Serious complication of large volume paracentesis (LVP) without a plasma expander that leads to faster reaccumulation of ascites, hyponatremia, renal impairment, and shorter survival.
- Clinical definition: 50% increase in the plasma renin activity (PRA) over the baseline on the 6th day after treatment, up to a value > 4 ng/mL per hour
Pathophysiology
Decreased systemic vascular resistance:
LVP causes mechanical decompression of the splanchnic vascular bed leading to splanchnic vasodilation, a further decrease in the arterial filling, and activation of neurohormonal systems.
Resulting effective hypovolemia due to arteriolar vasodilation in turn leads to a prolonged activation of the sympathetic nervous system and the rennin-angiotensin-aldosterone pathway. This results in free water and sodium retention. As a consequence, patients develop rapid reaccumulation of ascites, hyponatremia, renal injury, and encephalopathy.
Clinical features
PICD is a clinically silent syndrome, but an independent predictor of mortality in patients with massive ascites treated with large-volume paracentesis.
Re-emergence of symptoms:
Patients with PICD reaccumulate ascites and experience a return of symptoms more rapidly after paracentesis
- Rapid re-accumulation of ascites
- Dilutional hyponatremia
- Hepatorenal syndrome
- Decreased survival
Management
Plasma volume expanders:
Volume expansion with albumin infusion is the mainstay of treatment.
- Human albumin infusion (best option due to long half-life of 21 days and additional actions as an antioxidant, detoxification, immunoprotective, drug binding and delivery properties)
- Midodrine (α1-agonist): Acts on the α-adrenergic receptors of arteriolar and venous vasculature, producing an increase in vascular tone and elevation of blood pressure.
- Noradrenaline (potent α-agonist): Global vasoconstriction
