The pathogenesis of lung injury following pulmonary resection

Abstract

Postpneumonectomy pulmonary oedema (PPO) develops in~5% of patients undergoing pneumonectomy or lobectomy, and has a high associated mortality (>50%). In its extreme form, PPO follows a clinical and histopathological course indistinguishable from acute respiratory distress syndrome.Perioperative fluid overload, impaired lymphatic drainage following node dissection and trauma caused by surgical manipulation have been implicated in the pathogenesis of PPO. However, PPO more probably represents the pulmonary manifestation of a panendothelial injury consequent upon inflammatory processes induced by the surgical procedure, which involves collapse and re-expansion of the operative lung to permit hilar dissection and pulmonary resection.High inspired oxygen concentrations are required to overcome the effects of shunt. Animal studies have shown that pulmonary ischaemia/reperfusion can result in oedema formation, possibly due to the generation of pro-oxidant forces. Moreover, plasma taken from patients undergoing lobectomy or pneumonectomy (but not lesser resections) shows evidence of oxidative damage.Such evidence suggests either that the high inspired oxygen concentrations associated with one-lung ventilation, or ischaemia/reperfusion injury, may modulate postpneumonectomy pulmonary oedema. Mechanisms by which redox imbalance may result in tissue damage and postpneumonectomy pulmonary oedema are discussed. Eur Respir J 2000; 15: 790±799.

Step-by-step clinical management of one-lung ventilation: Continuing Professional Development

“…Reperfusion upon lung reexpansion leads to lung damage owing to the formation of ROS. 33 Prolonged OLV ([ 120 min) and generation of oxidative stress have been associated with increased rates of respiratory failure, cardiac arrhythmias, and pulmonary hypertension. 34 Moreover, high F I O 2 can lead to absorption atelectasis in poorly ventilated lung regions when oxygen absorption in denitrogenated alveoli results in alveolar collapse.…”

“…Based on animal experiments of lung recruitment in ALI, gradual re-expansion potentially induces less ALI in the operative lung. 33 The lung should therefore be re-expanded at a slow rate and to a lower plateau pressure. 47 Lung re-expansion may worsen lung injury due to ischemic reperfusion injury in the presence of ROS and oxidative stress.…”

“…La reperfusion lors de la réexpansion pulmonaire entraîne des lésions aux poumons en raison de la formation de DRO. 33 Une VUP prolongée ([ 120 min) et la génération de stress oxydatif ont été associées à des taux accrus d'insuffisance respiratoire, d'arythmies cardiaques et d'hypertension pulmonaire. 34 De plus, une F I O 2 élevée peut provoquer une atélectasie d'absorption dans les régions pulmonaires mal ventilées lorsque l'absorption d'oxygène dans les alvéoles dénitrogénées entraîne un collapsus alvéolaire.…”

“…33 Par conséquent, le poumon devrait être regonflé lentement et jusqu'à une pression de plateau plus basse. 47 La réexpansion pulmonaire pourrait aggraver les lésions pulmonaires en raison des lésions de reperfusion ischémique en présence de DRO et de stress oxydatif.…”

Perioperative tidal volume and intra-operative open lung strategy in healthy lungs: where are we going?

“…Causative factors of lung injury beside inflammatory processes induced by the surgical procedure are ventilatory trauma, transfusion, hypoxia-reoxgenation upon one-lung ventilation (OLV), etc. 42,43 . A prospective trial underlined the hypothesis that 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 14 alveolar hypoxia, followed by reoxygenation and re-expansion, respectively, triggers the release of inflammatory mediators 44 .…”