Case Study IV

Dx: Acute Peripheral Arterial Event

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Case Study IV Figure A

Inflammatory response at injection site with subsequent acute, localized ischemia; resultant full-thickness, necrotic wound.

Case Study IV Figure B

Clean, healthy granulating wound bed following debridement, HBO and negative pressure therapy; tendon, bone no longer visible.

Case Study IV Figure C

Progressive wound contraction, epithelialization following weekly Dermagraft application with concurrent HBO therapy.

Case Study IV Figure D

Wound fully epithelialized and limb preserved.

A 63-year-old female with a history of Sjogren's Syndrome and non-reconstructible lower extremity occlusive arterial disease presented to The Center For Wound Healing with an exquisitely painful, non-healing ulceration of the right great toe joint. She developed the wound two months prior to presentation following corticosteroid infiltration of the joint and surrounding soft tissue for relief of arthritic pain with rapid progression of tissue loss. Additionally, she complained of worsening lower extremity rest pain and claudication.

Upon presentation, a Wagner grade III ulceration over the dorsomedial aspect of the right first metatarsophalangeal joint was noted measuring 6cm x 4cm covered with a thick, adherent eschar. The patient demonstrated non-palpable pedal pulses with prior angiogram revealing large vessel occlusion of the right lower extremity with no run-off at the ankle level. As no revascularization options were available, the patient was at risk for amputation and significant disability if wound healing proved unsuccessful. Hyperbaric oxygen was immediately ordered to augment aggressive wound care by reversing persistent wound hypoxia and stimulating neovascularization and granulation tissue formation in an ischemic environment.

The patient initiated hyperbaric oxygen therapy (2.0 ATA, 90 minutes, full-body monoplace chamber) following orientation and medical clearance. Due to the severity of the patient’s pain, initial wound care consisted of a topical debriding agent. Pain management was consulted and sympathectomy was initially recommended to facilitate management of the wound. The patient refused this procedure but agreed to sympathetic nerve block series in order to allow more aggressive debridement and ensure compliance with treatment regimen. A total of 12 right lumber sympathetic nerve blocks were successfully performed in the two-month peri-operative period.

With pain controlled, bulk sharp debridement was then performed removing all remaining eschar and non-viable tissue from the wound bed. The dessicated long extensor tendon was observed as well as a portion of the distal first metatarsal. In the immediate post-operative period negative pressure therapy (KCI VAC) was initiated to stimulate granulation tissue formation and wound contraction. In addition, 11 weekly applications of a cryopreserved, human fibroblast-derived dermal substitute were performed to advance the formation of a granulation tissue base.

The patient had excellent response to the hyperbaric wound care regimen with steady improvement in wound granulation tissue, contraction and epithelialization as well as reduced rest pain within the limb. Following six months of intensive wound care, pain management and a total of 117 hyperbaric dives, the patient was discharged with the goal of limb salvage and improved quality of life met.

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