You are on page 1of 487

Seminar

in Radiology

Seminar
in Radiology

OP Sharma
MBBS, MD, PhD (Radiodiagnosis), FICR, MNAMS
Department of Radiodiagnosis and Imaging
Institute of Medical Sciences
Banaras Hindu University
Varanasi - 221005 India

JAYPEE BROTHERS
MEDICAL PUBLISHERS (P) LTD
New Delhi

Published by
Jitendar P Vij
Jaypee Brothers Medical Publishers (P) Ltd
EMCA House, 23/23B Ansari Road, Daryaganj
New Delhi 110 002, India
Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672
Fax: +91-11-23276490, +91-11-23245683 e-mail: jaypee@jaypeebrothers.com
Visit our website: www.jaypeebrothers.com

Branches
• 202 Batavia Chambers, 8 Kumara Krupa Road, Kumara Park East
Bangalore 560 001, Phones: +91-80-22285971, +91-80-22382956, +91-80-30614073
Tele Fax: +91-80-22281761 e-mail: jaypeemedpubbgl@eth.net
• 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza
Pantheon Road, Chennai 600 008, Phones: +91-44-28262665, +91-44-28269897
Fax: +91-44-28262331 e-mail: jpchen@eth.net
• 4-2-1067/1-3, Ist Floor, Balaji Building, Ramkote
Cross Road, Hyderabad 500 095, Phones: +91-40-55610020, +91-40-24758498
Fax: +91-40-24758499 e-mail: jpmedpub@rediffmail.com
• 1A Indian Mirror Street, Wellington Square
Kolkata 700 013, Phones: +91-33-22456075, +91-33-22451926
Fax: +91-33-22456075 e-mail: jpbcal@cal.vsnl.net.in
• 106 Amit Industrial Estate, 61 Dr SS Rao Road, Near MGM Hospital
Parel, Mumbai 400 012, Phones: +91-22-24124863, +91-22-24104532,
+91-22-30926896 Fax: +91-22-24160828 e-mail: jpmedpub@bom7.vsnl.net.in
• “KAMALPUSHPA” 38, Reshimbag Opp Mohota Science College,
Umred Road, Nagpur 440 009 (MS), Phone: +91-712-3945220, +91-712-2704275
e-mail: jpnagpur@rediffmail.com

Seminar in Radiology

© 2006, OP Sharma
All rights reserved. No part of this publication should be reproduced, stored in a retrieval
system, or transmitted in any form or by any means: electronic, mechanical, photocopying,
recording, or otherwise, without the prior written permission of the author and the publisher.

This book has been published in good faith that the material provided by author is original.
Every effort is made to ensure accuracy of material, but the publisher, printer and author
will not be held responsible for any inadvertent error(s). In case of any dispute, all legal
matters are to be settled under Delhi jurisdiction only.

First Edition: 2006
ISBN 81-8061-677-0

Typeset at JPBMP typesetting unit
Printed at Gopsons Papers Ltd, A-14, Sector 60, Noida 201 301, India

Foreword

PROF. SATISH KUMAR BHARGAVA E-03, GTB Hospital Campus
B.Sc, (Alld), MD (RD), MD (RT), Delhi – 110 095
DMRD (AMU), FICR, FIAMS, Tele: 22586606, 22586262/603 (Resi)
FCCP, FUSI, FAMS, FIMSA 22586262/401 (Off)
- Head, Department of Radiology & Imaging Fax: 011 22590495
University College of Medical Sciences & GTB Hospital
- Chairman, Board of Research Studies, FMS
Delhi Univ. (2001-2004)
- Visiting Professor – BP Koirala Instt. of Health Sciences, Nepal
- Ex-Chairman – Indian College of Radiology & Imaging (1999-2003)
- National President – Indian Radiological & Imaging Association
- Member – Delhi Medical Council (1998-2004)

In the last 2-3 decades medical sciences has shown a tremendous technological
development which is true for every branch of Medicine. However, the branch
of Radiology has shown revolution with the addition of many therapeutic
procedures and diagnostic modalities, i.e. ultrasound, CT, MRI, CT and PET,
color Doppler and other interventional procedures. This has resulted in the
change of nomenclature of department from Department of Radiology to
Department of Radiology and Imaging. The Radiologists help in making the
diagnosis in almost 70-80 percent of cases besides offering many other
therapeutic guided procedures with the availability of gamut of investigating
procedures. The purpose of book is to give comprehensive detail of the some
of the important topics which will be helpful to the residents and practicing
doctors in updating their knowledge. In the book entitled “Seminar in Radiology”
the complex and varied clinical presentation by disease processes, the
accompanying technical consideration and the aids to clinch the diagnosis
have been dealt with, all at one place in the most plausible and lucid manner.
Besides, interventional and therapeutic aspects are not left untouched.
Prof OP Sharma, an academician of repute has done an excellent job by writing
and giving an excellent presentation of the topics required in day-to-day practice.
I am sure the book will definitely find a space on the tables of postgraduate
students and Radiologists.

Prof. Satish K Bhargava
National President, IRIA

Preface

This book is primarily an effort to help all categories of Postgraduate students
for their preparations, appearing for final theory and practical examination of
MD/DMRD/DNB Radiodiagnosis.
Though this book at present has thirty chapters only and without
photograph. Inclusion of photo and X-ray prints have been omitted to avoid
the cost though I am sure all the students must be reading different books on
different imaging modalities. But in this book, I have tried to compile all the
possible most imaging feature of certain complex of sign and symptoms leading
to certain groups of diseases.
I shall be most happy if the readers demand more than this, provided they
feel satisfied, then 2nd edition will be more useful and fruitful for them.

OP Sharma

Acknowledgements

I am extremely thankful to Banaras Hindu University for providing all assistance
to publish this book. My thanks are also due to Shri OP Gupta, ex-Incharge
Art and Photography section of Institute of Medical Sciences BHU, my residents
especially Dr Rashmi Saraf and Mr Prashant Srivastava for computerized
help. In the last but not the least, I remain indebted to the readers of my book.

.

Role of Imaging in Gynecological Disorders 304 22. Genitourinary Tuberculosis 318 . Hepatobiliary Intervention 251 18. Contents SECTION 1: MUSCULOSKELETAL SYSTEM 1. Soft Tissue Calcification (Plain X-ray Appearance) 13 3. Osteoporotic Bone Disease 3 2. Inflammatory Arthropathy 34 4. Portal Hypertension 237 17. Diseases of White Matter Brain Substances 134 SECTION 3: CARDIOVASCULAR SYSTEM 11. Degenerative Disorders of Spine and Joints 65 7. Metabolic Bone Diseases 109 SECTION 2: CENTRAL NERVOUS SYSTEM 9. Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease 151 12. Abdominal Tuberculosis 265 19. Spinal Trauma 45 5. Uremia and Imaging 289 21. Imaging in Jaundice 221 16. Craniospinal Tuberculosis 125 10. PANCREAS AND HEPATOBILIARY TRACT 15. Valvular Heart Disease 171 SECTION 4: RESPIRATORY SYSTEM 13. Connective Tissue Disorders Involving Joints 59 6. Interstitial Lung Diseases 200 SECTION 5: GASTROINTESTINAL TRACT. Intestinal Polyposis 277 SECTION 6: GENITOURINARY SYSTEM 20. Osteolytic Bone Lesions 78 8. Pulmonary Infection 185 14.

Planning of Radiology Department 350 25. Common Radiopharmaceuticals Used in Various Systemic Disorders 374 26. Radiology of the Immunocompromised Patient 450 Index 465 . Radiation Hazard and Protection 397 27. Ultrasound and Color Doppler in Pelvic Masses 431 29. Medical Renal Diseases 331 24.xii Seminar in Radiology 23. Ultrasonography of Systemic Antenatal Abnormalities 412 28. Orbital Sonography 445 30.

SECTION 1 Musculoskeletal System .

.

After a short interval of balanced bone metabolism. there is impaired mineralization of osteoid and the ratio of organic matrix to mineral is increased. Skeletal growth is complete by the end of adolescence. The normal balance between bone formation and resorption results in maintenance of skeletal mass. The decrease in bone is also a consequence of ageing. spine (compression fractures). 1 Osteoporotic Bone Disease DEFINITION Osteoporosis is defined as decreased bone mass per unit volume without microstructural abnormality. It is the most frequent metabolic bone disease characterized by fractures especially in femur neck. the bone mass is decreased indicating that the rate of bone resorption must exceed than that of bone formation. PATHOGENESIS Bone remodeling (its formation and resorption) is a continuous process. distal radius (Colle’s fracture) and pubic symphysis. In osteoporosis. Radiologically there is: • Osteopenia (loss of bone density) • Spine shows ‘pencilling in’ of the vertebrae by the more radiographically- dense end plates • Biconcave vertebral bodies—Codfish vertebrae • Femoral neck reveals apparent increase in density of primary trabeculae with thinning of secondary trabeculae • Cortical thinning in appendicular skeleton. Bone quality is normal but quantity is reduced. but even after the closure of the enchondral growth plate. There is no abnormality in the structure of organic matrix (osteoid) nor there is any defect in mineralization while in osteomalacia. . It is normally regulated by systemic and locally produced agents. nutritional and mechanical factors. bone mass increases by radical growth until peak bone mass is achieved at about the age of 35 years. and metabolic. bone resorption begins to exceed bone formation and skeletal mass decreases.

Hypogonadism X. Genetic abnormalities in bone collagen synthesis – Homocystinuria – Osteogenesis imperfecta VII. Anemia XII.1. Generalized Osteoporosis I.g. Endocrine cause: – Glucocorticoid excess – Thyrotoxicosis – Hypogonadism – Hyperparathyroidism – Hyperprolactinemia – Diabetes mellitus III. Malignant diseases: – Multiple myeloma – Leukemia – Lymphoma IV. Involutional Osteoporosis Type I • Post-menopausal . Malnutrition/ deficiency states VIII. Chronic liver disease XI. Localized Osteoporosis – Immobilization – Post-fracture – Sudecks atrophy – Arthritis – Infection TYPES Various types of osteoporosis are given in Table 1. e. Unknown cause: – Primary/involutional osteoporosis – Juvenile osteoporosis II. Marrow packing disorders. Idiopathic B. Drugs: – Heparin – Ethanol VI. Glycogen storage disease XIII.4 Seminar in Radiology CLASSIFICATION A. Immobilization (Bed ridden) V. Gaucher’s disease XIV. Pregnancy IX.

Hyperprolactinemia 7. 50 to 65 years. level of activity. – Increase in fractures especially in vertebra and distal radius. – In vertebrae—loss of height and anterior wedging occurs. tibia. – Once osteoporosis is established. giving rise to rapid bone loss. Regional migratory osteoporosis – Age. Type II • Senile – Proportionate loss of cortical and trabecular bone. estrogen therapy does not affect the radiographic bone density. In both sexes >70 years with 2:1 female preponderance. Transient regional osteoporosis 9. Osteoporotic Bone Disease 5 Table 1. Glucocorticoid Excess • Cushing disease/steroid therapy • Biochemically—Negative calcium balance and hypercalciuria . not so in osteogenesis imperfecta) • Compression of vertebrae with kyphosis may results • Reduced bone density at areas of new bone growth and loss of height • Spontaneous recovery within 4 to 5 years but deformities may persist • Biochemical investigation are normal. skeletal size. Reflex sympathetic dystrophy syndrome 8.1: Types of osteoporosis 1. Idiopathic juvenile osteoporosis 3. – Disproportionate loss of trabecular bone. Involutional osteoporosis 2. Idiopathic Juvenile Osteoporosis • Rare self-limiting disease • Affects both sexes • Occurs before puberty (8—15 years) • Fractures characteristically seen in metaphysis of long bones with minimal trauma (metaphyseal fractures also seen in Battered Baby Syndrome. nutritional status and genetics. diminished adrenal function and secondary hyperparathyroidism may play a role. proximal humerus. pelvis.g. e. – Fracture—femoral neck. – Additional factors. – Cause—decreased oestrogen. which may lead to a marked kyphotic deformity. Glucocorticoid excess 4. Hypogonadism 5. – Cause is uncertain but reduced intestinal absorption. Thyrotoxicosis 6.

Girls (Turner’s syndrome) • Short stature • Increased carrying angle at elbow • Short fourth metacarpal • Changes of Blount’s disease at the knee (Medial tibial condyle is depressed and beak-like. a characteristic increased density of end-plates occurs • Avascular necrosis specially of femoral head (Leg-Calves-Perthes disease) • Multiple painless rib fractures • This all results in retarded growth of children. • Exophthalmos.6 Seminar in Radiology • Multiple fractures in long bones. Hyperprolactinemia • Due to reduced estrogen secretion. The medial femoral condyle may project downwards) • Congenital heart diseases especially coarctation of aorta Thyrotoxicosis • Increased metabolic ratio but bone formation is unable to match the rate of bone resorption which leads to reduced bone mass • Increased cortical striations of long bone seen besides osteoporosis • Thyroid therapy acropachy: – Rare. – Follows therapy for previous hyperthyroidism. Reflex Sympathetic Dystrophy Syndrome (Sudeck’s Atrophy/Algodystrophy/Reflux Neurovascular Dystrophy) . It must be distinguished from hypertrophic osteoarthropathy which is also found in the extremities but is usually exquisitely painful. ribs. – There is a characteristic periosteal thickening in the extremities and particularly in the hands. Hypogonadism Boys Delayed closure of epiphyseal plates—hence patients have long limbs with respect to their trunks. • Accelerated skeletal maturation in children. • Prelibial myxodema. vertebral bodies with exuberant callus formation • In compression fractures of vertebrae.

left hip is almost exclusively affected and the disease occurs in the third trimester of pregnancy • Some authors believe that it is a form of Sudeck’s atrophy • Symptoms resolve spontaneously in 4 to 10 months. Clinical Features • Pain • Swelling • Stiffness • Weakness • Hyperesthesia • Vasomotor changes. periarticular porosis. Osteoporotic Bone Disease 7 Causes • Prior trauma • Surgery • Infectious states • Vasculitis • Calcific tendonitis • Neoplasia • Disk herniation • Myocardial infarction • Degenerative cervical spine disease • Cardiovascular disorders. intracortical resorption and subchondral erosions are also seen. Transient (Regional) Osteoporosis • Rare condition of large joints where gross focal osteoporosis and pain occurs • Joint space is normal • Femoral head is commonest site • Young and middle aged • More common in men • No history of trauma or infection • In women. On X-ray • Endosteal bone resorption is the most prevalent form of demineralization in this condition • Subperiosteal resorption. It is thought to be related to abnormal neural refluxes. Regional Migratory Osteoporosis • Migratory condition .

and findings are: – Generalized osteopenia especially axial skeletal (vertebral column). INVESTIGATIONS With the advent by bone mass measurement.2: List of investigations 1. • Osteoporosis: A value for BDM or BMC 2. femur neck. – Thinning and accentuation of cortices.5 SD or more below young adult mean. calcaneum.2). vertebral bodies. Quantitative ultrasound 12. the fracture risk in osteoporosis can be quantified before the fracture occurs. the involvement of each joint lasting for approximately 9 months • Recurrence in other bones may occur successively by up to two years or more. • Severe osteoporosis: A value for BMD or BMC more than 2. Single X-ray technique 10. The various techniques for measuring the mineral content of bone are: Standared Radiography • Based on subjective criteria • The assessment usually done on metacarpal. Single energy photon absorptiometry 7. Standared radiography 2.5 SD below this value. Quantitative compound tomography 11. This is the major advancement in the field of osteoporosis (Table 1. talus. • Low bone mass (osteopenia): BMD or BMC more than 1SD below the young adult man but less than 2. ankle and foot • Commoner in men • Between 30 and 50 years • Clinically it is similar to transient osteoporosis of the hip. Table 1. MRI 13.5 SD below the young adult mean and the presence of 1 or more fragile fractures. Biochemical investigations WHO has classified osteoporosis on the basis of bone density measurements: • Normal: Bone mineral density (BMD) or bone mineral content (BMC) within 1SD of young male reference range. Comptom scattering 6.8 Seminar in Radiology • Hip is involved less frequently than other areas such as knee. Magnification radiography 3. Neutron activation analysis 5. . Dual energy X-ray absorptiometry 9. etc. Photodensitometry 4. Dual energy photon absorptiometry 8.

Photodensitometry • Images of bone of interest and reference aluminum wedge of known density are exposed on the same film. Common sites are sacrum. – Usually used at mid shaft of second metacarpal. The cortical thickness on either side of medullary space is measured with a measuring device and their sum expressed as the combined cortical thickness (CCT). the presence of overlying soft tissue and patient positioning • >3 percent bone loss is must. • Subperiosteal bone resorption. radiographic exposure. • Disadvantage: • Subjective • Affected by body habits. factors. – Change in shape of vertebral body—wedge-shape. • Disadvantage: – Does not reliably reflect bone mineral content – Conventional AP radiograph of a tubular bone is taken. Osteoporotic Bone Disease 9 – Accentuation of primary trabeculae with thinning of secondary trabeculae. com- pression – Insufficiency fractures due to normal stress on weakened bone. • This provides information comparable to SPA but with slightly lower precision. may be appreciated. to be appreciated on plain X-ray. even subtle. The optical density of the bone is then compared with that of the wedge with the photodensitometer. pubis hip. – It is particularly useful in serial studies and comparison with a large normal population can be made. As . The decay back to Ca-48 can be measured with a gamma counter. etc. Radiogrammetry • Advantage: – Simplest method. – Inexpensive. Neutron Activation Analysis • This technique uses high energy neutrons to active Ca-48 to Ca-49. Magnification Radiography • By either optical or as direct geometric means has a small but significant role in the assessment of osteoporosis. The fracture may be occult radiogrpahically and detected on CT or scintigraphy. sensitivity and accuracy. wrist. biconcave. – Easy to perform.

Dual Energy Photon Absorptiometry (DPA) • It uses gadolinium-153. This gives a reasonably accurate determination of total body calcium. No soft tissue correction done. assessment of regional calcium can also be made. Comptom Scattering • This technique measures the absolute density of a volume of tissue based on its electron density and is the only method other than CT that can measure purely trabecular bone. articular facet hypertrophy. it is largely a research tool. i. Single Energy Photon Absorptiometry (SPA) • This couples a monoenergetic photon source (Iodine-125). . a detector and intervening electronics that measure the beam attenuation through bone and express the result is bone mineral per cm2 scanned. kyphoscoliosis. which emits photon at two different energy levels. for soft tissue and bone.e. spine and redius. • The major disadvantage is that vertebral compression fractures with callus formation. as it is independent of variation in soft tissue of thickness. • Precision ≈ 2 percent Accuracy ≈ 6 percent • However. • Precision = 3 to 5 percent • Radiation dose varies form 200 to 2000 mrem • At present. • Lumbar spine from L1 to L4 is usually scanned. marginal osteophytes and extraosseous calcification (aorta) are also included in the integral measurement and may result in inaccurate and poorly reproducible vertebral measurements. • The major criticism is that it measures the mineral content of the appendicular skeleton (peripheral long bones). With modification.10 Seminar in Radiology approximately 98 percent of body calcium is in the bones. • Disadvantage: • Available in only few centers • Relatively large radiation does (200—300 mrem) • Precision and accuracy are in the order of 2 to 5 percent. end plates and posterior elements. because of dosemetric and statistical considerations. the low energy 1-125 source can not be used for body parts thicker than forearm. discogenic sclerosis. • This technique yields integral of all mineral within the scan path including the vertebral bodies. • This allows scanning of the spine and femur. • Usually radius is measured. • It is based on measurement of scattered radiation from a source of 100 to 700 keV gamma rays and is used for calcaneum.

thus enabling to measure small volumes of bone. • Either single energy (80 kVp) or dual energy (80 kVp/140 kVp) maybe used although the accuracy of single energy CT is variable and depends upon the amount of fat on the bone marrow • Precision of single energy method—1 to 3 percent and dual energy method —3 to 5 percent • Accuracy—5 to 10 percent • Radiation dose ≈ 200 mrem • At present CT analysis would appear to be most reliable and adaptable technique for bone density measurements . Osteoporotic Bone Disease 11 • The precision is in the order of 2 to 3 percent with accuracy of 4 to 10 percent. • There are two methods of generating dual energy X-ray spectrum. Single X-ray Technique • Uses X-rays instead of 1-125 in SPA. Then correction soft tissue is made. • P-DXA—DXA for scanning peripheral skeleton. – The use of a K-absorption edge filter to split polyenergetic X-ray beam into high and low energy components that mimics DPA. • DXA is single widely used technique. • Disadvantages—similar to DPA. In practice mid-portion of a vertebral body is used. • Advantage: – Ability to measure BMD in the spine and proximal femur-common sites of osteoporotic fractures. – Switching the high voltage generator between high and low kVp during alternate half cycles of the main supply. – Low radiation dose – Short scan time – High resolution images – Good precision and inherent stability of calibration. Dual Energy X-ray Absorptiometary (DXA) • The principle behind DXA is the measurement of transmission through the body of X-rays with high and low photon energies. A mineral reference phantom such as potassium phosphate solution is needed for calibration (multi-chamber phantom). Quantitative Computed Tomography (QCT) • CT is very effective for bone mineral content measurements and has the advantage of being able to measure small volumes of bone. thus enabling measurements of both cortical and cancellous bone. • Radiation dose ≈ 15 to 20 mrem • It is also used to determine total body mineral content.

except for T2 in women. The alkaline phosphates in uncomplicated instances is normal. • Disadvantage – No standardized methods of calibration and expression of measurement results since QUS employ diverse technology and different methods for calibration. Urinary excretion of peptides containing hydroxyproline is usually normal or slightly increased. – It has a potential for wider applicabilities. Magnetic Resonance Imaging (MRI) It has been suggested as another technique by virtue of the fact that T1 and T2 relaxation times for lumbar vertebral marrow have shown a decrease with increasing age. and the slope of the function is defined as broad band ultrasound attenuation index • Results suggest that this technique can be used to help differentiate between patients with osteoporosis and healthy patients and is comparable to DXA • Advantages – Lack of ionizing radiation – Less expensive than X-ray technology and is portable. to compensate for variations in signal sensitivity and magnetic field variations. Biochemical Investigations In osteoporosis. providing a measure of density. More rapid loss of bone mineral content in elderly women may explain the fact that T1 and T2 values are greater than in men of the same age.12 Seminar in Radiology • Advantage of QCT over other modalities – Transaxial display of data permitting identification of the anatomy and separate measurements of cortical. and bone therefore acts as frequency sensitive filter for ultrasound waves • The attenuation is an almost linear function of frequency. if the technique is to become an accurate method for determination of bone mineral content. cancellous or integral bone mineral. the ability to determine mineral content with high accuracy in the presence of variable fat and soft tissue content. This is based on the fact that attenuation is greater at higher frequencies. and calculates the attenuation index. Calibration phantoms will have to be designed. – In the dual energy node. – Capability of determining the linear absorption coefficient for a readily defined volume of bone thereby. but may increase after fractures. . including preventive screening for osteoporosis. however. Quantitative Ultrasound (QUS) (Broad Band Ultrasound Attenuation) • It measures the attenuation of ultrasound at various frequencies. This is explained by the replacement of active with fatty marrow. serum calcium and inorganic phosphorus are usually normal.

noncrystalline amorphous deposits + crystalline hydroxyapatite crystals 3. • Usually widespread and bilaterally symmetrical • Morphologically. amorphous clumps of Ca2+ and phosphate • May progress to ossification 2. dystrophic calcification is: • Ca2+ deposition in nonviable/dying tissues. Calcium pyrophosphate dihydrate b. the body responds by invoking a genetic inflammatory response reaction and sometimes ending with calcification of the damaged tissue So. PO43– levels. Calcification is: • Usually asymmetrical • More focal • Morphologically. If bony trabeculae are discernible within the mineralized focus. • Metastatic calcification – Occurs in normal viable tissues. the term ‘ossification’ is used. PO43– levels. PO43– levels . with • Normal serum Ca2+. Metastatic (1–2%) Occurs in cases of prolonged elevation of product of serum calcium and phosphate. with – Deranged serum Ca2+. can be classified into: 1. Calcium hydroxyapatite Soft tissue calcification. due to any cause. Dystrophic (95–98%) Whenever a tissue is damaged. 2 Soft Tissue Calcification (Plain X-ray Appearance) The deposition of amorphous calcium salts within the soft tissues is called mineralization/calcification. (serum Ca2+ × Serum PO43–). Idiopathic • Occurs in previously normal tissues • With normal serum Ca2+. Two forms of Ca2+ may be found in soft tissues: a. according to etiology.

Infection a. Malignant – Synovial sarcoma – Soft tissue osteosarcoma – Soft tissue chondrosarcoma vi. Arterial b. Bacterial – Tuberculosis – Leprosy b. Soft tissue necrosis . Benign – Haemangioma – Lipoma – Soft tissue chrondroma b. Trauma a. Crystal deposition disorders – CPPD (Calcium pyrophosphate dehydrate deposition disease) – HADD (Calcium hydroxyapetite deposition disease) – Haemochromatosis – Gout – Ochronosis (Alkaptonuria) v. Congenital – Fibrodysplasia ossificans progressiva – Ehler’s Danlos syndrome – Pseudoxanthoma elasticum – Werner’s syndrome b. Venous insufficiency ii. Connective tissue disorders a.14 Seminar in Radiology DIFFERENTIAL DIAGNOSIS OF VARIOUS CALCIFICATIONS A. Vascular a. Dystrophic i. Parasitic – Cysticercus – Dracunculosis – Loa loa – Armillifer iii. Neoplasia a. Acquired – Dermatomyositis – Progressive systemic sclerosis – CREST syndrome iv. Pseudohypoparathyroidism b. Metabolic disease a. Pseudopseudohypoparathyroidism c.

Severe secondary hyperparathyroidism 2. Hematopoietic malignancies o Multiple myeloma o Lymphoma c. Hypercalcemia a. Metastatic 1. Calcinosis circumscripta 4. Chondrocalcinosis (deposition of Ca pyrophosphate dihydrate crystals) – in 10-20 percent cases . Associated with renal .g. Primary hyperparathyroidism • Usually due to parathyroid adenomas (90%) or diffuse hyperplasia of the gland (10%) • ↑↑ Ca2+. Calcinosis universalis 3. Idiopathic 1. Haematoma c. Vitamin D intoxication . ↓ PO43– Calcification: a. Tumoural calcinosis 2. Calcific peritendinitis METABOLIC DISORDERS 1. Thiazides . Calcific bursitis 5. High bone turnover . Idiopathic hyperparathyroidism c. Immobilization . Vitamin D related . Hyperthyroidism . Solid tumor with metastasis (Breast ca) . Aluminium intoxication failure . Hypoparathyroidism C. Hyperphosphatemia a. Myositis ossificans traumatica d. Vitamin A intoxication e. Neurogenic heterotopic ossification B. Secondary hyperparathyroidism (e. Lithium therapy b. Parathyroid related . Idiopathic hypercalcemia of infancy d. CRF) b. Milk alkali syndrome . Primary hypercalcemia . Malignancy related . Soft Tissue Calcification 15 Injection granuloma – Thermal injuries – Fat necrosis b.

Hypoparathyroidism Deficiency of parathyroid hormone usually secondary to excision/ surgical trauma. Arterial b. Secondary hyperparathyroidism • ↑↑ PO43– levels • Commonest cause – Renal failure – Others—Osteomalacia due to various causes (pseudohypo- parathyroidism. Vitamin D deficiency) Calcification: a. 5th metacarpals and metatarsals – Small exostoses projected at right angle from the bone . Hyaline articular and fibrocartilage of knee . lungs. band-like ~ paraspinal calcification (as in DISH) • Basal ganglia calcification • Osteosclerosis • Premature closure of epiphysis ↓ Pseudohypoparathyroidism—Inherited disorder ↓ End organ resistance to parathyroid hormone (defective post-receptor mechanisms) • ↓ Ca2+. Arteries c.16 Seminar in Radiology ↓ Characteristically in . chondrocalcinosis is rare in secondary hyperpara- thyroidism 3. Periarticular calcification – In patients on long-term dialysis with renal transplant – May be large and globular – Otherwise. • Subcutaneous calcification • Usually. Symphysis pubis . kidney c. Renal calculi 2. Visceral—Heart. ↑ PO43– (and ↑ parathyroid levels) • Pseudopseudohypoparathyroidism (inherited disorder)—Patients with above radiographic abnormalities with normal Ca2+ levels—cause unknown • Both show following radiographic abnormalities: – Soft tissue calcifications – Short stature – Broad bones and cone epiphyses – Short 4th. Traiangular cartilage of wrist b.

Arterial i. popliteal) • Diabetics: Calcification more common in lower limbs • Generalized arterial calcification—associated with all causes of hypercalcemia (as enumerated above) • Aorta – Atheroma: Thick irregular calcification (usually involves the aortic arch) – Aortitis: Fine curvilinear calcification (usually confined to ascending aorta and sparing the arch) 2. pelvic and lower limb arteries ii. Atheroma – Irregular plaques to extensive tram track calcification – Common in aorta. Soft Tissue Calcification 17 4. Gout Monosodium urate deposits called as TOPHI which are not radio-opaque ↓ Secondary calcification may occur VASCULAR 1. Venous • Calcification is unusual in the wall of veins • Phleboliths: Single/ multiple oval opacities ~ < 3 mm length with translucent center . Monckeberg’s median sclerosis (intimal sclerosis) – Pipestem appearance – Also common in lower limb (femoral. Milk-alkali syndrome In peptic ulcer disease and renal impairment in whom increased ingestion or alkali (CaCO3) and milk ↓ Diffuse small—large masses of calcification in • Soft tissue (typically periarticulation) • Kidneys • Eyes 6. Hypervitaminosis D • Smooth lobulated amorphous masses of Ca2+ (ca hydroxyapatite) in – Periarticular region – Bursa – Tendon sheaths – Within the capsule and cavity of joints 5.

Leprosy – Rare cause of nerve calcification 2. Bacterial Diffuse calcification extremely rare in bacterial infection a. with a lucent centre. coiled curvilinear calcification ↓ . especially TB spine – Extensive calcified lymphadenitis b. Guinea worm: • Female form in subcutaneous tissue → Die ↓ Long. subcutaneous tissues and brain ↓ encyst Cysticercus cellulosae ↓ Classified dead cysts – Oval. upto 1 cm length and 2–3 mm broad. Parasitic a. Cysticercus cellulosae: • Prediliction of larval form to deposit in muscle. Tubercular – Resolving abscess. – Oriented in direction of muscle fibers – Number varies from 1–100 b.18 Seminar in Radiology ↓ • Common in: – Uterine and prostatic venous plexus – Varicose veins – Haemangiomas (cavernous) • Mafucci’s syndrome: – Haemangiomas (with phleboliths) + multiple enchondromas (Ollier’s disease) • Klippel-Trenaunay-Weber syndrome – Haemangiomas + Lymphatic involvement leading to limb hyper- trophy • Calcification in thrombus: – Band-like calcification in femoral vein following femoral vein thrombosis (differential diagnosis : ossified sacrotuberous ligament) • Chronic edema associated with venous incompetence: – Subcutaneous calcification – Organized periosteal new bone formation INFECTION 1.

autosomal dominant conditon) • Defect in collagen synthesis • Musculoskeletal features – Joint deformities – Post-vertebral scalloping – Archnodactyly – In 1/3 cases. subcutaneous calcification is seen ↓ Cause is local haemorrhage and fat necrosis On X-ray: Oval. Arteries – Media – Intima . d. Armillifer armillatus: • Crescentic calcification in muscles of trunk • Infected by snake meat e. aponeurosis. 2–15 mm densities with radiolucent centers predominantly affecting the forearms and shin of long bones: iii. Congenital i. Soft Tissue Calcification 19 May be crushed by muscle contraction— round. Fibrodysplasia ossifications progressiva (previously called as myositis ossificans progressiva) • Inherited autosomal disorder • Progressive swelling and ossification of the fascia. ligaments. Africa): • Long/coiled thread-like appearance. Pseudoxanthoma elasticum: Heterogeneous inheritance • Degeneration of the collagen—elastic tissues • Calcification seen in: a. Schistosomiasis: Calcification in urinary bladder CONNECTIVE TISSUE DISORDERS a. Ehlers-Danlos syndrome (rare. Loa loa (W. tendons and connective tissue of skeletal muscle (i. the ossification occurs in the perimuscular fascia and not in the muscles themselves). Hydatid cyst : Calcification in liver f. • Associated skeletal abnormalities may diagnose the condition before development of soft tissue swellings. • Large masses may bridge between bones—in thorax which may cause respiratory compromise.e. irregular mass c. best visualized in hand and foot. – Short 1st metacarpal. metatarsal – Small cervical vertebral bodies with relative prominence of pedicles ii.

e. tendons. periarticular structures iv. • “Milwaukee shoulder”: Extremely destructive arthritis of shoulder • May be associated with scleroderma and other connective tissue disorders iii. hip – CPPD may be associated with many conditions.Hyaline cartilage : Knee. Soft tissues – Commonest radiological abnormality – Linear calcinosis cutis (skin) – Ligaments. elbow. Oxalate crystal disease: • Ca-oxalate deposition in joints and other tissues. annulus fibrosis . HADD (Ca hydroxyapatite deposition disease) • Typically has a monoarticular presentation in the middle-aged and elderly • Joints—shoulders (commonest). gout. hips.Fibrocartilage: Menisci. symphysis pubis. dermal and ligamentous calcification v.Acute intermittent synovitis (pseudogout) . hyper- parathyroidism. which can occur in isolation / combination: . Weber-Christian disease • Subcutaneous calcified nodules b. Werner’s syndrome (Progeria) • Arterial. – There are 3 manifestations. cloud-like periarticular calcification is seen in and around supraspinatus tendon (shoulder) • Clinically : Pain in affected joint • Renal dialysis patents are at high risk of apatite deposition. knees and digits. ii.Chondrocalcinosis – Chondrocalcinosis—affects both . seen in renal failure patients on chronic haemodialysis • X-ray: Soft tissue calcifications and chondrocalcinosis DERMATOMYOSITIS (Called as Calcinosis Universalis in Older Textbooks) • Inflammation and degeneration of muscles . Wilson’s disease.Calcium pyrophosphate arthropathy . diabetes mellitus.20 Seminar in Radiology b. wrist. Acquired i. bursae involved • X-ray : Homogenous. Crystal deposition diseases • Calcium pyrophosphate dehydrate deposition disease (CPPD) – CPP deposition in and around joints + in annulus of intervertebral disc. triangular cartilage.g.

Acro-osteolysis : Terminal phallangeal resorption due to pressure atrophy b. ↓ • Differential diagnosis i.Sites of insulin Injection. Idiopathic calcinosis universalis ii.Blunt trauma – Radiation damage to tissue – Calcific myonecrosis : Calcification of atrophic muscles.Elher’s-Danlos syndrome . sheet. TRAUMA a. Hyperparathyroidism SCLERODERMA (Progressive Systemic Sclerosis) • Unknown etiology. Occasional intra-articular calcification • CREST syndrome (calcinosis cutis + Raynaud’s syndrome + esophageal dysmotility + sclerodactyly + Telangiectasia)—a related disorder—the only differentiations is that calcification may also involve the tendon sheaths. causes small vessel disease and fibrosis in various organs. . Soft Tissue Calcification 21 • X-ray: a. Scleroderma is the cutaneous manifestation of progressive systemic sclerosis.Frost bite : The commonest cause of calcification of pinna – Tuberculous lymph nodes – Fat necrosis causes calcification: . like calcification along fascial and muscle planes especially involving the proximal large muscles. Raynaud’s phenomenon and skin changes • X-ray – in hands : Typical features are: a. Calcinosis circumsctipta : Discrete dense plaques of calcification in the digits. c. Nonspecific subcutaneous calcification b. Soft Tissues Necrosis • Usually followed by calcification • Various examples: – Injection sites. (less common). • Clinically.Christian-Weber syndrome . 1—2 months after severe crush injury .Snake bites . especially quinine (oval ring shadows in gluteal region) and bismuth – Following .

which extends from normal skeleton into soft tissues and obscures the normal bony outlines (characteristically “woolly” appearance) • May occur in shoulder and elbows in cases of head/higher spinal injury • Surgical excision in associated with recurrence d. Acquired: Mainly traumatic i. Burns: .Bone formation not a direct result of burning as may develop at sites distal to the injury. Trauma: • Repeated minor trauma may cause ligament calcification i.22 Seminar in Radiology b. Fencer’s bone—Brachialis muscle iv. Dancer’s bone—Soleus muscle Note: Ossification of various ligaments may be a normal phenomenon of knee. Rider’s bone : adductor muscle ii. For example: • Ligamentum nuchae • Laryngeal cartilages . shoulders) .g. • Causes of heterotopic bone formation: a. Surgery: . may calcify. not necessarily result of a disease. • Pathologically: Inappropriate differentiation of fibroblasts into osteoblasts following in inflammatory lesions in soft tissues.In surgical scars. especially in subperiosteal location.Extensive ossification in related joints (hips. Paralysis : Neurogenic heterotopic ossification • In patients of paraplegia • X-ray : Common in pelvic bones and hip joints ↓ Periarticular new bone formation. Hematoma • Any hematomas. e. especially total hip arthropathy c. Pellegrini’s-Steida lesion—in medial collateral ligament of knee (medial to adductor tubercle) iii. elbows. Development – Fibrodysplasia ossificans progressiva – Melorrheostosis – Progressive osseous heteroplasia b. ii. cephalohematoma in neonates (due to birth trauma) OSSIFICATION • Many calcifying (amorphous) lesions may proceed to trabecular ossi- fication.

bursae and rarely tendon sheaths. but not done until left until maturation is complete TUMORS A. Loose bodies . Lipomas: • Radiolucent on X-rays • Calcification/ossification in long-standing cases b. Paraosteal osteosarcoma (presence of a thin lucency between the mass and bone differentiate it) b. tendons and fascia. • Surgical resection is best. Benign a. occurring in synovial joints. sacrotuberous ligaments. with reduction in size of the mass. • Iliosacral ligaments (angel wing sacrum) MYOSITIS OSSIFICANS • Heterotopic bone and sometimes cartilage formation in muscles. Bony erosions . Hemangioma . ↓ Finally . Synovial chondromatosis: Chondrometaplasia of the subsynovial connective tissue. following trauma. it resembles a soft tissue osteosarcoma. Pseudomalignant myositis ossificans = osseous tumor of soft tissue (in the absence of trauma) • Subsequently. appear as multiple opacities with flecks of calcifications and bony trabeculae. Soft Tissue Calcification 23 • Costal cartilages • Iliolumbar. • Multiple nodules of cartilage form in the synovium and project in the synovium ↓ Once mineralized. ossification occurs from peripheral to central. • Early biopsy should be avoided as pathologically. etc. Secodnary osteoarthritis c. • Pathologically : Trauma → Muscle damage → Hematoma ↓ Upto 2 weeks → Soft painful mass ↓ Next 2 weeks → Amorphous densities develop in the mass with periosteal reaction • Radiologically: Fine lacy calcification seen during this 4 weeks period D/D: a.

vaguely lobulated. pelvic girdle and shoulder – Areas/ nodules of faded radiopacity (due to tumoral osteogenesis) c. Soft Tissue Sarcomas a. shoulders. metabolic and collagen vascular disorders are ruled out) • Radiologically : Large. Rest are located closed to a joint (subfascial location) • D-ray : Dense intratumoral calcification and ossification b. Peripheral chondrosarcoma • A chondrosarcoma which originates outside the bone but implanted on the bone. with abundant calcification. Tumoral calcinosis: • Autosomal dominant • Any age • Majority have some biochemical defect of phosphorus metabolism • Serum calcium is normal (renal.24 Seminar in Radiology B. • X-ray: An extraosseous mass. Hemangiopericytomas 2. elbows or smaller joints (calcific fluid—carcinoma hydorxyapatite) ↓ Masses grow progressively ↓ May cause: – Bone erosions – Restricted joint movement – Superficial ulceration and secondary infection Differential diagnosis: – Renal osteodystrophy – Calcific myonecrosis . Thyroid adenomas—irregular peripheral egg shell calcifications C. multiocular. Soft tissue chondrosarcoma d. juxta-articular cystic lesions with/without fluid levels. Others 1. Idiopathic 1. frequently in hips. Soft tissue osteosarcomas • X-ray: – Located commonly in high. Synovial sarcoma • Common in young adults • Only 10 percent located within a joint cavity. Medullary carcinoma thyroid 3. bumpy (like cauliflower).

Secondary infection . unknown cause • Calcification in longitudinal bands in subcutaneous fat of extremities ↓ Subsequently. brucellosis) • Multiple scattered round densities • Presence of diffuse calcifications in lungs. cholangiocarcinoma) • Irregular patterns or multiple nodules . Parasitic a. renal osteo- dystrophy with secondary hyperparathyroidism 3. following . ligaments and tendons ↓ Calcific deposits coalesce and enlarge ↓ May break through the skin surface • Serum biochemistry—Normal • Differential diagnosis i. scleroderma.g. dermatomyositis. metastatic soft tissue calcification may be seen. Chronic amoebic abscess and pyogenic abscess (multiple lesions) • Mural calcification. hepatoblastoma. liver = pathognomic of histoplasmosis ii. Calcific bursitis ABDOMINAL CALCIFICATIONS 1. e. Calcinosis circumscripta: • Deposits of calcium in subcutaneous tissues in a circumscribed form in disease. Sarcoidosis: • Granulomatous disorder of unknown origin • Rarely. hepatoma. Soft Tissue Calcification 25 2.Surgical procedure iii. if contracted b. Hyperparathyroidism ii.Rupture and hemorrhage . spleen. Calcific peritendinitis 6. 5. histoplasmosis. secondary to hypercalcemia. Common i. Granuloma (TB. Liver a. Hydatid cyst • Fine curvilinear calcification in wall or dense and irregular. in muscles. Idiopathic calcinosis universalis: • Rare. Primary liver tumors (Hemangioma. Dermatomyositis 4.

Disseminated calcifications (usually <10 mm) a. Granulomatous diseases (TB. Pancreatic Calcification A. Calculi in Caroli’s disease v. Capsular + parenchymal calcificaiton: • Infarction • Pyogenic/ tubercular abscess • Hematoma 3. primary from colon or breast. Cystic (Congenital. Tumors • Cystadenoma Typical sunbrust appearance = • Cystadenocarcinoma pathognomic • Cavernous lymphangioma (rare tumor) . cystadeno- carcinoma of ovary) • Fine stippled (‘poppy seed’) calcifications b. Uncommon 2. Common 1. brucellosis) 4. post-traumatic. dermoid) 3. Hepatic artery aneurysm ii. Phleboliths (in splenic vein) b.26 Seminar in Radiology • Progressive increase in size and number of calcifications with enlarging liver—features of neoplasm iv. Vascular • Splenic artery athreoma (Tortuous corckscrew appearance—End- on view—thin-walled ring) • Splenic artery aneursym (thin-walled ring) 2. hydatid.Congenital .Acquired • Liver capsule calcification – Alcoholic cirrhosis – Pyogenic infection – Meconium peritonitis – Pseudomyxoma peritonei – Inadvertent introduction of barium into peritoneal cavity through a colonic perforation 2. Portal vein thrombosis iv. Chronic pancreatitis – Alcoholic (20-40%) – Secondary to gallstone • Multiple irregular small concretions B. Uncommon i. Cyst . histoplasmosis. Metastases (Mucinous. Calcified hematoma (post-traumatic) iii. Splenic Calcification 1. Acute pancreatitis (saponifications) 3.

Rarerly. Soft Tissue Calcification 27 4. Renal artery aneurysms: Circular. Gallbladder i. cracked egg shell calcification at the renal hilum. Gallstones (20% radio-opaque) ii. in mucous adenocarcinoma of gallbladder 5. Pseudocyst (rim of calcification) 7. Nephrocalcinosis iii. . Cystic fibrosis (fine granular calcification) 8. Hereditary pancreatitis (autosomal dominant) • Calcifications are rounded and enlarged clumps • Have high potency to develop pancreatic cancer 5. Milk of calcium bile (secondary to chronic cholecystitis with cystic duct obstruction) iv. Intraparenchymal hemorrhage (true intraparenchymal calcification) • Trauma • Infarction • Rupture of intraparenchymal aneurysm 9. Kidney i. Kwashiokar 4. Hyperparathyroidism • Pancreatic + renal clacification 6. Porcelain GB iii. Calculi ii.

Vas deferens a. Placental calcification (fine lace-like. Schistosomiasis 7. Calculi : 2-4 discrete. Female Genitourinary Tract A. irregular rims of calcification. Male Genitourinary Tract i. Uterus a. In degenerative condition in both (1) and (b) bilateral symmetrical. Ureter i. Tumors: Punctate/ coarse/ linear calcification in • Transitional cell and squamous cell carcinoma (epithelial tumors) • Less common in mesenchymal tumors – Leiomyosarcoma – Hemangioma 8. Chronic inflammation (TB. Schistosomiasis: UB wall calcification with normal capacity and distensibility b. nonspecific infections) ii. on either side of midline in elderlies. amorphous/ laminated/ speculated • Urethral calculi : Typically located in subpubic angle of pelvis/ close to midline. c. Leiomyosarcoma e. after 32 weeks of gestation) . Seminal vesicles • Infections like Neisseria gonorrhoae and TB • Multiple small concretions near proximal end of vas deferens iii. contracted UB with faint. Tuberculosis: Small. Urinary Bladder (UB)/Urethra i. iii. parallel tubular densities run medially and caudally to enter the medial aspect of seminal vesicles at base of prostate. Squamous cell carcinoma c. Prostate a. Fibroid : Mottled/ Mulberry type stippled calcification (Whorled appearance) b. c. Calculus (UB) : Circular/ oval.28 Seminar in Radiology 6. Post-irradiation ii. 9. Inflammatory disorders (UB) a. Lithopaedion f. Adenocarcinoma of endometrium d. In diabetics (young) b. Calculi ii.

proximal to stricture/ within diverticula a. outlining entire gland) . Stone in Meckel’s diverticulum ii. faceted. Appendiculoliths: with symptoms of acute appendicitis is S/o gangrenous appendicitis (may perforate) b. Neonatal hemorrhage (calcification form peripeheral—central) c. mottled deposits of calcium may occur • Leiomyomas (only 4%) v. Fallopian Tubes: Tubercular salpingitis (string of pearls appearance) C. Omental fat deposits (Mobile opaque nodules) Due to: – Interference of blood supply – Inflammation – Traumatic pancreatic fat necrosis vi. Alimentary Tract i. Appendices epiploaceae • Their infarction: cyst-like calcific shadows seen especially along the ascending colon iv. Soft Tissue Calcification 29 B. Ingested seeds/tablets 11. coarsely calcified mass in pelvis. which moves on serial films. TB (discrete stippled calcification. with relative radiolucency of lipid material in lesion = pathognomic ii. Spontaneous amputation of ovary • Small. with missing ovary by USG. Gonadoblastoma (rare) • Unilateral / bilateral. circumscribed/ mottled calcification iv. Tumors • Mucous adenocarcinomas of stomach and colon – Small. Enteroliths: Smooth. 10. Papillary cystadenomas and papillary cystadenocarcinomas • Psammomatous bodies ↓ Scattered fine amorphous calcification • Calcified metastatic deposits along lateral abdominal wall adjacent to peritoneal fat stripe—characteristic iii. Adrenals Common: a. Ovary: i. Idiopathic b. Mesentric/peritoneal cysts (especially chylous cysts) – Unilocular/multiocular calcification vii. Calcified mucocele of appendix iii. Dermoids (50% calcified) • Partial/ completely formed tooth.

Pseudomyxoma peritonei – Pseudomucinous cystadenoma of ovary – Mucocele appendix 3.30 Seminar in Radiology d. Retroperitoneum a. Lymphoma (postradiation) iii. Hydatid cyst 13. Tumors – Neuroblastoma – Phaeochromocytoma (mottled. Other tumors – Carcinoma – Adenoma – Adrneal choriostoma b. Wilm’s tumor (10%)—Peripheral and cystic ii. scattered densities) Uncommon: a. Sarcoidosis ii. Blastomycsis iv. Meconium peritonitis THORACIC CALCIFICATIONS A. Cavernous hemangioma c. Histoplasmosis ii. Undifferentiated abdominal malignancy 4. Generalized Abdominal Calcification 1. Psammomatous calcifications (from cystadenocarcinoma of ovary) 2. TB psoas abscess d. Teratomas b. Neuroblastoma (50%)—fine granular/stippled iii. Adrenal cyst 12. Neoplasms: i. TB peritonitis 5. Addison’s disease c. Solicosis • Uncommon i. Amyloidosis . Lymph Nodal Calcification Differential diagnosis of egg shell calcification • Common i.

Multiple large pulmonary nodules a. Bone formation • Primary . Hamartoma (Popcorn type calcification) c. Alveolar microlithiasis—Tiny dense stippled calcification (negative pleura sign) 2. Coccidiomycosis and other fungi iv. Rheumatic MS—Large ossific nodules. Infection a. Malignant i. Benign i. Coccidiomyosis b. Granuloma (TB. TB ii. Silicosis: – Pulmonary nodules may calcify – Baritosis and stanosis – denser nodules iii. Chickenpox c. Parenchymal Calcification 1. Widespread i. Histoplasmosis iii. Soft Tissue Calcification 31 B. Rarely – Schistosoma Armillifer (Very rare in military TB) ii. mainly at bases b. Pulmonary ossification a. Carcinoid type of bronchial adenoma d. Fine branching linear shadows usually involving a limited area of lung iv. Vascular Calcification 1. Metabolic disorders v. Calcified clot 3. AVM (arterovenous malformation) e. Rare – Primary pulmonary osteosarcomas – Seven percent of carcinomas 3. histoplasmosis) b. Solitary pulmonary nodule (SPN): a. Calcification of central pulmonary artery—in severe PAH C. Partly calcified nodules in – Rheumatoid arthritis – Multiple hamartochondromas b. Aneurysmal calcification – Aorta – Pulmonary artery 2.

sometime bilateral Empyema (usually TB) • Sheet-like calcification – en face—hazy – in profile—dense. well-defined outline • In mid and lower zone.32 Seminar in Radiology – Osteogenic sarcoma – Multiple chondrosarcomas • Secondary – Deposits of osteogenic sarcoma ii. Psammomas—Metastases from. PLEURAL CALCIFICATION Asbestosis (in parietal pleura mainly) • Calcification like—‘Holly leaf’. parallel to chest wall • TB—both parietal and visceral pleurae involved Hemothorax PERICARDIAL CALCIFICATION (CALCIFYING PERICARDIAL CONSTRICTION) 1. Uremic pericarditis Less common NECK • Tracheal ring calcification • Thyroid calcification – multinodular goiter. Hemopericardium 3. TB 2. psammomatous calcification. Post-irradiation—in Hodgkin’s disease. Mucoid calcification—Metastatic colloid carcinoma from carci- noma breast iv. linear. Pyogenic/viral pericarditis 4. Postoperative 5. thyroid carcinoma and papillary cystadenocarcinoma of ovary iii. seen in malignancy • Lymph node—TB/Lymphoma • Foreign body • Aneurysm of internal carotid artery INTRACRANIAL CALCIFICATION Physiological Calcification • Pineal gland (60% of adult) .

curvilinear in capsule of tumor • Pineal tumor—> 10 mm in diameter • Dermoid/Epidermoid/Teratoma • Colloid cyst • Choroid plexus papilloma • Chordoma Secondary • Occasional . neurocysticerosis. Congenital—Sturge-Weber syndrome. tuberose sclerosis 2. Infection—Healed brain abscess. medulloblastoma. Traumatic—Calcified hematoma 3. Tumor Primary • Lipoma of corpus callosum • Glioma—Amorphous bolb calcification or nodules or streaks • Glioblastoma multiforme—Astrocytoma. torch infection (Periventricular calcification) 4. isolated or conglomerated or homogeneous opacity • Pituitary macrodaenoma • Acoustic neuroma • Craniopharyngioma—Suprasellar calcification. oligodendroglioma • Meningioma—Nodule. ependymoma. Soft Tissue Calcification 33 • Habenular commissure (30%) • Choroid plexus (10%) • Basal ganglia • Dura mater – Falx cerebri (7%) – Superior sagittal sinus – Tentorium – Dural plaques (Parasagittal) – Petroclenoid ligament (12%) – Interclinoid ligament – Diaphragma sellae • Pituitary gland (Rare) • Carotid arteries (in elderly) Abnormal Calcification 1. tuberculosis.

• Soft tissues • Alignment • Cartilage space . Examination by standardized approach proposed by Forrester and Brown. 3 Inflammatory Arthropathy Inflammatory arthritides are group of different disorders with systemic manifestations with common factor being inflammatory pannus eroding cartilage and bone. should be taken. (Norgaard’s ballcatcher view). INVESTIGATIONS Plain X-ray Only films which will have impact on treatment. Initial screening : Rheumatoid series • PA hand Minimal requisite • Dorsiplantar feet • AP shoulder/ pelvic/knee • Lateral view in flexion of cervical spine Follow up—Only AP both hand.

Intervertebral disc spaces. fusion. Joint space narrowing. leakage of synovium into muscles. In delayed images (3 hours) → increased uptake at sites of increased bone turnover Ultrasonography High resolution ultrasonography shows capsule. bursa. Inflammatory Arthropathy 35 • Bone mineral integrity • Distribution pattern Plain X-ray of joint involved: • Permanent record of pathological process • Sequential radiographs disclose: – Progress of disease – Efficacy of treatment – Development of complication Arthrography Following arthroscopy/ joint aspiration Single/double air contrast technique → • To demonstrate status of synovium. . synovial effusion. with clarity especially in carpals/tarsals bone. subarticular bone • Distended capsule • Synovial proliferation and irregularity • Marginal erosion/ articular cartilage loss • Intra-articular loose bodies → “Floating Millet Seeds” • Geodes subarticular cyst • Ruptured capsule/Bakers cyst → leakage of contrast CT Scan Demonstrate erosions. Early / Blood pool phase → increased blood flow to synovium. cartilage. • Findings appear earlier than plain X-ray. loose bodies. facet joints are better demonstrated. Radio-nuclide Scan • High sensitivity but poor specificity (since relying on distribution of abnormal foci to make specific diagnosis). Magnetic Resonance Imaging When available/affordable—can be the investigations of choice for initial diagnosis and progress. erosions. 99mTc phosphate images. ruptured Baker’s cyst and Tendon tear.

. • Hormonal influence – decreased activity in pregnancy – men with RA have lower testosterone levels. Pathogenesis: Injury to synovial epithelial cells ↓ Synovitis with synovial hypertrophy ↓ Impaired nutrition and chondronecrosis Joint narrowing. metacarpophalangeal. Type III hypersensitivity/delayed hypersensitivity. RHEUMATOID ARTHRITIS Generalized connective tissue disease with extra-articular manifestations. • Tendonitis → tendon thickening surrounded by high signal edema on T2. With smaller peaks in extremes end of life M:F = 1:3 • Symmetric involvement of diarthrodial joints • Soft tissue changes Periarticular soft edema → fusiform Synovial hypertrophy /inflammation → widened joint space Effusion: • Bursitis → lobulated soft tissue density • Along tendon sheaths • Obliterations of normal fat planes. • Vascularised synovial proliferations → enhances after I/V Gadolinium. (especially wrist. • Swelling of ≥ 3 joints for ≥ 6 wks. 20-55 years.36 Seminar in Radiology • Marginal erosions seen earlier than in X-rays as “low signal defects”. • Craniovertebral junctions in spine cervical shows better visualized on MRI. subluxaiton and ankylosis Diagnostic criteria of American Rheumatism Association (minimum 4 points) • Morning stiffness ≥ 1 hr. metatarsophalangeal and proximal inter-phalangeal joint) • Symmetric involvement • Rheumatoid nodules • Positive rheumatoid factors • Radiological changes Age peak. Cause: • Genetic predisposition—DRW4 • Reaction to Ag from EBV/strains of E coli. • Pannus—soft tissue signal mass adjacent to eroded bone. Immune complex disease (Ag-Ab complex with complement fixation). • Subarticular cysts and bone edema → high signal on T2.

earlier and more common in feet than hand. Swan neck/Boutonnièrés deformity. 5th metatarsophalangeal joint (Lat > Medial) 2nd + 3rd metacarpophalangeal joint. especially hip joints • Enthesis changes—metabolically active site of ligament/tendon insertion into bone → soft tissue changes. – 5 basic types—flexion. Hitch hikers thumb Ulnar deviation and volar subluxation/dislocation at metacarpophalangeal joint. 3rd proximal interphalangeal joint (Radial > Ulnar) Proximal > distal (Metatarsal heads before phalangeal base) • Joint space changes – Increased due to in initial stages due to effusion Uniform narrowing due to chondronecrosis • Subchondral cysts/bone erosion – Due to pannus – Aggravated by mechanical factors → more in weightbearing larger joints • Joint malalignment/Deformity Due to: – capsular. (called as “main en lorgnette”) . subluxation. Inflammatory Arthropathy 37 • Osteoporosis: Periarticular due to hyperemia in acute stage Generalized due to disuse or immobilization. – Mid-shaft of phalanx/metacarpal – Near joint affected by synovitis. More common in small joints. Carplals appear like Telescoping of fingers. proximal interphalngeal joint All wrist joints + distal radioulnar joint Ulnar styloid process. dislocation • Secondary osteoarthritic changes In weightbearing joints. erosion • Periostitis = Local periosteal reaction – Less common in rheumatoid arthritis than sero-negative arthropathies. ligamentus and tendon laxity – cartilage and articular bone loss/ changes – fractures – rupture of tendons in region of roughened bones – irreversible in rheumatoid arthritis A and is progressive. Target Sites Hand and Wrist: Metacarpophalangeal joint. deviation. osteoporosis. – More common in feet → fluffy calcaneal spur in plantar aspect. • Erosions Marginal/Bare area → most important and diagnostic Central in location also seen. extension.

Hip joint: Protrusio-acetabuli Insufficiency facture neck of femur and avascular necrosis of head of femur head are important observations. Olecranon bursitis. Knee joint: Joint effusion → Lateral bulge of fat lines Distended suprapatellar space Increased patellofemoral space. Shoulder joint: Glenohumeral joint. . A very early change (35%)—apparent terminal phalangeal sclerosis due to osteopenia in surrounding. Bird’s beak appearance → due to gross bone loss especially at femoral head. Foot: Metatarsophalangeal joint especially 1st and 5th ones. subacromial space. acromioclavicular joint. Effusion → Elevation of anterior and posterior Fat pads. Rotator cuff tear/ atrophy—cranial migration of humeral head Pressure erosion of under surface of acromion. Enthesitis at Tendo-Achilles insertion/Plantar fascia in calcaneum. Resorption of acromial end of clavicle increase space and pencil tip erosion of calvicle. Elbow: Soft tissue abnormality seen earlier and may be the only finding. Ankle joint and heel: Rheumatoid nodule adjacent to Achilles tendon Focal erosion of calcaneous due to adjacent bursitis. Rheumatoid nodules on extensor surface. erosion of clavicle.38 Seminar in Radiology Extensor tendon rupture especially Extensio carpi ulnaris. Hallux valgus Dorsolateral subluxation/dislocation of proximal phalanges Hammer toes.THOMASIGN. Scapho-luntae ligament rupture → rotation and volar subluxation of scaphoid = called as TERRY. Enlarged subdeltoid bursa. Baker’s cyst → Soft tissue density posteriorily. Malalignment → Tibial subluxation Genu varum/valgum.

no parenchymal lesion. end plate irregularity. olecranon) without calcifications. fusion are commonest observations. cutaneous ulcerations. Apophyseal joints → erosion. brown pigmentation of exposed skin of extremities. peripheral. • Rheumatoid vasculitis—polyneuropathy. • Neurological sequeles Distal neuropathy (related to vasculitis) Nerve entrapment—Atlantoaxial subluxation. – Rheumatoid nodule (30%)—well-circumscribed. polymyopathy. Dryness of mouth due to functioning of salivary gland. Cervical spine may reveal Atlanto-axial joint → Subluxation Odontoid erosion Basilar invagination Odontoid fracture Erosion of spinous process → sharp and tapered. • Cardiovascular involvement – Pericarditis (20-50%) Myocardites (arrhythmia. fusion. cavitations – Caplan syndrome—hyperimmune reactivity to silica inhalation with rapidly developing multiple pulmonary nodules. – Pulmonary hypertension—secondary to arteritis. may remain without change for months – Interstitial fibrosis—lower lobe predominance. . gangrene. • Sjögren syndrome (15%) RA + keratoconjunctivitis + xerostomia (dryness of mouth due to decreased functioning of salivary galnd). Inflammatory Arthropathy 39 Temporomandibular Joint Crico-arytenoid involvement results in hoarseness of voice. • Pulmonary manifestations – Pleural effusion—mostly unilateral. heart block) Aortitis (5%) of ascending arota. Sarcoiliac joint: Erosion. subluxation. fusion Intervertebral disc spaces → narrowing. Aortic valve insufficiency. • Subcutaneous nodules (in 35% with active arthritis) over extensor surface (forearm) and pressure points (e. carpel tunnel syndrome • Lymphadenopathy (25%) Splenomegaly (1-5%). Extra-articular manifestations (75%) • Felty syndrome <1% RA of >10 yrs + splenomegaly + neutropenia with rapid weight loss. myocardial/visceral infarctions.g. therapy refractory leg ulcers. Less common in rheumatoid artheritis (=30%) than in seronegative arthritis.

) – Pausi articular type (≤ 4 joints) [esp. Chronic synovitis and hyperemia → osteopenia Epiphyseal overgrowth with squaring and angulation = balloon epiphysis Early closure of epiphyseal plate—growth disturbance (hypoplasia) Pathological fractures Small joints (hand and feet) • Enlarged carpal bones.N. Rheumatoid factor Clinical onset— As systemic disease 20 percent As joint disease 80 percent Radiological findings are late. Periosteal reaction → metacarpal/ phalangeal shaft = earliest larger joints involved (Elbow. malalignment subluxaiton uncommon. . 90% IgM –ve for RF – Still’s disease—acute systemic onset type with constitutional signs and symptoms + hepatosplenomegaly with little or no joint involvement + iridocyclitis (30% + L. Sholder.40 Seminar in Radiology JUVENILE CHRONIC POLYARTHRITIS • 10% IgM +ve for RF → Juvenile onset adult type RA. Erosion and ankylosis late feature → deformity. Cartilage and bone changes occur late and when severe → ankylosis. Cervical spine • Most commonly affected C2. Ankylosis affect both disc and apophyseal joints (2 or more veterbra) with wider than normal adjoining disc space. Erosions. Gracile bones. Growth disturbance and ankylosis → underdeveloped vertebral bodies. Mandibular growth disturbances. Enlarged metacarpal/phalangeal epiphysis. few >16 yrs. Synovitis and soft tissue findings → early. prominent and persistent for long time. Knee. Hip) Epiphyseal overgrowth → growth disturbance and length discrepancy Radial head enlargement Bowling of paired bones. Non-erosive disease. Knee/Wrist/Ankel/Metacarpo- phalangeal (MCP). C3. M<F Persistent arthritis of one or more joints for >6 weeks. rectangular phalanges. Proximal interphalangeal and Distal interphalangeal joint] – Polyarticular type (> 5 joints) • Age <16 yrs. Broadened articular ends of bones with smooth surface.

track” sign on AP view → Three vertical line due to calcified ALL. OA subluxation. Sclerosis Ankylosis Radio nucleide scan = Increased uptake ratio of more than 1. Age 20’s (15-35 yrs. more on iliac side. Loss of cortex Irregular cartilage space width Focal erosions. PLL and inter-spinous ligament. Inflammatory Arthropathy 41 Secondary degenerative changes occur late. – Anterior longitudinal ligament mineralization → fills the anterior Concavity of vertebral bodies. . S. knee) small joints. shoulder. Capsular calcification Spine: Involvement status: Lumbosacral region followed by thoracolumbar region. HLA–DR4 Target Joints: Spine and adjacent soft tissues Sacroiliac joints Temporomandibular joint → narrowing.4:1 Between SIJ and sarcum indicates sacroilitis. ANKYLOSING SPONDYLITIS Synonyms • Bekhterev’s disease • Marie-Strumpell disease Chronic progressive disease with insidious onset back pain and stiffness in young. rarely involved.I. joint involvement is not a feature of JRA. May be asymmetrical in early stage. Ligament mineralization → Anterior and Posterior longitudinal ligament Interspinous Apophyseal joint ankylosis Straightening “BAMBOO SPINE” Tram-Track line or “Trolley. Vertebral body squaring = characteristic feature and earliest due to Osteitis and erosions adjacent and end plate margins → shiny/Ivory corners ‘squared appearance’. Sacroiliac Joints: Symmetrical sacroiliitis. Syndesmophytes ossification of outer annular fibers.) M:F = 7:1 Caucasians : Blacks = 3:1 HLA – B27 +ve in 95%. ankylosis also affects peripheral large joints (hip.

wt. regional enteritis. Cardiac conductor defects Aortic incompetence Amyloidiosis Constitutional features → fever. PSORIATIC ARTHRITIS Etiology = unknown. . anorexia. SI Joint Peripheral joints — Hand [DIP.42 Seminar in Radiology Costotransverse joint erosion and fusion Synovitis of atlantoaxial joint → Subluxation which frequently becomes fixed → neural compression Osteopenic spine → Kyphoscoliosis/fracture with pseudoarthosis. Extra-articular Features Iritis (25%) Pulmonary fibrosis (B/L apical) with upward retraction of hila. (First described in 1822) Psoriasis affects 1% population → 7% have arthropathy HLA – B27 +ve (60%) Arthropathy – asymmetric • Usually after skin disease (65%) and 35 years. After • Along with skin change (25%) • Precedes skin changes (10%) • Five pattern of clinical presentation • Single joint or few random joints involved (70%) → oligoarticular type • RA like involvement (15%) → symmetric polyarthritis • Classical type (5%) – distal interphalangeal joint (DIPJ) + nail abnormality • Spondylitic type → with or without peripheral joint involvement • Arthritis mutilans → very aggressive variety → “Opera glass hand” + sacroiliities Target joints — Axial skeleton — Lumber spine. calcaneous Initially erosion → followed by healing and mineralization Shaggy/whiskered appearance Enthesophytes. loss. Associated with ulcerative colitis. fatigue. Sites = ischial tuberosity. PIP. MCP] Ankle and foot Hand and Foot • Sausage shape digit • Asymmetric erosive arthritis of DIPJ + osseous resorption + bony ankylosis in 10 percent. Enthesitis and ligament calcifications. iliac crest. greater trocanter.

Whipple’s disease. Separate from edge of vertebra. Target joints: MTPJ. Crohn’s disease. Behçet’s syndrome. IPJ of feet especially great toe. • Ivory phalanx → sclerosis of terminal phalanx (25%). • Squaring of vertebra in lumbar region • Sarcoiliitis → asymmetric/unilateral • Atlantoaxial subluxation + odontoid abnormality • Paraspinal ossifications REITER’S SYNDROME (Described in 1916) Infective origin—endemic/ venereal → non-gonococcal urethritis. vertically-oriented involving disc annulus (not end plate). Axial Skeleton • Floating syndesmophyte → single large. Inflammatory Arthropathy 43 • Pencil in cup deformity → erosion with ill-defined margins and adjacent proliferation of periosteal new bone—characteristic. PIP. DIPJ ENTEROPATHIC ARTHROPATHY In patients of ulcerative colitis. HLA – B27 +ve (60-80%) Age = young M:F = 5:1 Characterized by triad of Arthritis + Uveits + Urethritis + Pathognomonic skin change Keratoderma blenorrhagica affecting palm / sole. hemorrhagic cystitis Epidemic/ dysenteric → Shigella species. prostitis. • Erosions at superior/ posterior margin of calcanceus. Ankle joint/knee/hip joints SI Joint → asymmetric Also MCP. Peripheral asymmetric arthritis with predilection of joints of lower limb + Recurrent attacks. spine and peripheral joints Peripehral arthritis • Coincides with exacerbation/ severity of gut disease . • Diffuse wide-based fluffy calcaneal spur at attachment of Tendo-Achilles and plantar aponeurosis. intestinal bypass patients HLA – B27 +ve is 60 percent Involvement of SI joint. • Destructions of IPJ of 1st toe + exuberant peristeal reaction + bone formation at distal phalangeal base = pathognomonic → mouse ear appearance.

fungal. metacarpal joint: large wt. mild attacks of synovitis. I/V drug abuse Spread of infection from osteomyelitis in adjacent bone Etiology: Pyogenic—Streptococcus pyogenes. tuberculosis. viral Location: any joint—single.44 Seminar in Radiology Recurrent. H. influenzae. Staphylococcus aureus. Gonococci. bearing—hip/knee/spine X-Ray : Acute stage • May be normal • Soft tissue swelling and periarticular osteoporosis (less TB) • Joint effusion—distention/ subluxation in children • Joint space narrowing—irregular. rapid destruction (gradual TB) • Erosions—articular cartilage—pyogenic/small. peripheral—TB • Subchondral bone destruction and reactive sclerosis (less TB) Ankylosis—if entire cartilage lost Evidence of metaphyseal disease. soft tissue swelling and osteopenia Erosions rare Sacroiliitis and spondylitis • Independent of bowel disease M>F Bilateral and symmetrical Squaring of vertebras and syndesmophytes INFECTIVE ARTHRITIS Musculoskeletal infection: Cellulitis — soft tissues Osteomyelitis — bones Infectious arthritis — joints Route of infection: Direct invasion of synovium—penetrating/latrogenic injuries Infection from adjacent soft tissues—cellulitis. . Salmonella Non-pyogenic—M. acute. abscess Hematogenous spread—immunocompromised.

It is a major health problem in all countries with increasing pace of development.D12. Flexion injuries: • Commonest spinal injury • Stable • Usually results in wedge fractures/compression fractures (L1. According to type of traumatizing force/mechanism of injury: a.C5–C7) • Dislocation are common (esp. L2. – Fractures usually associated with dislocation – Shearing forces may cause chip or slice fracture of associated vertebra also. Twenty percent results in associated temporary or permanent neurological deficit. This is especially so because most of those affected are below the age of 40 years (more than 80%) leading to loss of productive years for the society. Etiology • Developed countries → Road traffic accident is the most common cause and is usually polytrauma in nature. C5 over C6) • Sprain observed in associated ligaments and muscles. 4 Spinal Trauma Spinal trauma is one of the surgical emergencies where an imageologist play the maximum role and utilize his skill to the best as there is so much to do for the patient within a limited time interval and resources. etc. Sufficient force can lead to tear in posterior ligaments and muscles. Classification 1. football players.  Flexion rotation injury: – Worst type of spinal injury as it is highly unstable and commonly affects the spinal cord. . rowers. • Developing countries → Fall from height • Other important causes are – Direct blow on spine as in medicolegal or industrial injury – Sports injury as in weight lifters.

b. discs and anterior longitudinal ligament. Unstable spine: • Cannot maintain relationships. Teetter-Totter fracture. Direct injury: • Rarer type of injury • Usually caused by a bullet or lathi blow • Usually fractures the spinous process e. d. 2. end plates. . further damage to nerve root and cord cannot be avoided. Extension injury: • Common in cervical and lumbar spine • May be stable or unstable • Results in chip fracture (Tear drop) of anterior vertebral rim. Violent muscle contraction: • Rare mode of injury • Sudden violent contraction of psoas muscle may lead to fracture of multiple transverse processes • Associated with a large retroperitoneal hematoma. Minor injury: • Patient is alert and co-operative • No neurological symptoms b. Smith fracture being specific types of it). Denis three column concept divides the spine in: a. – Horizontal fracture in vertebral body extending into posterior elements. b. Compression/Axial loading injury: • Commonly observed • Unstable • Vertical crushing leads to multiple fragments of vertebral bodies • Migration of fragments into spinal canal lead to neurological deficit esp. According to stability of spine: a. Stable spine: • One which can withstand physiological stresses (due to intact mechanical contacts) without progressive deformity and neurological deficit. Major injury: • Patient is unconscious and unco-operative • Neurological symptoms/deficit present • Associated with multisystem/multiorgan trauma 3. According to severity of injury: a. c.46 Seminar in Radiology  Flexion distraction injury: – Also known as seat-belt injury (Chance fracture. in cervical and upper dorsal spine. Anterior column: Anterior part of bodies.

Nexus Exclusion Criteria Excludes patient not be imaged. lamina. Costovertebral dislocation. Posterior: Pedicles. Denis further classified instability in Mechanical (if progressively deformable under physiological forces). Signs of Instability i.Increases distance of facet joint space iii. The involvement of middle column is especially responsible for instability.Disc pace narrowing (both D-L and cervical or widening in cervical) iv. 1. in cervical area) or even minimal in dorsolumbar area.Widened interspinous distance (known as Fanning) ii. Spinal Trauma 47 b. Mechanical injury may be either acute or chronic but neurological injury is usually acute. discs and posterior longitudinal ligament. The sensitivity of this criteria is 99 percent (a miss rate of 1 in 40000). end plates. spinous process and posterior ligamentous complex. Middle column: Posterior parts of bodies. Compression of vertebral height or more than 25 percent (cervical) or 50 percent. the choice of optimum views and methods is a must to bring out the maximum.87 in female INDICATIONS OF IMAGING As there is so little time allocated to radiologist in a traumatized patient. however. vii. vi. Focal angulation of more than 11° (cervical) and more than 40° (dorsal) v. The criteria are: – No midline spinal tenderness – No focal neurological deficit – No painful distracting injury – Normal alertness . Involvement of two or more columns leads to consequently increasing instability. Neurological (probability of production of new neuro-deficit or increasing of already existing deficit) or Combined. Also the condition of patients is such that he cannot be handled much nor can he co-operate and so the technique should be moulded accordingly. Subluxation of more than 3. be observed for 48 hours.5 mm (esp. This is more in dorsolumbar spine. rib and sternal fracture for dorsal spine. These patients should.80 in male T8 – T12 0. c. Anterior height Wedging ratio = Posterior height (N) = 0. articular processes.

e. Complications in delayed phase 4. appendix (Table 4. appendix (Table 4. cauda. etc. Associated with other injuries. bulge. Vandemark’s Risk Approach: Ref. The Spinal Cord • Shape • Size • Location within thecal sac. Para and Postvertebral muscles and fascial planes • Associated ligaments • Intervertebral discs (shape.) 4. The Vertebral Column • Shape of vertebra • Size of vertebra • Symmetry of vertebra • Cortical outline • End plates • Alignment • Curvature • Marrow • Posterior and lateral elements • Uncovertebral joints • Spinal canal 2. .2) AIM OF IMAGING To assess the: 1.3) Plain Film Radiography • Most useful initial technique is the Cross-table lateral view.1) 3. Positive in 70 to 90 percent of cases. ribs. Associated injury in cases of polytrauma Points to be Taken Care of: 1. thecal sac itself • Texture of cord • Size of central canal • Dura • Nerve roots. Dens. Appendix (Table 4. i. conus. ACR Appropriateness Criteria: Ref.48 Seminar in Radiology 2. texture. size. Stability of spine 3. filum 3. The Soft Tissue: • Pre. Severity of injury 2. occipital bone IMAGING MODALITIES Ref. Clivus.

C4 and rarely C2. therefore. Lateral spinal survey is mandatory. SPINAL INJURY – THE MEDICOLEGAL ASPECT • Under Section 320 of Indian Penal Code spinal injuries are considered “Grevious” in nature. • Evaluation of odontoid process may in additional be done by Kasabach’s method. • Spinal cord injury may be grevious even without fracture dislocation. Assessment of ligamentous injury – MR Compatible fiberglass. wrestling are causes of spinal laceration while pithing (B/W C1-C3) is common mode of infanticide in India. Clinical features out of proportion to imaging findings 3. • Spinous process fractures are highly specific while vertebral (D/L) body fracture/subluxation are moderately specific for Batterred baby syndrome. Graphite or Titanium apparatus should be used. “Any hurt that endangers life or which causes the sufferer to be in during the space of 20 days. FSE. can also decrease the time with equally good image quality. • Spinal concussion is quite commonly seen in Road/Railway accidents while compression may occur while one is suddenly banged. very rarely swimmer’s view (Twining/Fletcher view) may be required for cervicothoracic junction. • Flexion and extension views for instability may be performed but it is advisable to do it when muscle spasm has subsided (10 days) and to do it under supervision. Firearm injuries. Clinical evidence of spinal cord injury without bone injury 2. . Military posture is an indication of flexion being the cause of instability. i. in severe bodily pain or unable to follow his pursuit. RARE etc. • Patient maybe screened under fluoroscopy instead.e. Magnetic Resonance Imaging Has Four Basic Indications 1. • Pillar view for lamina and articular processes is performed sometimes. Progressive increase in neurological symptoms 4. – GRE sequences can form a Myelogram and are quite fast. in all such cases.” • Also a radiologist must remember that cervical spine injury is seen in hanging and not in strangulation. pull each other’s hairs. pushed or when ladies fighting. Judicial hanging leads to fracture of C3. Spinal Trauma 49 • May be followed by AP and open-mouth views (Three-film series) or additional oblique view (Five film series). 45° head rotation +15° caudal tube tilt.

iv. b. The location of edema is generally a less sensitive predictor for neurological level of initial injury. Cord hemorrhage: It is depicted very well on MRI and is more common in pediatric age group if occurring in isolation. . The neurological level of injury correlates well with the physical level of hemorrhage. Even large epidural hematomas may remain clinically silent and extend over multiple levels. Disruption of anterior and posterior longitudinal ligaments manifests as discontinuity in the normally low-signal intensity ligament. Symmetric/ asymmetric widening of disc space ii. Intervertebral disc injury i. ii. This type of injury is also known as Transaction without separation. Prevertebral soft edema is also very well shown. Type III injury is a combination of both. Spinal epidural hematoma: It occurs in 41 percent of spinal injuries. Frank protrusion of disc material into the epidural space v.50 Seminar in Radiology IMAGING FEATURES Nonosseous Injury a. Ligamentous and soft tissue edema are particularly well seen when imaging on low-field strength magnet. Early detection of ligamentous injury in trauma patients with neck pain and no evidence of fracture or subluxation on radiographs may obviate the need for delayed flexion and extension films. Intramedullary edema (Type II): The length of spinal cord with edematous change directly correlate with the degree of neurological impairment. Discontinuity of the outer annular fibers and/or longitudinal ligaments. Dorsal displacement of the posterior longitudinal ligament and epidural venous plexus. Location of hemorrhage is the most precise indicator of the neurological level of injury. This epidural collection is separated from CSF space by hypointense dura. Relative hyperintensity of one disc on sagittal T2W weighted image. Ligamentous injury MRI is the more sensitive method for detecting ligamentous injury. Spinal cord injury i. Presence of spinal cord hemorrhage signifies the most severe type (Type I) of damage of the spinal cord with a poor capacity to regain function below the level of damage. It follows the usually course of blood resolution. Root avulsion and dural tears: 1. Root avulsions are caused by traction injuries to arm or lower extremity. iv. The low-field open magnets are more easily used to image acute trauma patients. iii. Interspinous ligament injuries produce high T2 signal intensity within the ligament because of edema. iii. c.

5. Displacement of prevertebral fat stripe iii. Anterior wedging 2. Osseous Injuries ABC’s of Spinal Trauma Alignment 1. Disrupted posterior vertebral line 4. A delayed syrinx can be detected on MR well before clinical symptoms occur. Disruption of areas 2. Spinal Trauma 51 2. Interspinous/facet joint widening 2. 7. Rotation of spinous process 4. Loss of lordosis vi. A syrinx can result from nerve root avulsion. Laryngeal dislocation v. Retropharyngeal space widening ii. muscles shadow. airways may present as welling. CERVICAL SPINE INJURY Clark’s 12 Signs i. Spinal cord can herniate through the dural tear. 3. Dural tears are associated with central split fracture of spinous process or laminar fracture. CT myelography is the most sensitive investigation for identifying root avulsions and pseudomeningoceles. Focal kyphoscoliosis and loss of Lordosis 3. 6. Vacuum phenomenon Soft tissue swelling: Pre or paravertebral soft tissues. Tracheal deviation iv. which present usually after 18 months. Increased/decreases disc spaces 3. Disrupted C2 ring Cartilage Joint Space 1. Cortical buckling 3. fat strips. Acute kyphosis . Increased interpedicular distance Bone Integrity 1. Listhesis (Scottish Terrier Sign) 5. 4. Dural tears occur in 7 to 16 percent of lumbar fracture.

Plain films in flexion and extension are done. the ascending limb does not pass though spinolaminar line of C1 and dens tip does not lie within 5 mm of descending limb. This phenomenon is depicted beautifully on cine-kinematic MRI. The superior arc of the ring represents the superior articular facet. Harris ring of C2 is due to collection of images of overlying normal structures. CT images also show asymmetry of dens in relation to lateral mass of C1. Reformatted CT images clearly show the dislocation. Widened interspinous space ix. Rotation of vertebral bodies x. The predental space is increased and it is more than 3 mm in adults and 5 mm in children. Widened middle atlantoaxial joint xi. • Ascending limb. Harris ring is disrupted in fracture of body of C2. MRI depicts transection or cord contusion. Rotatory altalnoaxial dislocation Rotational injuries are uncommon in the cervical region. inferior arc of the ring is part of the foramen transversarium. Power’s Ratio • First line joints basion with middle of posterior arch of C1. Lee’s Method • Descending limb: basion to middle of spinolaminar line of C2. Widening of facet joint Verma’s 13th Sign: Antero or Retrolisthesis Cervical whiplash injury is depicted as Kyphosis of more than 10° between two vertebral bodies or isolated fanning of two spinous processes more than 12 mm or both. the posterior arc of the ring is the posterior vertebral body line. Torticollis viii. It is hyperextension and distraction injury of C1. C2. Two varieties may occur. In unstable atlantoaxial subluxation the predental space is more in the flexion than in the extension film.52 Seminar in Radiology vii. 3. Displaced fractures of body C2 produce widening of C2 in relation to width of C3. By Lee’s method. It occurs in less than 2 percent of cervical spine injuries. 2. This is called “fat C2 sign. Abnormal disc height xii.” 1. Predental space widening may be seen in sagittal reformatted CT images. Atlantoaxial Subluxation This is caused by flexion injury. Power’s ratio exceeds 1. • Second line joins opisthion with middle of anterior arch of C1. Occipitoaltantoaxial Injuries: – Traumatic atlantooccipital injuries This injury is usually fatal. the first . • Power’s ratio is the ratio between the two lines which normally is less than 1. Several methods have been used to assess if an abnormality exists. posteroinferior part of body of C2 to opisthion. anterior arc is formed by anterior vertebral body cortex.

C3-C7 Injury a. . Hangman’s fracture The anterior subluxation of C2 body and retrolisthesis of posterior elements of C2 relative to C3. This is true dislocation of C1 and C2 with locked facets. A frontal radiograph shows gross rotation of head. Flexion injuries They account for 50 to 80 percent of all cervical spine injuries. One or more anterior vertebral bodies may be involved without concomitant injury to posterior vertebral body. C1 Fractures Axial compression of C1 result in Jefferson fracture which involves unilateral/ bilateral anterior and posterior arches of atlas. CT scan through C2 shows no rotation. 2. The atlas is rotated more than 45°C with locked facts. Type I. Second type is the rotatory fixation of C1 and C2. In open mouth AP an overhanging of more than 3 to 9 mm is significant. CT shows the anterior and posterior arch fracture with lateral displacement of lateral masses of CI. CT is indicated to detect type 1 fracture as well as foramen transversarium involvement. If there is foramen transversarium involvement there be associated transaction of vertebral artery. : Horizontal fracture through C2 vertebral body  Type II is more common  In children. : Fracture at junction of dens and body of C2 III. 2. This may be diagnosed by the malalignment of the midline structures of the neck. Dens fracture: Dens fracture is usually associated with widening of prevertebral soft tissue shadow at C1–4 of more than 7 mm (C6 = 22 mm in adults and 14 mm in children). CT scan through C1 shows rotation. rupture of transverse ligament of dens is common while in adults the dens fracture. AP open mouth view shows eccentrically placed dens. Dens fracture is classified into 3 types. Spinal Trauma 53 is simple rotatory subluxation of C2. 1. Clay shoveler’s fracture There is oblique fracture spinous process of C6 or C7. : Oblique fracture through tip of dens II. Anterior vertebral body height reduction of more than 2 mm is significant in severe injuries there may be disruption of supraspinous and interspinous ligaments with increased interspinous distance. Wedge compression fracture This is due to flexion injury with axis of rotation through the posterior part of the vertebral body. C2 Fractures 1. The fracture line may be seen in lateral view.

widening of interspinous and interfacet spaces with focal kyphosis. Hyperextension injuries Hyperextension tear drop fractures belong to this category. These fractures are considered as stable one. Anterolisthesis can be demonstrated in upright lateral radiograph. Slight anterior wedging upto 20 percent of vertebral body height could be normal in T8–T12 vertebrae. and under tension.54 Seminar in Radiology 3. there may be widening of the interspinous distance. 4. Anterior height >2mm shorter than posterior vertebral body height indicated wedge fracture. CT shows the radially oriented fracture lines of the anterior endplate. Radiographically there is a triangular fragment at anteroinferior corner of vertebral body. Burst fracture 3. b. Hyperflexion sprain There is ligamentous injury with disruption of posterior ligamentous complex. Mild anterolisthesis with narrowing of anterior disc space and widening of interspinous distance is seen. The fragment is found at posteroinferior part of vertebral body. In occult hyperflexion sprain. The middle column remains intact and acts as a hinge. supine CT may be normal. and no posterior element fracture. Fracture dislocation 1. Flexion tear-drop fracture There is disruption of anterior and posterior ligamentous structures disc and apophyseal joints. slightly displaced fragments. Wedge fracture 2. THORACOLUMBAR SPINE INJURIES 1. Compression injuries represent a failure under compressive forces of the anterior column. the posterior column can fail. CT shows “nacked facet sign’ on axial sections. There is a decrease in vertebral body height anteriorly in lateral radiograph with maintained interpedicular distance in frontal radiograph and if the posterior column has failed under distraction. CT shows anterior subluxation with “bow-tie” sign oblique position of facets and articular processes. Wedge fracture (Compression fracture) This is the commonest type of injury in thoracolumbar spine comprising of 48 percent of all fractures and 58 percent of all major spine injuries. Bilateral facet lock There is disruption of middle and posterior columns. 5. Seat-belt injury 5. Cord damage is due to impingement and ligamentous sprain. MRI is the investigation of choice for elevation of cord impingement. CT is indicated in severe compression >50 percent to rule out burst fracture unless they result in severe kyphosis >40°. .

Burst fractures are considered unstable. pedicles. Axial CT scans are of limited value because of the horizontal nature of the fracture plane. Axial CT images . Spinal Trauma 55 2. transverse process. A fragment from the posterior aspect of the vertebral body may be retropulsed into the canal and may not be seen (vanishing line sign). occur in less than 10 percent of cases. even though there may be no neurological deficit (48-77% of the patients may have neurological deficit). The presence of “disappearing laminae” on the axial CT scan gives a clue to the presence of horizontal fracture though the laminae with associated diastasis. If the flexion part of the distraction is more severe. It comprises 14 percent of all spinal fractures. It comprises 5 percent of all fractures. It represents 10 percent of all spinal fracture. Fracture dislocation Fracture dislocation injuries are the most unstable type of injury representing failure of all the 3 columns under compression tension. rotation and shear. On frontal radiograph there is increase in interpedicular and a vertical laminal fracture may be present. a horizontally oriented fracture through the spinous process. The posterior vertebral body line is disrupted and there is abnormal posterior convexity of the vertebral body (posterior bow sign) and loss of vertebral body posteriorly. with increase of posterior vertebral body height and posterior disc space. There is an increase in the height of the neural foramina. laminae. Burst fracture Burst fracture represent failure under axial loading of anterior and middle columns. whether contiguous or not. The radiographic hallmark is vertebral subluxation or dislocation seen on the frontal or lateral radiogrpah. with extension into the posterior aspect of the vertebral body. 4. pedicles. 75 percent of the patients have neurological deficits. facet distraction becomes more pronounced. Two burst fractures. CT is used to show the size of the spinal canal and the degree of retropulsion of the posterior fragment. 3. A flexion injury with a initial fulcrum being at the seatbelt across the abdomen anteriorly is classically “Chance fracture”. most commonly occurring at thoracolumbar junction. Seat belt injury Seat belt injury represent a failure of both posterior and middle column under tension. the anterior column is considered intact because the anterior longitudinal ligament intact. Plain film shows fracture of lamina. Sagittal reconstruction CT images may demonstrate the nature and extent of the injury. with half occurring at L1. The articular facet of the vertebra above lie naked without their companion facets below. Though mild anterior wedging may be present. If the distraction forces act initially on the posterior ligamentous complex “smith injuries” are produced in which there is rupture of supra and interspinous ligaments. CT of facet distraction injuries shows the separation of the articular processes. Most burst fracture occur from T9-L5. Isolated involvement of superior vertebral endplate is most common.

open mouth. lateral. Low risk Mechanism of Injury unlikely to have exceeded physiological range of motion  Do A Three-View Series 3. Risk category Injury 1. lateral. Medium risk Injury likely to have exceeded physiological range of motion  Do A Five.View Series 4. The exact position of the dislocation can be made out on 3D reformatted CT images.2: Appropriateness rating for radiologic examinations Assessed by ACR Task Force (1995) Patient group Radiologic examination Score Asymptomatic and alert patients with AP. and open-mouth radiographs 1 normal physical examination with or Open-mouth and lateral radiographs only 1 without cervical collar AP. and oblique 1 radiographs Symptomatic patients with neurologic AP. No risk No historical or physical findings suggestive of spine injury  No Need for Imaging 2. No. lateral. High risk Injury very likely to have exceeded physiological range of motion Patient is unconscious or in an altered mental status  Do A Three.View Series Table 4. and open-mouth radiographs 9 signs or symptoms or cervical injury Open-mouth and lateral radiographs only 1 Oblique films * Symptomatic patients in whom Flexion and extension radiographs 9 ligamentous injury is suspected whose CT scan 1 plain films are normal MR imaging 1 CT scan Oblique radiographs * Patients with neurologic signs or MR imaging 9 symptoms whose plain films are CT myelography 9 normal Flexion and extension radiographs 1 Oblique radiographs * Patients whose screening plain films Conventional tomography 9 suggest injury at the occiput to C2 CT scan with reformation 9 levels MR imaging * CT myelography * Patients with impaired sensorium AP. and open-mouth radiographs 9 Open-mouth and lateral radiographs only * Oblique radiographs *  * = No consensus  1 = Least appropriate  9 = Most appropriate . lateral. APPENDIX Table 4.1: Vandemark’s risk—Tailored approach (For cervical spine) Sl.56 Seminar in Radiology may show naked facets or superiorly bilaterally locked facets.

laminar injury • More radiation Comupted tomography • Axial images with sagittal and • Costly coronal reforms possible • May miss horizontal • Soft tissues can be assessed fractures • Subtle fractures detected • Reforms are essential for • Better depiction of fractures displacements • Spinal Canal can be assessed • Poor resolution especially in • Can be combined to myelography reforms Myelography • Good to assess penetrating • Cannot be performed if injuries dural tear. C2. we have to wait for some time for contrast to spread Magnetic resonance • Good for soft tissue • Costly imaging • Best for cord • Time taking • Best for disc • Not easily available • Direct correlation to histo.3 Name of investigation Merits Limitations Plain radiography • Initial screening modality • Inadequate for C1. CV • Easy to access Junction • Portable • May miss subtle fractures • Cheap • Cannot evaluate non- • Radiation dose can be minimized osseous injury Conventional • Excellent for horizontally • Positioning for lateral tomography oriented fractures view is difficult • Better depiction of malalignment • Poor soft tissue delinea- • Excellent for CV junction tion • Cheap • Axial images not possible • Good for facet. Spinal Trauma 57 Table 4. • Apart from above archnoid space possible limitation. • Adverse reaction to con- meningocele trast media • Can detect CSF block due to • Complications of LP intrathecal blood clot or avulsed • Radiation does is high fragment • Patient has to be co- operatives movable CT myelography • Direct visualization of sub. root avulsion local infection present and meningocele/Pseudo. • Not good for bone study pathology • MR compatible venti- • No radiation lator fixators etc not • Multiplanner capability widely available • Spectroscopy can detect cord viability • For bleeding chronology Nuclear scan • Early detection of stress fracture USG • For associated STI • For intraoperative use .

58 Seminar in Radiology ALGORITHMS FOR IMAGING OF SPINAL TRAUMA .

5 Connective Tissue Disorders Involving Joints • Also known as collagen vascular diseases • This group of conditions comprise a number of chronic inflammatory autoimmune disorders. – Joints – Serous membranes – Blood vessels. vasculitis and immunological abnormalities such as circulating autoantibodies and immune complex deposition. • Conventionally. and – Telangiectasis • Some patients exhibit signs of more than one of the conditions. multisystem involvement. • May involve any tissue in any part of the body. secondary to vasoconstriction of the small blood vessels) – Esophageal abnormalities (dilatation and hypoperistalsis) – Sclerodactyly. the connective tissue disease comprises: – Rheumatoid arthritis – Systemic lupus erythematosus (SLE) – Systemic sclerosis (SS) – Polyarteritis nodosa (PAN) – Dermatomyositis/Polymyositis (PMS) – Mixed connective tissue disease (consists of combined features of SLE. • Antinuclear antibodies are widely used in the diagnosis of connective tissue diseases. SS and PMS) • CREST syndrome is a subgroup of systemic sclerosis characterized by : – Cutaneous calcinosis – Raynaud’s phenomenon (episodes of intermittent pallor of the finger and toes on exposure to cold. but frequently involves. and – Lungs and pleura The features are: arthritis or arthralgia. . The term ‘overlap syndrome’ has been extended to include almost any combination. • This is established by immunofluorescence against a rapidly dividing human tissue substrate such as Hep-2-cells.

representing a combination of joint effusion.” • Although such patients have an absence of rheumatoid factor. is an important diagnostic finding.60 Seminar in Radiology • Antibodies to double-standard DNA are virtually pathognomonic of SLE and their titer often approximates disease activity. osteoporosis is localized to periarticular areas. with progression of the condition. • Rheumatoid factor. and – Joint space pathology • The soft tissue swelling is the earliest sign and usually a fusiform. systemic inflammatory disease affecting primarily the synovial joints. • Anyone of the large weight-bearing and non-weight bearing joints can be affected by rheumatoid arthritis. periarticular osteoporosis. usually multicompartmental symmetric narrowing of the joint space associated with marginal or central erosions. and tenosynovitis. • Women are three times more often affected than the men. edema. • There is a striking tendency toward spontaneous remissions and exacerbations. a generalized osteoporosis can be observed. • It is periarticular in location. their clinical and radiographic picture is similar to seropositive rheumatoid arthritis. chronic. • Patients lacking the specific antibodies represented by RF are said to have “seronegative rheumatoid arthritis. representing specific antibodies in the patient’s serum. symmetric shape. unlike osteo- arthritis. • Osteoporosis is a striking feature of rheumatoid arthritis. and periarticular soft tissue swelling. Radiographic Features • Certain radiographic features can be identified which are characteristics of this inflammatory process. subchondral sclerosis—minimal or absent and formation of osteophytes is lacking. • In the early stage of the disease. • Other specific nuclear antigens have been defined including antibodies to- Sm (in SLE) Ro and La (in Sjögren’s syndrome) Centromere (in CREST) • Scl70 (in diffuse scleroderma) and • NRNP (in MCTD) RHEUMATOID ARTHRITIS • It is a progressive. These include: – Soft tissue swelling – Osteoporosis. • It is characterized by a diffuse. .

• In the cervical spine. • Narrowing in the hip joint leads to axial migration of the femoral head. which may be present only when secondary degenerative changes are superimposed on the underlying inflammatory process. • Rheumatoid arthritis characteristically affects the small joints of the wrist. and thus there is no evidence of subchondral sclerosis or osteophytosis. HitchHiker’s thumb are common. Boutonniere. which in more advanced stages may result in protrusio-acetabuli. • Fibrinoid (eosinophilic amorphous material) deposited along—blood vessels. a condition occurring predominantly in men. rheumatoid arthritis is characterized by erosion of the odontoid process associated with subluxation in the atlantoaxial joints and. arterioles and venules. • Hemotoxylin bodies seen in inflammatory infiltrates resulting from interaction between cell nuclei and antinuclear antibodies. • The erosive destruction of a joint may be central or peripheral in location. reparative processes are absent or very minimal. . • Subluxations and other joints deformities—Swan-neck. • Resoprtion of the distal end of the clavicle. Connective Tissue Disorders Involving Joints 61 • The joint space narrowing of rheumatoid arthritis is a symmetric process with concentric narrowing of the joint. • In addition to the characteristic changes exhibited in large joint involvement. multiple subcutaneous nodules. may also be observed. all three joint compartment are involved. It exhibits a characteristic lack of joint abnormalities. superior migration of C-2 and involvement of the apophyseal joints. • As a rule. • The subtalar joint is most often affected in the foot and a hallux valgus deformity is observed. • F > M. the small joints may also show radiographic features specific for these sites. frequently. as well as the metacarpophalangeal joints in the hand are spared although in advanced stages of the disease even these may be affected. • Pathology—Widespread vasculitis affecting capillaries. • Rheumatoid nodules. young adults • Black > whites • Multisystem disease with arthralgia and rashes are commonest clinical features and cerebral and renal diseases are the most serious problems. is a variant of rheumatoid arthritis. • In the knee. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) • It is a prototype of connective tissue diseases. • Cephalad migration of the humeral head may also be seen secondary to destructive changes in the shoulder joint and rupture of the rotator cuff. tissue fibers and synovium of joints. which assumes a pencil-like appearance. and a high titer of rheumatoid factor.

• Tendon involvement may be prominent. or • Vital role of the inflammatory process (vasculitis) in the development of this complication. The commonest presentation is joint or muscle pains. receiving high doses corticosteroids for long-standing SLE.62 Seminar in Radiology Musculoskeletal Features • The musculoskeletal system is a frequent site of involvement of SLE. • Joint involvement is the commonest clinical features (>90%). a patient develops a deforming arthritis. • Hands are the predominant site of involvement. leading to flexion contractures at the forearm and wrist in some cases. • Aspetic necrosis affecting the weight-bearing joints occurs in patients. The small joints are most commonly involved. which is frequently seen. A proximal myopathy occurs in 5 percent of patients. has been attributed to: • Complications of treatments with corticosteroids. . and • Interphalangeal joint of the thumb These pathognomonic deformities usually occur secondary to a loss of support from the ligamentous and capsular structures about the joint and at least in the early stage of disease are completely reducible. • Arthritis involvement is symmetric and articular deformities without fixed contractures are the hallmark. • Abnormalities are better demonstrated on the lateral projection. this differs steroid myopathy in that the shoulder girdle is more commonly involved and the serum muscle enzymes are usually elevated. In Lateral View Malalignments most commonly seen at the: • Metacarpophalangeal and proximal interphalangeal joints of the fingers. Seldom are. • Arthritis is symmetrical • Erosions are rare • Occasionally. Radiographic Features • SLE is characterized by flexible joint contractures and malalignments of the metacarpophalangeal and proximal interphalangeal joints. these abnormalities fixed and/or accompanied by articular erosions. since they can easily be reduced during positioning of the hand for the dorsovolar view. as a result of capsular and ligamentous laxity. Some patients present with • Sclerosis of the distal phalanges (acral sclerosis) or • With resorption of the terminal tufts (acro-osteolysis) Osteonecrosis.

corroborative findings are seen in the gastrointestinal tract. Radiographic Features Radiographic abnormalities are divided into two types: • Those involving soft tissues • Those involving joints. Polymyositis and Dermatomyositis • Polymyositis is a disorder of striated muscle characterized by diffuse. a connective tissue disorder. • When accompanied by a rash. it is called dermatomyositis. • Common in women • Peak incidence in adults aged between 30 and 60 years. with characteristic findings like– • Dilatation and hypomotility of the esophagus • Dilatation of the duodenum and small bowel with a pseudo-obstruction pattern • Pseudodiverticula of the colon. nonsuppurative inflammation and degeneration. The most characteristic soft tissue abnormality in both conditions are: Soft tissue calcifications- . with frequent involvement of the musculoskeletal system. In scleroderma. particularly the tips of fingers • Erosion and resorption of tufts of the distal phalanges • Subcutaneous and periarticular calcifications • Destructive changes of the small joints. • Primarily. a. usually in the interphalangeal joints. • Thirty to forty percent of patients have a positive serologic test for rheumatoid factor and positive antinuclear antibody test Radiographic Features Radiographically. • Proximal muscular weakness and wasting affecting shoulder and pelvic girdles. is characterized by thickening and fibrosis of skin and subcutaneous tissues. the musculoskeletal abnormalities associated with scleroderma are recognized as: • Atrophy of the soft tissues. • Dermatomyositis is associated with an increased incidence of carcinoma bronchus in men and ovarian cancer in women. Connective Tissue Disorders Involving Joints 63 Scleroderma (Progressive Systemic Sclerosis) • Generalized disorder of unknown etiology • Seen predominantly in young women • Usually becomes apparent in third and fourth decades of life.

• Patients in this group have prominent joint abnormalities. . Subcutaneous calcifications are seen similar to scleroderma b. • Soft tissue abnormalities are identical to those encountered in scleroderma. scleroderma.64 Seminar in Radiology The favorite sites of intermuscular calcification are the large muscles in the proximal portions of upper and lower extremities. Articular abnormalities are rarely seen Periarticular osteoporosis is commonly seen Destructive joint changes occurs occasionally and primarily in the distal interphalangeal articulations of the hands. dermatomyositis and rheumatoid arthritis. with typical involvement of the small articulations of the hand. • Joint deformities may simulate those seen in RA. Mixed Connective Tissue Disease • It is characterized by the clinical and radiologic features that combine the findings of SLE. wrist and foot.

lateral masses. Except for C1. c. spinous process and dens. 5 lumbar and 5 fused sacral coccyx vertebrae. Intervertebral disc: It separates two adjacent vertebral bodies. the disc have an attenuation value of 50 to 100 HU. Cervical canal: Triangular in shape. Lumbar canal: Round to oval shape and triangular shape caudally. pedicles. The spinal canal: Bounded anteriorly by vertebral bodies and intervertebral discs. measures 27 mm at C1 and 21 mm in lower cervical area in sagittal midline plane. C2 and sacrum each vertebra has similar osseous elements.5 mm anteroposteriorly and interpediculate distance of 16 mm. b. Thoracic canal: Canal is rounded in shape and constant in size. articular pillars and laminae. 3. The epidural space contains fat which outlines the nerve roots and epidural venous plexuses. The spinal cord and nerve roots: The cord descends from medulla and terminates at conus medullaris which lies between lower border of 12th dorsal and upper border of 3rd lumber vertebra where it becomes filum terminale. It consists of three parts • Central nucleus pulposus • Peripheral annulus fibers • Cartilaginous end plates . C2 has vertebral body. 6 Degenerative Disorders of Spine and Joints DEFINITION Normal ageing is a complex physiologic process that includes various degrees of gross anatomic and biochemical changes in the entire discovertebral complex. The nerve roots pass laterally from anterolateral and posterolateral margins of each segment. Normal Anatomy The spinal column includes 7 cervical. 12 thoracic. includes vertebral body. lateral masses and transverse processes. 1. The lowest normal diameter is 11. On CT. C1 (atlas) consists of anterior and posterior arches. • Anteriorly → Posterior longitudinal ligament • Posteriolaterally → Pedicles and laminae lined by ligamentum flava a. pedicles. 2.

c.66 Seminar in Radiology Complicated structures includes: • Nucleus pulposus • Annulus fibrosus – Outer – Inner Nucleus and inner portion of annulus plate show high signal intensity on T2-weighted images because of glycosaminoglycans and high water content than collagen fibers. e. After 30 Years of Age There is an indistinct boundary between nucleus pulposus and inner annulus fibrosus. Decrease in water binding capacity . superiorly by inferior margin of upper vertebral pedicle and inferiorly by superior pillars. These are: a. 5. Intervertebral foramina: It is bounded medially by posterior vertebral body and intervertebral disc. 4. so nucleus grossly appears. Posterior longitudinal ligament: It extends from C1 to S1 sacral vertebra. • Nuchal ligament: It connects the base of occipital bone to spinous processes of C1 to C7. Ligaments: a. d. Anterior longitudinal ligament: Ligament starts from the axis as atlantoaxial ligament and extends to sacral ligaments connecting the anterior aspects of vertebral bodies and disc spaces. b. homogenous except for small primitive notochord remnant. PLL does not adhere to vertebral body and widens laterally at intervertebral discs and attaches firmly to annulus fibrosus. In contrast to ALL. Physiological disc ageing in nucleus pulposus is related to specific chemical changes. Facet joints: These are joints between superior articular facet of lower and inferior articular facet of upper vertebra. Ligamentum flavum: It is attached to laminae (3 to 5 mm in thickness) and extends upto S1. Interspinous ligament: It connects the spinous processes. Normal joint space is 2 to 4 mm. and distinction between nucleus pulposus and annulus fibrosus is gradually lost because of fibrous tissue which develops near margin of nucleus pulposus. During 1st and 2nd Decades The notochordal remnants are—obliterated. In New Born Nucleus pulposus is fibrocartilagenous with little fibers.

inserted into ring apophysis Transverse and radial tears appear as increased signal intensity on T2-weighted images. Degenerative Disorders of Spine and Joints 67 b. there is gradual conversion of red marrow to yellow marrow. Type III: Decreased signal intensity on T1 and T2-weighted sequence due to extensive bone sclerosis. Increase in collagen content • In 1st decade → Nucleus pulposus contains 85 to 88 percent of H2O • In adulthood → Both contains 70 percent of H2O • With ageing → Collagen content increases Disc Degeneration Defined as diminished signal intensity on T2-weighted images with– a. . Usually annular tears enhance on administration of scar tissue during healing. Signal intensity changes in marrow adjacent to vertebral end palate is common on MR scan. Osteophytes are bony excrescences that originate near the margin of vertebral body of facet joints. Intradiscal gas (vacuum phenomenon) → Early degeneration may also occur without a loss in disc height or signal intensity. Three types of end pates changes: Type I: Decreased signal intensity on T1 and increased T2 signal intensity due to replacement of normal marrow by fibrovascular tissues with greater water content. Three types: Type I (concentric) : A concentric fluid space between annular lamellae. Osteophytes typically develop where Sharpey’s fibers attach to vertebral body. SPONDYLOSIS Etiology and Pathology The primary finding is osteophytosis: 1. Type II: Increased signal intensity is present on T1 and isointense to slightly increased on T2-weighted due to fatty marrow replacement. Vertebral End Plate Changes With Maturation. Disintegration of large molecular proteoglycans c. Loss of disc space height b. Annular Tears Tears of annulus fibrous also occur with ageing. Type II (radial) : Characterized by rupture of all layers Type III (transverse) : It involves rupture of Sharpey’s fibers.

Oblique view delineate encroach- ments of osteophytes into neural foraminas. Plain radiography AP. Conditions Predisposing to Early Osteoarthritis a. the lumbar and cervical areas are the most common sites. Location Although any spinal segment can be involved.68 Seminar in Radiology 2. It may be cause of low backache. a. The levels affected by both disc herniation and chronic spondylosis are C6—C7 (60% to 75%) and C5—C6 (20% to 30%) in cervical spine. frequently disc degeneration develops above or below the fused vertebra due to altered mechanics in spine. Cervical lordosis is reduced resulting in straightening of curvature b. Commonly in cervical spine. Sacralisation and lumbarization: Small or absent rib on T12 with large transverse process on L5 which fuses with sacrum and is known as sacralisation of L5 or cranial shift. The sacralised transverse process may form a pseudoarthrosis with ileum and degenerative sclerosis may occur around false joint. Disc herniaiton commonly seen at C6—C7 followed by C5—C6. Congenital vertebral fusion: Complete vertebral fusion is known as block vertebra. Age Incidence Increases with advancing age. oblique views are taken. example— Klippel-Feil syndrome. prevalence is 60 to 80 percent in patients of >50 years. In lumbar spine. . Vertebral end plates show sclerosis in late stages. In cervical spine: Clinical presentation: As • Radiculopathy • Myelopathy—UMN or LMN type of weakness • Neck pain • Vertebrobasilar insufficiency—because of intrusions of osteophytes into foramina transversarium. Schmorl’s nodes: It is herniation of disc material through end plate into vertebral body. thoracic spine is less frequently and less severely affected. C4—C5 and C3—C4 in decreasing order. b. Caudal shift implies presence of ribs on L1 and lumbarization of S1. 1. L4—L5 and L5—S1 are the most commonly and most severely affected sites. Imaging Techniques i. free disc above pseudoarthrosis show early degeneration. Secondly. lateral.

T11. AP b. iv. b. Intervertebral disc: Decreased height and decreased signal intensity on T2-weigted images and different degree of disc herniation can be assessed. Oblique views Radiological findings include – Disc space narrowing – Osteophytes formation – Facet joint hypertrophy . atrophy or myelomalacia. undergoes erosion and formation of osteophytes which causes foraminal stenosis. CT myelogram is useful to determine whether spinal cord compression is due to osteophytes or disc protrusion. Degenerative Disorders of Spine and Joints 69 c. For accurate localization of levels of stenosis and spinal canal diameter in sagittal plane can be assessed. Uncovertebral joints or joints of Luschka—When disc height decreases. show irregularity and sclerosis. Myelography Extradural deformity because of disc protrusion or indentation of thecal sac-filled with contrast can be noted. Small size of thoracic discs. Plain radiography a. Apophyseal joints—The changes include erosion. Imaging i. uncinate process approximate against vertebral body. Lateral c. CT Scan It accurately determines presence of osteophytes. MRI Sagittal and axial T1 and T2-weighted images are taken a. It can demonstrate damage to cord in the form of edema. c. Thoracic spine: Degenerative changes less frequently seen because of limited mobility of thoracic spine which is due to: a. d. The orientation of thoracic facet joints in coronal plane. Relative restraint placed on thoracic spine by ribs and sternum Location Majority of herniation are in lower thoracic spine. T12 and lower 4 or 5 disc space most commonly affected. and osteophyte formation. b. c. iii. ii. narrowing of canal. presence of prolapsed disc and compression of roots. Facet joint space is narrowed. 2.

disc versus ligamentous versus bony hypertrophy – For demonstration of lateral foraminal stenosis. CT scan: Findings are • Osteophytes – Vertebral – Facet . MRI: • Disc herniation are isointense or slightly hypointense on T1-weighted sequence and hypointense on T2-weighted sequences. Oblique • Disc space narrowing • Osteophytosis • Vertebral end plate changes • Schmorl’s nodes • Intradiscal gas or vacuum phenomenon and posterior elements • Facet joint hypertrophy • Spondylolysis associated with spondylolisthesis • Spinal stenosis AP diameter being <15 mm ii. Sensitivity is reduced at L5 to S1 level iii. Myelography Non-ionic media is commonly used. AP b. Plain radiography a.70 Seminar in Radiology – Kyphosis – Disc protrusion or extension can be seen ii. Lateral view c.e. • Large herniation result in partial or complete block of contrast column. iv. iii. • Large protrusion may occlude a root sheath or obstruct the theca. Lumbosacral Spine i. Disc prolapse displaces and usually causes tenting of the theca or deviation of corresponding nerve root sheath. Myelography • Mild to moderate ventral or ventrolateral indentation on contrast column is seen opposite to disc herniation. CT scan with myelography: • Detects encroachment on subarachnoid space or spinal cord • To differentiate an intradural component as well as lateral herniation of disc • To identify status of bony canal. i. • Limitation: – Does not delineate cause of narrowing.

Lateral or foraminal Facet Joint Disease and Synovial Cyst Etiology: Articular processes of spine are lined by synovium • Osteoarthritic changes are seen as fibrillation and erosion of articular cartilage. • MRI: Superior to CT because a. lower cervical and lower lumbar spine are commonly affected.Will be directly central or posterior – 10% disc herniation . • Approximately 10 percent disc herniation are calcified and some may contain gas secondary to vacuum phenomenon. nerve roots.Posterior lateral margins of disc – 30% disc herniation . Chronic disc herniations tend to have low signal intensity on T2-weighted due to loss of water content. . out of these lumbar is the most common site. Degenerative Disorders of Spine and Joints 71 • Schmorl’s nodes: Seen on CT scan as end plate sclerotic area and surrounding lucencies that represent interbody herniation of disc material. synovial cyst develop. Location: Middle. • Disc herniation : Protrusion. ligaments nerve roots. seen as high signal intensity on T2-weighted images and focal enhancement may be seen after gadolinium administration. Bone images are used to evaluate stenosis. thecal sac and spinal cord are clearly done but only disadvantage is lack of bony detail. • Adjacent to degenerated facet joint. • The signal intensity of herniated disc material is variable • Acute nucleus herniation may retain degree of hydration and produce high signal on T2-weighted images. • Annular tear is usually associated. Imaging: On plain films and NECT scans a. disc. spinal cord and disc bulge. and new bone formation. extension or sequestration can be seen – 60% disc herniation . • Joint space narrowing and facet hypertrophy: CT myelography gives better evaluation of thecal sac. Joint space narrowing b. Facet hypertrophy seen • Synovial cysts appear hypo/hyperdense compared to adjacent ligament flavum in NCCT scan and depending on contents. Osteophytosis c. It provides multiplanar imaging modality b. Distinction of bone. facet arthropathy and spondylolysis. containing contents as serous or mucinous fluid.

described as bilateral lower extremity radicular pains as sensorineural deficit. Morquio’s syndrome b. Spinal dysraphism f. Achondroplasia/hypochondroplasia d. however most thoracic herniations are central rather than lateral in location. . Scoliosis Acquired 1. Facet arthrosis c.72 Seminar in Radiology SPINAL STENOSIS Clinical Presentation Typically presents as neurological claudication. Metabolic—acromegaly. Ligamentous degeneration or spondylolisthesis d. Degenerative a. Posttraumatic 4. Disc herniation e. renal osteodystrophy. that occur when patients stand or walk. Other include: i. Short pedicle syndrome c. oxalosis Miscellaneous • Paget’s disease • Ankylosing spondylitis • Fluorosis • Rheumatoid arthritis • Diffuse idiopathic skeletal hyperostosis (Dish syndrome) Location The lumbar and cervical regions are most commonly affected. Ligamentous ossification/ calcification 2. Down’s syndrome e. Spondylosis with spondylolisthesis f. hypoparathyroidism. Low backache ii. Radiculopathies It can be: • Congenital • Acquired Congenital a. Spondylosis b. Postoperative 3. The incidence is less in thoracic spine due to limited mobility and because the weight-bearing axis does not intersect the posterior margins of vertebral bodies.

Discogenic Bony Origin i. becomes predisposed to either anterior (anterolisthesis) or posterior (retrolisthesis). Lateral recess stenosis: Bony overgrowth of lateral recess as part of degenerative processes resulting in entrapment of lateral roots. uncinate hypertrophy can lead to foraminal stenosis. Four grades of severity depending upon forward slippage [Meyerding’s classification (1932)]. ii. These changes predominantly seen in lower lumbar spine. resulting in erosion of articular cartilage and underlying bone. Non-discogenic – Body origin – Ligamentous origin b. Ossification of posterior longitudinal ligament: This entity is common in Japan. size and shape can narrow or focally impinge upon any part of neural canal. Disc herniation . Plain film: Seen as vertical band of ossified tissue along the posterior margin of vertebral bodies. vi. it can be of two types: a. Grade I : 25% Grade II : 50% Grade III : 75% Grade IV : 100% is slippage becomes more severe. Facet hypertrophy: There is repeated stress on apophyseal joints. Spondylolisthesis and spondylolysis: Spndylolysis is fibrous cleft within the pars interarticularis and spondylolisthesis is slippage of one vertebral body in relationship to an adjacent body. The ossified posterior longitudinal ligament can impinge upon spinal canal and can result in nerve root compression. Discogenic Spinal Stenosis Two types: i. On CT Scan: Involved portion of ligament is replaced by high density of calcium. In cervical spine. v. Osteophytes: Depending upon location. On MRI: Ossification is represented by low signal on both T1 and T2- weighted sequences. predisposed to slippage. iv. hypertrophies causing foraminal narrowing. Degenerative Disorders of Spine and Joints 73 According to cause. iii. slippage upon the vertebra inferior to it. Anterolisthesis is most common at L4/5 where the facets are oriented more sagittally than at any other level and are therefore. spinal canal is narrowed. Ligamentum flavum hypertrophy: It forms posterior wall of bony canal so hypertrophy contributes to narrowing. Disc bulge ii.

As the nucleus pulposus loses its turgor and elasticity of annulus diminishes. • Associated findings: Decreased disc height and signal intensity and annular tears can be seen as increased signal intensity on T2-weighted images. ii. mild bulging disc initially appears as loss of normal posterior disc concavity. Location In lumbar canal 93 percent are inside the spinal canal. asymmetric protrusion beyond the confines of annulus. non-focal protrusion of disc material beyond adjacent end plate usually circumferential and broad-based. • MRI: Focal. elevation. intact. Disc extrusion: When nucleus pulposus herniates through complete tear of annulus and is contained only by posterior longitudinal ligament. Disc Herniation Etiology and Pathology Herniation of nucleus pulposus through an annular defect causes focal protrusion of disc material beyond the margins of adjacent vertebral end plate. deviation or amputation of root sleeve and edema of affected nerve can be seen.74 Seminar in Radiology Disc Bulge Defined as extension of disc margin beyond the confines of adjacent end plate. nucleus can focally herniate through tear and called as protrusion. the disc bulges outward beyond the vertebral body margins. 3 percent are predominantly located in intervertebral foramen and 4 percent are extraforaminal. Imaging findings: On CT and MR scans. 2. Imaging • Myelography: Extradural deformity or displacement of contrast filled thecal sac. The herniated segment however remains attached to disc. Disc protrusion: When some of inner fibers of annulus tear but outer remains. Types of Disc Herniation i. This is the earliest type. Incidence Mild bulging of cervical disc is common incidental finding 1. Radial annual tear is usually associated and high signal in posterior annulus is seen on sagittal T2-weighted scans. . Moderate diffuse bulges are seen as diffuse. Enhancement following contrast administration is seen in some annular tears because of vascularized granulation tissue. • NCCT: Shows soft tissue mass with effacement of epidural fat and displacement of thecal sac.

OSTEOARTHRITIS (DEGENERATIVE/HYPERTROPHIC ARTHRITIS) OR OSTEOARTHRITIS • Degenerative condition affecting articulations particularly those bearing weight or these subjected to much wear and tear. Joint space remodeling: Joint narrowing is followed by loss of underlying bone in stressed areas and formation of new bone and cartilage in non- stressed area and at joint margins resulting in alteration of joint alignment. • The hands. knees and ankles of professional athletes. Two types—According to etiology: • Primary • Secondary Primary When no predisposing cause for joint change is found. . This is better appreciated on sagittal than on axial MR scan. but some intrinsic abnormality of cartilage causes it to degenerate. Disc tend to herniated posterolaterally because of posterior longitudinal ligament and annular fibers are thicker in midline and thinner laterally. joint space narrowing is result of cartilage destruction. Primary Osteoarthritis Pathophysiology It develops without evidence of an initiating factor. This change characteristically occurs in areas of excessive weight-bearing. for example. Degenerative Disorders of Spine and Joints 75 iii. large weight-bearing joints and spine are commonly involved • Usually polyarticular variety exists The radiological features of primary and secondary osteoarthritis are similar and major features are following: i. Sequestration: When an extruded nucleus breaks free of the parent disc called as sequestered or free segment. Secondary When degenerative changes develop in joints damaged as a result of previous disease example: trauma and inflammatory joints or when normal joints are subjected to repeated stress. Joint space narrowing: Normal width of joint space is due to radiolucent cartilage. is lack of connection between extruded segment of parent disc. ii. It appears that biomechanical forces across the joint are normal. The most important distinction. It may migrate superiorly or inferiorly to a different inter-space or even penetrate the dura.

usually on medial rather than lateral aspect of femoral neck. have pre-existing anomaly and some result from childhood. Localized increased in density is due to: a. Superior migration (78%): May occur laterally. and ossificaiton of cartilage debris. however when osteoarthritis results in pain and immobility. Knee Joint • Most commonly affected joint found in clinical practice • Consists of three compartments . • Cyst formation (Geode) in subarticular regions occurs in osteo- arthritis (D/D rheumatoid arthritis) and is found in weight-bearing areas. however different patterns are seen which depends on direction of migration of femoral head. osteoporosis and soft tissue wasting may result secondarily. however MR is preferred imaging modality for osteoarthritis in major joints. • There is no typical appearance of osteoarthritis of hip. • Congenital dysplasia • Congenital dislocation of hip • Acetabular dysplasia • Perthe’s disease : Some occur later as a result of Paget’s disease.76 Seminar in Radiology • Beneath areas of cartilage destruction. scoliosis. Medial migration (22%): May lead to protrusio acetabuli. Loose bodies: Formed by detachment of osteophytes. • Osteoporosis and bony ankylosis are not manifestation of degenerative disease and new bone formation is seldom seen in osteoporosis. rheumatoid arthritis and aseptic nercosis. a. b. Trabecular collapse. predominantly peripheral osteophytosis or within joint. Imaging: Plain X-ray and CT scan show osteophytes. joint space narrowing. eburnation results (increased change in exposed subchondral bone in degenerative disease in which it is converted to dense smooth substance like ivory). b. at joint margins. New bone is formed at the areas of low stress. erosions and cysts. central osteophytosis. medially or in intermediate direction. Osteoarthritis in Particular Joints a. acetabulum is dependent with narrowing of joint space. flattening and sclerosis results. Stress induced new bone formation. Hip joint: Patients developing premature osteoarthritis. capsular traction leads to new bone formation. • End result is femoral head shows bone loss in weight bearing areas and bone formation in non-weight bearing areas. 3.

joint narrowing osteophytosis and articular irregularities are seen particularly on lateral and skyline views especially at lateral facet of patella and patella often migrates outward. cysts and sclerosis of greater tuberosity. especially in severe cases. • The fabella may be enlarged and irregular in osteoarthritis. Sometimes erosive osteoarthritis seen in interphalangeal joints particularly patients who are seronegative (middle aged women). Degenerative Disorders of Spine and Joints 77 • A medial and lateral tibiofemoral and patellofemoral joint space narrowing. With malalignment following chronic rotator cuff tear Changes Include: • Erosions. Shoulder Joint Osteoarthritis changes does not usually occur at glenohumeral articulation in absence of predisposing factors. . • Distal interphalangeal joints are most commonly affected (in contrast to Rheumatoid arthritis) • Joint narrowing at distal interphalangeal joints with large osteophytes on distal phalangeal bases and overlying soft tissue swelling. joint space loss peripheral osteophytes. The radiological features are erosions which commence centrally. • In patellofemoral compartment. Sometimes scalloped defect of anterior distal femur is seen. The bone most commonly involved in osteoarthritic change is patella (which is subjected to large loads when knee is flexed in squatting positon). • Varus deformity is more common and is related to more common medial meniscus abnormalities. these factors include: a. Use of crutches b. sclerosis and cyst formation at articular surfaces. Joint narrowing affecting one or other compartment results in valgus/varus deformity opposite compartment may be widened. Hand and Wrist Joint • Commonly affected joint are carpometacarpal joint of thumb and trapezioscaphoid joint especially in women. • Spiking of tibial spines and osteophytes on articular margins are seen in early phase. • Irregular sclerosis along anatomic neck • Later atrophy of tuberosities and upward subluxation of humeral head • Acromioclavicular joint is also involved with irregularity. • These are prominence due to osteophytes. Bony ankylosis is an occasional feature and periosteal reaction may also be noted. Bouchard’s nodes and Heberden’s nodes are seen at proximal and distal interphalangeal joints respectively.

• CT scan: For extent of lesion. the points to be observed are site. 7 Osteolytic Bone Lesions Osteolytic lesions can be due to: • Non-neoplastic conditions • Benign neoplasm • Malignant neoplasm – Primary – Secondary Imaging Modalities to Study Lytic Lesions of Bones • Plain X-ray : Two views. matrix mineralization. LUCENT BONE LESION IN MEDULLA / WELL-DEFINED / NON- EXPANSILE / WITH SCLEROTIC MARGINS Suggest → Slow growth • Non-neoplastic Geode Brodie’s abscess Fibrous dysplasia • Healing benign/malignant bone lesions • Benign bone neoplasms Simple bone cyst Enchondroma Chondroblastoma GEODE = Subchondral cyst = synovial cyst = subarticular pseudocyst = necrotic pseudocyst. • MRI: For soft tissue extent and bone marrow involvement. • USG: High frequency probes are needed. bone expansion/ destruction. More sensitive and very early detection. at right angles. even before clinical/radiological evidence of lesion. soft tissue component and zone of transition.e. . periosteal reaction. soft tissue invasion. i. • Radio-nucleide: Bone scan – 99 mTc. AP/Lat for location. cortical break. margins.

often associated with joint narrowing Eburnation and collapse of bone BONE ABSCESS = Subacute localized pyogenic osteomyelitis (smoldering indolent infection) • Organism – most common Staphylococcus aureus • Age: common in children • Males more commonly affected than females. Polyostotic form (20-30%) . carpal. • Causes: Unknown? Gene mutation during embryogenesis • Age: 1st – 2nd decade (3-15 yrs) Disease progresses until growth ceases Sex: F>M Types A. Osteolytic Bone Lesions 79 • Etiology: Bone necrosis allows pressure induced intrusion of synovial fluid into subchondral bone seen in conditions with synovial inflammation. • Location: Predilection for cancellous tissue near ends of long bones proximal/ distal tibial metaphysis Metacarpal. Monostotic form (70-80%) Usually asymtomatic until 2nd –3rd decade B. known as TUNNELING – Periosteal new bone formation – Adjacent soft tissue swelling may or may not be present. osteonecrosis. hip • X-ray: Size usually 2 to 35 mm May be large and expansile In weight-bearing areas. RA. • Causes: OA. tarsal bones • X-ray appearance: Central area of lucency surrounded by dense rim of reactive sclerosis – Lucent channel-like/tortuous configuration extending towards the growth plate (PATHOGNOMIC). – May persist for many months • MRI: penumbra sign – Double line effect = high signal intensity of granulation tissue surrounded by low signal intensity of bone sclerosis in T2WI – Well-defined low to intermediate signal lesions outline by low signal on T1WI FIBROUS DYSPLASIA = LICHTENSTEIN – JAFFE DISEASE • Benign fibro-osseous developmental anomaly of osteoblastic differentiation and maturations. CPPD • Site: around knee.

pelvis. feet. inner table is spared – Obliteration of sphenoid and frontal sinus – Inferolateral displacement of orbit – Encroachment of orbital fissures . pathological fracture (75%) Abnormal veginal bleeding (25%) • Location: Unilateral and asymmetric Meta – diaphysis • Site: Femur. limp. skull and facial bones. upper extremity • Clinical features: – Leg length discrepancy – ‘Shepherds crook’ deformity – Facial asymmetry – Tibial bowing – Rib deformity C. spine. Cranofacial forms – LEONTIASIS OSSEA In 10-25 of Monostotic 50 percent of Polyostotic Isolated • Clinical features: – Cranial asymmetry – Facial deformity – Exophthalmos – Visual impairment • Location: facial bones • X-Ray appearances: – Unilateral over growth of facial and calvarial bones – Outward expansion of outer table with maintained convexity – Prominence of external occipital protuberance D. skull. Cherubism (special variant) AD with variable penetrance X-ray appearances: symmetrical involement of mandible and maxilla Site: metaphysis with extension into diaphysis • Usually unilateral/ asymmetrical X-ray Appearances • Radiolucent lesion in medullary cavity • Expansion of bones (ribs.80 Seminar in Radiology 2/3rd symptomatic by 1st decade C/F: leg pains. long bones) • Well-defined and smooth sclerotic margin of reactive bone = RIND OF ORANGE • Endosteal scalloping with cortical thinning • In skull– widened diploic space with displacement of outer table. tibia.

short stature – Bowing deformity and discrepancy of limb length – Shepherd’s crook deformity of neck of femur—coxavara – Premature onset of arthritis – Pathological fracture • Radionucleide Scan: Increased uptake by lesion SIMPLE BONE CYST Unicameral Bone Cyst = Solitary Bone Cyst Cyst filled with clear fluid under pressure. migrates to diaphysis with growth. calcaneum. small bones of hand Not in spine/calvaria Locaiton: Metaphysial—adjacent to epiphysis during active phase. Etiology: Trauma—synovial entrapment at capsular reflection Vascular anomaly blockage of interstitial drainages Age: 3-19 yrs (80%) occurs during active phase of bone growth M:F = 3:1 Clinical feature: asymptomatic Pathological fracture Site: Proximal femur/humerus (60-75%) Fibula. Bones preformed in cartilage are affected (not skull) Age: 10-30 yrs M:F = 1:1 Clinical features: • Usually asymptomatic • Painless swelling • Pathological fracture . the centrally displacement fragments fall into dependent portion Radionucleide Scan: Photopenic area with mild peripheral uptake Enchondroma: (If multiple – Enchondromatosis) = Benign cartilaginous growth in medullary cavity. ileum. Does not corss epiphysial plate X-ray Appearances • 2-3 cm oval lucency with its long axis parallel to long axis of bone • Fine sclerotic boundary • Scalloping and erosion of internal aspect of cortex • Fallen fragment sign: With fracture. Osteolytic Bone Lesions 81 • In pelvis and ribs – Cystic lesion – Protrusio acetabuli • In extremities – Premature fusion of ossificaiton center. rarely ribs. talus.

proximal. ulna.82 Seminar in Radiology Site: • Small bone of wrist and hand Distal and middle of metacarpals Proximal/middle phalanges • Femur. swelling. rings and arc pattern • Bulbus expansion of bone with cortical thinning • Madelung’s deformity—bowing deformity of limb with discrepancy of limb length • No cortical break/periosteal reaction CHONDROBLASTOMA = Codman tumor = cartilage containing GCT • Derived from primitive cartilage cells • Incidence 1 percent of primary bone neoplasms Age: Peak 2nd decade (10-26 yrs) M: F = 2:1 Clinical features: Mild joint pain. radius. subarticular location with open growth plate X-ray Appearances • Oval/round eccentric lytic lesion in epiphysis • 1-4 cm in diameter occupying less than ½ of epiphysis • Lobulated in 50 percent • Well-defined sclerotic margin . rib Locaiton: • Central and diaphyseal • Epiphysis only affected after closure of bone X-ray Appearances • Oval/ round lucency near epiphysis with fine marginal line • Scalloped endosteum • Ground glass appearance • Calcification—pin head. tibia. limitation of movement (may take months to year prior to diagnosis) Site: • Long bones (80%) Proximal femur and greater Trochanter Distal femur. proximal humerus 2/3 in lower extremity of which 50 percent above knee • Flat bones—near tri-radiate cartilage of innominate bone • Short tubular bones of hand/feet Location: Eccentric medullary. feet. tenderness. humerus. tibia. stippled.

Skull • 50 percent • Diploic space of parietal bone • Temporal bone Round/ovoid punched out lesions with serrated and beveiled edge of considerable size. Sharply marginated without sclerotic rim in active stage May have sclerotic margin during healing phase with slow reconstitution of bony structures. . thyroid • Multiple myeloma • Benign neoplasm Enchondroma Chondroblastoma EOSINOPHILIC GRANULOMA = Most benign type of histiocytsis-X Age: 5-10 yrs. • Hole within hole appearance—due to uneven involvements of inner and outer table • “Button sequestrum”—central bone density within lytic lesions • Overlying soft tissue mass. M : F = 3:2 Lesions arise within medullary canal of reticuloendothelial system— proliferation of histiosites and inflammatory cells. bronchus. Range = 2-30 years. kidney. Max. Site: Monostotic involvement in 50-75 percent Calvaria > Mandible > Long bones UL/ Ribs > Pelvis > Vertebrae If multiple – Then in different stages of evolution. Osteolytic Bone Lesions 83 • Punctate/irregular calcification • Intact cortical border • Thick periosteal reaction in metaphysis LUCENT BONE LESIONS IN MEDULLA / WELL-DEFINED/NO SCLEROSIS/NO EXPANSION = Absence of reaction bone formation = fast growth rate • Non-neoplastic • Eosinophilic granuloma • Brown tumor of hyperparathyroidism • Metastasis especially from breast. Eosinophils in blood and CSF.

ribs Metaphysis of long bone (femur) Facial bone Location: Often eccentric/cortical. Clinical feature: Tenderness and pain at the site of lesion “Bones. Frequently solitary .84 Seminar in Radiology Orbit • Benign focal mass +/. widening of medullary cavity • Cortical thinning. groans.infiltration of orbital bones Mastoid Process • Intractable otitis media with chronic ear discharge • Destructive lesion near mastoid antrum Jaw • Gingivial and surrounding soft time swelling • Floating teeth Axial Skeleton • Vertebra plana = “coin on edge” appearance = previously called as Calve’s disease (osteochondritis) Collapse of vertebral bodies—thoracic spine Preserved disc spaces Rare involvement of posterior elements No kyphosis Proximal Long Bones Painful bone lesion + swelling Mostly diaphyseal • Lytic lesion with ill-defined/sclerotic edge • Endosteal scalloping. psychic moans” Site: Jaw. intracortical tunneling • Erosion of cortex + soft tissue mass • Laminated periosteal reaction—may show interruption • May appear rapidly within 3 weeks • Lesion do not involve joint space and growth plate. BROWN TUMOR OF HYPERPARATHYROIDISM ≈ Osteoclastoma—a collection of osteoclasts Etiology: PTH stimulates osteoclastic activity—localised replacement of bone by vascularized fibrous tissue (Osteitis fibrosa cystica) Lesion becomes cystic following necrosis and liquifaction Frequent in primary hyperparathyroidism. stones. Rare. pelvis. 1.5 percent in secondary hyperparathyroidism.

lytic or well-marginated. proteinuria. Site: • Disseminated form Along normal sites of red bone marrow Axial skeleton Vertebra> Ribs> Skull > Pelvis > Long bone • Solitary form Vertebra> Pelvis> Skull > Sternum > Ribs • Spinal plasma cell myeloma – Sparing of posterior element – Paraspinal soft tissue mass with extradural extension – Scalloping of anterior margin of vertebral bodies (osseous pressure from adjacent enlarged lymph node) – Intervertebral disc and articular surfaces not affected. increased ESR. colon Multiple Myeloma Plasma cell infiltration of red bone marrow primary malignant neoplasm in adults Age: 40-60 yrs Rare < 30 yrs M:F = 2:1 Clinical features: Bone pain. pathological fracture Renal insufficiency. kidney. Bence Jones proteinuria Anemia. cystic lesion • Endosteal scalloping • Destruction of mid portions of distal phalanges with telescoping • Pathological fractures • Chondrocalcinosis Metastasis Metastatic lesion more common than primary bone neoplasm Osteolytic secondaries Causes • In childhood – neuroblastoma • Adult male – lung carcinoma • Adult female – breast carcinoma • Other site – thyroid. increased globulin production (monoclonal gammopathy) Hypercalcemia. Osteolytic Bone Lesions 85 X-ray Appearances • Expansile. .

edema LUCENT BONE LESION IN MEDULLA / WELL DEFINED/ECCENTRIC EXPANSION • Non-neoplastic • Benign neoplasm Non-ossifying fibroma and fibrous cortical defect Enchondroma Chondromyxoid fiobroma • Giant cell tumor Aneurysmal Bone Cyst (ABC) = Expansile lesions of bone containing thin-walled. Fluoride adminis- tration Poems Syndrome: Polyneuropathy Organomegaly—Liver. . Protein Skin change—Hirsutism. spleen Endocrinopathy—Diabetes mellitus M. Slow expansion of cortex • Extraosseous ABC—post-traumatic hemorrhagic cyst originating on surface of bone. sacrum) • Involvement of mandible (rare in secondary) • Skeletal form of multiple myeloma (1-3%) Solitary/diffuse Sclerosis may occur after chemotherapy (Radiotherapy). Pigmentation. Erosion through cortex into medulla. blood-filled cystic cavities Etiology: • Primary ABC (65-99%) Local circulatory disturbance as a result of trauma • Secondary ABC Arising in pre-existing bone tumor causing venous obstructive /arterio- venous fistula.86 Seminar in Radiology X-ray Appearance • In early stage—generalised osteoporosis with accentuation of trabecular pattern especially in spine. also post-fracture giant cell tumor Types • Intraosseous ABC—primary cystic/ telangiectatic tumor originating in bone marrow cavity rarely related to H/o trauma. • Punched out appearance of wide spread osteolytic areas with endosteal scalloping and uniform size in areas of red bone marrow • In skull—rain drop lesions • Diffuse osteolysis (pelvis.

Pathological fracture Site: Shaft of long bones. eccentric lucency. Multiple Fibroxanthoma: In 8-10 percent . • No perisosteal reaction (except when fracture) CT: Blood-filled. (10. fibula. pelvis X-ray Appearances • Purely lytic. Incidence = up to 40 percent of children > 2 yrs Etiology: Results from proliferative activity of a fibrous cortical defect that has expanded into the medullary cavity Age: 8-20 yrs. ± H/o trauma • Neurological sign if spine is also involved (from radiculopathy to quadriplegia) Site: Spine (12-30°) – with slight predilection for posterior elements Thoracic > Lumbar > Cervical Involvement of vertebral bodies May involve two contiguous vertebrae. • Long bones – eccentric . Clinical features: Usually asymptomatic.30 yrs) F>M Clinical features: • Pain of relatively acute onset with rapid increase in severity. metaphysis of femur. tibia. sponge-like with fluid—fluid level due to blood sedimentation MRI: • Multiple cysts of different signal intensity representing stages of blood byproducts • Low signal intensity rim = intact thickened periosteal membrane Radionucleide study: Dount sign = peripherally increased uptake Angiogram: Hypervascularity in lesion peripherally Non-Ossifying Fibroma Fibroxanthoma. Size : 2 – 20 cm • Aggressive expansile ballooning lesion or soap bubble pattern with thin internal trabe culation • Sclerotic inner portion • Almost invisible thin cortex – which is intact on CT • Epiphysial plate not envolved. mostly lower limb Especially about knee (distal femur and proximal tibia) Location: Eccentric metaphyseal region. humerus. Osteolytic Bone Lesions 87 Age: Peak 16 yrs.

88 Seminar in Radiology Associated with: Neurofibromatosis. Mostly before epiphysial closure Fibrous tissue from periosteum invades the underlying cortex. • Oval. ileum. lesion migrates towards diaphysis • Involvement over 2-4 yrs.overlying bulge of the cortex • Migrates towards center of diaphysis with skeletal maturity • Resolves with age • Minimum/mild uptake on bone scan Fibrous Cortical Defect Incidence = 30 percent of children M:F = 2:1 Age: Peak 7-8 yrs. fibula X-ray Appearances • Round when small. with sclerosis • Potential to grow and encroach on the medullary cavity leading to non- ossifying fibroma • Bone islands in adults may be the residues of incompletely involved cortical defects . V. Fibrous dysplasia Jaffi–Campenacci syndrome Non-ossifying fibroma with extraskeletal manifestation in children: • Mental retardation • Hypogonadism • Ocular defects • Congenital cardiovascular system defect • Café-au-lait spots X-ray Appearances • Multiocular ovoid bubbly osteolytic lesion • Aligned along long axis of bone approximately 2 cm in length • Dense sclerotic border towards medulla. ribs. extending parallel to long axis of bone • Cortical thinning and expansion • Smooth.or U-shaped at one end • Endosteal scalloping and thinning +/. average 1-2 cm. well-defined width sclerotic margin • Larger lesions are multiocular • With skeletal maturity. Clinical features: Asymptomatic Site: Metaphyseal cortex of long bones around knee Distal femur (postero-medially) Characteristic sites: Proximal tibia Proximal humerus. (2-10 yrs).

• Septations may mimic trabeculations • Stippled calcification within tumor in advanced (7%) stage • No periosteal reaction.7 cm in width) • Geographic bone destruction • Well-defined sclerotic overlying cortex • Bulged and thinned overlying cortex • Partial cortical erosions may / may not be present. Locaiton: Eccentric Metaphyseal 47-53% Metadiaphyseal 20-43% Metaepiphyseal 26% Diaphyseal 1-10% Epiphyseal 3% X-ray Appearances • Expansile void lesion with radiolucent center. along long axis of bone (1-10 cm length × 4 . distal femur > proximal tibia Upper limb away from elbow distal radius > proximal humerus . initially arising in cortex Incidence: < 1 percent of all bone tumors Composed of chondroid. mixoid and fibrous tissue in varying proportions Age: Peak 2-3rd decade (5-79 yrs. Arise after epiphyseal plate fusion M:F = 1:1 Clinical features: May be associated with Paget’s disease Local tenderness and pain Weakness and sensory deficit if in spine Site: • 85 percent in long bones In lower limb 50-60 percent about knee. Age: 20 – 40 yrs. Giant Cell Tumor = Osteoclastoma → probably arise from zone of intense osteoclastic activity in patient with mature skeleton. restricted movement Site: Long bones. ribs. swelling.2 percent of all primary bone tumors. Incidence: 4.) M:F = 1:1 Clinical features: Slowly progressive local pains. about knee joint 50 percent proximal tibia – distal femur Short-tubular bones of hand and feet 20 percent Flat bones—pelvis. Osteolytic Bone Lesions 89 CHONDROMYXOID FIRBROMA Rare benign cartilaginous tumor.

pheochromocytoma Plasmacytoma Central chondrosacroma Lymphoma of bone Fibrosarcoma Telangiectatic osteosacrcoma • Benign bone neoplasm ABC GCT Enchondroma • Non-neoplastic Fibrous dyplasia Hemophilic pseudotumor . Bronchus. hemorrhage) well-defined margin ± thin rim of sclerosis. Ribs. less commonly melanoma.90 Seminar in Radiology • 15 percent in flat bones Pelvis. • Crosses sacroiliac joint.Donut sign of central photopenia Angiography: Hypervascular lesion CT: Tumor of soft tissue attenuation with foci of low attenuation (necrosis. brest.5 percent are multifocal—in hand. Skull • 0. rarely may cross joint space in long bones Radionucleide study: Diffusely increased Uptake +/. thyroid. MRI: Heterogeneous signal intensity with low to intermediate intensity of T1 and T2 WI due to collagen and hemosidrein content Focal cystic areas. sacrum near sacroiliac joint > Thoracic > Cervical > Lumber. LUCENT BONE LESION /GROSSLY EXPANSILE • Malignant neoplasms Metastasis from renal cell carcinoma. Facial bones spread Location: Eccentric in metaphysis adjacent to articular cortex X-ray Appearances • Expansile solitary lytic lesion with “soap bubble” like trabeculation Conspicuous peripheral trabeculation without matrix/calcification • No sclerosis/periosteal reaction in absence of fracture • May break through bone cortex with cortical thinning Soft tissue invasions (25%) Pathological fracture • Destruction of vertebral body with secondary invasion of posterior elements – vertebral collapse • Involves adjacent vertebre and their discs spaces.

spine.P. Central Chondrosarcoma = Endosteal chondrosarcoma Incidence: 3rd most common primary bone tumor (1st – Multiple Myeloma. pubic rami. 2nd – Osteocarcoma) Arises from chondroblast Age: ≈ 45 yrs. sternum. ribs. Humerus X-ray Appearances • Solitary. mandible). Osteolytic Bone Lesions 91 Brown tumor of hyperparathyroidism Hydatid cyst Coccidiodomycosis Atypical Mycobacterium Cystic tuberculosis Brodies abscess Metastasis Grossly expansile metastasis RCC Thyroid Plasmacytoma Solitary myeloma of bone • Represents early stage of multiple myeloma • Localised destructive lesion in skeleton in region of RBM Age: 3rd to 7th decade Clinical features: Frequently asymptomatic Negative marrow aspirate No IgG spike in serum/urine Location: Thoracic/ Lumbar spine metacarpals Pelvis > Ribs > Sternum. • Poorly-defined margins without sclerosis • Swiss cheese pattern or soap bubble appearance • Pathological fractures frequent—collapse of vertebra. C. 10 percent occur in children M:F = 2:1 Clinical features: Hypercalcaemia as paraneoplastic syndrome (85%) Site: Neck of femur. skull (sphenoid. . proximal humerus. Femur. angle. grossly expansile osteolytic lesion with thinning of overlying cortex and internal trabeculations.

X-ray Appearances • Cancellous bone erosion (earliest sign) • Mottled permeative pattern of separate coalescent areas • Cortical destruction is late • Laminated/sunburst periosteal reaction (less than in Ewing’s) • Lytic/reactive new bone formation • Associated soft tissue mass without calcification • Synovitis of knee joint common • Pathological fracture and collapse of vertebra with anterior erosion. fibrous dysplasia . GCT. scapula.seclerotic margin which is well defined from host bone • +/. and vertebra Location: Dia-metaphysical 2/3rd sclerotic. ribs. FIBROSARCOMA Incidence = 40 percent of all primary bone tumor Etiology: • Primary fibrosarcoma 70 percent • Secondary fibrosarcoma 30 percent • Following RT for GCT/Lymphoma/Breast Cancer • Underlying bening lesions: Paget’s disease.small irregular punctate / snow flake calcification • In late cases – loss of definition and break through cortex • Endosteal cortical thickening • Presence of large soft tissue mass Lymphoma of Bone = Reticulum cell sarcoma = Histocytic lymphoma Incidence = 2-6 percent of all primary bone tumor in children In Hodgkin’s – 5-15 percent bone involvement In NHL – 25-40 percent Age: Any age. bone infactrs. 1/3 lytic. sclerotic lesion does not cause enlargement of bone. upper tibia. osteomyelitis Enchondroma. in diameter • Short transition zone +/. humerus. pelvis. Peak 3rd – 5th decade M: F = 2:1 Site: 40 percent above knee joint – Lower femur.92 Seminar in Radiology Location: Central in meta/diaphysis X-ray Appearances • Expansile osteolytic lesion one to several cms.

) M:F = 3:2 Sarcoma of bone with large blood-filled vascular channels Site: About knee 62% distal femur. spine Location: Eccentric at diaphyseal and metaphyseal junction: Intramedullary—Central type Periosteal—Parosteal type Central Type (More Common) • Well-defined with thin expanded cortex to aggressive osteolysis with geographic / permeative bone destruction and wide zone of transition • Intramedullary discontinuous spread • No calcification • Periosteal reaction uncommon and sparse. (3-67 yrs. Pelvis Rare in small bone of hands feet. Periosteal Type • Contour irregularity of cortical border • Periosteal reaction with perpendicular bone formation • Rarely may extend into medullary cavity Telangiectatic Osteosarcoma = Malignant bone aneurysm Frequency = 4-11 percent of all osteosarcoma Age: = Average 20 yrs. flat bone in older Femur tibia – about knee joint (80%). X-ray Appearances • Geographic bone destruction with wide zone of transition. Osteolytic Bone Lesions 93 Age: Predominant by 3rd – 6th decade M:F = 1:1 Clinical features: Metastases to lung. Jaw. proximal humerus Location: Metaphysis with extension into epiphysis. proximal tibia. lymph node Localized painful mass Tubular bone in young. . Bone scan: Donut sign = peripheral increased uptake with central osteopenia HEMOPHILIC PSEUDOTUMOR = Posthemorrhage cystic swelling within muscles and bones characterized by pressure necrosis and destruction due to subperiosteal bleeding. • Marked aneurysmal bone expansion • Fluid-filled levels • Nodular calcific foci of osteoid.

(Before epiphyseal closure).94 Seminar in Radiology • Juvenile form – usually multiple intramedullary expansile lesions without soft tissue mass in small bones of hand and feet. joints and periarticular structures. • Adult form – usually single intramedullary expansile lesion with large soft tissue mass in ileum/ femur. X-ray Appearances • Mixed cystic expansile lesion. medial end of clavicle. wrists. Bones—metaphysis of long bones. dog intermediate host. elbow. spine. HYDATID CYST = Echinococcus granulosus. • Bone erosion and pathological fracture • Hemophilic arthropathy • Synovial thickening and articular erosion. patella b. ankle. bearing joints—knee. Cystic Tuberculosis Well-marginated lytic lesion . osteopenia. • Destruction of vertebra with preserved disc space • Mono articular joint infection—Synoivial effusion. joint space narrowing destruction and ankylosis. Clinical features: X-ray Appearances COCCIDIODOMYCOSIS Chronic granulomatous lesion by fungi in bones. Wt. MRI: Hemorrhage of varying age. pelvis. initially marginal only • Periarticular osteoporosis (disuse and hyperemia) • Enlargement of growing epiphysis • Premature development of secondary degenerative changes. • Sclerosis surrounding osteolysis rare and late. Multiloculated cysts in bone adjacent soft tissue. X-ray Appearances • Focal areas of destruction and cavity formation = bubbly bone lesion. (Desert rheumatism). Site: a. • Proliferation of overlying periosteum. ribs. CT: Encapsulated mass lesion containing areas of low attenuation and calcification. Sheep definitive host.

• Lung infections • Dermal infection: direct spread from soft tissue lesion in diabetic foot. E. LUCENT BONE LESION IN MEDULLA/ILL-DEFINED = An aggressive pattern of destruction • Non-neoplastic – Osteomyelitis • Metastasis • Malignant lesions – Multiple myeloma – Lymphoma of bone – Long bone sarcomas  Osteosarcoma  Ewing’s Sarcoma  Central chondrosarcoma  Fibrosarcoma  Malignant fibrous histiocytoma Osteomyelitis Acute osteomyelitis Age: Children Organism: New born .. Children – S aureus M/C Adults – S aureus (60%) Enteric Op. • Direct implantation from traumatic/Iatrogenic source • Extension from adjacent soft tissue infection. Pathogenesis • Hematogenous spread most common. Osteolytic Bone Lesions 95 a. Staphylococcus aureus. In children frequent – in peripheral skeleton Symmetric distribution No sclerosis b. coli.Salmonella. Klebsiella. In adult – in skull/shoulder/ pelvis/ spine with sclerosis. Drug addicts – Pseudomonas (86%). Causes • Genitourinary tract infection most commonly. Streptococcus.Over pressure points in diabetics Vertebra-Lumbar > Thoracic > Cervical. Clinical features: Leukocytosis + fever Pathological fracture . Sickle cell disease .Group B Streptococcus. Site: Lower extremity 75 percent . Entrobacters.

• Serpigenous tracts with small sclerotic rim (Pathognomonic). d. c. – Joint involvement common. – Frequent joint involvement. – Subperiosteal abscess with extensive periosteal new bone formation therefore Periosteum loosely attached. Acute Osteomyelitis in Adults – Delicate periosteal new bone. – Little no systemic disturbance. • Sequestrum – detached devitalized necrotic cortical bone (>30 days). • Shortening of bone with destruction of epiphyseal cartilage. X-ray Appearances • Sequestration is frequent. Abscess formation in medulla with cortical spread. . – Spread to epiphysis because transepiphysel vessels cross growth plate into epiphysis.96 Seminar in Radiology a. • Periosteal elevation (with disruption of periosteal blood supply) • Small single/ multiple osteolytic areas in metaphysics. Acute Osteomyelitis in Childhood – Age : 2-16 years – Transepiphyseal vessels closed : Metaphyseal vessels forms ‘hair pin like’ bend near growth plate – Primary focus of infection locked in metaphysis. b. Acute Osteomyelitis in Infancy – Age < 18 months. • Area of bone destruction (>7-14 days)/ osteoporosis. • Involvement – Cloak of laminated/speculated periosteal reaction (>21 days). • Cloacae formation – space in which dead bone resides. X-ray Appearances • Radiogrpahic appearance is often normal in initial phase (< 10 days) • Localized soft tissue swelling adjacent to metaphysis with obliteration of fat plans ( >3-10 days). • Mid-shaft involvement less frequent. Acute Neonatal Osteomyelitis – Age Onset < 30 days of age. • Growth stimulation—by hyperemia and premature maturation of adjacent epiphysis. – Multicentric involvement more common. • Extensive periosteal reaction parallell to shaft (3-6 weeks) may be lamellar or nodular. • Joint infection again common because metaphyseal and epiphyseal vessels again connected. joints often involved. – Extensive soft tissue component.

Incidence = 15 percent of all bone tumors confirmed at biopsy. • Hyperintense halo surrounding cortex on T2WI – subperiosteal inflam- mation. Osteolytic Bone Lesions 97 CT: Dense bone fragments within area of bone destruction. chronic draining science. Types 1. – Hyperintense adjacent soft tissues on T2WI. • Image related to local blood and bone turnover. (Sequestrum). . Radionuclide Scanning Early diagnosis by 48 hours. elevated periosteum. Tc 99m labeled phosphonate and phosphate compound. • Focal /lineal cortical involvement – hyperintense on T2WI. Infant Children Adult Location Metaphysis . Chronic Osteomyelitis • Thick irregular sclerotic bone with radiolucencies. Primary Osteosarcoma – High grade intramedullary = central osteosarcoma = most common – Telangiectatic – Malignant bone aneurysm.Epiphysis Metaphysis Epiphysis Involucrum Common Common Not common Sequestrum Common Common Not common Joint involvement Common Not common Common Soft tissue abscess Common Common Not common Pathological fractures Not common Not common Common Fistulae Not common Variable Common OSTEOSARCOMA Second most common primary bone tumor (1st = multiple mycoma) derived from undifferentiated connective tissue and forms neoplastic osteoid. • Hyperintense line on T2WI extending from bone to skin surface and enhancement of borders-sinus tract. – Hyperintense fluid collection by hypointense pseudocapsule on T2WI and contrast enhancement of granulation tissue. • Abscess characteristics – Hyperintense rim (hyperemic zone) around a central low-intensity (=necrotic tissue) on CET1WI. MRI: • Bone marrow hypointense on T1WI and hyperintense on T2WI = water rich inflammatory tissue.

Bimodal distribution 10-25 years (70%0 and >60 years) related to previous conditions M:F . – Small cell. – Osteosarcomatosis–Multifocal osteosarcoma. – High grade surface. – Paget’s diseases (67-90%) – Sequele to irradiation – 2-40 years after related exposure dose (>1000 CGY).98 Seminar in Radiology – Low grade intraosseous lesion. • Sclerotic/Lytic/Mixed .5-7 percent occurs in spine. Surface/juxtacortical osteosarcoma. 4. fibrous dysplasia. osteonecrosis. Site: Long bones – 50-55 percent about knee . Location: Metaphysis (90-95%) Diaphysis/Epiphysis Doubling time = 20-30 days Three basic pattern- Sclerotic – 50% Purely lytic – 25% Mixed – 25% X-ray Appearances • Usually large bone lesion > 5-6 cm. – Per Osteal – origin from outer layer of periosteum.Femur/Tibia Proximal humerus 3. – Periosteal – from deep layer of periosteum. Central Osteosarcoma Arising from undifferentiated mesenchymal tissue forming neoplastic osteoid.2:1 Clinical features: • Painful swelling (1-2 months duration) • Fever • Slightly elevated alkaline phosphatase • Paraneoplastic syndrome in 25 percent – diabetes mellitus • Features of metastatic disease – lungs – multiple canon ball. – Chronic osteomyelitis. – Gnathic – Osteosarcoma of jaws. Secondary Osteosarcoma – Malignant transformation in benign process. 3. Extra skeletal – Localized within soft tissue without attachment to bone/ periosteum. Age . – Intra cortical. 2.

Radionuclide Scan • Intensely increased activity. Primitive primary malignant bone tumor derived from the connective issue framework of bone marrow. leukocytosis. • Cortical destruction – increased on T2WI. • Marrow involvement – decreased on T1WI. Location: Diaphyseal/Metadiaphyseal Usually no involvement of epiphysis as tumor originates in medullary cavity with invasion of Haversian system. Age: Peak =15 years. secondary anemia Site: Long bone 50 percent – Femur. Flat bones 40 percent – Pelvis. M:F = 2:1 Caucasians: 96 percent Clinical features: • Severe local pain • Soft tissue mass • Fever. Osteolytic Bone Lesions 99 • Aggressive periosteal reaction – Sun ray/Sun burst type often Codmans reactive triangle present. fibula. tibia. • Soft tissue extension demonstrated especially by SPECT. 95 percent between 4-25 yrs. • Transepiphyseal spread before plate closure. . ribs. humerus. • Low attenuation (high water content of chondroblastic component / hemorrhage/ necrosis) • High attenuation (mineralized matrix) MRI: • Tumor of intermediate intensity signal on T1WI and high intensity signal on T2WI. CT: • Soft tissue attenuation (non-mineralized portion) replacing fatty bone marrow. Ewing’s Sarcoma Incidence = 4-10 percent of all bone tumors. scapula. • Cortical disruption and soft tissue mass with tumor new bone formation. Most common malignant bone tumor in children. • Osteosclerotic zone – decreased on T1 and T2WI.

• Cortical thickening / destruction ± cortical sequestration. • Early fusiform laminated “onion skin” periosteal reaction. • Usually arises in association with another pre-existing benign bone disorder (therefore previously known as secondary firbosarcoma). • Penetration into soft tissues with preservation of tissue planes. chronic osteomyelitis. tibia. pelvis Location: Metaphysis can extend to diaphysis and some times to epiphysis. Bone scan: Increase tracer uptake around periphery CT: • Intraosseous/extraosseous extent of tumor • Relationship to major nerves and vessels. M:F = 1. 15% sclerotic). X-ray Appearances • Eccentric lytic lesion with cortical thinning. (62% lytic. 23% mixed. • In rib-disproportionately large inhomogeneous soft tissue mass with large intrathoracic and minimal extrathoracic component. humerus. e.g. . bone infarcts. • Moth eaten/permeative destruction with wide zone of transition. MRI: Marrow involvement ↑T2 ↓T1 Necrosis/cyst formation ↑T2 ↓T1 Hemorrhage ↑T2 ↓T1 Malignant Fibrous Hystiocytosis • Contain both histocytic and fibroblastic cells. • Cortical disruption. • No matrix calcification. • Destructive permeative lesion (with wide zone of transition). • Large soft tissue mass. uncommonly speculated “sun burst” type/ Codman’s triangle. Paget’s disease. Age: 30-60 yrs. enchondroma. previous radiation.5:1 Site: Distal femur. Clinical features: Painful swelling. therapy.100 Seminar in Radiology X-ray Appearances • 8-10 cm long lytic lesion in shaft of long bone.

Osteolytic Bone Lesions 101 MRI: Firbrous tissue—Intermediate intensity signal on T2WI Necrosis/hemorrhage—Increased on T2WI and decreases on T1WI. variable size lucencies. Neoplastic • Metastasis—including neuroblastoma in children. • Leukemia. • Cancellous and/or cortical bone involved. • Coalescence may occur. • Long bone sarcomas – Ewing’s sarcoma – Lymphoma of bone – Osteosarcoma – Chondrosarcoma – Fibrous sarcoma – Malignant fibrous histocytoma – Langerhans cell histocytosis Infective • Osteomyelitis OSTEOLYTIC LESION/POORLY DEMARCATED/ WITHOUT PERIOSTEAL REACTION OSTEOLYTIC LESIONS/POORLY DEMARCATED/ PERIOSTEAL REACTION • Osteomyelitis • Ewing’s sarcoma • Multiple myeloma . • Multiple myeloma. Moth Eaten Bone = Multiple Lytic Lesion • Multiple scattered.

.Rodent ulcer Hystocytoma .102 Seminar in Radiology Lucent Bone Lesion Unilocular Multilocular – Non-neoplastic • Simple unicameral bone cyst – GCT • ABC – ABC • Brown tumor of hyperparathyroidism – Fibrous dysplasia • Eosinophilic granuloma – Simple bone cyst • Post-traumatic/degeneration cyst • Pseudo-tumor of hemophilia • Intraosseous ganglion • Arthritic lesion • Endosteal pigmented villonodular synovites • Fibrous dysplasia • Infective lesions – Benign neoplasm • Fibrous cortical defect • Non-ossifying fibroma • GCT • Enchondroma • Histocytoma Lucent Lesion in Skull Vault Without Sclerosis With Sclerosis a. . Adults – Fibrous dysplasia • Neoplastic – Developmental – Multiple myeloma Epidermoid – Metastasis Meningocele – Hemangiomas – Neoplastic – Neurofibomatosis Hemangioma – Adjacent malignancy Langerhans’ cell- .Ca of ear – Infective – Paget’s sarcoma Chronic osteomyelitis • Traumatic Frontal sinus mucocele – Burr hole/Trephine – Leptomeningeal cyst • Idiopathic – Osteoporosis circumscripta Contd..

Vertebrae: 28 percent of all osseous haemangioma. F>M Site: Lower thoracic /upper lumber spine. Children • Neoplastic – Metastasis – Langerhans’ cell histocytosis Eosinophilic granuloma Hand Schuller Christian syndrome • Traumatic – Leptomeningeal cyst – Burr hole • Miscellaneous – Parietal foramina – Venous lakes – Benign neoplasm • Fibrous cortical defect • Non-ossifying fibroma • GCT • Enchondroma • Histocytoma Osseous Hemangiomas Mostly cavernous. .. Capillary Haemangioma Age: > 40 yrs. Osteolytic Bone Lesions 103 Contd. capillary type is rare Age: = 4-5th decade M:F = 2:1 Clinical features: Usually asymptomatic • Cavernous—20 percent of all hemangiomas Site: Frontal/Parietal region Location: Diploe X-ray Appearances • < 40 cm round osteolytic lesion • Sunburst /web-like appearance of trabecular thickening • Expansion of outer table > inner table producing a palpable lump. • Metabolic – Brown tumor of hyperparathyroidism · • Infective – TB osteomyelitis – Pyogenic osteomyelitis – Hydatid – Syphilis b..

CT: “Polka-dot” appearance with small punctate areas of sclerosed thickened vertical thickened vertical trabeculae. • CSF density cyst adjacent to/ in skull. • Bulging of posterior cortex. mandible.104 Seminar in Radiology X-ray Appearances • Coarse vertical trabeculae with osseous reinforcement adjacent to bone reabsorption caused by vascular channels. metaphyseal ends of long bones. clavicle. Leptomeningeal Cyst = Growing Fracture • Seen in 1 percent of pediatrics skull fracture. • Paravertebral soft tissue extension. zygoma. *Flat bones and long bones: Rare Ribs. Age = <3 yrs. may contain cerebral tissues. Lucent/Cystic Lesion Jaw • Dental – Peridontal/ Radicular/ Periapical cyst – Dentigerous cyst • Developmental/ Fissural cyst – Nasopalatine duct cyst/ Incisive canal cyst – Globulomaxillary cyst – Nasolabial cyst • Neoplastic – Ameloblastoma – GCT – Hemangioma – Metastasis . nasal bones. MRI: • Cyst isointense with CSF and communicating with subarchnoid space • Area of encephalomalacia underlying fracture • Intracranial tissue extending between fracture edges. MRI: Mottled pattern of low to high intensity on T1WI = very high intensity on T2WI. • Skull fracture—dural tear—arachnoid herniation into dural defect and CSF pulsation causes fracture diastasis and erosion of fracture margin. apparent 2-3 months after injury. X-ray Appearances • Skull defect with indistinct scalloped margins. • Extraosseous extension beyond bone lesion—cord compression.

posterior mandible. Site: Maxilla (may expand into maxillary sinus). Osteolytic Bone Lesions 105 • Langerhans’ cell histocytosis • Brown tumor of hyperparathyrodism • ABC • Simple bone cyst • Fibrous dysplasia Radicular Cyst Etiology: Deep carious lesion. maxilla 25 percent in region of bicuspids molars (therefore angle of mandible most common) X-ray Appearances • Uni/ multilocular lytic lesion with scalloped margin cortical expansion. • 1/3rd arise from dentigerous cyst. trauma. Ameloblastoma = Adamantinoma of jaw • Locally aggressive lesion from enamel type epithelial tissue elements around tooth. Site: Intimately associated with apex of non-vital tooth. Dentigerous Cyst • Epithelial lined cyst arising from odontogenic epithelium. developing around unerupted tooth. Age: 4-5th decade M:F = 1:1 Site: Mandible 75 percent. deep filling. • May be associated with impacted tooth/ resorption of the root of the tooth. Expansile Rib Lesions • Fibrous dysplasia • Eosinophilic granuloma • Enchondroma • Lymphoma • TB • Hematopoiesis • Ewing’s sarcoma • Chondromyxoid fibroma • Leukemia . X-ray: Apical lucency. X-ray: Cystic expansile lesion containing tooth.

Glomus body . .106 Seminar in Radiology • ABC • Metastasis • Plasmacytoma Lucent Lesions of Fingers • Benign neoplasm – GCT – ABC – Glomus tumor – Osteoblastoma – Enchondroma • Malignant neoplasm – Osteosarcoma – Fibrosarcoma – Metastatic – Multiple mychoma • Non-neoplastic – Brown tumor – Hemophilic pseudotumor – Epidermoid inclusion cyst – Geodes – Osteomyelitis – Fibrous dysplasia Glomus Tumor = Hamatroma composed of cells derived from neuromyoarterial apparatus (regulating blood flow in skin).encapsulated oval organ of ≈ 300 mm length. • Located in reticular dermis (=deepest layer of skin) • Concentrated in tips of digits • Composed of an afferent arteriole. Incidence: 1-5 percent of soft tissue tumors of hand Age: 4-5th decade Clinical features: • Joint tenderness and stabbing pain (≈ years prior to diagnosis) and sensitivity to cold • Love test : eliciting pain by applying precise pressure with a pencil tip.Hoyer canal lined by endothelium and surrounded by smooth muscle fibers). an anastomiotic vessel (= Sucquet . • Hildreth sign : disappearance of pain after application tourniquet proximally on area (= pathognomonic). a primary collecting vein.

scaphoid. (range 6-30 yrs. = rare benign tumor with unlimited growth potential and capability of malignant transformation Incidence: Age: Peak 15-20 yrs. worse at night. Site: • Spine: max is posterior element with extension into vertebral body C > T> L> Sacrum • Long bones: femur.) M : F = 2:1 Lesions: > 1. Subungual Glomus Tumor X-ray: Increased distance between dorsum of phalanx and under side of nail. smaller lesion known as osteoid osteoma Clinical features: • Dull localized pain of insidious onset. Extrinsic pressure erosion sharply marginated with sclerotic border. metacarpals.5 cm. paraparesis • Paraplegia (due to cord compression). tenderness. dorsal talus neck. decreased range of mobility • Asymptomatic rarely • Painful scoliosis (if located in ribs/ spine) due to muscles spasm • Parasthesia. USG: small hypoechoic tumor (>3 mm detectable) MRI: homogeneously high SI on T2WI (detectable if >2 mm) Angiogrpahy: Rich vascular tumor B. Glomus Tumor of Bone: Occasionally within bone • Resembles enchondroma Osteoblastoma = Giant osteoid osteoma = ossifying fibroma. • Response to salicylates • Localized swelling. fibula • Small bones of hand and feet. often of the terminal phalanx especially subungual portions.reactive sclerosis . humerus. mild muscle weakness.stippled/ small flecks of matrix calcification +/. tibia. may be periosteal X-ray Appearances • Radiolucent nidus > 2 cm size (2-12 cm) • Demarcated +/. metatarsals • Calvarium and mandible (=cementoblastoma) Location: Diaphyseal > metaphyseal Eccentric > centric Intracortical. Osteolytic Bone Lesions 107 Types A. radius.

108 Seminar in Radiology • Progressively expansile lesions—may rapidly increase in size. • Scoliosis • Osteoporosis due to disuse • Rapid calcification after radiotherapy. . thin osseous shell. thin shell of periosteal new bone.4th decade M>F Clinical featuers: • H/O skin penetrating trauma—implantation of epithelium under skin with secondary bone erosion • May be asymptomatic Location: superficially situated bones—calvarium. Nuclear scan: Intense focal uptake Angiography: Capillary tumor blush MRI: • Low to intermediate signal intensity on T1WI • Mixed intermediate to high on T2WI • Surrounding edema Epiderml Inclusion Cyst = Intraosseous keratin cyst = implantation cyst Age: 2nd. CT: • Multifocal matrix mineralization. cortical expansion/ destruction. phalanx (L>R hand) X-ray Appearances • Well-defined rounded osteolysis with sclerotic margins • Cortex expanded and thinned • No calcification/periosteal skin/soft tissue component • Pathological fracture often without periosteal skin. sclerosis • Expansile bone remodeling. sharply defined soft tissue component.

forming woven or lamellar bone. Apart from these histological bone types there are two grossly-visible types and can also be seen radiologically. nutritional status.e. 75 percent being formed by the cortical bone. has more Ca++ and cells with isotropic tensile property. Its basic structure comprises of a framework of ground substance consisting predominantly type I collagen called as osteoid matrix. Metabolism and Basic Structure Bone is a living tissue which is quite active metabolically. The medullary cavity predominantly has the trabecular bone white cortex is made up of compact bone. i. The bone turnover is much more at trabecular bone as compared to cortical bone. 10-18 percent of bone is turned over per year and trabecular bone exchange rate is @20 percent per year while cortical bone exchange rate is @4 percent per year.e. Woven bone is found at sites of active growth. Two . osteonection. Lamillar bone on the other hand has anisotropic property and is much stronger. sex. it has much more free surface area. It receives and returns approximately 200-400 ml blood/min to general circulation. site. Trabecular exchange is only at the surface while it is throughout in cortical bone. Depending upon age. proteoglycan and albumin.× (H3O)+2× (PO4-3)6]. and hydroxy- apatite crystals laid down upon the osteoid. osteocalcin. osteopontin. Collagens are laid down in woven (coarse fibered) or lamellar fashions. fibronectine sialoprotein. though trabecular bone constitute only 25 percent of bone. 8 Metabolic Bone Diseases Bone has three functions: • Mechanical • Metabolic • Hemopoitic Bone Physiology. It is found in mature skeleton. This collagen consists of a triple helix (2α1 + 1α2): also present in Ostoid are MGP and BGP having γ-carboxylic acid (γ-carboxylatin being accomplished by vitamin K). Trabecular or spongy or cancellous bone and cortical or compact bone are called as integral bone. etc. i. each measuring 20 nm × 6-7 nm [Ca++10.

Due to decreased osteoclast activity: • Calcitonin • Oestrogen via IL-6 • PGE2 • IFN-α (Interferon-α) • TGF-β (Tissue growth factor-β) Bone Destruction 1. Decreased Osteoblast • Corticosteroid . T4 • 1. Increased Osteoclast • IL-6 • IL-11 • IL 25DHD3 • PTH 2. 2. • IL-1 (Interleukin-I) • Growth hormone • Oestrogen • IGF-I (Insulin-like growth factor-I) • PGE2 (Prostaglandin E2) • TNF (Tissue necrosis factor). 25-Dihydrocholecalciferol). Osteoblasts Osteoblasts are the bone forming cells that line the bone surface and lay the osteoid. Due to increased osteoblast activity: • Parathyroid hormone • T3. physiology and embryology. It releases mineral from matrix and also dissolves the matrix. These finally turn to osteocytes when ample ground substance has been layed down. Bone Formation 1. Osteoclasts Osteoclasts are bone reabsorbing cells that are also found lining the surface forming sites called Howships lacunae. B.110 Seminar in Radiology cell types must be mentioned in relation to bone anatomy. • Both these cells function in a tanden osteoblasis starting within 2 weeks of osteoclasis and persisting upto 3 months. A. 25 DHD3 (1.

25 DHD3 ↑Ca ↓P ↑Ca absorption ↑ release of Ca Calcitonin ↑Ca ↓P ↓ excretion of Ca+ ↓ release of Ca Summarizing all these facts two conclusions are drawn: a. . b.g. cushing Bone Reabsorption 1. Bone cell function. Collagen framework. rickets 3. Osteofibrosa (mixed) Certain Terminologies are Considered Here 1. b. the phenomenon of normal bone formation and destruction are altered and hence radiological observations are either: a. e.g. Metabolic Bone Diseases 111 Blood Kidney Gut Bone PTH ↑Ca ↓P ↑PO4 excretion ↑ release of Ca ↑Ca absorption 1. Trabecular Classification of Metabolic Bone Disease • Metabolic bone disease in which there is altered bone metabolism. Alternation in bone structure is referred to as metabolic bone disease. Bone mineralization. It can be at the level of 1.e. Osteomalacia → osteoid > Ca iii. i.g. e. scurvy 2. 2. Intracortical 4. i. Endosteal 3.g. Osteoporosis (also known as osteopenia) → ratio of osteoid to Ca++ is normal ii. Osteoporosis – Bone quality is normal. Demineralization – Loss of mineral (halesteresis). Subperiosteal 2. e. Bone mass. Decreased bone density which again may be localized or generalized. idiopathic osteoporosis 4. e. Osteosclerosis (increased bone density) which may be localized or generalized. quantity is decreased.

Hypoparathyroid. 5. Regional migratory 5. Cushing disease 3.112 Seminar in Radiology 3. Osteoporosis 2. Pseudo and Pseudo-Pseudohypoparathyroidism 15. Juvenile idiopathic osteoporosis 12. Hyperpitutiarism 9. Gout 16. Sudeck’s 3. Disuse 2. Fluorosis 3. Osteomalacia 4. Pseudo and Pseudo-Pseudohypoparathyroidism. Hypogonadism 14. Pseudogout 17. Osteopenia – General/local decreased bone. Infections Generalized Increased Bone Density 1. 4. Deossification – Normal rate but increased resorption. Idiopathic chondrolysis 6. Scurvy 8. Primary ostolysis: Gorham’s disease. Hyperphosphatasia 13. 2. Transient 4. Undermineralization – Decreased deposition (Osteomalacia). Arthritides 8. Primary hyperparathyroidism 7. Generalized Decreased Bone Density 1. Osteogenesis imperfecta 11. Rickets 5. Carpotarsal syndrome 7. Hyperthyroidism/hypoparathyroidism 10. Hypervitaminois A and D Localized Increased Bone Density . Renal osteodystrophy 6. Oxalosis 18. Alkaptonuria Localized Decreased Bone Density 1. Neuromuscular disorders 9.

• Cortical thinning and prominence (Penciling in or picture frame). Fracture at hip and vertebra. humerus. Metabolic Bone Diseases 113 1. Drugs and others → Steroid. immunosuppressant d. alcohol. . Secondary Osteoporosis: a. hepatic insufficiency. Senile osteoporosis starts early in women and proceeds @ 3-20 percent per year. Chronic diseases → CRF. Type I (Postmenopausal) Especially trabecular bone loss Colle’s fracture and crush fracture of vertebra Type II (Senile) Both compact and trabecular bone loss Age > 75 years. malabsorption. Primary Osteoporosis • Involutional → Postmenopausal (Type I) → Senile (Type II) • Juvenile • Osteogenesis imperfecta 2. Thyroid acropachy 3. tibia. chronic inflammatory bowel disease Involutional osteoporosis is the most common metabolic bone disorder and may be due to postmenopausal state or senile. Radiological Features When > 30 percent bone lost • Decreased bone density especially at axial skeleton. Endocrine → Cushing’s disease: Addison’s disease → Hypogonadism : Postmenopausal → Acromegaly : Hypopituitarism → Diabetes mellitus → Hyperthyroidism : hypothyroidism → Hyperparathyroidism b. hepartin. Marrow expansion and replacement → Myeloma → Lymphoma → Leukaemia → Secondary deposits → Gaucher’s disease → Anaemias c. Hypervitaminosis A IMPORTANT FEATURES OF METABOLIC BONE DISEASES Osteoporosis Group 1. Heavy metal poisoning 2.

• Decreased skeletal maturation. etc. wrist.)—diagnosed by CT Scan. • Insufficiency fracture (sacrum. Primary 2. septic arthritis. vertebral index. • Rib fracture common • Mottled skull • Osteonecrosis especially in exogenous Cushings. • Fracture at non spinal sites (hip. Hyperparathyroidism In Osteofibrosa Group 1. Exogenous and Endogenous Cushing Disease • Pathological osteopenia • Exuberant callus with sclerosed vertebral end plates. • Diagnosis by exclusion of lymphoma. • Insufficiency fracture at metaphysis of long bones. scintigraphy. • Singh’s index. • Slipped capital femoral epiphysis. • Wedge. Hyperphosphatasia (Juvenile Paget’s Disease) • Autosomal recessive trait • Osteoporosis with bowed bones and Paget’s-like features. • Bowing and fracture. progressive • Male and female are equally affected. etc. short stature. Juvenile Osteoporosis • Initially. • Neuropathic joint. • Spinal disease commonly seen in dorsolumbar vertebra. osteogenesis imperfecta. • Excess formation of embryonic bone precursor which fails to mature to normal adult bone. ostoephytes. Secondary (renal osteodystrophy) 3. compressed vertebra (cod-fish). pubis).114 Seminar in Radiology • Accentuated primary trabecule. • Ground glass appearance especially at pelvis. Female before puberty. biconcave. metacarpal index. • Large mottled skull. leukemia. • Fuzzy cortex with prominent trabeculae followed by sclerosis. • Schmorl’s node. pubis. tenden rupture. • Endosteal and intracortical thinning. Tertiary .

• Brown tumor may become sclerotic or bone cyst. Features of ROD are seen more commonly on account of better management and survival of CRF patients: a. Metabolic Bone Diseases 115 1. Pepper – pot/salt – pepper skull. SI joint. 2. etc. Trochanter and tuberosities. Secondary (Renal Osteodystrophy): Adults – Chronic glomerulonephritis. • Erosive arthropathy involving distal interphalangeal joints. – Arteriovenous necrosis is usually due to steroid therapy and occurs even after transplant especially in femur. Aluminium toxicity: – Encephalopathy – Osteopenia . ribs. infection and fracture. knee and symphysis pubis. • Subperiosteal resorption (hand. • Intracortical resoption a sign of rapid absorption leading to basket work appearance of cortical meduallary junction. humerus. proximal clavicle. femur. slipped epiphysis and absorption forms a “rooting fense post appearance. Soft tissue calcifications is more common in secondary hyperparathyroidism due to ROD. • Subchondral bone absorption (pubis. expansile. arteriovenous necrosis: – Erosive arthropathy similar to Charcots joint’s without extensive loose bodies are seen especially noted in the shoulder and spine. lytic.” b. are usually the result of debilitated state. – Arthritis. Due to amyloid. • Chondrocalcinosis due to CPPD in wrist. vertebra). • Loss of lamina dura in mandible. • Findings suggestive of osteoporosis. CPPD infection. osteomyelitis. calcaneum. clavicle). well-defined lesions. • Subligamentous resorption in inferior surface of clavicle. Children – Chronic pyelonephritis • Occur as a result of persistant hypocalcemia in CRF and hence secondary hyperparathyrodism has become synonymous to ROD. metaphysis. c. • Osteosclerosis may be seen due to increased osteoblastic activity. talus and knee. • In children instead of osteomalacia frank rickets occurs wherein features of rickets. diaphysis) are multiocular. Due to chronic renal failure itself: – Osteoporosis – Osteosclerosis (due to increased osteoid) – Osteomalacia – Osteofibrosa • Sclerosis occurs especially at vertebral end plates producing Rugger – jersey spine. • Brown’s tumor (in epiphysis. tibia. Primary • Middle to old age especially in women.

• Increased sesamoid index. • Over all increase growth matter. i. • Changes are prominently seen at growing ends of bone. Scurvy • It is functional counterpart of osteoporosis in children more than 6 months. • At least 4-6 months of vitamin C deficiency is required for manifestations. • Overall bone density increases but transient osteopenic appearance on X-ray may be seen due to concomitant increased in osteoclastic activity. • Periosteal reaction positive. • Osteoporosis. • Frankle’s line (wide sclerotic zone of provisional calcification). • Prognathism. – Osteomalacia due to aluminium deposition on osteoid instead of calcium • Spondylosis with decreased disc space and marginal irregularity without paravertebral soft tissue.116 Seminar in Radiology – Fractures especially vertebre and 2/3/4 ribs. • Scalloped and A-P widened vertebra with spinal stenosis. • Thick irregular bones. Chondrocalcinosis also occurs. Hyperpituitarism: (Acromegaly and Gigantism) • Endochondral subligamentous and periosteal bone formation are increased.e. protein and cells. • Corner’s sing (Subphyseal bone infarction leading to epiphyseal to metaphyseal separation and hence subperiosteal haemorrhage). • Widended teeth. • Traummerfeld zone or scurvey line (a metaphyseal transverse zone below white line)–unmineralized osteoid. • Prominent bony ridges. . • Pelkan’s spur (metaphyseal spur due to marginal fracture). • Pneumatized air cells in sinuses. • Spade or spoon-shaped phalanges. • Cartilage growth leads to increased joint space. • Growth arrest lines can be seen in later part of life. Hypopituitarism • Decreased skeletal maturation and growth with osteoporosis. • Enlarged costochondral junction and discs due to increased endochondral growth. • Wimberger’s ring (small epiphysis with sclerotic margin). due to boiled milk. • Heal pad thickness increased.

• Osteoporosis with long limb. oxalate deposition in bone. • Homocysteinuria – AR: in the pyridoxine resistant variety (due to excess methionine in diet). Arachnodactyly. wormian bones. Miscellaneous • Drugs • Pregnancy • Multiple myeloma • Glycogen storage disease (G. juvenile myxedema and classical adult myxedema. valgus at knee and hip. Hypothyroidism may be primary or secondary and leads to Cretinism. • Turner’s syndrome like picture appear radiologically after 20 yrs. short trunk due to delayed epiphyseal closure. Metabolic Bone Diseases 117 Hyperthyroidism • Hypermetabolic state may lead to bony changes even in first year. • Osteoporosis with increased skeletal maturation as compared to hypothyroidism where osteoporosis with decreased skeletal growth and maturation with fragmented epiphysis. • Changes are commonly seen in hand. bullet shaped vertebrae etc. hypoplastic frontal sinus. • On the contrary brachycephaly. • Flat head of 3rd and 4th metacarpals • Hypoplastic sella. • Alkaptonuria – AR. sternal anomaly occurs. C1 vertebra.S. large epiphysis. Exophthalmos is a constant feature. . • Short 4th and 5th metacarpal (metacarpal sign).) • Gaucher’s disease • Chronic liver diseases • Oxalosis – AR. sclerosis. enlarged sella (bowl-sella or cherry sella). Calculi (recurrant leading to CRF). basilar impression are often noticed. And only in 50 percent. pelvis (android). • Decreased carpal angle (carpal sign). HGA a metabolite of tyrosine metabolism accumulates (as a result of enzyme deficiency) in connective tissue. pelvis. hypertelorism.D. which do not seem to be related with severity of disease. D-L spine. coxavara are seen in hypothyroidism as well as in slipped femoral epiphysis. clavicle. • Wilson’s disease → Osteomalacia. AR • Hemochromatosis • CPPD disease • Copper deficiency leads to rickets-like condition although zone of provisional calcification is maintained. Hypogondadism • Primary (Turner’s enuchoidism) or secondary to decreased Gonado-tropins. Osteoporosis.

• Progressive and painful even or rest. • > 40 years • Pelvis. • Severe osteoporosis. • Large joints involved. PVC Toxicity • Acro-osteolysis. Primary Osteolysis a. • Subchondral cyst formation may be seen. • Angiomatosis and altered pH. due to increased Purine metabolism. • Prominent around wrist. ankle. b. • Joint space is normal. Sudeck’s Osteodystrophy called as Algodystrophy or Reflux Sympathetic Dystrophy • Mainly endosteal part are involved. Regional Migratory Osteoporosis • Clinical setting similar but it migrates. Idiopathic multicentric carpotarsal osteolysis: • Associated nephropathy • Tapered adjacent bones Transient Regional Osteoporosis • Spontaneously resolving (4-10 months). knee. • Women in 3rd trimester. . hemangiosarcoma of liver. sacroilitis. Raynaud’s disease. Gorham’s disease: • Creeping disappearance of contiguous bones. Gout • In patient with raised uric acid. • Loss of hip. Idiopathic Chondrolysis • Young black girls more common. most commonly femoral head. • Joint destroyed. • Young → middle age man.118 Seminar in Radiology Disuse Phenomenon • Patchy with cyst (Subchondral) formation. shoulder are involved.

Renal factors → VDDR type I (Vit. Type II 1. Hepatic factors → liver cell failure → induced microsomal enzyme ii. Fibrogenesis ossium imperfecta • Looser’s zone and true fracture • Osteopenia and feature of porosis • Bowing of bones • Fraying.D. ankle. • Chronic tophi in gout presents as nonmineralized masses epicentered away from joint and appear as radiolucent mass. Axial osteomalacia 2. Fanconi syndrome 2. • Other joints involved are knee. RICKETS AND OSTEOMALACIA GROUP Type I A. Metaphyseal chondrodysplasia (schmid) 3. cupping • Widened growth plate • Rossary ricket • Craniotabes • Harrison’s sulcus • Pot belly • Pigeon chest • Protrusio acetabulii • Triradiate pelvis • Enthesopathy in FHVRR .O. Metabolic Bone Diseases 119 • Acute arthritis occur seen as erosive arthritis. Tumors producing parathrmone E. Infarcts and AVN may occur. splaying. sternoclavicular. Isolated phosphaturea C. Vitamin D metabolism deranged i. sacroiliac joint. Phosphate deficiency Conditions mimicking 1. D-dependent rickets) → VDDR type II → R. elbow. • Bone destruction due to intraosseus tophi in a cystic fashion is quite common in great toe and other small bones. B. Bone density. Vitamin D deficiency B. Renal tubular acidosis D. hip. Familial hypophosphatemic vitamin D refractory rickets. A. cartilage and joint alignment are present till date. Hypophosphatasia (AR) 4.

• Bone in bone appearance. • Soft tissue calcification. • Transverse metaphyseal and especially at knee (fibula) due to decreased blood supply. • Enthesiopathy. • Osteosclerosis (rarely porosis).120 Seminar in Radiology Hypoparathyroidism. • Cone epiphysis. • Soft tissue calcification. Hypervitaminosis D • Sclerosis of cortex and metaphysis with patchy porosis. Flurosis • Enthesiopathy and ligamentous calcification (interosseous ligament calcification) • Sclerosis in axial skeleton. • Short metacarpal and metatarsal. • Cupped and splayed metaphysis. . • Modelling deformity. hyperparathyroidism may occurs). • Basal ganglia calcification. • Abnormal hypoplastic tooth. Bismuth and Phosphorus. • Osteophytosis. • Exostosis. • Bowed limbs. • Widened suture. Hypervitaminosis A • Periosteal reaction similar to Caffey’s disease → seen in <1 year age especially ulna and metatarsal. • In Pseudo-Pseudo type blood chemistry in normal (Skeletal response preserved therefore. • Cervical osteophytes. • Calvarial thickening. Pseudo and Pseudo-Pseudo-Hypoparathyroidism • Autosomal dominant disease • Endogenous insensitivity due to defective adenylyl cyclase system. Heavy Metal Poisoning • Lead. • Widened suture. • Coxa vara and valga. • Premature epiphyseal closure.

DIAGNOSTIC TECHNIQUES IN METABOLIC BONE DISEASE 1. Markers of increased bone formation. Markers of increased bone resoption: • Hydroxylysine • Plasmatart rate resistant acid phosphatase. – Singh et al gave assessment of femoral neck trabeculae. – By Cameron and Sorensen. we can also measure the alternation in bone density using plain X-ray. . • Clubbing. • Chosslaps (degradation product collagen). Radiological • Plain X-ray Radiogrammetry – Apart from the typical radiological features of each disease. – The disadvantage of these techniques where that they could not do soft tissue correction. b. Metabolic Bone Diseases 121 Thyroid Acropachy • In thyrotoxic patients who are now Euthyroid due to treatment. • Asymmetric involvement of hand bones (radial aspect). • Alkaline phosphatase • Osteocalcin • Free bone Gla protein. D-Pyridinoline. 3. hip which are most commonly involved) was poor. – Correlation between peripheral (forearm. • Photodensitometry – Comparing density of ulna with an aluminum bar. – Cortical thickness of metacarpal. • Pyridinoline. Best method is Biopsy from anterior iliac crest. • LATS is the cause. The gold standard is however in vivo ash sampling. • Single Energy X-ray absorptiometry – Another technique using single energy source. • Osteomark (cross-links of collagen). Biochemical a. • Pretibial myxedema and diaphyseal periostitis. – Monoenergetic electron source (I25) with Nal Scientillation Counter which detects absorption by bone. • Single Photon Absorptiometry – For appendicular skeleton only and not in spine and hip. 2. – At distal non-dominant forearm. • ICTP (Carboxy terminal Pyridinoline cross-linked telopeptide of type I collagen). free pyridinolin. deoxypyridinoline. heal) and central (spine.

– Can assess Cancellous bone separately to monitor response to therapy. Interpretation: <1 SD (below the mean of Peak Bone Mass) = Normal 1-2. tibia used. – Heal. – Two X-ray beams used to scan the region of interest (spine and hip) quickly and then correction for soft tissue in made. i. – BUA = absorption and scattering. – SOS = elasticity and density.5 SD = Osteopenia > 2.e. – BUA and SOS measured. – LS spine (1-4 or 2-4) in PA or Lateral views is used. . Since. – Hip may be measured as a whole or in parts.5 SD = Osteoporosis • Quantitative CT Scan – Only technique that can differentiate cortical and cancellous bone. Z-score. lack of ref. – LS spine is used to select the ROI.122 Seminar in Radiology • Dual Energy X-ray Absorptiometry – The technique most in use. • Ultrasonometry – Only non-ionizing and radiation technique. variations may occur. stiffness index and BMD equivalent are calculated. data are the major draw backs. – A graph is plotted using amplitude loss of sound waves of various frequencies the slope of which is BUA. – Certain values are measured Bone mineral density (g/cm2) Bone mineral content (g) Bone mineral density % T-Score. But due to absence of artefacts and soft tissue hip is preferred. the distribution of cancellous bone here is not uniform therefore. – Also two derived coefficients. – Lack of standardized equipments and techniques. – Dexa can also be used to scan the peripheries hence also called as pDEXA.

SECTION 2 Central Nervous System .

.

they can present themselves for away from the spine along the fascial planes or neurovascular bundles. REGIONAL DISTRIBUTION OF TUBERCULAR LESIONS IN VERTEBRAL COLUMN Dorsal (T-11). evening rise of temperature. loss of appetite. Bilateral psoas abscess are also seen. • Equal in males and females. • Dorsolumbar and lumbar spine follow the well known pattern of tracking down the psoas sheath. 9 Craniospinal Tuberculosis • Commonest form of skeletal tuberculosis (T. lumbar triangle. intercostal spaces in the chest wall.) and consistutes 50 percent of all cases of TB of bones and joints. . • Rarely. in the upper part of thigh. cervical triangles. cervical sites (rare). caries spine causes REFERED PAIN Abdomen Spinal tumor Cervicodorsal spondylosis syndrome or disc syndrome ABSCESS AND SINUS • In the cervical or dorsal region. • Persistent backache once the active stage subsides. lumber (L1). The abscess may be palpable in the iliac fossa.B. • Most common during first 3 decades of life. lumbosacral. SYMPTOMS AND SIGNS • Symptoms are commonly insidious • In the active stage of the disease-loss of weight. night sweats. A cold abscess may be present clinically. stiff spine and localized kyphotic deformity. below the inguinal ligament or upto the knee. dorsolumbar. They may be seen in paraspinal region at the back.

Anterior types (involvement of anterior surface only) C. Spontaneous twitching of the muscles of lower limbs with exaggerated reflexes. D. b. Central cystic type: A lytic lesion with concentric collapse. B. Sudden complete paralysis. • Neurological involvement • Skipped lesions SIGNS AND SYMPTOMS OF POTT’S PARAPLEGIA Paraplegia of Slow Onsent a. c. Extreme cases—flaccid paralysis with loss of bladder and anal sphincter control. E. lamina and spinous process). d. Paradiscal lesions: Adjacent vertebral endplates destruction and diminition of the intervertebral disc space. • Associated extraspinal skeletal. glandular or visceral foci. c. Posterior spinal disease (involvement of pedicles. paraplegia in flexion. NEUROLOGICAL COMPLICATIONS Group A • During active phase of the disease (within 2 years) . spastic paraplegia in extension. Motor functions are affected first i.126 Seminar in Radiology SITE OF INVOLVEMENT IN A VERTEBRA A. Sense of position and vibration are last to disappear. ii. Spastic motor paraparesis. Paraplegia of Acute Onset a. atlantoccipital or atlantoaxial joints. Sensory involvement occurs lates in the disease and to a lesser degree than the motor involvement. More sensitive to compression. Diseased area in the spine lies anterior to the spinal cord and thus closer to the motor tracts. uncontrollable flexion spasm with involvement of bladder and anal spincters. Tuberculous synovitis of the apophyseal articulation. COMMON CLINICAL FEATURES OF SPINAL TUBERCULOSIS • Kyphoses • Palpable cold abscess • An active or healed TB sinus. b.

Inflammatory Causes Edema. X-RAY APPEARANCES The are four main sites where TB occurs in the vertebral bodies: A. Intrinsic Causes • Prolonged streching of the cord due to severe deformity. Anterior . • Cause of compression is mechanical like – tubercular debris. B. 2. Severe Moderate + with sensory deficit > 50% with sphincter involvement. CLASSIFICATION OF TUBERCULOUS PARAPLEGIA S. sequestra from vertebral body/disc. granulation tissue. Group B • Paraplegia associated with healed disease. C. Mild Patient aware but walks with support 3. Moderate Non-ambulatory with sensory deficit <50%. tubercular pus or casesous tissue. CAUSES OF NEUROLOGICAL DEFICITS A. Craniospinal Tuberculosis 127 • Early onset paraplegia. • Less favorable prognosis (needs surgical intervention). No. • TB meaningomyelitis • Infective thrombosis/endarteritis SPINAL TUMOR SYNDROME Diffuse extra-discal granuloma or tuberculoma even without any radiological evidence of tubercular involvement of the vertebera. • Syringomelic changes. 4. granulation tissue. • Cause of compression is inflammatory edema. • Favorable prognosis. • Internal gibbus formation. Paradiscal B. Mechanical Causes • Tubercular debris • Sequestra from vertebral body and disc • Constriction of cord due to stenosis of vertebral canal. caseous tissue and abscess. • Late onset paraplegia (>2 years). Negligible Patient unaware of neural deficit. Grade Clinical features 1. localized internal gibbus or kyphotic deformity causing stenosis of vertebral canal. physician detects plantar extension/clonus.

• In the mid and lower thoracic region – A fusiform shadow with shifting of the parapsinal line. Central D. • As 30-40 percent of calcium must be removed from a particular area to show radiolucent region on X-ray. • Due to more destruction of the vertebral body on one side. Anterior Type of Lesion • Infection starts beneath the anterior longitudnal ligament and periosteum. • Collapse of vertebral bodies and disc space reduction is minimal. . • Below the diaphragm – Unilateral or bilateral widening of psoas shadow. Central Lesion • Infection starts in the centre of the vertebral bodies (Reaches centre through Batson’s venous plexus or branches of posterior vertebral artery). spinous and transverse process. D. It is not until a lapse of 3-5 months after the beginning of the infectious process that the first tubercular destruction is identified on a radiograph. B. Paradiscal • The commonest type of involvement • Narrowing of the disc is the earliest radiological finding with loss of definition of the paradiscal margins. • Areas of destruction in the vertebrae may produce concentric collapse (vertebra plana). • In the cervical region – Increase in the retrotracheal and retropharyngeal space. Appendicial Lesion • Involvement of pedicles. Kyphotic deformity Due to destruction and anterior wedging of the involved vertebra. Appendicial type A. • In the upper thoracic region – Shifting of the apices laterally and downwards with a ‘v’ shaped shadow. lamina. • Disc spaces are intact. Paravertebral shadows It is produced by extension of tuberculous granulation tissue and collection of abscess in the paravertebral region. • Disc reduction may be minimal. • Aneurysmal phenomenon. • Paravertebral abscess may be present. LATERAL SHIFT AND SCOLIOSIS • A combination of lateral deviation and rotation of the spine.128 Seminar in Radiology C. • Peripheral portions of vertebral bodies show erosion in lateral view as shallow excavation. C. • Sometime the vertebra may be expanded or balloned like a tumor.

Adherence of the nerve roots of cauda equina. • A complete block below the level of conus medullaris will present as feathered. adherence of the nerve roots to theca – empty thecal sac. Craniospinal Tuberculosis 129 • Lower dorsal and lumbar spine are commonly involved. Severe kyphosis (Humpback) >3 vertebra involved (K > 60°) MYELOGRAM Features of Extradural Block • Identation of one side of the myelographic column. 3. Obliteration of nerve root sheaths. serrated interface of the myelographic column. • Angulation of the spinal cord with complete obstruction. RADIONUCLIDE BONE SCAN • Tc-99m – labelled bone seekers • Gallium – 67 – citrate • Indium – III or Tc-99m-labelled HMPAO ↓ Gamma Camera • Flow phase – low resolution angiogram. smoothing of thecal outline. c. Features of Arachnoiditis a. CLINICORADIOLOGICAL CLASSIFICATION OF TUBERCULAR SPONDYLITIS Stage Clinico radiological features 1. if paravertebral muscle involvement. • Blood pool phase – extent of soft tissue and bone hyperemia. shortening of sacral cul-de-sac. d. Irregularly narrowed theca with pocketing and cyst formation – delayed flow of contrast medium through subarachnoid space. increased uptake in the lower aspect of one vertebra and the upper aspect of the vertebra just below. Early destruction Diminished disc space and paradiscal area. Moderate angular kyphosis >3 vertebra involved (K = 30-60) 5. b. Predestruction Straighting of curvature. Mild-angular kyphosis 2-3 vertebra involved (K: 10-30) 4. • Possible involvement of posterior spinal articulation. 2. • On delayed scans. . Pott’s Spine Shows • Hypermia with increased blood pool activity. Shortening and incomplete filling of nerve root sheaths. • Delayed scan.

130 Seminar in Radiology COMPUTERIZED TOMOGRAPHY • Early changes within the bone is depicted as small areas of rarefaction in the subchondral bone. • Fibrocartilage in nucleous pulposus and central portion of annulus fibrosus has high signal intensity. • Cortical bone has negligible signal intensity. T2-Weighted Image • CSF has a high signal intensity “Myelogram effect”. • Gradient echo images are a supplement to spine-echo images (can be obtained with shorter acquisition time). • Proton density images. • Reformatted images may show changes in end plates. • T2-weighted images – Long TR (2000-4000 msec) and long TE (50-100 msec). • Advanced cases may result in a weakened vertebral body that may fragment and collapse. • Ligaments have intermediate signal intensity. bony ankylosis and sclerosis can be demonstrated. • Fat containing bone – higher signal intensity. • Fatty bone has a lower signal intensity. low to intermediate intensity. • Intravaneous contrast agents may add the paraspinal inflammatory tissue to enhance with better delineation of paraspinal abscess and their extent. • Cortex may demonstate small areas of irregularity or small areas of abscess which eventually may coalesce into large areas of destruction. • Inflammatory mass or bone fragments may displace and compress the thecal sac (CT myelo). • Intervertebral disc have nearly homogenous. MAGNETIC RESONANCE IMAGING • T1-weighted images of the spine – Spin echo pulse sequences with a short TR (200-1000) and TE (20-25 msec). T1-Weighted Image • The spinal cord has intermediate signal intensity. • In the healing phase. . Features • Decreased signal intensity with loss of delineation of the end plates from the intervertebral discs in T1-weighted images. • Increased intensity from the intervertebral disc and end plants on spin echo T2-weighted images. Peripheral portion (collagenous) has low-intensity. • Spinal cord has a lower signal intensity.

. • In TB spondyllitis. Hyperintense signal on T2 in the setting of chronic infection may be specific to MTB. 2. transverse process and ribs. TRAUMA • Traumatic compression fracture is wedge-shaped with intact disc spaces and paradiscal margins. – disc gives bright signal on T2-weighted – decreased signed of T1-weighted – enhancement after contrast administration. SYPHILITIC INFECTION • Arthralgic type or Gummatous type or Charcot’s disease of spine • Commonest sites are the lower dorsal and lumbar spine. • Paravertebral abscess may be seen in blastomycosis. DIFFERENTIAL DIAGNOSIS 1. • Multiple sinus formation with involvement of subcutaneous tissue. • There is bone destruction with rapid sclerosis and new bone. • Healing is by proliferative new born formation with bone ankylosis. • Demonstration of the fungus from the discharging sinus establishes the diagnosis. Mycotic spondylitis • Actinomycosis or blastomycosis • Involvement of vertebral body. • IV contrasts shows improved definition of epidural abscess and masses. • There may be sparring and ossceous bridging on both sides of disc with intradiscal calcification. • Sclerosis and destruction process go side by side. Pyogenic spondylitis • Follows infection or surgery of urogenital tract. Abscess show peripheral enhancement with cortical necrosis. Craniospinal Tuberculosis 131 • In chronic infection : T1-weighted images may show decreased or increased signal. cord and nerve root compression. • Extensive destruction with proliferative new bone formation which may extend into the paraspinal tissue. • Periosteal new born formation occurs in the anterior and lateral aspect of vertebral bodies (Saw tooth appearance). • Collapse of vertebral body is rare. • Varying degree of disc space reduction. Typhoid spine 3. • Diagnosis is confirmed by biopsy and serological tests. Brucella spondylitis 4.

• Hematogenous dissemination from a focus in the lungs or genitourinary tract.132 Seminar in Radiology SPONDYLOLISTHESIS • L4-L5. increase proteins. OSTEOPOROSIS Spinal Osteochondrosis • Adolescents • Rounded kyphosis • Several vertebrae involved with sclerotic epiphyseal plate. Tumorous Conditions • Hemangioma • GCT and ABC • Primary malignant tumors • Multiple myeloma • Secondary neoplastic deports Miscellaneous • Histocytosis X • Hydatid disease INTRACRANIAL TUBERCULOSIS • Leptomeningitis • Granulomas • Cerebritis/Abscess (Rare) • Extremes of age group. • Lumbar puncure – decreased glucose. headache. coma. L5/S1 • Forward displacement of one vertebra over another. ocasionally associated with decerebrate rigidity. pleocytosis and negative smears. Tubercular Meningitis • Clinical features – confusion. • Absence of constitutional symptoms. cranial nerve palsies and infarction. immunocompromised patients. stupor. lethargy. • Thick exudates in the basal cisterns – Communiating hydrocephalus – Vascular involvement  Leading to vasculitis  Infarctions . paravertebral shadows. etc.

ependymal TB. infarction. • Hydrocephalus. Tubercular Abscess • Central area of liquefaction and pus. CECT – ring/disc enhancement. • MRI shows better evaluation of infarcts. intraventricular. odema around the lesion is shown as hypoattenuated areas. • Histologically central area of necrosis with peripheral rim of Langerhans’ giant cells. lymphocytes and plasma cells. . MRI • Plain MRI – Mixed predominantly low signal intensity lesion with surrounding high signal intensity edema on T2-weighted images. • NCCT shows isodense. Tuberculomas • Can involve any cerebral compartment. ventriculitis and meningial enhancement. Target sign. hyperdense or mixed density lesion. Craniospinal Tuberculosis 133 CT Scan/MRI • NCCT / MRI – complete or partial obstruction of basal cisterns and sylvian fissures which have same density as the adjacent brain. • CECT / MRI – intense enhancement of the cisterns and leptomeninges. • Gd-MRI-Same pattern as CECT.

. It progresses from caudad to cephalad. tracts c. Three Months • Brachium points. NORMAL MYELINATION It is a dynamic process that begins during 5th fetal month and continues throughout life. Birth (Full Term) • Medullas • Dorsal midbrain • Inferior and superior cerebellar peduncles • Posterior limb of internal capsule • Ventrolateral thalamus b.10 Diseases of White Matter Brain Substances The white matter diseases are predominantly grouped into two classes. Eight Months • Centrum semiovale (complete except for some from temporal areas) • Subcortical U fibers (complete except for more rostral frontal areas) f. Six Months • Corpus callosum genu • Paracentral subcortical U fibers • Centrum semiovale (partial) e. Eighteen Months • Essentially like adult. Demyelinating: Disorder due to destruction of otherwise normal myelin. Dysmyelinating: Disorder with defective formation or maintenance of myelin. One Month • Deep cerebellar white matter • Corticospinal tracts • Pre-postcentral gyri • Optic nerves. 1. from dorsal to ventral and from central to peripheral (Table 10.1). cerebellar folia • Ventral brainstem • Optic radiations • Anterior limb of internal capsule • Occipital subcortical U fibers • Corpus callosum splenium d. Table 10.1: Normal myelination a. 2.

Pathology • Symmetrical demyelinaiton that spares subcortical ‘U’ fibers. deterioration of intellect. speech and co-ordination. Clinical Presentation • Motor signs of peripheral neuropathy. Occipital White Matter Most Involved • Adrenoleukodystrophy (also colossal splenium) iv. destruction or turn over of myelin. Enhancement following Contrast Administration • Alexander disease • ALD (1st calcification/ peripheral aim enhancement) vii. METACHROMATIC LEUKODYSTROPHY • Autosomal recessive • Lysosomal disorder caused by deficiency of catabolic enzyme Aryl sulfatase. Frontal White Matter Most Involved • Alexander disease iii. Strokes • Leigh syndrome • MELAS • MERRF • Homocystinuria. Macrocephaly • Alexander disease • Canvan disease • Mucopolysaccharidosis type I (Hurler) • Mucopolysaccharidosis type II (Hunter) v. Complete / Near Complete Lack of Myelination • Canavan disease • Pelizaeus-Merzbacher disease ii. Diseases of White Matter Brain Substances 135 LEUKODYSTROPHIES: DISTINCTIVE FEATURES i. INHERITED LEUKODYSTROPHIES These are dysmyelinating diseases and are a heterogeneous group of disorders characterized by enzyme deficiencies that result in abnormal formation. Thick Meninges • Hurler syndrome • High density basal ganglia • Krabbe disease vi. .

Late infantile age b.000 • Types – Infantile (most common) – Late infantile – Adult forms . seizures and cortical blindness. Adult form Approximately 80 percent occur between 1-2 year Location • Deep periventricular white matter that spares arcuate fibers Imaging Techniques • CT – NCCT o Low-density lesion progressive anteior to posterior within white matter o Mild to moderate ventricular enlargement – CECT: No enhancement • MRI – T2-weighted image show: Diffuse confluent high signal lesions in periventricular white matter.000 newborns Types according to age of onset a. – Increased signal of cerebellar white matter. KRABBE LEUKODYSTROPHY (GLOBOID CELL LEUKODYSTROPHY) • Autosomal recessive • Deficiency of lysosomal hydrolase (Galacto cerebroside betagalactosidase) Clinical Presentation • Psychomotor deterioration. Pathology • Brain is small and atrophic • Extensive symmetric dysmyelinaiton of centrum semiovale and corona radiata with sparing of subcortical ‘U’ fibers. irritability. optic atrophy. Juvenile form c. – Thalamus appears hypointense. Incidence: 1 in 50.136 Seminar in Radiology Incidence • Most common and present as → 1 in 100.

Pathology • Enlarged ventricles • Cerebral atrophy • Demyelination involves occipital lobes and corpus callosum in bilaterally symmetrical pattern Incidence • X-linked disorder • Seen in males • 3-10 years Location • Symmeteric white matter demyelinaiton occurs in peritrigonal regions and extends across corpus collosum splenium • Secondary changes are seen in posterior limb of internal capsule. B. Adrenomyeloneuropathy C. pons. Imaging Techniques • CT – NCCT o The thalamus and basal ganglia appear hyperdense o Diffuse low-density is present in periventricular white matter – CECT: No enhancement • MRI: – T2 WI : non-specific. pyramind and cerebellum. Acyl CoA synthetase which prevents break down of very long chain fatty acids which accumulates in tumorous tissues and plasma. hearing loss. confluent symmetrical periventricular white matter hyperintensities – Severe atrophy is seen in infantile form of GLD. . ADRENOLEUKODYSTROPHY (X-LINKED) • It is a group of three closely related paroxisomal disorders Clinical Presentation • Seizures. Adrenoleukodystrophy – Classic form casued by deficiency of single enzyme. Adrenoleukomyeloneuropathy. cerebral peduncles. visual behavioral disturbance. paraparesis A. Diseases of White Matter Brain Substances 137 Location • Centrum semiovale and periventricular white matter are involved.

symmetric low density lesion in parietoccipital region – CECT  Shows enhancement with advancing rim surrounded by non- enhancing edematous zone.138 Seminar in Radiology Imaging Techniques • Definitive diagnosis is made by plasma.  Hyperintense on T2 WI. 2. Intermediate zone of demyelination and inflammation  Enhances after contrast 3. nystagmus. Central necrotic zone  Low signal on T1 WI. Clinical Presentation • Poor head control. Classical – X-linked recessive b. cerebellar ataxia with abnormal eye movements. Types a.  High signal on T2 WI. • CT: – NCCT  Large. erythrocyte or cultured skin fibroblast assay of VLFA’s (very long chain fatty acids). Peripheral edematous zone  Hypointense on T1 WI. PEUZAEUS – MERZBACHER DISEASE • Linked with severe deficiency of myelin-specific lipids that lack lipid apoprotein (Lipophilin) which is necessary for oligodendrocyte differen- tiation and survival. • MRI: Three pathological zones are seen: 1. Connatal – X-linked / autosomal recessive Pathology • Brain and cerebellum are atrophic • Ventricles are large Incidence • Young boys • Type 1 is seen in infancy and early childhood • Type II–neonatal period .

loss of motor activity. megalencephaly . Diseases of White Matter Brain Substances 139 Imaging Techniques • NCCT: – Cerebral and cerebellar atrophy – White matter appears diffusely of low density • MR – T2 WI—shows diffuse high signal that extends peripherally – The brainstem. spasticity and seizures. Incidence • Rare disorder • Infants • Juvenile • Adult form Location • Predilection for frontal lobe white matter • Deposition of Rosenthal fibres in basal ganglia. psychomotor retardation. cerebellum and subcortical fibers are spared – The basal ganglia and thalamus appear hypointense (abnormal iron deposition) ALEXANDER DISEASE • Sporadic leukoencephalopathy of unknown etiology. • Inheritance is autosomal recessive Clinical Presentation • Hypotonia. thalamus and hypothalamus Imaging Techniques • NCCT: – Low attenuation in deep frontal white matter – Basal ganglia—shows low density lesions • CECT – Marked enhancement occurs in basal ganglia and periventricular regions CANNAVAN’S DISEASE (SPONGY DEGENERATION) • Deficiency of N-acetyl aspartylase—results in accumulation of N-acetyl aspartic acid in brain. Clinical Presentation • Early onset of megalencephaly.

ACQUIRED LEUKODYSTROPHIES MYELINOCLASTIC/ DEMYELINATING DISORDER MULTIPLE SCLEROSIS Etiology • Unknown • Autoimmune mediated demyelination • Most common (vascular and age-related) Clinical Presentation • Prolonged relapsing—remitting disease. . later on chronic progressive phase.140 Seminar in Radiology Pathology • Gross megalencephaly with increased brain weight and volume Incidence • Rare disorder • No gender predilection Location • Demyelination involves subcortical ‘U’ fibres • The occipital lobes are more involved than frontal and parietal lobes • Severe cases affect basal ganglia and thalami Imaging Techniques • NCCT – Diffuse low density throughout cerebral white matter • MR • T1 WI—homogenous diffuse symmetric low density throughout white matter • T2 WI—Near total high signal in white matter • Subcortical ‘U’ fibers are involved. Incidence • Young females (20-40 years) • Less common in children and adolescents. Pathology • Typical MS plaques are edematous pink-gray white matter lesions.

headache. foreign protein or autoantigen. initially mild fever.4 cm) o Low attenuation or isoattenuating lesions with contrast enhancement (acute / subacute lesions) o Low attenuation with and without contrast (chronic lesions). Imaging Techniques Normal in early phase of disease • CT – Ovoid periventriclular plaques (0.6 – 1. the virus propogates. Appearance is common in T1 and PD sequences – Variable o Enhancement o Solid o Ring o Punctuate/ nodular – Enhancement represents break in the blood brain barrier. drowsiness with advanced coarse symptoms ranging from seizures and focal neurological deficit to coma. • Corpus callosum (callososeptal interface is common location). VIRAL AND POSTVIRAL DEMYELINATION • The acute encephalitides may be secondary to a known causative agent or may be autoimmune response to non-specific viral illness or vaccinaiton • There is a hypersensitivity reaction caused by either a virus. unchecked and results in demyelination. . ADEM (ACUTE DISSEMINATED ENCEPHALOMYELITIS) • Immune mediated • Previous history of viral infection or vaccination Clinical Presentation • Abrupt onset. monophasic illness. • In immunocompromised patients. Diseases of White Matter Brain Substances 141 Location • Ovoid periventricular lesions oriented perpendicular to long axis of brain and lateral ventricles. – Atrophy – Mass effect (rare) • MRI – T1 WI—iso to hypointense lesions – T2 WI—hyperintense ovoid lesion – Beveled / target lesion.

Progressive Multifocal Leucoencephalopathy (PML) Etiology • Group B human papova virus • Papova virus infect and destroy oligodendroglia • Multifocal areas of myelin and arc loss involving deep and superficial matter. Lyme Disease – Multisystem disorder caused by thick borne Spirochete Borrelia burdofer – Pathogenesis o Vasculitis o Immune complex mechanism . Incidence and Age • 1-4 percent adults AIDS patients Location • Subcortical areas are first affected • Spread to deep white matter Imaging Technique • MR – Most-sensitive modality – T2 WI–multifocal oval/ sound subcortical white matter area – Late manifestation – confluent white matter disease with cavitatory change – Less commonly – unilateral white matter thalamic or basal ganglia lesions 2.142 Seminar in Radiology Pathology • Periventricular demyelinating foci Age • Children and young adults Imaging Technique • MR – T1-weighted image : Multifocal subcortical hyperintense foci – Bilateral / asymmetric lesion – On contrast: lesions may show contrast enhancement OTHER INFECTIVE CAUSES 1.

Central Pontine Myelinosis – Acute pontine demyelination – History of alcoholism associated with hyponatremia exacerbated by over-hydration and administration of diuretics. Imaging Techniques • CT: – Areas of decreased attenuation in the pons. Imaging Techniques • CT – Generalized atrophy – Bilateral symmetrical white matter hypodensity involving frontal lobe. • HIV virus is not only lymphotrophic but also neurotrophic and leads to demyeliniation. 3. cerebral edema. Other factors include systemic hypotension. – Extrapontine sites of involvement are basal ganglia. vascular myelo- pathy and peripheral neuropathy. Diseases of White Matter Brain Substances 143 Imaging Technique • MR – T2-weighted image shows extensive deep discrete and confluent white matter lesions – Enhance following contrast administration. AIDS-Related Leukoencephalopathy • CNS involvement in AIDS can manifest as acute encephalopathy. 2. METABOLIC CAUSES 1. – Asymmetrical patchy subcortical hyperintense lesions may be seen in parieto-occipital region. may show slight contrast enhancement • MR – T2WI: classical appearance: Triangular or trident-shaped central pontine hyperintensity due to sparing of corticospinal tracts in ventrolateral aspect of pons. characterized by involvement of corpus callosum demyelination and necrosis . Marchiafava – Bignami Disease • Poorly-nourished Italian men with history of chronic alcoholism • Pathologically. thalamus and subcortical white matter. – No contrast enhancement is noted • MR – T2-weighted image shows : punctate hyperintense foci. acute and chronic meningitis. subacute encephalitis. on larger focal and diffuse areas. etc. drugs.

Radiation induced demyelination • Radiation necrosis • Diffuse leukoencephalopathy A. e. • MR: – T2-weighted image show core of enhancing mass may be present – Diffuse white matter edema. Imaging Techniques • CT: – Abnormal low density white matter with mass effect. Radiation necrosis: • Coagulative necosis of white matter with fibrinoid necrosis of capillary blood vessels • Occurs after latent period of 4 months to several year. acqueduct and mammilary bodies. – Post-contrast T2 weighted image : Show enhancement around 3rd ventricle. 3. Wernicke Encephalopathy Etiology • Caused by nutritional thiamine deficiency • History of chronic alcoholism • Effects both gray and white matter Imaging • MR – T2-weighted Image : Hyperintense lesions around 3rd ventricle and acqueduct. on T1-weighted and hyperintense on T2-weighted sequences.g. TOXIC AND TRAUMATIC ENCEPHALOPATHIES Many toxic and traumatic processes may selectively destroy myelinated portions of brain.144 Seminar in Radiology • Cerebral hemispheric white matter and other commissural fibers may be affected Imaging Techniques • CT: – Hypoattenuating lesion seen involving corpus callosum • MR: – Callosal atrophy and focal necrosis as linear or punctuate hypointense lesions. B. Diffuse radiation induced leukoencephalopathy: • Involved all visible cerebral white matter . • Gamma radiation • Chemotherapeutic agents • Chemical toxins • Heavy metals • Specific surgical lesion 1.

2. well-defined hypodensity in centrum semiovale. internal and external capsules and periventricular white matter • MR – T2 and PD sequence : more-sensitive to detection of edema 3. strangulation. symmetrical. Imaging Technique • CT – Symmetrical hypodensity of white matter and lentiform nucleus – Loss of gray/white matter differentiation 2. • The white matter damage may be related to severity of systemic metabolic acidosis and systolic hypotension • The changes are prominent in arterial boundary watershed zones. • MR: – T2-weighted image shows symmetrical white matter involvement. Diseases of White Matter Brain Substances 145 • CT: – Diffuse low intensity white matter without contrast enhancement. carbon monoxide poisoning. Imaging Technique • CT – Extensive. anesthesia accidents. Global Hypoperfusion Syndrome Etiology • Prolonged hypoxia with accompanying systemic hypotension and acidosis • Important factors include : Drug overdose. postoperative shock. cardiac and respiratory arrest. Disseminated Necrotizing Leukoencephalopathy • Iatrogenic complication of intensive chemotherapy directed to central nervous system (most commonly methotrexate) • On CT/ MR: Diffuse symmetric white matter lesions similar to radiation therapy The leukoencephalopathy may be a result of longstanding hypertension or a single episode of hypotension. Hypertensive Encephalopathy Etiology • Hypertensive patients with rapidly rising blood pressure • Caused by vascular alterations which may lead to cerebral edema parenchymal microinfarcts and petechial hemorrhages. status epilepticus and vasospasm. profound hypoglycemia. 1. Eclampsia • Hypertensive disorder in third trimester of pregnancy • Involvement of posterior hemisphere .

Biswanger’s Disease (Subcortical Arteriosclerotic Encephalopathy) • Diffuse/ multifocal destructive process in central white matter resulting from generalized ischemic or vascular conditions • Clinically characterized by hypertensive dementia. gliosis and disturbance in myelinaiton • Periventricular leukomalacia—caused by ischemic infarction in premature infants in the periventricular white matter (water-shed zone in developing infants) • It reflects injury in 28-34 weeks of gestation. • MR – Generalized cerebral atrophy – Lacunar infarcts in basal ganglia and thalami – T2 WI shows—subcortical and periventricular lesions predominantly in frontal and occipital horns and centrum semiovale 5. seizures and syncopes.I. incompletely symmetrical hypodensity in central white matter more prominent in frontal lobes and centrum semiovale.146 Seminar in Radiology Imaging Technique • CT – White matter shows symmetric hypoattenuating areas • MR – T2 WI . Imaging Technique • MR – T2-weighted image show bilateral but asymmetric peritrigonal hyperintensities – Reduced white matter volume B. Term infants • In term infants. severe. Premature Infants • Developing brain is susceptible to injury and may lead to necrosis. regions and cell types to H. A. Imaging Techniques • CT – Diffuse. . injury. the ischemic lesion are in cortex and subcortical white matter • Deep gray nuclei may be affected.hyperintense lesions in deep white matter of occipital lobes. Hypoxic Ischaemic Encephalopathy Imaging manifestation depends on: • Length and severity of vascular insult • Age • Individual cerebral circulatory pathways • Inherent vulnerability of certain anatomic. 4.

putamen. AMINOACIDOPATHIES • Hereditary disorder of amino acid metabolism e. Imaging Technique • MR: T2 WI reveal focal hyperintensity subcortical in white matter. caudate nucleus. . brainstem or central white matter • Most characteristic foci of demyelinaiton are seen in lentiform nuclei. Vasculitis • SLE. pons and medulla.Phenylketonuria . parahippocamus area. . polyarteritis nodosa are potential causes. thalamus. cerebellum and brain stem nuclei D. Diseases of White Matter Brain Substances 147 C.g. MITOCHONDRIAL CYTOPATHIES Leigh’s disease (subacute necrotizing encephalopathy) • Low attenuation in basal ganglia. Sjögren’s syndrome. periaqueductal gray matter. Children and adults • Watershed infarction and neuronal necrosis within globus pallidus. cerebral peduncles. Behçet disease. MISCELLANEOUS Gangliosidoses • Tay Sach’s disease (GM2 gangliosidosis)—abnormality of myelin sphin- golipid metabolism Imaging Techniques • Macrocephaly • CT – Diminished attenuation of entire cerebral white matter • MR – Deep white matter demyelination – Thalamus may show flow void suggestive of calcification.Maple syrup urine disease .Ketolic hyperglycemia Imaging • Cerebral edema • Hypomyelinaiton • Diffuse white matter atrophy.

.

SECTION 3 Cardiovascular System .

.

11 Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease Cyanosis is a physical sign characterized by a slate-blue color of the mucous membranes. History 2. Cyanosis increases on crying. so that adequate life saving measures can be taken. cardiac abnormalities. However. whether congenital heart disease is the cause. 3. 5. nail beds and skin. It results from presence of deoxygenated hemoglobin in the blood at a concentration of >3-5 gm/dl which corresponds to PaO2 of less than 80 to 85 percent. In a newborn. Features of congestive heart failure. Conventional “five finger” approach is followed in diagnosis of any patient with heart disease: 1. X-ray chest . Physical examination 3. pulmonary disorders. Following features of heart disease are seen in a patient of congenital heart disease: 1. Following are the features characteristic of cyanosis of cardiac origin (associated with congenital heart disease). airway obstruction and very rarely methemoglobinemia). cyanosis may decrease but never disappears (as against cyanosis due to respiratory or CNS disorders) (Hyperoxia test). clubbing and polycythemia. Presence of central cyanosis indicates that heart disease is congenital. 2. Vigorous and labored respirations with tachypnea. Presence of murmurs. 1. cyanosis can be caused by a number of conditions (Central nervous system dysfunction. On giving 100% O2 inhalation. 4. 3. Presence of extracardiac congenital anomalies. most important consideration in evaluating cyanotic patient is to find out. 2. Murmurs apparent at birth or in the neonatal period (obstructive and regurgitant lesions become apparent at birth where as septal defects appear after sometime). Murmurs produced by congenital cardiac defects tend to be parasternal rather than apical. 4.

physiology. Classifications are based on morphology. embryology. Ground-glass appearance of the lungs with normal size heart → TAPVC with pulmonary venous obstruction. prominent hilar area with peripheral oligemia. increased and decreased .152 Seminar in Radiology 4. Boot shaped / ‘core en sabot’heart →TOF 4. Upper left border formed by ascending aorta → Corrected TGA 5. Ebstein’s anomaly – Massive cardiomegaly – Small main pulmonary artery segment – Ischemic lungs DIFFERENTIAL DIAGNOSIS OF CYANOTIC HEART DISEASE Several classifications have been suggested to categorize the patients of cyanotic heart disease to narrow down the differential diagnosis. 3. • It also gives idea of heart size. ‘Figure of 8’ or snowman appearance → Supracardiac total anomalous pulmonary venous connection. whether enlarged or not. Eisenmenger physiology → Cardiomegaly with prominent main pulmonary artery segment. • RVH – upturned apex • LVH – Broader apex which tends to dip below the left hemidiaphragm • Prominence of main pulmonary artery segment seen in – Left to Right shunts – Valvular pulmonary stenosis – PAH (Pulmonary artery hypertension) • Absence of main pulmonary artery segment seen in – Infundibular pulmonary stenosis (PS) – Transposition of great vessels (Where pulmonary artery is posteriorly placed) • Prominent aortic shadow – All conditions constituting fallots physiology – PDA (Patent Ductus Arteriosus) – Valvular aortic stenosis/ coarctation of aorta with post stenosis dilatation. 6. Few Diagnostic X-ray findings are: 1. Specific investigations – Cardiac catheterization – Echocardiography – Angiocardiography – Color Doppler imaging X-ray Chest • Most important information obtained by X-ray chest in cyanotic heart disease is about pulmonary blood flow-plethora or oligemia. Egg on side cardiac shape → TGA 2. ECG 5. • Typical patterns of cardiac silhouette in different congenital heart diseases.

Pulmonary stenosis is not included in 5T’s classification though based on physiology.g. Cyanosis: The more severe the cyanosis. Congestive failure: If a cyanosed patient is in CHF. mild cyanosis does not exclude severe lesion e. 2. 4. If there are more than one conditions in any of these six groups. 2 months baby with TGA with large VSD with increased pulmonary blood flow will have only mild cyanosis. fallot’s physiology or Eisenmenger physiology. Symptoms: If patient is symptomatic. We try to fit our patient into one of this group and then we can easily reach to a diagnosis by seeing that which of individual lesion has got that particular physiology. . X-ray and ECG usually solve the problem. the more severe is the lesion. Old system of classification was that of 5T’s. Assessment of Severity 1. Doppler Echo or cardiac catheterization. • Transposition of great arteries • Tetralogy of fallot • Truncus arteriosus • Tricuspid atresia (includes tricuspid valve atresia. tricuspid stenosis. For better understanding. it can be clubbed with Tricuspid atresia. This classification is based on physiology and results in six subgroups of cyanotic patients. Using this classification. Rest of the patients need to be evaluated by 2D echo. • Total anomalous pulmonary venous return.g. disease is severe. X-ray and ECG we can reach bedside diagnosis in 75 to 80 percent cases. more severe is the lesion.Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease 153 pulmonary blood flow. 3. and Ebstein’s anomaly). one should be well conversant with physiology. the disease is severe. hypoplastic RV. Age of onset of cyanosis: Earlier the onset of cyanosis. However. e.

2.8% Atriventricular septal defect (AVSD) . Acyanotic congenital heart disease B. INCIDENCE OF CONGENITAL HEART DISEASES Ventricular septal defect (VSD) .2% Patent ductus arteriosus (PDA) . 5. Right ventricular obstruction – Tetralogy of fallot – Pulmonary valve stenosis with VSD – Pulmonary infundibular stenosis with VSD .6% Single ventricle . 7. 36.6% Transposition of great arteries (TGA) . 6.6% Pulmonary atresia . CONGENITAL HEART DISEASES The incidence of CHD in live birth is estimated between 0.9% Coarctation of aorta . Cardiomegaly: Larger the heart size.5 and 1. 3.5% CLASSIFICATION OF CONGENITAL HEART DISEASE A. Pulmonary arterial hypertension: It’s presence suggests a more severe disease.7% Tetralogy of fallot (TOF) . Cyanotic CHD Group I : Right heart obstructions 1. Right atrial obstruction – Tricuspid atresia 2.1% Atrial septal defect (ASD) . 2. 4.2% Tricuspid atresia . 1. 5. more severe is the disease.9% Pulmonary stenosis (PS) .0 percent in various large series. 6. 8.154 Seminar in Radiology 5.9% Aortic stenosis . 3.

• VSD – RV is not markedly enlarged because the shunt from LV usually enters RV in its out flow so that RV main cavity does not receive the whole volume of blood. The heart chambers which enlarge are the right chamber which receives the shunt and those right heart chambers distal to it. The left heart chamber from which the shunt emerges enlarges. • If L-R shunt is extreme – left heart may fail causing pulmonary odema. Exceptions • ASD – in which LA does not enlarge as it immediately decompresses at low pressure through a large ASD into the RA. Others • Ebstein’s anomaly • Pulmonary valve stenosis • PAPVD • Hypoplastic left heart syndrome • Uhls anomaly L-R SHUNTS 1. Atria – TAPVD 2. Pulmonary arteriolar obstruction – Eisenmenger reaction Group II: Common cardiac chambers 1. ATRIAL SEPTAL DEFECT Types 1. as well as those left heart chambers proximal to it. 2. Abnormal conventional radiological features if pulmonary systemic blood flow ration is >2:1. • Complication of Eisenmenger reaction. Ventricles – Double outflow RV (DORV) – The Taussig Bing deformity 3. Persistent common truncus arteriosus Group III: Abnormal connections or discordance • TGA C.Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease 155 – Pulmonary valve stenosis with ASD – Pulmonary artery atresia with intact ventricular septum 3. Ostium secundum or fossa ovalis defect • 80-90 percent of all ASD • Upper part of atrial septum • Usually >1 cm and is not valvular unlike patent foramen ovale .

RADIOLOGY 1. LA does not enlarge as it is immediately decompressed at low pressure through a large ASD into the RA. lobar and segmental pulmonary arteries. Ascending aorta. Pulmonary plethora (pulmonary arterial overcirculation) • Enlargement of main pulmonary trunk. There is usually a cleft in the anterior mitral leaflet → MR. . • This is a very severe deformity with incompetence of both AV valves as well as combined ASD and VSD. The regurgitant jet usually passes directly through the low primum ASD into RA instead of entering LA. Ostium primum defect • Mildest form of ECD • Accompanied by an abnormal position and anatomy of mitral valve which results in an abnormal shape of LV best seen on frontal LV angiocardiography as the Goose neck deformity. central (hilar) pulmonary. – The diameter of enface pulmonary vessels exceeding the diameter of its companion bronchus – The visualization of enface vessels below the level of tenth posterior rib. B. If L → R shunt > 2:1 percent then heart is enlarged (RA and RV). • It is the most common CHD associated with Down’s syndrome A. • Both upper and lower lobe vessels are prominent • Semiquantitative guides: – Diameter of right inferior pulmonary artery exceeding the diameter of trachea.156 Seminar in Radiology 2. 3. 2. and its arch tend to appear smaller than normal (due to rotation of ascending aorta by enlarged RA and RV → sagittal malalignment of aortic arch) 3. Endocardial cushion defect (ECD) • 5-10 percent of all ASD • Situated low on the atrial septum immediately above the AV valves due to lack of fusion of septum primum with the AV cushions. Persistant AV canal • Ostium primum defect is accompanied by cleft leaflets of malformed mitral and tricuspid valves and by an inlet VSD. Sinus venosus defect • 5 percent of ASD • Due to incomplete incorporation of fetal sinus venosus into RA • Situated high on the septum immediately below the SVC opening • There is invariably aberrant drainage of right upper and some times middle lobe pulmonary veins into lower end of Superior Vena Cava.

An injection of contrast into LA shunt during the laevo phase is made. This is an abnormal anterior movement of interventicular septum during ventricular systole. 7. 5. 4. i. Aberrant pulmonary veins which often accompany ASD rarely be identified except Scimitar vein syndrome and in sinus venosus defect. • In ostium primum defect on LV angiography on the frontal films. – Pulmonary arteries and veins are enlarged in size and can be followed up to the outer third of the lung. ECHOCARDIOGRAPHY • Reliable method • Usually corrective surgery may be performed without the need for invasive diagnosis • 2D imaging shows the defect in almost all cases • Hemodynamics of ASD are demonstrated by Doppler echocardiography • The typical secundum defect is best seen from subcostal view. – The prominence of hilar vessels on the lateral view. ASD may present in middle aged or elderly. Presence of septal edema (Kerley B lines) in a case of ASD suggest an associated mitral valve anomaly (Lutembacher syndrome or ECD) → can get features of PVH. 6. Reversal of shunt. mitral orifice and aortic diameters and velocities • Doppler flow mapping identifies the spatial extent of shunting and helps in the assessment of its magnitude • Both pulsed and flow mapping Doppler methods often identify a tiny L-R atrial shunt which is not associated with chamber enlargement or a visible defect ANGIOCARDIOGRAPHY • Rarely indicated except for interventional therapy or to calculate shunt ratio accurately or to confirm or exclude some anatomic detail or for associated CHD. • A catheter from the leg visually passes from RA → ASD → LA. • Transoesophageal studies often used to demonstrate sinus venosus • The ratio of pulmonary to systemic blood flow may be estimated by assessing pulmonary artery. when heart failure or pulmonary hypertension can finally develop and cause symptoms for 1st time. . we get characteristic Goose neck appearance as the upper right border of the LV is deeply indented by a concavity caused by misplaced mitral valve.Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease 157 – Prominence of vessels situated below the crest of the diaphragm on frontal view. • Characteristic dilatation of right sided chambers is well seen and the dominance of right ventricular volume overload will often be seen as paradoxical septal motion. Eisenmenger reaction may develop in a minority of patients with large ASD usually after 30 years.e.

Treatment 1. Surgical closure – low mortality 2. Eisenmenger reaction D. E. Mid muscular/apical defect c. Membranous VSD – Most frequent – 2 types a. OR • A high VSD may be associated with an abnormal incompetent TV permitting LV → RV . This increases L-R shunt (not usually to major degree) • May be identified on angiocardiography. VENTRICULAR SEPTAL DEFECT • Most common CHD • Types A. Inlet or basal muscular defect b. B. Muscular VSD (Maladie de Roger abnormality) – Usually small and often multiple (Swiss cheese VSD) 3 types a. RV and LA) due to volume overload. Aberrant pulmonary veins • 10-20 percent • Pulmonary veins (usually from right lung) draining into RA. Lutembacher syndrome • Association of ASD usually of the secundum type with mitral stenosis either congenital or acquired. Outlet defect: Gerbode LV-RA Shunt • This unusual defect is due to maldevelopment of part of AV cushion and upper part of the ventricular septum which seperates LV from RA. Infracristal: b. Transcatheter occlusion of ASD is being developed. In large shunts heart size increases (LV. Radiology 1. Supracristal : Less frequent B. Holt-Oram Syndrome.RA. RV may not be as large as anticipated as it receives the shunt into its .158 Seminar in Radiology Atrial Septal Defect may be Associated with A. Pulmonary valve stenosis C.

Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease 159

outflow tract so RV cavity does not receive full shunt volume (unless LA is
noticeably enlarged, it is usually not possible to differentiate the cardiac
shape from ASD).
2. Pulmonary plethora: Main pulmonary trunk, right and left pulmonary artery
and lobar, segmental and peripheral pulmonary arteries enlarge.
3. Eisenmenger reaction: Due to pulmonary vascular resistance.
4. Infants with large VSD are often distressed with increasing L and R heart
failure and recurrent pulmonary infection.

Echocardiography
• 2D echo shows the site of defect and demonstrates chamber enlargement.
• Pulsed Doppler confirms the L-R shunt or may suggest R-L component
(Eisenmenger reaction).
• Estimation of pulmonary to systemic blood flow ratio is possible by
assessing aortic, mitral and pulmonary artery velocities and diameter.
• Doppler flow mapping, perhaps the most powerful of all tools, can identify
the site(s), extent and direction of shunt. The identification of a tiny muscular
VSD, too small to image directly, is most impressive application.

Angiocardiography
• Angiographic injection is done into LV or into the main pulmonary artery to
view the L-R shunt and opacification of RV.
• Frontal cine angiographic projections will demonstrate the size and anatomy
of the pulmonary arteries before and after surgery.
• IV Septum is curved in all directions (from front to back, from side to side
and from above downwards) so that no single projection will visualize the
entire IVS tangentially.
If biplane cine angiography is available, the best two views to select for
initial examination of septum are:
1. 65° LAO with 20 to 25° cranial tilt → for perimembranous, inlet and
midmuscular septum
2. 30° RAO → High anterior and conal septum.
If VSD is large, however, it may be obscuring additional defects, and
its dimensions in the foreshortened plane may not be apparent. If multiple
defects are shown, at least one additional view may be necessary to localize
the defects precisely.
• The study of VSD should not be concluded before consideration of
possible coexistance of PDA so it must be closed before the cardiac
bypass is setup. It often needs a separate aortogram.

VSD May be Associated with:
1. PDA and ASD (other L-R shunts)

160 Seminar in Radiology

2. Essential features of more complex anomalies
• TOF
• Persistent AV canal
• Persistent truncus arteriosus
3. Other congenital cardiac anomalies
• TGA
• Double outflow ventricle
• Pulmonary valve or infundibular stenosis
• AR may complicate a supracristal or high membranous VSD due to
possibly into and even obstructing RV outflow.
4. Eisenmenger reaction is most common with VSD.

AORTO PULMONARY SHUNTS
1. PDA - commonest
2. Others
a. Aortopulmonary window:
• Due to perforation of the septum dividing the fetal truncus into
pulmonary artery and aorta.
• PAH is commoner than PDA.
• There are separate, well formed arotic and pulmonary valves
differentiating it from persistent truncus arteriosus which has a
single semilunar valve.
b. Aortic sinus fistula:
A fistulous connection from the aortic sinuses is usually a complication
of aneurysmal dilatation of one of the sinuses of valsalva, and may be
congenital or acquired. Most commonly the right coronary or non-
coronary aortic cusp perforates a shunts into the RA or RV. A fistulous
left coronary cusp is most unusual and may shunt into the left heart or
pericardial sac.
c. Coronary artery arising from pulmonary Artery
i. Right coronary artery may arise from pulmonary Artery
• Rarely symptomatic
• Shunt from AO → LCA → via anastomosis, retrogradely through
anomalous RCA → PA.
• Diagnosis: Selective left coronary arteriography
ii. Left coronary artery may arise from Pulmonary Artery
• LV muscle oxygenation is grossly impaired → LVF
• If infant survives, large collateral develop between the two
coronary arteries, permitting shunt from aorta → Right coronary
Artery → Via anastomosis to left coronary Art. → Pulmonary
Art.
• Diagnosis: Selective right coronary arteriography.

Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease 161

Angiocardiography
• Rarely needed
• Injection of contrast medium into the aortic arch (Catheter introduced via
femoral artery; or through the ductus, it will demonstrate the anatomy of
the ductus).

PDA May be Associated with:
1. VSD and ASD (other L-R shunts)
2. Preductal coarctation of aorta
3. Pulmonary artery atresia or pseudotruncus in which PDA may be the
principal method of entry of blood the distal pulmonary arteries. An alternative
route is via enlarged bronchial arteries
4. Complete interruption of aortic arch and hypoplastic left heart syndrome
in which a large PDA transmits a large R-L shunt from the pulmonary
artery to the descending aorta. If there is atresia of the Ascending Aorta
and arch, the ductus may be the only supply of blood to the head and
coronary arteries.
5. Eisenmenger reaction
In 3,4 and 5 closure of ductus may be fatal unless complete repair of the
underlying anomaly is accomplished.
6. Vascular ring: If the arch is on the right side, the PDA may be on the left,
forming an arterial ring which may compress the trachea and/or esophagus,
particularly in childhood. Occasionally, normally seated left aortic arch
may be associated with PDA of unusual anatomy and location, perhaps on
the right, with potential compression of the trachea or esophagus.

CONGENITAL HEART DISEASE PRODUCING
CENTRAL CYANOSIS
1. Right Heart Obstructions
A. Right Atrial Obstruction

Tricuspid Atresia
• There is no tricuspid orifice
• There is obligatory flow of systemic venous return across an ASD to the
LA and LV. The LV is large as it carries both pulmonary and systemic
venous return. Some of the blood in the LV then crosses a VSD to reach
RV and PA.
• The VSD is often restrictive and there may be associated pulmonary
stenosis. The RV is often so underdeveloped that the condition is considered
as one of the ‘single ventricle’ group : There is often relatively low pulmonary
blood flow, although this is not invariable and the condition may be expressed

162 Seminar in Radiology

in various ways, depending on the state of the VSD and the right ventricular
outflow.
• Chest X-ray:
i. Pulmonary oligemia
ii. Markedly concave pulmonary bay. The main pulmonary artery and the
hilar arteries are much smaller than normal.
iii. Moderately large heart (↑ RA, LA and LV)
iv. Rounded contour of heart due to downward and leftward enlargement
of LV
v. The right heart border tends to be flat rather than convex and it lies
slightly more towards the midline than normal since the right atrium
although enlarged and moves to the left to occupy the space normally
occupied by the right ventricle.
vi. 10 percent patients—Right sided aortic arch.
B. Right Ventricular Obstruction

Tetralogy of Fallot
• It accounts for majority of cyanotic children who survive infancy and
about 12 percent of CHD.
• It is due to maldevelopment of the conotruncal septum which divides the
cephalad portion of bulbus cardis into pulmonary Artery and Ascending
Aorta.
• The conotruncal septum is displaced forward producing a small pulmonary
artery in front of a large ascending aorta. Deficiency of the proximal portion
of the conotruncal septum causes a large subaortic VSD. Abnormal
development of proximal bulbus cardis results in a narrow distorted
obstructed RV outflow.
• 4 classical features are:
i. Pulmonary stenosis
ii. Subaortic VSD
iii. Aortic origin overrides the VSD
iv. RV hypertrophy
• Cyanosis does not occur until infant is several months old. This is because
the VSD is the dominant lesion at birth and the original PS is often not
severe. There may be an L-R shunt. During the first few month of life,
progressive fibroelastosis increases the obstruction of the outflow of RV
to cause pulmonary oligemia. This causes increasing RV hypertrophy which
displaces the IV septum backwards so that aortic valve comes to be above
and astride the subaortic VSD. The aorta will now receive some of the
output of RV as well as LV and the ventricular shunt becomes R → L
because of increasing stenosis of RV outflow. This leads to cyanosis.

Radiology
1. At birth heart shape is nonspecific. Later shape is suggestive of diagnosis
in 25 percent the classic ‘Core en sabot’ appearance is due to combination

Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease 163

of deeply concave pulmonary bay and elevaion from the diaphragm of a
well rounded cardiac apex (RVH).
2. Central and hilar pulmonay arteries are small and there is pulmonary
oligemia.
• If pulmonary stenosis is severe, there may be a very prominent
bronchial arterial circulation producing a reticulonodular pattern in inner
third of lung with absence of the normal pulmonary arterial branching
pattern.
• The upper mediastinum may be abnormal due to a large branch from
the aorta or its main branches to supply the lungs.
• 25 percent cases have right sided aortic arch. The descending aorta
usually crossing to the left of the spine in the lower thorax. This type
of right arch is usually associated with mirror image branching (i.e. left
brachiocephalic, right common carotid and right subclavian in order of
branching).

Echocardiography
• It shows the VSD, the overriding aorta and RVH very clearly.
• The right ventricular outflow gradient and the pulmonary valve gradient
can be estimated using Doppler technique but there are possible error due
to the many levels at which obstruction can occur.
• R-L shunting across VSD can be seen on color-flow Doppler and pulsed
Doppler.

Angiocardiography
• This often required, in addition to, echocardiography, because precise
assessment of anatomy is essential in surgical planning. The size of the
pulmonary valve annulus as well as the size and anatomy of the more distal
pulmonary arteries must be determined. Injection of contrast into RV will
reveal the best disordered anatomy and circulation.
• The most common coronary artery variant occurring with TOF is anomalous
origin of left anterior descending coronary artery from the right coronary
artery. This vital artery runs over the surface of the right ventricle just
where the surgeon might make the incision, enlarge the right ventricular
outflow tract. So it must be detected by either opacification of aortic root
or by selective coronary arteriography.

Variants of TOF
1. The pulmonary valve may be absent (very uncommon) causing severe PR
and marked dilatation of main pulmonary artery and/or its R and L branches,
sufficient to compress neighboring structures.
2. The left main PA may be absent most frequently with a right sided ascending
aorta. The left lung may be slightly smaller and more oligemic than the
right but may have a more prominent bronchial collateral circulation.

164 Seminar in Radiology

3. ASD may be present (pentalogy of fallot) permitting R-L shunting at both
atrial and ventricular levels.
4. Pulmonary arterial atresia (pseudotruncus/ persistent truncus arteriosus
type IV).
C. Pulmonary Arteriolar Obstruction – Eisenmenger Reaction (ER)
• It is an important hemodynamic response to a large L-R shunt.
1. ASD
After 20-40 years of large L-R shunt → pulmonary arteriolar sclerosis
develops → increasing occlusion of pulmonary arteriolar bed → increase
peripheral pulmonary arteriolar resistance which exceeds systemic peripheral
resistance → reversal of shunt.
• The main pulmonary artery trunk, the right left main PA lobar and
segmental artery and the outflow of the RV are always markedly
enlarged; perhaps even to giant proportions.
• The heart size diminishes.
• Narrowing of peripheral pulmonary vessels.
• There is risk of paradoxical embolism.
• Calcificaiton of main and central pulmonary arteries.
2. VSD
The pulmonary arterioles and arteries retain their basic fetal structure and
their fetal high resistance to flow. Hence eisenmenger reaction may develop
in infancy or childhood without a prior massive L-R shunt. The heart,
common pulmonary trunk, Rt and Lt pulmonary artery are often only
slightly enlarged or may even be of almost normal size and shape unlike
Eisenmenger ASD.
3. PDA
• Heart may be minimally enlarged when eisenmenger reaction develops
in infancy.
• When eisenmenger reaction develops many years later – the heart is
considerably enlarged with large main pulmonary trunk and Rt. And Lt.
Branches. The segmental arteries are rarely and loabar arteries
uncommonly enlarged unlike extension of dilatation into segmental artery
in eisenmenger reaction in ASD.

COMMON CARDIAC CHAMBERS
A. ATRIA
Single Atria:
• Absence of development of interatrial septum
– Very rare
• TAPVD (total anomalous pulmonary venous drainage)
– More frequent variant of complete mixing of systemic and pulmonary
venous returns to the heart.
– In TAPVD all the pulmonary veins come to a confluence behind LA
and drain directly or indirectly into RA.
– There are 4 main pattern of TAPVD.

Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease 165

a. Supracardiac drainage
– Most frequent
– There is a large ascending vein on the left side which connects into the
left innominate vein which then enters SVC → RA.
b. Cardiac drainage into the right atrium either directly or via coronary sinus.
– Chest X-ray in supracardiac and cardiac TAPVD
i. Enlarged heart
ii. Pulmonary plethora
iii. In supracardiac TAPVD wide mediastinum due to left sided
ascending vein and in late cases “cottage loaf of bread heart” /
“figure of 8” / “showmon’s heart”.
c. Infradiaphragmatic or infracardiac drainage of confluence of pulmonary
veins via descending vein which passes through the diaphragm and enters
into portal vein or ductus venosus or rarely hepatic veins.
• 10 percent of TAPVD
• This variety is usually obstructed → severe pulmonary venous
congestion and edema and heart failure
• The heart is normal in size or only minimally enlarged as there is no
volume overload.
d. Drainage into combinations of above patterns.

B. Ventricles
• Single ventricle – Very rare
• More frequently there is one large ventricular chamber separated by a
rudimentary perforated ventricular septum from a second smaller
hypoplastic ventricle. The large ventricle may supply both aorta and
POA and hence is called double outflow ventricle—a term implying at
least 1½ semilunar valves arising from one ventricle.
– Double outlet RV (DORV) is more common
– Although both semilunar valves may clearly arise from one ventricle,
it is more frequent for one valve to lie astride the high VSD
(subpulmonary VSD) and therefore, receive blood from both
ventricles.
– Taussig—Bing deformity is an incomplete variant of DORV with a
transposed posteriorly displaced pulmonary artery arising astride a
subcristal VSD and receiving blood from both ventricles.

166 Seminar in Radiology

C. Persistent Common Truncus Arteriosus
• A single great artery arises from the heart due to failure of division of
the embryonic common truncus arteriosus. The common truncus arises
from above a large VSD and the pattern of division of the common
truncus varies.
• Types
• On X-ray Chest:
– Heart is enlarged to a varying degree with biventricular enlargement.
– Heart shape may be suggestive with a deeply concave pulmonary
bay with small hila and a rounded cardiac apex, elevated well above
the diaphragm.
– Truncus is a larger caliber than the normal aorta and rises high in
the mediastinum.
– Right sided aortic arch –30 to 40 percent.
– These features may produce the classic appearance of the ‘sitting
duck’ which is an extreme variant of ‘Coeur en sabot’.
– The lateral film shows an empty concavity at the site of the normal
pulmonary outflow tract and the main pulmonary artery.
– Lungs may be plethoric/oligemic/or may demonstrate PAH.
– Relatively narrow mediastinal shadow (as in TGA).
• Diagnosis
– Echocardiography is very helpful
– It is difficult to perform good angiography in these patients due to
the very fast blood flow through the heart which dilutes the contrast
medium. The patients are often very ill and catheterization with
angiography produces significant morbidity.
• Hemitruncus (or aortic origin of one PA)
– Occasionally only one lung is supplied from the truncus while the
other lung is supplied by a pulmonary artery arising from RV.
– It is frequently complicated by pulmonary artery stenosis, so that
the lung supplied by RV is oligemic while the other lung supplied
from aorta (truncus) may be very plethoric.

ABNORMAL CONNECTIONS OR DISCORDANCE : TGA
A. UTGA
• 75 percent of UTGA have dextrop loop
• There is ventriculoarterial discordance, i.e. RV gives rise to AO and LV
to PA.
• In order to sustain life mixing of blood must occur involving both L-R
shunt and an equal volume of R-L shunt.
• Both ASD and VSD are frequently present either above, together or
associated with PDA.

Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease 167

Radiology
• Heart is enlarged and rounded
• The right heart border is usually more convex and prominent due to RA
enlargement → globular heart like an egg on its side or apple on string.
• Narrow superior mediastinum on PA film and wide on lateral film → as
both ascending aorta and pulmonary artery lie in the midline.
• Pulmonary plethora as LV output is generally greater than RV output.
• The combination of unobtrusive central pulmonary arteries and pulmonary
plethora in a cyanotic child is highly suggestive of UTGA.
• 20 percent have pulmonary stenosis – then oligemic lung fields.

Diagnosis
Echocardiography is the investigation of choice but cardiac catheterization
and angiography is sometimes performed. It invasive procedure is required
(balloon septostomy - thin part of septum primum covering foramen ovale is
ruptured).

CORRECTED TRANSPOSITION OF GREAT ARTERIES
• 15 percent of all patients with transposition have CTGA with laevo loop
and inversion of ventricles.
• In CTGA the abnormal circulation of UTGA is corrected by second
developmental anomaly – artrioventricular discordance, which is due to
displacement of RV to the left of LV. This coronal malposition of the two
ventricles is called inversion of ventricles. The discordant connections
cancel each other in hemodynamic terms.
• Associated abnormalities, e.g. VSD, TR, PVS, or conduction defects
ultimately cause cardiac decompensation and symptoms.

Radiology
• On X-ray chest—the ascending aorta instead of forming a slightly convex
right border of the superior mediastinum, forms a long convexity along the
upper portion of the left cardiac border to reach the aortic arch which lies
to the left of trachea.

Echocardiography of TGA
• It is relatively straight forward in both types of TGA but care must taken
to correctly identify the two parallel great arteries as they may not be in
typical positions.
• The aorta can be identified specifically if the vessel is traced up to the
brachiocephalic artry origins.
• 2D imaging will show the smaller LV in D-loop TGA which pumps to the
pulmonary circuit, and the reversed curve of the interventricular septum
will be apparent.

On X-Ray • Enlarged globular or square cardiac silhouette with narrow vascular pedicle and pulmonary oligemia. Serious arrythmias • Clinical spectrum varies from severe cyanotic heart failure to minimal or absent symptoms with normal duration of life. These malpositioned cusps are malformed and permit TR of varying degree. The left border of the heart is also smoothly convex but . This results in considerable difficulty in RA emptying → enlarged RA. Various types of discordance (transposition) c. Patent foramen ovale or ASD → The raised RA pressure causes R- L shunt and central cyanosis of varying degree. b. • RV forward output is reduced because – Only its distal part can eject through PV – Tricuspid regurgitation – Impaired emptying of RA • Frequent associations: a.168 Seminar in Radiology • Associated conditions must be sought. • The right atrium is characteristically markedly enlarged causing a prominent smoothly convex right lateral border with increasing contact with the sternum anteriorly and a bulging posterior border as seen in lateral film. especially when the great arterial switch procedure is contemplated. • The proximal portion of the RV cavity is atrialized for it lies on the atrial side of the abnormally placed tricuspid valve but it contracts synchronously with the ventricle. Cardiac Catheterization and Angiocardiography • It will clearly show the abnormal connections and will also be useful for clarifying details of anatomy concerning associated anomalies. Ebstein’s Anomaly • Uncommon condition • The septal and posterior leaflets of tricuspid valve are attached to the middle of the right ventricular chamber instead of to the tricuspid ring at the atrioventricular junction. • It is important to assess coronary anatomy for surgical planning. OTHER CONGENITAL HEART DISEASES 1. • In L-loop TGA. the reversal of the morphologically L and R ventricles can be demonstrated by the reversed insertions of the AV valves. Others • Hypoplastic left heart syndrome • Pulmonary arteriovenous malformations.

curving in a crescent or scimitar course (convex to the right) undering as it approaches right cardiophrenic angle. The complete Scimitar syndrome involves presence of a. b. – The right lower and sometimes middle lobe veins form an abnormal vein which runs downwards and medially. It is often inadequately seen on X-ray (CT and US is better). 2. There is always and associated high ASD of the sinus venosus type. Anomalous Pulmonary Venosus Drainage • TAPVD • PAPVD PAPVD • It usually affects the right lung and the receiving chamber of one or more pulmonary veins may be RA. c. Heart may be normal or may have ASD. to pass through the diaphragm and drain into the upper IVC. SVC. The Scimitar vein runs posterior to RA and may be obscured by that chamber.Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease 169 superiorily it approaches the midline so that the vascular pedicle of the heart is narrow. due to the reduced cardiac pulsations. almost etched. • Lungs are noticeably oligemic • The cardiac outline is often very sharply defined. Scimitar vein and syndrome (Hypogenetic lung syndrome) or pulmonary venolobar syndrome. iii. There is often a substantial anomalous artery (best seen on aortography) passing upward from the abdominal aorta to supply the right lower lobe. ASD is frequently associated. d. . Echocardiography • PAPVD can be diagnosed by echocardiography by visualization of the individual veins draining into RA but the diagnosis can be more difficult if site of drainage is to IVC or SVC. Right bronchial tree may have abnormal branching and there may be bronchiectasis of the lower lobe. Veins of right lung—they may enter RA without any of above associations. Sinus venosus defect: The right upper lobe veins pass horizontally to enter the lower part of SVC which may be considerably dilated. A Scimitar pulmonary vein draining a small right lung with displacement of the mediastinum to right. i. especially as the heart is often displaced to the right because of the hypoplastic right lung. IVC or azygos vein in reducing order of frequency. ii. • There are few characteristic pattern of PAPVD. The main pulmonary artery and frequently its right and left branches are hidden by the enlarged heart. A hypoplastic right pulmonary artery which may be obscured by displaced heart.

And Rt. 3. • Very poor prognosis. Sometimes the direct injection of contrast medium into the suspected abnormal veins can be diagnostic.170 Seminar in Radiology Angiocardiography The delineation of individual pulmonary veins in PAPVD can be difficult and may require separate injections into Lt. . The principal components are MV atresia. carrying only reverse flow from the PD and aortic arch sufficient to fill the coronary arteries. The brachiocephalic branches are supplied retrogradely and the ascending aorta shows diminition in size. Hypoplastic Left Heart Syndrome (Aortic Atresia) There is a very small hypoplastic LV with an extremely low or absent LV output which is unable to sustain systemic circulation. In this condition the RV performs the entire systemic pumping function with systemic blood supply being directed through ductus arteriosus. aortic valve atresia and hypoplastic proximal aorta. but this approach can be surperisingly difficult to interpret as the contrast medium is rapidly diluted and the atrial anatomy is often unclear. Pulmonary arteries in oblique views.

The MV has three main components: • Leaflets (2) – anterior and posterior • Chordae attached to papillary muscles (‘subvalvular apparatus’) • Annulus (valve ring) 5. The two leaflets are attached at one end to the annulus and at the other (free) edge to the chordae which are fixed to the LV by the papillary muscles. 4. rheumatoid arthritis. 3. congenital. The MV opens during ventricular diastole when blood flows from LA into LV. Changes in MV Area in Relation to Severity of Mitral Stenosis (MS) Normal valve 4-6 cm2 Mild MS 2-4 cm2 Moderate MS 1-2 cm2 Severe MS <1 cm2 Investigations Radiology Plain Chest Skigram: PA View . During ventricular systole. the only common cause of MS is rheumatic heart disease. mucopolysaccharidoses (Hurler syndrome) and carcinoid. In practical terms. which is normally 4-6 cm2. 6. SLE. Mitral Stenosis Defenition: Reduction in the effective mitral valve orifice area.12 Valvular Heart Disease Mitral Valve (MV) : Anatomical Landmark 1. connective tissue disorders and infiltrations. The leaflets free edges meet at 2 points called the commissure. The MV is located between the LA and LV. 2. the MV closes as blood is ejected through LV. Much rarer causes include: Mitral annulus calcification.

Left atrial enlargement which may vary from trivial to gross. Long standing pulmonary venous hypertension gives rise to pulmonary arterial hypertension.172 Seminar in Radiology A. Typically in mitral stenosis a prominent left atrial appendage is also seen. If the pulmonary venous pressure is elevated. J. In long standing cases. In pure mitral stenosis. This sign is more obvious in expiration than in inspiration. . seen as widespread mottling. Mitral valve calcification indicates longstanding and severe MV disease. Splaying of carina and elevated left main bronchus and increased carina angle (normal = 57°). IN RAO VIEW Enlarged left atrium bulges backwards and obliterates the translucent retrocardiac space. H. septal lines and pleural effusions may appear. F. • Kerley A Line: Due to superficial lymphatic involvement and seen as vertical lines in upper field. This is reflected by enlarged main and central pulmonary arteries and peripheral pruning. tranverse cardiac diameter is often normal unless pulmonary hypertension develops. K. On Barium swallow. a bolus passes normally down to a point just below the left main bronchus when it seems to halt abruptly. B. the upper zone vessel is dilated due to upper lobe blood diversion and is brought into prominence by lower vascular constriction. D. C. seen as a : • Dense pear-shaped opacity lying transversely inside the cardiac shadow causing increased density due to left atrium. hemosiderin deposits may be found in the lungs. • Kerley C Line : seen as reticular pattern and due to involvement of all the groups of lymphatics. With higher pressures in the pulmonary veins. • Double heart shadow on the right of the spine (double right heart border). • Septal lines are Kerley B Lines: Transverse opaque lines of 1-2 cm length usually noted in pulmonary bases and are due to dilated deep lymphatics. This enlargement may vary from a simple straightening of the left heart border (called as mitralization) to a very gross local protrusion. best seen in lateral view between left atrium and left ventricle. Altered thoracic paraspinal line (Normal 8 mm). L. Lateral displacement of descending thoracic aorta. G. Barium bolus then fills slowly the lower third of the esophagus which is curved sharply backwards. Hemosiderosis and ossific nodules are the observation seen in advanced disease. I. E. More rarely seen in frontal view on an adequately penetrated film. Small aortic knuckle is caused partly by a true hypoplasia of aorta and partly by right ventricular rotation.

• The thickened leaflets return stronger echoes than normal. c. • The velocity of blood flow allows the pressure gradient across the mitral valve during diastole to be determined. • LA enlargement. • The ‘a’ wave is markedly diminished (absent with atrial fibrillation). M-mode Echocardiogram • The posterior leaflet moves forward in diastole in the same direction as the anterior leaflet. Assessment of left and right ventricular function. Direct measurement of the mitral valve orifice area using the parasternal short-axis view. Changes in the sizes of the four cardiac chambers. using the BERNOULLI PRINCIPLE (P1-P2 = 4V max2). and when calcification is present. multiple dense echoes are seen. commissural fusion causes abnormal movement of the mitral leaflets. b. Valvular Heart Disease 173 Echocardiography • Echocardiographic evaluation and Doppler studies have emerged as the most useful and essential investigation in the assessment of valvular heart disease. 2-D Echo • The two-dimensional echocardiogram enables visualization of the abnormal valve and its deranged movement. 2-D Parasternal Short Axis View (at the level of MV leaflets in end diastole) • Normally leaflets open and close in a ‘fish-mouth’ pattern. • Restricted leaflet motion. • Doming of one or more leaflets giving a characteristic ‘elbowing’ or ‘bent- knee’ appearance (particularly of AMVL). Doppler Echo Appearance • Continuous-wave Doppler is extremely useful in assessing the severity of mitral stenosis. • It allows— a. • In MS-leaflet tips are calcified and orifice size is reduced. • In mitral stenosis. 2-D Echo Parasternal Long Axis View • Thick and/or calcified leaflets. .

174 Seminar in Radiology • The mitral valve area can also be calculated by measuring the rate of decay of the Doppler-measured maximum velocity. which is usually associated with mild MR. In MR. In the occasional patient. • In late cases. • Gross enlargement of left atrium is noted in chronic rheumatic regurgitation with stenosis . catheterization is performed to assess changes in pulmonary artery pressure and pulmonary capillary wedge pressure during exercise. • Diastolic mitral regurgitation is rare and occurs when the left ventricular diastolic pressure exceeds left atrial pressure. allowing retrograde flow through the open mitral valve. mitral valve abnormalities. heart size may remain normal. and changes in ventricular function. Assessment of the severity of associated mitral regurgitation may also require left ventriculography. Left atrial dilation is usually obvious. to clarify the mechanism of exercise-induced symptoms. . shows C or J shaped appearance on plain chest film. moderate cardiac enlargement suggests left ventricular rather that right ventricular enlargement. MITRAL REGURGITATION Definition • Retrograde blood flow from the left ventricle to the left atrium. • Mitral regurgitation occurs usually during systole due to the ineffective closure of the mitral valve. MRI and CT • Both cardiac MRI and CT scan demonstrate chamber enlargement. there are changes in: • The function of the MV • The LV and LA which becomes dilated as there is volume and pressure load on LV and LA and in severe regurgitation a pressure load on RV. • Neither MRI nor CT provides any advantages over other imaging modalities and they are not indicated in the routine diagnosis and management of mitral stenosis. Cardiac Catheterization and Angiography • Unless information about the coronary arteries is required. Investigations Plain X-Ray Chest Skiagram • In mild regurgitation. • Mitral valve calcification. cardiac catheterization is unnecessary in most cases of mitral stenosis.

The width of the MR jet at the level of the leaflet tips (broad colour flow signal) correlates with severity (a wider jet represents more severe MR). a area >8 cm2 is likely to be severe. Papillary muscles—ruture. 4. scarring.g. Chordae—rupture. MV prolapse or flail posterior leaflet. 2. the cusps open and close again at end – systole when the aortic pressure exceeds the LV pressure. vegetations due to endocarditis. Wide jet. shortening. 2. 3. The aortic cusps form a central closure line in diastole. <4cm2 likely to be mild. vegetations. and two are located on the posterior wall (left and posterior cusps). The left atrium is enlarged. Leaflet abnormalities—rheumatic leaflets. In systole. 2-D echo helps to suggest an underlying cause and assess its consequences. volume-overloaded LV. flail leaflet. Valvular Heart Disease 175 Echocardiography M-Mode shows LV dimensions are increased as is velocity of motion of the posterior wall and interventricular septum (IVS). The area of color in the LA depends on the machine settings. the aortic wall bulges to form an aortic sinus of valsalva. Doppler echo features of severe MR 1. left coronary – left posterior sinus). 3. Jet fills a large area of LA. 5. The extent to which the MR jet fills the LA cavity is also a finding. LV abnormality—dilatation causing annular stretching and ‘functional’ MR. . e. This can be seen on color flow mapping and may also cause retrograde flow (LA to lungs) detected by pulsed wave Doppler with the sample volume in one of the pulmonary veins. hypertrophy. Aortic Valve (AV) The AV is located at the junction of the LV outflow tract and the ascending aorta. Raised pulmonary artery (PA) pressure is observed and is estimated by Doppler from tricuspid regurgitation (TR). prolapse. 4. Dense signal on continuous Doppler show intensity of the jet is greater with more severe MR since more red cells reflect ultrasound. to form a parallelogram shape. However. The parasternal long-and short-axis views and apical 4-chamber views are the most helpful and may show: 1. calcification. There may be features of an underlying cause of MR. The jet extends to the pulmonary veins. Valve has three cusps (leaflets)—one is located on the anterior wall (right cusp). The coronary arteries arise from the sinuses (right coronary-anterior sinus. Behind each cusps. Systolic flow reversal in pulmonary veins are seen. calcification. multiple echoes suggesting vegetations due to endocarditis. thickening. regional wall motion abnormality due to MI or ischemia.

Supravalvular AS Occurs in some congenital conditions such as William’s syndrome (which includes hypercalcemia. In adults. heart size remains within normal limits. plain chest skiagram shows normal sized heart. • There may also be evidence of associated pulmonary artery stenosis. Calcific (degenerative) AS associated with increasing age. the features observed are: . although occasionally post-stenotic dilation of aorta may be present. The LV ejection time can be measured from the point of cusp opening to cusp closing. Echocardiography A. 3. • In supravalvular AS. growth failure and mental retardation). • Recognizable left ventricular enlargement and raised pulmonary venous pressure are late signs indicating left ventricular failure. echoes from left coronary cusp may be seen within the parallelogram. with an inconspicuous aorta. absence of valve calcification suggests insignificant stenosis. Congenital bicuspid valve. Valvular AS has 3 main causes: 1. Rheumatic heart disease 2. chest skiagram is usually normal. It is possible to measure aortic root diameter and LA diameter from this M-mode image. C. B. Subvalvular AS: caused by obstruction proximal to the AV opening. • In subvalvular AS. It may occur at 3 levels • Valvular • Subvalvular • Supravalvular A. Investigations Plain Chest Radiograph The major features are: • In an uncomplicated AS. • Subaortic membrane • HCM • Tunnel subaortic obstruction • Upper septal bulge. • Post – stenotic dilation of ascending aorta-seen as a localized bulge to the right above the right atrium. On 2-D echo using parasternal long and short Axis views and apical 5-chamber views. Aortic Stenosis (AS) Definition: Narrowing of the left ventricular out-flow tract causing obstruction to systolic flow from the left ventricle to the aorta.176 Seminar in Radiology Rarely. • Aortic valve calcification – better detected by fluoroscopy.

0-2.0 > 64 > 40 Magnetic Resonance Imaging (MRI) and Computed Tomography (CT) 1. . Recordings of peak and mean velocity are made from apical. and in subvalvular stenosis. calcified.1.75 Peak velocity (m/s) Peak gradient Mean gradient (mmHg) (mmHg) Normal 1. while in supravalvular stenosis. B.5 Severe < 0. peak velocity peak pressure gradient and mean pressure gradient (often more accurate than peak). Features of Varying Degrees of AS Valve area (cm2) Normal 2. There may be LVH due to pressure overload 3. C. right parasternal and suprasternal sites. the pressure difference is between the supravalvular chamber and the aorta. it is within the LV. 3.5 Moderate 0. Doppler is most useful in determining the severity of AS by estimating the pressure gradient across the AV. have reduced motion or may ‘done’(latter is diagnostic of AS) 2. Post – stenotic dilatation of the aorta may be seen.2. MRI can also be used to measure aortic flow and transvascular gradient.0-4.3. Valvular Heart Disease 177 1.0 20-64 20-40 Severe > 4. Coronary arteriography is indicated preoperatively in patients with aortic stenosis with or without angina.0 < 20 < 20 Moderate 2. LV dilatation occurs if heart failure has developed (usually a poor prognostic feature) 4.75 .5 . Valve area can be calculated by use of the continuity equation. Severity of AS correlates with valve area. The corres- ponding pressure gradients are calculated using Bernaulli equation (gradient = 4 V2 max). there is a systolic pressure difference across the valve. 2. Cardiac catheterization is also indicated when the severity of aortic stenosis cannot be determined non-invasively. 2. The cusps may be seen to be thickened.5 Mild 1. Cardiac Catheterization and Angiography 1.0 < 10 < 10 Mild 1. A M-mode echocardiogram may show an eccentric closure line.5 . Both MRI and CT have been used to evaluate left ventricular function and left ventricular mass in patient with aortic stenosis. In valvular aortic stenosis.

Crohn’s. Left ventricular hypertrophy may be seen by contrast left ventriculography which. Rheumatic heart disease c. Aortic Regurgitation (AR) Definition: This is leakage of blood from the aorta into the left ventricle during diastole. Aortic root diseases: a. Usually there is generalized dilatation. SLE. Acute AR a. however. angiography may also reveal the thickening of the valve cusps with systolic doming and a central ejection jet. syphilis. ‘annulo-aortic ectasia’. but in Syphilis and Marfan’s Syndrome. 5. If AR is due to abnormalities of the aortic wall. Reiter’s disease. the ascending aorta is enlarged. pseudoxanthoma elasticum and aortitis. Distortion—Dissection (type I and II). angiography show the obstructive lesion above the sinuses of Valsalva. Ehler’s-Danlos syndrome. Associated aortic regurgitation can be demonstrated by aortography. hypertension. In valvular aortic stenosis. Connective tissue and inflammatory disease – Rheumatoid arthritis. Dissection c. In subvalvular aortic stenosis. b. 6. Endocarditis b. b. Trauma Investigations Plain Chest Skiagram a. the left ventricular angiogram shows the subvalvular obstruction or a more diffuse fibromuscular lesion. Chronic AR 1. 7. Endocarditis b. In supravalvular stenosis. 8. . a localized aneurysm of the ascending aorta may be seen.178 Seminar in Radiology 4. aortic annulus or aortic root. rupture of sinus of valsalva and aneurysm. Dilatation—Marfan’s syndrome. Whipple’s disease. is rarely required if echocardiographic evaluation is adequate. d. ankylosing spondylitis. 2. ankylosing spondylitis. subaortic and supraaortic stenosis. Congenital – bicuspid valve. Causes of AR: AR can result from intrinsic abnormalities of the valve leaflets. Valvular: a.

c. Echocardiography All the echo modalities are useful in diagnosis and evaluation. Valvular Heart Disease 179 c. Both suggest severe AR. along with the dilatation of the ascending aorta is characteristic. aliasing will occur. the LV dilates producing cardiac enlargement. d. b. rheumatic) • Vegetations • Dilated aortic root • Proximal aortic dissection • Abnormal indentation of anterior MV leaflet • Abnormal intraventicular septal motion. Colour flow mapping is helpful: The jet of AR can be seen entering the LV cavity on a number of views such as parasternal long-axis and apical 5-chamber. a. M-mode May Show • Vegetations on AV • Fluttering of AV cusps in diastole • Eccentric closure line of bicuspid valve • Dilation of Aortic root • Fluttering of anterior MC leaflet • Premature opening of AV because of raised left ventricular end-diastolic pressure (LVEDP) and premature closure of MV. . 2-D Echo May Show • LV dilation – correlates with severity of AR • Abnormal leaflets (Bicuspid. • Dilation of LV cavity due to volume overload. Pulsed Doppler can be used in the apical 5-chamber view with the sample volume just proximal to the AV: AR can be detected as a signal above the baseline but since velocity is usually high (>2m/s). Doppler Study This is useful both for detecting AR and assessing its severity. Continuous wave Doppler is then useful and the signal seen only above the baseline. Doppler and color flow mapping are especially helpful. e. M-mode and 2-D echo cannot directly diagnose AR but may indicate underlying causes and aid in the assessment of the effects of AR. • Exaggerated septal and posterior wall of LV wall motion (exaggerated septal early dip strongly suggests AR). In acute severe AR there may be pulmonary edema but the cardiac silhouette remains normal. In long standing AR. Linear calcification.

however. for quantitative measurement of regurgitation fraction and for evaluation of left ventricular volumes and function. it can be used for the diagnosis of aortic root disease and aortic dissection. mass and regurgitation index (RI= LV Stroke Volume/RV stroke volume). as its name suggests. Tricuspid Regurgitation (TR) Causes of TR are similar to MR – the commonest causes are secondary to RV dilatation. More severe TR is associated with a broad. . although cardiac output may remain normal. unlike the 2 of the MV. Cardiac Catheterization and Angiography In symptomatic patients with chronic AR. • An annulus or valve ring. along with a marked increase in left ventricular end-diastolic pressure. and primary causes include disease of the leaflets. In acute severe AR. Trans-tricuspid flow is best measured with pulsed Doppler in the apical 4-chamber view with the sample volume in the RV immediately below the TV. There is associated retrograde systole flow in the vena cava and hepatic vein. Angiography can be used for qualitative assessment of the severity of AR. Tricuspid Valve (TV) Tricuspid Stenosis (TS) The TV is structurally similar to the MV in having: • Leaflets – the TV has 3. and/or the subvalvular apparatus. M-mode and 2-D Echo findings are Analogous to MS • Thick and/or calcified leaflets • Restricted leaflet motion • Doming of one or more leaflets in diastole (especially the anterior leaflet). • Chordae attached to papillary muscles.180 Seminar in Radiology MRI AND CT Both can be used to assess left ventricular function. Echo assessment of TR severity is best achieved by Doppler as with MR. Pulmonary Valve (PV) The PV has 3 leaflets and sits at the junction of the RV outflow tract and the main pulmonary artery. left ventricular diastolic pressure is usually elevated. Doppler findings are similar to MS. cardiac output may be low. high-intensity jet filling the RA.

carcinoid). dilated PA. • The normal peak velocity across the valve is 1. Severity is indicated by the width of the jet at the valve level. Using pulsed wave Doppler. • Absent valve leaflets (congenital) • Pulmonary artery aneurysm. There may be evidence of : • Pulmonary hypertension: Dilated RV. Valvular Heart Disease 181 Pulmonary Stenosis (PS) May be valvular. • Increased intensity of the Doppler signal. and excellent in to right ventricle. Pulmonary Regurgitation (PR) Secondary causes are the most common M-mode and 2-D echo cannot detect PR directly but can show some evidence of the underlying cause and the effect.‘right ventricularization’ of IVS). • There may be post-stenotic dilatation of the PA or its branches and RV hypertrophy or dilatation due to pressure overload. it can be seen that the increase in velocity occurs in the RVOT below the level of the PV. • Vegetation on the valve in endocarditis. Doppler techniques show pulmonary regurgitation and help to assess severity. • The peak gradient across the valve can be estimated by Doppler sonography. To summarise the radiological findings. as with aortic regurgitation. calcified leaflets. Supravalvular PS can be due to stenosis of the main PA or any of its branches distal to the PV. abnormal IVS motion (behaves as though it ‘belongs’ to the RV rather than LV. It may be iaterogenic – post-surgical banding of the PA which is performed in left to right shunts. a table is being presented which divides the changes in three subgroups – . Valvular PS may be congenital or acquired (rheumatic. doming of the valve leaflets in systole and restricted motion.0 m/s. • Increased slop of the Doppler signal (deceleration time). Subvalvuler PS is most commonly congenital and is rarely acquired. Doppler indicators of severe pulmonary regurgitation are: • Colour flow – the regurgitant jet is visualized directly. • 2-D echo may show thickened. can be determined.show distance between the pulmonary valve and the level at which regurgitation is detected. • Thick immobile PV leaflets in rheumatic heart disease or carcinoid. • Pulsed wave Doppler . • Dilated PA – the diameter can be measured usually in parasternal short-axis view at AV level. supravalvular (peripheral) or subvalvular (infundibular). A jet at the lower infundibular region is severe.

In 25% cases confines of Rt. (normal 8 mm) obliteration is LVH – Calcification seen in (MS + MR) mitral valve.L. endo- cardinen. chus this bulge is to left side. obliteration in RVH – Lateral deviation of – Retrocardiac space T.1 Changes in heart Changes in lungs Changes in the mediastinum – Left atrial enlargement – Widening of carina angle Dorsal esophagus is bulged – Double density on right (normal 57°) to Rt side due to LA enlarge- side. carditendinae . cusp myocardican. – Small aortic knuckle – Long standing collapse – Fullness of pulmonary leads to bronchicctatic conus changes – Enlargement of left – Kerley ‘B’ line atrium appendage – Kerley ‘A’ line – Enlargement of Rt. left atrium compression of left main protrude through Rt bronchus resulting in coll- atrium. ment (75%). – Displacement followed by mal dilation. – Kerlay ‘C’ line ventricle – Milliary mottling – Straightening of left (Haemosiderosis) cardiac border – Calcification – Mitralisation of heart – Ossification – Lateral displacement – Pleural effusion of Descending – Retrosternal space Thoracic aorta. atrium. Never beyond the – Raising of left main bron. apse of Lt lower lung field.182 Seminar in Radiology Table 12. only in cases of aneuris.P.

SECTION 4 Respiratory System .

.

Each possesses morphologic findings sufficiently characteristic to be recognized. Pulmonary Vasculature c. 2. . Tracheobronchial tree b. Confirm the presumptive clinical diagnosis. radiological and pathological findings in pneumonia of different etiology. It is very difficult to describe them according to causative organism. and is characterized by inflammatory exudate in both the alveoli and interstitium. Detect complications such as cavitation. Pneumonia acquired via the tracheobronchial tree can be divided into three pathogenetic types. Identify underlying predisposing factors such as bronchiectasis and bronchial neoplasia. and development of empyema. abscess formation. each with different morphologic and roentogenographic characteristics. 3. mediastinum or across the diaphragm. Mycoplasma. may be important in determining the specific cause of the pneumonia. viruses and other microorganisms. Aims of Diagnostic Imaging 1. Monitor the radiologic progression and resolution of disease. Direct spread from chest wall.13 Pulmonary Infection PNEUMONIA Pneumonia is an infectious process involving pulmonary alveoli caused by bacteria. The clinical. are frequently very similar. pathologically and radiologically. 4. Infection Via the Tracheobronchial Tree Most commonly by aspiration or inhalation of microorganisms Or Direct physical implantation (bronchoscope). Pathology Route of entry to lung are followings— a. The pneumonias are frequently classified according to their etiology.

• Infection tends to occur predominantly in the basal areas. extend upto a well-defined pleural border. resulting in epithelial ulceration and formation of a fibrinopurulent exudate. Bronchopneumonia c.186 Seminar in Radiology a. In these cases. Air space (lobar pneumonia) b. It tends to localize initially in the periphery of the lung undercover of the visceral pleura. The larger bronchi usually remain patent and air containing. creating an air bronchogram. Infection by Direct Spread Direct spread across the chest wall or diaphragm or from the mediastinum may occur in extension of infection from an extrapulmonary source such as subphrenic abscess or acute mediastinitis secondary to esophageal rupture. . The initial assault occurs on the mucosa of the bronchi and bronchioles. which is quite characteristic. • Nodular appearance of the individual foci of infection is typical. Patent bronchi within homogeneous consolidation appear as linear branching lucencies (Positive air bronchogram). Bronchopneumonia (Lobular Pneumonia) Produced by Staphylococcus aureus. the pulmonary disease usually will be localized to an area contiguous with extrapulmonary source of infection and often takes the form of an abscess. at least in the early stages of disease. The fluid flows directly from alveolus to alveolus and acinus to acinus via communicating channels until the entire lobe is involved. Infection via the Pulmonary Vasculature Occurs in conjunction with an extrapulmonary focus of infection and resulting systemic septicemia. • Parenchymal involvement tends to be patchy and random in distribution. Interstitial pneumonia. with relative sparing of the bronchi and interstitium. This produces homogeneous consolidation. Air Space or Alveolar (Lobar) Pneumonia Characteristic of pneumococcal infection but can also occur with other organisms such as Klebsiella pneumoniae. Radiological Findings • Homogeneous opacification of the involved lobes or segments.

Radiological Findings • Multiple illdefined. Roentgenographic Manifestations • Homogeneous consolidation of lung parenchyma. Airspace nodules range from 3 to 10 mm in diameter and probably represent peribronchiolar consolidation. to fill them with hemorrhagic edema and pus. and focal confluent shadows in the peribronchiolar alveoli. It may indicate slight thickening of the interstitium or alveolar walls or partial filling of the alveoli. (A rare exception is spherical pneumonia) . invariably abuts against a viseral pleural surface. • Ground glass opacification is increase in pulmonary attenuation. Characterized by edema and inflammatory cellular infiltrate predominantly within interstitial tissue. These pneumonia begins in the lower lobes or posterior segments of the upper lobes. Rapidly air space edema spreads from acinus to acinus to involve varying amounts of lobar parenchyma. Interstitial pneumonia: Caused typically by viruses and Mycoplasma pneumoniae. • The nonhomogeneous pattern of ventilated and consolidated lobules results in sponge like pattern known as “Air alveologram”. confluent. nodular opacities. which is not associated with obscuration of underlying vessels. contiguous spread accounts for the homogenicity of consolidation and nonsegmental distribution observed both morphologically and roentgenologi- cally. Pneumonia Caused by Gram Positive Aerobic Bacteria Streptococcus pneumoniae is an oval lanceolate organism surrounded by a well defined capsule. The pattern of resolution or healing by tissue distruction with microabscesses or macroabscesses formation and fibrosis. Computed Tomography • High resolution CT findings of consolidation are homogeneous opacification with airbronchogram. Infiltration of the interstitium is manifested by thickening of the interlobular septa and of the peribroncho- vascular connective tissues. Earliest pathologic findings occur in relation to the terminal airways as in typical bronchopneumonia. Pulmonary Infection 187 Intense transmural inflammatory reaction quickly spreads into peribronchial and peribronchiolar alveoli. representing multiple secondary lobules filled with inflammatory exudate. Radiological Findings Inflammatory infiltration of the bronchial wall and interlobular septa leads to formation of linear and reticular opacities most marked in the perihilar zones. This centrifugal.

• Most frequently. Cavities may become permanent and mimic tuberculosis. In 1900. • Cavitation is common and there is healing with fibrosis. alcohol abuse. Klebsiella Pneumoniae • There is usually lobar consolidation more often right sided. • Pleural effusion. diabetes mellitus. • Cavitation is common and in children. causes bronchopneumonia with multiple patchy areas of consolidation. and frequently upper lobe. pneumatocele frequently develop. • Loss of volume is either slight or absent during the acute stage of the disease. tuberculosis. some degree of atelectasis is common. Mycobacterium bovis. empyema and areas of atelectasis are common complications. the disease is confined to one lobe but the infection may develop simultaneously in two or more lobes. Such as M. caused by exudate within airways and subsequent obstruction. The recent . the typical appearance is of multiple poorly defined rounded nodules that develop rapidly over a few days.000 per year. Today the disease is most commonly found in persons whose immune status is compromised by old age. steroid therapy or AIDS. • During resolution. • Infection due to inhalation. • When dissemination is hematogenous.188 Seminar in Radiology • Air bronchogram. The frontal chest radiograph remains the initial imaging investigation in tuberculosis. kansasii and M. Tuberculosis is classically divided into primary and postprimary disease. Tuberculosis The disease is worldwide in distribution. Primary Occurs in those. balnei can infect. • The volume of the affected lung is maintained. tuberculosis was worldwide epidemic with a mortality rate of approximately 250 per 100. Less commonly. In 95 percent of cases the causative organism is Mycobacterium tuberculosis hominis. not previously exposed to M. is frequently asymptomatic. and is therefore not detected clinically. • Cavitation is rare. atypical mycobacteria. Staphylococcus Aureus • May occur either as a primary respiratory tract infection or as a blood borne infection.

subapical acinonoduler foci). • Detect the sequele of healed tuberculosis such as cicatricial changes. epitheloid cells and langerhans giant cells. . These fine nodules are tubercles with caseous necrosis and surrounding granulation tissue. this primary complex “Ghon’s focus + regional lymphadenitis” heals with fibrosis and may calcify. Hematogenous Dissemination • May become disseminated to numerous extrapulmonary sites (urogenital system. surrounding granulation tissue rich in lymphocytes. Primary Complex Inhaled tubercle bacilli initially evoke a focal. • Caseous lymphadenitis may erode into an airway resulting in tuberculous dissemination through primary endobronchial spread. • Large infected lymph nodes may compress the bronchi resulting distal atelectasis. • Accurate interpretation of radiographic abnormalities. • Monitoring the response to therapy with serial imaging. Aims of Diagnostic Imaging • Adequate screening programme to detect early disease particularly in high risk group patients. • In the great majority of cases. Positive radiographic findings are present in only about 20 percent of children with positive tuberculin skin test. Pulmonary Infection 189 studies have emphasized the role of high resolution CT. • The most frequent manifestation of hematogenous dissemination is solitary tuberculous focus at the lung apex (The simon foci. bronchiectasis and cor pulmonale. (Ghon’s focus). Ghon’s focus is characterized by central necrosis also termed caseous necrosis. bones. emphysema. Assmann infiltrate. • Exudative pleurisy—Bacilli invade the pleura to form tubercles and results in pleural effusion. particularly in the detection of endobronchial spread. Spread of tubercle via lymphatics leads to a specific hilar lymphadenitis. Radiologic Findings Primary tuberculosis is rarely detected on the chest radiography. • Miliary tuberculosis are small nodules throughout the lung but displaying an upper zone predominance. nonspecific subpleural alveolitis that converts to a tuberculosis-specific inflammatory focus in about 10 days. meninges).

resembles effusion pleural. comprising caseous cone surrounded by a mantle of granulation tissue are also found. Productive Tuberculosis • Characterized by well defined solid nodular opacities of 1-2 mm in diameter correspond to the size of primary lobule. Tuberculomas measuring 1-3 cm in diameter. Dissemination of organisms by pulmonary vasculature can result in miliary tuberculosis consisting of spherical gray white nodules measuring 1-2 mm scattered more or less randomly throughout the parenchyma and on the pleura. • Miliary tuberculosis-mottled noduler pattern. . although suggested that impaired lymphatic drainage of these areas resulting from decreased pulmonary arterial blood flow is more important factor. The initial reaction is exudative and characterized by lobular caseous pneumonia consists of edema. fibrine and polymorphonuclear leuckocytes. • Infection occurs initially in the region of the terminal acinar airways. • Hilar and mediastinal Lymphadenitis leads to hilar enlargement and mediastinal widening respectively. • Coarse granular or “Snowstrom” pattern due to coalescence of nodules.Circumscribed small peripheral consolidation. Cavitating Tuberculosis Cavitation results from erosion of enlarging tubercles into airway leading to expulsion of the central necrotic material. this relates to the high PO2. Postprimary Tuberculosis Nearly all cases of postprimary tuberculosis occur in adults as a result of reactivation of a focus of infection acquired in earlier life.190 Seminar in Radiology • Ghon’s focus . The wall of the cavity contains infectious caseous material which provides the organism with the outside environment. giving the appearance of multiple parenchymal nodules. • Endobronchial spread of liquefied necrotic material from cavity can result in tuberculous infection. • Lymphangitic stranding connecting the primary focus with the hilar lymphadenitis from dumb-bell shaped opacity. • Exudative tuberculous pleuritis. representing the primary complex. Postprimary tuberculosis is localized initially to the apical and posterior segments of the upper lobes. • Histologically. the sequence of events in postprimary tuberculosis is similar to the primary infection except that necrosis probably occurs more rapidly as a result of the presence of hypersensitivity. The infection also extends towards the periphery of lung-and rupture into the pleural cavity results tuberculous empyema.

productive. Exudative Tuberculosis Patchy or confluent opacities with indistinct contours. • Arteries in the vicinity of chronic tuberculosis shows endarteritis obliterans a concomitant local increase in the number and size of bronchial artery branches. there is gradual healing with the formation of localized or extensive parenchymal scars. the definitive diagnosis requires culture of the organism. Although the identification of parenchymal disease in apical or superior segment of lower lobe strongly supports a roentgenologic diagnosis of tuberculosis. Fibrocavitatory Tuberculosis When host factors prevail. Mixed. 2. Vascular Abnormalities • Pulmonary arteries and vein in an area of active tuberculous infection may show vasculitis and thrombosis. .5 to 4 cm in diameter. In 80 percent cases shows small satelite lesions and calcifications. 2. Cicatricial bronchostenosis secondary to localized endobronchial infection. resulting in a healed cavity. Pulmonary Infection 191 Healing Occur in Two Ways • By opposition of granulation tissue at the mouth of the draining bronchus resulting in complete closure of the cavities. Most commonly by distruction and fibrosis of lung parenchyma resulting in retraction and irreversible bronchial dilatation. fibrotic changes. Bronchiectasis in postprimary tuberculosis can develop by two mechanisms: 1. gradually alter in appearance over a period of weeks in contrast to nonspecific pneumonia which may change within days. irregular polygonal opacities admixed with calcified granulomata. Productive Tuberculosis Produces sharply defined. Tuberculomas—Pulmonary nodules or masses of 0. and 5. accompanied by adjacent irregular emphysema and bronchiectasis. Exudative. • Tuberculous granulation tissue transform into fibrous tissue. have smooth margins and predilection for the upper zones. 4. 3. cavitatory. Roentgenographic Manifestations Produces a spectrum of radiographic manifestations: 1.

Paracicatricial emphysema. Cavities are frequently combined with disseminated acinar shadows due to endobronchial spread. Tuberculosis of the bronchial mucosa may be seen with perforation of tuberculous foci into airway and subsequent cavity formation. Computed Tomography Cavitation: HRCT has been shown to be superior to the chest radiograph in demonstrating cavitation.192 Seminar in Radiology Tuberculous Cavities Result from caseous necrosis of tuberculous pneumonia with subsequent expectoration of the contents. (Secondary infection). and poorly defined nodules. a fluid level may be identified in the cavity. Bronchography Bronchograms demonstrate both bronchial structures and extrinsic compression of the airways. . • Fibrocavitatory tuberculosis: Findings indicating chronic parenchymal changes including. bronchiectasis and broncho-vascular distoration may set in a thick pleural peel may encase the residual lung and lead to thoracic deformity with kyphoscoliosis. Cranial shift of hilar structures indicates fibrous contraction. parenchymal scarring. “Tree in bud” branching linear structures. calcification and fibrotic bands radiating from hilum to the apex. broncho-vascular distortion and cicatricial emphysema. fibrotic bands. caseating material within the terminal and respiratory bronchioles. Endobronchial Spread These include centrilobular nodules or linear structures. Poorly defined nodules represent peribronchiolar inflammation. particularly in cases complicated by fibrosis and architectural distoration. They are randomly distributed throughout the secondary lobule in contrast to the centrilobular nodules of endobronchial spread. • Miliary tuberculosis HRCT images show fine nodules which are uniformly distributed throughout the lungs. a cavity may disappear. Fibrotic Tuberculosis Include apical pleural thickening. These may be well or poorly defined and range in size from 1 to 4 mm in diameter. With adequete therapy. sometimes its wall become paper thin but it remains an air filled cystic space. The wall of cavity may be variably thin or thick and smooth or internally nodular.

Diffuse bilateral alveolar or mixred alveolar interstitial shadowing may be seen. The overall incidence of pulmonary fungal infections clinically and radiologically resemble bacterial pneumonias. Carcinoma 3. . and A. candidiasis) is caused by saprophytic fungi. blastomycosis and sporotrichosis. Parenchymal calcification of other etiology Fungal Diseases of the Lung Endemic disease. Primary Invasive Aspergillosis Develops when massive amounts of fungal spores are inhaled. Aspergillosis Aspergillus fumigatus. Opportunistic Fungal Infection (Asperigillosis. Nonspecific pneumonia 2. coccidioidomycosis. Secondary Angioinvasive Aspergillosis Occurs as an opportunistic infection in patients with severe debilitating illness particularly leukemia and lymphoma. histoplasmosis. Appearances may be indistinguishable from that of bacterial pneumonia with lobar. or segmental consolidation. which are usually present in the oral mucosa and become pathogenic in the immuno-compromised host. Candidiasis Candida albicans is part of the normal human microbial flora of the oral cavity. Radiological Findings A wide spectrum of radiolographic findings have been described in Candida pneumonia. The hosts have normal immunity. They include. Therefore. Pulmonary condidiasis occurs only in the immunocompromised patients. difinitive diagnosis is based on identification of the fungus at microscopy and culture. Pulmonary Infection 193 Differential Diagnosis 1. The diagnosis may be established by demonstration of Candida on trans- bronchial biopsy. caused by pathogenic fungi in an otherwise healthy individual. niger (They constitute part of the flora of the healthy oral cavity). flavus. A.

precipitating antibodies to Aspergillus and elevated IgE titers. • Central bronchiectasis involving the inner two-thirds of the bronchial tree and showing an upper lobe predominance may develop. It occurs in hosts with normal immunity and the fungus colonizes preexisting cavities (cysts. Bronchoceles are also frequent manifestation of ABPA. Pathologically. The characteristic “air crescent” sign develops late in the course of disease. bilateral peribronchial consolidation. On standard T1 weighted sequences. segmental or subsegmental distribution that predominantly involve the upper lobes. . and centrilobular nodules less than 5 mm in diameter. thrombosis and hemorrhagic infarction with subsequent necrosis and cavitation.194 Seminar in Radiology Pathologically this disease is characterized by mycotic vascular invasion. a ‘halo’ of ground-glass opacification surrounds the dense parenchymal foci. This may erode the cavity wall and lead to hemoptasis. The halo sign precedes the air crescent sign by upto 2 weeks. The chest radiograph shows transient infiltrates of lobar. These vary in shape but classically present “gloved finger” appearance. which presents with rounded shape and probably infarcted parenchyma. Allergic Bronchopulmonary Aspergillosis Represents a hypersensitivity reaction usually in asthmatics and manifestations include asthma. Multiple foci of consolidation may be present.T. The rim enhances on administration of intravenous Gadolinium. This represents a rim of hemorrhage or coagulation necrosis surrounding an area of infarction. tuberculous cavities. The initial chest radiograph may be normal. rounded consolidations have target appearance with a hypointense center and hyperintense rim. eosinophilia. Aspergilloma: It is the most common form of aspergillosis. mycelial plugs develop in the proximal airways but in contrast to invasive aspergillosis of the airways. ground glass attenuation. findings include lobar consolidation. Computed Tomography In early invasive aspergillosis. Invasive Aspergillosis of the Airways Diagnosis is based on the presence of organisms deep to the basement membrane C. Magnetic Resonance Imaging May be helpful in early diagnosis of invasive aspergillosis. tissue invasion is minimal or absent. cystic bronchiectasis) and forms fungal ball.

manifestations include chronic cavitating pneumonia. • There is accompanying hilar and mediastinal lymphadenopathy. leaving residual pulmonary granulomas that undergo central calcification to produce target pattern. • These pneumonic consolidations heal. Localized pleural thickening may be seen. • Chronic progressive histoplasmosis is the consequence of reactivation and has a poor prognosis. . Radiologic Findings The chest radiograph shows nonsegmented predominantly peripheral consolidation that may cavitate. there is generalized micronodular pattern. Nocardiasis Aerobic saprophyte found in the soil. Consolidation typically crosses interlobar fissures. the intestinal tract and the lung. A circular or crescent-shapped air space may be visible between the mycetoma and the cavity wall. Coccidioidomycosis (Coccidioides Immitis) Endemic in the southwestern US. homogenous opacity mobile within the cavity. pleural empyema and chestwall invasion. Actinomycosis Actinomyces israelii is intermediate between mycelial fungi and bacteria and is a common saprophyte in the human mouth.T. C. • Progressive cavitation with fibrosis may progress. Pulmonary nocardiosis may be similar to actinomycosis in its radiographic appearance. contaminated by Bat or bird excreta. The chest radiograph shows pneumonic consolidations and pulmonary nodules (Coccidioidomas) that occasionally cavitate. In the thorax. rib osteomyelities with periosteal thickening. In disseminated coccidioidomycosis. Pulmonary fibrosis are associated with advanced disease. Nonhomogenous attenution and surrounding crescent of air within the cavity. Pulmonary Infection 195 The chest radiograph shows a round. Histoplasmosis is a fungal infection that occurs mainly in North America. Radiologic Findings • Multiple ill defined patches of consolidation throughout both lungs. Histoplasmosis: Caused by Histoplasma capsulatum. Pleuroesophageal and pleuropulmonary fistulae. pleural empyema. Involves the cervicofacial region. • Acute histoplasmosis develops as the result of air borne primary infection. and inflammatory soft tissue masses of the chest wall may develop.

• Sonography will show hepatic and pleural changes. it is manifested as lymphadenitis and occasionally as interstitial pneumonia. The chest radiograph shows small. in the lungs with formation of eosinophilic loeffler infiltrate. while CT will indentify and characterize pulmonary parenchymal abnormalities. Radiologic Finding • Chest radiograph shows opacification of the lower thorax due to pneumonic consolidation with pleural effusion. sporotrichosis and mycormycosis are extremely rare and present as non specific pneumonic infiltrate. other mycoses like blastomycosis. South America. Pneumocystis Carinii Pneumonia Originally described in premature infants. • Initially ill defined infiltrate may form an abscess. Radiological Findings Ill-defined opacities resumbling acute viral pneumonia associated hilar lymphadenopathy. Amebiasis They are ingested in contaminated food and initially induce a colitis. They reach the liver via the blood stream and form hepatic abscesses. foci of bronchopneumonia and round masses (Torulomas) which may cavitate. The causative organisms are protozoa and helminths. In adults. Parasites may colonize in the lungs and forms cysts. Africa.196 Seminar in Radiology Cryptococcosis (Torulosis) The spores of Cryptococcus neoformans are found in dust and excreta and cause pulmonary infection in immunocompromised hosts. Adult toxoplasmosis is relatively uncommon except in patients with AIDS. 60-70 percent of patients with AIDS with develop pneumocystis carinii pneumonia. granulomas and abscesses. Toxoplasmosis Congenital toxoplasmosis due to transplacental infection is the most important form and presents with encephalitis and chorioretinitis. . it is a frequent pathogen in the immunocompromised host. In the HIV-negative population. Parasitic Infections Parasitic infections are more prevalent in Asia. They induce hypersensitivity reactions. subpleural granulomas.

Ascariasis Radiographs show. cerebral and bone involvement occur in about 10 percent of cases. the chitin membrane of the endocyst may collapse and float on the residual fluid (waterlity sign). less commonly a mosaic pattern with scattered foci of parenchymal involvement interspersed with normal lung is found. regional confluent infiltrates similar to eosinophilic loeffler pneumonia. This is an indication of early rupture. Schistosomiasis Schistosomiasis hematopium is endemic in North Africa. The infective larvae penetrate the skin. Hilar adenopathy and pleural effusions are unusual. . kidney and urinary bladder. Radiological Findings Solitary. smooth. Cystic changes are frequently identified. Later following cyst rupture. Occasionally the parasites lodge in the precapillary pulmonary arterioles and initiate an obstructive endarteritis leading to pulmonary hypertension and chronic cor pulmonale. The larvae hatch in the intestine with subsequent hematogenous spread to the liver. Then they enter the pulmonary circulation and subsequently the systemic arterial system to reach the liver. enter the capillaries and migrate through the systemic venous system to the right heart. Computed Tomography HRCT finding are bilateral ground glass opacification. Radiologic Findings The chest radiograph shows transient pulmonary infiltrates representing an eosinophilic loeffler-type pneumonia which is associated with passage of the larvae through the pulmonary capillaries. Progression to diffuse air space consolidation may occur. Echinococcus granulosus Human ingest the ova the dog tapeworm taenia echinococcus in contaminated food. homogeneous. Pulmonary. round. They may involve the perihilar and lower zones. mass ranging from 1 to 10 cm in diameter occasionally a thin crescent of air is visible between the ectocyst and pericyst (menisus sign). Pulmonary Infection 197 Radiological Findings Initial chest radiograph may be normal but in 80 percent of cases it shows diffuse. bilateral granular or reticular infiltrates.

• Streaky basal linear shadows. Cavitation is unusual in the severely immuno-compromised patients. Viral pneumonia is uncommon in adults. 1. Acquired Immuno Deficiency Syndrome (AIDS) Organisms causing intrathoracic infection in AIDS include bacteria. Patchy or extensive consolidation. • The mediastinal and hilar nodes are commonly enlarged. In the acute phase of infection. Herpes Varicella Zoster Varicella pneumonia occurs more often in adults than in children. viral pneumonias not rare in infants and children. small proportion of these nodules calcify. Following recovery. Peribronchial shadowing 2. a fulminating hemorrhagic pneumonia may be seen with widespread consolidation indistinguishable from non cardiogenic pulmonary edema or ARDS. However. Mycobacteria • Tuberculosis in advanced AIDS in frequently aggressive and manifestations may be those of primary or miliary tuberculosis. but often include. Measles Giant-Cell Pneumonia Although a disease of childhood. • Mycobacterium avium complex is found in up to 20 percent of AIDS patients. the chest radiograph may show wide spread nodular shadows up to 1 cm in diameter.198 Seminar in Radiology Viral Pneumonia Viral pneumonia usually commences in distal bronchi and bronchioles with distruction of the epithelium. • The endobronchial spread and cavitation are seen in the mildly immunocompromised ones. extensive pulmonary fibrosis may develop. The radiological appearances of a viral pneumonia are very varied. typical and atypical mycobacteria. protozoa. . it has been recorded in adults. widespread reticular shadows and diffuse ill defined nodular opacities are seen. Reticulonodular shadowing 3. viruses and fungi. if the patient survives. Influenza Virus Primary viral pneumonia during influenza epidemics. edema and lymphocytic infiltration. Most pneumonias that complicate viral infections in adults are due to bacterial superinfection.

pleural effusion and focal alveolar and diffuse reticulonodular shadowing. . especially CMV are an infrequent cause of pneumonia in AIDS. Pulmonary Infection 199 They include parenchymal nodules. • Mycobacterium tuberculosis and MAL are the most frequently responsible for mediastinal adenopathy in AIDS. Fungi Cryptococcosis is the most common pulmonary infection in AIDS and frequently coexists with cryptococcal meningitis. Pleural effusions and adenopathy are absent. • Pneumocystis carinii pneumonia Viruses All viruses. Intrathorasic manifestations include mediastinal lymphadenopathy. masses and consolidation in association with mediastinal lymphadenopathy. Radiographic manifestations include diffuse parenchymal infiltration that may be indistinguishable from non cardiogenic pulmonary edema.

14 Interstitial Lung Diseases DEFINITION Interstitium is supporting strength of lung and consists of loose connective tissue throughout lung consisting of 3 subdivisions: a. Granulomatous disease • Sarcoidosis • Wegener’s Granulomatosis 4. ETIOLOGY 1. Sub pleural → between pleura and lung parenchyma and is continuous with interlobular septas and perivenous spaces. Pneumoconiosis • Coal workers pneumoconiosis • Asbestosis . Interstitial pneumonias • Usual Interstitial Pneumonitis/Cryptogenic fibrosing alveolitis/idiopathic pulmonary fibrosis 2. Malignant Disease • Lymphoma • Lymphangitis carcinomatosis • Leukemia 3. c. b. Parenchymal (acina) → between alveolar walls and capillaries. Diffuse interstitial pattern is a radiological descriptive term and does not imply that the disease process is confined to the interstitium. In many cases both the alveolar cavity and the interstitial tissue both are abnormal. Infectious disorders • Miliary tuberculosis • Fungal • Pneumocystis • Mycoplasma • Parasites 5. Histocytosis ‘X’ (Langerhans histiocytosis) 6. Axial → surrounding bronchovascular bundle from hila to secondary pulmonary nodule.

15% – Collagen vascular disease . Allergic disease • Hypersensitivity pneumonitis or extrinsic allergic alveolitis • Pulmonary eosinophilia 9. • Among the various interstitial lung diseases. Drugs • Antineoplastic drugs 10. 8% PATHOGENESIS • Earliest manifestations are alveolitis (ground glass haze) Alveolitis (accumulation of leucocytes) ↓ Distorted normal alveolar structure ↓ Release of inflammatory mediators ↓ Injury to parenchymal cells ↓ Fibrosis ↓ End stage fibrotic lung . the commonest causes are: – Environmental diseases . Others • Lipid storage disease • Pulmonary haemosiderosis • Pulmonary edema • Tuberous sclerosis • Lymphangiomyomotosis • Amyloidosis • Neurofibromatosis EPIDEMIOLOGY • Prevalence → 20-40 lac of population suffers from Interstitial lung disease. Interstitial Lung Diseases 201 • Silicosis • Berylliosis 7. Autoimmune disease/collagen diseases • Scleroderma • Rheumatoid arthritis • Systemic Lupus Erythematosus • Polymyositis • Sjögren’s syndrome • Polyarteritis nodosa 8. 24% – Sarcoidosis . 20% – Interstitial pulmonary fibrosis .

FINDINGS ON X-RAY CHEST AND CT SCAN Shadows are: 1. Conventional radiography • First modality of diagnosis • Correlation between radiographic changes and severity of respiratory distress is often poor.202 Seminar in Radiology • Radiologically Ground glass haze ↓ – Nodular – Reticular – Reticulonodular – Streaky opacities – Fibrosis ↓ Honey-combing or swiss cheese appearance CLINICAL FEATURES • H/O exposure • Clinical history – breathlessness – effort intolerance – dry cough without any other obvious cause IMAGING TECHNIQUES 1. 4. MRI • Not the modality of choice for chest diseases because of motion effect of heart and lungs and inability to visualize small branching pulmonary vessels and bronchi and lung parenchyma. (e. using a field of view (FOV) just large enough to encompass the reason of interest) results in clear depiction of the distribution and higher definition of the appearance of pulmonary parenchymal disease. HRCT – Diagnostic modality • Thin sections (1-3 mm) combined with high spatial resolution reconstruction algorithm. Nodular . • Sometimes even advanced cases of interstitial lung disease may present normal findings on X-ray chest. (i. the bone algorithm) • And targeting the scan to the lung. So it is Non Specific and of limited diagnostic value 2.g. Conventional CT Scan • Better modality 3.e.

X – Fibrosing alveolitis – Pneumoconiosis – Sarcoidosis – Rheumatoid lung – Scleroderma 7. • Can be seen in both interstitial or alveolar pattern. Linear • Thick or thin band like shadows • Irregular distribution • Because of fibrosis of lung 3. Ground glass haze (active inflammation) • Homogeneous haze (veil) with loss of definition of pulmonary vessels and diaphragm. • Most common complication is pneumothorax • Common causes are: – Histiocytosis .Non branching and radiating from hilum • (B) .Thin lines at lung bases perpendicular to pleura • Causes are: – Pulmonary edema – Mitral valve disease – Penumoconiosis – Lymphangitis carcinomatosis – Sarcoidosis – Lymphatic obstruction – Idiopathic – Lymphoma 9. 8. Miliary – size 2-4 mm 6. Interstitial Lung Diseases 203 2. Others • Peribronchial cuffing • Subpleural lines • Traction bronchiectasis SARCOIDOSIS • Multisystem noncaseating granulomatous disease • Young adults • Blacks > whites • Males > female . Reticulonodular 5. Honeycomb • Size 5-10 mm thin walled cystic lesion • It is the only dependable sign of interstitial fibrosis. Reticular – when these lines overlap and produce a meshwork like pattern 4. Kerley lines • (A) .

The resulting skin reaction is biopsied and is deemed positive if it displays typical sarcoid histology. • 70-80 percent patients also have paratracheal lymphnode (especially right side). 2. Stage 2 : Lymphadenopathy with parenchymal opacity. sometimes give a ground glass appearance. • Upper/middle zone predominance. 10-20 percent • Patchy consolidation • Opacities sometimes contain air-bronchograms and have ill defined margins that commonly break up into a nodular pattern. Stage 3 : Parenchymal opacity alone. 1/3 of parenchymal opacities progress to fibrosis – rest resolve completely. • < 5 percent calcify – sometimes by egg shell calcification. Parenchymal Opacity 1. oval or irregular in shape sometimes containing an air- bronchogram. 2 percent • Nodules of 1-4 cm size which are usually relatively illdefined and rounded. • Very small aggregated opacities. 3. • Multiple and bilateral and may rarely cavitate. • On imaging Stage 1 : Lymphadenopathy • Bilateral symmetrical hilar (tracheobronchial and bronchopulmonary) lymphnode. • Range from 1 cm to a segment or more are usually multiple. Fibrotic Shadowing • Coarse linear opacities with evidence of volume loss. well/ill defined and are predominantly peribronchovascular and subpleural in distribution.204 Seminar in Radiology • Clinical features – Erythema nodosum – Arthralgia – Abnormal chest X-ray and respiratory symptoms • Diagnosis – Transbronchial biopsy – Kveim test → Intradermal inoculation of an extract of sarcoid tissue. 75-90 percent commonest pattern • Rounded or irregular nodules of 2-4 mm diameter. • Smaller or larger opacities are not uncommon. – Ga-67 is taken up by involved lymph node (LN) and lung and is used to assess activity and extent of disease. .

• May calcify/cavitate Cavitating bronchial carcinoma • Differential diagnosis of PMF TB Caplan’s Syndrome • Patients with coal workers pneumoconiosis/silicosis and rheumatoid disease may develop Caplan’s syndrome. • Complications are – Cor-pulmonale – Pneumothorax – Myecetoma formation Unusual Manifestation • Pleural effusion • Basal septal lines • Bronchostenosis – segmental or lobar collapse Nodules at branch points of pulmonary vessels and bronchi may be seen and beading of bronchus is typical on HRCT. PNEUMOCONIOSIS • Caused by inhalation of inorganic dusts. Interstitial Lung Diseases 205 • Ring shadow caused by blebs. • History of exposure – Living near mines or factory – Living with exposed worker – Working directly with dust COAL WORKERS PNEUMOCONIOSIS Simple Pneumoconiosis • Small nodules of 1-5 mm size • Little associated fibrosis • Upper/middle zones are affected Progressive Massive Fibrosis (PMF) • Large fibrotic aggregations • 1-10 cm size • Usually bilateral/round or oval/with spiculated margins and linear strands extending from them. . bullae and bronchiectasis or honeycombing. • Tend to migrate towards hila creating peripheral areas of emphysema and bullae. • Multiple round. well defined opacities.

• Upper/middle zones are affected. → Comet tail of incurving vessels being characteristic. – Increased subpleural attenuation and honeycombing – Rounded atelectasis → Fibrosing condition most commonly associated with asbestosis. remain static. SILICOSIS Simple Silicosis • Multiple nodular shadows of 2-5 mm diameter in size. calcify or cavitate • The lesions may precede the development of overt rheumatoid arthritis. . → Other features o Adjacent pleural thickening o Airbronchogram within the lesion. sometimes resembling holly leaves – They tend to occur in the mid zones and over the diaphragm. Complicated Silicosis • Progressive massive fibrosis (PMF) ASBESTOSIS • Symptoms are often not apparent until 20-30 years after exposure. Pulmonary lesion • Lower zones • Similar to fibrosing alveolitis • Fine reticular or nodular ↓ Coarser and causes loss of clarity of heart and diaphragm (shaggy heart). • Hilar lymphnode is common (may have eggshell calcification). • Diffuse thickening • Pleural effusion: Large effusions suggest carcinoma or mesothelioma • Mesothelioma 2. 1. • HRCT clearly shows: – Subpleural curvilinear opacities (crescents) – Parenchymal bands – Thickened inter and intralobular lines. Pleural lesion • Plaques: often calcify and produce bizarre opacities.206 Seminar in Radiology • 1-5 cm size • Usually appear in crops • Nodules may regress.

Systemic Lupus Erythematosus (SLE) • More common in females • Pleural effusion – Usually bilateral and small in volume and associated with pleurisy and pain. On Imaging • Diffuse fine nodular opacities or generalized ground glass haze . Interstitial Lung Diseases 207 → Recognition of these features may prevent unnecessary pulmonary resection for a suspected carcinoma but biopsy may be necessary as both lung and pleural mesothelioma are commoner in these patients. • Upper / middle zones COLLAGEN VASCULAR DISEASE 1. Others • Peritoneal mesothelioma • Other malignancies especially of – Upper digestive tract (esophagus and oropharynx) – Larynx OTHERS • Berylliosis • Siderosis (iron oxide dust) • Stannosis (tin oxide) • Barytosis (barium sulphate) – dense nodulation EXTRINSIC ALLERGIC ALVEOLITIS (HYPERSENSITIVITY PNEUMONITIS) • Allergic inflammatory granulomatous reaction of the lungs caused by inhalation of dusts containing certain organisms or proteins (type III and also partly type IV type of hypersensitivity reaction) (< 10 µm). • Farmer’s lung → micropolyspora faeni from damp hay • Pigeon breeders and budgerigar fanclers lung → droppings dust • Baggassosis – mouldy sugarcane residue • Air conditioning systems may circulate fungal spores and amoebae. • Patchy consolidation and septal lines similar to pulmonary edema in acute attacks. • Later . . • Basal segmental collapse – Thick horizontal band shadows.Early stages.reticulonodular shadows / coarse linear opacities / honey combing / cyst formation / bronchiectasis. 3.

• Egg shell calcification of lymph nodes • Predisposition to lung cancer • Associated pleural disease is rare. 2. • As in other cases of fibrosing alveolitis – Basal reticulonodular shadow – honey combing. • Fibrosing alveolitis – Apparent in chest X-ray in 5 percent of patients. HRCT is better for detection. Rheumatoid Disease (chest changes more in males) • Pleural effusion or thickening – Unilateral or bilateral – Usually asymptomatic – Commonest thoracic manifestation – Larger than SLE and often asymptomatic • Rheumatoid pulmonary nodules (up to 7 cm) – Uncommon but characteristic – Well defined round opacities with may be single or multiple. Systemic Sclerosis (more in females) • Highest incidence of pulmonary fibrosis amongst the connective tissue diseases. . 4. 3. • Esophageal involvement resulting in abnormal motility may cause reflux and aspiration pneumonia. – Basal reticulonodular which may progress to honeycombing and severe volume loss. Others Ankylosing spondylitis (in 1-2%) • Upper lobe fibrosis → usually bilateral and associated with apical pleural thickening and often with bullae (may become colonized by aspergillus). • Pulmonary artery hypertension • Obliterative bronchiolitis: – Produce airflow obstruction – Lungs appear over inflated with decrease in size and number of vessels.208 Seminar in Radiology • Pulmonary consolidation – Secondary infection – cavitation may occur – Pulmonary edema – Cardiac failure – Renal disease – Lupus pneumonitis – rare-diagnosis by exclusion • Pericardial effusion • Diaphragmatic dysfunction • Diffuse interstitial shadowing rare (<5% of cases). – Caplan’s syndrome → rheumatoid nodules develop against a background of simple pneumoconiosis.

Interstitial Lung Diseases 209 Sjögren’s Syndrome • Triad of – Dry eyes – Dry mouth – One of the other connective tissue disorders • Also there are – Pleural effusion – Fibrosing alveolitis – Recurrent chest infections – Lymphocytic interstitial pneumonitis Dermatomyositis and polymyositis • Basal fibrosing alveolitis. • Pulmonary opacities are due to eosinophilic exudates (PIE syndrome – pulmonary infiltrates with eosinophilia). Simple Pulmonary Eosinophilia (Loeffler’s syndrome) – Mild transient condition. 1. SYSTEMIC VASCULITIDES E. • Primary lung involvement is unusual. They may wax and wane and frequently cavitate forming masses with thick irregular walls: Differential diagnosis – Rheumatoid disease – Metastasis • Pleural effusion • Unusual – hilar and mediastinal LN • Granulomas may grow in the trachea and bronchi causing tracheal stenosis and lobar collapse.g. • Involvement of pharyngeal muscles may predispose to aspiration pneumonitis. Wegener’s Granulomatosis • It is a necrotizing granulomatous vasculitis which involves – Upper respiratory tract (sinus and nose) – Lungs – Kidneys (GN) • More in Males • The typical necrotising granulomas are seen as single/multiple well defined pulmonary masses varying in size from less than one to several cm. . PULMONARY EOSINOPHILIA • Transient opacities on the chest radiograph in association with an excess of eosinophils in blood.

• Central bronchiectasis • As in any condition which results in lung destruction and cavity formation – mycetoma formation may occur.210 Seminar in Radiology Responsible allergens   Parasites Drugs Ascaris PAS Ankylostoma Aspirin Strongyloides Penicillin Taenia Nitrofurantoin Toxocara Sulfonamides On X-ray • Illdefined non-segmental consolidation which may change position over a few days but usually resolve within a month. 3. • Chest skiagram shows transient shadows but after repeated attacks there may also be signs of fibrosis and bronchiectasis. . Asthmatic Pulmonary Eosinophilia (Allergic Bronchopulmonary Aspergillosis) • Most commonly caused by Aspergillus fumigatus. Chronic Pulmonary Eosinophilia (Cryptogenic pulmonary eosinophilia) • Cause uncertain • Persists for a month or more • Areas of consolidation tend to be peripheral in distribution • A distinctive diagnostic pattern is a vertical band of consolidation paralleling the chest wall but separated from it. Tropical Pulmonary Eosinophilia (TPE) • Caused by filariasis • Fine bilateral diffuse nodular shadowing with occasional confluent areas • Diffuse reticulonodular shadowing occasionally associated with hilar lymphadenopathy. not being restricted by inter lobular fissures. Pulmonary Eosinophilia Associated with the Systemic Vasculitides. Upper lobe predominance. 5. FIBROSING ALVEOLITIS OR DIFFUSE INTERSTITIAL PNEUMONIA • Primary or secondary • It includes a number of conditions in which there is pulmonary fibrosis associated with a chronic inflammatory reaction in the alveolar walls. Most patients have long standing asthma prior to development of this complication but often no allergen is identified.g. 4. Wegeners. 2. e. PAN • X-ray features are those of underlying connective tissue disorder.

• Histologically → Most cases show fibrosis and cellular infiltrate confined to the alveolar walls. Secondary Fibrosing Alveolitis (also causes of diffuse pulmonary fibrosis) • Connective tissue diseases (SLE. Some cases show mononuclear cells in the alveoli and may be termed desquamatic interstitial pneumonitis. honey combing and bullae. Cryptogenic Fibrosing Alveolitis (or UIP – usual interstitial pneumonitis or primary). SS. • On Imaging → Bilateral basal ground glass shadowing followed by reticulonodular pattern and honey combing – Pleural effusions – rare – Hilar and mediastinal lymphnode may be present especially on CT – Complications:  Corpulmonale  Infection B. ring shadows. Interstitial Lung Diseases 211 A. . RA) • Drugs and poisons • Radiation • Organic and inorganic dusts – Pneumoconiosis – Silicosis – Extrinsic allergic alveolitis • Noxious gases • Infection • Sarcoidosis • Histiocytosis • Chronic pulmonary edema • ARDS • Neurofibromatosis • Tuberous sclerosis • Lymphangiomyomotosis HISTIOCYTOSIS ‘X’ (LANGERHANS CELL HISTIOCYTOSIS) • More in males • 3 variants – Letterer Siew disease – Hand Schuller Christian disease – Eosinophilic granuloma • Unknown etiology • Multiple organs are involved (lung in 20% of patients) • Eosinophilic granulomas usually involve skeleton but may be confined to the lungs when M:F = 5:1 • On imaging – Illdefined transient patchy consolidation – rarely seen – Followed by reticulonodular pattern bilaterally in upper and middle zones. – Coarse linear shadows.

lymphnodes and alveolar walls. In LAM and TS . • On radiography – Bilateral patchy alveolar opacities in first 24 hours which become more extensive over the next few days. lung vessels. – At this stage Gram negative pneumonia frequently develops and cavitation and pleural effusion may be seen. • However the distribution of muscle proliferation is initially perilymphatic and the disease may also involve the mediastinal and retroperitoneal lymph nodes. LYMPHANGIOMYOMATOSIS • Very similar radiologically and pathologically to tuberous sclerosis. ACUTE RESPIRATORY DISTRESS SYNDROME • Acute respiratory failure in patients without previous lung disease and usually follows major trauma or shock. Pleural effusions are unusual and heart does not enlarge. hence chylothorax and chyloperitoneum are commoner than tuberose sclerosis. • Premenopausal females • Imaging – same as tuberose sclerosis. – Recurrent pneumothorax – Chylous pleural effusions are rare but may be large bilateral and persistent. . NEUROFIBROMATOSIS • Pulmonary fibrosis occurs in approximately 10 percent of patients with NF-I. Pleural effusions are common especially in LAM (chylous effusion due to involvement of thoracic duct by leiomyomatous tissue). Difference between histiocytosis and lymphangiomyomatosis (LAM) and tuberose sclerosis (TS): 1. – HRCT shows Multiple thin walled cysts with normal intervening lung parenchyma. 2. – Patient is almost invariably female. lymphatics.there is female predominance.212 Seminar in Radiology TUBEROUS SCLEROSIS • Triad of: – Mental retardation – Epilepsy – Adenoma sebaceum • 1 percent of patients of Tuberous sclerosis develop lung involvement - reticulonodular shadowing and eventually honey combing. Lower zones are involved 3. – Diffuse hyperplasia of smooth muscle in bronchi.

Interstitial Lung Diseases 213 – Aggressive ventilatory support: o Pneumomediastinum o Pneumothorax o Subcutaneous emphysema – Later pulmonary fibrosis and reticular shadowing • Causes of ARDS – Major trauma – Hypovoluemic shock – Septicemia – Fat embolism – Near drowning – Mendelson syndrome – Burns – Viral pneumonia – Pancreatitis – Oxygen toxicity – Disseminated intravascular coagulopathy PULMONARY HEMORRHAGE AND HEMOSIDEROSIS • Hemorrhage into lungs and airways may complicate: – Carcinoma Lung – Pneumonia – Bronchiectasis – Blood dyscrasias – Anticoagulant therapy – Trauma • Multifocal bleeding into alveoli (not associated with any of these conditions) may be referred to as pulmonary hemosiderosis .

They may become confluent and demonstrate an airbronchogram.g.g.214 Seminar in Radiology • Imaging – During an acute episode of pulmonary hemorrhage. e. – When bleeding stops → opacities resolve within a few days. DRUG INDUCED PULMONARY DISEASE • Pulmonary fibrosis → often basal predominance – Cytotoxic drugs – Gold – Mineral oil and nitrofurantoin • Pulmonary eosinophilia – PAS – Asprin – Penicillin • ARDS – Cytotoxic drugs. patchy illdefined areas of consolidation appear on the chest radiograph. Infection – Asymmetrical. upper zone and lobar distribution – Lack of rapid change • Diagnosis of hemorrhage – Haemosiderin laden macrophages in sputum/bronchial lavage – Increased uptake of inhaled radioactive CO by leaked blood. – Following repeated episodes of bleeding – pulmonary fibrosis may develop and produce a diffuse hazy nodular or reticular pattern. • Patients with nephritis are prone to pulmonary edema and pneumonia and differentiation from pulmonary hemorrhage may be difficult. Septal lines are occasional. mitral stenosis. Oedema – Cardiac enlargement – Pleural fluid – Septal lines b. – IV injection of RBC lebelled with 99Tc. – Bleomycin – Busulphan – Cyclophosphamide • SLE reaction – Penicillin – INH – Methyl dopa . – Hemosiderosis is also well recognized in patients with chronically elevated left atrial pressure. e. a. – On imaging permanent miliary stippling is seen due to focal nature of bleeding.

e. – Radiologically The effects are of obstruction. Interstitial Lung Diseases 215 • Pulmonary oedema – Salicylates – Narcotic overdose – Overtransfusion of IV fluids – Hypersensitivity to transfused blood and blood products. Secondary form in lungs does not produce any radiographic abnormality as secondary amyloid does not invoke an inflammatory response in lungs. • Pulmonary thromboembolism • Opportunistic infection – Steroids – Anticancer drugs • Mediastinal adenopathy – Phenytoin – Amiodarone AMYLOIDOSIS • Amyloid may be deposited in lung in primary (30-70%) and secondary (10%) forms of disease. or it may grow down the trachea and into the bronchi in the form of nodular submucosal plaques. – Enlarged lymphnode (may be calcified). calcific bodies and ossifications. PULMONARY ALVEOLAR PROTEINOSIS • Rare disease of unknown etiology • A fat laden proteinaceous material probably secreted by the type II pneumatocyte fills the alveoli. • Histologically there is a striking lack of reaction within the alveolar walls. o Atelectasis o Distal bronchiectasis o Infection • Tracheo Pathia Osteoplastica It is a condition of cartilaginous masses lining most of trachea and major bronchi. It is thought to be an end-stage of tracheobronchial amyloidosis. i. The masses contain amyloid deposits. • M:F = 3:1 • Any age . • This is probably the result of a response by the lungs to an irritant. • On imaging – Multiple nodular opacities which can cavitate or calcify. – Diffuse reticulonodular shadowing or honey combing. • Tracheobronchial amyloid – Solitary endobronchial tumor mass/polyp.

216 Seminar in Radiology • On Imaging – Resembles pulmonary oedema with small acinar perihilar opacities present in both lungs. • May be associated with – Lymphoma – Leukemia – Immunoglobulin deficiency • Diagnosis by: – Lung biopsy – Bronchoalveolar lavage – 25 percent cases all fatal within 5 years PULMONARY ALVEOLAR MICROLITHIASIS • Unknown etiology • Familial tendency • Multiple fine sand-like calculi (≤ 1 mm) are present in the alveoli. • In its usual form the delicate branching or lacelike pattern of dystrophic bone formation in the lower parts of the lungs is sufficiently distinctive to suggest the diagnosis. The calculi are calcified and produce widespread minute but very dense opacities on the chest radiograph. • It predisposes to infection from both common respiratory pathogens and opportunistic organisms. • Pulmonary fibrosis later on with development of bullae and cor pulmonale IDIOPATHIC PULMONARY OSSIFICATION • Rare condition • Unknown cause • Also called as: – Ossifying pneumonitis – Bony metaplasia of lung – Abosiform pulmonary ossification. Changes are bilateral and perihilar and usually symmetrical. DIFFERENTIAL DIAGNOSIS Lower Zone • Rheumatoid arthritis • Systemic sclerosis . – There may be thickening of interlobular septa in addition to ground glass shadowing and consolidation on HRCT producing the ‘crazy paving appearance’ that is typical of this condition. • If profuse – produce a white out of lung and best demonstrated by overexposed film. These opacities may become confluent.

Interstitial Lung Diseases 217 • Dermatomyositis • Polymyositis • Lymphangio myomatosis • Fibrosing alveolitis • Asbestosis • Chronic aspiration • Tuberous sclerosis • Drug reactions Increased Lung Volume • Histocytosis • Tuberous sclerosis • Lymphangiomyomatosis • Cystic fibrosis Rapid Change on Sequential Films • Oedema • Haemorrhage • Eosinophilic lung states High Density Nodules • Alveolar microlithiasis • Histoplasmosis • Chickenpox pneumonia • Stannosis • Barytosis Bullae • Underlying emphysema • Histiocytosis • Tuberous sclerosis • Lymphangiomyomatosis • Neurofibromatosis • Pneumoconiosis Honey Combing • Fibrosing alveolitis • Asbostosis • Histiocytosis • Tuberous sclerosis • Lymphangiomyomatosis .

choriocarcinoma • Silicosis • Berylliosis • Coal workers penumoconicosis • Extrinsic allergic alveolitis • Oil embolism (post lymphangiography) Greater than Soft Tissue Density • Chickenpox • Histoplasmosis • Siderosis • Stannosis • Barytosis • Haemosiderosis Disseminated Large Nodules (1-6 cm) • Metastasis • Rheumatoid nodules • Wegener’s granuloma • Pyemic abscesses • Hydatid cysts • Pulmonary infarcts • Arteriovenous malformation • Fungal • Caplan syndrome • PMF • Amyloidosis • Lymphoma Pleural Effusions are Notably Absent in • Sarcoidosis • Fibrosing alveolitis Upper Zone Fibrosis • Tuberculosis • Histoplasmosis • Sarcoidosis • Allergic bronchopulmonary aspergillosis • Progressive massive fibrosis • Ankylosing spondylitis • Extrinsic allergic alveolitis .218 Seminar in Radiology Miliary opacities • Fungal (Coccidomycosis. renal cell carcinoma. Blastomycosis. Histoplasmosis) • Tuberculosis • Sarcoidosis • Metastasis from thyroid.

SECTION 5 Gastrointestinal Tract. Pancreas and Hepatobiliary Tract .

.

g.0 mg/dl. the albumin bound un-conjugated bilirubin dissociates into bilirubin and albumin. ii. Non-hemoglobin haem containing pigments e. Transport: Bilirubin on release circulates as unconjugated bilirubin in plasma tightly bound to albumin. Bilirubin Metabolism 1. Hepatic phase i. Hyperbilirubinemia can be: • Conjugated • Unconjugated Pathogenesis A. Intestinal phase: Excreted in stool as stercobilinogen or metabolized to urobilinogen by the action of intestinal bacteria which is reabsorbed from the small intestine and reaches the enterohepatic circulation. catalase. 3. iii. Secretion into bile and storage: Conjugated bilirubin excreted directly into the bile canaliculi and then passes into bile ducts and gets stored in the gallbladder. Increased bilirubin production due to: • Excessive hemolysis • Ineffective erythropoiesis ii. Hemoglobin (80-85%) b. myoglobin. Predominantly unconjugated hyperbilirubinemia produces medical jaundice i. cytochrome 2. On entering the hepatocyte. Conjugation: Unconjugated bilirubin is converted to water-soluble conjugated bilirubin by enzyme glucoronosyl transferase. Decreased hepatic uptake due to: • Prolonged starvation . 4.15 Imaging in Jaundice Jaundice is defined as yellow pigmentation of skin and /or sclera in response to increased serum bilirubin level more than 2. Source: From catabolism of a.

Due to mechanical obstruction of the extrahepatic biliary tree → Obstructive jaundice. e. Rifampicin iii. Predominantly conjugated hyperbilirubinemia (Cholestasis) i.222 Seminar in Radiology • Sepsis • Drug. Due to impaired hepatic excretion of bile Suggestive of defect within the biliary canaliculi or small intrahepatic ducts → Medical jaundice ii.e. it is amenable to surgery).g. Approach to Diagnose a Case of Jaundice . Decreased bilirubin conjugation due to: • Deficiency of enzyme glucoronosyl transferase • Inherited disorders – Gilbert’s syndrome – Crigglar-Nijjar syndrome • Acquired disorders due to – Drugs – Hepatitis – Cirrhosis B. (i. Differentiation of Hepatocellular Jaundice from Obstructive Jaundice Parentral administration of vitamin K shows improvement of the prolonged prothrombin time in obstructive jaundice whereas no improvement is noted in cases of hepaticellular jaundice.

Benign tumor. Post-inflammatory • Chronic pancreatitis • Gallstones (including Mirizzi’s syndrome) • Pancreatic pseudocyst • Duodenal ulcer c. Cholangiocarcinoma ii. Benign strictures a. Hepatic neoplasm extending into the EHBD Causes of Obstructive Jaundice in Neonates • Extrahepatic biliary atresia • Choledochal cyst • Biliary hypoplasia • Inspissated bile duct syndrome • Bile duct stenosis Causes of Obstructive Jaundice in Children • Choledochal cyst • Biliary calculi • Bile duct tumor • Lymphadenopathy • Pancreatic masses Causes of Obstruction of Extrahepatic Bile Duct at Different Levels A. Neoplastic i. Primary sclerosing cholangitis ii. Metastasis—to lymph node in porta hepatis region vi. Biliary calculus b. At hilum (region of porta) • Cholangiocarcinoma . Intraluminal a. Parasite (Hydatid/Ascariasis) c. leiomyoma B. Ampullary carcinoma iii. e. Non-neoplastic i. lipoma. Post-traumatic • Surgery and other trauma b. Imaging in Jaundice 223 Causes of Biliary Obstruction A. Carcinoma head of pancreas iv. Gallbladder carcinoma Due to • Infiltration • Lymph node involvement v.g.

Benign – Sclerosing cholangitis – Infective cholangitis – Surgery or trauma – Mirizzi syndrome – Lymphadenopathy secondary to inflammatory conditions ii.224 Seminar in Radiology • Hepatic neoplasm extending into hilum • Metastasis • Sclerosing cholangitis B. Distal CBD obstruction • Benign stricture Due to – Cholangitis – Pancreatitis • Distal CBD calculus • Carcinoma head of pancreas • Ampullary carcinoma • Lymphadenopathy secondary to inflammatory and malignant conditions. In suprapancreatic portion of CBD i. Radiological Investigation 1. Ultrasound • Detection of dilated IHBR and CBD dilatation • Calculus in CBD • Pericholedochal and portahepatis lymphadenopathy • Pancreatic mass lesion • Infiltrating GB neck mass Signs of Dilated Intrahepatic Biliary Radicles • Parallel channel sign • Double barrel shot gun sign • Too many tubes in liver • Stellate pattern near portahepatis • Acoustic enhancement distal to duct . Plain X-ray abdomen • Radioopaque calculus shadow in biliary tree • Pancreatic calcification • Cystic mass causing soft tissue shadow • Gas in the biliary tree • Position of stent if present 2. Malignant – Cholangiocarcinoma – Secondary involvement by tumors of gallbladder and liver – Lymphadenopathy secondary to malignancy C.

Direct cholangiography i. ERCP iii. 4. e.g. T-tube cholangiography – Preoperative – Postoperative i. Computed Tomography • Detects IHBR dilatation and CBD dilatation • Pancreatic mass lesion.g. • Dilated CBD: Seen as rounded hypodense (water density) structure anterior to IVC which gradually tapers. chronic pancreatitis • Old age • Postcholecystectomy • Stone in CBD causing a “ball value effect” 3. e. • Detailed anatomy of bile duct is provided prior to surgery and interventional procedures • Postcholecystectomy syndrome Contraindications: • Bleeding or coagulation disorder • Prothrombin time >3 sec • Presence of active cholangitis • Contrast media hypersensitivity • Hepatitis B infection . PTC ii. Carcinoma head of pancreas. chronic hepatitis or cirrhosis • In these case direct cholangiography is the gold standard Dilatation of the Biliary Tree without Jaundice • IHBR obstruction by tumor while other part are unobstructed • In chronic incomplete or slowly progressive obstruction. PTC: “Percutaneous Transhepatic Cholangiography” Indications • Provide precise definition of site and etiology of obstructive lesion. (best modality for pancreas) • Choledocholithiasis • Pericholedochal and portahepatis lymphadenopathy • Infiltrating gallbladder neck mass lesion Features of Dilated Intrahepatic Biliary Radicles and CBD on CT Scan • Dilated IHBR: Seen as branching. low-attenuating tubular structures showing increase in diameter as they radiate towards the protahepatis. Imaging in Jaundice 225 Obstruction without Dilatation of Intrahepatic Biliary Radicles • Recent onset obstruction • Fibrosis of CBD wall as in sclerosing cholangitis • Rigidity of the surrounding liver parenchyma.

esophageal stricture Complications: • Pancreatitis • Cholangitis • Duodenal perforation • Instrumental injury 5. ERCP “Endoscopic Retrograde Cholangiopancreaticography” • Rapidly replacing PTC • Safe procedure when prothrombin time is significantly prolonged • Additional advantage of biopsy. . Hepatobiliary scintigraphy • Radionuclide labeled 99mTc IDA is injected intravenously which are accumulated by the hepatocytes and secreted into bile and subsequently into small bowel.226 Seminar in Radiology Complications • Sepsis • Bile leakage • Peritoneal haemorrhage ii. duodenal stenosis. severe pulmonary disease • Hepatitis B/AIDS • Acute pancreatitis • Acute phase of ascending cholangitis • Pyloric stenosis. removal of calculus and placement of stent • Higher success when the ducts are not dilated. MRI • Shows dilated IHBR and CBD. Stationary bile appear hyperintense relative to the background Advantages • Whole biliary and pancreatic ducts are visualized even in the presence of obstruction • Non-invasive • No need for contrast medium • Where ERCP cannot be done Disadvantages • High cost • Limited availability 6. Bile seen as hypointense on T1 and hypertense on T2 • Pancreatic lesion • Pericholedochal and portahepatis lymphadenpathy • Infiltrating GB neck mass 7. Contraindications • Apprehensive and unconscious patient • Patient with recent myocardial ischaemia. sphincterotomy. MRCP “Magnetic Retrograde Cholangiopancreaticography” • Details IHBR dilatation and CBD dilatation and level of obstruction and length of stricture as it can visualize both sides of the obstruction • Based on heavily T2-weighted sequence which increase the contrast.

Imaging in Jaundice 227 • Variable in demonstrating site of obstruction • Liver can be imaged with 99mTc sulphur colloid or albumin colloid for focal tumor involvement. IHBR dilatation may also occur . And 99mTc-labeled DISIDA (di-isopropyl-phenyl carbamoyl iminodiacetic acid) are used. either primary or secondary metastasis. • Use of SPECT may delineate better liver pathology • For bile duct 99mTc-labeled N-substituted iminodiacetic acid compound (99mTc-HIDA). Secondary • Originating in gallbladder and passing through the cystic duct into the biliary tree • Usually calcium bilirubinate Clinical Features • Asymptomatic → If stone is free in the biliary tree • RUQ pain and jaundice → If stone is impacted in the biliary tree Radiological Features • Plain X-ray abdomen : May show opaque calculus in the region of the biliary tree Cholangiography • Rounded or faceted filling defects within the contrast column • Single or multiple • Mobile or impacted Impacted Stone in Distal Common Bile Duct • Complete obstruction • Shows typical concave border of the contrast column outlining the calculus → Meniscus sign • Proximal CBD dilatation initially • Later. The later shows multiple focal areas of increased uptake corresponding to dilated duct demonstrated on cholangiogram. SPECIFIC PATHOLOGIES Choledocholithiasis Primary • Originating in the hepatobiliary duct secondary to infection or obstruction with bile stasis • Usually cholesterol stone.

CT Scan • Only 20 percent of the biliary duct stone shows homogenous high attenuation foci • Cholesterol stone → Low attenuation → Difficulty to detect • Calcium bilirubinate stone → Higher attenuation. widening of the bile duct proximal to the obstructing calculus → funnel-shaped appearance • Later on. hence can be detected Findings • Sees as higher attenuation than the adjacent bile • Intraluminal soft tissue density surrounded by a halo of low density bile → Target appearance • Intraluminal soft tissue density in the dependent part of CBD with a crescent-shaped appearance of the duct .228 Seminar in Radiology Impacted Stone in the Cystic Duct (Mirizzi’s Syndrome) • Can cause obstruction of the bile duct at the level of cystic duct insertion by – Extrinsic compression – Secondary inflammation MRCP • Shows similar findings as cholangiography • Advantage – No use of contrast – Can visualize the biliary tree on both sides of obstruction Differential Diagnosis of Filling Defect in the Biliary Tree • Air-bubble • Blood clot • Spasm of the biliary shincters • Intraluminal parasite • HCC invading the CBD • Papillary protruding lesions from ampullary carcinoma or cholangio- carcinoma Ultrasonography • Echogenic focus with acoustic shadowing in the biliary tree • Initially. CBD dilatation and IHBR dilatation.

Imaging in Jaundice 229 • Faint rim of increased density along the periphery of stone • Punctate areas of increased density in the central portion of the stone Secondary Findings in the Bile Duct • Dilated CBD with abrupt cut off if stone impacted in lower CBD • Later IHBR dilatation may also occur • Focal concentric biliary duct wall thickening due to associated inflammatory stricture. USG • Tubular non-shadowing echogenic structures in the dilated bile duct • Central sonolucent stripe is seen when the parasite is alive – Represents the worm’s digestive tract. When multiple • Parallel echogenic surface produce a “spaghetti” like appearance When coiled: • Appear as a rounded echogenic focus Kla Bull’s eye but lacks distal acoustic shadowing . Differential Diagnosis of Abrupt Termination in Distal CBD • Carcinoma of head of pancreas • Ampullary carcinoma MRI • T2-weighted images show marked contrast of the signal intensity between the bile and calculus – Calculus → Signal void – Bile → High signal intensity PARASITES Most common • Ascaris lumbricoides • Liver fluke • Hydatid cyst Findings for Ascaris and Liver Flukes Cholangiogrpahy • Linear lucencies within the contrast column in the extrahepatic bile duct • Single or multiple If coiled within the CBD • May show rounded filling defect simulating calculus.

Cholangiography • Very short and tight strictures • Focal concentric smooth area of narrowing with obstructed end convex distally → funnel-shaped appearance • Proximal bile duct dilatation • Surgical clips are often visible.230 Seminar in Radiology CT Scan • Seen as hyperattenuating tubular structure surrounded by less attenuated bile. Radiological Features • Seen in the mid-common duct near the junction with the cystic duct. Biliary Hydatid Disease • Due to rupture of hepatic hydatid cyst into the biliary ducts. USG • Laminated hydatid membrane—seen s filiform linear material in CBD • Hydatid daughter cysts—seen as rounded filling defects • Mixture of hydatid membrane and daughter cyst—seen as Amorphous debris in the bile duct. . Secondary Changes • Proximal CBD dilatation ± IHBR dilatation POST-TRAUMATIC STRICTURE Usually secondary to: • Cholecystectomy (most common) • Gastrectomy • Hepatic resection Post-cholecystectomy stricture from: • Clamp injury • Inclusion of a portion of the common bile duct in the cystic duct stump ligature • Local duct ischemia due to injury to the ductal arteries after excessive dissection • Inflammation from biliary leak • Prolonged—T-tube placement in the bile duct.

Bismuth classified postsurgical stricture in 5 types: Type I : · Low CHD stricture · Hepatic stump >2 cm Type II: · Middle CHD stricture · Hepatic stump < 2 cm Type III: · High stricture · Preservation of the biliary confluence Type IV: · Hilar stricture involving the biliary confluence Type V: · Stricture involving an anomalous distribution of the segmental branches Ultrasound • Proximal dilatation of CBD with smooth tapering stenosis or abrupt cut off. POSTINFLAMMATORY STRICTURES Causes • Chronic pancreatitis • Gall stone • Penetrating duodenal ulcer Radiological Features Chronic Pancreatitis • Usually long (3-5 cm) structure • Smooth concentric tapering narrowing of the intrapancreatic portion of CBD • Mild to moderate proximal biliary dilatation • Occasionally chronic Pancreatitis with a focal mass can cause abrupt narrowing of the dilated duct • A pseudopancreatic cyst in the head of pancreas . Based on ERCP and PTC. CT Scan • Proximal dilatation of CBD with smooth tapering stenosis or abrupt cut off. Imaging in Jaundice 231 PTC Combined with ERCP will show the Level and Length of the Stricture MRCP • Shows similar findings • Both sides of stricture are visualized hence level and length of stricture can be assessed.

Complication • Cholangiocarcinoma Radiological Findings • Diffuse. Cholangiography Often short and sometimes web-like: • May be single or multiple • Involve any portion of the biliary tree • Smooth tapered stricture of the biliary duct with proximal dilatation. PRIMARY SCLEROSING CHOLANGITIS • Uncommon disease of uncommon etiology • Characterized by chronic inflammation and fibrosis of the intrahepatic and extrahepatic biliary tree • Occurs mainly in young male • Usually associated with inflammatory bowel disease. . Clinical Features Weakness and pruritis followed by jaundice. USG/CT Findings of Postinflammatory Stricture • Smooth tapered stricture of the biliary duct with proximal dilatation • Additional findings: – Pancreatic enlargement – Parenchymal abnormalities – Pseudocyst – Calcification Gallstone Stricture • Result from fibrosis secondary to adjacent inflammed gallbladder or extrinsic compression by an impacted cystic duct stone. edema has to be differentiated.232 Seminar in Radiology It causes: – Extrinsic compression of the distal CBD leading to o Displacement o Stenosis o Proximal dilatation of CBD • Acute pancreatitis can cause transient stricture of the distal CBD.and extrahepatic bile ducts which tend to be short (1-2 cm) and alternate with normal or mildly dilated duct segments → Beaded duct appearance. multifocal strictures of both intra.

dilated peripheral ducts with no apparent connection to the central duct → Skip dilatation • Stenosis. fluid-filled cyst arising from the CBD (diverticula) Type III : Localized cystic dilatation of the distal intraluminal duodenal portion of CBD (choledochocele) Type IVa : Multiple cystic dilatation of intra and extrahepatic bile ducts Type IVb : Multiple cystic dilatation of extrahepatic bile duct Type V : Single or multiple cystic dilatation of the intrahepatic bile duct CHOLANGIOCARCINOMA Uncommon neoplasm <1 percent of all malignancies More common in male Peak incidence 6-7th decade Conditions which increase the risk of development of cholangiocarcinoma • Ulcerative coilitis • Sclerosing cholangitis . CHOLEDOCHAL CYST • Uncommon congenital cysts of the bile ducts • Manifest in childhood Clinical Features Triad of: • Jaundice • RUQ pain • Palpable—subcostal lump Diagnosis by USG/CT/ERCP/MRCP Type I : Fusiform cystic dilatation of the CBD Type II : Eccentric. Imaging in Jaundice 233 • Abrupt termination of the peripheral intrahepatic duct branches result in a “pruned tree” appearance. USG /CT Scan • IHBD dilatation usually mild and focal • Intrahepatic stenosis depicted by the presence of scattered. • Extrahepatic bile duct can show: – Stenosis – Dilatation – Wall thickening – Mural modularity – Mural contrast enhancement. pruning and beading of the IHBD can be seen.

In Diffuse Infiltrating Type • Diffuse irregular narrowing of the lumen of the bile duct. In Klastkin’s Tumour Dilated Intrahepatic biliary radicles Abrupt cut off at confluence of hepatic ducts. . Radiological Features Cholangiography • Abrupt cut off of the distal end of CBD with a markedly irregular intraluminal polypoidal mass. USG/CT Common Duct Involvement IHBD and CBD dilatation with abrupt cut off Lobar atrophy with crowding of dilated ducts in the atrophic lobe • Bile duct wall thickening.234 Seminar in Radiology • Choledochal cyst • Liver fluke infestation Types—Diffuse infiltrating. causing distal CBD obstruction without a demonstrable mass. AMPULLARY CARCINOMA • Carcinoma of the ampullla of vater. pruritis. • Abrupt complete obstruction with proximal dilatation of the biliary duct. • Appears as irregular polypoid mass. nodular and papillary Common sites • CBD—30-40 percent • CHD—30 percent • Hepatic duct confluence—20 percent • Cystic duct < 5 percent Clinical Features • Jaundice. weight loss. anorexia Radiological Findings Cholangiography Reveal • Bluntly tapered stricture with complete or partial obstruction of the duct and proximal dilatation of biliary duct.

• Distended gallbladder usually seen • At confluence of hepatic ducts (Klatskin’s tumour) • Dilated IHBR • Soft tissue lesion at confluence may be seen. Imaging in Jaundice 235 • Proximal dilatation of CBD and intrahepatic biliary radicles • Dilated pancreatic duct • Distension of gallbladder USG/CT Scan • Abrupt cut off of the dilated CBD at its distal end • Proximal dilatation of CBD and IHBR • Dilated pancreatic duct • Intraluminal soft tissue mass lesion ±. Clinical Features • Upper abdominal pain and weight loss • Jaundice Radiological Features • Concomitant stricture of distal CBD and pancreatic duct with proximal dilatation → Double duct sign • Abruptly tapered stricture is usually seen in the distal CBD • Distended gallbladder USG/CT Scan • Mass lesion in region of head of pancreas • Dilated CBD with tapered stricture in the region of pancreas • Dilate IHBR • Distended gallbladder Gallbladder Carcinoma • Uncommon neoplasm in Western World. • But most common biliary tract neoplasm. • Predisposing factors – Gallstone—Commonest association – Chronic cholecystitis – Procelain GB . CARCINOMA HEAD OF PANCREAS • Adenocarcinoma arising from the ductal epithelium of the gland • More common is elderly males. but common North Indian particularly in Eastern belt.

Metastasis • To portahepatis may manifest as a biliary obstruction due to extrinsic mass effect on the CHD and CBD. Which can result from: • Direct invasion to portahepatis by gallbladder. vomiting. USG/ CT Scan • IHBR + CBD dilatation with abrupt cut off at the level of obstruction • Gallbladder mass • Enlarged pericholedochyal lymph nodes. USG/CT Scan • Proximal dilatation with abrupt cut off • May show enlarged lymph node • Abnormal invading organs. pancreatic or gastric carcinoma • Metastasis to lymph nodes by lymphoma or other carcinoma Radiological Features Cholangiography • Abrupt cut off of the common duct with proximal dilatation. .236 Seminar in Radiology Clinical Features • Usually elderly female • Pain RUQ • Nausea. • Extrinsic compression of the common duct by enlarged lymph nodes. weight loss • Jaundice Biliary Obstruction Occurs Due to: • Intraductal spread along the cystic duct into the common duct. Radiological Features Cholangiography • Abrupt cut off of the common duct in the region of cystic duct with proximal dilatation of the biliary duct • Non-filling of the gallbladder.

the changes in pressure (P1–P2) along blood vessel are a function of the interplay between blood flow (Q) and vascular resistance (R). while contrast L and n are constant. The components which contribute to increased portal venous pressure are resistance to flow and increased portal venous blood flow. The normal liver may be conceptualized as a huge and distensible vascular network with very low resistance. P1–P2 = Q × R Resistance Resistance to the flow of blood in vessels can be expressed by Poiscuille's law: 8nL R= πr4 where n = coefficient of viscosity L = length of the vessel r = its radius Under physiologic conditions.16 Portal Hypertension DEFINITION Portal hypertension is defined as a free portal vein pressure more than the normal of 5 to 10 mm Hg or persistent portal venous pressure more than 30 cm saline or more than 8 mm Hg above IVC pressure. Flow Block A flow block causes an increased resistance to flow and leads toward reversal (hepatofugal or backward flow) of blood. resistance is mainly a function of change in radius (r). Depending on the type and stage of disease. The movement of portal blood across the liver is dependent on the pressure gradient between the portal and hepatic veins. or hepatic wedge venous pressure measurement more than 4mm Hg above IVC. Pathogenesis of Portal Hypertension : Resistance and Flow Ohm's law states that. The volume of portal flow is regulated by the vascular resistance of the splanchnic arteries. both components may significantly contribute to increased portal venous pressure. This block can be a mechanical .

4. Patients have an increased cardiac output. (Elevation of portal pressure to value greater than 100 mm Hg has been observed during the Valsalva . all of which contribute to portal hypertension. a web in major vessels or an extrinsic inflammatory or tumor process. because of porta-systemic collateral development. 2. splanchnic vasodilataion and increased portal venous flow. which then flows toward the umbilical area. 3. particularly when the outflow of the liver is impaired by an increase in pressure at the venous side as the consequence of inflow obstruction into the right heart.238 Seminar in Radiology obstruction in the system. blocked by collagen deposition or enlargement of hepatocytes. However. Collateral Circulation When portal pressure reaches a critical value. Explosion theory in which esophagal wall tension reaches a critical level and then rupture occurs. Umbilical vein: Increased pressure in the portal venous system opens the embryonic left umbilical vein. which drain into the internal iliac venous circulation. 5. Rupture of Esophageal Varices The mechanisms for the rupture of esophageal varices have not been fully elucidated. Corrosion hypothesis: Reflux of gastric acid injures the mucosa of the lower part of the esophagus. It is found at the microcirculatory level in parenchyma. Splenorenal collaterals: A communciation between the splenic and left renal vein may become predominant. measurements of lower sphincter pressure and pH failed to show evidence. 1. Increased Flow Present in chronic liver parenchymal disease as the consequence of complex circulatory process secondary to metabolic changes leading to hyperdynamic circulation. The block can be a thrombus. Gastric varices: Short gastric vein arising from the splenic vein feed the development of gastric varices in the gastric fundus. Esophageal varices: Redirection of flow in the coronary vein results in esophageal varices. Anorectal varices: The superior and middle hemorrhoidal veins arising from the inferior mesentric venous system connect at the level of the rectum with the inferior hemaorrhoidal veins. arising from the Lt branch of portal vein. porto-systemic collaterals may develop in 5 mains territories. The presence of gastric varices without esophageal varices suggest the possibility of splenic vein thrombosis. Finally the block can be functional.

• Catheterization of the umbilical vein in newborns associated with the development of omphalitis. . • Invasion into portal vein by carcinoma of the head of pancreas/CBD resulting into cavernous malformation of the portal vein. Influence of Portal Hypertension on Other Organs • Hypersplenism • Alterations of the splenic microcirculation. • Hypoxemia : due to functional pulmonary arteriovenous shunting and vasodilatation of pulmonary capillaries. The genesis of variceal rupture may be related to daily events in which pressure rises abruptly to extremely high values. Portal Hypertension 239 maneuver). • Splenic vein thrombosis. white cells and platelets. favors entrapment of red cells. • Disorderd coagulation system. with fibrotic changes in the splenic sinusoids. Classification of Portal Hypertension • Presinusoidal – extrahepatic → portal vein thrombosis – Intrahepatic → Schistosomiasis → Sarcoidosis → Felty's syndrome → Arsenic poisoning → Idiopathic portal hypertension → Primary biliary cirrhosis • Sinusoidal – Alcoholic cirrhosis – Vitamin 'A' intoxication – Nodular regenerative hyperplasia • Postsinusoidal – Intrahepatic → Veno-occlusive disease → Alcoholic hepatitis – Extrahepatic Budd-Chiari syndrome Presinusoidal Most commonly due to portal vein thrombosis and causes are: • Myeloproliferative syndrome.

as it provides: • Vascular anatomy and changes in calibre of vessels. The nodules in this entity are delineated. not by fibrous tissue but by collapsed liver parenchymal cells. anterior displacement of duodenal loop (Clatworthy's sign +ve). jejunal. Obliteration of small portal venules are its characteristic feature and liver function is preserved.chiari syndrome. Noncirrhotic portal fibrosis (idiopathic portal hypertension) is a common cause of portal hypertension. Eggs shed into the splanchnic venous tributaries and lodge in the portal vein radicles within the liver. constrictive pericarditis. penetrated dorsal view of dorsal spine may reveal following observations: • Cardiomegaly • Altered paraspinal line • Calcification in liver and spleen which may show enlargement. Inflammatory infiltration of the portal triads coexist with splenomegaly in the conditions like Felty's syndrome. pulmonary hypertension.240 Seminar in Radiology Presinusoidal Intrahepatic Etiologies Schistosomiasis is the most common entity. lymphoma and sarcoids. . • Detection of flow and its direction • Characterization of flow and quantification • Evaluation of organ parameters and associated abnormalities secondary to disease. • Vascular patency and presence of thrombus. gastric. Such as Budd. Barium meal. Conventional radiological investigation—plain X-ray abdomen and chest. Sinusoidal Etiologies • Alcoholic liver disease. These varices are typically shown as round / oval-filling defect or serpentine filling defect particularly in esophagus. obstructing portal venous flow. with flow in the portal vein directed toward the collateral circulation (hepatofugal flow). • Esophageal. Postsinusoidal Etiologies A common pathophysiologic change is the transformation of the portal vein to an outflow vessel. SONOGRAPHIC AND COLOR DOPPLER FLOW IMAGING EVALUATION OF PORTAL HYPERTENSION It is one of the most useful clinical monitoring device. Iliac varices and hemorrhoids. • Detection of portosystemic collaterals. duodenal. fibrotic reaction develops around the eggs. A granulomatous. • Nodular regenerative hyperplasia.

• Decreased number of peripheral portal branches in the liver. Vascular Signs of Portal Hypertension • Dilatation of portal. • Spontaneous portosystemic shunts with detection of collaterals. • Sonographic ratio of right / left lobe of liver should be 1:3 or less. • Ascites. • The most reliable evidence of portal hypertension is presence of collaterals and the extent of the shunt flow. Other Signs • Thickened GB wall • Splenomegaly • Increased thickness of lesser omentum in children as a result of lymphatic stasis. a non-specific sign. • Calibre of gastric vein more than 7 mm indicates a portahepatic pressure gradient above 10 mm Hg. • Decreased flow volume in the portal vein. • Decreased respiratiory variations in superior mesenteric and splenetic vein and inspiratiory calibre change of less than 4 percent. Sonography shows: Increased parenchymal echogenicity and poorly delineated intrahepatic portal venous walls. splenic and superior mesenteric veins. 47 an 45 percent. • Accentuation of fissures and nodularity Color Doppler Flow Imagings CDFI is at present the modality of choice in workup of portal hypertension: It basically assesses three main types: . • Dilated hepatic artery and splenic artery. It is a chronic hepatic parenchymal disease of diverse etiologies in which injury and regeneration of parenchyma is. splenic vein 10 to 12 mm and Superior Mesenteric Vein 10 to 11 mm in internal diameter. These vessels increase in clibre by 13 to 33 percent during deep inspiration and post prandially by 28. Portal Hypertension 241 Sonographically the main portal vein measures 13 to 15 mm. accompanied by increase in connective tissue formation resulting in destruction of normal architecture which causes portal hypertension. Specific Changes • Cirrhosis of liver is the commonest cause of portal hypertension. • Abnormal Doppler waveform in the hepatic veins. has 80 percent sensitivity. • Caudate lobe / right lobe ratio maintains with that of 5:4 or more. • Hepatofugal flow.

which may be due to reduced compliance of fibrotic liver. as this creates a situation similar to surgical Portosystemic anastomosis. • Patent paraumbilical vein with hepatofugal flow is seen more in NCPF. .sectional area of PV and flow velocity and shows a definite increase in cirrhosis. • Reversal of flow in splenic vein with enlarged renal vein draining into the IVC. • Short-gastric veins with flow towards diaphragm.78. • Heaptic artery of more than 4 to 6 mm diameter with RI 0. homoplastic signal with minimal respiratory variation. • Congestive index has been shown to have significant correlation with predicting bleeding. Hepatofugal flow is indicative of very severe portal hypertension. Quantitative CDFI Findings • Quantification of portal vein flow with CDFI is reduction in velocity in cirrhosis. direction of flow and characteristic of flow. extent of collaterals flow diversion which varies from patient to patient and also limitation of technique. Presence of hepatofugal flow has been shown to significantly reduce incidence of GI bleeding. Risk of Hemorrhage • The incidence of variceal bleeding is significantly reduce in patients with doppler evidence of large Paraumbilical and hepatofugal flow. Characteristics of Doppler Spectra of Hepatic Vein in Portal Hypertension • The normal 3 phase tracing of hepatic vein may be completely abolished. • Significantly reduced PI value of superior mesenteric artery (SMA) is reported in cirrhotic PHT and not in NCPF. • A patent and dilated paraumbilical vein may be associated with increase in flow and velocity. whereas a major splenorenal collateral may cause reversal of flow. Congestive index above 0.13 cm/sec has 67 percent-sensitive. gastroepiploic and esophageal varices and flow reversal in SMV. Congestive index: It is a ratio of cross. • Doppler spectra in normal portal veins are generally of low velocity.242 Seminar in Radiology Qualitative: Presence of flow. Portosystemic Surgical Shunt Follow-up • Evaluation of potency of shunt. • The variceal bleeding significantly higher in the patients with heapatopetal flow. The exact reduction reported is variable depending upon stage and etiology of cirrhosis.

Techniques 1. evidence of hepatofugal flow in intrahepatic portal branches is considered and indirect sign of potency. Direct correlation with portal pressure and variceal size IMAGING OF PORTAL VENOUS THROMBOSIS • Sonography is the modality of first choice and shows a the traid of 1. 3. 4. Arterioportography 3. Non-visualization of extrahepatic portal vein. Portal Hypertension 243 • Flow can be visualized directly through the anastomosis in portocaval shunt. Identifying the site of bleeding varices. Umbilical portography Arterial Portography Injection of contrast medium into the splenic / celiac artery and SMA. Periportal collaterals. Endoscopic Doppler Ultrasound • It has made hemodynamic evaluation of gastric and per esophageal vascular bed and azygos vein. Prior to TIPS. 2. 2. Bright echogenic band representing either thrombus or periportal fibrosis. • 7. • Doppler azygos flowmetry reveals: 1. • Evidence of significant hepatopetal flow in late follow-up of shunt is suggestive of anastomotic thrombosis. • When actual anastomosis and flow cannot be seen. Postoperative determination of portosystemic shunt. Significant increase in flow in esophageal varices. Equivocal cases where adequate information is not available by a color Doppler study. Splenoportovenography (SPV) 2. 3. Transhepatic / transjugular portography 4. to opacify the portal venous system in its venous phase. • Azygos vein can be localised at a distance of 20 to 25 cm from incisors and is localised by first identifying aorta. Indication 1.5 MHz convex transducer with 100° visual angle incorporated longitudinally with a fiber-optic scope. 2. Portography: Roentogenographic visualization of the portal venous system achieved by introduction of contrast into the system. .

• The filming sequence is used to cover 31 seconds. 2. If SMA or CA injections fail to show patent PV. • The needle is inserted into the spleen. With celiac or splenic artery injection both splenic or portal vein are seen. and then 1 film every third second for 24 seconds. then it is significant. towards the splenic hilum. 4. • Rapid hand injection of 30 ml of contrast (10 to 12 ml / sec) is given but better to use pressure injector. followed by 1 film every 5 sec for 5 sec. • Contrast material is injected at the rate of 9 to 13 cc. . • The SMA injection shows the SMV and PV and no contrast enters the splenic vein./sec in amount ranging from 35 to 50 cc by means of a pressure injector. • Films are taken in the following sequence : 2 films per sec for 2 sec. Technique • Size of the spleen is assessed. Left gastric vein opacification on splenic artery injection suggests hepatofugal flow. • The normal splenic or celiac artery injection delineates the splenic and portal vein only. • Usually the ninth intercostals space in midaxillary line is selected and the puncture is performed during suspended respiration using a 16 to 18 gauge long aspiration needle connected with syringe through catheter. Points to be Observed During Interpretation 1. Splenoportovenography (SPV) Shows better opacification of portal axis than arterioportography.244 Seminar in Radiology Technique • Percutaneous Seldinger technique through right femoral or axillary artery. The superior mesenteric artery injection will be normal even if splenic vein is thrombosed. followed by 1 film every 2 sec for 8 sec. Opacification of inferior mesenteric vein or superior mesenteric vein is unequivocal evidence of hepatofugal blood flow. 5. 3. then wedge venogram or intrahepatic parenchymal injection is successful in demonstrating hepatofugal flow in portal vein. Visualization of left gastric vein on celiac artery injection is not significant however if gastric veins are clearly varicosed or if esophageal varices are seen. directing it in an upward and inward direction. • Celiac artery and / or superior mesenteric artery are selectively engaged using a preformed visceral catheter. usually 1 film/sec for 7 seconds. • The veins are best seen between 14-20 seconds. without opacification of collaterals.

Nonfilling of the splenic/portal vein. • Normally. 2. no reflux is seen into tributary channels (IMV. b. Obstruction at or near the splenic hilum. Portal Hypertension 245 • Immediately after the needle is withdrawn. Simultaneous measurement of splenic pulp pressure. Severe hepatic failure Complications 1. Filling up of bridging collaterals. Advantages of Splenoportogram 1. The Normal Splenic Vein / Portal Vein Anatomy • The splenic vein is 5 to 13 cm in length and 1to 1. b. 3. 2. 3. • The portal vein is 6 to 8 cm in length. 2.2 to 2 cm wide usually straight and forms an angle of 40 to 90 degree with the spine. Contraindications 1. Obstruction at the formation of portal vein. Splenic rupture/subcapsular injection. a. Filling up of collaterals/tributaries. . Arteriovenous fistula/trauma 5. a.5 cm in diameter. SMV. • Splenic and portal vein PV joins at angle 90 to 140° in 80 percent cases. left gastric) or collaterals. abscess 4. Coagulation disorder 3. Obstruction of distal portal vein. Nonpalpable spleen/splenectomy. Better opacification of splenoportal axis. Dilated splenic vein up to this site with nonvisualized portal vein. Intraperitoneal/intracolonic/intrapleural injection of contrast. Severe ascites 6. Abnormal Splenoportography Reveals 1. 2. Splenic pathologies such as tumor. Vital signs monitored for next 6 hrs and bed rest is advised for another 6 hrs. 1. Hemorrhage Percutaneous Transhepatic Portography Second most common procedures to investigate portal hypertension. pressure is to be maintained at punctured site.

2. Contrast density is much superior to any other portographic method. It gives superior detail of intrahepatic and extrahepatic PV and hepatic vein branches compared to other techniques. 5. A collimation of 3 mm is used and the pitch and table speed is selected to allow scanning of the region of interest within 30 seconds. It is noninvasive and easier to perform. the catheter can be placed into any part of the splenoportal axis.) Spiral CT Portography • Typically 160 ml of contrast is injected at the rate of 3 ml/sec through the intravenous route using a pressure injector. • Once the right portal vein punctured.246 Seminar in Radiology Advantages 1. MIP images are more acceptable to surgeons. Manometric studies can be conducted at any point in the portal venous system. 6. Intervention in bleeding varices is possible. 3. 4. SV. . • A guide wire is advanced through the sheath into right branch of portal vein and then on portal vein proper. It is effective in demonstrating occlusions of the PV. 4. Coagulopathy 2. 3. Severe ascites and local problems (subphrenic abscess hemangioma etc. Advantages 1. 2. CT angiography enables imaging of the SV and SMV from a single contrast injection. • Scanning is started at 55 to 60 seconds delay after the on set of the injection. Contraindications 1. Once catheterized. the inner needle is removed and contrast is injected. Technique • Under local anesthesia a 27 cm needle passed perpendicularly for a depth of 10 to 15 cm in the mid-axillary line through the ninth or the tenth intercostal space. It is particularly useful when occlusion is due to direct tumor invasion or thrombosis. or SMV because of opacification irrespective of the direction of flow.

Portal Hypertension 247

ROLE OF ANGIOGRAPHY IN MANAGEMET OF
PORTAL HYPERTENSION
Pre- and Postoperative Shunt Evaluation
Surgical portasystemic shunts are effective for decompressing hypertensive
portal system and for controlloing variceal haemorrhage.
1. Total shunts
• Portocaval shunts
• Mesocaval shunts
2. Selective shunts
• Splenorenal shunts
• Coronocaval shunts

Preoperative Evaluation
• Predominant hepatopetal circulation with prominent liver opacification is a
relative contraindication.
• Hepatofugal circulation with slight or absent liver blush, gastroesophageal
varices constitutes probably the ideal hemodynamic situation for the
construction of a portocaval shunt.
• Prior to surgery it is important to determine the patency of portal vein and
its tributaries, direction of flow of blood.

Postoperative Evaluation
• Total shunts cause a complete loss of hepatic venous collaterals and an
increase in splenic venous flow, the portal venous pressure fall with time.
• Selective shunts do not alter portal venous pressures and therefore, the
hepatopetal portal venous flow is generally maintained.
• Regular follow-up is required in post-shunt patients to determine shunt
patency.

Radiologic Interventions
a. Vasopressin infusion
1. The selective celiac or splenic angiography is done to evaluate the portal
venous anatomy.
2. The vasopressing is infused in the SMA at the rate of 0.1 mt for 24 hrs.
b. Angiographic embolization using metal coils or hemostatic sponges can be
done by transhepatic catheterisation of the coronary vein and other
collateral.

TIPS (Transjugular Intrahepatic Portosystemic Shunts)
Creation of portosystemic shunt, by transjugular insertion of an expandable
metallic stent between the hepatic and portal veins under radiologic guidance.

248 Seminar in Radiology

Indications
Treatment of portal hypertension and its complications.

NATIONAL DIGESTIVE DISEASE ADVISORY BOARD (1994)
RECOMMENDS
Acute variceal bleed that cannot be successfully controlled with medical
treatment. Recurrent variceal bleeding in patients who are refractory to
conventional medical therapy.

Promising Yet Unproven
• Refractory ascites
• Budd-Chiari syndrome

Unproven
As initial therapeutic intervention for acute variceal hemorrhage and to prevent
recurrance of hemorrhage. To reduce intraoperative morbidity during liver
transplant surgery.

Contraindications
Absolute – Right-sided heart failure
– Polycystic liver disease
– Severe hepatic failure
Relative – Active intrahepatic or systemic infection
– Severe hepatic encephalopathy
– Portal vein thrombosis

Technique
The transjugular approach to the portal venous system and creation of a porto-
systemic shunt developed by Cola pinto.
• The procedure can be performed under conscious state, sedation or general
anesthesia for uncooperative patient.
• A 10-F vascular sheath is advanced into the right atrium.
• A5-F catheter is then introduced coaxially and pressures are measured of
right atrium, IVC, and free and wedged hepatic veins.
• CO2 digital subtraction wedged hepatic venography is performed to see
the portal vein.
• A 16-guage Colapinto needle is advanced over 0, 035-inch Amplatz, superstill
guidewire into the right hepatic vein.
• The guidewire is removed and the needle is advanced with fluoroscopic
guidance into the expected position of the right main portal vein.

Portal Hypertension 249

• The 9-F catheter is advanced over the Cola pinto needle and guide wire
into the portal vein.
• The needle is removed and a 5-F catheter is advanced into the portal vein.
• The parenchymal tract is dilated with an 8 mm PTA balloon catheter and
10 mm diameter metallic stent is placed in the tract.
• Portal and systemic venous pressures are measured and another portal
venogram is obtained.
• A portasystemic gradient less than 12 mm Hg after creation of a TIP is
satisfactory.

Complications
Technical
• Bleeding (extrahepatic needle puncture)
• Stent related (shortening, migrations, occlusion)

Hemodynamic
• Hepatic encephalopathy (20-40%)
• Cardiac failure

Late Complication
Restenosis and thrombosis of the shunt (25%).

Hepatic Venous Outflow Tract Obstruction (HVOT)
Hepatic venous Outflow tract (HVOT) obstruction is a group of conditions
which impede the drainage of blood from the liver parenchyma.

Etiology
• Hepatic vein obstruction is usually thrombosis, where IVC obstruction is
usually to non-thrombosis.
• The thrombosis in hepatic vein is predisposed by hypercoagulable states,
myeloproliferative syndromes . Extrinsic compression by hepatic tambours
and liver abscesses.
• IVC obstruction is either due to membrane or long segment narrowing or
due to coarctation.

Imaging
Contrast studies are the gold standard and include.
Inferior vena cavography, hepatic venography, percutaneous transhepatic
venography or functional hepatography.

250 Seminar in Radiology

Inferior Vena Cavogram
Two major types:
a. A thin membrane just below the celiac trunk junction
b. Segmental narrowing below the celiac artery junction and involving
intrahepatic segment of the IVC for variable distance.
c. Dilated below the obstruction-associated hypertrophy of the caudate lobe.
In complete IVC obstruction extensive collateral network involving the
ascending lumber and paravertebral veins is seen.

MRI
MRI can be performed in obesity or in presence of bowel gas.
• On conventional T1, T2 MRI scan portal vein exhibits flow void phenomenon
• MRI are best used for evaluation of vascular encasement
• The presence of uniform signal free ring surrounding inner bright zone
indicates vascular patency
• On gradient echo images obtained with flip angle <30° flowing blood within
portal vein appears bright.
• Area of reduced signal within vessel may represent thrombus
• Shunt and collatrals are well seen.

17
Hepatobiliary Intervention
TRANSHEPATIC INTERVENTIONS
In recent years percutaneous transhepatic interventional technique has come
in a big way in the clinical management of biliary tract obstruction.
Percutaneous transhepatic biliary drainage (PTBD) for combined
external / internal catheter decompression, provides an effective method for
rapid non-operative biliary decompression and has become an alternative to
standard surgical biliary bypass.
The basic technique for PTBD involves transhepatic insertion of a drainage
catheter into the biliary ducts and through areas of bile duct stricture into the
duodenum. The catheter is so designed that multiple sideholes can be placed
above and below the stricture to allow drainage of bile in an antegrade fashion
into the duodenal lumen for internal drainage.
PTBD affords an initial catheter access to the biliary ducts through which
varieties of secondary therapeutic interventional procedures can be performed.
Transhepatic biliary interventions

Initial access Secondary procedures
– Endoprosthesis
– Stricture dilatation
– Biopsy
– Stone removal

PERCUTANEOUS BILIARY DRAINAGE
Indications
• General – Extrahepatic obstruction with
– Sepsis
– Pruritus
– Hepatic decompression
• Specific – Palliation–advanced malignant
obstruction

252 Seminar in Radiology

– Preoperative decompression
– Sepsis – cholangitis, liver abscess
– Failed biliary – enteric anastomosis
– Secondary therapeutic maneuvers
– Stricture dilatation
– Endoprosthesis
– Stone dissolution/extraction
– Posttranshepatic cholangiographic
prophylactic decompression

Contraindications
PTBD is employed in patients who are too ill to undergo scheduled surgical
exploration. Routine contraindication to PTBD are:
• Uncorrectable bleeding diathesis
• Massive replacement of the liver by metastatic disease
• Hepatic cirrhosis

Instrumentation
Commercially-prepared biliary drainage kits are now available;
• Well–equipped procedure rooms with an assortment of guide wires, catheter
systems, vessel dilators, adaptors, skin fixation devices, and collection
bags.
• Initial diagnostic cholangiography is performed with a standard 22-gauge,
thin-walled Chiba needle followed by a cannula puncture of appropriate
biliary radicle using a conventional 18-gauge sheathed needle assembly.

Guide Wires
Two special wire have been designed specifically for biliary catheter intervention:
i. Ring-lunderquist torque wire
ii. Lunderquist “Coat hanger” wire long malleable tip

Biliary Guide Wires: Clinical Characteristics
Guide wires (0, 38 in.) Advantages Disadvantages
Tight J (3 mm) Leads with curve good for May not go through tight
tight turns obstruction
Floppy J (15 mm) Leads with curve good for turns May not support catheter in all
cases
Ring-lunderquist (torque) Torque control supports May pierce duct wall difficult
catheter wall negotiating tight turns
Lunderquist “Coat hanger” wire supports Not good for searching
catheter extremely well

Hepatobiliary Intervention 253

Catheters
Various radiopaque multi-sidehole drainage catheters have been employed in
different centers.

Biliary Drainage Catheters: Clinical Characteristics
Catheter Advantages Disadvantages
Ring (8, 33/10 F) Angle/pigtail tip anchor in Not good for external drainage
duodenum
Muller (8, 3/9, 0F) External drainage catheter with Too few sideholes for internal
various curves fewer sideholes drainage
Argyle feeding tubes Soft, large caliber easier on Too pliable to use initially
(10, 12, 14 F) patient can tailor sideholes
Self-retaining (cope loop) Soft, large caliber (polyvinyle Too pliable to use initially, long
or silastic) anchor effect with term patency unclear
inner suture
Foley type Standard balloon anchor rubber Wall necrosis from balloon

Patient Preparation
• Survey of the bleeding parameters
– The prothrombin time should be within two minutes
– Platelets above 75,000/ cumm.
• Prophylactic antibiotic coverage – The day before the procedure.
The, drugs routinely given are ampicillin and gentamicin (80 mg IM early
on the day of the procedure. Antibiotic coverage is continued for minimum of
three days after catheter insertion.
• Premedication with narcotics and sedatives are crucial both to cut down
anxiety and to control local discomfort at the puncture site during catheter
introduction.
• Preoperative preparations also include completely sterile skin preparation
and sterile surgical drapping of the fluoroscopic table.
• The procedure is carried out with running intravenous fluids and blood
pressure is monitored at timely intervals.

Techniques
1. Fine-needle transhepatic cholangiography done at first step in all cases.
2. A separate skin puncture site is selected based on fluoroscopic observations
of the position of the opacified bile ducts with the 18-gauge cannula sheath.
3. With selective-18-gauge cannula successful entry into biliary duct system
is confirmed by observing flow of bile.
4. Guide wire through the cannula is advanced caudally, then the cannula is
advanced over the guide wire as for as possible.
5. If the guide wire has passed beyond the stricture, through the ampulla into
the duodenum, a ring pigtail catheter is selected. When the guide wire
cannot be advanced beyond the stricture, a Mueller variety is preferred.

254 Seminar in Radiology

6. Catheter position is adjusted so that the sideholes are located above the
obstruction.
7. The biliary drainage catheter then fixed to the skin.
8. The catheter is allowed to drain externally by gravity
9. The catheter is clamped on the third day or fourth post-procedure day,
causing bile to flow in an antegrade manner into the duodenum.

Complications
Early – Bacteremia and sepsis
– Venous intraductal bleeding
– Arterial bleeding
Late – Cholangitis and sepsis

External Drainage
External drainage is often viewed as a “failure” of an attempt at internal drainage
occurs in 20 to 25 percent of cases, in such cases, dense periportal malignant
infiltration causes complete biliary obstruction.

Two-stage Delayed Internal Drainage
In the presence of undecompressed dilated ducts and untreated infected bile,
the risks of sepsis, duct perforation and bile leakage are much more.
Placement of external drainage catheter may be carried out initially and
followed by a delayed second-stage attempt to catheterize the stricture for
internal drainage after two to three days.

Multiple Drainage Catheter
Periportal obstruction (due to malignancy—cholangiocarcinoma) often
produces isolated non-communicating obstructions of multiple duct segments,
effectively is helped by multiple dramage catheter system.

Selective Drainage of the Left Duct
In cases with selective obstruction of the left hepatic duct system the principal
modifications in technique include the use of an anterior horizontal subxiphoid
approach is required. But the disadvantage of this procedure is that success
rate of internal drainage is difficult because of the acute right angle bend and
considerable amount of radiation dose to the operator’s hand.

SECONDARY PROCEDURES
Endoprosthesis
Endoprosthesis does not pose the drawbacks of the drainage catheter which
include malfunctions due to occlusion or migration, bacterial colonization and

Hepatobiliary Intervention 255

secondary suppurative cholangitis, local plain and the disturbing psychological
impact of a permanent externally protruding device.

Technique
After an internal drainage catheter is placed in the way earlier described, the
endoprosthesis is advanced coaxially over the drainage catheter. A guide wire
is passed through the drainage catheter to the distal end of the stricture, a bend
is placed in the wire at the skin surface. The guide wire tip is then withdrawn
to the proximal end of the stenotic area and second bend is made in the guide
wire. The difference gives the necessary length of the prosthetic device. Prior
to insertion of the endoprosthesis the stricture is coaxially dilated by insertion
of a large “dilating” 14 french Teflon catheter. Then endoprosthesis is placed
over the 7 to 8 french catheter and inserted. Dilating catheter used to push the
prosthetic device into the bile duct. The drainage catheter is then withdrawn
to the proximal end of the prosthesis, and contrast material is injected to
confirm the patency.

Complications
Cholangitis, proximal and distal migration of the prosthesis, recurrent
obstruction by tumor growth.

Stricture Dilatation
Benign, iatrogenic, and biliary enteric anastomotic strictures can be effectively
managed by percutaneous transhepatic dilatation.
i. Balloon catheter dilatation has two distict advantage. Dilatation can be
carried out to a 16 to 20 french caliber via only 8F catheter placed
across the liver.
ii. Following an interval of protective catheter drainage, all catheters can be
withdrawn.

Technique
Balloon catheter dilatation is performed several days after placement of an
internal drainage catheter with opaque contrast material injected into the balloon,
the degree of stenosis can be determined visually by inflating the balloon across
the site of the stricture, gradually increasing the pressure in the attached syringe.
Dilatation is complete when fully inflated balloon passes smoothly across the
stricture and no balloon passes smoothly across the stricture.

Transhepatic Biliary Calculus Removal
Nonoperative transcatheter manipulation of biliary duct calculi through the
transhepatic tract can be an alternative technique to the more conventional
transfistula or transendoscopic techniques for calculus extraction.

Opacification of the biliary tree though gallbladder under ultrasound guidance is indicated when PTC and ERCP have failed. The yield of positive cytologic material with fine-needle aspiration techniques approaches 90 percent. • Cytologic examination of bile obtained following percutaneous catheter insertion. size. especially the cholesterol solvent monooctanoin. 10-20 ml bile sample are routinely sent for cytologic analysis. and transcatheter forceps biopsy. • Transcatheter forceps biopsy techniques have been infrequently reported. Direct transcatheter instillation of stone solvents. a steerable remote-control catheter can be introduced over a guide wire into the tract. this will be in the right subcostal area so that the needle will traverse liver parenchyma and enter the body of the gallbladder. To obtain a diagnostic aspirate ii. and larger calculi may be fragmented and the fragments engaged in the basket and directed caudally into the duodenum. . transcatheter brush biopsy. • Brush biopsy through the percutaneous catheter can be carried out with to-and-fro and rotary movement. depending on the number. Ideally. Tissue Biopsy Techniques Available methods for pathologic diagnosis include bile cytology. Cholangiogram iii. Technique • An initial assessment of the liver and biliary tree is made using real time ultrasound and the point for puncture selected. Indications i. TRANSCHOLECYSTIC INTERVENTION Diagnostic percutaneous puncture of the gallbladder. and location of the calculi. has also continuous infusion at 4 to 10 ml/hr may be required. percutaneous needle aspiration biopsy. • Fine-needle aspiration biopsy can be performed in the area of bile duct stricture under fluoroscopic control. for upto two to three weeks. Most calculi can be directly withdrawn through the transepatic parenchymal tract. A conventional biliary stone basket (Dormia) can then be introduced through the steerable catheter.256 Seminar in Radiology Following gradual maturation of the transhepatic tract to an adequate caliber relative to the observed size of calculi. Transcatheter Irradiation Local high dose irradiation of obstructing malignant tumors using a radioactive source (iridium 192) placed in an indwelling catheter with external beam therapy ultimately completed the treatment plan.

7 F Mc Gahan catheter has been placed and properly fixed internally and externally. • 6. one should not hesitate to consider a transperitoneal approach in which the gallbladder is punctured at the point where it lies closest to the anterior abdominal wall. Intraperitoneal bile leakage 2. remove stones. For cholangiography as much bile as possible is aspirated before injection of 60 percent contrast under fluoroscopic control. the percutaneous cholecystostomy can provide a quick and safe means of interim drainage. • No attempt should be made at this time to obtain a cholangiogram. although the needle tip is directed into the lesion while using USG. Bile leak ii. sepsis and leakage are always there. Complications 1. Technique (Transhepatic or Transperitoneal) • The puncture site is chosen with US guidance • If there are problems with a transhepatic route (hepatic metastases). Complications i. • With the needle tip in the lumen of the gallbladder a specimen of bile is aspirated and sent for gram stain and culture/ sensitivity. Sepsis iv. and skin is nicked with scalped blade. to do so risk of vasovagal reaction. Vasovagal reactions (during procedure) . The catheter is then attached to a gravity drainage bag. Hepatobiliary Intervention 257 • The abdominal wall is infiltrated with 1 percent xylocaine. • Under US guidance the body of the gallbladder is punctured with a 22- guage spinal needle. all the bile and contrast is aspirated from the gall bladder. Colonic and duodenal perforation iii. The technique of percutaneous fine-needle aspiration biopsy of the gallbladder is essentially the same as that for diagnostic puncture. Bleeding into GB GALLBLADDER DRAINAGE Indication In the patient who is very ill on presentation or who only requires short-term drainage.

Wound hematoma iii. resulting in a cavitation bobble. • T-tube tracts. Complications i. The spark vaporizes fluid. Technique • A small incision is made in the fundus just large enough to accept a 24 F Foley catheter. . an electrode and an EHL generator. Failure of catheter placement INTRACORPOREAL BILIARY LITHOTRIPSY Principle Intracorporeal biliary lithotripsy (IBL) requires two components. Technique We have used intracorporeal EHL from a variety of percutaneous access routes.5. and calculi within the gallbladder removed using standard interventional techniques. • The Foley balloon is inflated and the fundus sutured to the peritoneum and posterior rectus sheath. calls for a 4-week period of tract. Perforation of the cystic duct v.258 Seminar in Radiology CHOLELITHOTOMY BY CHOLECYSTOSTOMY Indication Cholelithotomy through a cholecystomy tract generally is indicated in patient who had a cholecystostomy performed for urgent decompression of the gall bladder and is subsequently believed to be a high-risk patient for chole- cystostomy. and directly into the gallbladder. transhepatic tracts. including T-tube tracts. 1 week after the initial cholecystostomy. Wound infection ii. • For removal of intact stones using forceps or a stone basket or fragmentation of large stones with subsequent extraction of the fragments. 9F diameters when a potential difference is introduced across the electrode. Cholangitis vi. The energy of the hydraulic shock wave is transferred to the stone at the fluid-stone interface and fragments the stone. a spark is produced at the tip of the electrode. Which in turn create a hydraulic shock wave in the fluid of the bile duct. Injury to the colon iv. • About the seventh postoperative day the Foley catheter is removed over a guide wire. • A transhepatic approach to the gallbladder will allow tract dilatation approximately. Electrodes are available in 3. a cholangiogram is performed.

Indications Treatment of portal hypertension and its complications. • Using direct vision with the choledochoscope. • The 18-F thin-walled Teflon sheath allows easy access to the biliary tree with the flexible 15-F choledochoscope. • The T-tube is removed over a guide wire. INTEVENTIONAL PROCEDURES IN PORTAL HYPERTENSION TIPS TIPS is the creation of an image-guided connection between a major right hepatic vein and major intraheaptic branch of the portal vein. . Promising yet unproven: • Refractory ascites • Budd-Chiari syndrome Unproven As initial therapeutic intervention for acute variceal hemorrhage. bring the electrode almost into contact with the stone and are careful to avoid contact with the wall of the bile duct. the tract is dilated to 18 F by using coaxial dilators (Dilators – Cook. Bloomington). Recurrent variceal bleeding in patients who are refractory to conventional medical therapy. Hepatobiliary Intervention 259 • Standard practice is to remove all biliary calculi using a choledochoscope with a combination of fluoroscopic guidance and direct visualization. National Digestive Disease Advisory Board (1994) Recommends Acute variceal bleed that cannot be successfully controlled with medical treatment. Therapy for prevention of variceal hemorrhage. Initial therapy to prevent recurrent variceal hemorrhage. To reduce intraoperatie morbidity during liver transplant surgery. Contraindications Absolute – Right-sided heart failure – Polycystic liver disease – Severe hepatic failure Relative – Active intrahepatic or systemic infection – Severe hepatic encephalopathy – Portal vein thrombosis Technique The transjugular approach to the portal venous system and creation of a portosystemic shunt developed by Colapinto. • The fragments subsequently are irrigated and flushed through the sheath.

035-inch Amplatz. Sclerosing cholangitis e. Stones b. IVC. • The needle is removed and a 5-F catheter is advanced into the portal vein. Jaundice of undetermined etiology • Extrahepatic biliary obstruction a. superstill guidewire into the right hepatic vein. Drug-induced cholestasis c. Diagnostic indications A. Cirrhosis d. and free and wedged hepatic veins. occlusion) Hemodynamic – Hepatic encephalopathy (20-40%) – Cardiac failure Late – Restenosis and thrombosis of the shunt (25%) ENDOSCOPIC RETROGRADE CHOLANGIOGRAPHY Indications I. migrations. • The parenchymal tract is dilated with an 8 mm PTA balloon catheter and 10 mm diameter metallic stent is placed in the tract. Strictures d. Complications Technical – Bleeding (extrahepatic needle puncture) – Stent related (shortening. • Portal and systemic venous pressures are measured and another portal venogram is obtained. sedation or general anesthesia for uncomperative patient. Hepatitis b. Sphincter of Oddi dysfunction • Intrahepatic biliary obstruction a. • A 10-F vascular sheath is advanced into the right atrium • A 5-F catheter is then introduced coaxially and pressures are measured of right atrium. Malignancy . • A 16-guage Colapinto needle is advanced over 0. • The guidewire is removed and the needle is advanced with fluoroscopic guidance into the expected position of the right main portal vein. • A portosystemic gradient less then 12 mm Hg after creation of TIPS is satisfactory.260 Seminar in Radiology • The procedure can be performed under conscious. • The 9-F catheter is advanced over the Colapinto needle and guidewire into the portal vein. Tumor c. • CO2 digital subtraction wedged hepatic venography is performed to see the portal vein.

The type of endoscope employed is generally side-viewing duodenoscope. . 3% Technique • ERCP is generally performed using fluoroscopic rooms in radiology department. dilute the contrast to concentration of 30 percent. Therapeutic indications A. 7-0. 6% • Instrumental injury – 0. contrast runs the dependent wall and fills the left intrahepatic ducts. Percutaneous cytology II. • When the pancreatic duct is studied. Endoscopic papillotomy • Stones • Sphincter of oddi dysfunction B. • Endoscopist is responsible for cannulation and management of the patients. 60 percent diatrizoate is employed. 3% • Cholangitis – 0. Frequently the films are taken with erect position. The radiologist and endoscopist work together closely to achieve adequate images of the ductal structures. 07-0. • A tilting fluoroscopic table is therefore necessary. 4% • Drug reaction – 0. Acute pancreatitis (generally avoided) iii. Clinically unstable patients (severe cardiopulmonary disease) ii. 5-1. Placement of nasobiliary catheters C. Contrast hypersensitivity Complications • Pancreatitis – 0. • ERCP is a team effort. • In prone position. • Radiologist is responsible for the filming sequence and directing the injection. Fluid collection cytology c. • ERCP is initially performed with the patient in the prone-oblique or supine position. 1-0. Hepatobiliary Intervention 261 • Endoscopic cytology and biopsy a. Brush cytology or biopsy b. 6% • Pancreatic sepsis – 0. Internal transpapillary stents D. • Carried out using flexible fiber optic endoscope. Balloon catheter dilatation Contraindications Contraindications to ERCP are limited i. 6-0. • When examining the biliary tree attempts should be made to fill the entire ductal system so that both the left and right intrahepatic ducts are filled. • In the biliary tree.

• Infiltrating process may lead to irregularity which makes confusing diagnosis of malignant stricture. strictures. • Cirrhosis is the most common entity produces bizarre appearance. in the absence of previous surgery. • Stones rarely completely obstruct the duct unless impacted. Intrahepatic Bile Duct Abnormalities • Observations on bile ducts that need to be made to interpret. caliber irregularities. presence or absence of stones. diameter. include. obstruction and mass effect. areas of stenosis and ectasia and ductal irregularities due to regenerating nodules and chronic fibrosis are marked. • Strictures of proximal duct.262 Seminar in Radiology ABNORMALITIES OF THE BILIARY TREE Extrahepatic Bile Duct Abnormalities • Most common are choledocholithiasis and stricture. the mucosal details should be examined in the region of the stricture. • Abscesses. • Benign strictures of the distal common duct are most commonly seen in chronic pancreatitis. • Strictures involving the distal CBD include pathology in the pancreas as differential diagnosis. malignant strictures may have a very smooth and symmetric appearance. • If a stricture is encountered. when persistent are almost always due to calculus. • The companion pancreatogram may be extremely useful in determining the etiology of the stricture primary carcinoma of the pancreas almost always is accompanied by ductal abnormalities. • There are several congenital abnormalities where ERCP is well suited for studying choledochoceles. • Complete obstruction of the extrahepatic bile ducts almost invariably due to some malignant lesion. may produce mass effect or may directly communicate with the biliary tree. communication with parenchymal spaces (abscess) and obstruction. • Stones do not locally expand the common duct. • The pancreaticgram may confirm the presence or absence of chronic pancreatitis. . • Unfortunately. • Metastatic disease – the most common change include stenosis. splaying separation or crowding. • Filling defects within the CBD. must be considered to represent malignant disease.

Previous biliary tract surgery (hepaticojejunostomy) b. • Can be perfused mono-octanoin or bile salts to reduce the size of stones • Catheter is used to perform repeat cholangiography. stone or tumor. • The bile duct can be perfused with antibiotics or the catheter can be connected to a drainage bag to decompress the biliary tree. • Pigtail catheter can be fashioned across bile duct strictures.5 cm • Acute pancreatitis Placement of Nasobiliary Catheter • A 300 cm catheter can be placed through the endoscope and into the common bile duct above a stricture. Endoscopic Sphincterotomy Indications • Residual or recurrent CBD stone following cholecystectomy • Chledocholithiasis in high risk patients • Sphincter of oddi dysfunction • Gallstone pancreatitis Contraindication • Coagulation disorders • Long strictures of distal bile ducts • Large stone > 2. . Contraindication for ERCP. Hepatobiliary Intervention 263 Endoscopic Cytology and Biopsy Brushing of the stricture directly or collection of bile for cytology can confirm the malignant of a stricture. Ampulla is located in duodenal diverticulum d. Indications 1. Procedure of choice when endoscopic cannulation is impossible Examples: a. Internal Transpapillary Stent This is usually done for benign or malignant strictures in high-risk patients. Gastric outlet obstruction c. PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY (PTC) First described by Huard and Do Duan in 1937.

Biliary obstruction at the liver hilum b. 45%). Procedure complementary to ERCP Examples: a. Technique Under antibiotic cover and following correction of any pre-existing coagulopathy the liver is punctured using a chiba needle under fluoroscopic control and. . 3. if necessary under US guidance. On slow withdrawal of the needle the injection of contrast the ducts are identified and finally 20-50 ml contrast injected. Complications • Common: Sepsis (1. If the only purpose is sufficient drainage for palliation. biliary peritonitis (1. Failure to cannulate papilla b. hemorrhage (0. 35%) • Less common: Pneumothorax. Procedure of choice because of underlying pathology Examples: a. Hilar tumor.264 Seminar in Radiology 2. 4%).

During this period. Intestinal tuberculosis became a common diagnosis in the early 20th century. In the beginning of 1985.18 Abdominal Tuberculosis Tuberculosis is an ancient disease. means “to decay”) appreciated the severity of tuberculous enteritis as a complication of pulmonary tuberculosis.. The incidence is about 50 percent in patients with AIDS. and HIV/ AIDS epidemic. a resurgence began in the total number of new cases and peaked in 1992 related to the emergence of multiple-drug-resistant (MDR) tuberculosis. From 1953 to 1985. However since .5 percent per year was reported in United States with the total number of annual cases of tuberculosis falling from 84304 to 22201. tuberculosis. die if diarrhea sets in” diarrhea attacking a person with phthisis is a mortal sign (Paustian 1985). the hairs of whose head fall off. an average annual decrement of 4. It is estimated that between 19 to 43 percent of the world’s population is infected with M. who called tuberculosis as “Phthisis” (derived from the Greek words ‘phthiein. whereas only 10 to 15 percent non-HIV infected patients have extra- pulmonary manifestations. WHO estimates that every year more than 8 million new cases of tuberculosis occur and approximately 3 million persons die from the disease. Hippocrates. Antitubercular drugs developed in 1940 and then incidence of tuberculosis began to decline in the 1950s with the pasteurization. increased by 20 percent above that period in the nadir 7 years earlier. 95 percent of tuberculosis occur in developing countries where few resources are available to ensure proper treatment and where HIV infection may be common. He noted that the “Phtisical persons. Epidemiology Tuberculosis remains one of the deadliest disease in the world. number of individual infected. The first well documentated case of tuberculous peritonitis was described from the New York Hospital in 1843. as most cases of small intestinal thickening and narrowing were attributed to the recently identified tubercle bacillus (Horvath 1998). Enteric involvement was found in 6 to 90 percent patients with pulmonary tuberculosis in necropsy and radiological series. Abdominal tuberculosis may mimic a variety of gastrointestinal disorders. Intestinal tuberculosis was recognized as the most common complication of active pulmonary tuberculosis in the first half of the 20th century.

Hematogenous spread of the tubercle bacillus from an extraintestinal focus c.g. Patient might develop one of the three main types of disease – • Intestine • Peritoneum • Mesentery and mesenteric lymph node Pathogenesis a. Bile containing tubercular bacilli d. bovis) b. Extension from contiguous organs. . e.000 population (CDC surveillance reports 2002). with a historical low in 2001. Peritoneal tuberculosis • Acute tubercular peritonitis • Chronic tubercular peritonitis Ascitic form Encysted form Fibrous form – Adhesive type – Plastic type 3. ingestion of tubercle bacilli (M. Tuberculosis of solid visceras • Liver. the number of tuberculosis cases in the United States has declined steadily. biliary tract and gallbladder • Pancreas • Spleen 5. Miscellaneous Retroperitoneal lymph node tuberculosis. Gastro intestinal tuberculosis • Ulcerative • Hypertrophic or hyperplastic • Sclerotic • Diffuse colitis 2. female adnexa. commonly in chest. Classification of Abdominal Tuberculosis 1.266 Seminar in Radiology 1992.6 cases per 100. Tuberculosis of mesentery and its contents • Mesenteric adenitis • Mesenteric cyst • Mesenteric abscess • Rolled up omentum 4. of 5. Infection may develop primarily in the GI tract or it may be secondary to a focus elsewhere in the body. GASTROINTESTINAL TUBERCULOSIS Abdominal tuberculosis is endemic in India.

The lumen is narrowed resulting in a ‘napkin – ring’ type of stricture. Site of Involvement – Ileocecal region is the commonest followed by ileum.6%) • Acute appendicitis (3. lymphatic infiltration and tubercle formation (caseous necrosis). Hypertrophic type – Ileocecal region is involved.6%) (from a series of Bhansali) • Peritonitis (13. Abdominal Tuberculosis 267 Histopathogenesis Marked inflammation. esophagus and appendix. • Diarrhea 11 to 20 percent mucus in stool.6%) Possible Routes of Infection 1. colon (ascending) duodenum. Commonest 20 to 40 yrs • Female predominance has been described in Indian series. cecum. don’t penetrate muscularis propria. napkin ulcer. showing marked inflammatory and fibroblastic reaction in submucosa and mucosal surface to present as mass lesion. Clinical Features • Diseases can affect any age group. jejunum. nodules. blood and frank pus rarely observed. lymphatic obstruction or bacterial over growth. Gross Appearance Ulcerative type – Secondary to hematogenous spread. hyperplasia and stenosis. Hematogenous spread . Diffuse colitis endoscopically very similar to ulcerative colitis and can not be differentiated on the basis of mucosal appearance alone. • Fever in 40 to 70 percent.2%) • Perforation (16. edema. • Nausea and vomiting • Malena • Constipation • Menstrual abnormalities (in about 1/3 pts) • Intestinal obstruction (66. • Abdominal pain – most common symptom and present in almost every case. Direct invasion by suggested organism 2. Ulcerohypertrophic type – Combines the features of ulcers. pseudopolyp. Transverse. occur due to endarteritis. • Diarrhea alterating with constipation 8 to 20 percent • Weight loss • Anorexia • Malabsorption due to extensive ulceration. stomach. • Moving lump in abdomen.

Secondary Intestinal Tuberculosis Secondary infection of gut may arise from contamination of intestinal chyme by bacteria from another site. Increased physiologic stasis 3. the female adnexa. This mode is no more significant however isolated cases of primary tubercular enteritis. diverticula. Extension from diseased adjacent organ Direct Invasion by Suggested Organism Primary intestinal tuberculosis can result from food containing tubercule bacilli specially milk. which cause colonic traction. Abdominal distension due to ascites or intestinal obstruction. Intestinal involvement after ingestion of infected material is related to number and virulence of the suggested organism and the nutritional status of the patients. Site of involvement is influenced by – 1. After ingestion. tubercle bacilli pass through the stomach (where it is protected against digestion by its fatty capsules) into the small bowel. A palpable mass . Infected bile 4. through swallowing of infected sputum. entero-cutaneous are encountered due to penetrating abscesses. can also occur. Minimal digestive activity Hematogenous Spread Indirect evidence of this route of infection is obtained from clinical studies demonstrating early intestinal lesions in submcosa with normal overlying mucosa. More commonly caused by adjacent tubercular lymphadenitis. Fistulae like entero-enteric. narrowing. entero-vesicular. Intestinal narrowing occur due to extrinsic compression by lymph node. Abundance of Lymphoid tissue 2. usually the lungs. Bile Containing Tuberculous Bacilli Sequestration of the bacillus by the liver and excretion in the bile are a potential source and route of infection but this remain unproved. fixation and sinus tract formation. With widespread pasturization of milk disappearance of bovine tuberculosis is observed. Extension from Contiguous Organs Enteric tuberculosis may occur by direct extension from infected adjacent organ and tissue e.268 Seminar in Radiology 3.g. Physical Signs Ill and Malnourished patient appearance. Increased rate of electrolyte and water absorption 4.

Raised up cecum. Fleischener’s sign – Broad based triangular appearance of terminal ileum with base at the cecum – this is not seen in Crohn’s disease. LN enlargement and rolled up omentum. 11. 10. Stellate ulcer. narrowing of cecum “PURSE STRING SHAPE”. Thickening of mucosal fold with scalloping and spicule formation. Free intestinal perforation presents as peritonitis. 5. hypertrophic. • Ulcerative. inflamatory mass). obliteration of ileocecal angle. classical doughly abdomen are seen in 6 to 11 percent. 4. Steirlin’s sign – lack of barium retention in the inflamed segment of ileum. Dilatation and stasis proximal to stenotic segment. incompetent ileocecal valve. diffuse tubercular colitis. • Short segment of colon is envolved (5-7 cm). 9. 3. Differential Diagnosis • Ulcerative colitis • Crohn’s disease • Ameboma • Carcinoma • Actinomycosis • Vascular occlusive disease Tuberculosis of Colon and Rectum Hematochezia was common presentation. 8. . Abdominal Tuberculosis 269 due to hyperplastic cecal tuberculosis. In healed stage – shortening. DCBE study is helpful. 2. cecum or ascending colon. 7. Disturbance in motility with accelerated transit time. String sign – A persistent narrow stream of barium. COMPLICATION Intestinal obstruction Perforation/abscess Fistula formation GI bleeding Enterolithiasis Traction diverticula Small Intestines and Ileocecal Tuberculosis Barium Meal follow through Observations 1. Enterolith. 6. effacement of terminal ileum mucosal pattern are other signs. Filling defects in the cecum (due to thickening of ilio-cecal valve. shortening of ascending colon. hyper-segmentation and flocculation of barium suggestive of malabsorpthin pattern.

fever 1 percent incidence at autopsy. • Tubercular ulcer are commonly seen in the Pylorus. Primary esophageal TB by Torek (1931). Stomach Clinical feature : abdomen pain. lupoid. exophytic growth • Esophageal stricture (common in upper part) when in lower esophagus – it is malignant stricture and achalasia. (2) Rapid transit of ingested organism (3) Scarcity of lymph follicle in gastric wall (4) Intact gastric mucosa. Pseudotumor mass • Common presentation are dysphagia. • Ulceration. • Fistula. nodularity of mucosa. Post inflammatory polyps comprise of excessively regenerated mucosa • Luminal narrowing and stenosis • Hypertrophic mass causing filling defect.270 Seminar in Radiology • Multifocally scattered shallow ulcers (aphthous ulcers) • Transverse ulcer. hematemesis. thickening of wall. weight loss. epigastric mass. vomiting. • Hypertrophic exophytic growth 16 percent tubercular fistula in ano. • Direct spread from caseating tubercular lymphnode in the mediastinum involving esophagus. • Inguinal lymph node. trachea or bronchus. • Ulcers and fissures common. • Traction diverticulum • Fistula between esophagus and mediastinum. odynophagia. miliary lesion. verrucus. • Extrinsic compression by lymph node • Exophytic mass Incidence—1 percent at necropsy. nausea. as shallow extensive ulcers • Fibrosis—Linitis Plastica like pattern leading to gastric outlet obstruction. pain. upper GI bleed. Duodenum 2. Inflammatory polyps are caused by ulceration surrounding and undermining portion of intact mucosa. Esophagus 1st report by Denonvilliers (1837). GI bleed. . “Rose thorn” ulcers • Thickened folds • Inflammatory or post inflammatory polyps. Anal Canal These ulcers are shallow with bluish undermined edge. Rare—cause (1) acid. abscess formation.5 percent incidence. Clinical features—dyspepsia. aspiration due to fistula.

hyperperistalsis proximal to stricture. cecum or ileocecal region. Lymphnode Involvement • CT shows enlarged LN with hypodense centre and peripheral enhancing rim • Diffuse enlargement • Mesenteric. Pseudokidney or target sign. Ascites – free or loculated ascites. 2. multiple fine. • Skip area of concentric mural thickening may be seen elsewhere in the bowel. 7. Occasionally eccenteric involvement of the medial rectal wall.N. Usually concentric thickening. 11. Graded compression technique can be used to displace dilated and air filled bowel loops from the region of interest. hyperechoic centre (Caseation). • Low density areas representing necrosis in the wall. Circumferential thickening of bowel wall (> 3 mm). peripancreatic. para-aortic lymphnodes are involved • Congulomerate mixed density nodal mass • Enlarged nodes of homogeneous density associated with low density nodes at other sites. peripancreatie round or oval in shape with echogenic capsule. TRUS and TVS helps for rectovaginal and rectovesical fistulae demonstration. Enteroliths appear as echogenic foci. Sonography – 2nd Modality of imaging 1. Demostrates all features of tuberculosis as patients tend to be emaciated which provides a good acoustic window for a thorough examination. Lymphadenopathy–mesenteric. 3. • Hypertrophic mucosa resembling polyps • Distorption of the C-loop by lymphadenopathy • Healing → Contraction → Stenosis → Obstruction. CT Scan – Most modern imaging techonology: CECT • Mural thickening limited to the terminal ileum. 10. Abdominal Tuberculosis 271 • Ulceration and stricture in III part of duodenum with narrowing of lumen. portal. Areas of narrowing representing stricture. floating bowel loops. 6. Deep ulceration can be detected as radial extension of echogenic luminal contents into thickened wall. complete or incomplete and mobile strands of fibrin and debris are seen. area of calcification. . porta hepatis. 4. 8. thickened medial wall of cecum 5. Matted L. 9.

Hematogenous spread of bacilli from active pulmonary lesions 2.1 to 3. • On CT scan low attenuating adenopathy with rim enhancement. Three Types of Tubercular Peritonitis a. 1st documented case was described in 1843 at autopsy of 43 old seaman (Dineen 1976). • Focal ascites—interloop fluid collection that appear on sonogram as “club sand witch” appearance resulting from alternate hyperechoic and hypoechoic layers of the serosa and bowel wall of two adjacent loops with intervening anechoic fluid. PERITONEAL TUBERCULOSIS Peritoneum is a common site of involvement in the abdominal tuberculosis. Tubercular peritonitis is a frequent cause of ascitis in underdeveloped countries. • Omental or ileocecal mass • Enteritis involving ileocecal region. Others – contiguous spread from lesions in intestine or fallopian tubes. echopoor peritoneal thickening of 2 to 6 mm or irregular thickening with tiny nodule of < 5 mm size. c. Clinical Features • Abdominal distension by ascites • Anorexia. USG Findings • Free or loculated ascites. • LN calcification. Activation of a long latent foci of tuberculous infection of the peritoneum. Free ascitic fluid is commonly seen. • Peritoneal thickening appears as a irregular sheet like hypoechoic layers. diffuse regular. Pathogenesis—Two accepted mechanisms: 1. b.N. Plastic type—enlarged mesenteric L. showed peritoneal thickening in 14 to 100 percent of cases. It may be anechoic or contain debris. May show tiny nodule.5 percent. Fibrotic—thickened omentam with a mass. Wet ascitic type—ascites with pockets of loculated fluid with a thickened mesentry. Incidence 0. with central caseational necrosis and adhesion of bowel loops. Lacy strands or fine septa and low level echoes are characteristic of exudative ascites. Chest skiagram – 50 percent had pulmonary tuberculosis and 1/6 will have active disease. (> 3 in once cut section) of normal size or mildly enlarged mesenteric nodes usually located along the mesenteric vessel.272 Seminar in Radiology • Increased no. . When involved.

B. Granulomatous disease (tuberculous hepatitis)—unexplained fever. hepatomegaly ±. With bile duct involvement causing obstructive jaundice either by enlarged L. mild jaundice. which is due to high protein and cellular content in tubercular exudates. caseating granuloma showing improvement with A.T. 3. • Peritoneal enhancement with uniform thickening of peritoneum • Nodular implants with irregular thickening are extremely uncommon and should suggest peritoneal carcinomatosis. or inflammatory stricture. right lumbar region and right lower quadrant. Localized hepatic tuberculosis— a. Sex ratio – 2:1 M:F Age – 11 to 50 years Clinical Features Abdominal pain (45-66%) Fever (63-90%) Weight loss (55-75%) . • Mesentery may show increased density with soft tissue strands. CT Scan • High density ascites (24-45 HV) is characteristic of T. Without bile duct involvement to include solitary or multiple nodules. • Increased echogenecity of the mesentery (lymphatic obstruction) and fat deposition. Hepatic tuberculosis have been classified into three: 1. In extensive involvement. tuberculoma or hepatic abscess b. there is diffuse infiltration of mesentery by soft tissue density masses with mesenteric abscesses. Hepatobiliary Tuberculosis Military tuberculosis of liver is most common and is said to occur in 50 to 80 percent of all patients dying of pulmonary tuberculosis (Morris 1930). thickened and crowded vascular bundles or “stellate sign”. • Involvement of omentum—‘omental cake’. • Mesenteric lymphadenopathy • Omental thickening with hypoechoic nodules – “Omental cake” appearance. Abdominal Tuberculosis 273 • Mesenteric thickening (13-47 mm) can be seen in left upper quadrant. Miliary form 2.N. paraumbilical region. nodularity or ‘smudged appearance’.T. Hepatic TB with large abscess and nodules or tuberculoma have been reported by leader (1952).

multiple abscess seen in HIV patients. FNAC differentiates Ca. .274 Seminar in Radiology Jaundice (11-35%) Hepatomegaly (80-96%) Splenomegaly (25-57%) Liver calcification ( -50%) LFT – alk phos raised but not diagnostic. Micronodular-diffuse hyperechogenicity  causing bright liver. Pancreatic Tuberculosis Rare. Sonographically liver is either Macronodular . lymphoma. Splenic Tuberculosis Present either as hypersplenism or abscess or rarely as solitary tumor (Sheen – chen 1995) fever. weight loss. sarcoidosis or chronic pancreatitis.single / multiple nodule which  may be hypoechoic or hyperechoic with or without calcification. It may present as either acute or chronic pancreatitis or may nimic malignancy. homogenous splenic enlargement or macronodular splenic enlargement. The patient may present either as miliary tuberculosis. Clinical Features Anorexia Malaise Low grade fever Weight loss Night sweat Malena Mass/abscess Obstructive jaundice Head of pancreas-most commonly involved. LUQ pain. diarrhea.uncommon Single hypoechoic well defined mass Peripancreatic lymphnode enlargement Rarely calcification seen. occurs more often in immunocompromised patient (Brusko 1995) result of lympho-hematogenous dissemination or direct spread from other adjacent organ. Body and tail .

T. Abdominal Tuberculosis 275 Small Bowel Mesentery Micro (< 5 mm) Mesenteric changes . Plain X-Ray Abdomen Calcified L. liver. 2. TRIAD .N. cystic lymphonode or abscess. Detection of DNA of M. Calcified granuloma in spleen. Fixed loops of bowel mesentery standing out as spoke radiating out from the mesenteric root – “stellate sign” echogenic thickened mesentery (>15 mm) with mesenteric L. Chest X-Ray • Active pulmonary TB • Pleural effusion • Healed/calcified pulm TB. Isolation/detection of M. dilated terminal ileum. Ascites Absence of gas shadow in right iliac fossa. DIAGNOSIS OF ABDOMINAL TUBERCULOSIS Diagnosis is based on one of the following criteria: 1.Nodular lesions  Macro (> 5 mm) Mesenteric thickening Loss of normal mesenteric configuration ↓ They are solid. Mesenteric thickness in healthy person ranging from 5 to 14 mm. Segmental dilatation of terminal ileum. 4. . pneumoperitoneum. pancreas and dilated loops with fluid level.T. tuberculosis from diseased tissue or exudates and secretion of diseases tissue. Non caseating granuloma are characteristic radiological features or characteristic laboratory finding or serologic positively with clinical response to A.N. Presence of caseating granuloma/non-caseating granuloma with Langerhan’s giant cell in diseased tissue. tuberculosis from diseased tissue or exudates and secretion of diseased tissue. Barium Studies – Discussed earlier in detail. 3. ascites.

Deformed ileocecal valve with dilatation of terminal ileum b. Contracted Cecum b. dilatation and muscosal thickening of small bowel loops Gr IV Normal study Double Contrast Barium Enema Tuberculous colitis Involvement was asymmetric Lesion is common in Ascending colon Terminal colon Transverse colon Descending colon Sigmoid colon Skipped lesion Transverse Multiple ulcer Circumferential Depth of ulcer (< 2 mm) deep Fistula Polyp Mass (mis diagnosed as malignancy) Thickening Deformity Incompetency of IC valve Angiographic Appearance Hyperemic L. Multiple areas of dilatation. Ulcerations or narrowing of terminal ileum c. Stricture of ascending colon with shortening and involvement of ileocecal region Gr II Suggestive of intestinal tuberculosis if one of the following features is present – a. Strictures of ascending colon d. Contracted cecum. adjacent to localized transmural inflammatory disease of cecum (Not seen in Crotn’s) Hypertrophic TB – Pooling of contrast media and and tumor like capillary blush Malignancy Colonoscopic Findings in Ileocecal TB • Hypertrophied—thickening and hypertrophy of mucosa • Ulcerative hypertrophic—ulcer with hypertrophy of mucosa • Ulcerative—single of multiple ulcers of variable size and shape • Ulcer constrictive—narrow segment of intestine with ulcer.N.276 Seminar in Radiology Ba meal Follow Through Finding in Intestinal TB Gr I Highly suggestive of intestinal tuberculosis if one or more of the following features are present – a. abnormal ileocecal valve and/or terminal ileum c. . narrowing and matting of small bowel loops Gr III Nonspecific changes Features of matting.

In practise. but colonoscopic surveys suggest no more than 40 percent. 2. • True prevalence of colorectal polyps in the general population is unknown. myxofibroma and pedunculated fibroma . fibrolipoma. autopsy studies suggest an overall polyp prevalence of 50 percent. vertical height about 50 to 80 percent of their transverse diameter. Sessile • Intraluminal tumors that project within the lumen when viewed in profile but do not demonstrate a stalk. Fibrovascular polyp— • Also called as fibroma. Barium studies 2. • Broad base.19 Intestinal Polyposis • Word “polyp” derived from Greek work “polypus” meaning “many footed”. • In United States. polyp is used to define a discrete mass of tissue that protrudes into the lumen of the bowel. Pedunculated • Presents as filling defect completely surrounded by contrast medium with the exception of its attachment to the bowel wall by a stalk (which is often invisible) • Move up and down the lumen for a distance approximately double the length of pedicle. • Polypoid lesions are most common in colorectal region. Endoscopy Biopsy or polypectomy and histopathologic analysis definitive diagnostic test. DIAGNOSIS 1. because large population studies using complete colonoscopy have not been conducted. ESOPHAGEAL POLYPS Can be 1. Barium Studies Polyp can be 1.

pyloric canal obstruction • Composed of overgrowth of superficial gastric epithelium. Diminishes in size and disappear during effective therapy for esophagitis. substernal discomfort • Barium swallow – large intraluminal filling defects. adipose cells and stroma that arise in the mucosa or submucosa and are covered by the epidermoid epithelium • Symptoms – Dysphagia.  DX - – Prolapsed gastric fold – Submucosal neoplasms – Retention cyst – Small carcinoma POLYPS OF THE STOMACH • Epithelial polyps account for 5 to 10 percent of gastric tumors • Typically seen on Barium meal examination as – well circumscribed filling defects that interrupt normal mucosal pattern and occasionally displace gastric folds • Can have superficial ulcerations. average diameter – 5 to 10 mm. • Radiographic examination (1) smoothly marginated circular or pedunculated lesions. sausage like masses with smooth or lobulated surface. of same size. Rounded sessile polyps. superficial erosions at tip may be present. with cystic dilation of elongated mucosal folbs. 2. Associated findings of esophagitis – reduction in esophageal distensibility and contour irregularity and erosion. Pedunculation is common. Hyperplastic (regenerative) polyp- • 75 percent of gastric polyps • Symptoms—bleeding. 1. 4. • Radiographic examination: 1. usually 0. • Common in fundus and body.5 to 2 cm in diameter. 3. fibrous polyps and eosinophilic granuloma • Response to reflux esophagitis • Sessile lesions consists of inflamed granulation and fibrous tissue. Inflammatory cells present • Multiple in 20 to 25 percent cases. 2. . located near esophagogastric junction and often on top of thickened gastric fold. Inflammatory polyp— • Also called as inflammatory pseudopolyps. prolapse. Oval shaped or elongated. Hiatus hernia and gastroesophageal reflux commonly present.278 Seminar in Radiology • Consists of varying amounts of fibrovascular tissue.

Multiple polypi. Heterotopic polyps a. Adenomatous polyp • True neoplasms that are composed of dysplastic glands and capable of continued growth • Definite tendency towards malignant transformation. Gastric polyps – 25 to 50 percent patients. b. occur mostly in antrum. • Fundic gastric polyp — composed of normal appearing fundic glands with increased number of parietal and chief cells. but in a disorganized and proliferative pattern • Usually occur in hereditary syndromes such as Peutz Jeghers syndrome. have malignant potential. producing papillary or villous appearance – Usually single. 5. Hamartomatous polyps • Contain histologic elements present in gastric wall. 3. Umbilication site of excretory duct. large (greater than 2 cm) with irregular surface. common in gastric antrum – Often ulcerate. – Minimal involvement with few small polyps. . Retention polyps • Rare gastric lesions composed of dilated cystic glands and stromal tissue • Middle aged individuals with Cronkhite Canada syndrome • Present as one of 3 appearances :- – Innumerable small polyps extending over a portion as all of gastric mucosa. – Scattered polyps of varying size with thick folds. Contrast material enters deep fissures and furrows in polyp. larger than adenomatous polyps. Intestinal Polyposis 279 2. 5 mm in diameter. Adenomyomas – Made of ducts epithelialized by columnar cells and arranged in haphazard pattern. 4. juvenile polyposis and fundic gland polyp • In Peutz Jeghers syndrome. lobulated surface • Gastric polyps occur in juvenile GI polyposis and such polyposis are limited to stomach — occur in children. predominantly seen in fundus and body of stomach typically multiple. can be single as multiple. with or without fold thickening. • Radiographic examination : – Usually sessile. Heterotopic pancreatic rests – 4 percent of polyoid lesions of stomach – Favoured site-prepyloric region – Barium examination – submucosal lesion elevating overlying mucosal surface and containing central barium collection. Glands are dilated referred as glandular cysts Seen as sessile masses.

intramural mass – Common. Stalk sign: The head of a polyp is mobile and hidden behind the barium pool. 2. neurofibroma. COLORECTAL POLYPS Can be divided into two major groups. – Primarily in duodenum. neurogenic tumors. Increased density sign: Polyp seen as area of increased density because X-ray beam has to pass through outer layers of barium and also depth of air passed by beam is reduced. Non-epithelial tumors as leiomyoma. 6. it is viewed and its relationship to the barium pool. Neoplastic polyps-Adenomatous and malignant polyps. which diverge slightly as the stalk flattens out to merge with the mucosa. Creating a ring shadow enface. carcinoid tumors may also present as filling defects. A. hemangioma. d. Clinical Features • Bleeding anemia • Intussusception • Obstruction – if large Detection Barium enema Colonoscopy Radiologiccal Features Depends on the angle of which. Polypoid lesions of epithelial origin 1. Polypoid lesion of subepithelial origin: lipoma. clearly defined inner border.280 Seminar in Radiology – Less than 2 cm in diameter – Smooth. outer margin fading into the normal mucosal coating. Inflammatory polyp c. Hamartomatous polyp – Cystic (Juvenile polyp) – Cellular (Peutz Jeghers polyp) B. Meniscus sign: meniscus forms around base of a polyp. rare in prepyloric region of stomach. b. Stalk is outlined by two parallel lines of barium. . leiomyoma. Hat sign: When viewed obliquely. Hyperplastic polyp b. oval meniscus around the base and thin line of barium over the surface of a polyp produce hat sign. lymphoma. sharply demarcated. c. Non neoplastic polyps- a. a.prepyloric area • Brunners gland hyperplasia – Polypoid lesions composed of tightly organized but normal Brunner’s gland. sarcoma.

Tubular—can be sessile/pedunculated. 2. 14 percent— transverse colon. Tend to be sessile. however probability of malignancy can be made on radiologic findings. 18 percent descending colon. • Adenomas in left colon – larger. square. 4. • 20 to 40 percent of polyps greater than 2 cm are cancerous. trapezoid.5 cm in diameter rarely malignant • Above 1 cm—incidence of malignancy rises. Growth rate Any increase in size of colonic polyp – indication for removal. 2. predilection for rectum and cecum. Pedunculation • Polyp with well defined pedicle – substantially lower incidence of malignancy than sessile lesion of comparable diameter. Assessment of polyp – Six S’s 1. Symmetry of base—indrawn/smooth/irregular 5. Singularity or otherwise. Adenomatous Polyps • Most common neoplasms of colon • Sharply circumscribed area of dysplastic epithelium • Most—polypoid. Size 3. . 1. Villous—10 percent of adenomatous polyp. Surface Contour • Triangular. • Malignant potentiality observed. polyhedral or bizarre configuration increase the probability of malignancy. Bull’s eye/Target sign: Created when head and stalk are superimposed. 8 percent ascending colon and cecum. Site 2. Intestinal Polyposis 281 e. • Discrete surface ulceration – highly suggestive of carcinoma. 3. Size • Less than 0. Shape-seesile/stalk 4. also flat lesions • 60 percent—Rectosigmoid. inner ring due to stalk and outer to the head of polyp. • If indentation of ployp base seen in tangential view – suggest malignancy due to infiltration and invasion of mucosa adjacent to the lesion. Potential for Malignancy Accurate diagnosis by histopathology. Surface texture—smooth/lobulated/nodular 6. Incidence of malignancy— < 1 percent for adenomas < 1 cm in size > 20 percent for adenomas > 2cm in size • Can be classfied as: 1.

5 to 6 cm in diameter. ied with ischemic colitis. Mixed. Classic FAP/Familial multiple polyposis b. 1. 2. Gardner’s syndrome . often pedunculated. lymphoma may bulge into tumor being seen as polyp covered by intact mucosa. common- rectum or sigmoid Inflammatory polyps – Pseudopolyps • Term used for reparative mucosal protrusions that develop after severe mucosal damage and ulceration. may occur in any part of colon • Usually smaller than 5 mm • Particularly. When multiple – seldom more than 2 or 3 in number. • Mostly rectosigmoid region. A colon carcinoma is present in patient less than 40 years old. Non Epithelial Tumors Lipomas. small and lack distinctive heads. some have slender. but also seen in Crohn’s disease. Hyperplastic Polyps • Also called as metaplastic polyps • Present as minute smooth surfaced elevations with sessile configuration. Can be: 1. • Solitary – 75 percent of cases. 3. arborescent configuration called as filiform polyps. Hereditary polyposis syndromes Familial adenomatous polyposis syndromes: a. Juvenile Polyps • Occur as isolated lesions in children < 10 years. • Most often accompanied ulcerative colitis. GI polyp is identified in a young patient. Multiple polyps are demonstrated in any patient. amebiasis. common after 40 years • Biopsy and histology confirmation – Diagnosis.282 Seminar in Radiology For a given size. 3. bacterial colitis. chronic schistosomiasis and diverticular disease • Can be focally/diffusely distributed • Often multiple. • Barium examination – round filling defects. POLYPOSIS SYNDROMES Considered when – 1. leiomyomas. hemangioma. villous tumor has a likelihood harboring carcinoma 10 times as great as that of tubular adenomas. Some may be giant.

2. 3. vague abdominal pain. rarely before 20 years. Some have pedicles • Carcinoma – polypoid filling defects. Cronkhite Canada syndrome b. • Diagnosis-by colonoscopy. 5. Usually between 20 to 40 years.weight loss. 4. Peutz Jeghers syndrome b. osteoma. Clinical feature–usually 3rd or 4th decade of life. Non familial polyposis syndromes a. Basal cell nevus syndrome e. diarrhea-bloody stool. Also presence of gastric and small bowel polyps. 100 percent of untreated patients. Turcot’s syndrome d. Cowden’s syndrome d. Affected patients are identified at young and prophylactic total colectomy with ileorectal anastomosis should be performed. a. Gardner’s Syndrome • A syndrome featuring an autosomal dominant inheritance. • Polyps – multiple punctate eminences that impart a serrated to saw tooth contour to the intraluminal column of barium or as larger filling defects 1 to 2 cm in diameter. Rectal polyps – requires cautery. Ravalcaba myhre smith syndrome 2. may be sessile or pedunculated. villous adenomas or inflammatory polyps present. polyposis coli and a potential for colon malignancy. Colon cancers arise about 50 years of polyposis. Occassionally. Inflammatory polyposis (Pseudo polyps) c. Muir-Torre syndrome Familial hamartomatous polyposis syndromes. Lymphoid polyposis Benign lymphoid polyposis Malignant Lymphoma Familial Multiple Polyposis 1. Intestinal Polyposis 283 c. multiple carcinoma – common • Family screening should be done. 6. . Rectum and left side of colon more involved than right side of colon. prolapse of polyp through rectum. polyposis coli and eventual development of a colon carcinoma. multiple soft tissue tumors. Juvenile polyposis c. areas of segmental narrowing. Radiographic examination: To document size. number and distribution of polyps and to search for carcinoma. or typical annular lesions with overhanging margins. Colonic polyps are numerous – pinhead to 1 cm or more in size. Characterised by hereditary transmission. Histologically – adenomatous polyp.

• 12 percent have lung or laryngeal cancer. hypertrophied scars. unerrupted supernumerary teeth. tendency towards numerous caries. Long bone especially. usually endometrial. Muir – Torre Syndrome • Characterized by multiple sebaceous neoplasm of skin. Osteomas – appearing as exostoses or enostoses. mammary fibromatosis. . Malignant sarcomas are uncommon. lipofibromas. Polyps • Limited to colon. mandible and skull. 90 percent have GI visceral malignancy 80 percent—Colon Carcinoma 5 percent—Gastric Carcinoma 8 percent—Duodenal Carcinoma • 50 percent patients have urogenital malignancy. leiomyomas and neurofibromas. hypercementosis. keloids. 2. with multiple visceral neoplasms • Present in 5th to 6th decade. Bony Lesions 1. strong family history • 40 percent patients have being intestinal polyps. bladder or renal carcinoma.284 Seminar in Radiology Soft Tissue Tumors 1. Cutaneous lesions consists of sebaceous or inclusion cysts over scalp and back. Benign mesenchymal tumors as fibromas. Dental abnormalities – odontomes. also on face or extremities. peritoneal adhesions. femur and tibia – localized cortical thickening. • Neural tumors gliomas and medulloblastoma • Polyps larger and fewer than typical FAP. Turcot’s Syndrome (Glioma – Polyposis) • Syndrome of familial colonic polyposis with primary tumors of Nervous system. increase during 3rd and 4th decades – carpeting of colon • 100 percent develop colon carcinoma. present in maxilla. lipomas. mesenteric fibrosis and retroperitoneal fibrosis. Extracolonic – 5 percent or less of patients • Lymphoid hyperplasia of terminal ileum – cobblestone appearance that simulates multiple adenomas • Appear in teen age group of patient. long bones may be shortened or bowed. 3. 3. 2. Fibrous tissue has tendency towards proliferation – desmoid tumors.

• Small bowel – 95 percent patients show colon and rectum involvement – 30 percent patients. oval or slightly irregular macules. Persistent obstruction b. thyroid cancer and hamartomatous polyps of stomach. Cowden’s Syndrome (Multiple hamartoma syndrome) • Consists of multiple cutaneous hamartomas. stomach 25 percent involvement. Sessile lesions > 1. 1 to 5 mm in diameter.1 to 3 cm. • Autosomal dominant mode of inheritance • GI symptoms and colorectal cancer-uncommon. intussusception and obstruction • May coexist with adenomatous polyps in some patients with familial multiple polyposis or Gardner’s syndrome • Risk of colon cancer increased in patients with familial juvenile polyposis • Juvenile polyp has a smooth.5 cm. hamartomatous without malignant potential • Incidence of cancer – 2 to 3 percent Occur in stomach. less common – face or volar aspect of hands and feet • Polyps – predominantly GI. lobulated appearance. nontoxic goiter. Surgery a. Generalized juvenile polyposis (Involving entire GI tract) • Present in childhood with GI bleeding. lesions showing rapid growth. round confirm as opposed to adenomatous polyps that has fissured. Familial juvenile polyposis of stomach 3. – Common site – lips and buccal mucosa. and annular lesions – suspicious for carcinoma. Intestinal Polyposis 285 Peutz Jeghers Syndrome • Autosomal dominant mode of inheritance • Characterized by mucocutaneous pigmentation and GI polyposis • Mucocutaneous lesions – – Present in all patients – Develop in infancy or early childhood – Brown or black. duodenum and colon. Severe bleeding c. fibrocystic disease and cancer of breast. Suspected malignancy. • Polyps – multiple. Rare – jejunum and ileum. but also in urinary or respiratory tract. Familial juvenile polyposis coli (limited to colon) 2. Juvenile Polyposis • Three varieties have been recorded – 1. • Managed by conservative treatment. . small intestine and colon. size – 0.

accompanied by thickened mucosal folds and increased intraluminal fluid. small bowel and colon • No evidence of malignant potential. • Genital skin lesions – hyperpigmented muscles present on glans and shaft of penis. Basal Cell Nevus Syndrome • Associated with multiple gastric hamartomatous polyps • Multiple odontogenic keratocysts – in maxilla and mandible • Multiple basal cell carcinoma • Present during 2nd decade of life • Bifid ribs are common. • Intestinal lesions – harartomatous polyps involving gastric antrum. dystrophic changes in the fingernails. weight loss. pigmented genital lesions in males. Lymphoma : • May presents as multiple gastrointestinal polyps • Require adequate biopsy to distinguish them from true epithelial polyps. lipid storage myopathy and subcutaneous lipomas may be noticed. cutaneous hyperpigmentation.286 Seminar in Radiology Ruvalcaba Myhre Smith Syndrome – Sotos Syndrome • Consist of macrocephaly. More than 50 percent patients have small bowel polyps. Cronkhite Canada Syndrome • Characterized by presence of diffuse gastrointestinal polyposis. duodenum. alopecia. diarrhea. Absent on scrotum or genitalia of females. abdominal pain and complications of malnutrition • Develops during middle or old age (42 to 75 years) • Radiographic examination – multiple gastric and colonic polyps. and intestinal polyposis with mental retardation. .

SECTION 6 Genitourinary System .

.

Pre-renal causes. Renal causes. Clinical Signs and Symptoms Depends Upon a.20 Uremia and Imaging Definition: Uremia is a Complex of symptoms resulting from failing renal function. 2. Progress of disease Serum creatinine determines the progress of disease Patient may present either in state of Uremic emergency Or Chronic renal disease Uremic Emergency Causes 1. Pre-Renal Causes • Absolute decrease of blood volume due to: – Gastrointestinal bleeding – Trauma – Dehydration • Decreased effective circulating volume due to: – Congestive heart failure – Hemolytic uremic syndrome – Shock • Renal vascular state – Artery-stenosis/obstruction – Vein-occlusion Renal Causes • Functional changes – Non-steroidal anti-inflammatory drugs – Angiotension converting enzyme inhibitors . Etiology of the specific renal disease b. caused by the retention of constituents of normal urine. 3. Post-renal causes.

. neuropathy) • Inflammatory stricture • Mass originating in genital organs Contd..290 Seminar in Radiology • Renal diseases • Interstitial nephritis • Hereditary disease – Autosomal dominant polycystic kidney disease – Alports diseases • Systemic diseases with renal involvement – Diabetes mellitus – Hypertension – SLE. PUJ Obstruction • Intrinsic stenosis • Segmental dysfunction/adynamic segment • Valve • Kink (or) angulation • Adhesion (or) band • Lower pole artery • High insertion 2. Ureteric Obstruction • Primary megaureter (juxtavesical) • Ureterocele (ectopic/orthotopic) • Ureteric valve • Distal ureteric stenosis • Ureteric atresia • Circumcaval ureter with variants • Bladder diverticulum 3. mostly congenital • In adults. mostly acquired In Children 1. atresia • Fecal impaction (habitual constipation.. anterior • Presacral mass dissecting inferiorly sacular. Urethral Obstruction Intrinsic lesion Extrinsic lesion • Valve (posterior. systemic sclerosis • Vasculitis • Microangiopathy – Hemolytic uremic syndrome – Infection – Drug – Postpartum – Accelerated hypertension Post Renal Causes • In children. diverticulum • Stenosis.

fungus ball) Ureteric Obstruction Intraluminal Extraluminal • Stone • Large pelvic tumors • Blood clot • Retroperitoneal tumors • Neoplasm • Stricture • Sloughed papilla • Retroperitoneal fibrosis. blood clot. squamous cell cacinoma • Benign (Polyp. periureteric fibrovenous entrapment (ovarian vein syndrome) Gynecological conditions: • Endometriosis • Prolapse uterus • Hydrohematocolpos • Carcinoma cervix Gastrointestinal conditions: • Crohn’s disease • Diverticulitis • Appendicitis • Pancreatitis INVESTIGATIONS FOR VISUALIZATION OF KIDNEYS TO RECOGNISE THE ABNORMALITIES OF ANATOMY AND PHYSIOLOGY It is essential to understand the physiological and functional basis of the investigation. hydrocolpos.. Uremia and Imaging 291 Contd. infection and inflammation. vasculitis • Fungus ball • Pelvic fibrosis secondary to: Pregnancy related problems: Hydronephrosis of pregnancy. mesodermal tumors) • Other intraluminal lesion (stone. Intrinsic lesion Extrinsic lesion • Traumatic stricture • Male : Prostate • Urethral tumors Rhabdomyosarcoma Female : Hydrometrocolpos. fused labia Adults PUJ Region : • Scarring (inflammation. and to appreciated the limitations and possible sources of error in each technique.. ovarian vein thrombophlebitis. meticulous technique. surgery. trauma) • Reflux • Malignant tumour (Primary – Transitional cell secondary – metastatic) carcinoma. papilla. .

Do not give further contrast media for 48 hrs. 1. Contrast study Contrast media: Ionic/ Non-ionic both contrast media can be used. 10 CC of diatrizoate • Older children 2 to 3 CC/Pound. 5.292 Seminar in Radiology Imaging Techniques Conventional Uro-radiology A. Risk factors: Risk factors for contrast medium nephrotoxicity Major • Impaired renal function especially secondary to diabetic nephropathy • Dehydration • High osmolality of contrast media • Large doses of contrast Other Factors • Concurrent nephrotoxic drugs • Congestive heart failure • Age over 70 • Hypertension • Multiple myeloma GUIDELINES Guidelines for avoiding contrast medium nephrotoxicity in patients with impaired renal function. Discontinue nephrotoxic drugs. body weight • Adults: 300 mg/kg of iodine body weight but up to a maximum of 150 CC only Note: Contrast medium nephrotoxicity defined as rise in serum creatinine by more than 25 percent (or) 44 μmol/liter occurring 3 days following I/V contrast: for which there is no other explanation. ureters and urinary bladder region. . Ensure well hydration of the patient. Dose • Infants under six months. Plain skiagram of abdomen for kidneys. 3. b. Keep the contrast media to the minimum dose necessary to achieve the diagnosis. Use of low osmolality contrast media. 4. 2. Intravenous Urography: a.

Uremia and Imaging 293

B. High Dose IV Urography:
High dose IV Urography was formerly the main stay for imaging the kidneys
in patients with impaired renal function.
• Used to obtain renal size and the presence or absence of renal obstruction
• Use is now limited to patients with mild renal impairment (Sr. Cr. < 250
μmol) in whom renal USG has excluded obstruction
• Dose of contrast medium increased to 600 mg iodine/kg, double that
used in standard urography. (because unfavorable effect on the urogram
of the decreased GFR and impaired renal concentration can be
counteracted by increasing the dose of the contrast media).

Findings in Chronic Renal Failure
• In many patients, findings are non-specific
• In chronic glomerulonephritis
i. Renal length is reduced
ii. The parenchyma is diffusely thinned
iii. Pelvicalyceal anatomy is normal
• Features indicating
iv. Reflux nephropathy
v. Multiple renal infarcts
vi. Papillary necrosis

Nephrogram Patterns in Acute Renal Failure
High dose urography is no longer performed as a diagnostic test in acute renal
failure. However when a patient with impaired renal function has been given
the contrast medium, and an abnormal persistent nephrogram, seen on IVU
films (or) CTU, suggests different pathologies:
1. Acute tubular necrosis : Immediate homogenous nephrogram, persists
unchanged for 24 hr (or) longer.
2. Acute obstruction (including intratubular block) : Acute ischemia, acute
Oliguric glomerulonephritis. Immediate nephrogram becoming increasingly
dense with time.
3. Acute pyelonephritis: Acute renal vein thrombosis, multiple renal infarcts.
Striated nephrogram which may persist.
4. Contrast medium nephropathy : Persistent homogenous nephrogram 24 hr.
after I/V contrast medium.
C. Retrograde pyelogrpahy
D. Anteropyelography (or) Antegrade pyelograph
E. Retrograde urethrogram
F. Suprapubic cystogram

294 Seminar in Radiology

X-ray Exposures
• Total dose delivered during an average IVU is 10-15 mGy.
• Moreover X-ray doses are cumulative, so repeated examinations are more
dangerous when started in infants and children.

Ultrasonography and Colour Doppler Study
Technique requires knowledge of surface anatomy of the organs.
Normal sonographic anatomy: In Sagittal plane
• Size measures between 10 to 12 cm in long axis
• Renal capsule thin brightly reflective structure from the surrounding perirenal
fat.
• Renal cortex : midlevel gray echoes
• Renal pyramids : less echoic/darker
• Differentiation of cortex from medulla decreases with age
• Renal sinus : Contains collecting system, variable amount of fat. Is highly
reflective with slight distal acoustic shadowing.
• Renal pelvis: Seen as echo-free structure passing medially and interiorly
from the kidney.
• Ureteric orifices: Identified as and discrete elevations at the base of bladder.
• Ureteric jets: Visualized emanating from the ureteric orifices on both USG
and colour flow indices. Represents bursts of urine entering the bladder.
Note: Normal anatomy of neonate kidney : has certain important differences
from that of adult.
• Relative size is greater
• Size of medullary pyramids is also relatively more
• Increased differentiation between cortex and medulla
• Size and reflectivity of renal sinus are decreased due to paucity of sinus
fat.

Characteristic of Normal Doppler Sonogram
Kidney is an extremely vascular organ receives > 20 percent of cardiac output.
Normal: Ski, slope pattern
High velocity in systole with gradual decrease of low velocity
in early diastole and flows continuously throughout the
diastole.
Parameters: Pulsatality Index : 0.8 to 1.4
Resistivity Index : 0.56 to 0.7
On Colour flow Doppler: Vascular supply of the kidney can be identified
Colour Popwer Doppler: Parenchymal perfusion can be demonstrated as blush.
USG Contrast Agents: Recent introduction of USG contrast media usually in
the form of microspheres that traverse the pulmonary bed, for the assessment
of renal perfusions: adding functional information in additional to the anatomical
information.

Uremia and Imaging 295

CT Scan
Offers the Advantage of
• Less operator dependency
• Better resolution
• Higher specificity

Disadvantages
• More expensive
• Use of I/V contrast media
• Utilizes ionizing radiation

Applications of CT Scan
• Evaluation of renal tumors
• Retroperitoneal pathology affecting upper tract
• Lower tract tumor staging especially prostatic and testicular tumor
MRI: Has as yet less to offer than CT in the imaging of upper urinary tract.

Angiography
• Flush aortography
• Selective renal angiography
• Digital Substraction Angiography (DSA)
• Applications
– Evaluations of arterio-venous malformations
– Renovascular hypertension
– Transplant donor

Radionuclide Imaging
Radioactivity labeled compounds are used, they provide information about the
renal function.
• Used to measure glomerular filtration rate (GFR)
• Provide an index of renal plasma flow (RPF)

ROLE IN RENAL FAILURE
Acute renal failure (ARF): Radionuclide study provides information about the
first pass renal perfusion.
• Handling of glomerular filtrate
• If there is sufficient urine flow into the collecting system
• Frequency with which kidneys are visualized by this when IVU fails is
variable, but this is quite high
• Also provides prognostic information.

296 Seminar in Radiology

In Chronic Renal Function (CRF)
• USG remains the initial investigation of choice in CRF and may reveal the
etiology
• Irregular scarred kidneys – pyelonephritis/reflux disease
• Enlarged kidneys of polycystic kidney disease
• Small uniformly contracted kidneys of chronic glomerulonephritis
• Dilated ureters, collecting system, enlarged kidneys of chronic obstruction.
Although radionuclide investigations certainly shows the chronically damaged
kidneys in this situation and to very limited extent, predicts the degree of
recoverable function, it is only occasionally of any clinical value, and then it is
best performed by (99ICM) DMSA.

IMAGING OF KIDNEYS IN RENAL FAILURE
Has two principle aims:
1. Demonstrate or exclude obstruction
2. Estimate the renal size/parenchyma.

Demonstrate or Exclude Obstruction
Why? Because it is one of the few causes of potentially reversible renal damage.
Definition: Obstruction is increased resistance to urine flow. (Pressure in
collecting system = Flow × Resistance)
Therefore to maintain flow against resistance (obstruction the pressure in
collecting system will rise.)
• Obstruction could be
– Anatomical
– Functional

Hydronephrosis
Dilatation of collecting system with (or) without obstruction.

Grading in Hydronephrosis
Grade I: Minimal dilation appreciable, slight blunting of caliceal fornices.
Grade II: Obvious blunting of calyceal fornices and enlargement of calices
(flattening).
Grade III: Rounding of calices with obliteration of papilla
Grade IV: Extreme calyceal ballooning.
Renal parenchymal thinning/atrophy is seen with grade 3 and 4, but there
is no fixed relationship between the degrees of dilatation and parenchymal
atrophy

Uremia and Imaging 297

Pathophysiology
• Normal urine is propelled in forward fashion from renal pelvis to bladder
by ureteric contractions called as peristalsis producing localized high
pressure areas.
• Normal renal pelvic pressure < 12 mm Hg, which remain low despite the
transient peristalsis.
• In obstruction/vesicoureteric reflux.

The renal pelvic pressure rises

Consequently kidney damage occurs

Morphological changes Functional/physiological
of which are described alterations are described
by ‘obstructive uropathy’ by ‘obstructive nephropathy’
• Effects of urinary obstruction or overall renal function are influenced by:
– Whether the obstruction is unilateral (or) bilateral
– Acute (or) chronic
– Partial (or) complete
– Intermittent (or) constant
– Pre-existing renal disease (or) coexisting infection

Diagnosis by Imaging Techniques
Excretory urography (IVU): Findings
1. Increasingly dense ‘obstructive’ nephrogram
• Due to high concentrations of radiopaque contrast material in the tubules.
• Obstructive nephrogram often displays fine, white lines arranged radially
in the parenchyma extending to the renal margin.
• An obstructive nephrogram may not develop in spite of acute
obstruction, if there is severe renal infection or other pre-existing renal
parenchymal disease.
• Obstructive nephrogram is a manifestation of acute obstruction and
will not develop after several weeks of high grade obstruction.
• Acute or chronic obstruction : dense nephrogram developing in acute
obstruction in a kidney that already had chronic partial obstruction.
• Segmental obstructive nephrogram : developing in a portion of kidney
with duplex system (or) blocked caliceal infundibulum.
2. Delayed contrast excretion
Depending upon the degree of obstruction and progress of urine and contrast
through the tubules, there is variable delay in opacification of the collecting
system ranging from few minutes caliceal delay to hours to ooze into the

298 Seminar in Radiology

colleting system to be recognized against the backdrop of the collecting
system.
• Standing column of radiopaque urine down to the point of obstruction.
• Persistence of opacification
• Layering of contrast medium in depending portion of static urinary
system
• Just after the passage of an obstructing lesion, there will be rapid fading
of the “obstructive nephrogram”.
3. Dilatation
• Acute obstruction of a previously normal ureter and kidney leads to
little dilatation within first several days
• Calyceal fornices are slightly rounded but imprints on renal papillae
present.
4. High versus low obstruction
High obstruction causes more pelvicaliectasis than lower ones.
5. Heterotopic excretion
Gall bladder opacification is sometimes visible on delayed imaging.
6. Extravasation
Demonstrable in about 24 percent of patients with acute obstruction.
Overdistension of the collecting system ruptures the calyceal fornix
(weakest point) where it attaches to the renal papilla. Thus contrast medium
enters the –
• renal sinus (Pyelosinus extravasation)
• space surrounding pelvicalyceal system
– Causes smudged appearance of one (or) more calices
– With extensive leakage – contrast medium leaks medially around
the renal pelvis coursing down along the psoas muscle and outlining
the ureter
– Rarely extravasation may be:
o Pyelolymphatic
o Pyelosubcapsular
o Perinephric tissues
• Spontaneous extravasation is always benign. Self limited process without
clinical sequalae unless there is infection or continuing obstruction and
leakage.
7. Urinoma
• Results when unrelieved obstruction with continuous urine extra-
vasation
• Forms an encapsulated retroperitoneal urine collection
• Typically kidney displaced upwards, anteriorly and laterally.
8. Parenchymal rupture
True rupture of the renal parenchyma is a rare complication.

Uremia and Imaging 299

Ultrasonography
• Demonstrates pelvicaliectasis
• Doppler USG measurement of Renal Resistive Index
• Colour doppler evaluation of ureteric jets into the bladder
• Ultrasonographic demonstration of “Split Renal Sinus” must be assumed
to be hydronephrosis until proved other wise.

Deviation from this will lead Acceptance will lead to 20 percent
to false negative sonograms false positive rate which is acceptable
for a sensitive but non-invasive
screening test
• Pelvicaliectasis takes 24 hrs. to develop after the onset of acute obstruction,
hence 1/3rd cases are missed.
• USG and Plain X-ray KUB in patients with suspected ureteric calculi yield
success in 95 percent.

CT Scan
Similar findings as in excretory urography.

CHRONIC OBSTRUCTION
Urography findings:
1. Renal size
• Large (Partial obstruction)
• Small (Complete obstruction)
2. Nephrogram density
• Normal (or) faint, greater degree of obstructive atrophy – more
impairment
• In extreme little (or) no nephrogram, no recognizable excretion of
contrast into the collecting system.
3. Parenchymal Thickness
• Measured from the edge of calices and the outer surface of the
nephrogram
• Gives rough estimate of recoverable renal function
• More precise quantification requires radionuclide imaging, best obtained
after several weeks of decompression.
4. Soap-bubbles, Rims and Shells
• End stage obstructive atrophy characterized by marked thinning of the
renal parenchyma, surrounding the ballooned collecting system
• Shell/rim nephrogram – opacification of rind of renal tissue surrounding
the ballooned calyx
• Portrays irretrievable loss of renal function.

300 Seminar in Radiology

5. Pyelogram
Negative pyelogram on nephrogram phase. “Ball” pyelogram.
6. Ureter
Dilation and tortuous (low obstruction).
7. Post-obstructive atrophy
Kidney
• With minimal post-obstructive atrophy
– Normal in size
– Slight recession of papilla
• Severe post-obstructive atrophy may be large (or) small.
• Variable caliceal blunting
• Parenchymal thinning
• Impaired concentration of contrast medium.

A Typical Form
• Kidney shrinks dramatically in the weeks after relief of obstruction.
• Papillae and calices resume their size and shape.
• Renal contour remains smooth.

NON-OBSTRUCTIVE DILATATION
Dilatation of upper urinary tract in absence of anatomical obstruction.
1. Reflux
• Massive hydronephrosis and hydroureter
• Upper tract distension peaks during reflux and is obvious on cystoure
- thrography than excretory urography.
2. Post-obstructive dilatation
• Redundant and partially collapsed, but shows remarkable distensibility
in response to diuresis, full bladder, abdominal compression
• Diuresis renogrpahy (or) Whitaker test is especially useful in these
cases.
3. Megacalices
• Non-obstrcutive enlargement of calices, secondary to hypoplasia of
the renal medulla
• Number of calices often increased to between 25 to 40
• Pelvis and ureter are normal
• Renal cortical thickness and function remain normal
• Unilateral
• More common in males.
4. Megaloureter
• Ureterectasis in absence of mechanical obstruction
• Consistent abnormality is relatively normal caliber but non-distensible
Juxta vesical ureteric segment that fails to transmit peristalsis.

Uremia and Imaging 301

RENAL PARENCHYMAL DISEASE
Involving chiefly the renal parenchyma causing various degrees of renal
dysfunction either acute/or chronic in nature.

Classification
1. Glomerular disease
2. Renovascular disease
3. Tubulointerstitial disease
4. Dialysis associated disease

Essential Features when Imaging Patients for the Evidence of
Presence of Parenchymal Disease are:
1. Renal calcification (or) calculi
2. Abnormality of kidney size (or) shape/asymmetry
3. Generalized thinning (or) focal loss of renal substance
4. Abnormality of the collecting system especially deformity of papillae (or)
calices.
5. Occasionally, abnormality of nephrogrpahic pattern.
The most valuable observations for differential diagnoses are the presence
(or) absence of:
Papillary/caliceal abnormality, which implies deformity of papilla

Renal substance Collecting systems
Papillary necrosis/ Obstructive nephropathy
Reflux nephropathy
Radiological appearance of renal parenchymal diseases are divided into 4
groups based on the above observations:

No Papillary or Caliceal Abnormality
a. With diffuse parenchymal loss
Bilaterally Unilaterally
• Chronic glomerulonephritis • Renal artery stenosis
• Diffuse small vessel disease • Post- irradiation
• Hereditary nephropathies • Rare hypoplastic post-obstructive
atrophy.
b. Focal parenchymal loss
• Infarct
• Trauma

• Radiological imaging of these patients is a key factor in appropriate management of their disease. • Pelvic USG may demonstrate the abnormality suggesting the cause of obstruction • Highly trabeculated. • If examination of patient fails to uncover and obvious cause. in the setting of acute obstruction. With diffuse parenchymal loss • Obstructive nephropathy • Generalized reflux nephropathy b. imaging of the course of ureters and bladder should be attempted to determine the cause of obstruction • Bilateral hydronephrosis usually indicates bladder outlet obstruction. thick walled bladder suggests: Either – mechanical obstruction of urethra (or) functional abnormality – dys-synergia of sphincter • Bladder that appears capacious but other wise normal : neuropathy causing flaccidity and chronic urinary retention .302 Seminar in Radiology Papillary (or) Caliceal Abnormality is Present a. which may be anatomical or neurological disorder leading to functional obstruction. No parenchymal loss • Papilliary necrosis • Tuberculosis • Pelvicaliceal cyst • Megacalices • Medullary sponge kidneys c. Renal Ultrasonogram Alone is usually sufficient to identify patients secondary to urinary tract obstruction. • Although the percentage of false negative USG examinations are substantial. then imaging should be promptly undertaken. Focal parenchymal loss • Focal reflux disease • Atrophic pyelonephritis • Tuberculosis • Calculus disease WORKING FORMULAE/PRINCIPLES OF IMAGING IN PATIENTS WITH RENAL INSUFFICIENCY New Onset Renal Failure • Patients with renal insufficiency but without a history of prior renal disease. renal failure caused by obstruction indicates a long standing process with resultant hydronephrosis • Once diagnosis is established.

. ACD. and no abnormality are present in the pelvis. suspected renal mass. solid renal neoplasms develop. hematuria. • Numerous scattered simple small cysts in the renal parenchyma are typical of acquired cystic disease of dialysis. • Reasonable screening in patients on dialysis for neoplasms. – Dialysis > 4 years. CT of abdomen/pelvis should be undertaken • If an obstructing process is seen and imaging features are nor characteristic of a specific disease such as retroperitoneal fibrosis. USG is useful in guiding biopsy of kidney for histological diagnosis. Renal Insufficiency in Patients with Chronic Renal Failure • In 7 percent of patients who have undergone long term dialysis. • Metastatic renal adenocarcinoma from the native kidneys (2%) are responsible for late deaths in patients with renal transplantation. either peritoneal/hemodialysis. CT can be used to guide biopsy of obstructing lesion • Initial evaluation by USG of patients with newly diagnosed renal insufficiency is also useful in diagnosing disease other than urinary tract obstruction. – To be repeated yearly (or) sooner should new symptoms develop. who have flank pain. Progressive Renal Failure • Patients with clinical evidence of unexpected progression of renal insufficiency may benefit from the imaging of urinary tract • Evaluation should also include an attempt to identify renal arteries • Renal artery stenosis is a common cause of progressive renal insufficiency and one that may be treatable. Uremia and Imaging 303 • Intrinsic bladder abnormalities which may lead to bilateral urethral obstruction are usually detected by pelvic USG • Finally bladder that appears normal in conjunction with bilaterally hydronephrosis is seen in patients with retroperitoneal pathology • If bilateral hdyronephrosis present. like autosomal dominant polycystic kidney disease • The etiology of the renal disease usually cannot be further identified with USG directly • However.

ovarian dermoid (mural or presence of teeth). omental or peritoneal deposits of cystadenocarcinoma and tuberculous pyosalpinx (amorphous) • Localization and identification of intrauterine contraceptive device (IUCD). tend to remain on their own side. deviation. Complications of hysterectomy • Partial or complete ureteric occlusion by a suture • Division of the ureter leading to extravasation of contrast into the pelvic fascia or formation of ureterovaginal fistula where contrast is visualized in the vagina • Vesico-vaginal fistula where contrast is seen in the bladder and vagina but ureters appear normal .21 Role of Imaging in Gynecological Disorders CONVENTIONAL RADIOGRAPHY Plain X-Rays 1. Pelvic mass leading to ureteric obstruction with resultant hydronephrosis 2. ovarian fibroma. 1. or obstruction of the urinary tract in the pelvis. uterine carcinoma) • Any features of pulmonary tuberculosis (tubercular endometritis or salpingitis) • Metastases (malignant ovarian and uterine tumors. INTRAVENOUS UROGRAPHY Used in gynecological disorders to demonstrate distortion. unless large. Chest X-ray • Pleural effusion (both malignant and benign ovarian lesions. Plain X-ray abdomen • Homogenous soft tissue density within the pelvis which may extend upward into the abdomen and displace gas-filled bowel loops. chorio-carcinoma). 2. • Calcification is noted in uterine fibroids (patchy/mural). Actual invasion of the urinary bladder or ureters by a pelvic malignancy 3. • Uterine masses tend to lie in the midline. whereas ovarian tumors.

. cervix and vagina. Prolapse uterus 2. to assess patency after: – Sterilization – Reversal of sterilization – Reconstructive tubal surgery • Abnormal uterine bleeding. deviation of the course of the ureters and dilatation of the renal pelvis and calyces. Stress incontinence 3. These include : • Uterus didelphys: Duplication affecting the whole of uterus. OBSERVATIONS Congenital anomalies: Occur due to partial or complete failure of fusion or atresia of the mullerian ducts. Role of Imaging in Gynecological Disorders 305 • Pelvic accumulation of blood (hematoma) or lymph (lymphocyst) which can cause distortion of the shape of the bladder. Contraindications • Active pelvic sepsis • Pregnancy • Recent dilatation and curettage or any other uterine or tubal surgery within last 6 weeks • Immediate pre and postmenstrual phases • Contrast medium sensitivity. Vesicoureteric reflux 4. CYSTOGRAPHY Useful in cases of : 1. Vesico-vaginal fistula HYSTEROSALPINGOGRAPHY Indications • Infertility • Recurrent abortion • Congenital abnormalities – Primary diagnosis – Following reconstructive surgery • Post-uterine surgery – Myomectomy – Adhesiolysis – Cesarean section • Posttubal surgery.

the findings which suggests the diagnosis. If HSG has been done in an asymptomatic woman. 6. giving speculated appearance.306 Seminar in Radiology • Uterus bicornis bicollis: Two separate uterine horns. are: • A rigid non-peristaltic pipe-like tube (lead pipe appearance) • Beaded appearance • Calcification in a tuberculous pyosalpinx • Cornual/fimbrial block • Jagged. Cervical incompetence: funnel shaped cervix with a patulous internal os. 5. FALLOPIAN TUBE: 1. the tube is dilated (hydrosalpinx). C. 3. • Septate uterus: A septum protrudes from the fundus • Arcuate uterus: Characterized by the shape of the fundus. • Infantile uterus: Small sized uterus. the mass will deflect the uterus to the opposite side and the ipsilateral tube will be stretched over the mass. • Subserous fibroids: if situated laterally in the parametrium. Endometrial carcinoma: Filling defect with ragged contours. B. cervical canal is long relative to the uterine body. • Uterus bicornis unicollis: Two separate uterine horns which share a single cervix. 3. fluffiness of the tubal outline • Vascular or lymphatic intravasation of the dye. Endometrial polyps: Single or multiple. Synechiae: Irregular filling defects which are seen even in the contrast filled uterine cavity. CERVIX: 1. • Interstitial fibroids: enlarged or distorted uterine cavity. Tubal occlusion: Can involve the proximal/ mid segment/ distal part of the tube. Proximal to the occlusion. Paratubal adhesions: Contrast tends to remain in separate spots and does not spread freely in the peritoneal cavity. . which projects moderately into the uterine cavity. well defined filling defects which do not enlarge the uterine cavity. 2. Adenomyosis: Irregularity of the endometrium with penetration of the contrast medium into the myometrium. UTERUS 1. Tubercular endometritis: Very small irregular contracted uterine cavity. HSG is not done. each with its own cervix. 2. Fibroids • Submucous fibroids: sessile or polypoid filling defects. Acquired Conditions A. • Unicornuate uterus: Single spindle-shaped uterine cavity. single vagina. Tubercular salpingitis: In a proven case of genital TB. in the contrast filled cavity. 4.

appear as serpentine high signal intensity structures with a discrete low signal intensity muscularis. Salpingitis isthmica nodosa: small diverticular outpouchings of tubal epithelium into the myosalpinx. cervix and vagina are poorly delineated by CT scans. the stroma remains of low signal intensity and fluid within the follicular cysts show high signal intensity. Normal tubes are usually not well depicted. or triangular soft tissue mass located dorsal to the bladder. 5. Role of Imaging in Gynecological Disorders 307 4. Complications • Pain • Bleeding • Venous intravasation of contrast • Vasovagal episodes • Exacerbation of pelvic infection • Pregnancy irradiation CT AND MRI Anatomy CT The uterus is seen as a homogenous. round. Tubal polyps: Small. Centrally. the vaginal wall shows low signal intensity compared to the high signal intensity of the mucus within the vaginal cavity. which may contain a central area of low attenuation. more cellular smooth – muscle zone with a lesser water content compared with the outer myometrium. These appearances are liable to change with age. seen as discrete structures and the tubes are only seen if markedly abnormal in size. . usually in the isthmic portion of the tube. This is sharply demarcated from the low signal intensity of the deeper myometrium. a stripe of high signal intensity represents mucus within the endocervical lumen and epithelial glands. The bulk of the myometrium appears as intermediate signal intensity tissue. oval. This represents a compact. Ovaries show homogenous low signal on T1 but on T2. oval bilateral filling defects. MRI A characteristics zonal anatomy of the uterus is seen on MR (T2). Similarly. The cervix demonstrates a very low signal intensity myometrium which is continuous with the JZ of the uterine corpus. The demarcations between uterus. The inner high signal intensity stripe represents the glandular tissue of the endometrium. so called junctional zone (JZ). Unless enlarged. the ovaries are not generally identified. during different phases of the menstrual cycle and with intake of drugs such OCPs or HRT. If they are dilated. smooth.

Arcuate V Septate a. cervical. Partial VI Diethylstillbestrol – related • Except for demonstrating anomalies in position. • Renal anomalies. Complete (down to internal os) b. Classification of Mullerian Anomalies (Buttram VC. particularly renal agencies or ectopia. tubal or combined) II Unicornuate uterus a. WE. are frequently associated. MRI Features • Fundal notch or indentation is diagnostic of a bicornuate uterus whereas a septate uterus has a smooth minimally indented fundal contour. Benign Endometrial • Focal areas of hyperplasia of both the glands and stroma of the basal endometrium. T-shaped endometrial cavity with marginal irregularity. hemato- metra or hematocolpos. With rudimentary horn b. found in 10 to 24 percent of hysterectomy specimens. . findings include hypoplastic uterus. • Obstruction due to a vaginal septum leading to hematosalpinx. • Unicornuate uterus has an elongated banana-like shape that is quite unlike the triangular shape of a normal uterus. • In women exposed to DES (diethylstilbestrol) in utero. fundal. Complete (down to internal os) b. Without rudimentary horn III Uterus didelphys IV Bicornuate uterus a.308 Seminar in Radiology CONGENITAL ANOMALIES • Seen in 9 percent of women with infertility or fetal loss. CT has little impact on the diagnosis of congenital anomalies. • Arcuate uterus has a heart-shaped endometrial cavity and flat fundal contour. Gibbons. 1979) Type Anomaly I Segmental mullerian agenesis or hypoplasia (vaginal. ACQUIRED CONDITIONS Uterus A. Partial c.

• Angular margins or distorted shape. – A signal void rim or signal void areas may be seen within the lesion because of hemosiderin-laden macrophages. • The normal uterine zonal anatomy is preserved. fallopian tube. CT Features • Thickening of the tissues adjacent to the ovaries or uterus or involvement of the bladder. dysmenorrhea or infertility. This responds to hormonal stimulation and undergoes repeated cycles of hmorrhage with the development of blood filled cysts called endometriomas. • A definitive CT diagnosis cannot be made without a typical history. Endometriosis • Defined as the presence of functioning endometrium. • Patients present with pelvic pain. • Difficult to detect on CT. uterosacral ligaments. • Sites of implantation of ectopic endometrium are ( in descending order of frequency) – ovary. MRI Features • Endometriomas appear as multiple cysts lesions with signal behavior consistent with the presence of varying stages of hemorrhage: – Most have high signal on both T1 and T2. posterior wall of lower uterine segment. which represents fibrous tissue within the pedunculated stalk. • Polyps enhance with gadolinium ‘the contrast media’ but less than the surrounding endometrium. MRI Features • Intermediate signal intensity mass is noted within the endometrial cavity on T2-weighted images. cul-de-sac. non-invasive endometrial carcinoma. • Increased incidence of polyp formation is seen in women on ‘Tamoxifen’ therapy. rectovaginal septum and sigmoid colon. • D/D: Submucosal leiomyomas. rectum. . located outside the uterus. Role of Imaging in Gynecological Disorders 309 • May be sessile/ pedunculated and are usually attached to the uterine fundus. • Linear low-signal area is seen peripherally. small bowel or abdominal wall by single or multiple solid masses or fluid-filled cysts. • Present most commonly in the fourth to sixth decade with vaginal spotting. some may hypointense on both T1 and T2 or even hyperintense on T1 and hypointense on T2. uterus may appear normal or demonstrate non- specific widening of the endometrial cavity.

• D/D: Hemorrhagic ovarian cysts.310 Seminar in Radiology • Thick. less than the surrounding myometrium and remain well marginated. infertility.3 cm. fibroids enhance heterogeneously. • Amorphous popcorn. . others may present menorrhagia. whorl like or rim like calcification. • Soft tissue which distorts or obliterates the uterine cavity. • Can identify lesions as small as 0. habitual second trimester abortion or pelvic pain. • Although many patients are asymptomatic. • Lesions larger than 3 to 5 cm have heterogeneous areas of increased signal intensity representing degeneration. Uterine Leiomyomas/Fibroids • Benign smooth muscle cell tumors containing varying amounts of fibrous tissue. • After gadolinium administration. • Irregular low density areas within uterine masses representing degeneration of a leiomyoma. Adenomyosis • Presence of heterotopic endometrium located within the myometrium. • May be hypodense/ isodense/ hyperdense relative to normal myometrium. occurring in 20 to 40 percent of all women during the reproductive years. dysmenorrhea. • Cyclical hemorrhage of normally functioning endometrium is infrequent because the heterotopic endometrium is usually resistant to hormonal stimulation. MRI Features • Sharply marginated homogenous areas of decreased signal intensity on T2-weighted images. • Lipoleiomyoma : Well-encapsulated uterine mass that shows predominantly fat density. Mild to moderate enhancement is noted after IV contrast administration. • These are of 3 types: – Intramural – Submucosal – Suberosal CT Features • A focal solid mass causing a lobulation/ protrusion from the outer margin of the uterus. low signal intensity rim which may enhance after gadolinium administration. • Mural thickening.

hypertensive and diabetic and usually present with postmenopausal bleeding. • One third to half the number of patients are obese. premenopausal women during the fifth decade and presenting features including dysmenorrhea. dyspareunia and an enlarged uterus on examination. poorly marginated area of low signal intensity within the myometrium but contiguous with the junctional zone. can detect an enlarged uterus.5 cm in diameter and heterogeneous cervical stroma. of the junctional zone. . 55 to 60 years of age. menorrhagia. triangular mass extending from the central neoplasm that obliterates the normal parametrial fat planes. small leiomyomas (<2-3 cm) may have ill-defined borders). • Involvement of rectum or bladder is seen as either asymmetric wall thickening or protrusion of the growth into the lumen. • Adnexal spread appears as a lobulated. • Common in multiparous. CT Features • Focal or global enlargement of the uterine body. • Small foci of increased signal intensity may be seen on both T1 and T2 due to hemorrhage. which interdigitates with the smooth muscle of the normal myometrium without forming a sharp border. distinguishing adenomyoma from leiomyoma (However. pelvic pain. • Involvement of the cervix is seen as cervical enlargement greater than 3. B. haematometra or pyometra. • CT cannot assess the depth of myometrial invasion. irregular and heavy cycles. MRI Features • Focal adenomyosis is seen on T2 as an ill-defined. purulent vaginal discharge or lower abdominal pain.5 cm are considered metastatic. • Diffuse adenomyosis characterized by generalized thickening. CT shows a symmetrically enlarged uterus containing a central water-density mass. Role of Imaging in Gynecological Disorders 311 • Foci of adenomyosis are surrounded by hypertrophied smooth muscle. • Hypodense mass within the endometrial cavity on contrast-enhanced CT scan. either even or uneven (>5 mm). Nodes larger than 1. • CT has little to offer. • Lymph nodal metastases involves both pelvic and retroperitoneal nodes. • The mass can occlude the internal cervical os resulting in hydrometra. Malignant Endometrial Carcinoma • Usually seen in perimenopasual women. • An ill-defined border is the hallmark of focal adenomyosis.

• With gadolinium enhanced T1-weighted images. • Enlarged. • Cervical involvement is seen as distension of the endocervical canal or when relatively high signal intensity tumor mass disrupts the low signal intensity of the fibrous cervical stroma. • Presence of a heterogeneous myometrial mass with an indistinct border. inhomogeneous uterus with a central area of low attenuation. CT Features • Normal size uterus with areas of hypodensity. CT Features • Uterine enlargement with areas of inhomogenity and zones of low attenuation. pelvic (20%). – Invasion of contiguous pelvic structures can be seen by both CT and MRI. • With parametrial extension. vaginal bleeding and pelvic mass. Gestational Trophoblastic Neoplasia (GTN) • It is a spectrum of proliferative abnormalities of trophoblasts ranging from partial and complete hydatiform mole to persistent (invasive) GTN and choriocarcinoma. vagina (30%). metastases to the lung (80%). disrupting the normal signal intensity of parametrial fat. the growth enhances but later than normal endometrium. • The intermediate signal intensity tumor is seen on T2 to disrupt the junctional zone when myometrial invasion occurs.5 cm are considered metastatic (same as CT). • Presenting features include pelvic pain. liver and brain may occur. Leiomyosarcoma • Occurs in perimenopausal women and arises either de novo or from sarcomatous degeneration of leiomyoma. • Ovarian metastases appear as masses of intermediate signal intensity replacing the normal signal intensity of the ovarian stroma. the tumor will penetrate the serosal surface. • In choriocarcinoma. . usually as a result of local extension. • Hypodense foci. surrounded by highly enhanced areas in the myometrium.312 Seminar in Radiology MRI Features • Homogeneously widened endometrial stripe or a heterogeneous mass distending the endometrial cavity with intact junctional zone (non-invasive endometrial carcinoma). • Peritoneal or omental tumor implants have an intermediate signal intensity on T1 and higher signal intensity on T2. • Lymph nodes >1.

MRI Features • Intermediate signal mass on T2-weighted images that may expand the endocervical canal. • Obstruction of the endocervical canal leads to uterine enlargement with an endometrial fluid collection. • Patients present with irregular vaginal bleeding. fixed and bleeds on touch on examination. Role of Imaging in Gynecological Disorders 313 • Presence of bilaterally enlarged ovaries containing multiple theca-lutein cysts. • CT of the brain. CT Features • Solid mass enlarging the cervix greater than 3. Myometrium remains intact. nodular indentations or serrations of the bladder/ rectal wall and an intra-luminal mass. • Foci of high signal on T1 suggest the presence of hemorrhage. MRI Features • Complete hydatidiform moles appear as heterogeneous masses with vesicular spaces distending the endometrical canal. . cervical carcinomas may display increased enhanced in the early dynamic phase with improved tumor to cervix contrast. predominantly high signal intensity masses invading the myometrium and distorting the uterine zonal anatomy are seen. heterogeneous. • With Gadolinium. • Detection of pelvic and retroperitoneal nodes and liver metastases. • Myometrial invasion is better picked up on Gadolinium contrast-enhanced images. chest and abdomen enables detection of distant metastases. discharge. prominent parametrial soft tissue stands. • Parametrial tumor invasion leads to disruption of the peripheral cervix margins. eccentric parametrial soft tissue mass and obliteration of periureteric fat planes. pain and the cervix is friable. disrupt the low signal intensity of the fibrous cervical stroma. CERVIX Cervical Cancer • Most frequent of all the genital tract cancers. • Pelvic side wall extension is seen as soft tissue mass extension to the obturator internus or piri formis muscles. • Bladder or rectal involvement leads to focal loss of the perivesical/ perirectal fat plane with focal wall thickening.5 cm in diameter with hypodense areas due to necrosis and ulceration. • In persistent or invasive GTN.

• Detection of metastatic nodes. May be a symptomatic or produce local discomfort. with a thin wall and signal intensity isointense to urine on all pulse sequences: low signal on T1 and high signal on T2. This may extend upto the pelvic side wall. parametrial mass or stranding within the parametrial fat. rupture or torsion. • Focal disruption of the normal low signal intensity of the bladder or rectal wall. • With vaginal invasion. complex adnexal masses with centers of low attenuation.enhanced images may help differentiate adherent clot from a mural nodule because clot will not enhance after administration of Gadolinium.0 to 1. • Simple serous cysts include follicular cysts. . These may be complicated by haemorrhage or infection. loss of perivesical/perirectal fat planes. Layering may be present. asymmetric nodular wall thickening or intraluminal masses are seen with bladder or rectal involvement. • Acute hemorrhagic cysts may be diagnosed because of the high density of blood within the cyst. corpus luteal cysts. theca luein cysts and paratubal cysts. Contrast. Tubo-Ovarian Abscess • Complication of pelvic inflammatory disease that occurs in about one third of women having acute salpingitis.5 cm are considered abnormal and those between 1. • Presence of air within the mass is diagnostic of abscess. serous ovarian cysts are homogenous.5 cm are considered suspicious. MRI Features • On MR. CT Features • Thick-walled. menstrual disturbances. septations and shaggy margins. OVARIES Ovarian Cysts • Usually seen in the child bearing age. those larger than 1. A rim of soft tissue surrounds the cyst.314 Seminar in Radiology • With parametrial extension. CT Features • Smooth walled masses having a central low density close to that of water. or rarely causes acute symptoms due to complications like hemorrhage. tumor invades the low signal intensity vaginal wall. • Hemorrhagic cysts may show high signal on both T1 and T2. there is full thickness invasion of the cervical stroma associated with irregularity or asymmetry of the lateral cervical margins.

Unclassified tumors viii. Gonadoblastoma vi. hair. • Solid projection (dermoid plug) arising from the cyst wall. Lipid cell tumors iv. undifferentiated. tubular configuration and tend to be heterogeneous and ill defined on T2 weighted images. Brenner. Germ cell tumors • Dysgerminoma. embryonal carcinoma. unclassified. Role of Imaging in Gynecological Disorders 315 MRI Features • Tubo-ovarian abscesses have serpiginous. choriocarcinoma. • Most occur in women after the age of 50 but sometimes in younger women. clear cell. iii. Tumor-like conditions CYSTADENOMAS CT Features • Purely cystic and unilocular or multilocular with internal septations. Sex cord tumors • Granulosa-stromal cell tumors. teratoma and mixed. mixed. • Calcifications (teeth or abortive bone). Internal septations appear hypointense on T2. WHO Classification i. Ovarian Neoplasms • Account for 5 percent of all gynecological cancers in India and 15 percent in the west. debris and fluid. endometroid. Common epithelial tumors • Serous. No mural nodularity is noted. ii. MRI Features • Cystic lesions which appear hypointense on T1 and hyperintense on T2. cachexia and ascites. • Fat fluid level is a diagnostic feature. Secondary (metastatic) tumors ix. polyembryoma. mucinous. gynandroblastomas. CYSTIC TERATOMAS/DERMOID CYSTS CT Features • Low density mass containing a mixture of fat. . May cause abdominal pain. endodermal sinus tumor. androblastomas. No wall thickening or internal solid papillary projections. abnormal uterine bleeding. unclassified. Soft tissue tumors not specific to the ovary vii. v.

peritoneal implants and retroperitoneal lymphadenopathy.316 Seminar in Radiology MRI Features • Presence of fat within an adnexal mass which shows high signal intensity on T1 and intermediate to high signal on T2. • Bladder/rectal invasion • Nodal metastasis. CT Features • Mass caudal to the uterus with areas of low attenuation representing necrosis. palm-tree like protrusions. • Loss of fat plane between the tumor and bowel/bladder or frank disruption of bowel/ bladder wall. enlarged lymph nodes and peritoneal implants. mural nodules and areas signal void due to calcifications. • Cystadenocarcinomas appear as large. MRI Features • Presence of solid components and thick. cul-de-sac lesions or as unilateral/bilateral adnexal masses. Tumor is readily diagnosed by clinical examination. • Ascites. chemical-shift artifact is seen at the fat-water interface. papillary projections and solid tumor components. • Findings include layering. MALIGNANT OVARIAN TUMORS CT Features • Primary and metastatic ovarian tumors appear as abdominal or pelvic masses. cystic tumors with CT attenuation ranging from 10 to 20 HU. • Ascites. irregular walls or septations. VAGINA Vaginal Neoplasms • 90 percent cases are due to squamous cell carcinoma. • Other ovarian tumors are seen as mixed solid-cystic or predominantly solid masses with CT attenuation ranging from 40 to 50 HU. • Pulse sequences which suppress the signal from fat are helpful. • Thickened wall or internal septations. • Tumor approaching the pelvic side wall or distorting the iliac vessels. MRI Features • Diffuse/focal area of increased signal intensity interrupting the normal low signal intensity of the vaginal wall. Marginal irregularity and internal soft tissue components are seen. . floating debris or hair balls.

Role of Imaging in Gynecological Disorders 317 • Invasion of bladder/rectum. • Nodal metastasis. recurrent tumor has increased signal intensity on T2 whereas radiation fibrosis shows low signal intensity on both T1 and T2 when imaged at least 12 months after therapy. • On MRI. RECURRENT TUMOR VERSUS RADIATION FIBROSIS • Cannot be differentiated on CT. .

22 Genitourinary Tuberculosis Genitourinary tuberculosis is a late manifestation of earlier symptomatic or asymptomatic pulmonary infection. • Causes destruction of parenchyma and formation of caseous mass (tuberculoma) with displacement of calyces. • Granulomas may coalesce and form cavities. then is asymmetrical. – Causes part of papilla to become necrotic and slough given rise to papillary necrosis. • Discharge of M. sometimes only. • Leads to formation of microscopic granuloma throughout the cortices of both kidneys.7 percent positive cases in a study of 2240 patients suspected of having renal tuberculosis reported during a survey by ICMR (1973). if bilateral. it may be primary pathology also. • Present as renal mass produced by localized hydrocalicosis as a result of stricture of infundibular or calyceal neck. – Which rupture and communicates with the pelvicalyceal system. tuberculosis into blood stream from active site of infection (more often pulmonary). • These bacilli form further granulomas within the medulla and papilla. • Less prevalent in 5th and 6th decade. • An initial tubercle may enlarge forming a granuloma which may rupture into a Nephron producing tuberculous bacilluria. • These tubercles either heal spontaneously or as a result of anti-TB treatment administrated to control the initial primary focus. • Nonuncommon in India. • Usually unilateral. • Occurs predominantly in 2nd – 4th decade. Pathogenesis • Causative agent is usually mycobacterium tuberculosis. • Is rarely a part of multisystem miliary tuberculosis. • Incidence of 10. • Female predominantly affected. .

Two types – Caseocavernous enlarged kidney converted into a caseous filled sac. Clinical Features Symptoms Suggestive of UTI • Colicky flank pain • Chronic cystitis (frequency. dysuria) • Hematuria with flank pain Constitutional Symptoms • Weight loss • Fever • Night sweat • Anorexia • E/o chronic renal failure • Hypertension • Chronic epididymitis presents with multinodular. ureter – producing initial mucosal inflammation with ulceration. Genitourinary Tuberculosis 319 • Bacilli which are shed into urine. • Alternatively parenchymal caseation. Complications of Renal TB • Perinephritis • Perinephric abscess • Fistula and sinus tract • Psoas abscesses Imaging of Renal TB: Plain X-ray Film • Chest skiagram : findings of pulmonary tuberculosis • In abdomen – Calcification of adrenal or lymph nodes – Calcification of Psoas abscesses – Calcified granuloma . followed by granuloma and ultimately fibrosis with stricture formations. with or without calcification. hard and localized nodules near the tail. pelvis. • Primary and secondary amenorrhoea or infertility in women in tubercular endometritis or oophoritis. infect the walls of calyces. called “autonephrectomy”. necrosis and calcification may cause destruction of the kidney leading to malfunctioning calcified kidney. – Shrunkened. fibrotic and often calcified kidney.

• Fibrotic stricture Three points where fibrosis can occur 1. of calyx neck → Hydrocalyx Fibrosis of infundibulum → Focal/regional hydrocalycosis of renal pelvis → hydronephrosis • In case of stricutre of inferior margin of renal pelvis. • Minimal erosion of single calyceal tip leading to fuzziness – Ragged. dense ground glass appearance (Putty kidney). – Extensive cavitation are also called as ulcerocavernous cavity which fails to excrete contrast media on IV Urography. • Calcified caseous tissue is homogenous moderately. • Lobar distribution of calcification with the calcific rims outlining the periphery of distorted renal lobes. These kinks are known as Kerr’s kink.V. PUJ 3. • Calcification may extend along the ureter. • Initial cavitation. I. moth- eaten or feathery appearance. Advanced findings of Renal Tuberculosis are: • Cavitation – Lipping type of cavity if the cavity projects in medial direction. Lower ureter 2. • PCS deformity caused by traction of stricture infundibulum and parenchymal fibrosis can kink the pelvis. • Calcification may be noted in liver and spleen. • Papillary necrosis. the cephalic retraction is called as “Hicked Pelvis”.320 Seminar in Radiology – Pattern of calcification:  Linear  Curvilinear  Streaky  Mottled  Amorphous  Combination of all. . Neck of calyx. Urogram EARLY AND ADVANCED FEATURES Early Features of Renal TB are: • Earliest sign is slight loss of sharpness of the calyces suggestive of mucosal edema. – Cavitation due to caseation of enlarging tuberculomas or conglo- meration of tuberculomas.

Genitourinary Tuberculosis 321 • Mass lesion It is either due to hdyronephrosis or tubercular granuloma. Two types i. • Fistula formation • Phantom kidney → Completely stenosed infundibulum or calyx results in complete failure of excretion by involved renal parenchyma. • Secondary infection into perinephric collection. This nonvisualized kidney at urography may be small/normal/enlarged kidney depending upon the balance of renal atrophy versus hydronephrosis. abscess or pyonephrosis into perinephric tissue. Caseo-cavernous autonephrectomised kidney–Enlarged kidney converted into caseous filled sac with or without evidence of calcification. ii. Shrunken. b. fibrotic and calcified kidney. Perinephric abscess results from: • Perforation of pyocalyx. . Ultrasound • Most common sonographic abnormality is a focal renal lesion. Nonfunctioning Kidney Seen in • Both types of autonephrectomised kidney. Fistula and sinus tract: Extension of perinephric abscess to adjacent viscera or tissue results into sinus/ fistula which may be • Nephrogastric (left side) • Pyeloduodenal (Right side) Ascending colon in right side • Nephrocolonic Descending colon in left side • Nephrocutaneous • Enteric – renal • Enteric – vesical fistulae • Psoas abscesses: Renal TB spread to psoas muscle via perinephric space. 1. do not show excretion of contrast so CT/US can help in differentiation. Small (5-15 mm) lesion either echogenic or have echogenic border with central hypoechoic area. • Obstructed kidney due to obstructed ureter. • Renovascular hypertension. Medial hypertrophy with intimal or subintimal sclerosis is common finding). and is nonfunctional. a. (Conical stenosis or compete obstruction of Renal artery. • Calcification • Autonephrectomy This is end stage of renal TB.

subcutaneous collection.322 Seminar in Radiology 2.The parenchymal and central architecture may be altered. • Inflammatory hypervascularity can be seen especially if there is chronic sinus with secondary infection. • Cavity with irregular outline accompanied by a thick illdefined wall. Large lesion (>15 mm) of mixed echogenicity with poorly defined margin. • Papillary involvement appear as echogenic nonshadowing mass localized to few of calyces. The communicating tract appears as sonolucent linear track entering the dilated calyx. retroperitoneal fibrosis and spinal involvement. The sloughed calyceal wall appears as echogenic flap separated from calyceal wall. C.T. • Narrowing of intrarenal vessels due to surrounding fibrosis. Renal Angiography • Shows no specific vascular changes • Initially vessels appear normal. Wall is illdefined and thickened. • Non-specific sonolucent swelling with semisolid echotexture. • To evaluate the adjacent retroperitoneal area for extension of disease. perinephritis. • Lobar nephronia like picture may be seen. • Caliectasis is readily demonstrated. Findings • Fine calcification. • Focal calcification seen as high echogenic areas with post acoustic shadows (healed granulomatous lesion). it shows zones of irregularities and even complete occlusion. • Greater help in determining how much viable renal tissue kept for planning of partial nephrectomy. • In advanced cases narrowing of intra renal vessels encasement by fibrosis requires D/D from neoplasm. . Later. • Focal caliectasis is frequently encountered suggestive of infundibular stenosis. • A tuberculous granuloma is seen as a solid mass with little or more enhancement after contrast administration. perinephric abscess. • Shows urothelial edema and thickening. • Due to multifocal TB. • Necrotic debris and scattered echogenic foci may be seen. psoas abscess and other peritoneal collection. • Abscess appear as nonspecific sonolucent swelling with semi solid echotexture with irregular outline. • Stricture of portion of pelvis or ureter may lead to more diffuse hydronephrosis or pyonephrosis. • Focally dilated collecting system containing debris or debris-fluid level are important findings.

Genitourinary Tuberculosis 323 TB OF URETER. • Ulceration predominantly surrounding ureteric orifices. • Chronic stages show fibrotic strictures. RADIOLOGY IV Urography • Bladder lumen is irregular due to localized deformity from cicatrisation or due to hyperplastic inflammatory lesion. • Stricture may be single/ multiple including the beaded and corkscrew ureter • Late terminal stage include – Pipe stem ureter with calcification of its wall – Ulcers are linear most distally – Multiple active ulcers give rise to ragged. • Edema of trigone mucosa causing ureteral obstruction. • TB of bladder is an interstitial cystitis producing thickened spastic bladder of small capacity. hematuria Earliest Manifestation • Mucosal edema. • Hematogenous spread or contiguous spread or lymphadenopathy. frequency. saw-tooth ureter due to multiple active ulcerations. • Early involvement of TB → Resolves completely without stricture formation including urethral dilatation due to edema at the UV junction or due to urethral atony and ulcerative ureteritis. BLADDER IMAGING STUDIES • Bladder involved in 1/3rd of cases • Infection coming from kidney via urine • Symptoms: Dysuria. Ultrasonography • Not significant in imaging ureter in acute phase • Small mucosal granulomas seen in few ureter • Dilated with distal strictures • Identifying perinephric spread. – Multiple intraluminal ulceration represent mucosal granulomas can be demonstrated. paraurethral nodes and other lesion adjacent to Psoas abscess. BLADDER AND URETHRA Ureter • Usually secondary to renal TB in the stage of Bacilluria. • Sometimes granuloma formation is noted .

• Rarely vesicorectal or a vesico-vaginal fistula may be seen. • The undermining ulcer may be seen as escape of contrast in the deeper layer of the bladder wall with overhanging mucosa. • Calcification of bladder is rare and when seen. . small. echogenic and mostly located at base of bladder simulating bladder tumors. there are widened and tortuous arteries of the thickened bladder wall simulating bladder tumors. • Diffuse cicatrical contraction poducces a symmetrical. Findings • Offer no significant contribution except detection of faint calcification. C. • Evidence of disease adjacent to genital tract (especially seminal vesical and prostate). Cystogram • Shows filling defects simulating the appearance of multiple polypoid neoplasm • Chronic ulceration and often hypertrophy of bladder wall. Ultrasound • Visualization of bladder scanning – Deformed shape of bladder – Small capacity and thick wall are seen • Focal nodular lesion seen – May be sessile.T. • Dilatation of upper tracts can result from bladder abnormalities due to small bladder capacity or constriction of the intramural portion of the ureter by thick vesicle wall. thick walled bladder called the Thimble” bladder. – Undermining ulcer of bladder wall seen as intravasation of urine into deeper layer of bladder wall with overhanging mucosa. • In hypervascular type. Angiography • Angiographic appearance are nonspecific • Lesion may be hypervascular or hypovascular – reflecting difficult stages of activity of infection.324 Seminar in Radiology • Tuberculoma of vesical wall can be large. being manifested radiologically as filling defects simulating malignancy. appears like multiple speckled or curvilinear areas of calcification. • Fibrosis of the region of trigone produces gapping uretric orifices and Vesicoureteral reflux.

Retrograde Urethrography • Strictures are often secondary to periurethral abscess formation. • Obtaining ‘early films’ when about 3 to 4 ml of contrast is already instilled à defining endometrial and tubal details and spillage pattern. occurs due to descending infection resulting from tuberculous involvement of kidneys. prostatic abscess. Hysterosapingography • Invaluable procedure for evaluating the internal architecture of female reproductive tract. • Differential diagnosis – Calcified presacral nodes – Calcified uterine myomas – Pelvic phleboliths – Opaque teeth of ovarian dermoid – Peritoneal tubercular calcification • Tubal calcification – Linear streaks – Faint or dense tiny nodules 2. pelviurethral abscess or fistula formation. • To balloon dilatation. Spread from the fallopian tube to the uterus can occur in 50 percent of tubal infection. Sonourethrography • Effective in assessing true extent of periurethral fibrosis or stricture. urethral stricture. Imaging Features 1. • Detect reduction of uterine luminal size due to scarring and intrauterine adhesion. • Fistulas may be numerous resulting in so called “watering – can perineum”. Plain X-ray • Shows calcification of tubes or ovaries – Linear streak in the course of fallopian tube. urethrotomy or surgical urethroplasty. appear as faint/dense tiny nodule. . CT and MRI have limited roles GENITAL TRACT TUBERCULOSIS TB of Female Genital Tract Source – acquired by hematogenous dissemination from extragenital source usually lung. Genitourinary Tuberculosis 325 Urethra • Rare cause of urethritis. Primary focus of genital tuberculosis is fallopian tube.

• Diverticular cavities may surround ampulla and give characteristic tufted appearance. entire tube becomes encased in a heavy connective tissue scar • Lumen develops a beaded rigid pipe stem appearance • Isthmus obstruction is very frequent and is characterized by irregular patulus lumen • Puckering. interfering with normal ovulation • Peritoneal adhesion seen • The normal smooth pattern of the filling defects produced by bowel loops is distorted • Synaechia or intrauterine adhesions are irregular. Sonosalpingography This test is used as a basic screening test for evaluation tubal patency. TB of the Male Genital Tract • Fifty percent of male with genitourinary tuberculosis have genital involvement Route of entry – Hematogenous spread – Urinary tract • Reactivation of renal tubercles and antegrade seeding of prostatic and seminal vesicles with subsequent retrograde extension to epididymis and testis. stricture. • Sequence of involvement – Epididymis : 42% – Seminal vesicle : 23% – Prostate : 21% . occlusion and fistula formation have been observed • Caseous ulceration of mucosa produces ragged contour and diverticular outpouching of both isthmus and the ampulla. angulated with demarcated borders. peritubal halo and fixity are other tubal findings • Walls of the tubes are markedly thickened and irregular with chronic hydro or pyosalpinx • Peritubal adhesion found as a result of inflammation • These adhesions disrupt the anatomic relationship between the tube and the ovary. They present with filling defects due to adhesion • Adhesion – at cornual region result in tubal occlusion – at cervicoisthmus region may completely obstruct and associated with secondary amenorrhea • Uterus shows characteristic T-shaped uterus.326 Seminar in Radiology • Tubercular tubal abnormalities are almost always bilateral but not symmetrical • Fallopian tube narrowing. • As tuberculosis heals.

In India 5 to 26 percent • Inflammatory process begins in the tail and then spread to body and head • May involves the testis • Leads to persistent thickening and fibrosis with extension superiorly into the cord Ultrasound • High resolution USG is required • Normal feature → similar or slightly increase echotexture to the testes • In epidedymitis usually enlarged and hypoechoic Color Doppler • Inflammatory hyperemia • Focal or diffuse involvement • Non-uniform affection in some tail in affected while in other head is affected • Often associated with scrotal wall thickening and a reactive hydrocoele • Focus of calcification seen within the hydrocoele Chronic Phase • Marked thickening of Epididymis appears heterogenous or hyperechoic • A small epididymis with a coarse echotexture and scattered areas of calcification • Cord thickening • Retention cyst. echofree space with distal enhancement. . Tubercular Orchitis — Rare Source • Contiguous extension from the epididymis • Hematogenous spread Ultrasound • Testis may be enlarged and hypoechoic focal areas of hypoechogenicity mimicking tumors. on USG. MRI • Enlarged in a focal or diffuse manner and assumes a darker signal intensity. rounded. it is clearly defined. Genitourinary Tuberculosis 327 – Testes : 15% – Vas deferens : 12% – Pelvic urethra : 1% Epididymitis • Incidence : Upto 54 percent. rapidly declined in the west. commonest at are multiple.

• Hydrocele is usually present which is anechoic but may reveal irregular. may be thickened. • Patchy involvement is irregular and may present as a mass indistinguishable from tumor. Echoes are increased in intensity and usually uniform. crescent shaped area of hyperechogencity adjacent to epididymis • Epididymis is also enlarged due to edema pus • Testicular artery may be compressed or occluded with focal areas of ischaemia or infarction. firbrosis and dilatation may be seen CT Finding • Enlargement of one or both vesicles • Intravesicle areas of variable attenuation with hyperdense borders and strands formation is seen • Bladder wall adjacent to SV abscess.328 Seminar in Radiology • Peripheral. hard and nontender. Prostate • Route of entry – Descending infection from urinary tract . thick septation with heterogeneous debris. diffusely or locally MRI • Endorectal balloon surface coil MR image shows detail anatomy. Presence of calcification in hydrocele is definite indication of tubercular etiology. • Color Doppler shows increased number and concentration and prominent blood vessels in the affected tests. MRI • Chronic tubercular orchitis – Testis is diffusely heterogeneous with low signal intensity on T2 weighted images without mass effect Seminal Vesicle • May be primary tubercular involvement • Secondary to involvement of upper urinary tract with downward extension Pathology • TB causes destruction of convolution of the seminal vesicles with abscess formation • Ejaculatory ducts may be obstructed and shows calcification or cystic changes • Stenosis. Chronic Orchitis • Testis is enlarged.

Vas Deferense • Involved in 12 percent of genital TB • Calcification are characteristic intraluminal concretion but intramural calcification has also been reported . – Irregularities of outline of the hypoechoic areas may be seen – Irregularities of external contour of the prostate is noted. Genitourinary Tuberculosis 329 – Lymphatic and hematogenous spread – Direct extension from neighbouring organs – Ascending infection from urethra – Occurs after intravesical BCG therapy for bladder carcinoma. more clearly on enhanced CT MRI • Areas of fibrosis or abscess may be seen as areas of decreased signal intensity on T2 weighted images. Pathology • Basically the gland is enlarged and contains intraprostatic lesions that represent foci of caseous necrosis and inflammation. • In chronic prostatitis – TRUS usually demonstrate a heterogeneous echotexture – Dystrophic calcification may be noted Color Doppler • May help in detection of increased vascularity in the inflammatory phase of prostatitis CT Scan • CT Scan shows intraprostatic lesions as low density areas with irregular borders. Cystourethrography and Retrograde Urethrogram • Bladder base elevation due to prostatic involvement with cavities communicating with the urethra TRUS • Prostatitis involves either the peripheral area or the central periurethral area – Reveals enlargement of the gland with solitary (rare) or multiple hypoechoic zones of varying sizes. • Tuberculous abscess and excavation produced in the prostate may also communicates with the urethra.

330 Seminar in Radiology • Vasovesiculogrpahy demonstrate obstruction of vas deferens which may show beaded appearance • On MRI – it is distinguished by its dark muscular wall and small high signal lumen. . Penis • Rare (1%) • Secondary to coexisting urinary tract infection • It presents as a painless (although sometimes tender) ulcer on the glans penis • Diagnosis is made by biopsy • No radiological findings.

Medical renal disease can be classified into various groups – CLASSIFICATION I. • Chronic glomerulonephritis.23 Medical Renal Diseases DEFINITION Consists of multiple renal disorders involving mainly the renal parenchyma causing decrease of various degree of renal function either acute or chronic in nature. Those presenting as nephritis : • Acute diffuse proliferative glomerulonephritis • Rapidly progressive glomerulonephritis. • Hereditary nephritis. Those presenting as nephrosis : • Minimal change disease. • Focal proliferative glomerulonephritis. Infection : • Infective endocarditis • Shunt nephritis • Malaria . Secondary glomerular involvement in : a. • Focal segmental glomerulonephritis b. • Membranous glomerulonephritis • Membranoproliferative glomerulonephritis. Glomerular Disease 1. • IgA nephropathy 2. Primary glomerular disease : a. Systemic disease : • Systemic lupus erythematosus • Polyarteritis nodosa • Wagener’s granulomatosis • Henoch schonlein purpura • Diabetes mellitus • Renal amyloidosis b.

Tubulointerstitial Disease a. Drug Toxicity : • Pencillamin • Gold • Probenicid • Mercury • Captopril • Phenidione • NSAIDS • Trimethadion • Above secondarily disease presents as nephritis.e. ATN (acute tubular necrosis) c. Medullary sponge kidney IV. chronic lymphatic leukemia • Wilm’s tumor d. Renal vein thrombosis b. Dialysis Associated Disease Since most of renal disease are multisystemic and hence we will stick to renal manifestation only. GLOMERULAR DISEASES • Glomerular disease is basically a clinicopathological entity nevertheless radiology can contribute significantly to the diagnosis • In acute glomerulonephritis the renal size increases or remains normal and this can be seen on plain X-ray. IVP and USG in chronic phase the size decreases • USG gives additional information about echogenicity. DCN (diffuse cortical necrosis) d. there is increased cortical echogenicity and hence enhanced corticomedullary differentiation in acute glomerulonephritis. While in chronic glomerulo-nephritis the medullary echogenicity is also increased with resultant loss of corticomedullary differentiation . i. II. Renal artery stenosis and renovascular hypertension III.332 Seminar in Radiology • Syphilis • Hepatitis ‘B’ virus • Human immunodeficiency virus c. reflux nephropathy and drug induced nephropathy. Renovascular Diseases a. Infarction and occlusion c. Tumors : • Carcinomas • Hodkin’s disease • Lukemias i.e. Nephrocalcinosis e. b. Pyelonephritis including infective group.

• Incidence of tumor (kaposy sarcoma & lymphoma) and infection (Candida. Cryptococcus. • Usually size of kidney is increased with increased echogenicity. CMV and Pneumocystis infections. AIDS OR HIV INFECTION • By in large Focal/segmental glomerulosclerosis develops. interstitial nephritis may also occurs. • All above findings though helpful but are not conclusive towards diagnosis due to low specificity. Renal failure is quite common. • SLE forms echopoor patches in an overall echogenic parenchyma. 50 percent cases of azotemia and 30 percent cases of nephritic syndrome have renal amyloidosis. • In this condition (diabetic nephropathy i. • Final stage is end stage kidney diseases. Pneumocystis. Mucormycosis. CONNECTIVE TISSUE DISORDERS • Leads to vasculitis and glomerulonephritis. • Tubular ectesia and cyst formation occurs. Medical Renal Diseases 333 • Plain bony skiagram support the diagnosis of renal disease by showing increase bone density. however ATN. . CMV) are increased. later it decreases especially the cortex as amyloid deposites mainly in cortex. DIABETES MELLITUS • Most common cause of CRF in adults • Renal involvement by diabetes may be in form of a vascular manifestation or in form of infection due to debilitated state. USG • Initially size increases symmetrically. vascular involvement) initially the GFR increases renal size and volume increases but later all of these decrease. • Partial nephrocalcinosis is typical of MAIC infection. • Rheumatoid arthritis presents as a case of renal amyloidosis. (ESRD). • Findings are nonspecific on imaging.e. AMYLOIDOSIS • Renal involvement is mostly in secondary amyloidosis and 90 percent cases of proteinuria. • When the size decreases the echogenicity is increased in cortex and hence Conticomedullary differentiation is either preserved or increased. This is the phase when diffuse intercapillary glomerulosclerosis develops. MAIC.

b. pancreatitis with or without pseudocyst formation. c. Trauma 2. steroid therapy. • Finally an end stage kidney is formed. Retroperitonel pathology like benign or malignant masses. lympha- denopathy. maternal diabetes. hemorrhage. This discrepancy is due to collateral vasculature in adults especially on left side. Extrarenal causes a. RENOVASCULAR DISORDERS Renal Vein Thrombosis Etiology : 1. polycythemia. • Foci of hemorrhage. • Masses may also be seen in bladder. ureter and pararenal area. Clinical Features • Usually unilateral but may be bilateral also • Adults usually have a subacute/chronic nephritic disease or may even be asymptomatic while in children acute presentation with fever + leukocytosis + loin pain + mass + hematuria + Proteinuria is very common. aneurysms. amorphous calcification may be seen as a late finding but nomspecific. IVC thrombosis. • Corticomedullary differention is normal or increased. fibrosis. Renal a. • Amyloidosis • Diabetes • Systemic lupus erythematosus b. . Primary renal diseases (presenting usually as nephrosis) • Glomerulonephritis especially memberanous as 50 percent of its cases are complicated by renal vein thrombosis. Hemodynamic conditions that increase coagulability to cause hypovolumia: • Dehydration (most common cause in infants) • Oral contraceptive pills ingestion. • In general causes that decreases renal perfusion oxygenation.334 Seminar in Radiology • Focal or diffuse echogenic masses with or without mass effect may be seen in cortex later on. congenital heart diseases. Neoplasms : • Renal cell carcinoma • Wilm’s tumors c. • Thirty-three percent patient may have associated or induced pulmonary embolism.

Contrast Enhanced CT Scan • The affected kidney is enlarged and more hypoattenuating than normal. • Initially for 10 to 14 days we find a swollen enlarged kidney which compresses the sinus and pelvicalyceal system. smooth kidney with absent corticomedullary differentiation is noted. this is not a very reliable method and now PCR. • Renal venous jet is absent Arteriography • Stretching of vessels. Phelbography: Selective renal or IVC. • In the vein there is no color flow while in the arteries decreased or even reversed diastolic flow is noted with increases in RI and PI. . • Filling defect in vein. • Corticomedullary differentiation is lost after 3 to 4 weeks. This thrombus may be anechoic in the acute phase. • Gradual and/or incomplete block — – Size is usually normal. persistent or increasingly dense nephrogram. no filling of vein and filling of collaterals are observed. • Overall the kidney is hypoechoic but we may find some patchy anechoic areas representing areas of hemorrhagic infarct to become echogenic over the next 1 to 2 months. • In very late stages a small. MRA dnd MRI are thought to be more reliable. – Poor. • Non visualization of vein or a filling defect in vein may be noted. MRI and MRA: Depicts the pathology more clearly but are not essential for diagnosis. absent or striated nephrogram – Sketchy filling or pelvicalyceal system. Although contributory. Slow circulation time. • Rapid re-establishment of normal flow may occur as the collaterals develop and this is again more rapidly on left side. USG with Color Doppler Study • An echogenic mass (representing the thrombus) inside the lumen of renal vein may be noted. faint nephrogram. Medical Renal Diseases 335 IMAGING IVP • Sudden and/or complete block — – Kidneys are swollen and increased in size but later decreased in size due to shrinking – Poor.

Radionuclide scan: Divided renal function study can assess post thrombosis function. In subtotal or segmental disease a focal nephrographic defect may be noted. Late stages – Shrinking of size.) → In HUS initially (phases of anemia) the kidney is enlarged showing an echogenic cortex/Enhanced CM . 2. • Four weeks onwards in total disease – small smooth. Imaging IVP Early Stages – No nephrogram or very faint nephrogram without the opacification of pelvicalyceal system both in total and partial disease. 3. Thrombosis due to hemorrhage in a fissured plaque.e. OCCLUSION AND INFARCTION Etiology 1. Embolism is the most common cause in adults. Aortic dissection 5. 4. There may be a subcapsular halo of hypoechoic tissue (representing edematous normally perfused tissue by subcapsular vessels. i.336 Seminar in Radiology Retrograde pyelogram Sketchy filling with notching due to collaterats. sub total disease – Scar which is broad based with no calyecal deformity or minimal deformity not related to degree of scarring USG and Doppler Early → Total → Renal size may be normal or increased with decrea- sed or no color flow. Clinical Features • Unilateral disease causes only pain and hematuria. Vascular spasm as in shock. kidney with normal PCS is seen. • According to the vessel involved the nature of infarct is decided. Hemolytic uremic syndrome is the most important and common cause in a child. • Bilateral disease presents with renal failure. the involvement of intertobar artery gives rise to a subtotal infarct (most common in adults) while in HUS the glomerular vessels are involved and associated with vasculitis of arterioles.

Color returns (before phase of diuresis) acting as a marker to stop peritoneal dialysis. renovascular hypertension but still we discuss so much about this tiny number. pheochromocytoma. CT scan: Focal or generalized hypoattenuating lesion with/without mass effect and a CAPSULAR RIM SIGN is noted. hydatid. Angiography : • Features are almost same as that in IVP. Renal artery arteritis as in . 2. smooth/scarred kidney with mormal pelvi calyceal system but loss of Corteco- medullary differentiation is noted. Renal artery occlusion 3. echogenic. Therefore prevents complication due to long PI. Echogenic thrombus inlumen may be noted. Late stage → Small. Subtotal disease → Eight to twenty four hrs after occlusion a hypoechaic wedge shapped mass which may become hyperechoic later and finally forms a scar with normal Pelvi Calyceal System is noted. • A filling defect and obstruction in vessel may be seen. • Congenital coarctation of aorta or renal artery. Renal artery aneurysm or arterio venous fistulae. → subcapsular fluid may be seen → final phases show scarring Radionuclide Scan : By dynamic DTPA study decreased flow in early phase and decreased uptake in late phases is noted. i. aneurysm. psoas muscle. lympho-sarcoma. because this occurs in young b.e. etc. RENAL ARTERY STENOSIS AND RENOVASCULAR HYPERTENSION • Essential idiopathic hypertension accounts for about 95 percent of hypertension and only about 5 percent cases are caused by renal diseases. why? a. tendinous bands. Renal Artery Stenosis • Atherosclerosis accounts for 66 percent cases and is the most common cause of main renal artery occlusion in adults • Fibromuscular dysplasia is the most common cause of renovascular hypertensin in child. 4. • Trauma • Radiation arteritis (in child) • External compression by diaphragmatic crura. Medical Renal Diseases 337 differentiation but absent color flow. Takayasu arteritis and neurofibromatosis cause occlusion at ostia. renal cell carcinoma. because this is a curable condition Etiology 1.

Strategy for Investigation If disease is clinically suspected by following criteria - 1. Spiral CT Angiography Magnetic Resonance Angiogram • At present with best of equipments only proximal 3 to 5 cm of main renal artery can be seen. • To confirm/refute presence of collaterals (from 1-4 lumbar arteries. First rule out parenchymal disease as reflux nephropathy Do IVDSA if . Selective Renal Angiography • Of both diseased and normal side small vessels study should be done. gonadal. Flush Aortogram • To rule out any other cause. • Not good for branch stenosis. • Fibromuscular dysplasia is seen more commonly in young females. abdominal bruit. thromboangi itis obliterans. Severe hypertension in age < 40 and female. High peripheral plasma rennin activity. internal ilterna iliac. 50 percent cases are bilateral and distal 2/3 and segmental arteries are involved forming a typical “STRING OF BEADS / SAUSSACE SIGN”. congenital rubella. 5. adrenal and intercostal arteries). 3. 2. 40 yrs. Takayasu’s arteritis. 4.5 in diseased side. IVDSA • > 90 percent atherosclerotic lesions are correctly graded and > 90 percent renal artery stenosis are diagnosed. Recent onset accelerated hypertension.338 Seminar in Radiology Polyarteritis nodosa. Do Angiogram if < 40 yrs Captopril scintigraphy (to assess function) : can also be done by rennin ratio > 1. No response to treatment. 30 percent cases are bilateral and affects the initial 2 cm (1/3) of main renal artery in an eccentric manner. syphilis. . • Atherosclerosis occurs commonly in old age males. aorta.

e. TC 99 – MAG 3 or I123 hippuran shows. Tardus (decreased accleration time >. • Captopril scintigraphy is a new sensitive and highly specific test for renal artery stenosis showing increased transit and decreased uptake after the injection of captopril IVP • Rapid sequence IVP. b. the latter being infective and envolving the pelvicalyceal system also. is no longer done due to high false negative result. a. a. f. specific but insensitive. Peat systolic volume > 180 cm/s at site of stenosis. >75 percent stenosis – severe.5. Size is normal or decreased b. .07 sec decreased acceleration index < 3 m/s2 ) and parvus wave form. though sensitive but not specific. TUBULO – INTERSTITIAL DISEASES (TID) Acute Pyelonephritis • disease of tubules and interstitium are very closely related and hence are grouped under the rubric of TID. Interstitial nephritis and pyelonephritis both of which refer to the similar pathological process with the only difference being in their etiologies. right > 20 mm smaller than left.e. small smooth kidney left (>15 mm smaller than right. increasingly dense pyelogram d. in downstream vessels. Decreased relative perfusion from 1st images b. Medical Renal Diseases 339 Radionuclide Scan • TC 99 DMSA static imaging shows decreased relative renal function (< 45% of total). b. i. c. Decreased relative function.5 c. c. Acute tubular necrosis and clnically similar condition known as diffuse cortical necrosis.10 minutes interval. Aorta : Renal artery peak systolic velocity ratio > 3-3.3. delayed visualization of pelvicalyceal system on affected side (Nephrographic anomaly is usually not well appreciated). Delayed (> 5 min) visualization of pelvicalyceal system. • > 60 percent stenosis – significance. d. notching due to collaterals USG and Doppler: [may add captopil] highly. Dampening just proximal. a. These include – a. • Now we take early films at 2. • Dynamic imaging using TC 99 – DTPA. Delayed intra renal transit d. Spectral broadening distally.

Increased echogenicity with poor medullary definition. CT scan. though focal scarring is usually asymptomatic especially in adults. CT Scan and IVP show rim or intracavitory enhancement apart – from above findings. v. vi. NCCT shows a swollen kidney with hypo/hyper attenuated areas and loss of Corticomedullary differentiation. Focal (called as lobar nehronia) or diffuse swelling of kidneys with compression of central sinus and pelvicalyceal system [seen on all modalities]. Imaging: IVP. CT scan is being increasingly used for this purpose and is said to be more sensitive than USG. Mass effect may be noted and these may be perirenal stranding. • Scar if not seen should not be taken as absent as a scar on anteromedial and posterolateral surface is out of profile and hence not seen. . if there is infection lower down with Vesicoureteral reflux. The scarring may be unilateral or bilateral.340 Seminar in Radiology • Diagnosis of pyelonephritis is mostly made on clinical grounds with imaging used only to rule out an element of obstruction if present and only in 25 percent cases definite features of this diseases is seen. ii. 6. USG shows a hypo or iso echoic foci or even totally normal par enchyma with loss of Corticomedullary differentiation – lobar nephronia presents as a hypoechoic mass and if hemorrhage is present the whole thing becomes hyperechoic. plain X-ray 1. hypertension. 2. focal or generalized but always assymetrical. USG. • Scarring of renal tissue may be severe enough to cause CRF. iii. 4. In adults it is usually the devitalized renal tissue which is usually involved. Distorsion of underlying calyx (rarely may be normal) with a broken interpapillary line. abnormal patchy enhancement with band or wedge shapped areas of poor early (dut may be good delayed enhancement in 3-6 hrs) enhancement corresponding to striated nephrogram is seen. IVP shows poor and /or delayed filling up of pelvicalyceal system with a dense persistant and striated nephrogram in severe cases. In CECT. even a normal kidney may be involved. Small scarred kidney. iv. 5. Chronic Pyelonephritis and Reflux Nephropathy • These two are closely related conditions and in young age. Decreased cortical thickness. Wall of Pelvicalyceal system and ureter is thickened due to edema while on doppler decreased or absent vascularity noted. etc. Hypertrophy of remaining parenchyma 3. Areas of abscess formation if present are seen as solid or cystic areas with thick wall irregular outline and internal debris. Distance of vertebral body from affected pole is increased usually upper pole and that of right side is more involved. i.

• The latter usually occurs in diabetes and immunocompromized patients (where it is usually florid associated with infection if acute or bilateral if chronic). Medical Renal Diseases 341 • Now there is an important and confusing term known as papillary necrosis. Other non-specific findings are clubbing. Such patients hardly if ever give a history of drug intake. acute pyelonephritis may be divided in: a. • Clinically the patient may present as hematuria. b. • Renal outline and size initially may be normal or increased. • Enhancement on contrast administration is usually normal and a sloughed papilla forms a filling defect. • Radiopathological sequence of events is – Papillae swells –shrinks – sloughs Cavity formation Normal papillae Sinus-formation calcification Calyceal/Cortical Deformity and Hypertrophy of Normal Tissue : Findings on Various Investigative Modalities are: • Tracks and horns originating from calyces egg-in-cup or ring shadows in calyces. • Pathologically. blunting and truncation of calyx and papilla respectively in plain X-ray and IVP. sterile pyuria and CRF. • Analgesics like indomethacin. that too of multiple bilateral papillae. The two kidneys are symmetrically involved and asymmetry means associated renalartery stenosis. obstruction and infection. • Other causes are sickle cell disease and trait. There may be multiple Pelvicalycead system tumors with it. severe ARF of infancy but most common cause (especially in old psychiatrically disturbed females) is ANALGESIC NEPHROPATHY. A process starting in interstitium and secondarily involving the tubules so that if obstructive element is severe pyonephrosis may develop later. severe acute infection. colic. • In the usual chronic form of disease papillae may show various degree of damage. phenytbulazone and phenacetin are commonly implicated and can cause both interstitial nephritis and papillary necrosis. later on the size may be decreased with smooth scarring leading to a wavy outline. obstruction with infection. what is it? This is as acute pyelonephritic disease where the size of kidney is normal or decreased. . cortical thickness is normal but papillary or calcyceal anomaly is noted. A process initiating as a chemico-coagulative necrotic phenomenon at papillary tips leading to what is known as papillary necrosis or necrotizing papillitis.

RENAL TUBERCULOSIS • Though bilateral involvement is the rule clinically significant disease is usually found to be unilateral. • Twenty to Fifty six percent diagnosed on urine examination in asymptomatic patient . etc. Reflux disease. UB. • USG is helpful in later phases only.B. Clinical Features • Twenty percent cases are diagnosed at operation or autopsy. stricture. Pathogenesis Mycobacterium tuberculosis (MTB) in blood → goes to small renal vessels granuloma formed in cortex Burst to give Silent MTB in PCT Can not be tackled by phagocyte ← MTB and debris trapped in LOH because of hypertonic environment In medulla Clinically significant disease starts from Medulla Granuloma may enlarge in medulla leading to caseation and necrosis Most commonly bursts in the calyx may persist as a space-occupying lesion ← damage to parenchyma PCS. when infection is present) the disease is usually unilateral and sysmmetric. In these cases (i. • Differential diagnosis to medullary sponge kidney. (similar to endobronchial spread) Fibrosis.. ureter. cyst and Megacalyx. T.342 Seminar in Radiology • Medulla may also be involved if there is associated diabetes with infection or obstruction with infection.e. etc.

• Similarly diabetic calcification of vas is in walls and is well defined linear “tram-track” like and that in TB is luminal and hence is amorphous. etc. described as fuzzy. just a speck to large areas.e. calcification in TB can be differentiated from that in schistosomiasis in that latter shows lower ureter calcification with a dilated ureter. Sometimes a cavity with fistula to calyx may be seen. Imaging • Tomographic evaluation of kidney is of particular significance in this condition. faint dense (may be so faint that it may be difficult to differentiate from normal renal tissue).] 4. Minimal erosion of single calyceal tip is the earliest sign (D/D pyelosinus back flow or normal variation). Medical Renal Diseases 343 • Seventy-five percent of symptomatic patient show sign of inflammation of urinary tract out of these less than 20 percent have constitution symptoms • Five percent may have hypertension • Super added infection may be seen in 12 to 50 percent • Nephrolithiasis seen in 7 to 18 percent • Obstructive uropathy may quite commonly be seen. Cicatrization of major or minor calyx or it’s infudibula. Parenchymal mass with or without punctate calcification (if > 5 cm then called as granuloma) D/D renal cen carcinoma. irregular. Caliectasis with irregular contour (implying cortical necrosis) and erosion of pyramids. • Also one should look for evidence of calcification elsewhere (10%) i. this can also lead to hydronephrosis/ . [In such cases it is difficult to differentiate it from a cavity with sinus. feathery or moth eaten. Plain KUB X-Ray • Fifty percent cases will show parenchymal calcification (renal calcification in TB is more common than bladder and ureter). IVP Shows evidence only when a lesion has bursted into Pelvicalyceal system forming papillary cavity or has led to changes in PCS 1. • Size may be normal or increased or decreased.e. 3. i. • In ureter. 5. spleen (more common in histiocytosis). 2. lymphnode. Ureter (always secondary involvement) is dilated early on with irregular outline because of inflamed mucosa. • Chest skiagram may show evidence of disease in 50 to 75 percent with 10 percent showing active and 40 to 50 percent showing healed lesions. adrenal and for disease elsewhere as in spine. chest. psoas. Specific features are that the calcification is indefinite. to the extent of autonephrectomy. irregular.

other being Pseudomonas. other present with fever. coli. • Inject slowly to avoid bacterimia Angiography • Just to confirm TB and refute renal cell carcinoma • Early disease whow small vessel occlusion and altered arterial pattern. • Also the incidence of obstruction is more in diabetics (75%) • Eighteen percent present with pyrexia of unknown oxigin. fistula. all being capable of gas formation. Klebsiella. etc. CT Scan • Is useful when very poor function prohibits use of contrast. • USG guided FNAC is an important tool. inflamed (cystitis) or have granulomas. 6. dehydration and electrolyte imbalance. → Emergency nephrectomy is the treatment of choice . acidosis. • Lesion may resolve or enlarge or cavitate and communicate to pelvicalyceal system. • Mostly (62-70%) infection is due to E. → more in hypovascular kidney. hyperglycemia. calcification sinus. • Deilitated (as diabetics 90%) and old age females (2:1 to males) are more prone. Retrograde Pyelogram • Poor renal function is an indication • Give prophylactic antibiotic • Examine two sides at an internal of 4 to 6 days. EMPHYSEMATOUS PYELONEPHRITIS (EPN) • Is an acute fulminating fatal necrotic pyelonephritis. • Chronic disease shows strictures with back pressure changes. proteus. • Changes secondary to granulomas are noted. USG • Five to fifteen mm lesions are echogenic or hypoechoic with echogenic rim or >15 mm lesion of ill defined borders and heterogenous echogenicity may be seen. Candida and Aerobacter.344 Seminar in Radiology hydro ureter. • EPN type I → Parenchymal destruction with gas → more severe and fatal (69%) → more in immuncompromised patient. Bladder may be fibrosed (thimble). flank pain. • Disease is bilateral is 5-10 percent. Last stage is a fibrosed pipe stem ureter. Strictures (most commons at ureterovesical or uretreropelvic junction) gives a beaded look while extreme dilatation forms a cork screw ureter. inflamed mucosa.

CT: is the best method to diagnose. Segmental – One or more hypoechoic masses associated to a calyx with calculi at the tip of related papilla. diabetic. segmental or generalized collection of fat laden foam or histiocytes giving a yellow appearance in gross section. X-Ray • Gas is renal fossa • Air pyelogram USG: dirty shadow with echogenic renal fossa. normal shape. → Less severe (18% mortality) → Percutaneous nephrostomy is the treatment. coli are common organism. corresponding to dialated calyces. Diffuse → Increased size. lost corticomedullary differentiation. Medical Renal Diseases 345 • EPN type II → Renal/perirenal fluid with gas bubbles. → Perinephric extension (best seen on CT) → a large complex thick walled cystic mass with fluid levels may sometimes be seen → On CT few areas have fat density and this is very important. → Though renal function is poor and inability to fill pelvicalyceal system in-spite of a normal thick cortex and signs of obstruction with infection are all suggestive finding. Imaging Focal – has to be differentiated with mass lesion or abscess as it is limited to cortex only and if rest of parenchyma is normal it forms a filling defect. E. loculi or gas in PCS (called as air pyelogram). → Central sinus is very echogenic usually with a staghorn calculi. mass. • Nephrolithiasis (75%) is very common and is the cause for obstructive uropathy • Usually unilateral but bilateral disease is also observed • More in middle aged. . XANTHOGRANULOMATOUS PYELONEPHRITIS • Is an uncommon chronic suppurative disease where chronic disease process leads to focal (called as tumefactive). • Proteus. → If perirenal extension present then outline is irregular. → Posterior enhancement behind necrosed areas. weight loss and UTI are usual symptoms while diffuse from may lead to non functional kidney. • Pain. female. → Many hypoechoic areas or masses.

fibroepithelial polyp. etc. venous or glomerular insufficiency. Leukoplakia • Metaplastic plaques formed.346 Seminar in Radiology OTHER INFECTIONS Fungal Infection • Seen in immunocompromised patient with involvement of other systems also • Candida is most commonly involved but actinomycosis (of tract) may also be seen • Abscesses with calcification or fungal balls in pelvicalyceal system seen as filling defects • Involvement of pelvicayceal system and perirenal space is quite common • Balls may cause obstructive uropathy and have to be differentiated with sloughed papilla. ACUTE TUBULAR NECROSIS (also known as acute reversible renal failure) • Is an acute oliguric renal failure that cannot be explained by obstruction. Schistosomiasis • Hydroneprhosis due to lower tract involvement. Usually lower tract affected. Hydatid Disease • Thick calcified walled cyst with hydatied sand and scolices. Filariasis • Pyelolymphatic backflow seen. clot. arterial. coli infection. cholesteatoma. • Usually old immunocompromised female are affected • In kidney the function normal and masses may be formed. lucent calculi.5-3 cm) seen as filling defects are noted. • It is a locally invasive disease. • Gas and papillary necrosis may be seen • Renal function is decreased. Malakoplakia • Rare granulomatous E. • Plaques of various sizes (. Cholesteatoma • Whorly conglomerate of desquamated epithelial cells. . • Poles more affectd • Retrograde pyelogram shows a goblet or cresent sign. leukoplakia. transitional call carcinoma.

. X-ray abdomen in 3 weeks a patchy but more typically pencil line or tramlike calcification developes. • According to nomur et al the ratio AP : L ∝ Number of dialysis required ∝ Length of recovery ∝ Level of serum Creatinine • Platt et al tried to differentiate between the two most common causes of ARF that is ATN and prerenal disease by Doppler and found that initially in ATN RI > .75 (except hepato renal syndrome). USG • Size may be normal in early stage • Cortex is hypoechoic initially with lost corticomedullary differentiation but later as calcification develops it becomes hyperechoic with a rim of peripheral hypoechoic tissue. • Etiology – severe ischemia as in – Pregnancy (complicated – HgCl toxicity – Hypotension – Ethyleneglycol toxicity – Dehydration – Contrast toxicity – Hemoglobinuria – Gentamycin toxicity – Postoperative • It slowly corrects on it’s own and is the most common cause of ARF in hospital patients. DIFFUSE CORTICAL NECROSIS OR ACUTE CORTICAL NECROSIS • A rare disease caused by similar conditions as above but late pregnancy hemorrhage is the most common cause. • Calcification is seen at interface of normal and dead tissue even at 6th day. NEPHROCALCINOSIS • Is deposition of calcium in renal parenchyma (as compared to nephrolithiasis which is deposition of calcium predominantly in renal pelvicalyceal system). Medical Renal Diseases 347 • Cellular debris (that form casts) is inside the tubules. X-ray Enlarged renal silhoutte.75 (in renal art. • More severe and irreversible involvement of cortex only (sparing a sub capsular rim). IVP and CT: Rim Sign. increased cortical echogenicity (in toxic ATC with increased CMD or enlarged prominent pyramids/in ischemic ATN). Imaging IVP Increasingly dense and persistant pyelogram.) while in prerenal disease it is >. USG Increased sized especially A-P size.

congenital hypertrophic pyloric stenosis. Increased intestinal absorption of Ca++ ii. hyperoxaluria. renal tubular acidosis. Autosomal dominant polycystic kidney. • Calculi initiation occurs in walls of tubules when hypercalciuria is present.C. horseshoe kidney. hypervitaminosis-D. parathyroid adenoma. idiopathic hypercalcemia. • Medullary nephrocalcinosis quite commonly leads to nephrolithiasis and UTI. distal renal tubular acidosis. sarcoidosis. tumors (10% cases of R. a. Marfan’s syndrome. Medullary * Acute cortical necrosis * Secondary to cortical (rare).348 Seminar in Radiology Etiology i. • Disease may be asymptomatic. tuberculosis. caroli’s disease. Imaging IVP – Increased papillary blush and persistant visualization of medulla. Cortical (> 5%) b. medullary sponge kidney. myelomatosis. Dystrophic calcification • Hyperparathyroidism. • The pathology as described is best seen on USG it may also be seen (though missed sometimes on X-ray-KUB) acoustic shadow may be feable or absent in early phases. may also be associated with cortical cysts . MEDULLARY SPONGE KIDNEY • Unilateral or bilateral. osteoporosis. . Ehler Danlos syndrome. * Transplant rejection * Cushing’s syndrome * Sickle cell disease * Pyelonephritis.) hydatid. Unifocal or multifocal • It is formed due to congenital ectesia of the tubules located in pyramids • May be associated with hemihypertrophy. Increased bone turnover iii. * Wilson’s disease • Medullary calcification in distal renal tubular acidosis is typically dense. trauma. • Kidney may be large especially in patients with hemihypertrophy. * GN with nephrosis * Hyperparathyroidism is the most common cause (16%) * Alport’s disease * Medullary sponge kidney (75% of MSK cases) * Haemolytic uremic syndroma * Papillary necrosis. diseases chistosoma renal atherosclerosis. * Ethylene glycol toxicity * Metastasis. may be seen in 5 to 25 percent patients with calculi which leads to symptoms.C. USG – Most useful tool. milk-alkalie syndrome. hyperthyroidism.

END STAGE KIDNEY So small and echogenic kidney that may be difficult to notice and is diagnosed only as a curvilinear silhoutte moving during respiration. few to many cysts with increase in renal size in severe cases is noted. etc can be evaluated by Doppler technique • It is said that after 5 yrs. representing tumor and echoes. USG • Minute to large (5-3cm). . • Both these conditions are taken together as acquired cysts are very commonly seen in dialysis patients. • Benign adenoma and renal cell carcinoma (4-10%) may developed secondarily. representing hemorrhage are quite commonly seen • Cysts involve both cortex and medulla • In dialysis patients shunt thrombosis. Incidence of a disease rises to 90 percent. echogenicity is increased. age. hematocrit value and nature of disease process • Such changes are prevented from occurring or even are reverted back by a normally functioning transplant • Mural Nodules. If very cysts present. • The gravity of problem depends directly upon duration of dialysis. function. Tumors may also form in the same way. Medical Renal Diseases 349 AQUIRED CYST AND DIALYSIS/ASSOCIATED CYST • It is postulated that proliferative changes in response to toxins in epithelium both in native and transplanted kidneys associated with fibrotic changes in end stage kidney can lead to obstruction and hence cyst formation. • It is said that 3 to 5 cysts in appropriate clinical setting and CRF are diagnostic. sex.

next is the moderate – size community hospital. . regardless of the size of the institution housing them. First is the X-ray facility located in a private office or small hospital. Table 24. Installation of equipment according to recommendation of AERB 3.. The factors which contribute to the reduction of doses are following: 1.1: Minimum room requirements for X-ray facilities according to type of institution Room Private office Community hospital General hospital Examination rooms R-F X X X Chest X X Mammography X Special procedures X Patient rooms Waiting area X X X Dressing X X X Toilets X X X Film rooms Dark room X X Cassette loading X Automatic processor X X Film conveyors X File X X X contd. Some types of rooms are common to all X-ray facilities. and last is the large general hospital located in a medical center complex that serves teaching and research functions in addition to caring for patients. according to their size. Qualified personnel PLANNING OF DIAGNOSTIC X-RAY DEPARTMENT Design of X-ray Facilities Three types of facilities are identified..24 Planning of Radiology Department INTRODUCTION The basic aim in planning the radiology department is to prevent the unwanted exposure of radiation to patients. Proper planning. designing of the rooms 2. radiation workers and surroundings.

1. If this number is divided into twenty. space requirement and radiation characteristics. 250 × 20% = 50 X-ray patients 50 × 5% = 3 X-ray patients 50 + 3 = 53 total examinations per day 50/20 = 3 X-ray rooms required . Designing Team The designing team should have a minimum of six members. The more prominent of these are as follows: Number of examinations per year = Required number of X-ray room 5000 Number of hospital bed = Required number of X-ray room 200 The rule that there should be one diagnostic X-ray room for every 5000 annual X-ray examinations is quite general. Hospital administrator — The person who has an overview for relationship of the radiology service to the rest of the hospital about allocated funds. Planning of Radiology Department 351 contd. Room Private office Community hospital General hospital Technologist rooms Office X X Viewing X X Conference X Library X The backbone of any X-ray department is. 4.. Knowing the number of out patient examinations per day. Architect — Responsible for construction details 3.. 2. radiographic fluoroscopic examination room. a general purpose room can easily accommodate. a film file room and space for necessary clerical support are also required for every X-ray facility. 5. If 20 percent of the patients are referred for X-ray examination and 5 percent of those are reexamined. and how to utilize the equipments. Equipment manufacturer — Provides the necessary specifications of power requirements. how many X-ray rooms are required. a film viewing area. Radiologic physicist — Responsible for radiation protection for radiation worker. Example – an average of 250 patients visit a medical clinic each day. Departmental Activity Various authors and designers developed rules for estimating required department activity. Radiologist and chief technologist — Provide the necessary information about workload and anticipated future requirements. A darkroom.

the radiographic supply storeroom. As the size of the X-ray examining room increases. Patient Reception Waiting room Technologist Dressing room Radiologist Film X-ray examination Darkroom Interpretation Film filing Patient interview Consolation The X-ray technologists spend most of their time in the examining room but also must have ready access to the patient preparation area. On ground level. In fact when the departments are located on upper levels the shielding requirements can be receded by positioning the X-ray examining rooms along out side walls. Large general hospitals and teaching hospitals have ten to fifteen rooms or more. On the average. Modern structural engineering designs allow X-ray departments to be located on any floor of the hospital.4 exams per patients Answer: = 34 exams per day 4 days 34 exams per day = 2 x-ray rooms required for inpatient load 20 In general. Plan Layout The plan layout of the X-ray facility must take into account the various traffic patterns. and the professional staff. the average radiation dose to employees decreases. The lounge must . some of which are diagramed.352 Seminar in Radiology Example: A 400 bed hospital has an 85 percent occupancy rate. the X-ray examining rooms are generally located to the inside. the darkroom. the emergency area and surgery. How many X-ray rooms are needed for inpatients care? 400 beds × 85 percent occupied × 0. Location of X-ray Department The principal requirements for the location of the X-ray department prescribe that it should be near the outpatient clinic. private office have one or two rooms. 40 percent of inpatients receive an X-ray examination during their four-day stay. Community hospitals with 200 beds or less have two rooms.

5 mm lead thickness can provide adequate protection. • Such a design should be located in the X-ray department in such a way that future expansion can be accommodated. If the radiologist’s activities are strictly clinical. In nearly every X-ray room the generator is located out of the way in the corner and positioned on the floor. The location of the chest stand is important if an out side wall is available. Room Size The room size should be such as to permit installation. The protective barrier enclosing the operating console should be positioned relative to radiographic tube head so that it is seldom in line with the beam. At this distance a protection barrier of 1. X-ray Examination Room Space and freedom from abstraction are key requirements in the design of an X-ray examination room. if the radiologist is involved in teaching and research. • The X-ray examining rooms are positioned to the center with a central processing A second central — core design show. his office should be located within the radiology area so that technologists and other physicians have easy access to him. it should be used for positioning the chest stand especially the examining room is located above ground level. Too many console barriers incorporate. On the other hand. the X-ray examining rooms located along the out side walls with the administrative areas located to the interior. then his office should be located in another part of the hospital so that he will be free of interruptions when not on clinical call. 12-inch square viewing windows. This leaves 3 to 7 feet available in the false ceiling for the storage of X-ray apparatus particularly the generator. Planning of Radiology Department 353 be located in the radiology area for the comfort and convenience of the technologists and also to discourage trips to the cafeteria or elsewhere for coffee breaks. The control area should be roomy enough to accommodate several persons and adequately store film. If the chest board must be positioned along an inside wall. . new medical buildings often have interfloor distances of 12 to 15 feet with 8 or 9 foot drop ceilings in the X-ray examining rooms. from all these consideration size has been worked out to be minimum of 24 square meter (6 m × 4 m). use and servicing of equipment with safety and convenience for operating personel • To keep control at reasonable safe which is minimum 2 meters from the machine. additional lead shielding will probably have to be placed directly behind it. Single corridor plan with reasonable merit is designed in such a way so that patients enter at one and exit at the other.

the control panel is located in separate room. Dark Room Radiography begins and ends in the darkroom. help reducing exposure to the gonads. if attached to the fluoroscopic screen. it must be located above a height of 2 meters from the ground level. room should be so designed that complete darkness can be produced during screening examination Control Panel and Waiting Area For machines operating at 125 or greater than 125 kV. where the films are loaded into suitable light proof holders and where they are returned for processing into a finished radiography. the control panel should be located in a separate room or behind a mobile protective barrier of 1. . – The radiologist or technicians should wear a protective apron of at least 0. If there are two or more radiographic room.5 mm lead equivalent. Illumination Control In case of fluoroscopy machines. – Protective glass (vinal lead compound) of at least 0. – In cases of CT machines. control panel should be located in separate room. the dark room should preferably be situated in central position. – A fluoroscopic chair of 1. Location The dark room should be located very close to the radiography room as it saves lot of time.25 mm lead equivalent should be used by radiologist during screening work. waiting area should be provided out side x-ray room. It may be between 2 to 3 mm lead equivalence. Use of Protective Devices • Protective barrier: In case of diagnostic tubes operating at 100 kV.5 mm lead equivalent or partition wall with a viewing window of lead glass of 1.50 mm lead equivalent. the viewing window should have the lead equivalence such that it may offer the same protection as the rest of the wall.5 mm lead equivalent should be used during vertical fluoroscopy – The protective flaps of 0.354 Seminar in Radiology Opening on Ventilation Unshielded opening like windows and ventilations if provided in the x-ray room.25 mm lead equivalent.

C. For this reason. easily cleaned. Protection against radiation: It is essential for the darkroom to be well protected against radiation. The preparation of processing solutions must always take place out-side the processing room. The wall should be covered with chemical resistance material such as special paint. Entrance to Dark Room • Single door—which must be made light tight and should have an inside lock. Ideal is 100 square feet floor space and 11 feet ceiling height. Air Conditioning is though ideal solution for the dark room. Floor: The floor should be durable. concrete or ceramic tiles. Electric Wiring The dark room is a place where electric shock can be dangerous because presence of electric wiring in the proximity of aqueous solutions. Planning of Radiology Department 355 Size and Installation of the Darkroom A dark room must be large enough to accommodate all the necessary equipment without overcrowding. It is essential to earth all exposed non-current carrying metallic objects. Typical pass box has two light tight and X-ray proof doors that are so interlocked that both cannot be opened at the same time. Building Essentials A. varnish. Ventilation Windows should be avoided because they do not render the rooms lightproof. Wall covering: The walls of the dark room do not have to be dark. the loading bench and the processing tanks are arranged along opposite sides of the room referred to as the dry and wet sides. The lead equivalence of the wall adjoining the radiographic room should be efficient to prevent the films from Fogging. . B. The colour chosen should first be judged under safelight illumination as it is important that there should be maximum reflection of safe-light. water pipes. It is essential for dry and wet work to be carried out at a safe distance from each other. not slippery and resistant to staining and corrosive substances. The passbox is divided into two compartments one for exposed and the other for unexposed films. Pass Box The most suitable location for the passbox is near the film loading bench. Ceramic tiles or natural clay are most satisfactory.

The Dry Side Various components of dry side are. Require large floor area. • Separate compartments for storing every size of cassette are essential. • Film hangers are best kept on brackets above the loading bench. Safe light: The dark room should have source which will not fog films and also provide adequate illumination. brackets for film hangers.2 meter and bulb wattage should preferably be less than 15 watts. 2. • Stainless steel of the proper alloy composition is the best material for the processing tanks because it does not only resist corrosion but also permits rapid equalization of the temperature. storage for reserve film. The simplest type consist of a three compartment tank. General Illumination: Needed for general purpose such as cleaning changing solutions 3. and washing tank should be about twice the size the fixing tank with special attention should be given to the water circulation in the rinsing and washing sections. The Wet Side The processing tanks comprise the major equipment of the side dark room.So designed that one door cannot be opened until the other is completely closed. in which the inlet is at the bottom and the overflow at the top. film bin. The bench to covering should be linoleum and color chosen under allow the object to be readily distinguishable under safelight illumination. one end-compartment being used for developing and the opposite one for fixing. The working distance should not be less than 1. The middle compartment serves both to rinse and wash the films and should be supplied with running water. Illumination The darkroom should have three types of illumination 1. • A fixing tank should have twice the volume of a developing tank. . • Maze .356 Seminar in Radiology • Interlocked doors . compartments for cassettes. loading bench. Radiographic illumination: A fluorescent illumination for viewing wet radiographic should be mounted over the washing compartment. • Revolving door . The middle compartment serves both to rinse and the opposite for fixing. • Reserve films should be stored in a cupboard or case line with lead. • A more satisfactory arrangement consists of a large insulated stainless steel double compartment master tank. • The length of the loading bench depends upon the volume of work and available space.Serves as light trap and does not require doors.The preferred entrance these days.

the thickness of the sheet of radiographic film ranges form 200 to 300 μm. Size of films: 17 × 14”. • Spectral absorption: One should use a film whose sensitivity to various colours of light is properly matched to the spectrum of light emitted by the screen. 3. • Contrast: High contrast film produces a very black and white image while a low contrast film image is more gray. The silver halide crystal is the active ingredient of the radiographic emulsion. The base is of uniform lucency during manufacture. b. Duplicating film: It is single emulsion film that is exposed to ultra-violet light through the exiting radiography to produce a copy. • Speed: The thicker the emulsion more sensitive the film and therefore the higher the speed. Screen film: There are three characteristics : contrast. Types of Films 1. Two types of bases are available — cellulose triacetate and polyester. 11 × 14”. 4. Latitude: The ability of an emulsion to display the radiologic image with reasonably long range of tones from white through various shades of gray to black. An emulsion should have two important characteristics. Speed or sensitivity: The relative ability of an emulsion to respond with light / X-ray. Mammography film: Fine grain single emulsion film designed to be exposed with a single intensifying screen. Film Construction • Radiographic film has two parts: The base and the emulsion. Driers are available in enamel or stainless steel cabinets provided with heating elements and a blower fan. 14 × 14” 2. dye is added to the base to provide blue tint to the film. The emulsion is enclosed by a protective covering of gelatin. . and light absorption. • The emulsion: Consists of a homogenous mixture of gelatin and silver halide crystals. a. 6½ × 8½”. 18 × 8”. Direct exposure or Nonscreen film • Has a thicker emulsion than screen film • About four times as fast as screen film therefore requires only about one fourth the exposure of screen film for equal blackening. 15 × 12”. • Various types of drying devices help speed up the drying of films. speed. 12 × 12”. 15 × 6”. Planning of Radiology Department 357 • The heating elements is thermostatically controlled. In the typical emulsion 95 percent of the silver halide is silver bromide. • The base: Maintains its size and shape. 12 × 10”.

Dental film: • Intra oral • Panoramic 7. Reflective layer: Between the phosphor and the base is a reflective layer approximately 25 μm thick. Phosphor: The active layer emits light during stimulation by x-rays. Top coat (gelatin and hardener) E. Intensifying Screens An intensifying screen is a device that converts the energy of the x-ray beam into visible light. a hinged lid with one or more flat springs. • One intensifying screen is mounted on front inside of the cassette. made of a substance such as magnesium oxide or titanium dioxide. stainless steel. Subtraction film 6.358 Seminar in Radiology 5. This visible light then interacts with the radiographic film. It makes the screen resistant to abrasion and damage caused by handling. d. The intensification factor Exposure without screens I’F = Exposure with screens . Polyester base B. The active substance of conventional phosphor is crystalline calcium tungstate. Use of an intensifying screen results in considerably lower radiation dose and on another hand increase the radiography contrast. Rare earth are the phosphor material in newer faster screens. Base: It is 1 mm thick and serves principally as a mechanical support or phosphor layer. or plastic frame. c. Protective: This is transparent layer of the screen. and the second screen is mounted on the back inside. Back layer is antiholo Cassette • A case measuring about one-half inch in thickness and having an aluminium. forming the latent image. Screen Speed A screen is said to be fast when a relatively small x-ray exposure produces a given output of light and causes certain degree of blackening of film. The intensifying screen act as an amplifier of the remnant radiation reaching the screen film cassette. A. • Size of the cassettes are available in the corresponding size of films. Emulsion D. There are four layers: a. b. Medical Imaging film: Single coated film and has got five layers. Substratum C.

• Organic reducing agents: ((Hydroquinone and metol) Hydroquinone is slow acting and is responsible for the blackest shades (contrast). The intensity of light emitted by the screen is very low and therefore difficult to see. • Preservative: Sodium sulfite-protects the reducing agents from oxidation by the air. Preservative: Sodium Sulfite 3.activator results in swelling the emulsion. Therefore fluorescent material used is zinc cadmium sulphide. • Restrainer: Potassium bromide and potassium iodide (antifogging agent) these compounds restrict the action of the developing agent only to those silver halide that have been irradiated. • Activator: Sodium carbonate or sodium hydroxide. To harden the emulsion • Fixing solution 1. • Fixation: The purpose of fixation is 1. Hardener: Chrome alum or potassium alum 4. Planning of Radiology Department 359 Conventional screens are available in five-speeds Ultra speed 200 High speed 100 Medium speed 50 Detail speed 35 Ultra detail 15 Fluorescent Screen In fluoroscopy. MANUAL PROCESSING • Development: The function of development is to convert the latent image to a visible image by means of a developing solution. • Developing solution: It contains four essential ingredients. Fixing agent: Hypo (sodium thiosulphate) 2. making easier penetration of developing agent. To remove the unexposed and undeveloped silver halides 2. and the eye is most sensitive to green part of spectrum. . Acid : Sulphide or acetic acid Drier: It is required to get the film dried properly within shortest possible time. the visible light emitted by screen is viewed directly by radiologist and give the corresponding x-ray pattern. Metal acts rapidly and influences the lighter shades of gray. Clip type Hanger Channel type The size of the hanger is corresponding to film size. To preserve the film image 3.

With three phase equipment. Increase the capacity of the radiology department. Processing chemicals: • Increased concentration of solutions Hydroquinone and phenidone are used as developing agents • Increased processing temperatures to help speed up processing • Hardening of Emulsion (qlutaraldehyde potassium bromide) • Control of emulsion thickness sulfates are added to developer. Three Phase Generators Three-phase generators produce an almost constant potential difference for the x-ray tube. Higher effective kV . to minimize swelling of the emulsion • Precise replenishment of the developer and fixer to maintain the proper alkalinity of the developer. Advantages 1. Improves quality of the film image due to more accurate temperature regulation. These are arranged in either a delta or a star configuration. radiography. especially useful in angiography. Circulation system: Agitation of chemicals is provided by a circulation system that continuously pumps the developer and the fixer. 2. Nearly constant potential characteristics 3. 3. It shortens total processing time. wash water temperature is 2. spotfilm.8°C lower 4. • Three-phase circuits have delta wound primary coils but differ in the form of secondary windings. High MA at very short exposures. Temperature control: Developer temperature 35°C. Transport mechanism: Series of rollers which transport the films through various sections 2. 2. Three-phase generator operates on three-phase current which consists of three single-phase currents out of step with each other.360 Seminar in Radiology AUTOMATIC PROCESSING — CORNER CUTLURE There are many advantages of automatic processors 1. three autotransformer are needed for KV selection one for each phase. Essentials of Automatic Processor 1. 3.

to decrease voltage High-Tension Transformer The x-ray tube Kilovoltage is provided by the high-tension transformer is a step-up transformer having a large number of turns in its primary winding.f. As long as target is cold. each consisting of many turn of wire wounded in an iron coil. The potential difference across the secondary coil may be as high as 150 kV so the step-up transformer is immersed in oil in the transformer assembly for maximum insulation. one of these coils is known as primary which is connected to an AC source. this magnetic field induces a current in the secondary coil. source of AC current from high voltage to low voltage and vice versa. . Construction It consist of two coils. Planning of Radiology Department 361 TRANSFORMER Transformer is a device which convert e. the x-ray tube itself suppresses the negative phase of alternating current. Secondary is connected to the electrical device • When current flows through the primary coil — it creates a magnetic field within the core. Law of Transformer The voltage in the two circuit is proportional to the number of turns in the two coils Np Vp = Ns Vs Np – Number of turns in the primary coil Ns – Number of turns in the secondary coil Vp – Voltage in the primary circuit Vs – Voltage in the secondary circuit Step up . Method of Rectification Self wave rectification: This is the simplest method and occurs when the high voltage terminal are connected directly to the terminal of the x-ray tube.m.to increase voltage Step down . • The current only flows in the secondary circuit when the magnetic field is increasing or decreasing. RECTIFICATION Defined as the process of changing alternating current to direct current.

allowing passages of current in one direction only. rotates during x-ray production. one valve or two valves are used.. Stationary: target is a button of tungsten set in a block of copper which has very high heat storage capacity. b. regardless of the polarity of transformer during the different valves of the AC cycle. • Supporting wires • Focusing cup (molybdenum) Anode: There is two main types 1. molybdenum is used as the base material on which a layer of tungsten-rhenium is coated. filament never charged positivity. 2. If two valves are used in the circuit. This makes it possible for a large current to pass from the cathode to the anode. . Rotating: 5-6 percent. By following the numbered portions of the circuits A and B. This anode attached to the shaft of a small induction motor. an x-ray tube. In this case only positive phase of alternating current function while negatives phase is suppressed. that is from cathode to anode. Valve Tube They are thermionic diode tube having the same general construction as x-ray tubes. Full wave rectification: Four valve tubes can be arranged to provide full- wave rectification. a. the current always reaches the x-ray tube used in same direction that is both half cycles. Rhenium mixed with tungsten to prevent development of cracks in the anode.362 Seminar in Radiology Valve tube rectification: A valve tube is a thermionic diode tube which resembles. Cathode: A tungsten filament measuring 0. but differing incertain details. It lies in the longitudinal axis of the tubes. Cathode Consists of a coil of tungsten wire which is larger and thicker than the filament of an x-ray tube.2 mm in diameter and 1 cm in length. Half wave rectification: For this. surrounds the filament. Anode Having a large surface and cylindrical shape (resembling a metal can). supported by a large molybdenum spiral. X-Ray Tube Is a diode consisting of a tungsten filament cathode and a tungsten target anode in a evacuated glass tube and two circuits to heat the filament and drive the space charge electrons from the cathode to the anode.

Short focus for short exposure 2. Wide beam used 3. Narrow beam used so extraradiation avoided more homogenous and less scattering effects 4. The detector does not form the image. Exposed a larger area 4. Mostly high voltage (more than 200 KV) 2. Large focus for larger exposure 3. and larger focal spot. Low voltage 100-150 KV 1. X-ray Therapy Tubes X-ray therapy tubes operate at low MA values of tubes current. It adds up the energy of all the transmitted photons. Difference Diagnostic machine (Tube) Therapy machine (Tube) 1. Long frequency so less penetrating 5. Low voltage 50-120 KV 2. The . to provide x-ray of four main KV therapy ranges. Intermediate voltage 130-150 KV 3.. a stationary anode. Mega voltage 4 MV A typical orthovoltage therapy tube has a larger filament.. by scanning a thin cross section of the body with a narrow x-ray beam and measuring the transmitted radiation with a sensitive radiation detector. Planning of Radiology Department 363 Glass Envelope The anode and the cathode are enclosed in a borosilicate glass envelope containing as perfect a vacuum as possible. Short frequency so more penetrating power and thus give more skin and power and. less skin and bony reactions bone reactions X-ray machines Portable Mobile Stationary With horizontal table 200 – 1200 mA With five positioned table X-ray machine } With biplane motorized With biplane table View Box COMPUTED TOMOGRAPHY Basic Principle The internal structure of an object can be reconstructed from multiple projections of the object. Orthovoltage 160-300 KV 4. 1. The ray projections are found. Exposed a particular area 5.

9 sec. The x-ray tube detector movements were both linear and rotary. radiation. When the electrons reach the anode. The cadmium tungstate (Cd W04) is the scintillation crystal most commonly used in CT units. Perfect alignment between two is essential. Second generation scanners produced a tomographic section in between 10 to 90 sec. A five view study of the head took about 25 to 30 minutes. Scintillation crystals: Materials that produce light when ionizing radiation reacts with them. Detectors: There are two types of detectors used in CT scanners. X-ray tubes: New fan beam units have a diagnostic type x-ray tube with a rotation anode and much smaller focal spot. Rotate-fixed (fourth generation) First generation: It employed a pencil like x-ray beam and a single detector. These tubes have large heat loading and heat dissipation capabilities to withstand the very high heat loads. The collimators regulate the thickness of the tomography slice and control the scatter. Second generation: Adopting a fan-shaped beam and multiple detectors. 1.364 Seminar in Radiology numerical data from multiple ray sums and then computer processed to reconstructs an image. The voltage will cause the electron to move toward the anode. they produce a small current in the anode. The x-ray beam is collimated into a fan beam. Scintillation crystals 2. one close to the x-ray tube and at the detectors. This small current is the output signal from the detector. Xenon gas ionization chambers 1. Second generation (translate-rotate multiple detectors) 3. 2. Rotate-Rotate (third generation): Both the x-ray tube and detectors rotating around the patient. The detector does not move. in some units down to 0. The movements of the x-ray tube detector are both linear and rotary. Collimators: The x-ray beam is collimated at two points. First generation (translate-rotate. CT scanner have gone through a number of design changes. Both the x-ray tube and detectors rotate about the patient. The x-ray tube rotates in a circle inside the detector ring and x-ray beam is collimated to form a fan beam. 1. Multiple detectors are aligned along the arc of a circle whose center is the x-ray tube focal spot. one detector) 2. Rotate fixed (fourth generation): The detectors form a ring that completely surrounds the patient. Both rotate-rotate and rotate-fixed CT units continue to give excellent results. with no clear advantage of one over the other. and the positive ion to move toward the cathode. Third generation (Rotate-rotate) 4. Xenon gas ionization chambers: The photon interacts with gas atom by ionizing the atom into an electron-ion pair. just like first generation.6 mm. . The unit produce a scan in 4.

(Increased by 30%). The linear attenuation coefficient (μ) is used to quantitate attenuation. the patient table is continuously driven at a rate of one slice thickness per one revolution of the gantry. Permits three dimensional (3D) renderings. As the gantry rotates. field uniformity. Increasing pitch will cover scan field but at the expense of resolution the selection of the collimator width strongly effects the spatial resolution and narrower collimation results in improved resolution. spiral CT permits maintenance of a higher concentration of intravascular contrast material. Planning of Radiology Department 365 Image Reconstruction In CT a cross-sectional layer of the body is divided into many tiny blocks then each block is assigned a number proportional to the degree that the block attenuated the x-ray beam. Compared to conventional CT. The analytic methods are used for image reconstruction. • Most image performance parameters are not affected by spiral scanning (spiral and contrast resolution. determine the degree of attenuation. CT Angiography Spiral CT angiography is new technique for noninvasive vascular imaging. • This should be helpful in reformatted sagittal and coronal image. Spiral Acquisition The ratio of the table speed to the collimator width denotes the scan pitch. patient dose). The individual blocks are called voxels. . Their composition and thickness along with the quality of the beam. • The one parameter that is affected is the apparent slice thickness. • An accepted advantage is that a patient volume can be scanned continuously without gaps. Single breath hold scans eliminate irregularities caused by ventilatory misregistration. Image Quality The important factors are: • Quantum mottle (Noise) • Resolution • Patient exposure Spiral CT Spiral CT is a recent innovation which incorporates slip-ring coupling to allow 360° gantry rotation and continuous data acquisition.

In the same time at narrower collimation leading to higher axial resolution. Collimator Design Since a wider area is scanned and overall x-ray beam thickness is four times that in single slice CT more scatter radiation is generated hence in multi slice CT. Data Acquisition System The data acquisition system for multi slice CT permits 4 slices to be acquired simultaneously per gantry rotation. the collimator design is modified to compensate for the increase in A scatter radiation. all in just a few seconds. The virtual endoscopy procedure can be performed and repeated as many times as desired on the same data with different navigation plans. that simulate the views seen through a vide endoscope. Basic Technology Combines a 0. Virtual endoscopy: An alternative and non-invasive diagnostic technique to conventional endoscopy is an innovative diagnostic imaging. The data thus acquired is able to create internal views. abdomen or other areas of the body. metallic implants. Detector Design The detector element is a solid state scintillator. MIP selected only the brightest pixel along each ray. Endoscopy could be replaced by this computerized technique known as virtual endoscopy. Multi-slice Computed Tomography A multi-slice CT system uses multiple detector rows and can therefore acquire multiple slice per rotation. Latest generation helical CT scanners Hi-speed CT is able to take hundreds of images of the chest.366 Seminar in Radiology Segmentation Before rendering maximum intensity protection (MIP) and some shaded surface display (SSD) images it is necessary to perform a process of segmentation to remove unwanted high-attenuating structures such as bone. simultaneous multi-slice acquisition by a slice selectable detector array.000 detector elements are placed in a 2D array in the channel direction and in the longitudinal direction. more than 30. Electronic switches are placed between the detector array and the data acquisition system (DAS) and these enable the user to use thick or thin slices by activating a chosen number of detector elements. . in single breathold.5 second gantry rotation. Also the speed of gantry rotation is increased resulting in an overall increase in scan speed.

Display of Images • A mode: Amplitude modulated scan echoes are displayed as spike projection from a base line. Phased array: About 32 transducer elements are pulsed to form a sector image. The frequency of the sound waves used in medical field may be between 1 – 5 MHz. Linear scanner: A number of transducer elements (64-200) are arranged in a line and excited in groups so a rectangular format is produced. the information is displayed as gray scale which depicts the amplitude of returning echoes in varying shades of gray between black and white. 2-D Real Time Scan In this. • B mode: It is a brightness modulated scan. the returning B-mode echoes are displayed in such a way that movement of scanned body part is demonstrated. Reflected US wave with different acoustic density are detected by same crystal and converted into electrical impulse. These waves pass into the body and are both reflected and refracted at tissue interface in the body. • M mode: Returning echoes are recorded as bright dots along the time base. Planning of Radiology Department 367 The virtual endoscopy-medical applications can be applied to many areas of the body like : virtual colonoscopy. ULTRASOUND Ultrasound is a non ionizing diagnostic imaging technique with high frequency sound waves. Spike height is proportional to echo intensity. When voltage is placed across the disc of the crystal it creates a pulse of high frequency sound waves. It is extensively used in echo-cardiography to show movement of structures. Black is due to weak signal and white signifies high amplitude. In a static B mode image. The impulses are displayed on TV monitor. Three types are: 1. The real time scanner produces images at a fast frame speed of 30 sec. the returning B-mode echoes are electronically coupled and focused. Fast frame rate can be achieved by mechanical scanner or electronic array transducer. 2. . Electronic Array In this. Principles US wave are generated from piezoelectric crystals like lead zirconate titanate. virtual bronchoscopy and virtual angioscopy etc.

Coupling material is needed to make the contact between transducer and skin surface properly.5 MHz transducer is used. which allows visualization of the needle after relatively little tissue penetration. Ultrasound transducers are used to convert an electric signal into ultrasonic energy that can be transmitted into tissues. Use of sonographic needle guidance system There are two major designs: a. For deeper structure 1. Holes or grooves built into the transducer to hold biopsy needle. Indirect ultrasound guidance 2. Transrectal 3. for superficial structure (musculo skeletal purpose) 15 MHz. The rectal. Electronic linear arrays (used in 1.368 Seminar in Radiology Transducers A transducer is a device that converts one form of energy into another. Mechanical 360° scanners (used 1. Transesophageal 2. transurethral and transvaginal scanners have a light rod. The inside electrode abuts against a thick backing block that absorbs sound waves transmitted back into the transducer. Electronic phased arrays (used in 1) In all these types the same techniques are used to generate US image. Attachable biopsy guided that may be easily fixed to the transducer. 1. b. Transvaginal 4. Usually 3 or 3. Endo Sonography The possible applications in the field of endosonography are various: 1. and to convert ultrasonic energy reflected back from the tissues into an electronic signal.5 mm) piezoelectric crystal.2. Linear or curved array transducers are frequently used for guiding procedures because of their good near field resolution. at the tip of which the one element transducer is mounted. Mechanical 90°-110° sector scanners (used in transvaginal) 3.2. Guidance Systems Ultrasound guided interventional procedure can be performed by 1.3. The front and back faces of the crystal are coated with a thin conducting film to ensure good contact with the two electrodes that will supply the electric field. . The most important component is a thin (0. Freehand real time needle placement 3. Transurethral In general the following kinds of US system are available on the market.5 or 2 MHz is required.4) 2.3) 4.

many of the new agents take advantage of low-solubility gases such as perfluorocarbons. • In rectal. the galactose disaggregates into microparticles. Albunex . They provide penetration up/to approximately 8 cm. filling the bladder with water makes the coupling between the transducer and the bladder. the coupling is performed by a water filled rubber balloon. capable of passing through the pulmonary capillary bed and stable enough for the duration of the examination. • Pass successfully through pulmonary capillary circulation and stable enough following injection. Echovist — a galactose agent that forms larger bubbles and has been used extensively without any evidence of toxicity. 5 microns ranging from 1 to 8 μm. The acoustic properties lasting 8 to 12 minutes. vaginal and transesophageal applications.1 percent palmitic acid upon dissolution and agitation in sterile water for injection.9 percent specially manufactured microcrystalline galactose microparticles and 0. • Instead of air. Planning of Radiology Department 369 • In transurethral applications. Levovist — is a stable mixture consisting of 99. . Intra-operative Sonography Intra-operative ultrasound CIOUS is a dynamic and rapidly growing imaging technique providing important real-time information to the radiologists and surgeon. non-toxic. velocity and direction of flow.is composed of air filled human albumin microspheres having a mean size approximately 3. To detect blood flow within arteries and veins. Doppler Ultrasound This is based on Doppler effect in which there is a change in frequency of a signal due to the relative movement of the source of signal and the observer. Most agents enhance the echo by producing differences in acoustic impendence between the agent and the surrounding medium. while pulsed Doppler give information both about depth. the continuous wave Doppler can only tell velocity. Dedicated ultrasonography transducers are small and high frequency linear array 7 MHz and 5 MHz intra-operative transducers have a clear near field of view and can be used on all intraabdominal organs. Ultrasound Contrast Media An ideal US contrast agent should be injectable intravenously. These microbubbles are highly echogenic and are sufficiently stable for transit though the pulmonary circuit.

boils electrons. Signal plate iii. i.370 Seminar in Radiology CLOSED — CIRCUIT TELEVISION The components of a television system are camera. Target • Light passes though face plate • The signal place is a thin transparent film of graphite. Video Signal When a globule absorbs light. • The coils extends almost the entire length of the tube and creates a constant magnetic field parallel to the long axis of the tube this field keeps the beam of electrons in a narrow bundle. camera control unit and monitor. photoelectrons are emitted. • It is a thin film of photoconductive material. Television Camera The Vidicon camera is usually employed for fluoroscopy. • The anode extends across the target of the tube as a fine wire mesh. The electron beam scans the electrical image stored on the target and fills in the holes left by the emitted photoelectrons thus discharging the tiny globule capacitors. Similar events occurs over the entire surface of the target. • The television image is made up of thousands of tiny dots of different brighteners. working together move the electron beam over the target in a repetitive scanning motion. . creating and electron cloud. It is an electrical conductor with positive potential. usually antimony sulfide. • The fluoroscopic image from the image intensifier is focused on to the target assembly which consists of three layers. The dot distribution is along horizontal line called horizontal scan line. • All four coils. The result is a mosaic of charged globules that store an electrical image that is an exact replica of the light image focused on to the target. The globule positively charged and behaves like a tiny capacitor. and with signal plate form a uniform decelerating field adjacent to target. The essential part of a vidicon camera are- Vacuum tube that measures only 1 in diameter and 6 in length • The tube is surrounded by coils. Glass face plate ii. and electromagnetic focusing coil and two pairs of electrostatic deflecting coils. • The cathode is located at the opposite end of vidicon tube is heated indirectly by an internal electrical coil the heating coil.

discharging all the globules on the target. Only a small cluster. 3. MRI The most important part of the MR machine is the main magnet. the shim coils are used. This is cooled down to super conducting temperature (-269°C). For this process which is called shimming. They have a special current carrying conductor. Television Monitor The last link in the television chain is the Monitor. It also receives the signal. limited field strength and its weight. Planning of Radiology Department 371 The globules are not all discharged at the same time. Shim Coils Better homogeneity can be achieved by electrical and mechanical adjustments. disadvantage – thermal instability. Super conducting magnet: Most widely used in MR machines at the present time. is discharged each instant in time. Advantages of super conducting magnets are high magnetic field strength and excellent magnets field homogeneity. The strength of a magnet is given in tesla. 2. The result is a series of video pulses. . In MRI different types of magnets are used. nitrogen) are used for cooling of these magnets and have to be refilled. Volume Coils Volume coils are used in all MR units. Low field system on the other hand often better tissue contrast are cheaper in price. Permanent magnets: Does not use any energy for work. The Coils In MRI radio frequency coils are necessary to send in the RF pulse. At this temperature the current conducting material loses its resistance for electricity creating a constant magnetic field so called cryogens (helium. Resistive magnets: An electrical current is passed through a loop of wire and generates a magnetic field (electromagnet). It is important. It contains the picture tube and the controls for regulating brightness’ and contrast. as it is the transmitter for all types of examinations. 1. • High field strength system have better spatial resolution and may be used for spectroscopy. The body coil is a permanent part of the scanner and surrounds the patients. Then the electron beam moves on to the next dot in an orderly sequence. a dot.

Surface Coils Are placed directly on the area of interest and have different shapes corresponding to the part to be examined. May be adjusted to low or high flow sensitivity. . Enhancement) Maximum intensity projection (MIP) images Obtained both of MRA and MRV by special technique 2.are used to systematically vary the magnetic field by producing additional linear electromagnetic fields. most of the received signal coming from tissues near by. thus making slice selection. TOF MRA: On SE Images: Following blood appears ‘Flow Void’ (Most commonly used) TOF MRA (Both 2D and 3D images) GRE T1 WI MTC T1W sequence Flowing blood seen as an area of To suppress background for ‘Increased signal intensity’ proper visualization of vessels due of flow related enhancement’ (Not to be confused with Gd. They are receiver coils only. MR ANGIOGRAPHY It is noninvasive assessment of extracranial and intracranial vessels without use of contrast agent ↓ 3 dimensional map of blood vessels with multiple viewing angles including oblique view TOF MRA MRA PC MRA 1. Phase contrast MRA i.372 Seminar in Radiology Gradient coils. So selective venous and arterial MRA images can be obtained. It reveals direction and velocity of blood flow along with anatomical detail like TOF MRA iii. Depends on phase rather than amplitude of MR signal ii.

15 microgram/kg • Magnetite (Resovit or SHU-555) is the other SPIO in phase III clinical trial. MR CONTRAST MEDIA Contrast enhancement in MR imaging is the process of maximizing the difference of signal either intensity between two tissue and is achieved by either increasing or decreasing the signal intensity of a tissue relative to another. ferumoxide or AMI-25 has completed clinical trials. Planning of Radiology Department 373 iv. Mechanism of Contrast Enhancement in MRI MR contrast agents work by altering the tissue relaxation rates by changing the local magnetic environment. Excellent suppression of background rhythm but longer acquisition time. T2 Agents Gd chelates can be used as T2 agents is used in sufficiently high concentration and studied with fast imaging (0. It is useful to classify two broad categories as T1 and T2 agents. 10 . • Given IV. ground normal tissue on T2 Wt images. This leads to loss of signal of the back. v. T2 agents are coated iron oxide (SPIO/VSPIO) particles of various sizes these agents contain ferrite particles of appropriate size and are phagocytosed by macrophages of the liver.1.N. spleen. bone marrow and L. the first contrast usually administered in a dose of 0.5 mmol/kg). . T1 Agents Gd – DTPA (gadopentetate dimeglumine or magnevist) –ionic Gd. mmol/kg Major use of these agents is in detection of cerebral capillary break or enhancement of tissue. Superparamagnetic small particles (SPIO). DTPA- BMA (gadodiamide or Ommiscan) Gd-HP-DO3A (gadoteridol or Prochance) ] Nonionic Gadalinium DTPA. Useful for evaluating altered hemodynamics such as flow reversal after major vessel occlusion or stenosis. The agents cross the disrupted blood brain barrier similar to iodinated contrast used in CT.

electron capture. Isotopes: Nucleides with same atomic number (Z) (chemical and biological behaviour).25 Common Radiopharmaceuticals Used in Various Systemic Disorders Radioactivity: The term radioactivity refers to rearrangement process that takes place within an excited nucleus in the form of radioactive decay (4 types: α decay.g. SPECT Two types PET SPECT: Involves detection of gamma rays emitted by single photon from radionucleide like Tc-99m and Th201. Radionucleides: Unstable nucleides which release energy to reach a stable state are called radionucleides or radioisotopes. Emission Computed tomography: Provides in vivo 3 dimensional distribution of radiopharmaceuticals within body. but different mass number and different energy state.7 x 1010 Bq Radiopharmaceutical: Pharmaceutical with appropriate biological behaviour bound to radioactive material. β decay. 123I and 131I are isotopes of iodine. e. and isomeric transition). Natural occurring Radio isotopes Nuclear neutron used to Man made reactor bombard stable excited state Nuclei Cyclotron Deutron to bombard Stable nuclei Units of Radioactivity Activity → Becquerel (Bq) = 1 disintegration/sec 1 curie = 3. generated from set of 2 dimensional projectional images. .

) diphosphonates (methylene i. Isotopes used are prepared by cyclotron (bombardment of (+) charge (protons with stable nucleus → positron). osteomyelitis. Mechanism of Action Tc is labelled to phosphonates and there is interaction of phosphate component of hydroxyapatite crystal with endogenous calcium to produce insoluble Tc- calcium phosphate complexes known as chemicabsorption. hypotension can occur after IV administration. organic pyrophosphates and low radiation dose (t½ short – 6 hrs. 2. bronchospasm and rarely anaphylaxis. Radiopharmaceuticals 1. Strontium-85: emits high radiations dose. 2. is of long t½ but poor imaging characteristics. To demonstrate early physiological changes. MDP and ethylene hydroxy EHDP). 2. Then distribution of radionucleide is identified with gamma camera. Metabolic alterations at 5 to 10 percent level detected. having hypersensitivity to albumin products. Factors Affecting Uptake of Radionuclide in Bone a. Albumin macroaggregates not indicated in pts. Very sensitive.Common Radiopharmaceuticals Used in Various Systemic Disorders 375 PET: Uses coincidence detection of two 511-kev annihilations photons from positron emitting radionucleides as C-11. COMMON CLINICAL APPLICATIONS IN DIFFERENT SYSTEMS Bone Imaging Functional changes in tissues precede anatomical derangements and therefore radiographs are insensitive until pathology is well established. Vaso Vagal reactions with syncope. Significant allergic reactions – urticaria. Tc -99m labelled agents: Inorganic –Tc polyphosphates. Blood supply → ↑ in fracture. Common Adverse Reactions 1. 3. O-15 and F-18. Fluorine-18: It has short t½ and requires cyclotrons. 3. Advantages 1.e. N-13. It measures concentration of radiopharmaceuticals in body that are labelled with positron. however non-specific – complimentary to other imaging modalities. vascular primary neoplasm (called as extended pattern) .

376 Seminar in Radiology → ↓ if ischemia → prevents radiotracer from reaching bone → appears “cold” on scan b. In areas with ↑ MDP uptake when Gallium uptake exceeds in bone or soft tissues indicates active species. 4. 3. Flow phase → sequential 3 to 5 sec images from start of injection ↓ Major vascular pathways show activity ↓ do not measure actual blood flow however relative perfusion and areas of ↑ or ↓ flow 2. 1. Delayed scan → ≥ 2 hrs.e. in areas of ↑ mechanical stress. Indium-111 or 99Tc-HMPAO labeled WBC’s: advantage over Gallium → true physiological location of WBC’s in sepsis false positive results → uptake in areas of fracture also. and also in response to neoplastic. After injection ↓ . 5. metabolic or hormonal stimuli. Intensity of uptake reflects → rate of bone metabolism (i. Technique 550-740 MB of 99mTc MDP IV (dose reduced in children according to weight) ↓ drink plenty of water (hydration reduces dose and accelerates soft tissue clearance) ↓ Micturate and bone scan (2-4 hrs. reparative response around traumatic and inflammatory lesions. Blood pool phase → 5 to 10 min of injection ↓ within vascular and interstitial compartment ↓ Images show extent of soft tissue and bony hyperemia Important in (a) demonstration of soft-tissue component of lesions as cellulitis / osteomyelitis (b) Soft tissue component of bony tumors (c) Synovial hyperemia in inflammatory arthritis. Gallium-67 citrate → Ga-phosphate complexes localizes active sepsis. osteoblastic activity). after injection) → soft tissue activity has cleared ↓ Better delineation of skeleton 3 phase bone scanning done for significant information. Cellular activity and mineral turnover →↑ in epiphysis (growth area).

Sternum In children. iv. Sensitivity > 95 percent. scapula. senile osteoporosis where it shows poor bone uptake. base of skull and anterior ribs can be seen. commonly in axial skeleton. Benign GCT and osteoid osteomas show intense hyperemia (so ↑ uptake) . Around nasal cavity d. Laryngeal cartilage f.Common Radiopharmaceuticals Used in Various Systemic Disorders 377 excretion of radiotracer (clearance of soft tissue background) ↓ uptake in bony (osseous activity) whole body survey or anterior and posterior scans taken • Normal bone scan → Understanding is important to avoid interpretative errors. Calcifying costochondral junction g. iii. If mixed lesion. Normally isotope distribution observed in a. Radiation dose is less for whole body scan but low specificity. APPLICATIONS Metastasis i. Multiple scattered focal hot spots (↑ uptake) on bone scan. Important for monitoring progression or regression of Metastasis – so useful in evaluating response to treatment. Disseminated metastasis shows generalized ↑ uptake known as super scan. v. Oral alveolar ridge h. Primary Bone Tumors Highly vascular on flow scan and very active on delayed scan. this can give false negative bone scan. uptake in lesion may be normal. Benign Tumors – low grade uptake because less vascular than primary Malignant Tumor (If ↑ in benign indicates complicated by fracture/ infection). proximal long bones and areas difficult to visualize radiographically sternum. so used as screening procedure with confirmatory radiographs to detect suspicious areas. Osteoblastic metastasis appears as hot spot on bone scan. Ends of long bones b. Osteolytic Metastasis destroy trabeculae and appears as cold spot. Tips of scapulae e. reliable indicator than conventional radiography. hot symmetrical epiphyseal growth zones are seen. ii. In elderly patients. Sacroiliac joints c.

The reparative response of normal bone adjacent to ischemic area will show increase uptake . If cold lesion present in acute osteomyelitis it suggests highly aggressive process or sequestrum formation. Avascular Necrosis Ischaemia of bone is due to loss of nutrient artery blood supply. early osteoblastic activity and in delayed phase of 48 hrs to next few weeks. there is callus formation so all 3 phases are intensely hot however activity subsides in late Remodelling phase. Degenerative arthritis: Synovial hyperemia is absent and only delayed scan shows positiveness along subchondral surface. Inflammation Acute osteomyelitis: Changes are not apparent on radiographs till 7 to 10 days of inoculation of bacteria. gout. a. costovertebral joint showing increased uptake and loss of vertebral segmentality due to bridging syndesmophytes. it shows focal uptake at cortical margins. Ischemic bone is cold on scan as tracer cannot enter avascular area. there are stress fractures (Microfractures) not usually detected by conventional radiographs. b. • First few hours after injury. distribution of involved joint indicate particular type e. Arthritis Both inflammatory and degenerative arthritis show increase uptake on bone scan. rheumatoid arthritis and Psoriatic arthropathy and ankylosing spondylitis involvement of SI joint. On bone scan all three phases show increase uptake. • Traumatic synovitis shows increase uptake on delayed scan. Cellulitis: There is soft tissue hyperemia on blood pool and flow images and no significant bone uptake on delayed scan. there is hyperemia so increase uptake in blood flow and blood pool images. Inflammatory arthritis: Hyperemia of synovium on flow and blood pool images and increased uptake in capsule on delayed scans. • In athletes and dancers.378 Seminar in Radiology (N) to mild uptake Moderate Marked • Bone cyst • Adamantinoma • ABC • Bone island • Non ossifying fibroma • Chondroblastoma • Enchondroma • GCT • Fibrous cortical defect • Osteoblastoma • Fibrous dysplasia Trauma • It is not a primary technique for fracture detection.g. • Within 24 hrs.

Glomerular filteration agents • 99Tc-DTPA (diethylene triamine penta-acetate) • To measure GFR b. osteomalacia. RENAL IMAGING Radiopharmaceuticals used to evaluate renal functions a. 1. commonly as spotty involvement rather than diffuse involvement (characteristic of Paget’s disease). Observed in following conditions. Total renal function . Myeloproliferative hematolgoical disorders. a. renal osteodystrophy. hyperparathyroidism.Common Radiopharmaceuticals Used in Various Systemic Disorders 379 which enhances cold focus. Tubular secretion and ERPF agents (effective renal plasma flow) • I-131 OIH (orthoiodhiupprate) • I-123 OIH (orthoiodhiupprate) • Tc-99m-MAG3 (mercaptylacetyl triglyceine) → Clearance is highly comparable with clearance of OIH c. Osteoblastic and osteoclastic activity are also increased resulting in weakened and deformed bones which are intensely hot on bone scan. e. Metabolic bone disease. Static renal scan 1. reduced urinary activity and less soft tissue background than expected for age. d. Dynamic Renal Scan: To measure i. Disseminated Metastasis. Cortical imaging agents • Tc-99m GHA (glucoheptonate) – (only 20% retained in cortex) • Tc-99m DMSA (Dimercaptosuccinate) (40-50% bound to cortex) and retained in kidney for long time. Paget’s Disease Aetiology of Paget’s disease is unknown but blood flow is markedly increased. Hypertrophic pulmonary osteoarthropathy. Dynamic renography (dynamic renal scan) Techniques 2.g. This produces characteristic “Doughnut appearance” of vascular necrosis of hip. b. Fibrous Dysplasia Affected bones show intense uptake and distribution. Super Scan Significantly greater radionucleide uptake throughout the skeleton. c.

Quantitative evaluation of rate of transit through outflow tract (renal transit time) Commonly used radiopharmaceuticals are a. . 99Tc DTPA b.380 Seminar in Radiology ii. Therefore activity of whole kidney is sum of activity in all nephrons. 123I-OIH c. following which sequential 5 second images are obtained during first pass to kidney. The functional image between one and three minutes should be used to assess divided and regional renal function. Activity in bladder is recorded at the end of study before and after micturition. Principle Quantity of radiotracer in nephron depends on blood flow and ability to extract it. Divided renal function iv. -99Tc MAG3 Procedure: Well hydrated patient lies supine with knees in flexed position. AB: First phase or vascular phase: The scan within 20 to 35 sec of injection represents vascular radioactivity within vessels of kidney (blood flow) even after nephrectomy denotes vascular channels over renal bed. Parenchymal and collecting system clearance time can be evaluated from subsequent images and time activity curves. Time activity curve: Representation of activity (counts/min) with time. A rapid bolus injection of 300 mBq of Tc DTPA is given. Differential renal blood flow iii. The regional (differential) and total renal blood flow should be assessed from first pass images including aorta. 1. Another image is obtained at approximately 3 minutes and then at every 5 minutes intervals for 30 minutes. Events are recorded by standard renogram (Time activity curve).

It will be reduced physiologically during diuresis and prolonged during dehydration and in diseases that increases tubular transit (e. c. To know site of obstruction and determine extent of severity. Obstructive uropathy: Primary investigation is excretory urography and a. 4. decreases in renal tubular failure and impaired renal perfusion in renal artery stenosis and shock. b. in dehydration. ureteric obstruction. Renal failure: Aim in acute renal failure is to determine whether the obstruction is reversible or not. it is relatively longer when urine flow rate falls e. renal failure and shorter in diuresis. CD (Excretory or III phase): It is roughly exponential fall over next 20 minutes. Peak (c): Normally sharp because rate of transit through all nephrons is roughly same.g. shock. BC: Secretory or II phase (3-5 min) It represents nephron accumulation and the slope of curve is related to rate of accumulation. chronic renal inflammation. Renography enables function and effect of obstruction to be measured on renal parenchyma. Scintigraphy has little role in chronic renal failure. in diffuse vascular parenchymal disease. Thus slope is steep during diuresis. hydronephrosis or severely reduced urine flow rate.g.g. Delayed images show whether activity in bladder is present or not. 5. Diuretic augmented renography to distinguish obstruction from non obstructive dilatation (e. This fall is abnormally slow when drainage from pelvis is impaired. e. hydronephrosis). 3. Rapid reduction of renal activity (no obstruction) If after diuresis No dramatic fall in activity → PUJ obstruction 2. Clinical Uses 1. .g. In this stage ureteric drainage is more than accumulation.g.5 mg/kg of frusemide IV given at 20 minutes after radionucleide injection and imaging for further 15 to 30 minutes then percentage rate of wash out is calculated. Mean transit time: Mean transit time refers to time taken for activity to fall ½ of its peak. Transit time (AC): In next 3 to 5 min. Peak is rounded where transit is unequal e. Characteristically falling curve is strong evidence against obstruction whereas slowly rising curve indicates acute obstruction or exacerbation of chronic renal disease. extra renal pelvis) 0. Peak is sharper in diuresis than dehydration. This time can be recorded either for kidney as a whole or for parenchyma or for renal pelvis.Common Radiopharmaceuticals Used in Various Systemic Disorders 381 2.

Infarction : Detected by avascularity during all phase and no counts. Static renal scan: (Renal morphology) 99Tc DMSA (dimercaptosuccinate) is compound of choice. . as there is no excretion. presence of dilated pelvicalcycal system and cortical scars or other renal defects. there is decrease perfusion pressure and renogram is lower and flatter and transit time is prolonged. c. b. Ureteric obstruction: There is excretion and delineation of proximal collecting system without visualization of bladder.382 Seminar in Radiology 3. difference of 15 to 20 percent compared with opposite side is significant. Renovascular conditions: • In Renal vein thrombosis. • Diagnostic quality of renogram in hypertension is improved by using ACE inhibitors (Captopril) • Captopril scan : 99Tc DTPA scan before and after 25 to 50 mg captopril (2-3 hrs. small scarred kidney with decrease in activity. Ratio of GFR more than 1. In initial flow phase study decrease or absent blood flow in affected area. In functionally significant renal artery stenosis there is decreased uptake and increased transit after captopril administration. • Images assessed for renal size. Chronic pyelonephritis : irregular. d. Clinical Uses 1. 4. Acute Tubular Necrosis. fixed in tubule cells and renal parenchyma with no significant excretion. Comparison of renogram made on time to peak greater than 10 minutes is positive. Procedure: 150 MBq of Tc MDSA IV given and after 3 hours. Renal Transplantation: To study the complications a. Urinoma: Accumulation of radioactivity outside both ureter and bladder is an indication of urinoma may be due to mild or severe leakage from ureter usually at the site of anastomosis.5 is positive. so decreased uptake and peripheral defects. position. there is decreased perfusion and filtration so hold up of activity in collecting system. Infection a. 5. axis (horse-shoe kidney).Commonest. so poor TcDTPA accumulation and tracer diffuses into extracellular space and renal activity disappears. Hypertension: In Renal Artery Stenosis. • Emboli causes infarction. posterior and posterior oblique views and delayed images (if obstruction present). e. kidneys are imaged in anterior. after standard renogram) orally or IV and another renogram after 1 hour. Rejection: is given by perfusion index Count rate in region of interest over kidney Perfusion index = Count rate in distal iliac artery Fall in index is earliest indication of reflection and recovery is accompanied by gradual return to normal.

All show filling defects (non-specific). Acute pyelonephritis: Localized renal parenchymal defects present even when urogram is normal. 3. Gastroesophageal reflux Technique: Patient is given standard radioactive meal (-99Tc-sulfur colloid labelled scrambled egg) and transit (or emptying) time is noted. The images are assessed for presence of ureteric and intrarenal reflux.Common Radiopharmaceuticals Used in Various Systemic Disorders 383 b. b. Residual bladder volume → 25 mBq 99Tc DTPA IV and activity is recorded in bladder in known time and bladder emptied. study to be continued and denotes delayed emptying. However.V. etc. diffuse esophageal spasm. The technique is otherwise the same but catheterization is not required. A. Tuberculosis: The size of defect depends on extent of disease. compared with cysts and hematoma. rapid sequence studies show relatively increased vascularity of carcinoma and fistulas. If there is long delay in transit time. • PET is used for staging esophageal carcinoma in conjunction with CT more sensitive than CT in identifying regional and particularly distant metastasis. volume measured and bladder reimaged for same length of time. c. Urine volume passed (ml) x bladder count after micturition ________________________________________ Residual volume (ml) = Bladder count before micturition –after micturition GASTROINTESTINAL TRACT oesophagus → Primary role of radionucleides in a. Indirect technique → At the end of standard renogram.g. cyst. Cystourethrography For (1) Vesicoureteric Reflux (VUR) a.5-37 mBq) then serial films or computer images taken by seeing bladder activity and ureteric reflux is seen (data is acquired at 5-10 min interval throughout filling and emptying). Motility disorders e. Procedure: Bladder is catheterized and 99mTc-Pertechnetate instilled to max bladder volume in saline solution (18. 2. hematoma. Incidence of VUR underestimated as bladder is not always fully distended. Direct technique – same as MCU but radiation does is less. when radionucleide reaches bladder. 2. Renal trauma: Renal contusion causes generalized decrease in function or localized filling defects. . However in urogram there is only delayed excretion. patient is asked to void and activity is seen. achalasia and scleroderma. fistula. b. Tumors: In static image no features to distinguish carcinoma.

3. Gastric emptying curves for solids and liquids 2. allows visualization and characterization of antral contractions and for correlation of antral frequency and amplitude with gastric motility i. Assessment of inflammatory bowel disease Investigation of GI Bleeding a. Suspected GI bleeding b.e. greater antral motility faster emptying. Gastric emptying scintigraphy: Radiolabelled eggs with 99Tc-sulphur colloid is given to patient and H2O labeled with 111In DTPA → digestion completed within 10 minutes and simultaneous anterior posterior images are taken at regular intervals up to 50 percent and 100 percent emptying.384 Seminar in Radiology Stomach 1. Solid and liquid data plotted as percent retention of food in stomach over time. Gastric emptying of solids is sigmoidal in shape and characterized by initial shoulder with little emptying called as lag phase followed by prolonged linear phase and finally slowed phase. Liquid phase follows single exponential phase. 99Tc-sulphur colloid Two radionucleide . Dynamic antral scintigraphy: Dynamic imaging of stomach. Small intestine: Indications: a. Detection of Meckel’s diverticulum c. The geometric mean of gastric counts is calculated.

Focal diminished uptake. hydatid cyst. This increases with each circulation and radioactivity is deposited at bleeding site.1 ml/min. the site is identified by extravasation of radiotracer. In patients with normal functioning liver. • 99Tc-labeled red cells : autologous red blood cells which constantly circulate and extravasation can be seen at bleeding site. Localized low activity (defect) → created by a lesion that does not contain reticuloendothelial cells. Large liver → Malignancy. If active bleeding is taking place. Small liver → Cirrhosis. • Normal liver is roughly triangular with curved margins following the contours of diaphragm and rib cage. Inflammatory Bowel Disease 111In – labeled leucocytes migrate to inflammatory site and estimate the extent of disease. Metastasis (90% sensitivity). partial hepatectomy 3.W. A small portion is also absorbed by bone marrow.Common Radiopharmaceuticals Used in Various Systemic Disorders 385 b. amyloidosis and hemo- chromatosis. Site of bleeding may be identified when bleeding rate is low as 0. spleen and bone marrow. Cleft is seen between Rt and (Lt) lobe. 80 to 90 percent dose taken up by Kupffer cells in liver and 5 to 10 percent by spleen. Technique: Two to fifteen mCi of Tc sulfur colloid is injected intravenously. 2. Uses 1. Liver: Radionucleide imaging of liver is performed by using 99Tc sulfur-colloid or albumin which target the reticuloendothelial system. early cirrhosis.) is used and concentrates in gastric mucosa (parietal cells ) in both stomach and diverticulum and subsequent images are taken at 5 to 10 minutes of injection. Meckel’s Diverticulum 99 Tc pertechnetate (IV 50-200 μ Ci/kg B. Observed in following conditions: Abscess. Tc-labelled autologous red cells • Tc-sulfur colloid is given IV and cleared from circulation by reticuloendothelial cells of liver. primary neoplasm angioma and hemangioma. • If patient is known to have compromised hepatic function. . optimal concentration of sulfur colloid will take longer time and imaging should not begin before 20 to 30 minutes after injection. imaging may begin 5 to 10 minutes after injection and anterior and posterior images of liver and spleen are recorded. near the surface and size more than 2 cm can easily be detected. Increased activity in lower abdomen usually on right side is recorded.

g. congenital deficiency of hepatocyte function.g. increased competition from enlarged spleen (e. portal vein occlusion) or from skeleton are observed. Persistent non-visualization of gall bladder is an indicator of cystic duct obstruction however liver. Neonatal and childhood jaundice → Scintigraphy has important role to define surgically correctable disease e. 99Tc HIDA to study the action of biliary tree. bile duct and gut are demonstrated. extensive metastasis. ↑ Splenic size + ↑ blood flow → seen in conditions as malaria. cyst and hematoma (most important following blunt trauma) represents zone of ↓ activity. myelosclerosis. 5. Obstruction of biliary tree if failure to demonstrate intestinal activity even at 24 hrs. Spleen: Radionucleide imaging is an important investigation of suspected morphological and functional abnormalities of spleen and 99Tc colloid is used for the purpose. Biliary tract: 99Tc-Iminodiacetic acid e. infarction or lymphoma. so marked fall in hepatic activity and relatively high activity in caudate lobe. 2. . i. biliary atresia. Delayed excretion → Impaired hepatic perfusion. takes place Precautions Inadequate period of starvation may give false positive results in normal subjects. Heart damaged 99Tc-labelled or Cr labelled RBC’s used for functional studies. Technique HIDA (80-160 mBq) IV scan gives information about hepatic parenchyma in Ist 10 minutes. metastasis. Budd chiari syndrome → There is occlusion of hepatic veins. extahepatic biliary tree is outlined by 20 minutes and excretion into bowel by 1 hr.g. iv. cirrhosis of chronic infection iii. 3. The activity will be lowered than would be expected from size of spleen. Diffuse low activity → Low activity is compared with other structures thus accumulation over the vertebral bodies is an indication of poor hepatic accumulation usually due to diffuse hepatocellular failure. ↑ Splenic size + No ↑ blood flow → e.386 Seminar in Radiology 4. This condition can be excluded if tracer enters small intestine. Acute cholecystitis → Scintigraphy has high sensitivity in diagnosis. leukemia. portal vein thrombosis). decreased hepatic perfusion (cirrhosis. Cirrhosis → increased activity in spleen as compared to liver ii.g. Localized filling defects → seen in conditions as infection. Indications 1. Other positive findings for acute cholecystitis includes.

Citric acid is given to see capacity of glands to discharge secretions. Cystic duct sign → ↑ uptake in cystic duct proximal to obstructing calculus. If there is persistent activity. denotes an air trapping e. RESPIRATORY SYSTEM Radionucleide scanning is of most value in diagnosis of pulmonary embolism. b. b. Portovenous shunts → Tc sulphur colloid is used to detect shunt patency. Partial obstruction and ectasia of ducts → there is symmetrical delay in discharge of secretions. Chronic cholecystitis → There is delayed gall bladder filling after 1 hr with otherwise normal visualization. Kr-81 is exclusive marker of ventilation rate. Symmetrical accumulation in glands at 5 min and in mouth for 20 to 30 minutes. Kr-81 → (Photoenergy 190 KeV and t½ = 13 sec) is generated by decay of cyclotron produced Rubidium and has short half life so administered continuously.g. Abdominal sepsis – e. Clinical Uses a. • Cholecysto-duodenal fistula • Cholecysto-colic fistula • Choledocho-duodenal fistula Miscellaneous a. Tumors – Localized filling defects are seen except Warthin’s Tumor which traps pertechnetate and cannot secrete it. 133 Xe (t½ 5-7 days) is inspired and 10 sec.g. . emphysematous bullae.Common Radiopharmaceuticals Used in Various Systemic Disorders 387 a. Chest film and ventilation scan are recommended. . so remains hot. subphrenic abscess 80 M Bq 67Ga citrate IV injection → 6 hr. Rim Sign → increase uptake within adjacent liver b. Salivary glands: 99Tc Pertechnetate 75 mBq IV given and serial images at 5 min interval are taken. Next the mixture of 133Xe is rebreathed with air to reach equilibrium and then rebreathing is discontinued. Ventilation Scan a. 5.g. Serial images are recorded during wash out phase. Dry mouth – poor or absent salivary gland activity. c. e.show localized accumulation in abscess. b. This record shows the distribution of inspired air with areas of low activity representing poor ventilation. Image after single deep inspiration is recorded. 4. later. Biliary leak: Following surgery or trauma loculated or free tracer can be demonstrated in peritoneal cavity in biliary fistula.

and cleared from lung over next 12 hrs and then metabolized in liver. 3. Anterior. the distribution of radioactivity is even and parallel in both ventilation and perfusion images. This pattern is distributed in many conditions. bronchial obstruction. Decreased perfusion is seen in mechanical artery obstructions. Pulmonary embolus). Bulla/ Collapsed segment). pneumonia or redistribution of blood flow in mitral stenosis with pulmonary hypertension. example chronic or reversible pulmonary tuberculosis.3 days • Energy (191 KeV) 81 KeV • Limited availability (generator shelf life 1 day) Self life (2 weeks) • Expensive Cheaper • Easy to use in children and dyspnea Required cooperative patient • Can be performed after perfusion Must be performed before study available perfusion study unless computer substraction available • Multiple projection for imaging Single projection only • Wash in phase only Wash in phase plus equilibrium and wash out phase (volume air trapping) • Good quality images Less good (low energy) • SPECT possible Not practicable 2. 99Tc microspheres of uniform size (40μm) are most widely used. . Pulmonary embolism: Perfusion scintigraphy is sensitive but not specific. they are injected intravenously. so ventilation scan is combined to improve specificity. etc. Diminished ventilation leads to corresponding impaired perfusion (e. posterior and lateral oblique images are taken. the more dependent part of lung is slightly more perfused than rest of the lung. Decreased perfusion and normal ventilation (e.g. Uses 1. alveolar hypoxia due to air trapping.388 Seminar in Radiology Comparison of Inert Gases for Ventilation Imaging 81m 133 Kr Ke • t½ = 13 sec (Parent 81 Rb 4. Any pathological process that causes complete replacement/destruction of lung parenchyma produces matched defects on ventilation/perfusion scan (where both ventilation and perfusion are decreased) seen in conditions as obstructive pulmonary disease.g. Ventilation/Perfusion Ratio (V/Q): In normal scan. Cardinal sign of pulmonary embolus is under perfused part of lung on perfusion scanning (segmental defect) while ventilation scan is normal known as mismatched perfusion defect. sarcoidosis. Lung activity is proportional to its perfusion. Perfusion studies: The principle of perfusion scanning is that particles greater than 80 to 100 μm size of lung capillaries trapped during first pass through lung.6 hr) 5.

paratracheal lymphnodes. dementia. Supplementary to CT & MRI where results are inconclusive.g. bronchiectasis. Solitary pulmonary nodule is detected (Benign vs malignant).g. Major use in cerebrovascular disorders and neuropsychiatric disorders e. 4. Minute peripheral embolization following clot breakdowns may be overlooked if emboli are distributed evenly. Indications 1. 2. Partial occlusion of both main pulmonary arteries by saddle embolus produces symmetric scan. Gallium has affinity for granulomatous lesions in lung. For detection of occult infection (directed extrathoracically). Other lesions causing localized perfusions defects: Lung tumor. 3. etc. Gallium scanning: It has photon energy of (240 KeV) and t½ of 78 hrs. First choice in detection of venous sinus thrombosis and early cerebritis. 3. 5. lung abscess. 3. CT and MRI unavailable. radiation pneumonitis and fibrosis. CENTRAL NERVOUS SYSTEM SPECT and PET using both blood flow and metabolic agents produce images of physiologic and biochemical processes in brain. mimics metastasis. parotid glands.Common Radiopharmaceuticals Used in Various Systemic Disorders 389 Reverse mismatched defects → Conditions where perfusion abnormalities are more than ventilation scan or vice versa. acute partial bronchial obstruction. 3.g. 2. Uses 1.g. ↑ FDG uptake in chest infection. V/Q perfusion studies are used for preoperative assessment of large bullae and assessment after lobectomy. metallic implants. possible also by CT scan. Important role in staging lung cancer. tuberculosis. 2. For staging of Ca bronchus. Uses of PET 1. pneumonia. granuloma of sarcoidosis increase uptake in hila. e.g. b. e. e. Gallium is taken up in the areas of inflammation. lobar consolidation/collapse. Chronic obstructive pulmonary diseases. • Scintigraphy underestimates embolic disease in two conditions: a. exacerbation of chronic infection. granulocyte activity and in some tumors. . metabolic and degenerative disease. Where CT and MR impractical and unsuccessful e. More sensitive than CT scan for mediastinal assessment of squamous cancer of lung and whole body imaging for distant metastasis. 2. 4.

iii. potentially at risk. To determine stroke etiology. symmetric in uptake and clearly evident. high photon yield (140 KeV) c.ethyl cysteinate dimer – more stable than HMPAO Normal study: Transaxial coronal and sagittal images of cortical and subcortical structures readily discernible. In . • In subacute phase (5-14 days) accuracy rate of SPECT decreases significantly because of luxury perfusion (limitation of SPECT) which may mask initial area of hypo or absent perfusion with an apparent normal or increase area of uptake b. ii. 99mTc-Clucohepatonate c.390 Seminar in Radiology Principle: Radionucleides reach brain tumors and lesions by breach in blood brain barrier due to ↑ vascularity.e. 99Tc. thalami. Another application of SPECT for TIA is to detect adequacy of cerebrovascular reserve which is given by acetazolamide challenge test carbonic anhydrase inhibitor augmented SPECT imaging. Identification of reversible ischemia. Tc as Naperteslmatate a. TIA (Transient Ischemic Attack) i. Identifying patients at risk-persistent focal decrease in cerebral blood flow on SPECT in post ictus is of clinical significance. 99Tc DTPA-faster renal clearance b. This suggests an area of ischemic brain tissue surrounding infarction i. it is important for planning of treatment and in differentiating patient with low flow state due to carotid disease from patient with thromboembolic disease. occipital lobe. I labelled Iodoamphetamine is lipo- (Sodium preteslmatate) philic and crosses blood brain barrier (passive by diffusion) and has high 1st pass extraction and retention by binding to amine receptor sties b. Radiopharmaceuticals Non-diffusible tracers Diffusible traces 99 123 a. visual cortex evident as areas of more intense activity. c. 99Tc labelled HMPAO is most widely used and determines regional cerebral perfusion determined t½ = 6 hrs. reactive edema and altered celleualr metabolism.. Detection of acute ischaemia →SPECT is more sensitive than CT in early detection of acute ischemia (85-95%) and defects are larger than CT study. abnormal permeability. basal ganglion. Frontal lobe is demarcated from temporal lobe by Sylvian fissures. midline structures. Cerebrovascular diseases a. Clinical Indications 1.

PET a. cerebritis – due to herpes. Poor or low uptake indicates necrosis. High grade glioma show ↑ FDG uptake (worse prognosis) • Important in differentiation of Tumor recurrence vs.hypoperfusion in interictal state and hyperperfusion in ictal state. increase carbondioxide causing vasodilatation and increase flow. Neuro-Psychiatric diseases • Alzheimer’s disease → SPECT shows diminished perfusion in temporal lobes and parietal lobes however multi infarct dementia shows patchy and irregular defects. 4. – To differentiate Depression from Dementia. e.g. if mature abscess ↑ activity ring with inactive center. Role of PET in stroke → Stage of early infarction (denotes neuronal injury and inactivity). In Ischemia Stage of misery perfusion Stage of luxury perfusion (↑ oxygen extraction fraction) (↓ Oxygen Extraction Fraction) Miscellaneous a. In areas of decrease flow where there is already maximum vasodilatation (loss of cerebrovascular reserve) and no augmentation of cerebral blood flow on acetazolamide administration and ↓ tracer uptake on SPECT. defects in primary cortex and deep structures show normal flow in SPECT study in patients of depression and decreases perfusion in dementia.g.there is deficit in frontal or fronto-temporal area • Huntingtion’s disease → the deficit is in caudate lobe. Inflammatory disorders. single ill defined ↑ uptake area in temporal lobe. 2. Meningioma and high grade glioma show increased uptake where as pituitary ademoma and low grade glioma show decrease uptake. necrosis → High FDG suggests recurrence. ↓ FDG metabolism in parietoccipital regions b. PET: FDG uptake is directly proportional to metabolic activity of brain.Common Radiopharmaceuticals Used in Various Systemic Disorders 391 patients with normal cerebrovascular reserve after acetazolamide administration. PET → Detects seizure focus and its accuracy is 85 percent. It is marker of tumour proliferation. 3. Cerebral Tumors SPECT study: Degree of uptake is directly proportional to neovascularization and edema e. Epilepsy SPECT → Useful for localization of seizure it’s site and type . FDG scan show hot seizure focus during ictal state (↑ uptake). It distinguishes different causes of dementia • Pick’s disease . Interictal scanning with SPECT is less sensitive than during Ictal state. Important for surgical resection of focus. . C11 methionine is used.

131I. Detection of localization of CSF rhinorrhea → pattern of radioactivity distribution localizes site of fistula. iv.3 hrs. Ectopic thyroid: Activity can be detected in lingual/thyroglossal duct and retrosternal area. 99mTc pertechnetate – the usual activity given to adult is 100 mBq intravenously and scanning begins 30 minutes later and serve as base line for detecting cold areas and determining vascularity of palpable nodules. Thallium 201 → used in various disorders of patients with residual or recurrent thyroid cancer. and surrounds hemispheres in 24 hr. warm (equal). If activity in dilated ventricles and absent activity over the cerebral hemispheres for more than 24 hr.392 Seminar in Radiology b. sylvian and interhemispeheric fissure in 3 to 6 hr.04 days. low radiation does (γ energy 364 KeV) (it is excellent for functional study of thyroid tissue) • Disadvantage → limited availability and high cost of production as it requires cyclotron. Uses 1.It has long t½ 8. activity is less than normal. Radionuclides i. only delayed appearance of activity 2. 123I – It has short t½ 13. iii. These nodules are usually cold (less). Obstructive hydrocephalus → Ventricular reflux is seen in early images and delayed clearance to hemispheres. however. ii. Radionuclide Cisternography 111In DTPA or 99Tc DTPA in Lumbar subarachnoid space. denotes obstruction. 2. Venous sinus thrombosis → failure to visualize superior sagital sinus or cut off transverse sinus. ENDOCRINE SYSTEM Thyroid gland: Principle → The ability of thyroid gland is to trap iodine or iodine analogues as Tc → pertechnetate forms basis of thyroid scanning. and emits high radiation dose (γ energy 364 KeV) so unsuitable for diagnostic purposes but it is valuable as therapeutic agent. there is visualization of cisterns in 1 to 3 hr. In non-communicating → No reflux. Shunt Patency 3. and hot (greater). Uses 1. . Thyroid nodule: Activity according to relative accumulation of radionucleide in comparison with rest of thyroid tissue.

Se-75)-6β- Selenomethyl norcholesterol) are used to identify mass in cortex. Almost all cancers → < 1 percent iodine collected after 24 hrs of injection. Bilateral involvement denotes hyperplasia. and the thyroid component is subtracted by doing 99Tc MIBI scan. Relative ‘hot’ area is due to hyperfunction of normal tissue in thyroid gland damaged by surgery/radiation/Hashimoto’s disease iii.Common Radiopharmaceuticals Used in Various Systemic Disorders 393 a. • Grave’s disease → There is uniform tracer distribution in enlarged gland. 3. a.g. Autonomous foci in toxic multinodular goitre c. Hot: Activity is greater than that of surrounding thyroid tissue i. Adreno cortical . In this test thallium 201Chloride is taken up by thyroid and parathyroid. In hyperparathyroidism Sensitivity is of 90 percent for single adenoma 75 percent of recurrent hyperparathyroidism. 3. Conn’s Tumor → usually due to aldosterone secreting adenomas give increase activity on lesion site. non-uniform patchy alteration in tracer distribution. hyperplastic or colloid nodule. Non thyroid masses → Parathyroid cyst or tumor/ lipoma/lymph nodes b. 4. Increased cortical function gives rise to increase activity. ii. Warm: Activity of nodule may be equal to that in remainder of gland and these nodules are rarely significant clinically. Generalized Disorders • Hashimoto’s Thyroiditis → There is enlargement of gland and generalized. Fifty percent functioning autonomous nodules ii. It is an analogue of guanethidine which is concentrated in sympathoadrenal tissue. iii. Cold: Activity is less than rest of surrounding thyroid tissue i. Uses a. In cushing syndrome – usually there is functioning adenoma which shows high activity over one adrenal only. Adrenal Gland Adreno cortical Radiopharmaceuticals Adreno medullay 1. Parathyroid gland → Thallium substraction scanning is widely used. 2. Benign cold nodules → Adenoma (35%) focal thyroiditis.131I or Se labelled cholesterol (e. Adrenomedullary agents – 131I labelled MIBG is used. leaving only parathyroid activity. .

(2) Vertical long axis. • Grading of defects → a. • Myocardial infarction → ↓ perfusion to region on both stress and rest images and appears fixed and defects can be seen. severity and degree of redistribution. This denotes resting coronary blood flow. . Severe defect → Activity that is not significantly different from background. Technique → Injection of thallium is given during final minute of peak exercise and image of heart are taken immediately known as stress images and patient is allowed to rest for 2 to 4 hr. so on imaging Lt ventricular lumen appears larger on stress images and wall will appear thinner. it is K+ analogue.394 Seminar in Radiology → Primary and Secondary Pheochromocytoma and neuroblastoma . Normal b. and then delay or redistribution images are taken. CARDIOVASCULAR SYSTEM Myocardial Perfusion Imaging • Perfusion agents → Thallium 201 is used. • SPECT images are displayed in three planes of heart (1) Short axis. In defects. and uptake is dependent on myocardial blood flow. d. Radionucleide scanning is also useful in monitoring response to neuroblastoma treatment. Increase end diastolic pressure causes increase in Lt atrial and pulmonary capillary pressure. • Severe disease or (Lt) ventricular dysfunction → Left ventricle may decompensate with exercise causing decrease in systolic function and stroke volume increase. we assess size. Mild defect → showing noticeable defect and in counts also but no definite wall thickening. so significant portion of thallium is seen into lungs and increased pulmonary activity is noted. (3) Horizontal long axis. c. This results in transient increase Lt ventricle end diastolic pressure and cavity size. • Normal lateral wall show greatest activity. Moderate defect → More reduction of count so that wall appears thin.↑ uptake in adrenal medulla. It is a cyclotron product and t½ is 73 hrs. Therefore used to assess hypoperfusion or ischemia in wall of heart. basal septum least and part of annulus fibrosus structure of heart does not take up perfusion agent. Uses • Exercise induced ischemia (Transient ischemia) Relative perfusion defect on stress images → fills or redistribution on delay or rest images.

It is an inotropic agent and increases myocardial O2 demand. not persistent enough to cause necrosis result in temporary failure of mechanical function which may recover with time. concentrates in inversibly damaged myocardium. Two conditions where. Thallium 201-SPECt is more cost effective and relatively simple procedure requiring standard reinjection of thallium before the resting scan. dipyridimole or adenosine in association with myocardial perfusion imaging.Common Radiopharmaceuticals Used in Various Systemic Disorders 395 • Patients who cannot perform physical exercise. Dobutamine is widely used. This is an alternative method. • Hibernating myocardium: Results from chronic severe ischemia when residual perfusion is enough to support life and membrane function but not contractile function which may recover when adequate perfusion is restorted. Two most important recent advances in cardiac scintigraphy • Gated SPECT Imaging This gives simultaneous assessment of myocardial perfusion and function – Accuracy in diagnosis of coronary artery disease and differentiation of attenuation conventional artifacts from coronary artery disease – Evaluation of ventricular wall motion in area of decrease perfusion. A positive concentration differentiates between infarcted and normal tissue. – Although PET is using 18F-fluorodeoxyglucose as gold standard in identifying metabolic activity in non-contractile myocardium in which function is likely to return. myocardium may appear nonviable but is only non-contractile • Stunned myocardium: In Acute reversible ischemia. pharmacological stress testing (with dobutamine. • Serial evaluation of infarct size. Uses • To differentiate old and recent infarction (12 hr to 1 week after infarction). • Visualization of Rt ventricular infarction. • Infarct imaging agents: Tc labelled phosphates are used. – Residual Lt ventricular function and perfusion following acute myocardial infarction. • Assessment of Myocardial Viability → Indications • Important in patients with multiple infarctions and left ventricular dysfunction and for prediction of degree of recovery of function with revascularization is crucial in deciding to attempt the state of revascu- larization. .

N to 13. Rb-82. Myocardial metabolism → To know viable/non-viable myocardium.g. i. Myocardial perfusion imaging: To detect coronary artery disease. Quantitative myocardial perfusion imaging → by using N to 13-NH3. 4.NH3 and 0 to 15 have been used. 2. reduced perfusion (NH3) and increased glucose metabolism (FDG) is suggestive of viable myocardium.396 Seminar in Radiology PET 1. FDG goes to ischemic but viable myocardium).e. 3. e. Here is 2 to 3 fold increase in blood flow with pharmacological stress. . A PET mismatch pattern or perfusion metabolism mismatch pattern. Cardiomyopathies and chronic heart disease. hibernating myocardium (viable but non-functional) protocol used for viability is resting NH3 and FDG scan (NH3 goes to normal myocardium.

while still allowing necessary activities from which radiation exposure might result. proteins or enzymes.5 Total (approximate) 200 RADIOBIOLOGY • Definition: Study of biological effects of ionizing radiation. At each stage.26 Radiation Hazard and Protection The ICRP (International Commission on Radiological Protection) described in its recommendation 26 – ‘Radiation protection is concerned with the protection of individuals. . This process is not irreversible. When ionizing particles interact directly with (transfer their energy to) vital biologic macromolecules such as DNA.1: Sources and approximate annual levels of radiation Sources Level (mrads/yr) Natural (Background) 96 – Terrestrial 40 – Cosmic 31 – Internal 25 Artificial Medical exposure 93 Diagnostic X-rays 77 Dental X-rays 1 Radiopharmaceuticals 14 Radiation therapy 1 Nuclear weapons testing 4 Nuclear power generation <1 Research activities <1 Consumer products 4 Air travel 0. Ionized atoms can become neutral again by attracting a free electron. Molecules can be mended by repair enzymes. RNA. it is possible to recover from radiation damage. Cells and tissues can regenerate and recover from radiation energy. • Mode of action: Ionizing radiation produces damage in living systems by ionizing (removing electrons from) the atoms composing the molecular structures of these systems. their progeny and mankind as a whole.’ Table 26. An ionized atom will not bond properly into molecules necessary for the normal functioning of an organ.

A substantial dose is required to produce biological effects after irradiation. b. LD50/30 (Lethal dose 50/30): It is the whole body radiation that can be lethal to 50 percent of exposed population within 30 days. hours. life span shortening. erythema. fatigue. • Effects at cellular level a. As 80 percent of the body weight is water so more destructive effect results from indirect action than from direct action. e. Early effects: Appear within minutes.398 Seminar in Radiology damage occurs as a result of what is called direct action. Cells are directly killed or are affected so as to prevent mitosis. Recovery or death It consists basically of three syndromes (a) Hematopoetic syndrome – decrease in all blood cells and their effects (1-10 Gy) (b) Gastrointestinal syndrome – Nausea. seizure. blood disorders. cataract formation embryological or birth effects. fatigue. days or weeks of radiation exposure. b. Acute radiation syndrome/radiation sickness: It occurs after whole body reception of large doses of ionizing radiation delivered over a short period of time. It manifests itself in 4 major stages i. fluid loss (6-10 Gy) (c) Central nervous system syndrome – Stupor. (50 Gy). The four major types of late somatic effects are carcinogenesis. electrolyte imbalance. depression of sperm count. Late effects: It becomes apparent years after exposure. nausea. vomiting. and leucopenia. vomiting. For adult humans. ataxia. intestinal disorders. temporary or permanent sterlity and injury to central nervous system. Manifest illness iv. • Types of effect Ionizing radiation produces the greatest amount of biological damage in the human body when a large dose of high ionizing (high LET) radiation is delivered to large or radiosensitive area of body. These effects are the same for normal and cancerous tissues in that they differ little in their individual response to irradiation. it is called indirect action.No symptoms — lasts for about a week iii. The local blood supply is damaged — cell deaths c. Latent period . infection. agitation. epilation (loss of hair).g. Somatic a. diarrhoea. When a vital molecule such as DNA is acted upon by free radicals previously produced by the interaction of radiation with water molecules. bleeding. diarrhea. etc. Diagnostic radiological procedures do not impart radiation doses sufficient to cause early effects. ii. . Prodromal phase — occurs within hours — may last for hours or few days — nausea. Damaged cells not directly killed but become victims of tissue defence systems. LD50/30 is about 3 Gy (300 rad).

The standard radiation by convention is 250 kVp X-rays. • Doses above the threshold inevitably produce the effect. Nonstochastic/Deterministic/Acute Effects • The effects are not subject to laws of chance or probability. it interacts with the medium.g. and as a result deposits energy along its path. genetic effects and induction of cancer or leukemia. e. Radiation Hazard and Protection 399 Genetic Effects • Caused by gonad irradiation • They effect population as a whole rather than individuals • Progeny of exposed person is affected • Irradiation causes gene mutation and leads to abnormalities e. • Severity of effect is unrelated to radiation dose and there is no threshold below which the effect does not occur. The average deposited energy per unit path length is called linear energy transfer. deafness.g. • RBE (relative biologic effectiveness): RBE describes the relative capability of radiations with various LET’s to produce a particular biologic reaction. congenital blindness. • LET (Linear Energy Transfer) and Its Relationship to Biological Damage – When ionizing radiation passes through a medium. cataract formation and reproductive cell damage.g. – Unit is keV of energy transferred per micrometer of track length in soft tissue. – With increasing LET the ability to produce a biological response increases. radiosensitivity is high – Radiosensitivity increases as the proliferation rate of cells and the growth rate for tissues increase. Dose of standard radiation necessary to produce given effect. • The risk of damaging effect increases with increased exposure but the effect is not inevitable. – Younger tissues and organs are more radiosensitive – When the level of metabolic activity is high. . short term somatic effects and radiation accidents. mental and physical abnormalities. e. • Law of Bergonie and Tribondeau – Undifferentiated cells are more radiosensitive than mature cells. – Alpha particles and ions of heavy nuclei have high LET. Its severity increases with radiation dose. Stochastic/Nondeterministic/Chronic • The effects obey the laws of chance or probability. RBE = Dose of test radiation necessary to produce same effect.

• Care rather than fear. hence it should be minimized by conducting procedures as quickly as possible.2: Groups of persons requiring protection and protective measures Groups of persons requiring Protective measures protection • Those outside department • Architectural problem • Definitive construction features – Thick walls – Barium plaster • Those within the X-ray dept. c. Table 26. Speed or exposure time: Where the radiation beam is produced continuously. This implies that actual absorbed dose equivalent values should be kept well below their recommended maximum limits. Hence the use of long exposure cables for the hand switch in mobile radiography. viz. the amount of radiation received will clearly be proportional to the length of exposure time. • Benefit vs risk ratio should be high. – Radiation workers • Remember inverse square law • Protective devices — lead apron gloves • Personal monitoring devices – Auxillary staff. or the use of remote control in fluoroscopy is always safe. Distance: Keeping adequate distance is an effective method to control radiation. are more susceptible to radiation damage than is the child or the adult. This concept was put forth by NCRP by 1954. Barriers/shielding: The protection problem in X-ray rooms include not only the primary radiation. but also leakage of radiation emerging through the shield of the X-ray tube. • Severity of harm is proportional to dose and dose rate. Cardinal Methods to Control Radiation — Basic Principles The three fundamental principles of radiation protection of staff are: a. b. and scatter radiation from all irradiated objects (especially the patient). It follows inverse square law (the intensity of radiation decreases as the square of the distance between the source and detector or body). or using short bursts of fluoroscopy and image storage facilities.400 Seminar in Radiology This law indicates that the embryo and the fetus which contain a large number of immature nonspecialized cells. clerks • Should not sit/stay/wait or work in a unprotected room – Patients • Judicious examinations • Gonadal shields • To follow instructions RADIATION PROTECTION • Principle of alara: To reduce radiation dose to value which is “as low as reasonably achievable” consistent with achieving the maximum benefit which the use of ionizing radiation can produce. . A.

Calculation of Thickness of Barrier It is done by HVL (half value layer). and during fluoroscopy all fixed barriers are considered secondary including control booth. Primary barriers: Any barrier that intercepts the useful X-ray beam e.g. 2 mm lead is equivalent of approx 25 mm layer of high quality barium plaster. gonad shields. Barium concrete iii. the ceiling is always considered a secondary barrier. and 150 mm concrete. It is the thickness of a specific substance which when introduced into the beam of radiation will reduce the exposure rate by half. Radiation Hazard and Protection 401 Types i. Lead (aprons. ½ inch barium plaster. Brick. e. Secondary barriers: Any barrier that intercepts leakage and scatter radiation. gloves. 1º barrier 2° barrier For ceiling U=0 U=1 For floor U=1 U=1 For walls Depends U=1 .g.1 rem/wk for a controlled area or is less than 0. Factors Determining Barrier Thickness 1. collimation systems and the shielding features of intensifier housing etc. goggles) ii. It should be considered while designing the room (by the radiation protection advisor) and by the equipments manufacturer in the design of tube housings. 225 mm solid brick. the floor is nearly always considered a primary barrier and anywhere from one to four walls may also be primary barriers. Use factor (beam direction factor – U) – The fraction or percent of time that the beam is directed to a barrier while energized is the use factor. Concrete iv. Materials i. 3.01 rem/wk for uncontrolled area. Distance of the barrier from the radiation source – Follows inverse square law – No barrier is required if total exposure at a point in question is less than 0. Primary radiation will generally require larger thickness of shielding material than scattered radiation. Quantity of X-ray generated per week or workload 2. ii.

it is most important that a radiation protection plan is worked out to supplement the layout drawings.g. Controlled area • Area where adult employee is likely to receive >3/10th of any relevant dose limit (e. rest rooms (T = 1/4) c. LE is that thickness of lead in mm which affords the same protection as the barrier in question for the same radiation quality kVp. etc. Classified person — staff who are likely to receive 3/10th of dose limit in the course of their work are described as classified workers.e. Patient undergoing therapy or diagnostic procedure. Partial occupancy – corridors. B. Occupancy factor (T) – It is an expression of the extent of time to which the area being protected is occupied. Occasional occupancy – outside areas. elevators.g. c. Supervised area • Area where any person would be likely to receive >1/3rd of the value required for designation of controlled area (e. Any other person under a written scheme or work. 5. full occupancy – office or laboratory adjacent to the X-ray department T = 1 X-ray room (T = 1) b. Designer/construction: When planning an X-ray department. within a. • Other barriers are compared to lead in terms of their lead equivalence. Tasks at Different Levels for Radiation Protection 1. Radiation protection plan distinguishes between controlled area and other areas. – An area that is always occupied will require more shielding than one which is rarely occupied. 5 mSv whole body dose / annum). b. 15 mSv whole body dose per annum) • It embraces all rooms with X-ray equipment • Permitted assess is to a. It is particularly effective in attenuating radiation by the process of photoelectric absorption and compton scattering. dealing with functional requirements as well as the installation and building drawings which is approved by relevant authority and is compliant with the national protection regulations and/ or international recommendations. . Type of radiation (primary or secondary) falling on the barrier Value of Lead as Barrier • Lead has high atomic number (Z-82) and high density.402 Seminar in Radiology 4. Levels of occupancy in areas adjacent to X-ray rooms as suggested by NCRP (National Council on Radiation Protection And Measurements) In controlled area i.

Rectification c. Tube shielding ii. radiography a pregnant patient. 3. • The administrative chain of authorities include: a. Administrator • Overall supervision and coordination of the radiation protection activities (like personnel monitoring) in the X-ray department. viz. Factors within radiographers control . waiting rooms. Radiation protection supervisor for immediate supervision on a day to day basis. • Radiographer: i. • The radiographic control console should always be located behind a fixed protective barrier. • Permitted access is to those whose presence is necessary. tube housings and tube transformer assemblies must be supplied with accompanying instructions containing all information—on safety. Factors not within radiographers control a. advice and guidance to radiographers as and when required. ICRP ↓ AERB (atomic energy regulation board) ↓ BARC (Bhabha atomic energy research center)   DRP (Division of Radiological DRPS (Division of radiological Physics) protection services) Users • Radiologist i. Avoid unnecessary radiography ii. Equipment manufacturer and installation • Should be AERB / BARC certified • X-ray tubes must posses proper filters • All X-ray tubes. offices. Beam filtration b. Radiation Hazard and Protection 403 • It embraces other rooms of X-ray department and other areas. Supervision. c. streets or gardens in close vicinity of X-ray room. viz. Radiation protection advisor—physicist d. Appointed doctor—for medical surveillance of classified persons. District health authority / state government—for monitoring of radiation protection. b. Often the barrier is equipped with leaded glass window. 2.

To re-examine fluoroscopic images. ii.g. the patient is not exposed to further radiation dosage. Measures in fluoroscopy a. Use of autotimers to control exposure time h. Measures during examination . Selection of appropriate grid j. Patients that require assistance during examination should never be held by X-ray personnel but by member of patients family or by mechanical devices. Provide adequate shielding of radiosensitive regions (e. Use of fast screen/film (consistent with required unsharpness) c. i. Meticulous film processing f. Correct operating factors—exposure rate to the patient is actually reduced by an increase in kV and filtration. d. Compression on obese patients k. b. Minimize the use of X-rays during pregnancy and shield the fetus. as may happen with some functional examinations or when the time factor is important. Careful centering d. gonads). and a corresponding decrease in mA to retain same image brightness. c. Examine the possibility of using alternative techniques (e. ultrasound). In fluoroscopy: 1. Highest practicable kV g. Confirm that the examination has not been already done at an outside clinic or hospital from which the patient has been referred. Optimum exposure parameters e. Use of gonadal shields as appropriate i. Use of image intensifier instead of fluoroscopy 3. an image storage unit should be used. Radiation not to be continuous / intermittent fluoroscopy 4.g. Optimum collimation b. Adequate dark adaptation 2.404 Seminar in Radiology a. Pre-examination measures: a. Restriction of field size—suitable collimation 5. In this way. It is to be carried out when it is expected that a radiograph will not supply the necessary information. General Precautions for Patient’s Protection In general it may be stated that almost anything which will help to reduce patient doses will also tend to reduce doses to the staff directly concerned with radiological examinations. b.

Rotational scheduling of personnel. Provision of lead aprons and lead gloves 4. ii. In order to avoid repeat exposures. should be allowed within the room 2. iii. Optimum collimation 2. Use of autotimers to control exposure time. Use of highest practicable kV 4. General Precautions-Staff 1. The individual workers lifetime effective dose should not exceed age in years × 10 mSv (1 rad). Deterministic effects: i. The effective dose in any one year should not exceed 50 mSv (5 rem) b. Do not hold the patient during radiographic examination 9. Stochostic effects: i. . Post-examination measures: Implement a strict quality control program to minimize repeats. 3. especially tube leakage which should give a dose rate in air of less then 1mGyh-1 at 1m. PERMISSIBLE DOSES • Limits for occupational exposure: NCRP recommends: a. 500 mSv (50 rem) for localized areas of skin and the hands and feet. Use image intensifier. Adequate personal monitoring 6. 150 mSv (15 rem) for lens of eye ii. 2. Testing the equipment for performance. Patient care—position properly and give instruction against moving (27% cases). following measures should be adopted: 1. not fluoroscopy 6. Film care—use proper film and processing techniques (15% cases). whose presence is essential. Keep exposure records for staff 7. Never stand in the primary beam 8. and no occupational exposure should be permitted until the age of 18 years. Use of correct beam filtration 3. Should remain behind a lead screen when radiographs are taken 3. Use proper exposure conditions—do not over-or underexpose (52%). Only those. Use carbon fiber table tops to reduce dose 5. 5. Radiation Hazard and Protection 405 1.

should not exceed 1 mSv (0.5 mSv (0. To replace the old MPD formula. infrequent 5 mSv/year Averaged over 5 years exposure – Dose equivalent limits of lens of 50 mSv/year eye.406 Seminar in Radiology • Summary of Recommended Dose Limits NCRP ICRP if different Occupational exposure – Cumulative 10 mSv × age 20 mSV/year averaged over 5 years – Annual 50 mSv/year – Lens 150 mSv/year – Skin. exposed as part of their educational experience. the NCRP recommends limiting the cumulative absorbed dose equivalent in rem to the occupationally exposed persons age in years. Eighteen-year-old students.05 rem) per month.5 mSv/month Total of 2 mSv to effective dose limit abdominal surface Public exposure (annual) – Effective dose limit. Therefore. skin and extremities Negligible individual dose (annual) 0.001 rem) has been set. The formula.01 mSv/year No statement • Recent changes in NCRP recommendations: Recommendation in NCRP report no. To reduce exposure for pregnant female members of the medical radiography team. This means that below this absorbed dose equivalent level it is not necessary to try to reduce individual exposure. an annual effective absorbed dose equivalent of 0. MPD = 5(N – 18) rem [MPD = 50 (n – 18) mSv].5 rem) “not be received at a rate greater than 0. the cumulative absorbed dose equivalent should not exceed the age of the individual in years × 10 mSV (years × 1 rem). To provide a low-exposure cut-off level so that regulatory agencies could dismiss a level of individual risk as negligible. 91 now supersede those contained in NCRP report no 39. Radiography students are another important absorbed dose equivalent limiting consideration. continuous or 1 mSv/year frequent exposure – Effective dose limit. A summary of some of the important changes follows.1 rem) annually. was abandoned by the NCRP (NCRP report #91). governing cumulative whole body occupational exposure. .01 mSv (0. the NCRP now recommends that the effective absorbed dose equivalent limit for the unborn child (5 mSv/0. hands and feet 500 mSv/year Embryo or fetus exposure: 0. skin and extremities Education and training exposure annual – Effective dose limit 1 mSv/year No statement – Dose equivalent limit for lens of 50 mSv/year No statement eye.

⇒ Also availability of rapid and easy tests to confirm pregnancy (viz. She may be provided with a second personnel radiation monitor with instructions to wear it at waist level under the protective apron. Early conception iii. urine test and USG) makes the value of 10-days rule controversial. Radiation Hazard and Protection 407 PREGNANCY • Procedures followed in radiological examination of reproductive age group – The 10-day rule: ⇒ Presently of historical value ⇒ It says that women of child-bearing age who are referred for X-ray examinations of the abdomen. a. If possible. Unnecessary postponement in majority of females. • Pregnant technologist – Arrange an interview with the radiation protection supervisor. a technologist receives less than 500 mrems annually. Miscalculation of the date of monthly periods ii. ⇒ Pitfalls — i. The radiation monitoring report associated with this badge should reflect that it is a fetal dose monitor. the exposure under the protective apron should not exceed 50 mrems annually and the resulting fetal dose should not exceed 25 mrems. – If examination does not involve radiation of the pelvis. – If the examination involves the pelvis of the woman in the reproductive age group. Under normal circumstances. and pelvis should have such examinations performed only during the first 10 days following the onset of menstruation. If answer is ‘Yes’. – Fetal MPD is 500 mrems. Thus. If answer is ‘No’ proceed with the examination b. – In a pregnant patient avoid X-ray examination of abdomen and pelvis in the 1st trimester—delay till third trimester or later if possible. call a staff radiologist—Calculate benefit Vs. b. under most circumstances additional radiation protective measures may not be necessary: – Two measures are easy to carry out. when it is certain that there is no pregnancy. risk and take patient into confidence and obtain her permission to proceed with the examination. – Consequently. as recorded by the personnel monitor. explaining the risks involved and giving the option of a transfer to some other department till term. . ask the patient if she might be pregnant a. then simply drape the pelvic region with lead fabric. she should not be assigned to fluoroscopy or portable radiography.

The equipment used for this purpose is called a “TLD reader”. and this has the same effect as storage for 24 hr. ii. It can have almost any desired shape. Almost tissue equivalent 3. the light output as a function of time follows the pattern shown below and is termed as a glow curve. These materials are available either in powder form. it is usual to delay the read-out for at least 24 hr and so that the response is independent of the actual time between exposure and read-out. . • Conclusion (from the curve) i. • Technique: The material is kept in the intended area. Small in size and chemically inert 2. • The glow curve: When a previously irradiated sample of LiF is heated at a constant rate. Read-out system consistent and suitable for automation 7. the material/after exposure but before read-out may be preheated to 100ºC for about 5 min. Radiation excites electrons from the material and are trapped at impurity trap sites.408 Seminar in Radiology DOSIMETRY The term refers to detection and measurement of ionizing radiation Thermoluminescent Dosimeter (TLD) • Principle: The quantity (brightness) of light emitted is directly proportional to the radiation dose. Maximum light emission occurs at temperatures 150 to 270°C. Heat releases trapped electrons and brings them back to the ground state in the form of light (bluish-green in case of LiF. Usable over a wide range of radiation qualities 5. in practice. Alternatively. Small change in sensitivity with radiation quality 4. Read-out is simple and quick (less than 1 min per sample). Therefore. • Thermoluminescent materials: As thermoluminescent materials. calcium sulfate and lithium fluoride are most commonly used. Sensitivity independent of dose rate 6. The response fades off somewhat in the initial 24 hr (later it remains constant). 9. It is a special miniature cassette that holds a tiny film. rods or as chips. The energy gets stored in proportion to radiation dose. 8. Apart from initial fading can store dose over long periods of time. The material is heated in a special oven to a temperature of about 300ºC. The area under the whole glow curve can be used to measure the dose. • Attractive features of a Dosimeter 1. Exposures can be made “in the field” away from the measuring laboratory. Film Badge It is a personnel radiation monitoring device used in photographic method of dosimetry.

the device will be discharged by an amount proportional to the ionization provided by the radiation and the pointer moves across the scale. Wearing Period and Further Procedure Each member of staff should wear a film badge usually for a period of 4 weeks. the film inside is changed. When the electroscope is charged. It has no lead foil backing ii. It is of two types: (i) the self reading type. It has a fast emulsion on one side of the base and a slow one on the other (fast emulsion facing the front of the badge). 2. The exposed film is sent to a radiation protection laboratory (viz. However. where it is processed and the assessed dose is recorded. If the gas around leaves is then ionized. the differences are: i. At the end of the period. the instrument will be discharged. Assessment of radiation dose—Done by measuring the density of the monitoring film from the badge. Types It is the most sensitive personnel monitoring device.000). BARC – Bombay). Film badges have a limited self-life and should be kept in a cool place. Automatic processor is a must for consistency. the leaves diverge because of electrostatic repulsion. Principle Fountain pen dosimeter is based on the principle of a gold leaf electroscope. The casing is usually too thick to allow low energy radiation to penetrate. which contains a built in . this dosimeter must be charged to a predetermined voltage so that the scale reading indicates zero. The fast and slow emulsions enable a wide range of doses to be recorded on one film (1 to 10. However. Radiation Hazard and Protection 409 • Principle: The degree of blackening of film (photographic density) is proportional to the radiation exposure. Requirements of the System 1. Fountain Pen Dosimeter It is a compact portable device which fits the top pocket and can provide a useful safeguard in an area where radiation levels may be high. When placed in a radiation field. it is infrequently used. It can be evaluated daily. Working Before it is used. • Radiation monitoring film: It is similar in appearance to a dental film.

Pocket Ionization Chamber Advantages • Small. • Decreased film sensitivity above and below 50 keV. . • Not effective as a monitoring device if not worn. compact units. only the exposure received in the body area in which it is worn.410 Seminar in Radiology electrometer (a device that measures electrical charge) (ii) The non-self reading type. legally acceptable record of personnel exposure. • Exposure cannot be determined on day of occurrence. • Cost-efficient monitoring for large numbers of people. • Filters contained in the badge make it possible to estimate the direction from which the radiation came. which requires a special accessory electrometer to read the device. reliable manner. • Self-reading chambers provides immediate exposure readout for radiation workers in high exposure areas. gamma. • Reasonably accurate and sensitive. and all but very low energy beta radiation in a reliable manner. durable. • Detects and records small and large exposures in a consistent. • Provides a permanent. • Can discriminate between type of radiation and energy of x-. • Temperature and humidity can cause film in the badge to fog over long periods of time. gamma. convenient to use. • Can be used to monitor x-. • Instrument performance is usually not affected by outside influences such as heat and humidity fluctuations and non-extreme mechanical shock. • Records radiation exposure accumulated at a low rate over a long period of time. and beta radiation. • Filters can indicate whether exposure was due to excessive amounts of scattered radiation as opposed to a single exposure from the primary beam • Control badge can indicate if a group of badges were exposed in transit to and/or from an institution. easy to carry. Disadvantages • Records. • Can be used as monitors for procedures that last relatively short periods of time. Summary of the Advantages and Disadvantages of Personnel Monitoring Devices Film Badge Advantage • Lightweight. • Limited in accuracy to + or –20 percent. easy to carry. causing inaccurate exposure reading.

• Records only the exposure received in the body area in which it is worn. hence. • Calibrated dosimeters must be prepared and read with each group of TLDs as they are processed. Disadvantages • Greater initial cost than film badge service. • Unit is discharged if subjected to some type of mechanical shock and give a false high reading. • Readout process destroys information stored in TLD. which prevents the “read” TLD from serving as a permanent. TLD crystals can be reused. . making the device somewhat cost-effective. pressure or normal temperature changes. Radiation Hazard and Protection 411 Disadvantages • Fairly expensive. • Records only the exposure received in the body area in which it is worn. • Not effective as a monitoring device if not worn. TLD determines dose more accurately. dosimeter must be read each day after it is used. legal record of exposure. • Not affected by humidity. • Readings must be carefully obtained or they may be lost • To avoid inaccurate reading. Thermoluminescent Dosimeter Advantages • Crystals contained in TLD interact with ionizing radiation as human tissue does. • After reading has been obtained. • No permanent. • Can be worn upto 3 months. • Readouts must be carefully obtained or results can be lost. legal record of exposure is provided. hence not cost-effective for large number of persons.

Cigarette smoking. shape resulting from mechanical forces – intrauterine compression from oligohydramnios. Lead • Infection—Rubella. 2. There are four clinically significant types of congenital anomalies 1. 3. Congenital Syphillis. TORCH. functional. Deformation—Abnormal form.27 Ultrasonography of Systemic Antenatal Abnormalities A congenital anomaly is a structural abnormality of any type however it may be structural. • Radiation Ultrasound in Prenatal Screening • To screen for and to detect congenital abnormalities is one of the primary goals of prenatal surveillance. Causes • Genetic factors—Chromosomal abnormalities • Environmental factors such as drugs and virus • Multifactorial inheritance—Genetic and environment factors acting together. HIV. Clinical Markers • Advanced maternal age . behavioral and hereditary. Antibiotic. Varicella. Androgen/ Progesterone. Malformation—Morphological defects of an organ/ part of an organ due to intrinsically abnormal development process. Thyroid drugs. metabolic. 4. • The optimal gestation time to scan for most of developmental abnormalities is 18-22 wks. Disruption—interference of originally normal developmental process due to teratogen. Teratogen • Drugs. Anticonvulsant. • Chemicals—Mercury. Dysplasia—Abnormal organization of cells into tissues (dishistogenesis) affect several organs because of nature of underlying cellular disturbance. Alcohol.

Ultrasonography of Systemic Antenatal Abnormalities 413

• Previous birth of a malformed fetus
• Family history of a malformed fetus
• Consanguinity
• Exposure to drugs/ Radiation
• Maternal Diabetes Mellitus
• Bad obstetric history
• Bleeding in early pregnancy

Sonographic Findings
• Oligoamniotic sac
• Embryonic bradycardia
• Abnormal yolk sac
• Increased nuchal translucency
• Date size discrepancy at 9-12 wks.
• Symmetrical IUGR
• Polyhydramnios
• Oligohydramnios
• Breech presentation
• Twins

Nonsonographic Findings
• Abnormal results from chorionic villus sampling and Aminocentesis
• Abnormal immunoglobulin profile
• Abnormal increase of maternal serum alfa fetoprotein.

FETAL HEAD ANOMALIES
Supratentorial Abnormalities
1. Acrania (excencephaly)
US:
• Absence of cranial vault or calvaria
• Occurs at 10 week
• Partial or complete absence of cranial vault
• Disorganized brain tissue always present
2. Anencephaly
• Occurs in about 1= 1000 birth
US:
• Absence of cranial vault
• Cerebral hemisphere and thalamus are replaced by flattened, amorphous
vascular neural mass covered by a vascular membrane.
Associated fetures:
• Polyhydramnios
• Spina bifida with or without meningomyelocoele
• Cleft lip and palate, club foot and omphalocele

414 Seminar in Radiology

3. Encephalocoele
• Herniation of intracranial structures through a defect in cranium
• Mostly occur in the midline in the occipital region but occasionally
occur in parietal and frontal regions
• Can occur as isolated lesions or associated with other anomalies —
hydrocephalus, agenesis of corpus collosum
• Dandy Walker malformation
US:
• Cystic mass at the surface of skull
• Common in midline
• Contains brain tissue or a visible bony defect
Differential diagnosis
• Cystic hygroma, hemorrhage, teratoma, branchial cleft/cyst and scalp
edema.
4. Holoprosencephaly
Group of disorders arising from failure of normal forebrain development
during the process of cleavage and diverticulation.
• It can be alobar, semilobal and lobar
• Always associated with midline facial abnormalities.
US Appearance
Alobar:
• Interhemispheric fissure and the falx cerebri are totally absent.
• There is a single primitive ventricle (holoventricle)
• Dorsal sac between skull and cerebral convexity
• Thalami are fused in the midline
• Third ventricle, neurohypophysis, olfactory bulbs and tracts are absent.
• The midbrain, brainstem and cerebellum are structurally normal.
Semilobar
• Monoventricular cavity with rudimentary occipital horn
• Falx and interhemispheric fissure form caudally with partial separation
of occipital lobes
• Thalami fused in midline
• Olfactory bulbs and corpus collosum usually absent.
Lobar
• Patient can have nearly normal intellectual development to severe mental
retardation.
• Outcome depends on severity of hydrocephalus.
US:
• Difficult to diagnose prenatally since it form lobes
• Absence of septum pellucidum with fusion or squaring of frontal horns.
5. Hydranencephaly: Seen by 24-26 weeks
• Result of destructive intrauterine insult rather than development anomaly.
• Vascular occlusion of supraclinoid part of internal carotid artery – leading
to destruction of cerebral hemisphere with replacement and sparing of

Ultrasonography of Systemic Antenatal Abnormalities 415

temporal and occipital lobes and basal ganglia with preservation of
brain stem, thalami and cerebellum.
• Falx cerebri may be absent or incomplete but choroids plexus is
preserved.
• Head is filled with CSF and lined with leptomeninges.
D/D:
• Severe hydrocephalus
• Alobar holoprosencephaly
• Massive congenital subdural hydroma
• Postanoxic and infective encephalopathy.
6. Agenesis of corpus collosum:
• Usually development → 12-20 weeks
• Ventricles are displaced laterally with indentation of medial walls
• Ventriculomegaly seen in atrial and occipital region because of poor
white matter development surrounding these areas (Tear drop
configuration).
• Absent cavum septum pellucidum.
• Enlarged 3rd ventricle between the hemisphere seen as in
interhemispheric cyst.
• In the 3rd trimester too many sulci perpendicular to the interhemispheric
fissure showing a ‘sun burst’ orientation radiating from 3rd ventricle.
7. Ventriculomegaly:
• Refers to enlargement of lateral ventricle
• ↑ Width of body, anterior horn and posterior horn of lateral ventricle
• Normal value < 8m, borderline 8 to 10 mm, >10 mm abnormal.
Causes:
• Choroid plexus papilloma
• Intracranial hemorrhage
• Agenesis of corpus collosum
• Dandy Walker malformation
• Congenital infection with TORCH.

Infratentorial Abnormalities
1. Chiari Malformation
• Associated with spina bifida
• Hydrocephalus on USG
• Abnormally pointed frontoparietal region also called “Lemon sign”.
Lemon sign associated with spina bifida causing overlapping of frontal
bones seen in 89 to 98 percent of fetus under 24 weeks.
Can occur in normal fetus and in diverse abnormality →
• Encephalocoele
• Dandy Walver malformation
• Chiari Malformation

416 Seminar in Radiology

Banana Sign
• With effacement of posterior fossa are the result of hypoplasia of posterior
fossa with spina bifida.
• Result in compression of cerebellum with displacement of cisterna magna
• Cerebellar tonsils and vermis herniated inferiorly through the foramen
magnum
• Cerebellum assume a ‘C shaped’ banana sign finding consistent with Chiari
malformation.
2. Dandy Walker Malformation
• Diagnosis made after 18 weeks
• Characterized by midline cyst in posterior cranial fossa communicating
with 4th ventricle
Defect in cerebral vermis — either absent, small or abnormally present
• Hydrocephalus is quite commonly seen
• Dandy Walker variant is more common than the full syndrome
• It has less vermian agenesis
• A small cyst and minimal lateral ventricular enlargement
Associated anomalies
• Agenesis of corpus callosum
• Congenital heart disease
• Genitourinary abnormalities
• Polydactyly
D/D: Posterior fossa arachnoid cyst, may be midline and associated with
ventriculomegaly
3. Posterior fossa Arachnoid cyst:
• Unilocular collection of CSF within layer of Arachnoid membrane does
not communicate with ventricle. No associated anomaly.
4. Megacisterna magna
• Enlargement of cisterna magna beyond 10 mm
• Vermis is intact
• Can be a normal feature or cause hydrocephalus
• Associated with trisomy 18
5. Iniencephaly
• Rare case of dysraphism
• Involving occipital bone and contiguous upper spine
• Associated with segmental errors of the upper spine
• The resulting deformity markedly shortens the neck
• Head is dorsi-flexed which is known as the “star-gazing” position
• Associated anomalies – anencephaly or Klippel – Feil syndrome
Intracranial calcification:
Occur late in gestation, associated with fetal infection.
• Cause area of cell necrosis and may line ventricles or occur in
parenchyma associated with severe CNS changes including
microcephaly, ventriculomegaly and porencephalic cyst.

Ultrasonography of Systemic Antenatal Abnormalities 417

D/D:
• Torch infection
• Teratomas
• Tuberous Sclerosis
• Sturge Weber syndrome
• Sinus Venous Thrombosis

Fetal Neck
• Evaluated with polyhydramnios to look for obstructive lesions and fluid
collection
• Thyroid mass — goiter
• Other neck masses — hemangioma, cystic hygroma, teratoma.
Cystic hygroma — Seen as early as 10 weeks.
US show large nuchal fluid collection with random septation and
characteristic by a thicker midline septum.

Fetal Nuchal Translucency
• Suggested as a screen for chromosomal disorder.
• Normal measurement under 2.5 mm between 10 to 13 wks.
• Maximum thickness between skin and soft tissue overlying cervical spine.
• Increased thickness is associated with Trisomy 21, 18 and 13, Triploidy
and Turner’s syndrome.
• Other defect – cardiac, diaphragmatic, renal and abdominal.

Nuchal Thickness
• Skin Thickening of 6 mm or more in the occipital region between 15 to 19
wks, is indicative of Down syndrome.
• This is due to subcutaneous edema and distinct fluid collection, some
associated with cystic hygroma.
Nuchal Thickness in axial view from outer surface of occipital to outer
surface of overlying skin.

Fetal Facial Abnormalities
Cleft Lip and Palate
US
• Diagnosis by viewing nose, upper lip and alveolar margin in the coronal
direction, seen by 16 week.
• Association with polyhydramnios and small stomach.
• The eyes can be identified by 10 weeks and by 24 wks structure of globe
becomes apparent.
• Anomalies of eye spacing are more common.
• Hypotelorism (below 2 S.D. of the mean).

418 Seminar in Radiology

• Reduced interorbital distance associated with holoprosencephaly with or
without chromosomal defect.
• Hypertelorism — increase orbital separation may be isolated or in
combination myelomeningocoele and Chiari II malformation.

Mandible
• Micrognathia – seen as small mandible with a receding chin associated
with multiple syndromes.

Fetal Chest
Bilateral Pleural Effusion
Causes - Hydrops
Fetal – infection
Congestive heart failure
Turner’s and Down syndrome

Unilateral Effusion
Causes - Right diaphragmatic hernia
Sequestration
Cystic adenomatoid malformation
Segmental pulmonary hypoplasia
Chylous effusion
Chromosomal abnormalities
US: Appears as a rim of fluid around the lungs, the tips of which produce a
“Bat wing” appearance.

Congenital Diaphragmatic Hernia
Foramen of Bochdaleck Hernia
• Located in posterior lateral side of chest
• Detected by 17 wks.
• Mediastinum deviation seen
• Content of hernia on left side may be stomach, omentum, intestine, left
kidney
• Associated anencephaly, hydrocephaly, encephalocoele, spina bifida

Foramen of Morgagni Hernia
• Partial or complete absence of central diaphragm behind the sternum
allowing liver or bowel to herniated into the anterior mediastinum.
• Right side is more common.
US: Colon is most frequent content but liver, stomach and small intestine
herniation have also been reported.

Ultrasonography of Systemic Antenatal Abnormalities 419

Cystic Adenomatoid Malformation
CAM involve just one lobe of the lung
Two groups
1. Microscopic less common,
Cyst that are larger than 5 mm.
2. Small cyst cannot be distinguished produce solid echogenic mass.
D/D: Congenital diaphragmatic hernia (large cyst of CAM does not show
peristalsis) Bronchial cyst, Cystic dilation of bronchus, pericardial teratoma.

Mediastinum Mass
• Normal thymus enlarges linearly with age from 14 wks and appears
hyperechoic before 27 wks.
US: Seen on transverse section of thorax at the level of great vessels in anterior
mediastinum.

Teratoma
• May arise from pericardial sac predominated soft tissue sometimes with
some cystic areas and contain foci of calcification.

Posterior Mediastinum
• Most common mass
• Neurogenic tumors-neuroblastoma appears on paravertebral areas as
echogenic mass with echolucent center.
• Enteric cyst, occurs in cystic mass
• Duplication cyst- originating from jejunum and traversing the diaphragm
into the chest accompanied by vertebral anomalies.

Fetal Abdomen
Stomach
Failure of visualization of stomach in the LUQ
• Sometime it may be a normal feature
• Displacement of stomach into chest
• Nonproduction of amniotic fluid and failure to reach amniotic activity (renal
agencies, PUV)
• Esophageal atresia and Microgastria
• Associated with cardiac, genitourinary and central nervous system
anomalies.
• Total situs inversus — fetal stomach found in RUQ and right sided heart
• Partial situs inversus — right sided stomach and left sided heart.

420 Seminar in Radiology

Esophageal Atresia
• Inability to visualize the stomach bubble after repeated scan and the
demonstration of polyhydramnious

Duodenal Atresia
• Produced by a large obstructed stomach and a distended proximal duodenal
segment.

US
• Seen as two echolucent structures corresponding to the double bubble
sign.
• Stomach is distinguished by its rugae
• Polyhydramnious is always associated
• Also associated with VACTERL complex [Vertebral defect, Anal atresia,
cardiac defects, Tracheo-Esophageal fistula with Esophageal atresia and
Renal and limbs defects (Radial dysplasia)].

Atresia of Small Bowel
Causes
• Sites are proximal jejunum, proximal or distal ileum
• Vascular impairment
• Volvulus, Malroation, Bands
US
• Multiple interconnecting overdistended bowel loops
• Lower the site of obstruction, more the number of dilated loops
• Polyhydraminous usually associated.

Meconium Ileus
• Refers to obstruction and subsequent dilation of the ileum that occurs, due
to impaction of the abnormally sticky and thick meconium with cystic
fibrosis.
• The ileum dilates above the obstruction and volvulus or perfection may
result in chemical meconium peritonitis..
US
• Ascitis
• Calcification
• Pseudocyst formation due to inflammatory response.

Hirschsprung’s Disease
• Congenital aganglionosis of a segment of the colon, cause in function
bowel obstruction.

Ultrasonography of Systemic Antenatal Abnormalities 421

US
• Polyhydramnios
• Multiple dilated loops of fetal bowel
• Intraluminal calcification

Anorectal Atresia
US
• Distal colon is dilated
• Round calcification representing intraluminal calcified meconium
• Associated with other anomalies especially of VACTREL.

Gallbladder and Biliary Ducts
• In biliary atresia GB is often tiny
• GB is enlarged in extrahepatic biliary obstruction.

Choledochal Cyst
• Congenital cyst of biliary system

US
(Most common) cystic, ovoid or tear drop structure seen inferior to umbilical
vein and anterior to right kidney in RUQ.

Liver
Hepatomegaly seen in
• Hemolytic disease of isoimmunised pregnancies
• Congenital infection

US
• Fetal liver shows diffuse echogenic foci suggest possible hepatitis.
• Fetal hydrops, fetal CHF
• Tumors — Mesenchymal hamartoma, hemangioendothelioma, and
hemangioma
• Hypoechoic mass in the fetal liver
Liver calcification occur in
• Hepatic tumors
• Intrauterine infection
• Vascular insult

Spleen
Splenomegaly seen in
• Intrauterine infection

stomach. • The umbilical cord is normally inserted to the left of the defect. liver seen to be herniated through. FETAL RENAL ANOMALIES Renal Agenesis US • No kidney seen in renal fossa or in an ectopic location • With bilateral renal agenesis. Turner’s syndrome and trisomy 18. • Less commonly crossed renal ectopia.422 Seminar in Radiology • Congenital syphilis • Cytomegalovirus infection • Simple splenic cyst • Multiple splenic cyst as in congenital lymphangiomatosis • Fetal hydrops. GIT. Omphalocoele US • Defect in the anterior abdominal wall in midline with extrusion of abdominal contents (bowel. FETAL ABDOMINAL WALL DEFECT Gastroschisis US • Right paraumbilical defect involving all layers of abdominal wall. Renal Ectopia • Kidney seen in chest. . • Umbilical cord attached to the tip of omphalocoele. • Polyhydramnios and associated anomalies seen. • Small bowel usually herniates through the defect and multiple loops of bowel can be seen floating freely in the amniotic fluid. • Large bowel. Gynecological defects. or with or without fusion. Horseshoe Kidney • Usually inferior poles of kidneys are fused • Demonstration of bridge of renal tissue connecting the kidneys • Associated with CNS. adjacent to urinary bladder or iliac wing. stomach. there is severe oligohydramnios and non- visualization of both kidneys and bladder. • Ascitis. CVS. liver). CVS and chromosomal abnormality. • Associated with skeletal.

can be total. intermittent or partial obstruction . US Shows hydronephrosis of upper pole with normal lower pole. Bladder outlet Nonobstructive After 20 wks: Normal AP diameter of renal pelvis is upto 6 mm Borderline 6-9 mm Hydronephrotic > 10 mm PUJ: Dilated pelvicalyceal system with or without caliectasis. US • Kidneys are normal • Fluid filled bladder not identified • Everted bladder with heaped up mucosa may be seen as an irregular mass Urethral Obstruction • Causes posterior urethral valve • Urethral atresia • Stricture • Cloacal malformation PUV • Most common. ureters not visualized Amniotic fluid volume in normal VUJ: Hydronephrosis with hydroureter seen Primary megaureter – An aperistaltic distal ureteral segment. • Associated with epispadias with wide separation of pubic bones (pubic diastasis). Duplication Anomalies • In duplication of pelvicalyceal system upper pole moiety obstructs whereas lower pole moiety reflux.000 – 40. Ultrasonography of Systemic Antenatal Abnormalities 423 Hydronephrosis Obstructive : Pelvi – ureteral junction (PUJ) Vesico – ureteral junction (VUJ) . Bladder Extrophy • Occur in 10. • Posterior wall of urinary bladder is visualized.000 population • In complete median closure of inferior portion of anterior abdominal wall and the anterior wall of urinary bladder.

destroyed uniform pattern may be normal or small in size. . • Renal pelvis and ureter are usually atretic and not visible. • Causes obstruction of the urinary tract leading to hydronephrosis or hydroureter. hydronephrotic or dysplastic. US • Malformed kidney usually seen as enlarged. • Multiple cysts of varying size not communicating with each other and are randomly distributed.424 Seminar in Radiology US • Thickening of bladder wall • Bilateral tortuous hydroureters • Hydronephrosis. Prune Belly Syndrome (Triad Syndrome) • Classic Triad of absent anterior abdominal musculature • Undescended testes • Very large bladder • Prostatic urethra dilated • Ureters tortuous and dilated • Kidneys normal. Hydrometrocolpos • Enlargement of obstructed uterus and vagina from retained secretions Causes • Vaginal or cervical atresia • Imperforate hymen • Vaginal membrane US • Ovoid mass either cystic / complex. Ovarian Cyst • Benign ovarian cyst resolves spontaneously within 6 months of birth. Renal Cystic Disease • Multicystic dysplastic disease results from severe urinary obstruction before 8 to 10 wks due to atresia of the proximal third of the ureter with pelvic infundibulum.

• The contents can be anaechoic (meningocoele) or show strands or inhomogenous tissue (meningomyelocele/ lipocoele). • Seen in lumbar or lumbosacral areas and also at cranio-vertebral junction. Ultrasonography of Systemic Antenatal Abnormalities 425 D/D • Cystic lesion. D/D for fetal suprarenal mass – include • Neuroblastoma • Hemorrhage in the adrenals • Pulmonary sequestration • Enteric duplications cyst • Mesoblastic nephroma. Anomalies of Fetal Spine Spina Bifida • Involves vertebral column and spinal cord with disruption of the cutaneous and subcutaneous elements. Renal Neoplasm • Rare • Most common is mesoblastic nephroma • US shows as solid mass completely replacing the kidney or localized to part of the kidney • May contain cystic areas due to hemorrhagic or cystic degeneration • Polyhydramnios is frequently associated. • Seen as widening of interpedicular distance. • Splaying of posterior ossification centres. when on longitudinal section the entire spine is not properly appreciated. • A disruption of normal triangular appearance. • Usually suspected. Scoliosis and Hemivertebra Ultrasound • Lateral curvature of spine seen. . Autosomal Recessive (Infantile) Polycystic Kidney Disease (ARPKD) • Diagnosed by 14 wks • Renal enlargement • Increased renal echogenicity • Amniotic fluid volume is usually normal. at times internal septa • Presence of fluid debris level • Refractory clot and solid component suggesting trauma or hemorrhage.

.426 Seminar in Radiology • Usually a part of spina bifida • Associated with hemivertebra which is suspected on a lateral deviation of the anterior ossification centre when compared with adjacent one. GIT. • Severe oligohydramnios and single umbilical artery are present. Diastomatomyelia • Implies a partial or complete cleft of the spinal cord or filum terminale associated with spina bifida or hdyromyelia. Fetal Skeletal Anomalies • Thanatophoric dysplasia – severe micromelia with rhizomelic predominance • Macrocrania with decreased thoracic circumference. • Sac composed of three layers. • Spina bifida not associated. Caudal Regression Syndrome • Partial or total sacral agenesis and abnormalities of lumbar spine. lower limbs. Myelocystocoele • Dilation of spinal cord’s central canal which herniates posteriorly through the spinal canal to form an exterior sac. Sirenomelia • Severe form characterized by absent sacrum. anorectal atresia or renal dysgenesis or agenesis. majority of cases associated with diabetes mellitus. anomalies of renal. fusion of lower extremities. CNS system chromosomal anomalies.hydromelia. meningeal layer and skin. US • Demonstrate a cyst within a cyst • Splaying of the lamina or pedicle may/ may not be present. Sacrococcygeal Teratoma US • Appears as mass inferior to sacrococcygeal area • Mass seen as mixed echopattern but can also appear solid or cystic • Associated with polyhydraminos. US • Hemicords split by bony spetrum • Associated spina bifida. pelvis.

Asphyxiated Thoracic Dystrophy US • Extremely narrow chest with secondary hypoplasia • Limbs could be mildly shortened or even of normal length • Polydactyly. . Ultrasonography of Systemic Antenatal Abnormalities 427 US • Telephone receiver shape of extremities showing. Bowed appearance with marked curves • Cloverleaf skull deformity with/ without hydrocephalus • Cutaneous hydrops Achondrogenesis US • Severely retarded and absent skeletal ossificaiton • Limb length reduction is quite severe • Short trunk and narrow thorax Type I • Severely short limbs • Short neck • Short trunk with a protruding abdomen • Ribs fracture • Poor skull and vertebral ossification Type II • Variable limbs shortening • No ribs fracture • Relatively normal skull ossification Osteogenesis Imperfecta US • Severe micromelia with crumpled irregular femur • Ribs are short and beaded secondary to fractures • Limb’s movement is limited • Protuberant fetal abdomen • Hypomineralisation of calvarium • Skull is compressible by ultrasound transducer.

congenital hydronephrosis Abdominal viscera for any organomegaly and calcification Placenta for any chorio-angioma. Ventricular septal defect (Most common) US: seen as discontinuity in the interventricular septum . Cardiac four-chamber view • Situs • Size i. Hypoplastic left ventricle or left heart ii. Fetal Cardiac Abnormalities 1. Cardio-thoracic ratio • Size of ventricle i. Atrial septal defect ii. M-mode ultrasound ii. Large diaphragmatic hernia Cranial malformation Urogenital malformation – large polycystic kidney. Hypoplastic right ventricle • Septal defects i.428 Seminar in Radiology Fetal Hydrops • Abnormal fluid accumulation within fetal extravascular compartments and body cavities US • Ascitis • Pleural effusion • Pericardial effusion • Subcutaneous edema • Placental edema • Arterial and venous Doppler abnormalities • Polyhdyramnios Causes • Immune – Rhesus incompatibility Other blood group incompatibility • Nonimmune – Chromosomal abnormalities Turners syndrome Cardiac anomalies Thoracic – CAM.

Viral and bacterial infection. diabetes mellitus. Change in echo pattern • Cardiomyopathy Cause . US shows hypertrophy of ventricular wall and septum And dilatation of one or more cardiac chamber Pericardial effusion 2. Focal thickening ii. Transposition of great vessels Relation of ventricular septum to the great vessels i. • Cardiac fibroma 12 percent. Long and Short Axis views Criss cross relation of great vessels i. Atrio-ventricular canal Deficiency of interatrial or interventricular septum US: a defect in atrial/ ventricular septum with associated single abnormal AV valve seen • Valvular abnormalities i. Tricuspid. US • Solid echogenic masses • Single or multiple arising from AV septum • Teratomas may be cystic/Solid masses. Tricuspid. inborn error of metabolism. Ultrasonography of Systemic Antenatal Abnormalities 429 Color Doppler shows bi-directional of interventricular shunting with a systolic Right to left shunt and a late diastolic left to right shunt iii. Tetralogy of Fallot US – VSD seen in perimembranous portion of septum RVH rarely occurs in utero Dilated aorta is reliably seen Pulmonary stenosis is a dilated pulmonary artery secondary to absence of valve Cardiac Tumors • Rare – 10 percent malignant. Pulmonary and Aortic stenosis ii. Bicuspid. • Seventy-five percent of tumors are Rhabdomyoma and teratomas. Double outlet right ventricle ii. Pulmonary and Aortic regurgitation • Cardiac musculature i. . Bicuspid. Diffuse thickening iii.

Agenesis of the corpus callosum Dandy-Walker malformation Holoprosencephaly Spine Meningomyelocele Facial Hypertelorism Microphthalmia Micrognathia Neck Cystic hygroma Large. Horseshoe Renal cortical cyst kidney Hydronephrosis. Overlapping Widely spaced first and Clenched hands digits second toes. Horseshoe kidney Skeletal Short femur and Humerus Clubfoot deformity Postaxial polydactyly Clinodactyly of fifth digit Generalized arthrogryposis Comptodactyly. Wide iliac angle Organ system Triploidy Trisomy XI Head and brain Ventriculomegaly. Cleft lip and/or palate. Mircrophthalmia Hypotelorism Neck Thickened nuchal skin fold Nuchal thickening Nuchal thickening Cystic hygroma Cardiac Ventricular septal defect Ventricular septal defect Atrial septal defects Atrial septal defect Atrioventricular canal Dextrocardia Echogenic cardiac focus Echogenic cardiac focus Gastro-intestinal Hyperechoic bowel Diaphragmatic hernia Omphalocele Esophageal atresia Omphalocele Duodenal atresia Esophageal atresia Diaphragmatic hernia Urogenital Renal pyelectasis Hydronephrosis.430 Seminar in Radiology CHROMOSOMAL ABNORMALITIES Organ system Trisomy 21 Trisomy 18 Trisomy 13 Head and brain Mild ventriculomegaly Dolicocephayly. Agenesis shaped skull of corpus collosum Large cisterna magna Ventriculomegaly Chroid plexus cysts Enlarged cisterna Magna Agenesis of corpus collasum Mircocephaly Facial Flace face Micrognathia Mircophthalmia Micrognathia. Strawberry Holoprosencephaly. cystic hygroma Thorax Pleural effusion Cardiac Septal defects Coarctation of the aorta Gastro-intestinal Omphalocele Ascites Urogenital Hydronephrosis Horseshoe kidney Skeletal Syndactyly of the third and fourth fingers Short femur Clubbed feet . septate. Sloping fore- head.

improving transmission of the ultrasound beam. probe increasing sensitivity and spatial resolution of image. Visualization of pelvic structures may be limited in obese patients and others with excessive bowel gas and those who are unable to hold the urine. ULTRASOUND TECHNIQUES Transabdominal Ultrasound Transabdominal ultrasound imaging is primary method for assessment of. there is less beam attenuation in superficial soft tissues and a higher frequency (5-7 MHz). High resolution ultrasound may also be performed by a transrectal route to assess local tumor spread in patients with carcinoma of cervix. Transvaginal Ultrasound Initially it was used to monitor infertility treatment and to assess. Transvaginal transducer is closer to the region of interest. In female patients. The full bladder is vital for successful scanning. Demonstration of abnormal vascularity by Doppler is suggestive of neoplastic process causing neoangeogenesis. displacing small bowel and behaving as an acoustic window. ovarian vascularity fluctuates during the menstrual cycle. Doppler USG It can provide useful additional information about vascular abnormality associated with pathological pelvic conditions. It is the preferred technique for assessing pelvic inflammatory or malignant conditions especially when the patient is obese or cannot achieve adequate bladder fully. Postmenopausal ovaries are relatively hypovascular. pushing the uterus upwards from behind the pubic symphysis. Low resistance to high flow occurring in presence of functioning corpus luteum. . Non gynecological masses or pseudomasses most commonly originate from gastrointestinal tract and urinary tract. The transducers used are of lower frequency (3 to 4 MHz). uterus and adnexa in female patients and prostate in male patients. The pregnancy only and its complications.28 Ultrasound and Color Doppler in Pelvic Masses Pelvic masses are the commonest pathology in females particularly affecting uterine and adnexal anatomy.

Advances in computing power have resulted in the recent production of a real time 3D US (ultrasound system) known as 4D ultrasound imaging. grating lobe. hematoma. distended with gas or appendicitis. which increases the sensitivity of ultrasound to detection of flow. cutter and other artifacts. especially when color Doppler is used. CLINICAL. Patency is inferred when fluid accumulates in peritoneal cavity. Echogenic ultrasound contrast agents containing stabilized microbubbles allow the full length of fallopian tubes to be visualized.432 Seminar in Radiology Sonohysterosalpingography Ultrasound can be used to evaluate tubal patency: Transvaginal ultrasound is performed while saline or contrast medium is injected via a thin cannula through the cervical canal. Three Dimensional Imaging (3D) Three D ultrasound is based on reconstruction algorithms and is therefore dependent on high quality 2D data which have been limited by problems such as speckle. • Bladeder diverticula retroperitoneal abscess . 3D imaging has several features as compared to conventional 2D ultrasound. Volume data can be viewed in multiple imaging planes and accurate measurement of lesion volume may be obtained. carcinoma feces colon Miscellaneous • Pelvic kidney • Abdominal wall • Urachal cyst abscess. PATHOLOGICAL AND RADIOLOGICAL FINDINGS OF PELVIC MASSES Differential Diagnosis of Pelvic Masses Organ Cystic Solid • Functional cysts • Neoplasm: Benign or malignant Ovary • Neoplastic cysts: Benign or malignant • Endometriosis • Tubo ovarian mass like • Tubo-ovarian abscess chronic pyosalpinx • Ectopic Pregnancy Fallopian tubes • Hydrosalpinx • Neoplasm • Parovarian cysts • Chronic interstitial salpingitis Broad ligament • Broad ligament cyst • Broad ligament fibroid • Hematoma Uterus • Intrauterine pregnancy in • Pedunculated or bicornuate uterus intramural fibroid Bowel • Sigmoid or caecum • Diverticulitis.

pedunculated. It allows better differentiation between a submucosal and an intramural lesion and its relationship to endometrial cavity. Sonographically • Fibroids have variable appearances. • Calcification appears as focal areas of increased echogenicity or curvilinear echogenic rim with shadowing. although frequently asymptomatic. . Sarcomatous degeneration occur in less than 0. females present with pain and uterine bleeding. Ultrasound and Color Doppler in Pelvic Masses 433 PELVIC MASSES OF GYNECOLOGICAL ORIGIN Uterine Masses Uterine neoplasms arise either from myometrium or endometrium. usually impinge on the endometrium. 2. • Classification: – Intramural: Confined to myometrium (most common) – Submucosal: Projecting into uterine cavity – Subserosal: Projecting from the peritoneal surface of the uterus • Estrogen dependent tumor : may increase in size during pregnancy although half of all fibroids show little significant change during pregnancy. They occur in approximately 20 to 30 percent of females over the age of 30 years. • Degeneration and necrosis produces areas of decreased echogenicity or cystic spaces. because of the limited field of view. subserosal fibroids that simulate adnexal masses however pedunculated fibroids may be missed if transvaginal approach is alone used. not appreciated on transabdominal study. It can detect small leiomyomas. It clearly demonstrate the uterine origin of large. • Fibroids can demonstrate areas of acoustic attenuation or shadowing without a discrete mass. distorting the lumen. infarction or infection may occur. • Single or multiple. Myometrium a. Transvaginal Sonography 1.1 percent cases. • They appear hypoechoic or heterogeneous in echotexture and frequently distort the external contour of uterus. Leiomyoma (fibroid) • Myomas are the most common neoplasms of the uterus. Uterus may be enlarged with globular outline and heterogeneous echotexture resulting from small diffuse leiomyomas. • Degeneration.

dysmenorrhea and menorrhagia. The size of fibroid may be accurately measured using volumetric data.434 Seminar in Radiology Color Doppler Ultrasonography Low resistance flow in uterine artery has been reported in association with uterine fibroids. Color flow and spectral Doppler findings are variable in fibroids reflecting their natural history with growth followed by degeneration. Transabdominal Sonography The diagnosis is suggested if there is diffuse uterine enlargement with normal contour and normal myometrium and endometrium echotexture. Sonographically The appearance is similar to that of a rapidly growing or degenerating leiomyoma. inhomogeneous hypoechoic areas occur within myometrium predominantly posterior wall. . The relationship of endometrium to fibroid may be assessed more accurately than with 2D USG. Transvaginal Sonography Transvaginal sonography is more accurate in diagnosing this condition. Role of 3D Ultrasonography The exact location of fibroids in the uterus can be identified by using the simultaneous orthogonal display provided by 3D USG. b. center of the lesion is often avascular and necrotic. • The most common presentation is uterine enlargement and nonspecific symptoms as pelvic pain. The vascularity is typically peripheral with very high velocities and low resistance. c. Thickening of posterior myometrium with the involved area being slightly more hypoechoic than myometrium can also occur. It is more extensive in posterior wall.3 percent of uterine malignancies and may arise from preexisting uterine leiomyoma. Adenomyosis • It is overgrowth of basal layer of endometrium into myometrium: pathologically by the presence of endometrial glands and stroma within the myometrium. Leiomyosarcoma It accounts for 1. Patients are usually asymptomatic or uterine bleeding may occur. Abnormalities of the Endometrium Endometriosis Here normal appearing glands and stroma are found to be implanted outside their normal uterine cavity. however there can be local invasion of adjacent structures or distant metastasis. Small myometrial cysts may also be present. In contrast.

Endometrial Carcinoma • Seventy five to eighty percent cases are reported in post menopausal women with uterine bleeding. Endometrial hyperplasia is most important prognostic indicator. endometrial thickening. The localized form is also known as endometrioma or chocolate cyst. echogenic mass may be seen within the endometrial cavity and this appearance is much more easily identified when there is fluid within the endometrial cavity outlining the mass. • Risk factors are obesity. diabetes. Color Doppler Sometimes a feeding artery may be seen in stalk of polyp with color Doppler. predominantly cystic mass containing diffuse homogenous. occurs commonly in ovary. Malignant degeneration is uncommon. Ultrasound and Color Doppler in Pelvic Masses 435 • Most commonly occurs in the ovary. • Cystic areas may be seen within a polyp. which may be diffuse or localized. round. low level. nulliparity. Endometrial Polyps • Commonly seen perimenopasual and post menopausal women • Usually presents with uterine bleeding • Polyps may be pedunculated and approximately 20 percent are multiple. Color Doppler Study The vessels at the periphery of the endometriotic cyst show relatively high impedance. . hypertension. fallopian tube. Sonohysterography is a valuable technique when transvaginal sonography is unable to differentiate endometrial polyp from a submucosa leiomyoma. dyspareunia and infertility. internal echoes. Sonographically • They appear as non-specific echogenic. • Focal. broad ligament and posterior cul-de-sac and the urinary bladder. • Two forms have been described: diffuse and localized (endometrioma). • It affects reproductive age group and presents as dysmenorrhea. The characteristic appearance is comprised of well defined unilocular or multiocular. characteristically by transvaginal sonography. Sonographically The localized form.

19 (normal 0.3 ± 3. It was evaluated that endometrial thickness to be a better method for discriminating normal and pathologic or benign and malignant endometrium than Doppler of uterine or subendometrial arteries.05) have been demonstrated. • Transvaginal sonography can be used to depict endometrial thickness. invasive mole and chorio- carcinoma are rare neoplasms of the endometrium. however.436 Seminar in Radiology • Thickened endometrium with inhomogenous echotexture and irregular or poorly defined margins.11) and RI of 0. whereas obliteration of the halo is indicative of deep invasion.56 ± 0. Abnormalities of Cervix The cervix lies low in pelvis and is better assessed with transvaginal sonography. there is low resistance flow in the uterine arteries as compared with high resistance flow in normal or benign endometria. Color Doppler There is significant increase in myometrial and endometrial flow. Presence of the subendo- metrial halo indicates superficial invasion. Subsequent reports. Differential Diagnosis of Endometrial Carcinoma • Endometrial polyp • Gestational trophoplastic disease: In a younger age group. endometrial proliferation related to normal or abnormal pregnancy represents trophoblastic disease. have shown no significant difference in uterine blood flow between benign and malignant processes. more marked in aggressive tumors. discharge and pain. Role of Color and Spectral Doppler Initially it was suggested in endometrial carcinoma. Role of 3D Ultrasonography It measures volume of endometrium. Doppler indices are altered in trophoblastic tumors a mean PSV of 57. Hydatidiform mole. which is superior to endometrial thickness in diagnosis of endometrial carcinoma. . accurately and assess myometrial infiltration. the lesser the need for prolonged treatment cycles.86 ± 0. Transrectal ultrasound also delineates the anatomy clearly. • Carcinoma cervix: Most common genital carcinoma. 3D USG is also superior to conventional USG both for myometrial invasion and cervix extension. The extent of intratumoral flow correlates with the prognosis. Thickening and inhomogenity of the endometrium are characteristic features with varying degree of vesicles within uterine cavity and assessment of degree of invasion.4 (normal 28. patient usually presents with irregular vaginal bleeding. the higher the resistance index. 5 ± 20.

initial site for intraperitoneal fluid collection. Transvaginal sonography can demonstrate echoes within the fluid more frequently because of its improved resolution. blood resulting from a ruptured ectopic pregnancy or hemorrhagic cyst. Transrectal Ultrasound It can demostrate cervical enlargement and parametrial extension but not the full extent of bulky tumors or assessment of lymphnode enlargement. It is located between the rectum and vagina. is also known as the pouch of Douglas. Mass can also occlude the cervical internal os resulting in hematometra or pyometra which appears as fluid collection with/without internal echoes in endometrial cavity. As little as 5 cc of fluid have been detected by transvaginal sonography. Ultrasound and Color Doppler in Pelvic Masses 437 • Transabdominal sonography: It does not contribute to staging to the primary cervical tumor. The most common cause of ovarian enlargement in young women. Sonographically These functional cysts are typically unilocular. Color Doppler Cervical carcinoma can be seen on endovaginal ultrasound and neovascularity can be demonstrated in mass lesion. . Corpus luteal cyst may be enlarged due to internal hemorrhage or cyst formation. ascites or hepatic metastasis in advanced disease. Theca lutein cysts iii. but can show urinary tract obstruction. anechoic with well defined thin walls and posterior acoustic enhancement. Posterior cul-De-sac It is the most posterior and inferior reflection of the peritoneal cavity. • They include i. Pathologic fluid collections may be seen in association with generalized ascites. Endometriotic cysts • Follicular cysts usually regress spontaneously. Ovarian Masses Functional Cysts • These are non-neoplastic cysts related to the process of ovulation. • Theca lutein cysts result from hyperstimulaiton of ovary by HCG and are often associated with hydatidiform mole and choriocarcinoma. Functional cysts of follicular or corpus luteal type ii. • Seen most commonly in reproductive age group. It is a potential space and because of its location.

sertoli- leydig cell tumor. • Malignant neoplasms Histologic Outline of Ovarian Neoplasms Type Incidence Example 1. Meigs syndrome is benign ovarian fibroma with ascites and hydrothorax. colon. extragenital primary. Mucinous variety tend to contain more septa and echogenic material. thick. Ovarian Neoplasms • Benign neoplasms are usually of connective tissue origin (fibroma. serous and mucinous are large masses. The internal characteristics are much better appreciated on transvaginal sonogrpahy because of its improved resoluion. granulosa cell. endo- metrioid carcinoma. multilocular and often very large.438 Seminar in Radiology Hemorrhagic cysts show spectrum of findings as a result of variable sonographic appearances of blood. • Brenners tumors are bilateral in only 6. thecoma and fibroma 4. Sonographically. • Cystadenocarcinomas. dermoid. mural nodules and solid echogenic elements favour malignancy. Sexcord stromal tumors 5-10% Yolk sac tumor. thecomas or uterine leiomyomas. Usually complete resolution within the approximately 6 weeks. . muci- tumors nous cystadenoma (carcinoma). irregular septations. thecoma and Brenner tumor). theca lutein cysts are usually bilateral. The presence of solid component suggests malignancy. multilocular and contain papillary projections and echogenic material. Pseudomyxoma peritonei commonly associated with adenocarcinomas. Metastatic 5-10% Genital primary uterus. clear cell carcinoma 2. breast lymphoma Sonographically Well defined. Another patterns include reticular type pattern and fluid-fluid level between the clot and fluid component. An acute hemorrhagic cyst appears hyperechoic and may mimic a solid mass. Surface epithelial stromal 65-75% Serous cystadenoma (carcinoma). They vary in size. includes stomach. dysgerminona 3. anechoic lesions with thin wall are more likely to be benign whereas lesions with irregular walls. teratoma.5 percent and account for 1 to 2 percent of ovarian neoplasms. Germ cell tumors 15-20% Transitional cell tumor. Sonographically hypoechoic solid masses that may contain calcifications and that appear similar to ovarian fibromas. Histopathologic – Ultrasonographic Correlation • Cystadenoma are usually large anechoic masses that may contain septations.

a protruberance from the inner wall of a cyst and tip of iceberg appearance can be seen in dermoid. multiple cortical follicles in an enlarged ovary is considered specific sign. • Thecomas and fibromas are hypoechoic masses with associated posterior acoustic shadowing. Ovarian Torsion It is an acute abdominal condition caused by partial or complete rotation of the ovarian pedicle on its axis. high diastolic flow are tuboovarian abscesses. • Transvaginal color and pulsed Doppler distinguishes benign from malignant ovarian masses. although they are not always present. It usually occurs during reproductive years. the other lesions which demonstrate low impedance. • Dermoid plug. • Absence of flow within lesion usually indicates a benign lesion but several studies have shown absent flow within malignant lesion as well. Hair.4. Metastasis to ovariers from stomach and occasionally colon. actively hemorrhagic corpus luteum and some of the dermoids. with malignant masses having PI less than 1.0 or RI of less than 0. Dermoid arise from all three germ layers. The tumor has homogenous echotexture and may resemble pedunculated fibroid in adnexa. • Malignant lesion have more central vessels (flow) where as benign lesions have peripheral flow. there are severe pelvic pain. Ultrasound and Color Doppler in Pelvic Masses 439 • Ovarian cystic teratomas or dermoids are benign neoplasms with 2 percent risk of malignant transmission. Visualization of diachrotic notch suggest the possibility of benign in nature. . The fat-fluid or hair fluid level is characteristic of a dermoid. nausea and vomiting. fat and fragments of bone or teeth within mass are echogenic and produce posterior acoustic shadowing. Sonographically The findings are variable depending on the degree of vascular compromise. breast and pancreas are known as Krukenberg tumors. • Metastatic ovarian neoplasms are bilateral masses and may be hypoechoic or echogenic and occasionally cystic degeneration is present. sebum hair. calcium and other elements can led to different sonographic appearances. Color Doppler Findings • Malignant tumor growth depends upon angiogenesis and development of abnormal tumor vessels leads to decreased vascular resistance and thus higher diastolic flow velocity. The ovary is enlarged. Clinically. • Dysgerminomas are sonographically usually solid masses that may contain cystic areas representing hemorrhage or necrosis.

• Most commonly adnexal masses secondary to tubal disease are inflammatory or representing ectopic pregnancy. Parovarian Cysts • Parovarian cysts account for about 10 percent of all adnexal masses. Sonographically These are multiloculated cystic pelvic mass. The diagnostic findings is presence of septations and fluid and an intact ovary.440 Seminar in Radiology Color and Spectral Doppler There is absence of flow in the affected ovary. PID and endometriosis. The fluid is usually anechoic but may contain echoes as a result of hemorrhage or proteinaceous fluid. Peritoneal Inclusion Cyst They occur predomintaly in premenopasual women with a history of previous abdominal surgery. Acute salpingitis: The fallopian tube is swollen and edematous with dilated vessels on the peritubal surface. Inflammatory Tubal Masses i. fluid may accumulate within the adhesions and entrap the ovaries resulting in large adnexal mass. trauma. Sonographically They have typical appearance of cysts and may contain internal echoes as a result of hemorrhage. • They are located in broad ligament and are usually mesothelial or paramesonephric origins. The ovary may be located centrally or displaced peripherally. • They are frequently located superior to uterine fundus. Doppler findings depend on the degree and chronicity of the torsion and whether or not there is an associated adnexal mass. In patients with peritoneal adhesions. Paraovarian cysts show no cyclic changes. The ovaries are main source of production of periotoneal fluid in women. The ovaries are also involved resulting . COLOR DOPPLER Tubal Masses • Neoplasms arising from fallopian tube are rare. • A specific diagnosis is possible only by demonstrating a normal ipsilateral ovary close to but separate from the cyst.

Pyosalpinx or hydrosalpinx–fluid filled fallopian tube with or without internal echoes. Periovarian inflammation-enlarged ovaries with multiple cysts and indistinct margins. iii. These masses manifest in the form of a. Tubo-ovarian abscess–complex. Ovarian . Abdominal b. Uterine . Chronic inflammatory disease: Failure of acute pelvic infection to resolve completely results in chronic tubo-ovarian masses. vi. However. Tubo-ovarian complex–fusion of the inflamed dilated tube and ovary. Ectopic pregnancy : Implantation occurs outside the normal uterine cavity. Tubo-ovarian cyst Sonographic Findings i. v. Interstitial . Ultrasound and Color Doppler in Pelvic Masses 441 in tubo-ovarian abscess. Endometritis – endometrial thickening or fluid. Cervical . Pus in the cul-de-sac. predominantly cystic masses often indistinguishable from other adnexal masses. Chronic pyosalpinx c. The ampullary end of the tube distends more than the isthmic portion resulting in retort shaped pyosalpinx. Transvaginal Sonography On transabdominal sonography. folded configuration and well defined echogenic walls. Tubal . dilated tubes appear as complex. Extrauterine . irregular margins and internal echoes. Color Doppler Sometimes useful in differentiating hydrosalpinx from a prominent pelvic pain. In an inflammatory mass. ovarian tissue can be seen separately by transvaginal sonography because ovaries are relatively resistant to the infection. Hydrosalpinx b. iv. ii. Low level internal echoes within fluid filled tube suggests pyosalpinx. multiloculated mass with variable septations. ii. Chronic interstitial salpingitis d. Types: a. Rudimentary horn of bicornuate uterus . TVS recognizes fluid filled tube by its tubular shape.

These tumors frequently show charcteristic target sign of a gastrointestinal mass. consisting of central echogenic focus caused by air within the lumen.442 Seminar in Radiology ECTOPIC PREGNANCY • Amenorrhea. surrounding by thickened hypoechoic wall. Pseudogestational sac . Non supportive features . Transvaginal sonography can usually distinguish the pseudomass from a true mass. Specific findings . Adnexal mass . Peritrophoblastic flow.8 in inactive trophoblast. Ectopic tubal ring c. Live intrauterine pregnancy . Particulate ascites . Bowel Neoplasms Especially those involving rectosignoid. Intradecidual sign . caecum and ileum may simulate an adnexal mass. On the right side this is most frequently caused by . which is of high velocity and low resistivity index. Non specific findings . Pelvic Abscesses Related to inflammatory disease of the gastrointestinal tract may also present as an adnexal mass. Gastrointestinal Tract Masses The most frequent pelvic pseudomasses are fecal matter in the rectum simulating a complex mass in the cul-de sac and fluid filled rectosigmoid colon presenting as cystic adnexal masses. Sonographically a. PELVIC MASSES OF NON-GYNECOLOGICAL ORIGIN Non-gynecologic pelvic masses or pseudomasses most commonly originate from the gastrointestinal or urinary tract or may develop in postoperative period. pain followed by vaginal bleeding are the commonest presentation of ectopic pregnancy. The flow within the trophoblast will yield pulsatile flow of low resistance index in excess of 0. Peritrophoblastic flow Color and Spectral Doppler It helps to distinguish a gestational sac from decidual cast. Empty uterus . Color flow imaging shows classical “fire ring” pattern within the trophoblast. Live embryo in adnexa b.

The non-glandular elements are the prostatic urethra and the anterior fibromuscular stroma. URINARY TRACT MASSES Pelvic Kidney It may present as a clinically palpable mass. Glandular prostate consists of • Outer • Inner components In total. . zonal anatomy consists of five components a. USG and Doppler Evaluation of the Prostate The prostate is histologically composed of glandular and non-glandular elements. Anterior fibromuscular stroma b. Bladder diverticula may also simulate a cystic adnexal mass • Dilated distal ureters may simulate adnexal cysts on transverse scans. Sonographically • Recognized by typical reniform appearance and the absence of kidney in the normal location. Central zone e. is performed with transrectal approach. Peripheral zone Imaging The prostate can be visualized from a suprapubic position with transabdominal transducers but detailed assessment of zonal anatomy. Transition zone d. whereas abscesses on the left side are usually caused by diverticular disease. When a cystic pelvic mass is identified. bladder should be seen separately. Appropriate roentgenographic and endoscopic studies are helpful in establishing the diagnosis • Retroperitoneal sarcoma. lymphomas and teratomas of the sacrococcygeal areas are commonly noted on rectovaginal examination and can be confused as an adnexal mass. however sagittal scans show their tubular appearance and continuity with bladder • Ileitis may present as right adnexal mass as the loops of thickened and inflammed ileum become fixed in pelvis • Large intestinal malignancies are usually seen on left side but carcinoma of caecum present as right sided adnexal mass. Ultrasound and Color Doppler in Pelvic Masses 443 appendicitis or Crohn’s disease. Periurethral glandular tissue c.

• The peripheral zone forms an area of uniform echogenecity surrounding the central gland. which are localized collection of urine. they become highly echogenic. • A significant number of prostate cancers are difficult to detect because they are isoechoic with glandular tissue. the central gland becomes distinguishable as a well demarcated area of heterogenecity which may contain visible nodules. Sonographically Lymphoceles are cyctic having appearance similar to that of urinomas. lymphoceles. the zones of prostate are not sonographically evident. • The seminal vesicles can be seen superolaterally encased in hyperechoic fat that is continuous with fat surrounding the prostate. • Hematomas: During the initial acute phase. This appearance may be caused by dermoplastic response of the surrounding glandular tissue to the presence of tumor. Variable internal echogenicity may be seen and high intensity echoes with shadowing caused by gas may be seen. hematomas. hematomas are anechoic. cysts or calcification. with complete lysis. anechoic masses with thick. Sonographically • Abscesses are ovoid shaped. Doppler Imaging Normal vascularity is categorized as minimal intraparenchymal flow with symmetric capsular vessels. urinomas. • Doppler is useful adjunct to define areas of neovascularity that correlate with high grade cancers. This is due to release of angiogenesis growth factors in malignant tumors. Postoperative Pelvic Masses Postoperative masses may be abscesses. Secondary signs such as asymmetry and capsular bulging may be helpful in diagnosis. Following organization and clot formation. hematomas are again anechoic. • Lymphoceles: Occur following surgical disruption of lymphatics usually after pelvic lymphnode dissection or renal transplantation. Prostatic Cancer • Small cancers are usually hypoechoic and better seen with transrectal USG. . irregular walls and posterior acoustic enhancement. • With the development of benign prostate hypertrophy.444 Seminar in Radiology • In normal young men.

c. lymphoma. Hypoechoic Lesions: Cellulitis. inflammatory diseases.29 Orbital Sonography ORBITAL SONOANATOMY AND TECHNIQUE – THE SALIENT FEATURES • 5-10 MHz pen type transducer • Patient examined both in sitting and supine position • Parocular or transocular approach used • Examine other related systems and consensual light reflex from other eye also • Baring exceptions all pathologies. PNS malignancy. optic nerve and muscles are hypoechoic. carotico-cavernous fistula. vascular diseases. . pericytoma. glioma. posterior lens capsule. abscess. attenuation and reflectivity. a. hematoma.5 MHz transducer used. meningioma. CCF. cysts. sarcoma. b. tumors. • Chief indications are : orbital trauma cases. rest all structures are echogenic • Aqueous and vitreous are anechoic. pseudotumor. neurilem- moma. Medium Echogenicity: Dermoid. capillary hemangioma. ORBITAL COLOR DOPPLER • 7. mucocele. MHF. Orbital Sonopathology Lesions of the eyeball are classified according to their echogenicity. Anechoic Lesions: Silicone implants. ULTRASOUND BIOMICROSCOPY • 40-100 MHz transducer used • For the microscopic evaluation of cornea. sclera and retina are echogenic while uvea and optic nerve are hypoechoic. anterior chamber and Iris • Anterior lens capsule and the angle of anterior chamber.

– Guiding the extraction. penetration with Retention – Sympathetic ophthalmitis • Findings – Hyphema – Angle widening and recession – Lens dislocation and signs of injury – Vetreous Hemorrhage and degeneration – Retinal detachment – Scleral injury – Choroidal detachment – Optic nerve avulsion – Associated soft tissue injury – Prephthisis – Phthisis Magnetic – Foreign body Nonmagnetic – Signs of sympathetic ophthalmitis (floaters in aqueous and vitreous. • Classification: – Non penetrating . cavernous hemangioma. metastasis.B. etc.) Indications of B-mode USG • Hazy media • Suspected intra-ocular • To ascertain the cause of retinal detachment • Examination of Vitreous • Localization of FB • Biometry • Proptosis • Vascular disease and vascular evaluation of tumours.). – Follow-up of the management. SONOLOGICAL FEATURES OF ORBITAL DISEASES Orbital Trauma • Clinical and plain X-ray are a must before USG • Indications: – Detection and localization of a radiolucent foreign body (F.B. pleomorphic adenoma. . foreign body..).B.extra ocular F. – Exact localization of a radio-opaque foreign body (F. Echogenic Lymphangioma. concussion. synechiae. Abrasion – Penetrating . contusion.).Penetrating wound only.B.446 Seminar in Radiology d. – Assessment of nature of foreign body (F. plastic exudates at pupil.

Persistent embryonic vitreous • Persistant embryonic vitreous appears echogenic with bands. Orbital Sonography 447 COMMON CONGENITAL CONDITIONS 1. Coloboma • Usually inferonasal. • Eyeball is just a cystic structure with no specialized differentiation. 6. Anophthalmia (Agenesis) • A fissure suggestive of lids and a small cyst in orbital fat suggestive of eyeball are seen. • Scleral ectasia and pseudopapilledema. it is a well defined homogenous lentiform hypoechoic lesion • May lead to RD. Melanoma • Usually in 5th or 6th decade of life • Eighty-five percent arise from choroids • Usually unilateral and posterior to the equator • Sonographically. COMMON OCULAR TUMORS 1. 2. Congenital cataract • Both shape and echogenicity are altered. Orbital Cysts 4. one from lens to optic disc. GIT • Retinal detachment may be associated. • Usually unilateral. PVD and vitreal degeneration • Differential diagnosis is from Fuch’s spots and disciform lesion. Retinoblastoma • Commonest primary intraocular malignancy in childhood and only second to melanoma in adults • Sonologically it is a well defined irregular hypoechoic mass with calcification • May be associated with retinal detachment • Differential diagnosis is from PHPV. 5. coat’s diseases. • Eye ball is small. testis. . There is a persistant Hyaloid vascular system. bronchus. kidney. 3. toxocara infection. retinopathy cysticercosis. • Usually anterior type. Cryptophthalmos • Lids are absent. premature. Metastasis • Are commoner than primary lesions • Usually located posteriorly • Commonly from breast. esp. 2. 3.

3. DISEASES OF LENS 1. subhyaloid hemorrhage. Disciform lesions • Heterogeneously hyperechoic rounded or flat elevation at macula • Has to be differentiated from melanoma. macular edema. intravitreal hemorrhage). Retinoschiasis • Presents as a thin echogenic membrane anterior to the equator • Starts at the periphery. inferonasal to disc • This may be a major differential diagnosis of retinal detachment. asteroid hyalosis. Hemangioma • A broad based echogenic lesion with blood filled spaces and calcification • May be associated with cutaneous lesions. DISEASES OF RETINA 1. membranes and adhesions. DISEASES OF VITREOUS • Senile degeneration • Vitreous detachment • Vitreous opacities (floaters. 2. Choristoma: • Well defined dense echogenic lesion with acoustic shadow • Usually bilateral • Common in peripapvilary area • D/D is from Drusen. macular degeneration. Ectopia Lentis. Cataract: • Increased echogenicity of lens • Nicely seen capsule • Thick posterior acoustic shadow • Two thin shadows • Thick posterior capsule • Rough capsule • Internal echoes • Anterior capsule seen • Distortion/dislocation of lens. . 5. 2.448 Seminar in Radiology 4. Retinal detachment • Appears as thin membrane attached at the ora serrata and optic disc • Ballooning and thickness are variable and depend on the age of retinal detachment • Any subretinal fluid should be scanned in both the sitting as well as supine positions • Partial retinal detachment has an atypical picture.

vortical vein exit and disc • Usually associated with signs of retinal and vitreous disease/injury • In significant injury it is very confusing as the vortical veins are avulsed • Has to be differentiated from retinal detachment. pseudopapilledema. Orbital Sonography 449 DISEASES OF THE CHOROID Choroidal Detachment • Presents as a slightly thicker membrane attached at ora. papilledema. drusen and melanocytoma • All present as increased echogenicity and protrusion of the nerve head. . DISEASES OF SCLEROCORNEA Staphyloma. it can reliably comment only on the optic nerve head • Important conditions that can be suspected are papillitis. pseudostaphyloma and ectesia are important conditions that present as a bluge in optic contour. DISEASES OF THE OPTIC NERVE • Papilla is best examined by a lateral approach • USG is not a very good modality to comment on the optic nerve • At the most.

Defects in Phagocytes • Phagocytes include monocytes. Non-AIDS D. the population of immunocompromised hosts has increased enormously reflecting the emergence of AIDS. Non-AIDS B. To be effective. the increased use of immunosuppressive agents for the treatment of tumors and collagen vascular diseases and for the prevention of rejection in organ transplant recipients.e. AIDS . Non-AIDS C. AIDS . AIDS . They defend the body against bacteria and fungi. Intra-abdominal manifestations . Many immunocompromised patients have multiple immune defects which not only reflect the underlying disease but also the immunosuppressive therapy.30 Radiology of the Immunocompromised Patient Sections A. macrophages and neutrophils. Thoracic disease in the immunocompromised patient . • The defects can be quantitative i. Musculoskeletal complications INTRODUCTION The term “immunocompromised host” is a patient who is at increased risk for life threatening infections as a consequence of abnormality of the immune system. Specific defects are associated with specific kinds of infection. decrease in the counts of these cells or qualitative in which the function of these cells is inadequate. engulf and kill the microorganisms. Neurological manifestations . . During the past few decades. Immune Defects There are 5 principal kinds of immune defects. these cells must migrate to the site of infections.

malaise and low grade fever. Complement System Defects • Complement activation serves to opsonize pathogens. The predominant pathogens are intracellular. • Patients with cell mediated immunodeficiency are susceptible to infections by bacteria. fungi. attract inflammatory cells and kill pathogens by creating pores in its membrane. • Defects in complement system result in recurrent infections with extracellular bacteria including encapsulated bacteria. SECTION A THORACIC DISEASE IN THE IMMUNOCOMPROMISED PATIENT Patients with AIDS Infections • Pneumocystis Carinii Pneumonia – This is the most common life threatening lung infection to occur in patients with AIDS. i. Radiology of the Immunocompromised Patient 451 Defects in Humoral Immunity • There are 3 principal ways in which antibodies protect the host against invading microorganisms. . Defects Caused by Splenectomy or Hyposplenism • The spleen produces bacteria specific opsonizing antibodies and removes antibody coated bacteria from the bloodstream. Patients with defective antibodies are especially vulnerable to infections by encapsulated bacteria. iii. Defects in Cell Mediated Immunity • CD8 cells kill host cells infected by pathogens. Opsonization — antibody coats the surface of bacteria to stimulate phagocyte cells to ingest and kill it. • Patients with impaired splenic function are at risk of developing over– whelming bacterial infections. viruses and protozoa. especially those caused by encapsulated bacteria. Neutralization — binding of the antibody to the virus before it can enter the host cell to replicate ii. Complement activation — enhances opsonization and can directly kill certain bacteria. • CD4 cells activate macrophages thus allowing them to destroy pathogens and also activate B cells to produce antibodies. – Its presentation varies from acute fulminant respiratory failure to a more insidious onset with nonspecific symptoms of nonproductive cough.

bronchogenic spread is seen in the form of poorly defined nodular opacities. • Increased interstitial markings because of interstitial fibrosis which develops as the infection heals. • With the use of prophylactic therapy (aerosolized pentamidine). — On chest X-ray and CT scan. diffuse infiltrates. Early disease (CD4 > 200/mm3): — Disease is confined to the lungs and presents with classic features of reactivation. CT Scan Varied patterns are noted- • Most common pattern is diffuse / patchy ground glass infiltrates that do not obscure bronchovascular markings. the usual findings are upper lobe infiltrates. • May be normal or show only minimal increased lung markings. tuberculosis may be the first indication that a patient is HIV infected. primary progressive TB or miliary TB. i. — The presentation is reminiscent of primary TB.452 Seminar in Radiology Radiological Features Chest X-ray • Bilateral perihilar or diffuse infiltrates which may progress to diffuse consolidation involving the entire lung. ii. . nodules. • Cystic form characterized by one or more thin walled cysts or cavities. After contrast administration.  Clinically. tuberculous lymph nodes demonstrate characteristic low attenuation necrotic centers and rim enhancement on CT. cavitary lesions and endobronchial spread. — On chest X-ray and CT. kidneys has been noted.  Radiology of tuberculosis in AIDS depends on the severity of immunocompromise especially the CD4 count. • Mycobacterial Infections – Mycobacterium Tuberculosis  Has emerged as a serious health problem throughout the world and is one of the index infections for surveillance of AIDS. spleen. On CT. extensive calcification involving mediastinal lymph nodes and abdominal viscera- liver. consolidation and lymphadenopathy are seen frequently. 3 to 10 mm in diameter and unevenly distributed. Late disease (CD4 < 200/mm3): — Disseminated disease is more common.

CT is especially useful in cases where chest X-ray is normal. — Most common causative organisms are S. Radiological features : In the form of focal pulmonary consolidation segmental or lobar in distribution. nodules. neoformans and C. pneumoniae. albicans. it is disseminated at the time of diagnosis. v. aureus. Acute bacterial bronchitis is seen on CT as bronchial wall thickening. almost always in conjunction with infection of the central nervous system. Fungal Infections — Any number of fungal species can cause pulmonary infection in the AIDS patient including H. iv. infiltrates or nodules are noted. Cytomegalovirus Infection • Usually coexists with other opportunistic infections like Pneumocystis carinii pneumonia or neoplasias like Kaposi’s sarcoma. Viral Infections A large number of viruses are known to infect the lungs in an HIV positive patient. Radiological findings : • Chest X-ray may be normal. CT shows a pattern of air space disease with alveolar opacities similar to those seen in pneumocystis carinii pneumonia. C. capsulatum. The nodules are usually small (<3mm) in size. influenzae and S. Occasionally. CMV is the commonest of these. immitis. C. Aspergillus does not occur frequently in AIDS. – Cryptococcal Infection: Most common fungal pathogen to affect the lungs. Radiological findings : Single/multiple discrete pulmonary nodules which may progress to either consolidation / cavitation and mediastinal lymphadenopathy. HIV positive patients may also show atypical features like infiltrates or cavitation. H.  Pulmonary disease is relatively uncommon (only 5% of cases) Radiological findings : In the form of pulmonary infiltrates. Radiological findings : Suggest disseminated nodular disease. typically. . Bacterial Infections — Often aggressive and recurrent bacterial infections occur. iii. – Histoplasmosis: Very common. Radiology of the Immunocompromised Patient 453 – Mycobacterium Avium Intracellulare  Seen at profound levels of immunosuppression (CD4 < 100 cells/ mm3). lymphadenopathy and even miliary disease.

Klebsiella Pneumonia Radiological pattern : • Lobar consolidation especially in right upper lobe. PULMONARY COMPLICATIONS IN IMMUNOCOMPROMISED PATIENTS–NON AIDS Bacterial Pneumonias • These are the most frequent pulmonary infections and rapid progression may occur. • Associated with a low CD4 count Radiological findings : • Chest X-ray shows diffuse bilateral alveolar/interstitial opacities with widespread poorly defined nodules. • These are mostly non-Hodgkin B cell lymphomas. Pleural effusion may be present but lymphadenopathy is uncommon. • CT can delineate the pattern of bronchovascular distribution of lesions. The pulmonary lesions due to Kaposi sarcoma radiate out from the pulmonary hila in a distinctive pattern often appearing to encase and coat the bronchi. Radiological findings : Solitary or multiple well defined pulmonary masses. Legionnaire’s Disease • Caused by legionella pneumophila Radiological pattern : • Solitary/multifocal homogenous opacities or lobar consolidation. • Cavitation is common • Volume of affected lung is maintained or may be increased causing bulging of fissures.454 Seminar in Radiology NEOPLASMS Kaposi’s Sarcoma • Most common AIDS related malignancy ≈ 25 percent of HIV positive patients. . Rapid progression is noted with spread to other lobes and the opposite lung. AIDS Related Lymphoma (ARL) • Seen at profound levels of immunosuppression when CD4 counts are <50-100 cells/mm3) in ≈ 2-5 percent of AIDS patients. Mediastinal adenopathy and pleural effusion may be present. • Almost all cases are seen in homosexual males.

Invasive Aspergillosis Radiological pattern : • Can present as lobar consolidation. Radiological features : • Filling defects are seen in the mid esophagus because of herpetic vesicles • Punched out ulcers develop on a background of normal mucosa when these vesicles burst. SECTION B INTRA-ABDOMINAL MANIFESTATIONS IN THE IMMUNO-COMPROMISED PATIENT Patients with AIDS Gastrointestinal Tract Infections A. Radiological features : . Cytomegalovirus • Can involve any segment of the GIT and presenting symptoms depend on the location and severity of infection. • Parenchymal infiltrates involve the apical/posterior segments of upper lobes or superior segments of lower lobes. Mycobacterium Tuberculosis • A pattern of post primary TB is seen. • Rarely. ‘Halo Sign’ is a specific sign consisting of a round pulmonary nodule with a surrounding halo of intermediate CT attenuation. bronchopneumonia or multiple nodules. Radiological features : • Diffuse mucosal nodularity with deep marginal ulceration is seen. Cavitation is a common feature. Radiology of the Immunocompromised Patient 455 Pseudomonas Aeruginosa and Escherichia Coli • Both usually present as a bronchopneumonia which is often basal. • Cavitation and endobronchial spread are common. a fungal mass protruding into the lumen or the tracking of barium beneath a sloughing pseudomembrane may be seen. Candida Albicans • Candida esophagitis occurs in advanced degrees of immunosuppression and is mostly associated with oral thrush. • On CT. B. Herpes Simplex • Herpes esophagitis is usually preceded by a prodromal flu like illness. • Double contrast studies can reveal mucosal plaques which lead to a nodular appearance of longitudinal esophageal folds simulating varices. This is because of hemorrhagic necrosis. C.

• Traction diverticulae. Mycobacterium Tuberculosis • Can involve any portion of the GIT along with involvement of lymph nodes and peritoneum. Associated with finding is mesenteric/retroperitoneal lymphadenopathy. pericolonic inflammation and ulcerations. Small bowel • Most common site of involvement is the ileocecal region. • Changes are more common in the stomach and smal bowel. D. ulcers and fistula formation may occur. ii. • It can show low attenuation bowel wall thickening. the GIT is the most frequently involved site. Scarring and stricture formation may result. ulceration and circumferential antral narrowing. superficial ulcers on a normal mucosal background. • Lymphoid nodular hyperplasia and ulceration occur. • Giant (>2 cm) ulcers may be seen in the distal esophagus which extend across the GE junction. . iii. marked shortening of caecal pole may occur. Stomach • Gastric involvement produces nodular wall thickening. Mycobacterium Avium Intracellulare Radiological features : • Small bowel  Produces bowel dilatation and fold thickening. • Radiological patterns include ulceration with associated spasm of the terminal ileum and proximal ascending colon. Esophagus • Discrete. E. Radiological features : i. In later stages. thickened folds and plaques.456 Seminar in Radiology i. Pancolitis may occur. Thickened folds with segmental narrowing may also be seen. large submucosal nodules with central umblication (bull’s eye or target lesions). Esophagus • Infection usually spreads from adjacent infected mediastinal lymph nodes. • A higher incidence of enteric fistulae and involvement of stomach/ duodenum is seen in AIDS patients. NEOPLASMS Kaposi’s Sarcoma • After skin and lymph nodal involvement. ii. Large bowel • Usually caecum and proximal ascending colon are involved. Radiological features : • Barium studies may show small nodules.

lymphoma has a greater tendency for extranodal disease and a worse prognosis. • Patient may present with right upper abdominal pain. Lymphoma • In AIDS patients. . marked hepatosplenomegaly with multifocal micro abscesses in the solid organs occur. BILIARY DISEASE OR AIDS CHOLANGIOPATHY • Inflammation of the biliary tract in the AIDS patient is usually due to Cryptosporidium or Cytomegalovirus. HEPATOSPLENIC INVOLVEMENT Mycobacterium Tuberculosis • Disseminated disease involves the liver and spleen. H. Radiology of the Immunocompromised Patient 457 AIDS Related Lymphoma • Usually non-Hodgkin’s type. nausea and vomiting. Fungal Infections • Causative fungi are Candida. • There are various patterns of presentation. Cryptococcus. • Stomach and small bowel are most frequently involved. capsulatum and C. immitis. Radiological features : • Characterized by nodular/circumferential wall thickening with or without ulceration. Mycobacterium Avium Intracellulare • In disseminated infection. • Multifocal lesions appear hypoechoic on USG and hypodense on CT. These include: i. Acalculus cholecystitis shows thickened GB wall with no calculus is seen on USG. • Enlarged lymph nodes and hepatosplenomegaly may be seen. sometimes showing a typical spokeswheel pattern. Bacterial Abscesses • Especially seen in AIDS patients who are IV drug abusers and prone to develop septic emboli particularly by staphylococcal organisms. • Imaging findings are hepatosplenemegaly with focal lesions. • Candidiasis causes microabscesses in the liver and spleen which appear as multiple small hypoechoic lesions on USG. • Spleen and liver are common sites of involvement.

avium intracellulare. The characteristic feature of this condition is global enlargement of kidneys without hydronephrosis or scarring. On USG. – USG. M. iii. an immunosuppressive regimen is necessary to combat rejection of the transplanted organ by the host • The effects of immunosuppression can be considered under 2 main headings • The increased incidence of infection • The increased incidence of neoplasia. On NCCT. a striated nephrogram is seen. etc. Infection Pneumatosis Intestinalis • The small or large bowel show the presence of gas filled cysts in the submucosa. CT and ERCP are complementary modalities for evaluation of AIDS cholangiopathy Pancreatic Disease • Infections with Cytomegalovirus. • Acute pancreatitis may result from the use of anti-HIV drugs like didanosine. the medullary density is increased and following contrast administration. • Radiological findings are similar to those seen in the immunocompetent population.458 Seminar in Radiology – Pericholecystic fluid may be present – Long standing disease may show thickening and enhancement of the walls of the extrahepatic biliary system. 2. M. Sclerosing cholangitis with focal strictures and dilatations of intra or extra hepatic bile ducts. ii. GI COMPLICATIONS AFTER TRANSPLANTATION • After transplantation. Infections – Pneumocystis carinii infection produces a pattern of punctate calcification which can be detected on USG or NCCT. the kidneys are large with increased echogenicity. Kaposi’s sarcoma and non-Hodgkin’s lymphoma can also involve the kidneys and present as focal lesions or bilateral masses. HIV nephropathy — can present with hypertension or progressive renal failure. . or less commonly the subserosa. may occur occasionally. Renal candidiasis can produce microabscesses are seen as small bull’s eye lesions on USG or hypodense on CT. Renal Disease Renal involvement can be in the form of: 1. Papillary stenosis with dilatation of the bile ducts and delayed clearance of contrast from the CBD. 3. Candida. tuberculosis.

liver. Radiological features : • Barium studies reveal bulky masses with central ulceration. circumferential and diffuse wall thickening. diarrhea Radiological features : • CT abdomen shows diffuse wall thickening. • Barium enema shows diffuse fold thickening and numerous plaque like lesions. • CT abdomen reveals prominent haustral folds. SECTION C NEUROLOGICAL MANIFESTATIONS IN THE IMMUNO- COMPROMISED PATIENT Patients with AIDS Neurological complications are in the form of: • AIDS dementia complex . pericolonic fluid and thickening of fascial planes. Pseudomembranous Colitis • Overgrowth of Clostridium difficile in the bowel produces a toxin which is responsible for this disease. Radiological features : • Plain X-ray abdomen shows varying degrees of colonic dilatation with haustral blunting. • CT abdomen shows a similar appearance with central areas of low attenuation due to necrosis and poorly defined margins. Radiology of the Immunocompromised Patient 459 Radiological features : • Plain X-ray abdomen shows submucosal cysts as a chain of bubble like translucencies • On barium enema. retroperitoneal lymph nodes and lungs. these impart a wavy serpigenous border to the bowel lumen. Neoplasms • Incidence of cancer increases after organ transplantation. Typhilitis • An inflammatory and/or necrotic process involving the caecum and/or terminal ileum or appendix. • Causes abdominal pain. Lymphoma • Most common site of involvement is central nervous system. Extracranial involvement occurs in GIT.

Toxoplasmosis • Most common opportunistic infection in patients with AIDS caused by the protozoan. Radiological features : • Both CT and MRI show diffuse brain atrophy • Typical of HIV encephalitis are bilaterally symmetrical white matter lesions. .460 Seminar in Radiology • Opportunistic infections • Tumors AIDS Dementia Complex: • Most common neurological problems in AIDS. • Lesions are usually multiple and bilateral. Perivascular spaces and choroid plexus are also involved. decreased memory and psychomotor retardation. Opportunistic Infections A. hypodense on CT and hyperintense on T2W MRI. Fungal Infections Cryptococcosis • Infection by C. Toxoplasma gondii. thalami and the midbrain. Radiological features : • Lesions are well defined. B. seizures and encephalopathy. headache. rounded foci which are hypodense on CT and hyperintense on T2 WMR • Sometimes a conglomerate of the fungus and mucoid material produces mass lesions called “gelatinous pseudocysts” or “cryptococcomas”. • Other fungal infections are uncommon although cases of H capsulatum. A flavus. A fumigatus. • Patients present with inability to concentrate. • Both solid and ring lesions may be seen in the same patients. etc have been documented. • Common sites of involvement are basal ganglia and the corticomedullary junction. Mucor. • Results from reactivation of latent infection or a recently acquired infection in an HIV patient presenting with fever. • Preferential involvement of meninges is seen producing meningitis or meningoencephalitis. Radiological features : • CT and MRI demonstrate the typical lesions to be either ring enhancing with central hypodensity on CT/hypointensity on T1W images or a solid enhancing mass with variable amounts of edema. • Also called AIDS encephalopathy or subacute encephalitis. neoformans is common. • These lesions involve the basal ganglia. • This condition shows a good response to antibiotic therapy.

• MR is more sensitive in demonstraing meningeal involvement especially at sites around pituitary infundibulum. optic chiasm. Progressive Multifocal Leukoencephalopathy (PML) • Caused by the JC Papova virus. • Predilection for parietooccipital region is noted. Spinal Involvement • May be in the form of vertebral body destruction. Tubercular abscesses • Seen as ring enhancing masses. Viral Infections i. ii. On MR. • Irregular granular destruction of white matter occurs ranging in size from a few mms to an entire lobe of the brain. D. cranial nerves. • Communicating hydrocephalus may occur. Typical features include T1 hypointense lesions involving two or more contiguous vertebrae and the intervening disk space. hypothalamic cerebral convexities and ventricular ependyma. i. Mycobacterial Infections • Infection of the meninges and brain with M. Tuberculoma • Can be solitary/multiple • Results from hematogenous spread • Both CECT and MR can demonstrate nodular/ring enhancing lesion. • MR is a very sensitive modality for the evaluation of spinal TB. myelitis or arachnoiditis may also occur. • Four patterns of involvement are seen. Cerebral Infarctions • Arteritis of small vessels results in infarcts. sylvian fissures and tentorium. • Calcification is better identified on CT iii. involvement of disc space. • Commonly seen in the region of basal ganglia • Seen on NCCT as hypodense lesions. paraspinal or epidural abscess. they appear as T1 hypointense and T2 hyperintense. Radiology of the Immunocompromised Patient 461 C. usually >3 cm in size. • Cord granulomas. These lesions are hyperintense on T2W images. . solitary. • Grey matter may be involved. Tubercular meningitis • Results from granulomatous infection of the leptomeninges with exudation. may be multioculated iv. avium intracellulare is infrequent but M. • CECT shows leptomeningeal enhancement and enhancing exudates along basal cisterns. tuberculosis is common and can result from either reactivation of a latent focus or a newly acquired infection. intra osseous.

Radiological Features : • On CECT. beginning at the corticomedullary junction and extending towards the ventricles. tumor spreads by hematogenous route. • Masks or decreases the contrast enhancement of tumors and infections as it stabilizes the blood-brain barrier. features of encephalitis and myelitis are prominent. • Usually B cell variety of Non Hodgkin’s lymphoma. Kaposi’s Sarcoma • Uncommon. • Common sites of involvement are periventricular white matter. Mucor. ii. Radiological Features : • CT shows diffuse hypodensities in the white matter. • MR is more sensitive and typical findings include asymmetric sub- cortical and deep white matter areas of increased T2 signal. NEUROLOGICAL COMPLICATIONS IN IMMUNOCOMPROMISED PATIENTS . subependymal contrast enhancement and focal nodular/ring enhancing lesions. Neoplasms A. .NON AIDS Steroids • Enlargement of ventricular system and cortical sulci because of an electrolyte shift in the extracellular spaces. • MR reveals periventricular and subependymal enhancing lesions. lymphomatous lesions in non-HIV setting appear slightly hyperdense and show homogenous contrast enhancement. In contrast.462 Seminar in Radiology Radiological Features : • CT shows hypodense white matter lesions. corpus callosum and basal ganglia. they appear hypointense on T1 and iso to hyperintense on T2. B. Cytomegalovirus • Involves both brain and spinal cord. Radiological Features : • Enhancement is homogenously and cannot be differentiated by CT or MR from other enhancing mass lesions. • Increases vulnerability to fungal infections by Aspergillus. iii. Primary CNS Lymphoma • Second only to toxoplasmosis as a cause of focal cerebral masses in AIDS patients. • Multicentric tumors and central necrosis are common features. Candida and pyogenic infections by Staph aureus. • Clinically. They show intense enhancement with Gadolinium. they appear as ring enhancing lesions. Contrast enhancement is absent or minimal. On MRI.

bondy destruction can be seen. confusion. C. motor and speech derangement. etc • CT and MR can reveal evidence of meningitis. hydrocephalus. Penetration of the arterial system occurs. A. • The affected sinuses may appear hyperdense on CT scans and low signal intensity on MRI studies. . most important of which is Mucormycosis. Infections A. Organ Transplantation Both immunosuppression and the underlying organ disease can lead to complications. meningitis and cerebral abscess may result. Neoplasms • An increased incidence of CNS lymphoma is noted. • Bones are commonly affected. C neoformans. • Fungi usually enter the nasal vault leading to sinusitis and orbital cellulitis. The tumor may become multicentric and subependymal spread occurs. • Encephalopathy occurs leading to seizures. Cryptococcus. Drug Related Neurotoxicity • Such an effect has been noticed with cyclosporine. Opportunistic Infections • Usually occur 1 to 4 months after transplantation • The organisms are Aspergillus. Chronic Granulomatous Disease of Childhood. In the later stages of infection. Radiology of the Immunocompromised Patient 463 Diabetes Mellitus • Increased incidence of CNS infections. If the internal carotid arteries are involved. • Leukocytes are unable to respond normally to infections leading to a chronic inflammatory process. cerebral infarction. Mucor. B. SECTION D MUSCULOSKELETAL COMPLICATIONS IN THE IMMUNOCOMPROMISED PATIENT • Both infection and neoplasms may be seen. Listeria. cerebral abscesses and infarcts. • MR shows high signal intensity regions involving the subcortical white matter of the occipital lobes. • MR & CT reveal a ring or solid enhancing mass lesion.

• Ulcers. soft tissue masses and marrow involvement may be seen. Tubercular Arthritis • Usually affects the major joints . Kaposi’s Sarcoma • In AIDS patients. • Radiological features include juxtarticular osteoporosis. this multifocal malignancy may rarely involve the skeletal system. periosteal reaction.especially the hip and knee. • Radiological features include blurring of fat planes. Septic Arthritis • Common causative organisms are staphylococci. Superimposed sepsis causes osteoporosis and acceleration of bone destruction. an immune defect/steroid intake should be ruled out. A sclerotic or mixed picture with ill defined zone of transition. often abutting onto epiphyseal plates are seen. C. pneumococci. B. D. . • If more than one joint is infected. Neoplasms A. • Soft tissue infection leads to swelling loss of fat planes and lucencies may be seen. reduction of joint space and bone destruction. peripheral osseous erosions and reduction of joint space. • Radiological features are those of permeative lytic lesions with cortical destruction. Osteomyelitis in Diabetes Mellitus • Infection of bone and soft tissue occurs. Streptococci. B.464 Seminar in Radiology Radiological Features : • Widespread small foci of osteolysis. Lymphoma • Primary lymphoma is rare but secondary involvement may occur. lead to involvement of underlying bones with the development of osteomyelitis. osteoporosis. • Healing is with florid new bone formation leading to sclerosis and expansion. seen as soft tissue radiolucent defects. • Radiologically presents as lytic lesions with cortical disruption and periosteal reaction.

457 primary invasive 193 AIDS-related leukoencephalopathy 143 secondary angioinvasive 193 Alexander disease 139 Asphyxiated thoracic dystrophy 427 Alveolar microlithiasis 216 Atresia of small bowel 420 Alveolar proteonosis 215 Atrial septal defect 155 Amebiasis 196 types 155 Ameloblastoma 105 Autosomal recessive polycystic kidney Aminoacidopathies 147 disease 425 Ampullary carcinoma 234 Avascular necrosis 378 . 333 Abdominal tuberculosis 265 Aneurysmal bone cyst 86 classification of 266 Ankylosing spondylitis 41 gastrointestinal tuberculosis 266 Anomalies of fetal spine 425 miscellaneous 266 Anorectal atresia 421 peritoneal tuberculosis 266 Antenatal abnormalities 412 tuberculosis of mesentery 266 causes 412 tuberculosis of solid visceras 266 clinical markers 412 epidemiology 265 nonsonographic findings 413 Abnormalities of cervix 436 sonographic findings 413 Abnormalities of the biliary tree 262 teratogen 412 Abscesses 444 ultrasound in prenatal screening 412 Achondrogenesis 427 Aortic regurgitation 178 Acquired immunodeficiency syndrome 198 Aortic stenosis 176 Acquired leukodystrophies 140 Aortic valve 175 Actinomycosis 195 Aortopulmonary shunts 160 Acute cholecystitis 386 Aquired cyst and dialysis 349 Acute cortical necrosis 347 Arachnoiditis 129 Acute disseminated encephalomyelitis Arthritis 378 141 degenerative 378 Acute osteomyelitis 378 inflammatory 378 Acute pyelonephritis 339 Asbestosis 206 Acute renal failure 293 Ascariasis 197 Acute respiratory distress syndrome 212 Ascaris lumbricoides 229 Acute tubular necrosis 346 Aspergilloma 194 Adenomatous polyps 281 Adenomyosis 310 Aspergillosis 193 AIDS 333 allergic bronchopulmonary 194 AIDS cholangiopathy 457 invasive 194 AIDS related lymphoma 454. Index A Amyloidosis 215.

466 Seminar in Radiology B retroperitoneum 30 Bacterial abscesses 457 splenic calcification 26 Bacterial pneumonias 454 ureter 28 Barium enema 276 urinary bladder urethra 28 Barriers 400 arterial 17 calculation of thickness of barrier 401 differential diagnosis 14 types 401 dystrophic 14 primary 401 idiopathic 15 secondary 401 metastatic 15 value of lead as barrier 402 infection 18 Basal cell nevus syndrome 286 bacterial 18 Biliary disease 457 parasitic 18 Biliary drainage 251 intracranial calcification 32 Biliary drainage catheters 253 abnormal 33 clinical characteristics 253 physiological 32 Biliary guide wires 252 neck 32 clinical characteristics 252 pericardial calcification 32 Biliary leak 387 pleural calcification 32 Biliary obstruction 223 asbestosis 32 Biliary tree without jaundice 225 empyema 32 Biswanger’s disease 146 hemothorax 32 Bladder extrophy 423 soft tissue calcification 13 Bone 109 dystrophic 13 basic structure 109 idiopathic 13 bone destruction 110 metastatic 13 bone formation 110 thoracic calcifications 30 bone reabsorption 111 lymph nodal 30 functions 109 parenchymal 31 hemopoietic 109 vascular 31 mechanical 109 vascular 17 metabolic 109 venous 17 metabolism 109 Candida albicans 193 physiology 109 Candidiasis 193 Bone abscess 79 Cannavan’s disease 139 Bony lesions 284 Capillary haemangioma 103 Brown tumor of hyperparathyroidism 84 Caplan’s syndrome 205 Carcinoma head of pancreas 235 C Cardiac chambers 164 Calcification 13 atria 164 abdominal calcifications 25 persistent common truncus arteriosus adrenals 29 166 alimentary tract 29 ventricles 165 female genitourinary tract 28 Cardiac tumors 429 gallbladder 27 Cardiovascular system 394 generalized abdominal calcification 30 Caudal regression syndrome 426 kidney 27 Causes of neurological deficits 127 liver 25 Cellulitis 378 male genitourinary tract 28 Central chondrosarcoma 91 pancreatic calcification 26 Central nervous system 389 .

Index 467 Central pontine myelinosis 143 segmentation 366 Cervical cancer 313 spiral acquisition 365 Cervical spine injury 51 spiral CT 365 Clark’s 12 signs 51 Congenital anomalies 412 Verma’s 13th sign 52 types 412 Cherubism 80 deformation 412 Cholangiocarcinoma 233 disruption 412 Choledochal cyst 233. 463 366 Diagnostic techniques in metabolic bone principle 363 disease 121 . 333 Coils 371 acquired 20 Collagen vascular disease 207 congenital 19 Color Doppler 440 Cowden’s syndrome 285 Colorectal polyps 280 Craniospinal tuberculosis 125 groups 280 symptoms and signs 125 polypoid lesion of subepithelial Cronkhite Canada syndrome 286 origin 280 Cryptococcosis 196. 460 polypoid lesions of epithelial origin Cushing disease 114 280 Cyanosis 151 Common congenital conditions 447 Cystadenomas 315 Common ocular tumors 447 Cystic adenomatoid malformation 419 choristoma 448 Cystic teratomas/dermoid cysts 315 hemangioma 448 Cystic tuberculosis 94 melanoma 447 Cystourethrography 383 metastasis 447 Cytomegalovirus infection 453 retinoblastoma 447 Complement system defects 451 D Complications of renal TB 319 Defects caused by splenectomy or Computed tomography 363 hyposplenism 451 basic technology 366 Defects in cell mediated immunity 451 collimator design 366 Defects in humoral immunity 451 CT angiography 365 Defects in phagocytes 451 detector design 366 Delayed excretion 386 image quality 365 Dentigerous cyst 105 image reconstruction 365 Dermatomyositis 20 multi-slice computed tomography Diabetes mellitus 333. 421 dysplasia 412 Choledocholithiasis 227 malformation 412 primary 227 Congenital cyanotic heart disease 151 secondary 227 assessment of severity 153 Cholelithotomy by cholecystostomy 258 classification 154 Cholesteatoma 346 acyanotic 154 Chondroblastoma 82 cyanotic 154 Chondromyxoid fibroma 89 others 155 Chromosomal abnormalities 430 differential diagnosis 152 Chronic cholecystitis 387 incidence of 154 Chronic obstruction 299 Congenital diaphragmatic hernia 418 Chronic pyelonephritis 340 foramen of Bochdaleck hernia 418 Chronic renal failure 293 foramen of Morgagni hernia 418 Closed-circuit television 370 Congenital heart disease 161 Coccidiodomycosis 94. 199. 195 Connective tissue disorders 19.

434 Diffusible traces 390 Endoscopic retrograde cholangiography 260 Dilated intrahepatic biliary radicles 224. 435 radiological 121 Endometrial polyps 435 Diastomatomyelia 426 Endometriosis 309. 379 Emphysematous pyelonephritis 344 Filariasis 346 Enchondroma 81 Film badge 408 End stage kidney 349 Flurosis 120 Endocrine system 392 Fountain pen dosimeter 409 .468 Seminar in Radiology biochemical 121 Endometrial 308 biopsy 121 Endometrial carcinoma 311. Features of metabolic bone diseases 113 opathy 145 Fetal abdomen 419 Doppler ultrasound 369 Fetal abdominal wall defect 422 Dosimetry 408 Fetal cardiac abnormalities 428 Drug induced pulmonary disease 214 Fetal chest 418 ARDS 214 Fetal head anomalies 413 mediastinal adenopathy 215 banana sign 416 opportunistic infection 215 fetal facial abnormalities 417 pulmonary eosinophilia 214 fetal neck 417 pulmonary fibrosis 214 fetal nuchal translucency 417 pulmonary oedema 215 infratentorial abnormalities 415 pulmonary thromboembolism 215 nuchal thickness 417 SLE reaction 214 supratentorial abnormalities 413 Duplication anomalies 423 Fetal hydrops 428 E Fetal renal anomalies 422 Ebstein’s anomaly 168 Fetal skeletal anomalies 426 Echinococcus granulosus 197 Fibrosarcoma 92 Eclampsia 145 Fibrosing alveolitis 210 Ectopic pregnancy 442 Fibrous cortical defect 88 Ectopic thyroid 392 Fibrous dysplasia 79. 225 Endosonography 368 Disc bulge 74 applications 368 Disc herniation 74 transesophageal 368 etiology and pathology 74 transrectal 368 imaging 74 transurethral 368 location 74 transvaginal 368 types 74 Enteropathic arthropathy 43 disc extrusion 74 Eosinophilic granuloma 83 disc protrusion 74 Epiderml inclusion cyst 108 sequestration 75 Escherichia coli 455 Discogenic spinal stenosis 73 Esophageal polyps 277 Diseases of lens 448 fibrovascular polyp 277 Diseases of retina 448 inflammatory polyp 278 disciform lesions 448 Esophageal varices 238 retinal detachment 448 Ewing’s sarcoma 99 retinoschiasis 448 Expansile rib lesions 105 Diseases of sclerocornea 449 Diseases of the choroid 449 F choroidal detachment 449 Facet hypertrophy 73 Diseases of the optic nerve 449 Facet joint disease and synovial cyst 71 Diseases of vitreous 448 Familial multiple polyposis 283 Disseminated necrotizing leukoencephal.

455 Hypogondadism 117 Gastrointestinal tract masses 442 Hypoparathyroidism 120 Generalized decreased bone density 112 Hypopituitarism 116 Generalized increased bone density 112 Hypoxic ischaemic encephalopathy 146 Genital tract tuberculosis 325 Genitourinary tuberculosis 318 I clinical features 319 Idiopathic chondrolysis 118 constitutional symptoms 319 Idiopathic pulmonary ossification 216 symptoms suggestive of UTI 319 Imaging in gynecological disorders 304 early and advanced features 320 conventional radiography 304 pathogenesis 318 CT 307 Gerbode LV-RA shunt 158 cystography 305 Gestational trophoblastic neoplasia 312 hysterosalpingography 305 GI complications 458 intravenous urography 304 Giant cell tumor 89 MRI 307 Global hypoperfusion syndrome 145 Imaging of kidneys in renal failure 296 Glomus tumor 106 Immune defects 450 Gout 118 Immunocompromised host 450 Granulomatous disease of childhood 463 Inert gases 388 Infective arthritis 44 H Inferior vena cavogram 250 H. influenzae 44 Inflammation 378 Hashimoto’s thyroiditis 393 Inflammatory arthropathy 34 Heavy metal poisoning 120 infective 34 Hematoma 22. Index 469 Functional cysts 437 grading in 296 Fungal diseases of the lung 193 Hydronephrosis 421 Fungal infection 346. 457 Hyperparathyroidism 114 Fungi 199 Hyperphosphatasia 114 Hyperpituitarism 116 G Hyperplastic polyps 282 Gallbladder carcinoma 235 Hypersensitivity pneumonitis 207 Gallbladder drainage 257 Hypertensive encephalopathy 145 Gangliosidoses 147 Hyperthyroidism 117 Gardner’s syndrome 283 Hypervitaminosis A 120 Gastrochisis 422 Hypervitaminosis D 120 Gastrointestinal tract 383. 229 Inflammatory tubal masses 440 Hydatid disease 346 Influenza virus 198 Hydrometrocolpos 424 International Commission on Radiological Hydronephrosis 296 Protection 397 . 444 investigations 34 Hemophilic pseudotumor 93 arthrography 35 Hemosiderosis 213 CT scan 35 Hepatobiliary tuberculosis 273 magnetic resonance imaging 35 Herpes varicella zoster 198 plain X-ray 34 High-tension transformer 361 radio-nuclide scan 35 Hirschsprung’s disease 420 ultrasonography 35 Histiocytosis ‘X’ 211 non-infective 34 Histoplasmosis 195 sero-negative 34 HIV infection 333 sero-positive 34 Horseshoe kidney 422 Inflammatory bowel disease 385 Hydatid cyst 94.

464 hypervitaminosis D 17 Klebsiella pneumonia 186.Bignami disease 143 obstructive jaundice in children 223 Measles giant-cell pneumonia 198 obstructive jaundice in neonates 223 Meckel’s diverticulum 385 pathogenesis 221 Meconium ileus 420 Juvenile chronic polyarthritis 40 Mediastinum mass 419 Juvenile osteoporosis 114 Medullary sponge kidney 348 Juvenile polyposis 285 Metabolic bone disease 111 Juvenile polyps 282 classification 111 Metabolic disorders 15 K gout 17 Kaposi’s sarcoma 454. 457. 454 hypoparathyroidism 16 L milk-alkali syndrome 17 Langerhans cell histiocytosis 211 primary hyperparathyroidism 15 Lateral recess stenosis 73 secondary hyperparathyroidism 16 Lateral shift and scoliosis 128 Metastasis 85. 459. 91. 456. 95 Interventional procedures in portal Lucent lesions of fingers 106 hypertension 259 Lucent/cystic lesion jaw 104 Intracorporeal biliary lithotripsy 258 Lumbosacral spine 70 Intracranial tuberculosis 132 Lyme disease 142 Intrahepatic biliary radicles 225 Lymphangiomyomatosis 212 Intra-operative sonography 369 Lymphoceles 444 Invasive aspergillosis 455 Lymphoma 286. 83. 86. 236. 464 Investigations for visualization of Lymphoma of bone 92 kidneys 291 M J Malakoplakia 346 Jaundice 221 Malignant fibrous hystiocytosis 100 approach to diagnose 222 Malignant ovarian tumors 316 hepatocellular jaundice 222 Mandible 418 obstructive jaundice 222 Marchiafava . 377 Law of Bergonie and Tribondeau 399 Migratory osteoporosis 118 Law of transformer 361 Mirizzi’s syndrome 228 Legionnaires’ disease 454 Mitochondrial cytopathies 147 Leigh’s disease 147 Mitral regurgitation 174 Leiomyosarcoma 312 Mitral stenosis 171 Leptomeningeal cyst 104 Mitral valve 171 Leukodystrophies 135 anatomical landmark 171 adenoleukodystrophy 137 changes in MV area 171 distinctive features 135 Mixed connective tissue disease 64 inherited 135 MR contrast media 373 .470 Seminar in Radiology Interstitial lung diseases 200 Krabbe leukodystrophy 136 clinical features 202 metachromatic 135 epidemiology 201 Leukoplakia 346 etiology 200 Ligamentum flavum hypertrophy 73 findings on X-ray chest and CT Liver fluke 229 scan 202 Localized decreased bone density 112 imaging techniques 202 Localized increased bone density 112 pathogenesis 201 L-R shunts 155 Intestinal polyposis 277 Lucent bone lesion 90 diagnosis 277 Lucent bone lesion in medulla 78.

132 Myocardial perfusion imaging 394 classification 4 Myositis ossificans 23 generalized 4 localized 4 N low bone mass 8 National Digestive Disease Advisory normal 8 Board 259 severe osteoporosis 8 Neonatal and childhood jaundice 386 investigations 8 Neoplasms 459 biochemical investigations 12 Nephrocalcinosis 347 comptom scattering 10 Neurofibromatosis 212 dual energy photon absorptiometry Neurological complications 126 10 group A 126 dual energy X-ray absorptiometry 11 group B 127 magnetic resonance imaging 12 Nocardiasis 195 magnification radiography 9 Nonepithelial tumors 282 neutron activation analysis 9 Non-obstructive dilatation 300 photodensitometry 9 Nonosseous injury 50 quantitative computed tomography Non-ossifying fibroma 87 11 Normal myelination 134 quantitative ultrasound 12 O radiogrammetry 9 Obstruction of extrahepatic bile 223 single energy photon Occlusion and infarction 336 absorptiometry 10 Omphalocoele 422 single X-ray technique 11 Opportunistic fungal infection 193 standard radiography 8 Orbital color Doppler 445 pathogenesis 3 Orbital sonoanatomy and technique 445 types 4 Orbital sonopathology 445 glucocorticoid excess 5 Orbital trauma 446 hyperprolactinemia 6 Organ transplantation 463 hypogonadism 6 Osseous hemangiomas 103 idiopathic juvenile 5 Osseous injuries 51 involutional 4 Ossification 22 reflex sympathetic dystrophy Ossification of posterior longitudinal syndrome 6 ligament 73 regional migratory 7 Osteoarthritis 68. 75 thyrotoxicosis 6 in particular joints 76 transient 7 hand and wrist joint 77 Osteoporosis group 113 . Index 471 Muir-Torre syndrome 284 knee joint 76 Mullerian anomalies 308 shoulder joint 77 Multiple lytic lesion 101 types 75 Multiple myeloma 85 primary 75 Multiple sclerosis 140 secondary 75 Mycobacteria 198 Osteoblastoma 107 Mycobacterial infections 461 Osteogenesis imperfecta 427 Mycobacterium avium 198 Osteolytic bone lesions 78 Mycobacterium avium intracellulare Osteolytic lesion 101 457 Osteomyelitis 95 Mycobacterium tuberculosis 455 Osteomyelitis in diabetes mellitus 464 Myelocystocoele 426 Osteophytes 73 Myelogram 129 Osteoporosis 3.

424 opening on ventilation 354 Ovarian masses 437 pass box 355 Ovarian neoplasms 315. 396 caused by gram-positive aerobic Peutz-Jeghers syndrome 285 bacteria 187 Peuzaeus-Merzbacher disease 138 infection by direct spread 186 Planning of diagnostic X-ray department 350 infection via the pulmonary vasculature automatic processing 360 186 building essentials 355 infection via the tracheobronchial tree 185 cassette 358 lobular pneumonia 186 control panel and waiting area 354 pathology 185 radiological findings 186 dark room 354 Pocket ionization chamber 410 departmental activity 351 POEMS syndrome 86 design of X-ray facilities 350 Polycystic kidney disease 425 designing team 351 Polymyositis and dermatomyositis 63 dry side 356 radiographic features 63 electric wiring 355 Polyposis syndromes 282 entrance to dark room 355 hereditary polyposis syndromes 282 film construction 357 nonfamilial polyposis syndromes 283 fluorescent screen 359 Polyps 284 illumination 356 Polyps of the stomach 278 illumination control 354 adenomatous 279 intensifying screens 358 hamartomatous 279 location 354 heterotopic 279 location of X-ray department 352 hyperplastic 278 . pathological and radiological X-ray examination room 353 findings of 432 Plasmacytoma 91 differential diagnosis 432 Pneumatosis intestinalis 458 pelvic masses of gynecological origin 433 Pneumoconiosis 205 Pelvic masses of non-gynecological coal workers pneumoconiosis 205 origin 442 simple pneumoconiosis 205 Perfusion index 382 Pneumocystis carinii pneumonia 196.472 Seminar in Radiology Osteosarcoma 97 manual processing 359 Ovarian cyst 314. 451 Perfusion studies 388 Pneumonia 185 Peritoneal inclusion cyst 440 aims 185 Peritoneal tuberculosis 272 air space or alveolar (lobar) pneumonia Permanent magnets 371 186 PET 391. 438 plan layout 352 Ovarian torsion 439 room size 353 P screen speed 358 Paget’s disease 379 size and installation of the darkroom 355 Pancreatic disease 458 types of films 357 Pancreatic tuberculosis 274 duplicating film 357 PAPVD 169 mammography film 357 Parasitic infections 196 nonscreen film 357 Parathyroid gland 393 screen film 357 Parovarian cysts 440 use of protective devices 354 Pelvic kidney 443 ventilation 355 Pelvic masses 432 wet side 356 clinical.

458 Pseudomembranous colitis 459 classification 331 Pseudomonas aeruginosa 455 dialysis associated 332 Pseudo-pseudo-hypoparathyroidism 120 glomerular 331 Psoriatic arthritis 42 renovascular 332 Pulmonary eosinophilia 209 tubulointerstitial 332 asthmatic 210 Renal ectopia 422 chronic 210 Renal failure 295 pulmonary 210 Renal imaging 379 simple 209 Renal insufficiency 302 tropical 210 Renal neoplasm 425 Pulmonary hemorrhage 213 Renal parenchymal disease 301 Pulmonary valve 180 classification 301 PVC toxicity 118 dialysis associated disease 301 R glomerular disease 301 Radiation hazard 397 renovascular disease 301 early effects 398 tubulointerstitial disease 301 genetic effects 399 Renal trauma 383 late effects 398 Renal tuberculosis 342 nonstochastic/deterministic/acute Renal vein thrombosis 334 effects 399 Renovascular disorders 334 . Index 473 non-epithelial tumors 280 stochastic/nondeterministic/chronic retention 279 399 Portal hypertension 237 Radiation protection 400 angiography in management of 247 Radicular cyst 105 classification 239 Radioactivity 375 postsinusoidal 239 units of 375 presinusoidal 239 Radiobiology 397 influence of 239 Radionucleide cisternography 392 pathogenesis 237 Radiopharmaceuticals used in various sonographic and color Doppler flow systemic disorders 374 imaging evolution of 240 applications 377 Portal venous thrombosis 243 bone imaging 375 Posterior mediastinum 419 clinical applications in different Postinflammatory strictures 231 systems 375 Postoperative pelvic masses 444 radionucleide in bone 375 Post-traumatic stricture 230 radiopharmaceuticals 375 Pott’s paraplegia 126 Rectification 361 paraplegia of slow onset 126 full wave rectification 362 Pott’s spine 129 half wave rectification 362 Pregnancy 407 method 361 Primary bone tumors 377 Recurrent tumor versus radiation fibrosis Primary osteolysis 118 317 Primary sclerosing cholangitis 232 Regional osteoporosis 118 Progressive massive fibrosis 205 Reiter’s syndrome 43 Progressive multifocal Renal agenesis 422 leucoencephalopathy 142 Renal artery stenosis 337 Prostatic cancer 444 Renal cystic disease 424 Prune Belly syndrome 424 Renal diseases 331.

240. 188 Simple bone cyst 81 Steroids 462 Sirenomelia 426 Streptococcus pyogenes 44 Small intestines and ileocecal tuberculosis Sudeck’s osteodystrophy 118 269 Super conducting magnet 371 diagnosis 275 Syphilitic infection 131 Soft tissue tumors 284 Systemic lupus erythematosus 61 Soft tissues necrosis 21 musculoskeletal features 62 Son-diffusible tracers 390 radiographic features 62 Sonological features of orbital diseases 446 Systemic vasculitides 209 SPECT imaging 395 Spinal column 65 T Spinal injury 49 T1 agents 373 imaging features 50 T2 agents 373 medicolegal aspect 49 TAPVD 169 Spinal stenosis 72 TB of female genital tract 325 . 63 Spinal tumor syndrome 127 radiographic features 63 Splenic tuberculosis 274 Scoliosis and hemivertebra 425 Spondylolisthesis 73.474 Seminar in Radiology Renovascular hypertension 337 clinical presentation 72 Residual bladder volume 383 acquired 72 Resistive magnets 371 congenital 72 Respiratory system 387 miscellaneous 72 Rheumatoid arthritis 36 location 72 cause 36 types 73 diagnostic criteria 36 discogenic 73 pathogenesis 36 non-discogenic 73 Rheumatoid arthritis 60 Spinal trauma 45 radiographic features 60 classification 45 Rickets 119 compression/axial loading injury 46 type I 119 direct injury 46 type II 119 extension injury 46 Room 450 flexion injuries 45 examination rooms 450 major injury 46 film rooms 450 minor injury 46 patient rooms 450 stable spine 46 technologist rooms 351 unstable spine 46 Ruvalcaba Myhre Smith syndrome 286 violent muscle contraction 46 etiology 45 S imaging 47 Sacrococcygeal teratoma 426 imaging modalities 48 Salivary glands 387 magnetic resonance imaging 49 Salmonella 44 plain film radiography 48 Sarcoidosis 203 signs of instability 47 Schistosomiasis 197. 346 Spinal tuberculosis 126 Scleroderma 21. 137 Scurvy 116 Spondylolysis 73 Secondary intestinal tuberculosis 268 Spondylosis 67 Septic arthritis 464 age incidence 68 Silicosis 206 etiology and pathology 67 complicated 206 location 68 simple 206 Staphylococcus aureus 44.

383 Telangiectatic osteosarcoma 93 benign 23 Teratoma 419 idiopathic 24 TGA 166 soft tissue sarcomas 24 Thermoluminescent dosimeter 408. 131. 378 Uterine leiomyomas 310 Tricuspid valve 180 Tubal masses 440 V Tubercular abscess 133 Vaginal neoplasms 316 Tubercular arthritis 464 Ventilation/perfusion ratio 388 Tubercular lesions 125 Ventricular septal defect 158 Tubercular meningitis 132 types 158 Tubercular orchitis 327 membranous 158 Tubercular peritonitis 272 muscular 158 Tubercular spondylitis 129 Vial and postviral demyelination 141 Tuberculomas 133 Viral infections 461 Tuberculosis 188 Viral pneumonia 198 cavitating 190 Viruses 199 exudative 191 fibrocavitatory 191 W fibrotic 192 Wegener’s granulomatosis 209 postprimary 190 White matter 134 productive 190. Index 475 TB of the male genital tract 326 Tubulo interstitial diseases 339 TB of ureter. bladder and urethra 323 Tumors 23. 411 Turcot’s syndrome 284 Thoracolumbar spine injuries 54 Turner’s syndrome 6 algorithms for imaging of spinal Typhilitis 459 trauma 58 burst fracture 55 U fracture dislocation 55 Ultrasound 367 seat belt injury 55 Ultrasound biomicroscopy 445 wedge fracture 54 Ultrasound contrast media 369 Thyroid acropachy 121 Ultrasound techniques 431 Thyroid gland 392 Doppler USG 431 Thyroid nodule 392 sonohysterosalpingography 432 Torulosis 196 three-dimensional imaging 432 Toxic and traumatic encephalopathies 144 transabdominal ultrasound 431 Toxoplasmosis 196 transvaginal ultrasound 431 Transcholecystic intervention 256 Uremia 289 Transducers 368 clinical signs 289 Transformer 361 symptoms 289 Transhepatic cholangiography 263 Uremic emergency 289 Transhepatic interventions 251 Urethral obstruction 423 Transposition of great arteries 167 Urinary tract masses 443 Trauma 21. 191 classes 134 Tuberculosis of colon and rectum 269 demyelinating 134 Tuberculous paraplegia 127 dysmyelinating 134 classification of 127 Tuberous sclerosis 212 X Tubo-ovarian abscess 314 Xanthogranulomatous pyelonephritis 345 .