Breast mastitis is acute or chronic infectious or non-infectious inflammation of breast tissue. When progressive, a breast abscess (localized purulent collection) may develop. It is most commonly seen during the lactational period (lactational mastitis — 2-10% of all lactating women); non-lactational mastitis includes periareolar (periductal mastitis / Zuska disease), granulomatous mastitis, and idiopathic forms. Lactational mastitis is typically caused by Staphylococcus aureus and develops in the setting of milk stasis. Non-lactational periductal mastitis is strongly associated with smoking. Skin thickening, diffuse edema, and rim enhancement in abscesses are characteristic on imaging. Differential diagnosis from inflammatory breast cancer is critically important.
Age Range
25-50
Peak Age
35
Gender
Female predominant
Prevalence
Uncommon
Lactational mastitis begins with bacterial invasion in the setting of milk stasis (inadequate breast emptying, nipple fissures). Staphylococcus aureus is the most common causative agent; it enters the ductal system retrograde through nipple fissures. Bacterial invasion triggers neutrophil and macrophage infiltration → acute inflammatory response → tissue edema, hyperemia, and local temperature increase. Increased vascular permeability (histamine, bradykinin, prostaglandins) reflects as dermal and subdermal edema on ultrasonography and produces restricted diffusion on diffusion-weighted MRI (increased cell density and protein content). When inflammation localizes, accumulation of neutrophils and bacteria surrounded by a fibrous capsule forms an abscess. Neovascularization of the abscess capsule causes characteristic rim (ring) enhancement on contrast-enhanced MRI — gadolinium enters the newly formed, permeable vessels in the capsule, increasing T1 signal. Necrotic debris and pus accumulation in the abscess center demonstrate high signal on T2 and markedly restricted diffusion on DWI (restricted water molecule movement due to viscous content). In non-lactational periductal mastitis, ductal ectasia and keratin plugs trigger periductal inflammation; toxic substances in cigarettes directly damage ductal epithelium.
The combination of thick rim-enhancing collection on contrast-enhanced MRI with markedly restricted diffusion in the same collection on DWI is the most reliable diagnostic finding pair for breast abscess. This combination is distinguishing from necrotic malignant tumors (necrotic cavities generally do not show diffusion restriction).
Increased skin thickness (>2 mm), increased echogenicity and reticular pattern in subcutaneous fat due to edema. Breast parenchyma in the mastitis area becomes diffusely hypoechoic or heterogeneous. Thickening of Cooper ligaments may be seen. These findings are the US reflection of the inflammatory process and typically show segmental distribution in lactational mastitis.
Report Sentence
Marked skin thickening and reticular echogenicity increase consistent with edema is seen in the subcutaneous fat; findings are consistent with an acute inflammatory process.
When abscess develops, a thick, irregularly walled, hypoechoic or mixed echogenicity fluid collection is seen. Internal echoes, debris, and septations may be seen within the contents. Reactive inflammatory tissue with accompanying hypervascularity surrounds the collection. May show mild compressibility with pressure. Size and location are determinative in treatment planning (percutaneous drainage vs surgical).
Report Sentence
A thick, irregularly walled, hypoechoic/mixed echogenicity fluid collection containing internal echoes and debris is seen in the breast parenchyma, consistent with breast abscess.
On contrast-enhanced MRI, the abscess appears as a collection with thick and irregular rim (ring) enhancement. Enhancement is prominent at the abscess wall; the center does not enhance (necrotic cavity). Diffuse enhancement (inflammatory hyperemia) in surrounding breast parenchyma may accompany. The thickness and irregularity of rim enhancement reflects the maturity stage of the abscess. In inflammatory breast cancer, diffuse non-mass enhancement is dominant.
Report Sentence
On contrast-enhanced MRI, a collection demonstrating thick, irregular rim enhancement with a non-enhancing hypointense center is seen, consistent with breast abscess.
Abscess contents demonstrate markedly high signal on DWI and low signal on ADC map (restricted diffusion). This finding reflects the restriction of free water molecule movement by viscous purulent material within the abscess cavity. Diffusion restriction is one of the most reliable MRI findings for abscess diagnosis and is distinguishing from necrotic tumor cavities (necrotic cavities generally do not show diffusion restriction).
Report Sentence
The collection contents demonstrate markedly high signal on DWI and low signal on ADC map consistent with restricted diffusion; this finding strongly suggests purulent abscess contents.
Diffuse skin thickening, trabecular thickening, and parenchymal density increase are seen on mammography. When abscess develops, it may appear as a round or oval high-density mass. Overlap with mammographic findings of inflammatory breast cancer is possible. In the acute mastitis clinical context, mammography is generally complementary rather than diagnostic; US is preferred.
Report Sentence
Diffuse skin thickening, trabecular thickening, and parenchymal density increase are seen on mammography; while consistent with an inflammatory process in clinical context, inflammatory breast cancer should be considered in the differential diagnosis.
Marked hypervascularity is seen around the abscess and in the mastitis area on color Doppler examination. Increased blood flow due to inflammatory hyperemia appears as arterial and venous vascular signals in the abscess wall and surrounding tissue. This vascularity pattern is also useful for monitoring treatment response — vascularity decreases with treatment.
Report Sentence
Marked hypervascularity is seen around the collection and in the inflammatory area on color Doppler examination, consistent with an acute inflammatory process.
Criteria
Develops during breastfeeding period (usually first 6 weeks) in the setting of milk stasis. S. aureus is the most common agent. Unilateral, peripheral location is typical.
Distinct Features
Rapid response to antibiotic therapy. Continued breastfeeding recommended (breast emptying). Low recurrence, complete resolution expected with appropriate treatment.
Criteria
Non-lactational, periareolar location. Strong association with smoking. Develops in the setting of subareolar ductal ectasia and keratin plugs. Chronic relapsing course is typical.
Distinct Features
Periareolar fistula may develop. Smoking cessation is an important component of treatment. Antibiotics alone may be insufficient; ductal excision may be needed. High recurrence rate (50%).
Criteria
Rare, lobule-confined non-caseating granulomatous inflammation of unknown etiology. More common in young parous women. Autoimmune mechanism is suspected.
Distinct Features
Strongly mimics malignancy (spiculated mass, skin retraction). Multiple abscesses and fistulae may develop. Steroid therapy is first-line. Spontaneous remission possible but slow course.
Distinguishing Feature
Inflammatory breast cancer shows diffuse non-mass enhancement, skin thickening and dermal lymphatic tumor embolization; does not respond to antibiotic therapy. Mastitis/abscess shows rim enhancement and DWI restricted diffusion; improves with antibiotics. Biopsy is mandatory if no improvement after 2 weeks of antibiotics.
Distinguishing Feature
Fat necrosis shows a fat-density containing lesion (oil cyst), coarse calcification or architectural distortion on mammography. Presence of fat signal on MRI (T1 high, signal loss on fat suppression) distinguishes fat necrosis from abscess. Usually has trauma/surgical history.
Distinguishing Feature
Complex cyst may contain thin septations and debris but wall thickening is minimal, no surrounding tissue inflammatory changes, and no vascularity on Doppler. Abscess is distinguished by thick irregular wall, surrounding edema, and perilesional hypervascularity.
Urgency
urgentManagement
medicalBiopsy
Not NeededFollow-up
3-monthMastitis resolves with antibiotic therapy in early stages; continued breastfeeding is recommended in lactational mastitis. When abscess develops, US-guided percutaneous drainage or surgical drainage is required. If no response to 2 weeks of antibiotic therapy, biopsy is mandatory — inflammatory breast cancer must be excluded. Steroid therapy and long-term follow-up are needed in granulomatous mastitis. Post-treatment 3-month follow-up US is recommended.
Mastitis is treated with antibiotics. If abscess forms, percutaneous drainage or surgical incision-drainage is required. If unresponsive to antibiotics, inflammatory breast cancer must be excluded — biopsy is indicated. Non-puerperal mastitis may be recurrent.