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Journal of the American Podiatric Medical Association Vol 95 No 2 March/April 2005171
Pyoderma gangrenosum was first described by Brun-sting et al
1
in 1930. The term
 pyoderma gangreno-sum
is actually a misnomer, because the lesions arenot infectious or gangrenous.
2
The typical lesion is a vesicle, pustule, or papulopustular lesion that ulcer-ates to form a wound with characteristic blue-to-pur- ple undermined borders surrounded by erythema.
2, 3
The lesions are usually painful and may appear any-where on the body; however, they most often ariseon the lower extremities. They vary in that they mayhave granular or necrotic wound beds with eitherserous or purulent exudates.
2-4
Diagnosis and Histopathology
Diagnosis of pyoderma gangrenosum is a diagnosisof exclusion. There are documented characteristichistologic findings associated with the disorder; how-ever, the diagnosis is conferred only when other pathologic processes such as infection, vasculiticsyndromes, and neoplasia have been ruled out.Histologically, the lesions vary by site of biopsyfrom central wound polymorphonuclear leukocyte in-filtration with scattered lymphocytes and epidermaland papillary dermal necrosis to lymphocytic vasculi-tis in the peripheral advancing wound margins.
2
Thorough examination is required if pyodermagangrenosum is suspected, because the diagnosis isassociated with comorbidities in approximately 50%of cases. The most common associated illness is in-flammatory bowel disease, followed by rheumatoidarthritis, seronegative arthropathies, malignancies,and paraproteinemias.
2
Treatment
The treatment of pyoderma gangrenosum is broadbut is primarily targeted at systemic control of the in-flammatory process. Therapy includes high-dose cor-ticosteroids or other systemic immunosuppressantagents including, but not limited to, cyclosporine, cy-clophosphamide, chlorambucil, and azathioprine.
5
Ulceration of Pyoderma Gangrenosum Treatedwith Negative Pressure Wound Therapy
Stephen M. Geller, DPM*James A. Longton, DPM*
Pyoderma gangrenosum is a skin disease characterized by wounds withblue-to-purple undermined borders surrounding purulent necrotic bases.This article reports on a patient with a circumferential, full-thickness, andpartially necrotic lower-extremity ulceration of unknown etiology. Resultsof laboratory tests and arterial and venous imaging studies were found tobe within normal limits. The diagnosis of pyoderma gangrenosum wasmade on the basis of the histologic appearance of the wound tissue afterbiopsy as a diagnosis of exclusion. Negative pressure wound therapy wasundertaken, which saved the patient’s leg from amputation. Althoughnegative pressure wound therapy has demonstrated efficacy in the treat-ment of chronic wounds in a variety of circumstances, this is the first doc-umented use of this technique to treat an ulceration secondary to pyo-derma gangrenosum. (J Am Podiatr Med Assoc 95(2): 171-174, 2005)
CLINICALLY SPEAKING
*Podiatry Program, Phoenix Baptist Hospital, Phoenix, AZ.
Corresponding author:
Stephen M. Geller, DPM, Podia-try Program, Phoenix Baptist Hospital, 1728 W Glendale, Ste103, Phoenix, AZ 85021.
 
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
 
Journal of the American Podiatric Medical Association Vol 95 No 2 March/April 2005173
a bridge of necrotic skin on the anterior tibial crest.The wound base was black eschar with yellow,necrotic, gelatinous slough. The wound edges ap- peared hyperemic with purplish discoloration. Alsonoted were periwound serous fluid–filled vesicles.Dorsalis pedis and posterior tibial pulses were palpa-ble. There was no associated lymphangitis. Homans’sign was absent. The patient’s right upper thigh exhib-ited no appreciable warmth, tenderness, or erythema.The wound was cleansed with normal saline, anddeep tissue was taken from the wound base and sentfor gram stain, culture, and sensitivity testing. Addi-tionally, a pie-shaped specimen including both healthyand involved tissue was taken from the proximalwound margin for appropriate biopsy. The initial hist-opathologicexamination revealed nonspecific find-ings of acute and chronic inflammation. Specifictests for acid-fast organisms and fungi were found tobe negative. The specimen obtained contained no ev-idence of vasculitis or neoplasm. A diagnosis of pyo-derma gangrenosum was suggested on subsequentreexamination of the slide preparations.Lower-extremity vascular testing was expanded toinclude arterial and venous duplex Doppler studies,which revealed adequate arterial circulation and noevidence of thrombophlebitis. A complete blood countwith differential count, comprehensive metabolic panel, and rheumatoid factor were obtained andfound to be within normal limits. The patient’s eryth-rocyte sedimentation rate was elevated at 70 mm/h.
Course of Treatment
Therapy focused first on reduction of the leg edemaand absorption of the wound exudate. Negative pres-sure wound therapy was ordered after careful con-sideration yielded no contraindications. Three daysafter the initial examination, the wound was debrid-ed of necrotic tissue using pulsed lavage and dressedwith Mesalt sodium chloride–impregnated dressing(Mölnlycke Health Care AB, Göteborg, Sweden). Thefollowing week, the wound was reexamined anddressed with four-layer compressive wrap to helpcontrol edema. Negative pressure wound therapywas begun 1 week later. Initially, the white polyvinyl-alcohol foam was used because the wound was pain-ful at a suction power of 175 mm Hg (Fig. 2). After the pain persisted and was eventually linked to the high pressures needed for the polyvinyl-alcohol sponge, atransition was made to the black polyurethane foam.Mepitel (Mölnlycke Health Care AB) was used as anonadherent dressing with the black foam to facili-tate pain-free dressing changes and limit the aggres-sive nature of this open-cell foam.The wound showed signs of progressive healing,including a decrease in size (Fig. 3). The large woundepithelialized to form two separate wounds that be-came progressively smaller. The patient concurrentlybegan a course of corticosteroid therapy, with slowtapering from 40 to 20 mg/day, and was referred to arheumatologist for evaluation and management of the systemic immunologic component of the disease.The negative pressure wound therapy was discon-tinued after 7 months of treatment, when only a smallisland of granulation tissue remained in the area of theoriginal wound (Fig. 4). The wound was then managedwith a series of absorptive primary dressings securedwith a three- or four-layered compressive wrap to con-trol edema. For a short period, the wound was com-
Figure 1.
Initial appearance of circumferential necro-tizing calf wound that was diagnosed as pyodermagangrenosum.
Figure 2.
Depiction of negative pressure wound ther-apy. Two TRAC pads (KCI, Inc) were used to ensureequal distribution of negative pressure. Note the Y-connector at left.

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