Extracorporeal Shockwave Therapy (ESWT) otherwise referred to as shockwave therapy, was first introduced into clinical practice in 1982 for the management of urologic conditions. The success of this technology for the treatment of urinary stones quickly made it a first-line, non-invasive, and effective method. Subsequently, ESWT was studied in orthopaedics where it was identified that it could loosen the cement in total hip arthroplasty revisions. Further, animal studies conducted in the 1980s revealed that ESWT could augment the bone-cement interface, enhance osteogenic response and improve fracture healing. While shockwave therapy has been shown to be beneficial in fracture healing, most orthopaedic research has focused on upper and lower extremity tendinopathies, fasciopathies, and soft tissue conditions. 

Shockwaves are sound waves that have specific physical characteristics, including nonlinearity, high peak pressure followed by low tensile amplitude, short rise time, and short duration (10 ms). They have a single pulse, a wide frequency range (0-20 MHz), and a high-pressure amplitude (0-120 MPa)

These characteristics produce a positive and negative phase of shockwave. The positive phase produces direct mechanical forces, whereas the negative phase generates cavitation and gas bubbles that subsequently implode at high speeds, generating a second wave of shockwaves.

In comparison to ultrasound waves, the shockwave peak pressure is approximately 1000 times greater than the peak pressure of an ultrasound wave.

The effects of ESWT treatment are unknown. However, the proposed mechanisms of action for ESWT include the following: promote neovascularization at the tendon-bone junction, stimulate proliferation of tenocytes and osteoprogenitor differentiation, increase leukocyte infiltration, and amplify growth factor and protein synthesis to stimulate collagen synthesis and tissue remodeling.

Shockwaves are transient pressure disturbances that propagate rapidly in three-dimensional space. They are associated with a sudden rise from ambient pressure to their maximum pressure. Significant tissue effects include cavitation, which are consequent to the negative phase of the wave propagation.

Direct shockwave and indirect cavitation effects cause hematoma formation and focal cell death, which then stimulate new bone or tissue formation.

Indications for Shockwave Therapy

Shockwave therapy is primarily used in the treatment of common musculoskeletal conditions. These include: 

• Upper and lower extremitytendinopathies
• Greater trochanteric pain syndrome
• Medial tibial stress syndrome
• Patellar tendinopathy
• Plantar fasciopathy.
• Adhesive capsulitis
• Non-union of long bone fracture
• Avascular necrosis of femoral head
• Osteoarthritis of the knee

Conditions that can be treated with Shockwave Therapy

• Planter Fasciitis
• Calcific Tendonitis
• Jumpers Knee
• Heel spurs/ Heel pain
• Myofascial Trigger points in muscle 
• Tennis/ Golfers elbow
• Achilles Tendonitis
• Rotator cuff 

• Hip:
  • Trochanteric bursitis
  • Piriformis syndrome
  • Hamstring
• Knee:
  • Patella tendinopathy
  • Osgood Schlatter
• Shin splints

Benefits

• Breakdown scar tissue and adhesions
• Increased blood flow
• Improved healing response
• Reduce muscle spasm 
• Decrease pain

Pain and Shockwave

Maier et al. (2003) showed that after shockwave pain initially increases (for the first 6 hours after shockwave application). This comes from an increase in release of substance P (through C fiber and A-delta fiber depolarization) and the subsequent inflammatory response from that release. Shockwave mechanically stimulates the release of substance P (Maier et al. 2003).

However this initial release is followed by a subsequent decrease in levels of substance P (and hence inflammation) at the 24-hour point as the nerve degenerates (Maier et al. 2003). This reduction in substance P release lasts for over 6 weeks (Maier et al. 2003) and may go on as long as 2 years (Maier et al. 2003).

Biological Effects of Radial Shockwave 

The exact mechanism of how radial extracorporeal shockwave therapy affects human tissue is poorly understood. However, Haupt (1997) postulated 4 reaction phases.

1. Physical Phase. Extracellular cavitation, ionization of molecules and an increase in cell membrane permeability.
2. Physical-Chemical Phase. An interaction between diffusible radicles and bio-molecules released from stimulated cells.
3. Chemical Phase. Intracellular reactions and molecular changes in the actual cells.
4. Biological Phase. Is only established if the changes occurring in the chemical phase persist.

The effects of radial shockwave can be categorized into two major areas:

• Direct effects
• Indirect effects

Both the direct and indirect effects produce a biological response in treated tissues (Ogden, To-th-Kischkat & Schultheiss, 2001, Schmitz et al., 2013, Ueberle, 2007).

Cavitation (indirect effect, in the physical phase):

The indirect effect of cavitation is probably best understood.  After the initial positive pressure wave of shockwave there is a rapid negative pressure phase (tensile phase). During this negative phase cavitation occurs.

Cavitation is the formation of vapour bubbles in a liquid wherever the pressure of the liquid falls below its vapour pressure (Moholkar & Pandit, 1997) (this is what happens when you click your knuckles – the gas in the liquid implodes). This indirect effect occurs in both radial and focused shock waves (Schmitz et al., 2013, Chitnis & Cleveland, 2006, Ueberle, 2007).

These vacuum bubbles induce local shear forces when collapsing at the end of the phase of negative pressure (Ogden, To´th-Kischkat & Schultheiss, 2001). This cavitation damages the affected tissues.

Although pictures of cavitation are hard to generate radial shockwave machines have been captured creating them. An example is seen below:

Cavitation bubbles 15mm head 4bar at 10 Hz in degassed water.

The cavitation appears to last 1ms per shock and appears to be greater with increased shock frequency (Schlaudraff et al., 2014). Lower frequencies (1hz) show less cavitation (Schlaudraff et al., 2014) whilst low frequencies (5hz) show good cavitation (Kiessling et al., 2015) and high frequencies (15hz) show almost black out with cavitation. Of note the higher the frequency the wider Schlaudraff et al. (2014) found the cavitation field to be, but they also found the pressure field to be lower (for direct effects). Examples can be seen below:

Cavitation bubbles 15mm head 4bar 1 Hz in degassed water

Cavitation bubbles 15mm head 4bar 5 Hz in degassed water

Cavitation bubbles 15mm head 4bar 15 Hz in degassed water

Shockwave is thought to act on real cells in a mechanical way with three main consequences:

1. Cell destruction
2. Cell permeabilization
3. Cell detachment

Destruction (direct and indirect effects in the physical phase):

Destruction of tissue by shockwave is still a debated topic (we know it happens as kidney stones are destroyed this way). There are 4 main ways shockwaves can destroy tissue:

1. Spalling/spall crack formation (direct effect in the physical phase)

This is due to the generation of tensile stress caused by shockwave reflections at a pressure-release boundary (Delius, 2000, Lokhandwalla & Sturtevant, 2000, Eisenmenger, 2001, Xi & Zhong, 2001, Zhu et al., 2002). Reflected tensile waves may be focused or superimposed with the initial tensile pulse (Gracewski et al., 1993, Dahake, 1997, Xi & Zhong, 2001).

2. Spalling (direct effect in the physical phase)

This can be referred to as fragmentation. If a high velocity impact (in this case a shockwave) is applied at one side of a tissue, and can reach the other side (to a point where 2 tissues meet), then spalling starts from the free end (the impacted side where the shockwave hits). The compressive pulse is reflected from one side of the structure to the other as a tensile pulse. If the tensile pulse is higher than the ultimate tensile strength of the material a spall is formed, and the opposite side of the structure breaks off (Tan, 2008, Yankelevsky & Avnon, 1998).

Imagine a bony heel spur. The shockwave hits the spur If the wave is stronger than the tissue and if it has sufficient depth to reach the opposite side of the scar tissue A small piece of the spur is broken off on the opposite side as the wave is reflected across the scar.

The reflected wave  if it has enough energy left  and can cross back to the other side  can now knock off another piece on the leading edge. And on and on providing there is enough energy.

A new free end is formed and the remaining original pulse is reflected from this new free end. Once again the structure breaks when the reflected tensile pulse exceeds the ultimate tensile strength of the material, and again a new free end is formed. In this way multiple spalling is generated (Tan, 2008, Yankelevsky & Avnon, 1998).