Abstract
A 41-year-old woman who had chronic renal failure required a simple mastectomy for infarction of one breast. On initial presentation her condition was managed as a skin ulcer. Arterial calcification is common in chronic renal failure and its pathogenetic connection with this uncommon event is relevant to the management of “skin ulcers” in general in this population.
Arterial calcification, including in the subcutis, is common in chronic renal failure (CRF). Although not specific, this lesion is characteristic: medial calcification with fibrocalcific intimal thickening causing significant narrowing of the lumen. 1 An uncommon complication is infarctive necrosis of the skin and subcutis, generally of the extremities or lower abdomen, or both.1 Acute infarction of a breast has not been documented. It is reported here because of its relevance to the diagnosis and surgical management of necrotic skin lesions in unusual sites in patients having CRF.
Case report
A 41-year-old woman with CRF had rejected a transplanted kidney 9 years earlier and had suffered from hypotension ever since. She was on long-term hemodialysis. Two years earlier she had sought, unsuccessfully, to have breast reductions. Two months before this admission, she noticed acute reddish discolouration and a burning sensation of the skin of her right breast. Over the next few days, part of the breast became hard and very tender, and then it ulcerated. Three weeks later, the ulcer was excised and the skin closed. However, over the next 4 weeks the closure broke down, exposing necrotic fat. On referral to our hospital, she weighed 70 kg and was 1.54 m tall (body mass index 29.2). The blood pressure was 70/30 mm Hg, the pulse rate 120/min and her body temperature 38 °C. The breasts were large and pendulous. The right breast was hard and tender, and much of the upper half was deeply ulcerated. The left breast was uninvolved. The serum creatinine level was 624 μmol/L, urea nitrogen 16.4 mmol/L (urea), calcium 2.38 mmol/L, phosphorus 1.77 mmol/L and albumin 25 g/L. The intact serum parathormone level was 47.7 pmol/L (normal 1.3 to 5.7 pmol/L). Mammography could not be performed satisfactorily because of severe pain. A simple mastectomy revealed that the breast subjacent to the ulcer was infarcted (Fig. 1). Radiographs and microscopic examination of the operative specimen revealed two patterns of calcification (Fig. 2): one was of arteries, which showed the characteristic histologic lesion; the other was granular, correlating with calcification in necrotic fat. Four hyperplastic parathyroid glands were excised 18 days later. Her recovery was uncomplicated.
Sagittal slice of simple mastectomy specimen, showing infarcted fat (darker area) and ulceration of overlying skin.
Radiographs of sagittal breast slice including both nonulcerated and ulcerated skin. (Left) Calcified vessels to right range from 1 to 3 mm in external diameter. Note patch of granular calcification pattern to right, part of which is magnified in right-hand portion of figure. (Right) Granular pattern of calcification in necrotic fat.
Discussion
The risk of soft-tissue calcification is high in CRF because of the associated hyperphosphatemia and secondary hyperparathyroidism.2 Small arteries and arterioles in the subcutis are commonly calcified.1 However, ischemic necrosis is uncommon. Similar arterial lesions in the breast have been described radiologically and histologically in CRF patients,3–7 but clinical signs of breast fat necrosis are rare, even in the presence of skin and fat necrosis in other body areas;3–6 and breast infarction has not been documented. Arterial calcification is also commonly found in the breast with increasing age in the absence of CRF,3 but its morphology is different in that it lacks the fibrocalcific thickening of the intima with luminal narrowing, which is seen in CRF.1
Since calcification of subcutaneous arteries in CRF is generally asymptomatic, other factors must trigger the infarctions,8 such as trauma, including that of surgery4 and of mammography. 6 Our patient gave no history of trauma, and mammography was attempted after the fact. The calcified vessels appear to be predisposed to thrombosis5 during a coincidental hypercoagulable state,5,9 which was absent in this case. Two other factors may be relevant to our case: reduced perfusion through narrowed calcified vessels during shock8 probably contributes to the ischemic necrosis. Additionally, the local biophysical effects of large adipose deposits may also include interference with blood flow in the calcified arteries.4,10 Our patient had both chronic hypotension and large pendulous breasts. The role of the secondary hyperparathyroidism in the development of the arterial calcification in CRF has provided a rationale for surgical parathyroidectomy.1 However, its role in the initiation of the necrosis has yet to be defined.
Necrosis of skin and subcutis as a complication of CRF is not well known outside the field of nephrology. An awareness that it may also be precipitated or aggravated by surgical procedures is important for surgeons, who may be asked to perform elective procedures — if done, the mammoplasties previously requested by our patient could have led to disastrous complications — or to carry out débridement and repair of necrotic sites in these patients. For pathologists, radiographs of excised tissues are useful in the localization and histologic sampling of the small calcified vessels.4
Addendum
Another patient with a similar lesion complex was described in Human Pathology 1995;26:1055–64.
- Accepted November 7, 1995.