T
he purpose of this Wound Care Guide is to create a RESOURCE that fosters a more wholistic approach to the management of pressure injuries by simultaneously treating supine and seating postures. Our goal is to give a better understanding of the critical role appropriate wheelchair configurations and equipment choices play in the prevention and treatment of pressure injuries. After reading this guide, you as a Health Care Provider will be able to:
-
1
Identify the role wheelchair support surfaces play in the prevention and healing of a pressure injury
-
2
Ensure simultaneous consideration of BOTH supine and seated postures in the prevention and treatment of pressure injuries by addressing pressure, shear, and microclimate
-
3
Define each team member's role in prescribing and obtaining the appropriate wheelchair models, skin protection cushions, back supports, and accessories to minimize the risk of and assist in the healing of existing pressure injuries
What are the new definitions for the pressure injury staging?
Stages of Pressure Injuries:
Stage 1
Stage 2
Partial-thickness skin loss or blister. The wound bed is viable, pink or red, moist. These injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel.
Stage 3
Stage 4
Unstageable
Deep Tissue Pressure Injury (DTI)
Intact or non-intact skin with
Beyond the Bed
What are the top areas of common pressure injury development in supine?
- Heel
- Toe
- Sacrum
- Coccyx
- Ischial Tuberosity
- Occiput
- Scapula
- Spinous Process of Vertebrae
- Elbow
What are we missing in the treatment of a pressure injury?
As health care providers—especially physicians, nurses, and specialized therapists in wound care—we understand bedside treatment well. We search for the most appropriate support surfaces and stay up-to-date with the most innovative technologies to promote healing and prevention of new pressure injuries.
However, too often we forgot a critical piece of the puzzle in the fight against pressure injuries: prevention and treatment at the wheelchair level!
The above words and concepts jump to mind when discussing pressure injuries and they are just as critical to understand from the seated posture as they are in supine.
Are the common areas of pressure injury different in supine vs the seated posture?
Most patients that develop a pressure injury spend the majority of their time in bed or in a wheelchair, placing the skin and tissue under the bony prominences at risk. These "at risk" areas are almost identical bedside and in the wheelchair making it imperative to simultaneously prevent and treat pressure injuries from the supine and seated posture.
Why are these common areas at such high risk to develop a pressure injury?
In the wound care world, we are in a constant battle against the extrinsic factors of pressure injury development.
The extrinsic factors and the threat they pose to the patient in relation to the bed is well understood, BUT...
Do we consider these factors in relation to the wheelchair?
WE SHOULD!
Why do the extrinsic factors pose such a threat to a patient in the seated posture?
While seated, our weight goes directly through the pelvis and spine, leaving the bony prominences very susceptible to pressure, shear, and microclimate. This is the nature of a seated posture. With the constant compression of the skin and tissues:
-
a pressure injury can develop in four to six hours after sustained loading and at times in as little as an hour
-
and by allowing our patients to sit all day with low-quality cushions and back supports, we run the risk of "un-doing" the advancements we made with bedside treatments
What should our goal be when treating a pressure injury?
Treatment at both surfaces need simultaneous attention to minimize the risk of development or assist in the healing of an existing pressure injury. Provide the best equipment possible for all support surfaces!
What is my role in the equipment ordering process?
No matter if you are the doctor, nurse, therapist, or ATP, you play a critical role in the recognition, treatment, and prevention of a pressure injury. Take a look at the following flow chart to understand your role and how it fits in the big picture of providing every patient with the appropriate equipment.
Understanding the Population
Why is a wheelchair user's skin more susceptible to a pressure injury?
Most wheelchair users are dealing with factors that compromise skin integrity due to:
○ multiple co-morbidities
○ disease processes known to directly affect skin integrity such as IDDM, vascular insufficiencies, etc
○ the natural progression of aging
What layers of skin become compromised with disease and/or aging?
Since changes occur at each layer of the skin through disease processes and/or natural aging, ALL the layers are compromised and make a patient more susceptible to a pressure injury.
It is our job to understand these skin changes in order to combat pressure injuries through our wheelchair configurations and equipment choices by:
○ maximizing pelvic, trunk, head, and neck stability
○ achieving even pressure redistribution
○ maintaining optimal alignment
What are some of the skin changes that increase susceptibility to a pressure injury?
○ Decreased overall skin thickness○ Decreased number of sebaceous glands and sweat glands
○ Decreased vasularization
○ Reduction and disorganization of collagen and elastin fibers
○ Loss in Langerhans cells
○ Flattening of the dermal-epidermal junction
○ Loss in effectiveness of the never endings
○ Redistribution of fat cells and loss of connective tissue of the Hypodermis
Skin Changes at Each Layer
Let's compare young/healthy skin to aged/diseased skin and see why our patient population is at higher risk for pressure injury.
Why does thinner skin increase the risk of developing a pressure injury?
Overall skin thickness decreases by 6.4% per decade, increasing:
○ the risk of skin tears with minimal pressure, trauma, and shear forces
○ the susceptibility of the deeper layers of skin to the extrinsic factors as the epidermal layer is broken open more easily
○ the amount of time needed to heal a pressure injury
Layers of skin changed: Epidermis, Dermis, Hypodermis
How does having a reduction in sebaceous glands and sweat glands increase the risk of developing a pressure injury?
Fewer Sebaceous Glands
Less sebum (oil) production removes the oily coating from the superficial layer of skin, therefore:
○ breaking down the waterproof barrier that prevents excess moisture from entering the skin
○ reducing the natural lubrication that coats and protects the skin from drying out and becoming brittle, making it easier to break the skin open with pressure, trauma, and shear forces
○ allowing excess moisture to macerate the skin, increasing accessibility of the deeper layer to pressure and shear forces
Fewer Sweat Glands
○ Prevents perspiration with the exposure to excessive heat
○ Prevents the evaporation of sweat and the ability to cool the skin's temperature at the skin-seat interface
How does decreased vacularization affect skin integrity?
Weaker blood vessels and compromised blood flow make skin more susceptible to a pressure injury by increasing:
○ risk of ischemia and tissue death due to constant pressure under a bony prominence
○
Why is it detrimental to our skin when collagen and elastin fibers become disorganized and reduced in number?
Loss of collagen and elastin fibers:
○ decrease skin's tensile strength and elasticity, making the skin unable to "snap back" to its original position after a load has been removed
○
Why does a loss in Langerhans cells increase out susceptibility to pressure and shear?
Langerhans cells act as the body's warning against infection or high-pressure. The epidermal layer will redden and/or get warm as a warning sign to patient or caregiver to make a change!
Loss of Langerhans cells from disease or age:
○ slows the natural immune response of skin reddening and/or temperature change that acts as the initial warning signs of injury to the skin with pressure and/or trauma
○ increases susceptibility to prolonged pressure without an obvious warning sign to take precaution
What role does the dermal-epidermal junction play in maintaining healthy skin?
The dermal-epidermal junction is the communication channel between the dermis and the epidermis, allowing nutrients, O2, and blood to feed the epidermis and maintain skin integrity.
The dermal-epidermal junction is joined by wavy, finger-like projections called Rete Ridges. Rete Ridges increase the surface area to allow the flow of
How does the flattening of the dermal-epidermal junction affect skin integrity?
With age, the dermal-epidermal junction flattens by 35%, decreasing blood flow, O2, and nutrient exchange between the dermis and epidermis,
○ Results in the thinning of both layers of the skin
○ Prevents the natural keratinization needed for maintenance and healing of the skin after injury
Thinner epidermal and dermal layers:
○ causes a reduction in the barrier between the bony landmark and the pressure source
○ increases the susceptibility of the epidermis to break open at the bony prominences with pressure or trauma with shear forces
Is sensation affected by disease and age?
Age causes nerve endings to lose their effectiveness to perceive and react to stimuli, decreasing the ability to perceive input from pressure, heat, and cold.
Did you know that loss in effectiveness of nerve endings decreases the ability to perceive pain from pressure build-up under bony prominences? This results in decreased reaction time in performing pressure relieving techniques, which can result in a pressure injury.
What happens to the hypodermis with age and disease that places the deeper tissues, muscles, and bone at risk of pressure injury?
There is a reduction in the thickness of the hypodermis (fatty layer) due to:
○ the redistribution of fat cells
○ the loss of connective tissue
We never lose the number of fat cells we have. With age, fat cells are redistributed to areas of greater surface areas such as the stomach and thighs, leaving the areas under bony prominences more susceptible to the extrinsic factors of a pressure injury. Redistribution of fat cells to areas of great surface areas such as the stomach and thighs reduces the insulation and protective "cushion" the hypodermis normally would provide. A loss in connective tissue causes skin to be less firm. The skin then:
○ loses its strength and shape, becoming more susceptible to prolonged pressure at the bony prominences
○ loses fibrous bands that connect the skin to deeper tissues, making the deep tissue more susceptible to shear forces with movement in the wheelchair system
○ has diminished thermoregulation and absorbs more heat than it dissipates, making tissue more susceptible to the effects of pressure, shear, and microclimate
Intrinsic vs Extrinsic Factors
Patients are susceptible to pressure injuries in a seated posture due to the effects of intrinsic and extrinsic factors of a pressure injury.
What are Intrinsic Factors?
Factors stemming from within the body that make an individual more susceptible to a pressure injury, such as:
○ Limited mobility
○ Impaired sensation
○ Age-related skin changes
○ Postural deformities
○ Poor nutrition and dehydration
○ Urinary and fecal incontinence
○ Obesity
○ Being underweight
○ Limited alertness
○ Muscle spasms
○ Smoking
○ Medical conditions affecting blood flow
What are Extrinsic Factors?
Factors that stem from the outside environment and/or seating surface. Pressure, shear, and microclimate are the extrinsic factors of a pressure injury.
The therapist can prevent harmful effects of extrinsic factors through proper wheelchair positioning and equipment choices.
The Three Extrinsic Factors
Let's take a look at the extrinsic factors and threat they pose to our patients while seated!
Pressure
Pressure is a continuous force applied on or against an object by something that it is in contact with. In seating, equipment such as the seat and/or back support surface are in constant contact with the body creating peak pressures.
Shear
Shear is defined as a combination of downward pressure AND friction and occurs while a patient is in movement in the wheelchair system.
How is the mechanism of pressure different from the mechanism of shear?
Tissue death can occur with both pressure and shear, but the mechanism is quite different.
The Mechanics of Pressure
 |
Patient sits in a static posture for prolonged periods of time.
|
|
Peak pressures develop at the bony prominences caused by the downward pressure from gravity plus the upward pressure from the seated surface.
|
|
|
The skin/soft tissue between the bony prominences and the seat surface is constantly being compressed.
|
|
 |
|
|
The lack of blood flow, O2, and nutrient delivery results in ischemia.
|
|
|
Result in tissue death. |
The Mechanics of Shear
 |
Gravity causes downward pressure from prolonged sitting.
|
|
The patient moves/slides in the chair, causing friction.
|
|
|
The skin/tissue at the seat surface DOES NOT move while the underlying bone structure DOES.
|
|
|
The skin/tissue is strained by the combined pressure and friction.
|
|
 |
Permanent cell deformation and distortion occurs at the deeper layers of tissue.
|
|
Blood vessel damage decreases oxygen delivery.
|
|
|
Ischemia.
|
|
| Result is tissue death. |
Microclimate
Microclimate is the climate of a very small or restricted area that differs from the climate of the surrounding area. It usually occurs under the bony prominence where pressure is at its peak, creating excessive heat and/or moisture build-up at the seat and/or back support surface.
How is microclimate created?
Increased body temperature at the skin surface, increased tissue temperature, and/or increased moisture at the skin surface due to:
○ sweat
○ urinary or fecal incontinence
○ drainage from wounds
○ sitting on a non-breathable seat surface preventing ventilation
What skin changes make a patient more susceptible to microclimate?
A decreased number of sweat glands.
Fewer sweat glands:
○ prevent perspiration with the exposure to excessive heat
○ prevent the evaporation of sweat and the ability to cool the skin's temperature at the skin-seat interface
A decreased number sebaceous glands.
Less sebum (oil) production removes the oily coating from the superficial layer of skin:
○ breaking down the waterproof barrier that prevents excess moisture from entering the skin
○ reducing the natural lubrication that coats and protects the skin from drying out and becoming brittle, making it easier to break the skin open with pressure, trauma, and shear forces
○ allowing excess moisture to macerate the skin, increasing accessibility of the deeper layer to pressure and shear forces
How does microclimate increase the effects of pressure and shear?
Raised skin temperature and excessive moisture weaken the outermost layer of skin, making the deeper layers, tissue, muscle, and bone more susceptible to pressure and shear forces.
Elevated body temperature:
○ increases metabolic rate, in turn increasing the demand of O2 to be delivered to the tissues
○ however, pressure and shear cut off O2 supply
○ so, as demand increases but supply decreases, ischemia occurs more quickly than when the body temperature is normal
Elevated moisture:
○ increases the skin's coefficient of friction, making the skin and deeper tissues "stick" more easily to the seat surface when shear forces are applied
○ weakens the collagen fiber connections between the dermis and the epidermis and increases the risk of maceration
○ increases risk of maceration of the superficial layers of skin, which exposes the blood vessels in the deeper layers. This makes the blood vessels more susceptible to tearing and damage from shear and pressure
Meet the Author
Ana Endsjo, MOTR/L, CLT
About Ana
Ana Endsjo has worked as an occupational therapist since 2001 in a variety of treatment settings. She has mainly worked with the geriatric population, dedicated to the betterment of the treatment of the elderly in LTC centers. Her focus has been on seating and positioning and contracture management of the nursing home resident. With this experience, her hope is to guide other therapists, rehab directors, nurses, and administrators through educational guides, blogs, webinars, and live courses in her role as Permobil's Clinical Education Manager of the Long Term Care Division.
