Ion Implantation and Synthesis of Materials - Studium

154 11 Si Slicing and Layer Transfer: Ion-CutFig. 11.10. High magnification bright field XTEM images of the implantation damage zonein the (a) as-implanted sample and (b) in the near surface region in the exfoliated layer afterion cutting. The microcavities are viewed in focus in the as-implanted sample and in underfocus in the exfoliated layerThe peaks near the newly-formed surfaces are much more pronounced than inthe as-implanted sample.The data presented here shows that the H implanted into Si evolves into Hplatelets, and that the H-platelet distribution follows the damage profile. It isobvious that the H platelets play an important role in the Ion-Cut process.However, to produce cleavage of the silicon crystal, the H atoms must ultimatelyagglomerate to produce highly pressurized H 2 gas bubbles, which provide theforce for crack propagation. Hydrogen platelets are apparently the nuclei for H 2gas bubbles. Figure 11.12 shows schematically the development of implantedhydrogen into hydrogen platelets and ultimately into H 2 gas bubbles. In silicon,implanted hydrogen is known to be trapped at various implantation-induced latticedefects, such as vacancies or silicon interstitials, passivating the dangling siliconbonds. A common location for hydrogen atoms in p-type Si is the bond-centeredsite between two Si atoms at their lattice site. The occupation of hydrogen in thebond centers of the silicon crystal results in the formation of {100} H planes.Studies have shown that ion irradiation damage in Si creates defects that in turnproduce in-plane compressive stresses (Volkert 1991) and an elastic out-of-planetensile strain; the peak in the strain distribution is collocated with the damage peak(Paine et al. 1987; Tkachev et al. 1984). The out-of-plane tensile strain facilitatesthe incorporation of hydrogen atoms into the bond-centered sites between twoneighboring silicon atoms by reducing the strain energy needed in replacing theSi–H–Si bond with the Si–Si bond. Prestraining the lattice with radiation damageresults in a smaller length change upon H incorporation, thereby reducing thestrain energy barrier to this process. This explains why the H-platelet densitypeaks at the depth of maximum implantation damage.