Hepatobiliary

Biliary Tract

ANATOMY

INVESTIGATION

Mode	Advantages	Disadvantages
Ultrasound	1st line, 90% accuracy of finding GS	x show exact site, inaccurate in obesity, previous surgery, ascites, gaseous distention of abdominal viscera
MRCP	detailed imaging of entire biliary tree, detects stone as small as 2mm even without dilation	Expensive
ERCP	Therapeutic - stone removal, nasobiliary drainage, stenting	High morbidity (6-10%), pancreatitis

GALLSTONE

Pathophysiology

Lithogenic Bile

• Supersaturation of bile with substances like cholesterol or calcium bilirubinate forming monohydrate crystals.
• The crystals are trapped in gallbladder mucus, producing gallbladder sludge.
• Over time, the crystals grow, aggregate, and fuse to form macroscopic stones.

Stasis

• Supersaturation of bile with substances like cholesterol or calcium bilirubinate forming mo

Type

1. Cholesterol (80%)

• contain >70% cholesterol, large, usually green, radiolucent
• Risk : female, fat, fertile, forties, fair (caucassian), DM, pancreatitis, malabsoption, terminal ileal resection, IBD, smoking, Native American (Pima tribe)

2.  Pigment stones (20%)

• < 20% cholesterol, small, dark, friable, irregular, may be radio opaque
• due to infection with B-glucuronidase bacteria
• Risk : haemolytic anemia, biliary tract infection, cirrhosis

3.  Mixed

• 30-70% cholesterol, faceted (calcium salts, pigment, cholesterol)

Prevalence

• 8% of those aged over 40
• 90% asymptomatic
• May present as biliary colic, acute cholecystitis, cholangitis, pancreatitis, GS ileus.

BILIARY COLIC

Presentation

Pain

• epigastric or RUQ pain
• constant (not colic/waxing and waning)
• starts suddenly, max. intensify in 60 min, resolves gradually over 6h. (Lasts 30min -6h)
• frequently happen at night or after fatty meal, relieved by morphine
• can radiate to back/scapula/right shoulder
• nausea/vomiting
• rolling about
• no systemic signs -eg. fever , chills

 

Pathophysiology

• The visceral pain is caused by impaction of gallstone in the cystic duct 
• This distention of cystic duct activates visceral afferent sensory neurons.
• The resultant pain is poorly localized in dermatomes T8/9 (mid epigastrium, RUQ) although it  may radiate to RUQ.
• Pain is relieved when the gallstone migrates back into GB, passes through the ampulla, or falls back into CBD.

Differential Diagnosis

Pancreatitis, PUD, hiatus hernia, gastritis, IBS, angina pectoris

Investigation

• In uncomplicated biliary colic,FBC, LFT(AST, ALT, Alk Phos) & amylase are normal
• US- sensitive(95%) - gallstones within GB with mild wall oedema

• Hepatobiliary scintigraph / HIDA scan- (if diagnosis is uncertain after US) – add cholecystokinin (CCK) and morphine to increase sensitivity

• ERCP - for unresolved biliary colic symptoms after cholecystectomy. Can perform sphincterotomy in type I and II Sphincter of Oddi Dysfunction (SOD)
• AXR – exclude eg. bowel obstruction, perforation

Management

• Pain – Meperidine (pethidine) IM.1mg/kg every 3h. Morphine is avoided
• Nausea/vomiting -  antiemetic eg. metoclopramide IV
• Uncomplited biliary colic resolves with conservative treatment.
• Elective cholecystectomy (95% success)
• Diet – after attack, avoid high fat meals., lose weight
• Bed rest

ACUTE CHOLECYSTITIS

Presentation

• Constant, severe RUQ/epigastric pain >6h, may refer to the tip of right scapula.
• Low grade fever, tachycardia,
• Vomiting, nausea
• Often have history of biliary colic (except for alcalculous cholecystitis)
• Murphy’s sign – tenderness and an inspiratory pause elicited during palpation of the RUQ.
• Tachycardia, fever
• Palpable GB (30-40%)
• Jaundice (15%)

Pathophysiology

• Acute calculous cholecystitis caused by obstruction of the cystic duct, leading to distention of the gallbladder.
• blood flow and lymphatic drainage are compromised, leading to mucosal ischemia and necrosis.

Differential Diagnosis

Perforated peptic ulcer, pancreatitis, MI, hiatus hernia, herpes zoster appendicitis.

Investigation

• Labs are not reliable
• FBC - ↑ WCC (left shift), CRP
• LFT - ↑  Alk Phosphatase(25%), ALT, AST, bilirubin
• amylase- rule out pancreatitis
• urinalysis –rule out pyelonephritis, renal calculi
• Pregnancy test in females of childbearing age.
• US (95% sensitive, 80% specific) best 8h after fast (bile-filled GB) – see GB wall thickening >4mm, pericholecystic fluid, sonographic Murphy sign.
• Hepatobiliary scintigraphy
• CT, MRI- wall thickening (>4 mm), pericholecystic fluid, subserosal edema (in the absence of ascites), intramural gas, and sloughed mucosa.

Complications

• gangrene, perforation
• empyema of GB
• cholecystoenteric fistula
• hydrops -mucus accumulation in GB
• gallstone ileus
• choledocholithiasis
• emphysematous GB

Management

bowel rest, IVI, NBM, analgesia, iv antibiotics (cefuroxime)

Emesis – antiemetics,

ERCP - for symptomatic GS, mandatory for poor-risk pt, pt with cholangitis, severe pancreatitis, failed lap chole

Lap Chole within 72h of onset of symptoms, or interval lap chole >6 weeks

Or open cholecystectomy (more complications, scar-Kocher incision)

Laparoscopic Cholecystectomy

Contraindications

    * High risk for general anesthesia 

    * Morbid obesity

    * Signs of gallbladder perforation, such as abscess, peritonitis, or fistula

    * Previous abdominal surgery

    * Giant gallstones or suspected malignancy

    * End-stage liver disease with portal hypertension and severe coagulopathy

Consent

Eg: You don't really need a GB. Digestion can still function. In OT, you will be given GA and undergo keyhole surgery that may leave you 4 little scars, Tummy filled with CO2 to avoid injury. And your GB is taken out in little bag.

There are small risk of complication: refer below:

Inpatient stay for 2-3 days.

Procedures

1. The patient is anesthetized in supine position.

2. A scalpel is used to make a small incision at the umbilicus.

3. The abdominal cavity is entered by using a Veress needle or Hasson technique

4. The abdominal cavity is inflated with CO2 to create working space.

5. The camera is placed through the umbilical port.

6. Additional ports are placed inferior to the ribs at the epigastric, midclavicular and anterior axillary positions.

7. The gallbladder fundus is identified, grasped, and retracted superiorly.

8. The gallbladder infundibulum is retracted laterally to expose and open Calot's triangle (the area bound by the, cystic artery, cystic duct, common hepatic duct.)

9  The triangle is dissected to clear the peritoneal covering and obtain a view of the underlying structures.

10. The cystic duct and the cystic artery are identified clipped with tiny titanium clips and cut.

11. The gall bladder is dissected away from the liver bed and removed from one of the ports

12. The gall bladder is sent for biopsy to confirm the diagnosis and look for cancer. If present, a reoperation to remove part of liver and lymph nodes will be required in most cases

Risk and Complication

GA complication : 1/30 000

1. Common bile duct injury(0.25%) --> bile leak (biloma)
2. conversion to open surgery: 5%
3. Abdominal peritoneal adhesions --> switch to open cholecystectomy
4. Injury to Ducts of Luschka (33% of population) --> biliary leak (bile peritonitis) --> require a temporary bile stent, confirm via HIDA scan. Manage pain and Antibiotic ASAP.
5. retained stone -causes jaundice- need ERCP or if a T-tube is in place by extraction with Doemia basket down the T-tube track (Burhenne manouvre), flushing or dissolution.
6. Fat digestion affected, no gall bladder to store and release high quantity.
7. Chronic diarrhoea.
8. Postcholecystectomy syndrome (eg. sphincter of oddi dysfunction-SOD), PCS (gastrointestinal distress and persistent RUQ pain)
9. Abscess, wound infection, hernia

Acalculous Cholecystitis

Causes : Diabetes. Sepsis, TPN, Debilitation, major surgery, prolonged fasting. cardiac events, sickel cell disease, salomonella, CMV, Aids

Chronic Cholecystitis

Symptoms: chronic indigestion, vague abd pain, belching, nausea

Long-standing GB irritation

Repeated attacks of AC

• Gallbladder becomes inflamed, fibrotic and shrunken
• Loses its function: storage and concentration of bile
• Lonstanding: Porcelain Gallbladder

CHOLANGITIS

Presentation

• Charcot’s triad – fever(95%), RUQ pain (90%), jaundice(80%)
• Reynold’s pentad : Charcot’s triad + confusion +hypotension

Pathophysiology

• CBD obstruction leads to biliary stasis,bacterial overgrowth, suppuration, and biliary sepsis.
• Causes: choledocholithiasis (60%), biliary tract manipulation, pancreatic or biliary neoplasm, strictures, choledochal cysts

Differential Diagnosis

Pancreatitis, PUD, hiatus hernia, gastritis, IBS, angina pectoris

Investigation

• FBC - ↑ WCC
• LFT-  ↑ Alk phos, AST, ALT bilirubin
• +ve blood culture in 50%
• PFA
• US –GS in GB + in bile ducts + dilated extrahepatic or intrahepatic bile ducts
• PTC

Management

• Goal: decompress biliary tree
• hydration, electrolyte correction, broad spectrum Ab.
• urgent ERCP – papillotomy to remove stome
• if ERCP unavailable/fails, use Percutaneous transhepatic cholangiography (PTC)
• if ERCP, PTC unavailable, surgery to decompress CBD à T-Tube

 

ERCP : scope seen

GALLSTONE PANCREATITIS

Presentation

• Epigastric, back pain
• vomiting, nausea

Pathophysiology

• gallstone impacted in common pancreatic duct, get stuck in the Ampulla of Vater can cause obstruction in the outflow of pancreatic juices from the pancreas into the duodenum. Juices causes lysis (dissolving) of pancreatic cells

Differential Diagnosis

AAA, Peptic ulcer disease,

Investigation

• FBC - ↑ amylase, lipase, CRP
• LFT-  ↑ liver enzymes
• US may sho multiple stones, edematous pancrease
• CT – to evaluate complications

Management

• supportive
• cholecystectomy during same admission after acute attack subsided (23-60% recurrence if no O.R)

GALLSTONE ILEUS

Presentation

• crampy, colicky, abdominal pain, with freedom from pain between spasms.
• nausea, vomiting(?may be faeculent)
• High pitch "tinkling" bowel sound

Pathophysiology

• Gall bladder perforation, cholecystoenteric fistula (usually duodenal) with large gallstone impacting most commonly at the ileacecal valve.
• not an ileus, but a true partial or complete small bowel obstruction.

Differential Diagnosis

intestinal obstruction, adhesion from previous surgery

Investigation

• FBC,U&E, Creatinine, LFT
• 3 views abdomen, shows dilated small intestine, gallstone in RLQ and air in biliary tree(15%) - pneumobilia
• 
• Riglers sign: double wall sign- air in either side of bowel wall
• Upper GI series in unclear

Management

• hydrate, operate to remove stone, (enterotomy), usually don’t have to remove GB
• fistula usually closes spontaneously
• Surgery: laparotomy and "milking" of stone through ileocaecal valve, enterolithotomy, lap chole.
• mortality 10-15% - due to large amount of co-morbidities

GALLBLADDER CANCER

Presentation

• RUQ pain, palpable mass (if tumor in CBD)
• systemic ; unremitting jaundice, pruritus, weight loss, anorexia.
• Jaundice
• Palpable GB (Courvoisiers sign)
• Sister Mary Joseph node- palpable nodule bulging into the umbilicus
• Virchows node- enlarged, hard, left supraclavicular lymph node

Epidemiology

age 50-70, highest incidence in India

pt with gallbladder wall calcicfication, cholecytoenteric fistula and adenoma

female:male = 2:1

inflammatory condition, gallstone >3cm, high BMI

Pathophysiology

• No clear cause
• K-ras mutation (35-59%), p53 mutation (90%)
• Most gallbladder cancer begins in the cells that line the inner surface of the gallbladder (adenocarcinoma)
• Location: 60% fundus, 30% body, 10% neck
• generally spreads via the lymphatic channels and venous drainage, and peritoneal metastasis is common.

Differential Diagnosis

intestinal obstruction, adhesion from previous surgery

Investigation

• FBC: anaemia
• LFTs: ↑ ALP, bilirubin but normal AST. Klatskin tumor (at common hepatic bile duct bifurcation)
• ↑ carbohydrate antigen CA 19-9, carcioembryonic antigen (CEA)
• US and CT (dilated bile ducts, polyploidy lesions), ERCP and PTC (depict tumour
• Guided biopsy (Percutaneous CT scan) or endoscopic US with FNA

A transaxial enhanced computed tomography (CT) scan of a 60-year-old man with right upper quadrant pain shows a partially calcified gallbladder (arrow). At laparotomy and histology, an infiltrating adenocarcinoma of the gallbladder was confirmed.

Stage

Tis: Ca in situ
T1:
1a: invades lamina propria
1b: invades muscle layer
T2: no extension beyond serosa
T3: perforates serosa, into liver
T4: invades PV or HA, or multiple organs

N0: no nodes involved
N1: mets in regional nodes

M0: no distant mets
M1: distant mets

Management

• in situ lesions required cholecystectomy only
• for advanced, cholecystectomy + wedge resection of liver and regional lymphadenectomy
• Suspicion of tumorous involvement of the right hepatic duct will require an extended right hepatectomy, excision of the extrahepatic biliary tree, and Roux-en-Y hepaticojejunostomy to the left hepatic duct.
• + stents for palliation
• radiation or Whipple’s if tumour at low end of CBD
• Chemotherapy(gemcitabine, capecitabine, or 5-fluorouracil) or radiotherapy if late end stage

Prognosis

5 y survival

• Localised: 40%
• Regional 15%
• Distant: 10% 

CHOLANGIOCARCINOMA

Presentation

• Obstructive jaundice, may be preded with pruritus
• weight loss
• Dull RUQ pain
• anorexia

Epidemiology

• Highest rate in N. america
• M:F= 1:2.5
• Age: highest prevalence in 70s

Pathophysiology

• arise from intra-hepatic or extra hepatic biliary epithelium
• usually adenocarcinoma

Aetiology

• Infection- Liver flukes, Clonorchis sinensis, Ascaris
• Inflammatory Bowel Disease- Especially with PSC
• Chemicals- Rubber and wood industry
• Congenital- Choledochal cyst
   

Investigation

• FBC: anaemia
• LFTs: ↑ ALP, bilirubin, GGT
• ↑ carbohydrate antigen CA 19-9, carcioembryonic antigen (CEA)
• US , CT, MRI, EUS:FNA, PET
• ERCP (Brush cytology, biopsy, stenting), PTC (cytology, drainage)

Stage

Tis: Ca in situ
T1:
1a: invades mucosa
1b: invades muscularis
T2: invades perimuscular CT
T3: pinvades liver, GB, duodenum, pancreas, stomach, colon

N0: no nodes involved
N1: mets in cystic duct or hilar nodes of hepatoduodenal ligament.

N2: mets in peripancreatic, periportal, coeliac, or superior mesenteric nodes

M0: no distant mets
M1: distant mets

Management

paliative

• Stenting: plastic or metal by ERCP/PTC
• Chemo-5-FU, Gemcitabine
• Radiotherapy

Proximal Tumours- Orthotopic Liver transplant
Distal Tumours- Whipples