Plasma oncotic pressure is principally generated by albumin. A patient with chronic liver disease has serum albumin of 1.8 g/dL (normal 3.5–5.0 g/dL). Using the Starling forces concept, explain the predominant mechanism of ascites in this patient.
- A Portal hypertension alone drives all fluid into the peritoneum; albumin has no role in cirrhotic ascites
- B Low albumin increases hepatic lymph production, which drains into the peritoneum directly
- C Reduced albumin increases blood viscosity, raising capillary hydrostatic pressure and causing ascites
- D Reduced plasma oncotic pressure lowers the force retaining fluid in hepatic sinusoids and mesenteric capillaries, promoting net filtration into the peritoneal cavity ✓
Explanation
Normal plasma oncotic pressure (~28 mmHg, mainly from albumin at 3.5 g/dL) opposes the outward filtration pressure at capillaries. When albumin falls to 1.8 g/dL, oncotic pressure drops to ~8–10 mmHg, substantially reducing the inward oncotic force. Combined with elevated portal hydrostatic pressure (portal hypertension from cirrhosis), net filtration across hepatic sinusoids and splanchnic capillaries exceeds lymphatic drainage capacity, accumulating fluid in the peritoneal cavity as ascites.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.