Malignant Biliary Obstruction

1. Definition

Malignant biliary obstruction (MBO) refers to obstruction of the biliary tract by cancer growth within or around the biliary tract. ^[1]

Let's break the name down:

• "Malignant" = caused by cancer (as opposed to benign causes like gallstones or strictures)
• "Biliary" = relating to bile or the bile ducts (from Latin bilis = bile)
• "Obstruction" = blockage of flow

The key consequence is that bile — which is produced by hepatocytes and normally drains through the intrahepatic ducts → common hepatic duct → common bile duct → ampulla of Vater → duodenum — cannot reach the intestine. This causes conjugated (direct) hyperbilirubinaemia and the clinical syndrome of obstructive jaundice.

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2. Epidemiology

Global & Hong Kong Context

• MBO is not a single disease — it is a clinical syndrome caused by various malignancies. Epidemiology therefore depends on the underlying cause.
• Pancreatic cancer (the most common cause of MBO) is the 4th–5th leading cause of cancer death globally and has been rising in Hong Kong.
• Cholangiocarcinoma: Perihilar cholangiocarcinoma (Klatskin tumour) is the most common subtype (≈60%) ^[3]. Intrahepatic cholangiocarcinoma has been increasing in incidence worldwide.
• Hepatocellular carcinoma (HCC): The 5th most common cancer in Hong Kong and 3rd in cancer mortality ^[4]. HCC is disproportionately common in HK due to endemic hepatitis B.
• Gallbladder carcinoma: Female predominance (M:F = 1:2–3) ^[5]. 95% have co-existing gallstones.
• Recurrent pyogenic cholangitis (RPC) — also known as "Hong Kong disease" / oriental cholangiohepatitis ^[6] — is a significant risk factor for cholangiocarcinoma in the local population due to chronic biliary inflammation and intrahepatic stone disease.

Age & Sex

• MBO as a whole predominantly affects older adults (> 60 years).
• Pancreatic cancer: Male predominance ^[7].
• Gallbladder cancer: Female predominance ^[5].
• Cholangiocarcinoma: slight male predominance overall.

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3. Anatomy & Function of the Biliary System

Understanding the anatomy is absolutely essential to understanding where obstruction occurs and what it causes.

3.1 The Biliary Tree — From Liver to Duodenum

1. Intrahepatic bile ducts: Small bile canaliculi between hepatocytes → interlobular ducts → segmental ducts → right and left hepatic ducts
2. Common hepatic duct (CHD): Formed by confluence (bifurcation) of right and left hepatic ducts at the hepatic hilum
3. Cystic duct: Drains the gallbladder and joins the CHD
4. Common bile duct (CBD): Formed by junction of CHD + cystic duct. Approximately 7–8 cm long, runs in the hepatoduodenal ligament (free edge of lesser omentum), passes behind the first part of duodenum, through the head of pancreas
5. Ampulla of Vater: Where CBD and main pancreatic duct converge, opening into the second part of the duodenum (D2) at the major duodenal papilla
6. Sphincter of Oddi: Circular smooth muscle around the ampulla — controls bile and pancreatic juice flow into the duodenum

3.2 Regional Classification (Critical for MBO Localisation)

The biliary tree is divided into regions, and the level of obstruction determines which structures are dilated and which clinical features arise:

3.3 Key Anatomical Relationships

• The hepatoduodenal ligament (part of lesser omentum) contains the "portal triad": CBD (anterolateral), hepatic artery proper (anteromedial), portal vein (posterior). Tumours here can compress all three.
• The head of the pancreas wraps around the distal CBD — this is why even small pancreatic head tumours cause early biliary obstruction.
• The ampulla of Vater is the most distal point — tumours here present earliest with jaundice (and therefore have the best prognosis among periampullary carcinomas) because even tiny tumours obstruct the narrow ampullary lumen ^[5].

3.4 Functions of Bile

Understanding bile function explains the clinical consequences of obstruction:

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4. Etiology (Causes of MBO)

4.1 Malignant Causes of Biliary Obstruction

These are the cancers that directly cause MBO. The lecture slides specifically list: ^{[1] [9]}

Pathology causing malignant biliary obstruction: ^[1]

• Carcinoma of duodenum
• Periampullary carcinoma
• Carcinoma of pancreas
• Lymphoma
• Carcinoma of gallbladder — cystic duct LN, direct infiltration of CBD, tumour fragments
• Cholangiocarcinoma at hilum, Klatskin tumour
• HCC — direct infiltration, compression, tumour fragments in CBD

Let me elaborate on each:

A. Periampullary Carcinomas (Grouped Together)

These four tumours are grouped because their presentation and management are similar ^[5]:

B. Cholangiocarcinoma (CC)

• Definition: Carcinoma of the bile duct; > 90% are adenocarcinoma ^{[3] [8]}
• Klatskin tumour: Specifically refers to cholangiocarcinoma at the CHD bifurcation (hepatic confluence) — usually perihilar type ^[3]
• Mechanism: Direct intrinsic obstruction of the bile duct lumen
• Obstruction of the bifurcation of left and right hepatic duct → jaundice in early stage ^[8]
• Intrahepatic cholangiocarcinoma will NOT cause jaundice since bilirubin can be reabsorbed and re-excreted through unaffected parts of the liver ^[8]
• Characterised by slow growth, high rate of local invasion, mucin production, and tendency to invade perineural sheath and spread along nerves ^[8]

Bismuth-Corlette Classification (for perihilar cholangiocarcinoma): ^[3]

C. Hepatocellular Carcinoma (HCC)

HCC causes MBO through several mechanisms ^[5]:

• Compression causing obstructive jaundice — usually when mass is situated near the confluence of left and right intrahepatic ducts
  • From anterior liver = Segment 4/5
  • From posterior liver = Caudate segment (uncommon)
• Spread to lymph nodes (porta hepatis) in liver hilum
• Direct infiltration of CBD
• Tumour fragments in CBD

D. Carcinoma of the Gallbladder

Mechanism of MBO ^[5]:

• Spread to cystic duct lymph nodes
• Direct infiltration of CBD
• Tumour fragments in CBD
• Direct extension into liver (adjacent segments IV & V) ^[10]

E. Secondary Causes

• Lymphoma ^[1]
• Secondary hilar lymphadenopathy from GI malignancy (e.g., colorectal cancer metastatic to porta hepatis nodes) ^[5]
• Carcinoma of stomach with metastatic lymph node in the porta hepatis ^[11]

4.2 Causes by Level of Obstruction

This is a clinically useful framework — when you see the imaging, you determine the level of dilatation and then generate your differential ^[5]:

4.3 Benign Causes of Biliary Obstruction (Important Differentials)

These must be distinguished from MBO ^[5]:

• Choledocholithiasis (CBD stones) — most common cause of biliary obstruction overall
• Benign strictures: TB, autoimmune, iatrogenic (post-surgical), RPC
• Primary biliary cholangitis (PBC)
• Primary sclerosing cholangitis (PSC)
• Chronic pancreatitis / Pancreatic cysts
• Mirizzi syndrome — CHD obstruction caused by extrinsic compression from an impacted stone in Hartmann's pouch/cystic duct ^[12]
• Blood clot (haemobilia) / mucus / foreign body / tumour thrombus

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5. Risk Factors for the Underlying Malignancies

Since MBO is caused by various cancers, we must understand the risk factors for each:

5.1 Cholangiocarcinoma Risk Factors [3] [8]

5.2 Pancreatic Cancer Risk Factors [7]

5.3 Gallbladder Cancer Risk Factors [5] [10]

• Gallstones (95% of patients have gallstones) — strongest risk factor; larger and symptomatic stones carry higher risk
• Gallbladder polyps > 1 cm — prophylactic cholecystectomy recommended
• Porcelain gallbladder — calcified GB wall from chronic cholecystitis → ALL porcelain gallbladders should be removed (absolute indication for cholecystectomy) ^[5]
• Primary sclerosing cholangitis
• Abnormal pancreaticobiliary junction — long common channel → reflux of pancreatic juice into biliary tree
• Choledochal cysts

5.4 HCC Risk Factors [4]

• Any cause of cirrhosis: HBV (most common in HK), HCV, ALD, NAFLD, Wilson's disease, PBC, PSC
• HBV is carcinogenic even without cirrhosis (HBV DNA integration → direct DNA damage)
• Aflatoxin exposure
• Smoking, alcohol, obesity, DM

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6. Pathophysiology

6.1 Normal Bile Flow and Barrier Mechanisms

To understand what goes wrong, we first need to know what keeps things working normally ^[13]:

• Continuous flushing action of bile — physically washes away bacteria
• Bacteriostatic activity of bile salts — bile salts are inherently antimicrobial
• Biliary mucous and secretory IgA — anti-adherence factors preventing bacterial colonisation
• Sphincter of Oddi — acts as a mechanical barrier to ascending duodenal reflux and bacterial infection

6.2 Consequences of Malignant Biliary Obstruction

When a tumour obstructs the biliary tree, a cascade of pathophysiological consequences follows:

6.3 Manifestations of Pathophysiological Disturbance

The lecture specifically highlights these consequences ^{[1] [9]}:

A. Bleeding Tendency [5]

• Why? Vitamin K is a fat-soluble vitamin (along with A, D, E). Bile salts are required for fat emulsification and absorption in the small intestine. Without bile reaching the gut, fat-soluble vitamins cannot be absorbed.
• Vitamin K is a cofactor for hepatic synthesis of clotting factors II, VII, IX, X (and proteins C and S).
• Vitamin K deficiency → impaired clotting factor synthesis → coagulopathy → bleeding tendency
• This is a correctable coagulopathy — give parenteral (IV/IM) vitamin K (not oral, because oral vitamin K still requires bile salts for absorption!)

B. Infection (Biliary Sepsis) [5] [9]

Causes of mortality in MBO include: biliary sepsis, cancer cachexia, and liver failure. ^[9]

• Endotoxaemia — the liver normally clears gut-derived endotoxins (lipopolysaccharide from Gram-negative bacteria) via the reticuloendothelial system (Kupffer cells). In biliary obstruction, this function is impaired.
• Impaired reticuloendothelial function — Kupffer cells in the obstructed liver are dysfunctional
• Impaired cell-mediated immunity — obstructive jaundice suppresses T-cell and NK cell function
• Combined with loss of the biliary barrier (bile salts, IgA, sphincter of Oddi function), there is high susceptibility to ascending cholangitis and bacteraemia

The common organisms are ^[13]:

• Gram-negative: E. coli, Klebsiella pneumoniae, Enterobacter spp., Bacteroides fragilis
• Gram-positive: Enterococcus spp.
• If stent present: Pseudomonas (biofilm former on foreign bodies)

C. Poor Wound Healing / Poor Anastomotic Healing [5]

• Impaired protein synthesis — the obstructed, cholestatic liver has reduced synthetic function
• Malnutrition from cancer cachexia + fat malabsorption compounds this
• This is why MBO patients are high-risk surgical candidates ^[1]

D. Liver Failure [9]

• Prolonged biliary obstruction → secondary biliary cirrhosis
• Progressive hepatocyte damage from retained bile acids (which are cytotoxic)
• Combined with biliary sepsis → hepatocellular damage → liver failure

E. Renal Failure (Hepatorenal Syndrome / Cholemic Nephrosis)

• Conjugated bilirubin and bile acids are directly nephrotoxic
• Endotoxaemia causes renal vasoconstriction
• Patients with obstructive jaundice are at high risk of post-operative acute kidney injury — this is why aggressive hydration and avoidance of nephrotoxins are critical peri-operatively

6.4 Why MBO Patients Are High-Risk Surgical Candidates

The lecture emphasises: operative risk and strategy to reduce the risk. ^[1]

The combination of:

1. Coagulopathy (vitamin K deficiency)
2. Immunosuppression (impaired reticuloendothelial function, impaired cell-mediated immunity)
3. Impaired wound/anastomotic healing (poor protein synthesis)
4. Renal vulnerability (cholemic nephrosis)
5. Malnutrition (cancer cachexia + fat malabsorption)
6. Liver dysfunction (cholestasis ± secondary biliary cirrhosis)

...makes these patients among the highest-risk in surgery. Perioperative optimisation is crucial.

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7. Classification

7.1 By Underlying Pathology

As detailed in Section 4.1 above.

7.2 By Level of Obstruction [5]

7.3 Bismuth-Corlette Classification (Perihilar Cholangiocarcinoma)

As detailed in Section 4.1B above. This classification guides surgical planning — determines how much liver and bile duct needs resection. ^[3]

7.4 Pathology Producing Jaundice AND Epigastric Mass [11]

The lecture slide specifically lists scenarios where a patient presents with both jaundice AND an epigastric mass:

Pathology producing jaundice and epigastric mass: ^[11]

• Hepatomegaly secondary to biliary obstruction
• Hepatomegaly due to metastases or HCC
• Lymph node metastases to the coeliac axis or porta hepatis
• Carcinoma of stomach with metastatic lymph node in the porta hepatis
• Distended stomach due to duodenal obstruction by tumour which obstructs the bile duct as well

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8. Clinical Features

8.1 Symptoms

8.2 Signs

8.3 Distinguishing Medical vs Surgical Jaundice on History [2]

8.4 Distinguishing Stone vs Tumour [2]

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9. Specific Clinical Features by Underlying Malignancy

9.1 Pancreatic Cancer [7] [14]

• Painless progressive obstructive jaundice (tumour at head — 70%)
• Severe epigastric pain radiating to the back (tumour at body/tail — retroperitoneal infiltration of coeliac plexus)
• Constitutional symptoms (weight loss, anorexia)
• Symptoms of pancreatic insufficiency: steatorrhoea, maldigestion, malabsorption, new-onset DM
• Acute pancreatitis / gastric outlet obstruction (GOO)
• Paraneoplastic manifestations: Trousseau syndrome (migratory superficial thrombophlebitis), paraneoplastic pemphigoid ^[14]
• Double duct sign on imaging — dilated pancreatic duct + dilated CBD (both ducts compressed by pancreatic head mass)
• Sites of metastasis: liver, peritoneum, lung, bone

9.2 Cholangiocarcinoma [3] [8]

• Jaundice: ONLY in extrahepatic (perihilar/distal) cholangiocarcinoma
• Intrahepatic cholangiocarcinoma will NOT cause jaundice (bilirubin reabsorbed and re-excreted through unaffected liver) — instead presents as a liver mass
• Dark urine and pale stools (extrahepatic cholestasis)
• Pruritus, RUQ pain, fever (if cholangitis), weight loss
• Haemobilia (UGIB from biliary tree) — uncommon ^[3]
• Hepatomegaly (intrahepatic type)
• Palpable GB (Courvoisier's law — if distal tumour) ^[3]

9.3 Gallbladder Cancer [5] [10]

• Early stage: often asymptomatic or mimics cholelithiasis/cholecystitis (biliary colic, RUQ pain)
• Late stage: obstructive jaundice, palpable mass, constitutional symptoms
• Metastasis: direct extension into liver (segments IV & V), peritoneal seeding ^[10]
• Ascites, dyspnoea/cough/haemoptysis (distant metastases) ^[5]

9.4 HCC [4]

• RUQ pain ± right shoulder pain (Glisson's capsule distension)
• Hepatomegaly
• Obstructive jaundice: NOT common — occurs only when mass near confluence or by tumour fragments/direct infiltration of CBD
• Deranged LFT in cirrhotic patients: encephalopathy, coagulopathy, portal HT (ascites, oedema, variceal bleeding)
• Paraneoplastic syndromes: erythrocytosis (EPO), hypoglycaemia (IGF-2), hypercalcaemia (PTHrP)
• Ruptured HCC (haemoperitoneum — surgical emergency)

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10. Important Concepts — Tying It Together

10.1 The "Why" Behind Painless Jaundice

The reason MBO causes painless jaundice is fundamentally about the speed of obstruction:

• Gallstones cause acute, sudden obstruction → rapid biliary distension → pain (visceral pain from stretching of bile duct wall)
• Malignant tumours grow slowly → gradual obstruction → bile ducts have time to dilate and accommodate → no acute pain
• The gallbladder similarly has time to distend gradually → painless, palpable GB

10.2 Why CA Ampulla Has the Best Prognosis

The ampulla of Vater is the narrowest point of the entire biliary/pancreatic drainage system. Even a tiny tumour here will cause obstruction → early jaundice → early presentation → earlier diagnosis → better stage at diagnosis → better prognosis ^[5].

In contrast, pancreatic body/tail tumours have no nearby duct to obstruct early, so they present late with pain and metastases.

10.3 Causes of Mortality in MBO [9]

The three main causes of death in MBO are:

1. Biliary sepsis
2. Cancer cachexia
3. Liver failure

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Active Recall - Malignant Biliary Obstruction

1. State Courvoisier's Law and explain the pathophysiological basis. Name three exceptions.

Your answer

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In painless jaundice, if the gallbladder is palpable, it is unlikely due to gallstones (points to MBO). Basis: chronic gallstones cause repeated cholecystitis leading to fibrosed, contracted GB that cannot distend; malignant obstruction occurs in a normal compliant GB that can distend. Exceptions: (1) Double impaction (stone at CBD + stone at cystic duct), (2) Mirizzi syndrome, (3) Recurrent pyogenic cholangitis (RPC).

2. List the pathophysiological disturbances caused by MBO and the mechanism for each.

Your answer

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(1) Bleeding tendency - Vitamin K deficiency from impaired fat-soluble vitamin absorption due to lack of bile salts in gut, leading to reduced synthesis of factors II, VII, IX, X. (2) Biliary sepsis/infection - endotoxaemia from impaired reticuloendothelial function and impaired cell-mediated immunity plus loss of biliary barrier. (3) Poor wound healing - impaired hepatic protein synthesis plus malnutrition. (4) Liver failure - prolonged obstruction causing secondary biliary cirrhosis and bile acid cytotoxicity. (5) Renal failure - conjugated bilirubin and bile acid nephrotoxicity plus endotoxaemia-mediated renal vasoconstriction.

3. List the malignant causes of biliary obstruction and the mechanism by which each causes obstruction.

Your answer

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(1) CA head of pancreas - direct compression/invasion of distal CBD. (2) Cholangiocarcinoma/Klatskin tumour - intrinsic obstruction at hilum. (3) HCC - compression near confluence, direct CBD infiltration, tumour fragments in CBD, porta hepatis lymphadenopathy. (4) CA gallbladder - cystic duct LN spread, direct CBD infiltration, tumour fragments. (5) Periampullary CA (ampulla, distal CBD, duodenum) - obstruction at ampullary/distal level. (6) Lymphoma. (7) Secondary hilar lymphadenopathy from GI malignancy.

4. Why does intrahepatic cholangiocarcinoma NOT typically cause jaundice while perihilar cholangiocarcinoma does?

Your answer

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Intrahepatic cholangiocarcinoma obstructs only segmental/sectoral ducts; bilirubin from those segments is reabsorbed into the blood and re-excreted through unaffected parts of the liver via patent ducts, so total bilirubin does not rise significantly. Perihilar cholangiocarcinoma (Klatskin tumour) obstructs the confluence of the right and left hepatic ducts, blocking drainage from both lobes, so bilirubin cannot be excreted at all, leading to jaundice.

5. Name the three main causes of mortality in MBO. For biliary sepsis, explain why MBO patients are particularly susceptible.

Your answer

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Three causes: (1) Biliary sepsis, (2) Cancer cachexia, (3) Liver failure. Susceptibility to biliary sepsis: biliary stasis removes the flushing action of bile, bile salts bacteriostatic effect is lost, secretory IgA reduced, sphincter of Oddi barrier may be disrupted (especially post-ERCP/stenting). Additionally, impaired reticuloendothelial (Kupffer cell) function reduces clearance of gut endotoxins, and impaired cell-mediated immunity (T-cell/NK cell suppression) from obstructive jaundice.

6. A 70-year-old presents with painless progressive jaundice and a palpable gallbladder. How would you differentiate between gallstone disease and malignant obstruction based on history and examination?

Your answer

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Tumour: painless, progressive jaundice, significant weight loss, palpable non-tender GB (Courvoisier's), new-onset DM (if pancreatic), no fever unless superimposed cholangitis. Stone: colicky episodic pain, fluctuating jaundice (ball-valve effect), fever and rigors (cholangitis), GB usually NOT palpable (fibrosed from chronic cholecystitis). Both have tea-coloured urine and pale stools, but in tumour these are persistent and progressive while in stone disease they may fluctuate.

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References

^[1] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p2–3 ^[2] Senior notes: maxim.md, Section 5.3 Obstructive jaundice ^[3] Senior notes: maxim.md, Cholangiocarcinoma section ^[4] Senior notes: maxim.md, Hepatocellular carcinoma section ^[5] Senior notes: felixlai.md, Malignant biliary obstruction section (pp. 498–505) ^[6] Senior notes: maxim.md, Recurrent pyogenic cholangitis section ^[7] Senior notes: felixlai.md, Pancreatic cancer section (p. 591) ^[8] Senior notes: felixlai.md, Cholangiocarcinoma clinical manifestation section (p. 548) ^[9] Lecture slides: Malignant biliary obstruction.pdf, p29 ^[10] Senior notes: maxim.md, CA gallbladder section ^[11] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p32 ^[12] Senior notes: maxim.md, Courvoisier's Law note (p. 130); felixlai.md, Courvoisier's Law (p. 567) ^[13] Senior notes: felixlai.md, Acute cholangitis section (p. 520) ^[14] Senior notes: maxim.md, Pancreatic carcinoma section (p. 146) ^[15] Senior notes: maxim.md, Gastric outlet obstruction section (p. 130)

Differential Diagnosis of Malignant Biliary Obstruction

The differential diagnosis of MBO is really about answering a series of nested clinical questions. When a patient walks in with jaundice, you don't jump straight to "cancer" — you systematically narrow down: Is this jaundice? → Is it obstructive? → Is the obstruction benign or malignant? → What is the specific malignant cause? Let's work through this framework from first principles.

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1. The Overarching Framework: Classifying Jaundice

Before you can diagnose MBO, you must first establish that the jaundice is obstructive (post-hepatic/surgical) rather than pre-hepatic or hepatic (medical). This is fundamental because the management pathways are completely different — medical jaundice goes to the gastroenterologist/physician; obstructive jaundice goes to the surgeon.

Why does this distinction matter? Because conjugated bilirubin is water-soluble — it is filtered by the kidneys and appears in urine (dark/tea-coloured). Unconjugated bilirubin is albumin-bound and NOT filtered by the kidneys — so urine stays normal in pre-hepatic jaundice. And if bile can't reach the gut, there's no stercobilin production → pale stool. These are bedside clues you can elicit in 30 seconds. ^[2]

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2. Differential Diagnosis of Obstructive Jaundice

Once you've established the jaundice is obstructive, the next question is: what is causing the obstruction? A clean way to think about this is by the anatomical relationship of the pathology to the bile duct wall ^[2]:

Differential diagnosis of obstructive jaundice: ^[2]

• Intraluminal: gallstone (choledocholithiasis, acute cholangitis), RPC
• Mural: cholangiocarcinoma, PSC
• Extramural: CA head of pancreas, lymphadenopathy, gallstone (Mirizzi's syndrome)

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3. Differentiating Benign vs Malignant Biliary Obstruction

This is the crux of the matter. The clinical approach is: Is this stone disease (benign) or cancer (malignant)? The distinction drives urgency and management.

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4. Differential Diagnosis by Level of Obstruction

This is clinically extremely useful. When you get imaging back (USG, CT, MRCP), you determine which parts of the biliary tree are dilated and this tells you WHERE the obstruction is. Then you generate a focused differential for that level ^[5]:

Why does the GB distend only in distal obstruction? Because the cystic duct enters the CBD approximately at the junction of the upper and middle thirds. If the obstruction is below the cystic duct junction (distal CBD), back-pressure transmits into the gallbladder via the cystic duct → GB distends. If the obstruction is above the cystic duct junction (hilum), the cystic duct is still patent and drains into a non-obstructed distal CBD → no GB distension. ^[5]

A special note on hilar obstruction: Obstruction of just ONE hepatic duct (e.g., only the right) will NOT cause jaundice because the contralateral lobe excretes bilirubin normally through its patent duct. The Klatskin tumour causes jaundice because it sits at the confluence and blocks BOTH ducts. ^{[5] [8]}

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5. The Specific Malignant Causes — Differentiating Between Them

Once you suspect MBO, the next step is: which cancer is it? This matters because treatment differs.

5.1 Pathology Causing Malignant Biliary Obstruction [1]

The lecture slide specifically lists:

Carcinoma of duodenum, periampullary carcinoma, carcinoma of pancreas, lymphoma, carcinoma of gallbladder (cystic duct LN, direct infiltration of CBD, tumour fragments), cholangiocarcinoma at hilum (Klatskin tumour), HCC (direct infiltration, compression, tumour fragments in CBD) ^[1]

5.2 Cystic vs Solid Pancreatic Mass

The senior notes highlight that the differential diagnosis for pancreatic cancer is broad and should be based upon whether the mass is cystic or solid on imaging ^[7]:

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6. Differential Diagnosis of "Jaundice + Epigastric Mass"

This is a specific clinical scenario highlighted by the lecture slides ^[11]. When both jaundice AND an epigastric mass are present, consider:

Pathology producing jaundice and epigastric mass: ^[11]

• Hepatomegaly secondary to biliary obstruction
• Hepatomegaly due to metastases or HCC
• Lymph node metastases to the coeliac axis or porta hepatis
• Carcinoma of stomach with metastatic lymph node in the porta hepatis
• Distended stomach due to duodenal obstruction by tumour which obstructs the bile duct as well

Why do these all cause BOTH jaundice AND a mass?

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7. Specific Benign Mimics of MBO That Must Be Excluded

A. Acute Cholangitis [13]

Charcot's triad (50–70%): Fever, RUQ pain, jaundice Reynold's pentad ( < 10%): above + shock + altered mental status ^[13]

• Usually caused by choledocholithiasis (most common), but MBO itself can cause cholangitis (stasis + bacteria)
• The presence of fever and pain distinguishes cholangitis from "pure" MBO. However, MBO can be complicated by cholangitis — so cholangitis doesn't exclude MBO, it just means there's superimposed infection.

B. Mirizzi Syndrome [12]

• CHD obstruction caused by extrinsic compression from an impacted stone in Hartmann's pouch/cystic duct ^[12]
• Can present as jaundice with palpable GB — an exception to Courvoisier's Law ^[12]
• Important to recognise because it can mimic cholangiocarcinoma on imaging — CT with contrast needed to rule out malignant causes (e.g., porta hepatis LN) ^[12]

C. PSC [16]

• Chronic progressive inflammation → fibrosis → "beading" of bile ducts on cholangiography
• Strong association with ulcerative colitis ^[16]
• Can itself be a risk factor for cholangiocarcinoma — so PSC and cholangiocarcinoma can coexist, making differentiation extremely difficult
• IgG4-associated cholangitis must be distinguished from PSC (elderly male, responds to steroids) ^[16]

D. PBC [17]

• T-lymphocyte attack on small intralobular bile ducts → intrahepatic cholestasis
• Extreme female predominance (90–95%), middle-aged ^[17]
• Anti-mitochondrial antibody (AMA) positive
• Does NOT cause extrahepatic duct dilatation — this is a key imaging distinction from MBO

E. Choledochal Cysts [19]

• Congenital dilatation of intra/extrahepatic biliary system
• Most diagnosed before age 10 (60%)
• Classic triad: RUQ mass + pain + jaundice + fever
• Important because they are a risk factor for cholangiocarcinoma — can undergo malignant transformation

F. IgG4-Related Sclerosing Cholangitis

• Infiltration of biliary system with IgG4-positive plasma cells; predominantly elderly male ^[16]
• Can mimic cholangiocarcinoma or PSC on imaging
• Serum IgG4 elevated; responds dramatically to corticosteroids (unlike cholangiocarcinoma)
• Must be distinguished from cholangiocarcinoma before committing to major surgery ^[8]

G. Autoimmune Pancreatitis

• IgG4-related disease affecting the pancreas → can cause a pancreatic head mass mimicking pancreatic cancer
• "Sausage-shaped" pancreas on CT; elevated IgG4; responds to steroids
• Critical to differentiate because treatment is medical (steroids), not surgical (Whipple's)

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8. The Clinical Approach — Systematic DDx Algorithm

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9. Differential Diagnosis of Specific Cholangiocarcinoma [8]

The senior notes specifically list the DDx for cholangiocarcinoma — which is essentially the DDx for any patient presenting with hilar or proximal biliary obstruction:

• Choledocholithiasis — stones cause intraluminal obstruction; fluctuating jaundice, pain, fever
• Viral hepatitis — hepatic cause; transaminases ↑↑; no duct dilatation on imaging
• HCC — AFP elevated; known CLD/HBV; usually hepatomegaly rather than obstructive jaundice
• Pancreatic cancer — distal CBD obstruction; double duct sign; CA 19-9
• Cancer of the ampulla of Vater — earliest jaundice; visible on OGD at ampulla
• PSC — beaded bile ducts on cholangiography; associated with UC; chronic course
• PBC — AMA positive; female; small duct cholestasis; no extrahepatic dilatation

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10. Summary Table: Key Differentials and How to Distinguish Them

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Active Recall - Differential Diagnosis of MBO

1. Classify the differential diagnosis of obstructive jaundice by the anatomical relationship to the bile duct wall. Give two examples for each category.

Your answer

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Intraluminal: choledocholithiasis, RPC. Mural: cholangiocarcinoma, PSC. Extramural: CA head of pancreas, Mirizzi syndrome (or lymphadenopathy).

2. A patient with painless progressive jaundice has dilated intrahepatic ducts but a NORMAL calibre CBD on imaging. The gallbladder is NOT distended. Where is the obstruction and what are the top three differential diagnoses?

Your answer

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Obstruction is at the hilum (above the cystic duct junction). Top 3: (1) Klatskin tumour (cholangiocarcinoma at CHD bifurcation), (2) CA gallbladder with hilar invasion/LN, (3) HCC near confluence (segment 4/5). Others: porta hepatis lymphadenopathy, Mirizzi syndrome, PSC, RPC.

3. Why does CA ampulla of Vater have the best prognosis among periampullary carcinomas? Explain from first principles.

Your answer

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The ampulla of Vater is the narrowest point of the biliary/pancreatic drainage system. Even a tiny tumour here causes obstruction and early jaundice, leading to early clinical presentation, earlier diagnosis, and better stage at diagnosis. Earlier stage means higher resectability rate and better survival.

4. List five causes of jaundice with an epigastric mass as per the lecture.

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(1) Hepatomegaly secondary to biliary obstruction, (2) Hepatomegaly due to metastases or HCC, (3) Lymph node metastases to coeliac axis or porta hepatis, (4) Carcinoma of stomach with metastatic lymph node in porta hepatis, (5) Distended stomach due to duodenal obstruction by tumour which also obstructs the bile duct.

5. How would you distinguish IgG4-related sclerosing cholangitis from cholangiocarcinoma? Why is this distinction critical?

Your answer

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IgG4-related: elderly male, elevated serum IgG4, may have autoimmune pancreatitis (sausage-shaped pancreas), responds dramatically to corticosteroids. CholangioCA: does not respond to steroids, progressive obstruction, tissue diagnosis shows adenocarcinoma. Distinction is critical because IgG4-disease is treated medically with steroids (avoid unnecessary major surgery like Whipple's or hepatectomy), whereas cholangiocarcinoma requires surgical resection.

6. Explain why obstruction of only the right hepatic duct does NOT cause jaundice, but a Klatskin tumour at the confluence does.

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Isolated right hepatic duct obstruction means the left hepatic duct still drains bile from the left lobe normally. Bilirubin from the obstructed right lobe is reabsorbed into blood and re-excreted through the unaffected left lobe's patent ducts, so total serum bilirubin does not rise significantly. A Klatskin tumour sits at the CHD bifurcation, blocking drainage from BOTH right and left hepatic ducts, so bilirubin has no route of excretion and accumulates in the blood, causing jaundice.

References

^[1] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p23 ^[2] Senior notes: maxim.md, Section 5.3 Obstructive jaundice ^[3] Senior notes: maxim.md, Cholangiocarcinoma section ^[4] Senior notes: maxim.md, Hepatocellular carcinoma section ^[5] Senior notes: felixlai.md, Malignant biliary obstruction section (pp. 498–502) ^[6] Senior notes: maxim.md, Recurrent pyogenic cholangitis section ^[7] Senior notes: felixlai.md, Pancreatic cancer section (p. 591) ^[8] Senior notes: felixlai.md, Cholangiocarcinoma clinical manifestation and DDx (p. 548) ^[10] Senior notes: maxim.md, CA gallbladder section ^[11] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p32 ^[12] Senior notes: maxim.md, Mirizzi syndrome section; felixlai.md, Courvoisier's Law ^[13] Senior notes: felixlai.md, Acute cholangitis section (p. 520); maxim.md, Acute cholangitis section ^[14] Senior notes: maxim.md, Pancreatic carcinoma section (p. 146) ^[15] Senior notes: maxim.md, Gastric outlet obstruction section ^[16] Senior notes: felixlai.md, Primary sclerosing cholangitis section ^[17] Senior notes: felixlai.md, Primary biliary cholangitis section ^[18] Lecture slides: Malignant biliary obstruction.pdf, p8 ^[19] Senior notes: maxim.md, Choledochal cyst section

Diagnosis of Malignant Biliary Obstruction — Criteria, Algorithm & Investigations

1. Diagnostic Approach — The Logic

There is no single "diagnostic criterion" for MBO the way there is for, say, acute cholangitis (Tokyo Guidelines) or PBC (AMA + ALP + histology). MBO is a clinical-radiological diagnosis — you put together the clinical picture (painless progressive jaundice, Courvoisier's sign) with biochemistry (cholestatic LFT) and imaging (dilated ducts + mass) to arrive at a diagnosis and then characterise the underlying malignancy.

The lecture frames the management approach in four sequential steps ^[20]:

Management of MBO: ^[20]

1. Establish diagnosis
2. Delineate level and cause of obstruction
3. Treat suppurative cholangitis
4. Definitive treatment

And the learning objectives explicitly state ^[1]:

Imagings for jaundice and epigastric mass ^[1]

So the diagnostic workup is systematically: Clinical assessment → Bloods → Imaging (anatomical → cholangiographic → tissue) → Staging. Let's go through each layer.

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2. Physical Examination — What to Look For and Why

Physical examination in MBO is not just "ticking boxes" — each finding tells you something about the disease and its stage.

2.1 General Examination [5]

2.2 Abdominal Examination [5]

Signs of inoperability ^[5]:

• Irregular surface hepatomegaly — suggests metastatic liver deposits; irregular nodular surface
• Troisier's sign (Virchow's node) — left supraclavicular lymph node; indicates distant lymphatic spread via thoracic duct
• Blumer's shelf — palpable mass on digital rectal exam; peritoneal metastasis seeding to the rectovesical/rectouterine pouch (most dependent peritoneal recess)
• Sister Mary Joseph nodules — umbilical nodule; peritoneal metastasis tracking along the obliterated umbilical vein (ligamentum teres)
• Ascites — peritoneal carcinomatosis (malignant ascites)

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3. Biochemical Investigations

3.1 Blood Tests — The Rationale for Each

3.2 Tumour Markers

This is an area where students often get confused. Let's be crystal clear:

Tumour markers such as AFP, CA 19-9, and CEA are NOT very useful for MBO as a screening tool and are not included in the initial testing. ^[5] Common tumour markers are neither sensitive nor specific for periampullary tumours. ^[5] Absence of an elevated tumour marker does not exclude underlying malignancy. ^[5]

The lecture slide provides a detailed marker table ^[18]:

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4. Imaging Investigations

This is the heart of the diagnostic workup. The lecture slide states ^[21]:

Imaging: ^[21]

• Ultrasound / CT
• Size of bile duct
• Level of obstruction
• Cause of obstruction
• Other associated features
• Malignant disease: staging
• Benign disease: gallstones > complications

4.1 Transabdominal Ultrasound (USG) — First-Line

Why USG first? It is non-invasive, widely available, cheap, no radiation, and excellent at detecting biliary dilatation and gallstones. It answers the first critical question: Is there biliary obstruction?

Key USG finding: Malignant obstruction is suggested by ductal dilatation ( > 6 mm in adults) in the absence of stones ^[8]

4.2 CT Abdomen with Contrast — The Workhorse

CT is the definitive cross-sectional imaging for MBO. It simultaneously assesses: the mass, the level of obstruction, vascular involvement, lymph node status, and distant metastases.

For pancreatic cancer specifically, the CT protocol is critical: ^[14]

CT abdomen with contrast (pancreatic protocol) — thin-sliced triphasic (arterial + pancreatic + portovenous phases) ^[14]

Key CT findings for different MBO causes:

Determine resectability: encasement of SMA, hepatic artery, celiac trunk, SMV, PV ^{[14] [3]}

4.3 Cholangiography — Delineating the Biliary Tree

Once USG/CT has confirmed obstruction and localised the level, you need detailed mapping of the biliary anatomy — this is essential for surgical planning.

A. MRCP (Magnetic Resonance Cholangiopancreatography) — Non-invasive [20]

• Non-contrast, T2-weighted MRI ^[20]
• Non-invasive imaging of biliary system and GB ^[20]
• Superior in delineating the anatomy of biliary tree especially if the system is not completely obstructed ^[7]
• Largely replaces ERCP as a diagnostic tool ^[5]
• Avoids complications associated with ERCP, but NOT therapeutic ^[20]
• When to use: Patients without high suspicion of biliary obstruction (mild bilirubin/ALP elevation, equivocal CT findings) ^[5]; when anatomy delineation is needed before surgery; when ERCP is not indicated therapeutically

B. ERCP (Endoscopic Retrograde Cholangiopancreatography) — Invasive, Diagnostic + Therapeutic

• ERCP is both diagnostic AND therapeutic ^[5]
• Diagnostic: Direct cholangiogram; brush cytology; forceps biopsy for tissue diagnosis
• Therapeutic: Biliary stent placement; sphincterotomy; stone extraction
• Preferred for distal tumours ^[3] — the scope goes through the mouth → oesophagus → stomach → D2 → accesses the ampulla → cannulates the CBD from below
• ERCP brush cytology / biopsy: can also relieve jaundice by placing temporary stent ^[14]
• Complications: Pancreatitis (most common), bleeding, cholangitis, perforation — this is why ERCP has evolved into a mainly therapeutic modality ^[7]

C. PTC / PTBD (Percutaneous Transhepatic Cholangiography / Biliary Drainage) — Invasive [20]

• Diagnostic: Visualisation of biliary tree by percutaneous needle insertion through the liver into a dilated intrahepatic duct, then injection of contrast
• Therapeutic: External bile drainage by catheter (PTBD) or insertion of indwelling stents
• Preferred to ERCP for stricture/obstruction at or above the level of confluence of hepatic ducts ^[20] — because ERCP approaches from below and may not be able to pass contrast above a complete hilar obstruction
  • Examples: cholangiocarcinoma, PSC, RPC ^[20]
• Complications: bacteraemia (thus antibiotic prophylaxis required), haemobilia ^[20]

4.4 Endoscopic Ultrasound (EUS) ± FNAC / Biopsy

EUS combines endoscopy (placing a probe in the duodenum/stomach) with high-frequency ultrasound — giving you extremely close-up, high-resolution images of the pancreas, bile duct, and surrounding structures.

4.5 Tissue Diagnosis — When Is It Mandatory?

This is a nuanced and commonly examined point:

Tissue diagnosis is NOT mandatory if potentially resectable ^[14]

Why not? Because:

1. If imaging is classic for pancreatic CA and the tumour is resectable, going to surgery provides both the definitive treatment AND the tissue diagnosis (histology from the resected specimen)
2. Delaying surgery for a biopsy can set back treatment
3. Percutaneous biopsy carries risk of tumour seeding along the needle tract

When IS tissue diagnosis indicated? ^{[7] [14]}:

• CT failed to demonstrate typical features (uncertain diagnosis)
• Before starting neoadjuvant chemotherapy (need confirmed malignancy before giving toxic treatment)
• Suspected secondary metastasis to pancreas (need to identify the primary)
• To exclude mimics like autoimmune pancreatitis or chronic pancreatitis (which respond to steroids/medical treatment, NOT surgery) ^[7]
• Local evidence of unresectability on staging (patient will receive palliative chemo → need tissue confirmation first)

Methods of tissue diagnosis:

• EUS-guided FNAC/biopsy — preferred (less seeding risk) ^[14]
• ERCP brush cytology / forceps biopsy — can also relieve jaundice simultaneously ^[14]
• CT-guided percutaneous biopsy — higher seeding risk; used when EUS not available or not feasible
• Mother-baby cholangioscopy (SpyGlass) — for biliary strictures where EUS cannot reach the duct lumen ^[5]

4.6 Staging Investigations

Once MBO is confirmed, staging determines resectability — this is the single most important question after diagnosis:

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5. The Diagnostic Algorithm — Putting It All Together

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6. Special Investigation Scenarios by Suspected Malignancy

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7. Specific Imaging Findings — Interpretation Guide

7.1 Ultrasound Findings

7.2 CT Findings

7.3 MRCP Findings

7.4 Cholangiographic Findings (ERCP/PTC)

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8. Criteria for Unresectability on Imaging [3] [7] [14]

This is critical because it determines whether the patient gets curative surgery or palliative care:

Unresectable if: ^[3]

• Invasion of major vessels (e.g., main PV, main hepatic artery, celiac trunk, SMA, SMV) ^{[3] [14]}
• Extensive involvement of biliary tree (bilaterally > 2° radicles) ^[3]
• LN metastasis (retropancreatic, paracoeliac, paraaortic) ^[3]
• Distal organ metastasis (lung, peritoneum) ^[3]

For pancreatic cancer specifically ^[14]:

• Borderline resectable: Tumour abutting ( ≤ 180° contact) SMA/celiac axis or short-segment encasement of hepatic artery (without extension to celiac); SMV/PV involvement with potential for reconstruction
• Unresectable (locally advanced): Tumour encasing ( > 180°) SMA/celiac axis; unreconstructable SMV/PV occlusion
• Unresectable (metastatic): Any distant metastasis

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9. Summary Table: Investigation Modalities at a Glance

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Active Recall - Diagnosis of MBO

1. List the four sequential steps in the management/diagnostic approach to MBO as stated in the lecture.

Your answer

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(1) Establish diagnosis, (2) Delineate level and cause of obstruction, (3) Treat suppurative cholangitis, (4) Definitive treatment.

2. What are the normal size limits for the intrahepatic ducts and CBD on USG? What constitutes pathological dilatation?

Your answer

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Intrahepatic ducts normally not visible on USG (less than 2-3 mm). CBD greater than 0.8 cm (8 mm) is pathological. Rule of thumb: 0.1 cm per 10 years of age as upper limit.

3. Explain the double-duct sign. What pathology does it suggest and why?

Your answer

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Double-duct sign = simultaneous dilatation of both the common bile duct and main pancreatic duct. Suggests CA head of pancreas because a mass in the pancreatic head compresses both ducts as they converge at the ampulla of Vater. Can also be seen in ampullary carcinoma or chronic pancreatitis.

4. When is tissue diagnosis NOT mandatory before surgery in suspected pancreatic cancer? When IS it indicated?

Your answer

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NOT mandatory if imaging is classic and tumour is potentially resectable - surgery provides both treatment and tissue diagnosis. IS indicated if: (1) CT findings atypical/uncertain, (2) before neoadjuvant chemotherapy, (3) suspected 2nd primary/metastasis to pancreas, (4) unresectable disease requiring palliative chemo confirmation, (5) differential includes autoimmune pancreatitis or chronic pancreatitis.

5. Compare ERCP and PTC: which is preferred for proximal vs distal obstruction, and why?

Your answer

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ERCP preferred for distal obstruction - approaches from below through the ampulla, can cannulate and stent the distal CBD, and provides direct visualisation. PTC preferred for proximal/hilar obstruction (e.g., Klatskin tumour, PSC, RPC) - approaches from above through the liver into dilated intrahepatic ducts, can pass contrast above a complete hilar obstruction that ERCP cannot traverse from below.

6. List four criteria for unresectability in cholangiocarcinoma/periampullary cancer.

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(1) Invasion of major vessels: main portal vein, main hepatic artery, celiac trunk, SMA, SMV. (2) Extensive biliary involvement bilaterally beyond secondary radicles. (3) Distant lymph node metastasis: retropancreatic, paracoeliac, paraaortic. (4) Distant organ metastasis: lung, peritoneum, liver.

References

^[1] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p3 ^[3] Senior notes: maxim.md, Cholangiocarcinoma section (investigations and management) ^[4] Senior notes: maxim.md, Hepatocellular carcinoma section ^[5] Senior notes: felixlai.md, Malignant biliary obstruction section (pp. 501–503) ^[7] Senior notes: felixlai.md, Pancreatic cancer section (pp. 596–598) ^[8] Senior notes: felixlai.md, Cholangiocarcinoma diagnosis section (pp. 549–551) ^[10] Senior notes: maxim.md, CA gallbladder section ^[13] Senior notes: felixlai.md, Acute cholangitis section; maxim.md, Acute cholangitis section ^[14] Senior notes: maxim.md, Pancreatic carcinoma section (p. 146) ^[18] Lecture slides: Malignant biliary obstruction.pdf, p8 ^[20] Senior notes: maxim.md, HBP investigations section; Lecture slides: Malignant biliary obstruction.pdf, p10 and p15 ^[21] Lecture slides: Malignant biliary obstruction.pdf, p10

Management of Malignant Biliary Obstruction

1. The Management Framework — Thinking From First Principles

The management of MBO follows a clear logical sequence. You cannot just "operate" — these patients are among the highest-risk in all of surgery. The lecture provides the overarching framework ^[20]:

Management: ^[20]

1. Establish diagnosis
2. Delineate level and cause of obstruction
3. Treat suppurative cholangitis
4. Definitive treatment

And a more granular decision-making algorithm from the lecture slides ^[22]:

MBO → Treat SEPSIS → (1) Assess tumour resectability, (2) Patient general fitness, (3) Liver function reserve → Resectable vs Non-resectable → Palliation ^[22]

The key decision point is a two-axis assessment ^[5]:

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2. The Master Management Algorithm

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3. Step 1 — Treat Sepsis First

Before ANY definitive treatment decision, you must address superimposed biliary sepsis (cholangitis), which is life-threatening:

Palliative care: Treat sepsis, Relieve obstruction (enteric/biliary), Pain control ^[23]

Antibiotics ^[5]:

• Augmentin (amoxicillin-clavulanate) OR Cefuroxime (Zinacef) + Metronidazole (Flagyl) ^[5]
• Why these agents? They cover the typical biliary pathogens: Gram-negative rods (E. coli, Klebsiella) + anaerobes (Bacteroides) + Enterococci ^[13]
• For severe sepsis/shock: escalate to IV Tazocin (piperacillin-tazobactam) ^[13]

Emergency biliary drainage ^[13]:

• Indicated if: Reynold's pentad (fever + jaundice + RUQ pain + shock + altered mental status) or not responding to antibiotics for 24 hours (because antibiotics cannot be adequately secreted into bile when the duct is obstructed) ^[13]
• QMH practice: ERCP → PTBD → surgical exploration (ECBD with T-tube) ^[13]

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4. Step 2 — Assess the Two Axes

4.1 Assessing General Status (Patient Fitness) [5]

4.2 Assessing Tumour Status (Resectability) [5]

Clinical signs of inoperability (found on physical exam) ^[5]:

• Irregular surface hepatomegaly → liver metastases
• Troisier's sign (Virchow's node) → distant lymphatic spread
• Blumer's shelf → peritoneal metastases
• Sister Mary Joseph nodules → peritoneal metastases
• Ascites → peritoneal carcinomatosis

Radiological signs of inoperability ^{[5] [3]}:

• LN metastasis (retropancreatic, paracoeliac, paraaortic)
• Distant metastasis (liver, lung, peritoneum)
• Arterial involvement (SMA / Celiac axis) — encasement > 180°
• Venous involvement (SMV / PV) — NOTE: Portal vein involvement is NOT an absolute contraindication ^[5]
  • Venous resection is appropriate to improve resectability and achieve R0 resection (absence of microscopic residual tumour) ^[5]
  • Depends on the extent of involvement and QMH may consider resection of portal vein ^[5]
• Extensive involvement of biliary tree (bilaterally > 2° radicles) ^[3]

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5. Step 3 — Pre-operative Optimisation

Why is malignant biliary obstruction so risky for operation? ^[24]

• Cancer cachexia → malnutrition
• Liver function impairment
• Superimposed biliary infection

These three problems must be addressed before taking a patient to theatre:

5.1 Pre-operative Biliary Drainage

This is a nuanced and commonly examined topic:

Relief of biliary obstruction before surgery ^[25]:

• ERCP and endoprosthesis
• Percutaneous transhepatic biliary drainage
• Target level: Serum bilirubin < 50 µmol/L or < 20 µmol/L for concomitant partial hepatectomy ^[25]

Why drain pre-operatively? ^[5]

• Minimise risk of developing cholangitis while awaiting surgery
• Relieve jaundice and pruritus
• Prevent complications of prolonged cholestasis (renal impairment, coagulopathy, immune dysfunction)
• Allow time for neoadjuvant therapy in locally advanced disease

The debate — to drain or not to drain? ^[5]

Theoretically: Do NOT need to drain if no sepsis + early surgery can be offered within 1–2 weeks ^[5]

• Pre-operative biliary drainage increases risk of serious complications (pancreatitis, cholangitis, stent occlusion) even in expert hands
• Surgical-related complications are comparable even without drainage

Practically (QMH): Drain ALL patients since QMH cannot offer early surgery ^[5]

• Whipple operation has to wait for 6–8 weeks and the chance of biliary sepsis will be very high without drainage while waiting ^[5]

Advantages of pre-op drainage ^[5]:

• Minimise cholangitis risk during the wait
• Relieve symptoms (jaundice, pruritus)
• Allow neoadjuvant therapy

Disadvantages of pre-op drainage ^[5]:

• Increase the number of interventions and associated costs
• Increase risk of procedure-related complications: cholangitis, pancreatitis, bleeding, perforation, stent blockage

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6. Curative Treatment — Surgical Resection

Role of surgery: ^[26]

• Oncological clearance — R0 resection
• Relieve obstruction
• Pain control

Laparotomy is indicated if patient's general status is good and tumour is confined ^[5]:

• No promise of resection until laparotomy findings document absence of spread ^[5]
• Look for peritoneal nodules after laparotomy before resection and send for frozen section to rule out malignancy if suspicious ^[5]

6.1 Surgical Treatment by Underlying Pathology

6.2 The Whipple Operation — Understanding Why It Removes So Much

Let's explain from first principles why the Whipple operation (pancreaticoduodenectomy) requires resection of so many structures:

The head of the pancreas, the duodenum (D1–D3), the distal CBD, and the gallbladder share an intimate blood supply (gastroduodenal artery, inferior pancreaticoduodenal artery) and anatomical connections (the CBD runs through the pancreatic head; the pancreatic duct and CBD converge at the ampulla in D2). You cannot remove the pancreatic head without devascularising the duodenum, and you cannot leave the distal CBD behind without leaving residual tumour. Therefore, all these structures must come out as a single specimen.

Three reconstruction anastomoses after Whipple:

1. Pancreaticojejunostomy — reconnects remaining pancreatic body/tail to jejunum (so pancreatic juice drains into bowel)
2. Hepaticojejunostomy — reconnects remaining hepatic duct to jejunum (so bile drains into bowel)
3. Gastrojejunostomy (or duodenojejunostomy if PPPD) — reconnects stomach to jejunum (so food can pass into bowel)

6.3 Cholangiocarcinoma — Additional Surgical Considerations [3]

• If FLR (future liver remnant) inadequate: portal vein embolisation (PVE) to induce atrophy of affected segment + hypertrophy of unaffected segments ^[3]
  • Why? Blocking the portal vein branch to the side with the tumour causes that side to atrophy while the healthy side hypertrophies over 4–6 weeks — increasing the volume of functional liver that will remain after resection. Without this, post-hepatectomy liver failure is a major risk.
• Pre-operative drainage (ERCP / PTBD) considered if biliary sepsis / poor LFT ^[3]

6.4 Gallbladder Cancer — Specific Surgical Approach [10]

• Open approach for cholecystectomy is generally recommended since port site recurrences and late peritoneal metastasis associated with bile spillage are reported with laparoscopic approach ^[10]
• Open cholecystectomy with intra-op frozen section ^[10]:
  • Stage I disease (T1N0, confined to mucosa): no further treatment required
  • Higher stage disease (extending to serosa/transmural): extended cholecystectomy ^[10]
    • En-bloc resection of gallbladder with rim of liver ≥ 2 cm adjacent to gallbladder bed
    • Segmental hepatectomy (segments IVb, V)
    • Extrahepatic bile duct resection (if cystic duct involved)
    • Regional lymphadenectomy (porta hepatis LN) ^[10]

Intra-op frozen section of cystic duct ^[10]:

• Positive → regional LN dissection + extrahepatic bile duct resection with Roux-en-Y hepaticojejunostomy ^[10]
• Negative → regional LN dissection only

Absolute contraindications for radical resection of CA gallbladder ^[10]:

• Liver metastasis
• Peritoneal metastasis
• Malignant ascites
• Encasement or occlusion of major vessels (hepatic artery / portal vein)
• Involvement of paraaortic, pericaval, SMA, or celiac artery lymph nodes (considered distant metastatic disease)
• Extensive involvement of the hepatoduodenal ligament

6.5 Adjuvant Therapy

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7. Palliative Treatment — For Unresectable Disease

Only 15–20% of patients with pancreatic cancer are surgical candidates due to late presentation ^[7]. For the majority, palliation focuses on three pillars ^{[23] [7]}:

Palliative care: Treat sepsis, Relieve obstruction (enteric/biliary), Pain control ^[23]

7.1 Relieving Biliary Obstruction — Stenting vs PTBD vs Surgical Bypass

A. ERCP with Endoprosthesis (Endoscopic Stenting) — First Line [5]

ERCP with endoprosthesis is ALWAYS 1st line regardless of the level of obstruction especially for periampullary carcinoma ^[5]

Exceptions (when ERCP is NOT feasible) ^[5]:

• Contraindications for ERCP (e.g., structural upper GI abnormalities, partial gastrectomy with Billroth II or Roux-en-Y anastomosis — altered anatomy prevents scope from reaching the ampulla)
• Multiple stenting required or difficulty in reaching intrahepatic bile ducts (proximal/hilar obstruction)

Types of stents ^{[3] [5] [27]}:

Complications of stenting ^{[5] [3]}:

• Stent occlusion — from bile sludge, tumour ingrowth (through uncovered mesh), or tumour overgrowth (tumour growing over the stent ends) → Managed by sweeping or placing a new stent ^[3]
• Stent migration ^[3]
• Cholangitis / Cholecystitis ^[5]

B. Percutaneous Transhepatic Biliary Drainage (PTBD) [5]

• Indicated when ERCP is unsuccessful, unavailable, or contraindicated ^[5]
• ERCP with endoprosthesis is preferred over PTBD because ^[5]:
  • PTBD is technically more difficult
  • Bleeding is common due to puncture of hepatic artery or portal vein before reaching the bile duct (Portal triad) ^[5]

Types of PTBD ^[5]:

• Simple external PTBD: Short-term drainage to bridge to surgery; prone to electrolyte and fluid loss due to bile output
• External-internal type PTBD: Long-term palliation; catheter passes through the obstruction into the duodenum; side-holes above AND below the obstruction allow internal drainage; can be capped to internalise flow ^{[5] [27]}

PTBD complication management ^[5]:

• If bleeding after PTBD insertion:
  1. Stabilise and resuscitate
  2. Clamp the PTBD catheter
  3. Perform cholangiogram by injecting contrast into PTBD to determine if catheter is in hepatic artery or portal vein
  4. Remove catheter slowly to control bleeding — do NOT remove immediately as this converts the situation into free haemoperitoneum ^[5]

Complications of PTBD ^[5]:

• Cholangitis / Biliary sepsis
• Haemobilia (communication of the tract with a major vascular structure)

C. Palliative Bypass Surgery [5]

Palliative bypass is used when endoscopic/percutaneous approaches fail or when unresectability is discovered at laparotomy ^[14]:

When tumour found unresectable during laparotomy ^[14]:

• Double bypass surgery (gastric bypass + biliary bypass)
• Obtain transduodenal trucut biopsy ± celiac plexus block ^[14]

D. Comparison: Stenting/PTBD vs Surgical Bypass [28]

Prospective randomised trials comparing percutaneous or endoscopic drainage with surgical biliary bypass: ^[28]

Clinical decision: If the patient has a short life expectancy ( < 3–6 months), stenting is preferred (lower initial morbidity, avoids major surgery). If the patient has longer expected survival or unresectability is found at laparotomy, surgical bypass gives better long-term palliation.

7.2 Relieving Enteric Obstruction (Gastric Outlet Obstruction) [7]

CA head of pancreas can compress the duodenum → GOO:

• Endoscopic duodenal wall stenting ^[7] — self-expanding metallic stent placed endoscopically across the duodenal stricture
• Gastrojejunostomy (GJ) — surgical bypass of the duodenal obstruction ^[5]
• Percutaneous endoscopic gastrostomy (PEG) placement for decompression ^[7] — in patients unfit for any other intervention

7.3 Pain Control [5] [7]

Pain in MBO is primarily from retroperitoneal tumour infiltration of the celiac plexus (especially in CA body/tail of pancreas):

• Step 1: Analgesic ladder — paracetamol → NSAIDs → opioids (morphine) ^[7]
• Step 2: Endoscopic USG / CT-guided celiac plexus neurolysis (celiac plexus block) ^{[5] [7]}
  • How it works: Injection of alcohol (ethanol) or phenol into/around the celiac plexus (located anterior to the aorta at T12–L1) → chemical destruction of the sympathetic nerve fibres that transmit visceral pain from the upper abdomen
  • Adequate pain control is explicitly listed as a component of palliative care ^[5]
• Step 3: Short-course radiotherapy for local pain relief ^[14]

7.4 Palliative Chemotherapy [7] [8]

7.5 Management of Pancreatic Insufficiency [14]

If the pancreatic duct is also obstructed or pancreatic parenchyma is destroyed:

• Exocrine insufficiency → Pancreatic enzyme replacement (Creon)
• Endocrine insufficiency → OHA / insulin for diabetes management ^[14]

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8. EUS-Guided Interventions — Advanced Approaches [27]

When both ERCP and PTBD fail (or are contraindicated), EUS-guided transmural drainage offers alternatives:

These are increasingly available at specialised centres (including QMH) as rescue techniques.

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9. Special Considerations — Pre-operative Drainage in Detail

9.1 Method Selection [5] [25]

9.2 Stent Placement for Hilar Obstruction

• Use of unilateral or bilateral stents is controversial for hilar obstruction ^[8]
• Unilateral: Drains only one side; simpler; lower complication rate; but may not adequately relieve jaundice if both lobes are obstructed (Bismuth Type IV)
• Bilateral: Drains both lobes; better jaundice relief; but technically more difficult; higher complication rate
• Endoscopic method is preferred due to less inconvenience without external drainage, lower risk of bile leaks and bleeding ^[8]
• Percutaneous method has a higher success rate of palliation of jaundice and lower risk of early cholangitis but external drainage is inconvenient ^[8]

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10. Summary — Decision Flowchart by Clinical Scenario

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Active Recall - Management of MBO

1. State the three reasons why MBO is high-risk for operation and the pre-operative measures to address each.

Your answer

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(1) Cancer cachexia leading to malnutrition — nutritional support (enteral feeding, albumin correction). (2) Liver function impairment leading to bleeding tendency — IV Vitamin K and FFP during surgery. (3) Superimposed biliary infection — broad-spectrum antibiotic cover (Augmentin OR Cefuroxime + Metronidazole).

2. What is the target bilirubin before surgery in MBO? Why is the target different for operations involving hepatectomy?

Your answer

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Target bilirubin less than 50 micromol/L for standard surgery (e.g. Whipple). Less than 20 micromol/L for surgery with concomitant partial hepatectomy. The stricter target for hepatectomy is because the remaining future liver remnant must be functional; operating on a cholestatic liver with high bilirubin dramatically increases the risk of post-hepatectomy liver failure due to impaired hepatic regenerative capacity.

3. Compare single, double, and triple palliative bypass. What does each bypass, and when is each indicated?

Your answer

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Single bypass = Hepaticojejunostomy — bypasses biliary obstruction only. Double bypass = Single + Gastrojejunostomy — bypasses biliary AND enteric obstruction (GOO); indicated especially for CA head of pancreas which compresses both CBD and duodenum. Triple bypass = Double + Pancreaticojejunostomy — additionally bypasses pancreatic duct obstruction; rarely performed because pancreatic duct is small and anastomosis carries high risk of anastomotic leakage.

4. ERCP stenting is always first line for palliative biliary drainage. State three situations where it cannot be used, and what alternative is employed.

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(1) Structural upper GI abnormalities or altered anatomy (e.g. Billroth II, Roux-en-Y reconstruction — scope cannot reach ampulla). (2) Multiple stenting required or difficulty reaching intrahepatic bile ducts (proximal/hilar obstruction). (3) Failed ERCP cannulation. Alternative: Percutaneous transhepatic biliary drainage (PTBD).

5. When should you use a plastic stent vs a metallic stent in MBO, and why?

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Plastic stent: temporary pre-operative drainage or uncertain diagnosis — because plastic stents can be removed and exchanged easily; allows flexibility if patient proceeds to curative surgery. Metallic stent (SEMS): confirmed inoperable malignancy — because metallic stents have longer patency (months vs weeks), are more durable, but cannot be removed. Uncovered metallic stents preferred to avoid occluding biliary branches.

6. What is the role of portal vein embolisation in the management of Klatskin tumour? Explain the mechanism.

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PVE is performed when the future liver remnant (FLR) is inadequate after planned major hepatectomy. Mechanism: the portal vein branch supplying the tumour-bearing side is embolised, cutting off its portal blood flow. This causes atrophy of the affected segments and compensatory hypertrophy of the unaffected segments over 4-6 weeks, thereby increasing the volume of functional liver that will remain post-resection and reducing the risk of post-hepatectomy liver failure.

References

^[3] Senior notes: maxim.md, Cholangiocarcinoma management section ^[5] Senior notes: felixlai.md, Malignant biliary obstruction section (pp. 503–506) ^[7] Senior notes: felixlai.md, Pancreatic cancer treatment section (pp. 598–600) ^[8] Senior notes: felixlai.md, Cholangiocarcinoma treatment section (pp. 550–551) ^[10] Senior notes: maxim.md, CA gallbladder section; felixlai.md, CA gallbladder treatment section (pp. 568–570) ^[13] Senior notes: felixlai.md, Acute cholangitis treatment section (pp. 522–525); maxim.md, Acute cholangitis section ^[14] Senior notes: maxim.md, Pancreatic carcinoma section (pp. 146–148) ^[20] Lecture slides: Malignant biliary obstruction.pdf, p15 ^[22] Lecture slides: Malignant biliary obstruction.pdf, p18–19 ^[23] Lecture slides: Malignant biliary obstruction.pdf, p30 ^[24] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p63 ^[25] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p67 ^[26] Lecture slides: Malignant biliary obstruction.pdf, p19 ^[27] Senior notes: maxim.md, Methods of biliary drainage section (p. 7) ^[28] Lecture slides: Malignant biliary obstruction.pdf, p35

Complications of Malignant Biliary Obstruction

Complications of MBO can be organised into three categories: (A) complications of the disease itself (i.e., what the biliary obstruction and cancer do to the patient), (B) complications of diagnostic/palliative interventions (stenting, PTBD, ERCP), and (C) complications of curative surgery. Each has a clear pathophysiological basis. Let's go through every one from first principles.

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1. Complications of the Disease Itself

1.1 Causes of Mortality in MBO

The lecture specifically highlights the three terminal pathways ^[9]:

Cause of mortality in MBO: ^[9]

• Biliary sepsis
• Cancer cachexia
• Liver failure

These are not random — they arise directly from the pathophysiology of biliary obstruction combined with advanced malignancy.

1.2 Biliary Sepsis (Acute Cholangitis)

Why does it happen?

Bile stasis from obstruction removes the normal protective mechanisms of the biliary tree — continuous flushing action, bacteriostatic bile salts, mucosal IgA, and the sphincter of Oddi barrier ^[13]. Bacteria ascend from the duodenum into the stagnant, obstructed bile. Once biliary pressure exceeds the secretory pressure of the hepatocytes (normal ductal pressure: 7–14 cm H₂O; increased biliary pressure > 25 cm H₂O), bacteria are forced into the hepatic venous and lymphatic system (cholangiovenous and cholangiolymphatic reflux), leading to bacteraemia and septic shock ^[29].

A critical additional point from the lecture: Excretion of antibiotics is impaired in biliary obstruction ^[29] — meaning even if you give IV antibiotics, they cannot concentrate in the obstructed bile where the infection is. This is why biliary drainage is mandatory ^[29] in cholangitis complicating MBO.

Clinical features ^[13]:

• Charcot's triad (50–70%): Fever, RUQ pain, jaundice
• Reynold's pentad ( < 10%): Charcot's triad + shock + altered mental status → indicates suppurative cholangitis (pus under pressure in bile duct) with multi-organ failure

Common organisms ^[13]:

• Gram-negative: E. coli, Klebsiella pneumoniae, Enterobacter spp., Bacteroides fragilis
• Gram-positive: Enterococcus spp.
• If stent present: Pseudomonas (biofilm on foreign body)

1.3 Cancer Cachexia

Why does it happen?

Cancer cachexia is a multifactorial syndrome driven by:

• Tumour-derived cytokines (TNF-α, IL-6, IL-1) → systemic inflammation → skeletal muscle proteolysis → wasting
• Anorexia — central appetite suppression from cytokines
• Fat malabsorption — bile salts cannot reach the gut → impaired emulsification of dietary fat → steatorrhoea → caloric loss
• Impaired protein synthesis — cholestatic liver has reduced synthetic capacity → hypoalbuminaemia, muscle wasting

Cancer cachexia → malnutrition is explicitly listed as a reason MBO is high-risk for surgery ^[24].

1.4 Liver Failure

Why does it happen?

Prolonged obstruction of bile flow has progressive hepatotoxic effects:

• Bile acid cytotoxicity — retained bile acids (hydrophobic bile acids like lithocholic acid) are directly toxic to hepatocyte membranes, causing apoptosis and necrosis
• Secondary biliary cirrhosis — chronic obstruction → periportal fibrosis → eventually cirrhosis
• Endotoxaemia — Kupffer cells are dysfunctional → gut-derived endotoxins enter systemic circulation → further hepatocyte injury
• Impaired gluconeogenesis and impaired ketogenesis ^[30] — the cholestatic liver cannot adequately perform its metabolic functions, leading to metabolic decompensation

1.5 Renal Failure (Cholemic Nephrosis)

Why does it happen?

• Conjugated bilirubin and bile salts are directly nephrotoxic — they cause tubular necrosis
• Endotoxaemia causes renal vasoconstriction → reduced renal perfusion
• Dehydration (poor oral intake, vomiting from GOO)
• Historical studies showed: higher anastomotic leak, haemorrhage, and renal failure in jaundiced patients undergoing surgery ^[31]

This is why the lecture specifically lists mannitol, dopamine to prevent renal failure as one of the measures to reduce surgical complications ^[32].

1.6 Coagulopathy

Why does it happen? Impaired clotting factor synthesis ^[30]:

• Vitamin K (fat-soluble) cannot be absorbed without bile salts in the gut
• Vitamin K is a cofactor for hepatic synthesis of clotting factors II, VII, IX, X (and protein C, S)
• → Prolonged PT/INR → increased bleeding risk

1.7 Immune Dysfunction

Pathophysiological effects of malignant biliary obstruction: ^[30]

• Endotoxaemia
• ↓ Reticuloendothelial function
• ↓ Cell-mediated immunity

This creates a state of functional immunosuppression — the patient is vulnerable to infection (not just biliary, but also wound infections, pneumonia, urinary infections post-operatively).

1.8 Metabolic Derangements [30]

1.9 Gastric Outlet Obstruction (GOO)

Occurs specifically with CA head of pancreas — the tumour compresses both the CBD (causing jaundice) AND the duodenum (causing GOO) ^[5]. Presents with non-bilious projectile vomiting of undigested food, early satiety, weight loss, and succussion splash on examination.

1.10 Acute Pancreatitis

Can occur when tumour obstructs the main pancreatic duct (especially in periampullary or pancreatic head cancers) → back-pressure → premature activation of pancreatic enzymes → autodigestion ^[7].

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2. Complications of Diagnostic and Palliative Interventions

2.1 Complications of ERCP [27] [5]

ERCP is the workhorse intervention for MBO, but it carries significant procedural risks:

2.2 Complications of Biliary Stenting [5] [3]

Plastic vs Metallic stent patency ^[33]:

• Metal stents: 15–39 weeks patency
• Plastic stents: 7–20 weeks patency
• Metallic stents have significantly less recurrent biliary obstruction prior to death ^[33]

2.3 Complications of PTBD [5]

2.4 Complications of Pre-operative Biliary Drainage [31] [34]

The lecture specifically highlights this debate:

Pre-op biliary drainage has increased risk of serious complications: ^[34]

• Pancreatitis (7%), cholangitis (26%), blocked stent (15%), bleeding (2%), perforation (2%)
• Surgery-related complications were comparable (with or without pre-op drainage)
• Routine pre-op biliary drainage in patients undergoing surgery for CA pancreas increases rate of complications ^[34]

The jaundice itself also causes problems if left undrained ^[31]:

Jaundice → coagulopathy, malabsorption, malnutrition, and immune dysfunction → higher anastomotic leak, haemorrhage, and renal failure ^[31]

This creates a therapeutic dilemma — drain (and risk procedure-related complications) vs. don't drain (and risk cholestasis-related complications). As discussed in the management section, the practical QMH approach is to drain all patients because surgery cannot be performed early ^[5].

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3. Complications of Curative Surgery

3.1 Post-Whipple (Pancreaticoduodenectomy) Complications

Historical data shows MBO carries a very high operative mortality ^[35]:

Malignant biliary obstruction postoperative mortality: ^[35]

• Nakayama 1978: 28%
• Dixon 1983: 26%
• Lai 1992: 27%

Modern mortality at high-volume centres is now 2–5%, but morbidity remains substantial (30–50%).

Early Complications [7] [14]

Measures to reduce complications related to surgery for MBO: ^[32]

1. Nutritional support
2. Vitamin K
3. FFP during surgery
4. Antibiotic cover
5. Mannitol, dopamine to prevent renal failure
6. H₂ antagonist

Why H₂ antagonist? ^[32] Patients undergoing major HPB surgery are at high risk of stress ulceration — the combination of physiological stress, fasting, and potential ICU admission creates a perfect storm for gastric acid hypersecretion and mucosal ischaemia. H₂ blockers (ranitidine) or PPIs reduce this risk.

Late Complications [7] [14]

Pancreatic Fistula — In Detail [14]

This deserves special attention because it is the most feared complication after pancreatic surgery:

Classification (International Study Group of Pancreatic Fistula — ISGPF) ^[14]:

Downstream consequences of pancreatic fistula ^[14]:

• Pseudocyst — walled-off collection of pancreatic juice
• High-output fistula → dehydration, malnutrition, metabolic acidosis (loss of HCO₃⁻ in pancreatic juice)
• GDA pseudoaneurysm → intraabdominal haemorrhage / UGIB (pancreatic enzymes erode the GDA stump)
• Portal vein thrombosis / Splenic vein thrombosis (peripancreatic inflammation)
• Pancreatic ascites (leak into peritoneal cavity)

3.2 Post-Hepatectomy Complications (for Klatskin Tumour / Intrahepatic CC)

3.3 Post-Cholecystectomy Complications (for CA Gallbladder)

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4. Complications Summary — Organised by Pathophysiology

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5. Prognosis

The prognosis of MBO depends entirely on the underlying malignancy, but overall it is grim ^[7]:

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Active Recall - Complications of MBO

1. Name the three causes of mortality in MBO and explain the pathophysiological basis for each.

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(1) Biliary sepsis — bile stasis removes barrier mechanisms (flushing, bile salts, IgA, sphincter of Oddi); bacteria ascend; when biliary pressure exceeds 25 cmH2O, bacteria reflux into hepatic veins and lymphatics causing bacteraemia/septic shock; antibiotic excretion is impaired in obstruction. (2) Cancer cachexia — tumour-derived cytokines (TNF-alpha, IL-6) drive systemic inflammation, muscle proteolysis, anorexia; compounded by fat malabsorption from lack of bile salts. (3) Liver failure — bile acid cytotoxicity to hepatocytes, secondary biliary cirrhosis from prolonged obstruction, impaired Kupffer cell function and endotoxaemia causing further hepatocyte injury.

2. List the six measures to reduce complications related to surgery for MBO as per the lecture slides.

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(1) Nutritional support, (2) Vitamin K (correct coagulopathy), (3) FFP during surgery, (4) Antibiotic cover, (5) Mannitol and dopamine to prevent renal failure, (6) H2 antagonist (prevent stress ulceration).

3. Define post-operative pancreatic fistula and classify it by the ISGPF system. What are three downstream complications of pancreatic fistula?

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Definition: drain output of any volume after post-op Day 3 with drain amylase greater than 3 times the upper limit of normal. Classification: Biochemical leak (elevated amylase but asymptomatic), Grade B (persistent drainage greater than 3 weeks, requiring change in management, signs of infection, no organ failure), Grade C (unstable, requires re-operation, risk of organ failure). Downstream complications: (1) GDA pseudoaneurysm leading to intraabdominal haemorrhage or UGIB, (2) Portal vein or splenic vein thrombosis, (3) Pancreatic ascites. Others acceptable: pseudocyst, high-output fistula with dehydration/metabolic acidosis.

4. Why is the pancreaticojejunostomy anastomosis the highest risk for leak after a Whipple operation? What is the quoted leak rate?

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PJ leak rate is approximately 30 percent, higher than CJ or GJ. Reasons: (1) Pancreatic juice contains activated digestive enzymes (trypsin, lipase, amylase) that erode the anastomosis. (2) The pancreatic duct is often small and soft (especially in a non-dilated duct without upstream obstruction), making a secure anastomosis technically difficult. (3) The remaining pancreatic body/tail may be soft and friable. Note: somatostatin analogue (octreotide) does NOT reduce the risk of pancreatic fistula.

5. A patient with a PTBD catheter for palliation of Klatskin tumour develops sudden bright red drainage from the catheter. What has likely happened, and what is the step-by-step management?

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Likely complication: haemobilia — the percutaneous tract has communicated with a major vascular structure (hepatic artery or portal vein branch). Step-by-step: (1) Stabilise and resuscitate the patient. (2) Clamp the PTBD catheter to tamponade the bleeding. (3) Perform cholangiogram by injecting contrast into the PTBD to delineate whether the catheter is in the hepatic artery or portal vein. (4) Remove the catheter slowly to control bleeding. Do NOT remove immediately because this converts the contained bleeding into free haemoperitoneum. May require angiographic embolisation if bleeding persists.

References

^[3] Senior notes: maxim.md, Cholangiocarcinoma management section ^[5] Senior notes: felixlai.md, Malignant biliary obstruction section (pp. 504–507) ^[7] Senior notes: felixlai.md, Pancreatic cancer prognosis section (p. 602) ^[9] Lecture slides: Malignant biliary obstruction.pdf, p29 ^[10] Senior notes: maxim.md, CA gallbladder section ^[13] Senior notes: felixlai.md, Acute cholangitis section (pp. 520–522) ^[14] Senior notes: maxim.md, Pancreatic carcinoma section — Whipple complications and pancreatic fistula (pp. 147–148) ^[24] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p63 ^[25] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p67 ^[27] Senior notes: maxim.md, ERCP complications section ^[29] Lecture slides: Malignant biliary obstruction.pdf, p16 ^[30] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p64 ^[31] Lecture slides: Malignant biliary obstruction.pdf, p24 ^[32] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p66 ^[33] Lecture slides: Malignant biliary obstruction.pdf, p36 ^[34] Lecture slides: Malignant biliary obstruction.pdf, p26 ^[35] Lecture slides: WCS 056 - Painless jaundice and epigastric mass - by Prof R Poon.ppt (1).pdf, p62