| How is anatomy of biliary tree? | Intrahepatic ducts converge to become the right and left hepatic ducts.
Right and left hepatic ducts converge, forming the common hepatic duct.
Cystic duct comes off the gallbladder and joins the common hepatic duct to become the common bile duct (CBD).
CBD empties into the duodenum via the ampulla of Vater.
Calot’s triangle: Inferior border of the liver, common hepatic duct, and cystic duct.
The cystic artery runs through it, and the associated lymph node is called Calot’s node.
The right hepatic artery is adjacent to the cystic duct in Calot’s triangle and, as such, is susceptible to injury during cholecystectomy
The proximal end of the gallbladder near the cystic duct is called the infundibulum (Hartman’s pouch), and the larger distal end of the gallbladder is called the fundus.
The gallbladder collects bile directly from the liver via small bile ducts called ducts of Luschka. |
| What are variations of cystic duct anatomy? | A. Low junction between the cystic duct and common hepatic duct.
B. Cystic duct adherent to the common hepatic duct.
C. High junction between the cystic and the common hepatic duct.
D. Cystic duct drains into right hepatic duct.
E. Long cystic duct that joins common hepatic duct behind the duodenum.
F. Absence of cystic duct.
G. Cystic duct crosses posterior to common hepatic duct and joins it anteriorly.
H. Cystic duct courses anterior to common hepatic duct and joins it posteriorly. |
| What are variations of blood supply of gall bladder? | A. Cystic artery from right hepatic artery, about 80% to 90%.
B. Cystic artery from right hepatic artery (accessory or replaced)from superior mesenteric artery, about 10%.
C. Two cystic arteries,one from the right hepatic, the other from the common hepatic artery, rare.
D. Two cystic arteries, one from the right hepatic, the other from the left hepatic artery, rare.
E. The cystic artery branching from the right hepatic artery and running anterior to the common hepatic duct, rare.
F. Two cystic arteries arising from the right hepatic artery, rare. |
| What is cholelithiasis? | DEFINITION
Stones in the gallbladder.
85% of stones are composed primarily of cholesterol, while the remaining 15% are pigmented.
INCIDENCE
Approximately 10% of the U.S. population has gallstones; incidence increases with age.
RISK FACTORS
The typical ones are: Female, fat, fertile, and forty; other risk factors include:
Pregnancy, oral contraceptives, Western diet, inflammatory bowel disease (IBD), hyperlipidemia, ileal resection, and total parenteral nutrition (TPN). |
| What are S&S of cholelithiasis? Dx? | Most patients are asymptomatic.
Symptomatic patients classically complain of severe RUQ pain that radiates to the back, epigastrium or left upper quadrant (LUQ)
The pain tends to be worse after eating (especially after fatty foods) and may be associated with nausea and vomiting.
The symptom complex is called biliary colic and typically resolves over a few hours.
DIAGNOSIS
Often incidental, as most patients are asymptomatic.
Abdominal Ultrasound: Procedure of choice; classic findings include an acoustic shadow (“headlight”) and gravity-dependent movement of gallstones with patient repositioning. |
| How is tx of cholelithiasis? | Asymptomatic cholelithiasis does not require cholecystectomy unless the patient:
Has a porcelain gallbladder (which has an increased incidence of carcinoma)
Has sickle cell anemia
Has a stone > 2 to 3 cm
Is a pediatric patient
A laparoscopic cholecystectomy can be performed on 95% of patients
Medical treatment of cholelithiasis involves chenodeoxycholic acid or ursodeoxycholic acid, drugs that can be used to dissolve cholesterol stones.
These are not effective as surgical management
PROGNOSIS
3 to 5% of patients with cholelithiasis develop complications |
| What is acute calculous cholecystitis? | DEFINITION
Inflammation of the gallbladder wall, usually due to obstruction of the cystic duct by gallstones.
In acute cholecystitis, the pain is similar in character to cholelithiasis but typically lasts longer (> 3 hours).
SIGNS AND SYMPTOMS
RUQ tenderness and guarding are present, distinguishing it from uncomplicated biliary colic.
Pain typically lasts > 3 hours.
Fever, nausea, vomiting, and anorexia are nonspecific and variable.
Murphy’s sign
Sonographic Murphy’s: Pain over RUQ when palpated with ultrasound probe (87% sensitivity). |
| How is dx of acute calculous cholecystitis? | Labs: Leukocytosis, with or without increased ALP, LFTs, amylase, and total bilirubin.
Ultrasound: Reveals inflammation of the gallbladder wall (> 4 mm), pericholecystic fluid and stones in the gallbladder.
Positive predictive value of all three is 90%. Will also see dilation of the CBD if the stone has passed.
HIDA scan (most sensitive) : A radionucleotide scan in which Technetium-99m labeled iminodiacetic acid is intravenously into hepatocytes.
A normal gallbladder would be visualized within 1 hour. |
| How is tx of acute calculous cholecystitis? | NPO.
IV fluids.
IV antibiotic.
IV analgesia.
Cholecystectomy within 24 to 48 hours.
Often done laparoscopically.
If inflammation prevents adequate visualization of important structures, convert to open cholecystectomy |
| What is acalculous cholecystitis? | DEFINITION
Acute cholecystitis without evidence of gallstones; thought to be due to biliary stasis.
INCIDENCE
Ten percent of cases of acute cholecystitis.
RISK FACTORS
Most often seen in intensive care unit (ICU) patients with multiorgan system failure, trauma (especially after major surgery), burns, sepsis, and TPN.
DIAGNOSIS
Labs: Leukocytosis, with or without increased ALP, LFTs, amylase, and total bilirubin.
Ultrasound: Biliary sludge and inflammation wall (> 4 mm); can also detect complications (e.g., gangrene, empyema, or perforation of the gallbladder).
HIDA scan: To confirm diagnosis
TREATMENT
Urgent cholecystectomy;
Percutaneous cholecystostomy
in patients with high surgical risk |
| What is emphysematous cholecystitis? | Severe variant of cholecystitis caused by gas-forming bacteria
Relatively rare
Often results in perforation of the gallbladder, high mortality and morbidity
Typically affects elderly diabetic men |
| What is choledocholithiasis? | DEFINITION
Obstruction of the common bile duct by a microstone.
INCIDENCE
Found in 6–15% of acute calculous cholecystitis and 1–2% of acalculous cholecystitis at surgery.
SIGNS AND SYMPTOMS
Epigastric or RUQ pain and tenderness, jaundice, cholangitis, or recurrent attacks of acute pancreatitis without other known risk factors. |
| How is dx of choledocholithiasis? | DIAGNOSIS
Labs: Increased ALP, LFTs, total and direct Bilirubin.
Ultrasound: Highly specific but not very sensitive for CBD stones.
It shows gallstones, dilated CBD (>6 mm), and CBD stones in only 20–30% of patients with choledocholithiasis
MRCP.
ERCP: provides a diagnostic and therapeutic options.
Intraoperative cholangiography (during cholecystectomy). |
| How is tx of choledocholithiasis? | ERCP with sphincterotomy and stone extraction followed by laparoscopic cholecystectomy (85–90% successful).
If ERCP fails:
Laparoscopic cholecystectomy with cholangiograpyh and stone extraction ( can necessitate a laparotomy)
A T-tube is placed so bile can drain externally. It is removed 2 to 3 weeks later on an outpatient basis. |
| What is acute ascending cholangitis? | DEFINITION
Bacterial infection of the bile ducts usually associated with obstruction of the CBD by a gallstone.
SIGNS AND SYMPTOMS
Fever, chills
Nausea, vomiting
Abdominal pain with or without altered mental status and septic shock
Charcot’s triad:
RUQ pain
Fever
Jaundice
Reynold’s pentad:
Charcot’s triad plus
Central nervous system(CNS) symptoms
Septic shock |
| How is dx of acute cholangitis? | Labs: Leukocytosis with increased Bilirubin, ALP, and LFTs, Creatinin, PTT TP INR.
Ultrasound: Should be the initial study; dilation of common and intrahepatic bile ducts is suggestive.
MRCP, ERCP: Provides a definitive diagnosis; can also be therapeutic.
Bile cultures: Obtain to facilitate proper antibiotic treatment; offending organisms are usually enteric gram negatives and enterococci. |
| How is tx of cholagitis? | It is an emergency
NPO, IV fluids, and IV antibiotics.
ERCP/ PTC (percutaneous transhep cholangiography) immediately to decompress bile duct and remove obstruction.
If unsuccessful, Surgery with intraoperative decompression with T-tube placement and cholecystectomy. |
| What is sclerosing cholangitis? | A chronic, progressive inflammatory process of the biliary tree of unknown etiology that slowly damages the bile ducts, results in strictures.
This causes bile to accumulate in the liver, where it gradually damages liver cells and in most cases, leads to cirrhosis, fibrosis of the liver.
As cirrhosis progresses and the amount of scar tissue in the liver increases, the liver slowly loses its ability to function.
The scar tissue may block drainage of the bile ducts leading to infection of the bile.
INCIDENCE
2:1 male predominance with median age of onset at 40 years
Seventy percent of patients with sclerosing cholangitis have Inflammatory Bowel Disease, whereas 3 to 7.5% of patients with IBD have sclerosing cholangitis |
| How is dx of sclerosing cholangitis? | SIGNS AND SYMPTOMS
Many patients are asymptomatic at the time of diagnosis, but symptoms can include fever, weight loss, fatigue, pruritus, jaundice, hepatomegaly, splenomegaly, and hyperpigmentation.
DIAGNOSIS
ERCP/PTC reveal a “beads on a string” appearance of the bile ducts (alternating strictures and dilation) inside and/or outside the liver.
ALP is almost always elevated.
MRCP (less aggressive)
Liver Biopsy (if available) |
| How is tx of sclerosing cholangitis? | There is no curative treatment, several clinical trials are underway that aim to slow progression of this liver disease
Balloon dilation with stent placement can be performed for palliative purposes, but definitive treatment varies depending on the location of the strictures.
Extrahepatic strictures: Hepatoenteric anastomosis with removal of the extrahepatic ducts and T-tube placement for external drainage of bile.
Intrahepatic strictures: Liver transplant. |
| What are complications of sclerosing cholangitis? | Cirrhosis.
Cholangitis.
Obstructive jaundice.
Cholangiocarcinoma (10%).
Primary sclerosing cholangitis is one of the major known risk factors for cholangiocarcinoma . This represents a 400-fold greater risk of developing cholangiocarcinoma compared to the general population.
Surveillance for cholangiocarcinoma is mandatory |
| What is gallstone ileus? | Small bowel obstruction caused by a gallstone; the ileocecal valve is the most common site of obstruction.
Most often a large stone has eroded a hole through the gallbladder wall to the duodenum, causing a cholecystenteric fistula. A gallstone escapes through this hole into the GI tract and eventually gets stuck in the ileum, causing small bowel obstruction.
INCIDENCE
Most common in women over 70.
SIGNS AND SYMPTOMS
Symptoms of acute cholecystitis followed by signs of small bowel obstruction (nausea, vomiting, abdominal distention, RUQ pain). |
| How is dx of gallstone ileus? Tx? | DIAGNOSIS
Abdominal plain films: May show the
pathognomonic features of pneumobilia,
dilated small bowel, and a
large gallstone in the RLQ.
Ultrasound: Useful to confirm cholelithiasis; may also identify the fistula.
CT Scan
TREATMENT
Exploratory laparotomy, removal of the gallstone, and possible small bowel resection with or without cholecystectomy and fistula repair |
| How is gallbladder carcinoma? | DEFINITION
Malignant neoplasm of the gallbladder, the majority of which are adenocarcinomas.
INCIDENCE
Extremely rare (< 1% of patients with cholelithiasis); incidence increases with age with a peak at 75 years; female:male ratio 3:1
RISK FACTORS
Include porcelain gallbladder, gallstones, choledochal cysts, gallbladder polyps, and typhoid carriers with chronic inflammation.
SIGNS AND SYMPTOMS
Most patients are asymptomatic until late in the course when findings may include abdominal pain, nausea, vomiting, weight loss, RUQ mass, hepatomegaly, or jaundice. |
| How is dx of gallbladder carcinoma? | Ultrasound shows gallbladder inflammation, gallstones, or both; occasional gallbladder mass.
CT or MRI shows gallbladder mass (90% sensitive) with occasional portal lymphadenopathy; livers metastasis, peritoneal carcinomatosis |
| How is tx of gallbladder carcinoma? | Surgical excision is the only potentially curative treatment for cholangiocarcinoma.(IF NO METASTASIS)
Cholecystectomy (for T1 tumors, limited to muscular wall).
Cholecystectomy with segment 4b, 5 liver resection and portal lymphadenectomy (for T2 tumors, invasion to perimuscular tissue but not to serosa).
Right extended hepatectomy and resection of CBD followed by hepaticojejunostomy (for invasion into CBD or liver; T3 tumors). |
| How is paliative tx of gallbladder carcinoma, Prognosis? | PALLIATIVE TREATMENT : If non resectable
Chemotherapy
Complicated cases:
Jaundice by invasion of the CBD
Endoscopic treatment : stent
PTC
Surgical biliojejunostomy: intra or extrahepatic
Duodenal Invasion
Gastrojejunostomy+ biliojejunostomy or endoscopic or PTC
PROGNOSIS:
5% overall survival.
17% 5-year survival with resection for curative intent,
>95% survival for T1 tumors treated with cholecystectomy.
70% to >90% survival for T2 and T3 tumors if at least 4b and 5 segment resections are performed and no nodal involvement. |
| What is cholangiocarcinoma? | An uncommon tumor that may occur anywhere along the intrahepatic or extrahepatic biliary tree but is most commonly located at the bifurcation (Klatskin Tumor) of the right and left hepatic ducts (60–70% of cases).
Nearly all are adenocarcinomas (Over 95%).
INCIDENCE
Increases with age with peak at 55 to 70 years.
1/100,000 people per year.
The male-to-female ratio is 1.3:1.
RISK FACTORS
Choledochal cyst, ulcerative colitis, sclerosing cholangitis, toxins, contrast dye, hepatolithiasis, biliary-enteric anastomosis |
| What are choledocal cysts? | Choledochal cysts are congenital bile duct anomalies. These cystic dilatations of the biliary tree can involve the extrahepatic biliary , the intrahepatic biliary radicles, or both. They may occur as a single cyst or in multiples within the biliary tree. More frequent in East Asian nations like Japan and China. |
| What are S&S of cholangiocarcinoma? Dx? | SIGNS AND SYMPTOMS
Painless jaundice, right upper quadrant pain, pruritus, anorexia, malaise, weight loss.
Hyperbilirubinemia,elevated alkaline phosphatase.
Elevated CA 19-9
DIAGNOSIS
Ultrasound shows dilated extrahepatic and intrahepatic biliary ducts (depending on level of tumor);
CT or MRCP shows proximal and distal extent of tumor;
PTC allows brushings for cytologic studies of tumor
CA 19-9 is a useful tumor marker. |
| How is tx of cholangiocarcinoma? | INTRAHEPATIC
Surgical excision is the only potentially curative treatment for cholangiocarcinoma.
No surgery if portal invasion, trunk of the hepatic veins invasion, metastasis.
Intrahepatic cholangiocarcinomas are treated like hepatocellular carcinoma, with hepatectomy when possible.
EXTRAHEPATIC
The tumor is unresectable.
both hepatic ducts extensively involved (type IV),
the main trunk of the portal vein extensively involved
metastasis,
Bismuth-Corlette type I or II :
common bile duct excision with portal lymphadenectomy, cholecystectomy,
with bilateral Roux-en-Y hepaticojejunostomies |
| What is palliative tx of cholangiocarcinoma? | Nonoperative biliary decompression for proximal tumors.
Percutaneous placement of expandable metal stents
drainage catheters is usually the appropriate approach
for distal bile duct tumors, endoscopic metal stents placement is often the preferred approach
For patients with distal bile duct cancer found to be unresectable on surgical exploration, Roux-en-Y hepaticojejunostomy, cholecystectomy, and gastrojejunostomy to prevent gastric outlet obstruction should be performed. |
| How is prognosis of cholangiocarcinoma? | Most patients with unresectable cholangiocarcinoma die within 1 year of diagnosis.
Patients with distal cholangiocarcinoma are more likely to have resectable disease and improved prognosis compared to perihilar cholangiocarcinoma.
The overall 5-year survival rate for resectable disease is 30% to 50%. |
