Font Size: a A A

Damage mechanisms in shock wave lithotripsy (SWL)

Posted on:2002-12-02Degree:Ph.DType:Thesis
University:California Institute of TechnologyCandidate:Lokhandwalla, MurtuzaFull Text:PDF
GTID:2464390011997872Subject:Engineering
Abstract/Summary:
Shock wave lithotripsy is a ‘non-invasive’ therapy for treating kidney stones. Focused shock waves fragment stones to a size that can be passed naturally. There is, however, considerable tissue injury, and the mechanisms of stone fragmentation and tissue injury are not well understood. This work investigates potential tissue damage mechanisms, with an aim towards enhancing stone fragmentation and minimizing tissue damage.; Lysis of red blood cells (RBC's) due to in vitro exposure to shock waves was investigated. Fluid flow-fields induced by a non-uniform shock wave, as well as radial expansion/implosion of a bubble was hypothesized to cause cell lysis. Both the above flow-fields constitute an unsteady extensional flow, exerting inertial as well as viscous forces on the RBC membrane. The resultant membrane tension and the membrane areal strain due to the above flow-fields were estimated. Both were found to exert a significantly higher inertial force (50–100 mN/m) than the critical membrane tension (10 mN/m). Bubble-induced flow-field was estimated to last for a longer duration (∼1 microsec) compared to the shock-induced flow (∼1 ns) and hence, was predicted to be lytically more effective, in typical in vitro experimental conditions. However, in vivo conditions severely constrain bubble growth, and cell lysis due to shock-induced shear could be dominant.; Hemolysis due to shock-induced shear, in absence of cavitation, was experimentally investigated. The lithotripter-generated shock wave was refocused by a parabolic reflector. This refocused wave-field had a tighter focus (smaller beam-width and a higher amplitude) than the lithotripter wave-field. Cavitation was eliminated by applying overpressure to the fluid. Acoustic emissions due to bubble activity were monitored by a novel passive cavitation detector (HP-PCD). Aluminum foils were also used to differentiate cavitational from non-cavitational mode of damage. RBC's were exposed to the reflected wave-field from the parabolic reflector and also from a flat reflector, the latter serving as a control experiment. Exposure to the wave-field from the parabolic reflector increased hemolysis four-fold compared to untreated controls and was twice that of cell lysis with the flat reflector. This result corroborated the hypothesis of shock-induced shear as a damage mechanism.
Keywords/Search Tags:Shock, Damage, Cell lysis, Reflector, Mechanisms
Related items