4. Case Description:
ī¨ 9 year old American Paint Horse gelding, discipline is western pleasure
ī¨ Presenting complaint: Sore back, poor performance during the western
lope
ī¨ Previous veterinary diagnostics
ī¤ Bilateral tarsus radiographs from 2 years ago
ī¤ Bilateral stifle radiographs from 2 years ago
īŽ Flattening of the medial femoral condyle, bilaterally
ī¤ Thoracolumbar radiographs from 1 month ago
īŽ No evidence of overriding dorsal spinous process
ī¨ Previous veterinarian therapeutics
ī¤ Bilateral hock injections
īŽ Corticosteroids + HA
ī¤ Bilateral stifle injections
īŽ HA only
ī¤ Sacroiliac injection
īŽ Corticosteroids
ī¤ Right front bicepital bursa injection
ī¤ Mesotherapy
5. Lameness Evaluation
ī¨ Passive examination
ī¤ Negative hoof testers bilaterally
ī¤ Mild church hill response bilaterally
ī¤ Conformation
īŽ Straight legged in hind with sickle & cow hock conformation
ī¤ Feet
īŽ Egg bar shoe both fronts, mild frog atrophy
ī¤ Neck & Back
īŽ Hypereasethetic response along neck musculature
īŽ Withdrawal response to palpation of caudal thoracic &
lumbar epaxial musculature
6. Lameness Evaluation
ī¨ Passive examination
ī¤ No medial patellar ligament palpated, right hind
īŽ Previous desmotomy?
ī¤ Asymmetric musculature in hind end, with
generalized reduced muscle mass in right hind
ī¨ Active examination, baseline
ī¤ Grade 2/5 right hind
ī¤ Grade 1/5 left front
ī¤ Grade 1/5 right front
7. Lameness Evaluation
ī¨ Active examination, baseline
ī¤ On soft surface, left & right circle
īŽ Forelimbs: no change from baseline
īŽ Right hindlimb: slight increase in right hindlimb lameness
ī¤ On hard surface, left & right circle
īŽ Right hindlimb: increased, noted by toe dragging and
reduced cranial phase of stride
ī¨ Flexions
ī¤ Forelimb flexions â all negative
ī¤ Hindlimb flexions
īŽ Distal limbs â negative
īŽ Upper limbs â mild positive bilaterally
īŽ Abduction & adduction â mild positive, right hind
13. What is Shockwave?
ī¨ âExtracorporeal shockwave
therapyâ
ī¤ def: âExtracorporealâ
īŽ Acoustic waves generated outside
the body
ī¤ Transient high peak pressures
alternating with negative
pressure
īŽ Varies with machine type and
settings
īŽ Wave rise time of 5 to 10
nanoseconds
īŽ Maximum peak pressure of 20 to
100 megapascals
īŽ 1 megapascal is 10x that of
14. Shockwave Generators
ī¨ Variables: pressure, energy level, frequency, depth
of penetration, quantity of pulses applied
ī¨ Two broad categories of shockwave generation
ī¨ 1) âFocusedâ shockwave
ī¨ 2) âRadialâ shockwave
ī¨ Focal volume: area affected by the shockwave
ī¨ With energy constant,
ī¨ Smaller focal volume = more energy concentrated
ī¨ Large focal volume = energy spread over greater area
15. Shockwave Generators
ī¨ Generator types
ī¨ Focused shockwave
ī¨ 1) Piezoelectric generators
ī¨ High current excites crystals which then produces a
pressure wave
ī¨ Small focal volume, high energy flux, low overall energy
transfer
ī¨ 2) Electromagnetic generators
ī¨ High voltage current transfer through a coil, which propels a
diaphragm, creating a pressure wave
ī¨ Small focal volume, high energy flux, less concentrated (vs.
piezo)
ī¨ 3) Electrohydraulic shockwave
ī¨ Pass high voltage through a spark gap in a fluid filled
ellipsoid reflector
ī¨ Expanding plasma & gas bubbles create pressure wave
16. Shockwave Generators
ī¨ Generator types contâĻ
ī¨ Radial shockwave
ī¨ Also known as âballisticâ
ī¨ Doesnât have rapid rise time or high energy typical of
shockwave
ī¨ Uses mechanical concussion
ī¨ No focusing system
ī¨ Energy of wave declines in proportion to distance from
source
17.
18. Mechanism of Action:
ī¨ Not entirely understood
ī¨ Shockwave energy has similar physics as sound waves
ī¨ Acoustic impedance
ī¤ Amount of wave energy transmitted into tissue depends on the difference in impedance
between two tissue types
ī¤ Impedance = wave pressure (p) / wave velocity (v)
ī¨ Tissues withâĻ
ī¤ air-fluid interface absorb greatest amount of energy
īŽ Lower acoustic impedance
ī¤ muscle-fat interface absorb least amount of energy
īŽ Higher acoustic impedance
ī¤ Near lungs
īŽ Induce pleural hemorrhage
19. Mechanism of Action:
ī¨ When the shock wave meets an interface of different
impedanceâĻ
ī¤ Pressure and shear forces occur
ī¤ Development within fluid media of cavitation bubbles
īŽ Collapse & expand
īŽ Large amount of energy released when bubble implodes
īŽ Is it this mechanical mechanism at work?
ī¨ Pressure waves effect on cells (in-vitro):
ī¤ Bone remodeling
īŽ Induce production of nitric oxide (Wang 2003)
ī¤ Cytostimulation
īŽ Increase concentrations of TGF-Î (Wang 2000)
īŽ Increased concentration of osteocalcin (Wang 2000)
īŽ Increased osteocyte cell division (Wang 2000)
ī¤ Stimulation of endochondral ossification
īŽ Increase in extracellular matrix proteins (Takahaski 2001)
20. Analgesic
ī¨ Provides pain relief
ī¤ Likely largest reason therapeutic contributes to positive clinical
outcome for the client
ī¤ Dramatic decrease for 3 to 4 days ī¨ resurgence of pain ī¨
gradual decrease after 3 to 4 weeks
ī¨ Studies have shown decreased nerve conduction following
shockwave application
ī¤ Bolt 2004, McClure 2005.
ī¤ Disruption of myelin sheath with no evidence of damage to
Schwann cell bodies or axons
ī¨ Concern that analgesia may reduce or eliminate pain, that
could lead to catastrophic injury with continued exercise
ī¤ Too high of energy has been shown to induce micro-cracks in
dorsal cortical surface of MC3
ī¤ Withdrawal time of 5-7 days prior to performing
īŽ Racing jurisdictions, FEI
21. Application
ī¨ General rule is that a good ultrasound image can
be attained of the injury, then shockwave energy
can reach the depth of the tissue
ī¨ Once shockwave pulse hits bone, approximately
65% transmitted (and 35% reflected)
ī¤ Approximately 80-90% reduction of energy by 1-2cm
of bone
ī¨ Sedation ī¨ apply ultrasound gel to target area ī¨
perform shockwave therapy
ī¨ Often multiple series of shockwave sessions,
separated by 2-3 week intervals
23. Complications
ī¨ Dose dependent action, but generally very safe
ī¤ Too little energy = no effect
ī¤ Too much energy = damage tissues
ī¨ In bones,
ī¤ Micro-fracture of cortical bone
ī¤ Medullary hemorrhage
ī¤ Sub-periosteal hemorrhage
ī¨ In tendons,
ī¤ Hematoma formation
ī¤ Tendon cell damage
ī¨ Generally attempt to avoid large vessels
ī¨ Avoid active physis
ī¤ Unless treating A.L.D.
ī¨ Avoid neoplastic or infected tissue
ī¤ Metastasis or spread of sepsis
25. Historical Use
ī¨ First utilized for lithotripsy in
humans 25 years ago
ī¨ Graff, 1986
ī¤ Shockwave induced up-
regulation of osteoblast cells
ī¨ Haupt, 1991
ī¤ Increased healing time of
humeral fractures in rats
ī¨ Human medicine
ī¤ Lateral epicondylitis (tennis
elbow
ī¤ Plantar calcaneal spurs (heel
spurs)
ī¨ First clinical report in animals
ī¤ in 1999
ī¤ Shockwave described as a
26. Research
ī¨ Variable between studies
ī¤ Energy level, pulse frequency, depth of
penetration, number of treatments
ī¤ Type of injured tissue being treated
ī¨ Conjunctive therapy
ī¤ Controlled exercise, NSAIDs, heat/cold therapy,
pressure wraps, platelet rich plasma, stem cells
īŽ Skews interpretation
īŽ Does shockwave therapy affect stem cells?
27. Research
ī¨ Studied tendon-bone junction following shockwave
ī¤ 8 dogs
ī¤ 1000 pulses, 0.18mJ/mm2
ī¤ One limb, biopsies compared to pre-shockwave sample
ī¨ Biopsies
ī¤ Two blinded pathologists independently reviewed
histology slides
ī¤ Pre-shockwave in medial 1/3rd of Achilles tendon
ī¤ at 4 weeks in middle 1/3rd of Achilles tendon
ī¤ at 8 weeks in lateral 1/3rd of Achilles tendon
ī¨ New capillary vessels seen in shockwave treated
groups, none noted in control groups
ī¤ Present at 4 weeks, no further increase at 8 weeks
ī¤ No concurrent inflammatory cells
ī¨ Arranged myofibroblasts seen in treated tendons
ī¨ No changes in osteocyte activity, bone matrix or bone
vascularity
28. Research
ī¨ Dogs with unresolved stifle lameness treated with
ECSWT or untreated controls
ī¨ Determined force plate and range of motion
measurements
ī¤ Baseline, every 3 weeks for 4 sessions, and 4 weeks following
final session
ī¨ Peak Vertical Force
ī¤ 4 of 7 dogs in ECSWT group improved
ī¤ 1 of 5 dogs in control group improved
ī¨ Range of Motion
ī¤ 5 of 7 dogs in ECSWT group improved
ī¤ 3 of 5 dogs in control group improved
29. Research
ī¨ 24 dogs with hip
osteoarthritis
ī¨ 18 received radial
shockwave therapy; 6
controls
ī¨ Force plate
ī¤ Prior to treatment
ī¤ 6 weeks after treatment
ī¤ 3 months after treatment
ī¤ 6 months after treatment
ī¨ Significant improvement in
peak vertical force &
vertical impulse noted at all
time points post-
30. Research
ī¨ Study 1:
ī¤ 4 horses with radiographically normal cannon bones
ī¤ One MC3
īŽ Control
ī¤ One MC3 & one MT3
īŽ 1000 pulses of 0.89mJ/mm2
ī¤ One MT3
īŽ 1000 pulses of 1.8mJ/mm2
ī¨ No damage to soft tissue structures
ī¨ Mild sub-periosteal and endosteal hemorrhage
ī¤ Extending 1-2mm into the cortical bone
ī¤ Walls in the vessels of the osteon disrupted
ī¤ No micro-fractures appreciated
ī¨ Osteogenesis
ī¤ Not likely due to microfractures
ī¤ Potentially due to bone marrow hypoxia, sub-periosteal hemorrhage,
increased regional blood flow, activation of osteogenic factors
31. Research
ī¨ Study 2:
ī¤ 2 horses with radiographically normal cannon bones
ī¤ One MC3
īŽ Control
ī¤ One MC3 & MT3
īŽ 2000 pulses of 0.89mJ/mm2
ī¤ One MT3
īŽ Periosteum elevated to create mechanical irritation
ī¨ Kept alive for 30 days, then euthanized
ī¨ Osteon activity evaluated by fluorescent microscopy
ī¨ Shockwave treated cannon bones:
ī¤ Activated osteons
ī¤ New bone formation on periosteal & endosteal surface
ī¤ Shockwave limbs had 30% more activated osteons than control
ī¤ Shockwave limbs had 56% more activated osteons than
periosteal elevation
32. Research
ī¨ n = 24 horses, distal radial carpal
osteochondral fragment
ī¨ 3 groups of 8 horses
ī¤ Placebo (sham shockwave), positive control
(PSGAG IM q4days), or ECSWT (day 14 & 28)
ī¤ 2000 pulses, 0.14 mJ/mm2
ī¤ Lameness scores in ECSWT group were
significantly lower compared to placebo group (at
day 28 & 70), and compared to PSGAG group (at
day 70)
ī¤ Reduced carpal flexion scores in ECSWT group
vs. placebo/PSGAG group (at day 70)
33. Research
ī¨ No significant differences in synovial fluid color,
clarity, mucin clot formation, WBC counts between
groups
ī¨ Total protein and PGE2 lower in ECSWT &
PSGAG group compared to placebo group
ī¨ No difference between groups in gross pathologic
scores (cartilage fibrillation, synovial membrane
hemorrhage) or histologic scores (cellular
infiltration, synovial intimal hyperplasia, subintimal
edema/fibrosis/vascularity)
ī¨ Improved lameness scores lasted up to 42 days
after final treatment
34. Research
ī¨ Four horses had suspensory ligament desmitis
induced in both forelimbs using collagenase
ī¤ 1 ligament per horse treated with 3 sessions of
shockwave, 3 weeks apart
ī¤ 0.14 mJ/mm2, 1500 pulses
ī¨ Ultrasound exams every 3 weeks (non-
blinded)
ī¨ Horses euthanized at 18 weeks for histology
35. Research
ī¨ Fiber alignment score decreased
faster in the shockwave treatment
group compared to controls
ī¤ Score of 0 = normal, score of 3 =
25% or less
ī¨ No change in echogenicity
ī¨ Metachromasia
ī¤ Occurs from proteoglycan deposition
ī¤ More focal in shockwave treated
ligaments
ī¨ Fibroblast & type 3 collagen
ī¤ No difference
36. Research
ī¨ 6 healthy horses without lameness
ī¨ Shockwave therapy
ī¤ Proximal suspensory, metacarpus
ī¤ Fourth metatarsal bone
ī¤ Opposing limb served as control
ī¤ 2000 pulses, 0.15mJ/mm2
ī¨ Bone scans performed as baseline, and on day 3, 16, 19.
ī¨ Euthanasia for histopathology performed on day 30
ī¨ No damage to soft tissue, no microfractures induced
ī¨ Shockwave significantly increased osteoblasts numbers
ī¨ Significant correlation between osteoblast numbers and
radiopharmaceutical uptake noted
ī¤ On day 3 & 16 for hindlimb
ī¤ On day 3 only for forelimb
ī¨ Suggests shockwave increases osteoblast numbers
ī¤ Shortly after therapy (by 3 days)
37. Research
ī¨ 10 horses
ī¨ Collagenase injected into both forelimbs to create
suspensory desmitis
ī¨ 2 weeks after collagenase injection
ī¤ Shockwave therapy, 1500 pulses, 0.15mJ/mm2
ī¤ 3 treatment sessions, separated by 3 weeks
ī¨ Greater amounts of small collagen fibrils present in
ECSWT group
ī¤ Represent new collagen fibril formation
īŽ (759 +/- 42) vs. (69 +/- 14)
ī¨ Cytoplasmic staining in fibroblasts for TGFβ-1
ī¤ Increased in ECSWT group compared to controls
ī¨ Suggests rate of tissue repair in shockwave treated
tissue is greater than tissue that does not receive
38. Research
ī¨ Naturally occurring forelimb lameness
in 9 horses
ī¤ Baseline force plate values of
lameness, followed by force plate
values following diagnostic analgesia
ī¤ ECSWT performed
īŽ 1000 pulses, 0.15mJ/mm2
ī¤ Force plate 8 hours later, followed by
daily force plate for 7 days
ī¨ Peak Vertical Force
ī¤ PVF increased 8 hours & 2 days
following shockwave, and was not
statistically different than previous
diagnostic analgesia measurements
ī¨ Vertical Impulse
ī¤ After 8 hours & 2 days VI increased,
but was statistically lower than previous
diagnostic analgesia measurements
40. Overview
ī¨ Shockwave is widely used in equine veterinary
medicine
ī¨ There are various different types of shockwave
machines, which apply energy through different
means
ī¨ The exact mechanism of how shockwave influences
healing is still relatively unknown
ī¨ Shockwave stimulates growth of cells, in-vitro
ī¨ Shockwave increases neovascularization and
promotes bone remodeling, in-vivo
ī¨ Shockwave provides immediate analgesia for the first
5-7 days. This immediate analgesia then regresses. A
second phase of analgesia is often seen 3-4 weeks
thereafter.
ī¨ Growing research to support the clinical application of
Hinweis der Redaktion
Variables: pressure, energy level, frequency, depth of penetration, quantity of pulses applied
Adams reference 6, 4, and 11
In the early phase of tissue repair, TGFβ-1 has a proinflammatory action and also modulates the deposition of extracellular matrix com- ponents and enhances collagen, fibronectin, and gly- cosaminoglycan synthesis from fibroblasts.16 Wang et ala have suggested that one of the possible mechanisms of action of ESWT is mediated through the action of TGFβ-1.