The recipient operation
While management of the donor is of great importance to subsequent graft function, factors operating in the recipient during operation and after reperfusion may be equally significant. Failure of blood flow to return uniformly to all portions of previously ischaemic tissues (no reflow phenomenon) is a recognized sequel of extended ischaemic damage to organs in situ, to autografts, and to allografts. This phenomenon has been described following ischaemia of kidney, heart, muscle, brain, and other tissues. In recent years much attention has therefore focused on potential damage suffered by the graft during the implantation operation, and in the early period after revascularization.
Delayed restoration of blood flow to the renal cortex after reperfusion can contribute significantly to delayed graft function. Reperfusion of the stored kidney, rather than marking the welcome end of its ischaemic insult, may exacerbate the effects of ischaemia and lead to further cellular damage and early acute tubular necrosis.
The severity of reperfusion injury is dependent on the events of retrieval and storage. Injury can follow prolonged warm ischaemia, or extended cold preservation by either static or perfusion storage. The pathophysiology relates to continuing effects or oligaemic (hypoxic) hypothermic events during organ retrieval and storage under the fresh stimulus of return of oxygenated blood flow: pretreating the recipient, as well as the donor, can obviate some of these effects. Reperfusion injury can be exacerbated by gradual rewarming of the organ during reimplantation. Grafts should be kept cold with moistened cold packs during the recipient operation, and vascular anastomoses performed expeditiously. Addition of interposition arterial or venous jump grafts or other vascular repairs should be done as bench surgery on the preserved chilled organ. Technical failures of vascular anastomoses, requiring reclamping and revision, are potent contributors to reperfusion injury.
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