Geriatric Dermatology



Geriatric Dermatology


Gregory L. Wells

Peter C. Schalock



With advances in medicine and nutrition, the aging population continues to grow. Common causes of geriatric dermatologic visits include a multitude of dermatoses that are related to the aging of the skin and human body. Some common causes of geriatric skin problems are benign keratoses such as seborrheic keratoses and cherry angiomas, as well as neoplastic problems such as basal cell/squamous cell carcinomas and melanomas. These are reviewed in their respective chapters. Other conditions that are seen more commonly in the older individual will be reviewed here and include angular cheilitis, generalized pruritus, Grover disease, xerosis, and neoplasm-related dermatoses. Stasis dermatitis and skin ulcerations are also frequently encountered in older individuals. These topics are covered in Chapter 20.


Angular Cheilitis



Background

Angular cheilitis (AC) is a common dermatosis affecting the corners of the lips and adjacent skin. The causes of this condition are multifactorial. AC is most commonly seen in older individuals, though any age may be affected. The risk of developing AC is three times higher for those wearing dentures, and it is estimated that 30% to 50% of those with upper and lower dentures will develop AC. Another group at higher risk for developing AC is acquired immunodeficiency syndrome (AIDS) patients with lower CD4+ counts, thus allowing more frequent candidal infections. Patients with anemia, malignancy, or diabetes mellitus are also at higher risk for developing this condition.



Pathogenesis

Angular cheilitis results from chronic inflammation most often caused by saliva contacting the angles of the mouth (maceration/irritant dermatitis also known as perlèche). In elderly patients, ill-fitting dentures or resorption and atrophy of the alveolar bone may lead to poor occlusion of the lips, allowing chronic saliva leakage. In many, a fine crease at the corners of the mouth allows saliva to move out of the mouth by capillary action, thus creating a moist
environment that is conducive for fungal or bacterial growth. The most commonly encountered organisms in AC are S. aureus and Candida albicans.






Figure 17-1 Angular cheilitis in an older man.

Another consideration is allergic contact dermatitis, often secondary to products being used to treat the primary AC. An example would be the patient who uses a neomycin and bacitracin-containing ointment to treat her AC, and who then develops pruritic dermatitis in addition to the primary AC (Fig. 17-2). Causes of AC are summarized in Table 17-1.






Figure 17-2 Angular cheilitis secondary to allergic contact dermatitis to applied neomycin.


Clinical Presentation

Angular cheilitis initially presents as bilateral fissuring, erythematous plaques, and scaling at the corners of the mouth (Figs. 17-1, 17-2). These changes sometimes extend laterally and inferiorly. In many cases, the cutaneous lip and cheek skin are fissured. Depending on the process causing this condition, there are often other findings. Honeycomb crusting would suggest bacterial impetigo, while satellite pustules and a deep red appearance and fine scale suggest a fungal infection. Symptoms include pain, pruritus, or burning.








Table 17-1 Causes of Angular Cheilitis




Allergic contact dermatitis
Atopic dermatitis
C. albicans infection
Iron deficiency
Irritant contact dermatitis
Mechanical trauma (lip licking/frequent flossing)
Plummer-Vinson syndrome (upper esophageal web, iron deficiency anemia, glossitis, cheilitis)
Poorly fitting dentures
Retinoid therapy (isotretinoin/acitretin, etc.)
S. aureus infection
Vitamin deficiency (folate, B12, riboflavin)



Diagnosis

Angular cheilitis is a clinical diagnosis. To evaluate for fungal infection, one should consider a KOH preparation or send a culture for fungus/yeast. Bacterial infection is appropriately evaluated by taking a swab for culture. In general, a skin biopsy or further invasive testing is not indicated.

In patients in whom an underlying systemic cause is suspected, appropriate further workup is recommended. Consider checking a complete blood count, blood glucose, vitamin levels, and in patients with risk factors, a human immunodeficiency virus (HIV) test. Nutritional status should be evaluated. If allergic contact dermatitis is suspected, simply discontinuing all topical medications other than white petrolatum for at least 3 weeks should show considerable improvement. If definite identification of an allergen is necessary, the patient should be referred to a dermatologist for patch testing.


Therapy

Therapy is based on the underlying cause of AC. In the patient with dentures, refitting problematic/ill-fitting prostheses should be helpful. Treat infections appropriately with agents such as topical antifungals (i.e., ketoconazole, clotrimazole, miconazole); topical antibiotics (i.e., mupirocin); or topical anti-inflammatory agents such as calcineurin inhibitors (i.e., tacrolimus and pimecrolimus). If there is a component of atopic or allergic dermatitis, the mainstay of therapy is low- to mid-potency topical steroids (i.e., desonide or triamcinolone acetonide). In cases of recalcitrant yeast infection, consider oral fluconazole therapy.

Once the acute dermatitis is controlled, one may consider zinc oxide or white petrolatum as a barrier for maintenance. In difficult cases, one may consider treating with injectable intradermal fillers such as hyaluronic acid to reshape the oral commissures.


“At a Glance” Treatment



  • Refit ill-fitting dentures.


  • Treat based on etiology of infection or irritation:



    • Bacterial infection: mupirocin ointment BID × 1 to 2 weeks then PRN


    • Atopic or allergic dermatitis: desonide 0.05% cream BID for up to 3 weeks


    • Fungal: ketoconazole 2% cream BID × 1 to 2 weeks then PRN


    • Recalcitrant yeast: fluconazole PO




Course and Complications

Angular cheilitis generally follows a benign course without significant complication. Identification of the underlying cause of AC is essential to prevent acute cases from becoming chronic and also treating/curing chronic cases of AC.

ICD9 Codes




































































528.5 Diseases of lips
692.0 Contact dermatitis and other eczema due to detergents
692.1 Contact dermatitis and other eczema due to oils and greases
692.2 Contact dermatitis and other eczema due to solvents
692.3 Contact dermatitis and other eczema due to drugs and medicines in contact with skin
692.4 Contact dermatitis and other eczema due to other chemical products
692.5 Contact dermatitis and other eczema due to food in contact with skin
692.6 Contact dermatitis and other eczema due to plants (except food)
692.70 Unspecified dermatitis due to sun
692.71 Sunburn
692.72 Acute dermatitis due to solar radiation
692.73 Actinic reticuloid and actinic granuloma
692.74 Other chronic dermatitis due to solar radiation
692.75 Disseminated superficial actinic porokeratosis (dsap)
692.76 Sunburn of second degree
692.77 Sunburn of third degree
692.79 Other dermatitis due to solar radiation
692.81 Dermatitis due to cosmetics
692.82 Dermatitis due to other radiation
692.83 Dermatitis due to metals
692.84 Contact dermatitis and other eczema due to animal (cat) (dog) dander
692.89 Contact dermatitis and other eczema due to other specified agents



Generalized Pruritus



Background

Pruritus or itch is the most common symptom of the skin. It can be caused by both cutaneous and systemic disorders. Systemic generalized pruritus is defined by the underlying disease that causes the symptom of cutaneous itch. Fifty percent of dialysis patients report cutaneous pruritus, as do 25% of those with jaundice. A thorough workup of primary pruritus patients is essential, considering an underlying systemic illness is found in 10% to 50% of primary pruritus patients. General categories of systemic pruritus include renal pruritus, cholestatic pruritus, hematologic pruritus, endocrine pruritus, pruritus related to malignancy, and idiopathic generalized pruritus.



Pathogenesis

Unmyelinated C and A-delta neurons in the epidermis respond to pruritogenic and thermal stimuli. These neurons synapse with central neurons in the dorsal ganglia and travel through the spinothalamic tracts to the thalamus and cerebral cortex. These signals are processed in various areas of the brain. Multiple mediators of pruritus are responsible for the cutaneous sensation of itch. These mediators include histamine, tryptase, prostaglandin E, substance P, opioid peptides, nerve growth factor, and interleukin-2. The pathogenesis of systemic pruritus is related to the underlying cause (Table 17-2).


Clinical Presentation

Patients with pruritus may have a primary dermatologic disease or a systemic disease leading to itch. In patients with generalized pruritus, or pruritus affecting the entire body, the practitioner must rule out a systemic source
for the sensation. Clinical findings may include skin without a primary lesion, or may demonstrate cutaneous changes due to scratching or rubbing, as shown in Figure 17-3, or prurigo nodularis/lichen simplex chronicus, as shown in Figure 17-4. These skin findings may include multiple crusted papules, plaques, and ulcers with surrounding or overlying erosions and excoriations. Affected areas may include the arms, legs, abdomen, chest, and buttocks with sparing of the back or other unreachable body sites.








Table 17-2 Pathogenesis of Systemic Pruritus























SYSTEM POTENTIAL PATHOGENESIS
Renal Possibly due to increased blood histamine levels, increased levels of calcium/magnesium, increased parathyroid hormone levels
Cholestatic Unknown. Possibly due to elevated systemic levels of bile salts, histamine, and opioid levels
Hematologic Iron deficiency may contribute to pruritus.
Polycythemia vera patients have increased mast cells and basophils. Degranulation causes increased levels of serotonin (an itch mediator in the skin).
Endocrine Hyperthyroid and hypothyroid states both are more susceptible to pruritus due to activated kinins and increased xerosis respectively.
Diabetes mellitus increase pruritus but the mechanism is not known.
Malignancy-related Hodgkin disease: increased leukopeptidase and bradykinin
Carcinoid syndrome: increased serum serotonin levels
Almost any other malignancy can cause generalized pruritus through unclear mechanisms.
Idiopathic generalized Idiopathic


Diagnosis

The differential diagnosis of generalized pruritus is large and covers a wide range of systemic illness (Table 17-3).






Figure 17-3 Excoriations and postinflammatory hyperpigmentation on the upper back of an elderly woman.






Figure 17-4 Prurigo nodularis.









Table 17-3 Differential Diagnosis of Generalized Pruritus











































  • Uremia


  • HIV


  • Cholestasis


  • Brain abscess


  • Primary biliary cirrhosis


  • Multiple sclerosis


  • Viral hepatitis


  • Drug hypersensitivity reactions


  • Hodgkin disease


  • Psychogenic pruritus


  • Non-Hodgkin lymphoma


  • Pregnancy


  • Hyperthyroidism


  • Xerosis


  • Hypothyroidism


  • Carcinoid syndrome


  • Iron deficiency anemia


  • Multiple myeloma


  • Systemic carcinoma


  • Sjögren syndrome


  • Diabetes mellitus


  • Gastrointestinal parasite infection


  • Leukemia
 


  • Polycythemia vera
 

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Jul 21, 2016 | Posted by in Dermatology | Comments Off on Geriatric Dermatology

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