Localized Liver Injury During Normothermic Ex Situ Liver Perfusion Has No Impact on Short-term Liver Transplant Outcomes

Abstract

Background: Normothermic ex situ liver perfusion (NESLiP) has the potential to increase organ utilization. Radiological evidence of localized liver injury due to compression at the time of NESLiP, termed cradle compression, is a recognized phenomenon but is poorly characterized.

Methods: A retrospective analysis of a prospectively collected database was performed of transplanted livers that underwent NESLiP and subsequently had a computed tomography performed within the first 14 d posttransplant. The primary study outcome was 1-y graft survival.

Results: Seventy livers (63%) were included in the analysis. Radiological evidence of cradle compression was observed in 21 of 70 (30%). There was no difference in rate of cradle compression between donor after circulatory death and donated after brain death donors ( P = 0.37) or with duration of NESLiP. Univariate analysis demonstrated younger (area under the receiver operating characteristic, 0.68; P = 0.008; 95% confidence interval [CI], 0.55-0.82) and heavier (area under the receiver operating characteristic, 0.80; P < 0.001; 95% CI, 0.69-0.91) livers to be at risk of cradle compression. Only liver weight was associated with cradle compression on multivariate analysis (odds ratio, 1.003; P = 0.005; 95% CI, 1.001-1.005). There was no difference in 1-y graft survival (16/17 [94.1%] versus 44/48 [91.6%]; odds ratio, 0.69; P = 0.75; 95% CI, 0.07-6.62).

Conclusions: This is the first study assessing the impact of cradle compression on outcome. We have identified increased donor liver weight and younger age as risk factors for the development of this phenomenon. Increasing utilization of NESLiP will result in the increased incidence of cradle compression but the apparent absence of long-term sequelae is reassuring. Routine postoperative axial imaging may be warranted.

FIGURE 1.

Donor characteristics associated with cradle compression. Box plots of CIT (A), donor age (B), and donor liver weight (C) against presence of CC. CC, cradle compression; CIT, cold ischemic time.

FIGURE 2.

Cradle compression and 1-year graft and recipient survival. A and B, Kaplan-Meier curves of 1-y graft and recipient survival according to presence of CC. CC, cradle compression.

FIGURE 3.

Histological specimens from a liver with evidence of cradle compression. Histological specimen from a transplanted liver that was explanted in the early posttransplant period (with super-urgent transplantation performed in the recipient) for an unrelated cause (hepatic artery thrombosis). Histology demonstrating cradle compression with radiological evidence linear defects and contusion diffusion. A, Overview of 3 sections of the liver showing cradle compression area of injury (area of cradle compression in middle section marked by dotted line). B, Image of the subcapsular injury (linear defect highlighted by arrows). C, Linear defect demonstrating microscopic features of a subcapsular band of necrosis (marked by dotted line).

FIGURE 4.

3C classification of cradle compression. Representative images demonstrating the radiological appearances used in the 3C classification of cradle compression. Patients did not undergo protocol CTs during the study period. The recovery from baseline images are from different patients. The CT scans demonstrating <50% improvement, a linear defect and complete resolution are taken from a single patient who had multiple interval postoperative scans. The >50% improvement is from a different patient. 3C, Cambridge Cradle Compression; CT, computed tomography.