CHAPTER 95
Gopal A. Patel
Skin Disease and Old Age
INTRODUCTION
Aging affects all organ systems, including the integument.
Cell replacement, sensory perception, thermal regula-
tory function, and immune defense systems are among the
many components compromised. The skin appearance
changes, depending on environmental and genetic factors.
The ­psychosocial impact, including cosmetic disfigurement
and social stigma, in addition to vulnerability to skin dis-
ease, must be addressed in elderly patients. The role of the
physician is to diagnose, treat, and guide patients through
this visible component of aging, while preventing avoidable
disease.
EPIDEMIOLOGY
The U.S. population that is older than 65 is greatly expand-
ing. Skin complaints constitute a significant and grow-
ing portion of geriatric ambulatory patient visits. A 2005
study in the United States demonstrated that 21% of all
patients seen by family practitioners had a skin problem.
Seventy two percent of the time it was their primary com-
plaint.1 Also in 2005, the National Ambulatory Medical
Care Survey showed that the number of outpatient visits
was highest in the 45-to-64-year-old age group, a shift up
from the 1995 survey, suggesting increasing medical use by
the baby-boomer population, which is now entering the
65-and-older bracket.2 Among all patient age groups, 1 in
20 visits to an outpatient office are of skin, hair, or nail
concern.2 Diseases such as cutaneous melanoma are on
the rise, with lifetime risks shifting from 1/250 in 1980 to
1/65 in 2002 based on a U.S. population study.3 These data
emphasize the importance of skin disease recognition in
the elderly.4 Skin cancer, for example, is often preventable
and with early diagnosis can be 100% curable. Also, the
role of cosmetic services and the impact on ­psychosocial
well-being that can be traced to skin disease is of added
­concern.
APPROACH TO THE PATIENT
A complete medical history is desirable for the skin dis-
ease patient, regardless of age. One should pay attention to
­medicines or chemicals used, including topical, systemic, cos-
metic, or complementary and alternative ones. The ­duration
of a complaint, previous therapy, close contacts, and patient
opinions on etiology may assist or obfuscate diagnosis and
treatment. Hygiene, including bathing and laundering hab-
its, should be assessed. Geriatric patients should undergo a
thorough skin evaluation under good lighting.
Older patients often have trouble with medication com-
pliance. Dermatologic treatments are further ­challenging
because of their frequent topical nature. Patients may
need to apply creams on difficult-to-reach areas (e.g., feet,
back) or may be immobilized. Shampooing, showering, or
­complicated treatment regimens can confuse and challenge
Gangaram Ragi
W. Clark Lambert
Robert A. Schwartz
geriatric patients. The clinician needs to be aware of all these
barriers and accommodate accordingly.
SELECTED SKIN CONDITIONS
KEY POINTS
Skin Disease and Old Age
• Skin diseases are common in the elderly, and though rarely deadly,
may degrade quality of life.
• Skin cancer is increasing in incidence in light-skinned Americans
and is curable if diagnosed early.
• Xerosis and pruritus are the most common complaints of the
elderly and may be manifestations of many systemic diseases.
• Early treatment, within 3 days of onset, is most effective for
herpes zoster patients.
• Tobacco use and unregulated sun exposure are major preventable
factors in skin cancer predisposition and skin aging.
Eczematous disorders
The geriatric patient population’s chief complaint is often
of a pruritic (itchy) rash or lesion that turns out to be an
eczematous disease. The prevalence of eczema is between
2.4% and 4.1% in the U.S. population.5 In the elderly,
­natural aging of the skin predisposes patients to ­eczematous
diseases. In a Turkish study of more than 4000 patients,
eczematous disorders constituted nearly 22% of diagnoses
in the 65-to-74-year-old age group.6
XEROSIS (ECZEMA CRAQUELÉ, ASTEATOTIC ECZEMA)
Xerosis describes rough or dry skin, which is seen in almost
all elderly persons. Conditions of low humidity, such as
artificially heated rooms, especially forced hot air heating,
exacerbate this condition. Xerosis is actually a misnomer, as
water is not absent throughout the entire thickness of the
skin. There is only diminished hydration in the superficial
corneum.7,8 Xerosis has also been misclassified as a sebaceous
gland disorder. Though sebaceous gland activity decreases
with age and thus depletes the skin’s moisture, it only plays
a partial role in xerosis development.9 Other factors include
an irregular epidermal surface caused by maturation abnor-
malities. Deficits in skin hydration and lipid content impair
normal desquamation, leading to formation of the skin scales
that characterize xerosis. Furthermore, old age results in
altered lipid profiles and in decreased production of filag-
grin, which are filament associated proteins that bind kerati-
nocytes. Both features contribute to xerosis.8
Xerosis may appear scaly with accentuated skin lines,
often occurring on the anterior legs, back, arms, abdomen,
and waist. The scales are a result of epidermal water loss, and
focal dryness may be deep enough to cause bleeding fissures.
801
802 Section II  /  Geriatric Medicine
Superimposed pruritus is possible, leading to secondary
excoriations, inflammation, and lichen simplex chronicus.8
Allergic and irritant contact dermatitis may also complicate
xerosis. Secondary infection may follow a break in the skin
barrier.10 Xerosis is also a secondary feature of many of the
selected conditions in this chapter.
Untreated xerosis progresses to flaking, fissuring, inflam-
mation, dermatitis, and infection. Topical emollients make
dry skin more comfortable and avoid such complications.
Alpha-hydroxy acids (e.g., 12% ammonium lactate) are
helpful because of their keratolytic nature, though some
patients report stinging and irritation.11 Formulations con-
taining ammonium lactate or other alpha-hydroxy acids help
to restore barrier function and improve xerosis.12 Liberal use
of ­moisturizers throughout the day is recommended. Topical
­steroids (classes III and VI) are recommended in moderate to
severe cases, along with antipruritics for symptomatic itch-
ing. Further recommendations include decreasing hot water
baths, reducing use of soap or harsh skin cleansers, avoiding
rough clothes on the skin, utilizing humidifiers in dry envi-
ronments, or adding emollient substances, such as oatmeal,
to bathwater.
Simple xerosis is a common cause of pruritus in the elderly.
Asteatotic eczema is a dermatitis superimposed on xerosis
that often flares in the winter. It is dry, scaly skin, sometimes
resembling, in extreme cases, cracked porcelain with bleed-
ing from damaged dermal capillaries. The cracked porcelain,
or “crazy paving,” pattern is best termed eczema craquelé.13
Asteatotic eczema is a common condition on the shins of
geriatric patients, though it is also seen on other regions of
the body. Several associations of asteatotic eczema exist: one
related to hard soaps, one to corticosteroid therapy, one to
neurologic disorders, and an idiopathic one often located on
the shins of elderly patients. Prevention is the key to con-
trolling this entity. Contributing factors include cleansers
used, frequency of showers, diet, medications, and tempera-
ture exposure. Specifically, patients should reduce hot show-
ers and irritant detergents. Creams, humidifiers, and topical
steroids can improve the effects of asteatotic dermatitis.13
Alcohol-based lotions feel good just after application but
eventually cause increased dryness and should be avoided.
SEBORRHEIC DERMATITIS
Seborrheic dermatitis typically manifests as an erythematous
and greasy-like scaling eruption, usually affecting areas with
abundant sebaceous glands, including the scalp, ears, central
face, central chest, and intertriginous spaces.14 When ­present
in the scalp, it tends to cause flaking known as dandruff. It
may also appear as marked erythema over the nasolabial
fold during times of stress or sleep deprivation. Seborrheic
­dermatitis is found in greater frequency with neurologic con-
ditions such as Parkinson’s disease, a concern in the geriatric
population.15 Facial nerve injury, spinal cord injury, syringo-
myelia, and neuroleptic treatment are also associated with
seborrheic dermatitis.
The pathogenesis of seborrheic dermatitis, though con-
troversial, has been attributed to the yeast Malassezia species
(Malassezia furfur, Malassezia ovalis), formerly known as Pityros-
porum.16 This yeast is a normal inhabitant in more than 90% of
healthy adults, but when overgrown it can be ­proportionally
related to the severity of seborrheic ­dermatitis. Treatment
options against Malassezia species have been effective for
seborrheic dermatitis, supporting a causal relationship.
Antifungals along with topical steroids are utilized, such as
ketoconazole cream or shampoo and hydrocortisone valer-
ate cream.14 Furthermore, topical ketoconazole has inherent
anti-inflammatory properties. One classic study comparing
these two agents determined that 2% ketoconazole cream
was 80.5% effective in resolving seborrheic dermatitis, as
opposed to 94.4% efficacy with 1% hydrocortisone cream.17
Though not as good as hydrocortisone, ketoconazole
serves as an effective steroid sparing agent. The calcineu-
rin ­inhibitors tacrolimus and pimecrolimus are macrolide
immunosuppressants that are alternative agents for use on
the face, to again reduce the use of steroids in this sensi-
tive area. A 2008 randomized prospective controlled study
comparing 1% pimecrolimus cream and 2% ketoconazole
cream showed equal efficacy between the two, but there
were greater side effects with pimecrolimus.18 Side effects
included burning, itching, and redness. Both tacrolimus and
pimecrolimus have a black box label by the U.S. Food and
Drug Administration (FDA) warning of skin cancer or lym-
phoma formation in some patients using this drug, though
an established link remains controversial.19 ­Shampoos with
ketoconazole, selenium sulfide, salicylic acid, zinc pyrithi-
one, or tar are also effective for seborrheic dermatitis in hair-
bearing regions.20
Pruritus
Elderly patients often experience localized or general-
ized pruritus, which can be severe. The cause of itching
in elderly patients is often difficult to determine. Renal,
hematologic, endocrine, cholestatic, allergic, infectious,
and malignant causes all potentially contribute to the
elderly patient’s itch.21,22 Some of these are addressed here
(Table 95-1).
Physiologically, specific C-fiber neurons that terminate
at the dermoepidermal junction transmit the itch sensation
to the brain. These fibers possess receptors sensitive to his-
tamine, neuropeptide substance P, serotonin, bradykinin,
proteases, and endothelin. Rubbing or scratching further
stimulates these receptors.23 As the itch and scratch cycle
progresses; the skin is driven to a point of barrier function
compromise, which is worrisome in elderly patients with
limited means of self-care.
Table 95-1. Systemic Diseases Causing Pruritus
Uremia
Cholestasis
Pregnancy
Cancers (including lymphoma, leukemia, and multiple myeloma)
Polycythemia vera
Thyroid disease
Iron deficiency anemia
Diabetes mellitus
HIV infection
Multiple sclerosis
Drug hypersensitivity
Psychogenic causes
Senile pruritus
Sjögren’s syndrome
Carcinoid syndrome
Dumping syndrome

Pruritus is one of the most distressing concerns of a patient
suffering from cholestasis. The exact cause of pruritus in
this disease is unknown, though an altered role of opioid
­receptor function has been suggested.24 Treatment of the
underlying disease process often resolves itching. However,
some ­diseases, such as primary biliary cirrhosis (PBC), can-
not easily be cured. Ursodeoxycholic acid (UDCA) treat-
ment for PBC often does not resolve the patient’s pruritus.25
Cholestyramine, rifampin, naloxone, and phenobarbital are
other agents utilized for pruritus, all of which have substan-
tial side effects in the elderly.26
Generalized pruritus is recognized as a key marker of
underlying malignancy, particularly lymphomas and leu-
kemias.27 Generalized pruritus is noted in up to 30% of
patients with Hodgkin’s disease and may be the only presen­
ting symptom.28,29 Pruritus is also a noted feature of multiple
myeloma, polycythemia rubra vera, Waldenström’s macro-
globulinemia, and malignant carcinoid.30
Pruritus is best resolved by identifying and treating the
underlying systemic etiology. Unfortunately, nonspecific
therapies must often be employed for elderly patients with
atypical disease presentation. Emollients are valuable inter-
ventions regardless of suspected etiology, as some level
of pruritus exacerbating xerosis is present in most elderly
patients. Topical use of alcohol, hot water, or harsh soaps
and scrubbing must be discouraged. Proper humidity, cool
compresses, nail trimming, and behavior therapy may all
improve the itch and scratch cycle.23 Topical anesthetics
such as benzocaine and dibucaine have been utilized for
relief. A trial of oilated soap and antihistamines may also be
helpful before an invasive workup, including hematologic
studies, imaging for malignancy, skin biopsy, skin scrapings,
skin culture, and HIV tests.30 Antihistamines should be used
with caution as they are not universally effective and may
cause sedation in the vulnerable and often highly medicated
elderly patient.
Vascular-related disease
STASIS DERMATITIS
Stasis dermatitis is a common condition affecting 15 to
20 million patients over age 50 in the United States.31 It
often presents as a circumscribing dermatitis around the calf
and ankle in patients with chronic venous insufficiency and
venous hypertension. However, any body area constantly
under pressure against a hard surface may be impacted. Pit-
ting edema may be present in addition to loss of hair, waxy
appearance and yellow-brown pigmentation.32 If untreated,
stasis dermatitis may progress to a chronic nonhealing
wound with erythema and oozing. Stasis dermatitis results
from poor function of the deep venous system in the legs,
which leads to backflow and hypertension in the superficial
venous system.33 Often both lower legs show stasis dermati-
tis. An associated self-perpetuating cutaneous inflammatory
response follows.33 Workup includes venous Doppler studies
to identify flow in the involved venous plexus.
Several treatment approaches are useful in resolving sta-
sis dermatitis. Compression of the legs to control superficial
venous hypertension is critical. This can be achieved by the
use of Unna boots, compression stockings, or elastic wraps.
In one study of more than 3000 patients, those with stasis
dermatitis had a compliance of 46% for the use of com-
pression stockings.34 Leg elevation 6 inches above the level
Chapter 95  /  Skin Disease and Old Age 803
of the heart during sleep also improves blood flow. Topi-
cal treatments include corticosteroids and the ­calcineurin
inhibitors, pimecrolimus and tacrolimus. Corticosteroids
have an associated risk of tachyphylaxis and must be used
carefully because of the high risk of infection in these
patients.35,36 Topical antibiotics such as bacitracin, neomy-
cin, or ­polymyxin B may be added if there is evidence of skin
barrier compromise and infection.
For more information on stasis ulcers please refer to
Chapter 38.
CHERRY ANGIOMAS (CHERRY HEMANGIOMAS,
CAMPBELL DE MORGAN SPOTS)
Cherry angiomas are the most common vascular prolifera-
tions of the skin and are nearly ubiquitous after age 30. They
appear as firm, smooth, and red colored papules ranging in
size from 0.5 mm to 5 mm. They may also appear as a ­myriad
of tiny spots resembling petechiae. Though patients may
be concerned with a new cherry angioma, the condition is
benign. Cosmetic concern may merit electrocautery or laser
coagulation treatment.37
VENOUS LAKES
Venous lakes are dark blue to violet colored papules that
occur on sun-exposed areas of elderly patients. They are
compressible lesions common on the face, lips, and ears.
The differential diagnosis includes blue nevus and malignant
melanoma. Venous lakes are benign lesions and treatment is
for cosmetic purposes or bleeding. Electrodesiccation, exci-
sion, or lasers may be used to remove venous lakes.38
Infectious diseases
HERPES ZOSTER (SHINGLES)
Herpes zoster (shingles) is a reactivation of the varicella-
zoster virus, the causative agent of varicella. It is a signifi-
cant ailment of the geriatric population, constituting 690
to 1600 cases per 100,000 person-years in the 60-and-older
age group.39–41 The varicella zoster virus remains latent in
the dorsal root ganglia of the nervous system after its initial
infection usually resolves in childhood.42,43 A weakening or
impaired immune system is thought to precede reactivation,
so underlying conditions such as lymphoma, leukemia, and
possible HIV disease should be considered. Local steroid
injection has also been associated with a herpes zoster flare.44
Herpes zoster begins as a prodromal sharp pain localized to
a dermatomal region, followed by a rash and vesicular erup-
tion. Itching, burning, and weakness of muscles associated
with the involved nerve may be noted. More than 20 vesi-
cles outside of the primary dermatome suggest disseminated
zoster, as may be seen in immunocompromised patients45
or patients with granulocytic lesions. The long-lasting pain
of zoster may be mistaken for gallbladder, kidney, or car-
diac pain depending on location. Chronic pain or chronic
pruritus localized to the dermatome may follow. These are
known as postherpetic neuralgia (PHN) or postherpetic
itch, ­respectively.46
Herpes zoster is diagnosed by a Tzanck smear of a sample
scraped from the base of an intact vesicle. Appearance of mul-
tinucleated giant cells may indicate a herpetic infection. Treat-
ment of herpes zoster includes early antiviral therapy, within
72 hours of onset. Acyclovir is a safe but variably efficacious
agent, though famciclovir is also used. In one double-blind,
804 Section II  /  Geriatric Medicine
randomized group study of 55 patients, it was found that fam-
ciclovir was well tolerated and had a more favorable adverse
event profile than acyclovir.47 ­Valacyclovir is an l-valanine
ester form of acyclovir and is converted to acyclovir in vivo.
It provides three to five times the oral bioavailability of acy-
clovir and has been shown in clinical trials to better reduce
pain severity.48 In 2006, the FDA approved the use of zos-
ter vaccine live (Zostavax) for the prevention of shingles in
immunocompetent patients over 60 years of age. ­According
to the multicenter Shingles Prevention Study, vaccine admin-
istration reduces incidence, burden, and PHN complications
in elderly patients.49 Oral antibiotics ­covering staphylococci
and streptococci are used to control ­secondary infection.42
PHN is most evident in the elderly, and 10% to 18%
of zoster patients develop this neuralgia according to a
­community-based study in the United States.50 Treatment is
more challenging for PHN and requires concomitant use of
pain medication, such as topical capsaicin. Prompt prescrip-
tion of analgesia, recommended when zoster is still active,
often reduces long-term negative outcomes for PHN.51
SCABIES
Scabies is among the oldest recognized infections to occur
in humans, with more than 300 million yearly cases detected
worldwide.52,53 A U.K.-based study showed an incidence
of 788 per 100,000 person-years of scabies.54 Risk fac-
tors include nursing home residence, especially older (>30
years) and poorly staffed (>10:1 bed to health care provider)
institutions.
The causative agent for scabies is the mite, Sarcoptes sca-
biei, whose life span is about 1 month. Transmission requires
direct skin contact or indirect contact with bedding or
clothing. Once the pregnant female mite is on a new host,
she digs into the skin to lay eggs. The eggs, saliva, feces,
and the mites themselves lead to a delayed type IV hyper-
sensitivity reaction from 2 to 6 weeks after contact so that,
at onset, multiple lesions are typically seen. These immune
reactions lead to intense pruritus. In previously infected
patients, the immune system response may present in 1 to 4
days after contact.55
Scabies manifests as papules, pustules, burrows, nodules,
and also urticarial plaques. Severe pruritus impacts most
patients unless they are immunocompromised.56 In the lat-
ter case, scabies may resemble psoriasis or a hyperkeratotic
dermatosis. The infection is not life-threatening but is often
debilitating and depressing. Common areas infected include
the finger webs, wrists, waistline, axillary folds, genitalia, but-
tocks, and nipples.57 An area of concern should be scraped
and microscopically examined for mites. Early confirmation
is imperative to avoid secondary infection and rapid spread
in the susceptible nursing home environment.58 Treatment
includes permethrin cream or rinse, which should be applied
to all areas of the body for an 8- to 14-hour period. Mild
burning, stinging, and rash may develop. Lindane cream,
crotamiton, and sulfur have been utilized previously but
with less efficacy. Ivermectin is an alternative agent with the
benefit of oral administration, but the FDA has not officially
approved its use for scabetic infection.56 It is particularly
helpful in cases of scabetic resistance to permethrin, though
cases of ivermectin resistance are also documented.59,60
­Pruritus and inflammation may be handled with steroids and
antihistamines.61
PEDICULOSIS
Parasitic lice are known to infest hair-bearing areas of the
human body. Louse infection, or pediculosis, affects up to
12 million Americans each year. The offending human agents
include Pediculosis humanus humanus, Pediculosis humanus capitis
(larger body louse), and Phthirus pubis (pubic louse).62 Similar
to scabies, transmission may be direct or indirect through
brushes, clothing, or bedding. Higher levels of crowding
increase transmission rates, as seen in some nursing homes.
Pathogenesis involves deposition of eggs (nits) on hair shafts
and subsequent hatching under conditions of 70% humidity
and temperatures of 28°C or higher.61
The main symptom of lice infestation is pruritus.21 Bite
reactions, excoriations, lymphadenopathy, and ­conjunctivitis
are other possible manifestations. Hair combing may be
associated with a “singing” sound because of the interaction
of the tines with the nits. Red bumps on the scalp that pro­
gress to crusting and oozing are noted in Pediculosis humanus
capitis. Pediculosis is further complicated by the potential of
co-transported infections. Diagnosis is established by visu-
alization of the lice or nits. This often requires a good light
source and use of a comb to expose the hair. The difficult-
to-remove nits on the hair shafts appear as white specks on
examination.62 Prevention is the best way to address lice
infestations, such as avoiding continued contact with an
infested individual. Chemical pediculicides—including per-
methrin, malathion, lindane, pyrethrin—are the main treat-
ment modalities. These treatments should be repeated every
7 to 10 days and, because of increasing resistance, must often
be rotated.63 “Bug busting” with a wet comb and conditioner
has limited efficacy. Dimethicone has recently been shown
to treat pediculosis in a randomized controlled study where
69% of patients were cured, and only 2% had irritant reac-
tions.64 More studies are necessary for widespread recom-
mendation of this treatment. All family members and contact
persons should be included in therapy and prevention during
patient treatment.
ONYCHOMYCOSIS
Fungal infections are among the most prevalent integumen-
tary concerns in the elderly, and onychomycosis is a lead-
ing entity. Defined as a fungal infection involving the nail
and nail plate, over 90% of onychomycosis is attributable
to dermatophytes, known as tinea unguium, and 10% to non-
dermatophytic molds or Candida. The prevalence of onycho-
mycosis has been estimated at almost 6.5% in the overall
Canadian population.65 Studies have shown that onychomy-
cosis increases with age, possibly because of poor circula-
tion, diabetes, trauma, weakened immunity, poor hygiene,
and inactivity.66 Some studies have shown the prevalence of
onychomycosis in patients over 60 years of age to be 20%.67
Several classifications of onychomycosis exist, includ-
ing distal-lateral subungual, superficial white, candidal, and
proximal subungual. Distal-lateral subungual onychomy-
cosis is the clinically most common type, often caused by
Trichophyton rubrum invasion of the hyponychium, the white
area at the distal edge of the nail plate. The nails become
yellow and thick with parakeratosis and hyperkeratosis lead-
ing to subungual thickening and onycholysis. Superficial
white onychomycosis is often associated with HIV infec-
tion and appears as a chalklike white plaque on the dorsum
of the nail.68 The proximal subungual type is also relatively

uncommon and may present in either immunocompetent or
­immunocompromised patients. In this case, the infection
penetrates near the cuticle and migrates distally resulting
in hyperkeratosis, leukonychia, and onycholysis. Trichophy-
ton rubrum is again the most causative agent. Candidal ony-
chomycosis is seen in patients with chronic mucocutaneous
candidiasis.66
A patient history, physical examination, microscopy, and
culture are all critical to diagnosis. Onychomycosis is best
diagnosed by clipping the toenail very proximally and scrap-
ing the newly exposed subungual debris for laboratory evalu-
ation. Toenails are 25 times more likely to be infected than
fingernails.66 Typical presentation involves two feet and one
hand (the dominant hand of a patient).
Treatment options include topical and systemic medi-
cations along with surgical approaches. A surgical trim-
ming and debridement may be effective initially. Systemic
therapy includes griseofulvin, fluconazole, itraconazole,
or terbinafine.69 Multiple double-blind controlled ­studies
have shown terbinafine to be more effective than flucon-
azole or itraconazole for dermatophyte infections.70–75
­Systemic antifungals may have significant contraindications
in patients on other medications. Topical treatments have
poorer penetration and thus are less effective. Newer treat-
ments are being investigated, such as AN-2690 by Anacor
Pharmaceuticals, which allows for deeper penetration of
topical therapy.76
Cutaneous cancer
KEY POINTS
Skin Cancer
• Current rates suggest that one in five people in the United States
will develop skin cancer in his or her lifetime.
• Basal cell carcinoma is the most common type of skin cancer and
the one least likely to metastasize.
• Melanoma comprises 4% of skin cancers, and suspicion is guided
by ABCDE criteria (asymmetry, border irregularity, color variega-
tion, depth, and evolution of lesion).
• Actinic keratosis is considered to be a precancerous form of
squamous cell carcinoma, though its classification as malignant
neoplasm is debated.
• All patients would use a dermatologist-­recommended sunscreen
appropriate for their skin type and should avoid sun exposure dur-
ing the peak hours of sunlight.
Skin cancer is an increasingly important public health
issue for the geriatric population. Current rates demonstrate
that one in five people in the United States develop skin can-
cer at some point in their lifetime, with melanoma incidence
increasing faster than any other cancer worldwide.77 The
economic burden of skin cancer is substantial in the United
States.77 The risk of skin cancer has been related to ultravio-
let exposure, which has varying roles in basal cell carcinoma,
squamous cell carcinoma, and melanoma pathogenesis. The
use of sunblock, avoidance of peak hours of sunlight, and
proper clothing are simple preventive measures all patients,
young and old, can follow. Early detection is critical in the
elderly patient, as a 100% cure rate is possible.78
Chapter 95  /  Skin Disease and Old Age 805
ACTINIC KERATOSIS
Actinic keratosis (AK), or solar keratosis, may be defined as
a premalignant precursor of squamous cell carcinoma or an
incipient cutaneous squamous cell carcinoma.79 There are
about 5.2 million physician visits annually for AKs in the
United States, 60% by the Medicare population.80 These
precancers are most common in light-skinned populations
with year-round sun exposure who have not used appropri-
ate sunscreens. Areas most affected include the forehead,
scalp, ears, lower lip, forearms, and dorsal aspect of the
hands.81
AK development is attributable to ultraviolet (UV) radi-
ation-induced DNA mutation in select keratinocyte genes.
With time, AKs may develop into invasive squamous cell
carcinomas. They appear as small, skin-colored to yellowish-
brown macules or papules, often with a dry adherent scale.
They may feel rough to palpation, reminiscent of sandpa-
per, though are asymptomatic in most patients.82 If an AK
becomes painful, indurated, eroded, or greatly erythematous,
squamous cell carcinoma transformation must be highly sus-
pect. AKs may also proliferate and become exophytic so as
to ­constitute a “cutaneous horn.” This is particularly evident
on the ear.83 Treatment for few and discrete AKs is best per-
formed with cryosurgery (liquid nitrogen), which approaches
near 100% effectiveness and is convenient and economical.
Topical treatment includes 5-fluorouracil, imiquimod, diclof-
enac, and photodynamic therapy with a light-sensitizing
compound.81 Sun safety practice is helpful for prevention,
such as proper coverage and limited outdoor activity between
10 am and 4 pm.
SQUAMOUS CELL CARCINOMA
Squamous cell carcinoma (SCC) is a cancer arising from
the epithelium, with an estimated 200,000 cases diagnosed
each year.84 SCC is often separated into two groups based
on malignant potential. The more common type develops
from sun-damaged skin and AKs and is less likely to metas-
tasize. For people in this group, the lifetime risk of hav-
ing SCC after developing a single AK is between 6% and
10%.85 The more aggressive type arises from areas of prior
radiation or thermal exposure, chronic drains, chronic ulcers
(Marjolin’s ulcer), and mucosal surfaces. In general, pro-
longed UV radiation ­exposure induces DNA damage and
subsequent ­carcinogenesis in select keratinocytes leading to
SCC ­formation.81
SCCs arising from AKs often appear with a thick adher-
ent scale. The tumor is soft to hard, locally movable, and
has an erythematous, inflamed base. SCCs are frequently
found on the same areas noted for AKs. If a SCC is diag-
nosed on a mucous membrane or on non-sun-damaged
skin, it may be aggressive and can rapidly metastasize to
regional lymph nodes. An SCC described as firm, movable,
and elevated with minimal scale and a sharp border is usu-
ally derived from actinically damaged skin but not typi-
cally from a precursor AK. The differential diagnosis for
SCC is wide, including seborrheic keratosis, melanocytic
nevus, AK, and chromomycosis. Diagnosis is established
by skin biopsy. When SCC is in situ, it is commonly known
as Bowen’s disease.81 However, what Bowen originally
described is slightly different and includes the presence
of large atypical cells (“Bowen’s cells”) within the lesion.86
Smaller SCCs are treated with electrodesiccation and
806 Section II  /  Geriatric Medicine
curettage, whereas larger tumors in sensitive locations such
as the face are often best handled with Mohs micrographic
surgery. Other treatment options include radiation therapy,
carbon dioxide laser, and oral 5-fluorouracil for refractory
lesions.87
KERATOACANTHOMA
Keratoacanthomas (KAs) are a common and distinct neo-
plasm with a histologic pattern resembling SCC, thus
challenging the diagnosis. They are often found in sun-
exposed areas of light-skinned elderly patients, peaking
at ages 50 to 70 years and increasing in incidence with
advancing age.88,89 The face, forearms, and hands are
­frequently afflicted sites, though any area is possible.
The etiology of KAs is unknown, though they are likely
derived from hair follicles, with UV light, chemical carcin-
ogens, immunocompromised status, and viruses contribu-
tory to incidence and progression. KAs are usually solitary
and appear as firm, round, skin-colored or erythematous
dome-shaped papules. They often have a central umbilica-
tion with a keratin plug. Diagnosis is best ­established by
incorporating affected tissue with normal ­lateral tissue in a
biopsy specimen so as to help distinguish SCC from KA.
KAs grow rapidly in a period of 2 weeks but may slowly
involute over a period as long as 1 year if no intervention
is implemented.90 The primary therapy for KA remains
­surgical excision.
BASAL CELL CARCINOMA
Basal cell carcinomas (BCCs) are the most common type of
cancer in pale-skinned individuals. It is estimated that more
than 1 million new diagnoses are made each year in the
United States, comprising 25% of all cancers diagnosed.91
People who burn easily and severely in the sun without tan-
ning are those at greatest risk for BCC. Fortunately, BCC
only rarely metastasizes and is better described as a local
infiltrator, with the potential of destroying underlying struc-
tures if unattended. However, our group and others have
described a rare variant of facial BCC that is extremely
aggressive and rapidly involves deep tissue, especially bone.
Ultraviolet light exposure is the main etiologic agent, but
x-rays, thermal injury, and scars may all contribute to BCC
formation.92
There are five major subtypes of BCC. Noduloulcerative
BCC is the most common with a pearly dome-shaped nod-
ule, central umbilication, and telangiectatic border. This
type enlarges slowly, with a 4-mm-sized tumor taking years
to develop. Pigmented BCCs may display a uniform dark
pigment and can resemble melanoma. Cystic BCCs are
uncommon and are described as bluish gray cystic nodules.
Superficial BCCs are flat plaques with pearly translucency
and thin borders. This subtype is most common on the
trunk, unlike the high occurrence on the face of other sub-
types. Sclerosing BCCs appear as fibrosing and infiltrating
plaques. When these resemble a scar, it is often an ominous
sign of deep invasiveness.92 Such “morpheiform” BCC must
be excised with wide margins.
After biopsy-proven diagnosis, several treatment options
are available. These include cryotherapy, curettage and
electrodesiccation, radiotherapy, and excisional or Mohs
micrographic surgery. For carefully selected thin and small
BCCs, topical treatment options include imiquimod and
5-­fluorouracil. A 2004 study of 5% imiquimod cream for
superficial BCCs showed clearance rates near 75% based on
clinical and histologic examination.93
MELANOMA
Melanoma, a malignancy of melanocytes, comprises 4% of
all skin cancers but is the leading cause of skin cancer deaths
worldwide.94 According to the American Cancer ­Society,
cutaneous melanoma accounts for 60,000 cases but about
9,000 deaths annually. Melanoma incidence per year peaks
at 30 to 50 years of age. The median age of diagnosis is
59 years, with 19.5% of cases diagnosed between 55 and
64 years of age; 17.8% diagnosed between 65 and 74 years
of age; 16.4% ­diagnosed between 75 and 84 years of age;
and 5.5% diagnosed at older than 85 years of age. The
median age for death is 68 years, with 15% dying between
45 and 54 years of age; 18.8% dying between 55 and
64 years of age; 21.3% dying between 65 and 74 years of
age; 23.6% dying between 75 and 84 years of age; and
11.0% dying when older than 85 years of age. Incidence is
18.5 to 28.5 per 100,000 for white persons and 0.9 to 1.1 per
100,000 for black persons for all types of melanoma.95
Malignant melanoma formation is a multistep process of
mutations with risk factors including blistering tendencies
in the sun, high number of dysplastic moles, actively chang-
ing mole, family history of melanoma, previous history of
melanoma, and older age.96
There are several subtypes of melanoma. Superficial
spreading melanoma is characterized as a flat or slightly
elevated dark brown lesion with variegate colors. ­Nodular
melanoma manifests as a rapidly growing dark brown or
black papule or nodule that is at risk for ulceration and
bleeding. Both are common on the trunk and legs.96 Len-
tigo maligna is a slower-growing subtype on the rise in
the United States, which when invasive is called lentigo
maligna melanoma.97 It is found on chronically sun-­
damaged areas of the head, also on the neck and arms
with a peak incidence at 65 years of age. It is character-
ized as a brown to tan colored macule with possible areas
of hypopigmentation and later raised blue-black nodules
with dermal invasion. The last major subtype, acral mela-
noma, is the least common, comprising 2% to 8% of all
melanomas in lightly pigmented people and 29% to 72%
in darkly pigmented people. Although the proportion is
higher in dark-skinned individuals, the incidence is simi-
lar across all skin types.98 Acral melanomas are noted on
the palms, soles, and subungual areas and thus are more
­difficult to identify with late diagnosis leading to poor
outcome. They most often appear dark brown to black
with irregular ­borders. The subungual type may show
­Hutchinson’s sign, or proximal nail fold dark pigmenta-
tion.99 Two percent to 8% of all melanomas are amela-
notic, showing no ­pigmentation.96
Diagnosis involves a proper history and physical exami-
nation, along with lymph node evaluation. The ABCDE
criteria frequently mentioned is a useful tool during the
initial examination, and all components must be used in
concert to establish a level of suspicion. The mnemonic
stands for asymmetry, border irregularity, color variega-
tion, diameter and evolution or change over time. A biopsy
with pathologic confirmation is essential to rule out mim-
icking lesions such as pyogenic granuloma and pigmented

basal cell carcinoma. After biopsy-confirmed diagnosis and
evaluation for metastasis, the primary mode of treatment is
surgery.96
ANGIOSARCOMA
Angiosarcomas are rare and malignant neoplasms of endo-
thelial origin. The age-adjusted incidence for soft tissue sar-
coma was 3.1 per 100,000 men and women per year in the
2000–2004 period, with angiosarcomas constituting 4.1%
of such sarcomas.100,101 Angiosarcomas have a peak inci-
dence in the seventh decade, though any age group may be
affected. Cutaneous angiosarcoma of the scalp and face is
the most common form and appears as an enlarging bruise,
dark blue to black nodule, or unhealed ulceration. After
biopsy and staging, treatment remains challenging with a
combination of surgery and radiation therapy most success-
ful. Studies have demonstrated beneficial activity of pacli-
taxel and liposomal doxorubicin against angiosarcoma of the
scalp and face.102
KAPOSI’S SARCOMA
Kaposi’s sarcoma (KS) is a tumor of endothelial origin in
which the classic form is usually found in men in their
60s. Human herpesvirus-8 is linked to the pathogenesis of
all types of KS, including the classic form. Classic KS is
found as a rare and indolent lesion in elderly men of Jew-
ish and Mediterranean descent. Specifically, it represents
about 0.2% of cancer in older American men of Mediter-
ranean and Central-Eastern European (Ashkenazi) Jewish
lineage in the United States.103 In Israel, rates of classic KS
of 2.07 in men and 0.75 in women per 100,000 persons were
calculated.104 Clinically, it is often apparent on the distal
extremities as a bluish-red hematoma resembling a macule.
It can develop into plaques and nodules and may become
hyperkeratotic and ulcerate. The disease progresses slowly,
and patients may live for decades with the tumor. There-
fore, death in these patients may well be from other causes
of aging.104 In localized disease, treatment can be handled
with ­radiotherapy and intralesional chemotherapy. System-
wide chemotherapy, including agents such as doxorubi-
cin, vincristine, and etoposide, are helpful in metastasized
or aggressive KS. Immunotherapy including imiquimod,
interferon-α and sirolimus have been utilized, but specific
health concerns of each elderly patient need to be care-
fully addressed.105,106 Other types of KS, including those
in immunocompromised and AIDS patients, do not occur
preferentially in the elderly.
Bullous pemphigoid
Bullous pemphigoid is an autoimmune blistering disease pri-
marily of the elderly. The average age of affected patients is
65 years, and incidence reports vary by region.107,108 Rates
of 0.7 cases per 100,000 have been reported in Germany in
1995 and up to 4.3 cases per 100,000 in the United Kingdom
in 2008.108,109 The disease is characterized by large tense bul-
lae on an erythematous base on flexor areas of the extremi-
ties, axillae, groin, and abdomen. Clear or ­sanguineous
exudates exist in these bullae. The size can range from half
a centimeter to 7 centimeters. Postinflammatory pigmen-
tary changes may follow rupture of these bullae. Mucosal
lesions are rare but heal quickly if present. There have been
­associations of bullous pemphigoid with other autoimmune
Chapter 95  /  Skin Disease and Old Age 807
conditions such as psoriasis, diabetes mellitus, and rheuma-
toid arthritis.110
Consistent with its autoimmune etiology, IgG and C3 have
been demonstrated in the epidermal basement membrane of
bullous pemphigoid. IgG autoantibodies specifically bind to
hemidesmosome adhesion complexes (components BP180
and BP230) of the basement membrane.111 A subepidermal
blister forms with eosinophils, and possible lymphocytes,
histiocytes, and neutrophils. Diagnosis is established with
clinical and histologic contribution. A fresh blister biopsy
shows eosinophils in a subepidermal cleft, whereas direct
immunofluorescence demonstrates IgG or C3 linearly
­depo­sited at the basement membrane zone.110
Topical or systemic corticosteroids are used for treatment,
with systemic therapy most effective for multiple lesion
­disease.112 Before the start of systemic corticosteroids, tet-
racyclines, with possible niacinamide, may be explored for
mild to moderate disease.112
The use of steroids in elderly patients should be cou-
pled with calcium and vitamin D to help prevent osteo-
porosis complications. Supplemental anti-inflammatory
agents such as dapsone are useful for tapering steroid
doses. Dapsone therapy requires close evaluation of liver
and bone marrow function as well as ruling out glucose-
6-phosphate dehydrogenase deficiency, and the adverse
effect profile is severe. Other ancillary treatments include
azathioprine, methotrexate,113 chlorambucil, cyclosporine,
cyclophosphamide, plasmapheresis, and mycophenolate
mofetil.112,114 The effectiveness of plasma exchange or aza-
thioprine as adjuncts has not been concluded.112 Metho-
trexate is an excellent option in patients according to a
2008 Swedish study of 138 patients comparing methotrex-
ate, prednisone, methotrexate plus prednisone, and topical
steroid groups.115
Bullous pemphigoid may be fatal if appropriate treatment
is not administered. The main predictors of poor prognosis
include old age, female gender, associated chronic morbidi-
ties, and poor hygiene.116,117 Mortality rates from 19% to
43% have been reported in some studies, and death may be
related to chronic high-dose steroid use.116,118–120
Systemic concerns of the elderly
with cutaneous complications
DIABETES MELLITUS
Diabetes mellitus (DM) is an endocrine disease of epidemic
proportions in the United States. The Centers for Dis-
ease Control in a 2005 study showed that individuals over
60 years had a diabetes prevalence of 20.9%.121 ­Diabetes
manifests in many organ systems including the nervous,
renal, ocular, integumentary, and cardiovascular. Elderly
patients suffer greatly from complications such as functional
­disability, depression, cognitive impairment, injury, and
­urinary incontinence.
Diabetic dermopathy, also known as shin spots, is found
in 9% to 55% of diabetics.121–125 It appears as round slightly
indented patches of brown to purplish skin. Diabetic der-
mopathy is the most common cutaneous complication of
DM and suggests advanced internal disease of the heart,
liver, or kidney.122
Diabetes mellitus is the cause of the greatest number of
nontraumatic amputations in the United States. This is a
result of nonhealing ulcers in diabetics with long-standing
808 Section II  /  Geriatric Medicine
neuropathy and reduced pain sensation. Up to 25% of dia-
betics suffer from leg ulcers in their lifetime.126 Proper and
frequent examination of the feet and immediate treatment of
ulcers is a critical component of diabetic patient care.
Perforating dermatosis is a condition found in ­diabetics
who suffer from severe renal disease or in patients with
chronic renal failure alone. This condition presents as hyper-
keratotic, pruritic, and umbilicated papules and nodules on
the extensor surfaces of the legs, trunk, and face.127
Acanthosis nigricans is probably the most recognized der-
matologic sign of diabetes. It reflects insulin resistance and is
common among the obese. This is a diffuse, darkened, and
velvet-like thickening seen on the skin of the neck, axilla,
groin, umbilicus, hands, submammary area, and areola. In
exuberant form, this condition can also be a signal of internal
malignancy; thus, thorough examination is critical.27
Necrobiosis lipoidica diabeticorum presents as a red pap-
ule that grows peripherally, becomes atrophic in the ­center,
assuming an “apple-jelly”–like coloration, and eventually
appears telangiectatic and porcelain like. Though rare, a
striking 75% of patients with necrobiosis lipoidica have or
will be diagnosed with diabetes.128 Patients may respond to
topical or intralesional corticosteroids among other medica-
tions, but strict diabetes management does not improve the
papules of necrobiosis lipoidica.
THYROID DISEASE
Thyroid diseases, including hypo- and hyperthyroidism,
impact up to 20% of elderly patients129 Cutaneous mani-
festations of thyroid disease also depend on over- or under-
production of thyroid hormones. There is an increased
incidence of alopecia areata and ­vitiligo associated with
autoimmune thyroid disease.
Characteristic features of hyperthyroidism include ­palmar
erythema, warm and moist skin, and fragile scalp hair or
­alopecia. These signs are often useful for diagnosis. ­Pretibial
myxedema is a specific dermopathy of hyperthyroidism in
Grave's disease (an antibody-mediated autoimmune thy-
roid reaction). Firm, nonpitting, nodules or plaques form on
both legs in an asymmetric pattern. The color may be pink,
purple, or fleshlike.130 An accumulation of mucopolysaccha-
rides in the dermis is suspected to lead to this appearance.
These signature features of hyperthyroidism should trigger
appropriate diagnosis and treatment of the underlying disease
process. Hypothyroidism is a condition occurring in about
10% of females and 2% of males over 60 years of age.131
It manifests with a cutaneous feature of myxedema that is
more prolonged and diffuse. In advanced cases, the overall
appearance of the skin becomes dry, scaly, and yellowish with
sparse hair.131 With progressing myxedema, the face may also
appear flat and expressionless. Palmoplantar keratoderma, or
hyperkeratosis on the palms and soles, is possible in severe
cases. Hair and fingernails are prone to break as well.129 Ony-
cholysis, or separation of the nail plate from the nail bed,
is found in patients with thyrotoxicosis and hypothyroidism
but decreases in incidence in patients over 60 years of age.130
RENAL/ADRENAL DISEASE
Cushing's syndrome and Addison's disease are two condi-
tions of the adrenal gland with cutaneous manifestations. In
Cushing's disease, the main cause of Cushing's syndrome,
there is hypersecretion of adrenocorticotropic hormone
(ACTH).132 ACTH levels may rise from neoplasms of the
pituitary gland or from ectopic neoplasms such as oat cell
lung cancer.133 The primary clinical features include hyper-
tension and weight gain. A “buffalo hump” or redistribution
of fat to the upper back is evident, along with purple striae
on the torso. Hypertrichosis, excessive bruising, poor wound
healing, and hirsutism are additional complications.132 In
Addison’s disease, autoimmune destruction of the adrenals
leads to adrenocortical insufficiency. The main dermatologic
feature is hyperpigmentation of skin creases, new scars, the
vermilion border, nipple, and areas of constant pressure.133
The mechanism is attributable to the stimulation of melano-
cytes by ACTH or the closely related melanocyte-stimulat-
ing hormone (MSH). This darkening of the skin may be the
presenting feature.134
Chronic kidney disease (CKD) is a life-threatening condi-
tion affecting more than a third of patients 70 years of age
and older according to the National Health and Nutrition
Examination Survey.135 Cutaneous examination of patients has
shown that 50% to 100% have at least one dermatologic symp-
tom.136 The list of cutaneous sequelae is extensive, including
pruritus, xerosis, ischemic ulcerations, prurigo nodularis, cal-
cinosis cutis, calciphylaxis, Kyrle disease, ­bullous disease of
dialysis, and nephrogenic fibrosing dermopathy. The majority
of these improve with ­appropriate renal management.
Pruritus and xerosis have been attributed to uremia in CKD
patients.137–139 Pruritus may be local or generalized, mild or
severe, or episodic or constant. Evidently, it is highly patient
specific with no demographic biases.136 Both xerosis and pruri-
tus may improve with kidney disease management, with xerosis
specifically responding to emollients.139 Calcinosis cutis is the
result of insoluble calcium deposition in the skin, appearing as
multiple, firm, whitish papules, plaques, or nodules. They may
ulcerate extruding a chalky white substance.140 Calciphylaxis
refers to vascular calcification with skin necrosis. Patients have
firm painful lesions with central necrosis along a vascular track.
These may begin initially as violaceous mottling.141 Kyrle dis-
ease is the occurrence of widespread papules with central kera-
tin and cellular debris plugs. It usually begins as a silvery scaled
papule.142 Bullous disease of dialysis resembles porphyria cuta-
nea tarda with blistering and mechanical fragility of the skin
in sun-exposed areas. The incidence is 1.2% to 9% in patients
with CKD on hemodialysis.143–146
Nephrogenic fibrosing dermopathy is a condition with
fibrosis of the skin and internal organs that is distinct but
reminiscent of scleroderma. Large areas of indurated skin,
brawny discoloration, and tightening occur. Nephrogenic
fibrosing dermopathy occurs almost exclusively in patients
with end-stage renal disease who have had imaging studies
with gadolinium.147
NUTRITION
Proper nutrition, including daily recommended levels of
essential vitamins and minerals, is critical in the elderly to
prevent diseases with cutaneous manifestations such as
scurvy and pellagra. Please find more information on these
topics in Chapter 74.
MENOPAUSE
Menopause leads to significant changes in skin biology. On
physical examination, the skin is thinner and less lubricated
than premenopausal skin. The risk of infection is higher, and

atrophy, pruritus, stiffness, alopecia, and dryness result.148
­Topical estrogen-based creams have shown some improve-
ment in elasticity and moisturization. Specifically, collagen
content and dermal thickness are improved with estrogen
use after menopause.149,150 The risks and benefits for each
individual patient must be assessed before initiating therapy
for moderate improvement.
TOBACCO USE
Tobacco use is a leading cause of preventable morbidity and
mortality in the United States. In addition to risks of lung
cancer, chronic obstructive pulmonary disease, and cardiac
disease, the skin suffers significant damage from smoking.
Early skin aging, SCC, melanoma, oral cancer, acne, and hair
loss are some problems faced by long-term smokers. One
Chapter 95  /  Skin Disease and Old Age 809
study of 63 volunteers noted that a 35 pack-years smoking
history led to a significantly greater skin furrow depth of the
volar forearm when compared to non-smokers (p < 0.05).151 A
few specific signs of tobacco smoking include harlequin nail,
which is a demarcation between the yellow and pink on the
nail of a recent quitter. Smoker’s face refers to a constellation of
deep lines and furrows at right angles from the lips and corners
of the eye, prominence of bony structures, and general gray-
ing of the skin. In vitro and epidemiologic evidence strongly
support premature aging of skin from tobacco smoke.152
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