Abstract
Postoperative remote lung injury is a complication following various surgeries and is associated with short and long-term mortality and morbidity. The release of proinflammatory cytokines, damage-associated molecular patterns such as high-mobility group box-1, nucleotide-biding oligomerization domain (NOD)-like receptor protein 3 and heat shock protein, and cell death signalling activation, trigger a systemic inflammatory response, which ultimately results in organ injury including lung injury. Except high financial burden, the outcome of patients developing postoperative remote lung injury is often not optimistic. Several risk factors had been classified to predict the occurrence of postoperative remote lung injury, while lung protective ventilation and other strategies may confer protective effect against it. Understanding the pathophysiology of this process will facilitate the design of novel therapeutic strategies and promote better outcomes of surgical patients. This review discusses the cause and pathology underlying postoperative remote lung injury. Risk factors, surgical outcomes and potential preventative/treatment strategies against postoperative remote lung injury are also addressed.
Highlights
There are more than 230 million surgical operations around the world each year [1]
Taking remote lung injury following kidney surgery as an example, kidney injury after surgical operation causes the release of cytokines and chemokines as well as damage-associated molecular patterns (DAMPs) which attract a large number of immune cells, such as polymorphonuclear leukocytes and T cells into the alveolar space [13] (Fig. 2)
This study indicated that the surgical lung injury prediction (SLIP) score is of inferior power in this high-risk population than SLIP-2, which is more accurate in diverse and acutely ill patients
Summary
There are more than 230 million surgical operations around the world each year [1]. surgery is an essential treatment pathway in many diseases, respiratory complications following surgery away from the lung, referred to as ‘remote lung injury’, are associated with high mortality and physical disability even 5 years post-surgery [2, 3]. It was reported that autophagy in alveolar macrophages contributed to the pathogenesis of lung injury during mechanical ventilation through activation of the NLRP3 inflammasome [32].
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