Difference between revisions of "Liver"

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[[File:Steatosis severity at histopathology.jpg|thumb|center|400px|Steatosis grading: a: none. b: mild. c: moderate. d: severe.]]
 
[[File:Steatosis severity at histopathology.jpg|thumb|center|400px|Steatosis grading: a: none. b: mild. c: moderate. d: severe.]]
 
*Signs of '''acute liver failure'''. ''Further information in section below.''
 
*Signs of '''acute liver failure'''. ''Further information in section below.''
 +
*Signs of '''malignancy'''. If a tumor is found: {{Further|Liver tumor|linebreak=no}}
 
*Signs of '''congestive hepatopathy''' (indicating heart failure). ''Further information in section below.''
 
*Signs of '''congestive hepatopathy''' (indicating heart failure). ''Further information in section below.''
 
If a tumor is found: {{Further|Liver tumor|linebreak=no}}
 
  
 
===Acute liver failure===
 
===Acute liver failure===
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*'''Acute hepatic congestion''' shows dilated sinusoidal capillaries predominantly in zone 3 of the hepatic acinus.<ref>{{cite web|url=http://www.pathwaymedicine.org/acute-hepatic-congestion|title=Acute Hepatic Congestion|website=Pathway Medicine|accessdate=2020-03-06}}</ref>
 
*'''Acute hepatic congestion''' shows dilated sinusoidal capillaries predominantly in zone 3 of the hepatic acinus.<ref>{{cite web|url=http://www.pathwaymedicine.org/acute-hepatic-congestion|title=Acute Hepatic Congestion|website=Pathway Medicine|accessdate=2020-03-06}}</ref>
 
*Typical findings of '''chronic hepatic congestion''' are atrophy of hepatocytes in zone 3, perisinusoidal edema, thrombosis and hemorrhage. Chronic congestion typically displays perivenous and perisinusoidal fibrosis, with fibrous septa that bridge central hepatic veins. In contrast, other causes of distortion and cirrhosis typically have fibrous septa predominantly between portal triads. However, nonalcoholic steatohepatitis also may show perisinusoidal fibrosis in early stages; in later stages, the fibrosis tends to be in the portal triad. Cirrhosis develops in the final stages of congestive hepatopathy. Regenerating hepatocytes tend to grow in a sleevelike pattern along portal tracts, resulting in a nodular liver with preserved portal triads and obliterated or fibrosed hepatic veins, a pattern called "reverse lobulation". This pattern can also be seen in venous obstruction due to Budd-Chiari syndrome.<ref name="WellsFenstad2016">{{cite journal|last1=Wells|first1=Michael L.|last2=Fenstad|first2=Eric R.|last3=Poterucha|first3=Joseph T.|last4=Hough|first4=David M.|last5=Young|first5=Phillip M.|last6=Araoz|first6=Philip A.|last7=Ehman|first7=Richard L.|last8=Venkatesh|first8=Sudhakar K.|title=Imaging Findings of Congestive Hepatopathy|journal=RadioGraphics|volume=36|issue=4|year=2016|pages=1024–1037|issn=0271-5333|doi=10.1148/rg.2016150207}}</ref>
 
*Typical findings of '''chronic hepatic congestion''' are atrophy of hepatocytes in zone 3, perisinusoidal edema, thrombosis and hemorrhage. Chronic congestion typically displays perivenous and perisinusoidal fibrosis, with fibrous septa that bridge central hepatic veins. In contrast, other causes of distortion and cirrhosis typically have fibrous septa predominantly between portal triads. However, nonalcoholic steatohepatitis also may show perisinusoidal fibrosis in early stages; in later stages, the fibrosis tends to be in the portal triad. Cirrhosis develops in the final stages of congestive hepatopathy. Regenerating hepatocytes tend to grow in a sleevelike pattern along portal tracts, resulting in a nodular liver with preserved portal triads and obliterated or fibrosed hepatic veins, a pattern called "reverse lobulation". This pattern can also be seen in venous obstruction due to Budd-Chiari syndrome.<ref name="WellsFenstad2016">{{cite journal|last1=Wells|first1=Michael L.|last2=Fenstad|first2=Eric R.|last3=Poterucha|first3=Joseph T.|last4=Hough|first4=David M.|last5=Young|first5=Phillip M.|last6=Araoz|first6=Philip A.|last7=Ehman|first7=Richard L.|last8=Venkatesh|first8=Sudhakar K.|title=Imaging Findings of Congestive Hepatopathy|journal=RadioGraphics|volume=36|issue=4|year=2016|pages=1024–1037|issn=0271-5333|doi=10.1148/rg.2016150207}}</ref>
 +
 +
===Report===
 +
*Even absence of signs of hepatitis or malignancy
 +
*At least if the patient had alcohol abuse, a quantification of cirrhosis.
 +
*Optionally, even absence of congestive hepatopathy and/or steatosis.
  
 
{{Bottom}}
 
{{Bottom}}

Revision as of 07:47, 6 March 2020

Author: Mikael Häggström [note 1]

Tissue sampling

Fixation

Generally 10% neutral buffered formalin. Non–formalin-fixed tissue may be needed for tests such as microbiological analysis or copper quantification studies.[1]

Gross processing in autopsy

Make consecutive liver slices, such as in the sagittal or coronal plane.

Basic gross examination

  • Inspect the color and texture of the surfaces, including external and cut surfaces. Potential pathologies:
  • Look for any focal change in the liver volume, mainly any tumor. If found: Further information: Liver tumor
  • Determine liver weight.

Gross report

  • Weight
  • Color and texture of cut surfaces
  • Any focal change

Microscopic evaluation in autopsy

Pathologies can be topographically classified by liver zones. P: portal tract. V: central vein.

A minimal screening of autopsy specimens include:

  • A severity grading of previously known liver diseases.
  • Commonly, this includes to quantify any cirrhosis, at least if the patient had alcohol abuse.

Further information: Cirrhosis

  • Steatosis is also common:
Steatosis grading: a: none. b: mild. c: moderate. d: severe.
  • Signs of acute liver failure. Further information in section below.
  • Signs of malignancy. If a tumor is found: Further information: Liver tumor
  • Signs of congestive hepatopathy (indicating heart failure). Further information in section below.

Acute liver failure

Acute liver failure has multiple etiologies, and hence various presentations. Regardless of etiology, the initial hepatic insult that leads to acute liver failure is “hepatitis” in the broadest sense, with extensive hepatocyte injury and necrosis. The initiating process may damage the liver by zonal necrosis (with a centrilobular or acinar zones 3 necrosis indicating mainly acetaminophen hepatotoxicity), or it may damage the liver by a diffuse hepatitis with necrosis and inflammation as exemplified by acute viral hepatitis A, B, or E infections or other drug hepatotoxicities.[2]

Congestive hepatopathy

Histopathology of congestive hepatopathy, with sinusoidal dilation in zone 3. As the severity of the lesion increases, the sinusoids around the central vein become distended with extravasated red cells and there is adjacent hepatocyte plate atrophy.[4]
  • Acute hepatic congestion shows dilated sinusoidal capillaries predominantly in zone 3 of the hepatic acinus.[5]
  • Typical findings of chronic hepatic congestion are atrophy of hepatocytes in zone 3, perisinusoidal edema, thrombosis and hemorrhage. Chronic congestion typically displays perivenous and perisinusoidal fibrosis, with fibrous septa that bridge central hepatic veins. In contrast, other causes of distortion and cirrhosis typically have fibrous septa predominantly between portal triads. However, nonalcoholic steatohepatitis also may show perisinusoidal fibrosis in early stages; in later stages, the fibrosis tends to be in the portal triad. Cirrhosis develops in the final stages of congestive hepatopathy. Regenerating hepatocytes tend to grow in a sleevelike pattern along portal tracts, resulting in a nodular liver with preserved portal triads and obliterated or fibrosed hepatic veins, a pattern called "reverse lobulation". This pattern can also be seen in venous obstruction due to Budd-Chiari syndrome.[6]

Report

  • Even absence of signs of hepatitis or malignancy
  • At least if the patient had alcohol abuse, a quantification of cirrhosis.
  • Optionally, even absence of congestive hepatopathy and/or steatosis.

Notes

  1. For a full list of contributors, see article history. Creators of images are attributed at the image description pages, seen by clicking on the images. See Patholines:Authorship for details.

Main page

References

  1. 1.0 1.1 1.2 1.3 Boyd, Alexander; Cain, Owen; Chauhan, Abhishek; Webb, Gwilym James (2020). "Medical liver biopsy: background, indications, procedure and histopathology ". Frontline Gastroenterology 11 (1): 40–47. doi:10.1136/flgastro-2018-101139. ISSN 2041-4137. 
    • "This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license"
  2. Lefkowitch, Jay H. (2016). "The Pathology of Acute Liver Failure ". Advances In Anatomic Pathology 23 (3): 144–158. doi:10.1097/PAP.0000000000000112. ISSN 1072-4109. 
  3. Xue, Ran; Zhu, Yueke; Liu, Hui; Meng, Qinghua (2019). "The clinical parameters for the diagnosis of hepatitis B virus related acute-on-chronic liver failure with sepsis ". Scientific Reports 9 (1). doi:10.1038/s41598-019-38866-3. ISSN 2045-2322. 
    -"This article is licensed under a Creative Commons Attribution 4.0 International License"
  4. Shah, Shailja C.; Sass, David A. (2015). "“Cardiac Hepatopathy”: A Review of Liver Dysfunction in Heart Failure ". Liver Research - Open Journal 1 (1): 1–10. doi:10.17140/LROJ-1-101. ISSN 23794038. 
    -"This is an open access article distributed under the Creative Commons Attribution 4.0 International License (CC BY 4.0),"
  5. . Acute Hepatic Congestion. Pathway Medicine. Retrieved on 2020-03-06.
  6. Wells, Michael L.; Fenstad, Eric R.; Poterucha, Joseph T.; Hough, David M.; Young, Phillip M.; Araoz, Philip A.; Ehman, Richard L.; Venkatesh, Sudhakar K. (2016). "Imaging Findings of Congestive Hepatopathy ". RadioGraphics 36 (4): 1024–1037. doi:10.1148/rg.2016150207. ISSN 0271-5333. 

Image sources