Cutaneous candidiasis as a cause of delayed surgical wound healing

Cutaneous candidiasis as a cause of delayed surgical wound healing

Journal of the AmericanAcademyof Dermatology Volume30, Number 6 al. Akute Niereninsuffizienz bei der Behandlung der Psoriasis mit Furnarsaureester, S...

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Journal of the AmericanAcademyof Dermatology Volume30, Number 6

al. Akute Niereninsuffizienz bei der Behandlung der Psoriasis mit Furnarsaureester, Schweiz Moo Wochenschr 1989;119:826-30. 3. DubielW, HappieR. Behandlungsversuch mit Fumarsauremonoethylester bei Psoriasis vulgaris. Z Haut-Geschl Kr 1972;13:545-50. 4. Raab W. Treatment of psoriasis withfumaric acidand fumarates. Z Hautkr 1959;10:671-9. 5. PetresJ, KalkoffKW, BaronD, et al. Der Einfluss von Fumarsauremonoethylester auf die Nucleinsaure und Proteinsynthese PHA-stimulierter menschlicher Lymphozyten. Arch Derm Forsch 1975;251:295-300. 6. Hagedorn M, KalkoffKW, Kiefer G, et al. Fumarsauremonoethylester: Wirkung auf DNA-Synthese und erste tierexperimentelle Befunde. Arch Derm Forsch 1975; 254:67-73. 7. vanDijk E. Fumaarzuurvoorde behandeling vanpatienten met psoriasis. Ned Tijdschr Geneesk 1985;129:485-6.

Giandoni and Grabski 8. BayardW, Hunziker Th, Krebs A, et al. Perorale Langzeitbehandlung der Psoriasis mit Fumarsiiurederivaten. Hautarzt 1987;38:279-85. 9. Nieboer C, de Hoop D, Van Loenen AC, et al.Systemic therapywith fumaric acid derivatives: new possibilities in the treatmentof psoriasis. JAM ACAD DERMATOL 1989; 20:601-8. 10. Nugteren-Huying WM, vanderSchroeff JG, Hermans J, et al. Fumaric acid therapy for psoriasis: a randomized, double-blind, placebo-controlled study. J AM ACAD DERMATOL 1990;22:311-2. 11. Fredriksson T, Petterson V. Severe psoriasis: oraltherapy with a newretinoid. Dermatologica 1978;157:238-44. 12. Matthes V, Pawlak F, Altmeyer P. Oraltherapy of severe psoriasis byderivatives offumaric acid: anopen long-term studyover oneyear[Abstract]. Presented atthe 18thWorld Congress of Dermatology, New York, June 12-18, 1992. 1992:146A.

Cutaneous candidiasis as a cause of delayed surgical wound healing Martin B. Giandoni, MD, and William J. Grabski, MD San Antonio, Texas Background: Reports in the literature of surgical wounds infected with Candida species are scant.

Objective: We describe a subset of patients with cutaneous candidiasis whose only clinical finding was delayed wound healing. Methods: Surgical wounds managed with moist occlusive postoperative dressings were observed for delayed healing. Results: Three patients are described who demonstrated delayed wound healing with failure to epithelialize. Fungal cultures from each patient revealed heavy growth of Candida. The problem resolved quickly with a modified wound care regimen and application of an antiyeast cream. Conclusion: Cutaneous candidiasis can be a cause of delayed wound healing, especially in surgical wounds treated with antibacterial ointments and occlusive dressings. (J AM ACAD DERMATOL 1994;30:981-4.)

Cutaneous candidiasis associated with a surgical wound is probablymore common than is generally recognized. I, 2 Cutaneous candidiasis usually appears as a brightly erythematous eruption with superficial erosions, crusting, and small pustules in both a central and satellite distribution. Occasionally this appearance is associated with a surgical wound, but fewreportsinthe literature describe this complication. We describe three illustrative paFrom the Dermatology Service, Brooke Army MedicalCenter. Presentedat the nationalmeetingofThe American Society forDermatologic Surgery, Charleston, S.C., March 18,1993. Reprints not available.


tients, although wehaveseen manymore, with surgicalwounds that failed to healcompletely after an extended period. We postulate that cutaneous candidiasis associated with a surgical wound that fails to reepithelialize is common. Thisphenomenon has beenbriefly notedpreviously.? andwebelieve that it should be emphasized further. We discuss the spectrum of clinical presentation of this condition, the factors that favor cutaneous candidiasis in a surgical wound, and a simple regimen to treat the condition. CASE REPORTS

Case 1. An Sl-year-old woman had a large basal cell carcinoma excised from her left cheek. The defect re-



Giandoni and Grabski

Journal of the American Academy of Dermatology June 1994

Fig. 1. Patient 1. Skin graft 3 months after surgery.

Fig. 2. Patient 1. Skin graft reepithelialized after 2 weeks of anticandidal treatment.

quired a complex closure that included a left cheek and neck rotation flap and a full-thickness skin graft. Wound care consisted of daily cleansing with hydrogen peroxide and application of bacitracin ointment and a nonadherent bandage. Wound healing initially progressed satisfactorily with removal of sutures at 1 week and continuing wound care for the graft. After 3 months the graft had failed to epithelialize (Fig. 1). No inflammation, exudate, or signs of clinical infection were present; and bacterial cultures were negative. Potassium hydroxide (KOH) and Gram stain were positive for pseudohyphae, and fungal cultures showed heavy growth of Candida albicans. The antibacterial ointment and the occlusive dressing were discontinued, and 1% clotrimazole cream was applied twice daily. The wound epithelialized within 2 weeks (Fig. 2). Case 2. An 85-year-old man underwent curettage and electrodessication of a superficial squamous cell carcinoma near his left elbow. Wound care consisted of daily cleansing with hydrogen peroxide and application of bacitracin ointment and a nonadherent dressing. At 6 weeks healthy granulation tissue was present in the wound but no evidence of epithelialization had occurred (Fig. 3). No inflammation or sign of infection was present. Bacterial

cultures were negative, but fungal cultures showedheavy growth of C. a/bieans. A regimen consisting of elimination of the antibacterial ointment and occlusivedressing, and twice-dailyapplication of 1% oxiconazolecream, was initiated. Complete epithelialization occurred within 2 weeks. Case 3. An 81-year-old woman underwent superficial dermabrasion of a full-thickness skin graft of the left nasal tip to improve the contour. Wound care consisted of daily cleaning with hydrogen peroxide and application of bacitracin ointment and a nonadherent dressing. At 5 weeks the wound had not epithelialized (Fig. 4). No apparent inflammation or signs of infection were present. Bacterial cultures were negative,but fungal cultures grew C. a/bieans. An anticandidal wound care regimen was initiated, and full epithelialization occurred within 2 weeks.

DISCUSSION Factors that predispose patients to cutaneous candidiasis are frequently divided into local and systemic.' The relative importance of these predisposing factors has been evaluated in several studies

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Fig. 3. Patient 2. Curettage site 6 weeks after procedure.

Fig. 4. Patient 3. Dermabrasion site 5 weeks after procedure.

in both animal and human models.t" The three factors that are most significant for cutaneous wounds are destruction of the epidermal barrier, use of a local antibacterial agent, and long-term occlusion, as occurs with the standard moist occlusive antibacterial postoperative wound care regimen that is believed to enhance wound healing. Of these three predisposing factors, experimental models indicate that long-term occlusion is the most important. The typical clinical presentation of cutaneous candidiasis is infrequently associated with a surgical wound. Our experience illustrated in the three case reports suggests that within the clinical spectrum of

surgical wound-associated cutaneous candidiasis exists a subset with no apparent inflammation or pustules, whose only clinical manifestation is delayed wound healing. Several factors may explain the paucity of reports of cutaneous candidiasis in surgical wounds. It is generally an innocuous condition that clears spontaneously without permanent sequelae. Fungal cultures and KOH examination are not often performed, and the condition passes unrecognized. Probably the most important factor is that a causeand-effect relationship is difficult to establish. C. albicans is part of the normal flora on mucous

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membranes and sometimes on the skin. Eightypercent of pathogenic yeast isolated from the human body is C albicans.' The isolation froma cutaneous lesion of an organism that ispart ofthe normalflora cannotestablish causeunless other pertinentcriteria are considered. In 1984 Siegle et at 1 reported three cases of cutaneous candidiasis as a complication of facial dermabrasion. Their criteriafor establishing the diagnosis included the presence of a favorable environment for Candida growth, the development of the characteristic pustular dermatitis, culture and KOH isolation of Candida, and rapid uncomplicated resolution with anticandidal therapy. We believe our patients represent a distinct subset in the spectrumof cutaneous candidiasis. Cultureof Candida alonefrom a wound that fails to reepithelialize strongly suggests a causative rolefor this organism. The presence ofa wound environment that enhances Candida growthand the rapid resolution ofthe condition with an anticandidaregimen further support the diagnosis of cutaneous candidiasis. Our approach to anticandidal therapyin wounds withthiscomplication has beendescribed. Actually, elimination of the occlusive dressing and the antibacterial ointment would probably suffice. This is

Journal of the American Academy of Dermatology June 1994

what usually occurs in cutaneous candidiasis associated with a suturedwound. Most cases of failure to epithelialize that we attribute to candidiasis have been wounds that heal by secondary intention. These, westill believe, healbest in a moist and partiallyoccluded environment. Our useof an anticandidalcreamrepresents a compromise between a dry Candida-inhibiting environment and a moist optimal wound-healing environment. REFERENCES

1. Siegle RJ, Chiararnonti A, Knox DW, et aL Cutaneous candidosis as a complication offacialdermabrasion. J DermatolSurg OncoI1984;10:891-4. 2. Selden ST.Candida: a common culprit[Letter]. J Dermatal Surg Oneal 1985;11:958. 3. Rosman N. Oropharyngeal and cutaneous candidosis in patients withdecreased resistance to infections. Acta Derm Venereol [Suppl] (Stockh) 1986;121:47-9. 4. Maibach HI, Kligman AM. The biology of experimental human cutaneous moniliasis (Candida a/bicans). Arch DermatoI1962;85:233-54. 5. Rebora A, Marples RR, Kligman AM. Experimental infection with Candida a/bieans. Arch Dermatol 1973; 108:69-73. 6. RayTL, Wuepper KD.Experimental cutaneous candidiasis in rodents. J Invest DermatoI1976;66:29-33. 7. Stenderup A. Ecology of yeastand epidemiology of yeast infections. Acta Derm Venereol [Suppl] (Stockh) 1986; 121:27-37.