atlas of diagnostic radiology

Atlas ofDIAGNOSTICRADIOLOGY

Khalid MahmoodMBBS, FCPS, MACG

Professor and ChairDepartment of Medicine

Dow University of Health SciencesKarachi, Pakistan

ForewordPaul 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 transmittedin any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the priorwritten permission of the author and the publisher.

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

First Edition: 2009ISBN: 978-81-8448-670-4Typeset at JPBMP typesetting unitPrinted at Ajanta Press

To

My parents,

all my achievements are because of

their affection, efforts, encouragement

and prayers

Contributors

Kashif Burney MBBS MRCS(Eng.) FRCRConsultant Interventional RadiologistSt Helier University HospitalWrythe Lane, CarshaltonSurrey, UK

Sikandar Rafique Qureshi MBBS MCPSChief/Head RadiologistCivil Hospital, Karachi, Pakistan

Zahid Anwar Khan MBBS MCPS FCPS FRCREx. ProfessorHead Radiology DepartmentSindh Institute of Urology and Transplant (SIUT)Karachi, Pakistan

Qurat-ul-Ain MBBS FCPS (Radiology)Consultant RadiologistAga Khan University HospitalKarachi, Pakistan

Asima Shakoor MBBS FCPS (Medicine)Registrar MedicineDow Medical College, Civil HospitalKarachi, Pakistan

Abdul Wahid ShaikhClinical Research FellowDepartment of MedicineDow University of Health SciencesKarachi, Pakistan

Farooq M HusainRegistrar MedicineDow University of Health SciencesCivil Hospital, Karachi, Pakistan

Foreword

Roentgen’s discovery of X-rays in 1895 heralded the modern age ofmedicine. Before that time, there was no way of examining the internalstructures of the body without resorting to surgery. Since that discovery,we have been able to look at in vivo anatomy and pathology inincreasingly exquisite detail using a variety of sophisticated techniques.Despite this, the mainstay of diagnostic imaging for many parts of thebody 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 theexaminer which in turn largely depends on experience.

But how can a student obtain this experience? Partly, this must bewith direct patient involvement, but this can be considerably assistedby well-presented museum cases.

This atlas provides such an archive in a readily accessible form andwith sufficient clinical details that each case assists in the building of theknowledge base. The case mix has been chosen to represent the prevalentdisease pattern. As such, this will not only be a valuable resource for itstarget audience of local undergraduate and postgraduate students butwill also be of inestimable value to post-graduate students of medicineand their tutors in the parts of the world where the conditions shownmay be less frequently encountered.

The brief but salient account of the radiological features of theconditions provides a good introduction to each section. The films includemany plain radiographs, contrast examinations, computed tomographyand a few magnetic resonance imaging scans. In each case the imagespresented show the abnormality clearly. Some of the studies are lessperfect than others but this is the reality of life. Too many books showonly perfect cases giving the impression that this is how we should expectto see the cases. In practice the quality of images obtained depends on alarge variety of factors including age of equipment, radiographic expertiseand the condition of the patient. These cases thus represent the mix of

x Atlas of Diagnostic Radiology

images that the student is likely to meet and provide a superb resourcewhich will help to hone the necessary interpretive skills.

Professor Mahmood must be congratulated on having collected suchan interesting and useful museum of films and the atlas is testament tohis excellent relationships with his radiological colleagues.

Professor Paul R GoddardBSc, MBBS, MD, DMRD, FRCR

(Retd.) Consultant and Head of Training BristolRadiology Training Scheme

Civil Consultant to the Royal Air Force(Honorary Air Commodore)

Past-President of the Radiology Section of theRoyal Society of Medicine

Visiting ProfessorUniversity of the West England

Preface

Three simultaneous roles as a physician, teacher and examiner propelledmy search for radiological films with definite findings. This led to avirtual treasure of films from not only my own patients but even mycolleagues. Practising for over twenty-five years, I now felt myself in aposition to meticulously plan an Atlas. An Atlas of medical radiologymay sound as a misnomer to many but significant and valuable technicalinput from my radiologists should make this book reader friendly.

As 20% of X-rays are more than 20 years old, they are not of highquality yet have been included to make the compilation complete. Diversepresentations of diseases have been illustrated by multiple X-rays ofsingle diseases. Tuberculosis being a case in point, its high prevalenceand multisystem involvement has many X-rays to present a completespectrum of disease. Salient features of common diseases have beenadded 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 IntravenousUrographies and lastly CT and MRIs of Brain. In this era of rapid advance-ment in radiology and imaging, this atlas would be considered moreconventional. As undergraduate and postgraduate students of medicineare targeted for readership, I hope it proves valuable. The newer imagingtechnologies are not covered as this would require a bulkier offering, buthave been indicated where of value.

Khalid Mahmood

Acknowledgements

It would be remiss if I did not thank all those who have helped me inputting together this atlas. The compilation of this Atlas would not havebeen possible without the hard work and sincere contribution of myjuniors Dr Uzma Ghaury, Dr Asima Shakoor, Dr Abdul Wahid Shaikhand 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 mustnot forget to thank Professor Paul R Goddard for taking out some of hisvery precious time to go through the manuscript and write its foreword.

Contents

1. Pulmonology ............................................................................. 1Introduction ....................................................................................................... 2Pulmonary tuberculosis ................................................................................... 17Aspergillosis .................................................................................................... 36Bronchiectasis .................................................................................................. 40Consolidation ................................................................................................... 45Hydatid cyst of lung ........................................................................................ 62Pleural effusion ................................................................................................ 64Pneumothorax .................................................................................................. 69Pulmonary neoplasm ....................................................................................... 74Interstitial lung disease .................................................................................... 95Diaphragm .................................................................................................... 100Chronic obstructive pulmonary disease ......................................................... 106Cavitating lesions .......................................................................................... 108Mediastinal mass ........................................................................................... 112Pulmonary miscellaneous .............................................................................. 118

2. Cardiology .............................................................................. 123Introduction ................................................................................................... 124Congenital heart disease ................................................................................ 132Valvular heart diseases .................................................................................. 138Pericardial diseases ........................................................................................ 142Heart failure and cardiomyopathy ................................................................. 145Aneurysm....................................................................................................... 148Cardiology miscellaneous .............................................................................. 153

3. Barium Studies and Oral Cholecystography ................... 157Introduction ................................................................................................... 158Barium esophagus .......................................................................................... 165Barium stomach ............................................................................................. 177Barium duodenum ......................................................................................... 192Barium follow through .................................................................................. 195Barium enema ................................................................................................ 203Cholecystography .......................................................................................... 213

4. Skeletal System ..................................................................... 217Introduction ................................................................................................... 218Skeletal congenital anomaly ........................................................................... 230Metabolic bone disorders ................................................................................ 234Inflammatory joint diseases ........................................................................... 245Bone infections ............................................................................................... 261Hematological bone diseases .......................................................................... 275Skeletal neoplasm ........................................................................................... 280Skeletal miscellaneous .................................................................................... 286

5. Plain Abdomen and Intravenous Pyelograms ................ 295Introduction ................................................................................................... 296Abdomen ........................................................................................................ 300Intravenous urographies ................................................................................ 312

6. Brain ........................................................................................ 321Introduction ................................................................................................... 322Infections ........................................................................................................ 331Cerebrovascular diseases ................................................................................ 340Brain neoplasms ............................................................................................. 352

Index .............................................................................................................. 365

xvi Atlas of Diagnostic Radiology

1Pulmonology

2 Atlas of Diagnostic Radiology

PULMONARY TUBERCULOSIS

PRIMARY TUBERCULOSIS

Chest radiograph may appear entirely normal. Predominant feature isunilateral hilar and adjacent mediastinal adenopathy. Pulmonary focusis randomly distributed and may range from a small ill-defined shadowto segmental or lobar consolidation, commonly on the right side.Pulmonary focus may show calcification and may rarely cavitate. Airwaynarrowing secondary to extrinsic nodal compression with resultantatelectasis may occur (e.g. Brock’s syndrome). Primary tuberculosis mayalso present as pleural effusion or pleural thickening. Miliary tuberculosiscan occur as a complication.

POST-PRIMARY/SECONDARY/REACTIVATION TB

Calcified primary complex may be identified. The disease can be unilateralor bilateral and apical/posterior segments of the upper lobes or superiorsegments of the lower lobes are most often involved. Patchy foci of air-space disease “cotton-wool shadows” are characteristic. Pulmonary focimay cavitate, and multiple cavities of varying sizes may be present.Fluid levels may aid in recognition of cavities, the walls of which maybe indistinct or obscured by overlying densities. Pneumothorax mayoccur.

Scattered calcifications, fibrous contraction leading to hilar retractionand lobar volume reduction are seen in chronic cases. Lobar consolidationmay 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 calcifiedpleura (fibrothorax).

Endobronchial tuberculosis—ulcers and strictures, bronchialobstruction leading to collapse or hyperinflation, may also present asbronchiectasis. Single or multiple tuberculomata of variable sizes canalso 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 immunodeficiencysyndrome. J Thorac Imag 1990;5:38-45.

3Pulmonology

3. Ip MSM, So SY, Lam WK, Mok CK. Endobronchial tuberculosis revisited. Chest1986;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;160:753-8.

5. Leung AN, Muller N, Pineda PR, Fitzgerald JM. Primary tuberculosis in child-hood: 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 diseasesof 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 airspace (Air-meniscus sign) separating fungus ball from cavity wall ischaracteristic.

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 presentwithin 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 invasiveaspergillosis represent focal infarctions and are typically round withindistinct margins.

ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS (ABPA)

Acute

Bronchial wall thickening and atelectasis, mucoid impaction pattern, orconsolidation are ususal. V or Y shaped central mucus plugs with ‘fingerin glove’ appearance may be seen in ABPA.

Chronic

Bronchiectasis with scarring/fibrosis (usually upper zone) is morecommon, mucus plugs no longer evident.


CT SCAN

Non-invasive (Aspergilloma)

Sponge-like mass containing irregular air spaces which change withpatient’s 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 theupper lobes is seen.

BIBLIOGRAPHY

1. Castagnone D, Radaelli P, Cortelezzi A. Radiological aspects of invasive pulmonaryaspergillosis. 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-fluidlevels, are seen.

Loss of vascular shadows due to adjacent peribronchial fibrosis maybe present.

5Pulmonology

Bronchiectasis may show over-inflation or atelectasis, or may manifestwith associated infectious consolidation, scaring, bullae and pleuralthickening.

Dilated airways filled with secretions give rise to band shadows ofvariable size. Band shadow may branch, giving V, Y, or more complexshaped opacities.

BIBLIOGRAPHY

1. Peter Armstrong, Alan G Wilson, Paul Dee, David M Hansell. Imaging of diseasesof 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 radiographyand high-resolution CT. Chest 1996; 109(3):608-11.

CONSOLIDATION

Consolidation when associated with a patent airway, an air bronchogramis often visible. This sign is produced by the radiographic contrastbetween the column of air in the airway and surrounding opaque acini.

When consolidation is secondary to bronchial obstruction, air in theairways is resorbed and replaced by fluid and the affected area is ofuniform density.

The volume of purely consolidated lung is similar to that of the normallung since air is replaced by a similar volume of fluid or solid.

Air lucencies within consolidated lung may be due to resolution ofthe process with intervening normal lung, necrosis of tissue withcavitation or pneumatoceles.

When consolidation is due to fluid, its distribution is influenced bygravity, so that in acute pneumonitis consolidation is often denser andmore clearly demarcated inferiorly by a pleural surface, and is less denseand more indistinct superiorly.

When air bronchograms are evident on the chest radiograph thesemay manifest as echogenic linear structures.

When bronchi become fluid filled they are more clearly demonstratedas 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 adjacentto 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, andmay obscure the right upper mediastinum.

• Right middle lobe consolidation: This is limited by the horizontal fissureabove and the lower half of the oblique fissure posteriorly, and mayobscure 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 obliquefissure posteriorly. Lingular consolidation lobe may obscure the aorticknuckle.

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. Squire’s Fundamentals of Radiology (6th edn), London: Harvard

University Press; 2004; 112-21.

ATELECTASIS/COLLAPSE

The usual findings are localised increase in lung density, crowding ofpulmonary vessels, displacement of fissure/hilum, mediastinal shift,cardiac rotation and approximation of ribs. Compensatory over inflationof normal lung can occur.

BIBLIOGRAPHY

1. Woodring JH, Reed JC. Types and mechanisms of pulmonary atelectasis. J ThoracImaging 1996;11:92-108.

2. Proto AV, Tocino I. Radiographic manifestations of lobar collapse. SeminRoentgenol 1980;15:117–73.

CAVITATING LESIONS

A cavity is a gas-filled space surrounded by a complete wall which is3 mm or greater in thickness. Thin walled cavities are called cysts orring shadows.

Cavitations occur when an area of necrosis communicates with apatent airway. Particular features of importance are location of the cavity,

7Pulmonology

its outline, wall thickness, the presence of fluid level, contents of thecavity, satellite lesions, the appearance of the surrounding lung andmultiplicity of lesions.

Fluid within a cavity can be demonstrated only when using ahorizontal beam.

Common cavitating lesions are tuberculosis, staphylococcal infectionsand carcinoma. The tumor mass itself or the distal lung may cavitate.

Tuberculous cavities are usually in the upper zones, in the posteriorsegments of the upper lobes or apical segments of the lower lobes.

The site of lung abscesses following aspiration depends on patient’sposition at that time but they are most often right-sided and in thelower zones.

Traumatic lung cysts are often sub-pleural. Amebic abscesses arenearly always at the right base, the infection being extended from theliver.

Pulmonary infarcts are usually in the lower zone and sequestratedsegments are left-sided.

BIBLIOGRAPHY

1. David Sutton. Text book of radiology and imaging. 7th Edition, ChurchillLivingstone 2003;1:22-2.

2. Nestor LM, Neil Colman, Paré 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 homogeneousdensity 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 of50 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 fissuresappear as a spindle shaped pseudotumor.

If subpulmonic; apparent diaphragmatic elevation with more lateralappearance to diaphragmatic peak, no lung marking below silhouette ofdiaphragm, increased distance between ‘diaphragm’ and stomach bubble(>2cm) if on left side is seen.

If large mediastinal shift to contralateral side and/or inversion ofthe ipsilateral hemidiaphragm (more common on left) is present.

The radiographic appearance of pleural fluid may be modified whenthere is associated lung atelectasis.

Loculated chest wall effusions tend to be convex to the lung andsharply demarcated on pulmonary aspect when viewed tangentially andare 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 collectsat the apex. The lung apex retracts towards the hilum and on a frontalchest film the sharp white line of the visceral pleura will be visible,separated from the chest wall by the radiolucent pleural space, which isdevoid of lung markings.

9Pulmonology

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 themediatinum, kinking of the great veins and acute cardiac and respiratoryembarrassment. Radiologically the ipsilateral lung may be squashedagainst the mediastinum, or herniated across the midline, and theipsilateral hemidiaphragm is depressed.

The usual appearance in loculated or encysted pneumothorax is anovoid air collection adjacent to the chest wall, and it may be radio-graphically indistinguishable from a thin-walled subpleural pulmonarycavity, cyst or bulla.

The usual radiological appearance of a hydropneumothorax is thatof a pneumothorax containing a horizontal fluid level which separatesopaque fluid below from lucent air above.

BIBLIOGRAPHY1. David Sutton. Text book of radiology and imaging. 7th Edition, Churchill

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 topresent as central tumors, whereas adenocarcinoma and large cell typestend to produce peripheral lesions.

Pancoast tumors are frequently squamous cell in type and canresemble pleural thickening in the superior sulcus, usually associatedwith erosions of adjacent ribs and bones.

Peripheral tumors present as solitary nodules with generally well-defined edges; they may be spherical or oval shaped and may belobulated, approximately 16% show cavitation (usually squamous cell).

An irregular edge or ‘corona radiata’ is suggestive but not specific ofa malignant tumor. A single band connecting the nodule to pleura (Pleuraltail sign) is seen with both malignant and benign lesions. Air broncho-grams are not seen within nodules on plain films (can be seen on thinsection CT).

The cardinal imaging signs of a central tumor are collapse andconsolidation of the lung distal to the tumor and the presence of hilar


enlargement and‘Golden S’ sign (bulge in fissure adjacent to collapsedsegment) indicating central tumor.

Visible calcification is virtually never identified on plain chestradiograph 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 than18 months. Tumors less than 1cm in size are rarely visible on plain chestradiographs. Alveolar cell carcinomas give rise to alveolar opacities andspread rapidly.

BIBLIOGRAPHY

1. ER Heitzman, B Markarian, BN Raasch, EW Carsky, EJ Lane, ME Berlow. Pathwaysof tumor spread through the lung; radiologic correlations with anatomy andpathology. Radiology 1982; 144:3-14.

2. Im JG, Choi Bl, Park JH, et al. Case report CT findings of lobar bronchioloalveolarcarcinoma. 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.

4. Peter Armstrong. Imaging of diseases of the chest (3rd edn) 2000;307.5. 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 ofthe breast, colon, kidney, uterus, prostate, head and neck.

The hallmark of blood-borne metastases to the lungs on imaging isone or more oval or spherical, discrete pulmonary nodules, usually inthe 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 ashighly specific.

Cavitation is most frequent in metastases from tumors of the uterinecervix, 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.

11Pulmonology

Lymphangitis carcinomatosa is usually bilateral. Coarse linearreticular 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 veryobvious on CT scan.

In addition, it is possible to show pulmonary vessels leading directlyto individual metastases.

BIBLIOGRAPHY

1. Coppage L, Shaw C, Curtis AM. Metastatic disease to the chest in patients withextrathoracic malignanc. J Thorac Imaging. 1987;2:24-37.

2. Davis SD. CT evaluation for pulmonary metastases in patients with extrathoracicmalignancy. Radiology 1991; 180(1):1-12.

3. Libshitz HI, North LB: Pulmonary metastases. Radiol Clin North Am.1982; 20(3):437-51.

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 Hodgkin’s than Non-Hodgkin’s lymphoma (NHL).

In Hodgkin’s disease adenopathy tends to be bilateral butasymmetric, involving two or more nodal groups, anterior mediastinaland paratracheal groups are most frequently involved and the posteriormediastinal nodes being infrequently involved. In NHL adenopathytends to be hilar and mediastinal and is more likely to involve only asingle nodal group.

Parenchymal involvement is unusual at presentation; it is more commonin Hodgkin’s 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 ofmediastinal nodes.

Other manifestations include: Pericardial effusion, chest wall invasionor thymic enlargement but rather rarely.


CT SCAN FINDINGS

CT is the current ‘gold standard’ for evaluating the extent of thoracicinvolvement in patients with Hodgkin’s disease and, when required,for those with NHL.

CT can demonstrate disease even in patients with a normal chestX-ray and is more useful for staging the disease.

Compression of the pulmonary arteries, superior vena cava and majorbronchi by the enlarged nodes may be seen on a CT chest.

BIBLIOGRAPHY

1. Castellino RA , Blank N, Hoppe RT, C Cho. Hodgkin’s disease contribution ofchest CT in initial staging evaluation, Radiology. 1986;160:603-5.

2. David Sutton. Text book of radiology and imaging. 7th Edition, ChurchillLivingstone 2003;1:527-59.

3. Marc Bazot, Jacques Cadranel,Sylvie Benayoun, Marc Tassart, Jean Michel Bigot,Marie France Carette. Primary Pulmonary AIDS-Related Lymphoma Radiographicand CT Finding. Chest. 1999;116:1282-6.

4. Ooi GC, Chim CS, Lie AK, Tsang KW. Computed tomography features of primarypulmonary non-Hodgkin’s lymphoma. Clin Radiol 1999; 54:438–43.

5. Romano M, Libshitz HI. Hodgkin disease and non-Hodgkin lymphoma: Plainchest radiographs and chest computed tomography of thoracic involvement inpreviously untreated patients. Radiol Med (Torino) 1998;95(1-2):49-53.

SARCOIDOSIS

Bilateral hilar adenopathy with paratracheal adenopathy is the classicalfinding of chest X-ray in sarcoidosis.

The degree of hilar node enlargement ranges from barely detectableto massive, eggshell calcification of nodes can be seen specific tosarcoidosis or silicosis. Nodes usually regress with increasingparenchymal involvement. Parenchymal sarcoidosis may manifest asreticulonodular opacities or alveolar opacities. The nodules range from1 mm to over 5 mm. Alveolar sarcoidosis is due to both filling of air-spaces with inflammatory cells and compression and obliteration of thealveoli by enlarging interstitial nodules.

End-stage sarcoidosis typically shows scaring from the hilum intoupper and mid zones especially the lower part of the upper lobes.

Sarcoidosis is second only to tuberculosis as a predisposing conditionfor mycetoma formation.

Bronchi may be narrowed by external compression or muralgranulomata and fibrosis with post-obstruction atelectasis.

13Pulmonology

BIBLIOGRAPHY

1. Gross BH, Schneider HJ, Proto AV. Eggshell calcification of lymph nodes: Anupdate, AJR 1980;135: 1265-8.

2. Peter Armstrong. Imaging of diseases of the chest (3rd edn) 2000;641.3. 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 followingthe onset of clinical symptoms.

Bilateral, wide spread, patchy, ill-defined densities resemblingcardiogenic 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 areinvolved both centrally and peripherally and air bronchograms may bea prominent feature. CT scans, however, show that the distribution ofthe pulmonary opacification is patchy. Signs of interstitial edema, likehilar 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; 1:1-10.3. Peter Armstrong. Imaging of diseases of the chest (3rd edn) 2000;450.

CYSTIC FIBROSIS

The pulmonary manifestations are progressive from birth but do notbecome radiologically apparent for months or years, so X-ray may becompletely normal initially.

The earliest changes are variable and may include focal atelectasis,recurrent pneumonia, diffuse peribronchial infiltration, emphysema andhilar lymphadenopathy.

In the fully developed form of the disease the radiographic findingsare remarkably uniform and include the following:

Emphysema, enlarged hilar shadows and increase in perihilarshadows, (reactive hyperplasia to chronic infection), bronchiectasis, eithertubular or cystic, and atelectasis and focal infiltration prominent in theupper zones, a reverse of the usual situation with bronchiectasis.


BIBLIOGRAPHY

1. Bradley J Phillips, Charles W Perry. Quick Review: Cystic Fibrosis. The InternetJournal of Internal Medicine 2002;3(1).

2. Don CJ, Dales RE, Desmarias RL, Neimatullah M. The radiographic prevalence ofhilar 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 initiallyor may show small opacities which may be nodular or reticulonodularusually in the basal areas. The shadowing is usually symmetric fromside-to-side, but atypical distributions can occur.

Another common pattern is hazy, ground-glass opacification whichmay be diffuse or patchy. Volume loss is characterized by diaphragmaticelevation and depression of the fissures. The loss of volume is usuallyconcentrated in the lower lobes but may be generalized. Pneumothoraxoccurs occasionally, pneumomediastinum is also a recognizedcomplication.

With progression of the disease, the initially fine shadowing becomescoarser, and small, cyst like transradiancies appear leading to a honey-comb pattern in one-third to one-half of patients, in later stages of thedisease.

With gross fibrosis, larger cyst and bullae may appear.

CT SCAN

CT scan is valuable in the diagnosis of early stages of the disease. Theearliest CT sign of fibrosing alveolitis is faint subpleural opacification inthe posterobasal segments of the lower lobes.

As the interstitial fibrosis progresses, a reticular pattern containingsmall cystic air-spaces becomes evident. Interlobular interstitial thickeningmanifest as very fine reticulation or areas of ground-glass opacification.Moderately enlarged mediastinal lymph nodes are a frequent findingon 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).

15Pulmonology

2. Turner-Warwick M, Burrows B, Johnson A. Cryptogenic fibrosing alveolitis: Clinicalfeatures and their influence on survival. Thorax 1980; 35: 171-80.

3. Wells A. Clinical usefulness of high resolution computed tomography in cryptogenicfibrosing alveolitis. Thorax 1998; 53(12): 1080-7.

EMPHYSEMA

Chest radiography is insensitive for the detection of mild-to-moderateemphysema.

The chest radiographic findings in emphysema may be divided intofour types: hyperinflation, vascular change, bullae, and increasedmarkings. Hyperinflation and vascular change are the usual predominantfinding, with hyperinflation reflecting functional abnormality andvascular change reflecting lung destruction.

Hyperinflation is indicated by a number of signs, e.g low flatdiaphragm, increased retrosternal airspace, obtuse costophrenic angleand cardiac diameter less than 11.5 cm, with a vertical heart.

Vascular signs include increased transradiancy, reduced size andnumber of vessels in middle and outer 1/3 of lung indicating prunningof pulmonary arteries due to pulmonary hypertension. Bullae arecommon 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: Radiologic–pathologic correlations. Radiographics1993;13:311–28.

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 septicemboli. Bacterial lung abscess generally form a thick-walled cavity witha shaggy inner lining. The wall may be thick at first, but with furthernecrosis and coughing up of necrotic material it becomes thinner.

BIBLIOGRAPHY1. 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.


HIATUS HERNIA

Hiatus hernias are frequently incidental findings on chest radiographsand CT.

A hiatus hernia appears as a round soft-tissue mass often containingeither gas or an air-fluid level behind the heart, usually to the left of themidline 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-fluidlevels.

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.

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FIGURE 1.1: Primary Pulmonary Tuberculosis. Tuberculousmediastinal lymphadenopathy. Superior mediastinalwidening is seen due to tuberculous lymphadenopathy.Inhomogeneous shadowing seen in right upper and midzones due to tuberculous infiltrates.

FIGURE 1.2: Primary Pulmonary Tuberculosis.Inhomogeneous opacities seen in right upper and mid zones(arrow) with right hilar lymphadenopathy.


FIGURE 1.3: Primary Pulmonary Tuberculosis. Nodularopacities seen in the right upper zone with mediastinallymphadenopathy on the right side (arrow).

FIGURE 1.4: Primary Tuberculosis. Patchy infiltration visiblein the left mid zone along with widening of the superiormediastinum due to lymphadenopathy.

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FIGURE 1.5: Primary Pulmonary Tuberculosis. Rightsided mediastinal lymphadenopathy.

FIGURE 1.6: Postprimary Tuberculosis. Bilateral tuberculous infiltration and mediastinal lymphadenopathy.


FIGURE 1.7: Postprimary Pulmonary Tuberculosis.Fibrocavitatory lesions in the right upper zone due totuberculosis (arrow). Bilateral emphysematous changes withnarrow tubular heart shadow.

FIGURE 1.8: Miliary Tuberculosis. Right para-tracheal andbilateral hilar lymphadenopathy also seen along with miliarymottling

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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 rightlower lobe is also seen due to secondary bacterial infection.


FIGURES 1.11A AND B: Miliary Tuberculosis. (A) Miliarymottling more on left side. Hilar and superior mediastinallymphadenopathy is also apparent. (B) An enlarged viewshowing miliary mottling.

A

B

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FIGURE 1.12: Miliary Tuberculosis. Wide spread nodularshadowing.

FIGURE 1.13: Chronic Pulmonary Tuberculosis. Partialconsolidation of right upper lobe and a large cavity in leftupper zone (arrow) with raised left dome of diaphragm;pleural thickening and calcification.


FIGURE 1.14: Chronic Pulmonary Tuberculosis.Fibrocavitatory lesions bilaterally more extensive in rightupper zone. Tenting of right hemidiaphragm. Trachea ispulled to the right side.

FIGURE 1.15: Reactivation Tuberculosis. A case of healedpulmonary tuberculosis apparent from fibrotic changes inboth the lungs. Reactivation is visible in the form of a thickwalled cavity in the left lung (arrows).

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FIGURE 1.16: Tuberculous cavity with secondary infection inleft lung (black arrow). Calcified granuloma is also visible inright middle zone (white arrow).

FIGURE 1.17: Calcified granuloma (Tuberculomas) in apatient treated for tuberculosis (arrows).


FIGURE 1.18: Pulmonary Tuberculosis. Tuberculoma inthe right lung (arrow).

FIGURE 1.19: Tuberculoma. A large well-defined soft tissuemass with some calcifications, in the mid zone on right side(arrow). Relatively smaller nodules seen above it (Biopsyproven tuberculoma).

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FIGURE 1.20: Post-tuberculous fibrosis of right lung withipsilateral shifting of mediastinum and elevation of rightdome of diaphragm. Pleural calcification and calcified lymphnodes at the right hilum.

FIGURE 1.21: Post-tuberculous fibrosis and scar ring (arrow)especially in left upper zone and tenting of left hemi-diaphragm.


FIGURE 1.22: Fibrocavitatory tuberculosis of left lung alongwith lobar pneumonia right upper lobe due to secondarybacterial infection.

FIGURE 1.23: Pulmonary Tuberculosis. Bilateral apicalfibrosis with punctate calcification secondary to tuberculosis,mediastinal, tracheobronchial and left hilar lymphadeno-pathy.

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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 apatient with multi-drug resistant tuberculosis. Thick walledcavitatory lesions in the upper and basal segments of rightupper lobe (arrows).


FIGURE 1.26: Post-tuberculous cavitations withfibrotic changes.

FIGURE 1.27: Thick walled tuberculouscavitations in the right lung (arrows).

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FIGURE 1.28: Post-tuberculous bands. Band atelectasis inright lower zone (white arrow). Emphysematous changesalso seen in both the lungs. Loculated pneumothorax inright costophrenic angle (black arrow).

FIGURE 1.29: Post-tubercular pleural calcification. Interlacingpattern of pleural calcification especially on the right side(arrow). Calcified pleural plaques also seen along the rightdome of diaphragm.


FIGURE 1.30A: Series of chest X-raysof biopsy proven case of tuberculosis:a) Massive left sided pleural effusionseen with shift of mediastinum to rightside. Hilar lymphadenopathy alsoseen on right side with some calcifica-tions (Fluid analysis showed exudatewith predominant lymphocytes but nogrowth of mycobacteria).

FIGURE 1.30B: Large oval opacitywith fuzzy margins seen in the leftmiddle and lower zones over-lapping left border of the heart.Elevated left dome of diaphragmwith volume loss seen on the leftside because of partial collapse ofleft lower lobe. Small left sidedpleural effusion also seen. A largeoval lobulated shadow with internalcalcifications seen in right hilarregion indicating lymphadenopathy(CT guided biopsy of the massshowed caseating granulomascompatible with tuberculosis).

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FIGURE 1.30C: Marked improvement seen in the form of reduction in thesize of mass on the left side with regression of hilar lymph nodes on rightside lung expansion also noted (Clinically patient also had hoarsenessof voice due to compression of left recurrent laryngeal nerve, whichimproved markedly with anti-tubercular drug treatment).

FIGURE 1.30D: Further improvement notedon this chest X-ray.


FIGURE 1.31: Tuberculous Bronchopneumonia. Patchyalveolar opacities seen due to bronchial spread. Cavitationsseen on the left side with left upper lobe consolidation withhilar and pleural calcifications.

FIGURE 1.32: Bilateral tuberculous bronchopneumoniawith loculated pneumothorax on right side (arrows).

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FIGURE 1.33: Tuberculous bronchopneumonia. Widespreadpatchy opacities with air-bronchogram in the right lung- upperand middle zones with mediastinal lymphadenopathy (arrow).

FIGURE 1.34: Tuberculous consolidation-collapse left upperlobe. Thickening of pleura seen in interlobar fissure on theright side (arrow).


FIGURE 1.35: Aspergilloma in a tuberculous cavity. Fibroticchanges 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 (whitearrow). Large thick walled cavity with a rounded opacity insidewith a translucent rim around (black arrow)

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FIGURE 1.37: Aspergilloma in a post-tuberculous cavity. Cavityin the left apex with soft tissue mass inside. Soft tissuedensity with air crescent around.

FIGURE 1.38: Aspergilloma. Bilateral post-tuberculous cavities with largefungus ball seen in one of the cavity surrounded by radiolucent crescent allaround. There is also pleural adhesion in the right lung with right hilarlymphadenopathy.


A

B

C

FIGURES 1.39A TO C: Invasive Broncho-pulmonary Aspergillosis.Multiple irregular and linear opacities seen bilaterally without anyhilar or mediastinal lymphadenopathy.

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FIGURE 1.40A: Early and Late Aspergillosis. Axial CT chest.Nodule on CT with surrounding peripheral ill-definedopacification-so-called “halo” sign in a patient with earlyaspergillus infection post-bone marrow transplant forlymphoma.

FIGURE 1.40B: Cavitating lesion at the left apex- angioinvasiveaspergillus infection in a patient with acute myeloid leukemiawho underwent bone marrow transplantation.


FIGURE 1.41: Cystic bronchiectasis in right middle and lowerzones with consolidation. Hyperinflated lung fields and tubularheart also visible due to emphysema.

FIGURE 1.42: Bilateral bronchiectasis involvingmiddle and lower zones, more on right side.

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FIGURE 1.43: Bronchography (Right Oblique View). Cysticbronchiectasis in right middle lobe and medial segment ofright lower lobe. Contrast seen in right lung airways (arrows).

FIGURE 1.44: Cystic Bronchiectasis. Multiple lucencieswith air fluid levels in middle and lower zones of left lung.


FIGURE 1.45: Cystic Bronchiectasis. Honey combing withcystic bronchiectasis in right middle and lower lobes and leftlingular and apical basal segments with associatedconsolidation. Bilateral hilar and right tracheobronchiallymphadenopathy also visible.

FIGURE 1.46: Post-tuberculous Bronchiectasis. CT scanchest axial section (lung window) showing bronchiectasis ofapical segment of right lower lobe with pleural thickening.

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FIGURE 1.47: CT Chest Axial Section (Lung Window).Bronchectasis. Multiple bronchiectatic cavities right apicaland left lingular segments. Pleural thickening of right lung isalso seen.

FIGURE 1.48: Bronchiectasis with Cor pulmonale. CT scanchest showing bilateral bronchiectasis and cardiomegaly dueto cor pulmonale.

FIGURE 1.49: Cystic Fibrosis. Thick walled bronchiwith bilateral cystic changes and fibrosis.


FIGURE 1.50: Cystic Fibrosis. Course and thick bronchial shadowsseen in both lower zones with cystic bronchiectatic changes.

FIGURE 1.51: Cystic Fibrosis. Bronchiectatic changes, thick walledbronchi, fibrosis and prominent hilar and emphysematous lungs.

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FIGURE 1.52: Staphylococcal pneumonia. Consolidationwith partial collapse seen in the left lower zone with elevatedleft dome of diaphragm. Multiple pneumatoceles seen aboveconsolidation (arrow).

FIGURE 1.53: Mycoplasma pneumonia. Reticulonodularshadowing is seen bilaterally but more clearly marked onthe right side.


FIGURE 1.54: Right Lower Lobe Pneumonia. Opacity dueto consolidation of right lower lobe. Right costophrenic angleis obliterated due to pleural effusion. Cardiomegaly is alsopresent due to underlying ischemic heart disease.

FIGURE 1.55: Atypical Pneumonia. Bilateral reticulonodularshadowing especially in the right lower zone. Smalll amountof pleural effusion seen on the right side. Air space shadowingright lower lobe and left lower lobe.

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FIGURE 1.56: Consolidation-collapse Right Upper Lobe.Right upper lobe consolidation with partial collapse. Airbronchogram sign is seen. Trachea is central but theinterlobar fissure has been pulled up.

FIGURE 1.57: Pneumonia Left Lower Lobe. Consolidationof left lower lobe with mild left pleural effusion


FIGURE 1.58: Post-pneumonic Pneumatoceles. Multiplecavities in the right middle and lower zones.

FIGURE 1.59: Pneumonia Right Lower Lobe. Consolidationand collapse of right lower lobe. Loss of translucency overthe lower thoracic vertebra obliterating posterior costophrenicangle indicating pleural effusion.

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FIGURE 1.60: Left Lower Lobe Pneumonia. Left lower lobeconsolidation with partial collapse due to pneumonia.

FIGURE 1.61: Left upper lobe consolidation due topneumonia.


FIGURE 1.62: Pneumonia Left Lower Lobe. Consolidationof left lower lobe with air bronchogram. Emphysematouschanges and narrow tubular heart shadow.

FIGURE 1.63: Collapse of left upper lobe, left dome of the diaphragm iselevated along with ipsilateral mediastinal shift. Compensatoryemphysema of right lung with herniation to the contralateral side.

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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. Rightlung is hyperinflated with nodular opacities in the apex, alsomediastinal widening due to lymphadenopathy.


FIGURE 1.66: Legionnaine’s Pneumonia. Cardiomegaly withbilateral inhomogeneous opacities silhouetting both heartborders. Obliterated right costophrenic angle due to smalleffusion.

FIGURE 1.67: Left Lower Lobe Pneumonia. Lingular and lowerlobe consolidation. Opacity along the left heart border withelevated diaphragm and reduced lung volume on left side.

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FIGURE 1.68: Consolidation of left lower lobe and part ofLingular 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 bilateralhoney combing and consolidation of right middle and lowerzones as well as left lingular and lower lobe segments.Klebsiella was grown from the sputum. Patient has been achronic smoker. Heart is enlarged with unfolding of aorticarch.


FIGURE 1.70: Segmental consolidation involving theright 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 ofdiaphragm is clearly visible.

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FIGURE 1.72: Bronchopneumonia. Showing bilateralinhomogeneous opacities in the lower zones more markedon the right side.

FIGURE 1.73: Bronchopneumonia with right pleural effusion.Patchy opacities in both middle and lower zones withobliteration of right costophrenic angle.


FIGURE 1.74: Right Lung Collapse. Opaque right hemithoraxwith ipsilateral shift of mediastinum due to complete collapseof right lung.

FIGURE 1.75: Lingular lobe consolidation.

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FIGURE 1.76: Pneumocystis carinii pneumonia in a patientwith AIDS. Diffuse inhomogeneous shadowing seen in bothlungs.

FIGURE 1.77: Pneumocystis Carinii Pneumonia.Cardiomegaly, pneumomediastinum and bilateral alveolarinfiltrates. The patient was undergoing chemotherapy foracute myeloblastic leukemia.


FIGURE 1.78: Pneumocystis carinii infection. Bilateral peri-hilar and ground glass changes, caused by pneumocystiscarinii pneumonia, the most common infectious cause ofinterstitial lung disease in AIDS patients.

FIGURE 1.79: CT Axial HRCT image, showing patchy groundglass appearance in the lungs bilaterally in a patient with apneumocystis carinii pneumonia.

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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 withdistorsion of air spaces and peri-bronchial thickenning.

A B

C D

FIGURE 1.81: Bilateral Pneumonia. Multiple air spaceshadows seen bilaterally due to bacterial pneumonia.


FIGURE 1.82: Consolidation left lower and lingular lobedue to pneumonia with small pleural effusion.

FIGURE 1.83: Collapse of the left lung caused by carcinomaof the left main bronchus with compensatory emphysemaon opposite side.

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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 lobeconsolidation due to pneumonia (air bronchogram sign positive),obliteration of left costophrenic angle and left dome of diaphragmbecause of parapneumonic effusion is also seen.


FIGURE 1.86: Pulmonary Hydatid Cysts. Two large roundedopacities partly over lapping each other seen in the rightlung. Anti-echinococcal antibody titers were markedly raisedbut no evidence of hydatid cyst elsewhere in the body waspresent.

FIGURE 1.87: Pulmonary Hydatid Cysts. A large hydatidcyst seen in the right lung (upper and middle zones) pressingtrachea and superior mediastinum. Patient presented withdysphagia, difficulty in breathing and stridor.

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FIGURES 1.88A AND B: Infected hydatid cyst left mid andlower zone with pleural reaction seen.

BA


FIGURE 1.89: Moderate right sided pleural effusion.Homogeneous opacity with concave upper margin andobliteration of right costophrenic angle.

FIGURE 1.90: Right sided pleural effusion, secondary tocarcinoma bronchus (Hemorrhagic on aspiration).

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FIGURE 1.91: Loculated Tuberculous Empyema. Rightsided loculated pleural effusion. Widening of mediastinumdue to lymphadenopathy.

FIGURE 1.92: Moderate left sided pleural effusion withcontralateral shift of mediastinum. Left heart order obliterated(silhouette sign) with mediastinal and right hilarlymphadenopathy.


FIGURE 1.93: Loculated empyema on right side with fibro-thorax. Large opacity in the right lung with sharp medial borderand right dense curvilinear band in the middle and lowerzones. Mediastinum is central.

FIGURE 1.94: Tuberculous Pleural Effusion. Moderate leftsided pleural effusion, with right mediastinal shift. Patchyinfiltration seen in the middle zone on the right side.

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FIGURE 1.95: Non-Hodgkin’s lymphoma with chylothorax. Massivepleural effusion on left side. Right sided hilar and para-tracheallymphadenopathy. Contralateral shift of mediastinum.

FIGURE 1.96: Massive right sided pleural effusion. Right hemithoraxis homogeneously opaque, obliterating costophrenic angle, domeof the diaphragm and cardiac border. No evidence of air-bronchogram. Heart is shifted to the contralateral side.


FIGURE 1.97: Malignant pleural effusion in a case ofcarcinoma bronchus with lymphangiitic spread in the rightupper zone.

FIGURE 1.98: Tuberculous Pleural Effusion. Dense opacityseen in the left mid and lower zones with concave upperborder, obliteration of the left costophrenic angle and leftborder of the heart. Mediastinum is shifted towards oppositeside.

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FIGURE 1.99: Tension pneumothorax on the right side withwidening of intercostal spaces and depression of right domeof diaphragm. Shifting of mediastinum to the left withcollapsed right lung giving ‘Fist sign’ at the right hilum.

FIGURE 1.100: Pockets of pneumothorax with pleuraladhesions on the right side. Left upper zone is showing post-tuberculous scarring and fibrosis.


FIGURE 1.101: Large hydropneumothorax on the right side.

FIGURE 1.102: Moderate pneumothorax with partial collapseof right lung which is also showing bulla in its upper part(arrow). Small pleural effusion on the right side.

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FIGURE 1.103: Left sided hydropneumothorax.

FIGURE 1.104: Large hydropneumothorax on right sidewith contralateral mediastinal shift.


FIGURE 1.105: Right sided hydropneumothorax with a large bullaseen in the partially collapsed right lung (white arrow). Consolidationof the left lower lobe with a thick walled cavity above is also seen.Linear translucency along the heart border bilaterally indicatepneumopericardium/pneumomediastinum (black arrows).

FIGURE 1.106: Large right sided hydro (pyo)pneumothorax.

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FIGURE 1.107: Hydropneumothorax right side. Patchyopacities in the left lung and right sided hydro-pneumothorax (due to tuberculosis)

FIGURE 1.108: Left sided partial pneumothorax.


FIGURE 1.109: Carcinoma bronchus with post-obstructiveconsolidation in the left upper lobe. Irregular mass seen atthe left hilum.

FIGURE 1.110: Carcinoma Bronchus. Large oval opacity seenin the right upper lobe. Eccentric cavitation also visible in theupper and lateral part.

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FIGURE 1.111: Carcinoma Bronchus. Large inhomo-geneous opacity seen in the right lung. Cavitations seenwithin the opacity. Superior mediastinal lymphadenopathypresent. Right lower zone is hypertransradiant.

FIGURE 1.112: Carcinoma bronchus with post-obstructivepneumonia. Non-homogeneous opacity in right upper lobe (anteriorand apical segments) sparing the posterior segments. Right hilarand mediastinal lymphadenopathy also present.


FIGURE 1.113: Pancoast Tumor. Large well-defined homogeneousopacity occupying whole of the right upper and mid zones, obliteratingthe right mediastinal border and partly right heart border. Elevated rightdome of diaphragm due to phrenic nerve palsy is visible. Also right 3rdand 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 isobliterated (Silhouette sign).

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FIGURE 1.115: Carcinoma Bronchus (Squamous CellCarcinoma). Large mass with irregular and lobulated marginsseen 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).


FIGURE 1.117: Carcinoma Bronchus. Irregular mass in theright hilar area with post-obstructive segmental consolidationseen in the right upper and middle zones. Horizontal fissureis prominent because of fluid (Inflammatory) (arrow).

FIGURE 1.118: Pancoast tumor involving the left apex with riberosions (white arrow). Extensive soft tissue mass (extrapulmonary) with erosion of the medial end of left clavicle(black arrow) is also seen.

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FIGURE 1.119: Alveolar Cell Carcinoma. Bilateral ill-definedmultiple opacities with pleural effusion on the right side.

FIGURE 1.120: Carcinoma Lung. Soft tissue mass fairly welldefined in left upper lobe with central translucenciesindicating cavity formation.


FIGURE 1.121: Pancoast Tumor. Soft tissue opacity in the rightapex and supraclavicular region (black arrow) with destruction of2nd and 3rd ribs (posterior ends) (white arrows).

FIGURE 1.122: Carcinoma Bronchus. Cavitating lesion inthe left lower zone (black arrow). Left hilar lymphadenopathy(white arrow).

81Pulmonology

FIGURE 1.123: Carcinoma bronchus with lymphangiitiscarcinomatosis and right phrenic nerve palsy. Soft tissuemass with spiculated margins at right hilum, prominentinterstitial markings and raised right hemi-diaphragm.

FIGURE 1.124: Squamous cell carcinoma with central necrosis.Thick walled cavitatory lesion with air-fluid level (arrow).


FIGURE 1.125: Carcinoma Bronchus. An oblong mass withspiculated margins seen in the right hilum. Left hilum isalso prominent due to lymphadenopathy.

FIGURE 1.126: Bronchial Adenoma. Large, well circums-cribed nodule in the right lower zone (arrows). The patientpresented with recurrent hemoptysis.

83Pulmonology

FIGURE 1.127: Carcinoma Bronchus. Large dense opacitywih irregular margins seen in the right hilar region. Rightupper lobe is partly consolidated due to post-obtructiveinfection.

FIGURE 1.128: Carcinoma bronchus with post-obstructivepneumonia. Large mass in the right hilar region with post-obstructive consolidation due to infection in the upper andmiddle zones.


FIGURE 1.129A: Malignant Mesothelioma.Lobulated masses seen in the right hilar andperi-hilar regions with widening of superiormediastinum. Moderate pleural effusion is alsopresent.

FIGURES 1.129B AND C: CT scan chest showing pleural effusion and a broadbased mass arising from pleura on the right side with pleural thickening and pre-tracheal and mediastinal lymphadenopathy.

B C

85Pulmonology

FIGURE 1.130: Pancoast tumor in right upper lobe with partialcollapse. Opacity in right upper zone, inferiorly limited byhorizontal fissure which is being pulled up. Destruction ofposterior ends of first three ribs.

FIGURE 1.131: Lymphangiitis Carcinomatosa. Disseminatedlinear and nodular shadowing partly coalescent with eachother.


FIGURE 1.132: Metastases from carcinomastomach. Multiple round and oval opacities whichare well-defined and of variable sizes.

FIGURE 1.133: Extensive Metastasis fromOsteosarcoma. Multiple large oval, confluentand overlapping dense opacities in both the lungfields and the mediastinum.

87Pulmonology

FIGURE 1.134: Metastasis from Unknown Primary. Multipleround and oval opacities of variable sizes scattered in boththe lung fields. Hilar lymphadenopathy also visible.

FIGURE 1.135: Hamartomas. Two rounded lesions involvingthe upper and middle zones of right lung with popcorncalcification in the larger lesion.


FIGURE 1.136: Metastasis from Carcinoma-Thyroid. Multiplebilateral nodular opacities of different sizes mainly in theright lung.

FIGURE 1.137: Metastases from Unknown Primary.Multiple well-defined masses in the right lung.

89Pulmonology

FIGURE 1.138: Metastasis from Carcinoma Colon. Multipleopacities of variable sizes especially on right side with hilarand superior mediastinal lymphadenopathy.

FIGURE 1.139: Metastases with Pleural Effusion. Manywell-defined opacities of different sizes seen in the lung. Righthemidiaphragm is elevated due to liver metastases. Rightsided pleural effusion also present.


FIGURE 1.140: Metastases Secondary to Carcinoma ofBreast. Bilateral pleural effusion with disseminated nodularshadows seen through out both lung fields.

FIGURE 1.141: Neurofibromatosis. Marked scoliosis(concavity facing left) of the spine with a large extrathoracicsoft tissue mass on the right side (black arrow). A roundedopacity seen in the right lung (white arrow), is actually due toa neurofibroma present on the posterior chest wall.

91Pulmonology

FIGURE 1.142: Pleural Fibroma. Large well-defined massinvolving the middle and lower zones of the left lung withmarginal calcification.

FIGURE 1.143: Metastases from Carcinoma Breast. Multipleconfluent opacities seen in both the lungs- mid and lowerzones with right hilar lymphadenopathy.


FIGURE 1.144: Carcinoma Bronchus. CT scan chestshowing soft tissue rounded mass in right upper lobe of thelung and pre-tracheal and pre-carinal lymphadenopathy.

FIGURES 1.145A AND B: Carcinoma of Bronchus. (A) Chest X-ray showingmild left sided pleural effusion with left hilar lymph nodes enlargement. (B) CTscan done few days later showed collapse of the left lung due to carcinoma ofleft main bronchus with mild pleural effusion.

A

B

93Pulmonology

FIGURES 1.146A AND B: Malignant Mesothelioma.Mediastinal window showing consolidation with collapse ofright lung with pleural effusion and the lung window isshowing consolidation and collapse of left lung with pleuraleffusion, lobulated pleural mass along with hilar andmediastinal lymphadenopathy.

A

B


FIGURE 1.147: Mesothelioma. IV contrast enhanced CTchest. The image shows lumpy areas of pleural thickeningwith mediastinal and right axillary lymphadenopathy in ahistologically proven mesothelioma.

Differential diagnosis of multiple roundpulmonary opacities

Varying size:Metastases (GIT, breast, thyroid, kidney)Inflammatory

Wegener’s granulomatosisRheumatoid arthritis

AV malformationsInfections:

TuberculosisHydatidStaphylococcus aureusHistoplasmosis

Size b/w 2-5 mm (typically)TuberculosisLymphomaSarcoidosisMetastases

Size b/w 0.5-2 mmTuberculosis (Miliary)SarcoidosisOccupational lung diseases

95Pulmonology

FIGURE 1.148: Fibrosing Alveolitis. Decrease lung volume,elevated dome of diaphragm with reticulonodular shadowingseen in the lower lobes.

FIGURE 1.149: Shrinking lung syndrome in a patient withSLE.


FIGURE 1.150: Fibrosing Alveolitis. Bilateral reticulonodularshadowing seen in the lower zones due to interstitial lungdisease.

FIGURE 1.151: Fibrosing Alveolitis. Typical honey-coombappearance seen in a patient with advanced fibrosingalveolitis.

97Pulmonology

FIGURE 1.152: Chronic extrinsic allergic alveolitis (Birdfanciers lung). Fibrosis and scarring in upper zonesespecially on left side. Irregular opacities and some cavitatinglesions are also seen.

FIGURE 1.153: Pneumoconiosis (Siderosis). Dense linearbranching opacities seen in both the lung fields more on theleft side in a young male who worked for 6 months in oremines.


FIGURES 1.154A AND B: Silicosis. (A) Chest X-ray showing bilateral multipleirregular opacities with calcifications, pleural reaction and fibrosis. (B) CT scan chestreveals bilateral hilar lymphadenopathy with calcification. Right soft tissue massadjacent to right main bronchus, which is speculated. Multiple irregular opacitiesalso seen in both lung fields.

A

B

99Pulmonology

FIGURE 1.155: Acute Respiratory Distress Syndrome.Bilateral air space shadowing in a patient exposed to smokeinhalation.

FIGURE 1.156: Acute Respiratory Distress Syndrome.Widespread, uniformly distributed air space shadowing in asepticemic patient with multiorgan faliure.


FIGURE 1.157: Eventration of right dome ofdiaphragm (medial part).

FIGURE 1.158: Eventration of right dome of diaphragm,mimicking a mass lesion.

101Pulmonology

FIGURE 1.159: Gross eventration of the left dome ofdiaphragm

FIGURE 1.160: Eventration of right dome of diaphragmgiving effect of mass lesion.


FIGURE 1.161: Eventration of the right dome of diaphragm

FIGURE 1.162: Guillain Barré Syndrome . Bilateral elevateddomes of diaphragm due to involvement of phrenic nerves.

103Pulmonology

FIGURE 1.163: Chilaiditi’s Syndrome. Chest X-ray of a 21-yearold female, mentally retarded, having bilateral exophthalmus(congenital) and scoliosis. X-ray reveals bilateral elevated domesof diaphragm with underlying colonic shadows displacing liver,stomach and spleen downwards.

FIGURE 1.164: Large Liver Abscess. Markedly elevatedright dome of diaphragm due to underlying liver abscess.Minimal right sided pleural effusion also visible.


FIGURE 1.165: Large Liver Abscess. Large thick walled cavity with airfluid level seen in the right subphrenic region with small pleural effusionand 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

105Pulmonology

FIGURES 1.166A TO D: (A) Chest X-ray showing marked elevation of left dome ofdiaphragm with enormously distended and air filled splenic flexture of the colon dueto underlying volvulous. (B to D) Volvulus of large intestine with distension of theproximal colon occupying most of the left hemithorax and causing marked elevationof the left dome of diaphragm with shifting of the mediastinum to opposite side.

A

C

B

D


FIGURE 1.167: Chronic Obstructive Pulmonary Disease.Bilateral emphysematous changes with flattened domes ofdiaphragm and narrow tubular heart.

FIGURE 1.168: Acute Asthma. Hyperinflated lungs in apatient with acute severe asthma.

107Pulmonology

FIGURE 1.169: Emphysematous Bullae. Hyperinflated lungfields, with flattening of domes of diaphragm and narrowtubular heart. Multiple large bullae are visible in the left lung.

FIGURE 1.170: Cor-pulmonale Secondary to COPD.Cardiomegaly with right ventricular hypertrophy pattern. Centralpulmonary artery dilatation with pruning of arteries distally.Hyperinflated lungs with flattening of domes of diaphragm.


FIGURE 1.171: Lung Abscess with Effusion. Thick walledcavity with air-fluid level seen in the right lower zone. Rightcostophrenic angle obliterated.

FIGURE 1.172: Lung Abscess. Large thick walled cavitywith an air-fluid level seen in the left lung.

109Pulmonology

FIGURE 1.173: Large lung abscess in the left upper lobewith prominent air-fluid level.

FIGURE 1.174: Wegener’s Granulomatosis. Bilateral thickwalled cavities (arrows) with mediastinal lymphadenopathyand consolidation in the right lower zone.


FIGURE 1.175: Post-pneumonic lung abscess seen in theright lower lobe with small pleural effusion.

FIGURE 1.176: Wegener’s Granulomatosis. Multiple well-definednodular opacities seen in the right lung and picture of lobarconsolidation in the left lung. Patient had history of non-resolvingpneumonia and ultimately cANCA was found to be positive.

111Pulmonology

Differential diagnosis of cavitatory lung Lesions

Neoplastic- Carcinoma of bronchus- Metastases- Hodgkin’s disease

Infections- Tuberculosis- Staphylococcus aureus

Inflammatory- Wegener’s granulomatosis- Rheumatoid nodules- Sarcoidosis

Vascular- Infarction

Abnormal lung:- Cystic bronchiectasis- Infected emphysematous bulla

FIGURE 1.177: Stage II Sarcoidosis.Bilateral hilar lymphadenopathy andreticular shadowing in lung fields.Cardiomegaly and aortic calcification(arrow).

FIGURE 1.178: Stage II Sarcoidosis.Bilateral massive hilar and mediastinallymphadenopathy with pulmonaryinfiltrates.


FIGURES 1.179A TO C: Hodgkin’s Lymphoma. (A) Chest X-ray showing a roundedsoft tissue mass in the posterior superior mediastinum indenting the trachea frombehind. (B, C) CT scan chest of the same patient showing a large mass with an areaof central necrosis. The mass is extending upto the vertebral column.

A

B

C

113Pulmonology

FIGURE 1.180: Histoplasmosis. Asymmetricalbilateral hilar lymphadenopathy with multiple smallnodular opacities in the lung fields.

FIGURE 1.181: Non-Hodgkin’s Lymphoma. Bilateralasymmetrical superior mediastinal lymphadenopathy.


FIGURE 1.182: Non-Hodgkin’s Lymphoma. Mass insuperior mediastinum. Elevated right dome ofdiaphragm. Right tracheobronchial lymphadenopathywith basal atelectasis and small pleural effusion.

FIGURE 1.183: Non-Hodgkin’s Lymphoma. Para-vertebral,low attenuation lobulated mass with destruction of vertebralbody and lesion extending up to the spinal cord and displacingit posteriorly.

115Pulmonology

FIGURE 1.184: Hodgkin’s Disease. Bilateral mediastinaland hilar lymphadenopathy.

FIGURE 1.185: Hodgkin’s Disease. Hilar and mediastinallymphadenopathy, showing large oval opacity in the righthilar region with widening of mediastinum. Lobulatedshadows seen above the arch of aorta on both sides.


FIGURE 1.186: Hydatid Cysts. Two large overlappingcalcified cystic shadows seen in the anterior and superiormediastinum. Hydatid cysts rarely occur in the mediastinum.

FIGURE 1.187: Dermoid Cyst. Two rounded calcifiedmasses in the anterior mediastinum.

117Pulmonology

FIGURE 1.189: Thymoma. CT chest showing anterior mediastinalmass due to thymoma in a patient with myesthenia gravis.

Differential diagnosis of mediastinal mass lesionsAnterior 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

FIGURE 1.188: Bronchogenic Cysts.Three well-defined opacities seen inthe retrosternal area (arrows).


FIGURE 1.190: Retrosternal Goiter. Trachea beingcompressed and shifted towards right side (black arrow),widened superior mediastinum (white arrow).

FIGURE 1.191: Subcutaneous emphysema (arrows) in apatient with acute severe asthma without any pneumothorax.

119Pulmonology

FIGURE 1.192: Toxic Multinodular Goiter.Punctate calcification seen in the right upper zonedue to calcification in a large toxic multinodulargoiter with retrosternal extension (widenedsuperior mediastinum) (arrow).

FIGURE 1.193: Pulmonary translucencycomparatively more prominent on left sidebecause of absent breast shadow.


FIGURE 1.194: Calcification of tracheal rings; bronchiand 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.

121Pulmonology

FIGURE 1.196: Inadvertent aspiration of barium into the lungfields 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 seeninvolving the right lower lobe simulating consolidation,tappering apex towards the right hilum is apparent.


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 pulmonaryartery consistent with a pulmonary embolus.

123Cardiology


VALVULAR HEART DISEASES

MITRAL STENOSIS

The chest radiograph demonstrates selective left atrial enlargement, whichcan vary in severity.

Left atrial appendage may form a bulge on the left heart border justbelow the main pulmonary artery making the pulmonary conusprominent.

The atrium is large but the left ventricular contour remains smalleven in late stages. Small aortic knob is seen due to decreased leftventricular output.

If the mitral stenosis is both severe and long-standing thencalcification of the valve can develop, best visualized in lateral position.

Often there is upper lobe blood diversion, with enlargement of themain and central pulmonary arteries indicating pulmonary arterialhypertension.

The right-sided cardiac chambers will often be considerably enlarged.‘Double right heart border’ is present due to considerable enlargementof both atria.

Hemosiderosis and pulmonary ossified nodules may occasionally beseen.

BIBLIOGRAPHY

1. Chiles C, Putman CE. Pulmonary and Cardiac Imaging New York: Marcel Dekker.1997.

2. David Sutton. Text book of radiology and imaging (7th edn), Churchill Livingstone2003;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 thepresence of a high left atrial pressure, but acute pulmonary edema canoccur.

In the chronic phase, the heart tends to enlarge with a left ventricularconfiguration, left atrial enlargement being proportionately less promi-nent. In long-standing cases, however, there can be marked left atrialenlargement. Calcification of the valve does not occur. The pulmonaryvascular appearances are very similar to those of mitral stenosis but theheart size is often larger.

125Cardiology

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: JPLippincott, 1992.

3. Perloff JK, Roberts WC. The mitral apparatus: Functional anatomy of mitralregurgitation. Circulation 1972; 46:227.

AORTIC STENOSIS

Significant aortic stenosis may present with a virtually normal heartshadow, although it is rare. Initially, concentric left ventricular hyper-trophy produces only some rounding of the cardiac apex (overall heartsize is normal), there is also dilatation of the ascending aortic arch.

The post-stenotic dilatation of aorta is variable. These appearancescan be difficult to detect in the older patient in whom the aorta oftenbecomes unfolded and slightly dilated.

On the lateral film, the presence of calcification in the position of theaortic valve is an important sign, usually indicating important valvestenosis.

In most cases of aortic stenosis the pulmonary vascularity is normalbut in advanced cases there will be left ventricular dysfunction andassociated changes of left heart failure.

BIBLIOGRAPHY1. David Sutton. Text book of radiology and imaging (7th edn). Churchill Livingstone;

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 rightventricular enlargement is visible with an upward turned apex.

The main pulmonary artery is often prominent, which is caused bypost-stenotic dilatation.Peripheral pulmonary vascularity is usuallynormal but oligemic lung fields may be seen.


2003;1: 378-9.2. Davies MJ. Pathology of Cardiac Valves. Butterworths. London, 1980; 131-7.


CONGENITAL HEART DISEASES

TETRALOGY OF FALLOT’S

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 hypoplasticmain pulmonary artery.

2. Upward prominence of the cardiac apex due to distortion by thelarge right ventricle.

3. Pulmonary oligemia.4. In some cases right sided aortic arch.

BIBLIOGRAPHY

1. David Sutton. Text book of radiology and imaging (7th edn). Churchill Livingstone;2003;1: 382-3.

2. Elliott LP. Cardiac Imaging in Infants, Children and Adults. Philadelphia: JBLippincott, 1991.

TRANSPOSITION OF THE GREAT ARTERIES

D-loop Transposition

The chest X-ray is often, but not always, characteristic. The heart isslightly enlarged and rounded, generally biventricular enlargement withan 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 heartborder due to the abnormal leftward origin of the aorta.

A significant proportion of these patients have chest X-raysindistinguishable 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; Textbookof Angiocardiography. London; Futura. 1197.

ATRIAL SEPAL DEFECT

The chest X-ray is usually normal if the pulmonary-to-systemic flowratio is less than 2:1.

127Cardiology

If ratio exceeds this level there will be pulmonary plethora and cardiacenlargement. The cardiac enlargement is mainly due to right atrial andright ventricular dilatation.

In patients with significant pulmonary arterial hypertension (usuallythe elderly untreated patients), the chest X-ray will show dramaticappearances of central dilated pulmonary arteries and peripheralpulmonary vascular ‘pruning’. Left atrium and left ventricle are normal.Aorta is small.

BIBLIOGRAPHY

1. David Sutton. Text book of radiology and imaging (7th edn), Churchill Livingstone;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 ininfancy with right heart failure and poor forward flow to the pulmonaryartery. The chest X-ray in these cases may show massive globular cardio-megaly with pulmonary oligemia. The mildest expression occurs in someadults who present with mild signs or symptoms and a virtually normalchest X-ray.

BIBLIOGRAPHY


2. Elliott LP. Cardiac Imaging in Infants, Children and Adults. Philadelphia: JBLippincott, 1991.

PULMONARY VENOUS HYPERTENSION

The chest X-ray appearances of pulmonary venous hypertension arecharacterized 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.


5. Chronic changes are associated with Kerley B lines (horizontalsubpleural 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 horizontaland 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 beassociated with the development of hemosiderosis (appears as finepunctate calcifications that are scattered throughout both lungs).

9. Pulmonary ossific nodules (small areas of bone formation) can developif 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 thiscondition, it is a useful adjunct. It will be normal in the acute phase inthe majority of patients.

The chest radiograph provides some insight into the severity of themyocardial infarction.

The most common feature identified is the development of pulmonaryedema. Pleural effusions can develop if the left heart failure is prolonged.Progressive enlargement of the heart can occur, more often in anteriormyocardial infarction.

Several of the important complications of an acute myocardialinfarction can be suggested from the plain chest radiograph. If a leftventricular-aneurysm develops it is revealed as a localised bulge on theleft 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.


129Cardiology

CONGESTIVE CARDIAC FAILURE

The usual signs are cardiomegaly with left ventricular enlargement, andpulmonary venous hypertension signs. Pleural effusion is common(bilateral or right sided; unilateral left sided effusions rare and suggestsanother 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 ofall four chambers or of just the left ventricle. In the untreated patientthere is often volume overload of the left atrium leading to engorgementof the pulmonary vasculature. The diagnosis cannot be made on thechest radiograph alone.

BIBLIOGRAPHY


PERICARDIAL EFFUSION

The appearances that can be identified on the plain film depend on theamount of fluid present. A very large fluid collection can cause massiveenlargement of cardiac shadow.

The cardiac shadow has a rounded, globular appearance with noparticular chamber enlargement being identified (water bottle cardiacsilhouette) and sharp cardiophrenic angles.

If large enough the effusion will lead to an obstruction of the venousreturn to the right heart, which produces clear rather than congested lungs.

A rapidly increasing heart size on serial films is seen as effusionaccumulates. On lateral view loss of retrosternal space and separationof retrosternal from epicardical fat “fat pad sign” could be seen.


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. Dresseler’s 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: ACompanion to Brauwald’s Heart Disease. 2nd Edition,Philadelphia; WB Saunders;1996.

CONSTRICTIVE PERICARDITIS

The heart is often normal in size but can be enlarged especially in effuso-constrictive form. Straightening of the right heart border and rougheningof the cardiac outline as a result of pleuro-pericardial adhesions couldbe seen. Calcification along the heart border is seen in approximatelyhalf 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 ofpericardial calcification and disease.

BIBLIOGRAPHY

1. Braunwald E, Lorell BH. Percardial disease. In braunwald E (Eds): Heart Disease. ATextbook of Cardiovascular Medicine. Saunders 1984;1470.

2. David Sutton. Text book of radiology and imaging (7th edn), Churchill Livingstone2003;1:307.

131Cardiology

Comment

The purpose of this book is to display mainly plain films and CT. Alsoother techniques of value in the investigation of cardiac abnormalityinclude:• Echocardiography• Magnetic resonance imaging• Selective coronary angiography• Radio-isotope studies.

The plain films, however, do remain the starting point for all theseinvestigations.


FIGURE 2.2: Coarctation of Aorta. Notching of the inferiorborders of the ribs posteriorly seen (arrows).

FIGURE 2.1: Coarctation of Aorta. Inferior rib notching moreon left side. Cardiomegaly with left ventricular prepon-derance.

133Cardiology

FIGURE 2.3: Coarctation of Aorta. Narrow arch anddescending 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 withprominent collateralization. CT oblique sagittal reconstruction demonstrating the CTappearances of coarctation with an associated calcified bicuspid aortic valve.

A B


FIGURE 2.5: Dextrocardia with scoliosis of the spine.

FIGURE 2.6: Dextrocardia with Situs Inversus. Stomachfundus visible under the right side of diaphragm

135Cardiology

FIGURE 2.7: Dextrocardia and Situs Inversus. Dextro-rotation of heart, fundal gas seen on right side.

FIGURE 2.8: Dextrocardia. Axial MRI T1 weightedimage showing dextrocardia.


FIGURES 2.9A AND B: Right Sided Aorta. (A) The shadowof the ascending aorta and aortic knuckle are clearly visibleon the right side of the mediastinum (arrow). The leftmediastinal shadow is devoid of aortic knuckle anddescending aortic shadow. (B) CT scan chest of the samepatient showing complete transposition of the aorta includingascending aorta, arch of aorta and descending aorta to theright side.

A

B

137Cardiology

FIGURE 2.10: Transposition of Great Arteries. Narrowmediastinum, pulmonary plethora with borderlinecardiomegaly.

FIGURE 2.11: Atrial Septal Defect (Ostium SecundumType). Cardiomegaly, prominent pulmonary conus, dilatedpulmonary vessels and pulmonary plethora seen.


FIGURE 2.12: Severe Mitral Stenosis. Cardiomegaly, dilatedpulmonary arteries, prominent pulmonary conus, upper lobediversion of blood vesseles and alveolar opacities (moremarked on the right side) due to pulmonary edema seen.

FIGURE 2.13: Prosthetic Valves (1) Mitral, (2) Aortic.Sternal sutures are also visible.

139Cardiology

FIGURE 2.14: Severe Aortic Stenosis. Marked cardio-megaly with left ventricular preponderance. Ground glassappearance of lung fields due to pulmonary edema. Post-stenotic dilatation of aorta is also seen (arrow).

FIGURE 2.15: Severe Mitral Stenosis. Cardiomegaly withprominent pulmonary conus, large pulmonary arteries, andupper lobe diversion with double atrial shadow visible.


FIGURE 2.16: Pulmonary Stenosis. Cardiomegaly with rightventricular 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. Prominentpulmonary conus and linear calcification seen in the area ofmitral valve (arrow).

141Cardiology

FIGURE 2.18: X-ray Barium Swallow (Lateral View).Indentation and displacement of the esophagus due toenlarged 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.


FIGURE 2.20: Post-tuberculous fibrothorax and constrictivepericarditis. Encasement of the heart in calcified pericardium.Calcified plaques are also visible in the right pleura.

FIGURE 2.21: Massive pericardial effusiondue to viral pericarditis.

143Cardiology

FIGURE 2.22: Massive pericardial effusion. Sharp margins ofthe heart shadow and clear lung fields. Pneumopericardiumis also seen, which was iatrogenic (arrow).

FIGURE 2.23: Constrictive Pericarditis. Linear rim ofpericardial calcification visible along anterior wall and apexof the heart (arrow).


FIGURE 2.24: Effusoconstrictive pericarditis due totuberculosis, Linear pericardial calcification are visible alongthe left border of the heart (arrow). Post-tuberculous scaringalso visible in right upper zone.

FIGURE 2.25: MRI of a patient with constrictive pericarditis,showing thickened pericardium and minimal pericardialeffusion, low signal on T-1 and high on T-2 images.

145Cardiology

FIGURE 2.26: Acute pulmonary edema due to left ventricularfailure 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 arteriesdistally. Hyperinflated lungs with flattening of domes ofdiaphragm.


FIGURE 2.28: Congestive Cardiac Failure. Cardiomegalywith pulmonary plethora and right sided pleural effusion.

FIGURE 2.29: Acute pulmonary edema due to left ventricularfailure giving bat’s wings appearance.

147Cardiology

FIGURE 2.30: Dilated Cardiomyopathy. Cardiomegaly withpulmonary plethora. Fluid is seen in transverse fissure(arrow).

Causes of gross cardiac enlargement

- Multiple valvular diseaseAortic, mitral valve (particularly with regurgitation)

- Pericardial effusion- Atrial septal defect (with Eisenmenger’s syndrome)- Cardiomyopathy- Ebstein’s anomaly


FIGURE 2.31: Dissecting Aneurysm of Aorta. Aneurysm ofthe arch and descending aorta (in a young patient) is seen.Associated conditions include Marfan’s and other connectivetissue disorders.

FIGURE 2.32: Dissecting Aneurysm. Aneurysm hasfurther progressed as compared to previous X-ray.

149Cardiology

FIGURES 2.33A AND B: (A) Aortic aneurysm causingwidening of superior mediastinum (PA view). (B) compressingthe esophagus (lateral view). The patient presented withdysphagia.

A

B


FIGURES 2.34A AND B: Aortic Aneurysm. Enlargement ofaortic arch almost reaching upto the anterior chest wallshowing calcification within it.

A

B

151Cardiology

FIGURE 2.35: Aneurysm of the ascending aorta seen as alarge rounded opacity in the right hilar region with wideningof mediastinum.

FIGURE 2.36: Left ventricular aneurysm following acutemyocardial infarction.


FIGURES 2.37A TO C: AorticDissection. Aneurysmal dilatationof the ascending aorta seen.Tortuousity and unfolding of aortacausing mediastinal wideningalso seen.

FIGURE 2.38: Left VentricularAneurysm. Coronal CT imagewith a calcified left ventricularaneurysm.

A

B

C

153Cardiology

FIGURES 2.39A TO C: Mediastinal and pericardiallipomatosis in an asthmatic patient with itrogenic Cushing’ssyndrome. (A) Chest X-ray shows cardiomegaly withobliteration of cardiophrenic angles bilaterally and smoothmediastinal widening. (B,C) CT chest shows fat depositionaround the heart and the mediastinum can be easilydistinguished from the anatomical structures.

A

B

C


FIGURE 2.40: Pneumopyopericardium. Massivecardiomegaly with air-fluid level seen within thepericardium bilaterally (arrows).

FIGURES 2.41A AND B: SVC Stent. (A) PA chest radiograph. There is an SVC stentin situ (arrow) with a soft tissue mediastinal mass. (B) Axial and coronal reconstructionCT images showing the stent in place with no evidence of flow within it and extensiveenhancing chest wall collaterals in keeping with recurring SVC obstruction syndrome.The patient was known to have a primary bronchogenic carcinoma.

A B

155Cardiology

FIGURE 2.42: Artificial pacemaker (Unipolar type) withcollapse-consolidation of left lung.

FIGURE 2.43: Single chamber ventricular pacemaker.PA chest radiograph with a single chamber ventricularpacemaker in situ, the tip of the lead is normallyprojected to the left of the spine.

157Barium Studies and Oral Cholecystography


REFLUX ESOPHAGITIS

The earliest changes of esophagitis are seen on endoscopy. It is onlywith more pronounced edema that the earliest change of a fine mucosalnodularity is seen on a double contrast barium swallow.

The collapsed esophagus show thickened longitudinal folds, whichwhen nodular, can give an appearance similar to that seen with varices.

Multiple fine ulcers give the mucosa a punctate or granular appearanceor larger discrete punched out ulcers develops.

Scaring produce permanent folds that radiate from the margins ofulcer. Severe scarring results in stricture formation which are usuallysmooth and long.

BIBLIOGRAPHY

1. Detection of reflux esophagitis on double-contrast esophagrams and endoscopyusing 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 bydegeneration of neurons of Auerbach’s plexus.

A barium swallow will show the gastroesophageal junction failing toopen fully and tapering to a ‘rat tail’ or ‘bird beak’ appearance. Intactmucosal folds can be traced through this narrowed segment. With time,the esophagus dilates, lengthens and becomes tortuous. Wheninvestigating achalasia by barium meal it is not always possible to excludegastric carcinoma as a cause.

BIBLIOGRAPHY

1. Kostic SV, Rice TW, Baker ME, et al. Timed barium esophagogram: A simplephysiologic assessment for achalasia. J Thorac Cardiovasc Surg 2000; 120(5): 935-43.

2. Radiographic evaluation of esophageal function. Gastrointest Endosc Clin N Am2005; 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, polypoidor plaque-like lesions.

In advanced esophageal carcinoma, barium radiology most frequentlyshows a stricture with an irregular lumen and rolled margins, unlike benignpeptic strictures which have a smooth lumen and tapered margins. Sometumors show pronounced ulceration, or are predominantly polypoid orspread submucosally; producing thick and irregular esophageal folds.

BIBLIOGRAPHY

1. Montesi A, Pesaresi A, Graziani L, Salmistraro D, Dini L, Bearzi I. Barium imagingof 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, mostlydue to matted hair (trichobezoar) or vegetable or fruit pith (phytobezoar),including chewed beetle nuts.

Barium outlines and often penetrates the mass, which often appearas 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 slightdepression in the form of an ulcer.

In advance carcinoma “meniscus sign” is produced by the margin ofthe 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 orfungating or may ulcerate or infiltrate. Some Adenocarcinoma producean excess of extra-cellular mucin, and such mucin–producing carcinomasmay show stippled calcification.


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 X-ray studies. Abdom Imaging. 2003; 28(4):486-91.

2. Ukrisana P, Wangwinyuvirat M. Evaluation of the sensitivity of the double-contrastupper 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 gastrointestinaltuberculosis. This feature is attributed to the abundance of lymphoidtissue (Peyer’s patches) in the distal and terminal ileum. Early changeson barium examinations reveal nodular thickening of mucosal folds withloss of symmetry in the fold pattern. Similar to Crohn’s disease, deepfissures, sinus tracts, enterocutaneous fistulae, and perforation can occur,although less commonly. A cobblestone appearance of the mucosa is afeature of Crohn’s disease rather than Tuberculosis. Ulceration may bedemonstrated on double-contrast examinations, typically perpendicularto the long axis of the bowel; these heal with the formation of shortannular strictures. The ileocecal angle is obliterated with a widely patentileocecal valve. Colonic involvement is characterized by a combinationof narrowings, deep ulcerations, and mucosal granulation producingnodularity and inflammatory polyps. Less common findings are aphthousulcers and a diffuse colitis. Changes are usually noted in the cecum,ascending and transverse colon. Bowel contour may be lost withasymmetry simulating Crohn’s disease. When a short segment isinvolved, the strictures are hour-glass shaped rather than the apple-core deformity associated with carcinoma. In some cases, they may beindistinguishable.

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 JGastroenterol 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 abnormalitiesforming the malabsorption pattern and include bowel dilatation, mucosalthickening, flocculations, segmentation and bowel dilution of barium inadvance cases. These patterns are mostly seen in small intestinal mucosaldisorders, but otherwise barium studies can absolutely be normal inconditions 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 thegluten (found in wheat, barley and rye).

The classical radiological feature is ‘jejunization’. Jejunal folds areeither widely separated or absent altogether and this feature isaccompanied by a paradoxical increase in ileal folds.

Unfortunately these classical features are often absent, and probablythe commonest feature is luminal dilatation.

Transient painless intussusception is common and may be seen duringfollow-through.

BIBLIOGRAPHY

1. La Seta F, Buccellato A, Albanese M, Barbiera F, Cottone M, Oliva L, et al. Radiologyand 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 ofadult celiac disease assessed by double-contrast small bowel enteroclysis. Eur JRadiol 1992;15(2):157-62.

3. Burrows FG, Toye DK. Coeliac disease. Barium studies. Clin Gastroenterol1974;3(1):91-107.

WORM INFESTATION

Ascaris lumbricoides appearance on contrast studies is characteristic oncethe worms have swallowed barium it is seen within their intestinal tractand worms appear as long narrow tubular defects.


Hookworm, Tapeworm, Strongyloides and Anisakis all parasite thesmall 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 andWilkins Company. 1981;411-38.

2. Reeder MM. The radiological evaluation of Ascariasis of gastrointestinal, biliaryand respiratory tracts. Semin Roentgenol 1998;33(1):57-78.

ULCERATIVE COLITIS

Double contrast barium enema is more accurate than the single contraststudy in revealing early disease and also to show the disease extent andseverity, but it cannot visualize alterations in mucosal vascular pattern.

There is inflammation and ulceration of the colon, the later being thecardinal radiological sign. The ulcers are usually widespread and shallow.There is loss of normal colonic haustra ‘Bamboo Colon’ in the affectedportions. Pseudopolyps can be seen in advance cases as projections intothe 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 ileumand incompetence of the ileo-caecal valve. Any barium examination isabsolutely contraindicated if there is evidence of toxic dilatation or whenthere 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.

CROHN’S DISEASE

Contrast studies remain the mainstay for the diagnosis and assessmentof both distribution and severity, predominantly because they are bestable to demonstrate mucosal pathology.

The radiological changes of Crohn’s disease can be generally groupedinto three categories; early, advanced and complicated.


Although the earliest endoscopic manifestation is hyperemiacombined with an altered vascular pattern, this cannot be demonstratedon contrast studies. Villous edema and blunting follow and are the earliestdetectable radiological change, manifested as a granular pattern on highquality contrast studies. Early ulceration is typically apthous, whichdescribes small, shallow, circular, discrete ulcers surrounded by anedematous halo. Again these are well demonstrated on high qualitycontrast studies. Granularity and apthous ulceration represent the earliestdetectable radiological changes and are the most challenging becausethey are subtle. As the features progress, ulceration becomes linear anddeeper, with typical transmural penetration accompanied by muralthickening. Mucosal edema and inflammation intervenes between theseulcers to cause characteristic ‘cobblestone’ appearance. Ulceration isfrequently patchy and also asymmetrical along the bowel circumference;indrawing at the site of ulceration may be accompanied by ballooningof the contralateral wall creating a characteristic pseudodiverticularappearance.

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 maybe 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 Crohn’s disease. J Fam Pract 1997;45(6):465-

6.

DIVERTICULAR DISEASE

The distribution and severity of diverticular disease remains bestdemonstrated by barium enema. The diverticula themselves appear asflask-like or rounded outpouchings. When seen en face they producering shadows. Differentiation form a polyp is a common problem butthe definitive signs are projection beyond the bowel wall and thepresence of a fluid level within it.


Muscular changes results in a serrated appearance, frequentlyaccentuated by pronounced and persistent spasm.

BIBLIOGRAPHY

1. Balthazar EJ. Diverticular disease. In: Textbook of Gastrointestinal Radiology. WBSaunders 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 Crohn’s disease. J Fam Pract 1997;45(6):465-6.

CARCINOMA COLON

Radiological diagnosis of the primary tumor occurs usually on bariumenema examination.

Any intraluminal shadow or line that cannot be confidently attributedto a normal feature must be viewed with suspicion. Frank carcinomatypically manifests as an annular, irregular, ulcerating lesion-giving riseto the classical “Apple-Core” appearance.

Carcinoma has abrupt, shouldered margins and as oppose to spasmnormal 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 spreadlocally in a plaque-like infiltrative fashion. Overall, barium enema detectsapproximately 85% of colorectal cancers.

Primary radiological diagnosis may also be achieved using othermodalities, notably CT.

BIBLIOGRAPHY

1. Gazelle GS, McMahon P, Scholz FJ. Screening for colorectal cancer. Radiology2000; 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 double-contrast barium enema: Its pathologic predictive value. AJR Am J Roentgenol1983; 141:965-70.


FIGURE 3.1: Achalasia of Cardia. Mega-esophaguswith abrupt termination is seen.

FIGURE 3.2: Achalasia of Cardia. Dilated and tortousesophagus with narrowing at lower end, no mucosalirregularity or shouldering is visible.


FIGURE 3.3: Achalasia of Cardia. There is agrossly dilated esophagus with narrowed distalend. No contrast seen in the stomach.

FIGURE 3.4: Aortic Aneurysm. A large aneurysm of descending aorta and aorticknuckle causing displacement of esophagus to the right side. Diverticulum is alsopresent in the upper esophagus on the left side (Zenker’s diverticulum). Hiatus herniais also seen.


FIGURE 3.5: Peptic Esophageal Stricture. There is smooth,long stricture in the mid and distal esophagus with proximalhold up of barium and gross dilatation, no ulceration, noshouldering, and no mucosal irregularity.

FIGURE 3.6: Peptic esophagitis showing, smooth shortstricture in distal esophagus. Granular mucosa is also seenabove the stricture (arrow).


FIGURE 3.7: Cork Screw Esophagus. There is narrowing ofdistal end of esophagus with proximal dilatation in lateralview. Tertiary contractions in AP view (Cork screw esophagus).

FIGURE 3.8: Esophagitis and paraesophageal hiatushernia. Mucosal irregularity at the distal end.


FIGURE 3.9: Hiatus hernia (paraesophageal) and a largeduodenal diverticulum is visible in the first part (arrows).

FIGURE 3.10: Carcinoma Esophagus. Narrow distal end,long irregular stricture and shouldering with dilated midthoracic and upper thoracic segments of esophagus.


FIGURE 3.11: Carcinoma Esophagus. Dilatedesophagus with irregular mucosa and fillingdefects seen in the lower half.

FIGURE 3.12: Carcinoma Esophagus. There ismarkedly dilated esophagus and incompletediverticulum seen in the upper part. Shoulderingand irregular short stricture distally.


FIGURE 3.13: Carcinoma Esophagus. Mucosal destructionand 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 theesophagus with filling defects. Shouldering is positive.


FIGURE 3.15: Carcinoma Esophagus. A growth is seen inthe upper thoracic segment of esophagus, as narrowing ofmucosal irregularity and barium hold up in proximal part.

FIGURE 3.16: Carcinoma Esophagus. Rat tail appearanceof distal esophagus with proximal dilatation and air fluid level.


FIGURE 3.17: Carcinoma Esophagus. A growth in theesophagus involving middle and distal parts with ‘rat-tail’appearance is visible.

FIGURE 3.18: Carcinoma Esophagus. There is a shortirregular stricture and dilated upper esophagus.


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, post-operatively. Gastric pull through with gastroesophagealanastomosis.


FIGURE 3.21: Carcinoma Esophagus. Long irregularstricture mid and lower esophagus with shouldering is visible.

FIGURE 3.22: Carcinoma Esophagus. Narrowing and ‘rattail’ appearance of distal esophagus with dilatation in themiddle and upper parts, air fluid level is visible. Spill over ofbarium into air passages on right side (arrow).


FIGURE 3.23: Esophagogastrostomy in a patient withcarcinoma-esophagus. Stomach has been pulled into thethoracic 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.Scarred–clover leaf shaped deformed duodenal cap withirregular and ill-defined duodenal mucosa (arrow).


FIGURE 3.26: Chronic Duodenal Ulcer and Duodenitis.Typical clover leaf /trifoliate shaped duodenal cap and ill-defined mucosal folds of duodenal loops (arrow).

FIGURE 3.27: Gastric ulcer. A gastric ulcer is visible in theupper part on the lesser curvature as an ulcer niche (arrow).


FIGURE 3.28: Gastric Outlet Obstruction. Dilated stomachwith food particles interspersed with barium.

FIGURE 3.29: Gastric outlet obstruction, markedly distended stomach is seen. There is no contrast beyond the antrum.


FIGURE 3.30: Calcified Hydatid Cyst. Normal barium mealwith multiple radiopaque gallstones, and a large calcifiedhydatid cyst is seen in the left lobe of liver (arrow).

FIGURE 3.31: Trichobezoars in a Psychiatric Patient. Well-defined rounded filling defects at the fundus, antrum andbody of the stomach (arrows).


FIGURE 3.32: Carcinoma Stomach. Narrow distalesophageal end with, non-distendibility of stomach withirregularity and destruction of gastric mucosa at greatercurvature and body of stomach.

FIGURES 3.33A TO C: Hernia of Morgagni. Herniation of stomach and part of intestineinto the thorax through a congenital defect in the left dome of diaphragm.

A B

C


FIGURE 3.34: Pseudopancreatic cyst, showing, J-shapedstomach, stretched and displaced to the left and inferiorlydue to smooth round to oval shaped mass in the lesser sac.

FIGURE 3.35: Carcinoma. Stomach extending up to the distalesophageal end. Irregular filling defect in the fundus withdistorted mucosal folds can be seen. A well-defined mass atlesser 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 ofdilated esophagus and in the stomach due to gastric outlet obstructionand irregularity at greater curvature with rounded filling defect.


FIGURE 3.38: Adenocarcinoma of the fundus ofstomach involving the distal esophagus. There isnarrowing of distal esophagus with shouldering andproximal dilatation of esophagus. Irregularity andmucosal destruction at fundus and at adjoining part ofthe body of stomach with nondistensibility.

FIGURE 3.39: Antral carcinoma with gastro-colic fistulaand dilated stomach. A filling defect in the lower part ofstomach prior to antrum with gastro-colic fistula.


FIGURE 3.40: Adenocarcinoma of stomach with Linitis-plasticus. A large filling defect in the fundus of stomach withnarrowing of stomach lumen.

FIGURE 3.41: Leiomyoma of Stomach. A well demarcated filling defect in the region of stomach fundus.


FIGURES 3.42A AND B: Carcinoma Stomach (LinitisPlastica) with Liver Metastasis. Grossly narrowed stomachlumen due to infiltrating carcinoma-Linitus Plasticus, and softtissue shadow due to enlarged liver also seen filling theconcavity of stomach at lesser curvature.

A

B


FIGURE 3.43: Carcinoma stomach (Linitus Plasticus) withmetastases in liver. Left lobe is enlarged and occupying theconcavity of the medial border of the stomach.

FIGURE 3.44: Carcinoma Stomach. A growth in the stomachwith distortion of mucosa involving greater curvature andbody of stomach.


FIGURE 3.45: Fistulus connection with biliary tree (post-endoscopic barium study, showing barium enetring inthe 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 stomachinvolving the body, antrum and greater curvature.

FIGURE 3.48: Pyloric stenosis (adult variety) due tocarcinoma. The growth is in the distal stomach andpylorus (arrow).


FIGURES 3.49A TO D: Duodenal Giardiasis. Multiple round nodules of uniformsize and shape distributed through out the duodenum.

A C

B D


FIGURE 3.50: Liver abscess in the left lobeexerting pressure over the lesser curvature andcompressing body and antrum of stomach.

FIGURE 3.51: Pneumoperitoneum. Free airunder left hemi-diaphragm (arrow). Barium spillin the peritoneum is also seen.


FIGURE 3.52: Duodenal diverticulum inpost-bulbar region.

FIGURE 3.53: A large duodenal diverticulum.


FIGURE 3.54: A diverticulum from 2nd part of duodenum canbe seen (arrow). Thickening of rugal folds of stomach.

FIGURE 3.55: Two Duodenal Diverticuli. One big anothersmall arising from 1st and 2nd part of duodenal looprespectively (arrows).


FIGURE 3.56: Carcinoma Duodenum. There is a spasticduodenal loop. Ill-defined irregular mucosa of duodenal loopcan be seen along with distended stomach.

FIGURE 3.57: Carcinoma Duodenum. A long filling defectwith 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 seenin small intestine on barium follow through (arrows).

FIGURE 3.59: Ascariasis. Long segmented tube like fillingdefect because of round worms seen in the small intestine(arrow).


FIGURE 3.60: Ileocecal Tuberculosis. Deformedcecum with terminal ileal loops showing narrowing andmucosal irregularity.

FIGURE 3.61: Intestinal Tuberculosis. Terminal ileumis showing multiple narrowings. Appendix is clearlyoutlined (incidental finding).


FIGURE 3.62: Ileocaecal Tuberculosis. There is deformity of cecum and irregularity of mucosa in the terminal ileum.

FIGURE 3.63: Crohn’s Disease. Multiple jejunal stricturesalternating with dilatations is seen (arrows).


FIGURE 3.64: Crohn’s Disease. Adherent small bowel loopsdisplaced in the pelvis with multiple strictures noted.

FIGURE 3.65: Crohn’s disease showing, multiplestrictures in jejunum with rose thorn ulcers(arrows) consistent with jejunitis.


FIGURE 3.66: Intestinal Tuberculosis. Deformed cecum, mucosal irregularity andnarrowing of terminal ileum and jejunum seen. Dilatation of ileal and jejunal loops,lobulated external compression on terminal ileum also seen (due tolymphadenopathy).

FIGURE 3.67: Intestinal tuberculosis, there is jejunal mucosal fold thickening and rose thorn appearance of proximal jejunal loops and multiple narrow segments.


FIGURE 3.68: Intestinal Tuberculosis. Multiple strictureswith dilatations of small intestine.

FIGURE 3.69: Malabsorption Syndrome. Multiplesegmented dilatations of small intestine with loss of villouspattern, clumping of barium (flocculations) and increaseddistance b/w loops of small bowel is seen.


FIGURE 3.70: Malabsorption syndrome due to coeliacdisease. Dilated edematous loops of small intestine,Thickened and blunt mucosal folds can be seen.

FIGURE 3.71: Intestinal Tuberculosis. Multipleintestinal strictures are seen.


FIGURES 3.72A AND B: Duodenal Lymphoma Barium Mealand Axial CT. Barium meal image showing luminal narrowingof the duodenum. Axial CT abdomen with oral contrast of thesame patient showing marked thickening of the duodenalwall with oral contrast passing through it. This was confirmedhistologically as a lymphoma in this AIDS patient.

A

B


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.

A B C


FIGURE 3.75: Ileocecal Tuberculosis. Distortion of terminalileum and cecum is visible on barium enema.

FIGURE 3.76: Chronic Ulcerative Colitis. Narrowing andloss of haustrations seen in the descending and sigmoidcolon with granular appearance of the mucosa.


FIGURES 3.77A AND B: Ulcerative Colitis. Hose pipeappearance, due to loss of haustrations and granularappearance of mucosa. Widened pre-sacral space.

A

B


FIGURE 3.78: Chronic Ulcerative Colitis. Ahaustral patternof transverse and descending colon with mucosal granularityand narrowing at hepatic flexure with irregularity indicatingmalignant change is visible.

FIGURE 3.79: Ulcerative Colitis. There is ahaustral, narroweddescending colon with serrated margins due to active ulcers.


FIGURE 3.80: Ulcerative Colitis. Loss of haustrations intransverse colon with granularity and pseudopolyps formation.

FIGURE 3.81: Ulcerative Colitis. Descending and sigmoidcolon show multiple ulcers and tube like appearance.


FIGURE 3.82: Imperforated anus seen on cologram.

FIGURE 3.83: Chronic Ulcerative Colitis. Narrow segmentdescending colon with proximal dilatation of transverse andascending colon can be seen.


FIGURE 3.84: Multiple Polyps. There are multiple filling defectsin 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 transversecolon is seen. Narrowing and ulcerations of transverse colon andhepatic flexure also present.


FIGURE 3.86: Non-rotation of the Gut. A large bowel-—rectosigmoid,descending colon, splenic flexure and transverse colon on the left side ofthe 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. Narrowedlumen; mucosal destruction (arrow), shouldering and soft tissue massinvolving cecum and proximal ascending colon and dilation of remainingascending and transverse colon up to splenic flexure.


FIGURE 3.88: Carcinoma Colon. Barium enema demons-trating, irregular and deformed cecum with annular narrowingand filling defects in ascending colon (arrow).

FIGURE 3.89: Carcinoma. Rectum showing narrow irregulardistorted lumen of rectum due to the growth.


FIGURE 3.90: Barium enema demonstrating, a growth that iscausing intussusceptions at recto-sigmoid junction. Meniscussign in the sigmoid colon.

FIGURE 3.91: Carcinoma Ascending Colon. A filling defectseen in proximal ascending colon with shouldering andmucosal distortion is seen.


Differential diagnosis of colonic strictures

Neoplastic- Carcinoma- Lymphoma- Peritoneal metastases

Inflammatory- Ulcerative colitis- Crohn’s disease- Pericolic abscess- Radiotherapy

Infectious- Tuberculosis- Ameboma- Schistosomiasis- Lymphogranuloma venereum

Ischemia/Infarction

Postsurgical

Extrinsic masses

FIGURE 3.92: Sclerosing Cholangitis. The gallbladder isopacified, intra-hepatic biliary duct dilatation and narrowingof pancreatic duct and proximal CBD (distal not visualized)also seen. A calcified hydatid cysts seen in the liver. Oralcholecystography (OCG) post-fatty meal.


FIGURE 3.93: Oral cholecystography in a patient withcholelithiasis. A filling defect at the fundus can be seen.There is air in the wall of the gallbladder (emphyse-matous cholecystitis) (arrow).

FIGURE 3.94: Oral cholecystography showingcholelithiasis. The gallbladder can be seen withmultiple filling defects.


FIGURE 3.95: Oral Cholecystography Gallstones. Few largenucleated filling defects in the region of fundus of gallbladderindicating multiple gallstones.

217Skeletal System


RHEUMATOID ARTHRITS

Bilateral, symmetric involvement of metacarpophalangeal, proximalinterphalangeal and carpal joints with similar involvement of the jointsof feet is the hallmark of rheumatoid arthritis, but any or every joint ofthe body can be involved. Atlantoaxial subluxation may develop due toweakening 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 dueto synovial inflammation in bursae, joint spaces and along tendonsheaths. Joint distension also follows an increase in synovial fluid.

2. Osteopenia:Interpretation is subjective and changes are seen only after loss of25-50% of the bone mineral has occurred.

Osteoporosis in rheumatoid arthritis may be generalized due tosteroids or prolonged recumbency, or localized due to synovialinflammation (juxta-articular osteopenia).

3. Joint space changes and alignment deformities:In the early stage a joint space may be widened by synovialhypertrophy, inflammation and an effusion.

In the later stage joint spaces narrow due to cartilage destructionby pannus. Alignment abnormalities at joints may result from localsynovitis weakening the capsule and tendonitis.

Deformities of the joints can be seen radiologically. Atlanto-axialsubluxation occur with loss of odontoid peg and narrowing of discspaces, potentiated by laxity of ligaments around the peg.

4. Periostitis:Local periosteal reactions occur either along the midshaft of a phalanxor metacarpal as a reaction to local tendonitis, or at the metaphysisnear a joint affected by synovitis.

5. Erosions:These are the most important diagnostic lesions but are not alwayspresent. Classic periarticular erosions occur at the so-called ‘bare areas’of bone between the edge of the articular cartilage and the attachmentof the joint capsule. Erosions appear earlier and are more often seenin the feet bones, involving typically the lateral side of the fifthmetatarsal.

219Skeletal System

BIBLIOGRAPHY

1. David Sutton. Text book of radiology and imaging (7th edn). Churchill Livingstone;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 isnot specific to osteoporosis and can be seen in a variety of conditions.In osteoporosis trabecular loss is most evident radiographically in thespine, where there is loss of density, which may be appreciated as‘penciling in’ of the vertebra by the more radiographically dense end-plates. Biconcave vertebral bodies (cod-fish vertebrae) may occur.Endosteal and intracortical resorption of bone is prominent, producingcortical thinning most evident in the appendicular skeleton. The loss ofbone mass gives rise to increased incidence of fractures, particularly inthe femoral neck, spine (compression fractures), distal radius and pubicsymphysis.

BIBLIOGRAPHY


2. Iqbal MM. Osteoporosis: Epidemiology, diagnosis, and treatment. South Med J2000; 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 MineralMetabolism. Fourth Edition. Hagerstown, MD: Lippincott Williams and Wilkins;1999;160-5.

OSTEOARTHRITIS

Classic features include non-uniform joint space loss, subchondralsclerosis, osteophytes formation, subchondral cysts, and absence oferosions. Herberden nodes (osteophytes at distal interphalangeal joints)and Bouchard nodes (osteophytes at proximal interphalangeal joints)are commonly seen.


Superior or superolateral migration of femur within hip joint withbuttressing of medial femoral cortex can occur. Medial femoro-tibialcompartment is most commonly involved in knee. Sclerosis andnarrowing of intervertebral apophyseal joints is also common. Commonlyinvolved joints are distal interphalangeal joints of the fingers; firstcarpometacarpal joint; hips; knees; first metatarsophalangeal joints; andspine.There may be differences in the radiological appearances ofosteoarthritis at different joints, degenerative disease has a number ofspecific features whenever it occurs i.e. joint space narrowing due tocartilage destruction and then joint remodeling with loss of underlyingbone in stressed areas, and formation of new bone and cartilage in non-stressed areas and at joint margins, so that joint alignment alters. Loosebodies are formed by detachment of osteophytes, crumbling of articularsurfaces or ossification of cartilage debris. When osteoarthritis resultsin pain and immobility, osteoporosis and soft tissue wasting may resultsecondarily.

BIBLIOGRAPHY


2. Lane NE, Kremer LB. Radiographic indices for osteoarthritis. Rheum Dis ClinNorth 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 orderof 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 mineralizedepiphyseal centers with delayed appearance, increased distance betweenend of a shaft and epiphyseal center, cupping and fraying of metaphysisare commonly seen.

‘Rachitic rosary’ at costochondral junctions of middle ribs; thoracickyphosis with a ‘pigeon chest’ and bossing of the skull may occur.

In late stages a generalized reduction in bone density is seen, and inlong-standing cases fractures may occur.

Skull may be affected if process begins early. Usual supine positionof infant causes posterior flattening; this produces craniotabes, orsquarrying of calvarium.

221Skeletal System

Deformity is most marked at long bones, where bowing is evidentsecondary to asymmetric musculotendinous pulls on weakened growthplate. Scoliosis and pelvic changes occur later in process.

BIBLIOGRAPHY


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. HospMed 1998; 59(5): 399-403.

4. Silverman FN, Kuhn JP. Metabolic abnormalities of the skeleton. In: Caffey’sPediatric X-ray Diagnosis: An Integrated Imaging Approach. Ninth Edition. Mosby-Year Book 1993;666-74.

OSTEOMALACIA

The hallmark of osteomalacia are pseudo-fractures or ‘Looser’s zoneswhich are narrow zones of lucency, usually running perpendicular ornearly perpendicular to the bone cortex. Initially Looser’s zones arepoorly defined, these zones become progressively more prominent, withsclerotic 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 thevertebral bodies, and loss of vertebral height in a characteristic ‘codfishvertebra’ pattern. Bowing of long bones may also occur. Compressionwedge fractures of the vertebra are less common than in osteoporosis.

BIBLIOGRAPHY

1. David Sutton. Text book of radiology and imaging (7th edn). Churchill Livingstone2003;2:1354.

2. Renton P. Radiology of rickets, osteomalacia and hyperparathyroidism. HospMed 1998; 59(5): 399-403.

3. Steinbach HL, Noetzli M. Roentgen appearance of the skeleton in osteomalaciaand rickets. AJR Am J Roentgenol 1964; 91: 955.

GOUT

Classic features include tophi, normal mineralization, preserved jointspaces, marginal punched-out erosions with overhanging borders andsclerotic edges, and asymmetrical polyarticular distribution.


Classic location is 1st metatarso-phalangeal joint, but any metatarso-phalangeal joint may be involved. Gout tends to attack the distal andproximal interphalangeal joints, whereas rheumatoid arthritis affects themetacarpophalangeal 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 precipitatesin juxta-articular soft tissue mass, usually along extensor surface ofjoint.

Bilateral olecranon bursa effusion is characteristic. Erosions tend toappear near joint margins. As they enlarge, they tend to involve moreof the cortex of the shaft rather than the articular surface. Cartilagedestruction is relatively late manifestation.

BIBLIOGRAPHY

1. Bloch C, Hermann G, Yu TF. A radiologic reevaluation of gout: A study of 2000patients. AJR Am J Roentgenol 1980; 134(4):781-7.

2. David Sutton. Text book of radiology and imaging (7th edn). Churchill Livingstone2003;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 themiddle phalanx of the middle and index finger, is virtually pathogno-monic. Intracortical bone resorption is another feature of hyperpara-thyroidism which gives rise to small oval or cigar-shaped lucencies withinthe cortex. In the skull, a characteristic granular or mottled appearancemay occur, giving rise to the so-called ‘pepper-pot’ or salt-and-pepper’skull.

Subperiosteal resorption is also seen at medial aspect of femoral neckand proximal tibia, humerus and the ribs.

Subchondral bone resorption is another common feature, being foundat the distal and sometimes proximal end of the clavicles, symphysispubis and sacroiliac joints. This may occur at he vertebral end-plates,which may permit disc herniation (Schmorl’s nodes).

Subligamentous resorption at ischial/humeral tuberosity, greater/lesser trochanter of femur also occur.

223Skeletal System

Brown tumor (osteoclastoma) is lytic, expansile lesion usually in thepelvis, jaw, rib, facial bones. It is more common in primary hyper-parathyroidism, but because secondary hyperparathyroidism is moreprevalent, it is usually seen in secondary hyperparathyroidism.

‘Rugger jersey’ spine; due to osteosclerosis of vertebral endplates isusually seen in secondary hyperparathyroidism.

Chondrocalcinosis is more common in primary HPT. Periostitis andsoft 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


2. Gleason DC, Potchen EJ. The diagnosis of hyperparathyroidism. Radiol Clin NorthAm 1967; 5(2): 277-87.

3. Mayo-Smith W, Rosenthal DI. Radiographic appearance of osteopenia. Radiol ClinNorth Am 1991; 29(1): 37-47.

4. Pugh DG. Subperiosteal resorption of bone, a roentgenologic manifestation ofprimary hyperparathyroidism and renal osteodystrophy. AJR Am J Roentgenol1951; 66: 577-86.

ANKYLOSING SPONDYLITIS

Changes are most prominent in the axial skeleton with bilateral symmetricdistribution. Initially small erosions and sclerosis of Sacroiliac jointpredominantly on iliac side occur with progression to sacral side andultimately ankylosis. Similar changes in pubic symphysis are seen. Spinalchanges without sacroiliac changes are very rare in this disease. Erosionof vertebral margins heal by proliferation of sclerotic bone, which standsout 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 evenbefore.


Marginal syndesmophytes formation are common. Atlantoaxialsubluxation is seen. Osteoporosis, erosions and joint space narrowingare less prominent in peripheral joints, but shaggy periostitis andankylosis 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):

147-50.4. David Sutton. Text book of radiology and imaging (7th edn). Churchill Livingstone;

2003;2:1218-20.

ACROMEGALY

The radiographic features of acromegaly include enlarged mastoid aircells and sinuses, frontal bossing and prognathism.

Pituitary fossa enlargement may be seen on the plain film, althoughCT or MRI is more helpful in evaluating a pituitary adenoma.

In the spine, enlargement of the vertebral bodies with posteriorscalloping is seen.

The hands show characteristic enlargement of the bones and softtissues with spade-like terminal tufts, or arrowhead distal phalanges.

Widening of joint spaces due to overgrowth of articular cartilagemay 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


2. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science 1998;332.

225Skeletal System

MULTIPLE MYELOMA

Radiology plays an important part in the initial diagnosis of the disease.The two cardinal features are generalized reduction in bone densityand localized areas of translucency in red marrow areas. The axialskeleton, therefore, is affected predominantly. Lesions may also beobserved in the shafts of long bones and in the skull. Within spine,vertebral body is usually affected, while pedicle is usually spared. Thisdifferentiates myeloma from metastatic disease which affects pediclemore frequently.

Mandibular involvement is more common than in metastases. Focal‘punched out’ lytic lesions of relatively uniform size with endostealscalloping are very suggestive of multiple myeloma. Larger coalescentlesions are more characteristic of metastases. Isotope bone scans aregenerally negative with no appreciable uptake. Periosteal reaction israre. Soft tissue mass may accompany lesion in vertebral body and ribs,resulting in paraspinal/extrapleural mass. Osteosclerosis is uncommonmanifestation; usually seen after chemotherapy or radiotherapy or afterpathologic fracture. Pathological fractures are very often the initiatingfactor in the diagnosis of the disease.

BIBLIOGRAPHY

1. Greenspan A. Malignant bone tumors II. In: Greenspan A (Eds): Orthopedicradiology: A practical approach (3rd edn). Philadelphia; Pa: Lippincott Williamsand Wilkins, 2000; 697-700.

2. Ludwig H, Kumpan W, Sinzinger H. Radiography and bone scintigraphy inmultiple 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. SkeletalAbnormalities 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, especiallyfemur, tibia, and humerus in decreasing order; 50-75% of cases occuraround the knee.

Metaphyseal location is characteristic; however, infrequently diaphysismay be primary site of involvement.

Mixed lytic and sclerotic pattern is most typical, a florid spiculatedperiosteal reaction is present, the so called ‘sunray appearance’; purely


lytic pattern is encountered in telangiectatic variety which is extremelyvascular, usually poorly defined with soft tissue component.

Elevation of the periosteum is associated with new bone formation,the so called Codman’s triangle. Transphyseal spread is common evenbefore closure.

BIBLIOGRAPHY

1. David Sutton. Textbook of radiology and imaging (7th edn). Churchill Livingstone;2003;2:1261-8.

2. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science;1998;310.

METASTATIC DISEASE

The later stages of many malignant neoplasms are associated withmetastasis, and the skeleton is very commonly affected. Bony metastasisis present in approximately 25% of all deaths from malignant disease.

CT or MRI can detect bone metastasis at an early stage as comparedto plain radiograph. Multiple lesions are more likely than solitary lesion.Solitary focus may simply mean that another lesion has not been imagedor is currently undetectable on plain radiograph.

The spine, pelvis and ribs are the most common sites involved, thenare proximal ends of humeri and femora and, less often, the skull. Theseareas 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 extendin all directions, destroying the cortex, usually without the developmentof much periosteal reaction. Osteoblastic lesions produce dense and oftenwell-circumscribed areas of increased radiopacity. Purely osteolyticlesions 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 themost frequently involved site, especially vertebral bodies and pediclesof thoracolumbar spine. When long, tubular bones are involved, it isusually the proximal metaphyseal region of femur and humerus whichare involved.

227Skeletal System

BIBLIOGRAPHY

1. Bellamy EA, Nicholas D, Ward M, Coombes RC, Powles TJ, Husband JE.Comparison of computed tomography and conventional radiology in theassessment of treatment response of lytic bony metastases in patients withcarcinoma 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 “POTT’S DISEASE”

Most of the lesions occur in or below the midthoracic spine andinvolvement of the cervical and upper thoracic spine is uncommon.

Vertebral bodies may be first affected at three places, i.e. the upperor 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 partsof the vertebrae are most affected, causing anterior collapse or wedgingand posterior gibbus formation.

Abscesses form early and are easily seen in the thoracic region incontrast to the radiolucent lungs. In the lumbar region, lateral bulgingof 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 spreadsunder the anterior common ligament. Disc destruction may be late andthe anterior erosions difficult to detect.

MRI is the most useful form of imaging for the diagnosis of Pott’sdisease, from early lesions to extensive form of the disease.

BIBLIOGRAPHY

1. Boxer DI, Pratt C, Hine AL, M McNicol. Radiological features during and followingtreatment of spinal tuberculosis. Br J Radiol 1992; 65:476-9.

2. Lindahl S, Nyman RS, Brismar J, et al. Imaging of tuberculosis. IV. Spinalmanifestations 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.


SINUSITIS

Acute sinusitis is often due to secondary bacterial infection following aviral infection of respiratory tract.

The infection causes swelling of the mucosa, which appears as anopaque rim around the periphery of the sinus. An opaque sinus on plainX-ray may indicate fluid level in the sinus for which a tilted view shouldbe obtained.

Rarely there is involvement of bone which results in loss of outlineof the sinus wall followed by frank osteolysis and bone destruction.

In chronic sinusitis, CT is the investigation of choice as this definesthe degree and extent of involvement of the paranasal sinuses and alsoprovides the surgeon anatomical information before surgery.

BIBLIOGRAPHY


2. Smam PM, Brandwein M. Sinonasal Cavities. Inflammatory diseases, Tumours,Fractures, and postoperative Findings in Head and Neck imaging. Eds Peter MSam, 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’ differentiatesosteopetrosis from the other sclerosing dysplasias.

The ‘bone within a bone’ may be vertical in the long bone shafts anddigits, transverse at the metaphyses or beneath the iliac crests.

In long bones the ‘Erlenmeyer flask’ deformity due to failure ofmetaphyseal remodeling, giving gross distal undertubulation, and thepresence of dense bone, vertical fine lucencies extending to metaphysesare also present.

The bones of the skull base are initially affected with sclerosis andthickening, prominent in the floor of the anterior cranial fossa.

The medulla in the proximal skeleton is primarily involved and theperiphery spared. Mild, uniform increase in density may be seen.

BIBLIOGRAPHY


2. El-Tawil T, Stoker DJ. Benign Osteopetrosis: A review of 42 cases showing twodifferent patterns. Skeletal Radiology 1993;22:587-93.

229Skeletal System

MYCETOMA (MADURA FOOT)

Mycetoma implantation occurs mainly in the (bare) feet in semi-desertregions throughout the tropics. The skull and knees may also beimplanted, 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 corticesand cause cystic defects in the medulla. With superadded infection viathe implantation track, gross bone destruction results.

Reactive sclerosis and a shaggy periostitis with bone resorption givean appearance of ‘melting snow’.

BIBLIOGRAPHY


2. Renton P. Radiology of the foot. In Klenerman L (Eds). The foot and its disorders,Third Edition. Oxford: Blackwell Scientific; 1993.


FIGURE 4.1: Spina Bifida – S1. Sacralizationof 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 increasedintracranial pressure.

231Skeletal System

FIGURE 4.3: Osteopetrosis (Marble Bone Disease). X-raydorso-lumbar spine. There is generalized increased bonedensity, ‘Bone within a bone’ appearance. Erlen-Mayer Flaskshaped deformity of proximal femur.

FIGURE 4.4: Osteopetrosis. There isgeneralized increased bone density.


FIGURE 4.5: Osteopetrosis. X-ray dorso-lumbar spine showinggeneralized increased bone density seen in vertebral bodies andribs. Central horizontal band of translucency noted givingappearance of a sandwich.

FIGURE 4.6: Osteopetrosis (Marble Bone Disease). Diffuseincrease in bone density spine ribs. Pelvic bones show bone withinbone appearance.

233Skeletal System

FIGURES 4.7A AND B: Mucopolysaccharidosis Type 4(Morquio’s Disease). Kyphosis seen in dorso-lumbar spine, everydistal vertebra is shifted posteriorly in relation to upper ones. Centralbeaking 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.

A B

C D E


FIGURE 4.8: Mucopolysaccharidosis. Biconvex lumbar vertebra,D-12 is slightly shifted forward in relation to L1 can be seen. Tonguelike 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.

235Skeletal System

FIGURES 4.10A AND B: Osteomalacia showing, deformity ofpelvis, rugger jersy spine, diasthesis of right sacroiliac joint andprotrusio – acetabuli.

FIGURE 4.11: Osteomalacia, showing Looser’s zone in superiorand inferior pubic rami (arrows) and deformed pelvis.

A B


FIGURES 4.12A AND B: Osteomalacia with secondaryhyperparathyroidism in a patient with malabsorption. Incompletefracture of fibula with pseudofracture (Looser’s zone) both fibularproximal shafts and osteopenia (arrows).

A

B

237Skeletal 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 skullwith thin calvarium.


FIGURE 4.15: Idiopathic Sub-cutaneous Calcification. X-rayhands and wrist, showing popcorn type subcutaneous calcificationaround terminal phalanges in multiple fingers. Serum calcium,phosphate, alkaline phosphatase, serum PTH, uric acid levels werenormal. Fingertips were swollen, tender and gritty on feeling.

FIGURE 4.16: Hyperparathyroidism. Grossly deformed pelvis withfracture of superior and inferior pubic rami and thinning of cortex offemur.

239Skeletal System

FIGURE 4.17: Pseudohypoparathyroidism showingshort 4th metacarpal of either ring fingers.

FIGURE 4.18: Renal osteodystrophy with secondary hyperpara-thyroidism. X-ray lumbosacral spine (Lateral view) showing,increased bone density especially in vertebral end plates withcentral lucent bands ‘Rugger-jersy spine’.


FIGURE 4.19: Acromegaly. Large frontal, ethmoid, maxillarysinuses. Enlarged mandible (Prognathism).

FIGURE 4.20: Acromegaly. Enlarged frontal and maxillary sinuses.Enlarged skull (Macrocephaly). Ballooning of pituitary fossa withthinning of dorsum sella.

241Skeletal System

FIGURES 4.21A AND B: Acromegaly. There is marked expansion of the frontalsinuses. The pituitary fossa appears to be larger than normal. Erosion of posteriorclinoid process also noted.

A B

FIGURE 4.22: Rickets. Metaphyseal cupping, splaying and wide zone of provisionalcalcification at upper end of humerus and distal end of radius and ulna, proximal endof tibia and fibula with bowing and soft tissue swelling at wrist and knee joints andricketic rosary – wide anterior rib ends and generalized osteopenia.


FIGURE 4.23: Rickets. Lower end of radius and ulnashowing splaying, fraying and cupping at themetaphyseal end along with soft tissue swelling.

FIGURE 4.24: Rickets. Osteopenia in the metaphysesof both forearms, hands and wrists and soft tissueswelling of wrist. There are also metaphysealtransverse lucent bands of distal ends of both the radiusand ulna.

243Skeletal System

FIGURE 4.25: Rickets. Cupping, splaying, and frayingseen at the metaphyseal ends of femur, tibia and fibulawith soft tissue swelling seen.

FIGURE 4.26: Rachitic Rosary. Broadening of the anteriorribs seen (overgrowth of cartilage at the costochondraljunction) (arrows).


FIGURE 4.27: Scurvy. X-ray lower extremities with knee joint AP.Generalized osteopenia is seen. Pencil sharp outline of epiphysealcortex (Wimberger sign??). Metaphyseal sclerotic band— densezone of periosteal calcification, also liner soft tissue calcificationseen near the above end of the fibula.

FIGURES 4.28A AND B: Paget’s Disease of Bone. (A) Osteolytic andosteoblastic activity noted in the vault of skull. (B) X-ray hip AP showingosteoporotic changes in proximal shaft of femur with thinning of cortex. Scleroticand lytic changes seen in upper end of femur (neck and trochanteric regions).

A B

245Skeletal System

FIGURE 4.29: Juvenile Paget’sDisease. Osteolytic and osteoblasticactivity noted. Well circumscribedrounded sclerotic areas with centralosteolysis seen. The interveningbone is showing osteoporosis.

FIGURE 4.30: Chronic RheumatoidArthritis. Reduced/absent inter-carpal, carpometacarpal, metacar-pophalangeal and interphalangealjoint spaces and radio-carpal jointsspaces. Juxta-articular osteopenia,erosions and secondary osteo-arthritic changes also seen in someof the joints.

FIGURE 4.31: Rheumatoid Arthritis(Erosive Arthropathy). X-ray bothhands (PA view), showing destruc-tive, erosive polyarthropathy affec-ting the radiocarpal, midcarpal andthe small joints of both hands.Marked osteoporosis with multiplejoint subluxation.


FIGURE 4.32: Rheumatoid arthritis both hip joints, bilateralavascular necrosis of femoral heads – Drug induced (steroids).There is osteopenia, sclerosis, and fragmentation of femoral headsbilaterally. Fracture of right femoral neck is noted.

FIGURE 4.33: Rheumatoid Arthritis. Proximal interphalangealjoints showing arthritic change, reduced joint space andosteoporotic changes in the bones around the joints.

247Skeletal System

FIGURE 4.34: Rheumatoid Arthritis. X-ray hand (AP and lateralview) showing, narrowing of the joint spaces and osteopenia aroundthe metacarpophalangeal and interphalangeal joints. Inflammatorychanges also seen in the wrist joint.

FIGURE 4.35: Rheumatoid Arthritis. Reduced bone density, fusionof carpal bones with significant reduction of joint spaces in between.Reduced Interphalangeal joint spaces also present.


FIGURE 4.36: Rheumatoid Arthritis. Almost complete fusion ofcarpal bones with loss of carpal, carpo-metacarpal, and radio-carpal joints. There is significantly decreased metacarpo-phalangeal and interphalangeal joint spaces. There is subcorticalerosions seen in the metacarpal and interphalangeal joints. Juxta-articular osteoporosis noted at wrist and interphalangeal joints.

FIGURE 4.37: Rheumatoid Arthritis (Advanced). Loss of jointspaces, subluxation, erosion and decreased bone density seenin the joint.

249Skeletal System

FIGURES 4.38A TO D: Rheumatoid Arthritis. Narrowed joint spaces at elbow jointwith erosive changes seen at articular surfaces of humerous and ulna. Bone densityis reduced. Soft tissue swelling is also seen. Joints of the hands and wrists are alsoinvolved.

A

C

B

D


FIGURES 4.39A TO C: Rheumatoid Arthritis. An advance case ofrheumatoid arthritis with erosions and deformation of joints.Extensive destruction of the articular cortex of the metacarpo-phalangeal joints seen.

A

B

C

251Skeletal System

FIGURES 4.40A TO C: Rheumatoid Arthritis. Narrowed joint spaceswith erosions seen at metacarpo-phalangeal joints. Almostcompelete loss of inter-carpal joints i.e. matting. Overall reducedbone density noted. Reduced bone density. Arthritic changes seenin Talo-tibial and talo-calcaneal joints with reduced joint space.Arthritic changes alongwith reduced joint spaces also noted intarsal joints.Reduced bone density, diminished joint spaces.Subarticular sclerosis noted at both knees.

A B

C


FIGURE 4.41: Erosive Arthropathy in Psoriasis. X-ray of hand. There is acro-osteolysis of distal phalanges, sclerosis at middle phalanges, new boneformation, and loss of joint space between proximal and distal interphalangealjoints with expansion at the bases of proximal phalanges with subchondralsclerosis and loss of joint spaces at carpo-metacarpal joints.

FIGURE 4.42: Advanced secondary osteoarthritis in a patient with rheumatoidarthritis of both hip joints (Female pelvis). Excessive sclerosis seen in both hipjoints with loss of joint space in both hips. Bilateral protusio-acetabuli alsonoted.

FIGURE 4.43: Gout. X-ray right foot (AP view). There is sclerosis atmetatarsophalangeal joint of big toe with loss of joint space. Soft tissue swellingand juxta-articular erosions also seen. Bone density is preserved.

253Skeletal System

FIGURE 4.44: Ankylosing Spondylitis. X-ray dorso-lumbar spine(Lateral view).Calcification of anterior spinal ligaments and posteriorlongitudinal ligaments. Calcification and annular fibrosis (Bamboospine).

FIGURE 4.45: Ankylosing Spondylitis. X-ray dorso-lumbar spineshowing sclerosis of sacroiliac joints, tramline appearance of spineand bamboo spine.


FIGURES 4.46A AND B: Ankylosing spondylitis involving dorso-lumbarspine and sacro-iliac joint. Ossification of lateral, anterior and posterior spinalligaments seen (Bamboo shaped spine). Loss of joint spaces in both sacro-iliac joints.

FIGURE 4.47: Bilateral Sacroiliitis. Bilateral oblite-ration of sacroiliac joint alongwith arthritic changes ina patient with Inflammatory bowel disease.

A B

255Skeletal System

Causes of sacroiliitis

Unilateral:Most commonly infection but can becaused by most of the bilateral causes.

Bilateral:Ankylosing spondylitisInflammatory bowel diseaseReiter’s diseasePsoriaticRheumatoid arthritis (rare)

FIGURE 4.48: Ankylosing Spondy-litis. X-ray lumbo-sacral spine,showing syndesmophytes at lumbarspine, bilateral sacroiliitis, irregular,fragmented and sclerosed bothfemoral heads-bilateral avascularnecrosis, obliteration of joint spacesin both hip joint are also noted.

FIGURE 4.49: Reiter’s Disease.Arthritic changes seen in metacarpo-phalangeal and inter-phalangealjoints. Marked scoliosis noted at thesejoints especially in index finger andthumb. Overall bone density is reducedand expansion of the bases ofphalanges is noted. Some erosionsalso noted in subchondral regions ofmetacarpophalangeal and inter-phalangeal joints.


FIGURES 4.50A AND B: Cervical Myelogram (A/Pand Lateral View). Cervical spondylitis. Obstructionat the level of C-7 can be seen (Patient had presentedwith quadriparesis more marked in the lower limbs).

A

B

257Skeletal System

FIGURE 4.51: Myositis ossificans progressiva in case ofmixed connective tissue disease. Calcification in muscularsheaths pelvis, buttocks and ischial tuberosity also.

FIGURE 4.52: Myositis ossificans in a case of mixedconnective tissue sisease. Sub-cutaneous calcification withcalcification in muscles of the thigh.


FIGURES 4.54A AND B: Mixed Connective Tissue Disease.Sub-cutaneous and intramuscular calcification around the kneejoint and thigh, with contracture of knee joint and secondaryosteoporosis of bones.

FIGURES 4.53A AND B: Osteoarthrosis of Knee Joint. There isreduced joint space of medial tibiofemoral compartment withosteophytes on femur and tibial articular surfaces. Osteophyteson patella also seen.

A B

A

B

259Skeletal System

FIGURES 4.55A AND B: Advanced Osteoarthrosis withOsteoporosis. Marginal osteophytes (non-bridging) seenanterolaterally in lumbar vertebrae with reduced disc spaces at alllumbar vertebral levels and lower dorsal vertebral levels.

FIGURE 4.56: Osteoarthrosis of Spine. Degenerative changesand decrease disc space at L5-S1posteriorly. Tubular calcificationis also seen in abdominal aorta.

A B


Casuse of monoarthritis

- Infection:TuberculosisStaphylococcus aureus

- Trauma- Osteoarthritis- Neuropathic (including diabetes)- Gout and calcium pyrophosphate dihydrate

crystal deposition disease (CPPD)

Casuse of polyarthritis

- DegenerativeOsteoarthritis.

- NeuropathicDiabetes melitus.

- InflammatoryCTDRheumatoid (including SLE, scleroderma)Seronegative arthritis

Ankylosisng spondylitis, Rieter’s, psoriatic.- Crystal arthritis

Gout, CPPD

FIGURES 4.57A AND B: Cervical Spondylosis. Osteophytes at disc vertebrallevel of C2-C6 with reduced disc spaces b/w C5-6 and C6-7.

A B

261Skeletal System

FIGURES 4.58A TO C: Progeria. (A, B) X-ray skull showing osteoporosis, thin cranialvault, wormian bones, and hypoplastic maxillae and mandible. (C) X-ray pelvisshowing osteoporosis, short slender femora, and Coxa valga.

FIGURE 4.59: Tuberculous Osteomyelitis. X-ray foot (AP and Latview), showing calcification below 5th metatarsal base, and softtissue swelling with erosion of tarso-metatarsal joints (arrow).

A B C


FIGURES 4.60A AND B: Bone Tuberculosis. Circumscribed osteolytic lesion withsclerotic margins seen in the upper end of left femur (arrow) with erosions of thecortex 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 bonedensity. Absent left radius is also noted.

A B

263Skeletal System

FIGURES 4.62A AND B: Treated case of Pott’s disease. Partialcollapse and wedging of D4–D5 with sclerosis of the adjacentvertebral end plates and early spondylolytic changes.

FIGURES 4.63A AND B: Tuberculosis upper end of left femur.Lytic and sclerotic lesion seen in the upper end of left femur.

A B

A B


FIGURE 4.64: Tuberculosis of the spine with paraspinal abscess.Narrowing of the intervertebral space between L2-L3 vertebralbodies with erosion of the adjoining edges anteriorly with somesclerosis is seen. There is minimal anterior wedging of L1, L2 andL3 vertebral bodies. Associated paravertebral soft tissue shadowingis also seen. AP view is also showing similar changes.

FIGURE 4.65: Tuberculous spine D8-9 with para-spinal 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, andalso reduced disc space b/w D6-D7 and D7-D8.

Differential diagnosis ofparavertebral mass

Trauma/hematoma

Abscess- Staphylococcus aureus- Tuberculosis

Neoplasms- Lymphoma- Metastases

A B

265Skeletal System

FIGURES 4.66A AND B: Pott’s Disease. (A) X-ray LS spine lateralview showing involvement of the bodies of L1-L2 alongwithintervertebral disc and wedging of the bodies anteriorly. (B) Pott’sdisease dorsal spine with paraspinal abscess.

FIGURES 4.66C AND D: MRI clearly demonstrating destruction ofbodies of L1-L2 with some paraspinal collection. Marked indentationof thecal sac is apparent.

A B

C D


FIGURES 4.67A TO D: Pott’s Disease. MRI of same patientshowing involvement of D6-D10 vertebral bodies, intervertebraldiscs alongwith paraspinal abscess formation.

A B

C D

267Skeletal System

FIGURE 4.68: Paranasal Sinusitis. Soft tissue opacities in bothmaxillary sinuses can be seen. Nasal mucosal thickening is alsopresent. Frontal sinuses are enlarged with mucosal thickening.

FIGURE 4.69: Acute sinusitis with nasal mucosal thickening andfrontal sinusitis. Thickening of maxillary sinuses and haziness ofboth frontal sinuses more on right side can be seen. Soft tissueopacity in left maxillary sinus with air fluid level is also noted.


FIGURE 4.70: Leprosy. Erosion of terminalphalanges (fall off) is seen.

FIGURE 4.71: Diabetic Foot. Destruction of meta-tarsophalangeal joints and IP joints and loss of 3rd phalanxwith acro-osteolysis 4th and 5th distal phalanges.

269Skeletal System

FIGURE 4.72: Madura Foot (Biopsy Proved). Multiple osteoporoticand sclerotic areas seen in the tarsal and metatarsal bones.Erosions of some metatarsal shaft giving the soap bubbleappearance.

FIGURE 4.73: Madura Foot. Soft tissue swelling with diffuseosteolytic lesions in meta-tarsals and phalanges. Shaggy periostitiswith reactive sclerosis. Bone resorption also noted. Appearancesmimic Melting Snow.


FIGURE 4.74: Acute Osteomyelitis. Bony destruction seen inforearm. Periosteal reaction noted. Destructive process hasreached up to the epiphysis with soft tissue swelling.

FIGURE 4.75: Chronic Osteomyelitis. Lytic and sclerotic changesnoted in distal shaft of tibia and fibula with evidence of periostealreaction.

271Skeletal System

FIGURE 4.76: Chronic osteomyelitis of calcanium showingdestructive and sclerotic changes with soft tissue swelling.

FIGURE 4.77: Chronic Osteomyelitis. Lytic lesions,involucrum, sequestrum with sclerotic changes.


FIGURE 4.78: Chronic osteomyelitis, showing allcardinal features, i.e. destructive changes, periostealreaction, involucrum, cloacae and new bone formation.

FIGURE 4.79: Chronic osteomyelitis, showing cardinalfeatures, i.e. destructive changes, periosteal reaction,cloacae and sequestrum.

273Skeletal System

FIGURE 4.80: Osteomyelitis. Destructive and sclerotic lesions areseen. Sparing of epiphysis of the head of humerous, there is softtissue swelling with gap between gleno-humeral joint (effusion).

FIGURE 4.81: Diabetic Foot with Charcot Joint. There is soft tissueswelling, erosion of metatarsal and phalangeal bones. Noteamputation of big toe (arrow).


FIGURES 4.82A AND B: Septic Arthritis. Plain film andradioisotope bone scan of the wrist demonstrating ill-defined,osteopenic, mid carpal and radio-carpal joints with overlying softtissue swelling with a corresponding area of increased isotopeuptake on the delayed bone scan. This patient had a pathologicaldiagnosis of Staphylococcal arthritis.

A

B

275Skeletal System

FIGURE 4.83: Myelofibrosis/ Myelosclerosis. X-ray pelvis (APview) showing, patchy increased bone density and increasedtrabeculations.

FIGURE 4.84: X-ray legs acute leukemia showing generalizedosteopenia, and thinned cortex. Transverse lucent metaphysealband at distal ends tibia and fibula.


FIGURE 4.85: Multiple Myeloma. X-ray skull (Lateral view). Multiplepunched out lytic lesion in skull and mandible with endostealscalloping of inner table.

FIGURE 4.86: Advanced Case of Multiple Myeloma. X-ray pelvisincluding hips and proximal femur (Adult male). There isgeneralized reduction in bone density, with lytic lesions all over thevisualized skeleton and endosteal scalloping. Bilateral protrusio-acetabuli with deformed pelvis.

277Skeletal System

FIGURES 4.87 A TO C: Multiple Myeloma. (A) X-ray skull showingmultiple punched out lytic lesions. (B) X-ray pelvis showing multiplelytic lesions in pelvic bone. (C) X-ray dorsal spine showing lyticlesions in the ribs, dorsal spine, and collapse of D10, there is alsomultiple rib fractures (pathological) in left 7th and right 11th ribs.

A

B

C


FIGURE 4.88: Multiple Myeloma. X-ray skull AP view. There isdecreased bone density, extensive lytic lesions in skull, mandible,orbits and maxilla are present.

FIGURES 4.89A TO C: Multiple Myeloma. Punched out lytic lesionsand increased trabecular pattern with meshed osteoprosis.

A B C

279Skeletal System

FIGURE 4.90A: Thalassemia. X-ray both hands and forearms of achild. Showing widened, stubby metacarpal and phalanges andthinned cortex, also there is increased trabeculations,intramedullary permeation and lucencies. Same changes arepresent in radius and ulna and carpal bones.

FIGURE 4.90B: Thalassemia. X-ray skull (Lateral view). There isthickening of skull vault, osteopenia, and hair end on appearance.


FIGURE 4.91: Enlarged pituitary fossa due to pituitary tumor. Erosionof posterior clinoid process. Depression of floor of hypophysealfossa. Thinning of the posterior wall is also noted.

FIGURE 4.92: Pituitary Tumor. Dorsum sella is completelyeroded with thinning of the posterior wall.

281Skeletal System

FIGURES 4.93A TO D: Metastasis Lumbar Spine. X-ray shows reduced intervertebralspace in L1-L2 along with erosion and collapse of vertebral body of L2. MRI showingmetastatic deposits in L2 and L3 vertebrae with partial collapse of L2 indenting thethecal sac.

A B

C D


FIGURE 4.94: Osteosarcoma/Fibrosarcoma. Permeative lesionsat proximal femoral shaft meta-diaphyseal region with soft tissuemass, wide zone of transition with smooth displacement of fatplanes.

FIGURE 4.95: Metastases from Carcinoma Thyroid. Generalizedosteoporosis with multiple lucencies of varying sizes.

283Skeletal System

FIGURE 4.96: Metastases from Carcinoma of Prostate. X-raypelvis including hip joints (Male), showing lucencies and scleroticpatchy increased densities. Pathological fracture of inter-trochanteric region of left femoral neck also noted.

FIGURE 4.97: Carcinoma Bronchus with Metastasis. Lyticchanges seen in left 6th rib posteriorly. Left hila is enlarged.Inhomogeneous shadowing seen in right apex. Small pleuraleffusion at left costo-pherenic angle.


FIGURE 4.98: Osteoblastic lesions due to metastasis from carci-noma of prostate showing, multiple osteoblastic/osteoscleroticareas with osteoporotic zones in the pelvic bones.

Bone metastases (radiological appearances)

Lung- Carcinomas lytic- Carcinoid lytic or mixedBreastGenitourinary tract- Renal cell carcinoma lytic, expansile- Wilms tumour lytic- Bladder lytic, occasionally sclerotic- Prostate scleroticThyroid lytic, expansileGastrointestinal tract- Stomach sclerotic or mixed- Colon lyticAdrenal lyticSkin- Squamous cell Ca lytic- Melanoma lytic, expansileReproductive organs- Cervix lytic or mixed- Uterus lytic- Ovary lytic- Testis lytic

285Skeletal System

FIGURES 4.99A TO D: Ewing’s Sarcoma. (A) X-ray chest is showing large amount ofpleural effusion on right side. (B to D) CT chest reveals a large mass adherent to theright chest wall, protruding outside as well as extending into the thoracic cavity withmoderate amount of pleural effusion, the mass is showing central areas of necrosis.Biopsy proved it to be Ewing’s sarcoma.

A B

C D


FIGURE 4.100: Calcaneal spur in a patientwith painful heel.

FIGURE 4.101: Young’s Perthes disease. Sclerosis of femoralhead with fragmentation and widened metaphysis.

287Skeletal System

FIGURE 4.102: Exostosis–mid shaft ofhumerus with pathological fracture.

FIGURE 4.103: Charcot’s joint secondary to repeated intra-articularsteroid injections. Deformed knee joint with osteoporosis of bonesis noted. Calcification seen in the supra-patellar bursa and insidejoint cavity


FIGURE 4.104: Adolescent Kyphosis with Ostochondritis. X-raydorso-lumbar vertebrae (Lateral view). Khyphosis seen at dorso-lumbar region, Partial collapse of upper lumbar vertebrae alsonoted. Lower dorsal vertebrae are biconcave. Herniation of nucleuspulposus seen in the lower dorsal spine.

FIGURE 4.105: X-ray Pelvis. Bilateral osteitis condensa (normalvariant). The sacroiliac joint space is preserved.

289Skeletal System

FIGURE 4.106: Scleroderma. There is minimal arthritic changes atwrist joint, metacarpophalangeal joints, proximal and distalinterphalangeal joints and terminal bone resorption (Acro-osteolysis) (arrows).

FIGURE 4.107: Calcaneal spurring with calcification of thetendo-Achillese.


FIGURES 4.108A TO D: Hyperparathyroidism. (A) Nephrocalcinosis due to hyper-parathyroidism. (B) Multiple calcified densities seen in cortex and medulla. Sclerosisseen at the metacarpophalangeal joints. (C) Overall bone density is reduced in thewrist and hand. (D) Hyperostosis seen in the vault of skull, marked in the frontalregion.

A B

C D

291Skeletal System

FIGURES 4.109A TO C: (A,B) Pseudohypoparathyroidism showingintracerebral calcification on X-ray skull. (C) CT scan brain plainshowing extensive intracerebral calcification. Heavy calcificationseen within the basal ganglion and dentate nuclei. Parenchymalcalcification also seen bilaterally. No midline displacement.

A B

C


FIGURE 4.110: Non-ossified Fibroma/Fibrous Dysplasia. Lucentoval shaped, lobulated lesion with sclerotic margins in distal tibia(arrow).

FIGURES 4.111A AND B: Fluorosis. Ribs and other bones appearmarble white, bone contour is wooly and blurred especially in ribsdue to bone expansion and merging of trabeculae.

A B

293Skeletal System

FIGURE 4.112: Post-traumatic collapse and wedgingof L-2 vertebral body with osteoporosis (arrow). Discspaces are preserved. (Patient a truck driver had h/ojumping from the roof of his vehicle)

295Plain Abdomen and Intravenous Pyelograms


NEPHROCALCINOSIS

Morphologically, three types of calcifications have been described. Themost prevalent is a single cortical and thin peripheral band, often withcalcified extensions into the necrotic septa of Bertin (placed perpendicularto the cortical calcification). The medullary pyramids are usually spared,retaining the attenuation of the soft tissue. Initially, this pattern ofnephrocalcinosis may be difficult to recognize because calcification isfaint.

However, the kidney margins appear well-defined and appearpenciled in.

The second pattern seen with cortical nephrocalcinosis is theappearance of hyperattenuating tram lines. These lines may be continuous.More often, they are interrupted, reflecting more patchy distribution ofcortical necrosis.

The third pattern is a more diffuse distribution of punctatecalcification. This punctate pattern of calcification is thought to representnecrotic calcified glomeruli and tubules.

Medullary nephrocalcinosis typically produces clusters of stippledcalcifications, mainly within the regions of the renal pyramids.

BIBLIOGRAPHY

1. Akhan O, Ozmen MN, Coskun M. Systemic oxalosis: Pathognomonic renal andspecific extrarenal findings on US and CT. Pediatr Radiol 1995; 25(1): 15-6.

2. David Sutton. Text book of radiology and imaging (7th edn), Churchill Livingstone2003;1: 977.

3. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science;1998;232-3.

RENAL CALCULI

Radiodense stones suggest either calcium or struvite composition, butstruvite stones are usually large and fill the calyceal system. Cystinestones appear to be radiodense, but less dense than calcium-containingstones. Small, radiolucent stones suggest uric acid composition. Uricacid stones appear as filling defects on intravenous pyelography. Fillingdefects that occupy the renal pelvis are staghorn stones and may be ofstruvite, uric acid, or cystine composition. Sludge may be of either uricacid or cystine, can fill the renal pelvis, and cause obstruction. Plainradiographs of the abdomen can identify stones of greater than 3 mmsize. 80% of ureteric calculi are radiopaque, seen at the anatomic


narrowing (ureto-pelvic, ureto-vesicle junctions and the site where theureter crosses the sacrum and iliac vessel).

Mostly are calcium oxalate and phosphate stones. Up to 10% of thestones are composed of struvite (magnesium, ammonium phosphate)which are usually poorly radiopaque.

BIBLIOGRAPHY

1. David Sutton. Text book of radiology and imaging (7th edn), Churchill Livingstone;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 radiographand 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 polycystickidney disease (APKD). Hyperdense cysts on CT in ADPKD are seen in68% of cases. On unenhanced CT, they are seen as multiple, sharplycircumscribed cysts, generally subcapsular in location with attenuationvalues ranging from 40 to 90 HU. They appear significantly denser thanuncomplicated cysts and the remaining renal parenchyma. Thehyperdense appearance is believed to result from cyst hemorrhage. Theydo not enhance and are usually isodense/hypodense on enhanced scans.

BIBLIOGRAPHY

1. David Sutton. Text book of radiology and imaging (7th edn). Churchill Livingstone;2003;1: 936.

2. High-density renal cysts in Autosomal Dominant Polycystic Kidney diseasedemonstrated by CT. Levine Errol, Jared Grantham. Radiology 1985;154: 477-82.

3. Peter L Choyke. Inherited cystic diseases of kidney. Radiologic Clinics of NorthAmerica 1996;34(5):925-43.

EMPHYSEMATOUS PYELONEPHRITIS

Emphysematous pyelonephritis (EPN) is a severe necrotizing infectionof the renal parenchyma, with formation of gas within the collectingsystem, 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. Gascan be rim like or crescent-shaped in the perinephric area. Gas can also


be seen in the renal vein, inferior vena cava, and along with the psoasmuscle. Perinephric abscess may also lead to significant gas in theperinephric 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 horseshoekidney. Findings on the initial tomogram may be deceptive because ofthe exclusion of the anteriorly lying isthmus. Renal axis abnormalitiesare confirmed, as seen on the plain radiographs. In midline fusion, thekidneys are symmetric, with the lower pole calyces lying closer to oractually overlying the spine. The lower calyces are usually mediallyrotated, and they may actually lie medial to the ureters. Some degree ofmalrotation of the kidneys is usually present. A renal pelvis is oftenextrarenal and large.

The degree of malrotation has been associated with the degree offusion. If the isthmus is narrow, the kidneys are usually less malrotated,with pelvis lying anteromedially in its near normal position. In cases ofa wide isthmus, the renal pelves lie anteriorly or laterally. AssociatedUPJ obstruction may be present because of the higher ureteric insertionpoint that leads to delayed pelvic emptying. Ureters may have the so-called flower- vase appearance in which the upper ureters divergelaterally 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

IVPPresents as local infiltration into the parenchyma with subsequentpapillary necrosis and as the disease progresses, there is multi-focalstricturing with impairment of drainage, formation of caseous pus andsubsequent 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 changesare more pronounced in upper urinary tract (kidneys and ureters) leadingto hydronephrosis, hydroureter, pyelonephrosis and ultimate auto-nephrectomy with calcification and small contracted bladder.

BIBLIOGRAPHY


2. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science 1998;245-6.

HYDRONEPHROSIS

Mild to severe dilataion of pelvi-calyceal system can be seen. The kidneysmay be small and smooth (post-obstructive renal atrophy).

Mostly caused by obstructive pathology, non-obstructive causesinclude reflux, bacterial endotoxin, pregnancy and nephrogenic diabetesinsipidus.

BIBLIOGRAPHY

1. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science 1998;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 bepresent in the rectum, and sometimes it becomes difficult to differentiatesuch cases from low large bowel obstruction.

Air fluid levels can be seen in the plain erect film.

BIBLIOGRAPHY

1. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science 1998;137-8.


FIGURE 5.1: Ureteric Stone. A large radiopaque stoneshadow seen in the left ureter (lower end).

FIGURE 5.2: Stag-horn Calculus. A large stag-horn calculuswith two small calculi seen in the hydronephrotic left kidney.


FIGURE 5.3: Bilateral Stag-horn calculi.

FIGURE 5.4: Nephrocalcinosis. Multiple calcifieddensities seen in cortex and medulla bilaterally.


FIGURE 5.5: Renal Dystrophy Secondary to Oxalosis. Smallleft kidney with cortical calcification (arrows). Left renal anddistal ureteric calculi.

FIGURE 5.6: Auto-nephrectomy due to Tuberculosis.Calcified left kidney (multiple rings) and proximal ureter isclearly visible (arrow).


FIGURES 5.7A AND B: Emphysematous Pyelonephritis (Right). Air is seen inpelvicalyceal system of the right kidney (arrows).

FIGURES 5.8A AND B: Adult Polycystic Kidney Disease. Bilateral enlarge kidneyswith multiple thin rounded cysts of variable sizes seen compresing pelvicalycealsystem.

FIGURE 5.9: X-ray Abdomen plain (erectview) in a patient with ruptured liverabscess, with pneumoperitoneum andpneumointestinalis. Air fluid levels in theright hypochondrium, haziness in thecentral abdomen is also visible (due tomasive hepatomegaly).

A B

A B


FIGURE 5.10: Liver Abscess. A large gas shadow with a fluid level isvisible in the area of liver which is also enlarged. Gaseous distension ofbowel 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 massin the central abdomen anteriorly. This patient presented with centralabdominal mass and fever for 2 months duration. CT scan showing largewalled off collection of pus in the abdomen.


FIGURES 5.13A AND B: Hepatic Metastases. Multipleirregular hypoechoeic areas seen in both lobes of the livercompatible with metastatic lesions (arrows).

FIGURE 5.12: Hepatic metastasis secondary to carcinoma ofstomach. CT scan abdomen showing multiple hypodense areas ofvariable sizes seen in both the lobes of the liver (arrows).

A

B


FIGURE 5.14: CT abdomen showing hepatomegaly withmultiple hypodense areas of variable sizes occupying almostwhole of the liver parenchyma due to metastases.

FIGURES 5.15A TO D: Portal Vein Thrombosis. Contrast CT scan showing afilling defect in the area of portal vein.

A B

C D


FIGURES 5.16A AND B: Pancreatic Calcification. Patchycalcification seen in the region of head and body of pancreas.

FIGURE 5.17: Cholelithiasis. Multiple large radiopaquestone shadows in the region of gallbladder.

A B


FIGURE 5.18: Post- tuberculous calcified para-aortic andmesenteric lymph nodes (arrows).

FIGURE 5.19: Paralytic ileus/low intestinal obstruction.Multiple gas filled bowel loops either due to paralytic ileus ordue to low intestinal obstruction.


FIGURE 5.20: Necrotizing Fascitis. There are multiple gasfilled bowel loops. Subcutaneous emphysema with rupturedpyocele of the gallbladder into anterior abdominal wallcausing infection of the skin and subcutaneous tissuesvisible as subcutaneous emphysema.

FIGURE 5.21: Small Bowel Obstruction due to Tuberculosis.Multiple air fluid levels are visible in the upper central, bothpara-colic gutters and iliac fossae.


FIGURE 5.22: Calcified Hydatid Cysts. Multiple roundeddense lesions in the right hypochondrium, right and leftlumbar regions and left hemi-pelvis are visible due to multiplecalcified hydatid cysts in the abdomen.

FIGURES 5.23A AND B: Ovarian Dermoid. (A) Plain abdominal radiograph with atooth like opacity projected over the left sacroiliac joint (arrow). (B) The pelvic CT ofthe same patient shows bilateral fat attenuation lesions with calcific densities withinthem. The appearances on CT are typical of a dermoid cyst.

A B


FIGURE 5.24: Calcified Fibroids. Plain abdominalradiograph with multiple, rounded, well-defined, calcifiedlesions, typical of uterine fibroids.

COMMENT

The plain abdomen radiography may be used as a starting point inabdominal investigation but further studies are frequently required.Earlier in this book (p 158-215) examples of barium studies and oralcholecystograpy. Intravenous pyelography are included. Otherradiological investigations of value in the abdomen include CT scan,ultrasound and MRI.


FIGURE 5.25: Enlarged prostate, indenting the urinarybladder and causing elevation of its base.

FIGURE 5.26: Diverticulum of Urinary Bladder. A largeoutpouching is seen on the right of urinary bladder due todiverticulum formation (arrow).


FIGURE 5.27: Hydronephrosis of Left Kidney. An enlargedleft kidney with dilated pelvi-calyceal system with minimalhydronephrosis on right side.

FIGURE 5.28: Big Staghorn calculus right kidney.


FIGURES 5.29A TO C: Bilateral Renal Calculi. (A) An elongated vertical opacityseen on right side at the level of D12-L1due to renal stone. Transversely lying opacityseen on left side at the level of L2 (left renal stone). Oval opacity seen in the upperpart of left pelvis-distal left ureteric calculus. (B and C) Bilateral hydronephrosis moremarked on left side with distended left sided pelvi-calyceal system.

A B

C


FIGURE 5.30: Horseshoe Kidney. Lower pelvis of bothkidneys are uniting each other in the midline (isthmus). Bothkidneys are showing normal calyceal pattern.

FIGURES 5.31A AND B: Intravenous Cystogram (AP and Oblique View).Diverticulated urinary bladder, in a case of bladder neck obstruction.

A B


FIGURE 5.32: Enlarged left kidney with cyst betweensuperior and middle calyx (arrow).

FIGURE 5.33: Bilateral Chronic Pyelonephritis. Smallkidneys with irregular outline. Distortion and clubbing of minorcalyces seen.


FIGURES 5.34A AND B: IVP (5, 20 mins film A and B).Emphysematous pyelonephritis.

FIGURE 5.35: Acute Pyelonephritis. Edematous kidney withdense nephrogram and attenuated pelvi-calyceal system onthe left side due to acute pyelonephritis.

A B


FIGURE 5.36: Acute Pyelonephritis. Swollen left kidneywith attenuated pelvi-calyceal system.

FIGURE 5.37: Tuberculosis right kidney with auto-nephrectomy.


FIGURE 5.38: Genitourinary Tuberculosis. Non-functioningleft kidney. Minimal calcification seen at the lower pole of leftkidney. 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 thruisthmus.

A B

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TUBERCULOMA

Intracranial tuberculomas may be single or multiple, of variable sizesand situated above or below the tentorium. Brainstem involvement isinfrequent (2.5-8%) other uncommon sites include cavernous sinus, sellaturcica, suprasellar cistern and hypothalamus.

Tuberculomas may be or may not be associated with tuberculousmeningitis. The tuberculous focus starts off as an area of cerebritis andat this stage it is of low density on CT scan, the cerebritis then progressesto a focal non-caseating granuloma, which is isodense or mildly hyper-dense on CT, surrounded by perilesional low-density edema. Post-contrast there is dense nodular enhancement. As caseation occurs, thegranuloma becomes isodense or slightly hypodense.

The lesion now shows ring-enhancement, and perilesional edemaremains.

The radiological differential diagnosis of such ring-enhancementlesion includes abscess, neurocysticercosis, glioma, metastases, lymphomaand other granulomatous processes such as sarcoidosis. With dissemi-nated miliary tuberculosis, multiple enhancing small (< 5 mm) granulomasare seen scattered throughout the brain.

Tuberculous abscesses are rare, and usually on imaging a singlesupratentorial abscess is seen at the grey-white matter interface, whichhas 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 withinthe cerebral substance. Typical locations are within the known territoryof major vessels (e.g. the middle or posterior cerebral arteries) or in theregion of the basal ganglia and internal capsule.

So called watershed infarcts may be seen at the margins of a majorvascular territory, e.g. the posterior frontal and parieto-occipital zones.

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Infarcts are often triangular in shape, although they can appear roundedin axial cross-section. They involve both the white and superficial greymatter, whereas vasogenic edema (around a tumor, for example) usuallyaffects mainly the white matter.

This area of diminishes density accompanied by mild mass effectmay be seen as early as 6 hours after the onset of symptoms, but inmany cases is not clearly visible during the first 24 hours depending onthe quality of the CT scan images.

At first the margins of the infarct are poorly defined, although a fewinfarcts are clearly marginated from the outset.

The density of the lesion becomes progressively lower over thesucceeding weeks, until it approaches that of cerebrospinal fluid in amature infarct. About two weeks after the onset, and corresponding tothe phase of resolution of edema and of macrocytic and vascularinfiltration, 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 lossof volume, with enlargement of the adjacent cerebrospinal fluid space inmost cases. Complete healing is very rare. Enhancement of the infarctmay be seen after a few hours from the onset of symptoms, but is oftennot seen until some days have passed. Such enhancements may be aroundthe lesion, suggesting hypervascularity of the adjacent brain, or withinit, indicating a breakdown of the blood-brain barrier. Patterns ofenhancements vary widely. They include total enhancement of theinfracted area, central enhancement and ring enhancement, and suchappearances can simulate a tumor or an abscess. In some cases corticalenhancement is seen and this is more specific. There is no clear relationshipbetween the type of enhancement and the prognosis. Infarcts whichflood with contrast medium will go on to marked necrosis. Since it ispossible 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. Suchinfarctions are one of the very few situations in which contrast mediuminjection may show previously undetected lesions. The majority of infarctswill show enhancement at some stage during the first 2 weeks thoughsome do not.


After 6 weeks, however, persisting enhancement should suggest analternative diagnosis, even though occasional cases are encountered withenhancement persisting at 12 weeks.

A type of infarct whose appearance differ markedly from thosedescribed above is the uncommon hemorrhagic infarct. This is commonestwith major embolus but may also be seen with patients on anticoagulants.There is patchy increased density throughout the affected region, oftenwith some mass effect, or there may be hemorrhage at the corticalmargins of the infarct.

The ability to differentiate this type of infarct is important in itscontraindication to the use of anticoagulant drugs. The CT appearancemay resemble those of a hemorrhage or hemorrhagic contusion ratherthan a simple infarct.

Venous and sinus thrombosis, either spontaneous or more commonlyin association with inflammatory process, may lead to infarction. In severecases the white mater is predominantly affected and the changes areoften bilateral, showing as areas of diminished density.

The affected cerebral hemispheres are frequently swollen and mayshow hemorrhages and marked contrast enhancements. Increaseddensity of dural sinus or cortical veins with lack of the normalintraluminal enhancements may be detected on CT.

Transient ischemic attacks (TIA) CT scan shows diffuse, rather non-specific, ischemic abnormalities in up to 40% of the cases, often in basalganglia and white matter, and their relevance to the clinical symptomsis speculative.

BIBLIOGRAPHY

1. Cassidy TP, Lewis S, Gray CS. Computerized tomography and stroke. Scott MedJ 1993; 38(5):136-8.

2. Cormier PJ, Long ER, Russell EJ. MR imaging of posterior fossa infarction: Vascularterritory and clinical correlates. Radiographics 1992; 12: 1079-96.

3. EC Sa de Camargo, WJ Koroshetz. Neuroimaging of Ischemia and InfarctionNeuroRx 2005; 2(2): 265-76.

4. Osborn AG. Diagnostic Imaging: Brain (1st edn). Amirsys Inc: Altona, 2004.5. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science 1998;

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 treatment—systematic review. Radiology 2005;235(2):444-53.

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INTRACEREBRAL HEMATOMA

The vast majority of spontaneous hemorrhages occur in the elderly andmiddle-aged and are due to rupture of a microaneurysm on a smallintracerebral artery, with hypertension and atheroma as predisposingfactors. Intracerebral hemorrhage may also occur in patients onanticoagulants or with hemorrhagic blood disorders.

Because of the clear distinction between the high attenuation ofextravasated blood and that of the surrounding brain, CT scanning isby far the most accurate radiological method for demonstrating theselesions.

Of intracerebral hemorrhages that are hypertensive in origin, around60% occur in the basal ganglia or center sylvian areas; the remaining40% involve the Pons (20%), cerebellum (10%), and less commonly thecerebral white matter.

On CT the hemorrhage shows as an area of increased attenuationand is surrounded by a thin low-attenuation ring which probably resultsfrom clot retraction and damage to the blood-brain barrier. Hemorrhagecan rupture into the subarachnoid space or ventricles.

The mass effect depends on the size of the bleed but is frequentlyless then with tumors of comparable size.

The high attenuation of intracerebral hematomas is seen immediatelyfrom the time of hemorrhage. It decreases slowly over the subsequentweeks, until eventually a low-density cystic area remains. Enhancementmay occur around a clot due to damage to the blood-brain barrier andneovascularity. At the stage where the clot is isodense or of low densitythere is clear danger of confusing the CT appearances with those of anabscess or tumor post-enhancement.

BIBLIOGRAPHY

1. Aronovich BD, Reider-Groswasser II, Segev Y. Early CT changes and outcome ofischemic 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.


SUBARACHNOID HEMORRHAGE

Extravasated blood may be identified anywhere in the subarachnoidspace from its high attenuation.

It is usually confined to the basal cisterns. If the subarachnoid bloodis localized, e.g. in the insula, this can be very helpful in identifyingwhich of multiple aneurysms is responsible for the hemorrhage.

The presence of blood in both the cisterns and ventricles has a graverprognosis and is associated with a higher mortality.

Small amounts of intaventricular blood usually gravitate to the occipitalhorns, where it is readily identified.

Low density areas representing infracted or ischemic brain arefrequently shown. It is thought that they are related to the arterial spasmwhich often accompanies subarachnoid hemorrhage.

Dilated ventricles are shown in 50% of patients scanned within 48hours of a subarachnoid hemorrhage, as communicating hydrocephalusmay develop quite rapidly, due to blood clot obstructing the CSF flow.

In the rare cases in which subarachnoid hemorrhage is a manifestationof a tumor, the main findings are those of the tumor itself, with anassociated hematoma.

BIBLIOGRAPHY1. 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. Farrés MT, Ferraz Leite H, Schindler E, Mühlbauer M. Spontaneous subarachnoid

hemorrhage with negative angiography: CT findings. J Comput Assist Tomogr1992; 16: 534-7.

3. Hijdra A, Brouwers PJ, Vermeulen M, van Gijn J. Grading the amount of blood oncomputed tomograms after subarachnoid hemorrhage. Stroke 1990; 21: 1156–61.

4. Latchaw RE, Silva P, Falcone SF. The role of CT following aneurysmal rupture.Neuroimaging Clin N Am 1997;7:693–708.

HYPOXIC ISCHEMIC BRAIN DAMAGE

Global hypoxia, hypotension or hypoglycemia can damage the wholebrain, usually but not always symmetrically.

Patterns vary from total cerebral infarction to predominantly whitematter infarction, cortical watershed or white matter terminal zoneinfarction, basal ganglia infarcts (especially globus pallidus ), and purecortical damage in cerebral hemisphere or cerebellum such as in severehypoglycemia. Severe clinical disability can occur with little or no changeson CT or MRI.

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BIBLIOGRAPHY1. Naidich TP. Brain Vascular Distribution: Classical patterns of stroke. Categorical

Course in Cerebrovascular Disease. American Society of Neuroradiology 1989;63-77.

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, leptomenin-gies (pia and arachnoid maters) and the cerebrospinal fluid within thesubarachnoid space.

It may be associated with underlying cerebral parenchymalinflammation–meningoencephalitis. The role of imaging in meningitis islargely to detect complications such as hydrocephalus, venous thrombosisand infarction, as often in early uncomplicated meningitis imaging maybe normal. In most cases of viral meningitis CT and MRI are normal,unless associated with viral encephalitis.Brain swelling and meningealenhancement may be seen in some cases.

In early cases of pyogenic meningitis there may be obliteration of thebasal cisterns and cerebral and cerebellar sulci due to the presence of aninflammatory exudates and brain swelling. After contrast administrationthere may be either dural or leptomeningeal enhancement.

Communicating hydrocephalus is the most common complicationassociated with meningitis, resulting from blockage of the CSF flow.

In tuberculous meningitis the basal cisterns are obliterated by anisodense or hyperdense exudates, and postcontrast there is avidenhancement of the basal meninges extending into the ambient, sylvian,pontine and chiasmatic cisterns. The meningeal enhancement may extendover the cerebral and cerebellar hemisphere. Hydrocephalus is presentin 45-87% of patients at the time of diagnosis.

BIBLIOGRAPHY1. Becker LE. Infections of the developing brain. Am J Neuroradiol 1992;13(2):537-49.2. David Sutton. Text book of radiology and imaging (7th edn). Churchill Livingstone;

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 Radiol2006;36(11):1182-5.

4. Osbourne A. Diagnostic Neuroradiology. Mosby, Chicago; 1994;680-6.


SUBDURAL ABSCESS (EMPYEMA)

These are usually secondary to bacterial or fungal disease of the calvariaand subdural space, and frontal sinusitis is in fact the most commoncause of a subdural empyema. The cerebral convexities and in hemisphericfissure are the most common locations.

On CT these are seen as crescentric or lentiform collections of variableattenuation (usually reduced), whose margins, and occasionally contents,enhance markedly. Hypodensity of the adjacent brain may result fromsecondary venous infarction.

BIBLIOGRAPHY

1. Stevens EA, Norman D, Kramer RA, Messina AB, Newton TH. Computedtomographic brain scanning in intraparenchymal pyogenic abscesses. Am JRoentgenol 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 illnesswith a mortality of 55%. The severity of the infection can lead tohemorrhagic necrosis and considerable mass effect.

The changes are bilateral but may appear predominantly unilateral inthe 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) andthe adjacent posterior frontal region, usually with the mass effect.

The changes may be minimal in the first 2-3 days despite severeneurological impairment and should be carefully sought. Hemorrhagerarely shows a clear hematoma but may give rise to patchy areas ofslightly increased density. After contrast medium, enhancement is seenin most cases and may be patchy, peripheral or gyral. In the chronicthere may be large low density areas with associated local atrophy inthe affected regions.

2. CYTOMEGALOVIRUS (CMV)

CT will show dilated ventricles due to atrophy with periventricular andcortical calcifications.

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BIBLIOGRAPHY1. 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 maybe seen with small round cell tumors, tumors with high nuclear tocytoplasmic ratio, or hemorrhagic lesions. Midline shift and/orcompression of ventricles may be visible. Marked surrounding edema isusually present.Renal, breast, melanoma and choriocarcinoma most likelyto bleed.

Cystic and calcified metastases are rare. Edema is often striking andmay be only abnormality seen before contrast.

Most metastases enhance strongly; both solid and ring like patterns.

BIBLIOGRAPHY1. Davis PC, Hudgins PA, Peterman SB, Hoffman JC. Diagnosis of cerebral metastases.

Double-dose delayed vs. contrast-enhanced MR imaging. American Journal ofNeuroradiology 1991; 12: 293-300.

2. Zimmerman HM. The ten most common types of brain tumour. Seminars inRoentgenology 1971;6:48-54.

PITUITARY TUMORS

MRI is the preferred imaging modality for assessing pituitary adenomasand can evaluate local tumor invasion and compression of criticalstructures such as the chiasma more accurately. CT will betterdemonstrate destruction of the sellar floor. Large adenomas producingchiasmal compression, CT will show the extent and relationships of thesuprasellar component as well as the enlarged sella. The tumor can alsoextend laterally into the cavernous sinuses and temporal lobe ordownward into the sphenoid sinus.

Pituitary adenomas normally show homogeneous density similar toor slightly greater than that of normal brain tissue, and enhanceuniformly after contrast medium.

The CT diagnosis of microadenomas requires high-resolution CT.


The typical microadenoma can be recognized as a small low densityarea within the enhancing gland. Other features which may be seen aredeviation of the infundibulum and upward bulging of the upward bulgingof the upper surface of the gland.

BIBLIOGRAPHY1. David Sutton. Text book of radiology and imaging (7th edn), Churchill Livingstone;

2003;2: 1749-51.2. Peter Armstrong. Diagnostic Imaging (4th edn). London: Blackwell Science;

1998;409.

CRANIOPHARYNGIOMA

These tumors of epithelial origin account for up to 3% of primaryintracranial 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%) growinto the pituitary fossa and can produce enlargement and deformity ofthe sella.


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

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FIGURES 6.1A TO C: Tuberculomas. Hydrocephalussecondary to TBM and multiple tuberculomas. Pre- and post-contrast CT images showing basal meningeal enhancementand multiple focal ring lesions with surrounding edemainvolving both cerebral hemisphere. There is also evidenceof moderate hydrocephalus with peri-ventricular edema.

A B

C


FIGURE 6.2: Intra-cranial TB. Axial post-gadolinium and T2weighted MRI images demonstrating abnormal meningealenhancement with a ring enhancing lesion in the left middlecerebral peduncle with associated surrounding edema.

FIGURES 6.3A TO C: Tuberculomata. Nodular enhancinglesions with intense white matter edema seen.

A B

C

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FIGURE 6.4: Toxoplasmosis. Axial MRIbrain. Post IV Gadolinium. Multiple,bilateral, ring enhancing lesions bothwithin the deep white matter and thebasal ganglia are shown in an AIDSpatient. Most commonly affected areasare the basal ganglia, corticomedullaryjunction, white matter or periventricularregions. These were diagnosed to besecondary to toxoplasmosis. Thedifferential diagnoses for ring enhancinglesions are given in Page 334 and 335.

FIGURES 6.5A TO E: Tuberculomas Brain. (A to D) Multiple dense, contrastenhancing lesions with marked surrounding edema due to tuberculomas in a patientwith pulmonary tuberculosis. (E) Chest X-ray of the same patient showing apical andperi-hilar opacities in left lung and widenning of superior mediastinum due tolymphadenopathy-pulmonary tuberculosis.

A B

D E

C


FIGURES 6.6A TO C: Tuberculous Meningitis (Pre- andPost-contrast Scan). There is evidence of diffuse meningealenhancement and gross hydrocephalus.

A B

C

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FIGURE 6.7: Basal Meningitis. Basal enhancement ofmeninges seen associated with effacement of cortical sulciin a patient with pyogenic meningitis.

FIGURE 6.8: Tuberculous Meningitis. Post-contrast scanshowing meningeal enhancement and hydrocephalus.


FIGURES 6.9A AND B: Postencephalic Cyst and Hydrocephalus. Small right middlecerebral artey infarction is also seen. Ventricles are grossly dilated with a cysticlesion communicating with the right lateral ventricle anteriorly (1). Low attenuationseen 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 temporo-parietal region associated with significant perifocal edema causing mass effect withmidline displacement.

A B

A B

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FIGURES 6.11A TO D: Subdural Empyema Secondary to Sinusitis. (A) There isevidence of sinusitis with fluid levels involving all the sinuses except left maxillarysinus. (D) There is evidence of intracranial spread of infection with subdural empyema(arrow) and extension into right frontal lobe and inter-hemispheric fissure (arrow, Band C respectively).

A B

C D


FIGURE 6.12: Cerebritis with Pneumoencephalus. Corticalprominence seen due to cerebritis and pneumoencephalus(probably secondary due to dural defect), ventricles arenormal.

FIGURES 6.13A AND B: Metastasic, Abscesses. Multiple well-defined lesions atthe gray and white matter junction in the right frontal, left parietal and on the rightcerebellar hemispheres. The lesions are associated with significant edema and areenhancing after contrast administration. No evidence of midline shift. There is alsoevidence of ethmoidal sinusitis.

A B

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FIGURES 6.14A AND B: Amebic Abcesses. Bilateral low attenuation areas seen inthe region of basal ganglion with ring enhancement and surrounding edema due toamebic abscesses developed in a patient with lung abscess secondary to a rupturedliver abscess.

FIGURES 6.15A AND B: Lung Metastasis and Cerebral Abscess. The lungmetastasis is ring enhancing with a thin rim and surrounding edema. This isindistinguishable from the cerebral abscess (A) T1 weighted axial and (B) DiffusionMRI image—the latter image show the restricted diffusion characteristic of an abscess,tumors have free diffusion.

A B

A B


FIGURES 6.16A AND B: Cerebellar Abscess. Well circumscribed hypointense lesionseen in the right cerebellar hemisphere on T1 image with surrounding edema causedby a large cerebellar abscess. The lesion appears isointense on T2 image withsurrounding edema which is hyperintense.

FIGURE 6.17: Right Middle Cerebral Artery Infarction(Contrast). Large low attenuation area due to infarct withsurrounding edema seen involving the right Middle cerebralterritory, compressing the ventricular system leading tomidline displacement.

A B

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FIGURE 6.18: Acute Cerebellar Infarcts. Axial CT headshowing bilateral acute cerebellar infarcts secondary tobasilar artery thrombosis, with the typical low attenuationpresent in the cerebellar hemispheres.

FIGURE 6.19: Old infarct in left frontoparietal region withwidened adjacent sylvian fissure and asymmetric dilatationleft frontal horn with mild diffuse brain atrophy.


FIGURE 6.20: Large acute ischemic infarction in left fronto-temporo-parietal region with mass effect and mild midlineshift. No acute bleed or mass lesion is noted.

FIGURES 6.21A AND B: Ischemic infarct both cerebellar hemispheres (CT scanbrain plain and contrast). (A, B) There is evidence of a low density mass lesion in theleft cerebellar fossa involving the white matter. A similar low density area also seen inthe right cerebellar fossa.

A B

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FIGURE 6.22: Ischemic Infarction. There is a large hypo-dense area occupying right temporo-parietal region.Compression of right lateral ventricle and attenuation of sulciand gyri on the right side.

FIGURE 6.23: Intracereberal Hemorrhage. There isevidence of extensive hemorrhage in the left thalamus andbasal ganglia which has dissected into the ventricular systemand into the cisterns as well. There is evidence of dilatationof the frontal horns with mass effect at the level of 3rd ventricle.


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 acutehematoma in cerebellum with obstructive hydrocephalus causingsignificant dilatation of all the ventricles.

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FIGURE 6.26: Pontine Hemorrhage. A largehemorrhage seen in the pontine region.

FIGURE 6.27: Cerebral Hemorrhage. A large hemorrhagein the right deep parietal region with mild surrounding edemaand spillage into both lateral ventricles.


FIGURE 6.28: Parietal Lobe Hemorrhage. A large hematomaseen in the right parietal lobe with surrounding edema,pressure effect and mild midline shift.

FIGURE 6.29: Hemorrhagic Contusion. Plain CT brainshowing bilateral gyriform high density areas with mildperifocal edema.

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FIGURES 6.30A AND B: Subarachnoid Hemorrhage. High density seen in theSylvain fissures, ventricles and the subarachnoid spaces with midline shift.

FIGURE 6.31: Subarachnoid hemorrhage with intraventricular extension leading toobstructive hydrocephalus.

A B

A B


FIGURE 6.32: Subarachnoid Hemorrhage (SAH). Axial CThead. Unenhanced scan showing extensive acutehemorrhage in the sylvian fissures and the ambient cistern inkeeping with subarachnoid hemorrhage.

Diagnostic features of subarachnoidhemorrhage on plain CT scan brain

- High density material within the basal cisternsand 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.

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FIGURES 6.34A AND B: Bilateral Chronic SubduralHematoma. (A) Axial T2 weighted MRI brain demonstratingbilateral chronic subdural collections (High intensity). (B) Theisodense attenuation of the chronic subdural hematoma isdemonstrated on CT.

FIGURES 6.33A TO C: Subdural Hematoma. Left fronto-parietal region with left sided effacement of ventricle andassociated midline shift.

A B

C

A B


FIGURE 6.35: Acute and acute on chronic subduralhematomas. Unenhanced CT images showing bilateral acuteon chronic subdural collections with low attenuation fluidwith areas of high attenuation inkeeping with acutehemorrhage.

FIGURE 6.36: Acute Subdural Hematoma. Irregular denseopacity seen in the fronto-parieto-occipital regions withpressure effects over the right lateral ventricle.

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FIGURE 6.37: Arteriovenous Malformation. Low densitywith patchy hyperdensities areas seen in the left parieto-occipital 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 Hounsetield’s 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


FIGURE 6.38: Craniopharyngioma. CT scan axial viewshowing supracellar mass with extensive calcificationcausing obstructive hydrocephalus.

FIGURE 6.39: Medulloblastoma.CT scan showing a midlinemixed density posterior cranial fossa mass with somecalcifications, causing hydrocephalus due to obstruction of4th ventricle.

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FIGURES 6.40A AND B: Glioblastoma Multiforma. Sagittal and coronal view of MRIcontrast showing a frontal mass of mixed intensity partly enhancing with non-enhancingcentral portion.

FIGURE 6.41: Malignant Glioma. CT scan axial view showinga large complex density (partly solid, partly cystic) mass inthe left cerebral hemisphere with surrounding edema andmidline shift.

A B


FIGURES 6.42A TO C: Acoustic Neuroma. MRI brain axial view (A) Non-contrastTW1 showing a hypointense mass in cerello-pontine angle. (B) TW2 image showinga hyperintense mass in the cerebello-pontine angle compressing the brainstem andthe 4th ventricle, extending into the internal auditory meatus. (C) Post-contrast imageshowing an enhancing mass in the cerebello-pontine angle causing compressionof the brainstem and obstructing the 4th ventricle.

A B

C

355Brain

FIGURES 6.43A AND B: Malignant Glioma. CT scan axial view showing right parietalpartially cystic, partially solid mass with mixed enhancement and surrounding edema.

FIGURES 6.44A AND B: Meningioma. (A) Bilateral frontal mass the right one showingextensive lamellar calcification, left one isodense on plain CT scan. (B) Post-contrastscan showing vivid enhancement, attachment to falx cerebri and surroundingvasogenic edema.

A B

A B


FIGURE 6.45: Pituitary Adenoma. CT brain plain showing arounded mass of increased density in the area of sellameasuring about 2 cm in diameter.

FIGURE 6.46: Pituitary Adenoma. A rounded massenhancing on contrast is seen in the suprasellar cistern.

357Brain

FIGURES 6.47A AND B: Pituitary Adenoma. (A) MRI TW1image sagittal view showing enlargement of sella tursicawith a uniform ISO intense mass. (B) Post-contrast imageshowing marked enhancement.

A

B


FIGURE 6.48: Hemangiopericytoma. The hemangiopericytomawhich looks like an atypical meningioma, intensely enhancing,extra-axial lesion with is displacing the frontal horns of the lateralventricles.

FIGURE 6.49: Post-IV contrast CT showing multiplemetastases from a bowel primary – solid enhancing noduleswith enhancement and extensive vasogenic edema.

359Brain

FIGURES 6.50A AND B: Melanoma. Pre- and post-IV contrastCT. The images show high attenuation lesion in the leftcerebral hemisphere is due to high melanin content withsome enhancement on contrast scan.

A

B


FIGURES 6.51A TO D: Metastases. Pre- and post-contrast CT images showingmultiple ring enhancing lesions with perifocal edema involving right thalamus, leftoccipital region and right CP angle. A large cerebllar midline lesion is compressingthe 4th ventricle leading to mild to moderate hydrocephalus.

FIGURES 6.52A AND B: (A) T1 weighted coronal image and (B) T2 weighted axialimage, show an epidermoid tumor in the suprasellar cistern. Imaging characteristicson MRI are not dissimilar to CSF.

A B

C D

A B

361Brain

FIGURE 6.53: Metastatic Deposits. Multipledense, well-defined enhancing masses visiblein both hemispheres with significant surroundingedema.

FIGURE 6.54: Acoustic Neuroma. Axial MRIbrain showing a soft tissue mass adjacent to theright internal acoustic meatus in keeping with anacoustic neuroma.


FIGURE 6.55: Diffuse Cerebral Atrophy. The ventricles aremildly dilated with widened Sylvian fissures, cerebral sulci,and interhemispheric space.

FIGURE 6.56: Diffuse Cerebral Atrophy. Grossly dilatedventricles with widening of interhemispheric and cerebralsulci.

363Brain

FIGURES 6.57A TO C: Binswanger’s Disease. Low densitypatches are seen in bilateral frontoparietal periventricular regionsinvolving the basal ganglia with generalized cortical atrophy.

FIGURES 6.58A AND B: Glioma. Pre- and Post-IV contrast CThead. The right parietal tumor with a thick rim, infiltrating andenhancing with necrotic core. Histologically proven to be a glioma.

A

B C

A B


FIGURE 6.59: Thyroid Metatasis MRI with IVGadolinium. Axial image. The thyroid metastasis isincluded because it looks like a meningioma of thepetrous ridge – extra-axial, enhancing.

Index

AAchalasia of cardia 166Acromegaly 224Acute asthma 106Acute myocardial infarction 128Acute pyelonephritis 317Adult polycystic kidney disease 297Adult respiratory distress syndrome 13Allergic bronchopulmonary aspergillosis

3acute 3chronic 3

Amoebic abscesses 339Ankylosing spondylitis 223, 253Aortic dissection 152Ascariasis 195Ascending colon 210Aspergilloma in a tuberculous cavity 36Atelactasis/collapse 6

BBamboo shaped spine 254Barium enema 212Bezoars 159Bilateral chronic pyelonephritis 316Binswanger’s disease 363Bronchiectasis 4Bronchogenic carcinoma 9

CCalcified hydatid cyst 180Carcinoma bronchus 74Carcinoma caecum 210Carcinoma colon 164Carcinoma esophagus 159Carcinoma lung 79Carcinoma stomach 159

Causes of raised diaphragm 104bilateral 104unilateral 104

Cavitating lesions 6Cavitatory lung lesions 111

differential diagnosis 111abnormal lung 111infections 111inflammatory 111neoplastic 111vascular 111

Cerebellar hematoma 344Cerebral infarction 322Cerebral metastases 329Charcot’s joint 287Chickenpox 61Chilaiditi’s syndrome 103Cholelithiasis 307Chronic duodenal ulcer and duodenitis

178Chronic obstructive pulmonary disease 106Chronic pulmonary tuberculosis 23Coarctation of aorta 132Coeliac disease 161Congenital heart diseases 126

atrial septal defect 126Ebstein anomaly 127tetralogy of Fallot 126transposition of great arteries 126

D-loop transposition 126L-loop transposition 126

Congestive cardiac failure 129Consolidation 5

lobar consolidation 5Consolidation-collapse 47Constrictive pericarditis 130Cork screw esophagus 168Craniopharyngioma 330Crohn’s disease 162, 197Cryptogenic fibrosing alveolitis 14Cystic bronchiectasis 41Cystic fibrosis 13, 43


DDextrocardia with situs inversus 134Diabetic foot 268Diffuse cerebral atrophy 362Dilated cardiomyopathy 129Dissecting aneurysm 148Diverticular disease 163Duodenal lymphoma barium meal 202

EEmphysema 15Emphysematous bullae 107Emphysematous pyelonephritis 297, 317Encephalitis 328

cytomegalovirus 328herpes simplex encephalitis 328

Ewing’s sarcoma 285

FFibrosing alveolitis 96

GGastric outlet obstruction 179Gout 221

HHemangiopericytoma 358Hemorrhagic contusion 346Hiatus hernia 16Hodgkin’s lymphoma 112Hodgkin’s disease 115Horse-shoe kidney 298Hydatid cysts 7Hydronephrosis 299Hyperparathyroidism 222

causes 223primary 223secondary 223

Hypoxic ischemic brain damage 326

IIleocecal tuberculosis 196Intestinal tuberculosis 160, 201

Intracerebral hematoma 325Intravenous cystogram 315

LLeft ventricular aneurysm 152Leiomyoma of stomach 185Leprosy 268Liver abscess 104Loculated tuberculosis empyema 65Lung abscess 15Lymphangitis carcinomatosa 85Lymphoma 11

MMalabsorption syndrome 200Malignant glioma 355Malignant mesothelioma 84Marble bone disease 228Mediastinal mass lesions 117

differential diagnosis 117anterior mediastinum 117middle 117posterior 117

Meningitis 327Metastatic disease 226Military tuberculosis 21Monoarthritis 260

causes 260Mucopolysaccharidosis 233Multi-drug resistant tuberculosis 29Multiple myeloma 225Mycetoma 229Mycoplasma pneumonia 45

NNephrocalcinosis 296Non-Hodgkin’s lymphoma 67

OOsteoarthritis 219Osteoarthrosis of spine 259Osteomalacia 221Osteoporosis 219Osteosarcoma 225

367Index

PPaget’s disease 245Pancoast tumor 76Paralytic ileus 299Paranasal sinusitis 267Pleural fibroma 91Peptic esophageal stricture 167Pericardial effusion 129

causes 130Pituitary adenoma 356Pituitary tumor 280, 329Pleural effusion 8Pneumoconiosis 97Pneumocystis carinii pneumonia 57Pneumothorax 8Pneumopyopericardium 154Polyarthritis 260

causes 260Portal vein thrombosis 306Postprimary pulmonary tuberculosis 20Post-tuberculous cavitations 29Pott’s disease 227, 266Prosthetic valves 138Pulmonary aspergillosis 3

plain film 3invasive 3non-invasive 3

Pulmonary hydatid cysts 62Pulmonary metastases 10Pulmonary tuberculosis 2

primary tuberculosis 2secondary tuberculosis 2

Pulmonary venous hypertension 127Pyloric stenosis 189Pyogenic meningitis 327

RRachitic rosary 243Reactivation tuberculosis 24Reflux esophagitis 158Reiter’s disease 255Renal calculi 296Renal tuberculosis 299Retrosternal goiter 118Rheumatoid arthritis 218Rickets 220

Ring enhancing lesions of the brain 330Romanus lesion 223

SSacroiliitis 255

causes 255bilateral 255unilateral 255

Sarcoidosis 12Sclerosing cholangitis 213Septic arthritis 274Severe mitral stenosis 138Sinusitis 228Squamous cell carcinoma 81Stag-horn calculus 300Subarachnoid hemorrhage 326, 347Subdural abscess 328

TThyroid metastasis 364Toxic multinodular goiter 119Trichobezoar 183Tuberculoma 26, 322Tuberculous bronchopneumonia 34Tuberculous meningitis 327Tuberculous pleural effusion 66

UUlcerative colitis 162, 207

VValvular heart diseases 124

aortic stenosis 125mitral regurgitation 124mitral stenosis 124pulmonary stenosis 125

WWegener’s granulomatosis 109Worm infestation 161

atlas of diagnostic radiology

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