BackgroundBacterial translocation (BT) has been proposed as a trigger for stimulation of the immune system with consequent hemodynamic alteration in patients with liver cirrhosis. However, no information is available regarding its hemodynamic and coagulation consequences during liver transplantation.MethodsWe screened 30 consecutive adult patients undergoing living-donor liver transplant for the presence of BT. Bacterial DNA, Anti factor Xa (aFXa), thromboelastometry, tumor necrosis factor-α TNF-α, and interleukin-17 (IL-17) values were measured in sera before induction of anesthesia. Systemic hemodynamic data were recorded throughout the procedures.ResultsBacterial DNA was detected in 10 patients (33%) (bactDNA(+)). Demographic, clinical, and hemodynamic data were similar in patients with presence or absence of bacterial DNA. BactDNA(+) patients showed significantly higher circulating values of TNF-α and IL-17, and had significantly higher clotting times and clot formation times as well as significantly lower alpha angle and maximal clot firmness than bactDNA(−) patients, P < 0.05. We found no statistically significant difference in aFXa between the groups, P = 0.4. Additionally, 4 patients in each group needed vasopressor agents, P = 0.2. And, the amount of transfused blood and blood products used were similar between both groups.ConclusionBacterial translocation was found in one-third of patients at the time of transplantation and was largely associated with increased markers of inflammation along with decreased activity of coagulation factors.Trial registrationTrial Registration Number: NCT03230214. (Retrospective registered). Initial registration date was 20/7/2017.

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Background: Patients with End-stage liver disease undergoing orthotopic liver transplantation are prone to serious hemodynamic and metabolic derangements. The study aimed to assess the validity of central and pulmonary veno-arterial CO2 gradients to predict fluid responsiveness and to guide fluid management during liver transplantation. Methods: In adult recipients of liver transplantation, ASA III to IV, pulse pressure variations (PPV) guided intraoperative fluid management. PPV of ≥15% (Fluid Responding Status-FRS) indicated fluid resuscitation with 250 ml albumin 5% boluses repeated if required to correct PPV to <15% (Fluid non-Responding Status-FnRS). Samples from central venous and pulmonary artery catheters (PAC) were collected simultaneously to calculate both the central venous to arterial CO2 gap [C(v-a) CO2 gap] and the pulmonary venous to arterial CO2 gap [Pulm(p-a) CO2 gap]. Results: Primary outcome was the sensitivity of central venous CO2 gap to differentiate between fluid responding and non-responding states with 67 data points recorded (20 FRS and 47 FnRS). The discriminative ability of central and pulmonary CO2 gaps between the two statuses (FRS and FnRS) was poor with AUC of ROC of 0.698 and 0.570 respectively. The central CO2 gap was significantly higher in FRS than FnRS (P=0.016), with no difference in pulmonary CO2 gap between both statuses. The central and pulmonary CO2 gaps were weakly correlated to PPV [r=0.291, (P=0.017) and r=0.367, (P=0.002) respectively]. No correlation between both CO2 gaps and both CO and lactate could be seen. Conclusion: The Central and the Pulmonary CO2 gaps cannot be used as valid tools to predict fluid responsiveness and to guide fluid management during liver transplantation. CO2 gaps also do not correlate well with the changes in PPV or CO.

Introduction: Liver transplantation is the standard form of treatment for patients with end stage liver disease, with the use of blood product as a standard method for transfusion. Recombinant factor VIIa (rVIIa) may help those patients to acquire less amount of transfusion. This will have an impact not only the morbidity and mortality of the recipient and the donor, but also on the economical aspect of this tremendously expensive procedure. We conducted this study to verify the possible beneficial effects of using rVIIa at a lower dose than the standard dosage, which could have an impact on the future use of rVIIa. Methods: Twenty-four patients scheduled for orthotropic liver transplantation, divided into 2 groups; a control group and an rVIIa group. Both groups received the same anesthetics enlisted in our protocol for liver transplantation. The rVIIa group received a loading dose of 30 ug/kg of rVIIa following the induction of anesthesia, followed by a maintenance dose of 5 ug/kg until the end of the dissection phase. Demographic data, coagulation profile [prothrombin time (PT), prothrombin concentration (PC), partial thromboplastin time (PTT), International normalized ratio (INR)], blood loss, transfusion requirements, the duration of the dissection phase, the duration of surgery, hemoglobin concentration (Hb), and platelet count were done immediately after induction and 1, 2, 3 and 6 hours post induction (dissection phase). Finally, a Doppler assessment of the graft vessels was performed subsequent to anastomosis Results: The rVIIa group had a lower PT in the first two hours of the dissection phase in relation to the baseline and significantly lower than the control group (P = 0.0002). The INR showed a significant improvement in the rVIIa group during the dissection phase compared to the control group, and during the first two hours compared with the baseline in the rVIIa group (P = 0.0002). When compared to the control group, the rVIIa group had a significant increase in the platelet count, in all samples taken during the dissection phase. There was a significant decrease in the intraoperative requirements of packed red blood cells (P = 0.014), platelets (P = 0.0005) and fresh frozen plasma (P = 0.01) in the rVIIa group compared to the control group Discussion: We conclude that administering low dose of rVIIa would be helpful during liver transplantation surgery. Improvement in the coagulation profile, transfusion requirements, and consequently postoperative morbidity and mortality could be achieved. References: Roberts HR, Monroe DM, White GC. The use of recombinant factor VIIa in the treatment of bleeding disorders. Blood 2004;104:3858-3864.