LAUSR

Calcinosis cutis (CC) is the deposition of insoluble calcium within soft tissue. Pathological calcification was reported as early as 1740, and has since been spilt into five main subtypes: metastatic, calciphylatic, dystrophic, idiopathic and iatrogenic. Iatrogenic CC is a consequence of medical treatment or procedures, such as parenteral administration of calcium. Metastatic CC and calciphylatic CC both occur in the presence of abnormal calcium and phosphate metabolism; while the former is associated with conditions such as hyperparathyroidism, the latter is most commonly observed in end-stage renal failure. The exact pathogenesis of calciphylatic CC is not fully understood; it is thought that abnormal calcium homeostasis results in small vessel calcification, mainly within in the dermis and subcutaneous fat, causing clots, ischaemia and necrosis. By contrast, idiopathic and dystrophic CC both arise in the absence of any identifiable metabolic abnormality. A distinguishing feature is that while idiopathic CC occurs in the absence of any known tissue injury, dystrophic CC develops in an area of damaged, inflamed, neoplastic or necrotic skin, and can occur many years after the initial insult. It often develops following minor trauma and presents as a nonhealing ulcer within the affected area, making Marjolin ulcer an important differential diagnosis to exclude. Small areas of CC have been successfully treated with warfarin, carbon dioxide laser, ceftriaxone and intravenous immunoglobulin, while topical sodium thiosulfate has been effective in patients with connective tissue disease and calciphylaxis. Large localized areas of CC have been treated successfully with surgical intervention. A variety of management approaches for dystrophic CC within burn scars have been described, including simple removal of the calcium deposit using forceps, excision and split-skin graft, and intralesional triamcinolone. A 69-year-old man presented 10 years ago with an area of recurrent ulceration on his left thigh within the area of a split-skin graft applied following extensive thermal burns in childhood. The calcium deposit was treated with curettage on two occasions without success. The residual calcification was treated by excision and left to heal by secondary intention. The wound was dressed three times weekly with polymyxin/bacitracin ointment (Polyfax ; Teva UK Ltd, Castleford, West Yorkshire, UK) and an occlusive hydrocolloid dressing (DuoDERM Extra Thin; ConvaTec, Sunderland, County Durham, UK). Healthy granulation tissue developed, and the defect healed successfully (Fig. 1) Further areas of calcinosis on the same thigh and upper arm were also successfully managed with excision and secondary intention wound healing. There was no infection or pain, and the patient was able to manage the wound himself at home. No recurrence has been seen after a follow-up of 3 years. The exact pathophysiology of CC is still unknown but one possibility is that calcium deposits may extend beyond what is visible, leading to incomplete removal, with residual deposits acting as a foreign body and triggering inflammation. This has led to the suggestion that dystrophic CC is best managed via excision and skin graft. Although it has been successfully managed in this way, this approach leads to the creation of a second wound, along with the risk that the graft may not take. Furthermore, in cases of extensive burns there may be a lack of donor skin available to use as a graft. We have demonstrated that excision and healing by secondary intention is a feasible treatment option for dystrophic calcinosis arising within burn scars. In this case it was associated with no complications, high levels of patient satisfaction and good cosmesis. Correspondence: Dr Thomas Oliphant, Department of Dermatology, Royal Victoria Infirmary, Newcastle-Upon-Tyne, NE1 4LP, UK Email: [email protected]