Chapter 2: Laser Treatment of Cutaneous Vascular Lesions

INTRODUCTION

Destruction of vascular lesions by laser treatment represents one of the earliest applications of selective photothermolysis, a principle elucidated by Anderson and Parrish.¹ The first reports of successful clinical laser treatment of vascular lesions were made by Goldman and colleagues in 1968.² Laser treatment of vascular lesions is accomplished most often using the principle of selective photothermolysis, using nonablative vascular-selective lasers that target hemoglobin in the vessel. Alternative choices such as ablative lasers or photodynamic therapy have also been used to destroy vessels. When the appropriate laser and settings are selected and applied, lasers demonstrate success in safely destroying cutaneous vessels of various types, sizes, and depths.

SELECTIVE PHOTOTHERMOLYSIS OF VESSELS

Vascular lesions are composed of endothelial cell–lined vessels containing colorless lymphatic fluid, blood colored by hemoglobin, or both. Vessels vary in diameter, thickness, and depth. Hemoglobin present may be in varying states of oxygenation, including deoxyhemoglobin, oxyhemoglobin, methemoglobin, or any combination of these forms. Selective photothermolysis (Figure 2-1) employs the observation that preferential absorption of a laser pulse by certain pigmented chromophores causes their heating and subsequent thermal destruction, with relative sparing of surrounding structures. Excess thermal energy absorbed by the pigmented target diffuses to surrounding targets in a process termed thermal relaxation. In order to selectively destroy vessels, the laser wavelength should be preferentially absorbed by the chromophore present in the vessel, which in the case of blood-filled lesions is hemoglobin in varying forms. The wavelength must also be sufficiently long to reach the targeted vessel depth. The pulse duration should be equal to or less than the vessel thermal relaxation time (τ_r) to avoid heat damage to the surrounding structures (for cylindrical vessels, τ_r = d²/16κ; κ = 1.3 × 10⁻³ cm²/s).¹ The energy delivered, or fluence, should be sufficient to damage the vessel(s) while also conservative enough to limit injury of surrounding tissue.

MECHANISM OF VASCULAR INJURY

The ultimate target is the vascular endothelium. Selective photothermolysis indirectly injures the endothelium by heating the chromophore hemoglobin within the vessel, leading to formation of an occlusive mass of photocoagulated erythrocytes, with subsequent heat transfer to the endothelium and endothelial cell destruction by coagulation necrosis (achieved at a critical temperature of >70°C for thermal denaturation).³ Photomechanical effects including cavitation (water vaporization with steam bubble expansion and collapse) may also damage endothelial cells.

Histologic evaluation after selective photothermolysis of cutaneous vessels (Figure 2-2) demonstrates immediate brown discoloration of the blood with a viscous decrease in flow, hemostasis, and formation of a coagulated erythrocyte mass. Vessel rupture with hemorrhage may be observed at purpuric settings.¹ By 24 hours, vasculitis-like changes of neutrophilic and lymphocytic ...