We thank Dr Palacios-Jaraquemada et al for their interest in our article and for contributing to the discussion on uterine closure after cesarean delivery.
Our article focused on one aspect of uterine repair that is directly modifiable by obstetrical surgeons, namely the method of hysterotomy closure. Surgical technique is an important determinant of healing, and optimization of closure remains a necessary and clinically relevant goal. At the same time, uterine repair after cesarean delivery depends not only on how the incision is closed but also on where the incision is placed, the labor status at the time of surgery, preexisting uterine conditions such as prior cesarean deliveries, and host factors that regulate wound repair, including infection, genetic, and epigenetic influences. Many of these host determinants of wound healing and scar formation have not been appropriately evaluated.
Randomized clinical trials have examined technical variables such as the number of layers. While this work has advanced understanding of closure techniques, it addresses only part of the process of uterine repair. Healing occurs within a variable anatomic and inflammatory environment that extends beyond the surgical technique itself. Pathologic inflammation, whether related to infection or severe sterile inflammatory responses, interferes with collagen deposition, angiogenesis, and myometrial remodeling. The role of infection in uterine wound healing has been recognized for decades and remains clinically relevant, particularly because much perioperative infection and inflammation in obstetrics is subclinical.
Observational studies based on transvaginal ultrasound examination of the uterine scar performed 6 to 9 months after cesarean delivery provide important insights into factors associated with incomplete healing. In these studies, the principal determinants of large scar defects were measures of labor advancement at the time of cesarean delivery. The risk of incomplete healing increased markedly when cesarean delivery was performed at advanced cervical dilatation or when the presenting part was low in the pelvis, whereas uterine closure technique was not an independent predictor in multivariable analyses.
Randomized data further support the importance of incision location. In a controlled trial comparing higher vs lower uterine incisions in women undergoing cesarean delivery in advanced labor, a low hysterotomy was associated with a higher frequency of large scar defects at follow-up despite use of a standardized closure technique.
The anatomic location of the uterine incision is therefore a major determinant of healing. Vascular density, oxygen delivery, collagen organization, and myometrial architecture differ across the uterine body, lower uterine segment, and cervix. These regional differences influence scar remodeling and long-term tensile strength and should be considered alongside closure technique when evaluating uterine repair.
Taken together, these data support a broader clinical framework. While surgical technique remains central and was the focus of our article, optimal outcomes will require recognition that uterine healing reflects the interaction among closure method, incision location, labor status, inflammatory conditions, preexisting uterine factors, and host biological characteristics that regulate wound healing and scar formation. Consideration of these factors may help reduce the risk of uterine rupture, placenta accreta spectrum disorders, and other long-term complications of cesarean delivery.
We appreciate the contribution of Dr. Palacios-Jaraquemada et al to this discussion and agree that continued progress will depend on integrating surgical technique with an improved understanding of the anatomic and biological factors that influence uterine repair.
The authors report no conflict of interest.
This work was supported, in part, by the Pregnancy Research Branch, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development , National Institutes of Health , United States Department of Health and Human Services ( NICHD / NIH / DHHS ) and, in part, by federal funds from NICHD / NIH / DHHS (Contract No. HHSN275201300006C).
Dr Romero has contributed to this work as part of his official duties as an employee of the United States Federal Government.
The funder had no role in the design or conduct of the study; collection, management, analysis, or interpretation of the data; preparation, review, or approval of the manuscript; or the decision to submit the manuscript for publication.
References
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