172March/April 2005 • Vol 95 • No 2 • Journal of the American Podiatric Medical Association
Surgical debridement should be judicious, becauseeven minor trauma often causes an increase in the de-structive process, a phenomenon known as pathergy.
2-5
Negative Pressure Wound Therapy
Negative pressure wound therapy was first describedin 1997 by Argenta and Morykwas
6
and Morykwas etal
7
in porcine animal models and human clinical ex- perimental trials. The V.A.C., or Vacuum AssistedClosure, wound therapy system (KCI, Inc, San Anto-nio, Texas) is a subatmospheric pressure system thatuses foam fit by the applicator to the wound geome-try. The foam comes in two varieties, Versafoam(KCI, Inc), a white, hydrophilic, dense polyvinyl-alco-hol foam that comes packaged in saline and is usedmainly on superficial or extremely painful ulcera-tions, and a hydrophobic, black polyurethane foamthat has larger open cells that enhance exudate re-moval. Noncollapsible suction tubing connected to a vacuum pump is either embedded directly into a slitcut into the foam by the practitioner or connected toa TRAC pad(KCI, Inc) sitting on top of two layers of foam, depending on the type of wound and the V.A.C.model. The foam dressing and tubing are secured in place by an adhesive drape to maintain an airtightseal. Continuous or intermittent (5 min on, 2 min off)subatmospheric pressure is distributed uniformlyacross thewound bed through the open foam cells ata manually adjusted pressure of 125 to 175 mm Hgaccording to the amount of wound drainage. Thedressing offers a closed wound environment, whichrequires less frequent dressing changes than tradition-al wet-to-dry dressings but requires more skill in ap- plication, as the periwound area must be appropriate-ly protected to avoid maceration from excess woundfluids.The physiologic effect of negative pressure woundtherapy on soft tissues is compared to the callus dis-traction theory or the tension/stress effect on bones.
In vitro
and limited
in vivo
studies have shownthatnegative pressure wound therapy may increase localtissue perfusion, increase the rate of granulation tis-sue formation, and reduce wound bacterial load.
7
Ithas also been theorized that negative pressure woundtherapy causes changes in the wound microenviron-ment by removing interstitial edema and wound exu-date containing substances that may impede woundhealing, including matrix metalloproteinases.
8
Theseeffects are currently being studied to determinewhether they can be substantiated with a significantnumber of patients in randomized controlled trials.Negative pressure wound therapy is also being stud-ied to determine its efficacy in venous stasis and neu-ropathic ulcers. The significance of these studies hasnot yet been determined.
6, 9, 10
The therapy has shown promise in other uses such as securing skin graftsafter transplantation and for reepithelialization of donor sites.
11, 12
Although negative pressure wound therapy is use-ful in many clinical situations, it is contraindicated incertain settings. It should not be used on necrotic tis-sue with eschar present. Wounds with associated os-teomyelitis must be treated with appropriate debride-mentand antibiotic therapy. It is also not appropriatein the presence of neoplasm because of its effect ontissue proliferation. Other contraindications includeorgan or body cavity fistulas and placement in prox-imity to vessels.
13
Case Report
An otherwise healthy 82-year-old woman presentedto the Wound Care and Hyperbaric Medicine Clinicat Paradise Valley Hospital, Phoenix, Arizona, by re-ferral after a 2-month history of a progressively en-larging, painful ulceration on the posterior aspect of her right lower extremity. The patient first noticed abrownish discoloration in the area, which opened afew days later with a moderate amount of yellowish,watery exudate. The patient initially applied 1% hydro-cortisone cream to the wound area, and the woundgrew larger and ulcerated. The patient’s primary-care physician then performed a swab culture of the woundand began administration of oral cephalexin. Localwound care was managed with triple antibiotic oint-ment and nonadherent dressing. After 6 weeks of cephalexin therapy with no improvement, the patientwas referred to a vascular surgeon, who discontin-ued the cephalexin and prescribed oral ciprofloxacinand metronidazole. The patient was also prescribed venous duplex ultrasound and referred to our clinicfor further evaluation.The patient’s medical and social histories werenoncontributory, with no chronic illnesses or medi-cations other than the ciprofloxacin and metronida-zole. Review of systems revealed no history of de- pendent edema of the lower extremities, varicose veins, trauma, prior ulceration, or known insect bites.The patient had no appreciable foot deformities orburning, tingling, numbness, weakness, or crampingsensations.Upon initial evaluation at our clinic, the patient’sright lower leg was markedly edematous from theknee to the toes. The wound was circumferential, ex-tending from the inferior aspect of the gastrocnemiusmuscle belly to just proximal to the malleoli and mea-suring 15 cm at its greatest width (Fig. 1). There was
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