Histological and modeling study of skin thermal injury to 2.0 μm laser irradiation

Abstract

Qualitative and quantitative gross histopathologic studies of skin damage were performed at 48 hours after irradiation with a 2.0 microm thulium CW laser to determine the mechanisms of laser effects in the skin under various exposure conditions. Pig skin lesions were created at, below and beyond the threshold irradiation conditions for grossly apparent thermal lesions. Histological sections of these lesions were studied. For each threshold lesion, four quantitative histopathological parameters were measured: the widths of (1) epidermal necrosis at the surface, (2) the outer boundary of the thrombosis zone, (3) the depth of vascular thrombosis, and (4) the depth of perivascular inflammation (increased infiltrates of inflammatory cells) and edema. The quantitative histopathologic data were compared with predictions using an optical-thermal-damage model. Histologically, the thermal damage mechanisms for grossly apparent threshold lesions of persistent redness at 48 hours included necrosis of the epidermal cells, intravascular thrombosis and perivascular inflammation and edema in dermal blood vessels. At irradiation levels just below 'gross threshold', non-lethal thermal effects, such as perivascular inflammation and edema were found in the histological sections. When the radiation reached about 1.5-2.5 times beyond the threshold, decrease of dermal collagen birefringence was observed. A sequence of damage endpoints was defined in the skin as power increased. By choosing rate process coefficients to match specific mechanisms of lethal thermal damage, the optical-thermal-damage model is capable of predicting various types of thermal injury in the skin, such as epidermal necrosis, vascular thrombosis, and dermal collagen coagulation.