Case
A 39-year-old Chinese female with a history of two lower uterine segment cesarean sections (2018 and 2021) and one surgical abortion (2015) presented with postcoital bleeding recurring for 12 months, abnormal vaginal bleeding persisting for 3 months outside menstrual cycles, and abdominal pain for 1 day. The abdominal pain was a persistent dragging pain of mild intensity. She experienced a small amount of vaginal bleeding, absence of systemic symptoms such as dizziness, fatigue, nausea or vomiting. The patient has no other surgical history, and family and personal histories are unremarkable.
On admission, her vitals were stable with blood pressure of 107/64mmHg, pulse rate of 97 beats per minute, oxygen saturation of 100% on room air, respiratory rate of 20 breaths per minute, and temperature of 36.5°C. She was admitted to the hospital for a systematic physical examination and had mild tenderness in the lower quadrants without rebound tenderness or guarding. During the gynecological examination, she had a small amount of blood in the vagina, cervical tenderness and swaying pain, obvious tenderness over the lower uterine segment, and no abnormality of bilateral fallopian tubes and ovaries.
Her complete blood count and C-reactive protein (CRP) showed a hemoglobin of 123 g/L, platelets of 212×10 9 /L, white blood cells of 7.35×10 9 /L, and C-reactive protein of 23.33 mg/L. Coagulation profile, sex hormone and thyroid function tests were all within normal limits whileβ- human chorionic gonadotropin (β-HCG) was negative. Laboratory examination of vaginal discharge showed negative results for Chlamydia trachomatis and Neisseria gonorrhoeae.
The patient underwent transvaginal ultrasonography, which identified a defect measuring approximately 1.7×0.9 cm at the anterior lower uterine segment, precisely at the site of the previous cesarean scar. The residual myometrial thickness overlying the pouch was 3.0 mm. The indentation communicated clearly with the uterine cavity, and a small amount of retained fluid was visualized within the pouch. Additionally, a anechoic space measuring approximately 5.0×2.9×2.7 cm was observed in the pelvis.
Pelvic magnetic resonance imaging (MRI) showed a fluid-filled, well-circumscribed defect measuring approximately 4.2×2.4 cm at the anterior lower uterine segment, with the thinnest portion of the myometrium measuring 1.0 mm; and the range of encapsulated hematocele beside the diverticulum was about 7.4×4.2 cm, which was suggestive of rupture of the uterine scar diverticulum ( Figure 1 ).
Figure 1 Report of MRI examination information can be found in cesarean scar diverticulum (the left) and rupture and collection in the right. A sagittal magnetic resonance image of the pelvis in grayscale with a black border. A single red horizontal label line is placed across the mid pelvic region, extending from left toward the right side. Red text at the right end of the line reads encapsulated hematocele. The image contains multiple rounded and lobulated soft tissue intensity structures in the central pelvic area. A large bright fluid filled region occupies the lower left pelvic area. Curved bony structures of the lower spine and sacral region form a segmented arc along the upper right margin. No additional label lines, arrows, legends, scales, or measurement markings are present. A sagittal magnetic resonance image of the pelvis with a red label line and red text on a gray background.
Report of MRI examination information can be found in cesarean scar diverticulum (the left) and rupture and collection in the right.
Based on the patient’s medical history, symptoms, physical signs, laboratory tests, and imaging findings, the differential diagnosis included pelvic inflammatory disease, ectopic pregnancy, and cesarean scar pregnancy. A preliminary diagnosis of rupture of the uterine scar diverticulum was established. Based on the current diagnosis, hysteroscopy combined with laparoscopy was performed. Before the operation, the patient was informed in detail of the surgical risks, and it was confirmed that she had no desire for future childbearing.
Intraoperatively, a soft, protruding mass measuring approximately 7×4 cm vesicouterine pouch was revealed ( Figure 2 ). The fallopian tubes and ovaries appeared normal bilaterally. Upon entering the uterovesical peritoneum space, purulent-blood tinged fluid was noted emanating from the vesicouterine fold. Further exploration revealed a 3×2 cm ruptured cesarean scar diverticulum with encapsulated purulent collection. Notably, dense fibrous adhesions tethered the bladder to the cervix, with focal purulent infiltration of the bladder wall at the adhesion site, resulting in attenuated and friable bladder tissue ( Figure 3 ). Following meticulous adhesiolysis, sharp dissection delineated the diverticular margins. The 3 cm full-thickness uterine defect was excised with cold-knife scalpel to preserve adjacent vascular supply. Two-layered closure was performed using absorbable sutures in a continuous fashion to restore the contour of the lower uterine segment ( Figure 4 ). Intraoperative cystoscopy confirmed intact bladder mucosa and unobstructed ureteral orifices. The purulent secretion was cultured using traditional bacterial culture methods, including aerobic and anaerobic cultures, indicating positive for E. coli , and an antimicrobial susceptibility testing was performed. Pathological examination of the excised tissue revealed fibromuscular tissue with chronic inflammation.
Figure 2 A soft, protruding mass measuring approximately 7×4 cm vesicouterine pouch was revealed. A clinical photograph showing a close-up internal surgical view of pelvic tissue. A rounded protruding mass occupies the lower central area of the frame, with surrounding folds of tissue extending upward and to both sides. Text in the upper right reads vesicouterine pouch mass, with a single line directed toward the protruding area. Context information states the mass measures approximately 7 times 4 centimeters. A clinical photograph showing a vesicouterine pouch mass.
Figure 3 Dense fibrous adhesions tethered the bladder to the cervix, with focal purulent infiltration of the bladder wall at the adhesion site, resulting in attenuated and friable bladder tissue. Laparoscopic surgical image of the female pelvis with labels identifying the bladder, cervix, and uterine region. Dense fibrous adhesions tether the bladder to the cervix, obscuring the normal tissue planes. The adhesion site contains focal purulent infiltration and inflamed tissue involving the bladder wall. A surgical instrument is positioned across the operative field near the area of adhesion. The bladder tissue at the adhesion site is attenuated and friable, with erythematous, irregular tissue and inflammatory changes surrounding the affected area. Laparoscopic view of dense bladder hyphen cervix adhesions with localized purulent inflammation.
Figure 4 Two-layered closure was performed using absorbable sutures in a continuous fashionto restore the contour of the lower uterine segment. An annotation labeled “After repair of uterine diverticulum” points to the repaired lower uterine segment. Two laparoscopic instruments are positioned at the repair site. The defect has been closed with a two-layer continuous absorbable suture technique to restore the contour of the lower uterine segment. Surrounding pelvic tissues are shown, and the repaired area shows approximation of tissue edges following reconstruction. Laparoscopic view after uterine diverticulum repair with two-layer continuous suture closure.
A soft, protruding mass measuring approximately 7×4 cm vesicouterine pouch was revealed.
Dense fibrous adhesions tethered the bladder to the cervix, with focal purulent infiltration of the bladder wall at the adhesion site, resulting in attenuated and friable bladder tissue.
Two-layered closure was performed using absorbable sutures in a continuous fashionto restore the contour of the lower uterine segment.
Postoperatively, the patient received supportive care including anti-infective therapy and fluid replacement. The patient remained afebrile and reported no abdominal pain or other discomfort. On postoperative day 1, routine blood tests revealed a white blood cell count of 13.06×10 9 /L and a CRP level of 52.90 mg/L. However, re-examination on postoperative day 5 showed normalization of these indices, with a white blood cell count of 8.29×10 9 /L and a CRP level of 2.51 mg/L. Given the bladder serosal injury resulting from purulent invasion, an indwelling urinary catheter was maintained for five days. No urinary discomfort was noted after catheter removal. The patient had an uneventful recovery and was discharged on postoperative day 5. At the same time, no adverse or unexpected events occurred in the patient after surgery. The patient attended gynecological outpatient follow-up visits at 1, 3, and 6 months postoperatively. Menstrual cycles were regular, with no intermenstrual or postcoital bleeding, and no lower abdominal pain or other discomfort. A follow-up ultrasound performed at 3 months postoperatively revealed no abnormalities.
Background
A uterine cesarean scar diverticulum (CSD) is a depression structure communicating with the uterine cavity, resulting from defective myometrial healing at the cesarean incision site. 1 It is characterized by thinning of the isthmus muscle layer of the uterus, forming a depression or lacuna with the uterine cavity 1 , 2 and caused by multiple factors, such as surgical factors (suturing technique/materials), obstetric variables (number of cesarean deliveries, uterine position), patient demographics (age, BMI), and pathological processes (infection, ischemia). 3–7 A multivariate research analysis showed that the frequency of cesarean section, uterine position, and abnormal menstruation were independent risk factors for the formation of uterine scar diverticula. 7
CSD rupture is a specific type of uterine rupture. Uterine rupture most commonly occurs in women during gestation and delivery, and numerous documented cases have described spontaneous uterine rupture in pregnant patients. 8 , 9 In non-pregnant women, most uterine ruptures result from iatrogenic causes or trauma. 10 Although cases of adenomyosis-induced spontaneous rupture in a non-gravid uterus have been reported, 11–13 spontaneous uterine rupture secondary to pelvic infection in a non-pregnant uterus remains a rare event. The rupture of CSD is one of the serious long-term complications after a cesarean section, and its occurrence is closely related to poor healing of the cesarean incision. We describe a rare case of CSD rupture caused by non-pregnant intrauterine infection and investigate the pathophysiology, diagnosis, and treatment of this disease.
Conclusion
In conclusion, this case demonstrates that intrauterine infection is a potential and dangerous precipitating factor in uterine scar diverticulum rupture. When women with a history of cesarean section present with acute lower abdominal pain and signs of infection, clinicians should broaden their diagnostic thinking, include uterine scar diverticular rupture in the differential diagnosis, and perform timely imaging evaluation and surgical intervention to avoid serious consequences. This case affirms that timely surgical intervention and targeted antimicrobial therapy are essential in managing this condition, while consistent, guideline-adherent management of pelvic inflammatory disease remains the cornerstone of prevention.
Discussion
Globally, the incidence of uterine rupture is 0.07%, and most cases of uterine rupture occur in the third trimester, especially after 37 weeks gestation. 14–16 In the absence of pregnancy, spontaneous uterine rupture typically results from pathological weakening of the uterine architecture. However, the most clinically significant mechanisms in non-gravid patients involve infectious or neoplastic processes. 10 Spontaneous rupture of a CSD in the nonpregnant state remains exceptionally rare. This case highlights the unique etiology of non-pregnancy-related CSD rupture, where intrauterine infection emerges as the direct causative factor. Several potential reasons accounted for this disease.
E. coli , a common opportunistic pathogen of the intestinal and urogenital flora, employs dual-colonization strategies: ascending translocation through the cervicovaginal axis or hematogenous dissemination via bacteremia. 17 , 18 The cesarean-induced isthmic niche—characterized by local blood supply deficiency, suture material, and ischemic necrosis—provides an ideal nidus for colonization. 19
E. coli strains possess a plethora of both structural (such as fimbriae, pili, curli, flagella), produces specific toxins and colonization factors, which contribute to their capacity to cause disease and trigger a strong local inflammatory response. 17 , 18 , 20 When inflammatory cells such as neutrophils infiltrate the CSD, a large amount of proteases and active oxygen free radicals are released. These substances not only kill bacteria but also directly dissolve tissue and culminate in loss of tissue integrity and mechanical failure. 21
In women with cesarean scar disorder, the proportion of endometrium present on the surface of CSD is lower, and there is a lack of healthy and normal endometrium. 22 At the same time, chronic inflammation occurs in the CSD, with elevated inflammatory cytokine levels. 23 Chronic infection may result in dense adhesion between the lower uterine segment and surrounding organs (such as the bladder and cervix), as described in this report. Such adhesion not only limits the localization of infection, makes the inflammation more prone to spread, but may also further compromise the stability of the wall of the pouch due to persistent traction and local circulatory disturbances, contributing to the rupture process.
The wall of the CSD is mainly composed of fibrous scar tissue, absence of normal myometrial contractility, and both of the tensile strength and healing ability are significantly reduced. 24 Prior cesarean deliveries (two in this case) resulted in structural weakness, with myometrial fibrosis, reduced capillaries, poor tensile strength and poor healing ability, which formed the “predisposing anatomical substrate” for rupture. Patients with CSD could cause the deformation of the uterine cavity and intrauterine inflammation. 23 In this relatively closed space of the diverticulum, bacterial proliferation and inflammatory exudation can rapidly form an abscess. The pressure within the abs continues to increase, which directly compresses the local blood vessels, causing tissue ischemia and necrosis. On the other hand, the pressure acts on the fragile divert wall, which is the direct mechanical factor leading to its “rupture under pressure”. 25 Once an infection occured, the uterine scar diverticulum’s inherent ability to resist bacterial invasion and tissue dissolution was far lower than that of normal, making the infection more likely to rapidly penetrate the full thickness. 26 As described in the case, the purulent material involved the adjacent bladder wall, which also corroborated the invasive and destructive power of the infection.
In view of the above cases, CSD rupture should be systematically considered in the differential diagnosis of acute abdominal pain among females with prior cesarean section history, irrespective of pregnancy status. Detailed medical history (cesarean section history, symptoms) is a crucial step in clinical diagnosis. Preoperative diagnosis is challenging. The clinical manifestations include abdominal pain, hemoperitoneum, vaginal bleeding, and pelvic effusion, which overlap with the symptoms of pelvic inflammatory disease (PID), ectopic pregnancy, and cesarean scar pregnancy. At present, there are many examination methods for the examination of uterine diverticular, including ultrasound, hysterography, magnetic resonance imaging, and hysteroscopy. 27
PID is an infection of the female upper genital tract, involving the uterus, fallopian tubes, ovaries, and/or pelvic peritoneum, and is usually caused by Chlamydia trachomatis, Neisseria gonorrhoeae , and bacterial vaginosis-associated pathogens. 28 PID symptoms include pelvic pain, abnormal vaginal discharge or bleeding, dyspareunia and pelvic organ tenderness (ie, cervical mo-tion, uterine or adnexal tenderness) on bimanual examination 29 And the following additional criteria may improve the specificity of the diagnosis: oral temperature greater than 101°F (38.3°C), abnormal cervical discharge, cervical friability, abundant leukocytes on microscopy, elevated erythrocyte sedimentation rate or CRP, and laboratory documentation of cervical infection with C. trachomatis and N. gonorrhoeae . 30
Ectopic pregnancy is a pregnancy that implants outside the normal uterine cavity. 31 The main symptoms of ectopic pregnancy include amenorrhea, pain abdomen, and vaginal bleeding. Abdominal tenderness and cervical motion tenderness are the common findings. 32 The current diagnostic standard for ectopic pregnancy includes ultrasound imaging and serum levels of β-hCG. A patient with a β-hCG level >2000 mIU/mL with no sign of intrauterine pregnancy is highly suspicious of ectopic pregnancy. 33
Cesarean scar pregnancy, a complication in which an early pregnancy implants in the scar from a previous cesarean delivery, is a rare form of ectopic pregnancy. Ultrasound is the primary imaging modality for cesarean scar ectopic pregnancy diagnosis. Ultrasound images of cesarean scar pregnancy may show an empty uterine cavity with a pregnancy sac on a thinned myometrium just over the previous cesarean incision line next to the bladder. 34 MRI images can demonstrate a gestational sac embedded within the lower uterine segment at the level of a previous cesarean scar niche and an empty endometrial cavity and endocervix. 35
Based on the clinical history, routine blood tests, CRP β-hCG, heterogeneous ultrasound images, MRI findings, and laboratory examination of vaginal discharge, pelvic inflammatory disease, ectopic pregnancy, and cesarean scar pregnancy could be excluded. Thus, an initial diagnosis of cesarean scar diverticulum rupture could be established with certainty in this case. This case not only offers critical clinical insight, but also underscores the necessity of considering this diagnosis even in patients lacking classic risk factors.
Once uterine rupture is clinically diagnosed or highly suspected, surgical intervention should be immediate. While the patient in this case has no future fertility, for women who do, detailed counseling on risks associated with future pregnancy, the appropriate mode of delivery, conception timing, and early pregnancy surveillance techniques is necessary. After full-thickness repair of CSD, the restoration of myometrial continuity significantly reduces the risk of adverse obstetric outcomes in subsequent pregnancies. 36 Laparoscopic management is an approach that allows for simultaneous repair and revision of the cesarean scar defect with minimal impact to subsequent fertility. For women desiring future childbearing, there is still a risk of recurrent caesarean scar pregnancy, placenta accreta spectrum, and uterine rupture, but it is substantially lowered following successful anatomical repair. 37 For conception time, it is recommended to have at 6 to 12 months interval after surgery to allow sufficient scar healing before attempting pregnancy. 38 However, many patients become pregnant at an early age without any adverse consequences. If a patient urgently needs to conceive after surgery, it is recommended to start trying pregnancy as early as 6 weeks later. 3 But this timeframe is further individualized depending on the size of the defect. Following full-thickness or laparoscopic niche repair, pregnant women should undergo structured sonographic surveillance to monitor uterine integrity and exclude recurrent scar pathology. For early pregnancy surveillance, the first transvaginal ultrasound evaluation should be performed at 6–7 weeks gestation to confirm the location of the gestational sac and to exclude caesarean scar pregnancy. 39 Regarding delivery management, a planned elective repeat caesarean section is strongly recommended, typically performed between 36 and 38 + 6 weeks of gestation, to minimize the risk of uterine rupture during labor. 40 Although some women had successful vaginal delivery after uterine scar repair, 8 it is usually not recommended due to the potential for scar dehiscence. 41
This case highlights that in reproductive-age women presenting with an acute abdomen, a negative pregnancy test, and a history of cesarean, spontaneous uterine rupture secondary to intrauterine infection should be considered as a differential diagnosis. Early recognition and prompt intervention are essential to prevent severe complications. However, there are certain limitations in this case. First, as a single or small series of case reports, they provide weak form of clinical evidence, lacking control groups or comparative data. Second, although an association between intrauterine infection and diverticulum rupture may be observed, temporal and causal relationships cannot be definitively proven without experimental or large cohort studies. Third, findings from individual case reports may not apply to broader populations with different infection pathogens, prior cesarean techniques, or diverticulum morphologies.
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