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The Final FRCR
Complete Revision Notes

Vincent Helyar and Aidan Shaw

CRC Press
Taylor & Francis Group
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Boca Raton, FL 33487-2742

© 2018 by Taylor & Francis Group, LLC

CRC Press is an imprint of Taylor & Francis Group, an Informa business

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Foreword

The transition from the FRCR Part 1 to FRCR Part 2 is always a challenge. The first part
of the examination demands encyclopaedic knowledge of several subjects. Although
understanding is important, there is no getting away from the fact that in order to pass
this examination a candidate needs to extensively read and absorb many details. Part
2 is very different—although wide reading and extensive knowledge would help, this
examination is mainly a test of a candidate’s ability to use his or her knowledge to make
appropriate clinical diagnoses and management decisions.
Many candidates find it difficult to switch from ‘MCQ mode’ to the pragmatic and
sensible approach required for the second part of the FRCR examination. Although there
is no substitute for clinical practice for making this necessary transition, this excellent
book by Dr. Aidan Shaw and Dr. Vincent Helyar will help FRCR Part 2 candidates to
focus on real clinical issues in a sensible way and to think like practising radiologists
in real clinical situations. It adopts a succinct, accessible style peppered with the kind
of pertinent points which trainees usually only pick up as they move through a sub-
specialty. Plain radiographs and cross-sectional imaging examinations of excellent
quality are annotated clearly and are accompanied by the main differential diagnoses
presented in a format that is easy to read and memorise.
I anticipate that the book will be used as an adjunct to major textbooks for the
purposes of revision, and as a self-testing aid as the examination approaches. It is
enjoyable to read and easy to use, and its authors can take pride in a challenging task
extremely well accomplished.

Andreas Adam, CBE

Professor of Interventional Radiology
Guy’s and St. Thomas’ NHS Foundation Trust
London, UK
Contents

Foreword vii
Acknowledgements ix
Introduction xi
Authors xiii

1 Cardiothoracic and Vascular 1

Cardiovascular 1
Respiratory 16

2 Musculoskeletal 61
General musculoskeletal 61
Paediatrics 103
MSK tumours 130

3 Gastrointestinal 151
Gastrointestinal tract 151
Peritoneum and mesentery 190
Liver 193
Pancreas 228
Spleen 237
Abdominal aids 241

4 Genitourinary, Adrenal, Obstetrics and Gynaecology and Breast 245

Urinary tract 245
Adrenal glands 267
Gynaecology 270
Male genital tract 277
Breast 281

5 Paediatrics 287
Central nervous system 287
ENT and orbits 307
Cardiovascular 310
Respiratory 319
vi Content s

Miscellaneous 330
Gastrointestinal 333
Genitourinary 349

6 Central Nervous System, Head and Neck 361

Trauma 361
Cerebrovascular disease 365
Miscellaneous central nervous system disease 380
Basics of brain tumours 385
Intra-axial tumours 389
Extra-axial tumours 397
Congenital intracerebral lesions 407
CNS infection 408
Demyelinating disease 417
Leukodystrophy 421
Metabolic disorders 423
Degenerative disorders 423
Head and neck 425
Ear 431
Thyroid, parathyroid and salivary glands 433
Orbits 436
Mandible and maxilla 441
Spine 443
Cord 446
Index 457
Acknowledgements

I dedicate this book to my family, my wife Sinéad and my daughters Clara and Elizabeth
for their love and support. I am very grateful to my parents for giving me my love of
words and to my mother for the inspiration to write.
Vincent Helyar

I would like to dedicate this book to my amazing wife Juliette and my son Edward
for their continuing love, support and understanding throughout the writing of this
book and my career. I would also like to thank my legendary parents, Bryn and Ozden.
Without their continual love and support, I would not be where I am today.
Aidan Shaw
Introduction

This book is the product of several years of hard labour, the aim being to produce a
definitive revision manual for the unfortunate souls preparing for the final Fellowship
of the Royal College of Radiologists (FRCR). The aim of the book is to support you in
preparation both for the written ‘2a’ exams as well as the oral and written ‘2b’ component.
In each topic covered in this book, we hope that you will find enough information to
understand the clinical context of a condition and its key imaging characteristics. Some
information that you may find particularly useful is highlighted throughout in boxes.
To help you pass the 2a modules, we suggest you:

1. Over-prepare—do not underestimate how much work these exams require!

2. Start early and read widely (expect about 3 months of preparation per module if
working in the evenings and occasional weekends).
3. Do as many multiple choice questions (MCQs) as you can and read up on everything
you do not know.

For the 2b modules, we suggest you:

1. Over-prepare.
2. Report lots of plain films.
3. Read some case study texts early on (e.g. 4–6 months pre-exam).
4. Focus on viva practice, especially in the last 2–3 months.
5. Avoid burnout—know when to have time out!
6. Do at least 70 dedicated rapid-reporting plain film packs.
7. Use a checklist for rapid reporting.
8. Rehearse spiels for classic cases—whether or not you use them, it will build your
confidence in presenting a case.
9. Practice with your peers.

The FRCR examination is a great challenge to prepare for, not least because of the sheer
volume of information. You will be expected to have both a breadth and depth of knowledge,
and in the dreaded final viva, you will be expected to assimilate all of this under pressured
conditions in order to proffer a handful of sensible differential diagnoses—good luck! Rest
assured that your hard work will pay off and you will emerge with a very robust qualification.
Authors

Dr Vincent Helyar, FRCR EBIR is a Consultant Interventional Radiologist at Hampshire

Hospitals NHS Foundation Trust. After a successful career in information technology,
Vincent graduated from Guy’s, King’s and St Thomas’ School of Medicine in 2009
with Distinction. He completed his Foundation years in the South West of England
and then began specialty training in Clinical Radiology at Guy’s and St Thomas’ NHS
Foundation Trust. He completed specialty training in 2017 following a 2-year Fellowship
in Interventional Radiology.
Vincent trained as an Interventional Radiologist at Guy’s and St Thomas’ NHS
Foundation Trust. His practice includes a broad range of both vascular and non-vascular
intervention. He has a keen interest in teaching and has authored several book chapters,
numerous articles and has presented widely at national and international conferences.
He is a member of the Royal College of Radiologists, the British Society of Interventional
Radiology, the European Society of Radiology and the Cardiovascular and Interventional
Radiological Society of Europe.

Dr Aidan Shaw, MRCS FRCR is a Consultant Interventional Radiologist at Maidstone

and Tunbridge Wells NHS Trust. He completed his specialty training at Guy’s and
St Thomas’ NHS Foundation Trust including a two-years Interventional Radiology
fellowship. He has a particular interest in uterine artery embolisation, ovarian vein
embolisation and prostate artery embolisation.
He has authored books as well as book chapters, has been published extensively in a
number of international peer-reviewed journals and has won awards and fellowships in
the field of surgery and radiology. He is a member of the Royal College of Radiologists,
the Royal College of Surgeons, the British Society of Interventional Radiology and the
Cardiovascular and Interventional Radiological Society of Europe.
 C H A P T E R 1

Cardiothoracic and Vascular

CARDIOVASCULAR

ABERRANT LEFT PULMONARY ARTERY

Occurs due to the failure of formation of the sixth aortic arch. Blood to the left lung arises
from an aberrant left pulmonary artery that arises from the right pulmonary artery. The
vessel passes between the trachea and oesophagus and causes narrowing of the trachea in
a caudal direction. Associated with other anomalies (e.g. patent ductus arteriosus).

PLAIN FILM
●● Bronchial obstruction causes lung emphysema (right lung, middle lobe, lower
lobes, left upper lobe)

BARIUM SWALLOW
●● Anterior indentation on the oesophagus, just above the level of the carina

AORTIC ANEURYSM
Considered either true (aneurysm bound by all three walls of the vessel) or false (i.e.
pseudoaneurysm, part of the wall of the aneurysm is formed by surrounding soft tissue).
Aneurysms are described as being saccular or fusiform.

●● Saccular aneurysms are eccentric in shape, the aneurysm only forming from
part of the circumference of the vessel wall. Associated with mycotic aneurysms
(Figure 1.1).
●● Fusiform aneurysms involve the full vessel circumference and feature cylindrical
dilatation. More commonly seen with atherosclerotic aneurysms (Figure 1.2).

CT
●● Thoracic aortic aneurysms are mostly atherosclerotic and calcified in 75%.
Other causes include cystic medial necrosis (a disorder of the large arteries with
2 C ardiothoracic and Vascular

Figure 1.1 Saccular aneurysm. CT angiogram demonstrating a saccular aneurysm arising from
the abdominal aorta.

Figure 1.2 Fusiform aneurysm. CT angiogram demonstrating a fusiform abdominal aortic

aneurysm.

formation of cyst-like lesions in the media, associated with e.g. Marfan and Ehlers–
Danlos syndromes) and syphilis (expect extensive calcification).
●● Abdominal aortic aneurysms (AAAs)—mostly atherosclerotic.
●● Popliteal aneurysms, associated with an AAA in 30%–50%.

INTERVENTION
●● Advised when diameter >5.5 cm (the risk of rupture is greatly increased over this).
●● Endovascular stents are generally oversized by 10%. The presence of perigraft air is
a common finding in the immediate post-operative period; however, if present >1
week after surgery, suspect infection.
●● Endoleak is defined as the continued perfusion of the aneurysm despite placement
of a stent graft (Table 1.1).
 C ardiovascular 3

Table 1.1 The classification of endovascular stent graft endoleaks

Type of endoleak Site

Type 1 Leak from the stent/graft attachment due to an inadequate seal

1a Proximal
1b Distal
Type 2 Filling of the sac from retrograde flow through aortic branches
(most common, 80%) (e.g. lumbar arteries, inferior mesenteric)
Type 3 Structural failure of the stent graft/leak from mid-graft component
junction
Type 4 Porosity of the graft (corrects with reversal of anticoagulation)
Type 5 Endotension (i.e. aneurysm sac enlargement without
demonstrable leak)

AORTIC COARCTATION
Narrowing of the aortic isthmus, mostly occurs in males (80%). Associated with multiple
congenital anomalies, most commonly a bicuspid aortic valve (seen in 80%). Other
associations include Turner syndrome (15%–20%), posterior fossa malformations–
hemangiomas–arterial anomalies–cardiac defects–eye (PHACE) syndrome and intracerebral
berry aneurysms and bleeds. Causes heart failure in infancy and hypertension later.

PLAIN FILM (FIGURE 1.3)

●● Cardiomegaly with left ventricular hypertrophy.
●● Look for the ‘reverse 3 sign,’ formed by pre-stenotic aortic dilatation, the
coarctation and post-stenotic dilatation.
●● Inferior rib notching (large collateral intercostal vessels), most commonly
affecting the fourth to eighth posterior ribs after 5 years of age.

AORTIC DISSECTION
Blood under arterial pressure enters a tear in the intima and tracks along in the media.
A total of 60% of dissections involve the ascending aorta (Stanford type A and DeBakey

Figure 1.3 Coarctation of the aorta.

Chest x-ray demonstrating cardiomegaly,
a reverse 3 sign (red arrow) and inferior
rib notching (white arrow).
4 C ardiothoracic and Vascular

Table 1.2 Stanford and DeBakey classifications of thoracic aortic dissection

Stanford DeBakey

Type A Type I
Affects the ascending aorta and/or arch and Involves ascending and descending aorta
possibly into the descending aorta Type II
Involves the ascending aorta only
Type B Type III
Affects the descending aorta and/or arch IIIA—descending aorta only without extension
beyond the left subclavian artery below the diaphragm
IIIB—descending aorta with extension below
the diaphragm

type I and II) and will require surgical management. They mostly originate from the
right anterolateral wall of the ascending aorta, just distal to the aortic valve. They are
associated with connective tissue disorders (Marfan and Ehlers–Danlos syndromes),
bicuspid aortic valves, coarctation, relapsing polychondritis, Behçet disease, Turner
syndrome, trauma and pregnancy (Table 1.2).

PLAIN FILM
●● Widened mediastinum (over 8 cm)
●● Double aortic contour
●● Displacement of aortic knuckle calcification by 10 mm
●● May manifest as lower lobe atelectasis

CT (FIGURE 1.4)
●● Dissection flap separating true and false lumens (can be hard to tell which is
which).
●● The false lumen tends to be larger, enhances more slowly and may be thrombosed.
The ‘beak’ sign (wedges around the true lumen) and ‘cobweb’ sign (remnant
ribbons of media appearing as slender linear areas of low attenuation) are also
clues.

Figure 1.4 Aortic dissection. CT

angiogram demonstrating a dissection
of the ascending and descending
thoracic aorta—Stanford type A and
DeBakey type I. Red arrow—false lumen
of the ascending aorta. White arrow—
true lumen of the descending thoracic
aorta.
 C ardiovascular 5

AORTIC TRANSECTION
Occurs following major blunt trauma, 90% in the proximal descending aorta at the level
of the isthmus (mobile aortic arch moves against the fixed descending aorta at the level
of the ligamentum arteriosum). The diaphragmatic hiatus and aortic root are other risk
areas.

PLAIN FILM (FIGURES 1.5 AND 1.6)

●● Widened mediastinum (over 8 cm above the level of the carina and more than 25%
of the width of the chest) or indistinct arch contour.
●● Left apical pleural cap is classic, due to pleural haematoma.
●● Look for rightward deviation of the trachea and depression of the left main
bronchus.

Figure 1.5 Transection of the aorta. Chest x-ray demonstrating widening of the mediastinum,
a left apical pleural cap with slight deviation of the trachea to the right. There is also a fracture
of the right second rib in keeping with high-energy trauma.

Figure 1.6 Transection of the aorta. CT demonstrating a transection of the aorta (white arrow)
with mediastinal haematoma and pleural haematoma (red arrow), which creates the apical
pleural cap on the chest x-ray.
6 C ardiothoracic and Vascular

AORTIC REGURGITATION
The causes are congenital (e.g. bicuspid aortic valve) or acquired. Acquired regurgitation
is more common and may be divided into processes affecting the valve (e.g. rheumatic
fever and endocarditis) or just the ascending aorta (e.g. syphilis, Reiter syndrome,
Takayasu arteritis, etc.).

PLAIN FILM
●● Non-specific cardiomegaly with left ventricular enlargement
●● Apex blunted and inferolateral displacement of the left heart border

AZYGOS CONTINUATION OF THE INFERIOR VENA CAVA

Absent hepatic segment of the inferior vena cava (IVC). Commonly associated with IVC
duplication, congenital heart disease and polysplenia syndromes.

Box 1.1 ANOMALIES ASSOCIATED WITH POLYSPLENIA SYNDROME

Pulmonary
●● Bi-lobed continuation of the lungs
●● Bilateral hyparterial bronchi
Cardiac
●● Bilateral superior vena cava (SVC)
●● Dextrocardia/cardiac malposition
●● Anomalous pulmonary venous return
●● Atrial septal defect/ventricular septal defect (ASD/VSD)
Abdominal
Small bowel malrotation
Absent gallbladder
Stomach malposition

BEHÇET DISEASE
Behçet disease is a multi-systemic immune-mediated vasculitis affecting both arteries
and veins, more common (by four- to five-fold) in young women. The classic presentation
is with a triad of oral ulceration, genital ulceration and ocular inflammation.

CT (FIGURES 1.7 AND 1.8)

●● Cardiovascular system involved in up to 30%. Look for aortic pseudoaneurysms
and occlusion/stenosis of distal vessels.
●● Pulmonary artery aneurysms and haemorrhage.

MRI
●● Central nervous system (CNS) involved in up to 20%.
●● The best indicator is a brainstem/basal ganglia lesion (bright on T2) in the right
clinical context.
 C ardiovascular 7

Figure 1.7 Behçet disease. Chest x-ray

demonstrating coil embolisation of a
pulmonary artery aneurysm and dense
airspace opacification in keeping with
haemorrhage.

Figure 1.8 Behçet disease. CT

pulmonary angiogram (CTPA)
demonstrating a right pulmonary artery
aneurysm (with arrow).

BUERGER DISEASE
Also known as thromboangiitis obliterans. It is a non-atherosclerotic vascular disease
affecting medium- and small-sized vessels of the upper and lower limbs. It affects the
distal vessels first and then progresses proximally.

INTERVENTION
●● Characteristic appearance on angiography of arterial occlusions with multiple
corkscrew shaped collaterals.
●● Skip lesions are also a recognised feature—occlusions with normal intervening
arteries.

CARDIAC TRANSPLANTATION
Complications post-cardiac transplantation include infection and post-transplant
lymphoproliferative disorder (PTLD).
8 C ardiothoracic and Vascular

INFECTION
This is the most common complication following cardiac transplant. Infections in the
first month post-transplant are more likely bacterial. After that, opportunistic viral and
fungal infections are more common.

Plain film
●● Single or multiple pulmonary nodules may represent Nocardia or Aspergillus infection.
●● Aspergillus is more common 2 months post-transplant. Nocardia tends to occur
later (e.g. 5 months).

PTLD
Non-specific complication mostly occurring within 1 year of transplant. Affects
about 10% of solid organ recipients. It is due to B- or T-cell proliferation, usually
following Epstein–Barr virus (EBV) infection. Responds rapidly to a reduction in
immunosuppression or alternatively rituximab.

Plain film
●● Single or multiple well-defined, slow-growing lung nodules
●● Consolidation less common
●● Hilar or mediastinal lymph node enlargement

CARDIAC ANGIOSARCOMA
More frequently affects middle-aged males. Typically involves the pericardium (80%) and
the right atrium, which explains the presentation with right heart failure or tamponade.

CT
●● Diffusely infiltrating mass extending along the pericardium and extending into the
cardiac chambers/pericardiac structures
●● Or, a low-attenuation mass in the right atrium showing heterogeneous
enhancement and central necrosis

CARDIAC LIPOMA
This is the second most common benign cardiac tumour of adulthood, usually discovered
incidentally. They can grow to a large size without causing symptoms.

CT
●● Homogeneous low-attenuation mass in the pericardium or a cardiac chamber

CARDIAC METASTASES
Most commonly from lung, breast or melanoma.

CARDIAC MYXOMA
This is the most common primary cardiac tumour of adulthood. It is typically found
in the left atrium (75%–80%). Associated with the Carney complex (a rare multiple
endocrine syndrome featuring multiple cardiac myxomas and skin pigmentation).
 C ardiovascular 9

ECHOCARDIOGRAPHY
●● Mobile echogenic mass with a well-defined stalk—may obstruct the mitral valve

PLAIN FILM/CT
●● Cardiomegaly with left atrial enlargement (splaying of the carina)
●● Signs of mitral valve obstruction (pulmonary hypertension and pulmonary oedema
from increased left atrial pressure)
●● Soft tissue mass within the left atrium (Figure 1.9)

Figure 1.9 Atrial myxoma. CT image

demonstrating a soft tissue mass within
the left atrium; this was proven to be an
atrial myxoma.

CARDIAC RHABDOMYOMA
Most common childhood cardiac tumour, mostly diagnosed incidentally (usually
asymptomatic) at <1 year of age. They tend to be multiple. Associated with tuberous sclerosis
(50% of patients with cardiac rhabdomyomas later diagnosed with tuberous sclerosis).

ECHOCARDIOGRAPHY
●● Hyperechoic mass, most commonly arising from the interventricular septum (can
be found anywhere)
●● May obstruct a valve

MRI
●● Useful for characterising an abnormality/aiding surgical planning

CARDIOMYOPATHY
ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA
Rare cause of fatal arrhythmia and sudden death, typically in young males. Familial
association. Variants described include a fatty (myocardium replaced by fatty tissue) and
a fibrofatty form (myocardium replaced by fibrofatty tissue).

MRI
●● High T1 infiltration of the right ventricular wall
●● Dilatation of the right ventricle with thinning of the ventricle, aneurysmal bulging
10 C ardiothoracic and Vascular

DILATED CARDIOMYOPATHY
This is a diagnosis of exclusion and relates to dilatation of the ventricles of unknown
aetiology. It implies systolic dysfunction.

HYPERTROPHIC CARDIOMYOPATHY
Asymmetric left ventricular hypertrophy (>12–15 mm, commonly located at the base
of the interventricular septum) leads to narrowing of the outflow tract. Affects flow
dynamics and gives rise to systolic anterior motion of the mitral valve.

MRI
●● Useful for assessing the distribution of disease and wall thickness.
●● Note—fibrotic tissue within the interventricular septum leads to patchy, delayed
enhancement post-contrast.

RESTRICTIVE CARDIOMYOPATHY
Any disease that restricts diastolic filling—restrictive cardiomyopathy is a diastolic
problem, so atria are large and ventricles small. Causes include sarcoidosis, amyloidosis
and haemochromatosis.

TAKOTSUBO CARDIOMYOPATHY
Transient cardiac syndrome predominantly involving postmenopausal women (90%).
There is left ventricular apical akinesis and dysfunction, with normal coronary arteries.
The typical presentation is with chest pain that mimics a myocardial infarction (troponin
enzymes are mildly elevated) following a physically/emotionally stressful event.

Plain film
●● Pulmonary oedema

MRI
●● Left ventricular dyskinesia and ballooning
●● High T2 signal (oedema) in the ventricular wall
●● No significant delayed contrast enhancement of the ventricular wall
(distinguishing from myocardial infarction)

CAROTID ARTERY STENOSIS

Box 1.2 CAROTID ARTERY STENTING

There are specific indications for carotid artery stenting (rather than endarterectomy;
e.g. restenosis following surgery, radiation stenosis and previous neck surgery on the
ipsilateral side). Stent is placed within 2 weeks of a stroke.

This is a major cause of stroke, typically caused by atherosclerosis at the carotid bulb
and the proximal segment of the internal carotid artery. Note that the internal carotid
artery is also the second most common site for fibromuscular dysplasia stenosis after the
kidneys.
 C ardiovascular 11

DOPPLER ULTRASOUND (US)

●● More than 70% stenosis increases systolic and diastolic flow velocity.
●● Systolic flow >230 cm/second and diastolic flow >110 cm/second are significant.

MYOCARDIAL ISCHAEMIA
HIBERNATING MYOCARDIUM
This is viable myocardial tissue that has adapted over time to reduced perfusion. The
tissue may be a target for revascularisation.

Nuclear medicine
●● Abnormal perfusion and abnormal wall motion

MYOCARDIAL INFARCTION
Nuclear medicine
●● Matched rest and stress perfusion defect, does not normalise.
●● Note: Myocardial ischaemia shows a perfusion abnormality that reverses on rest.

MRI
●● Infarcted tissue is indicated by delayed hyper-enhancement.
●● In the first few days after infarction, there is high T2 signal in the affected
myocardium.

STUNNED MYOCARDIUM
Temporary, acute severe ischaemia causes an abnormality of wall motion.

Nuclear medicine
●● Normal perfusion, abnormal wall motion.
●● Repeated stunning may cause
myocardial hibernation.

PERICARDIAL CYST
Mostly an incidental finding,
typically found at the right anterior
cardiophrenic angle.

PLAIN FILM (FIGURE 1.10)

●● Well-demarcated, rounded mass
at right cardiophrenic angle.

CT (FIGURE 1.11)
●● Low-attenuation (Hounsfield unit
[HU25]) rounded mass adjacent
to the pericardium
Figure 1.10 Pericardial cyst. Chest x-ray
MRI demonstrating a well-demarcated mass at the
●● Low T1 signal, high on T2 right cardiophrenic angle.
12 C ardiothoracic and Vascular

Figure 1.11 Pericardial cyst. Computed tomography image demonstrating a low-attenuation

mass adjacent to the pericardium.

PERICARDITIS
Most pericarditis is idiopathic and may be due to an undiagnosed viral infection.
Restrictive pericarditis is associated with myocardial thickening.

ACUTE PERICARDITIS
Look for evidence of a pericardial effusion. Symptoms (cardiac tamponade) relate to both
the volume of the effusion and speed of accumulation.

Plain film
●● Normal until fluid volume >250 mL.
●● Bilateral hila overlay sign, globular enlargement of the heart (gives a ‘water bottle’
appearance).
●● On a lateral chest x-ray, the signs are the epicardial fat pad sign (epicardial fat
separated from pericardial fat by a lucent line) and filling in of the retrosternal space.

CONSTRICTIVE PERICARDITIS
Thickened pericardium restricts diastolic ventricular filling, and the end result is cardiac
failure. The aetiology includes sarcoidosis, tuberculosis (TB), chronic renal failure,
rheumatic fever, trauma and radiation.

Plain film
●● Pericardial calcification (50%) and pleural effusions
●● Pericardial effusion
●● No pulmonary oedema

CT
●● Pericardial thickening >4 mm suggests pericarditis (normal 2 mm, excludes
pericarditis).
●● Pericardial effusion.
●● Findings may be isolated to one side of the heart.
●● Pericardial enhancement with contrast.
 C ardiovascular 13

MRI
●● Useful for distinguishing pericardial thickening from pericardial effusion.

POLYARTERITIS NODOSA
This is a vasculitis of the small- and medium-sized arteries and is more common in
males. Fever, malaise and weight loss are almost always present, due to ischaemic
complications. Most (80%) have renal involvement. The gastrointestinal (GI) tract is
affected in about 60%.

CT/INTERVENTION (FIGURES 1.12 AND 1.13)

●● 1–5-mm microaneurysms, typically peripheral and intra-renal.
●● Aneurysms tend to occur where vessels bifurcate.

Figure 1.12 Polyarteritis nodosa. Left

renal artery angiogram demonstrating
multiple small renal artery aneurysms
(white arrow).

Figure 1.13 Polyarteritis nodosa. Inferior

mesenteric artery angiogram demonstrating
multiple small aneurysms (white arrows).
14 C ardiothoracic and Vascular

●● Stenoses also occur.

●● Vasculitis causes distal ischaemia (renal infarcts, gut ischaemia, etc.).
●● May present with haemorrhage.

POPLITEAL ARTERY ENTRAPMENT SYNDROME

Symptomatic deviation and compression of the popliteal artery secondary to an abnormal
relationship with the medial head of gastrocnemius/popliteus (rare). Affects young
sportsmen and is bilateral in up to two-thirds. May present as intermittent claudication
or acute thrombosis. The management is surgical.

MRI
●● Most useful for demonstrating artery–muscle relationship and vessel lumen.

INTERVENTION
●● Medial deviation or compression of the artery on plantar or dorsi flexion of the
ankle.

POST-EMBOLISATION SYNDROME
This arises as a complication of transarterial chemoembolisation or arterial embolisation
(e.g. liver lesion treatment or uterine artery embolisation). Incidence increases with
increasing lesion size. It usually occurs within the first 3 days and eases over the next
3 days, and is usually self-limiting. The symptoms are mild fever, nausea/vomiting and
pain.

CT
●● Commonly demonstrates gas within the embolised lesion—does not imply
infection.

RENAL ARTERY STENOSIS

Accounts for <5% of hypertension in adults. In the elderly, it is mostly due to
atherosclerosis (90%); in the young, consider fibromuscular dysplasia. Presents with
severe refractory hypertension, renal impairment and raised intracranial pressure.
Biochemistry shows raised plasma renin (captopril test).

DOPPLER US
●● Raised peak systolic velocity, mild 100–200 cm/second and severe >200 cm/second.
●● Damped systolic waveform (‘parvus–tardus’).
●● Affected side may show an elevated resistive index if measured proximal to the
stenosis.

INTERVENTION
●● Focal or segmental stenosis, atherosclerotic lesions tend to be at the ostium or
proximal 2 cm.
●● Angioplasty effective in 80% for proximal lesions, 30% for ostial lesions.
 C ardiovascular 15

RHEUMATIC HEART DISEASE

Heart disease arising from rheumatic fever (a complication of a streptococcal
pharyngitis). May affect the myocardium, pericardium or valves (mitral valve affected
most often).

PLAIN FILM
●● Enlarged left atrial appendage/left atrium is classic (splaying of the carina with left
atrial enlargement).
●● Mitral stenosis—look for evidence of pulmonary oedema, left atrial enlargement,
alveolar haemorrhage and pulmonary ossification (due to pulmonary
haemosiderosis).
●● Mitral regurgitation—look for left ventricular enlargement.
●● Also look for pericardial calcification, valvular calcification and global
cardiomegaly.

SARCOIDOSIS
Suspected in patients with sarcoidosis and arrhythmias, affects about 5% of sarcoidosis
patients. Associated with poorer outcomes and up to a quarter of deaths from
sarcoidosis.

MRI
●● In acute sarcoidosis, there may be delayed enhancement (also with ischaemia) or
T2 hyperintense nodules at the base of the septum and left ventricle.
●● Look for high T2 signal in the epicardium with or without wall thickening
secondary to oedema; subendocardium is spared.
●● Pericardial effusion.

SUBCLAVIAN STEAL SYNDROME

Severe stenosis of the proximal subclavian artery causes retrograde flow in the ipsilateral
vertebral artery (to bypass the stenosis by collaterals). In partial steal, there is antegrade
flow in the vertebral artery in systole, with retrograde flow in diastole. Associated
with cerebral ischaemic symptoms (e.g. vertigo, dizziness and syncope). Mostly due to
atherosclerosis, but also linked to vasculitis. Mostly occurs on the left.

US
●● Retrograde ipsilateral vertebral artery flow with evidence of a subclavian stenosis
(parvus–tardus and monophasic waveform in the distal subclavian artery)

CT/MR ANGIOGRAPHY
●● Subclavian stenosis/occlusion
●● Delayed enhancement/retrograde flow in ipsilateral vertebral artery

INTERVENTION
●● Angioplasty and stenting preferred to surgical bypass in symptomatic patients
16 C ardiothoracic and Vascular

TAKAYASU ARTERITIS
This is a large-vessel arteritis tending to affect young women. There is granulomatous
inflammation of the vessel wall, with vessels ultimately becoming stenotic, occluded or
aneurysmal.

CT
●● Vessel wall thickening and enhancement.
●● Aorta (thoracic particularly) and its branches are mostly affected.
●● Pulmonary arteries affected in 50%, peripheral pulmonary arteries may be
‘pruned’, trunk dilated.
●● Vessels calcify in chronic disease (otherwise they are more likely to become
aneurysmal).

MRI
●● Look for high signal on the short tau inversion recovery (STIR) in the vessel wall,
indicating oedema.

RESPIRATORY

ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)

Box 1.3 THE BASIC PRINCIPLES OF HRCT OF THE THORAX

Why?
HRCT of the chest is the only way to demonstrate the secondary pulmonary lobule
(i.e. the basic anatomical structure responsible for gas exchange composed of acini,
bronchioles, lymphatics and vessels).
When?
Any diffuse lung disease including interstitial lung disease, pulmonary eosinophilias
and obstructive lung disease and to investigate patients with symptoms and a normal
chest x-ray.
How?
The key aspects of HRCT are thin collimation (1–2-mm slices) and high spatial
resolution reconstruction. Slices may be taken at staggered intervals (‘interspaced’;
e.g. six to eight images total) or as a volumetric dataset (e.g. every 10 mm)—the
merits of each are debatable. Patients are usually scanned supine; prone positioning
is useful to differentiate disease from ‘dependent’ changes (i.e. atelectasis in older
patients and smokers). Images are usually gathered in full inspiration. Expiratory
scans are used to demonstrate air-trapping or to differentiate between vascular and
airway disease as a cause of air-trapping.
Read more:
Kazerooni, E. 2001. High-resolution CT of the lungs. American Journal of
Roentgenology 177:501–519.

Box 1.4 WHAT IS GROUND-GLASS ATTENUATION?

An amorphous increase in lung attenuation that does not obscure vessels. Vessels
are obscured by consolidation.
 Respirator y 17

Also known as ‘acute respiratory distress syndrome’, this is an acute condition

characterised by bilateral pulmonary infiltrates and severe hypoxaemia in the absence of
cardiogenic pulmonary oedema. The underlying problem is diffuse alveolar damage.

PLAIN FILM
●● Normal for the first 24 hours, then septal lines and peribronchial cuffing, but no
effusions.
●● Unlike pulmonary oedema, infiltrates are initially peripheral rather than central,
and air bronchograms are more commonly seen.
●● May be complicated by pneumonia.

HIGH-RESOLUTION CT (HRCT)
●● After months, the consolidative pattern gives way to reticulation in the non-
dependent lung and, finally, honeycombing.

α1 ANTITRYPSIN DEFICIENCY
α1 antitrypsin is an inhibitor of a protease for elastin. The deficiency is also associated
with cirrhosis, necrotising panniculitis and Wegener granulomatosis. It causes a pan-
lobar emphysema in the lungs in young patients (aged 40–50 years).

PLAIN FILM (FIGURE 1.14)

●● Normal in mild disease
●● Later on, lucent, hyperinflated lungs in a young patient

Figure 1.14 α1 antitrypsin deficiency. Chest x-ray demonstrating hyperexpanded lungs and
predominant lower zone emphysema.
18 C ardiothoracic and Vascular

HRCT (FIGURE 1.15)

●● Pan-lobular emphysema (i.e. enlarged and destroyed secondary pulmonary lobule)
tending to affect the lower lobes bilaterally
●● Associated with bronchiectasis

Figure 1.15 α1 antitrypsin deficiency. Computed tomography image demonstrating marked

pan-lobular emphysema.

AMIODARONE LUNG DISEASE

Box 1.5 DIFFERENTIALS FOR A HYPERDENSE LIVER

Amiodarone
Gold
Thorotrast (old contrast agent)
Haemochromatosis
Haemsiderosis (spleen affected, too)
Glycogen storage disease

An interstitial lung disease affecting patients after amiodarone treatment. It occurs 1–12
months following at least 6 months of treatment.

HRCT
●● Peripheral, hyperdense consolidation and patchy ground-glass opacification (i.e.
alveolar infiltrates)
●● Peripheral/basal fibrosis
●● Hyperdense liver and heart—this is classic

ARTERIOVENOUS MALFORMATION (AVM)

Affects up to 15% of people with hereditary haemorrhagic telangiectasia (Osler–Weber–
Rendu syndrome). Patients may present with orthodeoxia (postural hypoxaemia
accompanied by breathlessness) or stroke due to paradoxical emboli.
 Respirator y 19

PLAIN FILM/CT
●● Well-defined, lobulated nodules with a feeding artery and draining vein
●● May contain phleboliths
●● Most are unilateral and two-thirds are in the lower lobes.

ASBESTOS-RELATED LUNG DISEASE

Box 1.6 CAUSES OF LOWER ZONE FIBROSIS

Asbestosis
Connective tissue diseases (rheumatoid, scleroderma and systemic lupus
erythematosus)
Idiopathic pulmonary fibrosis (usual interstitial pneumonia [UIP])
Drugs (methotrexate, bisulfan and bleomycin)
Look for soft tissue calcification, dilated oesophagus, distal clavicular osteolysis,
pleural plaques, diaphragmatic calcification and sympathectomy clips to help
diagnose the cause.

This refers to a spectrum of lung disease resulting from asbestos exposure. It may be a
benign pleural disease, usually occurring >20 years after exposure. More common in
males (occupational).

PLAIN FILM
●● Pleural effusion first.
●● Then, often (80%) pleural plaques affecting both parietal pleura (posterolateral/
lateral/costophrenic angles/mediastinal).
●● Diaphragmatic plaques are pathognomonic, the apices are spared.
●● Plaques are not always calcified.

CT (FIGURE 1.16)
●● Look for areas of round atelectasis (‘pseudotumour’ appearance) next to a pleural
plaque. The bronchovascular bundle typically converges into the lesion (‘comet tail’
sign).

Figure 1.16 Rounded atelectasis. CT images demonstrating calcified pleural plaques with
rounded atelectasis (pseudotumour; red arrow) overlying a calcified pleural plaque (white
arrow). The bronchovascular bundles form the comet tail sign (red arrow).
20 C ardiothoracic and Vascular

ASBESTOSIS
This is an interstitial lung disease due to asbestos exposure. There is progressive dyspnoea
and a strong association with malignancy (adenocarcinoma more likely).

Plain film
●● Lower zone fibrosis (due to inhalation gradient)
●● Pleural plaques
●● Effusions

HRCT
●● Initially small, sub-pleural, round or branching opacities a few millimetres from
the pleura—this is peri-bronchiolar fibrosis.
●● Sub-pleural curvilinear opacities, parallel to the chest wall—may represent
atelectasis or be associated with honeycombing later on.
●● Late disease is characterised by parenchymal bands and reticulation with distortion
of the lung parenchyma and traction bronchiectasis.
●● As the disease progresses, there is basal honeycombing, appearing similar to UIP.
●● No lymph node enlargement.

ASPERGILLOSIS
Aspergillosis refers to a spectrum of abnormalities caused by infection with the
Aspergillus fungus. The severity of the disease depends partly on the patient’s immune
status (Note: AIDS alone does not count).

ASPERGILLOMA
Affects patients with normal immunity but abnormal lungs. Fungal infection occurs
within a pre-existing cyst, cavity, bulla or area of bronchiectasis. Commonly referred to
as mycetoma.

Plain film (Figure 1.17)

●● Typically upper lobe abnormality, mass within a cavity frequently accompanied by
pleural thickening.
●● ‘Monad’/air crescent sign—the fungus ball is frequently surrounded by a crescent of air.

CT
●● Fungus ball (may calcify) lying dependently within a cavity or thin-walled cyst.

Intervention
●● Bronchial arteries supplying the abnormal lung become hypertrophied and are
liable to bleed.
●● Bronchial artery embolisation may be performed for haemoptysis.

ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS (ABPA)

Usually occurs in the context of chronic asthma or cystic fibrosis. Aspergillus organisms
are inhaled by an atopic host and cause a hypersensitivity reaction. It is the most common
pulmonary cause of an eosinophilia. Treatment is with steroids.
 Respirator y 21

Figure 1.17 Cystic fibrosis with

aspergilloma. Chest x-ray demonstrating
a right upper zone cavity with a soft
tissue focus outlined by a crescent
of air (Monad sign; white arrow) in
keeping with an aspergilloma. A further
aspergilloma is identified within the left
mid-zone (red arrow).

Plain film (Figure 1.18)

●● Migratory patchy foci of consolidation.
●● ‘Tram track’ appearance (i.e. gross bronchiectasis), central/upper zones is classic.
●● Tubular opacities are classic—these are dilated airways plugged with mucous,
known as the ‘finger in glove’ appearance.
●● Atelectasis from airway obstruction.

Figure 1.18 Allergic bronchopulmonary

aspergillosis. Chest x-ray demonstrating
gross central bronchiectasis with tubular
opacities. These represent mucous-filled
bronchi known as the ‘finger in glove’
appearance.

HRCT (Figure 1.19)

●● Hyperdense mucoid impaction of central and upper lobe airways giving rise to
bronchiectasis.
●● Bronchiectasis is varicose or saccular.
●● Centrilobular nodules and masses are features, not pleural effusions.
22 C ardiothoracic and Vascular

Figure 1.19 Allergic bronchopulmonary

aspergillosis. CT image demonstrating
gross central varicose bronchiectasis
(white arrow) with mucous-filled bronchi.

●● Chronic disease leads to upper zone fibrosis.

●● Air-trapping—gives a mosaic pattern of attenuation.

SEMI-INVASIVE PULMONARY ASPERGILLOSIS

Also known as ‘chronic necrotising pulmonary aspergillosis’. It may affect those with
mild immunosuppression; overall prognosis is good. Treatment is with anti-fungals.

CT
●● Typically upper zone nodules that then cavitate—a necrotic area then separates the
nodule from the surrounding lung (the ‘air crescent’ sign).

ANGIOINVASIVE ASPERGILLOSIS
The most common fungal infection to affect the severely immunosuppressed (commonly
post-transplant, leukaemia and post-chemotherapy). Invades blood vessels and causes
pulmonary infarction. Rapid progression and high mortality.

CT
●● Nodules with a rim of ground-glass opacification (haemorrhage)—known as the
‘halo’ sign

AIRWAY-INVASIVE ASPERGILLOSIS
Aspergillosis that affects the airways. It may manifest as acute tracheobronchitis,
bronchiolitis or bronchopneumonia. There is ulceration of the airways.

CT
●● Nodular opacities, centrilobular nodules or consolidation

ASPIRATION
Location depends on the position of the patient at the time of aspiration. The left lung
may be spared.
 Respirator y 23

PLAIN FILM
●● Most commonly the lower lobes are affected if erect; posterior upper lobe and
superior lower lobe are affected if supine.

CT
●● Consolidation, material in the airway
●● May be complicated by necrosis or abscess formation

BRONCHIECTASIS

Box 1.7 CAUSES OF BRONCHIECTASIS

Idiopathic
●● Most common cause overall
Congenital
●● Cystic fibrosis—most commonly congenital
Bronchial atresia
●● Primary ciliary dyskinesia
Acquired
●● Post-infectious (including ABPA)—most commonly acquired
●● Aspiration (including foreign body obstruction)
●● Inflammation—rheumatoid, sarcoid

Defined as abnormal, irreversible airway dilatation often associated with thickening of

the bronchial wall. Subtypes are cylindrical, varicose and cystic.

CYLINDRICAL
Relatively uniform, mild airway dilatation with parallel bronchial walls. Most common
and least severe. Causes include cystic fibrosis (pan-lobar), hypogammaglobulinaemia
(lower lobe) and Japanese pan-bronchiolitis (pan-lobar).

Plain film
●● Tram-track appearance (en face dilated airways) or ring shadows (axial appearance
of dilated airways)
●● Bronchial wall thickening

HRCT
●● ‘Signet ring’ sign describes the axial view of a dilated airway of larger diameter
than the accompanying artery.
●● Airways do not taper as they approach the lung periphery (airways can be seen in
the peripheral third of lung).

VARICOSE
Bronchial lumen assumes a beaded (‘string of pearls’) configuration with sequential
dilatation and constriction. Causes include ABPA.
24 C ardiothoracic and Vascular

Plain film
●● Beaded airway dilatation with or
without mucous impaction (‘finger
in glove’).
●● ABPA tends to affect the upper
lobes.

CYSTIC
A string or cluster of cyst-like bronchi,
the most severe kind of bronchiectasis.
Causes include post-infectious (e.g.
pertussis and unilobar), post-obstruction
and Mounier–Kuhn syndrome.
Figure 1.20 Cystic bronchiectasis. Chest x-ray
Plain film/HRCT (Figure 1.20) demonstrating ring shadows in keeping with
●● Cysts in clusters or strings cystic bronchiectasis.
●● Air-fluid levels commonly seen
within the cysts

BRONCHIOLITIS OBLITERANS

Box 1.8 MOSAIC PERFUSION OF THE LUNG

Subtle pattern of variable lung attenuation with a slight decrease in the calibre and
number of pulmonary vessels within the areas of low attenuation.
Expiratory HRCT differentiates between the two causes (i.e. small airways disease
vs. pulmonary vascular abnormalities).

Bronchiolar and peribronchiolar inflammation of the bronchioles leads to submucosal and

peribronchiolar fibrosis. This causes an obstruction of the bronchial lumen, also known
as obliterative bronchiolitis. Associated with transplantation (e.g. bone marrow/graft vs.
host—up to 10%; lung transplant), viral infection (known as Swyer–James or MacLeod
syndrome in children), toxin inhalation, rheumatoid arthritis, inflammatory bowel disease
and drug reactions (bleomycin, gold, cyclophosphamide, methotrexate and amiodarone).

HRCT
●● Air-trapping on expiratory scans (i.e. mosaic perfusion pattern)—this is classic and
due to obstruction of the small airways.
●● Bronchiectasis (i.e. dilated and thick-walled).
●● Centrilobular ground-glass opacification.

BRONCHOGENIC CYST
This is the most common foregut malformation in the thorax. It constitutes up to 20%
of mediastinal masses. It is an abnormality of the ventral diverticulum of the primitive
foregut and is associated with other congenital anomalies, spina bifida, extra-lobar
sequestration and congenital lobar emphysema.
 Respirator y 25

Box 1.9 CAUSES OF A MIDDLE MEDIASTINAL MASS

Look for:
●● Widened paratracheal stripe
●● Mass in the aortopulmonary window
●● Displacement of the azygo-oesophageal line

Common differentials include:

1. Foregut duplication cyst (bronchogenic or oesophageal)—most common
2. Lymph node
3. Lung cancer
4. Aortic aneurysm

PLAIN FILM
●● Posterior or middle mediastinal mass, typically subcarinal and more common on
the right
●● Can be intrapulmonary—most commonly located in the medial lower lobes

CT
●● Well-circumscribed spherical mass, usually with an internal density of 0–25 HU
(may be higher)
●● May contain an air–fluid level if communicating with an airway
●● Rim-enhancement may be seen, calcification is not typical

BRONCHOPLEURAL FISTULA
This is an abnormal communication between the pleural space and the bronchial tree
caused by lobectomy, pneumonectomy, lung necrosis, TB, etc.

PLAIN FILM
●● The pleural cavity is expected to fill with fluid post-pneumonectomy—a fistula is
suspected if this does not occur, if there is an abrupt decrease in the air–fluid level
or there is a new gas in a previously fluid-filled pleural cavity.
●● Contralateral shift of the mediastinum.

NUCLEAR MEDICINE
●● Xenon ventilation study will show activity in the pleural space.

CARCINOID TUMOUR (FIGURE 1.21)

Carcinoid tumours are neuroendocrine tumours with low malignant potential; overall
prognosis is good. They are associated with multiple endocrine neoplasia type-1. They are
well-vascularised, endobronchial lesions, so commonly present with haemoptysis. Cough
and recurrent pneumonia are also common.

●● Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia—may be a

precursor to a bronchial carcinoid. Characterised by small lung nodules, air-
trapping, ground-glass opacification and bronchiectasis.
26 C ardiothoracic and Vascular

Figure 1.21 Carcinoid tumour. CT image demonstrating an avidly enhancing central mass with
foci of calcification.

PLAIN FILM
●● Atelectasis commonly, a nodule (typically perihilar) may be seen.

CT
●● Avidly arterial enhancing endobronchial lesion.
●● Rounded appearance and mostly found centrally (20% are peripheral).
●● A third calcify, no fat content and rarely cavitate.
●● Check lymph nodes for evidence of metastasis—Note: Lymph nodes may be
enlarged from concurrent infection.

NUCLEAR MEDICINE
●● Cold on fludeoxyglucose positron emission tomography (PET).
●● Gallium 68 PET is used to stage carcinoid.

Box 1.10 A DIFFERENTIAL FOR ENHANCING LYMPH NODES

Benign
●● Castleman disease
●● Sarcoid
Neoplastic
●● Renal cell carcinoma
●● Thyroid
●● Small-cell carcinoma

CASTLEMAN DISEASE
Benign B-cell lymphoproliferation, more common in patients with HIV or AIDS.
 Respirator y 27

CT
●● Multiple, enhancing lymph nodes—usually axillary or supraclavicular
●● Mediastinal or hilar nodes—rare
●● Centrilobular lung nodules and ground-glass opacification that mimics
lymphocytic interstitial pneumonia (LIP)—rare

CHURG–STRAUSS SYNDROME
Also known as eosinophilic granulomatosis with polyangiitis, this is a variant of
polyarteritis nodosa affecting small to medium vessels. It is a necrotising vasculitis.
Almost all patients have asthma, and eosinophilia and p-ANCA is positive in 75%.
Cardiac involvement (including infarction) is common.
Diagnostic criteria (four required): asthma, eosinophilia, neuropathy, migratory
or transient pulmonary opacities, paranasal sinus abnormalities and/or extravascular
eosinophils at biopsy.

PLAIN FILM
●● Transient peripheral consolidation and small pleural effusions

HRCT
●● Non-segmental, transient peripheral consolidation/ground glass
●● Interlobular thickening
●● Centrilobular nodules (less commonly)

CYSTIC FIBROSIS
This is an autosomal recessive defect in
the gene regulating chloride transport,
resulting in thick secretions. The
lungs and pancreas are affected most
severely.

PLAIN FILM (FIGURE 1.22)

●● Bronchiectasis (cylindrical at
first).
●● Bronchial wall thickening.
●● Hyperinflation (due to
air-trapping).
●● Any part of the lungs may be
affected, but particularly central
Figure 1.22 Cystic fibrosis. Chest x-ray
zones, upper lobes and apical
demonstrating hyperexpanded lungs with upper
lower lobes.
zone fibrosis, bronchial wall thickening and
●● Look for mucous impaction with
bronchiectasis affecting the central and upper
atelectasis.
zones. There is a cavity with a soft tissue focus
●● Spontaneous pneumothorax.
outlined by a crescent of air (Monad sign; white
●● Pulmonary artery enlargement.
arrow) in keeping with an aspergilloma.
28 C ardiothoracic and Vascular

HRCT
●● Most sensitive for detecting early change

DIAPHRAGMATIC RUPTURE
Usually occurs due to blunt abdominal trauma, with the left side three-times more likely
to rupture (the liver shields the right side).

PLAIN FILM
●● Abnormal contour to the diaphragm, abdominal contents in the chest and
deviation of an enteral tube

CT
●● Discontinuity of the left hemidiaphragm.
●● ‘Collar’ sign describes a focal constriction of the herniating viscera at the site of
rupture.
●● The ‘dependent viscera’ sign is where abdominal viscera lie dependently against the
posterior ribs due to loss of diaphragmatic support.

EXTRINSIC ALLERGIC ALVEOLITIS

See ‘Hypersensitivity pneumonitis’ section.

EMPHYSEMA
Defined as abnormal, permanent enlargement of the airspaces distal to the terminal
bronchiole, accompanied by destruction of their walls without obvious fibrosis.

CENTRILOBULAR
This is the most common subtype, mostly caused by smoking.

Plain film
●● Normal unless advanced
●● Hyperinflated lucent lungs and flattened diaphragms
●● More common in the upper zones
●● Check for bullae

HRCT
●● Multiple small, round foci of abnormally low attenuation without visible walls that
are scattered throughout normal-appearing lung parenchyma

PAN-LOBULAR
Associated with various causes, including α1-antitrypsin deficiency and drug reaction
(e.g. Ritalin and intravenous drug users).

Plain film
●● Insensitive—look for diffuse simplification of the lung architecture.

HRCT
●● Diffusely low-attenuation lungs without clear demarcation of normal lung
●● Loss of vascular markings
 Respirator y 29

PARASEPTAL
Lucent, cystic spaces arranged beneath the pleural surfaces, including the interlobar
fissures. Associated mostly with smoking.

Plain film
●● Rarely detectable
●● May be complicated by pneumothorax

HRCT
●● Cystic spaces arranged beneath the pleural surfaces including the interlobar fissures.
●● The borders of the secondary pulmonary lobule are intact.

EOSINOPHILIC LUNG DISEASE

Idiopathic subtypes are described below: namely, simple pulmonary eosinophilia, acute,
chronic and hypereosinophilic syndrome.

SIMPLE PULMONARY EOSINOPHILIA (LÖFFLER SYNDROME)

Initially described as due to parasitic infection, may be associated with other pathology (e.g.
ABPA) or drug reaction. It is benign and self-limiting. There is mild blood eosinophilia.

Plain film
●● ‘Reverse bat’s wing’ appearance is classic (i.e. bilateral peripheral airspace
opacification).

HRCT
●● Peripheral ground-glass opacification/consolidation
●● Nodules with surrounding ground-glass opacity (‘halo’ sign)

ACUTE EOSINOPHILIC PNEUMONIA

Mean age of onset about 30 years, may be smoking related. Rapid onset of symptoms,
fever and hypoxaemia. Marked eosinophilia on bronchoalveolar lavage (BAL)/pleural
samples, but normal blood levels. Rapid response to steroids.

Plain film
●● Bilateral densities with effusions, with or without consolidation

HRCT
●● Bilateral, patchy, ground-glass opacities
●● Interlobular septal thickening and pleural effusions

CHRONIC EOSINOPHILIC PNEUMONIA

Insidious onset of night sweats, pyrexia, cough and weight loss. More common in middle
age and 50% have asthma. Mild blood eosinophilia and high eosinophilia on BAL.
Responds to steroids.

Plain film
●● Bilateral, non-segmental, upper peripheral lobe airspace opacification (so-called
‘photographic negative of pulmonary oedema’ or ‘reverse bat’s wing’ appearance)
30 C ardiothoracic and Vascular

Box 1.11 CAUSES OF THE BAT’S WING APPEARANCE

Simple pulmonary eosinophilia
Chronic eosinophilic pneumonia
Cryptogenic organising pneumonia
Pulmonary vasculitis
Pulmonary infarction
Pulmonary contusion

HRCT
●● Dense peripheral consolidation
●● With or without ground glass, nodules and reticulation
●● Rarely effusions

IDIOPATHIC HYPEREOSINOPHILIC SYNDROME

Rare condition with marked eosinophilia and end-organ eosinophilic infiltration and
damage. Heart (endocardial fibrosis, cardiomyopathy, etc.) and nervous system most affected.

Plain film
●● Non-specific findings—multiple opacities, usually related to pulmonary oedema

HRCT
●● Nodules with a ground-glass halo
●● Pleural effusions due to cardiac failure

FAT EMBOLUS
Lung embolus of fat-containing material (may also travel to the brain or skin), the vast
majority are in patients 1–2 days following severe trauma or long bone fracture. Resolves
in 1–4 weeks, often asymptomatic.

PLAIN FILM/CT
●● Bilateral, widespread, ill-defined peripheral infiltrates similar to ARDS in a patient
with a recent history of major trauma

FIBROSING MEDIASTINITIS
Non-malignant proliferation of fibrous tissue affecting the mediastinum. Wide range
of causes including infectious (histoplasmosis and TB), inflammatory (retroperitoneal
fibrosis and orbital pseudotumour) and iatrogenic (radiotherapy and drug reaction).
Tends to affect the young. Described as focal (80%—usually secondary to TB or
histoplasmosis) or diffuse (20%—mostly inflammatory). It is the most common benign
cause of SVC obstruction.

FOCAL
CT
●● 2–5-cm calcified (80% calcified) mass compressing pulmonary vasculature leading
to right heart strain
 Respirator y 31

●● Peribronchial cuffing, septal thickening and wedge-shaped areas of pulmonary

infarction

DIFFUSE FORM
CT
●● Soft tissue encasement of mediastinal structures with infiltration of fat planes

FLEISCHNER SOCIETY GUIDELINES FOR PULMONARY NODULES

The purpose of the guidelines is to help with the management of small lung nodules
detected incidentally. The likelihood of malignancy depends on nodule size and patient
factors.

●● A low-risk patient has minimal/no smoking history and no other known risk
factors (e.g. significant family history, asbestos exposure, etc.).
●● The likelihood of malignancy is thought to be 0.2% for nodules of <3 mm, 0.9% for
nodules of 4–7 mm and 18% for nodules of 8–20 mm (Table 1.3).

Table 1.3 Fleischner Society guidelines 2013

Size (mm) Low risk High risk

≤4 No follow-up 12 months
>4–6 12 months 6 months, then 18–24
months
>6–8 6–12 months, then 18–24 months 3–6 months, 9–12 and 24
months
>8 3, 9 and 24 months + positron Same as low risk
emission tomography ± biopsy
Solid nodules: McMahon, H. et al. 2005. Guidelines for management of small pulmonary nodules detected on CT scans: A
statement from the Fleischner Society. Radiology 237:395–400.
Sub-solid nodules: Naidich, D. et al. 2012. Recommendations for the management of subsolid pulmonary nodules
detected at CT: A statement from the Fleischner Society. Radiology 266:304–317.

Box 1.12 A DIFFERENTIAL FOR SOLITARY PULMONARY NODULES

Granuloma
Organising pneumonia
Bronchogenic cyst
Infection/inflammation
Tumour
Carcinoid
Hamartoma

GOODPASTURE SYNDROME
Autoimmune disease characterised by glomerulonephritis and pulmonary
haemorrhage—note that pulmonary features occur before renal manifestations. The
pathology is antiglomerular basement membrane antibodies; these attack the alveolar
32 C ardiothoracic and Vascular

basement membrane in the lung. Associated with a positive p-ANCA (anti-neutrophil

cytoplasmic antibody) or c-ANCA in about 30%.

PLAIN FILM
●● Bilateral consolidation with sparing of the costophrenic angles and lung periphery.
●● Progression to an interstitial/fibrotic pattern in chronic disease.

HRCT
●● Patchy ground-glass opacification with peripheral and costophrenic angle sparing.
●● Airspace disease clears within a couple of weeks.
●● Pulmonary fibrosis may develop in the long term.

HAMARTOMA
This is a common, benign lung neoplasm peaking in the sixth decade. A minority (10%)
are endobronchial.

PLAIN FILM
●● Smooth, marginated nodule, frequently calcified.
●● Two-thirds in the lung periphery.
●● Look for atelectasis/consolidation, suggesting an endobronchial lesion.

CT
●● Fat attenuation of the nodule (50%)
●● Or a combination of fat and calcification
●● Diffuse popcorn calcification (classic)

NUCLEAR MEDICINE
●● Note: Up to 20% are hot on PET

HEREDITARY HAEMORRHAGIC TELANGIECTASIA

Also known as Osler–Weber–Rendu syndrome. It is an autosomal dominant disorder
characterised by multiple AVMs with a classic triad of telangiectasia, epistaxis and
a positive family history. A total of 20% of patients have multiple pulmonary AVMs,
causing cyanosis, dyspnoea, stroke and brain abscess. Other sites of AVMs include the
brain, spinal cord, GI tract and liver.

PLAIN FILM/CT
●● Rounded/lobulated nodule with feeding vessels

HISTOPLASMOSIS
Fungal infection from North America and inhaled from bird and bat faeces. In
immunocompetent individuals, infection almost always resolves without treatment.

PLAIN FILM/CT
●● Calcified pulmonary nodules 2–5 mm in size (miliary appearance).
 Respirator y 33

●● Enlarged lymph nodes with peripheral ‘egg shell’ calcification is classic.

●● Look for a broncholith—this is a calcified lymph node that has eroded into the
airway.

Box 1.13 CAUSES OF CALCIFIED LYMPH NODES IN THE THORAX

The six ‘osis’s’
Silicosis
Sarcoidosis
Histoplasmosis
Amyloidosis
Coal worker’s pneumoconiosis
Blastomycosis
Treated lymphoma

HIV/AIDS—PULMONARY MANIFESTATIONS (TABLE 1.4)

Table 1.4 CD4 count narrows the differential for potential causes of pulmonary infection in the
context of HIV and AIDS
<200 cells/µL = AIDS, high
risk for opportunistic
>200 cells/µL infection and malignancy <50 cells/µL

Histiocytosis Pneumocystis pneumonia Mycobacterium avium

Lymphoma (non-Hodgkin mostly) Tuberculosis
Cytomegalovirus Kaposi’s sarcoma
Recurrent bacterial pneumonia
(AIDS-defining illness)

CRYPTOCOCCUS
Plain film/CT
●● Small pulmonary nodules (solitary or multiple) that may cavitate. Segmental and
lobar consolidation.
●● Check for hilar and subcarinal lymph node enlargement.
●● Pleural effusions are common.

KAPOSI’S SARCOMA
This is the most common AIDS-related neoplasm and is more common in men.

Plain film/CT (Figure 1.23)

●● Numerous ill-defined perihilar/peribronchovascular nodules, surrounded by
ground glass.
●● Less commonly, there is interlobular septal thickening.
●● Look for enhancing hilar lymph node enlargement.
●● Pleural effusions atypical.

Nuclear medicine
●● Note: Lymphoma is gallium avid, Kaposi lesions are not.
34 C ardiothoracic and Vascular

Figure 1.23 Kaposi sarcoma. Computed tomography image demonstrating the typical ill-
defined peribronchovascular ‘flame-shaped’ ground-glass opacities (white arrow).

LYMPHOMA
Mostly non-Hodgkin and usually associated with more disseminated extra-nodal disease
involving the CNS, GI tract and bone marrow.

Plain film/CT
●● The most common finding is multiple pleural or intrapulmonary masses.

PNEUMOCYSTIS PNEUMONIA (PCP) (FIGURE 1.24)

Fungal infection, the most common opportunistic infection.

Plain film
●● May be normal.
●● Look for diffuse, bilateral airspace opacification.
●● Check for a pneumothorax—this would be nearly pathognomic for PCP in the right
setting.

Figure 1.24 Pneumocystis pneumonia.

Computed tomography image
demonstrating diffuse, bilateral ground-
glass opacification.
 Respirator y 35

CT
●● Diffuse, ground-glass pattern of airspace opacification (most typical) with or
without reticulation.
●● Upper lobe cysts are common and prone to pneumothorax.
●● No lymph node enlargement or pleural effusion.

PNEUMONIA
Bacterial pneumonia is most common (Streptococcus or Haemophilus), though TB
infection is the most common worldwide.

Plain film
●● Focal or lobar consolidation

HODGKIN VERSUS NON-HODGKIN LYMPHOMA

Box 1.14 COTSWOLDS MODIFICATION OF THE ANN ARBOR STAGING SYSTEM

Staging lymphoma
I: Single node group affected
II: Multiple node groups, same side of diaphragm
III: Multiple node groups, both sides of the diaphragm
IV: Multiple extra-nodal sites of disease, or nodes and extranodal disease
X: Denotes mass >10 cm
E: Denotes extra-nodal extension or single extra-nodal site of disease
Hodgkin and non-Hodgkin lymphomas are staged using the same system.

HODGKIN LYMPHOMA
Most present with enlarged supraclavicular/cervical lymph nodes, often with no
symptoms. Diagnosis confirmed by presence of Reed–Sternberg cells. More common in
the chest than non-Hodgkin.

Plain film (Figure 1.25)

●● Masses, consolidation and nodules
●● Pleural effusions are common

Figure 1.25 Lymphoma. Chest

x-ray demonstrating mediastinal
lymphadenopathy with widening of the
paratracheal stripe (white arrow) and loss of
the aortopulmonary window (red arrow).
36 C ardiothoracic and Vascular

CT
●● Parenchymal disease accompanied by intrathoracic adenopathy
●● Expect enlarged mediastinal lymph nodes (paratracheal and anterior
mediastinum), hila nodes atypical

NON-HODGKIN LYMPHOMA
Tends to present with slowly growing lymph nodes and B symptoms (i.e. fever, night
sweats, weight loss). Far more common than Hodgkin lymphoma. About three-quarters
in the thorax are diffuse large B-cell lymphoma (DLBCL).

Plain film
●● Classic appearance is hilar or mediastinal lymph node enlargement with a pleural
effusion.

CT
●● Pattern of lymph node enlargement varies with lymphoma subtype (e.g. in DLBCL,
prevascular/pretracheal nodes are most commonly affected).
●● May present with miliary nodules.

HYDATID INFECTION
The lungs are the second most common site (about 15%) after the liver to be affected. Up
to 15%–25% show no symptoms. Diagnosis made with Casoni skin test or serological
antigens. Expect blood eosinophilia.

PLAIN FILM
●● Multiple well-defined, rounded masses (up to 20 cm).
●● More common in the lower lobes, may have an air–fluid level (due to
communication with the bronchial tree).

CT
●● Cyst with low-density contents, rarely calcification.
●● ‘Water lily’ sign describes the floating cyst membrane within cyst fluid.
●● ‘Empty cyst’ sign occurs where cyst contents have been expectorated.

HYPERSENSITIVITY PNEUMONITIS
Also known as extrinsic allergic alveolitis, it is a granulomatous response to an inhaled
antigen. The antigens involved include animal proteins (e.g. bird fancier’s lung), microbes
(e.g. farmer’s lung, hot tub lung, etc.), chemicals, etc. Presentation may be acute (e.g.
6–8 hours after exposure) or chronic after years of exposure.

PLAIN FILM
●● A normal chest radiograph is the most common finding.
●● Look for multiple poorly defined small opacities, patchy/diffuse airspace shadowing.
●● Pleural effusions are unusual.
●● In chronic cases, there may be fibrosis, typically in the upper zones.
 Respirator y 37

HRCT
●● Patchy ground-glass change and small ill-defined centrilobular nodules.
●● Look for air-trapping giving a mosaic pattern of attenuation (i.e. trapped air in
secondary lobules).

IDIOPATHIC INTERSTITIAL PNEUMONIA

Box 1.15 MAKE SENSE OF IDIOPATHIC INTERSTITIAL PNEUMONIA

Mueller-Mang, C. et al. 2007. What every radiologist should know about idiopathic
interstitial pneumonias. Radiographics 27:595–615.
Hansell, D. et al. 2008. Fleischner society: Glossary of terms for thoracic imaging.
Radiology 246:697–722.

This is a group of seven diffuse lung diseases. They are rare, and each has its own pattern
on HRCT that correlates with histological findings. Patients typically present with non-
specific cough or dyspnoea.
In approximate order of frequency:

USUAL INTERSTITIAL PNEUMONIA (UIP)

The UIP pattern is seen with idiopathic pulmonary fibrosis (IPF; the clinical syndrome).
It typically affects those >50 years of age, often with a smoking history. The UIP pattern
is also seen with rheumatoid lung, systemic sclerosis (can have UIP or non-specific
interstitial pneumonia [NSIP] pattern), asbestosis and other connective tissue diseases.
Response to steroids and prognosis is poor in IPF.

Plain film
●● Normal at first, then decreased lung volumes with sub-pleural, basal reticulation.

HRCT
●● The classic trio is: (1) apicobasal gradient of (2) sub-pleural reticular opacities, and
(3) macrocystic honeycombing and traction bronchiectasis.
●● Ground-glass attenuation less extensive than the reticular opacities.
●● Check for an irregular pleural surface.
●● Typically, abnormal lung is seen next to normal lung.
●● The pattern is typical, biopsy may not be required for diagnosis.
●● 10% of IPF patients develop lung cancer.

NON-SPECIFIC INTERSTITIAL PNEUMONIA (NSIP)

Primarily idiopathic, but the pattern may also be associated with connective tissue
disorders (e.g. systemic lupus erythematosus [SLE] and systemic sclerosis), other
autoimmune diseases (rheumatoid arthritis) and may be drug induced (e.g. gold). Affects
younger patients than IPF and responds well to steroid treatment.

Plain film
●● Normal at first, then diffuse airspace opacities.
38 C ardiothoracic and Vascular

HRCT
●● Bilateral, symmetrical, sub-pleural ground-glass change with reticular opacities.
●● Traction bronchiectasis and consolidation later in the disease.
●● Ground-glass opacification dominates—not reticulation as with UIP.
●● There may be honeycombing late in the disease (microcystic).

CRYPTOGENIC ORGANISING PNEUMONIA (COP)

Previously known as bronchiolitis obliterans organising pneumonia. It is characterised by
the onset of cough, dyspnoea and low-grade pyrexia over several weeks. Wide age range
affected, more common between 40 and 70 years of age.

Plain film
●● Bilateral, peripheral patchy consolidation.
●● Fleeting/migratory consolidation is classic.

HRCT
●● Typically multifocal, transient, patchy, dense consolidation with a predominantly
sub-pleural, mid-lower zone distribution (80%).
●● Small centrilobular nodules and peribronchial thickening.
●● The ‘atoll’ sign is characteristic (not pathognomic), lesion with central ground glass
and rim of consolidation.
●● Adenopathy (25%) and effusions (30%) are less common.
●● Dense consolidation helps to distinguish COP from desquamative interstitial
pneumonia (DIP)—ground-glass opacification dominates in DIP

RESPIRATORY BRONCHIOLITIS-ASSOCIATED INTERSTITIAL

LUNG DISEASE (RB-ILD)
This is the interstitial lung disease of smokers, more common in men aged 30–40 years.
Treatment is with steroids and smoking cessation.

HRCT
●● Centriolobular nodules with ground glass, bronchial wall thickening and
air-trapping.
●● Expect background centrilobular emphysema (due to smoking history).

DESQUAMATIVE INTERSTITIAL PNEUMONIA (DIP)

Strongly associated with smoking (90% are smokers), considered the end of the RB-ILD
spectrum. More common in men, the prognosis is good with steroids and smoking
cessation.

Plain film
●● Non-specific, hazy opacities

HRCT
●● Diffuse ground-glass opacification not respecting fissures—this is classic.
●● Deep parenchymal cysts.
●● More commonly a peripheral pattern.
 Respirator y 39

ACUTE INTERSTITIAL PNEUMONIA (AIP)

Unlike the other idiopathic interstitial pneumonias (IIPs), symptom onset is acute and
rapidly progressive to requiring ventilation in 3 weeks. Steroids are effective early on, but
mortality remains 50%.

Plain film
●● Diffuse patchy airspace disease (similar to ARDS), but sparing the costophrenic
angles.

HRCT
●● Ground-glass opacities and dependent consolidation (from oedema and
haemorrhage).
●● For survivors of the acute disease, there may be non-dependent honeycombing and
traction bronchiectasis (consolidation is thought to be protective against this).

LYMPHOCYTIC INTERSTITIAL PNEUMONITIS (LIP)

Very rare when idiopathic. The pattern is more commonly seen in patients with Sjögren
syndrome or who are immunocompromised (e.g. HIV) and have chronic, active hepatitis.
More common in women.

Plain film
●● Non-specific, reticular or reticulo-nodular opacities

HRCT
●● The classic duo is: (1) diffuse ground-glass opacification; and (2) thin-walled
perivascular cysts.
●● Centrilobular nodules, septal thickening and pleural effusions are less common.

KARTAGENER SYNDROME
This is a type of primary ciliary dyskinesia with autosomal recessive inheritance. It
comprises a triad of dextrocardia, bronchiectasis and sinusitis. The problem is due
to ciliary dysfunction; in the lungs, this leads to bronchitis, recurrent pneumonia,
etc. It usually presents in childhood and is associated with infertility, corneal
abnormalities, transposition of the great vessels, pyloric stenosis, post-cricoid web and
epispadias.

PLAIN FILM
●● Classic findings are bronchiectasis and dextrocardia.
●● Check also for bronchial wall thickening, collapse and consolidation.

LUNG CANCER
Lung cancer is the most common cause of cancer death worldwide. Mostly diagnosed
when the disease is advanced, a minority (about 10%) are picked up incidentally. Lung
cancer is divided broadly into two groups: non-small-cell lung cancer (NSCLC; 85%) and
small-cell lung cancer (SCLC) (Table 1.5).
40 C ardiothoracic and Vascular

Table 1.5 Basic staging of non-small-cell lung cancer

Management T Characteristics

Lobectomy 1 Up to 3 cm in size, no bronchial invasion

2 3–7 cm, >2 cm from carina, lobar atelectasis
Pneumonectomy 3 >7 cm, <2 cm from carina, whole lung collapse, nodules in
same lobe, invasion of chest wall, diaphragm, pericardium, etc.
Non-operative 4 Tumour in the carina, invasion of heart/great vessels and
nodules in ipsilateral lobes
Note: Ipsilateral nodes are considered N1–2, or N3 if contralateral or supraclavicular. Nodules in the contralateral lung are
classified M1a, or M1b if distant metastases.

NSCLC
This is further sub-divided into squamous cell carcinoma (SCC) (35%), adenocarcinoma
(30%) and large-cell carcinoma (15%).

Plain film
●● Lung mass.
●● Lung/lobar collapse denoting an obstructing endobronchial mass.
●● Pleural effusion.
●● SCC tends to cavitate, adenocarcinoma may appear as consolidation resistant to
antibiotics.
●● Check for mediastinal or hilar lymph node enlargement and bone destruction.

CT
●● Ill-defined, peripheral, spiculated and irregular nodules are high risk.
●● Air bronchogram and focal lucency in a nodule also suggest malignancy.
●● Cavitation is non-specific, but a cavity wall >15 mm thick is worrying.
●● Nodules enhancing >15 HU are 98% sensitive, 73% specific for malignancy.
●● Common sites for metastases include adrenal glands, liver, brain, bones and soft tissues.

Nuclear medicine
●● PET is superior for staging (92% accuracy, 25% for CT) and assessing bone disease
(92% vs. 87%).
●● False positives may arise due to inflammatory processes.

SCLC
This used to be known as oat-cell carcinoma. It is very aggressive and rapidly fatal
without treatment (chemotherapy/radiotherapy). It is a disease of smokers and typically
presents once systemic.

Plain film
●● Large central mass involving at least one hilum
●● Lung/lobar collapse, pleural effusion

CT
●● Large central/hilar mass with associated lymph node enlargement.
●● Encasement of the heart and great vessels—note that a quarter of all superior vena
cava obstruction is due to SCLC.
 Respirator y 41

Nuclear medicine
●● Bone scan is useful for detecting bone metastases.
●● PET is used for staging.

LUNG TRANSPLANT PULMONARY COMPLICATIONS

Box 1.16 COMPLICATIONS OF LUNG TRANSPLANTATION

Acute complications
●● Reperfusion syndrome
●● Acute transplant rejection
●● Anastomotic dehiscence
Any time
●● Infection
Chronic
●● Bronchiolitis obliterans
●● PTLD

REPERFUSION SYNDROME
This is the most common immediate complication and occurs within 48 hours of
transplant.

Plain film
●● Perihilar airspace opacification
●● Bibasal pleural effusions

ACUTE TRANSPLANT REJECTION

Occurs at approximately 10 days post-transplant.

Plain film
●● Normal in 50%
●● Otherwise heterogeneous peri-hilar opacification, septal thickening and right
pleural effusion
●● Absence of upper lobe blood diversion

BRONCHIOLITIS OBLITERANS
This is a leading cause of death after approximately 2 years; onset is chronic from about 3
months post-transplant. Cytomegalovirus (CMV) is a predisposing factor.

Plain film/CT
●● Normal chest x-ray initially, then decreased vascular markings and increasing
bronchiectasis
●● Hyperinflated lungs with bronchial thickening and dilatation
●● Air trapping, mosaic perfusion and bronchiectasis
 Another Random Document on
Scribd Without Any Related Topics
 Bartolomeo Bosco in his prime. From an engraving
in the Harry Houdini Collection.

But in attacking Pinetti, Robert-Houdin goes a step too far and falsifies,
not directly but by innuendo, when he permits the impression to go forth
that Pinetti was hounded and ruined both financially and professionally by
Torrini, as is set forth on page 104. He pictures Torrini as dogging the
footsteps of Pinetti through all Italy and finally driving him in a state of
abject misery to Russia, where he died in the home of a nobleman, who
sheltered him through sheer compassion. Robert-Houdin must have known
this was absolutely untrue, for he quotes Robertson, who published Pinetti’s
true experiences in Russia. Pinetti took a fortune with him to Russia,
acquired more wealth there, and then lost his entire financial holdings
through his passion for balloon experiments, as is set forth in chapter II. of
this book.
Then, to show his own inconsistency, after picturing Pinetti in his
“Memoirs” as a charlatan, a conjurer of vulgar, uncouth pretensions rather
than as a good showman of real ability, Robert-Houdin is forced to admit on
page 25 of “Secrets of Magic” that later conjurers employed Pinetti
programmes as a foundation upon which their performances were built!
Even here, however, Robert-Houdin fails to acknowledge an iota of the
heavy debt which he personally owed the despised Chevalier Pinetti.
Robert-Houdin devotes the greater part of chapter X., American edition
of his autobiography, to belittling Bosco, a conjurer whose popularity all
over Europe was long-lived. First, he pictures Bosco as a most cruel
creature who literally tortured to death the birds used in his performances.
Here, as in his attack on Pinetti, Robert-Houdin throws the responsibility
for criticism on the shoulders of another. His old friend Antonio
accompanies him to watch Bosco’s performance, and it is Antonio
throughout the narrative who inveighs against Bosco’s cruelty and Antonio
who insists upon leaving before the performance closes, because the cruelty
of the conjurer nauseates him.
At that time no society for the protection of animals existed, and, even if
it had, I doubt whether Bosco’s performance would have come under the
ban. Certain magicians of to-day employ many of Bosco’s tricks in which
birds and even small animals are used, but the conjuring is so deftly done
that the public of 1907, like that of 1838, thinks it is all sleight-of-hand
work and that the birds are neither hurt nor killed. Even in Bosco’s time the
bird trick was not in his répertoire exclusively. All English magicians
employed it. Apparently the head of the fowl was amputated, but often in
reality it was tucked under the wing, and the head and neck of another fowl
was shown by sleight-of-hand. Quite probably the Parisian public did not
consider Bosco cruel. Robert-Houdin and his friend Antonio, being versed
in sleight-of-hand and conjuring methods, read cruelty between the deft
movements. Certain it is that the name of Bosco has not been handed down
to posterity by other writers as a synonym of cruelty.
The animus of Robert-Houdin’s attack on Bosco is evident at every point
of the narrative. Now he accuses him of bad taste in appearing in the box-
office. Again he suggests that the somewhat impressive opening of Bosco’s
act savors of both charlatanism and burlesque, when in reality the secret of
showmanship consists not of what you really do, but what the mystery-
loving public thinks you do. Bosco undoubtedly secured precisely the effect
he desired, because Robert-Houdin devotes more than a page to a most
unnecessary attempt to explain away what he considered Bosco’s
undeserved popularity.
Bosco was not only a clever magician, but a man of many adventures, so
that his life reads like a romance. This soldier of fortune, Bartolomeo
Bosco, was born of a noble Piedmont family, on January 11th, 1793, in
Turin, Italy. From boyhood he showed great ability as a necromancer, but at
the age of nineteen he was forced to serve under Napoleon I. in the Russian
campaign. He was a fusilier in the Eleventh Infantry, and at the battle of
Borodino was injured in an engagement with Cossacks. Pierced by a lance,
he lay upon the ground apparently dead. A Cossack callously roamed
among the dead and dying, rifling pockets and belts. When he came to the
form of Bosco, that youth feigned death, knowing that resistance to the
ghoul meant a death wound. But while the Cossack robbed the Italian
soldier, the latter stealthily raised his unwounded arm and by sleight-of-
hand rifled the well-filled pockets of the ghoul, which fact was not
discovered by the Cossack until he was far from the field of the dead and
dying, where he had left one of the enemy considerably better off, thanks to
Bosco’s conjuring gifts.
Later Bosco was sent captive to Siberia, where he perfected his sleight-
of-hand while amusing fellow-prisoners and jailers. In 1814 he was released
and returned to his native land, where he studied medicine, but eventually
decided to become a public entertainer. He was not only a clever
entertainer, but a good business man, and he planned each year on saving
enough money to insure a life of ease in his old age. But events intervened
to ruin all his well-laid plans. The sins of his youth brought their penalty.
An illegitimate son, Eugene, became a heavy drag upon the retired
magician, who was compelled to pay large sums to the young man in order
to prevent his playing in either France or Germany or assuming the name of
Bosco. In a German antiquary’s shop at Bonn on the Rhine I found an
agreement in which Bosco agreed to pay this youth five thousand francs for
not using the name of Bosco. This agreement is too long for reproduction in
this volume, but unquestionably it is genuine and tells all too eloquently the
troubles which beset Bosco in his old age.
Eugene was said to be the superior of his famous father in sleight-of-
hand, but he was wild and given to excesses. Women and wine checked
what might have been a brilliant professional career. Disabled, poverty-
stricken, and respected by none, he soon disappeared from the conjuring
world, and according to Carl Willman in the “Zauberwelt” he died
miserably in Hungary in 1891.
 Only photograph of Madame Bosco, given to the
author by Mrs. Mueller, Madame Bosco’s niece, at
the funeral of Wiljalba Frikell.

The author at the grave of Bosco. From a

photograph in the Harry Houdini Collection.

In the mean time, Bosco and his wife lived in poverty in Dresden, where
the once brilliant conjurer died March 2nd, 1863. His wife died three years
later and was interred in the grave with her husband in a cemetery on
Friedrichstrasse. There was nothing on the tombstone to indicate the double
interment, and I discovered the fact only by investigating the municipal and
cemetery records. Here I also learned that the grave had merely been leased,
and as the lease was about to expire the bones of the great conjurer and his
faithful wife might soon be disinterred and reburied in a neglected corner of
the graveyard devoted to the poor and unclaimed dead. To prevent this, I
purchased the lot and tombstone, and presented the same to the Society of
American Magicians, of which organization, at the present writing, I am a
member.
A man of noble birth and brilliant attainments was the original Bosco,
and his name became a by-word all over the Continent as the synonym, not
of cruelty, but of clever deception, yet never has posterity put the name of a
great performer to such ignoble uses. For who has not heard the cry of the
modern Bosco, “Eat-’em-alive"?
To-day I can close my eyes and summon two visions. First I see myself
standing bareheaded before a neglected grave in the quiet cemetery on
Friedrichstrasse, Dresden, the sunlight pouring down upon the tombstone
which bears not only the cup-and-balls and wand, insignia of Bosco’s most
famous trick, but this inscription: “Ici repose le célèbre Bartolomeo Bosco.
—Né à Turin le 11 Janvier, 1793; décédé à Dresden le 2 Mars, 1863.” The
history of this clever conjurer, with all its lights and shadows, sweeps
before me like a mental panorama.
The second vision carries me into the country, to the fairs of England
and the side-shows of America:
“Bosco! Bosco! Eat-’em-alive Bosco. You can’t afford to miss this
marvel. Bosco! Bosco!”
Follow me into the enclosure and gaze down into a den. There lies a
half-naked human being. His hair is long and matted, a loin cloth does
wretched duty as clothing. Torn sandals are on his feet. The eulogistic
lecturer dilates upon the powers of this twentieth-century Bosco, but you do
not listen. Your fascinated gaze is fixed on various hideous, wriggling,
writhing forms on the floor of the den. Snakes—scores of them! Now the
creature, half-animal, half-human, glances up to make sure that attention is
riveted upon him, then grasps one of the serpents in his hideous hands and
in a flash bites off its head. The writhing body falls back to the ground.
You grip the railing in a sudden faintness. Has your brain deceived your
eyes, or your eyes your brain? If you are a conjurer you try to convince
yourself that it is all a clever sleight-of-hand exhibition, but in your heart
you know it is not true. This creature, so near a beast, has debauched his
manhood for a few paltry dollars, and in dragging himself down has
dragged down the name of a worthy, a brilliant, a world-famous performer.
 Of the twentieth-century Boscos there are, alas, many. You will find
them all over the world, in street carnivals, side-shows, fair-booths, and
museums, and why the public supports such debasing exhibitions I have
never yet been able to understand. I have seen half-starved Russians pick
food from refuse-barrels. I have seen besotted Americans creep out from
low dives to draw the dregs of beer-barrels into tomato cans. I have seen
absinthe fiends in Paris trade body and soul to obtain their beloved
stimulant. I have heard morphine fiends in Russia promise to exhibit the
effect of the needle in return for the price of an injection. But never has my
soul so risen in revolt as at sight of this bestial exhibition with which the
name of Bosco, a nobleman and a conjurer of merit, has been linked.

Anderson’s opening programme at the Strand

Theatre, Christmas week, 1848, showing that he
duplicated the tricks offered by Robert-Houdin,
who, in his “Memoirs,” claims that Anderson’s
programme was stale and uninteresting by
comparison with his own.

Even more despicable than his attack upon Bosco is Robert-Houdin’s

flaying of John Henry Anderson. In this he is both unmanly and untruthful.
Hinging his attack on his surprise at the press methods and advertising
adopted in England as opposed to the less spectacular means employed in
France, he insinuates that Anderson’s entire success was built not upon
merit, ability, originality, or diversified programmes, but solely upon
sensational advertising. On page 325 of the American edition of his
“Memoirs” Robert-Houdin writes thus of his competitor:
“On my arrival in England a conjurer of the name of Anderson, who
assumed the title of Great Wizard of the North, had been performing for a
long period at the little Strand Theatre.
“This artist, fearing, doubtlessly, that public attention might be divided,
tried to crush the publicity of my performances; hence he sent out on
London streets a cavalcade thus organized:
“Four enormous carriages, covered with posters and pictures
representing all sorts of witchcraft, opened the procession. Then followed
four-and-twenty merry men, each bearing a banner on which was painted a
letter a yard in height.
“At each cross-road the four carriages stopped side by side and presented
a bill some twenty-five yards in length, while all the men (I should say
letters), on receiving the word of command, drew themselves up in a line,
like the vehicles.
“Seen in front the letters formed this phrase:
THE CELEBRATED ANDERSON ! ! !
While on the other side of the banners could be read:
THE GREAT WIZARD OF THE NORTH.
 Handbill used by Anderson in Germany. January,
1848, when Robert-Houdin claimed that he was
playing in the English provinces. From the Harry
Houdini Collection.

“Unfortunately for the Wizard, his performances were attacked by a

mortal disease; too long a stay in London had ended by producing satiety.
Besides, his repertory was out-of-date, and could not contend against the
new tricks which I was offering. What could he present to the public in
opposition to the second sight, the suspension, and the inexhaustible bottle?
Hence he was obliged to close his theatre and start for the provinces, where
he managed, as usual, to make excellent receipts, owing to his powerful
means of notoriety.”
In the first place, Robert Houdin insinuates that when they played in
opposition John Henry Anderson’s répertoire was stale and uninteresting. Is
it possible that Robert-Houdin could not read Anderson’s bills, or were his
statements deliberate falsehoods, emanating from a malicious, wilful desire
to injure Anderson?
What did Anderson have to offer in opposition to Robert-Houdin’s
much-vaunted Suspension, Second Sight, and Inexhaustible Bottle? Consult
the Anderson programme, reproduced, and you will find that the great
Wizard of the North duplicated the French conjurer’s répertoire. “The
Ethereal Suspension” of Robert-Houdin’s programme was “Suspension
Chloroforeene” on Anderson’s. Second Sight appeared on both bills. “The
Inexhaustible Bottle” had wisely been dropped by Anderson because he had
been using it in one form or another for ten years preceding the date of
Robert-Houdin’s appearance in London, as is proven in chapter IX. of this
book.
Therefore, if Anderson’s programme was passé and uninteresting, so also
must have been the one offered by Robert-Houdin!

Poster used by Anderson during his closing week at

the Strand Theatre, London, January 11th, 1848.
From the Harry Houdini Collection.

Second, John Henry Anderson was not in London when Robert-Houdin

arrived there in May, 1848. He was on the Continent, and a bill reproduced
will show that he was in Germany in January, 1848, and did not open at the
Strand Theatre until December 26th, 1848. Then it was Robert-Houdin who
had just returned from the provinces, not Anderson. Anderson had been
playing the capitals of Europe. Robert-Houdin had been in Manchester,
England.
Robert-Houdin again skilfully twists the truth to suit his own ends. He
actually states that Anderson, returning from a tour of the provinces, used a
new poster, a caricature of the famous painting, “Napoleon’s Return from
Elba":
“In the foreground Anderson was seen affecting the attitude of the great
man; above his head fluttered an enormous banner bearing the words ‘The
Wonder of the World’; while, behind him and somewhat lost in the shade,
the Emperor of Russia and several other monarchs stood in a respectful
posture. As in the original picture, the fanatic admirers of the Wizard
embraced his knees, while an immense crowd received him triumphantly. In
the distance could be seen the equestrian statue of the Iron Duke, who, hat
in hand, bowed before him, the Great Wizard; and lastly, the very dome of
St. Paul’s bent towards him most humbly.
“At the bottom was the inscription,

Return of the Napoleon of Necromancy.

“Regarded seriously, this picture would be found a puff in very bad taste;
but as a caricature it is excessively comic. Besides, it had the double result
of making the London public laugh and bringing a great number of shillings
into the skilful puffer’s pockets.”

Eugene Bosco, son of the original Bosco. From the

Harry Houdini Collection.
 Reference to my collection of Anderson programmes and press clippings
proves that while on the Continent his performances had created such a
sensation that, according to the ethics and etiquette of his profession,
Anderson was quite justified in assuming the title of “The Napoleon of
Necromancy” and in depicting even kings and noblemen admiring his
abilities as a conjurer. But, alas, Robert-Houdin had played only before
English and French monarchs, not before the other crowned heads of
Europe, including the Czar of Russia and the German Kaiser!
It required weeks and months of browsing in old book- and print-shops,
national libraries, and rare collections on my part to prove that Anderson
had really played these engagements, when his bitter rival, Robert-Houdin,
his heart eaten with jealousy until his sense of honor and truth was
hopelessly blunted, was claiming that Anderson had just returned from a
trip in the English provinces.
It will be noted by reference to the Anderson programme that he had
been engaged only for the Christmas holidays, but despite Robert-Houdin’s
claim that he was a failure and was obliged to close and seek new fields of
conquest in the provinces, Anderson’s engagement was extended. He
remained at the Strand until January 11th, 1848, then after a brief provincial
tour he actually returned to London and played to big receipts. Again and
again he appeared in London. Far from being the unpopular, forgotten ex-
magician pictured by Robert-Houdin, he performed with great success at
the St. James Theatre, London, in 1851. Robert-Houdin appeared in London
for the last time in 1853, but in 1865 “the despised and forgotten Anderson”
was there again, creating a furor in his exposure of the Davenport Brothers.
 John Henry Anderson as he appeared in his later
years. From a cut in the Harry Houdini Collection.

Robert-Houdin might have been justified in criticising Anderson’s

sensational advertising methods, for these were entirely opposed to the
more elegant and conservative methods employed by the French conjurer.
But certainly he was not justified in picturing his rival as one who had
passed his prime, whose popularity had waned, whose répertoire no longer
attracted the public. For, in addition to duplicating Robert-Houdin’s entire
répertoire, Anderson offered tricks of which Robert-Houdin knew nothing,
and for years to come he constantly reconstructed his programmes, keeping
them strictly up-to-date.
Anderson did die a poor man, but this was not because the amusement-
loving public had wearied of him. A popular performer, like so many of his
class he did not know how to invest his huge earnings. It is known that he
gave $20,000 to various charities, while no record of Robert-Houdin’s
charities exists. He was burned out several times. He lost money through a
bad contract made for his Australian tour. Certain investments dropped in
value because of the Civil War in the United States, during which England
sympathized with the South. Finally, during his American tour after the
Civil War, Anderson played the Southern States, then steeped in bitterness
toward the North, and was unfortunate enough to bill himself as “The Great
Wizard of the North.” This roused the Southern prejudice to white heat, he
was almost mobbed, and was finally driven from that section of the country.
He went into bankruptcy, November 19th, 1866, and died at Darlington,
County Durham, England, Feb. 3rd, 1874. His remains were interred, in
accordance with his dying request, at Aberdeen, Scotland.
So ends the true history of Robert-Houdin. The master-magician,
unmasked, stands forth in all the hideous nakedness of historical proof, the
prince of pilferers. That he might bask for a few hours in public adulation,
he purloined the ideas of magicians long dead and buried, and proclaimed
these as the fruits of his own inventive genius. That he might be known to
posterity as the king of conjurers, he sold his birthright of manhood and
honor for a mere mess of pottage, his “Memoirs,” written by the hand of
another man, who at his instigation belittled his contemporaries, and
juggled facts and truth to further his egotistical, jealous ambitions.
But the day of reckoning is come. Upon the history of magic as
promulgated by Robert-Houdin the searchlight of modern investigation has
been turned. Credit has been given where it belongs, to those magicians
who preceded Robert-Houdin and upon whose abilities and achievements
Robert-Houdin built his unearned, unmerited fame. The dust of years has
been swept from names long forgotten, which should forever shine in the
annals of magic.
Thus end, also, my researches, covering almost two decades of time,
researches in which my veneration for old-time magicians grew with each
newly discovered bit of history; researches during which my respect for the
profession of magic has grown by leaps and bounds. And the fruits of these
researches I now lay before the only true jury, the great reading public. My
task is finished.

Typographical errors corrected by the etext transcriber:

Inventions and and Discoveries=> Inventions and Discoveries {pg 14}
from his autobigraphy=> from his autobiography {pg 34}
is supposed so have been engraved=> is supposed to have been
engraved {pg 59 illustration caption}
is his autobiography=> in his autobiography {pg 89 illustration
caption}
woudn=> wound {pg 160}
perfomances=> performances {pg 187}
though as far as maiming him for life=> though not as far as maiming
him for life {pg 281}
the frontispiese=> the frontispiece {pg 48 illustration caption}
 *** END OF THE PROJECT GUTENBERG EBOOK THE UNMASKING
OF ROBERT-HOUDIN ***

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knowledge seekers. We believe that every book holds a new world,
offering opportunities for learning, discovery, and personal growth.
That’s why we are dedicated to bringing you a diverse collection of
books, ranging from classic literature and specialized publications to
self-development guides and children's books.

More than just a book-buying platform, we strive to be a bridge

connecting you with timeless cultural and intellectual values. With an
elegant, user-friendly interface and a smart search system, you can
quickly find the books that best suit your interests. Additionally,
our special promotions and home delivery services help you save time
and fully enjoy the joy of reading.

Join us on a journey of knowledge exploration, passion nurturing, and

personal growth every day!

ebookbell.com