Difference between revisions of "Liver"

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{{Comprehensiveness}}
 
==Tissue sampling==
 
==Tissue sampling==
 
*'''[[Autopsy]]'''
 
*'''[[Autopsy]]'''
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===Basic gross examination===
 
===Basic gross examination===
*Inspect the color and texture of the surfaces, including external and cut surfaces. Potential pathologies:
+
*'''Inspect''' the color and texture of the surfaces, including external and cut surfaces. Potential pathologies:
<gallery mode=packed>
+
<gallery mode=packed heights=190>
 
File:Gross pathology of alcoholic liver cirrhosis.jpg|Diffuse areas of pallor in cirrhosis, see '''[[Cirrhosis]]'''
 
File:Gross pathology of alcoholic liver cirrhosis.jpg|Diffuse areas of pallor in cirrhosis, see '''[[Cirrhosis]]'''
 
File:Wątroba marska (Ultima Thule).jpg|Pale macronodules of cirrhosis, see '''[[Cirrhosis]]'''
 
File:Wątroba marska (Ultima Thule).jpg|Pale macronodules of cirrhosis, see '''[[Cirrhosis]]'''
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File:Human liver with metastatic lesions from primary pancreas carcinoma (2).jpg|Liver metastases
 
File:Human liver with metastatic lesions from primary pancreas carcinoma (2).jpg|Liver metastases
 
</gallery>
 
</gallery>
*Look for any focal change in the liver volume, mainly any tumor.
+
*Look for any '''focal change''' in the liver volume, mainly any tumor. If found: {{Further|Liver tumor|linebreak=no}}
*Determine liver weight.
+
*Determine liver '''weight'''. The standard reference range for men is 970–1,860 g (2.14–4.10 lb)<ref name="MolinaDiMaio2012">{{cite journal|last1=Molina|first1=D. Kimberley|last2=DiMaio|first2=Vincent J.M.|title=Normal Organ Weights in Men|journal=The American Journal of Forensic Medicine and Pathology|volume=33|issue=4|year=2012|pages=368–372|issn=0195-7910|doi=10.1097/PAF.0b013e31823d29ad|pmid=22182984|s2cid=32174574}}</ref> and for women 600–1,770 g (1.32–3.90 lb).<ref name="MolinaDiMaio2015">{{cite journal|last1=Molina|first1=D. Kimberley|last2=DiMaio|first2=Vincent J. M.|title=Normal Organ Weights in Women|journal=The American Journal of Forensic Medicine and Pathology|volume=36|issue=3|year=2015|pages=182–187|issn=0195-7910|doi=10.1097/PAF.0000000000000175|pmid=26108038|s2cid=25319215}}</ref>
  
 
===Gross report===
 
===Gross report===
*Weight
+
*'''Weight'''. If abnormally low or high, preferably include the reference range.
*Color and texture of cut surfaces
+
*'''Color and texture''' of cut surfaces
*Any focal change
+
*Any '''focal change'''
  
 
==Microscopic evaluation in autopsy==
 
==Microscopic evaluation in autopsy==
 
[[File:Histopathology of liver zones.jpg|thumb|Pathologies can be topographically classified by liver zones. P: portal tract. V: central vein.]]
 
[[File:Histopathology of liver zones.jpg|thumb|Pathologies can be topographically classified by liver zones. P: portal tract. V: central vein.]]
[[File:Cirrhosis of the liver (trichrome stain) (5690946257).jpg|thumb|Trichrome stain, showing cirrhosis as a nodular texture surrounded by fibrosis (wherein collagen is stained blue).]]
 
 
A minimal screening of autopsy specimens include:
 
A minimal screening of autopsy specimens include:
*A severity grading of previously known liver diseases. Quantify any cirrhosis, at least if the patient had alcohol abuse. ''Further information: '''[[Cirrhosis]]'''
+
*A severity grading of '''previously known liver diseases'''.  
*Signs of acute liver failure.
+
:*Commonly, this includes to quantify any '''cirrhosis''', at least if the patient had alcohol abuse.  
*Signs of congestive hepatopathy (indicating heart failure).
+
<gallery mode=packed heights=170>
 +
File:Histopathology of steatohepatitis with mild fibrosis in the form of fibrous expansion (van Gieson).jpg|Steatohepatitis with '''mild fibrosis''' (van Gieson's stain).<ref name="BoydCain2020"/>
 +
File:Histopathology of steatohepatitis with moderate fibrosis, with thin fibrous bridges (van Gieson).jpg|Histopathology of steatohepatitis with '''moderate fibrosis''' (van Gieson's stain).<ref name="BoydCain2020"/>
 +
</gallery>
 +
{{Further|Cirrhosis}}
 +
:*'''Steatosis''' is also common, (see 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 '''inflammation''' at least around the portal triads.
 +
 
 +
===Steatosis===
 +
At least classify steatosis by severity:
 +
[[File:Steatosis severity at histopathology.jpg|thumb|center|400px|Steatosis grading: a: none. b: mild. c: moderate. d: severe.]]
 +
 
 +
<gallery mode=packed heights=190>
 +
File:Histopathology of microvesicular steatosis.jpg|Note the presence of '''microvesicular''' steatosis, as it is usually more harmful. It shows foamy hepatocytes (two annotated by arrows), as opposed to the more common macrovesicular steatosis (insert).
 +
File:Histopathology of centrilobular steatosis of the liver.jpg|Note any particular pattern of the steatosis, mainly '''centrilobular''' (pictured) or periportal.
 +
</gallery>
  
 
===Acute liver failure===
 
===Acute liver failure===
body formation (arrow) and bilirubinostasis (H&E stain)<ref name="BoydCain2020"/>]]
+
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.<ref name="Lefkowitch2016">{{cite journal|last1=Lefkowitch|first1=Jay H.|title=The Pathology of Acute Liver Failure|journal=Advances In Anatomic Pathology|volume=23|issue=3|year=2016|pages=144–158|issn=1072-4109|doi=10.1097/PAP.0000000000000112}}</ref>
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 being typical of 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.<ref name="Lefkowitch2016">{{cite journal|last1=Lefkowitch|first1=Jay H.|title=The Pathology of Acute Liver Failure|journal=Advances In Anatomic Pathology|volume=23|issue=3|year=2016|pages=144–158|issn=1072-4109|doi=10.1097/PAP.0000000000000112}}</ref>
 
 
<gallery mode=packed heights=200>>
 
<gallery mode=packed heights=200>>
File:Histopathology of acute hepatitis.jpg|Histopathology of acute hepatitis with lobular disarray and associated lymphocytic inflammation, acidophil  
+
File:Histopathology of acute hepatitis.jpg|Histopathology of '''acute hepatitis''' with lobular disarray and associated lymphocytic inflammation, acidophil acidophil body formation (arrow) and bilirubinostasis.<ref name="BoydCain2020"/>
 +
File:Histopathology of centrilobular hepatic necrosis of shock liver (intermediate magnification).jpg|'''Shock liver''', showing its hallmark<ref name="pmid29868133">{{cite journal| author=Ciobanu AO, Gherasim L| title=Ischemic Hepatitis - Intercorrelated Pathology. | journal=Maedica (Bucur) | year= 2018 | volume= 13 | issue= 1 | pages= 5-11 | pmid=29868133 | doi= | pmc=5972787 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29868133  }}</ref> pathologic finding centrilobular necrosis but viable periportal hepatocytes. The necrotic hepatocytes are seen as slightly more eosinophilic (red) and discohesive.
 +
File:Histopathology of massive hepatic necrosis in hepatitis B.jpg|'''Massive hepatic necrosis''': Liver cell dropout, residual hepatocytes and intact portal tract pattern.<ref>{{cite journal|last1=Xue|first1=Ran|last2=Zhu|first2=Yueke|last3=Liu|first3=Hui|last4=Meng|first4=Qinghua|title=The clinical parameters for the diagnosis of hepatitis B virus related acute-on-chronic liver failure with sepsis|journal=Scientific Reports|volume=9|issue=1|year=2019|issn=2045-2322|doi=10.1038/s41598-019-38866-3}}<br>-"This article is licensed under a Creative Commons Attribution 4.0 International License"</ref>
 
</gallery>
 
</gallery>
 +
 
===Congestive hepatopathy===
 
===Congestive hepatopathy===
<gallery mode=packed heights=200>
+
[[File:Histopathology of congestive hepatopathy.jpg|thumb|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.<ref name=Shah2015>{{cite journal|last1=Shah|first1=Shailja C.|last2=Sass|first2=David A.|title=“Cardiac Hepatopathy”: A Review of Liver Dysfunction in Heart Failure|journal=Liver Research - Open Journal|volume=1|issue=1|year=2015|pages=1–10|issn=23794038|doi=10.17140/LROJ-1-101}}<br>-"This is an open access article distributed under the Creative Commons Attribution 4.0 International License (CC BY 4.0),"</ref>]]
File:Histopathology of congestive hepatopathy.jpg|Histopathology of congestive hepatopathy, with sinusoidal dilation in zone 3. As the severityof the lesion increases, the sinusoids around the central vein become distended with extravasated red cells and there is adjacent hepatocyte plate atrophy.<ref>{{cite journal|last1=Shah|first1=Shailja C.|last2=Sass|first2=David A.|title=“Cardiac Hepatopathy”: A Review of Liver Dysfunction in Heart Failure|journal=Liver Research - Open Journal|volume=1|issue=1|year=2015|pages=1–10|issn=23794038|doi=10.17140/LROJ-1-101}}<br>-"This is an open access article distributed under the Creative Commons Attribution 4.0 International License (CC BY 4.0),"</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>
 +
 
 +
===Common normal findings===
 +
<gallery mode=packed>
 +
File:Histology of hepatocyte lipofuscin.jpg|Hepatocyte '''lipofuscin''', is of no real pathologic importance and does not warrant a mention in the report.<ref>{{cite web|url=https://webpath.med.utah.edu/LIVEHTML/LIVER019.html|title=The Internet Pathology Laboratory for Medical Education|website=The University of Utah Eccles Health Sciences Library|accessdate=2020-12-18}}</ref>
 
</gallery>
 
</gallery>
 +
 +
===Report===
 +
*At least if the patient had alcohol abuse, a quantification of cirrhosis.
 +
*Optionally, even absence of hepatitis, malignancy, congestive hepatopathy and/or steatosis.
 +
 +
==Microscopic examination in excisions==
 +
Mainly look for tumors. {{further|Liver tumor}}
  
 
{{Bottom}}
 
{{Bottom}}

Revision as of 09:18, 9 September 2021

Author: Mikael Häggström [note 1]

Comprehensiveness

On this resource, the following formatting is used for comprehensiveness:

  • Minimal depth
  • (Moderate depth)
  • ((Comprehensive))

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. The standard reference range for men is 970–1,860 g (2.14–4.10 lb)[2] and for women 600–1,770 g (1.32–3.90 lb).[3]

Gross report

  • Weight. If abnormally low or high, preferably include the reference range.
  • 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, (see section below).
  • 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.
  • Signs of inflammation at least around the portal triads.

Steatosis

At least classify steatosis by severity:

Steatosis grading: a: none. b: mild. c: moderate. d: severe.

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.[4]

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.[7]
  • Acute hepatic congestion shows dilated sinusoidal capillaries predominantly in zone 3 of the hepatic acinus.[8]
  • 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.[9]

Common normal findings

Report

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

Microscopic examination in excisions

Mainly look for tumors. Further information: Liver tumor

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. Molina, D. Kimberley; DiMaio, Vincent J.M. (2012). "Normal Organ Weights in Men ". The American Journal of Forensic Medicine and Pathology 33 (4): 368–372. doi:10.1097/PAF.0b013e31823d29ad. ISSN 0195-7910. PMID 22182984. 
  3. Molina, D. Kimberley; DiMaio, Vincent J. M. (2015). "Normal Organ Weights in Women ". The American Journal of Forensic Medicine and Pathology 36 (3): 182–187. doi:10.1097/PAF.0000000000000175. ISSN 0195-7910. PMID 26108038. 
  4. 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. 
  5. Ciobanu AO, Gherasim L (2018). "Ischemic Hepatitis - Intercorrelated Pathology. ". Maedica (Bucur) 13 (1): 5-11. PMID 29868133. PMC: 5972787. Archived from the original. . 
  6. 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"
  7. 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),"
  8. . Acute Hepatic Congestion. Pathway Medicine. Retrieved on 2020-03-06.
  9. 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. 
  10. . The Internet Pathology Laboratory for Medical Education. The University of Utah Eccles Health Sciences Library. Retrieved on 2020-12-18.

Image sources