Infarct of Breast Tissue
An infarct is a coagulative necrosis of (breast-) tissue, caused by ischemia. This is mostly not a primary event in breast tissue but rather a secondary one, typically occurring after an invasive procedure or within a breast lesion such as a fibroadenoma, papilloma, or large neoplasm. In rare events, it can occur during late pregnancy or lactation.
Secondary breast infarction sometimes occurs as a complication following core needle biopsy, fine needle aspiration biopsy (FNAB), or a surgical procedure by altering the blood vessels of a breast lesion, which then undergoes infarction.
Age: Wide age distribution depending on underlying lesion. Primary infarction is more typical in pregnant women.
Sex: Only females, no reported male case.
Site: No site preference.
Treatment: Due to clinical presentation of an infarct, core needle biopsy is most often performed. Local excision of the infarcted area is necessary most of the time due to pain and depending on the underlying lesion itself.
Outcome: Depends on the infarcted lesion and the primary cause.
Infarction typically presents as a palpable mass that may be painful and varies between soft and hard in consistency. In this case, it can be mistaken for a carcinoma due to the firm consistency of the lesion. Infarcts usually occur as single lesions, localized to a breast lesion, or to hyperplastic lactating breast tissue during the puerperal period. The infarcted area can be well circumscribed (Han et al. 2015). Hemorrhage can be seen within most infarcts and sometimes a hyperemic outer border can also be observed.
On routine H&E sections, infarcted tissue is, like in other areas of the body, typically recognizable by the loss of nuclear staining with ghostlike nuclear contours in an early phase, independent of the underlying structures. Epithelial structures are more affected compared to mesenchymal areas. Structural integrity of an underlying breast lesion is in most cases still preserved. Localized hemorrhages and small groups of granulocytes and lymphocytes can be included, and thrombotic small vessels can be seen.
After days to weeks, the infarcted area can undergo different changes depending on the remaining surrounding tissue and its capability to repair the infarcted area. This mainly depends on the cause of the infarct and whether the surrounding tissue is well oxygenized by blood vessels. In the latter case, the infarct will be organized by a typical granulation tissue, which contains macrophages, fibroblasts, and capillaries, finally resulting in a fibrotic scar with more or less remaining macrophages or siderophages. In the opposite case, if the surrounding tissue is less oxygenized, then the infarcted area will undergo a more acellular, long-lasting degenerative process leading to a pseudocyst with macro- or microcalcifications.
In a chronic ischemic healing process, epithelial structures can be entrapped and can be distorted within marked fibrosis, which might be mistaken for a carcinoma. The appearance of squamous metaplasia has also been described (Flint and Oberman 1984).
When an infarct in the breast is seen, it is most important to think about a possible infarcted neoplasm, which might be recognized only in its silhouettes. Therefore, a thorough clinical history or additional information is also very important. In every infarcted area, it is critical to also evaluate the general architectural aspects within the infarct and to evaluate the margin toward vital areas. These two steps may lead to the recognition of an underlying lesion or neoplasm, respectively. Findings of the core needle biopsy should be cautiously interpreted if the sample size is small and only central areas are visible. Ultimately surgical excision should be performed to confirm the diagnosis of an underlying breast lesion.
Typical breast lesions that tend to undergo (partial) infarction are fibroadenoma, papilloma, adenosis, and highly proliferative breast carcinoma, mostly basal-like carcinoma.
Similar to an infarct is hemorrhagic necrosis of the skin and subcutis, which can occur as a side effect or complication of anticoagulant therapy. Most often, this situation occurs subsequent to thrombophlebitis treated with warfarin. A hypersensitivity reaction affecting small vessels might be the pathogenic reason. Another explanation could be heterozygous protein C deficiency promoting paradoxical coagulation under warfarin (Isenberg et al. 1996).
Although not applicable to an infarct by itself, it can be helpful to reconstruct infarcted breast lesions. Sometimes myoepithelial markers can be helpful, even in less preserved areas.
Clinically, a breast infarct can simulate a carcinoma through its tenderness, and even enlarged axillary lymph nodes may coexist due to the reactive inflammatory process as a result of the infarct. Nipple discharge of an infarcted papilloma is bloody and thus raises suspicion. In FNAB, infarcted areas can show highly reactive and thus atypical cells, which may be misleading.
On H&E, highly fibrotic areas containing high collagen content and low cellularity can be mistaken for an infarct, but there are still some remaining bland fibroblasts and typical collagen bundles.
Difficulties sometimes arise because of the presence of complete necrotic material of a highly proliferative carcinoma or another breast lesion in the background.