One of the most intriguing complications encountered following lung transplantation (LT) is the pulmonary reimplantation response (PRR). PRR develops in the immediate posttransplant period (4 to 6 h up to 72 h) and is characterized by the development of alveolar infiltrates in the graft(s), a reduction in lung compliance, and impairment in gas exchange.
Originally described in the animal model by Siegleman et al,1–
the spectrum of PRR is synonymous with many other terms, including reperfusion injury, ischemia-reperfusion injury, reperfusion edema, primary graft failure (PGF), and early or primary graft dysfunction. The presentation of PRR exhibits variable incidence and clinical presentation. In the mildest form, PRR may affect nearly 60% of transplant recipients to some degree.2–
The most severe form, more recently referred to as PGF, may have an incidence of up to 15%.3–
According to the 2002 registry of the International Society of Heart and Lung Transplantation,4
primary/nonspecific graft failure is one of the leading causes of early (within 30 days) mortality following LT, accounting for 16.4% of deaths in this time period.