Damage Mechanism and Damage Range in Ophthalmic Nd:YAG-Laser Surgery

Abstract

The damage mechanisms of intraocular Nd:YAG laser surgery and their respective damage ranges were investigated in vitro using bovine cornea specimens as a model tissue. The main damage mechanisms are plasma formation and expansion, emission of acoustic transients, and cavitation with jet formation. When a sequence of laser pulses is applied, the interaction of the acoustic transients with gas bubbles remaining from preceding laser exposures is also important. To distinguish the effects caused by the different physical mechanisms, laser pulses were aimed directly onto the cornea, through the cornea, and parallel to the cornea at various distances. Simultaneously, the cavitation bubble size was determined. The surface morphology and section of the same lesions were studied by light and electron microscopy. The primary surgical mechanism is tissue evaporation by the laser plasma, whereas the collateral damage from single laser pulses ins mainly caused by the cavitation and jet formation. The damage range after a 4 mJ laser pulse is 0.8 mm which is slightly larger than the corresponding cavitation bubble radius. The damage range of the acoustic transients produced by a 4 mJ laser pulse is several millimeters, when they can interact with small gas bubbles attached to the corneal endothelium. The damage range of the acoustic transients alone is smaller than that of cavitation. However, on a subcellular level they can possibly cause damage up to a much larger distance. The damage range varies with the cube root of the laser pulse energy. A reduction of collateral effec’s therefore requires the use of small pulse energies.