gall bladder

Dr Noori Henoon Jasim Consultant Surgeon and Ass. Professor Gall Bladder

The gall bladder and bile duct :Anatomy:Pear shape , 7.5 – 12 cm in length . Capacity > 50 ml . Fundus , body , neck & infundibulum . cystic duct ( 2.5 cm , 0,5 cm ) join common hepatic duct ( 2.5 cm ) to form CBD. ( 7.5 cm ) Blood supply : cystic artery from Rt. Hepatic artery .Caterpillar turn : Tortuous Rt. Hepatic artery in front of origin of cystic duct with short cystic Ar.Lymphatics : two ways ;1- To cystic L.node of lund →coeliac L. N.2- Directly to liver .Physiology : Bile →97% water →2% bile salt →1% bile acid and cholesterol.

Bile production : 40 ml / hour = 1000 ml /day .Gall bladder function :1- Reservoir & storage.2- Concentration of bile 5-10 times .3- secretion of mucin ; 20 ml / day .Investigations of biliary tract :Plain Xray :Radio opaque stone 10 – 20 %.Porcelain gall bladder .Limey bile .Gas in biliary tree.2) Oral cholecystography & iv. Cholangiography.Out of use . Historical interest.3) Ultrasonography : Prime test . Standard test . Quick , non-invassive test .4) ERCP. & endoscopic ultrasonography . 5) PTC .6) MRCP (standard, no contrast).

7) Radio isotope scanning : 99mTC labelled HIDA , IODIDA . Iv. given , excreted in bile, gall bladder visualised 30 minute if delayed to 1 hour suggest acute cholangitis or contracted gall bladder ( chronic ) . 8) CT. Scan : To detect liver and pancreatic lesion . Cancer extent and staging . L. Node enlargement . 9) Per operative cholangiography . 10) Per operative choledochoscopy : Flexible fibreoptic endoscope to localize and extract stone .

Congenital abnormalities of GB. & bile ducts :1- Abscence of G.B.2- Phryngian cap 2 – 6 % , phrygian cap like hats of people of phrygia (asia Minor). Suptum in G. bladder either complete or incomplete .3- Intra hepatic G.B.4- Floating G.B. → torsion .5- Double G.B 6- Cystic duct anomalies : Intra hepatic ;Accessory duct . Low insertion . Short or absent.Extra hepatic biliary Atresia :1/14000 live births . Occlusion of variable length . inflamation → destruction → fibrosis → obliteration .Out come :Biliary cirrhosis . Portal hypertension . Jaundice . Liver failure

Types :Type I occlusion of C.B.D.Type II C.B.D. + C.H.D.Type III C.B.D. + C.H.D. + Lt. & Rt. H.d.Clinical features :1- Jaundice at birth – progressive – 2- Pale muconium.3- Dark urine .4- Steatorrhoea leading to Osteomalacia( biliary rickets ).5- Clubbing of fingers .6- Portal hypertension .7- Another anomalies in 20% .DDx:1- Neonatal jaundice .2- Choledochal cyst .3- Inspissated bile syndrome .4- Neonatal hepatitis.Rx : Early surgery Roux-en-Y or liver transplant.Post op. Complications :1- Cholangitis in 40% .2- Portal hypertension 50% .

Choledochal cyst :Def.: Congenital cystic dilatation of biliary tract (particularly CBD).Clinical features :1- Jaundice .2- Rt. hypochondrial cystic mass .3- Cholangitis & pancreatitis .Dx :1- ultrasound diagnostic test .2- MRCP.Px : Premalignant → cholangiocarcinoma .Rx : Surgical excesion & Roux-en-Y .

Choledochal cyst :Def.: Congenital cystic dilatation of biliary tract (particularly CBD).Clinical features :1- Jaundice .2- Rt. hypochondrial cystic mass .3- Cholangitis & pancreatitis .Dx :1- ultrasound diagnostic test .2- MRCP.Px : Premalignant → cholangiocarcinoma .Rx : Surgical excesion & Roux-en-Y .

EpidemiologyFemale, Fatty, Fertile, FortyTypes 1. Cholesterol and 2. Mixed : 80% in US and Europe 3.Pigmented: 80% in AsiaAetiologyMetabolicStasisPregnancyInfection……H. pyloriOthers…….Sickle Cell Anaemia . Heriditry Spherocytosis (See the diagram below). Gall Stone
Features
Cholesterol stone
Mixed stone
Black Pigment S.
Brown pigment S.
location
Gall bladder
Gall bladder
Gall bladder
Bile Duct
Components
Hardened cholesterol (almost pure cholesterol)
Mostly cholesterol (51-99% of stone contents) + calcium salts, bile acids, bilirubin pigments & phospholipid
Mostly Bilirubin pigments+ Ca phosphate+ Ca carbonate+≤ 30% cholestrol Mainly Ca bilirubinate+Ca palmitate+ Ca stearate +≤ 30% cholestrol Gross Features
Large solitary, white
Small, hard, multiple, faceted, green or yellow
Small, black, irregular& multiple
Large, brown & single
common possible Aetiology
Same as mixed
Most common Cases in which chol increase or bile acid dec in bile associated with patients with obesity, high caloric diet, contraceptive pills, ileal resection, abnormal emptying of gall bladder
Highly associated with SCA, H spherocytosis& cirrhosis
Associated with bile stasis & infected bile due to FB in bile duct like stent or parasitic infestations like Chlonorichis sinensis or Ascaris lumbricoidis
World distribution
In US and Europe 80% cholesterol or mixed……around 10% of them is pure Cholestrol stone In US and Europe 80% cholesterol or mixed……..Around 70% of them is mixed stone In US and Europe, both types of pigment stones represent around 20% of total mostly in immigrant people from Asia and Africa. In Asia 80% of . stones are pigment stones (black more than brown
In US and Europe, both types of pigment stones represent around 20% of total mostly in immigrant people from Asia and Africa Common in Asia. In Asia 80% of stones are pigment stones.(black more than brown)


Gall Stone Aetiology

Effects & complications of stones :I : Gall bladder : 1) Silent, asymptomatic (mostly) 2) Dyspepsia, Flatulence, Food intolerance (Fat) 3) Biliary colic 4) Cholecystitis (acute and chronic) 5) Fistula….leading to Mirizzi syndrom (less than 0.1%) 6) Mucocele. 7) Empyema of gall bladder 8) Gangrene & perforation 9) Carcinoma of gall bladder.II : Bile ducts : 1- Jaundice 2- Acute Cholangitis 3- Acute pancreatitis III : Intestine : intestinal obstruction ( gall stone ileus ) .

+ and flatulent dyspepsia

+then chronic cholecystitis
8.Mucocele 9. Empyema 10. Gangrene and perforation

Outcome of Gall Stone

Clinical Features
Silent
Most of patients , Asymptomatic
Flatulant Dyspepsia
Hx: Dyspepsia; R hypochondrail Pain or epigastric pain (more often dull and constant) + flatulence+ intolerance of Fatty food
Biliary colic
10-20% of patients of gall stone,Hx: Several episodes of pain which is sever (minutes-hours)+ nausea &vomiting for few weeks –then period of relief for few months as the stone dis-impacted back into gall bladderEx: negative Murphy’s sign + No feverUlS: no signs of acute cholecystitis but there is stonesBlood invest.: no significant change in laboratory data (may be slight rise in liver enzyme and bilirubin) Acute cholecystitis
Hx: R hypo&/ or epigastric pain more sever Ex: Tenderness+ Murphy’s sign positive+ low grade feverUlS Scan: shows signs of acute cholecystitis: distended gall b.+ presence of stones+ thickened wall of gall bladder+ pericholecystic fluid collectionBlood invest.: leukocytosis +moderate elevation in LFT Empyema of Gall Bladder
Same of acute cholecystitis + history of acute attack that has not relieved + more pain+ More tenderness+ more fever+ inc in pulse rate+ might be palpable mass in R hypochondrial region (gall bladder surrounded by omentum)
Perforation
Sign and symptoms of peritonitis usuall localized.
Chronic Cholecystitis
Hx: History of acute attack that has already been relieved+ pain less in severity and frequency + might be flatulent dyspepsia+ nausea and vomitingEx: No fever or tenderness or Murphy’s sign negative (shrinkage gall bladder)U/S: shrinkage gall bladder+ presence of g. stone+ No sign of acuteBlood investing.: Often Normal


Cholecystitis :Acute & 2) chronic Calculous 85 – 95 % Acalculous 5 – 15 %Acute :Inflammation of gall bladder wall .M.O. : 1- E.coli . 2- klebsiella . 3- streptococcus faecalis .4- bacteroid .5- clostridia & typhoid (uncommon & serious).Causes of acute cholecystitis :1-Stone in 90% impacted in Hartmann’s pouch or obstructing cystic duct .2- Stasis 3- Pancreatic juice reflux 4 – CBD stone .5- Bacteremia .6 – Vascular effect of → D.M. → sickle → hypertension → collagen disease cystic artery thrombosis → ischemia .

Clinical features of acute cholecystitis :1- sudden onset .2- 30 – 70 years & > 60 years 25% - 35% .3- White caucasian > black people .4- Heavy fatty meal .5- Pain (colicky).6- Nausea & vomitting .7- Fever > 38̊ C .8- Boas’s sign .9- Jaundice ?10- Murphy sign .11- Tenderness & rigidity .12- Palpable tender mass .DDx :1- Appendicitis . 2- Perforated peptic ulcer .3- Acute Rt. Pyelonephritis 4- Liver abscess .5- Rt. Lower lobar pneumonia. 6- Hepatitis7- Pancreatitis 8- Herbes zoster .9- Myocardial infarction .

The sequelae of attack :1- Resolution ; disimpaction of the stone & drainage , slipping back of the stone.2- Impacted stone persist → gangrene , mucocele , empyema .3- Perforation .4- Chronic .Dx:.1- ultrasound . 2- Radio isotop scan ( HIDA ) . 3- L.F.T. 4- WBC ___ leucocytosis .Treatment :A- Conservative Rx followed by laparoscopic Cholecystectomy (after 6-8 weeks).B- Laparoscopic Cholecystectomy .A- Conservative :90% of cases the symptoms subside.1- N.G. tube & nil per mouth .2- Antibiotics e.g.; cefazolin , Cefotaxim , gentamicin .3- Analgesia & antispasmatic .

B- Cholecystoctomy : → Early 2 – 3 – 5 days . → Delayed ˃ 6 weeks .Laproscopic rarely Open (if laparoscopic is not accessible or in case of conversion) N.B. : Conversion rate in acute cholecystitis more than in elective ( delayed ) but still conversion not failure of laparoscopic cholecystectomyChronic cholycystitis :Thickened fibrotic wall of G.B. with stone(s) .Symptoms :1- Pain : episodes of Rt. hypochondrial pain of varying severity & interval ( 3 – 12 hours) after .2- Flatulent dyspepsia , fullness , belching , heartburn & distension .3- nausea & vomiting .Dx: As acute .Rx: Cholecystectomy

.Saint triad :1- Gall stone(s) .2- Diverticulosis .3- Hiatus hernia .It is important to find which one is the cause for dyspepsia Post cholecystoctomy complications :1- Bleeding .2- Jaundice .3- Adjacent organs injury.4- Biliary leak → fistula ; due to : a) Slipped ligature b) Accessory duct . c) CBD. Injury or ischemia . d) Mirizzi syndrome .5- Post cholecystectomy syndrome.Indications of cholecystoctomy.1- Symptomatic gall stones.2- Asymptomatic gall stone as prophylactic cholecystectomy (controversial) .

:

Indications of choledochotomy at cholecystectomy : 1- Stone in CBD.2- Jaundice now or history .3- Dilated CBD. ˃ 10 mm.4- ↑ alkaline phosphatase .5- Wide cystic duct & multiple small gall stones .Any way the trend now in this case is to continue in laparoscopic cholecystectomy and after operation send the patient to ERCP to remove the CBD stone

Treatment : 1- ERCP & sphineterotomy . 2- Choledochotomy : A- Supraduodenal choledochotomy stone removal and then T. tube or choledocho-duodenostomy . B- Transduodenal sphineterotomy & stone extraction .


Treatment :Cholecystectomy + excision of gall bladder liver bed + Hilar lymphadenectomy .Prognosis :Poor. 90% will die in one year . 2–5% is 5 year survival .

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