Postoperative Remote Lung Injury and Its Impact on Surgical Outcome

Lin Chen; Hailin Zhao; Azeem Alam; Emma Mi; Shiori Eguchi; Shanglong Yao; Daqing Ma

Disclosures

BMC Anesthesiol. 2019;19(30) 

In This Article

Pathology of Postoperative Remote Lung Injury

Postoperative remote lung injury shares the same pathological changes as ALI/ARDS. ARDS is characterized by increased permeability of the alveolar epithelium and capillary endothelium. The disruption of these barriers results in the accumulation of protein-rich fluid in the alveoli, causing pulmonary oedema.

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 DAMPs which attract a large number of immune cells, such as polymorphonuclear leukocytes (i.e., neutrophils) and T cells into the alveolar space[13] (Figure 2). Activated macrophages recruit neutrophils and circulating monocytes to the site of injury in the lung. Neutrophils at injured sites release proteases, ROS and other inflammatory mediators, which further damage the barrier, worsening the pulmonary oedema.[51] Moreover, the inflammatory mediators damage type II pneumocytes, which are responsible for producing surfactant. The destruction of these cells results in an increase in surface tension and subsequent collapse of alveoli.[52] Subsequently, the normal structure of lung tissue is disrupted. The injured lung is characterized by thickened alveolar septa, infiltration of neutrophils even red blood cells in lung tissue as well as the accumulation of protein-rich fluid in the alveolar spaces[13,53] (Figure 3). The combination of all these processes leads to impairment of gas exchange between the blood stream and alveolar space, resulting in hypoxemia.

Figure 2.

Primary kidney injury and remote lung injury. Primary kidney injury causes the release of DAMP molecules, which in turn results in the upregulation of inflammatory responses in the distant lung. Immune cells, such as neutrophils, monocytes and T cells, contribute to the exacerbation of remote lung injury (Modified and reproduced with permission) (Springer Nature; Nature Reviews Nephrology) [13]

Figure 3.

Lung oedema due to functional loss of kidney. Factors associated with the initiation of remote lung injury include the accumulation of toxic by-products, enhanced cytokine release and impaired metabolism due to an imbalance of mediators secreted in kidney injury. These insults cause an increase in pulmonary vascular permeability and, therefore, oedema. Key cytokines in the pathogenesis of remote lung injury following AKI are IL-6 and IL-8, which lead to endothelial dysfunction and pulmonary oedema (Modified and reproduced with permission) (Springer Nature; Nature Reviews Nephrology) [13]

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