Contributing factors: (1) portal hypertension, (2) hypoalbuminemia, (3) hepatic lymph, (4) renal sodium retention—secondary to hyperaldosteronism, increased sympathetic nervous system activity (renin-angiotensin production). Initiating event may be peripheral arterial vasodilation triggered by endotoxin and cytokines and mediated by nitric oxide.
Treatment: Cirrhotic Ascites - Rigid salt restriction (<2 g Na/d).
- For moderate ascites, diuretics usually necessary; spironolactone 100-200 mg/d PO (can be increased to 400 mg/d if low-sodium diet is confirmed and fluid not mobilized); furosemide 40-80 mg/d PO or IV may be added if necessary (greater risk of hepatorenal syndrome [HRS], encephalopathy), can increase to maximum of 120-160 mg/d until effect achieved or complication occurs.
- Monitor weight, urinary Na and K, serum electrolytes, and creatinine. If ascites is still present with the above measures, this is defined as refractory ascites. Treatment modalities include:
- Pharmacologic therapy: add midodrine or clonidine to diuretic therapy
- Repeated large-volume paracentesis (5 L) with IV infusions of albumin (6-8 g/L ascites removed)
- Consider transjugular intrahepatic portosystemic shunt (TIPS). While TIPS manages the ascites, it has not been found to improve survival and is often associated with encephalopathy.
Prognosis for pts with cirrhotic ascites is poor with <50% survival 2 years after onset of ascites. Consider liver transplantation in appropriate candidates with the onset of ascites (Chap. 154. Cirrhosis and Alcoholic Liver Disease). |