G.I.T.

1
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Salivary glands
Diseases of the salivary glands
A. Chronic non neoplastic enlargement of the salivary glands:

1. Chronic obstructive sialectasis

Causes:
A. Stones:- May be solitary or multiple.
Incidence:
* Much higher in the submandibular glands.
* Multiple calculi are more frequent in the parotid.
Plain:
Shows the majority of the opaque stones.
Sialograrphy:
1. Identification and location of the opaque and non-opaque calculi.
2. Proximal dilatation of the ducts in large stones (>3mm).
3. Associated strictures in the duct.
4. Secondary infection irregular collection of the contrast medium within
small cavities in the gland.

B. Strictures:
It may be single or multiple.
Causes:
1. Tooth extraction and ill-fitting dentures Common.
2. Post Traumatic, inflammatory and operative.
Sialography :
1. Dilatation of the main duct and its tributaries proximal to the point of
obstruction.
2. Retention of the C.M. in the after lemon films.
3. In multiple stricture appearance of a string of sausages.
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2. Chronic non obstructive sialectasis:

Includes:
a. Recurrent sialadenitis in children.
b. Recurrent pyogenic parotitis in adult.
c. Sjogrens syndrome.
d. Mikuliczs disease.
- All produce enlargement of the major salivary glands.
- All give similar radiographic appearance :
A. Plain :
1. Soft tissue swelling.
2. Fine, nodular calcific densities may be present.
B. Sialography :
Degree of sialectasis According to severity
1. Normal sialogram = grade I.
- The ducts are evenly distributed and gently tapered.
2. Pruned tree appearance = grade II.
- Stretched and tapered intraglandular ducts with non filling of the
acini.
- It is the earliest finding.
3. Punctate sialectasis = grade III.
- Punctate dilatation of the peripheral ducts (1mm in size).
- Numerous, small collections of the C.M. evenly distributed
throughout the gland.
4. Globular sialectasis = grade IV.
- Globular dilatation of the peripheral ducts (1-2 mm in size).
- Irregular, deformed and sparse intra-glandular ducts.
5. Cavitating sialectasis = grade V.
- Results from coalescence of the globules into Cavities.
6. Destructive sialectasis = grade VI.
- Is the final stage of the disease bizarre pattern of filling with
pooling of the contrast medium simulating malignant neoplasm.
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B. Tumours
- Uncommon, 80% occurring in the parotid gland. Types:
1. Mixed salivary tumour (pleomorphic adenoma & Adenolymphoma) incomplete
capsule. Is the most common and the majority are benign.
2. Carcinoma and adenoma (rare) malig mixed tumour, mucoepidermoid, sq cell &
undifferentiated.
A. Sialography :
Benign tumours :
- Displacement of the stretched ducts around a circumscribed filling defect in the
parenchyma of the gland (Devoid of ducts and acinar filling).
Malignant tumours :
Infiltrating neoplasm produce an irregular filling defect with duct distortion and
pooling of the C.M. like grade VI.

B. U/S, C.T. & Scintigraphy :

Aim : To show extent of the spread of the invasive tumours.

N.B.:
Schatzkia Ring :
Marks junction between the striatum Squamous epithelium of the oesophagus and the columnar
epithelium of the stomach.
Seen in prone - trendlenberge position.
Appearance :
as a narrow indentation 2-3 mm deep extending inwards from sides of the oesophagus:
Large ring > 18 mm No C/O.
Small < 12 mm Episodes of bolus obstruction
Very small ring < 6 mm Acute obstruction.
It is a pathological ring (in cases of HH).
It is significant if its transverse diameter > 13 mm & there is reflux to level of carina.

Prevent reflux :
1. High pressure zone.
2. Cardiac sphincter B.
3. Acute angle of Hiss.
4. phrenico oesophageal memior.
5. Pinch cock effect of Rt crus.
6. Ring A: rosettes of mucosal folds bulge.
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The Oesophagus
Anatomical parts :
1. Upper oesophagus.
2. Thoracic.
3. The region around G.O.J.
Normal sites of Narrowing :
1) C6: Cricoid lip.
2) T4 : Aortic knob.
3) T5 : Lt bronchus.
4) T11 : Diaphragm.
rugea : longitudinal folds when empty.
Upper oesophagus
- Consisting of the hypopharynx and the cervical oesophagus.
- The hypopharynx : extends from the epiglottis to the level of the cricoid cartilage (C6).

Diseases of the upper oesophagus :

1. Crico-pharyngeal dysfunction crico-pharyngeal achalasia
- Thickening of the transverse bands of the crico-pharyngeal muscle incomplete
relaxation of the upper oesophageal sphincter.
- Hypertrophy of this segment produces a prominent rounded extrinsic impression in the
posterior wall of the Ba. filled oesophagus.
2. Oesophageal webs :
- They are shelf like semicircular infoldings of the mucosa, 1-2 mm thick, consisting of
plications of the normal squamous mucosa.
- Commonly arise from the anterior wall of the cervical oesophagus.
- Best seen with the patient swallowing a large bolus of Barium in the lateral
position.
- Webs need to be differentiated from the slight infolding of the mucosa of the
anterior wall of the cervical oesophagus at the level of the cricoid cartilage, which is a
normal finding and is caused by lax mucosa over a venous plexus. This does not
produce a discrete shelf, but, an irregularity to the anterior margin of the barium
column which often changes the shape from frame to frame.
Types :
1. Non specific an incidental findings.
2. Plummer vinson webs (sideroplastic dysphagia.):
Females with iron deficiency Anaemia.
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Premalignant.
Associated with some diseases : e.g. Cancer larynx & cancer oesophagus.
3. Neoplasm
4. Retro-pharyngeal abscess :
An abscess located between the pharynx or the cervical oesophagus and cervical spine.
Causes :
1. Tonsillitis common.
2. Traumatic pharyngitis.
3. Infection of the cervical spine T.B..

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1. Achalasia.
2. Scleroderma.
3. Zenkers.
4. Post cricoid carcinoma.
Radiologically: Lateral soft tissue film of the neck:
A. Without Ba:
- Soft tissue mass widening of the prevertebral space, which may contain gas bubbles.
- TB of spine:
- Narrow disc space, bone destruction.
B. With Ba:
- An impression in the posterior wall of the hypophorynx or the cervical
oesophagus.
- Forward displacement of the pharynx, oesophagus and trachea.
5. Oesophageal diverticulae :
projection of a pouch of the mucosa through the muscularis:
Types :
1. Upper oesophagus: posterior pharyngeal diverticulum and lateral pharyngeal
diverticulum.
2. Thoracic oesophagus: pulsion diverticulum and traction diverticulum.
3. Epiphrenic diverticulum.

Posterior pharyngeal diverticulum (Zinkers diverticulum)

Definition:
Pulsion diverticulum which herniate between the oblique and transverse fibres of the
inferior constrictors:
C/P :1. Occurs in elderly.
2. If large dysphagia and regurgitation of the undigested food.
3. Aspiration pneumonia.
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Radiological appearance:
A. Plain erect, lateral view of the neck:
1. Increase prevertebral soft tissue space.
2. Anterior displacement of the trachea.
3. Air fluid level in the pouch.
4. If large ... appears as superior posterior mediastinal mass.
B. Ba. Swallow :
1. Posterior position of the pouch, usually to the left with anterior displacement of
the oesophagus.
2. The pouch may be filled with Ba. With multiple filling defects due to food reside
and may remain filled with Ba. After the rest of the swallowed bolus has passed.

Lateral pharyngeocele
- Bulge through the thyrohyoid membrane rare (Valsalva)
a. Congenital : Remnant of the 2nd brancial arch.
b. Acquired : Glass blower, trumpeter.
- These are small, bilaterally and symmetrical.
Complications of oesophageal diverticulae :
1. Ulceration.
2. Haemorrhage.
3. Perforation (medaistinitis, lung abscess, bronchial fistula).

Thoracic diverticulum
1. Pulsion D.
Upper flower 1/3rds due to increase intraluminal pressure.
Occurs in Elderly and motility disorders.
2. Traction D. :
At the level of the carina.
May be related to fibrosis after the treatment for mediastinal tuberculosis
lymphadenopathy.
They project at any direction except posterior due to the spine.
Usually with wide neck.
Epiplueritic diverticulum
Pulsion diverticulum at the lower end of the oesophagus, more on the right side.
Usually associated with sever tertiary contraction.
DD from para-oesoph. H.H.
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Oesophageal motility disorders

Primary : Secondary :

1. Achalasia 1. Reflux oesophagitis.

2. Diffuse oesophageal spasm. 2. Scleroderma.
3. Tertiary contractions. 3. Metabolic and endocrine disorders.
4. Presby-oesophagus. 4. Neuro-muscular disorders.
1. Achalasia cardiospasm
Pathology :
Defect in the myenteric (Auebach's) plexus of nerves failure of the cardio-
oesophageal sphincter to relax when the contraction wave arrives retention of food
inside the oesophagus progressive oesoph. dilatation.
C/P :
- Age : 30-50 ys.
- Dysphagia more to fluids and solids.
Radiological appearance :
A. Ba. studies :
- The GOJ never fully opens, and appears smoothly or bird beak appearance.
- Intact mucosal folds can be traced throughout this segment.
- NB:
Inhalation of Amylnitrate causes prompt relaxation of the sphincter and may be used as
a diagnostic test.
- In early cases: pronounced tertiary contractions may be seen, but with time, they
become less evident and the oesophagus dilates, lengthens and becomes tortous.
B. Plain CXR:
Mediastinal widening with mottled appearance due to mixing of air with food.
Mediastinal air fluid level.
Absent gastric fundal air buble.
Aspiration pneumonia which may lead to bronchiectasis, lung abscess or
empyema.
Biopsy:
Increased risk of carcinoma.
Treatment:
- Balloon dilatation.
- Hellars cardiomyotomy.
Both lead to oesophageal perforation and GO reflux.
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D.D. : Other cause of oesoph. strictures.

2. Diffuse oesophageal spasm

- Of unknown origin.
- Ch. ch by diffuse muscular spasm, mainly affects lower 2/3 intermittent chest pain &
dysphagia.
- Ba. swallow cork screw appearance, a series of assymetrical indentations.

3. Tertiary contractions
NB:
Peristaltic wave :
- Primary : begins with act of swallowing.
- Secondary : start at level of aortic knuckle and proceed rhythmically to the cardial
followed by a wave of relaxation.

4. Presby oesophagus :
Impaired motor function due to muscle atrophy in Elderly, slightly dilated oesophag.
Ba. swallow cork screw appearance if tertiary contractions occur.

5. Scleroderma :
Ba swallow :
- Absent or decrease peristalsis .
- Mild dilatation of the lower 1/2 of the oesoph with free reflux dysphagia
stricture.
Ba enema :
- Characteristic pseudodiverticulosis & functional obstruction
Characteristic bone and soft tissue changes in hands absorption of terminal phalanges
calcinosis.
Lung :Bilateral basal diffuse interstitial fibroses (honey coomb). also 2y to oesph lesions
aspiration.
6. Metabolic and endocrine disorders
Ba swallow :
- Decreased peristalsis.
- Delayed emptying
- Tertiary contraction.

CREST syndrome : (All dilatation)

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C Calcinosis circumscrepte.
R Raynauds phenomenon.
E Esoph dysphagia

S Scleroderma (diffuse sclerosis of ms of

oesoph).

T Telangectasia.

Functional oesophageal divecticulae :

Def.
Alterations in normal oesophageal contraction waves causing considerable functional disturbances.
Disordered 1ry or 2ry motility and tertiary comtracions may be seen as the result of any disordered
affencning the lower oesophagus, and not only in elderly.????
I. Tertiary contractions : Ripple oesophagus.
A symptomatic, incoordinated, non. propulsive con traction of the oesophagus.
Occur in elderly people.The (oesophageal outline) is indented as each side to transient (few
seconds) seris ring contractions precipitated by swallowing.
Seen as ripples along the wall of the oesophagus or when more pronounced, as a series of
contraction rings, these contractions are frequently intermittent, lasting only for a few
seconds, but occasionally, they are pronounced segm??? the Ba column or producing a cork
screw appearance.
II. Cork. screw oesophagus : [curling phenon = I + II]
Radiologically
1. Smooth pouches (pseudo diverticulae) appear inbetween contracted segments (3-5
pouches).
2. Pulsion diverticulae.
Barrets oesophagus :
Oesophagitis (oesophageal ulceration)
A. Inflammatory
B. Neoplastic: Carcinoma, lymphoma.- Leiomyoma, leiomyosarcoma.

A. Inflammatory : (reflux, infection, corrosive, radiotherapy, chronic, Behcet, drugs.

1. Reflux oesophagitis (peptic oesophagitis)
- Characterised by :
Radiological appearance :
a. Mild cases hyperaemia of the mucosa, detected by endoscopy.
- When edema of the mucosa is pronounced, the earliest radiological changes are:
1. Fine mucosal nodularity are seen with the double contrast Ba study.
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2. Thickened longitudinal folds (wider than 3 mm) which often become

nodular, giving an appearance similar to that seen with varicose veins.
3. With further progression, ulceration:
a. Multiple fine ulcers give the mucosa a punctate or granular appearance.
b. Larger discrete punched out ulcers develop.
Ulceration from RO is more pronounced in the lower oesophagus, and
particularly immediately above the GOJ.
Ulceration may cause local circular muscle spasm and transverse folds and
with time scarring will produce permanent folds radiating from the margins of
the ulcer. Pseudo diverticula are seen (representing dilated ducts of the
mucous glands flask shaped outpunchings)
4. Severe scarring results in stricture formation which is:
a. Short.
b. Smooth lumen.
c. Tapered margins
NB:
Long strictures in:
1. Prolonged nasogastric tube.
2. ZE syndrome.
- Reflux oesophagitis: columnar metaplasia in the distal esophagus (Paretts oesophagus)
(5) in 10% of patients, 15% of which develop adenocarcinoma.
Endoscopy:
- Reddish pink columnar mucosa is seen to extend above the leve of the GOJ.
- Ulceration occurs at the junction of the columnar and the normal squamous
esophageal mucosa, so ulcers and strictures in Barrets oesophagus often develop
some distance above the GOJ, and on occasions may be seen in the mid-thoracic or
even the cervical oesophagus.
- Islands of columnar mucosa may give the oesophagus wall a five reticular pattern,
resembling the area gastricae pattern of the stomach.
Radionucleide imaging:
NB:
- RO commonly associated with hiatus hernia (15%).
2. Infectious oesophagitis :
- Commonly produced by Candida Albicans and H.simplex.
- Moniliasis is the most common cause.
- Occurs in debilitated persons (D.M.)
Radiological appearance :
Ba. swallow :
1. Extensive mucosal irregularity.
2. Thickened mucosal folds and ulcers.
3. Nodular cobble stone appearance.
4. Disturbed motility.
5. No stricture.
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3. Corrosive oesophagitis :
Chemically induced oesophagitis mainly post-potash.
1. Acute phase :
A. Plain :
Gas filled oesophagus, indicating oesoph. atony impending perforation.
B. Gastro-graphine swallow :
1. Will show if there is oesophageal or gastric perforatin.
2. Narrow oesophagus: edema or spasm and ulceration.
3. Gastrograffin may track under the sloughed mucosa.
4. Atonic oesophagus, diffuse oesophageal spasm,
2. Chronic phase :
Ba. Swallow :
- 1 month after ingestion development of stricture with the following criteria :
I. Mainly affect middle and lower 1/3 irreg.
II. Long in length, increased strictures (develop as early as 2 weeks) and may
involve the entire length of the oesophagus.
III. Having funnel shaped upper end with smooth tapering.
IV. Loss of mucosal pattern.
Complication cancer oesophagus, achalasia (if damage to the myenteric plexus).
DD with other strictures :
1. Reflux 2. Traumatic 3. Malignant 4. Radiotherapy :
- Rare.
- commonly disturbed oesophageal motility
5. Drug induced : e.g. tetracycline.
6. Crohns disease.
7. Behcets disease.

Causes of haematemesis :
1. Oesoph. varices.
2. Peptic oesophigits (reflux), Mallory-Weis syndrome..
3. Cancer oesoph.
4. rupture aortic aneurysm.
5. Gastritis, PU (Acute & chronic).
6. Cancer stomach.
7. Purpra, leukaemia, haemophilia.
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Oesophageal varices
- Dilatation of the submucosal veins in the lower oesophagus as a consequence of
portal hypertension bet oesph. v & Lt gast veins = uphill varices.
- S.V.C. obstruction varices at the upper end oesophagus = down hill varices.
Technique of examination :
1. Ba swallow :
- Induce hypotonia by Buscopan.
- The use of fairly Ba (high density).
- Multiple spot films with the patient in various position :
~ Various projections. ~ Positions Erect, supine, prone, 45 semi ??.
~ Use of valsalva manoeuvre.
Radiological appearance:
Ba. swallow :
En face: beaded or serpiginous translucent filling defect, resembling worms lying
in the lumen of the oesophagus.
In profile: varices appear as a line of nodular or scaloped filling defects.
a. Early Cases :
1.
2. The disappearance of the filling defect with inspiration and the
reappearance with expiration is pathognomonic.
b. Late cases :
3. The lower oesophageal lumen may be dilated and tortuous due to
degeneration of the muscle layer by varices at vasc. stasis & hypoxia.
DD :
1. Oesophagitis: mucosal abnormality in addition to the thickened folds and
sliding HH, GO reflux in invariably pres??.
2. Varicoid form of oesoph. carcinoma: mixed thickened mucosal folds, with
rigidity and loss of peristalsis of the affected area.

2. Portal veno-graphy :
- Venous phase.
- Splenoportogrpahy .
3. Oesophagoscopy :
Direct demonstration of the varices.
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Tumours of the oesophagus

1. Benign tumours :
A. Epithelial : B. Non epithelial :
- Arise from the mucosa : - Arise from the wall :
Papilloma , Adenoma. Leiomyoma, Fibroma, Lipoma

NB. :
Mass arises from the oesophageal mucosa forms acute angle with the wall.
- Mass arises within the wall of the oesophagus forms right angle with the wall.
- Mass arises extrinsic to the oesophagus forms obtuse angle with the wall.

Radiological appearance :
1. Plain soft tissue mass.
2. Ba. swallow :
a. Smooth, rounded filling defects (May be irregular).
b. The oesophagus dilated around it.
c. Normal mucosal folds and peristalsis.
d. The Ba. may be collected at the angle between the mass and the
oesophageal wall forming a ring shadow ? pathognomonic.
D.D. :
1. Air bubble (mobile).
2. Oesophageal varices (change with respiration).

II. Malignant tumours :

- Primary carcinoma, sarcoma, non Hodgkin.
- 2ry Direct extension from mediastinal tumour.

Carcinoma of the oesophagus

Pathology :
Squamous cell carcinoma : 60% adenocarcinoma ?????????
1. Polypoidal fungating type filling defect.
2. Infilterative type stricture.
3. Ulcerative type malignant ulcer.
Radiological appearance:
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Ba. swallow and fluroscopy

1. Hold up of the Ba. stream :
- Variable from flecting delay to complete obliteration deflected suddenly through
an
irregular channel.
- ????Early esophageal carcinoma in the barium is depressed, polypoid or plaque
like lesions.
- Or spread submucosally producing thick and irregular esophageal fold simulating
varices (varicoid carcinoma).

2. The filling defect :

Occurs in the polypoidal type.
Criteria :
a. Constant, Irregular well-defined edges.
b. Lack of distensibilty of the oesophageal wall at site of the mass, no
peristalsis.
c. Destruction of the mucosa at site of the mass.
d. Lumen : Irregular, narrowed, eccentric.
3. Malignant stricture :
- Occurs in the infilterative type :
a. Tend to be irregular, and rolled margins (and shouldering) DD peptic
stricture (smooth, tapered margins).
d. Soft tissue mass.???
e. G.O.R. when including the cardia.
4. Malignant ulcer :
a. Superficial ulcer :
b. Deep ulcer :
2. Edges : Punched out with irregular margin.
4. Perforation may occur into the mediastinum.

CXR:
Mediastinal mass produced by tumor or enlarged lymph nodes.
NB:
Adenocarcinoma frequenlty involve the gastric fundus, in which case it would be
difficult to decide whether the tumor has arisen in the stomach and oesophagus. If the
buld of the tumor involves the fundus (then it is generally classified as gastric carinoma)
but if the majority of the tumor involves the oesophagus. Then it will be assumed that it
has risen in the oesophagus.
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Endoscopic US and CT are used to stage oesophageal caracinoma:

CT :
- Better in assessment of tumor invasion of adjacent structures.
- Superior in diagnosing distant metastases.
Focal thickening of oesophagus. wall or soft tissue density.
Obliteration of perioesoph, soft T. planes = local invasion.

Endoscopic U/S :
- Shows the layers of the oesophageal wall, so best for local tumor staging.

Cancer : = hypoechoic :
poarly echogenic mass.
EUS is more accurate than CT (where LN > 1 cm are considered malignant).
Malignant nodes are round, hypoechoic and well defined.
Benign nodes are elongated, have echogenic centers, and ill defined
margins.
to diffrentiate reactive from malig change size > 1cm.
Squamous carcinoma at special sites
1. Post-cricoid carcinoma:
(Squamous cell carcinoma at the pharyngeo-oesophageal junction)
Female > male.
Predisposing factors: plummer vinson disease.
a) Plain :
Lateral view of the neck :
- Soft tissue mass (1) Widening of the prevertebral soft tissues shadow >
adjacent vertebra. And, (2) Forward displacement of the larynx.
b) Ba. swallow :
1. Slight obstruction irregular channel (narrowing of the oesophagus)
through the soft tissue mass.
2. Dilatation of the hypo-pharynx and pyriform fossa.
3. Hold up of air column (trapping).
4. Bone erosin4.
5. Positive valicula sign : (constant filling of widened valicula) with
barium.
6. Tracheal spill over.
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2. Carcinoma lower end oesophagus :

NB:
May essentially be gastric cancer infiltrating lower oesoph. horizontal cardiac ampulla.

Post corrosive Achalasia Malig

Long seg. Short seg. Variable
dilat above marked dilatation no dilatation
funnel no sharp demarcation shouldering
smooth or fine irreg. smooth outline irreg.
middle 3rd. lower end any site

Causes of smooth oesophageal strictures ( Serial Films)

A. Inflammatory :
1. Peptic oesophagitis.
2. Scleroderma.
3. Corrosive.
4. Iatrogenic : Prolonged use of the naso-gastric tube.

B. Neoplastic :
2. Mediastinal tumour (Bronchial carcinoma, lymph nodes).
3. Leiomyoma.
C. Others :
1. Achalasia.
2. Skin disorders - Pemphigus, Epidemolysis bullosa.

Causes of irregular strictures

A. Neoplastic :
1. Carcinoma.
2. Leio-myo-sarcoma.
3. Lymphoma : Usually extension from gastric lymphoma.
B. Inflammatory :
2. Crohns disease rare.
C. Iatrogenic :
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1. Radiotherapy rare.
2. Fundo-plication.

Radiological approach to D.D. of oesophageal strictures :

1. Clinical history : Dysphagia, drinking of a corrosive substance.
2. Plain chest :
- Evidence of achalasia.
- Mediastinal mass.
- Secondary lug changes.
3. Ba. examination of the oesoph. and stomach : stricture :
- Site, length, shape extrinsic or intrinsic.
- State of mucosa intact, thickened or destroyed.
- Presence of intra-luminal filling defect.
- Presence or absence of H.H or G.O.R.
- Degree of the obstruction.
4. Oesophagoscopy and biopsy.
5. C.T. and Endo-luminal U/S evaluate degree of the tumour infiltration.

Tubular structure lesion

Stricture Proximal upper extent

Narrow segment Dilatation transitional zone
length with normal part
site funding
mucosa shouldering
outline

Causes of dysphagia
A. Congenital :
1. Atresia +/- T.O.F
2. Stenosis.
3. Short oesoph. H.H.
4. Macro-glossia, coanal atresia.
5. Vascular rings with Rt. sided aortic arch, Aberrant right subclivian
artery and CVS cause : Lt at +++
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6. Others : cleft palate

B. Acquired :
I. Intrinsic :
1. Reflux stricture 2. Tumour.
3. Ingestion : corrosive, F.B.
4. Plummer vison web, diverticulae
5. Iatrogenic : - Radiotherapy, prolonged nasogastric tube.
6. Monilia and skin disorders 7. Schatzki ring.
II. Extrinsic :
1. Tumour : lymph nodes, mediastinal tumours, bronchogenic.
2. Vascular : aortic aneurysm
3. Pharyngeal pouch. 4. Goitre.
5. Prevertebral abscess or haematoma.
6. Rolling H.H.
III. Neuro muscular :
1. Achalasia 2. Scleroderma 3. Bulbar palsy, diphresier, tetanus.
IV. Hysterical
Boerhaves syndrome: spontaneous thoracic oesophgeal perforation.???

Congenital abnormalities
Types :
1. Oesoph. atresia.
2. Oesohp. stricture.
3. Tracheo-oesophageal fistula.

Embryology :
Pathology :
The upper oesoph. end in a blind pouch usually at the level of T2.
In 70% of cases the oesophagus communicative with the trachea or one
of the main bronchi.

C/P :
New-born who is choking, regurgitating and getting blue on first food.
Radiological appearance :
1. Plain abdomen :
Absent gas in the stomach, intestine (except with tracheo-oesoph. fistula).
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2. Passage of no (8) soft rubber-catheter instillation of 1-2CC (lipidol) out

lining of the blind pouch may pass into trachea ?? instillation of lipidol during
withdrwal of the catheter
detect site of the fistula.
3. Cine radiography in lateral projection in the prone position is the best technique
to detect the fistula.
4. Looks for other congenital abnormalities e.g. Rt. sided aorta (the position of the
aorta will determine the side of surgical approach)

Diaphragmatic hernias
N.B: Empty film, partially filled, serial

Development (congenital) Acquired (Hiatus hernia)

1. Pleuroperitoneal (Bochdalek) 1. Sliding (axial).
2.Anterior diaphragmatic (Morgagni) 2. Para-oesophageal (rolling).
3. Mixed.
HH : more variable size, pugea (3 or more gastric folds) shows peristalsis.
DD : with phrenic ampulla.
GE junction : Stellate (tugea) : 1-2cm above or below diaphragm.
Hiatus Hernia
The mechanism at cardia see 1st part.
Definition : H.H. is herniation of a portion of the stomach through the oesoph. hiatus.
Types :
1. Sliding : axial : The cardiac orifice herniate upwards into the thorax. 15% may be
associated with G.O.R oesophagitis.
2. Para-oesophageal = rolling : The cardiac orifice remains in the normal position
while the fundus herniate. No reflux, No oesophagitis No C.O. Detected only by
paracardiac soft tissue mass, more on the left and air fluid level seen in the chest
film.
3. Mixed : Both a siding and para-oesophagaeal component.
Clinical picture:
Retrosternal pain, epigastric discomfort, asymptomatic.
CXR:
A rounded soft tissue mass containing an air flluid level behind the heart.

Radiology features of sliding H : (Ba. swallow meal)

Small sliding hernias require Trendlenberg and straining.
 G.I.T. 21
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Most of para-oesophageal hernias are not reducible.

1. A pouch of the stomach above the hiatus of more than 2cm.
2. Three or more gastric folds passing from the stomach across the hiatus (to
differentiate from phrenic ampulla).
3. Wide hiatus > 3cm in diameter.
4. Z-line and area gastriae are located above hiatus.
5. Comment on reflux oesophagitis.
Important points that must be mentioned :
1. Reflux.
2. Ulceration (oesoph. herniated stomach).
3. Narrowing of lower end of oesoph.
4. Mucosal pattern of the herniated portion.
5. Extent of herniation.
6. Fluid level.
CT: Diaphragmatic crurae separated by more than 15 mm, and the hernia is seen as soft
tissue density mass above the hiatus, which may be surrounded by mesenteric fat.
N.B. :
Absence of gas & fluid St incarcerated SI loop with HH.
1. One fluid level irreducible herniated portion.
2. Two fluid level volvulous herniated portion.
 G.I.T. 22
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Eventration of diaphragm (e hiatus hernia)

Petitis event Unilat. congenital elev.

Def. The diaphragm is intact, forming a continuous sheath But part of it is paralysed,
thinned or lacking, in ms fibres sucked up into the chest & filled with viscera.
- Frequently affects left side.
CP : asympt. no cl. significance.
DD: Acquired pharenic palsy Ht not displaced.
- Other causes of elevated copula.
Rad. PA view
The left copula (considerably elevated, project as a thin bowed line across mid part of
1r. lung field. limited movement. on N. insp paradoxical on deep insp. or sniffing.
* Stomach considerably distended with gas partial volvolus (org. ax.) (common
association): a. Fundus rotated.
a. Greater curve rotated so that it becomes the upper most part of the
stomach, and lies immediately beneath the raised copula.
b. Body directly almost vertically downwards.
c. Inverted duodenal cap.
* Heart : frequently displaced to the right (rarely seen in acquired phrenic palsy).
Complications :
1. Peptic (reflux) oesophagitis.
2. Ulceration, volvulus, strangultion and infarction (rare) with para-oesophageal
hernia.
3. Stricture. 4. Adeno-carcinoma.
DD.:
1. Encysted pericardial effusion. 3. Pad of far
2. Pericardial cyst. (or pleura). 3. Bronchial cyst at carina.
4. Pneumopericardium & hydro. 5. Dilated oesoph (acholasia).
6. Epiphrenic diverticula 7. Lower lobe collapse
9. HH & Morgagni
Post-operative treatment:
-Ba swallow after fundal plication shows angulation and narrowing of the lower
oesophagus and there is a pseudotumor at the cardia.
-Angelchik prosthesis can migrate over the stomach or oesophagus or can erode the
stomach.
 G.I.T. 23
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Sub-phrenic abscess :
Cause : Perforated viscous, pancreatitis pentimites, extension from liver abscess.
Radiological features :
1. Early stages (space inflam before abscess formation) limitation of
diaphragmatic movement esp. on forced inspiration.
2. Abscess formation (depression of liver edge or gastric fundus. Elevated fixed
diaphragm.
3. Pleural reaction with obliteration of costo-phrenic angles, the lung overlying
may show opacity due to collapse or consolidation.
4. Gas formation ? in the abscess fluid level sitting, erect, lat. decubitus.
5. U/S : easier on Rt. side. Abscess appears as transonic zone.
Diff. betn. subphrenic abscess & subpulmonary plural effusion.
6. CT.
DD :
1. Interposition of colon on Rt side (falciform colon). colonic haustrations replace
normal dense liver shadow (Chialiditis syndrome).
2. Free air under diaphragm from perforated bowel.
3. Perforation into lesser sac (DD. from sub-phrenic abscess in Lt. side).
4. Sub-pulmonary pleural effusion (fundal gas bubble, Ba swallow).

The Stomach
Q: Discuss the role of radiological and imaging modalities in the diagnosis and
management of acute bleeding from upper gut.

Gastric diverticulae
DD Gastric ulcer: (chch site and shape)
Absent of ulcer ma?? and radiating folds.
1. Congenital.
2. Acquired following penetration or local perfortion of an ulcer or arround
anastomatic line, after surgical resection of the stomach.
Criteria of congenital divertianlae :
a. Usually at the funuds near the cardia (at the post wall, single smooth wall pouch).
b. small in size. c. narrow neck.
d. Flask in shape. e. Mucosal folds radiate into the diverticulum.
 G.I.T. 24
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Volvulus of the stomach

Classification :
According to the axis on which rotation will occurs.
A. Organo - axial - cardio-pyloric):
- The commonest type.
- The rotation occurs on an axis between the cardia and the pyloric canal .
- The greater curvature of the stomach twisting upwards and to the right the
duodenal cap and pyloric antrum are directed downward and backward and the body
directed almost vertically downwards.
Causes :
1. 2ry to eventration of the left dome.
2. Large hiatus hernia : The presence of two fluid levels in a hiatus hernia
suggests a voluvlus of the stomach within the hernial sac.
3. Hepato-diaphragmatic interposition dragging of the greater curvature
upwards by the transverses meso-colon in front of the lesser curveature.

DD :
a. Cup and spill (cascade) stomach b. Gastric displacement
B. Mesentero axial V :
- Rotation arround a vertical acis passing through the cardia.
C. Transverse axis V. :
Rotation arround the coronal axis the antrum swing upward in front
of the body towards the left copula.
Criteria a. The fundus and antrum clue together.
b. The pylorus downwards and to the left of the spine.
c. 2 fluid levels and air pockets in the fundus and pylorus.
D. Acute type :
Associated with oesophageal obstruction due to torsion of the fundus.

Gastritis
A. Acute gastritis
1. Acute erosive gastritis 2. Corrosive gastritis.
3. Phlegmonous (suppurative) gastritis 4. Emphysematous gastrits.
B. Cronic gastritis
1. Chronic atrophic gastritis.
2. Chronic hypertrophic gastritis.
 G.I.T. 25
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Acute erosive gastritis

Characterized by :
- Mucosal oedema and Erosions (small pools of Ba en face) (an epithelial defect that not
penetrate the muscularis).
Causes : Stress, Analgesics, steroids, Bile reflux and Crohns disease.
Types:
1. Complete erosion (Double contrast enface view)
- Numerous erosions, about 1 cm in size, consisting of small central
collection of Ba. Surrounded by a translucent ring (surrounding oedema)
smudge sign.

2. Incomplete erosion: (no halo)

- The often lie on rugal folds, giving the folds a scalloped margin.

Corrosive gastritis
- Mucosal oedema, progress to fibrosis and contraction.
DD. from scirrhous carcinoma.

Phlegmonous gastritis
- Acute fulminating infection Necrosis suppuration. It may lead to emphysematous
gastritis Gas bubbles within the gastric wall (rare).

Chronic atrophic gastritis

Double contrast :
The stomach is somewhat narrowed and shows a loss of fold pattern.
Focal enlargement may indicate intestinal metaplasia or early carcinoma.
Endoscopy & biopsy : Is the most sensitive method.
There is a high incidence of gastric carcinoma.

Chronic hypertrophic gastritis

Double contrast : Thickening & Tortuousity of the mucosal folds.
- As a general rule : The width of folds is considered abnormal
If > 0.5 cm in the antrum.
> 1.5 cm along the greater curvature and the fundus.
 G.I.T. 26
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D.D. of thick stomach folds :

A. Non inflammatory :
1. Normal variants.
2. Varices : Occurs in funds. Usually associated with oesoph. Varices and multiple,
smooth serpiginous filling defects.
3. Menetriers disease :
- Localised chronic hypertrophic gastritis characterised by excessive
mucous secretion and loss of protein PLE.
- It affects the greater curvature and fundus.
- Radiologically, extensive localised thickening of the rugae simulating
mass.
Diffrential diagnosis:
1. Fundal varices.
2. Polypoidal cancer.
3. Mass of polyps.
4. Intragastric prolapse of sliding hiatus hernia (pseudotumor in erect position,
when prone reduction.
B. Inflammatory:
1. Zollinger Ellison syndrome gastrinomas":
- Non B, islet cell tumour of the Pancreas.
- Criteria: a. Thickened, coarse mucosal folds.
b. Post-bulbar ulcer :
- In 1st and 2nd parts suggestive.
- In the distal one diagnostic.
c. Small bowel dilatation 2ry to hyperacidity.
2. Acute pancreatitis.
3. Crohns disease : Mild thickening of the folds with aphthous ulceration.

C. Infiltrative / Neoplastic :
1. Lymphoma. 2. metast. 3. leuk 4. easinopneulic 5. granulomas.
6. Carcinoma : Irregular folds with rigid wall.

Antral gastritis
Characterised by :
1. Narrowing of the gastric antrum.
2. Obliteration of normal prepyloric shoulder Cone shaped antrum.
3. Thickened mucosa and erosions.
4. Duodenitis or duod ulcer.
 G.I.T. 27
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DD : 1. Peptic ulcer.
2. Antral carcinoma.

Peptic Ulceration
Sites :
1. Lower oesophagus (Barretts) 2. Stomach and duodenal bulb (1st" of 1st part)
3. Jejunum after gastrojejunostomy or ZE 4. Meckels diverticulum.
Age : 35-65ys.
Incidence : D.U. : G.U. 4:1

Chronic gastric ulcer

Site : 80% lesser curvature, 12% pylorus, less common sites are the posterior and
anterior walls and the cardia.
Greater curve (sump ulcer): large and loaded in the dependant part of the greater
curvature.
Pathogenesis :
Decreased mucosal resistance.
Radiological features :
I. Direct signs :
- A benign ulcer in profile protrudes outside the expected line of the stomach
wall (DD malignant ulcer lies within the outline of the stomach) = ulcer niche.
- Overhanging mucosa at the margins of the benign ulcer will be seen as a line
seperation Ba filled ulcer from Ba in the stomach (Hamptons lines) should the
margins of the ulcer be edematous, then this line will be thick = collar
(prominent collar = mound in severe cases).
- When seen en face:
An ulcer on the dependant wall of the stomach fills with barium (ulcer
crater) whereas an ulcer on the non-dependant wall appears as a ring.
Smooth folds can be seen radicating from the edge of the ulcer. If the
margins are edematous, then the folds may stop some millimiters short of
the margin.
- With healing:
The ulcer decreases in size and alter in shape changing from being round to
linear. Sometimes scarring can be pronounced particularly if there has been
recurrent ulceration at the same site, in which case persistant gastric
deformity may result and lead to an hour glass configuration to the stomach.
En face, scars are often seen as punctate or linear grooves from which
smooth folds evenly radiate. In profile, scarrig causes a localized flattening
of the mucosa.
II. Indirect signs:
A. Gastrospasm :
 G.I.T. 28
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1. Localised notch or incisura :

- Occurs on greater curvature opposite the crater, above or below it.
- May be shallow or may extends to the lesser curvature and produce
pure spastic hourglass stomach of B-type.
2. Pyloro-spasm and antral spasm :
- Occurs in cases of pyloric and Juxta-pyloric ulceration
lack of filling of the antrum.
B. Pyloric function, gastric tone and peristalsis :
Hurst classifies gastric ulcers as follow :
1. Ulcer with pyloric achalasia:
2. Ulcer with pylorospams:
3. Ulcer with pyloric abstruction.
C. Rate of gastric evacuation Fluoroscopy
Delayed due to Hypotonia and pylorospam or stenosis.
D. Localised tenderness on pressure Fluoroscopy:
Persistent localised tenderness over the ulcer crater.
E. Peristaltic Jump Frankles sign : (also in early malignancy)
Interruption of the peristaltic wave on the lesser curvature by the ulcerated
area.
NB: Sure signs of activity :
1. Crater. 2. Ulcer mound. 3. Localised tenderness
4. Frnakls sign 5. Hyperprestalsis of whole stomach
6. Spasm (converget rugae, notch).
7. Bleeding ulcer.
Healing shallow wide neck oedema & crater

III. Cicatricial signs of gastric ulcer:

A. Pyloric stenosis:
1st stage (compensated):
1. Little or not gastric dilatation.
2. Active peristalsis but not excessive.
3. Slow but effective evacuation.
4. Possible visualisation of the pyloric canal.
2nd stage (decompensated):
1. Considerable gastric dilatation.
2. Vigorous hyperistalsis, after a short time, the hyperperistalsis die down
and hypotonia sustain until the ingestion of another meal exits the
 G.I.T. 29
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peristalsis again.
3. In the hypotonic stage erect position pool of the barium at the lower
pole (wide & shallow), tapped by transparent fluid.
4. Impossible to see the pyloric canal.
5. Gastric residue at 24 h. is pathognomonic.
3rd stage (complicated):
1. Very, marked dilatation.
2. Complete atony.
3. Complete obstruction with emptying by vomiting.
B. Hour-glass contracture of the stomach Simple cicatricial:
- Bi-loculation of the stomach, iIt must be differentiated from malignant cortracture:

hour glass B-type malig hour glass x-type

1. Complication of chronic gastric ulcer Scirrhous carcinoma
2. Shape B-shaped X-shaped
3. Contracture - Involve the greater curvature - Involve both the greater
and lesser curvature
4. Isthmus In the middle 1/3 of the Filling defect having
stomach, being caused by a criteria of malignancy
healed ulcer below the active
one.
5. Sagging Of the upper pouch below the No sagging
level of the ulcer.
- Stasis may occur in the lower
loculus due to associated
pylorospasm or stenosis
6. Stenosed Seen Seen
communicating
channel

C. Circular contracture of gastero hepatic omentum dragging of lesser curve, pylorus

& duod bulb up.
D. Presudo diverticulae .
E. Gastric adhesions decrease motility displacement of stomach distortion of contour.
 G.I.T. 30
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Complications of peptic ulcer

1) Bleeding : H& M
Radiological signs :
a. Bergs nodules blood clot producing an irregular
translucent defect at
the base of the Ba. filled crater.
b. Bleeding artery is seen at base of ulcer as small,round, translucent defect.
c. Fluoroscopy. Active bleeding is shown to displace Ba. Like larva flow.
Endoscopy Determination of the site of bleeding
Coeliac Angiography ?The site of bleeder artery
2) Perforation: Either into peritoneal cavity acute abdomen or adjacent organs.
Standing P.A :
- Free air the peritoneal cavity.
- Anterior wall (st. or dud) ulcers: perforate into peritoneal cavity, while
posterior wall into lesser sac or into pancreas or retroperitoneum (A gas
shasow or air fluid level that lies behind the stomach.
- Air under the diaphragm.
Oral gastrographin: seen free in the peritoneal cavity.
3) Penetration:
- Of pancreas (DU) or liver (GU).
- Fistula may occur eroding the colon (splenic flexure)
4) Obstruction : (cicatricial signs)
- Juxta-pyloric ulcer, associated with fibrosis or spasm gastric flow out
obstruction Pyloric stenosis, pseudodiverticulae, hour glass stomach.
Standing view :
- Distended stomach with fluid & food
Ba. Examination is done after gastric aspiration & lavage

Gastric fistula
[1] External due to trauma, wounds, operation, perforated ulcer.
[2] Internal :
A. Gastro colic carcinoma (colon, st.) sumpl ulcer, TB ulcer of the
colon and
gastrojujenostomy.
B. Gastro-jejuno - colic tirade of diarrhoea, foecal vomiting and wasting.
C. Cholesysto-gastric
 G.I.T. 31
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- Ulceration of a gall stone through adherent walls of the two viscera.

NB. Mucosal relief pattern :

1. Complete absence Atrophic gastritis & linits plastica
2. Localised absence carcinoma
3. Interruption & puckering ulcer.
4. Increased size & tortuousity hypertrophic gastritis.
5. Abnormal persistent fleck or Ba. Rests ulcer crater.
6. Disorganised pressure from outside.

Hour glass contracture of the stomach : Biloculation of the

stomach.
Causes :
1. Physiological results from marked hypotonia.
2. Physiologically cascade stomach :
- Ba. passes to the fundal loculus (cup), then, it spills down into the lower part of the
stomach, a semielliptical pool remaining above.
Causes : 1. Distended splenic flexure with gas.
2. localised spasm or muscle hypertonia. (healing ulcer at lesser curve)
3. Extrinsic pressure from tumour spleen ie. pr. from outside.
4. Simple cicatricial pancreas smooth contour, intct mucosa.
5. Malignant cicatricial hour glass (scirrhous)

Gastric tumours
Benign Malignant
Epith Non epthelial 1ry 2ry invasion
Adenoma single or Leiomyoma Adenocarinoma
multiple (gastric Fibroma Leiomyosarcoma
polyposis) Neurofibroma Lymphosarcoma
haemorgioma (Hodgkin)
carcinod

Carinoma of the stomach

Precancerous lesions:
Benign tumor.
Chronic atrophic gastritis.
Chronic PU.
Group A.
Pernicious anemia.
 G.I.T. 32
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High intake of nitrate.

Grossly:
60% pyloric region.
20% lesser curvature.
20% greater curvature.

~ Carcinomas protruding into the stomach lumen may be polypoidal or fungating

producing irregular persistent filling defect. The tumor may ulcerate or infiltrate.
~ Some adenocarcinomas produce an excess of extra-cellular mucin, and may show
stippled calcification.
- Malignant ulcer: (DD Benign ulcer)
1. The folds around the ulcer may be thickened, clubbed, interrupted, nodular or
fused.
2. They do not reach the margin of the ulcer, but this may be seen with benign
ulcers, if there is a rim of edema around the ulcer.
- Ulcer on the non-dependant wall appear as a ring, and the folds can be sharply
defined, while those or the non-dependant wall fill with Ba and Ba pools in
between folds which are less sharply defined.
3. When viewed on profile and in single contrast the margin of an ulcerating
tumor may project into the lumen of the stomach producing a meniscus sign.
~ Submucosal infiltration makes the stomach wall rigid with loss of peristalsis and the
gastric lumen narrows. If the whole stomach is involved this is known as a leather
bottle or linitis plastica. Mucosa is often nodular and fold pattern is lost or deformed.
~ Cancers involving the distal antrum may have an apple core appearance. Carcinoma of
the fundus may infiltrate the distal oesophagus producing an appearance that simulates
achalasia.

N.B: Leather bottle stomach in

1. carcinoma (diffuse scirrhous)
2. Lymphoma.
3. Crohns.
Criteria :
1. Decreased size & capacity of the stomach.
2. Marked contraction of the stomach rigidity.
3. Aperistalsis.
4. Rapid emptying.
5. Nodular mucosa and fold pattern is lost or deformed.
6. Oesophageal dilation due to decreased capacity of the stomach.

Gastric target lesion : (Bulls eye)

1. Leiomyoma.
 G.I.T. 33
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2. Metastases esp from Melanoma.

3. Lymphoma.
3. Carcinomatous ulcer malig. gast. ulcer 5%
- adenocarcinoma, leimyosarcoma, lymphoma, less differentiated adenocarcinoma.
Must be differentiated from simple ulcer as follow :
A. Site :
Simple ulcer : lesser curvature distant from the pylorus.
Malignant ulcer: more in greater curvature (50 70%).
B. Size : Any ulcer > 2.5 cm in diameter is considered malignant till otherwise
proved.
C. Shape :
- Simple ulcer hemi-sherical, sharpely defined, and regular bulge.
- Malignant ulcer irregular, everted edge, raised.
D. Meniscus sign :
- It is a translucent zone, few mm in width separating the braium filled ulcer
from the barium mass within the stomach. It is due to the hard growing
malignant edge of the ulcer projecting into the lumen of the stomach.
N.B.: The same appearance may be seen in benign ulcer with very raised
oedematous edges.
E. Therapeutic test :
simple ulcer should heal in few weeks after medical treatment.
Malignant ulcer will not.
F. Rugae :
- Simple ulcer mucosal folds are converging to the edge of the crater.
- Malignant ulcer mucosal folds are interrupted, distorted or irregular
together with filling defect.
G. Peristalsis :
- Simple U active.
- Malignant U. Decreased or absent.
H. Pyloric function :
- Simple U. normal or spastic.
Malig. U. may be gaping with rapid emptying.
1. Tenderness on palpation :
Mostly with simple ulcer.
J. Achylorhydria : Mostly with malignant ulcer.
 G.I.T. 34
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Lymphoma of the stomach

It is the commonest site for development of the gastro-intestinal lymphoma.
Primary lymphoma is usually non-Hodgkin.
Criteria :
1. Ulcerative, infiltrative or polypoidal.
2. At any site. Pseudolymphoma : proliferated lymphoid tissue as a
reaction to PU.
3. Difficult to differentiate from carcinoma (extension into thepyrlorous is
suggestive).
Differential diagnosis:
A. Polypoidal lesions multiple.
B. If they show central ulceration giving them a bulls eye appearance.
C. Bulky tumor producing pronunced thickening of the gastric wall or
shaving significant growth outside the stomach wall.

Post operative stomach

Types of operations :
1. Bilroth I : Partial gastroectomy (antrectomy) (with more recurrence &
haemorrhage) gastro-duodenostomy.
2. Bilroth II : partial gastrectomy with gastro-jejunostomy.
3. Polya 4. Vagotomy : truncal or selective drainage procedure Pyloro-
plasty division of the pyloric ring or gastro-enterostomy.
Complications :
1) Early :
A) Leakage from suture line
b. Obstruction c. Disordered function
2. Late :
a. Bleeding e. Ulceration
b. Recurrence of the tumour f. Gastro-jejuno-colic fistula
c. Post-gastrectomy syndrome. g. Mechanical dumping
h. Late post-prandial hypoglycaema.
Value of abdominal films :
1. Air-fluid levels Obstruction or abscess.
2. Distended bowel.
3. Free intraperitoneal air.
 G.I.T. 35
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4. Metallic sutures & clips guide to the previous operation, suture lines & anastomosis.
5. Retained F.b. e.g. Instrument.

Immediate post-operative examination :

Gastrographin meal for :
1. Suspected leakage sub-phrenic abscess.
2. Obstruction Gastric outflow obstruction.
Causes :
a. Oedema & haematoma around the stoma.
b. Gastric stasis (> 5 days) due to gastric atony.
c. Efferent loop obstruction following gastro-enterostomy.

Late post-operative examination :

1) Single contrast (ba. meal):
- Looking for a fistula & Ba enema.
- For the direction and rate of the flow.
2) Double contrast method of choice for stomal ulceration.
NB. In the presence of a gastro-enterostomy it is necessary to examine both the
normal channel and the stoma. usually Ba. prefer leaving the stomach via the new route.
On turning the patient on the right side filling of the antrum & duodenum via the
normal route.
Late complications: (from surgery)
1) stomal obstruction by
- Prolapse of the gastric mucosa through the stoma.
- Jejunogastric intussucepts / stoma filling defect in stomach having coil spring
app y SI.
- Gastric bezoars mass of matted vegetables or fruit pith (phytobezoar or
tricholezoor).
2) Peptic esophagitis from G.O. Reflux.
3) Ulceration due to recurrence.
- Recurrence at the original site or at a new site in the jejunum just distal to the
anastomosis = marginal or stomal ulcer.
Signs of stomal ulcer : Crater, stomal narrowing, thick juj-mucosal fold,
irritability & spasm.
4) Fistula.
5) Post-gastrectomy syndrome.
6) Haemorrhage due to ulcer or hemorrhgic gastritis.
 G.I.T. 36
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Hypertrophic pyloric stenosis

Hypertrophy of circular ms fibers
- Congenital defficiency of the longitudinal ms of the pylorus
- Male : female = 4 : 1.
I. Infantile : (Projectile vomiting & palpable mass) : olive radiological features : plain
(air distended stomach no gas in SMALL INTESTINE.):
1. String sign (narrow pyrloric canal).
3. Double track sign: parallel mucosal folds extending through elongated
pyloric canal.
4. Shoulder sign (indentation of Ba. filled pyloric antrum by hypertrophied
muscle).
5. Inverted duodera cap base umbrella - like defect.
6. Dilated stomach with active peristabis later atony.
II. Adult hypertrophic pyloric stenosis :
1. Narrowed pyloric canal + elongated, stasis accounts for association
with antral gastritis and gastric ulcer.
2. Bulges into the base of the duodenal cap (umberella shaped defect).
3. Antral tapering and the presence of intact mucosal folds passin through
the pyloric canal help to differentiate the condition from an annular carcinoma.
Plain films:
Little gas in the small bowel.
U/S: 1st approach: a pylorus measuring > 15*15 mm is abnormal center (anechoic)
surrounded by relatively hyperechoic muscle.

Causes of adult pyloric obstruction :

1. Idiopathic muscle hypertrophy.
2. Fibrosis after healing of a pyloric ulcer.
3. Extrinisic pressure by enlarged L.N. or cancer head pancreas.
4. Pyloric cancer.
5. Antal diaphragm
6. Spasm.
Child : Sites of normal flecks :
- Duod. atresia. 1. Apex of cap.
- Volvulus 2. (2 lateral) fornices.
- Annular pancreas. 3. Site of entry of pyloric canal.
- Hypertrophic pyloric stenosis.
 G.I.T. 37
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- Choledocal cyst.

The Duodenum
Chronic duodenal ulcer
Sites :
Involve the anterior and posterior wall equally.
Less common on the right and left borders.
Rarely at the fornices.

Radiological features :
- Duodenal ulcers on the dependant wall, on a double contrast study, fill with
barium and show radiating folds which stop short of the margin of the ulcer crater if
there is a rim of edema.
- Ulcers on the non-dependant wall are detected by barium and appear as a ring.
Good coating of the anterior wall can be difficult to achieve and for this reason, prone
or erect compression views of the duodenal bulb should be obtained. Ulcers are
generally round, but as with gastric ulcers, may be linear, especially if healing.
- Spasm and scarring may draw in the margins of the duodenal cap, distorting its
shape and sometimes producing a characteristic trifoliate or clover appearance.
DD:
Giant DU (may replace the whole cap and if smooth be mistaken for a normal cap) and
cap:
- Ulcer maintains its shape, yet the normal cap is seen to contract (due to peristalsis)
also pseudo-diverticulae and outpouchings produced by deformity of cap change
shape with peristalsis.
NB:
- Bleeding ulcers may contain a central filling defect due to blood clot (in duodenum
or stomach).
- The duodenum does not always return to normal with healing of an ulcer, as
epithelium may cover the surface of the ulcer, but the niche may persist.
- Pyloric canal ulcer may simulate an annular carcinoma if surrounding edema
produces
rolled margins at either end of canal.
- Ulcers at distal antrum pyloric canal, base of the bulb produce gastric outflow
obstruction (2ry pyloric stenosis).

Duodenitis
(Coarse duodenal mucosal folds = cobble stone or nodular cap)
It occurs in some patients independent of duodenal ulcer, or it may proceed ulceration or
remain after ulcer has been healed.
Radiological appearance :
 G.I.T. 38
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Technique : double contrast Ba. examination with hypotonic duodenography :

1. Errosion en-face as tiny specks of Ba. without (incomplete erosion), with
(complete erosion) surrounding translucent halo and back ground of normal or thickened
mucosa.
2. Coarse mucosal folds in 2 forms :
a. Thickened folds (2-3 length, 1cm width).
b. Multiple round or oval translucent defects (0.5 cm) erosions and coarse folds may give
the duodenal cap a cobble stone appearance.
3. Irritable duodenum.

D.D. of cobble stone duodenal cap :

Big Polypoid
1. Oedmea : associated with an ulcer.
2. Hypertrophied brunners glands (uniform in size).
3. Crohons disease (usually at pyloric antrum)
4. Varices : base of the cap + oesphageal varices. (Rt gas V. + panc. duod. v).
5. Lymphoma and carcinoma and AIDS.
Small: nodular cap (multiple small nodules in the cap).
1. Nodular lymphoid hyperlasia in achalasia with Giardia infection multiple
round nodules uniform in size (about 2 mm), shape and evenly disturbed
throughout the duodenum.
2. Heterotropic gastric mucosa: multiple small nodules of various size ( 6 11
mm) and shape are present extending from the pylorus towards apex of cap.
DD of thickened duodenal folds :
A. Inflammatory
i. Dudenitis
ii. Crohns disase : aphthous.
iii. Pancreatitis.
iv. Z.E. syndrome.
B. Neoplastic :
1. Lymphoma 2. Metastasis : melanoma, breast.
C. Vascular :
1. Intra-mural haematoma due to trauma.
2. Ischaemia : vasculitis 2 ry to radiotherapy, collagenic disease.
D. Oedema :
1. Causes of hypo-protinaemia e.g. Nephrotic syndrome.
2. Venous obstruction e.g. cirrhosis, Budd-chiari S.
 G.I.T. 39
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3. Lymphatic obstruction.
E. Infestations :
1. Ankylostoma.
2. Tapeworm Taenia saginata filling defect.
3. Giardiasis thickened & distorted mucosal folds with spasm
narrowing.

Duodenal diverticulosis
1. Primary diverticulae: Usually old patient.
Pathology :
Site :
- Commonest 2nd part of the duodenum (peri-ampullary) or from the third or
fourth part of the duodenum, usually multiple.
Shape : flask shape.
Nature : Mucosal protrusion via the mucsular coat.
a. True : the wall is formed of all coats (congenital).
b. False : mainly of mucosa (acquired)
Sequalae :
1. Diverticulitis
2. Ulceration & perforation, adhesions with pancreas.
3. Hemorrhage.
4. Biliary obstruction
5. Periampullary: prevent cannulation or the increase the complications of
endoscopic papillotomy.
3. Mechanical compression on duodenum Ileus & C.B.D obst.J.
Radiological appearance : Ba. meal.
Screen :
- The pouch fills from and empties into the duodenum.
- One or more rounded Ba. shadows close to and communicating with the
duodenum.
- Tenderness overthe site of the pouch.
- Fixed pouch due to: peridiverticulitis or deeply embeded in pancreatic head.
- Horizontal gas-fluid level.
II. 2ry diverticulosis :
Site : only in the 1st part of the duodenum.
Cause : 2ndry to any adjacent lesion.
Type i. Pulsion :
 G.I.T. 40
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- Opposite the ulcer scar with wide neck.

- Proximal to cicatricial stenosis (post-stenotic divert. of Akerland)
ii. Traction : due to adhesion between the duodenum and G.B.

III. Ampullary diverticulatae :

Causes types :
1. Opening of the papillae of the C.B.D and pancreatic ducts into the funuds of a
small-dilated paillae.
2. Dilatation of the ampulla itself congenital or acquired (ch-pancreatitis)
Radiological appearance :
1. Small, oval or round Ba. filled pouch of few mm.
2. At 2nd part at the ampullary site.
3. Mobile, painless on pressure.
4. No fluid level.

Chronic duodenal ileus

(D.D. of dilated duodenum)
A. Non-obstructive Mega-duodenum
scleroderma
B. Obstructive :
A. Intrinsic - Congenital atresia. web or membrane
- Duodenitis.
- Diverticulae, Neoplasm

B. Extrinsic - Sup. mesentric syndrome

- Tumour, abscess, gall stones.
- Adhesions
- Annular pancreas.
Radialogical appearance :
1. Dilated duodenum.
2. Active peristalsis.
3. Duodenal stasis.
4. Bowel is flattened against the spine.

Duodenal tumours
A. Bengin neoplasms (40% of the duodenal cap tumours are benign)
1) Adenomas :
 G.I.T. 41
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- Highly potential malignancy. - The most common.

- The adenomatous polyp are les than 1cm in diameter.
- They either sessile or pedunculated.
Radiology : Lobulated filling defects.
2) Hamatomatous polyps:
small filling defects present with peutz-jegher syndrome.
3) Leiomyomas :
- Intra-luminal buliging into the lumen of the duodenum with intact mucosa
except if ulcerated.
4) Lipoma :
- Translucent, submucosal tumour change in shape.
5) Carcinoid tumour :
- Irregular, single, lobulated filling defect.
- mainly located in the dudenal cap. post-bulbar region.

B. Malignant duodenal tumours

1) Primary
A. Adenocarcinoma :
- Mainly involve the 3rd part of the duodenum.
Radiologically soft tissue mass and stricture of the lumen.
B. 1ry lymphoma : Rare, polypoidal mass, thickened folds and nodules.
2) Secondary :
- From adjacent organs.
- Haematogenos : especialy melanoma.
Radiologically :
- Multiple filling defects.
- Extensic soft tissue mass compressing lumen.
- Filling defect may have central necrosis (Fleck of Ba.) Target lesion.

Smooth filling defects in the duodenum Cobble stone

1. Retained food & effervescent salts.
2. Duodenitis
3. Hypertrophy of Brunners glands.
4. Polyps arising from Brunners glands.
5. Varices of duodenal cap : p, anatomises between Rt. gastric & panccreatico-
duodenal V at base of cap.
6. Aberrant pancreatic tissue.
7. 1ry carcinoma. of duodenum (rare).
 G.I.T. 42
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8. Lymphomatous duodenal infiltration.

9. Enlarged L.N. around head, of pancreas.
10. Cancer head of pancreas & pancreatitis.
11. Coeliac a. stenosis : with subsequent dil of arteries is the pancreatic duodenal
arcade 2nd part.
12. Gastric metaplasia 24-39 small nodules of various sizes & shapes from pylorus to
apex of cap.
13. Annular pancreas : overdevelop of uncinate process of the pancreas surround
duodenum comp.
Rad smooth filling defect indent lat aspect of duodenum eccentric narrowing of
lumen without ulceration
Target lesion (leimyoma, metastasis, myeloma metast., lymphma).
Lesions in the duodenum beyond the cap
1) Ectopic pancreas
- Pyloric antrum, , 2nd part of the duodenum
- Single filling defect similar to sessile polyp
- Central Ba. collection resemble an ulcer.
2) Annular pancreas :
- Over development of the uncinate process formation of a ring of pancreas
tissue surrounding duodenum.
- Radiologically : Notch-like defect in lat. wall 2nd part of the duod. may
lead to obstruction.
3) Papilla of vater :
- Enlargement of the papilla due to oedema result from impaction of a gall
stone in the distal C.B.D or pancreatitis.
4) Acholedochocle as before.
5) Duodenal varices serpiginous, thickening of the mucosal folds.
6) Duodenal haematona thumb print filling defects.
7) Pancreas carcinoma.

The small intestine

1. Congenital :
A. Malrotation
Either :1. Complete :
With the large bowel to the left side of the abdomen and the small bowel
to the right.
2. Partial : with the caecum and the ascending colon to the left.
B. Internal hernias: in para-duodenal fossae or other peritoneal pockets.
 G.I.T. 43
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C. Meckels diverticulum
- A remnant of the vittelo-intestinal duct.
- Lies in the anti-mesenteric border of the ileum, 2 feet from the ileo-cecal
junction and about 2 inches long. (present in 2% of population).
C/P.
- Picture like-appendicits due to inflammation.
- Intestinal obstruction due to intessuception.
Asymptomatic
- Perforation peritonitis
- PU (peptic epth melena)
Radiologically
1. Plain : Rarely it appear as a larger gas filled viscus with fluid level.
2. Ba. Enema: no significant hold up of Barium due to wide neck (small bowel
enema).
3. Isotopes.

II. Parasitic infestation :

Ankylostoma
Irregularity of the mucosal pattern of the 2nd part of the duodenum due to
reattachment of heads of the worm.
Ascaris
(1) Plain :
- Intestinal obstruction: rare (a large mass of worms obstructing the bowel ioop).
(2) Barium enema : woms appear as a linear filling defect due to the presence of
worms in the lumen of the bowel, and contrast within the
alimentary tract of worms may be visible.

III. Inflammatory diseases :

Regional enteritis (Crohns disease)
Age : Any age (usually 3rd decade) non specific granulomatous influm. of GTT
Pathology :
Site : any part of the Gut, especially the terminal ilium.
Gross picture :
1. Asymmetrical involvement and skip lesions are characteristic.
2. The disease predominates on the mesentic border.
3. Wall, thickened, rigid, congested with narrow lumen.
4. Ulceration with cobble stone appearance.
 G.I.T. 44
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5. Enlarged mesenteric lymph nodes.

6. Loops are matted togther & fistulate is common between loops.
Microscopic picture :
1. Chronic non caseating inflammatory granuloma.
2. Oedema & fibrosis affecting all coats of the intestinal wall.
3. Deep fissure ulcer my extend into submucosa & musculairs.
C/P :
Onset : Acute : resembling acute appendicitis.
Chronic : chronic ill-health.
Presentation :
Diarrhoea, colic.
Low grade fever, Anaemia, Anorexia, loss of wt.
Tender mass on the right iliac fossa.
Complications :
1. Subacute intestinal obstruction very common.
2. Complete intestinal obstuction rare.
3. Fistulae either between the loops or viscus.
4. Perforation abscess formation.
5. Toxic megacolon.
6. Carcinoma (800 x increased incidence).
7. Lymphoma.
8. Systemic complications of the disease: arthropathy, eye lesions (uveitis), skin
lesions (erythema nodosa).
9. Malabsorption.

Radiological appearance :
Ba. meal follow through
- The terminal ileum is the most commonly affected site radiologically.
1. Apthoid ulcers or nodules due to edema or lymphoid hyperplasia.
2. A granular pattern:
Non-specific appearance.
Due to edema of the mucosa and submucosa.
3. fold thickening and irregularity if the edematous changes become marked.
4. An ulcernodular pattern: either longitudinal or transverse in type if both forms
are found in the same area a cobble stone appearance is seen eoth normal
mucosa lying between the ulcers.
5. The string sign: This occurs due to spasm and edema on the affected area or in
a more permanent basis due to fibrosis and loss of mucosa.
6. Ulceration: In the initial stages, small lucent areas 5 10 mm in diameter with
a central pool of barium may be present - Bulls eye or target lesion
 G.I.T. 45
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(apthous ulcers). Later, large marginal ulcers which may be oval, round or
crescent shaped with associated edema, fold radiation or fibrosis are found.
7. Marginal spiking: As fine streaks of Ba which extend outward from the
thickened bowel wall. This represents Ba within intramural fissures (coarse
rose thorn, fine raspberry thorn).
8. Fuliform polyps: Fine polyps may occur in both ulcerative colitis and Crohns
disease; however they are rare in the small bowel.
9. Fistula and sinuses: They are common, and involve either adjacent segments
of bowel, the bladder or the skin surface.
10. Marked mesenteric thickening is sometimes present and leads to assymetry of
and angulation of a bowel loop with separation from the adjacent bowel. This
separation is accentuated in many ases by the presence of enlarged mesenteric
lymph glands. Marked muscle relaxation gives a fixed rounded appearance to
a bowel loop Omega sign.

Other radiological changes:

1. Artheritis: sacroilitis and ankylosing spondylitis.
2. Scelerosing cholangitis and increased frequancy of gall stone disease due to
the termed ileal disease leading to a fail in the bile lsalt pool and the
productionof lithogenic bile.
3. Obstruction of the right ureter either by fibrosis or inflammatory mass.
4. Oxalate stones due to hyperoxaluria.
5. Psoas abscess: one of the commonest causes.
CT :
- Thick mucosa > 5mm
- Adjacent LN++ or fibrofatty infiltration of mesentery
- Abscess & fistulae.
Oedema of the muscular layer :(granular pattern)
??? Ileo-ileal difficult to demonstrate.
Ileo-colic : seen by Ba. enema.
Fistulae between the gut and the U.B.
Sinuses to the Vagina or anterior abdominal wall.
Latter stages :
Inflamatory mass with internal or external fistula.
Uretric obstruction due to retro-peritoneal fibrosis
Colonic involvement : haustral loss, pseudo-sacculations and
inflammatory polyps.
Differential diagnosis:
* T.B. of the small intestine:
- Stenotic lesions are common (in continuity sterling sign)
- Fistulae and sinuses are common.
 G.I.T. 46
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- The caecum may be extremly contracted.

- Calcified mesentric lymph nodes.
*Yersenia enteracolits. Apthoid ulceration, lymphoid hyperplasia and thick folds
*Actinomycosis: fistulous track to the skin surface. (discharge sulpher granules) and
considerable deformity of ileocecal region.
2. Ulcerative colitis :
Diff. Diagnosis U.C. Crohns
A. Clinically
Rectal bleeding Always 50%
Abominal pain Uncommon 50%
Abdominal mass. Never Common
Colonic involvement Always distal Proximal > diatal
B. Radiologically
- Ulceration - Shallow & granular - Deep, rose-thorne
- Haustra - Lost early in the disease - Incomplete loss
- Skip lesions - If involved, incontinuity - Often discontinue (skin lesion)
- Small bowel (valve) - Ileocaecal valve patulous - Ileo-caecal valve narrow or
- Caecum and T. ileum normal
C. Complications
- Fistula - Never Common
- Perforation - Uncommon Rare ( the thickness of bowel wall)
- Carcinoma of the colon - High risk in total colitis Rare
-Associated onditon: - Common Rare

3. Lymphosarcoma of the small intestine

4. Carcinoid tumours:
- Common at the ileum., ileo-coecal vavle, Appendix and may
cause senotic lesions, nodules.
- Arise from enterochromaffin cells and produce serotonin.
- Mostly in the appendix, mainly ileum and metastatize to the lung and liver.
5. Carcinoid syndrome:
- Primary tumor metastatize to the liver.
- Serotonin and other chronically active substances pass unaltered into pulmonary and systemic
circulation. Patients complain of abdominal pain, diarrhea, flushing and asthma.
X-ray findings:
- Initially, the tumor presents as a small round filling defect in the bowel, commonly the ileum.
- As it enlarges, a mass effect with displacement, constriction, and angulation of bowel is seen,
which is accentuated gy the fibrosis or desmoplastic action of the tumor, which sometimes
constricts drawing veins or rarely the smaller arterial branches.
- The linear extension of the tumor has been demonstrated on ????
Angiography:
- Radiating vessels with a limited tumor blush.
- Outline liver metastases prior to surgery or chemotherapy or if tumor embolisation is planned.
 G.I.T. 47
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5. Segmental infarction & radiation ileitis.

Rapid oedema, ulceration and fibrosis.

Lymphoma of small intestine

- 50 70 years.
- >
- Distal small boel due to the presence of peyers patches in ileum.
- May be 1ry or part of a generalized disease.
C/P:
- Abdominal pain, diarrhea, melena, or in some cases malabsorption due to
extensive bowel infilteration or lymphatic obstruction.
- Increase incidence in patients with coeliac disease.
Radiologically:
Ba follow through:
- Nodules, either multiple or single, may be seen, after associated with fold
thickening or ulceration; the nodule may be sufficiently enlarged to cause
intussuception and obstruction.
- If the tumor mass is sufficiently large, considerable bowel displacement, loop
separation (Black area) and lymphatic obstruction will be present.
- In some cases, if the smaller nodules undergo ulceration, they simulate aphthoid
inflammatory ulcers.
- In Hodgkins disease: there is less evidence of large abdominal mass and
fistulation.
CT:
- Demonstrate the site of the primary lesion and may show the presence of disease
elsewhere.
1. Bowel wall thickening.
2. Folds are thickened and the bowel is slightly dilated.
3. Aneurysmal dilatation or the presence of endo-exoenteric lesion may also
be seen as well as glandular masses either in the mesentery or
retroperitoneum.
- A rare appearance, due to the preservation of perivascular fat, may be
demonstrated on CT, when enlarged glands surround the SMA or vein (the sandwich
sign).
U/S:
 G.I.T. 48
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- Thickening of bowel wall, giving a uniformly hypoechoic pattern, with loss of the
ability to identify different layers.

Ileo-caecal T.B.
Pathology :
Site : It starts at caecum then to ascending colon and lastly 1-2 inches of ileum.
Pathogenesis :
- T.B. by haematogenus route is trapped in the submucosa tubercle
formation this coalase together to form tuberculoms caseation
occurs healing by fibrosis thickening of the wall narrowing of the
lumen with gradually increasing obstruction.
- Enlargement of the adjacent mesentric lymph nodes.
- The hyperplastic mucosa show ulceration and polypoidal growthes within
the lumen.
C/P :
1. Night sweating.
2. Discomfort in the right iliac fassa.
3. dirrhoea and mucous in the stool (with ulceration)
4. Palpable mass in the right iliac fossa.

Radiological appearance :
A. Ba. meal follow through :
1. Sterling sign :
2. Ulceration is transverse and associated with spasm of the ileum and the lower
ascending colon.?
3. If fibrosis follows there is either segmental or diffuse narrowing of the bowel
with masked shortening of the cecal pole.
4. The presence of linear ulceration, cobblestoning, fistulation, and assymetry of
the changes in the bowel wall strongly favors a diagnosis of Crohns disease
rather than TB
5. Calcified mesenteric lymph nodes.
CT:
- Acute stage: delineates masses, detects ascites, and thickening of the bowel.
Glandular enlargement with iso or hypodense central areas and peripheral enhancement
are seen when necrosis occur.
D.D. :
1. Crohns disease 3. Cancer caecum
2. Appendicular abscess. 4. Actinomycosis.
 G.I.T. 49
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IV. Vascular diseases :

1. Acute ishaemia :
Causes : Arterial embolisim or trombosis.
Radiological appearance :
1. Plain :
- Dilatation and fluid filled loops with thumb priting due to submucosal
edema.
- Later gas in thebowel wall: necrotizing enterocolitis.
???- Lastly with gas forming organism gas within the portal vien and intra-
hepatic ducts.
2. Ba. : Absolutely contra-indicated.
3. Angiography : may detect the cause.

2. Chronic ischaemia intestinal angina

Causes :
- Arteritis.
- Fibro-muscular hyperplasia.
- Pressure on the coeliec artery by the crus of the diaphragm.
C/P :
- Regular attacks of pain at the meal times.
- Steatorrhoea with sever loss of weight.
Radiological appearance :
1. Plain : Normal or dilated loops.
2. Ba. : Dilated loops with thick oedematous folds.
Thumb printing, fold thickening and separation of bowel loops.
CT:
1. Confirms bowel dilatation and wall thickening.
2. Show the thrombus in artery or vein.
3. Confirms the presence of air in the bowel wall and portal venous system.

V. Malabsorption syndrome
Causes of malabsorption:
I. Lesions in the bowel wall:
A. Mucosal: Coeliac
Whipples disease
 G.I.T. 50
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B. Total wall: Crohns disease

Ischemia
Lymphoma
Amyloid

II. Infective:
A. Acute: Bacillary
Parasitic: giardiasis, ascaris.
Viral.
B. Chronic: TB

III. Digestive defects:

1. Pancreatic defficiency: chronic pancreatitis, pancreatic cancer.
2. Biliary defficiency: biliary atresia, obstructive jaundice, HCF.
3. Cystic fibrosis.
4. Zollingear ellison syndrome.
IV. Lymphatic:
1ry lymphngectasia, 2ry lymphngectasia due to obstruction by tumor.
V. Enzyme defficiencies:
Disaccharidase, cystinuria.
VI. Drugs:
Neomycin, cholecystramine.

Individual diseases
I- A (1)-Coeliac disease :
It is the commonest cause of absorption syndrome (gluten sensitive entropathy wheat,
barley, rye, oats, HLA B8 & DR3).
C/P : a. Steatorrhoea.
b. Iron or folate deficiency anaemia.
Pathology :
- Jej. biopsy reveals, subtotal villous atrophy hypokalaemia
Radiological appearance:
1. Dilatation of bowel loops:
Most manifest in the jejunum, may also be seen in the ileum, rare in the colon.
Minimal peristaltic activity seen on screen.
2. Excessive secretion (misnomer) as it is infact due to diminished absorption of
the causing dilution of the Ba in the bowel.
3. Segmentation: is no longer a finding, due to modern Ba mixtures.
4. Mucosal fold changes:
 G.I.T. 51
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The folds may appear thickened or thinned, depending on the degree of bowel
dilatation and the amount of secretion present on the degree of bowel dilatation
and the amount of secretion present.
No destruction of mucosa is seen.
5. Intussuception: this is not uncommon in celiac disease.
6. The moulagae sign: found in severe cases, where the loss of folds leads to a tube
like appearance of the bowel.
Complications:
A. Lymphoma:
70 80 fold increase in risk of lymph in patients with coeliac disease.
Recurrence of abdominal pain, distension, and weight loss despite strict diet.
B. Carcinomas: of the oesophagus (higher incidence in patients with coeliac
disease).
C. Rarely: small intestinal ulceration, particularly in the jejunum.
D. Splenic atrophy may occur.
(2)-Whipples disease (intestinal lipodystrophy):
- As C. disease.
- Enlarged abdominal lymph. nodes.
- Bone changes : Spine as in Rheumatoid arthritis.

B- Radiological features of total wall affection:

a. Localised or multiple lesions of small intestine:
1) Crohns disease :
- Causes of malabsorption in Crohns disease.
i. Stagnation of individual loops.
ii. Ulcerated lesions loss of protein.
iii. Surgical resection .
- Radiological appearance as before.
2) Lymphoma :
- It leads to villous atrophy.
3) Scleroderma : severe dilatation of the duodenum and jejunum with
thichkenning of the folds.

III- Digestive defects: Cystic fibrosis

- The exocrine changes are most marked in the lungs, but the disturbance in the
mucous and electrolyte secretion may lead to changes in small and large bowel.
Radiographically:
The duodenum is the site most likely to show changes, they may appear as
nodular indentation, fold thickening, ulceration, strictures or loss of the normal
fold pattern, most marked in the descending part of the duodenum.
Rarely, a fine nodular sand like appearance may extend throughout the small
 G.I.T. 52
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bowel, due to excess abnormal mucous adhering to the tips of villi producing
small round filling defects in the Ba filled bowel.
A plain abdominal film, may in severe cases, show evidence of obstruction
with dilated bowel and fluid levels due to the viscid frothy intestinal contents.

- With the introduction of high dose pancreatic enzymes replacement, s??? both short and
long, may occur due to initial ischemia and a later fibrotic reaction, mostly in the
ascending colon.
Generalized colonic wall thickening and haustral loss may occur.
A defect in the medial wall of the cecum due to enlarged appendix due to
mucous plugging (enlarged appendix intussception).

V. Tumours of the small intestine

A: Benign tumours:
- Leiomyomas. - Adenomas.
- Lipomas - Haemangiomas.
- Polyposis Peutz. J. syndrome.
B: Malignant tumours:
1. Carcinoid.
2. Lymphoma see before.
3. Carcinomas rare.
4. Metastatic seadling or haematogenous as in bronchogenic, cancir
breast and melanoma.
Disaccharidase def. (eg. lactase) sucrase & maltase) unsplitted disacchoride moleclae large not
absorpted by microvilli remain in SI osmotic diarrhae malapsorption.
Rad. (Test sugar added to barium)
1. Dilution of barium preparation.
2. Relative rapid barium transit to colon.

Common ileocecal valve lesions:

1. Lipomatosis, ischemia.
2. Neop.: carcinoid, lymphoma, carcinoma.
3. Inflammatory: UC, Crohns, TB, Actino, amobiasis, yerssinia.

Appendix
I. Inflammations :
 G.I.T. 53
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A. Acute appendicitis :
C/P :
1. Plain, w is at 1st generalised then become localised to right iliac fossa.
2. Tenderness over the Mcburny point.
3. Rovsings sign : Rebound pain on the right side when we suddenly
remove our hand from the left side.
4. Leucocytosis > 14,000.
5. Vomiting
6. Fever > 38 C.
Radiological appearance :
1) Plain : 1. Appendicular calculus.
2. Sentinal loop dilated atonic ileum, containing fluid level.
3. Dilated caecum.
4. Blurring of the properitoneal fat line.
5. Right lower quadrant haze due to fluid and oedema.
6. Scoliosis concave to the right.
7. Right lower quadrant mass indenting the caecum.
8. Blurring of the right psoas line (unreliable).
9. Gas in the appendix.
2)U/S : It may be of no value.

B. Chronic appendicitis
Cambies technique:
- Give Ba. meal by mouth.
- After 2hr. give oral concentrated saline solution of MgSo4 which helps
much in emptying of the appendix.
- Examination is carried out at :
6hr : to estimate ileal stasis.
24hr. : to estimate Appendicular filling.
> 24hr. : to estimate Appendicular stasis.
- Fluoroscopy should be carried out at each time.
- Comment on : site, size, lumen, mobility, tenderness, filling and emptying
of the appendix.
The classical appearance :
1. Blind tube : 3-4cm lenght, 2-4 mm calibre.
2. Lumen : Mainly uniform or narrowing towards the base.
3. Firely mobile on palpation.
 G.I.T. 54
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4. The position is variable.

Radiological signs of chronic appendicites :
1. Non-filling of the appendix due to fibrotic stenosis of the lumen.
2. Incomplete filling due to stenosis, transparent contents.
3. Appendicular concretions : may be :
a. Radio-opaque, single or multiple.
b. Transparent : formed of inspisated faeces.
4. Irregularity of the appendicular lumen constant.
5. Fixation of the appendix due to adhesions, tested by pressure on it.
6. Fixation of the caecum or ileum, result from peritoneal adhesions.
7. Tenderness on pressure over the appendicular shadow due to :
- Mobile app : due to visceral tension on the inflamatory appendix.
- Fixed app.: due to dragging on the parietal peritonium.
8. Appendicular stasis retention of Ba. in appendix after caecum is clean (3-4 days).
9. Ileal stasis dilatation : Stasis occur due to adhesions or reflex ileocaecal valve closure.
10. Gastric stasis : Ileal stasis reflex inhibition of the gastric evacuation.
11. Kincking of the appendix Ba. filled appendix is angulated due to adhesions
to the adjacent structures.

Mucocoele of the appendix

Pathogenesis :
The appendix becomes distended with mucous as a result of obstruction of its lumen in
absence of infection.
Radiological appearance :
- Round filling defect on a Ba enema examination similar in appearance to an
inverted appendix stump. A mucocele may rarely calcify or rupture, if ruptures
pseudomyxoma, with accumulation of massive ascites which appears as multiple
cystic masses on CT. the shed epithelial cells may calcify throughout the peritoneum
(Millet seed appearance).
- Both CT and US are of value in demonstrating the presence or absence of wall
calcification and whether obstruction of the urerter or lower small bowel is presnt.

Appendicular abscess
Radiological appearance :
1. Spastic contracture of the caecum.
2. Pressure defect in the Ba. filled caecum.
3. Irregularity of the caecum outline due to associated typhitis.
 G.I.T. 55
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4. Fixation and tenderness of the caecum on palpation.

5. Mucosal relieve pattern intact mucosa (D.D. carcinoma, T.B.)
6. Displacement of the ileum by a large extra-luminal mass with thining and
stretching of the mucosal folds may be visible.

II. Tumours
A. Adeno carcinoma :
- Extremely rare. - Early ulceration, infiltration, metstasis.
B. Carcinoid tumour :
- Locally invasive, does not spread beyond appendix (or terminal ileum).
- May metastasise liver & lung. - 1cm rounded filling defect.
- CT, MRJ, angio tumour blush, radiating vs.
III. Diverticulae
Rare, occur as a part of colonic diverticulosis or distal to stenosis in the appendix.
Dilated small bowel :
Calibre :
- Proximal Jejenum > 3.5cm.
- Mid. small bowel > 3cm.
- Illeum > 2.5cm.
A. With normal folds :
1. Mechanical obstruction + dilated large bowel.
2. Paralytic ileus dilated small and large bowel.
3. Coeliac disease.
4. Scleroderma.
5. Post vagotomy gastrectomy.
B. With thick folds :
1. Ischaemia.
2. Crohns disease (oedema, nephrotic, cirrhosis, Budd Chiari).
3. Radiotherapy
4. Lymphoma
5. Zollinger Eilson syndrome (hyperacidity).
6. Extensive small bowel resection compensatory dilatation.
7. Amyloidosis.

Strictures in the small bowel :

1. Adhesions
2. Radiation enteritis.
3. Crohns disease
4. Tumours lymphoma, carcinoid mass, carcinoma. Rare mass,
sarcoma, (lymphoma and leiomyoma), metastasis.
 G.I.T. 56
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5. TB.
Thick smooth, regular folds :
1. Vascular ischaemia.
2. Radiotherapy : may have a latent period up to 25 years.
3. Oedema adjacent inflammation, hypoproteinaemia e.g. nephrotic &
cirrhosis, venous obstruction cirrhosis, Budd-chiari syndrome and
lymphatic lymphoma, retroperitoneal fibrosis.
4. Infilteration amyloidosis.
5. Coeliac disease uncommon.
Thick, irregular, distorted folds :
a. Localised :
1. Inflammatory Crohns disease Z.E. syndrome.
2. Neoplastic lymphoma, metastasis and crcinoid (40% in the ileum).
3. Infective T.B.
B. Wide spread :
1. Infilterative amyloidosis, Wipples disease.
2. Inflammatory Crohns disease.
3. Giardiasis + Nodular lymphoid hyperplasia.
Lesions in the terminal ileum :
1. Inflammatory Crohns disease Ulcerative colitis.
2. Infective T.B., actinomycosis (rare, predominantly caecum + bone
destruction) and histo-plasmasis.
3. Neoplastic lymphoma, carcinoid (annular fibrotic stricture,
intralipomatosis.
4. Ischaemia cobble stone or thumb printing appearance due to
submucosal edema perforation & bleeding.

The Colon
1. Congenital lesions
A. Ano rectal anomalies
Imperforate anus: It is a comon deformity of the alimentary canal.
Classification:-
~ Ladd and gross classification
- Anal stenosis due to failure of formation of the proctoderm.
- Imperforate anal membrane with anal depression due to membrane separating the
blind pouch of the rectum.
 G.I.T. 57
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- Anal agenesis it is a severe type which is associated with fistula or bony

deformities of the sacrum.
~ Another classification I.P.C.I.M.
1) High.
2) Intermediate.
3) Low.
Usually with genito-urinary fistulae.
Depending whether the distal bowel terminate above, at, or below the levator ani.
C/P: Male high and intermediate:
- Abdominal distension (6-8 hr. after labor).
- Absent anal orifice.
- With fistula ---meconium pass with urine.
Female high and intermediate
- Late abdominal; distension.
- Passing stool from the vagina.
Male / Female low type
- Pyramidal fold, membrane bulge at the anal orifice.
- Microscopic anus.
Radiologically:
1. Invertogram
The examination is not done except after 12-18hours after delivery to allow
sufficient swallowed air to reach and fill the terminal rectal segment. The anal
dimple is identified by metallic marker. The baby is held in inverted position for few
minutes to allow swallowed air to distend the rectal segment completely. Plain films
are taken in A-P and lateral views with additional films in supine and erect.
Radiographic appearance:
On A-P view:
The distance between the metallic marker and the gas filled rectal pouch is
estimated:
<1.5cm low
=1.5cm intermediate.
>1.5cm high.
On the lateral view
A line is drawn between the terminal portion of the sacrum and the pubis
(representing the pelvic floor):
If the blind pouch is below this line ---- low.
If the blind pouch is above this line ---- high.
 G.I.T. 58
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In both
Air in the UB, uterus (fistula)----high.
Presence of sacral deformities----high.

Injection of C.M into the distal loop gives an idea about:

Anatomy of the fistula and genito-urinary tract.
State of distal bowel.
2. Prone lateral shoot radiograph:
With vertical film + horizontal beam ------ better identification of rectal gas shadow.
Radiographic appearance:
Treatment: Low --- perineal approach and reconstruction.
High --- abdominal approach + colostomy.
B. Hirschsprungs disease
It is a disorder resulting from absence of the ganglion cells in the mesenteric plexus of the
involved segment which mainly occurs in the distal large bowel.
Pathogenesis :
During foetal life, migration of the neuroblasts occur in the gut in a cranio-caudal
direction forming the myeneteric plexus, so if it is incomplete, the distal gut remains
aganglionic and lead to failure of relaxation and peristaltic activity.
C/P :
- Infancy intestinal obstruction with violent attacks of diarrhoea.
- Childhood & adult constipation.
Incidence : Male : female = 4:1.
Site : recto-sigmoid 70%, but may occur in any part of the large gut.
Causes of megacolon :
1. Congenital (hirshusprung).
2. Idiopathic.
3. Toxic megacolon (UC).
Radiological appearance :
a. Plain :Infancy :
a. Generalised dilatation of the intestine with gas.
b. Absence of gas in the rectum.
Adult : Mottled appearance, due to faeces mixed with the gas.
b. Ba. enema :
Infancy Ba enema.
Adults gastrographin enema to avoid faecal impaction.
We only fill the distal bowel to identify the segment.
 G.I.T. 59
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3-Important signs:
1. Change of the calibre between the narrow distal aganglionic segment and the
more dilated normal proximal segment.
2. Delayed evacuation after 24hrs retained Ba in Hirsch. disease.
3. Irregular serrated outline of the aganglionic segment (but not a stricture).

Rectal biopsy : absence of ganglionic cells is diagnostic.

* Demonstration of characteristic pressure wave changes on pressure studies.

C. Idiopathic megacolon
Rectal dilatation extend to the anorectal junction with no distal narrowed segment. Dont
fill with barium water, intoxication.
II. Inflammatory lesions = Colitis
(Infective, Ulcerative, Ischemic)
A. Colitis due to organism:
Actinomycosis
T.B
Bilharizasis
Ambiasis
Common radiological appearance :
1. Hyperaemia & cell infiltration loss of the mucosal pattern.
2. Polyps due to increase mucous secretion.
3. Ulceration spasm & loss of haurstral pattern.
4. Healing by fibrosis stenosis.

B. Ulcerative colitis
It is a mucosal disease which almost always involve the rectum and may then spreads
proximally through the colon for a variable distance.
Female > male.
20 40 yr.
Causes :
Unknown, stress and immunological response to unknown antigen may be the cause
Pathology :
It affects the distal segment > proximal one.
Cellular inflammatory infiltrate which is confined to the mucosa, with distortionof the
glandular pattern, goblet cell depletion, and numerous crypt abscess, subsequently, loss of
haustration occurs with shortening and narrowing of the bowel.
 G.I.T. 60
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By endoscopic examination :
1. Stage of onset :
C/P :
- Fever, abdominal colic, bloody diarrhoea.
- Decrease weight, anaemia, dehydration malabsorption.
- Blood, mucous in the stool.
- mass in the right iliac fossa.
Complications :
1. Acute toxic dilatation.
2. Perforation fistula - perianal abscess.
4. Carcinomatous changes
- The development of malignancy is related to duration of the disease.
- It develops diffusely in a flat mucosa.
- Occasionally, it may be multifocal.
- When develops, it is either plaque like or sccirrhous type.
5. Arthritis and dermaititis :
Radiological appearance:
- Early changes consists of (1) an alteration of the normal sharp mucosal ine (the
tengential viens of the mucosal surface) which becomes blumed and slightly
thickened. This is accompanied by a fine grannular appearance in the en face view.
- As the disease progresses more:
(2) Coarse granular appearance is seen and the mucosal line becomes frankly
beaded.
- If ulceration develops, it is usually (3) restricted to the mucosa and therefore
appears shallow. Deep ulceration, in contrast to Crohns disease, is distinctly
uncommon but when it does occur, the ulcers tend to assume a collar stud
configuration and may coalesce.
NB: Ulceration in ulcerative colitis, always occurs against a background of a
diffusely abnormal mucosa, and discrete ulceration with intervening normal mucosa
is never seen.
(5) Increased width of the presacral space > 1 cm.
(6) Varying degrees of post-inflammatory polyposis may occur. The pos-
inflammatory polp sometimes called the pseudopolyp (consisits of grannultior
fibrous tissue woth an epithelial covering. A polypoidal appearnce in acute disease
represents a combinationof post-inflammatory polyps and mucosal tags which,
together with acutely active and ulcerative disease, produces gross flored mucosal
changes.
(7) The mucosal changes are accompanied by haustral blunting, followed by
effacement, and as the disease progressess, the colon shortens and the lumen
narrows due to muscular abnormality rather than fibrosis, which is not a feature of
 G.I.T. 61
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this disease. In the fully developed state, it produces the tubular pipe stem colon
of late UC.
Backwash ilietis:
Spread of mild inflammation to the terminal ileum in acute total colitis.
It appears slightly dilated with a dilated snd incompetent ileocecal valve.
The mucosa of terminal ileum shows mild granularity over a length of 515
cm.

C. Ischaemic colitis
It is due to blood flow below the critical level of the cellular viability.
1. Non gangrenous form :
Plain : Segment of colon where intra-luminal gas shadow shows evidence of
pronounced mucosal edema (thumb printing).
Ba. enema :
Shows an abnormal segment of the colon, often abruptly demarcated from the
adjacent normal bowel.
The involved area is narrowed with loss of normal haustration, spasm rigidity,
with thumb printing in the early stages due to mucosal edema and hemorrhage
into the bowel wall.
Majority of cases complete resolution.
Occasionally ulceration is seen during the course of the disease, and a fibrous
stricture may develop.
Common at splenic flexure.
(2) Gangrenous form :
Plain : Marked dilatation of large bowel e subsequent presence of gas in portal vein.
Diverticulosis of GIT :
1. Pharyngeal (lat, ant, post : Zenkers) (epiphernic)
2. Oesophageal (cong, acquired : Pulsion, traction).
3. Gastric (congenital, acquired).
4. Duodenal (congenital, acquired : Akerland)
5. Small int (meckels, congenital int.)
6. Colonic (pulsion type).

III. Diverticular diseases of the colon

They are mucosal herniation (protrusions) via muscular wall
Theories :
1. Old theory : herniation at site of entrance of the arterial branches of the
colonic
 G.I.T. 62
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vessels via wall.

2. Recent : herniation occurs at the mucosal dimples in areas not
straightened by
muscular band or fatty infiltration at these points.
Pathology :
1. Age : > 40y, male : female 4:1
2. Site : caecum (rare), sigmoid (due to pulsion power).
3. Shape : V. Shaped globular flask shape.
4. Surface : rounded or smooth or sessile.
5. Nature : Pulsion diverticulae.
6. Wall : mucosa, submucosa and peritoneal coats (muscle itself atrophies).
7. It is liable to infection.
8. Thickening, coursing and confluencing of the circular muscle fibres concertina like
or serrated appearance of theaffected area saw tooth pattern.
9. Thickening & shortening of the long muscle fibres shortening and narrowing
of the pelvic and descending colon.
10. Size : from 2mm 2cm
Complications : see the paper
1. Perforation :
- pneumoperitonium
- pericolic abscess ( leakage of comfort media)
- para-colic abscess.
2. Fistula ;
- The commonest is colo-vesical one (difficult to see by Ba. enema).
- Plain film: Air in the bladder and fistula may be demonstrated by
contrast study.
- Less commonly fistual between the colon and the small intestine,
vagina or skin.
3. Haemorrhage :
- Sever bleeding may occur in the elderly.
- Bleeding is brisk and of short duration.
- Superior mesenteric arteriography detect bleeding site, thickening of the
intima and thinning of the media.
4. Inflammatory bowel disease:
UC (less common) superimposed granularity.
Crohns (more common) obvious ulcers and edema.
5. Malignant changes it is of stricture type coexist rather with mucosal
destruction and shouldering.
6. Colonic stricture
 G.I.T. 63
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Infection .
General peritonitis.
Radiological appearance : (Ba. enema & Ba. follow through).
Filling & post evacuation :
1. Stage of dirdiverticulosis :
a. Fine spastic notches at summites of haustral bulges.
b. Prediverticular spasm.
c. Sigmoid goes into spasm as the rectum is filled.
2. Stage of diverticulae:
- It is characterised by presence of Ba. filled diverticulae in form of rounded opacities
(2mm-2cm) connected to the colonic lumen by narrow neck.
- It is acute phase. Ba enema not done except after 2 weeks for fear of peritonitis.
1. Diverticulae:
Flask like or rounded outpouchings from the bowel wall. When seen en face, they
are ring shadows; a narrower neck may et al. visible producing a smaller and
usually eccentrically placed ring within the larger circle of the diverticulum itself
and the presence, in erect view, of a barium fluid level.

2.The muscle change:

This in the sigmoid colon, produces the concertina-like or serated appearnce of the
affected area.
Patients with marked diverticular disease, sustain a pronounced and persistant
spasm during the filling stage of the Ba enema.
CT is of value in quabtifying periodic disease, abscess formation, and adjacent organ
involvement. CT guided abscess drainage is now a therapeutic option.
- Useful in right sided diverticulitis to DD from appendicitis, Crohns.

Complications:
Narrowing & marked irritability of the affected segment.
Tenderness on palpation by fluoroscopy.
Periodic abscess produces an extrinsic filling defect which is usually
eccenteric. Leak of Ba outside the lumen may be seen.
Mucosa: narrow and distortead (but not destroyed; DD cancer).
If perforation occurs:
- Spread of gas into the retroperitoneal tissues = soap bubble appearance on
the plain film.
- Free gas if there is performation into the peritoneal cavity.
 G.I.T. 64
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IV. Tumours of the colon

A. Colonic polyps 1) Adenomatous :
a. Adenomas : 3 forms of dysplasia
- Simple tubular (most common).
Radiologically:
A sessile adenomatous polyp, depending on its size and projection, appears
a either an obvious large round mass projecting into the colonic lumen or as a
smalll shadow which projects as a circle, oval or ellipse. Ba coating the base of
the poly, oftern produces a asal rim or ellipse seperated from the dome of the
polyp itself.
A cardinal feature of a pedunculated polyp is its stalk or pedicle.
- Villous ( greatest malignant potential), less common than simple tubular.
Flat, sessile masses with the interslices of the villous frond Filled with
barium. Thus, they present a fairly characteristic appearnce of a tumor
composed of frond like stalks or lace work pattern.
- Tubulo-villous. (they are single or multiple, sessile or pedunculated).???
- Villous adenoma (common in the rectum and sigmoid colon) is the largest, they
are flat sessile masses with interslices of the villous fronds filled with barium
showing the most sever dysplasia and has the higest incidence of malignancy.
Signs suggestive of malignancy :
a. Size : > 1cm
b. Sessile with the base is greater than the height.
c. Puckering of the colonic wall at the base of the polyp.,
d. Irregular surface.
- They are fronded, sessile and poorly coated by barium because of their
mucous secretion protein-loosing gastroenteropathy.

b. Familial polyposis :
- Autosomal dominant.
- Start in adolescent.
- No. : 100 5000 polyps.
- Pre-cancerous (about 100%). All cases (untreated).
- It involves all the colon especially the rectum and the distal colon.
Radiological appearance :
- Early: mucosal nodules measuring 1 2 mm in diameter is seen.
- Multiple, rounded, well-defined filling defects extending from pinpoint to large masses.

c. Gardners syndrome :
- Autosomal dominant.
 G.I.T. 65
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- Precancerous.
- Consists of : adenomatous polyp in the colon, multiple osteoma in the skull, and
mandible, multiple skin tumours and epidermoid cysts and dental abnormalities.
- Changes is simillar to familial polyposis.

2. Hyper-plastic :
a. Solitary or multiple in the rectum.
b. Nodular lymphoid hyperplasia :
i. Occurs in children.
ii. Filling defects smaller than in familial polyposis.
3. Hamartomatous :
a. Juvenile polyps :
1. Familial, childrens (6 years).
2. Usually solitary in the rectum.
3. No malignant changes
- Double contrast smooth, rounded masses with well-defined pedicle.

b. Peutz jeghers syndrome :

1. Autosomal dominant.
2. Consists of : colonic polyposis 50% (also small intestinal), mucosal & circum-
oral pigmentation.
- Carcinoma of the stomach & ovary are common association.

4) Inflammatory:
Follow any severe ulceration in the bowel and are particularly seen in post
inflammatory polyps. Have no malignant potential even in ulcerative colitis.
1. Ulcerative colitis :
- Polyps can be seen in all stages of the activity of colitis (pseudo polyps).
2. Crohns disease: less common than ulcerative colitis.
3. Schistosomiasis
4. Dysenteries

5. Infective:
a. Bilarziasis :
- Mainly involve the rectum.
- With or without stricture.
- Bilharzial mass nerver turn malignancy.
 G.I.T. 66
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- Never cause intestinal obstruction (pericolic i.e subserosa).

b. Amoebiasis :
Mucosal oedema, ulcers, blunting haustration.
- Amoeboma : Intra-luminal , Annular, Irregularity of the lumen with lack of
dispensability.
- Pleural reaction & elevated Rt hemidiaphram.
6) Others :
Turcots syndrome : Autosomal recessive, Colonic polyps, Malignant CNS lesion.
Polyps

Benign Malignant
- Diameter < 1 cm - Size > 1 cm ( incidence)
- Pedunculatd _ long stalk - Sessile + brood base
- Smooth surface. - Irregular surface
- Colon contour & wall unaffected - Indentation of colonic wall at base of
polyp.

B. Carcinoma of the colon

Pathology :
PDF : - Adenomatous polyps
- Familial polyposis
- UC
C/P :
* Female > male.
* Local mucus + blood _ change bowel habit, intussception.
* Deposits jaundice, ascites, lung, liver metastasis (most common).
- General anaemia, loss wt.
- Spread: local, lumph, blood, transcoelemic.
1. Microscopic types :
1. Adeon carcinoma the commonest.
2. Malignant carcinoid polypi (small lesion) OR large tumor
indistinguishable from cancer.3. Mucinous (colloid carcinoma) as
adenocarcinoma but the primary & 2 ries tend to be calcified.
4. Carcinoma (undiff.)
2. Gross types of adenocarcinoma :
Grossly, adenocarcinoma asume one of four types:
Polypoid (encephaloid), annular (schirrous), ulcerative, or diffusely infiltrative forms.
1. Mucoid adenocarcinoma :
 G.I.T. 67
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- The commonest form.

- It arises from glands of liberkuhan.
- The gland tend to secret mucous giving rise to colloid containing tissue.
2. Scirrhous adenocarcinoma (annular):
- Tend to encircle the bowel stenosis.
- Ulceration & perforation may occur.
- Mainly affect the left side (mainly sigmoid).
- It may be affect a segament of the gut (2-3) or may be localised give rise to
string carcinoma
3. Encephaloid carcinoma :

Sites : in order of frequency :

- Pelvic colon caecum & ascending colon T. colon & splenie flexure hepatic
flexure & descending colon.

Radiological appearances :
1. A tumor mass projecing into the lumen of the colon (?? Finger print defect).
2. A marginal filling defect projecting into the colonic lumen separated from the
normal mucosa by a sharp margin because of its apearance, it is sometimes
referred to as saddle cancer. At an earlier stage, this tumor appears plaque like.
3. Mucosal destruction with a sharp margin of seperation from the normal mucosa.
4. A classical annular carcinoma (Apple core appearance), stricture is short (6 cm.)
irregular or annular mucosal destruction, shouldering.
5. Long segment stricture (linitis plastica).
6. Colonic obstruction.
7. Fixationof the gut.
- US, CT, MRI, Isotope, to detect liver metastases.
1. Filling defect. 4. Stricture with proximal dilatation.
2. Mucosal destruction 5. Colonic obstruction
3. Tumour mass 6. Fixation of the gut.
These are the CARDINAL radiological signs

DD :
1. Metastasis localised nodular defects, or long segments stricture indistinguishable
from linitis plastica
2. Local spread from the adjacent primary tumour
- Large extra-colonic component.
 G.I.T. 68
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- Fixed mucosal fold.

- Nodular defects & ulceration.
3. Adhesions ;
- Common around the T. colon following cholecystitis or pancreatitis.
- The involved segament is fixed, rigid, narrow with intact mucosa.
4. Infections Amoeba, T.B. Bilharziasis causing strictures.
5. Crohns diseases and ulcerative colitis:
Characteristic radiological signs of these conditions and absence of the cardinal
signs of malignancy allow ready differentiation.
- Normal mucosa, or showing ulceration.
- Absent shouldering.
- Involved length is greater than carcinoma.
- Evidence of regional ileitis.
5. Local segmental spasm intact mucosa.

Pneumatosis coli
- It is a gas filled in the colonic wall.
- If rupture pneumoperitonium.
DD : of gas in wall of the colon :
1. Toxic megacolon.
2. Pneumatosis coli: in Ba appears multiple submucosal cysts with characteristic
serpiginous margin of the lumen. In plain: a chain of bubble like
transluciencies.
3. Infarction 4. Necrotizing enterocolitis.
5. Leukaemia 6. Sclerodema.

Colonic strictures
1. Neoplastic :
A. Carcinoma irregular and annular, shorter than 6 cm with mucosal destruction
and shouldering.
B. Lymphoma 1ry (rare caecum, rectum) or 2ry (stomach & small intestine
must be involved - Diffuse nodularity - or polypoidal masses).
2. Inflammatory :
a. Ulcerative colitis.
b. Crohns disease.
 G.I.T. 69
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c. Periocolic absces.
d. Radiotherapy :
- Stiructure occurs several year after radiotherapy.
- Common site is recto-segmoid.
- Stricture smooth, narrow.
3. Ischaemic :
- Common at the splenic flexure.
4. Infective :
a. T.B. commonest in iloe- caecal region. short, hourglass stricture.
b. Amoeboma more common in the descending colon
- Multiple in 50.
- Rapid improvement after treatment.
c. Bilharizal commonly recto-sigmoid, caused by healing by granulation tissues
following acute stage (oedema, polyps) stricture.
5. Extrinsic masses :
- Inflammatory - Tumours
- Endometriosis.
6. Cathartic colon :
- Pseudo-strictures, which alter their configuration during Ba. enema.
- The colon may be atonic & dilated.
- Initially in the ascending colon progression to involve all of the colon.

Filling defect in the sigmoid colon:

A. Rounded filling defect all types of polypi.
B. Finger print (thumb print) defect :
1. Neoplastic - Encephaloid carcinoma
- Lymphoma.
- Metastasis : (stomach, pancreas).
2. Inflammatory Ulcerative colitis Crohns disease
- Ischaemic colitis.` - Amoebic
- Bilharzial colitis.
C. Napkin ring defect encephaloid carcinoma schirrhous.
D. String defect annular schirrhous carcinoma.
E. Double-encroachment defect ulcerating adenocarcinoma.

DD mass in the right iliac fossa :

A. Appendix appendicular mass.
 G.I.T. 70
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B. Ileocoecal region :
1. Inflammatory Crohns disease - Ulcerative colitis. - Radiotherapy
2. InfectiveTB, Bz, actinomycosis, histoplasmosis, ameoboma and yersinia
3. Neoplastic Lymphoma, carcinoid, metastasis and carcinoma of caecum.
4. Vascular Aneurysm of the iliac arteries rare. Expansile pulsations. Detected
by angiography
C. Others :
1. Acute intussusception (early).
2.Ascaris mass
3. Ileo-psoas cold abscess
D. Kidney : Diopped Kidney (detected by I.V.U)
E. U.B. : huge diverticulae.
F. G.B. : Huge enlarged G.B. (hydrops) with hepatomegally.
G. Pathological undescended testes
H. In females tubo-ovarian mass. ovarian cyst, tubal preg., hydro, pyosalpinic
I. Large pelvic abscess.

Megacolon
1- In adult :
- Colonic calibre > 5.5 cm
A. Non toxic (without mucosal abnormalities ) :
1. Distal obstruction carcinoma.
2. Ileus.
3. Pseudo-obstruction : Symptoms & signs of large bowel obstruction but no
organic lesion identified by Ba. enema.
4. Purgative abuse.
B. Toxic (with sever mucosal abnormalities):
Deep ulceration with extensive sloughing of the mucosa.
1. Inflammatory U.C. & Crohnss disease.
2. Ischaemic 3. Amoebiasis.

2- In a child
1. Hirschsprungs disease.
2. Functional / psychogenic: the rectum is distended with faeces.
3. Cretinism.
4. Mechanical obstruction stricture : post necrotizing entero-colitis.
- tumour : sacrococygeal teratoma.
 G.I.T. 71
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- Imperforated anus.
5. Neurogenic spina bifida.

Widening of the retro rectal space:

The post-rectal soft tissue space at S3-S5 is > 1.5cm (N= 1 cm at S4)
A. Normal variation : 40% in obese persons.
B. Inflammatory : U.C., Crohnss radiotherapy & diverticulitis.
C. Neoplastic:
1. Carcinoma of the rectum.
2. Metastasis : prostatic, ovary.
3. Sacral tumours metastasis, plasma-cytoma, chordema.
D. Others :
1. Anterior sacral meningocoele : A sac containing C.S.F protrudes through a
defect in the anterior wall of the sacrum myelography & CT diagnostic.
2. Pelvic lipomatosis
3. Enteric duplication cysts.

CT retroperitoneal cystic masses

A. Pancreas pseudo-cyst, cyst adenoma/carcinoma and von-hippel-Lindau.
B. Kidney cystic diseases.
C. Retroperitoneal cystic tumours lymphangioma, leiomyo-sarcoma and
haemangio-pericytoma.
D. Paraaortic cystic nodes testicular teratoma and cancer cervix.
E. Others :
1. Hamratoma. 2. Abscess.
3. Lymphocele. 4. Meningocoele.

The liver
Causes of hepatomegally :
A. Cardiovascular
1. CHF 2. Constrictive pericarditis.
B. Infective :
1. Viral 2. Bacterial
a. Viral hepatitis a. Brucellosis
b. Infective monomucelois b. Milliary T.B.
3. Parasitic 4. Protozoal
 G.I.T. 72
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a. Bilharziasis a. Amoeba.
b. Hydatid b. Malaria.
c. Fasciola c . Toxoplasmosis
5. Mycotic a. Action-mycosis b. Histo plasmosis.
C. Infiltration :
1. By cells 2. By iron 3. By Lipid
a. Leukaemia a. Haemo-chromatosis a. Gaucher
b. Lymphoma b. Amyloidosis.
c. Metastasis
D. Hepato - toxins :
1. Obstructive jaundice 2. Drugs
E. Tumours :
1.1ry hepatoma 2. Cholangio-carcinoma.
3. Multiple metastasis 4. Adenoma

Scheme in suspected liver mass

Plain x-ray
U/S
Cystic solid Mixed
Aspiration biopsy CT Aspiration
Follow up Angio & MRI .

1. Plain film in hepatic masses : (should include both the diaphragm and symphysis
pubis on the same film).
A. Radiological signs of liver enlargement :
Right lobe :
1. Elevated Rt. hemidiaphragm
2. Depression of the hepatic flexure.
3. May be depression of the Rt. kidney.
4. Bulging of the Rt. lateral preperitoneal fat line.
Left lobe : The gastric fundus diplaced downward & laterally.
B. Subphrenic gas collection :
- An air fluid level
- Usually associated with :
1. Pleural effusion (Irritation of the parietal pleura).
 G.I.T. 73
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2. Basal lung consolidation.

- Fluosrcopy raised, immobile diaphragm.
C. Calcification :
1. Parasitic : curvilinea, as in hydatid cyst.
2. Tumour faint, mottling or sunburst in :
- Primary carcinomas.
- Metastasis - medullary carcinoma of the thyroid.
- Mucous secretory adenocarcinoma
3. Infections Amorphous in old abscess or calicifed granuloma.
D. Gas shadow within the liver:
1. In abscess cavity.
2. Linear extending to periphery portal circulation (A) portal pyemia
(B) promatosis intestinal (C) dead bowel *ischemia).
3. Linear in biliary tree.
E. Bone :
1. Erosion by 2ries 2. Scoliosis abscess.
F. Ascites
2. U/S in hepatic masses :
1. It is the most coast-effective technique of choice.
2. It can differentiate mass into cystic, solid or mixed
- Cystic has the following ch. ch. well-defined echolucent lesion with
posterior wall enhancement.
- Solid echogenic lesion (well or ill-defined) without post-wall
enhancement.
Specific features :
a. Metastasis :
1. Multiple, well-defined lesions of poor echogenicity surrounded by a very sharply
defined, poorly echogenic halo (Target lesion) pathogenomoic for metastasis .
2. Adeno-carcinoma of the breast, bronchus and pancreas poorly echogenic.
3. Vascular or mucinous carcinoma of the Bowel, Bladder, stomach strongly
echogenic metastasis.
B. Hepatic carcinoma :
1. May be focal or diffuse.
2. Large, poorly echogenic, unhomogenous lesion with irregular outline.
3. Cystic changes may be present.
4. Invasion or displacement of the hepatic veins or P.V.
C. Abscess :
 G.I.T. 74
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1. Cystic lesion. 2. Well circumscribed.

3. Thick, smooth wall with fine internal echoes due to debris.
4. Gas may be found bright echoes.
5. U/S aspiration biopsy diagnostic.
D. Hydatid :
Any one or combinationof the following appearnce:
1. A simple cyst with a parallel line (a lamina membrane) inside the wall.
2. Cyst containing smaller daughter cysts.
3. Homogenous material filling the cyst or surrounding internal contents.
4. Calcification within the wall (curved or linear).
5. Collapsed cyst within the parent cyst.
6. Echogenic; with or without the other signs. There is poor acoustic
enhancement.
NB Amoebic :
- Rounded
- Subcapsular.
- Contain fine echoes.
- Rupture.
- Re-scan after flagyl.

E. Haemangioma :
- Sub-capsular, lobulated, highly echogenic, well-circumscribed with areas of
(lucency venous lakes).
F. Adenomas :
- Strongly echogenic, large, well defined.
- Haemorrhage appears as cavities of poor echogencity .

3. C.T. in liver masses :

A. Cystic lesions :
- As pyogenic abscess, hydatid cyst.
1. Central, homogenous, attenuation value with increased attenuation of the
surrounding wall (pre-contrast).
2. After contrast enhancement enhancement of the wall.
3. Well-circumscribed with smooth wall.
4. Thick, shaggy interior as in pyogenic or amoebic abscesses.
5. Calcification in the wall of hydatid.
6. CT guided aspiration diagnostic.
B. Solid lesions :
1.Usually hypodense, may be homogenous or non-homogenous.
 G.I.T. 75
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2.It enhances after contrast injection but less than the surrounding except
haemangioma.
3. Well defined adenoma, haemangioma.
4. Ill - defined margin Hepatoma.
5. Solitary or multiple.
6. Areas of density Haemorrhage & calcification or areas of density
necrosis in the tumour.
7. It can diagnose LNS enlargement at porta-hepatis.
8. It can diagnose the state of the biliary systems.

4. Isotope scan :
- It reveals generalised liver enlargement.
- Localised areas of uptake non specific as it may be 1ry malignancy, 2ry
malignancy or abscess.

5. Angio-graphy :
- Diagnostic and therapeutic selective catheterization of the coeliac axis followed by
the hepatic artery.
Angiography in haemangioma :
- Feeding vessel N. size.
- Slow how in tumour.
large vasc. spaces.
- No early A.V shunting.
- Blush in venous phase.
followed by the hepatic artery : indications :
1. Surgical mapping before partial hepatectomy.
2. Embolization of the tumour before surgery.
3. Localised chemotherapy infusion by selective injection in the hepatic artery.
Specific features:
1. Cystic lesions :
- A vascular.
- Smooth displacement of the vessels arround the lesion.
2. Solid lesion :
- Vascular lesions A. V shunt.
- Tumour blush Displacement or invasion of the venules
- Parasitic blood supply.
 G.I.T. 76
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6. MRI :
It can diagnose the lesion either by
- Local alteration of the anatomy.
- Change in the signal intensity.
- Not able to diagnose calcification.
- T1 : liver > panc > spleen > kid
- T2 : liver < panc < spleen < kid
Metastasis: low on T1, hig on T2, target sign.
Haemangioma: Low on T1, v. high on T2, lobulated, on contrast : enhancement
from out in.
Hepatoma: best on T1 pseudocapsule of low signal center of ( signal >
surrounding
Amaebic: double wall sign + surrounding edema.

7. Indirect studies :
- Ba. meal, Ba. enema & I.V.U.
- It is used to diagnose hepatic masses either by its displacement or invasion.

Causes of localised liver mass = (SOL in the liver)

A. Congenital: Solitary or polyscystic, usually associated with adult polycystic
kidney.
B. Traumatic: haematoma Traumatic- AV fistula
C. Parasitic: amaebic, hydaitd cyst.
D. Inflammatory :
- Pyogenic abscess - Fungal abscess
- Cholangetic abscess - Tuberculoma
E. Neoplastic :
1. Malignant :
i. Primary hepatoma, cholangio-carcinoma, lymphoma and Kupffer cell sarcoma.
ii. 2ry :
2. Benign :
- Adenoma - Haemangioma - Hamartoma
- Dermoid - Cholangioma.
 G.I.T. 77
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The pancreas Pancreatic lesions

Causes of pancreatic calcification :
- Ch. alcoholic pancreatitis.
- Hyperpara.
- Cystic tumours.
- Haemangioma.
- Hematoma.
- Pseudo cyst.

A. Congenital : Annular pancreas.

B. Inflammatory :
- Acute pancreatitis. - Chronic pancreatitis.
- Recurrent acute pancreatitis - Cyst : true or pseudocyst.
C. Neoplastic : - Benign fibroma, and neurofibroma.
- Malignant 1ry adenocarcinoma, iselts cells endocrine
tumour and lymphoma. 2ry very rare.
- Cystic neoplasm serous cyst adenoma (benign) and mucinous
cyst adenoma (potentially malignant).

Criteria of cystic neoplasm :

- Large masses.
- Hypervascular - Calcification
Scheme in suspected pancreatic lesion
Plain x. ray Ba. meal

U/S
Cystic Solid Mixed
Aspiration ERCP
CT
Isotope
Angio
1. Plain radiography abdomen :
A. Annular pancreas:
- There is dilatation of the stomach and proximal part of the duodenum with littel
gas in the intestine (Ba meal)
 G.I.T. 78
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B. Acute pancreatitis : (Acute abdomen).

1. Selective ileus of the 2nd part of the duodenum
2. Gasless abdomen (due to vomiting).
3. Retro-peritoneal oedema & obliteration of the psoas shadow.
4. Gall stone.
6. Fluid in the left costo-phrenic angle.
7. Boney changes : Bone infarction, avasc necrosis, lytic lesions due to
metastatic fat necrosis.
C. Chronic pancreatitis :
1. Calcification along the pancreas.
2. Gall stones.
3. Bulky foamy faces from pancreatic steatorrhoea.
D. Pancreatic cyst :
- May migrate to the mediastinum, lower abdomen mass displacing gas filled
intestine or stomach
E. cystic neoplasms :
- May give a large mass with calcification.

2. Ba. meal & hypotonic duodenography :

A. Annular pancreas :
- Shows annular constriction of the 2nd part of the duodenum by the pressure of
an encircling band of the normal pancreatic tissue.
B. Acute pancreatitis :
- Using gastrographin outlines the obvious swelling of the pancreatic head
within the duodenal loops, wide curve.
C. Pancreatic cysts :
- Displacement or smooth indentation on the lesser curvature of the stomach with
narrowing of the calibre.
D. Carcinoma of the ampulla of vater :
- Extrinisic filling defect at sits of ampulla & duodenal, invasion
- Inverted 3 sign (frostberg),.
E. Carcinoma of the pancreatic head :
- Widening of the C-loop of the duodenum unreliable sign.
- Obstruction of the pancreatic portion of the C.B.D.
 G.I.T. 79
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- Encroach up on the duodenal mucosa spiculation at the duodenal fold

destruction.
- Enchroach up on the pyloric antrum mucosa destruction.

3) U/S :
- U/S vary with the stage & severity of the disease.
A. Acute pancreatitis :
1. Oedema : the affected sagement enlarges with echogenicity.
2. Necrosis : Usually associated with a fluid collection.
3. Haemorrhage : Is echogenic.
4. Inflammation of the retro-peritoneal fat very strong echoes with loss of the
normal detalis
B. Chronic pancreatitis :
1. Gland size focal enlargement global with loss of the normal anatomicl details.
2. Contour irregular outlines of the gland due to interlobar fibrosis.
3. Parenchyma : hetrogenous echogenicity.
4. Duct changes : Increased echogenicity of the walls relative to the parenchyma
- Calibre 2mm is significance.
- Major duct calibre changes can be seen.
5. Gland atrophy : uncommon.
6. Calcui strong echogenicity within the duct or the parenchyma.
7. Cysts - < 5cm in mild or moderate.
- > 5cm in sever pancreatitis.
- They represent ectatic ducts intra or peri pancreatic
8. Calcification with or without postacoustic shadowing.

C. Pancreatic neoplasm :
1. Benign :
Adenoma - Serous cyst adenoma and mucinous cyst adenoma
- Slow growing, multilocular, thick walls.
- Blood pool mucous calcification strongly echogenic.
- Benign islets cell tumours :
Are infrequently seen by U/S
Insulinomas :
- Small, solitary or multiple.
- Malignant metastasis (10%) liver.
Gastrinomas :
 G.I.T. 80
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- Small , multiple
- Malignant to the duodenal wall.
2. Pancreatic carcinomas :
- Size : enlargement of the pancreas, commonly in the head.
- Contour normal .
- Parenchyma heterogeneous echogenicity.
- Margin well defined.
- Duct size dilatation of ducts with surrounding the parenchyma is atrophied.
- Atrophy of the pancreatic tissue with shortening of the gland
a. Tortuous ducts.
b. Double ducts dilatation of the C.B.D and pancreatic duct due to
strictures in both.
- Cysts uncommon.
- Calcification uncommon.
4. E.R.C.P.:
a. Annular pancreas difficulty in introduction of the end via the duodenum.
b. Acute pancreatitis it is contraindicated.
c. Carcinoma as in obstructive jaundice.
d. Ch. pancreatitis as in obstructive jaundice.

5. C.T.:
A. Acute pancreatitis :
1. Diffusely enlarged. 2. Irregular outline.
3. Heterogeneous density 4. Intra or extrapancreatic fluid collection

Complications pseud-cyst, Haemorrhage high attenuation, pancreatic abscess

Lesser sac fluid collection.

B. Chronic pancreatitis :
1. Gland size normal or enlarged (focal or diffuse).
2. Irregular outline.
3. Dilatation of the pancreatic duct Irregular outline with low att. value.
4. Calcified stones high att. area within the gland.
5. Pancreatic cysts low att. areas.
6. Pseudo cyst determine its location.
7. Obliteration of the facial planes.
 G.I.T. 81
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C. Carcinoma :
1. Localised mass, of variable attenuation value, distorting the local anatomy.
2. Vascularity enhancement can take any form hypodensity, losdensity or
hyperdensity.
3. The mass may encroaches on the surrounding structures.
4. In advanced cases metastasis liver.
- Enlarged abd. lymph nodes.
- Atropy of the gland distal to the tumour.
- Dilated C.B.D & intra-hepatic billiary radicls.
5. Calcification & Haemorrhage The attenuation value.
6. Necrosis low att. areas.

D. Benign tumours :
Both adenomas and endocrine tumours :
- Appear as mass of variable attenuation due to fluid content.
- Endocrine tumour multiple, small, of vailable att. value.

E. Pancreatic cysts :
- Appear as lesion of low attenuation value the about the fluid level (1-6 H.U)
displacing the stomach & the intestinal loops.
6. Isotope scanning : It is of low value in pancreatic lesion with no specifecity

7. Angiography :
a. Coeliac axis arteriography :
- It help to demonstrate pancreatic lesion by highly vascular tumour with
pathological Vs, displasment of Vs arround the tumour and tumour, blush.
b. Transhepatic portography :
It helps to diagnose endocrine tumour by venous sampling.

8. MRI.
- Tumour signal on T1, contrast democate : tumour.
- Cystic T on T1 & high on T2.
- Acute pancreas T1 & T2 + same criteria as CT (fluid coll.)
- Hgic panc. v. high on T1.
- Ch. pancreatitis. calcification > 5mm appear as ill defined. areas of low
signal on T1 & T2.
 G.I.T. 82
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Cysts of the pancreas

Types:
-True : lined by epithelium
- Pseudo cyst: not lined by epithelium (always acquired)

Congenital Acquired
1. Solitary cyst 1. Retention cysts. 2ry to obst. by stone, small tumour
2. Polcystic pancreas 2. Parasitic cysts (hydatid).
3. Mucovisidosis 3. Cystic tumours Cyst adenoma serous (B)
Mucinous (M).
Cyst adenocarcinoma
Cystic cavitation in malg. tumour
4. Demoid cyst 4. Lymphatic cyst (lymphoepithelial cyst)

Pseudo-cysts of the pancreas

It is a collection of fluid, blood, serum or extravasated pancreatic juice in peri-pancreatic
tissue or the lesser sac.
Aetiology :
1. Acute pancreatitis : the commonest :
1. Focal pancreatic necrosis is more likely to cause pseudopancreatic cyst with
maturation taking from 2--6 ws.
2. The most common site is anterior to the body and tail of the pancreas extending
to the lesser sac anterior para-renal space and root of the mesentery.
3. Disruption of the duct system, and spillage of the pancreatic juice may make the
cyst to dissect its way between the tissue planes its presence in the abdomen or
thorax.
4. Haemorrhage, superimposed infection formation of echogenic debris.
5. Maturation, when complete the cyst become echo-free and intimately related to
the underlying pancreatic tissue with a characteristic feature is projection of a segment
of the pancreas in the cyst lumen.
6. Inflammatory cyst of acute onset attain, a large size containing about 5 litters.
 G.I.T. 83
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2. Chronic pancreatitis :
- Small, multiple.
- Within the pancreatic substance.
- Usually associated with intra-ductal calculi
- It is better to be termed retention cysts.
3. Trauma to the pancreas :
- Blunt disruption of the main pancreatic duct pseudocyst large.
site : At which the pancreas is stretched over the aorta.
- Penetrating Fistula formation.
4. Pancreatic malignancy :
Fluid collection 2ry to obstruction.
Fate may enlarge or decrease in size & disappear.
Complication Haemorrhage
- Infection Pancreatic abscess.
- Rupture fistula or ascitis.

The Spleen
Plain :
Size N = 11cm, > 15cm = splenomegally.
Stomach med., diaph. up, also related to kid & splenic flexure.
Inf. loss of it psoas line
Accessory splenules
- Calcification
- Ascites.

Causes of sptenomegally :
1) Blood disorders : - Leukaemia - Polycthaemia - Haemolytic A.
2) Lymphoma : - Hodgkins and non Hodgkins.
3) R.E. disorders : - Histocytosis, Gauchers disease.
4) Infection : Acute : Bacterial, viral
Chronic : Bacteria TB.
- Malaria
- Hydatid
 G.I.T. 84
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5) Vascular portal hypertension :

6) Trauma Rupture, subcapsular haematoma.
7) Metastasis.
8) Miscellaneous : Sarcoid, S.L.E Amyloid.
9) Splenic cyst pseudocyst : following old haematoma or infarction,
epidermoid cyst and hydatid cyst.

Causes of splenic calcification :

- Curvilinear : splenic artery aterosclerosis and aneurysm or cysts (hydatid and
post-traumatic).
- Multiple, small nodules phlebolithes, Haemorrhage, T.B., histoplasmatic and
brucellosis.
- Diffuse homogenous or fine granular sickle cell anaemia.
- Solitary > 1cm (healed infarction, Haematoma, abscess and TB).
Accessory spleen :
- Lying along the splenic artery near the hilum
DD : 1. Renal mass 2. Pancreatic mass

Portal hypertension
Definition :
It is elevation of the portal venous pressure above the normal which is 10-15cm
H2O (7 11 mm Hg).
Causes :
a. Pre sinusiodal :
1. Intra-hepatic 2. Extra-hepatic
a. Bilharzias a. Splenic vein tombosis.
b. Granuloma (TB sarcoid) b. Splenomegally portal blood flow
c. Malig. lymphoma c. Portal vein thrombosis
d. Amyloidosis - Cirrhosis
- Post splenectomy complications.
B. Post sinusoidal :
1. Intrahepatic : 2. Extra-hepatic
- Liver cimbosis - C.H.F
- Budd-chiari syndrome
(thrombosed hepatic veins or IVC)
Effects of portal hypertension :
 G.I.T. 85
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1) Splenomegally : Due to
- Congestion, hypersplenism.
- Opening of A.V. shunts.
- Or thrombosis of the portal or hepatic vessels.
2) Opening of the A.V. shunts :
- Cephalic around the lower end oesophagus between the oesoph.
branch of the left gastric (portal) and oesoph. branch of azygos vein
(systemic) oesoph. varices haematemesis.
3) Ascites :
1. Hypoproteinaemia due to liver insufficiency.
2. Inactivation of ADH and aldosterone.
3. Portal hypertension.

4) On GIT :
- Dyspepsia and malnutrition due to congestion.
5) On blood :
- Anaemia, leukopania, thrombocytopenia d.t. hypersplenism pancytopenia

Radiological examination of portal hypertension :

1) Plain radiography :
Chest C.H.F, Chest T.B., Sarcoidosis, Bilharzial corpulmonal
- Splenomegally : left hypochondrial soft tissue mass with long axis > 15cm
- Elevation of the left hemidiaphragm.
- Loss of the left psoas margin.
- Calcification in the spleen.
- Visualization of the Ascites Haziness, and bulging of the fat planes.
- Raised diaphragmatic copula.
- Displacement of the gass shadow centrally.
2) Ba. swallow :
- For oesopageal varices & double contrast Ba. meal for gastric varices.
3) Angiography :
Via : a. Superior mesentric arterography venous phase.
b. Splenic arterography venous pahse.
c. Direct trans-splenic percutaneous splenoportography.

Value : 1. Measuring the width of the splenic and portal vessels.

 G.I.T. 86
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2. Patency of the splenic portal vessels.

3. Visualization of the varices in the lower end oesophagus.
4. Interventional in embolization of the bleeding varices.
5. Pre-operative for shunting operations.
4. U/S :
Left renal assessment before warns operation :
1. Can help in diagnosis of the cause as liver cirrohsis and B.H.F.
2. Showe dilated collaterals around the spleen, liver and left gastric.
3. Portal vein dilataion.
5.C.T. :
It can visualize patency of the main vesseles using bolus injection.
6. Interventional procedure :
- Liver biopsy (CT or us)
- Embolization of varices by percutaneous transhepatic portography (P.T.P)
- Embolization of the splenic artery in the treatment of hypersplenism.
7. Isotopes :

The Biliary System

A. Gall bladder diseases
1. Gall stones :
a. Causes:
- Infection.
- Stasis.
- Change in bile constituents.
b. Pathology : Types
1) Cholesterol stones :
i. Type pure cholesterol.
ii. Incidence not common.
iii. No solitary
iv. size floats (erect film).
v. Causes Acute cholecystitis.
vii. Shape Round or oval and white.
2) Pigmented stones :
i. Pure pigment . ii. Not common.
iii. Multiple iv. Small.
v. Lucent. vi. Haemolytic anaemia
vii. Irregular and black.
 G.I.T. 87
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3. Mixed :
i. Cholesterol, pigment and Ca.
ii. Very common.
iii. Multiple
iv. Medium and faceted.
v. Opaque and lamellated.
vi. Cholecystitis.
vii. Hexagonal, faceted, brownish.

b) C/P, complications : see general medicine OMUMI.

c) Radiological appearance see obstructive jaundice.

2. Cholecystitis
A. Acute :
i. Acute calcular 96% due to cystic duct obstruction by stone.
ii. acute non calcular due to burn, polyarthritis, steroid therapy, typhoid.

Acute Cholecystitis :
Gall stones in 20%
Duodenal ileus
Ileus of hepatic flexure of colon
Rt hypochodn mass due to enlarged GB
Gas within biliary system
Cystic duct obst failure of GB to fill in scintigraphy

B. Chronic :
- Wall thick, shrunken, filbrotic.
- Mucosa ulcer, papilloma.
- Chronic stone.

3. Cholesterosis and cholecystosis:

A. Cholesterosis : strawberry G.B.
- There is diffuse deposition of cholesterol on G.B. mucosa and when reaching 1-2 mm
thickness small fixed filling defects in the back ground mucosa Straw berry
surface.
- G.B. radiographic unsharpness in cholecystogram, patients develop cholesterol
stones.
 G.I.T. 88
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B. Cholecystosis : Adenomyomatosis :
- Unknown aetiology.
- Muscle hypertrophy mucosal packers.
Radiological appearance : (Oral cholecystography)
1. Fixed fundal nodular filling defect.
2. Stricture .
- Any where in the G.B., accentuated after gall bladder contraction, may be
sharply localised or diffuse narrowing
DD : phrygian cap and simple fold partial septum across fundus
3. Rokitansky - Aschoff sinuses :
- Only fill and become visible after G.B. contraction = contraction within small
mural diverticula.
- Common with stricture.

Gall bladder adenomyomatosis:

Hyperplastic mucosa and muscle of GB wall outpouching of the mucosa into or
through the muscularis mucosa diverticula, known as Rokitansky sinuses.

4. Tumours of the gall bladder

(Very very rare)
A. Carcinoma :
Associated with gall stones, chronic cholecystitis and poreceline gall-bladder
Radiological appearance in jaundice
B. Papilloma, adenoma :
Rare to be diagnosed, 80% present at surgical specimen.

B. Biliary tree diseases

1) Obstructive jaundice
Obstruction of the bile flow to the duodenum with back diffusion of the conjugated
bilirubin to the blood.
Causes : obstruction of the extra-hepatic ducts.
a. In the lumen :
1. gall stones. 2. Ascaris worms.
b. Wall of the bile duct :
1. Stricture of C.B.D bilharzial & malignant (sclerosing cholangitis).
2. Bile duct tumour. cholangiocorcinoma, klat skin tumour
3. Ampulla of Water tumour.
4. Spasm of sphincter of Oddi.
 G.I.T. 89
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c. Extra luminal pressure :

1. Cancer head of pancreas.
2. Pancreatitis.
3. Enlarged L.N. at porta-hepatis.
4. Parasites Hydatid cyst.
5. Duodenal diverticulae.
6. Choledochal cyst CBD cyst

Radiological techniques:
A. Direct study :
1. Plain abdomen radiography .
2. U/S.
3. C.T., MRI.
4. Direct contrast study operative cholangiogrophy, pre-operative P.T.C
and post-operative T-tube cholangiography.
5. ERCP

6. Indirect contrast study oral cholangiography is contra-indicated in

obstructive jaundice. iv cholandiography.
7. fine needle biopsy.
B. Indirect study Ba. meal I.V.P.
1. Plain film :
It can visualise the pathology which causes the obstruction :
a. Stones radio-opaque stone in G.B. or hartmanns pouch :
- Usually mixed.
- When they are widely separated suggest obstruction jaundice.
- Biliary sand (limy bile) is ca caronate deposits in G.B.
b. Calcification
Calcified bladder wall porcelain G.B potentially malignant
(consequent to chronic inflammatory change).
Calcification in he pancreas Chronic pancreatitis.
c. Gas in biliary tree see acute abdomen .
d. Paralytic ileus acute pancreatitis and acute cholecysitis.
e. Bone erosion, 2ries, malignancy.
f. Ascitis malignancy.
g. Fat planes Its obscuration or absence indicate there is abst. Jaundice.
 G.I.T. 90
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2. Oral cholecystography :
- Is contra-indicated in obstructive jaundice.
- Non-calcified Gall stone : Appear as single or multiple mobile filling defects.
- After fatty meal increased sensitivity in detecting gall stones.
- G.B. carcinoma : commonly ass. e gall stones or porcelain wall in females.

3. Direct contrast study :

A. Pre-operative cholangiogram
I- P.T.C. :
- It is used to - Visualise dilatation of the biliary duct.
- Level of obstruction.
- Causes of obstruction.
- Nature of the proximal part of the obstruction
i. Bile duct stones in P.T.C :
- Appear as radiolucent, mobile, single or multiple, filling defect with gross
dilatation of the proximal duct.
- When impacted meniscus sign.
ii. Malignant stricture in P.T.C :
- Due to pancreatic carcinoma, cholongio-carcinoma
- It is usually complete.
- Convex cut off.
- Moderate to gross dilatation of the C.B.D and bile channels.
- Incomplete stricture demonstrate length of the stricture shoulder sign and
irregularity.

iii. Benign stricture in P.T.C

a. Following cholecytstectomy :
- Stricture is very short and tight.
- Occurs at the level at which the cystic duct was ligated.
- Dilatation above is rarely impressive.
b. Chronic pancreatitis :
- Produce a rat tail appearance of the stricture.
- Several cm in length.
- With or without calcification in the pancreatic head.
iv. Parasites in P.T.C. :
a. Hydatid cyst : produce compression of the biliary duct.
b. Round worm : Ascaris worm in C.B.D
 G.I.T. 91
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2- E.R.C.P :
- It replaces P.T.C especially when prothrombin time is prolonged.
- It is used in obst. jaundice to detect nature of the distal part of the obstruction.
a. In carcinoma of the pancreas. :
Pancreatic duct :
1. Occlusion is the commonest finding, commonly accompanying with block of
the C.B.D.
2. Duct stricture uncommon, with displacement of the main side ducts around
the tumour.
Cavities :
Cavities in the tumour may be filled with contrast giving scrambelt-egg.
appearance.
Filling defect :
Non filling of the several side branches due to destruction by the carcinoma with
intact main duct.

b. In chronic pancreatitis :
- Dilatation of the pancreatic duct and its branches, beading.
- Block in the main duct complete or incomplete mimic carcinoma.
- Cavities is small and communicate with the main duct.
- Calcification and calculi pathognomonic.
All these are the hall-marks of ch. pancreatitis

B. Operative cholangiography :
- During cholecystectomy to ensure that no stones are present in the extra-hepatic
biliary ducts.
- Criteria of the normal 1. Non dilated ducts.
2. Absence of filling defects.
3. Free flow of contrast to the duodenum.

C. Post-operative cholangiography
1-T. tube cholangiography
- After exploration of the C.B.D a T tube is inserted and removed after 7-10 days.
Value :
1. To drain the bile.
2. Prevent stricture.
 G.I.T. 92
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3. Ensure presence of no stones after cholecystectomy displaced down in the

C.B.D.

4. U/S :
Value
1. Demonstration of dilated ducts.
2. Level of the obstruction.
3. Nature of the obstructed segment.
4. Deposits and Ascites.
a. Gall stones :
- Is diagnosed by strong echogenicity, post acoustic shadowing and moves on changing position.
b. Chronic cholecystitis :
- Gall stones as above.
- Wall thickening > 4 mm.
- Reflectivity of the wall.
- Contracted G.B. with no lumen.
c. Bile duct stones : stones as above, dilated C.B.D > 9mm
d. Acute pancreatitis see pancreas
e. Chronic pancreatitis see pancreas.
f. Benign tumour usually well circumscribed lesion highly echogenic.
g. Pancreatic carcinoma see the pancreas.
h. Pseudo-cysts displacement.

5- C.T. in obstructive jaundice :

1. It is of value in distinguishing between extra or intra-hepatic cholestasis.
2. Dilated bile ducts lower attenuation linear or circular structures which
dont enhance with contrast.
3.Dilated CBD dilated tubular structure in porta-hepatis or pancreatic head.
4. In acute pancreatitis.
5. In chronic pancreatitis.
6. In pancreatic carcinoma.
7. Lymph node in the porta-hepatis can be diagnosed early by C.T.

6- Scintigraphy :
- Material I131 rose bengin or Tc44m HIDA.
1. Its major application is to define extra-hepatic obstruction.
2. Diagnosis of acute cholecysitis.
 G.I.T. 93
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3. Diagnosis of entergastric reflux bile reflux.

4. Detection of bile leaks post-operative, malignancy, trauma.

7- Angiography :
- See pancreas - Now it is replaced by U/S, ERCP and CT.

8- Indirect studies (Ba. meal and enema and I.V.P).

a. Tumour in the pancreatic body and head may cause obstruction in the
pyloric antrum duodenal loop extrinsic invasion or compression.
b. Duodenography cancer head speculation on the mucosal folds.
c. Widening of the C. loop.
d. Inverted 3 sign in the 2nd part of the duodenum.
e. Duodenal or gastric ulcer penetrating Parcreatitis Jaundice
f. Lymphoma of the stomach LN at portahepatis Jaundice.
g. Ba. enema displacement of the transverse colon.
h. I.V.P. displacement or invasion of the ureter.

9- Interventional :
Biopsy : US or CT - Bile duct stone extraction
ERCP : sphincterotomy - Strictures : Stent by PTC or ERCP
Balloon dilation
10- MRI :
T1 GB depends on conc. of bile (low)
T2 GB hyperintense > liver.

2. Sclerosing cholangitis:
- The hall-mark of this condition multiple, intra or extrahepatic duct stricture and slight
to moderate dilatation of the intervening duct segments.
- Associated conditions (30% - ulcerative colitis).
- Retro. peritoneal fibrosis.
- Fibrosing mediastinits.
- Reidles thyroiditis.
- It is a pre-malignant condition cholangio-
carcinoma
3. Parasites
a. Hydatid disease :
 G.I.T. 94
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- Compression or displacement on the bilary tree.

- Calcification of the wall of the cyst.
b. Round worm :
- Ascaris from the duodenum bile ducts intermittent biliary obstruction.
Radiology :
- The characteristic multiple filling defects.
- If passed to the liver liver abscess

4. Acute suppurative cholangitis

- Bile duct obstruction predispose to ascending infection suppuration
multiple abscess cavities, communicating with intra-hepatic bile ducts.

5. Congenital abnormalities :
A. Choledochal cyst :
- It is smooth saccular gross dilatation of part of the billiary tree CBD.
- The most common site is the lower 1/3 of C.B.D.

B. Carolis disease :
- Congenital intrahepatic bile duct dilatation.
- Multiple saccular dilatation usually situated peripherally.
C. Choledochocoele :
- Rare dilatation of the terminal bile duct filling defect in the medial wall of
the duodenum at the Ba.meal
D. Choledochal diverticulae :
- Diverticulum extending from the medial side of the lower end of the bile duct.

Gas in the biliary tract

Irregularly branching gas shadows which do not reach to the liver edge, probably
because of the direction of the bile flow.
A) Within th bile ducts :
1. Incompetence of the sphincter of oddi :
a. Following sphincterotomy.
b. Following passage of a gall stone.
c. Patulous sphincter in the elderly.
2. Post operative :
a. Cholecystoenterostomy.
b. Choldochoenterostomy.
 G.I.T. 95
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3. Spontaneous biliary fistula :

a. Passage of gall stones directly from an inflamed G.B. into the bowel
b. Duodenal ulcer perforating into the C.B.D.
B. Within the gall bladder :
1. All of the above.
2. Emphysematous (intramural & intraluminal gas, common in DM).

Acute abdomen
Plain films :
1- Supine abdomen: allows distribution of gas & calibre of bowel tube determined.
- Obliteration of fat lines, normally visualized, e.g. psoas outlines, indicates fluid or
inflammatory exudate in these regions.
2- Lt. lat. decubites (Rt. up) :
1. Good in pancreatitis show gas & fluid accumulation in 2nd part of
duod. (local, ileus).
2. Fluid levels of pt. cant stand.,
3- Erect abdomen : fluid levels
4- Chest PA.
1. Gas under diaphragm (perforation)
2. Pneumonia & pulm infarction (mimic acute abd), also pneumothorax,
myocardial infarction, pericarditis, CHF.
5- Chest lat : aortic dissection or rutpure. ++Calcifications:

Causes of acute abdomen :

I. Trauma IV. Intestinal obstruction
II. Perforation pneumopret. V. Gastric dilat.
III. Infection (acute conditions: acute ch., acute app) VII. Vascular lesions
VII. Renel colic, leaking aorta VIII. Intraperitonal fluid or abscess
(subphrenic, paracolic)

I. Trauma
I. Duodenum : (common fixed position)
A. Perforation : Plain
1. Intra peritoneal (A) Free gas under diaghram (erect).
(B) Gas along
falciform lig or
circ. collection done sign
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2. Retro peritoneal.
B. Intramural heamtoma : Ba meal
1. Large complete obstruction.
2. Atild coil spring appearance as bl. spread between. mucosal folds.

C.T. Acute abd : 1. Detect fluid collection + abcess :

- Less a sac collection.
- Retroperitoneal fluid localization by fascial planes
- Psoas abscess.
2. Abd. vascular disease :
- Abd. Aov. Ar dilatation, thrombus, calcification, rutpure loss of periaortic fat plane.
- Major brs SMA renal A.

II. Small bowel and colon : fixed sites are descending & sigmoid :
1. Plain : gas under diaphragm (rare).
2. Ba enema : Thumb prints submucosal haemorrhage.
III. Diaphragm : Lt leaf usually :
Herniation of bowel (with subsequent strangulation) or solid viscus into chest.
IV. Surgical trauma : U/S, C.T. or angio. peri-renal, peri-splenic or extraheputic
hematoma.
II. Perforation
Radiological features :
1. Plain film : free gas (supine : dome sign, erect : gas under diaphragm, Lt. Lat.
Dec : between liver & lat abdominal wall).
2. Water soluble contrast : leak into peritoneum
Causes :
I. Peptic ulcer (commonest) :
- If no gas detected (20%) - A water 50 % of contrast meal is done leak into
peritoneum.
- If no leak is detected, a delayed film is taken after 3 hrs CM in bladder
(absorption from peritoneum).
II. Diverticulitis :
Gas is usually localised (para-colic).
III. Ulcerative colitis :
Gas is seen in necrotic gut wall before perforation.
IV. Specific inflammations (Typhoid & paratyphoid).
V. Malignant growth.

DD of free gas :
 G.I.T. 97
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1. After laparotomy (disappears after 5-10 days).

2. Intestinal pnuomatosis (gas bubbles in bowel wall).
3. Necrotising enteritis: linear gas streaks (intra-mural gas).
4. ischemic bowel lesions: linear gas streaks.
N.B. : Rigler sign = visualise of both sides of bowel wall = pneumoperitoneum

III. Infection Local ileus

I. Acute appendicits : commonest cause of acute abdomen.
Plain abd. film (A) No renal or ureteric stone
(B) Distension of ileal loop (local ileus)
(C) Appendicolith (oval calcification).
II. Cholecystis : radiologically
1. Plain abd. film Stones (10%)
Distension of duodenum ileal loops (ileus).
Gas in GB (gas forming org.)
2.U/S.

III. Acute pancreatitis ( serum amylase) due to excessive vomiting plain, Ba, US
I. Gas less abdomen .
2. Head inflam (A) Local duodenal ileus.
(B) Thickened duodenal folds (med. wall)
(C) Wide c. curve of duodenum.
3. Body & tail inflam (A) Upper jejunal mucosal distortion.
(B) Single or several
fluid levels .
4. Absent gas in mid trans colon (stewart sign).
5. Development of abscess or pseudo pancreatic cyst in lesser sac
(A) fluid level (B) U/S features.
IV. Pelvic inflammatory states:
~ Salpingitis & tubo ovarian abscess U/S.
Ileal involvement : slightly distended loops with fluid level.

Causes of paralytic ileus :

1. Post operative
2. Peritonitis (general) (local: appendicitis - cholecystitis - pancreatitis - salpingitis).
3. Trauma.
 G.I.T. 98
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4. Pneumonia.
5. Renal colic, failure.
6. Morphine.
7. Hypo K.
8. Vasc. occlusion.

IV Intestinal obstruction
Causes : Mechanical intestinal obstruction :
I. Lumen :
1. Faecal impaction.
2. Gall stone ileus.
3. Food bolus.
4. Meconium ileus.
II. wall :
1. Congenital atresia : Hirschsprung's & imperforate anus
2. Crohns disease
3. Divecticulitis inflammatory conduction
4. Tumours.
III. Outside the wall :
1. Strangulated hernia (into o. ext.)
2. Volvulus.
3. Adhesions.
4. Bands.
5. Intessusception.
6. Lymphomas

Causes of pseudo-intestinal obstruction:

1. Idiopathic (do Ba enema to exclude cause).
2. DM.
3. Collagen disease.
4. Amyloid.
5. Neurological.
Colonic distension without obstruction:
* Pseudo obstruction.
* Paralytic ileus.

Adynamic intestinal obstruction :

1. Vascular ischemia
2. Scleroderma.
 G.I.T. 99
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3. Toxic dil of colon.

4. Necrotising enterocolitis.
5. Post operative ileus, suspected when these is small & large bowel obstruction

Causes of massively dilated stomach :

1. Paralytic ileus (trauma, post operative, peritonitis, pancreatitis, cholecystitis, diabetic & hepatic comas).
2. Gastric volvolus.
3. Air swallowing
4. Intubation.
5. Gastric outlet obst (Du, cancer antrum, extrinsic compression).

Small bowel Large bowel

Valvulae conivents Present in jejunum Absent

No. of loops Many Few
Distribution of loops Central Peripheral
Haustrations Absent Present
Diameter 3-5 cm 5cm+
Radius of curvature small large
Solid faeces absent Present

N.B In dilated small bowel, which is almost completely filled with fluid, small bubbles
of gas may be trapped in rows between valvulae coniventes on horizontal ray film. This is
known as String of beads sign this sign if present, is virtually diagnostic of small bowel
obst bec it doesnt occur normally (multiple fluid levels alone not diagnostic).

Radiology: Intestinal obstruction Dilated proximal fluid levels, collapse distal.

Fluid levels, are produced by intestinal obstruction :
I. Site of obstruction :
I. Small intestine: short & central fluid levels.
Distended jejeunal loops circ. lines (valvulae coniventes distended) ileal
loops smooth mucosa.
2. L.I : large & periph. fluid levels. Distended colon haustrations.
II. Patency of ileal valve :
1. Shut : levels confined to colon, cecum markedly distended & may perforate
+ No dist. of SI. type IA. or dist. of SI type IB.
2. Incompetent : levels in small intestine only type II.
III. Complete or incomplete obstruction :
1. Complete : No gas beyond it ( plain film changes begin after 3-5hrs &
 G.I.T. 100
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completed or 12hrs).
2. Incomplete : some gas beyond it.
IV. High intestinal (No gas) obstruction :
- Obstruction of 1st foot of small intestine vomiting of contents No fluid
levels nor gas distended loops.
- May occur after gastroenterostomy due to herniation of small intestine loop
into lesser sac & strangulation.

DD of fluid levels :
1. Uraemia
2. Hypokalemia.
3. Retained enema (multiple & small levels, no distension).
4. Jejunal diverticulae (short levels, no distension) and intestinal obstruction,
abscess, sentinal loop, hernia or achalasia.

Child: - Hypertrophic pyloric stenosis

- Volvulus.
- Intusception
- Annular pancreas
- Choledocal cyst
Strangulation:
1. Hernia
2. Valvolus
3. MVD (true)
4. Intussuscesption.
5. Adhesion

A. Neonatal obstruction
After birth, air few mins stomach then.few hrs.. small intestine .6 hrs rectum.
- Neonatal obstruction causes delay in gas transit through gut, its absence beyond
obstruction & distension with fluid levels proximally.
Causes of intestinal obstruction in neonates:
1. Duodenal (most common)
a. Stenosis atesia.
b. Annular pancreas.
c. Congenital fibrous band (of Ladd)
d. Congenital web.
e. Choledochal cyst.
2. Jejunal:
a. Atesia.
b. Malarotation and volvulus.
 G.I.T. 101
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3. Ileal:
a. Meconium ileus.
b. Atresia.
c. Inguinal hernia.
d. Paralytic ileus.
e. Intesseception.
4. Colonic:
a. Hirschsprung disease.
b. Imperforate anus.
c. Atresia.
5. Miscelleneous:
Necrotizing enterocolitis of infancy.

Causes :
1. Duodenal stenosis & atresia & (annular pancreas):
Erect 2 fluid, levels distended duodenum & stomach (double bubble sign).
Supine distended stomach & duodenum (band of Ladd)
2. Malrotation of bowel : volvolus neonatorum (obstructive peritoneal bands) plain
distension & fluid levels in small intestine.
Ba enema position of caecum.
3. Meconium, ileus : SI obstruc. by a plug of insipissated meconium in terminal ileum.
Distended SI loops but (no fluid levels (viscid meconium).
Speckled appearance of meconium throughout colon (bubbly soap)
Therapeutic water sol. c.m. enema due to its hyper osmolarity draws water from
the body helping to soften the meconium relieving the obstruction (Complications
such as dehydration and mucosal necrosis must be considered).

B. Necrotising enterocolitis of infancy (NEC)

Bowel anoxia due to maternal infection or birth trauma.
- Occurs in premature or with Hirshsprung disease.
- Usually affects terminal ileum, caecum & Rt. colon.
Radiological features :
1. Gas in gut wall (linear or cystic).
2. Gas in portal v. within liver (not a grave sign us adults).
3. Pneumo peritoneum if perforation occurs.
4. Ba enema reveals stricture or aganglionosis that developed after 3-4 wks.

C. Gall stone ileus:

 G.I.T. 102
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Mech. obstruction of terminal ileum by cholesterol stone after eroding GB & adjacent
gut. History is very helpful reaching diagnosis.
Radiological features: 1. Incomplete low SI obstruction
2. Air in GB & large bile ducts (branching pattern).
3. Stone seldom seen (abnormal location + change position).

D-Intussusception:
Commoner in young male children (adeno virus ?)
Radiological features :
Plain : 1. Small bowel obstruction (incomplete)
2. Rounded soft tissue mass surrounded by a cresecent of gas
3. Absent gas & faeces from Rt. iliac fossa (empty quarter sign.)
Ba obstruction & coiled spring appearance

E. Closed loop obstruction & strangulation

2 limbs of SI loop pass through a narrow opening e.g. hernial sac to be mechanically
obstructed follower by ischemia, necrosis, perforation & peritonitis.
Radiological features :
1. SI obstruction
2. Single distended loop with fluid level, some distance away from other distended
loops.
f. Obstuction due to metastasis & spread of malignancy:
1. Metastasis on serosa of bowel wall produce smooth filling defects with smooth .:
stretched intact mucosa & angulated, fixed, slightly distended intestinal loops
2. Colon may be involved by direct spread from cancer ovary or uterus subacute
obstruction.
3. 1ry TR

G. Obstruction due to parasites :

Ascaris worms caput medusa appear. (gas streaks between coiled worm masses).

V. Volvulus
- Torsion of part of the gut (inverted U-shaped gas-filled loop devoid of haustrae
(ahaustral), prox. obstruction , distal collapse & impaired bl. supply of twisted part.
PDF: long mesentry, ruddiment sigmoid, megacolon, feacal stasis.

Acute volvulus of SI (common) ;

 G.I.T. 103
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May be associated with congenital malrotation.

Prox. obstruction & oedematous loops (may perforate).
Acute volvulus of sigmoid colon (common)
Often occurs in mentally defective elderly.
Gross sigmoid distension & oedema (may perforate).
Rest of colon shows moderate distension.
Ba enema (rectum fills normally but ends at a sickle-shaped point (cobra head (bird
of prey) , beak like obstruction, streaks of ba bet muc. folds.

Acute volvulus of caecum :

Occurs betn. 20-40 yrs.
Low level SI obstruction occurs early caecum is on Lt of mid line, distended &
oedematous (may perforate).
Distal colon is collapsed.

Acute volvolus of stomach (organo axial or mesenterico-axial)

Oesophagus usually obstructed at cardia
Left diaphragm usually high.
Ba meal oesophageal for pyloric obstruction st .....

DD: Cascade (cup & spill) st. in lat. view the dep. part of fundus (corp) is post. and
when the Ba level rise, it spills along lesser curve & post wall + Ext. adh. + Press
from outside.
Identification of the loop in sigmoid volvulus:
1. A haustral margin.
2. Left flank overlap sign.
3. Liver overlap sign.
4. Apex above ???
5. Apex under left hemidiaphragm.
6. Inferior convergence on the left.
7. Air fluid ratio > 2 : 1.

VI. Vascular lesions (from the causes of acute abdomen)

A. Superior mesenteric a. obstruction :
Complete obstruction of main stem is rare gangrene of all SI shown as gas less
abdomen in early stages.
Obstruction of one of its branches local ileus.
1. Plain distension & fluid levels of some loop
 G.I.T. 104
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2. Barium , Thick wall rigid thick folds oedema, thumb printing (submucosal
oedema & haemorrhage) decreased segmental activity.
3. Selective arteriography obstruction
B. Rupture aneurysm & dissecting aneurysm :
- Usually in elderly male.
Radiological features :
1. Plain soft tissue shadow (aneurysm or hematoma) obscuring ms. lines on
post. abd. wall. Calcified plaques displaced in aneurysmal wall (lat. view).
2. Angiography double lumen.
3. U/S.

Causes of diarrhoea
I. Acute diarrhea :
1. Diabetic indiscreation.
2. Food poisoning.
3. Infections e.g. bacillary dysentrey.
4. Exacerbation of chr. diarrhea.
II. Chronic diarrhea :
1. After operations such as gastrectomy & vagotomy.
2. SI lesions Crohn's disease. Malasorption synd.
3. Colon lesions calc., diverticultis, ulcerative colitis, amoebiasis.
4. Thyrotoxcosis.
5. Anxiety neurosis.

Causes of constipation :
I. Organic obst :
1. Cancer colon.
2. Diverticular disease stricture.
II. Adynamic bowel :
1. Hirschsprungs disease.
2. Spinal cord lesion = paralytic.
3. Senility.
4. Myxoedema .
III. Painful anal conditions. piles & fissures.
IV. habit and diet: dyschasia, dehydration, and lack of bulk in diet.
V. Drugs morphine & aspirin.

Swellings in epigastrium
Stomach : Cancer stomach.
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Lt lobe of liver :
1. Amoebic abscess .
2. Hydatid cyst.
3. Cirrhotic liver.
4. Liver tumors.
Transverse colon : Carc.
Pancreas : 1. Cancer head.
2. Pseudo pancreatic cyst.
Enlarged para aortic Lns :
1. Lymphosarcoma.
2. Metastases.
Aneurysm of abd. aorta .
Swellings of ant. abd. wall.

Swellings in Rt hypochondrium
Rt. lobe of liver :
1. Amoebic hepatitis & amoebic liver abscess.
2. malig. tumours.
3. Enlarged liver : Bilhariziasis, leukemia ...
4. Hydatid cyst.
Swellings in GB :
1. Mucocele & pyocele.
2. Carc.
Swellings in Rt. kid encroacting on hypochondrium :
1. Hydro nephrosis & pyonephrosis.
2. Hypernephroma.
3. Wilms tumours.
4. Polycstic kid.
Retro peritoneal sarcoma :
1. Fibro-sarcoma.
2. Lympho-sarcoma.
Swellings of ant. abd. wall.

Abd. calcifications ass. with acute abdomen :

1. Gall stones, acute cholecystitis, acute pancreatitis, biliary colic, empyema of
G.B. , G. stone ileus,
2. Pancreatic calculi acute, ch. pancreatitis.
3. Appendicular calculus, appendicitis.
4. Calculus in mechel's diverticulum perforation inflam.
5. Ureteric calculus ureteric colic.
 G.I.T. 106
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6. Calcified G.B wall cholecystitis.

7. Limy bile cholecystitis
8. Calcified aneurysms (aortic, splenic rupture, hepatic.
9. Teeth or bone in ovarian dermoid torsion.

Causes of pseudopneumoperitoneum :
1. Chialiditis syndrome (falciform colon).
2. Subdiaphragmatic fat.
3. Omental fat.
4. Subphrenic abscess.
5. Curvilinear pulmonary collapse.
6. Distended viscus.

Causes of pneumoperitoneum :
1. Perforation :
a. peptic ulcer
b. inflammation, diverticulitis, appendicitis.
c. Infarction.
d. Malig. neoplasm.
e. Obstruction
2. Peritoneal dialysis, post-operative, tubal insufflation, silent viscus perforation (e.g.
steroid therapy.
3. Pneumediastinum.
4. Pneumothorax.
5. Idiopathic.
6. Introduction per vagina.

Chest conditions mimic an acute abd :

1. Lower lobe pneumonia.
2. Myocardial infarction.
3. Pulmonary infarction.
4. CHF.
5. Pericarditis.
6. Dissecting thoraxic aorta aneurysm.

Causes of small bowel fluid levels: Normal <2 fluid levels

1. Small bowel obstruction
 G.I.T. 107
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2. Large bowel obstruction

3. Paralytic ileus.
4. Gastroenteritis
5. Mesenteric thrombosis.
6. Jejunal diverticulatis.
7. Uremia.
8. Hypokalemie
9. Cleaning enemas
10. CHF, serosal, metast .

Causes of gas less abdomen :

Adult Child
1. High obstruction 1. High obst :
2. Asites a. A. Duod. Atresia
3. Acute pancreatitis due to. Excess b. B. Annular pancreas.
vomiting c. C. Hypertrophic pyloric
4. Large abd mass. stenosis
5. Fluid filled bowel: closed loop obst,d. D. Choledoctal cyst.
early mesenteric infarction. e. E. Volvolus.
6. Normal 2. Vomiting
3. Fluid filled bowel.
4. Congenital diaph. hernia
5. Oesoph atresia.
Abdominal mass in a neonate In child
Renal : Renal :
i. Hydronephrosis i. Wilms
ii. Multicystic kid. ii. Hydronephrosis
iii. Infantile polycystic kid iii. Cysts (multiple cystic
iv. Renal ectopia disease)
v. Renal v. thrombosis iv. Renal vein thrombosis.
vi. Wilm's tumour v. Lymphoma.

Genital :
i. Hydrometrocolpols Genital : ovarian teratoma (dermoid)
ii. Ovarian cyst Hematocolpos
GIT : duplication (comment in
Mesenteric cyst GIT : appendicular abscess, duplicat,
Retro-peritoneal: adrenal haemorrhage teratoma, lymphoma, pancreatic
pseudocyst, mesenteric cyst.
Neuroblastoma.
Neuroblastoma, ganglioneuroma,
Teratoma adrenal he, adrenal cortical t.
Hepatospleno-biliary: hepato blastoma Teratoma.
 G.I.T. 108
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Hepatic cyst
Splenic haematoma Haemangioma
Choledocal cyst. Hepatoblastoma
Choledochal cyst.

Causes of intest. obstruction in neonates:

1. Duodenal most common 2. Jeujenal
- Stenosis atresia - atresia.
- Annular pancreas - Malrotaroom + volvulus
- Anular pancreas
- Congenital fibrotic bands (of Lodd).
- Congenital web., choledocal cyst
3. Ileal 4. Colonic
- Meconum ileaus - Hirschsprungs
- Atresia - Imperforate arus.
- Ingurnal hernia - Atrasia.
- Intussuseption.

Causes of pseudo intest obstruction :

1. Idiopathic (do Ba enema to exclude cause)
2. DM.
3. Collagen dis.
4. Amyloid and Neurological.
Duodenal ileus :
1. Superior mesenteric synd.: sup. mes. passes infront of 5rd part of duodenum
(instead of post). pt. relieved an lying prone.
2. Acute pancreatitis.
Hour-glass stomach :
1. Normal.
2. Compression from outside.
3. Healing of gustric ulcer.

Adrenal Gland :
Anatomy :
- Are composed of a cortex and medulla. Medulla arise from sympathetic nervous sysm.
- Hormons secreted by adrenal cortex :
- Glucocortiocids hydrocuortizone.
- Mineralocorticoids aldosterone.
 G.I.T. 109
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- Androgens.
- Hormones secreted by medulla :
Adrenaline
Noradrenaline
- Arterial supply : Inf. adra a from renal artery
Middle adr a from aorta
Superior adr a from inferior phrenic a.
- Venous drainage : Left adr vein to renal vein.
Right adr vein to I.V.C.

Imaging investigations : CT is first choice in adrenal tumours :

1. Plain X ray and tomography.
2. I.V.U and high dose IVU.
3. Arteriongraphy and phlebography.
4. Vena caval and adrenal vein blood sampling (not imaging).
5. Isotope scanning.
6. U/S. : most Tu law on T1 - high on T2
7. CT & MRI : low signal gland < against adjacent high signal fat.
8. Needle biopsy (Not imaging but guided by it).

Abdominal masses in childhood

1. Retro peritoneal renal (hydronephorosis, cystic dis, Wilms, renal v.th, lymphama, supra renal
(Neuroblastoma, ganglioneure, adrenal cortical, adrenal haemorrhage).
2. Hepatobiliary : hepatoblastoma, hemangiona, choledochal cyst.
3. Gastro intestinal masses:
Duplication cysts (commonest)
teratoma
lymphoma
panc. pseudo cyst.
mesentcric cyst.
4. Pelvic masses
ovarian dermoid
Haematocolpus.
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DD. Adrenal Masses

A. Neoplasm :
1. Cortical (carcinoma and adenoma).
2. Medullary (neuroblatoma, pheochromocytoma, ganglioneuroma).
3. Stromal (lipoma).
4. Metastasis esp. bronchogenic carcinoma.
B. Other mass lesion :
1. Granuloma : TB, histoplasmosis.
2. Bilateral hyperplasia.
3. Cysts.
4. Haematoma, esp, children.
Differential diagnosis :
1. Renal cysts or tumours.
2. Spleen and acessory spleen on left side.
3. Pancreatic cyst or tumour.
4. Liver mass.
5. Para-aortic glands.
6. Retroperitoneal tumour.
7. Stomach mass.

Neuroblastoma
(Occur in children (1-4 years)
Presentation : (abdominal mass) (secondary deposits manfiestation).
Origin : Over 1/2 of them arise in the adrenals > 50% neurodectodernal tissue From
sympathetic tissue any where in body (eye, brain, sympathetic chain, UB).
Investigation :
A.Plain:
1. Abdominal mass or pelvic mass (soft tissue shadow).
2. Downward displacement of kid.
3. Calcifcation in > 50% irregular, finally stippled and punctate.
B. IVU :
1. Confirm kidney displacement.
2. Downward dropping of pelvis and calyces.
3. Impression on bladder and ureteric obstruction (pelvic mass).
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C. U/S :
1. A solid supra renal mass with heterogenous echogenecity.
2. Increased echogenicity and aconustic shadowing means (calcification).
3. Characteristically, it encase and surround the great vessels elevation and
displacement of the aorta and IVC.
4. Liver scanning for metastases (hypoechoic).
D. CT :
1. Demonstrate ex\tent of tumour.
2. A lesion of variable density with calcification.
3. Liver and para aortic L.N. for metastases.
4. Detection of deposits elsewhere (bilat + symmetrical in bone).
E. Angiography :
1. Vascular tumour.
2. Sometimes poorly vascular.
E. Isotope MiBG
G. MRI Iso, hypo, hyper on T1, high on T2.

DD :
Wilms tumour Neuroblastoma
Calcification Less common + more common
Angiography more vascular - less vascular !!
DD : of metastases wof neuroblastoma with (osteomyclits, ewings sarcoma, luekemia).

Ganglioneuroma :
A mature form of neurogenic tumour, common in children may in adult .
Appearance :
1. Paraspinal mass and calcification diagnostic.
2. Occasionally, it invade the spinal canal an extraspinal as well as intrespinal
component, causing neurological symptoms either from :
- Cord compression.
- Involvement of cauda equina
DD : Dumb-bell neurofibroma ?? (rare cases)
- Neuroblastioma 50% adrenal , symp tissue elsewhers (eye, brain).
- Gangloneuroma 10% adrenal, parasymp, (esp. para spinal).

Pheochromocytoma
The commonest adrenal tumour :
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Clinical picture : Attacks of paroxysmal hypertension accompanied by headache,

sweating, palpitation and turmor, 50% of adult patients present with sustained
hypertension.
Site : - 90% of tumours arise in adrenals.
- 10% ectopic = extra - adrenal sites .
- Found anywhere in sympathetic system from neck to pelvis e.g.
a. At hilum of kidney or hbelow kidney.
b. medial to IVC.
c. at the aortic bifurcation (organs of Zuckerkandl)
d. Bladder wall :
- Attacks of hypertension brought on by micturation.
e. Thoracic tumours para-vertebral or in mediastinum.
- 10% of cases are familial, bilateral, multiple, and extra adrenal,
children, malignant.
- 5% of cases are associated with neurofibromatosis.
- Association with carcinoma of thyroid and hyperparathyroidism =
multiple endocrine neoplasia (MEN type 2).
Imaging investications :
Plain & I.V.U. :
- May leveal a large mass above kidney.
- +/- renal displacement.
- Calcification is rare.

Ultrasound :
Size : rarely less than > 3cm.
The majority are solid but internal haemorrhage cystic changes.
CT :
- An excellent method for diagnosis of pheochromocytoma.
- Ectopic tumours are easily identified :
- Normal adrenal glands with biochemical evidence of pheochromocytoma = high
indication of ectopic tumours.
Angiography : (mid stream aortography), selective adrenal 9difficult) and selective renal
angiography (best). They will show large vascular tumour.
Scintigraphy :
- Demonstrate functioning pheochromocytomas with a high degree of accuracy.
- False + ve or -ve results (disadvantage).
- Can cover all possible sites of ectopin (instead of venous
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Venous sampling :
- Sample should be obtained from internal jugular and innominate veins on
both sides.
- From SVC, high IVC and both renal veins.
- Low IVC and both iliac veins.
Method : Percutaneous catheterization of femoral vein.
Value: being abnormally high on tumour side & normal on other side.
MRI
Needle biopsy U/S or CT guided.
Retroperitoneal air insufflation (absolete).

Malignant pheochromocytoma
- 10% of pheoch.
- Metastases to lymph nodes, bone, liver and chest.
- Invasion of the peri-renal fascia.

Adrenal cortical adenoma

- Usually small and non functioning.
- Functioning adenoma
Cushings
Conns syndrome venous sampling of aldosterone + isotope

Adrenal cortical carcinoma

Age > 40 years.
- present either with abdominal mass or metastasis.
- Like adenoma may be non functioning of functioning (1.2.3)
Imaging :
1. Plain & I.V.U: large mass e downward displacement of kid, & calcification in 30%.
2. Ultrasonography : Solid large adrenal mass in 40 years person.
3. CT: - Shows spread in adjacent structures.
- Involvement of lymph nodes and liver.
- The opposite adrenal become involved in 10%.
4. Isotope.

Cushings syndrome
Etiology :
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A. Due to excess ACTH production :

1. Pit, dependent pituitary microadenoma, 80% basophil aderoma.
2. Excess ectopic ACTC eg malig tumours (paromalig synd.)
C.T. pituitary, adrenal.
Nelson $: patient e adrenalectomy may develop large adenomas that enlarge sella.

Q1: Gastro-oesophageal junction lesions:

Q2: Discuss & illustrate role of radiology and imaging modalities in imaging.
Q3:Discuss the role of radiology in diagnosis of neonatal intestinal
obstruction.
- Hiatus hernia
- Small bowel lymphoma.
- Hepatic hemangioma.
- Colonic polypi.
- U/S in hepatic focal lesions.
Q4: Discuss diaphragmatic hernia.
- Pyloric stenosis.
- Mucoviscidosis.
- Hydatid liver disease.
Q5: Ileocecal junction lesions:
Q6: Discuss and illustrate the role of imaging modatlities?? radiological and
imaging modalities in diagnosis of neonatal abdominal masses.
- Cholangiocarcinoma.
- Chronic pancreatitis.
- Ischemic colonic stricture.
How to comment ?!!
Oesophagus :
Caurse, caliber, outlinc, mucosa, Ba. passage, peristalsis.
Stomach :
Shape & tone, size, site, arround of fasting gastric juice, evacuation time (intial), casal
pattern, filling defects, ulcers.
Duodunal carp.
Shape, outline, mucosa, ulcers, bulbar Ba crater or ring, healing radiating folds
persist - preudodivers, deh post. bulbar (pars superior & 2nd part).
Small bowel :
caliber, outline (ineeth or irregular), mucosa, space teb, loops.
Colon :
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BA passage, (resistence or pain) , length, caliber, haustinbosis, duerticulas, ulcors,

filling defects, mucosa, reticrectal space cair bilhreozioun lymphoma
endometiosis, (space) chordoma (baric) (rectum)
G.B. :
Plain : calculer o. carciofication.
Oral cholecysteginphy.
C.T. :
Infection.
hamartoma.
Tumours (minigionia & glioma, carrnio, pharyngicma)
Angio :
Aorta 2 brs., carclkid vessels, peripheral arteries, veins incompetence 21 or vaicases
veins D.O.T.
Report on : course, pathological vessels (glicon). blush (capill, phase in menogicma),
abnormal a-v channels (malformations), displacement (sub dural hematoma).
Fluid levels :
- obstruction
- abscess.
- divertulae.
- sentinal loop : dilated atronic ileum + fluid peol
- Hernia or achalasis.
Ascites central location of intestinal loops.
DD : Anemia, hypokalemia, retained enema, jejunal diverticulae.
portion.