Ascites in Cirrhotic Portal Hypertension: Correct Statement Analysis

Statement (b) is correct: In diuretic-resistant (refractory) ascites, large-volume drainage paracentesis is the treatment of choice. 1, 2, 3

Analysis of Each Statement

The serum-ascites albumin gradient (SAAG) is ≥1.1 g/dL in portal hypertension-related ascites, not <1.1. 1
A SAAG ≥1.1 g/dL indicates portal hypertension with approximately 97% accuracy 1
This high gradient reflects the oncotic pressure difference between serum and ascitic fluid caused by portal hypertension 4
A SAAG <1.1 g/dL would suggest non-portal hypertensive causes such as peritoneal carcinomatosis or tuberculosis 1

Large-volume paracentesis (LVP) is the definitive treatment for refractory ascites that fails to respond to sodium restriction and high-dose diuretics. 1, 3
Intravenous albumin must be administered at 8g per liter of ascites removed to prevent post-paracentesis circulatory dysfunction 1, 2
LVP provides rapid relief and is associated with fewer complications than traditional diuretic escalation alone 3
After paracentesis, diuretic therapy should be resumed to prevent rapid reaccumulation 1, 3
Alternative options for refractory ascites include transjugular intrahepatic portosystemic shunt (TIPS) in selected patients, though this may worsen hepatic encephalopathy 3, 5

While cirrhotic patients with ascites often have systemic arterial vasodilation and relative hypotension, systolic blood pressure is not "usually" <100 mmHg 4, 6
The hemodynamic profile includes splanchnic arterial vasodilation, increased cardiac output, and reduced systemic vascular resistance 6, 7, 3
Blood pressure varies widely depending on disease stage and compensatory mechanisms 6, 7
Hypotension becomes more pronounced in advanced stages with hepatorenal syndrome, but this is not the typical presentation of all ascites patients 8, 3

This is dangerously wrong. Sodium restriction to 2000 mg/day (88 mmol/day) is the cornerstone of ascites management, not sodium administration. 1, 9, 10
Administering sodium-containing fluids would worsen ascites by promoting further fluid retention 1, 7
The pathophysiology involves inappropriate renal sodium retention due to activation of the renin-angiotensin-aldosterone system 4, 6, 7
Fluid restriction is generally unnecessary unless serum sodium drops below 120-125 mmol/L 1
Critical pitfall: NSAIDs and ACE inhibitors should be avoided as they worsen sodium retention and hypotension respectively 1, 10

Serum aldosterone levels are markedly ELEVATED, not reduced, in cirrhotic ascites. 4, 6, 7
The renin-angiotensin-aldosterone system (RAAS) is activated as a compensatory response to effective arterial hypovolemia from splanchnic vasodilation 6, 7, 8
This hyperaldosteronism drives renal sodium retention and is the reason spironolactone (an aldosterone antagonist) is first-line diuretic therapy 1, 9
Standard initial therapy is spironolactone 100 mg daily plus furosemide 40 mg daily 1, 10

Sodium restriction to 2000 mg/day 1, 9, 10
Combination diuretics: spironolactone 100 mg + furosemide 40 mg daily 1, 10
Daily weight monitoring: target 0.5 kg/day loss (no edema) or 1 kg/day (with edema) 1
Monitor electrolytes, creatinine, and assess urinary sodium excretion if inadequate response 1, 10

Development of ascites indicates decompensated cirrhosis with approximately 20% mortality in the first year 1, 10
Ascites is an indication for liver transplantation evaluation 4, 1, 10
In alcohol-related cirrhosis, abstinence provides 75% 3-year survival versus 0% with continued drinking 1, 9