Hi Decendar

Thank you for your question. Scott Robinson MD and I discussed it and here are some thoughts: application of traditional NPWT on a patient with calciphylaxis would be contraindicated if the patient presented with any of the previously described NPWT contraindications [e.g. osteomyelitis without current antibiotic therapy, wound malignancy, exposed organs, bowel, or blood vessels, use in thoracic or abdominal cavities, necrotic tissue with eschar present, unstable structures (e.g. flaps or grafts), patients at increased risk of bleeding, and non-enteric or unexplored fistulas (to clarify, NPWT can be applied around or in the vicinity of a fistula, but not applied to directly evacuate fistula contents)].[1] There are case reports in which NPWT was used as adjunctive therapy after debridement in patients with calciphylaxis. [2,3], It is essential to note however, that an estimated 50% of all patients with calciphylaxis will die within 1 year, commonly due to sepsis.[2] The progression to ulcerating skin lesions has been associated with more than 80% mortality.[2] Thus, a multispecialty approach (with nephrologists, etc) addressing the underlying causes and comorbidities causing the ulcers is critically important, as ulcers are just the tip of the iceberg.

Below is an excerpt from one of the case reports, by Solansky et al [2]. In addition to supportive and medical interventions, authors reported surgical debridement followed by application of cellular and/or tissue based product and NPWT to bolster the larger areas of debridement.

"Calciphylaxis, or calcific uremic arteriolopathy (CUA), is defined by a systemic calcification of the arterioles progressing to ischemia and subcutaneous necrosis. The condition is most often observed in patients with renal failure and secondary hyperparathyroidism, affecting up to 4% of patients on hemodialysis. However, the condition can also develop in conjunction with sufficient renal function. Calcific uremic arteriolopathy lesions are extremely painful and typically present on the lower limbs, trunk, or genital regions as tender red areas which progress to subcutaneous nodules, dermal plaques, and eschar.

There is currently no established cure for calciphylaxis and treatment often involves combination therapy. Medical treatments typically include drugs to reduce calcification-promoting mineral and hormone imbalances, such as parathyroid hormone (PTH)-reducing medications (eg, cinacalcet), bisphosphonates, use of low-calcium dialysate and calcium-free phosphate binding agents, and vitamin K supplementation (as vitamin K deficiency is common in haemodialysis patients and may be a trigger for calciphylaxis due to its role in activating a tissue inhibitor of calcification).[4] Sodium thiosulfate is also a notable broad-spectrum therapeutic for CUA thought to act as an antioxidant, vasodilator, and calcium chelator. Wound management therapies consist of nonsurgical wound cleansing and HBOT (investigational). Major surgical treatments include parathyroidectomy, although this is generally reserved for patients with known primary hyperparathyroidism. Surgical debridement to remove necrotic tissue and promote the healing of healthy tissue is more widely used, but its efficacy is controversial due to the possibility of causing further tissue damage. The conundrum of debridement followed by wound progression makes the question of when to further debride when visibly necrotic tissue is present difficult to answer."

[1] https://woundreference.com/app/topic?id=negative-pressure-wound-therapy#-contraindications
[2] Solanski Det al. https://www.hmpgloballearningnetwork.com/site/wounds/article/successful-surgical-treatment-severe-calciphylaxis-using-bilayer-dermal-replacement-matrix
[3] Emohare O et al. https://pubmed.ncbi.nlm.nih.gov/15091142/
[4] Successful treatment of calciphylaxis with vitamin K in a patient on haemodialysis. https://pubmed.ncbi.nlm.nih.gov/35145651/

Hope this helps!