Damage formation and annealing studies of low energy ion implants ...

collision cascade and are mobile at room temperature, in combination with the operation
of dynamic annealing. The migration and trapping of these point defects at the oxide
interface is the origin of the formation of the amorphous, near-surface damage layer. A
similar process in which the surface represents a trap capturing interstitials (of which
there is an excess over vacancies (27)), can also explain the formation of the damage
layer observed for the case of the low dose, low energy As implants. In this early stage
amorphisation will be nucleation limited (14, 16). At a later stage in the process, the
planar growth of the amorphous layer into the underlying bulk material is observed.
This phenomenon is due not only to the accumulation of mobile interstitials originating
from greater depths at the advancing amorphous/crystalline interface, but also to the
expansion of disordered regions due to the increasing density of coverage of the Si
crystal matrix by the growing number of collision cascades that ultimately overlap. The
type of planar growth seen here at room temperature has also been observed at elevated
temperatures in studies of amorphisation / recrystallisation of the Si matrix under higher
energy ion bombardment (11, 14-16). Similar processes to those described above were
considered to be responsible for the planar growth.
Considering next the development of the As profile and its correlation with the
displaced Si distribution, Figure 5.2 shows that at doses below 1 × 10 14 cm -2 the
implanted As profile is significantly shallower than the TRIM calculated one which is
also drawn in the figure. However for increasing doses the As profile peak shifts to
greater depths, from 3.6 nm at 4 × 10 14 cm -2 to 5.5 nm for 1.8 × 10 15 cm -2 , as indicated
by the arrows in the figure. At the same time the As profile broadens towards the
surface, as is clearly visible for doses of 4 × 10 14 cm -2 and above. The latter behaviour
can be explained on the basis of range shortening due to the changing composition of
the matrix through As accumulation, collisional redistribution and / or collective mass
flows to take account of the accommodation of the implanted ions. Sputtering can be
largely ignored, as a TRIM calculation shows that 2.5 keV implanted to a dose of 1.8 ×
10 15 cm -2 causes the removal of less than 0.3 nm oxide. The incident ions will of course
cause disorder to the native oxide which remains unnoticed by MEIS. Figure 5.2 clearly
shows that the movement of As to greater depth with increasing dose occurs in parallel
with the planar growth of the amorphous layer. This indicates that the two effects are
closely related. On the basis of ballistics arguments, there is no doubt that a substantial
fraction of the As is initially stopped beyond the amorphous /crystalline interface.
Since MEIS does not detect any clear presence of As at these depths, the
possibility of the dopant having moved into substitutional positions and therefore being
111