A-Z of Abdominal

Radiology

Gabriel Conder, MRCP, FRCR

Consultant Radiologist,

Northwick Park and Central Middlesex Hospitals, North West London

Hospitals NHS Trust, London

John Rendle, FRCS (Eng), FRCR

Consultant Radiologist

Mayday University Hospital, Mayday Healthcare NHS Trust, Croydon

Sarah Kidd, MRCP, FRCR

Specialist Registrar in Radiology

St. Mary’s Hospital, Imperial College Healthcare NHS Trust, London

Rakesh R. Misra, BSc (Hons), FRCS (Eng.), FRCR

Consultant Radiologist

Wycombe Hospital, Buckinghamshire Hospital NHS Trust, High Wycombe

Series Editor

R. R. Misra

CAMBRIDGE UNIVERSITY PRESS

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this

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CONTENTS

Acknowledgements

page ix

Preface

List of abbreviations

xii

Abdominal trauma

Abscesses within the abdomen

Achalasia

Adnexal masses

Adrenal masses

Aortic aneurysm

Appendicitis

Ascites

Bezoar

Biliary gas

Biliary obstruction

Bladder calculi

Bowel obstruction

Calcifications

Chilaiditi’s sign/syndrome

Cholecystitis

Cirrhosis

Colitis

Colonic carcinoma

110

Colonic diverticulitis

116

Colonic polyps

120

Crohn’s disease

126

Dermoid tumour

134

Ectopic pregnancy

136

Endometrial carcinoma

138

vii

Familial polyposis coli

142

Fistulae

144

Foreign bodies

150

Free intra-abdominal gas

156

Gallstones

162

Hepatic masses

168

Herniae of the abdomen and pelvis

190

Intussusception

200

Lines and devices

208

Lymphadenopathy

220

Lymphoma: abdominal

224

Omental secondary deposits

232

Pancreatic carcinoma

234

Pancreatitis

240

Portal vein thrombosis

248

Portal venous gas

252

Portal venous hypertension

256

Pyelonephritis

262

Renal artery stenosis

270

Renal calcification

276

Renal developmental anomalies

282

Renal masses: benign

290

Renal masses: malignant

300

Renal tract calculi

308

Retroperitoneal fibrosis

314

Splenomegaly

318

Testicular neoplasms

322

Transitional cell carcinoma

324

Tuberculosis of the abdomen and pelvis

330

Uterine fibroids

340

Volvulus

346

viii

PREFACE

The A-to-Z of Abdominal Radiology is a valuable addition to the A-to-Z of

Radiology series, continuing the theme of concise introductions to specific

fields of radiology. The text is concisely laid out, following a similar format

to the other title in this series, using a bullet point format to allow rapid

assimilation of relevant facts. The text is richly illustrated with images from

modern scanners.

The book will be a useful aid to medical students, radiographers,

surgical trainees, physicians and emergency doctors who wish to gain a

greater understanding of abdominal and pelvic imaging and how it can

improve their clinical practice. Radiology trainees will also find this a

helpful aide-mémoire to consolidate their knowledge.

G. C.

J. R.

S. K.

R. R. M.

ABBREVIATIONS

^99mTc

technetium-99m

AAA

Abdominal aortic aneurysm

ACE

Angiotensin-converting-enzyme

AIDS

Acquired immunodeficiency syndrome

Antero-posterior

ARDS

Adult respiratory distress syndrome

ATLS

Advanced trauma life support

AXR

Abdominal X-ray

CA19-9

Carbohydrate antigen 19-9

CECT

Contrast-enhanced computed tomography

CNS

Central nervous system

Computed tomography

CXR

Chest X-ray

ERCP

Endoscopic retrograde cholangiopancreatography

FDG

Fluorodeoxyglucose

FIGO

Federation international de gynaecologie et obstetrique

FNH

Focal nodular hyperplasia

Gastrointestinal

Gray

HCC

Hepatocellular carcinoma

Hodgkin’s disease

Hounsfield unit

IUCD

Intrauterine contraceptive device

Intravenous

IVC

Inferior vena cava

IVU

Intravenous urogram

KUB

Kidney-ureter-bladder

LBO

Large-bowel obstruction

LIF

Left iliac fossa

LUQ

Left upper quadrant

MALT

Mucosa-associated lymphoid tissue

MIBG

Meta-iodobenzylguanidine

Magnetic resonance

MRCP

Magnetic resonance cholangiopancreatography

MRI

Magnetic resonance imaging

NECT

Non-enhanced CT

xii

NHL

Non-Hodgkin lymphoma

Nuclear medicine

PET

Positron emission tomography

PID

Pelvic inflammatory disease

PTC

Percutaneous trans-hepatic cholangiogram

RAS

Renal artery stenosis

RIF

Right iliac fossa

RLQ

Right lower quadrant

RPF

Retroperitoneal fibrosis

RTA

Road traffic accident

RUQ

Right upper quadrant

SBO

Small-bowel obstruction

T1W

T1 weighted

T2W

T2 weighted

Trans-abdominal

Tuberculosis

TCC

Transitional cell carcinoma

TIPS

Transjugular intrahepatic porto-systemic shunt

TURBT

Transurethral resection of bladder tumour

TURP

Transurethral resection of prostate

Transvaginal

Ulcerative colitis

United Kingdom

Ultrasound

USS

Ultrasound scan

VIP

Vasoactive intestinal polypeptide

WBC

White blood cell count

xiii

Abdominal trauma

Clinical characteristics

• Ageneraldiscussion,followedbyorgan-specificsummaries,isgivenbelow.

• Abdominal trauma is managed as part of general trauma under the

ATLS (advanced trauma life support) algorithm, where basic care of

airway, breathing and circulation is followed by a secondary survey and

simultaneous management.

• Abdominal trauma is usually divided into blunt and penetrating trauma.

Penetrating trauma

•

Generally managed by surgical exploration and repair. Surgical repair

may be primary or secondary (delayed) according to a multitude of

factors, including degree of contamination, time since injury and gen-

eral health of the patient.

•

Where the patient is haemodynamically unstable, with signs of

obvious massive intra-abdominal haemorrhage, many of the investiga-

tions below are suspended, and the patient is managed surgically on

an emergency basis with coexistent haemodynamic monitoring and

management.

•

If the patient is haemodynamically stable, the usual radiological inves-

tigation is a contrast-enhanced computed tomography (CECT) scan.

This is usually performed following a radiographic primary survey

(lateral cervical spine, chest and pelvis radiographs).

•

It is now generally considered that diagnostic peritoneal lavage is rarely

indicated and has been superseded by CECT.

•

Emergency ultrasound (US) of the abdomen and pelvis is sometimes

performed and may be of use in determining the presence and location

of intra-abdominopelvic blood. Vascularity of abdominal viscera (e.g.

the kidneys) can also be assessed. US may also be used to monitor

patients who are being managed conservatively. However, CECT is

considered superior in the context of acute abdominal trauma.

Blunt trauma to the spleen

• Spleen is the most commonly injured solid intra-abdominal organ.

• Blunt trauma is the most common cause.

• Often (40%) associated with lower rib fractures and left renal injury.

• In 20% of patients with left rib fractures, there is a concomitant splenic

injury.

Radiological features

•

Abdominal X-ray (AXR):

• Poor sensitivity in identifying both the site and presence of intra-

abdominal haemorrhage.

• May show associated fractures, displaced air-filled bowel caused by

intra-abdominal blood or free air from associated bowel perforation.

•

CECT:

• In nearly all cases of abdominal trauma, a CECT of the abdomen and

pelvis is performed to ensure adequate coverage of injuries.

• Mottled splenic parenchymal enhancement may represent contusion.

NB. The spleen in the arterial phase of a CECT may normally appear

mottled.

• Splenic fracture may present as complete separation of unenhancing

splenic fragments.

• Subcapsular haematoma is shown by a crescentic region of low

attenuation compressing normal parenchyma.

• Intracapsular haematoma is demonstrated by a hypodense inhomoge-

neous region within the spleen.

• Splenic laceration is revealed as a hypoattenuating line connecting

opposite visceral surfaces. Associated with perisplenic fluid.

• Multiple lacerations represent a shattered spleen.

• Disruption of the splenic capsule with high-density fluid within

abdomen represents splenic rupture with free intraperitoneal

haemorrhage.

Complications

• Splenic pseudocyst formation.

• Delayed rupture - up to 10 days later.

• Infected subcapsular haematoma.

• Splenic artery pseudoaneurysm.

Blunt trauma to the liver

• Second most frequently injured intra-abdominal organ.

• Associated with splenic injury in 45%.

• Right lobe more frequently injured.

• When left lobe is involved, there may be associated injury to the

duodenum, pancreas and transverse colon.

Radiological features

• AXR:

• Increased density in RUQ, displacement of neighbouring organs, e.g.

right kidney displaced downwards and medially.

Large liver laceration (arrow).

Liver haematoma. Large haematoma within the superior aspect of the

right lobe of liver (arrowhead) with an additional subcapsular haematoma

(asterisk).

• CECT:

• Subcapsular haematoma - hypoattenuating lenticular configuration,

usually resolves in 6-8 weeks and generally managed conservatively.

• Hepatic laceration - irregular linear branching, single or multiple

stellate configurations of low density relative to enhancing

parenchyma.

• Focal hepatic devascularisation

- focal hypodense wedge lesion

extending to liver surface.

• Active haemorrhage - focal hyperdense area.

• Hepatic necrosis - intrahepatic or subcapsular gas.

Complications

• Occur in up to 20%.

• Haemobilia.

• Pseudoaneurysm/arteriovenous fistula formation.

• Biloma.

• Infection/necrosis.

• Delayed hepatic rupture - unusual.

Blunt trauma to the kidneys

• Occurs in 10% of blunt abdominal injury.

• Often caused by a direct blow (80%).

• Usually caused by laceration by lower ribs or devascularisation of the

renal pedicle in acceleration-deceleration injuries.

• Associated with other abdominal organ injury in 20%.

• Almost always presents with some degree of haematuria (over 95%).

• Main exception is with renal pedicle injuries, where 25% have no

haematuria due to devascularisation of kidney.

• Not usually accompanied by lower renal tract injury.

• Four degrees of injury, ranging from contusion and corticomedullary

laceration (grade I) to renal pedicle avulsion (grade IV).

Radiological features

• AXR: Plain film findings commonly seen in renal trauma include:

• Absent psoas shadow.

• Enlarged/distorted kidney and pelvicalyceal system

(following

administration of IV contrast).

• Fractures of the 10th, 11th and 12th ribs.

• Fractures of the transverse processes of the 1st, 2nd or 3rd lumbar vertebra.

• Scoliosis, concave towards the injured side, due to associated muscle

spasm.

• Localised small-bowel/colonic ileus.

• US:

• May show devascularisation, renal swelling from a diffuse haematoma,

peri- or pararenal haematoma, renal laceration or ureteric obstruction

from a ureteric clot.

• CECT:

• Renal contusion - focal areas of decreased contrast enhancement or

striated nephrogram.

• Renal laceration - irregular linear hypodense parenchymal areas.

• Renal fracture - laceration connecting two cortical surfaces.

• Shattered kidney - multiple separated renal fragments.

• Subcapsular haematoma - crescentic superficial hypodense area.

• Wedge infarction - wedge-shaped perfusion defect.

• Renal vein thrombosis - persistent delayed nephrogram.

• Delayed scans are also often performed to check for a ureteric leak.

Blunt trauma to pancreas

• Usually caused by compression against the vertebral column; often

associated with seat belt compression injuries.

• Usually associated with upper abdominal visceral injury.

• Graded from minor contusion and capsular haematoma (grade I) to

severe devascularising crush injury (grade IV).

• Usually damage occurs at most vulnerable segment of pancreas: the

junction of the body and tail.

Radiological features

• CECT:

• Laceration - area of intrapancreatic low attenuation, often difficult to see.

• Direct evidence of haemorrhage - fluid around superior mesenteric

artery and pancreas.

• Indirect evidence - thickening of anterior pararenal fascia.

• Often requires delayed scans to exclude/monitor complications of

pancreatitis and devascularised pancreas.

Complications

• Post-traumatic pancreatitis, with:

• peripancreatic fat stranding

• diffuse or focal pancreatic enlargement

• irregular pancreatic contour.

• Splenic vessel fistula or arterial pseudoaneurysm.

• Pancreatic abscess.

• Pancreatic pseudocyst.

Blunt Trauma to the gastrointestinal tract

• The proximal jejunum is most commonly affected, followed by the

duodenum and ascending colon at the ileocaecal valve region. The

descending colon is only rarely involved.

Radiological features

• CECT:

• Appearances range from mesenteric or intramural haematoma to

frank colonic laceration and perforation.

Less-common abdominal trauma injuries

• Gallbladder.

• Ureter.

• Stomach.

• Adrenals.

Trauma to the bladder

Aetiology and frequency

The probability of bladder injury varies according to the degree of bladder

distension; a full bladder is more likely to be injured than an empty one.

• Approximately 10-25% of patients with a pelvic fracture also have

urethral trauma. Conversely, 10-29% of patients with posterior urethral

disruption have an associated bladder rupture.

• External trauma: 80%.

• Blunt injury: 60-85%:

- road traffic accident (RTA), 85%.

- fall, 10%.

- assault, 5%.

• Penetrating trauma: 15-40%:

- gunshot wound, 85%.

- stabbing, 15%.

• Iatrogenic: 15%.

• Includes gynaecological (post-hysterectomy), urological (after trans-

urethral resection of prostate (TURP) or bladder tumour (TURBT))

and orthopaedic (post-fixation of pelvic fractures) procedures.

• Intoxication: 4%.

• Spontaneous: <1%.

Classification of bladder rupture

• Extraperitoneal rupture: 50-75%.

• Intraperitoneal rupture: 25-45%.

• Incidence higher in children because of the predominantly intra-

abdominal location of the bladder prior to puberty.

• The bladder descends into the pelvis usually by the age of 20 years.

• Combined extraperitoneal and intraperitoneal rupture: 5-10%.

Extraperitoneal bladder rupture

• Traumatic extraperitoneal ruptures are usually associated with pelvic

fractures in up to

90% of patients. Conversely, approximately

10% of patients with pelvic fractures also have significant bladder

injuries.

• Results from the shearing force of the deforming bony pelvic ring,

which causes a ‘burst’ injury.

• Bony fragments may also cause direct laceration of the bladder and

the degree of bladder injury is directly related to the severity of the

fracture.

Intraperitoneal bladder rupture

• Occurs as the result of a direct blow to a distended urinary bladder. The

resulting increased intravesical pressure causes a horizontal tear along the

intraperitoneal portion of the bladder wall. This type of injury is

common amongst alcoholic patients or those sustaining blunt trauma

following a RTA.

Clinical characteristics

• Clinical signs of bladder injury are relatively non-specific; however, a

triad of symptoms is often present:

• gross haematuria

• suprapubic pain or tenderness

• difficulty or inability to void.

• Abdominal examination may reveal distension, guarding or rebound

tenderness.

• Absent bowel sounds and signs of peritoneal irritation indicate a possible

intraperitoneal bladder rupture.

• If blood is present at the urethral meatus, suspect a urethral injury.

Radiological features

• CT:

• Often the first test performed in patients with blunt abdominal trauma.

• Provides information on the status of the pelvic organs and bony

pelvis.

• CT cystography:

- The most sensitive test for evaluating a bladder perforation.

- Contrast is instilled into the bladder via a urethral catheter (or supra-

pubic catheter if contraindicated) followed by an abdominopelvic CT

scan.

- Intraperitoneal and extraperitoneal nature of a rupture can be

accurately assessed.

• Cystogram:

• Standard imaging for a suspected bladder injury.

- Consists of an initial plain radiograph of the kidney-ureter-bladder

(KUB).

- Followed by AP and oblique views of the contrast-filled bladder.

- Further AP film obtained after drainage.

Extraperitoneal bladder perforation following a transurethral resection of

a bladder tumour. This CT cystogram clearly demonstrates contrast

extravasation into the perivesical soft tissues (arrows). Note the presence of

several bladder diverticula and a Foley balloon catheter within the bladder (B).

• Extraperitoneal rupture:

- Contrast extravasation around the base of the bladder is confined to

the perivesical space. The bladder may assume a tear-drop shape from

compression by a pelvic hematoma.

- With more complex injuries contrast may extend into the thigh,

penis, perineum or anterior abdominal wall.

• Intraperitoneal rupture:

- Contrast extravasation into the peritoneal cavity, often outlining

loops of bowel and the paracolic gutters.

• Combination of intra- and extraperitoneal rupture:

- Contrast outlines the abdominal viscera and perivesical space.

Abscesses within the abdomen

Peritoneal abcesses

Clinical characteristics

• Accumulation of collections of pus in the peritoneal spaces.

• Subphrenic abcesses are usually secondary to surgery.

• Paracolic abcesses are usually local to their cause, such as diverticulitis,

appendicitis or anastomotic failure.

• They present with raised inflammatory markers, swinging pyrexia, pain

and malaise.

Radiological features

• AXR: abscesses are often of soft tissue density and, therefore, difficult to

see. The presence of gas makes the identification easier. The finding

of gas pockets outside the bowel lumen, particularly if its appearance

does not change over time, is highly suggestive. A subphrenic gas-fluid

level on an erect chest X-ray (CXR) or erect AXR is suggestive of a

collection in this region.

• USS: an effective test for abdominal collections, being sensitive for fluid

collections or gas-fluid collections. It can also be used for guided

percutaneous drainage. Occasionally deep collections may be obscured

by overlying bowel gas.

• CECT: very sensitive for collections and may identify those obscured on

US. CT guidance can be utilised for percutaneous drainage.

• NM: using¹¹¹indium labelled white cell scans are very sensitive for

detecting peritoneal abscesses but are infrequently used as the use of CT

increases.

Perirenal and renal abscesses

Clinical characteristics

• A complication of renal infection (see Pyelonephritis).

•

80% of cases result from ascending infection; may be related to obstruction.

• Haematogenous spread causes 20%.

• Urine culture may be negative.

• A renal abscess that extends through the renal capsule becomes a

perinephric abscess.

Radiological features

• AXR: provides clues as to the presence of a perinephric abscess. These

include loss of psoas shadow, focal mass seen in the renal outline,

displacement of the renal outline and gas in the renal bed. Calculi

may also be seen.

• USS: a hypo- or anechoic irregular mass, ± gas bubbles, ± perinephric

extension, may be demonstrated. Guided drainage can be performed.

• Intravenous urogram (IVU): a renal abscess may distort the pelvic-

alyceal system, but any mass lesion, such as a simple cyst, can have this

effect and hence an IVU is poorly specific.

• CT: may demonstrate a mass lesion with a low-density centre, and an

enhancing wall. Perinephric spread will be demonstrated and causal

factors, such as calculi, identified. Guided drainage can be performed.

• NM: inflammatory change in the renal bed may be demonstrated with a

radiolabelled white cell scan.

Hepatic abscesses

Clinical characteristics

• Most commonly secondary to biliary sepsis.

• Other causes include sepsis arriving via the portal venous system (i.e.

portal pyaemia, e.g. appendicitis), direct spread, indwelling arterial lines

and direct contamination associated with trauma.

• Pyogenic organisms (88%), amoebic (10%), fungal (2%).

• Presentation may include pyrexia, vomiting, abdominal pain, jaundice

and positive blood cultures.

Achalasia

Clinical characteristics

• This is a motility disorder that results in failure of relaxation of the lower

oesophageal sphincter.

• The sphincter will only relax when the hydrostatic pressure of the

column of food, or liquid, in the oesophagus exceeds that in the

stomach, more usually in the erect position.

• May be of primary or secondary aetiology; most commonly primary.

Secondary achalasia occurs rarely in diseases such as malignancy, dia-

betes mellitus and Chagas’ disease.

• Peak age of incidence is 20-40 years, but it has been diagnosed in children.

• Most common presentation is dysphagia. Patients may also complain of

retrosternal chest pain from oesophageal distension and effortless regur-

gitation of undigested food.

• Complications include aspiration pneumonia and an increased inci-

dence of oesophageal cancer.

Radiological features

•

Plain X ray:

• An air-fluid level may be seen within the dilated oesphagus on the

chest radiograph.

• A small or absent gastric bubble may be present on the abdominal

radiograph, but this is non-specific and generally an AXR is not

helpful.

•

Barium studies:

• The barium swallow is the radiological investigation of choice.

• Findings include:

- Failure of oesophageal peristalsis to clear the oesphagus of barium.

- Failure of relaxation of the lower oesophageal sphincter.

- Poorly coordinated peristaltic activity.

- Oesophageal dilatation is a late feature.

- Narrowing of the oesophagus at the lower sphincter resulting in

characteristic ‘bird’s beak’ tapering.

• The barium study may be normal, particularly in the early stages of

the disease.

• Radiological findings should be confirmed by endoscopy and mano-

metry and, if necessary, biopsies to exclude a secondary cause such as

malignancy, or to exclude malignancy as a complication of long-

standing achalasia.

Adnexal masses

Clinical characteristics

•

In anatomical terms the adnexa are considered to include the uterine

(fallopian) tubes and ovaries. Each ovary lies posterolaterally on either

side of the uterus, attached to the broad ligaments by its own mesentery,

the mesovarium, and to the uterus by the ovarian ligament. The fallopian

tubes lie in the superior aspect of the broad ligament. Each tube is

approximately 10cm long and from the uterus runs posteriorly, laterally

and then inferiorly.

•

The presentation of ovarian disease includes pain, menstrual irregular-

ities, infertility, dyspareunia or abdominal distension, or it may be an

incidental finding.

•

Ovarian pathology can be divided into the following categories:

• Benign physiological cysts:

- follicular cysts

- corpus luteal cysts.

• Benign mixed solid/cystic lesions

- mucinous cystadenoma

- serous cystadenoma

- teratoma/dermoid

- endometriosis.

• Benign solid tumours

- granulosa cell tumour

- fibroma

- Brenner tumour.

•

Malignancy: primary/secondary.

•

Pathology of the uterine tubes can be caused by pelvic inflammatory

disease (PID), ectopic pregnancy or rarely carcinoma.

•

Acute PID will present with pain and fever and possibly a palpable mass

in the adnexa.

•

The chronic form is often asymptomatic and may only be diagnosed

during investigation for infertility or pelvic pain.

•

Non-gynaecological causes of adnexal masses include an appendix mass

or diverticular disease.

•

Imaging features of ovarian neoplasias are rarely definitively diagnostic.

Radiological features

•

AXR: plain films do not have a role in the diagnosis of adnexal

pathology. Any abnormality on an AXR is likely to be an incidental

finding (e.g. calcification within an ovarian dermoid cyst).

•

Contrast studies:

• The hysterosalpingogram is used to demonstrate the uterine tubes

using x-ray screening following the instillation of iodinated contrast

into the uterine cavity via the cervical os.

• It forms part of the investigation of infertility to assess tubal patency.

• The ovaries will not be visible on x-ray screening.

•

USS:

•

Trans-abdominal (TA) and transvaginal (TV) US is the modality of

choice for initial gynaecological imaging.

•

Because of the anatomy of the adnexa, the positions of the ovaries can

be very variable and dependent on the degree of distension of the

urinary bladder. Pregnancy also affects laxity of the ligaments.

•

The TA US is usually done with a full bladder and TV US with an

empty bladder.

•

For both TA and TV US, a good anatomical landmark for the ovaries

is the internal iliac artery.

•

Ovarian cysts are very common and are usually considered normal

unless >20-25mm in diameter (cut off varies between institutions) or

the patient is prepubertal, pregnant or postmenopausal.

•

Cysts

> 20-25mm in women of reproductive age are usually

rescanned at a different stage of the menstrual cycle, for example

2 weeks later, to document their physiological nature.

•

Malignant ovarian masses are usually more complex than benign

lesions and US is used to assess ovarian morphology.

•

Indicators of malignancy include larger size, thick cyst wall, internal

septations, solid components and mixed echogenicity cyst fluid.

Blood flow assessment and pulsed Doppler are also of use.

•

The normal non-dilated fallopian tube is not visible ultrasonically but

can be seen following the instillation of an US micro-bubble contrast

medium via the cervical os. This technique, known as hysterosalpingo-

contrast sonography (HyCoSy), is used as an alternative to the hystero-

salpingogram to assess tubal patency.

•

The abnormal dilated tube (a hydrosalpinx), in chronic PID for

example, appears as a serpiginous structure in the pelvis.

•

An important adnexal mass is that of ectopic pregnancy, of which

97% are tubal. The US findings in ectopic pregnancy are absence of

a uterine pregnancy, an adnexal mass and free intraperitoneal fluid.

•

CT:

• CT is of some use in diagnosing adnexal masses but US and MRI

provide more internal detail, owing to better soft tissue differentia-

tion, without the radiation dose.

• CT is sensitive for fat or calcification within a mass, for example in a

dermoid tumour.

•

MRI:

• Can provide excellent resolution of the pelvis and is very useful in the

assessment of gynaecological pathologies.

• Used with fat suppression, it is sensitive for the fat seen in dermoid

tumours.

• Sensitivity for different blood breakdown products means MRI is

sensitive for endometrial deposits where fluid-fluid levels, caused by

haemorrhage of different ages, are seen within endometriotic cysts.

•

MRI features that suggest malignancy in an ovarian cyst:

• size >4cm.

• soft tissue, non-fatty mural nodules.

• large soft tissue component.

• mural or septal thickness of >3mm.

• mural or septal irregularity.

• metastatic deposits or direct spread.

• presence of ascites and peritoneal nodules.

Adrenal masses

Clinical characteristics

• The adrenal glands have a ‘Y’ configuration with an anteromedial body

and two posterior limbs.

• The right adrenal gland lies between the right crus of the diaphragm and

IVC at the level of the upper pole of the kidney. The left adrenal

extends from the upper pole of the left kidney almost to the hilum. It

lies in front of the left crus of the diaphragm.

• Usually the limbs are 3-6mm thick and the width of the entire gland is

<1cm.

• The adrenal cortex produces glucocorticoids (cortisol), mineralocorti-

coids (aldosterone) and androgens. The adrenal medulla produces adre-

naline and noradrenaline.

Causes of adrenal masses

•

Functional:

• adenoma causing Conn’s or Cushing’s syndrome.

• phaeochromocytoma.

• adrenal carcinoma.

•

Malignant:

• metastases.

• carcinoma.

• lymphoma.

• neuroblastoma.

•

Benign:

• non-functioning adenoma.

• angiomyolipoma.

• cyst.

• haemorrhage.

•

The most common neoplasms are adenomata and metastastic disease.

A common indication for adrenal imaging is to differentiate between

these.

•

The presentation of adrenal masses depends upon whether the mass is

functional or not.

•

Non-functioning tumours such as adenoma are usually an incidental

finding when the patient is imaged for another reason.

(A)

(B)

Adrenal adenoma. ‘In-phase’ (A) and ‘out-of-phase’ (B) MRI confirms

loss of signal in a lipid-rich left adrenal adenoma (arrows) on the

out-of-phase image compared with the corresponding in-phase imaging.

Adrenal adenoma. Low-density non-functioning right adrenal adenoma

(arrow).

• With a functional adenoma, the presentation varies with the type of

hormone being produced in excess.

• Conn’s syndrome is caused by excess aldosterone and results in hyper-

tension, hypokalaemia and alkalosis.

• Cushing’s syndrome is caused by excess glucocorticoid and results in

myopathy, osteoporosis, water retention, obesity of the trunk, head

and neck, hypertension, predisposition to infection, easy bruising, and

hyperglycaemia.

• Phaeochromocytoma is a neuroendocrine tumour that secretes cat-

echolamines, resulting in hypertension, cardiomyopathy, weight loss

and hyperglycaemia. The ‘rule of 10s’ applies to phaeochromocy-

toma: 10% are adrenal, 10% are bilateral, 10% are malignant.

Radiological features

Adrenal adenomas versus metastatic deposits

•

USS:

• Although the adult adrenal glands may be visualised on US, it is

usually the surrounding fat that is visible.

• The adrenals appear hypoechoic relative to the fat but may only be

seen when abnormally enlarged.

• By contrast the neonatal adrenal is readily seen because of its larger

size relative to the other intra-abdominal organs, smaller patient size

and less retroperitoneal fat.

• Adrenal masses usually appear hypoechoic, but haemorrhage or

necrosis results in a heterogeneous appearance.

• It is important to differentiate adrenal masses from masses arising from

the adjacent liver, spleen, kidneys and pancreas.

•

CT:

• CT is a well-established modality for investigating adrenal masses

and uses the fact that the majority of adenomata have high lipid

content.

• A non-contrast CT is performed and the CT number (Hounsfield

units (HU)) of the mass measured. If the HU is ≤10 it is considered to

be a benign adenoma on the basis of its fat content.

• If the HU is >10, an enhanced 80-s and a 15-min delayed postcontrast

CT are obtained, and the enhancement washout calculated. The

washout is a measure of the percentage decrease between the

enhanced and delayed images.

• A large decrease is a high percentage washout and a small decrease is a

low percentage washout.

• If the enhancement washout is > 50%, the diagnosis of a benign lipid-

poor adenoma is made.

• If the washout is <50%, the mass is considered indeterminate, and a

biopsy may be necessary to make a diagnosis, particularly in a patient

with a new extra-adrenal primary neoplasm.

• Metastatic deposits are usually larger and more heterogeneous than

adenomata and do not have intracellular fat. Even in patients with

known malignant primaries, half of all adrenal masses will be benign.

• MRI:

• MRI also makes use of the lipid content of adenomata.

• In-phase and out-of-phase (also known as chemical shift) imaging

demonstrates a loss of signal in a lipid-rich adenoma, on the out-of-

phase image compared with the corresponding in-phase imaging.

• A metastatic deposit does not demonstrate this loss of signal.

• Chemical shift imaging only provides the same information about an

adrenal mass as CT by identifying the lipid-rich subset of adenomata.

Intervention

• Adrenal venous sampling can be performed to identify whether the

abnormal hormone production is unilateral or bilateral: most com-

monly in primary hyperaldosteronism (Conn’s syndrome).

Phaeochromocytoma

Radiological features

• US:

• Phaeochromocytoma may be visible as a well-defined mass, which

may be solid or cystic to variable degrees.

• Echogenicity will be variable.

• CT:

• Phaeochromocytomas are usually large with a homogeneous density,

although larger masses may appear heterogeneous owing to haemor-

rhage or necrosis.

• Show strong contrast enhancement.

• Some authors believe that IV contrast administration may precipitate

a hypertensive crisis and recommend alpha and beta blockade prior to

IV contrast.

• MRI:

• Phaeochromocytoma have very high signal intensity on T₂-weighted

(T2W) images, higher than adenoma or metastasis, and usually iso- or

hypointense on T₁-weighted (T1W) imaging.

• Strong enhancement which may be heterogeneous depending on the

degree of cystic change.

• NM:

• NM has a role in the diagnosis of phaeochromocytoma.¹³¹I-MIBG

and¹²³I-MIBG are concentrated in the sympathomedullary system

and focal uptake is seen in phaeochromocytoma. Whole-body imag-

ing will demonstrate extra-adrenal tumours.

Adrenocortical carcinoma

• A rare carcinoma of the 4th to 7th decade.

• May present with Cushing’s syndrome if hyperfunctioning.

• Other presentations include pain and a mass.

• Usually >5cm in diameter at presentation.

• One-third show calcification.

• Can invade adjacent structures including the IVC.

• May metastasise to nodes, bones and lungs.

Radiological features

• USS:

• Tumour necrosis and haemorrhage result in heterogeneous

echogenicity.

• CT:

• Central area is of low density owing to necrosis.

• May be calcification and areas of haemorrhage.

• Irregular peripheral enhancement following contrast.

• MRI:

• The mix of haemorrhage and necrosis results in heterogeneous signal on

both T1W and T2W imaging.

• Irregular peripheral enhancement.

Myelolipoma

• A benign tumour composed of haematopoietic tissue and fat. Unlike

adenomas, the fat is discrete fat rather than intracellular.

• Can present with painful haemorrhage.

Radiological Features

• AXR: not generally helpful but may demonstrate a discrete, lucent,

fatty mass or calcification caused by previous haemorrhage.

• USS: heterogeneous mass is a mix of fat and haematopoietic tissue.

• CT: discrete fat interspersed with fine bands of soft tissue.

• MRI: discrete fat is demonstrated by high signal in T1W that is sup-

pressed on fat-suppressed sequences.

Adrenal haemorrhage

• May be caused by trauma, physiological stress (such as sepsis), a bleeding

diathesis or haemorrhage into an underlying neoplasia.

Radiological features

• USS:

• Especially sensitive in neonates.

• Initially a solid mass that becomes heterogeneous through liquefac-

tion. No signal on Doppler interrogation.

• Chronically may have cystic appearance with echogenic calcific foci.

• CT:

• Oval mass with peri-adrenal fat stranding.

• Chronically, cystic change and calcification can occur.

• MRI: signal will depend on the age of haematoma and the associated

blood breakdown products.

Aortic aneurysm

Clinical characteristics

• Afocalwideningoftheabdominalaortaof>3cm,involvingalllayersof

the vessel wall.

• Usual caused by atherosclerosis but may be secondary to trauma, infec-

tion, vasculitis or connective tissue disorders.

• Often asymptomatic.

• May present with a pulsitile mass, vessel rupture or an embolic event.

• Rupture classically presents with hypovolaemic shock, a pulsatile mass

and back pain.

Radiological features

•

AXR:

• Calcification of the aortic wall is a common finding in atherosclerosis.

• Loss of parallelism of the aortic wall suggests aneurysmal dilatation.

• Rarely vertebral body erosions may be seen with long-standing

aneurysms.

• In the acute scenario, loss of the psoas outline is associated with

retroperitoneal rupture.

•

USS:

• Is useful in both diagnosis and monitoring the size of abdominal aortic

aneurysms (AAA).

• In the acute abdomen, US can confirm the presence of an AAA, and

the presence of free abdominal fluid suggests rupture.

• However as CT is more sensitive and specific, US is most useful in the

case of a patient too unstable to be transferred to CT.

•

CECT:

• CT is used as part of elective surgical planning in determining the

anatomy of the AAA, particularly in relation to visceral vessels such as

the renal arteries.

• Retroperitoneal fibrosis associated with an AAA may be seen as a

surrounding soft tissue mass.

• In the acute setting, CT is the investigation of choice, often demon-

strating the precise site of rupture and is very sensitive to intraperi-

toneal and retroperitoneal haemorrhage.

• Rarer complications such as aorto-caval or aorto-enteric fistulae, and

occlusion, can be detected.

Appendicitis

Clinical characteristics

• A common cause of an acute abdomen with a peak incidence in the

2nd and 3rd decades.

• The aetiology is probably related to luminal obstruction, often by

lymphoid hyperplasia or a faecolith.

• Typically presents with RIF pain, nausea, vomiting, fever and evidence

of inflammation such as raised WBC and CRP.

• However, one-third may have an atypical presentation.

• Complications include localised perforation, abscess formation and gen-

eralised peritonitis. Rarely an obstructed appendix becomes distended by

abnormal accumulation of mucus, forming an appendix mucocoele.

Radiological features

• AXR:

• Is neither sensitive nor specific but can provide clues.

• The presence of a calcified appendicolith in the RLQ, combined with

abdominal pain, has a high positive predictive value for acute

appendicitis.

• Other signs are less specific and include caecal wall thickening, small-

bowel ileus and decreased small-bowel gas in the RIF.

• Free peritoneal fluid can lead to loss of the psoas outline, loss of the fat

planes around the bladder and loss of definition of the inferior liver

outline.

Ascites

Clinical characteristics

Intra-abdominal free fluid that may be classified as:

• Exudate: >30g/dl of protein; causes include peritoneal TB, pancreati-

tis, Meig’s syndrome and carcinomatosis.

• Transudate: <30g/dl of protein; causes include hypoalbuminaemia,

congestive cardiac failure, chronic renal failure, Budd-Chiari syndrome

and cirrhosis.

Radiological features

• AXR:

• Initial signs relate to the dependent accumulation of free fluid in the

pelvis and may be subtle and overlooked.

• Later signs are medial displacement of both the lateral border of the

liver and ascending and descending colon, bulging flanks, centralised

bowel loops and a generalised ‘greying’ of the abdominal film.

• USS:

• This is the investigation of choice to confirm the presence of ascites,

without the use of ionising radiation.

• US may provide additional information about the ascites such as

loculation or the presence of debris within the fluid.

• In addition, US allows the siting of diagnostic taps or therapeutic

drains.

• Evidence as to the aetiology of the ascites can also be gained, such as

the presence of cirrhosis.

Biliary gas

Clinical characteristics

• Gas within the biliary tree is often an incidental finding secondary to

medical intervention, such as a sphincterotomy or cholecystoenterostomy.

• Other causes include:

• a lax sphincter of Oddi in the elderly.

• passage of a gallstone.

• biliary fistulae caused by stones, neoplasia or duodenal ulceration.

• Biliary gas may result in gas within the gallbladder.

• Gas within the gallbladder may be secondary to emphysematous chol-

ecystitis. This is an infection with gas-forming organisms, seen in

diabetics and leading to mural and intraluminal gallbladder gas.

Radiological features

• AXR: branching radiolucencies are seen within the liver. These radio-

lucencies do not extend to the liver edge: a feature that helps to differ-

entiate biliary gas from gas in the portal vein. Gas in the gallbladder may

result in a gas-fluid level on an erect film.

• USS: linear echogenic shadows, paralleling the portal venous system,

are the characteristic appearance of biliary gas. Biliary calculi may be

identified.

• CT: branching air densities that parallel the portal system will be seen.

Calculi, fistulae or neoplastic masses may be identified.

Biliary obstruction

Clinical characteristics

• Characterised by jaundice with a raised alkaline phosphatase and

.-glutamyl transferase.

• May be an acute or chronic presentation and may or may not be

accompanied by pain.

• In 75% of adult biliary obstruction, the cause is benign, including

calculi, strictures from previous trauma or surgery, pancreatitis and

sclerosing cholangitis.

• Malignant causes include pancreatic head carcinoma, ampullary and

duodenal malignancy, cholangiocarcinoma and metastases.

• The triad of a palpable, distended gallbladder, obstructive jaun-

dice and the absence of pain are highly suggestive of a malignant

cause.

• An obstructed, infected biliary tree is a medical emergency and occurs

more frequently with calculus than malignant obstruction (2:1).

Radiological features

• USS:

• Is the imaging modality of choice in establishing the mechanical cause

of biliary obstruction. The bile duct is usually easily visualised at the

hepatic hilum. Most normal ducts measure <5mm in diameter;

however, studies have shown that up to 4% of normal cases have a

duct that measures >7mm. Therefore a diameter of 6-8mm can be

non-specific and may require further investigation. Intrahepatic bili-

ary dilatation can be seen as dilated biliary radicals seen running along

the portal vessels.

• Will often establish the cause and level of biliary obstruction, with

visualisation of intraductal calculi or obstructing masses. Patient

factors (such as body mass index) or overlying bowel gas may obscure

the more distal biliary tree.

• CT: is sensitive for biliary tree dilatation and, although less sensitive for

calculi than US, has the advantage of visualising the distal biliary tree

when it is obscured on US. It can also detect, and often accurately stage,

obstructing tumours.

• Magnetic resonance cholangiopancreatography (MRCP): use of

very heavily T2W imaging sequences to outline the fluid-filled bile

ducts can demonstrate the level of biliary obstruction very well. Stones

are demonstrated as filling defects. The addition of conventional axial

T1W and T2W images can give further information regarding extrinsic

causes of obstruction such as tumours.

• Endoscopic retrograde cholangiopancreatography (ERCP): a

combined endoscopic/fluoroscopic procedure outlines the biliary tree

with similar effect to an MRCP, but it has the advantage of allowing

therapeutic procedures such as sphincterotomy with stone removal and

biliary stent placement.

• Percutaneous trans-hepatic cholangiography (PTC): the rise of

less-invasive techniques means that PTC is now performed less as a

diagnostic procedure. It is useful in patients who have had a failed

ERCP and in those who cannot have an MRCP. The use of PTC

has been extended to allow percutaneous trans-hepatic placement of

drainage catheters or stents, especially when this is not possible during

ERCP or in cases of an obstructed, infected system.

Bladder calculi

Clinical characteristics

• Bladder calculi may form around a foreign body such as prostatic

chippings, pubic hair, fragments of bone from penetrating injuries,

and pieces of Foley catheters.

• May migrate from the proximal urinary tract.

• May be caused by stasis such as outflow obstruction, neuropathic

bladders and vesicular diverticulae.

• Infection, especially with Proteus sp., can result in bladder calculi

formation.

Radiological features

• AXR: Seen as a calcified body projected over the bladder area. In

women, calcified fibroids may cause confusion although the latter

may be seen lying above, rather than over, the bladder area.

• USS: Confirms the position and nature of the calcified density.

Bowel obstruction

Although small- and large-bowel obstruction (SBO and LBO) have com-

mon clinical features of colicky abdominal pain, vomiting, absolute con-

stipation and abdominal distension, their aetiology and management are

quite different and, therefore, will be considered separately. Predominance

of certain signs depends on the level of the obstruction.

Small-bowel obstruction

Clinical characteristics

• SBO presents with colicky abdominal pain and vomiting, which occurs

earlier in more proximal obstruction and later in distal obstruction.

• The bowel distal to the obstruction empties by absorption or evacuation

of its contents, whereas the bowel proximal to the obstruction distends

with gas and fluid.

• This eventually results in fluid shifts into the bowel, causing hypovo-

laemia and electrolyte imbalances.

• If SBO is not reversed it may progress from a simple to strangulated

obstruction with compromise of bowel wall arterial supply with a risk of

perforation and peritonitis.

• The causes of SBO can be divided into intraluminal, luminal and

extrinsic causes:

• Intraluminal: foreign body, bezoar, parasites, gallstones, food bolus.

• Luminal: atresia, inflammatory stricture (Crohn’s disease, TB), hae-

matoma, tumour.

• Extrinsic: adhesions, congenital bands, malrotation, herniae,

intussusception.

• Adhesions, herniae and tumours cause the majority of SBO, with

postsurgical adhesions being the most common cause.

Radiological features

•

AXR:

•

The jejunum lies mainly in the left hypochondrium and the ileum in

the pelvic midline.

•

In complete SBO, the small-bowel loops will distend in 3 to 5h and

are usually seen in the central abdomen.

•

An intraluminal width of >3cm on the AXR is abnormal.

•

Distended loops containing mainly fluid will appear as soft tissue

density. Occasionally, small pockets of gas trapped within the valvulae

conniventes create a ‘string of beads’ appearance.

•

A less frequent occurrence is gallstone ileus, when an intraluminal

calcified stone is seen, usually in the terminal ileum, with proximal

SBO and gas in the biliary tree owing to a cholecysto-duodenal fistula.

•

A closed-loop obstruction occurs when a loop of bowel is not

decompressed by the caudal passage of gas and fluid. This usually

occurs from adhesions and can result in a U-shaped distended loop of

small bowel that does not move over time. If it contains fluid, it

produces a pseudotumour appearance on the AXR because of its soft

tissue density; if it contains gas, it has a coffee-bean shape.

•

In children with an intussusception, a soft tissue mass may be seen on

the AXR and there may be signs of proximal SBO.

•

Chronic SBO may result in massively dilated bowel loops.

•

Intramural gas, as a result of bowel wall ischaemia, is usually associated

with a poor prognosis.

•

Usually a supine AXR is sufficient for assessment of a patient with

suspected SBO, but if it is normal, and there is a strong clinical

suspicion of obstruction, an erect AXR may help by demonstrating

air-fluid levels in dilated loops of small bowel.

•

A lateral decubitus AXR is indicated to show free gas if an erect CXR

cannot be performed.

•

Small bowel enema (enteroclysis):

• This investigation is more appropriate for chronic SBO than acute

SBO and involves the placement of a nasojejunal tube and subsequent

instillation of a barium suspension.

• It will demonstrate a delay in the passage of barium and calibre change

at the site of obstruction.

•

USS:

• Distended fluid-filled loops of small bowel are clearly visible on US

and their peristaltic activity can be assessed.

• The distal bowel loses its muscular activity at the site of obstruction,

whereas proximally there is an initial increased peristalsis in an attempt

to overcome the obstruction. This distinguishes it from ileus, where

there is a generalised loss of peristalsis.

•

CT:

• When the AXR suggests SBO, CT can confirm the diagnosis,

indicate the level and may reveal a cause.

• IV contrast is given but oral contrast is not usually necessary as the

dilated loops contain fluid and gas, which act as intrinsic contrast.

• A small bowel diameter >2.5cm on CT is abnormal.

• A transition point, where the calibre of the bowel changes from

dilated to collapsed, indicates the level of obstruction.

• Adhesive bands are not visible on CT and the diagnosis is inferred on

the basis of a transition point and the lack of an identifiable cause.

• In closed-loop obstruction, CT will demonstrate a U-shaped loop of

bowel with a slightly twisted mesentery containing vessels.

• CT is also useful in assessing the presence of strangulation. The bowel

wall will appear thickened, with oedema and haemorrhage in the

mesentery. The use of IV contrast helps to assess bowel wall enhance-

ment, and in severe cases intramural gas will be present.

Large bowel obstruction

Clinical characteristics

• Abdominal distension predominates, with colicky abdominal pain, and

absolute constipation a feature of complete obstruction.

• Faeculent vomiting occurs if the ileocaecal valve is incompetent, when

the features of SBO are added to those of LBO.

• The most common causes of LBO are carcinoma of the colon, diver-

ticulitis and volvulus, with carcinoma being the most common.

• The clinical history may suggest the underlying cause: an abrupt onset of

symptoms suggests an acute event such as volvulus, a history of change

in bowel habit and weight loss suggests carcinoma, and a chronic history

of constipation suggests diverticulitis.

• Right-sided colonic lesions can become quite large before obstruction

develops owing to the soft stool consistency, whereas sigmoid and rectal

tumours obstruct earlier because of the narrower colonic calibre and

more solid stool.

Radiological features

• AXR:

• This may be diagnostic. The distended colon lies around the periph-

ery of the abdomen and is distinguished from small bowel by haustral

markings that do not traverse the entire bowel lumen.

• Bowel distal to the obstruction is collapsed and the rectum does not

contain gas.

• If there is a tumour of the caecum and ascending colon, with an

incompetent ileocaecal valve, only the small bowel may be distended.

• The typical appearance of a caecal or sigmoid volvulus may be

apparent (this is covered elsewhere).

• Intramural or free intra-abdominal gas may be seen.

• Water-soluble contrast enema:

• Awater-solublecontrastrather thanbariumisusedbecauseofthe risk

of intraperitoneal contamination when perforation has occurred; the

contrast is instilled rectally.

• It may confirm the diagnosis and indicate the level of obstruction.

• In most instances, contrast enemas have been replaced by abdominal

and pelvic CT studies.

• USS: may demonstrate fluid-filled loops of bowel and thickened bowel

wall, but the findings are often non-specific and generally not helpful.

• CT:

• This has advantages over contrast enema especially in elderly or frail

patients.

• It is usually performed with IV contrast; oral contrast may be helpful

to outline small-bowel loops.

• CT will confirm the obstruction, with a colonic diameter of >6cm

(9cm in the caecum) being considered abnormal.

• The identification of a transition point indicates the level and the

cause may also be apparent.

• As stated above, the most common cause is colonic carcinoma,

followed by diverticulitis and volvulus.

• One of the limitations of CT is the difficulty in differentiating

diverticulitis from colonic cancer in certain patients.

• CT will also assess the presence of complications, such as strangula-

tion, as indicated by congestive changes or haemorrhage in the

mesentery, bowel wall thickening, and intramural gas.

Pseudo-obstruction

Clinical characteristics

• Also known as Ogilvie syndrome, this is a clinical syndrome with the

signs, symptoms and radiographic appearance of LBO but with no

identifiable mechanical cause.

• Recognised causes are:

• recent surgery.

• severe pulmonary or cardiovascular disease.

• severe electrolyte disturbance: hyponatraemia, hypokalaemia, hypo-

magnesaemia, hypo/hypercalcaemia.

• malignancy.

• systemic infection.

• severe constipation.

• medications: opioids, anticholinergic drugs, clonidine, amphetamines,

phenothiazines, steroids.

Radiological features

• AXR:

• This does not differentiate pseudo-obstruction from mechanical

obstruction but will demonstrate distended loops of large bowel.

• Serial films may be useful to document the clinical course and mon-

itor the colonic diameter.

• Water-soluble contrast enema: a water-soluble contrast enema will

not only help to exclude a mechanical obstruction, by demonstrating

free passage of contrast, but may also be therapeutic when Gastrografin

is used, as its hyperosmolality causes a fluid shift into the bowel,

stimulating colonic motility.

• CT: further imaging is not usually necessary unless a mechanical

obstruction has not yet been excluded.

Ileus

Clinical characteristics

• Paralytic ileus usually occurs after intra-abdominal surgery but may also

occur in several other settings:

• Postoperative: most common.

• Inflammatory bowel disease.

• Inflammatory: pancreatitis, appendicitis, cholecystitis, diverticulitis,

peritonitis.

• Metabolic: hypokalaemia, hypocalcaemia, hypomagnesaemia.

• Medication: opioids.

• It occurs due to cessation of peristalsis, resulting in a functional

obstruction.

• It differs from pseudo-obstruction in that both the small and large bowel

are involved.

• The patient presents with abdominal distension and vomiting, usually

postoperatively.

• Colicky pain is not a feature and bowel sounds are absent, in contrast to

the high-pitched sounds of obstruction.

Radiological features

• AXR:

• Loops of both small and large bowel will be dilated with no apparent

transition point.

• Further imaging is only necessary if there is difficulty excluding a

mechanical obstruction.

Calcifications

Numerous structures can calcify within the abdomen and pelvis. Most of

these are of no importance, but raise clinical concern when the AXR is

viewed!

• Costochondral calcification: age-related calcification of the costo-

chondral junctions is a common finding in the lower ribs projecting

over the superior part of the AXR. Typically in men, the calcification is

parallel to the edge of the cartilage, while in women the calcification is

central.

• Fibroid calcification: degenerate uterine fibroids (leiomyomata) may

calcify, resulting in a rounded, lobulated calcific body projected over

the female pelvis.

• Haematoma: some haematomas heal leaving a residual area of calci-

fication. Haematomas that follow an intramuscular injection into the

buttocks often calcify and may project over the pelvis and lower abdo-

men, possibly leading to diagnostic concern. These haematomas are

usually well defined, rounded or oval with rim calcification.

• Mesenteric lymph nodes: postinflammatory nodes may calcify. If

mesenteric nodes are affected this may result in lobulated calcification,

which typically lies medially within the abdomen. This may cause

diagnostic confusion particularly in gallstone ileus. Calcified mesenteric

nodes are not evidence of active lymph node disease.

• Phleboliths: phleboliths are benign venous calcifications that com-

monly occur in the pelvic veins and may simulate distal ureteric stones.

A typical phlebolith is round with a slightly radiolucent centre.

However, they may be projected over the course of the lower ureter

and those with an atypical appearance may be indistinguishable from

ureteric stones. If this is a clinical concern, further imaging, such as an

IVU or non-enhanced CT, may be necessary.

• Transverse processes: clearly calcification is normal in the transverse

processes of the lumbar vertebrae. However, the tips often appear

denser on AXR than the remainder of the transverse processes and

can, on occasion, be misinterpreted as ureteric calculi, as the courses of

the ureters often overlie the lower four transverse processes.

• Vascular calcification: vascular calcification is a common finding,

particularly in the elderly. Typically is seen as parallel lines of calci-

fication running along the course of arterial structures, most commonly

the aorta and iliac arteries. Often in the elderly these vessels have an

ectatic course, but the parallel nature of the calcification remains.

If parallelism is lost, aneurysmal dilatation should be suspected. The

splenic artery is often seen as a calcified serpiginous vessel in the left

upper quadrant.

Chilaiditi’s sign/syndrome

Clinical characteristics

•

Pronounced ‘Ky-la-ditty’.

•

Refers to the usually asymptomatic interposition of bowel between

the liver and right hemidiaphragm; usually is hepatic flexure, less com-

monly small bowel.

•

Seen in up to 0.25% of chest CXRs.

•

Most frequently an incidental finding in males and almost always in

adults.

•

Contributing factors include:

• absence of normal suspensory ligaments of the transverse colon.

• abnormality or absence of the falciform ligament.

• redundant colon, as might be seen in chronic constipation.

• aerophagia (air ‘swallower’).

• paralysis or eventration of the right hemidiaphragm.

• chronic lung disease, cirrhosis and ascites.

•

Chilaiditi’s ‘sign’ refers to the asymptomatic presence of interposed

bowel.

•

Chilaiditi’s ‘syndrome’ may present with:

• abdominal pain.

• constipation.

• vomiting.

• respiratory distress.

• anorexia.

•

It is clinically important because it may simulate a pneumoperitoneum,

resulting in unnecessary surgery.

Radiological features

• CXR: the presence of haustral folds within the ‘air beneath the dia-

phragm’ confirms it is contained within large bowel.

• CT:

• May be required if there is diagnostic dilemma.

• Particularly useful if there is strong clinical suspicion of concomitant

pneumoperitoneum, as this may be more difficult to diagnose.

Cholecystitis

Clinical characteristics

• Inflammation of the gallbladder that presents with RUQ pain.

• May be acute or chronic; the most common aetiology is gallstones in

both.

• In acute cholecystitis, gallstones impact in the neck of gallbladder

or within the cystic duct, with spontaneous disimpaction in 85%.

• Complications include perforation, gallbladder necrosis and gallblad-

der empyema.

• acalculous cholecystitis may be caused by decreased flow in the cystic

artery, occurs more common in seriously ill patients, can be complicated

by perforation and has a 6% mortality rate.

Radiological features

• USS: mainstay of imaging in cholecystitis.

• Primary finding is of a thickened gallbladder wall (>3mm), which

may be poorly defined, with impacted calculi.

• A gallstone is identified as an echogenic body with posterior acoustic

shadowing.

• The presence of inflammatory fluid or exudate surrounding the

gallbladder is often seen.

• Inflammatory debris may be identified as coarse non-dependent

echogenic material that, unlike stones, has no acoustic shadow.

• Positive ultrasound Murphy’s sign in 85% Focal gallbladder tender-

ness upon direct pressure with the US probe.

• CT: should not be necessary in the investigation of cholecystitis but

may be utilised as part of the investigation of non-specific abdominal

pain.

• Again the primary finding is of gallbladder mural thickening.

Associated inflammatory changes may be seen, characterised by

stranding in the adjacent fat. Biliary calculi may be identified.

• CT may be used to assess for complications such as perforation or

necrosis.

• MRI: can be helpful in difficult cases.

• MRCP may demonstrate biliary calculi.

• Standard MRI sequences may demonstrate gallbladder wall thicken-

ing; T2W scans, with fat suppression, can show associated inflamma-

tory changes and pericholecystic fluid.

Cirrhosis

Clinical characteristics

•

Cirrhosis is defined as hepatic fibrosis with the formation of regener-

ative nodules lacking normal hepatic architecture; particularly lack of a

central vein.

•

The aetiology is varied but a common underlying factor is repeated or

chronic inflammation and tissue destruction, with subsequent disorgan-

ised repair and regeneration.

•

There is a huge variety of causative agents. In developed countries, the

most common are viral (hepatitis B) and toxic (chronic alcohol abuse).

In some cases, no cause is found (cryptogenic hepatic cirrhosis).

•

Other less-common causes include;

• infestation with Schistosomes.

• chronic biliary obstruction; inflammatory bowel disease, cystic fibrosis,

primary biliary cirrhosis.

• haemochromatosis.

• vascular insufficiency from hepatic veno-occlusive disease or congestive

heart failure.

• nutritional: intestinal bypass procedures, abetalipoproteinaemia and

steatosis.

• drug-induced: particularly with methotrexate, isoniazid and

methyldopa.

• genetic: Wilson’s disease, type IV glycogen storage disease and

,₁-antitrypsin deficiency.

•

A pseudo-cirrhotic picture is seen in patients with treated hepatic

metastatic disease and should not be confused with real hepatic cirrhosis.

•

Morphologically there are two main types of cirrhosis:

• Chronic sclerosing cirrhosis involves minimal regeneration

of hepatocytes with little nodule formation leading to a small hard

liver.

• Nodular cirrhosis shows significant regeneration, leading to the

formation of multiple small nodules. In the early stages, the liver

may be enlarged.

•

Deranged intrahepatic venous flow results in bypassing of portal venous

flow directly into the systemic vasculature, leading to the development

of submucosal porto-venous varices, most commonly in the distal

oesophagus and rectal mucosa.

•

Patients present with signs and symptoms of chronic liver failure and

complications from portal hypertension.

•

Clinical features include jaundice, low-grade fever, anorexia and weight

loss, and nephrotic syndrome caused by low serum albumin (deficient

production by the liver).

Cirrhosis. Shrunken liver with an irregular margin and coarsened

echotexture. Note the presence of caudate lobe hypertrophy (arrowhead)

and ascites (asterisk).

• Clinical features of portal hypertension include hepatic encephalopathy

(from bypassing of the liver’s detoxifying capability secondary to porto-

systemic shunts) and risk of significant, often life-threatening, haemor-

rhage from oesophageal or rectal varices.

• There is an association with hypogonadism, anaemia, pancreatitis,

coagulopathy and cholelithiasis.

Radiological features

• Radiological features include changes visible within the liver, changes

owing to portal hypertension and changes from chronic hepatic

insufficiency.

• AXR: some of these changes, such as initial hepatic enlargement, ascites

and splenomegaly, may be seen on plain radiography but this is not

sensitive or specific.

• USS:

• US has an overall sensitivity of 80% in the detection of changes from

cirrhosis.

• On US, the liver may be enlarged initially with subsequent shrinkage

noted.

• Because of differential portal supply, the right lobe is often more

affected than the left, with subsequent shrinkage of the right lobe

(including the quadrate lobe), with hypertrophy of the left lobe and

caudate lobe (segment 1).

• Surface nodularity, increased parenchymal echogenicity, a coarse

heterogeneous texture and surface indentations are all seen on USS.

• Coexisting splenomegaly and signs of portal hypertension such as

portal varices and ascites are common.

• On duplex imaging, there is generally increased hepatic arterial

resistance following a meal and so-called ‘portalisation’ of the hepatic

venous waveform.

•

CT:

• On CECT, a shrunken liver with an irregular drawn-in surface is

generally seen. Liver density and enhancement following IV contrast

is variable.

• Fatty infiltration as seen in early cirrhosis may lead to a hypodense

enlarged liver. Generally there is non-uniform enhancement owing

to areas of fatty infiltration and areas of hepatic fibrosis.

• Hypertrophy of the caudate lobe may be seen.

• Liver density may, however, be normal. Splenomegaly and ascites are

easily detected by CECT.

•

MRI: is often used as a problem-solving tool in liver imaging, and

cirrhosis is no exception.

• An irregular area within the liver, as seen on US and CECT, may

represent a regenerating cirrhotic nodule, a dysplastic nodule or a

frankly malignant nodule (cirrhosis is a strong risk factor for the

development of hepatocellular carcinoma, particularly if caused by

viral infection).

• Regenerating nodules are hypointense on T1W and T2W sequences

because of iron deposits within them. Malignant nodules tend to be

variable on T1W and hyperintense on T2W images. They show

marked early contrast enhancement following gadolinium on T1W

sequences.

Colitis

• Colitis is inflammation of the colon.

• Causes include inflammatory bowel disease, ischaemia and infection.

Ulcerative colitis

Clinical characteristics

• Ulcerative colitis (UC) is an idiopathic inflammatory bowel disease that

affects the colon and usually starts in the rectum. It causes circum-

ferential, continuous proximal inflammation of the colon and, unlike

Crohn’s disease, skip lesions are not a feature.

• The diagnosis is usually made using endoscopy and biopsy.

• There may be a backwash terminal ileitis but otherwise GI involvement

is limited to the colon.

• Presents with abdominal pain and bloody diarrhoea. May be accom-

panied by electrolyte imbalances and fevers.

• The usual pattern is of periods of disease activity interspersed with

periods of remission.

• There are extra-colonic manifestations, which include erythema nodo-

sum, iritis, primary sclerosing cholangitis, chronic active hepatitis,

peripheral arthritis and spondylitis.

• Complications include toxic megacolon, with its associated high risk of

perforation and death. More chronic complications include stricture

formation and markedly increased risk of colonic carcinoma.

Radiological features

• AXR: plain films may demonstrate hyperplastic ‘mucosal islands’; dif-

fuse colonic dilatation, with loss of the normal haustral pattern; and

paucity of faecal material owing to inflammation.

• Barium enema (acute phase): may demonstrate narrowing and

incomplete filling owing to spasm. Different types of ulcer may be

seen: undermining (collar stud) ulcers, shallow ulcers or longitudinal

submucosal ulceration, resulting in a double tract of barium. Fine

granularity of the mucosa may be seen owing to a combination of

mucosal oedema and fine ulceration. Oedematous haustra may result

in thumb printing. Pseudopolyps may be caused by oedematous areas of

mucosa separated by areas of denuded mucosa.

• Barium enemas (chronic stage): may demonstrate a featureless,

narrow-calibre lumen - ‘hose pipe’ colon. Malignant transformation

may be seen. Surveillance for malignant change is usually via endos-

copy, thus avoiding radiation in what is often a young population.

• CT: may demonstrate circumferential wall thickening >10mm. A

continuous distribution from the rectum is suggestive of UC.

Differential diagnosis

One of the main differential diagnoses for UC is Crohn’s disease

Differences between UC and Crohn’s disease

Feature

Crohn’s disease

Ulcerative colitis

GI tract

Can affect any segment Colon and reflux terminal ileitis

only

Skip lesions

Present

None; continuous starting at

distal colon

Colonic shortening None

Yes, plus loss of haustra in

chronic cases

Ulcers

Deep, fissuring

Shallow confluent

Fistulae

A feature

None

Pseudodiverticulum Yes

None

Toxic megacolon Rare

Relatively common

Carcinoma

Slight increase in colonic Marked increase in rate of

carcinoma rate

colonic adenocarcinoma

Pseudomembranous colitis

Clinical characteristics

• Colitis induced by a toxin produced by Clostridium difficile.

• Predisposing factors include antibiotic therapy, shock, proximal LBO,

intestinal ischaemia and renal transplantation.

• Results in profuse watery diarrhoea, abdominal pain and tenderness.

• Endoscopy shows pseudomembranes.

• Diagnosed by visualisation of the pseudomembranes and stool assay for

the toxin.

Radiological features

• AXR: may demonstrate an ileus with mild gaseous large and small

bowel distension. Thumb printing may be a feature. The haustra may

appear thickened owing to oedema and the pseudomembranes may

cause an irregular, shaggy mucosal appearance.

• Barium enema: generally not required and is contraindicated in severe

cases. May demonstrate barium within clefts in the pseudomembranes.

The pseudomembranes may cause a nodular or shaggy appearance.

• USS: may demonstrate non-specific colonic wall thickening and the

presence of ascites.

• CT: may demonstrate circumferential colonic wall thickening with

mucosal enhancement.

100

Ischaemic colitis

Clinical characteristics

• Ischaemic colitis is caused by interruption to the colonic blood supply.

• Aetiologies include thrombosis, bowel obstruction and trauma.

• Predisposing factors include age, oral contraceptives, sickle cell disease

and surgical ligation of the inferior mesenteric artery.

• Presents with acute lower abdominal pain and tenderness, usually out of

proportion to the clinical signs. There may be rectal bleeding or

diarrhoea.

• Most commonly affects the left side of the colon, especially at the

splenic flexure where there is a watershed between the territories of

the superior and inferior mesenteric arteries. The rectum is usually

spared.

• May be a transient condition with spontaneous resolution over a few

months. May lead to incomplete healing with smooth stricture forma-

tion. Severe disease can lead to colonic infarction, with a high associated

mortality.

Radiological features

• AXR: plain film is often normal; however, gas within the colon may

outline the characteristic thumb printing of thickened, oedematous

folds seen in this condition.

• Barium enema: single-contrast instant enema may demonstrate

thumb printing and ulceration associated with this condition. A double-

contrast enema shows these findings more reliably but should be used with

caution in an acutely ill patient. A smooth stricture may be demonstrated

on a delayed study.

• CT: contrast-enhanced spiral CT is the usual first-line investigation for

suspected ischaemic colitis. A dual phase scan, performed in the arterial

and portal phases, may demonstrate thrombus in both the mesenteric

arterial or venous systems. The affected colon may appear abnormally

circumferentially thickened and demonstrate poor contrast enhance-

ment. There may be a sharp cut off between normal and abnormal

colon at the boundary of vascular territories. Mural gas may be seen in

more advanced disease and, in severe cases, portal gas may be identified.

The latter is a poor prognostic factor.

• Angiography: a more limited role in the era of multislice spiral CT but

may demonstrate attenuated arterial flow or the presence of a thrombus.

102

Radiation colitis

Clinical characteristics

• A late complication of radiotherapy that may present many years after

therapy. Typically involves doses of >45Gy.

• The radiation causes an occlusive endarteritis.

• Most commonly occurs in the rectum following treatment of gynaeco-

logical malignancy.

• May cause rectal bleeding, tenesmus and diarrhoea.

Radiological features

• Changes are confined to the radiotherapy field.

• Barium enema: may show strictures; these will often be smooth and

symmetrical, but prior ulceration may lead to scarring and distortion of

colonic folds. Fistulae may also occur.

• CT: may demonstrate luminal narrowing and homogeneous colonic

wall thickening. There may be thickening of pararectal fascia by fibrosis.

The surrounding fat may show increased density, again from fibrosis.

104

Radiological features

• AXR: plain films demonstrate colonic distension/colonic ileus. This

may be localised or involve the whole colon. The loss of the normal

haustral pattern and development of mucosal islands suggests mucosal

ischaemia. Mural gas and free peritoneal gas are late complications.

• Serial AXR: may demonstrate increasing dilatation. Associated small-

bowel dilatation indicates poor prognosis for medical treatment.

• CT: demonstrates colonic dilatation, with distorted haustra and mucosal

islands. Late complications such as mural gas and free intraperitoneal air

are readily identifiable.

• Barium enema: contraindicated because of the risk of perforation.

108

Colonic carcinoma

Clinical characteristics

• Most common GI carcinoma. Causes 15% of cancer deaths.

• Predisposing conditions include familial polyposis coli, Gardner’s syn-

drome and inflammatory bowel disease.

• Presentations include weight loss, iron-deficiency anaemia, abdominal

pain, rectal bleeding, perforation, intussusception and colonic

obstruction.

• Common sites for secondary spread include liver, lung, lymph nodes

and adrenals.

Radiological features

• AXR: useful in secondary large-bowel obstruction but otherwise AXR

has a non-specific role in diagnosing colonic carcinoma.

• Barium enema: double-contrast barium enema has, in the past, been

the radiological investigation of choice. May demonstrate the classic

annular ‘apple core’ lesion or a fungating polypoid lesion. Rarely,

longitudinal and circumferential spread (scirrhous carcinoma) is seen,

especially related to chronic UC.

110

• USS: can detect large carcinomas, nodal and hepatic spread, but is

relatively insensitive for primary colonic carcinoma.

• CT pneumocolon: excellent investigation for demonstrating the

abnormal mural thickening of colonic carcinoma. It has the advantage

over barium enemas of being able to demonstrate extra-colonic

involvement, and incidental non-colonic pathology.

• Standard CECT:

• Can demonstrate the larger carcinomas, and oral contrast 24h prior to

the scan increases the sensitivity. Psammomatous calcification may be

seen in mucinous adenocarcinoma.

• Can accurately stage colonic carcinoma, including intrathoracic

spread.

• Complications such as perforation, obstruction and abscess formation

can be assessed.

112

Colonic diverticulitis

Clinical characteristics

• Diverticular disease of the colon occurs when overactive smooth muscle

causes herniation of the mucosal and submucosal layers of the colon

through the muscle layers. Predominantly seen within the sigmoid

colon, although diverticular disease may be present anywhere within

the colon.

• Colonic diverticular disease is very common in Western societies where

the diet is low in roughage. Approximately 50% of those over 60 will be

affected. Up to a quarter may suffer from diverticulitis.

• Diverticulitis occurs when a colonic diverticulum becomes inflamed,

often by a faecolith. This presents with abdominal pain, usually in the

LIF, fever and a raised WBC.

• Complications include perforation, abscess formation and fistula

formation into adjacent structures, such as the uterus or bladder.

• Treatment is often conservative with antibiotic therapy, but surgery or

radiological intervention, such as percutaneous abscess drainage, may be

required.

Radiological features

• AXR: plain films may demonstrate a localised ileus, gas in a fistula or

abscess, or occasionally a pneumoperitoneum.

• Barium enema: demonstrates colonic diverticula very well and may

also demonstrate complications such as fistulae, perforation and abscess-

eses. The lumen of the colon affected by diverticular disease is usually

narrowed owing to muscular hypertrophy.

• USS: detects thickened bowel and fluid collections, but the diverticula

themselves and small gas collections are very difficult to identify. US is

generally less sensitive than CT but can be used for percutaneous

drainage.

116

• CECT: CT is the best imaging modality for visualising diverticulitis.

Diverticular disease is seen as small outpouchings arising from the affected

colon. These are usually gas filled, but high density within them may be

from a previous barium enema or a calcified faecolith. The affected colon

is often thickened by smooth muscle hypertrophy. In diverticulitis, the

pericolic fat becomes ‘stranded’ and indistinct as a result of inflammatory

oedema. Fluid- and gas-filled abscesses may be seen, as may pockets

of free gas. Fistulae may be directly demonstrated or inferred through

the presence of gas within adjacent involved organs such as the bladder

and uterus. CT can be used to guide percutaneous drainage of fluid

collections.

• It is important to remember that a carcinoma can occur within a

segment of colon affected by diverticular disease, and this can lead to

diagnostic confusion. Carcinoma often causes a shorter segment of

bowel thickening with heaped-up margins - the so-called ‘apple core’

lesion seen in barium enemas.

118

Colonic polyps

Adenomatous colonic polyps

Clinical characteristics

• Adenomatous colonic polyps are often asymptomatic but have the

potential to undergo malignant change. Adenomatous polyps of 5-9mm

have a 1% incidence of malignant change while those >2cm have an

incidence of almost 50%. Polyps >10mm need to be excised.

• Symptoms include diarrhoea, abdominal pain, rectal bleeding and

hypokalaemia.

Radiological features

• Endoscopic examination of the colon has the advantage of allowing

biopsy and excision of any polyps, but it is an invasive procedure, and

examination of the whole colon may be incomplete in a percentage of

patients.

• Barium enema:

• Double-contrast barium enemas have been the mainstay in colonic

imaging in the past, having a false-negative rate of 7% for polyps <10mm.

• Colonic polyps have characteristic appearances on barium enema, the

main cause of diagnostic confusion being differentiation from colonic

diverticula.

• The table shows the features of colonic polyps.

120

Features of colonic polyps on barium enemas

Feature

Characteristics

Meniscus sign

Barium forms a meniscus around the base of a polyp. When

viewed en face, the inner border of the meniscus is well

defined and the outer less well defined. In the en face view

of a diverticulum, the outer border is the better defined.

Hat sign

The ‘hat sign’ results from an oblique viewing of a polyp. The

barium meniscus forms the rim of the ‘bowler hat’, and the

barium covered polyp the body of the hat

Target sign

An en face view of a pedunculated polyp will demonstrate a

‘bull’s eye’ appearance, caused by the meniscus around the

base superimposed on the view of the barium-covered head

of the polyp

Increased density

A polyp is an intraluminal soft tissue that is of increased density

sign

compared with the gas-filled lumen in a good-quality

double-contrast enema. When the polyp is coated in

barium, this can be seen as a focus of increased density

Negative filling

Barium pools dependently and if a polyp is sitting in this pool

defect

it may be visible as a negative filling defect

Stalk sign

An oblique view of a pedunculated polyp may show the

outline of the stalk as two parallel barium lines that flare

slightly where the stalk merges with the mucosa. The axis of

the stalk may change as the patient’s orientation does during

the study

• CT pneumocolonography:

• Increasingly is replacing barium enema as the radiological investiga-

tion of choice. With multislice CT scanners, polyps of 5mm can be

detected with high sensitivity.

• There are a number of advantages of CT pneumocolonography over

barium studies. Although the same bowel preparation is used, the

study is quicker and easier for patients. It involves a slightly higher

radiation dose but provides more diagnostic information, such as

staging information about a colonic carcinoma or demonstrating

incidental, but significant, pathology.

122

Crohn’s disease

Clinical characteristics

• An inflammatory condition that can affect any portion of the GI tract.

Skip lesions (normal areas between affected ones) are typical and help to

distinguish colonic Crohn’s disease from UC.

• The terminal ileum is the commonest site affected.

• The inflammation can affect all histological layers of the GI tract.

• Presentation may include weight loss, recurrent diarrhoea, anaemia,

abdominal pain, peri-anal fistulae, abscesses and malabsorption.

• Complications include fistulae and abscess formation, stenosis, SBO,

adenocarcinoma and lymphoma.

• The differential includes UC, enteric TB, Yersiniae infection, lymphoma

and radiation ileitis.

126

Radiological features

• AXR: may demonstrate bowel wall thickening, related to inflammatory

change, as well as complications such as perforation, toxic megacolon and

abscess formation. However these changes are non-specific.

• USS: as Crohn’s disease is a chronic condition that often affects

young patients, repeated high-dose radiation studies, such as barium

follow-through, raises the risks of long-term complications such as

radiation-induced lymphoma. US can be used to assess for the mural

thickening (>8mm) associated with active disease, in patients with

known Crohn’s disease, without exposing them to ionising radiation.

US can also detect abscesses and guides the placement of drains.

128

• Barium studies:

• Early features include shallow aphthoid ulcers, enlargement of

lymphoid nodules and thickening and distortion of the valvulae

conniventes of the small bowel.

• Later features include cobble-stoning of the mucosa, from serpigi-

nous ulcers with intervening oedema, and rigid and straightened

small-bowel loops, caused by spasm and oedema. Small-bowel

loops may also appear separated owing to increased mesenteric fat

and nodes. Post-inflammatory pseudopolyps may be seen. Fistulae

may be demonstrated: entero-colic, entero-cutaneous or to other

viscera. Pseudodiverticula are caused by outpouchings of normal

bowel opposite fibrosed areas.

• In the end stages, stenotic sections are seen with ‘strings’ of barium

running through them. These are most common at the terminal

ileum. Proximal dilated loops may be seen.

130

• CT: thickened bowel wall may show a double-halo configuration; the

halo is the lumen surrounded by low-density oedematous mucosa,

which in turn is surrounded by a higher density thickened and fibrotic

muscularis. The increase in mesenteric fat may also be seen. Oral

contrast outlines fistulae, strictures and abscesses; the latter can be drained

under CT guidance.

• MRI: demonstrates thickened, enhancing bowel loops. T2W fat-

suppressed MRI is especially useful in demonstrating the anatomy of

peri-anal fistulae prior to surgery. MR enteroclysis shows promise as a

radiation-free replacement for the barium follow-through and small-

bowel enema.

132

Dermoid tumour

Clinical characteristics

• Dermoid tumour is also known as a mature cystic teratoma.

• A benign ovarian tumour that contains mature ectodermal tissues, such

as fat, hair and teeth. Forms up to a quarter of ovarian tumours.

• May present as an abdominal mass or acute abdominal pain if torsion

occurs.

• Often an incidental finding on imaging.

• Malignant degeneration occurs in 1-2%.

Radiological features

• AXR: can be diagnostic when a soft-tissue-density mass is seen within

the pelvis containing focal areas of fat density, bone or teeth.

• CT: may show fat-fluid interfaces within the tumour. A soft-tissue

nodule (Rokitansky nodule) may project into the cyst. This is made up

of sebaceous material.

• USS: advantageous compared with CT as it incurs no radiation dose. It

may demonstrate a complex mass with echo-poor cystic areas, echo-

genic areas of fat, a fat-fluid level and highly echogenic areas from teeth

and other calcification.

• MRI: again has the advantage of no ionising radiation. Although not as

sensitive as CT for calcification, MRI is very sensitive for detecting the

diagnostic fat within a dermoid tumour.

134

Ectopic pregnancy

Clinical characteristics

• Ectopic pregnancy is implantation of an embryo outside the uterine

cavity.

• It is associated with a history of a previous ectopic pregnancy, tubal

surgery, pelvic inflammatory disease, endometriosis and use of an IUCD.

• Usually presents by the 7^th week of pregnancy.

• Most (95%) occur in the fallopian tube.

• Other sites are ovarian, intra-abdominal and cervical.

• Symptoms include vaginal bleeding, abdominal pain and an adnexal

mass.

• May present with hypovolaemic shock in a ruptured ectopic pregnancy.

Radiological features

• May be diagnosed by TA or TV US. The latter is more sensitive but also

more invasive.

• USS: only specific finding by TA/TV US is visualisation of a live

ectopic embryo but this is seen in less than 20% of cases. Supportive

findings include no intrauterine pregnancy at 6 weeks of gestation,

pelvic free fluid or hyperechoic clot, hydro- or haematosalpinx or

a thickened endometrium. A pseudogestational sac may be seen -

consisting of endometrial thickening with an anechoic centre composed

of haemorrhage.

• Extensive intra-abdominal and pelvic haemorrhage may be seen in

women with a ruptured ectopic pregnancy. This can be assessed on

both US and CECT.

136

Endometrial carcinoma

•

Endometrial carcinoma is the most prevalent female cancer of the

genital tract and 4th most prevalent cancer in women.

•

Adenocarcinoma make up 90-95%.

•

Tumours of epithelial and mesenchymal origin

(sarcomata) form

5-10%; such as Leiomyosarcoma, malignant mixed müllerian tumours,

adenosarcomas, gestational trophoblastic tumours.

•

Incidence in UK is 4900 per annum, 990 deaths annually.

•

Disease of postmenopausal women; peak age 55-62 years, 75% over the

age of 50 years.

•

Risk factors:

• exposure to unopposed oestrogens, such as extrinsic oestrogen ther-

apy and tamoxifen, is common risk.

• obesity.

• nulliparity.

• ovarian malfunction in polycystic ovaries.

• late menopause.

•

Other associations are:

• diabetes mellitus.

• smoking.

• hypertension.

• association with breast cancer.

•

90% arise within uterine epithelium: 90% of these are well-differentiated

adenocarcinoma (grade I).

•

Endometrial cancer arises in the glandular component of endometrial

epithelium.

•

Grows as a polypoid mass within the endometrial cavity, producing

ulceration and vaginal bleeding.

•

Spread is by:

• direct invasion of the myometrium and extension through to the

serosa.

• direct invasion of parametrium with serosal seeding.

• direct extension down endocervical canal.

•

Uterus has a rich blood and lymphatic supply, a common route of

spread.

•

Lymph node and haematogeneous metastases are common:

• upper uterine body tumours spread to common iliac and para-aortic

nodes.

• mid and lower uterine body tumours spread to parametrial, para-

cervical and obturator nodes.

• metastases via round ligament and vaginal extension produce inguinal

adenopathy.

•

Distant spread is to bone, lungs, liver and brain.

138

Radiological features

•

FIGO classification used to stage uterine cancer:

Stage I: tumour confined to endometrium or myometrium (A-C).

Stage II: invasion of cervix (A-B).

Stage III: invasion of serosa, adnexae (A) or vagina (B) with nodal

metastases (IIIC).

Stage IV: invasion of bladder/bowel (IVA) or distant metastases (IVB).

•

Depth of myometrial invasion is the most important prognostic factor:

incidence of nodal mestastases rises from 3% (stage IB) to 40% (stage IC).

•

TV US, CT and MRI are all capable of assessing myometrial invasion.

•

Early endometrial disease best assessed by direct visualisation and biopsy.

•

Cross-sectional imaging best for more advanced disease.

•

USS (TV/TA):

• TV/US in the preferred modality due to greater sensitivity.

• Increase in endometrial thickness >5mm, usually echogenic, irregu-

lar poorly defined boundary.

• Myometrial invasion demonstrated as disruption of the normally

smooth interface between the endometrium and myometrium.

• Depth of invasion assessed by proportion of myometrium occupied

by echogenic tumour.

• Accuracy is 77-91%.

• Cervical involvement often detected.

• Usually superior to CT, equivalent to MRI for myometrial invasion

assessment.

• Extra-uterine and nodal spread not accurately determined.

• Diagnostic value of Doppler blood flow measurements is

controversial.

•

CECT:

• Demonstrates endometrial tumour as a hypodense mass in the endo-

metrial cavity or myometrium, or fluid-filled uterus caused by

endocervical canal obstruction by the tumour. Not used for local

staging.

• Capable of detecting deep myometrial invasion.

• May show cervical extension but less accurate than TV US or MRI.

• Accuracy of 58-76%.

• Often cannot differentiate from benign uterine masses, so less useful

in early disease.

• Most useful for advanced disease and detection of distant metastases,

pelvic extension and nodal mestastases.

•

MRI:

• Excellent for local staging.

• Widening or heterogeneity of signal within endometrial canal may be

only sign in stage IA carcinoma (confined to endometrium).

• Endometrial tumour has lower signal than endometrium, and higher

signal than myometrium.

140

(A)

(B)

Endometrial carcinoma. Axial (A) and sagittal (B) T1 MRI of the pelvis

after intravenous contrast. Abnormal enhancing soft tissue is seen

expanding the endometrial cavity (asterisk). The body of uterus is markedly

thinned (arrow). B, bladder.

• Disruption or absence of junctional zone implies myometrial inva-

sion; however, junctional zone may not be visible in some post-

menopausal women.

• Myometrial invasion shown as areas of relatively high signal within

the low-signal myometrium.

• Contrast-enhanced T1W images clearly define zonal anatomy and

improve accuracy.

• Endometrial cancer enhances more slowly than endometrium (bright

on T1W) or myometrium (dark on T1W).

• Relationship of tumour to cervix is important prognostically.

• Multiple planes used to assess both longitudinal and radial tumour

spread.

• Cervical epithelium is hyperintense on T2W and late post-gadolinium

T1W images; disrupted in cervical extension.

• MRI is superior to TV US and CT in predicting cervical stromal invasion.

• MRI is inferior to hysteroscopy in detecting mucosal involvement.

• Overall sensitivity of MRI is 82-94% in detecting deep myometrial

invasion.

141

Familial polyposis coli

Clinical characteristics

• An autosomal dominant condition with 80% penetrance that is charac-

terised by a myriad of (~1000) colonic adenomatous polyps.

• The polyps develop at the age of puberty.

• Symptoms include vague abdominal pain, bloody diarrhoea and

protein-losing enteropathy.

• The main complication is malignant transformation. By 20 years fol-

lowing diagnosis, almost 100% will have developed colonic carcinoma.

There is also a lesser increase in the incidence of gastric and small-bowel

malignancy.

• The treatment is total colectomy in the late teens or early twenties.

Radiological features

• Generally now diagnosed in family members by colonoscopy, but

sporadic cases may present at barium enema with a myriad of small

polyps forming a ‘carpet’ throughout the colon. There may be evidence

of carcinoma, often with more than one synchronous tumour.

• CT colonography can reliably detect polyps of 5mm and smaller but

represents a significant radiation dose in patients who are usually in their

teens at the time of investigation.

142

Radiological features

• Imaging of a fistula is aimed at identifying its exact path and any

underlying disease to aid surgical repair.

• AXR:

• Plain radiography generally is not helpful in diagnosing fistulae.

• Fluoroscopy following the instillation of iodinated contrast into a

cutaneous fistula (fistulogram) can be useful to demonstrate the tract.

• Barium: similarly barium in the bowel, either as a small bowel follow-

through or barium enema, or water-soluble contrast in the bladder as a

cystogram, may be used to demonstrate a fistula.

• Nonetheless, it is important to be aware that the fistulous tract may be

very small and, therefore, difficult to see on these studies.

• Despite this, such studies may be of use in delineating the extent of

underlying bowel disease.

146

• US, CT and MRI:

• All these modalities may be of use in imaging fistulae.

• A mass may be seen associated with the fistula, particularly when it is

caused by an inflammatory condition such as diverticular disease or

inflammatory bowel disease.

• The tract may also be visible.

• Air may be seen within the bladder in a colo-vesical fistula.

• Usually CT is the most useful of these cross-sectional modalities.

• Angiography:

• Angiography may be necessary to help to diagnose an aorto-enteric

fistula between the aorta and bowel, most commonly the third or

fourth part of the duodenum.

• This usually occurs in a patient with a preexisting aortic graft who

presents with an upper GI bleed, pain or a pulsatile mass.

• Alternatively, an aorto-enteric fistula may be investigated with CT

pre- and postcontrast.

148

Foreign bodies

Clinical characteristics

• Foreign bodies may appear in abdominal imaging following trauma,

iatrogenic intervention, and patient ingestion or insertion - either

intentionally or accidentally.

• There is a wide range of presentation, ranging from asymptomatic to in

extremis.

• Children tend to swallow coins, marbles, disc batteries and crayons.

• Adults tend to swallow dentures, chicken and fish bones or may obstruct

on a food bolus.

• Bizarre ingestions are more likely with psychiatric patients and a sub-

group of prison inmates.

• Within the oesophagus there are three points of narrowing where a

foreign body is likely to impact: the cricopharyngeus, at the level of the

aortic arch and at the lower oesophageal sphincter.

• Once a foreign body has passed in to the stomach, there is an 80-90%

chance of it passing through the GI tract.

• The main obstacle to passage through the small bowel is the ileocaecal

valve.

• Complications include laceration, perforation, associated peritonitis,

abscess formation and infection. Disc batteries may cause oesophageal

erosion.

150

Radiological features of ingested foreign bodies

• The imaging of an ingested foreign body consists of a CXR to assess

whether the body lies in the oesophagus.

• In children, this should include the neck.

• For fish and chicken bones, a soft tissue lateral radiograph of the neck is

indicated.

• In adults, a lateral CXR may also be needed if the frontal radiograph is

negative.

• If the foreign body has passed into the stomach, the patient can be

reassured.

• Generally, AXR is not justified because of radiation dose. Two excep-

tions are singestion of sharp or poisonous objects, such as open safety

pins or batteries.

152

Radiological features of iatrogenic/inserted

and incidental foreign bodies

• AXR:

• Detects radioopaque foreign bodies, such as metallic materials and

some types of glass.

• Can be useful for checking the position of medical devices, for

example the ‘lost IUCD’, as well as screening postoperative patients

when a surgical item is unaccounted for.

• If an unexpected foreign body is found, always consider that it may be

within the patient’s clothes.

• Remember not all foreign bodies are radioopaque, for example

wood.

• USS: initial investigation for checking whether an IUCD is within the

endometrial cavity, thereby avoiding the radiation dose of an AXR.

• CT: useful for assessing secondary complications of foreign bodies.

154

Free intra-abdominal gas

Pneumoperitoneum

Clinical characteristics

• The aetiology of pneumoperitoneum includes perforation of a hollow

viscus, through trauma, iatrogenic intervention or from inherent bowel

disease, such as a perforated ulcer. Other causes include gas entering via

the peritoneal surface, such as trans-abdominal biopsy or catheter place-

ment, and via the female genital tract.

• Gas-forming peritonitis or the rupture of a gas-filled intraperitoneal

abscess can also lead to a pneumoperitoneum.

• Postoperative gas takes a variable amount of time to disappear but if it

remains for more than 3 days consider ongoing gas leakage.

Radiological features

• Erect CXR:

• Small amounts of free gas are generally seen first in the RUQ as a

single area of radiolucency lying between the right hemidiaphragm

and the liver.

• Volumes as small as 2ml may be identified.

• Gas may also be seen under the left hemidiaphragm.

• Be aware that the patient should be in the erect position for at least

5 min before the CXR is taken to allow free gas to accumulate under

the diaphragm.

• Decubitus AXR:

• On occasion, the patient may not be able to maintain an erect

position for long enough, in which case a left lateral decubitus

AXR (left side down) can be helpful.

• In this position, free gas will lie between the lateral aspect of the liver

and the diaphragm.

156

• AXR:

• The supine AXR can demonstrate free gas, although greater quanti-

ties are usually needed than with the erect CXR.

• Free gas against a soft tissue surface will outline that tissue more clearly

than usually seen on AXR: structures so outlined include the falci-

form ligament, the liver edge, the umbilical ligaments and diaphrag-

matic slips.

•

“Riggler’s sign” (the double-wall) sign represents air within the bowel

lumen outlining the inner surface, while free air outlines the outer wall.

• Plain film pitfalls include Chilaiditi’s syndrome, subdiaphragmatic fat,

adjacent gas-filled bowel loops simulating Riggler’s sign, subdiaph-

ragmatic abscess, and diverticula of the stomach or duodenum.

• CT:

• This is very sensitive for detecting free gas, but the radiation dose

involved means that plain films remain the mainstay investigation.

• On CT, areas of gas need to be carefully examined to establish

whether they represent free or bowel gas.

• May demonstrate likely site of perforation.

• USS: much less sensitive than the above techniques as differentiating

free air from bowel gas is difficult.

158

Gallstones

Clinical characteristics

•

Gallstones are common, affecting 10-20% of the population.

•

Two main components are cholesterol and calcium bilirubinate

•

There are three types of gallstone, based on their components: choles-

terol, pigment and mixed, of which mixed is the most common type.

• Cholesterol stones are caused by precipitation of supersaturated bile

and occur in the Western population.

• Pigment stones occur from excessive haemolysis, resulting in excess

unconjugated bilirubin and hence precipitation of calcium

bilirubinate.

•

Gallstones may be present for decades without causing symptoms or

complications, and usually do not require any treatment.

•

Biliary colic is the result of a gallstone impacting within the cystic duct

during gallbladder contraction, which then eases as the gallbladder

relaxes and the stone dislodges. The pain localizes to the RUQ and

epigastrium.

•

Acute cholecystitis occurs when persistent obstruction of the cystic duct

causes gallbladder distension and inflammation. This may progress to

pus collecting within the gallbladder, known as an empyema. If the

gallbladder perforates, a pericholecystic abscess may form.

•

Chronic cholecystitis occurs in the setting of long-standing gallstones

and results in a shrunken gallbladder with loss of function.

•

Gallbladder adenocarcinoma occurs in patients with gallstones, but gallstones are

not carcinogenic per se.

Radiological features

• AXR: 30% of gallstones are calcified and 10% are visible on AXR. This

is usually an incidental finding rather than a diagnostic one, owing to the

high false-negative rate.

• USS:

• The most important modality for imaging gallstones and their

complications.

• Patients must be fasted to avoid gallbladder contraction, thereby

reducing false-negative investigations.

• Gallstones appear as echogenic foci, with posterior acoustic shadow-

ing, that move within the gallbladder when the patient is turned.

162

•

Fluoroscopy: the oral cholecystogram has largely been replaced by US

for the investigation of gallstones. An oral cholecystographic agent is

given and AXRs are taken the following day. Gallstones appear as filling

defects in the opacified gallbladder.

•

CT:

• Calcified gallstones have a characteristic appearance on CT but are

not as clearly visualised when non-calcified.

• Complications such as biliary obstruction and cholecystitis may also

be seen, but US remains the first-line investigation.

•

ERCP:

• ERCP is performed by physicians or surgeons rather than radiologists.

A side-viewing endoscope is used and the ampulla of Vater

cannulated.

• Stones are visualised as filling defects within the contrast-filled bile

ducts.

• Therapeutic procedures, such as sphincterotomy and removal of

stones, may also be performed.

•

MRI:

• MRCP is an alternative when it is not possible to perform ERCP.

• MRCP utilises heavily T2W sequences to highlight the slow-moving

fluid in the biliary system.

• Gallstones will appear as defects of low signal intensity within the

high-signal-intensity bile.

164

• NM:

• Iminodiacetic acid labelled with technetium-99^m is used to assess

biliary excretion and gallbladder function (HIDA scan).

• Failure to visualise the gallbladder by 4h, with normal bowel activity,

indicates cystic duct obstruction in acute cholecystitis.

• Has now largely been replaced by US.

• Interventional radiology:

• Interventional procedures include drainage of a gallbladder empyema

and PTC.

• PTC is performed to access the biliary tree percutaneously, and

involves percutaneous cannulation of the intrahepatic bile ducts via

a transhepatic approach.

166

Hepatic masses

The differentiation of clinically significant hepatic masses from incidental,

non-significant, hepatic masses is an important aspect of abdominal imaging.

Simple hepatic cysts

Clinical characteristics

• Very common incidental finding.

• Increasing incidence with advanced age.

• Associated with tuberose sclerosis and polycystic kidney disease.

• Rarely symptomatic.

Radiological features

• USS:

• Investigation of choice to confirm presence of a simple cyst.

• Well-defined, anechoic lesion with no visible wall.

• Haemorrhage or infection may result in internal echoes.

• CT: fluid attenuation

(0-10HU) lesion with no visible wall or

enhancement

• MRI: very high signal on T2W imaging, low signal on T1W and no

enhancement are the features of a simple cyst on MRI.

168

Hepatic haemangioma

Clinical characteristics

• A common, benign, liver lesion made up of vascular channels with

slowly circulating blood.

• Most are clinically silent but larger ones may spontaneously haemor-

rhage or cause pain from haemangioma thrombosis.

• Kasabach-Merritt syndrome is the association of a large haemangioma

and thrombocytopenia.

Radiological features

•

USS:

• The majority of haemangiomas are uniformly hyperechoic on US.

The majority show through enhancement.

• Some may be heterogeneous owing to scarring, fibrosis or haemorrhage.

• Often have no Doppler signal. If detectable, the velocities are <50cm s-1

•

90% are unchanged in US appearance on follow-up.

•

CT:

• Many liver lesions are investigated with a three-phase CT scan.

• This comprises a precontrast series, an arterial phase series and a portal

phase series. Occasionally delayed series are required.

• Haemangiomas are low density on precontrast imaging. On early

postcontrast, there is nodular, peripheral enhancement. Delayed

imaging shows filling in from the periphery inwards. This results in

complete ‘in-fill’ in three-quarters of haemangiomas.

• Larger haemangiomas are more likely not to fill in completely owing

to increased incidence of central scaring.

• Small (<1cm) haemangiomas may not demonstrate classical periph-

eral, nodular enhancement, being seen as a homogeneous enhancing

lesion on early phase imaging.

• The differential includes hypervascular metastases but these wash out

on delayed imaging, and are then hypodense compared with normal

hepatic parenchyma. Haemangiomas remain hyperdense on delayed

images.

170

• MRI:

• MRI is increasingly used to delineate hepatic masses. It has the

advantage over CT of not incurring a radiation dose, particularly

important when compared with multiple-phase CT examinations.

• Masses are well defined, sometimes with lobulated, margins. Smaller

lesions are homogeneous but larger ones may be inhomogeneous

because of scarring.

• T1W sequences show iso- or hypointense lesions.

• On T2W sequences, haemangiomas are very bright because of the

slow-flowing blood. The hyperintensity characteristically remains

with increasing echo times.

• The post-gadolinium enhancement pattern mirrors that seen on CECT.

172

Hepatic adenomas

Clinical characteristics

• Benign proliferation of hepatocytes. Well defined with a pseudo-capsule

of compressed normal hepatic tissue.

• May undergo fatty change, haemorrhage and necrosis.

• A condition seen almost exclusively in young females; occurs in men

taking anabolic steroids.

• Hormone sensitive with an increased incidence with hormone

contraception.

• Diabetes mellitus is a further risk factor.

• Growth during pregnancy may result in rupture.

• One-fifth of patients are asymptomatic.

• May present with RUQ pain from bleeding or a mass effect. Hepatomegaly

may be clinically evident.

• Biopsy carries high bleeding risk.

175

Radiological features

•

USS:

• Well-defined mass of variable echogenicity.

• The pseudo-capsule may be seen as a hypoechoic rim.

• In larger examples, necrosis can lead to cystic regions.

•

CT:

• On precontrast series, adenomas are usually well defined.

• Necrosis may lead to decreased density, while haemorrhage may lead

to increased attenuation.

• Adenomas have a vascular supply from the hepatic artery and, on

arterial phase CT, show brief enhancement relative to normal hepatic

tissue. Often iso- or hypodense on portal phase so may be missed if

only a portal phase postcontrast series is performed.

•

MRI:

• As adenomas are largely composed of hepatocytes, they often have a

very similar signal intensity to normal liver parenchyma on standard

T1W and T2W sequences.

• The presence of haemorrhage and intracellular fat can lead to slight

hyperintensity on T1W and T2W series.

• The presence of intracellular fat means that T1W out-of-phase

sequences will lead to a drop in signal relative to liver parenchyma.

NB: Small (<2cm) hepatomas may also occasionally demonstrate this

feature.

• As with CECT, hepatic adenomas show transient arterial enhance-

ment and subsequent homogeneous washout.

176

Focal nodular hyperplasia

Clinical characteristics

• Focal nodular hyperplasia (FNH) is a benign congenital hamartoma of

the liver.

• Consists of multiple small lobules of hepatocytes. There is often a central

fibrous scar with an arteriovenous malformation, producing a spoke-

like pattern of radiating vessels. The lesion is non-encapsulated.

• Most are <5cm in diameter. Often subcapsular in position and some are

pedunculated.

• Not caused by oral contraceptives but may grow under the hormonal

influence.

• Can be seen at any age but most commonly in the 3rd and 4th decades.

• Usually an incidental finding and are asymptomatic, although discom-

fort from a mass effect can occur.

• Unlike adenomas, FNHs rarely undergo necrosis or haemorrhage, and

intracellular fat is rarely seen.

Radiological feature

• USS:

• US may demonstrate some specific features; the mass is usually

homogeneous and either hypoechoic or isoechoic to hyperechoic

relative to hepatic tissue. The central scar will only be seen in one-fifth

of patients.

• Doppler studies may demonstrate the central arterial supply and the

spoke-like pattern of draining vessels.

• Shunt vessels have high velocity and arterial pulsatility.

178

•

CT:

• Best assessed with three-phase enhanced CT.

• On non-enhanced CT (NECT), FNHs are slightly hypoattenuating

or isoattenuating to normal liver.

• Following contrast, there is peak enhancement at 30-60 seconds with

rapid subsequent washout.

• The central scar may enhance less on the early phase but may be

hyperattenuating on delayed imaging owing to delayed washout.

•

Nuclear imaging: sulphur colloid scans involve the uptake of isotope

by the Kupffer cells of the reticular endothelial system of the liver. FNH

are the only hepatic masses to contain enough of these cells to have

normal or increased uptake on this imaging.

•

MRI:

• FNH are usually homogeneously slightly hyper- or isointense on

T2W images, homogeneously hypo- or isointense on T1W images.

• The central scar is usually hyperintense on T2W and hypointense on

T1W images.

• Following gadolinium enhancement, there is intense, homogeneous,

arterial phase enhancement within the body of the FNH. This rapidly

washes out to reach portal phase isointensity.

• The scar shows late, long-lasting enhancement.

180

Hepatic metastatic deposits

Clinical characteristics

• Metastatic deposits are the most common malignant liver masses, and

the liver is the second most common site of metastatic deposits after

local lymph nodes.

• Common sites of origin include the colon, stomach, breast, pancreas

and lung.

• Often discovered during staging of known primary tumours, but they may

present with hepatomegaly, jaundice or deranged liver function tests.

Radiological features

•

These can be very variable owing to the many possible primary tumours

of origin.

•

Mucinous adenocarcinomas, classically from colon, breast, stomach or

ovary, may calcify.

•

Metastases from melanoma, pancreatic islet cell tumours, thyroid carci-

noma, carcinoid and renal cell carcinoma may be hypervascular.

•

Metastases from stomach, pancreas, breast, lung and colon are often

hypovascular.

•

Hyperechoic metastases are seen in colonic carcinoma and hepatoma.

•

Hypoechoic secondaries are seen in cervical carcinoma, lymphoma and

pancreatic adenocarcinoma.

•

CT:

• Very reliable at detecting metastases, especially those <10mm.

• Best performed with IV contrast, although a NECT may be helpful

when hypervascular deposits are suspected, as these may be obscured

postcontrast. NECT also helps to detect the fine calcification seen in

mucinous GI secondaries - classically colonic metastases.

• Dynamic contrast enhancement usually shows a pattern of initial,

peripheral rim enhancement with a relatively hypovascular centre,

leading to a ‘target’ appearance, with delayed washout. However

many patterns of enhancement may be seen, depending on type of

metastases, including non-enhancement.

182

•

MRI:

•

MRI is better than CT at both detecting and characterising liver

masses.

•

This is important if resection or ablation of liver metastases is being

considered, as the presence of multiple deposits may preclude such

interventions. Conversely, MRI may establish that lesions seen on

other modalities are benign.

•

Classically, metastases are slightly hypointense in T1W and hyper-

intense on T2W.

•

Haemorrhagic metastases may have mixed T1W and T2W signal,

depending on the stage of blood product breakdown.

•

Melanin has paramagnetic properties, leading to variable hyper-and

hypointensity on both T1W and T2W images in melanoma

metastases.

•

Metastases from mucinous carcinomas, such as ovarian mucinous

cystadenocarcinoma or mucinous carcinoma of the pancreas, may

also be high on T1W images owing to their proteinaceous content.

•

Standard extracellular gadolinium enhancement patterns are similar

to those of iodinated contrast enhancement in CECT.

•

Some gadolinium- and manganese-based MRI contrast agents are

selectively taken up by hepatocytes, so increasing T1W parenchymal

hyperintensity in those hepatic neoplasia containing hepatocytes,

such as hepatic adenomas, FNHs and some well-differentiated hep-

atomas. However neoplasias not containing hepatocytes, such as

metastatic deposits and haemangiomas, do not take up such agents.

Therefore, on late (>10min) imaging, such lesions are hypointense

against the contrast uptake by hepatic parenchyma. This can be

helpful in detecting small deposits when liver resection or ablation is

being considered.

Hepatocellular carcinoma

Clinical characteristics

• Hepatocellular carcinoma (HCC) is also known as hepatoma.

• A primary malignancy of hepatocytes.

• In the developed world, this is largely associated with liver cirrhosis.

• Other risk factors include chronic viral hepatitis, carcinogens such as

aflatoxin, thorotrast, sex hormones and metabolic disorders such as

Wilson’s disease, haemachromatosis and ,₁-antitrypsin deficiency.

• Much more common in Asia and sub-Saharan Africa.

• May present with RUQ pain, hepatomegaly, ascites, weight loss, fevers

and paraneoplastic symptoms.

• Often HCCs are detected on USS.

• HCCs are associated with elevated ,-fetoprotein, which is used as a

screening tool in at-risk patients.

184

• Metastases may occur to the lungs, adrenal glands, bones and lymph

nodes.

• Invasion of the hepatic veins can result in a Budd-Chiari syndrome.

Tumour can track along the venous system, involving the IVC and right

atrium.

• Portal vein invasion is also a feature.

Radiological features

•

USS:

• US can be used as a screening tool in at-risk patients and as an initial

investigation in those with raised ,-fetoprotein, but it is not specific.

• HCCs may be focal, where a discrete mass can be seen. These may be

of variable echogenicity, especially in larger HCCs when haemor-

rhage and necrosis are seen.

• HCC is a vascular tumour and Doppler studies may demonstrate high

velocities.

• Invasion of venous structures can be seen.

• Diffuse HCC is poorly defined and may be difficult to detect on US,

as the subtle changes in echogenicity are difficult to differentiate

against the coarse echotexture often seen in cirrhosis.

• HCCs usually occur in cirrhotic livers where cirrhotic nodules are

common. However cirrhotic nodules are rarely seen on US and any

focal lesion should be considered highly suspicious.

•

CT:

• Detects two-thirds of HCCs in cirrhotic livers and more in non-

cirrhotic livers.

• May be focal, usually poorly defined or diffusely infiltrating.

Multifocal lesions are well recognised.

• Usually hypodense on pre-enhancement imaging; 10% may show

calcification.

• Arterial enhancement shows a heterogeneous pattern, although

lesions <1.5cm may show homogeneous enhancement.

• Necrotic, non-enhancing areas may be seen.

• On delayed portal phase scans, the tumour is usually of low attenu-

ation compared with the liver parenchyma.

• Involvement and occlusion of the portal and/or hepatic venous

systems may be demonstrated, as may areas of poorly perfused liver

secondary to venous compromise.

• Metastatic deposits, ascites and the extent of any vascular involvement

can all be assessed on CT.

186

•

MRI:

•

More sensitive than CT for the detection of HCCs.

•

The signal characteristics vary but classically the lesions are hypoin-

tense on T1W and mildly hyperintense on T2W. Hyperintensity on

T1W is a known feature, caused by the presence of intracellular fat,

and is associated with early, well-differentiated HCCs with a better

prognosis.

•

Arterial phase gadolinium enhancement is the most sensitive

sequence for hepatomas. They demonstrate diffuse heterogeneous

enhancement, although, as with CECT, small lesions may enhance

homogeneously. In contrast, metastatic deposits classically show

peripheral, rather than diffuse, early enhancement.

•

On delayed (2min post-injection) imaging, HCCs are usually hypo-

intense in comparison with hepatic tissue. There may be an enhanc-

ing psuedocapsule surrounding the HCC during the late

enhancement phase.

•

Diffusely infiltrating HCC is seen as mottled areas of T2W hyper-

intensity and early gadolinium enhancement.

•

MRI can detect metastatic deposits and assess the extent of venous

complications.

•

The presence of hepatocytes means HCCs take up liver-specific

contrast agents, unlike metastatic deposits.

•

There are a number of other mass lesions seen in cirrhotic livers.

- Regenerative nodules are not neoplastic but represent local hep-

atocyte proliferation. These tend to be <1.5cm in diameter, are

generally iso- or slightly hypointense in T1W and T2W sequences

and show no significant enhancement post-gadolinium.

- Dysplastic nodules represent adenomatous hyperplasia and are

premalignant, often developing into HCCs. Both mildly dysplastic

nodules and severely dysplastic ones are usually <1.5cm and may

be mildly hypo- or hyperintense on both T1W and T2W images.

The mildly dysplastic nodules demonstrate only minimal enhance-

ment, while severely dysplastic ones demonstrate intense, but

homogeneous enhancement.

188

Radiological interventions in hepatic masses

• As well as the use of cross-sectional imaging to obtain accurate tissue

samples from liver lesions, there has been an increase in radiologically

supported therapies.

• Percutaneous ablations of individual metastatic deposits and HCCs

using chemical or thermal ablation have had encouraging results com-

pared with hepatic resection.

• Ablations are performed under CT, US or MRI. One advantage of

using MRI combined with thermal ablation is that changes in the signal

of tissues, as their temperatures change, means real-time mapping of the

burn can be performed, resulting in a more accurate ablation.

• In the future, focused high-intensity US may be used to ablate hepatic

masses in a truly non-invasive manner.

Hepatocellular carcinoma post-ablation. The ablation film is a

real-time T1 image. The faint low signal line running obliquely through the

liver (arrow) is the sheath containing the laser fibre. The posteromedial area

of very low signal (asterisk) is the thermal burn in the carcinoma.

189

Herniae of the abdomen and pelvis

Hiatus hernia

Clinical characteristics

•

The oesphagus normally passes through the diaphragm at the level of

the 10th thoracic vertebra, and the phrenico-oesphageal membrane

fixes the oesophagus to the surrounding diaphragm.

•

When this membrane is deficient, a hiatus hernia occurs.

•

Hiatus hernia is common and the prevalence increases with age.

•

Although the majority of hiatus herniae are small, they can be very large

with the entire stomach lying in the thorax.

•

There are two types of hiatus hernia: sliding and paraoesophageal:

• Sliding is by far the most common type when the gastro-oesophageal

junction slides through the hiatus.

• In paraoesophageal herniae, the gastro-oesophageal junction is in the

normal position and the proximal stomach moves into the thorax,

where it usually lies to the left of the oesophagus in the posterior

mediastinum.

•

Sliding herniae are more likely to vary in their size and position and are

more commonly associated with gastro-oesophageal reflux.

•

Paraoesophageal herniae are more prone to incarceration and, rarely,

volvulus, and reflux is not always an association.

•

Hiatus herniae are frequently asymptomatic but associated gastro-

oesophageal reflux may cause dyspepsia.

•

Chronic gastro-oesophageal reflux can result in Barrett’s oesophagus,

which is the development of columnar epithelium in the lower oeso-

phagus; this results in a much higher risk of adenocarcinoma of the

oesophagus.

190

Radiological features

•

Plain X-ray: hiatus hernia is often diagnosed on chest radiography by

the presence of a mass behind the heart, with or without an air-fluid

level dependent on the patient’s position.

•

Upper GI tract barium study:

•

This is the radiological study of choice for diagnosing a hiatus hernia.

•

A double-contrast study is performed using barium and gas to coat

and distend the oesophagus and stomach.

•

A sliding hiatus hernia is more easily diagnosed by endoscopy than

barium study as the key feature is identification of the squamocolum-

nar mucosal junction, which should normally lie at 40cm from the

incisor teeth. A sliding hiatus hernia is diagnosed if the squamoco-

lumnar junction is seen at 38cm or less (depending on patient height).

•

The mucosal junction is more difficult to visualise on barium study

and, therefore, secondary features are relied on. These features

include the Schatzki, or B, ring, which is seen as a circumferential

indentation in the distal oesophagus on the barium study and marks

the site of the squamocolumnar junction.

•

Other features are the incisural notch, which is an incomplete ring

marking the site of the mucosal junction, and the diameter of the

hiatus being larger than the distal thoracic oesophagus.

•

The less-common paraoesophageal hernia is more readily seen on

barium study as it does not depend upon the identification of the

mucosal junction. The key feature is that the gastro-oesophageal

junction lies in the abdomen.

•

When assessing for a sliding hiatus hernia, it is important to ensure

maximal distension of the distal oesphagus with the patient in the

prone position, and also to assess for associated gastro-oesophageal

reflux with the patient tilted to the right from the supine position.

•

CT: hiatus hernia is often an incidental finding on cross-sectional

imaging, but it may also provide more detailed information of the

hernial contents in a large hernia.

192

Types of abdominal and pelvic herniae

•

Epigastric: a hernia through the fibres of the linea alba.

•

Femoral: a hernia through the femoral canal, medial and inferior to the

inguinal canal.

•

Incisional: an iatrogenic hernia, occuring in 2-10% of all abdominal

operations, secondary to breakdown of the surgical closure site from

prior surgery. Recurrence rates approach 20-45% following repair.

•

Inguinal: can be subdivided into indirect and direct. An indirect inguinal

hernia passes along the inguinal canal and the hernial sac may or may not

be limited to the inguinal canal. The neck of the sac lies lateral to the

inferior epigastric artery. A direct inguinal hernia passes directly forward

through the defect in the posterior wall of the inguinal canal, and the

neck of the hernia lies medial to the inferior epigastric artery.

•

Internal: herniation of bowel through defects in the peritoneum,

omentum, mesentery or band of adhesions.

•

Lumbar: hernia through the lumbar triangle. These tend to have a

wide neck.

•

Obturator: the hernia passes through the obturator foramen, following

the path of the obturator nerves and muscles. Because of its anatomic

position, this hernia presents more commonly as a bowel obstruction

than as a protrusion of bowel contents.

•

Peri-umbilical: herniation of abdominal contents through the peri-

umbilical tissues.

•

Richter: occurs when only the antemesenteric border of the bowel

herniates through a fascial defect, and may lead to incarceration or

strangulation of the focal herniated segment. It may occur with any of

the various abdominal herniae and is particularly dangerous, as the

strangulated bowel may be reduced spontaneously, leading to perfora-

tion and peritonitis.

•

Spigelian: this rare form of abdominal wall hernia occurs through the

semilunar line along the lateral aspect of the rectus sheath.

•

Umbilical: herniation of abdominal contents through the umbilicus.

194

Clinical characteristics

• The clinical presentation of a hernia depends upon the site, size and

hernial sac contents. Complications include incarceration, irreducibi-

lity, obstruction and strangulation.

Radiological features

• Plain X-Ray: not usually the modality of choice for diagnosing her-

niae; however, it is of use when bowel obstruction, secondary to a

hernia, is suspected. Occasionally identified incidentally on a barium

study.

• USS: useful to localise herniae and for differentiating from other causes

of a palpable lump such as solid masses or a haematoma.

• CT and MRI: although US can provide good resolution of many

superficial herniae, CT may provide more information regarding inter-

nal herniae.

196

• Herniography/herniogram:

• This technique is less frequently used now as there are other less-

invasive modalities available.

• A spinal needle is introduced into the peritoneal cavity and radio-

graphic contrast injected.

• The patient is asked to cough and perform the valsalva manoeuvre to

demonstrate contrast in the hernial sac.

Herniogram following installation of water soluble contrast into the

peritoneal cavity. Peritoneal indentations and fossae of the anterior

abdominal wall and their relation to the sites of groin hernia.

1, median umbilical ligament (obliterated urachus); 2, medial umbilical

ligament (obliterated umbilical arteries); 3, lateral umbilical ligament

(containing inferior epigastric arteries). Sites of possible herniae: A, lateral

fossa (indirect inguinal hernia); B, medial fossa (direct inguinal hernia);

C, supravesical fossa (supravesical hernia).

198

Intussusception

• Invagination or prolapse of a segment of intestinal tract (= intussusceptum)

into the lumen of the adjacent intestine (= intussuscipiens)

•

90% are ileocolic and ileoileocolic.

• In adults, the majority are caused by a pathological lead point.

Paediatric intussusception

Clinical characteristics

• In 90% of all paediatric intussusceptions there is no pathological lead

point and they are thought to be associated with lymphoid hyperplasia

in Peyer’s patches of the ileum.

• In the remaining 10%, the lead point is:

• Meckel’s diverticulum (most common lead point)

• polyp or other tumour

• duplication cyst

• Intussusception usually occurs in the first 2 years and rarely in neonates.

• The patient presents with severe colicky pain and vomiting. Initial stools

passed at the start of symptoms are unremarkable; blood and mucus

(‘redcurrant jelly’) stools are passed after 24h or so.

• On examination, there may be a palpable sausage-shaped mass, most

often in the upper abdomen.

200

Serosal surfaces

Peritoneal

in contact

transudate

Serosal surfaces

in contact

intussuscipiens (receptor)

Mucosal surfaces

returning limb of intussusceptum

in contact

mesentery

entering limb of intussusceptum

bowel lumen

Intussusception.

Radiological features

• AXR: film is normal in 50%. A soft-tissue mass or intraluminal filling

defect, in a partially air-filled bowel loop (commonly at hepatic flexure),

may be seen.

• USS: a ‘target sign’ may be seen, appearing as concentric alternating

echogenic and echo-poor rings, representing compressed mucosal and

serosal surfaces and oedematous bowel wall, respectively. Colour

Doppler shows blood vessels dragged in between the entering and

exiting layers of the intussusception. Absence of blood flow indicates

devitalised bowel segments.

• Antegrade barium study: contraindicated in perforation. Barium

examinations have been generally superseded by US. May show a

‘coiled spring’ appearance with a beak-like distal string of barium as it

runs through the central column.

• Barium enema: contraindicated in perforation. Water soluble contrast

enemas may demonstrate a convex intraluminal mass, representing the

intussusceptum, surrounded by contrast. The ‘coiled spring’ sign is seen as

contrast flows over the oedematous fold of the reflected intussusceptum.

201

Radiological management

• An intussusception can be reduced radiologically under fluoroscopic

guidance with barium, water-soluble contrast or air.

• Contraindications include peritonitis and shock.

• Prior to attempting reduction, the child should be resuscitated and both

surgical and anaesthetic cover available.

• The pneumatic technique is preferred as it is faster and if perforation

complicates the procedure the tears tend to be smaller, and hence the

degree of peritoneal contamination lessened.

• Radiological reduction can also be attempted under US guidance using

saline.

• The complication rate for radiological reduction is less than 3% and

includes perforation, the reduction of infarcted bowel and the non-

detection of a pathological lead point.

202

Adult intussusception

Clinical characteristrics

• Unlike in the paediatric situation, the majority, approximately 80%,

have a defined lead point such as a neoplasia, inverted diverticulum,

foreign body, chronic ulcers or postsurgical changes.

• Intussusceptions are the cause of approximately 15% of bowel obstructions.

• Other presentations include bloody diarrhoea, recurrent colicky abdo-

minal pain, palpable mass and change in bowel habit.

Radiological features

• CT:

• This is the imaging modality of choice. The intussusception is iden-

tified by a series of concentric rings. The central component repre-

sents the lumen and the intussusceptum wall. The middle ring is of

mesenteric fat in which mesenteric vessels are usually visible. The

peripheral ring is made up of the reflected intussusceptum and the

intussuscipiens.

• May also demonstrate the pathological lead point and its extent.

• Complications such as obstruction or perforation are also well

visualised.

204

Lines and devices

• It is important to be able to recognise common lines and devices used in

the abdomen in order to confirm they are correctly positioned and to

avoid misinterpretation.

Radiological features

• Most lines and devices are visible on AXR; however, as this is only a

two-dimensional assessment, further imaging is sometimes necessary to

assess the position and patency of various lines and tubes.

• US can confirm the patency of ureteric and biliary stents by document-

ing the absence of hydronephrosis and biliary dilatation.

• US and/or CT may be needed to assess surgical drains.

• If there is concern regarding patency of a vascular line, radiographic

contrast can be directly injected into it under fluoroscopic guidance.

208

Types of line/device

Vascular lines

• In the neonate, umbilical arterial and venous lines are commonly used.

• The umbilical artery catheter is passed via the umbilical artery into

the internal iliac artery and the infrarenal aorta. On AXR, it is seen to

loop down into the pelvis before travelling in a cephalic direction to

the left of the midline. The tip of the line should lie either above or

below the renal arteries, between T8 and T12 or L3 and L4.

• The umbilical vein catheter should traverse the umbilical vein, the

portal sinus (junction of left and right portal vein), ductus venosus and

IVC and end in the right atrium. On the abdominal film the catheter

passes in a cephalic direction from its entry point and should lie above

the liver in the right atrium. The umbilical vein catheter is easily

misplaced in a portal or hepatic branch and the tip is then seen

projected over the liver on AXR.

• Femoral venous lines lie in the inguinal regions and pass in the iliac

veins to the IVC.

• Arterial stents within the abdominal aorta and iliac arteries have a

mesh-like appearance.

• IVC filters look like the spokes of an umbrella and lie to the right of the

midline on the abdominal film.

210

Urinary tract lines

• The most commonly seen tube relating to the urinary tract on AXR is

the urinary catheter, placed either via the urethra or the suprapubic

route.

• Ureteric stents have curled ends and lie lateral to the transverse

processes of the vertebral bodies. Transplant kidneys may also have

ureteric stents that lie in the pelvis.

• Nephrostomy tubes placed percutaneously to drain an obstructed

kidney are seen in the upper abdomen, with a coiled end in the renal

angle and an external component.

• Patients with renal failure on peritoneal dialysis have an intra-

abdominal catheter that is tunnelled under the skin before entering

the abdomen and usually lies in the lower abdomen, although its

position is variable.

212

Gastrointestinal tract lines

• Tubes commonly seen within the GI tract are nasogastric and naso-

jejunal tubes placed for feeding. To aid identification, the tips of the

tubes are radioopaque and the tips of both should lie in the LUQ. The

nasojejunal tube lies more distally within the bowel and follows the

C-shaped loop of the duodenum, crossing the midline into the left side

of the abdomen, to lie just distal to the duodenojejunal junction.

• Stents placed within the biliary system, for example within the com-

mon bile duct, are visible on the abdominal film, lying in the RUQ.

• Stoma devices. The position of these is naturally dependent on the

procedure performed.

216

Lymphadenopathy

Clinical characteristics

• Lymphadenopathy can have numerous causes, which can be broadly

divided into neoplastic, infective and inflammatory conditions:

• neoplastic: lymphoma, leukaemia, metastatic cancer.

• infective: TB, bacterial, viral, fungal.

• inflammatory and miscellaneous: Castleman’s disease, amyloid,

sarcoid, mesenteric lymphadenitis.

Radiological features

•

As part of the investigation of a patient with lymphadenopathy, which is

apparent elsewhere, abdominal imaging may be performed.

•

The main purpose is to assess the size and extent of the lymph node

enlargement (i.e. regional or widespread) as well as to identify an

underlying cause.

•

Imaging also plays an important role in the follow-up of treated patients.

Generally the smaller diameter (short axis diameter) of the node in the

axial plane is recorded and regional nodal groups have different upper

limits of normality. As a rule of thumb, a short axis diameter of <1cm is

considered within normal limits, although there is overlap between

benign and malignant adenopathy. However, using size as a criterion

of malignancy may overlook microscopic metastases when only part of a

node is involved. If a lower threshold is used to separate benign and

malignant, the sensitivity increases but the specificity decreases, and

when a higher threshold is applied the sensitivity drops and the specif-

icity rises.

•

AXR: may detect calcification within lymph nodes but overall is not

helpful.

•

USS:

• As well as confirming that a palpable swelling is caused by lymph node

enlargement, US can characterise and assess the extent of lymphaden-

opathy, although visualisation of the retroperitoneum can sometimes

be obscured by overlying bowel gas.

• Normal lymph nodes are usually oval and hypoechoic (dark) with

hilar vascularity. They often have an echogenic fatty hilum.

• Malignant disease alters the morphology of nodes so that they become

more rounded with peripheral vascularity.

• US is also useful for performing US-guided fine needle aspiration

cytology or biopsy.

220

Lymphoma. Multiple large-volume mesenteric lymph nodes (arrows),

with additional confluent retroperitoneal nodal masses (asterisk).

Necrotic ring-enhancing node secondary to a malignant gastric ulcer

(not shown). Extensive soft tissue stranding present in the left upper

quadrant from local tumour infiltration (asterisk).

• CT:

• CT is particularly useful in assessing the extent of lymphadenopathy,

identifying an underlying cause and any complications, for example

hydronephrosis secondary to enlarged lymph nodes.

• It is also useful as a method of following up patients known to have

lymphadenopathy, after treatment.

221

• IV contrast is routinely given to help to differentiate lymph nodes

from adjacent vessels and oral contrast or water to outline small-

bowel loops.

• As on US, benign nodes may also demonstrate a fatty hilum and

characteristic oval shape.

• Enlarged lymph nodes can be characterised further by their appear-

ance. For example, tuberculous nodes typically have a low-density

necrotic centre and rim enhancement after IV contrast.

• Squamous cell metastases are also typically necrotic. In contrast,

lymphomatous nodes have a homogeneous appearance with minimal

enhancement.

• The rare condition, Castleman’s disease demonstrates marked lymph

node enhancement.

•

MRI:

• Both normal and malignant lymph nodes have intermediate signal

intensity on T1W sequences, intermediate-high on T2W sequences

and enhance after IV gadolinium.

• The same size criteria as for CT are used with the same problems.

• There have been clinical trials using specific contrast agents for

lymphoid tissue, which demonstrate improved accuracy, but these

agents are not in widespread use.

•

Positron emission tomography (PET) and PET-CT:

• Both PET and PET-CT use the glucose analogue

¹⁸F-

Fluorodeoxyglucose (FDG), which is taken up by cells with an increased

rate of glycolysis, as in malignant lymph nodes.

• The disadvantage of PET is its lack of spatial resolution owing to

limited anatomical information.

• This has been improved by the combination of CT with PET to

create PET-CT. The patient is scanned sequentially by the PET and

CT scanners from skull base to mid-thigh and the images recon-

structed and coregistered for interpretation by the radiologist.

• PET-CT can now provide accurate anatomical information about a

region of increased uptake of isotope in the PET component.

• It is important to be aware that other conditions, such as infection,

inflammation and granulomatous disease, can also demonstrate

increased glycolysis. However, PET-CT has an important role in

the diagnosis and staging of malignant disease.

222

Lymphoma: abdominal

Clinical characteristics

•

Lymphomas are malignancies of the lymphoid tissues of the body and

are broadly divided into Hodgkin’s disease (HD) and non-Hodgkin

lymphoma (NHL). They are a diverse group of neoplasms with some

broad patterns of presentation and behaviour.

•

Lymphoma accounts for 5-6% of all adult and 10% of childhood

malignancies. NHL is more common than HD (60:40%); in the UK

in 2001, there were 4600 deaths from NHL and 260 deaths from HD.

•

HD classically shows a bimodal peak distribution: in the third decade

and subsequently in the 65-75 age group. NHL is a disease of children

and the elderly, with a median age at diagnosis of 65 years.

•

The different behaviour of HD and NHL is reflected in their clinical

staging (which is distinct from their pathological staging). While both

HD and NHL are essentially diseases of lymph nodes, both may present

as either localised nodal disease or as widely disseminated cancer.

•

Most patients with HD present with painless asymmetrical nodal

enlargement, accompanied by night sweats, fever, pruritus and weight

loss in 40% (B symptoms).

• The commonest site of nodal involvement is cervical, present in up to

80% of patients. Exclusive infradiaphragmatic disease occurs in under

10% of patients. Splenomegaly is present in about a third. HD spreads

contiguously from one nodal group to the next. Primary extra-nodal

HD is very rare.

•

Patients with NHL also present with nodal enlargement, though in this

case it is often non-contiguous and extra-nodal disease is common.

Associated B symptoms occur half as often as with HD.

•

HD disease is staged via the Cotswold classification, a modification of

the Ann Arbor classification. Early disease is treated with radiotherapy,

while more advanced disease is treated with radiotherapy and chemo-

therapy. Overall 10-year survival in patients treated with radiotherapy

for early-stage HD is >90%.

•

The prognosis in NHL is very variable. Unlike HD, histological subtype

(particularly the division into low- and high-grade disease) as well as

stage is the major determinant of treatment. Low-grade lymphoma is

often asymptomatic and surveillance or local radiotherapy may be

appropriate. In high-grade lymphoma, multidrug chemotherapy and

new antibody therapies are utilised. The 10-year survival for low-grade

NHL treated with radiotherapy approaches 90%.

224

Radiological features

• Abdominal lymphoma may involve both nodal and extra-nodal sites.

Retroperitoneal nodal involvement is present in up to 35% of patients

with HD and up to 55% in NHL. Mesenteric nodes are involved in >50%

of patients with NHL but only 5% in HD. In HD, coeliac, splenic hilar and

porta hepatis nodes are involved in 30% of patients. Involvement of

splenic nodes is invariably associated with splenic infiltration. There

may be contiguous spread from mediastinal nodes in HD. In NHL,

nodal involvement is often non-contiguous and may be associated with

visceral involvement as well as diffuse mesenteric and omental involve-

ment. In the pelvis, all nodal groups may be involved in both NHL and

HD. Involved nodes are typically rounded, homogeneously enhancing

and may form a matted nodal group particularly in NHL.

• Extra-nodal abdominal involvement in both HD and NHL may

include the liver, spleen, GI tract, pancreas, genitourinary system and

adrenal glands.

Liver

• Liver and invariably splenic involvement occurs in 5% of patients with

HD, with 15% of patients with NHL similarly affected. Large focal areas

of involvement are easily seen on CT, MRI and US as well-defined,

large hypodense (on both NECT and CECT) or hypoechoic areas, but

are present in only 10% of hepatic involvement. On MRI, these areas

are low on T1W and high on T2W images. Imaging is insensitive to the

more common diffuse microscopic involvement seen in both HD and

NHL. Diffuse hepatomegaly is strongly suggestive of liver involvement.

Spleen

• The spleen is involved in 30-40% of patients with HD, usually with

coexistent supradiaphragmatic disease. In 10%, it may be the only

infradiaphragmatic site of disease.

• Splenomegaly, however, is an insensitive indicator of splenic involve-

ment, with 33% of normal-sized spleens found to contain tumour at

laparotomy. Splenic lymphoma may present as a solitary lesion, miliary

splenic nodules or multiple low-attenuation masses on CECT and US.

Optimum CECT scanning of the spleen is in the porto-venous phase of

contrast enhancement. US assessment of splenic involvement is insen-

sitive. Splenic involvement is seen in 40% of patients with NHL.

• Splenomegaly and splenic infarction are more common in NHL than HD.

226

Gastrointestinal tract

•

This is the commonest site of primary extra-nodal lymphoma in NHL.

•

Involvement in HD is very rare.

•

Primary lymphoma usually only affects one site. It develops from

mucosa-associated lymphoid tissue (MALT tumours) and has a bimodal

distribution of under 10 years and between 50 and 60 years.

•

Secondary lymphoma of the GI tract is common, with stomach

involvement being the most common (50%), followed by small bowel

(33%), large bowel (15%) and oesophagus (1%).

•

Almost 50% of patients demonstrate multiorgan abdominal disease.

•

Primary lymphoma of the stomach arises in MALT. It may present as

multiple nodules with central ulceration, a large fungating solitary lesion

or, in 10%, diffuse gastric fold thickening. Diagnosis is best made by

endoscopy but cross-sectional imaging is needed to assess the deep tissue

extent, extra-gastric nodal involvement and multiorgan disease.

•

Small bowel:

• Lymphoma accounts for 50% of all small-bowel tumours and usually

affects the terminal ileum.

• Patients with AIDS are particularly prone to disease in this region.

Multifocal disease is present in up to half.

• As the lymphoma develops and destroys the layers of the bowel,

involved areas initially produce mural thickening, leading to subse-

quent wall destruction, with segments of alternating constriction and

dilatation.

• Less commonly, involvement remains submucosal, leading to polyp

formation and intussusception. Indeed, lymphoma is the commonest

cause of intussusception in children after infancy.

• T-cell lymphoma associated with gluten-sensitive enteropathy and

,-chain disease affects the proximal small bowel and may lead to

bowel perforation.

• The small intestine may also be affected secondary to direct extension

from mesenteric adenopathy, leading to encasement and displace-

ment of affected bowel loops, peritoneal enhancement and occasion-

ally ascites in advanced disease, which may be indistinguishable from

peritoneal carcinomatosis.

•

Colon: primary lymphoma of the large bowel is rare (0.05% of all

colonic neoplasms) and usually affects the rectum and caecum, together

with terminal ileum, and may present as a large mass indistinguishable

from colonic carcinoma. Secondary involvement is more diffuse or

segmental.

•

Oesophagus: involvement is very unusual and when present involves

the distal oesophagus resulting in a typically smooth tapered

oesophagus.

228

(A)

(B)

Renal lymphoma before (A) and after (B) treatment. Large hypodense

masses expanding the right kidney prior to treatment, with significant

reduction in volume of the lesions post-treatment.

Pancreas

• Primary pancreatic lymphoma is responsible for just over 1% of pan-

creatic neoplasms and is more common in NHL than HD.

• A large pancreatic mass, with only mild pancreatic duct and common

bile duct obstruction, associated with retroperitoneal nodal involve-

ment is highly suspicious of lymphoma.

Genitourinary tract

• Although rarely involved in early disease, involvement rises to 50% in

advanced lymphoma.

• The testicle is most commonly involved, followed by kidney and

perirenal space. Involvement of the prostate, bladder, uterus, vagina

and ovaries is documented but rare.

• Testicular lymphoma is the commonest form of testicular neoplasm in

patients over 60 years.

• It is found in 1% of men with NHL, almost never in HD. Many cases are

clinically silent and the testis is an important site of residual disease

following treatment at other sites (similar to CNS disease). US demon-

strates non-specific findings of focal areas of hypoechogenicity or diffuse

decreased testicular echogenicity. It is bilateral in over 20% of patients.

229

•

Renal involvement is a relatively late event, with disease remaining

clinically silent in many patients.

•

Renal function usually remains normal and in 90% is caused by high-

grade NHL.

•

Involvement usually produces multiple intrarenal masses (60%). On

CT, these show typical density reversal patterns on both NECT and

CECT. In 10-20%, a solitary mass, indistinguishable from carcinoma, is

noted.

•

Renal involvement occurs in the absence of retroperitoneal adenopathy

in over half of those affected. Direct infiltration of the kidneys from the

retroperitoneum via the renal hilum is the second commonest mode of

involvement.

•

A soft tissue mass in the perirenal space is also commonly seen, encasing

the kidney without apparently invading it.

•

Diffuse renal involvement and subsequent enlargement and patchy

non-enhancement are less commonly seen.

•

Secondary involvement of the bladder is found in 10-15% of patients:

on CT and MRI this appears either as diffuse widespread bladder wall

thickening or as a large nodular mass. Both of these are indistinguishable

from transitional cell carcinoma and result in haematuria.

•

Primary bladder lymphoma is a MALT type and is more common in

women with a history of cystitis, presenting as solitary or multiple sessile

masses.

•

Involvement of the prostate is usually diffuse, with direct extension

from pelvic side wall nodes, in advanced disease, being the most common

form.

•

Female genital tract involvement in advanced lymphoma is common,

though primary involvement is rare (1% of extra-nodal NHL).

•

Most cases involve postmenopausal women, presenting with postme-

nopausal bleeding. Lymphoma may affect the cervix or uterine body,

where it produces diffuse enlargement with homogeneous signal return

or enhancement. Characteristically, the uterine mucosa is uninvolved

and the low-signal-intensity junctional zone, seen on MRI, remains

intact.

•

Ovarian lymphoma is rare but carries a poor prognosis because of the

advanced stage of disease at this point. Lesions are characteristically

bilateral and show homogeneous enhancement without haemorrhage,

necrosis or calcification.

Adrenal glands

• Primary involvement is rare; however in diffuse lymphoma, secondary

involvement occurs in 4% as assessed on CT, and in 24% of postmortem

examinations.

• Occurs more commonly with NHL than HD.

230

Bilateral adrenal lymphoma in a patient with HIV. The coronal T2W

MRI demonstrates large, heterogeneous, faintly hyperintense adrenal

masses (arrows). Following the administration of gadolinium (Post Gad),

only minimal enhancement is demonstrated (arrowhead).

• Bilateral involvement is seen in 50% of patients.

• Usually characterized as an area of low signal intensity on T1W images

and as an area of heterogeneous high signal intensity on T2W images,

with minimal progressive enhancement after contrast.

New developments

• The recent introduction of¹⁸F-FDG PET-CT has contributed signifi-

cantly to the detection and assessment of lymphoma.

• Cross-sectional imaging (CT, MRI and US) depends on the detection

of abnormalities in size, appearance and enhancement for the diagnosis

of organ involvement in lymphoma.

• Lymphomatous involvement often does not lead to anatomical changes

on imaging.

• This is particularly important in the assessment of post-treatment poten-

tial residual/recurrent disease. Functional imaging with¹⁸F-FDG PET-

CT enables a semiquantitative assessment of functionally abnormal

tissue and has become increasingly central to imaging in lymphoma.

231

Omental secondary deposits

Clinical characteristics

• The omentum is a fold of visceral peritoneum related to the stomach

and transverse colon, containing a large amount of fat and a rich vascular

network.

• Secondary neoplasms of the omentum are more common than primary

neoplasms. Ovarian carcinoma is the most common primary neoplasm

metastasising to omentum.

• Spread is either direct along the transverse mesocolon, the gastrosplenic

or gastrocolic ligaments or via peritoneal or haematogenous spread.

• The patient may be asymptomatic but there may be indicators of

progression of their underlying malignancy, with rising levels of tumour

markers.

Radiological features

• Omental deposits are visible on both US and CT. They may be detected

earlier on CT as irregular soft tissue density in the omental fat.

• In more advanced disease, the deposits range from discrete nodules to

confluent solid masses known as omental cakes. These may enhance.

Additional peritoneal deposits may be seen.

• MRI using gadolinium enhancement with fat suppression is also sensi-

tive for omental and peritoneal secondaries; the deposits show as

enhancing soft tissue lesions against the background of the dark sup-

pressed fat.

232

Pancreatic carcinoma

Clinical characteristics

•

Subtypes include carcinoma arising from ductal elements (ductal carci-

noma), carcinoma arising from the glandular elements (pancreatic acinar

carcinoma), tumours arising from the endocrine component of the

pancreas (islet cell cancer, glucagonoma, gastrinoma, VIPoma, soma-

tostatinoma and non-functioning islet cell tumour). Metastases to the

pancreas occur but are uncommon.

•

This discussion will focus on pancreatic ductal carcinoma.

•

Ductal carcinoma accounts for 80-90% of non-endocrine pancreatic

cancer and is the fifth leading cause of cancer death in Western countries.

•

There is increased risk with alcohol abuse, diabetes, heredity and

African ancestry.

•

A number of oncogene mutations have been identified including p53

and k-ras mutations, as well as overexpression of growth factors such as

epidermal growth factor and transforming growth factor.

•

There is an increasing incidence with age, ductal carcinoma being most

common in the 7th decade.

•

Over 50% of lesions are located in the head, 25% in the body and

approximately 10% in the tail.

•

Spread is through the pancreas into adjacent structures, with local

nodal and subsequent metastases to liver (30%), lungs, pleura and

bone. Peritoneal carcinomatosis with ascites occurs in up to 10% of

patients.

•

Local extension is predominantly posterior, involving visceral vessels

and the retroperitoneum. Extension anteriorly or laterally into the

splenic hilum also occurs.

•

Local extension may result in a tumour mass involving pancreas, duo-

denum, porta hepatis, spleen, stomach, root of small-bowel mesentery

and particularly the left adrenal gland.

•

In 85% of patients presenting with ductal adenocarcinoma, there will be

extra-pancreatic extension at the time of presentation and the carci-

noma is incurable.

•

At presentation, 40% have lymph node metastases, 50% have hepatic

metastases and 35% have peritoneal implants.

•

Median survival is 12-18 months. It has the worst 5-year survival of

more than 60 human malignancies.

•

Clinical features depend on the extent of disease and the site of origin.

•

In general, tumours in the head produce earlier symptoms than more

distal tumours, because of early involvement of the common bile duct as

it passes through the head of the pancreas to empty into the second part

234

of the duodenum.

thrombophlebitis and thrombosis (direct extension into vein or para-

neoplastic syndrome ), diabetes (destruction of islet cells by tumour) and

fatigue, malaise and weight loss (pancreatic insufficiency and paraneo-

plastic disease).

Radiological features

•

The goals of imaging include accurate preoperative staging to identify

the small proportion of patients where curative pancreaticoduodenec-

tomy may be considered, and to diagnose mimics of ductal adenocarci-

noma that have a significantly better prognosis.

•

In patients with obvious extra-pancreatic extension (where curative

surgery is not possible), CT- or US-guided fine needle aspiration is

standard procedure to confirm imaging diagnosis. In small tumours,

endoscopic US-guided fine needle aspiration can be used to improve

diagnostic yield.

•

In general, MRI and CECT are the most widely used modalities for

imaging and are roughly equivalent in their accuracy for tumour iden-

tification, local staging and identification of distant metastases.

•

The role of¹⁸F-FDG PET is evolving and it may become more useful in

the differentiation of benign and malignant lesions, and the identifica-

tion of distant metastases.

•

Pancreatic ductal carcinomas are relatively avascular compared with

normal pancreatic tissue, while islet cell tumours are hypervascular.

These features are utilised by subsequent imaging techniques.

•

Patient preparation for CECT includes distension of stomach and

duodenum with 1000ml of water orally. Initial NECT of target area

is followed by a late arterial phase scan. This arterial phase improves

visualisation of ductal carcinoma through its relative hypoattenuation, a

result of its relatively hypovascular nature, compared with the normal

pancreatic tissue.

•

This phase also enhances visualisation of small hepatic metastases by

showing ring enhancement.

•

Islet cell tumours, which are hypervascular, readily show up against

pancreatic tissue during arterial phase.

•

Venous phase scanning at 70s serves to confirm liver metastases, portal

venous occlusion and venous collaterals in portal obstruction.

•

Curved planar reconstructions through the pancreas can demonstrate

the pancreatic duct, common bile duct and peripancreatic vasculature.

Of particular importance is involvement of the superior mesenteric

vasculature.

•

Arterial encasement by tumour is an absolute contraindication to sur-

gical resection.

•

Obliteration of fat planes around

50% of the circumference of a

vessel on both MRI and CECT is reliable in predicting vascular

236

involvement.

Carcinoma of the head of pancreas. Ill-defined mass replacing the

head of pancreas (arrow) seen on CECT, with extension into the adjacent

body and invasion of the second part of duodenum.

Pancreatic mucinous cystadenocarcinoma. Large, faintly septated,

cystic neoplasm (asterisk) effacing the body and tail of pancreas.

• Involvement of the portal venous system is controversial, with some

surgeons still opting for attempted curative surgery.

• Most tumours (except uncinate process tumours) lead to eventual

involvement and obstruction of the common bile duct. Tumours in

the head and uncinate process typically infiltrate along the superior

mesenteric artery and root of small-bowel mesentery, while tumours

within the tail extend into splenic hilar structures and coeliac and

hepatic vessels.

• Direct extension into bowel wall is often visualised as an infiltrating

hypovascular mass involving the strongly enhancing bowel wall.

237

•

Assessment of nodal involvement is difficult. Pancreatic carcinoma

drains to peripancreatic nodes, then to nodes in the porta hepatis and

root of small-bowel mesentery, and finally to peri-aortic and distal

superior mesenteric nodes. Nodes >1cm are considered involved.

However, there is a high propensity for micrometastases in pancreatic

carcinoma, with no subsequent nodal enlargement. In addition, reactive

adenopathy following coexistent pancreatitis or instrumentation

(ERCP) is common, and nodal evaluation by CT is poor.

•

Metastases to liver and peritoneal surfaces are the most frequently

observed intra-abdominal sites. Small hepatic metastases are detected

during late arterial enhancement by ring enhancement. Peritoneal

thickening, nodules and ascites are indications of peritoneal

involvement.

•

Fast MR techniques, such as echo planar imaging and three-dimensional

volumetric breath holding, have established MR as a CT equivalent tool

for initial diagnosis and staging. The most useful sequence is contrast-

enhanced T1W breath-hold gradient echo sequences. MRCP is useful

for visualising the pancreatic duct or common bile duct obstruction or

involvement.

•

Pancreatic ductal carcinoma generally has a lower signal intensity than

normal pancreatic tissue, particularly with fat-suppression techniques.

T2W images are utilised for detection of hepatic metastases, showing

little contrast difference within the pancreas itself. Fast spin-echo tech-

niques are utilised for pancreatic visualisation owing to their rapid

acquisition and gadolinium-enhanced T1W echo gradient sequences

are used to map vascular invasion.

•

Endoscopic US plays a useful role in local staging when there is no

CECT or MRI evidence of distant metastases. Carcinoma is typically

hypoechoic on US and ductal obstruction distal to the lesion is readily

visualised on endoscopic US. Where tumour is unresectable, a defini-

tive tissue diagnosis may be obtained by endoscopic US-guided fine

needle aspiration.

•

Use of¹⁸F-FDG PET is sensitive and specific for pancreatic malignancy,

with sensitivity of 88% and specificity of 83%. It is useful in differ-

entiating benign from malignant lesions, confirming possible liver and

peritoneal metastases as identified on CECT or MRI, and is useful in

the follow-up of patients in the context of a rising carbohydrate

antigen 19-9 (CA19-9) serology.

•

Upper GI tract contrast studies are currently less utilised for diagnosis

and generally are performed in the context of postsurgical or palliative

management. However, on occasion, they may be the first indicator of

pancreatic malignancy, which may be demonstrated as an irregular or

smooth nodular mass, in the case of an ampullary lesion, or spiculation

and traction of the duodenum, in the case of local extension from a head

or body cancer. Extrinsic indentation of the ampulla of the duodenum

may be seen.

238

Pancreatitis

Clinical characteristics

• Classified as acute and chronic.

• Alcohol and cholelithiasis account for 60-70% of cases.

• Cholelithiasis responsible for 75% of cases of acute pancreatitis.

• Alcohol responsible for 70% of chronic pancreatitis cases.

• In

20-30% less common causes are involved, including metabolic

disorders (often with hypercalcaemia and/or hyperlipidaemia as com-

mon factors), multiple myeloma, amyloidosis and sarcoidosis.

• Hereditary pancreatitis is an autosomal dominant disorder producing

early-onset recurrent pancreatitis, with 20-40% developing pancreatic

carcinoma.

• Other causes include trauma, surgery, viral infections, such as measles

and mononucleosis, parasites, structural abnormalities, such as pancreas

divisum, and drugs such as steroids and thiazide diuretics.

• Up to 20% of cases are idiopathic.

• Complications include:

• pancreatic necrosis.

• acute peripancreatic fluid collections (phlegmon).

• pseudocyst formation.

• pancreatic abscess.

Clinical presentation

• Mild acute pancreatitis presents with epigastric abdominal pain, often

radiating through to the back, associated with nausea, vomiting and

general malaise.

• Occasionally progresses to acute severe pancreatitis, with profound

systemic upset including shock, adult respiratory distress syndrome

(ARDS) and multiorgan failure, flank ecchymosis (Grey-Turner sign)

and peri-umbilical ecchymosis (Cullen sign).

• Chronic pancreatitis presents with chronic intermittent abdominal pain

and symptoms and signs of pancreatic insufficiency, including malab-

sorption, diabetes mellitus and occasionally obstructive jaundice.

• Patients may also present with complications of acute pancreatitis, such

as jaundice from oedema of the common bile duct or calculi, pain and

upper GI obstructive symptoms (from pseudocyst formation) and dia-

betes from islet cell destruction.

240

Pancreatitis. Sentinel loops in the left upper quadrant (asterisks)

secondary to pancreatitis.

Acute pancreatitis

Radiological features

• AXR:

•

‘Sentinel loop’ - localised segment of gas-filled small bowel caused by

peritonism - is typically seen in the upper abdomen.

•

‘Colon cutoff sign’: dilated transverse colon with abrupt change to a

gasless descending colon, caused by local inflammation resulting in

spasm of the splenic flexure.

• Mottled appearance of pancreatic region owing to fat necrosis.

• Gas-less abdomen: multiple loops of fluid-filled bowel.

• Ascites.

• Intrapancreatic gas bubbles caused by necrosis and abscess formation.

• Gallstones may be identified if calcified.

• None of these findings is specific and usually CT and/or US are more

helpful.

• CXR:

• Left-sided pleural effusion.

• Left-sided hemidiaphragmatic elevation.

• Left-sided basal atelectasis.

241

• Pulmonary oedema or infiltrates in ARDS.

• Occasionally a pericardial effusion complicates pancreatitis.

• None of these findings are specific.

•

USS:

• Hypoechoic enlarged gland, caused by diffuse oedema.

• The pancreatic duct may be dilated (not normally seen in the normal

gland).

• Complications of acute pancreatitis (vide infra).

•

Barium meal and follow through:

• Enlarged tortuous rugal folds.

• Widening of retrogastric space (from pancreatic enlargement/inflam-

mation in lesser sac).

• Diminished duodenal peristalsis from surrounding inflammation.

• Oedematous swelling of papilla of Vater: Poppel sign.

• These studies have been largely superseded by CT and US.

•

CECT:

• Normal appearance of pancreas in nearly 30%.

• Enlarged and indistinct gland as a result of oedema.

• Thickening of anterior pararenal fascia.

• Hyperdense intrapancreatic portion can represent haemorrhagic

pancreatitis.

• Hypodense intrapancreatic portion may be seen, representing

phlegmonous pancreatitis.

• Non-enhancing areas indicate necrotic pancreatitis.

•

MRI:

• Inflammatory change in the peripancreatic fat is well demonstrated

on T2W fat-saturated images. Areas of non-enhancement indicate

necrosis.

• MRI is generally used to investigate possible aetiologies, using

MRCP to demonstrate gallstones not identified on US or CT.

Chronic pancreatitis

Radiological features

• AXR: multiple irregular pancreatic calcifications are virtually patho-

gnomonic. More commonly seen in alcohol-related disease.

• USS:

• Atrophic, bright pancreas, often with focal or extensive irregular duct

dilatation.

• Intraductal calcifications.

• Less commonly focal or diffuse glandular enlargement, mainly caused

by mild biliary duct dilatation.

242

• CT (pre- and postcontrast):

• Similar findings to those with US.

• NECT is excellent for demonstrating minimal degrees of pancreatic

calcification.

• CECT allows further characterisation of necrotic areas or intra/peri-

pancreatic fluid collections.

• Allows assessment of regional damage caused by recurrent inflamma-

tion (e.g. damage to the duodenum).

• MRI:

• Loss of signal intensity on T1W fat-suppressed images results from loss

of aqueous protein from pancreatic acini owing to fibrosis.

• Suboptimal contrast enhancement on post-gadolinium T1W images

results from destruction of the vascular tree by fibrosis.

• Cholangiopancreatography:

• Increasing use of MRCP has to a degree supplanted the use of ERCP.

• Key finding is irregular dilatation of pancreatic duct (grade I-III).

• Ranges from slight duct ectasia to beading of main duct with intra-

ductal protein plugs.

• Filling defects may represent calculi.

Complications of pancreatitis

Pancreatic necrosis

• Release of proteolytic and procoagulant enzymes within the pancreas

leads to diffuse necrosis.

• CECT is 90% accurate for diagnosis, demonstrating non-enhancement

of necrotic tissue.

• Often associated with other complications, for example ARDS, wide-

spread fat necrosis.

• Prognosis depends on degree of necrosis, rising to 50% mortality with

90% glandular necrosis.

Infected pancreatic necrosis

• Necrotic pancreatic tissue that becomes infected.

• May occur at any time following pancreatitis.

• CECT: gas-forming organisms produce pockets of gas within non-

enhancing necrotic pancreatic tissue.

• Open surgical debridement and drainage required.

• Prognosis worse than for pancreatic abscess.

244

Acute fluid collections (phlegmon)

• Collections of enzyme-rich fluid anterior to pancreas.

• Occurs in ~40% of patients with acute pancreatitis.

• Usually anterior and peripheral to gland.

• No fibrous capsule, as opposed to pseudocyst formation.

• Because of the proteolytic nature of the fluid, the collection can readily

spread into the mediastinum, pararenal fascia and neighbouring organs

(e.g. liver and spleen).

• Resolution is spontaneous in 50% and only requires serial follow-up.

• In the other 50% pseudocysts develop or complications of superadded

infection or haemorrhage occur.

• Often only distinguishing factor from pseudocyst is resolution on serial

imaging.

• On CECT, the collection presents as a hypodense area of water density

(<10HU) within the pancreatic bed, which may persist for months.

Pancreatic pseudocyst

•

A collection of pancreatic fluid that is encysted in a fibrous wall.

•

Occurs approximately 1 month after the acute onset of pancreatitis.

•

Usually oval or round in configuration.

•

Two-thirds are located within the pancreas itself but can occasionally be

intraperitoneal, retroperitoneal, intraparenchymal or mediastinal.

•

Caused by microperforation of the pancreatic duct, leading to an

encapsulated collection of fluid and enzymes.

•

Follows acute pancreatitis in up to 10% of patients. May also been seen

in those with chronic pancreatitis.

•

Usually sterile but may become secondarily infected, leading to abscess

formation.

•

Of pseudocysts, 50% resolve spontaneously and pose no problems, 20%

are stable and 30% lead to complications including:

• severe haemorrhage caused by erosion into superior mesenteric

vessels.

• splenic vein thrombosis from adjacent inflammation and pressure.

• peritonitis caused by rupture into the peritoneal cavity, lesser or

greater sac.

• dissection into adjacent organs such as liver, spleen or posterior wall of

stomach.

• pressure obstruction of duodenum or common bile duct, leading to

jaundice and cholangitis.

• superadded infection.

• increasing size through communication with pancreatic duct or

haemorrhage and osmosis.

246

Chronic pancreatitis with pseudocyst formation. Multiple

peripancreatic pseudocysts (asterisks). Note the pancreatic calcification

typical of chronic pancreatitis.

• AXR:

• Indentation of posterior stomach wall by cyst.

• Indirect evidence of pancreatic mass (e.g. displacement of the splenic

flexure, downward displacement of duodenojejunal junction.

• Gastric outlet obstruction.

• Not sensitive or specific.

• USS:

• Usually a unilocular single hypoechoic cyst is seen in relation to

pancreas.

• Multilocular in under 10%.

• May contain internal echoes owing to debris, haemorrhage, cellular

debris.

• CECT: fluid-filled peripancreatic cyst of 0-30HU attenuation.

• ERCP: communication with pancreatic duct in 70%.

Pancreatic abscess

• Fluid collection, often in relation to the pancreas, containing bacteria

and pus.

• Usually occurs 4 weeks after acute pancreatitis.

• Enhancement of abscess capsule on CECT.

• Managed by percutaneous drainage.

247

Portal vein thrombosis

• In the majority of cases, no cause for portal vein thrombosis is evident, in

spite of extensive investigation.

• More common in children and young adults.

• Secondary causes include:

• trauma: accidental, intraoperative or following umbilical vein

cannulation.

• tumour invasion, typically in hepatocellular carcinoma, cholangio-

carcinoma and pancreatic carcinoma.

• blood dyscrasias leading to hypercoagulable states, such as sickle cell

disease and severe dehydration (again more common in children).

• intra-abdominal sepsis.

• cirrhosis and portal hypertension, presumably owing to altered hae-

modynamics and venous stasis.

• May be isolated with relatively few effects or may result in:

• portal hypertension, with its associated complications.

• extension of thrombosis into mesenteric vessels, with subsequent

small-bowel infarction.

• hepatic infarction: two-thirds of the hepatic blood flow is derived

from the portal vein.

Clinical characteristics

• Most commonly seen in children.

• Hepatic encephalopathy as a result of diversion of portal blood through

the systemic circulation.

• Abdominal pain.

• Haematemesis secondary to oesophageal varices.

Radiological features

• AXR:

• Shows hepatosplenomegaly.

• Not very sensitive.

248

•

USS:

• Best imaging modality for screening in high-risk cases (lack of radi-

ation is especially useful in the younger target age group).

• Portal thrombosis appears as intraluminal material, of variable echo-

genicity, in an enlarged portal vein.

• Presence of portal hypertension can be confirmed by direct Doppler

interrogation of the portal vein and presence of porto-systemic col-

laterals and ascites.

• Decrease in hepatic arterial resistive index - a value of <0.5 is highly

suggestive - as a result of a partial compensatory increase in arterial

flow. This may be helpful in differentiating acute from chronic portal

vein thrombosis, as a fall in the index is not seen in the chronic

condition or in non-occlusive thrombosis (e.g. malignant thrombus).

• Cavernous transformation may be evident in subacute or chronic

thrombosis: a thrombosed extrahepatic portal vein is seen, with

multiple cavernous channels at the porta hepatis.

•

CT: typical appearances of intraluminal thrombosis:

• hyperdense thrombus on non-enhancing CT.

• hypodense filling defect surrounded by contrast on CECT.

•

MRI:

• Collaterals appear as multiple tubular flow voids.

• Portal vein thrombus is bright on T1W images.

•

Angiography:

• Thrombus appears as a filling defect on mesenteric venography.

• Tumour thrombus may appear as streaky contrast-filled vessels within

the thrombus-filling defect.

250

Portal venous gas

•

Bacterial overgrowth and invasion of the colonic submucosal venous

plexus can lead to gas in the portal system. This results in portal venous

flow carrying gas to the liver.

•

In the adult, it is usually a result of bowel wall infarction and impending

gangrene, and carries a very poor prognosis. Often a pre-terminal event.

•

The aetiology usually involves intestinal necrosis from a variety of

causes. The most common include:

• arterial or venous occlusion leading to bowel infarction.

• any severe inflammatory colonic condition such as severe UC, severe

diverticular disease or intra-abdominal abscess.

• severe necrotising pancreatitis can also result in portal gas from sub-

sequent adjacent colonic inflammation.

• necrotising enterocolitis.

• perforated peptic ulceration.

•

In children, often accompanies bowel obstruction, most commonly

from some form of congenital atresia such as oesophageal or duodenal

atresia.

•

Also seen in relation to umbilical vein catheterisation in sick neonates.

•

A relatively common finding in neonatal necrotising enterocolitis,

where, in contrast to adults, it does not carry the same poor prognosis.

•

Other, less-common, causes include iatrogenic injection of gas during

colonoscopy, air embolism during barium enema procedures, pneumo-

nia and diabetes.

Clinical characteristics

• There are no distinct clinical features.

• Often just part of the picture in a severely ill adult or neonate.

• Its significance is as an indicator of severe sepsis or bowel infarction.

• It is a worse prognostic sign in adults than in neonates.

Radiological features

• AXR:

• Often a subtle finding, which may be transient, especially in neonates

with necrotising enterocolitis.

• Typically presents as peripheral hepatic branching linear lucencies.

• Gas may occasionally be seen in the intestinal wall (pneumatosis

intestinalis) and less commonly in the mesenteric vessels themselves.

252

• USS:

• Gas in the portal venules within the liver produces intensely echo-

genic foci, often described as a ‘snow storm’ appearance.

• Doppler US reveals sharp bidirectional spikes superimposed on the

normal portal vein signal, caused by almost total reflection of sound

waves from microscopic portal gas bubbles.

• CT:

• Both NECT and CECT are exceptionally sensitive to the presence

of air.

• Portal vein gas is often difficult to distinguish from pneumobilia. In

gas within the intrahepatic bile ducts, the gas is often seen in a more

central position within the liver. This is presumably because of the

central flow direction of bile, carrying gas bubbles towards the porta

hepatis, whereas the portal flow carries the gas towards the periphery

of the liver.

254

Portal venous hypertension

•

Defined as a portal venous pressure of more than 5-10mmHg.

•

Almost always caused by increased portal venous resistance.

•

Site of resistance may be pre-, intra- or post-hepatic.

•

Prehepatic causes include portal venous thrombosis and portal venous

compression from tumour, lymphadenopathy or pancreatic masses

including a pseudocyst.

•

Intrahepatic causes include obstruction at the pre-sinusoidal, sinusoidal

and post-sinusoidal levels:

• pre-sinusoidal: congenital hepatic fibrosis, idiopathic non-cirrhotic

fibrosis, primary biliary cirrhosis.

• sinusoidal: hepatitis, sickle cell disease.

• post-sinusoidal: cirrhosis and veno-occlusive hepatic disease.

•

Post-hepatic causes are increased resistance to hepatic venous outflow, as

in congestive heart failure, constrictive pericarditis and Budd-Chiari

syndrome.

•

The most common cause world wide is schistosomiasis. In Western

countries, it is probably alcohol-induced cirrhosis, followed by hepatitis

C-induced cirrhosis.

•

Less-common causes include hyperdynamic flow states through the

portal venous system. These are mainly caused by abnormal vascular

channels in either hepatocellular carcinoma, or congenital arteriovenous

fistulae in conditions such as Osler-Weber-Rendu syndrome or trau-

matic arteriovenous fistula formation.

•

Whatever the underlying aetiology, elevated portal venous pressure

leads to diversion of GI venous return from the portal system to the

systemic circulation via porto-systemic collateral vessels.

•

Porto-systemic collateral vessels include:

• Coronary vein to azygos or hemi-azygos system via lower oesopha-

geal veins.

• Superior and inferior mesenteric veins to iliac veins via mesenteric

varices.

• Para-umbilical and omental veins to superficial veins of chest and

anterior abdominal wall via caput medusae veins.

• Splenic vein to azygos system via gastric fundal veins in gastrosplenic

ligament, producing splenic hilar varices.

• Gastric veins to renal veins via gastro-renal anastomoses.

• Gastric veins to pulmonary veins via gastric and pericardiophrenic

collaterals.

• Inferior mesenteric veins to internal iliac veins via rectal haemorrhoi-

dal veins.

256

• Splenic veins to retroperitoneal venous system via duodenal and

retroperitoneal varices.

• Intrahepatic shunt from portal to hepatic veins.

• Portal venous congestion also produces splenomegaly, ascites and GI

congestion.

Clinical characteristics

• Dilated porto-systemic collaterals (varices), particularly in the lower

oesophagus and lower rectum, are submucosal in position, structurally

weak and easily traumatised, and may undergo torrential haemorrhage.

• Drainage of blood from the GI system, directly into the systemic venous

circulation, bypasses the detoxifying function of the liver and may lead

to hepatic encephalopathy.

• Increased portal pressure produces local GI mucosal congestion, leading

to GI bleeding, malabsorption, splenomegaly and ascites.

• Underlying liver damage potentiates the effects of malabsorption and

haemorrhage.

Radiological features

•

USS:

• Enlarged portal vein (abnormal >13mm diameter).

• Enlarged superior mesenteric and splenic veins (less useful).

• Presence of ascites, splenomegaly, evidence of liver disease such as

cirrhosis or fibrosis.

• Presence of porto-systemic collaterals, especially at the splenic hilum,

falciform ligament, ligamentum teres of liver

(recanalised para-

umbilical veins) and lower gasto-oesophageal varices.

• Important to identify patency of portal and splenic veins as this will

influence management.

• Increased echogenicity and thickening of intrahepatic portal veins.

• Loss of the normal portal venous pressure fluctuation with respiration;

normally portal velocity will increase in expiration.

• Reduction in portal venous velocity, normally 12-30cm s−1.

• Reversal of the normal portal venous flow towards the liver (i.e.

hepatofugal flow).

• Portal hypertension results in an absolute increase in hepatic arterial

flow to the liver. This manifests as a dilated hepatic artery with an

elevated resistive index, >0.78.

•

Angiography:

• Elevated portal pressures (hepatic wedge pressure minus IVC pres-

sure): normal is <5mmHg.

• Portal flow towards the liver and porto-systemic collaterals as seen

with US.

• Corkscrew hepatic arteries are fairly indicative.

258

Radiological management

•

The most serious complications are hepatic encephalopathy and massive

GI haemorrhage from bleeding porto-systemic varices.

•

Management is directed towards halting bleeding and reducing portal

hypertension.

•

Transjugular intrahepatic porto-systemic shunt (TIPS):

• An intrahepatic porto-sytemic shunt to reduce the portal hyperten-

sion is formed under radiological control. The procedure involves:

- percutaneous approach via right internal jugular vein.

- insertion of an expandable metallic stent between the hepatic and

portal veins within the liver substance.

• Shunt surveillance is with US at regular intervals of 3-6 months.

• The shunt and collateral morphology, as well as haemodynamics, are

assessed at each US assessment.

• TIPS is a valuable management tool especially in patients with upper

GI variceal haemorrhage or refractory ascites and hepatorenal

syndrome.

•

Complications of TIPS include shunt obstruction, dislodgement and

hepatic vein stenosis.

•

Operative complications include vascular injury, particularly to the

hepatic artery, subcapsular haematoma or intraperitoneal haemorrhage

and bile duct damage.

•

Although the procedure can lessen portal hypertension, it can worsen

hepatic encephalopathy as it will bypass the detoxifying effect of the

liver.

260

Pyelonephritis

•

Consists of upper urinary tract infection with concomitant pelvicalyceal

and parenchymal inflammation.

•

Subtypes include emphysematous pyelonephritis, tuberculous pyelo-

nephritis and xanthogranulomatous pyelonephritis.

•

Cause is infected urine from lower tract in 80% of adult cases.

•

An underlying anatomical abnormality is responsible for 5%:

• obstruction.

• ureteric or renal calculus.

• urinary stasis or reflux.

•

Produces wedges of infection extending from papillary tip to cortical

surface in patchy distribution, sharply demarcated from adjacent spared

parenchyma.

•

Escherichia coli and Proteus, Klebsiella, Enterobacter and Pseudomonas spp.

responsible for most infections.

•

Haematogenous spread with Gram-positive cocci cause 20%.

•

Far more common in women, probably because they have shorter urethrae.

•

Risk factors include:

• urinary obstruction (e.g. prostatic hypertrophy in adults).

• pelviureteric junction obstruction and posterior urethral valve syn-

drome in children.

• calculi in any age group.

• vesicoureteric reflux in children.

• pregnancy, through hormonal relaxation of ureteral smooth muscle

and pressure effects on the ureters.

• diabetes mellitus.

• instrumentation of urinary tract.

• immunosuppression.

• possibly environmental factors such as dehydration.

•

Medical treatment is usually initiated without any imaging.

•

Indication for imaging in acute situation:

• diabetes mellitus.

• history of renal calculi.

• underlying renal tract abnormality: anatomical (e.g. scarred kidneys)

or functional (e.g. outflow obstruction).

• growth of atypical organisms.

• poor clinical response to appropriate antibiotic treatment.

• frequent recurrences.

• more than one confirmed episode in a male.

•

Management is aimed towards rapid elimination of infecting organism

with use of antibiotics and fluid replacement.

262

• In the case of obstruction, this must be relieved as a matter of urgency

in the presence of infection, if scarring is to be prevented. This may involve

placement of percutaneous nephrostomy or surgical removal of calculi.

• Underlying contributing factors must be dealt with, for example benign

prostatic hypertrophy causing outflow obstruction or calculi.

• Medical contributing factors must be controlled (e.g. optimum blood

glucose control maintained).

Clinical characteristics

• Presents acutely with signs of generalised sepsis such as fever, chills,

leukocytosis.

• Signs of localised infection: flank pain, pyuria and sometimes haematuria,

typically microscopic.

Radiological features

•

Imaging is important to ensure resolution of acute changes and to

exclude anatomical predisposing factors. It is useful in:

• defining underlying contributing factors such as obstruction, calculi,

reflux and previous renal scarring.

• diagnosing complications including renal and perirenal abscesses and

emphysematous pyelonephritis.

• diagnosing late sequelae, for example scarring, reflux and obstruction.

•

Intravenous urogram:

• Renal tract stones ± obstruction may be identified.

• Normal in over 75% of those with acute uncomplicated pyelonephritis.

• Renal enlargement may be seen, but this is poorly sensitive.

• Immediate persistent dense nephrogram is seen, which may be

striated.

• Shows delayed opacification of a collecting system.

• Compression of collecting system occurs from pyramidal oedema.

• In severe disease, the kidney cannot be visualised: the aetiology is

multifactorial, including interstitial oedema, inflammation, vasculitis

and nephron function disruption.

•

USS:

•

Usually normal.

•

When abnormal, most common findings are calculi and evidence of

obstruction:

• enlarged kidney(s)

• decreased echogenicity: either focal or global.

• loss of central sinus echogenicity owing to fat infiltrated with inflam-

matory oedema.

• loss of corticomedullary differentiation.

• mild hydronephrosis and ureteral dilatation.

• perirenal fluid from localised perinephric exudates.

264

• abscesses or collections.

• CT:

• Often normal.

• Localised or generalised renal enlargement identified.

• Wedge areas of hypoattenuating cortex in early contrast phase owing

to hypoperfusion and oedema.

• Poor corticomedullary differentiation.

• Mild pelvicalyceal and ureteral dilatation.

• Thickening of Gerota’s fascia.

• Perirenal stranding, implying perirenal inflammatory changes.

• Persistent enhancement on delayed scans in areas of diminished

enhancement on early phase.

• Calculi may be seen, as may obstruction.

• MRI: wedge-shaped areas of high signal on T1W post-gadolinium

sequences.

• Renal cortical scintigraphy:

• Generalised or focal decreased uptake of tracer

(usually

^99mTc-

labelled DMSA).

• Reflects decreased nephron function.

Complications of pyelonephritis

Abscesses

•

Renal tract abscesses:

• Usually caused by E. coli or Proteus spp.

• Cause is an ascending infection in 80%.

• Cause is haematogenous in 20%; there is a relatively high incidence in

IV drug users, endocarditis, blood sepsis and diabetics.

•

Renal abscess:

• IVU: Focal mass displacing collecting system.

• CECT: non-enhancing low-attenuation intrarenal lesion with enhan-

cing capsule.

• Gas bubbles may be present and are pathognomonic but not invariable.

• Perinephric fat obliteration.

• USS: hypoechoic mass with a thickened wall and septations.

• NM: Localised hot spot on galium-67 imaging.

•

Perinephric abscess:

• Caused by extension of a renal abscess through the renal capsule.

• High incidence in diabetics.

• CT: Focal renal mass extending through capsule on cross-sectional

imaging.

• Occasionally gas in renal fossa.

• AXR: shows loss of psoas muscle margin with ipsilateral scoliosis

caused by localised muscle spasm, concave towards involved side.

266

Xanthogranulomatous pyelonephritis

• Chronic suppurative granulomatous infection in patients with chronic

obstruction.

• Usually patients have underlying diabetes mellitus.

• Characterised by parenchymal destruction and replacement with lipid-

laden macrophages.

• There is diffuse renal involvement in 90%, with 10% being localised.

• Females are more affected than males; 10% seen in diabetics.

• Large or staghorn calculus seen in 75%, but in 25% is caused by non-

calculus obstruction.

• Produces an enlarged non-functioning kidney.

• USS may show dilated calyces, low-echo masses, with internal echoes

replacing the renal parenchyma.

• CECT: the kidney is replaced by multiple non-enhancing low-

attenuation masses. The attenuation value of these masses varies

from −10 to 30HU, depending on the lipid content. Caluli are readily

apparent.

Emphysematous pyelonephritis

• Usually caused by Gram-negative infection in diabetics.

• Ranges from gas in collecting system alone (emphysematous pyelitis),

with a mortality of 20%, to gas in the renal parenchyma and collecting

system (emphysematous pyelonephritis), with a mortality of up to 80%.

• CT: most reliable in these cases and can detect small pockets of air

within the kidney, often extending beyond the capsule and into the

renal vein and retroperitoneum.

• USS:

• May demonstrate echogenic foci within the renal parenchyma and

sinus caused by gas. Occasionally gas in the perinephric space can

obscure the kidney.

• Treatment is with nephrectomy.

268

Renal artery stenosis

Clinical characteristics

•

Renal artery stenosis (RAS) is responsible for up to 4% of cases of

hypertension, rising to one in four patients with resistant hypertension

and half of those with malignant hypertension.

•

Approximately 80% is caused by atherosclerosis; 90% of atherosclerotic

stenoses are in the renal artery trunk, usually within 2cm of its origin.

•

The majority of the remainder results from fibromuscular hyperplasia.

This is the most common cause of elevated blood pressure in children

and young adults and can result in renal insufficiency. This can lead to

beading of the artery through alternating stenoses and aneurysmal

dilatations. It may also cause a smooth, tubular narrowing. These find-

ings can be subtle.

•

Rarer causes include dissection, vasculitis, thromboembolic events and

retroperitoneal fibrosis.

•

Screening for RAS should be considered in:

• severe hypertension in young patients.

• a unilateral atrophic kidney.

• worsening of renal function following use of an angiotensin-converting

enzyme (ACE) inhibitor.

• hypertension with associated renal impairment of unknown aetiology.

• long-standing hypertension that rapidly deteriorates.

• refractory hypertension.

• presence of abdominal bruit and renal impairment and/or hypertension.

• vasculopathies with renal impairment and/or hypertension.

270

Radiological features

•

USS:

• A useful imaging technique in assessing renal impairment and hyper-

tension as it can assess renal size, hydronephrosis, renal scarring and

masses. It is relatively insensitive for detecting RAS as visualising the

renal artery can be difficult in many patients. A further complicating

factor is the common occurrence of multiple renal arteries.

• US usually only helpful in children, very thin adults and in assessing

transplant arteries

(which are more accessible at US than native

arteries).

• US signs of RAS are:

- direct visualisation of the stenosis.

- apeaksystolicvelocityof>150cms−1withadopplerangleof<60°.

- peak renal artery velocity : peak aortic velocity >3.5.

- absent diastolic forward flow.

- spectral broadening, owing to turbulence.

- dampened waveforms: slow upstroke (pulsus tardus) and decreased

amplitude (pulsus parvus).

•

CECT:

• CT angiography using multislice scanners, fine collimation and arte-

rial phase IV enhancement can accurately delineate RAS, but at a

high radiation dose.

• Note that iodinated contrast is nephrotoxic and may cause deterio-

ration in the renal function. Patients should be well hydrated.

•

MR angiography:

• Now the first choice for assessing for RAS, with sensitivities of >95%

and specificities of >90%.

• Although phase contrast and time of flight studies have been used

in the past, generally gadolinium-enhanced MR angiography is now

used.

• Can be limited by the presence of a metallic stent. May have difficulty

assessing small arteries, either accessory vessels or more distal branches.

272

Renal calcification

• Calcification of the renal system may be partial, total, regional, unilateral

or bilateral. It may involve just the kidney, part of the organ, or it may

be widespread and involve the associated ureter, bladder and seminal

vesicles in the male. The causes of calcification are varied but may be

classified according to the pattern of involvement.

• Renal calculi are dealt with in a separate section.

• Calcification caused by regional/local disease may involve either part of

the kidney or the retroperitoneum.

Perirenal retroperitoneal calcification

•

This is usually caused by trauma, infection or neoplasm.

•

Traumatic retroperitoneal haematomas often resorb only partially, leav-

ing an area of dystrophic calcification behind.

•

The most common neoplasms associated with retroperitoneal calcifica-

tion are Wilm’s tumour, neuroblastoma, teratomas and cavernous

haemangioma.

• Wilms’ tumour is the most common solid renal tumour of childhood

and may be bilateral in 10%, arising from nephroblastomatosis. The

tumour is usually large at presentation, arising from the renal cortex

and associated with calcification in about 15%.

• Neuroblastoma is the most common abdominal malignancy in

infancy (cf. Wilms’ tumour, which is more common in childhood).

It arises from neural crest tissue and presents as a large solid mass, often

extending across the midline, encasing the aorta and IVC. It typically

produces fine amorphous or stippled calcification (in 85%).

• Teratomas may occasionally extend to the level of the kidneys. They

characteristically produce distinctive calcified structures such as

teeth, cartilage and even digits. The appearance is radiologically

characteristic.

• Cavernous haemangiomas of the retroperitoneum demonstrate

characteristic calcified phleboliths within their capacious sinusoidal

network.

276

Calcification associated with a distinct

renal mass

•

The differential lies between a renal tumour, cyst, infection or vascular

calcification.

•

A calcified renal mass should always be investigated further as it may be

malignant in up to 75% of cases. The pattern of calcification is also

important. Peripheral calcification is usually non-malignant (20%) and is

usually calcification in a renal cyst. Non-peripheral calcification is

malignant in nearly 90% of occurrences.

•

Renal tumours associated with calcification are Wilms’ tumour in

childhood and renal cell carcinoma in adulthood, where the calcifica-

tion is often non-peripheral.

•

Renal infection with TB often results in calcification of the resulting

abscess (see Tuberculosis). Characteristic calcifications in a lobar distribu-

tion are often seen in end-stage TB: TB autonephrectomy.

•

Pyogenic abscesses rarely calcify.

•

Hydatid disease affects the kidneys in under 5% of patients, but when

present calcifies in over 50%.

•

Renal cysts demonstrate a spectrum of calcification. Simple cysts very

rarely calcify (1%) but intracystic infection or haemorrhage often results

in areas of intracystic calcification. In multiple renal cysts, as in adult

polycystic disease, peripheral egg-shell calcification is common and

much of the kidney becomes replaced by multiple areas of thin egg-

shell calcification.

•

Vascular calcification associated with a mass may result from either RAS

or a renal artery aneurysm, in which case a soft tissue mass is associated

with curvilinear or circular egg-shell calcification.

278

Nephrocalcinosis

• This is renal parenchymal calcification, which may be cortical or medul-

lary in distribution. Overall incidence varies from under 1% to around 5%

of the population and it has a wide spectrum of causes: 95% is medullary

nephrocalcinosis with 5% presenting as cortical nephrocalcinosis.

Cortical nephrocalcinosis

• This presents as peripheral (cortical) calcification with sparing of both

the subcortical renal region and the medullary pyramids, producing

classical ‘tramline’ calcifications.

• On US the involved kidney demonstrates a highly echogenic cortex.

• The most common causes include:

• chronic glomerulonephritis.

• cortical necrosis, most commonly from pregnancy, renovascular

shock, infection and renal toxins such as ethylene glycol ingestion

(antifreeze).

• less common causes include Alport’s syndrome (hereditary nephritis

and deafness), rejected renal transplant and chronic hypercalcaemic

states (congenital, paraneoplastic).

Medullary nephrocalcinosis

• In medullary nephrocalcinosis, calcifications involve the distal convo-

luted tubules within the renal medullary regions.

• AXR: There is stippled calcifications of the medullary pyramids.

• USS: There is corresponding hyperechogenicity of the involved renal

pyramids. The earliest sign may be absence of the relatively hypoechoic

renal medulla.

• The most common causes include:

• hyperparathyroid states, producing chronic hypercalcaemia and

hypercalciuria.

• papillary necrosis (diabetes, cirrhosis, chronic renal obstruction, anal-

gesic abuse and sickle cell disease).

• medullary sponge kidney.

• chronic pyelonephritis.

• other causes of hypercalciuria such as milk alkali syndrome, hyper-

vitaminosis D, renal tubular acidosis, hyperthyroidism, Cushing’s

syndrome, diabetes mellitus and paraneoplastic syndrome.

• causes of hyperoxaluria such as hereditary hyperoxaluria and derange-

ments of bile acid metabolism.

280

Renal developmental anomalies

Horseshoe kidney

• Most common renal fusion anomaly, with an incidence of up to 1%.

• Caused by fusion of lower renal poles in 90% and by upper pole fusion

in 10%.

• Associations include:

• Turner’s syndrome.

• trisomy 18.

• cardiovascular, CNS, anorectal, genitourinary and musculoskeletal

anomalies.

• vesicoureteric reflux.

• pelviureteric junction obstruction with secondary hydronephrosis.

• Complications include renal calculi formation and infection, possibly

caused by urinary stasis.

Radiological features

• May be imaged with US, IVU, CT or MRI.

• Plain AXR may demonstrate absence of normal renal outlines.

• Long axes of the kidneys are medially orientated.

• Kidneys lie more inferiorly than the normal renal position, at L4/5,

lying between the aorta and the inferior mesenteric artery origin.

• The renal pelves point anteriorly.

282

Crossed renal ectopia

• The kidney is located on the opposite side from the insertion of its

ureter into the bladder.

• Usually the kidneys are fused (crossed fused renal ectopia).

• The crossed kidney lies more inferiorly.

• Associations include:

• obstruction.

• calculi.

• hypospadias.

• urethral valves.

Pelvic kidney

• Failure of renal ascent has an incidence of 1:750.

• Often associated with failure of rotation, with the renal pelvis facing

anteriorly.

• Associations include:

• contralateral renal agenesis.

• hydronephrosis due to a high PUJ.

• reflux and hypospadias.

• A common cause of ‘absent’ kidney as seen on USS.

Complete ureteral duplication

(duplex kidney)

• Duplex kidney is caused by two, rather than one, ureteral buds arising

from the mesonephric duct, resulting in ureteral duplication. Up to 40%

are bilateral.

• The lower moiety drains the lower pole and mid-kidney and distally

inserts into the trigone of the bladder. This moiety is prone to vesi-

coureteric reflux, owing to a short ureteral course through the bladder

wall, with an associated risk of secondary chronic pyelonephritis.

Pelviureteric junction obstruction is a further complication.

284

• The upper pole moiety’s ureter has an ectopic distal insertion, more

inferior and medially to the lower pole moiety ureter. In men, the

insertion is always proximal to the external sphincter, so enuresis does

not occur. It can insert into the seminal vesicles, prostatic urethra and

ejaculatory ducts as well as low in the bladder. Men with duplex kidneys

are more at risk of epidymo-orchitis. Women with a duplex system may

have distal insertion below the external sphincter, leading to enuresis.

Sites include the distal urethra, genital tract and rectum.

• In men and women, the upper pole moiety is prone to obstruction

because of its ectopic distal insertion. An increased incidence of uretero-

coele is seen, further increasing the risk of distal obstruction.

Radiological features

• IVU:

• If both moieties are functional, then the ureteric duplication and the

sites of insertion distally will be demonstrated.

• The upper moiety may opacify poorly owing to obstruction. The

associated hydronephrosis may displace the lower moiety calyces

inferiorly - ‘drooping lily sign’.

• The lower pole may demonstrate scarring and atrophy, with secon-

dary loss of function through reflux nephropathy. The lower moiety

ureter may be tortuous and dilated because of reflux.

• USS:

• The kidney may be enlarged.

• Two renal pelves separated by renal parenchyma may be seen.

• Complications such as hydronephrosis or scarring can be identified.

Partial duplex system

• Partial duplex system is a result of a single ureteric bud branching. In

distinction to a full duplex system, there is a single distal ureter and

bladder insertion.

• It can be associated with obstruction of the lower pole pelviureteric

junction.

•

‘Yo-yo’ reflux, when urine refluxes from lower moiety into upper or

visa versa, may occur.

• There is an increased risk of urinary tract infection.

286

Renal agenesis

• If there is failure of induction, the ureteral bud does not lead to

formation of metanephric tissue. This results in a blind-ending ureter.

• In formation failure, the ureteral bud does not form, with resultant

absent trigone, ureter and kidney.

• Bilateral agenesis, Potter’s syndrome, is invariably fatal in the first week

of life owing to associated pulmonary hypoplasia.

• Unilateral agenesis is associated with trisomies, Turner’s syndrome and

Fanconi’s anaemia.

• Renal agenesis is associated with other urogenital tract anomalies. In

men, there may be agenesis or hypoplasia of the gonads and vas defer-

ens. In women, 40% of patients with renal agenesis have uterine or

vaginal anomalies.

288

Renal masses: benign

Simple renal cysts

• The simple cyst is the most common renal mass, possibly caused by

tubular blockage.

• In those aged over 50 years, 50% have simple renal cysts.

• These cysts have no malignant potential.

Radiological features

• USS:

• Rounded outline.

• Smooth, well-defined walls.

• Anechoic contents with through enhancement.

• Accuracy of >90%.

• CT:

• Well-defined, thin walls with no enhancement.

• Fluid density <25HU.

• Accuracy of >90%.

• MRI:

• Well-defined lesion of water signal intensity.

• Low signal on T1W and high on T2W imaging.

• No solid components and no enhancement.

• IVU:

• Smooth displacement or indentation of collection system.

• Well-defined defect identified in the nephrogram.

• Well-defined, non-enhancing exophytic lesion.

• IVU lacks sensitivity and specificity.

Renal sinus cyst (parapelvic cyst)

• Rounded fluid-filled cyst within the renal pelvis, arising from the renal

parenchyma or renal sinus, but not connected to the collecting system.

• Can occasionally cause calyceal obstruction or rarely hydronephrosis.

Usually asymptomatic.

290

Radiological features

• USS: may be mis-diagnosed as hydronephrosis on US.

• On a contrast study, such as an IVU or CT urogram, the lack of contrast

within the parapelvic cyst will differentiate it from hydronephrosis.

• If symptomatic, they can be ablated with an ultrasound guided 95%

alcohol injection.

Atypical cysts

• Simple cysts may have atypical appearance following haemorrhage or

infection.

Radiological features

• USS:

• Rounded lesion but wall may appear thickened.

• Shifting debris seen within cyst.

• Internal septations may be identified.

• CT: increased density

(>25HU) but no enhancement, owing to

increased protein within cyst.

• MRI: the usual signal of a simple cyst, low on T1W and high on T2W,

is altered, with iso- or hyperintensity seen on T1W, as a result of the

increased protein or blood breakdown products. The T2W signal is

usually hyperintense but less so than in a simple cyst.

Adult polycystic kidney disease

Clinical characteristics

• Adult polycystic kidney disease is an autosomal dominant condition that

results in a collagen defect.

• Carrier frequency is 1:1000.

• Associations include:

• berry aneurysms.

• cysts in pancreas, liver and other organs.

• mitral valve prolapse.

• Presentation usually occurs in the 4th or 5th decade.

• Presents with loin masses, renal failure, hypertension, haematuria,

proteinuria and abdominal pain.

• Complications include:

• renal failure.

• cyst haemorrhage, a cause of abdominal pain.

• calculi, often urate.

• increased incidence of renal cell carcinoma.

292

Radiological features

• AXR: not a first-line investigation but may show enlarged renal shad-

ows and curvilinear cyst calcification.

• USS:

• Multiple, bilateral cortical cysts.

• Enlarged kidneys.

• Renal outline is indistinct and as disease develops less cortical paren-

chyma is seen.

• If complicated by haemorrhage, debris may be seen within the cysts.

• IVU:

• Multiple areas of poor opacification on the nephrographic phase.

• Distortion of collecting systems.

• CT and MRI:

• Thinned parenchyma.

• Multiple, thin-walled, cysts. Mural thickening raises possibility of

complicating carcinoma.

• Low attenuation on CT.

• On MRI, they are low signal on T1W and high on T2W imaging.

• Following haemorrhage, cyst attenuation increases on CT. On MRI,

the T1W signal increases and the T2W signal is variable.

Acquired cystic kidney disease

Clinical characteristics

• Chronic renal cysts develop in patients on haemodialysis.

• There is a 90% incidence after 10 years of haemodialysis.

• Complications and associations include:

• haemorrhage into the cysts.

• increased incidence of renal cell carcinomas, with up to 5% of patients

developing these.

Radiological features

• The diagnosis is made by the presence of more than three cysts in a patient

on haemodialysis, without history of inherited cystic renal disease.

• The kidney will usually be atrophic. The cysts are usually <3cm, thin

walled and will have similar appearances to those seen in polycystic

kidney disease, including the findings of intracystic haemorrhage.

• The importance of imaging is to detect developing renal cell carcinomas.

294

Angiomyolipomas

Clinical characteristics

• Angiomyolipoma is a benign renal mesenchymal tumour containing fat,

smooth muscle and thick-walled blood vessels.

• Incidence is up to 3%.

• The vessels do not have a complete elastic layer, predisposing to aneur-

ysms and haemorrhage. If the tumour is greater than >4cm, there is a

60% chance of haemorrhage.

• Angiomyolipoma is sporadic in 80% and associated with tuberose

sclerosis in

20%. There is an association with von Hippel-Lindau

syndrome and neurofibromatosis.

• These tumours are often incidental findings, but if haemorrhage occurs,

they may present with flank pain or haemodynamic shock.

Radiological features

• The presence of fat within a renal lesion is highly suggestive of angio-

myolipoma, although occasionally renal cell carcinoma contains fat, as

do renal lipomas and liposarcomas. All these differentials are rare and

interval follow-up scans should be considered.

• USS: characteristic fat appears as areas of increased echogenicity within

a mass, but this is non-specific as calcification can cause confusion.

• CT: demonstrates variable amounts of fat within the lesion and may

demonstrate the presence of haemorrhage.

• MRI: focal fat with high T1W and T2W signal, that show signal loss on

fat suppression sequences, is characteristic.

296

Oncocytomas

Clinical characteristics

• A well-defined tumour seen from the 3rd decade onwards with a peak

in the 7th.

• Contains oncoctyes and well-differentiated proximal tubular cells.

• Often has central scar.

• Usually asymptomatic and may be discovered incidentally; it can be up

to 10cm in diameter.

• Unfortunately, neither the radiological findings nor needle biopsy can

reliably differentiate oncocytomas from renal cell carcinomas, and

resection is usually necessary.

Radiological features

• USS:

• Well-defined mass, often with a hypoechoic central scar.

• No through enhancement.

• CT:

• Well-defined mass with homogeneous enhancement, but if there is a

central scar this will be seen as a stellate, poorly enhancing region.

• Pseudocapsule may be seen.

• MRI:

• Again a well-defined lesion.

• The pseudocapsule may be seen as a well-defined low-signal rim.

• Shows enhancement, although scar may not enhance if present, with

peripheral washout.

298

Renal masses: malignant

Renal cell carcinoma

Clinical characteristics

• Adenocarcinoma accounts for 85% of renal malignancies.

• However, 30% are incidental findings during imaging.

• Most commonly present in the 6th or 7th decade; rarely occur in

children.

• Presenting features include haematuria, weight loss, fevers, anaemia,

flank pain or an abdominal mass.

• Cystic change may occur through necrosis, involvement of preexisting

cysts or in the cystadenocarcinoma histological subtype.

• Predisposing factors:

• von Hippel-Lindau syndrome is associated with multiple renal cell

carcinomas, in a younger cohort than usually seen.

• smoking.

• haemodialysis (as well as acquired cystic disease of renal failure).

• Metastatic spread includes ‘cannon ball’ lesions to the lungs, secondary

lesions to the liver, adrenal glands and contralateral kidney, lytic skeletal

metastases and hypervascular metastases to the brain.

• Direct spread can occur through the capsule into the perinephric fat and

the liver.

• Tumour may extend along the renal vein and involve the IVC and right

atrium.

Radiological features

• IVU:

• Control film may demonstrate a distorted renal outline and occasional

renal calcification. Skeletal metastases may be evident.

• Following contrast, parenchymal and calyceal distortion may be

evident.

• If there is renal vein obstruction, the affected kidney may not

enhance.

• Generally IVUs are non-specific and, in particular, small tumours may

be indistinguishable from other renal masses, such as simple cysts.

• USS:

• Tumours may be hypoechoic, hyperechoic or isoechoic compared

with renal parenchyma; most are hyperechoic. Cystic areas may be

present.

300

• Well-differentiated tumours may appear well demarcated.

Renal cell carcinoma. IVU shows an ill-defined mass (asterisk)

expanding the upper pole of the right kidney with distortion of the

upper pole calyces.

Renal cell carcinoma. Large solid mass (M), seen by US, is replacing

the upper two thirds of the kidney (K) with tumour extension (arrow)

into IVC (arrowhead).

• Involvement of venous structures (renal vein and IVC) may be seen as

soft tissue distending the vessels.

• US is less sensitive than MRI or CECT.

• CECT:

• A three-phase (precontrast, arterial phase contrast and portal phase

contrast) CT is usually performed.

301

• On precontrast studies, the lesion may be homogeneous if <3cm.

They are of increased density (>20HU) compared with simple cysts.

When >3cm in size, they become increasingly heterogeneous owing

to the increased incidence of necrosis. Tumour calcification may be

seen.

• Following IV contrast, the tumour generally enhances less avidly than

adjacent normal parenchyma, enhancement may be heterogeneous

owing to necrosis and cystic elements.

• The boundary between tumour and normal parenchyma is often ill

defined.

• The delayed phase of the CECT is very accurate at determining

venous involvement; this is seen as low-density filling defects within

the renal vein, surrounded by contrast.

• CECT is first-line investigation for tumour staging. It is effective at

demonstrating local adenopathy and distant metastases. Direct exten-

sion through the capsule into the perinephric space is well

demonstrated.

•

MRI:

• MRI is the most accurate imaging technique for abdominal staging of

renal carcinoma.

• Renal cell carcinomas are generally hypointense compared with renal

parenchyma on T1W and mildly hyperintense on T2W. However,

the difference in the signal characteristics between the tumour and

parenchyma, on an unenhanced scan, may be small; consequently, as

with CECT, three-phase enhancement is required.

• The 85% of tumours that are hypervascular will show heterogeneous

enhancement. Small tumours may demonstrate homogeneous enhance-

ment and may be iso-intense with parenchyma on some phases of

enhancement, hence the need for more than one postcontrast phase.

• The hypovascular carcinomas are usually of the papillary subtype,

are often well defined, and on CT can be mistaken for cysts. MRI

will demonstrate the solid nature of the lesions, and the presence

of subtle areas of enhancement within such lesions is highly

suggestive.

Radiological therapies

• There is a growing interest in the use of radiologically guided percuta-

neous thermal ablation, to debulk or destroy renal cell carcinomas (small

tumours) and for patients not fit for conventional surgery.

• Thermal ablation has been performed using radiofrequency probes,

laser fibres, high-power focused US and cryotherapy. These can be

monitored using CT, US or MRI. MRI has an advantage as changes in

temperature affect the T1W relaxation times, which can be utilised to

make an accurate, real-time thermal map to assess the extent of thermal

injury.

302

Renal lymphoma

Clinical characteristics

• Primary renal lymphoma and Hodgkin’s lymphoma of the kidney are

rare, but secondary renal involvement in NHL is not uncommon,

especially in late disease.

• Spread to the kidneys may be by direct extension or haematogenous.

• Presents with a renal mass, haematuria, weight loss and flank pain, but

many are asymptomatic. May cause renal impairment.

• Other signs of lymphoma, such as splenomegaly, may be seen.

Radiological features

•

Lymphoma is bilateral in 75%.

•

Solitary masses in 20%.

•

There may be renal enlargement owing to diffuse infiltration but the

renal contour is maintained. Renal sinus involvement is common.

•

May be perinephric in position, and a kidney surrounded by tumour

mass, with no compression or renal function loss, is highly suggestive of

lymphoma.

•

Renal vessels that remain patent despite being surrounded by tumour

are also suggestive.

•

USS:

• Focal lymphomatous lesions are generally hypoechoic or anechoic,

but without the through enhancement seen in true cysts.

• Loss of echogenic renal sinus fat is a common finding.

• General hypoechoic renal enlargement.

• Other evidence of abdominal lymphoma may be seen.

•

CT:

• Single or multiple nodules within the kidneys can be identified. They

are of lower density and enhance less avidly than normal renal

parenchyma.

• Other evidence of abdominal or pelvic involvement is seen.

•

MRI: renal lymphoma is hypointense to renal parenchyma on T1W

imaging, and isointense or slightly hypointense on T2W. It shows

relatively poor gadolinium enhancement.

304

Metastases to the kidney

Clinical characteristics

• Usually a feature of advanced malignant disease and usually asympto-

matic. Does not change management.

• May originate in many types of malignancy but common primaries

include lung, breast and GI malignancies.

Radiological features

• Usually bilateral, small, masses in a patient with a known primary.

• May be solitary, especially from colonic carcinoma. Solitary lesions tend

to be more infiltrative and less exophytic than renal cell carcinoma.

• If confirmation of diagnosis is clinically necessary, a needle aspiration

under CT or US guidance can be performed.

Transitional cell carcinonma

See separate section.

306

Renal tract calculi

•

Calculous disease of the renal tract may affect the kidney, ureter or

bladder. It affects men four times as often as women and affects 1-2

per 1000 population in developed countries. The underlying causes are

many, with 70-80% of symptomatic patients having an underlying

metabolic abnormality.

•

Theories as to the pathogenesis include chronically raised levels of

calcium excretion, abnormalities in oxalate, cystine, urate and xanthine

metabolism, urological sepsis and urinary stagnation, and chronic

dehydration.

•

Renal calculi may be clearly visible on plain radiography, or non-

opaque depending on their mineral content and type.

•

Opaque stones include calculi composed of calcium oxalate/phosphate

and magnesium ammonium phosphate/calcium phosphate. Poorly

opaque stones are composed of cystine while uric acid, xanthine and

mucoprotein calculi are non-opaque.

•

Calcium-containing calculi either result from a raised level of serum

calcium, as in hyperparathyroidism, milk alkali syndrome and sarcoido-

sis, or occur with normal levels of calcium, as in urinary obstruction,

infection, renal tubular acidosis and medullary sponge kidney.

•

Similarly, oxalate stones may be associated with primary oxaluria, which

is a rare autosomal recessive condition leading to diffuse nephrocalci-

nosis, vascular calcification, urolithiasis, osteopenia and dense or lucent

bands within the metaphyses. Oxalate stones may also form in the

presence of abnormal bile acid metabolism, as in patients with small

bowel disease, Crohn’s disease or large segment small-bowel resection

at or near the terminal ileum (site of reabsorption of bile salts in the

hepatic-enteric cycle).

•

Uric acid stones may form in the presence of chronically raised serum

urate, as in gout or myeloproliferative disorders (increased cell break-

down and urate metabolism), particularly during treatment of such

conditions. Urate stones may also form in patients with ileostomies or

following chronic dehydration (hot climates). Finally, matrix stones are

seen in chronically infected kidneys.

•

Symptoms, clinical signs and radiological appearances depend to a

degree on whether a renal calculus causes incomplete or complete

obstruction, or does not obstruct the renal tract.

308

Clinical characteristics

• Renal tract calculi may be entirely asymptomatic. When a calculus

causes renal obstruction, this results in severe renal angle pain, typically

colicky in nature, radiating from loin to groin, and associated with

nausea and vomiting.

• Renal calculi predispose to urinary tract infection. The association of

obstruction and infection, unless relieved, rapidly leads to significant

irreversible renal damage and may lead to renal failure.

Radiological features

•

Plain AXR:

• Radiodense stones may be seen on plain films of the involved area. An

important differential within the pelvis is the presence of phleboliths

within pelvic venous plexuses. These may cause diagnostic difficulty,

particularly in the region of the ureterovesical angles. Hydronephrosis

from calculous obstruction may be seen as enlarged soft tissue renal

shadows on plain AXR.

•

IVU:

• IVU is an important investigative tool in suspected calculous disease.

The control film may show radiodensities along the renal tract. After

administration of IV contrast, subtotal obstruction leads to a pro-

longed, delayed, nephrogram and hydronephrosis, the degree of

which depends on the degree of obstruction.

• The site of obstruction may be identified by a standing column of

contrast within the ipsilateral ureter above the level involved.

• In the case of total obstruction, there is, classically, absence of a

nephrogram on the affected side with no contrast seen within the

collecting system.

• Occasionally, in cases of total obstruction, high pressure within the

renal cortex causes extravasation of contrast within the perinephric

tissues.

310

• USS:

• Hydronephrosis is easily identified on US; an important differential is

a parapelvic cyst. US may also identify upper and lower ureteric

dilatation, although it is less accurate at identifying the mid ureter.

• Identification of bilateral ureteric jets of urine is important to exclude

ureteric obstruction. Calculi may be identified within the bladder as

echogenic foci with posterior acoustic shadowing.

• CT:

• NECT is the most accurate method of identifying renal tract calculi;

these are seen as radio-opacities surrounded by a cuff of ureteric

soft tissue. In contrast to other modalities, CT identifies all types of

renal tract calculus, including xanthine- and mucoprotein-containing

calculi.

• CT is particularly useful in identification of small ureteric calculi and

may identify ureteric oedema, perinephric stranding and renal

enlargement.

• Following contrast administration, delayed and decreased cortical

enhancement of the affected kidney reflects altered vascular dynamics,

owing to increased pressure within the distal nephrons.

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Retroperitoneal fibrosis

• Retroperitoneal fibrosis (RPF) is the pathological formation of dense

fibrotic tissue in the retroperiteum, that can lead to complications

involving the vasculature, lymphatics and renal tracts.

• Primary RPF (60%) is:

• probably an autoimmune process, leading to a generalised vasculitis.

• associated with fibrotic changes in other organs in 10%, including:

- fibrosing mediastinitis.

- fibrosing thyroiditis.

- sclerosing cholangitis.

• may respond to steroid treatment.

• Secondary RPF (40%); causes include:

• radiation therapy.

• desmoplastic responses to great vessel aneurysms or neoplasias.

• drugs, including beta-blockers and amphetamines.

• response to retroperitoneal fluid collections.

• connective tissue disorders.

Clinical characteristics

• Non-specific symptoms such as weight loss, nausea, pyrexia and general

malaise.

• Dull pain in the back and abdomen.

• Renal impairment and/or hypertension.

• Lower limb oedema.

• Usually the fibrosis starts at the bifurcation of the aorta and extends

proximally to eventually involve the renal hilum. More rarely, it

extends distally into the pelvis.

314

Radiological features

• IVU:

• Classical triad of features:

- bilateral ectasia of the ureters superior to L4/5 from impaired

peristalsis.

- ureters pulled medially by the fibrotic tissue.

- gradual tapering of the ureters under extrinsic pressure from fibrotic

tissue.

• Generally mild hydronephrosis.

• USS:

• Homogeneous hypoechoic retroperitoneal soft tissue.

• Renal tract dilation may be seen.

• CECT: can show peri-aortic soft tissue, which may enhance if active

inflammation is present.

• MRI:

• Low to medium signal intensity in T1W image.

• May be high intensity in T2W image if there is active inflammation,

and low signal if fibrotic.

• NM: there is uptake of gallium during active inflammation.

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Splenomegaly

•

Abnormally enlarged spleen.

•

Various methods for assessing size. Most radiologists ‘eyeball’ spleen for

size.

•

Inferior tip of spleen extends below the tip of the right lobe of liver.

•

Splenic length is longer than 12cm on transverse diameter.

•

Splenic index is most accurate assessment: multiply the three dimensions

and a value >140cm³ is significant.

•

In children, the spleen is more than 1.25 times the length of adjacent

kidney.

•

Spleen longer than 12-14 cm in superior-inferior dimension in an adult.

•

Diameter of AP spleen more than two-thirds the abdominal diameter.

•

Causes of splenomegaly can be divided according to the degree of sple-

nomegaly they cause.

•

Huge spleen:

• malaria.

• kala azar, leischmaniasis, syphilis.

• extramedullary haemopoiesis (e.g. myelofibrosis).

• chronic myeloid leukaemia.

• lymphoma.

• Gaucher’s disease.

•

Moderately large spleen:

• glycogen storage diseases, Gaucher disease, Neimann-Pick disease.

• haemolytic anaemias, haemochromatosis, sickle cell disease (early on

in sequestration crises).

• portal hypertension, splenic vein thrombosis.

• causes of huge spleen, in less advanced stages.

• leukaemia.

•

Borderline splenomegaly:

• sarcoidosis.

• amyloidosis.

• rheumatoid arthritis (Felty syndrome).

• systemic lupus erythematosus.

• haemodialysis.

• viral infections: hepatitis, glandular fever.

• bacterial infections: brucellosis, typhoid, tuberculosis, generalised

bacterial septicaemia.

• rickettsial infections: typhus.

• fungal infections: histoplasmosis.

•

Neoplasms of the spleen such as secondaries and angiosarcoma generally

replace splenic tissue rather than cause splenomegaly.

•

NB: sickle cell disease causes splenomegaly early on in the disease, followed

318

by auto-splenectomy following infarction, leading to a small spleen.

Splenomegaly in a patient with portal hypertension. The lower

pole of the spleen (arrowheads) clearly extends below the lower costal

margin. Furthermore, there is a generalised ‘haze’ over the abdomen,

caused by ascites, and thickening of valvulae conniventes secondary to

fold oedema.

Clinical characteristics

• Splenomegaly can often be detected on clinical examination, if mod-

erate to large.

• May present with dull LUQ pain.

• Presentation is more often with features of the underlying disease

process.

• If the spleen is very large, presentation can be with obstructive symp-

toms such as gastric obstruction or left renal hydronephrosis.

• An enlarged spleen is also at increased risk of infarction and trauma.

319

Radiological features

•

AXR:

• Enlarged spleen is often seen as large soft tissue density mass in the

LUQ.

• Spleen extends downwards and medially towards centre of abdomen.

• Enlarged spleen may be inferred from displacement of gas-filled small

bowel loops.

• May cause left renal hydronephrosis on IVU.

•

USS:

• Imaging modality of choice in initial confirmation of splenomegaly.

• Usually homogeneous texture on US.

• Coarse spleen, with similar echo properties to liver in haemochro-

matosis.

•

CT and MRI:

• Splenomegaly is easily identified on both CT and MRI, especially if

multiplanar reconstructions are used.

• Early arterial enhancement of spleen leads to patchy contrast

enhancement on CECT and can be mistaken for pathology.

• Associated pathology is often identified, for example portal varices

and cirrhotic liver in portal hypertension or a high-attenuation spleen

on NECT in haemochromatosis (from iron deposition).

320

Testicular neoplasms

•

Testicular neoplasms form 1-2 % of all male cancers.

•

Peak age of occurrence is 25-35 years and it is the most common

malignancy in age group 15-35 years.

•

Risk factors are Caucasian origin, testicular maldescent and positive family

history.

•

Metastases occur to liver, lung, brain and bones. Nodal metastases are

usually unilateral; bilateral in 8%.

•

The contralateral testis is at increased risk of developing a metachronous

tumour.

•

Most (95%) testicular neoplasms are germ cell tumours:

• seminoma (40%): very radiosensitive with a good prognosis.

• embryonal carcinoma (10%): more aggressive than seminomas.

• teratoma (10%): occur in a younger age group (10-20 years) and have

good prognosis.

• choriocarcinoma (1%): most aggressive form.

• mixed tumours: teratocarcinoma is the most common type; may

undergo spontaneous regression.

•

Sex cord-stromal tumours are usually benign and hormonally active.

•

Metastases: common primary sites include prostate, lung, kidney, GI

tract and melanoma. Metastases from prostatic carcinoma account for

75% of bilateral metastases to the testis. Routes of spread include

haematogenous, lymphatic, retrograde extension from the vas deferens

or direct invasion from an adjacent mass.

Clinical characteristics

• Chronic pain, sensation of heaviness.

• Acute scrotal pain in 10%, from intratumoural haemorrhage.

• Enlarging testicular mass.

• Secondary hormonal effects: gynaecomastia, virilisation.

Radiological features

• USS:

• Sensitivity of 95% for the detection of testicular tumours.

• Seminomas tend to be hypoechoic; the remainder are heterogeneous

in echotexture.

• Metastases usually present as multiple, bilateral hypoechoic masses.

• Lymphoma presents as diffuse or multifocal testicular enlargement.

• CECT: used for staging the disease.

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Transitional cell carcinoma

Clinical characteristics

• Approximately 85% of urothelial malignancies are transitional cell car-

cinomas (TCC).

• Risk factors include:

• smoking.

• aniline dyes.

• chronic urinary infection.

• analgesic abuse.

• cyclophosphamide therapy.

• high ingestion of coffee.

• Bladder involvement is much more common than the upper tracts.

• Synchronous and metachronous tumours relatively common.

• Symptoms include haematuria, flank pain and renal colic if obstruction

occurs.

• Spread is most commonly to local lymph nodes, the peritoneum or

liver.

Radiological features

• Because synchronous tumours are relatively common, the entire renal

tract should be investigated radiologically or urologically.

Bladder

Radiological features

• IVU: shows irregular filling defect; may have a sessile appearance.

• CECT and USS: both demonstrate focal mural thickening and

an exophytic mass projecting into the bladder lumen or within a

diverticulum.

• MRI:

• Most accurate for staging of bladder TCC.

• TCC are isointense on T1W sequences and hyperintense on T2W.

• TCC show early enhancement post-gadolinium injection, allowing

accurate assessment of bladder wall involvement.

324

Kidneys

Radiological features

•

IVU:

• Occasionally punctate calcification may be seen on the control film.

• Sessile filling defects can be seen within the collecting systems.

Contrast trapped within the intersitium of a papilliform tumour

gives rise to a stippled appearance.

• Non-opacification of a calyx occurs when obstructed by tumour.

Renal obstruction may be from tumour at the pelviureteric junction.

This may result in renal atrophy.

• Tumour infiltrating the renal parenchyma results in decreased con-

trast excretion, with preservation of the normal renal outline; this is

often not the case in renal cell carcinoma.

•

USS:

• Tumour is usually isoechoic or hyperechoic in comparison with renal

parenchyma.

• Depending on tumour location, calyceal dilatation, with or without

renal pelvis dilatation, may be seen.

• Renal infiltration with preservation of renal outline may be seen.

•

CECT:

• CT urography is an excretory phase CT of the renal tract and is

increasingly replacing IVU. This results in opacification of the pelvi-

calyceal systems and ureters, allowing assessment of filling defects as

in IVU.

• Mass centred on the collecting system shows variable enhancement.

Associated thickening of collecting system wall may be visible.

• There may be punctuate calcification.

• Renal infiltration can be demonstrated.

• CECT is commonly used as a staging study.

•

MRI:

• MR urography, either using heavily T2W images, to utilise the hyper-

intensity of urine, or heavily T1W delayed images, post-gadolinium,

can give similar images to IVU but without ionizing radiation.

• TCC may show heterogeneous gadolinium enhancement, but usu-

ally less than the renal parenchyma.

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Ureters

Radiological features

• IVU:

• Variable number of irregular intraluminal filling defects can be seen.

• Irregular luminal stricturing.

• Variable degrees of obstruction can lead to hydroureter, hydroneph-

rosis or a non-functioning kidney.

• USS: may demonstrate features of renal tract obstruction but the ureter,

particularly the mid ureter, is often poorly visualised using this modality.

• CECT: intraluminal soft tissue mass can be seen. Local extension into

periureteric fat and beyond may be demonstrated.

• MRI: MR urography can again replicate the IVU findings, but addi-

tional sequences are required to stage the tumour.

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Tuberculosis of the abdomen

and pelvis

Clinical characteristics

• Caused by Mycobacterium tuberculosis, an acid-alkali-fast bacillus.

• Infections are most commonly pulmonary, but any organ system in the

body may be affected.

• Increasing incidence in the developed world as a result of increased

immigration from endemic areas and increased numbers of immuno-

compromised individuals.

• Presentation depends on affected organ systems. Commonly, there are

pulmonary symptoms including chronic cough and haemoptysis.

• Non specific symptoms such as weight loss, fevers and night sweats are

characteristic.

• Abdominal symptoms will include the above non-specific signs, with

abdominal pain, nausea and vomiting. Urinary tract involvement man-

ifests as non-specific symptoms as well as dysuria, haematuria and sterile

pyuria.

Abdominal tuberculous lymphadenopathy

Clinical characteristics

• Multiple lymph node groups are affected simultaneously, most com-

monly mesenteric and peri-pancreatic groups.

• The main differential is lymphoma, which does not tend to undergo

necrosis.

Radiological features

• In 40-70% of patients with lymphadenitis, there are enlarged nodes

with hypodense centres and peripheral hyperdense enhancing rims,

characteristic, but not pathognomic, of caseous necrosis.

• Other nodal patterns include conglomerate mixed density masses,

enlarged homogeneous-density nodes, and an increased number (>3)

of normal or mildly enlarged homogeneous nodes.

330

Tuberculous peritonitis

Clinical characteristics

• Usually occurs secondary to haematogenous spread or from the rupture

of a tuberculous lymph node.

Radiological features

• There are three types.

• Wet: most common, featuring large amounts of free loculated fluid

with a high protein density (20-45 HU).

• Fibrotic: large omental and mesenteric cake-like masses with matting

of bowel loops.

• Dry: mesenteric thickening, fibrous adhesions and caseous nodules.

• Varying degrees of omental and mesenteric involvement are seen.

• Omentum appears smudged, caked or thickened in equal frequency.

• CT: findings in TB peritonitis are non-specific, with disseminated

peritoneal malignancy, non-TB peritonitis and mesothelioma as differ-

ential diagnoses.

• One complication is small bowel obstruction, and evidence may be seen

on imaging.

Gastrointestinal tuberculosis

Clinical characteristics

• TB in the GI tract is rare, but when present usually (90%) involves the

ileocaecal region and/or right side of colon. The gastroduodenal

regions are affected less often. The oesophagus is the least common

GI location affected by TB.

Radiological features

• Skip areas of concentric mural thickening with luminal narrowing,

sometimes with proximal dilatation elsewhere in the small bowel, and

in the presence of ileocaecal involvement strongly suggests TB.

• Mucosal ulceration is a common feature. Fistulae may occur.

• CT:

• The most common CT finding is mural thickening, which is mostly

concentric.

• Commonly there is focal mural thickening involving the ileocaecal

valve and medial aspect of the caecum.

• Associated evidence of TB, such as necrotic lymphadenitis, may be seen.

332

• Barium studies:

• The terminal ileum may appear rigid with proximal dilatation. The

valve itself may be enlarged.

• The caecum may appear contracted owing to fibrosis and spasm. The

affected ileal segments tend to be shorter than those in Crohn’s disease

and cobble-stoning is not seen in TB.

• Gastroduodenal TB can result in pyloric stenosis, deep ulceration and

rugal hypertrophy as a result of the infiltration.

• The differential, on barium studies, includes inflammatory bowel

disease, lymphoma, carcinoma or other infections.

Hepatosplenic tuberculosis

Clinical characteristics

• Usually caused by haematogenous spread as part of miliary TB.

• Hepatosplenic involvement is categorised as:

• micronodular or miliary: characterised by innumerable nodules,

diameter 0.5-2.0mm (which may not be detected by CT)

• macronodular: associated with tuberculoma dissemination and very

rare.

Radiological features

• CT:

• When TB is present, CT shows an enlarged liver and spleen contain-

ing multiple non-specific, low-attenuation lesions.

• The presence of calcified granulomata on CT, in the absence of a

known primary tumour, in patients with known risk factors should

raise suspicion of TB. Calcified granulomata may represent old,

healed TB lesions.

334

Adrenal tuberculosis

Clinical characteristics

• Adrenal involvement is seen in up to 6% of patients with active TB.

• These patients almost always present with bilateral adrenal involvement

and an Addisonian type clinical picture.

Radiological features

• The CT signs of active tuberculous adrenalitis are enlarged glands

associated with large hypodense, necrotic areas, with or without dot-

like calcification.

• Old TB lesions can result in dense adrenal calcification visible on CT or

AXR.

Genitourinary tuberculosis

Clinical characteristics

• Genitourinary TB is the most common clinical manifestation of extrap-

ulmonary tuberculosis.

• M. tuberculosis reaches the prostate, seminal vesicles and, particularly, the

kidneys by hematogenous route from the lungs.

• All other genital organs, including the epididymis and bladder, become

involved by direct extension of infection.

• Clinical clues include history of TB, sterile pyuria, haematuria, fre-

quency and dysuria.

336

Radiological features

•

Renal TB involvement is unilateral in 75%.

•

The earliest urographic abnormality is a ‘moth-eaten’ calyx caused by

erosion. It may resemble papillary necrosis but the latter is more often

bilateral and symmetrical.

•

Renal parenchymal cavitation may be detected as irregular pools of

contrast material.

•

Dilated calyces with related infundibular stricture at one or more sites

within the collecting system may be seen.

•

Characteristic calcifications in a lobar distribution are often seen in end-

stage TB: known as TB autonephrectomy.

•

Ureteric manifestations, characterised by thickened ureteric wall or

strictures, occur in almost half of all those with renal TB, involvement

being most common in the distal third of the ureter. CT demonstrates

focal ureteric mural thickening and inflammatory change in the peri-

ureteric fat.

•

Sequential bladder involvement is manifested as interstitial cystitis with

wall thickening, ulceration and eventual scarring, with long-term loss of

cystic volume.

•

Genital tract TB almost always involves the fallopian tubes in women,

usually causing bilateral salpingitis. Tubo-ovarian abscesses may be seen

on US, CT or MRI but are non-specific.

•

Male involvement is confined to the seminal vesicles or prostate, which

are occasionally calcified.

•

CECT shows hypoattenuating prostatic lesions, which likely represent

foci of caseous necrosis and inflammation. However non-tuberculous

pyogenic prostatic abscesses have a similar CT appearance.

Musculoskeletal tuberculosis

• Musculoskeletal manifestation of TB may be identified. The most

common ones are infective discitis and psoas abscesses.

338

Uterine fibroids

Clinical characteristics

•

Fibroids (uterine leiomyomata) are the most common gynaecological

tumour and are present in up to 50% of women over 40 years of age.

•

Fibroids are benign tumours composed of smooth muscle and fibrous

tissue that are hormone dependent, enlarging during pregnancy and

hormone-replacement therapy.

•

They usually present well after puberty and shrink after the menopause.

•

The clinical presentation depends on the position and size of the

fibroids:

• intramural fibroids are the most common.

• submucosal fibroids are least common; they lie adjacent to the uterine

cavity are most likely to cause symptoms such as menorrrhagia and

dysmenorrhoea by enlarging and distorting the uterine cavity.

• a third, subserosal group, lie on the outer uterine surface.

•

Symptoms and complications of fibroids include:

• pain.

• abnormal bleeding.

• torsion of pedunculated subserosal fibroids.

• subfertility.

• problems in pregnancy and labour, such as spontaneous abortion,

premature and obstructed labour.

• sarcomatous degeneration of fibroids (rare: < 1%).

Radiological features

• AXR:

• Not a modality of choice, but calcified fibroids may be seen in the

pelvis.

• Circumferential calcification tends to follow pregnancy; punctate

calcification is usually postmenopausal.

340

•

Hysterosalpingogram:

• Performed to investigate infertility.

• Submucosal and larger intramural fibroids will be seen as smooth

filling defects outlined by contrast in the inverted triangular-shaped

endometrial cavity.

•

USS:

• The echogenicity of fibroids is variable on US, with areas of calcifi-

cation as described above.

• Fatty, haemorrhagic and cystic areas may also be seen.

• The uterus can be focally or diffusely enlarged, with individual

fibroids measuring a few millimetres to over 20cm.

• The uterus may have an irregular outline if there are subserosal

fibroids. Large fibroids may compress the ureters, and it is important

to check for the presence of hydronephrosis.

•

CT: not particularly helpful at diagnosing fibroids other than detecting

uterine enlargement, as fibroids have the same density and contrast

enhancement as the uterine myometrium, unless calcified.

•

MRI:

• MRI provides excellent visualisation of the uterus and is used to

demonstrate the exact size and location of fibroids, which are of

lower signal intensity than the myometrium on T2W sequences.

• Approximately one-third of fibroids have a high-signal rim on T2W

images from peritumoral oedema, lymphatics or veins.

• Fibroids may degenerate as they enlarge, resulting in heterogeneous

signal.

• Contrast-enhanced MRI is obtained if information is required about

the vascular supply of the fibroids, such as prior to uterine artery

embolisation (see below).

• Advantages of MRI are the ability to delineate the relationship of

fibroids to the endometrial lining when planning surgery, and to

distinguish adenomyosis from fibroids.

• Adenomyosis is the presence of ectopic endometrium in the myome-

trium, which causes similar symptoms to fibroids. The diagnosis is

made on MRI if the junctional zone (the inner myometrium) is >11 mm

thick.

342

Radiological management

•

Medical treatment is only a temporary measure because hormonal

manipulation may shrink fibroids but it will not remove them. Hence

it is used only in patients awaiting surgery or who are close to the

menopause.

•

Surgical options include myomectomy and hysterectomy, which can be

performed by laparotomy or by operative hysteroscopy. Myomectomy

is performed to conserve fertility whereas hysterectomy is the definitive

treatment of fibroids.

•

Interventional radiological techniques include uterine artery embolisa-

tion, where the uterine artery is catheterised via a percutaneous femoral

artery approach, and bilateral embolisation of the uterine arteries is

performed with polyvinyl alcohol foam particles. Reasons for proce-

dure failure include an aberrant arterial supply to the uterus, incomplete

embolisation, very large fibroids or a coexisting disorder such as

adenomyosis.

•

Newer techniques include MRI-guided focused US and laser ablation,

which both use heat to cause tissue necrosis within the fibroids. The

former uses thermal heating by US and the latter uses a percutaneous

approach to insert laser fibres into the fibroids. In both cases the heating

of the fibroid tissue is monitored by detecting changes in MRI sequen-

ces to create a real-time thermal map.

344

Volvulus

• Volvulus results from torsion along the mesenteric axis of a segment of

the alimentary tract.

• It produces partial or complete intestinal obstruction.

• The ensuing ischaemia results in gangrene and perforation.

• The sigmoid colon is most commonly affected, followed by the cae-

cum, transverse colon and stomach.

• Predisposing factors include redundant bowel loops (e.g. in the chroni-

cally constipated), an elongated mesentery, malrotation and chronic

colonic distension.

Clinical characteristics

• Colonic volvulus presents with features of bowel obstruction: abdomi-

nal pain and distension, vomiting and constipation. In gastric volvulus,

there is severe epigastric pain, vigorous attempts to vomit, with little

result, and an inability to pass a nasogastric tube.

• The duration, type and severity of symptoms depend upon the location

of the obstruction, i.e. location of volvulus.

Gastric volvulus

Clinical characteristics

• Often occurs as a complication of a hiatus hernia

• Two types described:

• organo-axial rotation about a line extending from cardia to pylorus

• mesentero-axial rotation around an axis extending from the lesser to

greater curvature.

• Complications include intramural emphysema and gastric perforation.

Radiological features

• AXR: shows massively distended stomach in LUQ.

• Barium swallow/meal: shows incomplete or absent passage of con-

trast into the stomach.

346

Caecal volvulus

Clinical characteristics

• Predisposing factors are malrotation and a congenitally long mesentery.

• Peak age is 20-40 years, more commonly in males.

Radiological features

• AXR: ‘kidney-shaped’ distended caecum rotates centrally towards the

LUQ.

• Instant enema: the tapered end of the barium column points towards

the torsion.

Sigmoid volvulus

Clinical characteristics

• Typically occurs in elderly constipated patients. The sigmoid colon

twists on its mesenteric axis.

Radiological features

• AXR:

• Greatly distended loop, with fluid-fluid levels, mainly on the left side,

extending towards diaphragm.

• Produces a typical ‘coffee bean sign’, with a distinct midline crease,

representing the mesenteric root, surrounded by a gaseous distended loop.

• Associated with proximal bowel obstruction.

• Instant enema: ‘bird of prey sign’: tapered hook-like end can be seen

on the barium column.

• CT: tightly torted mesentery, produced by twisted afferent and efferent

loops, produces the so-called ‘swirl sign’.

348