Benign biliary disease
Dr. Gili Halfteck
Department of General Surgury
Shaare Zedek Medical Center
January 2014
Anatomy
Calot’s triangle
Physiology
• Roles of bile secretion:
1. Excretion of toxins and cellular metabolites (bilirubin)
2. Lipids absorption
Components of bile:
1. Bile salts
2. Lipids (phospholipids and cholesterol)
3. proteins
4. pigments
Bile flow
Stimuli of bile secretion
1. Vagal activity
2. Secretin
3. CCK (bile secretion and gallbladder wall contraction)
• Fasting state:
- entero-hepatic circulation
- Accumulation of bile in the gallbladder
- Retrograde filling of the gallbladder - tonic activity of the
sphincter of Oddi
• Fed state:
- CCK (acid, fat and protein in duodenum)
- Vagal activity
Symptoms of biliary tree disease
• Pain
• Fever
• Juandice
Pain
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Biliary colic
Usually constant pain
Location: RUQ/epigatrium
Can be associated with meals (1 hour or more after a
meal)
• Caused by contraction of the gallbladder against an
obstructed neck
• Stasis + pressure + bacterial inoculum – infection and
inflammation (RUQ tenderness on palpation)
• Murphy’s sign
Fever
• Accompanies infection and inflammation of the gallbladder or
biliary tree
• Not present in biliary colic
Juandice
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Elevation of serum bilirubin
Surgical (obstruction) / medical (hepatocellular)
>2.5 mg/dl – scleral icterus
>5 mg/dl – cutaneous juandice
Pathogenesis: failure to excrete bile from the liver to the
intestine
• Charcot’s triade: fever, RUQ pain, juandice
• Reynold’s pentad: + hypotension and altered mental
status
Laboratory tests
• Bilirubin (conjugated/unconjugated)
• Alkaline phosphatase, GGT
• Serum transaminases (AST, ALT)
Imaging
1. US
• study of choice for initial evaluation of jaundice and
gallbladder or biliary disease
• Surgical/medical jaundice
• High sensitivity and specificity for gallstones
2. HIDA (hepatic iminodiacetic acid) scan
• Nuclear medicine test – demonstrated physiologic bile flow
but does not provide anatomic delineation
• Failure to fill the gallbladder 2 hours after injection – cystic
duct obstruction (cholecystitis)
• Obstruction of the biliary tree, bile leaks
3. CT scan
• Superior anatomic information
• Most gallstones are isodense to bile
• Identifies cause and site of biliary obstruction
• Preoperative planning in pancreatic/hepatic neoplastic processes
4. MRI/MRCP
• Superior anatomic definition of intra- and extrahepatic biliary tree
and pancreas
• Non-invasive
• No radiation exposure
5. ERCP (endoscopic retrograde cholangiopancreatography)
• Invasive test using endoscopy and fluoroscopy
• Contrast injection through the ampulla and imaging of the
biliary tree
• Able to diagnose and treat many biliary tree diseases
(choledocholithiasis, tissue sampleing, CBD stenting)
• Complication rate - 10%
Bacteriology
• Without previous biliary intervention bile is considered
sterile
• The presence of gallstones or obstruction and stasis
increases the likelihood of bacterial contamination
• Mostly gram-negative aerobes – passage of bacteria
upward from the duodenum into the biliary tree
• E. Coli, Klebsiella, Enterobacter, Enterococcus spp.
Gallstones
Types:
1. Mixed stones (70%) – cholesterol and calcium
2. Pure cholesterol stones (10%)
3. Pigment stones – brown/black (10%)
Gallstones formation:
- Supersaturation of bile
- Concentration of bile in the gallbladder
- Crystal nucleation
- Gallbladder dysmotility
Natural history of gallstones
• Vast majority are asymptomatic – incidentale finding
• Biliary colic – temporary obstruction of the cystic duct or
gallbladder neck
• 1% of patients with asymptomatic stones develop complications
before onset of symptoms - prophylactic cholecystectomy is not
warranted
• High risk patients:
- Hemolytic anemias
- Porcelain gallbladder
- Large (>2.5 cm) stones
- Long common channels of bile and pancreatic duct
- Bariatric surgery (sleeve, bypass)
- Immunocompromised patients
Non-operative treatment of cholelitiasis
• Generally unsuccessfull and rarely used!!!
- Oral dissolution
- Contact dissolution
- Shock-wave lithotripsy
• Up to 50% recurrence rate
Acute calculus cholecystitis
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Pathogenesis: unresolved cystic duct obstruction
Inflammation, edema, subserosal hemmorhage
Infection of stagnant bile pool
Can progress to ischemia and necrosis (gangrenous
cholecystitis)
Presentation:
Fever
RUQ pain
Tenderness to palpation
Laboratory finding: leukocytosis, mild elevation of bilirubin,
transaminases, alk-phos.
diagnosis
1. Transabdominal US
- sensitive, inexpensive and reliable
- Sensitivity – 85%, specificity – 95%
- Gallstones, gallbladder wall thickening, pericholic fluid,
sonographic murphy’s sign
2. Hida scan
- Atypical cases
- Cystic duct obstruction
3. CT scan
- Less sensitive then US
Treatment
• NPO
• IV fluids
• IV antibiotics (broad-spectrum)
• Pain control
• Cholecystectomy (open/lap.)
• Percutaneous cholecystostomy
Chronic cholecystitis
• Inflammation and scarring of the gallbladder neck and cystic
duct
• Pathogenesis: recurrent biliary colic which cause temporary
cystic obstruction and do not cause acute cholecystitis
• Presentation: recurrent biliary colic (usually after fatty meals),
nausea, vomiting
• RUQ/epigatric pain radiating to the scapula, usually resolves
within few hours
• Symptomatic cholelithiasis – indication for chlecystectomy
Diagnosis
• History
• Transabdominal US – stones, sludge
Treatment
• Elective cholecystectomy
• Curative in > 90% of patients
choledocholithiasis
1. Primary common duct stones
- De novo in the bile duct
- Usually brown pigment stones
- More common in Asian population
- Associated with bacterial bile duct infection
2. Secondary common duct stones
- Arising from the gallbladder
- Most common bile duct stones in the USA
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Retained common duct stones – found within 2 years of
cholecystectomy
Presentation
• 80-90% of common duct stones remain clinically silent
• Routine cholangiography – 10% choledocholithiasis
• Selective cholangiography (pain, abnormal liver function test)
– 1-2% of patients will present with retained stones
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Symptoms:
Biliary colic
Obstructive juandice
Ascending cholangitis (fever, pain, juandice)
Diagnosis
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Hepatic function panel abnormalities
Leukocytosis
US – choledocholithiasis, biliary ductal dilatation, gallstones
Bile duct dilatation (>8 mm) in the presence of biliary colic,
juandice or gall stones is suggestve of choledocholithiasis
• ERCP
- highly sensitive and specific
- Usually therapeutic
- Sphincterotomy, balloon stone extraction
- Complication rate – 5-8%
• MRCP
- highly sensitive and specific
- Does not provide therapeutic solution
treatment
1. ERCP
- Sphincterotomy and stone extraction
- Reasons for endoscopic failure: large stones, multiple stones,
intrahepatic stones, altered anatomy, duodenal diverticula,
impacted stones
- Does not eliminate the risk of recurrent biliary stone disease
(up to 50% recurrence)
2. Common bile duct exploration (lap./open)
- Intraoperative cholangiogram
- Trans-cystic/common duct incision
Ascending cholangitis
• Acute ascending bacterial infection of the biliary tree cause by
obstruction
• Obstruction: stones, malignancy
• Presentation: Charcot’s triad (fever, RUQ pain, jaundice),
Reynold’s pentad (+hypotension, altered mental status)
Diagnosis
• Tachycardia, shock symptoms
• Laboratory test: leukocytosis, abnormal liver panel
• US – dilatation of the biliary tree
• CT – site of obstruction
• ERCP/PTC – diagnostic as well as therapeutic
Treatment
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NPO
IV fluids
IV antibiotics
Most patients respond to medical therapy
• Emergent decompression of the biliary tree
(ERCP/PTC)
Questions?