Primary graft dysfunction (PGD) after lung transplantation represents a multifactorial injury to the transplanted lung that develops in the first 72 hours after transplantation; it is variously referred to as "ischemia-reperfusion injury", "early graft dysfunction", and "reimplantation edema." PGD is characterized by severe hypoxemia, lung edema, and the radiographic appearance of diffuse pulmonary opacities without other identifiable cause. The typical pathologic pattern of PGD is diffuse alveolar damage.
Despite significant advances in organ preservation, surgical technique, and perioperative care, PGD is responsible for significant morbidity and mortality after lung transplantation [1-4].
The pathophysiology, risk factors, diagnosis, grading, and strategies to prevent PGD are reviewed here. Postoperative management following lung transplantation, evaluation of acute lung transplant rejection, and immunosuppression following lung transplantation are reviewed separately. (See "Lung transplantation: Procedure and postoperative management" and "Evaluation and treatment of acute lung transplant rejection" and "Induction immunosuppression following lung transplantation".)
The incidence of PGD is reported to be in the range of 10 to 25 percent; it is the leading cause of early death after lung transplantation [1-6]. Survivors of PGD tend to have a longer duration of mechanical ventilation, longer hospital stay, and lower lung function over time . As an example, a retrospective study of 255 lung transplant procedures found that recipients with severe PGD (table 1) versus those without had a 30 day mortality of 63 versus 9 percent and duration of mechanical ventilation of 15 versus 1 day(s) .
PGD reflects the summation of injury inflicted on the donor lung by the transplant process (retrieval, preservation, implantation, and reperfusion) and by other factors such as acid aspiration, pneumonia, and microtrauma from mechanical ventilation  (figure 1). Recipient factors also play a role in the development of PGD. For example, recipients with pulmonary fibrosis and primary pulmonary hypertension have higher incidence of PGD compared with patients with emphysema.