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Excerpt
The growing discrepancy between demand and supply of organs for transplantation has triggered a renewed interest in the use of grafts from non-heart-beating (NHB) donors (1). Extensive research and improvements in preservation technique have contributed to improved outcome after transplantation of kidneys from NHB donors in recent years. However, the percentage of delayed graft function and primary nonfunction is still higher than after transplantation of kidneys from brain death donors with an intact circulation (1). The crucial factor for organ viability from NHB donors is the period of poor and no perfusion before organ procurement. In combination with the subsequent cold preservation and reperfusion injury, this initial warm ischemic injury can cause severe damage to the donor organ. Although kidneys may eventually recover from prolonged warm ischemic injury while the patient is kept alive with the use of dialysis, warm ischemia is a main obstacle in the liver and lung, where no alternative substitution therapies are available. Therefore, better graft preservation techniques are needed before liver and lung transplantation from NHB donors can be safely and widely used.
It is often believed that the cardiac standstill in NHB donors not only results in warm ischemic injury, but also leads to the formation of thrombi in the microvasculature of the donor organs (23). However, the clinical relevance of early postmortem thrombus and fibrin formation remains unclear. Very few studies have focused on blood coagulation after cardiac standstill, and the knowledge about postmortem fibrin formation is limited. Most information comes from forensic studies, which in fact have indicated that activation of platelets is reduced early after death, and that coagulation is altered with less stable clot formation (45). Furthermore, the fibrinolytic system is markedly activated (4). These observations suggest that intravascular fibrin formation does not occur at a very high rate during the early postmortem period. In contrast, perfusion of NHB donor organs is often associated with a high resistance and inadequate microperfusion, which suggests the presence of thrombi and fibrin deposits in the microcirculation (1). It is possible that microthrombi are formed in the period immediately before cardiac arrest occurs. This period is often characterized by low blood pressures and inadequate circulation in the presence of normal coagulation, which are known risk factors for intravascular thrombus formation.
To prevent formation of (micro-) thrombi in organs that will be used for transplantation, high dose heparin is routinely given during organ procurement in heart-beating (brain death) donors. However, in NHB donors adequate heparinization is hampered by the lack of an intact circulation at the time of organ procurement. In most centers with a clinical protocol for NHB donors, the majority of cases are so called “ventilated switch off” procedures (also known as “controlled,” or category 3 NHB donors). In these cases, administration of heparin before cardiac standstill is obtained would be a violation of the necessary separation between the treatment team and the transplant team (1). In case of an unsuccessful resuscitation (“uncontrolled” or category 2 NHB donors), it has been proposed to resume cardiac message and give i.v. heparin after a waiting period of 10 min, marking the transition from treatment to donation procedure (1). Some centers have added heparin to the preservation fluid, but the efficacy of this strategy is questionable. Heparin prevents new fibrin formation but will have no effect on preexisting thrombi.
