Abstract

Necrotizing soft tissue infections of the breast are exceptionally rare surgical emergencies with high mortality, and monomicrobial Escherichia coli (Type 3) necrotizing fasciitis is an uncommon, highly virulent form. We report a 23-year-old woman with insulin-treated Type 1 diabetes mellitus as her only comorbidity who developed extensive breast necrosis from a small pustule and presented with sepsis. Wound cultures were sterile while blood cultures grew E. coli. She underwent repeated debridement, sequential vacuum-assisted closure therapy and, after infection control, latissimus dorsi myocutaneous flap reconstruction, followed by revision for partial lateral flap necrosis, and was discharged in good condition. Even a minor skin breach in a diabetic patient may trigger fulminant gram-negative necrotizing fasciitis; early recognition, aggressive debridement, culture-guided antibiotherapy, vacuum-assisted closure, and staged flap reconstruction are critical for survival and functional recovery.

Introduction

Necrotizing soft tissue infections (NSTIs) are rapidly progressive, life-threatening infections marked by widespread necrosis of the fascia, subcutaneous tissue, and overlying skin, with a reported mortality of 15%–30% that rises sharply with any delay in surgery [1, 2]. NSTI of the breast is exceptionally rare, represented in the literature by only a small number of cases [3, 4].

Diabetes mellitus is the best-established predisposing condition. Chronic hyperglycemia impairs innate immunity, suppresses antimicrobial peptide production, and compromises wound healing, so that even a trivial skin breach can become a portal for virulent organisms [5, 6]. We present a 23-year-old woman whose only comorbidity was Type 1 diabetes mellitus (T1DM) and who developed fulminant Escherichia coli monomicrobial NSTI of the breast from a small pustule, managed with repeated debridement, vacuum-assisted closure (VAC) therapy, and latissimus dorsi (LD) flap reconstruction.

Case report

A 23-year-old woman with insulin-treated T1DM and no other comorbidity presented with a right breast abscess and extensive overlying necrosis that had developed from a small pustular lesion (Figs 1 and 2). On admission she was septic: temperature 39.0°C, heart rate 110 beats/min, and blood pressure 75/50 mmHg. Laboratory studies showed leukocytosis (white blood cell count 19.7 × 109/L), markedly elevated C-reactive protein (455 mg/L) and poor glycemic control (HbA1c 9.7%). Breast ultrasonography revealed no discrete mass.

Clinical photograph of a right breast almost entirely covered by black, full-thickness skin necrosis, surrounded by a rim of red erythematous skin.
Figure 1

Initial presentation. Extensive necrosis of the right breast arising from a small pustular lesion, with surrounding erythema and a sharply demarcated zone of full-thickness skin necrosis.

Close-up clinical photograph showing a dark necrotic eschar covering the breast, bordered by inflamed pink erythematous skin, before surgical debridement.
Figure 2

Initial presentation, second view. Eschar-covered necrotic breast with peripheral erythema, prior to the first debridement.

Wound cultures yielded no growth, whereas blood cultures grew E. coli, confirming gram-negative bacteremia, and Type 3 monomicrobial NSTI. Histopathology of the debridement specimens showed no additional pathology, excluding an underlying malignancy. The patient underwent urgent surgical exploration; intraoperative findings were consistent with necrotizing fasciitis, with necrotic subcutaneous tissue and liquefied fascia. Because of rapid progression, repeated debridements were performed, excising all necrotic tissue (Fig. 3). Infectious Diseases was consulted and intravenous piperacillin-tazobactam was started.

Intraoperative photograph of a debrided breast wound bed showing red, bleeding viable tissue at the margins, with the nipple-areola complex partially preserved.
Figure 3

After surgical debridement. Wound bed after excision of all necrotic tissue, with viable bleeding tissue at the margins and the nipple-areola complex partially preserved.

The large defect was managed with VAC therapy rather than primary closure, in keeping with evidence that VAC reduces mortality and promotes granulation compared with conventional dressings in NSTI [7] (Figs 4 and 5). Internal Medicine and Endocrinology optimized glycemic control. Resolution of fever, declining inflammatory markers, and a clean granulating wound bed confirmed control of the infection (Fig. 6).

Photograph of a breast wound bed covered with healthy red granulation tissue after the first negative-pressure therapy cycle.
Figure 4

Wound bed after the first VAC cycle. Healthy granulation tissue developing over the debrided bed, indicating control of the infective process.

Photograph of a black negativepressure foam dressing with a suction tube sealed over the breast wound.
Figure 5

VAC therapy in place. Negative-pressure wound therapy dressing applied to the breast defect to accelerate granulation and prepare the wound bed.

Photograph of a clean, wellgranulating breast wound bed prepared for reconstruction, with the nipple-areola complex preserved.
Figure 6

After debridement and VAC, before reconstruction. A clean, well-granulating wound bed prepared for definitive coverage, with the nipple-areola complex preserved.

Intraoperative photograph of a pedicled latissimus dorsi muscle-and-skin flap being transposed into the breast defect.
Figure 7

Latissimus dorsi flap reconstruction. Intraoperative transposition of the pedicled LD myocutaneous flap into the breast defect.

Photograph of the reconstructed breast immediately after surgery, with the flap skin paddle sutured in place and closed-suction drains beneath the flap and in the axilla.
Figure 8

Immediate postoperative result. Completed flap inset with the skin paddle sutured in place and closed-suction drains positioned beneath the flap and in the axilla.

During follow-up, partial necrosis developed in the lateral flap, and revision surgery was performed ~10 days after reconstruction, without further complications; the drain was removed on the third postoperative day (Fig. 9). Antibiotherapy was re-evaluated with Infectious Diseases and switched to oral therapy before discharge. With a clean wound and good general condition, the patient was discharged in recovery and advised to continue dressing changes and to return for redness, swelling, foul-smelling discharge, fever, or deterioration; follow-up appointments were arranged (Fig. 10).

Photograph of the reconstructed breast after revision of the lateral flap necrosis, showing a viable flap.
Figure 9

After flap revision. Appearance following revision of the lateral flap necrosis.

Photograph of the healed reconstructed right breast at follow-up, with a viable flap, intact skin, and preserved breast contour.
Figure 10

Final outcome. Healed reconstructed right breast at follow-up, with a viable flap and preserved breast contour.

Once the infection was controlled, the Plastic, Esthetic, and Reconstructive Surgery team reconstructed the defect with a pedicled LD myocutaneous flap, chosen for its reliable thoracodorsal pedicle and generous tissue volume [8, 9] (Figs 7 and 8). The patient was monitored in the intensive care unit for one postoperative day and transferred to the ward after stabilization. Postoperatively she was followed with daily dressing changes. After discharge developed at the wound, a culture was taken and antibiotherapy adjusted accordingly; the sutures were partially opened over that area and dressings continued. The sub-flap, donor-site, and axillary drains were removed on the fifth postoperative day and the urinary catheter on the second.

Discussion

This case is notable for the patient’s young age with T1DM as the sole risk factor, the E. coli monomicrobial etiology (Type 3 NSTI, the subtype with the highest mortality), the breast as an exceptionally rare site, and survival with successful reconstruction despite a bacteremic presentation [4, 6]. Breast NSTI may arise from minor skin trauma, breast procedures, or underlying systemic disease, and its early stages can mimic cellulitis, mastitis, or inflammatory breast carcinoma, contributing to diagnostic delay [3, 10]. In our patient, progression from a small pustule to extensive necrosis with sepsis over a short period illustrates how unforgiving this disease can be.

The immunological vulnerability of T1DM is central. Chronic hyperglycemia suppresses antimicrobial peptides, facilitates biofilm formation and impairs keratinocyte migration and angiogenesis [5, 6]. Despite insulin therapy, an HbA1c of 9.7% reflects suboptimal control, likely rendering the skin highly susceptible to opportunistic gram-negative invasion after a minor breach. The combination of sterile wound cultures and positive blood cultures carries a practical message: local wound cultures may be falsely negative early or after antibiotic exposure and should not, alone, guide management. Blood cultures are indispensable in any patient with sepsis and rapidly progressing soft tissue infection [11, 12].

VAC therapy bridged debridement and reconstruction by reducing edema, promoting granulation and maintaining a clean wound bed [7]. The pedicled LD flap remains a reliable option for large, contaminated breast defects [8, 9]; partial lateral necrosis requiring revision is recognized, and our staged approach prioritized flap safety in a diabetic wound. The favorable outcome reflects multidisciplinary coordination among general surgery, plastic surgery, internal medicine, endocrinology, and infectious diseases, consistent with current consensus on adult NSTI [2]. Any rapidly expanding skin lesion in a diabetic patient warrants urgent evaluation for NSTI, with early debridement, culture-guided antibiotherapy, VAC therapy, and staged reconstruction remaining the cornerstones of survival and functional recovery.

Conflicts of interest

The authors declare that they have no conflict of interest.

Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Consent

Written informed consent was obtained from the patient for publication of this case report and the accompanying images. All identifying information has been anonymized. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.

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