Fig. 8.1
Cyst (a) Spot tangential compression mammographic view of a palpable “lump” reported by this 45-year-old patient (the site of which is marked with a metallic BB on the skin) shows an equal density mass (between arrows) with partially circumscribed and obscured margins. (b) Targeted ultrasound demonstrates a cyst, defined as such because it is anechoic with circumscribed margins, has barely perceptible walls, and demonstrates posterior acoustic enhancement (between arrowheads). This is benign and warrants no further intervention if the patient is otherwise asymptomatic
Apocrine metaplasia—The diagnosis is suggested mammographically by groups of calcifications that appear round or amorphous (“smudgy”) on a craniocaudal (top to bottom) view, but curvilinear (concave up) or linear on a lateral (side to side) view (Fig. 8.2). This change in appearance is pathognomonic for milk of calcium and is due to the layering or sedimentation of calcium in suspension in the fluid of micro- or macrocysts. When viewed in the side-to-side projection, the calcifications appear like a meniscus, mimicking a “teacup.” Sonographically, apocrine metaplasia may present as clustered microcysts with thin septa (Fig. 8.2) [2].
Fig. 8.2
Clustered cysts/apocrine metaplasia (a) Clusters of microcysts separated by thin septa (arrows) seen at ultrasound. (b and c) Different patient with milk of calcium seen mammographically; the change in form of calcifications from amorphous on the craniocaudal view to linear or curvilinear in the lateral-medial projection is pathognomonic for this benign process. (d) Cysts lined by apocrine cells, with ample eosinophilic cytoplasm and uniform nuclei. Apocrine metaplasia is often associated with calcium oxalate (not shown), best seen with polarization
Sclerosing adenosis , ductal hyperplasia (without atypia), columnar cell changes—may appear as grouped or diffusely distributed punctate or amorphous calcifications (Fig. 8.3), sometimes with associated masses. Typically, for most morphologies of calcifications, more diffuse and bilateral calcifiations are more likely to reflect benign fibrocystic changes [14]. If isolated, new, or increasing, work-up, follow-up, and/or biopsy may be warranted for confirmation.
Fig. 8.3
Benign amorphous calcifications, spot compression magnification views. (a) Biopsy in this 46-year-old yielded fibrocystic change including sclerosing adenosis, columnar cell change, and pseudoangiomatous stromal hyperplasia. (b) Calcifications were associated with benign breast tissue on histology in this 53-year-old
Duct ectasia —may appear as large (>2–3 mm), rod-like, solid, linear and branching calcifications mammographically (Fig. 8.4); these are intraductal and the result of inspissated secretions (and therefore debunk the mammography myth that all linear/intraluminal calcifications signify DCIS). On ultrasound, one may see dilated, fluid-filled ducts that taper normally.
Fig. 8.4
Duct ectasia, plasma cell mastitis. Large rod-like calcifications are intraductal, the result of inspissated secretions
Fig. 8.5
Stromal fibrosis. (a) Coarse heterogenous and linear calcifications in a 50-year-old woman. (b) A round mass with indistinct margins on baseline screening mammogram and subsequent targeted ultrasound (c) in a 59-year-old. The mass appeared nearly anechoic (cystic), but when aspiration yielded no fluid (not shown), core biopsy of this solid mass was undertaken. (d) The needle core biopsy shows diffuse stromal fibrosis and focal microcalcifications (arrows)
High-Risk Lesions
These entities incur increased future lifetime risk, or have potential to be upstaged to malignancy at excision. Management is controversial. Whether or not these lesions are excised, patients may undergo additional screening and/or (endocrine) chemopreventive measures based on their cumulative lifetime risk of breast cancer. If resected, susbsequent radiation treatment is not indicated for these lesions (unless upstaged to cancer at surgery).
Atypical ductal hyperplasia (ADH)/flat epithelial atypia (FEA)—most commonly diagnosed in the work-up of calcifications (often punctate, amorphous). These entities can coexist in a spectrum of proliferative changes from (usual) hyperplasia to low-grade DCIS; upstage rates to malignancy ranging from 11 to 62% [6, 7, 10, 19]. We recommend excision as definitive treatment. Patients with ADH are considered at intermediate risk (15–20% lifetime risk) for future breast cancer [8].
Lobular neoplasia: atypical lobular hyperplasia (ALH) , lobular carcinoma in situ (LCIS) –these are proliferative processes of the lobules and are most commonly incidental findings on imaging-guided core needle biopsies; in other words, they have no associated radiological appearance or “classic” finding. Despite the name (another unfortunate misnomer), LCIS is considered a risk factor for future malignancy (in either breast) rather than a malignancy (or pre-malignancy) itself [9, 20, 21]. Historically, its management has therefore been one of the most controversial in breast health, ranging from no action to surgical excision. Our practice is mixed, but several of us recommend excision after a core biopsy yielding LCIS.
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