This document discusses gallbladder diseases including gallstones, cholecystitis, choledocholithiasis, and cholangitis. It provides details on the anatomy and physiology of the biliary tract. The main types and risk factors for gallstone formation are described. Signs and symptoms, investigations, and management are outlined for various gallbladder disorders including cholesterol gallstones, acute cholecystitis, obstructive jaundice, ascending cholangitis, and gallstone ileus. Surgical and endoscopic treatment options are mentioned.

1. GALLBLADDER
DISEASES
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2. introduction
• Brief anatomy…….
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3. Normal Biliary Physiology
Liver produces 500-1500 mL of bile/day
Major physiologic role of biliary tract and GB is to
concentrate bile and conduct it in well-timed aliquots to the
intestine.
In the intestine:
bile acids participate in normal fat digestion
Cholesterol and other endogenous/exogenous compounds in bile
excreted in feces.
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4. Gallbladder disorders
• Gallstones
• Cholecystitis
• Choledocholithiasis
• cholangitis
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5. Gall stones
• Most common disorders
• Its unusual for the gallbladder to be diseased without gall stones
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6. • Types of gallstone
• Cholesterol stones (20%)
• Pigment stones (5%)
• Mixed (75%)
• Epidemiology
• Fat, Female, Fertile, Fourty inaccurate, but reminder of the typical patient
• F:M = 2:1 (18-65yrs of age)
• 10% of British women in their 40s have gallstones
• Genetic predisposition – ask about family history
Gallstones
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7. Cholesterol Stones
Cholesterol:
 Insoluble in water
 Normally carried in bile solubilized by bile acids and phospholipids
 In most individuals, bile contains > cholesterol than can be maintained in
stable solution
“supersaturated” with cholesterol  microscopic cholesterol crystals form
Interplay of nucleation (mucus, stasis) and “anti-nucleating” (apolipoprotein A-I)
factors determine whether cholesterol gall stones form
Gradual deposition of cholesterol layers 
 macroscopic cholesterol stones
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8. Cholesterol Stones
Gallbladder:
 key to stone formation
 Area of bile stasis  slow crystal growth
 Provides mucus or other material to act as a nidus for initiating cholesterol crystal.
 Mexican Americans and several American Indian tribes, particularly the Pima Indians in the
Southwest
high prevalence rates of cholesterol gallstones
↓bile acid secretion is believed to be the common denominator in these ethnic groups
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9. Risk factors for cholesterol gallstones
Increased secretion
• Elderly
• Female
• Pregnancy
• Obesity
• Rapid weight loss
Impaired gallbladder emptying
• Pregnancy
• Gallbladder stasis
• Fasting
• Total Parenteral Nutrition
• Spinal cord injury
Decreased bile secretion
• Pregnancy
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10. • 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)
Pathogenesis
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11.  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
Pathogenesis
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12. • 90% Asymptomatic
• 10% develop complications and do so on recurrent basis
• Biliary colic
• Acute cholecystitis
• Chronic cholecystitis
Clinical features
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13. • Blood tests
• Abdominal XR (10% gallstones are radio-opaque)
• CXR (to exclude perforation )
• 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
• 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)
Investigations for gallstone disease
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14. Management
• Not usually treated when asymptomatic
• Symptomatic gall stones best treated surgically
• Medical dissolution by use of ursodoxycholic acid (its a bile acid)
• ERCP(Endoscopic retrograde cholangiopancreatography)
 Dissolve cholesterol stones:
Instill Methyl-tert-butyl-ether or ethyl propionate into GB
 Fragment stones:
extracorporeal shock wave lithotripsy
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15. • Biliary Colic
• Acute Cholecystitis
• Gallbladder Empyema
• Gallbladder gangrene
• Gallbladder perforation
• Obstructive Jaundice
• Ascending Cholangitis
• Pancreatitis
• Gallstone Ileus (rare)
• Fistula formation
• Pressure on or inflammation of the common bile duct (Mirizzi’s syndrome)
• Cancer of the gall bladder
Complications
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16. Pathogenesis
 Stone intermittently obstructing cystic duct (causing pain) and then dropping
back into gallbladder (pain subsides)
USS confirms presence of gallstones
Treatment
 antibiotics
 Analgesia (opiates, ketorolac, indomethacin)
 Fluid resuscitation if vomiting-antiemetics like metoclopramide,
prochlorperazine
 If pain and vomiting subside does not need admitting
Biliary Colic
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17. Pathogenesis:
• Due to obstruction of the gallbladder neck or cystic duct by gallstone:
• Cystic duct blockage by gallstone
• Obstruction to secretion of bile from gallbladder
• Bile becomes concentrated
• Chemical inflammation initially
• Secondarily infected by organisms released by liver into bile stream
• Obstruction by mucus, parasitic worms or tumors
Clinical features
• Pain in the right upper quadrant and also in the epigastric area, right shoulder tip or in the
interscapular region
• Examination shows right hypochondriac tenderness, rigidity worst on inspiration (Murphy’s sign) and
occassional gallbladder mass
• Fever
• Leucocytosis
• Jaundice
• Elevated transaminase
Acute Cholecystitis
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18. Investigations and treatment
USS confirms diagnosis (gallstones, thickened gallbladder wall, peri-cholecystic fluid)
CBC = leucocytosis
Plain radiograph = radio opage gallstones
Serum amylase or lipase= pancreatitis
Treatment
• Admit for monitoring
• Bed rest
• Analgesia (diclofenac, pethedine, morphine)
• Clear fluids initially, then build up oral intake as cholecystitis settles
• IVF
• Antibiotics (cephalosporin plus metronidazole)
• 95% settle with above management
• If do not settle then for CT scan
• Empyema  percutaneous drainage
• Gangrene/perforation with generalised peritonitis emergency
Surgery
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19. Complications of acute cholecystitis
•Empyema of gallbaldder
•Gangrene of gallbladder (rare)
•Perforation ofgallbaldder (rare)
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20. Pathogenesis:
• Stone obstructing CBD (bear in mind there are other causes for obstructive jaundice) – danger is progression to ascending cholangitis.
• USS
• Will confirm gallstones in the gallbladder
• CBD dilatation i.e. >8mm (not always!)
• May visualise stone in CBD (most often does not)
• MRCP
• In cases where suspect stone in CBD but USS indeterminate
• E.g.1 obstructive LFTs but USS shows no biliary dilatation and no stone in CBD
• E.g. 2 normal LFTS but USS shows biliary dilatation
• ERCP
• If confirmed stone in CBD on USS or MRCP proceed to ERCP which will confirm this (diagnostic) and allow extraction of stones and sphincterotomy (therepeutic)
Treatment
• Must unobstruct biliary tree with ERCP to prevent progression to ascending cholangitis
• Whilst awaiting ERCP monitor for signs of sepsis suggestive of cholangitis
Obstructive Jaundice
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21. Pathogenesis:
• Stone obstructing CBD with infection/pus proximal to the blockage
Charcoat’s traid= RUQ pain, Chills and Fever , Jaundice
Treatment
• ABC
• Fluid resuscitation (clear fuids and IVF, catheter)
• Antibiotics (Augmentin)
• HDU/ITU if unwell/septic shock
• Pus must be drained* - this is done by decompressing the biliary tree
• Urgent ERCP
• Urgent PTC – if ERCP unavailable or unsuccessful (percutaneous transhepatic cholangiography)
Ascending Cholangitis
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22. 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-nil by mouth
• 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.
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23. Choledocholthiasis
• Stones in the common bile duct
• Follows bacterial infection secondary to parasitic infections with
clonorchis senensis, ascaris lumbricoides or fasciola hepatica
Clinical features
• Asymptomatic
• RUQ abdominal pain
• Pruritus and dark urine may be present
• Fever and rigors
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24. Management
• Analgesics
• Fluids
• Antibiotics
• Surgery
• Endocospic sphinteretomy via ERCP
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