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Ascites pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

Overview

Overview

Ascites is the excess accumulation of fluid in the peritoneal cavity. The fluid can be defined as transudate or exudate. Amounts of up to 25 liters are fully possible. Roughly, transudates are a result of increased pressure in the portal vein (> 8 mmHg), such as cirrhosis; while exudates are actively secreted fluid due to inflammation or malignancy. The most useful measure is the difference between ascitic and serum albumin concentrations. A difference of less than 1.1 g/dl (10 g/L) implies an exudate. There is no genetic background for ascites. On gross pathology, clear to pale yellow fluid accumulation in peritoneal space are characteristic findings of ascites under normal condition, but it may be chylous, psudochylous, or bloody.

Pathophysiology

Pathophysiology

Pathogenesis

Serum Albumin Ascites Gradiant (SAAG)

  • The most useful measure is the difference between ascitic and serum albumin concentrations.
  • A difference of less than 1.1 g/dl (10 g/L) implies an exudate.

Cirrhotic Ascites

Non-Cirrhotic Ascites



 
 
Renin-angiotensin system
 
 
Sympathetic nervous system
 
 
Antidiuretic hormone
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Systemic circulation
 
 
 
Renal circulation
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Arterial vasoconstriction
 
↑Tubular Na and H2O reabsorbtion
 
Renal vasoconstriction
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Arterial hypertension
 
Na and H2O excretion
 
Hepatorenal syndrome
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Fluid overload
 
 
 
 
Dilutional hyponatremia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Ascites formation
 
 
 
 
 
 
Genetics

Genetics

Associated Conditions

Associated Conditions

Associated conditions with ascites are as following:[10]

Gross Pathology

Gross Pathology

Chylous ascites

Pseudochylous ascites

Bloody ascites

Microscopic Pathology

Microscopic Pathology

Cirrhosis with bridging fibrosis (yellow arrow) and nodule (black arrow) – By Nephron, via Librepathology.org[16]







References

References

  1. Runyon BA (2009). “Management of adult patients with ascites due to cirrhosis: an update”. Hepatology. 49 (6): 2087–107. doi:10.1002/hep.22853. PMID 19475696.
  2. Giefer, Matthew J; Murray, Karen F; Colletti, Richard B (2011). “Pathophysiology, Diagnosis, and Management of Pediatric Ascites”. Journal of Pediatric Gastroenterology and Nutrition. 52 (5): 503–513. doi:10.1097/MPG.0b013e318213f9f6. ISSN 0277-2116.
  3. La Villa, Giorgio; Gentilini, Paolo (2008). “Hemodynamic alterations in liver cirrhosis”. Molecular Aspects of Medicine. 29 (1–2): 112–118. doi:10.1016/j.mam.2007.09.010. ISSN 0098-2997.
  4. Leiva JG, Salgado JM, Estradas J, Torre A, Uribe M (2007). “Pathophysiology of ascites and dilutional hyponatremia: contemporary use of aquaretic agents”. Ann Hepatol. 6 (4): 214–21. PMID 18007550.
  5. Bichet, Daniel (1982). “Role of Vasopressin in Abnormal Water Excretion in Cirrhotic Patients”. Annals of Internal Medicine. 96 (4): 413. doi:10.7326/0003-4819-96-4-413. ISSN 0003-4819.
  6. Hennenberg, M.; Trebicka, J.; Kohistani, A. Z.; Heller, J.; Sauerbruch, T. (2009). “Vascular hyporesponsiveness to angiotensin II in rats with CCl4-induced liver cirrhosis”. European Journal of Clinical Investigation. 39 (10): 906–913. doi:10.1111/j.1365-2362.2009.02181.x. ISSN 0014-2972.
  7. Laine GA, Hall JT, Laine SH, Granger J (1979). “Transsinusoidal fluid dynamics in canine liver during venous hypertension”. Circ. Res. 45 (3): 317–23. PMID 572270.
  8. Goodman GM, Gourley GR (1988). “Ascites complicating ventriculoperitoneal shunts”. J. Pediatr. Gastroenterol. Nutr. 7 (5): 780–2. PMID 3054040.
  9. Pakdel, A.; van Arendonk, J.A.M.; Vereijken, A.L.J.; Bovenhuis, H. (2010). “Genetic parameters of ascites-related traits in broilers: effect of cold and normal temperature conditions”. British Poultry Science. 46 (1): 35–42. doi:10.1080/00071660400023938. ISSN 0007-1668.
  10. Moore KP, Aithal GP (2006). “Guidelines on the management of ascites in cirrhosis”. Gut. 55 Suppl 6: vi1–12. doi:10.1136/gut.2006.099580. PMC 1860002. PMID 16966752.
  11. Huang LL, Xia HH, Zhu SL (2014). “Ascitic Fluid Analysis in the Differential Diagnosis of Ascites: Focus on Cirrhotic Ascites”. J Clin Transl Hepatol. 2 (1): 58–64. doi:10.14218/JCTH.2013.00010. PMC 4521252. PMID 26357618.
  12. Fukunaga, Naoto; Shomura, Yu; Nasu, Michihiro; Okada, Yukikatsu (2011). “Chylous Ascites as a Rare Complication After Abdominal Aortic Aneurysm Surgery”. Southern Medical Journal. 104 (5): 365–367. doi:10.1097/SMJ.0b013e3182142b7d. ISSN 0038-4348.
  13. Tarn, A. C.; Lapworth, R. (2010). “Biochemical analysis of ascitic (peritoneal) fluid: what should we measure?”. Annals of Clinical Biochemistry. 47 (5): 397–407. doi:10.1258/acb.2010.010048. ISSN 0004-5632.
  14. Runyon BA, Akriviadis EA, Keyser AJ (1991). “The opacity of portal hypertension-related ascites correlates with the fluid’s triglyceride concentration”. Am. J. Clin. Pathol. 96 (1): 142–3. PMID 2069132.
  15. Runyon BA, Hoefs JC, Morgan TR (1988). “Ascitic fluid analysis in malignancy-related ascites”. Hepatology. 8 (5): 1104–9. PMID 3417231.
  16. “File:Cirrhosis high mag.jpg – Libre Pathology”.
  17. Mitchell, Richard (2012). Pocket companion to Robbins and Cotran pathologic basis of disease. Philadelphia, PA: Elsevier Saunders. ISBN 978-1416054542.

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