The goal of this study is to determine if a high energy laser pulse can cause internal injury that cannot be grossly visualized. High power lasers are currently in development such as the Medical Free Electron Laser (MFEL), the Anti-Ballistic Laser (ABL) and the Tactical High Energy Laser (THEL) and the potential exists for human exposure. Little is known about the effects of these high output lasers on internal organs when a thoracic exposure occurs. This study utilized a 3.8 micron single 8 microsecond pulse laser for all exposures. Yucatan miniature pigs were exposed to a single pulse over the sternum. In addition, some animals were also exposed in the axillary region. Creatine phosphokinase (CPK) and troponin levels were measured prior to and post exposure to assess cardiac muscle damage. Gross and histologic changes were determined for the porcine skin, lung tissue, and cardiac muscle. This study explores if a greater than class 4 laser classification is warranted based on the potential for thoracic injury.
As a consequence of the enormous expansion of laser use in medicine, industry and research, specific safety standards must be developed that appropriately address eye protection. The purpose of this study is to establish injury thresholds to the cornea for 3.8 micron 8 microsecond laser light pulses and to investigate a possible replacement model to live animal testing. Previous studies of pulsed energy absorption at 3.8 microns were performed using rhesus monkey cornea and were at pulse durations two orders of magnitude different than the 8 microsecond pulses used in this study. Ex-vivo pig eyes were exposed at varying energies and evaluated to establish the statistical threshold for corneal damage. Histology was used to determine the extent of damage to the cornea. It is expected that the results will be used to assist in the establishment of safety standards for laser use and offer an alternative to future animal use in establishment of safety standards.
Background and purpose: The purpose of this study is to determine the impact of melanin on skin response to single 3.8 micron, eight microsecond laser pulses and the difference in lesion formation thresholds for input into laser safety standards. Williams et al., performed a study examining laser tissue interaction from 3.8-micron lasers in lightly pigmented Yorkshire pigs (Sus scrofa domestica). However, studies performed by Eggleston et al comparing pigmented and lightly pigmented skin with human skin found that the Yucatan mini-pig is a superior model for laser skin exposures.
Methods: Five Yucatan mini-pigs under general anesthesia were exposed to 3.8 micron laser pulses ranging from 0.8 J/cm2 to 93 J/cm2. Gross examinations were done acutely and 24 hours after laser exposure. Skin biopsies were then collected at various times post exposure, and histologic examinations were conducted. Results: The 24 hour ED50 was determined to be 4.5 J/cm2 with fiducial limits of 6.2 and 2.2 J/cm2. As deposited energy was increased, the lesion presentation ranged from whitening of the epidermis (4 J/cm2) to whitening with inflammatory centers (14 J/cm2), and at the highest energy levels inflammatory areas were replaced with an epidermal ulcerated central area (>21 J/cm2).
Conclusion: Preliminary findings suggest pigmentation or melanin may play a minor role in the mechanism of laser-tissue damage. The ED50 of Yorkshire pigs was 2.6 J/cm2. The ED50 of the Yucatan mini-pig was found to be 3.6 J/cm2, and although it was higher, it is still within the 95% fiducial limits.
The purpose of this study was to evaluate the laser-tissue interactions of engineered human skin and in-vivo pig skin following exposure to a single 3.8 micron laser light pulse. The goal of the study was to determine if these tissues shared common histologic features following laser exposure that might prove useful in developing in-vitro and in-vivo experimental models to predict the bioeffects of human laser exposure. The minimum exposure required to produce gross morphologic changes following a four microsecond, pulsed skin exposure for both models was determined. Histology was used to compare the cellular responses of the experimental models following laser exposure. Eighteen engineered skin equivalents (in-vitro model), were exposed to 3.8 micron laser light and the tissue responses compared to equivalent exposures made on five Yorkshire pigs (in-vivo model). Representative biopsies of pig skin were taken for histologic evaluation from various body locations immediately, one hour, and 24 hours following exposure. The pattern of epithelial changes seen following in-vitro laser exposure of the engineered human skin and in-vivo exposure of pig skin indicated a common histologic response for this particular combination of laser parameters.
Five male Yorkshire pigs were exposed on their flank to 4 microsecond pulses of laser light from a Deuterium Fluoride 3.8 micron Laser at varying energies. A preliminary ED50 threshold for various skin reactions was determined for this laser exposure combination. The animal’s skin was assessed for injury immediately, 1 hour, 24 hours and 72 hours post exposure. In general, energies below 3.2 J/cm2 leave no lasting skin reaction. As energy increased above the threshold, erythema or skin reddening was easily visualized. High-energy pulses appear to produce a “rug burn” erythema without evidence of punctate hemorrage (bleeding) or coagulation. Laser exposure sites on the pigs were also biopsied to obtain histopathological results. These findings suggest that the principal effect of this type of in-vivo laser exposure is removal of the epithelium, while not damaging the papillary dermis or structures beneath the Basement Membrane Zone (BMZ).
Yucatan mini-pigs and Yorkshire pigs were exposed on their flanks to 1318 nm, 0.5 ms laser pulses. Injuries were readily visible on the Yorkshire pigs immediately, one hour, and 24 hours post exposure but difficult to locate at 3 days post exposure. The Yucatan mini-pig injuries were not seen immediately or at one-hour post exposure, but at 24 hours and three days post exposure they were easily identified. The Yorkshire injuries were round red, well demarcated, with a circular pink area of edema. It is hypothesized that skin pigmentation has an effect on the mechanism of 1318 nm laser energy absorption in skin. Pigmentation may have a significant effect on how infrared laser injuries present, develop and heal.
Yucatan Mini-pigs were exposed on their flank to 0.5 milli second 1318 nm pulses of laser light. The ED50 damage threshold was determined for this laser exposure combination. The skin was assessed for injury immediately, at 1 hour, 24 hours and three days post exposure. Generally, at least 24 hours was required for visible lesions to form. It was found that as the duration between exposure and assessment expanded the injury was more easily visualized. Tissue samples were collected for histology at one hour, 24 hours and three days. Histologic sections will be presented in future work. It was also found that the topical application of mineral oil to the area of interest was found to greatly increase the ease of identification of injuries.
An increasing number of industries, to include military, medicinal, and technological arenas, are using 1.3 micron laser systems for which current skin and eye guidelines are identical. No skin threshold, ED50 or exposure data are available. The mechanisms of laser-tissue interaction with skin at 1.3 microns are unknown. Together, these facts necessitate increased research to prevent future laser accidents and injuries. This study examines the method of interaction of 1.3 microns laser light with tissue in the Yorkshire pig. Our research addresses laser-tissue interaction through delivery using a Nd:YAG with an intracavity filter producing 1.3 micron light at 0.5 millisecond exposure time and in the range of 137 to 475 J/cm2. Laser exposure to Yorkshire pigs was evaluated for dermal lesion development. Lesions were appraised for acute, one-hour and 24-hour post exposure presentation.
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