Congenital diaphragmatic hernia (CDH) is a developmental defect of the diaphragm that allows herniation of abdominal viscera into the thorax, resulting in pulmonary hypoplasia and abnormal pulmonary vascular development. Despite improvements in prenatal risk stratification and neonatal critical care, CDH continues to carry substantial mortality and long-term morbidity driven mainly by persistent pulmonary hypertension (PH), ventilator-associated lung injury, and cardiovascular dysfunction.1,3,6 Over the past two decades, the management paradigm has shifted from immediate surgical correction toward preoperative stabilization, recognizing that CDH is primarily a cardiopulmonary disease rather than a surgically correctable defect alone.1,2 International and national guidance emphasizes gentle ventilation strategies, avoidance of barotrauma, targeted PH therapy, and structured stabilization goals before operative intervention.1–3 Stabilization commonly includes acceptable oxygenation and ventilation on lung-protective settings, adequate systemic perfusion with minimal vasoactive support, controlled pulmonary pressures (often guided by echocardiography), and improving oxygenation index (OI) trends.1,3,14 However, the question of when to proceed with repair once stability is achieved remains unresolved. “Early repair” proponents argue that timely restoration of anatomy may improve lung mechanics, reduce gastric distension, facilitate enteral feeding, and shorten exposure to mechanical ventilation—thereby lowering ventilator-associated complications and infection risk.14,20 Conversely, “delayed repair” advocates emphasize that surgical stress can destabilize fragile cardiopulmonary physiology; delaying surgery may allow PH to improve, reducing perioperative decompensation.1,3 In practice, timing varies widely across centers, reflecting uncertainty and heterogeneity in disease severity, access to ECMO, and differences in stabilization protocols.2,3,24 The debate is particularly complex in infants requiring ECMO. Some strategies favor repair after decannulation to reduce bleeding risk, while others support on-ECMO repair in selected cases to avoid non-repair mortality and prolonged ECMO exposure. Evidence remains mixed: early protocolized repair soon after cannulation has been associated with worse outcomes in some cohorts,8 whereas other studies suggest survival benefit with earlier repair in carefully selected ECMO patients.12 Furthermore, transfusion burden and coagulopathy appear strongly influenced by ECMO duration and timing of surgery.9 Given these uncertainties, the present study compares early versus delayed repair in a contemporary cohort, using clinically practical definitions based on timing after stabilization. We hypothesized that among stabilized non-ECMO infants, early repair (≤48 hours) would be associated with reduced morbidity without compromising survival, while ECMO-associated outcomes would depend on repair timing and transfusion exposure.

This retrospective cohort study was conducted in a tertiary neonatal surgical intensive care unit. Medical records of neonates with CDH treated from January 2018 to December 2024 were reviewed. Study population All neonates with radiologically confirmed CDH admitted within 24 hours of birth were screened. Inclusion criteria 1. Neonates (≤28 days of life) with confirmed Bochdalek-type CDH. 2. Isolated CDH or CDH with minor non-lethal anomalies. 3. Underwent surgical repair during index admission. 4. Availability of complete preoperative stabilization data (ventilator settings, OI, echocardiography). Exclusion criteria 1. Major chromosomal anomalies or syndromic CDH with expected non-survivable prognosis (e.g., lethal trisomy). 2. Severe congenital heart disease requiring primary cardiac surgery. 3. Morgagni hernia or late-presenting CDH (>28 days). 4. Patients who died before any surgical decision could be made (non-repair deaths) were excluded from timing comparison but described in screening log. Definitions • Stabilization: meeting unit criteria for ≥6 hours: SpO₂ 85–95% on lung-protective ventilation, acceptable PaCO₂ with permissive hypercapnia strategy, improving OI trend, lactate ≤3 mmol/L, urine output ≥1 mL/kg/hr, and decreasing vasoactive requirement. Criteria aligned with contemporary consensus approaches.1–3 • Early Repair: surgery performed ≤48 hours of life after achieving stabilization. • Delayed Repair: surgery performed >48 hours after achieving stabilization. • Pulmonary hypertension severity: graded by echocardiography (mild/moderate/severe) per unit practice consistent with guideline recommendations.3 • OI (oxygenation index): calculated as (FiO₂ × mean airway pressure × 100) / PaO₂. Outcomes • Primary outcome: survival to discharge. • Secondary outcomes: ventilator days, duration of inhaled nitric oxide (iNO), ECMO requirement, perioperative transfusion, postoperative sepsis, recurrence within 6 months, and length of hospital stay. Statistical analysis Continuous variables were summarized as mean ± SD or median (IQR) and compared with t-test or Mann–Whitney U test. Categorical variables were compared using χ² or Fisher exact test. Multivariable logistic regression assessed association of timing group with survival, adjusting for prenatal severity markers (liver-up), side of defect, preoperative OI, and PH severity. Statistical significance was set at p<0.05.

Table 1. Baseline characteristics Variable Early Repair (n=58) Delayed Repair (n=62) p-value Male, n (%) 34 (58.6) 36 (58.1) 0.96 Gestational age (weeks), mean ± SD 38.1 ± 1.6 37.9 ± 1.8 0.48 Birth weight (kg), mean ± SD 2.83 ± 0.42 2.79 ± 0.45 0.62 Left-sided CDH, n (%) 49 (84.5) 50 (80.6) 0.56 Liver herniation (“liver up”), n (%) 18 (31.0) 24 (38.7) 0.37 Prenatal observed/expected LHR <25%, n (%) 10 (17.2) 13 (21.0) 0.60 Groups were comparable at baseline; Delayed group showed a non-significant trend toward greater severity (more liver-up and lower o/e LHR). Table 2. Preoperative physiology at stabilization Variable Early Delayed p-value Age at stabilization (hours), median (IQR) 18 (12–26) 20 (14–30) 0.34 OI at stabilization, median (IQR) 9 (6–13) 10 (7–15) 0.29 Severe PH on echo, n (%) 12 (20.7) 18 (29.0) 0.29 Need for iNO pre-op, n (%) 22 (37.9) 28 (45.2) 0.41 Inotropes at stabilization, n (%) 19 (32.8) 25 (40.3) 0.39 Physiologic severity at the point of “stability” was similar, supporting a fair comparison of timing strategies. Table 3. Operative details Variable Early Delayed p-value Age at repair (hours), median (IQR) 36 (28–44) 96 (72–132) <0.001 Primary repair, n (%) 40 (69.0) 39 (62.9) 0.47 Patch repair, n (%) 18 (31.0) 23 (37.1) 0.47 Thoracoscopic approach, n (%) 9 (15.5) 10 (16.1) 0.93 Operative time (min), mean ± SD 92 ± 24 95 ± 28 0.55 Technique and operative complexity were similar; timing was the major differentiator. Table 4. Postoperative outcomes Outcome Early Delayed p-value Survival to discharge, n (%) 49 (84.5) 48 (77.4) 0.33 Ventilator days, median (IQR) 8 (5–14) 12 (7–20) 0.01 iNO duration (days), median (IQR) 2 (0–5) 4 (1–7) 0.03 Sepsis (culture proven), n (%) 6 (10.3) 14 (22.6) 0.07 Length of stay (days), median (IQR) 18 (14–28) 24 (16–38) 0.02 Early repair was associated with significantly fewer ventilator days and shorter hospitalization, with a trend toward less sepsis. Table 5. ECMO subgroup outcomes (among those requiring ECMO) Variable Early (n=12) Delayed (n=16) p-value Repair on ECMO, n (%) 8 (66.7) 6 (37.5) 0.13 PRBC transfusion (mL/kg), median (IQR) 80 (50–120) 140 (90–210) 0.01 Platelet transfusion (mL/kg), median (IQR) 70 (40–110) 95 (60–160) 0.04 Major bleeding needing re-operation, n (%) 1 (8.3) 3 (18.8) 0.61 Survival to discharge, n (%) 7 (58.3) 8 (50.0) 0.71 In ECMO-supported infants, timing strategy influenced transfusion burden and bleeding tendency, aligning with published observations that earlier repair windows may reduce transfusion exposure in selected protocols.9 Table 6. Multivariable model for survival to discharge Predictor Adjusted OR 95% CI p-value Early vs delayed repair 1.32 0.56–3.12 0.52 Liver-up 0.42 0.18–0.98 0.04 Severe PH 0.39 0.16–0.93 0.03 OI at stabilization (per +5) 0.78 0.62–0.98 0.03 Patch repair 0.66 0.27–1.60 0.35 After adjustment, timing itself was not an independent predictor of survival, while physiologic severity (PH, OI) and liver herniation remained key determinants—consistent with modern understanding that CDH outcome is driven mainly by cardiopulmonary disease.1–3,6

This study compared early versus delayed CDH repair using a pragmatic definition based on timing after stabilization. The primary finding was that early repair (≤48 hours after stability) did not worsen survival and was associated with reduced ventilator days, shorter iNO exposure, and shorter length of stay. These results support a stabilization-first approach while discouraging unnecessary delay once physiologic goals are achieved. Current consensus guidance emphasizes that surgery should follow stabilization rather than be performed emergently.1–3 Yet “stability” is variably defined, and some centers extend preoperative optimization for several days. Data from Cox et al. suggest that delaying repair beyond the period of early stability can increase ventilator days and discharge age without survival benefit, using OI as a temporally reliable marker.14 Our findings are directionally consistent: delayed repair was associated with longer ventilator support and hospitalization, even though survival differences were not statistically significant. The ECMO subgroup remains the most controversial. Robertson et al. reported that a protocolized early repair strategy soon after cannulation may be associated with increased mortality and longer ECMO runs, while acknowledging that early repair may still be reasonable for infants unlikely to decannulate before repair.8 Other work suggests benefit of earlier repair after cannulation in selected cases,12 and large collaborative studies highlight the importance of minimizing non-repair deaths and center variability.24 In our ECMO subgroup, survival was similar between strategies, but early-timed repairs were associated with lower transfusion requirements—an observation concordant with reports that transfusion burden may increase with prolonged ECMO exposure and coagulopathy.9 Importantly, our multivariable analysis shows that severity markers (OI, PH, liver herniation) were more predictive of survival than timing group. This matches the broader literature that focuses on cardiopulmonary physiology, prenatal severity assessment, and standardized postnatal pathways.1–3,7 It also underscores that timing should not be considered in isolation: early repair is appropriate only once stabilization criteria are met, and delayed repair may be necessary in infants with persistent PH crises, escalating vasoactive need, or worsening OI. The study has limitations: retrospective design, single-center practice patterns, and potential residual confounding (e.g., clinician choice to delay in sicker infants). Additionally, excluding non-repair deaths from the timing comparison may underestimate the consequences of excessive delay in the most severe cases—an issue highlighted by multicenter data supporting aggressive but individualized surgical management.24 Future work should incorporate standardized physiologic triggers for surgery (including dynamic OI and echocardiographic measures) and stratify analyses by ECMO candidacy and prenatal severity. Overall, our findings support a balanced approach: stabilize first, then repair without undue delay, while tailoring decisions to disease physiology and ECMO trajectory.

Early repair of CDH within 24–48 hours after achieving stabilization was associated with improved morbidity outcomes (shorter ventilation and hospitalization) without compromising survival. Delayed repair beyond stability increased resource utilization and may elevate infection-related complications. In ECMO-supported infants, timing should be individualized, with attention to transfusion burden, bleeding risk, and feasibility of decannulation prior to repair.

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