Fig. 1 shows the representative high-speed sequences of EHL-induced bubble oscillation both in water and inside silicone tubes at an output setting of 70%. Following each spark, a cavitation bubble was produced and expanded freely in water to a maximum size of 5 mm and then collapse. In comparison, the expansion of an EHL-induced bubble inside a 1.5 mm and 3.5 mm silicone tubes were significantly constrained by the tube wall, leading to a shortened expansion of the bubble and more rapid collapse. It is interesting to note that the smaller the tube size, the larger the relative dilation of the tube. However, no rupture of the silicone tubes was observed after 100 shocks. The AE signals measured simultaneously revealed the significant reduction in the collapse time of the bubble inside the silicone tubes compared with that in water (see Fig. 2a). However, in contrast to the strong collapse in water, the secondary peak pressure from bubble collapse inside the silicone tubes was greatly diminished because of the significantly reduced bubble expansion (see Fig. 2b).
2. Shock wave-induced bubble oscillation in tissue phantom and
mechanism of vessel rupture
To investigate the vascular injury during SWL, silicone tubes of 500
mm inner diameter and cellulose hollow fibers of 200 mm inner diameter
were used as tissue phantom. High speed imaging system (see Fig.
3) was also set up to visualize the shock wave-induced bubble dynamics
inside silicone tube and hollow fiber. Fig. 4 shows
the bubble oscillation in silicone tube and hollow fiber and the rupture
of the fiber. It can be seen that the expansion of the shock wave-induced
bubbles was significantly constrained by the tube wall. The smaller the
tube the shorter the collapse time of the bubble would be. On the other
hand, the expansion of the bubbles inside the tube also cause significant
dilation of the tube wall. In our experiments, no damage was observed in
the silicone tubes after several hundred shocks. This is partially attributable
to the large wall thickness (300 to 400mm) of the silicone tubes and partially
to their intrinsic tensile failure strength (sf
=
8.4 MPa) which is much higher than that of small blood vessels (sf=
1.47 ~ 5.07 MPa). However, for the hollow fiber (3 mm wall thickness),
only about 20 shocks generated by the XL-1 lithotripter at 16 KV were needed
to cause a rupture, with circulating fluid inside the hollow fiber leaking
out into the surrounding caster oil (Fig. 4c). The
number of shocks needed to cause a rupture varied with the output voltage
of the lithotripter (Fig. 5). The increased propensity
for rupture at a higher KV (thus a potentially larger bubble expansion)
indicated that the ratio between the potential bubble expansion and vessel
size is an important determinant for the rupture. Interestingly, when the
pressure waveform of the XL-1 generated shock wave was inverted by a pressure-release
reflector insert to suppress the large intraluminal bubble expansion, no
rupture of the hollow fibers could be observed up to 100 shocks at 20KV.
These results strongly support our hypothesis that large intraluminal bubble
expansion could rupture capillary and small blood vessels if adequate cavitation
nuclei exist in blood.
See following two papers for more and detail information.