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Crit Care. 2010; 14(Suppl 1): P537.
Published online 2010 March 1. doi:  10.1186/cc8769
PMCID: PMC2933988

Advanced haemodynamic assessment of patients with liver disease and abdominal compartment syndrome

Introduction

Intra-abdominal hypertension (IAH, >12 mmHg) and abdominal compartment syndrome (ACS, >20 mmHg) frequently complicate the disease course in critically ill patients with liver disease. There is a paucity of data describing the circulatory changes observed during ACS outside experimental studies. The aim of this study was to investigate baseline haemodynamic variables in patients with ACS and their response following abdominal decompression.

Methods

Patients admitted to the liver ICU of King's College Hospital with ACS were studied. Transpulmonary thermodilution cardiac output monitoring and calculation of volumetric indices of preload was performed with the PiCCO system. MAP, CVP, ITBVI, cardiac index (CI), stroke volume index (SVI) and intra-abdominal pressure (IAP) were analysed pre and post intervention.

Results

Eighteen patients (nine female), median age 43 (range (R) 20 to 65) were studied. Ten patients had decompensated Budd-Chiari syndrome (BCS), eight underwent orthotopic liver transplantation and two had surgical shunt procedures. Eight patients had cirrhosis (PC) with organ failure and severe ascites necessitating therapeutic paracentesis. Pre-intervention IAP was raised (median 24, R 17 to 40). As a whole, volumetric markers of pre-load were low (median ITBVI 674, R 453 to 1,619) but improved (median ITBVI 763, R 512 to 1,110) post intervention (P = 0.02). Reduction in CVP post intervention was not statistically significant (16, R 0 to 25 vs 14, R 5 to 29). Compared with the PC group, the BCS group had persistently low ITBVI (median 633, R 453 to 924) despite aggressive volume resuscitation prior to decompression (median positive fluid balance 10 l, R 0.5 to 39). Abdominal decompression resulted in a reduction in IAP (median 15, R 6 to 31, P < 0.0001), increase in preload (ITBVI) and improvement in CI (3.9, R 1.9 to 7.4 vs 4.6, R 2.7 to 7.7, P < 0.0001) and SVI (40, R 22 to 111 vs 44, 30 to 61, P = 0.001). There was an inverse relationship between IAP, CI (P = 0.003) and SVI (P = 0.004). ITBVI correlated with parameters of flow (CI P < 0.0001 and SVI P < 0.0001), CVP did not.

Conclusions

ACS leads to central hypovolaemia. Abdominal decompression restores preload in association with improvement in cardiac output.

References


Articles from Critical Care are provided here courtesy of BioMed Central