A 95 year-old woman presented with upper abdominal pain and jaundice; ultrasound demonstrated gallstones. Symptoms were short in duration, and jaundice began to clear rapidly. In view of her age and improving condition, she was treated conservatively for cholecystitis. However, she then developed protracted vomiting; endoscopy demonstrated several stones in the duodenum.

What is the most likely cause this type of complication?

a. Malignancy extending into duodenumb. Perforation of gallbladderc. Carolis syndromed. Metastasis from another primary tumor

Diseases of the Gallbladder and Biliary TractDriss Raissi, MDNew York State UniversityDownstate Lecture Series

Normal Biliary PhysiologyLiver produces 500-1500 mL of bile/dayMajor 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 digestionCholesterol and other endogenous/exogenous cmpds in bile excreted in feces.

Biliary PhysiologyComplex fluid secreted by hepatocytes

Passes through hepatic bile ducts into common hepatic duct

Tonic contraction of sphincter of Oddi during fasting diverts ~1/2 of bile through the cystic duct into the GB stored and concentrated.

CCK released after food ingestion GB contracts, sphincter of Oddi relaxesAllows delivery of timed bolus of bile into intestine.

Bile acids detergent moleculesHave both fat and water soluble moietiesConvey phospholipids and cholesterol from liver to intestine Cholesterol undergoes fecal excretion

Enterohepatic circulationBile acids solubilize dietary fat and promote its digestion and absorption

Enterohepatic circulation:Bile acids efficiently reabsorbed by SI mucosa (terminal ileum) recycled to liver for re-excretion

Cholelithiasis

Normal Gallbladder

Velvety green mucosa

Thin wall

Tall columnar cells lining mucosal folds (right)

Submucosa and muscularis at the left.

CholelithiasisGallstones:MCC biliary tract disease in US (20-35% by age 75)

2 types:Cholesterol (75%)Pigment Calcium bilirubinate and other calcium salts

Cholesterol StonesCholesterol: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 solutionsupersaturated with cholesterol microscopic cholesterol crystals formInterplay of nucleation (mucus, stasis) and anti-nucleating (apolipoprotein A-I) factors determine whether cholesterol gall stones formGradual deposition of cholesterol layers macroscopic cholesterol stones

Cholesterol StonesGallbladder:

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 Southwesthigh prevalence rates of cholesterol gallstonesbile acid secretion is believed to be the common denominator in these ethnic groups

Pigment stonesPathophysiology less well understood production of bilirubin conjugates (hemolytic states) biliary Ca2+ and CO32- CirrhosisBacterial deconjugation of bilirubin to less soluble form

Predisposing FactorsFactors that increase biliary cholesterol saturation:EstrogensMultiparityOCPsObesityRapid weight lossTerminal ileal disease (decreases bile acid pool)

Factors that increase bile stasis:Bile duct stricturesParenteral hyperalimentationFastingCholedochal cystsPregnancy (GB hypomotility)

Clinical ManifestationsMost are asymptomaticDuct obstruction - underlying cause of all manifestationsCystic duct obstruction distends GB biliary pain Superimposed inflamm/ifx acute cholecystitisCommon duct obstruction pain, jaundice, ifx(cholangitis), pancreatitis, and/or hepatic damage 2 to biliary cirrhosis

Asymptomatic Gallstones60-80% patients with gallstones in USOver 20-year period:18% of these develop biliary pain3% require cholecystectomy

Prophylactic cholecystectomy considered in 3 high-risk groups:1. Diabetics 10-15% greater mortality2. Calcified (porcelain) GB Associated w/CA of GB3. Sickle cell anemia hepatic crisis difficult to differentiate vs. acute cholecystitis

Porcelain Gallbladder

Treatment of Asx GallstonesChenodeoxycholic acid or Ursodeoxycholic acidDissolution of cholesterol stones

Expectant management then cholecystectomy if symptomatic disease develops = more cost effective

Alternatives:Dissove cholesterol stones: Instill Methyl-tert-butyl-ether or ethyl propionate into GBFragment stones:extracorporeal shock wave lithotripsy

Extracorporeal Shockwave Lithotripsy

Chronic Cholecystitis and Biliary PainNonacute sx. caused by presence of gallstonesBiliary Pain (misnamed biliary colic)GB from symptomatic patients may be grossly normal Mild histologic inflammation with fibrosis and thickening often from previous attacks of acute cholecystitis.

Symptoms:From contraction of GB during transient obstruction of cystic duct by gallstones.Steady ache in epigastrium or RUQ comes on quickly plateau over a few minutes subsides gradually over 30 min-several hoursReferred pain at tip of scapula or right shoulderN/V can accompany. (no fever, leukocytosis, or palpable mass)Attacks occur at variable intervals (days years)Nonspecific symptoms: Dyspepsia, fatty food intolerance, bloating and flatulence, heartburn, belching

DiagnosisUltrasonographySensitivity and specificity >95%

Oral cholecystograpy90% sensitivity, 75% specificityReserved for ensuring cystic duct patency in pts whom dissolution therapy or extracorporeal shock wave lithotripsy is planned

TreatmentLaparoscopic cholecystectomyTreatment of choice for recurrent biliary painMay need preoperative endoscopic or radiologic examination of CBD for concomitant choledocholithiasis

Open cholecystectomyMortality rate

Acute Cholecystitis

Acute Cholecystitis Acute right subcostal pain and tenderness from obstruction of cystic duct Distension, inflammation, and 2 ifx of GB

Acalculous cholecystitis (5%) Triad - Prolonged fasting, immobility, hemodynamic instabilityCritically ill patients (burns, trauma, sepsis)Parenteral hyperalimentation

Acute CholecystitisEpigastric or RUQ painGradually in severity and localizes to GB areaUnlike biliary pain, does not spontaneously resolveLow grade fever, anorexia, n/v, right subcostal tenderness(+)Murphys signsubhepatic tenderness and inspiratory arrest during deep breathTender enlarged gallbladder (1/3)Mild jaundice (20%) concomitant CBD stones or BD edema

Murphys Sign

Complications Onset of fever, shaking chills, leukocytosis, abdominal pain or tenderness, or persistent severe symptoms =progression of disease and development of complications

Emphysematous cholecystitis Diabetics with bacterial gas present in GB lumen and wallEmpyema of gallbladderGangrenePerforationMirizzis syndromeProfound jaundice in which extrinsic CBD compression occurs from impacted stone in GB neck

EmphysematousCholecystitis

Diagnosis Acute CholecystitisRadionuclide scanning after administration of 99mTc-DISIDA or HIDAMost accurate test to confirm cystic duct obstructionIf GB fills with isotope acute cholecystitis unlikelyIf bile duct visualized but gallbladder not Clinical diagnosis strongly supported

Images taken shortly after injection of the radiolabeled tracer. Gallbladder (black spot) fills as radioactive material is secreted into bile and floods in. Images after gallbladder filled.Emptying stimulated by an injection of CCKEnlarging black streak representing the CBD appears below the gallbladder. As streak becomes visible, black spot representing the GB in size and almost disappears as bile is squeezed into the small intestine.

Diagnosis Acute CholecystitisUltrasonagraphy:Gallstones (or sludge in acalculous) along with localized tenderness over the GB, pericholecystic fluid, and GB wall thickening strong supportive evidence for acute cholecystitis

Oral cholecystograms = no clinical use Unreliable in acutely ill patient

Management of Acute CholecystitisPatients may improve over 1-7 days with expectant managementNG suction for profound vomiting, and/or abdominal distensionIV fluids, ABX, and analgesics

CholecystectomyBecause of high risk of recurrent acute cholecystitisWithin first 24-48 hours after acute episodeEmergency surgery if advanced disease and complications, usually associated with infection and sepsis.

Cholecystostomy (operative or percutaneous)Alternative to cholecystectomy in patients with high operative risk

PrognosisMortality of acute cholecystitis = 5-10%Almost entirely confined to patients >60 with serious associated diseases and those with supparative complications

ComplicationsInfectionCholecystoenteric fistula results in gallstone ileus.

Choledocholithiasis and Cholangitis

Choledocholithiasis & Acute Cholangitis~15% of pts with gallstones have CBD stones (choledocholithiasis)CD stones usually originate from GBLess commonly stones form de novo in the biliary treeInternational incidence rate higher b/c primary CBD stones caused by parasitesAsians Ascaris lumbricoides and Clonorchis sinensis

Biliary tract lithiasis most often begins with a calculus (stone) in the gallbladder.

A small enough calculus (or part of a calculus) may become impacted in the neck of the gallbladder or cystic duct acute cholecystitis.

The stone may travel further down into the common bile duct, and impaction in this duct (choledocholithiasis) may produce obstruction with jaundice.

The stone may travel further down and, near the ampulla, obstruct the pancreatic duct, leading to acute pancreatitis.

The stone may pass through the ampulla and out into the duodenum.

Symptoms and SignsBiliary colicFrom rapid in CBD pressure due to obstructed bile flow

Charcots Triad = classic cholangitis1. RUQ pain frequently recurring, severe, persists for several hours2. Chills and Fever - associated with severe colic3. Jaundice - associated with abdominal pain

Hepatomegaly in calculous biliary obstruction

Tenderness RUQ and epigastrium

Pain = MC presenting symptomcolicky in nature, moderate in severity, and located in the RUQintermittent, transient, and recurrent and may be associated with nausea and vomiting.

Jaundice CBD becomes obstructed and conjugated bilirubin enters the bloodstream. History of clay-colored stools and tea-colored urine is obtained from such patients in approximately 50%The jaundice can be episodic.

Fever Indication of cholangitisCharcot triad: fever, jaundice, and RUQ pain strongly favors the diagnosis.

Pancreatitis Gallstones are responsible for 50% of all casesConversely, 4-8% of patients with gallstones develop pancreatitis. Pancreatitis can be precipitated if CBD obstruction occurs at the level of the ampulla of Vater.

Presentation of Choledocholithiasis

Primary CBD StonesCaused by conditions leading to bile stasis and chronic bactibilia.

Up to 90% of patients with brown pigment CBD stones have (+) bile culture results Usually brown pigment stones. Brown stones differ from black pigment stones by having a higher content of cholesterol. Brown stones are soft and earthy in consistency and take the shape of the duct.

In Western populations, biliary stasis is secondary to factors such as:sphincter of Oddi dysfunction, benign biliary strictures, sclerosing cholangitis, and cystic dilatation of the bile ducts.

In Asian populations, A lumbricoides and C sinensis promote stasis:Either blocking the biliary ducts or by damaging the duct wallsResults in stricture formation. Bactibilia is also common in these instances, probably secondary to episodic portal bacteremia.

Secondary CBD Stones

Arise from the gallbladder migrate to the CBDHave a typical spectrum of cholesterol stones and black pigment stones. Bacteria can be cultured from the surface of cholesterol and pigment stones but not from the core, suggesting that bacteria do not play a role in their formation.

Laboratory Diagnosis WBC nonspecific. Serum and urine bilirubin - indicate obstruction of the CBDthe higher the bilirubin level, the greater the predictive value. CBD stones are present in approximately 60% of patients with serum bilirubin levels greater than 3 mg/dL. Serum amylase and lipase acute pancreatitis complicating choledocholithiasis. Alkaline phosphatase and gamma-glutamyl transpeptidase obstructive choledocholithiasisgood predictive value for the presence of CBD stones. Prothrombin time In prolonged CBD obstruction, secondary to depletion of vitamin K (the absorption of which is bile-dependent). Liver transaminases choledocholithiasis complicated by cholangitis, pancreatitis, or both.Blood culture positive in 30-60% of patients with cholangitis.

Preoperative DiagnosisTransabdominal ultrasonography It is usually the first modality used in the diagnosis of patients with biliary-related symptoms. Ultrasonography findings are accurate in the diagnosis of gallbladder stones, but CBD stones are missed frequently (sensitivity 15-40%). On the other hand, CBD dilatation is identified accurately, with up to 90% accuracy.

Endoscopic ultrasonography Introduction of a high-frequency (7.5-12 MHz) ultrasonic probe advanced into the duodenum under endoscopic guidance. A water-filled balloon is used to provide an acoustic window. Sensitivity and specificity of CBD stone detection are reported in range of 85-100%. Invasive, $$$, need experienced enoscopist/ultrasonographer

Computed tomography scan very accurate in the detection of biliary tree obstruction and ductal dilatationsensitivity of 75-90% in the detection of CBD stones = essential in evaluation of jaundice. Capable of defining the level of the obstruction and provides information about the surrounding structures, especially the pancreas.

MRCP noninvasive tool with 97% accuracy, 92% sensitivity, and 100% specificity. $$$, inconvenience, and limitations (eg, obesity, presence of metal objects, eg, pacemakers)

Endoscopic Ultrasound (EUS)

MRCP

Cholangiography

Criterion standard for the detection of CBD stonesEndoscopic Retrograde Cholangiopancreatography (ERCP)The CBD is cannulated through the ampulla, contrast injected, and films are obtained. Experience of the endoscopist is best predictor of success, (90-95% in expert hands)Complications = hyperamylasemia and cholangitis.

Percutaneous Transhepatic Cholangiography (PTC) may be the modality of choice in patients in whom ERCP is difficult (eg, previous gastric surgery)percutaneously and transhepatically into an intrahepatic duct, and cholangiography is performed.

ComplicationsBiliary Cirrhosis:CBD obstruction >30 days liver damage cirrhosis

Hypoprothrombinemia:Pts may bleed excessively d/t PTResponds to 10mg parenteral vitamin K or water soluble oral vitamin K within 24-36h.

Treatment of CholedocholithiasisCBD stone in pt with cholelithiasis and cholecystitis:endoscopic papillotomy and stone extraction followed by laparoscopic cholecystectomy.

ERCP before cholecystectomy in patients with:Gallstones and jaundice (serum bili >2 mg/dL)Dilated CBD (>7mm)Stones in bile duct seen on ultrasound or CT

Primary Biliary Cirrhosis

Primary Biliary CirrhosisChronic disease of liver with autoimmune destruction of intrahepatic bile ducts and cholestasis

Insidious onsetOften detected by chance finding of Alkaline Phosphatase

Women aged 40-60

Disease is progressive and complicated by:Steatorrhea, xanthomas, xanthelasma, osteoporosis, osteomalacia, and portal hypertension

Associated with Sjgrens syndrome, scleroderma, hypothyroidism, and celiac disease

Infection with Chlamydia pneumoniae may be trigger or causative agent

Xanthoma in PBC

Clinical FindingsMany asymptomatic for years

Fatigue and pruritis

Hepatomegaly with progression

Xanthomatous lesionsIn skin and tendons and around eyelids

Jaundice and signs of portal HTN (late)

Risk of osteoporosis increased

Laboratory findings in PBCSigns of cholestasisAlkPhos, cholesterol (HDL), later bilirubin

Anti-mitochondrial Antibodies (95%)Directed against PDH in mitochondria

Serum IgM

Diagnosis of PBCBased on cholestatic liver chemistries and anti-mitochondrial antibodies in serum combined with characteristic histology in liver biopsy

Liver biopsyPermits histologic stagingStage I: Portal inflammation with granulomasStage II: Bile duct proliferationStage III: Interlobular fibrous septaStage IV: Cirrhosis

Biliary Fibrosis Portal area with marked ductular proliferation and minimal inflammation in a case of chronic biliary obstruction.

Treatment of PBCUrsodeoxycholic Acid Preferred medical treatmentslows progression, improves long-term survival, risk of esophageal varices

Symptomatic TreatmentCholestyramine or Colestipol - for pruritisCan aggravate steatorrha leading to vitamin A,D,K deficiencyRifampin inconsistently beneficialOpiod antagonistsNaloxone, naltrexone show promise for treating pruritis5-HT3 antagonistsOndansetron Calcium supplementationHelps prevent osteomalcia

Colchicine and MethotrexateSome benefit improving symptoms and serum levels of AP

Liver transplantTreatment of choice for advanced disease

Prognosis of PBCWithout transplant, survival = 7-10 years once symptoms developAdverse prognostic indicators:Older ageHigh serum bilirubinEdemaLow serum albuminProlonged PTVariceal hemorrhage

The Mayo risk score: R = 0.871 loge (bilirubin in mg/dL) + (2.53) loge (albumin in g/dL) + 0.039 age in years + 2.38 loge(prothrombin time in seconds) + 0.859 (edema score of 0, 0.5, or 1)

Primary Sclerosing Cholangitis

Primary Sclerosing CholangitisUncommon disease characterized by diffuse inflammation of biliary tract leading to fibrosis and strictures of biliary system.

Most common in men age 20-40 and closely associated with ulcerative colitis (present in ~2/3 of pts with PSC)Only 1-4% of patients with UC develop PSC.Like UC, smoking is associated with a risk of PSC

Associated with HLA-B8 and DR3 or DR4

ANCA (70%), with fluorescent staining characteristics and target antigens distinct from those in Wegeners

In AIDS, PSC may result from infections caused by CMV, cryptosporidium, or microsporum.

PSC is usually progressive, leading to cirrhosis, portal hypertension, and liver failure.

Symptoms and SignsProgressive obstructive jaundiceFrequently associated with malaise, pruritus, anorexia, and indigestion.

Complications of chronic cholestasisOsteoporosis Malabsorption of fat soluble vitamins

Laboratory Diagnosis of PSCAP or GGT MC abnormality

Serum transaminases can be normal or

serum bilirubinin advanced PSC

Hepatic synthetic tests (albumin, PT, etc) abnormal in advanced PSC

Serum cholylglycine (bile salt)out of proportion to the elevation of serum bilirubin.

p-ANCAsin 60-82% of patients with PSC. (Frequency in UC is similar.)

CA 19-9 level greater than 100 U/mL has 75% sensitivity and 80% specificity in identifying PSC patients with cholangiocarcinoma.

Imaging Diagnosis of PSCERCP Cholangiography remains criterion standardCholangiography remains the criterion standard for establishing the diagnosis of PSC.irregularly distributed, multifocal strictures and dilatations of the intrahepatic and extrahepatic bile ducts = beading

MRCPNoninvasive, but less sensitive (90%) than ERCP(97%) for visualizing intrahepatic ducts

Imaging of PSCThe radiographic pattern of PSC is that of strictures of varying lengths in the intrahepatic and extrahepatic ducts.

There may intervening areas of minimal dilatation of the ducts with a resulting "beaded" appearance.

Usually there are multiple areas of involvement. In this case almost all of the visualized ducts are abnormal in contour.

ERCPERCP image shows multifocal strictures and irregularity of the right intrahepatic bile ducts.

Treatment of PSCNo effective medical therapies existCiprofloxacinEpisodes of acute bacterial cholangitisUrsodeoxycholic acid (UDCA) improves symptoms and LFTs in adult patients with PSC.

ERCPBalloon dilation of localized strictures. Repeated procedures improves survival.If major stricture short term stent relieves symptoms and improves LFTs

Surgical resectionIn patients without cirrhosis, resection of dominant bile duct stricture may improve survival vs. ERCP because of risk cholangiocarcinoma.

Prognosis of PSCAverages 10 years once symptoms appearAdverse prognostic markers:Older ageHigher serum bilirubin and ASTLower albumin levelsHistory of variceal bleeding

Complications:Cholangiocarcinoma (10-15%) of adults with PSC. Colon CA/dysplasia In patients with ulcerative colitis, PSC is independent risk factorStrict adherence to colonoscopic surveillance program avised

Neoplasms in the Biliary Tract

Carcinomas of Biliary TractManifestationsweight loss (77%)nausea (60%)anorexia (56%)abdominal pain (56%)fatigue (63%)pruritus (51%)fever (21%)malaise (19%) diarrhea (19%)constipation (16%)abdominal fullness (16%)Symptomatic patients usually have advanced disease, with spread to hilar lymph nodes before obstructive jaundice occurs.

It is associated with a poor prognosis.

Carcinoma of the GallbladderUncommon malignancy 2.5/100,000

Most common of biliary tract cancers (54%)

>90% are adenocarcinomas

In Native Americans, GB carcinoma is the most commonly seen GI malignancy

Male:Female = 1:3

Overall mean survival rate = 6 months, 5-year survival rate is 5%

At diagnosis, most of the GB is replaced or destroyed by the cancer

Risk Factors for GB CancerCholelithiasis often large and symptomatic stones presentChronic infection of gallbladderSalmonella TyphiGenetic FactorsGB polyps >1cm in diameterMucosal calcification of GB (Porcelain GB) carcinoma in 25% Anomalous pancreaticobiliary ductal junctionCongenital biliary cystsEnvironmental carcinogens

Anabolic SteroidsNo hablo ingles!

Baseball be very good to meI'm not a crazy person. I'm not stupid.

Symptoms and SignsJaundice skin or icteric sclerae

Early Pain in RUQ with radiation into back

Anorexia, weight loss, fever and chills (cholangitis), supraclavicular LN

Courvoisiers Law Palpable GB with obstructive jaundice signifies malignant diseaseThis generalization accurate only 50% of time

HepatomegalyUsually present and associated with liver tenderness

Ascites Can occur with peritoneal implants

Hematemesis or melenaFrom erosion of tumor into blood vessel (hemobilia)

Carcinoma of GallbladderLocation: fundus (60%), body (30%), neck (10%)

Notoriously insidiousDiagnosis made incidently at surgery

Spread Early lymphatic spread retroperitoneal, right celiac, and pancreaticoduodenal nodes. Direct invasion of the liver, extrahepatic biliary ducts, and duodenum and colon (less common) occurs. Intraperitoneal seeding may occur.

TNM StagingTis = Carcinoma in situ

T1a = GB wall: invades lamina propriaT1b = GB wall: invades muscle layer

T2 = Perimuscular connective tissue

T3 = Perforates serosa or directly invades liver or adjacent organ

T4 = Invades main portal vein or hepatic artery or multiple organs

N1a = Hepatoduodenal ligament nodesN1b = Other regional lymph nodes

M0 = No distant metastasesM1= Distant metastasesStage 0: Tis N0 M0

Stage I: T1 N0 M0

Stage II: T2 N0 M0

Stage III: T1-2 N1 M0 T3 N0-1 M0

Stage IVA: T4 N0-1 M0

Stage IVB: T1-4 N2 M0 T1-4 N0-2 M1

Carcinoma of Bile Ducts (Cholangiocarcinoma)Tumor that arises from the intrahepatic or extrahepatic biliary epithelium

3% of all cancer deaths in the US

> 90% are adenocarcinomas, remainder are squamous cell CA

3 Geographic Locations:Intrahepatic Least commonExtrahepatic (ie, perihilar)Perihilar (Klatskin tumors) = Most commonAt bifurcation of R and L hepatic ducts

Distal extrahepaticUpper border of pancreas ampulla

The etiology of most bile duct cancers remains undetermined.

Possible EtiologiesInfectionsIn SE Asia, chronic infx with liver flukesClonorchis sinensis, Opisthorchis viverrini and Fasciola Hepatica

Inflammatory bowel diseaseCCC generally develops in patients with long-standing ulcerative colitis and PSC.

Chemical exposuresprimarily among workers in the aircraft, rubber, and wood finishing industries.Thorotrast

Congenital diseases of the biliary tree choledochal cysts and Caroli disease

Pathophysiology of CCCLong-standing inflammation as with PSC, chronic parasitic infection suggested to play a role by inducing hyperplasia cellular proliferation malignant transformation.

Grow slowly and infiltrate walls of the ducts, dissecting along tissue planes

Local extension: liver, porta hepatis, regional LN of the celiac and pancreaticoduodenal chains.

Symptoms and SignsProgressive jaundice MC manifestation of bile duct cancer The obstruction and subsequent cholestasis tends to occur early if the tumor is located in the common bile duct or common hepatic duct.Jaundice often occurs later in perihilar or intrahepatic tumors and is often a marker of advanced disease. The excess of conjugated bilirubin is associated with bilirubinuria and clay colored stools.

Pruritus usually is preceded by jaundice, but itching may be the initial symptom of CCC. related to circulating bile acids.

Weight loss

Abdominal pain common in advanced disease and often is described as a dull ache in the RUQ

Courvoisiers SignIf CCC located distal to the cystic duct takeoff the patient may have a palpable gallbladder, (Courvoisier sign)

Laboratory ExaminationBiliary Neoplasms Conjugated BilirubinTotal serum bilirubin from 5-30mg/dL

Alkaline Phosphatase and GGT

Serum Cholesterol

ASTnormal or mildly elevated

CA 19-9If elevated may help distinguish CCC from benign biliary stricture

Imaging in Biliary NeoplasmsUltrasonagraphy and CT:Show GB mass in GB CarcinomaIntrahepatic masses or biliary duct dilationCT also shows involved regional LN

MRI with MRCPVisualization of biliary treeDetection of vascular invasion

Positron Emission Tomography (PET)Can detect CCC as small as 1cm

The most helpful diagnostic studies before surgery are either PTC or ERCP with biopsy and cytology

Treatment of Biliary NeoplasmsCurative Surgery (Gallbladder CA)May be attempted in young and fit pts if tumor is well localized.5 year survival for localized (stage 1, T1a, N0, M0) is as high as 80% with laparoscopic cholecystectomyOnly 15% if muscular invasion (T1b)If tumor unresectable at laparotomyCholecystoduodenostomy or T-tube drainage of CBD

Curative Surgery (CCC)Curable in 12 months after surgery

A 95 year-old woman presented with upper abdominal pain and jaundice; ultrasound demonstrated gallstones. Symptoms were short in duration, and jaundice began to clear rapidly. In view of her age and improving condition, she was treated conservatively for cholecystitis. However, she then developed protracted vomiting; endoscopy demonstrated several stones in the duodenum.

What is the most likely cause this type of complication?

a. Malignancy extending into duodenumb. Perforation of gallbladderc. Carolis syndromed. Metastasis from another primary tumor

AnswerB. This stone could not be removed endoscopically. Surgery confirmed the suspicion that the gallbladder had perforated into the duodenum, releasing the stones into the duodenal lumen. Measurement of the largest stone after surgical removal revealed it to be over 5 cm in length (right).