In a physiological state, pleural fluid enters the pleural space through the parietal pleura via a filtering pressure gradient and it is removed via an absorptive pressure gradient through the visceral pleura, together with lymphatic drainage through the stomas of the parietal pleura. Thus, filtration and reabsorption of pleural fluid maintain a dynamic balance through a negative feedback system between visceral and parietal pleurae [14, 15].
However, the physiological state is inevitably perturbed by the systemic response and local changes due to thoracic surgery. A systemic response is usually induced by anesthesia, surgical injuries, inflammation, and stress. Local changes, including intrathoracic tissue injuries and changes such as residual lung over-inflation and alteration of the pulmonary circulation (blood re-distribution, the increase in blood flow, velocity, and hydrostatic pressure) can contribute to the development of pleural effusion [16–18].
Few previous studies aimed to assess the factors affecting PDV after thoracic surgery, Hristova R et al. reported that age, chronic obstructive pulmonary disease (COPD), and lower lobectomy were risk factors for large drainage volume on the second day after lobectomy [19]. Kosugi et al. proved that reduced creatinine clearance and thoracic duct resection were risk factors for larger PDV after transthoracic oesophagectomy [20]. However, these two studies included various factors that could affect the PDV, such as different surgical procedures, timing of operation, presence of pleural adhesion, and blood transfusion or complications intra-or postoperatively. In order to minimize the potential interference factors, all patients in the present study were analyzed based on the exclusion criteria and they uniformly underwent uniportal VATS lobectomy, although which procedure has been proved could reduce the PDV after operation [21]. It may be an effective way to identify the predictive factors of PDV in patients who are diagnosed with NSCLC and who undergo uniportal VATS lobectomy.
Age is the most representative indicator of the physical condition, and our research showed that it was an independent predictive factor for PDV. This finding was similar to that in the study by Hristova R et al [19]. The primary reason why PDV increases with age is increased microvascular dysfunction and hyperpermeability, which are caused by the destruction of endothelial cell adhesion and interstitial matrix-associated proteins [22].
Our research proved that FEV1% was another indispensable predictor of PDV. FEV1% is considered to be an effective indicator of bronchiole expansion function and pulmonary compliance, and reduction in FEV1% reflects the degree of alveolar hyperinflation and subsequent physiopathological decrease in the pulmonary vascular bed,which can aggravate postoperative microvascular filtration. A previous investigation on the operative patients also suggested a causative relationship between the decrease in compliance and the perturbation in pleuro-pulmonary fluid balance, which might lead to an increase in pleural effusion [17].
LVEF, an index of left ventricular systolic function, was also found to be a predictor of PDV. One possible explanation is that decreased left-sided cardiac function increased the hydrostatic pressure in the pulmonary circulation and pulmonary edema promoted pleural fluid filtration. In addition, secondary pulmonary edema could also aggravate the hypoxia and inflammation of the residual lung, which further increased the PDV [23–25].
The relationship between TP and pleural transudate has been adequately studied in previous researches. Lower serum protein decreased the serum colloid osmotic pressure, which resulted in a higher PDV as a result of increased filtration and decreased reabsorption [15, 26, 27].
Patients who underwent lower lobectomy had higher PDV in our research, and this finding was in accordance with that reported by Hristova R et al. and Kouritas VK et al [19, 28, 29]. Increased PDV after lower lobectomy might be due to larger residual space after removal of the lower lobe than the upper or middle lobe, subsequently causing a greater reduction in the vascular bed and pleural reabsorption area as well as greater over-inflation and blood flow redistribution in the residual lung, which resulted in greater filtration of the pleural fluid.
In any case, the amount of pleural drainage cannot be ignored while judging the timepoint of chest tube removal. This study presents the important factors associated with PDV, which can help in perioperative patient management. These factors could be beneficial for alerting the surgeons of incremental PDV and for increasing the awareness. Before the operation, the patients with high predictive PDV should be administered an individualized correction through preoperative therapy and exercise for an enhanced recovery after surgery. After the operation, these predictors can help identify the patients who can safely undergo early chest tube removal after the operation and can provide evidence for differentiated and individualized chest tube management.