The ion-cut technology used for the fabrication of Silicon-On-Insulator (SOI) substrates involves a thermally activated layer splitting process with the evolution of hydrogenated defect complexes into microcracks in H-implanted Si. Since the layer splitting process is highly correlated to the interaction of H atoms with defects, it is expected that the blistering kinetics arising from H implantation would vary with crystal plane orientation of Si substrates. This study presents a thorough investigation of the influence of crystal plane orientation on the blistering kinetics and defect evolution in H-implanted Si. Three Si substrates of Si(100), Si(111), and Si(110) were implanted with H2+ ions at an accelerated energy of 40 keV to a fluence of 2.5 × 1016 cm−2. After ion implantation, the blistering characteristics, defect complexes, and microstructure of the specimens were characterized by SIMS, in-situ OM observation system, Raman spectra, and XTEM. The results revealed that two limiting steps of H atom diffusion dominate the blistering process in different temperature intervals. The transformation of VH3 (or V2H6) defect complex into Si:H surface state is mainly prevailing in the low-temperature interval. The blistering characteristics of Si showed a high correlation with the crystal plane orientation of Si substrates due to the difference in planar atomic density. Si(110) having a largest planar atomic density corresponds to a highest threshold temperature and a longest onset time for blister formation, followed by Si(111) and Si(100) in turn. The correlation between blistering characteristics and substrate orientation can be attributed to the fact that H implantation leads to different densities of the H-terminated platelets in Si specimens with various planar atomic densities, thus affecting the efficiency of free H atom diffusion into platelets and the blister growth as well. A conclusive finding from this study is that substrate orientation diversifies the defect density in damage layer caused by hydrogen implantation, which could change the nucleation sites of platelets available for blister formation and eventually influence the blistering efficiency and microcrack extension.