Unilateral lung injury after minimally invasive cardiac surgery: more questions than answers

Pulmonary dysfunction has been a much-noticed postoperative complication since the early days of cardiac surgery. The increasing popularity of minimally invasive cardiac surgery (MICS) has again attracted attention to the interaction between the cardiac surgical procedure and the lung. Recently, several authors reported on patient cohorts who developed unilateral lung injury after MICS, requiring extracorporeal circulation and unilateral lung collapse [ 1–3 ]. The frequency of unilateral lung injury, which manifests clinically as lung oedema, was reported to be between 2.1 and 25%. The varying incidence may be due to different diagnostic criteria, as well as to differences in patient cohorts and perioperative management. Obviously, there is a similarity between unilateral lung injury after MICS and re-expansion pulmonary oedema. Lung collapse has been shown to be associated with the sequestration of polymorphonuclear leucocytes. Respiratory burst and inflammatory activity are triggered when oxygen is supplied during re-expansion (and concomitant reperfusion) of the lung [ 4 ]. One may hypothesize that this inflammatory response is enhanced by multiple factors during cardiac surgery. The authors of the above-mentioned studies tried to identify factors that were associated with the development of unilateral lung injury after MICS. However, the rare occurrence of this event, especially in the work of Irisawa et al. [ 1 ], is a limiting factor with respect to the validity of the results of multivariate analysis. Although it is beyond the scope of this comment to discuss the various conditions, that might be involved in the development of unilateral lung injury after MICS, some aspects should be mentioned. The inflammatory response to re-expansion and reperfusion may be aggravated by the generalized inflammatory response generated by cardiopulmonary bypass. This mechanism may explain the association between prolonged cardiopulmonary bypass time (including prolonged lung collapse) and unilateral lung injury [ 1 , 2 ]. In addition, ischaemia of the lung might be worsened by the restriction of bronchial artery blood flow during extracorporeal circulation [ 5 ]. Mechanical factors may promote the formation of lung oedema: an increase in pulmonary capillary pressure generates an increase in fluid flux into the interstitium of the lung in the presence of increased microvascular permeability [ 6 ]. Another point that should be taken into consideration is the impact of ventilatory management on pulmonary function after re-expansion of the lung. The application of lung protective ventilation, thus avoiding recurrent alveolar collapse and reopening, as well as overinflation of the lung, has been shown to be related to an improved pulmonary function and decreased concentrations of proinflammatory cytokines in the bronchoalveolar lavage fluid and plasma of patients undergoing cardiac and non-cardiac surgery [ 7 , 8 ]. Lung damage may be aggravated by hyperoxic conditions, which are known to increase pulmonary reperfusion injury [ 9 ]. It is not known, to which extent these factors might influence the generation of unilateral lung injury after MICS. Other factors, such as comorbidities, intraoperative blood transfusion or genetic polymorphism, can affect the inflammatory response. Likewise, the modulation of the inflammatory response by glucocorticoids may have impact on the incidence of postoperative lung injury. A recent study demonstrated a beneficial effect of preoperative corticoid treatment on lung injury after cardiac surgery [ 10 ]; however, further details, such as the optimal dose required, remain to be evaluated. Studies like that of Irisawa et al. [ 1 ] draw attention to phenomena, which are underappreciated up to now. Questions as to which of the various factors known to be related to lung injury might be a risk factor, and which factors might protect against the development of unilateral lung damage after MICS, remain to be evaluated.