- Poster presentation
- Open Access
Budd-Chiari syndrome complicated by abdominal compartment syndrome: evidence of central hypovolaemia?
© BioMed Central Ltd. 2010
- Published: 1 March 2010
- Compartment Syndrome
- Abdominal Compartment Syndrome
- Transpulmonary Thermodilution
- Cardiac Output Monitoring
- Thermodilution Cardiac Output
Budd-Chiari syndrome (BCS) is characterised by hepatic venous outflow obstruction (HVOO) leading to post-sinusoidal portal hypertension, congestion of the liver with caudate lobe hypertrophy. In addition to intra-abdominal hypertension (IAH), caused by severe ascites, HVOO may aggravate the cardiovascular disturbances seen in patients with decompensated disease. The aim was to study the haemodynamic response to abdominal decompression in BCS compared with patients with decompensated cirrhosis.
Ten patients with BCS admitted to the Liver ICU, King's College Hospital were studied. Transpulmonary thermodilution cardiac output monitoring and calculation of volumetric indices of preload was performed with the PiCCO system. Haemodynamic variables and IAP were analysed pre and post intervention. The control group comprised of cirrhotic patients with IAH requiring abdominal paracentesis (PC).
Ten patients with BCS were studied, median age 39 years (range (R) 20 to 52); eight had liver transplantation and two had a surgical shunt procedure. Eight patients (PC), median age 59 (33 to 65), underwent abdominal paracentesis for tense ascites. IAP was raised in both groups pre intervention (23, R 17 to 40, BCS vs 26, R 20 to 40, PC). ITBVI remained low in the BCS group (632, R 453 to 924) pre intervention despite aggressive volume resuscitation (median positive FB10L, R 0.5 to 39). Post intervention, a reduction in IAP was seen in both groups (BC P < 0.001, PC P < 0.0001). ITBVI increased (633, R 453 to 924 vs 736, R 512 to 1,110, P = 0.001) in BCS patients. No change in ITBVI was noted (pre 870, R 598 to 1,619 vs post 1,036, R 763 to 1,762) in the CP group despite albumin replacement. An increase in CI and SVI was noted in both groups: BCS (CI P = 0.003, SVI P = 0.007), CP (CI P = 0.005, SVI P = 0.02). There was an inverse relationship between IAP, CI (P = 0.003), SVI (P = 0.004) and ITBVI (P = 0.01) in BCS patients. In the CP group, IAP did not correlate with ITBVI.
Compared with cirrhotic patients with ascites, patients with BCS and IAH have evidence of central hypovolaemia. We postulate that in addition to raised IAP, hepatic venous obstruction and caudate lobe hypertrophy limit venous return in patients with BCS. Reduction in IAP restores preload with improvement in cardiac output.