Acute cholangitis is a bacterial biliary tract infection developing in the setting of bile duct obstruction. Charcot's triad (fever, jaundice, right upper quadrant pain) is the classic clinical presentation. In severe cases, Reynolds' pentad (triad + hypotension + confusion) indicates septic shock and multi-organ failure. The most common cause is choledocholithiasis (28-70%); other causes include benign/malignant stricture, stent occlusion, and PSC. Emergency biliary decompression (ERCP) is life-saving. Treatment is planned according to Tokyo Guidelines (TG18) severity grading.
Age Range
35-85
Peak Age
60
Gender
Equal
Prevalence
Common
Acute cholangitis pathogenesis results from the combination of two fundamental conditions: (1) biliary obstruction and (2) bacterial contamination. Under normal conditions, bile is sterile and the sphincter of Oddi prevents retrograde passage of duodenal bacteria. Obstruction (stone, stricture, tumor) disrupts bile flow increasing intraductal pressure — normal pressure of 7-14 cmH2O rises to >25 cmH2O. This elevated pressure causes cholangiovenous and cholangiolymphatic reflux allowing bacteria to enter systemic circulation (bacteremia → sepsis). Most common pathogens are E. coli, Klebsiella, Enterococcus. Imaging reflects obstructive biliary dilatation + duct wall enhancement (inflammatory hyperemia) + periportal edema. Wall enhancement results from increased capillary permeability and inflammatory neovascularization. In severe cases, intraluminal purulent material (pyobilia) may appear as high-density bile.
Prominent wall enhancement of dilated bile ducts (>1.5 mm thick smooth concentric hyperdense ring) + obstructive cause (stone/stricture) + periportal edema/tracking. This triple pattern is highly suggestive of acute cholangitis. Together with Charcot's triad, it confirms the clinical diagnosis.
Prominent enhancement of dilated bile duct wall on portal venous phase — smooth concentric wall thickening and enhancement. Wall thickness >1.5 mm. Both intra and extrahepatic ducts may be involved. Obstructive cause (hyperdense stone, stricture, mass) is usually identifiable on the same study. Periportal hypodensity (edema) and perihepatic fluid may accompany.
Report Sentence
Prominent wall enhancement of dilated bile ducts is noted; consistent with acute cholangitis in the clinical context.
Segmental or wedge-shaped transient hepatic attenuation differences (THAD) in liver parenchyma on arterial phase — reflecting portal venous flow changes due to cholangitis. Periportal inflammation disrupts portal flow creating arterioportal shunts. These transient arterial enhancement differences must be distinguished from abscess or metastasis — disappearance on delayed phase favors THAD.
Report Sentence
Transient segmental enhancement differences (THAD) in liver parenchyma on arterial phase reflecting portal flow changes related to cholangitis.
Hyperintense halo in periportal area on T2-weighted images — reflecting inflammatory edema and lymphatic congestion. Also called 'periportal tracking'. Dilated bile ducts are markedly hyperintense on T2. Intraluminal debris/pus may create heterogeneous appearance with lower T2 signal. Perihepatic and pericholecystic fluid may accompany.
Report Sentence
Periportal edema (hyperintense periportal halo) and dilated bile ducts are seen on T2-weighted series; consistent with acute cholangitis.
Dilated bile ducts (intrahepatic >2 mm, CBD >6 mm) with echogenic debris/sludge/stones on US. Duct wall thickened and echogenic (>1.5 mm). Stones and/or wall thickening in gallbladder (cholecystitis association) are frequently seen. Perihepatic fluid may accompany. Hyperechoic filling defect in CBD (stone) shows obstructive cause.
Report Sentence
Echogenic debris within dilated bile ducts is noted; consistent with acute cholangitis in the clinical context.
Multiple small (<2 cm) foci showing diffusion restriction in liver parenchyma on DWI — hepatic microabscesses developing as complication of cholangitis. Bright signal at high b-value (b=800-1000), low value on ADC map. Abscesses typically located around dilated bile ducts in periportal distribution. Must be investigated in treatment-refractory cholangitis.
Report Sentence
Multiple small foci showing diffusion restriction in periportal distribution in liver parenchyma on DWI; consistent with hepatic microabscesses as cholangitis complication.
Hyperdense stone within CBD lumen on non-contrast CT (obstructive cause). Stone usually located in distal CBD (at ampullary level). Proximal bile duct dilatation accompanies. Non-contrast CT has 72-87% sensitivity for bile stone detection (cholesterol stones may be isodense). Stones may also be seen in intrahepatic bile ducts.
Report Sentence
Hyperdense obstructive stone in distal CBD lumen with proximal biliary dilatation; consistent with choledocholithiasis as cholangitis etiology.
Criteria
Cholangitis responding to antibiotic therapy without organ dysfunction. Mild biliary dilatation and minimal wall enhancement on imaging. Elective biliary drainage can be planned.
Distinct Features
Minimal biliary dilatation, mild wall enhancement, minimal or no periportal edema, no abscess.
Criteria
Cholangitis not responding to initial antibiotic therapy but without organ dysfunction. WBC >12000 or <4000, fever >39°C, age >75. Biliary drainage required within 24 hours. Prominent dilatation and wall enhancement on imaging.
Distinct Features
Prominent biliary dilatation, prominent wall enhancement, periportal edema, perihepatic fluid may be present.
Criteria
Cholangitis with organ dysfunction — hypotension (vasopressor requirement), altered consciousness, renal failure, hepatic failure, coagulopathy, thrombocytopenia. Reynolds' pentad (triad + shock + confusion). EMERGENCY biliary drainage + intensive care.
Distinct Features
Prominent dilatation, pyobilia (high-density intraluminal material), hepatic abscesses, THAD, widespread periportal edema, peritoneal fluid, septic changes.
Distinguishing Feature
Choledocholithiasis shows obstruction + dilatation but without wall enhancement and periportal edema, cholangitis has not developed. In acute cholangitis, wall enhancement + periportal edema + clinical findings (fever, jaundice) are added.
Distinguishing Feature
Cholangiocarcinoma shows irregular mass/thickening of duct wall + DWI restriction, acute inflammatory findings (periportal edema, THAD) are not prominent. In acute cholangitis, wall enhancement is smooth concentric and inflammatory findings predominate.
Distinguishing Feature
PSC has chronic multifocal strictures + dilatations (beaded appearance). Acute cholangitis may develop on PSC background but the acute episode is distinguished by wall enhancement and clinical findings.
Distinguishing Feature
Recurrent pyogenic cholangitis (Oriental cholangitis) shows chronic, recurrent episodes with predominant intrahepatic stones and segmental atrophy/hypertrophy pattern. Acute cholangitis usually presents as single episode with extrahepatic obstruction.
Urgency
emergentManagement
interventionalBiopsy
Not NeededFollow-up
specialist-referralAcute cholangitis is a life-threatening condition requiring emergency biliary decompression. According to Tokyo Guidelines (TG18) severity grading: Grade I — antibiotics + elective ERCP, Grade II — urgent ERCP (within 24 hours) + antibiotics, Grade III — EMERGENCY ERCP (<12 hours) + intensive care + broad-spectrum IV antibiotics. If ERCP fails, percutaneous transhepatic biliary drainage (PTBD) is performed. Definitive treatment of obstructive cause (stone extraction, stent, surgery) is planned after stabilization. Mortality without treatment 50-100%; with early drainage 2-10%.
Acute cholangitis is a serious infection requiring urgent treatment. Reynolds pentad (Charcot triad + shock + confusion) indicates severe cholangitis. Antibiotic therapy and urgent biliary drainage (ERCP or percutaneous) are required. Untreated, it can result in sepsis and organ failure.