Differential Diagnosis for Mastitis: A Comprehensive Guide for Clinicians

Introduction

Acute mastitis, an inflammatory condition of the breast, is frequently encountered in clinical practice, particularly among breastfeeding women. While lactational mastitis is the most prevalent form, nonlactational mastitis, including periductal mastitis (PDM) and idiopathic granulomatous mastitis (IGM), also occurs and presents unique diagnostic challenges. Lactational mastitis typically arises from milk stasis and bacterial invasion through compromised skin, often manifesting within the initial postpartum weeks. Its symptoms are characterized by localized erythema, pain, swelling, and sometimes systemic symptoms such as fever. Management strategies range from self-care interventions to antibiotic therapy in more severe cases.[¹][²][³]

Nonlactational mastitis encompasses conditions like PDM and IGM, both recognized as chronic inflammatory breast diseases. PDM primarily affects the ducts near the nipple and is commonly observed in younger women, while IGM, a rare inflammatory condition that can mimic malignancy, is distinguished by granuloma formation predominantly within the lobular tissue, particularly in women within five years of childbirth.[⁴] Diagnosing nonlactational mastitis can be complex due to overlapping symptoms among different types of mastitis and other breast pathologies. Accurate differential diagnosis is crucial because treatment strategies vary significantly, and misdiagnosis can lead to complications.[⁵][⁶][⁷]

Evaluation of acute mastitis often involves breast imaging, histopathological examination, and bacterial culture to discern the underlying cause and guide appropriate treatment. Management is tailored to the specific etiology; PDM typically necessitates surgical excision of affected tissue, whereas IGM management may include observation, antibiotics, steroid therapy, immunosuppressants, or surgery in refractory cases.[⁵][⁸][⁴] Lactational mastitis is generally managed with supportive care and antibiotics.[¹][⁵] A critical complication of both lactational and nonlactational mastitis is breast abscess formation, which requires prompt medical intervention, potentially including antibiotic therapy or drainage procedures, to prevent further complications.[¹][⁹] For detailed information on breast abscess diagnosis and management, clinicians can refer to StatPearls’ resource, “Breast Abscess.”

Etiology of Mastitis

Understanding the etiology of mastitis is paramount for accurate differential diagnosis. Mastitis is broadly categorized into lactational and nonlactational forms, each with distinct underlying causes.

Lactational Mastitis

Lactational mastitis, a frequent concern for breastfeeding mothers, is often initiated by milk stasis, which occurs when breast milk is not efficiently removed from the breast. Factors contributing to milk stasis include nipple trauma, latch difficulties, milk oversupply, missed feedings, and the use of nipple shields. Clinically, it presents with inflammation, tenderness, redness, and systemic symptoms such as fever and chills.[¹][¹⁰]

The precise causes of lactational mastitis are multifaceted. Disruption of the mammary microbiome, termed mammary dysbiosis, is considered a significant factor, suggesting an imbalance of bacteria within the breast rather than a straightforward infection.[¹][²] While pathogenic bacteria like Staphylococcus and Streptococcus are commonly identified in mastitis cases, they are also present in the milk of healthy women, indicating a complex role in disease development.[²] Nipple damage can facilitate bacterial entry, but many women with mastitis do not exhibit visible nipple trauma.[¹⁰] This suggests that mastitis is not solely caused by bacteria entering through nipple cracks. Instead, a disrupted milk microbiome, influenced by factors like antibiotic use, probiotics, hyperlactation, ductal narrowing, and the mechanical stress of breastfeeding, is thought to contribute to this inflammatory condition.[¹]

Periductal Mastitis and Idiopathic Granulomatous Mastitis

PDM and IGM are characterized by complex interactions between ductal obstruction, infection, and immune responses. The exact etiologies of both remain unclear. Bacterial involvement is well-established in PDM, whereas IGM is often sterile, indicating different underlying mechanisms despite clinical similarities. Both conditions share complex origins and risk factors, but their precise mechanisms and causative factors are not fully understood, necessitating further research to improve diagnostic and therapeutic strategies.

Periductal Mastitis

Periductal mastitis (PDM), also known as plasma cell mastitis or periareolar mastitis, is a chronic inflammatory condition predominantly affecting the periareolar region, often involving nonlactational, subareolar abscesses.[⁸] Smoking is a major risk factor for PDM due to its detrimental effects on epithelial cells and ductal tissue, promoting bacterial colonization and anaerobic bacterial growth.[⁵] Other factors, including obesity, nipple inversion, and hormonal imbalances like hyperprolactinemia, have been implicated in duct dysfunction and inflammation, although evidence is primarily from small case studies.[¹¹][⁵]

The role of bacteria in PDM is debated. While some studies identify pathogens such as Staphylococcus aureus and anaerobic organisms, others report sterile lesions, suggesting that immune responses following bacterial infiltration may be more significant than the infection itself. Immune dysregulation, particularly involving T helper cells (Th1 and Th17), likely exacerbates inflammation in PDM.[⁵] Reproductive factors, such as late menarche and increased age at first childbirth, may also influence PDM risk. Pathophysiologically, chronic ductal obstruction and rupture lead to secondary bacterial invasion, inflammation, and abscess formation, resulting in persistent subareolar masses and fistulae that significantly impact patient quality of life.[⁵][¹²]

Idiopathic Granulomatous Mastitis

Idiopathic granulomatous mastitis (IGM), or granulomatous lobular mastitis, is a rare and poorly understood inflammatory breast condition characterized by noncaseating granulomas within breast lobules. Granulomatous mastitis can be classified as specific or nonspecific. Specific granulomatous mastitis has identifiable causes, such as infections or systemic autoimmune diseases. Nonspecific granulomatous mastitis is further categorized into IGM, where no clear cause is found, and cystic neutrophilic granulomatous mastitis, associated with Corynebacterium infection. However, many experts use the terms granulomatous lobular mastitis, idiopathic granulomatous lobular mastitis, and cystic neutrophilic granulomatous mastitis synonymously with IGM.[⁵][⁴]

Several factors have been linked to IGM development, including pregnancy, lactation, hyperprolactinemia, trauma, diabetes, and hormonal contraceptive use. These factors may increase breast secretions or disrupt the immune microenvironment, contributing to local inflammation. Pregnancy and lactation are consistently associated with IGM, likely due to residual milk stasis causing lobule damage and inducing hypersensitivity or immune reactions.[⁵][⁴]

Corynebacterium species, particularly C. kroppenstedtii, are increasingly recognized as potential pathogens in IGM, although their exact role is still under investigation, as they are part of normal skin flora. These bacteria may trigger inflammation when they penetrate deeper breast tissues, as seen in animal studies.[⁴] Corynebacterium is sometimes considered a contaminant in laboratory settings and is difficult to culture using standard methods, making definitive identification as an infectious agent challenging. However, advanced genomic techniques have recently detected Corynebacterium in a significant proportion of IGM cases, suggesting a possible infectious trigger in some patients.[⁵][⁴]

Other proposed mechanisms for IGM include autoimmune pathways, although direct evidence is limited. The coexistence of autoimmune disorders (e.g., erythema nodosum, arthritis) with IGM suggests an immune-mediated component. Additionally, alpha-1 antitrypsin deficiency has been linked to isolated cases, as it can promote lobular inflammation histologically similar to IGM.[⁵][⁴]

Epidemiology of Mastitis

Understanding the epidemiology of mastitis is crucial for assessing risk and implementing preventive strategies, which indirectly aids in differential diagnosis by considering prevalence in different populations.

Lactational Mastitis Epidemiology

Lactational mastitis is a common breastfeeding complication that can significantly influence a mother’s decision to stop nursing; approximately 25% of women cite mastitis as a reason for ceasing breastfeeding.[¹³] Despite its prevalence, robust epidemiological studies on lactational mastitis incidence and risk factors are limited.[²] Reported incidence rates vary widely, from 1% to 33% globally, depending on definitions and study parameters.[¹³] Older studies in the United States reported incidence rates of about 7% to 10%.[¹⁴][¹⁵]

Incidence of lactational mastitis often peaks early postpartum, within the first 25 weeks after delivery, and then declines.[⁹] Longitudinal studies following women from 3 to 12 months postpartum have reported mastitis incidence rates between 23.7% and 27.1%. Recurrence is also common, affecting 6.5% to 8.5% of women with a history of mastitis. About 3% to 11% of women with acute mastitis develop a breast abscess.[¹][¹³]

Periductal Mastitis Epidemiology

PDM predominantly affects women of reproductive age and those in perimenopause and is strongly linked to tobacco use.[⁹][⁵] Rare cases have been reported in children and males.[⁵] The incidence of periductal mastitis varies, with studies reporting ranges of 5% to 9% and 5% to 25% of all symptomatic breast disease in nonlactating women.[¹⁶][⁵]

Idiopathic Granulomatous Mastitis Epidemiology

IGM is relatively rare, and accurate incidence data are scarce. The estimated prevalence is 2.4 per 100,000 individuals.[⁴] Some experts believe the incidence is underestimated due to frequent misdiagnosis. While typically unilateral, bilateral cases have been reported. The average age of onset is 32 to 35 years, with cases ranging from 11 to 83 years old. IGM primarily affects women, with rare male cases reported.[⁴]

IGM is associated with a history of pregnancy and lactation, with over 50% of patients reporting pregnancy within 5 years of diagnosis.[⁴] Breastfeeding duration in affected individuals ranges from 3 to 36 months, with IGM often manifesting 6 months to 5 years post-lactation. Rare cases during pregnancy have been documented. IGM in nulliparous women related to pituitary tumors or medications has also been observed.[⁴]

IGM occurs across all racial groups but appears more prevalent in Asian, Hispanic, and Middle Eastern populations. Within the United States, studies indicate a higher incidence in Hispanic women.[¹⁷][¹⁸][¹⁹][²⁰] However, no single ethnicity is definitively at significantly greater risk.[⁴]

Pathophysiology of Mastitis

Understanding the pathophysiology helps in differentiating mastitis from other breast conditions and in guiding management strategies.

Lactational Mastitis Pathophysiology

Lactational mastitis is a complex inflammatory condition of the mammary gland common during breastfeeding, potentially leading to early lactation cessation if not effectively managed. It primarily results from ductal narrowing and alveolar congestion, often due to milk stasis and hyperlactation. These conditions promote inflammatory responses, potentially progressing to bacterial mastitis if microbial invasion occurs. This progression can lead to abscess formation, particularly with tissue trauma from vigorous breast massage or nipple fissures.[⁹][¹]

Mastitis development involves both host and microbial factors. Milk stasis is a widely recognized trigger, although its direct causal role is not definitively proven. The lactating breast’s dynamic state, influenced by hormones, increases susceptibility. Hyperemia and stromal edema from hyperlactation can exacerbate ductal obstruction, creating an environment conducive to bacterial growth.[⁹][¹]

Periductal Mastitis and Idiopathic Granulomatous Mastitis Pathophysiology

PDM and IGM are rare inflammatory breast conditions with unclear causes, though several pathogenic mechanisms have been proposed.[⁴][⁸] PDM is often linked to ductal obstruction from squamous metaplasia, where keratinized debris blocks lactiferous ducts. This blockage can cause duct dilation, stasis, and rupture, leading to inflammation, infection, and fistula formation.[⁸][¹²]

IGM pathophysiology is thought to involve damage to the epithelial lining of breast ducts, causing leakage of ductal contents into adjacent lobular connective tissue. This triggers a localized inflammatory response with lymphocytes and macrophages migrating to periductal areas, forming noncaseating granulomas. These granulomas, concentrated in lobules, contain immune cells like Langerhans giant cells, plasma cells, lymphocytes, and epithelioid histiocytes. Inflammation and loss of acinar structure can lead to microabscesses, which may coalesce into larger abscesses.[⁴]

Histopathology of Mastitis

Histopathology is crucial in differentiating nonlactational mastitis from other conditions, including breast cancer. Biopsy is not typically recommended for lactational mastitis diagnosis.

Histologic changes in lactational mastitis include persistent ductal narrowing with inflammation in surrounding tissues.[¹] Nonlactational mastitis, including PDM and IGM, exhibits distinct but overlapping histopathological features. Biopsy is the gold standard for diagnosing nonlactational mastitis, with core needle biopsy showing higher sensitivity (96%) than fine-needle aspiration (21%). Additional tests, such as culture, Gram stain, and special stains for fungi and acid-fast bacilli, are needed to rule out infectious causes.[²¹][¹¹][⁴][⁵]

Periductal Mastitis Histopathology

PDM is characterized by chronic inflammation localized to breast ducts, often near the areola. Key histological findings include ductal dilatation, plasma cell infiltration, and occasional abscess formation. Acute phases show neutrophil dominance, while subacute and chronic phases show increased lymphocytes, plasma cells, foam cells, and multinucleated giant cells. These lesions involve proinflammatory cytokines like IFN-γ and IL-12A. Ductal rupture, wall thickening, and increased secretion are more common in PDM than IGM. Granulomas may be present, but microabscesses are uncommon. Bacterial infections often involve mixed microbial communities.[²¹][¹¹][⁴][⁵]

Idiopathic Granulomatous Mastitis Histopathology

IGM is primarily a lobular inflammatory condition defined by noncaseating granulomas with epithelioid histiocytes, multinucleated giant cells, lymphocytes, plasma cells, and neutrophils. Fat necrosis and sterile microabscesses are common, with granulomas centered on lobules. Histology often shows an absence of microorganisms, confirmed by negative Gram, acid-fast, and fungal stains, helping differentiate IGM from infection-related granulomas. The condition can also involve loss of acinar structures in affected ducts and lobules, with inflammation potentially extending to adjacent lobules in severe cases. Microabscesses and lipid vacuoles are more frequent in IGM than PDM.[²¹][¹¹][⁴][⁵]

History and Physical Examination in Mastitis

A thorough history and physical examination are essential for initial diagnosis and differential considerations in mastitis.

Lactational Mastitis Clinical Features

Lactational mastitis often follows breast engorgement or a blocked duct. Patients may report these preceding symptoms before developing classic mastitis signs. Lactational mastitis is characterized by a focal, firm, erythematous, swollen, and painful area in one breast, accompanied by systemic symptoms such as fever ≥100.4 °F (38 °C), tachycardia, chills, myalgias, and malaise.[¹]

Nonlactational Mastitis Clinical Features

PDM presents with a periareolar or subareolar mass, often with pain and erythema. Patients may exhibit nipple inversion, thick nipple discharge, breast abscess, or draining fistulas. Clinical features vary with condition duration. Acute PDM resembles acute suppurative mastitis, with an erythematous, swollen, warm, and painful breast and frequent abscess formation. Systemic symptoms like fever and malaise may be pronounced, indicating a severe inflammatory response. Subacute PDM has subsided systemic symptoms but persistent localized signs. A palpable lump may remain, and skin may appear dark red. Chronic PDM involves deep-seated masses, often in the areolar region, with flare-ups and remissions; severe cases may develop chronic sinus tracts and persistent draining wounds.[⁵]

IGM typically presents as a tender, erythematous, unilateral soft breast mass in any quadrant except the areolar region. Common symptoms include nipple discharge, skin changes like ulcers or sinus formation, and axillary lymph node enlargement, especially in chronic cases. Approximately 34% of IGM patients experience systemic symptoms beyond the breast, such as joint swelling, joint pain, and nodular erythema, often in the lower extremities.[⁵]

A grading system correlates IGM severity with clinical features and breast mass size. Mild IGM involves a breast mass ≤5 cm, localized pain, and no fistulas or ulcers. Moderate IGM includes a mass of 5 to 10 cm, moderate pain, and single fistulas or ulcers discharging 10 cm, severe pain, multiple fistulas, and ulcers discharging >20 mL daily. This system is crucial for assessing disease extent and guiding treatment strategies.[⁵]

Evaluation of Mastitis

Evaluation strategies differ for lactational and nonlactational mastitis, reflecting variations in etiology and differential diagnoses.

Lactational Mastitis Evaluation

Lactational mastitis diagnosis is primarily based on clinical history and physical examination. Women with systemic symptoms (e.g., fever, tachycardia) lasting over 24 hours should be evaluated for mastitis. Mastitis should also be considered in those without systemic symptoms who do not respond to supportive measures.[¹] Further evaluation is warranted if symptoms persist after 48 hours of first-line antibiotic therapy. Milk culture can identify resistant pathogens (e.g., methicillin-resistant Staphylococcus aureus) in patients not improving symptomatically. Breast ultrasound is indicated if abscess is suspected.[¹]

In women under 30, breast ultrasound can be used to assess for suspected abscesses, which appear as irregular hypoechoic fluid collections.[²²] For nonpregnant, nonlactating individuals, mammography is recommended as the initial imaging for new breast symptoms in women 30 and older.[²²] Ultrasound-guided needle aspiration can be both diagnostic and therapeutic for suspected breast abscesses.[⁹] Breast milk culture can guide antibiotic selection for severe infections unresponsive to initial antibiotics, though it is not routinely necessary. Blood cultures are not routine but should be considered for suspected bacteremia in severe mastitis cases.[¹⁶][¹]

Nonlactational Mastitis Evaluation

Nonlactational mastitis evaluation involves imaging, pathology, and microbiology to distinguish PDM from IGM and exclude other diagnoses. Laboratory tests, including complete blood count and C-reactive protein, may support diagnosis in systemic infection or severe disease.[⁴][⁹][⁵]

Breast Imaging Studies

In nonlactational mastitis, mammography and ultrasound are initial imaging modalities to evaluate breast masses and inflammatory changes. Mammography can show masses, densities, or architectural distortions, while ultrasound assesses masses, fluid collections, and ductal changes. MRI is used for complex cases or to differentiate mastitis from malignancy, showing inflammatory extent and abscesses. Imaging helps exclude breast cancer and guide biopsies.[²²][²³]

Pathological Evaluation

Biopsy is the diagnostic gold standard for nonlactational mastitis. Given IGM’s clinical similarity to breast cancer, biopsy is essential for diagnosis. PDM typically shows chronic inflammation with ductal dilatation and plasma cell infiltration, while IGM is defined by necrotizing granulomatous inflammation centered on lobules without caseation. Key histological findings in IGM include epithelioid histiocytes, multinucleated giant cells, and neutrophil-dominated microabscesses. Negative microbiology helps confirm IGM as noninfectious. Histological classification systems guide clinical management.[²¹][¹¹][⁴][⁵][⁹] (Refer to the Histopathology section for detailed biopsy findings.)

Microbiological Studies

Fluid aspirates from abscesses or tissue samples are cultured to identify bacterial, fungal, or mycobacterial pathogens. Additional Gram stain and special stains for fungi and acid-fast bacilli are necessary to exclude infectious etiologies.[²¹][¹¹][⁴][⁵] PDM often involves polymicrobial infections, including Pseudomonas, Staphylococcus aureus, and Corynebacterium. In IGM, Corynebacterium is a significant pathogen, identified using advanced methods like 16S rRNA gene sequencing.[⁴][⁹][⁵] Proinflammatory cytokines, such as IL-6, IL-12A, and IL-22/23, may serve as biomarkers for disease severity in IGM. Elevated levels and neutrophil-to-lymphocyte ratio are associated with poorer outcomes.[⁴][⁹][⁵]

Treatment and Management of Mastitis

Management strategies vary significantly depending on the type of mastitis diagnosed.

Lactational Mastitis Management

Effective lactational mastitis management focuses on symptom relief, inflammation reduction, and addressing underlying causes with supportive care.[¹]

Supportive Measures

Many lactational mastitis cases resolve without antibiotics. Supportive care includes rest, hydration, continued on-demand breastfeeding, avoiding nipple shields, supportive bras, and lymphatic drainage massage. Breast pumps should be used only when necessary, with proper fit and moderate suction to avoid nipple trauma. NSAIDs and ice packs can alleviate pain and swelling. Therapeutic ultrasound, under professional supervision, may reduce inflammation and edema. Probiotics may support microbiome balance without altering milk composition, though evidence is still developing.[¹]

Antibiotic Treatment

Antibiotics are indicated for confirmed bacterial infections, persistent symptoms not improving with supportive care, or positive cultures. Prophylactic antibiotics are not recommended due to microbiome disruption and resistance promotion.[¹] Recommended regimens include:

• First-line: Dicloxacillin or cephalexin.
• MRSA suspicion: Clindamycin or trimethoprim-sulfamethoxazole.
• Penicillin allergy: Clindamycin or erythromycin.

Further evaluation is needed if symptoms persist after 48 hours of first-line antibiotics.[¹]

Periductal Mastitis Management

PDM, while rare, is painful and often resistant to conservative treatments. Surgery is the most common intervention, with techniques tailored to optimize outcomes, minimize recurrence, and ensure cosmetic acceptability. Acute PDM should be treated with broad-spectrum antibiotics to control inflammation, although antibiotics alone have shown poor outcomes.[²¹][⁸] PDM treatment is individualized based on disease severity, patient preference, and surgeon expertise. Breast duct irrigation and minor excision are preferred for less severe cases, while extensive excision or plastic surgery is better for advanced or recurrent PDM. Consistent data across studies on the best approach is lacking.[⁸][⁵]

• Targeted excision: Focal excision of affected ducts preserves healthy tissue and achieves low recurrence rates. Wound packing post-excision showed a low treatment failure rate of 2.1%, possibly due to reduced bacterial proliferation. Antibiotics with primary closure further reduced recurrence. These methods require longer healing and careful postoperative care.[⁸]
• Reconstructive methods: For extensive disease, dermo-glandular flap transfers offer therapeutic and cosmetic benefits, with treatment failure rates of 0% to 5.2%. These are ideal for significant tissue removal while prioritizing aesthetics.[⁸]

Treatment outcomes are affected by smoking, fistulas, and disease stage. Postoperative care, wound management, and infection control reduce recurrence. Broad-spectrum antibiotics and proper surgical timing (avoiding acute inflammation) are essential.[⁸][⁵]

Idiopathic Granulomatous Mastitis Management

IGM management includes observation, antibiotics, corticosteroids, immunosuppressants, and surgery. Corticosteroids are commonly used, often with other treatments. While IGM can be self-limiting, its prolonged course and impact on quality of life necessitate individualized treatment plans. An interprofessional approach tailored to disease severity and patient preferences is recommended to balance symptom control with minimal adverse effects.[⁷][⁵][⁴]

Observation

Expectant management is an option for mild cases with smaller lesions (≤5 cm) and minimal symptoms, as spontaneous remission can occur.[⁷][⁵][⁴]

Pharmacologic Therapy

Antibiotics in IGM are debated but sometimes used, especially with suspected Corynebacterium infections. Extended doxycycline or clarithromycin courses have shown promise even without confirmed infections, though the mechanism is unclear. Short-term antibiotics (5-7 days) are generally ineffective, highlighting the need for precise diagnostic criteria.[⁷][⁵][⁴]

Corticosteroids are frequently used, with oral forms achieving about a 72% remission rate. High-dose regimens tend to be more effective than low doses. Local steroid injections offer similar efficacy with fewer systemic side effects. However, recurrence rates post-steroid therapy range from 17% to 50%, and long-term use can cause adverse effects like weight gain and glucose intolerance.[⁷][⁵][⁴]

Surgical Treatment

Surgery is often used for persistent or severe cases, alone or after medical therapy to reduce lesion size. Wide excision is more effective than limited resection in preventing recurrence, but may cause cosmetic defects. Stage I breast reconstruction with implants has improved postsurgical aesthetics. Sequential corticosteroid and surgery use is effective, reducing recurrence to 2% to 4%. Steroids can be used preoperatively to enhance surgical outcomes or postoperatively to prevent recurrence.[⁷][⁵][⁴]

Alternative Treatments

For corticosteroid-unresponsive cases, methotrexate has shown efficacy, with remission rates up to 93%. It requires careful monitoring for side effects like myelosuppression. Hormonal imbalances, such as hyperprolactinemia, should be managed with agents like bromocriptine.[⁷][⁵][⁴]

Differential Diagnosis of Mastitis

The differential diagnosis is crucial for appropriate management and to rule out more serious conditions like breast cancer. The conditions to consider vary depending on the type of mastitis.

Differential Diagnosis for Lactational Mastitis

When evaluating lactational mastitis, clinicians should consider the following differential diagnoses:[¹]

• Breast engorgement: This condition involves bilateral breast swelling and discomfort due to milk accumulation. Unlike mastitis, engorgement typically lacks focal redness, warmth, and systemic symptoms like fever.
• Clogged duct: A clogged milk duct presents as a localized, tender lump, sometimes with mild redness. Fever and systemic symptoms are typically absent.
• Breast abscess: A breast abscess is a localized collection of pus, often a complication of mastitis. It is characterized by a fluctuant, tender mass, significant redness, warmth, and often systemic symptoms. Ultrasound can help differentiate abscess from mastitis.
• Breast cyst: Breast cysts are fluid-filled sacs, often palpable as smooth, mobile masses. They are usually not associated with inflammation or systemic symptoms, though they can become painful.
• Galactocele: A galactocele is a milk-filled cyst that can occur during or after lactation. It presents as a smooth, mobile, and often painless mass.
• Phlegmon: Phlegmon refers to diffuse inflammation of soft tissues, which, in the breast, can mimic mastitis. However, phlegmon may not be as clearly localized and might involve deeper tissues.
• Inflammatory breast carcinoma: This aggressive form of breast cancer can present with redness, swelling, and warmth of the breast, mimicking mastitis. However, inflammatory breast cancer often progresses rapidly and may involve skin changes like peau d’orange. Lack of response to antibiotics and atypical presentation should raise suspicion for malignancy.
• Fat necrosis: Fat necrosis is a benign condition resulting from trauma or surgery, leading to fat tissue damage. It can present as a firm, painless mass and sometimes with skin changes, potentially mimicking mastitis or even breast cancer.
• Lactating adenoma: This benign breast tumor can occur during lactation and present as a palpable mass. It usually lacks the inflammatory signs of mastitis but needs to be differentiated from other breast masses, including malignancy.

Differential Diagnosis for Periductal Mastitis

The differential diagnosis for periductal mastitis includes:[⁵]

• Duct ectasia: Duct ectasia involves dilated milk ducts, which can sometimes cause nipple discharge and periareolar inflammation, mimicking PDM. However, duct ectasia is usually less painful and lacks the acute inflammatory signs of PDM.
• Breast abscess: As with lactational mastitis, breast abscess is a key differential. In the context of PDM, abscesses are typically subareolar.
• Breast carcinoma: Breast cancer must always be considered, especially inflammatory or subareolar types, as PDM can present with masses and skin changes that can be concerning for malignancy. Biopsy is essential to rule out cancer.

Differential Diagnosis for Idiopathic Granulomatous Mastitis

The differential diagnosis for idiopathic granulomatous mastitis is broad due to its varied presentation and histologic features:[⁴][²³]

• Breast carcinoma: IGM can clinically and radiologically mimic breast cancer, particularly inflammatory carcinoma. Biopsy is crucial to differentiate IGM from malignancy.
• Autoimmune diseases (e.g., Wegener granulomatosis and Takayasu arteritis): Systemic granulomatous diseases can manifest in the breast. Evaluating for systemic symptoms and considering serological tests for autoimmune conditions is important if IGM-like histology is found.
• Tuberculosis mastitis: Tuberculosis can affect the breast, causing granulomatous inflammation. Clinical history, chest X-ray, and specific stains for acid-fast bacilli on biopsy specimens are essential to rule out tuberculosis.
• Sarcoidosis: Sarcoidosis, a systemic granulomatous disease, can rarely involve the breast. Evaluation for systemic sarcoidosis and histologic features can help differentiate it from IGM.
• Breast abscess: Abscess formation can complicate IGM and needs to be considered in the differential, although IGM itself is a distinct inflammatory process.
• Fat necrosis: Fat necrosis can sometimes elicit a granulomatous reaction, but the clinical context and more typical histologic features of IGM usually help differentiate them.
• Leprosy: In endemic regions, mammary leprosy should be considered as it can cause granulomatous mastitis.
• Cat scratch disease: This bacterial infection, typically causing lymphadenitis, can rarely present with granulomatous lesions in various organs, potentially including the breast.
• Fungal infections (e.g., Histoplasmosis and Cryptococcosis): Deep fungal infections can cause granulomatous mastitis. Special stains and cultures on biopsy specimens are necessary to exclude fungal etiologies, especially in immunocompromised patients or those from endemic areas.

Prognosis of Mastitis

Prognosis varies depending on the type of mastitis and the appropriateness of treatment.

Most lactational mastitis patients recover with proper treatment. Recurrence occurs in 6.5% to 8.5% of patients.[¹³] Repeated episodes in the same breast area should prompt consideration of differential diagnoses.[¹]

PDM and IGM prognosis varies with treatment. Surgery is primary for PDM, but recurrence is a challenge, with rates up to 50%. Smoking worsens this risk.[⁵] Without duct resection, recurrence reaches 79%, reduced by 28% with resection.

IGM has spontaneous remission in about half of cases within 14.5 months. Surgical outcomes depend on procedure extent. Corticosteroid treatment has a 17% to 50% recurrence rate upon discontinuation. Combining corticosteroids with surgery lowers recurrence to 2% to 4%, improving long-term control and aesthetics.[⁵] IGM is not linked to increased breast cancer risk.[⁴]

Complications of Mastitis

Untreated or poorly managed mastitis can lead to several complications.

Lactational mastitis, a common breastfeeding issue, can lead to early breastfeeding cessation. Breast infection and pain are major reasons for early weaning.[²⁴][²⁵] Breast abscess, a lactational mastitis complication, occurs in 3% to 11% of patients.[²⁶][²⁴] Abscess development is more likely if mastitis is not promptly treated.

PDM and IGM can be complicated by abscess or fistula formation. Both nonlactational mastitis forms are associated with recurrence and can cause breast tissue scarring and deformity. Prolonged steroid use, sometimes for IGM, can cause adverse effects like obesity and glucose intolerance.[⁵]

Deterrence and Patient Education for Mastitis

Prevention and patient education are vital in managing mastitis risk and improving outcomes.

Promoting symptom awareness, smoking cessation, breast hygiene, and regular follow-ups for high-risk individuals are crucial for effective acute mastitis management. Clinicians should encourage early medical assessment for timely evaluation and complication prevention.[⁵][¹]

For lactational mastitis, patients should practice regular and complete breast emptying during breastfeeding, alternate feeding positions for proper drainage, and address nipple damage promptly to prevent infections. Proper hygiene and early symptom recognition (localized pain, redness, swelling) are essential for timely treatment.[¹] PDM prevention focuses on smoking cessation, which significantly reduces recurrence risk, and considering breast duct resection for high-risk patients. Patients should be informed about PDM recurrence and the importance of follow-up.[⁵] For IGM, while the cause is unclear, early detection and appropriate management, including antibiotics for potential Corynebacterium infections, can prevent complications. Patients should be educated on possible spontaneous remission and individualized treatment plans involving steroids, surgery, or antibiotics, considering cosmetic outcomes post-surgery. Risks of long-term steroid use, like weight gain and glucose intolerance, should be discussed.[⁵]

Pearls and Other Important Considerations in Mastitis Management

Key points for clinicians managing acute mastitis include:

• Lactational mastitis can initially be managed conservatively with supportive measures for 24 hours. Antibiotics should be started if symptoms don’t improve.
• If lactational mastitis symptoms don’t improve in 48 hours, consider milk culture and breast ultrasound for abscess assessment.
• IGM is rare and often mistaken for breast carcinoma. Biopsy is essential for diagnosis and to rule out malignancy.
• Most mastitis patients can be managed as outpatients. Hospitalization may be needed for hemodynamic instability, oral intake intolerance, severe dehydration, or failed outpatient management of recurrent infection.

Enhancing Healthcare Team Outcomes in Mastitis Management

Effective acute mastitis management requires a coordinated interprofessional approach focused on patient-centered care, safety, and improved outcomes. Physicians and advanced practitioners diagnose mastitis, identify causes, and develop tailored treatment plans, including surgery or corticosteroids for complex cases. Nurses and lactation consultants educate on breastfeeding techniques, address risk factors, and support breastfeeding continuity. Pharmacists ensure medication safety and efficacy, guiding breastfeeding continuity during treatment.

Interprofessional communication ensures seamless care coordination, especially in emergencies where lactation support may be needed. Teams must address immediate and long-term patient needs, including recurrence prevention and managing treatment side effects. Collaborative surgical care, including preoperative imaging and postoperative support with reconstruction options, optimizes cosmetic outcomes and patient satisfaction. Integrating each professional’s expertise allows for comprehensive, evidence-based care for acute mastitis, enhancing patient safety, recovery, and well-being.

Review Questions

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References

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² Wilson E, Woodd SL, Benova L. Incidence of and Risk Factors for Lactational Mastitis: A Systematic Review. J Hum Lact. 2020 Nov;36(4):673-686. [PMC free article: PMC7672676] [PubMed: 32286139]

³ Costa Morais Oliveira V, Cubas-Vega N, López Del-Tejo P, Baía-da-Silva DC, Araújo Tavares M, Picinin Safe I, Cordeiro-Santos M, Lacerda MVG, Val F. Non-lactational Infectious Mastitis in the Americas: A Systematic Review. Front Med (Lausanne). 2021;8:672513. [PMC free article: PMC8378399] [PubMed: 34422853]

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