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==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, [[transudate]]s are a result of increased pressure in the [[hepatic portal vein|portal vein]] (> 8 mmHg), such as [[cirrhosis]]; while [[Exudate|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 cavity|peritoneal space]] are characteristic findings of ascites under normal condition, but it may be [[Chylous ascites|chylous]], psudochylous, or bloody.
==Pathophysiology==


==Pathophysiology==
=== Pathogenesis ===
* Ascites is the excess accumulation of fluid in the [[peritoneal cavity]]. The fluid can be defined as a [[transudate]] or an [[exudate]]. Amounts of up to 25 liters are fully possible.<ref name="pmid19475696">{{cite journal |vauthors=Runyon BA |title=Management of adult patients with ascites due to cirrhosis: an update |journal=Hepatology |volume=49 |issue=6 |pages=2087–107 |year=2009 |pmid=19475696 |doi=10.1002/hep.22853 |url=}}</ref>
* Roughly, [[transudate]]s are a result of increased pressure in the [[hepatic portal vein|portal vein]] (> 8 mmHg), such as [[cirrhosis]]; while [[Exudate|exudates]] are actively secreted fluid due to [[inflammation]] or [[malignancy]].
* '''Exudates:'''
** High [[protein]]
** High [[lactate dehydrogenase|lactate dehydrogenase (LDH)]]
** Low [[pH]] (< 7.30)
** Low [[glucose]] level
** High [[white blood cells]] count
* '''Transudates:'''
** Low [[protein]] (< 30 g/L)
** Low [[Lactate dehydrogenase|lactate dehydrogenase (LDH)]]
** High [[pH]]
** Normal [[glucose]]
** Fewer than 1 [[White blood cells|white blood cell]] per 1000 mm³


=== 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 ===
=== Cirrhotic Ascites ===
* The main pathophysiology of ascites in cirrhotic patients consists of three interrelated mechanisms, include:<ref name="GieferMurray2011">{{cite journal|last1=Giefer|first1=Matthew J|last2=Murray|first2=Karen F|last3=Colletti|first3=Richard B|title=Pathophysiology, Diagnosis, and Management of Pediatric Ascites|journal=Journal of Pediatric Gastroenterology and Nutrition|volume=52|issue=5|year=2011|pages=503–513|issn=0277-2116|doi=10.1097/MPG.0b013e318213f9f6}}</ref>
* The main [[pathophysiology]] of ascites in [[Cirrhosis|cirrhotic]] patients consists of three interrelated mechanisms, include:<ref name="GieferMurray2011">{{cite journal|last1=Giefer|first1=Matthew J|last2=Murray|first2=Karen F|last3=Colletti|first3=Richard B|title=Pathophysiology, Diagnosis, and Management of Pediatric Ascites|journal=Journal of Pediatric Gastroenterology and Nutrition|volume=52|issue=5|year=2011|pages=503–513|issn=0277-2116|doi=10.1097/MPG.0b013e318213f9f6}}</ref>
** Portal hypertension
** [[Portal hypertension]]
** Vasodilation
** [[Vasodilation]]
** Hyperaldosteronism
** [[Hyperaldosteronism]]
* There is a nitric oxide overload in cirrhotic patients from an unknown source. Therefore, they involved in hypovolemia secondary to the systemic vasodilation.<ref name="La VillaGentilini2008">{{cite journal|last1=La Villa|first1=Giorgio|last2=Gentilini|first2=Paolo|title=Hemodynamic alterations in liver cirrhosis|journal=Molecular Aspects of Medicine|volume=29|issue=1-2|year=2008|pages=112–118|issn=00982997|doi=10.1016/j.mam.2007.09.010}}</ref>
* There is a [[nitric oxide]] overload in [[Cirrhosis|cirrhotic]] patients from an unknown source. Therefore, they involved in [[hypovolemia]] secondary to the systemic [[vasodilation]].<ref name="La VillaGentilini2008">{{cite journal|last1=La Villa|first1=Giorgio|last2=Gentilini|first2=Paolo|title=Hemodynamic alterations in liver cirrhosis|journal=Molecular Aspects of Medicine|volume=29|issue=1-2|year=2008|pages=112–118|issn=00982997|doi=10.1016/j.mam.2007.09.010}}</ref>
* The visodialtion induced by nitric oxide would trigger the stimulation of juxta-glumerular system to upregulate antidiuretic hormone (ADH) and sympathetic drive.<ref name="pmid18007550">{{cite journal |vauthors=Leiva JG, Salgado JM, Estradas J, Torre A, Uribe M |title=Pathophysiology of ascites and dilutional hyponatremia: contemporary use of aquaretic agents |journal=Ann Hepatol |volume=6 |issue=4 |pages=214–21 |year=2007 |pmid=18007550 |doi= |url=}}</ref> Excess ADH causes water retention and volume overload.<ref name="Bichet1982">{{cite journal|last1=Bichet|first1=Daniel|title=Role of Vasopressin in Abnormal Water Excretion in Cirrhotic Patients|journal=Annals of Internal Medicine|volume=96|issue=4|year=1982|pages=413|issn=0003-4819|doi=10.7326/0003-4819-96-4-413}}</ref>
* The [[vasodilation]] induced by [[nitric oxide]] would trigger the stimulation of [[Juxtaglomerular apparatus|juxta-glumerular system]] to [[upregulate]] [[Antidiuretic hormone|antidiuretic hormone (ADH)]] and [[sympathetic]] drive.<ref name="pmid18007550">{{cite journal |vauthors=Leiva JG, Salgado JM, Estradas J, Torre A, Uribe M |title=Pathophysiology of ascites and dilutional hyponatremia: contemporary use of aquaretic agents |journal=Ann Hepatol |volume=6 |issue=4 |pages=214–21 |year=2007 |pmid=18007550 |doi= |url=}}</ref> Excess [[ADH]] causes [[water retention]] and volume overload.<ref name="Bichet1982">{{cite journal|last1=Bichet|first1=Daniel|title=Role of Vasopressin in Abnormal Water Excretion in Cirrhotic Patients|journal=Annals of Internal Medicine|volume=96|issue=4|year=1982|pages=413|issn=0003-4819|doi=10.7326/0003-4819-96-4-413}}</ref>
* Despite the normal physiology of vessels, angiotensin would not cause vasoconstriction in cirrhotic patients and vasodilation becomes perpetuated.<ref name="HennenbergTrebicka2009">{{cite journal|last1=Hennenberg|first1=M.|last2=Trebicka|first2=J.|last3=Kohistani|first3=A. Z.|last4=Heller|first4=J.|last5=Sauerbruch|first5=T.|title=Vascular hyporesponsiveness to angiotensin II in rats with CCl4-induced liver cirrhosis|journal=European Journal of Clinical Investigation|volume=39|issue=10|year=2009|pages=906–913|issn=00142972|doi=10.1111/j.1365-2362.2009.02181.x}}</ref>
* Despite the normal [[physiology]] of [[vessels]], [[angiotensin]] would not cause [[vasoconstriction]] in [[Cirrhosis|cirrhotic]] patients and [[vasodilation]] becomes perpetuated.<ref name="HennenbergTrebicka2009">{{cite journal|last1=Hennenberg|first1=M.|last2=Trebicka|first2=J.|last3=Kohistani|first3=A. Z.|last4=Heller|first4=J.|last5=Sauerbruch|first5=T.|title=Vascular hyporesponsiveness to angiotensin II in rats with CCl4-induced liver cirrhosis|journal=European Journal of Clinical Investigation|volume=39|issue=10|year=2009|pages=906–913|issn=00142972|doi=10.1111/j.1365-2362.2009.02181.x}}</ref>
* Portal hypertension leads to more production of lymph, to the extend of lymphatic system overload. Then, the lymphatic overflow will directed into to peritoneal cavity, forming ascites.<ref name="pmid572270">{{cite journal |vauthors=Laine GA, Hall JT, Laine SH, Granger J |title=Transsinusoidal fluid dynamics in canine liver during venous hypertension |journal=Circ. Res. |volume=45 |issue=3 |pages=317–23 |year=1979 |pmid=572270 |doi= |url=}}</ref>
* [[Portal hypertension]] leads to more production of [[lymph]], to the extend of [[lymphatic system]] overload. Then, the [[lymphatic]] overflow will directed into to [[peritoneal cavity]], forming ascites.<ref name="pmid572270">{{cite journal |vauthors=Laine GA, Hall JT, Laine SH, Granger J |title=Transsinusoidal fluid dynamics in canine liver during venous hypertension |journal=Circ. Res. |volume=45 |issue=3 |pages=317–23 |year=1979 |pmid=572270 |doi= |url=}}</ref>


=== Non-Cirrhotic Ascites ===
=== Non-Cirrhotic Ascites ===
*  
* [[Peritoneal]] malignancy produces some [[protein]] factors into the [[peritoneum]], which may lead to [[osmotic]] drainage of water and fluid accumulation. [[Tuberculosis]] and other forms of ascites are induced through the same mechanism and [[osmotic]] fluid shift.<ref name="pmid3054040">{{cite journal |vauthors=Goodman GM, Gourley GR |title=Ascites complicating ventriculoperitoneal shunts |journal=J. Pediatr. Gastroenterol. Nutr. |volume=7 |issue=5 |pages=780–2 |year=1988 |pmid=3054040 |doi= |url=}}</ref>
* Ascitic fluid can accumulate as a [[transudate]] or an [[exudate]]. Amounts of up to 25 liters are fully possible.
* [[Pancreatic]] and [[biliary]] ascites are induced through leakage of [[pancreatic]] secretions or [[bile]] into the [[peritoneal cavity]], which may lead to [[inflammatory]] fluid shift and accumulation.
* Roughly, [[transudate]]s are a result of increased pressure in the [[hepatic portal vein|portal vein]] (>8 mmHg), e.g. due to cirrhosis, while exudates are actively secreted fluid due to [[inflammation]] or malignancy. As a result, exudates are high in protein, high in [[lactate dehydrogenase]], have a low [[pH]] (<7.30), a low [[glucose]] level, and more [[white blood cell]]s. Transudates have low protein (<30g/L), low LDH, high pH, normal glucose, and fewer than 1 white cell per 1000 mm³.  Clinically, the most useful measure is the difference between ascitic and [[serum albumin]] concentrations. A difference of less than 1 g/dl (10 g/L) implies an exudate. Portal hypertension plays an important role in the production of ascites by raising capillary hydrostatic pressure within the splanchnic bed.
<br>
Regardless of the cause, sequestration of fluid within the abdomen leads to additional [[fluid retention]] by the kidneys due to stimulatory effect on blood pressure hormones, notably [[aldosterone]]. The [[sympathetic nervous system]] is also activated, and [[renin]] production is increased due to decreased perfusion of the kidney. Extreme disruption of the renal blood flow can lead to the feared [[hepatorenal syndrome]]. Other complications of ascites include [[spontaneous bacterial peritonitis]] (SBP), due to decreased antibacterial factors in the ascitic fluid such as [[Complement system|complement]].
<br>
 
{{family tree/start}}
{{family tree| | | A01 | | | A02 | | | A03 | |A01=↑[[Renin-angiotensin system]]|A02=↑[[Sympathetic nervous system]]|A03=↑[[Antidiuretic hormone]]}}
{{family tree| | | |`|-|-|-|-|+|-|-|-|-|'| | |}}
{{family tree| | | | |,|-|-|-|^|-|.| | | | | |}}
{{family tree| | | | B01 | | | | B02 | | | | |B01=[[Systemic circulation]]|B02=[[Renal]] [[circulation]]}}
{{family tree| | | | |!| | | |,|-|^|-|.| | | |}}
{{family tree| | | | C01 | | C02 | | C03 | | |C01=[[Arterial]] [[vasoconstriction]]|C02=↑Tubular Na and H2O reabsorbtion|C03=[[Renal]] [[vasoconstriction]]}}
{{family tree| | | | |!| | | |!| | | |!| | | |}}
{{family tree| | | | D01 | | D02 | | D03 | | |D01=[[Arterial]] [[hypertension]]|D02=Na and H2O excretion|D03=[[Hepatorenal syndrome]]}}
{{family tree| | | | | |,|-|-|+|-|-|.| | | | |}}
{{family tree| | | | | E01 | |!| | E02 | | | |E01=[[Fluid overload]]|E02=[[Dilutional hyponatremia]]}}
{{family tree| | | | | | | | |!| | | | | | | |}}
{{family tree| | | | | | | | F01 | | | | | | |F01='''Ascites formation'''}}
{{family tree/end}}
 
==Genetics==
*There is no [[genetic]] background for ascites.
*Ascites syndrome, also called [[pulmonary hypertension]], is in fact a [[genetic disorder]] in broilers and [[poultry]].<ref name="Pakdelvan Arendonk2010">{{cite journal|last1=Pakdel|first1=A.|last2=van Arendonk|first2=J.A.M.|last3=Vereijken|first3=A.L.J.|last4=Bovenhuis|first4=H.|title=Genetic parameters of ascites-related traits in broilers: effect of cold and normal temperature conditions|journal=British Poultry Science|volume=46|issue=1|year=2010|pages=35–42|issn=0007-1668|doi=10.1080/00071660400023938}}</ref>
==Associated Conditions==
Associated conditions with ascites are as following:<ref name="pmid16966752">{{cite journal| author=Moore KP, Aithal GP| title=Guidelines on the management of ascites in cirrhosis. | journal=Gut | year= 2006 | volume= 55 Suppl 6 | issue=  | pages= vi1-12 | pmid=16966752 | doi=10.1136/gut.2006.099580 | pmc=1860002 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16966752  }}</ref>
* [[Cirrhosis]]
* [[Heart failure]]
* [[Portal hypertension]]
* [[Kwashiorkor]]
* [[Viral hepatitis]]
* [[Pancreatic disease]]
* [[Biliary disease]]
 
==Gross Pathology==
*On [[gross pathology]], clear to pale yellow fluid accumulation in [[Peritoneal cavity|peritoneal space]] are characteristic findings of ascites under normal condition.<ref name="pmid26357618">{{cite journal| author=Huang LL, Xia HH, Zhu SL| title=Ascitic Fluid Analysis in the Differential Diagnosis of Ascites: Focus on Cirrhotic Ascites. | journal=J Clin Transl Hepatol | year= 2014 | volume= 2 | issue= 1 | pages= 58-64 | pmid=26357618 | doi=10.14218/JCTH.2013.00010 | pmc=4521252 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26357618  }}</ref>
 
=== Chylous ascites ===
*[[Chylous ascites]] [[gross pathology]] is milky presentation of ascites fluid, which is reflective of high amounts of [[chylomicrons]].<ref name="FukunagaShomura2011">{{cite journal|last1=Fukunaga|first1=Naoto|last2=Shomura|first2=Yu|last3=Nasu|first3=Michihiro|last4=Okada|first4=Yukikatsu|title=Chylous Ascites as a Rare Complication After Abdominal Aortic Aneurysm Surgery|journal=Southern Medical Journal|volume=104|issue=5|year=2011|pages=365–367|issn=0038-4348|doi=10.1097/SMJ.0b013e3182142b7d}}</ref>
*On [[gross pathology]], milky appearance of ascitic fluid is characteristics of the followings:<ref name="TarnLapworth2010">{{cite journal|last1=Tarn|first1=A. C.|last2=Lapworth|first2=R.|title=Biochemical analysis of ascitic (peritoneal) fluid: what should we measure?|journal=Annals of Clinical Biochemistry|volume=47|issue=5|year=2010|pages=397–407|issn=0004-5632|doi=10.1258/acb.2010.010048}}</ref>
**[[Cirrhosis]]
**[[Infection|Infections]] ([[parasitic]] and [[tuberculosis]])
**[[Malignancy]]
**[[Congenital defects]]
**[[Trauma]]
**[[Inflammatory processes]]
**[[Nephropathy|Nephropathies]]
**[[Cardiac disease|Cardiopathies]]
 
=== Pseudochylous ascites ===
*Pseudochylous is the condition in which on [[gross pathology]] the ascitic fluid appearance is cloudy and/or turbid.  
*The following conditions can lead to pseudochylous:<ref name="pmid2069132">{{cite journal |vauthors=Runyon BA, Akriviadis EA, Keyser AJ |title=The opacity of portal hypertension-related ascites correlates with the fluid's triglyceride concentration |journal=Am. J. Clin. Pathol. |volume=96 |issue=1 |pages=142–3 |year=1991 |pmid=2069132 |doi= |url=}}</ref>
**[[Bacterial infection]]
**[[Peritonitis]]
**[[Pancreatitis]]
**[[Perforated duodenal ulcer|Perforated bowel]]
 
=== Bloody ascites ===
*On [[gross pathology]], bloody appearance of ascitic fluid is characteristics of the followings:<ref name="pmid3417231">{{cite journal |vauthors=Runyon BA, Hoefs JC, Morgan TR |title=Ascitic fluid analysis in malignancy-related ascites |journal=Hepatology |volume=8 |issue=5 |pages=1104–9 |year=1988 |pmid=3417231 |doi= |url=}}</ref>
**[[Benign]] or [[malignant tumors]]
**Hemorrhagic [[pancreatitis]]
**[[Perforated ulcer]]
==Microscopic Pathology==
[[image:Cirrhosis.jpg|thumb|200px|Cirrhosis with bridging fibrosis (yellow arrow) and nodule (black arrow) - By Nephron, via Librepathology.org<ref name="urlFile:Cirrhosis high mag.jpg - Libre Pathology">{{cite web |url=https://librepathology.org/wiki/File:Cirrhosis_high_mag.jpg#filelinks |title=File:Cirrhosis high mag.jpg - Libre Pathology |format= |work= |accessdate=}}</ref>]]
*On [[microscopic]] [[histopathological]] analysis, characteristic findings of [[cirrhosis]], as the most common cause of ascites, are based on Robbins definition (all three is needed for diagnosis):<ref>{{cite book | last = Mitchell | first = Richard | title = Pocket companion to Robbins and Cotran pathologic basis of disease | publisher = Elsevier Saunders | location = Philadelphia, PA | year = 2012 | isbn = 978-1416054542 }}</ref>
** Bridging [[fibrosis]]
** [[Nodule]] formation
** Disruption of the [[hepatic]] architecture
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==References==
==References==
{{Reflist|2}}
{{Reflist|2}}


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Latest revision as of 13:38, 31 January 2018

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

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

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

Associated Conditions

Associated conditions with ascites are as following:[10]

Gross Pathology

Chylous ascites

Pseudochylous ascites

Bloody ascites

Microscopic Pathology

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







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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