Dong AL, Li HX, Jia LL, Sun Y, Gao W, Yu WL. Association between central venous pressure and postoperative pulmonary complications in living-donor liver transplantation for pediatric patients. World J Gastrointest Surg 2026; 18(9): 122362 [DOI: 10.4240/wjgs.122362]
Corresponding Author of This Article
Wen-Li Yu, PhD, Chief Physician, Department of Anesthesiology, Tianjin First Central Hospital, No. 24 Fukuang Road, Nankai District, Tianjin 300192, China. yzxwenliyu@163.com
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Gastroenterology & Hepatology
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Dong AL, Li HX, Jia LL, Sun Y, Gao W, Yu WL. Association between central venous pressure and postoperative pulmonary complications in living-donor liver transplantation for pediatric patients. World J Gastrointest Surg 2026; 18(9): 122362 [DOI: 10.4240/wjgs.122362]
Author contributions: Dong AL and Li HX contributed equally to all aspects of this manuscript including study conception and design, data acquisition, analysis, and interpretation, and drafting of the article; Jia LL and Sun Y contributed to study conception and design, data analysis and interpretation, and drafting of the article; Gao W contributed to data acquisition; and Yu WL supervised the research and approved the final draft.
AI contribution statement: Portions of this manuscript were edited using AI tools solely for language refinement. The authors carefully reviewed and verified all AI-assisted outputs and take full responsibility for the scientific content of the manuscript.
Supported by Tianjin Horizontal Research Project, No. YLGX-MZ-2022008; Tianjin Key Clinical Speciality (Anaesthesiology) Construction Project; and Tianjin Key Medical Construction Project, No. TJYXZDXK-3-022C.
Institutional review board statement: This retrospective study was approved by the Institutional Review Board of First Central Hospital of Tianjin Medical University No. KYAP2025-153.
Informed consent statement: The need for patient consent was waived due to the retrospective nature of the study.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: No additional data are available.
Corresponding author: Wen-Li Yu, PhD, Chief Physician, Department of Anesthesiology, Tianjin First Central Hospital, No. 24 Fukuang Road, Nankai District, Tianjin 300192, China. yzxwenliyu@163.com
Received: April 20, 2026 Revised: June 30, 2026 Accepted: August 25, 2026 Published online: September 27, 2026 Processing time: 152 Days and 3 Hours
Abstract
BACKGROUND
Perioperative lung injury and postoperative pulmonary complications (PPCs) contribute substantially to respiratory morbidity and mortality and adversely affect outcomes in pediatric patients undergoing liver transplantation. In several surgical populations, different fluid management strategies have been associated with postoperative complications, particularly PPCs; however, this relationship remains unclear in pediatric liver transplantation.
AIM
To investigate the association between central venous pressure (CVP) and PPCs in pediatric patients undergoing living-donor liver transplantation (LDLT).
METHODS
We retrospectively reviewed pediatric patients who underwent LDLT between January 2019 and December 2024. The primary outcome was the incidence of PPCs. Multivariate logistic regression and restricted cubic spline analyses were used to evaluate the association between CVP and PPC incidence.
RESULTS
A total of 426 patients met the inclusion criteria, of whom 210 developed PPCs. A nonlinear association was observed between CVP and PPCs in pediatric LDLT recipients. In multivariate logistic regression analysis, CVP was independently associated with PPC incidence. After adjustment for potential confounders, each 1-unit increase in CVP was associated with a 9% reduction in the risk of PPCs [odds ratio (OR) = 0.91; 95% confidence interval (95%CI): 0.85-0.97; P = 0.007]. Threshold analysis showed that the OR for PPCs was 0.834 (95%CI: 0.752-0.925; P = 0.0006) among patients with CVP < 9.3 cmH2O.
CONCLUSION
An inverse association between CVP level and PPC incidence is observed among pediatric LDLT recipients with CVP < 9.3 cmH2O. Prospective longitudinal studies are warranted to establish causality and clarify the underlying mechanisms.
Core Tip: This retrospective study identified a novel J-shaped association between intraoperative central venous pressure (CVP) and postoperative pulmonary complications (PPCs) in 426 pediatric living-donor liver transplant recipients. Multivariate analysis demonstrated that each 1-unit increase in CVP was associated with a 9% reduction in PPC risk [odds ratio (OR) = 0.91, 95% confidence interval: 0.85-0.97, P = 0.007], with the strongest association observed at CVP < 9.3 cmH2O (OR = 0.834, P = 0.0006). These findings may provide insight into CVP as a modifiable factor for PPC mitigation in pediatric transplantation.
Citation: Dong AL, Li HX, Jia LL, Sun Y, Gao W, Yu WL. Association between central venous pressure and postoperative pulmonary complications in living-donor liver transplantation for pediatric patients. World J Gastrointest Surg 2026; 18(9): 122362
Pediatric liver transplantation has emerged as an advanced and effective treatment for children with end-stage liver disease in recent years, substantially improving survival and quality of life[1,2]. However, perioperative pulmonary adverse events, particularly postoperative pulmonary complications (PPCs), remain a major concern because they increase morbidity and mortality and adversely affect postoperative outcomes[3,4]. PPCs are associated with high global mortality, with 14%-30% of affected patients dying within 30 days after surgery[5]. Notably, approximately half of the risk factors for PPCs are potentially modifiable and related to perioperative care, including surgical technique, anesthetic management, fluid and transfusion management, and hemodynamic monitoring[5,6]. Therefore, targeted lung-protective perioperative strategies that optimize oxygenation and reduce pulmonary injury are essential for improving short- and long-term outcomes in pediatric recipients[7].
Children with end-stage liver disease often present with hepatosplenomegaly, hypoalbuminemia, coagulopathy, and anemia, all of which may predispose them to intravascular volume depletion. This vulnerability can be exacerbated by prolonged operative times and substantial intraoperative fluid losses. Children with biliary atresia who have undergone Kasai portoenterostomy may develop severe intra-abdominal adhesions and require extensive dissection, thereby increasing the risk of major bleeding[8,9]. Pediatric patients, especially infants, have a narrow physiologic range for fluid balance and limited tolerance to both hypovolemia and fluid overload. Advanced hemodynamic monitoring is therefore needed to assess intravascular volume, guide fluid management, and optimize preload during surgery. Volume assessment in children is particularly challenging because cardiopulmonary and vascular compliance differ across developmental stages and age groups[10]. Central venous pressure (CVP) has been used for more than half a century as a surrogate marker of intravascular volume to guide fluid management. In adult liver transplantation, maintaining low CVP (LCVP) as an anesthetic technique has been associated with improved outcomes[11,12]. However, in pediatric populations, reliable indicators for fluid management remain limited, and CVP continues to be widely used to guide intraoperative volume management.
Despite the widespread use of CVP monitoring, large-scale studies evaluating its role in pediatric liver transplantation are scarce. Although existing evidence supports the clinical relevance of CVP[13-15], its relationship with PPCs in pediatric liver transplantation remains unclear. Therefore, this retrospective study analyzed clinical data from pediatric living-donor liver transplantation (LDLT) recipients to clarify the association between intraoperative CVP and PPCs and to inform evidence-based perioperative fluid management.
MATERIALS AND METHODS
This retrospective study was approved by the Institutional Review Board of First Central Hospital of Tianjin Medical University. Owing to the observational study design, the requirement for written informed consent was waived. The study was reported in accordance with the Strengthening the Reporting of Observational Studies in Epidemiology guidelines, and the manuscript adheres to the relevant reporting standards[16,17].
Study population and data collection
This retrospective analysis included patients who underwent liver transplantation at our center between January 2019 and December 2024. The exclusion criteria were age ≥ 18 years, severe underlying cardiopulmonary disease (particularly preoperative pneumonia), or repeat liver transplantation. Recipient variables included sex, age, weight, pediatric end-stage liver disease (PELD) score, and history of Kasai procedure. Preoperative laboratory variables included albumin (ALB), red blood cell (RBC) count, hemoglobin (HGB), platelet count, international normalized ratio, prothrombin time, activated partial thromboplastin time, alanine aminotransferase, aspartate aminotransferase, total bilirubin, direct bilirubin, alkaline phosphatase, gamma-glutamyl transferase, and creatinine. Intraoperative variables included graft-to-recipient weight ratio (GRWR), graft cold ischemia time, CVP, HGB, mean blood pressure, lactate level, blood loss, urine output, blood transfusion volume, fresh frozen plasma (FFP) transfusion, surgical duration, ischemia-reperfusion (IR) events, adrenaline administration, ascites volume, duration of the anhepatic phase and intraoperative fluid balance (defined as the total volume of infused crystalloids and blood products, minus the combined volume of ascites removed, intraoperative urine output and blood loss). Postoperative variables included duration of mechanical ventilation, intensive care unit (ICU) length of stay, total hospital stay, and incidence of unplanned intubation and pneumonia.
Study outcomes and definitions
PPCs were defined as a composite endpoint comprising fatal and non-fatal respiratory events during the postoperative period. The clinical spectrum ranged from mild conditions, such as atelectasis, to severe, life-threatening respiratory failure[18,19]. Although these events arise through different pathophysiological mechanisms, their combined effect on postoperative recovery is clinically important[20]. Accordingly, the primary outcome was the occurrence of any predefined respiratory event, including respiratory failure, pulmonary infection, pulmonary edema, clinically meaningful atelectasis, or pleural effusion, within 7 days postoperatively[18-20].
Anesthesia management
All pediatric patients underwent general anesthesia in accordance with standard preoperative fasting guidelines[21]. After admission to the operating room, continuous electrocardiographic and pulse oximetry monitoring was established. Anesthesia was induced with intravenous midazolam (0.15 mg/kg), propofol (2-3 mg/kg), fentanyl (2-5 µg/kg), and rocuronium (0.6-1.0 mg/kg). Mechanical ventilation was maintained with a tidal volume of 8-10 mL/kg, a respiratory rate of 20-24 breaths/minute, an inspiratory-to-expiratory ratio of 1:1.5-2.0, peak airway pressures of 10-20 mmHg, and no positive end-expiratory pressure. End-tidal CO2 was maintained between 30 mmHg and 45 mmHg throughout the procedure. FiO2 was set to 100%) during anesthetic induction, and 50% was maintained thereafter. Anesthesia was maintained with sevoflurane (1.5%-2.5% inspired concentration), continuous propofol infusion (9-15 mg/kg/hour), intermittent fentanyl (1-3 µg/kg), and cisatracurium infusion (0.12 mg/kg/hour). Ultrasound-guided radial artery cannulation was used for continuous arterial pressure monitoring, and right internal jugular vein catheterization was used for CVP measurement. Hemodynamic targets included a mean arterial pressure of 40-65 mmHg, urine output > 1 mL/kg/hour, and arterial oxygen saturation ≥ 98% during surgery. Core temperature was maintained between 35.5 °C and 37.5 °C using fluid warmers, active airway humidification, and forced-air warming systems. Fluid management consisted of 5% ALB and Ringer's solution and was adjusted dynamically according to real-time hemodynamic parameters and CVP trends. Hematologic management aimed to maintain HGB concentrations ≥ 80 g/L through protocolized RBC transfusion, while balancing oxygen delivery against transfusion risk. Coagulation was monitored using a Sonoclot® analyzer (Sienco, Arvada, CO, United States), and FFP was administered when Sonoclot parameters indicated clinically important coagulopathy (clot rate < 0.3 or activated clotting time > 200 seconds). Systolic blood pressure and heart rate were maintained within ± 20% of preoperative baseline values by adjusting anesthetic depth, titrating vasoactive infusions, and providing dynamic fluid resuscitation.
Surgical technique
Graft implantation was performed using the piggyback technique with partial clamping of the inferior vena cava. After portal vein anastomosis was completed, graft reperfusion was achieved by sequentially unclamping the hepatic venous outflow followed by the portal vein. Hepatic arterial reconstruction was performed before biliary anastomosis[22].
Statistical analysis
All statistical analyses were performed using R software (version 3.3.2; R Foundation for Statistical Computing) and Free Statistics software (version 2.2). A two-tailed P value < 0.05 was considered statistically significant. Continuous variables are expressed as the mean ± SD for normally distributed data or as the median [interquartile range (IQR)] for non-normally distributed data. Categorical variables are presented as n (%). Group comparisons were performed using one-way analysis of variance for normally distributed continuous variables and the χ2 test or Cochran-Armitage trend test for categorical variables. Multivariate logistic regression was used to estimate adjusted odds ratios (ORs) with 95% confidence intervals (95%CIs) for PPCs. Covariates were selected based on their association with the outcome of interest or if their inclusion altered the effect estimate by > 10%[23]. Three models were constructed: An unadjusted (crude) model; a minimally adjusted model including recipient age and sex; and a fully adjusted model that included recipient age, sex, graft cold ischemia time, intraoperative blood loss, urine output, infusion volume, surgical duration, IR events, ascites volume, duration of the anhepatic phase, GRWR, and ICU length of stay. Nonlinear associations between CVP and PPC incidence were assessed using restricted cubic spline functions. Threshold effects were evaluated using piecewise linear regression, with inflection points determined through likelihood maximization and validated by bootstrap resampling. Subgroup analyses were performed using logistic regression models to assess the robustness of the associations across strata defined by recipient age, sex, PELD score, adrenaline administration, HGB level, surgical duration, mechanical ventilation time, early allograft dysfunction, IR events, and pneumonia. The potential impact of unmeasured confounding between CVP groups and PPCs was assessed by calculating E-values[24]. Propensity score matching (PSM) was used to reduce imbalance and potential bias[25]. A logistic regression model was constructed using the following covariates: Age, sex, cold ischemia time, blood loss, urine, liquid transfusion, blood transfusion, IR events, anthepatic phase time and PELD score. To minimize conditional bias, 1:3 nearest-neighbor matching algorithm with a caliper width 0.2 was applied. Matching balance was evaluated using the standardized mean difference, with a value < 0.1 considered acceptable.
RESULTS
Demographics and baseline characteristics
Among the 426 eligible patients, 216 did not develop PPCs whereas 210 patients did, resulting in an overall PPC incidence of 49.3% (Figure 1). Table 1 summarizes the baseline demographics of the patients. The median age was 8 (IQR: 6.0-15.8) months, and 57.7% of the patients were female. Patients who developed PPCs had lower CVP (median: 5.0 cmH2O; IQR: 3.0-8.0 cmH2O) than those without PPCs (median: 7.0 cmH2O; IQR: 5.0-8.6 cmH2O; P < 0.001). The PPC group also had longer surgical and ICU durations, more frequent adrenaline use (55.7% vs 39.4%, P < 0.001), and higher proportions of IR procedures and unplanned intubation. Preoperative laboratory values did not differ significantly between the groups (Table 1).
In addition, the PPC group included a higher proportion of males and patients with a prior surgical history, including Kasai operation and exploratory laparotomy (78.1% vs 60.2%, P < 0.001; Table 1).
Association between CVP and PPCs
Multivariate logistic regression analysis (Table 2) revealed a negative association between CVP and PPC incidence. In the unadjusted model, each 1-unit increase in CVP was associated with 10% lower odds of developing PPCs (OR = 0.90; 95%CI: 0.85-0.96; P = 0.001), and this association persisted in the fully adjusted model (OR = 0.91; 95%CI: 0.85-0.97; P = 0.0017). The E-value of this cohort was 1.43. When CVP was dichotomized at 6 cmH2O, patients with CVP > 6 cmH2O had lower odds of PPCs than those with CVP ≤ 6 cmH2O in the fully adjusted model (OR = 0.55, 95%CI: 0.36-0.84, P = 0.005). Further stratified analysis showed that, compared with patients with CVP < 5 cmH2O, those with CVP between 5 cmH2O and 10 cmH2O had a significantly lower risk of PPCs (OR = 0.45, 95%CI: 0.28-0.72, P = 0.001), whereas the association for CVP > 10 cmH2O also remained statistically significant (P = 0.023). After PSM, 204 patients were well matched, with no significant differences between the matched groups (Supplementary Table 1). The OR for the incidence of PPCs was 2.27 (95%CI: 1.04-4.99, P = 0.040) after PSM.
Table 2 Multivariate logistic regression analysis for the study participants.
Figure 2 presents the subgroup analysis results. Stratification by age, sex, PELD score, adrenaline administration, fluid transfusion, surgical duration, mechanical ventilation time, history of Kasai operation, IR events and incidence of pneumonia revealed no significant interactions (all P > 0.05), indicating the applicability and robustness of CVP across these subgroups.
Figure 2 Subgroup analysis between central venous pressure and postoperative pulmonary complication.
Subgroup forest plot for the incidence of postoperative pulmonary complications. Adjusted for age, sex, pediatric end-stage liver disease, adrenaline administration, liquid transfusion, surgery duration, mechanical ventilation time, history of Kasai operation, ischemia-reperfusion events and incidence of pneumonia. OR: Odds ratio; 95%CI: 95% confidence interval; IR: Ischemia-reperfusion; PELD: Pediatric end-stage liver disease.
Nonlinear relationship between CVP and PPC incidence
After adjustment for relevant covariates, a nonlinear dose-response relationship between CVP and PPC incidence was observed (Figure 3). Using a two-piecewise linear regression model, the CVP threshold was estimated at 9.281 cmH2O. Below this threshold, each 1-unit increase in CVP was associated with a 16.6% reduction in PPC risk (OR = 0.834; 95%CI: 0.752-0.925; P < 0.001; Table 3). Above this threshold, a stable association was observed between CVP and PPC incidence (OR = 1.193; 95%CI: 0.847-1.680; P > 0.05; Table 3).
Figure 3 Nonlinear relationship between central venous pressure and postoperative pulmonary complications.
Adjustment factors included age + sex + cold ischemia time + blood loss + urine + liquid transfusion + blood transfusion + ischemia-reperfusion + anthepatic phase time + pediatric end-stage liver disease sore. Restricted cubic splines results for the incidence of postoperative pulmonary complications. Curves represent estimated adjusted odds ratios (ORs), and shaded ribbons represent 95% confidence intervals. The vertical dotted line represents the lowest point of the curve which represents the lowest OR. The horizontal dashed line represents a hazard ratio of 1.0. PPC: Postoperative pulmonary complication; CVP: Central venous pressure.
Table 3 Threshold effect analysis of central venous pressure on postoperative pulmonary complications.
This retrospective study showed that intraoperative CVP was significantly associated with PPC incidence in children undergoing LDLT. This finding aligns with that of Bar et al[26], who reported that intraoperative fluid overload during pediatric liver transplantation impaired postoperative pulmonary function. In the present cohort, patients who developed PPCs also required unplanned intubation more frequently and had longer ICU stays.
Recent clinical studies have demonstrated a significant association between prolonged liver transplantation surgery and PPC occurrence. Proposed mechanisms include longer mechanical ventilation, greater blood transfusion and fluid requirements, and impaired thermoregulation[27,28]. Consistent with these findings, our results showed that patients in the PPC group had longer surgical durations. Prolonged operative times are typically accompanied by longer mechanical ventilation, predisposing patients to ventilator-associated lung injury, atelectasis, impaired mucociliary clearance, and ventilator-associated infection. Furthermore, patients with a prior surgical history were more likely to develop PPCs, potentially due to abdominal adhesions that increase operative difficulty, bleeding risk, and surgical duration.
In adult liver transplantation and other hepatic resections, CVP is traditionally maintained below 5 mmHg. Restrictive fluid management strategies during adult liver transplantation have been shown to reduce pulmonary complications and perioperative bleeding. However, evidence in pediatric liver transplantation remains limited, and the optimal CVP target has not yet been established.
The optimal method for assessing volume status in pediatric patients remains controversial[29]. Although several indicators for assessing circulatory volume status are available, no universally validated gold standard exists. CVP monitoring remains widely used for intravascular volume management because it is accessible and clinically practical[30,31]. Although CVP measurements can be affected by patient positioning, intrathoracic pressure, and myocardial contractility, they remain useful for tracking changes in volume status and hemodynamic trends[30]. CVP fluctuates substantially during the anhepatic phase, particularly during clamping and subsequent release (reperfusion) of the portal vein and inferior vena cava. In contrast, CVP values during the neohepatic (post-reperfusion) phase are relatively stable and may more reliably reflect intraoperative volume status. Therefore, this study used the mean CVP measured during the neohepatic phase.
Fan et al[3] reported that pathologically elevated CVP was associated with prolonged mechanical ventilation and a higher risk of adverse postoperative outcomes in pediatric liver transplantation, which is consistent with the clinical relevance of CVP in our cohort. In the present study, CVP was negatively associated with PPC incidence, and this association remained significant after adjustment for potential covariates and confounders. To assess the potential impact of unmeasured confounding on the study conclusions, we calculated the E-value. For the observed primary endpoint (OR = 0.91), the corresponding E-value is 1.43. This indicates that, to fully explain away the observed effect, an unmeasured confounder would need to be associated with both the exposure and the outcome by at least a 1.43-fold risk ratio. Although an E-value of 1.43 represents a moderate level, it provides some support for the robustness of our findings.
Owing to developmental differences between infants and school-aged children, CVP reference ranges vary significantly[30]. Consequently, age represents a potential confounder in studies evaluating PPCs. Therefore, we adjusted for age and performed subgroup analyses. The results were consistent across age strata, including the 1- and 3-year cohorts, supporting the robustness of our findings.
In several surgical cohorts, fluid management strategies have been associated with postoperative complications, particularly PPCs[32-34]. These adverse outcomes may arise through two pathways: Restrictive approaches can induce organ hypoperfusion secondary to hypovolemia, whereas liberal approaches may provoke venous congestion, capillary leakage, and tissue edema[35,36]. Importantly, substantial clinical evidence identifies intraoperative fluid overload as a modifiable risk factor for PPCs, including pneumonia, pleural effusion, and pulmonary edema[8,37]. Acute respiratory distress syndrome can result from intraoperative hemodynamic instability, which induces hepatic hypoperfusion and IR injury (IRI), thereby amplifying systemic inflammatory responses[38]. Consistent with this mechanism, patients who developed PPCs in our cohort had a higher incidence of IR events (P < 0.001), greater vasopressor requirements (P < 0.001), and longer operative times (P = 0.001).
During liver transplantation, the pulmonary system is particularly vulnerable to graft IRI because the lungs are the first capillary bed to receive portal venous return[39]. IRI triggers a systemic inflammatory cascade that affects pulmonary tissue, causing vascular endothelial injury, increased pulmonary vascular resistance, enhanced microvascular permeability, and exacerbated alveolar edema[40]. Vasoactive agents, such as epinephrine, are used to improve microcirculation by inducing peripheral vasoconstriction, which elevates perfusion pressure[41].
Rational volume management is an important lung-protective strategy during the perioperative period of liver transplantation. Effective fluid management protocols can reduce PPC incidence[37]. In this retrospective study, intraoperative CVP was significantly associated with PPC occurrence in pediatric LDLT recipients. Rather than treating CVP as an indeterminate range, we aimed to identify a clinically relevant intraoperative CVP threshold that could help guide fluid management and mitigate PPC risk.
Our analysis revealed a nonlinear, non-equidistant relationship between CVP and PPC incidence, consistent with a dose-response pattern. Using a threshold of 9.3 cmH2O, we observed a significant association between CVP and PPCs. When CVP was below 9.3 cmH2O, PPC incidence decreased as CVP increased; however, the association was no longer statistically significant at CVP ≥ 9.3 cmH2O. These findings suggest a saturation effect in the CVP-PPC relationship. This J-shaped pattern may be consistent with several physiological mechanisms in pediatric patients. One possibility is that children may tolerate moderate degrees of right ventricular volume loading; during this period, right ventricular performance could help maintain pulmonary blood flow via the Frank-Starling mechanism. If CVP rises substantially and remains elevated, right ventricular dilation and interventricular septal shift may affect left ventricular filling through ventricular interdependence. Under such circumstances, cardiac output could decrease, and reduced systemic and pulmonary perfusion may impair pulmonary microcirculation—potentially contributing to the development of PPCs. Overall, these considerations offer plausible explanations consistent with the non-linear association observed in our study. Further prospective multicenter studies are warranted to validate the identified threshold effect and to evaluate whether CVP-guided management can reduce PPCs and improve clinical outcomes.
Although current LCVP protocols lack evidence-based thresholds, our exploratory analysis identified an association between CVP < 9.3 cmH2O and PPC incidence in this cohort. PPC incidence differed across CVP levels and the relationship appeared to attenuate at CVP values ≥ 9.3 cmH2O. These results may help inform risk stratification and the selection of candidate thresholds for further study. Prospective multicenter studies are required to validate any CVP threshold before it is adopted as a clinical safety target.
This study has certain limitations. First, because this was a retrospective observational study, changes in surgical techniques during the extended study period may have influenced the outcomes. Second, although rigorous statistical adjustment was performed, residual confounding from unmeasured variables may have persisted. Third, the 7-day postoperative observation period for pulmonary complications may be insufficient to capture major surgical outcomes; therefore, extended follow-up is warranted in future studies. Finally, this was a single-center retrospective study in China with specific surgical protocols and anesthetic management practices. The applicability of the findings to other centers, particularly those using different ventilation strategies or enhanced recovery after surgery protocols, may therefore be limited.
CONCLUSION
This retrospective cohort study revealed that CVP may be a modifiable perioperative factor associated with PPCs after pediatric liver transplantation. Prospective multicenter longitudinal studies are required to validate these findings.
ACKNOWLEDGEMENTS
The authors wish to thank all those who performed the pediatric liver transplantations in this study.
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Footnotes
Peer review: Externally peer reviewed.
Peer-review model: Single blind
Specialty type: Gastroenterology and hepatology
Country of origin: China
Peer-review report’s classification
Scientific quality: Grade B, Grade B, Grade B, Grade B
Novelty: Grade B, Grade B, Grade B, Grade B
Creativity or innovation: Grade B, Grade B, Grade B, Grade B
Scientific significance: Grade A, Grade B, Grade B, Grade B
P-Reviewer: Khurram MF, PhD, Professor, India; Ullah W, Associate Professor, Pakistan S-Editor: Lin C L-Editor: A P-Editor: Yang YQ
