Pleural effusion (PE) is a highly prevalent complication in patients following cardiac surgery, with some medical institutions reporting incidences exceeding 60% [1, 2, 3]. PE is classified into early and late categories based on the time of onset, with early PE occurring within the first postoperative month and accounting for the majority of PE cases after cardiac surgery [4]. PE etiology in this population is multifactorial, including pleural inflammatory reactions induced by cardiopulmonary bypass and surgical trauma, coagulopathy secondary to hemodilution, hypoalbuminemia, and most crucially, elevated capillary hydrostatic pressure resulting from cardiac congestion or suboptimal volume management [2, 4, 5, 6]. Moreover, PE is a significant factor contributing to intensive care unit (ICU) re-admission and poor prognosis outcomes [1, 7].

Minimal pulmonary effusion generally does not warrant further clinical intervention. Conversely, significant pulmonary effusion may induce hypoxia, necessitating thoracentesis to ensure effective drainage [8, 9, 10, 11]. This intervention serves two purposes: it alleviates pulmonary compression and provides an indirect way to assess hydrostatic equilibrium. For the majority of patients, maximum PE volumes are usually drained on the first day. Nevertheless, persistent PE production may require repeated daily drainage.

At present, no studies have analyzed the quantitative relationship between early daily PE drainage trajectories and clinical outcomes. We hypothesize that PE drainage volumes after cardiac surgery are associated with clinical prognosis outcomes, and patients with different PE drainage trajectories have different clinical outcomes. To verify this, we conducted this study.

In this study, we screened more than 15,000 patients, of which 386 had PE with at least one puncture and drainage issue. The most significant conclusion was that increased continuous thoracic drainage was significantly associated with poor patient outcomes after cardiac surgery. To our knowledge, this is the first study to explore the relationship between PE drainage volume (and associated dynamic trajectories) with prognoses in patients undergoing cardiac surgery.

We evaluated associations between PE dynamics and patient outcomes from two perspectives. First, regarding pleural fluid production, higher mean daily PE volumes during postoperative days 2–4 and 5–7 were significantly associated with worse clinical outcomes, indicating that increased fluid production correlated with a poorer prognosis. Second, an analysis of PE production trends revealed that a downward trajectory—whether rapid (resulting in persistently low levels) or gradual—was associated with improved outcomes. In contrast, patients with persistently high PE volumes over 1 week had higher mortality rates and a greater incidence of composite endpoint events. Correlation analyses between PE production rates and cardiac function indices suggested that both the magnitude and duration of postoperative PE potentially reflected underlying cardiac function. In patients with impaired cardiac function, prolonged and elevated PE may have indicated either a lack of therapeutic benefit from the surgical intervention or a sustained procedure-related injury. Notably, these differences in PE dynamics became apparent by postoperative day 3 following thoracentesis and were predictive of subsequent clinical outcomes.

Despite limited studies on PE trajectory, several studies have examined PE causes after cardiac surgery. In Labidi et al. [4], patients with very early PEs were hemorrhagic, had higher neutrophil counts, and elevated lactate dehydrogenase levels, and the authors suggested that early effusions were possibly due to pleura trauma, whereas late effusions were more likely due to immune-inflammatory processes related to postcardiac injury syndrome. Pleurotomy can impair the pleura to resorb pleural fluid and may also lead to inflammation contributing to PE formation, consistent with previous findings showing that pleural injury and immunological perturbations were two important PE formation mechanisms after cardiac surgery [15].

Although pleural injury is known to contribute to PE following cardiac surgery, interindividual differences in PE formation rates and duration may also be influenced by other factors. We hypothesize that variations in postoperative cardiac function, particularly left ventricular performance, may have key roles. In heart failure, the primary mechanism underpinning pleural fluid accumulation involves transudation from the pulmonary interstitium into the pleural space. Elevated left atrial and left ventricular end-diastolic pressures are retrogradely transmitted to the alveolar capillaries, promoting fluid leakage and subsequent PE formation. Elevated hydrostatic pressure in these capillaries increases interstitial fluid in the lungs [16]. The fluid then moves from the pulmonary interstitial space across the visceral pleura into the pleural space along a pressure gradient. Pleural fluid accumulates when its formation rate exceeds parietal lymphatic capacity to absorb it.

In this study, we hypothesized that in early PE stages, cardiac insufficiency or excessive circulation load may have triggered PE generation mechanisms. This caused different PE generation rates in different patients from day 3 after pleural puncture and drainage. One observation that could support this hypothesis are NT-proBNP levels. In recent years, circulating natriuretic peptide levels have become useful adjunctive tools in heart failure (HF) diagnostics [17]. Both BNPs and NT-proBNPs are secreted almost exclusively from ventricles in response to pressure and volume overload. Overall, as BNP or NT-proBNP levels increase, the likelihood of HF also increases. In our study, we did not test for BNP in pleural fluid, but collected serum NT-proBNP data. NT-proBNP levels were high in the “persistently high” trajectory group (median (IQR) = 5616 (2954–11,650 ng/mL)) and were associated with mean daily pleural fluid production on days 2–4. Although our analysis revealed a statistically significant correlation between PE drainage volume and serum NT-proBNP levels (R² = 0.051, p 0.001), the low coefficient of determination indicates that this linear relationship accounts for merely 5.1% of the observed variance in drainage volumes. The observed correlation probably reflects the shared underlying pathophysiology of cardiac dysfunction and fluid overload states, consistent with NT-proBNP’s established role as a ventricular stress marker rather than a direct mediator of pleural fluid accumulation.

In our study, another indicator closely related to PE generation was platelet levels. Similar to NT-proBNP, platelets were inversely correlated with average daily PE volumes from 2 to 4 days. Although a statistically significant but weak inverse correlation was observed (R² = 0.023, p = 0.003), suggesting that platelet levels may partially reflect disease severity and surgical trauma intensity in PE patients, the minimal explained variance indicates that other pathophysiological factors likely play more predominant roles in determining drainage volumes. In the “persistently high” trajectory group, platelet levels were significantly lower, and levels were highest in the “persistently low” control group. Cardiopulmonary bypass (CPB) used in cardiac surgery may decrease platelet counts in initial phases [18, 19, 20]. Postoperative thrombocytopenia may also occur due to CPB hemodilution and mechanical damage to platelets [21]. In Keles et al. [22], pump and cross-clamp times were negatively correlated with platelet counts. Beyond baseline fibrinolysis and inflammatory stimuli associated with blood exposure to cardiopulmonary bypass circuits, high-dose systemic heparin exposure may further increase heparin induced thrombocytopenia perioperative risks [23, 24]. For patients with normal preoperative platelet counts, postoperative decreases may not be necessarily related to cardiac function, but lower platelet counts mean that patients may have higher bleeding risks. In our study, at the time of PE, patients with lower platelet counts had greater pleural fluid production. Therefore, platelet counts may be contributing factors to PE generation and amplify PE effects caused by decreased cardiac function and pleural injury.

This study had several limitations. First, as a single-center, retrospective observational study, the generalizability of our findings may be limited, and the decision to perform thoracentesis and catheter drainage, based on attending physician judgement, may have introduced selection bias. Second, we analyzed PE drainage volumes for only the first 7 days after cardiac surgery, without assessing the long-term impact on patient outcomes or the biochemical/cellular composition of drained PE volumes, which may have highlighted underlying pathophysiology mechanisms. Finally, despite adjusting for potential confounders in logistic regression analysis, residual confounding factors may still have existed due to the observational nature of the study.

PE formation trends showed a strong correlation with mortality and poor outcomes in patients who underwent cardiac surgery. Patients with persistently high PE drainage volumes represent a population that require close monitoring and attention.

The datasets generated and analyzed during the current study are not publicly available due to restrictions imposed by the hospital’s institutional policies. However, they can be made available from the corresponding author upon reasonable request.

JZ, JCL, GWT, YX—Conception and design; YX, GWT—Provision of study material or patients; JZ, JCL, JLL, GWT, MHL—Collection and assembly of data; JZ, JCL, JG, KL, GWT—Data analysis and interpretation; all authors—Manuscript writing. All authors read and approved the final manuscript. All authors have participated sufficiently in the work and agreed to be accountable for all aspects of the work.

The study was conducted in accordance with the Declaration of Helsinki, and the protocol was approved by the Ethics Committee of Zhongshan Hospital, Fudan University (B2019-075R). Individual consent for this retrospective analysis was waived.

Thanks to all the research participates who provided data for this study.

This article was supported by the Science and Technology Commission of Shanghai Municipality (20DZ2261200).

The authors declare no conflict of interest. Guo-wei Tu is serving as one of the Editorial Board members , Ming-hao Luo and Guo-wei Tu are serving as Guest Editors of this journal. We declare that Ming-hao Luo and Guo-wei Tu had no involvement in the peer review of this article and has no access to information regarding its peer review. Full responsibility for the editorial process for this article was delegated to Michael Dandel.