To The Editor:
I read with great interest the article, "Electrohydraulic High-Energy
Shock-Wave Treatment for Chronic Plantar Fasciitis" by Ogden et al.
(2004;86:2216-28). I congratulate them for reporting the results of the FDA
trial, which, to a vast extent, had been published earlier6,7.
Some points remain open for discussion.
1. The alleged efficacy of this singledose, high-energy, anesthetically
based treatment has already been discussed exhaustively by Buchbinder et
al.3 in 2002. Regarding the HealthTronics-sponsored FDA
trial2, Buchbinder et al. made the criticism that the presence of
plantar fasciitis was determined solely on clinical grounds. Also, it was
uncertain whether the two groups in the trial were comparable at baseline. In
their previous paper, Ogden et al.6 defined overall success of
treatment at twelve weeks as fulfillment of four of the following criteria:
(1) a minimum 50% improvement over baseline in the investigator's assessment
of pain (with a dolorimeter) and a score of £4 cm on a visual analogue
scale; (2) a minimum 50% improvement over baseline in the subject's
self-assessment of pain on first walking in the morning and a score of
£4 cm on a visual analogue scale; (3) a minimum 1-point or greater
improvement on a 5-point scale of distance walked without heel pain, or
maintenance of a baseline assessment of no pain or minimal pain; and (4) no
prescription of analgesics for pain in the treated heel between ten and twelve
weeks after treatment. While success according to the three criteria other
than the investigator's assessment of pain favored the active treatment, no
difference was significant (subject's selfassessment of pain: 59.7% in the
shock-wave group compared with 48.2% in the placebo group, p = 0.08; subject's
self-assessment of activity level: 71.4% in the shock-wave group compared with
67.2% in the placebo group, p = 0.49; and use of pain medications: 69.7% in
the shock-wave group compared with 67% in the placebo group, p = 0.41). I
wonder why Ogden et al., who quoted the paper by Buchbinder et al. in their
article, did not specifically respond to the objections by those authors. How
is it possible that suddenly significant differences were calculated after
three months of follow-up while, in the original FDA paper2, no
significant difference had been observed after the same duration of
follow-up?
2. In their paper, Ogden et al. reported active shock-wave treatment with
an energy flux density of 0.22 mJ/mm2 to be high-energy. In a
recent article, my colleagues and I8 treated patients with an
energy flux density of 0.18 mJ/mm2 and called it
low-energy. I therefore question the labeling of the dose used by
Ogden et al. as high-energy. I would like to know whether the authors
are aware of any consensus regarding how to define low-energy and high-energy
treatment.
3. I found it interesting to read that 47% of the patients in the placebo
group, who had received three 1-mL subcutaneous injections of lidocaine,
reported >50% relief of morning heel pain at the three-month follow-up
examination. In a study scheduled for publication9, eighty-six
patients with chronic plantar fasciitis were randomly assigned to receive
either low-energy extracorporeal shock-wave therapy without local anesthesia
weekly for three weeks or identical extracorporeal shock-wave therapy with
local anesthesia applied to the insertion of the plantar fascia. Significantly
more patients had >50% reduction of pain during the first steps in the
morning after extracorporeal shock-wave therapy without local anesthesia than
after extracorporeal shock-wave therapy with local anesthesia (67% compared
with 29%). Local anesthesia applied prior to treatment reduced the efficacy of
low-energy extracorporeal shockwave therapy in this study. I wonder what
explanation Ogden et al. can provide for the surprisingly high rate of
satisfied patients after treatment with local anesthesia only in their
experimental design. With their close to 50% success rate in patients with
previously recalcitrant morning pain, should subcutaneous injections of
lidocaine not be given priority before shock-wave treatment?
4. I agree with Ogden et al. that the mechanism of shock-wave action in
soft tissues is still under investigation. When discussing a possible working
mechanism of shock-wave application, it is important to focus not only on
differences among shock-wave devices in clinical use but also on different
pathways for the effects of high compared with low-energy shock waves. It is
important to know that the current literature10-13 indicates that
shock waves may selectively lead to dysfunction of peripheral sensory
unmyelinated nerve fibers without affecting nerve fibers responsible for motor
function (large myelinated fibers). For "high-energy" treatment
with 0.9 mJ/mm2, this selective destruction of sensory unmyelinated
nerve fibers within the focal zone of the extracorporeal shock-wave therapy
may contribute to clinically evident long-term analgesia10. For
"low-energy" application with 0.1 mJ/mm2, analgesia may
be a result of a shock-wave-induced destruction of sensory nerve fibers and
release of neuropeptides, such as CGRP (calcitonin gene-related peptide),
resulting in a local neurogenic inflammation in the focal area with subsequent
prevention of sensory nerve endings from reinnervating this
area11,12. A second application accentuated these inflammatory
changes and therefore prevented reinnervation13. Centrally, the
common finding of a reduction in the number of neurons immunoreactive to CGRP
and substance P without a reduction of the total number of neurons within the
lower lumbar dorsal root ganglion probably is a secondary effect following the
(primarily induced) decrease in the number of sensory nerve fibers in the
focal zone of the shock-wave application12. Thus, the peripheral
and central nervous systems may both play a pivotal role in mediating
shock-wave-induced long-term analgesia. Recently, Wang et al.14
showed that shock-wave application of 0.12 mJ/mm2 increased
neovascularization at the tendonbone junction in rabbits. Chen et
al.15 treated rats with collagenase-induced Achilles tendinitis
with a single shock-wave treatment of 0, 200, 500, or 1000 impulses of 0.16
mJ/mm2. Shock-wave application with 200 impulses restored
biomechanical and biochemical characteristics of healing tendons twelve weeks
after treatment. However, shock-wave treatments with 500 and 1000 impulses
elicited inhibitory effects on tendinitis repair. Low-energy shock-wave
treatment effectively promoted tendon-healing. In my view, it is clear from
these experimental data that, with increasing energy applied, there is a
chance of side effects that may well harm an already diseased fascia or
tendon. It is also clear that even "low-energy" shock waves may
induce a positive local reaction regarding downregulation of pain transmitters
and upregulation of cell proliferation factors. The clinical results reported
by Ogden et al., after use of an energy flux density of 0.22
mJ/mm2, probably are due to these effects.
5. I agree with Ogden et al. and with Speed16 that some regimens
of extracorporeal shock-wave therapy are a potentially helpful addition to the
options for the management of soft-tissue conditions such as chronic plantar
fasciitis. I support their belief that, contrary to the opinion of
Buchbinder17, these regimens of extracorporeal shock-wave therapy,
which produce virtually no complications and which allow immediate full
weight-bearing without splints, should therefore be given priority before
surgery18.
The issues and comments raised both by Buchbinder et al. and by Rompe
reflect generic and specific problems related to this emerging orthopaedic
technology. Those investigators studied the use of extracorporeal shock-wave
therapy with electromagnetic devices that differ from the electrohydraulic
device used in our study. Unfortunately, there are no recognized ways of
defining high-energy or low-energy, nor are there physical
means of assessing how much energy actually affects the target tissue.
Furthermore, the energy was delivered in different manners in their studies
(transverse versus plantar surface). Efforts certainly must be made to better
define parameters, as they obviously will define improvements in treatment.
Perhaps the first step was taken by Gerdesmeyer et al., who compared high and
low-energy shock-wave therapy (using different device settings) with a placebo
for treatment of calcific tendinopathy of the
shoulder19. Both
energy levels were effective compared with the placebo. However, the
high-energy treatment was considerably superior to the low-energy
treatment.
Both Buchbinder et
al.3 and Rompe et
al.20 used devices
at energy settings usually considered to be low-energy. Yet their findings
were quite disparate. Buchbinder et al. found no difference between patients
treated with shock waves and those treated with a
placebo3, while
Rompe et al., in a study published in JBJS, found extracorporeal shock-wave
treatment to be
effective20. The
protocols were quite different regarding patient selection, treatment regimen
(including the amount of energy and number of doses), involvement of
orthopaedists, and outcome criteria. All of these factors make comparison of
the studies difficult. Obviously all of the studies were well planned and
conducted.
We will address the various specific issues.
First, in answer to Buchbinder et al.: the previous article that we
published involved preliminary data assessed at three months following
shock-wave
treatment1. Our
recent study included the complete patient cohort in phases 1 and 2. This
involved a larger number of randomized patients as well as nonrandomized
patients. Furthermore, all treated patients were assessed with a different
outcomes analysis, in which we used the criteria described by Roles and
Maudsley (which were used in many European studies of extracorporeal
shock-wave therapy). These different patient numbers and assessments led to
different p values. The data submitted to the FDA were derived with multiple
different statistical analyses, and we chose to report a limited number of
them. The data were critically reviewed by an independent statistician, by the
FDA statistician, by the orthopaedic FDA panel statistician, and by the JBJS
reviewer.
All felt that the data were appropriately significant, especially relative
to the post-treatment outcome analysis of pain by the orthopaedists. The
comments about energy levels and follow-up duration reflect differences in
protocols and the aforementioned problems in energy/dose comparisons between
different devices. Finally, none of our patients had ultrasound diagnosis. We
felt strongly that patients who were referred with the diagnosis as made by
well-trained orthopaedists and podiatrists and who were reevaluated by another
orthopaedist using a specific definition of plantar fasciitis and a detailed
number of inclusion criteria certainly had the disease. Ultrasound is not
unequivocal in the diagnosis of this disorder.
Theodore et
al.21 used the same
device as Buchbinder et al. However, they used a much higher energy setting
(all patients received the same dosage), ankle block anesthesia, and a placebo
group. This study was instrumental in obtaining FDA approval of the device.
Their study also reinforced the fact that differences in the
"intensity" of the energy delivered, even by the same device, may
be a major factor in the likelihood of success.
With regard to Rompe's comments, the treatment group and placebo group as
well as the nonrandomized group were all comparable at baseline. This is
reflected in the values given in our publication. We certainly agree that the
most significant parameter of success was the investigator's assessment of
direct heel pain using a dolorimeter. Such a method of pain measurement was
not used in either the study by Buchbinder et
al.3 or that by
Rompe et al.20. We
stated that use of pain medication was a poor differentiator between treatment
and placebo groups. Neither Buchbinder et al. nor Rompe et al. assessed the
use of post-treatment pain medications.
Rompe raises the most perplexing question regarding extracorporeal
shock-wave therapy. What is high energy versus what is low energy? Patients
can tolerate certain levels of energy administration with electromagnetic
devices. Very few can tolerate even the lowest-energy settings of the
electrohydraulic device.
We agree with Rompe that injection of lidocaine or even saline solution
prior to treatment may potentiate the effect of extracorporeal shock-wave
therapy, especially with regard to cavitation. However, our placebo group had
limited lidocaine administration at the level of the ankle, not into the
plantar fascia.
We agree completely with Rompe's comments in the final paragraph. These
reflect recent detailed animal studies directed at understanding neurologic
and vascular responses to extracorporeal shock-wave therapy. Additional
comparable studies are necessary to understand the biologic mechanisms of
action. At the same time, better definitions of the physics of differently
generated shock waves are essential, not only to comprehend levels of
penetration into subcutaneous and deeper target tissues, but also to be able
to compare devices and studies using such devices.
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