Early Intervention for
Deep Tissue Injuries
MIST® Ultrasound
Healing Therapy
Pre-MIST®
Post 5 MIST®
Treatments
Deep Tissue Injury
What is a Deep Tissue Injury (DTI)?
NPUAP DEFINITION:
Deep Tissue Injury
The National Pressure Ulcer Advisory Panel (NPUAP)
defines a suspected Deep Tissue Injury as a,“Purple or
maroon localized area of discolored intact skin or bloodfilled blister due to damage of underlying soft tissue from
pressure and/or shear. The area may be preceded by tissue
that is painful, firm, mushy, boggy, warmer or cooler as
compared to adjacent tissue.1”
Epidermis
Dermis
Adipose
Tissue
Initial Injury
Muscle
Bone
• DTIs are a form of pressure ulcer that can
form over any area of pressure, but are most
commonly seen on the sacrum and heels.2,3
• The tissue injury occurs from the inside out.
Changes on the surface are not seen until later,
when the tissue undergoes necrosis.3-5
Reprinted with permission from NPUAP
DTI on buttock
DTI on heel
• DTIs require rapid identification, as they may
quickly progress to Unstageable, Stage III and IV
pressure ulcers despite aggressive and optimal
treatment.4, 5
• It is difficult to confirm an injury is a deep tissue
injury until it runs its full course. The word
“suspected” may be used in front of DTI until
this confirmation takes place.
Who is at risk for a Deep Tissue Injury?
High Risk Populations 4,6,7
Things to look for:
DTIs usually occur in the most compromised patients, but
can be found in almost any care setting where a patient
is allowed to remain in one physical position for extended
periods of time.4
• Confinement for more than 3 hours in the OR or cath lab
Patients with a cognitive deficit that impairs their ability
to sense pressure (stroke, anesthesia, coma, spinal cord
injury, etc,) are at the greatest risk.
• Leg numbness from stroke or neuropathy
• History of being “down at the scene” prior to admission
• Unable to turn; leg immobile (due to total hip or total
knee), fractured hip, spinal cord injury
• Use of medical devices: O2 mask, CPAP, braces etc.
• Complex medical conditions: acute cardiac event,
pneumonia, obesity, etc.
How do Deep Tissue Injuries Differ from other Pressure Ulcers?
SUPERFICIAL PRESSURE ULCERS
Low Pressure – Extended Time
DEEP TISSUE INJURIES
High Pressure – Short Time
PRESSURE & SHEAR
PRESSURE
PRESSURE
PRESSURE
Extrinsic Factors
• Moisture (urine & stool)
• Heat
• Friction
• Shear
Intrinsic Factors
• Impaired motor-sensory
• Poor nutrition
• Infection
Pressure 8-10
Extrinsic Factors
• Posture/Positioning
• Time on hard surface
• Stiffness/Firmness of the support surface
Intrinsic Factors
• Impaired motor-sensory
• Muscle atrophy
Pressure 8-10
• Lower pressure
(<200mm Hg)
over long
periods of time
(10 hours)
• High pressure
(>300mm Hg)
over short
periods of time
(3 hours)
Superficial Pressure Ulcer
DTI - Progressive Necrosis
Reprinted with permission from NPUAP
Reprinted with permission from NPUAP
Damage is created from
OUTSIDE > IN
Damage is created from
INSIDE > OUT
The Science Behind a Deep Tissue Injury
ISCHEMIA
Ischemia is caused from a prolonged mechanical load that
reduces local perfusion by collapsing capillaries within
the skeletal muscle. This mechanical load also alters
the interstitial environment, causing fluids and nutrients
needed for cellular function and metabolism to shift to
adjacent lower pressure areas in the interstitial space.11,12
oxygen-derived free radicals, but production of higher
concentrations during sudden reperfusion of ischemic
tissue may overwhelm the antioxidant system, resulting in
irreversible cell damage.22
Oxygen free radicals also have the potential to damage
the vessel endothelium causing thrombosis which
further contributes to ischemia. In addition, they
produce inflammatory mediators and leukocyte adhesion
molecules which compromise blood flow by occluding
capillary openings. This congestion causes local capillaries
to become more permeable, which contributes to the
edema noted in tissue surrounding deep tissue injuries.22
:::::
SUSTAINED CELL DEFORMATION
Ongoing ischemia causes a shift to anaerobic metabolism,
increasing the production of lactic acid and other
metabolic wastes that lead to cellular and interstitial
acidosis and cellular death.12,13 While considered the
primary cause of cell death associated with deep
tissue injuries, the short time required to achieve cell
death in a DTI suggests that ischemia is not the only factor
contributing to tissue damage.13-17
:::::
ISCHEMIC REPERFUSION INJURY
Evidence is growing to support cellular deformation as
a key causative factor in the cell death associated with
deep tissue injury.13-18 As a specific pressure threshold is
exceeded, the cell is stretched and the pores of the cell
membrane allow an increase in metabolites to move into
and out of the cell until an imbalance occurs leading to cell
death. The degree of damage is determined by the level
of cell deformation and exposure time. In addition, the
combination of pressure and shear can compress the cell
membrane to the point of rupture.
Ischemic-reperfusion injury is a two-step process
that begins with the cessation of blood-flow to the
muscle, leading to an oxygen deficit and buildup of toxic
metabolites normally removed by the flowing blood.
Restoration of blood flow stops and reverses the ischemic
damage, but gives rise to a cascade of inflammatory
responses including free radical production from the
sudden influx of significant quantities of oxygen.17-20
Reintroduction of oxygenated blood into an ischemic
site may cause oxygen molecules to bind with the waste
products of anaerobic metabolism. This produces a variety
of oxygen-derived free radicals such as superoxide,
hydrogen peroxide, hypochlorous acid, and more.12,21,22
Normally antioxidants protect cells against these
:::::
SUMMARY
As research into the causative factors of deep tissue injury
expands, it is clear that the tissue damage previously
thought to be the result of ischemia alone is due to a
combination of factors. The damage process in skeletal
muscle tissue is caused by the level of deformation during
short loading periods, however, during prolonged loading,
ischemia and reperfusion will ultimately play a more
important role.15 This damage can result from a single
event or a series of ischemic cycles that results when the
tissue is not allowed to fully recover.18
What are the Treatments for Deep Tissue Injuries?
STANDARD TREATMENTS
• Pressure Relief/Off Loading
• Repositioning schedules with
side to side turning
• Support surfaces (i.e. low air-loss
mattress, static air overlay)
• Heels in off-loading boots
• Nutritional Support
ADVANCED TREATMENTS
• MIST® Ultrasound Healing Therapy
MIST® Therapy is low frequency ultrasound delivered through a
noncontact saline mist. The sound waves of this non-thermal, painless
treatment penetrate into and below the surface to mechanically stimulate
cells. As a result, healing barriers are removed and cells are stimulated
to accelerate the normal healing process.23-29
CAUSE OF DTI
IMPACT OF MIST®
ISCHEMIA
Increased Vasodilation
Improves perfusion by dilation of the
capillaries surrounding the wound bed to
increase circulation, enhancing healing on a
macro level.30
Laser Doppler Perfusion Effects
Pre-MIST
5 minutes
Relative Units (RU)
0
Increased Angiogenesis
The resulting stress placed on the capillaries
leads to the stimulation of new capillaries
on a micro level. Significantly more blood
vessels (p<0.05) were present in the
granulation tissue of mice treated with
MIST Therapy.31
ISCHEMIA
REPERFUSION
INJURY
Reduction in Inflammation
Reduces inflammation through the reduction of
pro-inflammatory cytokines 26,27 and increases
nitric oxide (NO) production which alleviates the
negative impact of oxygen free radicals.21
500
Post-MIST
10 minutes
(after treatment completed)
1000
Angiogenesis
5 treatments over 10 days
Dark Pink = Blood Vessels
Control (sham)
25.7 ± 20.3
MIST Therapy
41.2 ± 23.0
Reduction of Pro-Inflammatory Cytokines
Pro-inflammatory cytokines: Interleukins (IL-1a, IL-6, IL-8, IL-11);
Tumor Necrosis Factor (TNF-a)
CELL
DEFORMATION
Cell Stimulation
Cell stimulation is noted in cells treated with MIST Therapy by an increase of ERK
(extracellular regulated kinase) and JNK (c-Jun N-terminal kinase) and the ERK/JNK ratio,
which is thought to regulate cell proliferation and cell survival mechanisms.32
Clinical Outcomes Comparison
Even with the best standard of care, the majority of deep tissue injuries will break down to become full thickness
wounds requiring healthcare providers to deal with the associated negative outcomes.
DTIs Treated with Standard of Care (SOC) Alone
Baharestani Data
Retrospective 2009
(N=200) 2
North Carolina WOCNs*
Prospective2011
(N=42) 33
Honaker
Retrospective
2012 (N=63) 3
Spontaneously Resolved
1%
5%
2%
Progressed to Stage I/II
1%
Not Reported
20%
sDTI
26%
67%
30%
Progressed to Stage III/IV
27%
28%
8%
Progressed to Unstageable
45%
Not Reported
40%
N = 305
7%
32%
61%
*2 DTIs could not be assigned based on information provided
Sacral DTI 35
Unstageable
Reprinted with permission from NPUAP
61% of DTIs progress
to full thickness
wounds with standard
of care alone
The addition of MIST Therapy to standard of care treatment significantly reduces the number of DTIs that will
degrade to Unstageable, Stage III/IV Pressure Ulcers.
DTIs Treated with (SOC) plus MIST® Therapy
Honaker Retrospective 2012
(N=64) 3
Honaker Prospective 2013
(N=43) 34
Spontaneously Resolved
18%
14%
Progressed to Stage I/II
62%
54%
sDTI
5%
30%
Progressed to Stage III/IV
6%
0%
Progressed to Unstageable
9%
2%
Sacral DTI
Pre-MIST® 36
Healing, Stage II
Post-MIST®
(5x/wk for 27 days) 36
N = 107
75%
15%
10%
Only 10% of DTIs progress
to full thickness wounds
when MIST Therapy is
added to Standard of Care
Financial Benefit of Early DTI Intervention with MIST® Therapy
STANDARD OF CARE (SOC)
Spontaneously Resolved
Stage 2
sDTI
Unstageable
Stage 3-4
MIST® THERAPY + SOC
7%
Spontaneously
Resolved
Stage 2
$55,400 2,3,34,37
32%
61%
75%
PER
HOSPITALIZATION
$129,248 8
sDTI
15%
PER
HOSPITALIZATION
Unstageable
Stage 3-4
10%
Adding MIST Therapy provides $36,000 saving per DTI patient
COST ANALYSIS – 20 DTI PATIENTS
SOC
MIST® + SOC
Cost of Stage I/II/DTI
($55,400 / 20) / 39%
($55,400 / 20) / 90%
Cost of Stage III/IV/UN
($129,248 / 20) / 61%
($129,248 / 20) / 10%
$0
($100 / 10 / per patient)
$2,008,946
$1,275,696
Cost of MIST®
Total Overall Cost
$2,008,946 - $1,275,696 =
$733,250
$733,250/20 = $36,663
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1.
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Slomka N, Or-Tzadikario S, Sassun D,
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11.
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For more information, contact your local Celleration representative or call 866.307.MIST (6478).
6321 Bury Drive, Suite 15
Eden Prairie, MN 55346
Phone: 952-224-8700
Customer Service: 866.307.MIST (6478)
email: info@celleration.com
www.misttherapy.com
Please see full package insert for additional information on indications,
contradictions, warnings, precautions, and side effects.
MC-67149_A 11/13