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Additional clinical history: The patient was in a severe car accident approximately 8 months prior, resulting in significant bruising of the right breast.
Does that change your differential diagnosis?
Differential diagnosis:
Actual diagnosis: Probable fat necrosis with developing central oil cyst, given history of significant blunt trauma to right breast.
FINAL ASSESSMENT: BI-RADS Final Assessment Category 3 - PROBABLY BENIGN - Initial short interval followup suggested.
Discussion
Fat necrosis is a benign, nonsuppurative process of the breast that can cause a diagnostic dilemma for the radiologist. It usually results from breast trauma, but other etiologies include post-surgical (biopsy, lumpectomy, or TRAM flap – usually in the upper outer quadrant due to reduced blood supply), ischemia (often post-radiation vasculitis), or chemical irritation (ruptured cyst/ectatic duct or plasma cell mastitis). The presentation is highly variable, but almost always involves a palpable mass or masses (97%). These are usually non-tender, but up to 26% of patients report tenderness. The masses are usually firm and fixed. Up to 14% of women with fat necrosis may demonstrate skin thickening or dimpling, and 9% may have nipple retraction. In the early stages, the only finding may be ecchymosis or erythema.
Accidental injury remains the most common cause, and is usually due to blunt trauma, often from a seatbelt. Penetrating trauma can be a causative agent, as well. Iatrogenic causes include post-biopsy, surgery, radiation, or direct silicone injection. Patients with diabetes and collagen vascular disease may present with spontaneous fat necrosis, and it is important to remember that 35-50% of women with fat necrosis do NOT elicit a history of prior trauma or surgery.
In terms of pathogenesis, inflammation or hemorrhage into breast fat results in adipocyte injury, resulting in leakage of fat into the surrounding tissues. This leaked fat degrades into fatty acids, which induce an inflammatory response, including formation of a reactive fibrous capsule to quarantine the process. Saponification of the fatty acids eventually results in calcium deposition, although this tends to develop 1.5 to 5 years following the initial insult. Calcifications tend to coarsen with time. Non-encapsulated fatty acids result in a granulomatous, foreign body-like reaction, which can lead to fibrosis and skin retraction, often mimicking the desmoplastic reaction of cancer.
Most importantly, fat necrosis of the breast is a BENIGN process, with NO malignant potential. No treatment is usually required, although lesions may be excised if painful.
Radiologic overview of the diagnosis:
Fat necrosis is usually first evaluated with diagnostic mammography, given the typical presentation of a palpable lump. On mammography, a round, oval, or lobulated, usually lucent mass is seen. Associated oil cyst(s), with possible peripheral rim calcification are common, and an indistinct interface of the mass with the adjacent breast tissue is secondary to adjacent edema, fibrosis, and inflammatory infiltrate. There are usually associated calcifications, and corroborating their presence with timing of injury is critical, as calcifications are very unusual in the immediate 18 months following trauma. If calcifications occur earlier than 18 months post-trauma, malignancy must be considered. Early in their development, calcifications may be fine linear or pleomorphic, mimicking DCIS. Calcifications coarsen over time, compatible with dystrophic calcification. Associated oil cysts may demonstrate typical eggshell calcification.
Ultrasound provides a useful adjunct imaging modality, and the appearance of fat necrosis is dynamic, and evolving following trauma. In the acute phase (within days of injury), ultrasound can demonstrate edema of the breast fat, resulting in increased echogenicity. In the subacute phase, ill-defined complex cystic masses are encountered, and are associated with edematous surrounding fat. The masses are mixed hyper- and hypo echoic, and a thin echogenic cyst wall may be observed. Diffuse low level internal echoes are commonly seen, as is posterior acoustic enhancement. In the late phase (after 18 months), prominent wall calcification results in posterior acoustic shadowing. Masses are thick walled and frequently solid, and may have angular margins if post-surgical in etiology. Doppler interrogation is useful, and if there is increased internal flow, this should raise concern for residual or recurrent tumor in the setting of post-lumpectomy or post-biopsy fat necrosis. Of note, post-radiation hyperemia may persist for up to one year.
MRI also can provide a useful adjunct to diagnostic mammography, and fat necrosis demonstrates high central fat signal on T1WI and low signal on T2WI fat suppressed sequences. T2WI FS sequences will delineate high signal resulting from fat edema. On post-contrast T1WI FS sequences, variable enhancement patterns are encountered, including focal, diffuse, or peripheral enhancement, depending on the degree and intensity of the inflammatory process. A thin rim of peripheral enhancement can persist up to 18 months, and has been reported to persist for several years in some cases. The contrast kinetics curve can be confusing, with slow gradual enhancement, rapid enhancement, and washout described.
In terms of initial imaging recommendations, diagnostic mammography with spot magnification views of associated calcifications is the best first-line modality. Ultrasound and MRI may be useful adjunct modalities. Because of the overlap in appearance with malignant processes, it is often appropriate to give a BIRADS 3 category, with short interval repeat imaging recommended to ensure stability. Needle biopsy may be required to absolutely differentiate from malignancy.
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