Prospective Evaluation of Intraoperative Hemodynamics in Liver Transplantation with Whole, Partial
and DCD Grafts
M. Sainz-Barriga, K. Reyntjens,M. G. Costa, L. Scudeller, X. Rogiers, P. Wouters, B. De Hemptinne,
R.I.Troisi1
American Journal of Transplantation 2010;10(8): 1850–1860
Background. Liver failure patients have complex hemodynamic changes resulting in a typical hemodynamic
profile of high cardiac output (CO), low systemic vascular resistance and porto-systemic shunting. Liver
transplantation (LT) replaces the cirrhotic liver, which offers high resistance to splanchnic flow, with a normal
resistance, however the circulatory changes do not immediately correct exposing the graft to the altered
circulation, in particular the high CO and splanchnic volume. The hepatic arterial buffer response dictates
reciprocity between portal venous flow (PVF) and hepatic artery flow (HAF) thus a high post-LT portal flow
may result in compromised HAF and consequent complications in the biliary system as seen in the small-for-size
syndrome, most usually related to partial liver grafts (living donor (LDLT) or split (SLT). Graft inflow
modification (GIM) may be used to ameliorate such situations. In this study the authors measured PVF and HAF
during LT in patients receiving a variety of graft types.
Methods. Hemodynamic measurements were made at four set timepoints throughout LT in 103 patients – 76
full size grafts, 5 LDLT, 13 SLT and 9 deceased donor (DCD). PVF and HAF were measured by ultrasound
transit-time flow measurement. Flows were expressed as ml/min/100g liver tissue. All patients underwent a
caval preserving transplant with a temporary portocaval shunt. GIM was considered for cases of persistent low
HAF which improved with portal clamping. Temporal changes during transplant were compared as were
timepoint specific hemodynamics between different types of donor organ. Historical values for HAF and PVF
made during liver donation were used as ‘normal” comparators. Factors potentially influencing hepatic flows
were investigated by linear regression modelling.
Main Findings. During LT median PVF was low at baseline, more than doubled post reperfusion (to greater
than normal) and remained elevated, although less so, 1.5hrs after reperfusion. HAF was low initially (although
the P/F ratio was high), fell post-reperfusion and rose somewhat at 1.5hrs post-reperfusion. The highest postreperfusion PVF (expressed per 100g liver weight) were in the LDLT, then SLT groups, HAF were similar
between groups. All flows had very wide ranges (eg initial PVF 1.4-534). Variables independently associated
with hepatic flows were recipient portal hypertension, CO (positive); warm ischemia time and steatosis
(negative).
GIM was performed on 5 patients (2 LDLT, 1 SLT, 2 full-size). One year graft survival was 90%.
Shortcomings. The large range in all the flow measurements and the relatively small numbers of reduced size
grafts makes identifying significant factors somewhat problematic – in particular there were only 5 LDLT, one
of the groups of interest. The overall outcomes were good with few of the complications postulated to be linked
to PVF/HAF mismatch; whilst this is fortunate for the patients involved it does mean that no clinical outcome
correlate of the observed flow alterations can be made. Again, GIM was undertaken on 5 patients based on
intraoperative flow measurements, with resulting ‘improvement” in liver flow hemodynamics, but the effect of
this cannot be evaluated in the absence of a control group.
Conclusion/Lessons. This study does provide useful information about changes in liver flows during LT and
particularly documents the high portal flows and low HA flows in reduced size graft recipients; however without
demonstrated correlations between this and outcomes of clinical interest the significance of these findings is
unclear. Further investigation should be undertaken firstly to identify what, if any, is the relationship between
liver blood flows measured during LT and post-operative complications and also to determine the effects of
potential modifiers of liver blood flow (pharmacological as well as surgical) and whether these relate to
outcomes of interest.
James Y. Findlay, MB, ChB.