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CO 2 laser physics and tissue interactions in skin
Author(s) -
Fulton James E.,
Shitabata Paul K.
Publication year - 1999
Publication title -
lasers in surgery and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.888
H-Index - 112
eISSN - 1096-9101
pISSN - 0196-8092
DOI - 10.1002/(sici)1096-9101(1999)24:2<113::aid-lsm6>3.0.co;2-7
Subject(s) - dermis , laser , erythema , lesion , pathology , wound healing , skin lesion , medicine , dermatology , surgery , optics , physics
Background and Objectives The theoretical model of CO 2 laser tissue interaction appeared to be too simplistic. To explain the reactions seen in skin, a more complex model was needed. We hoped to correlate the clinical‐histologic patterns of CO 2 laser tissue interactions. Study Design/Materials and Methods The Ultrapulse CO 2 laser was used on normal and pathologic skin conditions. Clinical observations were correlated with histologic examinations of biopsies. Results It was possible to demonstrate cavitation at the dermal‐epidermal junction 2–3 diameters beyond the actual spot of CO 2 laser contact with the skin. Dermal heat damage was seen as homogenization of collagen 1–2 diameters beyond the spot of laser contact. This flow of energy laterally at the dermal‐epidermal junction and vertically down the skin follicles was both clinically beneficial and detrimental. Beneficially, superficial skin lesions separated at this junction and were easily removed. The heat coagulation of the dermis facilitated lesion removal without bleeding. The clinician had a better view of the pathology and could find focal zones of deeper pathology that could be easily re‐treated. Detrimentally, this extended damage delayed wound healing and led to persistent erythema. Conclusion These clinical‐histologic correlations have provided a better understanding of CO 2 laser tissue interactions in skin. It has been possible to take advantage of these findings to remove pathologic skin conditions more efficiently. Lasers Surg. Med. 24:113–121, 1999. © 1999 Wiley‐Liss, Inc.