How can the etiology be determined.
The etiology can be determined using the serum-ascites albumin gradient (SAAG) based on Starling's law.
SAAG = (albumin levels in serum) - (albumin levels in ascitic fluid)
Describe the etiology in High SAAG ascites
≥ 1.1 g/dL (obsolete term: transudate)
Portal hypertension
Presinusoidal
Splenic or portal vein thrombosis
Schistosomiasis
Sinusoidal
Hepatic (common)
Cirrhosis
Alcohol-related liver disease
Liver metastases
Postsinusoidal
Cardiac
Right heart failure
Constrictive pericarditis
Budd-Chiari syndrome
Describe the pathophysiology in High SAAG ascites
Arterial vasodilation hypothesis in cirrhosis :
Portal hypertension → vasodilation → reduced systemic vascular resistance and reduced mean arterial blood pressure
Activation of endogenous vasoconstrictors, renal sodium and water retention, and renal vasoconstriction → hyperdynamic circulation
Right-sided heart failure: backflow of blood obstructing the venous outflow of the liver
Budd-Chiari syndrome: congestion of the portal/hepatic collateral veins and hypertrophy of the caudate lobe of the liver → compression of the sinusoids and intrahepatic inferior vena cava
All result in ↑ pressure in portal vein → ↑ hydrostatic pressure in the hepatic vessels → pushing of fluid out from the intravascular space to the peritoneal cavity
Describe the etiology in Low SAAG ascites
< 1.1 g/dL (obsolete term: exudate)
Hypoalbuminemia
Nephrotic syndrome
Severe malnutrition
Protein-losing enteropathy
Malignancy
Infections (e.g., tbc)
Pancreatitis
Low SAAG ascites
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