Uterine Dehiscence and Abdominal Wall Necrotizing Fasciitis Following Cesarean Section: A Case Report

Introduction

NSTIs are typically caused by toxin-producing bacteria and are characterized clinically by very rapid progression of disease with significant local tissue destruction [1]. NSTIs include necrotizing forms of fasciitis, myositis, and cellulitis, with high mortality, ranging from 25% to 35% [2]. Rapidly progressive necrosis in tissues often causes systemic sepsis, toxic shock syndrome, and multi-organ failure [3]. It usually spreads along the fascial plane, which has a deficient vascular supply, thereby leaving the superficial tissues relatively unaffected in the initial stages, which can subsequently delay diagnosis and surgical intervention [4]. After the infection spreads, the clinical presentation can include tense edema outside the area of compromised skin, pain disproportionate to appearance, skin discoloration (ecchymosis), blisters/bullae and necrosis, crepitus, and/or subcutaneous gas. The majority of postoperative NF cases in obstetrics and gynecology were reported prior to the introduction of prophylactic antibiotics [5]. The correlation between necrotizing fasciitis and cesarean section has been reported to be 1.8 per 1000 women, but the pathogenesis is not fully understood.

Case Report

A 28-year-old G5 P4 term patient, with a language barrier due to not speaking Arabic, presented to the emergency room with an intense cramping pain in the abdomen that radiated to the groin, and membrane rupture, which began more than 8 hours before. Prior to this pregnancy, she had 2 non-consecutive cesarean births. Two years ago, she gave birth spontaneously via trial of labor after cesarean (TOLAC). Her medical history was unremarkable. Vital signs were within normal range and her body mass index (BMI) was 59. Abdominal examination showed an average-size fetus, cephalic presentation, and positive fetal heartbeat. Vaginal examination showed 5-cm dilated, 80% effected, vertex at 0 station. The plan was for emergency cesarean section. Her initial lab tests showed hemoglobin (Hb) 10 g/dl, white blood cells (WBC) 11.85 K/uL, and platelets (PLT) 362 K/uL. The results of the coagulation profile, liver function test, renal function test, and urine analysis were normal.

During the emergency cesarean section, severe adhesions were identified. The operation was complicated by a lower-segment leaf laceration at the middle of the uterotomy, which extended caudally up to 3 cm. Bladder injury was thought to have occurred, but an injection of methylene blue revealed no extravasation. The estimated blood loss was 1800 ml. She received 2 units of packed red blood cells (PRBCs) intra-operatively. Postoperative lab tests showed WBC 10.57, HB 8.7, and PLT 283. During her postoperative course, a computed tomography (CT) urogram was performed to confirm there was no urinary bladder injury. Antibiotic therapy with cefuroxime was administered for 3 days. On the second day, she was sent home.

She visited the emergency room on the ninth postoperative day with intense brownish discharge from the surgical site, which started 2 hours prior to arrival, with history of fever and abdominal pain for 3 days (Figure 1). Vital signs showed a positive shock index of 1.9, BP 71/40, MAP 82, temperature 36.9°C, heart rate 140 bpm, maintaining O2 saturation on room air, GCS 15/15. She was started on intravenous (IV) hydration with ringer lactate and IV albumin. The ICU team was contacted because she was still hypotensive, with MAP of 52. A central line was inserted.

On examination, the surgical site is covered by a pendulous abdomen, and there is a 2-cm wound defect with apparent profuse wound discharge. A swab culture was taken. Vaginal examination revealed the same discharge from the wound. Blood tests showed WBC 18.36 K/uL, PLT 466K/uL, Hb 8.3 g/dL, and C-reactive protein (CRP) 356.0mg/L. INR was 1.35.

Initial resuscitation was carried out by the ICU staff. IV antibiotic therapy began with meropenem, vancomycin, and clindamycin for suspected necrotizing fasciitis. General Surgery team members were involved and planned for abdominal CT with contrast. Preoperative imaging was not performed, as the patient was unstable.

She underwent emergency exploratory laparotomy. Intra-operative findings showed necrotic fascia of the lower anterior abdominal wall, complete dehiscence of the uterotomy, adherence of the lower segment to the abdominal wall, friable necrotic endometrium with cutaneous sinus, and no bowel perforation. Following this, the surgeons performed a bilateral salpingectomy and hysterectomy (Figure 2), thoroughly cleaned the wounds, and used VAC. She received 2 units of PRBCs.

Bacterial cultured showed methicillin-resistant Staphylococcus aureus (MRSA) and Enterococcus faecalis. Postoperative care in the surgical ICU lasted for 5 days, then she transferred to the ward. Several VAC dressing changes and abdominal wall debridements were performed. The rest of the hospital course was uneventful. The histopathology result confirmed the diagnosis of acute suppurative endometritis and bilateral acute salpingitis. Hemodynamic stability was maintained throughout the surgical period, infection markers declined, and her clinical condition improved during the hospital stay. She was discharged 22 after surgery. She was seen in the outpatient clinic 4 weeks after discharge (Figure 3).

Discussion

Postpartum endometritis is an infection of the decidua that can affect all layers of the uterus. The risk of organisms from the vaginal vault colonizing the uterine cavity increases as the cervix dilates and the fetal membranes rupture. Puerperal/postpartum endometritis is more frequently seen after cesarean section compared to normal vaginal delivery, and is polymicrobial in nature [6]. Postpartum endometritis can present as necrotizing myometritis and necrotizing fasciitis of the abdominal wall. Necrotizing fasciitis in postpartum patients is a rare condition that can be lethal, with reported mortality rates ranging from 13% to 25% [7,8]. Most of the available data come from case reports and case series.

Classification schemes of necrotizing fasciitis are not clinically relevant, except for the bacterial etiology. Because waiting for microbiological proof could result in the patient’s death, the clinical picture drives decisions in cases of necrotizing fasciitis. Depending on the severity, source, and systemic implications, necrotizing fasciitis (NF) frequently necessitates additional therapies (Table 1).

The bacterial causes of necrotizing fasciitis can be categorized into 3 types: Type I – Polymicrobial infections involving 2 or more bacterial species; Type II – Infections caused by Group A β-hemolytic Streptococcus and/or Staphylococcus aureus, including methicillin-resistant strains (MRSA); and Type III – Infections attributed to Clostridium species.

Enterococcus faecalis and Enterococcus faecium are part of the normal gastrointestinal flora, but are also typical opportunistic pathogens. In some specific body areas, such as the groin, the skin can also be colonized by enteric flora [9]. Surveillance studies have detected MRSA colonization rates of up to 10% in rectovaginal swab specimens and up to 2% of nasal swab specimens in asymptomatic pregnant women at term [10].

Our patient was found to have a ruptured anterior uterine wall, probably due to bacterial proliferation, as some bacteria produce toxins that can lead to thrombosis of larger venules and arterioles, with subsequent ischemic necrosis of all tissue layers, from the dermis to the deep muscles [11]. This can result in a utero-cutaneous fistula, which is an abnormal communication between the abdominal wall and the anterior wall of the uterus, thereby creating a conducive environment for the development of NSTIs.

The most difficult aspect of treating these illnesses is determining the diagnosis, which helps healthcare professionals intervene promptly and effectively. The patient initially presented nonspecific symptoms that overlap with multiple differential diagnoses. A high index of suspicion is crucial for early detection. Delayed surgical debridement due to delayed diagnosis can increase the risk of death. Intraoperative findings include gray necrotic tissue, thrombosed veins, non-contracting muscle, “dishwater” pus, no bleeding, and no resistance to finger dissection in normally adherent tissues. Imaging tests in these situations should not postpone surgical intervention because the treatment requires emergency surgical debridement. Surgical exploration is warranted when there is strong clinical suspicion.

According to a review of the literature (Table 2), there is inadequate pre-incident history documentation, as most case reports focused on management and patient recovery. While intervention plays an important role in determining the outcome, risk analysis is also important. Most cases involved a post-emergency cesarean section. As most case reports did not document preoperative antibiotic administration, it can be assumed that prophylactic antibiotics were given; however, necrotizing fasciitis still occurred. Even with the assumption that all patients received prophylactic antibiotics before surgery, necrotizing fasciitis still developed. The addition of azithromycin in nonelective cesarean delivery, as currently recommended, could lead to further decreases in reported cases.

In several reported cases, patients received antibiotics after cesarean section due to various conditions but did not suppress the bacterial pathway. Treatment success depends on completely removing the infected tissues. Consequently, unless bleeding from nearby healthy subcutaneous tissues occurs, surgical debridement should be performed. Because of the edema and secretions in the operative area, surgical wounds are frequently left open. In wounds that are sufficiently debrided, a negative-pressure device can encourage increased vascularization of the wound bed and avoid the need for regular dressing changes. Usually, a second check is required 24–48 hours later.

Our hospital’s empiric therapy regimen consists of 3 antimicrobials: meropenem, vancomycin, and clindamycin. Meropenem covers a broad range of bacteria, including many gram-positive and gram-negative pathogens. Empirical coverage for MRSA infection was given with vancomycin. Clindamycin is a broad-spectrum antibiotic that is particularly effective against many gram-positive and anerobic bacteria. The use of protein synthesis inhibitors, such as clindamycin, can help by controlling the inflammatory response. Clindamycin is used as an antitoxin agent and is effective against toxin-elaborating strains of beta-hemolytic streptococci and S. aureus. Patients should continue receiving antibiotics until their condition has improved and no more debridements are required. Eventually, the bacterial culture should determine which antibiotic is appropriate.

Finally, even though radical debridement is necessary to save the patient’s life, it is often difficult to preserve function and achieve acceptable cosmetic results. Plastic surgery consultation should consider the wishes of the patient.

Conclusions

Postpartum necrotizing fasciitis (NF) is rare but potentially fatal. Early recognition remains critical and should be guided by a high index of suspicion, especially in patients with nonspecific symptoms such as persistent fever or disproportionate pain. While surgical debridement and broad-spectrum antibiotics are the mainstays of treatment, adjunctive therapies may be considered in select cases. Given the limited evidence supporting these alternatives, further research is needed to clarify their role. Enhanced postpartum monitoring and multidisciplinary collaboration are essential to improve early diagnosis and outcomes in such complex cases.