vascular causes include double aortic arch, anomalous left pulmonary artery (pulmonary sling) and innominate artery compression syndrome. However, several other vascular causes such as dilatation of pulmonary artery (Figs 9A to C), enlargement of ascending aorta, midline descending aorta and right arch with aberrant left subclavian artery can also result in airway compression. A vascular ring encircling the airway occurs as a result of the failure of primitive vascular structures to fuse and regress normally during the development of the aortic arch, pulmonary arteries, and/or ductus arteriosus. Patients with vascular rings may have wheezing, stridor, feeding difficulties, choking episodes, or even aspiration pneumonia; depending on the degree of tracheal and esophageal narrowing.4 Plain radiographs and barium swallow cannot reliably distinguish among the types of vascular ring. Cross-sectional imaging, either with CT or MR, is helpful in delineating the anatomy and aiding in presurgical planning and postsurgical assessment.4,9,10

Vascular Rings Double aortic arch: Double aortic arch is a congenital arch anomaly, and is the most common vascular ring to cause airway compression. It is usually an isolated anomaly. Both right and left arches are seen to arise from the ascending aorta and join to form the descending aorta. Right arch is commonly larger and posterosuperior.1,2 The two arches surround and compress the trachea anteriorly, and esophagus posteriorly. The level of compression is mid to lower thirds of intrathoracic trachea.1,2 On radiography, lateral tracheal indentations are seen. On cross-sectional imaging, it is important to determine the dominant arch (side), as the surgical approach differs accordingly.

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Pulmonary sling: Pulmonary sling refers to a pulmonary artery anomaly wherein the left pulmonary artery arises from the proximal right pulmonary artery, forming a “sling” around the trachea. It subsequently passes between the trachea and esophagus as it courses towards the left lung. It may be associated with congenital heart disease and complete tracheal rings, worsening the airway compromise.1,2

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Figs 9A to C: Vascular compression. Chest radiograph (A) and CECT

C

(B and C) of a 5-month-old infant with ventricular septal defect, showing enlarged central pulmonary arteries with volume loss of the left lung. There is compression of the bilateral main bronchi by the enlarged pulmonary arteries, especially the left main bronchus (arrow)

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Frontal radiograph reveals asymmetric lung inflation. On lateral radiograph, there is posterior compression of the trachea with anterior esophageal impression. It is the only vascular ring to course between the trachea and esophagus, to be associated with asymmetric lung inflation and also the only one to cause anterior indentation on the esophagus.1,2 Innominate artery compression syndrome: Innominate artery (Brachiocephalic) crosses the trachea anteriorly, just below the thoracic inlet. In infants, it arises more to the left than adults. In addition the presence of a large thymus in the mediastinum and lack of rigidity of infantile trachea results in tracheal compression. The range of symptoms vary from none to stridor and dyspnea resulting from severe compression. Most children outgrow the disease and surgery is reserved only for those with severe compression. Lateral radiographs reveal focal anterior indentation of the trachea. CT and MRI detail the severity of the compression and exclude other causes.1, 2

the proximal descending aorta and courses to the left behind the esophagus. In 60% cases, there is dilatation of origin of the LSA (aortic diverticulum of Kommerell). It is commonly an asymptomatic finding with only 5% patients having symptoms.2 However, this anomaly may be associated with a constricting left ligamentum arteriosum, forming a vascular ring and causing airway compression. If the ligamentum arteriosum connects to LSA it forms a loose vascular ring, while if it extends to the aortic diverticulum of Kommerell, a tight ring is formed. On frontal radiograph, there is aortic arch indentation on the right wall of the trachea with tracheal deviation to the left (Figs 10A to C). Right sided descending aorta may also be seen. Lateral view reveals indentation on the posterior aspect of trachea. On barium swallow, frontal views show a filling defect coursing from right inferior to left superior. On lateral view, there is posterior esophageal indentation. Cross-sectional imaging is indicated when there is clinical or radiographic evidence of airway compression.

Right arch with aberrant left subclavian artery: This is an arch anomaly wherein the aortic arch is located to the right of trachea. The left subclavian artery (LSA) originates from

Midline descending aorta: In this anomaly, the descending aorta is positioned immediately anterior to the vertebral body, instead of the normal left paravertebral location.

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Figs 10A to C: Right sided aortic arch. Chest radiograph (A) of a

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5-year-old boy reveals a right sided aortic arch with hyperlucent left lung. CECT chest (B) shows indentation on the right wall of the trachea by the arch with an aberrant left subclavian artery (arrow). The descending aorta is in midline (C)

Chapter 128 Pediatric Airway

It may be an isolated lesion or be associated with hypoplastic right lung and hence mediastinal shift; or aortic arch anomalies. Malposition may result in airway compression due to crowding of structures. Radiographs are often normal, crosssectional imaging reveals the diagnosis.

Other neoplasms that tend to narrow the airway by extrinsic mass effect include infantile hemangiomas, germ cell tumors, rhabdomyosarcomas and neurogenic tumors (Figs 13A and B).

Vascular Malformations Vascular malformations may be venous, lymphatic, or mixed venolymphatic. Although these lesions are usually soft and compressible, giant malformations of the neck and/or chest can compress airway.

Intrinsic causes include those involving the wall which may be dynamic (tracheomalacia) or fixed (stenosis) and intraluminal lesions.

Bronchopulmonary foregut malformations: Bronchogenic cysts are among the most common cystic lesions in the pediatric chest. The most common location is around the carina. Hence, when large, these result in compression of the proximal bronchi. They can occur anywhere along the respiratory tract.4 The dilated proximal esophageal pouch in patients of esophageal atresia can also exert a mass effect on the adjoining airway4 (Fig. 11).

Tracheomalacia: Tracheomalacia refers to abnormal softening of the trachea due to abnormality of the cartilaginous rings. This results in intermittent (expiratory) collapse of the trachea. The narrowing of the tracheal lumen is most marked during forced expiration, coughing, or the Valsalva maneuver.4 It may be primary or secondary to compression by masses or vascular structures. Similar condition may involve the proximal bronchi. It may be congenital associated with syndromes such as cystic fibrosis, or even result from chronic inflammation, chronic extrinsic compression or prior intubation. The characteristic clinical presentation is of an expiratory wheeze. The diagnosis cannot be made on the basis of a single radiograph. Fluoroscopy, and typically fiberoptic bronchoscopy can demonstrate the characteristic dynamic collapse of the trachea. Airway fluoroscopy done in a lateral projection is the traditional radiographic method of diagnosing tracheomalacia. However, bronchomalacia is difficult to diagnose on fluoroscopy, and controlled-ventilation CT, cine CT, or cine MR imaging are preferred methods for this entity.4 On a single phase inspiratory CT the diagnosis is difficult, although the trachea may demonstrate an abnormal shape being flattened slightly posteriorly in the membranous part1,2 (Figs 14A to C). Paired inspiratory-expiratory MDCT/cine MDCT is more sensitive to demonstrate the expiratory collapse, and require the measurement of the area of trachea in both the phases.12

Inflammatory causes: Deep neck space infections, when they spread into the mediastinum, can compress the airway. Large paravertebral abscesses, even tubercular may result in significant airway compression (Fig. 2). Mediastinal lymphadenopathy, tubercular or fungal infections can also narrow the airway by mass effect (Figs 12A to D). Masses: Lymphoma is the most common childhood neoplasm to cause symptomatic airway compromise in children.11

Fig. 11: Esophageal atresia. CECT of a neonate with esophageal atresia, performed to evaluate respiratory distress shows the dilated proximal esophageal pouch (white arrow) causing significant compression of the trachea (black arrow)

Intrinsic Causes

Wall Abnormalities

Stenosis: Fixed trachea stenosis may be congenital or acquired. Congenital tracheal stenosis results from absence of the membranous portion of the trachea resulting in complete or near complete cartilaginous tracheal rings. The various patterns of tracheal stenosis include generalized stenosis, carrot- or funnel-shaped segmental stenosis, and focal stenosis. Focal stenosis usually involves the lower trachea. A tight focal stenosis causes more severe symptoms than a long, mild stenosis. It may be associated with congenital heart disease, pulmonary sling, TEF, or skeletal abnormalities.2,4 On axial imaging, trachea appears as a round or complete circle (O-shaped). Other findings include: circumferential narrowing of the entire length of the trachea and fusion of the cartilaginous tracheal rings posteriorly.4, 13

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Figs 12A to D: Tubercular lymphadenopathy. CECT of a 6-year-old boy reveals conglomerate, necrotic, calcific mediastinal lymphadenopathy with left upper lobe consolidation (A). A more caudal section mediastinal window (B), and lung window (C) and minIP (D) show narrowing of the left main (arrow) and upper lobe bronchii

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Figs 13A and B: Neuroblastoma. CECT (A) showing a large posterior mediastinal mass lesion causing displacement and compression of the major bronchi, especially the left main bronchus. Lung window (B) reveals a hyperlucent left lung

Chapter 128 Pediatric Airway

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Figs 14A to C: Tracheomalacia. Axial CT (A) of a neonate with stridor showing slight posterior flattening of the trachea; min IP (B) and VRT images (C) show narrowing of subglottic trachea. On bronchoscopy, this narrowing was found to be dynamic

Congenital tracheal web is a rare entity. The web is usually not associated with deformity of the tracheal cartilage or the tracheal wall. CT reveals a weblike structure traversing and narrowing the tracheal lumen,14 which is well demonstrated on coronal reformatted images and virtual bronchoscopy.4 Bronchopulmonary foregut malformations: Bronchopulmonary foregut malformations include a wide spectrum of disorders such as: tracheal agenesis, tracheal stenosis, tracheal fistula, branching anomalies, bronchial stenosis, or lung agenesis and hypoplasia; as well as bronchogenic cysts are also included in this group.3 These anomalies may present with respiratory distress in the newborn, recurrent pulmonary infections or mass lesions later in life. This chapter deals with anomalies affecting the major bronchi. Bronchial atresia and sequestration: Bronchial atresia most often involves the left upper lobe. On CT, a mucocele is identified as a hypo- or fluid-attenuating branching structure distal to the atretic bronchus near the hilum. The pulmonary parenchyma distal to the atretic segment is often lucent and demonstrates air trapping. The affected region may even be outlined by pseudofissures.4 Bronchial atresia may be isolated or associated with a retained systemic vascular connection, when it is referred to as intralobar sequestration. The imaging appearance is virtually identical to that of isolated bronchial atresia, except that the atretic bronchus is ectopically located at the margin of the lung. Rarely, such ectopic bronchi may not be atretic but have a connection with the gastrointestinal tract, usually the esophagus. Such cases are usually accompanied by bronchiectasis and accumulated secretions from impaired clearance of lung parenchyma. It is hence important to look for airway abnormalities, pulmonary parenchymal abnormalities, retained systemic vascular connections, anomalous

pulmonary venous drainage, and airway communication with the gastrointestinal tract in patients with suspected bronchopulmonary foregut malformations.4, 15,16 Tracheoesophageal fistula (TEF): Esophageal atresia with or without TEF is believed to result from a faulty separation of the embryonic trachea and esophageal remnants. The most common type of these is proximal esophageal atresia with distal TEF (up to 80–90%). H-shaped TEFs with no atresia constitute up to 5–8%.4 Typical clinical presentation includes failure to pass a feeding tube in a newborn with a history of polyhydramnios at prenatal US, excessive secretions from the mouth, and respiratory distress.4 Chest radiograph demonstrates the feeding tube catheter ending/coiling in the proximal thoracic esophagus. The presence of air in the distal gastrointestinal tract confirms the presence of a distal TEF. In such patients, it is important to observe the airway as there is frequently associated tracheomalacia.17 Also, a dilated proximal esophageal pouch can result in airway compression. Patients with H type fistula may present with recurrent aspiration or small airway disease. While contrast esophagogram is the investigation of choice, CT scan may demonstrate the fistula (Figs 15A and B). Tracheobronchial branching anomalies: Tracheobronchial branching anomalies may be seen as an isolated finding or accompanying heterotaxy syndromes, pulmonary sling, and conditions associated with pulmonary underdevelopment (agenesis, aplasia or hypoplasia). The most common amongst these is the tracheal bronchus or “pig bronchus” (Figs 16A and B). A tracheal bronchus arises from the trachea or mainstem bronchus and aerates either the entire upper lobe or a segment.4,18 An accessory cardiac bronchus or tracheal diverticulum are also relatively common anomalies. An accessory cardiac bronchus arises from the medial wall of the

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right mainstem bronchus or bronchus intermedius, grows toward the pericardium terminating as a blind-ending stump or branching further.19 Tracheal diverticula is seen arising with a narrow stalk from the right posterolateral wall of the trachea near the thoracic inlet.4 Other abnormal branching patterns include tracheal trifurcation, bilateral right-sided isomerism or bilateral left-sided isomerism. A detailed classification of tracheobronchial branching anomalies has been given in “Imaging of the tracheobronchial tree” in AIIMS-MAMCPGI Imaging Course Series, Diagnostic Radiology-Chest and Cardiovascular Imaging 3rd edition.20 Metabolic conditions: Hunter syndrome (a mucopolysaccharidosis) may cause the deposition of mucopolysaccharides in the walls of the major airways results in progressive airway narrowing due to wall thickening and anteroposterior collapse.4, 21

A

Acquired: Acquired tracheal or bronchial strictures usually result from chronic inflammation, often tubercular (Figs 17A to E). Another cause of acquired airway strictures is posttraumatic sequelae.

Intraluminal Causes A foreign body (FB) is the most common cause of bronchial obstruction. Soft tissue masses of the trachea and bronchi are rare. Foreign body: Foreign body aspiration is most often seen in infants and toddlers (8 months–3 years). The bronchi are the most common site of lodgement (76%), while laryngeal (6%) or tracheal (4%) lodgement is far less common. Right bronchus is more common (58%), than the left (42%). 2 The clinical presentation may be acute, while more often

B

Figs 15A and B: Tracheoesophageal fistula (TEF). Axial CT (A) of an infant reveals a communication between the trachea and esophagus with right upper lobe consolidation. Coronal MPR (B) also demonstrates the fistula

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Figs 16A and B: Tracheal bronchus. Axial lung window (A), coronal MPR (B) reveal an accessory bronchus arising from the trachea and aerating the posterior segment of right upper lobe (arrows)

Chapter 128 Pediatric Airway

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Figs 17A to E: Inflammatory stricture. Cranial to caudal CECT sections (A to C) reveal narrowing of the left main and lower lobe bronchii with ill-defined surrounding soft tissue and collapse of left lower lobe. VB images (D) also confirm the main bronchus stricture with nonvisualization of the distal airway. Coronal minIP (E) shows a long segment involvement

the symptoms remain indolent. The symptoms and signs can mimic asthma, upper respiratory infection, or pneumonia. The history of aspiration is often not elicited. Foreign body may lead to partial (“ball-valve” effect) or complete obstruction, resulting in hyperinflation or collapse respectively. Chest radiograph findings include asymmetric lung aeration, lung consolidation or atelectasis,

and even pneumothorax or pneumomediastinum1 (Figs 18 and 19). Metallic foreign bodies can be identified on plain radiographs (Fig. 18). However, commonly aspirated airway foreign bodies are food products, particularly nuts, and seeds, which are not radiopaque enough to be identified at conventional radiography (Figs 20A to D). These organic materials can swell following absorption of water and then

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Fig. 18: Foreign body. Chest radiograph demonstrates a radiopaque foreign body in the right lower lobe bronchus with consolidation in the distal lung

Fig. 19: Foreign body. Chest radiograph of a 2-year-old boy with history of foreign body aspiration and sudden onset respiratory distress reveals a hyperinflated left lung with spontaneous pneumothorax (arrows) and extensive subcutaneous emphysema

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Figs 20A to D: Foreign body. Chest radiograph (A) of a toddler with history of recurrent high grade fever reveals a hyperinflated left lung with tram-track lesions in the left lower zone. A subsequent chest radiograph (B) shows progression in the lung parenchymal lesions with decrease in the hyperinflation. CT scan (C, D) reveals abrupt cut-off of the left main bronchus with intraluminal contents, and distal bronchiectasis. A “neem fruit ball” was removed from the left main bronchus on bronchoscopy

Chapter 128 Pediatric Airway

rapidly change a partial airway obstruction to a complete obstruction.4 Inspiratory radiographs alone may be normal in up to a third of patients (14–35%) with foreign bodies. 1,2 The lung volume of the affected lung/segment may be normal, increased or decreased.1,2 Majority (up to 97%) of the foreign bodies are nonradiopaque.1 The characteristic radiographic finding is that the lung volume remains static with no change in different phases of respiration. This can be demonstrated by obtaining paired inspiratory-expiratory radiographs in cooperative children. In infants and uncooperative children bilateral decubitus radiographs of the chest or fluoroscopy can demonstrate the same finding.1,2 The differential diagnosis of an asymmetric, lucent lung include Swyer-James syndrome and pulmonary hypoplasia.1,2 However, air trapping may be seen in partial obstruction. CT is not routinely advocated in evaluation of a bronchial foreign body. It may, however, be performed as work-up for nonresolving pneumonia or collapse, or even stridor (Fig. 20). CT is also a good option when the clinical setting does not strongly warrant bronchoscopy or if bronchoscopy is not readily available.4 On CT, foreign bodies are well demonstrated as filling defects in the bronchus, besides detailing the changes in the distal lung. It can identify both opaque and nonopaque foreign bodies. Kosucu et al reported a 100% sensitivity and specificity of CT in the evaluation of endobronchial foreign bodies. 22 Applegate et al while evaluating low-dose helical CT found a sensitivity of 83% and specificity of 89% for visualizing plastic pieces in the airway. Peanuts however were not well visualized in the same study.23 Even esophageal foreign bodies can present acutely with symptoms related to airway compression or with complications consequent to perforation and neck and/or mediastinal infection.4 Inflammatory: Tuberculosis—Occasionally, enlarged lymph nodes erode into the bronchus and result in endobronchial fibrosis or luminal occlusion. Intraluminal granulomas may occur in the trachea or bronchi.4,24 In a series by Weber et al., airway involvement in tuberculosis was seen in up to 30% cases.25 Tumors: Tracheal soft tissue masses include tracheal papilloma; while bronchial masses may be carcinoid tumors.1 Carcinoid tumor is the most common amongst these. Rare lesions include adenoid cystic carcinoma, mucoepidermoid carcinoma, inflammatory myofibroblastic tumor, juvenile xanthogranuloma, and metastasis.4 Carcinoid tumors comprise about 80% of endobronchial neoplasms in children and adolescents. These present in children or young adults and may be associated with neuroendocrine secretion. 3,26 Most carcinoid tumors

occur in the mainstem or lobar bronchi, and patients present with dyspnea, wheezing, cough or hemoptysis. CT reveals typically intensely enhancing, ovoid lesions with a long axis parallel to the bronchovascular bundle.4 These lesions may have intraluminal, mural, and extrabronchial components. Associated collapse, consolidation, or air trapping is often seen (Figs 21A to C). They are relatively slow growing masses, and complete surgical resection offers the best chance of cure.27,28

Peripheral Airways Bronchiolitis/Small Airway Disease Acute: Acute inflammation of the bronchi and bronchioles is common in children, and is most often infective in etiology. Plain radiographs reveal hyperinflation with increased perihilar markings. This entity is covered in detail in the chapter on Pulmonary Infections. Chronic: The causes of chronic, small airway disease in children include: constrictive bronchiolitis, extrinsic allergic bronchiolitis, diffuse panbronchiolitis, follicular bronchiolitis and lung disease of prematurity.3 The chest radiograph and even CT findings are often nonspecific though the underlying etiologies may be quite variable. CT scan reveals ground glass opacities with mosaic attenuation and air trapping. Mild bronchiectasis with bronchial wall thickening may be seen (Figs 22 and 23). Constrictive bronchiolitis or bronchiolitis obliterans: Although constrictive bronchiolitis may present as a unilateral hyperlucent lung (Swyer James syndrome), it is more often bilateral. There are several causes of this entity including infection (viral or mycoplasma), toxic and fume exposure, collagen vascular diseases such as Rheumatoid arthritis; and complication of bone-marrow or heart-lung transplant.3,29 HRCT reveals a prominent mosaic attenuation with bronchial abnormalities including bronchiectasis; and airtrapping3,30 (Figs 22A and B). The pattern is similar to severe asthma or cystic fibrosis. Extrinsic allergic alveolitis: Extrinsic allergic alveolitis or hypersensitivity pneumonitis is a form of cellular bronchilitis. In the acute stage CT reveals multiple, ill-defined centriliobular nodules; while in the subacute or chronic stage mosaic alternation with expiratory air trapping are seen3,29 (Figs 23A and B). Areas of fibrosis may also be present. Diffuse panbronchiolitis: Diffuse panbronchiolitis is an exudative form of bronchiolitis seen in Eastern and SouthEastern Asia. CT reveals multiple small centrilobular nodules and linear opacities diffusely distributed in both the lungs.3

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A

B

C

Figs 21A to C: Carcinoid tumor. CT scout (A) of a 16-year-old boy with history of recurrent pulmonary infections reveals volume loss of left lung with extensive consolidation and bronchiectasis. Axial CECT (B) shows a homogeneous mass in the left main bronchus with mediastinal shift to left. minIP (C) demonstrates the entire extent of the mass with distal lung changes. Histopathology revealed a carcinoid tumor

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B

Figs 22A and B: Chronic bronchiolitis. Axial CT lung window (A) and minIP (B) of a 3-year-old girl with history of dyspnea reveals prominent mosaic attenuation with air-trapping and mild bronchiectasis

Chapter 128 Pediatric Airway

A

B

Figs 23A and B: Chronic bronchiolitis. HRCT (A and B) of 8-year-old child reveals multiple, ill-defined centriliobular nodules and bronchial wall thickening (arrow)

Follicular bronchiolitis: Follicular bronchiolitis or lung hyperplasia of the bronchus associated lymphoid tissue is also a cause chronic obstructive diffuse lung disease. In addition to expiratory air trapping, CT reveals areas of ground glass opacity.3, 31

Chest radiographs reveal multiple cystic, ring or tram-track lucencies with bronchial wall thickening. In case of secondary infection mucous plugging, air-fluid levels, bronchial wall thickening and even enlarged draining nodes may be seen (Figs 24 and 25).

Lung Disease of Prematurity

Asthma

This is a unique form of airway disease seen in premature infants with bronchopulmonary dysplasia. It is a destructive diffuse lung disease occurring in a background of rapid alveolar growth. CT helps in excluding other causes of chronic respiratory distress such as central airway lesions.3

The peak age of prevalence of asthma in children is 6–11 years, with a male predominance. 30% of these persist into adulthood.2 Chest radiographs are usually normal and are indicated in case of poor response to therapy, suspected complications or suspicion of an alternate diagnosis.2 Radiographs reveal hyperlucency of lungs or foci of atelectasis. The differential diagnosis includes viral bronchiolitis. CT is seldom indicated in asthma and reveals nonspecific findings of small airway disease (Figs 26A and B). Findings of secondary allergic bronchopulmonary aspergillosis (ABPA) may be seen (Figs 27A and B). Complications are more frequent in younger children as their bronchi are smaller and more easily occluded in an exacerbation. Complications include: lobar collapse, segmental or subsegmental atelectasis, pneumonia, air leaks (pneumomediastinum), subcutaneous emphysema and rarely pneumothorax or pulmonary interstitial emphysema (PIE). In conclusion, it is critical to evaluate the airway in all children presenting with acute, chronic or recurrent respiratory symptoms. Multiphasic imaging is essential. Plain radiographs and fluoroscopy form the initial methods of evaluation, with CT being required often for a complete diagnosis.

Bronchiectasis Bronchiectasis is a common cause of respiratory symptoms in children.28 It is often the result of chronic inflammation causing damage to the supporting structure of the airways. Also, chronic or recurrent inflammation due to immunodeficiency states may cause bronchiectasis. Other etiologies include, abnormal mucus as in cystic fibrosis and abnormal mucociliary clearance in children with ciliary dyskinesias (Figs 24A to C). Proximal bronchial obstruction due to an intrinsic or extrinsic cause may also lead to bronchiectasis in the distal lung. Aspiration secondary to gastroesophageal reflux due to its chronic, recurrent nature has also been postulated as a cause of bronchiectasis.3,32 Patients typically present with recurrent infections. Chest radiographs are relatively insensitive in detecting early changes, with HRCT being the imaging modality of choice.3

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B

Figs 24A to C: Cystic fibrosis. CT scout (A) of a 16-year-old

C

girl showing tubular, branching opacities in the right lung with paratracheal adenopathy. CT scan (B and C) reveals areas of fibrosis, bronchiectasis, bronchial wall thickening, air trapping and mucus plugging

A

B

Figs 25A and B: Bronchiectasis. Chest radiograph (A) showing cystic lucencies with air-space nodules in the right lower zone suggesting secondary infection. CT scan (B) at a different date shows tubular and cystic bronchiectasis in right lower lobe with air trapping

Chapter 128 Pediatric Airway

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B

Figs 26A and B: Asthma. CT scout (A) showing relative hyperlucency of left lower zone. CT scan (B) shows multiple areas of air trapping

A

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Figs 27A and B: ABPA. Chest radiograph (A) of a 16-year-old asthmatic boy showing multiple tubular, branching opacities in bilateral lung fields giving a “finger-in-glove” appearance. CT scan (B) confirms the presence of bilateral tubular bronchiectasis with bronchoceles

REFERENCES 1. ‘Airway’ in Fundamentals of Paediatric Radiology LF Donnelly. 2001 Saunders, Philadelphia, USA. 2. ‘Airway’ in Diagnostic imaging Paediatrics. LF Donnelly (Ed). Amirsys, Utah, USA, 2005. 3. Long FR. Paediatric airway disorders: Imaging evaluation. Radiol Cl N Am. 2005;43:371-89. 4. Yedururi S, Guillerman RP, Chung T, et al. Multimodality Imaging of Tracheobronchial Disorders in Children Radiographics. 2008;28(3):e29. 5. Kumar D, Seith A, Sharma R, et al. Unpublished data AIIMS, Postgraduate Thesis - Evaluation of tracheobronchial lesions by multi-detector row CT. 2003-06. 6. Suto Y, Tanable Y. Evaluation of tracheal collapsibility in patients with tracheomalacia using dynamic MR imaging during coughing. Am J Roentgenol. 1998;171:393-4.

7. John SD, Swischuk LE. Stridor and upper airway obstruction in infants and children. Radiographics. 1992;12:625-43. 8. Bitar MA, Moukarbel RV, Zalzal GH. Management of congenital subglottic hemangioma: trends and success over the past 17 years. Otolaryngol Head Neck Surg. 2005;132:226-31. 9. Choo KS, Lee HD, Ban JE, et al. Evaluation of obstructive airway lesions in complex congenital heart disease using composite volume-rendered images from multislice CT. Pediatr Radiol. 2006;36:219-23. 10. Swischuk LE. Cardiovascular system: imaging of the newborn, infant and child. 5th ed. Philadelphia, Pa: Lippincott Williams &Wilkins. 2003. pp. 303-17. 11. Glick RD, La Quaglia MP. Lymphomas of the anterior mediastinum. Semin Pediatr Surg. 1999;8:69-77. 12. Lee EY, Litmanovich D, Boiselle PM. Multidetector CT evaluation of tracheobronchomalacia Radiol Clin N Am. 2009;47(2):261-9.

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Section 5 Pediatric Imaging 13. Berrocal T, Madrid C, Novo S, Gutierrez J, Arjonilla A, GomezLeon N. Congenital anomalies of the tracheobronchial tree, lung, and mediastinum: embryology, radiology, and pathology. Radiographics. 2004;24:e17. 14. Legasto AC, Haller JO, Giusti RJ. Tracheal web. Pediatr Radiol. 2004;34:256-8. 15. Langston C. New concepts in the pathology of congenital lung malformations. Semin Pediatr Surg. 2003;12:17-37. 16. Newman B. Congenital bronchopulmonary foregut malformations: concepts and controversies. Pediatr Radiol. 2006;36:773-91. 17. Swischuk LE. Alimentary tract, imaging of the newborn, infant and child. 5th ed. Philadelphia, Pa: Lippincott Williams &Wilkins. 2003. pp. 350-6. 18. Ghaye B, Szapiro D, Fanchamps JM, Dondelinger RF. Congenital bronchial abnormalities revisited. Radiographics. 2001;21:105-19. 19. McGuinness G, Naidich DP, Garay SM, Davis AL, Boyd AD, Mizrachi HH. Accessory cardiac bronchus: CT features and clinical significance. Radiology. 1993;189:562-6. 20. Bhalla AS, Sharma R. Imaging of the tracheobronchial tree in AIIMS-MAMC-PGI Imaging Course Series, Diagnostic Radiology-Chest and Cardiovascular Imaging, 3rd edn, Jaypee Publishers, New Delhi. 2009. pp. 90-116. 21. Davitt SM, Hatrick A, Sabharwal T, Pearce A, Gleeson M, Adam A. Tracheobronchial stent insertions in the management of major airway obstruction in a patient with Hunter’s syndrome (type-II mucopolysaccharidosis). Eur Radiol. 2002;12:458-62. 22. Kosucu P, Ahmetoglu A, Koramaz I, et al. Low-dose MDCT and virtual bronchoscopy in pediatric patients with foreign body aspiration. Am J Roentgenol. 2004;183:1771-7.

23. Applegate KE, Dardinger JT, Lieber ML, et al. Spiral CT scanning technique in the detection of aspiration of LEGO foreign bodies. Pediatr Radiol. 2001;31:836-40. 24. Mukhopadhyay S, Gupta AK, Seith A. Imaging of tuberculosis in children in essentials of tuberculosis in children 3rd edn, Vimlesh Seth, SK Kabra (Eds) Jaypee Brothers, New Delhi. 2006. pp. 375-404. 25. Weber AL, Bird KT, Janower ML. Primary tuberculosis of childhood with particular emphasis on changes affecting the tracheobronchial tree. Am J Roentgenol. 1968;103:123-32. 26. Ferretti GR, Thony F, Bosson JL, et al. Benign abnormalities and carcinoid tumors of the central airways:diagnostic impact of CT bronchography. Am J Roentgenol. 2000;174: 1307-13. 27. Curtis JM, Lacey D, Smyth R, Carty H. Endobronchial tumours in childhood. Eur J Radiol. 1998;29:11-20. 28. Kothari NA, Kramer SS. Bronchial diseases and lung aeration in children. J Thorac Imaging. 2001;16:207-23. 29. Hansell DM. Small airways disease: detection and insights with computed tomography. Eur Respir J. 2001;17: 1294-313. 30. Lau DM, Siegel MJ, Hildebolt CF, et al. Bronchiolitis obliterans syndrome: thin section CT diagnosis of obstructive changes in infants and young children after lung transplantation. Radiology. 1998;208:783-8. 31. Kinane BT, Mansell AL, Zwerdling RG, et al. Follicular bronchitis in the paediatric population. Chest. 1993;104:1183-6. 32. Patterson PE, Harding SM. Gastroesophageal reflux disorders and asthma. Curr Opin Pulm Med. 1999;5:63-7.

Developmental Anomalies of Gastrointestinal Tract

129

CHAPTER

Alpana Manchanda, Sumedha Pawa

Derangement of embryological development can lead to malformations at any point along the gastrointestinal tract (GIT) from the oropharynx to the anorectum. Most of these abnormalities manifest clinically with GIT obstruction and present with vomiting and abdominal distention. Bilestained vomiting occurs when the obstruction is below the ampulla of Vater, whereas vomiting of clear gastric contents indicates obstruction above the second part of the duodenum. Abdominal distention indicates a low level of obstruction. However, one must remember that both vomiting and abdominal distention may occur in conditions like sepsis, increased intracranial pressure, etc. in the absence of anatomic abnormality of the GI tract.1 Infants who have undergone resuscitative efforts, or infants on continuous positive airway pressure, may swallow an excessive amount of air, leading to clinically significant abdominal distention. Since the distention is by air only, the walls of the distended loops on the abdominal radiograph are razor-sharp. Pathological conditions, involving the gut, such as ileus and obstruction, are characterized by dilatation with both air and fluid.2 Developmental lesions of the neonatal gastrointestinal tract can be grouped as follows:1

ANATOMICAL Attributed to embryological maldevelopment: zz Esophageal atresia with or without fistula zz Antropyloric atresia zz Antral diaphragm zz Duodenal atresia zz Duodenal stenosis —— Intrinsic: Windsock duodenum —— Extrinsic: Annular pancreas —— Midgut malrotation with peritoneal bands zz Anorectal atresia. Attributed to in utero catastrophic (ischemic) complication: zz Jejunoileal atresia zz Colonic atresia or stenosis zz Complicated meconium ileus.

FUNCTIONAL zz zz

Meconium plug syndrome and its variants Megacystis-microcolon-intestinal hypoperistalsis.

COMBINED ANATOMICAL: FUNCTIONAL zz zz zz zz

Hypertrophic pyloric stenosis Midgut volvulus (complicating midgut malrotation) Uncomplicated meconium ileus Colonic aganglionosis (Hirschsprung’s disease).

IMAGING MODALITIES The imaging methods available to investigate the gastrointestinal tract in the neonate include, plain film radiography, ultrasonography and contrast studies of the GI tract. Nuclear scintigraphy, computed tomography and magnetic resonance imaging are uncommonly required in infants.1

Plain Film Radiography It is the simplest, usually the first and sometimes the only examination performed. An anteroposterior supine radiograph may be sufficient, only if the purpose is to evaluate a palpable mass or the presence of calcification. If obstruction is suspected, additional films are required. A cross-table lateral projection with the infant in supine position is best in terms of leaving the patient virtually undisturbed. However, a left-lateral decubitus view with a horizontal beam has the advantage of better identification of free gas over the liver and better anatomical definition of bowel loops in a frontal projection. If only one film is desired, a prone radiograph will give the most information regarding free gas as well as defining the level of obstruction. Occasionally, a prone lateral film is valuable for detection of gas in the rectum.1 Within seconds after birth, air enters the gastrointestinal tract and it can be seen radiographically in the stomach.

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Air is seen in the small bowel within the first hour, it reaches the cecum within 3–4 hours, and appears in the sigmoid colon by 11 hours. Gas-fluid levels are generally absent except in the stomach and occasionally in the right colon. The normal bowel gas pattern in neonates is quite different from that seen in older children and adults. It is characterized by gas throughout the small and large bowel and little fluid with respect to air, so that bowel-air interfaces are thin and sharp, with few, if any loops identified; rather, the gas distribution is one of multiple, closely apposed, rounded or polyhedral structures. Small and large bowels cannot be distinguished.2 A gasless abdomen after the first few hours of life is occasionally seen in normal infants as well as in those with uncontrollable vomiting, continuous gastric aspiration, severe dehydration, esophageal atresia without a fistula and deficient air swallowing, secondary to CNS depression. Obstruction is manifested by distention of portion of the GI tract proximal to the obstruction, with little or no gas below. By observing the number and distribution of distended bowel loops and air-fluid levels, one can estimate the approximate level of obstruction (Figs 1A and B).

Barium is not used in the following circumstances: (i)  Suspected perforation, where preferably a non-ionic contrast medium should be used; (ii) Instances of lower smallbowel obstruction when retained fluid proximally is likely to cause oral barium suspension to precipitate and degrade the images; (iii) When a cleansing effect is also desired, as in attempted reduction of meconium ileus or meconium plug. Ionic water-soluble contrast media are ideal for stimulating evacuation of retained thick tenacious intestinal contents by virtue of their high osmolarity, which increases the intraluminal fluid and bulk. This, however, may cause water and electrolyte imbalance and appropriate patient hydration and electrolyte homeostasis should be carefully maintained. Ionic contrast media are contraindicated when investigating esophageal problems because aspiration may cause pulmonary edema. Non-ionic contrast media are ideal for most of the circumstances. In suspected Hirschsprung’s disease, in which the rate of evacuation has some potential diagnostic value, barium should be preferred. The radiologist should modify the routine use of contrast as needed in a particular case.

Contrast Studies

Ultrasonography

Air is the cheapest, easiest and most commonly available contrast medium. The presence of gas within the bowel can be very useful in delineating abnormalities, particularly, a proximal high atresia. Occasionally, one may require to inject air to delineate the bowel better and it can be instilled by nasogastric tube or per rectum.3

Ultrasonography (US) has been found to be highly accurate in the diagnosis of hypertrophic pyloric stenosis. It is useful in the diagnosis of gastric and duodenal duplications and in the detection of duodenal dilatation accompanying intrinsic or extrinsic duodenal obstruction, such as duodenal atresia and stenosis. Although duodenal dilatation is non-specific

A

B

Figs 1A and B:  Plain X-ray abdomen erect view reveals (A) few (three) air-fluid levels in proximal small bowel with absence of distal air

diagnostic of a high small bowel (jejunal) obstruction in a newborn presenting with bilious vomiting; (B) In contrast, multiple air-fluid levels seen in another neonate with abdominal distention, is indicative of a low small bowel (ileal) obstruction

Chapter 129 Developmental Anomalies of Gastrointestinal Tract

and additional contrast studies may be required to identify the specific cause, US is an excellent screening technique for localization of the site of obstruction. Ultrasound is valuable in the investigation of abdominal distention or palpable mass lesions because of easy and accurate detection of ascites as well as meconium peritonitis and intraperitoneal cystic lesions such as intestinal duplications and mesenteric or omental cysts.1

ESOPHAGUS Esophageal Atresia and Tracheoesophageal Fistula Esophageal atresia with or without tracheoesophageal fistula (TEF) is the most common congenital abnormality of the esophagus, manifesting itself during the neonatal period, occurring in about 1 in 2,500 to 4,000 livebirths.4 It is usually sporadic and its etiology is uncertain.3 No definite familial tendency has been documented in esophageal artesia, but more than one case in the same family has been noted.

Embryology The trachea and esophagus develop from the common foregut during the early first trimester. During the 5th and 6th weeks of gestation, the common foregut divides into trachea and esophagus. Incomplete separation results in esophageal atresia with or without associated tracheoesophageal fistula. Because separation of the trachea and esophagus occurs cranial to tracheal branching of the carina, Tracheoesophageal fistulas generally present above the carina.5

Clinical Features The presentation is usually in the first few hours of life, with the newborn having excessive oral secretions, choking and sometimes even cyanosis. Typically, symptoms become more pronounced during the first feed. The abdomen may be distended due to air passing through the distal fistula into the stomach or may be scaphoid or gasless in patients who

A

B

C

have atresia without a fistula or atresia with a proximal fistula. Patients with an H-fistula usually present later with history of choking while feeding, cough, cyanosis, recurrent or chronic pneumonias and a distended abdomen from tracheal gas passing through the fistula into the esophagus and stomach.5 Esophageal atresia may be diagnosed by antenatal ultrasound. It is suspected on the basis of maternal polyhydroamnios with an absent fluid-filled stomach, the proximal esophageal pouch seen as a central anechoic area in the fetal neck or upper chest. The presence and size of the tracheoesophageal fistula determines the amount of fluid in the stomach and gastrointestinal tract. Associated anomalies in the other systems may be identified. The atresias may be multiple and involve the esophagus, duodenum and anus.

Classification Esophageal atresia and tracheoesophageal fistula have been classified based on their anatomical and radiographic appearance, i.e. on the basis of presence (and location) or absence of a tracheoesophageal fistula (Figs 2A to E). They have been variously designated as types A to E (or 1 to 5) as follows:3 Type A: Esophageal atresia without fistula (7.8%) Type B: Esophageal atresia with proximal fistula (0.8%) Type C: Esophageal atresia with distal fistula (85.8%) Type D: E  sophageal atresia with fistula in both the pouches (1.4%) Type E: H-type fistula without atresia (4.2%) In the majority of patients, the atresia occurs between the proximal and middle thirds of the esophagus with a gap of varying length between the atretic pouches.3 Most commonly, there is a proximal esophageal atresia with a distal tracheoesophageal fistula. This occurs in approximately 85.8% of cases. Next most common, occurring approximately in 7.8% cases, is isolated esophageal atresia. H-type fistula occurs in approximately 4.2% of cases. Esophageal atresia with proximal tracheoesophageal fistula or with both proximal and distal tracheoesophageal fistulas are quite rare.6

D

Figs 2A to E:  Types of esophageal atresia/tracheoesophageal fistula. The plain radiographs for Types A and B are similar as in case for Types C and D

E

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Approximately 50–70% of patients with esophageal atresia have additional anomalies. The VACTERL syndrome is seen in 15–30% of patients. “V” is for vertebral and vascular abnormalities. Of these, a right-sided aortic arch is seen in 5% cases. “A” is for anal and auricular malformations. “C” is for cardiac abnormalities like ventricular septal defects, patent ductus arteriosus and complex cyanotic heart disease. “TE” is for tracheoesophageal fistula and esophageal atresia. “R” represents renal abnormalities. “L” is for limb malformations.7

Imaging Features Plain film of the chest taken soon after birth reveals proximal esophageal pouch distended with air, thereby indicating the diagnosis on plain radiographs. In unequivocal cases, a thin soft rubber nasogastric tube is passed into the proximal pouch and about 5 cc of air is injected. A frontal radiograph of the chest showing dilated proximal esophageal pouch with round distal margin and coiled nasogastric tube within is diagnostic. The distended air filled proximal esophageal pouch may make visualization of the lower cervical and upper dorsal spine more clear. A lateral radiograph though not routinely indicated, if obtained, shows considerable anterior bowing and narrowing of the trachea by the dilated blind esophageal pouch. 3 Plain radiograph of the chest should include the abdomen to evaluate the presence of air in the gastrointestinal tract. The presence of air in the stomach and the small bowel indicates esophageal atresia with a distal tracheoesophageal fistula. Absence of air in the stomach eliminates the possibility of a distal fistula. The possibility of proximal tracheoesophageal fistula, however, cannot be eliminated (Figs 3 and 4).

A

Air confined to the stomach raises the possibility of associated duodenal atresia and necessitates a follow-up plain film examination. Routine contrast examinations are not required in the neonate with esophageal atresia and TEF.3 Use of radiopaque contrast in the proximal pouch should be avoided, owing to the possibility of aspiration. Swallowed air or air through nasogastric tube is usually adequate for the diagnosis and to demonstrate the extent of the proximal pouch. If positive contrast examination is needed then isotonic nonionic contrast medium should be used in minimal amount under fluoroscopic monitoring. Immediately after the study, contrast should be aspirated out. Through H-type fistulas can be at any level, most are at the thoracic inlet, between C7 and T2 vertebral bodies. The connection is angulated superiorly from the esophagus to the trachea, thus accounting for the more precise but less popular appellation of the N-type fistula (Fig. 5). The best way to demonstrate H-type tracheoesophageal fistula is with careful injection of contrast medium via a nasogastric tube, first placed at GE junction and then gradually withdrawing the nasogastric tube with simultaneous injection of contrast under fluoroscopic guidance at various levels of the esophagus. The main reason that the H-type TEF is inconstantaly patent is that the normal esophageal mucosa is quite redundant and usually occludes the esophageal side of the fistula. Normal active swallowing may not distend the esophagus sufficiently to allow passage of contrast into the fistula.8 The patient should be viewed in the lateral or steep prone oblique projection with the right side down. Care should be taken to separate tracheal and esophageal lumens during the study so that fistula is readily identified between them.

B

Figs 3A and B:  Esophageal atresia. (A) Frontal radiograph of chest and abdomen showing a catheter in the proximal pouch. The abdomen is gasless; (B) Lateral film shows the tip of the nasogastric tube at the level of 4th dorsal vertebra

Chapter 129 Developmental Anomalies of Gastrointestinal Tract

Fig. 4:  Esophageal atresia with distal tracheoesophageal fistula.

Coiled nasogastric tube is seen in the proximal esophageal pouch. Air is seen in the stomach and bowel

Fig. 5:  Contrast esophagogram demonstrating an oblique tract of an

H-type tracheoesophageal fistula arising from the anterior wall of the esophagus and passing cephalad to the posterior tracheal wall, with contrast filling the tracheobronchial tree

If the contrast appears in the trachea or lungs, it is very important to be certain, if the contrast went through a fistula or was aspirated. If in doubt, then the investigation must be repeated once the trachea is cleared of the contrast. The side of the aortic arch should be determined. This information is important to the surgeon because the surgical approach to the mediastinum for repair of esophageal atresia with a distal TEF is from the side opposite to the aortic arch. When plain radiograph fails to indicate the side of the arch, computed tomography or a cardiac ultrasound can localize the arch. H-type fistulas are commonly demonstrated by contrast studies.3 However, bronchoscopy and endoscopy are more

sensitive methods and may be indicated to confirm the diagnosis, especially in a symptomatic older child where the contrast esophagogram is normal. Computed tomography (CT) is occasionally used in the preoperative evaluation of neonates with TEF and has proved to be a noninvasive and quick investigation. As compared with conventional bronchoscopy or catheterization, CT does not require any general anesthesia. The improved spatial and temporal resolution of new generation of scanners facilitates assessment of such small defects such as TEF. Either direct sagittal acquisition or axial acquisition with multiplanar reconstruction may help in demonstrating the precise location of fistula and the length of the gap between esophageal segments. Alternatively, length of the atretic segment can be assessed by passing a feeding tube from above and a metal bougie from below, via a gastrostomy. The knowledge of the origin of the fistula is helpful to the surgeon not only in deciding the side of the thoracotomy (right or left), but also in anticipating the gap to be bridged. The most important advantage of CT is that both esophagus and trachea are seen in their natural (unstretched) positions, and the interpouch gap can be measured accurately.9 High resolution CT scan on a 64-slice CT scanner has shown to provide definitive diagnosis and help in surgical planning in a critically ill neonate with H-Type TEF by distending the esophagus with air (by means of nasogastric feeding tube) during CT acquisition. Such a maneuver has proved to be very useful in optimizing the visualization of the fistula which may be totally or partially closed by a valve like mucosal flap or by a spasm of the muscular layer of the esophagus.10 When there is a proximal fistula, then it is located in the anterior wall of the esophagus. In esophageal atresia with a distal fistula, primary repair is possible as the length of the gap between the esophageal segments is usually short. When there is atresia with no distal fistula, there is usually a long gap (of the order of about five vertebral bodies) between the proximal and distal esophageal segments. The growth of the esophageal segments during the first few months of life tends to lessen the gap, thereby making a delayed primary repair feasible. A gastrostomy is established for feeding in the meantime.

Radiological Evaluation of Postoperative Complications Most patients of isolated esophageal atresia and tracheoesophageal fistula do well following surgical repair. Nevertheless, complications following surgery do occur and can be grouped under early and late complications. The early complications include: (i) Leakage at the anastomotic site (14–16%), (ii) Esophageal stricture, and (iii) Recurrent fistula. Oral feeding is not started for 1–2 weeks following surgery, till the edema subsides. A contrast study of the esophagus should be performed prior to the institution of

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oral feeds. A low-osmolal nonionic contrast should be used as leakage at the anastomotic site and is the most commonly identified early complication of surgical repair. Anastomotic leak increases the risk of esophageal stricture in the future. Donnelly et al. found that the appearance of an extrapleural fluid collection after esophageal atresia repair performed via an extrapleural approach was associated with a high incidence of anastomotic leakage.8 If an anastomotic leak is left untreated, it may eventually lead to diverticulum formation. Most anastomotic leaks have been seen to close spontaneously. Stricture is another common complication which can occur following esophageal atresia repair. Most often, the stricture or narrowing is slight at the site of anastomotic repair and may persist for years, even though the patient has no functional problem (Figs 6A and B). Those with true stricture at anastomotic site are symptomatic and generally respond to bougie dilatation, with reoperation generally not required. However, if a stricture is associated with gastroesophageal reflux, the stricture may not respond to dilatation if it continues to be exposed to the acidic gastric contents. Hence, patients with postoperative strictures should be evaluated for reflux by upper gastrointestinal series or pH monitoring. A tracheoesophageal fistula can recur (3–14% cases) again at the anastomotic site, following surgery and is believed to be related to anastomotic leakage with erosion into trachea caused by local inflammation. The late complications which can occur following repair of an esophageal atresia are dysmotitily, gastroesophageal reflux, tracheomalacia, rib fusion and scolosis. Dysmotility is present in nearly all patients who have had esophageal atresia.

A

Gastroesophageal reflux is also commonly associated and has been reported in 40–70% of cases. Reflux is thought to be related to the shortening of the intra-abdominal portion of the esophagus, or occur secondary to the surgical repair. Reflux may lead to peptic esophagitis and is likely to be the cause of more distal strictures in those who have had a history of repaired esophageal atresia. Tracheomalacia is thought to occur due to chronic intrauterine compression of trachea by a distended upper esophageal pouch.

STOMACH Microgastria Congenital microgastria is an extremely rare anomaly in which fetal rotation of the stomach fails to occur. There is no differentiation into fundus, body, antrum and pyloric canal and the lesser and greater curvatures also do not develop.8 It is believed to occur as a result of atresia of normal foregut development in the 5th week of embryonal development. Microgastria is often accompanied by other congenital anomalies such as malrotation, asplenia, renal, limb, vertebral and cardiac anomalies (VACTERL syndrome).4 The common association between microgastria and upper extremity limb reduction defects, has led to the term microgastria-limb reduction complex.8 The clinical presentation of microgastria depends on the stage at which gastric development has been arrested. On prenatal ultrasound it may mimic esophageal atresia due to failure to visualize a distended stomach. Postnatally, microgastria presents with postprandial vomiting, failure to

B

Figs 6A and B:  (A) Esophageal atresia with distal TEF in a neonate. Lateral radiograph shows contrast-filled dilated proximal esophageal pouch

bowing the trachea anteriorly; (B) Barium swallow following primary anastomosis of esophageal atresia demonstrates slight narrowing at the anastomotic site (D4 vertebral level). The child had mild respiratory distress with dysphagia

Chapter 129 Developmental Anomalies of Gastrointestinal Tract

thrive, developmental delay, growth retardation, malnutrition and aspiration pneumonia. Most of the symptoms are due to secondary gastroesophageal reflux (GER).4 An upper GI study shows a small tubular stomach in the midline. The esophagus is dilated and appears to take over the storage function of the small capacity stomach. The gastroesophageal junction is incompetent and GER is present. There is associated esophageal dysmotility, secondary to its massive dilatation.4 The treatment of microgastria depends on its severity. The less severe forms may be treated conservatively, with surgery reserved as the first line of treatment in severe cases. The surgical treatment consists of creation of a Hunt-Lawrence pouch as a gastric reservoir, which allows for the secondary esophageal changes to resolve.4

DEVELOPMENTAL OBSTRUCTIVE DEFECTS Congenital gastric obstruction is rare, as unlike the esophagus, the stomach undergoes little alteration in form during development. Gastric obstruction in the newborn may be due to: 1. Gastric atresia 2. Pyloric stenosis 3. Pyloric/prepyloric membrane/Antral web.

Gastric Atresia Isolated gastric atresia is very rare and accounts for less than 1% of all congenital obstructions.11 Almost all gastric atresias occur at the pylorus or antrum. They are thought to be due to localized vascular occlusion in fetal life and not to failure of recanalization of the intestinal tract.3 Gastric atresia is classified into three types:12 1. Complete atresia with no connection between the stomach and duodenum 2. Complete atresia with the fibrous band connecting the stomach and duodenum, and 3. A gastric membrane or diaphragm producing atresia. Gastric atresia may be familial or associated with epidermolysis bullosa. The newborn presents mainly with regurgitation of non-bilious vomitus within the first few hours after birth. As obstruction is complete, a plain radiograph of the abdomen reveals a “single bubble appearance” with marked dilatation of the stomach, proximal to the obstruction and absence of gas in the small bowel and colon. This appearance is diagnostic and most patients are taken directly to surgery without any contrast imaging.11

Pyloric Stenosis or Prepyloric Membrane or Antral Web A pyloric stenosis or prepyloric membrane or antral web is a rare cause of symptomatic gastric obstruction in the newborn.2

Patients with webs or stenosis of the pylorus, rather than complete atresia may present later in life or even in adulthood because the obstruction is incomplete.8 The most common presenting symptoms are cyclic postprandial vomiting and episodes of transient vomiting.9 Radiographically, the stomach is dilated with varying degrees of distal air, the extent of which depends on the degree of obstruction. In patients with incomplete obstruction, webs are more common than stenosis.4 It is difficult to diagnose an antral web on imaging studies. On UGI barium studies, a web is seen as a thin, 2–3 mm, linear circumferential filling defect traversing the barium column producing a reduction in the antral lumen, with a normal pyloric canal.11 On ultrasound, the membrane may be visible, if the stomach is filled with clear fluid and appears as echogenic band extending centrally from the lesser and greater curvatures in the prepyloric region. A mucus strand may be mistaken for an antral membrane. On the basis of clinical and radiographical findings, the definitive diagnosis of antral web can be made endoscopically.2

Ectopic Pancreas Ectopic pancreas is an uncommon anomaly in which pancreatic tissue is found in the antropyloric region, less commonly in the duodenum. It is seen as an incidental finding. Less commonly, it can cause symptoms of pain, GI bleeding or obstruction.8 An upper GI study shows a smooth, dome shaped filling defect, 1–3 cm in diameter on the greater curvature of stomach, with central umbilication at times. Ectopic pancreatic tissue may produce intermittent obstruction, if it prolapses into the pylorus.11

Hypertrophic Pyloric Stenosis Hypertrophic pyloric stenosis (HPS) is a common developmental condition affecting young infants. The incidence of HPS is approximately 3 in 1000 livebirths and boys are affected four to five times more commonly than girls. There is a familial disposition. Affected patients usually present between 2 and 6 weeks of age, with projectile nonbilious vomiting. Other conditions that can manifest with non-bilious vomiting include pylorospasm, hiatus hernia and preampullary duodenal stenosis.13 HPS is never seen beyond 3 months of age, except reported in premature infants, in whom, enteral feeding has been started late.14 Diagnosis can be made on appropriate history and palpation of an ‘olive’ mass in the subhepatic region of an infant. The mass is reported to be seen in up to 80% of cases. Antral peristaltic waves can also be observed.3 HPS is characterized by hypertrophy of pyloric circular muscle and redundancy of the pyloric mucosa. However, its etiology is unknown. Possible causes include hypersecretion with resulting duodenal irritation and pylorospasm. There is a constant association with hyperplasia of the antral mucosa.3

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Recent work has confirmed that the pylorus is abnormally innervated, and suggested that a lack of nitric oxide synthetase may be responsible for the pylorospasm that leads to gastric outlet obstruction and muscular hypertrophy.5 In most cases, a clinical diagnosis can be confidently made. However, further investigation may be required when the diagnosis remains in doubt. The diagnosis of HPS can be established by either barium studies or US. Ultrasonography has replaced barium examination being noninvasive and its ability to visualize the pyloric muscle directly to obtain measurements of muscle thickness.15,16

Ultrasonography Ultrasonography (US) is the imaging modality of choice in an infant suspected of having pyloric stenosis, with a reported accuracy approaching 100%.13 The examination is typically performed with a high frequency linear transducer (>5 MHz) as the stomach, pylorus and duodenum are very superficial in an infant.17 The gallbladder which is adjacent to the pylorus, serves as a good landmark.3 Longitudinal and transverse images through the pylorus are obtained with the infant in the right posterior oblique position while scanning the right upper quadrant just off the midline. In this position, any fluid in the fundus of the stomach moves into the antrum and pyloric region, distending these regions. The stomach should not be emptied prior to the examination as this makes identification of antropyloric area difficult. If there is inadequate distention of the antrum, the infant may be given a glucose solution or water, orally or via a nasogastric tube. If fluid is administered, then it should be removed at the end of the examination to prevent further vomiting and the risk of aspiration. In addition, if there is lot of gas, scanning the baby in the prone position may help in visualization of the pyloric region.17 The US evaluation of HPS includes assessment of both morphological and quantitative features. The classic findings are of a thickened echo-poor pyloric muscle and an elongated pyloric canal.15,16,18 The thickened muscle is seen as two curved bundles of mixed but generally low reflectivity bulging into the base of the duodenal cap and gastric antrum. The mucosal echoes are seen as one or two central bright lines. On transverse images, the hypertrophic pylorus has a doughnut appearance, representing the reflective central mucosa and submucosa surrounded by echo-poor muscle. The hypertrophic muscle may look non-uniform on transverse scanning of the pylorus. This is related to the sonographic artifact of anisotropic effect because of the orientation of the muscle fibers.3 Other signs include exaggerated peristaltic waves that terminate at the pylorus, esophageal reflux and little, if any gastric emptying. An experienced examiner can frequently make the diagnosis just by qualitative assessment of the thickness of the pyloric wall. The exact measurements that separate a normal pylorus from a hypertrophic one, are controversial.16,18-20

However, as a general guide, a pyloric canal length greater than 15 mm, muscle thickness greater than 3.0 mm, and transverse serosa-to-serosa diameter greater than 15 mm is consistent with HPS (Figs 7A and B). At least two values should be positive. A muscle thickness less than 2.0 mm is unequivocally normal. A muscle thickness between 2 and 2.9 mm is abnormal but nonspecific, and can be seen in gastritis and pylorospasm as well as in HPS. Though pylorospasm may mimic HPS on sonography as there is some pyloric muscle thickening and/or slight elongation of the pyloric canal, pylorospasm is transient and generally resolves in 30 minutes. An important pointer for diagnosing pylorospasm is that there is considerable variation in measurement or image appearance with time during the study.21 Borderline muscle thickness measurements are more likely to occur in premature than in term infants. A number of ancillary sonographic signs of HPS have been described.17 zz Shoulder sign—refers to an indentation upon the gastric antrum produced by hypertrophy of the pyloric muscle zz Double tract sign—this refers to fluid, trapped in the mucosal folds in the center of an elongated pyloric canal seen as two sonolucent streaks in the center zz Nipple sign is produced due to the evagination of redundant pyloric mucosa into the distended portion of the antrum. Color Doppler evaluation of the pylorus may reveal hyperemia within the muscle and mucosal layers. False negative diagnosis may be made, if the stomach is overdistended, because it can displace the pylorus posteriorly, making it difficult to visualize the pyloric canal. If the scan is not in the midline, or is tangential to the antrum, the antral wall can simulate a thickened pyloric muscle, leading to a false positive diagnosis.

Barium Study A barium study should be performed, if ultrasound is inconclusive or gastroesophageal reflux is suspected. 21 If gastric distention is severe, a nasogastric tube should be passed and the stomach emptied. With the patient in the prone oblique position, the tube is placed in the antrum and adequate barium is injected via the tube under fluoroscopic control and spot films are taken. Most of the infants, with and without HPS, show some degree of pylorospasm. In HPS, generally barium will pass through the antropyloric region within 1–10 minutes, but may be delayed as long as 20–25 minutes. The pyloric canal is narrowed (the “string sign”) and elongated and almost always curved upward posteriorly (Fig. 8). Combination of narrowing and elongation is the hallmark of HPS on barium study. Barium may be caught between folds overlying the hypertrophied muscle and parallel lines (the “double string sign”) may be seen (Fig. 9). The enlarged muscle mass looks much like an “apple-core lesion”, with undercutting of the

Chapter 129 Developmental Anomalies of Gastrointestinal Tract

A

B

Figs 7A and B:  (A) Hypertrophic pyloric stenosis. Longitudinal ultrasound image showing an elongated thickened pylorus seen as two curved

bundles of low reflectivity (m). The mucosal echoes are seen as central bright lines. Gallbladder (Gb) shows sludge within. Minimal fluid is present around the stomach; (B) Transverse section shows the muscle thickness as an echo poor rim—Bull’s eye sign. Serosa to serosa measures 15 mm (cursors)

Fig. 8:  Upper GI barium study in a child with pyloric stenosis. The

markedly narrowed pylorus curves upward and posteriorly to the duodenal bulb which shows an impression of the hypertrophied muscle in the base

distal antrum and proximal duodenal bulb. The “beak sign” is noted as the thick muscle narrows the barium column as it enters the pyloric canal. Virtually all of the above signs can be seen transiently in infants especially those with some degree of spasm. The study should be continued sufficiently long to document the persistence of the findings in order to assure the diagnosis of pyloric stenosis. Occasionally, an associated antral web or diaphragm may be identified.

Fig. 9:  Characteristic findings of HPS in a 6-week-old boy with history of vomiting. The pyloric canal is narrowed and elongated and the base of the duodenal bulb is stretched by the pyloric mass

Adult Idiopathic Hypertrophic Pyloric Stenosis (AIHPS) It is a mild form of hypertrophic pyloric stenosis (HPS) which may rarely present later in adult life. Its exact incidence is not known, as majority of these patients are asymptomatic for years. Around 80% of patients with the adult form of the disease are men which is in concordance with the male

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preponderance of congenital HPS. The primary form of AIHPS should be differentiated from the secondary form which is caused by diseases such as peptic ulcer disease, hypertrophic gastritis or malignancy.23 In AIHPS, the pylorus is bulbous or fusiform with its thickest portion at the pyloroduodenal junction. Patients present with symptoms of delayed gastric emptying not associated with any pain. The radiologic and endoscopic studies may be nonspecific. However, the diagnosis should be suspected, if there is elongation of the pyloric canal and is accompanied by marked dilatation of the stomach. In AIHPS, the “string sign” may be seen as an extremely thin line of barium on an upper GI study. A marked thickening of the pyloric muscle may produce a convex indentation at the base of the duodenal bulb, causing a mushroom-like deformity (“Kirklin’s sign”). The presence of a barium-filled cleft between the hypertrophied muscle and the fibers of the pylorus can project into either one or both sides of the pylorus, proximal to the base of the bulb (“Twining’s sign”). However, none of these signs are pathognomic and presence of two or more of them strengthens the radiologic diagnosis. Endoscopy may be useful and the classic finding that has been described is the “donut” or the cervix sign which consists of a fixed narrow pylorus with a smooth border. In the congenital type of HPS, pyloromyotomy is the preferred treatment. Normal emptying of the stomach occurs within 2–3 days after the procedure. However, muscle thickness gradually regresses to normal and may even take 6–8 weeks.3 In contrast, in AIHPS, pyloroplasty and recently, laparoscopic pyloromyotomy have been tried with successful results.22 An increased incidence of renal anomalies like pelviureteric junction obstruction, primary megaureter, duplex kidney, renal agenesis or ectopia and horse-shoe kidney have been reported in patients with HPS.23

DUODENUM Duodenal obstruction is a relatively common form of intestinal obstruction in the newborn (Table 1). It may be complete (duodenal atresia) or incomplete. Complete duodenal obstruction is seen more frequently than congenital gastric obstruction.11 Incomplete obstruction may be intrinsic, such as duodenal stenosis caused by a web Table 1:  Causes of duodenal obstruction in the newborn Intrinsic

Extrinsic

Duodenal atresia

Ladd’s bands

Duodenal stenosis

Midgut volvulus with malrotation

Duodenal web or diaphragm

Annular pancreas Duplication Preduodenal portal vein

or “windsock” membrane; or it is more often extrinsic, e.g. duodenal compression from bands, annular pancreas, etc. Intrinsic and extrinsic obstructions may coexist.

Duodenal Atresia and Stenosis Atresia is much more common than stenosis, but the etiology is the same. Atresia or stenosis occurs when the duodenum, which is a solid tube till about 3–6 weeks’ gestation, fails to recanalize partially or completely. Unlike jejunal and ileal atresia, it does not appear to be related to intrauterine ischemia.11 Atresia and stenosis almost always occur in the region of the ampulla of Vater (about 80% are just distal to the ampulla); thus they are frequently accompanied by abnormalities of the bile duct and pancreas. Annular pancreas occurs in 20% of patients with duodenal atresia or stenosis. It may contribute to the duodenal obstruction but is seldom or never found without intrinsic obstruction of the duodenum. Duodenal atresia and stenosis may be associated with other congenital anomalies, like intestinal atresia and congenital heart disease and may be part of VACTERL association. About 30% of the patients have Down’s syndrome.24-26 Duodenal atresia and stenosis occur with equal frequency in boys and girls. Prematurity and maternal polyhydramnios are common. Bilious vomiting in the first few hours of life is the cardinal symptom but those with duodenal stensois can present at variable times, because the clinical findings depend on the degree of stenosis. Bilious vomiting is a feature in 80% of neonates with duodenal atresia as the atresia is present distal to the ampulla of Vater. In the remaining 20%, the vomitus is non-bilious.3

Imaging Features In newborns with duodenal atresia, the abdominal radiograph is usually diagnostic. Air is present in the stomach and proximal duodenum, but there is no air distally in the gastrointestinal tract. Erect film shows two gas-fluid levels in which the higher, larger bubble to the left is the stomach and the other bubble is the dilated proximal duodenum which is seen above the region of obstruction.11 Thus, the typical appearance of a “double-bubble sign” represents air, or air and fluid-filled distended stomach and duodenal bulb (Fig. 10). In duodenal stenosis, the stomach and duodenal bulb usually are distended, but air is present in the distal bowel. In newborns with evidence of complete duodenal obstruction on abdominal radiograph, there is mostly no need for further radiologic investigation. If enough air is not present to adequately demonstrate the obstruction, one can introduce through a nasogastric tube.12 However, a contrast enema in patients with complete duodenal obstruction may be done to exclude additional, more distal atresia.7 A microcolon implies that there is a distal atresia or atresias.

Chapter 129 Developmental Anomalies of Gastrointestinal Tract

total at the time of birth, if a complete ring is formed. If the ring is incomplete, the obstruction may occur later in life or may never produce symptoms.11 With severe obstruction, patient presents as a neonate. Presenting symptoms with delayed presentation are usually pain and vomiting. Radiographs are normal. On upper GI studies, a persistent waist is seen, partially obstructing the second part of duodenum.3

Preduodenal Portal Vein

Fig. 10:  Duondenal atresia. Erect film of the abdomen demonstrating the “double bubble” sign

The newborn with congenital duodenal obstruction, complete or partial, requires surgery and is frequently taken to surgery without any more radiological investigation other than the plain film. However, further radiological study is required for making a preoperative diagnosis, specifically to distinguish between a cause of partial obstruction for which operation may be delayed, such as duodenal stenosis, from midgut volvulus, which requires emergent surgery. In these cases, when the infant is clinically stable, an upper gastrointestinal (UGI) series may be very useful. On UGI study, duodenal stenosis appears as dilatation of the duodenum proximal to the point of obstruction with abrupt caliber change.3

Duodenal Web In patients with duodenal webs, the findings on UGI vary. In some, the appearance is of complete obstruction, in others there is narrowing of the duodenum. In the latter, a web is indistinguishable from simple duodenal stenosis. The most diagnostic appearance of a web is that of a thin, convex, curvilinear defect extending for a variable distance across the lumen of the duodenum. The “windsock” appearance that a duodenal web may have in an adult or older child, the so called intraluminal duodenal diverticulum, is not seen in newborns. This appearance is probably due to stretching and redundancy of the web caused by years of peristalsis, proximal to an incomplete obstruction.27

Annular Pancreas Annular pancreas is due to anomalous pancreatic tissue encircling the second part of duodenum. It is believed to result from the failure of normal pancreatic tissue to rotate around the duodenum. The duodenal obstruction may be

Preduodenal portal vein is rarely the sole cause of duodenal obstruction and is rarely diagnosed preoperatively. It is thus important for the surgeon to be aware of the association of this anomaly with the other congenital lesions causing duodenal obstruction.3 A preduodenal portal vein (persistent left vitelline vein) results from normal situs asymmetry and is commonly seen in patients with heterotaxy. The resultant portal vein courses anterior to the pancreas and duodenum. The condition is diagnosed by identifying the prepancreatic course of the portal vein on sonography, CT and MR imaging. It is now believed that in most cases of duodenal obstruction associated with a preduodenal portal vein, the obstruction is due to a primary, obstructing duodenal lesion such as intraluminal membrane or web and such a lesion should be suspected in these patients, if duodenal obstruction is present.21

SMALL BOWEL Anomalies of Rotation and Fixation Embryology At approximately sixth week of gestation, the primitive midgut herniates into the extraembryonic celom in the umbilical cord. The proximal and distal portions of the midgut elongate and rotate 270o anticlockwise around the axis of the superior mesenteric artery. By the end of the third month of gestation, the bowel loops return to their final position in the abdominal cavity. Fixation of the duodenojejunal junction or the ligament of Treitz in left upper quadrant occurs. The cecum is the last part of the GIT to be fixed and it normally comes to lie in the right lower quadrant. When all or part of the physiological rotation of bowel fails to occur, a wide variety of anomalies of intestinal rotation and mesenteric fixation occurs which consist of nonrotation, malrotation or reversed rotation.12 1. Nonrotation: It is an asymptomatic condition in which the small bowel lies entirely on the right side and the colon on the left side. It is demonstrated incidentally on barium studies in older children or adults (Figs 11A and B). The bowel is not very mobile and volvulus is not a common complication of nonrotation of the bowel. 2. Malrotation: In malrotation of the bowel, final position of the GI tract is somewhere between normal and

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complete nonrotation.12 Malrotation is a general term that includes a wide spectrum of anomalies that occur when this intestinal rotation and fixation occurs in an abnormal fashion. It can also be referred to as “malfixation”. Most commonly, there is incomplete rotation, which leads to a shortened mesenteric root which may have a narrow rather than a broad base that has a tendency to twist on its axis. This leads to extrinsic compression of the bowel, causing bowel obstruction, and if the twist persists, it may lead to occlusion of the mesenteric vessels. This twist of malfixed intestines around the short mesentery

A

is called a midgut volvulus (Figs 12A to C). In patients with malfixation of the bowel, in addition to the absence of a normal mesentery, frequently there are aberrant peritoneal bands (Ladd’s bands). These bands extend from the malpositioned cecum across the duodenum and attach to the hilum of the liver, posterior peritoneum or abdominal wall and can cause extrinsic duodenal obstruction (Figs 13 and 14).24 3. Reversed intestinal rotation: It is a rare rotational anomaly which renders the hepatic flexure and left transverse colon posterior in position. These portions of the colon

B

Figs 11A and B:  Barium meal follow through study shows (A) jejunal loops on the right side of the abdomen and (B) colon and cecum on the left side, with the ileum seen crossing the midline from right to left—Non-rotation

A

B

C

Figs 12A to C:  Illustration of midgut volvulus. Narrow mesenteric attachment of nonrotation (A) or incomplete rotation (B) may lead to midgut volvulus (C)

Chapter 129 Developmental Anomalies of Gastrointestinal Tract

A

B

Figs 13A and B:  Diagrammatic representation of Ladd’s bands causing duodenal compression in patients with malrotation. The cecum is left sided (A) and midline (B) in position and has dense peritoneal bands crossing over the duodenum

with many of them presenting in the first week of life. About 15–20% of patients present in late infancy or early childhood. In the remaining patients, malrotation is seen as an incidental finding. The bowel obstruction may be caused by the volvulus, by Ladd’s bands, or both. The sudden onset of bilious vomiting in a newborn who has been normal for the first few days of life should be considered to be due to a midgut volvulus until proved otherwise.

Imaging Features

Fig. 14:  Midgut malrotation with Ladd’s bands. Barium study shows distended proximal duodenum with tapering at the level of obstruction indicative of extrinsic compression. The small intestine, distal to the usual site of the ligament of Treitz lies below the duodenum and to the right

lie behind the descending duodenum and the superior mesenteric artery. The cecum is usually malrotated and medially placed and the small bowel is more right-sided than normal. Obstructing bands and midgut volvulus can occur.12

Clinical Features Two-thirds of patients who are symptomatic present with an acute onset of bilious vomiting in the first month of life

Plain radiographs may show feature of duodenal obstruction due to partially obstructing Ladd’s bands. The duodenal bulb dilatation is less than that seen with duodenal atresia. There may be little distal bowel gas. When there is a volvulus, the plain films may show features of distal bowel obstruction. Bowel-wall thickening and pneumatosis may be present due to volvulus-induced ischemia. The fluid-filled bowel loops associated with volvulus can simulate an abdominal mass. The abdomen may be gasless, which may be due either to proximal obstruction or to diffuse bowel necrosis in midgut volvulus. Of all the congenital anomalies that result in bilious emesis, only malrotation is likely to produce a normal abdominal film.24 Upper gastrointestinal barium examination is performed to document the location of ligament of Treitz and to evaluate for duodenal obstruction. Normally, the duodenojejunal junction lies to the left of the body of the first or second lumbar vertebra at the level of the duodenal bulb. In malrotation, it is located lower and to the right of normal. It is

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important to remember that the duodenojejunal junction is mobile in children and may be pushed inferomedially by an overdistended stomach, chronic bowel dilatation, enlarged spleen or in the presence of a nasojejunal tube.3 A lateral view of the contrast-filled duodenum is an important additional view in the upper GI study when evaluating for malrotation. Normal duodenum being a retroperitoneal structure, on lateral views is seen to lie behind the level of the stomach, with the fourth part of the duodenum superimposed on the second part of duodenum. This superimposed relationship is lost in case of malrotation of duodenum as it is seen to course anteriorly. An abnormal position of the duodenojejunal flexure may be the only indication of malrotation, as in 16% of cases cecum occupies its normal position. In addition, in malrotation the jejunum is usually on the right side of the abdomen. However, this should not be taken as an indication of malrotation as the jejunum in a normal child is relatively mobile and may be seen to the right of the spine.3 When volvulus occurs, there may be complete or partial duodenal obstruction. With complete obstruction, a beaked tapering of the obstructed duodenum may be seen. More commonly, the volvulus is intermittent with incomplete bowel obstruction with contrast filling the proximal small bowel. Occasionally, the pathognomonic corkscrew pattern of the twisted duodenum and jejunum is seen due to their clockwise twisting around the superior mesenteric artery (Figs 15A and B). In malrotation, the cecum and right colon may have abnormal mobility. The cecum is in the right upper quadrant or in midline in malrotation. A colonic beak may be present in the right colon on barium enema in the presence of volvulus.24 In the past, a contrast enema was the first investigation performed to evaluate for malrotation.3 This has been replaced by an upper GI study due to its greater sensitivity and specificity for malrotation. The cecum may

A

be mobile in neonates and may be seen in the right upper quadrant in the absence of malrotation. A barium meal upper GI study should be done for suspected malrotation since a normal barium enema does not exclude malrotation. The position of the cecum may be normal in a significant number of patients with malrotation.21 Hence, the upper GI study is the investigation of choice for the diagnosis of malrotation. Ultrasound may be useful in the early detection of midgut malrotation as well as complicating midgut volvulus. A distended proximal duodenum with a tapered end in front of the spine is consistent with malrotation in the proper clinical set-up. If in addition, one finds peritoneal fluid and edematous bowel loops on the right, the diagnosis of volvulus can be made. A normal anatomical relationship, however, in no way excludes the possibility of malrotation. A UGI series is mandatory, if this diagnosis must be confirmed or excluded prior to surgery. Ultrasound and CT scan may be helpful in suggesting the diagnosis of malrotation owing to abnormal superior mesenteric artery (SMA) or superior mesenteric vein (SMV) anatomy. The SMV normally rests to the right and anterior to the SMA. When the SMV is to the left of the SMA, this is highly suggestive of volvulus. When the SMV is anterior to the SMA, this is suggestive of malrotation with possible volvulus. Color Doppler US demonstrates whirlpool sign due to clockwise spiralling of the mesentery and superior mesenteric vein around the superior mesenteric artery. Inversion of the mesenteric vessels or the SMV rotation sign is not a sensitive screening test, because it may be present in normal population, patients with situs inversus and patients with abdominal masses. Other CT findings of midgut malrotation complicated by midgut volvulus are: (1) The ‘whirl’ sign of small-bowel loops revolved around the SMA; (Fig. 16) (2) A dilated, fluid-filled, obstructed stomach and proximal

B

Figs 15A and B:  Upper GI barium study in two different patients showing classic “corkscrew” appearance of the duodenum in midgut volvulus

Chapter 129 Developmental Anomalies of Gastrointestinal Tract

A

B

C

D

Fig. 16:  Axial CECT of the abdomen showing characteristic “whirlpool”

Figs 17A to D:  Types of small bowel atresia

duodenum; (3) Thick-walled loops of ischemic right-sided small bowel loops with potential pneumatosis intestinalis and mesenteric edema; and (4) free intraperitoneal fluid.

dilated fluid-filled bowel loops. These findings are nonspecific and the diagnosis is usually not confirmed until after birth.3 Proximal atresia may present with bilious vomiting; whereas more distal atresias present with abdominal distention. There may be failure to pass meconium. It is commonly associated with prematurity. Meconium may be passed, if atresia is located in the jejunum or occurred later in intrauterine life.

sign of clockwise twisting of the SMV and mesentery around the SMA

Jejunoileal Atresia and Stenosis Small bowel atresias (i.e. jejunal, jejunoileal or ileal) are more common than duodenal or colonic atresia. They are more common in the proximal jejunum and distal ileum than in the intervening small intestine.24 Jejunal atresias comprise around 50% of small bowel atresias and may be associated with other jejunal and ileal atresias.2

Embryology Most jejunal and ileal atresias and stenoses, except those that are familial, are thought to be secondary to ischemic injury to the developing gut. The ischemia may be due to primary vascular accident, usually in the mid second trimester or secondarily to a mechanical obstruction, as may occur in case of an in utero volvulus.24 There is no solid core phase in the development of jejunum and ileum, so recanalization is not thought to be involved. Jejunoileal atresia may involve the bowel anywhere from the ligament of Treitz to the ileocecal valve with the majority of cases of atresia occurring at the extremes of the small bowel. The devascularized bowel becomes necrotic and is resorbed leaving an atretic area of varying length with its attached mesentery. Several forms of atresia have been described surgically, but it is not possible to differentiate them by imaging studies.4

Clinical Features Antenatal diagnosis of small bowel atresia may be suggested on ultrasound by the presence of polyhydramnios and

Classification Small bowel atresia usually occurs as an isolated anomaly of the gastrointestinal tract. There are four types of small bowel atresia3 (Figs 17A to D): Type 1: Membranous or web-like atresia, composed of mucosal and submucosal elements with no interruption of the muscularis. Type 2: Atresia with a solid fibrous cord connecting the atretic bowel ends, but the mesentery is intact. All the three layers of the intestinal wall are interrupted. Type 3: Complete absence of a segment of bowel (total atresia) as well as a portion of the mesentery (V-shaped defect in the mesentry). Type 4: The familial form of multiple atresias. There are two unusual forms of atresia that are inherited.24 1. “Apple peel” or “Christmas tree” atresia 2. A syndrome of multiple intestinal atresias Apple peel or Christmas tree atresia is a rare variant of Type 3 atresia which consists of proximal jejunal atresia with absence of the distal superior mesenteric artery, shortening of the small bowel distal to the atresia and absence of the dorsal mesentery. This type of atresia is probably caused by prenatal occlusion of the SMA, distal to the origin of the midcolic artery. The distal small intestine spirals around its vascular supply giving the characteristic apple peel appearance (Fig. 17D).

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The result is a very short intestine with a propensity towards necrotizing enterocolitis.28 The syndrome of multiple intestinal atresias with intraluminal calcification is transmitted as an autosomal recessive pattern. There are multiple atresias from stomach to rectum. The radiological hallmark of this syndrome is extensive calcification of intraluminal contents between the areas of atresia. Nonhereditary bowel atresias may also demonstrate intraluminal calcification.24

Plain radiograph of the abdomen demonstrates typical findings of small-bowel obstruction. The site (jejunal or distal ileal) of the atresia can be suspected by the number and location of gas-filled loops of bowel (Fig. 18).3 Proximal jejunal atresia may have a few markedly dilated loops, the so-called triple bubble sign, more distal atresia typically has a more uniform dilatation of small bowel with associated air-fluid levels. The loop just proximal to the site of atresia is frequently disproportionately distended, with a bulbous end. If the ischemic event that produced the atresia caused a perforation, there may be evidence of meconium peritonitis which is a chemical peritonitis occurring as a result of extruded bowel contents producing an intense peritoneal inflammatory reaction. It leads to the formation of dense fibrotic tissue which often calcifies, resulting in characteristic intraperitoneal calcifications. Peritoneal calcifications may be identified on plain films as a consequence of meconium peritonitis, wherein they are seen as linear or flocculent areas of calcification within the peritoneal cavity (Fig. 19). The most frequent finding is a linear calcification under the free edge of the liver, though any or all portions of the peritoneum may be involved.4 The calcification may extend into the scrotum through a patent vaginal process to produce a calcified mass in the scrotum.28 The association of meconium peritonitis

with small bowel obstruction is virtually diagnostic of small bowel atresia.4 Ultrasound depicts the calcifications of meconium peritonitis as highly echogenic linear or clumped foci in the abdomen or pelvis. The appearance of meconium peritonitis on US may be either generalized or cystic. In the generalized condition, highly echogenic material spreads throughout the abdomen and around the bowel loops to produce a characteristic “snowstorm” appearance. Encysted collections of meconium show a variable appearance from homogeneous to heterogeneous echogenicity and may be ill-defined or well defined. Sonography may also be useful in differentiating ileal atresia from meconium ileus. In ileal atresia, the bowel contents are echopoor while in meconium ileus, the dilated bowel loops are filled with echogenic material.21 Additional imaging is not required in the presence of a high intestinal obstruction. A contrast enema is required for further evaluation for low bowel obstruction to distinguish between a large or distal small bowel obstruction, as the differentiation of the two on plain radiographs may be difficult or impossible. The most common causes of neonatal distal small bowel obstruction are ileal atresia and meconium ileus.3 Contrast enema should be performed with water soluble low osmolar contrast media introduced via a soft rectal catheter. Care must be taken to perform the enema as the distal blind pouch is prone to perforation. The one diagnostic finding to be looked for in the contrast enema performed in a setting of low bowel obstruction, is the presence or absence of a microcolon (Fig. 20). A microcolon is a colon of very small caliber, generally less than 1 cm diameter, and the entire colon must be involved (i.e. not a portion as in small left colon syndrome). Normally, colonic measurements are not needed for diagnosing microcolon as it is usually obvious on inspection. The colon is small owing to lack of use rather

Fig. 18:  Small bowel atresia. Air is seen in the stomach and dilated

Fig. 19:  Plain radiograph of the abdomen in a case of meconium

Imaging Features

part of the jejunum proximal to the atresia

peritonitis shows curvilinear calcification in the right flank

Chapter 129 Developmental Anomalies of Gastrointestinal Tract

and cecum, occluding its lumen and resulting in high-grade distal small bowel obstruction. Meconium ileus can be complicated or uncomplicated, with complicated meconium ileus being seen in up to half of the patients which include intestinal atresia, volvulus of the distal intestinal loop and perforation with meconium or pseudocyst formation.3

Imaging Features

Fig. 20:  Small bowel atresia. Contrast enema demonstrates a microcolon

than anatomic or functional abnormality. The more distal the small bowel obstruction, the smaller the colon. A microcolon or unused colon occurs when no or little intestinal juices (succus entericus) reaches the colon and is highly suggestive of a distal small bowel obstruction (meconium ileus or ileal atresia). A normal sized colon almost always excludes these diagnoses.24 It is important to remember that the presence of micro­ colon is diagnostic of long-standing distal small bowel obstruction, but a normal colon does not exclude it in all cases. Also, microcolon on contrast enemas may be seen in premature infants and occasionally, in total colonic aganglionosis (long segment Hirschsprung’s disease). The rectum is distensible in distal ileal atresia, thereby distinguishing it from the microcolon of long segment Hirschsprung’s disease.3 Jejunal atresia does not lead to a microcolon because the remaining small bowel, distal to the atresia produces sufficient succus entericus to give a colon of normal caliber. Hence, a microcolon in the presence of a high bowel obstruction indicates a second, more distal atresia.3 Surgical treatment involves resection of the atretic portion of the intestine with reanastomosis. The proximal dilated bowel may remain dilated for sometime in the postoperative period, showing delayed motility with delayed passage of contrast across a widely patent anastomosis.

Meconium Ileus Meconium ileus is a low intestinal obstruction caused by inspissation of abnormal meconium in the distal ileum. 24 It is almost always associated with cystic fibrosis and is a presenting feature of cystic fibrosis in 5–10% of these patients.24 The lack of normal pancreatic enzymes leads to thick, tenacious meconium that collects in the distal ileum

Meconium ileus is the most common mimic of small bowel atresia clinically and on plain films.4 Plain radiograph may demonstrate a distal bowel obstructive pattern with air-fluid levels. Bowel loops may vary in size, a finding seen less often in atresia. The dilated small-bowel loops that contain air can mimic colon loops in size and course. In addition, some air mixes with the viscid meconium and results in a bubbly appearance in the right lower quadrant. This “soap-bubble appearance” is not specific and a similar fecal pattern can be seen with any cause of distal intestinal obstruction like ileal atresia, colonic atresia, aganglionosis of the terminal ileum and meconium plug syndrome.28 Patients with meconium ileus have fewer air-fluid levels than patients with small-bowel atresias. Meconium peritonitis may occur and be associated with peritoneal calcifications. However, this differential point is not specific in all cases. A localized perforation forms a meconium pseudocyst which may have peripheral curvilinear calcifications seen on plain radiographs. The term pseudocyst is also used to refer for a mass of necrotic, fluidfilled bowel loops with a fibrous wall which may be seen as a mass on radiographs.3 Ultrasound can detect abnormal bowel dilatation and echogenic bowel contents in infants with meconium ileus. Ultrasound can also pick-up complications of meconium peritonitis or pseudocyst which is seen as echogenic material lying outside the bowel loops, with or without associated calcification. The colon of babies with meconium ileus is often said to be the smallest of all colons, and is empty except for a few occasional pellets of meconium. The distal 10–30 cm of ileum appears dilated due to meconium within and may even displace the right colon to the left.24 Definitive diagnosis is made with a low osmolal water soluble contrast enema which demonstrates a microcolon with inspissated meconium pellets identified in the collapsed distal ileum with dilated small bowel proximal to the obstruction (Fig. 21). Uncomplicated cases of meconium ileus may be treated with multiple contrast enemas, i.e. one or two enemas per day. The aim is to introduce the contrast into the dilated small bowel, proximal to the obstructing inspissated meconium. But care must be taken not to overdistend the meconium. This leads to mechanical loosening of the meconium pellets. The patient should be well hydrated, if high osmolarity agents are

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Fig. 21:  Meconium ileus. Water-soluble contrast enema showing a

microcolon. Filling defects due to meconium are seen in colon and distal ileum

used because of fluid shifts. The therapy is largely mechanical and the osmotic load probably plays little role. Repeated enemas may be used only, if progress is seen in decreasing the obstructing pellets. In premature infants, isotonic non-ionic contrast medium is used. Enema has a success rate of about 50 to 60% in treating meconium ileus.3 If signs of obstruction are not relieved or perforation/peritornitis develop, further attempts at therapeutic enema should be abandoned. Surgery in such patients often reveals complicated meconium ileus.

Megacystis-microcolon-intestinal Hypoperistalsis Syndrome (Berdon’s Syndrome) Megacystis-microcolon-intestinal hypoperistalsis syndrome is a pseudoatresia. There is a functional small bowel obstruc­ tion with a microcolon, malrotation and a large unobstructed bladder. There is four-to-one female predominance with associated genitourinary and congenital heart malformation in up to 14% cases. Upper GI contrast study shows hypomotility of small bowel with retrograde peristalsis. Ultrasound reveals a dilated bladder with bilateral hydroureteronephrosis.21 The prognosis is poor for long-term survival.

Meckel’s Diverticulum Meckel’s diverticulum is a congenital blind pouch in the small bowel which results from an incomplete obliteration of the proximal part of the vitelline duct (omphalomesenteric duct) during the fifth week of gestation. It results in a true diverticulum arising from the antimesenteric border of the distal ileum.29 For Meckel’s diverticulum, the common rule by which it is known is the “rule of twos”, i.e. it is found in 2% of the population, twice as common in males, most

frequently found in those less than 2 years of age and usually 2 feet from the ileocecal valve. It may contain ectopic mucosa, usually gastric mucosa which is responsible for the adjacent ulceration in the ileum. Meckel’s diverticulum usually does not give rise to symptoms. Bleeding is the most common complication in children reported in over 50% of cases, while it is seen in only around 12% cases in adults. Bleeding is usually minor, resulting in chronic anemia.22 It may present with malena due to ulceration of ectopic gastric mucosa in its wall. In 20–30% of patients, it may give rise to symptoms such as inflammation, and or perforation which may often be indistinguishable from acute appendicitis. Obstructive symptoms have been seen to occur more frequently than hemorrhage in patients with Meckel’s diverticulum presenting in adulhood. The obstruction may occur due to intussusception, volvulus, inflammatory adhesions. The diverticulum may get obstructed with resulting diverticulitis, may present as a mass and initiate intussusception in childhood. Preoperative evaluation of a Meckel’s diverticulum is difficult, and routine and special radiological studies such as plain abdominal radiograph, barium meal follow through, arteriography and computed tomography are often nondiagnostic and often of limited diagnostic value. The diverticulum is seldom recognized on a small bowel followthrough study because there is no significant hold-up, and the barium residue remaining in it is very small because of its wide neck.29,30 In suspected symptomatic Meckel’s diverticulum, preoperative evaluation includes 99mTc (technetium-99m pertechnetate) scanning which relies on the presence of ectopic gastric mucosa. In this study, 99mTc is injected intravenously, and over time it accumulates in the gastric mucosa. As symptoms such as bleeding is caused by the ectopic gastric issue, 99mTc scanning may help in the diagnosis in symptomatic cases. In children, the scan has a sensitivity of 85% and specificity of 95%, but in adults the sensitivity is 62.5% and the specificity 9%. The accuracy of the scan can be improved with the use of pentagastrin or cimetidine. In patients with nondiagnostic scan or with nonbleeding presentation, ultrasonography could prove to be useful in achieving a diagnosis.

Enteric Duplication Gastrointestinal duplications are uncommon congenital abnormalities that may occur anywhere in the gastrointestinal tract. But the most common locations are the distal ileum (35%), distal esophagus (20%) and stomach (9%) followed by duodenum and jejunum. Colonic and rectal duplications are rare. Multiple duplications may be present in 15–20% cases.21 Enteric duplication occurs in the late first or early second trimester owing to abnormal canalization of the bowel. The duplication has smooth muscle in its wall with gastrointestinal

Chapter 129 Developmental Anomalies of Gastrointestinal Tract

A

B

Figs 22A and B:  Esophageal duplication. Chest PA showing a well-defined soft tissue mass in the left hemithorax (A) lying posteriorl in the lateral film (B). There is associated hyperinflation of the let lung. The vertebral bodies appear normal

mucosal lining. The wall thickness is 3–5 mm as seen in normal bowel. It is usually adjacent to and in most instances, does not communicate with the gastrointestinal tract. In most cases of hemorrhage or ulceration, gastric mucosa is present. Esophageal duplications are located at the posterior aspect of the esophagus. Gastric duplication is found along the greater curvature of the stomach interposed between the stomach and the transverse colon. Duplications may be spherical or tubular. Tubular duplication is more likely to communicate with the adjacent bowel. They typically occur along the mesenteric border of the intestine and share a common blood supply. Thus the tubular type of duplication may complicate bowelsparing surgery because of difficulty in preserving the enteric blood supply. Unlike neurenteric cysts, duplication cysts are usually not associated with vertebral segmental anomalies.29

Clinical Features Duplications can present with a variety of symptoms and signs depending on the site of duplication and its size. Upper esophageal duplications present with symptoms due to tracheal compression. Other symptoms include nausea and vomiting. In the presence of heterotopic gastric mucosa, patients may present with gastrointestinal hemorrhage or even perforation. Patient may also present with distention, ulceration, volvulus, an abdominal mass lesion or with obstruction, particularly when the duplication is in the region of the ileocecal valve or duodenum. About 40% of patients with enteric duplication present by one month of age, with 85% diagnosed during the first year of life.

Malrotation, genitourinary anomalies and jejunal or ileal atresias are also seen. Duplications are more common in boys except for gastric ones, which occur without gender predominance.

Imaging Features Plain radiographs may demonstrate a mass lesion, especially in the chest in the case of esophageal duplication, (Figs 22A and B). The bowel gas pattern may suggest an obstruction, particularly with duodenal or ileal duplications. Enteric duplication cysts may reveal mural calcifications. Occasionally, duplication may get filled with barium suspension during gastrointestinal examinations. In most cases, however, the duplications are not demonstrated in this manner. Barium study usually reveals extrinsic compression (Figs 23A and B) of the bowel or an obstruction. On ultrasonography, a duplication cyst appears as a well-defined, unilocular anechoic mass with good through transmission (Fig. 24). Rarely, the contents are reflective or contain septations secondary to hemorrhage or inspissated material within the lumen. A highly reflective mucosa and a surrounding echo poor muscular wall may be seen as the duplication is of gastrointestinal origin.31,32 This is most easily identified in the dependent portion of the cyst.21 The presence of this double-layered appearance (“gut wall signature”) is relatively specific for the diagnosis of duplication cyst and is useful to exclude other cystic masses, such as mesenteric or omental cyst, choledochal cyst, ovarian cyst, pancreatic pseudocyst or abscess. The reflective lining may be absent as a result of extensive mucosal ulceration by gastric enzymes.

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Section 5 Pediatric Imaging

A

B

Figs 23A and B:  Barium study shows extrinsic impression on the body of the stomach with effacement of the mucosa in AP and lateral views in a case of gastric duplication

LARGE BOWEL Colonic Obstruction Obstruction of the colon in the newborn may be either anatomical or functional. The first type includes atresia of the colon, anorectal atresia, and with a functional element, aganglionosis or Hirschsprung’s disease. A group of poorly understood disorders like meconium plug, neonatal small left colon syndrome, etc. cause transient self-limited functional obstruction.

Colonic Atresia Fig. 24:  Ultrasound abdomen reveals a well-defined, smooth rounded cystic lesion with inner echogenic mucosal stripe and outer hypoechoic muscle layer—enteric duplication

Radionuclide studies may be useful in 30% of patients, where the enteric duplications have gastric mucosa. Free pertechnetate is taken up and secreted by gastric mucosa, thus localizing the enteric duplication.5 CT or MRI may be useful in further characterizing the nature of enteric duplication cysts when the diagnosis is unclear, wherein they are seen as well-marginated, smoothwalled masses of fluid attenuation/signal not showing any contrast enhancement (Figs 25A and B).

Colonic atresia is quite rare as compared to atresias of the small bowel.24 It is thought to be secondary to vascular insult. Multiple atresia syndromes may involve the colon in addition to small bowel. Proximal location is more common than distal, with atresias beyond the splenic flexure being unusual. If atresia is located in the ascending colon, it may often be indistinguishable from obstruction of the distal ileum.28 The classification system based on the anatomic appearance is same as with jejunoileal atresia. Type 1 represents a diaphragmatic occlusion; type 2 represents a complete atresia with a blind, solid cord extending between the two ends of atretic segment; and type 3 represents a complete atresia with complete separation and an associated V-shaped mesenteric defect.

Chapter 129 Developmental Anomalies of Gastrointestinal Tract

A

B

Figs 25A and B:  CECT images of esophageal and gastric duplications of the two patients of the same case as in Figures 22 and 23 show sharply marginated, non-enhancing, homogeneous mass of water attenuation in the (A) posterior mediastinum and (B) along the greater curvature of stomach

Clinical Features

Embryology

Patients present with distension and failure to pass meconium. Presentation may be delayed up to 48 hours, if the atresia is proximal.

In normal intrauterine development, neuroenteric cells migrate from the neural crest to the upper end of the gastrointestinal tract by 5 weeks and then proceeds in a caudal direction. These cells reach the rectum by 12 weeks and commence the intramural migration from Auerbach’s (myenteric) plexus to the submucosal plexus. Hirschsprung’s disease is caused by abnormal neural crest cell migration, resulting in arrested distal migration of these cells.3 As the normal migration is continuous from proximal to distal, the part of the GI tract distal to the site of arrest is aganglionic.8 In the majority of cases (75–80%), the aganglionic segment is limited to the rectosigmoid region (short segment aganglionosis). The aganglionosis always involves the anus and internal sphincter and extends proximally for a variable distance. The transition from innervated to aganglionic bowel is found in the rectosigmoid region in 73% of patients, the descending colon in 14%, and more proximal colon in 10%, according to Swenson et al.8 Total colon aganglionosis involves the entire colon and part of the terminal ileum. It can very rarely involve the large as well as whole of the small bowel, which is incompatible with life. At the other end of the spectrum is ultrashort segment Hirschsprung’s disease which is also rare. In this type, the aganglionosis is limited to the region of the internal sphincter.3 The ultrashort segment can only be diagnosed by manometry (not biopsy or imaging) and is usually not diagnosed in the neonatal period.4 Skip lesions in Hirschsprung’s disease are believed to be unlikely to exist if one accepts the concept of neuronal migration down the GI tract. It is likely that such areas represent areas of intrauterine ischemic insult leading to destruction of ganglion cells.12 However, according to recently published literature, skip lesions in Hirschsprung’s disease, though a controvertial

Imaging Features Prenatal sonography may demonstrate dilatation of the colon proximal to the atresia. Plain radiograph may demonstrate a distal obstruction with multiple air-fluid levels and may be nonspecific. Occasionally, a hugely and disproportionately dilated loop of bowel may be present and render the plain film evaluation highly suggestive of the diagnosis. 2 A “soap-bubble” appearance of retained meconium may be seen. There is dilatation of the proximal colon up to the level of the atresia, unless multiple atresias are present. Contrast enema shows a microcolon, distal to the atresia with obstruction to the retrograde flow of barium at the site of atresia. The colon may have a hook or question-mark appearance at the site of atresia. The colon is often non-fixed or malpositioned in the midline. The distal colon segment may perforate into the peritoneal cavity during a contrast enema because often the blind end is covered with only mucosa.

Hirschsprung’s Disease (Aganglionosis of the Colon) Hirschsprung’s disease is a condition caused by absence of normal ganglion cells in a segment of the colon, leading to a form of low intestinal obstruction. It accounts for around 15–20% of cases of neonatal bowel obstruction.28

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Section 5 Pediatric Imaging

condition, is a definite entity, with 24 cases reported till date. Skip lesions have been found to occur predominantly in patients with total colonic aganglionosis (92%). The presence of a skip area of normally innervated colon in total colonic aganglionosis may influence the surgical management, enabling the surgeons to preserve and use the ganglionated skip area during pull through operations.33 Hirschsprung’s disease may be associated with certain congenital anomalies like intestinal atresia, malrotation. Down’s syndrome is present in 2–3% cases.

Clinical Features The absence of ganglion cells interrupts the normal propa­ gation of colonic peristalsis. Patients with Hirschsprung’s disease fail to pass meconium in the first 48 hours of life. They may present with abdominal distention, bilious vomiting, or enterocolitis. Over 80% of patients present within the first 6  weeks in life. Hirschsprung’s disease is about three to four times as common in boys as in girls. Older children may present with chronic constipation. Hirschsprung’s disease can be complicated by life-threatening enterocolitis which presents with diarrhea, abdominal distention and fever and may progress to perforation with peritonitis.3

Imaging Features Plain films may demonstrate features of distal bowel obstruction. However, a dilated colon proximal to the distal and smaller aganglionic segment is the more typical finding (Fig. 26). A small gas-filled rectum can be seen, especially on prone films and may help in the diagnosis. The absence of rectal gas is not specific for Hirschsprung’s disease as it

Fig. 26:  Plain X-ray abdomen showing a dilated proximal sigmoid colon with a smaller distal sigmoid with relatively little rectal gas in a neonate with Hirschsprung’s disease

is commonly seen in infants with sepsis and necrotizing enterocolitis. 21 At times, the bowel pattern may appear normal. Less commonly (4%), pneumoperitoneum may be seen in patients with long segment or total colonic disease secondary to colonic perforation. The radiographic diagnosis is made by contrast enema and is directed towards identifying the transition zone which is the most specific sign of Hirschsprung’s disease. This is where the normal-sized, distal aganglionic bowel changes in caliber to join the proximal ganglionic bowel.3 This findings may not be obvious in the newborn, hence, careful attention should be given to the technique of performing barium enema. Barium enema is performed on an unprepared patient by inserting a straight-tipped catheter to a point just beyond the anal sphincter. Balloon catheters are not used to avoid expanding a narrow segment of aganglionic colon, and may thus obscure the diagnosis. There is also risk of perforation of the stiff aganglionic rectum.24 Barium contrast should be prepared with normal saline to avoid possibility of water absorption from the large surface area of dilated colon.29 With the patient in the lateral position, barium suspension is introduced slowly by gravity drip infusion, under fluoroscopic monitoring. The infusion is stopped and restarted as serial spot radiographs are obtained. As filling progresses into the descending colon, the patient is rolled into the supine position. If the examination is positive, the diagnosis in most cases is made by the time the barium fills the proximal descending colon. Rapid infusion of barium suspension can distend and mask the transition zone. When the transition zone is observed, the examination should be discontinued because filling of the more proximal dialated bowel beyond the transition zone may lead to impaction. However, the distention of the bowel, proximal to the aganglionic segent is gradual, and a transition zone is seen in only 50% of neonates during the first week of life.28 The transition zone generally is funnel-shaped and it is an important diagnostic feature. In some instances, the transformation from dilated bowel to narrowed bowel is abrupt (Fig. 27). In other cases, the funneling of the bowel occurs incrementally over a long segment of bowel to appear almost imperceptible because of the gradual change in caliber. In long segment Hirschsprung’s disease, a variable portion of the colon proximal to the sigmoid colon is aganglionic (Fig. 28). The pathological transition zone is usually somewhat more proximal than the radiographical one. Under fluoroscopic visualization, irregular saw-toothed mucosal pattern may be seen due to disordered contractions in the aganglionic colon (Fig. 29). Another radiographic appearance of Hirschsprung’s disease that has been described in neonates and young infants in whom the rectosigmoid region appears normal, is the presence of straight transverse bands in the involved segment of colon. These bands are thought to represent areas of persistent spasm.12

Chapter 129 Developmental Anomalies of Gastrointestinal Tract

Fig. 27:  Hirschsprung’s disease: Barium enema shows an abrupt

transition from the narrow caliber rectosigmoid (aganglionic) to the larger caliber more proximal sigmoid colon

The rectosigmoid index can be used in the diagnosis of Hirschsprung’s disease confined to the rectum. This compares the ratio of the rectal diameter to the sigmoid diameter and is considered abnormal, if the sigmoid colon is more dilated than the rectum (R/S index 60°

< 55°

Stable

None

II

Concentric position a. Physiological immaturity (age < 3 mon) b. Delayed ossification (age > 3 mon) c. Concentric position d. Subluxation

50°–60°

77°

— — Labrum everted

Evaluation by orthopedic surgeon Evaluation by orthopedic surgeon Required

>70°

B o ny ro o f d e f i c i e n t Required labrum everted

III

Low dislocation

0.5 cm but acetabulum visible; 3 = center size large enough to prevent visualization) (Figs 23A to D). In the transverse plane, with the infant’s hip flexed, the hypoechoic cartilaginous femoral head is viewed between two echogenic limbs of a ‘V’ (in adduction) or U (in abduction). Stability can also be assessed in the coronal plane while pistoning the hip anteroposteriorly (knees flexed), (Fig. 24).

Fig. 22: USG—62% coverage of the femoral head within the

Fig. 21: USG old neglected CDH on the right with normal left hip

acetabular cup

A

B

C

D

Figs 23A to D: Harcke’s dynamic four step method. (A) Transverse neutral view (B) Transverse flexion view (C) Coronal flexion view (D) Coronal neutral view. Ant, anterior; Lat, lateral; P, pubis; I, ischium; Il, ilium

2307

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Section 5 Pediatric Imaging

Rosendahl and co workers in 1992 described a modified Graf’s method classifying hip morphology and hip stability separately. Hip morphology (alpha angle) was assessed using the standard coronal view with the femoral head centered. In cases of decentered or dislocated hips-Graf type 2c, D, 3, 4a, the femoral head was relocated by mild traction on the thigh before morphology could be studied. A Barlow maneuver was applied to assess a coexisting instability. A technique for assessing the degree of lateralization of the femoral head on the basis of Harcke’s coronal flexion view was proposed by Morin et al. in 1985. Based on two lines paralleling Graf’s baseline, one tangent to the lateral part of the femoral head and one tangent to the medial junction of the head and acetabular fossa were drawn, they measured distance between medial and iliac lines (d) and between the medial and lateral lines (D). The ratio of d to D multiplied by 100 indicated the percentage of the femoral head covered by the bony acetabulum.15

Pediatric radiologists are relying increasingly on the use of dynamic sonography as this allows real time observation of maneuvers allowing a more accurate depiction of the femoral head in relation to the acetabulum as the hip position is changed. Hence, it allows not only depiction of DDH but is also able to assess whether a particular closed reduction is appropriate. Sonography can also be used to monitor treatment of patients with DDH in a spica cast, brace or Pavlik harness. The long axis anterior approach may be useful in a patient with a spica cast in which a window cannot be cut for lateral scanning. The window should be repositioned and the cast repaired to avoid posterior hip dislocation. The sonographic follow-up of patients being treated in a Pavlik harness is however easy as it permits movement within a safe zone while the degree of restriction prevents subluxation or dislocation. Improvement should be seen within 3 weeks of treatment. Duplex Doppler US has been used to assess vascularity of the femoral head in an infant undergoing abduction treatment. The normal spectral waveform of arterioles in the femoral head of an infant is a slow flow, low resistance arterial pattern with resistive indices ranging from 0.2 to 0.68 (mean 0.48 ± 0.11).16 Power Doppler can be used to visualize blood flow in the cartilaginous femoral head to ensure that flow is not compromised during treatment.

COMPUTED TOMOGRAPHY

Fig. 24: USG—hip flexed transverse plane—femoral head viewed between two echogenic limbs of pubis and ischium in adduction (‘V’)

A

Computed tomography is useful for the evaluation of concentricity of closed reduction, detection of iliopsoas muscle deformity or intra-articular soft tissue obstacles such as hypertrophied fibrofatty pulvinar which can make it difficult to achieve concentric reduction by the closed method, for detection when the surgical procedures are to be performed and for the determination of femoral torsion and acetabular configuration. It can be performed even when the patient is casted (Figs 25 and 26). CT is most useful in

B

Figs 25A and B: CT-MPR (A) and VRT (B) shows right femoral epiphysis dislocated superiorly and posteriorly

Chapter 142 Imaging of Pediatric Hip

Fig. 26: CT case of DDH with hip spica

postoperative assessment of reduction. Injection of contrast medium into joint is often performed during intraoperative reduction. CT done soon after allows the contrast medium surrounding the nonossified femoral head to be identified. This helps in assessment of the alignment of the femoral head and its relationship to the acetabulum. The use of three-dimensional imaging allows direct assessment of the amount of anterior and posterior acetabular coverage. Standard CT protocols allow images to be obtained in the standard frog leg position. Even though the femoral head may not be ossified the position of the femoral metaphysis relative to the midportion of acetabulum can be evaluated. CT scanning allows differentiation of lateral from posterior hip dislocations. Lateral displacement shows the labrum and capsule unfolded secondary to a tight iliopsoas tendon. In posterior dislocation approximation of the femoral metaphysis and acetabulum, projection of a mass behind the ischium and posterior displacement of pregluteal fat plane is seen. Acetabular anteversion is measured by determining the angle of the anterior and posterior rim relative to the vertical axis of the pelvis (Figs 27A and B). Increased acetabular anteversion has been noted in dysplastic hips and also in some healthy volunteers. Acetabular sector angles are more specific to the presence of hip dysplasia (Figs 28A and B). Anterior and posterior sector angles reflect the degree of anterior and posterior acetabular support.17 The sector angles are determined by measurement of the angle drawn between the center of the femoral head and the anterior and posterior acetabular rim relative to the horizontal axis of the pelvis. A normal anterior angle is greater than 50° and a normal posterior angle is greater than 90°. These angles are reduced in developmental dysplasia, which reflects acetabular support.

A

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Figs 27A and B: Schematic diagram (A) and CT (B). Measurement of femoral anteversion from an axial CT slice. H, horizontal line through femoral head center; P, posterior margin of acetabulum; A, anterior margin of acetabulum; V, line perpendicular to line H through point PAC; AV, angle of anteversion

Measurements of acetabular angles, have however not been found predictive of the outcome of DDH.18

MAGNETIC RESONANCE Magnetic resonance is used in the evaluation of dysplasia of the hip when there is (i) a complex dysplasia, (ii) there has been inadequate response to treatment, (iii) in late presentation and (iv) teratological dislocation. Axial and coronal MR images are most useful and small surface coils with high spatial resolution are necessary to evaluate DDH.

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The value of MR imaging in preoperative planning is due to its ability to portray the cartilaginous part of the pelvis and also analyze the relationship of the femoral head to the acetabulum and labrum. The femoral head is variably laterally displaced in DDH, with posterior and superior reduction. MR shows femoral head coverage in both coronal and axial planes without need for complex radiographic projections or magnification correction. The degree of coverage by the cartilaginous acetabulum and labrum can be evaluated by MR. MR imaging can show changes in the shape of the acetabulum, not demonstrated on CT sonography or radiography. In DDH, the acetabulum becomes elongated posteriorly or superiorly. The rim of the acetabulum becomes

A

oval and the acetabular cartilage becomes thickened and may become displaced.19 Any obstruction to the reduction can be visualized, especially in cases where there is a history of failed closed reduction. These include a flipped labrum, prominent pulvinar and a redundant ligamentum teres; capsule or illiopsoas tendon or transverse acetabular ligament, which may be interposed into the joint (Figs 29A and B). Prominent pulvinar is visualized as fibro fatty material in the joint, which does not allow normal seating of the femoral head within the joint. There can be a small amount of pulvinar normally present with the head being slightly laterally displaced. If the head is encompassed by the confines of the acetabulum

B

Figs 28A and B: Schematic diagram (A) and CT (B). Measurement of acetabular sector angles. H, horizontal line through femoral head center; P, posterior margin of acetabulum; A, anterior margin of acetabulum; C, center of femoral head; HASA, horizontal sector angle; AASA, anterior sector angle; PASA, posterior sector angle

A

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Figs 29A and B: MRI T1 coronal (A) and T2 axial (B) shows dislocated femoral epiphysis with hypertrophied ligamentum teres preventing relocation

Chapter 142 Imaging of Pediatric Hip

and pointing at the triradiate cartilage, the pulvinar usually atrophies. Gadolinium enhanced magnetic resonance arthrography visualizes the labrum, ligamentum teres, transverse acetabular ligament and the pulvinar.20 In the immediate postoperative period, MR imaging is useful in evaluation of proper reduction of the dislocated femoral head and its vascular health. Recently dynamic interventional MRI in an open configuration scanner has been used in the management of developmental dysplasia. The hip can be visualized during reduction and spica can be applied within the scanner itself.21

Differential Diagnosis of DDH Radiographic features such as shallow acetabulam with high angled roof lateral and cephalad displacement of the upper end of the femur and small ossification center for the head can be seen in congenital hypothyroidism. Following appropriate therapy, spontaneous resolution may occur. Traumatic epiphyseal separation of the femoral neck in very young infants may simulate congenital dislocation. The possibility of trauma may be considered if there is history of an abnormal presentation/difficult labor. Acquired non traumatic dislocation may develop in pyoarthrosis of hip. In such a case clinical sign of infection will be present.

The Painful Hip Hip pain in a child is always potentially serious and presents a diagnostic challenge since clinical differentiation between septic arthritis; transient synovitis and Perthes’ disease may be difficult. The principle concern is to distinguish sepsis of the hip joint from an irritable hip, as untreated sepsis can destroy the hip within days. The presentation may be mild and atypical and therefore imaging plays an important role in the management of such cases.

Septic Arthritis Acute purulent infection of the joints is more common in infancy and early childhood because of greater blood flow to the joints during active growth. Hematogenous seeding is the most common cause related to an upper respiratory tract infection or pyoderma. Infection may also spread from adjacent osteomyelitis in metaphysis (specially in hip, where metaphysis is intra-articular) or from cellulitis, abscess, etc. During infancy, septic arthritis frequently complicates osteomyelitis because capillaries from the metaphysis traverses the physis into the epiphysis. Infants with immune dysfunction, indwelling cathetars, vascular lines are at increased risk. Over 90% of cases of septic arthritis are monoarticular with hip being one of the most commonly affected joints.

Staphylococcus aureus is the most common cause of bacterial arthritis, with group B Streptococcus seen in neonates. H. influenzae in the 1-4 years age group. Children with chickenpox are at increased risk of developing septic arthritis and other musculoskeletal infections secondary to group A Streptococcus. Pneumococcal joint infection may be seen in children with splenic dysfunction. Over 90% of cases of septic arthritis are monoarticular with the hip being most commonly involved. Clinically there is fever, joint pain and swelling. Boys are affected twice as frequently as girls. It is a medical emergency as it may lead to joint destruction and impairment, if not immediately and adequately treated.

Pathology The joint cartilage is vascular and the synovial fluid cushions, lubricates and nourishes the joint cartilage. Bacteria may seed into the synovial space through the highly vascular synovial membrane. Initially, there is edema and hypertrophy of the synovial membrane with joint effusion, which distends the joint. Hyperemia and immobilization leads to demineralization and osteoporosis. The ensuing inflammatory reaction results in destruction of the cartilage matrix leading to reduction of the joint space. Inflammatory pannus destroys the articular cortex, which is eroded. Severe cases are characterized by massive destruction, separation of bone ends, subluxation and dislocation. During recovery bones recalcify and bony and fibrous ankylosis may occur.

Imaging Imaging evaluation is initially by conventional radiography. Plain films may be normal or demonstrate joint space widening with adjacent soft tissue swelling and disruption of normal tissue planes. It may show joint space loss and erosions with relative preservation of mineralization (Fig. 30). Radionuclide imaging is more sensitive than radiographs. A bone scan localizes the site of infection and is positive as early as 2 days after the onset of symptoms. In septic arthritis there is increased articular activity in the blood flow and blood pool phases. Reduced uptake within the epiphysis may be as a result of ischemia. Ultrasonography can clearly delineate presence and nature of joint fluid by direct visualization22 and can be used to guide needle aspiration. The anterior approach along the plane of the neck is used as this is the most easily distensible part of the joint and fluid first accumulates in this area. In normal hip, the joint capsule is seen as a continuous concave reflective line paralleling the anterior aspect of the femoral neck and capital femoral epiphysis. Synovial thickening or an effusion causes the joint capsule to become convex and bulge anteriorly. A difference of 2 mm in the Anterior

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Fig. 30: X-ray pelvis erosions in right femoral head with dislocation

Fig. 31: USG—Collection with echogenic debris following infection

and widening of joint space septic arthritis

A

B

Figs 32A and B: X-ray (A)—Reduced right hip joint space with irregularity of articular outline. Ultrasound hip (B) of the same patient—shows disorganized joint with effusion that shows debris—a case of septic arthritis

Capsule Distance (ACD) is indicative of effusion. Asymmetry is an unreliable parameter as effusion may be bilateral. The normal ACD increases with age and the upper limit of normal are 5 mm (50%) separates the two main groups A and B.45 DWI may be a noninvasive means of distinguishing between Perthes disease with favorable and unfavorable prognosis. Femoral epiphysis showed increased diffusivity in the affected hip. Increased metaphyseal diffusivity was found in all cases with absent lateral pillar enhancement at dynamic post contrast MR,46 signifying poor prognosis. The main differential diagnosis of LCP are toxic synovitis, septic hip, juvenile chronic arthritis and juvenile osteonecrosis (AVN due to a known cause-sickle cell anemia, thalassemia).

Proximal Femoral Focal Deficiency (PFFD) PFFD is a malformation in which complete growth and development of upper femur fails to occur. It encompasses spectrum ranging from mild shortening of an otherwise normal femur to severe handicap of absent femur, except for condyles accompanied by acetabular aplasia and thigh muscular dysplasia.

Imaging The radiographic findings consist of failure of development and delayed ossification of a lesser or greater part of the proximal femur. Hence, a short femur that is laterally situated and proximally displaced is demonstrated at birth. The distal femur is by definition always present (Figs 48 and 49), there is a misshapen femoral head and neck, upper end of disconnected distal femur—either bulbous or pointed. The femoral head is situated low in the acetabulum with a woolly outline. Secondary deformity of the acetabulum may result. In later cases, the greater trochanter will be found to curve like a beak and it may articulate with the ilium. Pelvis may show enlarged obturator foramen with a supra acetabular

Chapter 142 Imaging of Pediatric Hip

Fig. 48: X-ray pelvis—focal femoral deficiency in the right side

Fig. 49: Aitken class A PFFD: Femoral head is present and connected to the shaft of femur

bump or horizontal/dysplastic roof of the acetabulum. If radiographs show a normal acetabulam at birth, presence of normal cartilaginous femoral head is likely. Hip sonography plays a role in the classification of PFFD and in confirming the location of the femoral head with respect to the acetabulum, especially when no proximal femur is seen on radiography. US may reveal a cartilaginous head and neck.47 Ultrasonography may be useful in prenatal diagnosis and in infants to identify the femoral head. Mobility of the femoral head within the acetabulum may also be assessed.48 MR imaging can identify correctly the size and position of the femoral head present. Thin section coronal and axial imaging is of use in locating a small femur head. Continuity to the rest of the femur may also be assessed. Presurgical evaluation is important to guide the orthopedic surgeon in reconstruction. There may be a wide variation in the gap between femoral head and subtrochanteric femur. The gap may be small with pseudoarthrosis or be filled with fibroosseous tissue. It can also be devoid of any connective tissue. This and the resultant coxa vara deformity cannot be adequately seen on a radiograph as the gap is radiolucent. On CT, the nonossified areas have soft tissue attenuation. On MRI, the femoral head, if present exhibits the intensity of yellow marrow, whereas fibrous tissue is low in signal intensity on all pulse sequence. The prognosis and treatment options depend on grading of the abnormalities. The most commonly used system is the Aitken classification which assigns types A to D to the abnormality depending in the presence or absence of the femoral head and the acetabulum and osseous integrity of the remainder of the femoral shaft. In patients with type A PFFD, the femoral is short. The femoral head and acetabulum are present. In type D the femur is very short and head and acetabulum are absent. Acetabular deformity is correlated

with the presence or absence of the femur which can be inferred from the relative development of the acetabulum. The differential diagnosis can be a congenital short femur (no specific abnormalities of head, neck and shaft), z Congenital coxa vara–Head, neck normal z Developmental dysplasia of hip-Graf type 4 Traumatic femoral capital epiphysiolysis in newborn – Pain plus edema of inguinal crease and upper thigh is noted.

Slipped Capital Femoral Epiphysis Slipped capital femoral epiphysis (SCFE) is an uncommon skeletal disorder of adolescence often overlooked because of its non-specific presentation. It is a unique disorder because no other bone shows similar changes. It is usually seen during adolescent growth spurt in overweight children, with the incidence of bilaterality being 25%. There is a morphological change in the relationship of the femoral head to the femoral neck centered at the physeal level probably caused by obesity. The femoral head becomes relatively retroverted at the physeal level placing the head and physis at a mechanical disadvantage when subjected to stress. It is Salter 1 fracture through the proximal femoral physis with displacement of the capital femoral epiphysis. In most cases, the displacement of the head is usually medial and posterior relative to the metaphysis. In a few cases, there may be a valgus slip with the head rotating superiorly and posteriorly relative to the neck. This term does not include traumatic Salter-harris 1 as the etiology and management are different. The most common sign/symptom is limp, painful limitation of hip motion while walking/running. It coincides with adolescent growth and is related to endocrine disorders like hypothyroidism, pituitary dysfunction.

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A

B

Figs 50A and B: Schematic representation: (A) of hip shows Klein’s line that normally intersects lateral 1/3rd of the femoral epiphysis on the left, whereas in slipped epiphysis, no part of the epiphysis is lateral to it as seen on the right. X-ray pelvis. (B) Depicting the normal position of the femoral head in relation to the Klein’s line

The slip is classified as stable or unstable with the criterion being the ability to bear weight with or without crutches. The incidence of complications is higher with unstable variety.

Imaging Radiographs remain the prime method of diagnosing SCFE, though it may be difficult to diagnose on anterior projection alone. Medial displacement of the capital epiphysis is seen on the antero posterior projection. A line drawn along the lateral border of the femoral neck (Klein’s line) in a normal individual intercepts the epiphyseal ossification center so that a small portion of the head remains lateral to this line (Fig. 50A and B). With SCFE, no part of femoral head ossification center is seen lateral to the line. On the anterior projection, there may be mild widening, lucency and irregularity of the physis. The femoral head may appear foreshortened and there may be apparent sclerosis in the regional femoral neck as the femoral head rotates posteriorly. In the frogleg or true lateral position, the anterior and posterior corners of the epiphysis and metaphysis line up closely in a normal patient, whereas they are displaced in SCFE (Figs 51 and 52). Posterior displacement is seen on frog lateral radiograph as medial displacement of epiphysis relative to metaphysis. Approximately 90° external rotation of femur on frog-lateral means what is actually a posterior displacement of epiphysis looks like medial displacement on radiograph. On the cross table lateral radiograph with 25 flexion, it is seen as true posterior displacement of epiphysis. Metaphysis shows scalloping, irregularity, sclerosis and posterior beaking. One needs to be careful when using opposite asymptomatic hip as control for radiographic evaluation of painful one as the opposite side may have unrecognized SCFE.

Fig. 51: X-ray pelvis—Slipped capital epiphysis left side

Staging of radiographic findings is mild-moderate- severe based on the displacement of ossification center by 2/3 metaphyseal diameter. Ultrasound may suggest malalignment of the capital femoral epiphysis relative to the metaphysis.4 The alignment of the epiphysis relative to the metaphysis should be assessed as part of hip ultrasound study. Joint effusion, which may accompany SCFE, is recognized by US. US can be used as follow-up of SCFE due to risk of slippage in the contralateral hip.49 CT demonstrates the slip and the reduced femoral anteversion, which may be quantified. CT head/neck angles range from 4 to 57 degrees in symptomatic and 0 to 14 degrees in asymptomatic patient.50 It may also demonstrate metaphyseal scalloping and beaking (Figs 53A to C).

Chapter 142 Imaging of Pediatric Hip

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B

Figs 52A and B: X-ray frog’s leg view (A) and AP view (B) show medial and inferior displacement of the right capital epiphysis with widening of the physis

A

B

B

Figs 53A to C: CT—Coronal MPR (A), Axial (B) and VRT (C) Medial and posterior slip of the femoral epiphysis of the right hip with complication of avascular necrosis as seen by flattened head of femur

MR imaging relies on identification of the morphological change at head/neck function and the abnormal signal intensity centered on the physis, indicating stress and edema. Physeal widening is a constant feature and can be seen on MR

before being apparent on radiographs. 3D volume acquisition can be used to reconstruct sagittal oblique images along the axis of the femoral neck to identify any retroversion. MR image can be oriented to a plane orthogonal to the plane of

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A

B

Figs 54A and B: (A) MRI—T1 weighted coronal and (B) STIR coronal depicting widening and irregularity of the physis on the left side with physeal slip—Slipped capital femoral epiphysis

the physis to assess the width of the same. Physeal widening is seen on T1 weighted MRI, whereas synovitis and marrow oedema are appreciated on T2 weighted images (Figs 54A and B). MRI can also demonstrate physeal widening in the center or posteromedial origin of the physis in a contralateral asymptomatic hip, providing for prophylactic treatment of the same.51 Hyperintensity on fluid sensitive images at the physis is indicative of a chronic slip condition. Subtle abnormalities include edema on the metaphyseal side, usually at the extreme medial end of the physis. The complications of SCFE are avascular necrosis, occurring in 20–45% of cases and chondrolysis. Treatment consists of preventing further displacement and to cause closure of the physis. Chondrolysis is less common than AVN and is recognized by progressive thinning of the medial joint space on the radiographs. Premature closure of the physis of the greater trochanter is considered as predictive sign for chondrolysis. Premature osteo arthritis may develop in ¼-1/3 of patient with SCFE. Prognosis is poorer with unstable variety.

Differential Diagnosis z

z z z

Legg-Calve-Perthes’s disease—the patient is younger with irritable hip progressing to sclerosis and collapse of epiphysis, there is a hairline fracture with marrow edema: Hip joint inflammation Osteoid osteoma Traumatic SCFE

Developmental Coxa Vara The normal femoral neck shaft angle changes from about 150 degrees in the infant decreasing to 120 degrees in the

Fig. 55: Right coxa vara

adult. The femoral neck is valgus in infants because of relatively increased growth in the medial portion of the physis in the perinatal period. During childhood there is a greater amount of growth in the lateral portion of the femoral physis that is influenced by weight bearing. Coxa vara is defined as femoral neck shaft angle of less than 120 degrees.52 True coxa vara may be secondary to congenital anomalies, osteomalacia, or syndromes. Functional coxa vara occurs as a result of overgrowth of the greater trochanter secondary to AVN, infection or trauma. Developmental coxa vara, bilateral in 40% of cases, presents at 2 years of age with an abnormal gait. It is caused by an abnormality of bone growth at the physis with a greater rate of growth of the lateral aspect of the physis causing the physis to be more vertical than usual. Radiographs show a widened and an abnormally oriented physis (Fig. 55). As stress occurs along the physis multiple

Chapter 142 Imaging of Pediatric Hip

A

B

Figs 56A and B: X-ray pelvis (A)—Traumatic posterosuperior dislocation of the left femur, MRI-T1 coronal (B) depicting the superior and posterior dislocation

small steps occurs and small triangular corner fractures develop along the medial aspect of the physis. MR imaging demonstrates widening of the physis with expansion of the cartilage.

Pediatric Hip Trauma Traumatic hip dislocations rarely occur in childhood. Posterior hip dislocations comprise majority of such dislocations.53 A soft pliable acetabulum and ligamentous laxity may predispose the immature hip joint to a dislocation secondary to minimal trauma. Potential associated injuries include fracture and neurovascular injury while avascular necrosis and degenerative joint disease are potential sequelae. Osteochondral fractures may be difficult to recognize on plain radiography. CT is useful in the definition of the extent and displacement of complex and impacted fractures around the hip joint. Growth plate injuries are important to recognize as they have potential implications for growth arrest. Growth disturbance of the proximal femur can be post-traumatic or may be secondary to ischaemia following hyperabduction for DDH, Legg-Calve-Perthes’ disease and rapidly developing effusions. The proximal femur physis is particularly vulnerable because the epiphyseal artery is intraarticular. Physeal widening or narrowing may be seen on radiographs. MR imaging is the modality of choice. T1 weighted images demonstrate low signal intensity growth recovery line and variable signal intensity bony bridge on GRE sequences, a bridge appears as a low signal intensity interruption in high signal physeal cartilage. Physeal widening on GRE and T2 weighted images implies physeal dysfunction. Medial physeal impairment leads to a short wide femoral neck and coxa vara deformity whereas vertex arrest causes Coxa valga54 (Figs 56 and 57).

Fig. 57: X-ray pelvis—Fracture right femoral neck

Neuromuscular Hip Dysplasia Children who suffer from cerebral palsy or other neuromuscular disorders, who are unable to walk have a 58% incidence of hip dislocations. With muscle imbalance and lack of weight bearing, there is a coxa valga deformity with persistence of a straight neck shaft angle, which leads to hip dislocation. Simulated standing radiographs show pelvic tilt, valgus deformity of the femoral neck, abnormal shape and placement of the femoral head. CT is helpful for evaluation of the shape of the acetabulum and the degree of femoral articulation.

Childhood Idiopathic Chondrolysis of the Hip This is a rare disorder, which causes progressive destruction of the articular cartilage of the hip joint with associated bone

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remodeling. Cartilage loss, bone remodeling, and small joint effusions along with muscle wasting are seen.55

Calcification of Cartilage and Joints Idiopathic calcification of the cartilages of the hips, i.e. acetabular rims and femoral hands has been reported in children and the patients may be asymptomatic or have a limp with restricted hip movements. This is believed to be an acquired pathology due to local chemical trauma from partial extravasation of an intravenous injection via the femoral route. On serial studies, calcification may remain unchanged, increase, or show gradual resorption with early fusion of the femoral head and neck. The hip joint may also be involved as part of a large number of skeletal dysplasias or systemic disorders as in nutritional disorders, neoplasia like leukemia, metastatic neuroblastoma. Developmental and acquired abnormalities of the hip are relatively common in childhood. Radiographs, ultrasonography, MR imaging, computed tomography and nuclear medicine play an important role in the diagnosis and management of these disorders.

Femoroacetabular Impingement The geometry of femoral neck and acetabulum plays a role in the etiology of degenerative disease.56,57 Normally, the femoral neck has a definite narrowing or waist which allows the femur to abduct fully without impingement on the lateral aspect of the acetabulum. In patients with FAI, the femoral neck is not tabulated normally. Instead of having an identifiable constriction, a pistol grip deformity is seen in which tabulation is lacking. A small bump or protuberance may be identified on the anterior femoral neck. Slipped capital femoral epiphysis may be a contributing factor (Fig. 58). Axial oblique images prescribed along the axis of the femoral neck or reconstruction of 3D volume acquisition into axial oblique plane allows for measurement of D angle. First the center of the femoral head is identified using the contour of the head to fit a circle to outline and define the position of the center of the head. Two lines are extended from the center point of the head, one down the axis of the femoral neck and the second to the intersection point between the head and the neck, when the convexity of the femoral head becomes the concavity of the femoral neck. Angles less than 55 degrees are abnormal or if the head-neck line measures greater than the radius of the circle defining the femoral head, then a femoral waist deficiency is present. FAI may also be caused by over coverage of the femoral head and neck. This may be caused by acetabular retroversion. Normally the acetabulum has its lateral opening directed slightly anteriorly. In abnormal cases, the anterolateral

Fig. 58: CT—Oblique axial image shows evidence of CAM impingement with a bump at the femoral neck

edge of the acetabulum extends further laterally than the posterolateral edge so that the acetabular opening is directed posteriorly. On radiographs,this is visualized as the cross over sign. This is present when the anterior lip of the acetabulum crosses over the posterior lip on a standard frontal film. This limits the ability to flex at the hip as the femoral neck impinges on the anterior acetabulum. Abnormal morphology in the pediatric age group may not reflect the pathological abnormalities seen in adulthood, however subtle osseous abnormalities can help guide prognosis.

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of the hip-comparison with conventional arthrography. Radiology. 1999;212(2):519-25. Aubry S, Belanger D, Giguere C. Magnetic resonance arthrography of the hip: Insights Imaging. 2010;1:72-82. Klisie PJ. Congenital dislocation of the hip: A misleading term. J Bone Joint Surg Br. 1981;63:38-42. Kuhn JP, et al. Caffey’s Pediatric Diagnostic Imaging. 10th edn 2277-9,2004: Mosby. The joints BabynPS, RansOm MD 2435-93. Havije HT, Waller RS. Ultrasound screening for dysplasia of the hip (Letter). Pediatrics. 1995; 95:799-800. Zieger M. Ultrasound of the infant hip Part 2 validity of the method. Pediatric Radiol. 1986;16:488-92. Graf R. Classification of hip joint dysplasia by means of sonography. Arch Orthop Trauma Surg. 1984;102:248. Harcke HT, Lee MS, Born P, et al. Examination of the infant hip with real time ultrasonography. J Ultrasound Med. 1984;3:131. Harcke HT, Grissom LE. Performing dynamic sonography of the infant hip. AJR Am J Roentgenol. 1990;155:837. Rosendahl K, Toma P. Ultrasound in the diagnosis of developmental dysplasia of the new borns. The European approach. A review of methods, accuracy and clinical validity: Eur Radiol. 2007;17:1960-7. Schwartz DS, Kellar MS, Fields JM, et al. Arterial waveforms of the femoral heads of healthy neonates. AJR Am J Roentgenol. 1998;170:465-6. Browing WH, Rosenkrantz H, Tarquinio T. Computed Tomography in congenital hip dislocation. J Bone Joint Surgery (AM). 1982;64:27-31. Hubbard AM. Imaging of pediatric hip disorders. Rad Clin North Am. 2001;39(4). Dwek JR. The Hip: MR Imaging of Uniquely Pediatric Disorders: Radiol Clin North Am. 2009;47:997-1008. Kawaguchi AT, Otsuka NY, Deigado ED, et al. Magnetic resonance arthrography in children with developmental hip dysplasia. Clin Orthop. 2000;374:235-46. Tennant S, Kinmant C, Lamb G, et al. The use of dynamic interventional MRI in developmental dysplasia of the hip. J Bone Joint Surg B. 1999;81(3):392-7. Jawin J, Hoffer F, Rand F, et al. Joint effusion in children with an irritable hip: Ultrasound diagnosis and aspiration. Radiology. 1993;1987:459. Strouse PJ, Di Pietro MA, Adler RS. Hip Effusions: Evaluation with Power Doppler Sonography. Radiology. 1998;206:731-5. Hopkins K, Li K, Bergmon G. Gadolinium DTPA enhanced magnetic resonance imaging of musculoskeletal infections processes. Skeletal Radiol. 1995;24:325. Lee SK, Suh KJ, Kim YW, et al. Septic arthritis, versus transient synovitis at MR imaging preliminary assessment with signal intensity alterations in bone marrow. Radiology. 1999;211:459. Park JK, Kim BS, Choi G, et al. Distinction of reactive joint fluid from pyogenic abscess by diffusion–weighted imaging. J Magn Reson Imaging. 2007;25(4):859-61. Daldrup-Link HE, Steinbach L. MR imaging of Pediatric arthritis. Radiol Clin N Am. 2009;47:939-55.

28. Hong SH, Kim SM, Ahn JM, et al. Tuberculous versus pyogenic arthritis: MR imaging evaluation. Radiology. 2001;218:843-53. 29. Sawhney S, Jain R. Tuberculosis of the bones and joints. In Berry, Chowdhury, Suri (Eds): Diagnostic Radiology-Musculoskeletal and Breast imaging (1st edn). Jaypee Brothers 1998. 30. Chapman H, Murray RD, Stoken OJ. Tuberculosis of the bone and joints. Semin Roentgenol. 1979;19:26-282. 31. Murray RO, Jacobson HG. Infections: Radiology of Skeletal Disorders (2nd edn). Churchill Livingstone. 1997.p.1. 32. Jacobs P, Renton P. Avascular necrosis of bone: Osteochondritis: Miscellaneous bone lesions. In Sutton D (Ed): Textbook of Radiology and Imaging (4th edn). Churchill Livingstone. 1987; 1:77-94. 33. Caterall A. Legg-Calve-Perthes disease. New York, Churchill Livingston 1982. 34. O’hara SM. Benton C-abnormalities of hip in Diagnostic Imaging-Donelly. Amirsys 2005. 35. Doria AS, Guarniero R, Gunha FG, et al. Contrast enhanced power Doppler Sonography: Assessment of revascularization flow in Legg-Calve-Perthes’ disease. Ultrasound Med Biol. 2002;28(2):171-82. 36. Strouse PJ. Musculoskeletal system. In Haaga JR, Lanzieri, Gilkeson (Eds): CT and MR Imaging of the Whole Body (4th edn). 2002;2:2095-122. 37. Ha As, Wells J, Jaramillo D. Importance of sagittal MR imaging in nontraumatic femoral head osteonecrosis in children. Pediatr Radiol. 2008;38(ii):1195-200. 38. Jaramillo D, Galen TA, Winalski CS, et al. Legg-Calve-Perthes’ disease: MR imaging evaluation during manual positioning of the hip. Comparison with conventional arthrography. Radiology. 1999;212(2):519-25. 39. Dillman JR, Hernandez RJ. MRI of Legg-Calve-Perthes disease. AJR. 2009;193:1394-1407. 40. Mahnken AH, Staatz G, Ihme IV, et al. MR signal intensity characteristics in Legg-Calve-Perthes’ disease value of fat suppressed (STIR) images and contrast enhanced T1 weighted images. Acta Radiol. 2002; 43(3):329-35. 41. Lamer S, Dogeret S, Khairouni A, et al. Femoral head vascularization in Legg-Calve-Perthes’ disease Comparison of dynamic gadolinium enhanced substraction MRI with bone scintigraphy. Pediatric Radiol. 2002;32(8):580-85. 42. Menezes NM, Olear EA, Li X, et al. Gadolinium enhanced MR images of the growing piglet skeleton: Ionic versus. Nonionic contrast agent. Radiology. 2006;239(2):406-14. 43. Menezes NM, Connolly SA, Shapiro P, et al. Early ischemia in growing piglet skeleton. MR diffusion and perfusion imaging. Radiology. 2007;242(1):129-36. 44. Lahdes-Vasama T, Lamminen A, Merikanto J, et al. The Value of MRI in early Perthes’ disease: An MRI study with a 2 year follow up. Pediatric Radiol. 1997;27(6):517-22. 45. De Sanctis N, Rega AN, Rondinella F. Prognostic evaluation of Legg-Calve-Perthes’ disease by MRI—Pathomorphogenesis and new classification. J Pediatr Orthop. 2000;20(4):403-70.

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Section 5 Pediatric Imaging 46. Merlinic L, Combescure C, De Rosa V, et al. Diffusion— weighted imaging findings in perthes disease with dynamic gadolinuim–enhanced subtracted (DGS) with MR correlation— a preliminary study Pediatr Radiol. 2010;40(3):31. 47. Grissom LE, Harcke HT. Sonography in congenital deficiency of the femur. J Paediatr Orthop. 1994;14:29-33. 48. Kayser R, et al. Proximalfocal femoral deficiency—rare entity in the sonographic differential diagnosis of developmental dysplasia of the hip. J Pedia tr. 2005;146(1):141. 49. Castriota-Scandfrberg A, Orsi E. Slipped capital femoral epiphysis ultrasonographic findings skeletal. Radiol. 1993; 22(3):191-93. 50. Umans H, Liebling MS, Moy L, et al. Slipped capital femoral epiphysis: A physeal lesion diagnosed by MRI with radiographic and CT correlation. Skeletal Radiol. 1998;27(3):139-44. 51. Futami T, Suzuki S, Seto Y, et al. Sequential magnetic resonance imaging in slipped capital femoral epiphysis, assessment of prestep in the contralateral hip. J Paediatr Orthop B. 2001; 10(4):298-303.

52. Ozonof MB. Pediatric Orthopaedic. Radiology Philadelphia: WB Saunders 1992. 53. Petrie SG, Harris MB, Willis RB. Traumatic hip dislocation during childhood. A case report and review of the literature. Am J Ortho. 1996;25(a):645-9. 54. Ecklund K, Jaramillo D. Imaging of growth disturbance in children. Radiol Clin North Am. 2001;39(4):823-42. 55. Johnson K, Haigh SF, Ehtisham S, et al. Childhood Idiopathic Chondrolysis of the hip: MRI features. Paediatr Radiol. 2003; 33(3):194-9. 56. Pfirrmann CW, Mengiardi B, Dara C, et al. Ca M and pincer femora acetabular impingement: Characteristic MR authrographic findings in 50 patients. Radiology. 2006;240(3): 778-85. 57. Gam R, Parvizi J, Beck M, et al. Femoracetabular impingement: A cause of osteo arthritis of the hip. Clin Orthop Relat Res. 2003; 417:112-20.

Benign Bone and Soft Tissue Tumors and Conditions

143

CHAPTER

Mahesh Prakash, Kushaljit Singh Sodhi

INTRODUCTION

CARTILAGINOUS TUMORS

Benign bone tumor and tumor-like lesions are very common in children. More than half of all childhood bone neoplasms are benign.1 It is important that radiologists recognize the typical imaging features of benign tumors so that patient can avoid unnecessary diagnostic and surgical procedures. The differential diagnosis of bone tumors can be narrowed, based on knowledge of age of the patient, gender, constitutional complaints, location of the lesion in body and bone and general radiographic characteristics.2 Plain film radiographs remain the primary tool for evaluating bone tumors. However, other imaging methods, particularly magnetic resonance imaging (MRI) and in some cases computed tomography (CT) and nuclear studies, provide support for initial diagnosis by demonstrating specific features.1,2 Common benign bone lesions in children are osteochondroma, nonossifying fibroma, Langerhans’ cell histiocytosis, unicameral bone cyst and aneurysmal bone cyst. Benign bone tumors and tumor like lesions in children may be classified as follows:1 zz Cartilaginous tumors —— Osteochondroma —— Enchondroma —— Chondroblastoma —— Chondromyxoid fibroma zz Osseous tumors —— Osteoid osteoma —— Osteoblastoma zz Fibrous tumors —— Nonossifying fibroma —— Fibrous dysplasia —— Osteofibrous dysplasia zz Langerhans cell histiocytosis zz Giant cell tumor zz Tumor-like lesions —— Simple bone cyst —— Aneurysmal bone cyst —— Pseudotumor of hemophilia

Osteochondroma Osteochondromas are common lesions of the growing skeleton, occurring in approximately 1% of the general population. It is the most common benign neoplasm and constitutes 20–50% of all benign tumors.3 They arise from bony metaphysis with cartilage cap covering (Fig. 1). These tumors are either pedunculated or sessile. The long axis of the osteochondroma pedicle or stalk is almost always directed away from the adjacent joint. The direct communication between the osteochondroma and the cortex and marrow cavity of the bone from which it arises is a distinctive feature, that is particularly well demonstrated on computed tomography and magnetic resonance imaging. T2-weighted MR images is useful to demonstrate an cartilaginous cap (Fig. 2). The cap can be quite thick in early childhood and like the normal physis, becomes thinner with age. After epiphyseal closure, growth of the osteochondroma ceases. Multiple

Fig. 1:  Osteochondroma—Radiographs of lower end of femur (AP and lateral view) show large well-defined bony outgrowth, with broad based attachment to femur

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Fig. 2:  MRI (T1W fat sat), Axial section of the same patient shows clear demonstration of continuity of marrow and cortex of host bone into osteochondroma with covering cartilage cap

osteochondroma occur as a manifestation of diaphyseal aclasia, an inherited disorder with autosomal dominance (Fig. 3). Because most osteochondromas are asymptomatic, they are usually discovered incidentally. However, mechanical irritation of adjacent soft tissues or nerves, vascular injuries, fracture of the stalk, or malignant transformation can produce symptoms. Malignant transformation into low-grade chondro­ sarcoma occurs in 1% of osteochondromas, however, the risk is 10–30% in cases of multiple osteochondromatosis. 3,4 Malignant transformation should be considered when the osteochondroma grows after epiphyseal closure. Malignancy occurs in the cartilaginous cap, which becomes thickened. The cap of an osteochondroma usually measures less than 1 cm in thickness, whereas that of a chondrosarcoma often exceeds 2 cm.

Enchondroma Enchondromas accounts for 12% of benign bone tumors.3 These are most frequently located in the large and small tubular bones of the limbs, particularly those of the hand (Fig. 4). Like other cartilaginous tumors, enchondromas exhibit a lobulated growth pattern, that results in asymmetric expansion of the medullary cavity and endosteal scalloping. Tumor matrix may be radiolucent or show calcification. Characteristic cartilaginous ring and arc pattern of calcifications is seen on radiographs and CT images. On MR imaging, the tumor is isointense to muscle on T1-weighted and exhibits a heterogeneous, predominantly high T2-weighted signal.5 Contrast enhanced MRI may demonstrate a pattern of thin arcs and rings. Ollier’s disease is a nonheritable disorder of cartilage proliferation in which enchondromas involve multiple bones,

Fig. 3:  Diaphyseal aclasia—PA radiograph of bilateral hands show

multiple pedunculated osteochondromas, involving multiple bones of hands and forearm

Fig. 4:  Enchondroma—Radiograph shows a sharply demarcated

expansile lytic lesion with pathological fracture in the middle phalanx of index finger

especially those of the hands and may result in severe skeletal deformity. Enchondromatosis accompanied by multiple hemangiomas is known as Maffucci’s syndrome. Calcified phleboliths may be demonstrated radiographically in the hemangiomatous soft tissue masses. Lesions associated with both Ollier’s disease and Maffucci’s syndrome carry a significant risk of malignant degeneration (30–70%).6

Chondroblastoma It is less common than enchondroma. Chondroblastoma is composed of primitive cartilage cells, usually occurs in the age group of 10–20 years. It is typically located in epiphysis and apophysis of bone, most often the proximal humerus, distal

Chapter 143 Benign Bone and Soft Tissue Tumors and Conditions

Fig. 5:  Chondroblastoma—CT (coronal reformation) shows lytic

Fig. 6:  Chondromyxoid fibroma—Radiograph of right hip shows

femur, or proximal tibia. On plain X-ray, chondroblastoma is an eccentric, lucent, well-defined lesion with sclerotic borders. Periosteal reaction, far from the lesion is another common feature suggesting an accompanying inflammatory process. Approximately one third of chondrobastoma have a calcified matrix which can be better seen on CT scan (Fig. 5). The tumor shows signal intensity similar to that of muscle on MR imaging; however, the rim of the tumor has lower signal intensity. On T2-weighted images, the signal intensity of the tumor is low to intermediate. This tumor also shows extensive surrounding inflammation which may be confused with more aggressive lesion. Malignant transformation of chondroblastoma is extremely uncommon.7

usually affect boys in the second decade of life. Clinically most patients presents with pain that is especially severe at night and relieved by aspirin or other nonsteroidal antiinflammatory agents. More than half of tumors are located in proximal femur and tibia. They occur less frequently in the upper extremities than in the lower extremities. Osteoid osteomas also frequently affect the tubular bones of the hands and feet. They are however less common in the spine, where they affect the posterior arches of the vertebra. Histologically, the lesion consists of a nidus which is usually surrounded by dense sclerotic bone. The nidus contains interlacing trabeculae at various stages of ossification within a stroma of loose, vascular connective tissue. Osteoid osteoma can be cortical (the most common type), cancellous or medullary, and subperiosteal. The latter two types produce less sclerotic bone than those in the cortex do, making radiologic diagnosis difficult. Radiographically, the lesion appears as well-defined lytic lesion, surrounded by reactive sclerosis (Figs 7A and B). Solid or lamellated periosteal reaction is seen in 60% of patients. Nidus may be purely radiolucent or contain a dense center. Intra-articular osteoid osteomas may be either cancellous or periosteal and have little reactive bone or periosteal new bone formation. CT is very useful in showing the nidus, which can vary in its degree of ossification. CT appears to display the nidus better than MRI. The tumor nidus typically shows hypo to intermediate signal on T1W images and low-to-high signal on T2W images. The nidus shows enhancement with gadolinium.10 Intra-articular osteoid osteomas produce joint effusions and synovial proliferation. Radionuclide bone scans have been used for many years to help in diagnosis of osteoid osteomas. Bone scintigraphy, which is a highly sensitive method of detecting osteoid osteoma typically shows increased flow to the lesion on immediate images and a focus of increased activity on skeletal equilibrium images with

lesion in epiphysis of upper humerus with matrix calcification

Chondromyxoid Fibroma Chondromyxoid fibroma is less common than chondro­ blastoma, affecting predominantly males in the age group of 15–35 years.8 Histologically, it is composed of chondroid, myxoid and fibrous tissue in varying amounts. The common locations of tumor are ilium and the bones of the knee and foot. These tumors are located characteristically in metadiaphyseal location unlike chondroblastoma and do not cross an open growth plate. On plain radiograph, it appears as a well-marginated central or eccentric lucent lesion, with sclerotic margins and cortical expansion (Fig. 6). Half of the lesions may show parallel orientation to the long axis of the involved bone. Matrix calcification and periosteal new bone formation usually do not occur.

OSSEOUS TUMORS Osteoid Osteoma Osteoid osteoma is a fairly common tumor, accounting for approximately 10–12% of all benign tumors.9 These tumors

large expansile lesion with sclerotic border involving right acetabulum

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Section 5 Pediatric Imaging

A

B

Figs 7A and B:  Osteoid osteoma—(A) Radiograph of leg shows dense sclerosis and solid periosteal reaction in the diaphysis of tibia; (B) CT scan axial sections reveals well-defined lytic lesion with calcified nidus with gross adjacent sclerosis

A

B

Figs 8A and B:  Osteoblastoma (A and B)—MRI axial section, T1 and T2WI images reveal heterogeneous signal lesion, predominantly involving posterior elements of vertebra with extension into spinal canal and left paravertebral location

double density sign. Many times, osteomyelitis can mimick osteoid osteoma clinically as well radiographically; however, presence of soft tissue extension favors the diagnosis of osteomyelitis. The traditional treatment of choice has been surgical excision; however, it can also be successfully treated by radiofrequency ablation under image guidance.11

Osteoblastoma Osteoblastoma constitutes 2–6% of all bone tumors and most commonly occurs in patients in the second and third decade of life.12 This tumor is more common in males than in females. Histologically, the osteoblastoma is closely related to osteoid osteomas except that bony trabeculae are broader

and longer with absence of surrounding sclerotic halo. Size is an important consideration in distinguishing between these two types of tumors. If the size of lesion is less than 1.5 cm in diameter than it is likely to be osteoid osteomas, whereas tumors larger than 1.5 cm are usually osteoblastoma. The most common location of osteoblastoma is spine where it classically affects posterior elements (33%) (Figs 8A and B). 12 The other common locations are proximal femur and talus. On plain X-ray, spinal osteoblastoma is osteolytic lesion with destruction of overlying cortex and may extend to in the spinal canal. In the long bones, osteoblastoma appear radiologically as round or oval lucent tumors in the medulla. Periosteal reaction is common. Edema in the soft tissues or marrow appears hyperintense on T2-weighted images but the

Chapter 143 Benign Bone and Soft Tissue Tumors and Conditions

signal characteristics are not specific. Treatment is by surgical excision or curettage, but there is a moderate recurrence rate after these procedures.

FIBROUS TUMORS Nonossifying Fibroma Nonossifying fibroma is a benign fibroblastic mass that occurs in long bones of children and represents continuation of growth of fibrous cortical defect. It occurs eccentrically in the medullary cavity. The common location of lesion is in the bones around the knee joints. These lesions are usually asymptomatic and do not require specific treatment. On plain radiography, the lesion appears as well-marginated eccentric lytic lesion with scalloped margin (Fig. 9). Its inner border is often sclerotic and may appear multilocular due to corrugations. Differential diagnosis includes unicameral bone cyst, aneurysmal bone cyst, fibrous dysplasia, and chondromyxoid fibroma. The signal intensity of nonossifying fibroma is equal to or less than muscle on T1-weighted MR images and hypointense to fat on T2-weighted images. Postcontrast images usually show heterogeneous enhancement.

tubular bones, endosteal scalloping and trabeculation. The margin is sclerotic. The lesion may appear as ground glass or radiolucent, and this depends upon amount of fibrous tissue within the lesion. Bowing of the affected long bone may occur; when the affected bone is femur, the resulting deformity is called a “Shepherd’s crook” (Fig. 10). Thinning and destruction of the bony cortex may be seen on CT or MR images. Soft tissue extension of the lesion is unusual. On T1-weighted MR images, the signal intensity of fibrous dysplasia is similar to that of skeletal muscle. Although, the signal of pure fibrous tissue is hypointense on T2-weighted images, the signal of fibrous dysplasia is variable.

Osteofibrous Dysplasia It is a rare lesion that is usually confined to the tibia but can also involve the fibula. Most cases occur during the first decade of life. On plain X-ray, the lesion appears as an eccentric, lucent, solitary or multiloculated, lesion involving the anterior aspect of tibia. CT is very helpful in determining its intracortical location, an important feature in distinguishing osteofibrous dysplasia from fibrous dysplasia.14

Fibrous Dysplasia

HISTIOCYTOSIS X (LANGERHANS CELL HISTIOCYTOSIS)

Fibrous dysplasia is disorders where bone is replaced by abnormal fibrous tissue. Fibrous dysplasia can be monostotic, polyostotic, monomelic, or polymelic. It is more common in young females. It is occasionally seen in the first decade of life. In a small percentage of cases (2–3%), fibrous dysplasia is associated with endocrine disorders, especially precocious puberty in girls (McCune–Albright syndrome).13 Although it is not a true neoplasm, fibrous dysplasia involving a long bone may mimic a bone tumor or cyst. This type of fibrous dysplasia causes expansion of the medullary cavity of

Histiocytosis X is a syndrome that consists of group of clinical pathological entities: eosinophilic granuloma, Hand–Schüler–Christian disease and Letterer–Siwe disease. Eosinophilic granuloma is localized skeletal disease and is one of the commonly occurring bone tumors of boys in the first decade of life.15 The skull is the most frequent location, followed by the femur, mandible, pelvis, ribs and spine. The lesions are usually located in the medulla of the diaphysis and metaphysis and rarely involves the cortex and epiphysis. Multiple lesions occur in about 25% of cases.15 Pain is most

Fig. 9:  Nonossifying fibroma—Radiograph of knee joint (Lateral view)

Fig. 10:  Fibrous dysplasia—Radiograph of pelvis shows multiple

shows well-defined lytic lesion with sclerotic margin in characteristic location of lower end of femur

lytic lesions involving all the visualized bones with characteristic Shepherd’s crook deformity

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Section 5 Pediatric Imaging

common presenting problem with local tenderness and palpable mass. Histologically, the tumors are composed of Langerhans histiocytes containing their characteristic cleaved nuclei, and electron microscopy reveals Birbeck granules in the cytoplasm adjacent to the cell membrane. Radiographic appearance is variable. The lesion in calvarium typically appears as well defined lytic lesion with scalloped/beveled borders (Fig. 11). Sometimes, a button sequestrum may be seen in the lesion. Most of the lesions in long bones appear as lytic lesion with well-defined borders; however some of the lesions are permeative and associated with periosteal new bone formation (Fig. 12). The later findings suggest aggressive behavior. MRI is a very sensitive but nonspecific method of detecting eosinophilic granuloma. The lesion can be hypointense or hyperintense on T1 and hyperintense on T2W images, associated with extensive marrow and soft tissue edema. Occasionally, there is cortical disruption with

adjacent soft tissue seen on MRI (Fig. 13). The natural history of isolated lesion is gradual healing.16 Treatment depends upon the site, location and multiplicity of lesion.

Fig. 11:  Histiocytosis—Radiograph of skull (Lateral view) shows

Fig. 12:  Histiocytosis—Radiograph of the pelvis and upper femora

Fig. 13:  Histiocytosis—MRI of femur shows large heterogeneous

Fig. 14:  Giant cell tumor—Radiograph of knee (AP and Lateral

well-defined lytic lesion with beveled margins in frontal lobe

signal intensity lesion in diaphysis with cortical destruction, soft tissue and periosteal reaction

GIANT CELL TUMOR Giant cell tumors are very rare in children under 15 years of age, and commonly seen in girls.17 Radiographically, these tumors are well defined, eccentric lytic lesions usually located around the knee. The lesion usually shows nonsclerotic margin, cortical thinning without matrix calcification (Fig. 14). GCT is located in the metaphysis and do not cross the open physis, but may extend to the subchondral bone if the physis is closed. On MRI, the lesion shows generalized hypointensity on T2-weighted images. This T2 hypointensity may result from the tumor cellularity, or from recurrent hemorrhage within the lesion. The solid portions of GCT enhance diffusely

shows multiple well-defined and ill-defined lesions with associated periosteal reaction in both femora

view) show large grossly expansile lytic lesion in lower end of femur, extending up to subchondral region

Chapter 143 Benign Bone and Soft Tissue Tumors and Conditions

after gadolinium administration. Secondary, ABC formation can be seen in about 14% of GCT. 17

hemorrhage into the cyst can alter the signal characteristics of the lesion.5,18

TUMOR-LIKE LESIONS

Aneurysmal Bone Cyst

Simple Bone Cyst A bone cyst is a fluid filled lesion with fibrous lining. It occurs in metaphysis of long bones and adjacent to physis in children and young adults. Common locations are proximal humerus and femur.18 Calcaneum and ileum are less common sites. On plain radiograph, the lesion appears as moderately expansile, well marginated with or without sclerosis (Fig. 15). The cortex may be thinned out and may lead to pathological fracture. “Fallen fragment” sign may be seen, when there is piece of bone which migrates into the cavity and settles at the base. CT and MRI can confirm the cystic nature of the lesion. The fluid contents are usually of low intensity on T1-weighted images and hyperintensity on T2-weighted images. However,

Aneurysmal bone cyst is solitary, expansile radiolucent lesion and generally located in metaphysis of long bones. Other sites are dorsolumbar spine, small bones of hand, feet and pelvis. Pathologically, the lesion contains multiples cystic spaces containing various stages of blood. Radiologically, the lesion appears as expansile, lytic sharply circumscribed with thin cortex. The characteristic features are its ballooned out appearance and trabeculated appearance (Fig. 16). CT may demonstrate fluid-fluid level and thin rim of bone overlying the lesion. MRI shows the various stages of blood products which appear as layers of different signal intensity on both T1 and T2W images18 (Figs 17A and B). The differential diagnosis includes giant cell tumor, osteoblastoma, chondroblastoma, osteosarcoma and simple bone cyst.

Fig. 15:  Bone cyst—Radiograph of knee joint show mildly expansile

Fig. 16:  Aneurysmal bone cyst—Radiograph of shoulder joint shows

lytic lesion in metaphysis of tibia with thinning of cortex

A

multiloculated expansile lytic lesion, involving upper end of humerus

B

Figs 17A and B:  Aneurysmal bone cyst—MRI of the same patient, axial T1 and T2W images (A and B) show well-defined multiloculated expansile lesion with fluid-fluid/hemorrhage levels

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A

B

Figs 18A and B:  Pseudotumor of hemophilia—Radiograph of lower end of femur: (A) Shows lytic destruction of femur associated with large soft tissue component and bony spicules. MRI of the same patient, fat sat T2WI image; (B) Shows large soft tissue with various stages of blood components

Pseudotumor of Hemophilia Hemophilia is a bleeding disorder that occurs in males. Repetitive hemorrhage occurs close to muscle attachments without significant history of trauma. The common locations are iliopsoas and gastrocnemius muscles. Sometimes, there is intraosseous or subperiosteal hemorrhage, which can cause pressure erosion of bone. Plain X-ray shows pressure erosion/destruction of bone associated with large soft tissue component (Fig. 18A). Calcification within soft tissue hematoma may be seen. MRI shows variable heterogeneous signal, in form of various stages of blood products (Fig. 18B).

resonance imaging (MRI) should include the entire tumor so as to demonstrate its margins. MR images of soft tissue tumors have low specificity, are only occasionally helpful in differentiating between benign and malignant masses with certainty. Some MR imaging criteria have been postulated as indicators of malignancy, particularly in adults. These include size (>5–6 cm), absence of low signal on T2-weighted images, signal heterogeneity on T1-weighted images, early contrast enhancement, peripheral or heterogeneous enhancement, rapid initial enhancement followed by a plateau or a washout phase, and invasion of adjacent bone, neurovascular bundles, or both.19

SOFT TISSUE TUMORS

Vascular Lesions

The diagnosis of soft tissue tumors in children can be challenging due to broad spectrum of developmental anomalies, neoplasms, inflammatory conditions and pseudotumors. Ultrasonography (USG) and magnetic resonance imaging (MRI) are extremely useful in the characterization of these tumors. However, an accurate diagnosis can only be made by correlating with the patient’s age, clinical history and physical examination. Ultrasound is usually the modality of choice for the small and superficial soft tissue masses. It has the advantages of relatively low cost, portability, lack of radiation, no need for sedation, and widespread availability. Grayscale imaging should be performed with the highest frequency transducer available. Color Doppler should be performed to demonstrate the presence of vessels within the lesion. Due to its multiplanar imaging capabilities, high tissue contrast resolution, and lack of radiation, MR imaging is the modality of choice for the evaluation of large and deep masses or for those cases in which US is not adequate. Magnetic

Vascular lesions are the most common cause of soft tissue masses in children. Mulliken and Glowacki,20 divided them in two groups based on the findings on physical examination, clinical evolution, histology, and cellular kinetics: hemangiomas and vascular malformations. Hemangiomas are neoplastic lesions, whereas vascular malformations are errors of vascular morphogenesis. Categorization of a lesion into one of these two groups has significant implications for a patient’s management and prognosis.

Hemangioma Hemangiomas are considered to be true neoplasms and they account for 7–10% of all benign soft tissue tumors.20 Hemangiomas may be localized or diffuse and are histogically benign. Capillary (usually cutaneous), cavernous, venous and mixed types of hemangiomas have been described and classified according to the apparent origin of their vascular channels. Hemangiomas also contain variable amounts of

Chapter 143 Benign Bone and Soft Tissue Tumors and Conditions

nonvascular tissue and other elements, including fat, smooth muscle, fibrous tissue, myxoid stroma and hemosiderin. USG, CT, MRI and radiolabeled red cell scintigraphy, can facilitate preoperative diagnosis. Radiographs are important for detecting associated osseous abnormality, and the finding of calcified pheleboliths on radiographs or CT images is an indication of a hemangioma (Figs 19A and B). Ultrasound shows hemangioma as a well-defined mass of variable echogenicity.21 Color Doppler may show high flow pattern in proliferative phase; however, vascularity decreases in involuting phase. On T1-weighted MRI images, hemangiomas are either isointense or when they contain sufficient fat, hyperintense to muscle. On T2-weighted images, the lesions are well defined and markedly hyperintense with serpiginous high signal zones, that correlate with torturous vascular channels interlaced with lower intensity fibrous or fatty tissue. Phleboliths are hypointense on both T1 and T2-weighted sequences. Hemangiopericytoma is a rare soft tissue tumor of low but unpredictable malignant potential that is believed to arise from vascular endothelial pericytes. These tumors are usually located in the thigh or the pelvic retroperitoneum but can arise in any part of the body. Approximately 10% of hemangiopericytomas occur during childhood, and about one-third of these are congenital. 22 Congenital hemangiopericytoma can exhibit rapid initial growth, but spontaneous regression has also been reported. Microscopically, these tumors show endothelial proliferation with some similarity to hemangioma. Calcifications may be detected radiographically or by CT, and the tumors are well circumscribed. There may be partial destruction of adjacent bone. Hemangiopericytomas are very vascular lesions and show marked enhancement and frequently, central necrosis on contrast enhanced CT images. Like most soft tissue sarcomas, hemangiopericytomas are isointense to muscle on T1-weighted images and exhibit high

A

signal intensity on T2-weighted and STIR images, and they enhance moderately with gadolinium.

Vascular Malformations Vascular malformations occur due to errors in vascular development that are always present at birth. Based on the main vascular channel present within the lesion, they are classified as arteriovenous, venous, lymphatic, capillary, or mixed. Arteriovenous malformations are high-flow vascular malformations characterized by direct communication between the arterial and venous systems without an intervening capillary bed. These lesions may be detected at birth (40% of cases) and grow commensurately with the child.23 On US, they appear as multiple dilated tortuous channels diffusely involving subcutaneous soft tissues, which may not be apparent on gray scale but are easily demonstrated with color Doppler evaluation. These lesions have a high vascular density, and spectral Doppler analysis reveals high velocity in the arteries, but well-defined mass is usually not seen.21 On MR imaging, they appear as enlarged vascular channels associated with dilated feeding and draining vessels and without an associated well-defined mass. The high-flow vessels appear as signal void foci on spin echo images or as high signal intensity on flow-enhanced gradient-echo images. Venous malformations are characterized by the presence of anomalous ectatic venous channels. They may be small and localized or extensive. On US, venous malformations are usually of heterogeneous echogenicity, more commonly hypoechoic in comparison with the adjacent subcutaneous tissues phleboliths, may be present in 16% of cases. Doppler US usually detects slow venous flow within these lesions, although absence of flow is not uncommon which may reflect very slow flow or thrombosis. On MR imaging, they may appear as dilated tortuous veins or more often as lobulated masses, comprised of multiple locules reflecting dilated venous

B

Figs 19A and B:  Hemangioma—(A) Radiograph of shoulder joint shows large soft tissue around the joint with phleboliths; (B) MRI of same patient shows large lobulated soft tissue with multiple phleboliths

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Section 5 Pediatric Imaging

spaces separated by thin interstitial septa. They are iso- to hypointense to muscle on T1-weighted images, hyperintense on T2-weighted images, and show patchy enhancement after the administration of intravenous gadolinium.24 Lymphangioma usually visible at birth, is more frequent in the head and neck but also seen in the trunk, extremities, and in viscera. It may present clinically as, soft, smooth, translucent masses. On US, the macrocystic lymphatic malformations appear as well-defined, multicystic lesions. On MR imaging, the macrocystic lymphatic malformations appear as clearly defined cysts usually of low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, often with fluid-fluid levels. Postcontrast images show only septal enhancement without enhancement of the cystic spaces. This is a helpful feature in the differentiation from venous malformations.24

FIBROBLASTIC/MYOFIBROBLASTIC TUMORS Fibroblastic/myofibroblastic tumors comprise a large number of mesenchymal tumors with both fibroblastic and myofibroblastic features. Common lesions of this group are described here.

Nodular Fasciitis Nodular fasciitis is an idiopathic, self-limited focal fibrous proliferation, usually confined to the subcutaneous tissues. Common locations include the upper extremities and trunk. On US, nodular fasciitis is a well-defined lesion with, homogeneous/heterogeneous echotexture. The MR imaging appearance is variable, although more commonly, it appears as a fascia-based lesion of homogeneous isointense or slightly hyperintense to muscle on T1-weighted images, hyperintense on T2-weighted images, and homogeneous enhancement after gadolinium administration.25

Myositis Ossificans Myositis ossificans is a localized, self-limited, reparative hypercellular lesion, composed of reactive hypercellular fibrous tissue and bone. In most cases, a clear history of trauma is obtained. It often occurs in an area exposed to trauma, more commonly in the thighs and arms. Plain X-ray can show heterogeneous calcification, adjacent to bony attachment (Fig. 20). CT is the modality of choice for the evaluation of myositis ossificans. The appearance of the lesion changes with time. In the first 2 weeks after trauma, it appears as a noncalcified hypodense mass, with edema of surrounding soft tissues. Curvilinear peripheral calcification becomes evident after 4–6 weeks, with progressive internal ossification over the next several weeks and months.26

Fig. 20:  Myositis ossificans—Radiograph of pelvis shows soft tissue ossification adjacent to superior aspect of right acetabulum

Myofibroma/Myofibromatosis Solitary myofibroma is a common, benign fibrous tumor commonly seen in children 5 cm), the greater is the risk of rupture. Nevitt, et al. found that the risk of rupture after 8 years is 0% for aneurysms that are initially 3.5 cm, 5% for aneurysms between 3.5 cm and 4.9 cm, and 25% for aneurysms ( –2.5), osteoporosis (≤ –2.5), and severe osteoporosis (≤ –2.5 with a fragility fracture).8 This definition is applied to DXA measurements made (Table 1) in the lumbar spine, proximal femur, and forearm, but not to measurements made with other techniques (e.g. quantitative CT) or to DXA measurements made at other anatomic sites (e.g. calcaneus). Table 1:  The World Health Organization (WHO) definitions of osteoporosis and osteopenia by5 Terminology

T-score definition

Normal

: T ≥ –1.0

Osteopenia

: –2.5 < T < –1.0

Osteoporosis

: T ≤ –2.5

Severe osteoporosis

: T ≤ –2.5 in the presence of one or more fragility fractures

Chapter 191 Osteoporosis

Bone mineral density examinations have three principal roles, namely the diagnosis of osteoporosis, the assessment of patients’ risk of fracture, and monitoring response to treatment. BMD is a strong predictor of fracture risk, accounting for 75–85% of bone strength. The risk of fracture increases approximately 1.5-fold for each SD decrease from age-adjusted BMD.9 A helpful list of clinical indications for performing a bone density examination was published by the International Society for Clinical Densitometry (ISCD)10 and is summarized in Table 2. There are many advantages of central DXA as summarized in Table 3.11 Dual energy X-ray absorptiometry is the only procedure which can be used with fracture risk assessment tool or FRAX, which is particularly helpful in identifying patients who are at higher risk for fracture.12 The fracture risk assessment tool or FRAX provides an estimate of fracture risk on the basis of the BMD of the femoral neck; the patient’s age, sex, height, and weight; and seven clinical risk factors (previous fracture, having a parent who had a hip fracture, current smoking, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, and ingestion of three or more units of alcohol daily). If this information is entered along with the name of the manufacturer of the DXA scanner used and the algorithm estimates the 10-year probability of a major osteoporotic fracture (hip, spine, proximal humerus, or distal forearm).12 Table 2:  Indications for bone mineral density (BMD) testing •  Women aged 65 and older •  Postmenopausal women under age 65 with risk factors •  Men aged 70 and older •  Adults with a fragility fracture •  Adults with a disease or condition associated with low bone mass or bone loss •  Adults taking medication associated with low bone mass or bone loss •  Anyone being considered for pharmacological therapy •  Anyone being treated, to monitor treatment effect •  Anyone not receiving therapy in whom evidence of bone loss would lead to treatment

Table 3:  Clinical advantages of hip and spine DXA •  Proven ability to predict fracture risk •  C onsensus that BMD results can be interpreted using WHO T-scores •  Proven for effective targeting of antifracture treatments •  Effective for monitoring response to treatment •  Basis of new WHO algorithm for predicting fracture risk •  Short scan times •  Easy patient set-up •  Low radiation dose •  Good precision •  Acceptable accuracy •  Availability of reliable reference ranges •  Stable calibration •  Effective instrument quality control procedures

Recently, a study was published to establish age-specified bone mineral density (BMD) reference range for Indian females using dual-energy X-ray absorptiometry.13 Peak BMD was observed between 30 and 35 years at the hip, lumbar spine and radius. Compared with age-matched US females, BMD of lumbar spine was significantly lower for our subjects in all age groups. Prevalence of osteoporosis among women aged older than 50 years was significantly higher based on Caucasian T-scores as opposed to using peak BMD/standard deviation values from the population under review at lumbar spine but not at femoral neck. However, DXA, a two-dimensional technique, has some inherent limitations. It cannot distinguish between cortical and trabecular bone or discriminate between changes due to bone geometry (e.g. increases in the third dimension). Nor can it help those due entirely to increased bone density (within a fixed volume of bone). Apart from axial skeleton (lumbar spine and proximal femur) DXA scan can also be done at peripheral sites like distal radius and calcaneus. The calcaneus is particular useful for monitoring changes in BMD secondary to treatment as it contains high percentage (95%) of metabolically active trabecular bone. According to ISCD guidelines measurement by validated peripheral DXA (pDXA) devices can be used to assess vertebral and global fragility fracture risk in postmenopausal women, however its ability to predict vertebral fracture is weaker than central DXA and heel QUS. There is not sufficient evidence yet to support this position for men. Radius pDXA in conjunction with clinical risk factors can be used to identify a population at very low fracture probability in which no further diagnostic evaluation may be necessary. Central DXA measurements at the spine and femur are the preferred method for making therapeutic decisions and should be used if possible. However, if central DXA cannot be done, pharmacologic treatment can be initiated if the fracture probability, as assessed by radius pDXA (or DXA) using device specific thresholds and in conjunction with clinical risk factors, is sufficiently high. However, pDXA devices are not clinically useful in monitoring the skeletal effects of presently available medical treatments for osteoporosis.10 ISCD has also issued guidelines for use of DXA in children and adolescents.10 Table 4 lists comparison of different bone densitometry techniques.11

Quantitative Computed Tomography Quantitative computed tomography (QCT) is an addition to the field of bone mineral analysis. Quantitative CT differs from DXA as it provides separate estimates of trabecular and cortical bone BMD as a true volumetric mineral density in milligrams per cubic centimeter. This method uses a mineral calibration phantom that is placed in the CT scanner with the patient and provides corrections for machine drifts. A lateral computed radiograph (scout view) is first obtained for localization and then single axial scans are obtained through

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Section 7 Musculoskeletal and Breast Imaging

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Table 4:  Comparison of different bone densitometry techniques Central DXA

Peripheral DXA

QCT

QUS

Compatible with WHO T-scores

√

X

X

X

Proven to predict fracture risk

√

√

√

√

Compatible with new WHO fracture risk algorithm

√

X

X

X

Proven for effective targeting of treatment

√

?

?

?

Suitable for patient follow-up

√

X

√

X

Stable calibration

√

√

√

X

Good precision

√

√

√

X

Reliable reference ranges available

√

?

?

?

Keys: (√) Indicates where an alternative technique is known to perform in a comparable manner to central DXA. (?) Indicates where our knowledge is limited by an absence of suitable studies. (X) Indicates that alternative types of measurement are definitely unsuitable in these roles.

Fig. 2:  Lateral topogram (scout view) shows automatic

Fig. 3:  Midvertebral slice on QCT shows automatic contour

the midplane of two to four lumbar vertebral bodies (Figs 2 and 3). Quantitative readings are obtained from a region of interest over trabecular bone encompassing 3–4 cm3 of each vertebral body and from four different reference solutions in the phantom. These readings are averaged and used to calculate the mineral density of trabecular bone in mineral equivalents of K2HPO4 (mg/cm3).14,15 In addition to estimating the bone mineral density, QCT now, can also determine the future risk of osteoporotic fractures. The precision of this method is 1–3% for single energy (80 kVp) and 3–5% for dual energy (80 kVp/140 kVp) techniques with accuracy of 5–10%. The radiation dose is approximately 2 Sv. The theoretic advantages of QCT over other modalities include: (i) transaxial display of data permitting identification of the anatomy and separate measurement of cortical, cancellous, or integral bone mineral, (ii) capability of determining the linear absorption coefficient for a readily defined volume of bone and thereby, providing a measure

of density, and (iii) in the dual energy mode, the ability to determine mineral content with high accuracy in the presence of variable fat and soft tissue content.16 Quantitative CT is excellent for predicting vertebral fractures in postmenopausal women and serially measuring bone loss, generally with better sensitivity than projectional methods (such as DXA) because it selectively assesses the metabolically active and structurally trabecular bone in the center of the vertebral body. This selective assessment of trabecular bone also makes quantitative CT sensitive in measuring changes over a short follow-up period. The main theoretic advantages of quantitative CT over DXA are (a) the exclusion from the measurement of structures that do not contribute to spine mechanical resistance, yet contribute to DXA BMD values and (b) the possibility of selectively measuring trabecular tissue, the most metabolic active tissue and the main determinant of compressive strength in the vertebrae.17 Spine trabecular BMD by QCT can be used to monitor age-, disease- and treatment-related changes.18

determination of midvertebral slices of L1–L3

determination separating cortical (outer semicircle) and trabecular bone (inner semicircle). Note the phantom and calculation marker

Chapter 191 Osteoporosis

There have been fewer fracture prediction studies using QCT than those where DXA is applied, thus this area requires more research. In postmenopausal females QCT of the spine has been found to perform as well as, if not better than, DXA in the prediction of vertebral fractures.19 However, the use of spine QCT to predict hip fracture has not been substantiated yet.18 The ISCD position statements regarding QCT is that spinal trabecular BMD as measured by QCT has at least the same ability to predict vertebral fractures as AP spinal BMD measured by central DXA in postmenopausal women. There is lack of sufficient evidence to support this position for men. There is lack of sufficient evidence to recommend spine QCT for hip fracture prediction in either women or men. Central DXA measurements at the spine and femur are the preferred method for making therapeutic decisions and should be used if possible. However, pharmacologic treatment can be initiated if the fracture probability, as assessed by QCT of the spine in conjunction with clinical risk factors, is sufficiently high. Trabecular BMD of the lumbar spine measured by QCT can be used to monitor age, disease, and treatment related BMD changes. The disadvantage of QCT is that accuracy of BMD decreases to 20–25% in elderly osteoporosis populations.20 The authors analyzed bone mineral content in 100 normal Indian females (unpublished data) with mean age of 38.27 ± 11.12 years using QCT in their institute by linear regression. Normal Indian female has BMD of 217.87 – (1.6 × age of the patient) and normal Indian male has BMD of 221.01 – (1.5

× age of the patient). BMD is bone mineral density in mg/ cm3. The mean annual rate of trabecular bone loss was 1.10% for normal Indian females and showed more than two fold increase in 50–60-years range (1st menopausal decade). The trabecular bone loss at age 70 reached 3.19% (Figs 4 and 5). In a study of 55 patients of prostate cancer who underwent orchidectomy the author found that a statistical reduction in vertebral trabecular bone mineral density was observed in all patients within six months of orchidectomy.21 Average BMD decreased by 16.5 ± 8.6 mg/cc (13.8%) (Figs 6 and 7). In another group of female patients of progressive systemic sclerosis (n = 17), who were to undergo low dose steroid therapy, a pre- and post-therapy QCT was done to determine the effect of low dose steroids on bone mineral density. The author found a significant decrease in trabecular bone mineral density at all vertebral levels with an average decrease of 26.54% (unpublished data). The authors also studied the correlation between biochemical bone markers and bone mineral density (BMD) by using both QCT and DXA scanners of the same subjects done on the same day and to compare their findings in diagnosing them as osteoporotic or normal. They found that in the total population there is strong correlation only between bone marker osteocalcin and DXA-lateral. In males only there was no correlation between the bone markers and BMD findings by QCT and DXA scanners. In females both pre- and postmenopausal, there is strong correlation only between osteocalcin and DXA-AP and lateral but not with QCT and crosslaps. Whereas, in only postmenopausal

Fig. 4:  QCT determination of BMD of a normal 36 years old female

Fig. 5:  QCT determination of BMD of a osteopenic 50 years old female

with mean BMD of 152.8 mg/cc with T-score of –0.9 and Z-score of –0.7

with mean BMD of 120.3 mg/cc with T-score of –2.0 and Z-score of –0.7

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Section 7 Musculoskeletal and Breast Imaging

females there is strong correlation between osteocalcin and all the densitometric modalities, e.g. QCT, DXA-AP and DXAlateral but no correlation with crosslaps.22

Fig. 6:  Lateral topogram (scout view) shows midvertebral slices taken at L1–L3 vertebrae. Collapsed vertebra (L2 in this case) can be skipped manually

Another study has been done by the authors regarding comparison between the QCT and the DXA scanners in the evaluation of BMD in the lumbar spine. In both the scanning modalities there is direct correlation between age and osteoporosis as with increasing age the incidence of osteoporosis increased in all the groups. But QCT has been found to be more efficacious than DXA scan in the diagnosis of osteoporosis, i.e. QCT helps discriminate between normal subjects and those with osteoporosis better than DEXALateral and DEXA-AP.23 Although spinal quantitative CT has several advantages with respect to DXA technique, it also has several disadvantages, including a high radiation dose (Table 5), poor precision that limits its applicability to longitudinal assessments, high costs for quantitative CT scanners, a high degree of operator dependence, the need for a considerable amount of space and limited scanner access. Moreover, axial quantitative CT is used only for the assessment of spine volumetric BMD because the complexity of the hip architecture has precluded the development of reliable methods of densitometric assessment in this clinically important region. The World Health Organization (WHO) has defined osteoporosis in terms of bone densitometry

A

B

C

Figs 7A to C:  QCT determination of BMD of a 65-year-old postorchidectomy male patient at an individual vertebra (A) and average of 3 lumbar vertebrae (B and C)

Chapter 191 Osteoporosis

Table 5:  Radiation exposure of QCT protocols18 and other procedures involving ionizing radiation for comparison Technique

Voltage (kV)

Time current product (mAs)

Approximate effective dose (mSv)

Single slice QCT spine L1–L3 10 mm slice thickness

80

120