Pyogenic liver abscess pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Development of pyogenic liver abscess is the result of [[infection]] through the following routes like [[portal vein]] (also from [[pylephlebitis]] of [[portal vein]]), [[hepatic artery|hepatic arteries]] as [[abscess|metastatic abscesses]], direct spread from nearby [[infection]], [[trauma]] and [[retroperitoneal]] extension from [[appendix]].<ref name="pmid17861705">{{cite journal| author=Munro JC| title=VII. Lymphatic and Hepatic Infections Secondary to Appendicitis. | journal=Ann Surg | year= 1905 | volume= 42 | issue= 5 | pages= 692-734 | pmid=17861705 | doi= | pmc=1425980 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17861705 }} </ref><ref name="pmid8651751">{{cite journal| author=Huang CJ, Pitt HA, Lipsett PA, Osterman FA, Lillemoe KD, Cameron JL et al.| title=Pyogenic hepatic abscess. Changing trends over 42 years. | journal=Ann Surg | year= 1996 | volume= 223 | issue= 5 | pages= 600-7; discussion 607-9 | pmid=8651751 | doi= | pmc=1235191 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8651751 }} </ref><ref name="pmid15578367">{{cite journal| author=Rahimian J, Wilson T, Oram V, Holzman RS| title=Pyogenic liver abscess: recent trends in etiology and mortality. | journal=Clin Infect Dis | year= 2004 | volume= 39 | issue= 11 | pages= 1654-9 | pmid=15578367 | doi=10.1086/425616 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15578367 }} </ref><ref name="pmid10462653">{{cite journal| author=Lam YH, Wong SK, Lee DW, Lau JY, Chan AC, Yiu RY et al.| title=ERCP and pyogenic liver abscess. | journal=Gastrointest Endosc | year= 1999 | volume= 50 | issue= 3 | pages= 340-4 | pmid=10462653 | doi=10.1053/ge.1999.v50.98065 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10462653 }} </ref>Ascending [[biliary tract|biliary]] [[infection]] is the most common source of pyogenic liver abscess. | |||
==Pathophysiology== | |||
*Development of pyogenic liver abscess is the result of extension of [[infection]] through the following:<ref name="pmid17861705">{{cite journal| author=Munro JC| title=VII. Lymphatic and Hepatic Infections Secondary to Appendicitis. | journal=Ann Surg | year= 1905 | volume= 42 | issue= 5 | pages= 692-734 | pmid=17861705 | doi= | pmc=1425980 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17861705 }} </ref><ref name="pmid8651751">{{cite journal| author=Huang CJ, Pitt HA, Lipsett PA, Osterman FA, Lillemoe KD, Cameron JL et al.| title=Pyogenic hepatic abscess. Changing trends over 42 years. | journal=Ann Surg | year= 1996 | volume= 223 | issue= 5 | pages= 600-7; discussion 607-9 | pmid=8651751 | doi= | pmc=1235191 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8651751 }} </ref><ref name="pmid15578367">{{cite journal| author=Rahimian J, Wilson T, Oram V, Holzman RS| title=Pyogenic liver abscess: recent trends in etiology and mortality. | journal=Clin Infect Dis | year= 2004 | volume= 39 | issue= 11 | pages= 1654-9 | pmid=15578367 | doi=10.1086/425616 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15578367 }} </ref><ref name="pmid10462653">{{cite journal| author=Lam YH, Wong SK, Lee DW, Lau JY, Chan AC, Yiu RY et al.| title=ERCP and pyogenic liver abscess. | journal=Gastrointest Endosc | year= 1999 | volume= 50 | issue= 3 | pages= 340-4 | pmid=10462653 | doi=10.1053/ge.1999.v50.98065 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10462653 }} </ref> | |||
:*[[Portal vein]] (also from [[pylephlebitis]] of [[portal vein]]) | |||
:*[[Hepatic artery|Hepatic arteries]] as [[metastasis|metastatic]] [[abscesses]] | |||
:*Direct spread from nearby [[infection]] | |||
:*[[Trauma]] | |||
:*[[Retroperitoneal]] extension from [[appendix]] ([[appendicitis|suppurative appendicitis]] most frequent source of [[infection]]) | |||
*Ascending [[biliary tract|biliary]] [[infection]] is the most common source of pyogenic liver abscess. | |||
*Right lobe of [[liver]] is most commonly involved due to its greater blood supply than [[Caudate lobe of liver|caudate]] and [[Left lobe of liver|left lobes]]. | |||
*[[Bacteria]] involved in pyogenic liver abscess include: | |||
{{familytree/start}} | |||
{{familytree | | | | | | | | | | | | A01 | | | | A01='''Pyogenic liver abscess'''}} | |||
{{familytree | | | | | | | | | | | | |!| | | | |}} | |||
{{familytree | | | | | | | | | | | | B01 | | | | B01='''Bacteria'''}} | |||
{{familytree | | | |,|-|-|-|-|-|v|-|-|^|-|-|v|-|-|-|-|-|.|}} | |||
{{familytree | | | C01 | | | | C02 | | | | C03 | | | | C04 |C01=[[Gram-positive]] [[aerobes]]|C02=[[Gram-negative]] enterics|C03=[[Anaerobic]] organisms|C04=[[Acid fast|Acid fast bacilli]]}} | |||
{{familytree | | | |!| | | | | |!| | | | | |!| | | | | |!|}} | |||
{{familytree | | | D01 | | | | D02 | | | | D03 | | | | D04 | D01=[[Streptococcus|Streptococcus sp]] <br> ''[[Staphylococcus aureus]]'' / ''[[Staphylococcus epidermidis]]'' <br> ''[[Actinomyces|Actinomyces sp]] <br>[[Enterococcus|Enterococcus sp]] <br> ''[[Streptococcus milleri]]''|D02=''[[Escherichia coli]]'' <br> ''[[Salmonella typhi]]'' <br> ''[[Yersinia enterocolitica]]'' <br> ''[[Klebsiella|K.pneumonia]]'' <br> [[Pseudomonas|Pseudomonas sp]] <br> [[Proteus|Proteus sp]] <br> ''[[Eikenella corrodens]]'' <br> Others|D03=[[Bacteroides|Bacteroids sp]] <br> [[Fusobacterium]] <br> [[Anaerobic]]/ [[Microaerophilic]] [[streptococci]] <br> Other [[anaerobes]]|D04=''[[Mycobacterium tuberculosis]]''}} | |||
{{familytree/end}} | |||
==Pathogenesis== | |||
* In healthy patients the [[reticuloendothelial system|reticuloendothelial cells]] ([[kupffer cells]]) of [[liver]] control the transient portal [[bacteremia]] but in elderly and [[immunocompromised]] the [[bacteria]] can overwhelm the [[kupffer cells]] and lead to an [[abscess]].<ref name="pmid1863218">{{cite journal| author=Stain SC, Yellin AE, Donovan AJ, Brien HW| title=Pyogenic liver abscess. Modern treatment. | journal=Arch Surg | year= 1991 | volume= 126 | issue= 8 | pages= 991-6 | pmid=1863218 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1863218 }} </ref> | |||
==Gross Pathology== | |||
*Single or multiple cavities, filled with fowl smelling, creamy yellow [[necrosis|necrotic]] material, usually in [[right lobe of liver]]. | |||
*The [[abscess]] may have [[fibrous capsule]] which is a centimeter or more thick and gradually merges into the [[parenchyma|liver parenchyma]]. | |||
== | ==Microscopic Pathology== | ||
* | *Multiple [[neutrophil|neutrophilic]] [[abscesses]] with areas of [[necrosis]] are seen in the [[parenchyma|liver parencyma]].<ref name=abscess>https://librepathology.org/wiki/Liver_pathology Accessed on February 22, 2017</ref><ref name="pmid11882760">{{cite journal| author=Lublin M, Bartlett DL, Danforth DN, Kauffman H, Gallin JI, Malech HL et al.| title=Hepatic abscess in patients with chronic granulomatous disease. | journal=Ann Surg | year= 2002 | volume= 235 | issue= 3 | pages= 383-91 | pmid=11882760 | doi= | pmc=1422444 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11882760 }} </ref> | ||
*[[Suppuration]], [[liquefaction]] with presence of fibrino-purulent debris, and [[fibrosis]] are seen depending on stage. | |||
*The edges of the cavities are composed of a [[chronic]] [[inflammation|inflammatory]] infiltrate consisting of [[lymphocytes]], [[macrophages|epithelioid macrophages]], [[eosinophils]], and [[neutrophils]]. | |||
*Adjacent [[hepatocytes]] appear reactive. | |||
* | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
[[Category:Emergency mdicine]] | |||
[[Category:Disease]] | |||
[[Category:Up-To-Date]] | |||
[[Category:Infectious disease]] | |||
[[Category:Gastroenterology]] | |||
[[Category:Hepatology]] | |||
Latest revision as of 23:55, 29 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]
Overview
Development of pyogenic liver abscess is the result of infection through the following routes like portal vein (also from pylephlebitis of portal vein), hepatic arteries as metastatic abscesses, direct spread from nearby infection, trauma and retroperitoneal extension from appendix.[1][2][3][4]Ascending biliary infection is the most common source of pyogenic liver abscess.
Pathophysiology
- Development of pyogenic liver abscess is the result of extension of infection through the following:[1][2][3][4]
- Portal vein (also from pylephlebitis of portal vein)
- Hepatic arteries as metastatic abscesses
- Direct spread from nearby infection
- Trauma
- Retroperitoneal extension from appendix (suppurative appendicitis most frequent source of infection)
- Ascending biliary infection is the most common source of pyogenic liver abscess.
- Right lobe of liver is most commonly involved due to its greater blood supply than caudate and left lobes.
- Bacteria involved in pyogenic liver abscess include:
Pathogenesis
- In healthy patients the reticuloendothelial cells (kupffer cells) of liver control the transient portal bacteremia but in elderly and immunocompromised the bacteria can overwhelm the kupffer cells and lead to an abscess.[5]
Gross Pathology
- Single or multiple cavities, filled with fowl smelling, creamy yellow necrotic material, usually in right lobe of liver.
- The abscess may have fibrous capsule which is a centimeter or more thick and gradually merges into the liver parenchyma.
Microscopic Pathology
- Multiple neutrophilic abscesses with areas of necrosis are seen in the liver parencyma.[6][7]
- Suppuration, liquefaction with presence of fibrino-purulent debris, and fibrosis are seen depending on stage.
- The edges of the cavities are composed of a chronic inflammatory infiltrate consisting of lymphocytes, epithelioid macrophages, eosinophils, and neutrophils.
- Adjacent hepatocytes appear reactive.
References
- ↑ 1.0 1.1 Munro JC (1905). "VII. Lymphatic and Hepatic Infections Secondary to Appendicitis". Ann Surg. 42 (5): 692–734. PMC 1425980. PMID 17861705.
- ↑ 2.0 2.1 Huang CJ, Pitt HA, Lipsett PA, Osterman FA, Lillemoe KD, Cameron JL; et al. (1996). "Pyogenic hepatic abscess. Changing trends over 42 years". Ann Surg. 223 (5): 600–7, discussion 607-9. PMC 1235191. PMID 8651751.
- ↑ 3.0 3.1 Rahimian J, Wilson T, Oram V, Holzman RS (2004). "Pyogenic liver abscess: recent trends in etiology and mortality". Clin Infect Dis. 39 (11): 1654–9. doi:10.1086/425616. PMID 15578367.
- ↑ 4.0 4.1 Lam YH, Wong SK, Lee DW, Lau JY, Chan AC, Yiu RY; et al. (1999). "ERCP and pyogenic liver abscess". Gastrointest Endosc. 50 (3): 340–4. doi:10.1053/ge.1999.v50.98065. PMID 10462653.
- ↑ Stain SC, Yellin AE, Donovan AJ, Brien HW (1991). "Pyogenic liver abscess. Modern treatment". Arch Surg. 126 (8): 991–6. PMID 1863218.
- ↑ https://librepathology.org/wiki/Liver_pathology Accessed on February 22, 2017
- ↑ Lublin M, Bartlett DL, Danforth DN, Kauffman H, Gallin JI, Malech HL; et al. (2002). "Hepatic abscess in patients with chronic granulomatous disease". Ann Surg. 235 (3): 383–91. PMC 1422444. PMID 11882760.