Acute Mastitis

Etiology

Lactational Mastitis

Lactational mastitis, a common complication during breastfeeding, is often triggered by milk stasis, which occurs when milk is not effectively removed from the breast. This condition can result from factors such as nipple injury, latch difficulties, oversupply, skipped feedings, or the use of nipple shields. It manifests with inflammation, tenderness, redness, and systemic symptoms like fever and chills.[1][10]

The underlying causes of lactational mastitis are multifactorial. One potential contributor is the disruption of the breast microbiome, known as mammary dysbiosis, which may involve an imbalance of bacteria rather than a straightforward infection.[1][2] Pathogenic bacteria (eg, Staphylococcus and Streptococcus) are more frequently isolated from women with mastitis, but these bacteria are also present in healthy milk microbiomes, making their role complex.[2] Nipple trauma can facilitate bacterial entry, but studies show that many women with mastitis do not have visible nipple damage.[10] This evidence suggests that mastitis is not solely caused by retrograde bacterial spread through nipple cracks. Instead, a disrupted milk microbiome, influenced by factors like antibiotics, probiotics, hyperlactation, ductal narrowing, and the mechanical stress of breastfeeding, contributes to this inflammatory condition.[1]

Periductal Mastitis and Idiopathic Granulomatous Mastitis

PDM and IGM involve complex interactions of ductal obstruction, infection, and immune responses; the exact underlying etiologies of both conditions are unclear. While bacterial involvement is well-documented in PDM, IGM often remains sterile, highlighting differing underlying mechanisms despite overlapping features. Both disorders share complex origins and risk factors, although their precise mechanisms and causative factors remain incompletely understood. Further research is needed to define these conditions better and improve treatment strategies. 

Periductal mastitis

PDM, also known as plasma cell mastitis or periareolar mastitis, is characterized as a chronic inflammatory process primarily within the periareolar area that often involves nonlactational, subareolar abscesses.[8] Smoking is a significant risk factor for PDM due to its harmful effects on epithelial cells and ductal tissue, which promote bacterial colonization and anaerobic growth.[5] Conditions like obesity, nipple inversion, and hormonal disturbances, including hyperprolactinemia, have also been cited in studies as contributing to duct dysfunction and inflammation. However, these associations are primarily based on small case studies, lacking robust evidence.[11][5]

Bacterial involvement in PDM remains controversial. Although some studies identify common pathogens like Staphylococcus aureus and anaerobic organisms, others have reported sterile lesions, suggesting that immune responses following bacterial infiltration may play a more prominent role than the infection itself. Immune dysregulation, particularly mediated by T helper cells (Th1 and Th17), likely amplifies the inflammation in PDM.[5]

Reproductive factors, including late menarche and increased age at first childbirth, may also influence PDM risk. In terms of pathophysiology, chronic ductal obstruction and rupture promote secondary bacterial invasion, inflammation, and abscess formation. This results in persistent subareolar masses and fistulae, significantly impacting patient quality of life.[5][12]

Idiopathic granulomatous mastitis

IGM, or granulomatous lobular mastitis, is an uncommon and poorly understood inflammatory breast condition characterized by noncaseating granulomas within breast lobules. Granulomatous mastitis generally may be classified as specific or nonspecific. Specific granulomatous mastitis is associated with identifiable causes like infections or systemic autoimmune diseases. In some studies, nonspecific granulomatous mastitis is subcategorized into IGM, where no clear etiology is determined, and cystic neutrophilic granulomatous mastitis, which is associated with Corynebacterium infection. However, many experts use granulomatous lobular mastitis, idiopathic granulomatous lobular mastitis, and cystic neutrophilic granulomatous mastitis interchangeably with the term IGM.[5][4]

Several factors have been implicated in the development of IGM, 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. Among these, pregnancy and lactation have been consistently linked to IGM, likely due to residual milk stasis that damages lobules and induces hypersensitivity or immune reactions.[5][4]

Corynebacterium species, particularly C. kroppenstedtii, are increasingly recognized as possible pathogens in IGM, although their precise role is debated, as they are part of the normal skin flora. However, these bacteria may incite an inflammatory response when infiltrating deeper breast tissues, as demonstrated in livestock studies.[4] Because Corynebacterium is sometimes considered a normal colonizer in laboratory testing and is resistant to conventional culture methods, definitive identification as an infectious agent is difficult. Recently, though, advanced genomic techniques have detected Corynebacterium in a significant proportion of IGM cases, suggesting a possible infectious trigger for some patients.[5][4]

Other proposed mechanisms include autoimmune pathways, though direct evidence is limited. Autoimmune disorders (eg, erythema nodosum or arthritis) sometimes coexist with IGM, supporting an immune-mediated component. Additionally, alpha-1 antitrypsin deficiency has been linked to isolated cases, as it can promote lobular inflammation resembling IGM histology.[5][4]

Epidemiology

Lactational Mastitis

Lactational mastitis is a common complication of breastfeeding and can significantly influence the decision to discontinue nursing, with 1 in 4 women indicating mastitis as the deciding factor.[13] Despite this, epidemiological studies regarding lactational mastitis incidence and risk factors are lacking.[2] Reported rates of mastitis vary widely depending on definitions and study parameters, with estimates ranging from 1% to as high as 33% globally.[13] Older studies have reported an incidence of approximately 7% and 10% in the United States.[14][15]

In some studies, the incidence of lactational mastitis peaks during the early postpartum period, particularly within the first 25 weeks after delivery, and declines thereafter.[9] Longitudinal studies tracking women from 3 to 12 months postpartum have found mastitis incidence rates between 23.7% and 27.1%. Recurrence is also relatively common, affecting 6.5% to 8.5% of women who have previously experienced the condition. About 3% to 11% of women with acute mastitis progress to develop a breast abscess.[1][13]

Periductal Mastitis

PDM is most often found in reproductive-aged and perimenopausal females and is almost exclusively associated with tobacco use.[9][5] Rare cases have been documented 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

IGM is a relatively rare condition; therefore, studies reporting an accurate incidence are sparse. The condition has an estimated prevalence of 2.4 per 100,000 individuals.[4] However, some experts believe the incidence is underestimated due to frequent misdiagnosis. While the condition typically presents unilaterally, bilateral cases have been reported. The average age of onset ranges from 32 to 35 years, although cases have been documented in individuals aged 11 to 83. IGM primarily affects women, but rare cases have been reported in males.[4]

Furthermore, IGM is associated with a history of pregnancy and lactation, as >50% of patients report having been pregnant within 5 years of diagnosis.[4] Breastfeeding duration among affected individuals averaged between 3 and 36 months, with IGM often manifesting 6 months to 5 years after lactation ends. Rare case reports of IGM occurring during pregnancy have also been documented. IGM in nulliparous women due to pituitary tumors or medications has been observed.[4]

IGM occurs across all racial groups but appears to have a higher prevalence in individuals of Asian, Hispanic, and Middle Eastern descent. Within the United States, several studies have shown a higher incidence of IGM in Hispanic populations.[17][18][19][20] However, no single ethnicity has been definitively identified as being at significantly greater risk.[4]

Pathophysiology

Lactational Mastitis

Lactational mastitis is a multifaceted inflammatory condition of the mammary gland, frequently observed during breastfeeding, that can lead to early cessation of lactation if not effectively managed. Mastitis arises primarily due to ductal narrowing and alveolar congestion, often linked to milk stasis and hyperlactation. These conditions create an environment conducive to inflammatory responses, which may escalate to bacterial mastitis if microbial invasion occurs. This progression can result in complications such as abscess formation, particularly in the presence of tissue trauma from factors like vigorous breast massage or nipple fissures.[9][1]

The development of mastitis involves both host and microbial factors. Milk stasis is widely regarded as a trigger, though not definitively proven as a causal factor. The lactating breast’s dynamic nature, shaped by hormonal stimuli, further contributes to susceptibility. Hyperemia and stromal edema associated with hyperlactation can exacerbate ductal obstruction, fostering conditions for bacterial growth.[9][1]

Periductal Mastitis and Idiopathic Granulomatous Mastitis

PDM and IGM are rare inflammatory breast conditions with an uncertain cause, though several mechanisms have been proposed to explain their pathogenesis.[4][8] PDM is frequently linked to ductal obstruction caused by squamous metaplasia, where keratinized debris blocks lactiferous ducts. This blockage can lead to duct dilation, stasis, and subsequent rupture, resulting in inflammation, infection, and fistula formation.[8][12] 

The pathophysiology of IGM is thought to involve damage to the epithelial lining of the breast ducts, leading to the leakage of ductal contents into adjacent lobular connective tissue. This may trigger a localized inflammatory response characterized by the migration of lymphocytes and macrophages to periductal areas, resulting in the formation of noncaseating granulomas. These granulomas, concentrated in the lobules, consist of immune cells such as Langerhans giant cells, plasma cells, lymphocytes, and epithelioid histiocytes. Inflammation and loss of acinar structure can lead to microabscesses, which may coalesce to form larger abscesses.[4]

Histopathology

A biopsy is not recommended to evaluate lactational mastitis. However, histologic changes that characterize lactational mastitis include persistent ductal narrowing with inflammatory changes in surrounding tissues.[1] Nonlactational mastitis, encompassing PDM and IGM, demonstrates distinct yet overlapping histopathological features. A biopsy is the gold standard for diagnosing nonlactational mastitis, with core needle biopsy showing higher sensitivity (96%) than fine-needle aspiration (21%). Additional testing, such as culture, Gram stain, and special stains for fungi and acid-fast bacilli, is necessary to exclude infectious etiologies.[21][11][4][5]

Periductal Mastitis

PDM is characterized by chronic inflammation localized to the ducts of the breast, often near the areola. Key histological findings include ductal dilatation, infiltration by plasma cells, and occasional abscess formation. In the acute phase, neutrophils dominate, while subacute and chronic phases show increased lymphocytes, plasma cells, foam cells, and multinucleated giant cells. These lesions typically involve proinflammatory cytokines such as IFN-γ and IL-12A. Ductal rupture, wall thickening, and increased secretion are more prevalent in PDM compared to IGM. While granulomas may be present, microabscesses are uncommon. Bacterial infections often involve mixed microbial communities rather than a single pathogen.[21][11][4][5]

Idiopathic Granulomatous Mastitis

GLM is primarily a lobular inflammatory condition defined by noncaseating granulomas that include epithelioid histiocytes, multinucleated giant cells, lymphocytes, plasma cells, and neutrophils. Fat necrosis and sterile microabscesses are common, with granulomas centered on the lobules. Histological findings often reveal an absence of microorganisms, verified by negative Gram, acid-fast, and fungal staining, which helps differentiate granulomatous mastitis 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 more severe cases. Microabscesses and lipid vacuoles are more frequent in IGM than in PDM.[21][11][4][5]

History and Physical

Lactational Mastitis Clinical Features

Lactational mastitis is often preceded by either engorgement or a focally blocked duct. Patients may give a history of these associated symptoms before developing the classic features of mastitis. Lactational mastitis is characterized by a focal, firm, erythematous, swollen, and painful area of 1 breast and systemic symptoms, including fever with a temperature ≥100.4 °F (38 °C), tachycardia, chills, myalgias, and malaise.[1]

Nonlactational Mastitis Clinical Features

Features of PDM include a periareolar or subareolar mass, which may be associated with pain and erythema. Patients may present with nipple inversion, a thick nipple discharge, a breast abscess, or draining fistulas. The clinical features of PDM vary based on the duration of the condition. Acute PDM resembles acute suppurative mastitis as the affected breast is erythematous, swollen, warm, and painful, with abscesses often forming. Systemic symptoms, including fever and malaise, may be pronounced, reflecting a more severe inflammatory response. Subacute PDM typically has systemic symptoms which have subsided, but localized signs persist. A palpable lump may remain, and the overlying skin may appear dark red. Long-standing PDM cases are characterized by deep-seated masses, frequently located in the areolar region, with cycles of flare-ups and remission; in severe cases, chronic sinus tracts and persistent draining wounds may develop.[5]

IGM typically presents as a tender, erythematous, and unilateral soft breast mass that can occur in any breast quadrant except for the region beneath the areola. Common symptoms include nipple discharge, skin changes such as ulcers or sinus formation, and enlargement of the axillary lymph nodes, particularly in chronic cases. Approximately 34% of individuals with IGM experience systemic symptoms beyond the breast, including joint swelling, joint pain, and nodular erythema, often affecting the lower extremities.[5]

A grading system was developed that correlated the severity of IGM with clinical features and breast mass size. Mild IGM is characterized by a breast mass <2 cm with no associated ulcers or fistulas and minimal pain. Moderate IGM involves a breast mass measuring between 2 and 5 cm, with fluid collections that may require aspiration drainage, 1 fistula, and a small amount of discharge. Severe IGM is identified by a breast mass >5 cm, severe pain, the presence of multiple fistulas, and ulcers that discharge >20 mL daily. This system is instrumental in evaluating the extent of the disease and determining appropriate treatment strategies.[5]

Evaluation

Lactational Mastitis Evaluation

Lactational mastitis is primarily diagnosed based on history and clinical findings. Patients with systemic symptoms (eg, fever and tachycardia) lasting longer than 24 hours should be evaluated by a clinician for mastitis. Clinicians should also consider mastitis in those without systemic symptoms unresponsive to supportive measures.[1] Following 48 hours of first-line antibiotic therapy, clinicians should consider further evaluation. A milk culture to evaluate for resistant pathogens (eg, methicillin-resistant Staphylococcus aureus) in patients without symptomatic improvement. A breast ultrasound can be obtained if an abscess is suspected.[1]

In women younger than 30, if a breast abscess is suspected, a breast ultrasound can be obtained. Irregular hypoechoic fluid collections of purulent material will be seen if an abscess is present.[22] When considering imaging in nonpregnant nonlactating individuals, mammography is recommended as the initial imaging modality for women aged 30 years or older who have a new breast symptom.[22] Alternatively, ultrasound-guided needle aspiration can be performed for diagnostic and therapeutic purposes in women with clinical features of a breast abscess.[9] A breast milk culture can guide appropriate antibiotic selection for patients with a severe infection unresponsive to initial antibiotic therapy. However, this is not typically necessary. Similarly, blood cultures should be obtained to assess for suspected bacteremia in a patient with severe mastitis; however, blood cultures are not a part of routine workups.[16][1]

Nonlactational Mastitis Evaluation

The evaluation of nonlactational mastitis involves a combination of imaging studies, pathological examination, and microbiological testing to differentiate between PDM and IGM and exclude differential diagnoses. Laboratory studies, including complete blood counts and C-reactive protein, may provide supportive information in patients with systemic infection or severe disease.[4][9][5]

Breast imaging studies

• Ultrasonography: Ultrasound is commonly used in the initial assessment of mastitis. Lesions in PDM and IGM may appear irregular. Ductal dilatation >3 mm in PDM with internal echoes or mobile secretions is a typical finding. IGM is usually characterized by hypoechoic, irregular masses with features like tubular extensions, edema of the parenchyma, sinus tracts to the skin, ductal dilatation, and axillary lymphadenopathy. Ultrasound helps distinguish benign conditions from malignancies and guides therapeutic interventions (eg, abscess drainage).[4][9][23]

• Mammography: Mammographic findings in acute mastitis, particularly in younger women with dense breast tissue, are often nonspecific. They may include solitary masses, asymmetry, skin thickening, or axillary lymphadenopathy. Chronic mastitis and inflammatory breast cancer may present with similar imaging features, raising the potential for misdiagnosis.[4][9][5]

• Magnetic resonance imaging (MRI): MRI is more sensitive than mammography or ultrasound for detecting and characterizing lesions in nonlactational mastitis. It reveals distinct features such as heterogeneous or rim enhancement in inflammatory lesions, distinguishing them from malignancies. MRI can detect abscesses as thick-walled ring-enhancing masses and helps assess disease severity and response to treatment. However, distinguishing IGM from breast cancer may still require a biopsy.[5][4][9]

Pathological evaluation

A biopsy is the diagnostic gold standard for nonlactational mastitis. Given the clinical features of IGM overlap with those of breast cancer, a breast biopsy must be performed to make this 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 microbiological results help confirm IGM as a noninfectious condition. Classification systems provide clinical guidance based on histological features.[21][11][4][5][9] (Please refer to the Histopathology section for more information on biopsy findings.)

Microbiological studies

Fluid aspiration from abscesses or tissue samples is cultured to identify bacterial, fungal, or mycobacterial pathogens. Additional testing, including Gram stain and special stains for fungi and acid-fast bacilli, is also necessary to exclude infectious etiologies.[21][11][4][5] PDM often involves polymicrobial infections, with organisms such as Pseudomonas, Staphylococcus aureus, and Corynebacterium. In IGM, Corynebacterium is a significant pathogen, identifiable through advanced methods like 16S rRNA gene sequencing.[4][9][5] Additionally, studies suggest that proinflammatory cytokines, including IL-6, IL-12A, and IL-22/23, may serve as biomarkers for assessing disease severity in IGM. Elevated levels of these cytokines, along with the neutrophil-to-lymphocyte ratio, have been associated with poor outcomes.[4][9][5]

Treatment / Management

Lactational Mastitis Management Approaches

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

Supportive measures

Many cases of lactational mastitis resolve without antibiotics. Supportive care includes rest, hydration, continued on-demand breastfeeding, avoidance of nipple shields, supportive bra use, and lymphatic drainage massage. Additionally, patients should use breast pumps only when necessary, ensure a proper fit, and avoid nipple trauma by using moderate suction levels. The use of NSAIDs and ice packs can improve pain and swelling. Therapeutic ultrasound has been reported to alleviate inflammation and edema when supervised by a trained professional. While evidence is evolving, some studies have shown probiotics may support microbiome balance without altering milk composition.[1]

Antibiotic treatment

Antibiotics are indicated to treat bacterial infections confirmed by persistent symptoms that are not improving with supportive care or cultures. Prophylactic use of antibiotics is not recommended, as this can disrupt the breast microbiome and promote resistance.[1] The following regimens are recommended:

• First-line treatments: Dicloxacillin, flucloxacillin, or cephalexin for 10 to 14 days, targeting gram-positive organisms.[1]
• Second-line treatments: Clindamycin 300 mg 4 times daily for 10 to 14 days or trimethoprim-sulfamethoxazole double-strength twice daily for 10 to 14 days are alternatives, particularly for resistant infections if not contraindicated (eg, patients with G6PD deficiency).[1]
• Hospitalization: Reserved for severe cases necessitating intravenous antibiotics, with rooming-in encouraged to maintain breastfeeding.[1] If a patient requires hospitalization, empiric treatment with vancomycin should be initiated until culture and sensitivity results return. Studies on the appropriate duration of outpatient antibiotic treatment are lacking, but most sources recommend a 10- to 14-day course.[9]

Following 48 hours of first-line antibiotic therapy, clinicians should consider further evaluation.[1]

Periductal Mastitis Management Approaches

Although rare, PDM is a painful condition often resistant to conservative treatments. Surgery is the most common intervention, with various techniques tailored to optimize outcomes, minimize recurrence, and ensure cosmetic acceptability. In addition to surgical treatments, acute PDM should be treated with broad-spectrum antibiotics to control inflammation; however, antibiotic therapy alone was shown in a study to have poor outcomes.[21][8] PDM treatment should be individualized, considering the disease's severity, patient preferences, and the surgeon's expertise. Breast duct irrigation and minor excision techniques are preferred for less severe cases, while extensive excision or plastic surgery is more suitable for advanced or recurrent PDM. However, determining the best of the following approaches is challenging due to inconsistent data across studies.[8][5] (A1)

• Minimally invasive procedures: These methods, including incision and drainage, simple incision, and breast duct irrigation, have shown mixed results. Incision and drainage, with a pooled treatment failure rate of 75.6%, is considered unsuitable due to risks like mammary fistulas and disease progression. In contrast, breast duct irrigation demonstrated promise as a first-line treatment with a low treatment failure rate (19.4%) and faster healing time compared to other minimally invasive options.[8][5]
(A1)

• Targeted excision: Focal excision, targeting only the affected ducts, preserves healthy tissue and achieves low recurrence rates. Wound packing after excision showed a notably low treatment failure rate of 2.1%, possibly due to reduced bacterial proliferation. Adding antibiotic coverage to primary closure further reduced recurrence rates. However, these methods require extended healing periods and careful postoperative care.[8]
(A1)

• Complete excision: This procedure removes all affected ducts and offers the most definitive treatment for refractory PDM. Techniques that excise the entire affected area yielded low treatment failure rates. However, these procedures are invasive and best reserved for advanced or complex cases.[8]
(A1)

• Reconstructive methods: For extensive disease, reconstructive procedures such as dermo-glandular flap transfers provide both therapeutic and cosmetic benefits. These techniques achieved treatment failure rates of 0% to 5.2% and are ideal for patients requiring significant tissue removal while prioritizing aesthetic appearance.[8]
(A1)

Treatment outcomes are influenced by factors including smoking, the presence of fistulas, and disease stage. Postoperative care, including wound management and infection control, reduces recurrence. Broad-spectrum antibiotics and proper surgical timing (avoiding acute inflammation stages) are also essential.[8][5](A1)

Idiopathic Granulomatous Mastitis Management Approaches

The management of IGM involves various approaches, including observation, antibiotics, corticosteroids, immunosuppressants, and surgery. Corticosteroid therapy is commonly employed, often in conjunction 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](B2)

Observation

Expectant management is an option for mild cases with smaller lesions (<1–2 cm), as IGM can resolve spontaneously within 6 to 12 months. NSAIDs may be used for symptom relief during this period. Up to half of untreated cases may achieve remission within approximately 14.5 months.[7][5][4](B2)

Pharmacologic therapy

While the role of antibiotics in IGM remains debated, they are sometimes used, particularly when bacterial infections like Corynebacterium are suspected. Extended courses of certain antibiotics, eg, doxycycline or clarithromycin, have shown promise even in cases without confirmed infections, although the underlying mechanism is unclear. Short-term antibiotic treatments (5 to 7 days) are generally ineffective, emphasizing the need for precise diagnostic criteria.[7][5][4](B2)

Corticosteroids are frequently used, with oral forms achieving a remission rate of about 72%. High-dose regimens tend to yield better outcomes than low doses. Localized steroid injections offer comparable effectiveness while minimizing systemic side effects. However, recurrence rates following steroid therapy range from 17% to 50%, and long-term use may lead to adverse effects like weight gain and glucose intolerance.[7][5][4](B2)

Surgical treatment

Surgical intervention is often employed for persistent or severe cases, either alone or following medical therapy to reduce lesion size. Techniques include wide excision, which is more effective than limited resections in preventing recurrence, though outcomes may include significant cosmetic defects. Recent advancements, such as stage I breast reconstruction with implants, have improved postsurgical aesthetic results.[7][5][4] Sequential use of corticosteroids and surgery is an effective strategy, significantly reducing recurrence rates to 2% to 4%. Steroids can also be used preoperatively to enhance surgical outcomes or postoperatively to prevent recurrence.[7][5][4] (B2)

Alternative treatments

For cases unresponsive to corticosteroids, methotrexate has shown efficacy, with remission rates as high as 93%. Its use requires careful monitoring for side effects like myelosuppression. Hormonal imbalances, such as hyperprolactinemia, should be managed with specific agents like bromocriptine.[7][5][4](B2)

Differential Diagnosis

The differential diagnoses associated with the primary forms of mastitis include: 

• Lactational mastitis
  • Breast engorgement
  • Clogged duct
  • Breast abscess
  • Breast cyst
  • Galactocele
  • Phlegmon
  • Inflammatory breast carcinoma
  • Fat necrosis
  • Lactating adenoma [1]
• Periductal mastitis
  • Duct ectasia
  • Breast abscess
  • Breast carcinoma
• Idiopathic granulomatous mastitis 
  • Breast carcinoma
  • Autoimmune disease (eg, Wegener granulomatosis and Takayasu arteritis)
  • Tuberculosis mastitis
  • Sarcoidosis
  • Breast abscess
  • Fat necrosis
  • Leprosy
  • Cat scratch disease
  • Fungal infections (eg, Histoplasmosis and Cryptococcosis) [4][23]

Prognosis

Most patients with lactational mastitis will recover with appropriate treatment. According to some studies, lactational mastitis recurrence occurs in between 6.5% and 8.5% of patients.[13] However, repeated episodes of lactational mastitis in the same breast area should prompt the evaluation of differential diagnoses.[1]

The prognosis for PDM and IGM varies based on the treatment approach, with both conditions showing a risk of recurrence. Surgery is the primary treatment for PDM, yet recurrence remains a significant challenge, with rates reported as high as 50%. Smoking further exacerbates this risk.[5] Without breast duct resection, recurrence rates can reach 79%, but resection reduces this risk by 28%.

IGM has a tendency for spontaneous remission in about half of cases, typically within 14.5 months. However, surgical resection outcomes depend on the extent of the procedure. Treatment with corticosteroids, commonly used for IGM, has a variable recurrence rate (17% to 50%) upon discontinuation. Combining corticosteroids with surgery significantly lowers recurrence rates to 2% to 4%, offering better long-term control and improved aesthetic results.[5] Importantly, IGM has not been linked to an increased risk of future breast cancer.[4]

Complications

One of the most common breastfeeding complications is lactational mastitis, which can result in early termination of breastfeeding. Breast infection and associated pain are the most commonly cited reasons for early cessation.[24][25] A breast abscess is a complication of lactational mastitis and occurs in 3% to 11% of patients.[26][24] The development of a breast abscess is more common if mastitis is not treated early in its course.

Periductal mastitis and IGM can be complicated by an abscess or fistula formation. Both forms of nonlactational mastitis are associated with recurrence and can lead to scarring and deformity of the breast tissue. Prolonged steroid use, sometimes used to treat IGM, is associated with adverse effects like obesity and glucose intolerance.[5]