Download The Science of Pressure Ulcer Development

The Science of Pressure Ulcer
Development, Prevention and
Treatment with a View of New
Approaches to Predict and
Model
______________________________________________________________________
White Paper
Dr. James G. Spahn, MD, FACS
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©2015 James G. Spahn
ABSTRACT
The purpose of this article is to identify key scientific principles relating to pressure ulcer development and
analyze how the information can be used to extrapolate the most effective clinical decisions regarding
prevention and treatment measures. Pressure ulcers occur because of soft tissue distortion, and
incidence rates are on the rise in the healthcare arena. To better understand the issue, I first address the
many scientific factors relating to pressure ulcer development. I then elaborate on the current options in
place for prevention and treatment, such as the well-known support surface options and new-age
technologies which include predictive modeling and infrared thermography. Upon analysis, it can be
understood that knowledge of scientific principles and a clear understanding of the physiologic status of
the patient ultimately assist caregivers in the proper selection of treatment and prevention means that
lead to lower pressure ulcer incidence. The understanding of the physiologic status of patients is of
utmost importance in specific patient populations such as end of life, spinal cord injury, and severe
trauma patients relating to both goals for curative or palliative wound care (1).
INTRODUCTION
As pressure ulcer occurrence continues to rise, there is an ongoing search among caregivers for
improved methods of prevention and treatment with a goal of identifying the most effective practices for
addressing pressure ulcer care (2, 3, 4, 101, 102, 103). Support surfaces remain key factors in both
areas, yet with so many product choices, the selection process can be overwhelming. Pressure ulcers are
a significant problem across all healthcare settings in the United States. Annually, 2.5 million patients are
treated in acute-care facilities for pressure ulcers (5). Patients with pressure ulcers are three times more
likely to be discharged to a long-term care facility than those who do not have pressure ulcers (5).
Additionally, pressure ulcers are more likely to occur among those over age 65. Since the U.S. population
aged 65 and older is expected to double within the next 25 years, pressure ulcer risk and subsequent
prevalence is expected to increase (4). The older a person becomes the more frail they become. Because
frailty and pressure ulcers share important risk factors such as incontinence, falls, delirium and functional
decline, this will add to the growing concern of pressure ulcer risk in the aging baby boomer population
(6). If proactive assessments, prevention and early intervention are not implemented for the growing, high
risk geriatric population, it could pose a serious threat to the quality of health care delivered and our
already worrisome financial burdens (7). For example, the average cost associated with Stage IV
treatment was $129,248 (8).
Since pressure ulcer prevention, early intervention, treatment and care has become a quality indicator
used by federal/state agencies for regulatory oversight and litigation proceedings, avoidance of the
pressure ulcer problem must occur at all levels of care delivery and by all caregivers (7). [Figure 1]
Costs Related to Pressure Ulcers
Federal/Financial Fines for Non-compliance
•$3,050 to $10,000 per day for development of an avoidable Stage IV Pressure Ulcer (8)
Legal Issues Relating to Pressure Ulcers
•Long-term care legal cases per year increased from an average of 7 (1984 to August 31, 1999) to 18
(September 1, 1999) (8)
•Recovery costs increased 403% from $3,359,259 in 1999 to $13,554,168 in 2002 (8).
•Trend of plaintiffs winning verdicts is increasing which suggests facilities are being held to a higher
standard of care. (7)
[Figure 1]
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©2015 James G. Spahn
Along with the aging population, pressure ulcer occurrence relating to other comorbidities (ex: spinal cord
injury) is increasing in the younger population (7). It is essential that caregivers look to scientific principles
and the physiologic status of a patient when selecting routine surfaces, as well as adopting the new,
breakthrough technologies for pressure ulcer prevention and treatment. End-of-life care for terminal
patients also presents special and significant physiologic challenges in prevention and treatment be it
curative or palliative (1). Prior to the patient’s death, the body system starts shutting down. This can occur
within 24 hours or up to a 10 to 14-day time frame. This decrease in blood flow and tissue perfusion,
either acting alone or with other comorbidities, may explain the Kennedy Terminal Ulcer Occurrences and
SCALE as a predictor to the death of the patient (9) (10) (11).
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Part One
Back to Basics: Anatomy, Physiology, Physics, Chemistry, Pathology, etc.
Scientific Principles Relating to Pressure Ulcers & Proper Surface Selection
Gaining an understanding of the body’s response to tissue distortion and its effect on the tissue at risk to
develop a pressure ulcer can greatly simplify the tasks of support surface selection and comprehensive
prevention [Figure 2a] (12, 13, 14, 15). Pressure ulcer development is a combination of pressure, friction
and shear forces (16). These forces cause soft tissue distortion that results in ischemia, cell distortion,
impaired lymphatic drainage, impaired interstitial fluid flow and reperfusion injury (17, 18) [Figure 2b]. As
the scientific and mechanical principles relating to support surfaces stresses and the resulting soft tissue
strain are addressed, one must question the past concepts used in support surface selection, such as
relying solely on the absolute value of interface pressure readings and accepting reactive hyperemia as
an assured beneficial event (NPUAP/EPUAP Guidelines [19]) (12).
Anatomical properties of the body which have a direct effect on the body’s reaction
(strain) to a surface’s mechanical stresses.







Body type
Tissue type
Viscoelastic quality (stiffness)
Thickness
Blood supply (quantity and quality)
Skeletal press
Wedge-shape design of bony prominence
[Figure 2a]
Facts





Pressure ulcers are the result of the soft tissue distortion which causes:
Ischemia
Cell distortion
Abnormal interstitial fluid function
Lymphatic flow disruption
Reperfusion injury
[Figure 2b]
A cell is the complex, structural unit of all animals and plants. Cells and cellular products compose all
tissues of the body. Intercellular communication and cell division regulate all body functions and tissue
development; therefore, injury to cells can lead to significant tissue destruction or result in a diseased
state to the body (20). Cellular injury and death often result from events such as hypoxia and mechanical
stress, which cause ischemia and lead to impairment of normal cellular permeability, metabolism, protein
synthesis or phagocytosis, as well as other associated conditions listed in [Figure 2b] (21).
As patients lay or sit on a support surface, the surface media (Ex. gas, liquid, solid) and delivery method
(Ex. non – powered – static; powered – dynamic) dictate the amount of pressure and shearing forces that
are created (12). These mechanical stresses can cause distortion of the soft tissue and will most likely
result in crimping of the blood vessels, which then leads to decreased blood supply (ischemia) (104), and
a diminished supply of oxygen to the cells (hypoxia) (22). Hypoxia is the most common cause of cellular
injury (21). Therefore, in choosing support surface therapy, we must select products that minimize shear
and gradient pressure, thus preventing soft tissue distortion.
If a state of hypoxia is interrupted, meaning that blood supply and oxygen are restored, an increase in
blood flow and oxygen is rushed out to the hypoxic area as a compensatory reaction to the ischemic
event. This reaction is called reactive hyperemia (12, 22). Although this seems to be a logical solution to
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the problem, we must realize that tissues temporarily deprived of their blood supply do not always
achieve complete restoration of blood flow when reconnected to a normal supply (22, 23).
It is also known that during ischemia, an enzymatic conversion of xanthine dehydrogenase to xanthine
oxidase occurs within the cells, resulting in a dangerous superoxide anion (14, 23, 24). This “free radical”
is toxic to tissues and may generate other types of free radicals if blood flow is restored. The free radical
is a highly reactive molecule with unpaired electrons, thus it seeks reactions with other molecules to
achieve more electrical stability. As these reactions take place, the free radicals multiply, thereby
increasing the risk for tissue damage and cell death. Therefore, a sudden restoration of oxygen and blood
supply can actually cause damage. The resultant damage is known as reperfusion injury (14, 21, 23, 24).
With this scientific data in mind, one must question why it would be beneficial in prevention or treatment
efforts to place patients on support surfaces that rely on reactive hyperemia to occur. Large cell
alternating pressure support surfaces should be used cautiously and small cell alternating support
surfaces should not be used at all (Guidelines of NPUAP/EPUAP [19]).
A hypoxic event may cause reversible or irreversible damage (14, 21, 24). Reactive hyperemia is the
body’s attempt at saving the cells when blood flow is restored. What happens, however, if blood flow is
not restored and the cell injury is irreversible as in cases of prolonged soft tissue distortion? A damaging
cascade of events will likely occur.
Normal laminar blood flow allows leukocytes, erythrocytes and platelets to flow freely and smoothly within
the center of a vessel. They are surrounded by plasma and the layer of cells called the endothelium,
which is covered by a basement membrane (21). As soft tissue distortion occurs, blood vessels may
crimp or become blocked, resulting in decreased laminar flow and decreased velocity of flow. As the
laminar flow is disrupted, a turbulent flow begins, causing neutrophils to come in contact with the
endothelium. As the flow velocity decreases, the neutrophils will come in contact with endothelium. This
process is known as margination and results in an inflammatory response, development of free radicals,
release of proteolytic enzymes and stasis resulting in a microthrombotic condition of the small vessels
(13, 21, 22, 25).
Junctions between the endothelial cells then begin to develop and allow the blood cells to leak out into
the tissues. Once again, the enzymatic conversion that occurs during ischemia creates free radicals. As
the neutrophils leak into the tissues, they create a “respiratory burst” with their further release of free
radicals, thus causing more cellular damage. This cascade of events can progress if no circulation is
restored, if incomplete circulation is restored, or if a reperfusion injury occurs due to the body’s inability to
neutralize free radicals. This is called oxidative stress and it is a balancing act dictated by an individual’s
general health, age, nutritional status and quantity of free radicals (12, 21).
Aging itself plays a very significant role in pressure ulcer susceptibility. In aging skin, the epidermis and
dermis thin and elasticity decreases. There is a decrease in collagen synthesis, tensile strength and
moisture, making the skin stiffer (26, 27). These changes increase the skin’s susceptibility to pressure
ulcer development and decrease its ability to repair.
The first line of defense in pressure ulcer prevention is to select support therapy and repositioning
schedules that minimize soft tissue distortion caused by shear and gradient pressure to ultimately prevent
cellular necrosis as well as pain control in palliative care end of life patients (28). In order to do so,
caregivers must simply keep scientific principles in mind and understand the true effects of the support
surface media and container design being chosen.
The basic principles of physics, chemistry and mechanics define why this predicable outcome of soft
tissue strain occurs with support surface stress (stress to strain reaction). These principles are the kinetic
molecular theory, the ideal gas law, Archimedes principle, Hooke’s Law, and the physical properties
relating to a static fluid (non-powered), dynamic fluid (powered), solid media, and the mechanical
advantage of the simple inclined plane machine as relating to a wedge-shaped structure (29). Utilizing
these basic scientific principles, one can explain the clinical presentation of cellular necrosis (pressure
ulcer) occurring secondary to placing a human body on a surface (30, 31, 32). [Figure 3a and 3b]
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Basic scientific principles relating to chemistry explain the effects of various support surfaces
Physical properties of media




Static (non-powered) Gas
o Minimal molecular bonding
Liquid
o Moderate molecular bonding
Solid
o Strong molecular bonding
Dynamic (powered) Gas
o Forced molecular motion
[Figure 3a] (30)
Basic scientific principles relating to mechanics and physics explain the effects of various
support surfaces
Basic physics laws and principles


200 BC
o Archimedes Buoyancy Principle: Any object immersed in a fluid will be lighter
(Ex. it will be buoyed up) by an amount equal to the weight of the fluid it
displaces.
th
17 Century
o Force: A push or pull exerted on a body. It is a vector quantity, having
magnitude and direction.
o Boyle’s Law: The volume (V) of given quantity of any gas varies inversely with
the pressure (P)
o Pascal Principle: An external pressure applied to a fluid (liquid or gas) which is
confined within a container is transmitted undiminished throughout the entire
fluid. It equalizes in all directions and acts via forces perpendicular to the
retaining walls
o Newton’s 3rd Law: For every action there is an equal and opposite reaction
o Hooke’s Law of Elasticity: This can be stated in terms of stress and strain. If the
system obeys Hooke’s law, then stress  strain. We then define a constant,
called the modulus of elasticity, by the relation Modulus of elasticity =
stress/strain. The modulus has the same units as stress. A large modulus
means that a large stress is required to produce a given strain.



Young’s Modulus:
Shear Modulus:
Bulk Modulus*:
𝑭
( 𝑮𝒓𝒂𝒅𝒊𝒆𝒏𝒕 𝑷𝒆𝒓𝒑𝒊𝒏𝒅𝒊𝒄𝒖𝒍𝒂𝒓 𝑭)
𝑨
∆ 𝑳/𝑳°
𝑭
(𝑷𝒂𝒓𝒂𝒍𝒍𝒆𝒍 𝑭)
𝑨
𝑨𝒏𝒈𝒍𝒆 𝒐𝒇 𝑺𝒉𝒆𝒂𝒓
𝑭
(𝑵𝒐𝒏−𝒈𝒓𝒂𝒅𝒊𝒆𝒏𝒕∗∗ 𝑷𝒆𝒓𝒑𝒊𝒏𝒅𝒊𝒄𝒖𝒍𝒂𝒓 𝑭)
𝑨
∆ 𝑽/𝑽
*Volume Change
**Static fluid pressure
[Figure 3b] (30, 31, 32)
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©2015 James G. Spahn
Maintaining volumetric, three-dimensional configuration of the soft tissue at risk can be accomplished by
delivering non-gradient, perpendicular pressure by floating the body in a static fluid media (non-powered).
Flotation therapy is the most effective therapy to prevent and treat ulcer problems. The benefit of
maintaining volumetric support by utilizing flotation therapy is that the bony prominence is not able to sink
into the surrounding soft tissue [Figure 4a]. If this unwanted impaling occurs, then vertical shearing
(immersion), secondary to pressure gradiency, occurs with subsequent tissue distortion, ischemia, tissue
injury and ultimate cellular necrosis. This sequential event explains the crater-like wounds that occur
around, not only under, the bony prominence. Thus, the impaling of the wedge-like bony prominence into
the surrounding soft tissue creates force amplification following the mechanical advantage of a wedgeinclined plane machine. Examples of common areas where this event can take place include the lower
back, buttocks, and trochanter. [Figure 4b].
[Figure 4a]
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©2015 James G. Spahn
1
2
4
3
5
[Figure 4b]
This mechanical advantage is better understood when one compares a high-heel shoe versus a flat-heel
shoe. The pressure under the high-heel shoe is greater than that of the flat-heel shoe based on the
smaller area of support contact. But the force of the high-heel shoe is magnified when the high-heel
impales into a viscoelastic material (e.g. warm asphalt). Upon impaling the wedge-like structure, the
smaller surface of contact becomes a surface into which a wedge is being driven with the force
amplification of the weight of the body. This is comparable to the unwanted occurrence of a bony
prominence impaling into the surrounding viscoelastic soft tissue when shear strain (distortion), not
volumetric support (equalized compression), is delivered to the body by a support surface [Figure 5a]. An
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example of a common area where this type of event can take place are the heels [Figure 5b]. This is why
a static-fluid system is the ideal media to float the body.
[Figure 5a]
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©2015 James G. Spahn
1
2
3
4
5
[Figure 5b]
We have relied on interface pressure readings for some time now. Interface pressure is the intensity of
the perpendicular mechanical stress which is being applied externally to the skin (16, 33, 106). Relying
solely on these pressure readings in support surface selection can be dangerous and misleading due to
the fact that the body is three-dimensional, not two-dimensional (12, 29, 30, 34). We must consider the
depth, in addition to length and width, when assessing support surface needs. Ulcers develop at the bony
prominence level, requiring knowledge of all that is happening at that level. Is the bony prominence
impaling into the soft tissue? Is shearing causing the soft tissue to stretch over the bony prominence? For
example, if we place a body on a board, the interface pressure will most likely be fairly high. In contrast, if
we place a body on a foam surface, we would expect the interface pressure to be lower. However, as
discussed earlier, the other major component causing tissue damage is shearing stress resulting in soft
tissue distortion. An interface pressure reading does not tell us anything about these factors unless the
gradiency of the pressure is evaluated along with the absolute value (NPUAP/EPUAP Guidelines) (19,
33).
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Perhaps the only way to eliminate all pressure and tissue distortion would be to float in space where there
is no gravity. Due to the laws of gravity, there will always be some mechanical stress between a body and
the surface supporting it (12, 30, 34). With that said we must choose a support surface which provides
equalized pressure over the greatest area of contact with the body, without delivering shear and gradient
pressure and causing distortion of the soft tissue (19). A brief review of physics can help us choose. A
solid material is composed of many tightly bound molecules that adhere together. This physical property
allows shear forces to be sustained, which means they can also be delivered. Foam is an example of a
solid. A fluid, which may be a gas or a liquid, is composed of loosely bound molecules that tend not to
adhere so closely together, resulting in no shearing forces sustained or delivered (12, 29, 30, 34). Air and
water are examples of a fluid that delivers non-gradient pressure. In a pursuit of a support surface that will
deliver the least shear, it is scientifically clear that a static air product is the best choice due to its ability to
equally redistribute the weight of the body by compression and displacement (15). Water is denser and
has a greater viscosity. Thus, water can only achieve the desired three-dimensional body support by
displacement. The greater the density and viscosity of a fluid, the greater the risk is for the distortion of
tissue to occur on immersion of the surface. The density of viscosity of static (non-powered) air is
minimal, water moderate and sol (flowing gel) is extensive.(29, 30, 34) It is important to remember that
over inflation (air) and over filling (water) of the container will negate the beneficial properties of these two
forms of fluids that are frequently used as media in medical support surfaces.
Keeping in mind our goal of eliminating tissue distortion secondary to shear and gradient pressure, we
must consider the delivery method of the air. The delivery may be powered (Ex. alternating pressure, low
air loss) or non-powered (static air, water, sol).
The term powered air means that the air is moving or being pumped into a container (16, 29, 30, 34). If air
is being pumped into an empty container, it must provide enough air to make the container taut;
otherwise, a body would sink into the center, which is obviously not therapeutic with our goal. This taut
container may now be delivering shear forces much like a solid would. Again, we must think about what is
happening at the bony-prominence level. Also, moving air actually causes shearing of the tissue due to
the physical properties of a dynamic fluid system [Figure 6].
Physical Properties of Media
Solid
Static Fluid
(nonpowered)
Powered Air
•Board
•Foam
•Non-Flowing
Gel
•Air
•Water
•Sol
•Low Air Loss
•Alternating
Mechanical Stress
Gradient
Non-Gradient
Pressure and
Pressure
Shear
X
X
X
Soft Tissue Strain
Distortion
Volumetric
X
X
X
X
X
X
X
X
[Figure 6]
X
X
X
X
X
Low air loss therapy not only fills a container taut, thus delivering shear forces, but the method also blows
air out of the container. In addition to the high risk of tissue distortion, new risks are introduced as a result
of the circulating air. For example, continuous airflow on a patient’s skin can have a dangerous drying
effect on already dry skin. In cases of incontinence, the drying effect of the air may actually increase the
concentration of the urine and feces directly on the skin, thus increasing the likelihood of chemical
induced dermatitis and subsequent skin breakdown. Lastly, consider the existing contamination risk as
bacteria, viruses, funguses, etc. are being blown into the air (35-47).
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Static air is motionless or non-powered air (29, 30, 34). The loose molecules of static air actually
compress and displace when a body is placed on a relevant static air surface. As previously stated, the
molecules redistribute in a manner that provides non-gradient or equalized support to the entire surface
area of contact with the body. As a result, the chances of shearing and resultant soft tissue distortion are
minimized. Based on the basic principles of physiology and physics, static air is the media and delivery of
choice in our goal of pressure ulcer prevention and treatment [Figure 7] (48).
Three Properties of Pressure in a Fluid



The forces of a fluid at rest exerts on the walls of its container, and vice versa, always act
perpendicular to the walls.
An external pressure exerted on a fluid is transmitted uniformly throughout the volume of the
fluid.
The pressure on a small surface in a fluid state is the same regardless of the orientation of the
surface.
[Figure 7]
Gel products need to be placed in two different product categories. The non-flowing gels have physical
properties of a solid. The flowing gels (sols) have properties of a fluid. The problem is that sols have
higher viscosity and density properties than water. These physical properties cause the sols to deliver
greater shear forces with resulting soft tissue distortion as long as there is flowing motion and or depth of
emersion occurring (30) [Figure 6].
The thermal conductivity and the ability of different substances, particularly water and gels, must be
considered when protecting patients against “too cold” or “too hot” core temperature variance. This is
particularly important in the care of elderly and physiologically unstable patients. When considering the
above risks and recognizing the fact that the human body’s shell temperature acclimates to the
contiguous ambient temperature by physiologic temperature control processes over a short time frame,
turning and repositioning of the patient is beneficial for micro-environment, as well mechanical stress
management (49). The benefits of socialization for the patient resulting from more frequent caregiver
interactions is often forgotten as a valuable part of individualized care planning (50). The ability and ease
for the patient to turn independently or with caregiver assistance should be considered when selecting a
support surface product (51).
As pressure ulcer occurrence and associated treatment costs continue to increase while reimbursement
dwindles, protocols must be revised to maintain financial solvency (AHRQ [5]). It is imperative that funds
and time are not misused in facilities’ efforts. Responsibility must be taken to formulate informed
decisions based on scientific principles and outcome studies. Product utilization choices based on the
aforementioned principles should free up many dollars in the future, allowing available funds for additional
bedside caregiver staffing (52) [Figure 8]. It is apparent that prevention is the key, as it has been
reported that pressure ulcer treatment costs are 2.5 times greater than prevention costs (53). If funds are
budgeted appropriately and wise decisions are made early in targeting the key contributing factors to
pressure ulcer development, enormous impact can be made financially, and more importantly, in the lives
of patients.
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All Support Surfaces Should:
 Minimize pressure, shear, and friction injury
o Redistribute weight equally in a three-dimensional manner
o Aid in patient transferring and mobilization

Assist in moisture and temperature control
o Aid in patient transferring and mobilization

Minimize risk for product contamination of surface and/or media
o Be easy to clean




Minimize bio-aerosol spread
Be compatible with multiple surfaces
Be cost effective
Fulfill regulatory requirements
o Flame retardant
o Bio-compatibility
o Antimicrobial
o FDA regulations
o Good manufacturing process (ISO)
Address safety and comfort of patient
o Lightweight
o Pliable but durable
o Latex free
o Minimize hospital bed entrapment and falls

[Figure 8]
When the deep tissue injury component is considered in pressure ulcer staging, heel pressure ulcers are
now first in occurrence (54). It is important to remember that no support surface can protect the
ankle/foot/heel from pressure ulcers at all times. This is not because the products are not beneficial, but
because of recumbent physiological changes, hemodynamics (decreased circulatory perfusion and
venous congestion), and the anatomy (multiple bony prominences with minimal underlying tissue
attached to the legs which acts as a fulcrum) of the region creates a unique and challenging need that
frequently exceeds the capabilities of a support surface to protect the ankle/foot/heel from mechanical
stress injury. [Figure 9]
Medical devices (EX: pillows, splints, and heel elevators) used to offload the heel and other bony
prominences must be scrutinized relating to the risk of product surface and internal media contamination.
Open wounds, incontinence soiling, and normal skin colonization of the foot creates an environment for
occult device contamination.
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Ankle/Foot/Heel Products Should:
 Elevate heel (off of surface)
 Protect sides of foot and ankle
 Neutralize weight of lower extremity (Delever)
 Maintain and promote circulation
 Address foot drop and lateral rotation of ankle
 Allow access to the foot for inspection/treatment
 Facilitate the musculoskeletal pump
 Minimize risk for product contamination of surface or media
o Be easy to clean
 Fulfill regulatory requirements
o Flame retardant
o Bio-compatibility
o Antimicrobial
o FDA regulations
o Good manufacturing process (ISO)
 Address safety and comfort of patient
o Lightweight
o Pliable but durable
o Latex free
[Figure 9]
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Part Two
Seamless Continuum of Care: Computer Science, Informatics, Image
Analysis, etc.
New Approaches to Wound Care: Predictive Modeling, Infrared Thermography & Visual Imaging
Over the last century, clinicians have utilized medical devices that assist them in their delivery of patientcentered care. The common function of these devices is to add new scientific data to be evaluated and
not to replace the clinical judgment of the clinician. This fulfills the dictum that evidence-informed/best
practice is clinical judgment assisted by scientific data and patient-centered practice (55-58).
Entering into the era of computer science and sophisticated electronics, clinicians have the opportunity to
be supported by data and information in a statistically significant and timely fashion. These advancements
have allowed more extensive and useful collection of meaningful data that can be acquired, analyzed and
applied in conjunction with the knowledge and expertise of the clinician (59).
Predictive modeling is a relatively new area of activity when it comes to patient analysis, management
and overall treatment. During this process, a software solution is generated to assist the caregiver in
designing an acceptable outcome for the patient, a practice in which caregivers utilize tools such as
decision trees, support vector machines, neural networks and more. The result is assessments that
are correlated with standardized assessment tools, weighted government assessment tools, highly
specific analysis of attributes, and cross integration of co-morbidity factors. Ideally, these refined data
processes can be implemented into a system that gives healthcare prescribers the freedom and
confidence to authorize treatment for their individual patient needs. The solution might lie in enhanced
risk tools in the form of a data system that allows clinicians the freedom to apply their considerable skills
in combination with the power of accurate and current patient data.
Established assessment tools utilize linear regression or a simple addition of numerical risk factors.
Support Vector Machine (SVM), Probabilistic Neural Network (PNN), Feed Forward
Backpropagation Neural networks (BPN), Decision Trees (DT), and as many as 12 additional types
of models are available for consideration. In the development of predictive modeling modern
statistical methods can analyze interactions between the acquired data (e.g. gender, age, race and
other risk factors) that varies in different patient populations which can have non-linear
contributions. A perfect example of the benefits for using the predictive model concept is when a
comprehensive assessment is acquired and analyzed to determine the risk of pressure ulcer
development. This can also be used for assessing many other risk factors relating to the individual
patient’s condition. This confirms the belief of the author that pressure ulcers are the core quality
indicator for many risk factors that need to be analyzed [Figure 10].
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[Figure 10]
This development of a new method of predictability incorporates expert input by way of extensive
clinical experience in wound care, as well as extensive literature review to identify risk factors
described by other clinicians. From this information, identification of co-morbid conditions can be
highlighted. Numerical value correlations of an expert ranking metric for each question can also be
established, and used as a calculator, to assist the clinician in determining an individual’s
percentage risk level relating to each co-morbid category, based solely on the answers to the
questions posed to them. Serving as an enhancement to current technologies, protocols and processes
that caregivers are following today, predictive modeling delivers effective, real-time analysis of data and
helps produce useful knowledge bedside. Upon the review of the properly organized and trended data,
caregivers can understand the patient’s health in a holistic manner; a capability that is extremely unique,
as current techniques merely gather data without offering any knowledge to the provider based on that
data (60-73) [Figure 11].
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Addressing Nine Risk Factor Categories
1. Cognition
2. Mobilization & ambulation (motor and/or sensory)
3. Nutrition and hydration
4. Moisture (excessive & dryness) and incontinence (urinary/fecal/combination)
5. General medical co-morbidities (medication use)
6. Existing pressure ulcers (suspected DTI, Stage I, II, III, IV and Unstagable)
7. Previous pressure ulcers (closed Stage III, IV, Unstagable and DTI)
8. Contact with medical devices (Ex. braces, orthotics, cannulas, tubing), and/or an
object in contact with the body
9. Patient chooses not to accept part or all of the suggested medical treatment
[Figure 11] (51, 74, 75, 76, 77)
The recent recognitions of deep tissue injury under intact skin have resurrected a condition that has been
recognized to occur since the 1800s (1, 5, 6, 9). Pressure ulcer staging systems went from not defining
the occurrence to recognizing a specific stage of suspected deep tissue injury by the NPUAP in 2007 (2).
The clinical findings are referenced in the NPUAP guidelines (3). Since the injury of the underlying tissue
precedes the skin injury, clinical recognition can be delayed depending on the depth of the
pathophysiologic event (78). Clinicians and industry have been seeking and researching medical device
technology to identify the deep tissue injury prior to skin involvement. One of the approaches to identify
deep tissue injury has been long-wave infrared (IR) thermography [Figure 12]. This has been proven to
be beneficial in the evaluation of thermal heat intensity and gradiency relating to the abnormalities of the
skin and underlying tissue (SUT) [Figure 13] (79-92,107-122). Although this technology has expanded to
other areas of medical evaluation (93, 94, 105), the scope of this document is limited to the SUT
abnormalities. These abnormalities include the formation of deep tissue injury (DTI) and subsequent
necrosis caused by mechanical stress, infection, auto-immune condition and vascular flow problems. DTI
caused by mechanical stress (pressure, shear and frictional force) can be separated into three
categories.
Features of Long-wave IR Imager
What it is
•A non-contact medical device
•An adjunct tool used to identify areas of
interest to assist clinicians
•Portable and lightweight
What it is NOT
◦Is not a substitute for clinical judgment
◦Is not invasive, diagnostic, treatment, or therapy
tool
◦Is not an ionizing radiation or sound wave device
(EPA.gov, 2011)
[Figure 12]
Soft Tissue at Risk
Epithelial - covering
-skin-epidermis/dermis
-endothelium-lining of the vessels
Adipose tissue
Connective – support
Muscle – movement
Nervous - control
[Figure 13]
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The first category is a high magnitude/short duration mechanical stress represented by traumatic and
surgical wounds. The second category is low magnitude/long duration mechanical stress represented by
pressure ulcer development, which is also a factor in the development of ischemic and neuropathic
wounds. The third category is a combination of categories one and two represented by pressure ulcer
formation in the bariatric patient.
The pathophysiologic conditions that occur with DTI and subsequent necrosis of the affected tissue are
ischemia, cell distortion, impaired lymphatic drainage, impaired interstitial fluid flow and reperfusion injury
(12, 21). Category one is dominated by cell distortion and even destruction. Category two is dominated by
ischemia. Category three is a combination of cell distortion and ischemia (95-97).
Hypoxia causes aerobic metabolism to convert to anaerobic metabolism. This occurrence causes lactic
acidosis followed by cell destruction, release of enzymes and lytic reactions. The release of these
substances causes additional cell injury and destruction, and initiation of the inflammatory response.
It is very important to recognize that ischemic-reperfusion injury is associated with all of the above
mechanical stress-induced SUT injuries. This condition is caused by a hypoxia induced, enzymatic
change, as well as the respiratory burst associated with phagocytosis when oxygen returns after an
ischemic event.
The result of ischemic reperfusion injury is the formation of oxygen-free radicals (hydroxyl, superoxide,
and hydroxide peroxide) that cause damage to healthy and already injured cells leading to extension of
the original injury (14, 21, 23, 24, 52).
SUT injury and subsequent necrosis can also be caused by vascular disorders. Hypoxia can be caused
by an arterial occlusion or by venous hyperextension. Lymphatic flow or node obstruction can also create
vascular induced injury by creating fibrous restriction to venous drainage and subsequent cellular stasis in
the capillary system. These disorders are also accentuated by reperfusion injury and oxygen-free radical
formation.
Infection of the skin (impetigo), underlying tissue (cellulitis), deep tissue (fasciitis), bone (osteomyelitis)
and cartilage (chondritis) causes injury and necrosis of the affected tissue. Cells can be injured or
destroyed by the microorganism directly, by toxins released by the microorganism and/or the subsequent
immune and inflammatory response. These disorders are also accentuated by reperfusion injury and
oxygen-free radical formation.
Autoimmune morbidities of the skeletal joints (rheumatoid arthritis), underlying tissue (tendonitis, myelitis,
dermatitis) and blood vessels (vasculitis) cause similar dysfunction and necrosis of the tissue being
affected by the hypersensitivity reactions on the targeted cells and the subsequent inflammatory
response. Again, these conditions are accentuated by reperfusion and oxygen-free radical formation.
The common event that addresses all of the above SUT injuries is the inflammatory response. This
response has two stages. The first stage is vascular and the second is cellular. The initial vascular
response is vasoconstriction which will last a short time. The constriction causes a decrease in blood flow
to the area of injury, which causes vascular “pooling” of blood (passive congestion) in the proximal arterial
vasculature in the region of injury and intravascular cellular stasis occurs along with coagulation.
The second vascular response is extensive vasodilation of the blood vessels in the area of necrosis. This
dilation along with the “pooled” proximal blood causes increased blood flow with high perfusion pressure
into the area of injury. The high pressure flow can cause damage to endothelial cells. Leakage of plasma,
protein and intravascular cells causes more cellular stasis in the capillaries (micro-thrombic event) and
hemorrhage into the area of injury. When the perivascular collagen is injured, intravascular and
extravascular coagulation occurs. The rupture of the mast cells causes release of histamine which
increases the vascular dilation and the size of the junctions between the endothelial cells. This is the
beginning of the cellular phase. More serum and cells (mainly neutrophils) enter into the area of the
mixture of injured and destroyed cells by the mechanisms of margination, emigration (diapedesis) and
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chemotaxic recruitment (chemotaxic gradiency). Stalling of the inflammatory stage can cause the area of
necrosis (ring of ischemia) to remain in the inflammatory stage long past the anticipated time of two to
four days. This continuation of the inflammatory stage leads to delayed resolution of the ischemic necrotic
event.
The proliferation stage starts before the inflammatory stage recedes. In this stage, angiogenesis and the
formation of granulation and collagen deposition occur. Contraction also occurs, and peaks anywhere
from five to 15 days post injury.
Re-epithelialization occurs by various processes depending on the depth of injury. Partial thickness
wounds can resurface within a few days. Full thickness wounds need granulation tissue to form the base
for re-epithelialization to occur. The full-thickness wound does not heal by regeneration due to the need
for scar tissue to repair the wound. The repaired, scarred wound has less vascularity and tensile strength
of normal, regional and uninjured SUT. The final stage is remodeling, where collagen changes from type
III into a stronger type I and is arranged into an organized tissue.
All stages of wound healing require adequate vascularization to prevent ischemia, deliver nutrients and
remove metabolic waste. Following the vascular flow and metabolic activity of a necrotic area is currently
monitored by patient assessment and clinical findings of swelling, pain, redness, increased temperature,
and loss of function. Medical devices are now available to assist the clinician in defining the presence,
type and status of the SUT injury.
An IR and visual imaging device is a non-contact and non-radiating device that can be utilized bedside.
The combination of imagers allows both visible and invisible radiation from the body to be evaluated.
This allows both the anatomical and physiologic status of the SUT to be evaluated for injuries or disorders
that are not yet clinically recognizable. By visualizing the IR thermal intensity, the clinician can evaluate
the gradiency of the IR radiation emitted from the body region being imaged. The ability to visualize the
thermal gradiency allows the clinician to evaluate the metabolic activity and blood flow of the region being
imaged [Figure 14]. The normal SUT can be used as a control for that specific imaging procedure.
Why LWIT and Visual Imaging?
Obtains
Measures
Benefits
LWIR
Infrared thermal intensity
gradiency
Physiological status view
Recognition of skin and
underlying tissue abnormalities
prior to clinical recognition
Identifies visually whether the IR
image is either normal or
abnormal
Documentation of IR thermal
presenting the findings in a
trending fashion
[Figure 14]
Visual
Visible light
Anatomical view
Image that represents visual
status of skin and/or underlying
tissue
Creates awareness of site with
abnormality to allow sequential
evaluation of a condition
Documentation of visual
presentation of the findings in a
trending fashion
Having a real-time control (unaffected SUT) allows an area of interest (AOI) [either an open wound or
intact skin with underlying tissue abnormality] to be recognized. The AOI can be of greater intensity
(hotter) or less intensity (cooler) than the real-time SUT control of that region of the body. The AOI can
then be evaluated by the clinician relating to the degree of metabolism, blood flow, perfusion, necrosis,
inflammation and the presence of infection. This is done by comparing the hotter or cooler thermal
intensity of the AOI or wound base and peri-AOI or wound area to the real-time SUT control of the
location being imaged. Serial imaging can also assist the clinician in the ability to recognize improvement
or regression of the AOI or wound over time.
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©2015 James G. Spahn
The use of a long-wave infrared and visual imaging device is a useful adjunct tool for clinicians to
recognize physiologic and anatomical changes in an AOI before it presents clinically. It also gives
clinicians the ability to quantitatively document the status of the AOI/wound in a trending format. By
combining the knowledge obtained from the images with a comprehensive assessment, skin and
underlying tissue evaluation, along with an AOI or wound evaluation, will assist the clinician in analyzing
the etiology, improvement or deterioration, as well as the presence of infection affecting the AOI or
wound.
According to EF Ring, “Thermography, along with X-ray, CT, MRI, mammography, ultrasonography and
other imaging procedures, is not a standalone diagnostic tool. Like other imaging procedures, it is an
adjunctive tool, which while reliable should be utilized by the treating physician along with other tests and
analyses to arrive at a provisional or more complete diagnosis. No diagnosis should be based on thermal
imaging alone. Additional diagnostic procedures, which depend on the nature of the condition and/or body
region, are needed to achieve a final diagnosis. Thermography provides physiological imaging. X-ray, CT,
MRI, mammography, and ultrasonography provide anatomical imaging [Figure 15] (98, 99).”
[Figure 15]
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©2015 James G. Spahn
CONCLUSION
By understanding and utilizing basic science principles, a sound and justified decision can be made
regarding the ideal support surface (ex. bed, chair, ER surface, etc.) for each individual patient.
As new innovations for pressure ulcer prevention and detection are adopted throughout the continuum of
care, the opportunity for improved, individualized care plans continues to arise. Although these are new
approaches to wound care, they are in no way intended to replace facilities’ individualized care protocols
relating to pressure ulcer prevention and treatment. Instead, they are meant to provide caregivers with a
holistic view into each patient’s physiologic status to better define and portray the differing effects support
surfaces or related wound care initiatives have on each patient. As a result, individualized care plans can
then be extrapolated to ensure the proper matching of support surface and intervention methods to each
individual patient’s needs (100).
James G. Spahn, MD, FACS, is the CEO of EHOB, Inc., manufacturer of the WAFFLE® Brand Products
for the prevention and treatment of pressure ulcers, as well as founder and Chairman of the Board for
WoundVision, a leader in advanced wound detection through the use of thermal imaging and predictive
modeling software. For more information, call (800) 899-5553 (EHOB) or (888) 851-0098 (WoundVision),
email [email protected] or [email protected], or visit www.ehob.com and
www.woundvision.com.
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©2015 James G. Spahn
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©2015 James G. Spahn
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Understand Solve. “Home Health Care Management & Practice 19.4 (2007): 285-93.
101) Tippett, Aletha W., MD. "Reducing the Incidence of Pressure Ulcers in Nursing Home Residents:
A Prospective 6-Year Evaluation." Ostomy Wound Management (2009): 52-58. Print.
102) Johnson, Jane, Darcie Peterson, Betty Campbell, Regina Richardson, and Dana Rutledge.
"Hospital-Acquired Pressure Ulcer Prevalence-Evaluating Low-Air-Loss Beds."JWOCN (2011): 55-60.
Print.
103) Vermette, Sophie, RN, Isabelle Reeves, RN, and Jacques Lemaire, PhD. "Cost Effectiveness of
an Air-inflated Static Overlay for Pressure Ulcer Prevention: A Randomized, Controlled
Trial." Wounds 24.8 (2012): 207-14. Print.
104) Herrman, Eric C., MS, Charles F. Knapp, PhD, James C. Donofrio, PhD, and Richard Salcido,
MD. "Skin Perfusion Responses to Surface Pressure-induced Ischemia: Implication for the
Developing Pressure Ulcer." Skin Perfusion Responses to Surface Pressure-induced Ischemia:
Implication for the Developing Pressure Ulcer. N.p., n.d. Web. 01 Nov. 2012.
<http://www.rehab.research.va.gov/jour/99/36/2/herrman.htm>.
105) Williams, D. T., Jane R. Hilton, and K. G. Harding. "Diagnosing Foot Infection in
Diabetes."Clinical Infectious Diseases (n.d.): n. pag. Print.
106) Hanson, Darlene S., RN, Diane Langemo, PhD, Julie Anderson, RN, Pat Thompson, RN, and
Susan Hunter, RN. "Can Pressure Mapping Prevent Pressure Ulcers?" Nursing50-51 39.6 (n.d.): n.
pag. Print.
107) Iaizzo, Paul A., PhD. "Temperature Modulation of Pressure Ulcer Formation: Using a
Swine."Archives of Physical Medicine and Rehabilitation (1995): 666-73. Print.
108) Ratovoson, D., F. Jourdan, and V. Huon. "A Study of Heat Distribution in Human Skin: Use of
Infrared Thermography." EPJ Web of Conferences 6 (2010): 21008. Print.
109) Nakagami, Gohiro, PhD. "Combination of Ultrasonographic and Thermographic Assessments for
Predicting Partial-thickness Pressure Ulcer Healing." Wounds (2011): 285-92. Print.
110) Bird, H. A., and E. F. J. Ring. "Thermography And Radiology In The Localization Of
Infection." Rheumatology 17.2 (1978): 103-06. Print.
111) Roback, Kerstin. "An Overview of Temperature Monitoring Devices for Early Detection of
Diabetic Foot Disorders." Expert Review of Medical Devices 7.5 (2010): 711-18. Print.
112) Mirabella, Carlo, MD, Serene Bellandi, MD, Gabrielle Graziana, MD, Leonardo Tolomei, PhD,
Leonardo Manetti, PhD, and Damiano Fortuna, DVM. "Hemodynamic 3D Infrared Thermal
Stereoscopic Imaging (TSI) Investigation in Chronic Vascular Leg Ulcers: A Feasibility
Study." Wounds (2011): 276-84. Print.
113) Trandel, Richard S., PhD, David W. Lewis, PhD, and Phyllis J. Verhonick, Ed. D.
"Thermographical Investigation of Decubitus Ulcers." Bulletin of Prosthetics Research (1975): n. pag.
Print.
114) "Skin Deep: Imaging Technologies May Detect Pressure Ulcers And Deep-tissue Injuries That
Healthcare Workers May Miss." World Health. Georgia Institute of Technology, n.d. Web. 15 Aug.
2006. <http://www.worldhealth.net/news/skin_deep_imaging_technologies_may_detec/>.
115) Farid, Karen J., DNP, Chris Winkelman, PhD, Adel Rizkala, PharmD, and Katherine Jones, PhD.
"Using Temperature Pressure-related Intact Discolored Areas of Skin to Detect Deep Tissue Injury:
An Observational, Retrospective, Correlational Study." Ostomy Wound Management (2012): 20-31.
Print.
116) Goller, Herbert, PhD, David W. Lewis, PhD, and Robert E. McLaughling, MD. "Thermographic
Studies of Human Skin Subjected to Localized Pressure." University of Virginia (1971): 749-54. Print.
117) Havenith, G. "Temperature Regulation and Technology." Gerontechnology 1.1 (2001): 41-49.
Print.
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118) "Temperature of a Healthy Human (Body Temperature)." Temperature of a Healthy Human
(Body Temperature). N.p., n.d. Web. 01 Nov. 2012.
<http://hypertextbook.com/facts/LenaWong.shtml>.
119) Baharestani, Mona, Joyce Black, Kerylin Carville, Michael Clark, Janet Cuddigan, Carol Dealey,
Tom Deflorr, Amit Gefen, Keith Harding, Nils Lahmann, Maarten Lubbers, Courtney Lyder, Takehiko
Ohura, Heather Orsted, Vinoth Ranganathan, Steven Reger, Marco Romanelli, Hiromi Sanada, and
Makato Takahashi. "International Review: Pressure Ulcer Prevention: Pressure, Shear, Friction and
Microclimate in Context." International Review: Pressure Ulcer Prevention: Pressure, Shear, Friction
and Microclimate in Context. KCI, 01 Sept. 2012. Web. 05 Nov. 2012.
<http://www.woundsinternational.com/clinical-guidelines/international-review-pressure-ulcerprevention-pressure-shear-friction-and-microclimate-in-context>.
120) Patel S, Knapp C, Donofrio J, Salcido R. Temperature effects on surface pressure-induced
changes in rat skin perfusion: Implications in pressure ulcer development. J Rehabil Res Dev.
28(3):188-201
121) Bhargava A, Chanmugam A, and Herman C. Heat transfer model for deep tissue injury: a step
towards an early thermographic diagnostic capability. Diagnostic Pathology 2014, 9:36
122) Hildebrandt C, Raschner C, and Ammer K. An Overview of Recent Application of Medical
Infrared Thermography in Sports Medicine in Austria. Sensors (Basel). 2010; 10(5): 4700–4715.
PEER REVIEWED POSTERS FOR INTERNATIONAL/NATIONAL CONFERENCES:
1. Tippett, Aletha W., MD. A Simple Way to Prevent and Treat Pressure Ulcers. Rep. N.p.: n.p., n.d.
Print.
2. Tippett, Aletha W. Wounds Treated with Static Air Overlays. Rep. N.p.: n.p., n.d. Print.
3. Tippett, Aletha W., MD. Taking Pressure Ulcer Incidence to Zero: One Nursing Home's
Experience. Rep. N.p.: n.p., n.d. Print.
4. Stafford, Amy B., RN. Effectiveness of an Air Mattress Overlay and Seat Cushion for the
Prevention of Pressure Ulcers: A Quantitative Study. Rep. N.p.: n.p., n.d. Print.
5. Harwood, Judith K., RN, JoAnn Christiason, and Kaiser Permanente. Improving Quality of Life in
the LTC Hemodialysis Patient. Rep. N.p.: n.p., n.d. Print.
6. Hobba, Lisa, RN, and Michelle Kieninger, RN. Decreasing Pressure Ulcer Nosocomial Rates at a
Large Metropolitan Teaching Hospital. Rep. N.p.: n.p., n.d. Print.
7. Dunzweiler, Susan, RN, Karen Gammons, RN, and Lauren Hinson, RN. Taking the Pressure off
in the ICU. Rep. N.p.: n.p., n.d. Print.
8. Gute, Rebecca, RN. Versatility of a Static Air Overlay: Brought in for One Purpose, It Was Soon
Accomplishing FIVE! Rep. N.p.: n.p., n.d. Print.
9. Stow, Jean, RN. Reduction of Pressure Ulcer Incidence and Specialty Bed Rental Dollars Across
the Continuum of Care. Rep. N.p.: n.p., n.d. Print.
10. Cobb, Gladys A., RN, Linda H. Yoder, RN, and Joseph B. Warren, RN. Pressure Ulcers Patient
Outcomes on a Kinair Bed or EHOB Mattress. Rep. N.p.: n.p., n.d. Print.
11. Quality Improvement Skin Care Task Force. Methodist Hospital Pressure Ulcer Prevalence
Survey. Rep. N.p.: n.p., n.d. Print.
12. D'Andrea, Stephanie, RN, David A. Forreser, PhD, Denise Brenner, RN, Patricia P. Cupka, RN,
Angela N. Ryan, RN, Toni McTigue, APRN, and Janet Doyle-Munoz, RN.Initiating Pressure Ulcer
Prevention in the High Risk Population of the Emergency Department. Rep. N.p.: n.p., n.d. Print.
13. Azzaro, Margaret-Ann, RN. Decreasing Hospital Acquired Pressure Ulcers in the Acutely Ill MedSurg Patient. Rep. N.p.: n.p., n.d. Print.
14. Hobbs, Terry, RN. A Lift Team's Approach to Selecting Transferring and Positioning Devices.
Rep. N.p.: n.p., n.d. Print.
15. Gloeckner, Mary, RN, and Mary McLaughlin, RN. PATS...A Positioning and Turning Study. Rep.
N.p.: n.p., n.d. Print.
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TEXT BOOKS REVIEWED:
1. Corwin, E. J. (n.d.). Handbook of Pathophysiology Second Edition. Lippincott, Williams, and
Wilkins.
2. Price, S.A. & Wilson, L.M. (n.d.) Pathophysiology – Clinical Concepts of Disease Processes.
3. Krasner, D.L., Rodeheaver, G.T., & Sibbald, R.G. (2007). Chronic Wound Care: A Clinical Source
Book for Health Professionals. 4th Edition.
4. Morison, M.J. (2000). The Prevention and Treatments of Pressure Ulcers, 1st edition. Elsevier
Health Services.
5. Guyton, A.C., & Hall, J.E. (1996). Textbook of Physiology Ninth Edition. W.B. Saunders
Company.
6. Bullock, B.L. (1995). Pathophysiology-Adaptations and Alterations in Function, Fourth Edition.
Lippincott, Williams, and Wilkins.
7. Roades, R.A., & Tanner, G.A. (2003). Medical Physiology, 1st edition. Lippincott, Williams, and
Wilkins.
8. Morison, M.J., Ovington, L.G. & Wilkie, K. (2004). Chronic Wound Care – A Problem-Based
Learning Approach. Mosby.
9. Sussman, C, & Bates-Jensen, B. (2007). Wound Care – A Collaborative Practice Manuel For
Health Professionals Third Edition. Walters Kluwer.
10. Sussman, Carrie, and Barbara M. Bates-Jensen. Wound Care: A Collaborative Practice Manual.
4th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007.
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©2015 James G. Spahn