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  Vol. 129 No. 8, August 1993 TABLE OF CONTENTS
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Skin Graft Take and Healing Following 193-nm Excimer, Continuous-Wave Carbon Dioxide (CO2), Pulsed CO2, or Pulsed Holmium:YAG Laser Ablation of the Graft Bed

Howard A. Green, MD; Elizabeth E. Burd, MB, ChB, FRCS(Ed); Norman S. Nishioka, MD; Carolyn C. Compton, MD, PhD

Arch Dermatol. 1993;129(8):979-988.


Abstract

Background
Ablative lasers have been used for cutaneous surgery for greater than two decades since they can remove skin and skin lesions bloodlessly and efficiently. Because full-thickness skin wounds created after thermal laser ablation may require skin grafting in order to heal, we have examined the effect of the residual laser-induced thermal damage in the wound bed on subsequent skin graft take and healing. In a pig model, four different pulsed and continuous-wave lasers with varying wavelengths and radiant energy exposures were used to create uniform fascial graft bed thermal damage of approximately 25,160, 470, and 1100 µm. Meshed split-thickness skin graft take and healing on the thermally damaged fascial graft beds were examined on a gross and microscopic level on days 3 and 7, and then weekly up to 42 days.

Results
Laser-induced thermal damage on the graft bed measuring greater than 160±60 µm in depth significantly decreased skin graft take. Other deleterious effects included delayed graft revascularization, increased inflammatory cell infiltrate at the graft-wound bed interface, and accelerated formation of hypertrophied fibrous tissue within the graft bed and underlying muscle.

Conclusions
Ablative lasers developed for cutaneous surgery should create less than 160 ±60 µm of residual thermal damage to permit optimal skin graft take and healing. Pulsed carbon dioxide and 193-nm excimer lasers may be valuable instruments for the removal of full-thickness skin, skin lesions, and necrotic tissue, since they create wound beds with minimal thermal damage permitting graft take comparable to that achieved with standard surgical techniques.

(Arch Dermatol. 1993;129:979-988)



Author Affiliations

From the Department of Dermatology, Boston (Mass) University School of Medicine (Dr Green); University of Bristol (England) Department of Pathology and Microbiology, Bristol Royal Infirmary (Dr Burd); Wellman Laboratory of Photomedicine, Massachusetts General Hospital, Boston (Dr Nishioka); and Department of Pathology, Harvard Medical School, Shriners Institute, Massachusetts General Hospital, Boston (Dr Compton).



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