Breast cellulitis and other skin disorders of the breast

INTRODUCTION — Breast cellulitis is a skin infection that occurs as a result of bacterial entry via breaches in the skin barrier. Issues related to breast cellulitis and other skin disorders of the breast will be reviewed here. Issues related to breast abscess and lactational mastitis are discussed separately, as are issues related to breast reconstruction. (See "Primary breast abscess" and "Lactational mastitis" and "Overview of breast reconstruction".)

ACUTE BREAST CELLULITIS

Epidemiology — Breast cellulitis is relatively uncommon. A prospective study including 3762 patients evaluated in a dedicated breast center during a 14-month interval found that 0.6 percent presented with erythema of the breast and, of those 22 patients, only 2 had cellulitis [1]. Among patients managed for breast cancer with breast-conserving surgery and radiation therapy, breast cellulitis occurs in 1 to 8 percent of patients [2-7].

Risk factors for breast cellulitis include [1-5,7-10]:

●Prior breast cellulitis or infection

●Breast surgery within previous 30 days (surgical site infection)

●Lactation

●Trauma (eg, bites, nipple piercing, tattoos)

●Lesions in breast skin (eg, eczema, intertrigo, dermatitis, epidermolysis bullosa)

Issues related to delayed cellulitis following breast conservation therapy are discussed below. (See 'Delayed cellulitis after breast conservation therapy' below.)

Microbiology — Beta-hemolytic streptococci are common causes of breast cellulitis [3,9,11]. Group B beta-hemolytic streptococci have a proclivity to produce soft tissue infections in the setting of venous and/or lymphatic compromise [12]; in one case-control study, for example, breast cancer was identified as a risk factor associated with the development of group B beta-hemolytic streptococcal infection [13].

Staphylococcus aureus, including methicillin-resistant S. aureus (MRSA), can also be an important pathogen.

Clinical manifestations — Clinical manifestation of breast cellulitis include pain, diffuse erythema, tenderness, and warmth [2,4,5,8,14,15]. Pain can occur before onset of erythema. Systemic symptoms, such as fever or chills, are uncommon, occurring in only 6 of 50 cases in one series [4]. The physical examination of the breast demonstrates localized or diffuse erythema, edema, marked tenderness, and warmth. Axillary nodes can be enlarged and tender. Spread of infection along lymphatic pathways (lymphangitis) can also be seen (picture 1).

Diagnosis — The diagnosis of breast cellulitis is based on clinical manifestations [6,16-21]. The evaluation includes obtaining a clinical history to assess for trauma, underlying skin condition, breastfeeding, and previous breast surgery, breast cancer diagnosis, and/or local radiation treatment. A breast examination should be performed to assess the extent of erythema and swelling as well as for presence of tender and/or enlarged axillary lymph nodes.

No laboratory testing is diagnostic. Blood cultures are warranted in patients with rapidly progressive local changes of infection and/or evidence of systemic infection that includes hemodynamic instability, fever, chills, or malaise; otherwise, blood cultures are not necessary.

Radiographic imaging is useful if there is clinical suspicion of an underlying fluid collection, abscess, malignancy, or if there is no clinical improvement within 48 hours of appropriate antibiotic treatment. Ultrasound may demonstrate skin and subcutaneous edema; mammography may demonstrate mild skin thickening [22]. Magnetic resonance imaging (MRI) may demonstrate skin thickening and separation or septation of subcutaneous adipose tissue [23].

Differential diagnosis — Breast cellulitis must be distinguished from other inflammatory processes of the breast. Disruption of cutaneous lymphatics and/or circulation in the absence of an infectious process, such as a malignancy or an inflammatory process, can lead to a diffuse pattern of erythema that mimics cellulitis [24-26].

●Breast abscess – A breast abscess is a localized collection of pus in the breast tissue. Patients with breast abscess present with localized painful inflammation of the breast associated with fever and malaise, along with a fluctuant, tender, palpable mass. The diagnosis is based on clinical manifestations and ultrasonography. (See "Primary breast abscess".)

●Skin abscess overlying the breast – Skin abscesses involving the skin overlying the breast are usually related to an infected epidermoid cyst or related to hidradenitis suppurativa. (See 'Epidermoid cyst' below and 'Hidradenitis suppurativa' below.)

●Inflammatory breast cancer – Inflammatory breast cancer (IBC) should be considered if infection does not resolve with antimicrobial treatment. IBC may be distinguished by clinical manifestations of skin thickening due to edema, erythema, and peau d'orange appearance (picture 2 and picture 3 and picture 4). It is often associated with axillary lymphadenopathy. The diagnosis is established via biopsy. (See "Inflammatory breast cancer: Clinical features and treatment".)

●Other breast malignancy – Comedo ductal carcinoma in situ can become infected and present with inflammation or an abscess [27]. In addition, advanced breast cancer can present with skin ulceration, malodorous necrosis, and secondary infection. These diagnoses are established via biopsy. (See "Diagnostic evaluation of suspected breast cancer".)

●Paget disease of the breast – Paget disease of the breast (PDB) is a scaly, raw, vesicular, or ulcerated lesion that begins on the nipple and can spread to the areola (picture 5). The diagnosis is established by biopsy; the pathologic hallmark is the presence of malignant intraepithelial adenocarcinoma cells (Paget cells) within the epidermis of the nipple. Most cases are associated with an underlying invasive or noninvasive breast cancer. (See "Paget disease of the breast (PDB)".)

●Superficial thrombophlebitis of the breast – Superficial thrombophlebitis of the breast, also known as Mondor disease, is a self-limiting disease involving the superficial veins of the breast and anterior chest wall (picture 6) [28]. Clinical manifestations include a thickened, tender cord with pain, erythema, and swelling; the syndrome can occur following surgery, core biopsy of the breast, radiation treatment, trauma, or unrelated to any antecedent event [29-34]. The condition usually resolves in four to six weeks with symptomatic treatment using analgesics.

●Morphea – Morphea (localized scleroderma) is an idiopathic inflammatory skin disorder associated with fibrosis (picture 7). It may be associated with radiation therapy (picture 8), trauma, breast implants, or autoimmune disease [35]. The initial sign of morphea is often abrupt onset of an erythematous patch or edematous plaque. Some patients may note pain or itching at the site prior to the development of a clinically evident lesion. Clinical manifestations include inflammation with hyperpigmentation, retraction, skin thickening, and fibrosis extending into the subcutaneous adipose tissue [36]. (See "Pathogenesis, clinical manifestations, and diagnosis of morphea (localized scleroderma) in adults".)

●Postoperative dermal lymphedema – Postoperative dermal lymphedema presents with cutaneous erythema and induration in the absence of tenderness, fever, or leukocytosis [3,29,37]. The breast involvement may be localized or diffuse. Lymphedema is a manifestation of lymphatic obstruction, which can occur following surgery alone or in conjunction with radiation treatment for breast cancer [38,39]. Clinical evaluation and surveillance are adequate; a biopsy should be performed if malignancy is suspected.

●Radiation-induced dermatitis – Clinical manifestations of radiation-induced dermatitis include erythema, edema, pigment changes, epilation, and dry or moist desquamation (picture 9). These findings are strictly confined to the irradiated region and are not associated with fever or leukocytosis [29]. The diagnosis is established based on clinical manifestations. (See "Radiation dermatitis".)

●Issues related to delayed cellulitis after breast conservation therapy are discussed below. (See 'Delayed cellulitis after breast conservation therapy' below.)

●Radiation-induced fibrosis – Radiation-induced fibrosis can develop as a late effect of radiation treatment. Clinical manifestations include induration, thickening, and lymphedema in the skin and subcutaneous tissue of the breast. The diagnosis is established based on clinical manifestations. (See "Clinical manifestations, prevention, and treatment of radiation-induced fibrosis".)

●Spontaneous gangrene of the breast – Spontaneous gangrene of the breast with secondary infection can occur [16]. This is very rare; risk factors include diabetes and renal failure (picture 10). Spontaneous gangrene of the breast has also been reported in some patients within the first few days of receiving large doses of warfarin (picture 11) [40]. (See "Warfarin and other VKAs: Dosing and adverse effects", section on 'Skin necrosis'.)

●Bite wound – Clinical manifestations of bite wound infections may include tenderness, erythema, swelling, purulent drainage, lymphangitis, and fever. Management of human bites includes wound care, antibiotic therapy, and tetanus vaccination. (See "Human bites: Evaluation and management", section on 'Management'.)

Treatment — Treatment of breast cellulitis includes antibiotics, symptomatic relief, and management of underlying predisposing conditions.

General measures — To reduce local pain and swelling, we suggest nonsteroidal anti-inflammatory agents (eg, ibuprofen) along with cold compresses.

Skin conditions that predispose to the development of cellulitis, such as eczema or intertrigo (see 'Skin disorders of the breast' below), should be optimally managed. Diagnosis and treatment of such conditions are discussed elsewhere. (See "Treatment of atopic dermatitis (eczema)" and "Intertrigo".)

Antibiotic therapy — Selection of antibiotic therapy is based on the suspected bacterial etiology as well as the patient’s severity of illness and underlying medical conditions. In general, the approach to antibiotic choice for acute breast cellulitis is the same as for cellulitis located elsewhere on the body, with the exception of dosing adjustments in certain cases. (See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Selecting an antibiotic regimen'.)

Certain soft tissue infections of the breast have distinct microbiology and specific treatment approaches. Treatment of such infections is discussed elsewhere:

●Cellulitis in the setting of breast implants (see "Breast implant infections")

●Breast abscess (see "Primary breast abscess")

●Mastitis, including lactation-associated mastitis (see "Nonlactational mastitis in adults" and "Lactational mastitis")

●Cellulitis following localized trauma such as human bites, tattoos, or piercing (see "Human bites: Evaluation and management" and "Tattooing in adolescents and young adults" and "Body piercing in adolescents and young adults")

Indications for parenteral therapy — Most patients have uncomplicated infection that can be treated with oral antibiotics. However, some individuals warrant initial therapy with parenteral antibiotics.

We suggest initial parenteral therapy for individuals with the following clinical features:

●Systemic symptoms (eg, fever >100.5°F/38°C, hypotension, or sustained tachycardia)

●Rapid progression of erythema (eg, doubling the affected area within 24 hours; in particular, expansion over a few hours with severe pain should prompt consideration of a necrotizing infection) (see "Necrotizing soft tissue infections", section on 'Typical findings')

●Extensive erythema or edema (eg, involving >50 percent of the breast)

●Immunocompromised state

●Inability to absorb oral antibiotics

Initial parenteral regimens — When parenteral therapy is indicated, it should be started promptly. If possible, blood cultures should be obtained prior to initiation of parenteral antibiotics. Regimen selection is based on the likely microbiology and depends on the immune status of the patient.

●Immunocompetent patients without sepsis and without MRSA risk factors — Most patients do not need empiric MRSA coverage, and antibiotics directed against streptococci and methicillin-sensitive S. aureus are effective. We suggest one of the following regimens:

•Cefazolin 1 to 2 g intravenously every 8 hours

•Nafcillin 1 to 2 g intravenously every 4 hours

•Oxacillin 1 to 2 g intravenously every 4 hours

•Flucloxacillin 2 g intravenously every 6 hours (not available in the United States)

Although many patients have reported beta-lactam allergies, most do not have allergies that would prohibit the use of beta-lactams. In particular, many with penicillin allergies can still take a cephalosporin with or without a test dose. Evaluation of antibiotic allergies is particularly important for patients with breast cellulitis because they are at risk of subsequent infections (of the breast and elsewhere). Discussion of evaluation and management of reported penicillin allergies is presented in detail elsewhere. (See "Choice of antibiotics in penicillin-allergic hospitalized patients" and "Allergy evaluation for immediate penicillin allergy: Skin test-based diagnostic strategies and cross-reactivity with other beta-lactam antibiotics".)

•For patients with serious beta-lactam allergies that preclude use of the above regimens, intravenous vancomycin (table 1) is an alternative. Clindamycin (600 to 900 mg intravenously every 8 hours) is another alternative, but risk of resistance or C. difficile may limit its utility. Local rates of streptococcal and staphylococcal resistance to clindamycin should be considered before prescribing.

●Immunocompetent patients with sepsis or MRSA risk factors – Coverage of MRSA in addition to streptococci should be included when patients have sepsis or risk factors for MRSA, such as prior MRSA colonization or recent exposure to health care settings (table 2). For such patients, we suggest the following:

•Intravenous vancomycin (see table for dosing (table 1))

●Immunocompromised patients – These patients should receive antimicrobials with broadened activity that includes coverage against aerobic Gram-negative bacilli, including Pseudomonas aeruginosa. Additionally, we suggest empiric coverage with an agent active against MRSA. Example regimens include:

•Intravenous vancomycin 15 to 20 mg/kg every 8 to 12 hours (table 1)

PLUS

•Ceftazidime (2 g every 8 hours) or cefepime (2 g every 8 hours)

Other agents that cover P. aeruginosa are discussed elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Intravenous antibiotics'.)

When close follow-up is available, use of outpatient parenteral antimicrobial therapy (OPAT) may be favored due to its numerous benefits, including avoiding hospitalization. With this approach, patients are often seen initially in the hospital setting and are subsequently discharged on OPAT. Sometimes patients are transitioned directly to OPAT from an emergency department or clinic, although arranging OPAT from an outpatient setting can be logistically challenging. OPAT is discussed in greater detail elsewhere. (See "Outpatient parenteral antimicrobial therapy".)

Once there is evidence of clinical improvement, regardless of whether a patient is being treated in the hospital setting or at home receiving OPAT, parenteral antibiotics should be switched to oral antibiotics with comparable antimicrobial coverage. (See 'Initial oral regimens' below.)

Initial oral regimens — Most patients with breast cellulitis can be managed successfully with oral antibiotics in the outpatient setting. We recommend one of the following agents:

●Dicloxacillin 500 mg orally every 6 hours

●Flucloxacillin 500 to 1000 mg every 6 hours (not available in the United States)

●Cephalexin 500 mg orally every 6 hours

Certain situations warrant an alternative or adjusted oral regimen:

●Patients with breast edema or prior radiation therapy who do not meet criteria for parenteral antibiotics – Because these patients may have diminished local drug penetration, we increase the dose of dicloxacillin or cephalexin to 1000 mg orally every 6 hours for the first 48 hours, after which we reduce the dose to 500 mg orally every 6 hours.

●Patients with beta-lactam allergy – We suggest clindamycin (300 mg to 450 orally every 8 hours).

Because clindamycin is associated with elevated risk of C. difficile infection and antimicrobial resistance, careful evaluation of beta-lactam allergies should occur before choosing clindamycin. Most patients with reported beta-lactam allergies do not have allergies that would prohibit the use of beta-lactams. Evaluation of antibiotic allergies is particularly important for patients with breast cellulitis because they are at risk of subsequent infections (of the breast and elsewhere). Discussion of evaluation and management of reported penicillin allergies is presented in detail elsewhere. (See "Allergy evaluation for immediate penicillin allergy: Skin test-based diagnostic strategies and cross-reactivity with other beta-lactam antibiotics".)

●Patients with a history of MRSA or other MRSA risk factors (table 2) – We suggest trimethoprim-sulfamethoxazole (one double-strength tablet orally twice daily), or the combination of amoxicillin (875 mg orally twice daily) plus doxycycline (100 mg orally twice daily). In general, clindamycin (450 mg orally every 8 hours) is an acceptable alternative, although we avoid using clindamycin due to risk for C. difficile infection and the possibility of streptococcal and staphylococcal resistance.

●Immunocompromised patients – For immunocompromised patients, we include coverage for both MRSA and Pseudomonas by adding ciprofloxacin 500 to 750 mg orally twice daily to one of the oral regimens for immunocompetent patients with MRSA risk factors.

Monitoring response to therapy — Upon clinical presentation, we suggest outlining the area of cellulitis with a marker to help follow the clinical response to treatment (picture 12). Often, patients report improvement in pain before there is a noticeable decrease in erythema and edema. Clinical improvement should occur within 48 to 72 hours of treatment initiation. Absence of clinical response within this timeframe should prompt imaging (eg, ultrasound) to assess for abscess, re-evaluation of antibiotic coverage (including changing oral to parenteral therapy), and treatment of underlying predisposing conditions. Alternative diagnoses, such as necrotizing soft tissue infection or inflammatory breast cancer, should also be considered. (See "Necrotizing soft tissue infections" and "Inflammatory breast cancer: Clinical features and treatment".)

Duration of therapy — The optimal duration of antibiotic therapy is uncertain. In general, antibiotics are continued until clinical signs of infection have resolved which usually takes 5 to 14 days. Longer durations may be warranted for patients with breast cellulitis after breast-conserving surgery or prior radiation therapy.

Recurrence of infection

Management of recurrent infection — In general, the same approach and antibiotic regimens are used for recurrences as for initial episodes. If available, microbiologic data from prior episodes should guide antibiotic management for recurrences. (See 'Antibiotic therapy' above.)

Prevention of recurrent infection — Interventions to prevent recurrent infections include management of underlying predisposing conditions and prophylactic antibiotic therapy.

The presence of edema can limit the response to antibiotic therapy and can be challenging to treat. Although compression therapy is helpful for edematous cellulitis of the extremities, compression of breast edema is usually not feasible. Chronic skin conditions that predispose to cellulitis should be treated, with input from dermatologic specialists if necessary. We advise patients to keep the skin as clean and dry as possible by washing the area in a shower or bath and then patting the area dry with a cotton towel; if necessary, using a hair dryer (on a low or no-heat setting to prevent burn injury) may help with drying. For individuals with recurrence of proven S. aureus cellulitis, attempting decolonization is reasonable. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Prevention and control", section on 'Targeted decolonization'.)

The role of prophylactic antibiotics for prevention of recurrent breast cellulitis is unclear. Management of these patients should be done in concert with infectious disease specialists or others with relevant expertise. Some studies suggest benefit for patients with recurrent cellulitis, but these studies did not include patients with breast cellulitis. Prophylactic antibiotics for cellulitis are discussed in detail elsewhere. (See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Prevention of recurrences'.)

DELAYED CELLULITIS AFTER BREAST CONSERVATION THERAPY

Epidemiology — Following breast conservation treatment for breast cancer (breast conserving surgery and radiation therapy), cellulitis may occur months to years later.

Risk factors include [5,41]:

●Obesity

●Hematoma formation

●Postoperative bruising

●Breast edema

●Large resected volume

●Need for multiple seroma aspiration

●Connective tissue disorders

Pathogenesis — Delayed breast cellulitis may reflect an inflammatory process; bacteria may contribute to its development and to the chances of recurrence [41]. The microbiology of delayed breast cellulitis is the same as that of acute breast cellulitis. (See 'Microbiology' above.)

Clinical manifestations and diagnosis — Delayed breast cellulitis typically occurs within a few months following completion of radiotherapy. In most women, erythema subsides within a year, but breast edema can remain long term.

Clinical manifestations of delayed breast cellulitis are similar to those of acute cellulitis (picture 13). Pain tends to be greatest at the end of the day and least in the morning. (See 'Clinical manifestations' above.)

It can be a challenge to differentiate delayed breast cellulitis from postoperative infection, radiation cellulitis, and recurrent inflammatory carcinoma. (See 'Differential diagnosis' above.)

Treatment — The optimal approach to treatment of delayed breast cellulitis is uncertain. Some have suggested that delayed breast cellulitis may be noninfectious in origin and that anti-inflammatory therapy may be sufficient [41]; however, such patients typically present with systemic manifestations (fever, chills) and often respond to antibiotic therapy with activity against beta-hemolytic streptococci and S. aureus [3]. (See 'Antibiotic therapy' above.)

Improving lymphatic stasis and its consequences by manual lymphatic drainage, massage, and skin care may help improve this condition.

If the erythema and edema persist, a punch or core biopsy should be performed to exclude recurrent breast cancer.

SKIN DISORDERS OF THE BREAST — Some skin disorders of the breast may be associated with cellulitis [42].

Eczema — Eczema is characterized by thickened skin, increased skin markings (lichenification), and excoriated and fibrotic papules. The diagnosis is established based on clinical manifestations. Patients with eczema involving the skin overlying the breast may develop secondary cellulitis (picture 14). (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)

Epidermoid cyst — An epidermoid cyst is a discrete, freely movable nodule. The diagnosis of an epidermoid cyst is based upon clinical appearance and palpation. These cysts are common within the skin of the breast and can become secondarily infected (picture 15). (See "Overview of benign lesions of the skin", section on 'Epidermoid cyst'.)

Hidradenitis suppurativa — Hidradenitis suppurativa is a chronic inflammatory condition of the apocrine sweat glands; it can be associated with infection and abscess formation of the axilla or skin of the lower half of the breast (picture 16) [16,27,43-46]. Lesions frequently contain both aerobic and anaerobic bacteria. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis".)

Intertrigo — Intertrigo refers to inflammation at the site of two closely opposed skin surfaces (intertriginous area), often due to moisture and maceration (picture 17) [47,48]. The diagnosis is based on clinical manifestations. Intertrigo can be a recurrent problem in women with large ptotic breasts that make contact with the chest wall, usually affecting the skin of the lower half of the breast.

Pilonidal sinus — A pilonidal sinus is a cavity in the skin with a narrow opening on the surface that contains hair and skin debris. Pilonidal sinuses affecting the nipple have been described in hairdressers and sheep shearers and occur as a result of small pieces of cut hair that accumulate in clothing and penetrate the skin, causing inflammation and infection [16,44,49-52].

Piercing — Nipple rings can cause subareolar breast abscess and recurrent nipple infections, particularly in smokers (picture 18) [53]. In a study of 68 patients with a primary breast abscess, nipple piercing was a risk factor for a subareolar breast abscess (odds ratio [OR] 20, 95% CI 2.01-204.28) in addition to smoking (OR 11, 95% CI 4.41-29.94). (See "Body piercing in adolescents and young adults", section on 'Localized infection'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Evaluation of breast problems".)

SUMMARY AND RECOMMENDATIONS

●Clinical presentation – Patients with acute breast cellulitis present with a tender, warm, erythematous, and edematous breast. Pain often precedes other symptoms. Clinical presentation can overlap with multiple other breast conditions that should be considered at the time of diagnosis. (See 'Clinical manifestations' above and 'Differential diagnosis' above.)

●Microbiology – Most cases of breast cellulitis are caused by beta-hemolytic streptococci or Staphylococcus aureus, including methicillin-resistant S. aureus (MRSA). (See 'Microbiology' above.)

●Treatment – Patients with acute breast cellulitis are treated with antibiotics, symptomatic relief, and management of underlying conditions (eg, eczema). (See 'Treatment' above.)

•Indications for parenteral therapy – Similar to the general approach to cellulitis, for patients with signs of systemic toxicity, extensive disease, or rapidly progressive erythema, we collect blood cultures then treat with parenteral antibiotics. Otherwise, oral antibiotics are usually sufficient. (See 'Indications for parenteral therapy' above and "Acute cellulitis and erysipelas in adults: Treatment", section on 'Indications for parenteral therapy'.)

•Regimen selection:

-Immunocompetent patients without sepsis and without MRSA risk factors (table 2) – Parenteral options include cefazolin 1 to 2 g intravenously every 8 hours or nafcillin 1 to 2 g intravenously every 4 hours. Oral options include dicloxacillin 500 mg orally every 6 hours or cephalexin 500 mg orally every 6 hours.

-Immunocompetent patients with sepsis or MRSA risk factors (table 2) – Parenteral options include intravenous vancomycin (table 1). Oral options for patients with MRSA risk factors who are not septic include trimethoprim-sulfamethoxazole (one double-strength tablet orally twice daily), the combination of amoxicillin (875 mg orally twice daily) plus doxycycline (100 mg orally twice daily), or clindamycin (450 mg orally every 8 hours).

-Immunocompromised patients – We use broader antimicrobial therapy for these individuals given their elevated risk of atypical pathogens and rapid progression. Parenteral options include the combination of intravenous vancomycin (table 1) plus cefepime 2 g every 8 hours. For oral therapy, we add ciprofloxacin (500 to 750 mg orally twice daily) to the oral regimens for immunocompetent patients with MRSA risk factors.

-Patients with beta-lactam allergy – Many patients with reported beta-lactam allergies do not have allergies that prohibit the use of beta-lactams. In particular, many with penicillin allergies can still take a cephalosporin with or without a test dose. Careful evaluation to confirm the presence of serious beta-lactam allergies should occur before selecting alternative agents. Parenteral options include intravenous vancomycin (table 1) or clindamycin 600 to 900 mg intravenously every 8 hours. Oral options include clindamycin 300 to 450 mg orally every 8 hours. (See "Allergy evaluation for immediate penicillin allergy: Skin test-based diagnostic strategies and cross-reactivity with other beta-lactam antibiotics".)

•Duration of antimicrobial therapy – The duration of therapy is usually 5 to 14 days, depending on response to treatment.

●Monitoring response to therapy – Absence of clinical response to antibiotic therapy within 48 to 72 hours should prompt ultrasound to assess for abscess, re-evaluation of antibiotic choices, treatment of underlying predisposing conditions, and consideration of alternative diagnoses such as necrotizing soft tissue infection or inflammatory breast cancer. (See 'Monitoring response to therapy' above and 'Differential diagnosis' above.)