Protein-kinetic and haemodynamic studies in patients with liver cirrhosis. Evidence of a lymph-imbalance theory of ascites formation

Summary. Lymph drainage, splanchnic vascular pressures, plasma volume (PV), plasma renin (PRC) and aldosterone (PAC) concentrations were studied in different groups of patients with cirrhosis: I, patients who had never had ascites (n=17), II, patients with former but no actual ascites (n= 19), III, patients with slight or moderate ascites (n= 25), and IV, patients with tense ascites (n = 27). Lymph drainage, determined as TER_alb (the fraction of intravascular albumin mass (IVMaib), which leaves/returns into the vascular space per hour) was significantly elevated in cirrhotic patients (11.5% IVM_alb-h^-1) as compared to normal controls (5.9,P<0.001). TER_alb in patients with tense ascites (group IV) was on the average 8-4% IVMaib-h^-1, a value which is significantly above normal (P<0.05), but significantly below those of groups I, II and III (12.5,13.4,12.6,P<0.01). Wedged hepatic venous pressure increased from group I to IV: 16, 22, 25 and 34 mmHg, respectively (P<0.01). Inferior vena caval pressure in group IV (15 mmHg) was significantly above those of group III (8 mmHg) and group I+11 (6 mmHg), (P<0–01). From group I to III, PV increased significantly (3125, 3610, 3870 ml, P<0.01). In the ascitic patients PV was constant or fell slightly in patients with tense ascites (3730 ml). PRC in untreated patients with tense ascites (IV) was 287 mIU-1^-1, as compared to group III, I and normal controls (94, 50, 15, P<0.01). A similar pattern was found with respect to PAC. The results suggest that an imbalance between enhanced protein and fluid filtration (consequent on portal hypertension) on one side, and a relatively insufficient lymphatic drainage on the other side plays a substantial role in the pathogenesis of ascites in cirrhosis. The results do not support a progressive plasma volume expansion as the main cause of cirrhotic ascites.