Acute Cholangitis

1. Definition

Acute cholangitis is a clinical syndrome of bacterial infection of the biliary tract arising from a combination of biliary obstruction and bacterial contamination ^[1][2][3]. The name itself is instructive:

• "Chol-" = bile (Greek: cholē)
• "-ang-" = vessel/duct (Greek: angeion)
• "-itis" = inflammation

So cholangitis literally means "inflammation of the bile ducts." In clinical practice, we use the term to mean infection of the bile ducts — because the inflammation here is driven by bacteria, not autoimmunity or chemicals.

Acute cholangitis is one of the two most common complications of CBD stones, the other being acute biliary pancreatitis ^[1]. It ranges from a mild, self-limiting illness responsive to antibiotics and fluid resuscitation to fulminant suppurative cholangitis with septic shock and multi-organ failure requiring emergency biliary drainage.

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2. Epidemiology

2.1 Global Epidemiology

• Acute cholangitis accounts for approximately 1–9% of hospital admissions for gallstone-related disease.
• The incidence rises with age (peak in the 6th–7th decade) because gallstone prevalence increases with age and biliary instrumentation/stenting becomes more common.
• Males and females are affected roughly equally when corrected for the underlying cause; however, because gallstones are more common in females (the classic "4 F's" — Fair, Fat, Fertile, Forty), the raw numbers skew slightly female for stone-related cholangitis.

2.2 Hong Kong Context

In Hong Kong and Southeast Asia, the following epidemiological features are particularly relevant:

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3. Relevant Anatomy and Function of the Biliary System

Understanding acute cholangitis demands a solid grasp of biliary anatomy and the normal defence mechanisms that keep bile sterile.

3.1 Anatomy of the Biliary Tree

Key anatomical points:

• The gallbladder consists of fundus, body, infundibulum (Hartmann's pouch), and neck. The neck tapers into the cystic duct, which joins the CHD to form the CBD ^[1].
• The CBD is approximately 7–8 cm long and runs in the free edge of the lesser omentum (hepatoduodenal ligament) alongside the portal vein (posterior) and hepatic artery proper (left). It passes behind the first part of the duodenum and through the head of the pancreas before entering the second part of the duodenum at the major duodenal papilla (of Vater).
• The Sphincter of Oddi is a muscular sphincter at the distal end of the CBD/ampulla of Vater. It controls the flow of bile (and pancreatic juice) into the duodenum and acts as a mechanical barrier preventing duodenal-biliary reflux ^[1][3].
• Normal CBD diameter: ≤ 6–8 mm on ultrasound (may be up to 10 mm in elderly or post-cholecystectomy patients). Dilatation > 8 mm suggests obstruction.
• Normal ductal pressure: 7–14 cm H₂O ^[3]. This is a critical number — when obstruction raises ductal pressure above 25 cm H₂O, bacteria reflux into hepatic veins and peribiliary lymphatics, causing bacteraemia and potentially septic shock ^[3].

3.2 Normal Biliary Defence Mechanisms

The bile duct is normally sterile despite its connection to the bacteria-laden duodenum. This is maintained by several mechanisms ^[1]:

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4. Etiology (Causes of Biliary Obstruction)

Acute cholangitis requires obstruction + infection. The causes of obstruction are therefore the etiological framework ^[1][2][3][5]:

4.1 Causes — Tabulated by Frequency

4.2 Focus on Hong Kong-Specific Etiologies

4.2.1 Recurrent Pyogenic Cholangitis (RPC) — "Hong Kong Disease"

• Definition: Recurrent syndrome of bacterial cholangitis associated with intrahepatic pigment stones and intrahepatic biliary strictures ^[1][4].
• Pathophysiology — a vicious cycle:
  1. Initiating event: Parasitic infestation (e.g., Clonorchis sinensis from raw freshwater fish) → epithelial damage → bacterial translocation → stricture formation → biliary stasis ^[4].
  2. Stone formation: Bacteria (especially E. coli, Klebsiella) produce β-glucuronidase → cleaves conjugated bilirubin glucuronide → unconjugated bilirubin → complexes with calcium → calcium bilirubinate (brown pigment) stones ^[1][4].
  3. Malnutrition: Low-protein diet historically common in Asia → relative enzyme deficiency → favours formation of unconjugated bilirubin ^[4].
  4. Vicious cycle: Stone formation → obstruction → stasis → recurrent infection → more inflammation → more stricturing → more stones ^[1][4].
• Key differences from typical gallstone disease: Stones form de novo within intrahepatic ducts (not in gallbladder), are brown pigment (not cholesterol), and predominantly affect the left intrahepatic ducts ^[4].
• Complications: Biliary sepsis, liver abscess, secondary biliary cirrhosis, cholangiocarcinoma ^[4].

4.2.2 Clonorchis sinensis Infection

• Lifecycle: Humans are the definitive host; adult flukes reside in the biliary tract and lay embryonated eggs that pass in faeces ^[4].
• Transmission: Consumption of poorly cooked freshwater fish (淡水魚) ^[4].
• Clinical spectrum: Asymptomatic → acute cholangitis → RPC → increased risk of cholangiocarcinoma ^[4].
• Diagnosis: Stool microscopy for eggs, duodenal aspirate, USG for adult flukes, intra-operative choledochoscopy ^[4].
• Treatment: Praziquantel 25 mg/kg PO TDS × 1 day ^[4].

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5. Pathophysiology

This is the crux of understanding acute cholangitis. Let's build it from first principles.

5.1 The Two-Hit Model

Acute cholangitis requires the combination of: (1) biliary obstruction AND (2) significant bacterial contamination ^[1][2][3].

Why does obstruction alone not cause cholangitis? Because without bacteria, you simply have sterile bile building up → obstructive jaundice. The bile becomes concentrated and stagnant, but there is no infection.

Why does bactobilia alone not cause cholangitis? Because in the absence of obstruction, the continuous flow of bile washes bacteria into the duodenum, and bile salts kill remaining organisms. Up to 16% of patients undergoing biliary surgery have positive bile cultures without clinical infection ^[1].

5.2 Step-by-Step Pathophysiology

5.3 Bacteriology

The organisms responsible reflect the gut flora (since infection ascends from the duodenum) ^[1][2][3]:

High-Yield: The most common organism in acute cholangitis is E. coli. If a stent is present, think Pseudomonas in addition to the standard organisms. Anaerobes are more common in severe disease and post-biliary-enteric surgery ^[2].

5.4 Disrupted Barrier Mechanisms

In addition to the primary two-hit model, the normal barrier mechanisms described above can be disrupted iatrogenically ^[1]:

• After endoscopic sphincterotomy: Permanent loss of sphincter of Oddi function → free duodenal-biliary reflux.
• Biliary stent insertion: Foreign body serves as a nidus for bacterial biofilm + stent occlusion causes incomplete drainage.
• Choledochal surgery / biliary-enteric anastomosis: Surgical disruption of the normal anatomy removes the anti-reflux mechanism.

In these patients, the threshold for developing cholangitis is much lower because one of the two "hits" (bacterial contamination) is essentially always present.

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6. Classification

6.1 Anatomical Classification

6.2 Pathological Classification

6.3 Tokyo Guidelines (TG18/TG24) Severity Grading

The Tokyo Guidelines are the internationally accepted severity grading system for acute cholangitis. They stratify patients to guide the urgency of biliary drainage ^[6]:

6.4 Other Classifications

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7. Clinical Features

7.1 Symptoms

The clinical presentation of acute cholangitis follows directly from the pathophysiology: biliary obstruction + infection → pain (from ductal distension) + jaundice (from obstruction) + fever (from infection/bacteraemia).

7.1.1 Charcot's Triad (present in 50–70% of patients) [1][2]

7.1.2 Reynolds' Pentad (present in < 10% of patients) [1][2]

This represents Charcot's triad PLUS two additional features indicating progression to suppurative cholangitis with septic shock:

High-Yield: Reynolds' pentad = Charcot's triad + Shock + Confusion. It indicates suppurative cholangitis, a surgical emergency requiring immediate biliary drainage. Mortality without drainage is extremely high (approaching 50–100%) ^[1][2].

7.1.3 Other Symptoms

7.2 Signs

7.2.1 General Examination

7.2.2 Abdominal Examination

7.2.3 Signs of Complications / Severity

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8. Summary of Pathophysiology → Clinical Feature Connections

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Active Recall - Acute Cholangitis (Definition to Clinical Features)

1. What two conditions must coexist for acute cholangitis to develop?

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Biliary obstruction AND significant bacterial contamination. Obstruction alone causes sterile obstructive jaundice; bacteria alone causes asymptomatic bactobilia.

2. What is the normal biliary ductal pressure, and at what threshold do bacteria reflux into the bloodstream?

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Normal: 7-14 cm H2O. Cholangiovenous/lymphatic reflux occurs when pressure exceeds 25 cm H2O, leading to bacteraemia and potentially septic shock.

3. Name the components of Charcot's triad and Reynolds' pentad, and state the approximate percentage of patients presenting with each.

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Charcot's triad (50-70%): Fever, RUQ pain, Jaundice. Reynolds' pentad (less than 10%): Charcot's triad plus Hypotension and Altered mental status (confusion). Reynolds' pentad indicates suppurative cholangitis.

4. Why are antibiotics alone insufficient to treat moderate-to-severe acute cholangitis?

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Antibiotic excretion into bile is impaired when the biliary system is obstructed. Therefore, therapeutic antibiotic concentrations cannot be achieved at the site of infection. Biliary drainage is mandatory to decompress the system and allow source control.

5. A patient with a biliary stent develops acute cholangitis. What additional organism should you cover for, compared to standard cholangitis, and why?

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Pseudomonas aeruginosa. Biliary stents act as foreign bodies that serve as nidus for biofilm formation; Pseudomonas is commonly associated with healthcare-associated/foreign body-related infections and requires broader-spectrum antibiotic coverage.

6. Explain the pathophysiology of recurrent pyogenic cholangitis (RPC) and state why it is called 'Hong Kong disease'.

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RPC involves intrahepatic pigment stone formation due to bacterial beta-glucuronidase cleaving conjugated bilirubin to unconjugated bilirubin, which complexes with calcium to form calcium bilirubinate stones. Parasitic infection (e.g., Clonorchis sinensis) initiates epithelial damage leading to strictures, stasis, and recurrent infection in a vicious cycle. Called 'Hong Kong disease' because it is found exclusively/predominantly in Southeast Asian populations.

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References

^[1] Senior notes: felixlai.md (Acute cholangitis, Recurrent pyogenic cholangitis, Primary sclerosing cholangitis, Mirizzi syndrome sections) ^[2] Senior notes: maxim.md (Acute cholangitis, Choledocholithiasis, Recurrent pyogenic cholangitis sections) ^[3] Lecture slides: Malignant biliary obstruction.pdf (p16 — Cholangitis: biliary pressure, cholangiovenous reflux, impaired antibiotic excretion, mandatory drainage) ^[4] Senior notes: felixlai.md and maxim.md (Recurrent pyogenic cholangitis, Clonorchis sinensis sections) ^[5] Lecture slides: HCC and Gallstone acute cholangitis_Prof TT Cheung.pdf ^[6] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p7 — Acute Cholangitis pathogenesis)

Differential Diagnosis of Acute Cholangitis

Framing the Problem

The classic presentation of acute cholangitis — fever, RUQ pain, and jaundice — is not unique to cholangitis. Several other conditions in the right upper quadrant and hepatobiliary system can present with overlapping features. The differential diagnosis essentially asks: "What else could cause fever + abdominal pain + jaundice (or any combination thereof)?" ^[1][7].

The key to narrowing the differential lies in understanding which component dominates and what the timeline and associated features are. Let's work through this systematically.

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Approach to the Differential

Think about acute cholangitis as sitting at the intersection of three clinical domains:

1. Causes of RUQ pain (hepatobiliary, duodenal, thoracic referred pain)
2. Causes of obstructive jaundice (intraluminal, mural, extramural)
3. Causes of fever with abdominal pain (intra-abdominal sepsis)

The differential includes conditions that share at least two of the three Charcot's triad features.

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Detailed Differential Diagnosis

The conditions listed below are explicitly mentioned in the senior notes as the differential diagnosis of fever and abdominal pain in the context of suspected cholangitis ^[1][7][8]:

1. Acute Cholecystitis [1][7][8][9]

Why the confusion arises: Both conditions involve gallstones and present with RUQ pain and fever. The critical distinction is jaundice (prominent in cholangitis, rare in cholecystitis) and Murphy's sign (positive in cholecystitis, negative in cholangitis). Also, both can coexist — a patient can have a stone in the cystic duct (cholecystitis) AND a stone in the CBD (cholangitis) simultaneously.

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2. Choledocholithiasis (without infection) [7][10]

• Definition: Obstruction of CBD/CHD by gallstone without superimposed infection ^[10].
• Presentation: RUQ pain, obstructive jaundice (dark urine, pale stools), cholestatic LFT — but no fever and no rigors.
• Why it mimics cholangitis: Same stone, same duct, same jaundice. The difference is the absence of infection — no fever, no leukocytosis, no positive blood cultures. Essentially, this is "one hit" (obstruction) without the "second hit" (bacteria).
• Why it matters: Choledocholithiasis can progress to cholangitis if the obstruction persists and bacteria colonise the stagnant bile. Urgent treatment prevents this progression.
• USG: Dilated CBD ( > 8 mm), gallstone in CBD visible in only ~1/3 of cases due to obscuring duodenal gas ^[10].

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3. Liver Abscess [1][7][8][11]

This is a critical differential because it can present almost identically to cholangitis and requires entirely different management.

Why the confusion arises: Both present with fever and RUQ pain. The route of spread for pyogenic liver abscess is often ascending biliary infection (20–30% of cases) ^[11] — meaning cholangitis and liver abscess can coexist. In fact, liver abscess is a recognised complication of untreated cholangitis.

High-Yield: USG abdomen should always rule out liver abscess when cholangitis is suspected — the presentations are similar, and abscess requires image-guided drainage, not ERCP ^[2][8].

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4. Acute Biliary Pancreatitis [1][7][8][12]

• Mechanism: A gallstone migrates down the CBD and impacts at the ampulla of Vater, obstructing both the CBD and the pancreatic duct (of Wirsung) → pancreatic enzyme activation → autodigestion → acute pancreatitis ^[12].
• Overlap: Shares RUQ/epigastric pain and fever with cholangitis; obstructive jaundice may be present if the CBD remains obstructed.
• Key distinguishing features:
  • Pain: Classically epigastric, radiates straight through to the back, relieved by sitting up or leaning forward ^[12]. Cholangitis pain is more purely RUQ.
  • Amylase/Lipase: Markedly elevated ( > 3× upper limit of normal). In cholangitis, amylase may be mildly elevated but not to this degree.
  • Nausea and vomiting: More prominent in pancreatitis.
  • CT findings: Pancreatic inflammation, peripancreatic fat stranding, ± necrosis. In cholangitis, the pancreas is normal.
• Co-existence: Pancreatitis and cholangitis can occur simultaneously from the same impacted ampullary stone. Always check amylase/lipase in suspected cholangitis ^[2][8].

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5. Recurrent Pyogenic Cholangitis (RPC) [1][4][7][8]

• Definition: Recurrent bacterial cholangitis due to intrahepatic pigment stones and intrahepatic strictures ^[4].
• Why it's a separate differential: RPC presents with recurrent episodes of Charcot's triad (1–2 episodes/year), but the underlying pathology is intrahepatic (left lobe predilection), not simply a CBD stone.
• Key clues: Southeast Asian patient ("Hong Kong disease"), middle-age onset (30s–40s), history of recurrent cholangitis episodes, CT showing central dilated bile ducts with peripheral tapering and left lobe atrophy ^[4].
• Why it matters: Management is fundamentally different — standard ERCP may be inadequate (cannot access intrahepatic strictures); may require PTBD, hepaticojejunostomy, or hepatobiliary resection of the affected segment ^[4].

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6. Mirizzi Syndrome [7][8][13]

• Definition: CHD obstruction caused by extrinsic compression from an impacted stone in Hartmann's pouch or cystic duct ^[13].
• Presentation: Can present identically to cholangitis — fever, RUQ pain, jaundice. In fact, acute cholangitis is one of the presenting manifestations of Mirizzi syndrome ^[13].
• Key clue: Jaundice with palpable gallbladder — this is an exception to Courvoisier's Law ^[13].
• Chronic inflammation from the impacted stone can erode the bile duct wall, causing a cholecystobiliary fistula (Csendes classification) ^[13].
• Imaging: USG shows dilated biliary tree above the level of stone impaction + stone at GB neck + contracted GB. ERCP may demonstrate the fistula ^[13].
• Why it mimics cholangitis: The obstruction of the CHD leads to stasis, which predisposes to ascending infection — the mechanism is the same, just the cause of obstruction is different (external compression vs. intraluminal stone).

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7. Infected Choledochal Cyst [7][8]

• Definition: Congenital dilatation of the intra/extrahepatic biliary system that becomes secondarily infected.
• Presentation: RUQ mass + pain + jaundice + fever — the classic triad of choledochal cyst includes RUQ mass, pain, and jaundice ^[8].
• Key clue: Young patient (most diagnosed before age 10, ~60%), palpable RUQ cystic mass.
• Risk: Untreated cysts carry significant risk of cholangiocarcinoma — hence radical excision + Roux-en-Y reconstruction is the definitive management.

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8. Biliary Leak [1][7]

• Context: Usually post-operative (e.g., after laparoscopic cholecystectomy, liver resection, or biliary surgery). Bile leaks from the cystic duct stump, hepatic duct injury, or accessory ducts.
• Presentation: Fever, abdominal pain, ± jaundice, ± bile-stained drain output.
• Why it mimics cholangitis: Bile is irritant to the peritoneum and becomes secondarily infected → localised or generalised peritonitis with fever and RUQ pain.
• Key clue: Recent biliary surgery and clinical deterioration in the post-operative period.

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9. Malignant Biliary Obstruction (MBO) [2][3][5]

• Causes: Pancreatic head carcinoma, cholangiocarcinoma, periampullary carcinoma, porta hepatis lymph node metastasis ^[2][3].
• Typical presentation: Painless progressive obstructive jaundice in an elderly patient — this is the classic "textbook" presentation of MBO ^[14]. Weight loss, anorexia, and a palpable non-tender gallbladder (Courvoisier's sign) are suggestive.
• When it mimics cholangitis: MBO can cause secondary cholangitis when the obstructed bile becomes infected. In this scenario, the patient with known or occult malignancy develops superimposed fever and sepsis on top of their obstructive jaundice.
• Biliary obstruction + infection → cholangitis, and the principles of management are the same: biliary drainage is mandatory ^[3]. However, the underlying cause requires entirely different oncological management.

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10. Non-Biliary Mimics

These conditions can occasionally present with RUQ pain and/or fever, mimicking biliary pathology:

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Summary Table — Quick Differentiation

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Systematic Approach to Narrowing the Differential

When a patient presents with features suggestive of cholangitis, use this step-by-step approach:

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Active Recall - Differential Diagnosis of Acute Cholangitis

1. A patient presents with fever, RUQ pain, and jaundice. Murphy's sign is positive. What is the most likely diagnosis and why does Murphy's sign help differentiate?

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Acute cholecystitis with possible co-existing CBD stone causing jaundice (or Mirizzi syndrome). Murphy's sign is positive in cholecystitis because the inflamed gallbladder is tender when pressed against the examining hand during inspiration. In pure cholangitis, the gallbladder is not the primary inflamed organ, so Murphy's sign is typically negative.

2. How do you distinguish a liver abscess from acute cholangitis at the bedside and on investigations?

Your answer

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Liver abscess: swinging fever, tender hepatomegaly, jaundice is minimal (focal lesion, rest of liver compensates). Cholangitis: Charcot's triad with prominent jaundice, cholestatic LFT. On imaging, USG/CT in liver abscess shows a focal rim-enhancing cystic lesion (double-target sign on CT), while cholangitis shows dilated CBD with or without stone. Both may have positive blood cultures.

3. A patient with RUQ pain and fever has markedly raised AST/ALT (>1000 IU/L) with only mildly raised ALP. Is this more likely cholangitis or hepatitis? Explain using LFT pattern.

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Hepatitis. Cholangitis produces a cholestatic LFT pattern (ALP and GGT raised disproportionately to transaminases, with raised conjugated bilirubin). A hepatocellular pattern (AST/ALT much greater than ALP) points to hepatitis (viral, drug-induced, autoimmune). However, note that very early acute biliary obstruction can cause a transient transaminase spike, so clinical correlation is needed.

4. Why should you always check amylase/lipase and order a CXR when working up suspected acute cholangitis?

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Amylase/lipase: to rule out acute biliary pancreatitis, which can coexist with cholangitis (same impacted ampullary stone). Amylase greater than 3 times upper limit of normal suggests pancreatitis. CXR: to rule out right basal pneumonia (diaphragmatic irritation can cause referred RUQ pain mimicking biliary pathology) and to look for free air under diaphragm (perforated viscus).

5. Name three conditions where jaundice occurs with a palpable gallbladder, and explain why this is an exception to Courvoisier's Law.

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1. Malignant biliary obstruction (the gallbladder is non-fibrosed and distends - this is actually Courvoisier's Law itself, not the exception). Exceptions include: 2. Double impaction (stone in CBD causing jaundice plus stone in cystic duct causing mucocele of a fibrosed GB). 3. Mirizzi syndrome (impacted stone in Hartmann's pouch compresses CHD externally). 4. RPC (pathology is in bile ducts, not GB, so GB is not fibrosed and can distend). In these exceptions, despite gallstone disease, the gallbladder is palpable because either the obstruction pattern is unusual or the gallbladder itself is not chronically inflamed.

References

^[1] Senior notes: felixlai.md (Acute cholangitis — clinical manifestation, differential diagnosis) ^[2] Senior notes: maxim.md (Acute cholangitis — urgent investigations, management) ^[3] Lecture slides: Malignant biliary obstruction.pdf (p16 — Cholangitis: biliary pressure, impaired antibiotic excretion, mandatory drainage) ^[4] Senior notes: felixlai.md and maxim.md (Recurrent pyogenic cholangitis sections) ^[5] Lecture slides: Malignant biliary obstruction.pdf (malignant causes of biliary obstruction) ^[7] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p6–7 — Acute Cholangitis clinical manifestations, pathogenesis) ^[8] Senior notes: felixlai.md (Mirizzi syndrome — differential diagnosis list: choledocholithiasis, acute cholecystitis, liver abscess, infected choledochal cysts, biliary leaks, acute pancreatitis, acute appendicitis, RPC) ^[9] Senior notes: felixlai.md (Acute cholecystitis — Murphy's sign, LFT findings, USG cardinal signs) and maxim.md (Acute calculous cholecystitis) ^[10] Senior notes: maxim.md (Choledocholithiasis) ^[11] Senior notes: felixlai.md (Liver abscess) and maxim.md (Liver abscess) ^[12] Senior notes: felixlai.md (Acute pancreatitis — clinical manifestation, differential diagnosis) ^[13] Senior notes: maxim.md (Mirizzi syndrome) ^[14] Senior notes: maxim.md (Obstructive jaundice — painless progressive obstructive jaundice)

Diagnostic Criteria

The Tokyo Guidelines (TG18) — The Standard Framework

The Tokyo Guidelines (originally TG07, revised TG13, and most recently TG18) are the internationally accepted diagnostic criteria for acute cholangitis. They provide a structured, stepwise approach: first determine whether cholangitis is present (diagnosis), then grade its severity (which dictates urgency of drainage). Let's break this down from first principles ^[1][7].

The logic is straightforward: acute cholangitis = systemic inflammation/infection + biliary obstruction/cholestasis. The criteria are designed to capture both components, then confirm with imaging.

TG18 Diagnostic Criteria for Acute Cholangitis

Interpretation ^[1]:

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Severity Grading (TG18) — Determines Urgency of Drainage

Once the diagnosis is established, severity grading determines how urgently you need to drain:

High-Yield: Grade III = Reynolds' pentad territory. Any organ dysfunction = Grade III = emergency drainage. Don't wait.

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Diagnostic Algorithm

The following algorithm integrates clinical assessment, laboratory workup, imaging, and severity grading into a systematic approach:

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Investigation Modalities — Detailed Breakdown

Overview: What We Need to Know and Why

When investigating suspected acute cholangitis, we need to answer four questions:

1. Is there systemic infection? → Bloods (CBC, CRP, blood cultures)
2. Is there biliary obstruction/cholestasis? → LFT, bilirubin
3. Where is the obstruction and what is causing it? → Imaging (USG → MRCP/CT → ERCP)
4. How severe is it? → Organ function markers (RFT, clotting, ABG, lactate)

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A. Laboratory Investigations

A1. Complete Blood Count with Differential (CBC D/C)

A2. Liver Function Tests (LFT)

This is arguably the most important blood test in suspected cholangitis because it distinguishes cholestatic (obstructive) from hepatocellular patterns.

Note on early biliary obstruction: In the very early hours of acute obstruction (e.g., a stone suddenly impacts), AST/ALT can spike transiently ( > 1000 IU/L) before the cholestatic pattern declares itself. This is because acute rise in intraductal pressure causes direct hepatocyte injury. Don't be misled — repeat LFT in 24–48h and the cholestatic pattern will emerge ^[15].

A3. Inflammatory Markers

A4. Clotting Profile (PT/INR)

A5. Renal Function Tests (RFT)

A6. Serum Amylase and Lipase

High-Yield: Always check amylase in suspected cholangitis — cholangitis and pancreatitis can coexist from the same stone ^[2].

A7. Blood Culture — The Most Important Microbiological Investigation

A8. Bile Culture

A9. Urinalysis

A10. Other Blood Tests

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B. Radiological Investigations

The imaging strategy is stepwise — start with the simplest, most available test and escalate if needed.

B1. Erect Chest X-Ray (CXR) and Abdominal X-Ray (AXR)

These are baseline investigations, not primarily to diagnose cholangitis, but to exclude mimics and detect complications ^[2]:

B2. Transabdominal Ultrasound (USG) — The First-Line Imaging

B3. Magnetic Resonance Cholangiopancreatography (MRCP)

High-Yield: MRCP has largely replaced ERCP as the diagnostic tool for choledocholithiasis/cholangitis when therapeutic intervention is not immediately needed. ERCP is now reserved primarily for therapeutic indications ^[1][10][15].

B4. CT Abdomen (with IV contrast)

B5. Endoscopic Ultrasound (EUS)

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C. Invasive Cholangiographic Investigations (Diagnostic + Therapeutic)

C1. Endoscopic Retrograde Cholangiopancreatography (ERCP) — 1st Line for Drainage

ERCP is the cornerstone investigation/intervention in acute cholangitis because it is both diagnostic and therapeutic ^{[1][2][7][14]}.

Post-ERCP management of concerns ^[16]: If a patient develops fever and tachycardia after ERCP, the differential includes: persistent cholangitis (unsuccessful drainage, migrated/blocked stent, resistant organisms), or ERCP complications (flare-up sepsis, pancreatitis, perforation). Investigate with AXR (stent position) and bloods ^[16]. If abdominal pain develops post-ERCP, consider perforation (CT: retroperitoneal free gas) or post-ERCP pancreatitis (amylase) ^[16].

C2. Percutaneous Transhepatic Biliary Drainage (PTBD)

C3. Percutaneous Transhepatic Cholangiography (PTC)

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D. Summary of Investigation Modalities — When to Use What

E. Comparison Table of Cholangiographic Modalities

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F. Key Imaging Findings to Recognise

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Active Recall - Diagnosis and Investigations of Acute Cholangitis

1. State the TG18 diagnostic criteria for 'suspected' and 'definite' acute cholangitis.

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Suspected: ONE item from Category A (fever/chills OR lab evidence of inflammation such as abnormal WBC/raised CRP) AND ONE item from Category B (jaundice OR abnormal liver chemistries such as raised ALP/GGT/AST/ALT). Definite: meets suspected criteria PLUS imaging evidence (biliary dilatation OR etiology such as stone, stricture, stent).

2. What LFT pattern is expected in acute cholangitis and why? How does it differ from acute hepatitis?

Your answer

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Cholestatic pattern: ALP and GGT markedly elevated, conjugated bilirubin elevated, AST/ALT mildly elevated. This is because biliary obstruction induces ALP synthesis from cholangiocytes and canalicular membranes. In hepatitis, the pattern is hepatocellular: AST/ALT markedly elevated (hepatocyte necrosis) with ALP only mildly elevated.

3. Why is blood culture considered the most critical microbiological investigation in acute cholangitis?

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Blood culture identifies the causative organism and its antibiotic susceptibility, enabling targeted therapy and de-escalation from empirical antibiotics. Must be taken BEFORE starting antibiotics (as antibiotics can sterilise blood quickly). Bacteraemia occurs because raised intraductal pressure (greater than 25 cm H2O) causes cholangiovenous reflux of bacteria into the bloodstream.

4. A patient with suspected cholangitis has a normal USG abdomen but your clinical suspicion remains high. What is your next investigation and why?

Your answer

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MRCP. USG has limited sensitivity for distal CBD stones (only 33-50% visible due to duodenal gas) and may be falsely negative in early obstruction (duct not yet dilated). MRCP is non-invasive, non-contrast T2-weighted MRI that provides excellent biliary visualisation and can detect stones as small as 2-3mm. It does not allow therapeutic intervention, so if a stone is found, ERCP would still be needed for treatment.

5. In the acute setting of cholangitis, what is the primary role of ERCP? Why should bile be aspirated before injecting contrast?

Your answer

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Primary role is biliary drainage and decompression, NOT stone removal. Bile should be aspirated first to decompress the biliary tree and reduce intraluminal pressure, thereby reducing the risk of inducing further bacteraemia during contrast injection. Stone removal can be deferred to interval ERCP after sepsis resolves.

6. When is PTBD preferred over ERCP? What is the preferred access route and why?

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PTBD is preferred when ERCP is unsuccessful, unavailable, or contraindicated (e.g., altered GI anatomy such as Billroth II or Roux-en-Y, poor respiratory function). Also preferred for obstruction at or above the hepatic duct confluence (e.g., Klatskin tumour, RPC). The left hepatic duct is preferred because the subcostal approach is less painful than the intercostal route for the right duct and is less likely to transgress the pleural space.

References

^[1] Senior notes: felixlai.md (Acute cholangitis — diagnostic criteria, biochemical tests, radiological tests, ERCP, PTBD, surgical drainage) ^[2] Senior notes: maxim.md (Acute cholangitis — urgent investigations, ERCP, PTBD, management) ^[3] Lecture slides: Malignant biliary obstruction.pdf (p16 — Cholangitis: biliary pressure, impaired antibiotic excretion, mandatory drainage) ^[4] Senior notes: felixlai.md and maxim.md (Recurrent pyogenic cholangitis — investigations, imaging findings) ^[7] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p6–7 — clinical manifestations, pathogenesis; p13–15 — management, ERCP, surgical treatment) ^[10] Senior notes: maxim.md (Choledocholithiasis — investigations, MRCP, EUS, ERCP) ^[11] Senior notes: felixlai.md (Liver abscess) and maxim.md (Liver abscess — imaging findings) ^[14] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p14 — ERCP as first line, complications, relative contraindications) ^[15] Senior notes: felixlai.md (Choledocholithiasis — LFT, USG, MRCP, ERCP; Malignant biliary obstruction — biochemical tests, tumour markers, imaging) and maxim.md (HBP investigations — USG, EUS, CT, MRCP, PTC, ERCP) ^[16] Senior notes: maxim.md (HBP investigations — MRCP, PTC/PTBD, ERCP; Post-ERCP complications management)

Management of Acute Cholangitis

Guiding Principles — Why We Treat the Way We Do

Before diving into specifics, let's ground the entire management framework in the pathophysiology we've already established. Acute cholangitis = obstructed + infected biliary tree. Therefore, management must address three pillars simultaneously ^{[1][2][3][17][18]}:

1. Resuscitate the patient — they are septic; support the circulation and organs.
2. Kill the bacteria — IV antibiotics to control the infection.
3. Relieve the obstruction — biliary drainage to decompress the system (because antibiotics alone cannot work in an obstructed system — their excretion into bile is impaired ^[3]).

After the acute episode is controlled, a fourth pillar becomes relevant:

4. Treat the underlying cause — to prevent recurrence (e.g., cholecystectomy for gallstones, stent for malignant stricture, hepatectomy for RPC).

The mnemonic from the senior notes captures this perfectly:

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Master Management Algorithm

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Pillar 1: Resuscitation (R)

This is standard sepsis management — the same principles you'd apply to any patient with sepsis from any source. The biliary focus simply adds specific nuances ^{[1][2][17][18]}.

High-Yield: Recognize signs of shock — hypotension, oliguria, changes in mental status, cold and clammy skin, and metabolic acidosis — these are signs that the patient is moving towards Grade III and requires emergency intervention ^[1].

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Pillar 2: Antibiotics (A)

Why Antibiotics Matter — But Aren't Enough

Antibiotics target the bacteria driving the infection. However, recall the critical pathophysiology: excretion of antibiotics into bile is impaired in biliary obstruction ^[3]. This means that even with the correct antibiotic given IV, therapeutic concentrations at the site of infection (within the obstructed biliary tree) may not be achieved. This is why biliary drainage is mandatory — you must open the system for the antibiotics to work ^[3].

That said, antibiotics are essential to control the systemic sepsis (bacteraemia) and prevent progression to multi-organ failure while drainage is being arranged.

Empirical Antibiotic Regimens

Empirical antibiotics must cover the expected biliary pathogens: Gram-negative rods (E. coli, Klebsiella) + Enterococci + Anaerobes ^[1][7].

Duration and De-escalation

• Empirical antibiotics for 7 days ^[2], or until the source is controlled (drainage achieved) and clinical response is seen.
• De-escalate to targeted therapy once blood/bile culture and sensitivity results are available.
• In mild cases that respond quickly to drainage, shorter courses (3–5 days) may be adequate per TG18 recommendations.

Antibiotic Prophylaxis for Procedures

• Antibiotics are recommended before ERCP, especially in acute cholangitis — the biliary tract is normally sterile, and instrumentation can introduce or exacerbate infection ^[16][20].
• If ERCP results in incomplete drainage, antibiotics should be continued after the procedure ^[20].

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Pillar 3: Drainage (D) — Biliary Decompression

This is the most critical pillar. Without drainage, the obstructed, infected biliary tree acts like an undrained abscess — no amount of antibiotics will clear the infection if the pus (infected bile) remains under pressure ^[3].

When to Drain — Guided by Severity

Drainage Modalities — The Escalation Ladder

The QMH practice drainage escalation is: ERCP → PTBD → ECBD ^[1]. Let's detail each step.

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D1. Endoscopic Retrograde Cholangiopancreatography (ERCP) — 1st Line

ERCP +/- biliary stenting is the first-line approach for biliary drainage in acute cholangitis ^[2][7][14].

Breaking down the name: "Endoscopic" = using an endoscope; "Retrograde" = going backwards (against the normal flow of bile, from the duodenum up into the duct); "Cholangio-" = bile duct; "Pancreatography" = imaging of the pancreatic duct. So ERCP = using an endoscope to image and access the bile and pancreatic ducts from below.

Papillary Balloon Dilatation (Balloon Sphincteroplasty) — an alternative to sphincterotomy:

• Dilates the ampulla with a balloon rather than cutting it, attempting to preserve the biliary sphincter ^[1].
• Lower risk of bleeding than sphincterotomy.
• Safety has been questioned (higher risk of pancreatitis in early studies); endoscopic sphincterotomy remains the method of choice ^[1].

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D2. Percutaneous Transhepatic Biliary Drainage (PTBD) — 2nd Line

Management of cholangitis: Resuscitation → Treat sepsis with intravenous antibiotic → Decompression of biliary system: Endoscopic vs percutaneous → Definitive management ^[3][17][18].

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D3. Surgical Drainage — Exploration of Common Bile Duct (ECBD) — Last Resort

Surgical drainage is reserved for patients in whom other methods of biliary drainage cannot be performed or have failed ^[1][7][15].

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D4. Therapeutic EUS (EUS-Guided Biliary Drainage) — Emerging Option

• EUS-guided cholangiopancreatography is an emerging technique when ERCP fails ^[2].
• The echoendoscope is used to puncture the bile duct from the stomach or duodenum under ultrasound guidance, and a stent is placed transmurally.
• Still requires specialised expertise and equipment; not universally available but increasingly used as a rescue option before resorting to surgery or PTBD.

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Summary: Drainage Escalation

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Pillar 4: Definitive Management — Treating the Underlying Cause

Definitive treatment should be deferred until cholangitis has been treated and the proper diagnosis is established ^[1][18]. Once the acute sepsis is controlled and the patient is stable, address the underlying etiology to prevent recurrence.

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Management According to Clinical Scenario — Synthesis

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Post-ERCP Monitoring — Detecting Complications

After ERCP, watch for ^[16]:

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Complications of Sphincterotomy — Short-Term and Long-Term

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Active Recall - Management of Acute Cholangitis

1. State the RAD mnemonic for acute cholangitis management and explain each component.

Your answer

Grade

Show mark scheme

R = Resuscitation (NPO, IV fluids, monitor vitals and I/O Q1h, blood cultures before antibiotics, correct coagulopathy). A = Antibiotics (IV broad-spectrum: mild = Augmentin or Cefuroxime + Metronidazole; severe = Piperacillin-Tazobactam for 7 days). D = Drainage (biliary decompression: urgency based on TG18 severity grading; escalation ERCP then PTBD then ECBD).

2. What is the primary role of ERCP in acute cholangitis, and why should bile be aspirated before injecting contrast?

Your answer

Grade

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Primary role is biliary drainage and decompression, NOT stone removal in unstable patients. Bile should be aspirated first to decompress the biliary tree and reduce intraluminal pressure, thereby reducing the risk of inducing further bacteraemia during contrast injection. Stone removal can be deferred to interval ERCP after sepsis resolves.

3. A patient with acute cholangitis fails ERCP due to Billroth II anatomy. What are the next two drainage options in order, and what are the key considerations for each?

Your answer

Grade

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1st: PTBD - percutaneous transhepatic biliary drainage via intrahepatic duct (not CBD), left hepatic duct preferred (less painful subcostal approach, avoids pleural transgression). Similar efficacy to ERCP. Risk: fluid/electrolyte loss, bleeding, pneumothorax. 2nd: Surgical ECBD (exploration of common bile duct) with T-tube placement. Open approach for emergency. Mortality approximately 30%. Reserved as last resort when both ERCP and PTBD fail.

4. Why are antibiotics alone insufficient to treat moderate-to-severe acute cholangitis? Connect this to the pathophysiology.

Your answer

Grade

Show mark scheme

Antibiotic excretion into bile is impaired when the biliary system is obstructed. Therefore, even with correct IV antibiotics, therapeutic concentrations cannot be achieved at the site of infection within the obstructed biliary tree. Biliary drainage is mandatory to decompress the system, allow source control, and restore antibiotic penetration. Additionally, the obstructed system acts like an undrained abscess - pus under pressure - which antibiotics alone cannot sterilise.

5. After resolving acute cholangitis from a CBD stone, what is the definitive management plan? Why is ascending cholangitis still possible even after cholecystectomy?

Your answer

Grade

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Definitive: ERCP for stone removal (sphincterotomy plus wire basket or balloon extraction or mechanical lithotripsy) followed by early laparoscopic cholecystectomy (same admission preferred). Ascending cholangitis is still possible after cholecystectomy because: (1) ERCP-induced CBD dilatation leads to biliary stasis; (2) ageing-related CBD dilatation; (3) sphincterotomy permanently ablates the sphincter of Oddi barrier, allowing free duodenal reflux. Approximately 5% risk of recurrent biliary events.

6. List three potential complications of ERCP sphincterotomy and explain the difference between intraperitoneal and retroperitoneal perforation in terms of CXR findings and management.

Your answer

Grade

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Complications: (1) Post-ERCP pancreatitis, (2) Perforation, (3) Bleeding from papillotomy. Intraperitoneal perforation (duodenal wall): free gas under diaphragm on erect CXR, requires operative treatment (will not seal spontaneously). Retroperitoneal perforation (bile duct at ampulla): NO free gas under diaphragm on CXR but retroperitoneal gas may be seen on CT, managed conservatively (usually seals spontaneously).

References

^[1] Senior notes: felixlai.md (Acute cholangitis — treatment: general principles, medical treatment, ERCP, PTBD, surgical drainage) ^[2] Senior notes: maxim.md (Acute cholangitis — acute management RAD, ERCP technique, PTBD, surgical drainage, long-term management) ^[3] Lecture slides: Malignant biliary obstruction.pdf (p16 — Cholangitis: impaired antibiotic excretion, biliary drainage mandatory; p17 — Management of cholangitis: resuscitation, antibiotics, decompression, definitive management) ^[4] Senior notes: felixlai.md and maxim.md (Recurrent pyogenic cholangitis — management, PTBD, hepatobiliary resection) ^[7] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p13 — NPO, IVF, antibiotics: Cefuroxime, Metronidazole, Piperacillin-Tazobactam; p14 — ERCP first line, complications, contraindications; p15 — Surgical ECBD indications) ^[10] Senior notes: maxim.md (Choledocholithiasis — ERCP stone removal methods, surgical exploration, T-tube) ^[14] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p14 — ERCP first line, potential complications, relative contraindications for ERCP) ^[15] Senior notes: felixlai.md (Malignant biliary obstruction — ERCP with endoprosthesis, PTBD, stent types, palliative management) ^[16] Senior notes: maxim.md (Post-ERCP management, ASGE antibiotic prophylaxis guidelines, ERCP procedure details) ^[17] Lecture slides: Malignant biliary obstruction.pdf (p15 — Management: establish diagnosis, delineate level/cause, treat suppurative cholangitis, definitive treatment) ^[18] Lecture slides: Malignant biliary obstruction.pdf (p17 — Management of cholangitis: resuscitation, treat sepsis, decompression endoscopic vs percutaneous, definitive management) ^[19] Senior notes: maxim.md (Acute pancreatitis management — avoid morphine, analgesic choice) ^[20] Senior notes: maxim.md (ASGE guideline for antibiotic prophylaxis before GI endoscopy — ERCP in cholangitis)

Complications of Acute Cholangitis

Framework — Why Complications Occur

To understand the complications of acute cholangitis, think about the disease as an escalating cascade with three domains of damage:

1. Local complications — direct consequences of infected bile under pressure within the biliary tree and surrounding structures.
2. Systemic complications — consequences of bacteraemia and sepsis once bacteria and endotoxins reflux from the biliary system into the circulation (when intraductal pressure exceeds 25 cm H₂O ^[3]).
3. Iatrogenic complications — consequences of the interventions (ERCP, PTBD, surgery) used to treat cholangitis.

Additionally, there are long-term complications from recurrent or inadequately treated cholangitis.

Let's work through each systematically.

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A. Local Complications — Direct Extension of Biliary Infection

These result from the infected bile under pressure eroding into, or extending beyond, the bile duct into adjacent structures.

A1. Liver Abscess (Pyogenic)

A2. Gallbladder Empyema

A3. Biliary Stricture Formation

A4. Biliary Fistula

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B. Systemic Complications — Consequences of Bacteraemia and Sepsis

These complications arise when the infection is no longer contained within the biliary tree and has spilled into the systemic circulation. The pathophysiology is: increased biliary pressure > 25 cm H₂O → bacteria reflux to hepatic veins and lymphatics → bacteraemia and septic shock ^[3].

B1. Sepsis and Septic Shock (Biliary Sepsis)

B2. Multi-Organ Failure

When sepsis is not controlled, it progresses to multi-organ dysfunction syndrome (MODS) — the sequential or simultaneous failure of multiple organ systems:

High-Yield: Multi-organ failure is the cause of death in fatal cholangitis. The progression is: cholangitis → bacteraemia → SIRS → sepsis → septic shock → MODS → death. Early drainage interrupts this cascade.

B3. Disseminated Intravascular Coagulation (DIC)

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C. Complications Related to Biliary Obstruction Itself

Even before sepsis develops, the obstruction component of cholangitis causes its own set of problems:

C1. Acute Biliary Pancreatitis

C2. Coagulopathy from Vitamin K Deficiency

C3. Malnutrition and Fat Malabsorption

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D. Iatrogenic Complications — From the Treatments We Use

The drainage procedures themselves carry risks. These are important to know for exams because they frequently come up in the context of "complications of ERCP/PTBD."

D1. Complications of ERCP

Potential complications of ERCP ^[7][14][16]:

D2. Complications of PTBD

D3. Complications of Surgical ECBD

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E. Long-Term Complications of Recurrent / Chronic Cholangitis

These are particularly relevant in the context of recurrent pyogenic cholangitis (RPC) ^[4]:

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F. Summary Table — All Complications at a Glance

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Active Recall - Complications of Acute Cholangitis

1. A patient with cholangitis develops a swinging fever despite biliary drainage. What complication should you suspect, how do you diagnose it, and how do you manage it?

Your answer

Grade

Show mark scheme

Suspect pyogenic liver abscess. Diagnose with CT abdomen with contrast showing double-target sign (rim-enhancing lesion with central hypodensity). Manage with prolonged IV antibiotics (4-6 weeks) plus image-guided percutaneous drainage (aspiration if less than 5cm, catheter placement if greater than 5cm). If Klebsiella is isolated, consult ophthalmology to rule out endophthalmitis.

2. Explain the pathophysiology of how acute cholangitis leads to septic shock and multi-organ failure, starting from intraductal pressure.

Your answer

Grade

Show mark scheme

Biliary obstruction raises intraductal pressure above 25 cm H2O. At this pressure, bacteria and endotoxins reflux into hepatic veins and peribiliary lymphatics (cholangiovenous reflux), causing bacteraemia. Gram-negative endotoxins (LPS) activate the innate immune system, triggering massive cytokine release (TNF-alpha, IL-1, IL-6) leading to SIRS then sepsis. Sepsis causes vasodilation, capillary leak, myocardial depression leading to distributive shock. Organ hypoperfusion causes ARDS, AKI, DIC, hepatic failure, encephalopathy. Antibiotics alone are insufficient because their excretion into bile is impaired in obstruction, so biliary drainage is mandatory.

3. Name the most common complication of ERCP and explain how it occurs. What measures can prevent it?

Your answer

Grade

Show mark scheme

Post-ERCP pancreatitis (2-5% incidence). Occurs due to manipulation of the papilla causing oedema at the ampulla, obstructing the pancreatic duct orifice, leading to premature enzyme activation. Also from inadvertent contrast injection into the pancreatic duct. Prevention: rectal NSAIDs (diclofenac or indomethacin), pancreatic duct stent placement, guidewire cannulation before contrast injection to avoid injection into the pancreatic duct.

4. Differentiate intraperitoneal and retroperitoneal perforation after ERCP in terms of mechanism, CXR findings, and management.

Your answer

Grade

Show mark scheme

Intraperitoneal perforation: perforates the duodenal wall; CXR shows free gas under the diaphragm (pneumoperitoneum); requires operative treatment because it will not seal spontaneously. Retroperitoneal perforation: perforates the bile duct at the ampulla (retroperitoneal portion of D2); CXR shows NO free gas under diaphragm but CT may show retroperitoneal gas; managed conservatively as it usually seals spontaneously.

5. Why does recurrent pyogenic cholangitis predispose to cholangiocarcinoma and secondary biliary cirrhosis?

Your answer

Grade

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Cholangiocarcinoma: chronic inflammation of biliary epithelium from recurrent infection causes chronic cell turnover and repair, leading to the inflammation-dysplasia-carcinoma sequence (malignant transformation of biliary epithelium). Secondary biliary cirrhosis: chronic repeated biliary obstruction causes persistent cholestasis, periductal fibrosis extends into hepatic parenchyma, progressive fibrosis leads to cirrhosis. Called secondary because the cause (obstruction) is identified, distinguishing it from primary biliary cholangitis (autoimmune).

6. A patient develops fever and tachycardia after ERCP for cholangitis. What are the possible causes and how do you investigate?

Your answer

Grade

Show mark scheme

Differential: (1) Persistent cholangitis from unsuccessful drainage, migrated or blocked stent, or resistant organisms. (2) ERCP complications including flare-up sepsis, post-ERCP pancreatitis, or perforation. Investigations: AXR to check stent position (migration, blockage). Blood cultures, repeat bloods (CBC, LFT, CRP, amylase). If abdominal pain is prominent, CT abdomen to look for retroperitoneal free gas (perforation) or evidence of pancreatitis.

References

^[1] Senior notes: felixlai.md (Acute cholangitis — treatment, ERCP complications, PTBD, surgical drainage; Mirizzi syndrome — biliary fistula) ^[2] Senior notes: maxim.md (Acute cholangitis — acute management RAD, ERCP, PTBD, long-term management; post-cholecystectomy complications) ^[3] Lecture slides: Malignant biliary obstruction.pdf (p16 — biliary pressure, cholangiovenous reflux, impaired antibiotic excretion, mandatory drainage; p17 — management of cholangitis) ^[4] Senior notes: felixlai.md and maxim.md (Recurrent pyogenic cholangitis — complications: biliary sepsis, pancreatitis, abscess, fistula, cirrhosis, cholangiocarcinoma) ^[7] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p7 — pathogenesis; p14 — ERCP complications: perforation, bleeding from papillotomy, pancreatitis; p15 — surgical ECBD indications) ^[10] Senior notes: maxim.md (Choledocholithiasis — T-tube complications, stone removal methods) ^[11] Senior notes: felixlai.md (Liver abscess — overview, microbiology, route of spread) and maxim.md (Liver abscess — pathogens, investigations, management, complications) ^[14] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p14 — ERCP potential complications, contraindications) ^[15] Senior notes: felixlai.md (Malignant biliary obstruction — ERCP stent complications, PTBD bleeding management) ^[16] Senior notes: maxim.md (ERCP complications, post-ERCP management, PTC/PTBD complications, ASGE antibiotic prophylaxis) ^[21] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p5 — Complications of gallstone disease: acute cholangitis, liver abscess, acute pancreatitis) ^[22] Senior notes: felixlai.md (Acute pancreatitis — ERCP indications, biliary pancreatitis management) ^[23] Senior notes: felixlai.md (ERCP complications table — post-ERCP pancreatitis most frequent, cholangitis, bleeding, perforation, papillary stenosis, stent stenosis/migration)