Necrotizing Soft Tissue Infection of the Breast: Case Report and Literature Review

Case Reports

Case 1

A 55-year-old woman was diagnosed with invasive ductal carcinoma of the breast (stage T₂N₁M₀) three years earlier but had refused treatment. She returned to the clinic with a 15-cm ulcerated lesion (Fig. 1A) associated with ipsilateral aim lymphedema. Evaluation showed hepatic metastases (stage T₄bN₂M₁). She was overweight (body mass index [BMI] 28 kg/m²) and had mild arterial hypertension. Because of the extent of the disease and tumor ulceration, she was considered unfit for neoadjuvant chemotherapy, and she underwent modified radical mastectomy with axillary dissection and reconstruction using a latissimus dorsi myocutaneous flap. She was given prophylactic antibiotic consisting of 2 g of cefazolin intravenously at the time of induction of anesthesia, followed by 1 g intravenously every 8 h for 24 h. She was discharged on the first post-operative day.

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FIG. 1.

Images from Case 1. (A) Resected locally advanced breast cancer. (B) Necrotizing soft tissue infection after mastectomy. (C) Area of debridement. (D) Final result.

On the fourth post-operative day, she returned with fever, pain at the surgical site, and purulent secretion in the operative wound, with a fetid smell (Fig. 1B). She had stable hemodynamics, with slight dehydration. She was hospitalized and started on intravenous ceftriaxone, ampicillin, and gentamicin. She underwent extensive surgical treatment, with resection of the necrotic area (Fig. 1C), and was sent to the intensive care unit even though she did not demonstrate severe sepsis and her laboratory test results were acceptable. She remained in intensive care for two days, and, because she had a favorable evolution, she was discharged on the fifth day. Culture of the material from the infection site yielded Pseudomonas aeruginosa that was sensitive to gentamicin, but resistant to ampicillin and ceftriaxone. Dehiscence of the operative wound occurred, and she underwent debridement and local resuturing in the fourth week. Adequate local healing was achieved after eight weeks (Fig. 1D).

Case 2

A 57-year-old woman had a history of cancer in her right breast 18 years earlier. She presented a nodule 5 cm in diameter in her left breast, and biopsy showed invasive ductal carcinoma (stage T₂N₁M₀). Her BMI was 27.5 kg/m², and she had mild arterial hypertension and type II diabetes mellitus. She underwent modified radical mastectomy with axillary dissection and was given 2 g of cefazolin intravenously at the time of induction of anesthesia, followed by 1 g intravenously every 8 h for 24 h. She was discharged on the first post-operative day.

On the seventh post-operative day, the drain was removed, and a recurrent axillary seroma was found. The patient then underwent seroma aspiration in her city of origin. On the 32nd post-operative day, she came back to our hospital with a history of a seroma aspiration one day earlier, chest pain at the surgical site, fever, and vomiting. On physical examination, she was pallid, dehydrated, tachycardic, and dyspneic, with ketone halitosis. Local cellulitis without fluctuation was seen in the surgical scar. A hemogram showed leukopenia (3,300 leukocytes/cm³) with large immature cells, hyperglycemia (150 mg/dL), and a serum creatinine concentration of 2.0 mg/dL. The patient was hospitalized under intensive care, and broad-spectrum antibiotic therapy composed of vancomycin, metronidazole, and cefepime was given.

On the first day in the intensive care unit, her condition worsened, with worsening carbohydrate intolerance, and she developed skin necrosis (Fig. 2A). She therefore underwent surgery for local debridement (Fig. 2B). She developed respiratory dysfunction, acute kidney injury necessitating dialysis (peritoneal), septic shock, cyanosis, and necrosis of the extremities (Fig. 2C–E), and died of multiple organ dysfunction syndrome on the tenth day of hospitalization. Blood culture showed gram-positive cocci, with growth of Streptococcus pyogenes that was sensitive to penicillin G, cefepime, and vancomycin.

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FIG. 2.

Images from Case 2. (A) Cutaneous flap with necrotizing soft tissue infection after mastectomy. (B) Surgically debrided area. (C) Abnormality of peripheral perfusion at time of admission. (D) Evolution of debrided area. (E) Evolution of peripheral perfusion.

Discussion

Necrotizing soft tissue infection is a clinical entity considered to be a syndrome of progressive infectious gangrene of the skin and subcutaneous tissue [2]. It is called Fournier gangrene when it occurs in the perineum [19], and it is rare in breast tissue. The diagnosis of NSTI is clinical, and cases can be divided into the fulminating form, which is associated with septic shock and a high mortality rate, and the acute form, in which symptoms occur after several days followed by large areas of necrosis [20].

Table 1 summarizes all the breast cases in the literature (PubMed; Lilacs) [3–15] and the present report. The differential diagnosis of acute breast NSTI is made in relation to pyoderma gangrenosum, which is a rare, non-infectious, idiopathic necrotizing cutaneous disorder associated with systemic diseases in which the immune system plays a part [21–23]. It evolves as a complication of surgical procedures [21].

Regarding the anatomopathological characteristics in the initial stages, we observed extensive necrosis in the fascia and subcutaneous fat, acute perivascular inflammatory infiltrates within the dermis, and acute inflammatory infiltration of the muscles without necrosis [24]. Concomitant thrombosis of the microcirculation may occur. In the final stages, we observed necrosis involving the skin, subcutaneous fat, and fascia (Fig. 3).

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FIG. 3.

Histopathologic findings in soft tissue necrosis. (A) Necrosis of dermis and epidermis. (B) Necrosis of subcutaneous adipose tissue. (Hematoxylin and eosin; original magnification ×400.)

From an etiologic point of view, necrotizing fasciitis can be divided into three types [8,14,20,25]. Type I is associated with polymicrobial etiology and may involve gram-positive, gram-negative, and anaerobic bacteria. It is related to abdominal and pelvic surgery in patients with co-morbidities such as diabetes mellitus, obesity, and atherosclerosis, as observed in our Case 1. In this form, NSTI caused by P. aeruginosa is rare. Infection with this organism has been described after cesarean section, after colonization of devitalized tissue, and in immunosuppressed individuals [21,22], but it has never before been described in NSTI of the breast. The predisposing factor in our patient was the extensive ulcerated breast lesion and metastatic disease. Type II is found in association with Streptococcus spp. and, in some cases, Staphylococcus aureus or S. epidermidis. It is associated with small injuries, as observed in our Case 2, which is the first report of NSTI of the breast after mammary seroma aspiration. Some authors classify clostridial NSTI separately as Type III. Analyzing Table 1, we observed that NSTIs of the breast are frequently Type II (10/16), occurring mainly after breast procedures (9/16), in breast cancer (6/9), or as a complication of spontaneous mastitis (6/16). Only a single case of Type III NSTI has been reported following breast surgery [18].

Early diagnosis and immediate treatment are the most important factors for favorable evolution, given that delayed therapy may be associated with a high mortality rate. Once the disease has been identified, material needs to be gathered for culture (blood and tissue from the infected site). The choice of antibiotic therapy must be based on the fact that NSTIs are more frequently polymicrobial and may involve anaerobic and anaerobic gram-positive and gram-negative pathogens [26], so several single-agent regimens probably are effective, including imipenem-cilastatin, meropenem, ertapenem, piperacillin-tazobactam, ticarcillin-clavulanic acid, and tigecycline. Because of the increasing resistance of gram-negative bacilli to ampicillin-sulbactam, this regime must be considered only after local sensitivities are known. Other combinations of agents probably are equally effective, but changes to the initial antibiotic therapy should be made according to the results of the cultures and antibiogram and based on the evolution of the patient.

The surgeon's participation in controlling the focus of the infection is of fundamental importance, just as important as the broad-spectrum antibiotic therapy and the support measures, such as maintenance of volume, correction of electrolytic disorders, and treatment of any sepsis and septic shock. The surgical treatment consists of full local debridement to resect all of the necrotic tissue. Skin and fat are excised if the infection is under the fascia, and the muscle can be preserved. Repeated debridement may be necessary. In patients with breast cancer, five had previous mastectomies, and one had a previous quadrantectomy and was treated with mastectomy. Mastectomy was necessary in five of ten patients without breast cancer, whereas extensive debridement was performed in the other cases. Once the infection has been brought under control, skin grafting or soft tissue flaps can be considered [8]. Table 1 shows the infectious agents observed in cultures in reported cases, the antibiotic treatment that was instituted, and the evolution of the NSTI.

The mortality rate of NSTI in general ranges from 33% to 73%, whereas it is 18.7% (3/16) in the breast infections. The factors associated with the high mortality rate are age, trunk involvement, diabetes mellitus, delayed diagnosis, atherosclerosis, and inadequate surgery [6]. All of deaths from NSTI of the breast were in patients with the fulminating form; i.e., Type II associated with beta-hemolytic streptococci (Table 1). The surgical oncologist and breast surgeon must be alert to the possibility of this rare condition, for which broad-spectrum antibiotic therapy, intensive care support, and, in particular, early surgical intervention are fundamental for favorable evolution.