U.S. patent application number 10/096216 was filed with the patent office on 2002-12-12 for method and apparatus for cartilage growth stimulation.
Invention is credited to Rose, Emery, Ryaby, John P., Talish, Roger J., Urgovitch, Kenneth SR., Winder, Alan A..
Application Number | 20020188229 10/096216 |
Document ID | / |
Family ID | 21893969 |
Filed Date | 2002-12-12 |
United States Patent
Application |
20020188229 |
Kind Code |
A1 |
Ryaby, John P. ; et
al. |
December 12, 2002 |
Method and apparatus for cartilage growth stimulation
Abstract
A kit of elements including an ultrasonic generator (12),
transducers (402) with connecting cables (407, 408), and a means
(405, 406) for locating the transducers over areas of the body
containing cartilage, is provided with the surgical instruments for
post-surgical application to ultrasonically stimulate the cartilage
growth, thus relieving the effects of surgical intervention.
Inventors: |
Ryaby, John P.; (Essex
Falls, NJ) ; Talish, Roger J.; (Hillsborough, NJ)
; Rose, Emery; (Astoria, NJ) ; Winder, Alan
A.; (Westport, CT) ; Urgovitch, Kenneth SR.;
(Clifton, NJ) |
Correspondence
Address: |
CHIEF PATENT COUNSEL
SMITH & NEPHEW, INC.
1450 BROOKS ROAD
MEMPHIS
TN
38116
US
|
Family ID: |
21893969 |
Appl. No.: |
10/096216 |
Filed: |
March 11, 2002 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
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10096216 |
Mar 11, 2002 |
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09436999 |
Nov 9, 1999 |
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6355006 |
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60037367 |
Feb 6, 1997 |
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Current U.S.
Class: |
601/2 |
Current CPC
Class: |
A61B 17/1677 20130101;
A61N 7/00 20130101; A61B 18/20 20130101; A61B 17/16 20130101 |
Class at
Publication: |
601/2 |
International
Class: |
A61H 001/00 |
Claims
What is claimed is:
1. A kit for ultrasonically stimulating cartilage growth, which
comprises: means for initiating a biological healing response at or
adjacent a cartilaginous site; an ultrasonic transducer assembly
having at least one ultrasonic transducer; a placement module
configured to be worn by a patient, said placement module being
configured to receive said transducer assembly such that when said
placement module is worn said at least one ultrasonic transducer is
positioned in proximity to the channels; an ultrasonic signal
generator positioned in said ultrasonic transducer assembly; and a
main operating unit.
2. The kit according to claim 1, wherein the means for initiating
the biological healing response includes a drill assembly.
3. The kit according to claim 1, wherein the means for initiating
the biological healing response includes a laser drill
assembly.
4. The kit according to claim 1, wherein the means for initiating
the biological healing response includes a scraping assembly.
5. The kit according to claim 1, wherein the means for initiating
the biological healing response includes a chemical substance for
irradiating the cartilaginous site.
6. The kit according to claim 1, wherein said ultrasonic signal
generator includes signal generator circuitry and an internal power
source connected to said signal generator circuitry, a display
coupled to said signal generator circuitry to display treatment
sequence data, and said signal generator circuitry including a
processor and means for generating a pulsed RF signal.
7. The kit according to claim 1, further comprising safety
interlock means to prevent inadvertent excitation of said at least
one ultrasonic transducer.
8. The kit according to claim 1, wherein said placement module
includes a locking mechanism which when worn by the patient
prevents the patient from bending or extending the limbs.
9. The kit according to claim 1, wherein the placement module is
constructed from a conductive material and said at least one
ultrasonic transducer is provided on said placement module is
electrically coupled to said main operation unit via said
conductive material.
10. The kit according to claim 1, wherein the placement module is
custom molded for a particular joint of the patient.
11. The kit according to claim 1, wherein at least one ultrasonic
transducer includes means for receiving reflected diagnostic
data.
12. A method for ultrasonically stimulating a healing response for
the regeneration of cartilage comprising the following steps:
initiating a biological healing response at or adjacent a
cartilaginous site; providing a main operating unit having an
internal power source coupled to an ultrasonic transducer assembly,
said ultrasonic transducer assembly includes at least one
ultrasonic transducer, an ultrasonic signal generator and signal
generator circuitry therein; providing a placement module
configured to receive said transducer assembly such that when said
placement module is secured to a patient's body said at least one
ultrasonic transducer is positioned in proximity to the channels;
and exciting said at least one ultrasonic transducer to impinge
ultrasonic waves towards the cartilaginous site.
13. The method according to claim 12, wherein the step of
initiating the biological healing response includes drilling at
least one channel within the bone joint walls at the cartilaginous
site.
14. The method according to claim 12, wherein the step of
initiating the biological healing response is selected from the
group consisting of scraping the cartilaginous site, applying a
chemical substance to the cartilaginous site, and inducing a
fracture at the cartilaginous site.
15. The method according to claim 12, further comprising the step
of transplanting non-weight bearing cartilage to the cartilaginous
site prior to treatment.
16. The method according to claim 12, further comprising the step
of transplanting autologous cultured chondrocytes to the
cartilaginous site prior to treatment.
17. The method according to claim 12, further including the step of
receiving reflected diagnostic data by said at least one ultrasonic
transducer.
18. The method according to claim 12, wherein the step of exciting
said at least one ultrasonic transducer to impinge ultrasonic waves
towards the cartilaginous site causes the regenerated cartilage to
integrate with the non-regenerated cartilage present at the
cartilaginous site.
19. A method for ultrasonically stimulating a healing response for
the regeneration of cartilage comprising the following steps:
initiating a biological healing response at or adjacent a
cartilaginous site; releasably securing at least one ultrasonic
transducer coupled to a signal generator to a band; affixing the
band on a patient such that said at least one transducer is in
proximity to an area where the regeneration of cartilage is
desired; and exciting said at least one ultrasonic transducer by
actuating said signal generator to impinge ultrasonic waves towards
the cartilaginous site.
20. The method according to claim 19, further including the step
of: connecting said at least one ultrasonic transducer to an
operating unit, said operating unit having an internal power
source.
21. The method according to claim 19, further including the step of
receiving reflected diagnostic data by said at least one ultrasonic
transducer.
Description
[0001] This application claims priority to a U.S. Provisional
Application No. 60/037,367 filed on Feb. 6, 1997.
BACKGROUND OF THE INVENTION
[0002] 1. Field of the Invention
[0003] The present invention relates to methods and apparatus for
therapeutically treating injuries using ultrasound. More
particularly, the present invention relates to methods and
apparatus which utilize an ergonomically constructed ultrasonic
transducer assembly configured to cooperate with a placement module
for placement in proximity to a cartilage and/or osteochondral
injury and/or defect to stimulate cartilage growth.
[0004] 2. Description of the Related Art
[0005] The use of ultrasound to therapeutically treat and evaluate
bone injuries is known. Impinging ultrasonic pulses having
appropriate parameters, e.g., frequency, pulse repetition, and
amplitude, for suitable periods of time and at a proper external
location adjacent to a bone injury has been determined to
accelerate the natural healing of, for example, bone breaks and
fractures.
[0006] U.S. Pat. No. 4,530,360 to Duarte describes a basic
non-invasive therapeutic technique and apparatus for applying
ultrasonic pulses from an operative surface placed on the skin at a
location adjacent a bone injury. To apply the ultrasound pulses
during treatment an operator must manually hold the applicator in
place until the treatment is complete.
[0007] The Duarte patent as well as U.S. Pat. No. 5,520,612 to
Winder et al. describe ranges of RF signal for creating the
ultrasound, ultrasound power density levels, ranges of duration for
each ultrasonic pulse, and ranges of ultrasonic pulse
frequencies.
[0008] U.S. Pat. No. 5,003,965 to Talish et al. relates to an
ultrasonic body treatment system having a body-applicator unit
connected to a remote control unit by sheathed fiber optic lines.
The signal controlling the duration of ultrasonic pulses and the
pulse repetition frequency are generated apart from the
body-applicator unit. Talish et al. also describes a mounting
fixture for attaching the body-applicator unit to a patient so that
the operative surface is adjacent the skin location.
[0009] While the systems described in these patents relate to
therapeutic methods and apparatus for ultrasonic treatment of hard
and soft tissue injuries and defects, there is a need for
ergonomically configured signal generators and transducers for the
treatment of cartilage and/or osteochondral injuries and/or
defects. Further, a need exists for an apparatus which optimizes
the treatment of cartilage and/or osteochondral injuries and/or
defects.
[0010] A cartilage and/or osteochondral injury and/or defect
typically involves damage to the cartilage which lines articulating
bones (articular cartilage), such as the bones of the knee, elbow,
shoulder and ankle. Osteochondral injuries can be treated by
chondral and/or osteochondral drilling causing blood flow at the
site. The aim of chondral drilling is to stimulate cartilage
regeneration as part of the healing process. However, the resulting
nonhyaline or fibrocartilage produced is biomechanically inferior
to articular cartilage, does not have comparable proteoglycan
content, and may consist primarily of a thin unorganized layer of
collagen. Further, it has been observed that degeneration of the
new tissue generally occurs over time, requiring the need for
additional reconstructive surgical treatment.
[0011] Other methods of treatment include: the transplantation of
non-weight bearing cartilage to the injury and/or defect site;
inducing a fracture at the injury and/or defect site; placing a
carbon fiber matrix to induce cartilage formation; and autologous
chondrocyte implantation (ACI). ACI entails removing chondrocytes
capable of regenerating hyaline-like cartilage from the body and
culturin them for several weeks. During the culture process, the
number of cells increases approximately 15 times that of the
original tissue sample. The cultured cells are then transplanted
through an arthrotomy. A small piece of periosteum, the skin
covering a bone, is taken from the patient's tibia. The periosteum
is then sutured over the defect to provide a protective cover for
the cultured cells. The cultured cells are injected under the
periosteum into the defect where they will continue to multiply and
produce a durable repair tissue. However, ACI increases the healing
time since the chondrocytes need to be cultured before they are
transplanted to the patient.
[0012] Therefore, there is a further need for a method and
apparatus to stimulate cartilage regeneration which produces
fibrocartilage which is biomechanically equal or superior to
articular cartilage, has comparable proteoglycan content, and
consists of a thick organized layer of collagen. Further still, a
need also exists for an apparatus which stimulates cartilage
regeneration and where the regenerated cartilage does not
degenerate over time requiring additional treatment or
reconstructive surgery. Further, there is a need for an apparatus
which stimulates cartilage regeneration and significantly reduces
the healing time.
SUMMARY OF THE INVENTION
[0013] The ultrasonic treatment apparatus of the present invention
is used for therapeutically treating cartilage and/or osteochondral
injuries and/or defects using ultrasound. The apparatus includes an
ergonomically constructed placement module configured for mounting
at least one ultrasonic transducer assembly with an integral signal
generator which provides excitation signals to at least one
ultrasonic transducer within the transducer assembly. Timing
control circuitry as well as monitoring circuitry for the proper
attachment and operation of the transducer assembly are housed
within a portable main operating unit which may be fit within a
pouch worn by the patient. In operation, the placement module is
positioned against a part of the patient's body such that at least
one transducer is positioned over the cartilage and/or
osteochondral injury and/or defect. At least one transducer is then
excited for a predetermined period of time to impinge ultrasonic
waves against the damaged cartilage area to stimulate the
regeneration of new articular cartilage.
[0014] Preferably, the main operating unit has an internal power
source for powering the signal generator circuitry, a display
coupled to the signal generator circuitry to display treatment
sequence data, a keypad coupled to the signal generator circuitry
to permit user operation and/or entry of data. The signal generator
circuitry includes a processor, means for generating a pulsed
control signal, and a switch coupled to the processor for
regulating the pulsed control signal. A communication interface may
be connected between a communication port and the processor to
provide a communication link between the ultrasonic signal
generator and an external computer or modem. Preferably, the
communication interface is a serial communication interface,
however, a parallel interface is also contemplated. An alarm is
provided to indicate to the user that the treatment time has
expired. The alarm is coupled to the processor such that when
ultrasonic treatment is completed the processor activates the alarm
and terminates ultrasound generation.
[0015] The present invention also provides a kit for ultrasonically
treating cartilage and/or osteochondral injuries and/or defects.
The kit includes an ultrasonic transducer assembly, a placement
module configured to be worn by a patient and to receive the
ultrasonic transducer assembly, an integrated ultrasonic signal
generator located in the ultrasonic transducer assembly, and a main
operating unit (MOU) or controller. The MOU has an internal power
source thereby providing patient mobility. A MOU envisioned for use
with the present invention is described in U.S. Pat. No. 5,556,372
to Talish et al. which is hereby incorporated by reference.
[0016] The MOU is electrically coupled to at least one transducer
secured to the placement module. The activation of the signal
generator corresponding to each transducer excites at least one
ultrasonic transducer for impinging ultrasonic waves to the
cartilage and/or osteochondral injury and/or defect.
[0017] A method for ultrasonically treating cartilage and/or
osteochondral injuries and/or defects is also provided. Once the
location of the cartilage and/or osteochondral injury and/or defect
is ascertained, the body's own natural healing processes are
stimulated adjacent the injury. This can be accomplished by
chondral drilling on the defect to form a series of channels to
stimulate blood flow and induce the biological reconstructive
healing response of the underlying area at the cartilage site.
Other methods of stimulating this response includes laser drilling,
induce fracture, scraping, chemical or biochemical treatments, etc.
Once the healing response has been sufficiently facilitated, a
placement module containing an ultrasonic transducer assembly
having at least one transducer and one signal generator is
positioned adjacent to the injured part of the body such that at
least one transducer is in proximity to the cartilage and/or
osteochondral injury and/or defect for the treatment of the injury.
The signal generator is then activated to excite the at least one
transducer for impinging ultrasonic waves to the cartilage and/or
osteochondral injury and/or defect. The ultrasonic waves impinge
upon the injury site to stimulate and accelerate the biological
healing properties of the body to regenerate cartilaginous
material. The present method can also be used in conjunction with
the transplantation of autologous cultured chondrocytes to the
injury site to increase the healing time.
[0018] In an alternative embodiment, a placement module is provided
for securing a plurality of transducers thereto in a plurality of
configurations. The placement module is then secured to a cartilage
and/or osteochondral injury and/or defect site, for example, at the
ankle or wrist, to stimulate cartilage regeneration. Further, the
present invention also provides an embodiment having a placement
module which contains a locking structure for locking the
articulating bones in a particular position. This embodiment
prevents the patient from moving his limbs, for example, moving the
femur with respect to the tibia, during treatment.
BRIEF DESCRIPTION OF THE DRAWINGS
[0019] Preferred embodiments of the invention are described below
with reference to the drawings, which are described as follows:
[0020] FIG. 1 is a perspective view of a patient wearing a portable
ultrasonic treatment apparatus of a first embodiment according to
the present invention having a main operating unit or controller
and a placement module;
[0021] FIG. 2A is an exploded view of the placement module of the
portable ultrasonic treatment apparatus illustrated by FIG. 1;
[0022] FIG. 2B is a rear underside view of the placement module of
the portable ultrasonic treatment apparatus illustrated by FIG.
1;
[0023] FIG. 3 is a cross-sectional view illustrating the transducer
assembly impinging ultrasonic waves to articular cartilage within
the knee where an ultrasonic conducting gel is positioned between
the transducer assembly and the patient's knee;
[0024] FIG. 4 is a block diagram of one embodiment of the circuitry
for the ultrasonic transducer assembly;
[0025] FIG. 4A is a block diagram of an alternative embodiment of
the circuitry for the ultrasonic transducer assembly;
[0026] FIG. 5 is a perspective view of a second embodiment of the
portable ultrasonic treatment apparatus, illustrating a main
operating unit or controller and a placement module for treating
osteochondral injuries within the elbow region;
[0027] FIG. 6 is a perspective view of a third embodiment of the
portable ultrasonic treatment apparatus, illustrating a main
operating unit or controller and a placement module for treating
osteochondral injuries within the shoulder region;
[0028] FIG. 7 is a perspective view of a fourth embodiment of the
portable ultrasonic treatment apparatus illustrating a main
operating unit or controller and a placement module;
[0029] FIG. 8 is a perspective view of the portable ultrasonic
treatment apparatus illustrated by FIG. 7 mounted on a patient's
ankle;
[0030] FIG. 9 is a perspective view of a fifth embodiment of the
portable ultrasonic treatment apparatus, illustrating a main
operating unit or controller and a placement module for treating
osteochondral injuries within the knee region;
[0031] FIG. 10A is an exploded view of the portable ultrasonic
treatment apparatus illustrated by FIG. 9;
[0032] FIG. 10B is a perspective view of a support member of the
portable ultrasonic treatment apparatus illustrated by FIG. 9;
[0033] FIG. 11 is a flow-chart depicting the steps for stimulating
a healing response at the site of an osteochondral injury according
to the present invention;
[0034] FIG. 12A is a perspective view showing the drilling of
channels within the joint walls of the femur and tibia;
[0035] FIG. 12B is a cross-sectional view showing ultrasonic waves
"bouncing off" the channels within the joint walls of the femur and
tibia; and
[0036] FIGS. 13A-19D are photomicrographs illustrating the
postoperative appearance of cartilage and/or osteochondral defects
created at the patellar groove region of rabbits according to a
study conducted to demonstrate that daily ultrasound therapy
accelerated cartilage and/or osteochondral defect healing as early
as four weeks in both gross and histologic analysis.
DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS
[0037] The ultrasonic treatment apparatus of the present invention
is used for the surgically non-invasive utilization of ultra
high-frequency acoustic energy in the treatment of cartilage and/or
osteochondral injuries and/or defects. Even though this detailed
description discusses the treatment of cartilage and/or
osteochondral injuries and/or defects caused by an injury, the
ultrasound treatment apparatus can be used to treat osteochondral
defects caused by other means, such as medication, infection or
metabolic processes.
[0038] The apparatus includes an ergonomically constructed
placement module having a strap or other fastening means for being
secured adjacent an injured part of a patient's body. At least one
ultrasonic transducer assembly is attached or imbedded within the
placement module and properly positioned in proximity to the
cartilage and/or osteochondral injury and/or defect. Different
types of ultrasonic transducers and signals can be provided, such
as those described and schematically depicted in U.S. Pat. No.
5,520,612 to Winder et al. which is hereby incorporated by
reference. Particularly, the transducers and arrangements
schematically depicted by FIGS. 7-11 of the patent in which at
least one transducer is used to provide acoustic energy to the site
of the injury. The apparatus may also utilize a portable,
ergonomically constructed main operating unit (MOU) worn by the
patient which provides control signals to the ultrasonic
transducers. The MOU which is utilized is preferably the one
described in U.S. Pat. No. 5,556,372 to Talish et al. which is
hereby incorporated by reference.
[0039] Turning to the figures, in particular FIG. 1, one embodiment
of the portable ultrasonic treatment apparatus 10 of the present
invention is shown. The ultrasonic treatment apparatus 10 includes
a MOU 12, a placement module 14, and ultrasonic transducer
assemblies 16.
[0040] The placement module 14 comprises a placement support 20
which includes at least two or three channels 22 each having an
extension 24 mounted therein. Each extension has a transducer
pocket 26 at one end for holding one ultrasonic transducer assembly
16. It is contemplated for each extension 24 to have several range
of movements besides longitudinal motion, such as articulating
motion transverse to the longitudinal motion.
[0041] The placement module 14 further includes a placement band 28
cooperating with slot 30 for securing the placement support 20 to
the patient. The placement band 28 is configured to firmly secure
the placement module 14 to the patient. A sponge-like material 32
preferably lines the inner surface of the placement support 20 for
providing comfort to the patient (FIGS. 2A and 2B). The placement
support 20 may be constructed of hard plastics which may be custom
molded for a particular body part of the patient.
[0042] With reference to FIGS. 2A and 2B, the extensions 24 are
mounted to the placement support 20 via screws 33 and thumb screws
34. The screws 33 are passed through slots 35 and holes 36 on the
extensions 24 and are threaded to the thumb screws 34. The
extensions 24 can be moved to different positions to accommodate
patients of all sizes by unthreading the thumb screws 34 and
shifting the screws 33 along the slots 35 and threading the screws
33 to the thumb screws 34 at the new position.
[0043] The transducer assembly 16 may include circuitry,
schematically illustrated by FIGS. 4 and 4A and described below,
for exciting at least one transducer therein and is coupled to the
MOU by cable 37 and wires 39. The wires 39 are coupled to the
placement support 20. The cable 37 is preferably a multiconductor
cable capable of transmitting relatively low frequency RF or
optical signals, as well as digital signals. The cable 37 may
include coaxial cable or other types of suitable shielded cable.
Alternatively, the cable 37 may include fiber optic cable for
transmitting optical signals. The signals may be transmitted
continuously or as a series of pulses.
[0044] In operation, the placement module 14 is positioned and
secured to the patient's body as shown by FIG. 3, such that each
transducer assembly 16 lies over the cartilage and/or osteochondral
injury and/or defect. A locating ring such as the one disclosed in
U.S. patent application Ser. No. 08/389,148 may be used for
determining the location of injured bone, if the patient desires to
have one of the transducer assemblies overlying a bone injury,
before the placement module 14 is secured to the patient. Once the
placement module 14 is properly positioned, the transducer within
the transducer assembly 16 is excited for a pre-determined amount
of time. An ultrasound conducting gel 38 is positioned between the
transducer assembly 16 and the injured part of the patient's body
to prevent attenuation of the ultrasonic waves as they travel to
the articular cartilage 40, as shown by FIG. 3.
[0045] It is also contemplated that one or more transducers can be
converted to receive reflected diagnostic data from the treatment
site. This permits real time evaluation of the injury site and
healing process.
[0046] With reference to FIG. 4, a block diagram of one embodiment
of the ultrasonic transducer assembly circuitry is shown. The
transducer assembly circuitry 17 includes a receiver/RF oscillator
50 which receives the signals transferred by a signal generator
within MOU 12 via cable 37. The receiver/RF oscillator 50 is
connected to transducer driver 52 which excites transducer 16.
[0047] An alternative embodiment of the transducer assembly
circuitry 17 is shown in FIG. 4A. In this embodiment, the
ultrasonic transducer assembly 16 includes an internal battery 60
which supplies power to the components within the transducer
assembly 16. For example, battery 60 supplies power to signal
monitoring circuit 62 and signal driver 66. The signal monitoring
circuit 62 provides, preferably, a digital output signal 68 which
represents the waveform characteristics of the output of transducer
driver 70. These characteristics can be displayed on a digital
display and may include, for example, the frequency, pulse
repetition frequency, the pulse width and the average output power
of the transducer 16. The output signal 68 of signal monitoring
circuit 62 is transferred to the signal generator within MOU 12 via
driver 66 and cable 37. The signal generator may include a
processor and a switch for regulating the signal characteristics.
Control signals from the MOU 12 are received by receiver 72 via
cable 37. Safety or fixture interlock 74, which may include
switches on the outer surface of the placement module 14 or
transducer assembly 16, ensures that the placement module 14 is
properly positioned before providing power to the internal
components of the transducer assembly 16.
[0048] A second embodiment of the portable ultrasonic treatment
apparatus of the present invention is illustrated by FIG. 5 and
designated generally by reference numeral 200. The treatment
apparatus 200 includes MOU 12 and transducer assemblies 202 affixed
to a placement module 204 via extensions 206 for ultrasonically
stimulating the generation of cartilage in the elbow region. Each
transducer assembly 202 includes a power transducer 212 connected
to the MOU 12 by cable 218. An ultrasonic conducting gel 212 is
positioned between the transducer assemblies 202 and the
osteochondral injury to prevent attenuation of the ultrasonic waves
as they travel to the articular cartilage. In order to accommodate
various patients, the extensions 206 can be adjusted to several
positions by unthreading thumb screws 220. The circuitry for each
transducer assembly 202 may be similar to that disclosed for the
first embodiment and schematically illustrated by FIGS. 4 and
4A.
[0049] It is envisioned that the placement module 204 be
constructed from suitable conductive plastics, such as conductive
ABS plastics with either carbon, stainless steel, nickel or
aluminum fibers to forego the use of wires for connecting the
transducer assemblies 202 to the cable 218. In such an embodiment,
the conductive placement module 204 would be used to electrically
connect the transducer assemblies 202 to the MOU 12 via cable
218.
[0050] With reference to FIG. 6, a third embodiment of the portable
ultrasonic treatment apparatus of the present invention is
illustrated. In this embodiment, the treatment apparatus 300
includes a MOU 12, a placement module 304, and ultrasonic
transducer assemblies 306. The placement module 304 is configured
for placement on the shoulder region and includes a placement band
310 and a placement support 312. Each transducer assembly 306 is
connected to the MOU 12 by cable 318 to power transducer assembly
circuitry within each assembly 306. The circuitry (not shown) may
be similar to that disclosed for the first and second embodiments
and schematically illustrated by FIGS. 4 and 4A.
[0051] In operation, transducers within transducer assemblies 306
are excited for a pre-determined period of time to impinge
ultrasonic waves to articular cartilage within the shoulder
region.
[0052] A fourth embodiment of the portable ultrasonic treatment
apparatus of the present invention which is primarily suitable for
the treatment of cartilage and/or osteochondral injuries and/or
defects is illustrated by FIGS. 7 and 8. In this embodiment, the
apparatus 400 includes at least one ultrasonic transducer assembly
402 positioned within pockets 404 on a strip 406. The transducer
assemblies 402 may be arranged in a plurality of configurations
within pockets 404 to accommodate many patients' anatomical
differences. The strip 406 is secured in proximity to a cartilage
and/or osteochondral injury and/or defect as shown by FIG. 8 by a
self-tieing material 405. The strip 406 is connected via wires 407
and cable 408 to a MOU 12 which contains circuitry for exciting the
at least one ultrasonic transducer assembly 402 affixed to the
strip 406.
[0053] In operation, at least one transducer assembly 402 is
excited to impinge ultrasonic waves to the cartilage and/or
osteochondral injury and/or defect as shown by FIG. 8. It is
contemplated that during treatment an ultrasonic conducting gel is
positioned between the strip 406 and the patient's body to prevent
attenuation of the ultrasonic waves.
[0054] It is also contemplated to manufacture the strip 406 from
suitable conductive plastics such as conductive. ABS plastics with
either carbon, stainless steel, nickel or aluminum fibers to forego
the use of wires for electrically connecting the at least one
ultrasonic transducer 402 to the cable 408.
[0055] A fifth embodiment of the portable ultrasonic treatment
apparatus of the present invention which is primarily suitable for
the treatment of cartilage and/or osteochondral injuries and/or
defects is illustrated by FIGS. 9-10B. In this embodiment, the
apparatus 500 includes a MOU 12 and three ultrasonic transducer
assemblies 502 positioned within pockets 504 on an inner surface of
a concave plate 506 as shown by FIG. 10B. The concave plate 506 is
positioned at one end of a vertical bar 508 having a slot 509 at a
lower portion. The apparatus 500 further includes a locking support
module 510 having a thigh support 512 and a leg support 514.
[0056] As shown by the exploded view of FIG. 10A, the thigh support
512 includes a thigh support plate 516, a securing band 518, and
two horizontal locking extensions 520 affixed to the thigh support
plate 516 by screws 522 and thumb screws 524. The leg support 514
includes a leg support plate 526, a securing band 528, and two
vertical locking extensions 530 affixed to the leg support plate
526. The vertical bar 508 is configured to mount within a channel
532 on the leg support 514. The vertical bar 508 is secured to the
channel 532 by screw 534 and thumb screw 536. The vertical bar 508
can be moved vertically along the channel 532 by unthreading the
thumb screw 536 to accommodate various patients.
[0057] The thigh support 512 and the leg support 514 are locked to
each other by locking the horizontal locking extensions 520 and the
vertical locking extensions 530 by screws 538 and thumb screws 540
to prevent the patient from moving the thigh with respect to the
leg during treatment and to ensure that the transducer assemblies
502 remain fixed in their proper positions. The transducer
assemblies 502 are connected via a cable 542 which is plugged in to
hole 544 to the MOU 12 which contains circuitry for exciting the
ultrasonic transducer assemblies 502. It is contemplated that
during treatment an ultrasonic conducting gel is positioned between
the transducers 502 mounted in concave plate 506 and the patient's
body to prevent attenuation of the ultrasonic waves.
[0058] A method for treating a cartilage and/or osteochondral
injury and/or defect is depicted by the flow-chart of FIG. 11. The
method entails stimulating blood flow to induce a biological
reconstructive healing response of the underlying area at the
cartilage and/or osteochondral injury site (step A), and
irradiating the cartilage and/or osteochondral injury site with
ultrasonic waves for a time sufficient to accelerate the healing
response (step B). Step A entails mechanically drilling, induced
fracture, laser drilling, administering chemical or biochemical
treatments, scraping the injury site to stimulate the growth of
cartilaginous tissue. Step B preferably entails propagating a
primary directional lobe of acoustic energy in body tissue and/or
fluids about a central or longitudinal axis, and this primary
directional lobe is concentrically surrounded by primary shearwave
lobes of acoustic energy. The carrier frequency is sufficiently
elevated to establish a standing-wave condition in one or more
spaces between confronting surfaces adjacent or at the cartilage
and/or osteochondral injury site, as long as the space is
dimensionally characterized by at least a quarter-wavelength at the
carrier frequency, thereby enabling demodulation of the carrier
frequency. Within a matter of days, healing proceeds at an
accelerated pace in the environment of such demodulation, with
resultant cartilage development in reduction of the space; but the
pattern of carrier wave propagation in body tissue and/or fluids
surrounding the central axis of acoustic propagation is rich in
therapeutically beneficial shear waves of acoustic energy.
[0059] It is also contemplated to use the present method in
conjunction with the transplantation of autologous cultured
chondrocytes to the injury site to increase the healing time.
[0060] With reference to FIGS. 12A and 12B, there are illustrated
steps A and B, respectively. FIG. 12A is a perspective view showing
the drilling of channels 600 within the defect using a drill 608 to
stimulate blood flow and induce the biological reconstructive
healing response of the underlying area at the cartilage and/or
osteochondral injury site. FIG. 12B is a cross-sectional view
showing the ultrasonic waves "bouncing off" the channels 600 within
the joint walls 602 of the femur 604 and tibia 606 for a time
sufficient to accelerate the healing response.
[0061] FIGS. 13A-19D are photomicrographs illustrating the
postoperative appearance of cartilage and/or osteochondral defects
created at the patellar groove region of rabbits according to
studies (EXI095-01R and EXI096-01R) conducted to demonstrate that
daily ultrasound therapy accelerated cartilage and/or osteochondral
defect healing as early as four weeks in both gross and histologic
analysis. Defects treated with ultrasound demonstrated more hyaline
cartilage properties compared to nontreated sites at four, eight,
and twelve weeks postoperative. In addition, greater subchondral
bone restoration was also noted.
[0062] The second study, EXI096-01R, confirmed the results of the
initial study, EXI095-01R, and added longer term (12 weeks)
analysis. The four week postoperative ultrasound treated defects
received higher gross and histologic scores compared to the
nontreated defects, indicating accelerated tissue regeneration and
higher levels of proteoglycan formation and cartilage like
morphology and greater integration of the repair cartilage with the
surrounding host cartilage. The mean gross grade for the ultrasound
treated defects was 6.92/8 versus 4.8318 for the nontreated defects
at four weeks. The mean histologic grade for the ultrasound defects
was 15.11/24 versus 9.28/24 for the nontreated defects at four
weeks. At eight weeks postoperative, differences were more subtle
both grossly and histologically between treated and nontreated
defects. The mean gross grade for the ultrasound defects was 7.5018
compared to 6.33/8 for the nontreated defects at eight weeks. The
mean histologic grade for the ultrasound defects was 15.83/24
compared to 13.60/24 for the nontreated defects at eight weeks.
However, at twelve weeks postoperative, dramatic differences were
observed grossly between the treated and nontreated defects (7.17/8
gross grade for ultrasound defects versus 5.50/8 for nontreated
defects). This may represent the initial degeneration of the
inferior cartilage produced in the nontreated defects. The mean
histologic grade for the ultrasound treated defects was 19.06/24.
The mean grade for the nontreated defects was 15.06/24.
[0063] Overall, ultrasound treated sites demonstrated earlier and
greater amounts of cartilage and subchondral bone regeneration.
With time ultrasound sites demonstrated more extensive subchondral
bone regeneration, less degeneration of adjacent cartilage, and
greater chondral layer thickness and a greater amount of
integration of the repair cartilage with surrounding host
cartilage. These characteristics indicate a better quality of
repair cartilage, that may be better able to withstand loading and
degeneration over time.
[0064] A total of 18 male New Zealand White rabbits weighing five
to nine pounds at acquisition were utilized. Specific attention was
paid in selecting animals of uniform size to limit variability in
loading the osteochondral defects. Bilateral 3 mm diameter by 5 mm
deep osteochondral defects were created surgically in the patellar
groove of each femur. Daily 20 minute ultrasound therapy was
applied to the right knee defects only until sacrifice. The left
defects were not treated. In an initial pilot study of six animals
(EXI095-01R) three were sacrificed at four weeks postoperative and
three were sacrificed at eight weeks postoperative. Each defect was
evaluated grossly and histologically for the quality and extent of
cartilage regeneration. Based on the four and eight week gross and
four week histologic results, a second similar study was undertaken
(EXI096-01R) consisting of 12 rabbits. A gross pathologic
examination was made of all vital organs and systems. A summary of
the surgery and treatment schedule for both studies appears in
Table 1.
1TABLE 1 Treatment Schedule (EXI095-01R and EXI096-01R) Animal
Right Knee Left Knee Number Treatment Treatment Surgery Date
Duration EXI095-01R: G200 20 minute daily none May 16, 1996 4 weeks
G203 20 minute daily none May 16, 1996 4 weeks G217 20 minute daily
none May 16, 1996 4 weeks G198 20 minute daily none May 16, 1996 8
weeks G201 20 minute daily none May 16, 1996 8 weeks G202 20 minute
daily none May 16, 1996 8 weeks EXI096-01R: H155 20 minute daily
none July 26, 1996 4 weeks H156 20 minute daily none July 26, 1996
4 weeks H160 20 minute daily none July 26, 1996 4 weeks H152 20
minute daily none July 26, 1996 8 weeks H153 20 minute daily none
July 26, 1996 8 weeks H162 20 minute daily none July 26, 1996 8
weeks H154 20 minute daily none July 26, 1996 12 weeks H157 20
minute daily none July 26, 1996 12 weeks H161 20 minute daily none
July 26, 1996 12 weeks H163 20 minute daily none July 26, 1996 12
weeks H164 20 minute daily none July 26, 1996 12 weeks H165 20
minute daily none July 26, 1996 12 weeks
[0065] The right knees received 20 minute daily ultrasound therapy
with the Sonic Accelerated Fracture Healing (SAFHS) device six days
weekly beginning on postoperative day four. The left knees received
no treatment. SAFHS units were randomly chosen each day for
treatment. Due to the large number of animals in the study
EXI096-01R, some devices were used twice each day on two different
animals. Animals were sedated by intramuscular injection of Ketaset
and Rompun (83 mg/ml Ketamine and 17 mg/ml xylazine) at the dosage
of 0.3 mg/kg body weight in order to administer the therapy. This
dosage is approximately one half the anesthetic dosage intended to
provide sedation only. The ultrasound transducer was placed on the
distal femur at the lateral condyle with ample ultrasound coupling
gel. The sites were periodically shaved to ensure contact between
the transducer, coupling gel and skin.
[0066] The SAFHS device is a noninvasive FDA approved external
device indicated for the accelerated healing of fresh fractures.
SAFHS delivers a low level acoustic pressure wave signal with an
intensity of 30 milliwatts per square centimeter (equivalent to the
intensity used for diagnostic ultrasound) to the skin at the
fracture site for twenty minutes daily.
[0067] Using standard aseptic techniques, surgery was performed
under halothane gas anesthesia and was monitored by
electrocardiogram and heart rate monitors. Anesthesia was
administered by intramuscular injection of Ketaset and Rompun (83
mg/ml Ketamine and 17 mg/ml xylazine) at the dosage of 0.6 mg/kg
body weight. Both hind limbs were prepped and draped in sterile
fashion. The defect in the knee joint was made though a median
parapatellar incision. The connective tissue securing the patella
was partially released to dislocate the patella and expose the
media] femoral condyle and patellar groove (FIG. 13A). Using a
drill bit, a 3 mm diameter by 5 mm deep osteochondral defect in the
patellar sulcus of the femur was created (FIG. 13B). After
irrigation with saline, the joint was closed in layers (FIG. 13C).
Routine anterior-posterior radiographs were taken after surgery to
insure proper defect location.
[0068] Butorphanol tartrate (0.2 mg/kg body weight) was
administered subcutaneously as required. Animals were administered
intramuscular antibiotics for four days postsurgery. Animals were
kept in recovery cages postoperatively until fully conscious and
demonstrated weight bearing, after which they were transferred to
standard cages and allowed unrestricted motion. Halo collars were
utilized as needed to prevent the animal from removing sutures.
[0069] Osteochondral healing was evaluated grossly and
histologically. Radiographs were utilized as necessary to evaluate
healing. Animals were observed daily by qualified personnel for any
signs of ill health or adverse reaction to the experimental
procedures.
[0070] Both right and left distal femurs were harvested en bloc,
carefully labeled, and kept in cool saline until gross grading and
microphotography was completed. The specimens were then placed in
formalin based fixative and labeled with all necessary
identifications. A gross pathological exam of vital organs was
conducted by the in-house veterinarian. Microscopic pathologic
examination was performed on any tissues determined to be grossly
abnormal.
[0071] Each harvested defect knee was graded for gross appearance
based upon the scheme of Moran et. al. (The Journal of Bone and
Joint Surgery, 74-B, 659-667, 1992) by an observer blinded to the
treatment group. This analysis apportions points based upon the
formation of intra-articular adhesions, restoration of articular
surface, erosion and appearance of the cartilage. A total of eight
points is the best possible grade (Table 2.)
2TABLE 2 Gross Grading Scale Grades Intra-articular adhesions None
= 2 Minimal/fine loose fibrous tissue = 1 Major/dense fibrous
tissue = 0 Restoration of articular surface Complete = 2 Partial =
1 None = 0 Erosion of cartilage None = 2 Defect site/site border =
1 Defect site and adjacent normal cartilage = 0 Appearance of
cartilage Translucent = 2 Opaque = 1 Discolored or irregular = 0
TOTAL SCORE 8 possible points
[0072] All specimens were prepared for histologic evaluation. The
individual specimens were fixed by immersion in either 10% formalin
solution or 4% paraformaldehyde solution. Following fixation, the
specimens were slowly decalcified in EDTA. The defect area was
bisected across the diameter of the defect. The resulting halves
and surrounding tissue were embedded in paraffin and sectioned
across the defect site. Three sections, 5-7 um thick, from three
levels were cut from each block. Level 1 was closest to the defect
center. Level 3 was closest to the defect perimeter and level 2 was
centered between levels 1 and 3. Three sections from each level
were stained with hematoxylin and eosin, Goldner's trichrome, and
safranin-O and Fast Green stains (to indicate glycosaminoglycan
content in the matrix).
[0073] Decalcified histologic sections were evaluated by an
observer blinded to treatment group. Sections were graded base upon
the scheme of Moran et. al. which apportion points based upon the
nature of the repair cartilage, structural characteristics, and
cellular changes (Table 3.)
3TABLE 3 Histology Grading Scale NATURE OF THE PREDOMINANT TISSUE:
Cellular morphology Hyaline articular cartilage = 4 Incompletely
differentiated = 2 Fibrous tissue or bone = 0 Safranin-O staining
of the matrix Normal/near normal = 3 Moderate = 2 Slight = 1 None =
0 STRUCTURAL CHARACTERISTICS: Surface regularity Smooth/intact = 3
Superficial horizontal lamination = 2 Fissures, 25-100% of
thickness = 1 Severe disruption, fibrillation = 0 Structural
integrity Normal = 2 Slight disruption, including cysts = 1 Severe
disintegration = 0 Thickness 100% of normal cartilage thickness = 2
50-100% = 1 0-50% = 0 Bonding to the adjacent cartilage Bonded at
both ends of the defect = 2 Bonded at one end or partially bonded
at both ends = 1 Not bonded = 0 FREEDOM FROM CELLULAR CHANGES OF
DEGENERATION: Hypocellularity None = 3 Slight = 2 Moderate = 1
Severe = 0 Chondrocyte clustering None = 2 <25% of cells = 1
>25% of cells = 0 Freedom from degenerative changes in adjacent
cartilage Normal cellularity, no clusters, normal staining = 3
Normal cellularity, mild clusters, moderate staining = 2 Mild or
moderate hypocellularity, slight staining = 1 Severe
hypocellularity, poor or no staining = 0
[0074] Immunohistochemical staining of cartilage sections from
twelve week ultrasound treated and nontreated defects was performed
to identify Type I and Type II collagen. Goat antihuman polyclonals
obtained from Southern Biotechnology, Inc. were used.
Immunohistochemical staining identifies the critical components of
articular cartilage necessary for correct regeneration and
maintenance of the tissue phenotype. In addition, the presence of
other tissues reflective of inappropriate tissue formation is
identified. In hyaline articular cartilage Type II collagen should
be localized only in the cartilage layer above the subchondral
bone. Staining for Type I collagen should be restricted to the
subchondral bone region.
[0075] All surgeries were uneventful with no postoperative
complications. Pathologic examination of internal organs
demonstrated no adverse response to the daily ultrasound treatment
or experimental procedures.
[0076] A summary of the gross evaluation grades from studies
EXI095-01R and EXI096-01R appears in Table 4. FIGS. 2 through 4
demonstrate the typical gross appearance of the treated and
nontreated sites at four, eight, and twelve weeks
postoperative.
4TABLE 4 Mean Gross Evaluation Grade .+-. standard deviation (n =
6) NONTREATED ULTRASOUND 4 WEEKS 4.83 .+-. 1.72 6.92 .+-. 1.02 8
WEEKS 6.33 .+-. 0.82 7.50 .+-. 0.45 12 WEEKS 5.50 .+-. 1.22 7.17
.+-. 0.98
[0077] At four weeks postoperative the ultrasound treated defects
demonstrated more complete and uniform covering of the defect,
although typically the new cartilage had an opaque appearance.
Incompletely covered lesions were present at the center of many of
the nontreated sites and the tissue regenerated was irregular in
color (FIG. 14). By eight weeks both the ultrasound and nontreated
defects were covered uniformly with new tissue. The ultrasound
treated defects demonstrated less erosion of the new cartilage and
surrounding intact cartilage (FIG. 15). At twelve weeks
postoperative the defect borders in the ultrasound treated defects
were difficult to appreciate and the new cartilage had the
appearance of the adjacent tissue (FIG. 16) and it was well
integrated with the adjacent host cartilage. New cartilage had a
more transparent appearance compared to the nontreated defects and
clearly demonstrated significantly less erosion of the adjacent and
newly formed cartilage.
[0078] A summary of the mean histologic grades from studies
EXI095-01R and EXI096-01R appears in Table 5. One half of each
twelve week specimen has been submitted for tissue typing analysis
aimed at identifying the collagen type and percent tissue
composition.
5TABLE 5 Mean Histologic Grades for the four, eight, and twelve
weeks postoperative sites .+-. standard deviation (sample size) for
both EXI09S-01R and EXI096-01R. 4 Weeks Postoperative 8 Weeks
Postoperative 12 Weeks Postoperative Nontreated Ultrasound
Nontreated Ultrasound Nontreated Ultrasound Nature of the 1.11 .+-.
1.02 4.06 .+-. 2.44 3.87 .+-. 1.77 3.72 .+-. 1.81 3.50 .+-. 2.09
5.61 .+-. 1.20 Predominant (18) (18) (15) (18) (18) (18) Tissue
Structural 5.78 .+-. 1.86 6.78 .+-. 1.29 6.27 .+-. 1.49 7.28 .+-.
1.07 6.22 .+-. 1.99 7.17 .+-. 1.65 Characteristics (18) (18) (15)
(18) (18) (18) Freedom From 2.39 .+-. 1.72 4.28 .+-. 1.67 3.47 .+-.
1.73 4.83 .+-. 1.79 5.33 .+-. 2.52 6.28 .+-. 1.02 Cellular (18)
(18) (15) (18) (18) (18) Changes of Degeneration TOTAL 9.28 .+-.
3.61 15.11 .+-. 4.80 13.60 .+-. 3.68 15.83 .+-. 2.81 15.06 .+-.
6.30 19.06 .+-. 2.73 (out of 24 (18) (18) (15) (18) (18) (18)
possible points)
[0079] FIGS. 17, 18, and 19 demonstrate the typical histologic
appearance of both treated and nontreated defects at four, eight,
and twelve weeks postoperative.
[0080] At four weeks postoperative differences between the
ultrasound treated and nontreated defects were substantial. Intense
safranin-O staining of the matrix, extensive chondroblast activity,
and earlier subchondral bone formation in the ultrasound treated
defects was in sharp contrast with the lack of activity and
chondroblast phenotype present in the nontreated defects. Early
degenerative changes of the nontreated defects was also
evident.
[0081] At eight weeks the histologic results were similar to the
gross results. Generally, safranin-O staining was not as intense at
eight weeks postoperative in both the ultrasound treated and
nontreated defects. However, subchondral bone regeneration was
complete in the ultrasound treated sites and the repair cartilage
showed less signs of degenerative changes. The nontreated sites
showed less subchondral bone regeneration and organization of the
repair tissue.
[0082] Again at twelve weeks the ultrasound treated site had
greater mean histologic scores than the nontreated defects. In most
cases, subchondral bone regeneration was complete. However, the
chondral layer repair tissue in ultrasound treated sites
demonstrated more articular cartilage characteristics than the
nontreated sites. The majority of the nontreated sites were covered
with superficial layer of maturing fibrous tissue. The intensity of
safranin-O stain was slight or not present in the surface repair
layer of nontreated defects. Adjacent intact cartilage was
hypocellular and in several cases large clusters of greater than 20
chondrocytes were present at the junction between the repair tissue
and the host cartilage. Safranin-O staining was more intense in the
ultrasound treated sites, however, variations within the repair
cartilage of individual defects were observed. Regions of columnar
arrangement of chondrocytes, near normal chondral layer thickness
and safranin-O staining intensity were present in ultrasound
treated defects.
[0083] Strong Type II collagen staining of the newly regenerated
cartilage layer was found in ultrasound treated defects that showed
good repair, whereas nontreated defects sections with poor repair
showed less intensive staining or staining of cartilage deep within
the defect reflective of inappropriate tissue formation.
[0084] Positive staining for Type I collagen in the regenerated
bone showed very little or no localization in the regenerated
cartilage layer of the ultrasound treated samples. Presence of Type
I collagen in the non-bone areas would be an indication of fibrosis
or formation of fibrocartilage.
[0085] An additional study, EXI097-01R, was conducted on 66 rabbits
which received bilateral osteochondral defects in the femurs
according to the study design described above. A summary of the
gross grading results from this study pooled with those from
studies EXI095-01R and EXI096-01R are presented in "Gross Grading
Results" in Table 6.
6TABLE 6 Gross Grading Results Treatment Group Evaluation Period
TOTAL Abrasion Defects 4 weeks Mean 5.7 20 mins. ultrasound Std.
Dev. 1.0 Sample Size 6 Control Mean 4.8 Std. Dev. 0.8 Sample Size 6
Medial Condyle 4 weeks Mean 4.9 Defects Std. Dev. 1.4 20 mins.
ultrasound Sample Size 6 Control Mean 4.8 Std. Dev. 0.6 Sample Size
6 Patellar Groove 4 weeks Mean 5.5 Defects Std. Dev. 1.0 20 mins.
ultrasound Sample Size 6 Control Mean 5.8 (paired) Std. Dev. 0.3
Sample Size 6 Patellar Groove 4 weeks Mean 6.7 Defects Std. Dev.
1.0 20 mins. ultrasound Sample Size 6 5 mins. ultrasound Mean 5.8
Std. Dev. 1.0 Sample Size 6 Patellar Groove 4 weeks Defects ONGOING
20 mins. ultrasound 5 mins. ultrasound Patellar Groove 4 weeks
Defects ONGOING 20 mins. ultrasound 10 mins. ultrasound Patellar
Groove 4 weeks Defects ONGOING 20 mins. ultrasound 40 mins.
ultrasound Patellar Groove 4 weeks Mean 6.6 Defects Std. Dev. 1.0
20 mins. ultrasound (pooled) Sample Size 18 Control Mean 5.3
(pooled) Std. Dev. 1.3 Sample Size 18 Patellar Groove 4 weeks Mean
6.6 Defects Std. Dev. 1.0 20 mins. ultrasound Sample Size 12
Control Mean 5.0 (paired) Std. Dev. 1.5 Sample Size 12 Patellar
Groove 8 weeks Mean 7.0 Defects Std. Dev. 1.2 20 mins. ultrasound
(paired) Sample Size 11 Control Mean 5.8 (paired) Std. Dev. 1.4
Sample Size 11 Patellar Groove 12 weeks Mean 6.5 Defects Std. Dev.
1.1 20 mins. ultrasound (paired) Sample Size 11 Control Mean 5.6
(paired) Std. Dev. 1.1 Sample Size 11 Patellar Groove 24 weeks
Defects ONGOING 20 mins. ultrasound for first 12 weeks
postoperative Control (paired) Patellar Groove 24 weeks Defects
ONGOING 20 mins. ultrasound for first 18 weeks postoperative
Control (paired)
[0086] It will be understood that various modifications can be made
to the various embodiments of the present invention herein
disclosed without departing from its spirit and scope. For example,
various modifications may be made in the structural configuration
of the placement modules and the configuration of the components
used to excite the ultrasonic transducer. Therefore, the above
description should not be construed as limiting the invention but
merely as presenting preferred embodiments of the invention. Those
skilled in the art will envision other modifications within the
scope and spirit of the present invention as defined by the claims
presented below.
* * * * *