Definitive guide to Third year radiology course featuring X-ray, CT, MRI features for basic pathologies, for medical students - third year Plovdiv medical university

1. CONTENT:
PULMONARY:
Bronchial Foreign body
Bronchitis
Emphysema - subtypes
Atelectasis
Bronchiectasis
Pancoast tumour
Tuberculosis – Primary, Secondary and
disseminated.
Pneumoconiosis – silicosis, asbestosis.
Lung cancer; peripheral and central
Pulmonary Edema
Pleural effusion
Pleural tumours
Pneumonia: A. Bronchopneumonia, B.
Lobar and C. interstitial and lung abscess
Pneumothorax: Tension, open/closed
Hemothorax, Hemopneumothorax
CARDIAC:
Cardiomegaly
Aortic aneurysm
Intracranial (berry) aneurysm
Aortic dissection
Atherosclerosis
Pulmonary thromboembolism
Myocarditis
Cardiomyopathy
Pericarditis
Cardiac tamponade
Aortic regurgitation
Aortic stenosis
Mitral stenosis
Mitral regurgitation
Myxedematous Carcinoma heart
GIT 1 –Luminal organs
Atresia
Esophageal diverticulum
Hiatal Hernia and intrathoracic
stomach
Achalasia and Megaoesophagus
Esophageal varices
Esophageal stricture
Esophageal tear/rupture
Esophageal foreign body
Esophageal Carcinoma
Gastric ulcer
Duodenal ulcer
Acute abdomen free gas (Pneumoperitoneum)
Gastric carcinoma
Ileus/ bowel obstruction
volvulus
Appendicitis
Ulcerative colitis
Crohn’s disease
Colorectal cancer
Sigmoid diverticulosis
GIT 2 – Accessory organs
Liver steatosis
Liver cirrhosis
Primary liver cancer (HCC)
Liver echinococcal cysts
Liver cyst
Secondary liver metastasis
Liver Haemangioma:
Cholecystitis
Cholelithiasis
Gallbladder polyp
Cholangiocarcinoma
Acute and chronic pancreatitis
Pancreatic cysts and cancer

2. RENAL:
Congenital anomalies of the kidney
Nephrolithiasis
Hydronephrosis
Tumours of the kidneys (RCC), ureters and
Bladder (Transitional cell carcinoma)
Prostate gland tumours
OBGYN:
Ovarian cysts
Fetal Ultrasound
Breast tissue types
Calcified mammary gland
Breast cancer
HEAD/NECK and CNS:
Arachnoid Cyst
Ischemic stroke
Intracranial haemorrhages
Brain tumours
Contusion
Multiple sclerosis
Herniated disc
Trauma injury of spine
MUSCULOSKELETAL:
Osteonecrosis
Osteosclerosis
Lytic lesions
Periosteal reactions
Bone cyst
Osteoporosis
Osteomalacia
Osteopoikilosis
Ankylosing spondylitis
Rheumatoid arthritis
Intervertebral osteochondrosis and
Spondylosis.
Coxarthrosis
Gonarthrosis
Osteomyelitis (sequestrum)
Benign:
Osteoma (sinuses/ osteoid osteoma)
Chondromas (enchondromas)
Osteochondroma
Osteoclastoma (giant cell tumour)
Haemangioma
Malignant:
Osteosarcoma
Ewing sarcoma
Chondrosarcoma
Multiple myeloma
Congenital hip dysplasia
Fractures; types
- Greenstick fracture
- Fissure fracture
- Hairline fracture
- Compression fracture
- Compound fracture
- Avulsion fracture
- Crush
Dislocations (subluxation)

3. How to correctly and efficiently examine an entire chest X-ray?
FIRST: Assess X-ray quality! Don’t assume the radiology department has
delivered an adequate radiograph. Mistakes do happen. Is the x-ray “RIPE”?
Rotation – this should be avoided. Patients should be imaged “head on”
with spine centrally/ without any natural spinal curvature visible. The mid
clavicular line on both sides should be equidistant to the sternum and spine.
Inspiration – has the patient taken a sufficiently deep inspiration before
imaging. When viewing x-rays we want maximum visibility of all parenchyma
and structures. There should be a minimum of 5/6 anterior ribs or 9
posterior ribs visible above the diaphragm. As well as clearly visible
costophrenic angles. Any less is not adequate.
Projection – Which way was the radiograph taken? Normal is PA (posterior
to anterior) but sometimes they are taken AP (anterior to posterior –
important because the heart appears enlarged in AP projection when in fact
it is not.)
Exposure – X rays must be adjusted to have adequate penetration of the full
chest thickness so that structures are clearly differentiated. Can you see the
cardiac silhouette and vertebral column superimposed. If you cannot see
the spine through the cardiac silhouette the penetration was not sufficient.
R
R
*
*
*
*
*
I
P
E
E vertebrae
seen through
cardiac shadow

4. PART II of reading a chest X ray. Now that you’re confident in the quality of the image you can assess for abnormalities.
There is no specific order to do this but unless you have decided on a consistent procedure of some form you’re bound to miss
something! The following is a commonly used order of examination because it is fluid in progression, logical and addresses the
most important observations early on:
Its tempting to point out the obvious first, or to flit back and forth between the heart and lungs. But start procedurally with
one system, complete you evaluation and ONLY THEN move on to the other. This way you will have examined all possible
features.
1). AIRWAY – Trachea: deviated? Mass effect? Any inserted tubes? Obstructions or foreign bodies?
2). CARINA and BRONCHI – Foreign body, obstruction, thickening or displacement, tracheostomy tube?
3). HILUM – Masses? Bilateral (think sarcoidosis or TB). Unilateral (think tumour), Consolidation?
4). Sectional evaluation of EACH LUNG from top to bottom. Look for ANY asymmetry between left and right.
- Apical zone - masses? (Pancoast tumour), Cavities (TB, Cysts etc), consolidation.
- Upper zone – consolidation, cavities, masses, fibrosis, nodules, cysts
- Middle zone – consolidation, cavities, masses, fibrosis, nodules, cysts
- Lower zone/ lung bases – consolidation (pneumonia), atelectasis, hydro/hemothorax, pulmonary effusion?
5). *PLEURA (easily forgotten because it shouldn’t be visible normally) – thickened plaques? Mass (mesothelioma).
Ensure that the lung markings reach out all the way to the chest wall. Hyperlucent periphery suggests atelectasis.
6) COSTOPHRENIC ANGLES – should be sharp, clear and acute. If not this is known as “costophrenic angle blunting”
7). DIAPHRAGM– flattened? Abnormally raised? Visible? Fluid levels below? Free air? Continuous or divided by
pericardium? The right diaphragm should be normally a little higher than the left on account of the liver.
8). HEART: a). Cardiothoracic ratio? b). Right border c). Left border d). Valves and great vessels e). General shape
9). EVERYTHING ELSE: Ribs and collar bone fractures, dislocations, chest tubes, spinal deformities, pacemakers etc.

5. 1
2
3
4a
5
6
7
8
9
3
4a
b b
c
c
d d
7
Order of inspection as
outlined on previous
slide:

6. Bronchial Foreign body
• Most common in children under 4 years of age and
elderly with poor swallowing reflex.
• Right lung more commonly affected as the right main
bronchus is wider and more acute in angle.
• Different materials show up differently on x ray:
Metal (except aluminium) = opaque
Glass, animal bones = opaque
Wood, plastic and fishbones = lucent
• Unfortunately the majority of foreign bodies are
radiolucent.
Radiographic features:
- Patient should be imaged on expiration to exaggerate
lung differences.
- Interrupted bronchus sign – airway seems to truncate
or be “cut off” suddenly along its course.
- Affected lung is hyperinflated (less dense, hyperlucent
and larger) than the normal lung.
- Diaphragm on affected side is depressed.
- Findings will be normal in around one third of cases.
- Parenchyma distal to the obstruction may collapse
(unilateral atelectasis)

7. Bronchitis:
Inflammation of the large airways
Acute form = less than three months but typically 1 week – 10 days
Chronic form = 3 months in 2 consecutive years.
Acute:
 often caused by viral infection. Arely bacterial. May be caused by exposure
to irritants; dust, chemicals.
 hacking cough with expectoration – usually yellow or clear, green or pink
indicate lower RTI
 Wheezes, shortness of breath, chest pain and headache, runny nose, sinus
infection.
Plain radiograph: Not usually indicated for acute bronchitis. But if tachypnea,
tachycardia, fever and vocal fremitus are observed than it is indicated to rule
out pneumonia.
Only thing that may or may not be visible; Bronchial wall thickening
Chronic:
 Long-term smokers or heavy air pollution
 Overproduction and secretion of mucus by goblet cells and sustained
bronchial wall thickening.
 Other conditions that lead to chronic cough should be ruled out; heart
failure, TB, lung cancer.
Acute bronchitis; slight thickening of
bronchial walls but otherwise
relatively normal lung features

8.  Leads eventually to exertional
dyspnoea,
hypoxemia, cyanosis and cor pulmonale.
Radiographic features:
-Bronchial wall thickening
-Enlarged vessels
-Broncho-vascular irregularity – due to
repeated scarring
-Pulmonary fibrosis
-Late stage: Cardiomegaly
*Chronic bronchitis rarely occurs in strict
isolation so look for signs of emphysema
also (COPD)
CT: With contrast offers higher definition
of the same clinical findings
COPD: Features of chronic
bronchitis; thickened
bronchial walls and fibrosis

9. Emphysema:
 Permanently enlarged airspaces distal to terminal bronchioles,
destruction of the alveolar walls without obvious fibrosis
 Best evaluated on CT but radiograph can be suggestive
 Etiology: Smoking, alpha-antitrypsin deficiency and Ritalin
(methylphenidate) injection drug use.
 Emphysema patients are known as “pink puffers” (hypocapneic) as
opposed to those with chronic bronchitis “Blue bloaters” (hypoxic)
 Tachypnea, pursed lip breathing, barrel chest, hyper-resonant with
reduced lung sounds.
 Late stage: Cor pulmonale
Radio finding: Lateral view is particularly useful for “barrel chest”
-Signs of Hyper inflation; 1). Flattened hemidiaphragm is most specific/
reliable feature of this 2). Widely spaced ribs 3). Sternal bowing 4).
Widening (obtuse) costophrenic angles 5). Increased radiolucency of lung
parenchyma 6). Narrowing of intrathoracic trachea.
-Vascular changes; Diminished number of blood vessels, peripheral
vascular pruning while increased calibre of central arteries.
Right ventricular hypertrophy
CT: It is possible to identify the subtype (3) of emphysema with HRCT
scanning
Lateral x ray showing flattening of
the diaphragm and increased depth
of the retrosternal space (white
shape); increased anteroposterior
dimensions of the chest in
emphysema

10. CT specific findings of emphysema:
Centrilobular type:
-Upper zones of each lobe.
-Most common type
-Patchy distribution of focal lucencies
Panacinar type:
-lower lobes
-Uniform distribution
Paraseptal type:
-Peripheral, just beneath pleura by septal lines
-Small subpleural blebbing.
Above: Panacinar emphysema
Above; Centrilobular emphysema
Right:
Paraseptal
emphysema

11. Atelectasis;
Loss of lung volume secondary to collapse
Cause: Bronchial obstruction and secondary
diffusion of distal gas.
Types: sub-segmental, segmental, lobar or
involving the entire lung.
Bronchial obstruction can be caused
A) Intrinsically – foreign body, infection,
inflammation, cancer
B) Extrinsically – via compression of the lung
parenchyma by a tumour, vascular or
lymphatic abnormality or accumulation of
fluid or air in the pleural space.
Radiograph:
-Opacification of collapsed lung
-Mediastinal shift towards side of collapse
-Obstructive lesion may be clearly visible
-Elevation of diaphragm on affected side.
CT: Offers more detail.
Above and Above right: Lower left lobe
atelectasis; Frontal X ray shows
abnormal opacity in the base of the
lung with elevated hemidiaphragm. CT
shows mucus obstructing the lower
bronchioles (white arrows) and
displacement of the left major fissure
(dotted white arrow)
Left: Entire left lung collapse.
Mediastinal shift to affected side and
full opacification.

12. Pancoast Tumour (Apical tumour):
 Rare primary bronchogenic tumour of apex of lung with invasion into
soft tissue at the base of the neck.
 Only 3-5% of all bronchogenic carcinomas
 Pancoast syndrome: Shoulder/arm pain, paraesthesia and paresis with
atrophy of the thenar muscles of the hand as well as Horner’s triad:
miosis, ptosis and anhidrosis. Weight loss is also frequent.
 Type was squamous cell carcinoma but now bronchogenic
adenocarcinoma is more frequent. Pancoast tumours are typically Non-
small cell carcinomas (NSCC).
Plain radiograph:
- Soft tissue opacity at apex. May invade supraclavicular fossa or involve a
rib.
US: Only used to guide biopsy via a supraclavicular or intercostal acoustic
window.
CT: excellent for investigating bony involvement but poor for staging.
MRI: Excellent for soft tissue involvement and staging. Visualisation of
brachial plexus.
PET-CT: Good for assessing distant metastasis
Coronal lung window - CT
Coronal Bone window CT

13. Differential diagnosis of Pancoast tumour:
-Mesothelioma
-Pulmonary metastasis
-Chest wall metastasis
-Carotid pseudoaneurysm
-Pleural thickening due to TB

14. Tuberculosis
 Lungs are most common site of primary infection.
 Most cases are asymptomatic, some result in
haematological spread which may result in miliary TB.
 In immunosuppressed or compromised patients TB can
progress with constitutional symptoms of fever, malaise and
weight loss and a productive bloody cough.
 Primary TB can appear in any part of the lung in children
but usually either the apex or base in adults.
 Secondary flare-ups strongly prefer the upper lobe.
 Miliary type occurs diffusely throughout the lung and has
poor prognosis.
Radiographic features:
Primary TB
- Variable appearance from not visible through patchy to
entire lobar consolidation anywhere in the lung.
- Cavitation is uncommon
- Caseating necrotic granuloma (tuberculoma) form and then
calcify into a “ghon lesion”.
- Paratracheal and hilar lymphadenopathy (children), can
sometimes enlarge suficently to induse distal atelectasis.
- Pleural effusion in adults.
- Calcification of lymph nodes occurs in 30%
Primary TB cases

15. Secondary (Post-primary) TB:
 Reactivation of TB years later, often in the setting of
weakened immune system.
 Most commonly it attacks the posterior segments of the
upper lobe and superior parts of the lower lobes.
 More likely to cavitate.
 “Tree-in-bud” sign = endotracheal spread from one area to
another with the formation of nodules along the way (CT).
 Hilar node enlargement is less common (1/3 cases), lobar
consolidation and formation of tuberculoma can also occur
but less commonly than primary TB.
 When Tuberculomas do occur, they're almost always
solitary and located in the upper lobe.
 Rarely, calcified lymph node can erode and break off into a
bronchus and be coughed up (lithoptysis).
Miliary TB (disseminated):
 Demonstrates rampant and uncontrolled spread of TB
throughout the entire lung. Has poor prognosis
 Nodules are 1-3mm and diffuse. Also there is infiltration in
other systems and parts of the body. Miliary TB can occur
in both primary and secondary TB
Right: Miliary TB
Post
primary TB
with
cavitation’s
in upper
lobes

16. Pneumoconiosis:
• A broad spectrum of inhalation lung diseases or occupational lung diseases due to exposure to small particles of
aggravating substances. Particles between 2 – 5 microns are the worst offenders – as they are too small to be captured
by the nasal hairs and mucous but too large to be exhaled.
1). Silicosis:
 Classic form is chronic and more common. Acute form occurs only when sudden large doses of silicon dioxide (quartz/
glass dust/ sands) are inhaled especially in combo with heavy metals or carbon.
 Classic form can take on two typical appearances:
- Simple silicosis: pattern of small round or irregular opacities.
- Complicated silicosis: conglomerates forming massive pulmonary fibrosis.
Radiologic findings:
Acute cases;
- Bilateral consolidation
- Ground glass opacities
- Appear mostly around hilar area
of the lungs.
CT: Bilateral centrilobar nodular
ground glass opacities.
Multifocal patchy ground glass opacities
Consolidation
Chronic cases:
X-RAY; Multiple nodular opacities that are well defined and nodular in shape.
Range from 1mm – 1cm
Calcifications of nodules. Nodules appear mostly in upper lobes.
Sub-pleural pseudoplaques – thickened nodules at lung surface look like melted
candlewax.
CT: Same features as above but hilar lymphadenopathy can also be visualised –
eggshell calcifications.
In complicated cases: masses are larger, irregular in shape and progress from
periphery towards hilum leaving emphysematous and fibrotic tissue in wake.

17. CTs: Complicated silicosis with
progressive massive fibrosis
Axial (above) and frontal
(below) CT: Simple silicosis
Fibrosis at apex
of lung
Diffuse massive fibrosis with large
silicotic nodules especially in apex

18. 2). Asbestosis:
 Occurs usually 15-20 years post exposure.
 More common in men in occupational settings
Radiographic features:
 No pathognomonic changes specific to
asbestosis
 Calcified and non calcified pleural plaques may
be observed
 Irregular opacities
 Fine reticular pattern of fibrosis
CT:
 Centri-lobular dot-like opacities
 Peri-bronchial fibrosis
 Intralobular linear opacifications = reticular
fibrosis
 Subpleural curvilinear lines
 Changes similar to atelectasis – traction
banding, uneven shrinkage and receding of
parenchyma from chest wall, bronchiectasis.
CTs showing pleural plaques, fine reticular fibrosis and multiple dot-like opacities
Diffuse reticular fibrosis on
x-ray

19. Pulmonary edema
• Abnormal accumulation of fluid in the extravascular space of the lungs.
• Acute breathlessness, orthopnoea, paroxysmal nocturnal dyspnea
(PND), foaming at the mouth and general distress.
• Alveolar flooding typically occurs when Pulmonary Wedge Pressure
(PWP) increases to above 25mmhg.
• 2 pathological etiologies: 1). Increased hydrostatic pressure edema –
cardiogenic. (interstitial or alveolar flooding). Eg. Fluid overload or
heart failure, mitral regurgitation, aortic stenosis, arrythmia,
myocarditis/ cardiomyopathy.
• 2). Increased permeability edema – non cardiogenic (diffuse alveolar
damage – toxic or corrosive gases, infections, asthma, Acute lung injury,
ARDS and high altitude etc).
Plain radiograph:
-Cardiomegaly (cardiogenic causes )
-Venous redistribution to upper lobes (stag antler sign)
-Interstitial edema: Kerley lines (septal thickening) and peri-bronchial
cuffing, Hilar “haze”/ obscurity of hilum.
Kerley A = oblique, from periphery to hilum, longer than B.
Kerley B = Horizontal, peripheral, straight lines.
-Alveolar edema: airspace opacification
-Pulmonary effusion: fluid in interlobar fissures
Non-cardiogenic pulmonary edema: No cardiomegaly,
absence of pulmonary effusion into pleural space. Central
alveolar disease in “Bat wing” configuration.

20. CT:
-Ground glass opacification
-Thickening of bronchovascular bundles due
to a). Peribronchial thickening b). Vascular
engorgement and thus increased diameter.
US: Resonance artefacts called “B lines” due
to increased fluid density. Lung appears more
“solid-tissue-like” (hepatisation) – when
alveoli are flooded.
-More than 3 lines = pathological
-Close together (3mm or less) indicates
ground glass opacification.
-More distant (7mm apart) indicates
interstitial edema.
Differential diagnosis:
-Pulmonary haemorrhage
-Diffuse pneumonia
Alveolar edema: Diffuse, bilateral airspace disease with minor
fissure congestion- Kerley B lines (blue arrow) and pulmonary
effusion – seen at the base of the lung as blunting of the
normally visible costophrenic angles. Heart = slightly enlarged.

21. Signs of congestive heart failure: Kerley B lines (yellow
circle), Central alveolar disease (White arrows) and
Thickening of accessory fissure at base of lungs (Red
arrow) which indicates effusion.
Above: Kerley B lines. Small, horizontal
peripheral. Represents fluid leakage into
interlobular spaces. Seen often in
cardiogenic edemas
Above – CT axial
projection: pulmonary
alveolar edema. -
demonstrates bilateral
central peri-hilar
airspace disease.
Almost symmetrical.
Septal thickening in
periphery and pleural
effusion – larger on
right side (white
banding surrounding
lung parenchyma.)

22. Kerley A line
Above: Near drowning
– CT axial

23. Pleural Effusion:
• Is an umbrella term for any abnormal accumulation of fluid in the pleural space.
• Can be due to various pathological processes and so can be subdivided into:
-Empyema (septic/purulent effusions)
-Haemothorax (Blood accumulation in pleural space)
-Hydrothorax (Fluids eg. bilothorax – bile, urothorax – urine: both very rare, chemothorax or “infusothorax” – anti-cancer
drugs etc.)
• Can be a combo: hydropneumothorax.
• Clinical presentation: Non-specific Dyspnea, non- productive cough, chest pain. Specific: hemoptysis, night sweats and
fever and weight-loss = TB.
• Peripheral edema, orthopnoea and PND = Congestive heart failure.
Can be Transudative or Exudative.
Transudate = Low LDH, Low Protein concentration, low cellularity, normal glucose (same as plasma), specific gravity is
normal and PH is higher that exudative. Is NON-INFLAMMATORY in nature.
Causes include: Trauma/surgery, heart failure, nephrotic syndrome, cirrhosis, asbestosis.
Exudate = INFLAMMATORY, increased permeability and obstruction of lymphatic drainage. Exudate High protein content –
readily clots due to fibrinogen content, High cellularity – neutrophils, mafs, parenchymal cells etc, high LDH (indicates tissue
damage), Glucose is low. Specific gravity (density) is high, PH is low.
Causes include: Carcinoma, lymphoma, embolism and pulmonary infarction, Pneumonia, TB, Mesothelioma (aggressive
pleural cancer), connective tissue disorders: RA, SLE.

24. Sub-pulmonic effusion: costophrenic
angle is obscured on right side with
elevation of apparent hemi-diaphragm.
Above: Large Malignant bilateral effusion
Left and top
left corner:
Lateral and
frontal view
respectively –
large
pulmonary
effusion
Left. CT – axial
projection of
right sided
effusion.

25. Pneumonia:
 Very broad term used to describe infection of the lung. But it has
a widely varied etiology and appearance which can be classified
several ways
 Not to be confused with pneumonitis which is generally used to
describe non-infectious causes of inflammation.
Classification:
*According to radiographic appearance:
1). Atypical
2). Round
3). Cavitating
4). Haemorrhagic
Etiology: Viral, Bacterial, mycobacterial, Fungal
Method of spread: Bronchopneumonia, lobar pneumonia, multi-
lobar pneumonia, Interstitial Pneumonia and confluent pneumonia.
Setting of infection: 1). Community acquired, 2). Hospital acquired
pneumonia (HAP) = a). Ventilator associated b) Healthcare assoc. 3).
Aspiration pneumonia.
According to exudate: serous-desquamative, fibrinous, purulent,
haemorrhagic, putrefactive.
Duration: Acute and chronic

26. A) . Bronchopneumonia:
Plain radiograph:
- Multiple small nodular or reticulonodular (“web and ball”) opacities
- Patchy and /or confluent
- Often bilateral and asymmetric spread
- *Predominantly involves lung bases
CT:
- Multiple focal opacities arranged in lobular pattern
- Usually more common at centrilobar bronchioles giving appearance of a tree blossoming (buds along a branch).
- Confluence leads to “Patchwork quilt” appearance.

27. B). Lobar Pneumonia:
Clinical picture; Productive cough, dyspnoea, fever, rigors,
malaise, pleuritic pain and occasionally haemoptysis
-Bronchial breathing, dullness of percussion, pleuritic pain
-Additional breath sounds: Crackles, Rhonchi and wheezes.
-Streptococci pneumoniae = most common cause
OTHERS: Klebsiella pneumoniae, haemophilus influenzae, TB
STAGES: 1). Congestion
2). Red hepatisation – hemorrhage
3) Grey hepatisation – fibropurulent exudate
4). Resolution
Plain radiograph:
- Homogenous opacification of a lobe
- Fissures mark sharply defined border between affected and
unaffected areas
- Segmental bronchial consolidation
- “Air bronchograms” – unaffected bronchi are made visible by
surrounding consolidation of lung tissue.
- Atelectasis of small bronchioles can occur
Right Middle lobe
Pneumonia seen on
frontal and lateral
projection – X ray
See right –CT coronal
projection; Lobar
pneumonia of left
lung

28. CT:
- Opacification of entire lobe with sparing of large bronchi
- Ground glass opacities
Complications: Abscess, empyema and fibrinous pleuritis, dissemination – bacteraemia. Sepsis and multi-organ failure
Differential diagnosis:
- Atelectasis
- Pulmonary malignancy (lobar lymphoma).
Various lower left lobe pneumonias

29. C. Interstitial Pneumonia
 Has pattern of idiopathic pulmonary fibrosis.
 Lung volume loss, peripheral septal thickening, bronchiectasis and
“honeycombing” – characteristic diffuse cystic appearance of pulmonary fibrosis.
Etiology:
-Chronic interstitial pneumonitis
-Connective tissue lung disease: Rheumatoid arthritis, Scleroderma, chronic
hypersensitivity pneumonitis, radiation, asbestosis.
Plain radiographic features: X ray is non-specific. Only indicates advanced disease –
fine to course basal reticulation.
CT:
- Honeycombing; if over 8% of lung is highly specific to this disease
- Reticular opacities; in subpleural lung surfaces along with traction bronchiectasis
and ground-glass opacities
- Distortion of lung architecture
- Loss of lung volumes particularly in lower lung
Classic lung window CT scans showing interstitial
pneumonia – note the reticular fibrous structure
and cystic honeycombing of the parenchyma

30. Lung Abscess:
• A well circumscribed collection of
pus, difficult to manage/treat and
may be life-threatening.
• Advent of Abs has made this
uncommon except for in vulnerable
groups: elderly, malnourished,
debilitated and immunocompromised
• May be acute (<six weeks) or chronic
>six weeks).
• Aspiration = most common cause.
Plain radiographic features:
 Cavity containing gas-fluid level
 Usually round, clearly visible on all
projections.
US: Not indicated
CT:
 Contrast should be used, luminal wall
is thick and irregular
 Vary in size, may only contain fluid,
usually round.

31. Pneumothorax, Hemothorax and hemopneumothorax:
• Pneumothorax is a potentially serious life-threatening condition where
air accumulates in the pleural space displacing lung parenchyma
(atelectasis) and sometimes mediastinal structures too (tension).
• Asymptomatic, mild dyspnoea, pleuritic chest pain.
• Primary spontaneous pneumothorax is more common in young people
(>35) often due to congenital abnormalities of the lung, hyperinflation
or connective tissue disorders while secondary (to COPD, lung abscess,
tumour etc.) spontaneous pneumothorax is more common in people
over 45.
• Open and tension pneumothoraces are more common in trauma
(especially penetrating trauma of the chest cavity).
• Pneumothorax is usually easily identifiable on diagnostic images.
Radiographic findings:
 Thin sharp white line = visceral pleural edge
 No lung markings (total radiolucency) seen outside this line.
 Subcutaneous emphysema (maybe)
 No mediastinal shift (unless tension pneumothorax)
 Signs of pneumomediastinum
Ultrasound:
- Motion (m) setting can be used in the intercoastal spaces to visualise
whether there is movement of the lung parenchyma against the chest
wall.
Right: Left hemi-
thorax is
radiolucent due
to complete
collapse of the
lung, the
mediastinum is
slightly displaced
to the
contralateral side.

32. No movement indicates collapse.
- For small pneumothorax – anterior/supine
- For large pneumothorax – mid axillary line/ lateral
position (gas rises).
CT: The findings are very obvious.
Additional features in Tension pneumothorax:
- More severe clinical presentation: unilateral
decreased breathe sounds, severe dyspnea and use
of accessory muscles, hypotension, distended
jugular veins and signs of obstructive shock.
- Radiograph/CT: Deviated trachea, mediastinal shift,
bowing of ribcage – more horizontal course.
Non-tension Tension
Tension
Hemothorax:
• A type of pleural effusion where the fluid in the pleural cavity is blood.
Tension Hemothorax is due to massive internal bleeding
Bottom left: Ultrasound features of
pneumothorax; normal sliding of
the visceral pleura against the
chest wall causes a transitionary
hyper echoic line (waves on
seashore). When the pleura is
depressed by air this line cannot
occur and instead you see perfectly
flat uninterrupted echo lines
(barcode).

33. • Causes of Hemothorax: penetrating trauma,
malignancy, anticoagulant therapy, vascular
rupture, pulmonary infarction etc
Radiographic features: Only sensitive to large ones and
cannot differentiate between other pleural effusions.
US: Homogenous and echogenic fluid.
CT: Can determine whether the fluid is Edematous or
haemorrhagic by the attenuation value. Visualisation
of soft tissue damage such as contusions and
lacerations of the lung parenchyma or chest wall.
Above: two left-
sided Hemothorax
chest x-rays. Left:
CT showing a
large right sided
Hemothorax
Left: Two CTs
of
hemopneumo
thorax.
Right:
Hemothorax
only

34. Normal heart contour and Cardiomegaly:
• Causes include: Any of the four main valvular diseases, cardiomyopathy, hypertension, anemia, congestive heart failure
as well as lung diseases that lead to pulmonary hypertension and cor pulmonale (COPD, pulmonary embolism,
pulmonary fibrosis), renal failure and physiological states: athleticism and pregnancy.
• Normally it is easy to identify cardiomegaly but in some cases it can be either/or and then we measure the
cardiothoracic ratio. Normal = 2:1 [thoracic diameter vs. widest diameter of heart @ full inspiration].
Radiograph:
Normal contours from top are;
RIGHT SIDE:
1). Ascending aorta
2). Small indentation (between
aorta and right atrium – sight
of double density sign of L.
atrial enlargement.)
3). Right Atrium – forms right
contour of heart.
Normal LEFT SIDE:
1). Aortic knob
2). Main pulmonary artery
3). Slight indentation – also
the site of left atrial
enlargement.
4). Left ventricle makes up
the rest of the left contour.

35. Right V. enlargement
Biventricular Enlargement
Left V. Enlargement

36. Aneurysms:
• A focal abnormal dilatation (more than 150% of normal diameter) of
a vessel typically occurring in arteries (aneurysms in veins are rare
due to the lower blood pressures).
• Most often they occur in either the thoracic (TAA) or abdominal
aorta (AAA) but can also occur in the brain, iliac arteries or any other
major vessel and can even occur in the heart wall after an infarction.
• Types include: saccular or fusiform, true (involving all three wall
layers or false (pseudoaneurysm – involving only 2 or 1 layer of the
wall.
• Etiology of aneurysms: Hypertension, vasculitis, atherosclerosis,
congenital connective tissue disorders, trauma.
• MR and CT angiography are the methods of choice for aneurysms.
Ultrasound can be used only for Abdominal AA’s as the ribcage
prevents its use in TAA’s. Radiography can often easily visualise an
aortic aneurysm but differential diagnosis is difficult with other
possible masses. MRI should not be done in those with pacemakers.
• 1). Aortic Aneurysm:
• Saccular aneurysms involve asymmetric dilatation on one side of the
artery, bulging out like a “berry on a branch”. Fusiform aneurysms
are circumferential symmetric dilatation of all parts of the wall.
• Thoracic Aortic aneurysm (TAA) is less common than abdominal
aortic aneurysm (AAA)
CTA’s of
fusiform
abdominal
aortic
aneurysms

37. Radiographic features:
Thoracic:
• Aortic calcifications (indicating atherosclerosis/
chronic aortitis).
• Bulging mediastinal mass
Abdominal:
• Primary identification of mass.
• Monitoring growth rate
CTA:
Thoracic:
• Dilation of the arterial lumen
• Thickening or thinning of the wall
• Mural thrombus #
• Calcifications
• Hematoma in left mediastinum or pericardial
effusion/ tamponade (if ruptured)
Abdominal:
• Fat stranding (hyperintense) around aorta
• Retroperitoneal hematoma
• Contrast extravasation (rupture)
• Interruption in mural calcifications
DSA:
Used to be gold standard but it is an invasive method and so has
additional risks. It also cannot visualise extravascular soft tissues so has
been replaced by CT and MRI methods.
DSA gives superb resolution of the involved branches but can mask the
true size of an aneurysm with mural thrombus.
Ultrasound:
Thoracic: Not indicated
Abdominal: A great choice – fast, widely available. High sensitivity and
specificity. Pulsatile dilatation of aorta is visualised. Interference with
diagnosis can occur by overlying gas filled bowel.
MRA:
Thoracic: Similar findings as CTA but with enhanced resolution of soft
tissues and so is advantageous in young patients with Marfans/ Ehler-
danlos syndromes.
Abdominal: High resolution and good in cases where radiation must be
avoided.

38. Ultrasound of abdominal aortic aneurysms, colour doppler; RED = blood coming towards
transducer, BLUE = Blood going away from transducer
Left: DSA of TAA. Above – CTS of thoracic aortic aneurysms

39. 2). Cerebral saccular aneurysm (Berry aneurysm):
• Most common cause of non-traumatic subarachnoid
hemorrhage.
• Typically a true aneurysm with very round shape, may
contain a mural thrombus.
• Location: Anterior circulation (Anterior and middle cerebral
arteries, anterior portion of circle of Willis) is much more
common (90%) than Posterior circulation (Basilar artery,
superior cerebellar etc.).
Radiographic: is uninformative.
CTA:
 Hyperintense lesion
 Calcifications
 Filling defect with rim enhancement in the case of
thrombosed aneurysm.
MRA Similar findings as CTA.
MRI:
 T1 – flow void and heterogenous signal. Visualisation of
thrombus.
 T2 – Hypointense, thrombi have hyperintense rim
DSA (catheter angiography): Good for detection of small
aneurysms. Careful eval because 3D reconstructions can
sometimes overestimate dimensions.

40. Aortic Dissection:
• Most common form of acute aortic syndromes (others being
aneurysm, mural thrombus, aortic atherosclerotic ulcers etc)
• Blood enters between the intima and media through a tear and
tracks longitudinally along the vessel.
• Causes include: atherosclerosis, arterial hypertension, congenital
connective tissue disorders (Marfan’s and Ehler-danlos), aortic
coarctation, bicuspid aortic valve, syphilis, Turners syndrome (missing
X chromosome females), cardiac surgery complication.
• Clinical presentation can be acute (14 days), subacute (up to three
months) or chronic (more than three months) = abdominal organ
ischemia, limb ischemia, strokes and thrombotic incidences, ECG
changes (ST elevation)
Radiographic features:
• 60% of dissections involve the proximal aorta (DeB Type I + II/
Stanford A). Stanford A is based on whether the dissection involves
the ascending aorta or not.
• Pleural effusions are commonly seen with aortic dissection.
• Doubled or irregular aortic contour
• Widened mediastinum
• Deviation of mediastinal structures especially Esophagus and trachea
= > the right side.
• Left main bronchus pushed more horizontal in course
CT/ CT angiography: A good/ fast method for
diagnosis: offers soft tissue visualisation. Aortic
dissection is an emergency.
• Specificity and sensitivity of close to 100% for this
condition.
• Contrast CT is preferable for full visualisation.

41. • CT features of aortic dissection include;
- Intimal flap in the centre of the aortic lumen – dividing the lumen into two
semicircles – the true and false lumens.
- Dilation of the aorta due to increased resistance to blood flow
- Displacement of calcified atherosclerotic plaques into the lumen
- Aortic intramural hematoma
- End-organ ischemic changes
- “Windsock sign” – contrast tapers off like a windsock or traffic cone because of
uneven blood pressures and distribution between the two hollows.
- “Mercedes Benz” or “peace” sign when lumen is tripled barrelled (double
dissection).
- Chronic cases = intimal flap is much thicker due to attempted repair by
endothelium.
Which lumen is which?
The true original lumen is:
- More collapsed then the higher pressure false lumen
- Has calcifications in its exterior walls
- Continues from aortic root
The false lumen:
- Often the larger dilated lumen
- Lower contrast density
- Thinner, stretch wall, at risk of rupture
- Sometimes contains a thrombus

42. Ultrasound: Transoesophageal echocardiography
• Good method for visualisation but often has limited
access and is invasive so CT methods are still
preferred.
MRI: usually reserved as a follow-up method but can be
useful in those with renal impairment (contraindication
for contrast in CT method)
DSA: Digital subtraction angiography
Used to be the gold standard but it is invasive. DSA is
also more risky due to those associated with
catheterisation and potential rupture of the false lumen.
Treatment: a), Control Blood pressure b). Control Heart
rate (pain – sympathetic trigger) c) surgical repair.
Complication:
- Distal thromboembolism
- Distal ischemia and tissue damage
- Rupture and massive haemothorax/
hemoperitoneum
- MI secondary to coronary artery occlusion
- Cardiac tamponade

43. Atherosclerosis:
• A systemic vascular disease characterised by chronic
inflammatory processes and remodelling of large and
medium sized arteries leading to thickening and stiffening
of the intima with plaques made of cholesterol, necrotic
tissue, fibrose deposition and calcifications.
• Most common sites are around branching points, bends
and bifurcations in the arterial tree due to low turbulence/
shear stress exerted on the wall at these points.
• Risk factors: Hypertension, dyslipidemia, smoking, alcohol
use, family history, metabolic syndrome.
DSA (a fluoroscopic method using continuous
x-ray beam), CT angiography (contrast) and
Doppler Ultrasound are good choices to
visualise atherosclerosis. If not available MR
angiography with contrast is also good:
Atherosclerosis appears with the following:
- Segmental narrowing of the lumen of the
artery
- Uneven vascular wall
- Calcifications (opacities) in wall
- Engorged collateral vessels
1) Lerichs syndrome:
 Obliteration/ occlusion of the distal aorta and common iliac
arteries. Due to the presence of collaterals the obstruction is
bypassed and blood flow to the lower limbs is maintained,
although at reduced capacity.
 It is a chronic peripheral arterial insufficiency. Symptoms:
Impotence (males), intermittent claudication (pain) and
decreased or absent femoral pulse, paraesthesia, pallor,
coolness of the extremity.
CT angiograph

44. 2). Thoracic Aortic Atherosclerosis

45. 3). Renal Artery stenosis
(atherosclerosis =75% cases):
DSA –
fluoroscopy
Right: colour doppler, the green
indicates high velocity turbulent flow
across the stenotic area of the renal A.
DSA
CT angiography

46. 4). Coronary artery disease (mostly
atherosclerosis):

47. 5). Carotid and intracranial Stenosis:
Atherosclerosis can
affect virtually any large
to medium sized artery
in the body but most
common areas are the
aortic, popliteal, renal,
carotid, coronary and
circle of willis.

48. Pulmonary Thromboembolism:
 A life-threatening emergency whereby the pulmonary vessels
are occluded, commonly at the bifurcation of the pulmonary
trunk (saddle thrombus) but can happen anywhere within
either or both lungs, with predilection for the lower lobes.
 Non-thrombotic emboli include; gas bubbles, fat embolus,
amnion, septic, parasitic, tumour fragment, and calcific
emboli.
 DVT is a common source of a PTE, immobilised patients which
are female, on hormone therapy, post operatively/
hypercoagulative state are at high risk.
 Clinical presentation of PTE includes: Pitting edema of lower
limb (asymmetric), tachycardia, pleuritic chest pain, dyspnoea
and haemoptysis.
Radiograph: Not very sensitive/ specific for PTE but can rule out
pneumonia and pneumothorax.
 Fleischner sign Enlarged pulmonary artery
 Lung infarction – peripheral wedge shaped opacity
 Pleural effusion (1/3rd of cases)
 “Sudden cut-off” of either of the main branches of the P.
arteries
 Elevated diaphragm and vascular redistribution to upper lobes
Two radiographs
showing elevated
diaphragm and
two wedge
shaped
infarctions
(indicated)
secondary to PTE

49. Computed Tomography (contrast
enhanced):
 Filling defect in Pulmonary
arteries.
 Thrombus is often serpentine in
shape – taking the form of the
vessel in which it formed
 Polo mint sign – occluding
thrombus surrounded by ring of
peripheral contrast enhancement
 Affected vessel is dilated
 Chronic cases tend to be calcific,
or affecting the peripheral end of
the artery with collateralisation of
blood-flow.
Ultrasound:
 Right ventricular dysfunction
(dilated and hypocontractile)
 Interventricular septum
dyskinesia
 Thrombus in transit.
Below: US of thrombus
(white arrow) in transit
Right: Ultrasound of
Right ventricular
dilation due to
increased
pulmonary outflow
tract pressure

50. Myocarditis:
• Inflammation of the myocardium.
• Variable presentation (from asymptomatic to life-threatening cardiogenic
shock).
• Usually appears with fever, malaise and angina.
• Lab tests assist in diagnosis: increased ESR, leucocytosis, CK and troponin may
also be elevated mimicking MI
• ECG: sinus tachycardia, prolonged QRS complex, ST elevation can be present.
• Causes: Viral infections (Coxsackie B, Echovirus, arbovirus), bacterial: strep.
Pyogenes, staph. Aureus, diphtheria, fungal – candida albicans. SLE,
scleroderma.
• Drug induced: Anti- TB medications, Antibiotics, anticonvulsants, diuretics as
well as radiation and acute transplant rejection.
CT: Not highly informative. Early contrast enhancement of myocardium suggests
inflammation. US: Systolic and diastolic dysfunction and motion abnormalities.
MRI:
 Cine: Wall motion abnormalities throughout the heart
 Pericardial effusion in almost half of cases.
 T2 weighting (blood = black); myocardial hyperintensity suggests edema.
 Areas of early contrast enhancement (vasodilation/ inflammation)
 Areas of late contrast enhancement (gadolinium) suggests necrosis and
fibrosis
Pericarditis and cardiomegaly on a
radiograph may suggest myocarditis but
radiographs are of low diagnostic value
in this disease.

51. Myocardial Edema
Left: T2 weighted MRI
(A) showing mid-wall
septal and posterior
wall edema. C and D
(CT) show the same.
Late contrast
enhancement is seen
in B (MRI), suggests
necrosis.

52. Pericarditis:
 Inflammation of the pericardium, unlikely to occur by
itself and is usually secondary to some other systemic
disease.
 Diagnosis is mostly based on clinical presentation (
friction rub, chest pain, ECG – ST elevation PR
depression, etc) and diagnostic images are only
supplementary.
 Acute manifestations can be of several types: Fibrinous,
serous, haemorrhagic, tuberculous or purulent. Chronic
forms tend to be constrictive or adhesive.
 Ultrasound is a great choice. Radiographic and CT
evidence are suggestive but of less diagnostic value.
Ultrasound findings:
 Pericardial thickening
 Pericardial effusion
 Elevated filling pressures
 Cardiac tamponade
Chronic cases:
 L + R Atrial enlargement
 Doppler reveals increased filling pressures (diastolic
dysfunction) but no increase in blood velocity.
Radiograph:
 Increased cardiothoracic ratio
 “Flask-shaped” outline – effusion
 Pulmonary edema ( pulmonary venous congestion)
CT/MRI:
 Soft tissues and blood; jugular venous congestion,
pulmonary venous congestion, pulmonary edema, widening
of cardiac margins, narrowing of the root of great vessels
due to external pressure
CT: pericardial
thickening and
effusion clearly
visible,
enlargement
of heart
diameter

53. Cardiac Tamponade:
 Built up of fluids: blood, puss, lymph/ exudate,
gases or malignant tissue in the pericardial space
and can occur rapidly of progressively but in both
cases leads to diminished Cardiac Output.
 It shares many of features with pericarditis.
 Clinical presentation: Becks Triad
Ultrasound signs: Echocardiography is gold standard
for diagnosis!
- Pericardial effusion
- Collapse of right atria and then ventricle (pressures
here are lower than those exerted by the effusion,
first during diastole and then during systole.
- Abnormal changes to blood-flow with respiration.
(normally increased with inspiration).
Radiographic signs:
- Cardiomegaly that isn’t caused by build up of
epicardial fat with narrowed outflow tracts (water-
bottle sign)
- Decreased size of cardiac silhouette in cases where
the effusion pressure becomes severe (later
stages).
CT: (MRI has limited role in emergency setting)
- Engorgement of sup. and inf. vena cavae.
• Enlargement of Liver and kidneys (congestion)
- Periportal edema
- Pericardial thickening
- Interventricular septum becomes angled and compressed
- Collapse of right ventricle
Coronal
radiograph:
Water bottle
sign – orange
lines showing
acute narrowing
of cardiac base
with
cardiomegaly
(purple) and
dilation of the
pulmonary
vessels (blue
arrow)

54. Cardiac tamponade axial CT
CT: Enlarged liver, abdominal effusions,
cardiomegaly, large pericardial effusion
inferior to apex
Ultrasound: the best diagnostic
tool for this emergency

55. Aortic Regurgitation:
 Often asymptomatic, sometimes dyspnea and angina,
biphasic pulse wave, volume-loaded thrusting apex
beat, decrescendo early diastolic murmur (EDM).
Mostly chronic and rarely acute version.
 Etiology: Syphilis, Bicuspid valve, marfans syndrome,
Aortic dissection, infective endocarditis, iatrogenic (
catheterisation), Traumatic.
Plain Radiograph:
- Variable appearance
- Displacement of apex left and inferiorly
- LV hypertrophy and entire aortic enlargement.
- Occasionally an aneurysmal dilatation can be seen.
- Signs of congestive Heart Failure
CT: Failure of aortic cusps to align properly during diastole
MRI: Detailed analysis of aortic root and valve: estimated
ejection fraction, regurgitant jet volume, LV size.
CineMRI: White blood technique shows signal loss during
diastole ( darker area = regurgitant jet)
Left:
CineMRI
showing
regurgitant
“black
void” at
aortic
valve.

56. Aortic Stenosis
 Present in 1/4th of all patients with a valvopathy, often seen in
conjunction with mitral regurgitation.
 Most often degenerative
 Classic triad: Angina pectoris, dyspnoea and syncope
 Pulsus parvus et tardus (weak and delayed)
 Mid systolic crescendo-decrescendo murmur radiating to carotid
artery.
Plain Radiograph:
EARLY: normal heart size but dilated ascending aorta –
differentiated with hypertension in that the entire descending
portion of the aorta is also enlarged in hypertension.
LATE STAGE: Valve calcifications, cardiomegaly, pulmonary features:
cephalisation, interstitial and alveolar edema, features of heart
failure.
US (Echocardiography): Can assess location of stenosis:
supravalvular, valvular or sub-valvular as well as assess the aortic jet
velocity and pressure gradient
CT: Particularly good for visualisation of aortic valvular calcifications
Post stenotic dilatation of Ascending
aorta (above and below)
MRI

57. MRI: Detailed structural assessment
-Congenital deformity: Biscuspid or unicuspid aortic valve.
-Post-stenotic dilatation of aorta
-Increased Left ventricular mass
-LV wall thickening >12mm
-Dynamic changes: (cineMRI)
-Thickened valve leaflets and reduced excursion (movement outwards)
Complications:
• Congestive heart failure
• Aortic regurgitation
• Calcific emboli (Cerebral/ systemic)
• Sudden cardiac death
Left: Enlarged aorta
but heart size is
normal
Below-central: Left
image shows
enlarged aorta and
LV hypertrophy.
Right image (lateral
view shows the line
in blue that divides
the aortic valve
above from the
mitral valve below:
above this line
calcifications can
often be seen.
Far left: Aortic
Calcifications.

58. Mitral Stenosis
 Left atrial outflow obstruction
 99% due to rheumatic fever
 Focus on changes in the lung and right ventricle
Plain radiographic:
 Left atrial enlargement – convex or straightening of left heart
contour just below pulmonary artery.
 “Double density sign” – secondary contour visible over right
heart due to left atrial enlargement
 Carina – splayed/ more obtuse angle and left main bronchus is
elevated upwards.
 Cephalisation of upper lung vessels with pulmonary edema.
 Diffuse hemorrhage of alveoli.
 Late stage: pulmonary hemosiderosis and pulmonary
ossification.
Ultrasound (Echocardiography):
Early = area of mitral valve larger than 1.5cm2/ pressure gradient =
less than 5mmhg
Moderate = area 1-1.5cm2/ pressure gradient = 5-10mmhg
Late stage: area less than 1cm2/ pressure gradient = >10mmhg
Pulmonary
edema and
fibrosis
secondary to
mitral
stenosis

59. Ultrasound features: decreased leaflet mobility, increased
leaflet thickening, sub-valvular thickening (chordae) and
calcifications.
MRI/CT: same changes as plain radiograph but in more
detail.
Complications of mitral stenosis:
-congestive heart failure
-pulmonary edema
-atrial fibrillation
-Thromboembolic events
-Sudden death (arrythmia)
-Mitral regurgitation
cephalisation
Straightened
upper heart
border
Normal heart
size
Cephalisation of upper lung
vessels

60. Small Aorta due to decreased
cardiac output
Double-density
sign on right
side of heart
due to left
atrial
enlargement
into lung
parenchyma
(Left)
Elevated
Left main
bronchus
due to
left atrial
enlargem
ent

61. Mitral valve/annulus
calcifications secondary to
mitral stenosis

62. Mitral regurgitation:
• Acute type: due to decompensating congestive heart
failure and cardiogenic shock
• Thrusting apex beat/ holosystolic murmur radiating to
left axilla.
• Causes: Acute: Trauma, MI and papillary rupture,
Chronic: infective endocarditis, dilated
cardiomyopathy, rheumatic fever
Plain Radiograph:
 Left atrial enlargement
 “Double-density sign”
 Elevation of L. main bronchus and splaying of carina
 Left Ventricular enlargement (volume overload)
 Cephalisation of pulmonary vessels (Pulmon. HT)
 Signs of congestive heart failure
CT/MRI: same as plain radiograph/ better resolution.
US Echocardiogram: Increasing flow convergence,
enlarging regurgitant orifice, increased regurgitant jet
fraction.
Large Left
atrium
Markedly enlarged
heart
Normal pulmonary
vasculature – has
not yet cephalized

64. Above: Unilateral pleural edema
(cardiogenic) secondary to acute mitral
regurgitation
LV
LA
Left: Signal void
during systole in
CineMRI

65. Esophageal Diverticulum
 Esophageal diverticulum: sacs and outpouchings from the
Esophagus.
 True type = All three layers of the wall.
 False type = Only mucosa and submucosa (not adventitia).
 Can also be pulsion or traction type.
 Single or double contrast studies can be done with a substance
that produces gas “air” along with the barium swallow.
 “Biphasic exams” involve both single and double contrast studies.
Classification:
Upper esophageal – Zenkers diverticulum, Killian- jamieson divert.
Middle esophageal – traction are common due to inflammatory
processes in the mediastinum eg. Tuberculosis of the nodes which
pull on the Esophagus
Pulsion diverticula from processes that increase intraluminal
pressure and weaken the wall eg. Achalasia where food backs up
against the non-opening cardiac sphincter of the stomach or
esophageal dysmotility.

66. (left) Zenkers diverticulum:
- Pharyngoesophageal
- Older women
- It is a “pulsion diverticulum”.
- Site: superior boundary is
thyropharyngeal muscle and inferior
boundary is cricopharyngeal muscle.
- Seen posteriorly
- False diverticulum = herniation of
mucosa and submucosa through
muscular layer
(left) Mid-oesophageal Diverticulum:
- May be formed in response to pull
from fibrous adhesions following
lymph node infection (usually TB)
-True diverticulum = contains all 3
esophageal layers
-Or, may form from increased
intraluminal pressure and be pulsion
diverticula
(left) Epiphrenic diverticulum:
-Location is usually in distal
esophagus on lateral
esophageal wall, right > left
- Often associated with hiatal
hernia
-Pulsion diverticulum
-False diverticulum
**Pulsion = means pushed out
by internal pressure originating
from within hollow organs.
Essentially a herniation. Other
form = “traction” – the pulling
and retraction of tissues from
external pressure exerted by
fibrous tissue/ scarring.

68. Two main types: sliding and paraesophageal
 Most are acquired
 Incidence increases with age
 About 1/5 of patients with a hiatal hernia, usually the sliding type, have associated
gastro-esophageal reflux (GERD).
 Sliding hernias = 99%, lies at esophagogastric junction just above the diaphragm.
 Incidence increases with age. Most are asymptomatic but there is an assoc. with
GERD.
 Gerd can occur without any hiatal hernia and the same sphincteric dysfunction
that causes GERD can lead to a sliding hernia.
Radiologic findings:
-Bulbous area at distal end of Esophagus with failure of the Esophagus to narrow as
it passes through the diaphragm.
-Distal Esophagus should not measure more than 50%/ half the diameter of the
tubular Esophagus.
-Mucosal folds may roll out onto the diaphragm and cause small filling defects:
Schatzki’s rings – mark the postion of the esophagogastric junction
(above) Sliding hiatal hernia
with mucosal folds and
Schatzki rings
Hiatal Hernia

69. Paraesophageal Hernia:
 Worse of the two – Part of the stomach (fundus/antrum) rises up and
pushes through the diaphragm.
 The EGJ remains subdiaphragmatic however and is often “incarcerated” or
“Strangulated”.
 NOT associated with GERD.
 Often incidental finding
 CT, MRI, Chest X-ray with barium swallow
 Also esophagogastroduodenoscopy can be used.
 Treatment: medications to constrict the sphincter, failing this surgery,
especially if a lot of the stomach has passed superiorly.
Intrathoracic stomach:
 Cardia may still be subdiaphragmatic
 Greater curvature may be on left
or right side. See right (X- ray) and below (CT)

70. 3 images above and
left: Paraesophageal
hernias
4 images above/left:
Sliding hernias. More
common.

71. Megaoesophagus:
 Etiology: A). esophageal dysmotility caused by Chagas disease
(Trypanosoma cruzi), achalasia, scleroderma
Or B). Distal obstructions: malignant strictures caused by esophageal or
gastric carcinomas. Benign strictures and compression eg.
Lymphadenopathy.
 Is the diffuse dilatation of the esophageal wall.

72. Esophageal Varices:
 They are dilated submucosal veins between the portal and azygos venous
system due to increased collateral flow usually due to portal hypertension.
 Can be either uphill or downhill depending on the net flow of veinous
blood.
 Uphill = More common, usually only mid-lower 2/3rds of Esophagus
because distal Esophagus drains via the gastric vein. They extend upward
until the level of the tracheal carina. Most often caused secondary to liver
cirrhosis. Also due to splenic or portal thrombosis and rarely massive
splenomegaly.
 Downhill = upper 1/3rd of Esophagus. Caused by obstruction of azygos
drainage or superior vena cava by lung cancers, lymphoma, retrosternal
goiter, thymoma and mediastinal fibrosis.
 Can be seen with CT, UGI (upper gastrointestinal series -contrasted X-ray),
*DD= Chronic esophagitis or varicoid esophageal cancer.
Complications:
Bleeding (hematemesis) – approx. ¼ of patients within 2-3 years
Massive Exsanguination and death – 10-15%
CT scan axial and
coronal/ frontal

73. Image findings Esophageal Varices:
-Small amounts of barium are used to line the
mucosa. Patient is asked to avoid swallowing to
prevent peristaltic wave (lasts 20-30s) which would
obscure image.
Plain X ray – lobulated mass in posterior
mediastinum (not alsways visible)/ silhouetting of
aorta/ azygoesophageal recess is abnormally convex.
UGI (w/contrast): Thickened and interrupted
mucosal folds/ twisting or tortuous radiolucencies of
variable size and location.
Smooth lobulated filling defects -“Worm-eaten”
CT Thickened wall and lobulated outer contour.
Pleated/ bunched together esophageal luminal
masses.
Treatment: Tieing off the veins with elastic bands.
Vasopressors to reduce blood-flow into the veins.
Balloon tamponade – places internal compression to
prevent bleedinf. Liver transplant.

75. Esophageal Stricture:
 An esophageal stricture is an abnormal tightening of
the Esophagus, limit or block food and liquid on way to
stomach. Swallowing difficult/ lump in throat but
cancer and other issues can also cause them. A dilation
procedure can widen the Esophagus and reduce
symptoms.
 GERD – Barrett's Esophagus, is the most common
cause. Others: corrosive substance ingestion,
esophagitis, esophageal cancers, radiation therapy,
surgery, NSAIDS.
 Can be cancerous or benign. Cancerous type causes
rapid worsening of symptoms.
 Usually affect people over 40.
Radiologic finding:
BENIGN: smooth, tapering, concentric narrowing, may
only involve half of the wall – asymmetrical wall
contraction
MALIGNANT: sudden onset, nodular mucosa, irregular
shape/ eccentric and asymmetric.
Post -Corrosive
Malignant

77. Esophageal tear/ rupture/ perforation:
 Rare, medical emergency, people over 60/ male
predominance
 Chest or epigastric pain, dysphagia or dyspnoea,
subcutaneous emphysema and risk of bleeding
 Mostly iatrogenic: radiation therapy, surgical trauma
(penetrating or blunt)
 Other causes: corrosives, foreign body, cancer and
post vomitus (Boerhaave syndrome)
Radiologic Findings:
Plain x ray: Pneumomediastinum, pneumothorax, pleural
effusion are all clues. Abnormal cardio-thoracic outline.
Widening of mediastinal shadow.
CT: Extraluminal gas locules which can be found
anywhere from adjacent to the Esophagus to the
mediastinum and even abdomen/ pleural or mediastinal
fluid. Pericardial or pleural effusions.
Fluoroscopy: water soluble contrast shows mucosal
deformity or even leaks out of the Esophagus.
*Barium is contraindicated as it should never leave a
hollow organ as it induces inflammation.
Extravasated contrast
Diffuse Pneumomediastinum
Pneumomediastinum with L.
pleural effusion
Esophageal tear visible

78. Esophageal Foreign Body:
 Most common site of foreign bodies.
 Most common foods are a). Long, rubbery, smooth foods
like steak, hotdogs b). Fish bones
 Common in paediatrics: Grapes, peanuts, coins and
batteries.
 Usually lodge at a natural narrowing especially round
objects: cardiac sphincter but also commonly get stuck
on pathologic narrowing's – strictures, cancer etc.
 Complications: Obstruction (partial – less serious, or
total – not even swallowed saliva can pass), pressure
necrosis leading to perforation
 Swallowing batteries is dangerous as well as multiple
magnets.
Radiological findings:
Depending on the foreign body; metals and glass – show up
brightly radioopaque on X-ray, if suspected – no MRI!
US: Most foreign bodies are hyperechoic
CT: use all window options available; soft tissue, bone and
lung as the density of foreign bodies can vary widely.
*Some plastics may not show up on CT or MRI!
MRI: does not show wood; splinters, toothpicks etc. use US
for these.
Above; patient has
ingested a crucifix.
Pacemaker is also clearly
visible with leads

79. Esophageal Carcinoma:
 Relatively uncommon. Begins with increasing dysphagia,
hoarseness, heartburn and indigestion.
 Rare 1-4% of all cancers, 10% of GIT cancers, male
predominance, African ethnicity at increased risk, Most
common type is squamous cell carcinoma then
adenocarcinoma.
Radiological features:
**Combo: CT, US (Transesophageal) and PET scan are
classically used in order to make the diagnosis.
Chest radiograph: Deviation or indentation of trachea,
retrocardiac or posterior mediastinal mass. Esophageal air
fluid level. Aspiration pneumonia (reccurent). Widened
esophago-azygos recess.
CT: circumferential wall thickening/ dilated Esophagus
proximal to obstruction/ may contain fluid/ invasion into
either trachea or aortic and mass defect.
Fluoroscopy: Irregular Stricture with “hold-up” of fluids
trying to pass through. Shouldering may also be seen.

80. Ultrasound: Most effective for specific staging of the cancer.
T defines the layers of the esophageal wall hence can
differentiate T1, T2, and T3 tumours.
On US, the Esophagus consists of five layers.
1) Hyperechoic - interface between the transducer probe
and the superficial mucosa.
2).Hypoechoic layer represents the lamina propria and
muscularis mucosae.
3). Hyperechoic layer represents the submucosa
4). Hypoechoic layer represents the muscularis propria
5). Represents the interface between the adventitia and
surrounding tissues
Left: Pet
scan
showing
increased
uptake of
sugar by
cells:
suggests
cancer
Complications of Esophageal cancer: Trachea-
esophageal Fistula, fistula to bronchi or
mediastinum, perforation.

81. Peptic ulcer disease: 1). Gastric Ulcer
• Peptic ulcer is defined as a mucosa break of greater than 3mm.
• Gastric ulcer = a small subclass (only 5% of cases) of peptic ulcer
disease.
• Cause: Helicobacter pylori and increased gastric acid secretion.
• More common in males and older people
• “Gnawing” epigastric pain relieved after eating or taking antacids,
melena, hematemesis.
• Endoscopy is now more common than barium meal as a preferred
diagnostic approach (95% sensitivity) however with acute
abdominal pain, CT is first choice.
Complications: perforation, penetration (pancreatitis) and obstruction.
Plain radiograph: Not particularly useful but can demonstrate free-air
(pneumoperitoneum).
Fluoroscopy: Double contrast is used (barium and effervescent).
Pocket of barium indicates ulcer.
- Round ulcer most of the time and occasionally linear.
- If gastric folds are thickened and ulcer is post bulbar = suggestive of
Zollinger-Ellison syndrome.
- Radiating gastric folds
- Swollen border

82. CT features:
Use of an I.V contrast with multi-phase scan (non-
contrast, arterial and delayed) can visualise active
bleeding into the lumen of the stomach.
Ultrasound
Right: CT
axial
projection
perforated
gastric ulcer
Left:
Fluoro-
scopic
image
Right: CT
- Axial
Large
Gastric
ulcer

83. 2). Duodenal ulcer
 10% of adults, accounts for 2/3rds of all
peptic ulcers.
 Unlike gastric ulcers where 5 % are
malignant, duodenal ulcers are virtually
always benign.
 Causative agents: H. Pylori infection and
NSAID use, same as for gastric ulcers.
 Endoscopy: high sensitivity
 Double-contrast barium studies: High
sensitivity (but single contrast is poor).
Double contrast upper GIT series showing posterior wall duodenal ulcer
 3:1 Male to female ratio
 Bulbar location = 95%, anterior wall most common = 50% of
these.
 Post-bulbar location = 3-5% most common wall = medial.
Tendency to haemorrhage.
 Small round, ovoid or linear craters.

84. Upper GIT double- contrast fluoroscopy;
Collection of barium on represents crater.

85. Free Gas/ Pneumoperitoneum:
 Free gas in the peritoneal cavity due to several severe diseases.
 Most common cause: disruption of wall of hollow organs (tears,
perforations, trauma) secondary to:
- Peptic ulcer disease
- Ischemic bowel
- Bowel obstruction
- Appendicitis
- Diverticulitis
- Malignancy
- IBD
- Trauma: colonoscopy, surgery, foreign bodies, mechanical ventilation.
Plain chest X-ray:
Subdiaphragmatic free gas
“Leaping dolphin sign” – the hemidiaphragms are acutely concave due to
pressure from free gas.
“Continuous diaphragm sign” – normally central diaphragm is obscured
by cardiac silhouette. If we can see a continuous diaphragm through the
mediastinum it is suggestive of free gas.
US: Discreet hyperechoic foci – trapped air bubbles. Reverberation Lines.
No change with respiration. Moves when patient is repositioned. Moves
when pressure is applied caudally.
Chest radiograph: subdiaphragmatic
air clearly visible

86. Above: Continuous diaphragm sign on a
chest x ray. Normally the central part
(orange arrow) is connected to the
cardiac silhouette
CT axial projections
showing collection of
air superiorly US: Little gas bubbles (yellow
arrow) and reverberation lines
(2nd pic) indicate free air.

87. Gastric carcinoma;
 2nd most common cancer in the world after lung cancer.
 Uncommon before 40 years of age
 50% of people are asymptomatic. Symptoms may include dyspepsia,
anorexia and weight loss.
 5 year survival rate less than 20%. Poor prognosis
 95% = adenocarcinomas. H. pylori is a risk factor as well as GERD,
recurrent gastric ulcers, chronic gastritis, obesity, smoking and diet low
in fibre, fruit and vegetables.
 Pre-cancerous conditions: polyps, mucosa atrophy, pernicious anaemia.
 Examination: Full medical history, Full blood count and DBC, stool
sample – occult bleeding.
Endoscopy is good for visualisation/ biopsy
CT is good for staging of metastatic disease.
**Plain radiograph and ultrasound are of limited value.
CT: with Negative contrast (H20/gas)
- Polypoid mass protruding out into lumen of stomach
- Focal wall thickening
- Ulceration – gas filled crater in mass.
Positive contrast agent = high atomic number
= radioopaque (bright) = eg. barium, iodine
Negative contrast agent = lower atomic
number = radiolucent (dark) = water, air etc.
N.B! Benign peptic
ulcers tend to be on
the lesser curvature
whilst a greater
curvature lesion is
highly suspect of
carcinoma

88. Gastric Adenocarcinoma – most common stomach cancer
 Often asymptomatic when curable
 Anorexia, dyspepsia and weight loss when tumour becomes bulky
and obstructs stomach lumen
 Virchow's node (or trosier sign – left supraclavicular node
enlargement), Sister Mary-Joseph node (Umbilicus), Krukenbergs
node (Ovarian metastasis).
Endoscopy; Most appropriate primary investigation. Elicits; location,
extent, and can perform biopsy.
Radiological methods are only used to stage the metastasis.
Fluoroscopy
 Type I = elevated lesion (polyploid)
 Type II = Plaque/ raised plate like mucosal nodularity
 Type III = Ulcerative – crater with fusion of gastric folds, shallow
irregular shape
Advanced cancer: Can be lobulated, posterior wall - filling defect,
anterior wall - etched outline of trapped barium.
Penetration deep into wall (70% cases)
Ultrasound: Not useful unless of endoscopic type or tumour is large.
CT: preferred staging modality
We are looking for polyploid mass with/without
ulceration, focal wall thickening, irregular mucosal
folds, infiltration – loss of folds, gas filled ulcerative
crater.
Clinical stages:
STAGE 0: Limited to mucosa. Treatment mucosal
resection with radiation therapy/ chemo usually not
indicated.
STAGE 1: A – penetration into second and third layer
of stomach wall. Treatment is removal of part of
omentum. B – spread to local lymph nodes.
Radiation and chemo are now indicated.
STAGE 2: All four layers of wall penetrated. Or
superficial 2 layers) penetration and distant lymph
node metastasis.
STAGE 3: Three layers plus distant metastasis
STAGE 4: Diffuse metastasis to other organs and
tissue infiltration. Cure is rare at this stage.

89. Right: Fluoroscopy - Double-barium
contrast meal showing
adenocarcinoma of greater
curvature.
Above - Ultrasound:
loss over normal
alternating hyper- and
hypo- echoic bands of
GIT wall (long white
arrows show dark
shadow of carcinoma
penetrating serosa)
Enlarged perigastric
lymphnodes can also
be seen (small pointer
arrows)
Below: Double contrast-
Advanced Cancer filling the
body of the stomach
Above – CT showing adenocarcinoma of antro-pyloric
tract; note thickening of wall, visible ulcerative crater
and irregularity in shape

90. Bowel Obstruction
• Account for 20% of surgical abdomens
• Clinical presentation; Colicky abdominal pain , vomiting (more
predominant in small bowel obstruction), abdominal distension,
absolute constipation.
Plain Radiographic features: Can differentiate true mechanical
obstruction from ileus or constipation, localise the site of obstruction,
identify cause, assess for complications – ischemia and perforation,
assess viability of the bowel segments.
3-6-9 rule! A good way to assess for normal diameters of the bowel.
3cm = small intestine
6 cm = Large bowel and appendix
9 cm = cecum
Any change in this ratio indicates distension.
+ Fluid levels
Note: absence of these findings on abdominal x ray do not exclude
bowel obstruction.
CT: We are looking for;
A). Transitional point with abrupt change in bowel diameters
B). Dilated bowel loops before the obstruction
Left: Small
bowel
obstruction –
see visible
distension and
multiple air-
fluid levels
Left; CT shows air-
filled distended
transverse colon
with abrupt
termination in left
upper quadrant –
cause was
intussusception

91. C). Collapsed bowel distal to transitional point.
D). Bowel wall thickening (edema)
E). Stranding/ splaying of surrounding mesenteric fat – indicates
inflammation.
+ Complications:
1. Free gas – perforation
2.Ischemia
3.Strangulation – if herniation is seen.
These are general feature but radiologically we can further divide/
specify for small or large bowel obstruction.
Small Bowel Obstruction:
• More common site for mechanical obstruction than large intestine
(80%).
• Cramping pain, nausea and vomiting.
• Causes are congenital; atresia, midgut volvulus, mesenteric cyst,
Meckel diverticulum
or acquired; EXTRINSIC – adhesions, herniation, compression by
neoplasms/ aneurysms or hematomas
INTRINSIC – Inflammation (Chrons/ TB), luminal tumours, radiation,
ischemia , intussisception, foreign bodies and gallstones
Right: Bowel
obstruction with
massive
pneumoperitoneum
CT – frontal
projection
Small bowel
obstruction
secondary to
caecal
tumour

92. Radiographic features of small bowel obstruction:
• Dilated loops usually central ones
• Gas-fluid levels
• Plicae circulares are clearly visible (kerckring folds)
• “String of beads”
CT features: Same features as radiograph
Plus; Small bowel faeces sign – impaction of intestinal content
until it looks more like that seen in the large bowel.
Large intestinal obstruction:
• Most common cause = colorectal carcinoma (50%)
• 2nd most common = colonic diverticulitis
• Others: volvulus – sigmoid and caecal, ischemic stricture due
to colitis, faecal impaction (elderly) and intussusception.
Plain Radiograph:
• Proximal colonic distension
• Collapsed distal colon
• Small bowel dilatation
• No air in rectum
• Mural gas, free peritoneal gas or port venous gas (advanced
stage)

93. CT findings large bowel obstruction;
Most common modality for diagnosis as well as identification of
cause.
• Transition point
• Distended diameter with thinning and stretching of walls
• Complication: perforation or ischemia.
Volvulus:
Torsion of the gut around its mesentery
There are four types;
1 Gastric volvulus
2 Midgut volvulus
3 Cecal Volvulus
4 Sigmoid Volvulus (most common = 60%)
Complications: Torsion compresses blood supply - Venous
infarction occurs first followed by arterial ischemia if not corrected
and subsequent absolute infarction of the affected intestine.
Sigmoid Volvulus:
• Coffee-bean/ Kidney-bean or “Horseshoe” sign
• Unlike caecal volvulus – it lacks visible haustra with lower end
pointing into pelvis
• Liver overlap and absent rectal gas
Sigmoid
volvuli;
CT features of sigmoid volvulus:
• X marks the spot sign – where
the mesentery is twisted we see
an overlap.
• Whirl sign
• With contrast the sigmoid curves
and tapers like a birds beak

94. Appendicitis:
• Inflammation of the vermiform appendix
• Most common reason for abdominal surgery in young people. CT
is the most sensitive method for appendicitis.
• Most often caused by obstruction of the appendiceal lumen
resulting in fluid accumulation , suppurative inflammation,
secondary infection and finally ischemia, necrosis and perforation.
Radiographic features: (low diag. value)
 Most difficult part is finding it as its position is highly variable
 The appendix can have any length between 2-20cm
 Ascending behind the caecum is most common (66%), inferior to
the caecum (30%).
 Appendicolith might be observed as well as free gas (perforation)
or small bowel obstruction with multiple air-fluid levels.
Ultrasound:
 Round, aperistaltic, non-compressible dilated appendix.
 Appendicoliths are hyperechoic.
 Peri-appendiceal fluid accumulation
 Peri-appendiceal reactive enlargement of lymphnodes
 Thickened wall; Hyperaemia and necrosis

95. CT findings acute appendicitis:
First identify ileocecal valve, and then
look inferiorly on the ipsilateral side for
the appendix
 Appendix lumen dilation greater than
6mm
 Wall thickening of more than 3mm
 Periappendiceal inflammation: fat
stranding (abnormally increased
attenuation – opacification – of fat
tissue due to hyperaemia and
edema. Also occurs in peritonitis,
inflammation, ischemia and necrosis
of the bowel, pancreatitis, GIT
cancers and trauma)
 Abscess
 Peri-appendiceal fluid accumulation
 Focal non-enhancing wall– necrosis
MRI: is reserved only for pregnant
patients.
Left: Visible fluid filled
(black) lumen of
distended appendix in
an axial T2 weighted
MRI, fat stranding
(bright curvilinear
edge) can be seen
around the appendix
as well as two
appendicoliths

96. Right: CT - Distal
inflammation of the
appendix, calcified
appendicolith – white
obstruction – in neck of
appendix where it
connects to cecum (C ).
Notice the multiple air-
fluid levels in the small
intestine

97. Ulcerative colitis:
• Inflammatory bowel disease that primarily
affects the colon.
• Young adults (15-40), more common in males,
second peak after 50, less prevalent in
smokers (nicotine has protective effect).
• Symptoms: tenesmus (feeling like you still
need to void bowels despite having done so),
pain, fever.
• Differences with crohn’s:
- Ulcerative colitis only effects
mucosa/submucosa whilst crohns affects
entire wall.
- Restricted to distal colon/ rectum, crohns can
affect any part of the GIT mostly ileum.
- No strictures, fistulas and rectum is involved
unlike crohns.
- U. colitis causes bloody stool whilst crohns
doesn’t tend to.
- Obstruction and weight-loss is uncommon in
U. colitis.
- Nausea and vomiting uncommon.
Radiographic features: uninformative
Fluoroscopy: Double contrast barium enema – great
detailing of colonic mucosa. Contraindicated in severe
cases due to risk of perforation.
- Granular appearance
- Haustral thickening
- Mucosal ulcerations (button shape – pseudopolyp)
- Featureless and narrow in chronic cases – “lead pipe
sign”
Computed tomography:
- Abnormal thinning of colon wall.
- Various areas of thickened wall with inflammatory
pseudopolyps
- Mural stratification.
- Fat halo sign – rectum (submucosal fat deposition)
MRI:
Increased enhancement wall.
Thickening
Loss of haustral markings

98. Left : MRI
showing
rectal wall
thickening
Right: CT
showing the
same rectal
wall
thickening
Ulcerative colitis

99. Crohn’s disease:
• Idiopathic inflammatory bowel disease characterised by
widespread discontinuous (segmental) GIT inflammation which
can occur at any point along its course from mouth to anus.
Extra-intestinal disease is common.
• The terminal ileum and proximal colon however are the most
common sites.
• No gender predilection and the disease has geographic
variability.
• Symptoms include:
- Skin rash
- Pyoderma gangrenosum (purulent non-infectious ulceration of
skin)
- Stomatitis
- Fistulas between skin and GIT
- Arthritis and spondylarthrosis
- Episcleritis, iritis and uveitis
- Cirrhosis and pancreatitis
- Gallstones and renal calculi.
Radiographic evidence:
- ”Skip lesions” and discrete ulcerations.
- Small bowel = 70-80%, Small and large = 50%, Large only = 20%.
Fluoroscopy (with barium):
- Mucosal ulcers, longitudinal fissures,
cobblestone appearance.
- Widely separated loops due to fibrofatty
accumulation
- Leakage of barium through fistulae
- Thickened oedematous folds
- String sign; Stricture and spastic narrowing.
- Pseudodiverticula
- Partial obstruction
Ultrasound: (limited value but highly available)
- Wall thickening in small bowel (>3-4mm)
- Segmental loss of peristalsis
- Loss of clearly stratified wall layers
- Mural hyperaemia
- Hyperechoic fat stranding external to bowel
wall
- Mesenteric lymphadenopathy
- Hydroperitoneum (free fluid)
Doppler reveals increased arterial flow.

100. CT findings in Crohn’s disease:
 Hyperintensity of wall
 Fat-halo sign – submucosal fat
deposition
 Bowel wall thickening
 Comb sign – engorgement of vasa
recta (straight veins of mesentery)
 Fat stranding
 Strictures and fistulae
 Abscesses, peri-anal disease and
hepatobiliary manifestations
MRI: (MR enterography)
 Segmental mural hyper-
enhancement
 Wall thickening
 Intramural edema
 Strictures
 Ulcerations
 Decreased peristalsis
 Mesenteric venous thrombosis
 Lymphadenopathy
 abscess
Rose-thorn ulcers
Above: enteroscopy visualises ulcers. Right;
Fluoroscopy with barium

101. Crohns with duodenal
involvement
Fluoroscopic
visualisation of cobble
stoning
Ultrasound
showing
difference
between
normal bowel
loop and
Crohns bowel
loops
Left: CT showing bowel
strictures with mucosal
enhancement (white
arrows) and bowel wall
thickening. Stars
localise dilations of
proximal bowel
indicating obstruction

102. Colorectal carcinoma:
 Umbrella term for any cancer of the large bowel, caecum,
appendix or rectum.
 Second most commonly diagnosed malignancy in adults. Five
year survival rate of only 40-50%.
 Risk factors; low-fibre, high meat diet, IBD, obesity, smoking.
 Symptoms; constipation or diarrhea, iron-def. anemia, bowel
obstruction. Symptoms specific to sites of metastasis. Often
insidious nature.
 Most common locations are:
- Rectosigmoid (55%)
- Caecal/ ascending colon (20%)
- Transverse (10%)
- Descending colon (5%)
 Develops from adenomatous polyps which are usually benign.
 Preferred mode of investigation; Colonoscopy or DCBE
(Double contrast barium enema).
Fluoroscopy:
Double contrast is more sensitive than single contrast
“Apple-core sign” – a narrow circumferential protruding band of
tissue which may partially or totally obstruct the lumen.
Fistulas – to bladder, vagina, bowel.
“Apple-core sign” visible at right colic flexure
on contrast enhanced radiograph

103. Diverticulosis/ Diverticular disease:
 Diverticula are outpouchings of the bowel that result in
close ended sacs that communicate with the main lumen.
 They can arise almost anywhere in the small or large
bowel but are most common in the sigmoid colon.
*Also occur in Esophagus and stomach.
 Diverticula are susceptible to becoming infected due to
faecal trapping, stasis as well as harbouring bacteria and
gas accumulation which all lead to inflammation and
subsequent diverticulitis and diverticular hemorrhage.
 Most people are asymptomatic.
 Complications include; perforation and peritonitis,
intestinal obstruction, fistula, abscess, rectorrhagia and
stricture.
 TYPES;
Small intestine =
- Duodenal diverticula
- Meckel's diverticulum
- Jejunoileal Diverticulum
Large intestine =
- Sigmoid diverticulum
- Colonic (Transverse, descending etc)
Barium double
contrast studies;
Sigmoid
diverticula

104. Meckel diverticulum:
 Most common congenital structural abnormality of the
GIT.
 It is due to the fibrous degeneration of the umbilical
end of the omphalomesenteric (or “Vitelline”) duct that
occurs around the distal ileum.
 Slight male predilection
 Most complications occur in first two years of life.
 Clinical presentation: GIT hemorrhage, Small bowel
obstruction, intussusception, perforation, diverticulitis.
 It is characteristically difficult to visualise on most
radiographic images. Fluoroscopy and US

105. CT investigations:
• Better for visualisation and staging of metastasis.
• Soft tissue densities in lumen can sometimes be seen with
ulcerations
• Calcifications may be visible
• Complications may be seen: intussusception, perforation
etc.
MRI:
• Staging of lymph node involvement.
Differential Diagnosis:
Diverticulosis, IBD.
Left: 3 CT images
showing A= sigmoid
Polyp
B = Asymmetrical wall
thickening
C=Infiltration with
local node
involvement
Fluoroscopy

106. Liver Steatosis:
 Increase in intracellular fat content of the liver.
 Radiographically divided into 3 groups:
1). Focal Hepatic Steatosis
2). Diffuse hepatic steatosis
3). Multifocal nodular steatosis
Focal hepatic steatosis
US: *features only become apparent after fat conc.
reaches 15-20%*
- Increased liver echogenicity (brighter)
- Mild positive mass effect
- No distortion of vessels
- Inability to see portal vein walls.
Compare the liver and kidney parenchyma on Ultrasound
NORMAL FATTY LIVER
CT: Decreased attenuation (non-contrast as well as post
contrast).
Liver and spleen should be of comparable similarity in
density normally.
Intra-hepatic Vessels are highlighted/ stand out against
the fatty parenchyma in fatty liver disease
MRI: Modality of choice if diagnosis isn’t certain
Increased T1 signal

107. NORMAL
LIVER
FATTY
LIVER
CT
 Compare with
spleen
 Look at hepatic
vessels
 Search for fatty
nodules/ infiltrates

108. Liver Cirrhosis;
 Common end-point for most Liver diseases
 Typical etiology; Alcohol, hepatitis viruses B + C, drugs/
toxins, Biliary disease, storage diseases, autoimmune
and cystic fibrosis.
 Clinical presentation:
- Liver failure
- Portal Hypertension
- Ascites
- Hepatocellular carcinoma (HCC)
 Pathological stages are; a. fibrosis -> b. Nodular
regeneration -> c. Distortion of hepatic architecture
Radiographic features:
• Hypertrophy of the left and caudate lobe and atrophy of
the right lobe due to changes in blood-flow.
Ultrasound:
- Surface nodules and course heterogenous texture
- Changes in relative proportion of lobes
- Enlarged portal vein (specific finding)
- Cavernous transformation of intrahepatic vessels
- Other features: Splenomegaly, ascites and fatty changes
Below; various
US echoic
textures seen
in different
liver diseases.

109. CT features;
**Insensitive in early cirrhosis
• Regenerative nodules – either iso-dense or
hyperdense are visible on hepatic surface
• Features of fatty change
• Lobar hypertrophy or atrophy
• Signs of portal hypertension – portal vein
dilation, thrombosis, splenomegaly,
enhanced Porto-systemic collaterals.
MRI; Also insensitive in early cirrhosis but is
very good at screening for hepato-cellular
carcinoma.
- Same changes as US and CT.
- T1 – nodules are iso dense or hyperdense,
no early enhancement (arterial) because
there is mostly venous supply.
T2 – nodules are iso-dense but can be
hypodense if siderotic.
MR angiography – Can be used to assess
venous flow and portocaval anastomosis.
Healthy Cirrhotic

110. CT – axial projection Liver cirrhosis; Notice
a). The heterogenous nodularity b).
Splenomegaly 2nd to portal hypertension
Above: Enlarged spleen and
nodular liver on T1 weighted
MRI

111. Hepatocellular Carcinoma (Primary cancer):
 5% of all cancers. Strongly associated with cirrhosis and hepatitis viral
infections. Others: hemochromatosis, biliary cholangitis, porphyria and DM.
 Fatigue, cachexia, and other constitutional symptoms, jaundice, portal
hypertension, hepatomegaly and hemorrhage
 Marker = Alpha fetoprotein (AFP)
Radiographic features;
 Focal type; Large mass with necrosis, calcification of fat infiltrate
 Multifocal nodular type; variable attenuation with central necrosis.
 Diffuse type; difficult to distinguish from cirrhosis.
Ultrasound:
- Small hypoechoic foci
- Larger tumours – heterogenous due to fibrosis, haemorrhage, necrosis, fatty
change or calcifications.
- Sometimes hypoechogenic halo.
- Contrast enhanced: Arterial phase= enhancement (neovascularisation),
Portal phase = hypoechoic “Wash out”.
CT features:
• Later arterial enhancement followed by rapid washout – quickly becoming
indistinct from the remaining liver during venous phase.
• Wedge-shaped perfusion abnormalities
MRI features:
 T1 = hypodense usually
 T2 = variable, moderately hyperdense
 T1 with gadolinium contrast; Arterial
enhancement, persistent rim
enhancement thereafter “Capsule”
Digital subtraction angiography (DSA);
Hyper-vascular area = tumour
Portal vein tumour induced thrombi may
be visible.
Hypo-echoic mass on ultrasound

112. ABOVE CT axial; Arterial phase … and portal venous phase
Diffuse HCC with malignant portal
thrombosis
T1 weighted MRI RIGHT CT –
axial
projection
showing HCC
with
peritoneal
involvement

113. Echinococcal Cyst in Liver (Hydatid disease);
 Caused by parasitic tapeworm Echinococcus Granulosus
 Common in N. America and Australia. Most often the cysts will appear
in the liver, muscle, lungs and less commonly brain and other organs.
 Characterised by a fibrose rimmed, well circumscribed sphere with
little to no surrounding immune reaction.
 Dogs are the main host.
Radiographic features:
• Classically a curvilinear, semi-lunar calcific ring is seen “Egg-shell”
calcifications.
US: Cysts with septae and echo-genic material separating them from
smaller daughter cysts.
CT:
Fluid in cysts variably attenuates due to proteinaceous material.
Undulating membranous folding may be seen in the cyst = detached
endocyst. Peripheral focal calcifications. Hyperdense septae, changes to
intrahepatic ducts – compression, distension, rupture etc
MRI: T1 w/ contrast = enhancement of capsule.
CT Axial Contrast enhanced Portal Venous Phase
LEFT-
Coronal
projection
MRI T2
weighted
large
hydatid
cyst.

114. Calcified hydatid cyst
Ultrasound
images
clearly
show
undulating
membrane
Eggshell calcification seen on a
plain x ray
CT images of
cysts

115. Secondary Liver Metastasis;
• Much more common than primary hepatic cancer
• Symptoms; stretching of capsule leads to localised pain and
tenderness, also liver dysfunction, metabolic disorders, ascites,
low grade fever.
• Most common sites of primary malignancy;
- Gastrointestinal tract; esophageal, gastric, pancreatic ductal
adenocarcinoma (cancer cells travel by portal system).
- Others; Lungs, Breasts, ovaries/ testicular, sarcomas,
melanomas.
Important* It is difficult to accurately assess/ stage liver metastasis
due to the common presence of other more benign lesions –
haemangiomas, fatty deposits, fatty sparing, nodules, venous
malformations etc which can be confused for tumours.
Ultrasound:
- Rounded/ well circumscribed.
- Positive mass effect and distortion of nearby vessels
- Most often hypoechoic
- Hypoechoic halo due to compression of liver parenchyma and
decreased fat accumulation there.
- Cystic, calcified, echogenic variations are all possible
- N.B! The state of the background (Fatty or normal) can impact
on the relative echogenicity of the parenchyma.
Above; Axial CT – contrast
enhanced Arterial Phase
Axial CT contrast enhanced
Portal Venous phase
ABOVE; A case of multiple hyperechoic tumours
on ultrasound. Normally hypoechoic

116. CT findings:
• Liver Mets typically = Hypoattenuating
• Enhances less than rest of liver on contrast studies
• Contrast enhancement is peripheral
• There is delayed portal venous washout unlike
Haemangiomas.
MRI;
T1 – moderately hypointense
T1 + Contrast – peripheral enhancement or lesional
enhancement.
T2 – a little hyperdense.
Classical ultrasound findings; hypoechoic tumour with
dark hypoechoic halo/shadow.
Hypoattenuating Mets on a CT
LEFT quadrant: Various weightings
on MRI; upper = fat suppressed T2
weighted, below contrast enhanced
arterial phase
ABOVE: Solitary hypointense mass.

117. Liver Haemangioma:
• Common benign vascular malformation
• Five times more common in females and rarely seen in
children.
Ultrasound:
- Well defined hyperechoic lesions
- In fatty liver (hyperechoic) the haemangioma may look
hypoechoic.
- Colour doppler may show feeding vessels peripherally
Computed tomography:
- Hypoattenuating
- Bright dot sign – small focal hyperintense area in the
hypointense lesion.
- Contrast:
a). Arterial phase = peripheral enhancement
b). Portal venous phase = progressive peripheral
enhancement
c). Delayed phase = iso/hyper-attenuating to liver
parenchyma
MRI: T1: Hypointense , T2 Hyperintense
Axial CT; A – Arterial phase B – Delayed Phase
A B
C D
A = unenhanced
(hypodense), B =
Arterial phase –
peripheral
nodular
enhancement. C
= Portal phase
D =delayed
phase
(equilibrium
phase).

119. Cholecystitis and Cholelithiasis:
• Cholelithiasis can be acute or chronic. Primary cause is cholelithiasis, causes acute
and constant pain in the right upper quadrant that often radiates the right
shoulder.
• Cholelithiasis Mnemonic “The Five F’s” : Female, Fertile, Fat, Fair complexion
(Caucasian), over Forty.
Ultrasound: Gold standard for evaluation.
- Gallbladder wall thickening greater than 3mm.
- Peri-cholecystic fluid
- Gallbladder distension
- Possibly stones (hyperechoic) with an acoustic shadow (hypoechoic) and sludge
(hypoechoic, moves slowly with changed position of patient, can form a fluid-fluid
level with the anechoic bile above.)
CT: Less diagnostic than US but good for other related pathologies.
** Gallstones will not be seen in CT – they are iso-dense to the bile
- Gallbladder distension and wall thickening
- Mucosa is hyperdense
- Bile appears hyperdense
- Liver is enhanced due to reactive hyperaemia
- Gallbladder fundus pushes against anterior abdominal wall due to increased
pressure and swelling.
- MRCP (Magnetic resonance Cholangiopancreatography): Contrast flow stops due
to impacted stones in the neck of the gallbladder. Otherwise, MRI shows similar
findings to the other imaging techniques.
Gallstones
Acoustic
shadowing

120. Stone Distended gallbladder
with fundus pressing
Ant. abdo. wall

121. Gallbladder polyp
 Elevated lesions on the mucosal surface of the
bladder.
 Best characterised on ultrasound but can also be
diagnosed via CT and MRI
 Over 90% are benign but they are relatively frequent
( around 1 in every 10 people) as so its wise to be
aware of their findings.
 Gallbladder polyps can be adenomas, inflammatory
reactions or cholesterol polyps – most common
type, common in middle aged women. They are
cholesterol deposits in the gallbladder wall.
Ultrasound findings:
 Small size (less than 5mm)
 No shadowing and slightly echogenic
 Bigger polyps are more hypoechoic
 Immobile (unlike most free-stones)
 Smooth, solitary.
CT:
- Solitary soft tissue density in the lumen of the
gallbladder. Hyperintense lesions suggest increased
blood flow and cancer should be suspected then.
Multiple cholesterol
polyps in “strawberry
gallbladder”
Isointense when
compared to soft
tissues

122. Cholangiocarcinoma
• Cancers of the bile duct/ biliary tree. Second most common
primary hepato-biliary cancer after HCC.
• Male predilection , over 65, typically presents with
obstructive jaundice.
• Risk factors: Cirrhosis, sclerosing cholangitis, toxins, hepatitis,
gallstones.
• They usually follow one of three courses;
• Ultrasound, CT and ERCP are the most indicated techniques.
1). Mass forming intrahepatic
2). Peri-ductal infiltrating – at hilum
3). Intraductal
Ultrasound:
Mass forming: homogenous, intermediated echogenicity,
peripherally hypoechoic halo = compressed ischemic liver
Well circumscribed. Can cause retraction of liver capsule.
Periductal: narrowing of duct with well defined mass
Intraductal: Hyperechoic compared to surrounding liver,
narrowing of lumen, mass may or may not be seen.
CT:
Mass forming: low attenuation (dark) homogenous mass with
peripheral enhancement Dilated bile ducts distal to mass.
Capsular retraction and central fibrosis
Peri-ductal: Regions of duct wall thickening. Narrowed lumen
most commonly at hilum. Contrast enhancement.
Intraductal: Hypoattenuating (dark) polyploid mass
Direct cholangiography techniques eg ERCP:
- Risk of pancreatitis
- Risk of perforation
- Less preferred by patients
But good diagnostic value as well as in planning and treatment
Intrahepatic cholangiocarcinoma on Ultrasound

123. US: Tumour compressing common bile
duct with dilatation of duct
CT: Intrahepatic mass
forming

124. Pancreatitis
ACUTE: Potentially life-threatening disease, deep severe
epigastric pain, poorly localised, radiates to the back. Elevated
serum lipase and amylase. Cullen's and Grey-turner signs.
Causes: gallstones, alcohol, hypertriglyceridemia/
hypercalcemia, idiopathic, autoimmune, malignancy
cholangioscopy.
Plain X ray: Insensitive for acute pancreatitis. Can demonstrate
systemic effects.
- Localised small intestinal ileus (air-fluid levels)
- Spasm of descending colon
- Pleural effusion and pulmonary edema (ARDS)
- Hemidiaphragm elevation and basal atelectasis.
- Free air (acute abdomen)
Ultrasound:
- Can identify causative gallstones
- Vascular complications: Thrombosis
- Necrosis: hypoechoic areas
- Free air pockets in peritoneal cavity
- Decreased echogenicity of pancreas due to increased
volume
- Displacement of adjacent stomach and colon.
Computed Tomography:
Focal or diffuse enlargement of pancreas
Edematous changes in density.
Loss of clear pancreatic margin
Later on: necrosis (lack of parenchymal enhancement)
Abscess formation – well circumscribed, fluid filled.
High attenuation (bright) fluid occupying retroperitoneal
space and peri-pancreatic tissue indicates hemorrhage.
CHRONIC: Prolonged inflammation, irreversible fibrosis,
morphological change and endocrine/ exocrine dysfunction of
the pancreas, most commonly due to chronic alcoholism.
Presentation: Jaundice, malabsorption and diabetes type 2.
Ultrasound:
- Atrophic (small irreg. shape), fibrotic (hyperechoic – often
diffuse) and calcifications (very hyperechoic).
- Pseudocysts or pseudoaneurysms
- Presence of ascites
- Pancreas may be enlarged in the case of autoimmune
diseases.
CT: Main pancreatic duct is Dilated.

125. - Multiple calcifications can be observed.
- Atrophy and cysts
MRI:
- T1 – low signal intensity (dark)
- Decreased and delayed contrast enhancement – suggests impairment
of hemodynamic of the organ due to inflammation.
- Dilated branching vessels – shunting of blood.
- Parenchymal shrinkage and irregularity (atrophy)
“Chain of lakes” sign – pancreatic duct has several dilations alternating
with stenotic segments, often with calcifications.
Above. Ultrasound showing Acute
pancreatitis: enlargement with peri-
pancreatic fluid.
Left: Ultrasound demonstrating peri-
pancreatic effusion (hypoechoic
areas demonstrated by yellow
arrows) as well as parenchymal
hetero-echogenicity (necrosis,
hyperemia and active inflammation).

126. Above: 3 Acute pancreatitis CT’s: Enlarged,
peri-parenchymal fluid, edema, loss of
margins,
Below: 3 Chronic pancreatitis CT’s – atrophy/ shrinkage, multiple calcifications,
formation of hollow hypointense pseudocysts and abscesses of varying size

127. Pancreatic cancer (ductal adenocarcinoma):
• Pancreatic cancers can be of both the endocrine and exocrine
type however exocrine cancers of the pancreatic head/ proximal
body are by far the most common – 90-95% all cancers of the
organ.
• The most common of these exocrine cancers is ductal
adenocarcinoma. Others include cystic neoplasms, intraductal
papillary mucinous neoplasms.
• Endocrine cancers are on the other hand rare and include
insulinoma, gastrinoma and somatostatinoma.
• Pancreatic cancer has a poor prognosis = 22% of all deaths due to
GIT malignancy. 80% of cases are in the over 60s.
• Risk factors: smoking, fatty diet with red meat, obesity, family
history. Unlike pancreatitis it has a weak association with alcohol.
Fluoroscopy (barium swallow):
Distortion or wide sweeping of the duodenum due to displacement
by a mass, thinning or obliteration of the medial mucosa = “Frostberg
inverted 3 sign”
Ultrasound:
- Hypoechoic mass
- Double duct sign (dilation of both the common and pancreatic
ducts)
Frostberg inverted 3 sign on
fluoroscopic image

128. CT: The gold standard/ workhorse of
diagnosis
• Poorly defined masses
• Desmoplastic reaction (growth of
fibrous tissue around a malignant
process) – hypodense on arterial
phase scans
• Double-duct sign
• Calcifications are rare
• Used to establish whether the
tumour is resectable or not. If it has
grown to encapsulate more than
180 degrees around the celiac
plexus/ superior mesenteric artery
it is untreatable surgically.
MRI:
T1 hypointense compared with normal
pancreas
(with gadolinium contrast) = the
cancer has slower enhancement than
regular tissue.
T1 variable appearance
CBD
PD
D

129. Pancreatic pseudocysts:
• Most common cystic lesion of the pancreas.
• Often a result of prior acute and chronic pancreatitis.
• They develop roughly in the first four weeks after
inflammation and consist of encapsulated peri-pancreatic/
remote fluid collections.
• Clinical presentation: can be asymptomatic, mass effect
leading to obstructive jaundice, gastric outlet syndrome or
can cause secondary infection.
X ray: Not sensitive unless the pseudocyst is very large.
Increases distance from stomach top colon.
US: Fluid is hypoechoic or anechoic
CT: Well circumscribed, round, oval, homogenous low-
attenuating fluid surrounded by
hyper-attenuating wall.
MRI:
T1 Hypointense fluid
T2 Hyperintense fluid
MRI
CT CT
CT

130. RENAL RADIOLOGY
Congenital abnormalities of the kidneys:
1). Hypoplastic Kidney
2). Displaced/ Rotated kidney
3). Horseshoe (fusion anomaly) kidney
4). Polycystic kidney
1) Hypoplastic kidney:
Congenitally small kidney. Differs from renal atrophy in that
atrophy is the shrinkage of once normally sized/ well developed
kidneys.
Hypoplastic
kidneys on CT

131. 2). Displaced/ Malrotated Kidney:
Pelvic kidney, L shaped kidneys