Skin undergoes structural and physiological changes resulting from both the natural aging process and being exposed to damaging environmental elements. Over a lifetime, skin is observed to progressively degenerate. Most notable are the changes and deterioration in the structure of the skin which are due to losses and/or a disordering of collagen, the protein primarily responsible for the tensile strength of skin, and elastin fibres (Farage et al. 2009). The elderly therefore, have an increased susceptibility to skin injuries such as pressure ulcers, and a decreased healing response.
Pressure ulcers are common among individuals with SCI, and typically occur over boney prominences, such as the ischial tuberosities and malleoli. Damage to the skin and underlying tissue caused by pressure, shearing, and/or friction due to continuous sitting are the primary causes of pressure ulcers. As collagen metabolism increases as a result of SCI, these individuals may be more susceptible to pressure ulcers than non-SCI individuals (Claus-Walker & Halstead 1982a; Claus-Walker & Halstead 1982b). As a result of the combined effects of pressure, from sitting, and reduced skin integrity, due to collagen degradation, it is estimated that 85% of individuals with SCI will experience a pressure ulcer in their lifetime (Gunnewicht 1995). Given that the mean cost of healing a wound is approximately $50,000, which translates into an annual cost of 3.6 billion dollars in the United States (Beckrich & Aronovitch 1999), there is a strong need to understand age-related changes to the skin following SCI in order to help minimize the occurrence of wounds.
In this section, 2 longitudinal studies and 2 cross-sectional studies (see Table 8) on skin and subcutaneous tissues after SCI are reviewed.
Over a 2 year period, one-quarter of individuals with SCI experienced a pressure ulcer (Rodriguez & Garber 1994). Understanding how skin changes post-SCI is important, not only because of the implication of pressure ulcers, but because of other non-life threatening skin complications that commonly occur after SCI, which include local fungal infection, seborrheic dermatitis, and chronic acne vulgaris (Rubin-Asher et al. 2005; Stover et al. 1994). As well, attenuated immune response following SCI facilitates skin infections and lack of cutaneous sensation increases the incidence of pressure ulcers.
Park and colleagues (2011) found that the biomechanical skin properties were significantly altered following SCI in men, and these changes were directly influenced by regional sympathetic denervation rather than somatic sensory denervation. They found that age significantly correlated with all biomechanical skin parameters in their AB controls. However, in men with motor and sensory complete SCI, YPI rather than age was shown to be the most important factor influencing skin changes. Since the amount of dermal thickening is positively correlated with YPI, Park et al. (2011) hypothesized that the thickening process following SCI may be strong enough to overwhelm the impact of aging on biomechanical skin properties.
There is Level 2 evidence (Vaziri et al. 1994) suggesting that plasma fibronectin, as an indicator of wound healing, may rise in SCI male patients with fast healing ulcers but not in SCI patients with poor healing ulcers.
There is Level 5 evidence that the biomechanical skin properties are significantly influenced by sympathetic paralysis rather than somatic sensory paralysis. Furthermore, in men with complete SCI, YPI may be the influential factor on the biomechanical properties of the skin (Park et al. 2011).
Males with SCI have higher levels of collagen metabolite, glu-gal Hyl, than the able-bodied population, which may be a sign of premature aging of the skin. Further work is needed to conclusively demonstrate this.
Behavioural factors play a stronger role in the development of pressure ulcers in persons with SCI than either age or YPI.
In men with complete SCI, YPI may be the influential factor on biomechanical properties of the skin.