Postreperfusion syndrome: Hypotension after reperfusion of the transplanted liver

Aggarwal, Shushma; Kang, Yoogoo; Freeman, J. A.; Fortunato, Frank L.; Pinsky, Michael R.

doi:10.1016/0883-9441(93)90021-c

Cited by 187 publications

(142 citation statements)

References 9 publications

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“…The role of serum potassium as an underlying mechanism of PRS occurrence has been the subject of considerable debate [35,36]. In the present study, serum potassium levels measured before graft reperfusion were not significantly different between the PRS group and the No-PRS group.…”

Section: Discussioncontrasting

confidence: 48%

Sympathetic withdrawal is associated with hypotension after hepatic reperfusion

et al. 2013

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Objective Post-reperfusion syndrome (PRS), severe hypotension after graft reperfusion during liver transplantation, is an adverse clinical event associated with poorer patient outcomes. The purpose of this study was to determine whether alterations in autonomic control in liver transplant recipients prior to graft reperfusion are associated with the subsequent development of PRS. Methods Heart rate variability (HRV), systolic arterial blood pressure (SBP) variability, and baroreflex sensitivity of 218 liver transplant recipients were evaluated using 5 min of ECG and arterial blood pressure signals 10 min before graft reperfusion along with other clinical parameters. Logistic regression analyses were performed to assess predictors of PRS occurrence. Results Seventy-seven patients (35 %) developed PRS while 141 did not. There were significant differences in SBP (110 ± 16 vs. 119 ± 16 mmHg, P \ 0.001) and the ratio of low frequency power to high frequency power (LF/ HF) of HRV (1.0 ± 1.4 vs. 2.1 ± 3.7, P = 0.003) between the PRS group and No-PRS group. In multivariate logistic regression analysis, predictors were LF/HF (odds ratio 0.817, P = 0.028) and SBP (odds ratio 0.966, P \ 0.001).Interpretation Low LF/HF and SBP measured before hepatic graft reperfusion were significantly correlated with subsequent PRS occurrence, suggesting that sympathovagal imbalance and depressed SBP may be key factors predisposing to reperfusion-related severe hypotension in liver transplant recipients.

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Section: Discussioncontrasting

confidence: 48%

Sympathetic withdrawal is associated with hypotension after hepatic reperfusion

et al. 2013

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“…Previous reports on intermittent measurements during liver transplantation revealed a marked reduction in cardiac output levels after caval clamping [2,3,19,20] and almost a doubling in cardiac output after reperfusion of the graft [2,3,[19][20][21]; both findings are consistent with the present intermittent cardiac output data. In contrast, when cardiac output measurements were obtained using indocyanine green dye dilution, the cardiac output after reperfusion tended to increase from the immediate pre-reperfusion value but was found to be still lower than the baseline values [18]. If intermittent cardiac output is compared with bio-impedance cardiac output monitoring, the latter also reflects the decrease after caval clamping but after reperfusion it does not show the same marked increase observed with intermittent cardiac output [2].…”

Section: Discussionmentioning

confidence: 78%

“…Due to the signal processing algorithm, the displayed continuous cardiac output represents the mean of the measurements of the last 3-6 min [10]. If cardiac output decreases or increases suddenly, as occurs after caval clamping and reperfusion of the graft [1][2][3][18][19][20][21], continuous cardiac output measurements initiated within 6 min may reflect mixed data from before and after the event. However, in the present study, continuous cardiac output was recorded as the mean of two continuous cardiac output values obtained before and after intermittent cardiac output measurements.…”

Section: Discussionmentioning

confidence: 99%

Continuous versus intermittent thermodilution cardiac output measurement during orthotopic liver transplantation

et al. 1997

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SummaryWe evaluated intermittent and continuous thermodilution cardiac output data in 12 patients undergoing orthotopic liver transplantation. Measurements were performed at 16 predefined time points between induction of anaesthesia and 3 h after reperfusion of the liver graft. Cardiac output measurements yielded 192 data pairs (intermittent cardiac output range: 1.8-18.9 l.min ¹1 , continuous cardiac output range: 3.3-20.0 l.min ¹1 ). During most of the procedure the correlation between intermittent and continuous cardiac output measurements was significant (r = 0.87, p < 0.0001), accompanied with a bias of ¹0.240 l.min ¹1 and a degree of precision of 1.789 l.min ¹1 (< 10.0 l.min ¹1 : 1.137 l.min ¹1 , Ն10.0 l.min ¹1 : 2.220 l.min ¹1 ). However, in the early phases after caval clamping and after reperfusion, accuracy was not acceptable. Only during these phases did the difference between the mean values of pulmonary artery blood temperature and rectal temperature increase (after caval clamping) or decrease (after reperfusion). In conclusion, despite acceptable levels of accuracy and precision between intermittent and continuous cardiac output measurement under stable conditions, both methods showed markedly decreased accuracy and precision in the early phases after caval clamping and after reperfusion, possibly owing to increased thermal noise.

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“…Washing out the potassium by flushing 500 mL of portal vein blood through the liver graft eliminated cardiac arrest due to severe hyperkalemia. 4 In contrast, Aggarwal et al 5 stated that hyperkalemia does not appear to be a major cause of reperfusion hypotension. Other investigators have reported that many factors other than hyperkalemia are involved with death in the postrecirculation period.…”

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confidence: 98%

Hyperkalemia and liver transplantation

Perkins

2008

Liver Transpl

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Background: Hyperkalemia poses serious hazards to patients undergoing orthotopic liver transplantation (OLT), and its predictors have not been thoroughly examined. Methods: We retrospectively studied 1124 consecutive adult patients who underwent OLT. Hyperkalemia was defined as serum Kϩ Ͼ or ϭ5.5 mmol/L. A total of 47 recipient, donor, intraoperative, and laboratory variables were initially analyzed in univariate analyses. Independent predictors of hyperkalemia in three periods of OLT (prereperfusion, early postreperfusion, and late postreperfusion) were determined in multivariate logistic regression analyses. Results: Of 1124 patients, 10.2%, 19.1%, and 7.9% had hyperkalemia in the prereperfusion, early postreperfusion, and late postreperfusion periods, respectively. Higher baseline Kϩ and red blood cell transfusion were independent predictors of prereperfusion hyperkalemia. Higher baseline Kϩ (or prereperfusion Kϩ) and donation after cardiac death donor were independent predictors of early postreperfusion hyperkalemia. Higher baseline Kϩ, longer warm ischemia time, longer donor hospital stay, lower intraoperative urine output, and the use of venovenous bypass were independent predictors of late postreperfusion hyperkalemia. Conclusions: Several laboratory, intraoperative, and donor variables were identified as independent predictors of hyperkalemia in the different periods. Such information may be used for more targeted preemptive interventions in patients who are at risk of developing hyperkalemia during adult OLT. COMMENTSHyperkalemia has always been a problem in liver transplantation. Most concerns have been associated with severe hypotension, hypokalemia, and subsequent deaths in the reperfusion period. The occurrence of hyperkalemia in the period just following recirculation of blood during the liver transplant operation has been correlated with death. It has been thought that severe hyperkalemia may induce myocardial depression and the postreperfusion syndrome.2 Fukuzawa et al. 3 found a potassium concentration of 40 Ϯ 2 Meq/L in the first 100 mL of discarded blood following portal vein flush. These authors also observed that 500 mL of discarded blood contained 8.3 Ϯ 0.04 Meq, which was correlated with the graft liver weight. Washing out the potassium by flushing 500 mL of portal vein blood through the liver graft eliminated cardiac arrest due to severe hyperkalemia. 4 In contrast, Aggarwal et al.5 stated that hyperkalemia does not appear to be a major cause of reperfusion hypotension. Other investigators have reported that many factors other than hyperkalemia are involved with death in the postrecirculation period.6 Nakasuji and Bookallil 7 concluded that the occurrence of hyperkalemia after revascularization is correlated with serum potassium concentrations and metabolic acidosis due to insufficient cardiac output during the anhepatic phase. There have been several accounts of treating impending hyperkalemia with insulin infusion during the anhepatic phase. 8,9 In this article, Xia et al. r...

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Postreperfusion syndrome: Hypotension after reperfusion of the transplanted liver

Cited by 187 publications

References 9 publications

Sympathetic withdrawal is associated with hypotension after hepatic reperfusion

Sympathetic withdrawal is associated with hypotension after hepatic reperfusion

Continuous versus intermittent thermodilution cardiac output measurement during orthotopic liver transplantation

Hyperkalemia and liver transplantation

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