Biliary - The Biliary Tract
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Biliary - The Biliary Tract

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  • 1420 AntonisBenevieni had the first published case of gallstones after an autopsy of a female patient died after complaining of abdominal pain where he found a grossly inflamed and gangrenous gallbladder filled with stones.In 1687 Stal Pert Von DerWiel while operating on a patient with purulent peritonitis accidentally found gallstones, but did not know what to do with them.In 1733 Jean Louis Petit suggested removal of gallstone and drainage of the gallbladder through a cutaneous fistula. His first successful surgery was in 1743, after several failed attempts. His rigid criteria of surgical intervention was modified over the years. It involved adhering the gallblader to the abdominal wall and introduction of an indwelling trochar to remove stones and bile. This continued until 1859 when JLW Thudichum proposed a two stage elective cholecystostomy.In the 1st stage, the inflamed gallblader was sewed to the anterior abdominal wall. The second stage infolved making a direct incision over that site and removing stones.In 1867, a gynecologist fron Indiana, Dr John StoughBobbs, while operating a patient with suspected ovarian cysts. Found a inflamed and adherant sac containing “bullet like structures”. He opened it and removed the stones, then closed it primairly and left it in the abdominal cavity. Thus the first recorded cholecystostomy. The patient recovered and actually outlived Dr Bobbs.
  • Dr’s Zambecari & Teckoff, independent of one another, determined through experiments on pigs and dogs, that the gallbladder was not essential to life.1878, Dr Kocher refined the cholecystostomy procedure.Dr Langenbuch, having observed the reports of Dr’s Kocher, Bobbs and Thudichum, observd that all these measures were only temporary andc rallied to find a definate solution to the disease.On july 15, 1882, at the age of only 27. Dr Langenbuch successfully removed the gallbladder of a 43 year old man who had been suffering from the disease for over 16 years.His initial report was ignored by the medical community. He continued with his work and tallied up a mortality report. By 1886, it showed that his procedure had only a 12% mortality vs a 27% mortality with the traditional cholecystotomy. Thus, his procedure became the gold standard.Fast forward to 1940 when Mirizzi introduced cholangiography.
  • Trocartertroise quarts describes a 3 faced perforator enclosed in a metal canula. Objects like this have been discovered in Roman ruins such as Pompeii. Dimitri—exam through posterior vaginal fornix. He wore a head mirror to reflect light.
  • “normal” anatomyThe gallbladder lies between segment 4 & 5.The cystic artery is a branch off the right hepatic artery, found in the triangle of calot (cystic duct-lateral, CBD medial & liver-superiorLymphatics are on the R side of the CBD.Parasympatheic fibers from the left (anterior) trunk of the vagus nerve.Sympathetic fibers from the T7-T10 nerves coursing through the splanchnic and celiac ganglions. Thus the shoulder pain.Multiple variations of the R hepatic artery—2nd most common is off the SMA in 17% population--ABSITE

Biliary - The Biliary Tract Biliary - The Biliary Tract Presentation Transcript

  • The Biliary Tract
    Raymond W Pryor III M.D.
    July 31, 2008
  • History
  • History
    Circa 200 AD – Galen – the gallbladder as a subsidiary organ for the liver & responsible for yellow bile
    Renaissance period – Gallbladder seat of many emotions (gall)
    1652 - Thomas Bartholin – gallbladder part of bile tract from liver to intestine
    1654 - Thomas Glisson – formed more detailed anatomy of liver & biliary tract
  • More relevant history
    1420 - Antonio Benevieni – 1st account of gallstones
    1687 - Stal Pert Von DerWiel – 1st operation on gallstones
    1733 – Jean-Louis Petit -1st successful removal of gallstones with fistula formation
    1859 – J.L.W. Thudichum – Two stage cholecystostomy
    July 15, 1867 – Dr John StoughBobbs – Single stage cholecystostomy
  • Still More relevant History
    1630 & 1667 – Zambecarri & Teckoff – proved the gall bladder not essential to life
    1878 - Theodor Kocher – refined cholecystostomy procedure
    July 15, 1882 – Dr Langenbuch – 1st open cholecystectomy
    1886 – cholecystotomy 27% mortality vs 12% mortality for Langenbuch’s cholecystectomy – became gold standard
    1940’s – Mirizzi introduced cholangiography for CBD stones
  • Into the Laparoscopic Age
    Trocar insertion 1st described by Ezekiel and Celsus – 25 BC – AD 50
    Term “Trocar” coined in 1706
    “trocartertroise-quarts”
    1901 Dimitri OH – gynaecologist, performed 1st endoscopic exam
    1911 – Dr Bernheim published “Organoscopy” in Annals of Surgery
    1938 Veress developed spring-loaded needle
  • Laparoscopic development
    1952 – quartz rod to project light
    1959 – closed circuit television
    1966 – Kurt Semm – automatic insufflator device, thermo coagulation, irrigation & aspiration system and endoloop applicator
    1978 – Dr Hasson – direct placement of trochar
    1982 – Liver biopsy via laparoscopy
    1987 – Dr Mouret – 1st laparoscopic cholecystectomy on human
    By 1989, procedure being done in US
    1992 – NIH concluded Laparoscopic cholecystectomy treatment of choice
  • Anatomy
  • Anatomy
  • Variations in Bile Ducts
  • Biliary Physiology
    Overall, the purpose is to modify, store and regulate the flow of bile
    The gallbladder concentrates & stores bile, then releases bile in response to a meal
    Biliary duct secretion of chloride-rich fluid controled by secretin, cholecystokinin (CCK) and gastrin.
  • Gallbladder physiology
    Gallbladder wall has no muscularis mucosa or submucosa
    Predominantly columnar epithelial cells
    Rokitansky-Aschoff sinuses
    Ducts of Luschka
  • Gallbladder physiology
    Normal capacity of 40-50 mL
    Liver secretes >600 mL of bile daily
    Gallbladder mucosa has greatest absorptive capacity per unit area of any structure in body
    Concentrates bile 5-10 fold
    NaCl transport by epithelium is driving force and water passively absorbed
  • Composition of Bile
  • Biliary Motility
    Filling is facilitated by contraction of ampullary sphincter (Sphincter of Otti)
    Goes through cycles of partial emptying of 10-15% of volume to mix & concentrate bile
    After meal, sphincter of Oddi relaxes & CCK released—causing contraction of gallbladder
    When stimulated, 50-70% of contents ejected over 30-40 minutes
    Refills over next 60-90 minutes
  • Bacteriology
    Under “normal” conditions, the biliary tract is sterile
    Positive cultures found:
    11-30% symptomatic stones & chronic cholecystitis
    46% of acute cholecystitis
    58% with gallstones & CBD stones without cholangitis
    94% with gallstones, CBD stones and cholangitis
  • Organisms
    Gram-negative aerobes most common
    E. coli
    Klebsiella
    Pseudomonas
    Enterobacter
    Gram-positive aerobes
    Enterococcus
    Streptococcus viridans
    Anaerobes (~25%)
    Bacteroidesfragilis
    Clostridium
    Fungal
    Candida sp.
    Parasitic
    Opisthorchis sp. (Thailand) (Liver fluke)
    Clonorchis sp. (China)
    Approximately 50% of positive cultures will have 2 or more different bacteria species present
  • Antibiotic Choice 2008 Sanford Guide
    Cholecystitis (E. coli, Klebsiella, Enterococci)
    meropenem (Merrem)
    piperacillin/tazobactam (Zosyn)
    cefepime (Maxipime)
    cefazolin + ampicillin (Ancef + ampicillin)
    ciprofloxacin + metrodazole (Cipro + Flagyl)
    Emphysematous Cholecystitis (Clostridium perfringens +/- E. coli)
    meropenem (Merrem)
    piperacillin/tazobactam (Zosyn)
    ertapenem (Invanz)
    ticarcillin./clavulanate (Timentin)
    Cholangitis
    meropenem (Merrem)
    cefepime (Maxipime)
    piperacillin/tazobactam (Zosyn)
    Tigecycline (Tygacil)
    ampicillin/sulbactam (Unasyn)
    imipenem/cilstatin (Primaxin)
    cefoperazone (Cefobid)
  • Antibiotics (cont’d)
    PO Treatment of cholecystitis or cholangitis
    clindamycin (Cleocin)
    ciprofloxacin + metronidazole (Cipro + Flagyl)
    levofloxacin (Levoquin)
    moxifloxacin (Avelox)
    Opisthorchis sp. & Clonorchis sp. (Liver fluke)
    praziquantel (Biltricide)
    albendazole (Albenza) **poor response to above organisms
  • Gallstones
  • Cholelithiasis
    Formation represents failure to maintain bile components (cholesterol, Ca, bile pigments) in a solubilized state
    Majority of those with stones are asymptomatic
    1-2% of asymptomatic individuals develop symptoms per year
    Approx 65% of asymptomatic patients remain symptom free after 20 years
  • Cholesterol Gallstones
    75% of all gallstones in United States
    3 stages of formation
    Cholesterol supersaturation
    Crystal nucleation
    Stone growth
    Risk factors
    Female
    Multi gravid
    Estrogen use
    Old age
    Obesity
    Rapid weight loss
    Prolonged TPN
  • Pigment gallstones
    25% of stones in US, 65% in Japan
    Black Pigment
    Made of Ca bilirubinate, bilirubin polymers & bile acids
    Increased concentration of bilirubin & Ca
    Hemolytic disorders & cirrhosis
    Chronic TPN
    Ileal resections
    Exact mechanism unclear, may be due to presence of bacterial b-glucuronidase that deconjugatesbilirubin
    Brown Pigment
    Asian populations
    Infection & bacterial hydrolysis of bilirubin
    More commonly found in bile ducts
  • Biliary Sludge
    Viscous bile
    Precursor to gallstone formation
    Associated with prolonged TPN and fasting
    Often found during ultrasound evaluation
    Usually asymptomatic
  • Is Everyone Still Awake?
  • Diagnosis of cholelithiasis
    Abdominal plain film
    rarely useful as 10-15% of stones radiopaque enough to be seen
    Ultrasound
    Non-invasive and cost-effective
    95-98% sensitive, 98% specific for documenting presence of gallstones
    80-95% sensitive, 78-80% specific for cholecystitis
    Operator dependant
    Radionuclide scan – hepatobiliaryiminodiacetic acid (HIDA)
    Good for detecting cystic duct obstruction or CBD obstruction
    Also very useful in determining bile leaks after cholecystectomy
    Acute cholecystitis: 94% sensitive, 65-85% specific
    Chronic cholecystitis: 65% sensitive, 6-10% specific
    Overall false positive (no filling of cystic duct or gallbladder) 15-20%
    This is lowered with administration of morphine to 2-5%
    CT scan
    Less sensitive than ultrasound for detecting stones (50-70%) or cholecystitis.
    More expensive
    MRCP
    Cost prohibitive
    Most often used to detect common bile duct obstruction
  • Ultrasound
  • More images
  • CT Scan
  • MRCP
  • MRCP with morphine
  • Chronic Calculous Cholecystitis
    Recurrent cystic duct obstruction & inflammation
    Presents with biliary colic
    Association with meals present in only 50%
    Symptoms
    Pain duration 1-5 hours (rare >24 hrs or <1 hr)
    Nausea & vomiting present 60-70% of time
    Bloating & belching in 50%
    Fever & jaundice rare
    Exam may be normal unless during attack
    Laboratory values usually normal
    Differentials include: GERD, PUD, IBS, pancreatitis
    Treatment is elective laparoscopic cholecystectomy
  • Chronic Calculous Cholecystitis
  • Xanthogranulomatous cholecystitis
    Variant of chronic cholecystitis
    lipid-laden inflammatory process comparable to xanthogranulomatouspyelonephritis
    Marked wall thickening with intramural nodules visible on CT and US
    Cannot distinguish radiographically from gallbladder carcinoma
  • Porcelain gallbladder
    Rare disorder where chronic cholecystitis causes mural calcification of gallbladder wall
    Cholecystectomy is warranted as there is a 30-65% risk of underlying gallbladder carcinoma
  • Acute Calculous Cholecystitis
    Related to gallstones 90-95% of cases
    Non-resolving obstruction of cystic duct usually triggering event
    Can lead to ischemia and necrosis of gallbladder wall in 5-18%
    46% will have positive bile cultures
    75% will have had previous, less severe, attack of biliary colic
    Symptoms:
    RUQ pain lasting hours to days
    Pain usually unremitting
    Nausea, vomiting, anorexia & fevers common
    Positive Murphy’s sign
    Elevated alkaline phosphatase & WBC
    Management:
    NPO and IV fluids
    Pain control (avoid narcotics if possible)
    Antibiotics
    Treatment is Laparoscopic cholecystectomy
    Delayed vs immediate
  • Acute Calculous Cholecystitis
  • Acute Acalculous Cholecystitis
    5-10% of all patients with acute cholecystitis
    occur in absence of stones
    Frequently progresses to gangrene, empyema or perforation
    Common following trauma, burns, long-term TPN, AAA repair or cardiac bypass
    Exact etiology unclear, but may be related to ischemia & stasis
    Symptoms similar to Acute Calculous cholecystitis
    HIDA scan has 40% false positive rate
    Emergency cholecystectomy or percutaneouscholecystostomy is treatment of choice
    Mortality as high as 40% in some studies, due to concomitant illnesses
  • Acute Acalculous Cholecystitis
  • Complications of cholecystitis
    Suppurative cholecystitis may lead to sepsis and shock
    Perforation in 3-10% of cases (most contained by surrounding structures)
    Emphysematous cholecystitis
    Most common in poorly controlled diabetics
    Usually caused by Clostridium perfringens
    Gas seen in gallbladder wall
  • Gallstone Ileus
    Large gallstone the obstructs small bowel (distal ileum at ileocecal valve)
    Fistula between gallbladder and duodenum (can be colon or stomach)
    Most commonly in elderly (>70) females
    History of gallstone-related symptoms present in only 50%
    Only account for <1% of SBO cases
    <0.1% of those with gallstones will develop
    Up to 25% of SBO in elderly patients who have not had previous abdominal surgery or have a hernia
    Treat with Ex-lap and enterotomy with removal of stone. Take back for takedown of biliary-enteric fistula & cholecystectomy when more stable
    On the ABSITE every year!!!
  • Gallstone Ileus
  • Intrahepatic Stones
    AKA Hepatolithiasis
    Most common in East Asian population
    Most associated with biliary strictures, primary sclerosing cholangitis, choledochal cysts & biliary tract tumors
    Spontaneous in <10% of cases
    Treatment depends on location & underlying condition(s)
  • Choledocholithiasis
    7-15% of patients undergoing cholecystectomy have CBD stones
    Findings of jaundice, lightening of stool & dark urine
    Fevers & elevated WBC indicate cholangitis
    Serum Bilirubin has PPV of 28-50%
    Biliary obstruction may be partial or transient, so labs may be normal in up to 30%
  • Choledocholithiasis (cont’d)
    May have overlying pancreatitis (up to 45% of all cases of pancreatitis)
    Dilated CBD in 58% of patients
    Ultrasound only 60-70% sensitive for CBD stones
    MRCP 95% sensitive & 89% specific
    ERCP Gold Standard
    Can both diagnose and treat 90% of time
    Pancreatitis occurs in up to 5% of Patients
    If unable to remove stone with ERCP (or none available) need to do laparoscopic or open CBD exploration
    Stone found in CBD within 2 years of cholecystectomy is termed retained, >2 years is recurrent
  • Cholangitis
    Acute bacterial infection of biliary tract
    Most common cause of biliary obstruction as often associated with choledocholithiasis
    Occurs in 4-7% of ERCP and PTC (Percutaneoustranshepaticcholangiography)
    Other causes of obstruction associated with cholangitis:
    Strictures, neoplasms (rare), chronic pancreatitis, congenital cysts, duodenal diverticula
    Presentation of fever, RUQ pain, jaundice
    Charcot’s triad
    May also have Hypotension & mental status change
    Reynold’s pentad
    Lab findings: Leukocytosis, elevated alkphos, AST, ALT, Bilirubin (direct)
    Blood cultures positive 40-50%
    CT scan or Ultrasound can help make diagnosis
  • Treatment of Cholangitis
    Immediate IV antibiotics and fluid resuscitation
    If no response within 24 hours (15%), or in those with toxic cholangitis, emergency biliary decompression necessary
    Endoscopic or percutaneous
    May need open CBD exploration & T-tube placement (higher mortality)
    Overall mortality 2% (5% with toxic cholangitis)
    On ABSITE every year
  • Primary Sclerosing Cholangitis
    Choleststic liver disease characterized by fibrotic strictures in the intrahepatic and extrahepatic biliary tree in ABSENCE of any known cause.
    Associated with HLA B8/DR3, IDDM, Graves’ Disease, Sjögren’s syndrome, & Myasthenia gravis
    Clinical presentation highly variable
    Jaundice, pruritus, fatigue, abnormal LFT’s
    Mean age 40-45 years
    Male : female 3:1
    Diagnosis by ERCP
    Median survival after diagnosis 10-12 years
    Primary treatment is liver transplantation
  • Sclerosing cholangitis
    Sclerosing cholangitis caused by stones, cholangitis or operative trauma termed Secondary sclerosing cholangitis
  • Choledochal cysts
    Rare congenital dilation of biliary tract
    1 : 150,000 incidence in Western countries
    Much more common in Japan
    Female : male 8:1
    Most often diagnosed in infancy
    Treatment is resection
  • Biliary Strictures & Bile duct injury
    80-90% caused by iatrogenic injuries
    Laparoscopic cholecystectomy most common
    Present days to weeks after surgery
    May be years after surgery as scar tissue obstructs duct
    Treatment is decompression, drainage, possible surgical resection.
    Stenting being used with increasing frequency
    With ligation of CBD & strictures, need Roux-en-Y hepaticojejunostomy
  • Gallbladder Cancer
    5th most common GI tract malignancy
    2-3 times more common in females
    75% over age 65
    5,000 new cases in US annualy
    Found incidentally in 1% to 3% of cholecystectomy specimens
    Majority of the time, diagnosed in late stages with distant mets
    Cholelithiasis present in 75-90% of cases
    Only 0.4% of those with gallstones develop cancer
  • Gallbladder Cancer
    Over 90% are adenocarcinoma
    60% scirrhous, 25% papillary, 15% mucoid
    Squamous cell, oat cell, undifferentiated, adenosquamous & carcinoid tumors less common
    Only 10% are correctly diagnosed preoperatively
    1-3 out of every 100 cholecystectomy specimens will show carcinoma at pathology
    At diagnosis:
    25% contained to gallbladder wall
    35% metastases to regional lymph nodes
    40% have metastasized to distant sites
    Average survival is 6 months after diagnosis
  • Lymphatic drainage & spread
    Initial drainage to cystic duct node
    Descents along CBD nodes
    Nodes at posterior head of pancreas
    Interaortocaval nodes
    Can also spread by direct invasion into liver
  • Gallbladder Cancer
    Most commonly presents with RUQ pain
    Weight loss, jaundice, palpable mass very late findings
    Many report change in quality or frequency of biliary colic episodes
    US sensitivity 70-99%
    CT approx 75% sensitive
    MRI 90-99% sensitive
  • Management & Prognosis
    Tumor confined to mucosa or submucosa (T1a) or to muscularis (T1b) have overall 5-year survival of 100% & 85%
    Spillage of bile during cholecystectomy can seed abdomen
    Invasion beyond muscularis (T2 & T3) need extended cholecystectomy with lymph node dissection
    Stage III has ~15% 5-year survival
    Stage IV has median survival of 1-3 months from diagnosis
    Majority of cases, therapy is palliative
    Chemo & radiation hot been shown to increase survival
    Survival following radical resection of T2 gallbladder cancer vssimple cholecystectomy
  • Cholangiocarcinoma
    Uncommon tumor anywhere along intrahepatic or extrahepatic biliary tree
    60-80% occur at bifurcation
    Most present with obstructive jaundice, hepatomegaly, palpable gallbladder (Courvoisier’s sign) or cirrhosis (advanced disease)
    2,500-3,000 new cases in US annualy
    Mean age in 50’s, men & women equal
    Increased risk with choledochal cysts, intrahepatic stones, Liver flukes, dietary nitrosamines & exposure to dioxin
    Following biliary-enteric anastomosis, 5% will develop
    Tend to spread by direct extension
  • Staging & classification
    Intrahepatic tumors (Klatskin tumors)treated like hepatocellular carcinoma (hepatectomy)
    Perihilar treated with resection with local hepatic resection
    Distal treated like periampullary tumors with pancreatoduodenectomy (Whipple)
    TNM staging
  • Diagnosis
    Intrahepatic easily visualized on CT scan
    Perihilar & distal tumors difficult to visualize on US and CT
    ERCP & MRCP have near equal sensitivity (85-95%)
    Most patients have serum Bilirubin >10, elevated AlkPhos & CA 19-9
  • Treatment
    Preoperative placement of stents in hepatic & hilar tumor
    Resected Left lobe & hilum with reconstruction
  • Prognosis
    Long-term survival highly dependant on stage & treatment
    For resectable intrahepatic tumors, overall 5-year 30-40%
    Resectable peri-hilar tumors 10-20%
    Resectable distal tumors 28-45%
    Median survival for all unresectable tumors is 6-7 months
  • Miscellaneous Biliary Pathologies
    Biliary atresia
    Most common cause of persistent jaundice in newborn
    Treat with hepatic portoenterostomy (Kasai procedure) or transplantation
    Hemobilia
    Most cases in US due to trauma or iatrogenic injury
    Diagnosis often requires arteriography
    Treatment of persistent hemobilia includes embolization or surgical ligation
    Benign polyps of gallbladder
    From cholesterol laden macrophages in mucosa
    Papilloma of bile duct
    Very rare, only ~90 cases in literature
  • Mirizzi Syndrome
    Rare cause of biliary duct obstruction
    Large stone contained within gallbladder compresses the CBD
    Local spread of inflammation from gallbladder to CBD may also result in duct narrowing
  • The End