Objectives: The most widely used definition of postreperfusion syndrome in liver transplant is a 30% decrease in mean arterial pressure during the first 5 minutes after vascular unclamping. With these criteria, increased postoperative morbidity has been reported. Vasoactive drugs could prevent this syndrome. The main objective of our study was to determine the incidence and complications associated with postreperfusion syndrome in patients who received vasoactive support.
Materials and Methods: We studied 246 patients who received norepinephrine infusions to maintain mean arterial pressure ≥60 mm Hg and who were monitored with a Swan-Ganz catheter. Patients received a bolus of adrenaline after vascular unclamping in cases of insufficient response to norepinephrine.
Results: Among the study patients, 57 (23.17%) developed postreperfusion syndrome. Patients who developed postreperfusion syndrome did not present with more postoperative complications in terms of renal dysfunction (P = .69), repeat surgery (P = .15), graft rejection (P = .69), transplant replacement surgery (P = .76), hospital stay (P = .70), or survival (P = .17) compared with patients without postreperfusion syndrome.
Conclusions: In patients who underwent orthotopic liver transplant, in whom vasoactive drugs were administered, a diagnosis of self-limited postreper-fusion syndrome during the first 5 minutes after unclamping may not be associated with postoperative complications. The administration of vasoconstrictors may have a preventive effect on the postoperative complications associated with postreperfusion syndrome or they may mask the real incidence of postreperfusion syndrome. A broader definition of postreperfusion syndrome should be accepted.

Key words : Liver transplant, Posttransplant complications, Vasoconstrictors

Introduction

During the liver reperfusion stage of liver transplant, many inflammatory mediators flood the systemic circulation from the liver graft, producing a sudden load of cold and acidotic blood. At this stage of graft revascularization, there is an increase in the pulmonary vascular resistance index and pulmonary arterial pressure (PAP), along with a reduction in the systemic vascular resistance (SVR) index, heart rate (HR), cardiac index (CI), and arterial blood pressure.^1-3 Because of these fluctuations, some patients develop postreperfusion syndrome (PRS).

Postreperfusion syndrome was first defined by Aggarwal and colleagues4 as a 30% or greater decrease in mean arterial pressure (MAP) for at least 1 minute during the 5 minutes after unclamping of the portal vein and was found to be associated with several preoperative risk factors and postoperative complications. The variety of risk factors presented in previous studies suggests that the occurrence of PRS is unpredictable. These risk factors have been described in relation to the organ donor, such as donor age,^5-7 cold ischemia time,^5,8,9 presence of hepatic steatosis,¹⁰ and organs considered to be larger than their expected size.⁶ Other risk factors have been described in relation to the recipient of the liver graft, which include recipient age,11 Model for End-Stage Liver Disease (MELD) score,^10,12 increased creatinine levels,^10,12 increased potassium levels,¹³ low calcium levels,¹⁴ low hemoglobin levels,¹⁰ the presence of preoperative left ventricular diastolic dysfunction,8 and elevated HR.^10,14,15 Additional risk factors have been described to be related to the surgical technique, such as prolonged ischemia time,¹¹ the use of the classical technique, and rapid graft reperfusion.¹⁶ Studies have also reported that PRS is associated with an increase in intraoperative transfusion needs,^6,11,16 postoperative kidney injury,^10,12 longer intensive care unit (ICU) and hospital stays,^6,16 and mortality.^10,12,17

The incidence of PRS has been shown to vary widely among studies, ranging from 12% to 77%.^15,16 This variability depends not only on preoperative and intraoperative factors associated with anesthetic-surgical practice, but also on the various criteria for the definition of PRS, as well as the administration of vasoactive drugs to prevent or treat the syndrome. Misdiagnosis, however, occurs because PRS shares similar hemodynamic characteristics with some forms of shock, especially in terms of decreased MAP and SVR.

In this study, we evaluated patients who presented with PRS based on the Aggarwal definition,⁴ which is the most extended definition used for the diagnosis of PRS, and patients who received vasoactive support, which most frequently occurs among patients presenting with decreased MAP and/or SVR. Because some risk factors and hemodynamic variables are now corrected before and during vascular unclamping, an abolition or decrease in the incidence of PRS and the-refore associated complications could be expected.

Materials and Methods

The present single-center retrospective observational study was approved by the Ethics Committee of University Hospital and registered in the ClinicalTrials.gov database (NCT05658120). Patients gave their written informed consent to have their clinical data recorded and included in research studies. The protocol for the present study followed good clinical practice and was conducted in accordance with the ethical guidelines of the 1975 Helsinki Declaration.

Anesthesia
Patients received intravenous anesthesia, which included fentanyl (2 μg/kg), propofol (2 mg/kg), and atracurium (0.5 mg/kg). Mechanical ventilation was initiated with a volume control mode at a tidal volume of 8 mL/kg and a frequency of 12/minute; mechanical ventilation was adjusted to maintain an end-tidal carbon dioxide concentration between 33 and 38 mm Hg, positive end-expiratory pressure of 5 mm Hg, and inspired oxygen fraction between 0.55 and 0.6. Anesthesia was maintained with desflurane (3%-8%) in an air-oxygen mixture and a continuous infusion of atracurium (0.4 mg/kg/h) and fentanyl (4 μg/kg/h). Implanted lines were inserted into the radial artery for continuous arterial pressure monitoring and a triple-lumen Swan-Ganz catheter was inserted into the right internal jugular vein.

Prior to the anhepatic phase, an infusion of nore-pinephrine was administered in patients to maintain a MAP ≥ 60 mm Hg, and a bolus of adrenaline was administered after vascular unclamping in cases of insufficient response to norepinephrine. Vasoactive support was withdrawn for patients with MAP ≥60 mm Hg at the end of the neohepatic phase. Anesthetic management was intended to correct the cardiac preload, MAP, and metabolic status, especially before graft revascularization. For ionized calcium levels <4 mg/dL, patients were treated with calcium chloride. Patients with a base deficit >10 mmol/L were treated with sodium bicarbonate, and patients with hyperkalemia (>5 mmol/L) were treated with glucose and insulin.

From January 12, 2010, to October 13, 2019, our center used the following transfusion criteria: platelet infusion to maintain a count above 50 × 10⁹/L, packed red blood cells administered to maintain a hemoglobin blood level above 9 g/dL, and fresh frozen plasma administered in cases of significant bleeding. From October 13, 2019, to July 21, 2022, our center’s criteria were guided by viscoelastic testing by rotational thromboelastometry analysis.

Surgical technique
Liver graft anastomoses were performed using the piggyback technique, with or without temporary portocaval shunting. Immediately before the hepatic vein anastomosis was completed, the liver graft was perfused with albumin through the portal vein. All patients were transported postoperatively, still intubated, to the ICU.

Eligibility criteria and patient selection
The population of interest included 466 adult patients (346 men and 120 women) aged ≥18 years who underwent liver transplant from January 12, 2010, to July 21, 2022. From the total population of interest, we selected patients who were monitored with a Swan-Ganz catheter (n = 246). All donors of transplant recipients were deceased. The exclusion criteria were as follows: orthotopic liver transplant for acute liver failure, combined liver and kidney transplant, retransplant, moderate-to-severe vascular and valvular heart disease, chronic kidney disease (serum creatinine >1.5 mg/dL), moderate and severe hepatopulmonary syndrome, moderate and severe portopulmonary syndrome, and patients who were not monitored with a Swan-Ganz catheter. Figure 1 shows the flow diagram of the inclusion and exclusion process.

Study outcomes
The primary objective of our study was to determine the incidence of PRS, as defined by Aggarwal and colleagues,⁴ in liver transplant patients treated with norepinephrine, and to determine the clinical predictors of the occurrence of PRS. The secondary objective was to determine the complications associated with PRS, in terms of the need for transfusions, renal dysfunction, increased hospital stay, graft rejection, need for retransplant, and mortality.

Data collection
The following preoperative variables were collected and analyzed: ages of both recipient and donor, sex of the recipient, etiology of cirrhosis, recipient’s pathology, Child-Pugh classification, MELD score, presence of hepatocarcinoma, diabetes mellitus, hypertension, treatment of hypertension, renal dysfunction (serum creatinine >1.5 mg/dL), and presence of portal thrombosis.

Intraoperative variables were recorded at each stage of surgery and included the following: pulmo-nary capillary pressure (PCP), mean PAP, MAP, HR, CI, SVR index, central venous pressure (CVP), total blood loss, need for transfusions, doses of vaso-constrictors, global requirements for bicarbonate and calcium chloride, presence of malignant arrhythmias (fibrillation, flutter, ventricular tachycardia), and ischemic electrocardiographic abnormalities. The duration of each surgical phase, duration of cold ischemia, and weight of the liver (donor/recipient) were also recorded.

Postoperative data collected included the fol-lowing: graft rejection statistics, additional surgery related to the liver transplant, need for retransplant, renal dysfunction (glomerular filtration rate <60 mL/min/1.73 m²), hospital stay, and survival.

All items that could be used to identify the patient (clinical record number or name) were removed, to avoid the use of protected health information.

Data measurement
Patients had collection of hemodynamic parameters (MAP, HR, SVR, CVP, CI, PCP, and PAP) at each stage of liver transplant surgery, including during the dissection phase, during the anhepatic phase before unclamping of the inferior vena cava, 1 and 5 minutes after graft reperfusions, and during the neohepatic phase after completion of the vascular anastomosis.

The criteria for diagnosis of PRS included the following: ≥30% decrease in MAP during the first 5 minutes after unclamping of the inferior portal vein, decrease in CI and SVR with respect to baseline (anhepatic phase), and increase in PCP, CVP, and PAP with respect to baseline.

Data sources and management
The operative variables were prospectively collected by the research team during liver transplant. The research team retrospectively collected preoperative and postoperative data from the patients’ medical records. Postoperative data were collected from the complications that occurred during the postoperative hospital stay. Data regarding the need for a new transplant and survival were collected from medical records at 3 months after transplant.

Statistical analyses
The association between PRS and the preoperative, intraoperative, and postoperative variables was analyzed and compared between the 2 groups (with and without PRS).

We calculated the frequencies and percentages of categorical variables for the total sample and for the 2 groups with and without PRS. Differences between the 2 groups for each categorical parameter were assessed using the Pearson nonparametric chi-square test. For continuous variables, the median and interquartile range are shown. Differences between the 2 groups for each continuous parameter were assessed using the Mann-Whitney test (nonparametric). To check the evolution of hemodynamic parameters, we calculated repeated-measures general linear models with powerful estimation to handle violations of model assumptions (robust covariances). These models, adjusted for both sex and age, provided information on the evolution of the parameters over time, as well as on the influence of PRS on these evolutionary patterns. Values estimated by the models are presented as marginal means and 95% confidence intervals in tables and figures. The significance level used in the analyses was set at 5% (P = .05).

Results

Of the 246 patients included in the present study, 57 (23.17%) developed PRS. No clinical predictors of PRS were identified, and no differences were observed between the groups in with regard to non-hemo-dynamic intraoperative variables (P > .05) except for adrenaline consumption (Table 1 and Table 2).

The time evolutions of the different hemodynamic variables in the 2 groups are shown in Table 3 and Figure 2. Significant differences in the evolution times for MAP, SVR, and CI were shown between the groups. The filling pressures increased from the anhe-patic to the neohepatic phase, without differences between the groups (CVP, P = .11; and PCP, P = .59). In both groups, PAP showed a progressive increase from the anhepatic phase to the neohepatic phase (P = .88). Systemic vascular resistance decreased sharply during graft reperfusion and remained stable during the neohepatic phase (P = .001). Cardiac index progres-sively increased from the anhepatic to the neohepatic phase, and patients with PRS presented with a decrease in CI on graft reperfusion compared with patients without PRS (P = .03). Heart rate increased from the anhepatic to the graft reperfusion phase and remained stable during the anhepatic phase (P = 0.41).

Patients with PRS did not exhibit more posto-perative complications than patients without PRS in terms of renal dysfunction, repeat surgery, graft rejection, need for a new transplant surgery, hospital stay, and survival (P > .05) (Table 4).

Discussion

The primary finding of our study was that, in patients who required vasoactive drugs to prevent steep drops in MAP and in patients who had correction of some potential risk factors before vascular unclamping, the diagnosis of self-limited PRS in the first 5 minutes had no more negative clinical repercussions than shown in patients without PRS. This result could lead to 2 observations. First, it is possible that the administration of vasoconstrictors had a preventive effect on postoperative complications associated with PRS. Second, the true incidence of PRS may be masked by the administration of vasoactive drugs and may appear later than during the first 5 minutes, with the need to increase the doses of these drugs.

Patients in our study were diagnosed with PRS based on hemodynamic criteria during the first 5 minutes after vascular unclamping.⁴ However, the definition of this syndrome cannot be limited to the decrease in MAP in the first 5 minutes; rather, it must encompass a set of signs and symptoms that lead to a disease. Therefore, it is likely that prolonged hypotension, persistence or increase in vasoactive drug requirements, and the appearance of hemostatic changes or acid-base imbalance beyond 5 minutes after vascular unclamping are more reliable criteria for diagnosis of PRS and, therefore, better predictors of poor PRS outcomes.

A central problem in the diagnosis of PRS is the lack of unified criteria, which leads to significant variability in the published incidence. In the present study, we defined PRS using the most widely accepted definition, as described in 1987 by Aggarwal and colleagues.⁴ In addition, we observed PRS diagnoses in association with an increase in PCP pressures, as obtained by Swan-Ganz catheter monitoring, as well as an increase in CVP.^1-3 The hemodynamic profile during the different phases of transplant surgery for patients with and without PRS varied with regard to MAP, CI, and SVR, as was expected in our study.

According to Aggarwal and colleagues,⁴ PRS involves a 30% or greater decrease in MAP of at least 1-minute duration during the 5 minutes after portal unclamping. Under these circumstances, the authors observed a negative effect on patients who presented with PRS. However, with the consideration of the advances in surgical and reperfusion techniques,^18-22 the correction of PRS risk factors, and the admi-nistration of vasoconstrictors to control the intra-venous volume during liver transplant,²³ the diagnosis of PRS during the first 5 minutes may not have a negative clinical effect, as we noted in our study. Therefore, it may be necessary to broaden the definition of PRS, extending it to include hemodynamic involvement that lasts beyond the first 5 minutes after unclamping the portal vein, with the need to increase vasoactive support. In this sense, the definitions of Hilmi and colleagues¹¹ and Fukazawa and colleagues⁵ for severe PRS should be more acceptable in defining the syndrome.

Hilmi and colleagues¹¹ proposed a classification system, mild and severe, based on the severity of PRS. In mild reperfusion syndrome, the decrease in MAP does not reach 30% during the minute after portal unclamping and responds favorably to adrenaline (≤100 μg) without the need to continue vasopressors and/or intravenous boluses of calcium chloride (1 g). In severe reperfusion syndrome, the decrease in MAP exceeds 30% of the previous value, in conjunction with severe arrhythmias or asystole, or the need to start an intravenous infusion of vasopressors during the intraoperative and/or postoperative periods. Hilmi and colleagues11 added to their definition the appearance of prolonged fibrinolysis for >30 minutes or recurrent, if it reappears within 30 minutes after resolution, with the need to administer antifibrinolytics.

Fukazawa and colleagues⁵ established 3 phases of PRS. The first phase, the first 5 minutes after portal reperfusion, is characterized by sudden hypotension that frequently requires the administration of vasopressors and intravenous fluids. The second phase runs from 5 minutes after portal vein reperfusion through hepatic artery reperfusion and is characterized by a decrease in the MAP until the arterial reperfusion is restored. The third phase runs from arterial reperfusion to 240 minutes after portal vein reperfusion and is characterized by a norma-lization of the various hemodynamic parameters.

Some studies have demonstrated the role of boluses of chronotropic or vasoactive drugs in the prevention of PRS. The first such study was conducted by Acosta and colleagues²⁴ who used atropine before reperfusion to avoid triggeringthe Bezold-Jarisch reflex by preloading the right ventricle at the time of reperfusion. Their results showed no occurrence of bradycardia after reperfusion, although no effects were observed on MAP or hypotension in patients who developed PRS. Later, in a randomized controlled trial, Ryu and colleagues¹⁶ tested the preemptive use of phenylephrine (100 μg) or epinephrine (10 μg) at reperfusion and its association with the occurrence and severity of PRS. Their results showed a significant reduction in the occurrence of PRS in both treatment groups, associated with a reduced need for vasopressors in the postreperfusion period and showing no effects on mortality rates or length of hospital stay. Fayed and colleagues²⁵ replicated similar results using the goal-directed administration of ephedrine starting 5 minutes before reperfusion, aiming for a MAP between 85 and 100 mm Hg. Their results showed a reduction in the incidence of PRS, no hemodynamic overshooting episodes, and a reduction in the duration of posto-perative me-chanical ventilation, which the authors considered to be a preventive effect of vasoactive drugs against the occurrence of PRS in the first 5 minutes after unclamping. We agree in that we did not observe a worse prognosis in patients with PRS in terms of graft dysfunction, need for retransplant, renal insufficiency, days of hospita-lization, and mortality.

Other authors, however, have reported a higher number of postoperative complications in patients with PRS. Xu and colleagues⁸ reported increased renal dysfunction and mortality in patients with PRS. Khosravi and colleagues²⁶ observed more bleeding, an increased need for blood transfusions, increased fibrinolysis, and longer hospital stays in the group with severe PRS. Hilmi and colleagues¹¹ also found a higher frequency of complications associated with the appearance of PRS, including increased fibrinolysis, the need for transfusion and cryopreservation, longer mechanical ventilation, longer stays in the ICU, and greater need for a second transplant.

The present study had some limitations. We did not find perioperative factors that could be related to the appearance of PRS, but it was not possible to study all possible predictors, such as graft macrovesicular steatosis, the presence of intraoperative cardiac dysfunction in all patients and its relationship with PRS,^27-31 and the effects of rapid reperfusion.¹⁰ Given the most widely used definition of PRS, which only addresses the decrease in MAP during the first 5 minutes after vascular unclamping,⁴ it is likely that cardiovascular factors are the most involved in the generation of the syndrome. Thus, with vascular releases that are produced slowly or progressively, a lower incidence of PRS is expected. At the same rate of vascular unclamping, larger liver grafts would be expected to produce more PRS. Likewise, the incidence of PRS could be associated with individual differences in the degree of vascular reactivity, determined by the state of the vascular smooth muscle and the capacity of the vascular endothelium to generate arterial vasodilation or vasoconstriction.³² The determination of endothelial factors, such as nitric oxide, pros-tacyclin, endothelin 1, and angiotensin II before and after vascular unclamping, could indicate the role of the vascular endothelium in the generation of PRS.

Given the retrospective nature of the present study, we could not determine which patients required an increase in vasoactive drugs (relative to the anhepatic phase) during and after the first 5 minutes after vascular unclamping, which could be indicative of the progression and severity of PRS. For our study, we only recorded the total dose of noradrenaline administered, not its variations over time.

Conclusions

In patients who underwent OLT, in whom noradrenaline/adrenaline was administered and some of the potential risk factors were corrected prior to vascular unclamping, the diagnosis of self-limited PRS during the first 5 min after unclamping may not be associated with postoperative complications. The administration of vasoconstrictors may have a preventive effect on the postoperative complications associated with PRS, or they may mask the real incidence of PRS. Therefore, the authors of the present study advocate for the creation of a single definition of PRS that considers a time frame beyond 5 min, and the need for the maintenance of vasoactive drugs.

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