Cesarean scar defect-A rising concern or a physiological healing process?

Abstract

Sir, We read the study by Pan et al with great interest.1 They performed a prospective study among a Chinese population of patients undergoing elective cesarean section, evaluating the prevalence and predictors of cesarean scar defect (CSD) at 6 weeks postpartum. Although the authors meticulously address this important issue, several important points warrant further clarification. First, the definition of CSD was made on transvaginal ultrasound (TVS) scan. Although TVS was considered an accurate method for detecting CSD in the first studies performed on the topic, contrast-enhanced sonohysterography (SHG) may facilitate superior detection and measurement to TVS, resulting in higher prevalence and identification of larger CSD. Currently, SHG is considered to be the gold standard for the diagnosis of CSD,2 and definition of CSD by transvaginal ultrasound may be out of date. Secondly, the authors performed the diagnosis of CSD 6 weeks after the incision. As obstetric complications associated with CSD, usually occur after the next conception, we consider the relevance of CSD diagnosis to be higher in relation to the recommended minimal inter-pregnancy interval (IPI) period after cesarean section (ie, at least 12 months).3 This concurs with most previous studies which have evaluated CSD 6-12 months after the incision.2 Hence, diagnosis of CSD after 6 weeks may be irrelevant, as future healing of myometrium and endometrium would probably take place and the diagnosis of CSD will be reversed or altered, and thus the clinical relevance of this early sonographic diagnosis is debatable. Thirdly, in their discussion, the authors state that their study is the first to indicate that post-CS infection plays an important role in the pathogenesis of CSD. However, the authors do not elaborate on the definition of post-CS infection (diagnosis, symptoms, physical examination findings, time of onset of fever, etc.) Moreover, the authors refer to subfebrile temperature as a post-CS infection. Postoperative morbidity should be regarded as a body temperature >38°C starting 24 hours after the operation, as reported in a similar study on CSD.4 It is important to underline that in their study, the authors mention that cases of body temperature >38°C were comparable between CSD and no CSD groups. Fourthly, the authors state that administration of calcium channel blockers (CCB) post-CS may affect wound healing and contribute to the development of CSD. We question this assumption as it is based on a very small sample size and it is known from basic science and animal models that CCB improve wound healing.5 Fifthly, the authors state that higher fibrinogen level is a predictor of CSD and speculate that factors which promote wound healing may be decreased during pregnancy due to internal structural changes of platelets. This is questionable, as fibrinogen has a central role in wound healing and the cut-off value used by authors is arbitrary. A proper statistical analysis of means should be performed to evaluate the role of higher fibrinogen in the setting of CSD formation. Finally, we believe that the authors should be more cautious in drawing the conclusion that perioperative infection and hypercoagulability should be considered predictors of CSD. CSD are frequently identified after cesarean delivery. At present we can relate CSD to a wide variety of gynecological and obstetrical complications. However, there is a great deal of debate concerning how to act on this information. It must be questioned whether it is appropriate to measure CSD as early after delivery as was done in this study. More well-designed research on risk factors is needed to obtain tools to prevent future CSD development.