Atlas of Diagnostic Radiology

Atlas of
DIAGNOSTIC
RADIOLOGY
Atlas of
DIAGNOSTIC
RADIOLOGY
Khalid Mahmood
MBBS, FCPS, MACG
Professor and Chair

Department of Medicine
Dow University of Health Sciences
Karachi, Pakistan
Foreword
Paul R Goddard
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Atlas of Diagnostic Radiology

2009, Jaypee Brothers Medical Publishers
All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted
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First Edition: 2009

ISBN: 978-81-8448-670-4
Typeset at JPBMP typesetting unit
Printed at Ajanta Press
To
My parents,
all my achievements are because of
their affection, efforts, encouragement
and prayers
Contributors
Kashif Burney
MBBS MRCS(Eng.) FRCR
Consultant Interventional Radiologist

St Helier University Hospital
Wrythe Lane, Carshalton
Surrey, UK
Sikandar Rafique Qureshi
MBBS MCPS
Chief/Head Radiologist
Civil Hospital, Karachi, Pakistan
Zahid Anwar Khan
MBBS MCPS FCPS FRCR
Ex. Professor
Head Radiology Department
Sindh Institute of Urology and Transplant (SIUT)
Karachi, Pakistan
Qurat-ul-Ain
MBBS FCPS (Radiology)
Consultant Radiologist
Aga Khan University Hospital
Karachi, Pakistan
Asima Shakoor
MBBS FCPS (Medicine)
Registrar Medicine
Dow Medical College, Civil Hospital
Karachi, Pakistan
Abdul Wahid Shaikh
Clinical Research Fellow

Department of Medicine
Karachi, Pakistan
Farooq M Husain
Registrar Medicine
Civil Hospital, Karachi, Pakistan
Foreword
Roentgens discovery of X-rays in 1895 heralded the modern age of
medicine. Before that time, there was no way of examining the internal
structures of the body without resorting to surgery. Since that discovery,
we have been able to look at in vivo anatomy and pathology in
increasingly exquisite detail using a variety of sophisticated techniques.
Despite this, the mainstay of diagnostic imaging for many parts of the
body still remains the humble plain radiograph.
Even though the techniques of medical imaging are widely available,
their interpretation skill relies on the knowledge and ability of the
examiner which in turn largely depends on experience.
But how can a student obtain this experience? Partly, this must be
with direct patient involvement, but this can be considerably assisted
by well-presented museum cases.
This atlas provides such an archive in a readily accessible form and
with sufficient clinical details that each case assists in the building of the
knowledge base. The case mix has been chosen to represent the prevalent
disease pattern. As such, this will not only be a valuable resource for its
target audience of local undergraduate and postgraduate students but
will also be of inestimable value to post-graduate students of medicine
and their tutors in the parts of the world where the conditions shown
may be less frequently encountered.
The brief but salient account of the radiological features of the
conditions provides a good introduction to each section. The films include
many plain radiographs, contrast examinations, computed tomography
and a few magnetic resonance imaging scans. In each case the images
presented show the abnormality clearly. Some of the studies are less
perfect than others but this is the reality of life. Too many books show
only perfect cases giving the impression that this is how we should expect
to see the cases. In practice the quality of images obtained depends on a
large variety of factors including age of equipment, radiographic expertise
and the condition of the patient. These cases thus represent the mix of

images that the student is likely to meet and provide a superb resource
which will help to hone the necessary interpretive skills.
Professor Mahmood must be congratulated on having collected such
an interesting and useful museum of films and the atlas is testament to
his excellent relationships with his radiological colleagues.
Professor Paul R Goddard

BSc, MBBS, MD, DMRD, FRCR
(Retd.) Consultant and Head of Training Bristol

Radiology Training Scheme
Civil Consultant to the Royal Air Force
(Honorary Air Commodore)
Past-President of the Radiology Section of the
Royal Society of Medicine
Visiting Professor
University of the West England
Preface
Three simultaneous roles as a physician, teacher and examiner propelled
my search for radiological films with definite findings. This led to a
virtual treasure of films from not only my own patients but even my
colleagues. Practising for over twenty-five years, I now felt myself in a
position to meticulously plan an Atlas. An Atlas of medical radiology
may sound as a misnomer to many but significant and valuable technical
input from my radiologists should make this book reader friendly.
As 20% of X-rays are more than 20 years old, they are not of high
quality yet have been included to make the compilation complete. Diverse
presentations of diseases have been illustrated by multiple X-rays of
single diseases. Tuberculosis being a case in point, its high prevalence
and multisystem involvement has many X-rays to present a complete
spectrum of disease. Salient features of common diseases have been
added at the beginning of the chapters for the benefit of students.
Detailed description was beyond the scope of this book.
The atlas has been divided into chapters on Pulmonology, Cardiology,
Barium Studies, Musculoskeletal System, Abdomen including Intravenous
Urographies and lastly CT and MRIs of Brain. In this era of rapid advancement in radiology and imaging, this atlas would be considered more
conventional. As undergraduate and postgraduate students of medicine
are targeted for readership, I hope it proves valuable. The newer imaging
technologies are not covered as this would require a bulkier offering, but
have been indicated where of value.
Khalid Mahmood
Acknowledgements
It would be remiss if I did not thank all those who have helped me in
putting together this atlas. The compilation of this Atlas would not have
been possible without the hard work and sincere contribution of my
juniors Dr Uzma Ghaury, Dr Asima Shakoor, Dr Abdul Wahid Shaikh
and Dr Farooq M Husain for which I will remain thankful to them.
I cannot forget the technical help extended by Dr Sikandar Qureshi,
Dr Qurat-ul-Ain and Dr Kashif Burney for which I am grateful. I must
not forget to thank Professor Paul R Goddard for taking out some of his
very precious time to go through the manuscript and write its foreword.
Contents
1. Pulmonology ............................................................................. 1
Introduction ....................................................................................................... 2
Pulmonary tuberculosis ................................................................................... 17
Aspergillosis .................................................................................................... 36
Bronchiectasis .................................................................................................. 40
Consolidation ................................................................................................... 45
Hydatid cyst of lung ........................................................................................ 62
Pleural effusion ................................................................................................ 64
Pneumothorax .................................................................................................. 69
Pulmonary neoplasm ....................................................................................... 74
Interstitial lung disease .................................................................................... 95
Diaphragm .................................................................................................... 100
Chronic obstructive pulmonary disease ......................................................... 106
Cavitating lesions .......................................................................................... 108
Mediastinal mass ........................................................................................... 112
Pulmonary miscellaneous .............................................................................. 118
2. Cardiology .............................................................................. 123

Introduction ................................................................................................... 124
Congenital heart disease ................................................................................ 132
Valvular heart diseases .................................................................................. 138
Pericardial diseases ........................................................................................ 142
Heart failure and cardiomyopathy ................................................................. 145
Aneurysm ....................................................................................................... 148
Cardiology miscellaneous .............................................................................. 153
3. Barium Studies and Oral Cholecystography ................... 157

Introduction ................................................................................................... 158
Barium esophagus .......................................................................................... 165
Barium stomach ............................................................................................. 177
Barium duodenum ......................................................................................... 192
Barium follow through .................................................................................. 195
Barium enema ................................................................................................ 203
Cholecystography .......................................................................................... 213
xvi

4. Skeletal System ..................................................................... 217
Introduction ................................................................................................... 218
Skeletal congenital anomaly ........................................................................... 230
Metabolic bone disorders ................................................................................ 234
Inflammatory joint diseases ........................................................................... 245
Bone infections ............................................................................................... 261
Hematological bone diseases .......................................................................... 275
Skeletal neoplasm ........................................................................................... 280
Skeletal miscellaneous .................................................................................... 286
5. Plain Abdomen and Intravenous Pyelograms ................ 295

Introduction ................................................................................................... 296
Abdomen ........................................................................................................ 300
Intravenous urographies ................................................................................ 312
6. Brain ........................................................................................ 321

Introduction ................................................................................................... 322
Infections ........................................................................................................ 331
Cerebrovascular diseases ................................................................................ 340
Brain neoplasms ............................................................................................. 352
Index .............................................................................................................. 365
Pulmonology

PULMONARY TUBERCULOSIS
PRIMARY TUBERCULOSIS
Chest radiograph may appear entirely normal. Predominant feature is
unilateral hilar and adjacent mediastinal adenopathy. Pulmonary focus
is randomly distributed and may range from a small ill-defined shadow
to segmental or lobar consolidation, commonly on the right side.
Pulmonary focus may show calcification and may rarely cavitate. Airway
narrowing secondary to extrinsic nodal compression with resultant
atelectasis may occur (e.g. Brocks syndrome). Primary tuberculosis may
also present as pleural effusion or pleural thickening. Miliary tuberculosis
can occur as a complication.
POST-PRIMARY/SECONDARY/REACTIVATION TB
Calcified primary complex may be identified. The disease can be unilateral
or bilateral and apical/posterior segments of the upper lobes or superior
segments of the lower lobes are most often involved. Patchy foci of airspace disease cotton-wool shadows are characteristic. Pulmonary foci
may cavitate, and multiple cavities of varying sizes may be present.
Fluid levels may aid in recognition of cavities, the walls of which may
be indistinct or obscured by overlying densities. Pneumothorax may
occur.
Scattered calcifications, fibrous contraction leading to hilar retraction
and lobar volume reduction are seen in chronic cases. Lobar consolidation
may occur. Dissemination via the airways presents as bronchopneumonia.
Dissemination via the blood can cause miliary infiltrates.
Involvement of pleura can cause diffuse pleural thickening, effusions,
empyema, pneumothorax, bronchopleural fistula and eventually calcified
pleura (fibrothorax).
Endobronchial tuberculosisulcers and strictures, bronchial
obstruction leading to collapse or hyperinflation, may also present as
bronchiectasis. Single or multiple tuberculomata of variable sizes can
also occur.
BIBLIOGRAPHY
1. Delacourt C, Mamou Mani T, Bonnerot V, De Blic J, Sayeg N, Lallemand D, et al.
Computed tomography with normal chest radiograph in tuberculous infection,
Arch Dis Childhood. 1993; 69:430-2.
2. Goodman PC. Pulmonary tuberculosis in patients with acquired immunodeficiency
syndrome. J Thorac Imag 1990;5:38-45.
Pulmonology
3. Ip MSM, So SY, Lam WK, Mok CK. Endobronchial tuberculosis revisited. Chest
1986;89:727-30.
4. Lee KS, Song KS, Lim TH, Kim PN, Lee BH. Adult-onset pulmonary tuberculosis:
Findings on chest radiographs and CT scans. AJR Am J Roentgenol. 1993;160:7538.
5. Leung AN, Muller N, Pineda PR, Fitzgerald JM. Primary tuberculosis in childhood: Radiographic manifestations. Radiology 1992;182:87-91.
6. Palmer PES. Pulmonary tuberculosis: Usual and unusual radiographic presentations.
Semin Roentgenol 1979;14(3):204-43.
7. Peter Armstrong. Alan G. Wilson, Paul Dee, David M Hansell, Imaging of diseases
of the chest (3rd edn). 2000; 191.
PULMONARY ASPERGILLOSIS
PLAIN FILM
Non-invasive (Aspergilloma)
Solid round mass within a thick walled cavity with a crescent shaped air
space (Air-meniscus sign) separating fungus ball from cavity wall is
characteristic.
Pleural thickening of up to 2 cm adjacent to the cavity may be seen.
Fungus ball may show rim calcification. An air fluid level may be present
within the cavity.
Invasive
The radiographic findings are varied depending upon the stage, severity,
and extent of disease.
Single or multiple areas of consolidation or disseminated miliary/
nodular pattern may be seen. Areas of consolidation in invasive
aspergillosis represent focal infarctions and are typically round with
indistinct margins.
ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS (ABPA)
Acute
Bronchial wall thickening and atelectasis, mucoid impaction pattern, or

consolidation are ususal. V or Y shaped central mucus plugs with finger
in glove appearance may be seen in ABPA.
Chronic
Bronchiectasis with scarring/fibrosis (usually upper zone) is more

common, mucus plugs no longer evident.

CT SCAN
Non-invasive (Aspergilloma)
Sponge-like mass containing irregular air spaces which change with

patients position is characteristic.
Air crescent sign and wall of pre-existing cavity are clearly visible.
Invasive
CT halo sign is a band of increased attenuation in the surrounding lung.

The CT halo progresses to the air crescent sign which is a lucent
crescent of air around the margin.
Hilar adenopathy is not a feature.
Effusions occur only if hemorrhagic infarction results in bleeding
into the pleural space.
Chest wall or mediastinal invasion is rare.
Peribronchial consolidation or ground-glass opacity, centrilobular
micronodules and even bronchiectasis can occur.
ABPA
Characteristic proximal pattern of bronchiectasis predominantly in the

upper lobes is seen.
BIBLIOGRAPHY
1. Castagnone D, Radaelli P, Cortelezzi A. Radiological aspects of invasive pulmonary
aspergillosis. Radiol Med (Torino) 1984:70(1-2):1-6.
2. Freundlich IM, Israel HL. Pulmonary aspergillosis. Clin Radiol 1973;24(2):248-53.
3. Irwin A. Radiology of Aspergillosis. Clin Radiol 1967;18(4):432-8.
4. Libinski JK, Atkinson EW, Israel HI. Pleural thickening as a manifestation of
Aspergillus superinfection. Am J Roentgenol Ther Nucl Med 1974;120(4):883-6.
5. Zizzi G, Melillo L, Cammisa M. Carotenuto M. Invasive pulmonary aspergillosis.
Radiol Med Torino 1994;87(4):435-40.
BRONCHIECTASIS
Bronchial wall visible as single or parallel linear opacities (Tram-track),
ring and curvilinear opacities (bronchial end-on), may contain air-fluid
levels, are seen.
Loss of vascular shadows due to adjacent peribronchial fibrosis may
be present.
Pulmonology
Bronchiectasis may show over-inflation or atelectasis, or may manifest
with associated infectious consolidation, scaring, bullae and pleural
thickening.
Dilated airways filled with secretions give rise to band shadows of
variable size. Band shadow may branch, giving V, Y, or more complex
shaped opacities.
BIBLIOGRAPHY
1. Peter Armstrong, Alan G Wilson, Paul Dee, David M Hansell. Imaging of diseases
of the chest (3rd edn). 2000; 904.
2. Smith IE, Flower CD. Review article: Imaging in bronchiectasis. Br J Radiol 1996;
69(823): 589-93.
3. Van der Bruggen-Bogaarts BA, van der Bruggen HM, van Waes PF, Lammers JW.
Screening for bronchiectasis. A comparative study between chest radiography
and high-resolution CT. Chest 1996; 109(3):608-11.
CONSOLIDATION
Consolidation when associated with a patent airway, an air bronchogram
is often visible. This sign is produced by the radiographic contrast
between the column of air in the airway and surrounding opaque acini.
When consolidation is secondary to bronchial obstruction, air in the
airways is resorbed and replaced by fluid and the affected area is of
uniform density.
The volume of purely consolidated lung is similar to that of the normal
lung since air is replaced by a similar volume of fluid or solid.
Air lucencies within consolidated lung may be due to resolution of
the process with intervening normal lung, necrosis of tissue with
cavitation or pneumatoceles.
When consolidation is due to fluid, its distribution is influenced by
gravity, so that in acute pneumonitis consolidation is often denser and
more clearly demarcated inferiorly by a pleural surface, and is less dense
and more indistinct superiorly.
When air bronchograms are evident on the chest radiograph these
may manifest as echogenic linear structures.
When bronchi become fluid filled they are more clearly demonstrated
as echo-free branching structures.
LOBAR CONSOLIDATION
Consolidation of complete lobe produces a homogeneous opacity,
possibly containing an air bronchogram, delineated by the chest wall;

mediastinum, inter lobar fissure or diaphragm and mediastinum adjacent
to the non-aerated lung is obscured.
Right upper lobe consolidation: This is confined by the horizontal fissure
inferiorly and the upper half of the oblique fissure posteriorly, and
may obscure the right upper mediastinum.
Right middle lobe consolidation: This is limited by the horizontal fissure
above and the lower half of the oblique fissure posteriorly, and may
obscure the right heart border.
Lower lobe consolidation: This is limited by the oblique fissure anteriorly,
and may obscure the diaphragm.
Left upper lobe and lingular consolidation: These are limited by the oblique
fissure posteriorly. Lingular consolidation lobe may obscure the aortic
knuckle.
BIBLIOGRAPHY
1. Reed JC. Chest radiology: Plain film patterns and differential diagnosis (3rd edn).
Chicago: Mosby-year Book; 1987.
2. Peter Armstrong. Imaging of diseases of the chest (3rd edn) 2000;77.
3. Robert AN. Squires Fundamentals of Radiology (6th edn), London: Harvard
University Press; 2004; 112-21.
ATELECTASIS/COLLAPSE
The usual findings are localised increase in lung density, crowding of
pulmonary vessels, displacement of fissure/hilum, mediastinal shift,
cardiac rotation and approximation of ribs. Compensatory over inflation
of normal lung can occur.
BIBLIOGRAPHY
1. Woodring JH, Reed JC. Types and mechanisms of pulmonary atelectasis. J Thorac
Imaging 1996;11:92-108.
2. Proto AV, Tocino I. Radiographic manifestations of lobar collapse. Semin
Roentgenol 1980;15:11773.
CAVITATING LESIONS
A cavity is a gas-filled space surrounded by a complete wall which is
3 mm or greater in thickness. Thin walled cavities are called cysts or
ring shadows.
Cavitations occur when an area of necrosis communicates with a
patent airway. Particular features of importance are location of the cavity,
Pulmonology
its outline, wall thickness, the presence of fluid level, contents of the
cavity, satellite lesions, the appearance of the surrounding lung and
multiplicity of lesions.
Fluid within a cavity can be demonstrated only when using a
horizontal beam.
Common cavitating lesions are tuberculosis, staphylococcal infections
and carcinoma. The tumor mass itself or the distal lung may cavitate.
Tuberculous cavities are usually in the upper zones, in the posterior
segments of the upper lobes or apical segments of the lower lobes.
The site of lung abscesses following aspiration depends on patients
position at that time but they are most often right-sided and in the
lower zones.
Traumatic lung cysts are often sub-pleural. Amebic abscesses are
nearly always at the right base, the infection being extended from the
liver.
Pulmonary infarcts are usually in the lower zone and sequestrated
segments are left-sided.
BIBLIOGRAPHY
1. David Sutton. Text book of radiology and imaging. 7th Edition, Churchill
Livingstone 2003;1:22-2.
2. Nestor LM, Neil Colman, Par PD. Diagnosis of Diseases of the Chest(4th edn),
Philadelphia: WB Saunders, 1999.
HYDATID CYSTS
PLAIN FILM
One or more spherical or oval well-defined smooth mass of homogeneous
density in otherwise normal lung is apparent.
Cyst is usually located in middle or lower zone.
Multiple cysts are seen in about one-third of patients and are bilateral
in 20%.
There is a predilection for the lower lobes, the posterior segments,
and the right lung.
Calcification, which is a common feature of hydatid cysts in the liver,
is extremely rare in cysts arising in the lungs.
If the cysts ruptures, an air-fluid level is seen.
Hydatid cyst may also be present in the pleura, but mediastinal cysts
are relatively rare.

CT SCAN
CT scanning reveals fluid contents within the cyst.
The daughter cysts when present appear as curved septations.
On a CT the cyst wall ranges in thickness from 2 to 1 cm.
BIBLIOGRAPHY
1. Balikian JP, Mudarris FF. Hydatid disease of the lungs: A roentgenologic study of
50 cases. AJR 1974; 122:692-707.
2. Beggs I. The radiology of hydatid disease: A review. AJR 1985; 145:639-48.
PLEURAL EFFUSION
Blunting of posterior than lateral costophrenic angles on upright studies,
with meniscus like upper border is usual. Loculated fluid in fissures
appear as a spindle shaped pseudotumor.
If subpulmonic; apparent diaphragmatic elevation with more lateral
appearance to diaphragmatic peak, no lung marking below silhouette of
diaphragm, increased distance between diaphragm and stomach bubble
(>2cm) if on left side is seen.
If large mediastinal shift to contralateral side and/or inversion of
the ipsilateral hemidiaphragm (more common on left) is present.
The radiographic appearance of pleural fluid may be modified when
there is associated lung atelectasis.
Loculated chest wall effusions tend to be convex to the lung and
sharply demarcated on pulmonary aspect when viewed tangentially and
are typically greater in length than height.
BIBLIOGRAPHY
1. Amlyn L Evans, Fergus V Gleeson. Radiology in pleural disease: State of the art.
Respirology 2004; 9: 300-12.
2. Felson B. Chest roentgenology. Philadelphia: WB Saunders, 1973.
3. Fleischner FG. Atypical arrangement of free pleural effusion. Radiol Clin North
Am 1963;1:347-6.
PNEUMOTHORAX
A small pneumothorax in a free pleural space in an erect patient collects
at the apex. The lung apex retracts towards the hilum and on a frontal
chest film the sharp white line of the visceral pleura will be visible,
separated from the chest wall by the radiolucent pleural space, which is
devoid of lung markings.
Pulmonology
A large pneumothorax may lead to complete retraction of the lung,
with some mediastinal shift towards the normal side.
Tension pneumothorax may lead to massive displacement of the
mediatinum, kinking of the great veins and acute cardiac and respiratory
embarrassment. Radiologically the ipsilateral lung may be squashed
against the mediastinum, or herniated across the midline, and the
ipsilateral hemidiaphragm is depressed.
The usual appearance in loculated or encysted pneumothorax is an
ovoid air collection adjacent to the chest wall, and it may be radiographically indistinguishable from a thin-walled subpleural pulmonary
cavity, cyst or bulla.
The usual radiological appearance of a hydropneumothorax is that
of a pneumothorax containing a horizontal fluid level which separates
opaque fluid below from lucent air above.
BIBLIOGRAPHY
Livingstone 2003;1:131.
2. Greene R, McCloud TC, Stark P. Pneumothorax. Seminars in Roentgenolog.
1977;12:313-25.
3. Moskowitz PS, Griscom NT. The medial pneumothorax. Radiolog 1976;120(1):
143-7.
BRONCHOGENIC CARCINOMA
Squamous cell and small cell types of bronchogenic carcinoma tend to
present as central tumors, whereas adenocarcinoma and large cell types
tend to produce peripheral lesions.
Pancoast tumors are frequently squamous cell in type and can
resemble pleural thickening in the superior sulcus, usually associated
with erosions of adjacent ribs and bones.
Peripheral tumors present as solitary nodules with generally welldefined edges; they may be spherical or oval shaped and may be
lobulated, approximately 16% show cavitation (usually squamous cell).
An irregular edge or corona radiata is suggestive but not specific of
a malignant tumor. A single band connecting the nodule to pleura (Pleural
tail sign) is seen with both malignant and benign lesions. Air bronchograms are not seen within nodules on plain films (can be seen on thin
section CT).
The cardinal imaging signs of a central tumor are collapse and
consolidation of the lung distal to the tumor and the presence of hilar
10

enlargement andGolden S sign (bulge in fissure adjacent to collapsed
segment) indicating central tumor.
Visible calcification is virtually never identified on plain chest
radiograph but is seen in a small proportion of cases on CT.
Doubling of size of tumor is rare in less than one month or more than
18 months. Tumors less than 1cm in size are rarely visible on plain chest
radiographs. Alveolar cell carcinomas give rise to alveolar opacities and
spread rapidly.
BIBLIOGRAPHY
1. ER Heitzman, B Markarian, BN Raasch, EW Carsky, EJ Lane, ME Berlow. Pathways
of tumor spread through the lung; radiologic correlations with anatomy and
pathology. Radiology 1982; 144:3-14.
2. Im JG, Choi Bl, Park JH, et al. Case report CT findings of lobar bronchioloalveolar
carcinoma. J Computer Assist Tomogr 1986;10:320-2.
3. KS Lee, Y Kim, J Han, EJ Ko, CK Park, SL Primack. Bronchioloalveolar carcinoma:
Clinical, histopathologic and radiologic findings. Radiographics 1997; 17:1345-56.
5. Sider L. Radiographic manifestations of primary bronchogenic carcinoma. Radiol
Clinics N Am 1990;28:583-596.
6. Stark P. Multiple independent bronchogenic carcinomas. Radiology 145:599-601,
1982.
PULMONARY METASTASES
PLAIN FILM
The most common sources of pulmonary metastases include tumors of
the breast, colon, kidney, uterus, prostate, head and neck.
The hallmark of blood-borne metastases to the lungs on imaging is
one or more oval or spherical, discrete pulmonary nodules, usually in
the outer portions of the lung. They vary in size, are usually multiple,
and have well defined smooth or irregular outlines, with irregular,
sometimes frankly nodular thickening of the interstitial pulmonary septa.
This finding labeled as the beaded septum sign and is regarded as
highly specific.
Cavitation is most frequent in metastases from tumors of the uterine
cervix, colon, and head and neck.
Detectable calcification in metastases is very unusual.
Miliary nodulation, a pattern of innumerable tiny nodules resembling
miliary tuberculosis, is occasionally encountered.
Very rarely, metastases present as pulmonary consolidation. This
pattern has been seen with melanoma.
Pulmonology
Lymphangitis carcinomatosa is usually bilateral. Coarse linear
reticular or nodular basal shadowing often with pleural effussion is seen.
CT SCAN
All of the features which can be appreciated on plain X-ray are very
obvious on CT scan.
In addition, it is possible to show pulmonary vessels leading directly
to individual metastases.
BIBLIOGRAPHY
1. Coppage L, Shaw C, Curtis AM. Metastatic disease to the chest in patients with
extrathoracic malignanc. J Thorac Imaging. 1987;2:24-37.
2. Davis SD. CT evaluation for pulmonary metastases in patients with extrathoracic
malignancy. Radiology 1991; 180(1):1-12.
3. Libshitz HI, North LB: Pulmonary metastases. Radiol Clin North Am.1982; 20(3):43751.
4. Peter Armstrong. Diagnostic Imaging. Fourth Edition. London: Blackwell Science;
1998;96-8.
LYMPHOMA (CHEST)
PLAIN FILM
Cardinal features are mediastinal and hilar lymph node enlargement
(more frequent in Hodgkins than Non-Hodgkins lymphoma (NHL).
In Hodgkins disease adenopathy tends to be bilateral but
asymmetric, involving two or more nodal groups, anterior mediastinal
and paratracheal groups are most frequently involved and the posterior
mediastinal nodes being infrequently involved. In NHL adenopathy
tends to be hilar and mediastinal and is more likely to involve only a
single nodal group.
Parenchymal involvement is unusual at presentation; it is more common
in Hodgkins disease and almost always associated with adenopathy.
Parenchymal disease alone can occur in 50% of patients with NHL.
Parenchymal opacities vary from multiple nodules resembling
metastatic disease to air-space consolidations resembling pneumonia,
and diffuse interstitial thickening due to lymphatic spread or obstruction.
Pleural effusions may ocur which resolve with irradiation of
mediastinal nodes.
Other manifestations include: Pericardial effusion, chest wall invasion
or thymic enlargement but rather rarely.
11
12

CT SCAN FINDINGS
CT is the current gold standard for evaluating the extent of thoracic
involvement in patients with Hodgkins disease and, when required,
for those with NHL.
CT can demonstrate disease even in patients with a normal chest
X-ray and is more useful for staging the disease.
Compression of the pulmonary arteries, superior vena cava and major
bronchi by the enlarged nodes may be seen on a CT chest.
BIBLIOGRAPHY
1. Castellino RA , Blank N, Hoppe RT, C Cho. Hodgkins disease contribution of
chest CT in initial staging evaluation, Radiology. 1986;160:603-5.
Livingstone 2003;1:527-59.
3. Marc Bazot, Jacques Cadranel,Sylvie Benayoun, Marc Tassart, Jean Michel Bigot,
Marie France Carette. Primary Pulmonary AIDS-Related Lymphoma Radiographic
and CT Finding. Chest. 1999;116:1282-6.
4. Ooi GC, Chim CS, Lie AK, Tsang KW. Computed tomography features of primary
pulmonary non-Hodgkins lymphoma. Clin Radiol 1999; 54:43843.
5. Romano M, Libshitz HI. Hodgkin disease and non-Hodgkin lymphoma: Plain
chest radiographs and chest computed tomography of thoracic involvement in
previously untreated patients. Radiol Med (Torino) 1998;95(1-2):49-53.
SARCOIDOSIS
Bilateral hilar adenopathy with paratracheal adenopathy is the classical
finding of chest X-ray in sarcoidosis.
The degree of hilar node enlargement ranges from barely detectable
to massive, eggshell calcification of nodes can be seen specific to
sarcoidosis or silicosis. Nodes usually regress with increasing
parenchymal involvement. Parenchymal sarcoidosis may manifest as
reticulonodular opacities or alveolar opacities. The nodules range from
1 mm to over 5 mm. Alveolar sarcoidosis is due to both filling of airspaces with inflammatory cells and compression and obliteration of the
alveoli by enlarging interstitial nodules.
End-stage sarcoidosis typically shows scaring from the hilum into
upper and mid zones especially the lower part of the upper lobes.
Sarcoidosis is second only to tuberculosis as a predisposing condition
for mycetoma formation.
Bronchi may be narrowed by external compression or mural
granulomata and fibrosis with post-obstruction atelectasis.
Pulmonology
BIBLIOGRAPHY
1. Gross BH, Schneider HJ, Proto AV. Eggshell calcification of lymph nodes: An
update, AJR 1980;135: 1265-8.
3. Rabinowicz JG, Ulreich S, Soriano C. The usual unusual manifestations of sarcoidosis
and the hilar haze- A new diagnostic aid. AJR 1974;120:821-31.
ADULT RESPIRATORY DISTRESS SYNDROME

The radiographic changes may be delayed by 12 hours or more following
the onset of clinical symptoms.
Bilateral, wide spread, patchy, ill-defined densities resembling
cardiogenic pulmonary edema occur usually without cardiomegaly.
The densities progress in severity to produce confluent opacification,
the distribution of which is variable, but usually all lung zones are
involved both centrally and peripherally and air bronchograms may be
a prominent feature. CT scans, however, show that the distribution of
the pulmonary opacification is patchy. Signs of interstitial edema, like
hilar haze and lack of clarity of lung vessel, may also be present.
BIBLIOGRAPHY
1. Joffe N. The adult respiratory distress syndrome. AJR 1974; 122:719-32.
2. Lannuzzi M, Petty TL. The diagnosis, pathogenesis, and treatment of adult
respiratory distress syndrome. J Thorac Imaging 1986; 1:1-10.
CYSTIC FIBROSIS
The pulmonary manifestations are progressive from birth but do not
become radiologically apparent for months or years, so X-ray may be
completely normal initially.
The earliest changes are variable and may include focal atelectasis,
recurrent pneumonia, diffuse peribronchial infiltration, emphysema and
hilar lymphadenopathy.
In the fully developed form of the disease the radiographic findings
are remarkably uniform and include the following:
Emphysema, enlarged hilar shadows and increase in perihilar
shadows, (reactive hyperplasia to chronic infection), bronchiectasis, either
tubular or cystic, and atelectasis and focal infiltration prominent in the
upper zones, a reverse of the usual situation with bronchiectasis.
13
14

BIBLIOGRAPHY
1. Bradley J Phillips, Charles W Perry. Quick Review: Cystic Fibrosis. The Internet
Journal of Internal Medicine 2002;3(1).
2. Don CJ, Dales RE, Desmarias RL, Neimatullah M. The radiographic prevalence of
hilar and mediastinal adenopathy in adult cystic fibrosis. Can Assoc Radiol J 1997;
48:265-9.
CRYPTOGENIC FIBROSING ALVEOLITIS

PLAIN FILM
Even symptomatic patients may have a normal chest radiograph initially
or may show small opacities which may be nodular or reticulonodular
usually in the basal areas. The shadowing is usually symmetric from
side-to-side, but atypical distributions can occur.
Another common pattern is hazy, ground-glass opacification which
may be diffuse or patchy. Volume loss is characterized by diaphragmatic
elevation and depression of the fissures. The loss of volume is usually
concentrated in the lower lobes but may be generalized. Pneumothorax
occurs occasionally, pneumomediastinum is also a recognized
complication.
With progression of the disease, the initially fine shadowing becomes
coarser, and small, cyst like transradiancies appear leading to a honeycomb pattern in one-third to one-half of patients, in later stages of the
disease.
With gross fibrosis, larger cyst and bullae may appear.
CT SCAN
CT scan is valuable in the diagnosis of early stages of the disease. The
earliest CT sign of fibrosing alveolitis is faint subpleural opacification in
the posterobasal segments of the lower lobes.
As the interstitial fibrosis progresses, a reticular pattern containing
small cystic air-spaces becomes evident. Interlobular interstitial thickening
manifest as very fine reticulation or areas of ground-glass opacification.
Moderately enlarged mediastinal lymph nodes are a frequent finding
on CT. Honey comb appearance is very apparent on CT chest.
BIBLIOGRAPHY
1. Armando J Huaringa, Francisco J Leyva. Diffuse Parenchymal Lung Disease:
A Practical Approach. The Internet Journal of Pulmonary Medicine 2000;1(1).
Pulmonology
2. Turner-Warwick M, Burrows B, Johnson A. Cryptogenic fibrosing alveolitis: Clinical
features and their influence on survival. Thorax 1980; 35: 171-80.
3. Wells A. Clinical usefulness of high resolution computed tomography in cryptogenic
fibrosing alveolitis. Thorax 1998; 53(12): 1080-7.
EMPHYSEMA
Chest radiography is insensitive for the detection of mild-to-moderate
emphysema.
The chest radiographic findings in emphysema may be divided into
four types: hyperinflation, vascular change, bullae, and increased
markings. Hyperinflation and vascular change are the usual predominant
finding, with hyperinflation reflecting functional abnormality and
vascular change reflecting lung destruction.
Hyperinflation is indicated by a number of signs, e.g low flat
diaphragm, increased retrosternal airspace, obtuse costophrenic angle
and cardiac diameter less than 11.5 cm, with a vertical heart.
Vascular signs include increased transradiancy, reduced size and
number of vessels in middle and outer 1/3 of lung indicating prunning
of pulmonary arteries due to pulmonary hypertension. Bullae are
common and diagnostic in the presence of the above mentioned findings.
BIBLIOGRAPHY
1. Foster WL Jr, Gimenez EI, Roubidoux MA, Sherrier RH, Shannon RH, Roggli VL,
et al. The emphysemas: Radiologicpathologic correlations. Radiographics
1993;13:31128.
2. Pugatch RD. The radiology of emphysema, Clin Chest Med 1983, 4:433-42.
3. Simon G. Radiology and emphysema. Clin Radiol 1964; 15:293-306.
4. Thurlbeck WM, Simon G. Radiographic appearance of the chest in emphysema.
American Journal of Roentgenology 1978;134, 225-32.
LUNG ABSCESS
Lung abscess is seen as an area of lucency within an area of consolidation,
may have an air-fluid level. If multiple, consider possibility of septic
emboli. Bacterial lung abscess generally form a thick-walled cavity with
a shaggy inner lining. The wall may be thick at first, but with further
necrosis and coughing up of necrotic material it becomes thinner.
BIBLIOGRAPHY
1. David Sutton. Text book of radiology and imaging (7th edn), Churchill Livingstone
2003;(1):138-9.
2. Hood MR. Bacterial diseases of the lung. In: Shields TW (Eds): General Thoracic
Surgery (4th edn). Philadelphia, Pa: Lea and Febiger; 1989; 751-71.
15
16

HIATUS HERNIA
Hiatus hernias are frequently incidental findings on chest radiographs
and CT.
A hiatus hernia appears as a round soft-tissue mass often containing
either gas or an air-fluid level behind the heart, usually to the left of the
midline in the posterior mediastinum.
The larger hernias can also contain small intestine, colon and liver.
The diagnosis is readily confirmed by a lateral film, or a barium
meal, which shows the stomach above the diaphragm.
The diagnosis is also often confirmed by CT which shows the contrast
medium-filled stomach above the diaphragm surrounding fatty tissue.
With large paraesophageal hernias, the stomach not infrequently
undergoes organoaxial rotation and may, therefore contain two air-fluid
levels.
BIBLIOGRAPHY
1. David Sutton. Text book of radiology and imaging (7th edn). Churchill Livingstone;
2003;1:75-6.
2. Peter Armstrong. Imaging of diseases of the chest (3rd edn) 2000; 874.
Pulmonology
FIGURE 1.1: Primary Pulmonary Tuberculosis. Tuberculous

mediastinal lymphadenopathy. Superior mediastinal
widening is seen due to tuberculous lymphadenopathy.
Inhomogeneous shadowing seen in right upper and mid
zones due to tuberculous infiltrates.
FIGURE 1.2: Primary Pulmonary Tuberculosis.

Inhomogeneous opacities seen in right upper and mid zones
(arrow) with right hilar lymphadenopathy.
17
18
FIGURE 1.3: Primary Pulmonary Tuberculosis. Nodular

opacities seen in the right upper zone with mediastinal
lymphadenopathy on the right side (arrow).
FIGURE 1.4: Primary Tuberculosis. Patchy infiltration visible

in the left mid zone along with widening of the superior
mediastinum due to lymphadenopathy.
Pulmonology
FIGURE 1.5: Primary Pulmonary Tuberculosis. Right

sided mediastinal lymphadenopathy.
FIGURE 1.6: Postprimary Tuberculosis. Bilateral tuberculous infiltration and mediastinal lymphadenopathy.
19
20
FIGURE 1.7: Postprimary Pulmonary Tuberculosis.

Fibrocavitatory lesions in the right upper zone due to
tuberculosis (arrow). Bilateral emphysematous changes with
narrow tubular heart shadow.
FIGURE 1.8: Miliary Tuberculosis. Right para-tracheal and

bilateral hilar lymphadenopathy also seen along with miliary
mottling
Pulmonology
FIGURE 1.9: Miliary tuberculosis and left sided pneumothorax

(white arrows) and pneumomediastinum (black arrow)
(Pneumothorax rarely seen in miliary tuberculosis).
FIGURE 1.10: Miliary Tuberculosis. Consolidation of the right

lower lobe is also seen due to secondary bacterial infection.
21
22
B
FIGURES 1.11A AND B: Miliary Tuberculosis. (A) Miliary
mottling more on left side. Hilar and superior mediastinal
lymphadenopathy is also apparent. (B) An enlarged view
showing miliary mottling.
Pulmonology
FIGURE 1.12: Miliary Tuberculosis. Wide spread nodular

shadowing.
FIGURE 1.13: Chronic Pulmonary Tuberculosis. Partial

consolidation of right upper lobe and a large cavity in left
upper zone (arrow) with raised left dome of diaphragm;
pleural thickening and calcification.
23
24
FIGURE 1.14: Chronic Pulmonary Tuberculosis.

Fibrocavitatory lesions bilaterally more extensive in right
upper zone. Tenting of right hemidiaphragm. Trachea is
pulled to the right side.
FIGURE 1.15: Reactivation Tuberculosis. A case of healed

pulmonary tuberculosis apparent from fibrotic changes in
both the lungs. Reactivation is visible in the form of a thick
walled cavity in the left lung (arrows).
Pulmonology
FIGURE 1.16: Tuberculous cavity with secondary infection in

left lung (black arrow). Calcified granuloma is also visible in
right middle zone (white arrow).
FIGURE 1.17: Calcified granuloma (Tuberculomas) in a

patient treated for tuberculosis (arrows).
25
26
FIGURE 1.18: Pulmonary Tuberculosis. Tuberculoma in

the right lung (arrow).
FIGURE 1.19: Tuberculoma. A large well-defined soft tissue

mass with some calcifications, in the mid zone on right side
(arrow). Relatively smaller nodules seen above it (Biopsy
proven tuberculoma).
Pulmonology
FIGURE 1.20: Post-tuberculous fibrosis of right lung with

ipsilateral shifting of mediastinum and elevation of right
dome of diaphragm. Pleural calcification and calcified lymph
nodes at the right hilum.
FIGURE 1.21: Post-tuberculous fibrosis and scar ring (arrow)

especially in left upper zone and tenting of left hemidiaphragm.
27
28
FIGURE 1.22: Fibrocavitatory tuberculosis of left lung along

with lobar pneumonia right upper lobe due to secondary
bacterial infection.
FIGURE 1.23: Pulmonary Tuberculosis. Bilateral apical

fibrosis with punctate calcification secondary to tuberculosis,
mediastinal, tracheobronchial and left hilar lymphadenopathy.
Pulmonology
FIGURE 1.24: Post-tuberculous Cavitations. Such cavities

are a good site for Aspergilloma formation (arrows).
FIGURE 1.25: Multi-drug Resistant (MDR) Tuberculosis.

Fibrocavitatory pulmonary tuberculosis of both lungs in a
patient with multi-drug resistant tuberculosis. Thick walled
cavitatory lesions in the upper and basal segments of right
upper lobe (arrows).
29
30
FIGURE 1.26: Post-tuberculous cavitations with

fibrotic changes.
FIGURE 1.27: Thick walled tuberculous

cavitations in the right lung (arrows).
Pulmonology
FIGURE 1.28: Post-tuberculous bands. Band atelectasis in

right lower zone (white arrow). Emphysematous changes
also seen in both the lungs. Loculated pneumothorax in
right costophrenic angle (black arrow).
FIGURE 1.29: Post-tubercular pleural calcification. Interlacing

pattern of pleural calcification especially on the right side
(arrow). Calcified pleural plaques also seen along the right
dome of diaphragm.
31
32
FIGURE 1.30A: Series of chest X-rays

of biopsy proven case of tuberculosis:
a) Massive left sided pleural effusion
seen with shift of mediastinum to right
side. Hilar lymphadenopathy also
seen on right side with some calcifications (Fluid analysis showed exudate
with predominant lymphocytes but no
growth of mycobacteria).
FIGURE 1.30B: Large oval opacity

with fuzzy margins seen in the left
middle and lower zones overlapping left border of the heart.
Elevated left dome of diaphragm
with volume loss seen on the left
side because of partial collapse of
left lower lobe. Small left sided
pleural effusion also seen. A large
oval lobulated shadow with internal
calcifications seen in right hilar
region indicating lymphadenopathy
(CT guided biopsy of the mass
showed caseating granulomas
compatible with tuberculosis).
Pulmonology
FIGURE 1.30C: Marked improvement seen in the form of reduction in the

size of mass on the left side with regression of hilar lymph nodes on right
side lung expansion also noted (Clinically patient also had hoarseness
of voice due to compression of left recurrent laryngeal nerve, which
improved markedly with anti-tubercular drug treatment).
FIGURE 1.30D: Further improvement noted

on this chest X-ray.
33
34
FIGURE 1.31: Tuberculous Bronchopneumonia. Patchy

alveolar opacities seen due to bronchial spread. Cavitations
seen on the left side with left upper lobe consolidation with
hilar and pleural calcifications.
FIGURE 1.32: Bilateral tuberculous bronchopneumonia

with loculated pneumothorax on right side (arrows).
Pulmonology
FIGURE 1.33: Tuberculous bronchopneumonia. Widespread

patchy opacities with air-bronchogram in the right lung- upper
and middle zones with mediastinal lymphadenopathy (arrow).
FIGURE 1.34: Tuberculous consolidation-collapse left upper

lobe. Thickening of pleura seen in interlobar fissure on the
right side (arrow).
35
36
FIGURE 1.35: Aspergilloma in a tuberculous cavity. Fibrotic

changes seen bilaterally with a large cavity (left side)
containing a dense mass with air-crescent around (arrow).
FIGURE 1.36: Aspergilloma in a tuberculous cavity (white

arrow). Large thick walled cavity with a rounded opacity inside
with a translucent rim around (black arrow)
Pulmonology
FIGURE 1.37: Aspergilloma in a post-tuberculous cavity. Cavity

in the left apex with soft tissue mass inside. Soft tissue
density with air crescent around.
FIGURE 1.38: Aspergilloma. Bilateral post-tuberculous cavities with large

fungus ball seen in one of the cavity surrounded by radiolucent crescent all
around. There is also pleural adhesion in the right lung with right hilar
lymphadenopathy.
37
38
C
FIGURES 1.39A TO C: Invasive Broncho-pulmonary Aspergillosis.
Multiple irregular and linear opacities seen bilaterally without any
hilar or mediastinal lymphadenopathy.
Pulmonology
FIGURE 1.40A: Early and Late Aspergillosis. Axial CT chest.

Nodule on CT with surrounding peripheral ill-defined
opacification-so-called halo sign in a patient with early
aspergillus infection post-bone marrow transplant for
lymphoma.
FIGURE 1.40B: Cavitating lesion at the left apex- angioinvasive

aspergillus infection in a patient with acute myeloid leukemia
who underwent bone marrow transplantation.
39
40
FIGURE 1.41: Cystic bronchiectasis in right middle and lower

zones with consolidation. Hyperinflated lung fields and tubular
heart also visible due to emphysema.
FIGURE 1.42: Bilateral bronchiectasis involving

middle and lower zones, more on right side.
Pulmonology
FIGURE 1.43: Bronchography (Right Oblique View). Cystic

bronchiectasis in right middle lobe and medial segment of
right lower lobe. Contrast seen in right lung airways (arrows).
FIGURE 1.44: Cystic Bronchiectasis. Multiple lucencies

with air fluid levels in middle and lower zones of left lung.
41
42
FIGURE 1.45: Cystic Bronchiectasis. Honey combing with

cystic bronchiectasis in right middle and lower lobes and left
lingular and apical basal segments with associated
consolidation. Bilateral hilar and right tracheobronchial
lymphadenopathy also visible.
FIGURE 1.46: Post-tuberculous Bronchiectasis. CT scan

chest axial section (lung window) showing bronchiectasis of
apical segment of right lower lobe with pleural thickening.
Pulmonology
FIGURE 1.47: CT Chest Axial Section (Lung Window).

Bronchectasis. Multiple bronchiectatic cavities right apical
and left lingular segments. Pleural thickening of right lung is
also seen.
FIGURE 1.48: Bronchiectasis with Cor pulmonale. CT scan

chest showing bilateral bronchiectasis and cardiomegaly due
to cor pulmonale.
FIGURE 1.49: Cystic Fibrosis. Thick walled bronchi

with bilateral cystic changes and fibrosis.
43
44
FIGURE 1.50: Cystic Fibrosis. Course and thick bronchial shadows

seen in both lower zones with cystic bronchiectatic changes.
FIGURE 1.51: Cystic Fibrosis. Bronchiectatic changes, thick walled

bronchi, fibrosis and prominent hilar and emphysematous lungs.
Pulmonology
FIGURE 1.52: Staphylococcal pneumonia. Consolidation

with partial collapse seen in the left lower zone with elevated
left dome of diaphragm. Multiple pneumatoceles seen above
consolidation (arrow).
FIGURE 1.53: Mycoplasma pneumonia. Reticulonodular

shadowing is seen bilaterally but more clearly marked on
the right side.
45
46
FIGURE 1.54: Right Lower Lobe Pneumonia. Opacity due

to consolidation of right lower lobe. Right costophrenic angle
is obliterated due to pleural effusion. Cardiomegaly is also
present due to underlying ischemic heart disease.
FIGURE 1.55: Atypical Pneumonia. Bilateral reticulonodular

shadowing especially in the right lower zone. Smalll amount
of pleural effusion seen on the right side. Air space shadowing
right lower lobe and left lower lobe.
Pulmonology
FIGURE 1.56: Consolidation-collapse Right Upper Lobe.

Right upper lobe consolidation with partial collapse. Air
bronchogram sign is seen. Trachea is central but the
interlobar fissure has been pulled up.
FIGURE 1.57: Pneumonia Left Lower Lobe. Consolidation

of left lower lobe with mild left pleural effusion
47
48
FIGURE 1.58: Post-pneumonic Pneumatoceles. Multiple

cavities in the right middle and lower zones.
FIGURE 1.59: Pneumonia Right Lower Lobe. Consolidation

and collapse of right lower lobe. Loss of translucency over
the lower thoracic vertebra obliterating posterior costophrenic
angle indicating pleural effusion.
Pulmonology
FIGURE 1.60: Left Lower Lobe Pneumonia. Left lower lobe

consolidation with partial collapse due to pneumonia.
FIGURE 1.61: Left upper lobe consolidation due to

pneumonia.
49
50
FIGURE 1.62: Pneumonia Left Lower Lobe. Consolidation

of left lower lobe with air bronchogram. Emphysematous
changes and narrow tubular heart shadow.
FIGURE 1.63: Collapse of left upper lobe, left dome of the diaphragm is
elevated along with ipsilateral mediastinal shift. Compensatory
emphysema of right lung with herniation to the contralateral side.
Pulmonology
FIGURE 1.64: Consolidation of Right Middle Lobe.

Homogenous opacity overlying the heart.
FIGURE 1.65: Tubercular Pneumonia Left Upper Lobe.

Consolidation of left upper lobe with air bronchogram. Right
lung is hyperinflated with nodular opacities in the apex, also
mediastinal widening due to lymphadenopathy.
51
52
FIGURE 1.66: Legionnaines Pneumonia. Cardiomegaly with

bilateral inhomogeneous opacities silhouetting both heart
borders. Obliterated right costophrenic angle due to small
effusion.
FIGURE 1.67: Left Lower Lobe Pneumonia. Lingular and lower

lobe consolidation. Opacity along the left heart border with
elevated diaphragm and reduced lung volume on left side.
Pulmonology
FIGURE 1.68: Consolidation of left lower lobe and part of

Lingular lobe. Homogenous opacity in left lower zone (arrow),
silhouetting left hemi-diaphragm partly with air bronchogram.
FIGURE 1.69: Fibrocavitating lesion in left apex with bilateral

honey combing and consolidation of right middle and lower
zones as well as left lingular and lower lobe segments.
Klebsiella was grown from the sputum. Patient has been a
chronic smoker. Heart is enlarged with unfolding of aortic
arch.
53
54
FIGURE 1.70: Segmental consolidation involving the

right lower lobe in a patient with COPD.
FIGURE 1.71: Consolidation of the right middle lobe,

obliterating the rigth border of the heart but right dome of
diaphragm is clearly visible.
Pulmonology
FIGURE 1.72: Bronchopneumonia. Showing bilateral

inhomogeneous opacities in the lower zones more marked
on the right side.
FIGURE 1.73: Bronchopneumonia with right pleural effusion.

Patchy opacities in both middle and lower zones with
obliteration of right costophrenic angle.
55
56
FIGURE 1.74: Right Lung Collapse. Opaque right hemithorax

with ipsilateral shift of mediastinum due to complete collapse
of right lung.
FIGURE 1.75: Lingular lobe consolidation.
Pulmonology
FIGURE 1.76: Pneumocystis carinii pneumonia in a patient

with AIDS. Diffuse inhomogeneous shadowing seen in both
lungs.
FIGURE 1.77: Pneumocystis Carinii Pneumonia.

Cardiomegaly, pneumomediastinum and bilateral alveolar
infiltrates. The patient was undergoing chemotherapy for
acute myeloblastic leukemia.
57
58
FIGURE 1.78: Pneumocystis carinii infection. Bilateral perihilar and ground glass changes, caused by pneumocystis
carinii pneumonia, the most common infectious cause of
interstitial lung disease in AIDS patients.
FIGURE 1.79: CT Axial HRCT image, showing patchy ground

glass appearance in the lungs bilaterally in a patient with a
pneumocystis carinii pneumonia.
Pulmonology
FIGURES 1.80A TO D: Bronchiolitis Obliterans with Organizing Pneumonia. (A,B)

Chest X-rays show bilateral progressively increasing multiple alveolar opacities.
(C,D) CT scan shows multiple bilateral alveolar opacities with air bronchogram with
distorsion of air spaces and peri-bronchial thickenning.
FIGURE 1.81: Bilateral Pneumonia. Multiple air space

shadows seen bilaterally due to bacterial pneumonia.
59
60
FIGURE 1.82: Consolidation left lower and lingular lobe

due to pneumonia with small pleural effusion.
FIGURE 1.83: Collapse of the left lung caused by carcinoma

of the left main bronchus with compensatory emphysema
on opposite side.
Pulmonology
FIGURE 1.84: Chickenpox. Small calcified opacities seen in

both lung fields following a previous chickenpox infection.
FIGURE 1.85: Consolidation Left Lower Lobe. Left lower lobe

consolidation due to pneumonia (air bronchogram sign positive),
obliteration of left costophrenic angle and left dome of diaphragm
because of parapneumonic effusion is also seen.
61
62
FIGURE 1.86: Pulmonary Hydatid Cysts. Two large rounded

opacities partly over lapping each other seen in the right
lung. Anti-echinococcal antibody titers were markedly raised
but no evidence of hydatid cyst elsewhere in the body was
present.
FIGURE 1.87: Pulmonary Hydatid Cysts. A large hydatid

cyst seen in the right lung (upper and middle zones) pressing
trachea and superior mediastinum. Patient presented with
dysphagia, difficulty in breathing and stridor.
Pulmonology
B
FIGURES 1.88A AND B: Infected hydatid cyst left mid and
lower zone with pleural reaction seen.
63
64
FIGURE 1.89: Moderate right sided pleural effusion.

Homogeneous opacity with concave upper margin and
obliteration of right costophrenic angle.
FIGURE 1.90: Right sided pleural effusion, secondary to

carcinoma bronchus (Hemorrhagic on aspiration).
Pulmonology
FIGURE 1.91: Loculated Tuberculous Empyema. Right

sided loculated pleural effusion. Widening of mediastinum
due to lymphadenopathy.
FIGURE 1.92: Moderate left sided pleural effusion with

contralateral shift of mediastinum. Left heart order obliterated
(silhouette sign) with mediastinal and right hilar
lymphadenopathy.
65
66
FIGURE 1.93: Loculated empyema on right side with fibrothorax. Large opacity in the right lung with sharp medial border
and right dense curvilinear band in the middle and lower
zones. Mediastinum is central.
FIGURE 1.94: Tuberculous Pleural Effusion. Moderate left

sided pleural effusion, with right mediastinal shift. Patchy
infiltration seen in the middle zone on the right side.
Pulmonology
FIGURE 1.95: Non-Hodgkins lymphoma with chylothorax. Massive

pleural effusion on left side. Right sided hilar and para-tracheal
lymphadenopathy. Contralateral shift of mediastinum.
FIGURE 1.96: Massive right sided pleural effusion. Right hemithorax

is homogeneously opaque, obliterating costophrenic angle, dome
of the diaphragm and cardiac border. No evidence of airbronchogram. Heart is shifted to the contralateral side.
67
68
FIGURE 1.97: Malignant pleural effusion in a case of

carcinoma bronchus with lymphangiitic spread in the right
upper zone.
FIGURE 1.98: Tuberculous Pleural Effusion. Dense opacity

seen in the left mid and lower zones with concave upper
border, obliteration of the left costophrenic angle and left
border of the heart. Mediastinum is shifted towards opposite
side.
Pulmonology
FIGURE 1.99: Tension pneumothorax on the right side with

widening of intercostal spaces and depression of right dome
of diaphragm. Shifting of mediastinum to the left with
collapsed right lung giving Fist sign at the right hilum.
FIGURE 1.100: Pockets of pneumothorax with pleural

adhesions on the right side. Left upper zone is showing posttuberculous scarring and fibrosis.
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70
FIGURE 1.101: Large hydropneumothorax on the right side.
FIGURE 1.102: Moderate pneumothorax with partial collapse

of right lung which is also showing bulla in its upper part
(arrow). Small pleural effusion on the right side.
Pulmonology
FIGURE 1.103: Left sided hydropneumothorax.
FIGURE 1.104: Large hydropneumothorax on right side

with contralateral mediastinal shift.
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72
FIGURE 1.105: Right sided hydropneumothorax with a large bulla

seen in the partially collapsed right lung (white arrow). Consolidation
of the left lower lobe with a thick walled cavity above is also seen.
Linear translucency along the heart border bilaterally indicate
pneumopericardium/pneumomediastinum (black arrows).
FIGURE 1.106: Large right sided hydro (pyo)

pneumothorax.
Pulmonology
FIGURE 1.107: Hydropneumothorax right side. Patchy

opacities in the left lung and right sided hydropneumothorax (due to tuberculosis)
FIGURE 1.108: Left sided partial pneumothorax.
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74
FIGURE 1.109: Carcinoma bronchus with post-obstructive

consolidation in the left upper lobe. Irregular mass seen at
the left hilum.
FIGURE 1.110: Carcinoma Bronchus. Large oval opacity seen

in the right upper lobe. Eccentric cavitation also visible in the
upper and lateral part.
Pulmonology
FIGURE 1.111: Carcinoma Bronchus. Large inhomogeneous opacity seen in the right lung. Cavitations seen
within the opacity. Superior mediastinal lymphadenopathy
present. Right lower zone is hypertransradiant.

pneumonia. Non-homogeneous opacity in right upper lobe (anterior
and apical segments) sparing the posterior segments. Right hilar
and mediastinal lymphadenopathy also present.
75
76
FIGURE 1.113: Pancoast Tumor. Large well-defined homogeneous

opacity occupying whole of the right upper and mid zones, obliterating
the right mediastinal border and partly right heart border. Elevated right
dome of diaphragm due to phrenic nerve palsy is visible. Also right 3rd
and 4th ribs show lytic lesions posteriorly.
FIGURE 1.114: Carcinoma Bronchus (Squamous Cell Carcinoma).

Mass in the right middle and lower zone with right hilar lymphadenopathy.
Right dome of diaphragm in medial 3/4th and right heart border is
obliterated (Silhouette sign).
Pulmonology
FIGURE 1.115: Carcinoma Bronchus (Squamous Cell

Carcinoma). Large mass with irregular and lobulated margins
seen in the left lung.
FIGURE 1.116: Carcinoma Bronchus. Oval shaped opacity in left upper

mid zone with ill-defined margins and erosion of the ribs (arrow).
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78
FIGURE 1.117: Carcinoma Bronchus. Irregular mass in the

right hilar area with post-obstructive segmental consolidation
seen in the right upper and middle zones. Horizontal fissure
is prominent because of fluid (Inflammatory) (arrow).
FIGURE 1.118: Pancoast tumor involving the left apex with rib
erosions (white arrow). Extensive soft tissue mass (extra
pulmonary) with erosion of the medial end of left clavicle
(black arrow) is also seen.
Pulmonology
FIGURE 1.119: Alveolar Cell Carcinoma. Bilateral ill-defined

multiple opacities with pleural effusion on the right side.
FIGURE 1.120: Carcinoma Lung. Soft tissue mass fairly well

defined in left upper lobe with central translucencies
indicating cavity formation.
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80
FIGURE 1.121: Pancoast Tumor. Soft tissue opacity in the right

apex and supraclavicular region (black arrow) with destruction of
2nd and 3rd ribs (posterior ends) (white arrows).
FIGURE 1.122: Carcinoma Bronchus. Cavitating lesion in

the left lower zone (black arrow). Left hilar lymphadenopathy
(white arrow).
Pulmonology
FIGURE 1.123: Carcinoma bronchus with lymphangiitis

carcinomatosis and right phrenic nerve palsy. Soft tissue
mass with spiculated margins at right hilum, prominent
interstitial markings and raised right hemi-diaphragm.
FIGURE 1.124: Squamous cell carcinoma with central necrosis.

Thick walled cavitatory lesion with air-fluid level (arrow).
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82
FIGURE 1.125: Carcinoma Bronchus. An oblong mass with

spiculated margins seen in the right hilum. Left hilum is
also prominent due to lymphadenopathy.
FIGURE 1.126: Bronchial Adenoma. Large, well circumscribed nodule in the right lower zone (arrows). The patient
presented with recurrent hemoptysis.
Pulmonology
FIGURE 1.127: Carcinoma Bronchus. Large dense opacity

wih irregular margins seen in the right hilar region. Right
upper lobe is partly consolidated due to post-obtructive
infection.

pneumonia. Large mass in the right hilar region with postobstructive consolidation due to infection in the upper and
middle zones.
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84
FIGURE 1.129A: Malignant Mesothelioma.

Lobulated masses seen in the right hilar and
peri-hilar regions with widening of superior
mediastinum. Moderate pleural effusion is also
present.
FIGURES 1.129B AND C: CT scan chest showing pleural effusion and a broad
based mass arising from pleura on the right side with pleural thickening and pretracheal and mediastinal lymphadenopathy.
Pulmonology
FIGURE 1.130: Pancoast tumor in right upper lobe with partial

collapse. Opacity in right upper zone, inferiorly limited by
horizontal fissure which is being pulled up. Destruction of
posterior ends of first three ribs.
FIGURE 1.131: Lymphangiitis Carcinomatosa. Disseminated

linear and nodular shadowing partly coalescent with each
other.
85
86
FIGURE 1.132: Metastases from carcinoma

stomach. Multiple round and oval opacities which
are well-defined and of variable sizes.
FIGURE 1.133: Extensive Metastasis from

Osteosarcoma. Multiple large oval, confluent
and overlapping dense opacities in both the lung
fields and the mediastinum.
Pulmonology
FIGURE 1.134: Metastasis from Unknown Primary. Multiple

round and oval opacities of variable sizes scattered in both
the lung fields. Hilar lymphadenopathy also visible.
FIGURE 1.135: Hamartomas. Two rounded lesions involving

the upper and middle zones of right lung with popcorn
calcification in the larger lesion.
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88
FIGURE 1.136: Metastasis from Carcinoma-Thyroid. Multiple

bilateral nodular opacities of different sizes mainly in the
right lung.
FIGURE 1.137: Metastases from Unknown Primary.

Multiple well-defined masses in the right lung.
Pulmonology
FIGURE 1.138: Metastasis from Carcinoma Colon. Multiple

opacities of variable sizes especially on right side with hilar
and superior mediastinal lymphadenopathy.
FIGURE 1.139: Metastases with Pleural Effusion. Many

well-defined opacities of different sizes seen in the lung. Right
hemidiaphragm is elevated due to liver metastases. Right
sided pleural effusion also present.
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90
FIGURE 1.140: Metastases Secondary to Carcinoma of

Breast. Bilateral pleural effusion with disseminated nodular
shadows seen through out both lung fields.
FIGURE 1.141: Neurofibromatosis. Marked scoliosis

(concavity facing left) of the spine with a large extrathoracic
soft tissue mass on the right side (black arrow). A rounded
opacity seen in the right lung (white arrow), is actually due to
a neurofibroma present on the posterior chest wall.
Pulmonology
FIGURE 1.142: Pleural Fibroma. Large well-defined mass

involving the middle and lower zones of the left lung with
marginal calcification.
FIGURE 1.143: Metastases from Carcinoma Breast. Multiple

confluent opacities seen in both the lungs- mid and lower
zones with right hilar lymphadenopathy.
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92
FIGURE 1.144: Carcinoma Bronchus. CT scan chest

showing soft tissue rounded mass in right upper lobe of the
lung and pre-tracheal and pre-carinal lymphadenopathy.
B
FIGURES 1.145A AND B: Carcinoma of Bronchus. (A) Chest X-ray showing
mild left sided pleural effusion with left hilar lymph nodes enlargement. (B) CT
scan done few days later showed collapse of the left lung due to carcinoma of
left main bronchus with mild pleural effusion.
Pulmonology
B
FIGURES 1.146A AND B: Malignant Mesothelioma.
Mediastinal window showing consolidation with collapse of
right lung with pleural effusion and the lung window is
showing consolidation and collapse of left lung with pleural
effusion, lobulated pleural mass along with hilar and
mediastinal lymphadenopathy.
93
94
FIGURE 1.147: Mesothelioma. IV contrast enhanced CT

chest. The image shows lumpy areas of pleural thickening
with mediastinal and right axillary lymphadenopathy in a
histologically proven mesothelioma.
Differential diagnosis of multiple round

pulmonary opacities
Varying size:
Metastases (GIT, breast, thyroid, kidney)
Inflammatory
Wegeners granulomatosis
Rheumatoid arthritis
AV malformations
Infections:
Tuberculosis
Hydatid
Staphylococcus aureus
Histoplasmosis
Size b/w 2-5 mm (typically)
Tuberculosis
Lymphoma
Sarcoidosis
Metastases
Size b/w 0.5-2 mm
Tuberculosis (Miliary)
Sarcoidosis
Occupational lung diseases
Pulmonology
FIGURE 1.148: Fibrosing Alveolitis. Decrease lung volume,

elevated dome of diaphragm with reticulonodular shadowing
seen in the lower lobes.
FIGURE 1.149: Shrinking lung syndrome in a patient with

SLE.
95
96
FIGURE 1.150: Fibrosing Alveolitis. Bilateral reticulonodular

shadowing seen in the lower zones due to interstitial lung
disease.
FIGURE 1.151: Fibrosing Alveolitis. Typical honey-coomb

appearance seen in a patient with advanced fibrosing
alveolitis.
Pulmonology
FIGURE 1.152: Chronic extrinsic allergic alveolitis (Bird

fanciers lung). Fibrosis and scarring in upper zones
especially on left side. Irregular opacities and some cavitating
lesions are also seen.
FIGURE 1.153: Pneumoconiosis (Siderosis). Dense linear

branching opacities seen in both the lung fields more on the
left side in a young male who worked for 6 months in ore
mines.
97
98
B
FIGURES 1.154A AND B: Silicosis. (A) Chest X-ray showing bilateral multiple
irregular opacities with calcifications, pleural reaction and fibrosis. (B) CT scan chest
reveals bilateral hilar lymphadenopathy with calcification. Right soft tissue mass
adjacent to right main bronchus, which is speculated. Multiple irregular opacities
also seen in both lung fields.
Pulmonology
FIGURE 1.155: Acute Respiratory Distress Syndrome.

Bilateral air space shadowing in a patient exposed to smoke
inhalation.
FIGURE 1.156: Acute Respiratory Distress Syndrome.

Widespread, uniformly distributed air space shadowing in a
septicemic patient with multiorgan faliure.
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100
FIGURE 1.157: Eventration of right dome of

diaphragm (medial part).
FIGURE 1.158: Eventration of right dome of diaphragm,

mimicking a mass lesion.
Pulmonology
FIGURE 1.159: Gross eventration of the left dome of

diaphragm
FIGURE 1.160: Eventration of right dome of diaphragm

giving effect of mass lesion.
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102
FIGURE 1.161: Eventration of the right dome of diaphragm
FIGURE 1.162: Guillain Barr Syndrome . Bilateral elevated

domes of diaphragm due to involvement of phrenic nerves.
Pulmonology
FIGURE 1.163: Chilaiditis Syndrome. Chest X-ray of a 21-year

old female, mentally retarded, having bilateral exophthalmus
(congenital) and scoliosis. X-ray reveals bilateral elevated domes
of diaphragm with underlying colonic shadows displacing liver,
stomach and spleen downwards.
FIGURE 1.164: Large Liver Abscess. Markedly elevated

right dome of diaphragm due to underlying liver abscess.
Minimal right sided pleural effusion also visible.
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104
FIGURE 1.165: Large Liver Abscess. Large thick walled cavity with air
fluid level seen in the right subphrenic region with small pleural effusion
and consolidation in the right lower lobe.
Causes of raised diaphragm

Unilateral:
- Phrenic nerve palsy
- Pulmonary collapse
- Pulmonary infarction
- Splinting of diaphragm
- Eventration
- Subphrenic inflammatory disease
- Scoliosis
- Pleural disease
Bilateral:
- Bilateral basal pulmonary collapse
- Small lungs
- Ascites
- Pregnancy
- Hepatosplenomegaly
- Large intra-abdominal tumor
- Bilateral subphrenic abscess
Pulmonology
FIGURES 1.166A TO D: (A) Chest X-ray showing marked elevation of left dome of
diaphragm with enormously distended and air filled splenic flexture of the colon due
to underlying volvulous. (B to D) Volvulus of large intestine with distension of the
proximal colon occupying most of the left hemithorax and causing marked elevation
of the left dome of diaphragm with shifting of the mediastinum to opposite side.
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106
FIGURE 1.167: Chronic Obstructive Pulmonary Disease.

Bilateral emphysematous changes with flattened domes of
diaphragm and narrow tubular heart.
FIGURE 1.168: Acute Asthma. Hyperinflated lungs in a

patient with acute severe asthma.
Pulmonology
FIGURE 1.169: Emphysematous Bullae. Hyperinflated lung

fields, with flattening of domes of diaphragm and narrow
tubular heart. Multiple large bullae are visible in the left lung.
FIGURE 1.170: Cor-pulmonale Secondary to COPD.

Cardiomegaly with right ventricular hypertrophy pattern. Central
pulmonary artery dilatation with pruning of arteries distally.
Hyperinflated lungs with flattening of domes of diaphragm.
107
108
FIGURE 1.171: Lung Abscess with Effusion. Thick walled

cavity with air-fluid level seen in the right lower zone. Right
costophrenic angle obliterated.
FIGURE 1.172: Lung Abscess. Large thick walled cavity

with an air-fluid level seen in the left lung.
Pulmonology
FIGURE 1.173: Large lung abscess in the left upper lobe

with prominent air-fluid level.
FIGURE 1.174: Wegeners Granulomatosis. Bilateral thick

walled cavities (arrows) with mediastinal lymphadenopathy
and consolidation in the right lower zone.
109
110
FIGURE 1.175: Post-pneumonic lung abscess seen in the

right lower lobe with small pleural effusion.
FIGURE 1.176: Wegeners Granulomatosis. Multiple well-defined

nodular opacities seen in the right lung and picture of lobar
consolidation in the left lung. Patient had history of non-resolving
pneumonia and ultimately cANCA was found to be positive.
Pulmonology
Differential diagnosis of cavitatory lung Lesions
Neoplastic
- Carcinoma of bronchus
- Metastases
- Hodgkins disease
Infections
- Tuberculosis
- Staphylococcus aureus
Inflammatory
- Wegeners granulomatosis
- Rheumatoid nodules
- Sarcoidosis
Vascular
- Infarction
Abnormal lung:
- Cystic bronchiectasis
- Infected emphysematous bulla
FIGURE 1.177: Stage II Sarcoidosis.

Bilateral hilar lymphadenopathy and
reticular shadowing in lung fields.
Cardiomegaly and aortic calcification
(arrow).
FIGURE 1.178: Stage II Sarcoidosis.

Bilateral massive hilar and mediastinal
lymphadenopathy with pulmonary
infiltrates.
111
112
C
FIGURES 1.179A TO C: Hodgkins Lymphoma. (A) Chest X-ray showing a rounded
soft tissue mass in the posterior superior mediastinum indenting the trachea from
behind. (B, C) CT scan chest of the same patient showing a large mass with an area
of central necrosis. The mass is extending upto the vertebral column.
Pulmonology
FIGURE 1.180: Histoplasmosis. Asymmetrical

bilateral hilar lymphadenopathy with multiple small
nodular opacities in the lung fields.
FIGURE 1.181: Non-Hodgkins Lymphoma. Bilateral

asymmetrical superior mediastinal lymphadenopathy.
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114
FIGURE 1.182: Non-Hodgkins Lymphoma. Mass in

superior mediastinum. Elevated right dome of
diaphragm. Right tracheobronchial lymphadenopathy
with basal atelectasis and small pleural effusion.
FIGURE 1.183: Non-Hodgkins Lymphoma. Para-vertebral,

low attenuation lobulated mass with destruction of vertebral
body and lesion extending up to the spinal cord and displacing
it posteriorly.
Pulmonology
FIGURE 1.184: Hodgkins Disease. Bilateral mediastinal

and hilar lymphadenopathy.
FIGURE 1.185: Hodgkins Disease. Hilar and mediastinal

lymphadenopathy, showing large oval opacity in the right
hilar region with widening of mediastinum. Lobulated
shadows seen above the arch of aorta on both sides.
115
116
FIGURE 1.186: Hydatid Cysts. Two large overlapping

calcified cystic shadows seen in the anterior and superior
mediastinum. Hydatid cysts rarely occur in the mediastinum.
FIGURE 1.187: Dermoid Cyst. Two rounded calcified

masses in the anterior mediastinum.
Pulmonology
FIGURE 1.188: Bronchogenic Cysts.

Three well-defined opacities seen in
the retrosternal area (arrows).
FIGURE 1.189: Thymoma. CT chest showing anterior mediastinal

mass due to thymoma in a patient with myesthenia gravis.
Differential diagnosis of mediastinal mass lesions
Anterior mediastinum
- Lymphadenopathy (TB, lymphoma)
- Tumors (Thymoma, teratoma, etc.)
- Goiter
- Pericardial cyst
- Morgagnian hernia
Middle
- Lymphadenopathy
- Aortic aneurysm
- Hydatid cyst
- Carcinoma bronchus
- Causes of cardiomegaly (in children)
Posterior
- Neuroblastoma (in children)
- Metastases and myeloma
- Paraspinal abscess (TB)
- Hiatus hernia
117
118
FIGURE 1.190: Retrosternal Goiter. Trachea being

compressed and shifted towards right side (black arrow),
widened superior mediastinum (white arrow).
FIGURE 1.191: Subcutaneous emphysema (arrows) in a

patient with acute severe asthma without any pneumothorax.
Pulmonology
FIGURE 1.192: Toxic Multinodular Goiter.

Punctate calcification seen in the right upper zone
due to calcification in a large toxic multinodular
goiter with retrosternal extension (widened
superior mediastinum) (arrow).
FIGURE 1.193: Pulmonary translucency

comparatively more prominent on left side
because of absent breast shadow.
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120
FIGURE 1.194: Calcification of tracheal rings; bronchi

and costal cartilages in an old age patient.
FIGURE 1.195: Azygos lobe fissure (black arrow) with azygos

vein (white arrow) in the lower margin of fissure.
Pulmonology
FIGURE 1.196: Inadvertent aspiration of barium into the lung

fields in a patient with pharyngeal and vocal cord paralysis.
Bilateral nodular opacities more marked in the lower zones
(Snowfall appearance).
FIGURE 1.197: Pulmonary Embolism. Large infarct seen

involving the right lower lobe simulating consolidation,
tappering apex towards the right hilum is apparent.
121
122
FIGURE 1.198: Pneumomediastinum (arrows), a chest tube

is seen placed in the pericardium from the right side.
FIGURE 1.199: Pulmonary Emboli. CT pulmonary angiogram

(CTPA) showing a filling defect in a right lower lobe pulmonary
artery consistent with a pulmonary embolus.
Cardiology
123
124

VALVULAR HEART DISEASES
MITRAL STENOSIS
The chest radiograph demonstrates selective left atrial enlargement, which
can vary in severity.
Left atrial appendage may form a bulge on the left heart border just
below the main pulmonary artery making the pulmonary conus
prominent.
The atrium is large but the left ventricular contour remains small
even in late stages. Small aortic knob is seen due to decreased left
ventricular output.
If the mitral stenosis is both severe and long-standing then
calcification of the valve can develop, best visualized in lateral position.
Often there is upper lobe blood diversion, with enlargement of the
main and central pulmonary arteries indicating pulmonary arterial
hypertension.
The right-sided cardiac chambers will often be considerably enlarged.
Double right heart border is present due to considerable enlargement
of both atria.
Hemosiderosis and pulmonary ossified nodules may occasionally be
seen.
BIBLIOGRAPHY
1. Chiles C, Putman CE. Pulmonary and Cardiac Imaging New York: Marcel Dekker.
1997.
2003;1:301-2.
3. Hammer WJ, Roberts WC, DeLeon AC Jr. Mitral stenosis secondary to combined
massive metal annular calcific deposits and small, hypertrophied left ventricles:
Hemodynamic documentation in four patients. Am J Med 1978; 64:371.
MITRAL REGURGITATION
In the acute phase, the heart size is likely to remain normal even in the
presence of a high left atrial pressure, but acute pulmonary edema can
occur.
In the chronic phase, the heart tends to enlarge with a left ventricular
configuration, left atrial enlargement being proportionately less prominent. In long-standing cases, however, there can be marked left atrial
enlargement. Calcification of the valve does not occur. The pulmonary
vascular appearances are very similar to those of mitral stenosis but the
heart size is often larger.
Cardiology
BIBLIOGRAPHY
1. David Sutton. Text book of radiology and imaging (7th edn), Churchill Livingstone;
2003;302-3.
2. Higgins CB. Essentials of Cardiac Radiology and Imaging. Philadelphia, Pa: JP
Lippincott, 1992.
3. Perloff JK, Roberts WC. The mitral apparatus: Functional anatomy of mitral
regurgitation. Circulation 1972; 46:227.
AORTIC STENOSIS
Significant aortic stenosis may present with a virtually normal heart
shadow, although it is rare. Initially, concentric left ventricular hypertrophy produces only some rounding of the cardiac apex (overall heart
size is normal), there is also dilatation of the ascending aortic arch.
The post-stenotic dilatation of aorta is variable. These appearances
can be difficult to detect in the older patient in whom the aorta often
becomes unfolded and slightly dilated.
On the lateral film, the presence of calcification in the position of the
aortic valve is an important sign, usually indicating important valve
stenosis.
In most cases of aortic stenosis the pulmonary vascularity is normal
but in advanced cases there will be left ventricular dysfunction and
associated changes of left heart failure.
BIBLIOGRAPHY
2003;1: 381-2.
2. Edwards JE. Calcific aortic stenosis: Pathologic features. Proc. Staff Meet. Mayo
Clin 1961; 36:444.
3. Edwards JE. Pathology of acquired valvular disease of the heart. Semin Roentgenol
1979;14:96.
PULMONARY STENOSIS
Initially the heart size is normal. If severe stenosis is present the right
ventricular enlargement is visible with an upward turned apex.
The main pulmonary artery is often prominent, which is caused by
post-stenotic dilatation.Peripheral pulmonary vascularity is usually
normal but oligemic lung fields may be seen.
BIBLIOGRAPHY
2003;1: 378-9.
2. Davies MJ. Pathology of Cardiac Valves. Butterworths. London, 1980; 131-7.
125
126

CONGENITAL HEART DISEASES
TETRALOGY OF FALLOTS
Many cases of tetralogy of Fallot have a nearly normal chest film.
In the classical appearance there will be:
1. Concavity on the left heart border in the region of the hypoplastic
main pulmonary artery.
2. Upward prominence of the cardiac apex due to distortion by the
large right ventricle.
3. Pulmonary oligemia.
4. In some cases right sided aortic arch.
BIBLIOGRAPHY
2003;1: 382-3.
2. Elliott LP. Cardiac Imaging in Infants, Children and Adults. Philadelphia: JB
Lippincott, 1991.
TRANSPOSITION OF THE GREAT ARTERIES

D-loop Transposition
The chest X-ray is often, but not always, characteristic. The heart is
slightly enlarged and rounded, generally biventricular enlargement with
an oval or egg-shaped configuration. There is pulmonary plethora.
L-loop Transposition
The chest X-ray may show a characteristic long curve to the left heart
border due to the abnormal leftward origin of the aorta.
A significant proportion of these patients have chest X-rays
indistinguishable from normal.
BIBLIOGRAPHY
1. David Sutton. Textbook of radiology and imaging (7th edn), Churchill Livingstone;
2003;1: 385-7.
2. Freedom RM, Mawson JB, Yoo SJ, Benson LN. Congenital Heart Disease; Textbook
of Angiocardiography. London; Futura. 1197.
ATRIAL SEPAL DEFECT

The chest X-ray is usually normal if the pulmonary-to-systemic flow
ratio is less than 2:1.
Cardiology
If ratio exceeds this level there will be pulmonary plethora and cardiac
enlargement. The cardiac enlargement is mainly due to right atrial and
right ventricular dilatation.
In patients with significant pulmonary arterial hypertension (usually
the elderly untreated patients), the chest X-ray will show dramatic
appearances of central dilated pulmonary arteries and peripheral
pulmonary vascular pruning. Left atrium and left ventricle are normal.
Aorta is small.
BIBLIOGRAPHY
2003;1: 374.
2. Ronald L. Eisenberg, Clinical Imaging, an atlas of differential diagnosis (4th edn).
2003; 248.
EBSTEIN ANOMALY
The clinical presentation varies considerably, severe cases presenting in
infancy with right heart failure and poor forward flow to the pulmonary
artery. The chest X-ray in these cases may show massive globular cardiomegaly with pulmonary oligemia. The mildest expression occurs in some
adults who present with mild signs or symptoms and a virtually normal
chest X-ray.
BIBLIOGRAPHY
2003;1: 398.
2. Elliott LP. Cardiac Imaging in Infants, Children and Adults. Philadelphia: JB
Lippincott, 1991.
PULMONARY VENOUS HYPERTENSION

The chest X-ray appearances of pulmonary venous hypertension are
characterized by:
1. Mild haziness in the lower zones with attenuation of the lower zone
vessels.
2. Prominence of the upper zone vessels upper lobe diversion.
3. The central pulmonary arteries are dilated, tapering to normal caliber
as they proceed distally.
4. There may be slight loss of definition of the heart and mediastinal
contours.
127
128

5. Chronic changes are associated with Kerley B lines (horizontal
subpleural lines, identified at the costophrenic angles).
6. Interstitial edema may cause thickening of the interlobar fissures,
seen in the horizontal fissure in the PA film and in both horizontal
and oblique fissures in the lateral film.
7. Pulmonary effusions may also develop.
The effusion is usually bilateral and can be large in amount.
8. Long-standing pulmonary venous hypertension can occasionally be
associated with the development of hemosiderosis (appears as fine
punctate calcifications that are scattered throughout both lungs).
9. Pulmonary ossific nodules (small areas of bone formation) can develop
if pulmonary hypertension remains severe for a long period of time.
BIBLIOGRAPHY
1. David Sutton. Textbook of radiology and imaging (7th edn), Churchill Livingstone;
2003;1: 288-90.
2. Peter Armstrong, Imaging of diseases of the chest (3rd edn). 2000; 431.
3. Simon M. The pulmonary vessels: Their hemodynamic evaluation using routine
radiographs. Radiol Clin North Am 1963; 11:362.
ACUTE MYOCARDIAL INFARCTION

Chest radiography is not the primary method for diagnosing this
condition, it is a useful adjunct. It will be normal in the acute phase in
the majority of patients.
The chest radiograph provides some insight into the severity of the
myocardial infarction.
The most common feature identified is the development of pulmonary
edema. Pleural effusions can develop if the left heart failure is prolonged.
Progressive enlargement of the heart can occur, more often in anterior
Several of the important complications of an acute myocardial
infarction can be suggested from the plain chest radiograph. If a left
ventricular-aneurysm develops it is revealed as a localised bulge on the
left heart border on chest radiograph.
The wall of long-standing aneurysm may show calcification.
BIBLIOGRAPHY
1. Chiles C, Putman CE. Pulmonary and Cardiac Imaging New York. Marcel Dekker.
1997.
2003;1: 296.
Cardiology
CONGESTIVE CARDIAC FAILURE
The usual signs are cardiomegaly with left ventricular enlargement, and
pulmonary venous hypertension signs. Pleural effusion is common
(bilateral or right sided; unilateral left sided effusions rare and suggests
another cause).
BIBLIOGRAPHY
1. Ronald L Eisenberg. Clinical Imaging, an atlas of differential diagnosis (4th edn).
2003; 238.
DILATED CARDIOMYOPATHY
The plain film is often abnormal, demonstrating cardiac enlargement of
all four chambers or of just the left ventricle. In the untreated patient
there is often volume overload of the left atrium leading to engorgement
of the pulmonary vasculature. The diagnosis cannot be made on the
chest radiograph alone.
BIBLIOGRAPHY
2003;1: 299.
PERICARDIAL EFFUSION
The appearances that can be identified on the plain film depend on the
amount of fluid present. A very large fluid collection can cause massive
enlargement of cardiac shadow.
The cardiac shadow has a rounded, globular appearance with no
particular chamber enlargement being identified (water bottle cardiac
silhouette) and sharp cardiophrenic angles.
If large enough the effusion will lead to an obstruction of the venous
return to the right heart, which produces clear rather than congested lungs.
A rapidly increasing heart size on serial films is seen as effusion
accumulates. On lateral view loss of retrosternal space and separation
of retrosternal from epicardical fat fat pad sign could be seen.
129
130

Causes of pericardial effusion
Transudative:
Heart failure
Hypoalbuminemia
Uremia
Exudative:
Viral infection (pericarditis or myocarditis)
Acute or chronic bacterial infection including tuberculosis
Inflammation (e.g. Dresselers syndrome)
Hemopericardium:
Post-cardiac surgery
Perforation of the heart by catheter (angiogram, pacemaker or angioplasty).
Bleeding disorders (including anticoagulation)
BIBLIOGRAPHY
1. Chiles C, Putman CE. Pulmonary and Cardiac Imaging New York: Marcel Dekker.
1997.
2. David Sutton. Textbook of radiology and imaging (7th edn). Churchill Livingstone;
2003;1: 305-7.
3. Skorton DJ, Schelbert HR, Wolf G L, Brundage BH. Marcus Cardiac Imaging: A
Companion to Brauwalds Heart Disease. 2nd Edition,Philadelphia; WB Saunders;
1996.
CONSTRICTIVE PERICARDITIS
The heart is often normal in size but can be enlarged especially in effusoconstrictive form. Straightening of the right heart border and roughening
of the cardiac outline as a result of pleuro-pericardial adhesions could
be seen. Calcification along the heart border is seen in approximately
half of the cases, more clearly visible on lateral view.
The lungs are usually clear due to constriction over the right heart,
although pleural effusion is not uncommon.
CT and MRI are helpful in revealing extent and distribution of
pericardial calcification and disease.
BIBLIOGRAPHY
1. Braunwald E, Lorell BH. Percardial disease. In braunwald E (Eds): Heart Disease. A
Textbook of Cardiovascular Medicine. Saunders 1984;1470.
2003;1:307.
Cardiology
Comment
The purpose of this book is to display mainly plain films and CT. Also
other techniques of value in the investigation of cardiac abnormality
include:
Echocardiography
Magnetic resonance imaging
Selective coronary angiography
Radio-isotope studies.
The plain films, however, do remain the starting point for all these
investigations.
131
132
FIGURE 2.1: Coarctation of Aorta. Inferior rib notching more

on left side. Cardiomegaly with left ventricular preponderance.
FIGURE 2.2: Coarctation of Aorta. Notching of the inferior

borders of the ribs posteriorly seen (arrows).
Cardiology
FIGURE 2.3: Coarctation of Aorta. Narrow arch and

descending aorta and inferior rib notching due to coarctation.
cardiomegaly is also present.
FIGURES 2.4A AND B: Coarctation of Aorta. MIP (Maximum intensity projection)

oblique sagittal MRI image showing the typical appearance of aortic coarctation with
prominent collateralization. CT oblique sagittal reconstruction demonstrating the CT
appearances of coarctation with an associated calcified bicuspid aortic valve.
133
134
FIGURE 2.5: Dextrocardia with scoliosis of the spine.
FIGURE 2.6: Dextrocardia with Situs Inversus. Stomach

fundus visible under the right side of diaphragm
Cardiology
FIGURE 2.7: Dextrocardia and Situs Inversus. Dextrorotation of heart, fundal gas seen on right side.
FIGURE 2.8: Dextrocardia. Axial MRI T1 weighted

image showing dextrocardia.
135
136
B
FIGURES 2.9A AND B: Right Sided Aorta. (A) The shadow
of the ascending aorta and aortic knuckle are clearly visible
on the right side of the mediastinum (arrow). The left
mediastinal shadow is devoid of aortic knuckle and
descending aortic shadow. (B) CT scan chest of the same
patient showing complete transposition of the aorta including
ascending aorta, arch of aorta and descending aorta to the
right side.
Cardiology
FIGURE 2.10: Transposition of Great Arteries. Narrow

mediastinum, pulmonary plethora with borderline
cardiomegaly.
FIGURE 2.11: Atrial Septal Defect (Ostium Secundum

Type). Cardiomegaly, prominent pulmonary conus, dilated
pulmonary vessels and pulmonary plethora seen.
137
138
FIGURE 2.12: Severe Mitral Stenosis. Cardiomegaly, dilated

pulmonary arteries, prominent pulmonary conus, upper lobe
diversion of blood vesseles and alveolar opacities (more
marked on the right side) due to pulmonary edema seen.
FIGURE 2.13: Prosthetic Valves (1) Mitral, (2) Aortic.

Sternal sutures are also visible.
Cardiology
FIGURE 2.14: Severe Aortic Stenosis. Marked cardiomegaly with left ventricular preponderance. Ground glass
appearance of lung fields due to pulmonary edema. Poststenotic dilatation of aorta is also seen (arrow).
FIGURE 2.15: Severe Mitral Stenosis. Cardiomegaly with

prominent pulmonary conus, large pulmonary arteries, and
upper lobe diversion with double atrial shadow visible.
139
140
FIGURE 2.16: Pulmonary Stenosis. Cardiomegaly with right

ventricular preponderance and upward turned apex.
Prominent main pulmonary artery with post-stenotic dilatation.
FIGURE 2.17: Calcified Mitral Valve. Double atrial shadow,

straightening of the left border of the heart. Prominent
pulmonary conus and linear calcification seen in the area of
mitral valve (arrow).
Cardiology
FIGURE 2.18: X-ray Barium Swallow (Lateral View).

Indentation and displacement of the esophagus due to
enlarged left atrium of the heart caused by mitral stenosis
(arrows).
FIGURE 2.19: Ebstein Anomaly. Cardiomegaly with globular

heart. Pulmonary oligemia with small pulmonary arteries.
141
142
FIGURE 2.20: Post-tuberculous fibrothorax and constrictive

pericarditis. Encasement of the heart in calcified pericardium.
Calcified plaques are also visible in the right pleura.
FIGURE 2.21: Massive pericardial effusion

due to viral pericarditis.
Cardiology
FIGURE 2.22: Massive pericardial effusion. Sharp margins of

the heart shadow and clear lung fields. Pneumopericardium
is also seen, which was iatrogenic (arrow).
FIGURE 2.23: Constrictive Pericarditis. Linear rim of

pericardial calcification visible along anterior wall and apex
of the heart (arrow).
143
144
FIGURE 2.24: Effusoconstrictive pericarditis due to

tuberculosis, Linear pericardial calcification are visible along
the left border of the heart (arrow). Post-tuberculous scaring
also visible in right upper zone.
FIGURE 2.25: MRI of a patient with constrictive pericarditis,

showing thickened pericardium and minimal pericardial
effusion, low signal on T-1 and high on T-2 images.
Cardiology
FIGURE 2.26: Acute pulmonary edema due to left ventricular

failure following acute myocardial infarction.
FIGURE 2.27: Cor-pulmonale Secondary to COPD.

Cardiomegaly with right ventricular hypertrophy pattern.
Central pulmonary artery dilatation with pruning of arteries
distally. Hyperinflated lungs with flattening of domes of
diaphragm.
145
146
FIGURE 2.28: Congestive Cardiac Failure. Cardiomegaly

with pulmonary plethora and right sided pleural effusion.
FIGURE 2.29: Acute pulmonary edema due to left ventricular

failure giving bats wings appearance.
Cardiology
FIGURE 2.30: Dilated Cardiomyopathy. Cardiomegaly with

pulmonary plethora. Fluid is seen in transverse fissure
(arrow).
Causes of gross cardiac enlargement

-
Multiple valvular disease

Aortic, mitral valve (particularly with regurgitation)
Pericardial effusion
Atrial septal defect (with Eisenmengers syndrome)
Cardiomyopathy
Ebsteins anomaly
147
148
FIGURE 2.31: Dissecting Aneurysm of Aorta. Aneurysm of

the arch and descending aorta (in a young patient) is seen.
Associated conditions include Marfans and other connective
tissue disorders.
FIGURE 2.32: Dissecting Aneurysm. Aneurysm has

further progressed as compared to previous X-ray.
Cardiology
B
FIGURES 2.33A AND B: (A) Aortic aneurysm causing
widening of superior mediastinum (PA view). (B) compressing
the esophagus (lateral view). The patient presented with
dysphagia.
149
150
B
FIGURES 2.34A AND B: Aortic Aneurysm. Enlargement of
aortic arch almost reaching upto the anterior chest wall
showing calcification within it.
Cardiology
FIGURE 2.35: Aneurysm of the ascending aorta seen as a

large rounded opacity in the right hilar region with widening
of mediastinum.
FIGURE 2.36: Left ventricular aneurysm following acute

151
152
FIGURES 2.37A TO C: Aortic

Dissection. Aneurysmal dilatation
of the ascending aorta seen.
Tortuousity and unfolding of aorta
causing mediastinal widening
also seen.
FIGURE 2.38: Left Ventricular

Aneurysm. Coronal CT image
with a calcified left ventricular
aneurysm.
Cardiology
C
FIGURES 2.39A TO C: Mediastinal and pericardial
lipomatosis in an asthmatic patient with itrogenic Cushings
syndrome. (A) Chest X-ray shows cardiomegaly with
obliteration of cardiophrenic angles bilaterally and smooth
mediastinal widening. (B,C) CT chest shows fat deposition
around the heart and the mediastinum can be easily
distinguished from the anatomical structures.
153
154
FIGURE 2.40: Pneumopyopericardium. Massive

cardiomegaly with air-fluid level seen within the
pericardium bilaterally (arrows).
FIGURES 2.41A AND B: SVC Stent. (A) PA chest radiograph. There is an SVC stent
in situ (arrow) with a soft tissue mediastinal mass. (B) Axial and coronal reconstruction
CT images showing the stent in place with no evidence of flow within it and extensive
enhancing chest wall collaterals in keeping with recurring SVC obstruction syndrome.
The patient was known to have a primary bronchogenic carcinoma.
Cardiology
FIGURE 2.42: Artificial pacemaker (Unipolar type) with

collapse-consolidation of left lung.
FIGURE 2.43: Single chamber ventricular pacemaker.

PA chest radiograph with a single chamber ventricular
pacemaker in situ, the tip of the lead is normally
projected to the left of the spine.
155
Barium Studies and Oral Cholecystography
157
158

REFLUX ESOPHAGITIS
The earliest changes of esophagitis are seen on endoscopy. It is only
with more pronounced edema that the earliest change of a fine mucosal
nodularity is seen on a double contrast barium swallow.
The collapsed esophagus show thickened longitudinal folds, which
when nodular, can give an appearance similar to that seen with varices.
Multiple fine ulcers give the mucosa a punctate or granular appearance
or larger discrete punched out ulcers develops.
Scaring produce permanent folds that radiate from the margins of
ulcer. Severe scarring results in stricture formation which are usually
smooth and long.
BIBLIOGRAPHY
1. Detection of reflux esophagitis on double-contrast esophagrams and endoscopy
using the histologic findings as the gold standard. Abdom Imaging 2004;29(4).
421-5.
2. Marsot-Dupuch K, Meyer B, Tiret E, Tubiana JM. Barium imaging of the esophagus.
Normal and pathologic aspects. Ann Radiol 1994;37(7-8):457-70.
ACHALASIA
Achalasia is a motor disorder of the esophagus and is caused by
degeneration of neurons of Auerbachs plexus.
A barium swallow will show the gastroesophageal junction failing to
open fully and tapering to a rat tail or bird beak appearance. Intact
mucosal folds can be traced through this narrowed segment. With time,
the esophagus dilates, lengthens and becomes tortuous. When
investigating achalasia by barium meal it is not always possible to exclude
gastric carcinoma as a cause.
BIBLIOGRAPHY
1. Kostic SV, Rice TW, Baker ME, et al. Timed barium esophagogram: A simple
physiologic assessment for achalasia. J Thorac Cardiovasc Surg 2000; 120(5): 93543.
2. Radiographic evaluation of esophageal function. Gastrointest Endosc Clin N Am
2005; 15(2):231-42.
3. Sezgin O, Ulker A, Temucin G. Barium findings in achalasia. J Clin Rad 2001; 29(1):
31-40.

CARCINOMA ESOPHAGUS
Early esophageal cancer on barium studies appear as depressed, polypoid
or plaque-like lesions.
In advanced esophageal carcinoma, barium radiology most frequently
shows a stricture with an irregular lumen and rolled margins, unlike benign
peptic strictures which have a smooth lumen and tapered margins. Some
tumors show pronounced ulceration, or are predominantly polypoid or
spread submucosally; producing thick and irregular esophageal folds.
BIBLIOGRAPHY
1. Montesi A, Pesaresi A, Graziani L, Salmistraro D, Dini L, Bearzi I. Barium imaging
of the esophagus. Normal and pathologic aspects. Ann Radiol 1994;37(7-8):457-70.
2. Nahum H, Reysseguier JC, Prandi D, Conte-Marti J, Benasse S, Lortat-Jacob JL.
Tumors of the esophagus. A radiological study of 11 cases. Ann Radiol (Paris)
1972;15(7):581-90.
BEZOARS
A bezoar is a mass of ingested material built up in the stomach, mostly
due to matted hair (trichobezoar) or vegetable or fruit pith (phytobezoar),
including chewed beetle nuts.
Barium outlines and often penetrates the mass, which often appear
as a filling defect with a mottled appearance.
BIBLIOGRAPHY
1. Gastric trichobezoar: Barium findings. Radiology 1986;161(1):123-4.
2. Small bowel phytobezoars: Detection with radiography. Radiology 1989;172(3):
705-7.
CARCINOMA STOMACH
Early carcinomas of the stomach may appear as slight elevation or slight
depression in the form of an ulcer.
In advance carcinoma meniscus sign is produced by the margin of
the ulcer. Infiltration of the whole of stomach is known as leather bottle
or Linitis plastica appearance.
Carcinoma may protrude into the stomach lumen and be polypoid or
fungating or may ulcerate or infiltrate. Some Adenocarcinoma produce
an excess of extra-cellular mucin, and such mucinproducing carcinomas
may show stippled calcification.
159
160

BIBLIOGRAPHY
1. Nishimata H, Maruyama M, Shimaoka S, Nishimata Y, Ohi H, Niihara T, et al.
Early gastric carcinomas in the cardiac region: Diagnosis with double-contrast Xray studies. Abdom Imaging. 2003; 28(4):486-91.
2. Ukrisana P, Wangwinyuvirat M. Evaluation of the sensitivity of the double-contrast
upper gastrointestinal series in the diagnosis of gastric cancer. J Med Assoc Thai.
2004; 87(1):80-6.
INTESTINAL TUBERCULOSIS
Ileocecal involvement is seen in 80-90% of patients with gastrointestinal
tuberculosis. This feature is attributed to the abundance of lymphoid
tissue (Peyers patches) in the distal and terminal ileum. Early changes
on barium examinations reveal nodular thickening of mucosal folds with
loss of symmetry in the fold pattern. Similar to Crohns disease, deep
fissures, sinus tracts, enterocutaneous fistulae, and perforation can occur,
although less commonly. A cobblestone appearance of the mucosa is a
feature of Crohns disease rather than Tuberculosis. Ulceration may be
demonstrated on double-contrast examinations, typically perpendicular
to the long axis of the bowel; these heal with the formation of short
annular strictures. The ileocecal angle is obliterated with a widely patent
ileocecal valve. Colonic involvement is characterized by a combination
of narrowings, deep ulcerations, and mucosal granulation producing
nodularity and inflammatory polyps. Less common findings are aphthous
ulcers and a diffuse colitis. Changes are usually noted in the cecum,
ascending and transverse colon. Bowel contour may be lost with
asymmetry simulating Crohns disease. When a short segment is
involved, the strictures are hour-glass shaped rather than the applecore deformity associated with carcinoma. In some cases, they may be
indistinguishable.
BIBLIOGRAPHY
1. Gupta SK, Jain AK, Gupta JP, et al. Duodenal tuberculosis. Clin Radiol 1988; 39(2):
159-61.
2. Marshall JB. Tuberculosis of the gastrointestinal tract and peritoneum. Am J
Gastroenterol 1993; 88(7): 989-99.
3. Segal I, Tim LO, Mirwis J. Pitfalls in the diagnosis of gastrointestinal tuberculosis.
Am J Gastroenterol 1981; 75(1): 30-5.

MALABSORPTION
Barium studies of the small intestine can reveal the typical abnormalities
forming the malabsorption pattern and include bowel dilatation, mucosal
thickening, flocculations, segmentation and bowel dilution of barium in
advance cases. These patterns are mostly seen in small intestinal mucosal
disorders, but otherwise barium studies can absolutely be normal in
conditions like pancreatic insufficiency, post-gastrectomy stae, etc.
BIBLIOGRAPHY
1. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science.
1998;173-74.
COELIAC DISEASE
Coeliac disease reflects hypersensitivity to the gliadin fractions of the
gluten (found in wheat, barley and rye).
The classical radiological feature is jejunization. Jejunal folds are
either widely separated or absent altogether and this feature is
accompanied by a paradoxical increase in ileal folds.
Unfortunately these classical features are often absent, and probably
the commonest feature is luminal dilatation.
Transient painless intussusception is common and may be seen during
follow-through.
BIBLIOGRAPHY
1. La Seta F, Buccellato A, Albanese M, Barbiera F, Cottone M, Oliva L, et al. Radiology
and adult celiac disease. Current indications of small bowel barium examinations.
Radiol Med (Torino). 2004;108(5-6):515-21.
2. La Seta F, Salerno G, Buccellato A, Tine F, Furnari G. Radiographic indicants of
adult celiac disease assessed by double-contrast small bowel enteroclysis. Eur J
Radiol 1992;15(2):157-62.
3. Burrows FG, Toye DK. Coeliac disease. Barium studies. Clin Gastroenterol
1974;3(1):91-107.
WORM INFESTATION
Ascaris lumbricoides appearance on contrast studies is characteristic once
the worms have swallowed barium it is seen within their intestinal tract
and worms appear as long narrow tubular defects.
161
162

Hookworm, Tapeworm, Strongyloides and Anisakis all parasite the
small bowel, eliciting non-specific findings of fold thickening, nodularity,
mild dilatation and flocculation on contrast studies.
BIBLIOGRAPHY
1. Reeder MM, Palmer PES. Radiology of Tropical Diseases. Baltimore, Williams and
Wilkins Company. 1981;411-38.
2. Reeder MM. The radiological evaluation of Ascariasis of gastrointestinal, biliary
and respiratory tracts. Semin Roentgenol 1998;33(1):57-78.
ULCERATIVE COLITIS
Double contrast barium enema is more accurate than the single contrast
study in revealing early disease and also to show the disease extent and
severity, but it cannot visualize alterations in mucosal vascular pattern.
There is inflammation and ulceration of the colon, the later being the
cardinal radiological sign. The ulcers are usually widespread and shallow.
There is loss of normal colonic haustra Bamboo Colon in the affected
portions. Pseudopolyps can be seen in advance cases as projections into
the lumen of the bowel between the ulcers.
Strictures are rare and usually indicate malignant transformation.
Involvement of the whole colon results in dilatation of the terminal ileum
and incompetence of the ileo-caecal valve. Any barium examination is
absolutely contraindicated if there is evidence of toxic dilatation or when
there is risk of perforation.
BIBLIOGRAPHY
1. Carucci LR, Levine MS. Radiographic imaging of inflammatory bowel disease.
Gastroenterol Clin North Am 2002; 31(1): 93-117.
2. Eisenberg RL. Gastrointestinal Radiology: A Pattern Approach. Philadelphia:
Lippincott-Raven; 1998;602-8.
3. Peter Armstrong. Diagnostic Imaging. Fourth Edition. London: Blackwell Science;
1998;180.
CROHNS DISEASE
Contrast studies remain the mainstay for the diagnosis and assessment
of both distribution and severity, predominantly because they are best
able to demonstrate mucosal pathology.
The radiological changes of Crohns disease can be generally grouped
into three categories; early, advanced and complicated.

Although the earliest endoscopic manifestation is hyperemia
combined with an altered vascular pattern, this cannot be demonstrated
on contrast studies. Villous edema and blunting follow and are the earliest
detectable radiological change, manifested as a granular pattern on high
quality contrast studies. Early ulceration is typically apthous, which
describes small, shallow, circular, discrete ulcers surrounded by an
edematous halo. Again these are well demonstrated on high quality
contrast studies. Granularity and apthous ulceration represent the earliest
detectable radiological changes and are the most challenging because
they are subtle. As the features progress, ulceration becomes linear and
deeper, with typical transmural penetration accompanied by mural
thickening. Mucosal edema and inflammation intervenes between these
ulcers to cause characteristic cobblestone appearance. Ulceration is
frequently patchy and also asymmetrical along the bowel circumference;
indrawing at the site of ulceration may be accompanied by ballooning
of the contralateral wall creating a characteristic pseudodiverticular
appearance.
Advanced disease may also be complicated by strictures, fistulation,
and abscess formation and, rarely by tumor.
Strictures are generally easy to demonstrate using contrast studies.
Massive small-bowel dilatation secondary to stricture can occur and may
be complicated by bacterial overgrowth.
BIBLIOGRAPHY
1. Carucci LR, Levine MS. Radiographic imaging of inflammatory bowel disease.
Gastroenterol Clin North Am 2002; 31(1): 93-117.
2. Diagnostic approach to IBD. Hepatogastroenterology. 2000;47(31):44-8.
3. Eisenberg RL. Gastrointestinal Radiology: A Pattern Approach. Philadelphia:
Lippincott-Raven 1998;602-8.
4. Marshall RC. Radiologic evaluation of Crohns disease. J Fam Pract 1997;45(6):4656.
DIVERTICULAR DISEASE
The distribution and severity of diverticular disease remains best
demonstrated by barium enema. The diverticula themselves appear as
flask-like or rounded outpouchings. When seen en face they produce
ring shadows. Differentiation form a polyp is a common problem but
the definitive signs are projection beyond the bowel wall and the
presence of a fluid level within it.
163
164

Muscular changes results in a serrated appearance, frequently
accentuated by pronounced and persistent spasm.
BIBLIOGRAPHY
1. Balthazar EJ. Diverticular disease. In: Textbook of Gastrointestinal Radiology. WB
Saunders Co; 1994;1072-97.
2. Hulnick DH, Megibow AJ, Balthazar EJ. Diverticulitis: Evaluation by contrast enema.
AJR Am J Roentgenol 1987; 149:644-6.
3. Marshall RC. Radiologic evaluation of Crohns disease. J Fam Pract 1997;45(6):4656.
CARCINOMA COLON
Radiological diagnosis of the primary tumor occurs usually on barium
enema examination.
Any intraluminal shadow or line that cannot be confidently attributed
to a normal feature must be viewed with suspicion. Frank carcinoma
typically manifests as an annular, irregular, ulcerating lesion-giving rise
to the classical Apple-Core appearance.
Carcinoma has abrupt, shouldered margins and as oppose to spasm
normal mucosal fold cannot be traced through the stricture lumen,
indicating both a mucosal origin and destruction.
Many cancers present as an eccentric tumor mass and some spread
locally in a plaque-like infiltrative fashion. Overall, barium enema detects
approximately 85% of colorectal cancers.
Primary radiological diagnosis may also be achieved using other
modalities, notably CT.
BIBLIOGRAPHY
1. Gazelle GS, McMahon P, Scholz FJ. Screening for colorectal cancer. Radiology
2000; 215:327-35.
2. MacCarty RL. Colorectal cancer: The case for barium enema. Mayo Clin Proc 1992;
67:253-57.
3. Ott DJ, Gelfand DW, Wu WC, Ablin DS. Colon polyp morphology on doublecontrast barium enema: Its pathologic predictive value. AJR Am J Roentgenol
1983; 141:965-70.
FIGURE 3.1: Achalasia of Cardia. Mega-esophagus

with abrupt termination is seen.
FIGURE 3.2: Achalasia of Cardia. Dilated and tortous

esophagus with narrowing at lower end, no mucosal
irregularity or shouldering is visible.
165
166
FIGURE 3.3: Achalasia of Cardia. There is a

grossly dilated esophagus with narrowed distal
end. No contrast seen in the stomach.
FIGURE 3.4: Aortic Aneurysm. A large aneurysm of descending aorta and aortic
knuckle causing displacement of esophagus to the right side. Diverticulum is also
present in the upper esophagus on the left side (Zenkers diverticulum). Hiatus hernia
is also seen.
FIGURE 3.5: Peptic Esophageal Stricture. There is smooth,

long stricture in the mid and distal esophagus with proximal
hold up of barium and gross dilatation, no ulceration, no
shouldering, and no mucosal irregularity.
FIGURE 3.6: Peptic esophagitis showing, smooth short

stricture in distal esophagus. Granular mucosa is also seen
above the stricture (arrow).
167
168
FIGURE 3.7: Cork Screw Esophagus. There is narrowing of

distal end of esophagus with proximal dilatation in lateral
view. Tertiary contractions in AP view (Cork screw esophagus).
FIGURE 3.8: Esophagitis and paraesophageal hiatus

hernia. Mucosal irregularity at the distal end.
FIGURE 3.9: Hiatus hernia (paraesophageal) and a large

duodenal diverticulum is visible in the first part (arrows).
FIGURE 3.10: Carcinoma Esophagus. Narrow distal end,

long irregular stricture and shouldering with dilated mid
thoracic and upper thoracic segments of esophagus.
169
170
FIGURE 3.11: Carcinoma Esophagus. Dilated

esophagus with irregular mucosa and filling
defects seen in the lower half.
FIGURE 3.12: Carcinoma Esophagus. There is

markedly dilated esophagus and incomplete
diverticulum seen in the upper part. Shouldering
and irregular short stricture distally.
FIGURE 3.13: Carcinoma Esophagus. Mucosal destruction

and irregular narrowing seen in the middle part of esophagus.
FIGURE 3.14: Carcinoma esophagus involving the upper part.

There is narrowing and irregular margins in the upper part of the
esophagus with filling defects. Shouldering is positive.
171
172
FIGURE 3.15: Carcinoma Esophagus. A growth is seen in

the upper thoracic segment of esophagus, as narrowing of
mucosal irregularity and barium hold up in proximal part.
FIGURE 3.16: Carcinoma Esophagus. Rat tail appearance

of distal esophagus with proximal dilatation and air fluid level.
FIGURE 3.17: Carcinoma Esophagus. A growth in the

esophagus involving middle and distal parts with rat-tail
appearance is visible.
FIGURE 3.18: Carcinoma Esophagus. There is a short

irregular stricture and dilated upper esophagus.
173
174
FIGURE 3.19: Carcinoma Esophagus, showing an irregular

filling defect in the middle 2/3rd of the esophagus.
FIGURE 3.20: A case of carcinoma esophagus, postoperatively. Gastric pull through with gastroesophageal
anastomosis.
FIGURE 3.21: Carcinoma Esophagus. Long irregular

stricture mid and lower esophagus with shouldering is visible.
FIGURE 3.22: Carcinoma Esophagus. Narrowing and rat

tail appearance of distal esophagus with dilatation in the
middle and upper parts, air fluid level is visible. Spill over of
barium into air passages on right side (arrow).
175
176
FIGURE 3.23: Esophagogastrostomy in a patient with

carcinoma-esophagus. Stomach has been pulled into the
thoracic cavity after resection of esophagus (Anastomosis).
Causes of esophageal strictures

Inflammatory:
- Reflux and hiatus hernia
- Scleroderma
- Corrosives
- Iatrogenic (prolonged use of nasogastric tube)
Neoplastic:
- Carcinoma (squamous)
- Mediastinal tumors (Ca bronchus)
- Leiomyoma
Others:
- Achlasia
- Skin disorders (pemphigus, epidermolysis bullosa)
FIGURE 3.24: Nonspecific duodenitis and proximal jejunitis.

Gastric ulcer filled with barium at fundal region (arrow).
FIGURE 3.25: Chronic duodenitis and chronic duodenal ulcer.

Scarredclover leaf shaped deformed duodenal cap with
irregular and ill-defined duodenal mucosa (arrow).
177
178
FIGURE 3.26: Chronic Duodenal Ulcer and Duodenitis.

Typical clover leaf /trifoliate shaped duodenal cap and illdefined mucosal folds of duodenal loops (arrow).
FIGURE 3.27: Gastric ulcer. A gastric ulcer is visible in the

upper part on the lesser curvature as an ulcer niche (arrow).
FIGURE 3.28: Gastric Outlet Obstruction. Dilated stomach

with food particles interspersed with barium.
FIGURE 3.29: Gastric outlet obstruction, markedly distended

stomach is seen. There is no contrast beyond the antrum.
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FIGURE 3.30: Calcified Hydatid Cyst. Normal barium meal

with multiple radiopaque gallstones, and a large calcified
hydatid cyst is seen in the left lobe of liver (arrow).
FIGURE 3.31: Trichobezoars in a Psychiatric Patient. Welldefined rounded filling defects at the fundus, antrum and
body of the stomach (arrows).
181
FIGURE 3.32: Carcinoma Stomach. Narrow distal

esophageal end with, non-distendibility of stomach with
irregularity and destruction of gastric mucosa at greater
curvature and body of stomach.
C
FIGURES 3.33A TO C: Hernia of Morgagni. Herniation of stomach and part of intestine
into the thorax through a congenital defect in the left dome of diaphragm.
182
FIGURE 3.34: Pseudopancreatic cyst, showing, J-shaped

stomach, stretched and displaced to the left and inferiorly
due to smooth round to oval shaped mass in the lesser sac.
FIGURE 3.35: Carcinoma. Stomach extending up to the distal

esophageal end. Irregular filling defect in the fundus with
distorted mucosal folds can be seen. A well-defined mass at
lesser curvature due to enlarged left lobe of the liver.
FIGURE 3.36: Antral-carcinoma with gastro-colic fistula. Distended

stomach with irregularities and soft tissue mass at lesser curvature.
FIGURE 3.37: Trichobezoar. Hold up of contrast in the distal 1/3rd of

dilated esophagus and in the stomach due to gastric outlet obstruction
and irregularity at greater curvature with rounded filling defect.
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184
FIGURE 3.38: Adenocarcinoma of the fundus of

stomach involving the distal esophagus. There is
narrowing of distal esophagus with shouldering and
proximal dilatation of esophagus. Irregularity and
mucosal destruction at fundus and at adjoining part of
the body of stomach with nondistensibility.
FIGURE 3.39: Antral carcinoma with gastro-colic fistula

and dilated stomach. A filling defect in the lower part of
stomach prior to antrum with gastro-colic fistula.
FIGURE 3.40: Adenocarcinoma of stomach with Linitisplasticus. A large filling defect in the fundus of stomach with
narrowing of stomach lumen.
FIGURE 3.41: Leiomyoma of Stomach. A well demarcated

filling defect in the region of stomach fundus.
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186
B
FIGURES 3.42A AND B: Carcinoma Stomach (Linitis
Plastica) with Liver Metastasis. Grossly narrowed stomach
lumen due to infiltrating carcinoma-Linitus Plasticus, and soft
tissue shadow due to enlarged liver also seen filling the
concavity of stomach at lesser curvature.
FIGURE 3.43: Carcinoma stomach (Linitus Plasticus) with

metastases in liver. Left lobe is enlarged and occupying the
concavity of the medial border of the stomach.
FIGURE 3.44: Carcinoma Stomach. A growth in the stomach

with distortion of mucosa involving greater curvature and
body of stomach.
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FIGURE 3.45: Fistulus connection with biliary tree (postendoscopic barium study, showing barium enetring in
the biliary tree)
FIGURE 3.46: Carcinoma Stomach Antral Region.

Growth in the distal stomach with shouldering.
FIGURE 3.47: Carcinoma Stomach. A growth in the stomach

involving the body, antrum and greater curvature.
FIGURE 3.48: Pyloric stenosis (adult variety) due to

carcinoma. The growth is in the distal stomach and
pylorus (arrow).
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190
FIGURES 3.49A TO D: Duodenal Giardiasis. Multiple round nodules of uniform

size and shape distributed through out the duodenum.
FIGURE 3.50: Liver abscess in the left lobe

exerting pressure over the lesser curvature and
compressing body and antrum of stomach.
FIGURE 3.51: Pneumoperitoneum. Free air

under left hemi-diaphragm (arrow). Barium spill
in the peritoneum is also seen.
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192
FIGURE 3.52: Duodenal diverticulum in

post-bulbar region.
FIGURE 3.53: A large duodenal diverticulum.
FIGURE 3.54: A diverticulum from 2nd part of duodenum can

be seen (arrow). Thickening of rugal folds of stomach.
FIGURE 3.55: Two Duodenal Diverticuli. One big another

small arising from 1st and 2nd part of duodenal loop
respectively (arrows).
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FIGURE 3.56: Carcinoma Duodenum. There is a spastic

duodenal loop. Ill-defined irregular mucosa of duodenal loop
can be seen along with distended stomach.
FIGURE 3.57: Carcinoma Duodenum. A long filling defect

with irregular mucosa is seen in the 1st part of the duodenum
(black arrow) with a pseudo-diverticulum in the 2nd part
(white arrow).
FIGURE 3.58: Ascariasis. Long vermiform filling defects seen

in small intestine on barium follow through (arrows).
FIGURE 3.59: Ascariasis. Long segmented tube like filling

defect because of round worms seen in the small intestine
(arrow).
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196
FIGURE 3.60: Ileocecal Tuberculosis. Deformed

cecum with terminal ileal loops showing narrowing and
mucosal irregularity.
FIGURE 3.61: Intestinal Tuberculosis. Terminal ileum

is showing multiple narrowings. Appendix is clearly
outlined (incidental finding).
FIGURE 3.62: Ileocaecal Tuberculosis. There is deformity

of cecum and irregularity of mucosa in the terminal ileum.
FIGURE 3.63: Crohns Disease. Multiple jejunal strictures

alternating with dilatations is seen (arrows).
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FIGURE 3.64: Crohns Disease. Adherent small bowel loops

displaced in the pelvis with multiple strictures noted.
FIGURE 3.65: Crohns disease showing, multiple

strictures in jejunum with rose thorn ulcers
(arrows) consistent with jejunitis.
FIGURE 3.66: Intestinal Tuberculosis. Deformed cecum, mucosal irregularity and

narrowing of terminal ileum and jejunum seen. Dilatation of ileal and jejunal loops,
lobulated external compression on terminal ileum also seen (due to
lymphadenopathy).
FIGURE 3.67: Intestinal tuberculosis, there is jejunal mucosal fold thickening and
rose thorn appearance of proximal jejunal loops and multiple narrow segments.
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FIGURE 3.68: Intestinal Tuberculosis. Multiple strictures

with dilatations of small intestine.
FIGURE 3.69: Malabsorption Syndrome. Multiple

segmented dilatations of small intestine with loss of villous
pattern, clumping of barium (flocculations) and increased
distance b/w loops of small bowel is seen.
FIGURE 3.70: Malabsorption syndrome due to coeliac

disease. Dilated edematous loops of small intestine,
Thickened and blunt mucosal folds can be seen.
FIGURE 3.71: Intestinal Tuberculosis. Multiple

intestinal strictures are seen.
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202
B
FIGURES 3.72A AND B: Duodenal Lymphoma Barium Meal
and Axial CT. Barium meal image showing luminal narrowing
of the duodenum. Axial CT abdomen with oral contrast of the
same patient showing marked thickening of the duodenal
wall with oral contrast passing through it. This was confirmed
histologically as a lymphoma in this AIDS patient.
FIGURES 3.73A TO C: Diverticulosis Coli. Multiple outpouchings of different sizes

(filled with barium) in recto-sigmoid, descending and transverse colon are seen.
FIGURE 3.74: Diverticular disease of colon.
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FIGURE 3.75: Ileocecal Tuberculosis. Distortion of terminal

ileum and cecum is visible on barium enema.
FIGURE 3.76: Chronic Ulcerative Colitis. Narrowing and

loss of haustrations seen in the descending and sigmoid
colon with granular appearance of the mucosa.
B
FIGURES 3.77A AND B: Ulcerative Colitis. Hose pipe
appearance, due to loss of haustrations and granular
appearance of mucosa. Widened pre-sacral space.
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206
FIGURE 3.78: Chronic Ulcerative Colitis. Ahaustral pattern

of transverse and descending colon with mucosal granularity
and narrowing at hepatic flexure with irregularity indicating
malignant change is visible.
FIGURE 3.79: Ulcerative Colitis. There is ahaustral, narrowed

descending colon with serrated margins due to active ulcers.
FIGURE 3.80: Ulcerative Colitis. Loss of haustrations in

transverse colon with granularity and pseudopolyps formation.
FIGURE 3.81: Ulcerative Colitis. Descending and sigmoid

colon show multiple ulcers and tube like appearance.
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FIGURE 3.82: Imperforated anus seen on cologram.
FIGURE 3.83: Chronic Ulcerative Colitis. Narrow segment

descending colon with proximal dilatation of transverse and
ascending colon can be seen.
FIGURE 3.84: Multiple Polyps. There are multiple filling defects

in the rectum and at recto-sigmoid junction due to polyps.
FIGURE 3.85: Diverticular disease with malignant transformation.

Narrowing; filling defects and diverticulae in recto-sigmoid colon,
with proximal dilatation of splenic flexure and part of transverse
colon is seen. Narrowing and ulcerations of transverse colon and
hepatic flexure also present.
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210
FIGURE 3.86: Non-rotation of the Gut. A large bowel-rectosigmoid,

descending colon, splenic flexure and transverse colon on the left side of
the abdomen and small bowel in the lower abdomen and pelvis is seen.
Hepatic flexure of colon lies in the right iliac fossa.
FIGURE 3.87: Carcinoma Cecum and Ascending Colon. Narrowed

lumen; mucosal destruction (arrow), shouldering and soft tissue mass
involving cecum and proximal ascending colon and dilation of remaining
ascending and transverse colon up to splenic flexure.
FIGURE 3.88: Carcinoma Colon. Barium enema demonstrating, irregular and deformed cecum with annular narrowing
and filling defects in ascending colon (arrow).
FIGURE 3.89: Carcinoma. Rectum showing narrow irregular

distorted lumen of rectum due to the growth.
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212
FIGURE 3.90: Barium enema demonstrating, a growth that is

causing intussusceptions at recto-sigmoid junction. Meniscus
sign in the sigmoid colon.
FIGURE 3.91: Carcinoma Ascending Colon. A filling defect

seen in proximal ascending colon with shouldering and
mucosal distortion is seen.

Differential diagnosis of colonic strictures
Neoplastic
- Carcinoma
- Lymphoma
- Peritoneal metastases
Inflammatory
- Ulcerative colitis
- Crohns disease
- Pericolic abscess
- Radiotherapy
Infectious
- Tuberculosis
- Ameboma
- Schistosomiasis
- Lymphogranuloma venereum
Ischemia/Infarction
Postsurgical
Extrinsic masses
FIGURE 3.92: Sclerosing Cholangitis. The gallbladder is

opacified, intra-hepatic biliary duct dilatation and narrowing
of pancreatic duct and proximal CBD (distal not visualized)
also seen. A calcified hydatid cysts seen in the liver. Oral
cholecystography (OCG) post-fatty meal.
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214
FIGURE 3.93: Oral cholecystography in a patient with

cholelithiasis. A filling defect at the fundus can be seen.
There is air in the wall of the gallbladder (emphysematous cholecystitis) (arrow).
FIGURE 3.94: Oral cholecystography showing

cholelithiasis. The gallbladder can be seen with
multiple filling defects.
FIGURE 3.95: Oral Cholecystography Gallstones. Few large

nucleated filling defects in the region of fundus of gallbladder
indicating multiple gallstones.
215
Skeletal System
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RHEUMATOID ARTHRITS
Bilateral, symmetric involvement of metacarpophalangeal, proximal
interphalangeal and carpal joints with similar involvement of the joints
of feet is the hallmark of rheumatoid arthritis, but any or every joint of
the body can be involved. Atlantoaxial subluxation may develop due to
weakening of the transverse ligaments from synovial inflammation.
Radiographic changes may be summarized as follows:
1. Soft-tissue changes:
Soft-tissue swelling is due to edema of periarticular tissues and due
to synovial inflammation in bursae, joint spaces and along tendon
sheaths. Joint distension also follows an increase in synovial fluid.
2. Osteopenia:
Interpretation is subjective and changes are seen only after loss of
25-50% of the bone mineral has occurred.
Osteoporosis in rheumatoid arthritis may be generalized due to
steroids or prolonged recumbency, or localized due to synovial
inflammation (juxta-articular osteopenia).
3. Joint space changes and alignment deformities:
In the early stage a joint space may be widened by synovial
hypertrophy, inflammation and an effusion.
In the later stage joint spaces narrow due to cartilage destruction
by pannus. Alignment abnormalities at joints may result from local
synovitis weakening the capsule and tendonitis.
Deformities of the joints can be seen radiologically. Atlanto-axial
subluxation occur with loss of odontoid peg and narrowing of disc
spaces, potentiated by laxity of ligaments around the peg.
4. Periostitis:
Local periosteal reactions occur either along the midshaft of a phalanx
or metacarpal as a reaction to local tendonitis, or at the metaphysis
near a joint affected by synovitis.
5. Erosions:
These are the most important diagnostic lesions but are not always
present. Classic periarticular erosions occur at the so-called bare areas
of bone between the edge of the articular cartilage and the attachment
of the joint capsule. Erosions appear earlier and are more often seen
in the feet bones, involving typically the lateral side of the fifth
metatarsal.
Skeletal System
BIBLIOGRAPHY
2003;2:1201- 6.
2. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science;
1998;335-7.
3. Ronald L Eisenberg. Clinical Imaging: An atlas differential diagnosis (4th edn).
2003;812.
OSTEOPOROSIS
Osteoporosis is appreciated radiographically as loss of bone density,
best described as osteopenia.
The radiographic appearance of generalized osteopenia however is
not specific to osteoporosis and can be seen in a variety of conditions.
In osteoporosis trabecular loss is most evident radiographically in the
spine, where there is loss of density, which may be appreciated as
penciling in of the vertebra by the more radiographically dense endplates. Biconcave vertebral bodies (cod-fish vertebrae) may occur.
Endosteal and intracortical resorption of bone is prominent, producing
cortical thinning most evident in the appendicular skeleton. The loss of
bone mass gives rise to increased incidence of fractures, particularly in
the femoral neck, spine (compression fractures), distal radius and pubic
symphysis.
BIBLIOGRAPHY
2003;2:1356-7.
2. Iqbal MM. Osteoporosis: Epidemiology, diagnosis, and treatment. South Med J
2000; 93(1): 2-18.
3. Jergas MD, Genant HK. Radiology of osteoporosis. In: Favus MJ, Goldring SR,
Christakos S (Eds). Primer on the Metabolic Bone Diseases and Disorders of Mineral
Metabolism. Fourth Edition. Hagerstown, MD: Lippincott Williams and Wilkins;
1999;160-5.
OSTEOARTHRITIS
Classic features include non-uniform joint space loss, subchondral
sclerosis, osteophytes formation, subchondral cysts, and absence of
erosions. Herberden nodes (osteophytes at distal interphalangeal joints)
and Bouchard nodes (osteophytes at proximal interphalangeal joints)
are commonly seen.
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Superior or superolateral migration of femur within hip joint with
buttressing of medial femoral cortex can occur. Medial femoro-tibial
compartment is most commonly involved in knee. Sclerosis and
narrowing of intervertebral apophyseal joints is also common. Commonly
involved joints are distal interphalangeal joints of the fingers; first
carpometacarpal joint; hips; knees; first metatarsophalangeal joints; and
spine.There may be differences in the radiological appearances of
osteoarthritis at different joints, degenerative disease has a number of
specific features whenever it occurs i.e. joint space narrowing due to
cartilage destruction and then joint remodeling with loss of underlying
bone in stressed areas, and formation of new bone and cartilage in nonstressed areas and at joint margins, so that joint alignment alters. Loose
bodies are formed by detachment of osteophytes, crumbling of articular
surfaces or ossification of cartilage debris. When osteoarthritis results
in pain and immobility, osteoporosis and soft tissue wasting may result
secondarily.
BIBLIOGRAPHY
2003;2:1222-3.
2. Lane NE, Kremer LB. Radiographic indices for osteoarthritis. Rheum Dis Clin
North Am 1995;21:379-394.
3. Ronald L Eisenberg. Clinical Imaging, an atlas of differential diagnosis (4th edn).
2003;812.
RICKETS
Ricketic changes are most obvious at regions of active growth; in order
of decreasing frequency, middle rib costochondral junctions, distal femur,
proximal humerus, both ends of tibia, and distal ulna and radius.
Widened growth plates (earliest change), poorly mineralized
epiphyseal centers with delayed appearance, increased distance between
end of a shaft and epiphyseal center, cupping and fraying of metaphysis
are commonly seen.
Rachitic rosary at costochondral junctions of middle ribs; thoracic
kyphosis with a pigeon chest and bossing of the skull may occur.
In late stages a generalized reduction in bone density is seen, and in
long-standing cases fractures may occur.
Skull may be affected if process begins early. Usual supine position
of infant causes posterior flattening; this produces craniotabes, or
squarrying of calvarium.
Skeletal System
Deformity is most marked at long bones, where bowing is evident
secondary to asymmetric musculotendinous pulls on weakened growth
plate. Scoliosis and pelvic changes occur later in process.
BIBLIOGRAPHY
2003;2:1353-4.
2. Do TT. Clinical and radiographic evaluation of bowlegs. Curr Opin Pediatr 2001;
13(1): 42-6.
3. Renton P. Radiology of rickets, osteomalacia and hyperparathyroidism. Hosp
Med 1998; 59(5): 399-403.
4. Silverman FN, Kuhn JP. Metabolic abnormalities of the skeleton. In: Caffeys
Pediatric X-ray Diagnosis: An Integrated Imaging Approach. Ninth Edition. MosbyYear Book 1993;666-74.
OSTEOMALACIA
The hallmark of osteomalacia are pseudo-fractures or Loosers zones
which are narrow zones of lucency, usually running perpendicular or
nearly perpendicular to the bone cortex. Initially Loosers zones are
poorly defined, these zones become progressively more prominent, with
sclerotic margins. These zones are frequently bilateral and symmetrical,
and occur at regular sites such as the pubic rami, proximal femur, scapula,
lower ribs and ulna. Osteopenia develops with penciling-in of the
vertebral bodies, and loss of vertebral height in a characteristic codfish
vertebra pattern. Bowing of long bones may also occur. Compression
wedge fractures of the vertebra are less common than in osteoporosis.
BIBLIOGRAPHY
1. David Sutton. Text book of radiology and imaging (7th edn). Churchill Livingstone
2003;2:1354.
2. Renton P. Radiology of rickets, osteomalacia and hyperparathyroidism. Hosp
Med 1998; 59(5): 399-403.
3. Steinbach HL, Noetzli M. Roentgen appearance of the skeleton in osteomalacia
and rickets. AJR Am J Roentgenol 1964; 91: 955.
GOUT
Classic features include tophi, normal mineralization, preserved joint
spaces, marginal punched-out erosions with overhanging borders and
sclerotic edges, and asymmetrical polyarticular distribution.
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Classic location is 1st metatarso-phalangeal joint, but any metatarsophalangeal joint may be involved. Gout tends to attack the distal and
proximal interphalangeal joints, whereas rheumatoid arthritis affects the
metacarpophalangeal and proximal interphalangeal joints.
Other locations include any joint of fingers, carpo-metacarpal, wrist,
elbow, knee, and shoulder.
Tophi are radiolucent, become radiopaque when calcium precipitates
in juxta-articular soft tissue mass, usually along extensor surface of
joint.
Bilateral olecranon bursa effusion is characteristic. Erosions tend to
appear near joint margins. As they enlarge, they tend to involve more
of the cortex of the shaft rather than the articular surface. Cartilage
destruction is relatively late manifestation.
BIBLIOGRAPHY
1. Bloch C, Hermann G, Yu TF. A radiologic reevaluation of gout: A study of 2000
patients. AJR Am J Roentgenol 1980; 134(4):781-7.
2. David Sutton. Text book of radiology and imaging (7th edn). Churchill Livingstone
2003;2:1229-30.
3. Ray MJ, Bassett RL. The radiologic manifestations of gout. Orthopedics 1985; 8(1):92,
95-8.
HYPERPARATHYROIDISM
Subperiosteal erosion of bone, particularly along the radial aspect of the
middle phalanx of the middle and index finger, is virtually pathognomonic. Intracortical bone resorption is another feature of hyperparathyroidism which gives rise to small oval or cigar-shaped lucencies within
the cortex. In the skull, a characteristic granular or mottled appearance
may occur, giving rise to the so-called pepper-pot or salt-and-pepper
skull.
Subperiosteal resorption is also seen at medial aspect of femoral neck
and proximal tibia, humerus and the ribs.
Subchondral bone resorption is another common feature, being found
at the distal and sometimes proximal end of the clavicles, symphysis
pubis and sacroiliac joints. This may occur at he vertebral end-plates,
which may permit disc herniation (Schmorls nodes).
Subligamentous resorption at ischial/humeral tuberosity, greater/
lesser trochanter of femur also occur.
Skeletal System
Brown tumor (osteoclastoma) is lytic, expansile lesion usually in the
pelvis, jaw, rib, facial bones. It is more common in primary hyperparathyroidism, but because secondary hyperparathyroidism is more
prevalent, it is usually seen in secondary hyperparathyroidism.
Rugger jersey spine; due to osteosclerosis of vertebral endplates is
usually seen in secondary hyperparathyroidism.
Chondrocalcinosis is more common in primary HPT. Periostitis and
soft tissue calcification usually seen in secondary hyperparathyroidism.
Causes of hyperparathyroidism
Primary:
- Parathyroid adenoma
- Hyperplasia of gland
- Carcinoma
Secondary:
- Chronic renal failure
- Malabsorption
- Rickets and osteomalacia
BIBLIOGRAPHY
2003;2:1362-4.
2. Gleason DC, Potchen EJ. The diagnosis of hyperparathyroidism. Radiol Clin North
Am 1967; 5(2): 277-87.
3. Mayo-Smith W, Rosenthal DI. Radiographic appearance of osteopenia. Radiol Clin
North Am 1991; 29(1): 37-47.
4. Pugh DG. Subperiosteal resorption of bone, a roentgenologic manifestation of
primary hyperparathyroidism and renal osteodystrophy. AJR Am J Roentgenol
1951; 66: 577-86.
ANKYLOSING SPONDYLITIS
Changes are most prominent in the axial skeleton with bilateral symmetric
distribution. Initially small erosions and sclerosis of Sacroiliac joint
predominantly on iliac side occur with progression to sacral side and
ultimately ankylosis. Similar changes in pubic symphysis are seen. Spinal
changes without sacroiliac changes are very rare in this disease. Erosion
of vertebral margins heal by proliferation of sclerotic bone, which stands
out in marked contrast to the rest of the vertebral body (Romanus lesion).
Bamboo spine with undulation of ligamentous calcification/ossification,
which are prone to fracture and pseudoarthrosis are late features.
Squaring and straightening of anterior vertebral bodies occurs even
before.
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Marginal syndesmophytes formation are common. Atlantoaxial
subluxation is seen. Osteoporosis, erosions and joint space narrowing
are less prominent in peripheral joints, but shaggy periostitis and
ankylosis are more common.
BIBLIOGRAPHY
1. Braun J, Sieper J, Bollow M. Imaging of sacroiliitis. Clin Rheumatol 2000; 19(1): 51-7.
2. Braunstein EM, Martel W, Moidel R. Ankylosing spondylitis in men and women:
A clinical and radiographic comparison. Radiology 1982;144(1): 91-4.
3. Cardenosa, Gilda. Ankylosing Spondylitis. Radiographic Highlights 1990; 42(1):
147-50.
2003;2:1218-20.
ACROMEGALY
The radiographic features of acromegaly include enlarged mastoid air
cells and sinuses, frontal bossing and prognathism.
Pituitary fossa enlargement may be seen on the plain film, although
CT or MRI is more helpful in evaluating a pituitary adenoma.
In the spine, enlargement of the vertebral bodies with posterior
scalloping is seen.
The hands show characteristic enlargement of the bones and soft
tissues with spade-like terminal tufts, or arrowhead distal phalanges.
Widening of joint spaces due to overgrowth of articular cartilage
may be seen.
The feet show evidence of increased thickness of heel pads.
The long bones of the feet are elongated, although the feet usually
remain slender.
Prominence of muscle attachments, and premature or exaggerated
degenerative changes may be seen.
Calcification of the pinna of the ear occurs.
Chondrocalcinosis has been reported as a rare variation.
BIBLIOGRAPHY
2003;2:1360-1.
2. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science 1998;
332.
Skeletal System
MULTIPLE MYELOMA
Radiology plays an important part in the initial diagnosis of the disease.
The two cardinal features are generalized reduction in bone density
and localized areas of translucency in red marrow areas. The axial
skeleton, therefore, is affected predominantly. Lesions may also be
observed in the shafts of long bones and in the skull. Within spine,
vertebral body is usually affected, while pedicle is usually spared. This
differentiates myeloma from metastatic disease which affects pedicle
more frequently.
Mandibular involvement is more common than in metastases. Focal
punched out lytic lesions of relatively uniform size with endosteal
scalloping are very suggestive of multiple myeloma. Larger coalescent
lesions are more characteristic of metastases. Isotope bone scans are
generally negative with no appreciable uptake. Periosteal reaction is
rare. Soft tissue mass may accompany lesion in vertebral body and ribs,
resulting in paraspinal/extrapleural mass. Osteosclerosis is uncommon
manifestation; usually seen after chemotherapy or radiotherapy or after
pathologic fracture. Pathological fractures are very often the initiating
factor in the diagnosis of the disease.
BIBLIOGRAPHY
1. Greenspan A. Malignant bone tumors II. In: Greenspan A (Eds): Orthopedic
radiology: A practical approach (3rd edn). Philadelphia; Pa: Lippincott Williams
and Wilkins, 2000; 697-700.
2. Ludwig H, Kumpan W, Sinzinger H. Radiography and bone scintigraphy in
multiple myeloma: A comparative analysis. Br J Radiol 1982; 55(651): 173-81.
3. ME Mulligan EJC, Angtuaco ABT, Fassas R, Walker R, Sethi, B Barlogie. Skeletal
Abnormalities in Multiple Myeloma. Radiology, January 1, 2005; 234(1): 313-314.
OSTEOSARCOMA
Osteosarcoma is the commonest primary malignant bone tumor,
accounting for 25% of all primary bone tumors.
Most common site of involvement is appendicular skeleton, especially
femur, tibia, and humerus in decreasing order; 50-75% of cases occur
around the knee.
Metaphyseal location is characteristic; however, infrequently diaphysis
may be primary site of involvement.
Mixed lytic and sclerotic pattern is most typical, a florid spiculated
periosteal reaction is present, the so called sunray appearance; purely
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lytic pattern is encountered in telangiectatic variety which is extremely
vascular, usually poorly defined with soft tissue component.
Elevation of the periosteum is associated with new bone formation,
the so called Codmans triangle. Transphyseal spread is common even
before closure.
BIBLIOGRAPHY
1. David Sutton. Textbook of radiology and imaging (7th edn). Churchill Livingstone;
2003;2:1261-8.
1998;310.
METASTATIC DISEASE
The later stages of many malignant neoplasms are associated with
metastasis, and the skeleton is very commonly affected. Bony metastasis
is present in approximately 25% of all deaths from malignant disease.
CT or MRI can detect bone metastasis at an early stage as compared
to plain radiograph. Multiple lesions are more likely than solitary lesion.
Solitary focus may simply mean that another lesion has not been imaged
or is currently undetectable on plain radiograph.
The spine, pelvis and ribs are the most common sites involved, then
are proximal ends of humeri and femora and, less often, the skull. These
areas correspond to sites of persistent hematopoiesis in the adult.
Lesions may appear purely osteolytic, osteosclerotic, or mixed.
Osteolytic lesions typically arise in the medulla and progressively extend
in all directions, destroying the cortex, usually without the development
of much periosteal reaction. Osteoblastic lesions produce dense and often
well-circumscribed areas of increased radiopacity. Purely osteolytic
lesions are from neuroblastoma, lung, breast, thyroid, kidney, and colon.
Purely osteosclerotic lesions include those from medulloblastoma,
bladder, carcinoid (of bowel), lymphoma (Hodgkin), and prostate.
Mixed lesions include breast, prostate and lymphoma. Expansile
bubbly lesions are seen from kidney and thyroid tumors. Spine is the
most frequently involved site, especially vertebral bodies and pedicles
of thoracolumbar spine. When long, tubular bones are involved, it is
usually the proximal metaphyseal region of femur and humerus which
are involved.
Skeletal System
BIBLIOGRAPHY
1. Bellamy EA, Nicholas D, Ward M, Coombes RC, Powles TJ, Husband JE.
Comparison of computed tomography and conventional radiology in the
assessment of treatment response of lytic bony metastases in patients with
carcinoma of the breast. Clin Radiol 1987; 38(4): 351-5.
2. Ell PJ. Skeletal imaging in metastatic disease. Curr Opin Radiol 1991; 3(6): 791-6.
3. Kagan AR, Bassett LW, Steckel RJ, Gold RH. Radiologic contributions to cancer
management. Bone metastases. Am J Roentgenol 1986; 147(2): 305-12.
4. Thrall JH, Ellis BI. Skeletal metastases. Radiol Clin North Am 1987; 25(6): 1155-70.
SPINAL TUBERCULOSIS POTTS DISEASE

Most of the lesions occur in or below the midthoracic spine and
involvement of the cervical and upper thoracic spine is uncommon.
Vertebral bodies may be first affected at three places, i.e. the upper
or lower disc margin, in the center, and anteriorly under the periosteum.
The disc substance is often eroded.
Adjacent vertebral bodies are commonly involved. The anterior parts
of the vertebrae are most affected, causing anterior collapse or wedging
and posterior gibbus formation.
Abscesses form early and are easily seen in the thoracic region in
contrast to the radiolucent lungs. In the lumbar region, lateral bulging
of the psoas outlines may be demonstrable radiologically.
Calcifications, when present, favor diagnosis of tuberculosis.
Affected vertebral bodies frequently become fused. The subperiosteal
type of infection begins anteriorly under the periosteum and spreads
under the anterior common ligament. Disc destruction may be late and
the anterior erosions difficult to detect.
MRI is the most useful form of imaging for the diagnosis of Potts
disease, from early lesions to extensive form of the disease.
BIBLIOGRAPHY
1. Boxer DI, Pratt C, Hine AL, M McNicol. Radiological features during and following
treatment of spinal tuberculosis. Br J Radiol 1992; 65:476-9.
2. Lindahl S, Nyman RS, Brismar J, et al. Imaging of tuberculosis. IV. Spinal
manifestations in 63 patients. Acta Radiol 1996; 37:506-11.
3. Shanley DJ. Tuberculosis of the spine: Imaging features. Am J Res 1995;164:659-64.
4. Weaver P, Lifeso R. The radiological diagnosis of tuberculosis of the adult spine.
Skeletal Radiol 1984; 12:178-86.
227
228

SINUSITIS
Acute sinusitis is often due to secondary bacterial infection following a
viral infection of respiratory tract.
The infection causes swelling of the mucosa, which appears as an
opaque rim around the periphery of the sinus. An opaque sinus on plain
X-ray may indicate fluid level in the sinus for which a tilted view should
be obtained.
Rarely there is involvement of bone which results in loss of outline
of the sinus wall followed by frank osteolysis and bone destruction.
In chronic sinusitis, CT is the investigation of choice as this defines
the degree and extent of involvement of the paranasal sinuses and also
provides the surgeon anatomical information before surgery.
BIBLIOGRAPHY
2003;2: 1519-20.
2. Smam PM, Brandwein M. Sinonasal Cavities. Inflammatory diseases, Tumours,
Fractures, and postoperative Findings in Head and Neck imaging. Eds Peter M
Sam, Hugh D Curtis (3rd edn), Mosby. 1996.
OSTEOPETROSIS (MARBLE BONE DISEASE)

Increased density and thickening of long bones, especially metaphyses,
can be seen in utero. The presence of a bone within a bone differentiates
osteopetrosis from the other sclerosing dysplasias.
The bone within a bone may be vertical in the long bone shafts and
digits, transverse at the metaphyses or beneath the iliac crests.
In long bones the Erlenmeyer flask deformity due to failure of
metaphyseal remodeling, giving gross distal undertubulation, and the
presence of dense bone, vertical fine lucencies extending to metaphyses
are also present.
The bones of the skull base are initially affected with sclerosis and
thickening, prominent in the floor of the anterior cranial fossa.
The medulla in the proximal skeleton is primarily involved and the
periphery spared. Mild, uniform increase in density may be seen.
BIBLIOGRAPHY
2003;2: 1128-9.
2. El-Tawil T, Stoker DJ. Benign Osteopetrosis: A review of 42 cases showing two
different patterns. Skeletal Radiology 1993;22:587-93.
Skeletal System
MYCETOMA (MADURA FOOT)
Mycetoma implantation occurs mainly in the (bare) feet in semi-desert
regions throughout the tropics. The skull and knees may also be
implanted, usually by thorns.
Lesions are usually localized as large, well defined black fungus balls,
which can be seen on soft-tissue radiographs. These erode the cortices
and cause cystic defects in the medulla. With superadded infection via
the implantation track, gross bone destruction results.
Reactive sclerosis and a shaggy periostitis with bone resorption give
an appearance of melting snow.
BIBLIOGRAPHY
2003;2: 1176-7.
2. Renton P. Radiology of the foot. In Klenerman L (Eds). The foot and its disorders,
Third Edition. Oxford: Blackwell Scientific; 1993.
229
230
FIGURE 4.1: Spina Bifida S1. Sacralization

of L5 with pseudoarthrosis.
FIGURE 4.2: Hydrocephalus. X-ray skull AP view

(Child). The skull is large, with widened sutures
(Sagittal, coronal, lambdoid) due to increased
intracranial pressure.
Skeletal System
FIGURE 4.3: Osteopetrosis (Marble Bone Disease). X-ray

dorso-lumbar spine. There is generalized increased bone
density, Bone within a bone appearance. Erlen-Mayer Flask
shaped deformity of proximal femur.
FIGURE 4.4: Osteopetrosis. There is

generalized increased bone density.
231
232
FIGURE 4.5: Osteopetrosis. X-ray dorso-lumbar spine showing

generalized increased bone density seen in vertebral bodies and
ribs. Central horizontal band of translucency noted giving
appearance of a sandwich.
FIGURE 4.6: Osteopetrosis (Marble Bone Disease). Diffuse

increase in bone density spine ribs. Pelvic bones show bone within
bone appearance.
233
Skeletal System
FIGURES 4.7A AND B: Mucopolysaccharidosis Type 4

(Morquios Disease). Kyphosis seen in dorso-lumbar spine, every
distal vertebra is shifted posteriorly in relation to upper ones. Central
beaking of vertebra (spine) seen.
FIGURES 4.7C TO E: Stubby Long Bones. Secondary deformity in the elbow.

Shortening of long bones seen. The skull is large. Ape like pelvis, shallow acetabulum,
and Coxa Vera deformity is seen. Epiphysis of femur are not well developed.
234
FIGURE 4.8: Mucopolysaccharidosis. Biconvex lumbar vertebra,

D-12 is slightly shifted forward in relation to L1 can be seen. Tongue
like protrusions in L1 and L2 inferiorly.
FIGURE 4.9: Hyperparathyroidism. Pathological fracture of tibia

(Lt) and fibula-proximal shaft in a case of hyperparathyroidism.
Generalized osteopenia is also noted.
235
Skeletal System
FIGURES 4.10A AND B: Osteomalacia showing, deformity of

pelvis, rugger jersy spine, diasthesis of right sacroiliac joint and
protrusio acetabuli.
FIGURE 4.11: Osteomalacia, showing Loosers zone in superior

and inferior pubic rami (arrows) and deformed pelvis.
236
B
FIGURES 4.12A AND B: Osteomalacia with secondary
hyperparathyroidism in a patient with malabsorption. Incomplete
fracture of fibula with pseudofracture (Loosers zone) both fibular
proximal shafts and osteopenia (arrows).
Skeletal System
FIGURE 4.13: Osteomalacia. X-ray pelvis including hip showing,

patchy increased density of bone and generalized osteopenia.
Loosers zones in both femoral necks (arrows).
FIGURE 4.14: Hyperparathyroidism. Pepper pot skull

with thin calvarium.
237
238
FIGURE 4.15: Idiopathic Sub-cutaneous Calcification. X-ray

hands and wrist, showing popcorn type subcutaneous calcification
around terminal phalanges in multiple fingers. Serum calcium,
phosphate, alkaline phosphatase, serum PTH, uric acid levels were
normal. Fingertips were swollen, tender and gritty on feeling.
FIGURE 4.16: Hyperparathyroidism. Grossly deformed pelvis with

fracture of superior and inferior pubic rami and thinning of cortex of
femur.
Skeletal System
FIGURE 4.17: Pseudohypoparathyroidism showing

short 4th metacarpal of either ring fingers.
FIGURE 4.18: Renal osteodystrophy with secondary hyperparathyroidism. X-ray lumbosacral spine (Lateral view) showing,
increased bone density especially in vertebral end plates with
central lucent bands Rugger-jersy spine.
239
240
FIGURE 4.19: Acromegaly. Large frontal, ethmoid, maxillary

sinuses. Enlarged mandible (Prognathism).
FIGURE 4.20: Acromegaly. Enlarged frontal and maxillary sinuses.

Enlarged skull (Macrocephaly). Ballooning of pituitary fossa with
thinning of dorsum sella.
Skeletal System
FIGURES 4.21A AND B: Acromegaly. There is marked expansion of the frontal

sinuses. The pituitary fossa appears to be larger than normal. Erosion of posterior
clinoid process also noted.
FIGURE 4.22: Rickets. Metaphyseal cupping, splaying and wide zone of provisional
calcification at upper end of humerus and distal end of radius and ulna, proximal end
of tibia and fibula with bowing and soft tissue swelling at wrist and knee joints and
ricketic rosary wide anterior rib ends and generalized osteopenia.
241
242
FIGURE 4.23: Rickets. Lower end of radius and ulna

showing splaying, fraying and cupping at the
metaphyseal end along with soft tissue swelling.
FIGURE 4.24: Rickets. Osteopenia in the metaphyses

of both forearms, hands and wrists and soft tissue
swelling of wrist. There are also metaphyseal
transverse lucent bands of distal ends of both the radius
and ulna.
Skeletal System
FIGURE 4.25: Rickets. Cupping, splaying, and fraying

seen at the metaphyseal ends of femur, tibia and fibula
with soft tissue swelling seen.
FIGURE 4.26: Rachitic Rosary. Broadening of the anterior

ribs seen (overgrowth of cartilage at the costochondral
junction) (arrows).
243
244
FIGURE 4.27: Scurvy. X-ray lower extremities with knee joint AP.
Generalized osteopenia is seen. Pencil sharp outline of epiphyseal
cortex (Wimberger sign??). Metaphyseal sclerotic band dense
zone of periosteal calcification, also liner soft tissue calcification
seen near the above end of the fibula.
FIGURES 4.28A AND B: Pagets Disease of Bone. (A) Osteolytic and

osteoblastic activity noted in the vault of skull. (B) X-ray hip AP showing
osteoporotic changes in proximal shaft of femur with thinning of cortex. Sclerotic
and lytic changes seen in upper end of femur (neck and trochanteric regions).
Skeletal System
FIGURE 4.29: Juvenile Pagets

Disease. Osteolytic and osteoblastic
activity noted. Well circumscribed
rounded sclerotic areas with central
osteolysis seen. The intervening
bone is showing osteoporosis.
FIGURE 4.30: Chronic Rheumatoid

Arthritis. Reduced/absent intercarpal, carpometacarpal, metacarpophalangeal and interphalangeal
joint spaces and radio-carpal joints
spaces. Juxta-articular osteopenia,
erosions and secondary osteoarthritic changes also seen in some
of the joints.
FIGURE 4.31: Rheumatoid Arthritis

(Erosive Arthropathy). X-ray both
hands (PA view), showing destructive, erosive polyarthropathy affecting the radiocarpal, midcarpal and
the small joints of both hands.
Marked osteoporosis with multiple
joint subluxation.
245
246
FIGURE 4.32: Rheumatoid arthritis both hip joints, bilateral

avascular necrosis of femoral heads Drug induced (steroids).
There is osteopenia, sclerosis, and fragmentation of femoral heads
bilaterally. Fracture of right femoral neck is noted.
FIGURE 4.33: Rheumatoid Arthritis. Proximal interphalangeal

joints showing arthritic change, reduced joint space and
osteoporotic changes in the bones around the joints.
Skeletal System
FIGURE 4.34: Rheumatoid Arthritis. X-ray hand (AP and lateral

view) showing, narrowing of the joint spaces and osteopenia around
the metacarpophalangeal and interphalangeal joints. Inflammatory
changes also seen in the wrist joint.
FIGURE 4.35: Rheumatoid Arthritis. Reduced bone density, fusion

of carpal bones with significant reduction of joint spaces in between.
Reduced Interphalangeal joint spaces also present.
247
248
FIGURE 4.36: Rheumatoid Arthritis. Almost complete fusion of

carpal bones with loss of carpal, carpo-metacarpal, and radiocarpal joints. There is significantly decreased metacarpophalangeal and interphalangeal joint spaces. There is subcortical
erosions seen in the metacarpal and interphalangeal joints. Juxtaarticular osteoporosis noted at wrist and interphalangeal joints.
FIGURE 4.37: Rheumatoid Arthritis (Advanced). Loss of joint

spaces, subluxation, erosion and decreased bone density seen
in the joint.
249
Skeletal System
FIGURES 4.38A TO D: Rheumatoid Arthritis. Narrowed joint spaces at elbow joint

with erosive changes seen at articular surfaces of humerous and ulna. Bone density
is reduced. Soft tissue swelling is also seen. Joints of the hands and wrists are also
involved.
250
C
FIGURES 4.39A TO C: Rheumatoid Arthritis. An advance case of
rheumatoid arthritis with erosions and deformation of joints.
Extensive destruction of the articular cortex of the metacarpophalangeal joints seen.
251
Skeletal System
C
FIGURES 4.40A TO C: Rheumatoid Arthritis. Narrowed joint spaces
with erosions seen at metacarpo-phalangeal joints. Almost
compelete loss of inter-carpal joints i.e. matting. Overall reduced
bone density noted. Reduced bone density. Arthritic changes seen
in Talo-tibial and talo-calcaneal joints with reduced joint space.
Arthritic changes alongwith reduced joint spaces also noted in
tarsal joints.Reduced bone density, diminished joint spaces.
Subarticular sclerosis noted at both knees.
252
FIGURE 4.41: Erosive Arthropathy in Psoriasis. X-ray of hand. There is acroosteolysis of distal phalanges, sclerosis at middle phalanges, new bone
formation, and loss of joint space between proximal and distal interphalangeal
joints with expansion at the bases of proximal phalanges with subchondral
sclerosis and loss of joint spaces at carpo-metacarpal joints.
FIGURE 4.42: Advanced secondary osteoarthritis in a patient with rheumatoid

arthritis of both hip joints (Female pelvis). Excessive sclerosis seen in both hip
joints with loss of joint space in both hips. Bilateral protusio-acetabuli also
noted.
FIGURE 4.43: Gout. X-ray right foot (AP view). There is sclerosis at
metatarsophalangeal joint of big toe with loss of joint space. Soft tissue swelling
and juxta-articular erosions also seen. Bone density is preserved.
Skeletal System
FIGURE 4.44: Ankylosing Spondylitis. X-ray dorso-lumbar spine

(Lateral view).Calcification of anterior spinal ligaments and posterior
longitudinal ligaments. Calcification and annular fibrosis (Bamboo
spine).
FIGURE 4.45: Ankylosing Spondylitis. X-ray dorso-lumbar spine

showing sclerosis of sacroiliac joints, tramline appearance of spine
and bamboo spine.
253
254
FIGURES 4.46A AND B: Ankylosing spondylitis involving dorso-lumbar

spine and sacro-iliac joint. Ossification of lateral, anterior and posterior spinal
ligaments seen (Bamboo shaped spine). Loss of joint spaces in both sacroiliac joints.
FIGURE 4.47: Bilateral Sacroiliitis. Bilateral obliteration of sacroiliac joint alongwith arthritic changes in
a patient with Inflammatory bowel disease.
Skeletal System
Causes of sacroiliitis
Unilateral:
Most commonly infection but can be
caused by most of the bilateral causes.
Bilateral:
Ankylosing spondylitis
Inflammatory bowel disease
Reiters disease
Psoriatic
Rheumatoid arthritis (rare)
FIGURE 4.48: Ankylosing Spondylitis. X-ray lumbo-sacral spine,

showing syndesmophytes at lumbar
spine, bilateral sacroiliitis, irregular,
fragmented and sclerosed both
femoral heads-bilateral avascular
necrosis, obliteration of joint spaces
in both hip joint are also noted.
FIGURE 4.49: Reiters Disease.

Arthritic changes seen in metacarpophalangeal and inter-phalangeal
joints. Marked scoliosis noted at these
joints especially in index finger and
thumb. Overall bone density is reduced
and expansion of the bases of
phalanges is noted. Some erosions
also noted in subchondral regions of
metacarpophalangeal and interphalangeal joints.
255
256
B
FIGURES 4.50A AND B: Cervical Myelogram (A/P
and Lateral View). Cervical spondylitis. Obstruction
at the level of C-7 can be seen (Patient had presented
with quadriparesis more marked in the lower limbs).
Skeletal System
FIGURE 4.51: Myositis ossificans progressiva in case of

mixed connective tissue disease. Calcification in muscular
sheaths pelvis, buttocks and ischial tuberosity also.
FIGURE 4.52: Myositis ossificans in a case of mixed

connective tissue sisease. Sub-cutaneous calcification with
calcification in muscles of the thigh.
257
258
FIGURES 4.53A AND B: Osteoarthrosis of Knee Joint. There is

reduced joint space of medial tibiofemoral compartment with
osteophytes on femur and tibial articular surfaces. Osteophytes
on patella also seen.
B
FIGURES 4.54A AND B: Mixed Connective Tissue Disease.
Sub-cutaneous and intramuscular calcification around the knee
joint and thigh, with contracture of knee joint and secondary
osteoporosis of bones.
259
Skeletal System
B
FIGURES 4.55A AND B: Advanced Osteoarthrosis with
Osteoporosis. Marginal osteophytes (non-bridging) seen
anterolaterally in lumbar vertebrae with reduced disc spaces at all
lumbar vertebral levels and lower dorsal vertebral levels.
FIGURE 4.56: Osteoarthrosis of Spine. Degenerative changes

and decrease disc space at L5-S1posteriorly. Tubular calcification
is also seen in abdominal aorta.
260

Casuse of monoarthritis
- Infection:
Tuberculosis
Staphylococcus aureus
- Trauma
- Osteoarthritis
- Neuropathic (including diabetes)
- Gout and calcium pyrophosphate dihydrate
crystal deposition disease (CPPD)
Casuse of polyarthritis
- Degenerative
Osteoarthritis.
- Neuropathic
Diabetes melitus.
- Inflammatory
CTD
Rheumatoid (including SLE, scleroderma)
Seronegative arthritis
Ankylosisng spondylitis, Rieters, psoriatic.
- Crystal arthritis
Gout, CPPD
FIGURES 4.57A AND B: Cervical Spondylosis. Osteophytes at disc vertebral

level of C2-C6 with reduced disc spaces b/w C5-6 and C6-7.
261
Skeletal System
FIGURES 4.58A TO C: Progeria. (A, B) X-ray skull showing osteoporosis, thin cranial
vault, wormian bones, and hypoplastic maxillae and mandible. (C) X-ray pelvis
showing osteoporosis, short slender femora, and Coxa valga.
FIGURE 4.59: Tuberculous Osteomyelitis. X-ray foot (AP and Lat

view), showing calcification below 5th metatarsal base, and soft
tissue swelling with erosion of tarso-metatarsal joints (arrow).
262
FIGURES 4.60A AND B: Bone Tuberculosis. Circumscribed osteolytic lesion with

sclerotic margins seen in the upper end of left femur (arrow) with erosions of the
cortex especially in the lateral view and speckled calcifications centrally.
FIGURE 4.61: Pyogenic arthritis. X-ray forearm and elbows

(AP view). There is erosion of olecranon process of ulna,
trochlear of humerus, periosteal reaction, and increased bone
density. Absent left radius is also noted.
Skeletal System
FIGURES 4.62A AND B: Treated case of Potts disease. Partial

collapse and wedging of D4D5 with sclerosis of the adjacent
vertebral end plates and early spondylolytic changes.
B
FIGURES 4.63A AND B: Tuberculosis upper end of left femur.
Lytic and sclerotic lesion seen in the upper end of left femur.
263
264
FIGURE 4.64: Tuberculosis of the spine with paraspinal abscess.

Narrowing of the intervertebral space between L2-L3 vertebral
bodies with erosion of the adjoining edges anteriorly with some
sclerosis is seen. There is minimal anterior wedging of L1, L2 and
L3 vertebral bodies. Associated paravertebral soft tissue shadowing
is also seen. AP view is also showing similar changes.
Differential diagnosis of
paravertebral mass
Trauma/hematoma
Abscess
- Staphylococcus aureus
- Tuberculosis
Neoplasms
- Lymphoma
- Metastases
FIGURE 4.65: Tuberculous spine D8-9 with paraspinal abscess. X-ray dorsal spine showing,
bilateral para-spinal soft tissue mass D4-D9.
There is loss of disc space b/w D8 and D9, and
also reduced disc space b/w D6-D7 and D7-D8.
Skeletal System
FIGURES 4.66A AND B: Potts Disease. (A) X-ray LS spine lateral

view showing involvement of the bodies of L1-L2 alongwith
intervertebral disc and wedging of the bodies anteriorly. (B) Potts
disease dorsal spine with paraspinal abscess.
FIGURES 4.66C AND D: MRI clearly demonstrating destruction of

bodies of L1-L2 with some paraspinal collection. Marked indentation
of thecal sac is apparent.
265
266
FIGURES 4.67A TO D: Potts Disease. MRI of same patient

showing involvement of D6-D10 vertebral bodies, intervertebral
discs alongwith paraspinal abscess formation.
Skeletal System
FIGURE 4.68: Paranasal Sinusitis. Soft tissue opacities in both

maxillary sinuses can be seen. Nasal mucosal thickening is also
present. Frontal sinuses are enlarged with mucosal thickening.
FIGURE 4.69: Acute sinusitis with nasal mucosal thickening and

frontal sinusitis. Thickening of maxillary sinuses and haziness of
both frontal sinuses more on right side can be seen. Soft tissue
opacity in left maxillary sinus with air fluid level is also noted.
267
268
FIGURE 4.70: Leprosy. Erosion of terminal

phalanges (fall off) is seen.
FIGURE 4.71: Diabetic Foot. Destruction of metatarsophalangeal joints and IP joints and loss of 3rd phalanx
with acro-osteolysis 4th and 5th distal phalanges.
Skeletal System
FIGURE 4.72: Madura Foot (Biopsy Proved). Multiple osteoporotic

and sclerotic areas seen in the tarsal and metatarsal bones.
Erosions of some metatarsal shaft giving the soap bubble
appearance.
FIGURE 4.73: Madura Foot. Soft tissue swelling with diffuse

osteolytic lesions in meta-tarsals and phalanges. Shaggy periostitis
with reactive sclerosis. Bone resorption also noted. Appearances
mimic Melting Snow.
269
270
FIGURE 4.74: Acute Osteomyelitis. Bony destruction seen in

forearm. Periosteal reaction noted. Destructive process has
reached up to the epiphysis with soft tissue swelling.
FIGURE 4.75: Chronic Osteomyelitis. Lytic and sclerotic changes

noted in distal shaft of tibia and fibula with evidence of periosteal
reaction.
Skeletal System
FIGURE 4.76: Chronic osteomyelitis of calcanium showing

destructive and sclerotic changes with soft tissue swelling.
FIGURE 4.77: Chronic Osteomyelitis. Lytic lesions,

involucrum, sequestrum with sclerotic changes.
271
272
FIGURE 4.78: Chronic osteomyelitis, showing all

cardinal features, i.e. destructive changes, periosteal
reaction, involucrum, cloacae and new bone formation.
FIGURE 4.79: Chronic osteomyelitis, showing cardinal

features, i.e. destructive changes, periosteal reaction,
cloacae and sequestrum.
Skeletal System
FIGURE 4.80: Osteomyelitis. Destructive and sclerotic lesions are

seen. Sparing of epiphysis of the head of humerous, there is soft
tissue swelling with gap between gleno-humeral joint (effusion).
FIGURE 4.81: Diabetic Foot with Charcot Joint. There is soft tissue
swelling, erosion of metatarsal and phalangeal bones. Note
amputation of big toe (arrow).
273
274
B
FIGURES 4.82A AND B: Septic Arthritis. Plain film and
radioisotope bone scan of the wrist demonstrating ill-defined,
osteopenic, mid carpal and radio-carpal joints with overlying soft
tissue swelling with a corresponding area of increased isotope
uptake on the delayed bone scan. This patient had a pathological
diagnosis of Staphylococcal arthritis.
Skeletal System
FIGURE 4.83: Myelofibrosis/ Myelosclerosis. X-ray pelvis (AP

view) showing, patchy increased bone density and increased
trabeculations.
FIGURE 4.84: X-ray legs acute leukemia showing generalized

osteopenia, and thinned cortex. Transverse lucent metaphyseal
band at distal ends tibia and fibula.
275
276
FIGURE 4.85: Multiple Myeloma. X-ray skull (Lateral view). Multiple

punched out lytic lesion in skull and mandible with endosteal
scalloping of inner table.
FIGURE 4.86: Advanced Case of Multiple Myeloma. X-ray pelvis

including hips and proximal femur (Adult male). There is
generalized reduction in bone density, with lytic lesions all over the
visualized skeleton and endosteal scalloping. Bilateral protrusioacetabuli with deformed pelvis.
Skeletal System
C
FIGURES 4.87 A TO C: Multiple Myeloma. (A) X-ray skull showing
multiple punched out lytic lesions. (B) X-ray pelvis showing multiple
lytic lesions in pelvic bone. (C) X-ray dorsal spine showing lytic
lesions in the ribs, dorsal spine, and collapse of D10, there is also
multiple rib fractures (pathological) in left 7th and right 11th ribs.
277
278
FIGURE 4.88: Multiple Myeloma. X-ray skull AP view. There is

decreased bone density, extensive lytic lesions in skull, mandible,
orbits and maxilla are present.
FIGURES 4.89A TO C: Multiple Myeloma. Punched out lytic lesions

and increased trabecular pattern with meshed osteoprosis.
Skeletal System
FIGURE 4.90A: Thalassemia. X-ray both hands and forearms of a

child. Showing widened, stubby metacarpal and phalanges and
thinned cortex, also there is increased trabeculations,
intramedullary permeation and lucencies. Same changes are
present in radius and ulna and carpal bones.
FIGURE 4.90B: Thalassemia. X-ray skull (Lateral view). There is

thickening of skull vault, osteopenia, and hair end on appearance.
279
280
FIGURE 4.91: Enlarged pituitary fossa due to pituitary tumor. Erosion

of posterior clinoid process. Depression of floor of hypophyseal
fossa. Thinning of the posterior wall is also noted.
FIGURE 4.92: Pituitary Tumor. Dorsum sella is completely

eroded with thinning of the posterior wall.
Skeletal System
FIGURES 4.93A TO D: Metastasis Lumbar Spine. X-ray shows reduced intervertebral

space in L1-L2 along with erosion and collapse of vertebral body of L2. MRI showing
metastatic deposits in L2 and L3 vertebrae with partial collapse of L2 indenting the
thecal sac.
281
282
FIGURE 4.94: Osteosarcoma/Fibrosarcoma. Permeative lesions

at proximal femoral shaft meta-diaphyseal region with soft tissue
mass, wide zone of transition with smooth displacement of fat
planes.
FIGURE 4.95: Metastases from Carcinoma Thyroid. Generalized

osteoporosis with multiple lucencies of varying sizes.
Skeletal System
FIGURE 4.96: Metastases from Carcinoma of Prostate. X-ray

pelvis including hip joints (Male), showing lucencies and sclerotic
patchy increased densities. Pathological fracture of intertrochanteric region of left femoral neck also noted.
FIGURE 4.97: Carcinoma Bronchus with Metastasis. Lytic

changes seen in left 6th rib posteriorly. Left hila is enlarged.
Inhomogeneous shadowing seen in right apex. Small pleural
effusion at left costo-pherenic angle.
283
284
FIGURE 4.98: Osteoblastic lesions due to metastasis from carcinoma of prostate showing, multiple osteoblastic/osteosclerotic
areas with osteoporotic zones in the pelvic bones.
Bone metastases (radiological appearances)

Lung
- Carcinomas
- Carcinoid
Breast
Genitourinary tract
- Renal cell carcinoma
- Wilms tumour
- Bladder
- Prostate
Thyroid
Gastrointestinal tract
- Stomach
- Colon
Adrenal
Skin
- Squamous cell Ca
- Melanoma
Reproductive organs
- Cervix
- Uterus
- Ovary
- Testis
lytic
lytic or mixed
lytic, expansile
lytic
lytic, occasionally sclerotic
sclerotic
lytic, expansile
sclerotic or mixed
lytic
lytic
lytic
lytic, expansile
lytic or mixed
lytic
lytic
lytic
Skeletal System
FIGURES 4.99A TO D: Ewings Sarcoma. (A) X-ray chest is showing large amount of
pleural effusion on right side. (B to D) CT chest reveals a large mass adherent to the
right chest wall, protruding outside as well as extending into the thoracic cavity with
moderate amount of pleural effusion, the mass is showing central areas of necrosis.
Biopsy proved it to be Ewings sarcoma.
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286
FIGURE 4.100: Calcaneal spur in a patient

with painful heel.
FIGURE 4.101: Youngs Perthes disease. Sclerosis of femoral

head with fragmentation and widened metaphysis.
Skeletal System
FIGURE 4.102: Exostosismid shaft of

humerus with pathological fracture.
FIGURE 4.103: Charcots joint secondary to repeated intra-articular

steroid injections. Deformed knee joint with osteoporosis of bones
is noted. Calcification seen in the supra-patellar bursa and inside
joint cavity
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288
FIGURE 4.104: Adolescent Kyphosis with Ostochondritis. X-ray

dorso-lumbar vertebrae (Lateral view). Khyphosis seen at dorsolumbar region, Partial collapse of upper lumbar vertebrae also
noted. Lower dorsal vertebrae are biconcave. Herniation of nucleus
pulposus seen in the lower dorsal spine.
FIGURE 4.105: X-ray Pelvis. Bilateral osteitis condensa (normal

variant). The sacroiliac joint space is preserved.
Skeletal System
FIGURE 4.106: Scleroderma. There is minimal arthritic changes at

wrist joint, metacarpophalangeal joints, proximal and distal
interphalangeal joints and terminal bone resorption (Acroosteolysis) (arrows).
FIGURE 4.107: Calcaneal spurring with calcification of the

tendo-Achillese.
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290
FIGURES 4.108A TO D: Hyperparathyroidism. (A) Nephrocalcinosis due to hyperparathyroidism. (B) Multiple calcified densities seen in cortex and medulla. Sclerosis
seen at the metacarpophalangeal joints. (C) Overall bone density is reduced in the
wrist and hand. (D) Hyperostosis seen in the vault of skull, marked in the frontal
region.
Skeletal System
C
FIGURES 4.109A TO C: (A,B) Pseudohypoparathyroidism showing
intracerebral calcification on X-ray skull. (C) CT scan brain plain
showing extensive intracerebral calcification. Heavy calcification
seen within the basal ganglion and dentate nuclei. Parenchymal
calcification also seen bilaterally. No midline displacement.
291
292
FIGURE 4.110: Non-ossified Fibroma/Fibrous Dysplasia. Lucent

oval shaped, lobulated lesion with sclerotic margins in distal tibia
(arrow).
B
FIGURES 4.111A AND B: Fluorosis. Ribs and other bones appear
marble white, bone contour is wooly and blurred especially in ribs
due to bone expansion and merging of trabeculae.
Skeletal System
FIGURE 4.112: Post-traumatic collapse and wedging

of L-2 vertebral body with osteoporosis (arrow). Disc
spaces are preserved. (Patient a truck driver had h/o
jumping from the roof of his vehicle)
293
Plain Abdomen and Intravenous Pyelograms
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296

NEPHROCALCINOSIS
Morphologically, three types of calcifications have been described. The
most prevalent is a single cortical and thin peripheral band, often with
calcified extensions into the necrotic septa of Bertin (placed perpendicular
to the cortical calcification). The medullary pyramids are usually spared,
retaining the attenuation of the soft tissue. Initially, this pattern of
nephrocalcinosis may be difficult to recognize because calcification is
faint.
However, the kidney margins appear well-defined and appear
penciled in.
The second pattern seen with cortical nephrocalcinosis is the
appearance of hyperattenuating tram lines. These lines may be continuous.
More often, they are interrupted, reflecting more patchy distribution of
cortical necrosis.
The third pattern is a more diffuse distribution of punctate
calcification. This punctate pattern of calcification is thought to represent
necrotic calcified glomeruli and tubules.
Medullary nephrocalcinosis typically produces clusters of stippled
calcifications, mainly within the regions of the renal pyramids.
BIBLIOGRAPHY
1. Akhan O, Ozmen MN, Coskun M. Systemic oxalosis: Pathognomonic renal and
specific extrarenal findings on US and CT. Pediatr Radiol 1995; 25(1): 15-6.
2003;1: 977.
1998;232-3.
RENAL CALCULI
Radiodense stones suggest either calcium or struvite composition, but
struvite stones are usually large and fill the calyceal system. Cystine
stones appear to be radiodense, but less dense than calcium-containing
stones. Small, radiolucent stones suggest uric acid composition. Uric
acid stones appear as filling defects on intravenous pyelography. Filling
defects that occupy the renal pelvis are staghorn stones and may be of
struvite, uric acid, or cystine composition. Sludge may be of either uric
acid or cystine, can fill the renal pelvis, and cause obstruction. Plain
radiographs of the abdomen can identify stones of greater than 3 mm
size. 80% of ureteric calculi are radiopaque, seen at the anatomic

narrowing (ureto-pelvic, ureto-vesicle junctions and the site where the
ureter crosses the sacrum and iliac vessel).
Mostly are calcium oxalate and phosphate stones. Up to 10% of the
stones are composed of struvite (magnesium, ammonium phosphate)
which are usually poorly radiopaque.
BIBLIOGRAPHY
2003;1: 965-9.
2. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science; 1998:
231-2.
3. Smith SL, Somers JM, Broderick N, Halliday K. The role of the plain radiograph
and renal tract ultrasound in the management of children with renal tract calculi.
Clinical Radiology 2000; 55: 708-10.
ADULT POLYCYSTIC KIDNEY DISEASE

CT scan is the imaging of choice for the diagnosis of adult polycystic
kidney disease (APKD). Hyperdense cysts on CT in ADPKD are seen in
68% of cases. On unenhanced CT, they are seen as multiple, sharply
circumscribed cysts, generally subcapsular in location with attenuation
values ranging from 40 to 90 HU. They appear significantly denser than
uncomplicated cysts and the remaining renal parenchyma. The
hyperdense appearance is believed to result from cyst hemorrhage. They
do not enhance and are usually isodense/hypodense on enhanced scans.
BIBLIOGRAPHY
2003;1: 936.
2. High-density renal cysts in Autosomal Dominant Polycystic Kidney disease
demonstrated by CT. Levine Errol, Jared Grantham. Radiology 1985;154: 477-82.
3. Peter L Choyke. Inherited cystic diseases of kidney. Radiologic Clinics of North
America 1996;34(5):925-43.
EMPHYSEMATOUS PYELONEPHRITIS
Emphysematous pyelonephritis (EPN) is a severe necrotizing infection
of the renal parenchyma, with formation of gas within the collecting
system, renal parenchyma, or perirenal tissues.
CT scan is the definitive test. Several patterns have been described,
including streaky, streaky plus mottled, and streaky plus bubbly. Gas
can be rim like or crescent-shaped in the perinephric area. Gas can also
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298

be seen in the renal vein, inferior vena cava, and along with the psoas
muscle. Perinephric abscess may also lead to significant gas in the
perinephric space. A stone may be seen in the collecting system.
BIBLIOGRAPHY
1. Ahlering TE, Boyd SD, Hamilton CL, et al. Emphysematous pyelonephritis:
A 5-year experience with 13 patients. J Urol 1985; 134(6):1086-8.
2. Michaeli J, Mogle P, Perlberg S, et al. Emphysematous pyelonephritis. J Urol 1984;
131(2): 203-8.
3. Shokeir AA, El-Azab M, Mohsen T, El-Diasty T. Emphysematous pyelonephritis:
A 15-year experience with 20 cases. Urology 1997; 49(3): 343-6.
HORSESHOE KIDNEY
IVU usually reveals the classical findings associated with horseshoe
kidney. Findings on the initial tomogram may be deceptive because of
the exclusion of the anteriorly lying isthmus. Renal axis abnormalities
are confirmed, as seen on the plain radiographs. In midline fusion, the
kidneys are symmetric, with the lower pole calyces lying closer to or
actually overlying the spine. The lower calyces are usually medially
rotated, and they may actually lie medial to the ureters. Some degree of
malrotation of the kidneys is usually present. A renal pelvis is often
extrarenal and large.
The degree of malrotation has been associated with the degree of
fusion. If the isthmus is narrow, the kidneys are usually less malrotated,
with pelvis lying anteromedially in its near normal position. In cases of
a wide isthmus, the renal pelves lie anteriorly or laterally. Associated
UPJ obstruction may be present because of the higher ureteric insertion
point that leads to delayed pelvic emptying. Ureters may have the socalled flower- vase appearance in which the upper ureters diverge
laterally over the isthmus and then converge inferiorly.
BIBLIOGRAPHY
1. Kolln CP, Boatman DL, Schmidt JD. Horseshoe kidney. A review of 105 patients.
J Urol 1972; 107(2): 203-4.
2. Nino-Murcia M, deVries PA, Friedland GW. Congenital anomalies of the kidneys.
Clin Uroradiol 2000; 1: 690-763.
3. Segura JW, Kelalis PP, Burke EC. Horseshoe kidney in children. J Urol 1972; 108(2):
333-6.

RENAL TUBERCULOSIS
IVP
Presents as local infiltration into the parenchyma with subsequent
papillary necrosis and as the disease progresses, there is multi-focal
stricturing with impairment of drainage, formation of caseous pus and
subsequent calcification.
Strictures affecting the calyceal system produce hydrocalysis.
Badly affected areas become non-functiong. Tuberculous lesion may
develop at any site in the urinary tract but generally radiological changes
are more pronounced in upper urinary tract (kidneys and ureters) leading
to hydronephrosis, hydroureter, pyelonephrosis and ultimate autonephrectomy with calcification and small contracted bladder.
BIBLIOGRAPHY
2003;1: 944-6.
245-6.
HYDRONEPHROSIS
Mild to severe dilataion of pelvi-calyceal system can be seen. The kidneys
may be small and smooth (post-obstructive renal atrophy).
Mostly caused by obstructive pathology, non-obstructive causes
include reflux, bacterial endotoxin, pregnancy and nephrogenic diabetes
insipidus.
BIBLIOGRAPHY
970.
PARALYTIC ILEUS
In generalized paralytic ileus both the large and small bowel are dilated.
the dilatation extends down into the sigmoid colon and gas may be
present in the rectum, and sometimes it becomes difficult to differentiate
such cases from low large bowel obstruction.
Air fluid levels can be seen in the plain erect film.
BIBLIOGRAPHY
137-8.
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300
FIGURE 5.1: Ureteric Stone. A large radiopaque stone

shadow seen in the left ureter (lower end).
FIGURE 5.2: Stag-horn Calculus. A large stag-horn calculus

with two small calculi seen in the hydronephrotic left kidney.
FIGURE 5.3: Bilateral Stag-horn calculi.
FIGURE 5.4: Nephrocalcinosis. Multiple calcified

densities seen in cortex and medulla bilaterally.
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302
FIGURE 5.5: Renal Dystrophy Secondary to Oxalosis. Small

left kidney with cortical calcification (arrows). Left renal and
distal ureteric calculi.
FIGURE 5.6: Auto-nephrectomy due to Tuberculosis.

Calcified left kidney (multiple rings) and proximal ureter is
clearly visible (arrow).
FIGURES 5.7A AND B: Emphysematous Pyelonephritis (Right). Air is seen in

pelvicalyceal system of the right kidney (arrows).
FIGURES 5.8A AND B: Adult Polycystic Kidney Disease. Bilateral enlarge kidneys
with multiple thin rounded cysts of variable sizes seen compresing pelvicalyceal
system.
FIGURE 5.9: X-ray Abdomen plain (erect

view) in a patient with ruptured liver
abscess, with pneumoperitoneum and
pneumointestinalis. Air fluid levels in the
right hypochondrium, haziness in the
central abdomen is also visible (due to
masive hepatomegaly).
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304
FIGURE 5.10: Liver Abscess. A large gas shadow with a fluid level is
visible in the area of liver which is also enlarged. Gaseous distension of
bowel loops and stomach seen due to paralytic ileus.
FIGURE 5.11: Ruptured Liver Abscess into the Peritoneal Cavity.

Abdominal CT showing well-defined low attenuation oval shaped mass
in the central abdomen anteriorly. This patient presented with central
abdominal mass and fever for 2 months duration. CT scan showing large
walled off collection of pus in the abdomen.
FIGURE 5.12: Hepatic metastasis secondary to carcinoma of

stomach. CT scan abdomen showing multiple hypodense areas of
variable sizes seen in both the lobes of the liver (arrows).
B
FIGURES 5.13A AND B: Hepatic Metastases. Multiple
irregular hypoechoeic areas seen in both lobes of the liver
compatible with metastatic lesions (arrows).
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306
FIGURE 5.14: CT abdomen showing hepatomegaly with

multiple hypodense areas of variable sizes occupying almost
whole of the liver parenchyma due to metastases.
FIGURES 5.15A TO D: Portal Vein Thrombosis. Contrast CT scan showing a

filling defect in the area of portal vein.
B
FIGURES 5.16A AND B: Pancreatic Calcification. Patchy
calcification seen in the region of head and body of pancreas.
FIGURE 5.17: Cholelithiasis. Multiple large radiopaque

stone shadows in the region of gallbladder.
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308
FIGURE 5.18: Post- tuberculous calcified para-aortic and

mesenteric lymph nodes (arrows).
FIGURE 5.19: Paralytic ileus/low intestinal obstruction.

Multiple gas filled bowel loops either due to paralytic ileus or
due to low intestinal obstruction.
FIGURE 5.20: Necrotizing Fascitis. There are multiple gas

filled bowel loops. Subcutaneous emphysema with ruptured
pyocele of the gallbladder into anterior abdominal wall
causing infection of the skin and subcutaneous tissues
visible as subcutaneous emphysema.
FIGURE 5.21: Small Bowel Obstruction due to Tuberculosis.

Multiple air fluid levels are visible in the upper central, both
para-colic gutters and iliac fossae.
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310
FIGURE 5.22: Calcified Hydatid Cysts. Multiple rounded

dense lesions in the right hypochondrium, right and left
lumbar regions and left hemi-pelvis are visible due to multiple
calcified hydatid cysts in the abdomen.
FIGURES 5.23A AND B: Ovarian Dermoid. (A) Plain abdominal radiograph with a
tooth like opacity projected over the left sacroiliac joint (arrow). (B) The pelvic CT of
the same patient shows bilateral fat attenuation lesions with calcific densities within
them. The appearances on CT are typical of a dermoid cyst.
FIGURE 5.24: Calcified Fibroids. Plain abdominal

radiograph with multiple, rounded, well-defined, calcified
lesions, typical of uterine fibroids.
COMMENT
The plain abdomen radiography may be used as a starting point in
abdominal investigation but further studies are frequently required.
Earlier in this book (p 158-215) examples of barium studies and oral
cholecystograpy. Intravenous pyelography are included. Other
radiological investigations of value in the abdomen include CT scan,
ultrasound and MRI.
311
312
FIGURE 5.25: Enlarged prostate, indenting the urinary

bladder and causing elevation of its base.
FIGURE 5.26: Diverticulum of Urinary Bladder. A large

outpouching is seen on the right of urinary bladder due to
diverticulum formation (arrow).
FIGURE 5.27: Hydronephrosis of Left Kidney. An enlarged

left kidney with dilated pelvi-calyceal system with minimal
hydronephrosis on right side.
FIGURE 5.28: Big Staghorn calculus right kidney.
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314
C
FIGURES 5.29A TO C: Bilateral Renal Calculi. (A) An elongated vertical opacity
seen on right side at the level of D12-L1due to renal stone. Transversely lying opacity
seen on left side at the level of L2 (left renal stone). Oval opacity seen in the upper
part of left pelvis-distal left ureteric calculus. (B and C) Bilateral hydronephrosis more
marked on left side with distended left sided pelvi-calyceal system.
FIGURE 5.30: Horseshoe Kidney. Lower pelvis of both

kidneys are uniting each other in the midline (isthmus). Both
kidneys are showing normal calyceal pattern.
B
FIGURES 5.31A AND B: Intravenous Cystogram (AP and Oblique View).
Diverticulated urinary bladder, in a case of bladder neck obstruction.
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316
FIGURE 5.32: Enlarged left kidney with cyst between

superior and middle calyx (arrow).
FIGURE 5.33: Bilateral Chronic Pyelonephritis. Small

kidneys with irregular outline. Distortion and clubbing of minor
calyces seen.
B
FIGURES 5.34A AND B: IVP (5, 20 mins film A and B).
Emphysematous pyelonephritis.
FIGURE 5.35: Acute Pyelonephritis. Edematous kidney with

dense nephrogram and attenuated pelvi-calyceal system on
the left side due to acute pyelonephritis.
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318
FIGURE 5.36: Acute Pyelonephritis. Swollen left kidney

with attenuated pelvi-calyceal system.
FIGURE 5.37: Tuberculosis right kidney with autonephrectomy.
FIGURE 5.38: Genitourinary Tuberculosis. Non-functioning

left kidney. Minimal calcification seen at the lower pole of left
kidney. Small capacity thick walled urinary bladder.
FIGURES 5.39A AND B: Horseshoe Kidney with Bilateral Hydronephrosis.

Significant changes on the left side seen. Lower poles almost joining each other thru
isthmus.
319
Brain
321
322

TUBERCULOMA
Intracranial tuberculomas may be single or multiple, of variable sizes
and situated above or below the tentorium. Brainstem involvement is
infrequent (2.5-8%) other uncommon sites include cavernous sinus, sella
turcica, suprasellar cistern and hypothalamus.
Tuberculomas may be or may not be associated with tuberculous
meningitis. The tuberculous focus starts off as an area of cerebritis and
at this stage it is of low density on CT scan, the cerebritis then progresses
to a focal non-caseating granuloma, which is isodense or mildly hyperdense on CT, surrounded by perilesional low-density edema. Postcontrast there is dense nodular enhancement. As caseation occurs, the
granuloma becomes isodense or slightly hypodense.
The lesion now shows ring-enhancement, and perilesional edema
remains.
The radiological differential diagnosis of such ring-enhancement
lesion includes abscess, neurocysticercosis, glioma, metastases, lymphoma
and other granulomatous processes such as sarcoidosis. With disseminated miliary tuberculosis, multiple enhancing small (< 5 mm) granulomas
are seen scattered throughout the brain.
Tuberculous abscesses are rare, and usually on imaging a single
supratentorial abscess is seen at the grey-white matter interface, which
has a hyperdense rim and low-density center on CT.
BIBLIOGRAPHY
1. Bhargava S, Tandon PN. Intracranial tuberculomas: A CT study. Br J Radiol 1980;
53(634):935-45.
2. Wasay M, Kheleani BA, Moolani MK, Zaheer J, Pui M, Hasan S, Muzaffar S, et al.
Brain CT and MRI findings in 100 consecutive patients with intracranial tuberculoma.
J Neuroimaging 2003;13(3):240-7.
3. Whelan MA, Stern J. Intracranial tuberculoma. Radiology 1981;138(1):75-81.
CEREBRAL INFARCTION
The cardinal sign of infarction is an area of decreased attenuation within
the cerebral substance. Typical locations are within the known territory
of major vessels (e.g. the middle or posterior cerebral arteries) or in the
region of the basal ganglia and internal capsule.
So called watershed infarcts may be seen at the margins of a major
vascular territory, e.g. the posterior frontal and parieto-occipital zones.
Brain
Infarcts are often triangular in shape, although they can appear rounded
in axial cross-section. They involve both the white and superficial grey
matter, whereas vasogenic edema (around a tumor, for example) usually
affects mainly the white matter.
This area of diminishes density accompanied by mild mass effect
may be seen as early as 6 hours after the onset of symptoms, but in
many cases is not clearly visible during the first 24 hours depending on
the quality of the CT scan images.
At first the margins of the infarct are poorly defined, although a few
infarcts are clearly marginated from the outset.
The density of the lesion becomes progressively lower over the
succeeding weeks, until it approaches that of cerebrospinal fluid in a
mature infarct. About two weeks after the onset, and corresponding to
the phase of resolution of edema and of macrocytic and vascular
infiltration, infarcts may be less evident than at other times.
Some infarcts may appear isodense at about the third week.
In the first week there is often some swelling of the affected part of
the brain, but persistent mass effect is rare, and eventually there is loss
of volume, with enlargement of the adjacent cerebrospinal fluid space in
most cases. Complete healing is very rare. Enhancement of the infarct
may be seen after a few hours from the onset of symptoms, but is often
not seen until some days have passed. Such enhancements may be around
the lesion, suggesting hypervascularity of the adjacent brain, or within
it, indicating a breakdown of the blood-brain barrier. Patterns of
enhancements vary widely. They include total enhancement of the
infracted area, central enhancement and ring enhancement, and such
appearances can simulate a tumor or an abscess. In some cases cortical
enhancement is seen and this is more specific. There is no clear relationship
between the type of enhancement and the prognosis. Infarcts which
flood with contrast medium will go on to marked necrosis. Since it is
possible that the contrast medium may have a deleterious effect/
administration in cases of obvious infarction in contraindicated.
Occasionally enhancement may be the only definite indication of ischemia,
the infarct itself being isodense with the surrounding brain. Such
infarctions are one of the very few situations in which contrast medium
injection may show previously undetected lesions. The majority of infarcts
will show enhancement at some stage during the first 2 weeks though
some do not.
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324

After 6 weeks, however, persisting enhancement should suggest an
alternative diagnosis, even though occasional cases are encountered with
enhancement persisting at 12 weeks.
A type of infarct whose appearance differ markedly from those
described above is the uncommon hemorrhagic infarct. This is commonest
with major embolus but may also be seen with patients on anticoagulants.
There is patchy increased density throughout the affected region, often
with some mass effect, or there may be hemorrhage at the cortical
margins of the infarct.
The ability to differentiate this type of infarct is important in its
contraindication to the use of anticoagulant drugs. The CT appearance
may resemble those of a hemorrhage or hemorrhagic contusion rather
than a simple infarct.
Venous and sinus thrombosis, either spontaneous or more commonly
in association with inflammatory process, may lead to infarction. In severe
cases the white mater is predominantly affected and the changes are
often bilateral, showing as areas of diminished density.
The affected cerebral hemispheres are frequently swollen and may
show hemorrhages and marked contrast enhancements. Increased
density of dural sinus or cortical veins with lack of the normal
intraluminal enhancements may be detected on CT.
Transient ischemic attacks (TIA) CT scan shows diffuse, rather nonspecific, ischemic abnormalities in up to 40% of the cases, often in basal
ganglia and white matter, and their relevance to the clinical symptoms
is speculative.
BIBLIOGRAPHY
1. Cassidy TP, Lewis S, Gray CS. Computerized tomography and stroke. Scott Med
J 1993; 38(5):136-8.
2. Cormier PJ, Long ER, Russell EJ. MR imaging of posterior fossa infarction: Vascular
territory and clinical correlates. Radiographics 1992; 12: 1079-96.
3. EC Sa de Camargo, WJ Koroshetz. Neuroimaging of Ischemia and Infarction
NeuroRx 2005; 2(2): 265-76.
4. Osborn AG. Diagnostic Imaging: Brain (1st edn). Amirsys Inc: Altona, 2004.
409-11.
6. Stevens JM, Barber CJ, Kerslake R, Broz M, Barter S. Extended use of cranial CT in
the evaluation of patients with stroke and TIAs. Neuroradiology 1991;33(3):200-6.
7. Wardlaw JM, Mielke O. Early signs of brain infarction at CT: Observer reliability
and outcome after thrombolytic treatmentsystematic review. Radiology 2005;
235(2):444-53.
Brain
INTRACEREBRAL HEMATOMA
The vast majority of spontaneous hemorrhages occur in the elderly and
middle-aged and are due to rupture of a microaneurysm on a small
intracerebral artery, with hypertension and atheroma as predisposing
factors. Intracerebral hemorrhage may also occur in patients on
anticoagulants or with hemorrhagic blood disorders.
Because of the clear distinction between the high attenuation of
extravasated blood and that of the surrounding brain, CT scanning is
by far the most accurate radiological method for demonstrating these
lesions.
Of intracerebral hemorrhages that are hypertensive in origin, around
60% occur in the basal ganglia or center sylvian areas; the remaining
40% involve the Pons (20%), cerebellum (10%), and less commonly the
cerebral white matter.
On CT the hemorrhage shows as an area of increased attenuation
and is surrounded by a thin low-attenuation ring which probably results
from clot retraction and damage to the blood-brain barrier. Hemorrhage
can rupture into the subarachnoid space or ventricles.
The mass effect depends on the size of the bleed but is frequently
less then with tumors of comparable size.
The high attenuation of intracerebral hematomas is seen immediately
from the time of hemorrhage. It decreases slowly over the subsequent
weeks, until eventually a low-density cystic area remains. Enhancement
may occur around a clot due to damage to the blood-brain barrier and
neovascularity. At the stage where the clot is isodense or of low density
there is clear danger of confusing the CT appearances with those of an
abscess or tumor post-enhancement.
BIBLIOGRAPHY
1. Aronovich BD, Reider-Groswasser II, Segev Y. Early CT changes and outcome of
ischemic stroke. Eur J Neurol 2004; 11(1): 63-5.
2. Cohen WA, Wayman LA. Computed tomography of intracranial hemorrhage.
Neuroimaging Clin N Am 1989; 2:75-87.
3. Gokaslan ZL, Narayan RK. Intracranial Hemorrhage in the Hypertensive Patient.
Neuroimaging Clinics of North America 1992; 2: 171-86.
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326

SUBARACHNOID HEMORRHAGE
Extravasated blood may be identified anywhere in the subarachnoid
space from its high attenuation.
It is usually confined to the basal cisterns. If the subarachnoid blood
is localized, e.g. in the insula, this can be very helpful in identifying
which of multiple aneurysms is responsible for the hemorrhage.
The presence of blood in both the cisterns and ventricles has a graver
prognosis and is associated with a higher mortality.
Small amounts of intaventricular blood usually gravitate to the occipital
horns, where it is readily identified.
Low density areas representing infracted or ischemic brain are
frequently shown. It is thought that they are related to the arterial spasm
which often accompanies subarachnoid hemorrhage.
Dilated ventricles are shown in 50% of patients scanned within 48
hours of a subarachnoid hemorrhage, as communicating hydrocephalus
may develop quite rapidly, due to blood clot obstructing the CSF flow.
In the rare cases in which subarachnoid hemorrhage is a manifestation
of a tumor, the main findings are those of the tumor itself, with an
associated hematoma.
BIBLIOGRAPHY
1. Avrahami E, Katz R, Rabin A, Friedman V. CT diagnosis of non-traumatic
subarachnoid hemorrhage in patients with brain edema. Eur J Radiol 1998; 28: 222-5.
2. Farrs MT, Ferraz Leite H, Schindler E, Mhlbauer M. Spontaneous subarachnoid
hemorrhage with negative angiography: CT findings. J Comput Assist Tomogr
1992; 16: 534-7.
3. Hijdra A, Brouwers PJ, Vermeulen M, van Gijn J. Grading the amount of blood on
computed tomograms after subarachnoid hemorrhage. Stroke 1990; 21: 115661.
4. Latchaw RE, Silva P, Falcone SF. The role of CT following aneurysmal rupture.
Neuroimaging Clin N Am 1997;7:693708.
HYPOXIC ISCHEMIC BRAIN DAMAGE

Global hypoxia, hypotension or hypoglycemia can damage the whole
brain, usually but not always symmetrically.
Patterns vary from total cerebral infarction to predominantly white
matter infarction, cortical watershed or white matter terminal zone
infarction, basal ganglia infarcts (especially globus pallidus ), and pure
cortical damage in cerebral hemisphere or cerebellum such as in severe
hypoglycemia. Severe clinical disability can occur with little or no changes
on CT or MRI.
Brain
BIBLIOGRAPHY
1. Naidich TP. Brain Vascular Distribution: Classical patterns of stroke. Categorical
Course in Cerebrovascular Disease. American Society of Neuroradiology 1989;6377.
2. Osborne AG. Stroke. In: Diagnostic Neuroradiology. Mosby; 1994:355-60.
3. Yee T, Gronner A, Knight RT. CT findings of hypoxic basal ganglia damage. South
Med J 1994;87(6):624-6.
MENINGITIS
This is an infective/inflammatory process of the dura mater, leptomeningies (pia and arachnoid maters) and the cerebrospinal fluid within the
subarachnoid space.
It may be associated with underlying cerebral parenchymal
inflammationmeningoencephalitis. The role of imaging in meningitis is
largely to detect complications such as hydrocephalus, venous thrombosis
and infarction, as often in early uncomplicated meningitis imaging may
be normal. In most cases of viral meningitis CT and MRI are normal,
unless associated with viral encephalitis.Brain swelling and meningeal
enhancement may be seen in some cases.
In early cases of pyogenic meningitis there may be obliteration of the
basal cisterns and cerebral and cerebellar sulci due to the presence of an
inflammatory exudates and brain swelling. After contrast administration
there may be either dural or leptomeningeal enhancement.
Communicating hydrocephalus is the most common complication
associated with meningitis, resulting from blockage of the CSF flow.
In tuberculous meningitis the basal cisterns are obliterated by an
isodense or hyperdense exudates, and postcontrast there is avid
enhancement of the basal meninges extending into the ambient, sylvian,
pontine and chiasmatic cisterns. The meningeal enhancement may extend
over the cerebral and cerebellar hemisphere. Hydrocephalus is present
in 45-87% of patients at the time of diagnosis.
BIBLIOGRAPHY
1. Becker LE. Infections of the developing brain. Am J Neuroradiol 1992;13(2):537-49.
2003;2: 1784-5.
3. ITheron S, Andronikou S, Grobbelaar M, Steyn F, Mapukata A, du Plessis J. Localized
basal meningeal enhancement in tuberculous meningitis. Pediatr Radiol
2006;36(11):1182-5.
4. Osbourne A. Diagnostic Neuroradiology. Mosby, Chicago; 1994;680-6.
327
328

SUBDURAL ABSCESS (EMPYEMA)
These are usually secondary to bacterial or fungal disease of the calvaria
and subdural space, and frontal sinusitis is in fact the most common
cause of a subdural empyema. The cerebral convexities and in hemispheric
fissure are the most common locations.
On CT these are seen as crescentric or lentiform collections of variable
attenuation (usually reduced), whose margins, and occasionally contents,
enhance markedly. Hypodensity of the adjacent brain may result from
secondary venous infarction.
BIBLIOGRAPHY
1. Stevens EA, Norman D, Kramer RA, Messina AB, Newton TH. Computed
tomographic brain scanning in intraparenchymal pyogenic abscesses. Am J
Roentgenol 1978;130(1):111-4.
2. Weisberg L. Subdural empyema. Clinical and computed tomographic correlations.
Arch Neurol 1986;43(5):497-50.
3. Zimmerman RD, Leeds NE, Danziger A. Subdural empyema: CT findings.
Radiology 1984; 150(2): 417-22.
ENCEPHALITIS
1. HERPES SIMPLEX ENCEPHALITIS
This involves predominantly the temporal lobes and is a grave illness
with a mortality of 55%. The severity of the infection can lead to
hemorrhagic necrosis and considerable mass effect.
The changes are bilateral but may appear predominantly unilateral in
the acute phase, and this may lead to a false diagnosis of tumor at imaging.
CT scan shows reduced density in the affected temporal lobe (s) and
the adjacent posterior frontal region, usually with the mass effect.
The changes may be minimal in the first 2-3 days despite severe
neurological impairment and should be carefully sought. Hemorrhage
rarely shows a clear hematoma but may give rise to patchy areas of
slightly increased density. After contrast medium, enhancement is seen
in most cases and may be patchy, peripheral or gyral. In the chronic
there may be large low density areas with associated local atrophy in
the affected regions.
2. CYTOMEGALOVIRUS (CMV)
CT will show dilated ventricles due to atrophy with periventricular and
cortical calcifications.
Brain
BIBLIOGRAPHY
1. Jordan J, Enzmann DR. Encephalitis. Neuroimaging Clin N Amer 1997; 1:17-38.
2. Osborn AG. Diagnostic Neuroradiology. Mosby; 1994.
3. Osborn AG. Infection, white matter abnormalities, and degenerative diseases.
Diagnostic Neuroradiology. St. Louis; Mosby, 1994; 694-6.
4. Shaw DW, Cohen WA. Viral infections of the CNS in children: Imaging features.
Am J Roentgenol 1993;160(1):125-33.
CEREBRAL METASTASES
Attenuation varies, but most are isodense with brain. Hyperdensity may
be seen with small round cell tumors, tumors with high nuclear to
cytoplasmic ratio, or hemorrhagic lesions. Midline shift and/or
compression of ventricles may be visible. Marked surrounding edema is
usually present.Renal, breast, melanoma and choriocarcinoma most likely
to bleed.
Cystic and calcified metastases are rare. Edema is often striking and
may be only abnormality seen before contrast.
Most metastases enhance strongly; both solid and ring like patterns.
BIBLIOGRAPHY
1. Davis PC, Hudgins PA, Peterman SB, Hoffman JC. Diagnosis of cerebral metastases.
Double-dose delayed vs. contrast-enhanced MR imaging. American Journal of
Neuroradiology 1991; 12: 293-300.
2. Zimmerman HM. The ten most common types of brain tumour. Seminars in
Roentgenology 1971;6:48-54.
PITUITARY TUMORS
MRI is the preferred imaging modality for assessing pituitary adenomas
and can evaluate local tumor invasion and compression of critical
structures such as the chiasma more accurately. CT will better
demonstrate destruction of the sellar floor. Large adenomas producing
chiasmal compression, CT will show the extent and relationships of the
suprasellar component as well as the enlarged sella. The tumor can also
extend laterally into the cavernous sinuses and temporal lobe or
downward into the sphenoid sinus.
Pituitary adenomas normally show homogeneous density similar to
or slightly greater than that of normal brain tissue, and enhance
uniformly after contrast medium.
The CT diagnosis of microadenomas requires high-resolution CT.
329
330

The typical microadenoma can be recognized as a small low density
area within the enhancing gland. Other features which may be seen are
deviation of the infundibulum and upward bulging of the upward bulging
of the upper surface of the gland.
BIBLIOGRAPHY
2003;2: 1749-51.
1998;409.
CRANIOPHARYNGIOMA
These tumors of epithelial origin account for up to 3% of primary
intracranial tumors.
Calcification is present in over 80% of the childhood cases.
They usually grow above the sella and adhere tightly to the floor of
the third ventricle and infundibulum. A small proportion (15%) grow
into the pituitary fossa and can produce enlargement and deformity of
the sella.
BIBLIOGRAPHY
2003;2: 1752-3.
Ring enhancing lesions of the brain

Neoplastic
- High grade gliomas
- Metastases
- Lymphoma
Infective
- Abscesses
Reparative
- Resolving hematoma or infarct
- Post-irradiation
Brain
C
FIGURES 6.1A TO C: Tuberculomas. Hydrocephalus
secondary to TBM and multiple tuberculomas. Pre- and postcontrast CT images showing basal meningeal enhancement
and multiple focal ring lesions with surrounding edema
involving both cerebral hemisphere. There is also evidence
of moderate hydrocephalus with peri-ventricular edema.
331
332
FIGURE 6.2: Intra-cranial TB. Axial post-gadolinium and T2

weighted MRI images demonstrating abnormal meningeal
enhancement with a ring enhancing lesion in the left middle
cerebral peduncle with associated surrounding edema.
C
FIGURES 6.3A TO C: Tuberculomata. Nodular enhancing
lesions with intense white matter edema seen.
333
Brain
FIGURE 6.4: Toxoplasmosis. Axial MRI

brain. Post IV Gadolinium. Multiple,
bilateral, ring enhancing lesions both
within the deep white matter and the
basal ganglia are shown in an AIDS
patient. Most commonly affected areas
are the basal ganglia, corticomedullary
junction, white matter or periventricular
regions. These were diagnosed to be
secondary to toxoplasmosis. The
differential diagnoses for ring enhancing
lesions are given in Page 334 and 335.
FIGURES 6.5A TO E: Tuberculomas Brain. (A to D) Multiple dense, contrast

enhancing lesions with marked surrounding edema due to tuberculomas in a patient
with pulmonary tuberculosis. (E) Chest X-ray of the same patient showing apical and
peri-hilar opacities in left lung and widenning of superior mediastinum due to
lymphadenopathy-pulmonary tuberculosis.
334
C
FIGURES 6.6A TO C: Tuberculous Meningitis (Pre- and
Post-contrast Scan). There is evidence of diffuse meningeal
enhancement and gross hydrocephalus.
Brain
FIGURE 6.7: Basal Meningitis. Basal enhancement of

meninges seen associated with effacement of cortical sulci
in a patient with pyogenic meningitis.
FIGURE 6.8: Tuberculous Meningitis. Post-contrast scan

showing meningeal enhancement and hydrocephalus.
335
336
FIGURES 6.9A AND B: Postencephalic Cyst and Hydrocephalus. Small right middle
cerebral artey infarction is also seen. Ventricles are grossly dilated with a cystic
lesion communicating with the right lateral ventricle anteriorly (1). Low attenuation
seen at the level of right Sylvian fissure.
FIGURES 6.10A AND B: Cerebral Abcess Secondary to Middle Ear Infection.

Large rounded thick smooth wall ring enhancing lesion is seen in left temporoparietal region associated with significant perifocal edema causing mass effect with
midline displacement.
Brain
FIGURES 6.11A TO D: Subdural Empyema Secondary to Sinusitis. (A) There is

evidence of sinusitis with fluid levels involving all the sinuses except left maxillary
sinus. (D) There is evidence of intracranial spread of infection with subdural empyema
(arrow) and extension into right frontal lobe and inter-hemispheric fissure (arrow, B
and C respectively).
337
338
FIGURE 6.12: Cerebritis with Pneumoencephalus. Cortical

prominence seen due to cerebritis and pneumoencephalus
(probably secondary due to dural defect), ventricles are
normal.
B
FIGURES 6.13A AND B: Metastasic, Abscesses. Multiple well-defined lesions at
the gray and white matter junction in the right frontal, left parietal and on the right
cerebellar hemispheres. The lesions are associated with significant edema and are
enhancing after contrast administration. No evidence of midline shift. There is also
evidence of ethmoidal sinusitis.
Brain
FIGURES 6.14A AND B: Amebic Abcesses. Bilateral low attenuation areas seen in
the region of basal ganglion with ring enhancement and surrounding edema due to
amebic abscesses developed in a patient with lung abscess secondary to a ruptured
liver abscess.
FIGURES 6.15A AND B: Lung Metastasis and Cerebral Abscess. The lung
metastasis is ring enhancing with a thin rim and surrounding edema. This is
indistinguishable from the cerebral abscess (A) T1 weighted axial and (B) Diffusion
MRI imagethe latter image show the restricted diffusion characteristic of an abscess,
tumors have free diffusion.
339
340
FIGURES 6.16A AND B: Cerebellar Abscess. Well circumscribed hypointense lesion

seen in the right cerebellar hemisphere on T1 image with surrounding edema caused
by a large cerebellar abscess. The lesion appears isointense on T2 image with
surrounding edema which is hyperintense.
FIGURE 6.17: Right Middle Cerebral Artery Infarction

(Contrast). Large low attenuation area due to infarct with
surrounding edema seen involving the right Middle cerebral
territory, compressing the ventricular system leading to
midline displacement.
Brain
FIGURE 6.18: Acute Cerebellar Infarcts. Axial CT head

showing bilateral acute cerebellar infarcts secondary to
basilar artery thrombosis, with the typical low attenuation
present in the cerebellar hemispheres.
FIGURE 6.19: Old infarct in left frontoparietal region with

widened adjacent sylvian fissure and asymmetric dilatation
left frontal horn with mild diffuse brain atrophy.
341
342
FIGURE 6.20: Large acute ischemic infarction in left frontotemporo-parietal region with mass effect and mild midline
shift. No acute bleed or mass lesion is noted.
FIGURES 6.21A AND B: Ischemic infarct both cerebellar hemispheres (CT scan
brain plain and contrast). (A, B) There is evidence of a low density mass lesion in the
left cerebellar fossa involving the white matter. A similar low density area also seen in
the right cerebellar fossa.
Brain
FIGURE 6.22: Ischemic Infarction. There is a large hypodense area occupying right temporo-parietal region.
Compression of right lateral ventricle and attenuation of sulci
and gyri on the right side.
FIGURE 6.23: Intracereberal Hemorrhage. There is

evidence of extensive hemorrhage in the left thalamus and
basal ganglia which has dissected into the ventricular system
and into the cisterns as well. There is evidence of dilatation
of the frontal horns with mass effect at the level of 3rd ventricle.
343
344
FIGURE 6.24: Parenchymal Hemorrhage. Plain CT brain showing

a large high attenuation area with mild perifocal edema.
FIGURE 6.25: Cerebellar Hematoma. There is evidence of acute

hematoma in cerebellum with obstructive hydrocephalus causing
significant dilatation of all the ventricles.
Brain
FIGURE 6.26: Pontine Hemorrhage. A large

hemorrhage seen in the pontine region.
FIGURE 6.27: Cerebral Hemorrhage. A large hemorrhage

in the right deep parietal region with mild surrounding edema
and spillage into both lateral ventricles.
345
346
FIGURE 6.28: Parietal Lobe Hemorrhage. A large hematoma

seen in the right parietal lobe with surrounding edema,
pressure effect and mild midline shift.
FIGURE 6.29: Hemorrhagic Contusion. Plain CT brain

showing bilateral gyriform high density areas with mild
perifocal edema.
Brain
FIGURES 6.30A AND B: Subarachnoid Hemorrhage. High density seen in the

Sylvain fissures, ventricles and the subarachnoid spaces with midline shift.
FIGURE 6.31: Subarachnoid hemorrhage with intraventricular extension leading to

obstructive hydrocephalus.
347
348
FIGURE 6.32: Subarachnoid Hemorrhage (SAH). Axial CT

head. Unenhanced scan showing extensive acute
hemorrhage in the sylvian fissures and the ambient cistern in
keeping with subarachnoid hemorrhage.
Diagnostic features of subarachnoid

hemorrhage on plain CT scan brain
- High density material within the basal cisterns
and cerebral fissures.
- Blood in the ventricles
- Blood within the brain parenchyma and
subdural space.
- Blood in sylvian fissure, occipital horn and
inter hemispheric fissure
- Mild communicating hydrocephalus.
Brain
C
FIGURES 6.33A TO C: Subdural Hematoma. Left frontoparietal region with left sided effacement of ventricle and
associated midline shift.
FIGURES 6.34A AND B: Bilateral Chronic Subdural

Hematoma. (A) Axial T2 weighted MRI brain demonstrating
bilateral chronic subdural collections (High intensity). (B) The
isodense attenuation of the chronic subdural hematoma is
demonstrated on CT.
349
350
FIGURE 6.35: Acute and acute on chronic subdural

hematomas. Unenhanced CT images showing bilateral acute
on chronic subdural collections with low attenuation fluid
with areas of high attenuation inkeeping with acute
hemorrhage.
FIGURE 6.36: Acute Subdural Hematoma. Irregular dense

opacity seen in the fronto-parieto-occipital regions with
pressure effects over the right lateral ventricle.
Brain
FIGURE 6.37: Arteriovenous Malformation. Low density

with patchy hyperdensities areas seen in the left parietooccipital region due to contrast filled grossly dilated vessels
(mostly enlarged veins).
Radiological features of subdural hematoma

Acute:
- Crescent shape parallel to skull vault
- Blood is homogeneous and hyperdense to
brain
- Bukling of the brain medially away from the
vault
- Progressive drop in the Hounsetields units
until the collection resembles water
Acute on chronic:
- Fluid-fluid level appearance (fresh blood is
heavier and sinks with gravity)
- Loculations may be present
- Dystrophic calcifications may develop later on
351
352
FIGURE 6.38: Craniopharyngioma. CT scan axial view

showing supracellar mass with extensive calcification
causing obstructive hydrocephalus.
FIGURE 6.39: Medulloblastoma.CT scan showing a midline

mixed density posterior cranial fossa mass with some
calcifications, causing hydrocephalus due to obstruction of
4th ventricle.
Brain
FIGURES 6.40A AND B: Glioblastoma Multiforma. Sagittal and coronal view of MRI
contrast showing a frontal mass of mixed intensity partly enhancing with non-enhancing
central portion.
FIGURE 6.41: Malignant Glioma. CT scan axial view showing

a large complex density (partly solid, partly cystic) mass in
the left cerebral hemisphere with surrounding edema and
midline shift.
353
354
C
FIGURES 6.42A TO C: Acoustic Neuroma. MRI brain axial view (A) Non-contrast
TW1 showing a hypointense mass in cerello-pontine angle. (B) TW2 image showing
a hyperintense mass in the cerebello-pontine angle compressing the brainstem and
the 4th ventricle, extending into the internal auditory meatus. (C) Post-contrast image
showing an enhancing mass in the cerebello-pontine angle causing compression
of the brainstem and obstructing the 4th ventricle.
Brain
FIGURES 6.43A AND B: Malignant Glioma. CT scan axial view showing right parietal
partially cystic, partially solid mass with mixed enhancement and surrounding edema.
FIGURES 6.44A AND B: Meningioma. (A) Bilateral frontal mass the right one showing
extensive lamellar calcification, left one isodense on plain CT scan. (B) Post-contrast
scan showing vivid enhancement, attachment to falx cerebri and surrounding
vasogenic edema.
355
356
FIGURE 6.45: Pituitary Adenoma. CT brain plain showing a

rounded mass of increased density in the area of sella
measuring about 2 cm in diameter.
FIGURE 6.46: Pituitary Adenoma. A rounded mass

enhancing on contrast is seen in the suprasellar cistern.
Brain
B
FIGURES 6.47A AND B: Pituitary Adenoma. (A) MRI TW1
image sagittal view showing enlargement of sella tursica
with a uniform ISO intense mass. (B) Post-contrast image
showing marked enhancement.
357
358
FIGURE 6.48: Hemangiopericytoma. The hemangiopericytoma

which looks like an atypical meningioma, intensely enhancing,
extra-axial lesion with is displacing the frontal horns of the lateral
ventricles.
FIGURE 6.49: Post-IV contrast CT showing multiple

metastases from a bowel primary solid enhancing nodules
with enhancement and extensive vasogenic edema.
Brain
B
FIGURES 6.50A AND B: Melanoma. Pre- and post-IV contrast
CT. The images show high attenuation lesion in the left
cerebral hemisphere is due to high melanin content with
some enhancement on contrast scan.
359
360
FIGURES 6.51A TO D: Metastases. Pre- and post-contrast CT images showing

multiple ring enhancing lesions with perifocal edema involving right thalamus, left
occipital region and right CP angle. A large cerebllar midline lesion is compressing
the 4th ventricle leading to mild to moderate hydrocephalus.
FIGURES 6.52A AND B: (A) T1 weighted coronal image and (B) T2 weighted axial
image, show an epidermoid tumor in the suprasellar cistern. Imaging characteristics
on MRI are not dissimilar to CSF.
Brain
FIGURE 6.53: Metastatic Deposits. Multiple

dense, well-defined enhancing masses visible
in both hemispheres with significant surrounding
edema.
FIGURE 6.54: Acoustic Neuroma. Axial MRI

brain showing a soft tissue mass adjacent to the
right internal acoustic meatus in keeping with an
acoustic neuroma.
361
362
FIGURE 6.55: Diffuse Cerebral Atrophy. The ventricles are

mildly dilated with widened Sylvian fissures, cerebral sulci,
and interhemispheric space.
FIGURE 6.56: Diffuse Cerebral Atrophy. Grossly dilated

ventricles with widening of interhemispheric and cerebral
sulci.
Brain
FIGURES 6.57A TO C: Binswangers Disease. Low density

patches are seen in bilateral frontoparietal periventricular regions
involving the basal ganglia with generalized cortical atrophy.
FIGURES 6.58A AND B: Glioma. Pre- and Post-IV contrast CT

head. The right parietal tumor with a thick rim, infiltrating and
enhancing with necrotic core. Histologically proven to be a glioma.
363
364
FIGURE 6.59: Thyroid Metatasis MRI with IV

Gadolinium. Axial image. The thyroid metastasis is
included because it looks like a meningioma of the
petrous ridge extra-axial, enhancing.
Index
A
Achalasia of cardia 166
Acromegaly 224
Acute asthma 106
Acute myocardial infarction 128
Acute pyelonephritis 317
Adult polycystic kidney disease 297
Adult respiratory distress syndrome 13
Allergic bronchopulmonary aspergillosis
3
acute 3
chronic 3
Amoebic abscesses 339
Ankylosing spondylitis 223, 253
Aortic dissection 152
Ascariasis 195
Ascending colon 210
Aspergilloma in a tuberculous cavity 36
Atelactasis/collapse 6
B
Bamboo shaped spine 254
Barium enema 212
Bezoars 159
Bilateral chronic pyelonephritis 316
Binswangers disease 363
Bronchiectasis 4
Bronchogenic carcinoma 9
C
Calcified hydatid cyst 180
Carcinoma bronchus 74
Carcinoma caecum 210
Carcinoma colon 164
Carcinoma esophagus 159
Carcinoma lung 79
Carcinoma stomach 159
Causes of raised diaphragm 104

bilateral 104
unilateral 104
Cavitating lesions 6
Cavitatory lung lesions 111
differential diagnosis 111
abnormal lung 111
infections 111
inflammatory 111
neoplastic 111
vascular 111
Cerebellar hematoma 344
Cerebral infarction 322
Cerebral metastases 329
Charcots joint 287
Chickenpox 61
Chilaiditis syndrome 103
Cholelithiasis 307
Chronic duodenal ulcer and duodenitis
178
Chronic obstructive pulmonary disease 106
Chronic pulmonary tuberculosis 23
Coarctation of aorta 132
Coeliac disease 161
Congenital heart diseases 126
atrial septal defect 126
Ebstein anomaly 127
tetralogy of Fallot 126
transposition of great arteries 126
D-loop transposition 126
L-loop transposition 126
Congestive cardiac failure 129
Consolidation 5
lobar consolidation 5
Consolidation-collapse 47
Constrictive pericarditis 130
Cork screw esophagus 168
Craniopharyngioma 330
Crohns disease 162, 197
Cryptogenic fibrosing alveolitis 14
Cystic bronchiectasis 41
Cystic fibrosis 13, 43
366
D
Dextrocardia with situs inversus 134
Diabetic foot 268
Diffuse cerebral atrophy 362
Dilated cardiomyopathy 129
Dissecting aneurysm 148
Diverticular disease 163
Duodenal lymphoma barium meal 202
E
Emphysema 15
Emphysematous bullae 107
Emphysematous pyelonephritis 297, 317
Encephalitis 328
cytomegalovirus 328
herpes simplex encephalitis 328
Ewings sarcoma 285
F
Fibrosing alveolitis 96
G
Gastric outlet obstruction 179
Gout 221
H
Hemangiopericytoma 358
Hemorrhagic contusion 346
Hiatus hernia 16
Hodgkins lymphoma 112
Hodgkins disease 115
Horse-shoe kidney 298
Hydatid cysts 7
Hydronephrosis 299
Hyperparathyroidism 222
causes 223
primary 223
secondary 223
Hypoxic ischemic brain damage 326
I
Ileocecal tuberculosis 196
Intestinal tuberculosis 160, 201
Intracerebral hematoma 325

Intravenous cystogram 315
L
Left ventricular aneurysm 152
Leiomyoma of stomach 185
Leprosy 268
Liver abscess 104
Loculated tuberculosis empyema 65
Lung abscess 15
Lymphangitis carcinomatosa 85
Lymphoma 11
M
Malabsorption syndrome 200
Malignant glioma 355
Malignant mesothelioma 84
Marble bone disease 228
Mediastinal mass lesions 117
differential diagnosis 117
anterior mediastinum 117
middle 117
posterior 117
Meningitis 327
Metastatic disease 226
Military tuberculosis 21
Monoarthritis 260
causes 260
Mucopolysaccharidosis 233
Multi-drug resistant tuberculosis 29
Multiple myeloma 225
Mycetoma 229
Mycoplasma pneumonia 45
N
Nephrocalcinosis 296
Non-Hodgkins lymphoma 67
O
Osteoarthritis 219
Osteoarthrosis of spine 259
Osteomalacia 221
Osteoporosis 219
Osteosarcoma 225
367
Index
P
Pagets disease 245
Pancoast tumor 76
Paralytic ileus 299
Paranasal sinusitis 267
Pleural fibroma 91
Peptic esophageal stricture 167
Pericardial effusion 129
causes 130
Pituitary adenoma 356
Pituitary tumor 280, 329
Pleural effusion 8
Pneumoconiosis 97
Pneumocystis carinii pneumonia 57
Pneumothorax 8
Pneumopyopericardium 154
Polyarthritis 260
causes 260
Portal vein thrombosis 306
Postprimary pulmonary tuberculosis 20
Post-tuberculous cavitations 29
Potts disease 227, 266
Prosthetic valves 138
Pulmonary aspergillosis 3
plain film 3
invasive 3
non-invasive 3
Pulmonary hydatid cysts 62
Pulmonary metastases 10
Pulmonary tuberculosis 2
primary tuberculosis 2
secondary tuberculosis 2
Pulmonary venous hypertension 127
Pyloric stenosis 189
Pyogenic meningitis 327
R
Rachitic rosary 243
Reactivation tuberculosis 24
Reflux esophagitis 158
Reiters disease 255
Renal calculi 296
Renal tuberculosis 299
Retrosternal goiter 118
Rheumatoid arthritis 218
Rickets 220
Ring enhancing lesions of the brain 330

Romanus lesion 223
S
Sacroiliitis 255
causes 255
bilateral 255
unilateral 255
Sarcoidosis 12
Sclerosing cholangitis 213
Septic arthritis 274
Severe mitral stenosis 138
Sinusitis 228
Squamous cell carcinoma 81
Stag-horn calculus 300
Subarachnoid hemorrhage 326, 347
Subdural abscess 328
T
Thyroid metastasis 364
Toxic multinodular goiter 119
Trichobezoar 183
Tuberculoma 26, 322
Tuberculous bronchopneumonia 34
Tuberculous meningitis 327
Tuberculous pleural effusion 66
U
Ulcerative colitis 162, 207
V
Valvular heart diseases 124
aortic stenosis 125
mitral regurgitation 124
mitral stenosis 124
pulmonary stenosis 125
W
Wegeners granulomatosis 109
Worm infestation 161

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