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On call radiology
1. ON CALL
RADIOLOGY
Gareth Lewis • Hiten Patel
Sachin Modi • Shahid Hussain
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ISBN: 978-1-4822-2167-1
9 781482 221671
90000
K22247
MEDICINE
On Call Radiology presents case discussions on the most common and important clinical
emergencies and their corresponding imaging findings encountered on-call. Cases are
divided into thoracic, gastrointestinal and genitourinary, neurological and non-traumatic
spinal, paediatric, trauma, interventional and vascular imaging. Iatrogenic complications are
also discussed.
Each case is presented as a realistic clinical scenario and includes a clinical history
and request for imaging. Multi-modality imaging examples and a case discussion on the
diagnosis and basic management, with emphasis on important radiological findings, are
also presented.
This book combines a case-based discussion format with practical advice on imaging
decision making in the acute setting. It also offers guidance on radiology report writing and
techniques, with a focus on relevant positive and negative findings to pass on to referring
clinicians. On Call Radiology offers invaluable knowledge and practical tips for any
on-call radiologist.
ON CALL
RADIOLOGY
K22247_Cover.indd All Pages 5/21/15 1:52 PM
5. ON CALL
RADIOLOGY
Gareth Lewis, MBChB, FRCR, Radiology Registrar, University Hospitals
Birmingham NHS Foundation Trust, Birmingham, UK
Hiten Patel, MBChB, FRCR Radiology Registrar, University Hospitals
Coventry and Warwickshire NHS Trust, Coventry, UK
Sachin Modi, BSc(Hons), MBBS, FRCR, Radiology Registrar, University
Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
Shahid Hussain, MA, MB, BChir, MRCP, FRCR, Consultant Cardiothoracic
Radiologist, Heart of England NHS Foundation Trust, Birmingham, UK
ON CALL
RADIOLOGY
Gareth Lewis, MBChB, FRCR, Radiology Registrar, University Hospitals
Birmingham NHS Foundation Trust, Birmingham, UK
Hiten Patel, MBChB, FRCR Radiology Registrar, University Hospitals
Coventry and Warwickshire NHS Trust, Coventry, UK
Sachin Modi, BSc(Hons), MBBS, FRCR, Radiology Registrar, University
Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
Shahid Hussain, MA, MB, BChir, MRCP, FRCR, Consultant Cardiothoracic
Radiologist, Heart of England NHS Foundation Trust, Birmingham, UK
K22247_FM.indd 1 16/05/15 3:05 AM
18. xiv
Clinical radiology is at the centre of modern medicine
and a high-quality service has repeatedly been shown
to significantly improve patient outcomes. Over the
last 10 years there has been a significant increase in
demand for radiology services, resulting in a 26.5%
increase in radiology examinations in England, from
just over 30 million in 2004/5 to almost 39 million
in 2010/11. Since 2004/5 the number of computed
tomographic (CT) examinations has increased by
86% (Department of Health, 2011). On-call work,
unsurprisingly, has followed this same trend with an
increase in both the number and the complexity of
scans now being performed out of hours as emergency
imaging. Understandably, starting on calls in radiology
can be a very daunting prospect. It marks a turning
point from having very few responsibilities within a
department to being integral to the work of both the
Radiology Department and to the Hospital as a whole.
On-call work presents a myriad of complex issues
including: identifying pathology that may never have
been seen before; coordinating scans and deciding scan
protocols; and communicating with clinicians at all
levels of seniority. Perhaps most importantly, on-call
work carries a significant amount of responsibility since
frequently, a decision on whether a patient needs to
go to theatre or whether he/she requires immediate
intervention will be dependent upon the findings of the
radiology examination.
PREFACE
The purpose of this book is to try to assist junior
radiology trainees who are starting their on calls.
We have presented here the commonest cases that
trainees are likely to encounter in an on-call situation.
An almost limitless number of cases could have been
included, since virtually anything can present in an
on-call situation. We have, however, tried to present
some of the most common cases as well as a host of tips
on how to approach emergency imaging situations.
Multiple images, as well as tips about reporting, have
been included with each case. The majority of on-call
work is CT work, and for this reason we have included
CT scan protocols where appropriate. Although
Radiology Departments have standard protocols for
imaging of non-emergency work, the out of hours types
of pathology sometimes require fine tuning of these
protocols to ensure that appropriate sequences have
been obtained.
We hope that this text will assist junior radiology
trainees in gaining some confidence as they start their
on calls and will help assuage some of their fears.
Gareth Lewis
Hiten Patel
Sachin Modi
Shahid Hussain
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19. xvACKNOWLEDGEMENTS
The authors acknowledge the following colleagues who kindly contributed images for use in this book:
Dr Ben Miller, Dr John Henderson, Dr Sarah Cooper, Dr Michelle Christie-Large, Dr Helen Williams,
Dr Adam Oates, Dr Martin Duddy, Dr Peter Riley, Dr Peter Guest and Dr Osama Abulaban. Special thanks
to Eloise Lewis, who provided the medical illustrations.
Gareth Lewis: To my wife Eli, thanks for all your help and support.
Hiten Patel: Special thanks to my parents for their continued support.
Sachin Modi: For my Mum, Dad and my wife Kaveeta.
Shahid Hussain: To my family and friends.
K22247_FM.indd 15 16/05/15 3:05 AM
20. xvi
HSV herpes simplex virus
Hu Hounsfield unit
IMA inferior mesenteric artery
IR interventional radiologist
ISS Injury Severity Score
IV intravenous/intravenously
IVC inferior vena cava
JVP jugular venous pressure
LBO large bowel obstruction
LP lumbar puncture
LV left ventricle
MIP maximum intensity projection
MRA magnetic resonance angiography
MRI magnetic resonance imaging
MTC major trauma centre
NG nasogastric (tube)
NICE National Institute for Health and Clinical
Excellence
NPSA National Patient Safety Agency
PA posterior-anterior
PACS picture archiving and communication
system
PCWP pulmonary capillary wedge pressure
PI pyloric index
RI Resistive Index
SAH subarachnoid haemorrhage
SBO small bowel obstruction
ABBREVIATIONS
AAA abdominal aortic aneurysm
AOM acute otitis media
AP anterior-posterior
ARDS acute respiratory distress syndrome
AXR abdominal radiograph
BTS British Thoracic Society
CAD carotid artery dissection
CFA common femoral artery
CIN contrast-induced nephropathy
CMD corticomedullary differentiation
CNS central nervous system
CSF cerebrospinal fluid
CT computed tomography
CTA computed tomography angiography/
angiogram
CTPA computed tomography pulmonary
angiography/angiogram
CTSI computed tomography Severity Index
CXR chest radiograph
DJ duodenojejunal (junction)
EDH extradural haematoma
ET endotracheal (tube)
EVAR endovascular aneurysm repair
EVD external ventricular drain
GCS Glasgow Coma Score
GFR glomerular filtration rate
GI gastrointestinal
HIV human immunodeficiency virus
HPS hypertrophic pyloric stenosis
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21. Abbreviations xvii
SDH subdural haematoma
SMA superior mesenteric artery
SMV superior mesenteric vein
SVC superior vena cava
SVS slit ventricle syndrome
TCC transitional cell carcinoma
TIA transient ischaemic attack
TIPS transjugular intrahepatic portosystemic
shunt
VP ventriculoperitoneal (shunt)
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23. 1
that radiographers and radiologists involved in the
administration of IV contrast have up to date life
support training; however, this should not deter them
from involving the on-call medical emergency team in
appropriate situations.
Systemic reactions
The commonest side-effects of acute contrast reactions
include nausea, vomiting and urticaria. Following
injection of contrast media, patients may also develop
a warm flushing sensation. These are usually self-
limiting and generally do not pose any danger for the
patient, although it is worthwhile documenting such
reactions in the medical records for future reference.
In some patients, symptomatic relief may be achieved
through the use of antihistamines.
Renal impairment
Contrast-induced nephropathy (CIN) is a deterioration
in renal function following the administration of
contrastmedia(AmericanCollegeofRadiology,2013).
Patients at increased risk of developing CIN include
thosewithpre-existingrenaldysfunction,dehydration,
nephrotoxic medication and multiple doses of contrast
media in a short space of time. In order to reduce the
incidence of complications, patients at risk of CIN
should be discussed with the referring team. This
may include pre-hydration or the decision not to use
contrast. A guide level of an estimated glomerular
filtration rate (GFR) below 60 ml/min has been used
to suggest renal impairment; however, local guidelines
should be used. Certainly the risks versus the benefits
of giving contrast should always be considered.
Following imaging, patients at risk of developing CIN
should have regular observation of renal function
for at least 72 hours to ensure no acute deterioration
in function.
ADVERSE REACTIONS TO
CONTRAST MEDIA
While reactions to IV contrast can be delayed, it is
the immediate, acute reaction that is more relevant to
the on-call radiologist. Reactions to contrast media
vary depending on the type of agent used, with higher
incidences of reactions occurring in ionic as opposed
to non-ionic agents. Although the use of IV contrast
media has become routine, it is always important to
remember that severe reactions, while rare, can occur
(1 in 170,000 people have a fatal reaction, Vamasivayam
et al., 2006). The use of IV contrast is often extremely
beneficial, if not necessary, in the interpretation of
computed tomography (CT) imaging; however, its use
should always be balanced with the potential risks of
contrast reaction.
Essential information that should be sought from
the patient before contrast administration includes
history of:
• Previous contrast reaction.
• Asthma.
• Renal impairment.
• Diabetes mellitus.
• Metformin therapy.
Clinical features of a contrast medium reaction are
varied, ranging from vomiting and mild urticaria to
acute anaphylaxis and cardiopulmonary collapse.
There are numerous risk factors that may predispose
an individual to contrast reactions, such as previous
reactions to contrast media, pre-existing renal failure,
nephrotoxic medication and advancing age amongst
others (Maddox, 2002). In such instances, radiologists,
in conjunction with the referring team, should
follow the departmental guidelines when making the
decision to use an IV contrast medium. It is important
INTRODUCTION
K22247_Introduction.indd 1 16/05/15 3:15 AM
24. Introduction2
Patients with progressively worsening symptoms,
reduced tissue perfusion, signs of skin ulceration/
blistering or altered sensation should be reviewed by
the local surgical/plastics team.
References and further reading
American College of Radiology (2013) ACR Manual
on Contrast Media. Version 9. ACR Committee on
Drugs and Contrast Media, pp. 33–41.
Department of Health (2011) Imaging and Diagnostics.
http://webarchive.nationalarchives.gov.uk/
20130107105354/http://www.dh.gov.uk/en/
Publicationsandstatistics/Statistics/Performance
dataandstatistics/HospitalActivityStatistics/
DH_077487.
Maddox TG (2002) Adverse reactions to contrast
material: recognition, prevention and treatment.
Am Fam Physician 66: 1229–1234.
Resuscitation Council (UK) (2010) Advanced life
support algorithm. In: Adult Advanced Life Support.
www.resus.org.uk/pages/alsalgo.pdf. Accessed on
23rd May 2014.
Royal College of Radiologists (2010) Standards for
Intravascular Contrast Agent Administration to
Adult Patients, Second Edition. Royal College of
Radiologists, London.
Vamasivayam S, Kalra MK, Torres WE et al. (2006)
Adverse reactions to intravenous iodinated
contrast media: a primer for radiologists. Emerg
Radiol 12: 210–215.
Anaphylactic reaction
An anaphylatic reaction is the most serious and life-
threatening side-effect of contrast administration
and requires immediate recognition and treatment.
Symptoms include bronchospasm and hypotension,
whichmayleadtocardiopulmonaryarrest.Management
of anaphylaxis should follow the advanced life support
algorithm and involve the medical emergency team
when appropriate (Resuscitaion Council, 2010).
If the anaphylactic reaction is mild (e.g. scattered,
protracted urticaria), an antihistamine orally,
intramuscularly or IV should be considered. Mild
bronchospasm can be treated with oxygen by mask
(6–10 litres/min)andabeta-2agonistinhaler(2–3 puffs).
If moderate (e.g. profound urticaria, laryngeal oedema
orbronchospasmnotresponsivetoinhalers),adrenaline
1:1000 (0.1–0.3 ml intramuscularly) may be required.
If severe, the resuscitation team should be called while
all the above measures are undertaken.
Contrast extravasation
Extravasation of contrast medium can occur with
both hand and pump injections and usually occurs
into the subcutaneous tissues. Patients may be
asymptomatic or develop erythema, swelling and
pain at the site of extravasation. Most cases are self-
limiting and do not require further intervention;
however, compartment syndrome or skin necrosis
may occur on rare occasions. Elevation of the limb
and the use of ice packs may help to ease symptoms.
K22247_Introduction.indd 2 16/05/15 3:15 AM
25. 3
Chapter 1
THORACIC IMAGING
ACUTE AORTIC SYNDROME
Acute aortic syndrome encompasses three closely
related pathologies: aortic dissection, intramural
haematoma and penetrating atherosclerotic ulcer. The
wall of the aorta consists of three layers: the innermost
intima, the middle media and the outermost adventitia.
Dissections can be caused both by an intimal tear
leading to propagation of blood within the media or by
primary intramural haematoma with resultant intimal
perforation (Macura et al., 2003). As this progresses,
an intimal flap is lifted away from the media, resulting
in two channels within the aortic lumen, referred to as
the true and false lumens. Propagation of the flap and
false lumen thrombosis can ultimately result in end-
organ ischaemia. Intramural haematoma is thought
to be the result of spontaneous bleeding of the vasa
vasorum into the media. A penetrating atherosclerotic
ulcer is defined as ulceration within atherosclerosis
that herniates into the media. This can also result in
intramural haematoma. Penetrating aortic ulcers and
intramural haematoma can both progress to aortic
dissection (Macura et al., 2003).
Spontaneous aortic dissection is usually seen in the
middle aged to elderly population, with spontaneous
cases commonly associated with hypertension and
atherosclerosis. Secondary causes include trauma
(usually preceded by intramural haematoma) and
collagen vascular diseases such as Marfan and
Ehlers–Danlos syndromes; these conditions should
be considered in younger patients presenting with
dissection.
Typical symptoms and signs of aortic dissection
include upper limb blood pressure asymmetry and
‘tearing’ chest pain that radiates through to the back,
although an absence of these findings does not exclude
MODALITY PROTOCOL
CT Unenhanced. No oral contrast. Scan from
just above aortic arch to diaphragm level.
Aortic angiogram: 100 ml IV contrast via
18G cannula, 4 ml/sec. Bolus track centred
on the descending thoracic aorta. Scan from
just above aortic arch to femoral head level.
Table 1.1 Acute aortic syndrome.
Imaging protocol.
the diagnosis. The mortality rate depends on both
the underlying pathology and the extent of aortic
involvement. However, the potential complications
are severe; as such, the on-call radiologist should have a
high index of suspicion for this pathology.
Radiological investigations
CT angiography (CTA), with corresponding
unenhanced imaging to identify intramural
haematoma, has a high sensitivity and specificity for
acute aortic syndrome and is the modality of choice.
The scanning area should extend from just above the
aortic arch to the femoral heads to prevent missing the
true extent of a dissection. Chest plain film imaging
may show signs such as an abnormal aortic contour or
widened mediastinum; however, plain film imaging is
neither sensitive nor specific for aortic dissection. (See
Table 1.1.)
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26. Chapter 14
Radiological findings
Computed tomography
The unenhanced phase should be scrutinised for
intramural haematoma, which appears as crescenteric
high attenuation material within the aortic wall. This
is best appreciated on a narrow image window setting
(Figure 1.1a) and can be difficult to appreciate on the
enhanced phase (Figure 1.1b). On contrast enhanced
CT aortography, intramural haematoma presents as a
low attenuation crescent or circumferential opacity (in
relation to the IV contrast) and can be confused with
non-calcified atherosclerotic disease.
When interpreting contrast enhanced CT
aortography,itisvitalthattheaortaisscrutinisedinaxial,
sagittalandcoronalplaneswithappropriatewindowing
(width 400, level 100), which aids visualisation of
the dissection flap (Figure 1.2a). This appears as a
serpiginous, linear filling defect extending across the
lumenoftheopacifiedaorta,dividingtheaortaintotwo
channels, the true and false lumen. Inspecting the aorta
onsofttissuewindowsettingsalonecanresultinafalse-
negativeresult,sincethedissectionflapcanbeobscured
by adjacent high attenuation IV contrast (Figure 1.2b).
Delineation of the true and false lumens can be helpful
as a guide to potential surgical or interventional
management. The true lumen is defined as the lumen
that is supplied by the aortic root. Generally, the
true lumen is smaller, demonstrates denser contrast
opacificationandissurroundedbyintimalcalcification,
whereas the false lumen is larger, less dense and in time
can become thrombosed. Distinguishing a thrombosed
falselumen(whichcanbeseeninaorticdissection)from
atherosclerotic intraluminal thrombus can be difficult;
the former may displace intimal calcifications away
from the aortic wall, a useful distinguishing feature.
The most cranial and caudal aspect of a dissection
flap/intramural haematoma should be identified;
this may involve re-scanning the patient if the extent
of dissection is not fully imaged initially. The major
branches of the aorta arch should be scrutinised;
propagationintotheaorticarchcanresultinthrombosis
and cerebral ischaemia (Figure 1.3). Involvement of
the aortic root may threaten the coronary arteries
and can rupture into the pericardium, resulting in
haemopericardium and cardiac tamponade; the former
is suggested by intermediate to high density (25 Hu)
fluid in the pericardial space (Figure 1.4). Cardiac
tamponade can occur with even a small volume of fluid
and is more dependent on the rate of accumulation.
Secondary signs (e.g. flattening/bowing of the LV
septum,refluxofcontrastintotheIVC/azygousveinand
distension of the SVC/IVC) can be unreliable. Clinical
review looking for a raised JVP and pulsus paradoxus
and further investigation with echocardiography is
Figures 1.1a, b Axial images: unenhanced and IV contrast enhanced scans of the aortic arch in the arterial
phase. The unenhanced image demonstrates a hyperdense crescenteric rim outlining the aortic arch, representing
intramural haematoma (arrow). On the contrast enhanced image, this is difficult to appreciate.
(a) (b)
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27. 5Thoracic imaging
Figure 1.3 Coronal image: IV contrast enhanced
CT scan of the thorax in the arterial phase. A dissection
flap can be seen extending from the aortic root and
involving the brachiocephalic trunk, which may
compromise distal blood flow into the right common
carotid artery and right subclavian artery.
Figure 1.4 Axial image: IV contrast enhanced CT scan
of the thorax in the arterial phase. A dissection flap is
shown within the aortic root. In addition, hyperdense
material is seen in the pericardium consistent with
haemopericardium (arrow). This may occur in coronary
artery rupture as a result of dissection.
Figures 1.2a, b Axial images: IV contrast enhanced CT scans of the thorax in the arterial phase. There is a
serpiginous, linear structure within the aortic arch containing flecks of calcification consistent with an aortic
dissection flap (arrow). Figure 1.2b demonstrates the importance of appropriate window width and level, as the
dissection flap is barely visible without image manipulation.
(a) (b)
K22247_C001.indd 5 16/05/15 3:06 AM
28. Chapter 16
required. Cardiac motion artefact, which commonly
occurs in the region of the aortic root, can be
misinterpreted as a dissection flap. Familiarity with this
artefact can prevent a false-positive result (Figure 1.5).
The dissection can also extend caudally into the
descending thoracic and abdominal aorta; the coeliac
axis, SMA and IMA should be closely inspected for
involvement. Furthermore, it is useful to identify which
of the main abdominal aortic branch vessels arise from
thefalselumen,astheseareatriskofischaemia.Coeliac
axisinvolvementcanresultin liver or splenic ischaemia,
whichtypicallypresentsasreducedenhancement.SMA
or IMA involvement can result in bowel ischaemia (see
Chapter 2:Gastrointestinalandgenitourinaryimaging,
Bowel ischaemia and enterocolitis).
Both intramural haematoma and aortic dissection
should be classified according to the Stanford or
DeBakey model; this has important prognostic and
management implications (Table 1.2).
LOCATION MANAGEMENT
Stanford A Involving thoracic aorta
proximal to origin of
left subclavian artery.
Surgical.
Stanford B Involving the aorta
distal to the left
subclavian artery.
Conservative.
DeBakey I Involving ascending
aorta, aortic arch and
descending aorta.
Surgical.
DeBakey II Involving ascending
aorta.
Surgical.
DeBakey III Involving descending
aorta only.
Conservative.
Table 1.2 Stanford and DeBakey systems.
Figure 1.5 Axial image: IV contrast enhanced CT scan
of the thorax in the arterial phase. Normal appearance
of the heart. An apparent, linear defect structure can be
seen in the ascending aorta. This is a normal appearance
in non-ECG-gated studies resulting from cardiac
motion during the scan.
A penetrating atherosclerotic ulcer is usually
associated with marked atherosclerotic disease and
appears as a focal bulging or out-pouching of the aortic
wall, usually separating atherosclerotic calcification
(Figure 1.6). Although sometimes subtle, this is an
important finding and can ultimately progress to
intramural haematoma, aneurysm and aortic rupture.
Comparison with previous imaging is useful to help
identify this important pathology.
Key points
• Acute aortic syndrome is a spectrum of
abnormality comprising aortic ulceration,
intramural haematoma and dissection.
• Contrast enhanced CT is the imaging
modality of choice to characterise aortic
dissection. Unenhanced CT imaging should be
performed to aid identification of intramural
haematoma.
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29. 7Thoracic imaging
• Careful windowing is required to identify
dissection flaps. Intramural haematoma appears as
crescenteric high attenuation material within the
aortic wall on the unenhanced phase.
Report checklist
• Presence or absence of intramural haematoma.
• Cranial and caudal extent of the dissection flap.
• Patency of great vessels/coeliac axis/SMA/IMA/
renal arteries.
• Presence of pericardial blood and any signs of
cardiac tamponade.
• Classification.
Reference
Macura JK, Corl FM, Fishman EK et al. (2003)
Pathogenesis in acute aortic syndromes: aortic
dissection, intramural hematoma, and penetrating
atherosclerotic aortic ulcer. Am J Roentgenol
181:309–316.
Figure 1.6 Axial image: IV contrast enhanced
CT scan of the thorax in the arterial phase. A small
outpouching of contrast can be seen through a defect
in the distal aspect of the aortic arch, representing an
atherosclerotic ulcer (arrow).
THORACIC AORTIC INJURY
Aorticinjuryisamajorconcerninthesettingofprimarily
blunt,butalsopenetrating,thoracictrauma.Traumatic
injury of the thoracic aorta is a spectrum of injury,
including aortic intramural haematoma and dissection,
laceration, pseudoaneurysm (in which a rupture is
containedbyperiaorticsofttissues)andcompleteaortic
transection and rupture (see Acute aortic syndrome
for discussion on aortic intramural haematoma and
dissection). Injury occurs most commonly at regions
of aortic tethering, such as the aortic isthmus. Classic
symptoms and signs include chest pain, dyspnoea
and upper limb hypertension with associated lower
limb hypotension. Ultimately, aortic transection and
rupture result in profound haemodynamic instability.
Mortality rates are high, estimated at 80–90% in
untreated aortic injury (Parmley et al., 1958). As such,
the on-call radiologist should have a high index of
suspicion for aortic injury in this scenario. Accurate and
swift diagnosis is vital, facilitating urgent surgical or
interventional repair.
Radiological investigations
CT is the most sensitive and specific modality for
aortic trauma. Both enhanced and unenhanced phases
should be performed, the latter aiding in identification
of intramural haematoma, although often the precise
protocol is determined by departmental polytrauma
guidelines. Depending on the clinical presentation
of the patient, chest plain film imaging can be used as
an initial screening test, although this modality is not
reliable enough to exclude more subtle injury and can
appear normal in up to 7% of significant aortic injuries
(Fabian et al., 1997). (See Table 1.3.)
MODALITY PROTOCOL
CT Unenhanced. Scan from aortic arch to
diaphragm level.
Aortic angiogram: 100 ml IV contrast via
18G cannula, 4 ml/sec. Bolus track centred
on the aortic arch. Scan from aortic arch to
diaphragm level.
Table 1.3 Thoracic aortic injury.
Imaging protocol.
K22247_C001.indd 7 16/05/15 3:06 AM
30. Chapter 18
as haematoma. Any loss of definition of the aortic wall
should also be treated with suspicion, as should focal
periaortic fat stranding. Focal filling defects within the
aortic lumen can indicate intraluminal clot and occult
injury, although comparison with previous imaging is
helpful to assess for pre-existing atheroma (Figure 1.9).
Aortic dissection and intramural haematoma can also
be seen in traumatic aortic injury (see Acute aortic
syndrome for these findings). Any suspicion of aortic
injury should be urgently communicated to the
referring team.
Plain films
While chest plain film imaging cannot exclude aortic
injury, it can yield helpful signs. Mediastinal widening
of 8cm canbeanindicator of mediastinal haematoma.
It should be noted that the sensitivity and specificity
of mediastinal widening for aortic injury varies from
53–100% and 1–60%, respectively (Groskin, 1992).
The most common cause of mediastinal haematoma
in trauma is the tearing of small mediastinal veins, as
opposed to aortic injury. Other signs of aortic injury
include an indistinct aortic contour, left apical pleural
cap, tracheal deviation and depression of the left main
bronchus.
Radiological findings
Computed tomography
As with all polytrauma cases, a ‘primary survey’ of
CT imaging should be performed in an attempt to
identify immediately life-threatening aortic injury.
The thoracic aorta should be scrutinised using
multiplanar reformatting and appropriate window
settings (window 400, level 100). Focal aortic
contour deformities (including focal aneurysms)
and mural discontinuity are direct signs of aortic
injury (Figures 1.7a, b). Familiarity with the normal
appearance of the aortic isthmus is essential, since this
canbemistakenforaorticinjury.Activeextravasationof
IVcontrast,commonlyintothemediastinumorpleural
spaces, is indicative of active bleeding.
There are more subtle signs of aortic injury. The
presence of mediastinal haematoma should always
make the on-call radiologist suspicious, although
other causes include venous injury (including the
azygous vein) and vertebral body fractures. Mediastinal
haematoma presents on CT as increased attenuation
material within the mediastinum (30 Hu). Periaortic
haematoma is extremely worrisome for an occult
aortic injury (Figures 1.8a, b). Both residual thymic
tissue and pericardial recesses can be misinterpreted
Figures 1.7a, b Axial and coronal images: IV contrast enhanced CT scans of the thorax in the arterial phase. Both
cases demonstrate contour abnormality of the thoracic aorta, in keeping with aortic injury (arrows).
(a) (b)
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31. 9Thoracic imaging
References
Fabian TC, Richardson JD, Croce MA et al. (1997)
Prospective study of blunt aortic injury: multicenter
trial of the American Association for the Surgery of
Trauma. J Trauma Acute Care Surg 42:374–380;
discussion 380–383.
Groskin SA (1992) Selected topics in chest trauma.
Radiology 183:605–617.
Parmley LF, Mattingly TW, Manion WC et al. (1958)
Nonpenetrating traumatic injury of the aorta.
Circulation 17:1086–1101.
Figure 1.9 Axial image: IV contrast enhanced CT scan
of the thorax in the arterial phase. There is a filling
defect within the aortic lumen, in keeping with a clot
(arrow). Periaortic haematoma is also present.
Figures 1.8a, 8b Axial images: IV contrast enhanced CT scans of the thorax in the arterial phase. There is
increased density material in the para-aortic regions consistent with haematoma (arrows). This can be seen tracking
inferiorly in the posterior mediastinum along the descending thoracic aorta. An aortic dissection flap can be seen
within the aortic lumen (1.8a).
Key points
• Aortic injury is a life-threatening complication of
both blunt and penetrating trauma.
• CT is the modality of choice to investigate aortic
injury but radiological signs may also be seen on
plain film radiographs.
Report checklist
• Document the relevant negatives of thoracic
aortic injury, including aortic contour abnormality,
mediastinal haematoma and active extravasation.
• Recommend urgent surgical and interventional
radiology opinion.
(a) (b)
K22247_C001.indd 9 16/05/15 3:06 AM
32. Chapter 110
PULMONARY EMBOLISM
Pulmonaryembolismisamedicalemergency,although
clinical presentation varies according to the degree of
arterial occlusion. Pulmonary emboli most commonly
arise from the deep venous system of the lower
extremities, but emboli can also occur from the upper
limbs, right-sided cardiac chambers and jugular venous
system. There are many risk factors for pulmonary
embolism,namelythosethatproduceahypercoagulable
state (Table 1.4). Occlusion of the pulmonary arteries
causes both respiratory and cardiovascular effects.
Respiratory effects include increased alveolar dead
space, hypoxaemia, hyperventilation and pulmonary
infarction. Cardiovascular effects include an increase
in pulmonary vascular resistance, which also results
in an increase in right ventricular afterload and right
ventricular failure (compounded by reflex pulmonary
arterial constriction). Symptoms and signs include
chest pain, dyspnoea, haemoptysis and collapse. Chest
pain is typically pleuritic in nature, although this classic
type of pain is only usually present in small peripheral
emboli that cause pleural inflammation and irritation.
Hypoxaemia is frequently, but not universally, present
on arterial blood gas analysis. Large emboli causing
proximal occlusion of the pulmonary arterial system
can result in profound haemodynamic instability,
leadingtocardiacarrest.Becauseofthisvariableclinical
presentation, it can be useful to clinically separate cases
into suspected massive and non-massive pulmonary
embolism, which in turn dictates further investigation
and urgency of diagnosis.
It is important to appreciate that radiology only
plays one part in the investigation pathway of suspected
non-massive pulmonary embolism, which also includes
clinical pre-test probability scoring and laboratory
D-dimer analysis. The National Institute for Health
and Clinical Excellence (NICE) in the UK has
published revised guidelines for the investigation and
managementofpulmonaryembolismbasedona2-level
WellsScoreratherthana3-levelWellsScore(Table1.5;
Figure 1.10, NICE, 2012). D-dimer analysis should be
performed only on patients with a low or intermediate
pre-test probability of pulmonary embolism; a normal
D-dimertestinthisscenariohasalmosta100%negative
predictive value and excludes the diagnosis. A positive
MAJOR RISK FACTORS (RELATIVE RISK 5–20)
Surgery (where appropriate
prophylaxis is used, relative
risk is much lower)
Major abdominal/pelvic
surgery.
Hip/knee replacement.
Postoperative intensive care.
Obstetrics Late pregnancy.
Caesarean section.
Puerperium.
Lower limb problems Fracture.
Varicose veins.
Malignancy Abdominal/pelvic.
Advanced/metastatic.
Reduced mobility Hospitalisation.
Institutional care.
Miscellaneous Previous proven venous
thromboembolus.
MINOR RISK FACTORS (RELATIVE RISK 2–4)
Cardiovascular Congenital heart disease.
Congestive cardiac failure.
Hypertension.
Superficial venous
thrombosis.
Indwelling central vein
catheter.
Oestrogens Oral contraceptive.
Hormone replacement
therapy.
Miscellaneous Chronic obstructive
pulmonary disease.
Neurological disability.
Occult malignancy.
Thrombotic disorders.
Long-distance sedentary
travel.
Obesity.
Other (inflammatory
bowel disease, nephrotic
syndrome, chronic dialysis,
myeloproliferative disorders,
paroxysmal nocturnal
haemoglobinuria, Behçet’s
disease).
Table 1.4 Risk factors for venous
thromboembolism (Campbell
et al., 2003).
K22247_C001.indd 10 16/05/15 3:06 AM
33. 11Thoracic imaging
performed within 24 hours (Campbell et al., 2003).
CTPA is now considered the initial imaging modality
of choice in suspected cases of non-massive pulmonary
embolism. The advantages of CTPA include its
relativelyhighsensitivityandspecificity,availabilityout
of hours and ability to identify alternative intrathoracic
pathologies. A negative CTPA study of diagnostic
quality effectively excludes the diagnosis of pulmonary
embolism. Limitations of CT include indeterminate
results owing to suboptimal contrast opacification
within the pulmonary arterial system, and a breathing
artefact, which can both limit interpretation of the
more distal arterial system. Isotope lung scanning
can be used as an alternative or adjunct to CT in the
absence of a co-existing structural lung abnormality,
although this modality is not readily available out of
hours in most centres. While a low probability result
from an isotope scan effectively excludes the diagnosis,
ahighprobabilitystudycanstillyieldasignificantfalse-
positive rate.
Both CTPA and echocardiography are considered
diagnostic for suspected cases of massive pulmonary
embolism. The exact modality often depends on local
protocol; however, it must be emphasised that imaging
CLINICAL FEATURES POINTS
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Heart rate 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative) 1
Clinical probability simplified score
PE likely More than 4 points
PE unlikely 4 points or less
Adapted from Wells PS, Anderson DR, Rodger M et al. (2000) Derivation of a simple clinical model to categorize patients probability of
pulmonary embolism: increasing the model’s utility with the SimpliRED D-dimer. Thromb Haemost 83:416–420, with permission.
DVT = deep pain thrombosis; PE = pulmonary embolism.
Table 1.5 Two-level Wells score.
result necessitates further radiological investigation to
exclude pulmonary embolism; however, false-positive
results can be seen secondary to infection, malignancy,
pregnancy and recent surgery. D-dimer analysis should
generally not be performed in patients with a high
pre-test probability, since a false-negative result can
occur in over 15% of cases (Stein PD et al., 2007). In
stable patients with suspected non-massive pulmonary
embolism, treatment in the form of anticoagulation
can be started prophylactically prior to radiological
confirmation or exclusion. The investigation pathway
is different for suspected cases of massive pulmonary
embolism, since urgent diagnosis is vital in order to
facilitate urgent thrombolytic therapy.
Radiological investigations
Due to the often non-specific presentation of
pulmonary embolism, all stable patients with suspected
pulmonary embolism should have chest plain film
imaging prior to further imaging. While this modality
cannot confirm the diagnosis, it may diagnose
alternativepathologiesthatcanaccountforthepatient’s
symptoms. British Thoracic Society (BTS) guidelines
recommend that diagnostic imaging should ideally be
K22247_C001.indd 11 16/05/15 3:06 AM
34. Chapter 112
Figure 1.10 Suggested algorithm for the diagnosis of acute pulmonary embolism (PE).
Patient with signs or symptoms of PE
Other causes excluded by assessment of general medical history, physical examination and chest X-ray
PE suspected
Two-level PE Wells score
PE likely (4 points)
Is CTPA* suitable** and available immediately?
Yes No
Offer CTPA
(or V/Q
SPECT or
planar
scan)
Immediate interim parenteral
anticoagulant therapy
CTPA (or V/Q SPECT or
planar scan)
PE unlikely ( 4 points)
D-dimer test
Was the D-dimer test positive?
Is CTPA* suitable** and available immediately?
Immediate interim
parenteral anticoagulant
therapy
Offer CTPA
(or V/Q
SPECT or
planar
scan) CTPA (or V/Q SPECT or
planar scan)
Was the CTPA (or V/Q SPECT or
planar scan) positive?
Advise the patient it is not likely that he/
she has PE. Discuss the signs and symptoms
of PE, and when and where to seek further
medical help. Take into consideration
alternative diagnoses.
Advise the patient
it is not likely that
he/she has PE.
Discuss the signs
and symptoms of
PE, and when and
where to seek further
medical help. Take
into consideration
alternative
diagnoses.
Consider a
proximal leg
vein ultrasound
scan.
Is deep vein thrombosis suspected?
Was the CTPA (or V/Q SPECT or planar scan) positive?
Yes
Yes
No
No
Diagnose PE and treat
Yes
No
Yes No
Yes No
*Computed tomography pulmonary angiogram
**For patients who have an allergy to contrast media, or who have renal impairment, or whose risk from irradiation is
high, assess the suitability of V/Q SPECT† or, if not available, V/Q planar scan, as an alternative to CTPA.
†Ventilation/perfusion single photon emission computed tomography
K22247_C001.indd 12 16/05/15 3:06 AM
≤
35. 13Thoracic imaging
should never delay urgent thrombolysis if massive
pulmonary embolism is suspected clinically. (See
Table 1.6.)
Radiological findings
Computed tomography pulmonary angiogram
Interpretation of CTPA studies should begin with
an assessment of the quality of the study, namely the
degree of pulmonary artery contrast opacification
and any potential breathing artefact. An average
attenuation of at least 250 Hu is required in the main
pulmonary trunk to accurately diagnose more distal
emboli. Opacification depends on the size and site of
IV access, rate of injection and exact scan protocol;
inspiration just prior to scanning can cause poorly
MODALITY PROTOCOL
CT Pulmonary angiogram: 100 ml IV contrast
via 18G cannula, 4 ml/sec. Bolus track
centred on main pulmonary artery. Scan
from thoracic inlet to diaphragm level.
Table 1.6 Pulmonary embolus.
Imaging protocol.
opacified blood to be introduced into the pulmonary
arterial system, resulting in the mixing and dilution of
contrast. The precise sensitivity of CTPA studies varies
according to both the quality of contrast opacification
and the degree of artefact (e.g. breathing). It may be the
case that contrast opacification centrally is adequate;
however, emboli more distal in the pulmonary arterial
system cannot be excluded. It is good practice to
quantify to what arterial level emboli can be excluded:
lobar, segmental or subsegmental.
Thepulmonaryarterialsystemshouldbescrutinised
systematically using multiplanar reformatting. A
rounded intraluminal filling defect within a pulmonary
artery, which may also cause slight vessel expansion, is
consistentwithanacuteembolus(Figure 1.11).Itcanbe
difficult to appreciate emboli if the pulmonary arteries
are inspected on standard soft tissue window settings,
since they can be obscured by the dense IV contrast.
Inspection on a relatively wide window setting (width
700, level 100) can alleviate this. A gradual decrease
in opacification of the distal segmental and sub-
segmental pulmonary arteries on a suboptimal study
should not be confused with multiple emboli. Poorly
opacified pulmonary veins can also be misinterpreted
as emboli within the arterial system. Findings seen
in association with pulmonary embolism include
Figure 1.11 Axial image: IV contrast enhanced
CT pulmonary angiogram. A filling defect is outlined by
intravenous contrast in the right main pulmonary artery
consistent with acute embolus (arrow).
K22247_C001.indd 13 16/05/15 3:06 AM
36. Chapter 114
narrowing due to recanalisation (Figures 1.14). A focal
linear intraluminal filling defect within a pulmonary
artery is suggestive of an arterial web, which can be seen
as a result of chronic emboli. Secondary pulmonary
artery hypertension can result from multiple chronic
emboli. The main sign of pulmonary hypertension
on CT is enlargement of the main pulmonary artery
(greater than 34 mm or larger than the corresponding
ascendingaorta;Figure 1.15).Mosaicattenuationofthe
lung parenchyma can also be seen in cases of chronic
pulmonary emboli, although this appearance has a wide
differential diagnosis (Figure 1.16).
pleural effusions, atelectasis and pulmonary infarcts.
The latter present as peripheral wedge-shaped areas of
consolidation,which inthesubacutephasemaycavitate
(Figures 1.12a–c, 1.13).
Chronic pulmonary embolism can provide a
diagnosticchallengefortheradiologist,althoughseveral
findings can be observed that imply this diagnosis.
Calcification of a filling defect suggests chronicity.
Otherradiologicalsignsincludefillingdefectsthatcause
narrowing (as opposed to expansion), eccentric filling
defects that form an obtuse (as opposed to acute) angle
with the pulmonary artery wall and an abrupt artery
Figures 1.12a–c Axial images: IV contrast enhanced
CT scans of the thorax in the arterial phase. Peripheral,
wedge-shaped area of consolidation shown. Over time,
the area of consolidation develops an irregular, thick
rind with areas of cavitation centrally due to infarction.
Note the associated pulmonary arterial filling defects in
1.12b and 1.12c consistent with pulmonary emboli.
(a) (b)(b)
(c)
K22247_C001.indd 14 16/05/15 3:06 AM
37. 15Thoracic imaging
Figure 1.13 PA chest radiograph. Area of peripheral
consolidation at the left mid zone representing an area
of peripheral lung infarction.
Figure 1.14 Axial image: IV contrast enhanced
CT scan of the pulmonary trunk in the arterial phase.
There are features of chronic pulmonary emboli with
recannalised embolic material seen along the walls of the
right main pulmonary artery (arrow).
Figure 1.15 Axial image: IV contrast enhanced
CT pulmonary angiogram. The diameter of the main
pulmonary trunk is greater than the diameter of the
ascending aorta at that same level, suggesting pulmonary
hypertension. The cause is chronic pulmonary emboli
completely occluding the right main pulmonary artery.
Figure 1.16 Axial image: IV contrast enhanced
CT scan of the thorax in the arterial phase. Mosaic
attenuation of the right upper lobe is shown as a result
of abnormal pulmonary perfusion in chronic embolic
disease.
K22247_C001.indd 15 16/05/15 3:06 AM
38. Chapter 116
CT studies can also yield information regarding
the severity of cardiovascular compromise secondary
to pulmonary emboli. Right ventricular dysfunction
and adverse outcome is indicated by a short-axis right
ventricle:left ventricle ratio of greater than 1.5 or
convex bowing of the interventricular septum towards
the left (Figure 1.17). This is an important finding and
if present may necessitate thrombolysis, although this
ultimately depends on the clinical condition of the
patient.
Whenever the scan is negative it is important to look
foranothercauseforchestpainorshortnessofbreathto
explainthepatient’ssymptoms.Theaortaandtheheart
should be assessed for aortic pathology or myocardial
infarction. A septal infarct on a CTPA scan is shown
(Figure 1.18).
Key points
• Radiology is only a part of the investigation
pathway for pulmonary embolism, which includes
pre-test probability scoring and D-dimer analysis
where appropriate.
• CTPA is the out of hours imaging modality of
choice in the investigation of pulmonary emboli.
• A Hu of greater than 250 in the main pulmonary
artery is required for an optimal study.
Figure 1.17 Axial image: IV contrast enhanced
CT scan of the thorax in the arterial phase. The right
ventricle:left ventricle ratio is increased with bowing of
the interventricular septum to the left.
Figure 1.18 Axial image: IV contrast enhanced
CT scan of the thorax in the arterial phase. There is
focal hypoenhancement in the LV septum suggestive of
an acute septal infarct (arrow).
• Pulmonary emboli appear as intraluminal filling
defects on CTPA.
• The severity of cardiovascular compromise
secondary to a large pulmonary embolus is best
assessed by the short-axis right ventricle:left
ventricle ratio.
Report checklist
• The presence or absence of any evidence of right
heart strain.
References
Campbell IA, Fennerty A, Miller AC (2003) British
Thoracic Society guidelines for the management
of suspected acute pulmonary embolism. Thorax
58:47–484.
National Institute of Health and Care Excellence
(NICE) Clinical Guideline 144 (2012) Venous
thromboembolic diseases: the management of
venous thromboembolic diseases and the role of
thrombophilia testing.
Stein P, Woodard P, Weg J et al. (2007) Diagnostic
pathways in acute pulmonary embolism:
recommendations of the PIOPED II Investigators.
Radiology 242:15–21.
K22247_C001.indd 16 16/05/15 3:06 AM
39. 17Thoracic imaging
auscultation. Co-existing signs, such as peripheral
pitting oedema and elevated JVP, imply congestive
cardiac failure.
Radiological investigations
Plain films are the first-line modality in the
investigation of pulmonary oedema; additional cross-
sectional imaging is not required to make the diagnosis.
However, because of the non-specific symptoms and
signs of pulmonary oedema, it can often be seen on CT
imaging performed for other indications, and therefore
the common CT findings are discussed subsequently.
Further investigation of the underlying aetiology often
involves cardiology input.
Radiological findings
Computed tomography and plain films
An understanding of the anatomy of the lung is
necessary to appreciate the spectrum of abnormality
seen in pulmonary oedema on both plain films and
CT. The secondary pulmonary lobule is the most
basic unit of pulmonary structure and is bordered
by a surrounding septum of connective tissue. It
is comprised of multiple acini (responsible for gas
exchange) with a central terminal bronchiole and
centrilobular artery. The peripheral septum contains
both the pulmonary veins and lymphatics, although
there is another central lymphatic network that courses
centrallythroughthesecondarypulmonarylobulewith
the bronchovascular bundle. Excess fluid can fill both
thealveolarairspaces(resultingingroundglassopacity,
whichcanprogresstoconsolidation)andthepulmonary
ACUTE PULMONARY OEDEMA
Pulmonary oedema is a medical emergency and can be
defined as an excess of fluid in the extravascular spaces
of the lung, occurring when there is imbalance of fluid
deposition and absorption. This complex balance is
affected by the hydrostatic and oncotic pressures of
the intravascular and extravascular compartments and
capillary membrane permeability (Gluecker et al.,
1999). Thus, any increases in capillary hydrostatic
pressure or membrane permeability can result in
pulmonary oedema.
The many causes of pulmonary oedema can
be broadly divided into cardiac and non-cardiac
(Table 1.7).Commoncausesincludepulmonaryvenous
hypertension secondary to left ventricular failure and
fluid overload. Damage to the capillary bed may also
result in pulmonary oedema. When associated with
respiratory failure and reduced lung compliance, this
is termed acute respiratory distress syndrome (ARDS)
(Table 1.8) and is characterised by a normal pulmonary
capillary wedge pressure (PCWP).
Symptoms and signs of pulmonary oedema include
rapid onset dyspnoea, hypoxia and crepitations on lung
CARDIOGENIC NON-CARDIOGENIC
Left heart failure.
Mitral valve disease.
Fluid overload.
Post-obstructive pulmonary oedema.
Pulmonary veno-occlusive disease.
Near drowning pulmonary oedema/
asphyxiation pulmonary oedema.
ARDS–pulmonary oedema with
diffuse alveolar damage.
Heroin-induced pulmonary oedema.
Transfusion-related acute lung injury.
High-altitude pulmonary oedema.
Neurogenic pulmonary oedema.
Pulmonary oedema following lung
transplantation.
Re-expansion pulmonary oedema.
Post lung volume reduction
pulmonary oedema.
Pulmonary oedema due to air
embolism.
Table 1.7 Causes of pulmonary oedema.
• Septicaemia.
• Shock.
• Burns.
• Acute pancreatitis.
• Disseminated intravascular coagulation.
• Drugs.
• Inhalation of noxious fumes.
• Aspiration of fluid.
• Fat embolism.
• Amniotic fluid embolism.
Table 1.8 Causes of ARDS.
K22247_C001.indd 17 16/05/15 3:06 AM
40. Chapter 118
interlobular septal thickening and visualisation of the
secondary pulmonary lobule (Figures 1.20a, b). This,
in combination with ground glass opacity, may form a
‘crazy paving’ appearance. This has a wide differential
diagnosis, which includes:
• Alveolar proteinosis.
• Oedema (heart failure/ARDS).
• Pulmonary haemorrhage.
• Infection (e.g. mycoplasma, Legionella,
Pneumocystis carinii/jiroveci pneumonia).
• Organising pneumonia.
• Acute interstitial pneumonitis/non-specific
interstitial pneumonitis.
As PCWP continues to increase, alveolar oedema will
occur, appearing as multifocal areas of ground glass and
airspace opacity in perihilar and dependent regions of
the lungs (Figure 1.21).
Distinguishing the underlying cause of pulmonary
oedema is helpful clinically, although often difficult.
Upper lobe blood diversion and Kerley lines are
most suggestive of pulmonary venous hypertension
secondary to cardiac failure. Associated findings such
as cardiomegaly and bilateral pleural effusions are also
suggestive of underlying left ventricular failure. In the
absence of cardiomegaly, other causes of pulmonary
oedema should be considered, such as fluid overload
or ARDS, although it should be noted that acute
myocardial infarction can cause pulmonary oedema
with a normal heart size in the absence of pre-existing
left ventricular failure. It is always useful to look at the
myocardial enhancement and attenuation of the left
ventricle on CT. This should be uniform; however,
in myocardial infarction the myocardium may
demonstrate decreased attenuation. This represents
decreased enhancement in acute infarction and fatty
deposition in chronic infarction (Figure 1.22).
Key points
• Pulmonary oedema is a medical emergency and
can cause rapid-onset respiratory failure.
• The commonest cause of pulmonary oedema is
pulmonary venous hypertension secondary to left
ventricular failure, although other causes include
fluid overload and ARDS. In the absence of
associated cardiomegaly, non-cardiogenic causes
should be considered.
interstitium (resulting in smooth interlobular septal
thickening).
Interpretation of chest plain films should begin
with an assessment of the quality and radiographic
technique. Anterior-posterior studies can overestimate
the size of the cardiac silhouette due to X-ray beam
divergence. Supine images, as opposed to erect images,
cancauseredistributionofbloodtotheupperzonesand
widening of the vascular pedicle, important signs of left
ventricularfailureandpulmonaryvenoushypertension,
respectively. Poorly inspired images (6 anterior ribs)
can cause crowding of the pulmonary vasculature
and apparent lung congestion. Therefore, a PA chest
radiograph is the best for identifying the appropriate
features.
The spectrum of findings seen on both plain films
and CT in pulmonary venous hypertension can be
correlated with a progressive increase in PCWP. A
mild increase in PCWP results in upper lobe blood
diversion. As PCWP increases, additional findings
such as peribronchial cuffing, loss of vascular definition
and Kerley lines can be seen, all of which indicate
excess fluid in the interstitium (Gluecker et al., 1999)
(Figure 1.19). On CT, the normal interstitium should
be imperceptible. Excess fluid can result in smooth
Figure 1.19 AP portable chest radiograph. Fluid
can be seen in the horizontal fissure, as well as within
the interstitium along the periphery of the thorax.
There is also loss of vascular definition due to venous
hypertension.
K22247_C001.indd 18 16/05/15 3:06 AM
41. 19Thoracic imaging
Report checklist
• Presence or absence of associated cardiomegaly.
Reference
GlueckerT,CapassoP,SchnyderPet al.(1999)Clinical
and radiologic features of pulmonary oedema.
Radiographics 19:1507–1531.
• Plain films are the first-line modality to investigate
pulmonary oedema. CT is NOT indicated in the
investigation of pulmonary oedema, although this
is frequently seen in acute CT chest examinations.
• Loss of vascular definition and Kerley lines imply
interstitial oedema. Alveolar oedema appears as
multifocal airspace opacities in the perihilar and
dependent regions of the lungs.
Figures 1.20a, b Axial images: IV contrast enhanced CT scans of the thorax. There is a combination of
interlobular septal thickening and patchy ground glass opacity, resulting in a crazy paving appearance.
Figure 1.21 AP chest radiograph. There are bilateral,
perihilar airspace opacities consistent with alveolar
oedema. The costophrenic angles are not visible due to
bilateral pleural effusions.
Figure 1.22 Axial image: IV contrast enhanced
CT scan of the thorax in the arterial phase. There is
subendocardial fat deposition at the LV apex in keeping
with previous myocardial infarction.
(a) (b)
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42. Chapter 120
familiarity with the wide variation of appearances of the
‘normal’ SVC is important. Any large extrinsic mass
significantly compressing the SVC is easily evident on
CT (Figures 1.23a–c). Difficulty comes in identifying
intrinsic SVC thrombus or tumour infiltration, since
flow in the SVC can often be turbulent. This is made
even more challenging by the dilution of IV contrast
material in the SVC by unenhanced blood from the
IVC, which can simulate intraluminal thrombus.
Thrombus should be suspected in the presence of a
focal filling defect in the SVC lumen, which may also
cause expansion of the lumen with localised stranding
of the adjacent fat. Thrombus may extend into the
brachiocephalic and subclavian veins, which should
also be inspected. Regardless of the cause, the length
and severity of obstruction should be considered; total
occlusion of the SVC lumen may require more urgent
treatmentthanpartialocclusion.Completeobstruction
of the SVC results in a significant hold up of contrast in
the venous system proximal to the level of obstruction.
Knowledge of the potential collateral pathways in
SVC obstruction is necessary in order to assess the
severity and duration of the obstruction. The main
collateral systems include the azygous-hemiazygous
(most important), internal mammary, long thoracic
and vertebral venous pathways (Sheth et al., 2009). In
normalconditions,antegradebloodflowshouldbeseen
SUPERIOR VENA CAVA OBSTRUCTION
Superiorvenacava(SVC)syndromereferstoaspectrum
of clinical findings that occur secondary to obstruction
of the SVC. The most common causes of SVC
obstructionarepulmonaryandmediastinalmalignancy.
Other causes include thrombosis of the SVC secondary
to central line placement, benign mediastinal tumours,
vascular aneurysms, mediastinal fibrosis and radiation
fibrosis. Symptoms and signs include neck and upper
limb swelling, distended superficial veins in the SVC
territory,dyspnoeaandheadache(secondarytocerebral
oedema from impaired venous drainage). The severity
of symptoms has been shown to depend on the level of
obstruction (above or below the azygous arch) and the
presence of a collateral network (Plekker et al., 2008).
Althoughtheseverityofthepresentationoftendepends
on the duration of obstruction, urgent diagnosis is
necessary to facilitate treatment such as radiotherapy
and interventional stenting.
Radiological investigations
Contrast enhanced CT allows visualisation of the SVC,
venous collateralisation and the potential cause of the
obstruction,andisconsideredthemodalityofchoicefor
initial assessment. Catheter venography is reserved for
therapeutic stent placement in confirmed cases. While
chest plain films have value in identifying potential
mediastinal and lung masses that may be a cause of
SVC obstruction, this modality cannot confirm venous
obstruction. Ultrasound with Doppler analysis of the
upper limb, subclavian brachiocephalic and internal
jugular veins can also be helpful. Dampening of the
normalvenouswaveformandlossofnormalrespiratory
variationareindirectsignsofSVCobstruction.Because
ofthelimitedacousticwindow,theSVCitselfcannotbe
imaged in its entirety with ultrasound. (See Table 1.9.)
Radiological findings
Computed tomography
Analysis of CT imaging should begin with the SVC
itself. The cross-sectional morphology of the SVC
varies according to circulating volume; as such,
MODALITY PROTOCOL
CT Post IV contrast: 100 ml IV contrast via
18G cannula, 3 ml/sec. Scan at 30 seconds
after initiation of injection. Scan from lung
apices to diaphragm level.
Table 1.9 Superior vena cava obstruction.
Imaging protocol.
K22247_C001.indd 20 16/05/15 3:06 AM
43. 21Thoracic imaging
in the azygous and hemiazygous veins, which provide
an accessory pathway of blood to the SVC and right
atrium. Collateral flow in the azygous system should be
suspected with abnormal venous distension, although
this can also be seen with other conditions (Table 1.10).
Venouscollateralvesselsappearasenlargedserpiginous
vessels containing dense IV contrast; these can be
seen in the chest wall, mediastinum, intercostal and
• Congestive heart failure.
• SVC obstruction.
• Azygous continuation of the IVC.
• Portal hypertension.
• Constrictive pericarditis.
Table 1.10 Causes of azygous distension.
Figures 1.23a–c Axial and
coronal images: IV contrast
enhanced CT scans of the thorax
in the arterial phase. There is a
spiculated mediastinally invasive
lung tumour, which is compressing
the SVC to a narrow slit.
(a) (b)
(c)
K22247_C001.indd 21 16/05/15 3:06 AM
44. Chapter 122
Report checklist
• Document the degree of SVC obstruction.
• Consider the underlying cause, such as an
obstructing mass or intraluminal thrombus.
• Document the degree of collateralisation.
References
Gosselin M, Rubin G (1997) Altered intravascular
contrast material flow dynamics: clues for
refining thoracic CT diagnosis. Am J Roentgenol
169:1597–1603.
Plekker D, Ellis T, Irusen EM et al. (2008) Clinical
and radiological grading of superior vena cava
obstruction. Respiration 76:69–75.
Sheth S, Ebert M, Fishman E (2009) Superior vena
cava obstruction evaluation with MDCT. Am J
Roentgenol 194:336–346.
paravertebral regions (Figure 1.24). Obstruction of the
SVC above the level of the azygous arch results in flow
through chest wall collaterals into the azygous venous
system. Obstruction distal to the level of the azygous
arch results in retrograde flow in the azygous vein,
presentingasdensecontrastmaterialwithintheazygous
venous system on CT, which is normally unenhanced
in physiological antegrade flow (Gosselin et al., 1997)
(Figures 1.25a, b). The presence of collateral vessels
implies a significant long-standing venous obstruction.
Key points
• SVC obstruction is a medical emergency. The
most common causes include malignancy and
iatrogenic related thrombosis.
• Although catheter venography is more sensitive
in subtle cases, CT is non-invasive and provides
useful information of both the degree of
obstruction and the underlying cause.
Figure 1.24 Axial image: IV contrast enhanced
CT scan of the thorax in the arterial phase. There are
multiple, serpiginous enhancing vessels adjacent to the
diaphragm consistent with venous collaterals, some
of which drain into the IVC (arrow). Incidental note is
made of a chronic left-sided pleural effusion.
K22247_C001.indd 22 16/05/15 3:06 AM
45. 23Thoracic imaging
Figures 1.25a, b Axial images: IV contrast enhanced CT scans of the thorax in the arterial phase. Both cases
demonstrate reflux of IV contrast from the SVC into the azygous vein. A hypoattenuating mass can be seen in the
anterior mediastinum causing obstruction of the SVC proximally (1.25a).
(a) (b)
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47. 25
Chapter 2
GASTROINTESTINAL AND
GENITOURINARY IMAGING
ABDOMINAL AORTIC
ANEURYSM RUPTURE
Abdominal aortic aneurysms (AAAs) are a vascular
surgical emergency. A true aneurysm is defined as
focal dilatation of the artery (an increase of at least
50% of the normal vessel diameter) that involves
the intima, media and adventitia. In comparison, a
pseudoaneurysm is a focal collection of blood that
connects with the vessel lumen, but is bound only by
adventitia or local soft tissues. AAA rupture occurs
more commonly with advancing age, and is estimated
to occur in 2–4% of the population over 50 years of
age (Bengtsson et al., 1992).
The most common cause of AAA rupture is
degeneration of the vessel wall, traditionally attributed
to atherosclerosis, although inflammatory, mycotic
and traumatic pseudoaneurysms can also occur.
Aneurysms are also associated with connective tissue
disease, particularly in younger patients. The classic
sign of a pulsatile abdominal mass may not always
be present. Symptoms and signs may be more non-
specific, including abdominal pain, collapse and
haemodynamic instability. In practice, the on-call
radiologist should have a high index of suspicion for
this condition in any elderly patient presenting with
abdominal pain. The mortality rate is high; at least
65% of patients with aortic aneurysm rupture and
die before reaching hospital. Urgent diagnosis is
vital in order to facilitate life saving open surgical or
endovascular aneurysm repair.
Radiological investigations
Ultrasound and CT can both accurately assess the
size of the abdominal aorta. Ultrasound has a well-
established role in the long-term follow up of known
cases of AAA; however, it also has a role in the acute
MODALITY PROTOCOL
CT Aortic angiogram: 100 ml IV via
18G cannula, 4 ml/sec. Bolus track centred
on mid-abdominal aorta. No oral contrast.
Scan from just above diaphragm to femoral
head level.
Table 2.1 Abdominal aortic aneurysm rupture.
Imaging protocol.
setting. Ultrasound can be performed initially in
suitable patients who are stable and who do not have
a known history of aortic aneurysm; a normal calibre
aorta is unlikely to rupture spontaneously. The
gross signs of aortic rupture, such as retroperitoneal
haematoma, would be expected to be present,
although the more subtle signs of impending rupture
are difficult to assess with ultrasound.
CT is the imaging modality of choice in assessing
potential aortic aneurysm rupture and should be
performed in unstable patients with a strong clinical
suspicion without delay. CT not only has a high
sensitivity and specificity for AAA rupture, but it
is also useful in identifying alternative abdominal
pathologies to account for the presentation. Both
unenhanced and arterial phases should be obtained.
(See Table 2.1.)
Radiological findings
Computed tomography
In cases where AAA rupture is strongly suspected
clinically, it can be helpful to review the initial images
locally when the patient is still in the radiology
department. This allows prompt communication of
a rupture to the referring team. Comparison with
previous imaging is extremely helpful in cases of
known AAA.
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48. Chapter 226
Degenerative aneurysms are usually fusiform in
shape. Small, focal dissections within degenerative
AAAs are not uncommon (Figure 2.2). A saccular
aneurysm or lobulated contour should prompt a
suspicion of infection (mycotic aneurysm). Additional
findings suggestive of infection include significant
periaortic inflammation, local fluid collections,
vertebral body destruction and fistulation with adjacent
structures (Figure 2.3).
The presence of retroperitoneal or periaortic
haematoma is indicative of aneurysmal rupture and
shouldbeurgentlycommunicatedtothereferringteam
(Figure 2.4). It is sometimes possible to identify the
exactsiteofrupture;thisappearsasafocaldiscontinuity
in the aortic wall. Active contrast extravasation can
also sometimes be identified in the presence of IV
contrast.
An AAA is confirmed when the maximum diameter
of the abdominal aorta exceeds 3 cm (Figure 2.1).
The size, morphology and location of the aneurysm is
best characterised on the arterial phase. Aneurysms can
be infrarenal (originating below the level of the renal
arteries) or suprarenal/renal; the location determines
potential treatment. In infrarenal cases, the distance
between the renal arteries and the most cranial aspect
of the aneurysm should be measured; this information
can dictate if a case is suitable for endovascular repair.
For aortic ruptures where the aneurysm involves the
renal arteries, endovascular repair is less suitable than
an open approach, since an adequate ‘landing zone’
is required for stent placement. Further relevant
contraindications of an endovascular approach include
angulated, tortuous or narrowed (8 mm) iliac arteries
or tapering of the aneurysmal neck.
Figure 2.1 Axial image: IV contrast enhanced CT scan
of the abdomen in the arterial phase. The abdominal
aorta is aneurysmal, with contrast seen within the lumen
of the vessel. Hypodense thrombus can also be seen
along the left aortic wall, in addition to a thin rim of
calcification around the vessel.
Figure 2.2 Axial image: IV contrast enhanced CT scan
of the abdomen in the arterial phase. The abdominal
aorta is aneurysmal, and a linear dissection flap can be
seen traversing the lumen.
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49. Gastrointestinal and genitourinary imaging 27
Figure 2.3 Coronal image: IV contrast enhanced
CT scan of the abdomen in the arterial phase. A saccular
aneurysm is seen arising from the abdominal aorta,
which is fistulating with the left common iliac vein.
Figure 2.4 Axial image: IV contrast enhanced CT scan
of the abdomen in the arterial phase. There is large
volume retroperitoneal haematoma, which can be seen
outlining the right Gerota’s fascia, extending into the
paracolic spaces.
Figure 2.5 Axial image: IV contrast enhanced CT
scan of the abdomen in the arterial phase. The aorta
is aneurysmal and contains thrombus. Ill-defined,
crescenteric high attenuation material can be seen
within the thrombus consistent with contained contrast
extravasation/fissuring into the thrombus (arrow).
There is a spectrum of more subtle CT findings
that are important to appreciate. Contained rupture
should be suspected if the posterior wall of the aorta
is ill-defined or cannot be clearly delineated from
the vertebral bodies, termed the ‘draped aorta’ sign
(Halliday et al., 1996). High attenuation material
in a crescenteric distribution within thrombus in
the aneurysm sac, best appreciated on wide window
settings, can represent infiltration of blood into the
thrombus wall and is suggestive of impending rupture
(Gonsalves, 1999) (Figure 2.5). Further signs that can
indicate impending rupture include aneurysms larger
than 7 cm with increasing abdominal pain, a rapid
increase in the size of an AAA (10 mm per year) and
fissuring of thrombus or mural calcification (Rakita
et al., 2007).
An additional complication of AAA is aortoenteric
fistulation, in which a communication is formed
between the aorta and bowel, usually in the region
of the second or third part of the duodenum. This is
suggested by gas within the aortic lumen, although
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50. Chapter 228
this can also be seen with mycotic aneurysms. Active
extravasation of aortic contrast into the bowel, or a
history of melaena, can be useful distinguishing factors
(Figures 2.6a, b).
Key points
• CT is the optimum imaging modality in the
assessment of potential AAA rupture.
• An aneurysm is confirmed when the maximum
diameter of the aorta exceeds 3 cm. Rupture is
confirmed in the presence of retroperitoneal or
periaortic haematoma.
• More subtle signs of impending aneurysm rupture
include increasing pain, an increase in size greater
than 10 mm per year and crescenteric high
attenuation within aortic thrombus.
Report checklist
• Presence or absence of haemorrhage and active
contrast extravasation.
• Presence or absence of dissection flap.
Figures 2.6a, b Axial images: IV contrast enhanced CT scans of the abdomen in the arterial phase. Ill-defined
contrast can be seen extending from the aorta into a loop of bowel anteriorly, consistent with an aortoenteric fistula
(arrow). The aorta is seen to be aneurysmal more cranially.
(a) ( b)
• Anatomical location of the aortic aneurysm:
infrarenal or juxtarenal.
• Renal vessel involvement or renal hypoperfusion.
• Signs of significant intravascular volume depletion
e.g. IVC flattening.
• Patency of coeliac axis/SMA/IMA/renal arteries.
References
Bengtsson H, Bergqvist D, Sternby NH (1992)
Increasing prevalence of abdominal aortic
aneurysms: a necropsy study. Eur J Surg 158:19–23.
Gonsalves CF (1999) The hyperattenuating crescent
sign. Radiology 211:37–38.
Halliday KE, Al-Kutoubi A (1996) Draped aorta: CT
sign of contained leak of aortic aneurysms. Radiology
199:41–43.
Rakita D, Newatia A, Hines J et al. (2007) Spectrum
of CT findings in rupture and impending rupture
of abdominal aortic aneurysms. Radiographics
27:497–507.
K22247_C002.indd 28 16/05/15 3:07 AM
51. Gastrointestinal and genitourinary imaging 29
is more helpful in cases of occult or intermittent GI
bleeding). CTA is increasingly being used as the first-
line imaging modality of choice and is a useful adjunct
in cases where endoscopy has failed to identify a source
of bleeding. The sensitivity of CT decreases if bleeding
is intermittent and timing the scan with the clinical
signs of active bleeding is essential. Utilising triple-
phase CTA (unenhanced, arterial and delayed phases)
increases sensitivity and specificity when compared
with using a single phase only. Oral contrast may mask
the potential site of bleeding and should therefore be
omitted. It is also important to consider whether the
patient has had any recent oral contrast examinations,
since this can also lead to a false-positive result. Barium
enemas are of particular importance, since the oral
contrast can remain in diverticulae for months or even
years.Catheterangiographyisinvasiveandisnowadays
lesssensitivethanCTA;assuchitisgenerallyperformed
once CTA has identified a bleeding point, with an aim
to embolisation and treatment. (See Table 2.3.)
Radiological findings
Computed tomography
The GI tract should be scrutinised systematically, with
careful attention being paid to the locations that are
common sources of bleeding (stomach, duodenum
and colon). The focus of acute GI bleeding is located
by identifying high attenuation material (90 Hu)
within the bowel lumen on the arterial phased scan,
which represents active extravasation of IV contrast.
ACUTE GASTROINTESTINAL BLEEDING
Acute gastrointestinal (GI) bleeding is a medical and
surgical emergency, with an associated mortality of
up to 40% (Walsh et al., 1993). GI bleeding has many
causes (Table 2.2) and can be divided into upper and
lower tract bleeding, according to its location in
relation to the ligament of Treitz. Upper tract bleeding
is more common than lower tract bleeding, comprising
approximately 75% of cases (Ernst et al., 1999).
Symptoms such as haematemesis and melaena usually
indicateanuppertractsource,whereasfreshperrectum
bleeding usually signifies bleeding from the lower GI
tract. Profound bleeding can result in haemodynamic
instability and therefore urgent localisation of the
source is vital. Endoscopy has traditionally been
considered the first-line investigation for suspected GI
bleeding, especially in cases of suspected upper tract
bleeding. Limitations of endoscopy include an inability
to visualise the upper tract distal to the fourth part of
theduodenumanddifficultyinvisualisingbleedingfoci
because of profound intraluminal haemorrhage. With
the increasing sensitivity of CT and ease of access,
radiological investigations are increasingly being
considered as the first-line investigation.
Radiological investigations
Radiological investigations that play a part in the
management of GI bleeding include CTA, catheter
angiography and radionucleotide imaging (the latter
UPPER LOWER
Mallory–Weiss tear Angiodysplasia
Oesophageal varices Diverticulitis
Gastric/duodenal ulcer Colitis
Gastritis Malignancy
Malignancy
Table 2.2 Causes of gastrointestinal bleeding.
MODALITY PROTOCOL
CT Unenhanced. No oral contrast. Scan from
above diaphragm to femoral head level.
Aortic angiogram: 100 ml IV contrast via
18G cannula, 4 ml/sec. Bolus track centred on
mid-abdominal aorta. No oral contrast. Scan
from above diaphragm to femoral head level.
Delayed phase. IV contrast as above, scan at
120 seconds after start of contrast injection.
No oral contrast. Scan from above diaphragm
to femoral head level.
Table 2.3 Acute gastrointestinal bleeding.
Imaging protocol.
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52. Chapter 230
This is usually more apparent and accumulates on
the delayed phase (Figures 2.7, 2.8). It is vital to
scrutinise the unenhanced phase to assess for pre-
existing foci of high attenuation within the bowel
lumen that may lead to false positives; these can
include ingested tablets, foreign bodies and suture
material. Previous imaging should also be reviewed in
this regard. Cone beam artefact is another common
false positive, occurring at interfaces between fluid and
air within the bowel.
Bleeding in the distal oesophagus may be secondary
to oesophageal varices, a complication of portal
hypertension. These may be visualised as dilated,
• Splenomegaly.
• Ascites.
• Varices: splenic/oesophageal.
• Underlying cause (i.e. liver cirrhosis with atrophy and
nodular/irregular contour).
• Contrast enhancement of para-umbilical vein.
Table 2.4 Computed tomographic signs of
portal hypertension.
Figure 2.7 Axial image: contrast enhanced CT scan of
the abdomen in the arterial phase. Hyperdense material
can be seen in a dependent position within the lumen of
the ascending colon (arrow), consistent with an acute,
arterial haemorrhage.
Figure 2.8 Axial image: contrast enhanced CT scan of
the abdomen in the delayed phase. On delayed imaging,
further contrast has accumulated within the lumen
of the ascending colon as a result of continued, active
haemorrhage at this site.
serpiginous enhancing vessels in the region of the distal
oesophagus. Findings suggestive of liver cirrhosis
and portal hypertension, such as an irregular liver
outline and splenic enlargement, should prompt
the search for oesophageal varices (Table 2.4;
Figures 2.9, 2.10).
IfGIbleedingisidentified,itisimportantto consider
anunderlyingcause.Muralthickeningcanbemalignant,
inflammatory, ischaemic or infective in nature, all of
whichcanbecomplicatedbybleeding.Itisalsoimportant
to appreciate that GI bleeding is often intermittent and
it is not uncommon for CTA to be normal, even in
haemodynamically compromised patients.
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53. Gastrointestinal and genitourinary imaging 31
Figure 2.9a, b Axial and coronal images: unenhanced
CT scans of the abdomen. A transjugular intrahepatic
portosystemic shunt (arrow) and coiled oesophageal
varices are shown.
Figures 2.10a–c Axial images: unenhanced, arterial
and delayed phase CT scans of the abdomen. This
sequence of images demonstrates a contrast blush
on the arterial phase within the stomach (arrow). No
corresponding density is seen on the unenhanced scan.
Findings are in keeping with acute gastric bleeding.
The spleen is enlarged, suggestive of underlying portal
hypertension.
(a)
( b)
(c)
( b)(a)
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54. Chapter 232
BOWEL PERFORATION
GI perforation is an emergency condition requiring
urgent surgical intervention. Clinical diagnosis of the
site of bowel perforation is difficult as the symptoms
may be non-specific. Diagnosis depends mostly on
imaging investigations, and a correct diagnosis of the
presence of, site and cause is crucial for appropriate
management and for planning surgery.
Breach of the GI tract wall can be due to peptic
ulcer disease, inflammatory disease, blunt or
penetrating trauma, iatrogenic factors, a foreign body
or a neoplasm. Clinical presentation is usually that of
abdominal pain and nausea and vomiting, with signs of
peritonitis including rebound tenderness and guarding
on palpation. Patients can be extremely unwell with
signs and symptoms of shock. Inflammatory markers
(C-reactive protein) and raised white cells may be
present on laboratory blood analysis.
Radiological investigations
The first-line imaging investigations for suspected
bowel perforation are plain films, including an erect
CXR and a plain abdominal film, but these are only
sensitive in 50–70% of cases. Contrast studies are
no longer indicated in the acute setting. As well as
having a suboptimal sensitivity, plain films will not
demonstrate the site of perforation, which is useful
to know prior to surgery. CT is the imaging modality
of choice, as it provides the most information
for planning surgery, with a sensitivity of 86% in
identifying the site of perforation. The goal of imaging
is to identify extraluminal leakage and the subsequent
inflammatory reaction around the perforation site.
(See Table 2.5.)
Key points
• CTA and catheter angiography are useful in
conjunction with oesophagogastroduodenoscopy
and colonoscopy in the investigation of acute GI
bleeding, although the sensitivity is reduced when
bleeding is intermittent.
• Triple-phase CTA increases the sensitivity
of detection of acute bleeding and should be
performed without oral contrast.
• Active bleeding appears as a high attenuation focus
within the bowel lumen on the arterial phase,
which becomes more pronounced on the portal
venous phase. Scrutiny of the unenhanced images
reduces false positives.
Report checklist
• Identify the bleeding vessel where possible, and
the large artery of which it is a branch.
• Consider underlying causes.
• Look for signs of significant intravascular volume
loss (e.g. flattening of the IVC).
• Emphasise that bleeding can be intermittent and
therefore a ‘normal’ scan does not exclude GI
bleeding.
• Recommend urgent interventional radiology
referral.
References
Ernst AA, Haynes ML, Nick TG et al. (1999)
Usefulness of the blood urea nitrogen/creatinine
ratio in gastrointestinal bleeding. Am J Emerg
Med 17:70–72.
Walsh RM, Anain P, Geisinger M et al. (1993) Role
of angiography and embolization of massive
gastroduodenal haemorrhage. J Gastrointest
Surg 3:61–65.
MODALITY PROTOCOL
Plain film imaging AP supine abdominal radiograph to include the liver. A left lateral decubitus film can be performed with
the patient lying on their left and the right side up.
Erect chest radiograph to include the diaphragms. Patient should be upright for at least 10 minutes
prior to image acquisition.
CT Post IV contrast, portal venous phase: 100 ml IV contrast, 4 ml/sec via 18G cannula. Scan at 70 seconds.
Scan from above diaphragm to femoral head level.
Table 2.5 Bowel perforation. Imaging protocol.
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55. Gastrointestinal and genitourinary imaging 33
Radiological findings
Plain films
The presence of free air under the diaphragm
on an erect chest plain film is diagnostic of free
intraperitoneal air (Figure 2.11). As little as 1 ml of air
can be identified under the diaphragm. Care should be
taken not to confuse the stomach bubble under the left
hemidiaphragm with free air.
Aplainabdominalfilmcanrevealabowelperforation,
with the presence of Rigler’s sign (gas outlining both
sides of the bowel wall) (Figure 2.12). Other abdominal
plain film signs of free air include football sign (oval-
shaped peritoneal gas), which is more common in
children (Figure 2.13), increased lucency over the right
upper quadrant (gas accumulating anterior to the liver)
or the triangle sign (gas accumulating between three
loops of bowel). Free gas can also be seen outlining
ligaments in the abdomen, such as the falciform
ligament (Figure 2.14). A left lateral decubitus film can
also be used in the detection of small amounts of free
air that may be interposed between the free edge of the
liver and the lateral wall of the peritoneal cavity.
Figure 2.11 AP semi-erect chest radiograph. Large
volumes of gas can be seen underneath the diaphragm
consistent with pneumoperitoneum.
Figure 2.13 AP supine abdominal radiograph.
A large, rounded lucency is seen projected in the
mid-abdomen representing free intra-abdominal gas in a
non-dependent location. The falciform ligament is also
seen outlined clearly by free gas (arrow).
Figure 2.12 AP supine abdominal radiograph. Gas
can be seen within the peritoneum on both sides of the
bowel wall (Riggler’s sign), highlighting multiple loops
of dilated small bowel.
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