Gallstones form when there is an imbalance in bile that allows cholesterol to precipitate out of solution. Gallstones can cause complications like biliary colic, cholecystitis, obstructive jaundice, cholangitis, and pancreatitis. Ultrasound is often the first imaging test used to detect gallstones in the gallbladder. For gallstones causing symptoms, laparoscopic cholecystectomy is the standard treatment, while asymptomatic gallstones may sometimes be dissolved medically with bile acids if surgery is declined.

1. Presented by :
Osama Soudi Abd El-zahir
Supervised :
Prof. Dr. Khaled Mahran
GALLSTONES

2. ANATOMY
The Gallbladder:
 Pear-shaped sac.
 30-50 ml.
 Located in the fossa on the inferior surface of the liver
 4 anatomic areas.
 Blood supply: cystic artery ( triangle of calot).
 Venous drainage: small veins enter directly to the liver.
 Lymphatic: nodes at the neck of the GB.

3. Anatomy of Gallbladder
The gall bladder is
located in the junction
of the right ninth costal
cartilage and lateral
border of the rectus
abdominis .
 It is a pear shaped sac
lying on the inferior
surface of the liver in a
fossa between the right
and quadrate lobes
with a capacity of about
30 to 50 mL.

4. Anatomy of Gallbladder
 The gallbladder is in direct contact to
the superior part of the duodenum
and transverse colon.
 The gall bladder has three parts the
neck which tapers into the narrow
cystic duct which connects with the
common duct.
 Body: contacts the visceral surface of
the liver the transverse colon and
superior part of the duodenum
 Fundus: The wide end of the organ
projects 1-2 cm from the inferior
border of the liver.

5. Anatomy of Gallbladder
The cystic duct (3-4 cm long) connects the neck of the
gallbladder to the common hepatic duct .
The spiral fold helps keep the cystic duct open ;thus bile can
easily be diverted into the gallbladder when the distal end of
the bile duct is closed by the sphincter of the bile duct.
The spiral fold also offers additional resistance to sudden
dumping of bile when the sphincters are closed, and intra-
abdominal pressure is suddenly increased, as during a
sneeze or cough.
The cystic duct passes between the layers of the lesser
omentum, usually parallel to the common hepatic duct, which
it joins to form the bile duct.

6. Blood Supply of the Gall
Bladder
The cystic artery,
supplying the
gallbladder and
cystic duct
commonly arises
from the right
hepatic artery.

8. PHYSIOLOGY
Bile Formation and composition:
 Produced by the liver ( 500-1000 ml/day).
 Production is stimulated by vagus, food particles in the duodenum,
and secretin.
 Composed of water, electrolytes, bile salts, bile pigments, protein,
lipids.
 Cholesterol -> primary bile acids -> ( conjugation + Na) -> bile salts ->
small intestine :
*80% absorbed in terminal ileum.
*deconjugated (secondary bile acids) -> absorbed in colon
 95% of the bile acid pools is reabsorbed (enterohepatic circulation)

10. G.B Function:
 Store and concentrate bile.
 Secrete glycoprotein and hydrogen ion.
 Contraction stimulated by CCK and vagus nerve and inhibited
by sympathetic stimulation, VIP, and somatostatin
Sphincter of oddi:
 Regulates bile flow, prevents back flow, and diverts bile into
G.B.
 Basal resting pressure of 13 mm Hg above duodenal pressure.
 CCK causes relaxation

11. P r o t o p o r p h y r in
H a e m G l o b i n
H a e m o g l o b i n
E r y t h r o p l a s t
A m i n o A c id
C O
B i l e
S t e r c o b i l i n o g e n
u r o b i l i n o g e n
B i l i r u b i n
g l u c u r o n i d e s
B i l i r u b i n
I r o n
T r a n s f e r r in
L i v e r
Bilirubin synthesis

12. Adult human produce 400 – 800 ml of bile
daily .
BILE SECRETION :
Occur in two stages :
1- Active secretion from hepatocytes to the
canaliculi , bile duct .
2- Modification in the bile duct through
addition of H2O & HCO3
During fasting state , bile will be stored in the
gallbladder .

13. Gallstones
Types of gallstone
– Cholesterol stones (20%)
– Pigment stones (5%)
– Mixed (75%)
Epidemiology
– Fat, Fair, Female, Fertile, Fourty inaccurate, but reminder
of the typical patient
– F:M = 2:1
– 10% of British women in their 40s have gallstones
– Genetic predisposition – ask about family history

14. Pathogenesis
Composition of bile:
– Bilirubin (by-product of haem degradation)
– Cholesterol (kept soluble by bile salts and lecithin)
– Bile salts/acids (cholic acid/chenodeoxycholic acid):
mostly reabsorbed in terminal ileum(entero-hepatic
circulation).
– Lecithin (increases solubility of cholesterol)
– Inorganic salts (sodium bicarbonate to keep bile alkaline
to neutralise gastric acid in duodenum)
– Water (makes up 97% of bile)

15. Pathogenesis
Cholesterol
– Imbalance between bile salts/lecithin and cholesterol allows cholesterol to
precipitate out of solution and form stones
Pigment
– Occur due to excess of circulating bile pigment (e.g. Heamolytic anaemia)
Mixed
– Same pathophysiology as cholesterol stones
Other Factors
– Stasis (e.g. Pregnancy)
– Ileal dysfunction (prevents re-absorption of bile salts)
– Obesity and hypercholesterolaemia

16. Complications of Gallstones
80% Asymptomatic
20% develop complications and do so
on recurrent basis

17. Complications of Gallstones

18. Complications of Gallstones
Biliary Colic
Acute Cholecystitis
– Gallbladder Empyema
– Gallbladder gangrene
– Gallbladder perforation
Obstructive Jaundice
Ascending Cholangitis
Pancreatitis
Gallstone Ileus (rare)

19. Gallstone ileus
Pathogenesis:
 Gallstone causing small bowel obstruction (usually obstructs in terminal ileum)
 Gallstone enters small bowel via cholecysto-duodenal fistula (not via CBD)
AXR – dilated small bowel loops
 May see stone if radio-opaque
Treatment
 NBM
 Fluid resuscitation + catheter
 NG tube
 Analgesia
 Surgery (will not settle with conservative management) – enterotomy +
removal of stone
Diagnosis of gallstone ileus usually made at the time of surgery.

20. Acute Biliary Pancreatitis
 Gallstones are the most
common cause of acute
pancreatitis (AP), a potentially
life-threatening condition,
worldwide.
 accounting for at least one half
of the 4.8-24.2 cases of
pancreatitis per 100,000
people that occur in Western
countries. About 80,000 cases
occur in the USA; 17 per
100,000 new cases.

21. Investigations for gallstone disease
 Bloods (already discussed)
 AXR (10% gallstones are radio-opaque)
 E-CXR (to exclude perforation – MUST!)
 ECG (to exclude MI)
 USS: first line investigation in gallstone disease
– Confirms presence of gallstones
– Gall bladder wall thickness (if thickened suggests cholecystitis)
– Biliary tree calibre (CBD/extrahepatic/intrahepatic) – if dilated suggests stone in CBD (normal CBD <8mm).
– Sometimes CBD stone can be seen.
 MRCP: To visualise biliary tree accurately (much more accurate than USS)
– Diagnostic only but non-invasive
– Look for biliary dilatation and any stones in biliary tree
 ERCP: Diagnostic and therepeutic in biliary obstruction
– Diagnostic and therepeutic but invasive
– Look for biliary tree dilatation and stones in biliary tree
– Stones can be extracted to unobstruct the biliary tree and perform sphincterotomy
– Risk of pancreatitis, duodenal perforation
 PTC
– To unobstruct biliary tree when ERCP has failed
– Invasive – higher complication rate than ERCP
 CT: Not first line investigation. Mainly used if suspicion of gallbladder empyema, gangrene, or
perforation and in acute pancreatitis (USS not good for looking at pancreas)

22. Treatment
 Symptomatic
– Laparoscopic cholecystectomy for symptomatic stones
– Open cholecystectomy, which involves a large
abdominal incision and direct exploration, is safe and
effective. Its overall mortality rate is about 0.1% when
done electively during a period free of complications.
 Asymptomatic
– For patients who decline surgery, or are at high risk of
surgical complications, but want to remove
asymptomatic stones; these gallstones can sometimes
be dissolved by ingesting bile acids orally for many
months.

23. Thanks