Study concept and design: Dr Sarin, Dr Sharma, Dr Ashish, and Dr Hitendra
Hepatic and systemic hemodynamic derangements predict early mortality and recovery in patients with acute-on-chronic liver failure
Version of Record online: 22 JUL 2013
© 2013 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd
Journal of Gastroenterology and Hepatology
Volume 28, Issue 8, pages 1361–1367, August 2013
How to Cite
Garg, H., Kumar, A., Garg, V., Kumar, M., Kumar, R., Sharma, B. C. and Sarin, S. K. (2013), Hepatic and systemic hemodynamic derangements predict early mortality and recovery in patients with acute-on-chronic liver failure. Journal of Gastroenterology and Hepatology, 28: 1361–1367. doi: 10.1111/jgh.12191
Acquisition of data: Dr Hitendra and Dr Vishal
Analysis and interpretation of data: Dr Hitendra, Dr Ashish, Dr Manoj, and Dr Ramesh
Drafting of the manuscript: Dr Hitendra, Dr Ashish, Dr Sarin
Critical revision of the manuscript for important intellectual content: Dr Sarin and Dr Ashish
Statistical analysis: Dr Hitendra, Dr Ashish, and Dr Manoj
Study supervision: Dr Sarin
Conflict of interest: None.
Source(s) of support (grants, equipment, drugs): None.
- Issue online: 22 JUL 2013
- Version of Record online: 22 JUL 2013
- Accepted manuscript online: 11 MAR 2013 08:53PM EST
- Manuscript Accepted: 25 FEB 2013
- acute-on-chronic liver failure;
- hepatic venous pressure gradients;
- pulmonary hemodynamics;
- systemic hemodynamics
Background and Aims
Acute-on-chronic liver failure (ACLF) is a clinical entity where there is a potential for reversibility of hepatic dysfunction once the acute hepatic insult resolves. The portal and systemic hemodynamics in ACLF patients to study its relevance in determining the clinical outcomes was studied.
Clinical, laboratory, portal, and systemic hemodynamic assessments were done at admission and after 3 months. Standard medical care was given to all the patients.
Fifty-seven patients with ACLF were enrolled, and they underwent baseline hepatic venous pressure gradient (HVPG) measurement. Twenty-six (46%) patients died during the 3-month follow-up. Presence of high HVPG and hepatic encephalopathy were found to be independent baseline predictors of mortality. Of the 31 surviving patients, 24 consented for a repeat HVPG. The baseline HVPG reduced from 16 (range 12–30) to 13 (range 6–21) mmHg; (P < 0.05). The reduction in HVPG correlated with clinical and biochemical recovery, and reduction in Child–Turcotte–Pugh score score (P < 0.05), while the aortic mean arterial pressure, cardiac index and systemic vascular resistance index improved significantly (< 0.05). Six (25%) patients developed upper gastrointestinal bleed; the median HVPG between bleeders and non-bleeders was not different possibly because of early onset of bleed (median 20 [15–45 days]).
Baseline HVPG is an independent predictor of mortality in ACLF patients. The portal and systemic circulatory anomalies regress substantially by 90 days and correlate with clinical recovery. However, in the initial phase, the raised portal pressure predisposes these patients to high risk of variceal bleeding.