PBL Patient case 12: Obstructive
Jaundice
Basic Anatomy
Signs and Symptoms
-
N+V
Fever
Abdo pain –
o RUQ, radiating to R shoulder, back
Local peritonism
GB mass
+ve Murphy’s sign
Sites of Obstruction
1.
-
Gall Bladder or Cystic Duct
ASx (70%)
RUQ Pain (++ fatty foods)
Biliary Colic (Colicky epigastric P)
Cholecystitis (RUQ P + Fever)
- Empyema of GB
- Porcelain GB (Calcification)
- Rarely perforation – biliary
peritonitis
2. CBD (Choledocholithiasis)
- Cholestatic Jaundice
- Ascending Cholangitis (Rigors,
Jaundice, RUQ pain)
3. Pancreatitis
- Migration of stones down CBD thru
ampulla of Vater
- Epigastric Pain radiating to back
Risk Factors of Cholesterol Stones
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Female
Forties (unusual < 30 yrs)
Fat
Multiparity
Diet (High animal fat)
Contraceptive pill
Ileal disease or resection
Diabetes
Acromegaly Rx with octreotide
Consequences of Gall Stones
1. Asymptomatic gallstones
2. In Gall Bladder
- Biliary Colic
o Obstruction at any part of billary tree (cystic duct to Sphincter of Oddi)
o Severe constant pain RUQ radiate shoulder/subscapular, N&V, fevers, rigors,
- Cholecystitis (Acute and Chronic)
o Can cause empyema – spread infection or burst (but rare due to dual blood supply)
- Empyema/Mucocele
o Obstructed GB fills with pus/mucous
- Carcinoma
- Mirizzi’s Syndrome
o Jaundice with acute cholecystitis without CBD stone put compression of CBD due to
stone in cystic duct
3. In the bile ducts
- Cholangitis
- Pancreatitis
- Obstructive jaundice
4. In the gut
- Gallstone Ileus – SB obstruction
o Large stone erodes through GB into duodenum can obstruct T.I. @ ileocecal valve
o (X-ray: pneumobilia, small bowl fluid levels, stone)
Bile
Consists of:
- Bile acids
- Cholesterol
- Phospholipids
- Conjugated bilirubin
- Water and electrolytes
Synthesis of Bile Acids
- Bile acids are not present in the diet, and are synthesized in the liver by enzymes
- Primary bile acids are synthesized in the liver from cholesterol (cholic acid and
chenodeoxycholic acid)
- Secondary bile acids are synthesized from primary bile acids in the intestine by colonic
bacterial enzymes (deoxycholic acid and lithocholic acid)
- Bile acids will be conjugated to form tauro or glyco- conjugated bile acids  secreted into
duodenum in bile
Synthesis of Conjugated Bilirubin
- Produced mainly from breakdown of mature RBC in the Kupffer cells of the liver and RES
- Biliverbin is formed from haem and is reduced to form bilirubin
- Br is unconjugated and water- insoluble  transported to liver attached to albumin
- Bilirubin dissociates from albumin and taken up by hepatic cells where it is conjugated with
glucuronic acid and excreted into bile
Role of Bile in Digestion
- Bile acids help to emulsify fats in food by forming micelles  increases surface area for the
action of pancreatic lipase (digestion)
- Increases absorption of fat soluble vitamins (A,D,E,K)
- Bile also serves as a route of excretion for bilirubin (RBC degradation by- product)
- Neutralizes excess stomach acid before entering ileum
- Bile salts also act as bacteriocides  kills bacteria that may be present in food
Enterohepatic Circulation
- Primary bile acids are synthesized in the liver from cholesterol  conjugated pass into
duodenum and aid digestion and absorption of fat
- Reabsorption of bile acids occur mainly in the ileum by an active transport mechanism 
return back to the liver via the portal vein (enterohepatic circulation)
- 95-98% of total circulating bile acids are absorbed each day
- Only a small quantity escapes reabsorption and is excreted in the faeces
- To maintain status quo, the liver will then synthesize enough bile acids to match the faecal
loss
- At the terminal ileum, free Br is reduced to urobilinogen  some will be excreted as
stercobilinogen and urobilinogen  remainder will be reabsorbed and passed to the liver via
E.C
Pathophysiology
Types of Gallstones
- Cholesterol gallstones (80% in western countries)
- Pigment stones (predominantly calcium bilirubinate or polymer- like complexes with
calcium, copper and some cholesterol)
Cholesterol Gallstones
Due to cholesterol crystallization from gall bladder bile
1. Excess of cholesterol and deficit of bile salts in bile  imbalance between ratio of
cholesterol and bile salts
2. Crystallization- promoting factors within bile
3. Motility of gall bladder
Bile Pigment Gallstones
Black pigment stones:
- Seen in patients with haemolytic conditions eg sickle cell disease  excessive secretion of Br
Brown Pigment stones:
- Presence of bile stasis and/ or biliary infection
Obstructive Jaundice
Gradual Obstruction of CBD over weeks/months
- Gallstones
- Carcinoma of CBD
- Carcinoma of head of pancreas
- Inflammatory stricture of CBD
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Biliary obstruction causes progressive dilatation of intrahepatic bile ducts as intrabiliary
pressures rise
Hepatic bile flow is suppressed reabsorption and regurgitation of conjugated Br into the
blood stream
Leads to jaundice accompanied by dark urine and light- colored stools
ALP is raised with only slight elevation in aminotransferases
If biliary obstruction persists, there is a risk the static bile will become infected causing acute
cholangitis and eventually liver abscesses
Lack of bile in small intestine causes malabsorption of fat and fat- soluble substances
Investigations
Liver Function Tests:
• Serum bilirubin – elevated
• AST, ALT – normal or slightly elevated
• ALP – elevated (4-10x normal)
• Albumin – usually normal
• GGT – elevated
• PTT, INR – usually normal
Abdominal Ultrasound
- Size of biliary tracts
- Degree of obstruction
- Can determine cause of obstruction
Abdominal CT
- Can visualise biliary tree
- Very good at detecting calcified stones and malignancies
ERCP (Endoscopic retrograde cholangiopancreatography)
An endoscope is passed through the mouth, esophagus and stomach to the 2nd part of the
duodenum. A catheter is passed up the ampulla of vater into the CBD, and dye is injected.
- Allows visualisation and access to the biliary and pancreatic ducts
- Sphincterotomy and stone extraction can be performed
- Has a significant risk of pancreatitis (5%)
- Current gold standard imaging for pancreatobiliary tree.
MRCP (Magnetic resonance cholangiopancreatography)
An MRI method of visualising the pancreatobiliary tree.
- Non-invasive (no contrast is required)
Management
Cholelithiasis
- Asymptomatic stones: attempt dissolution (ursodeoxycholic acid).
o Reduce Risk factors
- Symptomatic stones : laparoscopic cholecystectomy.
Complications
- Cholecystitis
- Choledocolithiasis,
- Cholangitis
- Fistula formation
- Pancreatitis.
Prognosis
Asymptomatic gallstones become symptomatic at about 2%/year, once symptoms (biliary colic)
begin they recur at 40%/year and progress to a complication at 2%/year.
Choledocolethiasis
Endoscopic Retrograde Cholangiopancreatography
Indications: Cholangitis, jaundice + dilated intrahepatic ducts, jaundice + normal calibre
ducts + non-diagnositic liver biopsy, recurrent pancreatitis, post-cholecystectomy pain
Therapeutic ERCP: Sphincterotomy (CBD stones), Stenting of malignant strictures
Prophylaxis:
o Check LFTs clotting + platelets
o Antibiotics (Ciprofloxacin)
o Analgesic (Morphine/Metoclopramide)
o Sedation (Midazolam)
Complications:
o Pancreatitis, bleeding, cholangitis, perforation
Acute Cholecystitis
Medical: NBM nil by mouth, Pain relief, IVI + Cefuroxime (1.5g/8h IV)
Surgical: consider cholescystectomy (laporoscopic) within 72hours OR after 6/12 weeks
Mortality < 1%
Relapse (18%) - if not within time frame
Complications
Gall bladder perforation/rupture
Ascending cholangitis
Pancreatitis
Peritonitis
Prevention
Removal of the gallbladder and gallstones will prevent further attacks.
Following a low-fat diet if prone to gallstone attacks.
Cholangitis
Quick diagnosis and treatment are very important.
Antibiotics to cure infection are tried first for most patients. ERCP or other surgical procedure is
done when the patient is stable.
Patients who are very ill or are quickly getting worse may need surgery right away.
Complications
Sepsis
Prevention
Treatment of gallstones, tumors, and infestations of parasites may reduce the risk for some people.
A metal or plastic stent within the bile system may be needed to prevent recurrence.
Patient Case – Mr P
Presentation
 31 y.o plumber
 22/4 – presented to ED
◦ Sudden onset epigastric pain
◦ 8/10, colicky
 Ix –
◦ ECG: ST elevation in leads II and III
◦ Cardiac enzymes: normal
◦ AST: 44U/L
(10-40)
◦ Lipase: 62U/L (10-55), *amylase not done
 Pain resolved, discharged 23/4
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25/4 – presented via ambulance
◦ Epigastric pain
◦ Increasing severity  10/10, radiating to back
◦ SOB (but not O/E)
◦ Noted ‘tingling’ in L arm
◦ N+V (3x)
◦ Jaundiced (not marked)
Ix –
◦ FBE, U+Es, LFTs, troponin, CK, amylase, lipase
◦ Upper abdo US
DDx
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Cardiac –
◦ Acute coronary syndrome
Abdo –
◦ Pancreatitis
◦ Cholecystitis, Biliary colic
◦ Acute hepatitis
◦ Peptic ulcer disease
Resp –
◦ Pneumonia
Past Hx
 Jan 2011 – similar episode of abdo pain
 2/52 ago – N+V, ? ‘food poisoning’
 1986 – tonsillectomy
 1998 – L shoulder reconstruction
 Otherwise fit and healthy
◦ NKA
◦ No current Rx
FHx
 Mum
◦ Cholecystectomy 2010
◦ Hypertension
 Dad
◦ Thyroidectomy 2009 (benign nodules)
 Sister – A+W
Social Hx
 Never smoked
 etOH
◦ 4-6 SDs daily (regular beers)
◦ no AFDs
 Lives with partner (nurse)
 Runs own plumbing business
Ix Results
 Cardiac enzymes – normal
 FBE – mild neutrophilia
 LFTs:
◦ T Bilirubin – 30 umol/L
(4-20)
◦ ALP – 112 U/L
(35-110)
◦ GGT – 325 U/L
(5-50)
◦ ALT – 182 U/L
(5-40)
◦ AST – 264 U/L
(10-40)
 Upper abdo US
◦ Thickened gallbladder wall (4.2mm)
◦ Multiple immobile calculi and sludge
◦ No ductal dilatation
 Normal CBD (3.9mm)
◦ Mild fatty infiltration of liver
◦ Normal spleen, pancreas and kidneys
Rx

Surgery:
◦ Laparoscopic cholecystectomy
◦ Intra-op cholangiogram
◦ Umbilical hernia repair
 (incidental finding on pre-operative Ex)
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Pt reports some abdominal tenderness, poor appetite, no N+V
Dressings over 4x lap ports
Mildly jaundiced (skin and sclera)
◦ Pt’s partner reports this is resolving
F/U