Postpneumonectomy pulmonary oedema (PPO) develops in similar to 5% of patie
nts undergoing pneumonectomy or lobectomy, and has a high associated mortal
ity (>50%). In its extreme form, PPO follows a clinical and histopathotogic
al course indistinguishable from acute respiratory distress syndrome.
Perioperative fluid overload, impaired lymphatic drainage following node di
ssection and trauma caused by surgical manipulation have been implicated in
the pathogenesis of PPO, However, PPO more probably represents the pulmona
ry manifestation of a panendothelial injury consequent upon inflammatory pr
ocesses induced by the surgical procedure, which involves collapse and re-e
xpansion of the operative lung to permit hilar dissection and pulmonary res
ection.
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 f
orces. Moreover, plasma taken from patients undergoing lobectomy or pneumon
ectomy (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 imba
lance may result in tissue damage and postpneumonectomy pulmonary oedema ar
e discussed.