Cirrhotic ascites. Pathophysiology, diagnosis, and management

V. K. Rocco, A. J. Ware

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Cirrhotic ascites occurs via both overflow and underfill mechanisms. Intrahepatic hypertension activates a hepatic baroreceptor reflex that enhances renal sodium absorption; plasma volume is expanded. As cirrhosis progresses, the hepatoportal Starling forces become sufficiently disturbed to sequester this 'overflow' in the peritoneal cavity, which results in ascites formation. 'Underfill' of the vascular system occurs and eventually dominates the clinical picture. Finally, intrahepatic hypertension also activates the renin-angiotensin system, which causes renal vasoconstriction; the increase in renal prostaglandin synthesis maintains renal blood flow. Although cirrhotic ascites is traditionally classified as a transudate, the serum-ascites albumin gradient may be a better indicator of ascites secondary to portal hypertension than other causes. General management of patients with cirrhotic ascites includes severe restriction of dietary sodium intake and bed rest; diuretics are added if spontaneous diuresis does not occur after 3 to 4 days.

Original languageEnglish (US)
Pages (from-to)573-585
Number of pages13
JournalAnnals of Internal Medicine
Volume105
Issue number4
StatePublished - 1986

Fingerprint

Ascites
Hypertension
Dietary Sodium
Kidney
Starlings
Bed Rest
Baroreflex
Plasma Volume
Renal Circulation
Diuresis
Peritoneal Cavity
Portal Hypertension
Exudates and Transudates
Renin-Angiotensin System
Vasoconstriction
Diuretics
Serum Albumin
Prostaglandins
Blood Vessels
Fibrosis

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Cirrhotic ascites. Pathophysiology, diagnosis, and management. / Rocco, V. K.; Ware, A. J.

In: Annals of Internal Medicine, Vol. 105, No. 4, 1986, p. 573-585.

Research output: Contribution to journalArticle

@article{7670b95d2a004ffaa8c31c3d16c893aa,
title = "Cirrhotic ascites. Pathophysiology, diagnosis, and management",
abstract = "Cirrhotic ascites occurs via both overflow and underfill mechanisms. Intrahepatic hypertension activates a hepatic baroreceptor reflex that enhances renal sodium absorption; plasma volume is expanded. As cirrhosis progresses, the hepatoportal Starling forces become sufficiently disturbed to sequester this 'overflow' in the peritoneal cavity, which results in ascites formation. 'Underfill' of the vascular system occurs and eventually dominates the clinical picture. Finally, intrahepatic hypertension also activates the renin-angiotensin system, which causes renal vasoconstriction; the increase in renal prostaglandin synthesis maintains renal blood flow. Although cirrhotic ascites is traditionally classified as a transudate, the serum-ascites albumin gradient may be a better indicator of ascites secondary to portal hypertension than other causes. General management of patients with cirrhotic ascites includes severe restriction of dietary sodium intake and bed rest; diuretics are added if spontaneous diuresis does not occur after 3 to 4 days.",
author = "Rocco, {V. K.} and Ware, {A. J.}",
year = "1986",
language = "English (US)",
volume = "105",
pages = "573--585",
journal = "Annals of Internal Medicine",
issn = "0003-4819",
publisher = "American College of Physicians",
number = "4",

}

TY - JOUR

T1 - Cirrhotic ascites. Pathophysiology, diagnosis, and management

AU - Rocco, V. K.

AU - Ware, A. J.

PY - 1986

Y1 - 1986

N2 - Cirrhotic ascites occurs via both overflow and underfill mechanisms. Intrahepatic hypertension activates a hepatic baroreceptor reflex that enhances renal sodium absorption; plasma volume is expanded. As cirrhosis progresses, the hepatoportal Starling forces become sufficiently disturbed to sequester this 'overflow' in the peritoneal cavity, which results in ascites formation. 'Underfill' of the vascular system occurs and eventually dominates the clinical picture. Finally, intrahepatic hypertension also activates the renin-angiotensin system, which causes renal vasoconstriction; the increase in renal prostaglandin synthesis maintains renal blood flow. Although cirrhotic ascites is traditionally classified as a transudate, the serum-ascites albumin gradient may be a better indicator of ascites secondary to portal hypertension than other causes. General management of patients with cirrhotic ascites includes severe restriction of dietary sodium intake and bed rest; diuretics are added if spontaneous diuresis does not occur after 3 to 4 days.

AB - Cirrhotic ascites occurs via both overflow and underfill mechanisms. Intrahepatic hypertension activates a hepatic baroreceptor reflex that enhances renal sodium absorption; plasma volume is expanded. As cirrhosis progresses, the hepatoportal Starling forces become sufficiently disturbed to sequester this 'overflow' in the peritoneal cavity, which results in ascites formation. 'Underfill' of the vascular system occurs and eventually dominates the clinical picture. Finally, intrahepatic hypertension also activates the renin-angiotensin system, which causes renal vasoconstriction; the increase in renal prostaglandin synthesis maintains renal blood flow. Although cirrhotic ascites is traditionally classified as a transudate, the serum-ascites albumin gradient may be a better indicator of ascites secondary to portal hypertension than other causes. General management of patients with cirrhotic ascites includes severe restriction of dietary sodium intake and bed rest; diuretics are added if spontaneous diuresis does not occur after 3 to 4 days.

UR - http://www.scopus.com/inward/record.url?scp=0022451912&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022451912&partnerID=8YFLogxK

M3 - Article

VL - 105

SP - 573

EP - 585

JO - Annals of Internal Medicine

JF - Annals of Internal Medicine

SN - 0003-4819

IS - 4

ER -