Acute Cholangitis

Acute bacterial infection of the biliary tract due to obstruction, classically presenting with Charcot's triad of fever, jaundice, and right upper quadrant pain.

2. Epidemiology

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

Feature	Relevance to Hong Kong
Choledocholithiasis	Remains the most common cause worldwide and in Hong Kong ^[1]^[2].
Recurrent pyogenic cholangitis (RPC)	Also known as "Hong Kong disease" / oriental cholangiohepatitis — a uniquely Southeast Asian entity involving recurrent cholangitis from intrahepatic pigment stones and strictures ^[1]^[4]. Peak prevalence in the 30s–40s, equal sex distribution.
Clonorchis sinensis	Liver fluke endemic to areas where raw/undercooked freshwater fish is consumed; causes chronic biliary inflammation predisposing to RPC and cholangiocarcinoma ^[1]^[4].
Hepatitis B	Highly prevalent in Hong Kong; chronic liver disease and cirrhosis contribute to altered bile composition and immunocompromise.
Ageing population	Increased biliary stenting and ERCP procedures → rising incidence of post-procedural/stent-related cholangitis.
Malignant biliary obstruction	Pancreatic head carcinoma, cholangiocarcinoma, and periampullary tumours are important causes of cholangitis in the elderly ^[3]^[5].

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.

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

Defence Mechanism	How it works
Continuous flushing action of bile flow	Antegrade bile flow physically washes bacteria back into the duodenum — like a river current preventing upstream migration.
Bacteriostatic activity of bile salts	Bile salts are detergents; they disrupt bacterial cell membranes and inhibit growth.
Biliary mucus and secretory IgA	These act as anti-adherence factors, preventing bacteria from colonising the ductal epithelium (similar to the mucosal immune barrier in the gut).
Sphincter of Oddi	A mechanical barrier at the ampulla that prevents duodenal reflux and ascending bacterial contamination ^[1]^[3].

Why does cholangitis occur after sphincterotomy?

After endoscopic sphincterotomy (done during ERCP to remove CBD stones), the Sphincter of Oddi is permanently divided. This ablates the mechanical barrier, allowing free reflux of duodenal contents into the biliary tree. That is why patients with prior sphincterotomy, biliary stents, or choledochal surgery are at increased risk of recurrent cholangitis — the normal barrier is permanently disrupted ^[1]^[2].

4. Etiology (Causes of Biliary Obstruction)

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

Cause	Details	Relative Frequency
Choledocholithiasis (CBD stones)	Most common cause worldwide and in Hong Kong ^[1]^[2]^[3]. Stones migrate from gallbladder via cystic duct or form de novo in CBD.	Most common (~30–70% of cases)
Benign biliary strictures	Post-surgical injury (e.g., after cholecystectomy), chronic pancreatitis, PSC, post-radiation.	Common
Malignant biliary obstruction (MBO)	Pancreatic head carcinoma, cholangiocarcinoma, periampullary carcinoma, porta hepatis lymph node metastases ^[2]^[3]^[5].	Common in elderly
Indwelling biliary stents / post-instrumentation	Stent occlusion by sludge/biofilm → obstruction proximal to stent; foreign body serves as nidus for bacterial colonisation ^[1]^[2]. Disrupted sphincter post-sphincterotomy.	Increasingly common
Parasitic infection	Clonorchis sinensis, Opisthorchis viverrini, Ascaris lumbricoides — adult worms or eggs obstruct bile ducts ^[1]^[4]. Particularly important in Hong Kong/Southeast Asia.	Important regionally
Recurrent pyogenic cholangitis (RPC)	Intrahepatic pigment stone formation + strictures → stasis → recurrent infection. "Hong Kong disease" ^[1]^[4].	Important in Hong Kong
Choledochal cysts	Congenital dilatation of bile ducts → stasis → risk of cholangitis (and cholangiocarcinoma) ^[1].	Rare
Mirizzi syndrome	Large stone impacted in cystic duct/Hartmann's pouch compressing the CHD externally → obstruction → cholangitis ^[1].	Rare
Primary sclerosing cholangitis (PSC)	Chronic fibrosing inflammation of bile ducts → strictures → stasis → cholangitis. Strong association with ulcerative colitis ^[1].	Rare in Asia
Biliary-enteric anastomosis stricture	Stricturing at the site of surgical anastomosis (e.g., hepaticojejunostomy) → stasis → ascending infection.	Post-surgical

4.2 Focus on Hong Kong-Specific Etiologies

5. Pathophysiology

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

Step	Event	Mechanism
1	Biliary obstruction occurs	Stone impaction, tumour compression, stricture, stent occlusion, or parasites block bile flow.
2	Bile stasis develops	Loss of the flushing action of bile. Stagnant bile loses its bacteriostatic effect. IgA and mucus barrier become overwhelmed.
3	Bacterial colonisation	Bacteria ascend from the duodenum (most common route) or arrive via portal venous haematogenous spread ^[1].
4	Intraductal pressure rises	Normal: 7–14 cm H₂O ^[3]. With obstruction, pressure rises progressively.
5	Pressure exceeds 25 cm H₂O	Bacteria and endotoxins reflux into hepatic veins and peribiliary lymphatics → bacteraemia → systemic inflammatory response (SIRS) → sepsis ^[3].
6	Impaired antibiotic penetration	Excretion of antibiotics into bile is impaired in biliary obstruction — this is why antibiotics alone are often insufficient and biliary drainage is mandatory ^[3].
7	Septic shock / suppurative cholangitis	If undrained, purulent bile (pus) fills the ducts under high pressure → overwhelming sepsis → multi-organ failure → death.

Why Antibiotics Alone Are Not Enough

A common exam mistake is thinking that antibiotics alone can treat cholangitis. In biliary obstruction, antibiotic excretion into bile is impaired ^[3] — so even if the right antibiotics are given IV, they cannot reach therapeutic concentrations in the obstructed biliary tree. That is why biliary drainage is mandatory in moderate-to-severe cholangitis. Think of it like trying to put out a fire in a locked room — you need to open the door (decompress the duct) before the water (antibiotics) can reach the flames.

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

Category	Organisms	Notes
Gram-negative rods (most common)	Escherichia coli, Klebsiella pneumoniae, Enterobacter sp.	These are the dominant pathogens ^[1]^[2]^[3]. They produce endotoxins (lipopolysaccharide) which drive the septic response.
Enterococci (Gram-positive)	Enterococcus faecalis, E. faecium	The most common Gram-positive organisms in biliary infections ^[1]^[2]^[3].
Anaerobes	Bacteroides fragilis, Clostridium sp.	More common in severe/complicated infections and in patients with prior biliary-enteric anastomosis ^[1]^[3].
Pseudomonas aeruginosa		More common in patients with biliary stents — important because it requires broader-spectrum antibiotic coverage ^[2].

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].

6. Classification

Type	Description
Ascending cholangitis	Infection ascending from the duodenum → most common type in clinical practice ^[2].
Descending cholangitis	Infection spreading from the liver/portal system → less common, seen in liver abscess or haematogenous seeding.

Type	Description
Non-suppurative (simple) cholangitis	Infected bile without frank pus. Responds to antibiotics + elective drainage.
Suppurative cholangitis	Frank purulent bile under pressure. This is the severe, life-threatening form. Requires emergency biliary decompression. Characterised by Reynolds' pentad.

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

Grade	Severity	Criteria	Management Implication
Grade I	Mild	Acute cholangitis that does not meet criteria for Grade II or III. Responds to initial medical treatment (antibiotics + supportive care). No organ dysfunction.	May respond to antibiotics alone initially; early elective biliary drainage.
Grade II	Moderate	Associated with any TWO of: WBC > 12,000 or < 4,000/mm³; fever ≥ 39°C; age ≥ 75; bilirubin ≥ 5 mg/dL; albumin < 0.7 × lower limit of normal. Does not meet Grade III. Does not respond to initial medical treatment.	Requires early biliary drainage (within 24–48 hours).
Grade III	Severe	Associated with organ dysfunction in any ONE system: cardiovascular (hypotension requiring vasopressors), neurological (altered consciousness), respiratory (PaO₂/FiO₂ < 300), renal (oliguria, Cr > 2.0 mg/dL), hepatic (PT-INR > 1.5), haematological (Plt < 100,000/mm³).	Requires urgent/emergency biliary drainage + organ support (ICU).

Tokyo Guidelines Severity Grading — Exam Must-Know

Grade I (Mild): No organ dysfunction, responds to antibiotics.
Grade II (Moderate): Does not respond to initial treatment OR has risk factors (high WBC, high fever, elderly, high bilirubin, low albumin).
Grade III (Severe): Organ dysfunction — this is suppurative cholangitis / biliary sepsis. Emergency drainage is life-saving.

Classification	Details
By etiology	Stone-related vs. non-stone (malignant, stricture, stent, parasitic) ^[2].
Primary vs. Secondary	Primary cholangitis = PSC (autoimmune). Secondary = all other causes (obstruction-related). The term "primary" distinguishes PSC from secondary sclerosing cholangitis ^[1].
IgG4-associated cholangitis	Infiltration of biliary system with IgG4-positive plasma cells, mostly in elderly males. Part of the IgG4-related disease spectrum. Responds to corticosteroids ^[2].

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).

Symptom	Pathophysiological Basis
Fever (with or without rigors/chills)	Bacteraemia: when intraductal pressure exceeds ~25 cm H₂O, bacteria and endotoxins reflux into hepatic veins and lymphatics → systemic inflammatory response → fever. Rigors (shaking chills) indicate bacteraemia with endotoxaemia — the body's thermoregulatory "reset" to a higher set-point ^[3].
Right upper quadrant (RUQ) / epigastric abdominal pain	Distension of the bile duct wall by impacted stone or increased intraductal pressure stimulates visceral afferent pain fibres (carried via the coeliac plexus and splanchnic nerves to T6–T9 dermatomes). The pain is typically constant and dull (unlike the colicky pain of biliary colic which is from gallbladder contraction against a stone in the cystic duct).
Jaundice	Biliary obstruction → conjugated bilirubin cannot be excreted into the duodenum → accumulates in the blood → deposits in skin and sclerae (yellow). Conjugated bilirubin is water-soluble → excreted by the kidneys → dark urine (tea-coloured). Reduced bilirubin reaching the gut → less stercobilinogen → pale/clay-coloured stools.

Charcot's Triad

A useful mnemonic: "F-A-J" — Fever, Abdominal pain, Jaundice. Named after Jean-Martin Charcot (1877), the famous French neurologist who also described Charcot-Marie-Tooth disease and Charcot joints. Present in 50–70% but NOT in all patients — absence does not exclude the diagnosis ^[1]^[2].

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

Additional Feature	Pathophysiological Basis
Hypotension (shock)	Overwhelming bacteraemia → massive release of endotoxins (LPS from Gram-negative bacteria) → activation of inflammatory cascade (TNF-α, IL-1, IL-6) → systemic vasodilation + increased capillary permeability + myocardial depression = distributive (septic) shock. This is the same pathway as any Gram-negative sepsis.
Altered mental status (confusion)	Cerebral hypoperfusion from shock + direct neurotoxic effects of systemic endotoxaemia + metabolic encephalopathy (hepatic dysfunction from cholestasis, renal dysfunction from shock) → decreased consciousness ranging from confusion to obtundation.

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].

Symptom	Mechanism
Nausea and vomiting	Visceral afferent stimulation from biliary distension triggers the vomiting centre via vagal afferents. Also common in any systemic sepsis.
Dark urine	Conjugated (water-soluble) bilirubin excreted renally → urine becomes tea/cola-coloured. This is conjugated hyperbilirubinaemia because the obstruction is post-hepatic.
Pale stools (acholic stools)	Reduced bilirubin entering the gut → less conversion to stercobilinogen/stercobilin → clay/putty-coloured stools.
Pruritus	Bile salt deposition in the skin due to cholestasis → activates itch receptors (pruritoceptors). More common in chronic/subacute obstruction than in acute cholangitis.
Anorexia and malaise	Systemic inflammatory response + hepatic dysfunction.

7.2 Signs

Sign	Pathophysiological Basis
Fever (often high-grade, > 38.5°C, with rigors)	Bacteraemia with endotoxin release → pyrogenic cytokines (IL-1, TNF-α, IL-6) act on the hypothalamic thermoregulatory centre → febrile response. Rigors indicate the temperature is being "reset" to a higher set-point.
Jaundice (scleral icterus first)	Conjugated hyperbilirubinaemia. Sclera have high elastin content with affinity for bilirubin → icterus visible when serum bilirubin > 34 μmol/L (~2 mg/dL). Best detected in natural daylight.
Tachycardia	Systemic inflammatory response → increased sympathetic drive + if hypovolaemic from sepsis → compensatory tachycardia.
Hypotension (in severe cholangitis)	Septic shock — see above.
Dehydration	Poor oral intake + fever + third-space losses from sepsis.

Sign	Pathophysiological Basis
RUQ tenderness	Palpation over the distended, inflamed bile duct and surrounding peritoneum → localised somatic pain. The gallbladder fossa and CBD lie beneath the right costal margin at the intersection with the lateral border of the rectus abdominis (the hepatic point).
Murphy's sign — typically NEGATIVE (important distinguishing feature)	Murphy's sign is positive in acute cholecystitis (inflammation of the gallbladder), NOT in cholangitis. In cholangitis, the primary pathology is in the bile duct, not the gallbladder. However, if concurrent cholecystitis is present (e.g., from a stone impacted at the cystic duct), Murphy's sign may be positive.
Hepatomegaly	Biliary obstruction → bile duct distension → secondary hepatic congestion and inflammation → liver may be palpably enlarged and tender. In chronic/recurrent cholangitis (e.g., RPC), hepatomegaly may be more pronounced due to parenchymal changes.
No peritonism (usually)	Cholangitis is an intraductal infection. Unlike perforated viscus or appendicitis, there is no peritoneal soiling — so generalised peritonitis with guarding and rigidity is typically absent unless there is perforation or concomitant pathology.

Cholangitis vs. Cholecystitis — Don't Confuse Them

Cholangitis = infection of the bile duct → Charcot's triad (Fever + Pain + Jaundice); Murphy's sign typically negative; jaundice is prominent.
Cholecystitis = inflammation of the gallbladder → Murphy's sign positive; fever; RUQ pain; jaundice is uncommon (only ~20%, usually from Mirizzi syndrome or co-existing CBD stone).

The key differentiator: Jaundice is much more prominent in cholangitis. Murphy's sign is positive in cholecystitis but not cholangitis.

Sign	Significance
Altered mental status	Part of Reynolds' pentad — indicates suppurative cholangitis / septic encephalopathy.
Oliguria	Renal hypoperfusion from septic shock → acute kidney injury.
Cold, clammy skin	Late sign of distributive shock → compensatory peripheral vasoconstriction.
Metabolic acidosis (on ABG)	Tissue hypoperfusion → anaerobic metabolism → lactic acidosis.
Petechiae / bleeding	Disseminated intravascular coagulation (DIC) from sepsis + impaired hepatic synthesis of clotting factors from biliary obstruction + reduced vitamin K absorption (fat-soluble vitamin requiring bile salts for absorption).

Pathophysiology	Clinical Feature
Biliary obstruction → ↑ intraductal pressure → ductal distension	RUQ / epigastric pain
Obstruction → conjugated bilirubin retention	Jaundice, dark urine, pale stools, pruritus
Bacterial contamination + stasis → infection → bacteraemia	Fever, rigors, raised WBC, positive blood cultures
Intraductal pressure > 25 cm H₂O → cholangiovenous reflux ^[3]	Bacteraemia → SIRS → sepsis → septic shock
Septic shock → organ hypoperfusion	Hypotension, altered mental status, oliguria, metabolic acidosis
Impaired antibiotic excretion in obstructed system ^[3]	Failure of antibiotics alone → need for biliary drainage
Cholestasis → reduced bile salt in gut	Fat malabsorption, vitamin K deficiency → coagulopathy

High Yield Summary

Definition: Acute cholangitis = bacterial infection of biliary tract due to obstruction + bacterial contamination (both required).

Most common cause: Choledocholithiasis (CBD stones). In Hong Kong, also think of RPC and Clonorchis sinensis.

Normal biliary defences: Bile flow flushing, bile salt bacteriostasis, mucosal IgA, Sphincter of Oddi barrier.

Pathophysiology: Obstruction → stasis → bacterial overgrowth → raised intraductal pressure → cholangiovenous/lymphatic reflux when pressure > 25 cm H₂O → bacteraemia → sepsis. Antibiotic excretion is impaired in obstruction → biliary drainage is mandatory.

Bacteriology: Gram-negative rods (E. coli, Klebsiella) most common; Enterococci; anaerobes in severe cases; Pseudomonas if stent present.

Clinical features:

Charcot's triad (50–70%): Fever + RUQ pain + Jaundice
Reynolds' pentad ( < 10%): Charcot's triad + Hypotension + Altered mental status = suppurative cholangitis = surgical emergency

Tokyo Guidelines severity:

Grade I (Mild): Responds to antibiotics
Grade II (Moderate): Does not respond / has risk factors
Grade III (Severe): Organ dysfunction → emergency drainage

Key distinguishing point: Murphy's sign is positive in cholecystitis, NOT cholangitis. Jaundice is prominent in cholangitis, often absent in cholecystitis.

Active Recall - Acute Cholangitis (Definition to Clinical Features)

Differential Diagnosis of Acute Cholangitis

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]:

Feature	Acute Cholecystitis	Acute Cholangitis
Primary pathology	Inflammation of the gallbladder (from cystic duct obstruction)	Infection of the bile duct (from CBD obstruction)
Jaundice	Uncommon (~20%) — only if Mirizzi syndrome or co-existing CBD stone	Prominent — because the CBD itself is obstructed
Murphy's sign	Positive (inspiratory arrest on RUQ palpation — gallbladder is inflamed and tender)	Typically negative (the gallbladder is not the inflamed organ)
Fever	Present but usually lower-grade initially (chemical → secondary bacterial infection over 48h)	Often high-grade with rigors from the outset (bacteraemia from cholangiovenous reflux)
Pain character	Starts as biliary colic that persists > 6 hours, becomes constant with peritoneal signs	Constant RUQ/epigastric pain, less peritoneal involvement
LFT	Usually normal or mildly deranged (obstruction limited to gallbladder) ^[9]	Cholestatic pattern (↑ ALP, ↑ GGT, ↑ conjugated bilirubin) — because the CBD is obstructed
USG	5 cardinal signs: gallstones, distended GB, wall thickening > 3 mm, pericholecystic fluid, sonographic Murphy's sign ^[9]	Dilated CBD ± stone, ± dilated intrahepatic ducts

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.

Exam Pearl — Cholecystitis vs Cholangitis

Students commonly conflate these two. Remember:

Cholecystitis = gallbladder problem → Murphy's positive, jaundice rare, LFT often normal.
Cholangitis = bile duct problem → Charcot's triad, Murphy's negative, cholestatic LFT. If the LFT shows a significantly cholestatic pattern (markedly raised ALP/GGT/bilirubin), think duct, not gallbladder ^[9].

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

Feature	Liver Abscess	Acute Cholangitis
Fever pattern	Swinging fever (high spikes followed by remission — "picket-fence" pattern), chills, rigors ^[11]	High-grade fever with rigors, but usually more constant
Pain	RUQ pain, tender hepatomegaly	RUQ pain, hepatomegaly less prominent
Jaundice	Not significant (abscess is focal — the unaffected liver parenchyma continues to excrete bilirubin) ^[11]	Prominent (entire biliary outflow is obstructed)
LFT	Mildly deranged, ALP may be elevated, but bilirubin often near-normal	Cholestatic pattern (markedly raised ALP, GGT, bilirubin)
Imaging	CT abdomen with contrast: double-target sign (rim-enhancing lesion with central hypodensity), cluster sign ^[11]. USG: multiloculated cystic mass.	USG: dilated CBD ± stone. CT shows dilated ducts.
Aetiology clues	Klebsiella (especially in > 60 years old + DM in Hong Kong); ascending biliary infection itself; portal venous spread from appendicitis/diverticulitis ^[11]	CBD stone, stent, stricture, tumour

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].

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

Condition	Key Distinguishing Feature	Why It Can Mimic
Acute Appendicitis ^[1]^[7]^[8]	Pain starts peri-umbilical, migrates to RLQ (McBurney's point). No jaundice. Rovsing's sign positive.	Early appendicitis can cause vague upper abdominal pain before localising. High appendix (retrocaecal/subhepatic) may cause RUQ pain.
Peptic Ulcer Disease ^[8]^[12]	Epigastric pain, relationship to meals, ± GI bleeding. No jaundice.	Perforated posterior duodenal ulcer can mimic biliary/pancreatic pathology with referred pain.
Acute Hepatitis ^[8]	Prodromal symptoms (malaise, anorexia), hepatocellular LFT pattern (markedly raised AST/ALT >> ALP), viral serology positive.	Causes jaundice + RUQ tenderness + fever. But the LFT pattern is hepatocellular (transaminases dominant), not cholestatic.
Right lower lobe pneumonia ^[8]^[9]	Cough, dyspnoea, pleuritic chest pain, crackles on auscultation. CXR infiltrate.	Diaphragmatic irritation from basal pneumonia can cause referred RUQ pain and fever — a classic "trap" in exams.
Myocardial infarction ^[8]^[12]	Inferior MI can cause epigastric/RUQ pain. ECG changes, troponin elevation.	Vagal stimulation from inferior MI causes nausea, vomiting, and epigastric discomfort that mimics biliary colic or pancreatitis.

The Right Basal Pneumonia Trap

In exams, a patient with fever, RUQ pain, and raised WBC may have a right basal pneumonia rather than a biliary problem. Always examine the chest and order a CXR — this is why an erect CXR is part of the standard workup for RUQ pain ^[2].

Diagnosis	Pain	Jaundice	Fever	Murphy's	Key Investigation	Key Distinguishing Feature
Acute Cholangitis	RUQ, constant	✅ Prominent	✅ High + rigors	−	USG: dilated CBD	Charcot's triad, cholestatic LFT
Acute Cholecystitis	RUQ, > 6h	± Rare (~20%)	✅ Lower-grade	+	USG: 5 cardinal signs	Murphy's sign, GB wall thickening
Choledocholithiasis	RUQ	✅	✗ No fever	−	USG: dilated CBD	No infection — just obstruction
Liver Abscess	RUQ, tender hepatomegaly	± Minimal	✅ Swinging	−	CT: rim-enhancing lesion	Focal liver lesion, blood cultures
Acute Pancreatitis	Epigastric → back	±	✅	−	Amylase/lipase > 3× ULN	Sits up/leans forward, marked amylase
RPC	RUQ	✅	✅ Recurrent	−	CT: left lobe intrahepatic duct dilatation	Recurrent episodes, SE Asian, intrahepatic stones
Mirizzi Syndrome	RUQ	✅	✅	±	ERCP: extrinsic CHD compression	Palpable GB + jaundice, fistula
Hepatitis	RUQ	✅	✅ Low-grade	−	Hepatocellular LFT, viral serology	AST/ALT >> ALP (hepatocellular pattern)
Pneumonia	RUQ (referred)	✗	✅	−	CXR: consolidation	Respiratory symptoms, CXR findings

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

Always Order These in Suspected Cholangitis

When working up a patient with possible cholangitis, the following investigations help differentiate the differential:

Bloods: CBC, LFT (cholestatic vs hepatocellular pattern), amylase/lipase (r/o pancreatitis), blood culture ^[2]
Erect CXR (r/o pneumonia, free air under diaphragm from perforation) ^[2]
USG abdomen (dilated duct? Stone? Liver abscess? GB wall thickening?) ^[2]
If inconclusive: MRCP, CT abdomen with contrast (r/o liver abscess or malignant obstruction), or EUS ^[2]

High Yield Summary

Core differential of acute cholangitis (conditions sharing fever + RUQ pain ± jaundice):

Acute cholecystitis — Murphy's positive, jaundice rare, GB pathology on USG
Choledocholithiasis — jaundice without fever (no infection yet)
Liver abscess — swinging fever, tender hepatomegaly, CT double-target sign; similar presentations, must rule out on USG ^[2]
Acute biliary pancreatitis — epigastric pain radiating to back, amylase > 3× ULN
RPC — recurrent episodes, Southeast Asian, intrahepatic pigment stones, left lobe
Mirizzi syndrome — palpable GB + jaundice (exception to Courvoisier's Law)
Infected choledochal cyst — young patient, RUQ mass
Biliary leak — post-operative context
Malignant biliary obstruction — painless progressive jaundice in elderly, superimposed infection = cholangitis
Non-biliary mimics: Right basal pneumonia, acute hepatitis, inferior MI, peptic ulcer, appendicitis

Key differentiating tools: LFT pattern (cholestatic vs hepatocellular), Murphy's sign (cholecystitis vs cholangitis), amylase (pancreatitis), CXR (pneumonia), USG (ductal dilatation vs focal liver lesion vs GB pathology), blood cultures.

Active Recall - Differential Diagnosis of Acute Cholangitis

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

Category	Criteria
A. Systemic inflammation	A-1. Fever ( > 38°C) and/or shaking chills OR A-2. Laboratory evidence of inflammatory response: abnormal WBC count ( < 4,000 or > 10,000/mm³), ↑ CRP, or other changes indicating inflammation
B. Cholestasis	B-1. Jaundice (total bilirubin ≥ 2 mg/dL / ~34 μmol/L) OR B-2. Abnormal liver chemistries: ↑ ALP, ↑ GGT, ↑ AST, ↑ ALT (beyond 1.5× upper limit of normal)
C. Imaging	C-1. Biliary dilatation on imaging OR C-2. Evidence of an etiology on imaging (e.g., stone, stricture, stent)

Interpretation ^[1]:

Diagnostic Level	Criteria Required
Suspected diagnosis	ONE item from A (systemic inflammation) AND ONE item from B (cholestasis)
Definite diagnosis	Meets criteria for suspected diagnosis PLUS ANY item from C (imaging evidence)

Why This Structure Makes Sense

Think about it: a patient with fever + cholestatic LFT could have cholangitis, but they could also have acute hepatitis with secondary bacterial infection, or even cholecystitis with mild LFT derangement. Adding the imaging criteria (dilated duct, visible stone/stricture/stent) confirms that the problem is truly in the biliary tree. That is why a "definite" diagnosis requires imaging confirmation.

Exam Must-Know — Diagnostic Criteria

A common exam pitfall: students remember Charcot's triad but forget the formal Tokyo Guidelines criteria. The TG18 criteria are more sensitive than Charcot's triad (which is only present in 50–70% of cases). You can diagnose cholangitis even without jaundice — as long as you have systemic inflammation + abnormal liver chemistries + imaging findings ^[1].

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

Grade	Severity	Criteria	Clinical Implication
Grade I	Mild	Does not meet Grade II or III criteria. Responds to initial antibiotics + supportive care.	May attempt antibiotics first; early biliary drainage planned.
Grade II	Moderate	Meets ≥ 2 of: WBC > 12,000 or < 4,000; fever ≥ 39°C; age ≥ 75; total bilirubin ≥ 5 mg/dL (~85 μmol/L); albumin < 0.7 × lower limit of normal. Does not respond to initial medical treatment.	Requires early biliary drainage (within 24–48 h).
Grade III	Severe	Organ dysfunction in ≥ 1 system: Cardiovascular (hypotension needing vasopressors), Neurological (altered consciousness), Respiratory (PaO₂/FiO₂ < 300), Renal (oliguria or creatinine > 2.0 mg/dL), Hepatic (PT-INR > 1.5), Haematological (platelets < 100,000/mm³)	Urgent/emergency biliary drainage + ICU admission + organ support. This is suppurative cholangitis.

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

Investigation Modalities — Detailed Breakdown

A. Laboratory Investigations

Finding	Interpretation	Pathophysiological Basis
Leukocytosis with neutrophil predominance	Active bacterial infection / systemic inflammation	Bone marrow releases neutrophils in response to bacterial endotoxins and pro-inflammatory cytokines (IL-1, TNF-α, G-CSF). Neutrophils are the "first responders" to bacterial infection.
Left shift (↑ band forms)	Marrow is "ramping up" — pushing immature neutrophils into circulation	When demand exceeds the marrow reserve of mature neutrophils, immature forms (bands) are released. Indicates significant bacterial infection.
Leukopenia ( < 4,000)	Paradoxically indicates severe sepsis	Overwhelming infection consumes neutrophils faster than the marrow can replenish them, OR endotoxin-mediated marrow suppression. This is a bad prognostic sign — part of TG18 Grade II/III criteria.
Thrombocytopenia	DIC from sepsis OR hypersplenism from underlying cirrhosis	Important to check before any invasive procedure (ERCP, PTBD) — coagulopathy increases bleeding risk ^[1]^[15].

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

Marker	Expected Finding	Interpretation
↑ ALP (Alkaline Phosphatase)	Elevated, often markedly	ALP is concentrated in the bile duct epithelium (cholangiocytes) and the canalicular membrane of hepatocytes. Biliary obstruction causes bile to back up → cholestasis induces synthesis and release of ALP into blood. This is the hallmark of an obstructive/cholestatic pattern ^[1]^[2]^[15].
↑ GGT (Gamma-Glutamyl Transferase)	Elevated, often markedly	GGT is found in biliary epithelium and hepatocyte canalicular membranes. Rises with ALP in cholestasis. GGT confirms that a raised ALP is of biliary origin (vs. bone, pregnancy, etc.) ^[1]^[2].
↑ Conjugated (direct) bilirubin	Elevated	The obstruction prevents conjugated bilirubin from being excreted into the duodenum → it refluxes back into the blood. It is water-soluble → filtered by kidneys → dark urine ^[1]^[2].
↑ AST/ALT	Mildly to moderately elevated	In cholangitis, transaminases may be elevated (hepatocyte injury from back-pressure of bile, ischaemia from sepsis), but ALP and GGT rise disproportionately more than AST/ALT. If AST/ALT >> ALP, think hepatocellular cause (hepatitis), not cholangitis ^[1]^[15].

LFT Pattern Recognition — Exam Must-Know

Cholestatic pattern (cholangitis, choledocholithiasis, MBO): ALP ↑↑, GGT ↑↑, conjugated bilirubin ↑↑, AST/ALT mildly ↑.

Hepatocellular pattern (hepatitis, drug injury): AST/ALT ↑↑↑, ALP mildly ↑.

This pattern distinction alone can differentiate cholangitis from hepatitis at a glance ^[1]^[2].

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].

Marker	Finding	Notes
↑ CRP	Elevated (often markedly)	Hepatic acute-phase reactant produced in response to IL-6. Useful for monitoring treatment response (falls with successful drainage). Part of TG18 Criterion A.
↑ ESR	Elevated	Less specific than CRP; takes days to rise and fall.
Procalcitonin	Elevated in bacterial sepsis	More specific for bacterial infection than CRP. Increasingly used in severe sepsis to guide antibiotic duration. Not yet universally adopted in TG18 criteria.

Finding	Interpretation
Prolonged PT / elevated INR	Two mechanisms: (1) Vitamin K deficiency — bile salts are needed for absorption of fat-soluble vitamins (A, D, E, K) in the gut; biliary obstruction → no bile salts in gut → impaired vitamin K absorption → reduced synthesis of factors II, VII, IX, X ^[1]^[15]. (2) Hepatic synthetic dysfunction from sepsis-related hepatic injury or underlying liver disease.
Corrects with IV vitamin K	Confirms the cause is vitamin K malabsorption (obstructive), not intrinsic liver failure. If it does not correct, suspect severe hepatic dysfunction or DIC.

Pre-Procedure Check

Always check clotting and platelets before ERCP or PTBD. Coagulopathy from vitamin K deficiency is common in obstructive jaundice and needs correction (IV vitamin K) to reduce procedural bleeding risk ^[1]^[15].

Finding	Interpretation
↑ Creatinine, ↑ Urea	Acute kidney injury from sepsis-induced renal hypoperfusion (pre-renal), OR hepatorenal syndrome in patients with underlying chronic liver disease. Part of TG18 Grade III criteria.
Electrolyte abnormalities	Metabolic acidosis (lactic acid from tissue hypoperfusion), hyperkalaemia (from renal dysfunction).

Finding	Interpretation
Mildly elevated amylase	Common in cholangitis — mild pancreatic irritation from a stone near the ampulla.
Markedly elevated ( > 3× ULN)	Suggests concurrent acute biliary pancreatitis — an impacted ampullary stone obstructing both CBD and pancreatic duct ^[2]^[10]^[15].

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

Detail	Rationale
Must be taken BEFORE starting antibiotics	Antibiotics can sterilise the blood quickly, making cultures falsely negative.
At least 2 sets from different sites	Increases sensitivity, helps distinguish true bacteraemia from contaminant.
Request aerobic AND anaerobic bottles	Anaerobes (e.g., Bacteroides fragilis) are common in severe cholangitis ^[1]^[7].
Request antibiotic susceptibility testing	Guides de-escalation of empirical antibiotics to targeted therapy ^[1].
Positive in ~20–70% of cases	Depends on timing relative to antibiotic administration and severity. Positive cultures are common in the presence of bile duct stones and other obstructive causes ^[1].

Blood Culture — Absolutely Must Do

Blood culture is highlighted as a critical investigation in both senior notes and lecture slides ^[2]^[7]. In the acute setting, blood cultures are the only way to identify the causative organism and its antibiotic sensitivities. Take them before antibiotics. This is a frequent exam point.

Detail	Rationale
Obtained at the time of ERCP or PTBD	When bile is aspirated during drainage, it should be sent for culture and sensitivity ^[1].
Higher sensitivity than blood cultures	Bile cultures are positive in up to 80–100% of cholangitis cases (vs. 20–70% for blood cultures).
Organisms may differ from blood cultures	Polymicrobial infection is common; bile cultures may reveal additional organisms not detected in blood.

Finding	Interpretation
Conjugated bilirubin in urine (bilirubinuria)	Conjugated bilirubin is water-soluble → filtered by kidneys → appears in urine. Indicates post-hepatic (obstructive) jaundice. Absent urobilinogen (because bilirubin never reaches the gut to be converted).

Test	Rationale
Arterial blood gas (ABG)	In severe cholangitis: metabolic acidosis (lactic acidosis from tissue hypoperfusion), respiratory compensation. Part of severity assessment.
Lactate	Marker of tissue hypoperfusion. Elevated lactate ( > 2 mmol/L) indicates sepsis-related organ dysfunction.
Blood glucose	Infection can cause hyper- or hypoglycaemia. DM is a risk factor for liver abscess (important differential).
Group and save / cross-match	Pre-procedural preparation for ERCP/PTBD/surgery.
Tumour markers (CEA, CA 19-9)	If malignant biliary obstruction is suspected as the underlying cause. Not diagnostically useful (lack sensitivity and specificity) but serial assay after resection may detect recurrence ^[15].

B. Radiological Investigations

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

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

Modality	Findings	Rationale
Erect CXR	Right basal consolidation → pneumonia (mimics RUQ pain); right-sided pleural effusion (complication of subphrenic/hepatic abscess); free gas under diaphragm (perforation — unlikely in cholangitis but must exclude) ^[2]	Rule out non-biliary causes of fever + RUQ pain.
AXR	Aerobilia (gas in biliary tree — seen as branching radiolucencies over the liver) → indicates communication between bowel and biliary tree (prior sphincterotomy, biliary-enteric anastomosis, cholecystoenteric fistula, gas-forming infection) ^[2]; radio-opaque gallstones (~15% visible); pancreatic calcification (chronic pancreatitis)	Aerobilia in a septic patient suggests ascending infection through a disrupted sphincter.

Detail	Explanation
Why first-line	Readily available, non-invasive, no radiation, bedside (can be done in a sick patient in the emergency department), quick ^[1]^[2].
What to look for	1. CBD dilatation ( > 8 mm, or > 10 mm post-cholecystectomy / elderly) — indicates distal obstruction. 2. Intrahepatic duct dilatation — indicates obstruction at or above the hilum. 3. CBD stone — echogenic focus with posterior acoustic shadow within the CBD. 4. Gallstones in the gallbladder — suggests choledocholithiasis as the likely cause. 5. Liver abscess — hypoechoic/anechoic collection in liver parenchyma → important differential to rule out ^[2]. 6. Gallbladder abnormalities (wall thickening, distension, pericholecystic fluid → cholecystitis).
Limitations	Distal CBD is poorly visualised due to overlying duodenal gas — CBD stones are only visible in ~33–50% of cases on USG ^[1]^[10]^[15]. Early obstruction may not yet have caused visible ductal dilatation. Operator-dependent. Body habitus (obesity) limits visualisation ^[15].

USG Is Not Perfect — Understand Its Limitations

A normal USG does not exclude cholangitis. Small CBD stones can be missed, and early obstruction may not yet have caused ductal dilatation. If clinical suspicion remains high despite a negative USG, proceed to MRCP ^[1]^[2].

Detail	Explanation
What it is	Non-contrast, T2-weighted MRI sequence that makes bile and pancreatic fluid appear bright white against dark surrounding tissue ^[15]^[16]. Essentially a non-invasive "cholangiogram" without needing to inject contrast into the ducts.
Indications	Normal or equivocal USG but high clinical suspicion for cholangitis ^[1]. Intermediate pre-test probability of CBD stone. Need to evaluate for alternative diagnoses missed on USG.
Advantages	Non-invasive, no radiation, no contrast injection into ducts (no risk of introducing infection), excellent visualisation of both intrahepatic and extrahepatic ducts, can detect stones as small as 2–3 mm ^[1]^[15]^[16].
Limitations	Does NOT permit therapeutic intervention — if you find a stone, you still need ERCP to remove it ^[1]^[4]^[16]. Can miss very small stones ( < 3 mm). Requires patient cooperation (lying still for ~15 min). Contraindicated in patients with certain metallic implants/pacemakers.
Key findings	Filling defect (dark) within a bright bile-filled duct = stone. Abrupt duct cutoff = stricture or tumour. Ductal dilatation upstream of obstruction. "Double duct sign" (both CBD and pancreatic duct dilated) → periampullary pathology (e.g., pancreatic head cancer).

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].

Detail	Explanation
Indications	Rule out liver abscess (double-target sign, rim enhancement) ^[2]^[11]. Rule out malignant biliary obstruction (pancreatic mass, cholangiocarcinoma, lymphadenopathy) ^[2]^[3]. Evaluate for RPC (central dilated bile ducts with peripheral tapering, left lobe atrophy) ^[4]. Evaluate for complications (abscess formation, perforation).
Advantages	Excellent anatomical detail, can detect mass lesions, staging of malignancy, available in emergency setting.
Limitations	Less sensitive than MRCP for detecting small CBD stones. Radiation exposure. IV contrast risks (allergy, nephrotoxicity — especially relevant if AKI from sepsis).
Key cholangitis-specific findings	Dilated CBD ± visible stone, periductal enhancement (inflamed duct walls "light up" with contrast), intrahepatic duct dilatation, ± liver abscess.

Detail	Explanation
What it is	An endoscope with an ultrasound transducer at its tip, positioned in the duodenum to image the CBD, pancreatic head, and ampulla from very close range, eliminating bowel gas interference ^[10]^[15].
Indications	Alternative to MRCP when MRCP is contraindicated (e.g., metallic implants) or when MRCP is equivocal ^[2]^[10]. High suspicion for CBD stone despite negative MRCP. Suspected periampullary/pancreatic malignancy (allows FNAC or trucut biopsy for tissue diagnosis) ^[15].
Advantages	Superior sensitivity for small CBD stones (comparable to MRCP). Can obtain tissue biopsy (FNAC). EUS-guided therapeutic interventions increasingly available (EUS-guided cholangiopancreatography as rescue when ERCP fails).
Limitations	Invasive (endoscopic procedure), requires sedation, operator-dependent, limited availability.

C. Invasive Cholangiographic Investigations (Diagnostic + Therapeutic)

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

Aspect	Detail
Procedure	Side-viewing duodenoscope is passed into the second part of the duodenum → the major duodenal papilla (ampulla of Vater) is identified → a catheter is introduced into the bile duct → contrast is injected → fluoroscopic images delineate the biliary tree.
Diagnostic role	Confirms the level and cause of obstruction (stone, stricture, tumour) ^[1]^[7]. Allows bile aspiration for culture ^[1]^[2]. Direct visualisation of the ampulla (detect periampullary tumours).
Therapeutic role	Biliary drainage and decompression — this is the primary goal in acute cholangitis ^[2]^[14]. Sphincterotomy (cutting the sphincter of Oddi to widen the opening). Stone extraction (wire baskets, stone extraction balloons, mechanical lithotripsy) ^[10]. Plastic stent placement (to maintain duct patency and drainage) ^[2]. In the acute setting, the role is biliary drainage and decompression in unstable patients, NOT necessarily stone removal — stone removal can be deferred to interval ERCP after sepsis resolves ^[2].
Technique in cholangitis	Aspirate bile duct first to remove bile and pus → decompress the biliary tree → reduce risk of inducing bacteraemia during contrast injection ^[2]. Then inject contrast and place a plastic stent.
Potential complications	Perforation, bleeding from papillotomy, pancreatitis ^[7]^[14]. Post-ERCP pancreatitis occurs in ~3–5% of cases.
Relative contraindications	Altered GI anatomy (e.g., Billroth II gastrectomy, Roux-en-Y reconstruction) — the duodenoscope cannot reach the papilla in these configurations ^[7]^[14]. Poor respiratory function (sedation risk). Coagulopathy (bleeding risk from sphincterotomy).

ERCP in Cholangitis — Critical Concept

The primary role of ERCP in acute cholangitis is BILIARY DRAINAGE AND DECOMPRESSION, not stone removal ^[2]^[14]. In an unstable septic patient, the goal is to decompress the obstructed, infected biliary system as quickly and safely as possible. Stone removal can wait until the patient is stable. Think of it as draining the abscess — you don't need to find and remove every stone in a sick patient; you need to relieve the pressure.

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].

Aspect	Detail
When used	Indicated when ERCP is unsuccessful, unavailable, or contraindicated ^[1]^[2]^[7].
Procedure	Under USG or fluoroscopic guidance, a needle is inserted percutaneously through the liver into a dilated intrahepatic bile duct (not the CBD directly) ^[2]. Position is confirmed with contrast injection. A drainage catheter is then placed over a guidewire.
Route	Left hepatic duct is preferred — accessed via a subcostal approach, which is less painful than the intercostal approach for the right duct and less likely to transgress the pleural space ^[1].
Advantages	Easy output monitoring (external drainage catheter allows measurement of bile output and assessment of adequacy of drainage) ^[2]. Can be internalised later (internal-external drainage). Similar efficacy and complication rates as ERCP ^[2]. Can access hilar and intrahepatic obstruction that ERCP cannot reach (e.g., Klatskin tumour, RPC with intrahepatic strictures) ^[4]^[15]^[16].
Limitations	More invasive than ERCP (traverses liver parenchyma). Risk of bleeding (haemobilia), biliary peritonitis, pneumothorax (right-sided approach), catheter dislodgement. Risk of fluid and electrolyte loss through external drainage ^[2]. Requires dilated ducts for safe access.
Confirmation of adequate drainage	Steady decline in serum bilirubin concentration over subsequent days ^[1].
Complications	Bacteraemia (thus antibiotic prophylaxis required), haemobilia ^[16].

Aspect	Detail
What it is	The diagnostic component of the percutaneous transhepatic approach — contrast is injected through the percutaneous needle to opacify the biliary tree ^[16].
Preferred over ERCP when	Obstruction at or above the level of confluence of hepatic ducts (e.g., Klatskin tumour, PSC, RPC) ^[16] — ERCP opacifies the ducts from below and may not visualise above a complete obstruction, whereas PTC accesses from above.
Therapeutic extension	After diagnostic PTC, the procedure can be extended to PTBD (drainage catheter), stone extraction, stricture dilatation, or stent placement across malignant strictures ^[1]^[16].

Feature	MRCP	ERCP	PTC / PTBD	EUS
Invasiveness	Non-invasive	Invasive (endoscopic)	Invasive (percutaneous)	Invasive (endoscopic)
Diagnostic	✅ Excellent	✅ Excellent	✅ Good	✅ Excellent for distal CBD
Therapeutic	❌ No	✅ Yes (1st line)	✅ Yes	✅ Emerging (EUS-guided drainage)
Sensitivity for CBD stones	~90–95%	~95%	~95%	~95%
Risks	Minimal (MRI contraindications)	Pancreatitis, perforation, bleeding	Bleeding, haemobilia, pneumothorax, bacteraemia	Sedation, perforation (rare)
Access to hilar/intrahepatic ducts	✅ Good	❌ Limited (from below)	✅ Excellent (from above)	❌ Limited
Bile culture	❌ No	✅ Yes	✅ Yes	❌ No
Preferred for	Diagnostic workup	Therapeutic drainage (1st line)	Failed ERCP / hilar obstruction	MRCP contraindicated / tissue biopsy

Finding	Modality	Significance
Dilated CBD > 8 mm	USG, CT, MRCP	Biliary obstruction
Intrahepatic duct dilatation	USG, CT, MRCP	Proximal/hilar obstruction
Filling defect in CBD	MRCP, ERCP	CBD stone
Abrupt duct cutoff	MRCP, ERCP	Stricture or tumour
Double duct sign	CT, MRCP	Simultaneous dilatation of CBD + pancreatic duct → periampullary pathology (pancreatic head cancer)
Aerobilia	AXR, CT	Gas in biliary tree — prior sphincterotomy, biliary-enteric anastomosis, gas-forming infection ^[2]
Periductal enhancement	CT with contrast	Inflamed bile duct walls in cholangitis
Double-target sign	CT with contrast	Liver abscess — rim-enhancing lesion with central hypodensity
Central duct dilatation with peripheral tapering + left lobe atrophy	CT	RPC ^[4]

High Yield Summary

Diagnostic Criteria (TG18):

Suspected: Systemic inflammation (fever OR raised WBC/CRP) + Cholestasis (jaundice OR abnormal LFT)
Definite: Suspected criteria + Imaging evidence (biliary dilatation OR etiology such as stone/stricture/stent)

Severity Grading: Grade I (mild) → antibiotics; Grade II (moderate) → early drainage 24–48h; Grade III (severe, organ dysfunction) → emergency drainage

Key bloods: CBC, LFT (cholestatic pattern: ALP ↑↑, GGT ↑↑, conjugated bilirubin ↑↑), RFT, CRP, clotting, amylase, blood culture before antibiotics

Imaging ladder: USG abdomen (1st line) → MRCP (if USG equivocal, high suspicion) → ERCP (1st line therapeutic — diagnostic + therapeutic) → PTBD (if ERCP fails/contraindicated) → Surgical ECBD (last resort)

ERCP key points: In acute cholangitis, role is biliary drainage and decompression, NOT stone removal initially. Aspirate bile first to decompress before injecting contrast. Complications include perforation, bleeding, pancreatitis. Contraindicated in altered GI anatomy (Billroth II, Roux-en-Y).

PTBD: Access via intrahepatic ducts (not CBD), left hepatic duct preferred (subcostal, less pain, avoids pleura). Similar efficacy to ERCP. Preferred for hilar/intrahepatic obstruction.

QMH escalation: ERCP → PTBD → ECBD

Active Recall - Diagnosis and Investigations of Acute Cholangitis

Management of Acute Cholangitis

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].

Intervention	Rationale	Details
Keep the patient fasting (NPO)	Bowel rest reduces cholecystokinin (CCK) release → reduces gallbladder contraction and bile flow → reduces pressure in the obstructed system. Also prepares the patient for potential ERCP/surgery ^[2]^[7]^[17].	"Keep the patient fast" ^[7].
Intravenous fluid resuscitation	Sepsis causes vasodilation + capillary leak + third-space losses → intravascular volume depletion → tissue hypoperfusion. Aggressive IV crystalloid restores circulating volume and supports organ perfusion ^[1]^[2]^[17]^[18].	Target urine output > 0.5 mL/kg/h as a marker of adequate renal perfusion.
Monitor vitals and I/O Q1h	Continuous monitoring of vitals to look for signs of failure of conservative treatment ^[1]^[2]: ↑ Temperature/Pulse; ↓ BP/Consciousness level/Urine output; increased abdominal tenderness and guarding.	These are red flags indicating deterioration — triggers for escalation to urgent drainage.
Blood cultures × 2 before antibiotics	Identify the causative organism and guide de-escalation from empirical to targeted therapy ^[2]. Must be taken before antibiotics (antibiotics sterilise blood quickly).	Aerobic + anaerobic bottles, from two different venepuncture sites.
Correct coagulopathy	Obstructive jaundice → impaired bile salt delivery to gut → reduced absorption of fat-soluble vitamin K → deficiency of clotting factors II, VII, IX, X → coagulopathy ^[1]. Must correct before any invasive procedure (ERCP, PTBD).	IV Vitamin K (phytomenadione) 10 mg slow IV. Effect takes ~6–12 hours. For urgent procedures, consider fresh frozen plasma (FFP) for immediate correction.
Analgesics	Pain control is humane and reduces sympathetic drive (which worsens tachycardia and vasoconstriction).	Paracetamol, NSAIDs (with caution if renal function impaired), opioids if needed. Avoid morphine if concurrent pancreatitis suspected (potential sphincter of Oddi spasm) ^[19].
Organ support if needed	Grade III (severe) cholangitis with organ dysfunction may require ICU admission.	Vasopressors for refractory hypotension (noradrenaline first-line in septic shock), mechanical ventilation for respiratory failure, renal replacement therapy for AKI.

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].

Pillar 2: Antibiotics (A)

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

Regimen	Components	When to Use	Rationale
IV Cefuroxime + Metronidazole	2nd-gen cephalosporin (Gram-neg cover) + nitroimidazole (anaerobic cover)	Mild-to-moderate cholangitis ^[7]	Cefuroxime covers most community-acquired Gram-negatives; metronidazole ("metro" = uterus in Greek, but the drug targets anaerobes by forming toxic free radicals in anaerobic bacteria that lack protective enzymes).
IV Augmentin (Amoxicillin-Clavulanate)	Aminopenicillin + β-lactamase inhibitor	Mild cholangitis ^[2]	Covers Gram-positives (including Enterococci), many Gram-negatives, and some anaerobes. The clavulanate inhibits bacterial β-lactamase enzymes that would otherwise destroy the amoxicillin.
IV Piperacillin-Tazobactam (Tazocin)	Extended-spectrum penicillin + β-lactamase inhibitor	Severe cholangitis ^[2]^[7]	Broader spectrum than Augmentin — covers Pseudomonas aeruginosa (critical if stent-related cholangitis), Enterococci, Gram-negatives, and anaerobes. Tazobactam inhibits a wider range of β-lactamases.
Metronidazole + 3rd-gen cephalosporin (Ceftriaxone)	As described	Alternative regimen ^[1]	Ceftriaxone provides excellent Gram-negative cover including many resistant organisms; add metronidazole for anaerobes. Note: ceftriaxone does not cover Enterococci.
Metronidazole + Fluoroquinolone (Ciprofloxacin/Levofloxacin)	As described	Alternative regimen (e.g., penicillin allergy) ^[1]	Fluoroquinolones provide Gram-negative and some Gram-positive cover. Use with caution due to increasing resistance and side effects (tendon rupture, QT prolongation).

Antibiotic Choice Summary from Lecture Slides

Lecture slide antibiotics for acute cholangitis ^[7]:

Cefuroxime
Metronidazole
Piperacillin + Tazobactam

Senior notes ^[2]:

Mild: IV Augmentin
Severe: IV Tazocin
Duration: × 7 days (adjust based on culture results and clinical response)

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].

TG18 Grade	Drainage Timing	Rationale
Grade I (Mild)	Elective/early — antibiotics first, drain when available	Most respond to antibiotics initially. However, early drainage is still recommended to prevent deterioration.
Grade II (Moderate)	Early drainage within 24–48 hours	Does not respond to initial medical treatment, or has risk factors for deterioration. Delay increases morbidity.
Grade III (Severe)	URGENT/EMERGENCY drainage	Organ dysfunction present. Urgent if Reynolds' pentad, not responding to antibiotics for 24h ^[2]. Every hour of delay increases mortality.

15% Rule

15% of patients will NOT respond to antibiotics and require emergency biliary decompression ^[1]. This is why you must continuously monitor — if the patient is not improving within 24 hours, escalate to drainage regardless of severity grade.

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.

Aspect	Detail
Role in acute cholangitis	Biliary drainage and decompression in unstable patients — NOT stone removal ^[2]. The priority is to decompress the infected system, not to clear every stone.
Technique	1. Aspirate bile duct first → removes bile and pus → decompresses biliary tree → reduces risk of inducing bacteraemia during contrast injection ^[2]. 2. Inject contrast → delineate anatomy, level and cause of obstruction. 3. Place plastic stent (temporary, requires scheduled change) to maintain duct patency and drainage ^[2]. 4. ± Sphincterotomy (cut the sphincter of Oddi with electrocautery to facilitate drainage/stone extraction).
Stone removal timing	Remove stone now OR interval ERCP after sepsis resolves ^[2]. In a sick, unstable patient, just stent and drain. Come back for definitive stone removal when the patient is stable.
Stent types	Plastic stent — for acute drainage (temporary, cheaper, requires scheduled replacement every 3 months as they occlude). Self-expanding metal stent (SEMS) — for malignant obstruction (more durable, longer patency, but more expensive and difficult to remove) ^[1]^[15].
Mortality	< 5% with endoscopic drainage ^[2] — compared to ~30% mortality with surgical exploration of CBD ^[2].
Methods of stone retrieval (when stable)	Wire baskets — literally a wire cage that captures the stone. Stone extraction balloon — inflated below the stone and pulled down to sweep it out. Mechanical lithotripsy — crushes large stones too big to extract whole ^[10].

Potential complications ^[7]^[14]	Mechanism
Perforation	Intraperitoneal perforation: duodenal wall perforated → free gas under diaphragm on CXR → requires operative treatment (will not seal spontaneously). Retroperitoneal perforation: bile duct perforated when cutting the ampulla (retroperitoneal portion of D2) → no free gas under diaphragm, but retroperitoneal gas may be present on CT → usually conservative treatment (seals spontaneously) ^[1].
Bleeding from papillotomy (sphincterotomy)	Electrocautery incision through the sphincter may transect a blood vessel at the papilla. Usually controlled endoscopically (adrenaline injection, clips, cautery).
Post-ERCP pancreatitis	Occurs in ~3–5% of ERCPs. Cannulation and contrast injection can traumatise the pancreatic duct orifice → oedema at the ampulla → obstruction of pancreatic duct → enzyme activation → pancreatitis. Prevention: pancreatic duct stent placement, rectal NSAIDs (diclofenac/indomethacin) ^[16].
Infection (flare-up sepsis)	Injecting contrast into an obstructed system can worsen bacteraemia. That's why aspirate first before injecting contrast ^[2].

Relative contraindications for ERCP ^[7]^[14]	Rationale
Altered GI anatomy — Billroth II gastrectomy, Roux-en-Y	The side-viewing duodenoscope cannot reach the papilla when the normal duodenal anatomy has been surgically altered. In Billroth II, the duodenal stump is closed; in Roux-en-Y, the efferent limb is too long for a standard scope. May require balloon-assisted enteroscopy ERCP or surgical approach.
Unstable patient (absolute)	Cannot tolerate sedation/prone position. Stabilise first, then drain. If too unstable for ERCP, consider bedside PTBD.
Uncorrected coagulopathy	Sphincterotomy carries bleeding risk. Either correct coagulopathy first, or use nasobiliary drain or direct stent placement without sphincterotomy as an alternative in patients with coagulopathy ^[1].
Contrast allergy (absolute)	Risk of anaphylaxis.

Nasobiliary Drain — The Coagulopathy Option

In patients where sphincterotomy cannot be performed (e.g., due to coagulopathy), a nasobiliary drain catheter can be placed during ERCP without cutting the sphincter. This permits active decompression of the CBD by aspiration and provides a route for irrigation of the biliary system. The catheter exits through the nose, allowing bedside monitoring of bile output ^[1].

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].

Aspect	Detail
When used	Indicated when ERCP is unsuccessful, unavailable, or contraindicated (e.g., altered GI anatomy, poor respiratory function preventing sedation/prone position) ^[1]^[2].
Procedure	Under USG/fluoroscopic guidance, a needle is inserted percutaneously through the liver into a dilated intrahepatic bile duct (NOT the CBD directly) ^[2]. Guidewire → catheter placement → external drainage.
Preferred access	Left hepatic duct — subcostal approach is less painful than intercostal route for right duct and less likely to transgress the pleural space ^[1].
Efficacy	Similar efficacy and complication rates as ERCP ^[2].
Advantages	Easy output monitoring — external drainage catheter allows direct measurement of bile output ^[2]. Can be internalised later (internal-external drainage). Can access hilar and intrahepatic obstruction that ERCP cannot reach from below (e.g., Klatskin tumour, RPC) ^[4].
Limitations	More invasive (traverses liver parenchyma). Risk of bleeding (haemobilia), pneumothorax (right-sided approach), bile leak, catheter dislodgement. Risk of fluid and electrolyte loss through external drainage ^[2].
Confirmation of adequate drainage	Steady decline in serum bilirubin over subsequent days ^[1].

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

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

Aspect	Detail
Indications ^[7]^[15]	Failure of endoscopic drainage OR Deterioration despite endoscopic drainage.
Approach	Open approach for emergency case; laparoscopic approach in selected elective cases ^[7]^[15].
Procedure	Open/laparoscopic ECBD → choledochotomy (incision into CBD) → removal of stones → placement of T-tube for post-operative drainage and subsequent cholangiogram ^[1]^[2].
Mortality	~30% in the emergency setting — significantly higher than endoscopic drainage ( < 5%) ^[2]. This is precisely why surgery is the last resort.
T-tube	A T-shaped rubber tube placed in the CBD after exploration. The horizontal limb sits inside the CBD; the vertical limb exits through the abdominal wall. Allows post-operative bile drainage + subsequent T-tube cholangiogram to check for residual stones. However, T-tubes are associated with complications (infection, bile leak, tube dislodgement) and are falling out of favour ^[10].

Surgical Treatment — Key Slide Points

Decompression by exploration of common bile duct (ECBD) ^[7]^[15]:

Indications: failure of endoscopic drainage; deterioration despite endoscopic drainage
Open approach for emergency case
Laparoscopic approach in selected elective case

This is the last step in the QMH escalation: ERCP → PTBD → ECBD ^[1].

Step	Modality	Mortality	When
1st line	ERCP +/- biliary stenting	< 5%	Standard approach for all grades
2nd line	PTBD	Similar to ERCP	ERCP fails/contraindicated
Emerging	EUS-guided biliary drainage	Data evolving	ERCP fails, expertise available
3rd line (last resort)	Surgical ECBD + T-tube	~30%	Both ERCP and PTBD fail

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.

Underlying Cause	Definitive Management	Key Points
Choledocholithiasis (gallstones)	ERCP for stone removal (lithotripsy) + Laparoscopic cholecystectomy ^[2]^[10]	Early cholecystectomy (during the same admission, rather than interval) is now preferred — reduces risk of recurrent biliary events. Stone removal at ERCP: sphincterotomy + wire basket / balloon extraction / mechanical lithotripsy ^[10]. Note: ascending cholangitis is still possible after cholecystectomy due to biliary stasis from ERCP-induced CBD dilatation or ageing-related CBD dilatation ^[2].
Stent occlusion	Stent removal and replacement ^[1]	Patients with indwelling stents and cholangitis usually require repeated imaging and stent exchange. Plastic stents occlude every ~3 months; metal stents last longer but can also occlude (sludge, tumour ingrowth/overgrowth).
Benign biliary stricture	Endoscopic stent placement / balloon dilatation ^[2]	Serial dilatation and stenting over months may be needed. If refractory, surgical biliary-enteric anastomosis (hepaticojejunostomy).
Malignant biliary obstruction (MBO)	Determined by resectability ^[1]^[3]^[17]^[18]	Establish diagnosis → Delineate level and cause of obstruction → Treat suppurative cholangitis → Definitive treatment ^[3]^[17]. Resectable: Surgical resection (e.g., Whipple operation for pancreatic head/periampullary tumour). Unresectable: Palliative stenting (metallic stent preferred for durability) or palliative surgical bypass (hepaticojejunostomy / choledochojejunostomy) ^[1].
RPC	Regular ductal clearance + surgical resection ^[2]^[4]	ERCP is difficult for intrahepatic access → PTBD, T-tube drainage, hepaticocutaneojejunostomy (HCJ) for acute drainage ^[4]. Long-term: regular USG surveillance, ERCP stone clearance/stricture dilatation. Resection of affected hepatobiliary segment + biliary-enteric anastomosis (hepaticojejunostomy) — indicated for atrophic liver segment, failed non-operative treatment, or suspected cholangiocarcinoma ^[4].
Parasitic infection	Praziquantel (for Clonorchis sinensis: 25 mg/kg PO TDS × 1 day) ^[4]	Eradicate the parasite to break the cycle of epithelial damage → stricture → stasis → stone formation.

Scenario	Acute Management	Drainage Approach	Definitive Management
Grade I cholangitis from CBD stone	NPO, IVF, IV Augmentin, monitor	Elective ERCP (sphincterotomy + stone extraction)	Early laparoscopic cholecystectomy
Grade II cholangitis from CBD stone	NPO, IVF, IV Tazocin, monitor closely	Early ERCP within 24–48h (stent ± stone extraction)	Interval stone removal if deferred + cholecystectomy
Grade III cholangitis (Reynolds' pentad)	Aggressive resuscitation, IVF, vasopressors if needed, IV Tazocin, ICU	URGENT ERCP → PTBD if fails → ECBD if both fail	Once stable: definitive treatment of cause
Cholangitis from malignant obstruction	NPO, IVF, IV antibiotics, correct coagulopathy	ERCP stenting (plastic → metal when diagnosis confirmed) OR PTBD if hilar obstruction	Staging workup → resection if operable; palliative stenting/bypass if not
Cholangitis from stent occlusion	NPO, IVF, IV Tazocin (cover Pseudomonas)	ERCP: stent removal and replacement	Evaluate for underlying cause of stent dysfunction; regular stent exchange programme
RPC with acute cholangitis	NPO, IVF, IV antibiotics	PTBD (ERCP often inadequate for intrahepatic access)	Regular ductal clearance; hepatobiliary resection + HJ if indicated

After ERCP, watch for ^[16]:

Complication	Clinical Clue	Investigation	Management
Persistent cholangitis	Ongoing fever, tachycardia post-ERCP	AXR (stent migration/blockage), bloods	Unsuccessful drainage, migrated/blocked stent, or resistant organisms → repeat ERCP or PTBD ^[16]
Flare-up sepsis	Fever spike immediately post-procedure	Blood cultures, repeat bloods	Continued antibiotics, ensure adequate drainage ^[16]
Post-ERCP pancreatitis	Epigastric pain, elevated amylase ( > 3× ULN)	Amylase/lipase, CT if severe	Supportive (NPO, IVF, analgesics)
Perforation	Abdominal pain, peritonism, surgical emphysema	CT abdomen: retroperitoneal free gas ^[16]	Intraperitoneal: surgery. Retroperitoneal: usually conservative (seals spontaneously) ^[1].
Bleeding	Haematemesis, melaena, drop in Hb	OGD	Endoscopic haemostasis (adrenaline injection, clips, cautery)

Time Frame	Complication	Mechanism
Short-term	Acute pancreatitis	Ampullary oedema → pancreatic duct obstruction → enzyme activation
	Perforation (intraperitoneal or retroperitoneal)	Electrocautery cut extends beyond the sphincter
	Bleeding	Transection of papillary vessels
	Infection	Introduction of bacteria during instrumentation
Long-term	Recurrent cholangitis	Loss of sphincter of Oddi barrier → free duodenal reflux → ascending infection, especially if biliary stasis persists
	Stone recurrence	Altered biliary dynamics post-sphincterotomy; ~5% risk of recurrent biliary events even after cholecystectomy ^[10]
	Papillary stenosis	Scarring at the sphincterotomy site → re-stenosis → obstruction

High Yield Summary

Management Framework = RAD:

R: Resuscitation — NPO, IV fluids, monitor vitals & I/O Q1h, blood cultures before antibiotics, correct coagulopathy
A: Antibiotics — Mild: IV Augmentin or Cefuroxime + Metronidazole; Severe: IV Piperacillin-Tazobactam (Tazocin) × 7 days
D: Drainage — urgency by TG18 severity:
- Grade I → antibiotics first, plan early ERCP
- Grade II → early ERCP within 24–48h
- Grade III → URGENT ERCP
Drainage escalation (QMH): ERCP → PTBD → ECBD

ERCP Key Points:

1st line for drainage; mortality < 5%
Role: biliary drainage and decompression, NOT stone removal in unstable patients
Aspirate bile first before injecting contrast
Complications: perforation, bleeding from papillotomy, pancreatitis
Contraindications: altered GI anatomy (Billroth II, Roux-en-Y), coagulopathy, contrast allergy

PTBD: 2nd line; access via intrahepatic ducts (not CBD), left hepatic duct preferred; similar efficacy to ERCP

Surgical ECBD: Last resort; indications = failure or deterioration despite endoscopic drainage; open for emergency, laparoscopic for selected elective; mortality ~30%

Definitive Management (after acute episode):

Gallstones → ERCP stone removal + early laparoscopic cholecystectomy
Stricture → endoscopic stenting/dilatation
MBO → staging → resection (Whipple) or palliative stent/bypass
Stent occlusion → stent exchange
RPC → regular ductal clearance ± hepatobiliary resection + HJ

Key principle: antibiotics alone are insufficient because antibiotic excretion is impaired in biliary obstruction → biliary drainage is mandatory

Active Recall - Management of Acute Cholangitis

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

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.

Aspect	Detail
Mechanism	Infected bile under high pressure in the intrahepatic ducts → bacteria disseminate into the surrounding hepatic parenchyma → focal collection of pus forms → pyogenic liver abscess ^[4]^[11]^[21]. This is essentially the "path of least resistance" — the infected bile breaks through the duct wall into the liver tissue.
Why right lobe is more common	The right hepatic lobe is larger and receives a greater proportion of portal blood flow, making it more susceptible to haematogenous and biliary seeding ^[11].
Clinical clue	Patient with cholangitis who develops swinging (spiking) fever despite adequate biliary drainage — fever pattern shifts from the constant high fever of cholangitis to a "picket-fence" swing pattern typical of an abscess. Tender hepatomegaly with minimal jaundice improvement ^[11].
Diagnosis	CT abdomen with contrast: double-target sign (rim-enhancing lesion with central hypodensity) ^[11]. USG: hypoechoic collection in liver parenchyma — which is why USG should always be performed in cholangitis workup to rule out co-existing abscess ^[2].
Management	IV antibiotics (prolonged course, 4–6 weeks) + image-guided percutaneous drainage (aspiration if < 5 cm, catheter placement if > 5 cm) ^[11].

Liver Abscess — Common Complication to Watch For

Liver abscess is listed as a complication of gallstone disease ^[21] and is a well-recognised sequela of cholangitis. In Hong Kong, Klebsiella pneumoniae liver abscess is particularly important in patients > 60 years old with DM — if Klebsiella is identified, urgently consult ophthalmology to rule out endophthalmitis (metastatic infection of the eye) and monitor for meningitis ^[11].

Aspect	Detail
Mechanism	If the cystic duct is simultaneously obstructed (e.g., by a stone in the cystic duct while another stone obstructs the CBD), the gallbladder becomes a closed, infected space. Stagnant bile becomes infected → pus fills the gallbladder = empyema ("em-" = in, "pyema" = pus).
Clinical clue	Tender, palpable RUQ mass + septic-looking patient. Essentially, this is severe acute cholecystitis superimposed on cholangitis.
Management	Percutaneous cholecystostomy for drainage in the acutely septic patient; definitive cholecystectomy once stable.

Aspect	Detail
Mechanism	Repeated episodes of cholangitis cause chronic inflammation → fibrosis → stricturing of the bile duct wall. Each episode of infection and healing lays down more scar tissue, narrowing the duct lumen progressively ^[4]. This is the fundamental pathology in recurrent pyogenic cholangitis (RPC) — stasis + stricturing + recurrent infection in a vicious cycle ^[4].
Consequence	Strictures perpetuate obstruction → predispose to further cholangitis episodes → more stricturing. Without definitive treatment (e.g., resection, biliary-enteric anastomosis), the cycle is self-reinforcing.
Long-term risk	Chronic inflammation from recurrent stricturing is a risk factor for cholangiocarcinoma (malignant transformation of biliary epithelium) ^[4].

Aspect	Detail
Mechanism	Chronic inflammation and high intraductal pressure can erode the bile duct wall into adjacent structures, creating abnormal communications: cholecystobiliary fistula (between gallbladder and CBD, as in Mirizzi syndrome) ^[1], or cholecystoenteric fistula (between gallbladder and bowel — can cause gallstone ileus).
Clinical significance	Fistulae allow free passage of duodenal bacteria into the biliary tree (further perpetuating infection) and can cause complications such as gallstone ileus (large stone passes through fistula into bowel and impacts at the ileocaecal valve).

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].

Aspect	Detail
Mechanism	Gram-negative bacteria (especially E. coli, Klebsiella) release endotoxin (lipopolysaccharide, LPS) into the bloodstream → activates the innate immune system → massive release of pro-inflammatory cytokines (TNF-α, IL-1, IL-6) → systemic inflammatory response syndrome (SIRS) → if uncontrolled → sepsis → septic shock ^[1]^[3].
Pathophysiology of septic shock	Distributive shock: cytokines cause systemic vasodilation (loss of vascular tone) + increased capillary permeability (fluid leaks into interstitium) + myocardial depression (cytokine-mediated) → profound hypotension refractory to fluids alone → requires vasopressors.
Clinical presentation	Reynolds' pentad — Charcot's triad (fever, RUQ pain, jaundice) + hypotension + altered mental status (confusion) ^[1]^[2]. This represents suppurative cholangitis — frank pus under pressure in the bile duct with overwhelming sepsis. Present in < 10% of patients but carries very high mortality without emergency drainage ^[1]^[2].
Recognition	Signs of shock: hypotension, oliguria, changes in mental status, cold and clammy skin, metabolic acidosis ^[1].
Why drainage is life-saving	Excretion of antibiotics is impaired in biliary obstruction ^[3] — antibiotics alone cannot sterilise the obstructed, infected system. You must remove the source (decompress the bile duct) to break the septic cycle. Biliary drainage is mandatory ^[3].

Biliary Sepsis — The Critical Complication

Septic shock from cholangitis (Grade III, TG18) is a surgical emergency. Mortality without drainage approaches 50–100%. With timely endoscopic drainage, mortality drops to < 5% ^[2]. Every hour of delay matters.

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

Organ System	Manifestation	Mechanism
Cardiovascular	Refractory hypotension, need for vasopressors	Vasodilation, myocardial depression from cytokines, capillary leak
Respiratory	Acute respiratory distress syndrome (ARDS)	Cytokine-mediated alveolar-capillary membrane damage → non-cardiogenic pulmonary oedema → severe hypoxaemia. Neutrophils activated by sepsis marginate in the pulmonary vasculature and release proteases/oxidants that damage the alveolar epithelium.
Renal	Acute kidney injury (AKI) — oliguria, rising creatinine	Renal hypoperfusion from shock + direct nephrotoxicity from endotoxins + potential nephrotoxicity from antibiotics (aminoglycosides). Also, obstructive jaundice itself predisposes to hepatorenal syndrome via bile salt-mediated renal vasoconstriction.
Hepatic	Worsening liver function (rising bilirubin, falling albumin, prolonged PT)	Direct hepatocyte injury from biliary back-pressure + sepsis-related ischaemic hepatitis ("shock liver") + pre-existing cholestasis.
Haematological	Disseminated intravascular coagulation (DIC)	Endotoxin activates the coagulation cascade → widespread microvascular thrombosis → consumption of clotting factors and platelets → paradoxical bleeding (consumption coagulopathy). Clinically: petechiae, oozing from IV sites, bleeding from mucosal surfaces. Lab: ↓ platelets, ↓ fibrinogen, ↑ D-dimer, prolonged PT/APTT.
Neurological	Altered mental status, confusion, coma	Cerebral hypoperfusion + metabolic encephalopathy (hepatic, uraemic) + direct endotoxin neurotoxicity. Part of Reynolds' pentad.

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.

Aspect	Detail
Mechanism	Endotoxin (LPS) from Gram-negative bacteria activates tissue factor on endothelial cells and monocytes → triggers the extrinsic coagulation cascade → widespread activation of thrombin → microvascular fibrin deposition → consumption of clotting factors (especially fibrinogen) and platelets → bleeding tendency. Simultaneously, fibrinolysis is activated to dissolve the microthrombi → D-dimer rises.
Clinical significance	DIC compounds the coagulopathy already present from vitamin K deficiency (biliary obstruction → impaired bile salt delivery to gut → impaired absorption of fat-soluble vitamin K → reduced synthesis of factors II, VII, IX, X). The combination makes haemorrhagic complications particularly dangerous.
Lab findings	↓ Platelets, ↓ fibrinogen, ↑↑ D-dimer, prolonged PT and APTT, fragmented red cells (schistocytes) on blood film.

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

Aspect	Detail
Mechanism	If the obstructing stone is impacted at the ampulla of Vater, it blocks both the CBD and the main pancreatic duct (of Wirsung) → pancreatic enzyme stasis → premature intrapancreatic activation of trypsinogen → autodigestion of pancreatic tissue → acute pancreatitis ^[1]^[21].
Why it's a complication of cholangitis	Cholangitis and biliary pancreatitis share the same underlying cause (impacted ampullary stone). They frequently coexist — always check amylase/lipase in cholangitis ^[2].
Clinical clue	Epigastric pain radiating straight through to the back, relieved by sitting forward. Amylase/lipase > 3× upper limit of normal.
Management	ERCP within 24–72 hours for sphincterotomy and stone extraction when cholangitis and pancreatitis coexist ^[1]^[22].

Aspect	Detail
Mechanism	Biliary obstruction → bile salts do not reach the duodenum → impaired emulsification and absorption of fats → impaired absorption of fat-soluble vitamins (A, D, E, K) → vitamin K deficiency → reduced hepatic synthesis of clotting factors II, VII, IX, X (the "vitamin K-dependent factors") → prolonged PT/INR → bleeding tendency ^[1].
Clinical significance	Must be corrected before any invasive procedure (ERCP, PTBD, surgery) — IV vitamin K takes 6–12h to take effect; for urgent procedures, give FFP for immediate correction.

Aspect	Detail
Mechanism	Chronic/recurrent biliary obstruction → bile salts don't reach the gut → impaired fat emulsification → steatorrhoea (pale, fatty, foul-smelling stools that float) + malabsorption of fat-soluble vitamins (A, D, E, K). Patients become malnourished, particularly with recurrent episodes (as in RPC).

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."

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

Complication	Incidence	Mechanism	Management
Post-ERCP pancreatitis	~2–5% (most frequent complication) ^[16]^[23]	Manipulation of the papilla → oedema at the ampulla → obstruction of pancreatic duct orifice → premature enzyme activation → pancreatitis. Injection of contrast into the pancreatic duct increases risk.	Supportive (NPO, IVF, analgesics). Prevention: rectal NSAIDs (diclofenac/indomethacin), pancreatic duct stent, guidewire cannulation before contrast injection ^[16].
Ascending infection / flare-up sepsis	~1% ^[16]	Injection of contrast into an obstructed system → increases intraductal pressure → forces more bacteria into the bloodstream → transient worsening of bacteraemia. This is why aspirate bile first before injecting contrast ^[2]. Also occurs from unsuccessful drainage, migrated/blocked stent, resistant organisms ^[16].	Ensure adequate drainage; if stent blocked/migrated → repeat ERCP or PTBD; broaden antibiotic coverage. Investigation: AXR (check stent position) ^[16].
Post-sphincterotomy bleeding	~2% ^[16]	Electrocautery incision through the sphincter transects a blood vessel at the papilla. Risk factors: intra-operative bleeding, coagulopathy, initiation of anticoagulants within 3 days, active cholangitis ^[16].	Resuscitation → localisation → endoscopic haemostasis (injection of 1:10,000 adrenaline, clip application). Prevention: correct coagulopathy, cut along the right axis within the safety zone ^[16].
Perforation	~1% ^[16]	Intraperitoneal perforation (duodenal wall): free gas under diaphragm on CXR → requires operative treatment (will not seal spontaneously) ^[1]. Retroperitoneal perforation (bile duct at ampulla — retroperitoneal portion of D2): no free gas under diaphragm; retroperitoneal free gas on CT → usually conservative treatment (seals spontaneously) ^[1]^[16].	Intraperitoneal: laparotomy + repair. Retroperitoneal: NPO, IV antibiotics, monitoring.
Papillary stenosis	Late complication	Scarring at the sphincterotomy site → fibrosis → re-stenosis of the ampulla → biliary obstruction → recurrent cholangitis.	Repeat sphincterotomy or balloon dilatation.
Stent occlusion	Expected with plastic stents (~3 months)	Sludge (bile sludge/biofilm), tumour ingrowth (through the stent mesh in metal stents), or tumour overgrowth (tumour grows over the ends of the stent) ^[15]^[21].	Stent exchange (routine for plastic stents); sweeping or re-stenting for metal stents ^[21].
Stent migration	Variable	Stent moves from its intended position → loss of drainage → recurrent obstruction and cholangitis.	Endoscopic retrieval and repositioning/replacement. Investigation: AXR to check stent position ^[16].

Complication	Mechanism	Notes
Bleeding / Haemobilia	The percutaneous needle traverses liver parenchyma → may puncture a branch of the hepatic artery or portal vein (structures that run alongside bile ducts in the portal triad) → blood enters the biliary tree (haemobilia) or peritoneal cavity ^[15]^[16].	Management: stabilise + resuscitate; clamp the PTBD catheter; perform cholangiogram via PTBD to delineate whether catheter is in artery/vein; remove catheter slowly to control bleeding — do NOT remove immediately as this may convert to free haemoperitoneum ^[15].
Bacteraemia	Manipulation of the infected biliary system → bacteria reflux into the bloodstream.	Antibiotic prophylaxis is required for PTC/PTBD ^[16].
Bile leak / biliary peritonitis	Bile leaks from the percutaneous tract into the peritoneal cavity.	Usually self-limited if catheter drains adequately; may require peritoneal drainage if peritonitis develops.
Pneumothorax	Right-sided intercostal approach → needle transgresses the pleural space.	This is why the left hepatic duct is preferred (subcostal approach) — less likely to transgress the pleural space ^[1].
Fluid and electrolyte loss	External drainage catheter diverts bile externally → loss of bile salts, water, bicarbonate, electrolytes.	Monitor I/O carefully; replace losses; consider internalising the drainage (internal-external catheter) ^[2].
Catheter dislodgement	Catheter pulled out accidentally → loss of access.	Secure the catheter properly; if dislodged, may need re-insertion.

Complication	Detail
High mortality (~30%) in emergency setting	Due to operating on a septic, unstable patient with biliary obstruction. The anaesthetic risk, surgical stress response, and compromised hepatic/renal function all contribute ^[2].
Biliary leak	From the choledochotomy site or T-tube insertion site.
T-tube complications	Infection around the tube site, bile leak on removal, tube dislodgement, retained stone in the T-tube tract ^[10].
Wound infection	Operating in a contaminated field (infected bile).
Incisional hernia	Long-term complication of laparotomy.

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

Complication	Mechanism
Secondary biliary cirrhosis	Chronic, repeated biliary obstruction → persistent cholestasis → periductal fibrosis extends into hepatic parenchyma → progressive hepatic fibrosis → cirrhosis. This is "secondary" biliary cirrhosis because the cause is known (obstruction), as opposed to "primary" biliary cholangitis (autoimmune) ^[4].
Cholangiocarcinoma	Chronic inflammation of biliary epithelium → chronic cell turnover and repair → increased risk of malignant transformation (inflammation → dysplasia → carcinoma sequence). This is analogous to how chronic ulcerative colitis predisposes to colorectal cancer, or how Barrett's oesophagus predisposes to oesophageal adenocarcinoma. RPC, PSC, liver fluke infection (Clonorchis sinensis), and choledochal cysts all carry significantly elevated risk of cholangiocarcinoma ^[4].
Recurrent cholangitis	Even after definitive treatment (e.g., cholecystectomy), ascending cholangitis can recur due to: ERCP-induced CBD dilatation (loss of normal duct calibre → stasis); ageing-related CBD dilatation; permanent loss of Sphincter of Oddi barrier after sphincterotomy ^[2].
Hepatic atrophy	Segmental or lobar atrophy from chronic obstruction of the corresponding intrahepatic duct (the affected liver segment shrinks because bile cannot drain → chronic injury → fibrosis → atrophy). Particularly common in RPC affecting the left lobe ^[4].

Category	Complication	Key Feature
Local	Liver abscess	Swinging fever, tender hepatomegaly, CT double-target sign
	Gallbladder empyema	Tender RUQ mass + septic patient
	Biliary stricture	Recurrent obstruction, vicious cycle (RPC)
	Biliary fistula	Cholecystobiliary or cholecystoenteric communication
Systemic	Biliary sepsis / septic shock	Reynolds' pentad; Grade III cholangitis
	Multi-organ failure	ARDS, AKI, DIC, hepatic failure, encephalopathy
	DIC	↓ Plt, ↓ fibrinogen, ↑ D-dimer, bleeding
Obstruction-related	Acute biliary pancreatitis	Ampullary stone; amylase > 3× ULN
	Coagulopathy	Vitamin K malabsorption → ↑ PT/INR
	Fat malabsorption	Steatorrhoea, fat-soluble vitamin deficiency
Iatrogenic (ERCP)	Post-ERCP pancreatitis	Most common ERCP complication (~2–5%)
	Perforation	Intraperitoneal (surgery) vs retroperitoneal (conservative)
	Bleeding	Post-sphincterotomy; correct coagulopathy
	Flare-up sepsis	Failed drainage, blocked stent, aspirate bile before contrast
	Stent occlusion / migration	Recurrent obstruction; AXR to check position
Iatrogenic (PTBD)	Bleeding / haemobilia	Portal triad puncture
	Pneumothorax	Right intercostal approach → use left subcostal
	Fluid/electrolyte loss	External bile drainage
Long-term	Secondary biliary cirrhosis	Chronic obstruction → hepatic fibrosis
	Cholangiocarcinoma	Chronic inflammation → malignant transformation
	Recurrent cholangitis	Post-sphincterotomy/cholecystectomy; CBD dilatation
	Hepatic atrophy	Segmental chronic obstruction (RPC, left lobe)

High Yield Summary

Complications of acute cholangitis can be remembered as LOCAL → SYSTEMIC → IATROGENIC → LONG-TERM:

Local: Liver abscess, gallbladder empyema, biliary stricture, biliary fistula.

Systemic: Biliary sepsis / septic shock (Reynolds' pentad) → multi-organ failure (ARDS, AKI, DIC, hepatic failure, encephalopathy). Mechanism: biliary pressure > 25 cm H₂O → cholangiovenous reflux → bacteraemia → SIRS → sepsis → MODS. Biliary drainage is mandatory because antibiotic excretion is impaired in obstruction.

Iatrogenic: ERCP complications = pancreatitis (most common, ~2–5%), perforation (intraperitoneal = surgery; retroperitoneal = conservative), bleeding, flare-up sepsis, stent occlusion/migration. PTBD = bleeding/haemobilia, pneumothorax, bacteraemia, fluid loss. Surgical ECBD = high mortality (~30%).

Long-term (especially in RPC): Secondary biliary cirrhosis, cholangiocarcinoma, recurrent cholangitis, hepatic atrophy.

Key principle: The most dangerous complication is septic shock with multi-organ failure — early biliary drainage is life-saving and the single most important intervention to prevent this cascade.

Active Recall - Complications of Acute Cholangitis

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)

High Yield Summary

Definition: Acute cholangitis = bacterial infection of biliary tract due to obstruction + bacterial contamination (both required).

Most common cause: Choledocholithiasis (CBD stones). In Hong Kong, also think of RPC and Clonorchis sinensis.

Normal biliary defences: Bile flow flushing, bile salt bacteriostasis, mucosal IgA, Sphincter of Oddi barrier.

Bacteriology: Gram-negative rods (E. coli, Klebsiella) most common; Enterococci; anaerobes in severe cases; Pseudomonas if stent present.

Clinical features:

Charcot's triad (50–70%): Fever + RUQ pain + Jaundice
Reynolds' pentad ( < 10%): Charcot's triad + Hypotension + Altered mental status = suppurative cholangitis = surgical emergency

Tokyo Guidelines severity:

Grade I (Mild): Responds to antibiotics
Grade II (Moderate): Does not respond / has risk factors
Grade III (Severe): Organ dysfunction → emergency drainage

Key distinguishing point: Murphy's sign is positive in cholecystitis, NOT cholangitis. Jaundice is prominent in cholangitis, often absent in cholecystitis.

High Yield Summary

Core differential of acute cholangitis (conditions sharing fever + RUQ pain ± jaundice):

Acute cholecystitis — Murphy's positive, jaundice rare, GB pathology on USG
Choledocholithiasis — jaundice without fever (no infection yet)
Liver abscess — swinging fever, tender hepatomegaly, CT double-target sign; similar presentations, must rule out on USG ^[2]
Acute biliary pancreatitis — epigastric pain radiating to back, amylase > 3× ULN
RPC — recurrent episodes, Southeast Asian, intrahepatic pigment stones, left lobe
Mirizzi syndrome — palpable GB + jaundice (exception to Courvoisier's Law)
Infected choledochal cyst — young patient, RUQ mass
Biliary leak — post-operative context
Malignant biliary obstruction — painless progressive jaundice in elderly, superimposed infection = cholangitis
Non-biliary mimics: Right basal pneumonia, acute hepatitis, inferior MI, peptic ulcer, appendicitis

High Yield Summary

Diagnostic Criteria (TG18):

Suspected: Systemic inflammation (fever OR raised WBC/CRP) + Cholestasis (jaundice OR abnormal LFT)
Definite: Suspected criteria + Imaging evidence (biliary dilatation OR etiology such as stone/stricture/stent)

Severity Grading: Grade I (mild) → antibiotics; Grade II (moderate) → early drainage 24–48h; Grade III (severe, organ dysfunction) → emergency drainage

Key bloods: CBC, LFT (cholestatic pattern: ALP ↑↑, GGT ↑↑, conjugated bilirubin ↑↑), RFT, CRP, clotting, amylase, blood culture before antibiotics

QMH escalation: ERCP → PTBD → ECBD

High Yield Summary

Management Framework = RAD:

R: Resuscitation — NPO, IV fluids, monitor vitals & I/O Q1h, blood cultures before antibiotics, correct coagulopathy
A: Antibiotics — Mild: IV Augmentin or Cefuroxime + Metronidazole; Severe: IV Piperacillin-Tazobactam (Tazocin) × 7 days
D: Drainage — urgency by TG18 severity:
- Grade I → antibiotics first, plan early ERCP
- Grade II → early ERCP within 24–48h
- Grade III → URGENT ERCP
Drainage escalation (QMH): ERCP → PTBD → ECBD

ERCP Key Points:

1st line for drainage; mortality < 5%
Role: biliary drainage and decompression, NOT stone removal in unstable patients
Aspirate bile first before injecting contrast
Complications: perforation, bleeding from papillotomy, pancreatitis
Contraindications: altered GI anatomy (Billroth II, Roux-en-Y), coagulopathy, contrast allergy

PTBD: 2nd line; access via intrahepatic ducts (not CBD), left hepatic duct preferred; similar efficacy to ERCP

Surgical ECBD: Last resort; indications = failure or deterioration despite endoscopic drainage; open for emergency, laparoscopic for selected elective; mortality ~30%

Definitive Management (after acute episode):

Gallstones → ERCP stone removal + early laparoscopic cholecystectomy
Stricture → endoscopic stenting/dilatation
MBO → staging → resection (Whipple) or palliative stent/bypass
Stent occlusion → stent exchange
RPC → regular ductal clearance ± hepatobiliary resection + HJ

Key principle: antibiotics alone are insufficient because antibiotic excretion is impaired in biliary obstruction → biliary drainage is mandatory

High Yield Summary

Complications of acute cholangitis can be remembered as LOCAL → SYSTEMIC → IATROGENIC → LONG-TERM:

Local: Liver abscess, gallbladder empyema, biliary stricture, biliary fistula.

Long-term (especially in RPC): Secondary biliary cirrhosis, cholangiocarcinoma, recurrent cholangitis, hepatic atrophy.

Acute Cholangitis

1. Definition

2. Epidemiology

2.1 Global Epidemiology

2.2 Hong Kong Context

3. Relevant Anatomy and Function of the Biliary System

3.1 Anatomy of the Biliary Tree

3.2 Normal Biliary Defence Mechanisms

4. Etiology (Causes of Biliary Obstruction)

4.1 Causes — Tabulated by Frequency

4.2 Focus on Hong Kong-Specific Etiologies

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

4.2.2 Clonorchis sinensis Infection

5. Pathophysiology

5.1 The Two-Hit Model

5.2 Step-by-Step Pathophysiology

5.3 Bacteriology

5.4 Disrupted Barrier Mechanisms

6. Classification

6.1 Anatomical Classification

6.2 Pathological Classification

6.3 Tokyo Guidelines (TG18/TG24) Severity Grading

6.4 Other Classifications

7. Clinical Features

7.1 Symptoms

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]

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

8. Summary of Pathophysiology → Clinical Feature Connections

Active Recall - Acute Cholangitis (Definition to Clinical Features)

References

Differential Diagnosis of Acute Cholangitis

Framing the Problem

Approach to the Differential

Detailed Differential Diagnosis

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

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

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

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

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

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

7. Infected Choledochal Cyst [7][8]

8. Biliary Leak [1][7]

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

10. Non-Biliary Mimics

Summary Table — Quick Differentiation

Systematic Approach to Narrowing the Differential

Active Recall - Differential Diagnosis of Acute Cholangitis

References

Diagnostic Criteria

The Tokyo Guidelines (TG18) — The Standard Framework

TG18 Diagnostic Criteria for Acute Cholangitis

Severity Grading (TG18) — Determines Urgency of Drainage

Diagnostic Algorithm

Investigation Modalities — Detailed Breakdown

Overview: What We Need to Know and Why

A. Laboratory Investigations

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

A2. Liver Function Tests (LFT)

A3. Inflammatory Markers

A4. Clotting Profile (PT/INR)

A5. Renal Function Tests (RFT)

A6. Serum Amylase and Lipase

A7. Blood Culture — The Most Important Microbiological Investigation

A8. Bile Culture

A9. Urinalysis

A10. Other Blood Tests

B. Radiological Investigations

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

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

B3. Magnetic Resonance Cholangiopancreatography (MRCP)

B4. CT Abdomen (with IV contrast)

B5. Endoscopic Ultrasound (EUS)

C. Invasive Cholangiographic Investigations (Diagnostic + Therapeutic)

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

C2. Percutaneous Transhepatic Biliary Drainage (PTBD)