Miscellaneous

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
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Seminar in Radiology
2006, OP Sharma
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recording, or otherwise, without the prior written permission of the author and the publisher.
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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.
Contents
SECTION 1: MUSCULOSKELETAL SYSTEM

1. Osteoporotic Bone Disease 3
2. Soft Tissue Calcification (Plain X-ray Appearance) 13
3. Inflammatory Arthropathy 34
4. Spinal Trauma 45
5. Connective Tissue Disorders Involving Joints 59
6. Degenerative Disorders of Spine and Joints 65
7. Osteolytic Bone Lesions 78
8. Metabolic Bone Diseases 109
SECTION 2: CENTRAL NERVOUS SYSTEM

9. Craniospinal Tuberculosis 125
10. Diseases of White Matter Brain Substances 134
SECTION 3: CARDIOVASCULAR SYSTEM
11. Diagnostic Approach to a Case of Congenital
Cyanotic Heart Disease 151
12. Valvular Heart Disease 171
SECTION 4: RESPIRATORY SYSTEM
13. Pulmonary Infection 185
14. Interstitial Lung Diseases 200
SECTION 5: GASTROINTESTINAL TRACT, PANCREAS AND
HEPATOBILIARY TRACT
15. Imaging in Jaundice 221
16. Portal Hypertension 237
17. Hepatobiliary Intervention 251
18. Abdominal Tuberculosis 265
19. Intestinal Polyposis 277
SECTION 6: GENITOURINARY SYSTEM
20. Uremia and Imaging 289
21. Role of Imaging in Gynecological Disorders 304
22. Genitourinary Tuberculosis 318
xii Seminar in Radiology
23. Medical Renal Diseases 331

24. Planning of Radiology Department 350
25. Common Radiopharmaceuticals Used in
Various Systemic Disorders 374
26. Radiation Hazard and Protection 397
27. Ultrasonography of Systemic Antenatal Abnormalities 412
28. Ultrasound and Color Doppler in Pelvic Masses 431
29. Orbital Sonography 445
30. Radiology of the Immunocompromised Patient 450
Index 465
SECTION 1
Musculoskeletal
System
1
Osteoporotic Bone Disease
DEFINITION
Osteoporosis is defined as decreased bone mass per unit volume without
microstructural abnormality. Bone quality is normal but quantity is reduced. It
is the most frequent metabolic bone disease characterized by fractures especially
in femur neck, spine (compression fractures), distal radius (Colles fracture)
and pubic symphysis.
There is no abnormality in the structure of organic matrix (osteoid) nor
there is any defect in mineralization while in osteomalacia, there is impaired
mineralization of osteoid and the ratio of organic matrix to mineral is increased.
Radiologically there is:
Osteopenia (loss of bone density)
Spine shows pencilling in of the vertebrae by the more radiographically-
dense end plates
Biconcave vertebral bodiesCodfish vertebrae
Femoral neck reveals apparent increase in density of primary trabeculae
with thinning of secondary trabeculae
Cortical thinning in appendicular skeleton.
PATHOGENESIS
Bone remodeling (its formation and resorption) is a continuous process. It is
normally regulated by systemic and locally produced agents, and metabolic,
nutritional and mechanical factors. The normal balance between bone formation
and resorption results in maintenance of skeletal mass. In osteoporosis, the
bone mass is decreased indicating that the rate of bone resorption must exceed
than that of bone formation.
The decrease in bone is also a consequence of ageing. Skeletal growth is
complete by the end of adolescence, but even after the closure of the enchondral
growth plate, bone mass increases by radical growth until peak bone mass is
achieved at about the age of 35 years. After a short interval of balanced bone
metabolism, bone resorption begins to exceed bone formation and skeletal
mass decreases.
4 Seminar in Radiology
CLASSIFICATION
A. Generalized Osteoporosis
I. Unknown cause:
Primary/involutional osteoporosis
Juvenile osteoporosis
II. Endocrine cause:
Glucocorticoid excess
Thyrotoxicosis
Hypogonadism
Hyperparathyroidism
Hyperprolactinemia
Diabetes mellitus
III. Malignant diseases:
Multiple myeloma
Leukemia
Lymphoma
IV. Immobilization (Bed ridden)
V. Drugs:
Heparin
Ethanol
VI. Genetic abnormalities in bone collagen synthesis
Homocystinuria
Osteogenesis imperfecta
VII. Malnutrition/ deficiency states
VIII. Pregnancy
IX. Hypogonadism
X. Chronic liver disease
XI. Anemia
XII. Glycogen storage disease
XIII. Marrow packing disorders, e.g. Gauchers disease
XIV. Idiopathic
B. Localized Osteoporosis
Immobilization
Post-fracture
Sudecks atrophy
Arthritis
Infection
TYPES
Various types of osteoporosis are given in Table 1.1.
Involutional Osteoporosis
Type I
Post-menopausal
Osteoporotic Bone Disease 5
Table 1.1: Types of osteoporosis

1. Involutional osteoporosis
2. Idiopathic juvenile osteoporosis
3. Glucocorticoid excess
4. Hypogonadism
5. Thyrotoxicosis
6. Hyperprolactinemia
7. Reflex sympathetic dystrophy syndrome
8. Transient regional osteoporosis
9. Regional migratory osteoporosis
Age, 50 to 65 years.
Disproportionate loss of trabecular bone, giving rise to rapid bone loss.
Increase in fractures especially in vertebra and distal radius.
In vertebraeloss of height and anterior wedging occurs, which may
lead to a marked kyphotic deformity.
Causedecreased oestrogen.
Additional factors, e.g. skeletal size, level of activity, nutritional status
and genetics.
Once osteoporosis is established, estrogen therapy does not affect the
radiographic bone density.
Type II
Senile
Proportionate loss of cortical and trabecular bone.
Fracturefemoral neck, proximal humerus, tibia, pelvis.
In both sexes >70 years with 2:1 female preponderance.
Cause is uncertain but reduced intestinal absorption, diminished adrenal
function and secondary hyperparathyroidism may play a role.
Idiopathic Juvenile Osteoporosis

Rare self-limiting disease
Affects both sexes
Occurs before puberty (815 years)
Fractures characteristically seen in metaphysis of long bones with minimal
trauma (metaphyseal fractures also seen in Battered Baby Syndrome, 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.
Glucocorticoid Excess
Cushing disease/steroid therapy
BiochemicallyNegative calcium balance and hypercalciuria
Multiple fractures in long bones, ribs, vertebral bodies with exuberant callus
formation
In compression fractures of vertebrae, 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.
Hypogonadism
Boys
Delayed closure of epiphyseal plateshence patients have long limbs with
respect to their trunks.
Girls (Turners syndrome)

Short stature
Increased carrying angle at elbow
Short fourth metacarpal
Changes of Blounts disease at the knee (Medial tibial condyle is depressed
and beak-like. 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.
There is a characteristic periosteal thickening in the extremities and
particularly in the hands. It must be distinguished from hypertrophic
osteoarthropathy which is also found in the extremities but is usually
exquisitely painful.
Exophthalmos.
Prelibial myxodema.
Accelerated skeletal maturation in children.
Hyperprolactinemia
Due to reduced estrogen secretion.
Reflex Sympathetic Dystrophy Syndrome

(Sudecks Atrophy/Algodystrophy/Reflux Neurovascular Dystrophy)
Causes
Prior trauma
Surgery
Infectious states
Vasculitis
Calcific tendonitis
Neoplasia
Disk herniation
Myocardial infarction
Degenerative cervical spine disease
Cardiovascular disorders.
It is thought to be related to abnormal neural refluxes.
Clinical Features
Pain
Swelling
Stiffness
Weakness
Hyperesthesia
Vasomotor changes.
On X-ray
Endosteal bone resorption is the most prevalent form of demineralization
in this condition
Subperiosteal resorption, periarticular porosis, 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, 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 Sudecks atrophy
Symptoms resolve spontaneously in 4 to 10 months.
Regional Migratory Osteoporosis

Migratory condition
Hip is involved less frequently than other areas such as knee, ankle and
foot
Commoner in men
Between 30 and 50 years
Clinically it is similar to transient osteoporosis of the hip, the involvement
of each joint lasting for approximately 9 months
Recurrence in other bones may occur successively by up to two years or
more.
INVESTIGATIONS
With the advent by bone mass measurement, the fracture risk in osteoporosis
can be quantified before the fracture occurs. This is the major advancement in
the field of osteoporosis (Table 1.2).
Table 1.2: List of investigations
1. Standared radiography
2. Magnification radiography
3. Photodensitometry
4. Neutron activation analysis
5. Comptom scattering
6. Single energy photon absorptiometry
7. Dual energy photon absorptiometry
8. Dual energy X-ray absorptiometry
9. Single X-ray technique
10. Quantitative compound tomography
11. Quantitative ultrasound
12. MRI
13. 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.
Low bone mass (osteopenia): BMD or BMC more than 1SD below the
young adult man but less than 2.5 SD below this value.
Osteoporosis: A value for BDM or BMC 2.5 SD or more below young adult
mean.
Severe osteoporosis: A value for BMD or BMC more than 2.5 SD below the
young adult mean and the presence of 1 or more fragile fractures.
The various techniques for measuring the mineral content of bone are:
Standared Radiography
Based on subjective criteria
The assessment usually done on metacarpal, calcaneum, talus, femur neck,
vertebral bodies, etc. and findings are:
Generalized osteopenia especially axial skeletal (vertebral column).
Thinning and accentuation of cortices.
Accentuation of primary trabeculae with thinning of secondary

trabeculae.
Change in shape of vertebral bodywedge-shape, biconcave, com-
pression
Insufficiency fractures due to normal stress on weakened bone. The
fracture may be occult radiogrpahically and detected on CT or
scintigraphy. Common sites are sacrum, pubis hip, wrist, etc.
Disadvantage:
Subjective
Affected by body habits, radiographic exposure, factors, the presence of
overlying soft tissue and patient positioning
>3 percent bone loss is must, to be appreciated on plain X-ray.
Magnification Radiography
By either optical or as direct geometric means has a small but significant
role in the assessment of osteoporosis.
Subperiosteal bone resorption, even subtle, may be appreciated.
Radiogrammetry
Advantage:
Simplest method.
Inexpensive.
Easy to perform.
Disadvantage:
Does not reliably reflect bone mineral content
Conventional AP radiograph of a tubular bone is taken. 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).
Usually used at mid shaft of second metacarpal.
It is particularly useful in serial studies and comparison with a large
normal population can be made.
Photodensitometry
Images of bone of interest and reference aluminum wedge of known density
are exposed on the same film. The optical density of the bone is then
compared with that of the wedge with the photodensitometer.
This provides information comparable to SPA but with slightly lower
precision, sensitivity and accuracy.
Neutron Activation Analysis

This technique uses high energy neutrons to active Ca-48 to Ca-49. The
decay back to Ca-48 can be measured with a gamma counter. As
approximately 98 percent of body calcium is in the bones. This gives a

reasonably accurate determination of total body calcium. With modification,
assessment of regional calcium can also be made.
Disadvantage:
Available in only few centers
Relatively large radiation does (200300 mrem)
Precision and accuracy are in the order of 2 to 5 percent.
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.
It is based on measurement of scattered radiation from a source of 100 to
700 keV gamma rays and is used for calcaneum, spine and redius.
Precision = 3 to 5 percent
Radiation dose varies form 200 to 2000 mrem
At present, it is largely a research tool.
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. No soft tissue
correction done.
Usually radius is measured.
Precision 2 percent
Accuracy 6 percent
However, because of dosemetric and statistical considerations, the low
energy 1-125 source can not be used for body parts thicker than forearm.
The major criticism is that it measures the mineral content of the
appendicular skeleton (peripheral long bones).
Dual Energy Photon Absorptiometry (DPA)

It uses gadolinium-153, which emits photon at two different energy levels,
i.e. for soft tissue and bone.
This allows scanning of the spine and femur, as it is independent of variation
in soft tissue of thickness.
Lumbar spine from L1 to L4 is usually scanned.
This technique yields integral of all mineral within the scan path including
the vertebral bodies, end plates and posterior elements.
The major disadvantage is that vertebral compression fractures with callus
formation, kyphoscoliosis, articular facet hypertrophy, discogenic sclerosis,
marginal osteophytes and extraosseous calcification (aorta) are also included
in the integral measurement and may result in inaccurate and poorly
reproducible vertebral measurements.
The precision is in the order of 2 to 3 percent with accuracy of

4 to 10 percent.
Radiation dose 15 to 20 mrem
It is also used to determine total body mineral content.
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. Then correction soft
tissue is made.
There are two methods of generating dual energy X-ray spectrum.
The use of a K-absorption edge filter to split polyenergetic X-ray beam
into high and low energy components that mimics DPA.
Switching the high voltage generator between high and low kVp during
alternate half cycles of the main supply.
DXA is single widely used technique.
Advantage:
Ability to measure BMD in the spine and proximal femur-common
sites of osteoporotic fractures.
Low radiation dose
Short scan time
High resolution images
Good precision and inherent stability of calibration.
P-DXADXA for scanning peripheral skeleton.
Disadvantagessimilar to DPA.
Single X-ray Technique

Uses X-rays instead of 1-125 in SPA.
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
to measure small volumes of bone, thus enabling measurements of both
cortical and cancellous bone. In practice mid-portion of a vertebral body is
used. A mineral reference phantom such as potassium phosphate solution
is needed for calibration (multi-chamber phantom).
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 method1 to 3 percent and dual energy method
3 to 5 percent
Accuracy5 to 10 percent
Radiation dose 200 mrem
At present CT analysis would appear to be most reliable and adaptable
technique for bone density measurements
Advantage of QCT over other modalities

Transaxial display of data permitting identification of the anatomy and
separate measurements of cortical, cancellous or integral bone mineral.
Capability of determining the linear absorption coefficient for a readily
defined volume of bone thereby, providing a measure of density.
In the dual energy node, the ability to determine mineral content with
high accuracy in the presence of variable fat and soft tissue content.
Quantitative Ultrasound (QUS)

(Broad Band Ultrasound Attenuation)
It measures the attenuation of ultrasound at various frequencies, and
calculates the attenuation index. This is based on the fact that attenuation
is greater at higher frequencies, and bone therefore acts as frequency
sensitive filter for ultrasound waves
The attenuation is an almost linear function of frequency, 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.
It has a potential for wider applicabilities, including preventive screening
for osteoporosis.
Disadvantage
No standardized methods of calibration and expression of measurement
results since QUS employ diverse technology and different methods
for calibration.
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, except for T2 in women. This is explained by the replacement
of active with fatty marrow. 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. Calibration phantoms will have to be designed, however, to
compensate for variations in signal sensitivity and magnetic field variations, if
the technique is to become an accurate method for determination of bone
mineral content.
Biochemical Investigations
In osteoporosis, serum calcium and inorganic phosphorus are usually normal.
The alkaline phosphates in uncomplicated instances is normal, but may increase
after fractures. Urinary excretion of peptides containing hydroxyproline is
usually normal or slightly increased.
2 Soft Tissue Calcification
(Plain X-ray Appearance)
The deposition of amorphous calcium salts within the soft tissues is called
mineralization/calcification. If bony trabeculae are discernible within the
mineralized focus, the term ossification is used.
Two forms of Ca2+ may be found in soft tissues:
a. Calcium pyrophosphate dihydrate
b. Calcium hydroxyapatite
Soft tissue calcification, according to etiology, can be classified into:
1. Dystrophic (9598%)
Whenever a tissue is damaged, the body responds by invoking a genetic
inflammatory response reaction and sometimes ending with calcification
of the damaged tissue
So, dystrophic calcification is:
Ca2+ deposition in nonviable/dying tissues, with
Normal serum Ca2+, PO43 levels.
Calcification is:
Usually asymmetrical
More focal
Morphologically, amorphous clumps of Ca2+ and phosphate
May progress to ossification
2. Metastatic (12%)
Occurs in cases of prolonged elevation of product of serum calcium and
phosphate; (serum Ca2+ Serum PO43), due to any cause.
Metastatic calcification
Occurs in normal viable tissues, with
Deranged serum Ca2+, PO43 levels.
Usually widespread and bilaterally symmetrical
Morphologically, noncrystalline amorphous deposits + crystalline
hydroxyapatite crystals
3. Idiopathic
Occurs in previously normal tissues
With normal serum Ca2+, PO43 levels
DIFFERENTIAL DIAGNOSIS OF VARIOUS CALCIFICATIONS

A. Dystrophic
i. Vascular
a. Arterial
b. Venous insufficiency
ii. Infection
a. Bacterial
Tuberculosis
Leprosy
b. Parasitic
Cysticercus
Dracunculosis
Loa loa
Armillifer
iii. Connective tissue disorders
a. Congenital
Fibrodysplasia ossificans progressiva
Ehlers Danlos syndrome
Pseudoxanthoma elasticum
Werners syndrome
b. Acquired
Dermatomyositis
Progressive systemic sclerosis
CREST syndrome
iv. Metabolic disease
a. Pseudohypoparathyroidism
b. Pseudopseudohypoparathyroidism
c. Crystal deposition disorders
CPPD (Calcium pyrophosphate dehydrate deposition disease)
HADD (Calcium hydroxyapetite deposition disease)
Haemochromatosis
Gout
Ochronosis (Alkaptonuria)
v. Neoplasia
a. Benign
Haemangioma
Lipoma
Soft tissue chrondroma
b. Malignant
Synovial sarcoma
Soft tissue osteosarcoma
Soft tissue chondrosarcoma
vi. Trauma
a. Soft tissue necrosis
Soft Tissue Calcification 15
Injection granuloma
Thermal injuries
Fat necrosis
b. Haematoma
c. Myositis ossificans traumatica
d. Neurogenic heterotopic ossification
B. Metastatic
1. Hypercalcemia
a. Parathyroid related - Primary hypercalcemia
- Lithium therapy
b. Malignancy related - Solid tumor with metastasis (Breast ca)
- Hematopoietic malignancies
o Multiple myeloma
o Lymphoma
c. Vitamin D related - Vitamin D intoxication
- Idiopathic hypercalcemia of infancy
d. High bone turnover - Hyperthyroidism
- Immobilization
- Thiazides
- Vitamin A intoxication
e. Associated with renal - Aluminium intoxication
failure - Milk alkali syndrome
- Severe secondary hyperparathyroidism
2. Hyperphosphatemia
a. Secondary hyperparathyroidism (e.g. CRF)
b. Idiopathic hyperparathyroidism
c. Hypoparathyroidism
C. Idiopathic
1. Tumoural calcinosis
2. Calcinosis universalis
3. Calcinosis circumscripta
4. Calcific bursitis
5. Calcific peritendinitis
METABOLIC DISORDERS
1. Primary hyperparathyroidism
Usually due to parathyroid adenomas (90%) or diffuse hyperplasia of
the gland (10%)
Ca2+, PO43
Calcification:
a. Chondrocalcinosis (deposition of Ca pyrophosphate dihydrate crystals)
in 10-20 percent cases

Characteristically in - Hyaline articular and fibrocartilage of knee
- Symphysis pubis
- Traiangular cartilage of wrist
b. Arteries
c. Renal calculi
2. Secondary hyperparathyroidism
PO43 levels
Commonest cause
Renal failure
OthersOsteomalacia due to various causes (pseudohypo-
parathyroidism, Vitamin D deficiency)
Calcification:
a. Arterial
b. VisceralHeart, lungs, kidney
c. Periarticular calcification
In patients on long-term dialysis with renal transplant
May be large and globular
Otherwise, chondrocalcinosis is rare in secondary hyperpara-
thyroidism
3. Hypoparathyroidism
Deficiency of parathyroid hormone usually secondary to excision/ surgical
trauma.
Subcutaneous calcification
Usually, band-like ~ paraspinal calcification (as in DISH)
Basal ganglia calcification
Osteosclerosis
Premature closure of epiphysis

PseudohypoparathyroidismInherited disorder

End organ resistance to parathyroid hormone (defective post-receptor
mechanisms)
Ca2+, PO43 (and parathyroid levels)
Pseudopseudohypoparathyroidism (inherited disorder)Patients with
above radiographic abnormalities with normal Ca2+ levelscause
unknown
Both show following radiographic abnormalities:
Soft tissue calcifications
Short stature
Broad bones and cone epiphyses
Short 4th, 5th metacarpals and metatarsals
Small exostoses projected at right angle from the bone
4. Hypervitaminosis D
Smooth lobulated amorphous masses of Ca2+ (ca hydroxyapatite) in
Periarticular region
Bursa
Tendon sheaths
Within the capsule and cavity of joints
5. Milk-alkali syndrome
In peptic ulcer disease and renal impairment in whom increased ingestion
or alkali (CaCO3) and milk

Diffuse smalllarge masses of calcification in
Soft tissue (typically periarticulation)
Kidneys
Eyes
6. Gout
Monosodium urate deposits called as TOPHI which are not radio-opaque

Secondary calcification may occur
VASCULAR
1. Arterial
i. Atheroma
Irregular plaques to extensive tram track calcification
Common in aorta, pelvic and lower limb arteries
ii. Monckebergs median sclerosis (intimal sclerosis)
Pipestem appearance
Also common in lower limb (femoral, popliteal)
Diabetics: Calcification more common in lower limbs
Generalized arterial calcificationassociated 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. Venous
Calcification is unusual in the wall of veins
Phleboliths: Single/ multiple oval opacities ~ < 3 mm length with
translucent center

Common in:
Uterine and prostatic venous plexus
Varicose veins
Haemangiomas (cavernous)
Mafuccis syndrome:
Haemangiomas (with phleboliths) + multiple enchondromas (Olliers
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. Bacterial
Diffuse calcification extremely rare in bacterial infection
a. Tubercular
Resolving abscess, especially TB spine
Extensive calcified lymphadenitis
b. Leprosy
Rare cause of nerve calcification
2. Parasitic
a. Cysticercus cellulosae:
Prediliction of larval form to deposit in muscle, subcutaneous tissues
and brain
encyst
Cysticercus cellulosae

Classified dead cysts
Oval, with a lucent centre, upto 1 cm length and 23 mm broad.
Oriented in direction of muscle fibers
Number varies from 1100
b. Guinea worm:
Female form in subcutaneous tissue Die

Long, coiled curvilinear calcification

May be crushed by muscle contraction

round, irregular mass
c. Loa loa (W. Africa):
Long/coiled thread-like appearance, best visualized in hand and foot.
d. Armillifer armillatus:
Crescentic calcification in muscles of trunk
Infected by snake meat
e. Hydatid cyst : Calcification in liver
f. Schistosomiasis: Calcification in urinary bladder
CONNECTIVE TISSUE DISORDERS

a. Congenital
i. Fibrodysplasia ossifications progressiva (previously called as myositis
ossificans progressiva)
Inherited autosomal disorder
Progressive swelling and ossification of the fascia, aponeurosis,
ligaments, tendons and connective tissue of skeletal muscle (i.e. the
ossification occurs in the perimuscular fascia and not in the muscles
themselves).
Large masses may bridge between bonesin thorax which may
cause respiratory compromise.
Associated skeletal abnormalities may diagnose the condition before
development of soft tissue swellings.
Short 1st metacarpal, metatarsal
Small cervical vertebral bodies with relative prominence of
pedicles
ii. Ehlers-Danlos syndrome (rare, 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, 215 mm densities with radiolucent centers
predominantly affecting the forearms and shin of long bones:
iii. Pseudoxanthoma elasticum: Heterogeneous inheritance
Degeneration of the collagenelastic tissues
Calcification seen in:
a. Arteries
Media
Intima
b. Soft tissues
Commonest radiological abnormality
Linear calcinosis cutis (skin)
Ligaments, tendons, periarticular structures
iv. Werners syndrome (Progeria)
Arterial, dermal and ligamentous calcification
v. Weber-Christian disease
Subcutaneous calcified nodules
b. Acquired
i. Crystal deposition diseases
Calcium pyrophosphate dehydrate deposition disease (CPPD)
CPP deposition in and around joints + in annulus of intervertebral
disc.
There are 3 manifestations, which can occur in isolation /
combination:
- Acute intermittent synovitis (pseudogout)
- Calcium pyrophosphate arthropathy
- Chondrocalcinosis
Chondrocalcinosisaffects both
- Fibrocartilage: Menisci, triangular cartilage, symphysis pubis,
annulus fibrosis
- Hyaline cartilage : Knee, wrist, elbow, hip
CPPD may be associated with many conditions, e.g. hyper-
parathyroidism, gout, Wilsons disease, diabetes mellitus.
ii. HADD (Ca hydroxyapatite deposition disease)
Typically has a monoarticular presentation in the middle-aged and
elderly
Jointsshoulders (commonest), hips, knees and digits, bursae
involved
X-ray : Homogenous, 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.
Milwaukee shoulder: Extremely destructive arthritis of shoulder
May be associated with scleroderma and other connective tissue
disorders
iii. Oxalate crystal disease:
Ca-oxalate deposition in joints and other tissues, 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
X-ray:
a. Nonspecific subcutaneous calcification
b. (less common), sheet, like calcification along fascial and muscle planes
especially involving the proximal large muscles.

Differential diagnosis
i. Idiopathic calcinosis universalis
ii. Hyperparathyroidism
SCLERODERMA
(Progressive Systemic Sclerosis)
Unknown etiology, causes small vessel disease and fibrosis in various
organs. Scleroderma is the cutaneous manifestation of progressive systemic
sclerosis.
Clinically, Raynauds phenomenon and skin changes
X-ray in hands : Typical features are:
a. Acro-osteolysis : Terminal phallangeal resorption due to pressure atrophy
b. Calcinosis circumsctipta : Discrete dense plaques of calcification in the
digits.
c. Occasional intra-articular calcification
CREST syndrome (calcinosis cutis + Raynauds syndrome + esophageal
dysmotility + sclerodactyly + Telangiectasia)a related disorderthe only
differentiations is that calcification may also involve the tendon sheaths.
TRAUMA
a. Soft Tissues Necrosis
Usually followed by calcification
Various examples:
Injection sites, especially quinine (oval ring shadows in gluteal region)
and bismuth
Following
- Snake bites
- Frost bite : The commonest cause of calcification of pinna
Tuberculous lymph nodes
Fat necrosis causes calcification:
- Elhers-Danlos syndrome
- Christian-Weber syndrome
- Sites of insulin Injection.
- Blunt trauma
Radiation damage to tissue
Calcific myonecrosis : Calcification of atrophic muscles, 12
months after severe crush injury
b. Hematoma
Any hematomas, especially in subperiosteal location, may calcify, e.g.
cephalohematoma in neonates (due to birth trauma)
OSSIFICATION
Many calcifying (amorphous) lesions may proceed to trabecular ossi-
fication.
Pathologically: Inappropriate differentiation of fibroblasts into osteoblasts
following in inflammatory lesions in soft tissues.
Causes of heterotopic bone formation:
a. Development
Fibrodysplasia ossificans progressiva
Melorrheostosis
Progressive osseous heteroplasia
b. Acquired: Mainly traumatic
i. Burns:
- Extensive ossification in related joints (hips, elbows, shoulders)
- Bone formation not a direct result of burning as may develop at
sites distal to the injury.
ii. Surgery:
- In surgical scars, especially total hip arthropathy
c. Paralysis : Neurogenic heterotopic ossification
In patients of paraplegia
X-ray : Common in pelvic bones and hip joints

Periarticular new bone formation, 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. Trauma:
Repeated minor trauma may cause ligament calcification
i. Riders bone : adductor muscle
ii. Pellegrinis-Steida lesionin medial collateral ligament of knee
(medial to adductor tubercle)
iii. Fencers boneBrachialis muscle
iv. Dancers boneSoleus muscle
Note: Ossification of various ligaments may be a normal phenomenon of
knee, not necessarily result of a disease.
For example:
Ligamentum nuchae
Laryngeal cartilages
Costal cartilages
Iliolumbar, sacrotuberous ligaments, etc.
Iliosacral ligaments (angel wing sacrum)
MYOSITIS OSSIFICANS
Heterotopic bone and sometimes cartilage formation in muscles, tendons
and fascia, following trauma.
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. Paraosteal osteosarcoma (presence of a thin lucency between
the mass and bone differentiate it)
b. Pseudomalignant myositis ossificans = osseous tumor of soft
tissue (in the absence of trauma)
Subsequently, ossification occurs from peripheral to central, with reduction
in size of the mass.
Early biopsy should be avoided as pathologically, it resembles a soft tissue
osteosarcoma.
Surgical resection is best, but not done until left until maturation is complete
TUMORS
A. Benign
a. Lipomas:
Radiolucent on X-rays
Calcification/ossification in long-standing cases
b. Synovial chondromatosis:
Chondrometaplasia of the subsynovial connective tissue, occurring in
synovial joints, bursae and rarely tendon sheaths.
Multiple nodules of cartilage form in the synovium and project in
the synovium

Once mineralized, appear as multiple opacities with flecks of
calcifications and bony trabeculae.

Finally - Loose bodies
- Bony erosions
- Secodnary osteoarthritis
c. Hemangioma
B. Soft Tissue Sarcomas

a. Synovial sarcoma
Common in young adults
Only 10 percent located within a joint cavity. Rest are located closed
to a joint (subfascial location)
D-ray : Dense intratumoral calcification and ossification
b. Soft tissue osteosarcomas
X-ray:
Located commonly in high, pelvic girdle and shoulder
Areas/ nodules of faded radiopacity (due to tumoral osteogenesis)
c. Soft tissue chondrosarcoma
d. Peripheral chondrosarcoma
A chondrosarcoma which originates outside the bone but implanted
on the bone.
X-ray: An extraosseous mass, vaguely lobulated, bumpy (like
cauliflower), with abundant calcification.
Others
1. Hemangiopericytomas
2. Medullary carcinoma thyroid
3. Thyroid adenomasirregular peripheral egg shell calcifications
C. Idiopathic
1. Tumoral calcinosis:
Autosomal dominant
Any age
Majority have some biochemical defect of phosphorus metabolism
Serum calcium is normal (renal, metabolic and collagen vascular
disorders are ruled out)
Radiologically : Large, multiocular, juxta-articular cystic lesions
with/without fluid levels, frequently in hips, shoulders, elbows or
smaller joints (calcific fluidcarcinoma hydorxyapatite)

Masses grow progressively

May cause:
Bone erosions
Restricted joint movement
Superficial ulceration and secondary infection
Differential diagnosis:
Renal osteodystrophy
Calcific myonecrosis
2. Calcinosis circumscripta:
Deposits of calcium in subcutaneous tissues in a circumscribed
form in disease, e.g. scleroderma, dermatomyositis, renal osteo-
dystrophy with secondary hyperparathyroidism
3. Idiopathic calcinosis universalis:
Rare, unknown cause
Calcification in longitudinal bands in subcutaneous fat of extremities

Subsequently, in muscles, ligaments and tendons

Calcific deposits coalesce and enlarge

May break through the skin surface
Serum biochemistryNormal
i. Hyperparathyroidism
ii. Dermatomyositis
4. Sarcoidosis:
Granulomatous disorder of unknown origin
Rarely, metastatic soft tissue calcification may be seen, secondary
to hypercalcemia.
5. Calcific peritendinitis
6. Calcific bursitis
ABDOMINAL CALCIFICATIONS
1. Liver
a. Common
i. Granuloma (TB, histoplasmosis, brucellosis)
Multiple scattered round densities
Presence of diffuse calcifications in lungs, spleen, liver =
pathognomic of histoplasmosis
ii. Parasitic
a. Hydatid cyst
Fine curvilinear calcification in wall or dense and irregular,
if contracted
b. Chronic amoebic abscess and pyogenic abscess (multiple lesions)
Mural calcification, following
- Secondary infection
- Rupture and hemorrhage
- Surgical procedure
iii. Primary liver tumors
(Hemangioma, hepatoblastoma, hepatoma, cholangiocarcinoma)
Irregular patterns or multiple nodules
Progressive increase in size and number of calcifications with

enlarging liverfeatures of neoplasm
iv. Metastases (Mucinous, primary from colon or breast, cystadeno-
carcinoma of ovary)
Fine stippled (poppy seed) calcifications
b. Uncommon
i. Hepatic artery aneurysm
ii. Calcified hematoma (post-traumatic)
iii. Portal vein thrombosis
iv. Calculi in Carolis disease
v. Cyst - 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. Splenic Calcification
1. Vascular
Splenic artery athreoma (Tortuous corckscrew appearanceEnd-
on viewthin-walled ring)
Splenic artery aneursym (thin-walled ring)
2. Cystic (Congenital, post-traumatic, hydatid, dermoid)
3. Disseminated calcifications (usually <10 mm)
a. Phleboliths (in splenic vein)
b. Granulomatous diseases (TB, histoplasmosis, brucellosis)
4. Capsular + parenchymal calcificaiton:
Infarction
Pyogenic/ tubercular abscess
Hematoma
3. Pancreatic Calcification
A. Common
1. Chronic pancreatitis Alcoholic (20-40%)
Secondary to gallstone
Multiple irregular small concretions
B. Uncommon
2. Acute pancreatitis (saponifications)
3. Tumors
Cystadenoma Typical sunbrust appearance =
Cystadenocarcinoma pathognomic
Cavernous lymphangioma (rare tumor)
4. Hereditary pancreatitis (autosomal dominant)

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

i. Inflammatory disorders (UB)
a. Schistosomiasis: UB wall calcification with normal capacity and
distensibility
b. Tuberculosis: Small, contracted UB with faint, irregular rims of
calcification.
c. Post-irradiation
ii. Calculus (UB) : Circular/ oval; amorphous/ laminated/ speculated
Urethral calculi : Typically located in subpubic angle of pelvis/ close
to midline.
iii. Tumors: Punctate/ coarse/ linear calcification in
Transitional cell and squamous cell carcinoma (epithelial tumors)
Less common in mesenchymal tumors
Leiomyosarcoma
Hemangioma
8. Male Genitourinary Tract

i. Vas deferens
a. In diabetics (young)
b. In degenerative condition
in both (1) and (b) bilateral symmetrical, parallel tubular densities
run medially and caudally to enter the medial aspect of seminal
vesicles at base of prostate.
c. Chronic inflammation (TB, nonspecific infections)
ii. Seminal vesicles
Infections like Neisseria gonorrhoae and TB
Multiple small concretions near proximal end of vas deferens
iii. Prostate
a. Calculi : 2-4 discrete, on either side of midline in elderlies.
9. Female Genitourinary Tract

A. Uterus
a. Fibroid : Mottled/ Mulberry type stippled calcification (Whorled
appearance)
b. Squamous cell carcinoma
c. Adenocarcinoma of endometrium
d. Leiomyosarcoma
e. Lithopaedion
f. Placental calcification (fine lace-like; after 32 weeks of gestation)
B. Fallopian Tubes: Tubercular salpingitis (string of pearls appearance)

C. Ovary:
i. Dermoids (50% calcified)
Partial/ completely formed tooth, with relative radiolucency of
lipid material in lesion = pathognomic
ii. Papillary cystadenomas and papillary cystadenocarcinomas
Psammomatous bodies

Scattered fine amorphous calcification
Calcified metastatic deposits along lateral abdominal wall adjacent
to peritoneal fat stripecharacteristic
iii. Gonadoblastoma (rare)
Unilateral / bilateral, circumscribed/ mottled calcification
iv. Spontaneous amputation of ovary
Small, coarsely calcified mass in pelvis, which moves on serial
films, with missing ovary by USG.
10. Alimentary Tract

i. Enteroliths: Smooth, faceted, proximal to stricture/ within diverticula
a. Appendiculoliths: with symptoms of acute appendicitis is S/o
gangrenous appendicitis (may perforate)
b. Stone in Meckels diverticulum
ii. Calcified mucocele of appendix
iii. Appendices epiploaceae
Their infarction: cyst-like calcific shadows seen especially along
the ascending colon
iv. Tumors
Mucous adenocarcinomas of stomach and colon
Small, mottled deposits of calcium may occur
Leiomyomas (only 4%)
v. Omental fat deposits (Mobile opaque nodules)
Due to:
Interference of blood supply
Inflammation
Traumatic pancreatic fat necrosis
vi. Mesentric/peritoneal cysts (especially chylous cysts)
Unilocular/multiocular calcification
vii. Ingested seeds/tablets
11. Adrenals
Common:
a. Idiopathic
b. Neonatal hemorrhage (calcification form peripeheralcentral)
c. TB (discrete stippled calcification, outlining entire gland)
d. Tumors
Neuroblastoma
Phaeochromocytoma (mottled, scattered densities)
Uncommon:
a. Other tumors
Carcinoma
Adenoma
Adrneal choriostoma
b. Addisons disease
c. Adrenal cyst
12. Retroperitoneum
a. Neoplasms:
i. Wilms tumor (10%)Peripheral and cystic
ii. Neuroblastoma (50%)fine granular/stippled
iii. Teratomas
b. Cavernous hemangioma
c. TB psoas abscess
d. Hydatid cyst
13. Generalized Abdominal Calcification

1. Psammomatous calcifications (from cystadenocarcinoma of ovary)
2. Pseudomyxoma peritonei
Pseudomucinous cystadenoma of ovary
Mucocele appendix
3. Undifferentiated abdominal malignancy
4. TB peritonitis
5. Meconium peritonitis
THORACIC CALCIFICATIONS
A. Lymph Nodal Calcification
Differential diagnosis of egg shell calcification
Common
i. Sarcoidosis
ii. Solicosis
Uncommon
i. Histoplasmosis
ii. Lymphoma (postradiation)
iii. Blastomycsis
iv. Amyloidosis
B. Vascular Calcification
1. Aneurysmal calcification
Aorta
Pulmonary artery
2. Calcified clot
3. Calcification of central pulmonary arteryin severe PAH
C. Parenchymal Calcification
1. Widespread
i. Infection
a. Coccidiomyosis
b. Chickenpox
c. Rarely
Schistosoma
Armillifer
(Very rare in military TB)
ii. Silicosis: Pulmonary nodules may calcify
Baritosis and stanosis denser nodules
iii. Pulmonary ossification
a. Rheumatic MSLarge ossific nodules, mainly at bases
b. Fine branching linear shadows usually involving a limited area
of lung
iv. Metabolic disorders
v. Alveolar microlithiasisTiny dense stippled calcification (negative
pleura sign)
2. Solitary pulmonary nodule (SPN):
a. Granuloma (TB, histoplasmosis)
b. Hamartoma (Popcorn type calcification)
c. Carcinoid type of bronchial adenoma
d. AVM (arterovenous malformation)
e. Rare
Primary pulmonary osteosarcomas
Seven percent of carcinomas
3. Multiple large pulmonary nodules
a. Benign
i. TB
ii. Histoplasmosis
iii. Coccidiomycosis and other fungi
iv. Partly calcified nodules in
Rheumatoid arthritis
Multiple hamartochondromas
b. Malignant
i. Bone formation
Primary
Osteogenic sarcoma
Multiple chondrosarcomas
Secondary
Deposits of osteogenic sarcoma
ii. PsammomasMetastases from, thyroid carcinoma and papillary
cystadenocarcinoma of ovary
iii. Mucoid calcificationMetastatic colloid carcinoma from carci-
noma breast
iv. Post-irradiationin Hodgkins disease.
PLEURAL CALCIFICATION
Asbestosis (in parietal pleura mainly)
Calcification likeHolly leaf, well-defined outline
In mid and lower zone, sometime bilateral
Empyema (usually TB)

Sheet-like calcification
en facehazy
in profiledense, linear, parallel to chest wall
TBboth parietal and visceral pleurae involved
Hemothorax
PERICARDIAL CALCIFICATION
(CALCIFYING PERICARDIAL CONSTRICTION)
1. TB
2. Hemopericardium
3. Pyogenic/viral pericarditis
4. Postoperative
5. Uremic pericarditis Less common
NECK
Tracheal ring calcification
Thyroid calcification multinodular goiter, psammomatous calcification,
seen in malignancy
Lymph nodeTB/Lymphoma
Foreign body
Aneurysm of internal carotid artery
INTRACRANIAL CALCIFICATION
Physiological Calcification
Pineal gland (60% of adult)
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. CongenitalSturge-Weber syndrome, tuberose sclerosis
2. TraumaticCalcified hematoma
3. InfectionHealed brain abscess, tuberculosis, neurocysticerosis, torch
infection (Periventricular calcification)
4. Tumor
Primary
Lipoma of corpus callosum
GliomaAmorphous bolb calcification or nodules or streaks
Glioblastoma multiformeAstrocytoma, ependymoma, medulloblastoma,
oligodendroglioma
MeningiomaNodule, isolated or conglomerated or homogeneous opacity
Pituitary macrodaenoma
Acoustic neuroma
CraniopharyngiomaSuprasellar calcification, curvilinear in capsule of
tumor
Pineal tumor> 10 mm in diameter
Dermoid/Epidermoid/Teratoma
Colloid cyst
Choroid plexus papilloma
Chordoma
Secondary
Occasional
3
Inflammatory Arthropathy
Inflammatory arthritides are group of different disorders with systemic
manifestations with common factor being inflammatory pannus eroding
cartilage and bone.
INVESTIGATIONS
Plain X-ray
Only films which will have impact on treatment, should be taken.
Initial screening : Rheumatoid series
PA hand Minimal requisite
Dorsiplantar feet
AP shoulder/ pelvic/knee
Lateral view in flexion of cervical spine
Follow upOnly AP both hand. (Norgaards ballcatcher view).
Examination by standardized approach proposed by Forrester and Brown.
Soft tissues
Alignment
Cartilage space
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, cartilage, 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, with clarity especially in carpals/tarsals bone.
Joint space narrowing, erosions, fusion.
Intervertebral disc spaces, facet joints are better demonstrated.
Radio-nuclide Scan
High sensitivity but poor specificity (since relying on distribution of abnormal
foci to make specific diagnosis).
Findings appear earlier than plain X-ray.
99mTc phosphate images.
Early / Blood pool phase increased blood flow to synovium.
In delayed images (3 hours) increased uptake at sites of increased bone
turnover
Ultrasonography
High resolution ultrasonography shows capsule, synovial effusion, loose bodies,
bursa, leakage of synovium into muscles, ruptured Bakers cyst and Tendon
tear.
Magnetic Resonance Imaging

When available/affordablecan be the investigations of choice for initial
diagnosis and progress.
Marginal erosions seen earlier than in X-rays as low signal defects.

Pannussoft tissue signal mass adjacent to eroded bone.
Vascularised synovial proliferations enhances after I/V Gadolinium.
Subarticular cysts and bone edema high signal on T2.
Tendonitis tendon thickening surrounded by high signal edema on T2.
Craniovertebral junctions in spine cervical shows better visualized on MRI.
RHEUMATOID ARTHRITIS
Generalized connective tissue disease with extra-articular manifestations.
Type III hypersensitivity/delayed hypersensitivity. Immune complex disease
(Ag-Ab complex with complement fixation).
Cause:
Genetic predispositionDRW4
Reaction to Ag from EBV/strains of E coli.
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, subluxaiton and ankylosis
Diagnostic criteria of American Rheumatism Association (minimum 4 points)
Morning stiffness 1 hr.
Swelling of 3 joints for 6 wks. (especially wrist, metacarpophalangeal,
metatarsophalangeal and proximal inter-phalangeal joint)
Symmetric involvement
Rheumatoid nodules
Positive rheumatoid factors
Radiological changes
Age peak, 20-55 years. 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.
Osteoporosis:
Periarticular due to hyperemia in acute stage
Generalized due to disuse or immobilization.
Erosions
Marginal/Bare area most important and diagnostic
Central in location also seen.
More common in small joints; earlier and more common in feet than hand.
5th metatarsophalangeal joint (Lat > Medial)
2nd + 3rd 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, 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.
5 basic typesflexion, extension, deviation, subluxation, dislocation
Secondary osteoarthritic changes
In weightbearing joints, especially hip joints
Enthesis changesmetabolically active site of ligament/tendon insertion
into bone soft tissue changes, osteoporosis, erosion
Periostitis = Local periosteal reaction
Less common in rheumatoid arthritis than sero-negative arthropathies.
More common in feet fluffy calcaneal spur in plantar aspect.
Mid-shaft of phalanx/metacarpal
Near joint affected by synovitis.
Target Sites
Hand and Wrist:
Metacarpophalangeal joint, proximal interphalngeal joint
All wrist joints + distal radioulnar joint
Ulnar styloid process.
Swan neck/Boutonnirs deformity.
Hitch hikers thumb
Ulnar deviation and volar subluxation/dislocation at metacarpophalangeal
joint. Carplals appear like Telescoping of fingers. (called as main en lorgnette)
Extensor tendon rupture especially Extensio carpi ulnaris.

Scapho-luntae ligament rupture rotation and volar subluxation of scaphoid
= called as TERRY- THOMASIGN.
A very early change (35%)apparent terminal phalangeal sclerosis due to
osteopenia in surrounding.
Elbow:
Soft tissue abnormality seen earlier and may be the only finding.
Effusion Elevation of anterior and posterior Fat pads.
Olecranon bursitis.
Rheumatoid nodules on extensor surface.
Shoulder joint: Glenohumeral joint, acromioclavicular joint, subacromial space,
erosion of clavicle.
Resorption of acromial end of clavicle increase space and pencil tip erosion
of calvicle.
Rotator cuff tear/ atrophycranial migration of humeral head
Pressure erosion of under surface of acromion.
Enlarged subdeltoid bursa.
Hip joint:
Protrusio-acetabuli
Insufficiency facture neck of femur and avascular necrosis of head of
femur head are important observations.
Birds beak appearance due to gross bone loss especially at femoral
head.
Knee joint:
Joint effusion
Lateral bulge of fat lines
Distended suprapatellar space
Increased patellofemoral space.
Malalignment
Tibial subluxation
Genu varum/valgum.
Bakers cyst
Soft tissue density posteriorily.
Ankle joint and heel:
Rheumatoid nodule adjacent to Achilles tendon
Focal erosion of calcaneous due to adjacent bursitis.
Foot:
Metatarsophalangeal joint especially 1st and 5th ones.
Hallux valgus
Dorsolateral subluxation/dislocation of proximal phalanges
Hammer toes.
Enthesitis at Tendo-Achilles insertion/Plantar fascia in calcaneum.
Temporomandibular Joint
Crico-arytenoid involvement results in hoarseness of voice.
Cervical spine may reveal
Atlanto-axial joint
Subluxation
Odontoid erosion
Basilar invagination
Odontoid fracture
Erosion of spinous process sharp and tapered.
Apophyseal joints erosion, subluxation, fusion
Intervertebral disc spaces narrowing, end plate irregularity, fusion.
Sarcoiliac joint:
Erosion, fusion are commonest observations.
Less common in rheumatoid artheritis (=30%) than in seronegative arthritis.
Extra-articular manifestations (75%)
Felty syndrome <1%
RA of >10 yrs + splenomegaly + neutropenia with rapid weight loss, brown
pigmentation of exposed skin of extremities, therapy refractory leg ulcers.
Sjgren syndrome (15%)
RA + keratoconjunctivitis + xerostomia (dryness of mouth due to decreased
functioning of salivary galnd).
Dryness of mouth due to functioning of salivary gland.
Pulmonary manifestations
Pleural effusionmostly unilateral, no parenchymal lesion, may remain
without change for months
Interstitial fibrosislower lobe predominance.
Rheumatoid nodule (30%)well-circumscribed, peripheral, cavitations
Caplan syndromehyperimmune reactivity to silica inhalation with
rapidly developing multiple pulmonary nodules.
Pulmonary hypertensionsecondary to arteritis.
Subcutaneous nodules (in 35% with active arthritis) over extensor surface
(forearm) and pressure points (e.g. olecranon) without calcifications.
Cardiovascular involvement
Pericarditis (20-50%)
Myocardites (arrhythmia, heart block)
Aortitis (5%) of ascending arota.
Aortic valve insufficiency.
Rheumatoid vasculitispolyneuropathy; cutaneous ulcerations; gangrene;
polymyopathy; myocardial/visceral infarctions.
Neurological sequeles
Distal neuropathy (related to vasculitis)
Nerve entrapmentAtlantoaxial subluxation, carpel tunnel syndrome
Lymphadenopathy (25%)
Splenomegaly (1-5%).
JUVENILE CHRONIC POLYARTHRITIS

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

OA subluxation.
S.I. joint involvement is not a feature of JRA.
ANKYLOSING SPONDYLITIS
Synonyms
Bekhterevs disease
Marie-Strumpell disease
Chronic progressive disease with insidious onset back pain and stiffness in
young.
Age 20s (15-35 yrs.)
M:F = 7:1 Caucasians : Blacks = 3:1
HLA B27 +ve in 95%; HLADR4
Target Joints:
Spine and adjacent soft tissues
Sacroiliac joints
Temporomandibular joint narrowing, ankylosis
also affects peripheral large joints (hip, shoulder, knee) small joints, rarely
involved.
Sacroiliac Joints:
Symmetrical sacroiliitis. May be asymmetrical in early stage.
Loss of cortex
Irregular cartilage space width
Focal erosions, more on iliac side.
Sclerosis
Ankylosis
Radio nucleide scan = Increased uptake ratio of more than 1.4:1
Between SIJ and sarcum indicates sacroilitis.
Capsular calcification
Spine:
Involvement status: Lumbosacral region followed by thoracolumbar region.
Vertebral body squaring = characteristic feature and earliest due to
Osteitis and erosions adjacent and end plate margins shiny/Ivory corners
squared appearance.
Anterior longitudinal ligament mineralization fills the anterior
Concavity of vertebral bodies.
Syndesmophytes ossification of outer annular fibers.
Ligament mineralization Anterior and Posterior longitudinal ligament
Interspinous
Apophyseal joint ankylosis
Straightening BAMBOO SPINE
Tram-Track line or Trolley- track sign on AP view Three vertical line
due to calcified ALL, PLL and inter-spinous ligament.
Costotransverse joint erosion and fusion

Synovitis of atlantoaxial joint Subluxation which frequently becomes
fixed neural compression
Osteopenic spine Kyphoscoliosis/fracture with pseudoarthosis.
Enthesitis and ligament calcifications.
Sites = ischial tuberosity, greater trocanter, iliac crest, calcaneous
Initially erosion followed by healing and mineralization
Shaggy/whiskered appearance
Enthesophytes.
Extra-articular Features
Iritis (25%)
Pulmonary fibrosis (B/L apical) with upward retraction of hila.
Cardiac conductor defects
Aortic incompetence
Amyloidiosis
Constitutional features fever, anorexia, fatigue, wt. loss.
Associated with ulcerative colitis, regional enteritis.
PSORIATIC ARTHRITIS
Etiology = unknown. (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; SI Joint
Peripheral joints Hand [DIP, PIP, MCP]
Ankle and foot
Hand and Foot

Sausage shape digit
Asymmetric erosive arthritis of DIPJ + osseous resorption + bony ankylosis
in 10 percent.
Pencil in cup deformity erosion with ill-defined margins and adjacent

proliferation of periosteal new bonecharacteristic.
Ivory phalanx sclerosis of terminal phalanx (25%).
Destructions of IPJ of 1st toe + exuberant peristeal reaction + bone
formation at distal phalangeal base = pathognomonic mouse ear
appearance.
Diffuse wide-based fluffy calcaneal spur at attachment of Tendo-Achilles
and plantar aponeurosis.
Erosions at superior/ posterior margin of calcanceus.
Axial Skeleton
Floating syndesmophyte single large, vertically-oriented involving disc
annulus (not end plate). Separate from edge of vertebra.
Squaring of vertebra in lumbar region
Sarcoiliitis asymmetric/unilateral
Atlantoaxial subluxation + odontoid abnormality
Paraspinal ossifications
REITERS SYNDROME (Described in 1916)

Infective originendemic/ venereal non-gonococcal urethritis, prostitis,
hemorrhagic cystitis
Epidemic/ dysenteric Shigella species.
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.
Peripheral asymmetric arthritis with predilection of joints of lower limb +
Recurrent attacks.
Target joints:
MTPJ, IPJ of feet especially great toe.
Ankle joint/knee/hip joints
SI Joint asymmetric
Also MCP, PIP, DIPJ
ENTEROPATHIC ARTHROPATHY
In patients of ulcerative colitis, Crohns disease, Whipples disease, Behets
syndrome, intestinal bypass patients
HLA B27 +ve is 60 percent
Involvement of SI joint, spine and peripheral joints
Peripehral arthritis
Coincides with exacerbation/ severity of gut disease
Recurrent, acute, mild attacks of synovitis, 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 synoviumpenetrating/latrogenic injuries
Infection from adjacent soft tissuescellulitis, abscess
Hematogenous spreadimmunocompromised, I/V drug abuse
Spread of infection from osteomyelitis in adjacent bone
Etiology: PyogenicStreptococcus pyogenes, Staphylococcus aureus, H.
influenzae, Gonococci, Salmonella
Non-pyogenicM. tuberculosis, fungal, viral
Location: any jointsingle, metacarpal joint: large wt. bearinghip/knee/spine
X-Ray : Acute stage
May be normal
Soft tissue swelling and periarticular osteoporosis (less TB)
Joint effusiondistention/ subluxation in children
Joint space narrowingirregular, rapid destruction (gradual TB)
Erosionsarticular cartilagepyogenic/small, peripheralTB
Subchondral bone destruction and reactive sclerosis (less TB)
Ankylosisif entire cartilage lost
Evidence of metaphyseal disease.
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. It is a major health
problem in all countries with increasing pace of development. 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. Twenty percent
results in associated temporary or permanent neurological deficit.
Etiology
Developed countries Road traffic accident is the most common cause
and is usually polytrauma in nature.
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, rowers, football players, etc.
Classification
1. According to type of traumatizing force/mechanism of injury:
a. Flexion injuries:
Commonest spinal injury
Stable
Usually results in wedge fractures/compression fractures
(L1, L2,D12,C5C7)
Dislocation are common (esp, C5 over C6)
Sprain observed in associated ligaments and muscles. Sufficient
force can lead to tear in posterior ligaments and muscles.
Flexion rotation injury:
Worst type of spinal injury as it is highly unstable and commonly
affects the spinal cord.
Fractures usually associated with dislocation
Shearing forces may cause chip or slice fracture of associated
vertebra also.
Flexion distraction injury:

Also known as seat-belt injury (Chance fracture, Teetter-Totter
fracture, Smith fracture being specific types of it).
Horizontal fracture in vertebral body extending into posterior
elements.
b. Extension injury:
Common in cervical and lumbar spine
May be stable or unstable
Results in chip fracture (Tear drop) of anterior vertebral rim.
c. 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. in cervical and upper dorsal spine.
d. Direct injury:
Rarer type of injury
Usually caused by a bullet or lathi blow
Usually fractures the spinous process
e. 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.
2. According to severity of injury:
a. Minor injury:
Patient is alert and co-operative
No neurological symptoms
b. Major injury:
Patient is unconscious and unco-operative
Neurological symptoms/deficit present
Associated with multisystem/multiorgan trauma
3. 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.
b. Unstable spine:
Cannot maintain relationships, further damage to nerve root and
cord cannot be avoided.
Denis three column concept divides the spine in:
a. Anterior column: Anterior part of bodies, end plates, discs and anterior
longitudinal ligament.
Spinal Trauma 47
b. Middle column: Posterior parts of bodies, end plates, discs and posterior
longitudinal ligament.
c. Posterior: Pedicles, lamina, articular processes, spinous process and
posterior ligamentous complex.
Involvement of two or more columns leads to consequently increasing
instability. The involvement of middle column is especially responsible for
instability. This is more in dorsolumbar spine.
Denis further classified instability in Mechanical (if progressively deformable
under physiological forces), Neurological (probability of production of new
neuro-deficit or increasing of already existing deficit) or Combined.
Mechanical injury may be either acute or chronic but neurological injury is
usually acute.
Signs of Instability
i.Widened interspinous distance (known as Fanning)
ii.Increases distance of facet joint space
iii.Disc pace narrowing (both D-L and cervical or widening in cervical)
iv. Focal angulation of more than 11 (cervical) and more than 40 (dorsal)
v. Subluxation of more than 3.5 mm (esp. in cervical area) or even minimal
in dorsolumbar area.
vi. Compression of vertebral height or more than 25 percent (cervical) or
50 percent.
vii. Costovertebral dislocation, rib and sternal fracture for dorsal spine.
Anterior height
Wedging ratio =
Posterior height
(N) = 0.80 in male T8 T12

0.87 in female
INDICATIONS OF IMAGING
As there is so little time allocated to radiologist in a traumatized patient, the
choice of optimum views and methods is a must to bring out the maximum.
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.
1. Nexus Exclusion Criteria
Excludes patient not be imaged. The sensitivity of this criteria is 99 percent
(a miss rate of 1 in 40000). These patients should, however, be observed
for 48 hours.
The criteria are:
No midline spinal tenderness
No focal neurological deficit
No painful distracting injury
Normal alertness
2. Vandemarks Risk Approach: Ref. appendix (Table 4.1)

3. ACR Appropriateness Criteria: Ref. appendix (Table 4.2)
AIM OF IMAGING
To assess the:
1. Severity of injury
2. Stability of spine
3. Complications in delayed phase
4. Associated injury in cases of polytrauma
Points to be Taken Care of:

1. 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. The Spinal Cord
Shape
Size
Location within thecal sac, thecal sac itself
Texture of cord
Size of central canal
Dura
Nerve roots, cauda, conus, filum
3. The Soft Tissue:
Pre, Para and Postvertebral muscles and fascial planes
Associated ligaments
Intervertebral discs (shape, size, bulge, texture, etc.)
4. Associated with other injuries, i.e. ribs, Dens, Clivus, occipital bone
IMAGING MODALITIES
Ref. Appendix (Table 4.3)
Plain Film Radiography

Most useful initial technique is the Cross-table lateral view. Positive in
70 to 90 percent of cases.
Spinal Trauma 49
May be followed by AP and open-mouth views (Three-film series) or

additional oblique view (Five film series).
Evaluation of odontoid process may in additional be done by Kasabachs
method, i.e. 45 head rotation +15 caudal tube tilt, very rarely swimmers
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. Military posture is an indication of flexion being the
cause of instability.
Patient maybe screened under fluoroscopy instead.
Pillar view for lamina and articular processes is performed sometimes.

Has Four Basic Indications
1. Clinical evidence of spinal cord injury without bone injury
2. Clinical features out of proportion to imaging findings
3. Progressive increase in neurological symptoms
4. Assessment of ligamentous injury
MR Compatible fiberglass, Graphite or Titanium apparatus should be
used.
GRE sequences can form a Myelogram and are quite fast. FSE, RARE
etc. can also decrease the time with equally good image quality.
SPINAL INJURY THE MEDICOLEGAL ASPECT

Under Section 320 of Indian Penal Code spinal injuries are considered
Grevious in nature.
Spinal cord injury may be grevious even without fracture dislocation.
Any hurt that endangers life or which causes the sufferer to be in during
the space of 20 days, in severe bodily pain or unable to follow his pursuit.
Also a radiologist must remember that cervical spine injury is seen in hanging
and not in strangulation. Judicial hanging leads to fracture of C3, C4 and
rarely C2.
Spinal concussion is quite commonly seen in Road/Railway accidents while
compression may occur while one is suddenly banged, pushed or when
ladies fighting, pull each others hairs.
Firearm injuries, wrestling are causes of spinal laceration while pithing
(B/W C1-C3) is common mode of infanticide in India.
Spinous process fractures are highly specific while vertebral (D/L) body
fracture/subluxation are moderately specific for Batterred baby syndrome.
Lateral spinal survey is mandatory, therefore, in all such cases.
IMAGING FEATURES
Nonosseous Injury
a. Intervertebral disc injury
i. Symmetric/ asymmetric widening of disc space
ii. Relative hyperintensity of one disc on sagittal T2W weighted image.
iii. Discontinuity of the outer annular fibers and/or longitudinal ligaments.
iv. Frank protrusion of disc material into the epidural space
v. Dorsal displacement of the posterior longitudinal ligament and epidural
venous plexus.
b. Ligamentous injury
MRI is the more sensitive method for detecting ligamentous injury.
Disruption of anterior and posterior longitudinal ligaments manifests as
discontinuity in the normally low-signal intensity ligament. Interspinous
ligament injuries produce high T2 signal intensity within the ligament because
of edema. Prevertebral soft edema is also very well shown. Ligamentous
and soft tissue edema are particularly well seen when imaging on low-field
strength magnet. The low-field open magnets are more easily used to image
acute trauma patients. 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.
c. Spinal cord injury
i. Cord hemorrhage:
It is depicted very well on MRI and is more common in pediatric age
group if occurring in isolation. 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. The
neurological level of injury correlates well with the physical level of
hemorrhage. Location of hemorrhage is the most precise indicator of
the neurological level of injury. It follows the usually course of blood
resolution. This type of injury is also known as Transaction without
separation.
ii. Intramedullary edema (Type II):
The length of spinal cord with edematous change directly correlate
with the degree of neurological impairment. The location of edema is
generally a less sensitive predictor for neurological level of initial injury.
Type III injury is a combination of both.
iii. Spinal epidural hematoma:
It occurs in 41 percent of spinal injuries. Even large epidural hematomas
may remain clinically silent and extend over multiple levels. This epidural
collection is separated from CSF space by hypointense dura.
iv. Root avulsion and dural tears:
1. Root avulsions are caused by traction injuries to arm or lower
extremity.
Spinal Trauma 51
2. A syrinx can result from nerve root avulsion, which present usually
after 18 months.
3. A delayed syrinx can be detected on MR well before clinical
symptoms occur.
4. Dural tears occur in 7 to 16 percent of lumbar fracture.
5. Spinal cord can herniate through the dural tear.
6. Dural tears are associated with central split fracture of spinous
process or laminar fracture.
7. CT myelography is the most sensitive investigation for identifying
root avulsions and pseudomeningoceles.
Osseous Injuries
ABCs of Spinal Trauma
Alignment
1. Disruption of areas
2. Focal kyphoscoliosis and loss of Lordosis
3. Rotation of spinous process
4. Listhesis (Scottish Terrier Sign)
5. Increased interpedicular distance
Bone Integrity
1. Anterior wedging
2. Cortical buckling
3. Disrupted posterior vertebral line
4. Disrupted C2 ring
Cartilage Joint Space

1. Interspinous/facet joint widening
2. Increased/decreases disc spaces
3. Vacuum phenomenon
Soft tissue swelling: Pre or paravertebral soft tissues, fat strips, muscles
shadow, airways may present as welling.
CERVICAL SPINE INJURY

Clarks 12 Signs
i. Retropharyngeal space widening
ii. Displacement of prevertebral fat stripe
iii. Tracheal deviation
iv. Laryngeal dislocation
v. Loss of lordosis
vi. Acute kyphosis
vii. Torticollis
viii. Widened interspinous space
ix. Rotation of vertebral bodies
x. Widened middle atlantoaxial joint
xi. Abnormal disc height
xii. Widening of facet joint
Vermas 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. Harris ring of C2 is due to collection of images of overlying
normal structures. The superior arc of the ring represents the superior articular
facet; the posterior arc of the ring is the posterior vertebral body line, inferior
arc of the ring is part of the foramen transversarium, anterior arc is formed by
anterior vertebral body cortex. Harris ring is disrupted in fracture of body of
C2. Displaced fractures of body C2 produce widening of C2 in relation to
width of C3. This is called fat C2 sign.
1. Occipitoaltantoaxial Injuries:
Traumatic atlantooccipital injuries
This injury is usually fatal. It is hyperextension and distraction injury of
C1, C2. Several methods have been used to assess if an abnormality
exists. By Lees method, the ascending limb does not pass though
spinolaminar line of C1 and dens tip does not lie within 5 mm of
descending limb. Powers ratio exceeds 1. Reformatted CT images
clearly show the dislocation, MRI depicts transection or cord contusion.
Lees Method
Descending limb: basion to middle of spinolaminar line of C2.
Ascending limb; posteroinferior part of body of C2 to opisthion.
Powers Ratio
First line joints basion with middle of posterior arch of C1.
Second line joins opisthion with middle of anterior arch of C1.
Powers ratio is the ratio between the two lines which normally is
less than 1.
2. Atlantoaxial Subluxation
This is caused by flexion injury. The predental space is increased and it is
more than 3 mm in adults and 5 mm in children. Plain films in flexion and
extension are done. In unstable atlantoaxial subluxation the predental space
is more in the flexion than in the extension film. This phenomenon is
depicted beautifully on cine-kinematic MRI. Predental space widening may
be seen in sagittal reformatted CT images. CT images also show asymmetry
of dens in relation to lateral mass of C1.
3. Rotatory altalnoaxial dislocation
Rotational injuries are uncommon in the cervical region. It occurs in less
than 2 percent of cervical spine injuries. Two varieties may occur, the first
Spinal Trauma 53
is simple rotatory subluxation of C2. This may be diagnosed by the

malalignment of the midline structures of the neck. Second type is the
rotatory fixation of C1 and C2. This is true dislocation of C1 and C2 with
locked facets. The atlas is rotated more than 45C with locked facts. AP
open mouth view shows eccentrically placed dens. A frontal radiograph
shows gross rotation of head. CT scan through C1 shows rotation. CT
scan through C2 shows no rotation.
C1 Fractures
Axial compression of C1 result in Jefferson fracture which involves unilateral/
bilateral anterior and posterior arches of atlas. CT shows the anterior and
posterior arch fracture with lateral displacement of lateral masses of CI. In
open mouth AP an overhanging of more than 3 to 9 mm is significant.
C2 Fractures
1. Dens fracture:
Dens fracture is usually associated with widening of prevertebral soft tissue
shadow at C14 of more than 7 mm (C6 = 22 mm in adults and 14 mm in
children). Dens fracture is classified into 3 types.
Type
I. : Oblique fracture through tip of dens
II. : Fracture at junction of dens and body of C2
III. : Horizontal fracture through C2 vertebral body
Type II is more common
In children, rupture of transverse ligament of dens is common
while in adults the dens fracture.
2. Hangmans fracture
The anterior subluxation of C2 body and retrolisthesis of posterior elements
of C2 relative to C3. 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.
C3-C7 Injury
a. Flexion injuries
They account for 50 to 80 percent of all cervical spine injuries.
1. Clay shovelers fracture
There is oblique fracture spinous process of C6 or C7. The fracture
line may be seen in lateral view.
2. Wedge compression fracture
This is due to flexion injury with axis of rotation through the posterior
part of the vertebral body. One or more anterior vertebral bodies may
be involved without concomitant injury to posterior vertebral body.
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.
3. 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. In occult hyperflexion
sprain, supine CT may be normal. Anterolisthesis can be demonstrated
in upright lateral radiograph.
4. Bilateral facet lock
There is disruption of middle and posterior columns. CT shows anterior
subluxation with bow-tie sign oblique position of facets and articular
processes. CT shows nacked facet sign on axial sections.
5. Flexion tear-drop fracture
There is disruption of anterior and posterior ligamentous structures
disc and apophyseal joints. Radiographically there is a triangular fragment
at anteroinferior corner of vertebral body, widening of interspinous
and interfacet spaces with focal kyphosis.
b. Hyperextension injuries
Hyperextension tear drop fractures belong to this category. The fragment
is found at posteroinferior part of vertebral body. Cord damage is due to
impingement and ligamentous sprain. MRI is the investigation of choice
for elevation of cord impingement.
THORACOLUMBAR SPINE INJURIES

1. Wedge fracture
2. Burst fracture
3. Seat-belt injury
5. Fracture dislocation
1. 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.
Compression injuries represent a failure under compressive forces of the
anterior column. The middle column remains intact and acts as a hinge,
and under tension, the posterior column can fail. 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, there may be widening of the interspinous
distance.
Anterior height >2mm shorter than posterior vertebral body height
indicated wedge fracture. Slight anterior wedging upto 20 percent of
vertebral body height could be normal in T8T12 vertebrae. CT shows the
radially oriented fracture lines of the anterior endplate, slightly displaced
fragments, and no posterior element fracture. CT is indicated in severe
compression >50 percent to rule out burst fracture unless they result in
severe kyphosis >40. These fractures are considered as stable one.
Spinal Trauma 55
2. Burst fracture
Burst fracture represent failure under axial loading of anterior and middle
columns, most commonly occurring at thoracolumbar junction. It
comprises 14 percent of all spinal fractures. Burst fractures are considered
unstable, even though there may be no neurological deficit (48-77% of the
patients may have neurological deficit). Most burst fracture occur from
T9-L5, with half occurring at L1. Two burst fractures, whether contiguous
or not, occur in less than 10 percent of cases.
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. A fragment from the posterior aspect of the
vertebral body may be retropulsed into the canal and may not be seen
(vanishing line sign). On frontal radiograph there is increase in interpedicular
and a vertical laminal fracture may be present. Isolated involvement of
superior vertebral endplate is most common. CT is used to show the size
of the spinal canal and the degree of retropulsion of the posterior fragment.
3. Seat belt injury
Seat belt injury represent a failure of both posterior and middle column
under tension. A flexion injury with a initial fulcrum being at the seatbelt
across the abdomen anteriorly is classically Chance fracture, a horizontally
oriented fracture through the spinous process, laminae, pedicles, transverse
process, with extension into the posterior aspect of the vertebral body.
Though mild anterior wedging may be present, the anterior column is
considered intact because the anterior longitudinal ligament intact. It
comprises 5 percent of all fractures.
Plain film shows fracture of lamina, pedicles, with increase of posterior
vertebral body height and posterior disc space. There is an increase in the
height of the neural foramina. Axial CT scans are of limited value because
of the horizontal nature of the fracture plane. Sagittal reconstruction CT
images may demonstrate the nature and extent of the injury. 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. CT of
facet distraction injuries shows the separation of the articular processes.
The articular facet of the vertebra above lie naked without their companion
facets below. 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. If the flexion part of the distraction is more
severe, facet distraction becomes more pronounced.
4. 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.
It represents 10 percent of all spinal fracture. 75 percent of the patients
have neurological deficits. The radiographic hallmark is vertebral subluxation
or dislocation seen on the frontal or lateral radiogrpah. Axial CT images
may show naked facets or superiorly bilaterally locked facets. The exact
position of the dislocation can be made out on 3D reformatted CT images.
APPENDIX
Table 4.1: Vandemarks riskTailored approach (For cervical spine)
Sl. No. Risk category Injury
1. No risk No historical or physical findings suggestive of spine injury
No Need for Imaging
2. Low risk Mechanism of Injury unlikely to have exceeded physiological
range of motion
Do A Three-View Series
3. Medium risk Injury likely to have exceeded physiological range of motion
Do A Five- View Series
4. 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 4.2: Appropriateness rating for radiologic examinations

Assessed by ACR Task Force (1995)
Patient group Radiologic examination Score
Asymptomatic and alert patients with AP, lateral, and open-mouth radiographs 1
normal physical examination with or Open-mouth and lateral radiographs only 1
without cervical collar AP, lateral, open mouth, and oblique 1
radiographs
Symptomatic patients with neurologic AP, lateral, 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, lateral, and open-mouth radiographs 9
Open-mouth and lateral radiographs only *
Oblique radiographs *
* = No consensus
1 = Least appropriate
9 = Most appropriate
Spinal Trauma 57
Table 4.3
Name of investigation Merits Limitations

Plain radiography Initial screening modality Inadequate for C1, C2, 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, 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, root avulsion local infection present
and meningocele/Pseudo- 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- Apart from above
archnoid space possible limitation, 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- 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
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.
May involve any tissue in any part of the body, but frequently involves.
Joints
Serous membranes
Blood vessels, and
Lungs and pleura
The features are: arthritis or arthralgia, multisystem involvement, vasculitis
and immunological abnormalities such as circulating autoantibodies and immune
complex deposition.
Conventionally, the connective tissue disease comprises:
Systemic lupus erythematosus (SLE)
Systemic sclerosis (SS)
Polyarteritis nodosa (PAN)
Dermatomyositis/Polymyositis (PMS)
Mixed connective tissue disease (consists of combined features of SLE,
SS and PMS)
CREST syndrome is a subgroup of systemic sclerosis characterized by :
Cutaneous calcinosis
Raynauds phenomenon (episodes of intermittent pallor of the finger
and toes on exposure to cold, secondary to vasoconstriction of the
small blood vessels)
Esophageal abnormalities (dilatation and hypoperistalsis)
Sclerodactyly, and
Telangiectasis
Some patients exhibit signs of more than one of the conditions. The term
overlap syndrome has been extended to include almost any combination.
Antinuclear antibodies are widely used in the diagnosis of connective tissue
diseases.
This is established by immunofluorescence against a rapidly dividing human
tissue substrate such as Hep-2-cells.
Antibodies to double-standard DNA are virtually pathognomonic of SLE

and their titer often approximates disease activity.
Other specific nuclear antigens have been defined including antibodies to-
Sm (in SLE)
Ro and La (in Sjgrens syndrome)
Centromere (in CREST)
Scl70 (in diffuse scleroderma) and
NRNP (in MCTD)
RHEUMATOID ARTHRITIS
It is a progressive, chronic, systemic inflammatory disease affecting
primarily the synovial joints.
Women are three times more often affected than the men.
There is a striking tendency toward spontaneous remissions and
exacerbations.
Rheumatoid factor, representing specific antibodies in the patients serum,
is an important diagnostic finding.
Patients lacking the specific antibodies represented by RF are said to have
seronegative rheumatoid arthritis.
Although such patients have an absence of rheumatoid factor, their clinical
and radiographic picture is similar to seropositive rheumatoid arthritis.
It is characterized by a diffuse, usually multicompartmental symmetric
narrowing of the joint space associated with marginal or central erosions,
periarticular osteoporosis, and periarticular soft tissue swelling, subchondral
sclerosisminimal or absent and formation of osteophytes is lacking.
Anyone of the large weight-bearing and non-weight bearing joints can be
affected by rheumatoid arthritis.
Radiographic Features
Certain radiographic features can be identified which are characteristics of
this inflammatory process. These include:
Soft tissue swelling
Osteoporosis, and
Joint space pathology
The soft tissue swelling is the earliest sign and usually a fusiform, symmetric
shape.
It is periarticular in location, representing a combination of joint effusion,
edema, and tenosynovitis.
Osteoporosis is a striking feature of rheumatoid arthritis, unlike osteo-
arthritis.
In the early stage of the disease, osteoporosis is localized to periarticular
areas; with progression of the condition, a generalized osteoporosis can be
observed.
Connective Tissue Disorders Involving Joints 61
The joint space narrowing of rheumatoid arthritis is a symmetric process

with concentric narrowing of the joint.
In the knee, all three joint compartment are involved.
Narrowing in the hip joint leads to axial migration of the femoral head,
which in more advanced stages may result in protrusio-acetabuli.
Cephalad migration of the humeral head may also be seen secondary to
destructive changes in the shoulder joint and rupture of the rotator cuff.
Resoprtion of the distal end of the clavicle, which assumes a pencil-like
appearance, may also be observed.
The erosive destruction of a joint may be central or peripheral in location.
As a rule, reparative processes are absent or very minimal, and thus there
is no evidence of subchondral sclerosis or osteophytosis, which may be
present only when secondary degenerative changes are superimposed on
the underlying inflammatory process.
In addition to the characteristic changes exhibited in large joint involvement,
the small joints may also show radiographic features specific for these
sites.
Rheumatoid arthritis characteristically affects the small joints of the wrist,
as well as the metacarpophalangeal joints in the hand are spared although
in advanced stages of the disease even these may be affected.
Subluxations and other joints deformitiesSwan-neck, Boutonniere,
HitchHikers thumb are common.
The subtalar joint is most often affected in the foot and a hallux valgus
deformity is observed.
In the cervical spine, rheumatoid arthritis is characterized by erosion of
the odontoid process associated with subluxation in the atlantoaxial joints
and, frequently, superior migration of C-2 and involvement of the apophyseal
joints.
Rheumatoid nodules, a condition occurring predominantly in men, is a
variant of rheumatoid arthritis. It exhibits a characteristic lack of joint
abnormalities, multiple subcutaneous nodules, and a high titer of rheumatoid
factor.
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

It is a prototype of connective tissue diseases.
F > M; young adults
Black > whites
Multisystem disease with arthralgia and rashes are commonest clinical
features and cerebral and renal diseases are the most serious problems.
PathologyWidespread vasculitis affecting capillaries, arterioles and
venules.
Fibrinoid (eosinophilic amorphous material) deposited alongblood vessels,
tissue fibers and synovium of joints.
Hemotoxylin bodies seen in inflammatory infiltrates resulting from interaction
between cell nuclei and antinuclear antibodies.
Musculoskeletal Features
The musculoskeletal system is a frequent site of involvement of SLE. The
commonest presentation is joint or muscle pains.
Joint involvement is the commonest clinical features (>90%). The small
joints are most commonly involved.
Arthritis is symmetrical
Erosions are rare
Occasionally, a patient develops a deforming arthritis, as a result of capsular
and ligamentous laxity.
Tendon involvement may be prominent, leading to flexion contractures at
the forearm and wrist in some cases. A proximal myopathy occurs in
5 percent of patients; this differs steroid myopathy in that the shoulder
girdle is more commonly involved and the serum muscle enzymes are
usually elevated.
Aspetic necrosis affecting the weight-bearing joints occurs in patients,
receiving high doses corticosteroids for long-standing SLE.
SLE is characterized by flexible joint contractures and malalignments of
the metacarpophalangeal and proximal interphalangeal joints.
Arthritis involvement is symmetric and articular deformities without fixed
contractures are the hallmark.
Hands are the predominant site of involvement.
Abnormalities are better demonstrated on the lateral projection, since they
can easily be reduced during positioning of the hand for the dorsovolar
view.
In Lateral View
Malalignments most commonly seen at the:
Metacarpophalangeal and proximal interphalangeal joints of the fingers,
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.
Seldom are, these abnormalities fixed and/or accompanied by articular
erosions.
Some patients present with
Sclerosis of the distal phalanges (acral sclerosis) or
With resorption of the terminal tufts (acro-osteolysis)
Osteonecrosis, which is frequently seen, has been attributed to:
Complications of treatments with corticosteroids, or
Vital role of the inflammatory process (vasculitis) in the development of
this complication.
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.
Primarily, a connective tissue disorder, is characterized by thickening and
fibrosis of skin and subcutaneous tissues, with frequent involvement of
the musculoskeletal system.
Thirty to forty percent of patients have a positive serologic test for
rheumatoid factor and positive antinuclear antibody test
Radiographically, the musculoskeletal abnormalities associated with
scleroderma are recognized as:
Atrophy of the soft tissues, particularly the tips of fingers
Erosion and resorption of tufts of the distal phalanges
Subcutaneous and periarticular calcifications
Destructive changes of the small joints, usually in the interphalangeal joints.
In scleroderma, corroborative findings are seen in the gastrointestinal tract,
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.
Polymyositis and Dermatomyositis

Polymyositis is a disorder of striated muscle characterized by diffuse,
nonsuppurative inflammation and degeneration.
Proximal muscular weakness and wasting affecting shoulder and pelvic
girdles.
When accompanied by a rash, it is called dermatomyositis.
Common in women
Peak incidence in adults aged between 30 and 60 years.
Dermatomyositis is associated with an increased incidence of carcinoma
bronchus in men and ovarian cancer in women.
Radiographic abnormalities are divided into two types:
Those involving soft tissues
Those involving joints.
a. The most characteristic soft tissue abnormality in both conditions are:
Soft tissue calcifications-
The favorite sites of intermuscular calcification are the large muscles

in the proximal portions of upper and lower extremities.
Subcutaneous calcifications are seen similar to scleroderma
b. 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.
Mixed Connective Tissue Disease

It is characterized by the clinical and radiologic features that combine the
findings of SLE; scleroderma, dermatomyositis and rheumatoid arthritis.
Patients in this group have prominent joint abnormalities, with typical
involvement of the small articulations of the hand, wrist and foot.
Joint deformities may simulate those seen in RA.
Soft tissue abnormalities are identical to those encountered in scleroderma.
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.
Normal Anatomy
The spinal column includes 7 cervical, 12 thoracic, 5 lumbar and 5 fused
sacral coccyx vertebrae. Except for C1, C2 and sacrum each vertebra has
similar osseous elements, includes vertebral body, pedicles, articular pillars
and laminae. C1 (atlas) consists of anterior and posterior arches, lateral masses
and transverse processes. C2 has vertebral body, pedicles, lateral masses,
spinous process and dens.
1. The spinal canal: Bounded anteriorly by vertebral bodies and intervertebral
discs.
Anteriorly Posterior longitudinal ligament
Posteriolaterally Pedicles and laminae lined by ligamentum flava
a. Cervical canal: Triangular in shape, measures 27 mm at C1 and
21 mm in lower cervical area in sagittal midline plane.
b. Thoracic canal: Canal is rounded in shape and constant in size.
c. Lumbar canal: Round to oval shape and triangular shape caudally.
The lowest normal diameter is 11.5 mm anteroposteriorly and
interpediculate distance of 16 mm.
2. 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. The nerve roots pass laterally from anterolateral and posterolateral
margins of each segment.
The epidural space contains fat which outlines the nerve roots and
epidural venous plexuses.
3. Intervertebral disc: It separates two adjacent vertebral bodies. On CT, the
disc have an attenuation value of 50 to 100 HU.
It consists of three parts
Central nucleus pulposus
Peripheral annulus fibers
Cartilaginous end plates
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.
In New Born
Nucleus pulposus is fibrocartilagenous with little fibers, so nucleus grossly
appears, homogenous except for small primitive notochord remnant.
During 1st and 2nd Decades

The notochordal remnants areobliterated, and distinction between nucleus
pulposus and annulus fibrosus is gradually lost because of fibrous tissue which
develops near margin of nucleus pulposus.
After 30 Years of Age

There is an indistinct boundary between nucleus pulposus and inner annulus
fibrosus.
4. Facet joints: These are joints between superior articular facet of lower and
inferior articular facet of upper vertebra. Normal joint space is 2 to 4 mm.
5. Ligaments:
a. 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. Posterior longitudinal ligament: It extends from C1 to S1 sacral
vertebra. In contrast to ALL, PLL does not adhere to vertebral body
and widens laterally at intervertebral discs and attaches firmly to annulus
fibrosus.
c. Interspinous ligament: It connects the spinous processes.
Nuchal ligament: It connects the base of occipital bone to spinous
processes of C1 to C7.
d. Ligamentum flavum: It is attached to laminae (3 to 5 mm in thickness)
and extends upto S1.
e. Intervertebral foramina: It is bounded medially by posterior vertebral
body and intervertebral disc, superiorly by inferior margin of upper
vertebral pedicle and inferiorly by superior pillars.
Physiological disc ageing in nucleus pulposus is related to specific chemical
changes. These are:
a. Decrease in water binding capacity
Degenerative Disorders of Spine and Joints 67
b. Disintegration of large molecular proteoglycans

c. 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. Loss of disc space height
b. Intradiscal gas (vacuum phenomenon) Early degeneration may also
occur without a loss in disc height or signal intensity.
Vertebral End Plate Changes

With Maturation, there is gradual conversion of red marrow to yellow marrow.
Signal intensity changes in marrow adjacent to vertebral end palate is common
on MR scan.
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.
Type II: Increased signal intensity is present on T1 and isointense to slightly
increased on T2-weighted due to fatty marrow replacement.
Type III: Decreased signal intensity on T1 and T2-weighted sequence due to
extensive bone sclerosis.
Annular Tears
Tears of annulus fibrous also occur with ageing.
Three types:
Type I (concentric) : A concentric fluid space between annular lamellae.
Type II (radial) : Characterized by rupture of all layers
Type III (transverse) : It involves rupture of Sharpeys fibers, inserted
into ring apophysis
Transverse and radial tears appear as increased signal intensity on
T2-weighted images. Usually annular tears enhance on administration of scar
tissue during healing.
SPONDYLOSIS
Etiology and Pathology
The primary finding is osteophytosis:
1. Osteophytes are bony excrescences that originate near the margin of
vertebral body of facet joints. Osteophytes typically develop where
Sharpeys fibers attach to vertebral body.
2. Schmorls nodes: It is herniation of disc material through end plate into

vertebral body.
Age Incidence
Increases with advancing age, prevalence is 60 to 80 percent in patients of
>50 years.
Location
Although any spinal segment can be involved, the lumbar and cervical areas
are the most common sites, thoracic spine is less frequently and less severely
affected.
The levels affected by both disc herniation and chronic spondylosis are
C6C7 (60% to 75%) and C5C6 (20% to 30%) in cervical spine.
In lumbar spine, L4L5 and L5S1 are the most commonly and most
severely affected sites.
Conditions Predisposing to Early Osteoarthritis

a. Congenital vertebral fusion: Complete vertebral fusion is known as block
vertebra, frequently disc degeneration develops above or below the fused
vertebra due to altered mechanics in spine. Commonly in cervical spine,
example Klippel-Feil syndrome.
b. 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. Caudal shift implies presence of ribs on
L1 and lumbarization of S1. The sacralised transverse process may form a
pseudoarthrosis with ileum and degenerative sclerosis may occur around
false joint. It may be cause of low backache. Secondly, free disc above
pseudoarthrosis show early degeneration.
1. In cervical spine:
Clinical presentation: As
Radiculopathy
MyelopathyUMN or LMN type of weakness
Neck pain
Vertebrobasilar insufficiencybecause of intrusions of osteophytes into
foramina transversarium.
Imaging Techniques
i. Plain radiography
AP, lateral, oblique views are taken. Oblique view delineate encroach-
ments of osteophytes into neural foraminas.
a. Cervical lordosis is reduced resulting in straightening of curvature
b. Disc herniaiton commonly seen at C6C7 followed by C5C6,
C4C5 and C3C4 in decreasing order. Vertebral end plates show
sclerosis in late stages.
c. Apophyseal jointsThe changes include erosion, and osteophyte

formation. Facet joint space is narrowed, show irregularity and
sclerosis.
d. Uncovertebral joints or joints of LuschkaWhen disc height
decreases, uncinate process approximate against vertebral body,
undergoes erosion and formation of osteophytes which causes
foraminal stenosis.
ii. Myelography
Extradural deformity because of disc protrusion or indentation of thecal
sac-filled with contrast can be noted.
iii. CT Scan
It accurately determines presence of osteophytes, narrowing of canal,
presence of prolapsed disc and compression of roots, CT myelogram is
useful to determine whether spinal cord compression is due to osteophytes
or disc protrusion.
iv. MRI
Sagittal and axial T1 and T2-weighted images are taken
a. For accurate localization of levels of stenosis and spinal canal diameter
in sagittal plane can be assessed.
b. It can demonstrate damage to cord in the form of edema, atrophy or
myelomalacia.
c. Intervertebral disc: Decreased height and decreased signal intensity
on T2-weigted images and different degree of disc herniation can be
assessed.
2. Thoracic spine: Degenerative changes less frequently seen because of limited
mobility of thoracic spine which is due to:
a. Small size of thoracic discs.
b. The orientation of thoracic facet joints in coronal plane.
c. Relative restraint placed on thoracic spine by ribs and sternum
Location
Majority of herniation are in lower thoracic spine, T11, T12 and lower 4 or 5
disc space most commonly affected.
Imaging
a. AP
b. Lateral
c. Oblique views
Radiological findings include
Disc space narrowing
Osteophytes formation
Facet joint hypertrophy
Kyphosis
Disc protrusion or extension can be seen
ii. Myelography
Mild to moderate ventral or ventrolateral indentation on contrast
column is seen opposite to disc herniation.
Large herniation result in partial or complete block of contrast
column.
iii. 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.
iv. MRI:
Disc herniation are isointense or slightly hypointense on T1-weighted
sequence and hypointense on T2-weighted sequences.
Lumbosacral Spine
a. AP
b. Lateral view
c. Oblique
Disc space narrowing
Osteophytosis
Vertebral end plate changes
Schmorls nodes
Intradiscal gas or vacuum phenomenon and posterior elements
Facet joint hypertrophy
Spondylolysis associated with spondylolisthesis
Spinal stenosis AP diameter being <15 mm
ii. Myelography
Non-ionic media is commonly used. Disc prolapse displaces and usually
causes tenting of the theca or deviation of corresponding nerve root
sheath.
Large protrusion may occlude a root sheath or obstruct the theca.
Limitation:
Does not delineate cause of narrowing, i.e. disc versus ligamentous
versus bony hypertrophy
For demonstration of lateral foraminal stenosis. Sensitivity is
reduced at L5 to S1 level
iii. CT scan:
Findings are
Osteophytes
Vertebral
Facet
Schmorls nodes: Seen on CT scan as end plate sclerotic area and

surrounding lucencies that represent interbody herniation of disc
material.
Joint space narrowing and facet hypertrophy: CT myelography gives
better evaluation of thecal sac, nerve roots, spinal cord and disc
bulge. Bone images are used to evaluate stenosis, facet arthropathy
and spondylolysis.
Approximately 10 percent disc herniation are calcified and some
may contain gas secondary to vacuum phenomenon.
MRI: Superior to CT because
a. It provides multiplanar imaging modality
b. Distinction of bone, disc, ligaments nerve roots, thecal sac and
spinal cord are clearly done but only disadvantage is lack of bony
detail.
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. Chronic disc herniations tend
to have low signal intensity on T2-weighted due to loss of water
content.
Annular tear is usually associated, seen as high signal intensity on
T2-weighted images and focal enhancement may be seen after
gadolinium administration.
Disc herniation : Protrusion, extension or sequestration can be seen
60% disc herniation - Posterior lateral margins of disc
30% disc herniation - Will be directly central or posterior
10% disc herniation - 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, and new bone formation.
Adjacent to degenerated facet joint, synovial cyst develop, containing
contents as serous or mucinous fluid.
Location: Middle, lower cervical and lower lumbar spine are commonly affected,
out of these lumbar is the most common site.
Imaging: On plain films and NECT scans
a. Joint space narrowing
b. Osteophytosis
c. Facet hypertrophy seen
Synovial cysts appear hypo/hyperdense compared to adjacent ligament
flavum in NCCT scan and depending on contents.
SPINAL STENOSIS
Clinical Presentation
Typically presents as neurological claudication, described as bilateral lower
extremity radicular pains as sensorineural deficit, that occur when patients
stand or walk. Other include:
i. Low backache
ii. Radiculopathies
It can be:
Congenital
Acquired
Congenital
a. Morquios syndrome
b. Short pedicle syndrome
c. Achondroplasia/hypochondroplasia
d. Downs syndrome
e. Spinal dysraphism
f. Scoliosis
Acquired
1. Degenerative
a. Spondylosis
b. Facet arthrosis
c. Ligamentous degeneration or spondylolisthesis
d. Disc herniation
e. Spondylosis with spondylolisthesis
f. Ligamentous ossification/ calcification
2. Postoperative
3. Posttraumatic
4. Metabolicacromegaly, renal osteodystrophy, hypoparathyroidism, oxalosis
Miscellaneous
Pagets disease
Ankylosing spondylitis
Fluorosis
Diffuse idiopathic skeletal hyperostosis (Dish syndrome)
Location
The lumbar and cervical regions are most commonly affected. 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, however
most thoracic herniations are central rather than lateral in location.
According to cause, it can be of two types:

a. Non-discogenic
Body origin
Ligamentous origin
b. Discogenic
Bony Origin
i. Facet hypertrophy: There is repeated stress on apophyseal joints, resulting
in erosion of articular cartilage and underlying bone, hypertrophies causing
foraminal narrowing. These changes predominantly seen in lower lumbar
spine.
ii. Osteophytes: Depending upon location, size and shape can narrow or
focally impinge upon any part of neural canal. In cervical spine, uncinate
hypertrophy can lead to foraminal stenosis.
iii. 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, becomes predisposed to either
anterior (anterolisthesis) or posterior (retrolisthesis), 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,
predisposed to slippage.
Four grades of severity depending upon forward slippage [Meyerdings
classification (1932)].
Grade I : 25%
Grade II : 50%
Grade III : 75%
Grade IV : 100% is slippage becomes more severe, spinal canal is
narrowed.
iv. Ligamentum flavum hypertrophy: It forms posterior wall of bony canal
so hypertrophy contributes to narrowing.
v. Ossification of posterior longitudinal ligament: This entity is common
in Japan. The ossified posterior longitudinal ligament can impinge upon
spinal canal and can result in nerve root compression.
Plain film: Seen as vertical band of ossified tissue along the posterior
margin of vertebral bodies.
On CT Scan: Involved portion of ligament is replaced by high density of
calcium.
On MRI: Ossification is represented by low signal on both T1 and T2-
weighted sequences.
vi. Lateral recess stenosis: Bony overgrowth of lateral recess as part of
degenerative processes resulting in entrapment of lateral roots.
Discogenic Spinal Stenosis

Two types:
i. Disc bulge
ii. Disc herniation
Disc Bulge
Defined as extension of disc margin beyond the confines of adjacent end
plate. As the nucleus pulposus loses its turgor and elasticity of annulus
diminishes, the disc bulges outward beyond the vertebral body margins.
Incidence
Mild bulging of cervical disc is common incidental finding
1. Imaging findings: On CT and MR scans, mild bulging disc initially appears
as loss of normal posterior disc concavity.
2. Moderate diffuse bulges are seen as diffuse, non-focal protrusion of disc
material beyond adjacent end plate usually circumferential and broad-based.
Associated findings: Decreased disc height and signal intensity and
annular tears can be seen as increased signal intensity on T2-weighted
images. Enhancement following contrast administration is seen in some
annular tears because of vascularized granulation tissue.
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.
Location
In lumbar canal 93 percent are inside the spinal canal, 3 percent are
predominantly located in intervertebral foramen and 4 percent are extraforaminal.
Imaging
Myelography: Extradural deformity or displacement of contrast filled thecal
sac, elevation, deviation or amputation of root sleeve and edema of affected
nerve can be seen.
NCCT: Shows soft tissue mass with effacement of epidural fat and
displacement of thecal sac.
MRI: Focal, asymmetric protrusion beyond the confines of annulus. Radial
annual tear is usually associated and high signal in posterior annulus is seen
on sagittal T2-weighted scans.
Types of Disc Herniation

i. Disc protrusion: When some of inner fibers of annulus tear but outer
remains, intact, nucleus can focally herniate through tear and called as
protrusion. This is the earliest type.
ii. Disc extrusion: When nucleus pulposus herniates through complete tear
of annulus and is contained only by posterior longitudinal ligament. The
herniated segment however remains attached to disc.
iii. Sequestration: When an extruded nucleus breaks free of the parent disc
called as sequestered or free segment. It may migrate superiorly or
inferiorly to a different inter-space or even penetrate the dura.
The most important distinction, is lack of connection between extruded
segment of parent disc. This is better appreciated on sagittal than on
axial MR scan.
Disc tend to herniated posterolaterally because of posterior longitudinal
ligament and annular fibers are thicker in midline and thinner laterally.
OSTEOARTHRITIS (DEGENERATIVE/HYPERTROPHIC
ARTHRITIS) OR OSTEOARTHRITIS
Degenerative condition affecting articulations particularly those bearing
weight or these subjected to much wear and tear.
Two typesAccording to etiology:
Primary
Secondary
Primary
When no predisposing cause for joint change is found.
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, for example, knees and ankles of professional
athletes.
Primary Osteoarthritis
Pathophysiology
It develops without evidence of an initiating factor. It appears that biomechanical
forces across the joint are normal, but some intrinsic abnormality of cartilage
causes it to degenerate.
The hands, 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. Joint space narrowing: Normal width of joint space is due to radiolucent
cartilage, joint space narrowing is result of cartilage destruction. This
change characteristically occurs in areas of excessive weight-bearing.
ii. 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.
Beneath areas of cartilage destruction, eburnation results (increased

change in exposed subchondral bone in degenerative disease in which
it is converted to dense smooth substance like ivory).
Localized increased in density is due to:
a. Stress induced new bone formation.
b. Trabecular collapse, flattening and sclerosis results.
New bone is formed at the areas of low stress, at joint margins,
predominantly peripheral osteophytosis or within joint, central
osteophytosis.
Cyst formation (Geode) in subarticular regions occurs in osteo-
arthritis (D/D rheumatoid arthritis) and is found in weight-bearing
areas.
3. Loose bodies: Formed by detachment of osteophytes, and ossificaiton of
cartilage debris.
Osteoporosis and bony ankylosis are not manifestation of degenerative
disease and new bone formation is seldom seen in osteoporosis, however
when osteoarthritis results in pain and immobility, osteoporosis and
soft tissue wasting may result secondarily.
Imaging: Plain X-ray and CT scan show osteophytes, joint space narrowing,
erosions and cysts, however MR is preferred imaging modality for
osteoarthritis in major joints.
Osteoarthritis in Particular Joints

a. Hip joint: Patients developing premature osteoarthritis, have pre-existing
anomaly and some result from childhood.
Congenital dysplasia
Congenital dislocation of hip
Acetabular dysplasia
Perthes disease : Some occur later as a result of Pagets disease,
scoliosis, rheumatoid arthritis and aseptic nercosis.
There is no typical appearance of osteoarthritis of hip, however different
patterns are seen which depends on direction of migration of femoral
head.
a. Superior migration (78%): May occur laterally, medially or in intermediate
direction.
b. Medial migration (22%): May lead to protrusio acetabuli, acetabulum is
dependent with narrowing of joint space, capsular traction leads to new
bone formation, usually on medial rather than lateral aspect of femoral
neck.
End result is femoral head shows bone loss in weight bearing areas and
bone formation in non-weight bearing areas.
Knee Joint
Most commonly affected joint found in clinical practice
Consists of three compartments
A medial and lateral tibiofemoral and patellofemoral joint space narrowing.

The bone most commonly involved in osteoarthritic change is patella (which
is subjected to large loads when knee is flexed in squatting positon).
In patellofemoral compartment, 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. Sometimes
scalloped defect of anterior distal femur is seen, especially in severe cases.
Spiking of tibial spines and osteophytes on articular margins are seen in
early phase. Joint narrowing affecting one or other compartment results in
valgus/varus deformity opposite compartment may be widened.
Varus deformity is more common and is related to more common medial
meniscus abnormalities.
The fabella may be enlarged and irregular in osteoarthritis.
Shoulder Joint
Osteoarthritis changes does not usually occur at glenohumeral articulation in
absence of predisposing factors, these factors include:
a. Use of crutches
b. With malalignment following chronic rotator cuff tear
Changes Include:
Erosions, cysts and sclerosis of greater tuberosity.
Irregular sclerosis along anatomic neck
Later atrophy of tuberosities and upward subluxation of humeral head
Acromioclavicular joint is also involved with irregularity, sclerosis and cyst
formation at articular surfaces.
Hand and Wrist Joint

Commonly affected joint are carpometacarpal joint of thumb and
trapezioscaphoid joint especially in women.
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. Bouchards nodes
and Heberdens nodes are seen at proximal and distal interphalangeal joints
respectively.
These are prominence due to osteophytes. Sometimes erosive osteoarthritis
seen in interphalangeal joints particularly patients who are seronegative
(middle aged women). The radiological features are erosions which
commence centrally, joint space loss peripheral osteophytes. Bony ankylosis
is an occasional feature and periosteal reaction may also be noted.
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, at right angles, i.e. AP/Lat for location, the points
to be observed are site, margins, periosteal reaction, matrix mineralization,
bone expansion/ destruction, soft tissue component and zone of transition.
Radio-nucleide: Bone scan 99 mTc.
More sensitive and very early detection, even before clinical/radiological
evidence of lesion.
CT scan: For extent of lesion, cortical break, soft tissue invasion.
MRI: For soft tissue extent and bone marrow involvement.
USG: High frequency probes are needed.
LUCENT BONE LESION IN MEDULLA / WELL-DEFINED / NON-

EXPANSILE / WITH SCLEROTIC MARGINS
Suggest Slow growth
Non-neoplastic
Geode
Brodies 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.
Osteolytic Bone Lesions 79
Etiology: Bone necrosis allows pressure induced intrusion of synovial fluid

into subchondral bone seen in conditions with synovial inflammation.
Causes: OA, RA, osteonecrosis, CPPD
Site: around knee, hip
X-ray:
Size usually 2 to 35 mm
May be large and expansile
In weight-bearing areas, 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.
Location: Predilection for cancellous tissue near ends of long bones proximal/
distal tibial metaphysis
Metacarpal, carpal, 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), known as TUNNELING
Periosteal new bone formation
Adjacent soft tissue swelling may or may not be present.
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.
Causes: Unknown? Gene mutation during embryogenesis
Age: 1st 2nd decade (3-15 yrs)
Disease progresses until growth ceases
Sex: F>M
Types
A. Monostotic form (70-80%)
Usually asymtomatic until 2nd 3rd decade
B. Polyostotic form (20-30%)
2/3rd symptomatic by 1st decade

C/F: leg pains, limp, pathological fracture (75%)
Abnormal veginal bleeding (25%)
Location: Unilateral and asymmetric
Meta diaphysis
Site: Femur, tibia, pelvis, feet, skull and facial bones, spine, upper
extremity
Clinical features:
Leg length discrepancy
Shepherds crook deformity
Facial asymmetry
Tibial bowing
Rib deformity
C. 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. 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, skull, 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, inner
table is spared
Obliteration of sphenoid and frontal sinus
Inferolateral displacement of orbit
Encroachment of orbital fissures
In pelvis and ribs

Cystic lesion
Protrusio acetabuli
In extremities
Premature fusion of ossificaiton center- short stature
Bowing deformity and discrepancy of limb length
Shepherds crook deformity of neck of femurcoxavara
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.
Etiology: Traumasynovial 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
Site: Proximal femur/humerus (60-75%)
Fibula, calcaneum, talus, rarely ribs, ileum, small bones of hand
Not in spine/calvaria
Locaiton: Metaphysialadjacent to epiphysis during active phase, migrates
to diaphysis with growth. 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, 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. Bones preformed in cartilage
are affected (not skull)
Age: 10-30 yrs
M:F = 1:1
Clinical features:
Usually asymptomatic
Painless swelling
Site:
Small bone of wrist and hand
Distal and middle of metacarpals
Proximal/middle phalanges
Femur, tibia, humerus, radius, ulna, feet, 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
Calcificationpin head, stippled, rings and arc pattern
Bulbus expansion of bone with cortical thinning
Madelungs deformitybowing 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, tenderness, swelling, limitation of movement
(may take months to year prior to diagnosis)
Site:
Long bones (80%)
Proximal femur and greater Trochanter
Distal femur, proximal, tibia, proximal humerus
2/3 in lower extremity of which 50 percent above knee
Flat bonesnear tri-radiate cartilage of innominate bone
Short tubular bones of hand/feet
Location:
Eccentric medullary, subarticular location with open growth plate
X-ray Appearances
Oval/round eccentric lytic lesion in epiphysis
1-4 cm in diameter occupying less than of epiphysis
Lobulated in 50 percent
Well-defined sclerotic margin
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, bronchus, kidney, thyroid
Multiple myeloma
Benign neoplasm
Enchondroma
Chondroblastoma
EOSINOPHILIC GRANULOMA
= Most benign type of histiocytsis-X
Age: 5-10 yrs. Max.
Range = 2-30 years.
M : F = 3:2
Lesions arise within medullary canal of reticuloendothelial system
proliferation of histiosites and inflammatory cells. Eosinophils in blood and
CSF.
Site:
Monostotic involvement in 50-75 percent
Calvaria > Mandible > Long bones UL/ Ribs > Pelvis > Vertebrae
If multiple Then in different stages of evolution.
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.
Hole within hole appearancedue to uneven involvements of inner and
outer table
Button sequestrumcentral bone density within lytic lesions
Overlying soft tissue mass.
Orbit
Benign focal mass +/- 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 Calves
disease (osteochondritis)
Collapse of vertebral bodiesthoracic 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, widening of medullary cavity
Cortical thinning, intracortical tunneling
Erosion of cortex + soft tissue mass
Laminated periosteal reactionmay show interruption
May appear rapidly within 3 weeks
Lesion do not involve joint space and growth plate.
BROWN TUMOR OF HYPERPARATHYROIDISM

Osteoclastomaa collection of osteoclasts
Etiology: PTH stimulates osteoclastic activitylocalised replacement of bone
by vascularized fibrous tissue (Osteitis fibrosa cystica)
Lesion becomes cystic following necrosis and liquifaction
Frequent in primary hyperparathyroidism.
Rare, 1.5 percent in secondary hyperparathyroidism.
Clinical feature: Tenderness and pain at the site of lesion
Bones, groans, stones, psychic moans
Site: Jaw, pelvis, ribs
Metaphysis of long bone (femur)
Facial bone
Location: Often eccentric/cortical. Frequently solitary
X-ray Appearances
Expansile, lytic or well-marginated, 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, kidney, 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, proteinuria, Bence Jones proteinuria
Anemia, increased ESR, increased globulin production (monoclonal
gammopathy)
Hypercalcemia.
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.
X-ray Appearance
In early stagegeneralised osteoporosis with accentuation of trabecular
pattern especially in spine.
Punched out appearance of wide spread osteolytic areas with endosteal
scalloping and uniform size in areas of red bone marrow
In skullrain drop lesions
Diffuse osteolysis (pelvis, sacrum)
Involvement of mandible (rare in secondary)
Skeletal form of multiple myeloma (1-3%)
Solitary/diffuse
Sclerosis may occur after chemotherapy (Radiotherapy), Fluoride adminis-
tration
Poems Syndrome:
Polyneuropathy
OrganomegalyLiver, spleen
EndocrinopathyDiabetes mellitus
M. Protein
Skin changeHirsutism, Pigmentation, 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, 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, also post-fracture giant cell tumor
Types
Intraosseous ABCprimary cystic/ telangiectatic tumor originating in bone
marrow cavity rarely related to H/o trauma. Slow expansion of cortex
Extraosseous ABCpost-traumatic hemorrhagic cyst originating on surface
of bone. Erosion through cortex into medulla.
Age:
Peak 16 yrs. (10.30 yrs)
F>M
Clinical features:
Pain of relatively acute onset with rapid increase in severity, 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 . metaphysis of femur, tibia, humerus, fibula,
pelvis
X-ray Appearances
Purely lytic, eccentric lucency, 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.
No perisosteal reaction (except when fracture)
CT: Blood-filled, sponge-like with fluidfluid 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. 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.
Clinical features: Usually asymptomatic. Pathological fracture
Site: Shaft of long bones, mostly lower limb
Especially about knee (distal femur and proximal tibia)
Location: Eccentric metaphyseal region.
Multiple Fibroxanthoma: In 8-10 percent
Associated with: Neurofibromatosis,

Fibrous dysplasia
JaffiCampenacci syndrome
Non-ossifying fibroma with extraskeletal manifestation in children:
Mental retardation
Hypogonadism
Ocular defects
Congenital cardiovascular system defect
Caf-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; V- or U-shaped at one end
Endosteal scalloping and thinning +/- 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. (2-10 yrs). Mostly before epiphysial closure
Fibrous tissue from periosteum invades the underlying cortex.
Clinical features: Asymptomatic
Site: Metaphyseal cortex of long bones around knee
Distal femur (postero-medially)
Characteristic sites: Proximal tibia
Proximal humerus, ribs, ileum, fibula
X-ray Appearances
Round when small, average 1-2 cm.
Oval, extending parallel to long axis of bone
Cortical thinning and expansion
Smooth, well-defined width sclerotic margin
Larger lesions are multiocular
With skeletal maturity, lesion migrates towards diaphysis
Involvement over 2-4 yrs. 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
CHONDROMYXOID FIRBROMA
Rare benign cartilaginous tumor, 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.)
M:F = 1:1
Clinical features: Slowly progressive local pains, swelling, restricted movement
Site: Long bones, about knee joint 50 percent proximal tibia distal femur
Short-tubular bones of hand and feet 20 percent
Flat bonespelvis, ribs.
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 - 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.
Septations may mimic trabeculations
Stippled calcification within tumor in advanced (7%) stage
No periosteal reaction.
Giant Cell Tumor

= Osteoclastoma probably arise from zone of intense osteoclastic activity
in patient with mature skeleton.
Incidence: 4.2 percent of all primary bone tumors.
Age: 20 40 yrs. Arise after epiphyseal plate fusion
M:F = 1:1
Clinical features: May be associated with Pagets 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; distal femur > proximal tibia
Upper limb away from elbow distal radius > proximal humerus
15 percent in flat bones

Pelvis, sacrum near sacroiliac joint > Thoracic > Cervical > Lumber, Ribs,
Skull
0.5 percent are multifocalin hand. 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%)
Destruction of vertebral body with secondary invasion of posterior elements
vertebral collapse
Involves adjacent vertebre and their discs spaces.
Crosses sacroiliac joint; rarely may cross joint space in long bones
Radionucleide study: Diffusely increased Uptake +/- Donut sign of central
photopenia
Angiography: Hypervascular lesion
CT: Tumor of soft tissue attenuation with foci of low attenuation (necrosis,
hemorrhage) well-defined margin thin rim of sclerosis.
MRI: Heterogeneous signal intensity with low to intermediate intensity of T1
and T2 WI due to collagen and hemosidrein content
Focal cystic areas.
LUCENT BONE LESION /GROSSLY EXPANSILE

Malignant neoplasms
Metastasis from renal cell carcinoma, thyroid, less commonly melanoma,
Bronchus, brest, pheochromocytoma
Plasmacytoma
Central chondrosacroma
Lymphoma of bone
Fibrosarcoma
Telangiectatic osteosacrcoma
Benign bone neoplasm
ABC
GCT
Enchondroma
Non-neoplastic
Fibrous dyplasia
Hemophilic pseudotumor

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, Femur, Humerus
X-ray Appearances
Solitary, grossly expansile osteolytic lesion with thinning of overlying cortex
and internal trabeculations.
Poorly-defined margins without sclerosis
Swiss cheese pattern or soap bubble appearance
Pathological fractures frequentcollapse of vertebra.
Central Chondrosarcoma
= Endosteal chondrosarcoma
Incidence: 3rd most common primary bone tumor (1st Multiple Myeloma,
2nd Osteocarcoma)
Arises from chondroblast
Age: 45 yrs. 10 percent occur in children
M:F = 2:1
Clinical features: Hypercalcaemia as paraneoplastic syndrome (85%)
Site: Neck of femur, pubic rami, proximal humerus, ribs, skull (sphenoid, C.P.
angle, mandible), sternum, spine.
Location: Central in meta/diaphysis
X-ray Appearances
Expansile osteolytic lesion one to several cms. in diameter
Short transition zone +/- seclerotic margin which is well defined from host
bone
+/- 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 Hodgkins 5-15 percent bone involvement
In NHL 25-40 percent
Age: Any age. Peak 3rd 5th decade
M: F = 2:1
Site: 40 percent above knee joint Lower femur, upper tibia, humerus, pelvis,
scapula, ribs, and vertebra
Location: Dia-metaphysical
2/3rd sclerotic, 1/3 lytic, sclerotic lesion does not cause enlargement of bone.
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 Ewings)
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.
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:
Pagets disease, GCT, bone infactrs, osteomyelitis
Enchondroma, fibrous dysplasia
Age: Predominant by 3rd 6th decade

M:F = 1:1
Clinical features: Metastases to lung, lymph node
Localized painful mass
Tubular bone in young, flat bone in older
Femur tibia about knee joint (80%), Jaw, Pelvis
Rare in small bone of hands feet, spine
Location: Eccentric at diaphyseal and metaphyseal junction:
IntramedullaryCentral type
PeriostealParosteal 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.
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. (3-67 yrs.)
M:F = 3:2
Sarcoma of bone with large blood-filled vascular channels
Site: About knee 62% distal femur, proximal tibia, proximal humerus
Location: Metaphysis with extension into epiphysis.
X-ray Appearances
Geographic bone destruction with wide zone of transition.
Marked aneurysmal bone expansion
Fluid-filled levels
Nodular calcific foci of osteoid.
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.
Juvenile form usually multiple intramedullary expansile lesions without

soft tissue mass in small bones of hand and feet. (Before epiphyseal closure).
Adult form usually single intramedullary expansile lesion with large soft
tissue mass in ileum/ femur.
X-ray Appearances
Mixed cystic expansile lesion.
Bone erosion and pathological fracture
Hemophilic arthropathy
Synovial thickening and articular erosion, initially marginal only
Periarticular osteoporosis (disuse and hyperemia)
Enlargement of growing epiphysis
Premature development of secondary degenerative changes.
CT: Encapsulated mass lesion containing areas of low attenuation and
calcification.
MRI: Hemorrhage of varying age.
HYDATID CYST
= Echinococcus granulosus. Sheep definitive host, dog intermediate host.
Multiloculated cysts in bone adjacent soft tissue.
Clinical features:
X-ray Appearances
COCCIDIODOMYCOSIS
Chronic granulomatous lesion by fungi in bones, joints and periarticular
structures.
Site:
a. Bonesmetaphysis of long bones, medial end of clavicle, spine, ribs, pelvis,
patella
b. Wt. bearing jointsknee, ankle, wrists, elbow.
X-ray Appearances
Focal areas of destruction and cavity formation = bubbly bone lesion.
Proliferation of overlying periosteum.
Sclerosis surrounding osteolysis rare and late.
Destruction of vertebra with preserved disc space
Mono articular joint infectionSynoivial effusion, osteopenia, joint space
narrowing destruction and ankylosis. (Desert rheumatism).
Cystic Tuberculosis
Well-marginated lytic lesion
a. In children frequent in peripheral skeleton

Symmetric distribution
No sclerosis
b. In adult in skull/shoulder/ pelvis/ spine with sclerosis.
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
Ewings Sarcoma
Central chondrosarcoma
Fibrosarcoma
Malignant fibrous histiocytoma
Osteomyelitis
Acute osteomyelitis
Age: Children
Organism: New born - Group B Streptococcus, E. coli, Staphylococcus aureus.
Children S aureus M/C
Adults S aureus (60%) Enteric Op., Streptococcus.
Drug addicts Pseudomonas (86%); Klebsiella, Entrobacters.
Sickle cell disease - Salmonella.
Causes
Genitourinary tract infection most commonly.
Lung infections
Dermal infection: direct spread from soft tissue lesion in diabetic foot.
Pathogenesis
Hematogenous spread most common.
Direct implantation from traumatic/Iatrogenic source
Extension from adjacent soft tissue infection.
Site: Lower extremity 75 percent - Over pressure points in diabetics
Vertebra-Lumbar > Thoracic > Cervical.
Clinical features: Leukocytosis + fever
a. Acute Neonatal Osteomyelitis

Age Onset < 30 days of age.
Little no systemic disturbance.
Multicentric involvement more common, joints often involved.
b. Acute Osteomyelitis in Infancy
Age < 18 months.
Spread to epiphysis because transepiphysel vessels cross growth plate
into epiphysis.
Frequent joint involvement.
Extensive soft tissue component.
Subperiosteal abscess with extensive periosteal new bone formation
therefore Periosteum loosely attached.
c. 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. Abscess formation in medulla with cortical spread.
X-ray Appearances
Sequestration is frequent.
Periosteal elevation (with disruption of periosteal blood supply)
Small single/ multiple osteolytic areas in metaphysics.
Extensive periosteal reaction parallell to shaft (3-6 weeks) may be lamellar
or nodular.
Shortening of bone with destruction of epiphyseal cartilage.
Growth stimulationby hyperemia and premature maturation of adjacent
epiphysis.
Mid-shaft involvement less frequent.
Serpigenous tracts with small sclerotic rim (Pathognomonic).
Joint infection again common because metaphyseal and epiphyseal vessels
again connected.
d. Acute Osteomyelitis in Adults
Delicate periosteal new bone.
Joint involvement common.
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).
Area of bone destruction (>7-14 days)/ osteoporosis.
Involvement Cloak of laminated/speculated periosteal reaction (>21 days).
Sequestrum detached devitalized necrotic cortical bone (>30 days).
Cloacae formation space in which dead bone resides.
CT: Dense bone fragments within area of bone destruction. (Sequestrum).

MRI:
Bone marrow hypointense on T1WI and hyperintense on T2WI = water
rich inflammatory tissue.
Focal /lineal cortical involvement hyperintense on T2WI.
Hyperintense halo surrounding cortex on T2WI subperiosteal inflam-
mation.
Hyperintense line on T2WI extending from bone to skin surface and
enhancement of borders-sinus tract.
Abscess characteristics
Hyperintense rim (hyperemic zone) around a central low-intensity
(=necrotic tissue) on CET1WI.
Hyperintense fluid collection by hypointense pseudocapsule on T2WI
and contrast enhancement of granulation tissue.
Hyperintense adjacent soft tissues on T2WI.
Radionuclide Scanning
Early diagnosis by 48 hours. Tc 99m labeled phosphonate and phosphate

compound.
Image related to local blood and bone turnover.
Chronic Osteomyelitis
Thick irregular sclerotic bone with radiolucencies, elevated periosteum,
chronic draining science.
Infant Children Adult

Location Metaphysis - 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.
Incidence = 15 percent of all bone tumors confirmed at biopsy.
Types
1. Primary Osteosarcoma
High grade intramedullary = central osteosarcoma = most common
Telangiectatic Malignant bone aneurysm.
Low grade intraosseous lesion.

Small cell.
OsteosarcomatosisMultifocal osteosarcoma.
Gnathic Osteosarcoma of jaws.
2. Surface/juxtacortical osteosarcoma.
Per Osteal origin from outer layer of periosteum.
Periosteal from deep layer of periosteum.
High grade surface.
Intra cortical.
3. Extra skeletal Localized within soft tissue without attachment to bone/
periosteum.
4. Secondary Osteosarcoma Malignant transformation in benign process.
Pagets diseases (67-90%)
Sequele to irradiation 2-40 years after related exposure dose
(>1000 CGY).
Chronic osteomyelitis, osteonecrosis, fibrous dysplasia.
Central Osteosarcoma
Arising from undifferentiated mesenchymal tissue forming neoplastic osteoid.
Age - Bimodal distribution 10-25 years (70%0 and >60 years) related to previous
conditions
M:F - 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.
Site: Long bones 50-55 percent about knee - Femur/Tibia
Proximal humerus
3.5-7 percent occurs in spine.
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.
Sclerotic/Lytic/Mixed
Aggressive periosteal reaction Sun ray/Sun burst type often Codmans

reactive triangle present.
Cortical disruption and soft tissue mass with tumor new bone formation.
Transepiphyseal spread before plate closure.
Radionuclide Scan
Intensely increased activity.
Soft tissue extension demonstrated especially by SPECT.
CT:
Soft tissue attenuation (non-mineralized portion) replacing fatty bone
marrow.
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.
Marrow involvement decreased on T1WI.
Cortical destruction increased on T2WI.
Osteosclerotic zone decreased on T1 and T2WI.
Ewings Sarcoma
Incidence = 4-10 percent of all bone tumors.
Most common malignant bone tumor in children.
Primitive primary malignant bone tumor derived from the connective issue
framework of bone marrow.
Age: Peak =15 years.
95 percent between 4-25 yrs.
M:F = 2:1
Caucasians: 96 percent
Clinical features:
Severe local pain
Soft tissue mass
Fever, leukocytosis, secondary anemia
Site: Long bone 50 percent Femur, tibia, fibula, humerus.
Flat bones 40 percent Pelvis, ribs, scapula.
Location: Diaphyseal/Metadiaphyseal
Usually no involvement of epiphysis as tumor originates in medullary cavity
with invasion of Haversian system.
X-ray Appearances
8-10 cm long lytic lesion in shaft of long bone, (62% lytic; 23% mixed;
15% sclerotic).
Destructive permeative lesion (with wide zone of transition).
Penetration into soft tissues with preservation of tissue planes.
Early fusiform laminated onion skin periosteal reaction, uncommonly
speculated sun burst type/ Codmans triangle.
Cortical thickening / destruction cortical sequestration.
In rib-disproportionately large inhomogeneous soft tissue mass with large
intrathoracic and minimal extrathoracic component.
MRI:
Marrow involvement T2 T1
Necrosis/cyst formation T2 T1
Hemorrhage T2 T1
Malignant Fibrous Hystiocytosis

Contain both histocytic and fibroblastic cells.
Usually arises in association with another pre-existing benign bone disorder
(therefore previously known as secondary firbosarcoma), e.g. Pagets
disease, chronic osteomyelitis, bone infarcts, enchondroma, previous
radiation, therapy.
Clinical features: Painful swelling.
Age: 30-60 yrs.
M:F = 1.5:1
Site: Distal femur, tibia, humerus, pelvis
Location: Metaphysis can extend to diaphysis and some times to epiphysis.
X-ray Appearances
Eccentric lytic lesion with cortical thinning.
Moth eaten/permeative destruction with wide zone of transition.
Cortical disruption.
Large soft tissue mass.
No matrix calcification.
Bone scan: Increase tracer uptake around periphery
CT:
Intraosseous/extraosseous extent of tumor
Relationship to major nerves and vessels.
MRI: Firbrous tissueIntermediate intensity signal on T2WI

Necrosis/hemorrhageIncreased on T2WI and decreases on T1WI.
Moth Eaten Bone = Multiple Lytic Lesion

Multiple scattered, variable size lucencies.
Coalescence may occur.
Cancellous and/or cortical bone involved.
Neoplastic
Metastasisincluding neuroblastoma in children.
Multiple myeloma.
Leukemia.
Long bone sarcomas
Ewings 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
Ewings sarcoma
Multiple myeloma
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-
- Rodent ulcer Hystocytoma
- Ca of ear Infective
Pagets sarcoma Chronic osteomyelitis
Traumatic Frontal sinus mucocele
Burr hole/Trephine
Leptomeningeal cyst
Idiopathic
Osteoporosis circumscripta
Contd...
Contd...
Metabolic
Infective
TB osteomyelitis
Pyogenic osteomyelitis
Hydatid
Syphilis
b. Children
Neoplastic
Metastasis
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 type is rare
Age: = 4-5th decade
M:F = 2:1
Clinical features: Usually asymptomatic
Cavernous20 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.
Vertebrae: 28 percent of all osseous haemangioma.
Capillary Haemangioma
Age: > 40 yrs.
F>M
Site: Lower thoracic /upper lumber spine.
X-ray Appearances
Coarse vertical trabeculae with osseous reinforcement adjacent to bone
reabsorption caused by vascular channels.
Bulging of posterior cortex.
Extraosseous extension beyond bone lesioncord compression.
Paravertebral soft tissue extension.
CT: Polka-dot appearance with small punctate areas of sclerosed thickened
vertical thickened vertical trabeculae.
MRI: Mottled pattern of low to high intensity on T1WI = very high intensity
on T2WI.
*Flat bones and long bones: Rare
Ribs, clavicle, mandible, zygoma, nasal bones, metaphyseal ends of long bones.
Leptomeningeal Cyst = Growing Fracture

Seen in 1 percent of pediatrics skull fracture.
Skull fracturedural teararachnoid herniation into dural defect and CSF
pulsation causes fracture diastasis and erosion of fracture margin, apparent
2-3 months after injury.
Age = <3 yrs.
X-ray Appearances
Skull defect with indistinct scalloped margins.
CSF density cyst adjacent to/ in skull, may contain cerebral tissues.
MRI:
Cyst isointense with CSF and communicating with subarchnoid space
Area of encephalomalacia underlying fracture
Intracranial tissue extending between fracture edges.
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

Brown tumor of hyperparathyrodism
ABC
Simple bone cyst
Fibrous dysplasia
Radicular Cyst
Etiology: Deep carious lesion; deep filling; trauma.
Site: Intimately associated with apex of non-vital tooth.
X-ray: Apical lucency.
Dentigerous Cyst
Epithelial lined cyst arising from odontogenic epithelium, developing around
unerupted tooth.
Site: Maxilla (may expand into maxillary sinus), posterior mandible.
X-ray: Cystic expansile lesion containing tooth.
Ameloblastoma = Adamantinoma of jaw

Locally aggressive lesion from enamel type epithelial tissue elements around
tooth.
1/3rd arise from dentigerous cyst.
Age: 4-5th decade
M:F = 1:1
Site: Mandible 75 percent, 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.
May be associated with impacted tooth/ resorption of the root of the tooth.
Expansile Rib Lesions

Fibrous dysplasia
Enchondroma
Lymphoma
TB
Hematopoiesis
Ewings sarcoma
Chondromyxoid fibroma
Leukemia
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).
Glomus body - 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, an anastomiotic vessel
(= Sucquet - Hoyer canal lined by endothelium and surrounded by smooth
muscle fibers), a primary collecting vein.
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.
Hildreth sign : disappearance of pain after application tourniquet proximally
on area (= pathognomonic).
Types
A. Subungual Glomus Tumor
X-ray: Increased distance between dorsum of phalanx and under side of nail.
Extrinsic pressure erosion sharply marginated with sclerotic border, often
of the terminal phalanx especially subungual portions.
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.
= rare benign tumor with unlimited growth potential and capability of malignant
transformation
Incidence:
Age: Peak 15-20 yrs. (range 6-30 yrs.)
M : F = 2:1
Lesions: > 1.5 cm, smaller lesion known as osteoid osteoma
Clinical features:
Dull localized pain of insidious onset, worse at night.
Response to salicylates
Localized swelling, tenderness, decreased range of mobility
Asymptomatic rarely
Painful scoliosis (if located in ribs/ spine) due to muscles spasm
Parasthesia, mild muscle weakness, paraparesis
Paraplegia (due to cord compression).
Site:
Spine: max is posterior element with extension into vertebral body
C > T> L> Sacrum
Long bones: femur, tibia, humerus, radius, fibula
Small bones of hand and feet; dorsal talus neck, scaphoid, metacarpals,
metatarsals
Calvarium and mandible (=cementoblastoma)
Location: Diaphyseal > metaphyseal
Eccentric > centric
Intracortical, may be periosteal
X-ray Appearances
Radiolucent nidus > 2 cm size (2-12 cm)
Demarcated +/- stippled/ small flecks of matrix calcification
+/- reactive sclerosis
Progressively expansile lesionsmay rapidly increase in size, cortical

expansion/ destruction, sharply defined soft tissue component, thin shell
of periosteal new bone.
Scoliosis
Osteoporosis due to disuse
Rapid calcification after radiotherapy.
CT:
Multifocal matrix mineralization, sclerosis
Expansile bone remodeling, thin osseous shell.
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- 4th decade
M>F
Clinical featuers:
H/O skin penetrating traumaimplantation of epithelium under skin with
secondary bone erosion
May be asymptomatic
Location: superficially situated bonescalvarium, 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.
8
Metabolic Bone Diseases
Bone has three functions:
Mechanical
Metabolic
Hemopoitic
Bone Physiology, Metabolism and Basic Structure

Bone is a living tissue which is quite active metabolically. It receives and
returns approximately 200-400 ml blood/min to general circulation. Its basic
structure comprises of a framework of ground substance consisting
predominantly type I collagen called as osteoid matrix; and hydroxy-
apatite crystals laid down upon the osteoid, each measuring 20 nm 6-7 nm
[Ca++10. (H3O)+2 (PO4-3)6].
This collagen consists of a triple helix (21 + 12): also present in Ostoid
are MGP and BGP having -carboxylic acid (-carboxylatin being accomplished
by vitamin K), osteonection, osteopontin, osteocalcin, fibronectine sialoprotein,
proteoglycan and albumin.
Collagens are laid down in woven (coarse fibered) or lamellar fashions,
forming woven or lamellar bone. Woven bone is found at sites of active growth,
has more Ca++ and cells with isotropic tensile property. Lamillar bone on the
other hand has anisotropic property and is much stronger. It is found in mature
skeleton.
Apart from these histological bone types there are two grossly-visible types
and can also be seen radiologically, i.e. Trabecular or spongy or cancellous
bone and cortical or compact bone are called as integral bone. The medullary
cavity predominantly has the trabecular bone white cortex is made up of
compact bone. The bone turnover is much more at trabecular bone as compared
to cortical bone, i.e. it has much more free surface area. Depending upon age,
site, nutritional status, sex, etc. 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, though trabecular bone constitute only
25 percent of bone, 75 percent being formed by the cortical bone. Trabecular
exchange is only at the surface while it is throughout in cortical bone. Two
cell types must be mentioned in relation to bone anatomy, physiology and

embryology.
A. Osteoblasts
Osteoblasts are the bone forming cells that line the bone surface and lay
the osteoid. These finally turn to osteocytes when ample ground substance
has been layed down.
B. Osteoclasts
Osteoclasts are bone reabsorbing cells that are also found lining the surface
forming sites called Howships lacunae. It releases mineral from matrix and
also dissolves the matrix.
Both these cells function in a tanden osteoblasis starting within 2 weeks
of osteoclasis and persisting upto 3 months.
Bone Formation
1. Due to increased osteoblast activity:
Parathyroid hormone
T3, T4
1, 25 DHD3 (1, 25-Dihydrocholecalciferol).
IL-1 (Interleukin-I)
Growth hormone
Oestrogen
IGF-I (Insulin-like growth factor-I)
PGE2 (Prostaglandin E2)
TNF (Tissue necrosis factor).
2. Due to decreased osteoclast activity:
Calcitonin
Oestrogen via IL-6
PGE2
IFN- (Interferon-)
TGF- (Tissue growth factor-)
Bone Destruction
1. Increased Osteoclast
IL-6
IL-11
IL 25DHD3
PTH
2. Decreased Osteoblast
Corticosteroid
Metabolic Bone Diseases 111
Blood Kidney Gut Bone

PTH Ca P PO4 excretion release of Ca
Ca absorption
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. Alternation in bone structure is referred to as metabolic bone disease. It

can be at the level of
1. Collagen framework, e.g. scurvy
2. Bone mineralization, e.g. rickets
3. Bone mass, e.g. idiopathic osteoporosis
4. Bone cell function, e.g. cushing
Bone Reabsorption
1. Subperiosteal
2. Endosteal
3. Intracortical
4. Trabecular
Classification of Metabolic Bone Disease

Metabolic bone disease in which there is altered bone metabolism, i.e. the
phenomenon of normal bone formation and destruction are altered and
hence radiological observations are either:
a. Osteosclerosis (increased bone density) which may be localized or
generalized.
b. Decreased bone density which again may be localized or generalized.
i. Osteoporosis (also known as osteopenia) ratio of osteoid to Ca++
is normal
ii. Osteomalacia osteoid > Ca
iii. Osteofibrosa (mixed)
Certain Terminologies are Considered Here

1. Osteoporosis Bone quality is normal, quantity is decreased.
2. Demineralization Loss of mineral (halesteresis).
3. Undermineralization Decreased deposition (Osteomalacia).

4. Deossification Normal rate but increased resorption.
5. Osteopenia General/local decreased bone.
Generalized Decreased Bone Density

1. Osteoporosis
2. Cushing disease
3. Osteomalacia
4. Rickets
5. Renal osteodystrophy
6. Primary hyperparathyroidism
7. Scurvy
8. Hyperpitutiarism
9. Hyperthyroidism/hypoparathyroidism
10. Osteogenesis imperfecta
11. Juvenile idiopathic osteoporosis
12. Hyperphosphatasia
13. Hypogonadism
14. Pseudo and Pseudo-Pseudohypoparathyroidism
15. Gout
16. Pseudogout
17. Oxalosis
18. Alkaptonuria
Localized Decreased Bone Density

1. Disuse
2. Sudecks
3. Transient
4. Regional migratory
5. Idiopathic chondrolysis
6. Primary ostolysis: Gorhams disease,
Carpotarsal syndrome
7. Arthritides
8. Neuromuscular disorders
9. Infections
Generalized Increased Bone Density

1. Hypoparathyroid, Pseudo and Pseudo-Pseudohypoparathyroidism.
2. Fluorosis
3. Hypervitaminois A and D
Localized Increased Bone Density

1. Heavy metal poisoning

2. Thyroid acropachy
3. Hypervitaminosis A
IMPORTANT FEATURES OF METABOLIC BONE DISEASES

Osteoporosis Group
1. Primary Osteoporosis
Involutional Postmenopausal (Type I)
Senile (Type II)
Juvenile
Osteogenesis imperfecta
2. Secondary Osteoporosis:
a. Endocrine Cushings disease: Addisons disease
Hypogonadism : Postmenopausal
Acromegaly : Hypopituitarism
Diabetes mellitus
Hyperthyroidism : hypothyroidism
Hyperparathyroidism
b. Marrow expansion and replacement
Myeloma
Lymphoma
Leukaemia
Secondary deposits
Gauchers disease
Anaemias
c. Drugs and others
Steroid, hepartin, alcohol, immunosuppressant
d. Chronic diseases
CRF, malabsorption, hepatic insufficiency, chronic
inflammatory bowel disease
Involutional osteoporosis is the most common metabolic bone disorder
and may be due to postmenopausal state or senile. Senile osteoporosis starts
early in women and proceeds @ 3-20 percent per year.
Type I (Postmenopausal) Especially trabecular bone loss
Colles fracture and crush fracture of vertebra
Type II (Senile) Both compact and trabecular bone loss
Age > 75 years.
Fracture at hip and vertebra, humerus, tibia.
Radiological Features
When > 30 percent bone lost
Decreased bone density especially at axial skeleton.
Cortical thinning and prominence (Penciling in or picture frame).
Accentuated primary trabecule.

Wedge, biconcave, compressed vertebra (cod-fish).
Insufficiency fracture (sacrum, pubis, etc.)diagnosed by CT Scan,
scintigraphy, etc.
Fracture at non spinal sites (hip, wrist, pubis).
Endosteal and intracortical thinning.
Ground glass appearance especially at pelvis.
Singhs index, metacarpal index, vertebral index.
Schmorls node.
Juvenile Osteoporosis
Initially, progressive
Male and female are equally affected. Female before puberty.
Insufficiency fracture at metaphysis of long bones.
Spinal disease commonly seen in dorsolumbar vertebra.
Diagnosis by exclusion of lymphoma, leukemia, osteogenesis imperfecta.
Slipped capital femoral epiphysis.
Exogenous and Endogenous Cushing Disease

Pathological osteopenia
Exuberant callus with sclerosed vertebral end plates.
Rib fracture common
Mottled skull
Osteonecrosis especially in exogenous Cushings.
Neuropathic joint, tenden rupture, ostoephytes.
Decreased skeletal maturation, septic arthritis.
Hyperphosphatasia (Juvenile Pagets Disease)

Autosomal recessive trait
Osteoporosis with bowed bones and Pagets-like features, short stature.
Excess formation of embryonic bone precursor which fails to mature to
normal adult bone.
Fuzzy cortex with prominent trabeculae followed by sclerosis.
Bowing and fracture.
Large mottled skull.
Hyperparathyroidism
In Osteofibrosa Group
1. Primary
2. Secondary (renal osteodystrophy)
3. Tertiary
1. Primary
Middle to old age especially in women.
Findings suggestive of osteoporosis.
Subperiosteal resorption (hand, tibia, femur, ribs, clavicle).
Loss of lamina dura in mandible.
Subchondral bone absorption (pubis, proximal clavicle, SI joint,
vertebra).
Intracortical resoption a sign of rapid absorption leading to basket work
appearance of cortical meduallary junction, Pepper pot/salt pepper
skull.
Subligamentous resorption in inferior surface of clavicle, Trochanter
and tuberosities, calcaneum.
Browns tumor (in epiphysis, metaphysis, diaphysis) are multiocular,
expansile, lytic, well-defined lesions.
Brown tumor may become sclerotic or bone cyst.
Erosive arthropathy involving distal interphalangeal joints.
Osteosclerosis may be seen due to increased osteoblastic activity.
Chondrocalcinosis due to CPPD in wrist, knee and symphysis pubis.
2. Secondary (Renal Osteodystrophy): Adults Chronic glomerulonephritis;
Children Chronic pyelonephritis
Occur as a result of persistant hypocalcemia in CRF and hence
secondary hyperparathyrodism has become synonymous to ROD. Soft
tissue calcifications is more common in secondary hyperparathyroidism
due to ROD. Features of ROD are seen more commonly on account of
better management and survival of CRF patients:
a. 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.
In children instead of osteomalacia frank rickets occurs wherein features
of rickets, slipped epiphysis and absorption forms a rooting fense
post appearance.
b. Due to amyloid, CPPD infection, arteriovenous necrosis:
Erosive arthropathy similar to Charcots joints without extensive
loose bodies are seen especially noted in the shoulder and spine.
Arthritis, osteomyelitis, etc. are usually the result of debilitated
state, infection and fracture.
Arteriovenous necrosis is usually due to steroid therapy and
occurs even after transplant especially in femur, humerus, talus
and knee.
c. Aluminium toxicity:
Encephalopathy
Osteopenia
Fractures especially vertebre and 2/3/4 ribs.

Osteomalacia due to aluminium deposition on osteoid instead of
calcium
Spondylosis with decreased disc space and marginal irregularity without
paravertebral soft tissue.
Scurvy
It is functional counterpart of osteoporosis in children more than 6 months,
due to boiled milk.
At least 4-6 months of vitamin C deficiency is required for manifestations.
Osteoporosis.
Frankles line (wide sclerotic zone of provisional calcification).
Traummerfeld zone or scurvey line (a metaphyseal transverse zone below
white line)unmineralized osteoid.
Pelkans spur (metaphyseal spur due to marginal fracture).
Wimbergers ring (small epiphysis with sclerotic margin).
Periosteal reaction positive.
Growth arrest lines can be seen in later part of life.
Corners sing (Subphyseal bone infarction leading to epiphyseal to
metaphyseal separation and hence subperiosteal haemorrhage).
Changes are prominently seen at growing ends of bone.
Hyperpituitarism: (Acromegaly and Gigantism)

Endochondral subligamentous and periosteal bone formation are increased.
Over all increase growth matter, i.e. protein and cells.
Overall bone density increases but transient osteopenic appearance on
X-ray may be seen due to concomitant increased in osteoclastic activity.
Increased sesamoid index.
Enlarged costochondral junction and discs due to increased endochondral
growth.
Cartilage growth leads to increased joint space. Chondrocalcinosis also
occurs.
Heal pad thickness increased.
Prominent bony ridges.
Thick irregular bones.
Widended teeth.
Prognathism.
Pneumatized air cells in sinuses.
Scalloped and A-P widened vertebra with spinal stenosis.
Spade or spoon-shaped phalanges.
Hypopituitarism
Decreased skeletal maturation and growth with osteoporosis.
Hyperthyroidism
Hypermetabolic state may lead to bony changes even in first year, which
do not seem to be related with severity of disease. Exophthalmos is a
constant feature.
Osteoporosis with increased skeletal maturation as compared to
hypothyroidism where osteoporosis with decreased skeletal growth and
maturation with fragmented epiphysis, wormian bones, bullet shaped
vertebrae etc. Hypothyroidism may be primary or secondary and leads to
Cretinism, juvenile myxedema and classical adult myxedema.
Changes are commonly seen in hand, D-L spine, pelvis.
On the contrary brachycephaly, enlarged sella (bowl-sella or cherry sella),
hypoplastic frontal sinus, coxavara are seen in hypothyroidism as well as
in slipped femoral epiphysis.
Hypogondadism
Primary (Turners enuchoidism) or secondary to decreased Gonado-tropins.
Osteoporosis with long limb, short trunk due to delayed epiphyseal closure.
Short 4th and 5th metacarpal (metacarpal sign).
Decreased carpal angle (carpal sign).
Flat head of 3rd and 4th metacarpals
Hypoplastic sella, C1 vertebra, clavicle, pelvis (android), hypertelorism,
basilar impression are often noticed.
Turners syndrome like picture appear radiologically after 20 yrs. And
only in 50 percent.
Miscellaneous
Drugs
Pregnancy
Multiple myeloma
Glycogen storage disease (G.S.D.)
Gauchers disease
Chronic liver diseases
Oxalosis AR, Calculi (recurrant leading to CRF), oxalate deposition in
bone.
Alkaptonuria AR, HGA a metabolite of tyrosine metabolism accumulates
(as a result of enzyme deficiency) in connective tissue.
Wilsons disease Osteomalacia, AR
Hemochromatosis
CPPD disease
Copper deficiency leads to rickets-like condition although zone of provisional
calcification is maintained.
Homocysteinuria AR: in the pyridoxine resistant variety (due to excess
methionine in diet). Osteoporosis, Arachnodactyly, large epiphysis, sclerosis,
valgus at knee and hip, sternal anomaly occurs.
Disuse Phenomenon
Patchy with cyst (Subchondral) formation.
Prominent around wrist.
Sudecks Osteodystrophy called as Algodystrophy or

Reflux Sympathetic Dystrophy
Mainly endosteal part are involved.
Subchondral cyst formation may be seen.
Progressive and painful even or rest.
Severe osteoporosis.
Primary Osteolysis
a. Gorhams disease:
Creeping disappearance of contiguous bones.
Angiomatosis and altered pH.
> 40 years
Pelvis, shoulder are involved.
b. Idiopathic multicentric carpotarsal osteolysis:
Associated nephropathy
Tapered adjacent bones
Transient Regional Osteoporosis

Spontaneously resolving (4-10 months).
Young middle age man.
Women in 3rd trimester.
Large joints involved, most commonly femoral head, ankle, knee.
Joint space is normal.
Regional Migratory Osteoporosis

Clinical setting similar but it migrates.
Loss of hip.
Idiopathic Chondrolysis
Young black girls more common.
Joint destroyed.
PVC Toxicity
Acro-osteolysis, Raynauds disease, hemangiosarcoma of liver, sacroilitis.
Gout
In patient with raised uric acid, due to increased Purine metabolism.
Acute arthritis occur seen as erosive arthritis.

Chronic tophi in gout presents as nonmineralized masses epicentered away
from joint and appear as radiolucent mass. Bone density, cartilage and joint
alignment are present till date.
Bone destruction due to intraosseus tophi in a cystic fashion is quite common
in great toe and other small bones. Infarcts and AVN may occur.
Other joints involved are knee, ankle, elbow, sternoclavicular, hip, sacroiliac
joint.
RICKETS AND OSTEOMALACIA GROUP

Type I
A. Vitamin D deficiency
B. Vitamin D metabolism deranged
i. Hepatic factors liver cell failure
induced microsomal enzyme
ii. Renal factors VDDR type I (Vit. D-dependent rickets)
VDDR type II
R.O.D.
Type II
1. A. Familial hypophosphatemic vitamin D refractory rickets.
B. Isolated phosphaturea
C. Renal tubular acidosis
D. Tumors producing parathrmone
E. Fanconi syndrome
2. Phosphate deficiency
Conditions mimicking
1. Axial osteomalacia
2. Metaphyseal chondrodysplasia (schmid)
3. Hypophosphatasia (AR)
4. Fibrogenesis ossium imperfecta
Loosers zone and true fracture
Osteopenia and feature of porosis
Bowing of bones
Fraying, splaying, cupping
Widened growth plate
Rossary ricket
Craniotabes
Harrisons sulcus
Pot belly
Pigeon chest
Protrusio acetabulii
Triradiate pelvis
Enthesopathy in FHVRR
Hypoparathyroidism, Pseudo and

Pseudo-Pseudo-Hypoparathyroidism
Autosomal dominant disease
Endogenous insensitivity due to defective adenylyl cyclase system.
In Pseudo-Pseudo type blood chemistry in normal (Skeletal response
preserved therefore, hyperparathyroidism may occurs).
Calvarial thickening.
Basal ganglia calcification.
Soft tissue calcification.
Short metacarpal and metatarsal.
Coxa vara and valga.
Bowed limbs.
Cone epiphysis.
Premature epiphyseal closure.
Abnormal hypoplastic tooth.
Osteosclerosis (rarely porosis).
Exostosis.
Flurosis
Enthesiopathy and ligamentous calcification (interosseous ligament
calcification)
Sclerosis in axial skeleton.
Osteophytosis.
Hypervitaminosis D
Sclerosis of cortex and metaphysis with patchy porosis.
Soft tissue calcification.
Hypervitaminosis A
Periosteal reaction similar to Caffeys disease seen in <1 year age
especially ulna and metatarsal.
Widened suture.
Enthesiopathy.
Cervical osteophytes.
Cupped and splayed metaphysis.
Heavy Metal Poisoning

Lead, Bismuth and Phosphorus.
Modelling deformity.
Transverse metaphyseal and especially at knee (fibula) due to decreased
blood supply.
Widened suture.
Bone in bone appearance.
Thyroid Acropachy
In thyrotoxic patients who are now Euthyroid due to treatment.
LATS is the cause.
Pretibial myxedema and diaphyseal periostitis.
Clubbing.
Asymmetric involvement of hand bones (radial aspect).
DIAGNOSTIC TECHNIQUES IN METABOLIC BONE DISEASE

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

The technique most in use.
Two X-ray beams used to scan the region of interest (spine and
hip) quickly and then correction for soft tissue in made.
Dexa can also be used to scan the peripheries hence also called as
pDEXA.
LS spine (1-4 or 2-4) in PA or Lateral views is used.
Hip may be measured as a whole or in parts. Since, the distribution
of cancellous bone here is not uniform therefore, variations may
occur. But due to absence of artefacts and soft tissue hip is preferred.
Certain values are measured
Bone mineral density (g/cm2)
Bone mineral content (g)
Bone mineral density %
T-Score, Z-score.
Interpretation: <1 SD (below the mean of Peak Bone Mass) = Normal
1-2.5 SD = Osteopenia
> 2.5 SD = Osteoporosis
Quantitative CT Scan
Only technique that can differentiate cortical and cancellous bone.
Can assess Cancellous bone separately to monitor response to
therapy.
LS spine is used to select the ROI.
Ultrasonometry
Only non-ionizing and radiation technique.
Heal, tibia used.
BUA and SOS measured.
BUA = absorption and scattering.
SOS = elasticity and density.
A graph is plotted using amplitude loss of sound waves of various
frequencies the slope of which is BUA.
Also two derived coefficients, i.e. stiffness index and BMD equivalent
are calculated.
Lack of standardized equipments and techniques, lack of ref. data
are the major draw backs.
SECTION 2
Central
Nervous System
9
Craniospinal Tuberculosis
Commonest form of skeletal tuberculosis (T.B.) and consistutes 50 percent
of all cases of TB of bones and joints.
Most common during first 3 decades of life.
Equal in males and females.
SYMPTOMS AND SIGNS

Symptoms are commonly insidious
In the active stage of the disease-loss of weight, loss of appetite, night
sweats, evening rise of temperature, stiff spine and localized kyphotic
deformity. A cold abscess may be present clinically.
Persistent backache once the active stage subsides.
Rarely, caries spine causes REFERED PAIN
Abdomen Spinal tumor Cervicodorsal spondylosis

syndrome or disc syndrome
ABSCESS AND SINUS

In the cervical or dorsal region, they can present themselves for away
from the spine along the fascial planes or neurovascular bundles. They
may be seen in paraspinal region at the back, cervical triangles, intercostal
spaces in the chest wall.
Dorsolumbar and lumbar spine follow the well known pattern of tracking
down the psoas sheath. The abscess may be palpable in the iliac fossa,
lumbar triangle, in the upper part of thigh, below the inguinal ligament or
upto the knee. Bilateral psoas abscess are also seen.
REGIONAL DISTRIBUTION OF TUBERCULAR LESIONS

IN VERTEBRAL COLUMN
Dorsal (T-11), lumber (L1), dorsolumbar, lumbosacral, cervical sites
(rare).
SITE OF INVOLVEMENT IN A VERTEBRA

A. Paradiscal lesions: Adjacent vertebral endplates destruction and diminition
of the intervertebral disc space.
B. Anterior types (involvement of anterior surface only)
C. Posterior spinal disease (involvement of pedicles, lamina and spinous
process).
D. Central cystic type: A lytic lesion with concentric collapse.
E. Tuberculous synovitis of the apophyseal articulation, atlantoccipital or
atlantoaxial joints.
COMMON CLINICAL FEATURES OF SPINAL TUBERCULOSIS

Kyphoses
Palpable cold abscess
An active or healed TB sinus.
Associated extraspinal skeletal, glandular or visceral foci.
Neurological involvement
Skipped lesions
SIGNS AND SYMPTOMS OF POTTS PARAPLEGIA

Paraplegia of Slow Onsent
a. Spontaneous twitching of the muscles of lower limbs with exaggerated
reflexes.
b. Spastic motor paraparesis, spastic paraplegia in extension, paraplegia in
flexion, uncontrollable flexion spasm with involvement of bladder and anal
spincters.
c. Extreme casesflaccid paralysis with loss of bladder and anal sphincter
control.
Paraplegia of Acute Onset

a. Sudden complete paralysis.
b. Motor functions are affected first
i. More sensitive to compression.
ii. Diseased area in the spine lies anterior to the spinal cord and thus
closer to the motor tracts.
c. Sensory involvement occurs lates in the disease and to a lesser degree than
the motor involvement.
d. Sense of position and vibration are last to disappear.
NEUROLOGICAL COMPLICATIONS
Group A
During active phase of the disease (within 2 years)
Craniospinal Tuberculosis 127
Early onset paraplegia.

Cause of compression is inflammatory edema, granulation tissue, tubercular
pus or casesous tissue.
Favorable prognosis.
Group B
Paraplegia associated with healed disease.
Late onset paraplegia (>2 years).
Cause of compression is mechanical like tubercular debris, sequestra
from vertebral body/disc, localized internal gibbus or kyphotic deformity
causing stenosis of vertebral canal.
Less favorable prognosis (needs surgical intervention).
CLASSIFICATION OF TUBERCULOUS PARAPLEGIA

S. No. Grade Clinical features
1. Negligible Patient unaware of neural deficit, physician detects plantar
extension/clonus.
2. Mild Patient aware but walks with support
3. Moderate Non-ambulatory with sensory deficit <50%.
4. Severe Moderate + with sensory deficit > 50% with sphincter
involvement.
CAUSES OF NEUROLOGICAL DEFICITS

A. Inflammatory Causes
Edema, granulation tissue, caseous tissue and abscess.
B. Mechanical Causes
Tubercular debris
Sequestra from vertebral body and disc
Constriction of cord due to stenosis of vertebral canal.
Internal gibbus formation.
C. Intrinsic Causes
Prolonged streching of the cord due to severe deformity.
Syringomelic changes.
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.
X-RAY APPEARANCES
The are four main sites where TB occurs in the vertebral bodies:
A. Paradiscal
B. Anterior
C. Central
D. Appendicial type
A. Paradiscal
The commonest type of involvement
Narrowing of the disc is the earliest radiological finding with loss of
definition of the paradiscal margins.
As 30-40 percent of calcium must be removed from a particular area
to show radiolucent region on X-ray. 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.
Paravertebral shadows
It is produced by extension of tuberculous granulation tissue and collection
of abscess in the paravertebral region.
In the cervical region Increase in the retrotracheal and retropharyngeal
space.
In the upper thoracic region Shifting of the apices laterally and
downwards with a v shaped shadow.
In the mid and lower thoracic region A fusiform shadow with shifting
of the parapsinal line.
Below the diaphragm Unilateral or bilateral widening of psoas shadow.
Aneurysmal phenomenon.
Kyphotic deformity
Due to destruction and anterior wedging of the involved vertebra.
B. Central Lesion
Infection starts in the centre of the vertebral bodies (Reaches centre
through Batsons venous plexus or branches of posterior vertebral
artery).
Areas of destruction in the vertebrae may produce concentric collapse
(vertebra plana).
Sometime the vertebra may be expanded or balloned like a tumor.
Disc reduction may be minimal.
Paravertebral abscess may be present.
C. Anterior Type of Lesion
Infection starts beneath the anterior longitudnal ligament and periosteum.
Peripheral portions of vertebral bodies show erosion in lateral view as
shallow excavation.
Collapse of vertebral bodies and disc space reduction is minimal.
D. Appendicial Lesion
Involvement of pedicles, lamina, spinous and transverse process.
Disc spaces are intact.
LATERAL SHIFT AND SCOLIOSIS

A combination of lateral deviation and rotation of the spine.
Due to more destruction of the vertebral body on one side.
Lower dorsal and lumbar spine are commonly involved.

Possible involvement of posterior spinal articulation.
CLINICORADIOLOGICAL CLASSIFICATION OF
TUBERCULAR SPONDYLITIS
Stage Clinico radiological features
1. Predestruction Straighting of curvature, if paravertebral muscle
involvement.
2. Early destruction Diminished disc space and paradiscal area.
3. Mild-angular kyphosis 2-3 vertebra involved (K: 10-30)
4. Moderate angular kyphosis >3 vertebra involved (K = 30-60)
5. Severe kyphosis (Humpback) >3 vertebra involved (K > 60)
MYELOGRAM
Features of Extradural Block
Identation of one side of the myelographic column.
Angulation of the spinal cord with complete obstruction.
A complete block below the level of conus medullaris will present as
feathered, serrated interface of the myelographic column.
Features of Arachnoiditis
a. Shortening and incomplete filling of nerve root sheaths.
b. Obliteration of nerve root sheaths, shortening of sacral cul-de-sac,
smoothing of thecal outline.
c. Adherence of the nerve roots of cauda equina, adherence of the nerve
roots to theca empty thecal sac.
d. Irregularly narrowed theca with pocketing and cyst formation delayed
flow of contrast medium through subarachnoid space.
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.
Blood pool phase extent of soft tissue and bone hyperemia.
Delayed scan.
Potts Spine Shows

Hypermia with increased blood pool activity.
On delayed scans, increased uptake in the lower aspect of one vertebra
and the upper aspect of the vertebra just below.
COMPUTERIZED TOMOGRAPHY
Early changes within the bone is depicted as small areas of rarefaction in
the subchondral bone.
Cortex may demonstate small areas of irregularity or small areas of abscess
which eventually may coalesce into large areas of destruction.
Reformatted images may show changes in end plates.
Intravaneous contrast agents may add the paraspinal inflammatory tissue
to enhance with better delineation of paraspinal abscess and their extent.
Advanced cases may result in a weakened vertebral body that may fragment
and collapse.
Inflammatory mass or bone fragments may displace and compress the
thecal sac (CT myelo).
In the healing phase, bony ankylosis and sclerosis can be demonstrated.
MAGNETIC RESONANCE IMAGING

T1-weighted images of the spine Spin echo pulse sequences with a short
TR (200-1000) and TE (20-25 msec).
T2-weighted images Long TR (2000-4000 msec) and long
TE (50-100 msec).
Proton density images.
Gradient echo images are a supplement to spine-echo images (can be obtained
with shorter acquisition time).
T1-Weighted Image
The spinal cord has intermediate signal intensity.
Ligaments have intermediate signal intensity.
Intervertebral disc have nearly homogenous, low to intermediate intensity.
Cortical bone has negligible signal intensity.
Fat containing bone higher signal intensity.
T2-Weighted Image
CSF has a high signal intensity Myelogram effect.
Spinal cord has a lower signal intensity.
Fatty bone has a lower signal intensity.
Fibrocartilage in nucleous pulposus and central portion of annulus fibrosus
has high signal intensity. Peripheral portion (collagenous) has low-intensity.
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.
In chronic infection : T1-weighted images may show decreased or increased

signal. Hyperintense signal on T2 in the setting of chronic infection may be
specific to MTB.
In TB spondyllitis,
disc gives bright signal on T2-weighted
decreased signed of T1-weighted
enhancement after contrast administration.
IV contrasts shows improved definition of epidural abscess and masses,
cord and nerve root compression. Abscess show peripheral enhancement
with cortical necrosis.
DIFFERENTIAL DIAGNOSIS
1. Pyogenic spondylitis
Follows infection or surgery of urogenital tract.
There is bone destruction with rapid sclerosis and new bone.
Varying degree of disc space reduction.
Healing is by proliferative new born formation with bone ankylosis.
2. Typhoid spine
3. Brucella spondylitis
4. Mycotic spondylitis
Actinomycosis or blastomycosis
Involvement of vertebral body, transverse process and ribs.
Paravertebral abscess may be seen in blastomycosis.
Sclerosis and destruction process go side by side.
Periosteal new born formation occurs in the anterior and lateral aspect
of vertebral bodies (Saw tooth appearance).
Collapse of vertebral body is rare.
Multiple sinus formation with involvement of subcutaneous tissue.
Demonstration of the fungus from the discharging sinus establishes
the diagnosis.
SYPHILITIC INFECTION
Arthralgic type or Gummatous type or Charcots disease of spine
Commonest sites are the lower dorsal and lumbar spine.
Extensive destruction with proliferative new bone formation which may
extend into the paraspinal tissue.
Diagnosis is confirmed by biopsy and serological tests.
TRAUMA
Traumatic compression fracture is wedge-shaped with intact disc spaces
and paradiscal margins.
There may be sparring and ossceous bridging on both sides of disc with
intradiscal calcification.
SPONDYLOLISTHESIS
L4-L5, L5/S1
Forward displacement of one vertebra over another.
OSTEOPOROSIS
Spinal Osteochondrosis
Adolescents
Rounded kyphosis
Several vertebrae involved with sclerotic epiphyseal plate.
Absence of constitutional symptoms, paravertebral shadows, etc.
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, immunocompromised patients.
Hematogenous dissemination from a focus in the lungs or genitourinary
tract.
Tubercular Meningitis
Clinical features confusion, headache, lethargy, stupor, coma, ocasionally
associated with decerebrate rigidity, cranial nerve palsies and infarction.
Lumbar puncure decreased glucose, increase proteins, pleocytosis and
negative smears.
Thick exudates in the basal cisterns
Communiating hydrocephalus
Vascular involvement
Leading to vasculitis
Infarctions
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.
Hydrocephalus, infarction.
MRI shows better evaluation of infarcts, ventriculitis and meningial
enhancement.
Tuberculomas
Can involve any cerebral compartment, intraventricular, ependymal TB.
Histologically central area of necrosis with peripheral rim of Langerhans
giant cells, lymphocytes and plasma cells.
NCCT shows isodense, hyperdense or mixed density lesion.
CECT ring/disc enhancement, Target sign, odema around the lesion is
shown as hypoattenuated areas.
MRI
Plain MRI Mixed predominantly low signal intensity lesion with
surrounding high signal intensity edema on T2-weighted images.
Gd-MRI-Same pattern as CECT.
Tubercular Abscess
Central area of liquefaction and pus.
10 Diseases of White
Matter Brain Substances
The white matter diseases are predominantly grouped into two classes.
1. Dysmyelinating: Disorder with defective formation or maintenance of myelin.
2. Demyelinating: Disorder due to destruction of otherwise normal myelin.
NORMAL MYELINATION
It is a dynamic process that begins during 5th fetal month and continues
throughout life. It progresses from caudad to cephalad, from dorsal to ventral
and from central to peripheral (Table 10.1).
Table 10.1: Normal myelination
a. Birth (Full Term)

Medullas
Dorsal midbrain
Inferior and superior cerebellar peduncles
Posterior limb of internal capsule
Ventrolateral thalamus
b. One Month
Deep cerebellar white matter
Corticospinal tracts
Pre-postcentral gyri
Optic nerves, tracts
c. Three Months
Brachium points, cerebellar folia
Ventral brainstem
Optic radiations
Anterior limb of internal capsule
Occipital subcortical U fibers
Corpus callosum splenium
d. Six Months
Corpus callosum genu
Paracentral subcortical U fibers
Centrum semiovale (partial)
e. Eight Months
Centrum semiovale (complete except for some from temporal areas)
Subcortical U fibers (complete except for more rostral frontal areas)
f. Eighteen Months
Essentially like adult.
Diseases of White Matter Brain Substances 135
LEUKODYSTROPHIES: DISTINCTIVE FEATURES

i. Complete / Near Complete Lack of Myelination
Canavan disease
Pelizaeus-Merzbacher disease
ii. Frontal White Matter Most Involved
Alexander disease
iii. Occipital White Matter Most Involved
Adrenoleukodystrophy (also colossal splenium)
iv. Macrocephaly
Alexander disease
Canvan disease
Mucopolysaccharidosis type I (Hurler)
Mucopolysaccharidosis type II (Hunter)
v. Thick Meninges
Hurler syndrome
High density basal ganglia
Krabbe disease
vi. Enhancement following Contrast Administration
Alexander disease
ALD (1st calcification/ peripheral aim enhancement)
vii. Strokes
Leigh syndrome
MELAS
MERRF
Homocystinuria.
INHERITED LEUKODYSTROPHIES
These are dysmyelinating diseases and are a heterogeneous group of disorders
characterized by enzyme deficiencies that result in abnormal formation,
destruction or turn over of myelin.
METACHROMATIC LEUKODYSTROPHY
Autosomal recessive
Lysosomal disorder caused by deficiency of catabolic enzyme Aryl
sulfatase.
Motor signs of peripheral neuropathy, deterioration of intellect, speech and
co-ordination.
Pathology
Symmetrical demyelinaiton that spares subcortical U fibers.
Incidence
Most common and present as
1 in 100,000 newborns
Types according to age of onset
a. Late infantile age
b. Juvenile form
c. 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.
Increased signal of cerebellar white matter.
Thalamus appears hypointense.
KRABBE LEUKODYSTROPHY (GLOBOID

CELL LEUKODYSTROPHY)
Autosomal recessive
Deficiency of lysosomal hydrolase (Galacto cerebroside betagalactosidase)
Psychomotor deterioration, irritability, optic atrophy, seizures and cortical
blindness.
Pathology
Brain is small and atrophic
Extensive symmetric dysmyelinaiton of centrum semiovale and corona
radiata with sparing of subcortical U fibers.
Incidence: 1 in 50,000
Types
Infantile (most common)
Late infantile
Adult forms
Location
Centrum semiovale and periventricular white matter are involved.
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, 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
Seizures, visual behavioral disturbance, hearing loss, paraparesis
A. Adrenoleukodystrophy
Classic form casued by deficiency of single enzyme. Acyl CoA
synthetase which prevents break down of very long chain fatty
acids which accumulates in tumorous tissues and plasma.
B. Adrenomyeloneuropathy
C. Adrenoleukomyeloneuropathy.
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, cerebral
peduncles, pons, pyramind and cerebellum.
Imaging Techniques
Definitive diagnosis is made by plasma, erythrocyte or cultured skin fibroblast
assay of VLFAs (very long chain fatty acids).
CT:
NCCT
Large, symmetric low density lesion in parietoccipital region
CECT
Shows enhancement with advancing rim surrounded by non-
enhancing edematous zone.
MRI: Three pathological zones are seen:
1. Central necrotic zone
Low signal on T1 WI.
High signal on T2 WI.
2. Intermediate zone of demyelination and inflammation
Enhances after contrast
3. Peripheral edematous zone
Hypointense on T1 WI.
Hyperintense on T2 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.
Poor head control, nystagmus, cerebellar ataxia with abnormal eye
movements.
Types
a. Classical X-linked recessive
b. 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 IIneonatal period
Imaging Techniques
NCCT:
Cerebral and cerebellar atrophy
White matter appears diffusely of low density
MR
T2 WIshows diffuse high signal that extends peripherally
The brainstem, cerebellum and subcortical fibers are spared
The basal ganglia and thalamus appear hypointense (abnormal iron
deposition)
ALEXANDER DISEASE
Sporadic leukoencephalopathy of unknown etiology.
Early onset of megalencephaly, psychomotor retardation, spasticity and
seizures.
Incidence
Rare disorder
Infants
Juvenile
Adult form
Location
Predilection for frontal lobe white matter
Deposition of Rosenthal fibres in basal ganglia, thalamus and hypothalamus
Imaging Techniques
NCCT:
Low attenuation in deep frontal white matter
Basal gangliashows low density lesions
CECT
Marked enhancement occurs in basal ganglia and periventricular regions
CANNAVANS DISEASE (SPONGY DEGENERATION)

Deficiency of N-acetyl aspartylaseresults in accumulation of N-acetyl
aspartic acid in brain.
Inheritance is autosomal recessive
Hypotonia, loss of motor activity, megalencephaly
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 WIhomogenous diffuse symmetric low density throughout white
matter
T2 WINear total high signal in white matter
Subcortical U fibers are involved.
ACQUIRED LEUKODYSTROPHIES MYELINOCLASTIC/

DEMYELINATING DISORDER
MULTIPLE SCLEROSIS
Etiology
Unknown
Autoimmune mediated demyelination
Most common (vascular and age-related)
Prolonged relapsingremitting disease, later on chronic progressive phase.
Pathology
Typical MS plaques are edematous pink-gray white matter lesions.
Incidence
Young females (20-40 years)
Less common in children and adolescents.
Location
Ovoid periventricular lesions oriented perpendicular to long axis of brain
and lateral ventricles.
Corpus callosum (callososeptal interface is common location).
Imaging Techniques
Normal in early phase of disease
CT
Ovoid periventriclular plaques (0.6 1.4 cm)
o Low attenuation or isoattenuating lesions with contrast enhancement
(acute / subacute lesions)
o Low attenuation with and without contrast (chronic lesions).
Atrophy
Mass effect (rare)
MRI
T1 WIiso to hypointense lesions
T2 WIhyperintense ovoid lesion
Beveled / target lesion. 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.
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, foreign protein
or autoantigen.
In immunocompromised patients, the virus propogates, unchecked and
results in demyelination.
ADEM (ACUTE DISSEMINATED ENCEPHALOMYELITIS)

Immune mediated
Previous history of viral infection or vaccination
Abrupt onset, monophasic illness, initially mild fever, headache, drowsiness
with advanced coarse symptoms ranging from seizures and focal
neurological deficit to coma.
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. 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.
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 WImultifocal 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. Lyme Disease
Multisystem disorder caused by thick borne Spirochete Borrelia burdofer
Pathogenesis
o Vasculitis
o Immune complex mechanism
Imaging Technique
MR
T2-weighted image shows extensive deep discrete and confluent white
matter lesions
Enhance following contrast administration.
3. AIDS-Related Leukoencephalopathy
CNS involvement in AIDS can manifest as acute encephalopathy,
subacute encephalitis, acute and chronic meningitis, vascular myelo-
pathy and peripheral neuropathy.
HIV virus is not only lymphotrophic but also neurotrophic and leads to
demyeliniation.
Imaging Techniques
CT
Generalized atrophy
Bilateral symmetrical white matter hypodensity involving frontal lobe.
No contrast enhancement is noted
MR
T2-weighted image shows : punctate hyperintense foci, on larger focal
and diffuse areas.
Asymmetrical patchy subcortical hyperintense lesions may be seen in
parieto-occipital region.
METABOLIC CAUSES
1. Central Pontine Myelinosis
Acute pontine demyelination
History of alcoholism associated with hyponatremia exacerbated by
over-hydration and administration of diuretics. Other factors include
systemic hypotension, cerebral edema, drugs, etc.
Imaging Techniques
CT:
Areas of decreased attenuation in the pons, 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.
Extrapontine sites of involvement are basal ganglia, thalamus and
subcortical white matter.
2. Marchiafava Bignami Disease
Poorly-nourished Italian men with history of chronic alcoholism
Pathologically, characterized by involvement of corpus callosum
demyelination and necrosis
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, on T1-weighted and hyperintense on T2-weighted sequences.
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.
Post-contrast T2 weighted image : Show enhancement around 3rd
ventricle, acqueduct and mammilary bodies.
TOXIC AND TRAUMATIC ENCEPHALOPATHIES

Many toxic and traumatic processes may selectively destroy myelinated portions
of brain, e.g.
Gamma radiation
Chemotherapeutic agents
Chemical toxins
Heavy metals
Specific surgical lesion
1. Radiation induced demyelination
Radiation necrosis
Diffuse leukoencephalopathy
A. Radiation necrosis:
Coagulative necosis of white matter with fibrinoid necrosis of capillary
blood vessels
Occurs after latent period of 4 months to several year.
Imaging Techniques
CT:
Abnormal low density white matter with mass effect.
MR:
T2-weighted image show core of enhancing mass may be present
Diffuse white matter edema.
B. Diffuse radiation induced leukoencephalopathy:
Involved all visible cerebral white matter
CT:
Diffuse low intensity white matter without contrast enhancement.
MR:
T2-weighted image shows symmetrical white matter involvement.
2. 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.
1. Global Hypoperfusion Syndrome
Etiology
Prolonged hypoxia with accompanying systemic hypotension and
acidosis
Important factors include : Drug overdose, cardiac and respiratory
arrest, anesthesia accidents, profound hypoglycemia, strangulation,
postoperative shock, carbon monoxide poisoning, status epilepticus
and vasospasm.
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.
Imaging Technique
CT
Symmetrical hypodensity of white matter and lentiform nucleus
Loss of gray/white matter differentiation
2. 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.
Imaging Technique
CT
Extensive, symmetrical, 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. Eclampsia
Hypertensive disorder in third trimester of pregnancy
Involvement of posterior hemisphere
Imaging Technique
CT
White matter shows symmetric hypoattenuating areas
MR
T2 WI - hyperintense lesions in deep white matter of occipital lobes.
4. Biswangers Disease (Subcortical Arteriosclerotic Encephalopathy)
Diffuse/ multifocal destructive process in central white matter resulting
from generalized ischemic or vascular conditions
Clinically characterized by hypertensive dementia, seizures and
syncopes.
Imaging Techniques
CT
Diffuse, severe, incompletely symmetrical hypodensity in central
white matter more prominent in frontal lobes and centrum semiovale.
MR
Generalized cerebral atrophy
Lacunar infarcts in basal ganglia and thalami
T2 WI showssubcortical and periventricular lesions predominantly
in frontal and occipital horns and centrum semiovale
5. Hypoxic Ischaemic Encephalopathy
Imaging manifestation depends on:
Length and severity of vascular insult
Age
Individual cerebral circulatory pathways
Inherent vulnerability of certain anatomic, regions and cell types to
H.I. injury.
A. Premature Infants
Developing brain is susceptible to injury and may lead to necrosis,
gliosis and disturbance in myelinaiton
Periventricular leukomalaciacaused 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.
Imaging Technique
MR
T2-weighted image show bilateral but asymmetric peritrigonal
hyperintensities
Reduced white matter volume
B. Term infants
In term infants, the ischemic lesion are in cortex and subcortical white
matter
Deep gray nuclei may be affected.
C. Children and adults

Watershed infarction and neuronal necrosis within globus pallidus,
putamen, caudate nucleus, thalamus, parahippocamus area, cerebellum
and brain stem nuclei
D. Vasculitis
SLE, Sjgrens syndrome, Behet disease, polyarteritis nodosa are
potential causes.
Imaging Technique
MR: T2 WI reveal focal hyperintensity subcortical in white matter.
MISCELLANEOUS
Gangliosidoses
Tay Sachs 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.
MITOCHONDRIAL CYTOPATHIES
Leighs disease (subacute necrotizing encephalopathy)
Low attenuation in basal ganglia, brainstem or central white matter
Most characteristic foci of demyelinaiton are seen in lentiform nuclei,
cerebral peduncles, periaqueductal gray matter, pons and medulla.
AMINOACIDOPATHIES
Hereditary disorder of amino acid metabolism
e.g. - Maple syrup urine disease
- Phenylketonuria
- 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, 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, cyanosis can be caused by a number of conditions (Central
nervous system dysfunction, pulmonary disorders, cardiac abnormalities,
airway obstruction and very rarely methemoglobinemia). However, most
important consideration in evaluating cyanotic patient is to find out, whether
congenital heart disease is the cause, so that adequate life saving measures can
be taken.
Following are the features characteristic of cyanosis of cardiac origin
(associated with congenital heart disease).
1. Vigorous and labored respirations with tachypnea.
2. Cyanosis increases on crying.
3. On giving 100% O2 inhalation, cyanosis may decrease but never disappears
(as against cyanosis due to respiratory or CNS disorders) (Hyperoxia test).
4. Features of congestive heart failure.
5. Presence of murmurs, clubbing and polycythemia.
Following features of heart disease are seen in a patient of congenital heart
disease:
1. Murmurs apparent at birth or in the neonatal period (obstructive and
regurgitant lesions become apparent at birth where as septal defects appear
after sometime).
2. Murmurs produced by congenital cardiac defects tend to be parasternal
rather than apical.
3. Presence of central cyanosis indicates that heart disease is congenital.
4. Presence of extracardiac congenital anomalies.
Conventional five finger approach is followed in diagnosis of any patient
with heart disease:
1. History
2. Physical examination
3. X-ray chest
4. ECG
5. 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.
It also gives idea of heart size, whether enlarged or not.
Typical patterns of cardiac silhouette in different congenital heart diseases.
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.
Few Diagnostic X-ray findings are:
1. Egg on side cardiac shape TGA
2. Figure of 8 or snowman appearance Supracardiac total anomalous
pulmonary venous connection. Ground-glass appearance of the lungs with
normal size heart TAPVC with pulmonary venous obstruction.
3. Boot shaped / core en sabotheart TOF
4. Upper left border formed by ascending aorta Corrected TGA
5. Eisenmenger physiology Cardiomegaly with prominent main pulmonary
artery segment, prominent hilar area with peripheral oligemia.
6. Ebsteins 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. Classifications are
based on morphology, embryology, physiology, increased and decreased
Diagnostic Approach to a Case of Congenital Cyanotic Heart Disease 153
pulmonary blood flow. For better understanding, one should be well conversant
with physiology.
Old system of classification was that of 5Ts.
Transposition of great arteries
Tetralogy of fallot
Truncus arteriosus
Tricuspid atresia (includes tricuspid valve atresia, tricuspid stenosis,
hypoplastic RV, and Ebsteins anomaly).
Total anomalous pulmonary venous return.
Pulmonary stenosis is not included in 5Ts classification though based on
physiology, it can be clubbed with Tricuspid atresia.
This classification is based on physiology and results in six subgroups of

cyanotic patients. 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. If there are more than one conditions in any of
these six groups, e.g. fallots physiology or Eisenmenger physiology, X-ray
and ECG usually solve the problem. Using this classification, X-ray and ECG
we can reach bedside diagnosis in 75 to 80 percent cases. Rest of the patients
need to be evaluated by 2D echo, Doppler Echo or cardiac catheterization.
Assessment of Severity
1. Cyanosis: The more severe the cyanosis, the more severe is the lesion.
However, mild cyanosis does not exclude severe lesion e.g. 2 months baby
with TGA with large VSD with increased pulmonary blood flow will have
only mild cyanosis.
2. Age of onset of cyanosis: Earlier the onset of cyanosis, more severe is the
lesion.
3. Symptoms: If patient is symptomatic, disease is severe.
4. Congestive failure: If a cyanosed patient is in CHF, the disease is severe.
5. Cardiomegaly: Larger the heart size, more severe is the disease.

6. Pulmonary arterial hypertension: Its presence suggests a more severe
disease.
CONGENITAL HEART DISEASES

The incidence of CHD in live birth is estimated between 0.5 and 1.0 percent in
various large series.
INCIDENCE OF CONGENITAL HEART DISEASES

Ventricular septal defect (VSD) - 36.1%
Atrial septal defect (ASD) - 8.2%
Patent ductus arteriosus (PDA) - 7.9%
Pulmonary stenosis (PS) - 6.9%
Coarctation of aorta - 5.9%
Aortic stenosis - 5.7%
Tetralogy of fallot (TOF) - 4.6%
Transposition of great arteries (TGA) - 3.8%
Atriventricular septal defect (AVSD) - 3.6%
Pulmonary atresia - 2.6%
Single ventricle - 2.2%
Tricuspid atresia - 1.5%
CLASSIFICATION OF CONGENITAL HEART DISEASE

A. Acyanotic congenital heart disease
B. Cyanotic CHD
Group I : Right heart obstructions
1. Right atrial obstruction
Tricuspid atresia
2. Right ventricular obstruction
Tetralogy of fallot
Pulmonary valve stenosis with VSD
Pulmonary infundibular stenosis with VSD
Pulmonary valve stenosis with ASD

Pulmonary artery atresia with intact ventricular septum
3. Pulmonary arteriolar obstruction
Eisenmenger reaction
Group II: Common cardiac chambers
1. Atria
TAPVD
2. Ventricles
Double outflow RV (DORV)
The Taussig Bing deformity
3. Persistent common truncus arteriosus
Group III: Abnormal connections or discordance
TGA
C. Others
Ebsteins anomaly
Pulmonary valve stenosis
PAPVD
Hypoplastic left heart syndrome
Uhls anomaly
L-R SHUNTS
1. Abnormal conventional radiological features if pulmonary systemic blood
flow ration is >2:1.
2. 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, as well as those left heart chambers
proximal to it.
Exceptions
ASD in which LA does not enlarge as it immediately decompresses at
low pressure through a large ASD into the RA.
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.
If L-R shunt is extreme left heart may fail causing pulmonary odema.
Complication of Eisenmenger reaction.
ATRIAL SEPTAL DEFECT

Types
1. 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
2. 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.
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.
It is the most common CHD associated with Downs syndrome
A. 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. There is usually a
cleft in the anterior mitral leaflet MR. The regurgitant jet usually
passes directly through the low primum ASD into RA instead of entering
LA.
B. Persistant AV canal
Ostium primum defect is accompanied by cleft leaflets of malformed
mitral and tricuspid valves and by an inlet VSD.
This is a very severe deformity with incompetence of both AV valves
as well as combined ASD and VSD.
RADIOLOGY
1. If L R shunt > 2:1 percent then heart is enlarged (RA and RV). LA does
not enlarge as it is immediately decompressed at low pressure through a
large ASD into the RA.
2. Ascending aorta, 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. Pulmonary plethora (pulmonary arterial overcirculation)
Enlargement of main pulmonary trunk, central (hilar) pulmonary, lobar
and segmental pulmonary arteries.
Both upper and lower lobe vessels are prominent
Semiquantitative guides:
Diameter of right inferior pulmonary artery exceeding the diameter
of trachea.
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.
Prominence of vessels situated below the crest of the diaphragm

on frontal view.
The prominence of hilar vessels on the lateral view.
Pulmonary arteries and veins are enlarged in size and can be followed
up to the outer third of the lung.
4. Reversal of shunt, i.e. Eisenmenger reaction may develop in a minority of
patients with large ASD usually after 30 years.
5. 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. Aberrant pulmonary veins which often accompany ASD rarely be identified
except Scimitar vein syndrome and in sinus venosus defect.
7. ASD may present in middle aged or elderly, when heart failure or pulmonary
hypertension can finally develop and cause symptoms for 1st time.
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.
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. This is an abnormal anterior movement of
interventicular septum during ventricular systole.
Transoesophageal studies often used to demonstrate sinus venosus
The ratio of pulmonary to systemic blood flow may be estimated by
assessing pulmonary artery, 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. An injection
of contrast into LA shunt during the laevo phase is made.
In ostium primum defect on LV angiography on the frontal films, 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.
Atrial Septal Defect may be Associated with

A. Aberrant pulmonary veins
10-20 percent
Pulmonary veins (usually from right lung) draining into RA. This
increases L-R shunt (not usually to major degree)
May be identified on angiocardiography.
B. Pulmonary valve stenosis
C. Eisenmenger reaction
D. Lutembacher syndrome
Association of ASD usually of the secundum type with mitral stenosis
either congenital or acquired.
E. Holt-Oram Syndrome.
Treatment
1. Surgical closure low mortality
2. Transcatheter occlusion of ASD is being developed.
VENTRICULAR SEPTAL DEFECT

Most common CHD
Types
A. Membranous VSD
Most frequent
2 types
a. Infracristal:
b. Supracristal : Less frequent
B. Muscular VSD (Maladie de Roger abnormality)
Usually small and often multiple (Swiss cheese VSD)
3 types
a. Inlet or basal muscular defect
b. Mid muscular/apical defect
c. 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.
OR
A high VSD may be associated with an abnormal incompetent TV permitting
LV RV - RA.
Radiology
1. In large shunts heart size increases (LV, RV and LA) due to volume overload.
RV may not be as large as anticipated as it receives the shunt into its
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)
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.
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
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 patientsRight 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
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.
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.
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 / showmons 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 ventriclea term implying at
least 1 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.
TaussigBing 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.
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.
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 chestthe 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.
Associated conditions must be sought.

In L-loop TGA, the reversal of the morphologically L and R ventricles can
be demonstrated by the reversed insertions of the AV valves.
Cardiac Catheterization and Angiocardiography

It will clearly show the abnormal connections and will also be useful for
clarifying details of anatomy concerning associated anomalies.
It is important to assess coronary anatomy for surgical planning, especially
when the great arterial switch procedure is contemplated.
Others
Hypoplastic left heart syndrome
Pulmonary arteriovenous malformations.
OTHER CONGENITAL HEART DISEASES

1. Ebsteins 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. These malpositioned cusps are malformed
and permit TR of varying degree.
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. This results in considerable difficulty
in RA emptying enlarged RA.
RV forward output is reduced because
Only its distal part can eject through PV
Tricuspid regurgitation
Impaired emptying of RA
Frequent associations:
a. Patent foramen ovale or ASD The raised RA pressure causes R-
L shunt and central cyanosis of varying degree.
b. Various types of discordance (transposition)
c. Serious arrythmias
Clinical spectrum varies from severe cyanotic heart failure to minimal
or absent symptoms with normal duration of life.
On X-Ray
Enlarged globular or square cardiac silhouette with narrow vascular
pedicle and pulmonary oligemia.
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. The left border of the heart is also smoothly convex but
superiorily it approaches the midline so that the vascular pedicle of the

heart is narrow. The main pulmonary artery and frequently its right and
left branches are hidden by the enlarged heart.
Lungs are noticeably oligemic
The cardiac outline is often very sharply defined, almost etched, due to
the reduced cardiac pulsations.
2. 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, SVC, IVC or azygos vein in reducing order
of frequency. ASD is frequently associated.
There are few characteristic pattern of PAPVD.
i. Sinus venosus defect: The right upper lobe veins pass horizontally to
enter the lower part of SVC which may be considerably dilated. There
is always and associated high ASD of the sinus venosus type.
ii. Scimitar vein and syndrome (Hypogenetic lung syndrome) or pulmonary
venolobar syndrome.
The right lower and sometimes middle lobe veins form an abnormal
vein which runs downwards and medially, curving in a crescent or
scimitar course (convex to the right) undering as it approaches
right cardiophrenic angle, to pass through the diaphragm and drain
into the upper IVC. The Scimitar vein runs posterior to RA and may
be obscured by that chamber, especially as the heart is often
displaced to the right because of the hypoplastic right lung. It is
often inadequately seen on X-ray (CT and US is better).
The complete Scimitar syndrome involves presence of
a. A Scimitar pulmonary vein draining a small right lung with
displacement of the mediastinum to right.
b. A hypoplastic right pulmonary artery which may be obscured
by displaced heart.
c. Right bronchial tree may have abnormal branching and there
may be bronchiectasis of the lower lobe.
d. There is often a substantial anomalous artery (best seen on
aortography) passing upward from the abdominal aorta to supply
the right lower lobe.
iii. Veins of right lungthey may enter RA without any of above
associations. Heart may be normal or may have ASD.
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.
Angiocardiography
The delineation of individual pulmonary veins in PAPVD can be difficult and
may require separate injections into Lt. And Rt. Pulmonary arteries in oblique
views. Sometimes the direct injection of contrast medium into the suspected
abnormal veins can be diagnostic, but this approach can be surperisingly difficult
to interpret as the contrast medium is rapidly diluted and the atrial anatomy is
often unclear.
3. 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.
The principal components are MV atresia, aortic valve atresia and
hypoplastic proximal aorta. In this condition the RV performs the entire
systemic pumping function with systemic blood supply being directed
through ductus arteriosus. The brachiocephalic branches are supplied
retrogradely and the ascending aorta shows diminition in size, carrying
only reverse flow from the PD and aortic arch sufficient to fill the coronary
arteries.
Very poor prognosis.
12
Valvular Heart Disease
Mitral Valve (MV) : Anatomical Landmark
1. The MV is located between the LA and LV.
2. The MV opens during ventricular diastole when blood flows from LA into
LV.
3. During ventricular systole, the MV closes as blood is ejected through LV.
4. 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.
6. The leaflets free edges meet at 2 points called the commissure.
Mitral Stenosis
Defenition: Reduction in the effective mitral valve orifice area, which is normally
4-6 cm2.
In practical terms, the only common cause of MS is rheumatic heart disease.
Much rarer causes include:
Mitral annulus calcification, congenital, connective tissue disorders and
infiltrations, SLE, rheumatoid arthritis, mucopolysaccharidoses (Hurler
syndrome) and carcinoid.
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
A. Left atrial enlargement which may vary from trivial to gross, seen as a :
Dense pear-shaped opacity lying transversely inside the cardiac shadow
causing increased density due to left atrium.
Double heart shadow on the right of the spine (double right heart border).
B. Typically in mitral stenosis a prominent left atrial appendage is also seen.
This enlargement may vary from a simple straightening of the left heart
border (called as mitralization) to a very gross local protrusion.
C. Splaying of carina and elevated left main bronchus and increased carina
angle (normal = 57).
D. Small aortic knuckle is caused partly by a true hypoplasia of aorta and
partly by right ventricular rotation.
E. If the pulmonary venous pressure is elevated, the upper zone vessel is
dilated due to upper lobe blood diversion and is brought into prominence
by lower vascular constriction.
F. With higher pressures in the pulmonary veins, septal lines and pleural
effusions may appear.
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.
Kerley A Line: Due to superficial lymphatic involvement and seen as
vertical lines in upper field.
Kerley C Line : seen as reticular pattern and due to involvement of all
the groups of lymphatics.
G. Mitral valve calcification indicates longstanding and severe MV disease,
best seen in lateral view between left atrium and left ventricle. More rarely
seen in frontal view on an adequately penetrated film.
H. In long standing cases, hemosiderin deposits may be found in the lungs,
seen as widespread mottling. Hemosiderosis and ossific nodules are the
observation seen in advanced disease.
I. Long standing pulmonary venous hypertension gives rise to pulmonary
arterial hypertension. This is reflected by enlarged main and central
pulmonary arteries and peripheral pruning.
J. In pure mitral stenosis, tranverse cardiac diameter is often normal unless
pulmonary hypertension develops.
K. Lateral displacement of descending thoracic aorta.
L. Altered thoracic paraspinal line (Normal 8 mm).
IN RAO VIEW
Enlarged left atrium bulges backwards and obliterates the translucent
retrocardiac space.
On Barium swallow, a bolus passes normally down to a point just below
the left main bronchus when it seems to halt abruptly. Barium bolus then fills
slowly the lower third of the esophagus which is curved sharply backwards.
This sign is more obvious in expiration than in inspiration.
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.
In mitral stenosis, commissural fusion causes abnormal movement of the
mitral leaflets.
M-mode Echocardiogram
The posterior leaflet moves forward in diastole in the same direction as the
anterior leaflet.
The a wave is markedly diminished (absent with atrial fibrillation).
The thickened leaflets return stronger echoes than normal, and when
calcification is present, multiple dense echoes are seen.
2-D Echo
The two-dimensional echocardiogram enables visualization of the abnormal
valve and its deranged movement.
It allows
a. Direct measurement of the mitral valve orifice area using the parasternal
short-axis view.
b. Assessment of left and right ventricular function.
c. Changes in the sizes of the four cardiac chambers.
2-D Echo Parasternal Long Axis View

Thick and/or calcified leaflets.
Restricted leaflet motion.
Doming of one or more leaflets giving a characteristic elbowing or bent-
knee appearance (particularly of AMVL).
LA enlargement.
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.
In MS-leaflet tips are calcified and orifice size is reduced.
Doppler Echo Appearance

Continuous-wave Doppler is extremely useful in assessing the severity of
mitral stenosis.
The velocity of blood flow allows the pressure gradient across the mitral
valve during diastole to be determined, using the BERNOULLI PRINCIPLE
(P1-P2 = 4V max2).
The mitral valve area can also be calculated by measuring the rate of decay
of the Doppler-measured maximum velocity.
MRI and CT
Both cardiac MRI and CT scan demonstrate chamber enlargement, mitral
valve abnormalities, and changes in ventricular function.
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, cardiac
catheterization is unnecessary in most cases of mitral stenosis. In the
occasional patient, catheterization is performed to assess changes in
pulmonary artery pressure and pulmonary capillary wedge pressure during
exercise, to clarify the mechanism of exercise-induced symptoms.
Assessment of the severity of associated mitral regurgitation may also
require left ventriculography.
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.
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.
In MR, 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.
Investigations
Plain X-Ray Chest Skiagram
In mild regurgitation, heart size may remain normal.
In late cases, moderate cardiac enlargement suggests left ventricular rather
that right ventricular enlargement. Left atrial dilation is usually obvious.
Gross enlargement of left atrium is noted in chronic rheumatic regurgitation
with stenosis .
Mitral valve calcification, which is usually associated with mild MR, shows
C or J shaped appearance on plain chest film.
Echocardiography
M-Mode shows LV dimensions are increased as is velocity of motion of the
posterior wall and interventricular septum (IVS). The left atrium is enlarged.
There may be features of an underlying cause of MR, e.g. multiple echoes
suggesting vegetations due to endocarditis, MV prolapse or flail posterior leaflet.
2-D echo helps to suggest an underlying cause and assess its consequences.
The parasternal long-and short-axis views and apical 4-chamber views are the
most helpful and may show:
1. LV abnormalitydilatation causing annular stretching and functional MR,
regional wall motion abnormality due to MI or ischemia, volume-overloaded
LV.
2. Leaflet abnormalitiesrheumatic leaflets, vegetations due to endocarditis,
prolapse, flail leaflet.
3. Chordaerupture, thickening, shortening, calcification, vegetations.
4. Papillary musclesruture, hypertrophy, scarring, calcification.
Doppler echo features of severe MR
1. Wide jet. 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).
2. Jet fills a large area of LA. The extent to which the MR jet fills the LA
cavity is also a finding. The area of color in the LA depends on the machine
settings. However, a area >8 cm2 is likely to be severe, <4cm2 likely to be
mild.
3. Systolic flow reversal in pulmonary veins are seen. The jet extends to the
pulmonary veins. 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.
4. Dense signal on continuous Doppler show intensity of the jet is greater
with more severe MR since more red cells reflect ultrasound.
5. Raised pulmonary artery (PA) pressure is observed and is estimated by
Doppler from tricuspid regurgitation (TR).
Aortic Valve (AV)

The AV is located at the junction of the LV outflow tract and the ascending
aorta.
Valve has three cusps (leaflets)one is located on the anterior wall (right
cusp), and two are located on the posterior wall (left and posterior cusps).
Behind each cusps, the aortic wall bulges to form an aortic sinus of valsalva.
The coronary arteries arise from the sinuses (right coronary-anterior sinus,
left coronary left posterior sinus).
The aortic cusps form a central closure line in diastole. In systole, the
cusps open and close again at end systole when the aortic pressure exceeds
the LV pressure, to form a parallelogram shape.
Rarely, echoes from left coronary cusp may be seen within the
parallelogram. The LV ejection time can be measured from the point of cusp
opening to cusp closing. It is possible to measure aortic root diameter and LA
diameter from this M-mode image.
Aortic Stenosis (AS)

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

or may done(latter is diagnostic of AS)
2. There may be LVH due to pressure overload
3. LV dilatation occurs if heart failure has developed (usually a poor
prognostic feature)
4. Post stenotic dilatation of the aorta may be seen.
B. A M-mode echocardiogram may show an eccentric closure line.
C. Doppler is most useful in determining the severity of AS by estimating the
pressure gradient across the AV. Recordings of peak and mean velocity are
made from apical, right parasternal and suprasternal sites. The corres-
ponding pressure gradients are calculated using Bernaulli equation (gradient
= 4 V2 max). Valve area can be calculated by use of the continuity equation.
Severity of AS correlates with valve area, peak velocity peak pressure
gradient and mean pressure gradient (often more accurate than peak).
Features of Varying Degrees of AS

Valve area (cm2)
Normal 2.5 - 3.5
Mild 1.5 - 2.5
Moderate 0.75 - 1.5
Severe < 0.75
Peak velocity (m/s) Peak gradient Mean gradient
(mmHg) (mmHg)
Normal 1.0 < 10 < 10
Mild 1.0-2.0 < 20 < 20
Moderate 2.0-4.0 20-64 20-40
Severe > 4.0 > 64 > 40
Magnetic Resonance Imaging (MRI) and

Computed Tomography (CT)
1. Both MRI and CT have been used to evaluate left ventricular function and
left ventricular mass in patient with aortic stenosis.
2. MRI can also be used to measure aortic flow and transvascular gradient.

1. Coronary arteriography is indicated preoperatively in patients with aortic
stenosis with or without angina.
2. Cardiac catheterization is also indicated when the severity of aortic stenosis
cannot be determined non-invasively.
3. In valvular aortic stenosis, there is a systolic pressure difference across
the valve, while in supravalvular stenosis, the pressure difference is between
the supravalvular chamber and the aorta, and in subvalvular stenosis, it is
within the LV.
4. Left ventricular hypertrophy may be seen by contrast left ventriculography

which, however, is rarely required if echocardiographic evaluation is
adequate.
5. In valvular aortic stenosis, angiography may also reveal the thickening of
the valve cusps with systolic doming and a central ejection jet.
6. In supravalvular stenosis, angiography show the obstructive lesion above
the sinuses of Valsalva.
7. In subvalvular aortic stenosis, the left ventricular angiogram shows the
subvalvular obstruction or a more diffuse fibromuscular lesion.
8. Associated aortic regurgitation can be demonstrated by aortography.
Aortic Regurgitation (AR)

Definition: This is leakage of blood from the aorta into the left ventricle during
diastole.
Causes of AR: AR can result from intrinsic abnormalities of the valve leaflets,
aortic annulus or aortic root.
Chronic AR
1. Valvular:
a. Endocarditis
b. Rheumatic heart disease
c. Congenital bicuspid valve, subaortic and supraaortic stenosis.
d. Connective tissue and inflammatory disease Rheumatoid arthritis,
SLE, Crohns, ankylosing spondylitis, Whipples disease.
2. Aortic root diseases:
a. DilatationMarfans syndrome, hypertension, Ehlers-Danlos
syndrome, pseudoxanthoma elasticum and aortitis.
b. DistortionDissection (type I and II), syphilis, ankylosing spondylitis,
Reiters disease, rupture of sinus of valsalva and aneurysm.
Acute AR
a. Endocarditis
b. Dissection
c. Trauma
Investigations
Plain Chest Skiagram
a. If AR is due to abnormalities of the aortic wall, the ascending aorta is
enlarged.
b. Usually there is generalized dilatation, annulo-aortic ectasia, but in Syphilis
and Marfans Syndrome, a localized aneurysm of the ascending aorta may
be seen.
c. Linear calcification, along with the dilatation of the ascending aorta is

characteristic.
d. In long standing AR, the LV dilates producing cardiac enlargement.
e. In acute severe AR there may be pulmonary edema but the cardiac silhouette
remains normal.
Echocardiography
All the echo modalities are useful in diagnosis and evaluation. Doppler and
color flow mapping are especially helpful. 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.
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. Both suggest severe AR.
Dilation of LV cavity due to volume overload.
Exaggerated septal and posterior wall of LV wall motion (exaggerated septal
early dip strongly suggests AR).
2-D Echo May Show

LV dilation correlates with severity of AR
Abnormal leaflets (Bicuspid, rheumatic)
Vegetations
Dilated aortic root
Proximal aortic dissection
Abnormal indentation of anterior MV leaflet
Abnormal intraventicular septal motion.
Doppler Study
This is useful both for detecting AR and assessing its severity.
a. 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.
b. 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), aliasing will occur.
c. Continuous wave Doppler is then useful and the signal seen only above the
baseline.
MRI AND CT
Both can be used to assess left ventricular function, mass and regurgitation
index (RI= LV Stroke Volume/RV stroke volume).

In symptomatic patients with chronic AR, left ventricular diastolic pressure is
usually elevated, although cardiac output may remain normal. In acute severe
AR, however, cardiac output may be low, along with a marked increase in left
ventricular end-diastolic pressure. Angiography can be used for qualitative
assessment of the severity of AR, 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.
Tricuspid Valve (TV)

Tricuspid Stenosis (TS)
The TV is structurally similar to the MV in having:
Leaflets the TV has 3, as its name suggests, unlike the 2 of the MV.
Chordae attached to papillary muscles.
An annulus or valve ring.
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).
Doppler findings are similar to MS. 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.
Tricuspid Regurgitation (TR)

Causes of TR are similar to MR the commonest causes are secondary to RV
dilatation, and primary causes include disease of the leaflets, and/or the
subvalvular apparatus.
Echo assessment of TR severity is best achieved by Doppler as with MR.
More severe TR is associated with a broad, high-intensity jet filling the RA.
There is associated retrograde systole flow in the vena cava and hepatic vein.
Pulmonary Valve (PV)

The PV has 3 leaflets and sits at the junction of the RV outflow tract and the
main pulmonary artery.
Pulmonary Stenosis (PS)

May be valvular, supravalvular (peripheral) or subvalvular (infundibular).
Valvular PS may be congenital or acquired (rheumatic, carcinoid).
2-D echo may show thickened, calcified leaflets, doming of the valve
leaflets in systole and restricted motion.
There may be post-stenotic dilatation of the PA or its branches and RV
hypertrophy or dilatation due to pressure overload.
The normal peak velocity across the valve is 1.0 m/s.
The peak gradient across the valve can be estimated by Doppler sonography.
Supravalvular PS can be due to stenosis of the main PA or any of its
branches distal to the PV. It may be iaterogenic post-surgical banding of the
PA which is performed in left to right shunts.
Subvalvuler PS is most commonly congenital and is rarely acquired. Using
pulsed wave Doppler, it can be seen that the increase in velocity occurs in the
RVOT below the level of the PV.
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. There may be evidence of :
Pulmonary hypertension: Dilated RV, dilated PA, abnormal IVS motion
(behaves as though it belongs to the RV rather than LV- right
ventricularization of IVS).
Dilated PA the diameter can be measured usually in parasternal short-axis
view at AV level.
Vegetation on the valve in endocarditis.
Thick immobile PV leaflets in rheumatic heart disease or carcinoid.
Absent valve leaflets (congenital)
Pulmonary artery aneurysm.
Doppler techniques show pulmonary regurgitation and help to assess severity,
as with aortic regurgitation. Doppler indicators of severe pulmonary
regurgitation are:
Colour flow the regurgitant jet is visualized directly. Severity is indicated
by the width of the jet at the valve level, and excellent in to right ventricle.
Pulsed wave Doppler - show distance between the pulmonary valve and
the level at which regurgitation is detected, can be determined. A jet at the
lower infundibular region is severe.
Increased intensity of the Doppler signal.
Increased slop of the Doppler signal (deceleration time).
To summarise the radiological findings, a table is being presented which
divides the changes in three subgroups
Table 12.1
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. Never beyond the Raising of left main bron- ment (75%). In 25% cases
confines of Rt. atrium, chus this bulge is to left side.
only in cases of aneuris- Displacement followed by
mal dilation, left atrium compression of left main
protrude through Rt bronchus resulting in coll-
atrium. apse of Lt lower lung field.
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. 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. obliteration in RVH
Lateral deviation of Retrocardiac space
T.P.L. (normal 8 mm) obliteration is LVH
Calcification seen in (MS + MR)
mitral valve, cusp
myocardican, endo-
cardinen, carditendinae
SECTION 4
Respiratory
System
13
Pulmonary Infection
PNEUMONIA
Pneumonia is an infectious process involving pulmonary alveoli caused by
bacteria, Mycoplasma, viruses and other microorganisms, and is characterized
by inflammatory exudate in both the alveoli and interstitium.
The pneumonias are frequently classified according to their etiology. The
clinical, radiological and pathological findings in pneumonia of different etiology,
are frequently very similar. It is very difficult to describe them according to
causative organism.
Aims of Diagnostic Imaging

1. Confirm the presumptive clinical diagnosis.
2. Identify underlying predisposing factors such as bronchiectasis and
bronchial neoplasia.
3. Monitor the radiologic progression and resolution of disease.
4. Detect complications such as cavitation, abscess formation, and development
of empyema.
Pathology
Route of entry to lung are followings
a. Tracheobronchial tree
b. Pulmonary Vasculature
c. Direct spread from chest wall, mediastinum or across the diaphragm.
Each possesses morphologic findings sufficiently characteristic to be
recognized, pathologically and radiologically, may be important in determining
the specific cause of the pneumonia.
Infection Via the Tracheobronchial Tree

Most commonly by aspiration or inhalation of microorganisms Or
Direct physical implantation (bronchoscope). Pneumonia acquired via the
tracheobronchial tree can be divided into three pathogenetic types, each with
different morphologic and roentogenographic characteristics.
a. Air space (lobar pneumonia)

b. Bronchopneumonia
c. Interstitial pneumonia.
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,
at least in the early stages of disease.
Infection tends to occur predominantly in the basal areas.
Nodular appearance of the individual foci of infection is typical.
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.
In these cases, the pulmonary disease usually will be localized to an area
contiguous with extrapulmonary source of infection and often takes the form
of an abscess.
Air Space or Alveolar (Lobar) Pneumonia

Characteristic of pneumococcal infection but can also occur with other
organisms such as Klebsiella pneumoniae.
It tends to localize initially in the periphery of the lung undercover of the
visceral pleura. The fluid flows directly from alveolus to alveolus and acinus
to acinus via communicating channels until the entire lobe is involved, with
relative sparing of the bronchi and interstitium.
This produces homogeneous consolidation. The larger bronchi usually
remain patent and air containing, creating an air bronchogram, which is quite
characteristic.
Radiological Findings
Homogeneous opacification of the involved lobes or segments, extend upto
a well-defined pleural border. Patent bronchi within homogeneous
consolidation appear as linear branching lucencies (Positive air
bronchogram).
Bronchopneumonia (Lobular Pneumonia)

Produced by Staphylococcus aureus. The initial assault occurs on the mucosa
of the bronchi and bronchioles, resulting in epithelial ulceration and formation
of a fibrinopurulent exudate.
Pulmonary Infection 187
Intense transmural inflammatory reaction quickly spreads into peribronchial

and peribronchiolar alveoli, to fill them with hemorrhagic edema and pus. The
pattern of resolution or healing by tissue distruction with microabscesses or
macroabscesses formation and fibrosis.
Multiple illdefined, confluent, nodular opacities, representing multiple
secondary lobules filled with inflammatory exudate.
The nonhomogeneous pattern of ventilated and consolidated lobules results
in sponge like pattern known as Air alveologram.
Interstitial pneumonia: Caused typically by viruses and Mycoplasma
pneumoniae. Characterized by edema and inflammatory cellular infiltrate
predominantly within interstitial tissue.
Inflammatory infiltration of the bronchial wall and interlobular septa leads to
formation of linear and reticular opacities most marked in the perihilar zones,
and focal confluent shadows in the peribronchiolar alveoli.
Computed Tomography
High resolution CT findings of consolidation are homogeneous opacification
with airbronchogram.
Ground glass opacification is increase in pulmonary attenuation, which is
not associated with obscuration of underlying vessels. It may indicate
slight thickening of the interstitium or alveolar walls or partial filling of the
alveoli. Airspace nodules range from 3 to 10 mm in diameter and probably
represent peribronchiolar consolidation. Infiltration of the interstitium is
manifested by thickening of the interlobular septa and of the peribroncho-
vascular connective tissues.
Pneumonia Caused by Gram Positive Aerobic Bacteria

Streptococcus pneumoniae is an oval lanceolate organism surrounded by a
well defined capsule.
These pneumonia begins in the lower lobes or posterior segments of the
upper lobes. Earliest pathologic findings occur in relation to the terminal airways
as in typical bronchopneumonia. Rapidly air space edema spreads from acinus
to acinus to involve varying amounts of lobar parenchyma. This centrifugal,
contiguous spread accounts for the homogenicity of consolidation and
nonsegmental distribution observed both morphologically and roentgenologi-
cally.
Roentgenographic Manifestations
Homogeneous consolidation of lung parenchyma, invariably abuts against
a viseral pleural surface. (A rare exception is spherical pneumonia)
Air bronchogram.
Loss of volume is either slight or absent during the acute stage of the
disease.
During resolution, some degree of atelectasis is common, caused by exudate
within airways and subsequent obstruction.
Most frequently, the disease is confined to one lobe but the infection may
develop simultaneously in two or more lobes.
Cavitation is rare.
Staphylococcus Aureus
May occur either as a primary respiratory tract infection or as a blood
borne infection.
When dissemination is hematogenous, the typical appearance is of multiple
poorly defined rounded nodules that develop rapidly over a few days.
Infection due to inhalation, causes bronchopneumonia with multiple patchy
areas of consolidation.
Cavitation is common and in children, pneumatocele frequently develop.
Pleural effusion, empyema and areas of atelectasis are common
complications.
Klebsiella Pneumoniae
There is usually lobar consolidation more often right sided, and frequently
upper lobe.
The volume of the affected lung is maintained.
Cavitation is common and there is healing with fibrosis. Cavities may become
permanent and mimic tuberculosis.
Tuberculosis
The disease is worldwide in distribution. In 95 percent of cases the causative
organism is Mycobacterium tuberculosis hominis.
Less commonly, Mycobacterium bovis, atypical mycobacteria. Such as
M. kansasii and M. balnei can infect.
In 1900, tuberculosis was worldwide epidemic with a mortality rate of
approximately 250 per 100,000 per year.
Today the disease is most commonly found in persons whose immune
status is compromised by old age, alcohol abuse, diabetes mellitus, steroid
therapy or AIDS.
Tuberculosis is classically divided into primary and postprimary disease.
Primary
Occurs in those, not previously exposed to M. tuberculosis, is frequently
asymptomatic, and is therefore not detected clinically. The frontal chest
radiograph remains the initial imaging investigation in tuberculosis. The recent
studies have emphasized the role of high resolution CT, particularly in the
detection of endobronchial spread.
Aims of Diagnostic Imaging

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

Hilar and mediastinal Lymphadenitis leads to hilar enlargement and
mediastinal widening respectively.
Lymphangitic stranding connecting the primary focus with the hilar
lymphadenitis from dumb-bell shaped opacity, representing the primary
complex.
Miliary tuberculosis-mottled noduler pattern.
Coarse granular or Snowstrom pattern due to coalescence of nodules.
Exudative tuberculous pleuritis- resembles effusion pleural.
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.
Postprimary tuberculosis is localized initially to the apical and posterior
segments of the upper lobes, this relates to the high PO2, although suggested
that impaired lymphatic drainage of these areas resulting from decreased
pulmonary arterial blood flow is more important factor.
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 initial reaction is exudative and characterized by lobular caseous
pneumonia consists of edema, fibrine and polymorphonuclear leuckocytes.
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, comprising caseous cone surrounded by a mantle of granulation
tissue are also found.
Endobronchial spread of liquefied necrotic material from cavity can result
in tuberculous infection.
Infection occurs initially in the region of the terminal acinar airways, giving
the appearance of multiple parenchymal nodules. 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.
Cavitating Tuberculosis
Cavitation results from erosion of enlarging tubercles into airway leading to
expulsion of the central necrotic material. The infection also extends towards
the periphery of lung-and rupture into the pleural cavity results tuberculous
empyema. The wall of the cavity contains infectious caseous material which
provides the organism with the outside environment.
Healing Occur in Two Ways

By opposition of granulation tissue at the mouth of the draining bronchus
resulting in complete closure of the cavities.
Tuberculous granulation tissue transform into fibrous tissue, resulting in a
healed cavity.
Fibrocavitatory Tuberculosis
When host factors prevail, there is gradual healing with the formation of localized
or extensive parenchymal scars, accompanied by adjacent irregular emphysema
and bronchiectasis.
Bronchiectasis in postprimary tuberculosis can develop by two mechanisms:
1. Most commonly by distruction and fibrosis of lung parenchyma resulting
in retraction and irreversible bronchial dilatation.
2. Cicatricial bronchostenosis secondary to localized endobronchial infection.
Vascular Abnormalities
Pulmonary arteries and vein in an area of active tuberculous infection may
show vasculitis and thrombosis.
Arteries in the vicinity of chronic tuberculosis shows endarteritis obliterans
a concomitant local increase in the number and size of bronchial artery
branches.
Roentgenographic Manifestations
Produces a spectrum of radiographic manifestations: 1. Exudative, 2.
productive, 3. cavitatory, 4. fibrotic changes, and 5. Mixed.
Although the identification of parenchymal disease in apical or superior
segment of lower lobe strongly supports a roentgenologic diagnosis of
tuberculosis, the definitive diagnosis requires culture of the organism.
Exudative Tuberculosis
Patchy or confluent opacities with indistinct contours, gradually alter in
appearance over a period of weeks in contrast to nonspecific pneumonia which
may change within days.
Productive Tuberculosis
Produces sharply defined, irregular polygonal opacities admixed with calcified
granulomata.
TuberculomasPulmonary nodules or masses of 0.5 to 4 cm in diameter,
have smooth margins and predilection for the upper zones. In 80 percent
cases shows small satelite lesions and calcifications.
Tuberculous Cavities
Result from caseous necrosis of tuberculous pneumonia with subsequent
expectoration of the contents. The wall of cavity may be variably thin or thick
and smooth or internally nodular, a fluid level may be identified in the cavity.
(Secondary infection). With adequete therapy, a cavity may disappear,
sometimes its wall become paper thin but it remains an air filled cystic space.
Cavities are frequently combined with disseminated acinar shadows due to
endobronchial spread.
Fibrotic Tuberculosis
Include apical pleural thickening, parenchymal scarring, calcification and
fibrotic bands radiating from hilum to the apex. Cranial shift of hilar structures
indicates fibrous contraction. Paracicatricial emphysema, bronchiectasis and
broncho-vascular distoration may set in a thick pleural peel may encase the
residual lung and lead to thoracic deformity with kyphoscoliosis.
Computed Tomography
Cavitation: HRCT has been shown to be superior to the chest radiograph in
demonstrating cavitation, particularly in cases complicated by fibrosis and
architectural distoration.
Endobronchial Spread
These include centrilobular nodules or linear structures, Tree in bud branching
linear structures, and poorly defined nodules, caseating material within the
terminal and respiratory bronchioles. Poorly defined nodules represent
peribronchiolar inflammation.
Miliary tuberculosis
HRCT images show fine nodules which are uniformly distributed throughout
the lungs. These may be well or poorly defined and range in size from 1 to
4 mm in diameter. They are randomly distributed throughout the secondary
lobule in contrast to the centrilobular nodules of endobronchial spread.
Fibrocavitatory tuberculosis: Findings indicating chronic parenchymal
changes including, fibrotic bands, broncho-vascular distortion and cicatricial
emphysema.
Bronchography
Bronchograms demonstrate both bronchial structures and extrinsic
compression of the airways. Tuberculosis of the bronchial mucosa may be
seen with perforation of tuberculous foci into airway and subsequent cavity
formation.
Differential Diagnosis
1. Nonspecific pneumonia
2. Carcinoma
3. Parenchymal calcification of other etiology
Fungal Diseases of the Lung

Endemic disease, caused by pathogenic fungi in an otherwise healthy individual.
They include, histoplasmosis, coccidioidomycosis, blastomycosis and
sporotrichosis.
Opportunistic Fungal Infection

(Asperigillosis, candidiasis) is caused by saprophytic fungi, which are usually
present in the oral mucosa and become pathogenic in the immuno-compromised
host. The overall incidence of pulmonary fungal infections clinically and
radiologically resemble bacterial pneumonias. Therefore, difinitive diagnosis is
based on identification of the fungus at microscopy and culture.
Candidiasis
Candida albicans is part of the normal human microbial flora of the oral
cavity. Pulmonary condidiasis occurs only in the immunocompromised patients.
The diagnosis may be established by demonstration of Candida on trans-
bronchial biopsy.
A wide spectrum of radiolographic findings have been described in Candida
pneumonia. Appearances may be indistinguishable from that of bacterial
pneumonia with lobar, or segmental consolidation. Diffuse bilateral alveolar or
mixred alveolar interstitial shadowing may be seen.
Aspergillosis
Aspergillus fumigatus, A. flavus, and A. niger (They constitute part of the
flora of the healthy oral cavity).
Primary Invasive Aspergillosis

Develops when massive amounts of fungal spores are inhaled. The hosts have
normal immunity.
Secondary Angioinvasive Aspergillosis

Occurs as an opportunistic infection in patients with severe debilitating illness
particularly leukemia and lymphoma.
Pathologically this disease is characterized by mycotic vascular invasion,

thrombosis and hemorrhagic infarction with subsequent necrosis and cavitation.
The initial chest radiograph may be normal. Multiple foci of consolidation
may be present, which presents with rounded shape and probably infarcted
parenchyma. The characteristic air crescent sign develops late in the course
of disease.
Computed Tomography
In early invasive aspergillosis, a halo of ground-glass opacification surrounds
the dense parenchymal foci. This represents a rim of hemorrhage or coagulation
necrosis surrounding an area of infarction. The halo sign precedes the air
crescent sign by upto 2 weeks.

May be helpful in early diagnosis of invasive aspergillosis.
On standard T1 weighted sequences, rounded consolidations have target
appearance with a hypointense center and hyperintense rim. The rim enhances
on administration of intravenous Gadolinium.
Invasive Aspergillosis of the Airways

Diagnosis is based on the presence of organisms deep to the basement
membrane C.T. findings include lobar consolidation, bilateral peribronchial
consolidation, ground glass attenuation, and centrilobular nodules less than
5 mm in diameter.
Allergic Bronchopulmonary Aspergillosis

Represents a hypersensitivity reaction usually in asthmatics and manifestations
include asthma, eosinophilia, precipitating antibodies to Aspergillus and elevated
IgE titers.
Pathologically, mycelial plugs develop in the proximal airways but in contrast
to invasive aspergillosis of the airways, tissue invasion is minimal or absent.
The chest radiograph shows transient infiltrates of lobar, segmental or
subsegmental distribution that predominantly involve the upper lobes.
Bronchoceles are also frequent manifestation of ABPA. These vary in shape
but classically present gloved finger appearance.
Central bronchiectasis involving the inner two-thirds of the bronchial tree
and showing an upper lobe predominance may develop.
Aspergilloma: It is the most common form of aspergillosis. It occurs in hosts
with normal immunity and the fungus colonizes preexisting cavities (cysts,
tuberculous cavities, cystic bronchiectasis) and forms fungal ball. This may
erode the cavity wall and lead to hemoptasis.
The chest radiograph shows a round, homogenous opacity mobile within

the cavity. A circular or crescent-shapped air space may be visible between
the mycetoma and the cavity wall. Localized pleural thickening may be seen.
C.T. Nonhomogenous attenution and surrounding crescent of air within the
cavity.
Histoplasmosis: Caused by Histoplasma capsulatum. Histoplasmosis is a fungal
infection that occurs mainly in North America.
Acute histoplasmosis develops as the result of air borne primary infection.
contaminated by Bat or bird excreta.
Radiologic Findings
Multiple ill defined patches of consolidation throughout both lungs.
There is accompanying hilar and mediastinal lymphadenopathy.
These pneumonic consolidations heal, leaving residual pulmonary
granulomas that undergo central calcification to produce target pattern.
Chronic progressive histoplasmosis is the consequence of reactivation and
has a poor prognosis.
Progressive cavitation with fibrosis may progress.
Coccidioidomycosis (Coccidioides Immitis)

Endemic in the southwestern US. The chest radiograph shows pneumonic
consolidations and pulmonary nodules (Coccidioidomas) that occasionally
cavitate.
In disseminated coccidioidomycosis, there is generalized micronodular
pattern. Pulmonary fibrosis are associated with advanced disease.
Actinomycosis
Actinomyces israelii is intermediate between mycelial fungi and bacteria and is
a common saprophyte in the human mouth. Involves the cervicofacial region,
the intestinal tract and the lung. In the thorax, manifestations include chronic
cavitating pneumonia, pleural empyema and chestwall invasion.
Radiologic Findings
The chest radiograph shows nonsegmented predominantly peripheral
consolidation that may cavitate. Consolidation typically crosses interlobar
fissures.
Pleuroesophageal and pleuropulmonary fistulae, pleural empyema, rib
osteomyelities with periosteal thickening, and inflammatory soft tissue masses
of the chest wall may develop.
Nocardiasis
Aerobic saprophyte found in the soil. Pulmonary nocardiosis may be similar to
actinomycosis in its radiographic appearance.
Cryptococcosis (Torulosis)
The spores of Cryptococcus neoformans are found in dust and excreta and
cause pulmonary infection in immunocompromised hosts.
The chest radiograph shows small, subpleural granulomas, foci of
bronchopneumonia and round masses (Torulomas) which may cavitate, other
mycoses like blastomycosis, sporotrichosis and mycormycosis are extremely
rare and present as non specific pneumonic infiltrate.
Parasitic Infections
Parasitic infections are more prevalent in Asia, Africa, South America. The
causative organisms are protozoa and helminths. They induce hypersensitivity
reactions, in the lungs with formation of eosinophilic loeffler infiltrate. Parasites
may colonize in the lungs and forms cysts, granulomas and abscesses.
Amebiasis
They are ingested in contaminated food and initially induce a colitis. They
reach the liver via the blood stream and form hepatic abscesses.
Radiologic Finding
Chest radiograph shows opacification of the lower thorax due to pneumonic
consolidation with pleural effusion.
Initially ill defined infiltrate may form an abscess.
Sonography will show hepatic and pleural changes, while CT will indentify
and characterize pulmonary parenchymal abnormalities.
Toxoplasmosis
Congenital toxoplasmosis due to transplacental infection is the most important
form and presents with encephalitis and chorioretinitis. Adult toxoplasmosis is
relatively uncommon except in patients with AIDS.
In the HIV-negative population, it is manifested as lymphadenitis and
occasionally as interstitial pneumonia.
Ill-defined opacities resumbling acute viral pneumonia associated hilar
lymphadenopathy.
Pneumocystis Carinii Pneumonia

Originally described in premature infants. In adults, it is a frequent pathogen in
the immunocompromised host. 60-70 percent of patients with AIDS with
develop pneumocystis carinii pneumonia.
Initial chest radiograph may be normal but in 80 percent of cases it shows
diffuse, bilateral granular or reticular infiltrates. They may involve the perihilar
and lower zones. Progression to diffuse air space consolidation may occur.
Hilar adenopathy and pleural effusions are unusual.
Computed Tomography
HRCT finding are bilateral ground glass opacification, less commonly a mosaic
pattern with scattered foci of parenchymal involvement interspersed with
normal lung is found. Cystic changes are frequently identified.
Schistosomiasis
Schistosomiasis hematopium is endemic in North Africa. The infective larvae
penetrate the skin, enter the capillaries and migrate through the systemic venous
system to the right heart. Then they enter the pulmonary circulation and
subsequently the systemic arterial system to reach the liver, kidney and urinary
bladder.
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. Occasionally the parasites lodge in
the precapillary pulmonary arterioles and initiate an obstructive endarteritis
leading to pulmonary hypertension and chronic cor pulmonale.
Echinococcus granulosus
Human ingest the ova the dog tapeworm taenia echinococcus in contaminated
food. The larvae hatch in the intestine with subsequent hematogenous spread
to the liver. Pulmonary, cerebral and bone involvement occur in about
10 percent of cases.
Solitary, smooth, round, homogeneous, mass ranging from 1 to 10 cm in
diameter occasionally a thin crescent of air is visible between the ectocyst and
pericyst (menisus sign). This is an indication of early rupture. Later following
cyst rupture, the chitin membrane of the endocyst may collapse and float on
the residual fluid (waterlity sign).
Ascariasis
Radiographs show, regional confluent infiltrates similar to eosinophilic loeffler
pneumonia.
Viral Pneumonia
Viral pneumonia usually commences in distal bronchi and bronchioles with
distruction of the epithelium, edema and lymphocytic infiltration.
The radiological appearances of a viral pneumonia are very varied, but
often include.
1. Peribronchial shadowing
2. Reticulonodular shadowing
3. Patchy or extensive consolidation.
Viral pneumonia is uncommon in adults. Most pneumonias that complicate
viral infections in adults are due to bacterial superinfection. However, viral
pneumonias not rare in infants and children.
Influenza Virus
Primary viral pneumonia during influenza epidemics, a fulminating hemorrhagic
pneumonia may be seen with widespread consolidation indistinguishable from
non cardiogenic pulmonary edema or ARDS, if the patient survives, extensive
pulmonary fibrosis may develop.
Herpes Varicella Zoster

Varicella pneumonia occurs more often in adults than in children. In the acute
phase of infection, the chest radiograph may show wide spread nodular shadows
up to 1 cm in diameter. Following recovery, small proportion of these nodules
calcify.
Measles Giant-Cell Pneumonia

Although a disease of childhood, it has been recorded in adults.
The mediastinal and hilar nodes are commonly enlarged.
Streaky basal linear shadows, widespread reticular shadows and diffuse ill
defined nodular opacities are seen.
Acquired Immuno Deficiency Syndrome (AIDS)

Organisms causing intrathoracic infection in AIDS include bacteria, typical
and atypical mycobacteria, protozoa, viruses and fungi.
Mycobacteria
Tuberculosis in advanced AIDS in frequently aggressive and manifestations
may be those of primary or miliary tuberculosis. Cavitation is unusual in
the severely immuno-compromised patients.
The endobronchial spread and cavitation are seen in the mildly
immunocompromised ones.
Mycobacterium avium complex is found in up to 20 percent of AIDS
patients.
They include parenchymal nodules, masses and consolidation in association

with mediastinal lymphadenopathy.
Mycobacterium tuberculosis and MAL are the most frequently responsible
for mediastinal adenopathy in AIDS.
Pneumocystis carinii pneumonia
Viruses
All viruses, especially CMV are an infrequent cause of pneumonia in AIDS.
Radiographic manifestations include diffuse parenchymal infiltration that may
be indistinguishable from non cardiogenic pulmonary edema. Pleural effusions
and adenopathy are absent.
Fungi
Cryptococcosis is the most common pulmonary infection in AIDS and
frequently coexists with cryptococcal meningitis.
Intrathorasic manifestations include mediastinal lymphadenopathy, pleural
effusion and focal alveolar and diffuse reticulonodular shadowing.
14
Interstitial Lung Diseases
DEFINITION
Interstitium is supporting strength of lung and consists of loose connective
tissue throughout lung consisting of 3 subdivisions:
a. Axial surrounding bronchovascular bundle from hila to secondary
pulmonary nodule.
b. Parenchymal (acina) between alveolar walls and capillaries.
c. Sub pleural between pleura and lung parenchyma and is continuous
with interlobular septas and perivenous spaces.
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.
ETIOLOGY
1. Interstitial pneumonias
Usual Interstitial Pneumonitis/Cryptogenic fibrosing alveolitis/idiopathic
pulmonary fibrosis
2. Malignant Disease
Lymphoma
Lymphangitis carcinomatosis
Leukemia
3. Granulomatous disease
Sarcoidosis
Wegeners Granulomatosis
4. Infectious disorders
Miliary tuberculosis
Fungal
Pneumocystis
Mycoplasma
Parasites
5. Histocytosis X (Langerhans histiocytosis)
6. Pneumoconiosis
Coal workers pneumoconiosis
Asbestosis
Interstitial Lung Diseases 201
Silicosis
Berylliosis
7. Autoimmune disease/collagen diseases
Scleroderma
Systemic Lupus Erythematosus
Polymyositis
Sjgrens syndrome
Polyarteritis nodosa
8. Allergic disease
Hypersensitivity pneumonitis or extrinsic allergic alveolitis
Pulmonary eosinophilia
9. Drugs
Antineoplastic drugs
10. 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.
Among the various interstitial lung diseases, the commonest causes are:
Environmental diseases - 24%
Sarcoidosis - 20%
Interstitial pulmonary fibrosis - 15%
Collagen vascular disease - 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
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. Conventional radiography
First modality of diagnosis
Correlation between radiographic changes and severity of respiratory
distress is often poor.
Sometimes even advanced cases of interstitial lung disease may
present normal findings on X-ray chest.
So it is Non Specific and of limited diagnostic value
2. Conventional CT Scan
Better modality
3. HRCT Diagnostic modality
Thin sections (1-3 mm) combined with high spatial resolution
reconstruction algorithm, (e.g. the bone algorithm)
And targeting the scan to the lung, (i.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.
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.
FINDINGS ON X-RAY CHEST AND CT SCAN

Shadows are:
1. Nodular
2. Linear
Thick or thin band like shadows
Irregular distribution
Because of fibrosis of lung
3. Reticular when these lines overlap and produce a meshwork like pattern
4. Reticulonodular
5. Miliary size 2-4 mm
6. Honeycomb
Size 5-10 mm thin walled cystic lesion
It is the only dependable sign of interstitial fibrosis.
Most common complication is pneumothorax
Common causes are:
Histiocytosis - X
Fibrosing alveolitis
Pneumoconiosis
Sarcoidosis
Rheumatoid lung
Scleroderma
7. Ground glass haze (active inflammation)
Homogeneous haze (veil) with loss of definition of pulmonary vessels
and diaphragm.
Can be seen in both interstitial or alveolar pattern.
8. Kerley lines
(A) - 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. Others
Peribronchial cuffing
Subpleural lines
Traction bronchiectasis
SARCOIDOSIS
Multisystem noncaseating granulomatous disease
Young adults
Blacks > whites
Males > female
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.
The resulting skin reaction is biopsied and is deemed positive if it displays
typical sarcoid histology.
Ga-67 is taken up by involved lymph node (LN) and lung and is used to
assess activity and extent of disease.
On imaging
Stage 1 : Lymphadenopathy
Bilateral symmetrical hilar (tracheobronchial and
bronchopulmonary) lymphnode.
70-80 percent patients also have paratracheal lymphnode
(especially right side).
< 5 percent calcify sometimes by egg shell calcification.
Stage 2 : Lymphadenopathy with parenchymal opacity.
Stage 3 : Parenchymal opacity alone.
Parenchymal Opacity
1. 75-90 percent commonest pattern
Rounded or irregular nodules of 2-4 mm diameter, well/ill defined and
are predominantly peribronchovascular and subpleural in distribution.
Smaller or larger opacities are not uncommon.
Very small aggregated opacities, sometimes give a ground glass
appearance.
Upper/middle zone predominance.
2. 10-20 percent
Patchy consolidation
Opacities sometimes contain air-bronchograms and have ill defined
margins that commonly break up into a nodular pattern.
Range from 1 cm to a segment or more are usually multiple.
3. 2 percent
Nodules of 1-4 cm size which are usually relatively illdefined and
rounded; oval or irregular in shape sometimes containing an air-
bronchogram.
Multiple and bilateral and may rarely cavitate.
1/3 of parenchymal opacities progress to fibrosis rest resolve completely.
Fibrotic Shadowing
Coarse linear opacities with evidence of volume loss.
Ring shadow caused by blebs, bullae and bronchiectasis or honeycombing.

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.
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.
Tend to migrate towards hila creating peripheral areas of emphysema and
bullae.
May calcify/cavitate
Cavitating bronchial carcinoma
Differential diagnosis of PMF
TB
Caplans Syndrome
Patients with coal workers pneumoconiosis/silicosis and rheumatoid disease
may develop Caplans syndrome.
Multiple round, well defined opacities.
1-5 cm size
Usually appear in crops
Nodules may regress, remain static, calcify or cavitate
The lesions may precede the development of overt rheumatoid arthritis.
SILICOSIS
Simple Silicosis
Multiple nodular shadows of 2-5 mm diameter in size.
Hilar lymphnode is common (may have eggshell calcification).
Upper/middle zones are affected.
Complicated Silicosis
Progressive massive fibrosis (PMF)
ASBESTOSIS
Symptoms are often not apparent until 20-30 years after exposure.
1. Pleural lesion
Plaques: often calcify and produce bizarre opacities, sometimes
resembling holly leaves They tend to occur in the mid zones and over
the diaphragm.
Diffuse thickening
Pleural effusion: Large effusions suggest carcinoma or mesothelioma
Mesothelioma
2. Pulmonary lesion
Lower zones
Similar to fibrosing alveolitis
Fine reticular or nodular

Coarser and causes loss of clarity of heart and diaphragm (shaggy
heart).
HRCT clearly shows:
Subpleural curvilinear opacities (crescents)
Parenchymal bands
Thickened inter and intralobular lines.
Increased subpleural attenuation and honeycombing
Rounded atelectasis
Fibrosing condition most commonly associated with asbestosis.
Comet tail of incurving vessels being characteristic.
Other features
o Adjacent pleural thickening
o Airbronchogram within the lesion.
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.
3. 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 m).
Farmers 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.
On Imaging
Diffuse fine nodular opacities or generalized ground glass haze - Early
stages.
Patchy consolidation and septal lines similar to pulmonary edema in acute
attacks.
Later - reticulonodular shadows / coarse linear opacities / honey combing
/ cyst formation / bronchiectasis.
Upper / middle zones
COLLAGEN VASCULAR DISEASE

1. Systemic Lupus Erythematosus (SLE)
More common in females
Pleural effusion
Usually bilateral and small in volume and associated with pleurisy
and pain.
Basal segmental collapse
Thick horizontal band shadows.
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).
2. 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.
Caplans syndrome rheumatoid nodules develop against a
background of simple pneumoconiosis.
Apparent in chest X-ray in 5 percent of patients. HRCT is better for
detection.
Basal reticulonodular which may progress to honeycombing and
severe volume loss.
Pulmonary artery hypertension
Obliterative bronchiolitis:
Produce airflow obstruction
Lungs appear over inflated with decrease in size and number of
vessels.
3. Systemic Sclerosis (more in females)
Highest incidence of pulmonary fibrosis amongst the connective tissue
diseases.
Esophageal involvement resulting in abnormal motility may cause reflux
and aspiration pneumonia.
As in other cases of fibrosing alveolitis Basal reticulonodular shadow
honey combing.
Egg shell calcification of lymph nodes
Predisposition to lung cancer
Associated pleural disease is rare.
4. 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).
Sjgrens Syndrome
Triad of
Dry eyes
Dry mouth
One of the other connective tissue disorders
Also there are
Pleural effusion
Recurrent chest infections
Lymphocytic interstitial pneumonitis
Dermatomyositis and polymyositis
Basal fibrosing alveolitis.
Involvement of pharyngeal muscles may predispose to aspiration
pneumonitis.
Primary lung involvement is unusual.
SYSTEMIC VASCULITIDES
E.g. Wegeners 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. They
may wax and wane and frequently cavitate forming masses with thick
irregular walls:
Rheumatoid disease
Metastasis
Pleural effusion
Unusual hilar and mediastinal LN
Granulomas may grow in the trachea and bronchi causing tracheal stenosis
and lobar collapse.
PULMONARY EOSINOPHILIA
Transient opacities on the chest radiograph in association with an excess
of eosinophils in blood.
Pulmonary opacities are due to eosinophilic exudates (PIE syndrome
pulmonary infiltrates with eosinophilia).
1. Simple Pulmonary Eosinophilia (Loefflers syndrome)
Mild transient condition.
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.
2. 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, not being restricted by
inter lobular fissures.
3. Tropical Pulmonary Eosinophilia (TPE)
Caused by filariasis
Fine bilateral diffuse nodular shadowing with occasional confluent areas
Diffuse reticulonodular shadowing occasionally associated with hilar
lymphadenopathy.
4. Asthmatic Pulmonary Eosinophilia
(Allergic Bronchopulmonary Aspergillosis)
Most commonly caused by Aspergillus fumigatus. Most patients have
long standing asthma prior to development of this complication but
often no allergen is identified. Upper lobe predominance.
Chest skiagram shows transient shadows but after repeated attacks
there may also be signs of fibrosis and bronchiectasis.
Central bronchiectasis
As in any condition which results in lung destruction and cavity
formation mycetoma formation may occur.
5. Pulmonary Eosinophilia Associated with the Systemic Vasculitides, e.g.
Wegeners, PAN
X-ray features are those of underlying connective tissue disorder.
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.
A. Cryptogenic Fibrosing Alveolitis (or UIP usual interstitial pneumonitis or

primary).
Histologically Most cases show fibrosis and cellular infiltrate confined
to the alveolar walls. Some cases show mononuclear cells in the alveoli
and may be termed desquamatic interstitial pneumonitis.
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. Secondary Fibrosing Alveolitis (also causes of diffuse pulmonary fibrosis)
Connective tissue diseases (SLE, SS, 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
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, ring shadows, honey combing and bullae.
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.
Diffuse hyperplasia of smooth muscle in bronchi, lung vessels,
lymphatics, lymphnodes and alveolar walls.
Patient is almost invariably female.
HRCT shows Multiple thin walled cysts with normal intervening lung
parenchyma.
Recurrent pneumothorax
Chylous pleural effusions are rare but may be large bilateral and
persistent.
LYMPHANGIOMYOMATOSIS
Very similar radiologically and pathologically to tuberous sclerosis.
However the distribution of muscle proliferation is initially perilymphatic
and the disease may also involve the mediastinal and retroperitoneal lymph
nodes, hence chylothorax and chyloperitoneum are commoner than tuberose
sclerosis.
Premenopausal females
Imaging same as tuberose sclerosis.
Difference between histiocytosis and lymphangiomyomatosis (LAM) and
tuberose sclerosis (TS):
1. In LAM and TS - there is female predominance.
2. Lower zones are involved
3. Pleural effusions are common especially in LAM (chylous effusion due to
involvement of thoracic duct by leiomyomatous tissue).
NEUROFIBROMATOSIS
Pulmonary fibrosis occurs in approximately 10 percent of patients with
NF-I.
ACUTE RESPIRATORY DISTRESS SYNDROME

Acute respiratory failure in patients without previous lung disease and usually
follows major trauma or shock.
On radiography
Bilateral patchy alveolar opacities in first 24 hours which become more
extensive over the next few days. Pleural effusions are unusual and
heart does not enlarge.
At this stage Gram negative pneumonia frequently develops and
cavitation and pleural effusion may be seen.
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
Imaging
During an acute episode of pulmonary hemorrhage, patchy illdefined
areas of consolidation appear on the chest radiograph. They may become
confluent and demonstrate an airbronchogram. Septal lines are
occasional.
When bleeding stops opacities resolve within a few days.
Following repeated episodes of bleeding pulmonary fibrosis may
develop and produce a diffuse hazy nodular or reticular pattern.
Hemosiderosis is also well recognized in patients with chronically
elevated left atrial pressure, e.g. mitral stenosis.
On imaging permanent miliary stippling is seen due to focal nature of
bleeding.
Patients with nephritis are prone to pulmonary edema and pneumonia and
differentiation from pulmonary hemorrhage may be difficult.
a. Oedema
Cardiac enlargement
Pleural fluid
Septal lines
b. 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.
IV injection of RBC lebelled with 99Tc.
DRUG INDUCED PULMONARY DISEASE

Pulmonary fibrosis often basal predominance
Cytotoxic drugs
Gold
Mineral oil and nitrofurantoin
Pulmonary eosinophilia
PAS
Asprin
Penicillin
ARDS
Cytotoxic drugs, e.g.
Bleomycin
Busulphan
Cyclophosphamide
SLE reaction
Penicillin
INH
Methyl dopa
Pulmonary oedema
Salicylates
Narcotic overdose
Overtransfusion of IV fluids
Hypersensitivity to transfused blood and blood products.
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. Secondary form in lungs does not produce any
radiographic abnormality as secondary amyloid does not invoke an
inflammatory response in lungs.
On imaging
Multiple nodular opacities which can cavitate or calcify.
Diffuse reticulonodular shadowing or honey combing.
Enlarged lymphnode (may be calcified).
Tracheobronchial amyloid
Solitary endobronchial tumor mass/polyp, or it may grow down the
trachea and into the bronchi in the form of nodular submucosal plaques.
Radiologically
The effects are of obstruction, i.e.
o Atelectasis
o Distal bronchiectasis
o Infection
Tracheo Pathia Osteoplastica
It is a condition of cartilaginous masses lining most of trachea and major
bronchi. The masses contain amyloid deposits, calcific bodies and
ossifications. It is thought to be an end-stage of tracheobronchial
amyloidosis.
PULMONARY ALVEOLAR PROTEINOSIS

Rare disease of unknown etiology
A fat laden proteinaceous material probably secreted by the type II
pneumatocyte fills the alveoli.
This is probably the result of a response by the lungs to an irritant.
Histologically there is a striking lack of reaction within the alveolar walls.
M:F = 3:1
Any age
On Imaging
Resembles pulmonary oedema with small acinar perihilar opacities
present in both lungs. These opacities may become confluent. Changes
are bilateral and perihilar and usually symmetrical.
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.
It predisposes to infection from both common respiratory pathogens and
opportunistic organisms.
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. The
calculi are calcified and produce widespread minute but very dense opacities
on the chest radiograph.
If profuse produce a white out of lung and best demonstrated by
overexposed film.
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.
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.
DIFFERENTIAL DIAGNOSIS
Lower Zone
Systemic sclerosis
Dermatomyositis
Polymyositis
Lymphangio myomatosis
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
Neurofibromatosis
Pneumoconiosis
Honey Combing
Asbostosis
Histiocytosis
Tuberous sclerosis
Miliary opacities
Fungal (Coccidomycosis, Blastomycosis, Histoplasmosis)
Tuberculosis
Sarcoidosis
Metastasis from thyroid, renal cell carcinoma, choriocarcinoma
Silicosis
Berylliosis
Coal workers penumoconicosis
Oil embolism (post lymphangiography)
Greater than Soft Tissue Density

Chickenpox
Histoplasmosis
Siderosis
Stannosis
Barytosis
Haemosiderosis
Disseminated Large Nodules (1-6 cm)

Metastasis
Rheumatoid nodules
Wegeners granuloma
Pyemic abscesses
Hydatid cysts
Pulmonary infarcts
Arteriovenous malformation
Fungal
Caplan syndrome
PMF
Amyloidosis
Lymphoma
Pleural Effusions are Notably Absent in

Sarcoidosis
Upper Zone Fibrosis

Tuberculosis
Histoplasmosis
Sarcoidosis
Allergic bronchopulmonary aspergillosis
Progressive massive fibrosis
Ankylosing spondylitis
SECTION 5
Gastrointestinal
Tract, Pancreas and
Hepatobiliary Tract
15
Imaging in Jaundice
Jaundice is defined as yellow pigmentation of skin and /or sclera in response
to increased serum bilirubin level more than 2.0 mg/dl.
Bilirubin Metabolism
1. Source:
From catabolism of
a. Hemoglobin (80-85%)
b. Non-hemoglobin haem containing pigments e.g. myoglobin, catalase,
cytochrome
2. Transport: Bilirubin on release circulates as unconjugated bilirubin in plasma
tightly bound to albumin.
3. Hepatic phase
i. On entering the hepatocyte, the albumin bound un-conjugated bilirubin
dissociates into bilirubin and albumin.
ii. Conjugation: Unconjugated bilirubin is converted to water-soluble
conjugated bilirubin by enzyme glucoronosyl transferase.
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.
4. 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.
Hyperbilirubinemia can be:
Conjugated
Unconjugated
Pathogenesis
A. Predominantly unconjugated hyperbilirubinemia produces medical jaundice
i. Increased bilirubin production due to:
Excessive hemolysis
Ineffective erythropoiesis
ii. Decreased hepatic uptake due to:
Prolonged starvation
Sepsis
Drug, e.g. Rifampicin
iii. Decreased bilirubin conjugation due to:
Deficiency of enzyme glucoronosyl transferase
Inherited disorders
Gilberts syndrome
Crigglar-Nijjar syndrome
Acquired disorders due to
Drugs
Hepatitis
Cirrhosis
B. Predominantly conjugated hyperbilirubinemia (Cholestasis)
i. Due to impaired hepatic excretion of bile Suggestive of defect within
the biliary canaliculi or small intrahepatic ducts Medical jaundice
ii. Due to mechanical obstruction of the extrahepatic biliary tree
Obstructive jaundice, (i.e. it is amenable to surgery).
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.
Approach to Diagnose a Case of Jaundice

Imaging in Jaundice 223
Causes of Biliary Obstruction

A. Non-neoplastic
i. Benign strictures
a. Post-traumatic
Surgery and other trauma
b. Post-inflammatory
Chronic pancreatitis
Gallstones (including Mirizzis syndrome)
Pancreatic pseudocyst
Duodenal ulcer
c. Primary sclerosing cholangitis
ii. Intraluminal
a. Biliary calculus
b. Parasite (Hydatid/Ascariasis)
c. Benign tumor, e.g. lipoma, leiomyoma
B. Neoplastic
i. Cholangiocarcinoma
ii. Ampullary carcinoma
iii. Carcinoma head of pancreas
iv. Gallbladder carcinoma
Due to
Infiltration
Lymph node involvement
v. Metastasisto lymph node in porta hepatis region
vi. 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. At hilum (region of porta)
Cholangiocarcinoma
Hepatic neoplasm extending into hilum

Metastasis
Sclerosing cholangitis
B. In suprapancreatic portion of CBD
i. Benign
Infective cholangitis
Surgery or trauma
Mirizzi syndrome
Lymphadenopathy secondary to inflammatory conditions
ii. Malignant
Cholangiocarcinoma
Secondary involvement by tumors of gallbladder and liver
Lymphadenopathy secondary to malignancy
C. 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.
Radiological Investigation
1. 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. 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
Obstruction without Dilatation of Intrahepatic Biliary Radicles

Recent onset obstruction
Fibrosis of CBD wall as in sclerosing cholangitis
Rigidity of the surrounding liver parenchyma, e.g. 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, e.g. Carcinoma
head of pancreas, chronic pancreatitis
Old age
Postcholecystectomy
Stone in CBD causing a ball value effect
3. Computed Tomography
Detects IHBR dilatation and CBD dilatation
Pancreatic mass 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.
Dilated CBD: Seen as rounded hypodense (water density) structure anterior
to IVC which gradually tapers.
4. Direct cholangiography
i. PTC
ii. ERCP
iii. T-tube cholangiography
Preoperative
Postoperative
i. PTC: Percutaneous Transhepatic Cholangiography
Indications
Provide precise definition of site and etiology of obstructive lesion.
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
Complications
Sepsis
Bile leakage
Peritoneal haemorrhage
ii. ERCP Endoscopic Retrograde Cholangiopancreaticography
Rapidly replacing PTC
Safe procedure when prothrombin time is significantly prolonged
Additional advantage of biopsy, sphincterotomy, removal of calculus
and placement of stent
Higher success when the ducts are not dilated.
Contraindications
Apprehensive and unconscious patient
Patient with recent myocardial ischaemia, severe pulmonary disease
Hepatitis B/AIDS
Acute pancreatitis
Acute phase of ascending cholangitis
Pyloric stenosis, duodenal stenosis, esophageal stricture
Complications:
Pancreatitis
Cholangitis
Duodenal perforation
Instrumental injury
5. 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.
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. MRI
Shows dilated IHBR and CBD. Bile seen as hypointense on T1 and
hypertense on T2
Pancreatic lesion
Pericholedochal and portahepatis lymphadenpathy
Infiltrating GB neck mass
7. Hepatobiliary scintigraphy
Radionuclide labeled 99mTc IDA is injected intravenously which are
accumulated by the hepatocytes and secreted into bile and subsequently
into small bowel.
Variable in demonstrating site of obstruction

Liver can be imaged with 99mTc sulphur colloid or albumin colloid for
focal tumor involvement, 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). And 99mTc-labeled DISIDA (di-isopropyl-phenyl
carbamoyl iminodiacetic acid) are used. 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.
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
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, IHBR dilatation may also occur
Impacted Stone in the Cystic Duct (Mirizzis 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, widening of the bile duct proximal to the obstructing calculus
funnel-shaped appearance
Later on, CBD dilatation and IHBR dilatation.
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, 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
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.
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.
USG
Tubular non-shadowing echogenic structures in the dilated bile duct
Central sonolucent stripe is seen when the parasite is alive
Represents the worms digestive tract.
When multiple
Parallel echogenic surface produce a spaghetti like appearance
When coiled:
Appear as a rounded echogenic focus Kla Bulls eye but lacks distal acoustic
shadowing
CT Scan
Seen as hyperattenuating tubular structure surrounded by less attenuated
bile.
Biliary Hydatid Disease

Due to rupture of hepatic hydatid cyst into the biliary ducts.
USG
Laminated hydatid membraneseen s filiform linear material in CBD
Hydatid daughter cystsseen as rounded filling defects
Mixture of hydatid membrane and daughter cystseen 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
ProlongedT-tube placement in the bile duct.
Seen in the mid-common duct near the junction with the cystic duct.
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.
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.
Based on ERCP and PTC, 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.
CT Scan
Proximal dilatation of CBD with smooth tapering stenosis or abrupt cut
off.
POSTINFLAMMATORY STRICTURES
Causes
Chronic pancreatitis
Gall stone
Penetrating duodenal ulcer
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
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, edema
has to be differentiated.
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.
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.
Complication
Cholangiocarcinoma
Diffuse, multifocal strictures of both intra- and extrahepatic bile ducts
which tend to be short (1-2 cm) and alternate with normal or mildly dilated
duct segments Beaded duct appearance.
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, dilated peripheral
ducts with no apparent connection to the central duct Skip dilatation
Stenosis, pruning and beading of the IHBD can be seen.
Extrahepatic bile duct can show:
Stenosis
Dilatation
Wall thickening
Mural modularity
Mural contrast enhancement.
CHOLEDOCHAL CYST
Uncommon congenital cysts of the bile ducts
Manifest in childhood
Clinical Features
Triad of:
Jaundice
RUQ pain
Palpablesubcostal lump
Diagnosis by USG/CT/ERCP/MRCP
Type I : Fusiform cystic dilatation of the CBD
Type II : Eccentric, 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
Choledochal cyst
Liver fluke infestation
TypesDiffuse infiltrating, nodular and papillary
Common sites
CBD30-40 percent
CHD30 percent
Hepatic duct confluence20 percent
Cystic duct < 5 percent
Clinical Features
Jaundice, pruritis, weight loss, anorexia
Cholangiography Reveal
Bluntly tapered stricture with complete or partial obstruction of the duct
and proximal dilatation of biliary duct.
Abrupt complete obstruction with proximal dilatation of the biliary duct.
In Diffuse Infiltrating Type

Diffuse irregular narrowing of the lumen of the bile duct.
In Klastkins Tumour
Dilated Intrahepatic biliary radicles
Abrupt cut off at confluence of hepatic ducts.
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.
AMPULLARY CARCINOMA
Carcinoma of the ampullla of vater.
Appears as irregular polypoid mass, causing distal CBD obstruction without
a demonstrable mass.
Cholangiography
Abrupt cut off of the distal end of CBD with a markedly irregular intraluminal
polypoidal mass.
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 .
Distended gallbladder usually seen
At confluence of hepatic ducts (Klatskins tumour)
Dilated IHBR
Soft tissue lesion at confluence may be seen.
CARCINOMA HEAD OF PANCREAS

Adenocarcinoma arising from the ductal epithelium of the gland
More common is elderly males.
Clinical Features
Upper abdominal pain and weight loss
Jaundice
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 common North Indian
particularly in Eastern belt.
But most common biliary tract neoplasm.
Predisposing factors
GallstoneCommonest association
Chronic cholecystitis
Procelain GB
Clinical Features
Usually elderly female
Pain RUQ
Nausea, vomiting, weight loss
Jaundice
Biliary Obstruction Occurs Due to:

Intraductal spread along the cystic duct into the common duct.
Extrinsic compression of the common duct by enlarged lymph nodes.
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.
USG/ CT Scan
IHBR + CBD dilatation with abrupt cut off at the level of obstruction
Gallbladder mass
Enlarged pericholedochyal lymph nodes.
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, pancreatic or gastric
carcinoma
Metastasis to lymph nodes by lymphoma or other carcinoma
Cholangiography
Abrupt cut off of the common duct with proximal dilatation.
USG/CT Scan
Proximal dilatation with abrupt cut off
May show enlarged lymph node
Abnormal invading organs.
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, 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 changes in pressure (P1P2) along blood vessel are
a function of the interplay between blood flow (Q) and vascular resistance
(R).
P1P2 = Q R
Resistance
Resistance to the flow of blood in vessels can be expressed by Poiscuille's
law:
8nL
R=
r4
where n = coefficient of viscosity
L = length of the vessel
r = its radius
Under physiologic conditions, resistance is mainly a function of change in
radius (r), while contrast L and n are constant. The normal liver may be
conceptualized as a huge and distensible vascular network with very low
resistance. The movement of portal blood across the liver is dependent on the
pressure gradient between the portal and hepatic veins. The volume of portal
flow is regulated by the vascular resistance of the splanchnic arteries. The
components which contribute to increased portal venous pressure are resistance
to flow and increased portal venous blood flow. Depending on the type and
stage of disease, both components may significantly contribute to increased
portal venous pressure.
Flow Block
A flow block causes an increased resistance to flow and leads toward reversal
(hepatofugal or backward flow) of blood. This block can be a mechanical
obstruction in the system. It is found at the microcirculatory level in

parenchyma, blocked by collagen deposition or enlargement of hepatocytes.
The block can be a thrombus, a web in major vessels or an extrinsic
inflammatory or tumor process. Finally the block can be functional, 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.
Increased Flow
Present in chronic liver parenchymal disease as the consequence of complex
circulatory process secondary to metabolic changes leading to hyperdynamic
circulation. Patients have an increased cardiac output, splanchnic vasodilataion
and increased portal venous flow, all of which contribute to portal hypertension.
Collateral Circulation
When portal pressure reaches a critical value, porto-systemic collaterals may
develop in 5 mains territories.
1. Esophageal varices:
Redirection of flow in the coronary vein results in esophageal varices,
because of porta-systemic collateral development.
2. Gastric varices:
Short gastric vein arising from the splenic vein feed the development of
gastric varices in the gastric fundus. The presence of gastric varices without
esophageal varices suggest the possibility of splenic vein thrombosis.
3. Umbilical vein:
Increased pressure in the portal venous system opens the embryonic left
umbilical vein, arising from the Lt branch of portal vein, which then flows
toward the umbilical area.
4. Splenorenal collaterals:
A communciation between the splenic and left renal vein may become
predominant.
5. 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, which drain into the internal iliac venous circulation.
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. However, measurements of lower sphincter pressure
and pH failed to show evidence. Explosion theory in which esophagal wall
tension reaches a critical level and then rupture occurs. (Elevation of portal
pressure to value greater than 100 mm Hg has been observed during the Valsalva
Portal Hypertension 239
maneuver). The genesis of variceal rupture may be related to daily events in

which pressure rises abruptly to extremely high values.
Influence of Portal Hypertension on Other Organs

Hypersplenism
Alterations of the splenic microcirculation, with fibrotic changes in the
splenic sinusoids, favors entrapment of red cells, white cells and platelets.
Hypoxemia : due to functional pulmonary arteriovenous shunting and
vasodilatation of pulmonary capillaries.
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.
Catheterization of the umbilical vein in newborns associated with the
development of omphalitis.
Disorderd coagulation system.
Invasion into portal vein by carcinoma of the head of pancreas/CBD resulting
into cavernous malformation of the portal vein.
Splenic vein thrombosis.
Presinusoidal Intrahepatic Etiologies

Schistosomiasis is the most common entity. Eggs shed into the splanchnic
venous tributaries and lodge in the portal vein radicles within the liver. A
granulomatous, fibrotic reaction develops around the eggs, obstructing portal
venous flow.
Noncirrhotic portal fibrosis (idiopathic portal hypertension) is a common
cause of portal hypertension. Obliteration of small portal venules are its
characteristic feature and liver function is preserved. Inflammatory infiltration
of the portal triads coexist with splenomegaly in the conditions like Felty's
syndrome, lymphoma and sarcoids.
Sinusoidal Etiologies
Alcoholic liver disease.
Nodular regenerative hyperplasia. The nodules in this entity are delineated,
not by fibrous tissue but by collapsed liver parenchymal cells.
Postsinusoidal Etiologies
A common pathophysiologic change is the transformation of the portal vein to
an outflow vessel, with flow in the portal vein directed toward the collateral
circulation (hepatofugal flow). Such as Budd- chiari syndrome, constrictive
pericarditis, pulmonary hypertension.
Conventional radiological investigationplain X-ray abdomen and chest,
Barium meal; penetrated dorsal view of dorsal spine may reveal following
observations:
Cardiomegaly
Altered paraspinal line
Calcification in liver and spleen which may show enlargement.
Esophageal, gastric, duodenal, jejunal, Iliac varices and hemorrhoids, anterior
displacement of duodenal loop (Clatworthy's sign +ve). These varices are
typically shown as round / oval-filling defect or serpentine filling defect
particularly in esophagus.
SONOGRAPHIC AND COLOR DOPPLER FLOW IMAGING

EVALUATION OF PORTAL HYPERTENSION
It is one of the most useful clinical monitoring device, as it provides:
Vascular anatomy and changes in calibre of vessels.
Vascular patency and presence of thrombus.
Detection of portosystemic collaterals.
Detection of flow and its direction
Characterization of flow and quantification
Evaluation of organ parameters and associated abnormalities secondary to
disease.
Sonographically the main portal vein measures 13 to 15 mm, 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, 47 an 45 percent.
Vascular Signs of Portal Hypertension

Dilatation of portal, splenic and superior mesenteric veins.
Decreased respiratiory variations in superior mesenteric and splenetic vein
and inspiratiory calibre change of less than 4 percent, has 80 percent
sensitivity.
Dilated hepatic artery and splenic artery.
Spontaneous portosystemic shunts with detection of collaterals.
Decreased number of peripheral portal branches in the liver.
Decreased flow volume in the portal vein.
Abnormal Doppler waveform in the hepatic veins.
Hepatofugal flow.
Other Signs
Thickened GB wall
Splenomegaly
Increased thickness of lesser omentum in children as a result of lymphatic
stasis.
Ascites, a non-specific sign.
The most reliable evidence of portal hypertension is presence of collaterals
and the extent of the shunt flow.
Calibre of gastric vein more than 7 mm indicates a portahepatic pressure
gradient above 10 mm Hg.
Specific Changes
Cirrhosis of liver is the commonest cause of portal hypertension. It is a
chronic hepatic parenchymal disease of diverse etiologies in which injury
and regeneration of parenchyma is; accompanied by increase in connective
tissue formation resulting in destruction of normal architecture which causes
portal hypertension.
Sonography shows: Increased parenchymal echogenicity and poorly
delineated intrahepatic portal venous walls.
Sonographic ratio of right / left lobe of liver should be 1:3 or less.
Caudate lobe / right lobe ratio maintains with that of 5:4 or more.
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:
Qualitative: Presence of flow, direction of flow and characteristic of flow.

Hepatofugal flow is indicative of very severe portal hypertension. Presence
of hepatofugal flow has been shown to significantly reduce incidence of GI
bleeding, as this creates a situation similar to surgical Portosystemic
anastomosis.
Characteristics of Doppler Spectra of Hepatic Vein

in Portal Hypertension
The normal 3 phase tracing of hepatic vein may be completely abolished,
which may be due to reduced compliance of fibrotic liver.
Doppler spectra in normal portal veins are generally of low velocity,
homoplastic signal with minimal respiratory variation.
Heaptic artery of more than 4 to 6 mm diameter with RI 0.78.
Significantly reduced PI value of superior mesenteric artery (SMA) is
reported in cirrhotic PHT and not in NCPF.
Patent paraumbilical vein with hepatofugal flow is seen more in NCPF.
Reversal of flow in splenic vein with enlarged renal vein draining into the
IVC.
Short-gastric veins with flow towards diaphragm, gastroepiploic and
esophageal varices and flow reversal in SMV.
Quantitative CDFI Findings

Quantification of portal vein flow with CDFI is reduction in velocity in
cirrhosis. The exact reduction reported is variable depending upon stage
and etiology of cirrhosis, extent of collaterals flow diversion which varies
from patient to patient and also limitation of technique.
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: It is a ratio of cross- sectional area of PV and flow velocity
and shows a definite increase in cirrhosis. Congestive index above
0.13 cm/sec has 67 percent-sensitive.
Risk of Hemorrhage
The incidence of variceal bleeding is significantly reduce in patients with
doppler evidence of large Paraumbilical and hepatofugal flow.
The variceal bleeding significantly higher in the patients with heapatopetal
flow.
Congestive index has been shown to have significant correlation with
predicting bleeding.
Portosystemic Surgical Shunt Follow-up

Evaluation of potency of shunt.
Flow can be visualized directly through the anastomosis in portocaval shunt.

When actual anastomosis and flow cannot be seen, evidence of hepatofugal
flow in intrahepatic portal branches is considered and indirect sign of
potency.
Evidence of significant hepatopetal flow in late follow-up of shunt is
suggestive of anastomotic thrombosis.
Endoscopic Doppler Ultrasound

It has made hemodynamic evaluation of gastric and per esophageal vascular
bed and azygos vein.
7.5 MHz convex transducer with 100 visual angle incorporated
longitudinally with a fiber-optic scope.
Azygos vein can be localised at a distance of 20 to 25 cm from incisors
and is localised by first identifying aorta.
Doppler azygos flowmetry reveals:
1. Significant increase in flow in esophageal varices.
2. 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. Non-visualization of extrahepatic portal vein.
2. Bright echogenic band representing either thrombus or periportal fibrosis.
3. Periportal collaterals.
Portography: Roentogenographic visualization of the portal venous system
achieved by introduction of contrast into the system.
Indication
1. Equivocal cases where adequate information is not available by a color
Doppler study.
2. Identifying the site of bleeding varices.
3. Postoperative determination of portosystemic shunt.
4. Prior to TIPS.
Techniques
1. Splenoportovenography (SPV)
2. Arterioportography
3. Transhepatic / transjugular portography
4. Umbilical portography
Arterial Portography
Injection of contrast medium into the splenic / celiac artery and SMA, to opacify
the portal venous system in its venous phase.
Technique
Percutaneous Seldinger technique through right femoral or axillary artery.
Celiac artery and / or superior mesenteric artery are selectively engaged
using a preformed visceral catheter.
Contrast material is injected at the rate of 9 to 13 cc./sec in amount ranging
from 35 to 50 cc by means of a pressure injector.
The veins are best seen between 14-20 seconds.
The filming sequence is used to cover 31 seconds, usually 1 film/sec for
7 seconds, and then 1 film every third second for 24 seconds.
The normal splenic or celiac artery injection delineates the splenic and
portal vein only, without opacification of collaterals.
The SMA injection shows the SMV and PV and no contrast enters the
splenic vein.
Points to be Observed During Interpretation

1. With celiac or splenic artery injection both splenic or portal vein are seen.
Opacification of inferior mesenteric vein or superior mesenteric vein is
unequivocal evidence of hepatofugal blood flow.
2. 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, then it is significant.
3. Left gastric vein opacification on splenic artery injection suggests
hepatofugal flow.
4. The superior mesenteric artery injection will be normal even if splenic vein
is thrombosed.
5. If SMA or CA injections fail to show patent PV, then wedge venogram or
intrahepatic parenchymal injection is successful in demonstrating
hepatofugal flow in portal vein.
Splenoportovenography (SPV)
Shows better opacification of portal axis than arterioportography.
Technique
Size of the spleen is assessed.
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.
The needle is inserted into the spleen, directing it in an upward and inward
direction, towards the splenic hilum.
Rapid hand injection of 30 ml of contrast (10 to 12 ml / sec) is given but
better to use pressure injector.
Films are taken in the following sequence : 2 films per sec for 2 sec,
followed by 1 film every 2 sec for 8 sec, followed by 1 film every 5 sec
for 5 sec.
Immediately after the needle is withdrawn, pressure is to be maintained at

punctured site. Vital signs monitored for next 6 hrs and bed rest is advised
for another 6 hrs.
The Normal Splenic Vein / Portal Vein Anatomy

The splenic vein is 5 to 13 cm in length and 1to 1.5 cm in diameter.
The portal vein is 6 to 8 cm in length, 1.2 to 2 cm wide usually straight and
forms an angle of 40 to 90 degree with the spine,
Splenic and portal vein PV joins at angle 90 to 140 in 80 percent cases.
Normally, no reflux is seen into tributary channels (IMV, SMV, left gastric)
or collaterals.
Abnormal Splenoportography Reveals

1. Obstruction at or near the splenic hilum.
a. Nonfilling of the splenic/portal vein.
b. Filling up of bridging collaterals.
2. Obstruction at the formation of portal vein.
a. Dilated splenic vein up to this site with nonvisualized portal vein.
b. Filling up of collaterals/tributaries.
3. Obstruction of distal portal vein.
Advantages of Splenoportogram
1. Better opacification of splenoportal axis.
2. Simultaneous measurement of splenic pulp pressure.
Contraindications
1. Nonpalpable spleen/splenectomy.
2. Coagulation disorder
3. Splenic pathologies such as tumor, abscess
4. Arteriovenous fistula/trauma
5. Severe ascites
6. Severe hepatic failure
Complications
1. Splenic rupture/subcapsular injection.
2. Intraperitoneal/intracolonic/intrapleural injection of contrast.
3. Hemorrhage
Percutaneous Transhepatic Portography

Second most common procedures to investigate portal hypertension.
Advantages
1. Once catheterized, the catheter can be placed into any part of the splenoportal
axis.
2. Contrast density is much superior to any other portographic method.
3. Manometric studies can be conducted at any point in the portal venous
system.
4. Intervention in bleeding varices is possible.
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.
Once the right portal vein punctured, the inner needle is removed and
contrast is injected.
A guide wire is advanced through the sheath into right branch of portal
vein and then on portal vein proper.
Contraindications
1. Coagulopathy
2. Severe ascites and local problems (subphrenic abscess hemangioma etc.)
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.
Scanning is started at 55 to 60 seconds delay after the on set of the injection.
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.
Advantages
1. It is noninvasive and easier to perform.
2. MIP images are more acceptable to surgeons.
3. It is effective in demonstrating occlusions of the PV, SV, or SMV because
of opacification irrespective of the direction of flow.
4. CT angiography enables imaging of the SV and SMV from a single contrast
injection.
5. It is particularly useful when occlusion is due to direct tumor invasion or
thrombosis.
6. It gives superior detail of intrahepatic and extrahepatic PV and hepatic vein
branches compared to other techniques.
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.
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
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.
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.
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 Palliationadvanced malignant
obstruction
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;
Wellequipped 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.
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 malignancycholangiocarcinoma) 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 operators 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
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.
Following gradual maturation of the transhepatic tract to an adequate caliber

relative to the observed size of calculi, a steerable remote-control catheter can
be introduced over a guide wire into the tract. A conventional biliary stone
basket (Dormia) can then be introduced through the steerable catheter. Most
calculi can be directly withdrawn through the transepatic parenchymal tract,
and larger calculi may be fragmented and the fragments engaged in the basket
and directed caudally into the duodenum. Direct transcatheter instillation of
stone solvents, especially the cholesterol solvent monooctanoin, has also
continuous infusion at 4 to 10 ml/hr may be required, for upto two to three
weeks, depending on the number, size, and location of the calculi.
Tissue Biopsy Techniques

Available methods for pathologic diagnosis include bile cytology, percutaneous
needle aspiration biopsy, transcatheter brush biopsy, and transcatheter forceps
biopsy.
Cytologic examination of bile obtained following percutaneous catheter
insertion. 10-20 ml bile sample are routinely sent for cytologic analysis.
Fine-needle aspiration biopsy can be performed in the area of bile duct
stricture under fluoroscopic control. The yield of positive cytologic material
with fine-needle aspiration techniques approaches 90 percent.
Brush biopsy through the percutaneous catheter can be carried out with
to-and-fro and rotary movement.
Transcatheter forceps biopsy techniques have been infrequently reported.
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.
TRANSCHOLECYSTIC INTERVENTION
Diagnostic percutaneous puncture of the gallbladder.
Indications
i. To obtain a diagnostic aspirate
ii. Cholangiogram
iii. Opacification of the biliary tree though gallbladder under ultrasound
guidance is indicated when PTC and ERCP have failed.
Technique
An initial assessment of the liver and biliary tree is made using real time
ultrasound and the point for puncture selected. Ideally, this will be in the
right subcostal area so that the needle will traverse liver parenchyma and
enter the body of the gallbladder.
The abdominal wall is infiltrated with 1 percent xylocaine, and skin is

nicked with scalped blade.
Under US guidance the body of the gallbladder is punctured with a 22-
guage spinal needle.
With the needle tip in the lumen of the gallbladder a specimen of bile is
aspirated and sent for gram stain and culture/ sensitivity.
For cholangiography as much bile as possible is aspirated before injection
of 60 percent contrast under fluoroscopic control.
The technique of percutaneous fine-needle aspiration biopsy of the
gallbladder is essentially the same as that for diagnostic puncture, although the
needle tip is directed into the lesion while using USG.
Complications
1. Intraperitoneal bile leakage
2. Bleeding into GB
GALLBLADDER DRAINAGE
Indication
In the patient who is very ill on presentation or who only requires short-term
drainage, the percutaneous cholecystostomy can provide a quick and safe
means of interim drainage.
Technique (Transhepatic or Transperitoneal)

The puncture site is chosen with US guidance
If there are problems with a transhepatic route (hepatic metastases), 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.
6.7 F Mc Gahan catheter has been placed and properly fixed internally and
externally, all the bile and contrast is aspirated from the gall bladder. The
catheter is then attached to a gravity drainage bag.
No attempt should be made at this time to obtain a cholangiogram, remove
stones; to do so risk of vasovagal reaction, sepsis and leakage are always
there.
Complications
i. Bile leak
ii. Colonic and duodenal perforation
iii. Sepsis
iv. Vasovagal reactions (during procedure)
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.
Technique
A small incision is made in the fundus just large enough to accept a 24 F
Foley catheter.
The Foley balloon is inflated and the fundus sutured to the peritoneum and
posterior rectus sheath.
About the seventh postoperative day the Foley catheter is removed over a
guide wire, a cholangiogram is performed, and calculi within the gallbladder
removed using standard interventional techniques.
For removal of intact stones using forceps or a stone basket or fragmentation
of large stones with subsequent extraction of the fragments.
A transhepatic approach to the gallbladder will allow tract dilatation
approximately. 1 week after the initial cholecystostomy.
T-tube tracts, calls for a 4-week period of tract.
Complications
i. Wound infection
ii. Wound hematoma
iii. Injury to the colon
iv. Perforation of the cystic duct
v. Cholangitis
vi. Failure of catheter placement
INTRACORPOREAL BILIARY LITHOTRIPSY

Principle
Intracorporeal biliary lithotripsy (IBL) requires two components, an electrode
and an EHL generator. Electrodes are available in 3.5, 9F diameters when a
potential difference is introduced across the electrode, a spark is produced at
the tip of the electrode. The spark vaporizes fluid, resulting in a cavitation
bobble. Which in turn create a hydraulic shock wave in the fluid of the bile
duct. The energy of the hydraulic shock wave is transferred to the stone at the
fluid-stone interface and fragments the stone.
Technique
We have used intracorporeal EHL from a variety of percutaneous access routes,
including T-tube tracts, transhepatic tracts, and directly into the gallbladder.
Standard practice is to remove all biliary calculi using a choledochoscope

with a combination of fluoroscopic guidance and direct visualization.
The T-tube is removed over a guide wire, the tract is dilated to 18 F by
using coaxial dilators (Dilators Cook, Bloomington).
The 18-F thin-walled Teflon sheath allows easy access to the biliary tree
with the flexible 15-F choledochoscope.
Using direct vision with the choledochoscope, bring the electrode almost
into contact with the stone and are careful to avoid contact with the wall
of the bile duct.
The fragments subsequently are irrigated and flushed through the sheath.
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.
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
Unproven
As initial therapeutic intervention for acute variceal hemorrhage. Initial therapy
to prevent recurrent variceal hemorrhage. Therapy for prevention of 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 procedure can be performed under conscious, sedation or general

anesthesia for uncomperative patient.
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, 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.
The 9-F catheter is advanced over the Colapinto needle and guidewire 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 portosystemic gradient less then 12 mm Hg after creation of TIPS is
satisfactory.
Complications
Technical Bleeding (extrahepatic needle puncture)
Stent related (shortening, migrations, occlusion)
Hemodynamic Hepatic encephalopathy (20-40%)
Cardiac failure
Late Restenosis and thrombosis of the shunt (25%)
ENDOSCOPIC RETROGRADE CHOLANGIOGRAPHY

Indications
I. Diagnostic indications
A. Jaundice of undetermined etiology
Extrahepatic biliary obstruction
a. Stones
b. Tumor
c. Strictures
d. Sclerosing cholangitis
e. Sphincter of Oddi dysfunction
Intrahepatic biliary obstruction
a. Hepatitis
b. Drug-induced cholestasis
c. Cirrhosis
d. Malignancy
Endoscopic cytology and biopsy

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

Extrahepatic Bile Duct Abnormalities
Most common are choledocholithiasis and stricture.
Filling defects within the CBD, when persistent are almost always due to
calculus.
Stones rarely completely obstruct the duct unless impacted.
Stones do not locally expand the common duct.
Strictures involving the distal CBD include pathology in the pancreas as
differential diagnosis.
If a stricture is encountered, the mucosal details should be examined in the
region of the stricture.
Infiltrating process may lead to irregularity which makes confusing
diagnosis of malignant stricture.
Unfortunately, malignant strictures may have a very smooth and symmetric
appearance.
Benign strictures of the distal common duct are most commonly seen in
chronic pancreatitis.
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.
The pancreaticgram may confirm the presence or absence of chronic
pancreatitis.
Strictures of proximal duct, in the absence of previous surgery, must be
considered to represent malignant disease.
Complete obstruction of the extrahepatic bile ducts almost invariably due
to some malignant lesion.
There are several congenital abnormalities where ERCP is well suited for
studying choledochoceles.
Intrahepatic Bile Duct Abnormalities

Observations on bile ducts that need to be made to interpret, include,
diameter, splaying separation or crowding, caliber irregularities, strictures,
presence or absence of stones, communication with parenchymal spaces
(abscess) and obstruction.
Cirrhosis is the most common entity produces bizarre appearance, areas
of stenosis and ectasia and ductal irregularities due to regenerating nodules
and chronic fibrosis are marked.
Metastatic disease the most common change include stenosis, obstruction
and mass effect.
Abscesses, may produce mass effect or may directly communicate with
the biliary tree.
Endoscopic Cytology and Biopsy

Brushing of the stricture directly or collection of bile for cytology can confirm
the malignant of 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 > 2.5 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, 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.
Can be perfused mono-octanoin or bile salts to reduce the size of stones
Catheter is used to perform repeat cholangiography.
Internal Transpapillary Stent

This is usually done for benign or malignant strictures in high-risk patients.
Pigtail catheter can be fashioned across bile duct strictures.
PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY (PTC)

First described by Huard and Do Duan in 1937.
Indications
1. Procedure of choice when endoscopic cannulation is impossible
Examples:
a. Previous biliary tract surgery (hepaticojejunostomy)
b. Gastric outlet obstruction
c. Ampulla is located in duodenal diverticulum
d. Contraindication for ERCP.
2. Procedure of choice because of underlying pathology

Examples:
a. Biliary obstruction at the liver hilum
b. If the only purpose is sufficient drainage for palliation.
3. Procedure complementary to ERCP
Examples:
a. Failure to cannulate papilla
b. Hilar tumor.
Technique
Under antibiotic cover and following correction of any pre-existing
coagulopathy the liver is punctured using a chiba needle under fluoroscopic
control and, 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, 4%), biliary peritonitis (1, 45%), hemorrhage (0, 35%)
Less common: Pneumothorax.
18
Abdominal Tuberculosis
Tuberculosis is an ancient disease. Hippocrates, who called tuberculosis as
Phthisis (derived from the Greek words phthiein,, means to decay)
appreciated the severity of tuberculous enteritis as a complication of pulmonary
tuberculosis. He noted that the Phtisical persons, the hairs of whose head fall
off, die if diarrhea sets in diarrhea attacking a person with phthisis is a mortal
sign (Paustian 1985). The first well documentated case of tuberculous peritonitis
was described from the New York Hospital in 1843. Intestinal tuberculosis
became a common diagnosis in the early 20th century, as most cases of small
intestinal thickening and narrowing were attributed to the recently identified
tubercle bacillus (Horvath 1998).
Epidemiology
Tuberculosis remains one of the deadliest disease in the world. WHO estimates
that every year more than 8 million new cases of tuberculosis occur and
approximately 3 million persons die from the disease. 95 percent of tuberculosis
occur in developing countries where few resources are available to ensure
proper treatment and where HIV infection may be common. It is estimated
that between 19 to 43 percent of the worlds population is infected with
M. tuberculosis. Abdominal tuberculosis may mimic a variety of gastrointestinal
disorders, whereas only 10 to 15 percent non-HIV infected patients have extra-
pulmonary manifestations. The incidence is about 50 percent in patients with
AIDS. Intestinal tuberculosis was recognized as the most common complication
of active pulmonary tuberculosis in the first half of the 20th century. Enteric
involvement was found in 6 to 90 percent patients with pulmonary tuberculosis
in necropsy and radiological series. Antitubercular drugs developed in 1940
and then incidence of tuberculosis began to decline in the 1950s with the
pasteurization. From 1953 to 1985, an average annual decrement of 4.5 percent
per year was reported in United States with the total number of annual cases
of tuberculosis falling from 84304 to 22201. In the beginning of 1985, a
resurgence began in the total number of new cases and peaked in 1992 related
to the emergence of multiple-drug-resistant (MDR) tuberculosis; and HIV/
AIDS epidemic. During this period, number of individual infected, increased
by 20 percent above that period in the nadir 7 years earlier. However since
1992, the number of tuberculosis cases in the United States has declined steadily,
with a historical low in 2001, of 5.6 cases per 100,000 population (CDC
surveillance reports 2002).
Classification of Abdominal Tuberculosis

1. Gastro intestinal tuberculosis
Ulcerative
Hypertrophic or hyperplastic
Sclerotic
Diffuse colitis
2. Peritoneal tuberculosis
Acute tubercular peritonitis
Chronic tubercular peritonitis
Ascitic form
Encysted form
Fibrous form
Adhesive type
Plastic type
3. Tuberculosis of mesentery and its contents
Mesenteric adenitis
Mesenteric cyst
Mesenteric abscess
Rolled up omentum
4. Tuberculosis of solid visceras
Liver, biliary tract and gallbladder
Pancreas
Spleen
5. Miscellaneous
Retroperitoneal lymph node tuberculosis.
GASTROINTESTINAL TUBERCULOSIS
Abdominal tuberculosis is endemic in India. Patient might develop one of the
three main types of disease
Intestine
Peritoneum
Mesentery and mesenteric lymph node
Pathogenesis
a. Infection may develop primarily in the GI tract or it may be secondary to
a focus elsewhere in the body; commonly in chest, ingestion of tubercle
bacilli (M. bovis)
b. Hematogenous spread of the tubercle bacillus from an extraintestinal focus
c. Bile containing tubercular bacilli
d. Extension from contiguous organs, e.g. female adnexa.
Abdominal Tuberculosis 267
Histopathogenesis
Marked inflammation, edema, lymphatic infiltration and tubercle formation
(caseous necrosis).
Gross Appearance
Ulcerative type Secondary to hematogenous spread. Transverse, napkin
ulcer, dont penetrate muscularis propria, occur due to endarteritis. The lumen
is narrowed resulting in a napkin ring type of stricture.
Hypertrophic type Ileocecal region is involved, showing marked
inflammatory and fibroblastic reaction in submucosa and mucosal surface to
present as mass lesion.
Ulcerohypertrophic type Combines the features of ulcers, nodules,
pseudopolyp, hyperplasia and stenosis.
Diffuse colitis endoscopically very similar to ulcerative colitis and can not
be differentiated on the basis of mucosal appearance alone.
Site of Involvement Ileocecal region is the commonest followed by ileum,
jejunum, cecum, colon (ascending) duodenum, stomach, esophagus and
appendix.
Clinical Features
Diseases can affect any age group. Commonest 20 to 40 yrs
Female predominance has been described in Indian series.
Abdominal pain most common symptom and present in almost every
case.
Fever in 40 to 70 percent.
Diarrhea 11 to 20 percent mucus in stool, blood and frank pus rarely
observed.
Diarrhea alterating with constipation 8 to 20 percent
Weight loss
Anorexia
Malabsorption due to extensive ulceration, lymphatic obstruction or bacterial
over growth.
Moving lump in abdomen.
Nausea and vomiting
Malena
Constipation
Menstrual abnormalities (in about 1/3 pts)
Intestinal obstruction (66.2%)
Perforation (16.6%) (from a series of Bhansali)
Peritonitis (13.6%)
Acute appendicitis (3.6%)
Possible Routes of Infection

1. Direct invasion by suggested organism
2. Hematogenous spread
3. Infected bile
4. Extension from diseased adjacent organ
Direct Invasion by Suggested Organism

Primary intestinal tuberculosis can result from food containing tubercule bacilli
specially milk. With widespread pasturization of milk disappearance of bovine
tuberculosis is observed. This mode is no more significant however isolated
cases of primary tubercular enteritis, can also occur.
Secondary Intestinal Tuberculosis

Secondary infection of gut may arise from contamination of intestinal chyme
by bacteria from another site, usually the lungs, through swallowing of infected
sputum. Intestinal involvement after ingestion of infected material is related to
number and virulence of the suggested organism and the nutritional status of
the patients. After ingestion, tubercle bacilli pass through the stomach (where
it is protected against digestion by its fatty capsules) into the small bowel. Site
of involvement is influenced by
1. Abundance of Lymphoid tissue
2. Increased physiologic stasis
3. Increased rate of electrolyte and water absorption
4. 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.
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.
Extension from Contiguous Organs

Enteric tuberculosis may occur by direct extension from infected adjacent
organ and tissue e.g. the female adnexa.
Fistulae like entero-enteric, entero-vesicular, entero-cutaneous are
encountered due to penetrating abscesses. Intestinal narrowing occur due to
extrinsic compression by lymph node. More commonly caused by adjacent
tubercular lymphadenitis, which cause colonic traction, diverticula, narrowing,
fixation and sinus tract formation.
Physical Signs
Ill and Malnourished patient appearance.
Abdominal distension due to ascites or intestinal obstruction. A palpable mass
due to hyperplastic cecal tuberculosis, LN enlargement and rolled up omentum,

classical doughly abdomen are seen in 6 to 11 percent. Free intestinal perforation
presents as peritonitis.
COMPLICATION
Intestinal obstruction
Perforation/abscess
Fistula formation
GI bleeding
Enterolithiasis
Traction diverticula
Small Intestines and Ileocecal Tuberculosis

Barium Meal follow through Observations
1. Disturbance in motility with accelerated transit time, hyper-segmentation
and flocculation of barium suggestive of malabsorpthin pattern.
2. Thickening of mucosal fold with scalloping and spicule formation.
3. Stellate ulcer.
4. Steirlins sign lack of barium retention in the inflamed segment of
ileum, cecum or ascending colon.
5. String sign A persistent narrow stream of barium.
6. Dilatation and stasis proximal to stenotic segment.
7. Filling defects in the cecum (due to thickening of ilio-cecal valve,
inflamatory mass).
8. Fleischeners sign Broad based triangular appearance of terminal ileum
with base at the cecum this is not seen in Crohns disease.
9. In healed stage shortening, narrowing of cecum PURSE STRING
SHAPE, shortening of ascending colon, incompetent ileocecal valve.
10. Enterolith.
11. Raised up cecum, obliteration of ileocecal angle, effacement of terminal
ileum mucosal pattern are other signs.
Differential Diagnosis
Ulcerative colitis
Crohns disease
Ameboma
Carcinoma
Actinomycosis
Vascular occlusive disease
Tuberculosis of Colon and Rectum

Hematochezia was common presentation.
Ulcerative, hypertrophic, diffuse tubercular colitis.
Short segment of colon is envolved (5-7 cm), DCBE study is helpful.
Multifocally scattered shallow ulcers (aphthous ulcers)

Transverse ulcer, nodularity of mucosa. Rose thorn ulcers
Thickened folds
Inflammatory or post inflammatory polyps. Inflammatory polyps are caused
by ulceration surrounding and undermining portion of intact mucosa. Post
inflammatory polyps comprise of excessively regenerated mucosa
Luminal narrowing and stenosis
Hypertrophic mass causing filling defect.
Anal Canal
These ulcers are shallow with bluish undermined edge.
Ulcers and fissures common, lupoid, verrucus, miliary lesion.
Fistula, abscess formation.
Hypertrophic exophytic growth 16 percent tubercular fistula in ano.
Inguinal lymph node.
Esophagus
1st report by Denonvilliers (1837). Primary esophageal TB by Torek (1931).
Direct spread from caseating tubercular lymphnode in the mediastinum
involving esophagus.
Ulceration, thickening of wall, exophytic growth
Esophageal stricture (common in upper part) when in lower esophagus
it is malignant stricture and achalasia;
Traction diverticulum
Fistula between esophagus and mediastinum, trachea or bronchus.
Pseudotumor mass
Common presentation are dysphagia, odynophagia, aspiration due to fistula,
hematemesis.
Stomach
Clinical feature : abdomen pain, nausea, vomiting, GI bleed, fever 1 percent
incidence at autopsy.
Tubercular ulcer are commonly seen in the Pylorus, as shallow extensive
ulcers
FibrosisLinitis Plastica like pattern leading to gastric outlet obstruction.
Extrinsic compression by lymph node
Exophytic mass
Incidence1 percent at necropsy. Rarecause (1) acid, (2) Rapid transit
of ingested organism (3) Scarcity of lymph follicle in gastric wall (4) Intact
gastric mucosa.
Duodenum
2.5 percent incidence. Clinical featuresdyspepsia, pain, weight loss, upper

GI bleed, epigastric mass.
Ulceration and stricture in III part of duodenum with narrowing of lumen.

Hypertrophic mucosa resembling polyps
Distorption of the C-loop by lymphadenopathy
Healing Contraction Stenosis Obstruction.
Sonography 2nd Modality of imaging
1. Pseudokidney or target sign.
2. Demostrates all features of tuberculosis as patients tend to be emaciated
which provides a good acoustic window for a thorough examination.
3. Graded compression technique can be used to displace dilated and air
filled bowel loops from the region of interest.
4. Circumferential thickening of bowel wall (> 3 mm), thickened medial
wall of cecum
5. Deep ulceration can be detected as radial extension of echogenic luminal
contents into thickened wall.
6. Areas of narrowing representing stricture, hyperperistalsis proximal to
stricture.
7. Enteroliths appear as echogenic foci.
8. Lymphadenopathymesenteric, porta hepatis, peripancreatie round or
oval in shape with echogenic capsule.
9. Matted L.N. hyperechoic centre (Caseation), area of calcification.
10. TRUS and TVS helps for rectovaginal and rectovesical fistulae
demonstration.
11. Ascites free or loculated ascites, floating bowel loops, multiple fine,
complete or incomplete and mobile strands of fibrin and debris are seen.
CT Scan Most modern imaging techonology:
CECT
Mural thickening limited to the terminal ileum, cecum or ileocecal region.
Usually concentric thickening. Occasionally eccenteric involvement of the
medial rectal wall.
Low density areas representing necrosis in the wall.
Skip area of concentric mural thickening may be seen elsewhere in the
bowel.
Lymphnode Involvement
CT shows enlarged LN with hypodense centre and peripheral enhancing
rim
Diffuse enlargement
Mesenteric, peripancreatic, portal, para-aortic lymphnodes are involved
Congulomerate mixed density nodal mass
Enlarged nodes of homogeneous density associated with low density nodes
at other sites.
Increased no. (> 3 in once cut section) of normal size or mildly enlarged
mesenteric nodes usually located along the mesenteric vessel.
LN calcification.
On CT scan low attenuating adenopathy with rim enhancement.
Omental or ileocecal mass
Enteritis involving ileocecal region.
PERITONEAL TUBERCULOSIS
Peritoneum is a common site of involvement in the abdominal tuberculosis.
Tubercular peritonitis is a frequent cause of ascitis in underdeveloped countries.
1st documented case was described in 1843 at autopsy of 43 old seaman
(Dineen 1976). Incidence 0.1 to 3.5 percent.
When involved, showed peritoneal thickening in 14 to 100 percent of cases.
May show tiny nodule, diffuse regular, echopoor peritoneal thickening of
2 to 6 mm or irregular thickening with tiny nodule of < 5 mm size.
PathogenesisTwo accepted mechanisms:
1. Hematogenous spread of bacilli from active pulmonary lesions
2. Activation of a long latent foci of tuberculous infection of the peritoneum.
Others contiguous spread from lesions in intestine or fallopian tubes.
Clinical Features
Abdominal distension by ascites
Anorexia.
Three Types of Tubercular Peritonitis

a. Wet ascitic typeascites with pockets of loculated fluid with a thickened
mesentry.
b. Plastic typeenlarged mesenteric L.N. with central caseational necrosis
and adhesion of bowel loops.
c. Fibroticthickened omentam with a mass.
Chest skiagram 50 percent had pulmonary tuberculosis and 1/6 will have
active disease.
USG Findings
Free or loculated ascites. Free ascitic fluid is commonly seen. It may be
anechoic or contain debris. Lacy strands or fine septa and low level echoes
are characteristic of exudative ascites.
Focal ascitesinterloop 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 thickening appears as a irregular sheet like hypoechoic layers.
Mesenteric thickening (13-47 mm) can be seen in left upper quadrant,

paraumbilical region, right lumbar region and right lower quadrant.
Increased echogenecity of the mesentery (lymphatic obstruction) and fat
deposition.
Mesenteric lymphadenopathy
Omental thickening with hypoechoic nodules Omental cake appearance.
CT Scan
High density ascites (24-45 HV) is characteristic of T.B. which is due to
high protein and cellular content in tubercular exudates.
Peritoneal enhancement with uniform thickening of peritoneum
Nodular implants with irregular thickening are extremely uncommon and
should suggest peritoneal carcinomatosis.
Mesentery may show increased density with soft tissue strands, thickened
and crowded vascular bundles or stellate sign. In extensive involvement,
there is diffuse infiltration of mesentery by soft tissue density masses with
mesenteric abscesses.
Involvement of omentumomental cake, nodularity or smudged
appearance.
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).
Hepatic TB with large abscess and nodules or tuberculoma have been
reported by leader (1952).
Hepatic tuberculosis have been classified into three:
1. Miliary form
2. Granulomatous disease (tuberculous hepatitis)unexplained fever, mild
jaundice, hepatomegaly , caseating granuloma showing improvement with
A.T.T.
3. Localized hepatic tuberculosis
a. Without bile duct involvement to include solitary or multiple nodules,
tuberculoma or hepatic abscess
b. With bile duct involvement causing obstructive jaundice either by
enlarged L.N. or inflammatory stricture.
Sex ratio 2:1 M:F
Age 11 to 50 years
Clinical Features
Abdominal pain (45-66%)
Fever (63-90%)
Weight loss (55-75%)
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.
Sonographically liver is either
Macronodular - single / multiple nodule which

may be hypoechoic or hyperechoic with or
without calcification.
Pancreatic Tuberculosis
Rare, occurs more often in immunocompromised patient (Brusko 1995) result
of lympho-hematogenous dissemination or direct spread from other adjacent
organ.
Clinical Features
Anorexia
Malaise
Low grade fever
Weight loss
Night sweat
Malena
Mass/abscess
Obstructive jaundice
Head of pancreas-most commonly involved.
Body and tail - uncommon
Single hypoechoic well defined mass
Peripancreatic lymphnode enlargement
Rarely calcification seen.
It may present as either acute or chronic pancreatitis or may nimic
malignancy.
FNAC differentiates Ca, lymphoma, sarcoidosis or chronic pancreatitis.
Splenic Tuberculosis
Present either as hypersplenism or abscess or rarely as solitary tumor (Sheen
chen 1995) fever, weight loss, LUQ pain, diarrhea, multiple abscess seen in
HIV patients.
The patient may present either as miliary tuberculosis, homogenous splenic
enlargement or macronodular splenic enlargement.
Small Bowel Mesentery

Micro (< 5 mm)
Mesenteric changes - Nodular lesions
Macro (> 5 mm)
Mesenteric thickening
Loss of normal mesenteric configuration

They are solid, cystic lymphonode or abscess.
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.N.
Mesenteric thickness in healthy person ranging from 5 to 14 mm.
DIAGNOSIS OF ABDOMINAL TUBERCULOSIS

Diagnosis is based on one of the following criteria:
1. Isolation/detection of M. tuberculosis from diseased tissue or exudates
and secretion of diseased tissue.
2. Detection of DNA of M. tuberculosis from diseased tissue or exudates and
secretion of diseases tissue.
3. Presence of caseating granuloma/non-caseating granuloma with Langerhans
giant cell in diseased tissue.
4. Non caseating granuloma are characteristic radiological features or
characteristic laboratory finding or serologic positively with clinical response
to A.T.T.
Chest X-Ray
Active pulmonary TB
Pleural effusion
Healed/calcified pulm TB.
Plain X-Ray Abdomen

Calcified L.N.
Calcified granuloma in spleen, liver, pancreas and dilated loops with fluid level,
dilated terminal ileum, ascites, pneumoperitoneum.
TRIAD - Ascites
Absence of gas shadow in right iliac fossa.
Segmental dilatation of terminal ileum.
Barium Studies Discussed earlier in detail.
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. Deformed ileocecal valve with dilatation of terminal ileum
b. Contracted cecum, abnormal ileocecal valve and/or 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. Contracted Cecum
b. Ulcerations or narrowing of terminal ileum
c. Strictures of ascending colon
d. Multiple areas of dilatation, narrowing and matting of small bowel loops
Gr III Nonspecific changes
Features of matting, 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.N. adjacent to localized transmural inflammatory disease of cecum
(Not seen in Crotns)
Hypertrophic TB Pooling of contrast media and
and tumor like capillary blush
Malignancy
Colonoscopic Findings in Ileocecal TB

Hypertrophiedthickening and hypertrophy of mucosa
Ulcerative hypertrophiculcer with hypertrophy of mucosa
Ulcerativesingle of multiple ulcers of variable size and shape
Ulcer constrictivenarrow segment of intestine with ulcer.
19
Intestinal Polyposis
Word polyp derived from Greek work polypus meaning many footed.
In practise, polyp is used to define a discrete mass of tissue that protrudes
into the lumen of the bowel.
Polypoid lesions are most common in colorectal region.
True prevalence of colorectal polyps in the general population is unknown,
because large population studies using complete colonoscopy have not
been conducted.
In United States, autopsy studies suggest an overall polyp prevalence of 50
percent, but colonoscopic surveys suggest no more than 40 percent.
DIAGNOSIS
1. Barium studies
2. Endoscopy
Biopsy or polypectomy and histopathologic analysis definitive diagnostic
test.
Barium Studies
Polyp can be
1. 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.
2. Sessile
Intraluminal tumors that project within the lumen when viewed in profile
but do not demonstrate a stalk.
Broad base, vertical height about 50 to 80 percent of their transverse
diameter.
ESOPHAGEAL POLYPS
Can be
1. Fibrovascular polyp
Also called as fibroma, fibrolipoma, myxofibroma and pedunculated
fibroma
Consists of varying amounts of fibrovascular tissue, adipose cells and

stroma that arise in the mucosa or submucosa and are covered by the
epidermoid epithelium
Symptoms Dysphagia, substernal discomfort
Barium swallow large intraluminal filling defects. Oval shaped or
elongated, sausage like masses with smooth or lobulated surface.
Pedunculation is common.
2. Inflammatory polyp
Also called as inflammatory pseudopolyps, fibrous polyps and
eosinophilic granuloma
Response to reflux esophagitis
Sessile lesions consists of inflamed granulation and fibrous tissue.
Radiographic examination:
1. Rounded sessile polyps, usually 0.5 to 2 cm in diameter, located
near esophagogastric junction and often on top of thickened gastric
fold.
2. Associated findings of esophagitis reduction in esophageal
distensibility and contour irregularity and erosion.
3. Hiatus hernia and gastroesophageal reflux commonly present.
4. Diminishes in size and disappear during effective therapy for
esophagitis.
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.
1. Hyperplastic (regenerative) polyp-
75 percent of gastric polyps
Symptomsbleeding, prolapse, pyloric canal obstruction
Composed of overgrowth of superficial gastric epithelium, with cystic
dilation of elongated mucosal folbs. Inflammatory cells present
Multiple in 20 to 25 percent cases, of same size.
Radiographic examination (1) smoothly marginated circular or
pedunculated lesions, average diameter 5 to 10 mm, superficial
erosions at tip may be present.
Common in fundus and body.
Intestinal Polyposis 279
2. Adenomatous polyp
True neoplasms that are composed of dysplastic glands and capable of
continued growth
Definite tendency towards malignant transformation.
Radiographic examination :
Usually sessile, large (greater than 2 cm) with irregular surface.
Contrast material enters deep fissures and furrows in polyp,
producing papillary or villous appearance
Usually single, common in gastric antrum
Often ulcerate.
3. Hamartomatous polyps
Contain histologic elements present in gastric wall, but in a disorganized
and proliferative pattern
Usually occur in hereditary syndromes such as Peutz Jeghers syndrome,
juvenile polyposis and fundic gland polyp
In Peutz Jeghers syndrome, Gastric polyps 25 to 50 percent patients.
Multiple polypi, occur mostly in antrum, larger than adenomatous
polyps, lobulated surface
Gastric polyps occur in juvenile GI polyposis and such polyposis are
limited to stomach occur in children, can be single as multiple, have
malignant potential.
Fundic gastric polyp composed of normal appearing fundic glands
with increased number of parietal and chief cells. Glands are dilated
referred as glandular cysts
Seen as sessile masses, 5 mm in diameter, predominantly seen in fundus
and body of stomach typically multiple.
4. 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, with or without fold thickening.
Scattered polyps of varying size with thick folds.
Minimal involvement with few small polyps.
5. Heterotopic polyps
a. 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. Umbilication site
of excretory duct.
b. Adenomyomas
Made of ducts epithelialized by columnar cells and arranged in
haphazard pattern.
Less than 2 cm in diameter

Smooth, sharply demarcated, intramural mass
Common- prepyloric area
Brunners gland hyperplasia
Polypoid lesions composed of tightly organized but normal Brunners
gland.
Primarily in duodenum, rare in prepyloric region of stomach.
6. Non-epithelial tumors as leiomyoma, neurogenic tumors, carcinoid tumors
may also present as filling defects.
COLORECTAL POLYPS
Can be divided into two major groups.
A. Polypoid lesions of epithelial origin
1. Neoplastic polyps-Adenomatous and malignant polyps.
2. Non neoplastic polyps-
a. Hyperplastic polyp
b. Inflammatory polyp
c. Hamartomatous polyp
Cystic (Juvenile polyp)
Cellular (Peutz Jeghers polyp)
B. Polypoid lesion of subepithelial origin: lipoma, leiomyoma, neurofibroma,
hemangioma, lymphoma, sarcoma.
Clinical Features
Bleeding anemia
Intussusception
Obstruction if large
Detection Barium enema
Colonoscopy
Radiologiccal Features
Depends on the angle of which, it is viewed and its relationship to the barium
pool.
a. Meniscus sign: meniscus forms around base of a polyp. Creating a ring
shadow enface, clearly defined inner border, outer margin fading into the
normal mucosal coating.
b. Hat sign: When viewed obliquely, oval meniscus around the base and thin
line of barium over the surface of a polyp produce hat sign.
c. 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.
d. Stalk sign: The head of a polyp is mobile and hidden behind the barium
pool. Stalk is outlined by two parallel lines of barium, which diverge slightly
as the stalk flattens out to merge with the mucosa.
e. Bulls eye/Target sign: Created when head and stalk are superimposed,
inner ring due to stalk and outer to the head of polyp.
Assessment of polyp Six Ss
1. Site
2. Size
3. Shape-seesile/stalk
4. Symmetry of baseindrawn/smooth/irregular
5. Surface texturesmooth/lobulated/nodular
6. Singularity or otherwise.
Potential for Malignancy

Accurate diagnosis by histopathology, however probability of malignancy can
be made on radiologic findings.
1. Size
Less than 0.5 cm in diameter rarely malignant
Above 1 cmincidence of malignancy rises.
20 to 40 percent of polyps greater than 2 cm are cancerous.
2. Pedunculation
Polyp with well defined pedicle substantially lower incidence of
malignancy than sessile lesion of comparable diameter.
3. Surface Contour
Triangular, square, trapezoid, polyhedral or bizarre configuration
increase the probability of malignancy.
Discrete surface ulceration highly suggestive of carcinoma.
If indentation of ployp base seen in tangential view suggest malignancy
due to infiltration and invasion of mucosa adjacent to the lesion.
4. Growth rate
Any increase in size of colonic polyp indication for removal.
Adenomatous Polyps
Most common neoplasms of colon
Sharply circumscribed area of dysplastic epithelium
Mostpolypoid, also flat lesions
60 percentRectosigmoid, 18 percent descending colon, 14 percent
transverse colon, 8 percent ascending colon and cecum.
Adenomas in left colon larger.
Malignant potentiality observed.
Incidence of malignancy < 1 percent for adenomas < 1 cm in size > 20
percent for adenomas > 2cm in size
Can be classfied as:
1. Tubularcan be sessile/pedunculated.
2. Villous10 percent of adenomatous polyp.
Tend to be sessile, predilection for rectum and cecum.
For a given size, villous tumor has a likelihood harboring carcinoma

10 times as great as that of tubular adenomas.
3. Mixed.
Hyperplastic Polyps
Also called as metaplastic polyps
Present as minute smooth surfaced elevations with sessile configuration.
Mostly rectosigmoid region, may occur in any part of colon
Usually smaller than 5 mm
Particularly, common after 40 years
Biopsy and histology confirmation Diagnosis.
Juvenile Polyps
Occur as isolated lesions in children < 10 years.
Solitary 75 percent of cases. When multiple seldom more than 2 or 3 in
number.
Barium examination round filling defects, often pedunculated, common-
rectum or sigmoid
Inflammatory polyps Pseudopolyps
Term used for reparative mucosal protrusions that develop after severe
mucosal damage and ulceration.
Most often accompanied ulcerative colitis, but also seen in Crohns disease,
ied with ischemic colitis, bacterial colitis, amebiasis, chronic schistosomiasis
and diverticular disease
Can be focally/diffusely distributed
Often multiple, small and lack distinctive heads, some have slender,
arborescent configuration called as filiform polyps. Some may be giant.
1.5 to 6 cm in diameter.
Non Epithelial Tumors

Lipomas, leiomyomas, hemangioma, lymphoma may bulge into tumor being
seen as polyp covered by intact mucosa.
POLYPOSIS SYNDROMES
Considered when
1. GI polyp is identified in a young patient.
2. Multiple polyps are demonstrated in any patient.
3. A colon carcinoma is present in patient less than 40 years old.
Can be:
1. Hereditary polyposis syndromes
Familial adenomatous polyposis syndromes:
a. Classic FAP/Familial multiple polyposis
b. Gardners syndrome
c. Turcots syndrome
d. Muir-Torre syndrome
Familial hamartomatous polyposis syndromes.
a. Peutz Jeghers syndrome
b. Juvenile polyposis
c. Cowdens syndrome
d. Basal cell nevus syndrome
e. Ravalcaba myhre smith syndrome
2. Non familial polyposis syndromes
a. Cronkhite Canada syndrome
b. Inflammatory polyposis (Pseudo polyps)
c. Lymphoid polyposis
Benign lymphoid polyposis
Malignant Lymphoma
Familial Multiple Polyposis

1. Characterised by hereditary transmission, polyposis coli and eventual
development of a colon carcinoma.
2. Clinical featureusually 3rd or 4th decade of life, vague abdominal pain,
diarrhea-bloody stool,weight loss, prolapse of polyp through rectum.
3. Colonic polyps are numerous pinhead to 1 cm or more in size, may be
sessile or pedunculated.
4. Rectum and left side of colon more involved than right side of colon. Also
presence of gastric and small bowel polyps.
5. Histologically adenomatous polyp. Occassionally, villous adenomas or
inflammatory polyps present.
6. Colon cancers arise about 50 years of polyposis. Usually between 20 to 40
years, rarely before 20 years. 100 percent of untreated patients.
Diagnosis-by colonoscopy.
Radiographic examination: To document size, number and distribution of polyps
and to search for carcinoma.
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. Some have pedicles
Carcinoma polypoid filling defects, areas of segmental narrowing, or
typical annular lesions with overhanging margins, multiple carcinoma
common
Family screening should be done. Affected patients are identified at young
and prophylactic total colectomy with ileorectal anastomosis should be
performed. Rectal polyps requires cautery.
Gardners Syndrome
A syndrome featuring an autosomal dominant inheritance, multiple soft
tissue tumors, osteoma, polyposis coli and a potential for colon malignancy.
Soft Tissue Tumors

1. Cutaneous lesions consists of sebaceous or inclusion cysts over scalp and
back, also on face or extremities.
2. Benign mesenchymal tumors as fibromas, lipomas, lipofibromas,
leiomyomas and neurofibromas. Malignant sarcomas are uncommon.
3. Fibrous tissue has tendency towards proliferation desmoid tumors,
keloids, hypertrophied scars, mammary fibromatosis, peritoneal adhesions,
mesenteric fibrosis and retroperitoneal fibrosis.
Bony Lesions
1. Osteomas appearing as exostoses or enostoses, present in maxilla, mandible
and skull.
2. Long bone especially. femur and tibia localized cortical thickening, long
bones may be shortened or bowed.
3. Dental abnormalities odontomes, unerrupted supernumerary teeth,
hypercementosis, tendency towards numerous caries.
Polyps
Limited to colon, 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, increase during 3rd and 4th decades
carpeting of colon
100 percent develop colon carcinoma.
Turcots Syndrome (Glioma Polyposis)

Syndrome of familial colonic polyposis with primary tumors of Nervous
system.
Neural tumors gliomas and medulloblastoma
Polyps larger and fewer than typical FAP.
Muir Torre Syndrome

Characterized by multiple sebaceous neoplasm of skin, with multiple visceral
neoplasms
Present in 5th to 6th decade, strong family history
40 percent patients have being intestinal polyps, 90 percent have GI visceral
malignancy
80 percentColon Carcinoma
5 percentGastric Carcinoma
8 percentDuodenal Carcinoma
50 percent patients have urogenital malignancy, usually endometrial, bladder
or renal carcinoma.
12 percent have lung or laryngeal cancer.
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, oval or slightly irregular macules, 1 to 5 mm in diameter.
Common site lips and buccal mucosa, less common face or volar
aspect of hands and feet
Polyps predominantly GI, but also in urinary or respiratory tract.
Small bowel 95 percent patients show colon and rectum involvement
30 percent patients, stomach 25 percent involvement.
Polyps multiple, size 0.1 to 3 cm, hamartomatous without malignant
potential
Incidence of cancer 2 to 3 percent
Occur in stomach, duodenum and colon. Rare jejunum and ileum.
Sessile lesions > 1.5 cm, lesions showing rapid growth, and annular lesions
suspicious for carcinoma.
Managed by conservative treatment.
Surgery
a. Persistent obstruction
b. Severe bleeding
c. Suspected malignancy.
Juvenile Polyposis
Three varieties have been recorded
1. Familial juvenile polyposis coli (limited to colon)
2. Familial juvenile polyposis of stomach
3. Generalized juvenile polyposis (Involving entire GI tract)
Present in childhood with GI bleeding, intussusception and obstruction
May coexist with adenomatous polyps in some patients with familial multiple
polyposis or Gardners syndrome
Risk of colon cancer increased in patients with familial juvenile polyposis
Juvenile polyp has a smooth, round confirm as opposed to adenomatous
polyps that has fissured, lobulated appearance.
Cowdens Syndrome
(Multiple hamartoma syndrome)
Consists of multiple cutaneous hamartomas, fibrocystic disease and cancer
of breast, nontoxic goiter, thyroid cancer and hamartomatous polyps of
stomach, small intestine and colon.
Autosomal dominant mode of inheritance
GI symptoms and colorectal cancer-uncommon.
Ruvalcaba Myhre Smith Syndrome Sotos Syndrome

Consist of macrocephaly, pigmented genital lesions in males, and intestinal
polyposis with mental retardation, lipid storage myopathy and subcutaneous
lipomas may be noticed.
Genital skin lesions hyperpigmented muscles present on glans and shaft
of penis. Absent on scrotum or genitalia of females.
Intestinal lesions harartomatous polyps involving gastric antrum,
duodenum, small bowel and colon
No evidence of malignant potential.
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.
Cronkhite Canada Syndrome

Characterized by presence of diffuse gastrointestinal polyposis, dystrophic
changes in the fingernails, alopecia, cutaneous hyperpigmentation, diarrhea,
weight loss, abdominal pain and complications of malnutrition
Develops during middle or old age (42 to 75 years)
Radiographic examination multiple gastric and colonic polyps. More than
50 percent patients have small bowel polyps, accompanied by thickened
mucosal folds and increased intraluminal fluid.
Lymphoma :
May presents as multiple gastrointestinal polyps
Require adequate biopsy to distinguish them from true epithelial polyps.
SECTION 6
Genitourinary
System
20
Uremia and Imaging
Definition: Uremia is a Complex of symptoms resulting from failing renal
function, caused by the retention of constituents of normal urine.
Clinical Signs and Symptoms Depends Upon

a. Etiology of the specific renal disease
b. 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.
2. Renal causes.
3. Post-renal causes.
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
Renal diseases
Interstitial nephritis
Hereditary disease
Autosomal dominant polycystic kidney disease
Alports diseases
Systemic diseases with renal involvement
Diabetes mellitus
Hypertension
SLE, systemic sclerosis
Vasculitis
Microangiopathy
Hemolytic uremic syndrome
Infection
Drug
Postpartum
Accelerated hypertension
Post Renal Causes

In children, mostly congenital
In adults, mostly acquired
In Children
1. 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. Urethral Obstruction
Intrinsic lesion Extrinsic lesion
Valve (posterior, anterior Presacral mass dissecting inferiorly
sacular, diverticulum
Stenosis, atresia Fecal impaction (habitual constipation,
neuropathy)
Inflammatory stricture Mass originating in genital organs
Contd...
Uremia and Imaging 291
Contd...
Intrinsic lesion Extrinsic lesion
Traumatic stricture Male : Prostate
Urethral tumors Rhabdomyosarcoma
Female : Hydrometrocolpos, hydrocolpos,
fused labia
Adults
PUJ Region :
Scarring (inflammation, surgery, trauma)
Reflux
Malignant tumour (Primary Transitional cell secondary metastatic)
carcinoma, squamous cell cacinoma
Benign (Polyp, mesodermal tumors)
Other intraluminal lesion (stone, blood clot, papilla, fungus ball)
Ureteric Obstruction
Intraluminal Extraluminal
Stone Large pelvic tumors
Blood clot Retroperitoneal tumors
Neoplasm Stricture
Sloughed papilla Retroperitoneal fibrosis, infection and
inflammation, vasculitis
Fungus ball Pelvic fibrosis secondary to:
Pregnancy related problems:
Hydronephrosis of pregnancy, ovarian vein
thrombophlebitis, periureteric fibrovenous entrapment
(ovarian vein syndrome)
Gynecological conditions:
Endometriosis
Prolapse uterus
Hydrohematocolpos
Carcinoma cervix
Gastrointestinal conditions:
Crohns 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, meticulous technique, and to appreciated the limitations and
possible sources of error in each technique.
Imaging Techniques
Conventional Uro-radiology
A. Intravenous Urography:
a. Plain skiagram of abdomen for kidneys, ureters and urinary bladder
region.
b. Contrast study
Contrast media: Ionic/ Non-ionic both contrast media can be used.
Dose
Infants under six months, 10 CC of diatrizoate
Older children 2 to 3 CC/Pound, 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 mol/liter occurring 3 days following I/V contrast:
for which there is no other explanation.
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
Age over 70
Hypertension
Multiple myeloma
GUIDELINES
Guidelines for avoiding contrast medium nephrotoxicity in patients with impaired
renal function.
1. Use of low osmolality contrast media.
2. Keep the contrast media to the minimum dose necessary to achieve the
diagnosis.
3. Ensure well hydration of the patient.
4. Do not give further contrast media for 48 hrs.
5. Discontinue nephrotoxic drugs.
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
mol) 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
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.
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.
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
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
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.
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.
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.
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
Papillary (or) Caliceal Abnormality is Present

a. With diffuse parenchymal loss
Obstructive nephropathy
Generalized reflux nephropathy
b. No parenchymal loss
Papilliary necrosis
Tuberculosis
Pelvicaliceal cyst
Megacalices
Medullary sponge kidneys
c. 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.
Radiological imaging of these patients is a key factor in appropriate
management of their disease.
If examination of patient fails to uncover and obvious cause, then imaging
should be promptly undertaken.
Renal Ultrasonogram
Alone is usually sufficient to identify patients secondary to urinary tract
obstruction.
Although the percentage of false negative USG examinations are substantial,
in the setting of acute obstruction, renal failure caused by obstruction
indicates a long standing process with resultant hydronephrosis
Once diagnosis is established, imaging of the course of ureters and bladder
should be attempted to determine the cause of obstruction
Bilateral hydronephrosis usually indicates bladder outlet obstruction, which
may be anatomical or neurological disorder leading to functional obstruction.
Pelvic USG may demonstrate the abnormality suggesting the cause of
obstruction
Highly trabeculated, 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
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, and no abnormality are present in the
pelvis, 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, 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,
like autosomal dominant polycystic kidney disease
The etiology of the renal disease usually cannot be further identified with
USG directly
However, USG is useful in guiding biopsy of kidney for histological
diagnosis.
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.
Renal Insufficiency in Patients with Chronic Renal Failure

In 7 percent of patients who have undergone long term dialysis, either
peritoneal/hemodialysis, solid renal neoplasms develop.
Metastatic renal adenocarcinoma from the native kidneys (2%) are
responsible for late deaths in patients with renal transplantation.
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, who have flank pain, hematuria, ACD, suspected
renal mass.
To be repeated yearly (or) sooner should new symptoms develop.
21 Role of Imaging in
Gynecological Disorders
CONVENTIONAL RADIOGRAPHY
Plain X-Rays
1. Plain X-ray abdomen
Homogenous soft tissue density within the pelvis which may extend
upward into the abdomen and displace gas-filled bowel loops.
Uterine masses tend to lie in the midline, whereas ovarian tumors, unless
large, tend to remain on their own side.
Calcification is noted in uterine fibroids (patchy/mural), ovarian dermoid
(mural or presence of teeth), ovarian fibroma, omental or peritoneal
deposits of cystadenocarcinoma and tuberculous pyosalpinx
(amorphous)
Localization and identification of intrauterine contraceptive device
(IUCD).
2. Chest X-ray
Pleural effusion (both malignant and benign ovarian lesions, uterine
carcinoma)
Any features of pulmonary tuberculosis (tubercular endometritis or
salpingitis)
Metastases (malignant ovarian and uterine tumors, chorio-carcinoma).
INTRAVENOUS UROGRAPHY
Used in gynecological disorders to demonstrate distortion, deviation, or
obstruction of the urinary tract in the pelvis.
1. Pelvic mass leading to ureteric obstruction with resultant hydronephrosis
2. Actual invasion of the urinary bladder or ureters by a pelvic malignancy
3. 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
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, deviation of the course
of the ureters and dilatation of the renal pelvis and calyces.
CYSTOGRAPHY
Useful in cases of :
1. Prolapse uterus
2. Stress incontinence
3. Vesicoureteric reflux
4. Vesico-vaginal fistula
HYSTEROSALPINGOGRAPHY
Indications
Infertility
Recurrent abortion
Congenital abnormalities
Primary diagnosis
Following reconstructive surgery
Post-uterine surgery
Myomectomy
Adhesiolysis
Cesarean section
Posttubal surgery, to assess patency after:
Sterilization
Reversal of sterilization
Reconstructive tubal surgery
Abnormal uterine bleeding.
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.
OBSERVATIONS
Congenital anomalies: Occur due to partial or complete failure of fusion or
atresia of the mullerian ducts.
These include :
Uterus didelphys: Duplication affecting the whole of uterus, cervix and
vagina.
Uterus bicornis bicollis: Two separate uterine horns, each with its own
cervix, single vagina.
Uterus bicornis unicollis: Two separate uterine horns which share a single
cervix.
Septate uterus: A septum protrudes from the fundus
Arcuate uterus: Characterized by the shape of the fundus, which projects
moderately into the uterine cavity.
Unicornuate uterus: Single spindle-shaped uterine cavity.
Infantile uterus: Small sized uterus, cervical canal is long relative to the
uterine body.
Acquired Conditions
A. UTERUS
1. Fibroids
Submucous fibroids: sessile or polypoid filling defects; in the contrast
filled cavity.
Interstitial fibroids: enlarged or distorted uterine cavity.
Subserous fibroids: if situated laterally in the parametrium, the mass
will deflect the uterus to the opposite side and the ipsilateral tube
will be stretched over the mass.
2. Adenomyosis: Irregularity of the endometrium with penetration of the
contrast medium into the myometrium, giving speculated appearance.
3. Endometrial polyps: Single or multiple, well defined filling defects which
do not enlarge the uterine cavity.
4. Tubercular endometritis: Very small irregular contracted uterine cavity.
5. Synechiae: Irregular filling defects which are seen even in the contrast
filled uterine cavity.
6. Endometrial carcinoma: Filling defect with ragged contours.
B. CERVIX:
1. Cervical incompetence: funnel shaped cervix with a patulous internal
os.
C. FALLOPIAN TUBE:
1. Tubal occlusion: Can involve the proximal/ mid segment/ distal part of
the tube. Proximal to the occlusion, the tube is dilated (hydrosalpinx).
2. Paratubal adhesions: Contrast tends to remain in separate spots and
does not spread freely in the peritoneal cavity.
3. Tubercular salpingitis: In a proven case of genital TB, HSG is not
done. If HSG has been done in an asymptomatic woman, the findings
which suggests the diagnosis, are:
A rigid non-peristaltic pipe-like tube (lead pipe appearance)
Beaded appearance
Calcification in a tuberculous pyosalpinx
Cornual/fimbrial block
Jagged, fluffiness of the tubal outline
Vascular or lymphatic intravasation of the dye.
4. Tubal polyps: Small, smooth, oval bilateral filling defects.

5. Salpingitis isthmica nodosa: small diverticular outpouchings of tubal
epithelium into the myosalpinx, usually in the isthmic portion of the
tube.
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, oval, or triangular soft tissue
mass located dorsal to the bladder, which may contain a central area of low
attenuation. The demarcations between uterus, cervix and vagina are poorly
delineated by CT scans. Unless enlarged, the ovaries are not generally identified,
seen as discrete structures and the tubes are only seen if markedly abnormal in
size.
MRI
A characteristics zonal anatomy of the uterus is seen on MR (T2). The inner
high signal intensity stripe represents the glandular tissue of the endometrium.
This is sharply demarcated from the low signal intensity of the deeper
myometrium, so called junctional zone (JZ). This represents a compact, more
cellular smooth muscle zone with a lesser water content compared with the
outer myometrium. The bulk of the myometrium appears as intermediate signal
intensity tissue. The cervix demonstrates a very low signal intensity myometrium
which is continuous with the JZ of the uterine corpus. Centrally, a stripe of
high signal intensity represents mucus within the endocervical lumen and
epithelial glands. Similarly, the vaginal wall shows low signal intensity compared
to the high signal intensity of the mucus within the vaginal cavity. These
appearances are liable to change with age, during different phases of the
menstrual cycle and with intake of drugs such OCPs or HRT.
Ovaries show homogenous low signal on T1 but on T2, the stroma remains
of low signal intensity and fluid within the follicular cysts show high signal
intensity. Normal tubes are usually not well depicted. If they are dilated, appear
as serpentine high signal intensity structures with a discrete low signal intensity
muscularis.
CONGENITAL ANOMALIES
Seen in 9 percent of women with infertility or fetal loss.
Renal anomalies, particularly renal agencies or ectopia, are frequently
associated.
Classification of Mullerian Anomalies

(Buttram VC, Gibbons, WE; 1979)
Type Anomaly
I Segmental mullerian agenesis or hypoplasia (vaginal, cervical, fundal, tubal or
combined)
II Unicornuate uterus
a. With rudimentary horn
b. Without rudimentary horn
III Uterus didelphys
IV Bicornuate uterus
a. Complete (down to internal os)
b. Partial
c. Arcuate
V Septate
a. Complete (down to internal os)
b. Partial
VI Diethylstillbestrol related
Except for demonstrating anomalies in position, CT has little impact on the

diagnosis of congenital anomalies.
MRI Features
Fundal notch or indentation is diagnostic of a bicornuate uterus whereas a
septate uterus has a smooth minimally indented fundal contour.
Arcuate uterus has a heart-shaped endometrial cavity and flat fundal contour.
Unicornuate uterus has an elongated banana-like shape that is quite unlike
the triangular shape of a normal uterus.
Obstruction due to a vaginal septum leading to hematosalpinx, hemato-
metra or hematocolpos.
In women exposed to DES (diethylstilbestrol) in utero, findings include
hypoplastic uterus, T-shaped endometrial cavity with marginal irregularity.
ACQUIRED CONDITIONS
Uterus
A. Benign
Endometrial
Focal areas of hyperplasia of both the glands and stroma of the basal
endometrium, found in 10 to 24 percent of hysterectomy specimens.
May be sessile/ pedunculated and are usually attached to the uterine fundus.
Present most commonly in the fourth to sixth decade with vaginal spotting.
Increased incidence of polyp formation is seen in women on Tamoxifen
therapy.
Difficult to detect on CT; uterus may appear normal or demonstrate non-
specific widening of the endometrial cavity.
MRI Features
Intermediate signal intensity mass is noted within the endometrial cavity
on T2-weighted images.
Linear low-signal area is seen peripherally, which represents fibrous tissue
within the pedunculated stalk.
The normal uterine zonal anatomy is preserved.
Polyps enhance with gadolinium the contrast media but less than the
surrounding endometrium.
D/D: Submucosal leiomyomas, non-invasive endometrial carcinoma.
Endometriosis
Defined as the presence of functioning endometrium, located outside the
uterus. This responds to hormonal stimulation and undergoes repeated
cycles of hmorrhage with the development of blood filled cysts called
endometriomas.
Patients present with pelvic pain, dysmenorrhea or infertility.
Sites of implantation of ectopic endometrium are ( in descending order of
frequency) ovary, uterosacral ligaments, cul-de-sac, posterior wall of
lower uterine segment, fallopian tube, rectovaginal septum and sigmoid
colon.
CT Features
Thickening of the tissues adjacent to the ovaries or uterus or involvement
of the bladder, rectum, small bowel or abdominal wall by single or multiple
solid masses or fluid-filled cysts.
A definitive CT diagnosis cannot be made without a typical history.
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; some may hypointense on
both T1 and T2 or even hyperintense on T1 and hypointense on T2.
A signal void rim or signal void areas may be seen within the lesion
because of hemosiderin-laden macrophages.
Angular margins or distorted shape.
Thick, low signal intensity rim which may enhance after gadolinium
administration.
D/D: Hemorrhagic ovarian cysts.
Uterine Leiomyomas/Fibroids
Benign smooth muscle cell tumors containing varying amounts of fibrous
tissue, occurring in 20 to 40 percent of all women during the reproductive
years.
Although many patients are asymptomatic, others may present menorrhagia,
dysmenorrhea, infertility, habitual second trimester abortion or pelvic pain.
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.
Soft tissue which distorts or obliterates the uterine cavity.
Mural thickening.
Amorphous popcorn, whorl like or rim like calcification.
May be hypodense/ isodense/ hyperdense relative to normal myometrium.
Mild to moderate enhancement is noted after IV contrast administration.
Irregular low density areas within uterine masses representing degeneration
of a leiomyoma.
Lipoleiomyoma : Well-encapsulated uterine mass that shows predominantly
fat density.
MRI Features
Sharply marginated homogenous areas of decreased signal intensity on
T2-weighted images.
Can identify lesions as small as 0.3 cm.
Lesions larger than 3 to 5 cm have heterogeneous areas of increased signal
intensity representing degeneration.
After gadolinium administration, fibroids enhance heterogeneously, less
than the surrounding myometrium and remain well marginated.
Adenomyosis
Presence of heterotopic endometrium located within the myometrium.
Cyclical hemorrhage of normally functioning endometrium is infrequent
because the heterotopic endometrium is usually resistant to hormonal
stimulation.
Foci of adenomyosis are surrounded by hypertrophied smooth muscle,

which interdigitates with the smooth muscle of the normal myometrium
without forming a sharp border.
Common in multiparous, premenopausal women during the fifth decade
and presenting features including dysmenorrhea, menorrhagia, pelvic pain,
dyspareunia and an enlarged uterus on examination.
CT has little to offer, can detect an enlarged uterus.
MRI Features
Focal adenomyosis is seen on T2 as an ill-defined, poorly marginated area
of low signal intensity within the myometrium but contiguous with the
junctional zone.
An ill-defined border is the hallmark of focal adenomyosis, distinguishing
adenomyoma from leiomyoma (However, small leiomyomas (<2-3 cm)
may have ill-defined borders).
Diffuse adenomyosis characterized by generalized thickening, either even
or uneven (>5 mm), of the junctional zone.
Small foci of increased signal intensity may be seen on both T1 and T2 due
to hemorrhage.
B. Malignant
Endometrial Carcinoma
Usually seen in perimenopasual women, 55 to 60 years of age.
One third to half the number of patients are obese, hypertensive and diabetic
and usually present with postmenopausal bleeding, irregular and heavy
cycles, purulent vaginal discharge or lower abdominal pain.
CT Features
Focal or global enlargement of the uterine body.
Hypodense mass within the endometrial cavity on contrast-enhanced CT
scan.
CT cannot assess the depth of myometrial invasion.
Involvement of the cervix is seen as cervical enlargement greater than 3.5
cm in diameter and heterogeneous cervical stroma.
Adnexal spread appears as a lobulated, triangular mass extending from the
central neoplasm that obliterates the normal parametrial fat planes.
The mass can occlude the internal cervical os resulting in hydrometra,
haematometra or pyometra. CT shows a symmetrically enlarged uterus
containing a central water-density mass.
Lymph nodal metastases involves both pelvic and retroperitoneal nodes.
Nodes larger than 1.5 cm are considered metastatic.
Involvement of rectum or bladder is seen as either asymmetric wall
thickening or protrusion of the growth into the lumen.
MRI Features
Homogeneously widened endometrial stripe or a heterogeneous mass
distending the endometrial cavity with intact junctional zone (non-invasive
endometrial carcinoma).
The intermediate signal intensity tumor is seen on T2 to disrupt the junctional
zone when myometrial invasion occurs.
With gadolinium enhanced T1-weighted images, the growth enhances but
later than normal endometrium.
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.
With parametrial extension, the tumor will penetrate the serosal surface,
disrupting the normal signal intensity of parametrial fat.
Ovarian metastases appear as masses of intermediate signal intensity replacing
the normal signal intensity of the ovarian stroma.
Peritoneal or omental tumor implants have an intermediate signal intensity
on T1 and higher signal intensity on T2.
Lymph nodes >1.5 cm are considered metastatic (same as CT).
Leiomyosarcoma
Occurs in perimenopausal women and arises either de novo or from
sarcomatous degeneration of leiomyoma.
Presenting features include pelvic pain, vaginal bleeding and pelvic mass.
CT Features
Uterine enlargement with areas of inhomogenity and zones of low
attenuation.
Presence of a heterogeneous myometrial mass with an indistinct border.
Invasion of contiguous pelvic structures can be seen by both CT and
MRI.
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.
In choriocarcinoma, metastases to the lung (80%), vagina (30%), pelvic
(20%), usually as a result of local extension, liver and brain may occur.
CT Features
Normal size uterus with areas of hypodensity.
Enlarged, inhomogeneous uterus with a central area of low attenuation.
Hypodense foci, surrounded by highly enhanced areas in the myometrium.
Presence of bilaterally enlarged ovaries containing multiple theca-lutein

cysts.
CT of the brain, chest and abdomen enables detection of distant metastases.
MRI Features
Complete hydatidiform moles appear as heterogeneous masses with vesicular
spaces distending the endometrical canal. Myometrium remains intact.
In persistent or invasive GTN, heterogeneous, predominantly high signal
intensity masses invading the myometrium and distorting the uterine zonal
anatomy are seen.
Foci of high signal on T1 suggest the presence of hemorrhage.
Myometrial invasion is better picked up on Gadolinium contrast-enhanced
images.
CERVIX
Cervical Cancer
Most frequent of all the genital tract cancers.
Patients present with irregular vaginal bleeding, discharge, pain and the
cervix is friable, fixed and bleeds on touch on examination.
CT Features
Solid mass enlarging the cervix greater than 3.5 cm in diameter with
hypodense areas due to necrosis and ulceration.
Obstruction of the endocervical canal leads to uterine enlargement with an
endometrial fluid collection.
Parametrial tumor invasion leads to disruption of the peripheral cervix
margins, prominent parametrial soft tissue stands, eccentric parametrial
soft tissue mass and obliteration of periureteric fat planes.
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, nodular indentations or serrations of
the bladder/ rectal wall and an intra-luminal mass.
Detection of pelvic and retroperitoneal nodes and liver metastases.
MRI Features
Intermediate signal mass on T2-weighted images that may expand the
endocervical canal, disrupt the low signal intensity of the fibrous cervical
stroma.
With Gadolinium, cervical carcinomas may display increased enhanced in
the early dynamic phase with improved tumor to cervix contrast.
With parametrial extension, there is full thickness invasion of the cervical

stroma associated with irregularity or asymmetry of the lateral cervical
margins, parametrial mass or stranding within the parametrial fat. This
may extend upto the pelvic side wall.
With vaginal invasion, tumor invades the low signal intensity vaginal wall.
Focal disruption of the normal low signal intensity of the bladder or rectal
wall, loss of perivesical/perirectal fat planes, asymmetric nodular wall
thickening or intraluminal masses are seen with bladder or rectal
involvement.
Detection of metastatic nodes, those larger than 1.5 cm are considered
abnormal and those between 1.0 to 1.5 cm are considered suspicious.
OVARIES
Ovarian Cysts
Usually seen in the child bearing age. May be a symptomatic or produce
local discomfort, menstrual disturbances, or rarely causes acute symptoms
due to complications like hemorrhage, rupture or torsion.
Simple serous cysts include follicular cysts, corpus luteal cysts, theca
luein cysts and paratubal cysts. These may be complicated by haemorrhage
or infection.
CT Features
Smooth walled masses having a central low density close to that of water.
A rim of soft tissue surrounds the cyst.
Acute hemorrhagic cysts may be diagnosed because of the high density of
blood within the cyst.
MRI Features
On MR, serous ovarian cysts are homogenous, with a thin wall and signal
intensity isointense to urine on all pulse sequences: low signal on T1 and
high signal on T2.
Hemorrhagic cysts may show high signal on both T1 and T2. Layering
may be present. Contrast- enhanced images may help differentiate adherent
clot from a mural nodule because clot will not enhance after administration
of Gadolinium.
Tubo-Ovarian Abscess
Complication of pelvic inflammatory disease that occurs in about one third
of women having acute salpingitis.
CT Features
Thick-walled, complex adnexal masses with centers of low attenuation,
septations and shaggy margins.
Presence of air within the mass is diagnostic of abscess.
MRI Features
Tubo-ovarian abscesses have serpiginous, tubular configuration and tend
to be heterogeneous and ill defined on T2 weighted images.
Ovarian Neoplasms
Account for 5 percent of all gynecological cancers in India and 15 percent
in the west.
Most occur in women after the age of 50 but sometimes in younger women.
May cause abdominal pain, abnormal uterine bleeding, cachexia and ascites.
WHO Classification
i. Common epithelial tumors
Serous, mucinous, endometroid, clear cell, Brenner, mixed,
undifferentiated, unclassified.
ii. Sex cord tumors
Granulosa-stromal cell tumors, androblastomas, gynandroblastomas,
unclassified.
iii. Lipid cell tumors
iv. Germ cell tumors
Dysgerminoma, endodermal sinus tumor, embryonal carcinoma,
polyembryoma, choriocarcinoma, teratoma and mixed.
v. Gonadoblastoma
vi. Soft tissue tumors not specific to the ovary
vii. Unclassified tumors
viii. Secondary (metastatic) tumors
ix. Tumor-like conditions
CYSTADENOMAS
CT Features
Purely cystic and unilocular or multilocular with internal septations. No
wall thickening or internal solid papillary projections.
MRI Features
Cystic lesions which appear hypointense on T1 and hyperintense on T2.
Internal septations appear hypointense on T2. No mural nodularity is noted.
CYSTIC TERATOMAS/DERMOID CYSTS

CT Features
Low density mass containing a mixture of fat, hair, debris and fluid.
Calcifications (teeth or abortive bone).
Solid projection (dermoid plug) arising from the cyst wall.
Fat fluid level is a diagnostic feature.
MRI Features
Presence of fat within an adnexal mass which shows high signal intensity
on T1 and intermediate to high signal on T2. chemical-shift artifact is seen
at the fat-water interface.
Pulse sequences which suppress the signal from fat are helpful.
Findings include layering, floating debris or hair balls, palm-tree like
protrusions, mural nodules and areas signal void due to calcifications.
MALIGNANT OVARIAN TUMORS

CT Features
Primary and metastatic ovarian tumors appear as abdominal or pelvic
masses, cul-de-sac lesions or as unilateral/bilateral adnexal masses.
Thickened wall or internal septations, papillary projections and solid tumor
components.
Cystadenocarcinomas appear as large, cystic tumors with CT attenuation
ranging from 10 to 20 HU. Marginal irregularity and internal soft tissue
components are seen.
Other ovarian tumors are seen as mixed solid-cystic or predominantly
solid masses with CT attenuation ranging from 40 to 50 HU.
Ascites, peritoneal implants and retroperitoneal lymphadenopathy.
MRI Features
Presence of solid components and thick, irregular walls or septations.
Tumor approaching the pelvic side wall or distorting the iliac vessels.
Loss of fat plane between the tumor and bowel/bladder or frank disruption
of bowel/ bladder wall.
Ascites, enlarged lymph nodes and peritoneal implants.
VAGINA
Vaginal Neoplasms
90 percent cases are due to squamous cell carcinoma. Tumor is readily
diagnosed by clinical examination.
CT Features
Mass caudal to the uterus with areas of low attenuation representing necrosis.
Bladder/rectal invasion
Nodal metastasis.
MRI Features
Diffuse/focal area of increased signal intensity interrupting the normal low
signal intensity of the vaginal wall.
Invasion of bladder/rectum.
Nodal metastasis.
RECURRENT TUMOR VERSUS RADIATION FIBROSIS

Cannot be differentiated on CT.
On MRI, 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.
22
Genitourinary Tuberculosis
Genitourinary tuberculosis is a late manifestation of earlier symptomatic or
asymptomatic pulmonary infection.
Is rarely a part of multisystem miliary tuberculosis, sometimes only, it may
be primary pathology also.
Nonuncommon in India.
Incidence of 10.7 percent positive cases in a study of 2240 patients
suspected of having renal tuberculosis reported during a survey by ICMR
(1973).
Occurs predominantly in 2nd 4th decade.
Less prevalent in 5th and 6th decade.
Female predominantly affected.
Pathogenesis
Causative agent is usually mycobacterium tuberculosis.
Discharge of M. tuberculosis into blood stream from active site of infection
(more often pulmonary).
Leads to formation of microscopic granuloma throughout the cortices of
both kidneys.
These tubercles either heal spontaneously or as a result of anti-TB treatment
administrated to control the initial primary focus.
Usually unilateral, if bilateral, then is asymmetrical.
An initial tubercle may enlarge forming a granuloma which may rupture
into a Nephron producing tuberculous bacilluria.
These bacilli form further granulomas within the medulla and papilla.
Granulomas may coalesce and form cavities.
Which rupture and communicates with the pelvicalyceal system.
Causes part of papilla to become necrotic and slough given rise to
papillary necrosis.
Causes destruction of parenchyma and formation of caseous mass
(tuberculoma) with displacement of calyces.
Present as renal mass produced by localized hydrocalicosis as a result of
stricture of infundibular or calyceal neck.
Genitourinary Tuberculosis 319
Bacilli which are shed into urine, infect the walls of calyces, pelvis, ureter
producing initial mucosal inflammation with ulceration, followed by
granuloma and ultimately fibrosis with stricture formations.
Alternatively parenchymal caseation, necrosis and calcification may cause
destruction of the kidney leading to malfunctioning calcified kidney, called
autonephrectomy.
Two types
Caseocavernous enlarged kidney converted into a caseous filled sac,
with or without calcification.
Shrunkened, fibrotic and often calcified kidney.
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, hard and localized nodules
near the tail.
Primary and secondary amenorrhoea or infertility in women in tubercular
endometritis or oophoritis.
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
Pattern of calcification:
Linear
Curvilinear
Streaky
Mottled
Amorphous
Combination of all.
Calcified caseous tissue is homogenous moderately, dense ground glass
appearance (Putty kidney).
Lobar distribution of calcification with the calcific rims outlining the
periphery of distorted renal lobes.
Calcification may extend along the ureter.
Calcification may be noted in liver and spleen.
I.V. 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.
Minimal erosion of single calyceal tip leading to fuzziness Ragged, moth-
eaten or feathery appearance.
Papillary necrosis.
Initial cavitation.
Advanced findings of Renal Tuberculosis are:

Cavitation
Lipping type of cavity if the cavity projects in medial direction.
Cavitation due to caseation of enlarging tuberculomas or conglo-
meration of tuberculomas.
Extensive cavitation are also called as ulcerocavernous cavity which
fails to excrete contrast media on IV Urography.
Fibrotic stricture
Three points where fibrosis can occur
1. Lower ureter
2. PUJ
3. Neck of calyx.
of calyx neck Hydrocalyx
Fibrosis of infundibulum Focal/regional hydrocalycosis
of renal pelvis hydronephrosis
In case of stricutre of inferior margin of renal pelvis, the cephalic retraction
is called as Hicked Pelvis.
PCS deformity caused by traction of stricture infundibulum and parenchymal
fibrosis can kink the pelvis. These kinks are known as Kerrs kink.
Mass lesion
It is either due to hdyronephrosis or tubercular granuloma, do not show
excretion of contrast so CT/US can help in differentiation.
Calcification
Autonephrectomy
This is end stage of renal TB, and is nonfunctional.
Two types
i. Caseo-cavernous autonephrectomised kidneyEnlarged kidney
converted into caseous filled sac with or without evidence of
calcification.
ii. Shrunken, fibrotic and calcified kidney.
Fistula formation
Phantom kidney Completely stenosed infundibulum or calyx results in
complete failure of excretion by involved renal parenchyma.
Nonfunctioning Kidney Seen in

Both types of autonephrectomised kidney.
Obstructed kidney due to obstructed ureter.
Renovascular hypertension. (Conical stenosis or compete obstruction of
Renal artery. Medial hypertrophy with intimal or subintimal sclerosis is
common finding).
This nonvisualized kidney at urography may be small/normal/enlarged kidney
depending upon the balance of renal atrophy versus hydronephrosis.
a. Perinephric abscess results from:
Perforation of pyocalyx, abscess or pyonephrosis into perinephric tissue.
Secondary infection into perinephric collection.
b. 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.
Ultrasound
Most common sonographic abnormality is a focal renal lesion.
1. Small (5-15 mm) lesion either echogenic or have echogenic border
with central hypoechoic area.
2. Large lesion (>15 mm) of mixed echogenicity with poorly defined

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

Ureter
Usually secondary to renal TB in the stage of Bacilluria.
Hematogenous spread or contiguous spread or lymphadenopathy.
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.
Chronic stages show fibrotic strictures.
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, saw-tooth ureter due to multiple
active ulcerations.
Multiple intraluminal ulceration represent mucosal granulomas can be
demonstrated.
Ultrasonography
Not significant in imaging ureter in acute phase
Small mucosal granulomas seen in few ureter
Dilated with distal strictures
Identifying perinephric spread, paraurethral nodes and other lesion adjacent
to Psoas abscess.
BLADDER IMAGING STUDIES

Bladder involved in 1/3rd of cases
Infection coming from kidney via urine
Symptoms: Dysuria, frequency, hematuria
Earliest Manifestation
Mucosal edema.
Ulceration predominantly surrounding ureteric orifices.
Edema of trigone mucosa causing ureteral obstruction.
TB of bladder is an interstitial cystitis producing thickened spastic bladder
of small capacity.
RADIOLOGY
IV Urography
Bladder lumen is irregular due to localized deformity from cicatrisation or
due to hyperplastic inflammatory lesion.
Sometimes granuloma formation is noted
Tuberculoma of vesical wall can be large, being manifested radiologically

as filling defects simulating malignancy.
Cystogram
Shows filling defects simulating the appearance of multiple polypoid
neoplasm
Chronic ulceration and often hypertrophy of bladder wall.
The undermining ulcer may be seen as escape of contrast in the deeper
layer of the bladder wall with overhanging mucosa.
Diffuse cicatrical contraction poducces a symmetrical, small, thick walled
bladder called the Thimble bladder.
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.
Fibrosis of the region of trigone produces gapping uretric orifices and
Vesicoureteral reflux.
Calcification of bladder is rare and when seen, appears like multiple speckled
or curvilinear areas of calcification.
Rarely vesicorectal or a vesico-vaginal fistula may be seen.
Ultrasound
Visualization of bladder scanning
Deformed shape of bladder
Small capacity and thick wall are seen
Focal nodular lesion seen
May be sessile, echogenic and mostly located at base of bladder
simulating bladder tumors.
Undermining ulcer of bladder wall seen as intravasation of urine into
deeper layer of bladder wall with overhanging mucosa.
C.T. Findings
Offer no significant contribution except detection of faint calcification.
Evidence of disease adjacent to genital tract (especially seminal vesical and
prostate).
Angiography
Angiographic appearance are nonspecific
Lesion may be hypervascular or hypovascular reflecting difficult stages
of activity of infection.
In hypervascular type, there are widened and tortuous arteries of the
thickened bladder wall simulating bladder tumors.
Urethra
Rare cause of urethritis, occurs due to descending infection resulting from
tuberculous involvement of kidneys, prostatic abscess, urethral stricture,
pelviurethral abscess or fistula formation.
Fistulas may be numerous resulting in so called watering can perineum.
Retrograde Urethrography
Strictures are often secondary to periurethral abscess formation.
Sonourethrography
Effective in assessing true extent of periurethral fibrosis or stricture.
To balloon dilatation, urethrotomy or surgical urethroplasty.
CT and MRI have limited roles
GENITAL TRACT TUBERCULOSIS

TB of Female Genital Tract
Source acquired by hematogenous dissemination from extragenital source
usually lung.
Primary focus of genital tuberculosis is fallopian tube. Spread from the
fallopian tube to the uterus can occur in 50 percent of tubal infection.
Imaging Features
1. Plain X-ray
Shows calcification of tubes or ovaries Linear streak in the course of
fallopian tube, appear as faint/dense tiny nodule.
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. Hysterosapingography
Invaluable procedure for evaluating the internal architecture of female
reproductive tract.
Obtaining early films when about 3 to 4 ml of contrast is already
instilled defining endometrial and tubal details and spillage pattern.
Detect reduction of uterine luminal size due to scarring and intrauterine
adhesion.
Tubercular tubal abnormalities are almost always bilateral but not

symmetrical
Fallopian tube narrowing, occlusion and fistula formation have been
observed
Caseous ulceration of mucosa produces ragged contour and diverticular
outpouching of both isthmus and the ampulla.
Diverticular cavities may surround ampulla and give characteristic tufted
appearance.
As tuberculosis heals, 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, stricture, 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, 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, angulated with
demarcated borders. 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.
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.
Sequence of involvement
Epididymis : 42%
Seminal vesicle : 23%
Prostate : 21%
Testes : 15%
Vas deferens : 12%
Pelvic urethra : 1%
Epididymitis
Incidence : Upto 54 percent, rapidly declined in the west. 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, on USG, it is clearly defined, rounded, echofree space with
distal enhancement; commonest at are multiple.
MRI
Enlarged in a focal or diffuse manner and assumes a darker signal intensity.
Tubercular Orchitis Rare

Source
Contiguous extension from the epididymis
Hematogenous spread
Ultrasound
Testis may be enlarged and hypoechoic focal areas of hypoechogenicity
mimicking tumors.
Peripheral, 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.
Color Doppler shows increased number and concentration and prominent
blood vessels in the affected tests.
Chronic Orchitis
Testis is enlarged, hard and nontender. Echoes are increased in intensity
and usually uniform.
Patchy involvement is irregular and may present as a mass indistinguishable
from tumor.
Hydrocele is usually present which is anechoic but may reveal irregular,
thick septation with heterogeneous debris. Presence of calcification in
hydrocele is definite indication of tubercular etiology.
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, 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, may be thickened, diffusely or locally
MRI
Endorectal balloon surface coil MR image shows detail anatomy.
Prostate
Route of entry
Descending infection from urinary tract
Lymphatic and hematogenous spread

Direct extension from neighbouring organs
Ascending infection from urethra
Occurs after intravesical BCG therapy for bladder carcinoma.
Pathology
Basically the gland is enlarged and contains intraprostatic lesions that
represent foci of caseous necrosis and inflammation.
Tuberculous abscess and excavation produced in the prostate may also
communicates with the urethra.
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.
Irregularities of outline of the hypoechoic areas may be seen
Irregularities of external contour of the prostate is noted.
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, more clearly on enhanced CT
MRI
Areas of fibrosis or abscess may be seen as areas of decreased signal
intensity on T2 weighted images.
Vas Deferense
Involved in 12 percent of genital TB
Calcification are characteristic intraluminal concretion but intramural
calcification has also been reported
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.
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.
Medical renal disease can be classified into various groups
CLASSIFICATION
I. Glomerular Disease
1. Primary glomerular disease :
a. Those presenting as nephrosis :
Minimal change disease.
Membranous glomerulonephritis
Membranoproliferative glomerulonephritis.
Focal segmental glomerulonephritis
b. Those presenting as nephritis :
Acute diffuse proliferative glomerulonephritis
Rapidly progressive glomerulonephritis.
Focal proliferative glomerulonephritis.
Hereditary nephritis.
Chronic glomerulonephritis.
IgA nephropathy
2. Secondary glomerular involvement in :
a. Systemic disease :
Systemic lupus erythematosus
Polyarteritis nodosa
Wageners granulomatosis
Henoch schonlein purpura
Diabetes mellitus
Renal amyloidosis
b. Infection :
Infective endocarditis
Shunt nephritis
Malaria
Syphilis
Hepatitis B virus
Human immunodeficiency virus
c. Tumors :
Carcinomas
Hodkins disease
Lukemias i.e. chronic lymphatic leukemia
Wilms tumor
d. Drug Toxicity :
Pencillamin Gold
Probenicid Mercury
Captopril Phenidione
NSAIDS Trimethadion
Above secondarily disease presents as nephritis.
II. Renovascular Diseases

a. Renal vein thrombosis
b. Infarction and occlusion
c. Renal artery stenosis and renovascular hypertension
III. Tubulointerstitial Disease

a. Pyelonephritis including infective group, reflux nephropathy and drug
induced nephropathy.
b. ATN (acute tubular necrosis)
c. DCN (diffuse cortical necrosis)
d. Nephrocalcinosis
e. Medullary sponge kidney
IV. 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, i.e. 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
Medical Renal Diseases 333
Plain bony skiagram support the diagnosis of renal disease by showing

increase bone density.
All above findings though helpful but are not conclusive towards diagnosis
due to low specificity.
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.
In this condition (diabetic nephropathy i.e. vascular involvement) initially
the GFR increases renal size and volume increases but later all of these
decrease.
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.
Final stage is end stage kidney diseases. (ESRD).
AIDS OR HIV INFECTION

By in large Focal/segmental glomerulosclerosis develops, however ATN,
interstitial nephritis may also occurs.
Tubular ectesia and cyst formation occurs.
Partial nephrocalcinosis is typical of MAIC infection, CMV and
Pneumocystis infections.
Usually size of kidney is increased with increased echogenicity.
Incidence of tumor (kaposy sarcoma & lymphoma) and infection (Candida,
Mucormycosis, Cryptococcus, MAIC, Pneumocystis, CMV) are increased.
CONNECTIVE TISSUE DISORDERS

Leads to vasculitis and glomerulonephritis.
Findings are nonspecific on imaging.
SLE forms echopoor patches in an overall echogenic parenchyma.
Rheumatoid arthritis presents as a case of renal amyloidosis.
AMYLOIDOSIS
Renal involvement is mostly in secondary amyloidosis and 90 percent cases
of proteinuria, 50 percent cases of azotemia and 30 percent cases of nephritic
syndrome have renal amyloidosis. Renal failure is quite common.
USG
Initially size increases symmetrically, later it decreases especially the cortex
as amyloid deposites mainly in cortex.
Focal or diffuse echogenic masses with or without mass effect may be

seen in cortex later on.
Corticomedullary differention is normal or increased.
Foci of hemorrhage, amorphous calcification may be seen as a late finding
but nomspecific.
Masses may also be seen in bladder, ureter and pararenal area.
Finally an end stage kidney is formed.
RENOVASCULAR DISORDERS
Renal Vein Thrombosis
Etiology :
1. Renal
a. Primary renal diseases (presenting usually as nephrosis)
Glomerulonephritis especially memberanous as 50 percent of its
cases are complicated by renal vein thrombosis.
Amyloidosis
Diabetes
Systemic lupus erythematosus
b. Neoplasms :
Renal cell carcinoma
Wilms tumors
c. Trauma
2. Extrarenal causes
a. Retroperitonel pathology like benign or malignant masses, lympha-
denopathy, hemorrhage, aneurysms, fibrosis, pancreatitis with or
without pseudocyst formation.
b. IVC thrombosis.
c. Hemodynamic conditions that increase coagulability to cause
hypovolumia:
Dehydration (most common cause in infants)
Oral contraceptive pills ingestion, steroid therapy, maternal diabetes,
congenital heart diseases, polycythemia.
In general causes that decreases renal perfusion oxygenation.
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.
This discrepancy is due to collateral vasculature in adults especially on left
side.
Thirty-three percent patient may have associated or induced pulmonary
embolism.
IMAGING
IVP
Sudden and/or complete block
Kidneys are swollen and increased in size but later decreased in size
due to shrinking
Poor, absent or striated nephrogram
Sketchy filling or pelvicalyceal system.
Gradual and/or incomplete block
Size is usually normal.
Poor, persistent or increasingly dense nephrogram.
USG with Color Doppler Study

An echogenic mass (representing the thrombus) inside the lumen of renal
vein may be noted. This thrombus may be anechoic in the acute phase.
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. Although
contributory, this is not a very reliable method and now PCR, MRA dnd
MRI are thought to be more reliable.
Rapid re-establishment of normal flow may occur as the collaterals develop
and this is again more rapidly on left side.
Initially for 10 to 14 days we find a swollen enlarged kidney which
compresses the sinus and pelvicalyceal system.
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.
Corticomedullary differentiation is lost after 3 to 4 weeks.
In very late stages a small, smooth kidney with absent corticomedullary
differentiation is noted.
Contrast Enhanced CT Scan

The affected kidney is enlarged and more hypoattenuating than normal.
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.
Phelbography: Selective renal or IVC.
Filling defect in vein.
Renal venous jet is absent
Arteriography
Stretching of vessels, faint nephrogram. Slow circulation time, no filling
of vein and filling of collaterals are observed.
Retrograde pyelogram Sketchy filling with notching due to collaterats.

Radionuclide scan: Divided renal function study can assess post thrombosis
function.
OCCLUSION AND INFARCTION

Etiology
1. Embolism is the most common cause in adults.
2. Thrombosis due to hemorrhage in a fissured plaque.
3. Hemolytic uremic syndrome is the most important and common cause in a
child.
4. Aortic dissection
5. Vascular spasm as in shock.
According to the vessel involved the nature of infarct is decided, i.e.
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.
Clinical Features
Unilateral disease causes only pain and hematuria.
Bilateral disease presents with renal failure.
Imaging
IVP
Early Stages
No nephrogram or very faint nephrogram without the opacification of
pelvicalyceal system both in total and partial disease.
In subtotal or segmental disease a focal nephrographic defect may be noted.
Late stages
Shrinking of size.
Four weeks onwards in total disease small smooth, kidney with normal
PCS is seen, 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. There may be a subcapsular
halo of hypoechoic tissue (representing edematous
normally perfused tissue by subcapsular vessels.)
In HUS initially (phases of anemia) the kidney is
enlarged showing an echogenic cortex/Enhanced CM
differentiation but absent color flow. Color returns

(before phase of diuresis) acting as a marker to stop
peritoneal dialysis. Therefore prevents complication
due to long PI.
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.
Echogenic thrombus inlumen may be noted.
Late stage Small, echogenic, smooth/scarred kidney with
mormal pelvi calyceal system but loss of Corteco-
medullary differentiation is noted.
CT scan: Focal or generalized hypoattenuating lesion with/without
mass effect and a CAPSULAR RIM SIGN is noted.
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.
Angiography : Features are almost same as that in IVP.
A filling defect and obstruction in vessel may be seen.
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,
i.e. renovascular hypertension but still we discuss so much about this tiny
number, why?
a. because this occurs in young
b. because this is a curable condition
Etiology
1. 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.
Congenital coarctation of aorta or renal artery, Takayasu arteritis and
neurofibromatosis cause occlusion at ostia.
Trauma
Radiation arteritis (in child)
External compression by diaphragmatic crura, tendinous bands, psoas
muscle, pheochromocytoma, renal cell carcinoma, aneurysm, hydatid,
lympho-sarcoma, etc.
2. Renal artery occlusion
3. Renal artery aneurysm or arterio venous fistulae.
4. Renal artery arteritis as in
Polyarteritis nodosa, Takayasus arteritis, congenital rubella, syphilis,

thromboangi itis obliterans.
Atherosclerosis occurs commonly in old age males, 30 percent cases are
bilateral and affects the initial 2 cm (1/3) of main renal artery in an eccentric
manner.
Fibromuscular dysplasia is seen more commonly in young females, 50
percent cases are bilateral and distal 2/3 and segmental arteries are involved
forming a typical STRING OF BEADS / SAUSSACE SIGN.
Strategy for Investigation

If disease is clinically suspected by following criteria -
1. Severe hypertension in age < 40 and female.
2. Recent onset accelerated hypertension.
3. No response to treatment.
4. High peripheral plasma rennin activity.
5. abdominal bruit.
First rule out parenchymal disease as reflux nephropathy
Do IVDSA if . 40 yrs.
Do Angiogram if < 40 yrs
Captopril scintigraphy (to assess function) : can also

be done by rennin ratio > 1.5 in diseased side.
IVDSA
> 90 percent atherosclerotic lesions are correctly graded and > 90 percent
renal artery stenosis are diagnosed.
Not good for branch stenosis.
Flush Aortogram
To rule out any other cause.
To confirm/refute presence of collaterals (from 1-4 lumbar arteries, aorta,
internal ilterna iliac, gonadal, adrenal and intercostal arteries).
Selective Renal Angiography

Of both diseased and normal side small vessels study should be done.
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.
Radionuclide Scan
TC 99 DMSA static imaging shows decreased relative renal function
(< 45% of total), though sensitive but not specific.
Dynamic imaging using TC 99 DTPA, TC 99 MAG 3 or I123 hippuran
shows.
a. Decreased relative perfusion from 1st images
b. Decreased relative function.
c. Delayed intra renal transit
d. Delayed (> 5 min) visualization of pelvicalyceal system.
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. is no longer done due to high false negative result.
Now we take early films at 2,3,5,10 minutes interval.
a. delayed visualization of pelvicalyceal system on affected side
(Nephrographic anomaly is usually not well appreciated).
b. small smooth kidney left (>15 mm smaller than right, right > 20 mm
smaller than left.
c. increasingly dense pyelogram
d. notching due to collaterals
USG and Doppler: [may add captopil] highly, specific but insensitive.
a. Size is normal or decreased
b. Aorta : Renal artery peak systolic velocity ratio > 3-3.5
c. Tardus (decreased accleration time >.07 sec decreased acceleration
index < 3 m/s2 ) and parvus wave form, in downstream vessels.
d. Peat systolic volume > 180 cm/s at site of stenosis.
e. Spectral broadening distally.
f. Dampening just proximal.
> 60 percent stenosis significance, >75 percent stenosis severe.
TUBULO INTERSTITIAL DISEASES (TID)

Acute Pyelonephritis
disease of tubules and interstitium are very closely related and hence are
grouped under the rubric of TID, These include
a. Interstitial nephritis and pyelonephritis both of which refer to the similar
pathological process with the only difference being in their etiologies,
i.e. the latter being infective and envolving the pelvicalyceal system
also.
b. Acute tubular necrosis and clnically similar condition known as diffuse
cortical necrosis.
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.
i. Focal (called as lobar nehronia) or diffuse swelling of kidneys with
compression of central sinus and pelvicalyceal system [seen on all
modalities].
ii. IVP shows poor and /or delayed filling up of pelvicalyceal system with
a dense persistant and striated nephrogram in severe cases.
iii. 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.
iv. Wall of Pelvicalyceal system and ureter is thickened due to edema while
on doppler decreased or absent vascularity noted.
v. NCCT shows a swollen kidney with hypo/hyper attenuated areas and
loss of Corticomedullary differentiation. In CECT, 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.
CT scan is being increasingly used for this purpose and is said to be
more sensitive than USG.
vi. Areas of abscess formation if present are seen as solid or cystic areas
with thick wall irregular outline and internal debris. Mass effect may be
noted and these may be perirenal stranding. CT Scan and IVP show
rim or intracavitory enhancement apart from above findings.
Chronic Pyelonephritis and Reflux Nephropathy

These two are closely related conditions and in young age, even a normal
kidney may be involved, if there is infection lower down with Vesicoureteral
reflux. In adults it is usually the devitalized renal tissue which is usually
involved.
Scarring of renal tissue may be severe enough to cause CRF, hypertension,
etc. though focal scarring is usually asymptomatic especially in adults.
Imaging: IVP, USG, CT scan, plain X-ray
1. Small scarred kidney. The scarring may be unilateral or bilateral, focal
or generalized but always assymetrical.
2. Hypertrophy of remaining parenchyma
3. Distorsion of underlying calyx (rarely may be normal) with a broken
interpapillary line.
4. Distance of vertebral body from affected pole is increased usually upper
pole and that of right side is more involved.
5. Decreased cortical thickness.
6. Increased echogenicity with poor medullary definition.
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.
Now there is an important and confusing term known as papillary necrosis,

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.
Pathologically, acute pyelonephritis may be divided in:
a. A process starting in interstitium and secondarily involving the tubules
so that if obstructive element is severe pyonephrosis may develop later.
b. A process initiating as a chemico-coagulative necrotic phenomenon at
papillary tips leading to what is known as papillary necrosis or
necrotizing papillitis.
The latter usually occurs in diabetes and immunocompromized patients
(where it is usually florid associated with infection if acute or bilateral if
chronic).
Other causes are sickle cell disease and trait, obstruction with infection,
severe acute infection, severe ARF of infancy but most common cause
(especially in old psychiatrically disturbed females) is ANALGESIC
NEPHROPATHY. Such patients hardly if ever give a history of drug intake.
There may be multiple Pelvicalycead system tumors with it.
Analgesics like indomethacin, phenytbulazone and phenacetin are commonly
implicated and can cause both interstitial nephritis and papillary necrosis,
that too of multiple bilateral papillae.
Clinically the patient may present as hematuria, colic, sterile pyuria and
CRF.
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. Other non-specific findings are clubbing, blunting and truncation
of calyx and papilla respectively in plain X-ray and IVP.
In the usual chronic form of disease papillae may show various degree of
damage. The two kidneys are symmetrically involved and asymmetry means
associated renalartery stenosis, obstruction and infection.
Renal outline and size initially may be normal or increased, later on the size
may be decreased with smooth scarring leading to a wavy outline.
Enhancement on contrast administration is usually normal and a sloughed
papilla forms a filling defect.
Medulla may also be involved if there is associated diabetes with infection

or obstruction with infection. In these cases (i.e. when infection is present)
the disease is usually unilateral and sysmmetric.
USG is helpful in later phases only.
Differential diagnosis to medullary sponge kidney, T.B., Reflux disease,
cyst and Megacalyx.
RENAL TUBERCULOSIS
Though bilateral involvement is the rule clinically significant disease is
usually found to be unilateral.
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, ureter, UB, etc.
(similar to endobronchial spread)
Fibrosis, stricture, etc.
Clinical Features
Twenty percent cases are diagnosed at operation or autopsy.
Twenty to Fifty six percent diagnosed on urine examination in asymptomatic
patient
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.
Imaging
Tomographic evaluation of kidney is of particular significance in this
condition.
Plain KUB X-Ray

Fifty percent cases will show parenchymal calcification (renal calcification
in TB is more common than bladder and ureter). Specific features are that
the calcification is indefinite, irregular, faint dense (may be so faint that it
may be difficult to differentiate from normal renal tissue), just a speck to
large areas, i.e. to the extent of autonephrectomy.
Size may be normal or increased or decreased.
In ureter, calcification in TB can be differentiated from that in
schistosomiasis in that latter shows lower ureter calcification with a dilated
ureter.
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, irregular.
Also one should look for evidence of calcification elsewhere (10%) i.e.
spleen (more common in histiocytosis), lymphnode, psoas, adrenal and
for disease elsewhere as in spine, chest, etc.
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.
IVP
Shows evidence only when a lesion has bursted into Pelvicalyceal system
forming papillary cavity or has led to changes in PCS
1. Minimal erosion of single calyceal tip is the earliest sign (D/D pyelosinus
back flow or normal variation).
2. Caliectasis with irregular contour (implying cortical necrosis) and erosion
of pyramids, described as fuzzy, feathery or moth eaten. Sometimes a
cavity with fistula to calyx may be seen.
3. Cicatrization of major or minor calyx or its infudibula. [In such cases it is
difficult to differentiate it from a cavity with sinus.]
4. Parenchymal mass with or without punctate calcification (if > 5 cm then
called as granuloma) D/D renal cen carcinoma.
5. Ureter (always secondary involvement) is dilated early on with irregular
outline because of inflamed mucosa, this can also lead to hydronephrosis/
hydro ureter. Strictures (most commons at ureterovesical or uretreropelvic

junction) gives a beaded look while extreme dilatation forms a cork screw
ureter. Last stage is a fibrosed pipe stem ureter.
6. Bladder may be fibrosed (thimble), inflamed (cystitis) or have granulomas.
Retrograde Pyelogram
Poor renal function is an indication
Give prophylactic antibiotic
Examine two sides at an internal of 4 to 6 days.
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.
Changes secondary to granulomas are noted.
CT Scan
Is useful when very poor function prohibits use of contrast.
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.
Lesion may resolve or enlarge or cavitate and communicate to pelvicalyceal
system.
Chronic disease shows strictures with back pressure changes, inflamed
mucosa, calcification sinus, fistula, etc.
USG guided FNAC is an important tool.
EMPHYSEMATOUS PYELONEPHRITIS (EPN)

Is an acute fulminating fatal necrotic pyelonephritis.
Mostly (62-70%) infection is due to E. coli, other being Pseudomonas,
Klebsiella, proteus, Candida and Aerobacter, all being capable of gas
formation.
Deilitated (as diabetics 90%) and old age females (2:1 to males) are more
prone.
Disease is bilateral is 5-10 percent.
Also the incidence of obstruction is more in diabetics (75%)
Eighteen percent present with pyrexia of unknown oxigin, other present
with fever, flank pain, hyperglycemia, acidosis, dehydration and electrolyte
imbalance.
EPN type I Parenchymal destruction with gas
more severe and fatal (69%)
more in immuncompromised patient.
more in hypovascular kidney.
Emergency nephrectomy is the treatment of choice
EPN type II Renal/perirenal fluid with gas bubbles, loculi or gas in

PCS (called as air pyelogram).
Less severe (18% mortality)
Percutaneous nephrostomy is the treatment.
X-Ray
Gas is renal fossa
Air pyelogram
USG: dirty shadow with echogenic renal fossa.
CT: is the best method to diagnose.
XANTHOGRANULOMATOUS PYELONEPHRITIS
Is an uncommon chronic suppurative disease where chronic disease
process leads to focal (called as tumefactive), segmental or generalized
collection of fat laden foam or histiocytes giving a yellow appearance in
gross section.
Proteus, E. coli are common organism.
Nephrolithiasis (75%) is very common and is the cause for obstructive
uropathy
Usually unilateral but bilateral disease is also observed
More in middle aged, diabetic, female.
Pain, mass, weight loss and UTI are usual symptoms while diffuse from
may lead to non functional kidney.
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.
Segmental One or more hypoechoic masses associated to a calyx with calculi
at the tip of related papilla.
Diffuse Increased size, normal shape, lost corticomedullary
differentiation.
Many hypoechoic areas or masses, corresponding to dialated
calyces.
Posterior enhancement behind necrosed areas.
Central sinus is very echogenic usually with a staghorn calculi.
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.
If perirenal extension present then outline is irregular.
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, clot, lucent calculi, transitional call carcinoma,
fibroepithelial polyp, leukoplakia, cholesteatoma, etc.
Gas and papillary necrosis may be seen
Renal function is decreased.
Malakoplakia
Rare granulomatous E. coli infection. Usually lower tract affected.
Plaques of various sizes (.5-3 cm) seen as filling defects are noted.
Usually old immunocompromised female are affected
In kidney the function normal and masses may be formed.
It is a locally invasive disease.
Cholesteatoma
Whorly conglomerate of desquamated epithelial cells.
Leukoplakia
Metaplastic plaques formed.
Schistosomiasis
Hydroneprhosis due to lower tract involvement.
Filariasis
Pyelolymphatic backflow seen.
Hydatid Disease
Thick calcified walled cyst with hydatied sand and scolices.
Poles more affectd
Retrograde pyelogram shows a goblet or cresent sign.
ACUTE TUBULAR NECROSIS (also known as acute reversible renal
failure)
Is an acute oliguric renal failure that cannot be explained by obstruction,
arterial, venous or glomerular insufficiency.
Cellular debris (that form casts) is inside the tubules.

Etiology severe ischemia as in
Pregnancy (complicated HgCl toxicity
Hypotension Ethyleneglycol toxicity
Dehydration Contrast toxicity
Hemoglobinuria Gentamycin toxicity
Postoperative
It slowly corrects on its own and is the most common cause of ARF in
hospital patients.
Imaging
IVP Increasingly dense and persistant pyelogram.
X-ray Enlarged renal silhoutte.
USG Increased sized especially A-P size, increased cortical echogenicity (in
toxic ATC with increased CMD or enlarged prominent pyramids/in ischemic
ATN).
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 (in renal art.) while in prerenal disease it is >.75 (except
hepato renal syndrome).
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.
More severe and irreversible involvement of cortex only (sparing a sub
capsular rim).
X-ray abdomen in 3 weeks a patchy but more typically pencil line or tramlike
calcification developes.
IVP and CT: Rim Sign.
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.
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).
Etiology
i. Increased intestinal absorption of Ca++
ii. Increased bone turnover
iii. Dystrophic calcification
Hyperparathyroidism, idiopathic hypercalcemia, renal tubular acidosis,
medullary sponge kidney, sarcoidosis, hyperoxaluria, hypervitaminosis-D,
milk-alkalie syndrome, osteoporosis, myelomatosis, hyperthyroidism,
trauma, tuberculosis, tumors (10% cases of R.C.C.) hydatid, diseases
chistosoma renal atherosclerosis.
a. Cortical (> 5%) b. Medullary
* Acute cortical necrosis * Secondary to cortical (rare).
* GN with nephrosis * Hyperparathyroidism is the
most common cause (16%)
* Alports disease * Medullary sponge kidney
(75% of MSK cases)
* Haemolytic uremic syndroma * Papillary necrosis.
* Transplant rejection * Cushings syndrome
* Sickle cell disease * Pyelonephritis.
* Ethylene glycol toxicity * Metastasis.
* Wilsons disease
Medullary calcification in distal renal tubular acidosis is typically dense.
Medullary nephrocalcinosis quite commonly leads to nephrolithiasis and
UTI.
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.
MEDULLARY SPONGE KIDNEY

Unilateral or bilateral, Unifocal or multifocal
It is formed due to congenital ectesia of the tubules located in pyramids
May be associated with hemihypertrophy, Autosomal dominant polycystic
kidney, Marfans syndrome, Ehler Danlos syndrome, distal renal tubular
acidosis, horseshoe kidney, parathyroid adenoma, congenital hypertrophic
pyloric stenosis, carolis disease.
Disease may be asymptomatic, may be seen in 5 to 25 percent patients
with calculi which leads to symptoms, may also be associated with cortical
cysts .
Calculi initiation occurs in walls of tubules when hypercalciuria is present.
Kidney may be large especially in patients with hemihypertrophy.
Imaging
IVP Increased papillary blush and persistant visualization of medulla.
USG Most useful tool.
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. Tumors
may also form in the same way.
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.
It is said that 3 to 5 cysts in appropriate clinical setting and CRF are
diagnostic.
USG
Minute to large (5-3cm), few to many cysts with increase in renal size in
severe cases is noted. If very cysts present, echogenicity is increased.
The gravity of problem depends directly upon duration of dialysis, age,
sex, 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, representing tumor and echoes, representing hemorrhage
are quite commonly seen
Cysts involve both cortex and medulla
In dialysis patients shunt thrombosis, function, etc can be evaluated by
Doppler technique
It is said that after 5 yrs. Incidence of a disease rises to 90 percent.
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.
24 Planning of
Radiology Department
INTRODUCTION
The basic aim in planning the radiology department is to prevent the unwanted
exposure of radiation to patients, radiation workers and surroundings.
The factors which contribute to the reduction of doses are following:
1. Proper planning, designing of the rooms
2. Installation of equipment according to recommendation of AERB
3. Qualified personnel
PLANNING OF DIAGNOSTIC X-RAY DEPARTMENT

Design of X-ray Facilities
Three types of facilities are identified, according to their size. First is the
X-ray facility located in a private office or small hospital; next is the moderate
size community hospital; 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. Some types of rooms are common to all X-ray facilities,
regardless of the size of the institution housing them.
Table 24.1: 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...
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, radiographic fluoroscopic

examination room. A darkroom, a film viewing area, a film file room and space
for necessary clerical support are also required for every X-ray facility.
Designing Team
The designing team should have a minimum of six members.
1. Hospital administrator The person who has an overview for relationship
of the radiology service to the rest of the hospital about allocated funds.
2. Architect Responsible for construction details
3. Radiologist and chief technologist Provide the necessary information
about workload and anticipated future requirements.
4. Radiologic physicist Responsible for radiation protection for radiation
worker, and how to utilize the equipments.
5. Equipment manufacturer Provides the necessary specifications of power
requirements, space requirement and radiation characteristics.
Departmental Activity
Various authors and designers developed rules for estimating required
department activity. 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.
Knowing the number of out patient examinations per day. If this number is
divided into twenty, a general purpose room can easily accommodate.
Example an average of 250 patients visit a medical clinic each day. If 20
percent of the patients are referred for X-ray examination and 5 percent of
those are reexamined, how many X-ray rooms are required.
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
Example: A 400 bed hospital has an 85 percent occupancy rate. On the average,
40 percent of inpatients receive an X-ray examination during their four-day
stay. How many X-ray rooms are needed for inpatients care?
400 beds 85 percent occupied 0.4 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, private office have one or two rooms. Community hospitals
with 200 beds or less have two rooms. Large general hospitals and teaching
hospitals have ten to fifteen rooms or more. As the size of the X-ray examining
room increases, the average radiation dose to employees decreases.
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, the emergency area and surgery.
Modern structural engineering designs allow X-ray departments to be
located on any floor of the hospital. 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. On ground level, the X-ray
examining rooms are generally located to the inside.
Plan Layout
The plan layout of the X-ray facility must take into account the various traffic
patterns, some of which are diagramed.
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, the radiographic
supply storeroom, the darkroom, and the professional staff. The lounge must
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.
If the radiologists activities are strictly clinical, his office should be located
within the radiology area so that technologists and other physicians have easy
access to him. On the other hand, if the radiologist is involved in teaching and
research, 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.
Single corridor plan with reasonable merit is designed in such a way so
that patients enter at one and exit at the other.
Such a design should be located in the X-ray department in such a way
that future expansion can be accommodated.
The X-ray examining rooms are positioned to the center with a central
processing
A second central core design show, the X-ray examining rooms located
along the out side walls with the administrative areas located to the interior.
X-ray Examination Room

Space and freedom from abstraction are key requirements in the design of an
X-ray examination room.
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.
Too many console barriers incorporate, 12-inch square viewing windows.
The control area should be roomy enough to accommodate several persons
and adequately store film.
The location of the chest stand is important if an out side wall is available,
it should be used for positioning the chest stand especially the examining room
is located above ground level. If the chest board must be positioned along an
inside wall, additional lead shielding will probably have to be placed directly
behind it.
In nearly every X-ray room the generator is located out of the way in the
corner and positioned on the floor, 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. This leaves 3 to 7 feet available in the false ceiling for the storage of
X-ray apparatus particularly the generator.
Room Size
The room size should be such as to permit installation, 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. At this distance a protection barrier of 1.5 mm lead thickness can
provide adequate protection, from all these consideration size has been
worked out to be minimum of 24 square meter (6 m 4 m).
Opening on Ventilation
Unshielded opening like windows and ventilations if provided in the x-ray
room, it must be located above a height of 2 meters from the ground level.
Illumination Control
In case of fluoroscopy machines, 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, control panel should be
located in separate room, waiting area should be provided out side x-ray
room.
Use of Protective Devices

Protective barrier: In case of diagnostic tubes operating at 100 kV, the
control panel should be located in a separate room or behind a mobile
protective barrier of 1.5 mm lead equivalent or partition wall with a viewing
window of lead glass of 1.5 mm lead equivalent.
Protective glass (vinal lead compound) of at least 0.25 mm lead
equivalent should be used by radiologist during screening work.
A fluoroscopic chair of 1.5 mm lead equivalent should be used during
vertical fluoroscopy
The protective flaps of 0.50 mm lead equivalent, if attached to the
fluoroscopic screen, help reducing exposure to the gonads.
The radiologist or technicians should wear a protective apron of at
least 0.25 mm lead equivalent.
In cases of CT machines, the control panel is located in separate room,
the viewing window should have the lead equivalence such that it may
offer the same protection as the rest of the wall. It may be between
2 to 3 mm lead equivalence.
Dark Room
Radiography begins and ends in the darkroom, where the films are loaded into
suitable light proof holders and where they are returned for processing into a
finished radiography.
Location
The dark room should be located very close to the radiography room as it
saves lot of time. If there are two or more radiographic room, the dark room
should preferably be situated in central position.
Size and Installation of the Darkroom

A dark room must be large enough to accommodate all the necessary equipment
without overcrowding. Ideal is 100 square feet floor space and 11 feet ceiling
height.
It is essential for dry and wet work to be carried out at a safe distance
from each other. For this reason, the loading bench and the processing tanks
are arranged along opposite sides of the room referred to as the dry and wet
sides.
The preparation of processing solutions must always take place out-side
the processing room.
Building Essentials
A. Protection against radiation: It is essential for the darkroom to be well
protected against radiation. The lead equivalence of the wall adjoining the
radiographic room should be efficient to prevent the films from Fogging.
B. Floor: The floor should be durable, easily cleaned, not slippery and resistant
to staining and corrosive substances.
Ceramic tiles or natural clay are most satisfactory.
C. Wall covering: The walls of the dark room do not have to be dark. The
colour chosen should first be judged under safelight illumination as it is
important that there should be maximum reflection of safe-light. The wall
should be covered with chemical resistance material such as special paint,
varnish, concrete or ceramic tiles.
Ventilation
Windows should be avoided because they do not render the rooms lightproof.
Air Conditioning is though ideal solution for the dark room.
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, water pipes.
It is essential to earth all exposed non-current carrying metallic objects.
Pass Box
The most suitable location for the passbox is near the film loading bench.
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. The passbox is
divided into two compartments one for exposed and the other for unexposed
films.
Entrance to Dark Room

Single doorwhich must be made light tight and should have an inside
lock.
Interlocked doors - So designed that one door cannot be opened until the
other is completely closed.
Maze - Serves as light trap and does not require doors. Require large floor
area.
Revolving door - The preferred entrance these days.
Illumination
The darkroom should have three types of illumination
1. Safe light: The dark room should have source which will not fog films and
also provide adequate illumination. The working distance should not be
less than 1.2 meter and bulb wattage should preferably be less than 15
watts.
2. General Illumination: Needed for general purpose such as cleaning changing
solutions
3. Radiographic illumination: A fluorescent illumination for viewing wet
radiographic should be mounted over the washing compartment.
The Dry Side

Various components of dry side are; loading bench, compartments for cassettes,
film bin, storage for reserve film, brackets for film hangers.
The length of the loading bench depends upon the volume of work and
available space. The bench to covering should be linoleum and color chosen
under allow the object to be readily distinguishable under safelight
illumination.
Separate compartments for storing every size of cassette are essential.
Reserve films should be stored in a cupboard or case line with lead.
Film hangers are best kept on brackets above the loading bench.
The Wet Side

The processing tanks comprise the major equipment of the side dark room.
The simplest type consist of a three compartment tank, one end-compartment
being used for developing and the opposite one for fixing. The middle
compartment serves both to rinse and the opposite for fixing. The middle
compartment serves both to rinse and wash the films and should be supplied
with running water.
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.
A more satisfactory arrangement consists of a large insulated stainless
steel double compartment master tank.
A fixing tank should have twice the volume of a developing tank, 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, in which the inlet is at the bottom and the overflow at the top.
The heating elements is thermostatically controlled.

Various types of drying devices help speed up the drying of films. Driers
are available in enamel or stainless steel cabinets provided with heating
elements and a blower fan.
Film Construction
Radiographic film has two parts: The base and the emulsion. The emulsion
is enclosed by a protective covering of gelatin, the thickness of the sheet
of radiographic film ranges form 200 to 300 m.
The base: Maintains its size and shape. The base is of uniform lucency
during manufacture, dye is added to the base to provide blue tint to the
film.
Two types of bases are available cellulose triacetate and polyester.
The emulsion: Consists of a homogenous mixture of gelatin and silver
halide crystals. The silver halide crystal is the active ingredient of the
radiographic emulsion. In the typical emulsion 95 percent of the silver
halide is silver bromide. An emulsion should have two important
characteristics.
a. Speed or sensitivity: The relative ability of an emulsion to respond with
light / X-ray.
b. 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.
Types of Films
1. Screen film: There are three characteristics : contrast, speed, and light
absorption.
Contrast: High contrast film produces a very black and white image
while a low contrast film image is more gray.
Speed: The thicker the emulsion more sensitive the film and therefore
the higher the speed.
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.
Size of films: 17 14, 15 12, 12 12, 12 10, 18 8, 6 8,
15 6, 11 14, 14 14
2. 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.
3. Mammography film: Fine grain single emulsion film designed to be exposed
with a single intensifying screen.
4. Duplicating film: It is single emulsion film that is exposed to ultra-violet
light through the exiting radiography to produce a copy.
5. Subtraction film
6. Dental film:
Intra oral
Panoramic
7. Medical Imaging film: Single coated film and has got five layers.
A. Polyester base B. Substratum
C. Emulsion D. Top coat (gelatin and hardener)
E. Back layer is antiholo
Cassette
A case measuring about one-half inch in thickness and having an aluminium,
stainless steel, or plastic frame, a hinged lid with one or more flat springs.
One intensifying screen is mounted on front inside of the cassette, and the
second screen is mounted on the back inside.
Size of the cassettes are available in the corresponding size of films.
Intensifying Screens
An intensifying screen is a device that converts the energy of the x-ray beam
into visible light. This visible light then interacts with the radiographic film,
forming the latent image.
The intensifying screen act as an amplifier of the remnant radiation reaching
the screen film cassette.
Use of an intensifying screen results in considerably lower radiation dose
and on another hand increase the radiography contrast.
There are four layers:
a. Protective: This is transparent layer of the screen. It makes the screen
resistant to abrasion and damage caused by handling.
b. Phosphor: The active layer emits light during stimulation by x-rays. The
active substance of conventional phosphor is crystalline calcium tungstate.
Rare earth are the phosphor material in newer faster screens.
c. Reflective layer: Between the phosphor and the base is a reflective layer
approximately 25 m thick, made of a substance such as magnesium oxide
or titanium dioxide.
d. Base: It is 1 mm thick and serves principally as a mechanical support or
phosphor layer.
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 intensification factor
Exposure without screens
IF =
Exposure with screens
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, the visible light emitted by screen is viewed directly by
radiologist and give the corresponding x-ray pattern. The intensity of light
emitted by the screen is very low and therefore difficult to see, and the eye is
most sensitive to green part of spectrum. Therefore fluorescent material used
is zinc cadmium sulphide.
Clip type
Hanger
Channel type
The size of the hanger is corresponding to film size.
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.
Organic reducing agents: ((Hydroquinone and metol) Hydroquinone is slow
acting and is responsible for the blackest shades (contrast). Metal acts
rapidly and influences the lighter shades of gray.
Activator: Sodium carbonate or sodium hydroxide- activator results in
swelling the emulsion, making easier penetration of developing agent.
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.
Preservative: Sodium sulfite-protects the reducing agents from oxidation
by the air.
Fixation: The purpose of fixation is
1. To remove the unexposed and undeveloped silver halides
2. To preserve the film image
3. To harden the emulsion
Fixing solution
1. Fixing agent: Hypo (sodium thiosulphate)
2. Preservative: Sodium Sulfite
3. Hardener: Chrome alum or potassium alum
4. Acid : Sulphide or acetic acid
Drier: It is required to get the film dried properly within shortest possible time.
AUTOMATIC PROCESSING CORNER CUTLURE

There are many advantages of automatic processors
1. It shortens total processing time.
2. Improves quality of the film image due to more accurate temperature
regulation.
3. Increase the capacity of the radiology department.
Essentials of Automatic Processor

1. Transport mechanism: Series of rollers which transport the films through
various sections
2. 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, to minimize
swelling of the emulsion
Precise replenishment of the developer and fixer to maintain the proper
alkalinity of the developer.
3. Temperature control: Developer temperature 35C, wash water temperature
is 2.8C lower
4. Circulation system: Agitation of chemicals is provided by a circulation system
that continuously pumps the developer and the fixer.
Three Phase Generators

Three-phase generators produce an almost constant potential difference for
the x-ray tube.
Three-phase generator operates on three-phase current which consists of
three single-phase currents out of step with each other.
These are arranged in either a delta or a star configuration.
Three-phase circuits have delta wound primary coils but differ in the form
of secondary windings.
With three phase equipment, three autotransformer are needed for KV
selection one for each phase.
Advantages
1. High MA at very short exposures, especially useful in angiography, spotfilm,
radiography.
2. Nearly constant potential characteristics
3. Higher effective kV
TRANSFORMER
Transformer is a device which convert e.m.f. source of AC current from high
voltage to low voltage and vice versa.
Construction
It consist of two coils, each consisting of many turn of wire wounded in an
iron coil, one of these coils is known as primary which is connected to an AC
source.
Secondary is connected to the electrical device
When current flows through the primary coil it creates a magnetic field
within the core, this magnetic field induces a current in the secondary coil.
The current only flows in the secondary circuit when the magnetic field is
increasing or decreasing.
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 - to increase voltage
Step down - 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.
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.
RECTIFICATION
Defined as the process of changing alternating current to direct current.
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. As
long as target is cold, the x-ray tube itself suppresses the negative phase of
alternating current.
Valve tube rectification: A valve tube is a thermionic diode tube which

resembles, an x-ray tube, allowing passages of current in one direction only,
that is from cathode to anode.
a. Half wave rectification: For this, one valve or two valves are used. If two
valves are used in the circuit, filament never charged positivity. In this
case only positive phase of alternating current function while negatives
phase is suppressed.,
b. Full wave rectification: Four valve tubes can be arranged to provide full-
wave rectification.
By following the numbered portions of the circuits A and B, regardless of
the polarity of transformer during the different valves of the AC cycle, the
current always reaches the x-ray tube used in same direction that is both half
cycles.
Valve Tube
They are thermionic diode tube having the same general construction as x-ray
tubes, but differing incertain details.
Cathode
Consists of a coil of tungsten wire which is larger and thicker than the filament
of an x-ray tube. It lies in the longitudinal axis of the tubes; supported by a
large molybdenum spiral.
Anode
Having a large surface and cylindrical shape (resembling a metal can), surrounds
the filament. This makes it possible for a large current to pass from the
cathode to the anode.
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.
Cathode: A tungsten filament measuring 0.2 mm in diameter and 1 cm in
length.
Supporting wires
Focusing cup (molybdenum)
Anode: There is two main types
1. Stationary: target is a button of tungsten set in a block of copper which
has very high heat storage capacity.
2. Rotating: 5-6 percent. Rhenium mixed with tungsten to prevent development
of cracks in the anode, molybdenum is used as the base material on which
a layer of tungsten-rhenium is coated. This anode attached to the shaft of
a small induction motor, rotates during x-ray production.
Glass Envelope
The anode and the cathode are enclosed in a borosilicate glass envelope
containing as perfect a vacuum as possible.
X-ray Therapy Tubes

X-ray therapy tubes operate at low MA values of tubes current, to provide
x-ray of four main KV therapy ranges.
1. Low voltage 50-120 KV
2. Intermediate voltage 130-150 KV
3. Orthovoltage 160-300 KV
4. Mega voltage 4 MV
A typical orthovoltage therapy tube has a larger filament, a stationary anode,
and larger focal spot.
Difference
Diagnostic machine (Tube) Therapy machine (Tube)
1. Low voltage 100-150 KV 1. Mostly high voltage (more than 200 KV)
2. Short focus for short exposure 2. Large focus for larger exposure
3. Wide beam used 3. Narrow beam used so extraradiation
avoided more homogenous and less
scattering effects
4. Exposed a larger area 4. Exposed a particular area
5. Long frequency so less penetrating 5. 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. The ray projections are found, 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. The detector does not
form the image. It adds up the energy of all the transmitted photons. The
numerical data from multiple ray sums and then computer processed to
reconstructs an image.
CT scanner have gone through a number of design changes.
1. First generation (translate-rotate, one detector)
2. Second generation (translate-rotate multiple detectors)
3. Third generation (Rotate-rotate)
4. Rotate-fixed (fourth generation)
First generation: It employed a pencil like x-ray beam and a single detector.
The x-ray tube detector movements were both linear and rotary. A five view
study of the head took about 25 to 30 minutes.
Second generation: Adopting a fan-shaped beam and multiple detectors. The
movements of the x-ray tube detector are both linear and rotary, just like first
generation. Second generation scanners produced a tomographic section in
between 10 to 90 sec.
Rotate-Rotate (third generation): Both the x-ray tube and detectors rotating
around the patient. The unit produce a scan in 4.9 sec. Multiple detectors are
aligned along the arc of a circle whose center is the x-ray tube focal spot. The
x-ray beam is collimated into a fan beam. Both the x-ray tube and detectors
rotate about the patient.
Rotate fixed (fourth generation): The detectors form a ring that completely
surrounds the patient. The detector does not move. The x-ray tube rotates in
a circle inside the detector ring and x-ray beam is collimated to form a fan
beam. Both rotate-rotate and rotate-fixed CT units continue to give excellent
results, with no clear advantage of one over the other.
X-ray tubes: New fan beam units have a diagnostic type x-ray tube with a
rotation anode and much smaller focal spot, in some units down to 0.6 mm.
These tubes have large heat loading and heat dissipation capabilities to withstand
the very high heat loads.
Collimators: The x-ray beam is collimated at two points, one close to the
x-ray tube and at the detectors. Perfect alignment between two is essential.
The collimators regulate the thickness of the tomography slice and control the
scatter, radiation.
Detectors: There are two types of detectors used in CT scanners.
1. Scintillation crystals
2. Xenon gas ionization chambers
1. Scintillation crystals: Materials that produce light when ionizing radiation
reacts with them. The cadmium tungstate (Cd W04) is the scintillation
crystal most commonly used in CT units.
2. Xenon gas ionization chambers: The photon interacts with gas atom by
ionizing the atom into an electron-ion pair. The voltage will cause the electron
to move toward the anode, and the positive ion to move toward the cathode.
When the electrons reach the anode, they produce a small current in the
anode. This small current is the output signal from the detector.
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. The individual blocks are called voxels. Their
composition and thickness along with the quality of the beam, determine the
degree of attenuation. The linear attenuation coefficient () is used to quantitate
attenuation.
The analytic methods are used for image reconstruction.
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. As the gantry rotates,
the patient table is continuously driven at a rate of one slice thickness per one
revolution of the gantry.
Most image performance parameters are not affected by spiral scanning
(spiral and contrast resolution, field uniformity, patient dose).
The one parameter that is affected is the apparent slice thickness. (Increased
by 30%).
An accepted advantage is that a patient volume can be scanned continuously
without gaps.
This should be helpful in reformatted sagittal and coronal image.
CT Angiography
Spiral CT angiography is new technique for noninvasive vascular imaging.
Compared to conventional CT, spiral CT permits maintenance of a higher
concentration of intravascular contrast material. Single breath hold scans
eliminate irregularities caused by ventilatory misregistration. Permits three
dimensional (3D) renderings.
Spiral Acquisition
The ratio of the table speed to the collimator width denotes the scan pitch.
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.
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, metallic implants.
MIP selected only the brightest pixel along each ray.
Multi-slice Computed Tomography

A multi-slice CT system uses multiple detector rows and can therefore acquire
multiple slice per rotation. Also the speed of gantry rotation is increased resulting
in an overall increase in scan speed. In the same time at narrower collimation
leading to higher axial resolution.
Basic Technology
Combines a 0.5 second gantry rotation, simultaneous multi-slice acquisition
by a slice selectable detector array.
Detector Design
The detector element is a solid state scintillator; more than 30,000 detector
elements are placed in a 2D array in the channel direction and in the longitudinal
direction. 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.
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, the collimator design is modified to compensate for the increase in A
scatter radiation.
Data Acquisition System

The data acquisition system for multi slice CT permits 4 slices to be acquired
simultaneously per gantry rotation.
Virtual endoscopy: An alternative and non-invasive diagnostic technique to
conventional endoscopy is an innovative diagnostic imaging. Endoscopy could
be replaced by this computerized technique known as virtual endoscopy. Latest
generation helical CT scanners Hi-speed CT is able to take hundreds of images
of the chest, abdomen or other areas of the body, all in just a few seconds, in
single breathold.
The data thus acquired is able to create internal views, that simulate the
views seen through a vide endoscope. The virtual endoscopy procedure can
be performed and repeated as many times as desired on the same data with
different navigation plans.
The virtual endoscopy-medical applications can be applied to many areas

of the body like : virtual colonoscopy, virtual bronchoscopy and virtual
angioscopy etc.
ULTRASOUND
Ultrasound is a non ionizing diagnostic imaging technique with high frequency
sound waves. The frequency of the sound waves used in medical field may be
between 1 5 MHz.
Principles
US wave are generated from piezoelectric crystals like lead zirconate titanate.
When voltage is placed across the disc of the crystal it creates a pulse of high
frequency sound waves. These waves pass into the body and are both reflected
and refracted at tissue interface in the body. Reflected US wave with different
acoustic density are detected by same crystal and converted into electrical
impulse. The impulses are displayed on TV monitor.
Display of Images
A mode: Amplitude modulated scan echoes are displayed as spike projection
from a base line. Spike height is proportional to echo intensity.
M mode: Returning echoes are recorded as bright dots along the time base.
It is extensively used in echo-cardiography to show movement of structures.
B mode: It is a brightness modulated scan. In a static B mode image,
the information is displayed as gray scale which depicts the amplitude of
returning echoes in varying shades of gray between black and white. Black is
due to weak signal and white signifies high amplitude.
2-D Real Time Scan

In this, the returning B-mode echoes are displayed in such a way that movement
of scanned body part is demonstrated. The real time scanner produces images
at a fast frame speed of 30 sec.
Fast frame rate can be achieved by mechanical scanner or electronic array
transducer.
Electronic Array
In this, the returning B-mode echoes are electronically coupled and focused.
Three types are:
1. Linear scanner: A number of transducer elements (64-200) are arranged in
a line and excited in groups so a rectangular format is produced.
2. Phased array: About 32 transducer elements are pulsed to form a sector
image.
Transducers
A transducer is a device that converts one form of energy into another.
Ultrasound transducers are used to convert an electric signal into ultrasonic
energy that can be transmitted into tissues, and to convert ultrasonic energy
reflected back from the tissues into an electronic signal.
The most important component is a thin (0.5 mm) piezoelectric crystal.
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 inside electrode abuts against a thick backing block that absorbs
sound waves transmitted back into the transducer.
Usually 3 or 3.5 MHz transducer is used. For deeper structure 1.5 or 2
MHz is required, for superficial structure (musculo skeletal purpose) 15 MHz.
Coupling material is needed to make the contact between transducer and skin
surface properly.
Guidance Systems
Ultrasound guided interventional procedure can be performed by
1. Indirect ultrasound guidance
2. Freehand real time needle placement
3. Use of sonographic needle guidance system
There are two major designs:
a. Holes or grooves built into the transducer to hold biopsy needle.
b. Attachable biopsy guided that may be easily fixed to the transducer.
Linear or curved array transducers are frequently used for guiding
procedures because of their good near field resolution, which allows
visualization of the needle after relatively little tissue penetration.
Endo Sonography
The possible applications in the field of endosonography are various:
1. Transesophageal
2. Transrectal
3. Transvaginal
4. Transurethral
In general the following kinds of US system are available on the market.
1. Mechanical 360 scanners (used 1,2,3,4)
2. Mechanical 90-110 sector scanners (used in transvaginal)
3. Electronic linear arrays (used in 1,2,3)
4. Electronic phased arrays (used in 1)
In all these types the same techniques are used to generate US image.
The rectal, transurethral and transvaginal scanners have a light rod, at the
tip of which the one element transducer is mounted.
In transurethral applications, filling the bladder with water makes the

coupling between the transducer and the bladder.
In rectal, vaginal and transesophageal applications, the coupling is performed
by a water filled rubber balloon.
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.
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. They provide penetration
up/to approximately 8 cm.
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.
To detect blood flow within arteries and veins, the continuous wave Doppler
can only tell velocity, while pulsed Doppler give information both about depth,
velocity and direction of flow.
Ultrasound Contrast Media

An ideal US contrast agent should be injectable intravenously, non-toxic, capable
of passing through the pulmonary capillary bed and stable enough for the
duration of the examination. Most agents enhance the echo by producing
differences in acoustic impendence between the agent and the surrounding
medium.
Albunex - is composed of air filled human albumin microspheres having a
mean size approximately 3, 5 microns ranging from 1 to 8 m. The acoustic
properties lasting 8 to 12 minutes.
Pass successfully through pulmonary capillary circulation and stable enough
following injection.
Levovist is a stable mixture consisting of 99.9 percent specially
manufactured microcrystalline galactose microparticles and 0.1 percent palmitic
acid upon dissolution and agitation in sterile water for injection, the galactose
disaggregates into microparticles. These microbubbles are highly echogenic
and are sufficiently stable for transit though the pulmonary circuit.
Echovist a galactose agent that forms larger bubbles and has been used
extensively without any evidence of toxicity.
Instead of air, many of the new agents take advantage of low-solubility
gases such as perfluorocarbons.
CLOSED CIRCUIT TELEVISION

The components of a television system are camera, camera control unit and
monitor.
The television image is made up of thousands of tiny dots of different
brighteners. The dot distribution is along horizontal line called horizontal
scan line.
Television Camera
The Vidicon camera is usually employed for fluoroscopy.
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, and electromagnetic focusing coil and
two pairs of electrostatic deflecting coils.
The fluoroscopic image from the image intensifier is focused on to the
target assembly which consists of three layers.
i. Glass face plate
ii. Signal plate
iii. Target
Light passes though face plate
The signal place is a thin transparent film of graphite. It is an electrical
conductor with positive potential.
It is a thin film of photoconductive material, usually antimony sulfide.
The cathode is located at the opposite end of vidicon tube is heated indirectly
by an internal electrical coil the heating coil, boils electrons, creating and
electron cloud.
The anode extends across the target of the tube as a fine wire mesh, and
with signal plate form a uniform decelerating field adjacent to target.
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.
All four coils, working together move the electron beam over the target in
a repetitive scanning motion.
Video Signal
When a globule absorbs light, photoelectrons are emitted. The globule positively
charged and behaves like a tiny capacitor. Similar events occurs over the
entire surface of the target. 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 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.
The globules are not all discharged at the same time. Only a small cluster,
a dot, is discharged each instant in time. Then the electron beam moves on to
the next dot in an orderly sequence, discharging all the globules on the target.
The result is a series of video pulses.
Television Monitor
The last link in the television chain is the Monitor. It contains the picture tube
and the controls for regulating brightness and contrast.
MRI
The most important part of the MR machine is the main magnet. The strength
of a magnet is given in tesla.
In MRI different types of magnets are used.
1. Permanent magnets: Does not use any energy for work, disadvantage
thermal instability, limited field strength and its weight.
2. Resistive magnets: An electrical current is passed through a loop of wire
and generates a magnetic field (electromagnet).
3. Super conducting magnet: Most widely used in MR machines at the present
time. They have a special current carrying conductor. This is cooled down
to super conducting temperature (-269C). At this temperature the current
conducting material loses its resistance for electricity creating a constant
magnetic field so called cryogens (helium, nitrogen) are used for cooling
of these magnets and have to be refilled. Advantages of super conducting
magnets are high magnetic field strength and excellent magnets field
homogeneity.
High field strength system have better spatial resolution and may be
used for spectroscopy.
Low field system on the other hand often better tissue contrast are
cheaper in price.
The Coils
In MRI radio frequency coils are necessary to send in the RF pulse.
Volume Coils
Volume coils are used in all MR units. The body coil is a permanent part of the
scanner and surrounds the patients. It is important, as it is the transmitter for
all types of examinations. It also receives the signal.
Shim Coils
Better homogeneity can be achieved by electrical and mechanical adjustments.
For this process which is called shimming, the shim coils are used.
Gradient coils- are used to systematically vary the magnetic field by producing
additional linear electromagnetic fields, thus making slice selection.
Surface Coils
Are placed directly on the area of interest and have different shapes
corresponding to the part to be examined. They are receiver coils only, most
of the received signal coming from tissues near by.
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. 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. Enhancement)
Maximum intensity projection (MIP) images

Obtained both of MRA and MRV by special technique
2. Phase contrast MRA
i. Depends on phase rather than amplitude of MR signal
ii. It reveals direction and velocity of blood flow along with anatomical
detail like TOF MRA
iii. May be adjusted to low or high flow sensitivity. So selective venous
and arterial MRA images can be obtained.
iv. Useful for evaluating altered hemodynamics such as flow reversal

after major vessel occlusion or stenosis.
v. Excellent suppression of background rhythm but longer acquisition
time.
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.
Mechanism of Contrast Enhancement in MRI

MR contrast agents work by altering the tissue relaxation rates by changing
the local magnetic environment.
It is useful to classify two broad categories as T1 and T2 agents.
T1 Agents
Gd DTPA (gadopentetate dimeglumine or magnevist) ionic Gd. DTPA-
BMA (gadodiamide or Ommiscan)
Gd-HP-DO3A (gadoteridol or Prochance) ]
Nonionic
Gadalinium DTPA, the first contrast usually administered in a dose of 0.1.
mmol/kg
Major use of these agents is in detection of cerebral capillary break or
enhancement of tissue. The agents cross the disrupted blood brain barrier
similar to iodinated contrast used in CT.
T2 Agents
Gd chelates can be used as T2 agents is used in sufficiently high concentration
and studied with fast imaging (0.5 mmol/kg).
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, spleen, bone marrow and L.N. This leads to loss
of signal of the back, ground normal tissue on T2 Wt images.
Superparamagnetic small particles (SPIO), ferumoxide or AMI-25 has
completed clinical trials.
Given IV. 10 - 15 microgram/kg
Magnetite (Resovit or SHU-555) is the other SPIO in phase III clinical
trial.
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: decay, decay, electron capture, and isomeric transition).
Radionucleides: Unstable nucleides which release energy to reach a stable
state are called radionucleides or radioisotopes, e.g. 123I and 131I are isotopes
of iodine.
Isotopes: Nucleides with same atomic number (Z) (chemical and biological
behaviour), but different mass number and different energy state.
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 = 3.7 x 1010 Bq
Radiopharmaceutical: Pharmaceutical with appropriate biological behaviour
bound to radioactive material.
Emission Computed tomography: Provides in vivo 3 dimensional distribution
of radiopharmaceuticals within body, generated from set of 2 dimensional
projectional images.
SPECT
Two types
PET
SPECT: Involves detection of gamma rays emitted by single photon from
radionucleide like Tc-99m and Th201.
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, N-13, O-15 and F-18. It measures
concentration of radiopharmaceuticals in body that are labelled with positron.
Isotopes used are prepared by cyclotron (bombardment of (+) charge (protons
with stable nucleus positron).
Common Adverse Reactions

1. Vaso Vagal reactions with syncope, hypotension can occur after IV
administration.
2. Significant allergic reactions urticaria, bronchospasm and rarely
anaphylaxis.
3. Albumin macroaggregates not indicated in pts. having hypersensitivity to
albumin products.
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.
Advantages
1. To demonstrate early physiological changes.
2. Metabolic alterations at 5 to 10 percent level detected.
Very sensitive, however non-specific complimentary to other imaging
modalities.
Radiopharmaceuticals
1. Strontium-85: emits high radiations dose, is of long t but poor imaging
characteristics.
2. Fluorine-18: It has short t and requires cyclotrons.
3. Tc -99m labelled agents: Inorganic Tc polyphosphates, organic
pyrophosphates and low radiation dose (t short 6 hrs.) diphosphonates
(methylene i.e. MDP and ethylene hydroxy EHDP).
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. Then distribution
of radionucleide is identified with gamma camera.
Factors Affecting Uptake of Radionuclide in Bone

a. Blood supply in fracture, osteomyelitis, vascular primary
neoplasm (called as extended pattern)
if ischemia prevents radiotracer from reaching bone

appears cold on scan
b. Cellular activity and mineral turnover in epiphysis (growth area),
reparative response around traumatic and inflammatory lesions, in areas of
mechanical stress, and also in response to neoplastic, metabolic or
hormonal stimuli. Intensity of uptake reflects rate of bone metabolism
(i.e. osteoblastic activity).
4. Gallium-67 citrate Ga-phosphate complexes localizes active sepsis. In
areas with MDP uptake when Gallium uptake exceeds in bone or soft
tissues indicates active species.
5. Indium-111 or 99Tc-HMPAO labeled WBCs: advantage over Gallium
true physiological location of WBCs in sepsis false positive results
uptake in areas of fracture also.
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. after injection) soft tissue activity has
cleared

Better delineation of skeleton
3 phase bone scanning done for significant information.
1. 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. 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.
3. Delayed scan 2 hrs. After injection

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. Normally isotope distribution observed in
a. Ends of long bones
b. Sacroiliac joints
c. Around nasal cavity
d. Tips of scapulae
e. Laryngeal cartilage
f. Calcifying costochondral junction
g. Oral alveolar ridge
h. Sternum
In children, hot symmetrical epiphyseal growth zones are seen. In elderly
patients, senile osteoporosis where it shows poor bone uptake.
APPLICATIONS
Metastasis
i. Multiple scattered focal hot spots ( uptake) on bone scan, commonly
in axial skeleton, proximal long bones and areas difficult to visualize
radiographically sternum, scapula, base of skull and anterior ribs can be
seen.
ii. Sensitivity > 95 percent, reliable indicator than conventional radiography.
Radiation dose is less for whole body scan but low specificity, so used
as screening procedure with confirmatory radiographs to detect
suspicious areas.
iii. Osteoblastic metastasis appears as hot spot on bone scan. Osteolytic
Metastasis destroy trabeculae and appears as cold spot.
If mixed lesion, uptake in lesion may be normal, this can give false
negative bone scan.
iv. Disseminated metastasis shows generalized uptake known as super
scan.
v. Important for monitoring progression or regression of Metastasis so
useful in evaluating response to treatment.
Primary Bone Tumors

Highly vascular on flow scan and very active on delayed scan.
Benign Tumors low grade uptake because less vascular than primary
Malignant Tumor (If in benign indicates complicated by fracture/
infection). Benign GCT and osteoid osteomas show intense hyperemia (so
uptake)
(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.
First few hours after injury, there is hyperemia so increase uptake in blood
flow and blood pool images.
Within 24 hrs, 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.
In athletes and dancers, there are stress fractures (Microfractures) not
usually detected by conventional radiographs, it shows focal uptake at
cortical margins.
Traumatic synovitis shows increase uptake on delayed scan.
Inflammation
Acute osteomyelitis: Changes are not apparent on radiographs till 7 to 10 days
of inoculation of bacteria. On bone scan all three phases show increase uptake.
If cold lesion present in acute osteomyelitis it suggests highly aggressive process
or sequestrum formation.
Cellulitis: There is soft tissue hyperemia on blood pool and flow images and
no significant bone uptake on delayed scan.
Arthritis
Both inflammatory and degenerative arthritis show increase uptake on bone
scan.
a. Inflammatory arthritis: Hyperemia of synovium on flow and blood pool
images and increased uptake in capsule on delayed scans.
b. Degenerative arthritis: Synovial hyperemia is absent and only delayed scan
shows positiveness along subchondral surface, distribution of involved
joint indicate particular type e.g. gout, rheumatoid arthritis and Psoriatic
arthropathy and ankylosing spondylitis involvement of SI joint, costovertebral
joint showing increased uptake and loss of vertebral segmentality due to
bridging syndesmophytes.
Avascular Necrosis
Ischaemia of bone is due to loss of nutrient artery blood supply. Ischemic
bone is cold on scan as tracer cannot enter avascular area. The reparative
response of normal bone adjacent to ischemic area will show increase uptake
which enhances cold focus. This produces characteristic Doughnut

appearance of vascular necrosis of hip.
Pagets Disease
Aetiology of Pagets disease is unknown but blood flow is markedly increased.
Osteoblastic and osteoclastic activity are also increased resulting in weakened
and deformed bones which are intensely hot on bone scan.
Fibrous Dysplasia
Affected bones show intense uptake and distribution, commonly as spotty
involvement rather than diffuse involvement (characteristic of Pagets disease).
Super Scan
Significantly greater radionucleide uptake throughout the skeleton, reduced
urinary activity and less soft tissue background than expected for age. Observed
in following conditions.
a. Metabolic bone disease, e.g. hyperparathyroidism, renal osteodystrophy,
osteomalacia;
b. Myeloproliferative hematolgoical disorders;
c. Disseminated Metastasis;
d. Hypertrophic pulmonary osteoarthropathy.
RENAL IMAGING
Radiopharmaceuticals used to evaluate renal functions
a. Glomerular filteration agents
99Tc-DTPA (diethylene triamine penta-acetate)
To measure GFR
b. 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. 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.
1. Dynamic renography (dynamic renal scan)
Techniques
2. Static renal scan
1. Dynamic Renal Scan: To measure
i. Total renal function
ii. Differential renal blood flow

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

1. 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.
2. BC: Secretory or II phase (3-5 min)

It represents nephron accumulation and the slope of curve is related to rate
of accumulation. Thus slope is steep during diuresis, decreases in renal
tubular failure and impaired renal perfusion in renal artery stenosis and
shock.
3. Peak (c): Normally sharp because rate of transit through all nephrons is
roughly same. Peak is rounded where transit is unequal e.g. in diffuse
vascular parenchymal disease. Peak is sharper in diuresis than dehydration.
4. Transit time (AC): In next 3 to 5 min, it is relatively longer when urine flow
rate falls e.g. in dehydration, shock, renal failure and shorter in diuresis.
5. CD (Excretory or III phase): It is roughly exponential fall over next 20
minutes. In this stage ureteric drainage is more than accumulation.
This fall is abnormally slow when drainage from pelvis is impaired, e.g.
ureteric obstruction, hydronephrosis or severely reduced urine flow rate.
Mean transit time: Mean transit time refers to time taken for activity to fall
of its peak. This time can be recorded either for kidney as a whole or for
parenchyma or for renal pelvis. It will be reduced physiologically during diuresis
and prolonged during dehydration and in diseases that increases tubular transit
(e.g. chronic renal inflammation, hydronephrosis).
Clinical Uses
1. Obstructive uropathy: Primary investigation is excretory urography and
a. Renography enables function and effect of obstruction to be
measured on renal parenchyma.
b. To know site of obstruction and determine extent of severity.
c. Diuretic augmented renography to distinguish obstruction from non
obstructive dilatation (e.g. extra renal pelvis)
0.5 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.
Rapid reduction of renal activity (no obstruction)

If after diuresis
No dramatic fall in activity PUJ obstruction
2. Renal failure: Aim in acute renal failure is to determine whether the

obstruction is reversible or not.
Characteristically falling curve is strong evidence against obstruction
whereas slowly rising curve indicates acute obstruction or exacerbation of
chronic renal disease. Delayed images show whether activity in bladder is
present or not.
Scintigraphy has little role in chronic renal failure.
3. Hypertension: In Renal Artery Stenosis, there is decrease perfusion pressure

and renogram is lower and flatter and transit time is prolonged, difference
of 15 to 20 percent compared with opposite side is significant.
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. after standard renogram) orally or IV and another renogram
after 1 hour. In functionally significant renal artery stenosis there is
decreased uptake and increased transit after captopril administration.
Comparison of renogram made on time to peak greater than 10 minutes
is positive. Ratio of GFR more than 1.5 is positive.
4. Renovascular conditions:
In Renal vein thrombosis, there is decreased perfusion and filtration so
hold up of activity in collecting system.
Emboli causes infarction. In initial flow phase study decrease or absent
blood flow in affected area, so decreased uptake and peripheral defects.
5. Renal Transplantation: To study the complications
a. Acute Tubular Necrosis- Commonest, as there is no excretion, so poor
TcDTPA accumulation and tracer diffuses into extracellular space and
renal activity disappears.
b, 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.
c. Ureteric obstruction: There is excretion and delineation of proximal
collecting system without visualization of bladder.
d. 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.
e. Infarction : Detected by avascularity during all phase and no counts.
Static renal scan: (Renal morphology)
99Tc DMSA (dimercaptosuccinate) is compound of choice, fixed in tubule
cells and renal parenchyma with no significant excretion.

Procedure: 150 MBq of Tc MDSA IV given and after 3 hours, kidneys are
imaged in anterior, posterior and posterior oblique views and delayed images
(if obstruction present).
Images assessed for renal size, position, axis (horse-shoe kidney), presence
of dilated pelvicalcycal system and cortical scars or other renal defects.
Clinical Uses
1. Infection
a. Chronic pyelonephritis : irregular, small scarred kidney with decrease
in activity.
b. Tuberculosis: The size of defect depends on extent of disease.

c. Acute pyelonephritis: Localized renal parenchymal defects present even
when urogram is normal.
2. Tumors: In static image no features to distinguish carcinoma, cyst,
hematoma, A.V. fistula. All show filling defects (non-specific). However,
rapid sequence studies show relatively increased vascularity of carcinoma
and fistulas, compared with cysts and hematoma.
3. Renal trauma: Renal contusion causes generalized decrease in function or
localized filling defects. However in urogram there is only delayed excretion.
Cystourethrography
For (1) Vesicoureteric Reflux (VUR)
a. Direct technique same as MCU but radiation does is less.
Procedure: Bladder is catheterized and 99mTc-Pertechnetate instilled to max
bladder volume in saline solution (18.5-37 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).
The images are assessed for presence of ureteric and intrarenal reflux.
b. Indirect technique At the end of standard renogram, when radionucleide
reaches bladder, patient is asked to void and activity is seen. Incidence of
VUR underestimated as bladder is not always fully distended. The technique
is otherwise the same but catheterization is not required.
2. Residual bladder volume 25 mBq 99Tc DTPA IV and activity is
recorded in bladder in known time and bladder emptied, volume
measured and bladder reimaged for same length of time.
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. Motility disorders e.g. diffuse esophageal spasm, achalasia and scleroderma,
etc.
b. Gastroesophageal reflux
Technique: Patient is given standard radioactive meal (-99Tc-sulfur colloid
labelled scrambled egg) and transit (or emptying) time is noted.
If there is long delay in transit time, study to be continued and denotes
delayed emptying.
PET is used for staging esophageal carcinoma in conjunction with CT
more sensitive than CT in identifying regional and particularly distant
metastasis.
Stomach
1. 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. The geometric
mean of gastric counts is calculated. 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.
Gastric emptying curves for solids and liquids
2. Dynamic antral scintigraphy: Dynamic imaging of stomach, allows

visualization and characterization of antral contractions and for correlation
of antral frequency and amplitude with gastric motility i.e. greater antral
motility faster emptying.
3. Small intestine:
Indications: a. Suspected GI bleeding
b. Detection of Meckels diverticulum
c. Assessment of inflammatory bowel disease
Investigation of GI Bleeding
a. 99Tc-sulphur colloid
Two radionucleide
b. Tc-labelled autologous red cells

Tc-sulfur colloid is given IV and cleared from circulation by
reticuloendothelial cells of liver, spleen and bone marrow. If active
bleeding is taking place, the site is identified by extravasation of
radiotracer. This increases with each circulation and radioactivity is
deposited at bleeding site. Site of bleeding may be identified when
bleeding rate is low as 0.1 ml/min.
99Tc-labeled red cells : autologous red blood cells which constantly
circulate and extravasation can be seen at bleeding site.
Meckels Diverticulum
99
Tc pertechnetate (IV 50-200 Ci/kg B.W.) 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. Increased activity in lower
abdomen usually on right side is recorded.
Inflammatory Bowel Disease

111In labeled leucocytes migrate to inflammatory site and estimate the extent
of disease.
Liver: Radionucleide imaging of liver is performed by using 99Tc sulfur-colloid
or albumin which target the reticuloendothelial system.
Technique: Two to fifteen mCi of Tc sulfur colloid is injected intravenously,
80 to 90 percent dose taken up by Kupffer cells in liver and 5 to 10 percent by
spleen. A small portion is also absorbed by bone marrow. In patients with
normal functioning liver, imaging may begin 5 to 10 minutes after injection
and anterior and posterior images of liver and spleen are recorded.
Normal liver is roughly triangular with curved margins following the
contours of diaphragm and rib cage. Cleft is seen between Rt and (Lt)
lobe.
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.
Uses
1. Large liver Malignancy, early cirrhosis, amyloidosis and hemo-
chromatosis.
2. Small liver Cirrhosis, partial hepatectomy
3. Localized low activity (defect) created by a lesion that does not contain
reticuloendothelial cells. Focal diminished uptake, near the surface and
size more than 2 cm can easily be detected.
Observed in following conditions: Abscess, hydatid cyst, Metastasis (90%
sensitivity), primary neoplasm angioma and hemangioma.
4. 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, extensive
metastasis, decreased hepatic perfusion (cirrhosis, portal vein thrombosis),
increased competition from enlarged spleen (e.g. myelosclerosis, portal
vein occlusion) or from skeleton are observed.
5. Budd chiari syndrome There is occlusion of hepatic veins, so marked
fall in hepatic activity and relatively high activity in caudate lobe.
Spleen: Radionucleide imaging is an important investigation of suspected
morphological and functional abnormalities of spleen and 99Tc colloid is used
for the purpose.
i. Cirrhosis increased activity in spleen as compared to liver
ii. Splenic size + blood flow seen in conditions as malaria, cirrhosis
of chronic infection
iii. Splenic size + No blood flow e.g. leukemia, infarction or lymphoma.
The activity will be lowered than would be expected from size of spleen.
iv. Localized filling defects seen in conditions as infection, metastasis,
cyst and hematoma (most important following blunt trauma) represents
zone of activity. Heart damaged 99Tc-labelled or Cr labelled RBCs
used for functional studies.
Biliary tract: 99Tc-Iminodiacetic acid e.g. 99Tc HIDA to study the action of
biliary tree.
Technique
HIDA (80-160 mBq) IV scan gives information about hepatic parenchyma in
Ist 10 minutes, extahepatic biliary tree is outlined by 20 minutes and excretion
into bowel by 1 hr. takes place
Precautions
Inadequate period of starvation may give false positive results in normal subjects.
Indications
1. Neonatal and childhood jaundice Scintigraphy has important role to
define surgically correctable disease e.g. biliary atresia. This condition can
be excluded if tracer enters small intestine. Obstruction of biliary tree if
failure to demonstrate intestinal activity even at 24 hrs.
2. Delayed excretion Impaired hepatic perfusion, congenital deficiency of
hepatocyte function.
3. Acute cholecystitis Scintigraphy has high sensitivity in diagnosis.
Persistent non-visualization of gall bladder is an indicator of cystic duct
obstruction however liver, bile duct and gut are demonstrated. Other positive
findings for acute cholecystitis includes.
a. Rim Sign increase uptake within adjacent liver

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

81m 133
Kr Ke
t = 13 sec
(Parent 81 Rb 4.6 hr) 5.3 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. Perfusion studies: The principle of perfusion scanning is that particles

greater than 80 to 100 m size of lung capillaries trapped during first pass
through lung. 99Tc microspheres of uniform size (40m) are most widely
used, they are injected intravenously; and cleared from lung over next 12
hrs and then metabolized in liver. Lung activity is proportional to its
perfusion, the more dependent part of lung is slightly more perfused than
rest of the lung. Anterior, posterior and lateral oblique images are taken.
Decreased perfusion is seen in mechanical artery obstructions, alveolar
hypoxia due to air trapping, bronchial obstruction, pneumonia or
redistribution of blood flow in mitral stenosis with pulmonary hypertension.
3. Ventilation/Perfusion Ratio (V/Q): In normal scan, the distribution of
radioactivity is even and parallel in both ventilation and perfusion images.
This pattern is distributed in many conditions.
Diminished ventilation leads to corresponding impaired perfusion (e.g. Bulla/
Collapsed segment).
Decreased perfusion and normal ventilation (e.g. Pulmonary embolus).
Uses
1. Pulmonary embolism: Perfusion scintigraphy is sensitive but not specific,
so ventilation scan is combined to improve specificity. 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.
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, example chronic or reversible pulmonary
tuberculosis, sarcoidosis, etc.
Reverse mismatched defects Conditions where perfusion abnormalities are

more than ventilation scan or vice versa, e.g. Chronic obstructive pulmonary
diseases, bronchiectasis, lobar consolidation/collapse, acute partial bronchial
obstruction.
Scintigraphy underestimates embolic disease in two conditions:
a. Minute peripheral embolization following clot breakdowns may be
overlooked if emboli are distributed evenly.
b. Partial occlusion of both main pulmonary arteries by saddle embolus
produces symmetric scan.
2. Other lesions causing localized perfusions defects: Lung tumor, pneumonia,
exacerbation of chronic infection, e.g. tuberculosis, lung abscess, radiation
pneumonitis and fibrosis.
3. V/Q perfusion studies are used for preoperative assessment of large bullae
and assessment after lobectomy.
Gallium scanning: It has photon energy of (240 KeV) and t of 78 hrs.
Gallium is taken up in the areas of inflammation, granulocyte activity and in
some tumors.
Uses
1. For detection of occult infection (directed extrathoracically).
2. For staging of Ca bronchus, possible also by CT scan.
3. Gallium has affinity for granulomatous lesions in lung, e.g. granuloma of
sarcoidosis increase uptake in hila, paratracheal lymphnodes, parotid glands,
etc.
Uses of PET
1. Important role in staging lung cancer.
2. FDG uptake in chest infection, mimics metastasis.
3. Solitary pulmonary nodule is detected (Benign vs malignant).
4. More sensitive than CT scan for mediastinal assessment of squamous
cancer of lung and whole body imaging for distant metastasis.
CENTRAL NERVOUS SYSTEM

SPECT and PET using both blood flow and metabolic agents produce images
of physiologic and biochemical processes in brain.
Indications
1. First choice in detection of venous sinus thrombosis and early cerebritis.
2. Supplementary to CT & MRI where results are inconclusive.
3. Where CT and MR impractical and unsuccessful e.g. metallic implants.
4. CT and MRI unavailable.
5. Major use in cerebrovascular disorders and neuropsychiatric disorders
e.g. dementia, metabolic and degenerative disease.
Principle: Radionucleides reach brain tumors and lesions by breach in blood

brain barrier due to vascularity, abnormal permeability, reactive edema and
altered celleualr metabolism.
Non-diffusible tracers Diffusible traces
99 123
a. Tc as Naperteslmatate a. 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. 99Tc DTPA-faster renal clearance b. 99Tc labelled HMPAO is most widely used
and determines regional cerebral perfusion

determined t = 6 hrs., high photon yield
(140 KeV)
c. 99mTc-Clucohepatonate c. 99Tc- ethyl cysteinate dimer more

stable than HMPAO
Normal study: Transaxial coronal and sagittal images of cortical and subcortical
structures readily discernible. Frontal lobe is demarcated from temporal lobe
by Sylvian fissures, occipital lobe, visual cortex evident as areas of more
intense activity, midline structures, basal ganglion, thalami, symmetric in uptake
and clearly evident.
Clinical Indications
1. Cerebrovascular diseases
a. 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. This suggests an area of ischemic brain tissue surrounding
infarction i.e. potentially at risk.
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. To determine stroke etiology, it is important for planning of treatment
and in differentiating patient with low flow state due to carotid disease
from patient with thromboembolic disease.
c. TIA (Transient Ischemic Attack)
i. Identification of reversible ischemia.
ii. Identifying patients at risk-persistent focal decrease in cerebral
blood flow on SPECT in post ictus is of clinical significance.
iii. 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. In
patients with normal cerebrovascular reserve after acetazolamide

administration, increase carbondioxide causing vasodilatation and
increase flow. 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.
2. Neuro-Psychiatric diseases
Alzheimers disease SPECT shows diminished perfusion in temporal
lobes and parietal lobes however multi infarct dementia shows patchy
and irregular defects.
To differentiate Depression from Dementia, defects in primary
cortex and deep structures show normal flow in SPECT study in
patients of depression and decreases perfusion in dementia.
PET
a. FDG metabolism in parietoccipital regions
b. It distinguishes different causes of dementia
Picks disease - there is deficit in frontal or fronto-temporal area
Huntingtions disease the deficit is in caudate lobe.
3. Cerebral Tumors
SPECT study: Degree of uptake is directly proportional to neovascularization
and edema e.g. Meningioma and high grade glioma show increased uptake
where as pituitary ademoma and low grade glioma show decrease uptake.
PET: FDG uptake is directly proportional to metabolic activity of brain.
High grade glioma show FDG uptake (worse prognosis)
Important in differentiation of Tumor recurrence vs. necrosis High
FDG suggests recurrence. C11 methionine is used. It is marker of tumour
proliferation. Poor or low uptake indicates necrosis.
4. Epilepsy
SPECT Useful for localization of seizure its site and type - hypoperfusion
in interictal state and hyperperfusion in ictal state. Interictal scanning with
SPECT is less sensitive than during Ictal state.
PET Detects seizure focus and its accuracy is 85 percent. Important
for surgical resection of focus. FDG scan show hot seizure focus during ictal
state ( uptake).
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. Inflammatory disorders, e.g. cerebritis due to herpes, single ill defined
uptake area in temporal lobe, if mature abscess activity ring with inactive
center.
b. Venous sinus thrombosis failure to visualize superior sagital sinus or cut

off transverse sinus.
Radionuclide Cisternography
111In DTPA or 99Tc DTPA in Lumbar subarachnoid space, there is visualization
of cisterns in 1 to 3 hr. sylvian and interhemispeheric fissure in 3 to 6 hr. and

surrounds hemispheres in 24 hr. If activity in dilated ventricles and absent
activity over the cerebral hemispheres for more than 24 hr. denotes obstruction.
Uses
1. Obstructive hydrocephalus Ventricular reflux is seen in early images
and delayed clearance to hemispheres.
In non-communicating No reflux, only delayed appearance of activity
2. Shunt Patency
3. Detection of localization of CSF rhinorrhea pattern of radioactivity
distribution localizes site of fistula.
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.
Radionuclides
i. 131I- It has long t 8.04 days, and emits high radiation dose ( energy
364 KeV) so unsuitable for diagnostic purposes but it is valuable as
therapeutic agent.
ii. 123I It has short t 13.3 hrs. low radiation does ( energy 364 KeV) (it
is excellent for functional study of thyroid tissue)
Disadvantage limited availability and high cost of production as it
requires cyclotron.
iii. 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.
iv. Thallium 201 used in various disorders of patients with residual or
recurrent thyroid cancer.
Uses
1. Ectopic thyroid: Activity can be detected in lingual/thyroglossal duct and
retrosternal area, however, activity is less than normal.
2. Thyroid nodule: Activity according to relative accumulation of radionucleide
in comparison with rest of thyroid tissue. These nodules are usually cold
(less), warm (equal), and hot (greater).
a. Cold: Activity is less than rest of surrounding thyroid tissue

i. Almost all cancers < 1 percent iodine collected after 24 hrs of
injection.
ii. Benign cold nodules Adenoma (35%) focal thyroiditis,
hyperplastic or colloid nodule.
iii. Non thyroid masses Parathyroid cyst or tumor/ lipoma/lymph
nodes
b. Hot: Activity is greater than that of surrounding thyroid tissue
i. Fifty percent functioning autonomous nodules
ii. Relative hot area is due to hyperfunction of normal tissue in
thyroid gland damaged by surgery/radiation/Hashimotos disease
iii. Autonomous foci in toxic multinodular goitre
c. Warm: Activity of nodule may be equal to that in remainder of gland and
these nodules are rarely significant clinically.
Generalized Disorders
Hashimotos Thyroiditis There is enlargement of gland and generalized,
non-uniform patchy alteration in tracer distribution.
Graves disease There is uniform tracer distribution in enlarged gland.
3. Parathyroid gland Thallium substraction scanning is widely used. In
this test thallium 201Chloride is taken up by thyroid and parathyroid, and
the thyroid component is subtracted by doing 99Tc MIBI scan, leaving
only parathyroid activity.
Uses
a. In hyperparathyroidism
Sensitivity is of 90 percent for single adenoma
75 percent of recurrent hyperparathyroidism.
4. Adrenal Gland
Adreno cortical
Adreno medullay
1. Adreno cortical - 131I or Se labelled cholesterol (e.g. Se-75)-6-

Selenomethyl norcholesterol) are used to identify mass in cortex.
Increased cortical function gives rise to increase activity.
a. In cushing syndrome usually there is functioning adenoma which
shows high activity over one adrenal only. Bilateral involvement
denotes hyperplasia.
2. Conns Tumor usually due to aldosterone secreting adenomas give
increase activity on lesion site.
3. Adrenomedullary agents 131I labelled MIBG is used. It is an analogue
of guanethidine which is concentrated in sympathoadrenal tissue.
Primary and Secondary Pheochromocytoma and neuroblastoma -

uptake in adrenal medulla. Radionucleide scanning is also useful in
monitoring response to neuroblastoma treatment.
CARDIOVASCULAR SYSTEM
Myocardial Perfusion Imaging
Perfusion agents Thallium 201 is used, it is K+ analogue, and uptake is
dependent on myocardial blood flow. Therefore used to assess
hypoperfusion or ischemia in wall of heart. It is a cyclotron product and
t is 73 hrs.
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. and then delay or redistribution images are taken. This
denotes resting coronary blood flow.
SPECT images are displayed in three planes of heart (1) Short axis; (2)
Vertical long axis; (3) Horizontal long axis.
Normal lateral wall show greatest activity, 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.
Myocardial infarction perfusion to region on both stress and rest
images and appears fixed and defects can be seen. In defects, we assess
size, severity and degree of redistribution.
Grading of defects
a. Normal
b. Mild defect showing noticeable defect and in counts also but no
definite wall thickening.
c. Moderate defect More reduction of count so that wall appears thin.
d. Severe defect Activity that is not significantly different from
background.
Severe disease or (Lt) ventricular dysfunction
Left ventricle may decompensate with exercise causing decrease in systolic
function and stroke volume increase. This results in transient increase Lt
ventricle end diastolic pressure and cavity size, so on imaging Lt ventricular
lumen appears larger on stress images and wall will appear thinner. Increase
end diastolic pressure causes increase in Lt atrial and pulmonary capillary
pressure, so significant portion of thallium is seen into lungs and increased
pulmonary activity is noted.
Patients who cannot perform physical exercise, pharmacological stress

testing (with dobutamine, dipyridimole or adenosine in association with
myocardial perfusion imaging. This is an alternative method. Dobutamine
is widely used. It is an inotropic agent and increases myocardial O2 demand.
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.
Two conditions where, myocardium may appear nonviable but is only
non-contractile
Stunned myocardium: In Acute reversible ischemia, not persistent enough
to cause necrosis result in temporary failure of mechanical function which
may recover with time.
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.
Although PET is using 18F-fluorodeoxyglucose as gold standard in
identifying metabolic activity in non-contractile myocardium in which
function is likely to return. Thallium 201-SPECt is more cost effective
and relatively simple procedure requiring standard reinjection of thallium
before the resting scan.
Infarct imaging agents: Tc labelled phosphates are used, concentrates in
inversibly damaged myocardium. A positive concentration differentiates
between infarcted and normal tissue.
Uses
To differentiate old and recent infarction (12 hr to 1 week after infarction).
Serial evaluation of infarct size.
Visualization of Rt ventricular infarction.
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.
Residual Lt ventricular function and perfusion following acute
myocardial infarction.
PET
1. Quantitative myocardial perfusion imaging by using N to 13-NH3. Here
is 2 to 3 fold increase in blood flow with pharmacological stress.
2. Myocardial perfusion imaging: To detect coronary artery disease, Rb-82,
N to 13- NH3 and 0 to 15 have been used.
3. Myocardial metabolism To know viable/non-viable myocardium, e.g.
hibernating myocardium (viable but non-functional) protocol used for
viability is resting NH3 and FDG scan (NH3 goes to normal myocardium,
FDG goes to ischemic but viable myocardium). A PET mismatch pattern
or perfusion metabolism mismatch pattern, i.e. reduced perfusion (NH3)
and increased glucose metabolism (FDG) is suggestive of viable
myocardium.
4. Cardiomyopathies and chronic heart disease.
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, their progeny and mankind as a whole, while still allowing
necessary activities from which radiation exposure might result.
Table 26.1: 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 0.5
Total (approximate) 200
RADIOBIOLOGY
Definition: Study of biological effects of ionizing radiation.
Mode of action: Ionizing radiation produces damage in living systems by
ionizing (removing electrons from) the atoms composing the molecular
structures of these systems. An ionized atom will not bond properly into
molecules necessary for the normal functioning of an organ.
This process is not irreversible. At each stage, it is possible to recover
from radiation damage. Ionized atoms can become neutral again by attracting
a free electron. Molecules can be mended by repair enzymes. Cells and tissues
can regenerate and recover from radiation energy.
When ionizing particles interact directly with (transfer their energy to)
vital biologic macromolecules such as DNA, RNA, proteins or enzymes,
damage occurs as a result of what is called direct action. When a vital molecule
such as DNA is acted upon by free radicals previously produced by the
interaction of radiation with water molecules, it is called indirect action. As
80 percent of the body weight is water so more destructive effect results
from indirect action than from direct action.
Effects at cellular level
a. Cells are directly killed or are affected so as to prevent mitosis.
b. The local blood supply is damaged cell deaths
c. Damaged cells not directly killed but become victims of tissue defence
systems. These effects are the same for normal and cancerous tissues
in that they differ little in their individual response to irradiation.
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.
Somatic
a. Early effects: Appear within minutes, hours, days or weeks of radiation
exposure. A substantial dose is required to produce biological effects after
irradiation. Diagnostic radiological procedures do not impart radiation doses
sufficient to cause early effects, e.g. nausea, fatigue, erythema, epilation
(loss of hair), blood disorders, intestinal disorders, depression of sperm
count, temporary or permanent sterlity and injury to central nervous system.
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. Prodromal phase occurs within hours may last for hours or few
days nausea, vomiting, diarrhoea, fatigue, and leucopenia.
ii. Latent period - No symptoms lasts for about a week
iii. Manifest illness
iv. 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, vomiting, diarrhea, electrolyte imbalance, bleeding,
infection, fluid loss (6-10 Gy) (c) Central nervous system syndrome
Stupor, agitation, ataxia, seizure, etc. (50 Gy).
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. For adult humans,
LD50/30 is about 3 Gy (300 rad).
b. Late effects: It becomes apparent years after exposure. The four major
types of late somatic effects are carcinogenesis, life span shortening, cataract
formation embryological or birth effects.
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.g. congenital
blindness, deafness, mental and physical abnormalities.
Stochastic/Nondeterministic/Chronic
The effects obey the laws of chance or probability.
The risk of damaging effect increases with increased exposure but the
effect is not inevitable.
Severity of effect is unrelated to radiation dose and there is no threshold
below which the effect does not occur, e.g. genetic effects and induction
of cancer or leukemia.
Nonstochastic/Deterministic/Acute Effects
The effects are not subject to laws of chance or probability,
Doses above the threshold inevitably produce the effect. Its severity increases
with radiation dose, e.g. short term somatic effects and radiation accidents,
cataract formation and reproductive cell damage.
LET (Linear Energy Transfer) and Its Relationship to
Biological Damage
When ionizing radiation passes through a medium, it interacts with the
medium, and as a result deposits energy along its path. The average
deposited energy per unit path length is called linear energy transfer.
With increasing LET the ability to produce a biological response
increases.
Unit is keV of energy transferred per micrometer of track length in soft
tissue.
Alpha particles and ions of heavy nuclei have high LET.
RBE (relative biologic effectiveness): RBE describes the relative capability
of radiations with various LETs to produce a particular biologic reaction.
Dose of standard radiation necessary to produce given effect.
RBE =
Dose of test radiation necessary to produce same effect.
The standard radiation by convention is 250 kVp X-rays.
Law of Bergonie and Tribondeau
Undifferentiated cells are more radiosensitive than mature cells.
Younger tissues and organs are more radiosensitive
When the level of metabolic activity is high, radiosensitivity is high
Radiosensitivity increases as the proliferation rate of cells and the growth
rate for tissues increase.
This law indicates that the embryo and the fetus which contain a large
number of immature nonspecialized cells, are more susceptible to radiation
damage than is the child or the adult.
Table 26.2: 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.
Radiation workers Remember inverse square law
Protective devices lead apron gloves
Personal monitoring devices
Auxillary staff, viz. 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. This implies that actual
absorbed dose equivalent values should be kept well below their
recommended maximum limits. This concept was put forth by NCRP by
1954.
Care rather than fear.
Severity of harm is proportional to dose and dose rate.
Benefit vs risk ratio should be high.
A. Cardinal Methods to Control Radiation Basic Principles
The three fundamental principles of radiation protection of staff are:
a. Distance: Keeping adequate distance is an effective method to control
radiation. It follows inverse square law (the intensity of radiation
decreases as the square of the distance between the source and detector
or body). Hence the use of long exposure cables for the hand switch in
mobile radiography, or the use of remote control in fluoroscopy is
always safe.
b. Speed or exposure time: Where the radiation beam is produced
continuously, the amount of radiation received will clearly be
proportional to the length of exposure time, hence it should be minimized
by conducting procedures as quickly as possible, or using short bursts
of fluoroscopy and image storage facilities.
c. 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, and scatter radiation from all irradiated
objects (especially the patient).
Types
i. Primary barriers: Any barrier that intercepts the useful X-ray beam e.g.
the floor is nearly always considered a primary barrier and anywhere
from one to four walls may also be primary barriers. It should be
considered while designing the room (by the radiation protection advisor)
and by the equipments manufacturer in the design of tube housings,
collimation systems and the shielding features of intensifier housing etc.
Primary radiation will generally require larger thickness of shielding
material than scattered radiation.
ii. Secondary barriers: Any barrier that intercepts leakage and scatter
radiation, e.g. the ceiling is always considered a secondary barrier, and
during fluoroscopy all fixed barriers are considered secondary including
control booth.
Materials
i. Lead (aprons, gloves, gonad shields, goggles)
ii. Barium concrete
iii. Concrete
iv. Brick.
2 mm lead is equivalent of approx 25 mm layer of high quality barium
plaster, 225 mm solid brick, inch barium plaster, and 150 mm concrete.
Calculation of Thickness of Barrier

It is done by HVL (half value layer). It is the thickness of a specific substance
which when introduced into the beam of radiation will reduce the exposure
rate by half.
Factors Determining Barrier Thickness

1. Quantity of X-ray generated per week or workload
2. 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
0.1 rem/wk for a controlled area or is less than 0.01 rem/wk for
uncontrolled area.
3. 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.
1 barrier 2 barrier
For ceiling U=0 U=1
For floor U=1 U=1
For walls Depends U=1
4. Occupancy factor (T)

It is an expression of the extent of time to which the area being protected
is occupied.
An area that is always occupied will require more shielding than one
which is rarely occupied.
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.e. within a. full occupancy office or laboratory adjacent to
the X-ray department T = 1 X-ray room (T = 1)
b. Partial occupancy corridors, rest rooms (T = 1/4)
c. Occasional occupancy outside areas, elevators, etc.
5. 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. It is particularly
effective in attenuating radiation by the process of photoelectric absorption
and compton scattering.
Other barriers are compared to lead in terms of their lead equivalence. LE
is that thickness of lead in mm which affords the same protection as the
barrier in question for the same radiation quality kVp.
B. Tasks at Different Levels for Radiation Protection
1. Designer/construction: When planning an X-ray department, it is most
important that a radiation protection plan is worked out to supplement
the layout drawings, 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. Radiation protection plan distinguishes
between controlled area and other areas.
Controlled area
Area where adult employee is likely to receive >3/10th of any relevant
dose limit (e.g. 15 mSv whole body dose per annum)
It embraces all rooms with X-ray equipment
Permitted assess is to
a. Classified person staff who are likely to receive 3/10th of dose
limit in the course of their work are described as classified workers.
b. Patient undergoing therapy or diagnostic procedure.
c. Any other person under a written scheme or work.
Supervised area
Area where any person would be likely to receive >1/3rd of the value
required for designation of controlled area (e.g. 5 mSv whole body
dose / annum).
It embraces other rooms of X-ray department and other areas, viz.

offices, waiting rooms, streets or gardens in close vicinity of X-ray
room.
Permitted access is to those whose presence is necessary.
2. Equipment manufacturer and installation
Should be AERB / BARC certified
X-ray tubes must posses proper filters
All X-ray tubes, tube housings and tube transformer assemblies
must be supplied with accompanying instructions containing all
informationon safety.
The radiographic control console should always be located behind
a fixed protective barrier. Often the barrier is equipped with leaded
glass window.
3. Administrator
Overall supervision and coordination of the radiation protection
activities (like personnel monitoring) in the X-ray department.
The administrative chain of authorities include:
a. Appointed doctorfor medical surveillance of classified persons.
b. Radiation protection supervisor for immediate supervision on a
day to day basis.
c. Radiation protection advisorphysicist
d. District health authority / state governmentfor monitoring of
radiation protection.
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. Supervision, advice and guidance to radiographers as and when required,
viz. radiography a pregnant patient.
Radiographer:
i. Factors not within radiographers control
a. Beam filtration
b. Rectification
c. Tube shielding
ii. Factors within radiographers control
a. Optimum collimation
b. Use of fast screen/film (consistent with required unsharpness)
c. Careful centering
d. Optimum exposure parameters
e. Meticulous film processing
f. Highest practicable kV
g. Use of autotimers to control exposure time
h. Use of gonadal shields as appropriate
i. Selection of appropriate grid
j. Compression on obese patients
k. Patients that require assistance during examination should never be
held by X-ray personnel but by member of patients family or by
mechanical devices.
In fluoroscopy:
1. Adequate dark adaptation
2. Use of image intensifier instead of fluoroscopy
3. Radiation not to be continuous / intermittent fluoroscopy
4. Restriction of field sizesuitable collimation
5. Correct operating factorsexposure rate to the patient is actually
reduced by an increase in kV and filtration, and a corresponding decrease
in mA to retain same image brightness.
General Precautions for Patients 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.
i. Pre-examination measures:
a. Confirm that the examination has not been already done at an outside
clinic or hospital from which the patient has been referred.
b. Examine the possibility of using alternative techniques (e.g.
ultrasound).
c. Minimize the use of X-rays during pregnancy and shield the fetus.
d. Provide adequate shielding of radiosensitive regions (e.g. gonads).
Measures in fluoroscopy
a. It is to be carried out when it is expected that a radiograph will not
supply the necessary information, as may happen with some
functional examinations or when the time factor is important.
b. To re-examine fluoroscopic images, an image storage unit should be
used. In this way, the patient is not exposed to further radiation
dosage.
ii. Measures during examination
1. Optimum collimation
2. Use of correct beam filtration
3. Use of highest practicable kV
4. Use carbon fiber table tops to reduce dose
5. Use image intensifier, not fluoroscopy
6. Use of autotimers to control exposure time.
iii. Post-examination measures: Implement a strict quality control program
to minimize repeats.
General Precautions-Staff
1. Only those, whose presence is essential, should be allowed within the
room
2. Should remain behind a lead screen when radiographs are taken
3. Provision of lead aprons and lead gloves
4. Testing the equipment for performance, especially tube leakage which should
give a dose rate in air of less then 1mGyh-1 at 1m.
5. Adequate personal monitoring
6. Keep exposure records for staff
7. Never stand in the primary beam
8. Do not hold the patient during radiographic examination
9. Rotational scheduling of personnel.
In order to avoid repeat exposures, following measures should be adopted:
1. Use proper exposure conditionsdo not over-or underexpose (52%).
2. Patient careposition properly and give instruction against moving (27%
cases).
3. Film careuse proper film and processing techniques (15% cases).
PERMISSIBLE DOSES
Limits for occupational exposure: NCRP recommends:
a. Stochostic effects:
i. The individual workers lifetime effective dose should not exceed
age in years 10 mSv (1 rad), and no occupational exposure
should be permitted until the age of 18 years.
ii. The effective dose in any one year should not exceed 50 mSv (5
rem)
b. Deterministic effects:
i. 150 mSv (15 rem) for lens of eye
ii. 500 mSv (50 rem) for localized areas of skin and the hands and
feet.
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, hands and feet 500 mSv/year
Embryo or fetus exposure: 0.5 mSv/month Total of 2 mSv to
effective dose limit abdominal surface
Public exposure (annual)
Effective dose limit, continuous or 1 mSv/year
frequent exposure
Effective dose limit, infrequent 5 mSv/year Averaged over 5 years
exposure
Dose equivalent limits of lens of 50 mSv/year
eye, 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, skin and extremities
Negligible individual dose (annual) 0.01 mSv/year No statement
Recent changes in NCRP recommendations: Recommendation in NCRP

report no. 91 now supersede those contained in NCRP report no 39. A
summary of some of the important changes follows. The formula, MPD =
5(N 18) rem [MPD = 50 (n 18) mSv], governing cumulative whole
body occupational exposure, was abandoned by the NCRP (NCRP report
#91). To replace the old MPD formula, the NCRP recommends limiting
the cumulative absorbed dose equivalent in rem to the occupationally exposed
persons age in years. Therefore, the cumulative absorbed dose equivalent
should not exceed the age of the individual in years 10 mSV (years 1
rem).
To reduce exposure for pregnant female members of the medical radiography
team, the NCRP now recommends that the effective absorbed dose equivalent
limit for the unborn child (5 mSv/0.5 rem) not be received at a rate greater
than 0.5 mSv (0.05 rem) per month.
Radiography students are another important absorbed dose equivalent
limiting consideration. Eighteen-year-old students, exposed as part of their
educational experience, should not exceed 1 mSv (0.1 rem) annually.
To provide a low-exposure cut-off level so that regulatory agencies could
dismiss a level of individual risk as negligible, an annual effective absorbed
dose equivalent of 0.01 mSv (0.001 rem) has been set. This means that below
this absorbed dose equivalent level it is not necessary to try to reduce individual
exposure.
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, and pelvis should have such
examinations performed only during the first 10 days following the
onset of menstruation, when it is certain that there is no pregnancy.
Pitfalls
i. Miscalculation of the date of monthly periods
ii. Early conception
iii. Unnecessary postponement in majority of females.
Also availability of rapid and easy tests to confirm pregnancy (viz.
urine test and USG) makes the value of 10-days rule controversial.
If the examination involves the pelvis of the woman in the reproductive
age group, ask the patient if she might be pregnant
a. If answer is No proceed with the examination
b. If answer is Yes, call a staff radiologistCalculate benefit Vs.
risk and take patient into confidence and obtain her permission to
proceed with the examination.
If examination does not involve radiation of the pelvis, then simply
drape the pelvic region with lead fabric.
In a pregnant patient avoid X-ray examination of abdomen and pelvis in
the 1st trimesterdelay till third trimester or later if possible.
Pregnant technologist
Arrange an interview with the radiation protection supervisor, explaining
the risks involved and giving the option of a transfer to some other
department till term.
Fetal MPD is 500 mrems. Under normal circumstances, a technologist
receives less than 500 mrems annually, as recorded by the personnel
monitor.
Consequently, the exposure under the protective apron should not exceed
50 mrems annually and the resulting fetal dose should not exceed 25
mrems.
Thus, under most circumstances additional radiation protective
measures may not be necessary:
Two measures are easy to carry out.
a. If possible, she should not be assigned to fluoroscopy or portable
radiography.
b. She may be provided with a second personnel radiation monitor
with instructions to wear it at waist level under the protective apron.
The radiation monitoring report associated with this badge should
reflect that it is a fetal dose monitor.
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.
Thermoluminescent materials: As thermoluminescent materials, calcium
sulfate and lithium fluoride are most commonly used. These materials are
available either in powder form, rods or as chips. It can have almost any
desired shape.
Technique: The material is kept in the intended area. The energy gets stored
in proportion to radiation dose. Radiation excites electrons from the material
and are trapped at impurity trap sites. The material is heated in a special
oven to a temperature of about 300C. Heat releases trapped electrons and
brings them back to the ground state in the form of light (bluish-green in
case of LiF. The equipment used for this purpose is called a TLD reader.
The glow curve: When a previously irradiated sample of LiF is heated at a
constant rate, the light output as a function of time follows the pattern
shown below and is termed as a glow curve. The area under the whole
glow curve can be used to measure the dose.
Conclusion (from the curve)
i. Maximum light emission occurs at temperatures 150 to 270C.
ii. The response fades off somewhat in the initial 24 hr (later it remains
constant). Therefore, in practice, 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. Alternatively, the material/after exposure
but before read-out may be preheated to 100C for about 5 min, and
this has the same effect as storage for 24 hr.
Attractive features of a Dosimeter
1. Small in size and chemically inert
2. Almost tissue equivalent
3. Small change in sensitivity with radiation quality
4. Usable over a wide range of radiation qualities
5. Sensitivity independent of dose rate
6. Read-out system consistent and suitable for automation
7. Read-out is simple and quick (less than 1 min per sample).
8. Apart from initial fading can store dose over long periods of time.
9. 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. It is a special miniature cassette that holds a tiny film.
Principle: The degree of blackening of film (photographic density) is

proportional to the radiation exposure.
Radiation monitoring film: It is similar in appearance to a dental film.
However, the differences are:
i. It has no lead foil backing
ii. 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). The fast and slow
emulsions enable a wide range of doses to be recorded on one film (1
to 10,000).
Requirements of the System

1. Automatic processor is a must for consistency.
2. Film badges have a limited self-life and should be kept in a cool place.
Wearing Period and Further Procedure

Each member of staff should wear a film badge usually for a period of 4
weeks. At the end of the period, the film inside is changed. The exposed film
is sent to a radiation protection laboratory (viz. BARC Bombay), where it is
processed and the assessed dose is recorded.
Assessment of radiation doseDone by measuring the density of the monitoring
film from the badge.
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. It can be
evaluated daily. The casing is usually too thick to allow low energy radiation to
penetrate.
Principle
Fountain pen dosimeter is based on the principle of a gold leaf electroscope.
When the electroscope is charged, the leaves diverge because of electrostatic
repulsion. If the gas around leaves is then ionized, the instrument will be
discharged.
Working
Before it is used, this dosimeter must be charged to a predetermined voltage
so that the scale reading indicates zero. When placed in a radiation field, the
device will be discharged by an amount proportional to the ionization provided
by the radiation and the pointer moves across the scale.
Types
It is the most sensitive personnel monitoring device. However, it is infrequently
used. It is of two types: (i) the self reading type, which contains a built in
electrometer (a device that measures electrical charge) (ii) The non-self reading
type, which requires a special accessory electrometer to read the device.
Summary of the Advantages and Disadvantages of

Personnel Monitoring Devices Film Badge
Advantage
Lightweight, durable, easy to carry.
Cost-efficient monitoring for large numbers of people.
Records radiation exposure accumulated at a low rate over a long period
of time.
Provides a permanent, legally acceptable record of personnel exposure.
Detects and records small and large exposures in a consistent, reliable
manner.
Instrument performance is usually not affected by outside influences such
as heat and humidity fluctuations and non-extreme mechanical shock.
Filters contained in the badge make it possible to estimate the direction
from which the radiation came.
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.
Can be used to monitor x-, gamma, and all but very low energy beta
radiation in a reliable manner.
Can discriminate between type of radiation and energy of x-, gamma, and
beta radiation.
Disadvantages
Records, only the exposure received in the body area in which it is worn.
Not effective as a monitoring device if not worn.
Temperature and humidity can cause film in the badge to fog over long
periods of time, causing inaccurate exposure reading.
Decreased film sensitivity above and below 50 keV.
Exposure cannot be determined on day of occurrence.
Limited in accuracy to + or 20 percent.
Pocket Ionization Chamber

Advantages
Small, compact units, easy to carry, convenient to use.
Reasonably accurate and sensitive.
Can be used as monitors for procedures that last relatively short periods of
time.
Self-reading chambers provides immediate exposure readout for radiation
workers in high exposure areas.
Disadvantages
Fairly expensive, hence not cost-effective for large number of persons.
Readings must be carefully obtained or they may be lost
To avoid inaccurate reading, dosimeter must be read each day after it is
used.
Unit is discharged if subjected to some type of mechanical shock and give
a false high reading.
No permanent, legal record of exposure is provided.
Records only the exposure received in the body area in which it is worn.
Thermoluminescent Dosimeter
Advantages
Crystals contained in TLD interact with ionizing radiation as human tissue
does; hence, TLD determines dose more accurately.
Not affected by humidity, pressure or normal temperature changes.
Can be worn upto 3 months.
After reading has been obtained, TLD crystals can be reused, making the
device somewhat cost-effective.
Disadvantages
Greater initial cost than film badge service.
Readouts must be carefully obtained or results can be lost.
Readout process destroys information stored in TLD, which prevents the
read TLD from serving as a permanent, legal record of exposure.
Calibrated dosimeters must be prepared and read with each group of TLDs
as they are processed.
Records only the exposure received in the body area in which it is worn.
Not effective as a monitoring device if not worn.
27
Ultrasonography of Systemic
Antenatal Abnormalities
A congenital anomaly is a structural abnormality of any type however it may
be structural, functional, metabolic, behavioral and hereditary.
There are four clinically significant types of congenital anomalies
1. MalformationMorphological defects of an organ/ part of an organ due
to intrinsically abnormal development process.
2. Disruptioninterference of originally normal developmental process due
to teratogen.
3. DeformationAbnormal form, shape resulting from mechanical forces
intrauterine compression from oligohydramnios.
4. DysplasiaAbnormal organization of cells into tissues (dishistogenesis)
affect several organs because of nature of underlying cellular disturbance.
Causes
Genetic factorsChromosomal abnormalities
Environmental factors such as drugs and virus
Multifactorial inheritanceGenetic and environment factors acting
together.
Teratogen
Drugs, Cigarette smoking, Thyroid drugs, Alcohol, Androgen/ Progesterone,
Antibiotic, Anticonvulsant.
ChemicalsMercury, Lead
InfectionRubella, TORCH, Varicella, HIV, Congenital Syphillis.
Radiation
Ultrasound in Prenatal Screening

To screen for and to detect congenital abnormalities is one of the primary
goals of prenatal surveillance.
The optimal gestation time to scan for most of developmental abnormalities
is 18-22 wks.
Clinical Markers
Advanced maternal age
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
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
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
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
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.
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 Turners 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).
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
Turners 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.
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.
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.
Hirschsprungs Disease
Congenital aganglionosis of a segment of the colon, cause in function
bowel obstruction.
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
Congenital syphilis
Cytomegalovirus infection
Simple splenic cyst
Multiple splenic cyst as in congenital lymphangiomatosis
Fetal hydrops.
FETAL ABDOMINAL WALL DEFECT

Gastroschisis
US
Right paraumbilical defect involving all layers of abdominal wall.
Small bowel usually herniates through the defect and multiple loops of
bowel can be seen floating freely in the amniotic fluid.
The umbilical cord is normally inserted to the left of the defect.
Large bowel, stomach, liver seen to be herniated through.
Polyhydramnios and associated anomalies seen.
Omphalocoele
US
Defect in the anterior abdominal wall in midline with extrusion of abdominal
contents (bowel, stomach, liver).
Umbilical cord attached to the tip of omphalocoele.
Ascitis.
FETAL RENAL ANOMALIES

Renal Agenesis
US
No kidney seen in renal fossa or in an ectopic location
With bilateral renal agenesis, there is severe oligohydramnios and non-
visualization of both kidneys and bladder.
Renal Ectopia
Kidney seen in chest, adjacent to urinary bladder or iliac wing.
Less commonly crossed renal ectopia, or with or without fusion.
Associated with skeletal, CVS, GIT, Gynecological defects.
Horseshoe Kidney
Usually inferior poles of kidneys are fused
Demonstration of bridge of renal tissue connecting the kidneys
Associated with CNS, CVS and chromosomal abnormality, Turners
syndrome and trisomy 18.
Hydronephrosis
Obstructive : Pelvi ureteral junction (PUJ)
Vesico ureteral junction (VUJ)
- 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,
ureters not visualized
Amniotic fluid volume in normal
VUJ: Hydronephrosis with hydroureter seen
Primary megaureter An aperistaltic distal ureteral segment.
Duplication Anomalies
In duplication of pelvicalyceal system upper pole moiety obstructs whereas
lower pole moiety reflux.
US
Shows hydronephrosis of upper pole with normal lower pole.
Bladder Extrophy
Occur in 10,000 40,000 population
In complete median closure of inferior portion of anterior abdominal wall
and the anterior wall of urinary bladder.
Posterior wall of urinary bladder is visualized.
Associated with epispadias with wide separation of pubic bones (pubic
diastasis).
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, can be total, intermittent or partial obstruction
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, hydronephrotic or dysplastic.
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.
US
Malformed kidney usually seen as enlarged, destroyed uniform pattern
may be normal or small in size.
Multiple cysts of varying size not communicating with each other and are
randomly distributed.
Renal pelvis and ureter are usually atretic and not visible.
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.
Causes obstruction of the urinary tract leading to hydronephrosis or
hydroureter.
Ovarian Cyst
Benign ovarian cyst resolves spontaneously within 6 months of birth.
D/D
Cystic lesion, at times internal septa
Presence of fluid debris level
Refractory clot and solid component suggesting trauma or hemorrhage.
Autosomal Recessive (Infantile) Polycystic

Kidney Disease (ARPKD)
Diagnosed by 14 wks
Renal enlargement
Increased renal echogenicity
Amniotic fluid volume is usually normal.
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.
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.
A disruption of normal triangular appearance.
Seen as widening of interpedicular distance.
Splaying of posterior ossification centres.
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.
Scoliosis and Hemivertebra

Ultrasound
Lateral curvature of spine seen.
Usually suspected, when on longitudinal section the entire spine is not
properly appreciated.
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.
Myelocystocoele
Dilation of spinal cords central canal which herniates posteriorly through
the spinal canal to form an exterior sac.
Spina bifida not associated.
Sac composed of three layers- hydromelia, meningeal layer and skin.
US
Demonstrate a cyst within a cyst
Splaying of the lamina or pedicle may/ may not be present.
Diastomatomyelia
Implies a partial or complete cleft of the spinal cord or filum terminale
associated with spina bifida or hdyromyelia.
US
Hemicords split by bony spetrum
Associated spina bifida.
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, anomalies of renal, GIT, CNS system
chromosomal anomalies.
Caudal Regression Syndrome

Partial or total sacral agenesis and abnormalities of lumbar spine, pelvis,
lower limbs, majority of cases associated with diabetes mellitus.
Sirenomelia
Severe form characterized by absent sacrum, fusion of lower extremities,
anorectal atresia or renal dysgenesis or agenesis.
Severe oligohydramnios and single umbilical artery are present.
Fetal Skeletal Anomalies

Thanatophoric dysplasia severe micromelia with rhizomelic predominance
Macrocrania with decreased thoracic circumference.
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
Limbs movement is limited
Protuberant fetal abdomen
Hypomineralisation of calvarium
Skull is compressible by ultrasound transducer.
Asphyxiated Thoracic Dystrophy

US
Extremely narrow chest with secondary hypoplasia
Limbs could be mildly shortened or even of normal length
Polydactyly.
Fetal Hydrops
Abnormal fluid accumulation within fetal extravascular compartments and
body cavities
US
Ascitis
Pleural 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, Large diaphragmatic hernia
Cranial malformation
Urogenital malformation large polycystic kidney, congenital
hydronephrosis
Abdominal viscera for any organomegaly and calcification
Placenta for any chorio-angioma.
Fetal Cardiac Abnormalities

1. Cardiac four-chamber view
Situs
Size
i. M-mode ultrasound
ii. Cardio-thoracic ratio
Size of ventricle
i. Hypoplastic left ventricle or left heart
ii. Hypoplastic right ventricle
Septal defects
i. Atrial septal defect
ii. Ventricular septal defect
(Most common)
US: seen as discontinuity in the interventricular septum
Color Doppler shows bi-directional of interventricular shunting

with a systolic Right to left shunt and a late diastolic left to right
shunt
iii. 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. Bicuspid, Tricuspid, Pulmonary and Aortic stenosis
ii. Bicuspid, Tricuspid, Pulmonary and Aortic regurgitation
Cardiac musculature
i. Focal thickening
ii. Diffuse thickening
iii. Change in echo pattern
Cardiomyopathy
Cause - Viral and bacterial infection, inborn error of metabolism, diabetes
mellitus.
US shows hypertrophy of ventricular wall and septum
And dilatation of one or more cardiac chamber
2. Long and Short Axis views
Criss cross relation of great vessels
i. Double outlet right ventricle
ii. Transposition of great vessels
Relation of ventricular septum to the great vessels
i. 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.
Seventy-five percent of tumors are Rhabdomyoma and teratomas.
Cardiac fibroma 12 percent.
US
Solid echogenic masses
Single or multiple arising from AV septum
Teratomas may be cystic/Solid masses.
CHROMOSOMAL ABNORMALITIES
Organ system Trisomy 21 Trisomy 18 Trisomy 13

Head and brain Mild ventriculomegaly Dolicocephayly, Strawberry Holoprosencephaly, 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, Sloping fore-

head, 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, Horseshoe Renal cortical cyst

kidney Hydronephrosis, Horseshoe
kidney
Skeletal Short femur and Humerus Clubfoot deformity Postaxial polydactyly

Clinodactyly of fifth digit Generalized arthrogryposis Comptodactyly, Overlapping
Widely spaced first and Clenched hands digits
second toes, Wide iliac angle
Organ system Triploidy Trisomy XI
Head and brain Ventriculomegaly, Agenesis of the corpus

callosum
Dandy-Walker malformation
Holoprosencephaly
Spine Meningomyelocele
Facial Hypertelorism Microphthalmia

Micrognathia
Neck Cystic hygroma Large, septate, 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
28 Ultrasound and Color
Doppler in Pelvic Masses
Pelvic masses are the commonest pathology in females particularly affecting
uterine and adnexal anatomy. Non gynecological masses or pseudomasses
most commonly originate from gastrointestinal tract and urinary tract.
ULTRASOUND TECHNIQUES
Transabdominal Ultrasound
Transabdominal ultrasound imaging is primary method for assessment of,
uterus and adnexa in female patients and prostate in male patients. The full
bladder is vital for successful scanning, pushing the uterus upwards from
behind the pubic symphysis, displacing small bowel and behaving as an acoustic
window, improving transmission of the ultrasound beam. The transducers
used are of lower frequency (3 to 4 MHz). 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.
Transvaginal Ultrasound
Initially it was used to monitor infertility treatment and to assess. The pregnancy
only and its complications. It is the preferred technique for assessing pelvic
inflammatory or malignant conditions especially when the patient is obese or
cannot achieve adequate bladder fully. Transvaginal transducer is closer to the
region of interest, there is less beam attenuation in superficial soft tissues and
a higher frequency (5-7 MHz), probe increasing sensitivity and spatial resolution
of image. High resolution ultrasound may also be performed by a transrectal
route to assess local tumor spread in patients with carcinoma of cervix.
Doppler USG
It can provide useful additional information about vascular abnormality
associated with pathological pelvic conditions. In female patients, ovarian
vascularity fluctuates during the menstrual cycle. Low resistance to high flow
occurring in presence of functioning corpus luteum. Postmenopausal ovaries
are relatively hypovascular. Demonstration of abnormal vascularity by Doppler
is suggestive of neoplastic process causing neoangeogenesis.
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. 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, especially when color
Doppler is used, which increases the sensitivity of ultrasound to detection of
flow.
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, grating lobe, cutter and other artifacts. 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. Advances in computing power have resulted in the recent
production of a real time 3D US (ultrasound system) known as 4D ultrasound
imaging.
CLINICAL, 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,
distended with gas or appendicitis, carcinoma
feces colon
Miscellaneous Pelvic kidney Abdominal wall
Urachal cyst abscess, hematoma,
Bladeder diverticula retroperitoneal abscess
Ultrasound and Color Doppler in Pelvic Masses 433
PELVIC MASSES OF GYNECOLOGICAL ORIGIN

Uterine Masses
Uterine neoplasms arise either from myometrium or endometrium.
Myometrium
a. Leiomyoma (fibroid)
Myomas are the most common neoplasms of the uterus. They occur
in approximately 20 to 30 percent of females over the age of 30 years.
Single or multiple, although frequently asymptomatic, females present
with pain and uterine bleeding.
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.
Degeneration, infarction or infection may occur. Sarcomatous
degeneration occur in less than 0.1 percent cases.
Sonographically
Fibroids have variable appearances. Uterus may be enlarged with globular
outline and heterogeneous echotexture resulting from small diffuse
leiomyomas.
They appear hypoechoic or heterogeneous in echotexture and frequently
distort the external contour of uterus.
Fibroids can demonstrate areas of acoustic attenuation or shadowing
without a discrete mass.
Calcification appears as focal areas of increased echogenicity or curvilinear
echogenic rim with shadowing.
Degeneration and necrosis produces areas of decreased echogenicity or
cystic spaces.
Transvaginal Sonography
1. It allows better differentiation between a submucosal and an intramural
lesion and its relationship to endometrial cavity, usually impinge on the
endometrium, distorting the lumen.
2. It can detect small leiomyomas, not appreciated on transabdominal study.
It clearly demonstrate the uterine origin of large, pedunculated, subserosal
fibroids that simulate adnexal masses however pedunculated fibroids may
be missed if transvaginal approach is alone used, because of the limited
field of view.
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. The
vascularity is typically peripheral with very high velocities and low resistance.
In contrast, center of the lesion is often avascular and necrotic.
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. The relationship of
endometrium to fibroid may be assessed more accurately than with 2D USG.
The size of fibroid may be accurately measured using volumetric data.
b. Leiomyosarcoma
It accounts for 1.3 percent of uterine malignancies and may arise from
preexisting uterine leiomyoma. Patients are usually asymptomatic or uterine
bleeding may occur.
Sonographically
The appearance is similar to that of a rapidly growing or degenerating leiomyoma,
however there can be local invasion of adjacent structures or distant metastasis.
c. Adenomyosis
It is overgrowth of basal layer of endometrium into myometrium:
pathologically by the presence of endometrial glands and stroma within
the myometrium. It is more extensive in posterior wall.
The most common presentation is uterine enlargement and nonspecific
symptoms as pelvic pain, dysmenorrhea and menorrhagia.
Transabdominal Sonography
The diagnosis is suggested if there is diffuse uterine enlargement with normal
contour and normal myometrium and endometrium echotexture. Thickening
of posterior myometrium with the involved area being slightly more hypoechoic
than myometrium can also occur.
Transvaginal sonography is more accurate in diagnosing this condition,
inhomogeneous hypoechoic areas occur within myometrium predominantly
posterior wall. Small myometrial cysts may also be present.
Abnormalities of the Endometrium

Endometriosis
Here normal appearing glands and stroma are found to be implanted outside
their normal uterine cavity.
Most commonly occurs in the ovary, fallopian tube, broad ligament and
posterior cul-de-sac and the urinary bladder.
Two forms have been described: diffuse and localized (endometrioma).
The localized form is also known as endometrioma or chocolate cyst.
It affects reproductive age group and presents as dysmenorrhea,
dyspareunia and infertility.
Sonographically
The localized form, occurs commonly in ovary. The characteristic appearance
is comprised of well defined unilocular or multiocular, predominantly cystic
mass containing diffuse homogenous, low level, internal echoes,
characteristically by transvaginal sonography.
Color Doppler Study

The vessels at the periphery of the endometriotic cyst show relatively high
impedance.
Endometrial Polyps
Commonly seen perimenopasual and post menopausal women
Usually presents with uterine bleeding
Polyps may be pedunculated and approximately 20 percent are multiple.
Malignant degeneration is uncommon.
Sonographically
They appear as non-specific echogenic, endometrial thickening, which
may be diffuse or localized.
Focal, round, 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.
Cystic areas may be seen within a polyp. Sonohysterography is a valuable
technique when transvaginal sonography is unable to differentiate
endometrial polyp from a submucosa leiomyoma.
Color Doppler
Sometimes a feeding artery may be seen in stalk of polyp with color Doppler.
Endometrial Carcinoma
Seventy five to eighty percent cases are reported in post menopausal women
with uterine bleeding.
Risk factors are obesity, hypertension, diabetes, nulliparity. Endometrial
hyperplasia is most important prognostic indicator.
Thickened endometrium with inhomogenous echotexture and irregular or

poorly defined margins.
Transvaginal sonography can be used to depict endometrial thickness,
accurately and assess myometrial infiltration. Presence of the subendo-
metrial halo indicates superficial invasion, whereas obliteration of the halo
is indicative of deep invasion.
Role of Color and Spectral Doppler

Initially it was suggested in endometrial carcinoma, there is low resistance
flow in the uterine arteries as compared with high resistance flow in normal or
benign endometria. Subsequent reports, however, have shown no significant
difference in uterine blood flow between benign and malignant processes. 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.
Role of 3D Ultrasonography
It measures volume of endometrium, which is superior to endometrial thickness
in diagnosis of endometrial carcinoma. 3D USG is also superior to conventional
USG both for myometrial invasion and cervix extension.
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. Hydatidiform mole, invasive mole and chorio-
carcinoma are rare neoplasms of the endometrium. Thickening and
inhomogenity of the endometrium are characteristic features with varying
degree of vesicles within uterine cavity and assessment of degree of invasion.
Color Doppler
There is significant increase in myometrial and endometrial flow, more marked
in aggressive tumors. Doppler indices are altered in trophoblastic tumors a
mean PSV of 57. 5 20.4 (normal 28.3 3.11) and RI of 0.56 0.19 (normal
0.86 0.05) have been demonstrated. The extent of intratumoral flow correlates
with the prognosis, the higher the resistance index, the lesser the need for
prolonged treatment cycles.
Abnormalities of Cervix
The cervix lies low in pelvis and is better assessed with transvaginal sonography.
Transrectal ultrasound also delineates the anatomy clearly.
Carcinoma cervix: Most common genital carcinoma, patient usually presents
with irregular vaginal bleeding, discharge and pain.
Transabdominal sonography: It does not contribute to staging to the primary

cervical tumor, but can show urinary tract obstruction, ascites or hepatic
metastasis in advanced disease. 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.
Transrectal Ultrasound
It can demostrate cervical enlargement and parametrial extension but not the
full extent of bulky tumors or assessment of lymphnode enlargement.
Color Doppler
Cervical carcinoma can be seen on endovaginal ultrasound and neovascularity
can be demonstrated in mass lesion.
Posterior cul-De-sac
It is the most posterior and inferior reflection of the peritoneal cavity. It is
located between the rectum and vagina, is also known as the pouch of Douglas.
It is a potential space and because of its location, initial site for intraperitoneal
fluid collection. As little as 5 cc of fluid have been detected by transvaginal
sonography. Pathologic fluid collections may be seen in association with
generalized ascites, blood resulting from a ruptured ectopic pregnancy or
hemorrhagic cyst. Transvaginal sonography can demonstrate echoes within
the fluid more frequently because of its improved resolution.
Ovarian Masses
Functional Cysts
These are non-neoplastic cysts related to the process of ovulation. The
most common cause of ovarian enlargement in young women.
Seen most commonly in reproductive age group.
They include
i. Functional cysts of follicular or corpus luteal type
ii. Theca lutein cysts
iii. Endometriotic cysts
Follicular cysts usually regress spontaneously. Corpus luteal cyst may be
enlarged due to internal hemorrhage or cyst formation.
Theca lutein cysts result from hyperstimulaiton of ovary by HCG and are
often associated with hydatidiform mole and choriocarcinoma.
Sonographically
These functional cysts are typically unilocular, anechoic with well defined thin
walls and posterior acoustic enhancement.
Hemorrhagic cysts show spectrum of findings as a result of variable

sonographic appearances of blood. The internal characteristics are much better
appreciated on transvaginal sonogrpahy because of its improved resoluion. An
acute hemorrhagic cyst appears hyperechoic and may mimic a solid mass.
Another patterns include reticular type pattern and fluid-fluid level between
the clot and fluid component. Usually complete resolution within the
approximately 6 weeks. Sonographically, theca lutein cysts are usually bilateral,
multilocular and often very large.
Ovarian Neoplasms
Benign neoplasms are usually of connective tissue origin (fibroma, thecoma
and Brenner tumor). They vary in size. Meigs syndrome is benign ovarian
fibroma with ascites and hydrothorax.
Malignant neoplasms
Histologic Outline of Ovarian Neoplasms

Type Incidence Example
1. Surface epithelial stromal 65-75% Serous cystadenoma (carcinoma), muci-
tumors nous cystadenoma (carcinoma), endo-
metrioid carcinoma, clear cell carcinoma
2. Germ cell tumors 15-20% Transitional cell tumor, teratoma, dermoid,
dysgerminona
3. Sexcord stromal tumors 5-10% Yolk sac tumor, granulosa cell, sertoli-
leydig cell tumor, thecoma and fibroma
4. Metastatic 5-10% Genital primary uterus, extragenital
primary, includes stomach, colon, breast
lymphoma
Sonographically
Well defined, anechoic lesions with thin wall are more likely to be benign
whereas lesions with irregular walls, thick, irregular septations, mural nodules
and solid echogenic elements favour malignancy.
Histopathologic Ultrasonographic Correlation

Cystadenoma are usually large anechoic masses that may contain septations.
Mucinous variety tend to contain more septa and echogenic material.
Cystadenocarcinomas, serous and mucinous are large masses, multilocular
and contain papillary projections and echogenic material. The presence of
solid component suggests malignancy. Pseudomyxoma peritonei commonly
associated with adenocarcinomas.
Brenners tumors are bilateral in only 6.5 percent and account for 1 to 2
percent of ovarian neoplasms. Sonographically hypoechoic solid masses
that may contain calcifications and that appear similar to ovarian fibromas,
thecomas or uterine leiomyomas.
Ovarian cystic teratomas or dermoids are benign neoplasms with 2 percent

risk of malignant transmission. Dermoid arise from all three germ layers,
sebum hair, calcium and other elements can led to different sonographic
appearances. Hair, fat and fragments of bone or teeth within mass are
echogenic and produce posterior acoustic shadowing. The fat-fluid or hair
fluid level is characteristic of a dermoid.
Dermoid plug, a protruberance from the inner wall of a cyst and tip of
iceberg appearance can be seen in dermoid.
Dysgerminomas are sonographically usually solid masses that may contain
cystic areas representing hemorrhage or necrosis.
Thecomas and fibromas are hypoechoic masses with associated posterior
acoustic shadowing. The tumor has homogenous echotexture and may
resemble pedunculated fibroid in adnexa.
Metastatic ovarian neoplasms are bilateral masses and may be hypoechoic
or echogenic and occasionally cystic degeneration is present. Metastasis
to ovariers from stomach and occasionally colon, breast and pancreas are
known as Krukenberg tumors.
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.
Transvaginal color and pulsed Doppler distinguishes benign from malignant
ovarian masses, with malignant masses having PI less than 1.0 or RI of
less than 0.4. the other lesions which demonstrate low impedance, high
diastolic flow are tuboovarian abscesses, actively hemorrhagic corpus
luteum and some of the dermoids. Visualization of diachrotic notch suggest
the possibility of benign in nature.
Absence of flow within lesion usually indicates a benign lesion but several
studies have shown absent flow within malignant lesion as well.
Malignant lesion have more central vessels (flow) where as benign lesions
have peripheral flow.
Ovarian Torsion
It is an acute abdominal condition caused by partial or complete rotation of the
ovarian pedicle on its axis. It usually occurs during reproductive years. Clinically,
there are severe pelvic pain, nausea and vomiting.
Sonographically
The findings are variable depending on the degree of vascular compromise.
The ovary is enlarged, multiple cortical follicles in an enlarged ovary is
considered specific sign, although they are not always present.
Color and Spectral Doppler

There is absence of flow in the affected ovary. Doppler findings depend on
the degree and chronicity of the torsion and whether or not there is an associated
adnexal mass.
Parovarian Cysts
Parovarian cysts account for about 10 percent of all adnexal masses.
They are located in broad ligament and are usually mesothelial or
paramesonephric origins.
They are frequently located superior to uterine fundus.
Sonographically
They have typical appearance of cysts and may contain internal echoes as a
result of hemorrhage. Paraovarian cysts show no cyclic changes.
A specific diagnosis is possible only by demonstrating a normal ipsilateral
ovary close to but separate from the cyst.
Peritoneal Inclusion Cyst

They occur predomintaly in premenopasual women with a history of previous
abdominal surgery, trauma, PID and endometriosis.
The ovaries are main source of production of periotoneal fluid in women.
In patients with peritoneal adhesions, fluid may accumulate within the adhesions
and entrap the ovaries resulting in large adnexal mass.
Sonographically
These are multiloculated cystic pelvic mass. The diagnostic findings is presence
of septations and fluid and an intact ovary. The ovary may be located centrally
or displaced peripherally. The fluid is usually anechoic but may contain echoes
as a result of hemorrhage or proteinaceous fluid.
COLOR DOPPLER
Tubal Masses
Neoplasms arising from fallopian tube are rare.
Most commonly adnexal masses secondary to tubal disease are inflammatory
or representing ectopic pregnancy.
Inflammatory Tubal Masses

i. Acute salpingitis: The fallopian tube is swollen and edematous with dilated
vessels on the peritubal surface. The ovaries are also involved resulting
in tubo-ovarian abscess. The ampullary end of the tube distends more

than the isthmic portion resulting in retort shaped pyosalpinx.
ii. Chronic inflammatory disease: Failure of acute pelvic infection to resolve
completely results in chronic tubo-ovarian masses. These masses manifest
in the form of
a. Hydrosalpinx
b. Chronic pyosalpinx
c. Chronic interstitial salpingitis
d. Tubo-ovarian cyst
Sonographic Findings
i. Endometritis endometrial thickening or fluid.
ii. Pus in the cul-de-sac.
iii. Periovarian inflammation-enlarged ovaries with multiple cysts and
indistinct margins.
iv. Pyosalpinx or hydrosalpinxfluid filled fallopian tube with or without
internal echoes.
v. Tubo-ovarian complexfusion of the inflamed dilated tube and ovary.
vi. Tubo-ovarian abscesscomplex, multiloculated mass with variable
septations, irregular margins and internal echoes.
On transabdominal sonography, dilated tubes appear as complex, predominantly
cystic masses often indistinguishable from other adnexal masses. However,
TVS recognizes fluid filled tube by its tubular shape, folded configuration and
well defined echogenic walls. Low level internal echoes within fluid filled tube
suggests pyosalpinx.
In an inflammatory mass, ovarian tissue can be seen separately by
transvaginal sonography because ovaries are relatively resistant to the infection.
Color Doppler
Sometimes useful in differentiating hydrosalpinx from a prominent pelvic pain.
Ectopic pregnancy : Implantation occurs outside the normal uterine cavity.
Types:
a. Extrauterine - Tubal
- Ovarian
- Abdominal
b. Uterine - Interstitial
- Rudimentary horn of bicornuate uterus
- Cervical
ECTOPIC PREGNANCY
Amenorrhea, pain followed by vaginal bleeding are the commonest
presentation of ectopic pregnancy.
Sonographically
a. Specific findings - Live embryo in adnexa
b. Non specific findings - Empty uterus
- Pseudogestational sac
- Particulate ascites
- Adnexal mass
- Ectopic tubal ring
c. Non supportive features - Live intrauterine pregnancy
- Intradecidual sign
- Peritrophoblastic flow
Color and Spectral Doppler

It helps to distinguish a gestational sac from decidual cast. Peritrophoblastic
flow, which is of high velocity and low resistivity index. The flow within the
trophoblast will yield pulsatile flow of low resistance index in excess of 0.8 in
inactive trophoblast. Color flow imaging shows classical fire ring pattern
within the trophoblast.
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.
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. Transvaginal sonography can usually
distinguish the pseudomass from a true mass.
Bowel Neoplasms
Especially those involving rectosignoid, caecum and ileum may simulate an
adnexal mass. These tumors frequently show charcteristic target sign of a
gastrointestinal mass, consisting of central echogenic focus caused by air
within the lumen, surrounding by thickened hypoechoic wall.
Pelvic Abscesses
Related to inflammatory disease of the gastrointestinal tract may also present
as an adnexal mass. On the right side this is most frequently caused by
appendicitis or Crohns disease, whereas abscesses on the left side are usually
caused by diverticular disease.
URINARY TRACT MASSES

Pelvic Kidney
It may present as a clinically palpable mass.
Sonographically
Recognized by typical reniform appearance and the absence of kidney in
the normal location. When a cystic pelvic mass is identified, bladder should
be seen separately. Bladder diverticula may also simulate a cystic adnexal
mass
Dilated distal ureters may simulate adnexal cysts on transverse scans,
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. 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.
USG and Doppler Evaluation of the Prostate

The prostate is histologically composed of glandular and non-glandular
elements. The non-glandular elements are the prostatic urethra and the anterior
fibromuscular stroma.
Glandular prostate consists of
Outer
Inner components
In total, zonal anatomy consists of five components
a. Anterior fibromuscular stroma
b. Periurethral glandular tissue
c. Transition zone
d. Central zone
e. Peripheral zone
Imaging
The prostate can be visualized from a suprapubic position with transabdominal
transducers but detailed assessment of zonal anatomy, is performed with
transrectal approach.
In normal young men, the zones of prostate are not sonographically evident.
With the development of benign prostate hypertrophy, the central gland
becomes distinguishable as a well demarcated area of heterogenecity which
may contain visible nodules, cysts or calcification.
The peripheral zone forms an area of uniform echogenecity surrounding
the central gland.
The seminal vesicles can be seen superolaterally encased in hyperechoic
fat that is continuous with fat surrounding the prostate.
Doppler Imaging
Normal vascularity is categorized as minimal intraparenchymal flow with
symmetric capsular vessels.
Prostatic Cancer
Small cancers are usually hypoechoic and better seen with transrectal USG.
This appearance may be caused by dermoplastic response of the
surrounding glandular tissue to the presence of tumor.
A significant number of prostate cancers are difficult to detect because
they are isoechoic with glandular tissue. Secondary signs such as asymmetry
and capsular bulging may be helpful in diagnosis.
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, hematomas, lymphoceles, urinomas.
Sonographically
Abscesses are ovoid shaped, anechoic masses with thick, irregular walls
and posterior acoustic enhancement. Variable internal echogenicity may
be seen and high intensity echoes with shadowing caused by gas may be
seen.
Hematomas: During the initial acute phase, hematomas are anechoic.
Following organization and clot formation, they become highly echogenic,
with complete lysis, hematomas are again anechoic.
Lymphoceles: Occur following surgical disruption of lymphatics usually
after pelvic lymphnode dissection or renal transplantation.
Sonographically
Lymphoceles are cyctic having appearance similar to that of urinomas, which
are localized collection of urine.
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, optic nerve and muscles are hypoechoic,
rest all structures are echogenic
Aqueous and vitreous are anechoic; posterior lens capsule, sclera and
retina are echogenic while uvea and optic nerve are hypoechoic.
ULTRASOUND BIOMICROSCOPY
40-100 MHz transducer used
For the microscopic evaluation of cornea, anterior chamber and Iris
Anterior lens capsule and the angle of anterior chamber.
ORBITAL COLOR DOPPLER

7.5 MHz transducer used.
Chief indications are : orbital trauma cases, inflammatory diseases, vascular
diseases, tumors, carotico-cavernous fistula.
Orbital Sonopathology
Lesions of the eyeball are classified according to their echogenicity, attenuation
and reflectivity.
a. Anechoic Lesions:
Silicone implants, hematoma, cysts, mucocele, PNS malignancy.
b. Hypoechoic Lesions:
Cellulitis, abscess, glioma, lymphoma, sarcoma, pseudotumor, neurilem-
moma, MHF, pericytoma, CCF, capillary hemangioma.
c. Medium Echogenicity:
Dermoid, meningioma.
d. Echogenic
Lymphangioma, cavernous hemangioma, pleomorphic adenoma, foreign
body, metastasis.
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.).
Exact localization of a radio-opaque foreign body (F.B.).
Assessment of nature of foreign body (F.B.).
Guiding the extraction.
Follow-up of the management.
Classification:
Non penetrating - extra ocular F.B., concussion, contusion, Abrasion
Penetrating - Penetrating wound only, 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,
plastic exudates at pupil, synechiae, 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.
Orbital Sonography 447
COMMON CONGENITAL CONDITIONS

1. Persistent embryonic vitreous
Persistant embryonic vitreous appears echogenic with bands, esp. one
from lens to optic disc. There is a persistant Hyaloid vascular system.
Usually unilateral.
Usually anterior type.
Eye ball is small.
2. Congenital cataract
Both shape and echogenicity are altered.
3. Orbital Cysts
4. Cryptophthalmos
Lids are absent.
Eyeball is just a cystic structure with no specialized differentiation.
5. Anophthalmia (Agenesis)
A fissure suggestive of lids and a small cyst in orbital fat suggestive of
eyeball are seen.
6. Coloboma
Usually inferonasal.
Scleral ectasia and pseudopapilledema.
COMMON OCULAR TUMORS

1. 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, toxocara infection, coats diseases,
premature, retinopathy cysticercosis.
2. Melanoma
Usually in 5th or 6th decade of life
Eighty-five percent arise from choroids
Usually unilateral and posterior to the equator
Sonographically, it is a well defined homogenous lentiform hypoechoic
lesion
May lead to RD, PVD and vitreal degeneration
Differential diagnosis is from Fuchs spots and disciform lesion.
3. Metastasis
Are commoner than primary lesions
Usually located posteriorly
Commonly from breast, bronchus, testis, kidney, GIT
Retinal detachment may be associated.
4. Choristoma:
Well defined dense echogenic lesion with acoustic shadow
Usually bilateral
Common in peripapvilary area
D/D is from Drusen.
5. Hemangioma
A broad based echogenic lesion with blood filled spaces and calcification
May be associated with cutaneous lesions.
DISEASES OF LENS
1. Ectopia Lentis.
2. 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.
DISEASES OF VITREOUS
Senile degeneration
Vitreous detachment
Vitreous opacities (floaters, asteroid hyalosis, subhyaloid hemorrhage,
membranes and adhesions, intravitreal hemorrhage).
DISEASES OF RETINA
1. 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.
2. Disciform lesions
Heterogeneously hyperechoic rounded or flat elevation at macula
Has to be differentiated from melanoma, macular edema, macular
degeneration.
3. 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.
Orbital Sonography 449
DISEASES OF THE CHOROID

Choroidal Detachment
Presents as a slightly thicker membrane attached at ora, 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.
DISEASES OF SCLEROCORNEA
Staphyloma, 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, it can reliably comment only on the optic nerve head
Important conditions that can be suspected are papillitis, papilledema,
pseudopapilledema, drusen and melanocytoma
All present as increased echogenicity and protrusion of the nerve head.
30
Radiology of the
Immunocompromised Patient
Sections
A. Thoracic disease in the immunocompromised patient - AIDS
- Non-AIDS
B. Intra-abdominal manifestations - AIDS
- Non-AIDS
C. Neurological manifestations - AIDS
- Non-AIDS
D. 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.
During the past few decades, the population of immunocompromised hosts
has increased enormously reflecting the emergence of AIDS; 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.
Immune Defects
There are 5 principal kinds of immune defects. Specific defects are associated
with specific kinds of infection. Many immunocompromised patients have
multiple immune defects which not only reflect the underlying disease but also
the immunosuppressive therapy.
Defects in Phagocytes
Phagocytes include monocytes, macrophages and neutrophils. They defend
the body against bacteria and fungi. To be effective, these cells must migrate
to the site of infections, engulf and kill the microorganisms.
The defects can be quantitative i.e. decrease in the counts of these cells or
qualitative in which the function of these cells is inadequate.
Radiology of the Immunocompromised Patient 451
Defects in Humoral Immunity

There are 3 principal ways in which antibodies protect the host against
invading microorganisms.
i. Neutralization binding of the antibody to the virus before it can
enter the host cell to replicate
ii. Opsonization antibody coats the surface of bacteria to stimulate
phagocyte cells to ingest and kill it.
iii. Complement activation enhances opsonization and can directly kill
certain bacteria.
Patients with defective antibodies are especially vulnerable to infections by
encapsulated bacteria.
Complement System Defects

Complement activation serves to opsonize pathogens, 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.
Defects in Cell Mediated Immunity

CD8 cells kill host cells infected by pathogens.
CD4 cells activate macrophages thus allowing them to destroy pathogens
and also activate B cells to produce antibodies.
Patients with cell mediated immunodeficiency are susceptible to infections
by bacteria, fungi, viruses and protozoa. The predominant pathogens are
intracellular.
Defects Caused by Splenectomy or Hyposplenism

The spleen produces bacteria specific opsonizing antibodies and removes
antibody coated bacteria from the bloodstream.
Patients with impaired splenic function are at risk of developing over
whelming bacterial infections, especially those caused by 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.
Its presentation varies from acute fulminant respiratory failure to a
more insidious onset with nonspecific symptoms of nonproductive
cough, malaise and low grade fever.
Chest X-ray
Bilateral perihilar or diffuse infiltrates which may progress to diffuse
consolidation involving the entire lung.
May be normal or show only minimal increased lung markings.
CT Scan
Varied patterns are noted-
Most common pattern is diffuse / patchy ground glass infiltrates that do
not obscure bronchovascular markings.
Increased interstitial markings because of interstitial fibrosis which develops
as the infection heals.
Cystic form characterized by one or more thin walled cysts or cavities.
With the use of prophylactic therapy (aerosolized pentamidine), extensive
calcification involving mediastinal lymph nodes and abdominal viscera-
liver, spleen, kidneys has been noted.
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.
Clinically, tuberculosis may be the first indication that a patient is
HIV infected.
Radiology of tuberculosis in AIDS depends on the severity of
immunocompromise especially the CD4 count.
i. Early disease (CD4 > 200/mm3):
Disease is confined to the lungs and presents with classic
features of reactivation.
On chest X-ray and CT scan, the usual findings are upper
lobe infiltrates, cavitary lesions and endobronchial spread.
On CT, bronchogenic spread is seen in the form of poorly
defined nodular opacities, 3 to 10 mm in diameter and
unevenly distributed.
ii. Late disease (CD4 < 200/mm3):
Disseminated disease is more common.
The presentation is reminiscent of primary TB, primary
progressive TB or miliary TB.
On chest X-ray and CT, diffuse infiltrates, nodules,
consolidation and lymphadenopathy are seen frequently. After
contrast administration, tuberculous lymph nodes
demonstrate characteristic low attenuation necrotic centers
and rim enhancement on CT.
Mycobacterium Avium Intracellulare

Seen at profound levels of immunosuppression (CD4 < 100 cells/
mm3).
Pulmonary disease is relatively uncommon (only 5% of cases)
Radiological findings :
In the form of pulmonary infiltrates, nodules, lymphadenopathy and
even miliary disease.
iii. Bacterial Infections
Often aggressive and recurrent bacterial infections occur.
Most common causative organisms are S. pneumoniae, H.
influenzae and S. aureus.
Radiological features :
In the form of focal pulmonary consolidation segmental or lobar in
distribution. HIV positive patients may also show atypical features like
infiltrates or cavitation. Acute bacterial bronchitis is seen on CT as
bronchial wall thickening.
iv. Fungal Infections
Any number of fungal species can cause pulmonary infection
in the AIDS patient including H. capsulatum, C. immitis, C.
neoformans and C. albicans. Aspergillus does not occur
frequently in AIDS.
Cryptococcal Infection: Most common fungal pathogen to affect the
lungs, almost always in conjunction with infection of the central nervous
system.
Single/multiple discrete pulmonary nodules which may progress to either
consolidation / cavitation and mediastinal lymphadenopathy.
Histoplasmosis: Very common, typically, it is disseminated at the time
of diagnosis.
Suggest disseminated nodular disease. CT is especially useful in cases
where chest X-ray is normal. The nodules are usually small (<3mm) in
size.
v. Viral Infections
A large number of viruses are known to infect the lungs in an
HIV positive patient. CMV is the commonest of these.
Cytomegalovirus Infection
Usually coexists with other opportunistic infections like Pneumocystis
carinii pneumonia or neoplasias like Kaposis sarcoma.
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.
Occasionally, infiltrates or nodules are noted.
NEOPLASMS
Kaposis Sarcoma
Most common AIDS related malignancy 25 percent of HIV positive
patients.
Almost all cases are seen in homosexual males.
Associated with a low CD4 count
Chest X-ray shows diffuse bilateral alveolar/interstitial opacities with
widespread poorly defined nodules. 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.
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.
These are mostly non-Hodgkin B cell lymphomas.
Solitary or multiple well defined pulmonary masses. Mediastinal adenopathy
and pleural effusion may be present.
PULMONARY COMPLICATIONS IN IMMUNOCOMPROMISED

PATIENTSNON AIDS
Bacterial Pneumonias
These are the most frequent pulmonary infections and rapid progression
may occur.
Klebsiella Pneumonia
Radiological pattern :
Lobar consolidation especially in right upper lobe.
Cavitation is common
Volume of affected lung is maintained or may be increased causing bulging
of fissures.
Legionnaires Disease
Caused by legionella pneumophila
Solitary/multifocal homogenous opacities or lobar consolidation. Rapid
progression is noted with spread to other lobes and the opposite lung.
Pseudomonas Aeruginosa and Escherichia Coli

Both usually present as a bronchopneumonia which is often basal.
A pattern of post primary TB is seen.
Parenchymal infiltrates involve the apical/posterior segments of upper lobes
or superior segments of lower lobes.
Cavitation and endobronchial spread are common.
Invasive Aspergillosis
Can present as lobar consolidation, bronchopneumonia or multiple nodules.
On CT, Halo Sign is a specific sign consisting of a round pulmonary
nodule with a surrounding halo of intermediate CT attenuation. This is
because of hemorrhagic necrosis. Cavitation is a common feature.
SECTION B
INTRA-ABDOMINAL MANIFESTATIONS IN
THE IMMUNO-COMPROMISED PATIENT
Patients with AIDS
Gastrointestinal Tract
Infections
A. Candida Albicans
Candida esophagitis occurs in advanced degrees of immunosuppression
and is mostly associated with oral thrush.
Diffuse mucosal nodularity with deep marginal ulceration is seen.
Double contrast studies can reveal mucosal plaques which lead to a
nodular appearance of longitudinal esophageal folds simulating varices.
Rarely, a fungal mass protruding into the lumen or the tracking of
barium beneath a sloughing pseudomembrane may be seen.
B. Herpes Simplex
Herpes esophagitis is usually preceded by a prodromal flu like illness.
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.
C. Cytomegalovirus
Can involve any segment of the GIT and presenting symptoms depend
on the location and severity of infection.
i. Esophagus
Discrete, superficial ulcers on a normal mucosal background.
Giant (>2 cm) ulcers may be seen in the distal esophagus
which extend across the GE junction.
ii. Stomach
Gastric involvement produces nodular wall thickening,
ulceration and circumferential antral narrowing.
iii. Large bowel
Usually caecum and proximal ascending colon are involved.
Pancolitis may occur.
Lymphoid nodular hyperplasia and ulceration occur.
It can show low attenuation bowel wall thickening,
pericolonic inflammation and ulcerations.
D. Mycobacterium Tuberculosis
Can involve any portion of the GIT along with involvement of lymph
nodes and peritoneum.
i. Esophagus
Infection usually spreads from adjacent infected mediastinal lymph
nodes.
Traction diverticulae, ulcers and fistula formation may occur.
Scarring and stricture formation may result.
ii. Small bowel
Most common site of involvement is the ileocecal region.
Radiological patterns include ulceration with associated spasm of
the terminal ileum and proximal ascending colon. In later stages,
marked shortening of caecal pole may occur. Thickened folds with
segmental narrowing may also be seen.
A higher incidence of enteric fistulae and involvement of stomach/
duodenum is seen in AIDS patients.
E. Mycobacterium Avium Intracellulare
Small bowel
Produces bowel dilatation and fold thickening. Associated with
finding is mesenteric/retroperitoneal lymphadenopathy.
NEOPLASMS
Kaposis Sarcoma
After skin and lymph nodal involvement, the GIT is the most frequently
involved site.
Changes are more common in the stomach and smal bowel.
Barium studies may show small nodules, large submucosal nodules with
central umblication (bulls eye or target lesions), thickened folds and
plaques.
AIDS Related Lymphoma

Usually non-Hodgkins type.
Stomach and small bowel are most frequently involved.
Characterized by nodular/circumferential wall thickening with or without
ulceration.
Enlarged lymph nodes and hepatosplenomegaly may be seen.
HEPATOSPLENIC INVOLVEMENT
Disseminated disease involves the liver and spleen.
Multifocal lesions appear hypoechoic on USG and hypodense on CT.
Mycobacterium Avium Intracellulare

In disseminated infection, marked hepatosplenomegaly with multifocal
micro abscesses in the solid organs occur.
Bacterial Abscesses
Especially seen in AIDS patients who are IV drug abusers and prone to
develop septic emboli particularly by staphylococcal organisms.
Spleen and liver are common sites of involvement.
Fungal Infections
Causative fungi are Candida, Cryptococcus, H. capsulatum and C. immitis.
Candidiasis causes microabscesses in the liver and spleen which appear as
multiple small hypoechoic lesions on USG, sometimes showing a typical
spokeswheel pattern.
Lymphoma
In AIDS patients, lymphoma has a greater tendency for extranodal disease
and a worse prognosis.
Imaging findings are hepatosplenemegaly with focal lesions.
BILIARY DISEASE OR AIDS CHOLANGIOPATHY

Inflammation of the biliary tract in the AIDS patient is usually due to
Cryptosporidium or Cytomegalovirus.
Patient may present with right upper abdominal pain, nausea and vomiting.
There are various patterns of presentation. These include:
i. Acalculus cholecystitis shows thickened GB wall with no calculus is
seen on USG.
Pericholecystic fluid may be present

Long standing disease may show thickening and enhancement of
the walls of the extrahepatic biliary system.
ii. Sclerosing cholangitis with focal strictures and dilatations of intra or
extra hepatic bile ducts.
iii. Papillary stenosis with dilatation of the bile ducts and delayed clearance
of contrast from the CBD.
USG, CT and ERCP are complementary modalities for evaluation of
AIDS cholangiopathy
Pancreatic Disease
Infections with Cytomegalovirus, M. tuberculosis, M. avium intracellulare,
Candida, etc. may occur occasionally.
Acute pancreatitis may result from the use of anti-HIV drugs like didanosine.
Radiological findings are similar to those seen in the immunocompetent
population.
Renal Disease
Renal involvement can be in the form of:
1. HIV nephropathy can present with hypertension or progressive renal
failure. The characteristic feature of this condition is global enlargement of
kidneys without hydronephrosis or scarring. On USG, the kidneys are
large with increased echogenicity. On NCCT, the medullary density is
increased and following contrast administration, a striated nephrogram is
seen.
2. Infections Pneumocystis carinii infection produces a pattern of punctate
calcification which can be detected on USG or NCCT.
Renal candidiasis can produce microabscesses are seen as small bulls eye
lesions on USG or hypodense on CT.
3. Kaposis sarcoma and non-Hodgkins lymphoma can also involve the
kidneys and present as focal lesions or bilateral masses.
GI COMPLICATIONS AFTER TRANSPLANTATION

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

Most common neurological problems in AIDS.
Also called AIDS encephalopathy or subacute encephalitis.
Patients present with inability to concentrate, decreased memory and
psychomotor retardation.
Both CT and MRI show diffuse brain atrophy
Typical of HIV encephalitis are bilaterally symmetrical white matter lesions,
hypodense on CT and hyperintense on T2W MRI.
Opportunistic Infections
A. Toxoplasmosis
Most common opportunistic infection in patients with AIDS caused by
the protozoan, Toxoplasma gondii.
Results from reactivation of latent infection or a recently acquired
infection in an HIV patient presenting with fever, headache, seizures
and encephalopathy.
This condition shows a good response to antibiotic therapy.
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.
Both solid and ring lesions may be seen in the same patients.
Lesions are usually multiple and bilateral.
Common sites of involvement are basal ganglia and the corticomedullary
junction.
B. Fungal Infections
Cryptococcosis
Infection by C. neoformans is common.
Preferential involvement of meninges is seen producing meningitis or
meningoencephalitis. Perivascular spaces and choroid plexus are also
involved.
Lesions are well defined, 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.
These lesions involve the basal ganglia, thalami and the midbrain.
Other fungal infections are uncommon although cases of H capsulatum,
A flavus, A fumigatus, Mucor, etc have been documented.
C. Mycobacterial Infections
Infection of the meninges and brain with M. avium intracellulare is
infrequent but M. tuberculosis is common and can result from either
reactivation of a latent focus or a newly acquired infection.
Four patterns of involvement are seen.
i. Tubercular meningitis
Results from granulomatous infection of the leptomeninges
with exudation.
CECT shows leptomeningeal enhancement and enhancing
exudates along basal cisterns, sylvian fissures and tentorium.
MR is more sensitive in demonstraing meningeal involvement
especially at sites around pituitary infundibulum, optic chiasm,
cranial nerves, hypothalamic cerebral convexities and
ventricular ependyma.
Communicating hydrocephalus may occur.
ii. Tuberculoma
Can be solitary/multiple
Results from hematogenous spread
Both CECT and MR can demonstrate nodular/ring enhancing
lesion.
Calcification is better identified on CT
iii. Tubercular abscesses
Seen as ring enhancing masses, usually >3 cm in size,
solitary, may be multioculated
iv. Cerebral Infarctions
Arteritis of small vessels results in infarcts.
Commonly seen in the region of basal ganglia
Seen on NCCT as hypodense lesions. On MR, they appear
as T1 hypointense and T2 hyperintense.
Spinal Involvement
May be in the form of vertebral body destruction, involvement of
disc space, intra osseous, paraspinal or epidural abscess.
Cord granulomas, myelitis or arachnoiditis may also occur.
MR is a very sensitive modality for the evaluation of spinal TB.
Typical features include T1 hypointense lesions involving two or
more contiguous vertebrae and the intervening disk space. These
lesions are hyperintense on T2W images.
D. Viral Infections
i. Progressive Multifocal Leukoencephalopathy (PML)
Caused by the JC Papova virus.
Irregular granular destruction of white matter occurs ranging in
size from a few mms to an entire lobe of the brain.
Grey matter may be involved.
Predilection for parietooccipital region is noted.
Radiological Features :
CT shows hypodense white matter lesions, beginning at the
corticomedullary junction and extending towards the ventricles.
MR is more sensitive and typical findings include asymmetric sub-
cortical and deep white matter areas of increased T2 signal. Contrast
enhancement is absent or minimal.
ii. Cytomegalovirus
Involves both brain and spinal cord.
Clinically, features of encephalitis and myelitis are prominent.
CT shows diffuse hypodensities in the white matter, subependymal
contrast enhancement and focal nodular/ring enhancing lesions.
MR reveals periventricular and subependymal enhancing lesions.
iii. Neoplasms
A. Primary CNS Lymphoma
Second only to toxoplasmosis as a cause of focal cerebral masses
in AIDS patients.
Usually B cell variety of Non Hodgkins lymphoma.
Multicentric tumors and central necrosis are common features.
Common sites of involvement are periventricular white matter,
corpus callosum and basal ganglia.
On CECT, they appear as ring enhancing lesions. In contrast,
lymphomatous lesions in non-HIV setting appear slightly hyperdense
and show homogenous contrast enhancement. On MRI, they appear
hypointense on T1 and iso to hyperintense on T2. They show intense
enhancement with Gadolinium.
B. Kaposis Sarcoma
Uncommon, tumor spreads by hematogenous route.
Enhancement is homogenously and cannot be differentiated by CT
or MR from other enhancing mass lesions.
NEUROLOGICAL COMPLICATIONS IN
IMMUNOCOMPROMISED PATIENTS - NON AIDS
Steroids
Enlargement of ventricular system and cortical sulci because of an electrolyte
shift in the extracellular spaces.
Masks or decreases the contrast enhancement of tumors and infections as
it stabilizes the blood-brain barrier.
Increases vulnerability to fungal infections by Aspergillus, Mucor, Candida
and pyogenic infections by Staph aureus.
Diabetes Mellitus
Increased incidence of CNS infections, most important of which is
Mucormycosis.
Fungi usually enter the nasal vault leading to sinusitis and orbital cellulitis.
Penetration of the arterial system occurs. If the internal carotid arteries are
involved, cerebral infarction, meningitis and cerebral abscess may result.
The affected sinuses may appear hyperdense on CT scans and low signal
intensity on MRI studies. In the later stages of infection, bondy destruction
can be seen.
Organ Transplantation
Both immunosuppression and the underlying organ disease can lead to
complications.
A. Opportunistic Infections
Usually occur 1 to 4 months after transplantation
The organisms are Aspergillus, Mucor, Cryptococcus, Listeria,
C neoformans, etc
CT and MR can reveal evidence of meningitis, hydrocephalus, cerebral
abscesses and infarcts.
B. Drug Related Neurotoxicity
Such an effect has been noticed with cyclosporine.
Encephalopathy occurs leading to seizures, confusion, motor and speech
derangement.
MR shows high signal intensity regions involving the subcortical white
matter of the occipital lobes.
C. Neoplasms
An increased incidence of CNS lymphoma is noted.
MR & CT reveal a ring or solid enhancing mass lesion. The tumor may
become multicentric and subependymal spread occurs.
SECTION D
MUSCULOSKELETAL COMPLICATIONS IN THE

IMMUNOCOMPROMISED PATIENT
Both infection and neoplasms may be seen.
Infections
A. Chronic Granulomatous Disease of Childhood.
Leukocytes are unable to respond normally to infections leading to a
chronic inflammatory process.
Bones are commonly affected.
Widespread small foci of osteolysis, often abutting onto epiphyseal
plates are seen.
Healing is with florid new bone formation leading to sclerosis and
expansion.
B. Osteomyelitis in Diabetes Mellitus
Infection of bone and soft tissue occurs.
Soft tissue infection leads to swelling loss of fat planes and lucencies
may be seen.
Ulcers, seen as soft tissue radiolucent defects, lead to involvement of
underlying bones with the development of osteomyelitis. Superimposed
sepsis causes osteoporosis and acceleration of bone destruction.
C. Tubercular Arthritis
Usually affects the major joints - especially the hip and knee.
Radiological features include juxtarticular osteoporosis, peripheral
osseous erosions and reduction of joint space.
D. Septic Arthritis
Common causative organisms are staphylococci, pneumococci,
Streptococci.
If more than one joint is infected, an immune defect/steroid intake
should be ruled out.
Radiological features include blurring of fat planes, osteoporosis,
reduction of joint space and bone destruction.
Neoplasms
A. Lymphoma
Primary lymphoma is rare but secondary involvement may occur.
Radiological features are those of permeative lytic lesions with cortical
destruction. A sclerotic or mixed picture with ill defined zone of
transition, periosteal reaction, soft tissue masses and marrow
involvement may be seen.
B. Kaposis Sarcoma
In AIDS patients, this multifocal malignancy may rarely involve the
skeletal system.
Radiologically presents as lytic lesions with cortical disruption and
periosteal reaction.
Index
A Amyloidosis 215, 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, 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
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
Biswangers 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 Cannavans disease 139
Bony lesions 284 Capillary haemangioma 103
Brown tumor of hyperparathyroidism 84 Caplans 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
Clarks 12 signs 51 Congenital anomalies 412
Vermas 13th sign 52 types 412
Cherubism 80 deformation 412
Cholangiocarcinoma 233 disruption 412
Choledochal cyst 233, 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, 195 Connective tissue disorders 19, 333
Coils 371 acquired 20
Collagen vascular disease 207 congenital 19
Color Doppler 440 Cowdens 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, 199, 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, 463
366 Diagnostic techniques in metabolic bone
principle 363 disease 121
biochemical 121 Endometrial 308

biopsy 121 Endometrial carcinoma 311, 435
radiological 121 Endometrial polyps 435
Diastomatomyelia 426 Endometriosis 309, 434
Diffusible traces 390 Endoscopic retrograde cholangiography 260
Dilated intrahepatic biliary radicles 224, 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 Ewings 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- 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
Ebsteins 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, 379
Emphysematous pyelonephritis 344 Filariasis 346
Enchondroma 81 Film badge 408
End stage kidney 349 Flurosis 120
Endocrine system 392 Fountain pen dosimeter 409
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
Gardners syndrome 283 Hypervitaminosis A 120
Gastrochisis 422 Hypervitaminosis D 120
Gastrointestinal tract 383, 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
Hashimotos thyroiditis 393 Inflammatory arthropathy 34
Heavy metal poisoning 120 infective 34
Hematoma 22, 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
Hirschsprungs 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, 229 Inflammatory tubal masses 440
Hydatid disease 346 Influenza virus 198
Hydrometrocolpos 424 International Commission on Radiological
Hydronephrosis 296 Protection 397
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, 83, 86, 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, 457, 459, 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 - Bignami disease 143
obstructive jaundice in children 223 Measles giant-cell pneumonia 198
obstructive jaundice in neonates 223 Meckels 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
Kaposis sarcoma 454, 456, 464
hypervitaminosis D 17
Klebsiella pneumonia 186, 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, 91, 236, 377
Law of Bergonie and Tribondeau 399 Migratory osteoporosis 118
Law of transformer 361 Mirizzis syndrome 228
Legionnaires disease 454 Mitochondrial cytopathies 147
Leighs 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
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, 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
Osteosarcoma 97 manual processing 359

Ovarian cyst 314, 424 opening on ventilation 354
Ovarian masses 437 pass box 355
Ovarian neoplasms 315, 438 plan layout 352
Ovarian torsion 439 room size 353
P screen speed 358
Pagets 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, 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, 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, 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
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
Potts paraplegia 126
Rectification 361
paraplegia of slow onset 126
full wave rectification 362
Potts 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
Reiters 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, 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
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, 240, 346
Spinal tuberculosis 126
Scleroderma 21, 63
Spinal tumor syndrome 127
Splenic tuberculosis 274
Scoliosis and hemivertebra 425
Spondylolisthesis 73, 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, 188
Simple bone cyst 81
Steroids 462
Sirenomelia 426
Streptococcus pyogenes 44
Small intestines and ileocecal tuberculosis
Sudecks 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
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
Index 475
TB of the male genital tract 326 Tubulo interstitial diseases 339

TB of ureter, bladder and urethra 323 Tumors 23, 383
Telangiectatic osteosarcoma 93 benign 23
Teratoma 419 idiopathic 24
TGA 166 soft tissue sarcomas 24
Thermoluminescent dosimeter 408, 411 Turcots syndrome 284
Thoracolumbar spine injuries 54 Turners 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, 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 Wegeners granulomatosis 209
postprimary 190 White matter 134
productive 190, 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

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Seminar

First Edition: 2006

Typeset at JPBMP typesetting unit

PROF. SATISH KUMAR BHARGAVA E-03, GTB Hospital Campus

Prof. Satish K Bhargava

This book is primarily an effort to help all categories of Postgraduate students

I am extremely thankful to Banaras Hindu University for providing all assistance

SECTION 1: MUSCULOSKELETAL SYSTEM

SECTION 2: CENTRAL NERVOUS SYSTEM

SECTION 5: GASTROINTESTINAL TRACT, PANCREAS AND

23. Medical Renal Diseases 331

Table 1.1: Types of osteoporosis

Idiopathic Juvenile Osteoporosis

Girls (Turners syndrome)

Reflex Sympathetic Dystrophy Syndrome

Transient (Regional) Osteoporosis

Regional Migratory Osteoporosis

WHO has classified osteoporosis on the basis of bone density measurements:

Accentuation of primary trabeculae with thinning of secondary

Neutron Activation Analysis

approximately 98 percent of body calcium is in the bones. This gives a

Single Energy Photon Absorptiometry (SPA)

Dual Energy Photon Absorptiometry (DPA)

The precision is in the order of 2 to 3 percent with accuracy of

Dual Energy X-ray Absorptiometary (DXA)

Single X-ray Technique

Quantitative Computed Tomography (QCT)

Advantage of QCT over other modalities

Quantitative Ultrasound (QUS)

Magnetic Resonance Imaging (MRI)

DIFFERENTIAL DIAGNOSIS OF VARIOUS CALCIFICATIONS

May be crushed by muscle contraction

CONNECTIVE TISSUE DISORDERS

B. Soft Tissue Sarcomas

Progressive increase in size and number of calcifications with

4. Hereditary pancreatitis (autosomal dominant)

7. Urinary Bladder (UB)/Urethra

8. Male Genitourinary Tract

9. Female Genitourinary Tract

B. Fallopian Tubes: Tubercular salpingitis (string of pearls appearance)

10. Alimentary Tract

13. Generalized Abdominal Calcification

Empyema (usually TB)

Habenular commissure (30%)

Bone mineral integrity

Magnetic Resonance Imaging

Marginal erosions seen earlier than in X-rays as low signal defects.

Extensor tendon rupture especially Extensio carpi ulnaris.

JUVENILE CHRONIC POLYARTHRITIS

Secondary degenerative changes occur late.

Costotransverse joint erosion and fusion

Hand and Foot

Pencil in cup deformity erosion with ill-defined margins and adjacent

REITERS SYNDROME (Described in 1916)

Recurrent, acute, mild attacks of synovitis, soft tissue swelling and

Flexion distraction injury:

(N) = 0.80 in male T8 T12

2. Vandemarks Risk Approach: Ref. appendix (Table 4.1)

Points to be Taken Care of:

Plain Film Radiography

May be followed by AP and open-mouth views (Three-film series) or

Magnetic Resonance Imaging

SPINAL INJURY THE MEDICOLEGAL ASPECT

Cartilage Joint Space