(1) gastro

X-RAYSX-RAYS
By
Prof Dr IBRAHIM DAWOUD
Prof of Surgery
Mansoura University

PREFACE TO THEPREFACE TO THE
SECOND EDITIONSECOND EDITION

This type of work has been prepared to meet the compelling
needs of the under and postgraduate medical students.
To promote its accessibility this work is presented in 2 CDs,
each one contains 6 chapters.
The 1st
one includes (Barium Series in GIT–Portal Venography
– Plain X-ray Abdomen and Biliary).
The 2nd
one includes ( Vascular Surgery – Chest – Urology –
Varieties and Orthopedic).
In fact no effort has been spared in trying to eliminate the
difficulties encountered by medical students during their
studies and training surgery.
Waiting hardly for your comments you can contact me at:
 E-mail dawoud2004@hotmail.com
 Tel 0123471715 -- 0502252882
 Clinic:
‫الثانى‬ ‫الدور‬ - ‫الوقاف‬ ‫عمارة‬ – ‫الطميهى‬ ‫ميدان‬ – ‫المنصورة‬

How to read
 Plain X-ray
 Plain x-ray (describe the region).
 View (PA, lat, oblique).
 Position (erect, supine).
 Quality.
 Exposure.
 Chest: Centralization, Bony frame work. Costophrenic angle,
Soft tissue shadow.
 Abdomen: well prepared or not, radio-opaque shadow, gas
shadow.
 Bone: Fracture, tumor, inflammation.
 Soft tissue mammogram.

How to read
 X-RAY with dye
G.I.T.
 Upper GIT: Barium Swallow.
 Stomach: Barium meal, or Gastrographin meal.
 Duodenum: Hypotonic duodenography.
 Small intestine: Barium Follow through.
 Large intestine: Barium Enema.
 Sinus: Sinogram.
 Fistula: Fistulography.

How to read
 X-RAY with dye
Portal tract
 Percutaneous trans-splenic portography.
 Percutaneous transhepatic portography.
 Transfemoral splenic artery angiography.
 Transfemoral SMA angiography.
 Transfemoral IMA angiography.
 CT.
 US.

How to read
 X-RAY with dye
Biliary
 Plain X-ray Rt hypochondrium.
 Oral cholecystography.
 I.V. Cholangiography.
 PTC (Percutaneous Transhepatic Cholangiography)
 ERCP.
 MRCP.
 T-Tube Cholangiography.

How to read
 X-RAY with dye
Urology
 UTP (Urinary Tract Plain).
 IVU (Intravenous Urography).
 MRU.
 Urethrography.
 Ascending Cystography.
 CT scan.
 US.

How to read
 X-RAY with dye
Vascular
 Plain X-Ray.
 Venography (Phlebography)
 Arteriography.
 DVI ( Digital Venous Image).
 DSA ( Digital Subtraction Angiography).
 CT scan.
 Duplex US.
 MRA.

 Barium Swallow showing the esophagus in serial
films.
 It revealed mild dilatation of the esophagus
with multiple persistent filling defects in the lower
third of the esophagus and/or longitudinal furrows.
 Diagnosis most probably
Esophageal Varices.
BARIUM SWALOW
How to read

 Etiology of esophageal varices.
 Anatomy of esophageal varices.
 Complications.
 What are the other Porto systemic collaterals?
- Hepatopetal collaterals - Hepatofugal collaterals
 Why EV is considered the most serious problem in
Porto systemic collaterals.
 Management:
(1) Clinical picture.
(2) Other investigations should be done.
(3) Treatment: - silent varices.
- Bleeding varices ---- Acute attack.
---- In between attacks.
Questions

 The left gastric, short gastric, and terminal branches of
the splenic vein provide the main venous drainage.
 They are arranged into 4 layers with a series of
perforating veins.
 In Portal Hypertension they are all dilated with
reversed or bidirectional blood flow.
 Dilated intraepithelial and sub epithelial V may lead to
varices on varices----» “Cherry red spot” or “Red wale”.
 Grades of varices.
Anatomy of E.V.

SM
MP
Esophagus
XX
◄◄◄◄◄ Bl flow
M
liver
►►►►►--------------------------------------◄◄◄----------------
Esophagus
Bl flowBl flow
liver
--------------
--------------
Intraepith veins
Subepith veins
Varices on varices
VARICES
VARICES
M

 It is present in the lower end of the chest, the bleeding
is severe and may be fatal due to.
1- Negative intrathoracic pressure.
2- Shearing movement of the diaphragm.
3- Increased acidity and reflux.
4- Present in inaccessible area.
5- Chronic liver CF with coagulation defect.
 The amount and time of bleeding are not expected.
 The blood is digested by Hcl of the stomach, and
fermented by E coli with liberation of huge amount of
ammonia  liver – more liver failure
 Brain -- Ammoniacal encephalopathy.
Why EV is considered the most
serious problem

How to read
 Barium swallow
 It revealed that the barium-filled diverticulum
extends below the level of the cricopharyngeus
posterior to the proximal cervical esophagus.
 A large diverticulum may protrude to the left or
compress the cervical esophagus.
Zenker's diverticulum
(posterior hypopharyngeal diverticulum)

 Zenker's diverticulum (posterior hypopharyngeal
diverticulum) is an acquired mucosal herniation
through an area of anatomic weakness in the region
of the cricopharyngeus muscle (Killian's dehiscence).
 This area of anatomic weakness has been variably
described as between the thyropharyngeus and
cricopharyngeus muscles or between the oblique and
horizontal fibers of the cricopharyngeus.
 Patients complain of coughing following swallowing,
food regurgitation, or halitosis. Many patients with
have an associated hiatal hernia and/or
gastroesophageal reflux.

 Rarely, these diverticula are complicated by ulceration
or malignancy.
 During swallowing, a Zenker's diverticulum appears
as a posterior bulging of the distal pharyngeal wall
above an anteriorly protruding cricopharyngeus.
 At rest, the barium-filled diverticulum extends below
the level of the cricopharyngeus posterior to the
proximal cervical esophagus.
 A large diverticulum may protrude to the left or
compress the cervical esophagus.
 Treatment: ?

How to read
 Barium swallow showing dilatation of the esophageal
body.
 With short segment stricture.
 A “bird-beak” like tapering of the esophagus at the GE
junction. OR
 A Sigmoid “ Mega esophagus”
 Absence of air-bubble in the fundus of the stomach.
 Diagnosis most probably Achalasia of the esophagus.

Questions
Describe the pathology.Describe the pathology.
-Absence of peristaltic contractions within the
esophageal body & incomplete relaxation of the HPZ.
-The cause of neuropathy and the site of the primary
lesion still unknown.
- It is due to damage to the parasympath. Innervations
of the esophagus. Also impairment of the non-
adrenergic non-cholinergic N.F. of the LES.
-Anatomical lesions in the brain stem “ reduction in No
and abnormalities of the cells of the DMN of the vagus”.
- Also in Auerbach´s intramural plexus.
- Complications: *Inhalation pneumonia *Toxic RH. A.
*Starvation *Perforation *Diverticulae *Carcinoma

Management
 Clinical picture.
 Other Investigations:
* Chest X-ay. * Endoscopy and biopsy.
* Manometry. * Radionuclide esoph transit study.
 Treatment:
- Medical– long acting nitrites or Ca channel blockers.
- Frequent dilatation.
- Surgery:
* Heller's esophago-cardiomyotomy.
* Esophagogastrectomy.

 Barium swallow shows irregular areas of
narrowing and dilatation ----- “Shish kebab”
“corkscrew” “rosary bead” esophagus.
 The esophageal muscle is hypertrophied, but
histologically normal.
 Treatment:
- Medical– long acting nitrites or Ca channel
blockers.
- Frequent dilatation.
- Long esophageal myotomies.
What are other types of myotomies in GIT?
Diffuse esophageal spasm

 Barium swallow shows mild dilatation
of the esophagus with irregular stenotic
lesion in the lower end of the
esophagus “moth eaten appearance”
 With shouldering.
 The stenotic segment is long giving a
“rat-tail” appearance.
 Diagnosis most probably
Cancer esophagus
Cancer esophagus

Questions
 How to DD between Achalasia and Cancer esophagus?.
 Pathology of Cancer esophagus .
 What is “ Barrett's esophagus”
 Diagnosis of cancer esophagus.
 Treatment.

ACHALASIA CANCER ESOPHAGUS
Middle aged female Old aged male
Long history of dysphagia Short history
Dysphagia more to fluids Dysphagia more to solids
Dysphagia is intermittent Dysphagia is progressive
No Gas bubble in stomach Presence of Gas bubble
Barium- moderate to huge
dilatation, with smooth short
segment stricture
Barium- mild dilatation, with
irregular long segment
stricture, and shouldering
Endoscopy as you enter a
cave
difficult to pass the stricture
Pathology: absent or
degenerated N plexus
Pathology: Malignant cells

Pathology
 N/E: Polypoid (fungating) mass- Stenotic – Ulcerative.
 M/E: Sq CC- Adenocarcinoma- Sarcoma .
 TNM:
-Tx: can not be assessed. * Nx: can not be assessed.
-T0: no evidence of 1ry . * No: no nodal involvement.
-Tis: In situ. * N1: Regional LN involved.
-T1: Submucosa.
-T2: Muscularis propria. * Mx: can not be assessed
-T3: Adventitia. * M0: no evidence
-T4: Adjacent structures * M1: Presence of metasta
 Spread

Barrett's Esophagus
 Columnar cell metaplasia >3cm in the distal tub esoph
 3 types ( intestinal- junctional- fundic) .
 It is common in pts with GERD and peptic stricture of
the esophagus.
 I t is considered as a premalignant.
 Treatment. Regular follow up by endoscopy and
histopathology.
 Low grade dysplasia: continue medical ttt and follow
up
 High grade dysplasia: treated as carcinoma in situ.

Treatment
Cervical
esophagus
Sup
mediastinum
Middle and
lower third
Cardia
Pharyngolar
yngoesopha
gectomy.
Split sternum
esophagectomy
Lewis-tanner
operation
Transhiatal
esophagectomy
Free jejunal
transfer
Three phase
esophagectomy
Transhiatal
esophagectomy
Esophagogastr
ectomy
Three phase
esophagectomy
Abdominal
Gastrectomy
Bypass Kischner
gastric bypass
Colon bypass Jejunum
bypass

Normal
Barium in Trendlenberg position

*Barium meal in Trendlenberg position.
*Displacement of the cardio-esophageal
junction above the esophageal hiatus.
*Part oh the stomach is present in the chest.
*Reflux of barium into the esophagus.
• Diagnosis:
Type I ( Axial – Sliding ) Hiatal Hernia
With Reflux esophagitis
( GERD)
(Gastroesophageal Reflux Disease)

Questions
 Types of H.H.
 Pathology of Reflux Esophagitis.
 Complications of GERD.
 What is “ Barrett's esophagus”
 Diagnosis.
 Treatment.

Pathology
The normal PH of the lower esophagus is 5 - 6.5.
 With GERD PH falls below 4 with direct chemical
damage to epithelium.
 Also pepsin, trypsin, bile salts, and lysolecithin.
 Inflammatory cells appear in the epithelium.
 The total epithelial thickness is reduced.
 Ulceration – which is healed by fibrosis
or -- Columnar cell metaplasia
 Complications: - Chronic blood loss
- Deep ulceration with periesophagitis
- Formation of stricture and web
- Columnar cell changes

Clinical Picture
Symptom Grade Description
Heartburn
None 0 No heart burn
Minimal 1 Occasional episode
Moderate 2 Reason for medical ttt
Severe 3 Interfere with activity
Regurgitation
None 0 No regurgitation
Moderate 2 On position or straining
Severe 3 Asp pneum., Noct cough
Dysphagia
None 0 No dysphagia
Moderate 2 Require fluid to clear
Severe 3 Require medical ttt

Investigations
Category Test Indications
Radiological
Chest X-ray Aspiration pneumonia, perforation
Barium Dysphagia, perforation, motility
disorder
Cine radiology Motility disorder, reflux disease
CT Staging of malignant disease
US External Diaphragmatic screening
Endoscopic Staging of malignant disease
Isotope Liquid or solid T³³ for esoph transit and reflux
Endoscopy All esophageal pathology
Physiological
Manometry Motility disorder and GERD
Bernstein test Esophageal sensitivity to acid
Acid reflux test Reflux disease
24 hr PH monit Reflux disease

TREATMENT
Uncomplicated Disease
 Wt reduction and stop smoking and alcohol.
 Avoid tight closes.
 Frequent small meals.
 The last meal is 3 hrs before sleep.
 Antacids 1 hr after meal and at bed time.
 The pt is advised to sleep on several pillows with
elevation of foot of the bed.
Indications of Surgery:
- Failure of medical ttt
- Presence of mechanically defective LES
- Development of complications
- Pts with neutral or alkaline reflux

TREATMENT
* Nissen Fundoplication:
 Laparoscopic approach.
 Transabdominal.
 Transthoracic.
* Belsey Mark IV Partial Fundoplication:
* Hill Gastropexy
* Angle chick Prosthesis
Complicated Cases
- Acquired short esophagus--- Collis Gastroplasty
- Benign stricture--- Fundic patch
- Barrett esophagus--- follow up
---- as in situ carcinoma

CORROSIVE ESOPHAGEAL STRICTURE

*Barium meal of an infant.
*Dilatation of the stomach.
*Double-track appearance( enfolding of the mucosa
into the pyloric canal.
*String sign. (convex narrow elongated pyloric
canal.
*Mushroom effect of the pyloric mass indenting the
duodenal cap.
*Diagnosis most probably
“Infantile Hypertrophic Pyloric Stenosis”

Questions
 Pathology (incidence, Etiology. NE, MP, Complications).
 D.D.
1- Pylorospasm
2-Gastroenteritis
3- GERD
4- Increased ICT
5-Infection (pneumonia, meningitis)
 Treatment.
1- Medical
2- Surgical: Ramstedt´s pyloromytomy

Types
 Hernia through foramen of Bochdalek.
(Persistence of the pleuroperitoneal canal)
 Hernia through foramen of Morgagni or Magendie.
(Parasternal through a triangular defect lateral to the
sternum)
 Herniation through the central tendon.
 Congenital H.H.
 Congenital short esophagus.
 Eventration of the diaphragm
 Traumatic diaph H

*Barium meal and follow-through.
*Showing pylorus, pylorodudenal junction, duodenal
cap, and 1st
, 2nd
,and 3rd
parts of the duodenum in
serial films.
*Persistent ulcer niche in the 1st
part of the
duodenum.
*The niche appeared as a barium-filled crater at the
upper border of the duodenum.
*Persistent deformity of the duodenal cap.
*in end-on view “Trefoil Deformity”
“Chronic Duodenal Ulcer”

Questions
 How to DD bet Chr gastric ulcers and Chr DU.
 Pathology of DU.
 Clinical picture:
(Quality- Radiation- Rhythmicity- Periodicity).
 Investigations
1- Laboratory.
2- Endoscopy
3- Gastric FT ( FTM – Basal secretion – Maximum sec. )
4- Serum Gastrin
 Treatment.
1- Medical .
2- Surgical.
3- Treatment of complications.

Gastric Ulcer Duodenal Ulcer
Age Older Younger
Sex Equal Male : female 10:1
Bl Gp - ve O
Family H +ve +ve
Constitution Careless Hyperactive
Acidity Normo or Hypo Hyperacididty
Motility Hypomotility Hypermotility
Etiology ▼mucosal
resistance
▲parietal cell mass
▲vagal tone
▼regen power of
G mucosa
Endocrine dysfunction
Liver cirrhosis

Gastric Ulcer Duodenal Ulcer
Pain Soon after eating
Not on lying down
2 hrs after eating
Hunger & night pain
Vomiting Considerable No vomiting
Periodicity Present Well marked
Appetite Afraid to eat Good
Weight Weight loss No loss of weight
Hemorrhage Hematemesis more Melena more

 Medical:
1- Diet:
2- Drugs
{1} Antacids {2} Anticholenergic drugs
{3} Sucralfate {4} Bismuth compounds
{5} H2 receptor blockers {6} Proton-pump inhibitors
3-Mnagement of Acute exacerbations
{1} Hospitalization {2} Ryle tube
{3} Sedation {4} Anticholenergic
{5} H2 receptor blockers {6} Proton-pump inhibitors
Treatment

 Surgical:
{1} Vagotomy with or without drainage
{2} Subtotal Gastrectomy
 Treatment of Complications:
{1} Bleeding
{2} Perforation
[a] acute perforation.
[b] subacute perforation
{3} Pyloric obstruction
{4} Recurrent ulceration:
[a] Incomplete vagotomy [b] Z-E syndrome
[c] Retained gastric antrum [d] Hypercalcemia
[e] Inadequate resection

 Vagotomy:
[a] Trunkal vagotomy------------------- need drainage procedure
[b] Selective vagotomy----------------- need drainage procedure
[c] Super selective----------------------- no
[e] Tailor operation---------------------- no
Drainage:
{1} pyloroplasty
{2} Gastrojejunostomy
{3} Antrectomy
[a] Billroth I------------------ Gastro-duodenostomy
[b] Billroth II ---------------- Gastro jejunostomy
 Subtotal Gastrectomy:
[a] Billroth I-------------- Gastro-duodenostomy
[b] Billroth II ------------ Gastro jejunostomy (side to side)
[c] Polya ---------------- “ “ (end to side )
[d] Hofmeister---------- “ “ (end to side ) with valve

*Barium meal.
*Showing the stomach is mildly dilated with
obstruction of its outlet.
*A large ulcer is present in the lesser curve.
*The ulcer lies inside the wall of the stomach.
*Associated with a notch on the greater curvature .
“Malignant Gastric Ulcer”

Questions
 How to DD radiologically bet benign and malignant
gastric ulcers.
 Pathology.
 Investigations.
 Treatment.
1- Operable.
2- Inoperable

Benign Vs Malignant Ulcer
Benign Ulcer Malignant Ulcer
No Single or Multiple Usually single
Site Ulcer-bearing area Outside ulcer-bearing area
Size Less than 1 inch More than 1 Inch
Shape Regular,rounded,oval Irregular
Edge Sharp Everted (Carmen's Meniscus s)
Base Lies outside the wall
(Ulcer niche)
Lies inside the wall
(Polypoid or ulcerative mass)
Margin Radiating mucosal
folds (fibrosis)
Rigidity of the gastric wall
around ulcer (infiltration)
Ass ulcer notch G C no
duodenal deformity no

TNM Staging
 T1- limited to the mucosa and submucosa
 T2- The muscularis or subserosa.
 T3- Tumor penetrates the serosa.
 T4- Contiguous structures.
 N0- No metastasis.
 N1- Perigastric LN ≤ 3cm of the tumor
 N2- Perigastric LN ≥ 3cm of the tumor including Gastric,
Common hepatic, splenic, and celiac
 Mo- No metastasis
 M1- Distant metastases

*Barium meal.
*Showing the stomach is hugely dilated with
obstruction of its outlet.
“soup-plate” - “Tea-pot” - “Hour-glass” stomach
*The stomach is mostly located in the pelvis.
*A fluid level is present.
*Delayed emptying of the stomach.
*Deformity of the duodenum .
“Gastric outlet obstruction”

 Barium Enema showing the Rectum, sigmoid
colon descending colon, and part of the
transverse colon.
 It revealed abrupt stoppage of dye at the
transverse colon with a filling defect
Giving Claw-shape sign.
Spring-coil sign.
Egg-on-cake sign.
INTUSSUSCEPTION.
BARIUM ENEMA
How to read

 Definition.
Invagination of one loop of the gut into the other
 Pathogenesis
Partial obstruction initiates hyper peristaltic activity of
the proximal segment, so that instead of pushing the
obstructing agent it pushes the wall of the gut itself
invaginating one loop into the other.
 Pathology.
3 layers (entering- returning- ensheathing)
 Types.
5 types *ileo-ileal *ileo-caecal
*ileo-colic *ileo-ileo-caecal
*colo-colic
Questions

 Clinical types.
1- Infantile type (always acute)
2- Adult type ( acute – chronic)
 Other Investigations.
 DD.
Acute entero-colitis - Henoch purpura
Rectal prolapse
 Treatment:
Resuscitation
Ryle tube
Removal of obstruction

colon, and part of the transverse colon.
 It revealed Multiple, smooth, regular, rounded
filling defects localized to the rectum and sigmoid
colon
BILHARZIAL POLYPOSIS
BARIUM ENEMA
How to read

 Pathology.
1- Etiology: Common in Egypt, caused by S Mansoni.
2- Site: Heaviest affection in the sigmoid and rectum.
3- Pathological types
{a} Submucous type.
{b} Diffuse type.
4- Pathogenesis.
5- Complications:
Hge, anemia, rectal prolapse
 Clinical Picture.
 D.D.
 Investigations.
 Treatment.
Questions

colon, descending colon and part of the
transverse colon.
 It revealed Multiple, smooth, regular, rounded
filling defects localized to the rectum and sigmoid
colon
Giving
( Honey-comb appearance)
VILLOUS ADENOMA
BARIUM ENEMA
How to read

 Pathology:
Also called PAPILLARY ADENOMA
1- Age: above 45y
2- Site: rectum and sigmoid
3- N/E: sessile bulky soft mass with smooth or
velvety surface and numerous frond-like
projections.
4- MP: Core of CT covered with a single layer of
columnar epithelium.
5- the tumor is a precursor of papilliferous carcinoma
Questions:

 Clinical picture
 Discharge of blood and mucous from the rectum
 Feeling of incomplete evacuation
 Mucous diarrhea with K loss and Ms weakness
 Diagnosis
 Sigmoidscopy and biopsy
 Treatment
 Low anterior resection for tumors > 7 cm
 Abdominoperineal resection for tumors < 7 cm,
and proved to be malignant.
 Complete local excision for other sites
Questions:

 Barium Enema showing the Rectum, sigmoid colon,
descending colon and part of the transverse colon.
 It revealed Multiple, smooth, regular, rounded filling
defects
With
Large irregular mass at the rectosigmoid with
shouldering and moth-eaten appearance
VILLOUS ADENOMA
with Cancer Rectosigmoid
BARIUM ENEMA
How to read

 TRUE POLYPS:
(1) Juvenile polyps:
 It is a hamartomatous polyp
 It occurs in children, usually single
 In the rectum, never turn malignant
 Spontaneous auto amputation
(2) Villous Adenoma:
(3) Adenomatous polyp:
 The commonest tumor
 The polyps are pedunculated, firm tumors, with
irregular surface, rarely turn malignant.
 Bleeding per rectum, anemia, prolapse.
 Treatment by Endoscopic polypectomy
Types of colonic polyposis

(4) Familial Polyposis:
 It is a hereditary disease transmitted from both sexes
to both sexes.
 Large No of polyps in the colon and rectum before
puberty, that turn malignant before 40 y.
 They may be sessile or pedunculated.
 Pain, diarrhea, tenesmus, blood and mucous in stool.
 Treatment by total or subtotal colectomy, or
abdominoperineal for malignant tumors.
(5) Syndromes.
 Gardner syndrome
 Cronkhite- Canada syndrome.
 FALSE POLYPS:
Hyperplastic epithelium ( Bilharzial – Ulcerative colitis –
at the edge of TB ulcer, and dysenteric ulcer

 Barium Enema showing the Anal canal, Rectum,
Sigmoid colon, Descending colon.
 Marked dilatation of the colon, with the presence of
funnel shaped segment below it, and spastic
collapsed segment extending distally to the anorectal
region.
 Diagnosis:
Most probably HIRCHSPRUNG DISEASE
- The dilated segment --- (Megacolon)
- The funnel segment ---- ( Transition zone)
- The stenosed segment– ( Spastic segment)
How to read

 Pathology:
 Etiology
 N/E:
 MP:
 Complications:
 Investigations: ---- Biopsy
 Treatment:
1. Swenson's
2. Soave's
3. Duhamel´s
4. Lynn´s
Questions

 Barium Enema showing the Anal canal, and
Rectum.
 It revealed abrupt stoppage of dye at the upper
end of the rectum with narrowing, with
characteristic
“Twisted bird's peak”
OR “Ace of Spade” Sign
 DIAGNOSIS
Volvulous of the Sigmoid
How to read

 Plain X-ray abdomen.
 It revealed marked dilatation of the sigmoid colon
occupying the greater part of the abdomen, and
displacing the diaphragm.
Giving the characteristic sign
Omega- shape sign
Diagnosis most probably
Volvulous of the Sigmoid
How to read

 Etiology:
 Chr. Constipation  Abnormal elongation of pelvic
mesocolon.
 Hyperperistaltic activity  twist
 Pathology:
 The upper loop falls in front of the lower loop, and the
twist occurs in Anticlock-wise direction.
 The veins are compressed  congestion.
 Lib. of huge amount of Co2 & N2 severe distention.
 Gangrene, perforation, with fatal peritonitis.
of Acute Intestinal Obstruction
Questions

 Investigations:
 Treatment
 Resuscitation
 Ryle
 Removal of obstruction
{A} Proctoscopic decompression
With the pt in Knee-elbow position
Sigmoidopexy after few days
{B} Immediate laparotomy
(1) Manual Untwist if the loop is viable
( In a CLOCK-WISE direction )
(2) Resection by the Paul Mikulicz method
or Hartmann procedure

 Barium enema showing the rectum, sigmoid
colon, descending colon, transverse colon, and
part of the ascending colon.
 It revealed a large irregular filling defect, with
destruction of the wall (moth-eaten appearance).
 Failure of passage of the dye proximal to the mass
Cancer Ascending Colon
How to read

colon, descending colon, and part of the
transverse colon.
 It revealed an irregular filling defect, with stricture
and shouldering (Apple- core appearance).
 Failure of passage of the dye proximal o the mass
(in the last film)
Cancer Transverse Colon
How to read

descending colon.
 It revealed an irregular stricture at the lower end
of the descending colon (Moth- eaten
appearance).
Cancer Descending Colon
How to read

colon, and part of the descending colon.
 It revealed an irregular filling defect, with stricture
and shouldering (Apple- core appearance).
Cancer Rectosigmoid Colon
How to read

 Pathology
(1) Etiology
(2) Incidence------------------------------------>
(3) N/E:
* Polypoidal (Cauliflower) mass
* Stenotic schirrus
* Malignant ulcer
(4) MP
* Adenocarcinoma * Spheroidal CC * Colloid carcinoma
(5) Spread
* Intramural * Direct * Lymphatic
* Blood * Transperit spread * Local implantation
(6) Complications
* Bleeding * Perforation * Fistula
* Intussusception * Acute Int Obst
Questions

 Investigations
 Treatment
{A} Without Int Obst
Operable
1. Caecum  Rt hemicolectomy
2. Hepatic Flexure  Extended Rt hemicolectomy
3. Transverse colon  Transverse colectomy
4. Descending colon  Lt hemicolectomy
5. Splenic Flexure  Extended Lt Hemicolectomy
6. Sigmoid colon  Pelvic colectomy
Inoperable
1. Palliative resection
2. Palliative Bypass

{B} With Int Obst
Resectable
(1) One Stage operation
* Tumors of the Rt side  Rt hemicolectomy
* Tumors of the Lt side  Lt hemicolectomy, with 1ry
resection anastomosis after on table lavage
(2) Two Stages Operations
* Tumors on the Rt side  Ileotransverse colostomy,
then after 2 weeks  Rt hemicolectomy
* Lt side  Proximal colostomy then 2 w  resection
 Immediate resection with terminal colostomy
(3) Three stages operation
Unresectable
 Ileotransverse anastomosis
 Palliative transverse or pelvic colostomy

descending colon.
 It revealed an irregular stricture at the rectum
(Moth- eaten appearance).
Cancer Rectum
How to read

 Pathology
(1) Etiology
(2) Incidence– upper 1/3 (35%) middle 1/3 (30%) lower 1/3 (35%)
(3) N/E:
* Malignant ulcer (commonest)
* Polypoidal (Cauliflower) mass
* Annular (Stenotic) lesion at the rectosigmoid
(4) MP
* Adenocarcinoma * Spheroidal CC * Colloid carcinoma
(5) Spread
* Intramural * Direct * Lymphatic
* Blood * Transperit spread * Local implantation
(6) Complications
* Bleeding * 2ry piles * Fistula
* Acute or chr int obst * Toxemia and cachexia
Questions

(7) Staging
Duke's classification
(A) The tumor limited to the rectal wall
(B) Extrarectal tissue but no LN
(C) Regional LN involved  {C1} Pararectal LN alone {C2} Central LN
(D) Distant metastases
TNM
T0: no tumor Nx: can not be assessed
Tx: can not be assessed No: not involved
Tis: In situ carcinoma N1: involved
T1: Confined to mucosa
T2: Musculosa or serosa
T3: Adjacent structures with no fistula Mx: not assessed
T4: Fistula with any of the above Mo: no known metastases
T5: Direct extension to other M1: Distant metastases

 Investigations
 Treatment
{A} Without Int Obst
Operable
(1) Radical resection with colostomy
[a] Abdomino-perineal [b] Perineo-abdominal
[c] Combined [d] Abdominal
[e] perineal [f] pelvic exentration
(2) Radical resection without colostomy
[a] Sphincter-saving operation
* For tumors 10 cm above the anus
* Excision with 5 cm safety margin with end to end
anastomosis either manual or by stapler

[b] Rectum-saving operation
1. Early growth situated in the lower 10 cm.
2. Polypoidal or sessile growth, mobile
3. Well differentiated
4. No LN
 Local excision
 Electrocoagulation
 Endocavitary contact irradiation
Inoperable
 Palliative resection
 Radiotherapy
 Chemotherapy
{B} With Int Obst
Proximal loop colostomy in the transverse colon then
treat acc whether operable or inoperable

 Barium enema showing sigmoid colon,
descending colon, and transverse colon.
 It revealed that most of the colon is present in the
chest cavity
Eventration of the Diaphragm
How to read

descending colon.
 It revealed a narrowed sigmoid colon, with
multiple globular shadows in relation to the colon
with serrations of the bowel wall
(saw-teeth appearance).
DIVERTICULOSIS COLI
How to read

 Definition
Acquired herniations of colonic mucosa (pulsion Diverticulae), through the
circular Ms at the points of Bl V enter.
 Pathology
1. Incidence
2. Etiology
3. Pathogenesis
 Management
1. Diverticulosis Coli
2. Diverticulitis
3. Perforation
4. Fistula
5. Obstruction
6. Bleeding
Questions

ascending colon.
 It revealed a narrow contracted short colon with
loss of haustrations
(pipe- stem appearance).
ULCERATIVE COLITIS
How to read

 Definition
Non-specific ulceration of mucosa and submuc of rectum and colon.
 Etiology
*Infection *Autoimmune * Allergic *Genetic *Emotional stress.
 Pathology
*Starts in the rectum and spreads proximally.
*Abscess in the crypts  burst to form small ulcers  coalesce to form
large ulcer
*The ulcers  reflex Ms spasm  intramural fibrosis.
*The colon is reduced in length and the m.m. bet ulcers  hyperplasic
 Pseudopolyps.
 Complications
*Local ( toxic megacolon– hge– stricture– abscess– fistula- carcinoma)
*Systemic ( skin- eye- liver- kidney- Joints- DVT )
Questions

 Clinical Picture
1. Acute fulminant type
2. Chronic intermittent type
3. Chronic continuous type
 Investigations
 Treatment
{1} Medical treatment {2} Surgical treatment
 Antidiarrheal agent 1. One stage procto-colectomy with
 Intestinal antiseptic terminal ileostomy
 Corticosteroids 2. Total procto-colectomy with
 Supportive therapy ileo-anal pouch
 Dieting 3. Ileostomy alone in emergency
 Immunosuppressive 4. Total colectomy with ileo-rectal
anastomosis

 Inflammatory Bowel Diseases
(1) Regional Enteritis (Crohn´s disease).
(2) Ulcerative colitis.
(3) TB of the intestine ( ulcerative type – hyperplastic TB).
(4) Bilharziasis of the colon.
(5) Ileo-caecal actinomycosis.
 Surgical complications of Typhoid Fever:
(1) Paralytic ileus.
(2) Intestinal he (at the 3rd
week).
(3) Perforation ( at the 3rd
week) – ulcers in antimesenteric border-
mortality 30% - fistula may develop )
(4) Cholecystitis.
(5) Phelebitis ( esp. lt common iliac V ).
(6) Genito-urinary complications.
(7) Joints : arthritis
(8) Bone : osteomyelitis & typhoid spine.

 Plain X-ray chest, abdomen & pelvis of an infant,
with the patient upside down, and a coin inserted
at the anal dimple.
 The gas shadow is distal to the level of Ano-
coccegeal line (level of pelvic floor Ms- levator
ani).
 Diagnosis
Low imperforate Anus
How to read

 Plain X-ray chest, abdomen & pelvis of an infant,
with the patient upside down, and a coin inserted
at the anal dimple.
 The gas shadow is proximal to the level of Ano-
coccegeal line (level of pelvic floor Ms- levator
ani).
 Diagnosis
High imperforate Anus
How to read

 Plain X-ray abdomen & pelvis of an infant, with the
patient upside down, and a metal rod is inserted at the
anal canal.
 The metal rod ends at the level of Ano-coccegeal line
and the gas shadow is proximal to the level of Ano-
coccegeal line (level of pelvic floor Ms- levator ani).
 With no communication between the gas shadow and
the metal rod
 Diagnosis
High imperforate Anus
( RECTAL ATRESIA)
How to read

 Types:
Low anomalies High anomalies
1. Covered anus 1. Ano-rectal agenesis
2. Membranous anus 2. Rectal atresia
3. Stenosed anus 3. Cloaca
4. Ectopic anus
 Embryology
 DD of Neonatal Intestinal Obstruction
 Treatment
Questions

 Gastric:Gastric:
1-Pyloric atresia 2. Antral web
 DuodenalDuodenal
1- Atresia 2. Malrotation
3- Annular pancreas 4- Anterior portal vein
 Small bowelSmall bowel
Structural (1) Atresia (2) Internal hernia
(3) Duplication cyst (4) Vitelline duct remnant
Mechanical Meconium ileus
Acquired (1) Sepsis (2) Necrotizing enterocolitis
 ColonicColonic
1- colonic Atresia 2 - Anorectal atresia
3- Hirchsprung disease 4- Meconium blug
Neonatal Intestinal Obstruction

 Plain X-ray abdomen & pelvis
 Postero-anterior view
 Erect position
 It revealed multiple air-fluid levels arranged in
Step-ladder pattern
Acute Intestinal Obstruction
How to read

 Supine position
 It revealed dilated intestinal loop
with a characteristic
Vulvulae Conneventes
(Jejunal Obstruction)
How to read

 Supine position
 It revealed dilated intestinal loop
with a characterless pattern
No Vulvulae Conneventes
No Haustrations
(Ileal Obstruction)
How to read

 Supine position
 It revealed hugely dilated intestinal loop
with a characteristic
Haustrations (Sacculations)
(Colonic Obstruction)
How to read

 Definition
Failure of intestinal contents to progress
 Types
 Pathology
(1) Proximal segment
* Hyperperistaltic phase * Antiperistaltic phase
* Stage of dilatation
(2) Distal segment
 Pathophysiology
* Source of fluid * source of air
Questions
Dynamic Adynamic
Simple occlusion Pure strangulation
Occlusion with strangulation Paralytic ileus

 Investigations
 Treatment
R R R
(Resuscitation) (Ryle tube) (Removal of obstruction)
Mesenteric Vascular Occlusion
 Etiology
* Arterial embolism * Arterial thrombus * Venous thrombus
 Investigations
* Leucocytosis * ▲serum amylase * distension of small & large int
* Paracentesis  serosanguinous fluid
 Treatment
* Viable Gut * Non-viable Gut

Paralytic Ileus
 Etiology
* Reflex symp ↑↑: after op or trauma * Toxic↓↓ in peritonitis
* Anoxic ↓↓: prolonged distension * Biochemical ↓↓: hypokalemia
 Investigations
• Enema is retained
• Air-fluid level
 Treatment
Treatment of the primary cause
(1) IV fluids
(2) Ryle
(3) Intestinal stimulants
(4) Frequent enemas

 Erect position
 It revealed Air under both copulae of the
diaphragm
for
Differential Diagnosis
How to read

 Physiological after abdominal operations or laparoscopy.
 After utero-tubal insufflations.
 Penetrating stab wound abdomen
 Closed abdominal trauma with rupture gut
 Perforated viscous
{1} Perforated peptic ulcer (gastric- duodenal- Meckel).
{2} Perforated typhoid ulcer.
{3} Perforated diverticulum.
{4} Iatrogenic perforation.
{5} Perforated malignant ulcer
 Subphrenic abscess with air-forming organisms.
 Old method (pneumoperitoneum) for treatment of TB.

 Percutaneous Trans-splenic Portal Venography.
 It revealed
Splenic sinusoids
Splenic vein.
Portal vein with its 2ry and 3ry branches
Inferior mesenteric vein.
Portal Hypertension
Grade I
How to read

 Grades of Portal Hypertension.
* Grade O:
Good perfusion, with visualization of the portal vein, and
its all branches up to fine arborization, with no collaterals
* Grade I:
Fair perfusion, with visualization of the portal vein up to
3ry branches
* Grade II:
Poor perfusion with visualization of the portal vein up to
2ry branches, with collaterals.
* Grade III:
Poor visualization, only the portal vein, Rt & Lt branches.
* Grade IV:
Non visualization of the portal vein, with hepatofugal circ

 Value of portography
1. It reveals the site of obstruction in the portal tree.
2. It reveals the dilated collaterals.
3. It reveals the suitable vein for shunt operation.
4. It reveals direction of blood flow (Hepatopetal – Fugal).
5. We can estimate the portal pressure at the same time.
6. We can estimate the portal flow (Grades).
7. Postoperative for patency of the shunt.
 Methods:
Direct
*PT splenic *PT hepatic *Umb v *Operative
*Postop (after portocaval shunt through femo V)
Indirect
* Arterial portography *DVI

 Indirect Portal Venography.
 Arterial Portography (Through the splenic artery )
 It revealed
Splenic sinusoids
Splenic vein.
Portal vein with its branches
up to fine arborization
Absence of collaterals.
Normal Portal Venography
How to read

 Arterial Portography (Through the splenic artery
and SMA)
 It revealed
Splenic sinusoids
Splenic vein.
up to 3ry branches
presence of collaterals.
G I
Portal Hypertension
How to read

and SMA)
 It revealed
Splenic sinusoids
Splenic vein.
up to 2ry branches
presence of collaterals.
G II
Portal Hypertension
How to read

and SMA)
 It revealed
Splenic sinusoids
Splenic vein.
Portal vein with its Rt & Lt branches
presence of many collaterals.
G III
Portal Hypertension
How to read

and SMA)
 It revealed
No vein from the hepatic circulation
All the blood is directed away from
the liver.
( Hepato-fugal circulation)
G IV
Portal Hypertension
How to read

 Definition of portal hypertension
 Etiology
 Pathology of Portal Hypertension
*Liver *Spleen
*Congestive gastroenteropathy
*Development of Collaterals
*Ascites
 Complications of PH.
 Investigations
Child (Pough) classification
 Treatment
Questions

 Hepatic Angiography.
 Through Percutaneous Transfemoral catheter
 It revealed
* Irregular tortuous arteries feeding the tumor
(Tumor Blush & Tumor Encasement).
* A large No of new vessels around the tumor
(neovascularization) ( thread and streaks sign)
* Tumor staining in the venous phase
Hepatocellular Carcinoma
How to read

 Through the splenic artery and SMA
 It revealed
No vein from the hepatic circulation
All the blood is directed away from
the liver.
( Hepato-fugal circulation)
Obstructed Shunt
How to read

 Plain X-ray abdomen ( Rt hypochondrium).
 The patient is more or less well prepared.
 It revealed
* A radio-opaque shadow (s) in the rt hypochondrium.
* A rim of translucency (in the 1st
film) (Signet ring).
* Dilated ileal loop near to the GB (Sentinel loop).
* Colon filled with gas near to GB ( Colon Cut-off sign).
* Calcification of the GB wall (6th
film) (Porcelain GB)
Diagnosis
Radio-opaque Shadow
in the Rt hypochondrium for DD
most probably
Gall Stone (s) with Chronic calcular cholecystitis
How to read

 DD of radio-opaque shadow
{1} Gall stone ------- Shape of the stone
------ In lat view in front of the spine
{2} Renal stone ------ Cholecystography or IVU
{3} Calcified LN
{4} Fecolith or FB in the small intestine
{5} Phlebolith
{6} Atherosclerotic renal artery
{7} Hydatid cyst in the liver
{8} Calcified TB kidney or suprarenal gland
{9} Calcified costal cartilage
{10} Fracture transverse process of lumbar vertebra
Questions

 Value of plain X-ray in GB diseases
{1} It may reveal radio-opaque shadow in 15%
shape of the stone ( faceted – signet-ring)
{2} It may reveal Gas-containing fissures within the stone
(Mercedes Benz –sea-gull sign)
{3} Calcification of the wall of the GB (Porcelain GB)
{4} GB may contain bile with high concentration of Ca CO3
(Limey GB)
{5} GB may contain gas (Emphysematous GB)
{6} Dilated ileal loop (sentinel loop)
{7} Colon filled with gas (Colon cut-off sign)
{8} Soft tissue shadow in the Rt hypochondrium (omentum)
{9} Exclude other conditions ( Perforated DU )
Questions

 Oral cholecystography
 It revealed
* The dye is well concentrated by the GB.
* Normal size and shape of the GB.
* No filling defect or effect.
* The GB is well contracted after fatty meal.
* No other signs of chr inflammation
Diagnosis
Normal oral Cholecystography
How to read

 It revealed
* The dye is well concentrated by the GB.
* The shape of the GB is distorted.
Diagnosis
Pharygian Cap
Q: Other anomalies in the Biliary tree
How to read

 It revealed
* Faint concentration of the dye.
* Non visualization of the GB (obstructed).
* filling effect.
* The GB is not contracted after fatty meal.
* Other signs of chr inflammation
Diagnosis
Chr Calcular Cholecystitis
Porcelain GB ,
Obstructed by a stone in the neck
Q: Causes of non visualized GB
How to read

 It revealed
* Faint concentration of the dye.
* filling defect.
* The GB is not contracted after fatty meal.
* Other signs of chr inflammation
Diagnosis
Chr Calcular Cholecystitis
? Cholesterol stone
How to read

 Types of Chronic Cholecystitis
 Types of Gall stones
 Complications of Gall stones
 Other investigations
 Treatment
Questions

 Types of Chronic Cholecystitis
(1) Chronic calcular cholecystitis.
(2) Chronic non calcular cholecystitis.
(3) Cholecystosis.
Chr inflam. With hyperplasia of all tissue elements
(4) Cholesterosis (Strawberry GB).
Metabolic disturbances  deposition of cholesterol crystals in the
mucosa  red streaked mucosa with cholesterol polyps ( strawberry
appearance)
(5) Cholecystitis glandularis proliferans.
*Thickening and hyperplasia of all layers (Adenomatosis)
*Mucosal polyps * Diverticular stone  abscess & fistula
(6) Biliary Dyskinesia
*Due to spasm in the Oddi sphincter
Questions

meal and follow through
Gall bladder----------------

meal and follow through
Gall bladder---------------------- 

PTC
---------------------Gall bladder----------------
cannula--------------
---------------duodenum---------------

 Gastrographin meal and follow through
shows filling of the Biliary ductal system
via a fistula from the post-bulbar duodenum
to the neck of the small, shrunken gallbladder
(Film .2, arrow).
 A PTC
(Film .3) also demonstrated
the connection between
the neck of the gallbladder
and the duodenum. No gallstone is seen.
Cholecysto-duodenal fistula
How to read

 Types of Cholangiography
(1) IV Cholangiography.
(2) Excretion scan (HIDA or PIPIDA).
(3) PTC
(4) ERCP
(5) MRCP
(6) Operative :.
*Pre-exploratory
*Post exploratory  Through choledocoscope
 Through T- tube
(7) Postoperative
*2 weeks after exploration CBD through T- tube
*Through a biliary fistula
Questions

 T- tube cholangiography
It revealed
 * normal calibre CBD.
 * normal IH Biliary radicals.
 * no filling defect or effect in the CBD.
 * smooth tapered lower end CBD.
 * The dye is passed to the duodenum
Diagnosis
Normal T – tube cholangiography
Q: Criteria of normal
T–tube cholangiography
How to read

 Indications of exploration CBD
 Preoperative
 Operative
 Postoperative
 Methods of exploration CBD
 Supra duodenal portion
 Retro & infraduodenal portion
 Intra duodenal portion
Questions

 T- tube cholangiography
It revealed
 * dilated CBD.
 * dilated IH Biliary radicals.
 * filling defect or effect in the CBD.
 * abrupt stoppage of dye in lower end CBD.
 * The dye is not passed to the duodenum
Diagnosis
Residual stone CBD
Q: Criteria of missed stone
in T–tube cholangiography
How to read

 In the immediate postoperative period:
Leave the T- tube for 4-6 weeks
 * dissolution of the stone.
 Heparin (25000 u in 250 ml saline/8h for 1 week
 Chenodeoxycholic acid
 Monoglyceride mono octanion
 Methyl tetra butyl ether
 * Extraction of the stone by Dormia basket.
 * Fiber optic choledocoscope.
 * Second operation for sphincteroplasty.
 * Second operation for Choledochlithotomy
Treatment of Residual stone

 After removal of the T- tube
 * Endoscopic sphincterotomy.
and remove the stone by
Dormia basket or balloon catheter
Associated with high morbidity and mortality
 Late (months or years)
 * Endoscopic sphincterotomy.
Treatment of Residual stone

 Endoscopic Retrograde
Cholangio-pancreatography
It revealed
 * dilated CBD.
 * filling defect in the CBD.
Diagnosis
Residual stone CBD
during extraction by endoscope
How to read

 IV Cholangiography
It revealed
 * dilated CBD.
 * filling defect in the CBD.
Diagnosis
Primary stones CBD
How to read

 Indications of Transduodenal
Sphincterotomy
Open the 2nd
part of the duodenum longitudinally and
pass a grooved probe in the duodenal papilla and
divide the papilla and all of the sphincter at 10 O
clock
 * Stone impacted at the duodenal papilla.
 * CBD dilated and filled with stones.
 * Stenosed or fibrosed papilla.
 * Stones in CBD in pt had undergone
cholecystectomy.
Questions

 Indications of Transduodenal Sphincteroplasty
or Choledochoduodenostomy
 Stones
* 1ry stones. * Large stones (>1.5 cm).
* Multiple stones. * Multiple intrahepatic stones
* Recurrent stones * Impacted stones
 Strictures
* CBD stricture. * Stricture with chr pancreatitis
* Iatrogenic stricture. * Stricture from stone impaction
 Severe dilatation CBD > 1inch
 Biliary Dyskinesia
Questions

 Intraoperative cholangiography
through cystic duct
It revealed
 * normal caliber CBD.
 * normal IH Biliary radicals.
 *no filling defect or effect in the CBD.
 * smooth tapered lower end CBD.
 * The dye is passed to the duodenum
Diagnosis
Normal cholangiography
How to read

 Fistulogram Cholangiography
It revealed
 * dilated CHD.
 * abrupt stoppage of dye in lower end CHD.
CHD stump > 2cm
 * Failure of passage of the dye to the CBD
or to the duodenum
Diagnosis
Benign Biliary Stricture
with obstruction at the CHD
Type I Bismuth classification
How to read

Hepatico-jejunostomy
With entero-anastomosis

 IV Cholangiography
It revealed
 * dilated CHD.
 * abrupt stoppage of dye in lower end CHD.
CHD stump < 2cm
 * Failure of passage of the dye to the CBD
or to the duodenum
Diagnosis
Type II Bismuth classification
How to read

 MRCP
It revealed
 * abrupt stoppage of dye at the confluence
of rt and lt HD
 * Failure of passage of the dye to the CHD or CBD
Diagnosis
Type III Bismuth classification
How to read

End to side Hepatico-jejunostomy
with entero anastomosis

End to end Hepatico-jejunostomy
with Roux-en Y

 T- tube Cholangiography
It revealed
 * abrupt stoppage of dye at the lower end
of rt and lt HD
 * Failure of passage of the dye to the CHD or CBD
Diagnosis
Malignant Biliary Stricture
Klatskin tumor
How to read

 ERCP
It revealed
 * 1st
film  injection of the dye.
 * 2nd
film  introduction of the stint.
 * 3rd
film  injection of the dye through the stint.
 * 4th
film  the cholangiogram after insertion of
the stint
Diagnosis
Malignant Biliary Stricture
Klatskin tumor
with stinting of the CBD
How to read

 PTC
 define the extent of ductal involvement.
 The films show high grade obstruction of the
CHD near the hilus with medial displacement
of the duct by adjacent tumor mass.
 The intrahepatic ducts are markedly dilated.
 Diagnosis
 The findings of a mass partially filling the
gallbladder lumen and extending into the liver
with ductal obstruction at level of the porta
hepatis and the presence of a gallstone are
characteristic of gallbladder carcinoma
How to read

 Pathology and staging
 Diagnosis
 DD
 Treatment
Questions

 ERCP
It revealed
 Retrograde filling of the CBD shows the cyst
as an abrupt fusiform cystic dilatation of the
CBD. The intrahepatic ducts are normal in
caliber. The CBD joins the pancreatic duct
near the ampulla; the pancreatic duct is
otherwise normal.
Diagnosis
Choledochal cyst
How to read

 Anatomy and pathology
 Type I * Dilatation of extra hepatic BT
1- cystic 2- focal 3- fusiform
 Type II * Saccular diverticulum
of extra hepatic bile duct
 Type III * Choledochocele.
 Type IV
{a} * Dilatation Intra and extra hepatic BT
{b} * Multiple extra hepatic dilatations.
 Type V * Dilatation confined to the
Intrahepatic BT
Questions

 Etiology
 Clinical Presentation
 DD
 Diagnostic studies.
 Complications.
 Management
Questions

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