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Liver Function and Splanchnic Ischemia in Critically III Patients

Nicholas D. Maynard; Robert C. Mason; David J. Bihari; R. Neil Dalton; Richard Beale; Mark N. Smithies
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Affiliations: From the Department of Surgery, Guy's Hospital, London, United Kingdom,  From the Department of Intensive Care, Guy's Hospital, London, United Kingdom,  From the Department of Paediatrics, Guy's Hospital, London, United Kingdom

Affiliations: From the Department of Surgery, Guy's Hospital, London, United Kingdom,  From the Department of Intensive Care, Guy's Hospital, London, United Kingdom,  From the Department of Paediatrics, Guy's Hospital, London, United Kingdom

Affiliations: From the Department of Surgery, Guy's Hospital, London, United Kingdom,  From the Department of Intensive Care, Guy's Hospital, London, United Kingdom,  From the Department of Paediatrics, Guy's Hospital, London, United Kingdom


1997 by the American College of Chest Physicians


Chest. 1997;111(1):180-187. doi:10.1378/chest.111.1.180
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Abstract

Study objective: To investigate the concept that splanchnic ischemia leads to hepatic dysfunction in the critically ill.

Design: Prospective study and analysis of patient data.

Setting: A general ICU in an inner-city London teaching hospital.

Patients: Twenty-seven consecutive critically ill patients with evidence of inadequate tissue perfusion requiring pulmonary artery catheterization and mechanical ventilation.

Measurements: In all patients, we measured the hepatic metabolism of lidocaine (lignocaine) to monoethylglycinexylidide (MEGX) and the clearance of indocyanine green (both dynamic, flow-dependent tests of hepatic function) over the first 3 days following admission to the ICU. These were compared with results of standard liver function tests and related to tonometric assessment of gastric intramucosal pH (pHim) and outcome.

Results: There were no significant differences in bilirubin, aspartate aminotransferase, alkaline phosphatase, and prothrombin levels, or in indocyanine green clearance between survivors and nonsurvivors. On day 3, the median MEGX level was higher in survivors than in nonsurvivors (16 vs 2.4 ng/mL, p<0.001), and the median MEGX level in nonsurvivors fell over the 3 days (20.6 to 2.4 ng/mL, p<0.002). MEGX levels were significantly correlated with pHim (Spearman rank correlation coefficient [Rs]=0.69, p<0.001) as were the changes in the two measurements over the 3 days (Rs=0.46, p<0.02). The MEGX formation test and gastric pHim were the most discriminatory with regard to death and survival.

Conclusions: Our findings suggest that critically ill patients develop significant hepatic dysfunction that is associated with a poor outcome. This is likely to be due to a mismatch between hepatic metabolic demand and blood flow, and the MEGX formation test appears to be an extremely effective means of assessing liver function and flow in this group of patients.


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