Dear Editors,
Pyoderma gangrenosum (PG) is a rare neutrophilic dermatosis as part of a complex systemic autoinflammatory process.1 It usually begins as a pustule or nodule, which rapidly evolves into a painful ulcer, with purpuric edges, perilesional erythema, and sloughy and necrotic wound bed. Even if diagnostic criteria have been suggested, PG diagnosis is mainly based on the exclusion of other possible causes.2 Treatment of PG is based on topical and systemic immunomodulatory and/or immunosuppressant agents. PG lesions typically worsen after trauma, which is referred as the pathergy phenomenon. Consequently, mechanical debridement and surgical procedures should be avoided in ulcers secondary to pyoderma gangrenosum. However, once inflammation is controlled by systemic immunosuppresion, these wounds may benefit from invasive treatments.3, 4, 5 We present a case of pyoderma gangrenosum under immunosuppression, with no clinical signs of inflammation that responded successfully to negative pressure therapy and punch grafting.
A 31 year old woman, with systemic lupus erythematosus with renal disease, treated with low dose prednisone, cyclosporine, and hydroxicloroquine presented for 2 months an ulcer located on the anterior aspect of her left leg. She presented with a 4 × 5 cm ulcer with well defined undermining dark‐red to livid edges, with sloughy wound bed. The surrounding skin was erythematous and indurated (Figure 1). Histological findings supported clinical suspicion and intravenous metilprednisolone 1 mg·kg−1·d−1 was started. She required hospitalisation and systemic antibiotics due to sepsis of cutaneous origin. Few weeks later, signs of inflammation had disappeared, oral dose of prednisone was progressively reduced, and both compression therapy with a multicomponent bandage and negative pressure therapy (Vacuum‐Assisted Closure) was started. When adequate granulation tissue was present in the wound bed (Figure 2), 5 weeks after starting the negative pressure therapy and under low doses of prednisone, punch grafting was performed in an outpatient basis. The grafted wound was covered with a single‐use negative pressure therapy device and a multicomponent bandage. Two weeks later, with a unique dressing change in between, complete epithelialisation was achieved.
Figure 1.

Ulcer with clinical signs of inflamation
Figure 2.

A, Wound bed with granulation tissue and edges without signs of inflammation. B, Complete epithelialisation 2 weeks after punch grafting
Complete healing rates with classical immunosuppressive treatments (predominantly oral corticosteroids and cyclosporine) do not reach 50% at 6 months.3, 4 Although different biologic agents may be an effective alternative in nonresponders, the problem is not only controlling pyoderma activity but also repairing all lost tissue.
Once the inflammatory activity is controlled, the strategy to facilitate the formation of granulation tissue and promote epithelialization will be similar to that used in wounds of other aetiologies.5 Therefore, negative pressure therapy and thin split‐thickness grafts will be good alternatives, either alone or in combination, to accelerate healing.3, 4, 5
Punch grafting is a traditional and minimal invasive technique to enhance wound healing, which may be performed in an outpatient basis. These thin split‐thickness skin grafts, which contain epidermis and papillary dermis, are obtained under local anaesthesia with a punch, curette, or surgical blade and are placed directly on the wound bed. The donor site is usually anterior‐lateral thigh. Local pressure and immobilisation during the first 3 to 4 days after the procedure are essential for graft taking.5
When grafting a wound bed with optimal granulation tissue, as in this case, a 100% graft uptake may be obtained. However, if the wound bed conditions are not perfect and grafts do not adhere, the procedure is still useful as grafts will release growth factors and cells that promote epithelialization and reduce pain.5
The combined use of negative pressure therapy and punch grafting has several advantages considering graft taking. On the one hand, their sequential use is of great interest, as the application of negative pressure promotes the formation of granulation tissue, with reduction of exudate and bacterial load, and therefore prepares the wound bed to facilitate graft taking. On the other hand, its synchronous use can improve the percentage of graft taking.6, 7
Compression therapy was also used because despite the absence of reflux or an obstructive disorder, the large inflammation found in pyoderma gangrenosum can trigger a state of venous hypertension that may hinder healing. In fact, any leg ulcer, except for cases with advanced peripheral arterial occlusive insufficiency, will benefit from the antigravity and anti‐inflammatory effect of compression (bandages, hosiery or compression wraps). Since the application of the compression bandage may be painful initially, the recommendation is to start with 20 mm Hg and increase the compression depending on patient's tolerance. With progressive reduction of inflammation, tolerance will increase.5
Once clinical inflammation has been controlled by systemic immunosuppression, local wound treatment in PG should be similar to any other wound. Compression therapy will help to control inflammation in PG, but it should be adapted to pain. Advanced therapies such as negative pressure therapy and punch grafting will speedup healing time.
REFERENCES
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