Acute cholangitis
Updates to Article Attributes
Acute cholangitis, or ascending cholangitis, is a form of cholangitis and refers to acute bacterial infection of the biliary tree secondary to bile duct obstruction. It is a condition with high mortality that necessitates emergent biliary decompression.
Clinical presentation
The classical presentation is the Charcot triad of fever, right upper quadrant abdominal pain, and jaundice, which is only seen in ~40% of patients. Patients can also present with Reynolds pentad, which is the Charcot triad (fever, pain and jaundice) plus shock and delirium (and/or lethargy) 1-3.
Pathology
Gram-negative enteric bacteria, most commonly Escherichia coli, are the primary pathogens 3.
Acute cholangitis is seen in the setting of biliary tree obstruction 1,2:
choledocholithiasis
(~80causing obstruction of the common bile duct by calculi in 80%)of cases.malignancymalignant disease (~20%)biliary tree procedures or instrumentation, e.g. ERCP
Complications include sepsis, hepatic abscesses, portal vein thrombosis and biliary peritonitis.
Radiographic features
Acute cholangitis is typically a clinical diagnosis with imaging performed to determine if there is evidence of 1,3:
intrahepatic and/or extrahepatic duct dilatation (indicating obstruction/stasis)
bile duct wall thickening or focal outpouchings
Ultrasound
A hallmark finding of ascending cholangitis on ultrasound is thickening of the walls of the bile ducts in the appropriate clinical setting 4. Ultrasound may also show biliary dilatation with calculi, with or without pus, which appears as debris material within the common bile duct. In the setting of acute cholangitis, sensitivity to detect choledocholithiasis is reduced 5,6.
CT
Inhomogeneous liver enhancement on arterial-phase CT. This is a non-specific sign and should be interpreted in the correct clinical context 2,7.
Treatment and prognosis
Treatment involves appropriate antibiotic therapy and biliary tree decompression (usually either via ERCP or PTC). Mortality rates are between 50-90% for severe acute cholangitis 8,9.
Various factors suggestive of poor prognosis include 5,10-12:
high fever >39°C
organ dysfunction
advanced age >75 years
malignancy as aetiology
medical comorbidities
hyperbilirubinaemia ≥2.2 mg/dL
reduced platelet count <150 × 109/L
hypoalbuminaemia <3.0 mg/dL
prolonged prothrombin time >1.5 s
leucocytosis >20,000/mm3
bacteraemia
endotoxemia
elevated serum creatinine
elevated urea/BUN
dilated common bile duct (≥11 mm diameter)
Complications
sepsis, and
biliary peritonitis.
History and etymology
Jean-Martin Charcot (1825-1893) was trained as a pathologist, but he was also a skilled practicing physician, and for many the "father of neurology", who also made important contributions to psychiatry. He also has the distinction of probably having more medical eponyms named after him than any other individual in history 13,14.
-<p><strong>Acute</strong> <strong>cholangitis</strong>, or <strong>ascending cholangitis</strong>, is a form of <a href="/articles/cholangitis">cholangitis</a> and refers to acute bacterial infection of the <a href="/articles/biliary-tree-anatomy">biliary tree</a>. It is a condition with high mortality that necessitates emergent biliary decompression. </p><h4>Clinical presentation</h4><p>The classical presentation is the <a href="/articles/charcot-triad">Charcot triad</a> of <a href="/articles/pyrexia">fever</a>, right upper quadrant abdominal pain, and <a href="/articles/jaundice">jaundice</a>, which is only seen in ~40% of patients. Patients can also present with <a href="/articles/reynolds-pentad-1" title="Reynolds pentad">Reynolds pentad</a>, which is the Charcot triad plus <a href="/articles/shock">shock</a> and <a href="/articles/delirium">delirium</a> (and/or lethargy) <sup>1-3</sup>. </p><h4>Pathology</h4><p>Gram-negative enteric bacteria, most commonly <em>Escherichia coli</em>, are the primary pathogens <sup>3</sup>. </p><p>Acute cholangitis is seen in the setting of biliary tree obstruction <sup>1,2</sup>:</p><ul>-<li><p><a href="/articles/choledocholithiasis">choledocholithiasis</a> (~80%)</p></li>-<li><p>malignancy (~20%)</p></li>-<li><p><a href="/articles/primary-sclerosing-cholangitis">sclerosing cholangitis</a></p></li>-<li><p>biliary tree procedures, e.g. <a href="/articles/endoscopic-retrograde-cholangiopancreatography">ERCP</a></p></li>-</ul><h4>Radiographic features</h4><p>Acute cholangitis is typically a clinical diagnosis with imaging performed to determine if there is evidence of <sup>1,3</sup>:</p><ul>-<li><p><a href="/articles/bile-duct-dilatation" title="Bile duct dilatation">intrahepatic and/or extrahepatic duct dilatation</a> (indicating obstruction/stasis)</p></li>-<li><p><a href="/articles/bile-duct-wall-thickening-differential">bile duct wall thickening</a> or focal outpouchings</p></li>-<li><p><a href="/articles/gallstones-1">cholelithiasis</a>/<a href="/articles/choledocholithiasis">choledocholithiasis</a></p></li>-</ul><h5>Ultrasound</h5><p>A hallmark finding of ascending cholangitis on ultrasound is thickening of the walls of the bile ducts in the appropriate clinical setting <sup>4</sup>. Ultrasound may also show biliary dilatation with calculi, with or without pus, which appears as debris material within the common bile duct. In the setting of acute cholangitis, sensitivity to detect choledocholithiasis is reduced <sup>5,6</sup>. </p><h5>CT </h5><p>Inhomogeneous liver enhancement on arterial-phase CT. This is a non-specific sign and should be interpreted in the correct clinical context <sup>2,7</sup>.</p><h4>Treatment and prognosis</h4><p>Treatment involves appropriate antibiotic therapy and <a href="/articles/biliary-tree-decompression">biliary tree decompression</a> (usually either via <a href="/articles/endoscopic-retrograde-cholangiopancreatography">ERCP</a> or <a href="/articles/percutaneous-transhepatic-cholangiography">PTC</a>). Mortality rates are between 50-90% for severe acute cholangitis <sup>8,9</sup>.</p><p>Various factors suggestive of poor prognosis include<sup> 5,10-12</sup>:</p><ul>-<li><p><a href="/articles/pyrexia">high fever</a> >39°C</p></li>-<li><p><a href="/articles/shock">shock</a></p></li>-<li><p>organ dysfunction</p></li>-<li><p>advanced age >75 years</p></li>-<li><p><a href="/articles/delirium">mental confusion</a></p></li>-<li><p>malignancy as aetiology</p></li>-<li><p>medical comorbidities</p></li>-<li><p>hyperbilirubinaemia ≥2.2 mg/dL</p></li>-<li><p>reduced platelet count <150 × 10<sup>9</sup>/L</p></li>-<li><p>hypoalbuminaemia <3.0 mg/dL</p></li>-<li><p>prolonged prothrombin time >1.5 s</p></li>-<li><p>leucocytosis >20,000/mm<sup>3</sup></p></li>-<li><p>bacteraemia</p></li>-<li><p>endotoxemia</p></li>-<li><p>elevated serum creatinine</p></li>-<li><p>elevated urea/BUN</p></li>-<li><p><a href="/articles/bile-duct-dilatation">dilated common bile duct</a> (≥11 mm diameter)</p></li>-<li><p><a href="/articles/choledocholithiasis">bile duct stones</a></p></li>-<li><p><a href="/articles/hepatic-abscess-1">liver abscesses</a></p></li>-</ul><h5>Complications</h5><ul>-<li><p><a href="/articles/hepatic-abscess-1">hepatic abscess</a></p></li>-<li><p><a href="/articles/portal-vein-thrombosis">portal vein thrombosis</a></p></li>- +<p><strong>Acute</strong> <strong>cholangitis</strong>, or <strong>ascending cholangitis</strong>, is a form of <a href="/articles/cholangitis">cholangitis</a> and refers to acute bacterial infection of the <a href="/articles/biliary-tree-anatomy">biliary tree</a> secondary to bile duct obstruction. It is a condition with high mortality that necessitates emergent biliary decompression. </p><h4>Clinical presentation</h4><p>The classical presentation is the <a href="/articles/charcot-triad">Charcot triad</a> of <a href="/articles/pyrexia">fever</a>, right upper quadrant abdominal pain, and <a href="/articles/jaundice">jaundice</a>, which is only seen in ~40% of patients. Patients can also present with <a href="/articles/reynolds-pentad-1" title="Reynolds pentad">Reynolds pentad</a>, which is the <strong>Charcot triad (fever, pain and jaundice) </strong>plus <a href="/articles/shock">shock</a> and <a href="/articles/delirium">delirium</a> (and/or lethargy) <sup>1-3</sup>. </p><h4>Pathology</h4><p>Gram-negative enteric bacteria, most commonly <em>Escherichia coli</em>, are the primary pathogens <sup>3</sup>. </p><p>Acute cholangitis is seen in the setting of biliary tree obstruction <sup>1,2</sup>:</p><ul>
- +<li><p><a href="/articles/choledocholithiasis">choledocholithiasis</a> causing obstruction of the common bile duct by calculi in 80% of cases.</p></li>
- +<li><p>malignant disease (~20%)</p></li>
- +<li><p><a href="/articles/primary-sclerosing-cholangitis">sclerosing cholangitis</a></p></li>
- +<li><p>biliary tree procedures or instrumentation, e.g. <a href="/articles/endoscopic-retrograde-cholangiopancreatography">ERCP</a></p></li>
- +</ul><p>Complications include sepsis, hepatic abscesses, portal vein thrombosis and biliary peritonitis.</p><h4>Radiographic features</h4><p>Acute cholangitis is typically a clinical diagnosis with imaging performed to determine if there is evidence of <sup>1,3</sup>:</p><ul>
- +<li><p><a href="/articles/bile-duct-dilatation" title="Bile duct dilatation">intrahepatic and/or extrahepatic duct dilatation</a> (indicating obstruction/stasis)</p></li>
- +<li><p><a href="/articles/bile-duct-wall-thickening-differential">bile duct wall thickening</a> or focal outpouchings</p></li>
- +<li><p><a href="/articles/gallstones-1">cholelithiasis</a>/<a href="/articles/choledocholithiasis">choledocholithiasis</a></p></li>
- +</ul><h5>Ultrasound</h5><p>A hallmark finding of ascending cholangitis on ultrasound is thickening of the walls of the bile ducts in the appropriate clinical setting <sup>4</sup>. Ultrasound may also show biliary dilatation with calculi, with or without pus, which appears as debris material within the common bile duct. In the setting of acute cholangitis, sensitivity to detect choledocholithiasis is reduced <sup>5,6</sup>. </p><h5>CT </h5><p>Inhomogeneous liver enhancement on arterial-phase CT. This is a non-specific sign and should be interpreted in the correct clinical context <sup>2,7</sup>.</p><h4>Treatment and prognosis</h4><p>Treatment involves appropriate antibiotic therapy and <a href="/articles/biliary-tree-decompression">biliary tree decompression</a> (usually either via <a href="/articles/endoscopic-retrograde-cholangiopancreatography">ERCP</a> or <a href="/articles/percutaneous-transhepatic-cholangiography">PTC</a>). Mortality rates are between 50-90% for severe acute cholangitis <sup>8,9</sup>.</p><p>Various factors suggestive of poor prognosis include<sup> 5,10-12</sup>:</p><ul>
- +<li><p><a href="/articles/pyrexia">high fever</a> >39°C</p></li>
- +<li><p><a href="/articles/shock">shock</a></p></li>
- +<li><p>organ dysfunction</p></li>
- +<li><p>advanced age >75 years</p></li>
- +<li><p><a href="/articles/delirium">mental confusion</a></p></li>
- +<li><p>malignancy as aetiology</p></li>
- +<li><p>medical comorbidities</p></li>
- +<li><p>hyperbilirubinaemia ≥2.2 mg/dL</p></li>
- +<li><p>reduced platelet count <150 × 10<sup>9</sup>/L</p></li>
- +<li><p>hypoalbuminaemia <3.0 mg/dL</p></li>
- +<li><p>prolonged prothrombin time >1.5 s</p></li>
- +<li><p>leucocytosis >20,000/mm<sup>3</sup></p></li>
- +<li><p>bacteraemia</p></li>
- +<li><p>endotoxemia</p></li>
- +<li><p>elevated serum creatinine</p></li>
- +<li><p>elevated urea/BUN</p></li>
- +<li><p><a href="/articles/bile-duct-dilatation">dilated common bile duct</a> (≥11 mm diameter)</p></li>
- +<li><p><a href="/articles/choledocholithiasis">bile duct stones</a></p></li>
- +<li><p><a href="/articles/hepatic-abscess-1">liver abscesses</a></p></li>
- +</ul><h5>Complications</h5><ul>
- +<li><p><a href="/articles/hepatic-abscess-1">hepatic abscess</a></p></li>
- +<li><p><a href="/articles/portal-vein-thrombosis">portal vein thrombosis</a></p></li>
- +<li><p>sepsis, and </p></li>
- +<li><p>biliary peritonitis.</p></li>
Tags changed:
- acute ascending cholangitis