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Lung injury is the leading cause of death after thoracic surgery. Initially recognized after pneumonectomy, it has since been described after any period of 1-lung ventilation (OLV), even in the absence of lung resection. Overhydration and high tidal volumes were thought to be responsible at various points; however, it is now recognized that the pathophysiology is more complex and multifactorial. All causative mechanisms known to trigger ventilator-induced lung injury have been described in the OLV setting. The ventilated lung is exposed to high strain secondary to large, nonphysiologic tidal volumes and loss of the normal functional residual capacity. In addition, the ventilated lung experiences oxidative stress, as well as capillary shear stress because of hyperperfusion. Surgical manipulation and/or resection of the collapsed lung may induce lung injury. Re-expansion of the collapsed lung at the conclusion of OLV invariably induces duration-dependent, ischemia-reperfusion injury. Inflammatory cytokines are released in response to localized injury and may promote local and contralateral lung injury. Protective ventilation and volatile anesthesia lessen the degree of injury; however, increases in biochemical and histologic markers of lung injury appear unavoidable. The endothelial glycocalyx may represent a common pathway for lung injury creation during OLV, because it is damaged by most of the recognized lung injurious mechanisms. Experimental therapies to stabilize the endothelial glycocalyx may afford the ability to reduce lung injury in the future. In the interim, protective ventilation with tidal volumes of 4 to 5 mL/kg predicted body weight, positive end-expiratory pressure of 5 to 10 cm H2O, and routine lung recruitment should be used during OLV in an attempt to minimize harmful lung stress and strain. Additional strategies to reduce lung injury include routine volatile anesthesia and efforts to minimize OLV duration and hyperoxia.

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Interesting concepts have emerged from case reports and small studies on the treatment and prediction of hypoxemia during OLV. Definitive studies on the most effective ventilatory mode remain elusive. End-organ effects of OLV are an exciting new concept that may shape clinical practice and research going forward.

Preoperative risk factors for AKI after lung resection surgery overlap with those established for other surgical procedures. Perioperative management seems to influence the risk of AKI after lung resection; in particular, the use of synthetic colloids may increase the risk, whereas thoracoscopic procedures may decrease the risk of AKI. Early postoperative AKI is associated with respiratory complications and prolonged hospitalization.

The morbidity and mortality after esophagectomy remains high despite significant improvements over the last decades. Enhanced recovery pathways appear promising in achieving further marginal gains but at present are lacking large scale, prospective, multicenter evidence.

Ultrasound-based measurements of skin-to-epidural depth show acceptable agreement with the actual depth observed during epidural catheterization; however, the limits of agreement are wide, which restricts the predictive value of ultrasound-based measurements. Further study is required to delineate the role of ultrasound in thoracic epidural catheterizations.