Association between intraoperative fluid volume and 30-day mortality in patients undergoing lung transplantation: a retrospective cohort study

Introduction

Lung transplantation (LTx) has achieved broad clinical acceptance as a treatment for end-stage pulmonary disease. According to the 2022 report from the International Society for Heart and Lung Transplantation (ISHLT) registry, approximately 70,000 adult LTxs have been performed globally, with over 4,000 procedures conducted annually in recent years (1). Despite advancements in surgical techniques, organ preservation, and perioperative management, mortality among lung transplant recipients remains high (2). A study reported a 30-day postoperative mortality rate of approximately 21.6% following LTx in China (3). The primary causes of early mortality include primary graft dysfunction (PGD), infection, and multiple organ dysfunction syndrome (4). The 30-day postoperative mortality rate reflects the quality of perioperative management and the incidence of early complications, serving as a critical indicator of transplant success and patient prognosis. Therefore, improving 30-day survival is essential for enhancing long-term outcomes and quality of life in lung transplant recipients.

Perioperative fluid management is critical for maintaining circulatory stability and adequate organ perfusion. Previous studies have explored the relationship between perioperative fluid management and early complications after LTx. A retrospective study showed that each additional liter of intraoperative fluid increased the risk of developing severe PGD by approximately 22% (5). As PGD is one of the primary causes of early mortality, this finding suggests that excessive intraoperative fluid administration may indirectly increase the risk of early mortality (6-8). Additionally, another study identified perioperative positive fluid balance as a risk factor for acute kidney injury (AKI) within 72 h postoperatively, which may also contribute to increased 30-day mortality (9). However, existing literature primarily focuses on the relationship between intraoperative fluid management and short-term complications such as PGD and AKI, with limited research directly examining its association with 30-day mortality. Given that 30-day all-cause mortality is a crucial indicator for objectively and comprehensively assessing postoperative recovery and prognosis, there is a need for studies that directly evaluate the relationship between intraoperative fluid volume and 30-day mortality.

This study aimed to investigate the independent effects of intraoperative fluid volume on 30-day mortality after LTx to provide evidence-based guidance for perioperative fluid management to reduce early mortality and improve short-term survival in this population. We present this article in accordance with the STROBE reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-aw-2349/rc).

Methods

Setting and study population

This retrospective study included adult patients who underwent LTx at The Second Affiliated Hospital of Zhejiang University School of Medicine between 2021 and 2023. Approval for this study was granted by the Ethics Committee of The Second Affiliated Hospital of Zhejiang University School of Medicine (No. 2022 0352), and all procedures were performed in accordance with the Declaration of Helsinki and its subsequent amendments. The requirement for informed consent was waived by the Ethics Committee due to the single-center retrospective design.

Patient eligibility

The inclusion criteria encompassed adult patients who had undergone LTx during the study period. Patients were excluded if they (I) underwent multi-organ transplantation or re-transplantation; (II) had missing data on 30-day mortality; or (III) had intraoperative fluid volumes outside the mean ± 3 standard deviation (SDs) range.

Endpoints

The primary endpoint was 30-day mortality after LTx. The secondary endpoints were the incidence of grade 3 PGD within 72 h postoperatively, incidence of AKI within 7 days postoperatively, duration of mechanical ventilation (h), total intensive care unit (ICU) stay (h), and hospital stay (h). Grade 3 PGD was diagnosed when the arterial oxygen partial pressure to fraction of inspired oxygen (PaO₂/FiO₂) ratio fell below 200 mmHg in conjunction with bilateral pulmonary infiltrates evident on chest radiographs (10). AKI was defined as the development of AKI within 7 days postoperatively, based on the Kidney Disease: Improving Global Outcomes (KDIGO) consensus definition (11).

Data extraction

Clinical information was collected through review of the electronic medical record and comprised the following variables: (I) preoperative variables such as demographic characteristics [age, sex, and body mass index (BMI)], primary diagnoses, comorbidities (cardiac dysfunction, respiratory failure, pulmonary hypertension, and diabetes mellitus), American Society of Anesthesiologists (ASA) classification, preoperative life support [mechanical ventilation or extracorporeal membrane oxygenation (ECMO)], and laboratory values (hemoglobin, albumin, serum creatinine and arterial lactate); (II) donor-related variables such as donor age, sex, cause of death, duration of mechanical ventilation, PaO₂/FiO₂ ratio, and cold ischemia time; (III) intraoperative variables such as type of LTx, operative duration, use and type of intraoperative ECMO, need for intraoperative hemodialysis, norepinephrine dose, and intraoperative fluid volume; and (IV) early postoperative variables such as requirement for ECMO support and its duration.

Intraoperative fluid volume was quantified as the cumulative amount of fluid administered from anesthesia induction to the end of surgery, including crystalloid solutions, colloid solutions (albumin), and allogeneic blood products [red blood cells (RBCs) and fresh frozen plasma (FFP)]. The administration of blood products was decided upon collaboratively by the surgical and anesthesia teams. The anesthesia team guided intraoperative fluid management by assessing volume status based on arterial blood gas analysis, thromboelastography (TEG), and pulse contour cardiac output monitoring (PiCCO). Hemodynamic stability was maintained through the administration of vasoactive agents, including phenylephrine, norepinephrine, and vasopressin, in accordance with real-time hemodynamic parameters. Fluid volume was extracted from anesthesia and transfusion records and expressed in L.

Statistical analysis

R software (version 4.3.3) was used for statistical analyses. Baseline characteristics of 30-day survivors and non-survivors were compared. Distributional assumptions were examined with the Shapiro-Wilk test. Normally distributed continuous data were summarized as mean ± SD, and non-normal data as median [interquartile range (IQR)]. Categorical variables were expressed as counts (n) and percentages. Between-group differences were tested with independent t-tests or Mann-Whitney U tests for continuous data, and with χ² or Fisher’s exact tests for categorical data.

Logistic regression models were constructed to assess the association between intraoperative fluid volume and 30-day mortality, with outcomes reported as odds ratios (ORs) and 95 % confidence intervals (CIs). Covariate selection was based on clinical literature. Four logistic regression models were progressively developed to account for confounding factors: Model 1, without adjustment; Model 2, accounted for demographic factors, including age, sex, and BMI; Model 3, further accounted for preoperative factors, such as primary diagnosis, pulmonary hypertension, diabetes mellitus, preoperative ECMO support, serum creatinine, and lactate levels; and Model 4, further accounted for intraoperative factors, including operative duration, type of LTx, norepinephrine dose, intraoperative blood loss, intraoperative ECMO type, and cold ischemia time. Model 4 results are presented as the primary findings. To assess dose-response relationships, intraoperative fluid volumes were divided into quartiles [from the lowest quartile (Q1) to the highest quartile (Q4)], and trends across quartiles were analyzed using Chi-squared test for trends.

Each fluid component (crystalloids, colloids, RBC, and FFP) was individually analyzed in place of total fluid volume to assess its independent associations with 30-day mortality. The significance of the associations between total intraoperative fluid volume and 30-day mortality was set at P<0.05. To control false-positive risk from multiple comparisons, significance levels for fluid components were adjusted using Bonferroni correction.

Subgroup analyses were performed to assess the relationship between the intraoperative fluid volume and 30-day mortality across different demographic characteristics. ORs and 95% CIs for each subgroup were summarized in forest plots. Interaction terms were included in the models to test for heterogeneity, and P values for interaction were reported.

Furthermore, we applied multivariable logistic regression to assess the relationship between intraoperative fluid volume and grade 3 PGD, controlling for age and sex, BMI, primary diagnosis, pulmonary hypertension, operative duration, transplantation type, intraoperative ECMO type, donor sex, donor cause of death, cold ischemia time, and donor PaO₂/FiO₂ ratio. Cox proportional hazards models, incorporating identical covariates, were employed to assess the impact of intraoperative fluid volume on the length of mechanical ventilation, total ICU stay, and hospital stay. Death before discharge was treated as the endpoint.

Variance inflation factors (VIFs) were used to assess multicollinearity among covariates in Model 4. Restricted cubic splines (RCSs) were utilized to investigate nonlinear relationships between intraoperative fluid volume and 30-day mortality. The significance of nonlinearity was assessed using likelihood ratio tests. Receiver operating characteristic (ROC) curves were plotted to quantify the discriminative performance of intraoperative fluid volume for 30-day mortality.

Assuming a 30-day mortality rate of 12.8%, with a relative risk ratio of 1.2 for each additional liter of perioperative fluid volume, and a SD of 2.5, a minimum sample size of 320 patients is required to achieve 80% test power at a two-tailed α level of 0.05.

Results

Figure 1 outlines the eligibility and exclusion criteria of the study. A total of 398 adult patients underwent LTx during the study period. Exclusions were made for 11 patients who received multi-organ transplants, 4 who underwent re-transplantation, and 1 patient with missing 30-day mortality. Additionally, 11 patients with intraoperative fluid volumes beyond the mean ± 3 SDs were excluded, leaving 375 patients for the final analysis.

Figure 1 Flow chart of the study. SD, standard deviation.

Among the 375 patients, 48 died within 30 days of transplantation, resulting in a 30-day mortality rate of 12.8%. Among the 48 non-survivors, the primary causes of death were septic shock (n=19, 39.6%), cardiogenic shock (n=17, 35.4%), and hemorrhagic shock (n=10, 20.8%), followed by cerebrovascular accidents (n=2, 4.2%). Compared to survivors, non-survivors had significantly higher preoperative lactate levels (1.85 vs. 1.60 mmol/L, P=0.047), longer surgery durations (353 vs. 310 min, P<0.001), higher intraoperative norepinephrine doses (6.00 vs. 4.00 mg, P=0.04), higher intraoperative blood loss (0.80 vs. 1.20 L, P=0.006), and longer cold ischemia times (7.70 vs. 7.50 h, P=0.03). Non-survivors also received significantly higher intraoperative fluid volumes than survivors (4.92 vs. 3.00 L, P<0.001). Between-group comparisons showed no significant difference in age, sex, BMI, primary diagnosis, diabetes mellitus, and preoperative ECMO support (Table 1).

Four logistic regression models were established to assess the association between intraoperative fluid volume and 30-day mortality (Table 2). Intraoperative fluid volume, when considered as a continuous variable, was significantly linked to 30-day mortality across all models (Model 1, OR =1.43, 95% CI: 1.26–1.64; Model 2, OR =1.50, 95% CI: 1.30–1.73; Model 3, OR =1.64, 95% CI: 1.38–1.95; Model 4, OR =2.70, 95% CI: 1.89–3.87; all P<0.001). VIF for Model 4 remained below 10, confirming that multicollinearity among the included covariates was negligible (Figure S1). RCS analysis did not demonstrate significant nonlinear relationship (P for nonlinearity =0.84; Figure S2). The ROC curve for intraoperative fluid volume predicting 30-day mortality yielded an area under the curve (AUC) of 0.72 (95% CI: 0.64–0.80) with a cut-point of 4.79 L (Figure S3). After adjusting the fluid volume based on patient weight, we found a positive correlation between the total intraoperative fluid volume per kilogram of body weight and the 30-day mortality rate (OR =1.05, 95% CI: 1.03–1.07, P<0.001). When intraoperative fluid volume was divided into quartiles, 30-day mortality increased from Q1 to Q4 (P for trend <0.001). In the Model 4 with full covariate adjustment, the ORs (95% CIs) for Q2, Q3, and Q4 compared to Q1 were: Q2, OR =1.28, 95% CI: 0.37–4.42, P=0.69; Q3, OR =1.79, 95% CI: 0.51–6.25, P=0.36; Q4, OR =14.31, 95% CI: 3.65–56.38, P<0.001).

Regression analyses indicated significant associations between intraoperative volumes of crystalloids, RBC, and FFP with 30-day mortality (Table 3). After Bonferroni correction, each additional liter of crystalloids increased mortality risk by approximately 74% (P=0.01), RBC by 2.59-fold (P<0.001), and FFP by 3.21-fold (P<0.001). In contrast, colloid volume was not significantly associated with mortality (P=0.56). Stratified analyses by age, pulmonary hypertension, preoperative ECMO support, transplant type, operative duration, and cold ischemia time showed consistent trends across subgroups (Figure 2). Interaction terms were not statistically significant (all P for interaction >0.05). However, among patients aged ≥65 years or those with a surgical duration of less than 300 minutes, the link between intraoperative fluid volume and 30-day mortality did not achieve statistical significance (P>0.05).

Figure 2 Subgroup analysis of the associations between intraoperative fluid volume and 30-day mortality. CI, confidence interval; ECMO, extracorporeal membrane oxygenation; OR, odds ratio.

Eighty patients developed grade 3 PGD, and 208 patients developed AKI. An additional liter of intraoperative fluid raised the risk of grade 3 PGD by 18% (OR =1.18, 95% CI: 1.01–1.40, P=0.04) and the risk of AKI by 30% (OR =1.30, 95% CI: 1.11–1.53, P=0.001). Durations for mechanical ventilation, total ICU stay, and hospital stay were 35 h (IQR, 19–111.5 h), 141 h (IQR, 68.4–434.5 h), and 864 h (IQR, 624–1,392 h), respectively. In the multivariate Cox proportional hazards models, each additional liter of intraoperative fluid was linked to a 22% delay in extubation [hazard ratio (HR) =0.78, 95% CI: 0.72–0.83, P<0.001], 19% longer total ICU stay (HR =0.81, 95% CI: 0.74–0.88, P<0.001), and 20% longer hospital stay (HR =0.80, 95% CI: 0.73–0.89, P<0.001) (Figure 3).

Figure 3 Multivariable associations between intraoperative fluid volume and secondary outcomes adjusting for covariates. AKI and PGD effects are presented as OR, while time to ICU extubation, ICU length of stay, and hospital length of stay effects are presented as HR. AKI, acute kidney injury; CI, confidence interval; HR, hazard ratio; ICU, intensive care unit; OR, odds ratio; PGD, primary graft dysfunction.

Discussion

This study enrolled 375 adult lung transplant recipients and is the first to assess the independent associations between intraoperative fluid volume, including its individual components, and 30-day mortality. After adjustment for confounders, intraoperative fluid volume was significantly associated with 30-day mortality, whether treated as a continuous or categorical variable. Additionally, intraoperative volumes of crystalloids, RBC, and FFP were significantly associated with increased 30-day mortality, while colloid volume showed no significant correlation.

Previous studies have linked intraoperative fluid administration to early complications. Geube et al. prospectively analyzed 492 lung transplant recipients at the Cleveland Clinic and reported that each additional liter of fluid was associated with a 22% higher risk of grade 3 PGD (5). As PGD is a key driver of early mortality, this finding corroborates our observed significant association between fluid volume and 30-day mortality (12). Shen et al. found that positive perioperative fluid balance increases the risk of postoperative AKI, which may increase early postoperative mortality (9). These studies underscore the importance of avoiding excessive fluid administration to improve early outcomes after LTx. While previous investigations have focused on complications such as PGD and AKI, few have directly examined 30-day mortality. Our study extends prior work by quantifying the independent effects of total intraoperative fluid volume and its components on mortality, and by establishing a 4.79 L cutoff, offering a clear clinical reference for perioperative fluid management. Notably, our study identified cardiogenic shock and septic shock as the primary causes of death. These findings align with pathophysiological mechanisms wherein fluid overload precipitates circulatory failure by increasing cardiac burden and worsening pulmonary edema, while simultaneously exacerbating severe infection via tissue edema and perfusion impairment.

The association between fluid management and outcomes observed in lung transplant recipients aligns with findings in other surgical populations. In a multicenter prospective cohort study of 479 high-risk elective surgery patients admitted to the ICU, Silva et al. reported that non-survivors had significantly higher intraoperative fluid balances than survivors, with each 100 mL increment associated with a 2.4% increase in mortality (13). In cardiac surgery, a retrospective analysis of 1,358 patients by Pradeep et al. found that patients receiving intraoperative fluid volumes above the median (3.9 L) had significantly lower 90-day survival (14). Similarly, Smith et al. reported in 2,327 aortic valve replacement patients that positive fluid balance was associated with increased risks of myocardial infarction, AKI, and 30-day mortality (15). Collectively, these findings and ours underscore the need for precise intraoperative fluid restriction to mitigate early postoperative mortality across surgical specialties.

Several pathophysiological mechanisms may explain how excessive fluid administration increases mortality risk in lung transplant recipients. First, large-volume fluid administration raises pulmonary capillary pressure and exacerbates pulmonary edema. In the background of impaired lymphatic drainage and increased vascular permeability in the transplanted lung, excessive fluid administration during reperfusion further exacerbates endothelial barrier disruption, precipitating acute non-cardiogenic pulmonary oedema and elevating postoperative early mortality (16). Our findings showed that each additional liter of crystalloid was associated with an 74% increase in 30-day mortality, whereas colloids had no significant impact. This discrepancy may be explained by the small molecular size of crystalloids, which readily diffuse into the interstitium, while colloids, such as albumin, remain predominantly intravascular. A secondary analysis of the PROPPR trial in patients with hemorrhagic trauma found that each 500 mL increment in crystalloid administration increased acute respiratory distress syndrome risk by 9% within 6 h postoperatively (17). These data support our findings that excessive crystalloid administration significantly increases mortality risk in lung transplant recipients and suggests to prioritize colloids for intraoperative volume resuscitation to minimize pulmonary edema and related complications.

Excessive intraoperative fluid administration may also exacerbate ischemia-reperfusion injury through inflammatory mechanisms. Large-volume fluid administration can damage pulmonary capillary endothelium, disrupt the basement membrane, increase vascular permeability, and promote protein extravasation. Transfusion of RBC and FFP may trigger transfusion-related acute lung injury, a non-cardiogenic pulmonary edema occurring within 6 h of transfusion that is typically triggered by human neutrophil antigen or human leukocyte antigen antibodies in donor blood (18). Microparticles and hemoglobin fragments from packed RBC can activate complement system and immune cells, while FFP contains high levels of antibodies and cytokines that can amplify a cytokine storm (19). Two multicenter cohort studies (n>500) independently associated large intraoperative RBC transfusions with early PGD (20,21). Furthermore, several retrospective cohort studies involving over 5,000 patients have consistently demonstrated that perioperative blood transfusion increases postoperative complications and mortality after cardiac surgery (22,23). These findings are consistent with our results, which associate RBC and FFP administration with increased 30-day mortality.

Dilutional anemia induced by large-volume crystalloid administration can reduce arterial oxygen saturation, leading to tissue hypoxia, increased lactate, and impaired organ perfusion. Hemodilution has been linked to elevated lactate levels, AKI, and increased mortality (14). Fluid overload also causes systemic tissue edema, impeding oxygen and metabolite diffusion. Encapsulated organs like the kidneys and liver are particularly vulnerable due to limited interstitial volume, which compromises perfusion pressure and organ function (24). Lung transplant recipients often present with pulmonary hypertension or right ventricular dysfunction, making them highly sensitive to changes in cardiac preload and afterload. Excessive intraoperative fluid administration not only markedly elevates right ventricular preload and pulmonary arterial pressure but also predisposes to or exacerbates right heart failure. This, in turn, worsens systemic and hepatic-renal venous congestion, creating a vicious cycle that ultimately increases postoperative complications and mortality risk.

In summary, excessive intraoperative fluid administration significantly increases mortality risk after LTx through multiple pathophysiological pathways. A restrictive or goal-directed fluid strategy is recommended to prevent fluid overload (25). Hemodynamic parameters, such as central venous pressure, pulmonary artery wedge pressure, and right ventricular end-diastolic volume, should be closely monitored to assess fluid responsiveness. Dynamic indicators, such as pulse pressure variation, stroke volume variation, and systolic pressure variation, can help optimize tissue perfusion management. Infusion rates and volumes must be strictly controlled, with vasoactive drugs prioritized to stabilize circulation. Patients receiving >4.79 L intraoperatively should be classified as high risk and considered for early ECMO or continuous renal replacement therapy to support vital organ oxygenation. Based on the results of this study, we recommend prioritizing the use of human albumin for fluid resuscitation in appropriate cases, in order to enhance plasma colloid osmotic pressure, reduce capillary leakage, and protect the endothelial glycocalyx.

The use of transesophageal echocardiography can further guide goal-directed fluid strategy. Finally, in terms of blood transfusion management, it is recommended to minimize blood loss and transfusion requirements to improve patient prognosis. Surgical teams should prioritize minimally invasive and precise hemostatic techniques to reduce bleeding, employ restrictive transfusion thresholds, and use coagulation monitoring (e.g., ROTEM) to guide targeted transfusions and limit exposure to RBC and FFP. Bleeding due to coagulopathy can be managed using fibrinogen concentrates, prothrombin complex concentrates, or antifibrinolytic agents (26).

There are several limitations in this study. First, despite adjusting for multiple confounders, this single-center retrospective observational study may still be affected by potential biases and unmeasured confounders, and cannot establish causality. Second, our analysis focused solely on intraoperative fluid volume and did not include postoperative fluid volume. Future studies should investigate fluid intake and balance during the first 72 h postoperatively to provide a more comprehensive understanding. Finally, as this study examined only 30-day outcomes, the impact of intraoperative fluid administration on long-term survival and chronic graft function remains unclear. Future multicenter, prospective, randomized controlled trials are required to validate the impact of intraoperative fluid volume on 30-day mortality and to develop individualized fluid management protocols to optimize both short- and long-term outcomes in LTx recipients.

Conclusions

This study demonstrates a significant association between intraoperative fluid volume and 30-day mortality after LTx. These findings support the use of restrictive fluid administration strategies combined with dynamic targeted monitoring to avoid unnecessary blood product administration.

Acknowledgments

During the preparation of this manuscript, the authors utilized ChatGPT to assist with language editing. After using this tool, the authors reviewed and edited the content as needed and take full responsibility for the content of the publication.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-aw-2349/rc

Data Sharing Statement: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-aw-2349/dss

Peer Review File: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-aw-2349/prf

Funding: This study was supported by the National Natural Science Foundation of China (Nos. U24A200213, 82371217, and 82071227), the National Clinical Key Specialty Construction Project of China 2021 (No. 2021-LCZDZK-01), the Key Research and Development Program of Zhejiang Province (No. 2024C03091), the Zhejiang Clinovation Pride (No. CXTD202501020), and the Leading Health Talents of Zhejiang Province, Zhejiang Health Office [No. 18 (2020)].

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-aw-2349/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was approved by the Ethics Committee of The Second Affiliated Hospital of Zhejiang University School of Medicine (No. 2022 0352). The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The requirement for informed consent was waived by the Ethics Committee due to the single-center retrospective design.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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