Fracture mechanics model of stone comminution in ESWL and implications for tissue damage

Focused shock waves administered during extracorporeal shock-wave lithotripsy (ESWL) cause stone fragmentation. The process of stone fragmentation is described in terms of a dynamic fracture process. As is characteristic of all brittle materials, fragmentation requires nucleation, growth and coalescence of flaws, caused by a tensile or shear stress. The mechanisms, operative in the stone, inducing these stresses have been identified as spall and compression-induced tensile microcracks, nucleating at pre-existing flaws. These mechanisms are driven by the lithotripter-generated shock wave and possibly also by cavitation effects in the surrounding fluid. In this paper, the spall mechanism has been analysed, using a cohesive-zone model for the material. The influence of shock wave parameters, and physical properties of stone, on stone comminution is described. The analysis suggests a potential means to exploit the difference between the stone and tissue physical properties, so as to make stone comminution more effective, without increasing tissue damage

Mechanical haemolysis in shock wave lithotripsy (SWL): I. Analysis of cell deformation due to SWL flow-fields

This work analyses the interaction of red blood cells (RBCs) with shock-induced and bubble-induced flows in shock wave lithotripsy (SWL), and calculates, in vitro, the lytic effects of these two flows. A well known experimentally observed fact about RBC membranes is that the lipid bilayer disrupts when subjected to an areal strain (ΔA/A)c of 3%, and a corresponding, critical, isotropic tension, Tc, of 10 mN m-1 (1 mN m-1 = 1 dyne cm-1). RBCs suspended in a fluid medium tend to deform in accordance with the deformation of the surrounding fluid medium. The fluid flow-field is lytically effective if the membrane deformation exceeds the above threshold value. From kinematic analysis, motion of an elementary fluid particle can always be decomposed into a uniform translation, an extensional flow (e.g. vec u∞(x,y,z) = (k(t)x,-k(t)y,0)) along three mutually perpendicular axes, and a rigid rotation of these axes. However, only an extensional flow causes deformation of a fluid particle, and consequently deforms the RBC membrane. In SWL, a fluid flow-field, induced by a non-uniform shock wave, as well as radial expansion/implosion of a bubble, has been hypothesized to cause lysis of cells. Both the above flow-fields constitute an unsteady, extensional flow, which exerts inertial as well as viscous forces on the RBC membrane. The transient inertial force (expressed as a tension, or force/length), is given by Tiner~ρrc3k/τ, where τ is a timescale of the transient flow and rc is a characteristic cell size. When the membrane is deformed due to inertial effects, membrane strain is given by ΔA/A~kτ. The transient viscous force is given by Tvisc~ρ(ν/τ)1/2rc2k, where ρ and ν are the fluid density and kinematic viscosity. For the non-uniform shock, the extensional flow exerts an inertial force, Tinerapprox64 mN m-1, for a duration of 3 ns, sufficient to induce pores in the RBC membrane. For a radial flow-field, induced by bubble expansion/implosion, the inertial forces are of a magnitude 100 mN m-1, which last for a duration of 1 µs, sufficient to cause rupture. Bubble-induced radial flow is predicted to be lytically more effective than shock-induced flow in typical in vitro experimental conditions

Design and characterization of a research electrohydraulic lithotripter patterned after the Dornier HM3

An electrohydraulic lithotripter has been designed that mimics the behavior of the Dornier HM3 extracorporeal shock wave lithotripter. The key mechanical and electrical properties of a clinical HM3 were measured and a design implemented to replicate these parameters. Three research lithotripters have been constructed on this design and are being used in a multi-institutional, multidisciplinary research program to determine the physical mechanisms of stone fragmentation and tissue damage in shock wave lithotripsy. The acoustic fields of the three research lithotripters and of two clinical Dornier HM3 lithotripters were measured with a PVDF membrane hydrophone. The peak positive pressure, peak negative pressure, pulse duration, and shock rise time of the focal waveforms were compared. Peak positive pressures varied from 25 MPa at a voltage setting of 12 kV to 40 MPa at 24 kV. The magnitude of the peak negative pressure varied from -7 to -12 MPa over the same voltage range. The spatial variations of the peak positive pressure and peak negative pressure were also compared. The focal region, as defined by the full width half maximum of the peak positive pressure, was 60 mm long in the axial direction and 10 mm wide in the lateral direction. The performance of the research lithotripters was found to be consistent at clinical firing rates (up to 3 Hz). The results indicated that pressure fields in the research lithotripters are equivalent to those generated by a clinical HM3 lithotripter

Mechanical haemolysis in shock wave lithotripsy (SWL): II. In vitro cell lysis due to shear

In this work we report injury to isolated red blood cells (RBCs) due to focused shock waves in a cavitation-free environment. 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, as characterized by a membrane hydrophone. Cavitation was eliminated by applying overpressure to the fluid. A novel passive cavitation detector (HP-PCD) operating at high overpressure (up to 7 MPa) was used to measure acoustic emission due to bubble activity. The typical 'double-bang' emission measured in the lithotripter free-field was replaced by a continuum of weak signals when the fluid was enclosed in a pressure chamber. No acoustic emissions were measured above an overpressure of 5.5 MPa. Aluminium foils were used to study shock wave damage and had distinct deformation features corresponding to exposure conditions, i.e. pitting and denting accompanied by wrinkling. Pitting was eliminated by high overpressure and so was due to cavitation bubble collapse, whereas denting and wrinkling were caused by the reflected shock wave refocused by the parabolic reflector. RBCs suspended in phosphate-buffered saline (PBS) were exposed to the reflected wave field from a parabolic reflector and also from a flat reflector. Exposure to the wave field from the parabolic reflector increased haemolysis four-fold compared with untreated controls and was twice that of cell lysis with the flat reflector. Recently we analysed deformation and rupture of RBCs when subjected to a flow field set up by a focused shock. The cell lysis results presented here are in qualitative agreement with our theoretical prediction that haemolysis is directly related to the gradient of shock strength and validates shearing as a cell lysis mechanism in SWL

Damage mechanisms in shock wave lithotripsy (SWL)

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