Current evidence on posthepatectomy liver failure: comprehensive review

Abstract

Introduction: Despite important advances in many areas of hepatobiliary surgical practice during the past decades, posthepatectomy liver failure (PHLF) still represents an important clinical challenge for the hepatobiliary surgeon. The aim of this review is to present the current body of evidence regarding different aspects of PHLF.

Methods: A literature review was conducted to identify relevant articles for each topic of PHLF covered in this review. The literature search was performed using Medical Subject Heading terms on PubMed for articles on PHLF in English until May 2022.

Results: Uniform reporting on PHLF is lacking due to the use of various definitions in the literature. There is no consensus on optimal preoperative assessment before major hepatectomy to avoid PHLF, although many try to estimate future liver remnant function. Once PHLF occurs, there is still no effective treatment, except liver transplantation, where the reported experience is limited.

Discussion: Strict adherence to one definition is advised when reporting data on PHLF. The use of the International Study Group of Liver Surgery criteria of PHLF is recommended. There is still no widespread established method for future liver remnant function assessment. Liver transplantation is currently the only effective way to treat severe, intractable PHLF, but for many indications, this treatment is not available in most countries.

Fig. 1

Schematic overview of normal and dysfunctional liver regeneration Left side shows functional liver regeneration. Major hepatectomy induces drastic changes in the haemodynamic environment of the liver. An increase in shear stress leads to activation of liver sinusoidal endothelial cells, which in turn release nitric oxide (NO). NO together with cytokines released from Kupffer cells, such as tumour necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6 promote liver regeneration. Right side shows dysfunctional liver regeneration. An overwhelming increase in portal pressure can cause ‘small-for-flow‘ syndrome. Excessive shear stress induces an overshooting inflammatory response, followed by neutrophil recruitment into the liver. This causes inhibition of liver regeneration, parenchymal necrosis, and hepatocyte apoptosis. LSEC, liver sinusoidal endothelial cells; ROS, reactive oxygen species.

Fig. 2

Regional distribution of liver function assessed with hepatobiliary scintigraphy ^99mTc-mebrofinin scan showing poor drainage of the right posterior sector, as can be seen by the higher (yellow signal) compared with low (blue).

Fig. 3

Methods to increase future liver remnant size Contrast-enhanced CT of patients subject to different treatments. a PVE. b Rescue ALPPS after insufficient effect of PVE. c PVE/HVE. Before (1) and after (2) images are shown in each case. All patients with left lateral segment (plus/minus segment 1) as FLR marked with red before intervention and green at evaluating radiology. PVE, portal vein embolization; ALPPS, associating liver partition and portal vein ligation for staged hepatectomy; HVE, hepatic vein embolization; FLR, future liver remnant.