“…More importantly, the pathophysiological basis of UPE to date remains unclear, with various suggested mechanisms. These include direct insults from atelectasis and hydrostatic forces leading to an alveolar-capillary barrier disruption, compounded by an indirect injury following ischemia-reperfusion, mediated by oxidative free radicals and chemo-toxic inflammatory cells [ 1 , 4 , 5 ].…”