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Review
. 2023 Mar 18;13(3):58-85.
doi: 10.5500/wjt.v13.i3.58.

Primary graft dysfunction following lung transplantation: From pathogenesis to future frontiers

Sanjeet Singh Avtaar Singh  1   2 , Sudeep Das De  3 , Ahmed Al-Adhami  4   5 , Ramesh Singh  6 , Peter Ma Hopkins  7 , Philip Alan Curry  8
Affiliations
Review

Primary graft dysfunction following lung transplantation: From pathogenesis to future frontiers

Sanjeet Singh Avtaar Singh et al. World J Transplant. .

Abstract

Lung transplantation is the treatment of choice for patients with end-stage lung disease. Currently, just under 5000 lung transplants are performed worldwide annually. However, a major scourge leading to 90-d and 1-year mortality remains primary graft dysfunction. It is a spectrum of lung injury ranging from mild to severe depending on the level of hypoxaemia and lung injury post-transplant. This review aims to provide an in-depth analysis of the epidemiology, patho physiology, risk factors, outcomes, and future frontiers involved in mitigating primary graft dysfunction. The current diagnostic criteria are examined alongside changes from the previous definition. We also highlight the issues surrounding chronic lung allograft dysfunction and identify the novel therapies available for ex-vivo lung perfusion. Although primary graft dysfunction remains a significant contributor to 90-d and 1-year mortality, ongoing research and development abreast with current technological advancements have shed some light on the issue in pursuit of future diagnostic and therapeutic tools.

Keywords: Extracorporeal membranous oxygenation; Lung transplantation; Pathophysiology; Primary graft dysfunction; Risk factors.

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Conflict of interest statement

Conflict-of-interest statement: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Pathophysiological mechanisms that lead to ischaemic-reperfusion injury and subsequently chronic lung allograft dysfunction. CLAD: Chronic lung allograft dysfunction.
Figure 2
Figure 2
Pathophysiology of lung ischemia-reperfusion injury. ROS: Reactive oxygen species.
Figure 3
Figure 3
Nicotinamide adenine dinucleotide phosphate oxidase system and the generation of superoxide anion. NADPH: Nicotinamide adenine dinucleotide phosphate.
Figure 4
Figure 4
Example of an ex vivo lung perfusion circuit. ICU: Intensive care unit.
See this image and copyright information in PMC

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