KEY WORDS: acute lung injury, acute respiratory distress syndrome, esophagectomy, pathophysiology, postoperative complications.Esophagectomy is widely considered to be a high risk surgical approach. While improvements in surgical technique, perioperative monitoring, and postoperative care have led to a reduction in mortality following esophagectomy, early mortality remains between 5% and 10%. 1,2 Moreover, postoperative complications, involving predominantly the cardiorespiratory system, occur in up to 50% of patients. 3 Of the numerous respiratory complications that are associated with esophagectomy, acute lung injury (ALI) and its more severe form acute respiratory distress syndrome (ARDS) are of notable significance due to their prevalence and impact on early morbidity and mortality. 4 Reported rates of ALI and ARDS following esophagectomy are 23.8% and 14.5% respectively, the latter associated with 50% mortality. 4 While the existence of an accepted clinical definition for ALI/ARDS 5 has greatly contributed to the wider study of ALI/ARDS, continued variability in reporting practices has meant that the pathophysiology of this syndrome in the context of esophagectomy remains incompletely understood. Notwithstanding, patient-specific factors, the extent and nature of surgical trauma, and frequent requirement for periods of one-lung ventilation (OLV) are all anticipated to contribute to the development of ALI/ARDS following esophagectomy through their influence on systemic and local inflammatory responses. Consequently, the aim of this review is to define the pathophysiology of ALI/ARDS in the setting of esophagectomy and to explore potential strategies for prediction and prevention of this complication.
PATHOPHYSIOLOGY OF ALI/ARDSAs first described by Ashbaugh et al. in 1967, ALI/ ARDS is recognized as a constellation of clinical, radiological, and physical abnormalities that collectively define an underlying picture of diffuse damage to the alveolar capillary unit and associated pulmonary gas exchange disturbance. 6 Central to this process is disruption of vascular endothelial and pulmonary epithelial linings and subsequent flooding of the alveolar and interstitial spaces with proteinaceous fluid, rich in inflammatory mediations and leukocytes. 7 Causes of ALI/ARDS can be broadly divided between those that result in either direct or indirect lung injury. Common sources of direct lung injury include: pneumonia, aspiration, trauma, reperfusion, and inhalation injury. Alternatively, sepsis, shock, polytrauma, and blood transfusion are common sources of indirect lung injury. 8 In patients undergoing esophagectomy precipitants of ALI/ARDS may reflect both local and systemic insults.