Uterine necrosis during pregnancy following exploratory laparotomy
- Anna Hirsch ,
- Rachel Newman and
- Mariam Naqvi
- Obstetrics and Gynecology, Cedars-Sinai Medical Center, Los Angeles, California, USA
- Correspondence to Dr Anna Hirsch; anna.hirsch@cshs.org
Abstract
Uterine necrosis is an infrequent event and is most commonly reported as a complication of interventions for postpartum haemorrhage management. Cases of uterine necrosis in pregnancy are rare. The mainstay of treatment for uterine necrosis is hysterectomy, and the data regarding conservative management are limited. A gravida 3, para 2 presented at 33 weeks gestation with ovarian torsion and underwent an exploratory laparotomy with ovarian cystectomy. The surgery was complicated by excess bleeding, which was controlled with the placement of sutures along the uterine body. She had multiple subsequent presentations for severe abdominal pain without clear aetiology. Four weeks after the initial surgery, she underwent caesarean delivery, at which time uterine necrosis was diagnosed. Her uterus was preserved. She received postoperative intravenous antibiotics and was closely observed. She continued to do well 10 months postpartum. In patients with uterine necrosis during pregnancy who are haemodynamically stable, conservative management may be an option.
Background
Uterine necrosis is a condition most commonly seen in the postpartum period as a complication of surgical methods used to control postpartum haemorrhage, including uterine artery embolisation, compression sutures and uterine artery ligation.1–3 The risk of uterine necrosis appears to be increased when a combination of these methods is used simultaneously.1 As this condition is rare, its precise incidence is uncertain. A review by Poujade et al identified 19 cases of uterine necrosis following pelvic embolisation for postpartum haemorrhage spanning from 1985 to 2013, of which four cases had partial uterine involvement.4 In these cases, management typically included total (78%) or subtotal (10%) hysterectomy, with 15% also undergoing partial cystectomy for associated bladder necrosis. A more recent review of complications of uterine artery embolisation after postpartum haemorrhage demonstrated uterine necrosis in 11 of 117 patients. Of these, two patients required hysterectomy, and the remainder were managed with serial pelvic ultrasound every 6–12 months.2
Antepartum uterine necrosis has been described as a theoretical complication of incarceration of the retroverted uterus between the symphysis pubis and sacral promontory.5 Otherwise, cases of its occurrence during pregnancy are scarce. Accordingly, the natural history and optimal management of uterine necrosis occurring during pregnancy remain unknown. In this report, we describe a case of uterine necrosis occurring as a complication of laparotomy for ovarian torsion during pregnancy.
Case presentation
A gravida 3, para 2 at 33 weeks and 4 days of gestation presented to a community hospital with right-sided abdominal pain. Physical examination was notable for right lower quadrant guarding and rebound, and pelvic ultrasound showed an 8 cm adnexal mass, concerning for adnexal torsion. She underwent exploratory laparotomy, which confirmed ovarian torsion. On entry into the abdomen, haemoperitoneum was noted. A haemorrhagic ovarian cyst was dissected off the ovary and uterus, after which haemostatic sutures were placed into the uterine wall to control surface bleeding adjacent to the dissection. Additional bleeding from engorged uterine vessels along the right uterine sidewall was controlled by suture placement, and electrocautery was also used to manage serosal bleeding. Estimated blood loss was 750 mL; given postoperative haemoglobin drop from 102 g/L to 67 g/L, this was thought to be an underestimation. She received three units of packed red cells for symptomatic acute blood loss anaemia and her haemoglobin stabilised. She also received antenatal corticosteroids for fetal lung maturity on postoperative days 0 and 1. Fetal monitoring was reassuring throughout this hospitalisation. She was discharged on postoperative day 4. Pathological examination of the surgical specimen confirmed an 8.7 cm haemorrhagic mucinous cystadenoma.
The patient presented to our institution on postoperative day 7, at 34 weeks and 3 days of gestation, with persistent, severe right abdominal pain. At the time of presentation, she had normal vital signs: the temperature was 36.7°C, blood pressure was 119/69 mm Hg, pulse was 96 beats/min, respiratory rate was 18 breaths/min and SpO2 was >96% on room air. On physical examination, her abdomen was diffusely tender to palpation without rebound or guarding. External fetal heart monitoring was reassuring. Regular contractions were noted on tocometry and correlated with the worsening of her abdominal pain. Her cervix was 1 cm dilated and remained stable over serial cervical examinations.
Investigations
Complete blood count (CBC), comprehensive metabolic panel (CMP), lipase, haptoglobin and urinalysis were obtained, notable for mild transaminitis (aspartate aminotransferase 89 U/L and alanine transaminase 76 U/L). The remainder of her laboratories were normal. She underwent a CT abdomen/pelvis with intravenous contrast, which revealed mild stranding adjacent to the right uterine body at the prior surgical site and moderate stool burden. No clear cause of her pain was identified. The patient was admitted and received intravenous opioids along with stool softeners and laxatives; she had a bowel movement and her pain improved significantly. Her transaminitis spontaneously resolved on follow-up. She was discharged home after 3 days.
The patient initially did well at home, though she continued to have intermittent episodes of abdominal pain requiring acetaminophen and hydrocodone. At 35 weeks and 5 days of gestation, the patient had a fetal growth ultrasound performed that showed normal amniotic fluid volume and an estimated fetal weight of 3219 g (90th percentile for gestational age by Hadlock formula). No pelvic free fluid or abnormalities of the uterus, cervix, ovaries or adnexa were seen.
Differential diagnosis
The differential diagnosis of postoperative abdominal pain in a pregnant patient included intra-abdominal bleeding, haematoma, bowel or bladder injury, surgical site infection or pelvic abscess. Uterine rupture due to myometrial injury was considered given the involvement of the uterine body during the initial surgery, but felt to be less likely in the setting of reassuring fetal heart tracing and no prior uterine surgery. Preterm labour was also considered; however, the patient had no cervical change over serial examinations. Once laboratory results showed a mild transaminitis, the team also considered liver injury, cholelithiasis, pre-eclampsia and HELLP syndrome. The patient met no blood pressure or laboratory criteria for a pregnancy-induced hypertensive disorder. Additionally, a CT scan demonstrated expected inflammatory changes at the surgical site, without definitive evidence to support any of the differential diagnoses. After several days of admission for serial abdominal examinations, pain control and a bowel regimen, her symptoms improved enough for discharge. She did well in the intervening 2 weeks, further supporting a benign cause of her abdominal pain; uterine necrosis was not suspected by the treating team prior to diagnosis.
Treatment
The patient presented to our institution again at 36 weeks and 6 days with regular painful contractions and worsened abdominal pain. Her cervix was 1 cm dilated, and she had no peritoneal signs on abdominal examination. CBC, CMP, lipase and urinalysis were normal. Fetal heart tracing was notable for intermittent late decelerations. She was admitted for delivery due to category II fetal heart tracing near term. Induction was initiated with the cervical ripening balloon, oxytocin infusion and artificial rupture of membranes. After 12 hours, the fetal heart rate was non-reassuring, with tachycardia up to 180 beats/min, minimal variability, intermittent late decelerations and pseudo-sinusoidal pattern. Despite resuscitative measures and initiation of empirical ampicillin and gentamicin for suspected chorioamnionitis, the patient ultimately underwent emergent low transverse caesarean delivery for prolonged fetal bradycardia. A male neonate weighing 3110 g was delivered with Apgar scores of 7, 8 and 9 at 1, 5 and 10 min of life, respectively.
At the time of uterine exteriorisation for hysterotomy repair, a 5 cm region of apparent myometrial necrosis with surrounding hyperaemia was noted within the right uterine body (figure 1). Cultures and biopsy of this area were collected. Intraoperative consultation with a gynecologic-oncologist was obtained, and the decision was made to leave the uterus in situ without resection of the necrotic area. The remainder of the caesarean delivery was complicated by uterine atony requiring intramuscular methylergonovine, carboprost and placement of a B-Lynch suture, with an estimated blood loss of 800 mL.
A focal area of uterine necrosis noted at the time of caesarean delivery.

Postoperatively, the patient continued empirical intravenous antibiotics, consisting of ampicillin, gentamicin and clindamycin. On postoperative day 2, she had a transient fever of 39.2°C, but then remained afebrile for the remainder of her postpartum hospitalisation. Pathological examination of uterine biopsy confirmed necrosis. Cultures from this region grew Staphylococcus lugdunensis and blood cultures resulted in no bacterial growth. On repeat CT scans, no abscess or alternative source of infection was identified. With input from infectious disease, her antibiotic regimen was continued for 7 days postoperatively.
Outcome and follow-up
Maternal
The patient was discharged home on postoperative day 7 after the completion of all intravenous antibiotics. She was seen for follow-up visits at 2 weeks, 6 weeks, 3 months and 7 months postpartum, with normal postoperative recovery. To assess for recurrence of the adnexal mass, she underwent pelvic ultrasound at her 3-month follow-up visit, which showed an 8-week sized uterus with homogeneous echogenicity and unremarkable ovaries. She was started on combined hormonal contraceptives for ovulation suppression.
Neonatal
The baby met all newborn milestones and was admitted to the general nursery. He was discharged on the day of life 7 with his parents. As of his 9-month follow-up visit with his paediatrician, he has been meeting all appropriate growth and developmental milestones.
Discussion
This report details an unusual case of antepartum uterine necrosis following laparotomy for ovarian torsion in the third trimester. Typically, collateral flow between the ovarian, uterine, cervical and vaginal arteries provides a protective mechanism to prevent myometrial necrosis from occurring if the blood supply is diminished.4 Anatomic variation with the absence of utero-ovarian anastomoses has been described in a case of uterine necrosis following uterine artery embolisation.3 It is possible that a similar anatomic variation could have contributed to the development of the condition described here. Additionally, the use of suture placement and electrocautery to achieve haemostasis—though sometimes essential—is not without risk. Specific surgical challenges in this case included difficult visualisation due to haemoperitoneum, and though not explicitly noted by the surgeons, likely adhesions between the adnexal mass and the uterine serosa. Careful surgical technique, optimisation of visualisation, use of non-crushing vascular clamps when appropriate, and seeking additional assistance from surgical colleagues, all have the potential to minimise the risk of uterine necrosis as a complication of pelvic surgery.
Diagnosis of uterine necrosis in this patient was challenging, and ultimately the diagnosis was delayed by almost 4 weeks due to the broad differential diagnosis of postoperative abdominal pain. Prior studies note that uterine necrosis often presents with fever, abdominal pain, menorrhagia and leucorrhoea occurring a mean of 21 days following embolisation.4 The most common imaging findings were the presence of gas within the myometrium, absence of myometrial enhancement after gadolinium contrast, peripherally enhancing rim around the region of necrosis and enlarged uterus; however, no finding was consistently seen in the majority of cases identified.4 In pregnancy, imaging diagnosis is especially challenging due to the avoidance of contrast agents and physiological changes of the gravid uterus that may mask radiological clues. Outside of pregnancy, contrast-enhanced MRI or CT is the preferred imaging modality, although their respective sensitivities for the diagnosis of this condition are unclear. Therefore, in any patient who undergoes pelvic surgery during pregnancy and has persistent postoperative pelvic pain, it is necessary to maintain a high level of clinical suspicion for the interruption of uterine blood supply and uterine necrosis.
Necrotic tissue can be susceptible to invasion and colonisation with bacteria, particularly from the urogenital and gastrointestinal tracts. Various pathogens have been described in cases of uterine necrosis, including Escherichia coli, Citrobacter koseri and Fusobacterium necrophorum.6 7 Tanaka et al describes a case of Finegoldia magna myometritis in a patient with uterine necrosis diagnosed 11 weeks after uterine artery embolisation for postpartum haemorrhage.8 She underwent hysterectomy and recovered without the need for prolonged antibiotic therapy. In our case, cultures from the necrotic area of the uterus were obtained at caesarean delivery and grew S. lugdunensis, which was likely introduced during the course of her initial open surgery. This coagulase-negative staphylococcal species has been found on the skin of the inguinal region and has been implicated in skin and soft tissue infections, septic arthritis and infective endocarditis.9 Most isolates of S. lugdunensis are widely susceptible to antimicrobials, although like Staphylococcus aureus, resistance to penicillin derivatives is increasing.9
Much remains unknown regarding the long-term implications of uterine necrosis on fertility and pregnancy outcome, as many cases described in the literature were treated with hysterectomy. With necrotic disruption of the myometrial layer, impaired fertility, abnormal implantation, and abnormal placentation are all potential concerns that should be considered prior to future attempts at conception. Concern for uterine rupture at the region of necrosis due to myometrial weakening may dictate optimal mode and timing of delivery, and the patient was counselled regarding this potential risk. Although more data are needed, a conservative approach with uterine preservation may be considered in cases of uterine necrosis when close inpatient surveillance and follow-up are possible, and when future fertility is desired. If conservative management is pursued, a low threshold to pursue operative management via hysterectomy should be maintained if clinical improvement is not observed.
Learning points
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Uterine necrosis can be a rare cause of persistent postoperative abdominal pain after pelvic surgery during pregnancy.
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Antepartum uterine necrosis is challenging to diagnose and may not always be visible on routine imaging.
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Surgical technique involving the use of electrocautery and suture placement on the gravid uterus may play a role in the risk of uterine necrosis.
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Conservative management with close observation and treatment of concurrent infection may be safe in haemodynamically stable patients with uterine necrosis who desire uterine preservation.
Ethics statements
Patient consent for publication
Footnotes
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Contributors All three authors were involved in the care of this patient during her admissions. AH obtained consent from the patient, reviewed the medical record, drafted the report and incorporated edits to produce the final manuscript. RN drafted sections of the report and contributed edits throughout the writing process. MN oversaw the production of the report, contributed edits and provided expertise and guidance.
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Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
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Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
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Competing interests None declared.
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Provenance and peer review Not commissioned; externally peer reviewed.
- © BMJ Publishing Group Limited 2022. No commercial re-use. See rights and permissions. Published by BMJ.
References
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