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

Siniscalchi, Antonio; Gamberini, Lorenzo; Laici, Cristiana; Bardi, Tommaso; Ercolani, Giorgio; Lorenzini, Luca; Faenza, Stefano

doi:10.3748/wjg.v22.i4.1551

Cited by 88 publications

(87 citation statements)

References 78 publications

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“…21 However Another clinical challenge that anesthesiologists may encounter during graft reperfusion is hemodynamic instability. 23 In our study, median MAPs remained stable in both groups with adequate increase in the noradrenaline dose. 22 In this study we did not observe PRS in the DHOPE group.…”

Section: Discussionsupporting

confidence: 61%

Opposite acute potassium and sodium shifts during transplantation of hypothermic machine perfused donor livers

Burlage

Hessels

Rijn

et al. 2019

American Journal of Transplantation

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Liver transplantation is frequently associated with hyperkalemia, especially after graft reperfusion. Dual hypothermic oxygenated machine perfusion (DHOPE) reduces ischemia/reperfusion injury and improves graft function, compared to conventional static cold storage (SCS). We examined the effect of DHOPE on ex situ and in vivo shifts of potassium and sodium. Potassium and sodium shifts were derived from balance measurements in a preclinical study of livers that underwent DHOPE (n = 6) or SCS alone (n = 9), followed by ex situ normothermic reperfusion. Similar measurements were performed in a clinical study of DHOPE‐preserved livers (n = 10) and control livers that were transplanted after SCS only (n = 9). During DHOPE, preclinical and clinical livers released a mean of 17 ± 2 and 34 ± 6 mmol potassium and took up 25 ± 9 and 24 ± 14 mmol sodium, respectively. After subsequent normothermic reperfusion, DHOPE‐preserved livers took up a mean of 19 ± 3 mmol potassium, while controls released 8 ± 5 mmol potassium. During liver transplantation, blood potassium levels decreased upon reperfusion of DHOPE‐preserved livers while levels increased after reperfusion of SCS‐preserved liver, delta potassium levels were ‐0.77 ± 0.20 vs. +0.64 ± 0.37 mmol/L, respectively (P = .002). While hyperkalemia is generally anticipated during transplantation of SCS‐preserved livers, reperfusion of hypothermic machine perfused livers can lead to decreased blood potassium or even hypokalemia in the recipient.

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Section: Discussionsupporting

confidence: 61%

Opposite acute potassium and sodium shifts during transplantation of hypothermic machine perfused donor livers

Burlage

Hessels

Rijn

et al. 2019

American Journal of Transplantation

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“…Liver IRI has significant effects on liver function and causes systemic injury . The liver‐specific and systemic effects of IRI have important implications for the practice of liver transplantation …”

Section: Introductionmentioning

confidence: 99%

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Dar

Sullivan

Bynon

et al. 2019

Liver International

261

245

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Liver disease causing end organ failure is a growing cause of mortality. In most cases, the only therapy is liver transplantation. However, liver transplantation is a complex undertaking and its success is dependent on a number of factors. In particular, liver transplantation is subject to the risks of ischaemia‐reperfusion injury (IRI). Liver IRI has significant effects on the function of a liver after transplantation. The cellular and molecular mechanisms governing IRI in liver transplantation are numerous. They involve multiple cells types such as liver sinusoidal endothelial cells, hepatocytes, Kupffer cells, neutrophils and platelets acting via an interconnected network of molecular pathways such as activation of toll‐like receptor signalling, alterations in micro‐RNA expression, production of ROS, regulation of autophagy and activation of hypoxia‐inducible factors. Interestingly, the cellular and molecular events in liver IRI can be correlated with clinical risk factors for IRI in liver transplantation such as donor organ steatosis, ischaemic times, donor age, and donor and recipient coagulopathy. Thus, understanding the relationship of the clinical risk factors for liver IRI to the cellular and molecular mechanisms that govern it is critical to higher levels of success after liver transplantation. This in turn will help in the discovery of therapeutics for IRI in liver transplantation – a process that will lead to improved outcomes for patients suffering from end‐stage liver disease.

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“…The latter is responsible for the post-reperfusion syndrome (PRS), which is an intra-operative complication, whose definition is still under debate, that may influence morbidity and mortality of recipients. PRS involves intra-operative events such as reduction of mean arterial pressure (MAP), presence of haemodynamic arrhythmias, need for inotropic drugs during transplantation[7]. This condition promotes multi-organ damage, with particular kidney involvement through systemic inflammatory and haemodynamic mechanisms in addition to a direct damage with tubular cell death.…”

Section: Introductionmentioning

confidence: 99%

Acute kidney injury and post-reperfusion syndrome in liver transplantation

Umbro¹,

Tinti²,

Scalera³

et al. 2016

WJG

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In the past decades liver transplantation (LT) has become the treatment of choice for patients with end stage liver disease (ESLD). The chronic shortage of cadaveric organs for transplantation led to the utilization of a greater number of marginal donors such as older donors or donors after circulatory death (DCD). The improved survival of transplanted patients has increased the frequency of long-term complications, in particular chronic kidney disease (CKD). Acute kidney injury (AKI) post-LT has been recently recognized as an important risk factor for the occurrence of de novo CKD in the long-term outcome. The onset of AKI post-LT is multifactorial, with pre-LT risk factors involved, including higher Model for End-stage Liver Disease score, more sever ESLD and pre-existing renal dysfunction, either with intra-operative conditions, in particular ischaemia reperfusion injury responsible for post-reperfusion syndrome (PRS) that can influence recipient’s morbidity and mortality. Post-reperfusion syndrome-induced AKI is an important complication post-LT that characterizes kidney involvement caused by PRS with mechanisms not clearly understood and implication on graft and patient survival. Since pre-LT risk factors may influence intra-operative events responsible for PRS-induced AKI, we aim to consider all the relevant aspects involved in PRS-induced AKI in the setting of LT and to identify all studies that better clarified the specific mechanisms linking PRS and AKI. A PubMed search was conducted using the terms liver transplantation AND acute kidney injury; liver transplantation AND post-reperfusion syndrome; acute kidney injury AND post-reperfusion syndrome; acute kidney injury AND DCD AND liver transplantation. Five hundred seventy four articles were retrieved on PubMed search. Results were limited to title/abstract of English-language articles published between 2000 and 2015. Twenty-three studies were identified that specifically evaluated incidence, risk factors and outcome for patients developing PRS-induced AKI in liver transplantation. In order to identify intra-operative risk factors/mechanisms specifically involved in PRS-induced AKI, avoiding confounding factors, we have limited our study to “acute kidney injury AND DCD AND liver transplantation”. Accordingly, three out of five studies were selected for our purpose.

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

Cited by 88 publications

References 78 publications

Opposite acute potassium and sodium shifts during transplantation of hypothermic machine perfused donor livers

Opposite acute potassium and sodium shifts during transplantation of hypothermic machine perfused donor livers

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Acute kidney injury and post-reperfusion syndrome in liver transplantation

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