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Aspergillosis Presenting As Koebner's Phenomenon in a Healed Scaldp Burns 26 (2000) 92±96 www.elsevier.com/locate/burns Aspergillosis presenting as Koebner's phenomenon in a healed scald p G. Williams, N. Moiemen, J.D. Frame* St Andrews Centre for Plastic Surgery and Burns, Broom®eld Hospital, Court Road, Chelmsford CM1 7ET, UK. Accepted 18 May 1999 Abstract Koebner's phenomenon is an uncommon postburn complication. The following report describes a female child who sustained an 80% total body surface area scald which healed with conservative treatment. She developed a cutaneous Aspergillus infection involving only the previously scalded areas. The uninjured skin remained normal. She went on to develop systemic aspergillosis and died of multi-organ failure. # 2000 Elsevier Science Ltd and ISBI. All rights reserved. Keywords: Koebner's phenomenon; Aspergillus; Burn wound infection 1. Introduction susceptibility of healed thermally injured skin to infec- tious dermatoses. It may also be that the incidence of Koebner's phenomenon was ®rst published in 1877 Koebner's phenomenon in burns is underreported. by the German dermatologist, Heinrich Koebner (1838±1904) [1]. It is now de®ned as the development of lesions in previously normal skin that has been trau- 2. Case report matised either externally or internally. The original and most widely described disease exhibiting A four year old female black child was admitted to Koebner's phenomenon is psoriasis but it has also the regional burns unit with an 80% total body surface been described in a number of other skin disorders area scald following immersion in a hot bath. Her face including lichen planus and vitiligo. There is only one and patches on the abdomen, chest, left thigh, dorsal previous report of Koebner's phenomenon in burns left upper limb and both knees posteriorly were and this involved an outbreak of viral warts con®ned spared. The majority of the scald was assessed as to an area of skin previously scalded [2]. The aetiology super®cial partial thickness. (Fig. 1). She was managed of Koebner's phenomenon is unknown although a var- conservatively and resuscitated with intravenous ¯uids. iety of theories have been proposed including vascular, Early in the second week she became unwell and dermal, neural, genetic, hormonal and enzymatic fac- underwent tangential excision of deep dermal areas on tors. In burns, it may be that antigen presenting cells her buttocks, right hand and right shoulder. In the (Langerhan's cells) are reduced in number at the site third and fourth weeks postadmission, she had mul- of injury. This may oer a possible explanation for the tiple septic episodes with positive blood cultures for gram-negative and gram-positive organisms, for which she received a variety of antibiotics. During this period p This paper was presented at the 10th Congress of the her scald completely healed and her discharge home International Society for Burn Injuries in Jerusalem, November was planned. However, she suddenly developed fulmi- 1998. * Corresponding author. Tel.: +44-1245-516-199; fax: +44-1245- nant gram-negative sepsis from an unidenti®ed source 516-219. and required ventilation and haemo®ltration. She was 0305-4179/00/$20.00 # 2000 Elsevier Science Ltd and ISBI. All rights reserved. PII: S0305-4179(99)00100-X G. Williams et al. / Burns 26 (2000) 92±96 93 Fig. 1. Appearance of partial thickness scald on admission to hospital. transferred to a paediatric intensive care unit as her 3. Discussion healed scald was not thought to be the source of her illness. There she was treated symptomatically with Until 1967, only ®ve cases of fungal burn wound antibiotics, inotropes and jet ventilation. She returned infection had been reported. The introduction of to the burns unit o cardiopulmonary support and topical antimicrobials such as mafenide acetate and sil- systemically much improved. However, her healed ver sulfadiazine had a major in¯uence on the reduction scald had started to break down with widespread, of gram-negative burn wound infection but was associ- small, dark necrotic ulcers. These were biopsied and ated with an increased incidence of opportunistic infec- shown to contain Aspergillus on the surface. (Fig. 2). tions by yeasts and fungi. She was started on intravenous Amphotericin B but Aspergillus species are ubiquitous, commonly occur- deteriorated quickly. Within 4 days, the ulcers had ring in soil, water and the decaying of vegetation. coalesced to cover the entire 80% originally scalded. Reservoirs in hospitals from which these fungi have (Fig. 3). The unscalded skin remained healthy. She been cultured include un®ltered air, ventilation sys- underwent fascial excision of all involved tissue and all tems, contaminated dust dislodged during construc- areas were covered with Integra (Integra Lifesciences, tion, carpeting, food and ornamental plants [3]. Plainsboro, NJ 08536). Biopsies taken at this time In any deteriorating burn wound, the diagnosis of a showed the Aspergillus not only in®ltrating to a much fungal infection should be kept in mind but especially deeper level, but also present in the walls and lumens with the appearance of dark, ulcerated areas. Biopsy of blood vessels indicating blood borne dissemination. and histological examination is crucial as only thirty (Fig. 4). She went on to develop multi-organ failure percent of histologically proven infections are con- and died forty ®ve days following admission. Post ®rmed with culture[4]. mortem examination showed both lungs extensively Radical wide local excision is recommended once in®ltrated with Aspergillus. diagnosis is con®rmed and this may be best achieved 94 G. Williams et al. / Burns 26 (2000) 92±96 by amputation if infection is con®ned to the limbs [5]. As systemic antifungals have serious toxic side eects, their use should be limited to those patients with disse- minated fungal infections or those who have microvas- cular involvement detected on wound biopsy specimens [6]. In addition, systemic antifungals may be useful perioperatively to prevent local extension of dis- ease from seeding after radical debridement [7]. Epidemics within burns units have been associated with contaminated air-conditioning systems and there- fore installation of high ecacy particulate air ®lters with regular maintenance and microbiological surveil- lance is important. In units where fungal burn wound infection is prevalent, prophylaxis with topical Nystatin has been found to be eective [8]. This case study is interesting because the Aspergillus infection occurred after the scald had healed although it is not possible to say when the wound was inocu- lated with the fungus. In addition, it involved only the injured skin and those areas not originally scalded remained healthy. Previously, progression of tissue involvement with fungi has been described from con- tamination to colonisation of the surface, eschar pen- etration, subeschar infection and invasive infection [9]. There was a similar progression in this case, con®rmed on histology, from surface involvement to subcu- taneous spread with vascular invasion and dissemina- tion. The decision to perform radical excision is easier to Fig. 2. Haematoxylin and Eosin stain of biopsy from ulcerated area make when the infection is con®ned to small areas or showing Aspergillus on the surface. single limbs. In this case, there were widespread lesions Fig. 3. Appearance of Aspergillus infected scald prior to fascial excision. Note healthy appearance of uninjured skin. G. Williams et al. / Burns 26 (2000) 92±96 95 Fig. 4. Grocott silver stain of biopsy from ulcerated area showing invasive Aspergillus within the wall and lumen of a subcutaneous blood vessel. involving the trunk and all limbs from the onset and thermal injury on the immunological skin defence eradication of involved tissue required fascial excision mechanisms is required. of 80% of the total body surface area. This case is also particularly tragic because one month following the injury it appeared as if the scald References had healed. There was no evidence from the patient's clinical history that she suered from any pre-existing [1] Miller RAW. The Koebner phenomenon. Int J Dermatol primary immunode®ciency. The fact that the sub- 1982;21:192±7. sequent infection involved only the thermally injured [2] Khan JI, Frame JD. Koebner's phenomenon in burns: another complication following thermal injury. Burns 1993;19(3):249±50. skin is the basis for presenting this as an example of [3] Fridkin SK, Jarvis WR. Epidemiology of nosocomial infections. Koebner's phenomenon. Further work on the eect of Clin Microbiol Rev 1996;9(4):499±511. 96 G. Williams et al. / Burns 26 (2000) 92±96 [4] Bruck HM, Nash G, Pruitt BA. Opportunistic fungal infection [7] Burdge JJ, Rea F, Ayers L. Noncandidal, fungal infections of of the burn wound with phycomycetes and Aspergillus. Arch the burn wound. J Burn Care Rehabil 1980;9(6):599±602. Surg 1971;102:476±82. [8] Levenson C, Wohlford P, Djou J, Evans S, Zawacki B. [5] Stone HH, Cuzzell JZ, Kolb LD, Moskowitz MS, McGowan JE. Preventing postoperative burn wound aspergillosis. J Burn Care Aspergillus infection of the burn wound. J Trauma Rehabil 1991;12(2):132±5. 1979;19(10):765±7. [9] Salisbury RE, Silverstein P, Goodwin MN. Upper extremity fun- [6] Becker WK, Cio WG, McManus AT, et al. Fungal burn gal invasions secondary to large burns. Plast Reconstr Surg wound infection. Arch Surg 1991;126:44±8. 1974;54(6):654±9..
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