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Common Skin Disorders in the Elderly
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Xerosis- Dry Skin
What is xerosis?
Xerosis is also known as dry skin.
Characterized by itchy, dry, cracked, and fissured skin with scaling.
Occurs most often on the legs of elderly patients, but may be present on the hands and the body.
Why is it common in the elderly?
Incidence increases with age and is most common in the elderly with more than 50% of older adults
being affected.
Primarily due to the fact that aged individuals have decreased sebaceous (oil secreting glands) and
sweat gland activity which predisposes aged skin to moisture depletion.
Causative factors include cold, dry weather, such as in winter or air conditioning.
o Daily use of cleansers and/or bathing without replacing natural skin emollients.
Palliative factor includes warm, humid weather.
Preexisting disease states, therapies, and medications make the elderly more susceptible to dry
skin and include:
o Radiation
o End-stage kidney disease
o Nutritional deficiency; especially zinc and essential fatty acids
o Hypothyroidism
o Neurologic disorders with decreased sweating
o Antiandrogen medications (ex. Bicalutamide, Flutamide; for prostate cancer)
o Diuretic therapy
o HIV
What are some non-prescription treatment options for dry skin?
Keratolytics, moisturizers, and steroids are the primary components of treatment.
Additional management suggestions include:
o Avoid excessive bathing; take brief (3-5 minute) full body bathes 2-3 times per week,
using bath oil.
o Use lukewarm (not hot) water to bathe because hot water increases dryness.
o If possible, take sponge baths on other nights, using warm water to maintain skin
hydration.
o Drink plenty of water daily (unless patient has a diagnosis of heart failure and is water
restricted).
o Minimize the use of soap, and instead use nonirritating soaps such as Cetaphil, Oil of
Olay, or Dove
o Avoid harsh skin cleansers
o Apply moisturizers directly to skin that is still damp
o Liberal amounts of moisturizer should be applied 3-4 times daily and continued as long as
dry skin persists
{AmLactin, Aveeno, Eucerin, Lubriderm, Aquaphor, Cetaphil}
o Avoid friction from washcloths, rough clothing, and abrasives.
o Avoid caffeine, spices, and alcohol (perfumes) as these can contribute to dehydration.
o Use a humidifier in dry environments to minimize evaporation from the skin.
Add products such as oilated oatmeal or bath oil near the end of your bath to enhance skin
hydration; if used on a regular basis may clog plumbing pipes and can leave the tub VERY slick, so
use caution especially with elderly patients who are prone to falls.
{Aveeno Bath Treatment}
Ointments tend to hydrate the skin better than creams or lotions because they draw moisture to the
skin for a longer period of time. If ointments are not an option because of their “greasy” texture,
creams are still a better option than lotions for hydration.
For more severe cases of dry skin, use a product that contains urea or lactic acid
Apply topical hydrocortisone ointment to reduce inflammation and itching; this medication
should not be used for more than 7 days.
Pressure Ulcers
What are pressure ulcers?
A pressure ulcer is an area of skin that breaks down when you stay in one position for too long
without shifting your weight.
Often happens if you use a wheelchair or you are bedridden, even for a short period of time (for
example, after surgery or an injury). The constant pressure against the skin reduces the blood
supply to that area, and the affected tissue dies.
A pressure ulcer starts as reddened skin but gets progressively worse, forming a blister, then an
open sore, and finally a crater. The most common places for pressure ulcers are over bony
prominences (bones close to the skin) like the elbow, heels, hips, ankles, shoulders, back, and the
back of the head.
Pressure sores are categorized by severity, from Stage I (earliest signs) to Stage IV (worst):
Diabetic Ulcers
What causes diabetic ulcers?
Longstanding high blood sugar can damage blood vessels, decreasing blood flow to the foot. This
poor circulation can weaken the skin, contribute to the formation of ulcers, and impair wound
healing. Some bacteria and fungi thrive on high levels of sugar in the bloodstream, and bacterial
and fungal infections can break down the skin and complicate ulcers.
In addition, high blood sugar can damage the nerves of the foot, decreasing a patient's ability to
notice pain and pressure. Without these sensations, it is easy to develop callused pressure spots
and accidentally injure the skin, soft tissue, bones, and joints.
Why are they such a big deal?
The most important underlying cause leading to foot ulceration is diabetic peripheral neuropathy,
which is present to some degree in more than 50% of diabetic persons older than 60 years old.
The prevalence of diabetic foot ulcers is reported at 2-10%.
Lesions typically first appear on an average of 14 years after initial manifestation of DM.
Although researchers don't understand exactly how damage occurs, a high blood sugar level
seems to impair your nerves' ability to transmit signals to your brain.
The most common cause of ulceration is repetitive mechanical forces of gait, which lead to callus,
the most important pre-ulcerative lesion in the neuropathic foot.
How do you treat Pressure & Diabetic Ulcers?
Wound debridement is an important element of ulcer treatment as necrotic tissue promotes
bacterial growth and impairs wound healing. There are several approaches to debridement
available and they allow for removal of all dead tissue, greater visual assessment of the wound
base, and promote the release of growth factors.
Debridement should remove all necrotic tissue in order to achieve a red, granular, wound bed, and
the gold-standard includes using the sharp technique, which requires using a scalpel blade.
The overall aim is to redistribute pressure evenly to the affected area. The extent of infection in the
soft tissue or bone surrounding the ulcer affects management and may include local debridement
and topical antibiotics or the use of systemic antibiotics.
Actinic Keratoses
What are actinic keratoses?
Actinic keratoses (AKs) are premalignant lesions that develop only on sun-damaged skin, in
contrast to basal cell carcinomas (BCC), which, although most common on sun-exposed areas, can
occur on skin that is not exposed to the sun.
How are they formed?
AKs result from a clone of abnormal squamous cells caused by UV light-induced gene alteration;
invasive squamous cell carcinoma (SCC) then develops after further gene alteration due to
additional UV exposure and damage; although the risk of malignant transformation within one year
is only 1 in 1000.
What do they look like?
AKs appear as patches of hyperkeratosis with some surrounding inflammation
and redness on sun-exposed areas of the head and neck, forearms and hands,
and upper back.
What are the treatment options?
The treatment of AKs begins with prevention. Avoiding sun exposure is one approach and in
addition, sunscreens have been shown to reduce the number of AKs over two years by 51%.
Active treatment of AKs depends upon the size of the lesion and the number of lesions present.
Some clinicians treat all AKs, while others treat only the ones that are enlarging and becoming a
threat for the development of SCC, and some AKs may spontaneously regress.
Liquid nitrogen cryotherapy is a widely utilized and effective treatment for AKs that are small and/or
shallow.
Chemotherapy with topical 5-fluorouracil has been used with good success in patients with multiple
actinic keratoses. It causes inflammation and, after weeks, destruction of the lesions. Four to six
weeks are generally required for the skin to progress through redness, blistering, necrosis with
erosion, and reepithelialization. Topical 5-fluorouracil is effective in more than 90 percent of
patients who can tolerate it.
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