CO2-LASER DEBRIDEMENT OF SULFUR MUSTARD (BIS-2-CHLOROETHYL-SULFIDE) INDUCED CUTANEOUS LESIONS ACCELERATES PRODUCTION OF A NORMAL EPIDERMIS WITH ELIMINATION OF CYTOLOGICAL ATYPIA
Kj. Smith et al., CO2-LASER DEBRIDEMENT OF SULFUR MUSTARD (BIS-2-CHLOROETHYL-SULFIDE) INDUCED CUTANEOUS LESIONS ACCELERATES PRODUCTION OF A NORMAL EPIDERMIS WITH ELIMINATION OF CYTOLOGICAL ATYPIA, British journal of dermatology, 137(4), 1997, pp. 590-594
Sulphur mustard (bis-2-chloroethyl sulphide; HD) exposure acutely prod
uces lesions that vary from mild erythema, to blister formation, to ne
crosis, When blisters occur, with or without necrosis, healing of the
lesions is delayed. Weanling pigs exposed to a mild erythema-producing
dose of HD and to a moderate erythema-producing dose that consistentl
y gave microblister formation were treated with CO2 laser (Tru-Pulse)
debridement at 6, 24 or 48h after exposure. The histopathological feat
ures observed at 14 days after exposure in control skin and skin expos
ed to both HD doses were compared with the features observed in CO2 la
ser-debrided skin in non-exposed and HD-exposed skin sites, The overly
ing epidermis in the non-laser treated lesions was thin, with of cytol
ogical atypia and squamoid changes within the basal cell layer, as wel
l as scattered apoptoticinecratic keratinocytes. An increased inflamma
tory infiltrate and necrobiotic changes in the dermis were seen al the
higher HD dose, AU. laser-treated lesions appeared identical, with a
thick, differentiated epidermis and a well-formed basal cell layer. Th
ere was minimal inflammatory infiltrate. In the papillary dermis there
were increased stromal cells. Laser debridement of mild clinical lesi
ons induced by HD produced a more functional epidermis by 14 days as w
ell as clearing the epidermis of damaged keratinocytes.