Post reperfusion syndrome during liver transplantation: From pathophysiology to therapy and preventive strategies

Table 2 Pathophysiology

Year	Ref.	Title	Type of study	No. subjects	Findings	Jadad score
1993	De Wolf et al[22]	Right ventricular function during orthotopic liver transplantation	Prospective	20	RVEF maintained throughout the OLT procedure	1
1994	Ronholm et al[36]	Complement system activation during orthotopic liver transplantation in man	Prospective	16	The complement cascade activation demonstrated during OLT is located in the gut and triggered by hypoperfusion of the gut due to clamping of the portal and caval veins. There was a significant correlation between activation of complement with high concentration of C3a anaphylatoxin and development of PRS	1
1995	Blanot et al[41]	Circulating endotoxins and postreperfusion syndrome during orthotopic liver transplantation	Prospective	15	No correlation between plasma endotoxins detectable with the LAL (limulus amoebocyte lysate) test and PRS. However the endotoxenemia is still an important risk factor	1
1995	Scholz et al[38]	Activation of the plasma contact system and hemodynamic changes after graft revascularization in liver transplantation	Prospective	17 (19 OLT procedures)	Liver graft reperfusion was associated with a significant increase in Kallikrein activity with a concomitant drop in antiprotease activity and high molecular weight kininogen. Hemodynamic changes correlated with the plasmatic concentrations	0
1997	Bellamy et al[33]	Changes in inflammatory mediators during orthotopic liver transplantation	Prospective	10	After reperfusion SVRI decreased and CI increased; these were accompanied by increases in TNF-α , TNF-α-R, IL-1β, IL-1 receptor antagonist, IL-6, IL-8; no changes in PAF and Thromboxane B2; Leukotriene C4, D4, E4 decreased	1
1999	Acosta et al[21]	Effect of reperfusion on right ventriculoarterial coupling in liver transplantation	Prospective	52	Similar ↑ in CI, RVEDVI, RVSWI in both PRS and non PRS patients, better ventriculo-arterial coupling in non PRS patients due to a decrease in pulmonary vascular elastance	1
1999	Acosta et al[31]	Changes in serum potassium during reperfusion in liver transplantation	Retrospective	106	No correlation between changes in serum potassium and PRS	1
2004	Bellamy et al[37]	Complement membrane attack complex and hemodynamic changes during human orthotopic liver transplantation	Prospective	40	The formation of MAC complex and degradation of C3,C4 increased markedly at the time of liver graft reperfusion. Concomitantly SVRI decreased and CI increased, with changes correlated to the activation of the MAC	1
2008	Ripoll et al[25]	Cardiac dysfunction during liver transplantation: incidence and preoperative predictors	Retrospective	209	22.5% abnormal cardiac response to reperfusion, predictive factors: hyponatremia, lower PAP and lower CVP and PCWP, at the beginning of the intervention. Preoperative echocardiography couldn't predict abnormal response	1
2011	Bezinover et al[34]	Release of cytokines and hemodynamic instability during the reperfusion of a liver graft	Prospective	17	The concentration of TNF-α correlated directly with the amount of catecholamines used to treat hemodynamic instability. No correlation between any cytokine levels and the duration of CIT, the surgical technique, and the quality of the liver graft	1
2012	Xu et al[23]	Evaluation of the right ventricular ejection fraction during classic orthotopic liver transplantation without venovenous bypass	Prospective	30	RV function is impaired during the anhepatic and early reperfusion stages, particularly in the high MELD score patients	1
2013	Siniscalchi et al[18]	Hyperdynamic circulation in cirrhosis: predictive factors and outcome following liver transplantation	Retrospective	242	Hyperdynamic circulation is associated to ↓ MAP, SVI and ↑ PCWP and PVRI 10 min after reperfusion	1
2013	Escobar et al[26]	Stroke volume response to liver graft reperfusion stress in cirrhotic patients	Prospective	271	Non-responder patients (35.7%) had higher MELD score, left atrial diameter and low SVRI at the beginning of the intervention. These patients experienced more early cardiovascular events and ICU stay	1
2014	Tsai et al[35]	Ischemic reperfusion injury-induced oxidative stress and pro-inflammatory mediators in liver transplantation recipients	Prospective	14	Malondialdehyde (MDA) is one of the intermediate metabolites from lipid peroxidation and representing a indirectly measure of oxidative stress-induced liver injury. Recipients with higher values of preoperative bilirubin, AST, ALT, MELD score, INR, and blood loss tended to have significantly higher levels of MDA and may suffer more injury from this insult	1

RVEF: Right ventricular ejection fraction; OLT: Orthotopic liver transplantation; C3a: Complement anaphylatoxin 3a; PRS: Post reperfusion syndrome; SVRI: Systemic vascular resistance index; CI: Cardiac index; TNF: Tumor necrosis factor; IL: Interleukin; PAF: Platelet activating factor; RVEDVI: Right Ventricular end-diastolic volume index; RVSWI: Right ventricular stroke work index; MAC: Complement membrane attack; PAP: Pulmonary arterial pressure; CVP: Central venous pressure; PCWP: Pulmonary capillary wedge pressure; CIT: Cold ischemia time; RV: Right ventricular; MELD: Model for end-stage liver disease; MAP: Mean arterial pressure; SVI: Stroke volume index; PVRI: Pulmonary vascular resistance index; SVRI: Systemic vascular resistance index; ICU: Intensive care unit.