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Ascites
‘’abnormal collection of fluid in the peritoneal cavity, a common complication
of portal hpt secondary to cirrhosis’’
 Na+ & H20 retention, due to peripheral arterial vasodilation particularly the
splanchnic circulation. This reduces BP and activates the rennin-angiotensin system
and sympathetic nervous supply  increased H20 and Na+ retention
 Local hydrostatic pressure increase due to portal hpt, which increase lymph
production in the hepatic and splanchnic areas. Transudation of the fluid ascites
 Hypoalbuminaemia due to decreased liver synthesis, resulting in a low plasma
oncotic pressure
 2° hyperaldosteronism  with reduced catabolism of the salt-retaining hormone. 
Spironolactone (aldosterone antagonist) used as Tx.
Causes:
Portal Hpt:
 Cirrhosis
 CCF
 Constrictive Pericarditis
 Budd-Chiari Syndrome
 IVC obstruction
Hypoalbuminaemia:
 Nephrotic Syndrome
 Protein losing enteropathy
Neoplasms:
 Peritoneal carcinomatosis
 Pseudomyxoma
Miscellaneous:
 Pancreatic ascites
 Nephrogenic – ass with dialysis
 Myxoedema
 Meigs’s syndrome
Clinical Features:
 Abdo distension
 Fluid thrill
 Shifting Dullness
Tense ascites can cause; pain, difficulty
breathing, eversion of the umbilicus, hernias
& scrotal odeama.
If rapid onset think  Ca, GI bleeding,
infection, portal venous thrombosis
What is the Ascites made of?
Look at serum: asites albumin gradient  shows oncotic pressures and correlates
with portal venous pressures
Management:
 Dietary Na+ restriction (1-1.5g/day)
 Diuretics – spironlactone
 Stop alcohol
 Monitor renal and liver function
 Potential complications – encephalopathy, hypokaleamia, hyponatreamia,
hypochloraemic alkalosis and azotaemia.
 If tense ascites  paracentesis
 If no response  serial therapeutic paracentesis, peritoneovenous shunt,
transjugular intrahepatic portosystemic shut & liver transplant.
Transudate : low protein ( <30 g/L)
Exudate : high protein
High gradient >11g/l - (ass with portal hpt)
 Cirrhosis
 Alcoholic Hepatitis
 Cardiac Ascites
 Fulminant hepatic failure
 Budd-Chiari
 Portal vein thrombosis
 Veno-occlusive disease
Low gradient <11g/l
 Peritoneal carcinomatosis
 TB
 Pancreatic Ascites
 Biliary Ascites
 Nephrotic Syndrome

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Ascities overview

  • 1. Ascites ‘’abnormal collection of fluid in the peritoneal cavity, a common complication of portal hpt secondary to cirrhosis’’  Na+ & H20 retention, due to peripheral arterial vasodilation particularly the splanchnic circulation. This reduces BP and activates the rennin-angiotensin system and sympathetic nervous supply  increased H20 and Na+ retention  Local hydrostatic pressure increase due to portal hpt, which increase lymph production in the hepatic and splanchnic areas. Transudation of the fluid ascites  Hypoalbuminaemia due to decreased liver synthesis, resulting in a low plasma oncotic pressure  2° hyperaldosteronism  with reduced catabolism of the salt-retaining hormone.  Spironolactone (aldosterone antagonist) used as Tx. Causes: Portal Hpt:  Cirrhosis  CCF  Constrictive Pericarditis  Budd-Chiari Syndrome  IVC obstruction Hypoalbuminaemia:  Nephrotic Syndrome  Protein losing enteropathy Neoplasms:  Peritoneal carcinomatosis  Pseudomyxoma Miscellaneous:  Pancreatic ascites  Nephrogenic – ass with dialysis  Myxoedema  Meigs’s syndrome Clinical Features:  Abdo distension  Fluid thrill  Shifting Dullness Tense ascites can cause; pain, difficulty breathing, eversion of the umbilicus, hernias & scrotal odeama. If rapid onset think  Ca, GI bleeding, infection, portal venous thrombosis
  • 2. What is the Ascites made of? Look at serum: asites albumin gradient  shows oncotic pressures and correlates with portal venous pressures Management:  Dietary Na+ restriction (1-1.5g/day)  Diuretics – spironlactone  Stop alcohol  Monitor renal and liver function  Potential complications – encephalopathy, hypokaleamia, hyponatreamia, hypochloraemic alkalosis and azotaemia.  If tense ascites  paracentesis  If no response  serial therapeutic paracentesis, peritoneovenous shunt, transjugular intrahepatic portosystemic shut & liver transplant. Transudate : low protein ( <30 g/L) Exudate : high protein High gradient >11g/l - (ass with portal hpt)  Cirrhosis  Alcoholic Hepatitis  Cardiac Ascites  Fulminant hepatic failure  Budd-Chiari  Portal vein thrombosis  Veno-occlusive disease Low gradient <11g/l  Peritoneal carcinomatosis  TB  Pancreatic Ascites  Biliary Ascites  Nephrotic Syndrome