The Mysterious Calciphylaxis: Wounds with Eschar — To Debride or Not to Debride?

Rosalia Martin, MSN, RN, CNS, CWOCN

C alciphylaxis (CPX) is a potentially fatal complication of end-stage renal disease.1 Many authors have called calciphylaxis a rare phenomenon, a potentially fatal condition, and a syndrome that leads to ischemic ulcerations. Throughout the years, this mysterious disease has been described in the literature by a variety of names such as uremic gangrene syndrome,1,2 calcifying panniculitis, and calcific uremic arteriolopathy.3,4 According to Bliss and others,1,5 the most functional term may be the most recent: vascular calcification-cutaneous necrosis syndrome.

The pathogenesis of CPX is uncertain.1 Just as perplexing is wound care treatment, which is limited to aggressive surgical debridement of necrotic tissue. Srikureja6 states that debridement and regular wound care are necessary to promote healing and prevent serious complications from overwhelming secondary infection. Hadler7 recommends topical wound care products to facilitate debridement. Acknowledging the fact that these ischemic ulcerations of the skin are due to metastatic calcification of subcutaneous tissue and small arteries,8 debridement of ischemic wounds with stable eschar is contraindicated until perfusion status is determined.9 Furthermore, preventing wound infection is critical because sepsis related to wound infection is the leading cause of death for patients with CPX.10

According to Nunley,11 the obscure pathogenesis of CPX is likely the result of a multiplicity of comorbid factors or events. It is believed that patients develop this condition as a result of a hypersensitivity reaction to sensitizers such as increased parathyroid hormone (PTH), hypercalcemia, and hyperphosphatemia.3,12,13 According to Ledbetter,3 underlying vascular damage is present within the small vessels that may be related to the cause of renal failure; this predisposes patients to metastatic calcification in the setting of an elevated PTH level with an elevated calcium and phosphate product. Yet some patients with CPX have normal calcium, phosphate, and PTH concentrations.14 Also, the exact role of parathyroid hormone is uncertain because CPX may occur after total parathyroidectomy in the absence of measurable PTH levels.11

Exposure to challenging agents such as blood transfusions, albumin administration, corticosteroids, immunosuppressive agents, and local trauma are also thought to be responsible for the precipitating events of CPX.8,15 This belief is based on the experimental studies performed on rats by Selye16 that included exposing the subjects to challengers such as blood products, metals salts, and trauma. Functional protein C abnormality or protein S deficiency could be likely causes of thrombotic events, representing the cause of ischemia in clients who are susceptible to developing CPX.1,3,17


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