Acute inflammation and infection within the bile duct, usually in association with biliary tree obstruction.
Discusses manifestations and management of cholangitis.
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Increases with age
Peaks 50-60y
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Physiology Notes
Normal sterility of the biliary tract maintained by several factors:
- intact SOO; prevents reflux of duodenal contents.
- unimpeded efflux of bile
- immunoglobulin A in bile
- bacteriostatic properties of bile salts
Cholangitis can ensue when these factors breached / diminished; or if FB present in the duct.

Congenital duct lesions

Infection, often following FB / stone impaction.
- most common bugs: E coli, then Klebsiella and Enterobacter.
- contribution of anaerobes (bacteroides, clostridium) more common if older / instrumented and should be covered.
Strictures & causes
- pancreatic Ca
- cholangioca
- porta hepatis tumours / mets
Blocked endobiliary stent 2nd most common cause.
Biliary instrumentation
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In our referral base, stones usually originate in GB; cf in SEA, where stones often originate in duct.
Infection often occurs after nidus sets up in duct (eg. stone).
- (access is from direct ascent of bacteria from duodenum into the bile duct).
- haematogenous seeding via portal vein path likely to play a much more minor role.
Duct wall ischaemia can contribute in choledocholithiasis.
Leads to localised pain as inflammation spreads transmurally.
Bacteria multiply

E. coli

Presence of foreign bodies (e.g. stents) can provide a niche for bacteria including E. Coli.
Of special interest because it secretes Beta-glucuronidase.
- this deconjugates bilirubin glucuronide
--> results in poorly soluble unconjugated bilirubin that precipitates in bile, adding to the foreign body load and leading to brown pigment microstones.


Systemic sepsis
Repeated bouts of cholangitis may lead to strictures
--> and ultimately liver parenchymal destruction & fibrosis (i.e. 2ndary biliary cirrhosis).
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As for choledocholithiasis / cholecystitis.
Major systemic upset common.

Charcot's triad; pain, jaundice, fever
- only present in 50% or so
- but jaundice quite common at 90%
- fever and abdo pain less prevalent 66%
Beware absence of pain in the elderly

'Reynolds pentad'
= ridiculous eponymous nonsense
- means also hypotension and mental status derangement.
--> suggestive of cholangitis with severe sepsis.
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The 'Tokyo guidelines' bring an evidence-based approach to definition, diagnosis and management.
Diagnosis can be 'suspected' or 'definite' based on testing criteria.
Then perform a severity grading.

Tokyo Guidelines Diagnostic Criteria
A. Clinical hx and manifestations
- hx of biliary disease
- fever /chills
- juandice
- abdo pain
B. Lab data
- inflammatory response (WCC / CRP)
- abnormal LFTs (ALP, GGT, ALT, AST)
C. Imaging Findings
- biliary dilatation or evidence of etiology (stricture, stone, stent)
Suspected = Two or more in A
Definite = Charcot's triad or 2 or more in A plus B and C.

Tokyo Guidelines Severity Criteria
Responds to initial medical therapy
Doesn't respond to initial medical treatment
Not assoc. with organ dysfunction
Onset of dysfunction in one or more of:
- cardiovascular: requiring dopamine >5ug/kg/min or any dobutamine
- nervous: disturbance of consciousness
- resp: PaO2/FiO2 ratio <300
- renal: creat >2.0 mg/dL
- liver: INR>1.5
- haem: platelets < 100,000


LFTs - esp GGT and ALP.
Raised bilirubin.
Amylase elevated mildly in 30%

Routine blood cultures


First investigation.
Non-invasive, rapid, cost effective and highly sensitive.
Bright echo with acoustic shadowing if stones found.
Ducts may be dilated.
- normal = <4mm + 1mm every decade >40y
False negative in ~5% of examinations.

Generally follows USS
Allows direct chonagiography and therapeutic intervention.
- check coags first
- ensure consent re post op pancreatitis obtained.

If ERCP not possible.

Allows abdo assessment but insensitive for CBD stones.
MRCP much better for ducts but prolonged duration means unsuitable if unstable.
- prefer ERCP for cholangitis

Radioisotope Scans
Eg with HIDA, DIDA - extracted from the blood and rapidly excreted into the biliary tree.
Good for identifying cystic duct obstruction, and assessing gallbladder function if given with CCK.
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Acute management
1. Resuscitation
Attend to ABCs, may be shocked.
2. Antibiotics

Broad spectrum
- commonly triples
- alternatively tazocin if wanting to avoid gentamicin-induced nephrotoxicity.
- not ceftriaxone alone due to poor activity against enterococcus species.
3. Coagulopathy
Correct with Vitamin K

85%+ will respond to resuscitation and empiric antibiotic therapy.
- duration based on response.
As per Tokyo
-  moderate not responding; e.g. continuing pain or leukocytosis
- severe shows organ failure usually requiring ICU
Effective in 90-98%.
- bile aspirated from CBD then decompressed before contrast cholangiography
- else can set off bacteraemia
Sphincterotomy contraindicated in coagulopathy
- stent the duct as a temporary measure.

More invasive; in those failing ERCP or lacking access
- e.g. if reconstructed.

Surgical Drainage
Has fallen out of favour due to poorer outcomes with more invasive procedures.
Mainly of historical interest.
- wen needed, usually involves a choledochotomy, placement of 16Fr+ T-tube in bile duct.
Delay definitive tehrapy until a later date.
May play a role in Mirizzi, cholelithiasis, benign and malignant biliary strictures.

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