Cholangitis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2], Farwa Haideri [3]

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Overview

Cholangitis involves two main factors: an increased bacterial presence and elevated intraductal pressure in the bile duct, both of which allow for translocation of bacteria or endotoxins in the vascular system. Bacterial contamination alone does not usually result in cholangitis. Increased pressure in the biliary system, from obstruction in the bile duct, widens the spaces between the cells lining the duct, which brings bacterially contaminated bile into the bloodstream.

Pathophysiology

By BruceBlaus Source- https://commons.wikimedia.org/wiki/File:Gallstones.png[1]

The onset of cholangitis involves two factors: increased bacteria in the bile duct and elevated intraductal pressure in the bile duct that allows translocation of bacteria or endotoxins into the vascular system. Because of its anatomical characteristics, the biliary system is likely to be affected by elevated intraductal pressure. With the elevated intraductal biliary pressure, the bile ductules tend to become more permeable to bacteria and toxins. This can result in serious;even fatal infections, such as hepatic abscesses and sepsis.[2] Functional changes in sinusoidal lining cells are also common.[3][2]

Pathogenesis

Bile, which is produced by the liver, serves to eliminate cholesterol and bilirubin from the body, as well as to emulsify fats to make them more soluble in water and aid in their digestion. It is formed in the liver by hepatocytes and excreted into the common hepatic duct. Some bile is stored in the gallbladder and can be released at time of digestion. All bile reaches the duodenum through the common bile duct and the ampulla of Vater.[4]

The biliary tree is usually relatively free of bacteria because of certain protective mechanisms:

  • The sphincter of Oddi acts as a mechanical barrier.
  • The biliary system normally has low pressure and allows bile to flow freely through. This flushes bacteria, if present, into the duodenum, and does not allow for the establishment of an infection.[4]

Increased pressure within the biliary system resulting from obstruction in the bile duct widens spaces between the cells lining the duct, bringing bacterially contaminated bile in contact with the bloodstream. Increased biliary pressure decreases production of immunoglobulins (e.g., IgA) in the bile. This results in bacteremia and gives rise to the systemic inflammatory response syndrome (SIRS), which is comprised of fever (often with rigors), tachycardia, increased respiratory rate, and increased white blood cell count.[5][6][2]

Bacterial contamination alone, in absence of obstruction, does not usually result in cholangitis.

Gross Pathology

Duodenoscopy image of ampulla of Vater with pus extruding from it, indicative of cholangitis.[7]
  • On gross pathology following are characteristic findings of cholangitis[8]:
    • Thickening of bile ducts
    • Bile stasis (cholestasis) as shown by greenish discoloration of parenchyma
    • Abscesses or pus in bile duct, as seen in the picture (seen more commonly in acute suppurative cholangits)
    • Erosions or ulcers in the bile duct

Microscopic Pathology

On microscopic histopathological analysis, following features are characteristic findings of acute cholangitis[9]:

  • Acute cholangitis in a patient with multiple bile duct procedures. After the biopsy, removal of bile duct stones released pus.[10]
  • Patient with sepsis and acute cholangitis.[10]

References

  1. , CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=56630024
  2. 2.0 2.1 2.2 Kimura Y, Takada T, Kawarada Y, Nimura Y, Hirata K, Sekimoto M, Yoshida M, Mayumi T, Wada K, Miura F, Yasuda H, Yamashita Y, Nagino M, Hirota M, Tanaka A, Tsuyuguchi T, Strasberg SM, Gadacz TR (2007). "Definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis: Tokyo Guidelines". J Hepatobiliary Pancreat Surg. 14 (1): 15–26. doi:10.1007/s00534-006-1152-y. PMC 2784509. PMID 17252293.
  3. Kawada, N., Takemura, Y., Minamiyama M. (1996). "Pathophysiology of acute obstructive cholangitis". Journal of Hepato-Biliary-Pancreatic Surgery. 3 (1): 4–8. doi:10.1007/BF01212771.
  4. 4.0 4.1 Kinney TP (2007). "Management of ascending cholangitis". Gastrointest. Endosc. Clin. N. Am. 17 (2): 289–306, vi. doi:10.1016/j.giec.2007.03.006. PMID 17556149.
  5. Sung JY, Costerton JW, Shaffer EA (1992). "Defense system in the biliary tract against bacterial infection". Dig. Dis. Sci. 37 (5): 689–96. PMID 1563308.
  6. Navaneethan U, Jayanthi V, Mohan P (2011). "Pathogenesis of cholangitis in obstructive jaundice-revisited". Minerva Gastroenterol Dietol. 57 (1): 97–104. PMID 21372774.
  7. https://commons.wikimedia.org/wiki/Category:Ascending_cholangitis#/media/File:Cholangitis.jpg
  8. Fyfe, Billie (2016). Diagnostic pathology. Philadelphia, PA: Amirsys/Elsevier. ISBN 978-0323376761.
  9. Fyfe, Billie (2016). Diagnostic pathology. Philadelphia, PA: Amirsys/Elsevier. ISBN 978-0323376761.
  10. 10.0 10.1 "Medical liver disease - Libre Pathology".


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