U.S. patent application number 16/736672 was filed with the patent office on 2020-05-07 for treatment systems and methods for affecting glands and other targeted structures.
The applicant listed for this patent is Zeltiq Aesthestics, Inc.. Invention is credited to Leonard DeBenedictis, George Frangineas, JR., Kerrie Jiang, Gurvinder Singh Nanda, Linda Pham, Kristine Tatsutani, Bryan J. Weber, Peter Yee.
Application Number | 20200138501 16/736672 |
Document ID | / |
Family ID | 52469360 |
Filed Date | 2020-05-07 |
United States Patent
Application |
20200138501 |
Kind Code |
A1 |
DeBenedictis; Leonard ; et
al. |
May 7, 2020 |
TREATMENT SYSTEMS AND METHODS FOR AFFECTING GLANDS AND OTHER
TARGETED STRUCTURES
Abstract
Treatment systems, methods, and apparatuses for treating acne,
hyperhidrosis, and other skin conditions are described. Aspects of
the technology can include cooling a surface of a patient's skin
and detecting changes in the tissue. The tissue can be cooled a
sufficient length of time and to a temperature low enough to affect
glands or other targeted structures in the skin.
Inventors: |
DeBenedictis; Leonard;
(Dublin, CA) ; Frangineas, JR.; George; (Fremont,
CA) ; Tatsutani; Kristine; (Redwood City, CA)
; Weber; Bryan J.; (Livermore, CA) ; Jiang;
Kerrie; (Foster City, CA) ; Yee; Peter; (San
Ramon, CA) ; Pham; Linda; (Pleasanton, CA) ;
Nanda; Gurvinder Singh; (Fremont, CA) |
|
Applicant: |
Name |
City |
State |
Country |
Type |
Zeltiq Aesthestics, Inc. |
Pleasanton |
CA |
US |
|
|
Family ID: |
52469360 |
Appl. No.: |
16/736672 |
Filed: |
January 7, 2020 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
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15115503 |
Jul 29, 2016 |
10575890 |
|
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PCT/US2015/013971 |
Jan 30, 2015 |
|
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16736672 |
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61934549 |
Jan 31, 2014 |
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61943250 |
Feb 21, 2014 |
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61943257 |
Feb 21, 2014 |
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Current U.S.
Class: |
1/1 |
Current CPC
Class: |
A61F 7/00 20130101; A61H
1/008 20130101; A61F 2007/0093 20130101; A61F 2007/0096 20130101;
A61B 2018/00291 20130101; A61F 2007/0019 20130101; A61F 2007/0045
20130101; A61F 2007/0047 20130101; A61B 2090/065 20160201; A61F
2007/0004 20130101; A61F 7/007 20130101; A61F 2007/0003 20130101;
A61B 2018/00714 20130101; A61F 2007/0052 20130101; A61B 2018/00791
20130101; A61H 1/006 20130101; A61B 18/0206 20130101; A61B
2090/0463 20160201; A61F 2007/0075 20130101; A61N 7/00 20130101;
A61B 2018/00875 20130101; A61F 2007/0087 20130101; A61B 18/02
20130101; A61B 2018/0237 20130101; A61F 2007/0056 20130101; A61K
31/047 20130101; A61B 2018/00464 20130101; A61F 2007/0036 20130101;
A61K 31/045 20130101; A61B 2018/0262 20130101; A61B 2018/00994
20130101; A61B 90/04 20160201 |
International
Class: |
A61B 18/02 20060101
A61B018/02; A61B 90/00 20060101 A61B090/00; A61K 31/047 20060101
A61K031/047; A61K 31/045 20060101 A61K031/045; A61F 7/00 20060101
A61F007/00; A61H 1/00 20060101 A61H001/00; A61N 7/00 20060101
A61N007/00 |
Claims
1. A method for treating a subject's exocrine glands, comprising:
cooling a surface of a subject's skin with a cooling device to
produce a freeze event in a portion of the skin with exocrine
glands, the surface of the skin being cooled to a temperature
higher than about -40 degrees C.; detecting the freeze event in the
patient's skin; and controlling the cooling device and other
treatment parameters to continue to cool the subject's skin after
detecting the freeze event and to maintain at least a partially
frozen state of the portion of the skin for a period of time long
enough to alter a level of production by the exocrine glands, the
partially frozen state of the portion of the skin is maintained
without injuring the epidermis underlying the cooling device, and
the period of time being longer than about 10 seconds.
2. The method of claim 1, wherein the exocrine glands are sebaceous
glands and/or sweat glands, wherein the cooling device and
treatment parameters are controlled so as to not cause either or
both hypopigmentation or hyperpigmentation more than a day
following the treatment.
3. The method of claim 1, wherein the period of time is shorter
than about 1 minute, 2 minutes, 3 minutes, 4 minutes, 5 minutes, or
10 minutes.
4. The method of claim 1, wherein the period of time and
temperature are selected so that lipid rich cells in a subcutaneous
layer are not substantially affected by the skin cooling.
5. The method of claim 1, wherein the period of time and
temperature are selected so that lipid rich cells in a subcutaneous
layer are substantially affected by the skin cooling.
6. The method of claim 1, further comprising thawing the subject's
frozen skin after the period of time has transpired to control
freeze damage caused by the skin cooling.
7. The method of claim 1, further comprising controlling the
cooling device so that the freeze event causes more apoptotic
damage to the subject's tissue than necrotic damage.
8. The method of claim 1, further comprising controlling the
cooling device and treatment parameters so that the freeze event
causes apoptotic damage to the subject's glands and does not cause
necrotic damage to epidermal and/or subcutaneous tissue.
9. The method of claim 1, further comprising controlling the
cooling device and treatment parameters so that the freeze event is
short enough to prevent equilibrium temperature gradients from
being established in the cooled skin.
10. The method of claim 1, further comprising controlling the
cooling device so that the freeze event begins within a second
predetermined period of time after the cooling device begins
cooling the surface of the skin, the second predetermined period of
time being shorter than about 30 seconds, or about 1, 2, 3, 4, 5,
6, 7, 8, 9, or 10 minutes.
11. The method of claim 1, wherein the cooling device is controlled
to supercool the skin, and further comprising heating a surface of
the skin to warm an epidermis to a temperature above freezing, then
delivering a substance, energy, or pressure to the skin to aid in
formation of nucleation sites in the supercooled skin to initiate
the freeze event.
12. The method of claim 1, further comprising delivering a
cryoprotectant to the surface of the subject's skin for a period of
time which is short enough to prevent the cryoprotectant from
significantly inhibiting initiation of the freeze event in dermal
tissue but is long enough to allow the cryoprotectant to provide
substantial freeze protection to epidermal tissue so as to prevent
either hypopigmentation or hyperpigmentation more than a day
following the treatment.
13. The method of claim 1, wherein the subject is affected by acne
in the portion of the skin with exocrine glands, and wherein the
method alters a level of secretion by sebaceous glands in the
portion of the skin, whereby an appearance of the acne is improved
in the portion of the skin.
14. The method of claim 1, wherein the subject is affected by
hyperhidrosis in the portion of the skin with exocrine glands, and
wherein the method alters a level of sweat secretion by sweat
glands in the portion of the skin, whereby hyperhidrosis is treated
in the portion of the skin.
15. A method for treating glands of a subject, comprising: cooling
a surface of a subject's skin to produce a cooling event at a
target region with the glands, the surface of the skin being cooled
to a temperature higher than -40 degrees C.; and controlling a
cooling device and other treatment parameters to cool the surface
of the skin for a period of time and to a temperature sufficiently
low to injure the subject's dermis and the glands therein but
without injuring the subject's epidermis and without injuring the
subject's subcutaneous adipose tissue, the period of time being
less than about 30 minutes.
16. The method of claim 15, wherein the cooling device and other
treatment parameters are controlled to sufficiently protect an
epidermis so as to not cause either or both hypopigmentation or
hyperpigmentation more than a day following the treatment.
17. The method of claim 15, wherein the treatment is for treating
acne by injuring sebaceous glands.
18. The method of claim 15, wherein the treatment is for treating
hyperhidrosis by injuring sweat glands.
19. The method of claim 15, further comprising delivering a
cryoprotectant to the skin to protect the subject's epidermal
tissue.
20. The method of claim 15, further comprising delivering thermal
energy to the surface of the skin before, during, and/or after skin
cooling to protect an uppermost region of the skin from freeze
damage, and optionally delivering thermal energy to the subject's
subcutaneous tissue transcutaneously through the skin to protect
the subject's subcutaneous layer.
21. The method of claim 20, further comprising cooling the skin to
a supercooled temperature, then warming an epidermis to a
non-freezing temperature, and then nucleating the skin to initiate
the freeze event in the supercooled skin.
22. The method of claim 15, further comprising cooling the skin
sufficiently to a cause a freeze event, detecting the freeze event,
and controlling the cooling device so that the freeze event lasts a
second period of time which is longer than 10 seconds and shorter
than 10 minutes.
23. The method of claim 15, wherein the cooling device is
controlled so that a most significant tissue injury cooling zone is
centered at a depth between about 0.5 mm to about 2.0 mm.
24. The method of claim 15, wherein the freeze event damages mostly
dermal tissue.
25. The method of claim 15, wherein the skin is facial skin or
located on either a palm of a hand, a sole of a foot, brow, scalp,
or axilla region.
Description
CROSS-REFERENCE TO RELATED APPLICATIONS
[0001] This application is a Divisional of U.S. patent application
Ser. No. 15/115,503, filed Jul. 29, 2016, now pending, which is a
35 U.S.C. .sctn. 371 U.S. National Phase application of
International Application No. PCT/US2015/013971, filed Jan. 30,
2015, which claims priority to U.S. Provisional Patent Application
No. 61/934,549, filed Jan. 31, 2014, entitled "COMPOSITIONS,
TREATMENT SYSTEMS AND METHODS FOR IMPROVED COOLING OF LIPID-RICH
TISSUE;" U.S. Provisional Patent Application No. 61/943,250, filed
Feb. 21, 2014, entitled "TREATMENT SYSTEMS, METHODS, AND
APPARATUSES FOR IMPROVING THE APPEARANCE OF SKIN;" and U.S.
Provisional Patent Application No. 61/943,257, filed Feb. 21, 2014,
entitled "TREATMENT SYSTEMS, METHODS AND APPARATUS FOR REDUCING
SKIN IRREGULARITIES CAUSED BY CELLULITE." All of these patent
applications are incorporated herein by reference in their
entireties.
INCORPORATION BY REFERENCE OF COMMONLY-OWNED APPLICATIONS AND
PATENTS
[0002] The following commonly assigned U.S. Patent Applications and
U.S. Patents are incorporated herein by reference in their
entirety:
[0003] U.S. Patent Publication No. 2008/0287839 entitled "METHOD OF
ENHANCED REMOVAL OF HEAT FROM SUBCUTANEOUS LIPID-RICH CELLS AND
TREATMENT APPARATUS HAVING AN ACTUATOR";
[0004] U.S. Pat. No. 6,032,675 entitled "FREEZING METHOD FOR
CONTROLLED REMOVAL OF FATTY TISSUE BY LIPOSUCTION";
[0005] U.S. Patent Publication No. 2007/0255362 entitled
"CRYOPROTECTANT FOR USE WITH A TREATMENT DEVICE FOR IMPROVED
COOLING OF SUBCUTANEOUS LIPID-RICH CELLS";
[0006] U.S. Pat. No. 7,854,754 entitled "COOLING DEVICE FOR
REMOVING HEAT FROM SUBCUTANEOUS LIPID-RICH CELLS";
[0007] U.S. Patent Publication No. 2011/0066216 entitled "COOLING
DEVICE FOR REMOVING HEAT FROM SUBCUTANEOUS LIPID-RICH CELLS";
[0008] U.S. Patent Publication No. 2008/0077201 entitled "COOLING
DEVICES WITH FLEXIBLE SENSORS";
[0009] U.S. Patent Publication No. 2008/0077211 entitled "COOLING
DEVICE HAVING A PLURALITY OF CONTROLLABLE COOLING ELEMENTS TO
PROVIDE A PREDETERMINED COOLING PROFILE";
[0010] U.S. Patent Publication No. 2009/0118722, filed Oct. 31,
2007, entitled "METHOD AND APPARATUS FOR COOLING SUBCUTANEOUS
LIPID-RICH CELLS OR TISSUE";
[0011] U.S. Patent Publication No. 2009/0018624 entitled "LIMITING
USE OF DISPOSABLE SYSTEM PATIENT PROTECTION DEVICES";
[0012] U.S. Patent Publication No. 2009/0018623 entitled "SYSTEM
FOR TREATING LIPID-RICH REGIONS";
[0013] U.S. Patent Publication No. 2009/0018625 entitled "MANAGING
SYSTEM TEMPERATURE TO REMOVE HEAT FROM LIPID-RICH REGIONS";
[0014] U.S. Patent Publication No. 2009/0018627 entitled "SECURE
SYSTEM FOR REMOVING HEAT FROM LIPID-RICH REGIONS";
[0015] U.S. Patent Publication No. 2009/0018626 entitled "USER
INTERFACES FOR A SYSTEM THAT REMOVES HEAT FROM LIPID-RICH
REGIONS";
[0016] U.S. Pat. No. 6,041,787 entitled "USE OF CRYOPROTECTIVE
AGENT COMPOUNDS DURING CRYOSURGERY";
[0017] U.S. Pat. No. 8,285,390 entitled "MONITORING THE COOLING OF
SUBCUTANEOUS LIPID-RICH CELLS, SUCH AS THE COOLING OF ADIPOSE
TISSUE";
[0018] U.S. Provisional Patent Application Ser. No. 60/941,567
entitled "METHODS, APPARATUSES AND SYSTEMS FOR COOLING THE SKIN AND
SUBCUTANEOUS TISSUE";
[0019] U.S. Pat. No. 8,275,442 entitled "TREATMENT PLANNING SYSTEMS
AND METHODS FOR BODY CONTOURING APPLICATIONS";
[0020] U.S. patent application Ser. No. 12/275,002 entitled
"APPARATUS WITH HYDROPHILIC RESERVOIRS FOR COOLING SUBCUTANEOUS
LIPID-RICH CELLS";
[0021] U.S. patent application Ser. No. 12/275,014 entitled
"APPARATUS WITH HYDROPHOBIC FILTERS FOR REMOVING HEAT FROM
SUBCUTANEOUS LIPID-RICH CELLS";
[0022] U.S. Patent Publication No. 2010/0152824 entitled "SYSTEMS
AND METHODS WITH INTERRUPT/RESUME CAPABILITIES FOR COOLING
SUBCUTANEOUS LIPID-RICH CELLS";
[0023] U.S. Pat. No. 8,192,474 entitled "TISSUE TREATMENT
METHODS";
[0024] U.S. Patent Publication No. 2010/0280582 entitled "DEVICE,
SYSTEM AND METHOD FOR REMOVING HEAT FROM SUBCUTANEOUS LIPID-RICH
CELLS";
[0025] U.S. Patent Publication No. 2012/0022518 entitled "COMBINED
MODALITY TREATMENT SYSTEMS, METHODS AND APPARATUS FOR BODY
CONTOURING APPLICATIONS";
[0026] U.S. Publication No. 2011/0238050 entitled "HOME-USE
APPLICATORS FOR NON-INVASIVELY REMOVING HEAT FROM SUBCUTANEOUS
LIPID-RICH CELLS VIA PHASE CHANGE COOLANTS, AND ASSOCIATED DEVICES,
SYSTEMS AND METHODS";
[0027] U.S. Publication No. 2011/0238051 entitled "HOME-USE
APPLICATORS FOR NON-INVASIVELY REMOVING HEAT FROM SUBCUTANEOUS
LIPID-RICH CELLS VIA PHASE CHANGE COOLANTS, AND ASSOCIATED DEVICES,
SYSTEMS AND METHODS";
[0028] U.S. Publication No. 2012/0239123 entitled "DEVICES,
APPLICATION SYSTEMS AND METHODS WITH LOCALIZED HEAT FLUX ZONES FOR
REMOVING HEAT FROM SUBCUTANEOUS LIPID-RICH CELLS";
[0029] U.S. patent application Ser. No. 13/830,413 entitled
"MULTI-MODALITY TREATMENT SYSTEMS, METHODS AND APPARATUS FOR
ALTERING SUBCUTANEOUS LIPID-RICH TISSUE";
[0030] U.S. patent application Ser. No. 13/830,027 entitled
"TREATMENT SYSTEMS WITH FLUID MIXING SYSTEMS AND FLUID-COOLED
APPLICATORS AND METHODS OF USING THE SAME";
[0031] U.S. Provisional Patent Application No. 61/943,251 entitled
"TREATMENT SYSTEMS AND METHODS FOR TREATING CELLULITE"; and
[0032] U.S. Provisional Patent Application No. 61/943,257 entitled
"TREATMENT SYSTEMS, METHODS, AND APPARATUS FOR REDUCING
IRREGULARITIES CAUSED BY CELLULITE."
TECHNICAL FIELD
[0033] The present disclosure relates generally to treatment
systems and methods for affecting target structures in a subject's
body. In particular, several embodiments are directed to treatment
systems and methods for affecting glands to treat acne,
hyperhidrosis, cysts, or other conditions.
BACKGROUND
[0034] Exocrine glands found in the skin have a role in maintaining
skin health including lubricating, waterproofing, cleansing and/or
cooling the skin or hair follicles of the body by excreting
water-based, oily and/or waxy substances through skin pores or hair
follicles. Overproduction and/or over-secretion of these substances
by certain exocrine glands, such as sebaceous glands and
sudoriparous glands (e.g., sweat glands), can cause unappealing
skin disorders that have proved to be difficult to treat. For
example, overproduction of sebum, a waxy substance produced and
secreted by sebaceous glands, can lead to formation of comedones
(e.g., blackheads, whiteheads, etc.) as well as other inflammatory
conditions of the skin associated with acne (e.g., inflamed
papules, pustules, nodules, etc.) and can potentially lead to
scarring of the skin. Overproducing sebaceous glands associated
with hair follicles can be mostly found in highly visible regions
of the body, such as on the face, neck, upper chest, shoulders and
back, and demand for effective treatments has been and remains
quite high.
[0035] Hyperhidrosis is a condition associated with excessive
sweating and results from the overproduction and secretion of sweat
from sweat glands in the skin of mammals. Excessive sweating from
eccrine sweat glands, which are distributed almost all over the
body, can cause discomfort and embarrassment. For example, focal
hyperhidrosis can occur on the palms of the hands, soles of the
feet, face and scalp. Apocrine sweat glands, particularly in the
axilla (i.e., armpits), have oil-producing cells that can
contribute to excessive production and undesirable odor. Treatment
for these conditions are often ineffective, non-lasting, and/or
have undesirable side-effects.
BRIEF DESCRIPTION OF THE DRAWINGS
[0036] In the drawings, identical reference numbers identify
similar elements or acts. The sizes and relative positions of
elements in the drawings are not necessarily drawn to scale.
[0037] FIG. 1 is a schematic cross-sectional view of the skin,
dermis, and subcutaneous tissue of a subject.
[0038] FIG. 2 is a schematic cross-sectional view of the skin,
dermis, and subcutaneous tissue of the subject in FIG. 1 after
treating sebaceous glands.
[0039] FIG. 3 is a partially schematic, isometric view of a
treatment system for non-invasively treating targeted structures in
a human subjects body in accordance with an embodiment of the
technology.
[0040] FIG. 4 is a cross-sectional view of a conduit of the
treatment system of FIG. 3.
[0041] FIG. 5 is a cross-sectional view of a treatment device
applied to a treatment site in accordance with an embodiment of the
technology.
[0042] FIGS. 6A to 6C are schematic cross-sectional views of
treatment devices in accordance with embodiments of the
technology.
[0043] FIG. 6D is a side view of an applicator for treating
discrete features in accordance with embodiments of the
technology.
[0044] FIGS. 6E and 6F are cross-sectional views of a distal end of
the applicator of FIG. 6D.
[0045] FIGS. 7 to 10 are flow diagrams illustrating methods for
affecting target regions in accordance with embodiments of the
technology.
[0046] FIG. 11 is a schematic block diagram illustrating computing
system software modules and subcomponents of a computing device
suitable to be used in treatment systems in accordance with
embodiments of the technology.
DETAILED DESCRIPTION
A. Overview
[0047] The present disclosure describes treatment systems and
methods for affecting target structures in tissue. The systems and
methods disclosed herein can be used to target glands (e.g.,
exocrine glands, sebaceous glands, sudoriparous glands, etc.),
structures in the skin (e.g., hair follicles, superficial nerves,
etc.), and/or layer(s) of tissue (e.g., dermal layer, epidermal
layer, layer(s) of the epidermis, etc.). Several of the details set
forth below are provided to describe the following examples and
methods in a manner sufficient to enable a person skilled in the
relevant art to practice, make, and use them. Several of the
details and advantages described below, however, may not be
necessary to practice certain examples and methods of the
technology. Although described examples and methods target glands,
the technology can target other structures or features and may
include other examples and methods that are within the scope of the
technology but are not described in detail. The treatment systems
and treatment devices disclosed herein can perform a wide range of
cryotherapy procedures.
[0048] Reference throughout this specification to "one example,"
"an example," "one embodiment," or "an embodiment" means that a
particular feature, structure, or characteristic described in
connection with the example is included in at least one example of
the present technology. Thus, the occurrences of the phrases "in
one example," "in an example," "one embodiment," or "an embodiment"
in various places throughout this specification are not necessarily
all referring to the same example. Furthermore, the particular
features, structures, routines, blocks, stages, or characteristics
may be combined in any suitable manner in one or more examples of
the technology. The headings provided herein are for convenience
only and are not intended to limit or interpret the scope or
meaning of the technology.
[0049] Various aspects of the technology are directed to treatment
systems and methods for affecting target structures in a human
subject's body. The target structures can be glands, hair
follicles, nerves (e.g., superficial nerves), or one or more layers
of tissue (e.g., dermal layer, epidermal layer, layer(s) of the
epidermis, etc.). To treat acne, the surface of the subject's skin
can be cooled to produce a temperature at or below 0, 5, 10, 15, or
20 degrees C. and to produce either a cooling event or a freeze
event in a targeted portion of the skin with sebaceous glands. The
skin can be cooled to maintain the cooled state or frozen state of
the targeted portion of the skin for a period of time long enough
to alter a level of secretion production by the sebaceous glands.
The characteristics of the cooling event or freeze event can be
controlled to manage thermal injury. Such characteristics include,
without limitation, the amount of cooling or freezing, density and
distribution of ice crystals, freezing rate, etc. Cryotherapy can
affect, without limitation, glandular function, structures of
glands (e.g., gland portions, duct portions, etc.), number of
glands, and/or sizes of glands.
[0050] Freeze events can include partially or completely freezing
liquids or lipids proximate to or within glands to destroy, reduce,
disrupt, modify, or otherwise affect glands or the supporting
anatomical features (e.g., ducts, pores, hair follicles, etc.). In
some embodiments, to treat exocrine glands, a subject's skin can be
cooled to produce a partial freeze event in a portion of skin with
exocrine glands. The level of freezing can be controlled to limit
tissue damage, such as tissue damage to non-targeted tissue, damage
of targeted tissue (e.g., to avoid excess damage to targeted
tissue), and so forth. The subject's skin can be continuously or
periodically cooled/heated to adjust the level of freezing. For
example, the skin surface can be cooled or heated to increase or
decrease, respectively, the number and/or sizes of ice crystals at
the target region.
[0051] In some embodiments, a method comprises cooling a subject's
skin to produce a cooling event in the skin, but not a freeze
event. After the cooling event begins, the subject's skin is cooled
to maintain the cooling event to alter glands (e.g., gland
function, gland size, gland structure, gland number, etc.). The
cooling event can alternatively be a freeze event that involves at
least partially or totally freezing a target region with the glands
so as to alter secretion levels of the glands. In acne treatments,
the freeze event can injure sebaceous glands to reduce sebum
production. In hyperhidrosis treatments, the freeze event can
injure sweat glands to reduce sweating. The location and
characteristics of the freeze event can be selected based on
treatments to be performed.
[0052] Aspects of the technology can include a method for treating
a subject's exocrine glands by cooling a surface of a subject's
skin with a cooling device to produce a partial or total freeze
event in a portion of the skin with exocrine glands. The partial or
total freeze event in the patient's skin can be detected. The
cooling device and other treatment parameters can be controlled to
continue to cool the subject's skin after detecting the partial or
total freeze event and to maintain a partially or totally frozen
state of the portion of the skin for a period of time long enough
to alter a level of production by the exocrine glands. In one
embodiment, the period of time is longer than a predetermined
threshold period of time, such as 10 seconds, 20 seconds, or other
selected period of time. If the epidermis is overly frozen,
hyperpigmentation (skin darkening) or hypopigmentation (skin
lightening) can result, which is often undesirable. The cooling
device and treatment parameters can be controlled so as to not
cause either or both hypopigmentation or hyperpigmentation more
than a day following treatment.
[0053] At least some embodiments are systems and methods for
selective non-invasive cooling of tissue sufficiently deep to
affect glands. Axilla apocrine sweat glands or eccrine sweat glands
on the palms of the hands can be at different tissue depths than
sebaceous glands within acne-prone regions (e.g., regions along the
face, chest, shoulders, or back). The systems and methods disclosed
herein can controllably cool tissue at specific depths for injuring
targeted glands. In various embodiments, a zone of maximum cooling
or maximum freezing can occur at depths between about 1 mm to about
5 mm, between about 2 mm and about 5 mm, between about 3 mm and
about 5 mm, or between about 4 mm and about 5 mm. Other depths can
be selected based on the location of the targeted structures. In
some embodiments, a treatment site can be cooled to a temperature
equal to or lower than about 0.degree. C., -5.degree. C.,
-10.degree. C., -15.degree. C., -20.degree. C., or -25.degree. C.
for a treatment period, and either be in a supercooled state, a
partial frozen state, or totally frozen state. The treatment period
can be equal to or greater than about 1 second, 2 seconds, 3
seconds, 5 seconds, 30 seconds, 1 minute, 5 minutes, 10 minutes, 30
minutes, or other time periods selected based on the desired
thermal injury. In some supercooling embodiments, the skin is
cooled to a supercooled temperature and the epidermis is then
warmed to a non-freezing temperature. After warming the epidermis,
supercooled tissue is nucleated to initiate the freeze event in the
supercooled skin. A freezing point of a material is most reliably
ascertained by warming frozen material slowly and measuring a
temperature at which melting begins to occur. This temperature is
generally not ambiguous if the material is slowly warmed. Partial
melting will begin to occur at the freezing/melting point.
Conversely, if a non-frozen material is cooled, its
freezing/melting point is harder to ascertain since it is known
that many materials can simply "supercool," that is they can be
cooled to a bulk temperature below their freezing/melting point and
still remain in a non-frozen state. As used herein, "supercooling,"
"supercooled," "supercool," etc., refers to a condition in which a
material is at a temperature below its freezing/melting point but
is still in an unfrozen or mostly unfrozen state.
[0054] With or without freezing, at least some embodiments of the
technology are directed to controlling a cooling device or
providing other means for sufficiently protecting the epidermis
from injuries that cause hyperpigmentation (skin darkening) or
hypopigmentation (skin lightening). The other means for protection
can include, without limitation, heating the epidermis to a
non-freezing temperature while deeper tissue remains cold to induce
injury thereto and/or applying a cryoprotectant to a surface of the
skin to provide freeze protection to the epidermis while allowing
deeper tissue or structures to be more affected by the cooling/cold
treatment.
[0055] Applicators disclosed herein can include one or more
elements (e.g., resistive heaters, electrodes, transducers,
vibrators, etc.) for delivering energy, such as thermal energy,
electromagnetic energy, infrared energy, light energy, ultraviolet
energy, radiofrequency energy, microwave energy, ultrasound energy
(e.g., low frequency ultrasound, high frequency ultrasound, etc.),
mechanical massage, and/or electric fields (e.g., AC or DC electric
fields). The energy can inhibit or reduce freeze damage or cooling
damage in non-targeted regions. Thermal energy can be used to
protect non-targeted tissue, such as facial subcutaneous fat, when
cryogenically treating superficial facial dermal structures.
Additionally or alternatively, non-targeted regions can be
protected by a chemical cryoprotectant. In addition to targeting
glands (e.g., exocrine glands such as sebaceous glands, apocrine
sweat glands, eccrine sweat glands, etc.), applicators can be
configured to target other structures, such as collagen and/or
elastin for skin tightening and dermal thickening, nerve tissue
(e.g., superficial nerves), and/or hair follicles.
[0056] At least some aspects of the technology are directed to
systems and methods that enable supercooling of target regions.
Aspects of the disclosure are further directed to systems or
methods for protecting non-targeted cells, such as cells in the
dermal and/or epidermal skin layers, by preventing or limiting
thermal damage (e.g., cooling or freeze damage) during
dermatological and related aesthetic procedures that require
sustained exposure to cold temperatures. For example, treatment
systems can supercool treatment sites without causing nucleation
and freezing. Non-targeted tissue can be heated to localize the
supercooling, and after localizing the supercooled tissue,
supercooled body fluids/lipids can be nucleated by various methods
to initiate a partial or total freeze and to damage, reduce,
disrupt, modify or otherwise affect targeted cells.
[0057] In some supercooling embodiments, regions with glands can be
supercooled either with or without using any cryoprotectant.
Non-targeted region(s) can be heated above their freezing points
before initiating crystallization of the supercooled tissue. In
certain embodiments for affecting glands in the dermal layer, the
skin can be supercooled either with or without affecting the
subcutaneous layer. After heating the epidermal layer so that
mostly dermal tissue is supercooled, nucleation in the dermal layer
can be initiated. Freezing of the supercooled region can be
promoted without damaging non-targeted tissue or non-targeted
anatomical features. Nucleation can be induced by delivering an
alternating current to the tissue, applying a nucleating solution
onto the surface of the skin (for example one that includes
bacteria which initiate nucleation), applying fields (e.g.,
electric fields), and/or by creating a mechanical perturbation to
the tissue, such as by use of vibration, ultrasound energy,
etc.
B. Treatment Sites
[0058] FIG. 1 is a schematic cross-sectional view of tissue of a
subject in accordance with one embodiment. The subject's skin 10
includes the dermis 12 located between the epidermis 14 and the
subcutaneous layer 16. The dermis 12 includes sebaceous glands 17
that produce sebum for moisturizing the skin and hair. Acne is a
skin condition typically characterized by excess sebum that may
plug hair follicles and/or pores. The level of sebum production may
vary between individuals and may vary by body location depending on
the number and sizes of the sebaceous glands. Sebum can flow along
the healthy hair follicle 20 to moisturize the hair 23 and/or
epidermis 14. When the sebaceous glands 17 produce excess sebum, it
can collect and/or become trapped in hair follicles. Overproduction
and/or entrapment of sebum, the waxy substance produced and
secreted by sebaceous glands 17, can lead to formation of comedones
(e.g., blackheads, whiteheads, etc.) as well as other inflammatory
conditions of the skin associated with acne (e.g., inflamed
papules, pustules, nodules, etc.). In some individuals, inflamed
follicles and pores can become infected and the condition can
potentially lead to scarring of the skin. The illustrated hair
follicle 22 is clogged with excess sebum to form a pimple or red
spot. Other medical conditions associated with overactive sebaceous
glands which produce an excess of sebum include sebaceous cysts,
hyperplasia and sebaceous adenoma. Non-medical, but cosmetically
unappealing, conditions associated with overactive sebaceous glands
include oily skin and/or oily hair (e.g., on the scalp).
[0059] Hyperhidrosis is a skin condition characterized by abnormal
sweating due to high secretion levels of sweat glands 26. Eccrine
sweat glands are controlled by the sympathetic nervous system and
regulate body temperature. When an individual's body temperature
rises, eccrine sweat glands secrete sweat (i.e., water and other
solutes) that flows through a gland tubule 28. The sweat can
evaporate from the skin surface to cool the body. Apocrine sweat
glands (not shown) secrete an oil-containing sweat into hair
follicles 20. The axilla (e.g., armpit) and genital regions often
have a higher concentration of apocrine sweat glands. Hyperhidrosis
occurs when sweat glands produce and secrete sweat at levels above
that required for regulation of body temperature, and the condition
can be generalized or localized (i.e., focal hyperhidrosis) to
specific body parts (e.g., palms of hands, soles of feet, brow,
scalp, face, underarms, etc.).
[0060] FIG. 2 is a schematic cross-sectional view of the skin 10 in
FIG. 1 showing a reduction of acne after treatment in accordance
with aspects of the present technology. A treatment device in the
form of a thermoelectric applicator 104 ("applicator 104") has been
applied to and cooled the skin 10 to produce a freeze-induced
injury that affected the sebaceous glands 17. Although the
reduction in acne is shown while the applicator 104 is applied to
the skin 10, it may take a relatively long period of time (e.g.,
days, weeks, months, etc.) for acne to be reduced after treatment.
The sebum production level of the two sebaceous glands 17 along the
hair follicle 22 has been substantially reduced to inhibit clogging
to minimize, reduce, or eliminate acne. The sweat gland 26 can also
be targeted. For example, the applicator 104 can produce a partial
or total freeze event or non-freezing cooling event or supercooling
event to injure the sweat gland 26 and/or duct 28 in a region of
the skin located along the hands, armpits, or other locations with
excess sweating. Cryotherapy can be performed any number of times
at the same site or different sites to treat acne, hyperhidrosis,
or other conditions.
C. Cryotherapy
[0061] FIG. 3 and the following discussion provide a general
description of an example of a suitable non-invasive treatment
system 100 in which aspects of the technology can be implemented.
The treatment system 100 can be a temperature-controlled cooling
apparatus for cooling tissue at a targeted treatment site to
perform cryotherapy. Physiological characteristics affected by
cryotherapy can include, without limitation, cellular stability,
cell/tissue elasticity, cell size, cell number, and/or gland size
or secretion ability (e.g., size/diameter of the duct portion). For
example, the treatment system 100 can cool the epidermis, dermis,
subcutaneous fat, or other targeted tissue to modify glandular
function, reduce gland size, etc. Non-targeted tissue, such as
subdermal tissue or tissue adjacent the targeted exocrine glands,
can remain generally unaffected. In various embodiments, the
treatment system 100 can be configured to cool the skin of the
patient to selectively affect (e.g., injure, damage, kill)
secreting exocrine glandular cells. In a particular example,
cooling can produce a cold shock response to modify a secretion
volume from a targeted exocrine gland of the epidermis and/or
dermis by affecting protein proliferation and other cellular
functions. Those skilled in the relevant art will appreciate that
other examples of the disclosure can be practiced with other
treatment systems and treatment protocols, including invasive,
minimally invasive, other non-invasive medical treatments.
[0062] In one example, lipid-producing cells residing in or at
least proximate to sebaceous glands (e.g., glandular epithelial
cells) present in the dermis of a target region can be targeted by
the treatment system 100 for the treatment of acne or other skin
condition. The lipid-producing cells residing in or proximate to
sebaceous glands contribute to production of sebum, the waxy and
oily secretion that can contribute to acne. For example, the
treatment system 100 can be configured to reduce a temperature of a
dermal layer of skin to reduce the temperature of lipid-producing
cells residing in or at least proximate to sebaceous glands such
that the targeted lipid-producing cells excrete a lower amount of
sebum, such that there are fewer lipid-producing cells resulting in
less sebum production within the targeted sebaceous glands, or in
another embodiment, such that the sebaceous glands are destroyed.
The treatment system 100 can be configured, for example, to reduce
a subject's acne by cooling acne-prone regions of the body.
[0063] In another example, secreting glandular cells residing in
axilla apocrine sweat glands can be targeted by the treatment
system 100 for the treatment of hyperhidrosis. Apocrine sweat
glands comprise a coiled secretory portion located at the junction
of the dermis and the subcutaneous fat, and a duct portion that
funnels the secreted sweat substance into a portion of a hair
follicle. Secreting glandular cells residing in the coiled
secretory portion between the dermis and the subcutaneous layers
produce an oily compound and create a secretion substance that also
includes water and other solutes, such as minerals, lactate and
urea to form apocrine sweat. The treatment system 100 can be
configured to reduce a temperature of a dermal layer of skin (e.g.,
at or near the axilla) to reduce the temperature of secreting
glandular cells residing in the coiled portion of the apocrine
sweat glands such that the targeted cells excrete a lower amount of
oil-containing sweat, such that there are fewer sweat-producing
cells resulting in less sweat/oil production within the targeted
apocrine sweat glands, or in another embodiment, such that the
apocrine sweat glands are destroyed. In yet another embodiment,
secreting glandular cells residing in or proximate to eccrine sweat
glands (e.g., in the palms of the hands, soles of the feet, scalp,
face, axilla region, etc.) can be targeted by the treatment system
100 for the treatment of focal hyperhidrosis at those treatment
sites.
[0064] Referring to FIG. 3, the applicator 104 is suitable for
altering a function of a gland residing in skin without affecting
subcutaneous tissue (e.g., subcutaneous adipose tissue, etc.). The
applicator 104 can be suitable for modifying a secretion volume,
level, biochemical content, or other factor from targeted exocrine
glands (e.g., sebaceous glands 17 or sweat glands 26 shown in FIG.
1) by cooling the skin without permanently altering cells of
non-targeted tissue (e.g., deep dermal tissue, subdermal tissue,
etc.). Without being bound by theory, the effect of cooling
selected cells (e.g., glandular secreting cells, hair follicles,
etc.) is believed to result in, for example, protein alteration
(e.g., synthesis of heat shock proteins, stress proteins, etc.),
cell size alteration, cell division, wound remodeling (e.g.,
thickening of the epidermis, contraction of the epidermis, etc.),
fibrosis, and so forth. By cooling the skin to a sufficient low
temperature, target cells that contribute to the presence of
undesired features can be selectively affected while non-targeted
tissue can be unaffected.
[0065] The applicator 104 can be used to perform a wide range of
different cryotherapy procedures. One cryotherapy procedure
involves at least partially freezing tissue (e.g., cellular
structures, intracellular fluid, extracellular fluid, connective
tissue etc.) in a target tissue region to form crystals that alter
targeted cells to modify a glandular secretion characteristic
(e.g., volume, content, etc.) without destroying a significant
amount of cells in the skin. To avoid destroying skin cells in a
partial freeze embodiment and in an embodiment where tissue is not
partially frozen, the surface of the patient's skin can be cooled
to temperatures no lower than, for example, -40.degree. C. for a
duration short enough to avoid, for example, excessive ice
formation, permanent thermal damage, or lightening or darkening
skin, such as significant hypopigmentation (including long-lasting
or permanent hypopigmentation) or hyperpigmentation (including
long-lasting or permanent hyperpigmentation) in a period of time
following a treatment, such as several hours; one, two, three days;
or one, two, three weeks; and longer periods of time following a
treatment. In another embodiment, undue destruction of skin cells,
epidermal cells in particular, can be avoided by applying heat to
the surface of the patient's skin to heat these skin cells above
their freezing temperature. The patient's skin can be warmed to at
least about -30.degree. C., -25.degree. C., -20.degree. C.,
-15.degree. C., -10.degree. C., 0.degree. C., 10.degree. C.,
20.degree. C., 30.degree. C., or other temperature sufficient to
avoid, for example, excessive ice formation, permanent thermal
damage, or significant hypopigmentation or hyperpigmentation of the
non-targeted and/or epidermal tissue. In some treatments, skin can
be cooled to produce partial or total freeze events that cause
apoptotic damage to skin tissue without causing significant damage
to adjacent subcutaneous tissue. Apoptosis, also referred to as
"programmed cell death", of the skin tissue can be a
genetically-induced death mechanism by which cells slowly
self-destruct without incurring damage to surrounding tissues.
Other cryotherapy procedures may cause non-apoptotic responses.
[0066] In some tissue-freezing procedures, the applicator 104 can
controllably freeze tissue (e.g., organic matter, inorganic matter,
etc.) within a tissue region and can detect the freeze event. After
detecting the freeze event, the applicator 104 can periodically or
continuously remove heat from the target tissue to keep a volume of
target tissue frozen for a suitable predetermined length of time to
elicit a desired response and yet a short enough period of time to
not cause any unwanted or undesired side effects, such as
hypopigmentation and/or hyperpigmentation. The detected freeze
event can be a partial freeze event, a complete freeze event, etc.
In some embodiments, the controlled freezing causes tightening of
the skin, thickening of the skin, and/or a cold shock response at
the cellular level in the skin. In one tissue-freezing treatment,
the applicator 104 can produce a partial or total freeze event that
includes, without limitation, partial or full thickness freezing of
the patient's skin for a relatively short limit to avoid cooling
the adjacent subcutaneous tissue to a low enough temperature for
subcutaneous cell death. The freezing process can include forming
ice crystals in intracellular and/or extracellular fluids, and the
ice crystals can be small enough to avoid disrupting membranes so
as to prevent significant permanent tissue damage, such as
necrosis. Some partial freeze events can include freezing mostly
extracellular material without freezing a substantial amount of
intercellular material. In other procedures, partial freeze events
can include freezing mostly intercellular material without freezing
a substantial amount of extracellular material. The frozen target
tissue can remain in the frozen state long enough to affect the
target tissue but short enough to avoid damaging non-targeted
tissue or damaging an undue amount of the target tissue. For
example, the duration of the freeze event can be shorter than about
20 seconds, 30 seconds, or 45 seconds or about 1, 2, 3, 4, 5 or 10
minutes. The frozen tissue can be thawed to prevent necrosis and,
in some embodiments, can be thawed within about 20 seconds, 30
seconds, or 45 seconds or about 1, 2, 3, 4, 5, or 10 minutes after
initiation of the freeze event.
[0067] The mechanisms of cold-induced tissue injury in cryotherapy
can also involve direct cellular injury (e.g., damage to the
cellular machinery) and/or vascular injury in embodiments where
freezing occurs and in embodiments where freezing does not occur.
For example, cell injury can be controlled by adjusting thermal
parameters, including (1) cooling rate, (2) end (or minimum)
temperature, (3) time held at the minimum temperature (or hold
time), (4) temperature profile, and (5) thawing rate. In one
example, increasing the hold time can allow the intracellular
compartments to equilibrate with the extracellular space, thereby
increasing cellular dehydration. Another mechanism of cold-induced
injury is cold and/or freeze-stimulated immunologic injury. Without
being bound by theory, it is believed that after cryotherapy, the
immune system of the host is sensitized to the disrupted tissue
(e.g., lethally damaged tissue, undamaged tissue, or sublethally
injured tissue), which can be subsequently destroyed by the immune
system.
[0068] One mechanism to selectively affect oil and/or
sebum-producing and secreting glandular cells is to cool the
targeted tissue to temperatures that affect lipid-rich cells (which
generally freeze or are damaged at temperatures which are higher
than temperatures at which non-lipid rich cells are damaged) but
that do not negatively affect non-lipid rich cells, such as other
cells in the epidermal and dermal layers at or proximate to the
treatment site which have lower temperature damage thresholds. The
treatment system 100 can be configured to cool the subject's skin
for a period of time long enough so that lipid-rich cells (sebum or
oil-producing cells residing in or at least proximate to exocrine
glands) in the dermal layer are substantially affected to cause,
for example, apoptosis. Apoptosis of lipid-rich cells may be a
desirable outcome for beneficially altering (e.g., reducing)
glandular function that may contribute to an undesirable appearance
(e.g., acne, hyperhidrosis, etc.). Apoptosis of glandular
lipid-rich cells can involve ordered series of biochemical events
that induce cells to morphologically change. These changes include
cellular blebbing, loss of cell membrane asymmetry and attachment,
cell shrinkage, chromatin condensation, and chromosomal DNA
fragmentation. Injury via an external stimulus, such as cold
exposure, is one mechanism that can induce apoptosis in cells.
Nagle, W. A., Soloff, B. L., Moss, A. J. Jr., Henle, K. J.
"Cultured Chinese Hamster Cells Undergo Apoptosis After Exposure to
Cold but Nonfreezing Temperatures" Cryobiology 27, 439-451 (1990).
One aspect of apoptosis, in contrast to cellular necrosis (a
traumatic form of cell death causing, and sometimes induced by,
local inflammation), is that apoptotic cells express and display
phagocytic markers on the surface of the cell membrane, thus
marking the cells for phagocytosis by, for example, macrophages. As
a result, phagocytes can engulf and remove the dying cells (e.g.,
the lipid-rich cells) without eliciting an immune response.
[0069] Without being bound by theory, one mechanism of apoptotic
lipid-rich cell death by cooling is believed to involve localized
crystallization of lipids within the adipocytes at temperatures
that may or may not induce crystallization in non-lipid-rich cells.
The crystallized lipids may selectively injure these cells,
inducing apoptosis (and may also induce necrotic death if the
crystallized lipids damage or rupture the bilayer lipid membrane of
the glandular cell). Another mechanism of injury involves the lipid
phase transition of those lipids within the cell's bilayer lipid
membrane, which results in membrane disruption, thereby inducing
apoptosis. This mechanism is well documented for many cell types
and may be active when lipid-rich cells, are cooled. Mazur, P.,
"Cryobiology: the Freezing of Biological Systems" Science, 68:
939-949 (1970); Quinn, P. J., "A Lipid Phase Separation Model of
Low Temperature Damage to Biological Membranes" Cryobiology, 22:
128-147 (1985); Rubinsky, B., "Principles of Low Temperature
Preservation" Heart Failure Reviews, 8, 277-284 (2003). Other
possible mechanisms of lipid-rich cell damage, described in U.S.
Pat. No. 8,192,474, relates to ischemia/reperfusion injury that may
occur under certain conditions when such cells are cooled as
described herein. For instance, during treatment by cooling as
described herein, targeted glandular tissue may experience a
restriction in blood supply and thus be starved of oxygen due to
isolation while pulled into, e.g., a vacuum cup, or simply as a
result of the cooling which may affect vasoconstriction in the
cooled tissue. In addition to the ischemic damage caused by oxygen
starvation and the build-up of metabolic waste products in the
tissue during the period of restricted blood flow, restoration of
blood flow after cooling treatment may additionally produce
reperfusion injury to the glandular cells due to inflammation and
oxidative damage that is known to occur when oxygenated blood is
restored to tissue that has undergone a period of ischemia. This
type of injury may be accelerated by exposing the glandular cells
to an energy source (via, e.g., thermal, electrical, chemical,
mechanical, acoustic or other means) or otherwise increasing the
blood flow rate in connection with or after cooling treatment as
described herein. Increasing vasoconstriction in such glandular
tissue by, e.g., various mechanical means (e.g., application of
pressure or massage), chemical means or certain cooling conditions,
as well as the local introduction of oxygen radical-forming
compounds to stimulate inflammation and/or leukocyte activity in
glandular tissue may also contribute to accelerating injury to such
cells. Other yet-to-be understood mechanisms of injury may also
exist.
[0070] In addition to the apoptotic mechanisms involved in
lipid-rich cell death, local cold exposure may induce lipolysis
(i.e., fat metabolism) of lipid-rich cells. For example, cold
stress has been shown to enhance rates of lipolysis from that
observed under normal conditions which serves to further increase
the volumetric reduction of lipid-rich cells. Vallerand, A. L.,
Zamecnik. J., Jones, P. J. H., Jacobs, I. "Cold Stress Increases
Lipolysis, FFA Ra and TG/FFA Cycling in Humans" Aviation, Space and
Environmental Medicine 70, 42-50 (1999).
[0071] Without being bound by theory, the effect of cooling on
lipid-rich cells is believed to result in, for example, membrane
disruption, shrinkage, disabling, destroying, removing, killing, or
another method of lipid-rich cell alteration. For example, when
cooling glandular tissue in the dermal layer to a temperature lower
than 37.degree. C., lipid-rich cells (e.g., sebum-producing cells
within sebaceous glands, oil-producing cells within sweat glands)
can selectively be affected. In general, the remaining cells in the
epidermis and dermis of the subject 101 have lower amounts of
lipids compared to the secreting lipid-rich cells forming portions
of the glandular tissue. Since lipid-rich cells are more sensitive
to cold-induced damage than non-lipid-rich cells, it is possible to
use non-invasive or minimally invasive cooling to destroy
lipid-rich cells without destroying the overlying or surrounding
skin cells. In some embodiments, lipid-rich cells within secretory
glands are destroyed while the appearance of overlying skin is
improved.
[0072] Lipid-containing cells are more easily damaged by low
temperatures than the non-lipid rich dermal and epidermal cells,
and as such, the treatment system 100 can be used to cool the
desired layers of skin at the treatment sites to a temperature
above the freezing point of water, but below the freezing point of
fat. It is believed that the temperatures can be controlled to
manage damage in the non-lipid-rich cells of the epidermis and/or
dermis via, for example, intracellular and/or extracellular ice
formation. Excessive ice formation may rupture the cell wall and
may also form sharp crystals that locally pierce the cell wall as
well as vital internal organelles. Ice crystal initiation and
growth can be managed to avoid cell death in the non-targeted
portions of the skin. When extracellular water freezes to form ice,
the remaining extracellular fluid becomes progressively more
concentrated with solutes. The high solute concentration of the
extracellular fluid may cause intracellular fluid to be driven
through the semi-permeable cellular wall by osmosis resulting in
cell dehydration. The applicator 104 can reduce the temperature of
the lipid-rich cells found in the targeted glandular tissue such
that the lipid rich cells are destroyed while the temperature of
the remaining skin cells are maintained at a high enough
temperature to produce non-destructive freeze events in the skin.
Cryoprotectants and/or thermal cycling can prevent destructive
freeze events in the non-targeted skin tissue.
[0073] At least some aspects of the technology are directed to
systems and methods of treating a patient by cooling a surface of
the patient's skin to a temperature sufficiently low to cause
supercooling of targeted tissue below the skin surface. The surface
of the skin can then be heated to a non-supercooled temperature
while the targeted tissue remains in a supercooled state. After
heating the non-targeted tissue, the supercooled targeted tissue
can be controllably frozen. In some embodiments, nucleation can be
controlled to cause partial or total freezing. The applicator 104
can be kept generally stationary relative to the treatment site
during cooling to avoid pressure changes that would cause
nucleation. After heating non-targeted tissue, the applicator can
cause nucleation in the supercooled targeted tissue by, for
example, varying applied pressures, delivering energy (e.g.,
ultrasound energy, RF energy, ultrasound energy), applying fields
(e.g., electric fields), or providing other perturbations (e.g.,
vibrations, pulses, etc.), as well as combinations thereof. Because
the non-targeted tissue has been warmed to a non-supercooled state,
it does not experience a freeze event. In some embodiments, the
applicator can include one or more movable plates (e.g., plates
movable to vary applied pressures), rotatable eccentric masses,
ultrasound transducers, electrical current generators, or other
elements capable of providing nucleating perturbations. Vacuum
applicators can increase and decrease vacuum levels to massage
tissue, vary applied pressures, etc.
[0074] Once catalyzed, the partial or total freeze event can be
detected, and a cooling device associated with the treatment system
100 can be controlled to continue cooling the patient's skin so as
to maintain a frozen state of targeted tissue for a desired period
of time. The skin can be periodically or continuously cooled to
keep a sufficient volume of the tissue in a frozen state. In some
embodiments, the targeted tissue can be kept frozen for longer or
shorter than about, for example, 1 second, 5 seconds, 10 seconds,
20 seconds, 30 seconds, 1 minute, several minutes, or other time
period selected to reduce or limit frostbite or necrosis. Further,
the temperature of the upper tissue of the skin can be detected,
and the treatment system can be controlled to apply heat to the
surface of the patient's skin for a preselected period of time to
prevent freezing of non-targeted tissue. The preselected period of
time can be longer or shorter than about 1, 2, 3, 4, or 5 seconds.
Accordingly, non-targeted tissue can be protected without using a
chemical cryoprotectant that may cause unwanted side effects.
Alternatively, a cryoprotectant can also be used if an additional
margin of safety for some tissue, such as the epidermis, is
desired.
D. Treatment Systems and Methods of Treatment
[0075] FIG. 3 is a partially schematic, isometric view of a
treatment system for non-invasively treating targeted structures in
a human subjects body in accordance with an embodiment of the
technology. The treatment system 100 can include the applicator
104, a connector 103, and a base unit 106. After applying the
applicator 104 to a subject 101, it can cool cells in or associated
with targeted glands. For example, the applicator 104 can be
applied to acne-prone regions and can transcutaneously cool skin to
reduce the temperature of lipid-producing cells residing in or at
least proximate to sebaceous glands (e.g., glandular epithelial
cells) to lower the amount of secreted sebum and thereby eliminate,
reduce, or limit acne. The applicator 104 can also cool sweat
glands and associated structures to treat hyperhidrosis.
[0076] The connector 103 can be an umbilical cord that provides
energy, fluid, and/or suction from the base unit 106 to the
applicator 104. The base unit 106 can include a fluid chamber or
reservoir 105 (illustrated in phantom line) and a controller 114
carried by a housing 125 with wheels 126. The base unit 106 can
include a refrigeration unit, a cooling tower, a thermoelectric
chiller, heaters, or any other devices capable of controlling the
temperature of coolant in the fluid chamber 105 and can be
connectable to an external power source and/or include an internal
power supply 110 (shown in phantom line). The power supply 110 can
provide electrical energy (e.g., a direct current voltage) for
powering electrical elements of the applicator 104. A municipal
water supply (e.g., tap water) can be used in place of or in
conjunction with the fluid chamber 105. In some embodiments, the
system 100 includes a pressurization device 117 that can provide
suction and can include one or more pumps, valves, and/or
regulators. Air pressure can be controlled by a regulator located
between the pressurization device 117 and the applicator 104. If
the vacuum level is too low, tissue may not be adequately (or at
all) held against the applicator 104, and the applicator 104 may
tend to move along the patient's skin. If the vacuum level is too
high, undesirable patient discomfort and/or tissue damage could
occur. A vacuum level can be selected based on the characteristics
of the tissue and desired level of comfort.
[0077] An operator can control operation of the treatment system
100 using an input/output device 118 of the controller 114. The
input/output device 118 can display the state of operation of the
applicator 104 and treatment information. In some embodiments, the
controller 114 can exchange data with the applicator 104 via a
wired connection or a wireless or an optical communication link and
can monitor and adjust treatment based on, without limitation, one
or more treatment profiles and/or patient-specific treatment plans,
such as those described, for example, in commonly assigned U.S.
Pat. No. 8,275,442. In some embodiments, the controller 114 can be
incorporated into the applicator 104 or another component of the
system 100.
[0078] Upon receiving input to start a treatment protocol, the
controller 114 can cycle through each segment of a prescribed
treatment plan. Segments may be designed to freeze tissue, thaw
tissue, supercool tissue, nucleate supercooled tissue, and so on.
In so doing, the power supply 110 and the fluid chamber 105 can
provide power and coolant to one or more functional components of
the applicator 104, such as thermoelectric coolers (e.g., TEC
"zones"), to begin a cooling cycle and, in some embodiments,
activate features or modes such as vibration, massage, vacuum, etc.
The controller 114 can receive temperature readings from
temperature sensors, which can be part of the applicator 104 or
proximate to the applicator 104, the patient's skin, a patient
protection device, etc. It will be appreciated that while a target
region of the body has been cooled or heated to the target
temperature, in actuality that region of the body may be close but
not equal to the target temperature, e.g., because of the body's
natural heating and cooling variations. Thus, although the system
100 may attempt to heat or cool tissue to the target temperature or
to provide a target heat flux, a sensor may measure a sufficiently
close temperature or heat flux. If the target temperature or the
flux has not been reached, power can be increased or decreased to
change heat flux to maintain the target temperature or "set-point"
selectively to affect targeted tissue.
[0079] FIG. 4 is a cross-sectional view of the connector 103 taken
along line 4-4 of FIG. 3 in accordance with at least some
embodiments of the technology. The connector 103 can be a
multi-line or multi-lumen conduit with a main body 179 (e.g., a
solid or hollow main body), a supply fluid line or lumen 180a
("supply fluid line 180a"), and a return fluid line or lumen 180b
("return fluid line 180b"). The main body 179 may be configured
(via one or more adjustable joints) to "set" in place for the
treatment of the subject. The supply and return fluid lines 180a,
180b can be tubes made of polyethylene, polyvinyl chloride,
polyurethane, and/or other materials that can accommodate
circulating coolant, such as water, glycol, synthetic heat transfer
fluid, oil, a refrigerant, and/or any other suitable heat
conducting fluid. In one embodiment, each fluid line 180a, 180b can
be a flexible hose surrounded by the main body 179. Referring to
FIGS. 3 and 4, coolant can be continuously or intermittently
delivered to the applicator 104 via the supply fluid line 180a and
can circulate through the applicator 104 to absorb heat. The
coolant, which has absorbed heat, can flow from the applicator 104
back to the base unit 106 via the return fluid line 180b. For
warming periods, the base unit 106 (FIG. 3) can heat the coolant
such that warm coolant is circulated through the applicator 104.
Referring now to FIG. 4, the connector 103 can also include one or
more electrical lines 112 for providing power to the applicator 104
(FIG. 3) and one or more control lines 116 for providing
communication between the base unit 106 (FIG. 3) and the applicator
104 (FIG. 3). To provide suction, the connector 103 can include one
or more vacuum tubes or lines 119.
[0080] FIG. 5 is a schematic cross-sectional view of a treatment
device in the form a non-invasive applicator 204 suitable for the
treatment system 100 in accordance with an embodiment of the
present technology. The applicator 204 can cool tissue to produce a
thermal event (e.g., supercooling event, freezing event, cooling
event, etc.) in a targeted cooling or event zone 232 (shown in
phantom line). The controller 114 can be programmed to cause the
applicator 204 to cool the subject's skin after detecting the
thermal event (e.g., freeze event, supercooling event, reaching a
target temperature with or without causing a freeze event, or other
detectable thermal event) so that the thermal event lasts a
sufficient period of time to substantially alter secretion
production levels of the glands. In some procedures, a cooling
event can last long enough to permanently decrease production
levels of the glands in the event zone 232 in which most
significant damage occurs. For example, most or substantially all
the sebaceous glands 17 in the event zone 232 can be destroyed,
reduced, or otherwise altered to reduce or otherwise modify sebum
production.
[0081] A central region 234 of the event zone 232 can be deeper
than most of the epidermal layer 14 to avoid or limit damage to
epidermal tissue which could lead to undesired skin coloration
changes. A distance 237 between the surface of the skin and the
event zone 232 can be generally equal to or greater than the
thickness of the epidermis 14 and, in some embodiments, can be
between about 0.1 mm to about 1.5 mm, between about 0.5 mm to about
1.5 mm, or other distances selected to keep thermal damage to
epidermal tissue at or below an acceptable level. The event zone
232 can be at a maximum depth 239 between about 0.25 mm to about 5
mm, between about 0.25 mm to about 6 mm, between about 0.3 mm to
about 5 mm, between about 0.3 mm to about 6 mm, between about 0.5
mm to about 5 mm, between about 0.5 mm to about 6 mm, or other
depths selected to avoid or limit injures to deeper non-targeted
tissue (e.g., subcutaneous tissue 16) or structures. The height 241
of the event zone 232 can be between about between about 0.1 mm to
about 6 mm, between about 0.1 mm to about 3.5 mm, between about 0.3
mm to about 5 mm, between about 1 mm to about 3 mm, or other
heights selected based on the thickness of the dermis 12. For
example, the height 241 can be slightly greater than the thickness
of the dermis 12 to keep thermal-injuries, if any, to the epidermis
14 and/or subcutaneous layer 16 at an acceptable level. In some
embodiments, the event zone 232 can be generally centered in the
dermis 12, and the height 241 can be less than the thickness of the
dermis 12. Adjacent epidermal and subdermal tissue may also be
cooled but can be at a sufficiently high temperature to avoid or
limit thermal injury. The location and dimensions (e.g., height
241, width, length, etc.) of the event zone 232 can be selected
based on the location of the targeted structures, tissue
characteristics at the target site, etc. In some embodiments, the
event zone 232 can comprise significant amounts of epidermal and
dermal tissue. For example, the event zone 232 can comprise most of
the tissue located directly between the cooled heat-exchanging
surface 219 and the subcutaneous tissue 16. In some procedures, at
least about 60%, 70%, 80%, 90%, or 95% of the tissue directly
between the heat-exchanging surface 219 and the subcutaneous layer
16 can be located within the event zone 232. Heating,
cryoprotectants, and/or supercooling techniques can be used to
avoid injury to the epidermal tissue.
[0082] The applicator 204 can include a cooling device 210 and an
interface layer 220. The cooling device 210 can include, without
limitation, one or more thermoelectric coolers 213, each including
one or more the thermoelectric elements (e.g., Peltier-type TEC
elements) powered by electrical energy from a treatment tower or
base unit (e.g., base unit 106 of FIG. 3) or another power source.
The thermoelectric coolers 213 can also include controllers,
temperature regulators, sensors, and other electrical components.
For example, each thermoelectric cooler 213 can include an array of
individually controlled thermoelectric elements and a controller.
In some embodiments, the controller 114 can be programmed to
control operation of the thermoelectric coolers 213 to remove heat
from tissue at a sufficient rate to produce a cooling event (e.g.,
a freeze or non-freeze event) that can cause destruction of
targeted cells. In freeze event embodiments, ice crystals may
nucleate and grow in the event zone 232 and can damage cells to
inhibit or otherwise affect gland function, but they may also
locally pierce a sufficient amount of the cell walls to destroy the
glands.
[0083] The applicator 204 can include sensors configured to measure
tissue impedance, pressure applied to the subject, optical
characteristics of tissue, and/or tissue temperatures. As described
herein, sensors can be used to monitor tissue and, in some
embodiments, to detect events. The number and types of sensors can
be selected based on the treatment to be performed. In some
embodiments, the applicator 204 can include a communication
component 215 that communicates with the controller 114 to provide
a first sensor reading 242, and a sensor 217 that measures, e.g.,
temperature of the cooling device 210, heat flux across a surface
of or plane within the cooling device 210, tissue impedance,
application force, tissue characteristics (e.g., optical
characteristics), etc. The interface layer 220 can be a plate, a
film, a covering, a sleeve, a substance reservoir or other suitable
element described herein and, in some embodiments, may serve as the
patient protection device described herein.
[0084] The interface layer 220 can also contain a similar
communication component 225 that communicates with the controller
114 to provide a second sensor reading 244 and a sensor 227 that
measures, e.g., the skin temperature, temperature of the interface
layer 220, heat flux across a surface of or plane within the
interface layer 220, contact pressure with the skin of the patient,
etc. For example, one or both of the communication components 215,
225 can receive and transmit information, such as temperature
and/or heat flux information as determined by one or both of
sensors 217, 227. The sensors 217, 227 are configured to measure a
parameter of the interface without substantially impeding heat
transfer between the applicator 204 and the patient's skin.
[0085] In certain embodiments, the applicator 204 can include a
sleeve or liner 250 (shown schematically in phantom line) for
contacting the patient's skin 230, for example, to prevent direct
contact between the applicator 204 and the patient's skin 230, and
thereby reduce the likelihood of cross-contamination between
patients, minimize cleaning requirements for the applicator 204,
etc. The sleeve 250 can include a first sleeve portion 252 and a
second sleeve portion 254 extending from the first sleeve portion.
The first sleeve portion 252 can contact and/or facilitate contact
of the applicator 204 with the patient's skin 230, while the second
sleeve portion 254 can be an isolation layer extending from the
first sleeve portion 252. The second sleeve portion 254 can be
constructed from latex, rubber, nylon, Kevlar.RTM., or other
substantially impermeable or semi-permeable material. The second
sleeve portion 254 can prevent contact between the patient's skin
230 and the applicator 204, among other things. Further details
regarding a patient protection device may be found in U.S. Patent
Publication No. 2008/0077201.
[0086] The applicator 204 can be manually held against the
subject's skin and can also include a belt or other retention
devices (not shown) for holding the applicator 204 against the
skin. The belt may be rotatably connected to the applicator 204 by
a plurality of coupling elements that can be, for example, pins,
ball joints, bearings, or other types of rotatable joints.
Alternatively, retention devices can be rigidly affixed to the end
portions of the interface layer 220. Further details regarding
suitable belt devices or retention devices may be found in U.S.
Patent Publication No. 2008/0077211. In conjunction with or in
place of a retention device, a vacuum can assist in forming a
contact between the applicator 204 (such as via the interface layer
220 or sleeve 250) and the patient's skin 230.
[0087] The sensors 217, 227 can serve as event detect sensors that
provide output (e.g., sensor readings 242, 244) collected in
real-time because real-time processing of such output can help
correctly and efficaciously administer treatment. The output can be
detected temperatures, heat fluxes, optical characteristics of
tissue, mechanical characteristics of tissue, etc. In one example,
real-time data processing is used to detect cooling events and to
determine a period of time to continue cooling the patient's skin
after one or more cooling events are detected. Tissue can be
monitored to keep a desired region or volume of tissue in the
cooled state (e.g., at least partially or totally frozen state) for
a period of time selected by the controller 114 or an operator. The
period of time can be equal to or longer than about, for example, 5
seconds, 10 seconds, 30 seconds, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 30
minutes, 1 hour, or other suitable period of time. In some
procedures, the cooling event is a freeze event that lasts a period
of time which is longer than 10 seconds and shorter than 10
minutes.
[0088] Optionally, the applicator 204 can include one or more
features used with supercooling. For example, the interface layer
220 can include one or more nucleation elements 231, 233 in the
form of positive and negative electrodes for heating the skin using
alternating current heating. For radiofrequency induced nucleation,
the nucleation elements 231, 233 can be radiofrequency electrodes.
The power supply 110 (FIG. 3) can include an RF generator for
driving the elements 231, 233. The nucleation elements 231, 233 can
also be configured to provide changes in applied pressure to cause
nucleation. Any number of different types of nucleation elements
can be incorporated into the interface layer 220 or other
components of the applicator 204 to provide the ability to
controllably nucleate supercooled tissue.
[0089] Although the thermoelectric elements 213 can heat tissue,
the applicator 204 can also include dedicated heating elements used
to, for example, thaw tissue. FIG. 5 shows the interface layer 220
including heaters 235 for generating heat delivered to the surface
of the skin 230. The heaters 235 can be resistive heaters, Peltier
devices, or other thermoelectric elements. Optionally, the
nucleation elements 231, 233 can also be used to control the
temperature of the skin 230. For example, the nucleation elements
231, 233 can include RF electrodes that cooperate to deliver RF
energy to heat the skin 230 or deeper tissue.
[0090] Multiple applicators may be concurrently or sequentially
used during a treatment session, and such applicators can include,
without limitation, vacuum applicators, belt applicators, and so
forth. Each applicator may be designed to treat identified portions
of the patient's body, such as the chin, cheeks, forehead, back,
shoulders, arms, pectoral areas, armpits, genital region, palms of
hands, soles of feet and so forth. For example, a vacuum applicator
may be applied at the back region, and the belt applicator may be
applied around the thigh region, either with or without massage or
vibration. Exemplary applicators and their configurations usable or
adaptable for use with the treatment system 100 are described in,
e.g., U.S. Pat. No. 8,834,547 and commonly assigned U.S. Pat. No.
7,854,754 and U.S. Patent Publication Nos. 2008/0077201,
2008/0077211, and 2008/0287839, which are incorporated by reference
in their entireties.
[0091] FIGS. 6A to 6C illustrate treatment devices suitable for use
with treatment systems disclosed herein in accordance with
embodiments of the technology. FIG. 6A is a schematic,
cross-sectional view illustrating an applicator 260 for
non-invasively removing heat from target areas of a subject 262.
The applicator 260 can include a heat-exchanging unit or cooling
device 264 (shown in phantom line) and an interface layer 265
(shown in phantom line). The interface layer 265 can have a rigid
or compliant concave surface 267. When the applicator 260 is held
against the subject, the subject's tissue can be pressed against
the curved surface 267. In some treatments, the compliant concave
surface 267 can be suitable for being applied to a subject's chin,
cheek, forehead, or other contoured body area. One or more vacuum
ports can be positioned along the surface 267 to draw the skin 262
against the surface 267. The configuration of the applicator 260
can be selected based on the treatment site.
[0092] FIG. 6B is a schematic, cross-sectional view illustrating an
applicator 270 that can include a heat-exchanging unit 274 having a
rigid or compliant convex surface 276 configured to be applied to
concave regions of the subject. Advantageously, the convex surface
276 can spread tissue to reduce the distance between the convex
surface 276 and targeted tissue under the convex surface 276. In
some treatments, the applicator 270 can be applied to the axilla
(i.e., armpit) region to affect apocrine sweat glands.
[0093] FIG. 6C is a schematic, cross-sectional view illustrating an
applicator 280 including a surface 282 movable between a planar
configuration 284 and a non-planar configuration 285 (shown in
phantom). The surface 282 is capable of conforming to the treatment
site to provide a large contact area. In some embodiments, the
surface 282 can be sufficiently compliant to conform to highly
contoured regions of a subject's face when the applicator 280 is
pressed against facial tissue. In other embodiments, the applicator
280 can include actuators or other devices configured to move the
surface 282 to a concave configuration, a convex configuration, or
the like. The surface 282 can be reconfigured to treat different
treatment sites of the same subject or multiple subjects.
[0094] FIG. 6D is a side view of an applicator 289 configured to
treat a targeted feature. Targeted features can be, without
limitation, cysts, glands, or other discrete features. The
applicator 289 can include a main housing 290, a cooling assembly
291, and a control element 292. The main housing 290 can be a
tubular member that surrounds and protects the cooling assembly
291. The cooling assembly 291 can include, without limitation, a
cooling device or element 293 ("cooling element 293") and a
connector 294. The cooling element 293 can be connected to another
device (e.g., a control tower or base unit) by the connector 294.
The connector 294 can be a rod that is moved distally (indicated by
arrow 295) or proximally (indicated by arrow 296) to move the
cooling element 293 along a passageway of the housing 290. The
connector 294 can include one or more conduits, wires, passageways,
or other features for providing energy (e.g., electrical energy,
radiofrequency energy, etc.), coolant, a vacuum, or the like. In
some embodiments, the connector 294 can be an umbilical rod that
provides energy, fluid, and/or suction. The applicator 289 can
include sensors or other applicator components disclosed herein.
For example, the applicator 289 can include sensors configured to
measure tissue impedance, pressure applied to the subject, optical
characteristics of tissue, and/or tissue temperatures in order to
monitor tissue and, in some embodiments, to detect events, such as
partial or complete freeze events.
[0095] FIG. 6E is a cross-sectional view of a distal portion of the
applicator 289. The cooling element 293 is spaced apart from an
opening 303 for receiving a feature 297 to be treated. The
connector 294 can be pushed distally (indicated by arrow 299) to
move the cooling element 293 relative to a longitudinal axis 305 of
the applicator 289. In some embodiments, the connector 294 is
manually moved through the housing 290. In other embodiments, the
applicator 289 can include or be used with a drive device
configured to move the connector 294. The drive device can include,
without limitation, one or more motors (e.g., drive motors, stepper
motors, etc.), sensors (e.g., position sensors), controllers, or
other components.
[0096] FIG. 6F is a cross-sectional view of the applicator 289
after the cooling element 293 thermally contacts the target feature
297. In some embodiments, the cooling element 293 can have a
generally concave surface 301 for contacting a large area of the
protruding target feature 297, such as a sebaceous cyst,
sudoriferous cyst, cyst of Zeis, hidrocystoma, bulging gland, acne,
or other treatable feature.
[0097] The control element 292 can be used to adjust the cooling
element 293 by, for example, bending or otherwise adjusting the
configuration of the cooling element 293. The curvature of the
surface 301 can be increased or decreased by moving the control
element 292 inwardly or outwardly, respectively. The control
element 292 can include, without limitation, one or more clamps,
bands, locking features, etc. for adjusting the configuration of
the distal end of the main housing 290 and cooling element 293. The
cooling element 293 can be flexible to comfortably engage the
target features, such as a bulging cyst. In rigid embodiments, a
physician can select a curved cooling element 293 with a
configuration (e.g., a partially spherical shape, partially
elliptical shape, etc.) selected based on, for example, the shape
and/or configuration of targeted feature(s). The cooling element
293 can include, without limitation, one or more cooling devices,
thermoelectric coolers, cooling channels, electrodes, heating
elements, or other features for treating the target feature 297.
After the cooling element 293 contacts the skin 307, the cooling
element 293 can actively cool the target feature 297.
[0098] The applicator 289 can be used to cool/heat relatively small
features that may be near sensitive non-targeted tissue. The size
of the cooling element 293 can be selected to minimize treatment of
non-targeted tissue. To treat features around the eyes, the
applicator 289 can be selected such that most of the tissue
received by the cooling element 293 is targeted tissue to avoid
affecting surrounding tissue. In some procedures, the applicator
289 can be applied to the subject such that the targeted feature is
positioned within the opening 303 (FIG. 6E). The cooling element
293 can be moved through the housing 290 and into thermal contact
with the subject's skin 307. In some procedures, the cooling
element 293 can be moved back and forth to adjust the applied
pressure, provide a massaging effect, promote nucleation, or the
like. The applicator 289 can treat a wide range of features or
areas at various locations along the subject's body.
[0099] FIGS. 7 and 8 are flow diagrams illustrating methods for
treating sites in accordance with embodiments of the technology.
Although specific example methods are described herein, one skilled
in the art is capable of identifying other methods that could be
performed using embodiments disclosed herein. The methods are
generally described with reference to the treatment system 100 of
FIG. 3, but the methods may also be performed by other treatment
systems with additional or different hardware and/or software
components.
[0100] FIG. 7 is a flow diagram illustrating a method 350 for
treating exocrine glands in accordance with embodiments of the
technology. Generally, a subject's skin can be cooled to thermally
affect a target region containing exocrine glands. Treatment can be
monitored in order to keep tissue cooled for a sufficient length of
time to affect the exocrine glands. Details of method 350 are
discussed below.
[0101] At block 352, a treatment device is applied to a subject by
placing its heat-exchanging surface or other feature in thermal
contact with the subject's skin. The surface of the subject's skin
can be continuously or periodically cooled to produce at least one
cooling event (e.g., a partial freeze event, a complete freeze
event, supercooling event, etc.) in a portion of the skin with
exocrine glands. In treatments for acne, the targeted glands can be
sebaceous glands and/or supporting structures, which may be in the
epidermis and/or dermis. In treatments for excessive sweating, the
targeted glands can be sweat glands and/or supporting
structures.
[0102] Rapid cooling can create a thermal gradient with the coldest
temperatures in the region of skin near the treatment device
whereas rapid heating can create a thermal gradient with the
highest temperatures in the region of skin near the treatment
device. During cooling, skin can be frozen for a short enough
duration to not establish a temperature equilibrium across the skin
and adjacent subcutaneous tissue. Cryoprotectant(s) and/or warming
cycle(s) can be used to inhibit freezing of the uppermost
non-targeted layer or layers of skin (e.g., layers of the
epidermis). In some procedures, a cryoprotectant can be applied to
the treatment site to inhibit damage to the epidermis while cooling
and freezing the dermal layer without causing freeze damage to
subcutaneous tissue. As such, the combination of cryoprotectant and
controlled cooling can produce a desired cooling zone, and cooling
of the cooling zone can be controlled to either have a non-freeze
cooling event, a partial freeze event or a total brief freeze
event. In some embodiments, the treatment device can non-invasively
produce a freeze event that begins within a predetermined period of
time after the applicator begins cooling the patient's skin. The
predetermined period of time can be equal to or shorter than about
10 seconds, 30 seconds, 60 seconds, 90 seconds, 120 seconds, or 150
seconds or longer periods and, in some embodiments, can be from
between about 10 seconds to about 150 seconds, between about 30
seconds to about 150 seconds, or between about 60 seconds to about
150 seconds. In some embodiments, the predetermined period of time
can be shorter than about 1, 2, 3, 4, 5, 6, 7, 8, 9, or 10 minutes.
A controller (e.g., controller 114 of FIG. 2) can select the
predetermined period of time for producing a cooling event based on
the treatment temperatures, treatment sites, and/or cryotherapy to
be performed. Alternatively, an operator can select the period of
time for cooling and can enter it into the controller 114.
[0103] In some embodiments, the subject's skin can be cooled to
produce a partial freeze event that includes at least some
crystallization (e.g., formation of microscopic ice crystals) in
intercellular material (e.g., fluid, cell components, etc.) and/or
extracellular fluid. By avoiding extensive ice crystal formation
that would cause frostbite or necrosis, partial freeze events can
occur without excessive tissue damage. In some embodiments, the
surface of the patient's skin can be cooled to a temperature no
lower than about -40.degree. C., -30.degree. C., -20.degree. C.,
-10.degree. C., -5.degree. C., or -3.degree. C. to produce a
partial freeze event in the skin without causing irreversible skin
damage. In one example, the surface of the skin can be cooled to
from about -40.degree. C. to about 0.degree. C., from about
-30.degree. C. to about 0.degree. C., from about -20.degree. C. to
about 0.degree. C., or from about -15.degree. C. to about 0.degree.
C. or below about -10.degree. C., -20.degree. C., -20.degree. C.,
-30.degree. C., or -40.degree. C. It will be appreciated that the
surface of the skin can be cooled to other temperatures that are
selected based on the mechanism of action.
[0104] At block 354, one or more events (e.g., freeze events) can
be detected using one or more electrical components of the
treatment device. During cooling, targeted tissue can reach a
temperature below the freezing point of its biological tissue and
fluids (e.g., approximately -1.8.degree. C.). As tissue, fluids,
and lipids freeze, crystals can form and energy associated with the
latent heat of crystallization is released. The treatment system
can determine the extent of freezing based on the detected
temperature changes caused of crystallization. A relatively small
positive change in tissue temperature can indicate a partial or
total freeze event whereas a relatively large positive change in
tissue temperature can indicate a complete freeze event. The sensor
167 (FIG. 2) and the sensor 227 of FIG. 5 can be freeze detect
sensors capable of detecting the positive change in tissue
temperature, and the treatment system can identify it as a freeze
event. The treatment system can be programmed so that small
temperature variations do not cause false alarms with respect to
false events. Additionally or alternatively, the treatment systems
may detect changes in the temperature of its components or changes
in power supplied to treatment devices, or other components, to
identify freeze events.
[0105] The treatment system 100 of FIG. 3 can use optical
techniques to detect cooling events at block 354 of FIG. 7. For
example, sensor 167 of FIG. 2 and sensors 217, 227 of FIG. 5 can be
optical sensors capable of detecting changes in the optical
characteristics of tissue caused by freezing. Optical sensors can
include, without limitation, one or more energy emitters (e.g.,
light sources, light emitting diodes, etc.), detector elements
(e.g., light detectors), or other components for non-invasively
monitoring optical characteristics of tissue. In place of or in
conjunction with monitoring using optical techniques, tissue can be
monitored using electrical and/or mechanical techniques. In
embodiments for measuring electrical impedance of tissue, the
sensors (e.g., sensor 167 of FIG. 2 and sensors 217, 227 of FIG. 5)
can include two electrodes that can be placed in electrical
communication with the skin for monitoring electrical energy
traveling between the electrodes via the tissue. In embodiments for
measuring mechanical properties of tissue, the sensors disclosed
herein can comprise one or more mechanical sensors which can
include, without limitation, force sensors, pressure sensors, and
so on.
[0106] At block 356, the treatment device and other treatment
parameters can be controlled to control the temperature in the
target region and, in some embodiments, includes periodically or
continuously cooling the patient's tissue to keep a target region
of skin in a cooled state (e.g., a frozen state) for a period of
time. The treatment parameters can include, for example,
cryoprotectant protocols, temperature profiles, treatment
durations, number of cooling zones, characteristics of cooling
zones, energy delivered to tissue, control parameters (e.g.,
control parameters for features such as vibration, massage, vacuum,
and other treatment modes), or the like. For example, the skin
within the cooling zone (e.g., event zone 232 of FIG. 5) can be
kept frozen for a length of time selected based on the desired
severity of the freeze injury. In short treatments, the period of
time can be equal to or shorter than about 5, 10, 15, 20, or 25
seconds. In longer treatments, the period of time can be equal to
or longer than about 25 seconds, 30 seconds, 45 seconds or 1, 2, 3,
4, 5, or 10 minutes. In some procedures, the treatment device can
be controlled so that the skin is partially or completely frozen
for no longer than, for example, 5 minutes, 10 minutes, 20 minutes,
30 minutes, 45 minutes, or 1 hour. In some examples, the skin is
frozen for about 1 minute to about 5 minutes, about 5 minutes to
about 10 minutes, about 10 minutes to about 20 minutes, about 20
minutes to about 30 minutes, or about 30 minutes to about 1
hour.
[0107] In some embodiments, the treatment system can control the
treatment device so that the freeze event causes apoptotic damage
to targeted glands but does not cause such damage to non-targeted
tissue. In one example, the treatment device produces a partial
freeze event short enough to prevent establishing equilibrium
temperature gradients in the patient's skin. This allows freezing
of shallow targeted tissue without substantially affecting deeper
non-targeted tissue. Moreover, cells in the dermal layer can be
affected to a greater extent than the cells in the subdermal layer
(e.g., subcutaneous adipose tissue). In some procedures, the
subdermal layer can be kept at a sufficiently high temperature
(e.g., at or above 0.degree. C.) while the shallower dermal tissue
experiences the partial or total freeze event. The treatment system
can also control operation of the treatment devices to thermally
injure tissue to cause fibrosis, which increases the amount of
connective tissue in a desired tissue layer (e.g., epidermis and/or
dermis) to increase the firmness and appearance of the skin. In
other treatments, the treatment system controls one or more
applicators to supercool and freeze dermal tissue.
[0108] At block 358, the frozen region can be thawed by heating it
and/or applying a topical substance in order to minimize, reduce,
or limit tissue damage. The applicator can thaw the patient's skin
after the freeze event occurs and after a period of time has
transpired. The period of time can be equal to or shorter than
about 5, 10, 15, 20, or 25 seconds or about 1, 2, 3, 4, 5, 6, 7, 8,
9, or 10 minutes. In one example, the uppermost skin layer(s) can
be periodically heated to a temperature above the skin's freezing
point to provide freeze protection thereto. The applicator can
include one or more thermal elements (e.g., resistive heaters,
electromagnetic energy emitters, Peltier devices, etc.) for heating
tissue. For example, a cooling element 109 of FIG. 2 can be a
Peltier device or one or more resistive heaters capable of
generating heat for thawing tissue. In some embodiments, the
applicator 104 of FIGS. 2 and 3 can have separate and independently
controlled cooling elements and heating elements that can cooperate
to provide precise temperature control for freezing and
thawing/warming cycles. In some embodiments, applicators may stop
cooling tissue to allow frozen tissue to passively warm and
thaw.
[0109] The treatment systems disclosed herein can monitor the
location and/or movement of the treatment devices and may prevent
false or inaccurate determinations of treatment events based on
such monitoring. During treatment, the treatment device may move
which may cause it to contact a warmer area of skin, to no longer
contact the skin, and so on. This may cause the treatment system to
register a difference in temperature that is inconsistent with a
normal treatment. Controllers (e.g., controller 114 of FIG. 3) may
be programmed to differentiate between these types of temperature
increases and a temperature increase associated with freezing. U.S.
Pat. No. 8,285,390 discloses techniques for monitoring and
detecting freeze events and applicator movement and is incorporated
by reference in its entirety. Additionally, treatment systems can
provide an indication or alarm to alert the operator to the source
of this temperature increase. In the case of a temperature increase
not associated with an event, the system may also suppress false
indications, while in the case of a temperature increase associated
with freezing, the system take any number of actions based on that
detection.
[0110] FIG. 8 is a flow diagram illustrating a method 400 in
accordance with an aspect of the present technology. Generally, a
substance can be applied to the treatment site. The applicator can
be applied to the treatment site and can cool tissue while the
cryoprotectant protects non-targeted tissue. A cooled region (e.g.,
a frozen or non-frozen region) can be warmed (e.g., thawed) to
inhibit or limit thermal damage to tissue. In some embodiments, the
treatment site can be monitored to keep tissue frozen or non-frozen
but yet cold for a sufficient length of time to affect glands.
Details of method 400 are discussed below.
[0111] At block 402, a substance can be applied to the subject's
skin to improve heat transfer between the treatment device and the
subjects skin, selectively protect non-target tissues from thermal
damage (e.g., freeze damage due to crystallization), and/or
initiate/control thermal events. In one embodiment, the substance
can be a cryoprotectant that prevents, inhibit, or limits damage to
non-targeted tissue. Additionally or alternatively, the
cryoprotectant can allow, for example, the treatment device to be
pre-cooled prior to being applied to the subject for more efficient
treatment. Further, the cryoprotectant can also enable the
treatment device to be maintained at a desired low temperature
while preventing ice formation on the cooled surface of the
treatment device, and thus reduces the delay in reapplying the
treatment device to the subject. Yet another aspect of the
technology is the cryoprotectant may prevent the treatment device
from freezing to the subject's skin. Certain cryoprotectants can
allow microscopic crystals to form in the tissue but can limit
crystal growth that would cause cell destruction and, in some
embodiments, can allow for enhanced uptake or absorption and/or
retention in target glands and/or surrounding tissue prior to and
during cooling.
[0112] Some embodiments according to the present technology may use
a cryoprotectant with a freezing point depressant that can assist
in preventing freeze damage that would destroy cells. Suitable
cryoprotectants and processes for implementing cryoprotectants are
described in commonly-assigned U.S. Patent Publication No.
2007/0255362. The cryoprotectant may additionally include a
thickening agent, a pH buffer, a humectant, a surfactant, and/or
other additives and adjuvants as described herein. Freezing point
depressants may include, for example, propylene glycol (PG),
polyethylene glycol (PEG), dimethyl sulfoxide (DMSO), or other
suitable alcohol compounds. Cryoprotectant can be delivered to the
surface of the patient's skin for a period of time which is short
enough to not significantly inhibit the initiation of the partial
freeze event in dermal tissue but which is long enough to provide
substantial protection to non-targeted tissue epidermal. Multiple
cryoprotectants can be used to protect different tissue layers. For
example, a first cryoprotectant for protecting deep tissue can be
applied before a second cryoprotectant for protecting shallow
tissue because the first cryoprotectant may require a longer
delivery time to reach the deeper tissue.
[0113] The rate of cryoprotectant delivery can be selected based on
the characteristics of the cryoprotectant and the desired amount of
tissue protection. In one specific treatment, an interface member
is placed directly over the target area, and the treatment device
with a disposable sleeve or liner is placed in contact with the
interface member. The interface member can be a cotton pad, a gauze
pad, a pouch, or a container with a reservoir containing a volume
of cryoprotectant or other flowable conductive substance. The
interface member can include, for example, a non-woven cotton
fabric pad saturated with cryoprotectant that is delivered at a
desired delivery rate. Suitable pads include Webril.TM. pads
manufactured by Covidien of Mansfield, Mass. Further details
regarding interface members and associated systems and methods of
use are described in commonly-assigned U.S. Patent Publication No.
2010/0280582.
[0114] In block 404, the subjects skin can be cooled using a
treatment device in thermal contact with the subject's skin. The
surface of the subject's skin can be continuously or periodically
cooled to produce a freeze event (e.g., partial freeze event,
complete freeze event, etc.). The description of block 352 in FIG.
7 applies equally to block 404 in FIG. 8.
[0115] In block 406, thermal energy can be delivered to the surface
of the skin before, during, and/or after skin cooling to protect
non-targeted tissue in the uppermost region of the skin. In some
embodiments, the dermal tissue with glands below the epidermis can
be frozen/supercooled. The treatment device can heat the surface of
the skin to warm the epidermis or portions thereof to prevent,
inhibit, or limit damage to non-targeted epidermal tissue while the
region of dermal tissue with glands remains in a frozen/supercooled
state. If the targeted region is supercooled, it can be
controllably frozen using one or more nucleation initiators (e.g.,
mechanical perturbation such as vibration, ultrasound pulse, change
in pressure, etc.).
[0116] Heat can be delivered transcutaneously to the subcutaneous
layer to protect the subcutaneous tissue. For example, subcutaneous
tissue can be heated prior to tissue cooling the subject's skin at
block 404. In some procedures, the subcutaneous tissue can be
periodically heated (e.g., heated using radiofrequency energy)
during skin cooling. Some embodiments, the skin can be
alternatingly heated and cooled. The heating cycles can be used to
keep the subcutaneous tissue at or above a threshold temperature
(e.g., above its freezing point) to avoid freeze damage to the
subcutaneous layer. The cooling cycles can be used to periodically
cool the targeted dermal tissue and/or epidermal tissue. In some
embodiments, the topical substance can be applied in order to
minimize, reduce, or limit tissue damage.
[0117] At block 408, the frozen region can be warmed (e.g.,
thawed). In freeze event embodiments, the applicator can thaw the
patient's skin after the freeze event occurs and after a period of
time has transpired. The thawing process at block 408 can be the
same as the thawing process of block 358 of FIG. 7.
E. Treatments using Supercooling
[0118] FIGS. 9 and 10 are flow diagrams illustrating methods for
supercooling regions in accordance with embodiments of the
technology. Generally, a surface of a human subject's skin can be
cooled to a temperature no lower than -40.degree. C. to avoid
unwanted skin damage and so that the temperature of at least a
portion of tissue is in a supercooled state. The surface of the
skin can be heated to bring shallow non-targeted tissue out of the
supercooled state while the deeper targeted region remains in the
supercooled state. The supercooled targeted region can be nucleated
due to a perturbation that causes at least partial or total
freezing that destroys or damages targeted cells, for example, due
to crystallization of intracellular and/or extracellular fluids. In
one embodiment, mechanical perturbation and/or other catalyst for
nucleation (e.g., RF energy, alternating electric fields, etc.)
within the target tissue can be provided only following a
protective increase of a temperature of non-targeted epidermal
layers. The mechanical perturbations can be vibrations, ultrasound
pulses, and/or changes in pressure. The non-targeted layers can be
warmed enough to avoid freezing of non-targeted tissue upon
nucleation. The treatment system 100 (FIG. 3) can utilize
applicators disclosed herein to perform such supercooling
methods.
[0119] FIG. 9 is a flow diagram illustrating a method 450 in
accordance with an aspect of the present technology. An early stage
of the method 450 can include cooling a surface of a human
subject's skin to a first temperature (block 452). The first
temperature can be, for example, between about -10.degree. C. and
-40.degree. C. such that a portion of tissue below the surface is
in a supercooled state. In other embodiments, the first temperature
can be a temperature between about -15.degree. C. and -25.degree.
C., a temperature between about -20.degree. C. and about
-30.degree. C., or other temperature below a freezing
temperature.
[0120] In block 454, the surface of the human subject's skin is
heated an amount sufficient to raise the skin surface temperature
from the first temperature to a second temperature, which can be a
non-supercooled temperature, while the targeted region remains in
the supercooled state. For example, the treatment system can be
used to heat the surface of the skin to a temperature higher than
about 0.degree. C., higher than about 5.degree. C., higher than
about 10.degree. C., higher than about 20.degree. C., higher than
about 30.degree. C., or higher than about 35.degree. C. There can
be a temperature gradient between the targeted tissue and the skin
surface such that most of the non-targeted tissue (e.g., epidermis)
is at a non-supercooled temperature.
[0121] In block 456, the supercooled portion of tissue below the
skin surface can be nucleated to cause at least some fluid and
cells in the supercooled tissue to at least partially or totally
freeze. In one embodiment, nucleation of the supercooled tissue is
caused by a mechanical perturbation, ultrasound, massaging, or
other suitable nucleation initiator. Warmed cells residing at the
surface of the human subject's skin do not freeze at block 456. As
such, cells at the skin surface are protected without using a
chemical cryoprotectant. The chemical cryoprotectants can be
selected to inhibit or limit hyperpigmentation or
hypopigmentation.
[0122] In block 458, the supercooled tissue can be maintained in
the at least partially or totally frozen state for a predetermined
period of time longer than, for example, about 10 seconds, 12
seconds, 15 seconds, or 20 seconds. In various arrangements, the
supercooled tissue in a cooling zone (e.g., event zone 232 of FIG.
5) can be maintained in the at least partially or totally frozen
state for a duration of time sufficient to treat acne, improve a
quality of hair, treat hyperhidrosis, etc. In certain embodiments,
the skin is cooled/heated to maintain targeted tissue in at least a
partially or totally frozen state for the predetermined time longer
than about 10 seconds, longer than about 12 seconds, longer than
about 15 seconds, or longer than about 20 seconds.
[0123] FIG. 10 illustrates a method 500 for affecting a target
region in a human subject's body in accordance with another
embodiment of the present technology. The method 500 can include
transdermally removing heat from tissue at a target region such
that the target region is cooled to a supercooled temperature
(block 502). The supercooled temperature can be, for example, below
about 0.degree. C. or within a range from about 0.degree. C. to
about -20.degree. C., from about -10.degree. C. to about
-30.degree. C., from about -20.degree. C. to about -40.degree. C.,
or no lower than about -40.degree. C. Cryoprotectants can be used
when cooling tissue to very low temperatures, including
temperatures lower than -40.degree. C.
[0124] In block 504, the method 500 includes applying heat to an
epidermis of the target region to warm epidermal cells in the
target region to a temperature above freezing while glands in the
dermis are at or near the supercooled temperature. For example, the
step of applying heat can include warming a portion of most of the
epidermal layer under the treatment device to a temperature above
about 0.degree. C., about 5.degree. C., about 10.degree. C., about
20.degree. C., about 25.degree. C., or about 32.degree. C. Warming
can be accomplished by thermal heaters (e.g., heaters 235 in FIG.
5) disposed on a surface of the applicator contacting or
confronting a skin surface. Alternatively, if deeper tissue is not
targeted, such tissue could be warmed using focused electrical
currents which focus their energy below the skin surface, focused
ultrasound which has a focal point for its energy below the skin
surface, or RF energy. In such embodiments, the elements 235 of
FIG. 5 can be electrodes or transducers.
[0125] In block 506, a freeze event in the dermal layer can
selectively affect the targeted glands while epidermal cells are
not affected by the freeze event. The method 500 can include
providing at least one of vibration, mechanical pressure, and
ultrasound pulses to the target region to cause such a freeze
event. In various arrangements, the freeze event can cause at least
partial crystallization of a plurality of gland cells in the target
region. Beneficially, the epidermal cells are protected to avoid or
limit freeze damage to those cells.
[0126] In some methods 500, supercooled temperatures of the
targeted tissue can be achieved without initiating nucleation by
cooling the treatment site at a relatively slow rate (e.g., the
temperature profile can cause a slow cooling of the tissue at the
target region) at block 502. For example, the rate of cooling can
be either equal to, slower or faster than about 0.5, 1, 2, 3, 4, 5,
6, 7, 8, 9 or 10 degrees C. per minute. A preferred rate of cooling
is about either 2, 4, or 6 degrees C. per minute. Additionally or
alternatively, a treatment device can apply a generally constant
pressure during cooling to the supercooled temperature range to
avoid pressure changes that would cause inadvertent nucleation. In
a further embodiment, the targeted tissue can be cooled while the
patient is held still (e.g., without movement of the treatment
site) to avoid mechanically disturbing the supercooled tissue and
unintentionally causing crystallization. At block 504, the
temperature of the non-targeted surface tissue can be warmed to a
non-freezing temperature and/or a non-supercooled temperature prior
to perturbation and subsequent freezing. In one embodiment, the
warming cycle of the temperature profile can occur quickly such
that the underlying and/or targeted tissue remains in the
supercooled state throughout the warming cycle. The supercooled
tissue can then be nucleated at block 506.
[0127] Various aspects of the methods disclosed herein can include
cosmetic treatment methods for treating the target region of a
human subject's body to achieve a cosmetically beneficial
alteration of a portion of tissue within the target region. Such
cosmetic methods can be administered by a non-medically trained
person. The methods disclosed herein can also be used to (a)
improve the appearance of skin by tightening the skin, improving
skin tone and texture, eliminating or reducing wrinkles, increasing
skin smoothness, thickening the skin, (b) improve the appearance of
cellulite, and/or (c) treat sebaceous glands, hair follicles,
and/or sweat glands.
F. Suitable Computing Environments
[0128] FIG. 11 is a schematic block diagram illustrating
subcomponents of a computing device 700 suitable for the system 100
of FIG. 3 in accordance with an embodiment of the disclosure. The
computing device 700 can include a processor 701, a memory 702
(e.g., SRAM, DRAM, flash, or other memory devices), input/output
devices 703, and/or subsystems and other components 704. The
computing device 700 can perform any of a wide variety of computing
processing, storage, sensing, imaging, and/or other functions.
Components of the computing device 700 may be housed in a single
unit or distributed over multiple, interconnected units (e.g.,
though a communications network). The components of the computing
device 700 can accordingly include local and/or remote memory
storage devices and any of a wide variety of computer-readable
media.
[0129] As illustrated in FIG. 11, the processor 701 can include a
plurality of functional modules 706, such as software modules, for
execution by the processor 701. The various implementations of
source code (i.e., in a conventional programming language) can be
stored on a computer-readable storage medium or can be embodied on
a transmission medium in a carrier wave. The modules 706 of the
processor can include an input module 708, a database module 710, a
process module 712, an output module 714, and, optionally, a
display module 716.
[0130] In operation, the input module 708 accepts an operator input
719 via the one or more input/output devices described above with
respect to FIG. 5, and communicates the accepted information or
selections to other components for further processing. The database
module 710 organizes records, including patient records, treatment
data sets, treatment profiles and operating records and other
operator activities, and facilitates storing and retrieving of
these records to and from a data storage device (e.g., internal
memory 702, an external database, etc.). Any type of database
organization can be utilized, including a flat file system,
hierarchical database, relational database, distributed database,
etc.
[0131] In the illustrated example, the process module 712 can
generate control variables based on sensor readings 718 from
sensors (e.g., sensor 167 of FIG. 2, the temperature measurement
components 217 and 227 of FIG. 5, etc.) and/or other data sources,
and the output module 714 can communicate operator input to
external computing devices and control variables to the controller
114 (FIGS. 3 and 5). The display module 816 can be configured to
convert and transmit processing parameters, sensor readings 818,
output signals 720, input data, treatment profiles and prescribed
operational parameters through one or more connected display
devices, such as a display screen, printer, speaker system, etc. A
suitable display module 716 may include a video driver that enables
the controller 114 to display the sensor readings 718 or other
status of treatment progression.
[0132] In various embodiments, the processor 701 can be a standard
central processing unit or a secure processor. Secure processors
can be special-purpose processors (e.g., reduced instruction set
processor) that can withstand sophisticated attacks that attempt to
extract data or programming logic. The secure processors may not
have debugging pins that enable an external debugger to monitor the
secure processor's execution or registers. In other embodiments,
the system may employ a secure field programmable gate array, a
smartcard, or other secure devices.
[0133] The memory 702 can be standard memory, secure memory, or a
combination of both memory types. By employing a secure processor
and/or secure memory, the system can ensure that data and
instructions are both highly secure and sensitive operations such
as decryption are shielded from observation. The memory 702 can
contain executable instructions for cooling the surface of the
subject's skin to a temperature and controlling treatment devices
in response to, for example, detection of a partial or complete
freeze events. The memory 702 can include thawing instructions
that, when executed, causes the controller to control the
applicator to heat tissue. In some embodiments, the memory 702
stores instructions that can be executed to control the applicators
to perform the methods disclosed herein without causing undesired
effects, such as significantly lightening or darkening skin one of
more days after the freeze event ends. The instructions can be
modified based on patient information and treatments to be
performed. Other instructions can be stored and executed to perform
the methods disclosed herein.
[0134] Suitable computing environments and other computing devices
and user interfaces are described in commonly assigned U.S. Pat.
No. 8,275,442, entitled "TREATMENT PLANNING SYSTEMS AND METHODS FOR
BODY CONTOURING APPLICATIONS," which is incorporated herein in its
entirety by reference.
G. CONCLUSION
[0135] It will be appreciated that some well-known structures or
functions may not be shown or described in detail, so as to avoid
unnecessarily obscuring the relevant description of the various
embodiments. Although some embodiments may be within the scope of
the technology, they may not be described in detail with respect to
the Figures. Furthermore, features, structures, or characteristics
of various embodiments may be combined in any suitable manner. The
technology disclosed herein can be used for improving skin and skin
conditions and to perform the procedures disclosure in U.S.
Provisional Application Ser. No. 61/943,250, filed Feb. 21, 2014,
U.S. Pat. No. 7,367,341 entitled "METHODS AND DEVICES FOR SELECTIVE
DISRUPTION OF FATTY TISSUE BY CONTROLLED COOLING" to Anderson et
al., and U.S. Patent Publication No. US 2005/0251120 entitled
"METHODS AND DEVICES FOR DETECTION AND CONTROL OF SELECTIVE
DISRUPTION OF FATTY TISSUE BY CONTROLLED COOLING" to Anderson et
al., the disclosures of which are incorporated herein by reference
in their entireties. The technology disclosed herein can target
tissue for tightening the skin, improving skin tone or texture,
eliminating or reducing wrinkles, increasing skin smoothness as
disclosed in U.S. Provisional Application Ser. No. 61/943,250.
[0136] Unless the context clearly requires otherwise, throughout
the description, the words "comprise," "comprising," and the like
are to be construed in an inclusive sense as opposed to an
exclusive or exhaustive sense; that is to say, in a sense of
"including, but not limited to." Words using the singular or plural
number also include the plural or singular number, respectively.
Use of the word "or" in reference to a list of two or more items
covers all of the following interpretations of the word: any of the
items in the list, all of the items in the list, and any
combination of the items in the list. In those instances where a
convention analogous to "at least one of A, B, and C, etc." is
used, in general such a construction is intended in the sense of
the convention (e.g., "a system having at least one of A, B, and C"
would include but not be limited to systems that have A alone, B
alone, C alone, A and B together, A and C together, B and C
together, and/or A, B, and C together, etc.). In those instances
where a convention analogous to "at least one of A, B, or C, etc."
is used, in general such a construction is intended in the sense of
the convention (e.g., "a system having at least one of A, B, or C"
would include but not be limited to systems that have A alone, B
alone, C alone, A and B together, A and C together, B and C
together, and/or A, B, and C together, etc.).
[0137] Any patents, applications and other references, including
any that may be listed in accompanying filing papers, are
incorporated herein by reference. Aspects of the described
technology can be modified, if necessary, to employ the systems,
functions, and concepts of the various references described above
to provide yet further embodiments. While the above description
details certain embodiments and describes the best mode
contemplated, no matter how detailed, various changes can be made.
Implementation details may vary considerably, while still being
encompassed by the technology disclosed herein. The various aspects
and embodiments disclosed herein are for purposes of illustration
and are not intended to be limiting, with the true scope and spirit
being indicated by the following claims.
* * * * *