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THE
IMPORTANCE OF THE MICRO-ENVIRONMENT OF SUPPORT SURFACES IN THE MANAGEMENT
OF PRESSURE ULCERS
Dr
Steven I. Reger
with Vinoth K. Ranganathan and Vinod Sahgal
Introduction
Soft tissue breakdown is a major cause of disablement in the United States
affecting an estimated 1.3 to 3 million patients1,2 and the total cost
of associated health care is $8 billion/yr.3 There are more than one hundred
biome-chanical and pathophysiological factors identified as contributing
to the formation of ischaemic necrosis of the skin and soft tissues.1
External pressure has been the most frequently discussed stress factor
in the formation of ulcers. Other primary stress factors associated with
ulcer formation are shear,4 friction and the resulting deformation of
the soft tissues. The secondary or environmental factors important in
bed immobility are temperature, moisture, duration of the applied load,
atrophy, and posture. These factors influence tissue quality by reducing
the strength and the stiffness of soft tissues and increasing the coefficient
of friction of the skin.

Table 1: Pressure-Induced
Tissue Injury accelerates with increasing body temperature
At
different anatomical regions the prevalence of the ulcers and the corresponding
body- interface pressures are highly variable, depending on the tissue
health, thickness, support characteristics, and the method of measurement.
A recently completed survey of publications on the prevalence of pressure
ulcers and interface pressures at anatomical sites5 indicated a non-linear
(inverse) relation between prevalence and interface pressure for the general
and the spinal cord injured populations. The prevalence6,7,8 of pressure
ulcers is plotted in Figures 1 and 2 as a function of the peak interface
pressure measured at the indicated anatomic sites normalized to the number
of subjects reported by various authors.9–15 Figure 1 shows a low
non-linear correlation for the general population while a definitely negative
correlation is shown in Figure 2 for the spinal cord injured population.
(Note: If peak pressure and pressure ulcer prevalence information for
the same anatomical sites were unavailable for both the general and spinal
cord injured population, the values may not be shown in both figures).
The dotted lines in both figures indicate the hypothetical trend of direct
association between the prevalence of ulcers and the reported interface
pressures. This lack of direct relation of pressure to the frequency of
ulcers at anatomical sites suggests the major influence of secondary factors
on ulcer formation and mandates the control of these factors at the microenvironment
of the support surface. This environment at the contact of the body and
the support is characterized by the interface pressure, shear, temperature,
moisture and friction. These factors will be discussed here to aid in
the selection of support surfaces for the effective management of pressure
ulcers.

Figure 1: The
graph shows a low non-linear correlation between
pressure ulcer prevalence and peak pressure for the general population.

Figure 2: The graph shows a negative correlation between
pressure ulcer prevalence
and peak pressure for the spinal-cord injured population.
Effect
of Shear Stress
Shear stress is generated in the soft tissues by the tangential force
component of the body weight on the contact area externally and by the
parallel and opposite tangential force on the bony prominence internally.
Tangential forces acting on the skin develop shear stress in the tissues
through friction and cause the tissue layers to slide with respect to
each other. A simple algebraic equation describes this relationship as:
Tangential component of gravity force
Shear = ––––––––––––––––––––––––––––––––––
Contact Area
The
amount of sliding depends on the looseness of the connective fibres between
the tissue layers. If the fibres are tight, the skin and subcutaneous
tissue will be subjected to higher shear stress; if the fibres are loose,
there will be more sliding and lower shear stress. Shear stress is reduced
by a decrease in the tangential force and an increase in the contact area.
Loose covers and increased immersion in the support medium also increase
contact area and further reduce shear stresses. When shear-induced tissue
sliding is present, vessels approaching the skin surface perpendicularly
will bend and occlude at the connective layers between the tissue planes.
Thus, shear will increase the effect of pressure in reducing flow through
the blood vessels.16 Conversely, if shear stress is reduced, tissues can
tolerate higher pressures without blood flow occlusion.

Figure
3: The illustration shows the lack of skin stretch in the case
of
low coefficient of friction between the cover and the bed.
Figure
4: The illustration shows the skin stretch on one side and folding of
tissues on the side opposite
to the direction of movement (see inset) in the case of high coefficient
of friction between the cover and the bed.
Effect
of Friction
Friction is a phenomenon that describes the surface’s ability to
prevent motion due to forces tangential to the contact area. The tangential
or friction force depends on the perpendicular force and the coefficient
of friction and it is independent of the contact area. When the cover
of the support surface is designed to allow movement over its foundation,
due to lower coefficient of friction, the slippage occurs between the
cover and the bed and not within the tissue layers and the tension in
the skin is decreased without stretch and occlusion of blood vessels (Figure
3). The tangential force is reduced most effectively by decreasing the
coefficient of friction on the support surface. The effect of a high coefficient
of friction is shown in Figure 4. The effectiveness of properly inflated
air, water, and viscous fluid or gel supports rests on these principles.
Combinations of these biomechanical principles are commonly used in modern
support surfaces to create a better physical environment for tissue survival.
Effect
of Temperature
Elevating body temperature increases the metabolic activity of the tissues
by 10% per degree Celsius of temperature rise, thus increasing the need
for oxygen and energy source at the cellular level. If the patient has
impaired circulation from local pressure and shear then the tissues will
starve and release contents of lysozymes inducing autodigestion of cytoplasm.
The metabolic activity may also cease from lack of energy and the accumulation
of waste products. It has been shown17 that pressure induced tissue injury
accelerates with increasing body temperature (see Table 1). An equally
significant effect of increases in skin temperature is the induction of
the sweat response and the potential accumulation of moisture in the skin
at the skin-support interface.
Effect
of Moisture
Hydration of the weight-bearing skin opens a new set of destructive influences
on skin integrity. Moisture from sweating or from incontinence will hydrate
the skin, dissolve the molecular collagen cross links of the dermis and
soften the stratum corneum (maceration). Skin maceration results in the
reduction of stiffness, nearly complete loss of connective tissue strength
and in erosion of the dermis under the action of shear forces. Another
result of skin hydration is the rapid increase of the coefficient of friction
of the epidermis, which promotes adhesion of the skin to the support surface
and produces elevated shear, easy sloughing and ulceration. Compounding
the destructive effect of stress is hydration diluting the natural skin
acidity, reducing antibacterial properties of the epidermis leading to
easier sepsis.
The clinician has two excellent technologies for controlling the microclimate
at the skin-support surface interface. The low? and high?air?loss18 and
the air-fluidized support systems are designed to reduce stress and temperature,
evaporate moisture and prevent heat accumulation at the interface with
the support surface. The evaporation of one kilogram of water from the
skin at the support surface will remove 580 Kcal of heat from the body
through the ‘latent heat of vaporization’.19 Thus the cooling
power at the rate of the total water loss through the skin for an average
person with 1.8m2 skin surface and 26.7g/m2hr water loss is 27.9Kcal/hr.
With proper design and nursing care aimed to maintain physiologic water
balance, dynamic air loss supports are able to control interface pressure,
shear, and the temperature and moisture of the support environment.
Effect
of Pressure
The pressure stress in the soft tissues arises from the force component
perpendicular to the external contact area and from the body weight acting
through the nearest bony prominence. Algebraically, this relationship
can be stated as:
Perpendicular component of gravity force
Pressure = –––––––––––––––––––––––––––––––––––––
Contact Area
In
the design of support surfaces the objective is to increase contact area
by greater ‘immersion’ allowing the body to sink more deeply
into the support, distributing the force and reducing the pressure. The
cyclic transfer of weight from high-pressure areas is the main principle
underlying alternating pressure support systems. The alternating pressure
creates pressure gradients, which are related to shear stress and may
damage adipose tissues and capillaries that are lacking tensile strength.4,16
The effects of pressure and shear stress on the blood flow to the tissues
are similar. Both stresses reduce blood flow and hence, tissue perfusion.20
Pressure is nearly two times as potent as shear in occluding the arteriolar
blood flow to the cutaneous skin.16 Thus, a simple reduction of tissue
stretching can nearly double the tissues’ ability to withstand pressure.
Many support surfaces take advantage of this fact to reduce shear, improving
the weight?bearing tolerances of the soft tissues.21
Summary
A variety of support surfaces are available for treating patients with
pressure ulcers. The available support surfaces tend to focus mainly on
pressure relief and fail to address all the other factors contributing
to the formation of ischemic necrosis. The challenge for the clinician
is to choose from the spectrum of available products, the one that best
meets most of the patient’s needs. Here, we have reviewed the effects
of microenvironment and the related principles of support surface function
to aid the clinician in choosing the most appropriate support for each
patient.
References:
1. Lyder CH. Pressure ulcer prevention and management. JAMA 2003; 289(2):
223–26.
2. Allman RM. Pressure sores among the elderly. N Engl J Med. 1989; 320(13):
850–53.
3. Kuhn BA and Coulter SJ. Balancing the pressure ulcer cost and quality
equation. Nurs Econ. 1992; 10(5): 353–9.
4. Reichel SM. Shear force as a factor in decubitus ulcers in paraplegics.
J Am Med Assoc. 1958; 166(7): 762–3.
5. Reger SI, Sahgal V. Tissue stress and the management of skin microclimate.
In: Proceedings of The Ad-visory Panel on TheraKair; International Wound
Healing Foundation, Positif Press, Oxford, 2004; 38–42.
6. Noble PC. The Prevention of Pressure Sores in Persons with Spinal Cord
Injuries. Monograph No. 11. World Rehabilitation Fund Inc. New York, N.Y.
1981; 2.
7. Yarkony GM, Heinemann AW. ‘Pressure Ulcers’. In: Stover
SL. et al (eds) Spinal Cord Injury: Clinical Outcomes from the Model Systems.
Gaithersburg, MD. 1995; 100–119.
8. Pressure Ulcers in America: Prevalence, Incidence and Implications
for the Future. In: Cuddigan J, Ayello EA, Sussman C, Baranoski S (eds):
National Pressure Ulcer Advisory Panel. Reston, VA. 2001; 52.
9. Berijan RA, Douglas HO, Holyoke ED et al. Skin pressure measurements
on various mattress surfaces in cancer patients. Am J Phys Med. 1983;
62(5): 217–26.
10. Allen V, Ryan DW and Murray A. Repeatability of subject/bed interface
pressure measurements. J Biomed Eng. 1993; 15(4): 329–32.
11. Bar CA. Evaluation of cushions using dynamic press measurement. Prosthet
Orthot Int. 1991; 15(3): 232–240.
12. Lilla JA, Friedrichs RR and Vistnes LM. Floatation mattresses for
preventing tissue breakdown. Geriatrics. 1975; 30(9): 71–75.
13. Allen V, Ryan DW and Murray A. Measurements of interface pressure
between body sites and the surfaces of four specialized air mattresses.
British Journal of Clinical Practice 1994; 48(3): 125–129.
14. Collier ME. Pressure-reducing mattresses. Journal of Wound Care 1996;
5(5): 207–211.
15. Sachse RE, Fink SA and Klitzman B. Multimodality evaluation of pressure
relief surfaces. Plastic and Reconstructive Surgery 1998; 102(7): 2381–87.
16. Bennett L, Kavner D, Lee BY, Trainor FS. Shear vs. pressure as causative
factors in skin blood flow occlusion. Arch Phys Med Rehabil. 1979; 60:
309–14.
17. Kokate JY, Leland KJ, Held AM, et al. Temperature-modulated pressure
ulcers: a porcine model. Arch Phys Med Rehabil. 1995; 76(7): 666–73.
18. Reger SI, Adams TC, Maklebust JA, Sahgal V Validation test for climate
control on air-loss supports. Arch Phys Med Rehabil 2001; 82 (5): 597–603.
19. Scott J W. The body temperature. In: Best CH, Taylor B (eds): The
Physiological Basis of Medical Practice. Baltimore: The Williams and Wilkins
Co. 1961: 895.
20. Cherry GW, Ryan TJ. Pathophysiolgy In: Parish L.C., Witkowski J.A,
Crissey J T. (eds). The decubitus ulcer in clinical practice. Berlin:
Springer-Verlag, 1997; 33–43.
21. Jay R. Pressure and Shear: their effects on support surface choice.
Ostomy Wound Manage 1995; 4(8): 36–45.
Experimental pig model:
100mmHg pressure applied for five hours.17
Body Temperature Outcome
25°C no break down
35°C partial thickness injury
45°C full thickness breakdown
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