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Transient elastography with the XL probe rapidly identifies patients with nonhepatic ascites

Authors Kohlhaas A, Durango E, Millonig G, Bastard C, Sandrin L, Golriz M, Mehrabi A, Buchler, Seitz H, Mueller S

Received 26 January 2012

Accepted for publication 19 March 2012

Published 1 May 2012 Volume 2012:4 Pages 11—18

DOI https://doi.org/10.2147/HMER.S30256

Review by Single-blind

Peer reviewer comments 3

Anna Kohlhaas1, Esteban Durango1, Gunda Millonig1, Cecile Bastard2, Laurent Sandrin2, Mohammad Golriz3, Arianeb Mehrabi3, Markus W Büchler3, Helmut Karl Seitz1, Sebastian Mueller1
1Department of Medicine and Center for Alcohol Research, Liver Disease and Nutrition, Salem Medical Center, University of Heidelberg, Heidelberg, Germany; 2Department of Research and Development, Echosens, Paris, France; 3Department of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg, Germany

Background: In contrast with other elastographic techniques, ascites is considered an exclusion criterion for assessment of fibrosis stage by transient elastography. However, a normal liver stiffness could rule out hepatic causes of ascites at an early stage. The aim of the present study was to determine whether liver stiffness can be generally determined by transient elastography through an ascites layer, to determine whether the ascites-mediated increase in intra-abdominal pressure affects liver stiffness, and to provide initial data from a pilot cohort of patients with various causes of ascites.
Methods and results: Using the XL probe in an artificial ascites model, we demonstrated (copolymer phantoms surrounded by water) that a transient elastography-generated shear wave allows accurate determination of phantom stiffness up to a water lamella of 20 mm. We next showed in an animal ascites model that increased intra-abdominal pressure does not affect liver stiffness. Liver stiffness was then determined in 24 consecutive patients with ascites due to hepatic (n = 18) or nonhepatic (n = 6) causes. The cause of ascites was eventually clarified using routine clinical, imaging, laboratory, and other tools. Valid (75%) or acceptable (25%) liver stiffness data could be obtained in 23 patients (95.8%) with ascites up to an ascites lamella of 39 mm. The six patients (25%) with nonhepatic causes of ascites (eg, pancreatitis, peritoneal carcinomatosis) had a significantly lower liver stiffness (<8 kPa) as compared with the remaining patients with hepatic ascites (>30 kPa). Mean liver stiffness was 5.4 kPa ± 1.3 versus 66.2 ± 13.3 kPa.
Conclusion: In conclusion, the presence of ascites and increased intra-abdominal pressure does not alter underlying liver stiffness as determined by transient elastography. We suggest that, using the XL probe, transient elastography can be used first-line to identify patients with nonhepatic ascites at an early stage.

Keywords: ascites, liver stiffness, transient elastography, liver cirrhosis, noncirrhotic ascites, congestion, peritoneal carcinomatosis, intra-abdominal pressure, alcoholic liver disease

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