103 - Clinical Features of Decompensated Cirrhosis in Patients Without Clinically Significant Portal Hypertension

Purpose: There is limited data available on patients with clinically decompensated cirrhosis in the apparent absence of clinically significant portal hypertension. We aimed to examine the natural history of patients with decompensating events, but without clinically significant portal hypertension.

Materials and Methods: We evaluated 1210 patients who underwent portal pressure assessment between 2014 and 2022. 41/1210 patients had biopsy proven cirrhosis with a clinical decompensation despite an HVPG < 10mmHg. Clinical and laboratory variables were assessed at the time of portal pressure assessment and were followed up for 14±20 months after HVPG measurement.

Results: Of the 41 decompensated cirrhosis patients with low HVPG, 35 were men (85%) and 36 were White (88%). The mean free hepatic venous pressure was 15±6mmHg, wedge hepatic venous pressure was 21±6mmHg, and HVPG was 6±3mmHg. Alcohol related liver disease and non-alcoholic steatohepatitis were the most common causes of cirrhosis (21 and 8 patients, respectively). 16 patients were on beta-blockers. The most common decompensating events were hepatic encephalopathy and ascites (25 patients, 61%) each, and esophageal varices (11 patients (27%) - 6 non-bleeding and 5 bleeding); 21 patients had more than one decompensating event. 27 patients were Child Pugh score B (11) or C (16). The mean MELD score at baseline was 18±9. During followup, (28 patients, 68%, had follow-up of at least 6 months and were further analyzed), only 4 (of 28) patients did not experience a further decompensating event. New onset ascites was noted in 7 patients (25%), esophageal varices and hepatic encephalopathy in 5 patients (18%) each (Table). Five-year mortality in those followed > 6 months was 33% (9/28).

Conclusion: Despite being uncommon, patients with clinically decompensated cirrhosis and low HVPG ( < 10mmHg) are likely to further decompensate and have a high mortality rate. These patients may also have a unique clinical phenotype in which elevated central venous pressure contributes to portal hypertension. These findings signify the need for refined definitions of portal hypertension in cirrhosis patients and moreover to be cognizant of substantial mortality risk in patients with a decompensating event, regardless of HVPG.