PhysiologyTier 1Medical Sciences concept

Serum-ascites albumin gradient (SAAG) interpretation

Core concept2 exam ›

  • SAAG = serum albumin - ascitic albumin, both drawn the same day
    • Measures portal pressure, not the ascites protein content
    • High oncotic gradient is needed to balance a high hydrostatic portal pressure -> the gap widens
  • SAAG >=11 g/L = portal hypertension (~97% accurate)
  • SAAG <11 g/L = non-portal-hypertensive - peritoneal or lymphatic disease
  • Not affected by diuresis, therapeutic paracentesis, or infection - the gradient holds
  • Total ascitic protein is the second axis, not a competing test - it separates sinusoidal from post-sinusoidal causes

Key detail

Two-axis classification
Ascitic protein <25 g/LAscitic protein >=25 g/L
SAAG >=11Cirrhosis (sinusoidal), late Budd-Chiari, fulminant hepatic failureCardiac ascites, constrictive pericarditis, early Budd-Chiari, IVC obstruction, sinusoidal obstruction syndrome
SAAG <11Nephrotic syndrome, protein-losing enteropathyPeritoneal carcinomatosis, TB peritonitis, pancreatic ascites, serositis, chylous
  • Cirrhosis leaks a low-protein fluid - damaged sinusoids are already leaky, so albumin is lost upstream
  • Cardiac ascites leaks a high-protein fluid - sinusoids intact, hydrostatic backpressure only
    • The classic exam pairing: high SAAG + high protein = the heart, not the liver
  • Mixed ascites (cirrhosis + peritoneal TB or malignancy) occurs in ~5% - SAAG stays high
Adjuncts on the same tap
  • PMN >=250/mm3 = SBP, treat before culture returns
  • Ascitic amylase >>serum -> pancreatic ascites
  • Triglycerides >200 mg/dL -> chylous
  • Cytology ~97% sensitive for peritoneal carcinomatosis, but near-useless for hepatocellular carcinoma or massive liver metastases - those cause ascites by portal hypertension, not by seeding
  • ADA / mycobacterial culture for TB peritonitis (low yield in cirrhotics)

Clinical relevance1 exam ›

  • A high SAAG mandates a portal-pressure answer - do not chase cytology first
    • dec sodium intake + spironolactone/frusemide works only for high-SAAG ascites; diuretics are ineffective and harmful in malignant ascites
  • Low SAAG + high protein + lymphocytes = TB or carcinomatosis -> laparoscopy with peritoneal biopsy
  • Nephrotic ascites is the low-SAAG low-protein exception - loss, not leak
Pleural equivalent (same logic, different cutoffs)
  • Light's criteria overcall exudate in diuresed heart failure - use a gradient to rescue
    • Serum - pleural protein >31 g/L -> transudate
    • Serum - pleural albumin >12 g/L -> transudate (most sensitive; useful in hepatic hydrothorax)
  • Hepatic hydrothorax - transudate crossing diaphragmatic defects, usually right-sided, may occur without clinically detectable ascites

Correlations

  • Cirrhosis and portal hypertension; SBP; hepatorenal syndrome; TIPS
  • Budd-Chiari and sinusoidal obstruction syndrome
  • Constrictive pericarditis vs restrictive cardiomyopathy
  • Peritoneal carcinomatosis; ovarian malignancy (Meigs)
  • Pleural effusion - Light's criteria and transudate/exudate
  • Nephrotic syndrome; protein-losing enteropathy

Study aid only. These notes are written with the help of AI. Not for guiding clinical decisions.