Damage Mechanisms in Shock Wave Lithotripsy (SWL)

Citation

Lokhandwalla, Murtuza (2001) Damage Mechanisms in Shock Wave Lithotripsy (SWL). Dissertation (Ph.D.), California Institute of Technology. doi:10.7907/VZWS-7Z85. https://resolver.caltech.edu/CaltechETD:etd-03162005-130412

Abstract

NOTE: Text or symbols not renderable in plain ASCII are indicated by [...]. Abstract is included in .pdf document. 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 associated with this treatment, and the mechanisms of stone fragmentation and tissue injury are not well understood. This work investigates potential tissue damage mechanisms, with an aim towards modifying the wave-field parameters, so as to enhance stone fragmentation and minimize tissue damage. Lysis of red blood cells (RBC's) due to in vitro exposure to shock waves was considered as a model of cellular level damage. Fluid flow-fields induced by a non-uniform shock wave, as well as radial expansion/implosion of a bubble was hypothesized to cause lysis of cells. 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 ([Delta]A/A) 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 ([...]) compared to the shock-induced flow ([...]) 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. A novel passive cavitation detector (HP-PCD) operating at high overpressure (upto 7 MPa) was used to measure acoustic emission due to bubble activity. Aluminum foils were also used to differentiate cavitational from non-cavitational mode of damage. RBC's suspended in phosphate-buffered saline PBS) 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 cell damage mechanism in the absence of cavitation.

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