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GALLBLADDE

R STONES
Presented by:

Amer AlQaisi
Faisal AlEnezi

:Supervised by
Prof. Kamal Gharaibeh

OUTLINES
1.Anatomy

of gallbladder
2.Anatomy of biliary tree
3.Physiology of biliary system
4.Bilirubin metabolism cycle.
5.Congenital abnormalities
6.Gallstones
7.Complications of gallstones
8.Clinical presentation & Management
9.Choledocolithiasis & cholangitis
10.
Neoplasms

Anatomy of Gallbladder
Gallbladder is a pear-shaped sac lying
on the undersurface of the live which is
7.5-12 cm long and it has a capacity
of 30-50 ml.
It is divided to :
- Fundus
- Body
- Neck
The Hartmann's pouch : is a dilatation
in the gallbladder just before the
origin of cystic duct .

Relation:
Anteriorly :
the anterior abdominal wall and
.the inferior surface of the liver
Posteriorly

:
the transverse colon(proximal)
.1st and 2nd part of duodenum

The

fundus is usually projects inferiorly (at the level of the 9 th


costal cartilage in the midclavicular line) and the neck directed
upward backward.

Blood supply:
- by the cystic artery , a branch from the
right hepatic artery .
- cystic vein which drain directly into the
portal vein.

The lymph drainage:


- into the cystic lymph node of Lund which
situated near the neck of the gallbladder.

Nerve supply:
supplied by 3 types of innervation,Theceliac
plexus supplies sympathetic innervation,
thevagus nervesupplies parasympathetic
innervation, and theright phrenic
nerveconveys sensory information.

ANATOMY OF BILIARY TREE

The ducts of biliary tree are :


The common hepatic duct :
it is about 4 cm (result from the union of.Rt.& Lt hepatic duct)
Cystic duct :
it is about 3.8 cm, somewhat S shapedwhich connect the neck of the
gallbladder with the common hepatic
.duct
The common bile duct :
it is about 8 -10 cm that is result from theunion of the common hepatic duct with
.the cystic duct

The common bile duct descends behind the duodenum


and pancreas and usually joined by pancreatic duct, and
together, they open into a small ampulla in the
duodenal wall ( ampulla of vater ).

There are a small ducts that drain bile directly into the
. gallbladder from the liver, called Duct of Luschka

Cystohepatic triangle an anatomic space bordered by


thecommon hepatic ductmedially, thecystic
ductlaterally and the inferior edge of the liver
superiorly.

Calot's Triangle : cystic duct, the common hepatic duct,


and the cystic artery

PHYSIOLOGY

Gallbladder is under control of Cholecystokinin (CCK ) and its functions


are :
Contraction of the gallbladder
Relaxation of the Sphincter of Oddi
Slowing gastric emptying
increase pancreatic enzyme secretion

The gall bladder is a reservoir for bile. During fasting, resistance


to flow through the sphincter is high, and bile excreted by the
liver is diverted to the gall bladder. After feeding, the resistance
to flow through the sphincter of Oddi is reduced, the gall bladder
contracts, and the bile enters the duodenum. These motor
responses of the biliary tract are in part effected by the hormone
CCK.

PHYSIOLOGY
The second main function of the gall bladder is concentration of
bile by active absorption of water, sodium chloride and
bicarbonate by the mucous membrane of the gall bladder. The
hepatic bile that enters the gall bladder becomes concentrated
510 times, with a corresponding increase in the proportion of
bile salts, bile pigments, cholesterol and calcium.
The third function of the gall bladder is the secretion of mucus
approximately 20 ml is produced per day. With total obstruction
of the cystic duct in a healthy gall bladder, a mucocele develops
on account of this function of the mucosa of the gall bladder.

Bile
Components of bile:
Water 95%
electrolytes
bile salts (like cholic acid & chenodeoxycholic acid )
phospholipids ( like licithin)
bilirubin (conjugated)
fatty acids

The function of bile is to emulsify fat.

Absence of bile causing malabsorption of fat


and fat soluble vitamins ( A , D , E , K )

95% of bile salts are reabsorbed in the terminal


ileum , pass back via the portal venous
drainage to the liver and once again secreted in
the bile (EHC). So, resection of terminal ileum
will decrease bile salts that will cause GB
stones formation.

BILIRUBIN PRODUCTION
Heme proteins
myoglobin, cytochromes
(to 25% 20)

Hemoglobin
(to 80% 70)
Heme

Heme oxygenase
Biliverdin
Biliverdin reductase
Bilirubin

albumin

indirect
unconjugated
pre-hepatic

BILIRUBIN PROCESSING
albumin-Bilirubin

albumin

ligandin

hepatocyte
ligandin-Bilirubin
UDP-Glucuronyl
transferase
ER

Bilirubin diglucuronide

bile (gall bladder)

direct
conjugated
post-hepatic

BILIRUBIN EXCRETION
Bilirubin diglucuronide
glucuronate 2

liver 90%

Bacterial enzyme
Bilirubin
Bacterial enzyme

intestines
Urobilinogen

<-------kidneys 10%
20%
Bacterial enzymes

80%
Stercobilinogen

Stercobilin

Urobilin

urine

feces

CONGENITAL ABNORMALITIES
Absence of the gall bladder
Occasionally, the gall bladder is absent. Failure to
visualise the
gall bladder is not necessarily a pathological problem.
The Phrygian cap
present of septum that incompletely divides the GB.
(SINGLE OR MULTIPLE)

Floating gall bladder


The organ may hang on a mesentery, which makes it liable
to undergo torsion of GB to occur with consequent
gangrene & rupture

Double gall bladder


Rarely, the gall bladder is duplicated. One may be
intrahepatic
Absence of the cystic duct
This is usually a pathological, the GB open directly
ino the side of common bile duct
A long cystic duct travelling alongside the common
hepatic duct to open near the duodenal orifice
( occur in 10% of cases )

CHOLEDOCHAL CYST :

Presence of cystic dilation in the biliary tree (most commonly in CBD)


Classification according to the site of the cyst or dilatation

Type I:Most common variety (80-90%) involving saccular or fusiform


dilatation of a portion or entirecommon bile duct(CBD) with normal
intrahepatic duct.
Type II:Isolated diverticulum protruding from the CBD.
Type III or Choledochocele:Arise from dilatation of duodenal portion of
CBD or wherepancreatic ductmeets.
Type IVa:Characterized by multiple dilatations of the intrahepatic and
extrahepaticbiliary tree.
Type IVb:Multiple dilatations involving only the extrahepatic bile ducts.
Type V:Cystic dilatation of intra hepatic biliary ducts.

BILLIARY ATRESIA
- Biliary atresia (BA) is a progressive, idiopathic, fibroobliterative disease of the extrahepatic biliary tree that
presents with biliary obstruction exclusively in the neonatal
period.
- The extrahepatic bile ducts are progressively destroyed by
an inflammatory process, which starts around the time of
birth. The aetiology is unclear. The inflammatory destruction
of the bile ducts has been classified into three main types :
type I: atresia restricted to the common bile duct;
type II: atresia of the common hepatic duct;
type III: atresia of the right and left hepatic ducts.
-Associated anomalies include, in about 20% of cases, cardiac
lesions, polysplenia, situs inversus, absent vena cava and a
preduodenal portal vein.

COMPLICATIONS :
-Ascending cholangitis
Intrahepatic changes can occur and eventually
result in biliary cirrhosis and portal hypertension.
Untreated, death from the consequences of liver
failure occurs before the age of 3 years.

Liver transplantation is the main


choice of treatment .

GALLSTONES

Cholelithiasis means stones in the gallbladder. (the most


common biliary pathology)
affect more than 15% of adult in USA .
Asymptomatic (most common) >80 %
Symptomatic (complicated) 10-20% : pain, jaundice,
pruritus, feveretc.
10% of gallstones are radio-opaque .

Risk factors :
The big 5 : five Fs : female 3:1 , forty (>40) , fat ,
fertile,fair.

less common :
-Oral Contraceptives. - Rapid weight loss.
-Hyperlipidemia -Gallbladder stasis.
-Family history
-Ileal diseases or resection
Types of GB stones :
1. Cholesterol 20 %.
2. Pigmented ( Black , Brown ) 5 %.
3. Mixed 75 %

Pathogenesis:
When bile is supersaturated
with cholesterol, unstable
unilamelar phospholipid
vesicles are formed.
(Cholesterol > 80%)
This leads to formation of
cholesterol crystals.
Characteristics :
Yellowish

, greasy.

Ovoid

, firm

Single

or multiple

Most

are radiolucent.

CHOLESTEROL
STONES

Contains less than 30% cholesterol. Contain bilirubin and


calicium

Two types : Black and Brown.


Black

stones :

Accompanies hemolysis (hereditary spherocytosis , sickle cell


anemia).

Brown

Stones :

Form

in bile duct and related to bile stasis and infected

bile.
Associated

with the presence of foreign bodies within the


bile ducts such as stents, or parasites .

PIGMENTED STONES

Characteristic :

Anywhere in the biliary tree.

Black: in sterile GB bile ,small, numerous, friable, 50-75% are


radio-opaque

Brown: in infected intra- or extrahepatic ducts, single or few,


soft & greasy, radiolucent

MIXED STONES

Is the most common 75%


cut surface is laminated with alternate dark &light
zones of pigment & cholesterol respectively

WHAT ARE THE


COMPLICATIONS
OF GALLSTONES?

In gallbladder :
- Acute cholecystitis.
- Chronic cholecystitis
- Biliary Colic
- Empyema.
- Mucocele.
- Perforation
- Carcinoma (0.08%)

In the Bile Ducts:


- Obstructive jaundice
- Ascending cholangitis
- Acute pancreatitis

In the intestine
- Gallstone ileus
(intestinal obstruction)

BILIARY COLIC

It is a misnomer because the pain increases in


intensity then reaches a plateau then decreases but
never disappears . So

not a true colic

Caused by:
- Transient obstruction of the GB by a stone in
Hartmanns pouch or cystic duct , which leads to
spasm in the wall of GB

Presentation:
pain:
S:Right upper quadrant.
O: suddenly after fatty meals
C: gripping pain, dull.
R: referred to the tip of the right shoulder and
radiate to the back
A: Associated with - Nausea, vomiting, flatulence,
dyspepsia .
T: Less than 6 hours, if more then it is acute
cholecystitis.

ACUTE CHOLECYSTITIS

1-acute calculous cholecystitis 95%


2-acute Acalculous cholecysitis 5%

ACUTE CALCULOUS CHOLECYSTITIS

Definition:
Inflammation of the gallbladder that
develops over hours, usually resulting from a
cystic duct obstruction by a gallstone.
This form of gallbladder disease usually
subsides within 1 to 7 days with a
conservative plan of treatment .

Not everyone who has gallstones will go on


to develop cholecystitis .

inflammation of the mucosa by the congested bile


salt. This will lead to edema and distention in the
wall causing increased intraluminal pressure and
compromises blood flow to mucosa.

- Stasis and Concentrated bile , with superimposed


bacterial infection

- A stone obstructing the gallbladder neck


(Hartmanns pouch) or anywhere in cystic duct.

Pathophysiology

Unrelieved obstruction , without infection and


continuous mucus secretion >> Mucocele

Unrelieved obstruction with infection and


pus formation >> Empyema

- Gangrene may cause perforation (causing


abscess and chemical peritonitis )

- Decrease blood flow with infection lead to


gangrene that cause softness of GB wall

5
4

CLINICAL PRESENTATION
(ACUTE CHOLECYSTITIS)
Age : Typically 30-60 year old.
Presentation in younger patients, may be due
to congenital hemolytic anemia(sickle-cell
disease often form pigment stones, which
may precipitate an attack of acute
cholecystitis).
Gender : Females are more commonly affected

Analysis of Pain:
S: RUQ
O: sudden onset
C: sharp
R: radiates to the back (close to the inferior angle of
right scapula)
A: associated with nausea , vomiting and fever
T: continuous , Duration of pain usually >6 hours
E: aggravated by movements and breathing
S: severe
*The patient May have previous history of flatulent
dyspepsia or biliary colic .

PHYSICAL EXAMINATION

General Examination :
_ Patient appears ill
_ shallow breathing
_ Tachycardia +ve, Pyrexia +ve

** few patients with AC have jaundice by two mechanisms :


1- stone passed to the CBD obstuctive jaundice
2- Mirrizi syndrome :
occur when the cystic duct is densely adhered to the CBD .
the stone in the cystic duct cause compression of the CBD .

PHYSICAL EXAMINATION

Abdominal Examination :

RHC mass and tenderness, guarding/rigidity


Zackary-cope's sign : RHC fullness
Boas Sign : hyperaesthesia (increased or altered sensitivity)
below the right scapula.
Murphy's sign : Cessation of breath at deep inspiration during
the deep palpation at the tip of 9th rib
Bowel sounds are normally present except in biliary
peritonitis(GB has infarcted/ruptured ) rare complication

What are the differences in the clinical presentation


between biliary colic
and Acute cholecystitis ???
Biliary colic :
pain duration < 6 hrs
Afebrile patient
vomiting once or twice
mild tenderness
Acute cholecystitis :
pain duration > 6 hrs
febrile patient
repeated vomiting
severe tenderness

INVESTIGATION

5.

Full blood count - reveals leukocytosis


KFT
LFT bilirubin (to detect bile duct obstuction)
Amylase and lipase level ( for acute pancreatitis)
US abdomen ( THE GOLD STANDARD)

6.

HIDA scan ( if US is not diagnostic)

7.

X-ray (not useful,only10-15% of stones are visible)


MRCP
ERCP

1.
2.
3.
4.

8.
9.

What are the ultrasonic features of


??Acute Cholecystitis
1)

Distended gall bladder

2)

Fluid surrounding the gall bladder

3)

Gall bladder wall thickening (>3mm)

4)

Dilated cystic duct

5)

Stones in the gall bladder

MRCP : magnetic resonance


cholangiopancreatography

ERCP : endoscopic retrograde


cholangiopancreatography

Both are used for diagnosis .

ERCP used also for therapy of CBD stones .

HIDA scan : reveal non-opacification of the


gallbladder from obstruction of the cystic duct.

ACUTE ACALCULOUS CHOLECYSTITIS

Inflammation of the gallbladder in the absence of gall


stone , usually seen in seriously ill patients after :
major surgeries, trauma, burns, sepsis

It occurs because of :
1) Dehydration
2) GB stasis
3) Vascular compromise
4) Bacterial contamination
( mostly Gram ve: E-coli , Klebsiella , Enterobacter )

CHRONIC CHOLECYSTITIS

Chronic inflammation of the gall bladder because


of recurrent attacks of acute cholecystitis or biliary
colic ending in thickening and fibrosis of its wall.

Stones are almost always present.

Supersaturation of bile predisposes to chronic


inflammation & stone formation.

Bacteria are isolated in 1/3 of the cases.

PRESENTATION
-Upper abdominal pain after eating.
((begins 15 to 30 mins after a meal,
and last for 30 to 90 mins))
(most common complaint).
- flatulent dyspepsia(post-prandial belching)
- Heartburn

PHYSICAL EXAMINATION

Signs of jaundice
Abdomen looks normal
RHC mass and tenderness
Percussion and auscultation should be normal

: DDX OF RUQ PAIN


Common:
1. Perforated peptic ulcer
2. High appendicitis
3. Acute pancreatitis
Uncommon:
4. Acute pyelonephritis
5. Right lower lobe pneumonia
6. MI(inferior)

MANAGEMENT

Conservative management : ( >90% of cases will respond)


1) Nil by mouth [NPO]
2) Gain IV access, give IV fluids
3) Administration of antibiotics
4)Administration of analgesics
5) Monitoring of vital signs
6) If symptoms subsided, initially oral fluid intake is allowed,
then followed by fat-free diet, and lastly regular diet
7) US - to evaluate whether there's any local complications
8) Plan for cholecystectomy ( open or laparoscopic )
A) Early (within 72 hours).
B) Late ( after 2-3 months).
*Sometimes we do Cholecystostomy in case of empyema

CHOLECYSTECTOMY
Usually we do it by laparoscopy,
but in the following cases we do it by Laparotomy :
1.
2.
3.

not well defined anatomy


uncontrolled bleeding
bile duct injury

POST OPERATIVE
COMPICATIONS
1- hemorrhage
**usually the source is from cystic artery.
** the patient complains of persistent abdominal pain,
or features of hypovolemic shock

2- wound infection
3- bile leak
4-bile duct stricture
**the most dangerous complication , leads to :
cholangitis , obstructive jaundice ,
secondary biliary cirrhosis and hepatic failure.

5-post cholecystectomy syndrome

NEOPLASMS

Benign tumors of the GB:


papilloma , myxoma , fibroma ,
adenomyoma , lipoma , carcinoid .
Malignant tumors of the GB :
80 % of the tumors are adenocarcinoma
90 % of pts have cholelithiasis
Porcelain GB Carry a risk of 50 % of malignancy
(calcification of GB due to excessive stones).

PORCELAIN GB

CHOLEDOCOLITHIASIS
- Stones present within the biliary tree.
- Stones may be:
1) derived from gallbladder
2) primary ductal & intrahepatic stone formation

- Asymptomatic in 10%
- Symptoms due to:
1) cholangitis (Charcots triad), biliary obstruction
(Obstructive Jaundice , Dark urine , Pale stool ,itching)
2) pancreatitis
3) Liver abscess
4) chronic liver disease with secondary biliary cirrhosis
5) acute cholecystitis

CHOLEDOCHOLITHIASIS CAN BE
PRIMARY OR SECONDARY

u/s , ERCP are the diagnostic modalities


Liver function test are consistent with
obstructive jaundice
Surgical TT :
Cholecystectomy , choledocotomy , CBD
exploration , T tube placement &
operative cholangiogram .

CHOLANGITIS : INFECTION OF THE BILLIARY TREE


- Etiology :
1. CBD stones.
2. post.op stricture.
3. Neoplasm
4. sclerosing cholangitis.
5. billiary contrast studies .
.

Treatment : NPO , IV antibiotics ,


relief of the obstruction

CHOLANGIOCARCINOMA

Malignant tumors of the bile duct may be


associated with :
1- Sclerosing cholangitis.
2- chronic parasitic infection of the bile duct.
3- Gall stones.

The tumor may be located in :


distal CBD , common hepatic duct , cystic duct ,
left or right hepatic duct (most common site)

Treatment by : Whipple procedure.