Haemodynamic response to abdominal decompression in acute Budd–Chiari syndrome
Article first published online: 17 JUN 2011
© 2011 John Wiley & Sons A/S
Volume 31, Issue 8, pages 1171–1178, September 2011
How to Cite
Joshi, D., Saha, S., Bernal, W., Heaton, N., Wendon, J. and Auzinger, G. (2011), Haemodynamic response to abdominal decompression in acute Budd–Chiari syndrome. Liver International, 31: 1171–1178. doi: 10.1111/j.1478-3231.2011.02557.x
- Issue published online: 7 AUG 2011
- Article first published online: 17 JUN 2011
- Received 16 November 2010, Accepted 12 May 2011
- abdominal compartment syndrome;
- Budd-Chiari syndrome;
- intra-abdominal hypertension;
- intra-abdominal pressure
Background: Intra-abdominal hypertension (IAH) and abdominal compartment syndrome commonly occur in patients with liver disease.
Aims: We compared haemodynamic variables pre- and post-abdominal decompression in patients with acute Budd–Chiari syndrome (BCS) and patients with chronic liver disease (CLD), ascites and IAH.
Methods: Patients with IAH admitted to the Liver ICU, King's College Hospital were studied. Transpulmonary thermodilution cardiac output (CO) monitoring was performed with the PiCCO® system.
Results: Ten patients with decompensated BCS (median age 39 years, 20–52) and eight patients with CLD (59 years, 33–65) and tense ascites requiring paracentesis were studied. Intra-abdominal pressure (IAP) was raised in both groups pre-intervention (BSC 23 mmHg, 17–40; CLD 26, 20–40). Intrathoracic blood volume (ITBVI) was persistently low in the BCS group (632 ml/m2, 453–924) despite volume resuscitation. Post-intervention, reduction in IAP was noted in both groups (BCS P<0.001, CLD P<0.0001). The ITBVI increased (P=0.001) in the BCS group only. An increase in cardiac index (CI) and stroke volume index (SVI) was noted in both groups (BCS: CI P=0.003, SVI: P=0.007; CLD: CI P=0.005, SVI P=0.02). The central venous pressure did not change in either group and did not correlate with markers of flow (CI, SVI) or IAP. Both groups demonstrated an inverse relationship between IAP, CI and SVI.
Conclusion: Patients with BCS and IAH have evidence of central hypovolaemia. In addition to raised IAP, hepatic venous obstruction and caudate lobe hypertrophy limit venous return in patients with BCS. Reduction in IAP and re-establishment of caval flow restores preload with improvement in CO.