Haemodynamic Response to Abdominal Decompression in Acute Budd–Chiari Syndrome

Deepak Joshi; Sujit Saha; William Bernal; Nigel Heaton; Julia Wendon; Georg Auzinger


Liver International. 2011;31(8):1171-1178. 

In This Article

Abstract and Introduction


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.


Intra-abdominal hypertension (IAH), (sustained elevation of intra-abdominal pressure, IAP, ≥12 mmHg) and abdominal compartment syndrome (ACS) (IAP≥20 mmHg with evidence of new organ dysfunction) are associated with decreased survival and a high prevalence of multiorgan failure in critically ill patients.[1–3] IAP is affected by the volume of intra-abdominal organs, presence of space occupying lesions (solid or liquid) within the abdomen and conditions limiting abdominal wall expansion. ACS left untreated can result in pulmonary, renal and liver dysfunction.[4–7] ACS can complicate the disease course of decompensated chronic liver disease (CLD) if portal hypertension, ascites, and less frequently bleeding from abdominal wall or intra-abdominal varices leads to an acute increase in IAP. Recent guidelines published by the World Society of the Abdominal Compartment Syndrome (WSACS), provide physicians with a diagnostic and therapeutic management algorithm.[2,3]

Intra-abdominal hypertension can negatively affect abdominal, as well as extra abdominal organ function including the respiratory, renal, intestinal, cerebral and in particular the cardiovascular system,[8,9] where it is associated with a reduction in cardiac preload caused by reduced venous return from intra-abdominal venous capacitance vessels. Studies have demonstrated that static filling pressures such as central venous pressure (CVP) and pulmonary artery occlusion pressure correlate poorly with true cardiac filling.[10] They may be falsely raised in critical illness because of changes in thoraco-abdominal compliance such as during positive pressure ventilation with high levels of positive end expiratory pressure (PEEP), or in cases of IAH and ACS.[11] More recently studies have confirmed both the superiority and reliability of volumetric markers of preload such as right-ventricular end diastolic-volume index, global end diastolic volume index and intrathoracic blood volume index (ITBVI) over pressure-derived variables, with the exception being where transmural pressures were calculated.[12,13]

Budd–Chiari syndrome (BCS) is characterised by obstruction of the hepatic venous outflow at any level from the small hepatic veins to the right atrium.[14] It leads to post-sinusoidal portal hypertension and congestion of the liver with caudate-lobe hypertrophy. Ascites occurs because of post-sinusoidal portal hypertension as opposed to sinusoidal or presinusoidal portal hypertension, which frequently complicates most forms of cirrhosis.

In a recently published study of 21 patients with BCS, the haemodynamic profile differed significantly from that in cirrhotic patients.[15] BCS patients demonstrated normal cardiopulmonary haemodynamics with an expanded plasma volume, with no evidence of systemic vasodilatation. One hypothesis offered by the authors suggested that the acute/subacute obstruction to the hepatic blood flow may promote the release of vaso-constrictive stimuli such as plasma renin, aldosterone and norepinephrine, which compensate for the release of vasodilatory factors triggered by portal hypertension. The BCS patients in that study had relatively preserved synthetic liver function (Child–Pugh score 8.2±1.8) and the authors provided no data on the influence of abdominal hypertension on preload, cardiac output (CO) and other haemodynamic variables. We postulate that IAH and ACS in combination with caudate lobe hypertropy lead to a critical reduction in venous return and is responsible for reduced CO.

We therefore aimed to compare haemodynamic variables at baseline and following abdominal decompression by means of a surgical shunt procedure or liver transplantation in critically ill patients with acute BCS complicated by ACS. A group of patients with decompensated cirrhosis and ascites with similar elevation in IAH before and after paracentesis served as controls.