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Many wounds, despite their relation to the many pathophysiological processes defined in this handbook, defy simple description. Thus, the miscellaneous wounds discussed in this chapter may have some underlying tendencies of other diagnoses, e.g. an immune component, but have a different unique primary etiology, or even unknown pathophysiology. Because of their unique pathological manifestations, often multidisciplinary approaches will be required to both diagnose and treat the patient and the wound. Elusive and challenging pathways to both wound healing and subsequent return to optimal function are the only common factors in this group of wounds.



  • Is caused by calcific occlusion of the small vessels to the skin and subcutaneous tissue

  • Is classified as calcific uremic arteriolopathy (CUA) or non-uremic calciphylaxis (NUC)1 with the risk factors shown in Table 10-1.

  • Is not well understood, but CUA appears to be related to deficiencies in vascular calcification inhibitors (e.g. fetuin-A and matrix Gla protein) and dysregulation of extra-skeletal mineralization1

  • Has the following three-step progression

    • Calcification within the media layer of the vessel causing narrowing of the lumen

    • Proliferation of endothelial cells and fibrosis underneath the intima (termed subintimal fibroplasia)

    • Thrombosis of the vessel lumen resulting in ischemic injury to the skin and hypodermis2

TABLE 10-1Risk factors for calcifylaxis

Clinical presentation

  • Presents initially as livedo reticularis, plaques, or nodules

  • Progresses to skin and subcutaneous necrosis with dark eschar

  • Causes erythema, induration, and severe pain

  • Usually occurs on bilateral lower extremities (especially thighs) and abdomen, areas where there is more adipose tissue

  • May occur in areas where patient gives daily insulin injections, due to the repeated trauma2


(A) Early presentation of calciphylaxis. (B) Progression of calciphylaxis to full thickness, necrotic wounds.

Medical management

  • Confirm diagnosis with a punch biopsy using the double trephine technique2

  • Treat to halt the vascular calcification2

    • Increase phosphate removal and decrease phosphate intake (ideal phosphate level is 3 mg/dL)

    • Increase calcium removal by dialysis and decrease calcium intake (ideal calcium level is 8 mg/dL)

    • Lower levels of parathyroid hormone with cinacalcet (in mild cases) or parathyroidectomy in refractory cases3

    • Discontinue Vitamin D supplements4

    • Discontinue warfarin and substitute alternative anticoagulants5

    • Transition from peritoneal dialysis to hemodialysis if possible

    • Administer ...

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