Skin Matters: Xerosis and Pruritus in Elderly Patients, Part 1

    Dry skin (xerosis) is a common dermatological skin condition characterized by pruritic, dry, cracked, and fissured skin with scaling. Xerosis occurs most often on the legs of elderly patients but also may be present on the hands and trunk. Xerotic skin looks like a pattern of cracked porcelain. These cracks or fissures are caused by epidermal water loss. The skin splits and cracks deeply enough to disrupt dermal capillaries; fissures may bleed. Pruritus, or itching, leads to secondary lesions.

    Scratching and rubbing produce excoriation (an inflammatory response), lichen simplex chronicus (leather-like skin), and edematous patches.¹ Subsequently, environmental allergens and pathogens can easily penetrate the skin, increasing the risk of allergic and irritant contact dermatitis as well as infection. Allergic and irritant contact dermatitis may cause persistent and possibly more extensive dermatitis, despite therapy.¹ Eczematous changes can occur with a delayed hypersensitivity response, even in advanced age.² Secondary infection is an inherent risk with any break in the skin barrier.
A recent study of nursing home patients in the author’s care found that the two most common skin problems are xerosis and pruritus (see Table 1). Given these results, the importance of comprehensive treatment of these problems to prevent stasis dermatitis and ulcer formation cannot be underestimated.

Prevalence and Predisposing Factors

    Xerosis affects the elderly primarily because they have decreased sebaceous and sweat gland activity, which predisposes their skin to moisture depletion. A number of additional factors help deplete the skin’s moisture. Xerosis tends to relapse in the winter when environmental humidity is lower.³ The daily use of cleansers and/or bathing without replacing natural skin emollients affects skin moisture.⁴ Plus, elderly patients are more susceptible to xerosis because of pre-existing disease states, therapies, and medications – these include end-stage renal disease, nutritional deficiency (especially zinc and essential fatty acids), thyroid disease, neurological disorders with decreased sweating, human immunodeficiency virus, malignancy, radiation, anti-androgen medications, and diuretic therapy.^5-7

Pathology

    In healthy skin, skin cells called corneocytes detach from neighboring cells and are replaced by younger cells from deeper skin layers. This orderly process, called desquamation, leads to corneocyte or skin cell loss from the skin surface. Desquamation is controlled primarily by two intercellular components - corneodesmosomes and lipids. The intercellular actions of these components help preserve tissue thickness.

    Corneodesmosomes bind the corneocytes to maintain intercellular cohesion and tissue integrity. Effective desquamation requires that corneodesmosomes eventually be broken down. Although this process, called corneodesmolysis, effectively eliminates the corneodesmosomes in healthy skin,³ this is not the case with xerotic skin. Corneodesmosomes persist and disturb the orderly desquamation process. In chronic and acute dry skin conditions, this disturbed process is manifested by the formation of visible, powdery flakes on the skin surface.⁸

    Another important consideration is that free water is necessary to control the corneodesmolysis process. Adequate lipid content is required to retain the free water. Inadequately hydrated skin cannot provide this free water. Therefore, deficits in both skin hydration and lipid content play a key role in xerosis.³ Consequently, the skin’s inability to retain moisture and provide an effective barrier directly impacts the development of xerosis in aged skin.^9,10

Treatment

    Once the stage is set for xerosis development, flaking, fissuring, inflammation, dermatitis, and infection can develop. The vicious xerotic cycle must be broken to disable the process and prevent complications.^11,12 This is precisely the goal of xerosis treatment – to break the xerotic cycle.

    Keratolytics, moisturizers, and steroids are the primary substances used to achieve this goal. Several studies^13,14 have demonstrated the keratolytic effect of ammonium lactate 12% lotion in reducing the severity of xerosis. However, individuals with sensitive skin may not tolerate some products formulated with alpha-hydroxy acids (AHAs) due to unacceptable levels of stinging and irritation; in such cases, a sensitive skin variant formulation should be substituted.¹⁵ Liberal use of moisturizers reduces scaling and enhances the corneodesmosome degradation process.^16-18 Additional treatment via application of topical steroids (class 3-6) is recommended in moderate to severe cases.⁴ Antipruritics should be added if severe itching is present.¹²

    Additional management suggestions include:
•  Reduce frequency of bathing
•  Bathe with lukewarm (not hot) water
•  Use nonirritant soaps, such as Cetaphil® soap (Galderma Laboratories, Fort Worth, Tex), Oil of Olay® (Procter & Gamble, Cincinnati, Ohio), and Dove® (Lever Fabrege Limited, UK), minimally
•  Avoid harsh skin cleansers
•  Apply a moisturizer, such as Sween 24 (Coloplast Corp., Marietta, Ga), directly to damp skin
•  Avoid friction from washcloths, rough clothing, and abrasives
•  Use air humidification in dry environments.^4,19

Conclusion

    Aged skin is susceptible to the development of xerosis. The pathophysiology of xerosis is related to abnormal keratin production; elderly persons have decreased skin fatty acids, which results in decreased skin barrier and hydration. The vicious cycle of the xerotic process puts elderly patients at risk for xerosis-related complications. The treatment goal focuses on breaking the xerotic cycle to prevent secondary complications.

    This article was adapted from Norman RA. Xerosis and pruritus in elderly patients, part 1. ECPN. March 2005.

1. Anderson CK, Miller F III, Cooper S. Asteatotic eczema. eMedicine Journal. Available at: http://www.emedicine.com/derm/ topic538.htm. Accessed February 23, 2005.

2. Aoyama H, Tanaka M, Hara M, Tabata N, Tagami H. Nummular eczema: an addition of senile xerosis and unique cutaneous reactivities to environmental aeroallergens. Dermatology. 1999;199(2):135–139.

3. Harding R, Mayo C, Rawlings A. Stratum corneum lipids: the effect of ageing and the seasons. Arch Dermatol Res. 1996;288(12):765–770.

4. Huntley AC. Eczematous diseases. Available at: http://matrix.ucdavis.edu/tumors/eczema/eczema.html. Accessed February 14, 2005.

5. Nunley JR. Dermatologic manifestations of renal disease. Available at: http://www.emedicine.com/derm/topic550.htm. Accessed February 14, 2005.

6. Weismann K, Wadskov S, Mikkelsen HI, Knudsen L, Christensen KC, Storgaard L. Acquired zinc deficiency dermatosis in man. Arch Dermatol. 1978;114(10):1509–1511.

7. Rowe A, Mallon E, Rosenberger P, Barrett M, Walsh J, Bunker C. Depletion of cutaneous peptidergic innervation in HIV-associated xerosis. J Invest Dermatol. 1999;112(3):284–289.

8. Simon M, Bernard D, Minondo AM, et al. Persistence of both peripheral and non-peripheral corneodesmosomes in the upper stratum corneum of winter xerosis skin versus only peripheral in normal skin. J Invest Dermatol. 2001;116(1):23–30.

9. Engelke M, Jensen JM, Ekanayake-Mudiyanselage S, Proksch E. Effects of xerosis and ageing on epidermal proliferation and differentiation. Br J Dermatol. 1997;137(2):219–225.

10. De Paepe K, Derde MP, Roseeuw D, Rogiers V. Incorporation of ceramide 3B in dermatocosmetic emulsions: effect on the transepidermal water loss of sodium lauryl sulphate-damaged skin. J Eur Acad Dermatol Venereol. 2000;14(4):272–279.

11. Seidenari S, Giusti G. Objective assessment of the skin of children affected by atopic dermatitis: a study of pH, capacitance and TEWL in eczematous and clinically uninvolved skin. Acta Derm Venereol. 1995;75(6):429–433.

12. Thaipisuttikul Y. Pruritic skin diseases in the elderly. J Dermatol. 1998;25(3):153–157.

13. Jennings MB, Alfieri D, Ward K, Lesczczynski C. Comparison of salicylic acid and urea versus ammonium lactate for the treatment of foot xerosis. A randomized, double-blind, clinical study. J Am Podiatr Med Assoc. 1998;88(7):332–336.

14. Kempers S, Katz HI, Wildnauer R, Green B. An evaluation of the effect of an alpha hydroxy acid-blend skin cream in the cosmetic improvement of symptoms of moderate to severe xerosis, epidermolytic hyperkeratosis, and ichthyosis. Cutis. 1998;61(6):347–350.

15. Wolf BA, Paster A, Levy SB. An alpha hydroxy acid derivative suitable for sensitive skin. Dermatol Surg. 1996;22(5):469–473.

16. El Gammal C, Pagnoni A, Kligman AM, El Gammal S. A model to assess the efficacy of moisturizers—the quantification of soap-induced xerosis by image analysis of adhesive-coated discs (D-Squames). Clin Exp Dermatol. 1996;21(5):338–343.

17. Harding C, Watkinson A, Rawlings A, Scott IR. Dry skin, moisturization and corneodesmolysis. Int J Cosmet Sci. 2000;22(1):21–52.

18. Rawlings A, Harding C, Watkinson A, Banks J, Ackerman C, Sabin R. The effect of glycerol and humidity on desmosome degradation in stratum corneum. Arch Dermatol Res. 1995;287(5):457–464.

19. Lazar AP, Lazar P. Dry skin, water, and lubrication. Dermatol Clin. 1991;9(1):45–51.

Resource
Norman RA. Xerosis and pruritus in the elderly: recognition and management. Dermatol Ther. 2003;16(3):254–259.