Postpneumonectomy pulmonary oedema revisited.

Postoperative pulmonary oedema occurs early post-operatively (>6 h) and is associated with a net fluid overload. A recent survey of 8,195 major operations showed an incidence of 7.6%, with a mortality of 11.9% [1]. Post-pneumonectomy pulmonary oedema (PPO) occurs after pneumonectomy [2] or lung resection [3], in the absence of left ventricular dysfunction or infection. The overall incidence is 5.1% with a mortality of 3.6% [4]. Although PPO has not yet been well defined, there is a growing body of evidence suggesting that increased pulmonary perfusion flow and the subsequent rise in net filtration pressure [5], a restricted capillary volume [2], endothelial damage, amputation of the lymphatic system [6] and hyperinflation [7] are the main causes of this poorly understood clinical entity [8]. PPO occurs more often after pneumonectomy than after partial lung resection and right pneumonectomy seems to be more frequently involved [9, 10]. Prior radiotherapy and intraoperative fluid overload are independent risk factors in cancer patients [3]. Transfusion of fresh frozen plasma and higher mechanical ventilation pressures during surgery are also independent factors [11]. Prognosis varies according to the presentation. Although some studies report a high mortality (~100%) [12], others found different degrees of lung impairment, from acute lung injury (mild-to-moderate) to adult respiratory distress syndrome (ARDS) (severe), the latter being associated with a poor prognosis [3, 4, 11]. Experimental and clinical studies suggest that factors other than fluid overload contribute to disease severity [10]. In dogs, pneumonectomy does not acutely increase susceptibility to extravascular lung water formation (EVLW) caused by haemodynamic challenge [13]. PPO occurs after contralateral pneumonectomy and mediastinal lym-phatic interruption [6]. The simple procedure of thor-acotomy results in an increase in EVLW, and the addition of manual compression of the lung facilitates this increase in EVLW even further [14]. Postoperative pulmonary function, assessed by means of the forced expiratory volume in one second, is reduced for $2 weeks, irrespective of the extent of pulmonary resection [15]. Pulmonary endothelial permeability is increased after pneumonect-omy [16, 17]. All these data suggest that the pulmonary blood/gas barrier is somewhat altered in PPO because of endothelial or epithelial injury, or both. In this issue of the European Respiratory Journal, JORDAN et al. [18] present a review of PPO with emphasis on some hypotheses regarding its pathogenesis. Among different pathogenic factors, the authors focus on the role played by ischaemia, or more precisely hypoxaemia, and reperfusion injury of the remaining …