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".)
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 . 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 [1-5,7-9]:
●Prior breast cellulitis or infection
●Breast surgery within previous 30 days (surgical site infection)
●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 [3,9,10]. Group B beta-hemolytic streptococci have a proclivity to produce soft tissue infections in the setting of venous and/or lymphatic compromise ; 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 .
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 [2,4,5,8,13,14]. 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 . 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 [6,15-20]. 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 . Magnetic resonance imaging (MRI) may demonstrate skin thickening and separation or septation of subcutaneous adipose tissue .
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 [23-25].
●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 . 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) . 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 [28-33]. 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 . 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 . (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 [3,28,36]. 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 [37,38]. 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 . 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 . 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) . (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'.)
Clinical approach — Management of cellulitis includes symptomatic relief and antibiotic therapy. Nonsteroidal anti-inflammatory agents (eg, ibuprofen) along with cold compresses or ice packs reduce local pain and swelling.
Patients with uncomplicated cellulitis may be treated with oral dicloxacillin or cephalexin. For most patients with breast cellulitis (including those with minimal or no edema and absence of systemic symptoms), we give 500 mg orally every 6 hours. For patients with extensive cellulitis, underlying breast edema, and/or prior radiation therapy (which may be associated with diminished drug penetration), we give 1000 mg orally every 6 hours for the first 48 hours, then reduce the dose to 500 mg orally every 6 hours. In the setting of beta-lactam allergy, clindamycin (300 mg to 450 orally every 8 hours) may be administered. Outlining the area of cellulitis with a marker to assess response is a valuable indicator of progress (picture 12).
Patients with rapidly progressing erythema (picture 12) or signs of systemic toxicity warrant collection of blood cultures followed by parenteral treatment with oxacillin (2 g intravenously every 6 hours) or cefazolin (1 to 2 g intravenously every 8 hours). In the setting of beta-lactam allergy, vancomycin (table 1) or clindamycin (600 mg intravenously every 8 hours) may be administered. In the setting of risk for MRSA (table 2), vancomycin (table 1) is warranted. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Treatment of skin and soft tissue infections".)
Once there is evidence of clinical improvement, treatment should be switched to oral therapy (dicloxacillin 500 mg oral every six hours or cephalexin 500 mg orally every six hours). Clindamycin (450 mg orally every eight hours) is an option in patients who are allergic to beta-lactam antibiotics; however, it is associated with increased risk for Clostridioides difficile infection. Patients with known or suspected MRSA infection may transition to oral treatment with clindamycin, trimethoprim-sulfamethoxazole (1 double-strength tab orally twice daily), or linezolid (600 mg orally twice daily) (table 3).
For patients who have received recent chemotherapy and/or are neutropenic, the antibiotic regimen must be broadened to include coverage for aerobic gram-negative bacilli, including Pseudomonas aeruginosa. (See "Treatment of neutropenic fever syndromes in adults with hematologic malignancies and hematopoietic cell transplant recipients (high-risk patients)".)
The optimal duration of oral antibiotic therapy is uncertain; 5 to 14 days is appropriate for most patients, but the duration must be tailored and based on individual clinical circumstances. Longer durations may be warranted in patients with breast cellulitis after breast-conserving surgery and radiotherapy. In general, antibiotics are continued until clinical signs of infection have resolved, including pain, fever, erythema, and edema. Frequently, patients report improvement in pain before there is a noticeable decrease in erythema and swelling.
In the absence of clinical response to antibiotic therapy within 48 to 72 hours, ultrasound should be performed to assess for abscess. Alternative diagnoses such as inflammatory breast cancer should also be considered.
Recurrent cellulitis — Management of recurrent breast cellulitis consists of antibiotic therapy and management of edema with compressive therapy [40,41].
Patients with breast cellulitis are at risk for recurrent infection. Antibiotic management of a recurrent episode should be guided, in part, by microbiologic data obtained during a prior episode, if available. Otherwise, the choice of antibiotic therapy is the same as the approach to treatment of an initial episode of cellulitis (table 3). Chronic dermatologic conditions that predispose to cellulitis should be treated aggressively, and the skin should be kept as clean and dry as possible.
For some patients with multiple recurrent episodes, long-term suppressive antibiotic therapy may be appropriate. Management of these patients should be done in concert with infectious disease specialists or others with extensive expertise in the management of patients with breast cellulitis. Penicillin skin testing may be reasonable in patients with a history of penicillin allergy to determine if a beta-lactam can be used for long-term suppressive therapy. (See "Penicillin skin testing".)
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 [5,42]:
●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 . 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 ; 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 . (See 'Clinical approach' 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 .
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 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) [15,26,44-47]. 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) [48,49]. 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 [15,45,50-53].
Piercing — Nipple rings can cause subareolar breast abscess and recurrent nipple infections, particularly in smokers (picture 18) . 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".)
●Patients with breast cellulitis present with a tender, warm, erythematous, and edematous breast. (See 'Clinical manifestations' above.)
●Beta-hemolytic streptococci are common causes of breast cellulitis. Staphylococcus aureus, including methicillin-resistant S. aureus, can also cause breast cellulitis. (See 'Microbiology' above.)
●Patients with uncomplicated breast cellulitis may be treated with empiric oral antibiotic therapy. Patients with signs of systemic toxicity or rapidly progressing erythema warrant collection of blood cultures followed by treatment with parenteral therapy. The duration of therapy is usually 5 to 14 days, depending on response to treatment. (See 'Clinical approach' above.)
●In the absence of clinical response to antibiotic therapy within 48 to 72 hours, ultrasound should be performed to assess for abscess. In addition, alternative diagnoses such as inflammatory breast cancer should be considered. (See 'Clinical approach' above and 'Differential diagnosis' above.)
●Treatment of recurrent breast cellulitis consists of antibiotic therapy and management of edema with compressive therapy. Antibiotic selection should be guided by microbiologic data (if available); otherwise, the approach is the same as for an initial episode of cellulitis. (See 'Recurrent cellulitis' above.)
●Some skin disorders of the breast may be associated with cellulitis. (See 'Skin disorders of the breast' above.)