Abstract
Primary graft dysfunction (PGD) is the clinical syndrome of acute lung injury after lung transplantation (LTx). However, PGD is an umbrella term that encompasses the ongoing pathophysiological and -biological mechanisms occurring in the lung grafts. Therefore, we aim to provide a focused review on the clinical, physiological, radiological, histological and cellular level of PGD. PGD is graded based on hypoxemia and chest X-ray (CXR) infiltrates. High-grade PGD is associated with inferior outcome after LTx. Lung edema is the main characteristic of PGD and alters pulmonary compliance, gas exchange and circulation. A conventional CXR provides a rough estimate of lung edema, while a chest computed tomography (CT) results in a more in-depth analysis. Macroscopically, interstitial and alveolar edema can be distinguished below the visceral lung surface. On the histological level, PGD correlates to a pattern of diffuse alveolar damage (DAD). At the cellular level, ischemia-reperfusion injury (IRI) is the main trigger for the disruption of the endothelial-epithelial alveolar barrier and inflammatory cascade. The multilevel approach integrating all PGD-related aspects results in a better understanding of acute lung failure after LTx, providing novel insights for future therapies.
Highlights
Primary graft dysfunction (PGD) is the clinical syndrome of acute lung injury in the first 72 h after lung transplantation (LTx) defined by hypoxemia and alveolar infiltrates on chest X-ray (CXR) [1]
PGD can be considered as a distinct phenotype of acute respiratory distress syndrome (ARDS) with LTx being the clinical insult [15]
The latter could be attributed to the finding that in some centers the incidence of bronchiolitis obliterans syndrome (BOS)—one phenotype of chronic lung allograft dysfunction (CLAD)—was increased in patients who developed PGD grade 3 after LTx [24–27]
Summary
Primary graft dysfunction (PGD) is the clinical syndrome of acute lung injury in the first 72 h after lung transplantation (LTx) defined by hypoxemia and alveolar infiltrates on chest X-ray (CXR) [1]. The pathophysiological hallmarks of PGD are lung edema with decreased compliance, impaired gas exchange and increased pulmonary vascular resistance (PVR) [1–3] These are the result of multiple injuries to the lung grafts, starting in the organ donor and lasting during and after implantation. Terms as ischemia-reperfusion injury (IRI), reperfusion edema, pulmonary reimplantation response, early allograft dysfunction and primary graft failure have all been used interchangeably to describe acute lung injury after LTx [1,4,10,16,17] This use of terminology lacks uniformity and clarity. After LTx, clinicians are confronted with patients presenting with hypoxemia and bilateral alveolar infiltrates on CXR This is called PGD and its heterogeneous presentation required a grading system to estimate the extent of the ongoing acute lung injury. Airway (stenosis or dehiscence of bronchial anastomoses, impaction), vascular (obstruction of the anastomoses), cardiac (left heart failure, dyssynchrony), parenchymal (infection, rejection, aspiration, atelectasis, hemorrhage) and pleural (effusion, hemothorax, pneumothorax, open chest) complications have to be considered [1]
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