(1) gastro

X-RAYSX-RAYS

By

Prof Dr IBRAHIM DAWOUD

Prof of Surgery

Mansoura University

PREFACE TO THE PREFACE 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 [email protected] Tel 0123471715 -- 0502252882 Clinic:

المنصورة – ميدان الطميهى – عمارة الوقاف - الدور الثانى

mailto:[email protected]

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.


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. Fistula: Fistulography.

How to read

X-RAY with dye

Urology UTP (Urinary Tract Plain). IVU (Intravenous Urography). MRU. Urethrography. Ascending Cystography. CT scan. US. Fistula: Fistulography.

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

Mliver

►►►►►--------------------------------------◄◄◄----------------

Esophagus

Bl flowBl flow

liver

----------------------------

Intraepith veinsSubepith 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

Cervicalesophagus

Sup mediastinum

Middle and lower third

Cardia

Pharyngolaryngoesophagectomy.

Split sternum esophagectomy

Lewis-tanner operation

Transhiatal esophagectomy

Free jejunal transfer

Three phase esophagectomy

Transhiatal esophagectomy

Esophagogastrectomy

Three phase esophagectomy

Abdominal Gastrectomy

Bypass Kischner gastric bypass

Colon bypass Jejunum bypass

NormalBarium 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

InvestigationsCategory Test Indications

RadiologicalChest 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

PhysiologicalManometry Motility disorder and GERD

Bernstein test Esophageal sensitivity to acid

Acid reflux test Reflux disease

24 hr PH monit Reflux disease

TREATMENTUncomplicated 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

Laparoscopic repair of H.H.

CORROSIVE ESOPHAGEAL STRICTURE

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). Clinical picture. 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 eatingNot 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

PYLOROPLASTY

Gastrojejunostomy

Gastrojejunostomy

*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. Clinical picture. 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

Chr DU

Malignant ulcer

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”

Claw-shape sign.

Spring-coil sign.

Egg-on-cake sign

Egg-on-cake sign

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) Clinical picture. Other Investigations. DD. Acute entero-colitis - Henoch purpura Rectal prolapse Treatment: Resuscitation Ryle tube Removal of obstruction

Barium Enema showing the Rectum, sigmoid 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

Barium Enema showing the Rectum, sigmoid 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: Clinical picture: 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


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. Clinical picture:

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

Barium enema showing the rectum, sigmoid 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) Diagnosis most probably

Cancer Transverse Colon

How to read

Barium enema showing the rectum, sigmoid colon, descending colon, transverse colon, and descending colon.

It revealed an irregular stricture at the lower end of the descending colon (Moth- eaten appearance).


Cancer Descending Colon

How to read

Barium enema showing the rectum, sigmoid 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

Clinical picture Investigations Treatment {A} Without Int Obst Operable1. Caecum Rt hemicolectomy2. Hepatic Flexure Extended Rt hemicolectomy3. Transverse colon Transverse colectomy4. Descending colon Lt hemicolectomy5. Splenic Flexure Extended Lt Hemicolectomy6. Sigmoid colon Pelvic colectomy Inoperable1. Palliative resection2. 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


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

TNMT0: 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

organs or structures

Clinical picture 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 operation1. 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


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.

Pathology1. Incidence

2. Etiology

3. Pathogenesis

Management

1. Diverticulosis Coli

2. Diverticulitis

3. Perforation

4. Fistula

5. Obstruction

6. Bleeding

Questions

Barium enema showing the rectum, sigmoid colon, descending colon, transverse colon, and ascending colon.

It revealed a narrow contracted short colon with loss of haustrations

(pipe- stem appearance).


ULCERATIVE COLITIS

How to read

DefinitionNon-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 Picture1. 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

CLOACA

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

Vulvulae Conneventes


Plain X-ray abdomen & pelvis Postero-anterior view Supine position It revealed dilated intestinal loop

with a characteristic




(Jejunal Obstruction)

How to read

Plain X-ray abdomen & pelvis Postero-anterior view Supine position It revealed dilated intestinal loop with a characterless pattern No Vulvulae Conneventes No Haustrations Diagnosis most probably


(Ileal Obstruction)

How to read

Plain X-ray abdomen & pelvis Postero-anterior view 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

Clinical picture 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

Clinical picture Investigations• Enema is retained • Air-fluid level

TreatmentTreatment of the primary cause(1) IV fluids(2) Ryle(3) Intestinal stimulants(4) Frequent enemas

Plain X-ray abdomen & pelvis Postero-anterior view 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.


Portal tract Percutaneous trans-splenic portography. Percutaneous transhepatic portography. Transfemoral splenic artery angiography. Transfemoral SMA angiography. Transfemoral IMA angiography. CT. US.

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 portography1. 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. Diagnosis most probably

Normal Portal Venography

How to read

Indirect Portal Venography. Arterial Portography (Through the splenic artery

and SMA) It revealed Splenic sinusoids Splenic vein. Portal vein with its branches up to 3ry branches presence of collaterals. Diagnosis most probably

G I Portal Hypertension

How to read


and SMA) It revealed Splenic sinusoids Splenic vein. Portal vein with its branches up to 2ry branches presence of collaterals. Diagnosis most probably

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. Diagnosis most probably

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) Diagnosis most probably

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. Clinical picture 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 Diagnosis most probably

Hepatocellular Carcinoma

How to read

Indirect Portal Venography. 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) Diagnosis most probably

Obstructed Shunt

How to read

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. Fistula: Fistulography.

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

Mercedes Benz

Mercedes Benz

Mercedes Benz

Mercedes Benz

Emphysematous GB

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

Oral cholecystography 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

Oral cholecystography 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

Oral cholecystography 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

Cholecysto-duodenal fistula

Gall bladder----------------

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 * Second operation for sphincteroplasty. * Second operation for Choledochlithotomy

Associated with high morbidity and mortality

Late (months or years) * Endoscopic sphincterotomy. * Second operation for sphincteroplasty.

* Second operation for Choledochlithotomy

Treatment of Residual stone

Endoscopic Retrograde Cholangio-pancreatography It revealed * dilated CBD. * dilated IH Biliary radicals. * filling defect in the CBD. * abrupt stoppage of dye in lower end CBD. * The dye is not passed to the duodenum Diagnosis Residual stone CBD during extraction by endoscope

How to read

IV Cholangiography It revealed * dilated CBD. * dilated IH Biliary radicals. * filling defect in the CBD. * abrupt stoppage of dye in lower end CBD. * The dye is not passed to the duodenum 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 Juxtapapillary Diverticulum

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 IH Biliary radicals. * 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-jejunostomyWith entero-anastomosis

IV Cholangiography It revealed * dilated IH Biliary radicals. * 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 II Bismuth classification

How to read

Hepatico-jejunostomyWith entero-anastomosis

MRCP It revealed * dilated IH Biliary radicals. * abrupt stoppage of dye at the confluence of rt and lt HD * Failure of passage of the dye to the CHD or CBD

Diagnosis Benign Biliary Stricture with obstruction at the CHD Type III Bismuth classification

How to read

Type III

End to side Hepatico-jejunostomy with entero anastomosis

End to end Hepatico-jejunostomy with Roux-en Y

T- tube Cholangiography It revealed * dilated IH Biliary radicals. * 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 with obstruction at the CHD Klatskin tumor

How to read

1ST FILM

1ST FILM

1ST FILM

2ND FILM

2ND FILM

2ND FILM

3ND FILM 4TH FILM

3ND FILM

3ND FILM

3ND FILM

4TH FILM

4TH FILM

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

with obstruction at the CHD

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

Education

(1) gastro