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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
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.

Fig 1: Pressure Ulcer Prevalence vs. Peak Pressure for the general population
Figure 1: The graph shows a low non-linear correlation between
pressure ulcer prevalence and peak pressure for the general population.

Fig 2: Pressure Ulcer Prevalence vs. Peak Pressure for the spinal cord injured 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.

Fig 3: Effect of low coefficient of friction on skin and soft tissues

Figure 3: The illustration shows the lack of skin stretch in the case of
low coefficient of friction between the cover and the bed.



Fig 4: Effect of high coefficient of friction on skin and soft tissues

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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