Encyclopedia of Pathology

Living Edition
| Editors: J.H.J.M. van Krieken

Breast Fat Necrosis

  • Inta Liepniece-Karele
  • Sergejs IsajevsEmail author
Living reference work entry
DOI: https://doi.org/10.1007/978-3-319-28845-1_4748-1



Breast fat necrosis is a benign nonsuppurative inflammatory process of adipose tissue usually complicating breast trauma, breast surgery, or radiation treatment. It was initially described in 1920 by Lee, BE & Munzer, JT.

Clinical Features

The etiological factors include trauma or microtrauma, radiotherapy, biopsy, anticoagulation (warfarin), surgery, duct ectasia, and breast infections (Tan et al. 2006; Kaplan et al. 2005). The breast can be injured in a motor vehicle accident, which occurs in 16% of cases of seat belt-restrained victims. Fat necrosis was observed secondary to the direct injection of silicone or paraffin into the breast. Transplantation of a large amount of autologous fat can result in fat necrosis, because fat cells are not nourished adequately until neovascularization occurs. Other rare causes include polyarteriitis nodosa, Weber-Christian disease, and granulomatous angiopanniculitis. Sometimes, the cause of fat necrosis is unknown (Tan et al. 2006; Kaplan et al. 2005).

Fat necrosis of the breast may be a challenging diagnosis on mammography, ultrasound, CT, PET-CT, and MRI. The extent of associated fibrosis, liquefied fat, and calcifications determine the imaging findings of fat necrosis. The diagnosis of fat necrosis using fine needle aspiration cytology (FNAC) is limited by inadequate samples. Core biopsy is more sensitive.

Clinical presentation of fat necrosis is variable (Chala et al. 2004) ranging from an incidental benign finding (indolent single or multiple round oil cysts or nodules on imaging) to a lump highly suggestive of cancer (palpable and radiologically visible irregular masses with overlying skin retraction). It can be associated with pain, skin or nipple retraction, erythema and lymphadenopathy. The lesion characteristically is situated near the skin or areola, since these are the sites within the breast that are most vulnerable to trauma. The average period for patients to present with a breast lump from time of trauma is 68.5 weeks (Tan et al. 2006; Kaplan et al. 2005).
  • Incidence

    The incidence of the disease is estimated to be up to 0.6% in the breast, representing 2.75% of all benign lesions. Fat necrosis is found in 0.8% in surgical specimens of breast tumors and in 1% of breast reduction surgery cases (Tan et al. 2006; Kaplan et al. 2005).

  • Age

    Variable, the average age of clinical presentation is 50 years.

  • Sex

    Mainly described in female breast.

  • Site


  • Treatment

    In patients with a new palpable finding, the history of a traumatic event can be helpful in making the diagnosis of fat necrosis. Management includes short-term follow-up with imaging and physical examination, including mammographic follow-up. Fat necrosis often resolves on its own. If the lump does not disappear over time, or increase in size, operation may be recommended to remove the affected area. Excisional biopsy is required when the clinical and radiological features resembles carcinoma.

  • Outcome

    Edema is characteristic in the hyperacute inflammatory phase. Fat cell necrosis releases cytoplasmic triglycerides into the interstitial space leading to a fat-containing cavity called “oil cyst”. The fatty acids can react with calcium ions, which accumulate around the cavity forming “calcified oil cyst.” Non-encapsulated fatty acids or granulation tissue can be attacked by the immune system and reabsorbed leaving a fibrous scar (Tan et al. 2006; Kaplan et al. 2005; Taboada et al. 2009).


Initially fat necrosis appears as an area of hemorrhage in fat. After several weeks, the affected area becomes bright yellow (saponification), chalky white (calcification) or yellow-gray (fibrosis). Cystic degeneration may occur.


Microscopic appearance of the fat necrosis depends on the age of the lesion. Initial changes are disruption of fat cells accompanied by hemorrhage and lipid laden histiocytes (Figs. 1, 2, and 3 H&E). Progression of the lesion is marked by the formation of multinucleated histiocytes, hemosiderin deposits, and calcification. Variable amount of lymphocytes, plasma cells, sometimes with eosinophils is present at this stage. Fibrosis develops peripherally as the demarcation. In some cases, the area of necrotic fat and cellular debris may become cystic. Dystrophic calcification may occur in older lesions.
Fig. 1

Magnification × 200, ME staining

Fig. 2

Magnification × 40, ME staining

Fig. 3

Magnification × 100, ME staining


In rare cases, immunohistochemical stains for cytokeratin may be necessary to exclude an underlying carcinoma. Foamy histiocytes may be confirmed by positive CD68 and negative pancytokeratin immunostains (Tan et al. 2006; Kaplan et al. 2005).

Differential Diagnosis

Breast Tuberculosis

Breast tuberculosis (tuberculous mastitis) is more frequent in premenopausal women. In younger patients, the lesion is more likely to have signs and symptoms of an abscess, whereas in older women tuberculosis tends to cause a mass that simulates carcinoma. The patients usually have ipsilateral axillary granulomatous lymphadenitis. The most common form of tuberculous mastitis is nodular mastitis with slowly growing solitary mass. Macroscopically, the lesion consists of nodular, indurated gray or tan tissue with yellow-to-white foci of caseous necrosis, which may simulate noninfective fat necrosis. Microscopically granulomatous lesions are present with Langhans giant cells and caseous necrosis containing typical bacteria detected by Ziehl Neelsen stain. The granulomas tend to be associated with ducts (Tan et al. 2006; Kaplan et al. 2005), while fat necrosis is not specifically associated to glandular structures. Similarly to fat necrosis, the chronic evolution is fibrosis.


Breast abscess commonly seen in lactating women, frequently caused by Staphylococcus aureus that penetrates through a nipple fissure (Tan et al. 2006; Kaplan et al. 2005). Lactational mastitis and abscess formation develop as a result of obstruction to the flow in one or more major lactiferous ducts. The histologic appearance varies from acute inflammation that may be accompanied by focal necrosis, to organized chronic abscesses.

Subareolar abscesses usually occur in nonlactating premenopausal women. The process is characterized by repeated episodes of abscess formation in subareolar region as the result of duct obstruction caused by squamous metaplasia in terminal portion of lactiferous ducts.

Breast Infarction

Breast infarction (Kaplan et al. 2005) most frequently occurs during pregnancy or postpartum (Tan et al. 2006). The lesion presents clinically as a discrete mass that usually is asymptomatic, but sometimes pain and tenderness are reported. The breast infarction usually occurs in women less than 35 years. The gross appearance of the infarcted tissue is variable: hemorrhage in acute onset and pallor or yellow discoloration in older infarcts similar to fat necrosis. Microscopic findings depend on the duration of the infarct. Early lesions are characterized by hemorrhage. Ischemic changes involve glandular tissues, a feature not seen in fat necrosis. Infarction is demarcated by a zone of granulation tissue with variable inflammatory reaction, hemosiderin deposits, and fibrosis.

Lupus Mastitis

Lupus mastitis can occur in 2% cases of patients with systemic lupus erythematosus. Lupus mastitis is a form of lupus panniculitis characterized by nodular lesions clinically and by fat necrosis in various stages of evolution histologically. It can present as palpable nodules accompanied by calcifications on mammography reflecting the evolution from local panniculitis to fat necrosis (Tan et al. 2006; Kaplan et al. 2005).

Breast Lipoma

Breast lipoma with central necrosis is uncommon; just few cases have been reported. Lipoma appears as a round or oval radiolucent mass with a thin capsule. Mammography shows eggshell calcifications.

Mondor’s Disease or Superficial Thrombophlebitis

The cause of this lesion is trauma, physical exertion, operations performed on the breast or chest wall (Tan et al. 2006; Kaplan et al. 2005). At difference with fat necrosis, physical examination shows a subcutaneous cord. Microscopically, the characteristic feature is thrombophlebitis (Tan et al. 2006; Kaplan et al. 2005).

References and Further Reading

  1. Bowman, E., Oprea, G., Okolo, J., Rizzo, M., Garram-Mendola, S., Manne, U., Smith, G., Pambuccian, S., & Bumpers, H. L. (2012). Pseudoangiomatous stromal hyperplasia (PASH) of the breast: A series of 24 patients. Breast, 18, 242–247.CrossRefGoogle Scholar
  2. Chala, L. F., de Barros, N., de Camargo Moraes, P., Endo, E., Kim, S. J., Pincerato, K. M., Carvalho, F. M., & Cerri, G. G. (2004). Fat necrosis of the breast: Mammographic, sonographic, computed tomography, and magnetic resonance imaging findings. Current Problems in Diagnostic Radiology, 33, 106–126.CrossRefGoogle Scholar
  3. Kaplan, V., Kelley, C. J., & Babu, E. D. (2005). Fat necrosis of the breast – A review. The Breast, 15, 313–318.PubMedGoogle Scholar
  4. Lee, B. E., & Munzer, J. T. (1920). Fat necrosis of the female breast and its differentiation from carcinoma. Annals of Surgery, 37, 188–195.CrossRefGoogle Scholar
  5. Taboada, J. L., Stephens, T. W., Krishnamurthy, S., Brandt, K. R., & Whitman, G. J. (2009). The many faces of fat necrosis in the breast. American Journal of Roentgenology, 192, 815–825.CrossRefGoogle Scholar
  6. Tan, P. H., Lai, L. M., Carrington, E. V., Opaluwa, A. S., Ravikumar, K. H., Chetty, N., Kaplan, V., Kelley, C. J., & Babu, E. D. (2006). Fat necrosis of the breast – A review. The Breast, 15, 313–318.CrossRefGoogle Scholar

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© Springer Nature Switzerland AG 2018

Authors and Affiliations

  1. 1.Riga East University Hospital, Centre of Pathology/Faculty of MedicineUniversity of LatviaRigaLatvia