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Sensitivity to

–Foods

–Drugs: neomycin, quinolones, acetaminophen, and oral contraceptives

–Contact and dietary: nickel (more common in young women), chromate (more common in men), and cobalt (1)

–Smoking

GENERALPREVENTION

Control emotional stress.

Avoid excessive sweating.

Avoid exposure to irritants.

Avoid diet high in metal salts (chromium, cobalt, nickel).

Avoid smoking.

COMMONLYASSOCIATED CONDITIONS

Atopic dermatitis

Allergic contact dermatitis

Parkinson disease HIV (2)

DIAGNOSIS

HISTORY

Episodes of pruritic rash

Recent emotional stress

Familial or personal history of atopy

Exposure to allergens or irritants (3)

–Occupational, dietary, or household

–Cosmetic and personal hygiene products

–Vesicular eruption typically occurs 24 hours after allergen challenge (1).

Costume jewelry use

IV immunoglobulin therapy

HIV

Smoking

PHYSICALEXAM

Transient, often recurrent, symmetrical vesicular eruptions located on volar

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and plantar surfaces and lateral fingers. Lesions may not heal completely between flares (1).

Prodrome: Intense pruritus may occur prior to vesicular eruption. Early findings

–1 to 2 mm, clear, nonerythematous, deep-seated vesicles (lasting 2 to 3 weeks)

–Has a “tapioca” appearance

Late findings

–Unroofed vesicles with inflamed bases

–Desquamation (terminal phase)

–Peeling, rings of scale, or lichenification common

DIFFERENTIALDIAGNOSIS

Vesicular tinea pedis/manuum

Vesicular id reaction

Contact dermatitis (allergic or irritant)

Scabies

Chronic vesicular hand dermatitis

Drug reaction

Dermatophytid

Bullous disorders: dyshidrosiform bullous pemphigoid, pemphigus, bullous impetigo, epidermolysis bullosa

Pustular psoriasis

Acrodermatitis continua

Erythema multiforme

Herpes simplex infection

Pityriasis rubra pilaris

Vesicular mycosis fungoides

DIAGNOSTIC TESTS & INTERPRETATION

Follow-Up Tests & Special Considerations

Skin culture in suspected secondary infection (most commonly,

Staphylococcus aureus) (4)

Consider antibiotics based on culture results and severity of symptoms.

Diagnostic Procedures/Other

Diagnosis is based on clinical exam.

Potassium hydroxide (KOH) wet mount (if concerned about dermatophyte

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infection)

Patch test (if suspecting allergic cause) (4)

Test Interpretation

Fine, 1- to 2-mm spongiotic, intraepidermal vesicles with little to no inflammatory change

No eccrine glandular involvement Thickened stratum corneum

TREATMENT

GENERALMEASURES

Avoid possible causative factors: stress, direct skin contact with irritants, nickel, occlusive gloves, household cleaning products, smoking, sweating.

Use moisturizers/emollients for symptomatic relief and to maintain effective skin barrier (4).

Skin care

–Wear shoes with leather rather than rubber soles (e.g., sneakers).

–Wear socks and gloves made of cotton and change frequently.

–Wash infrequently, carefully dry, and then apply emollient.

–Avoid direct contact with fresh fruit (5)[C].

MEDICATION

First line

Mild cases: topical steroids (high potency) (2)[B]

–Considered cornerstone of therapy but limited published evidence

–Limited use for 2 weeks due to risk of infection (4)[B]

Moderate to severe cases

–Ultrahigh-potency topical steroids with occlusion over treated area (4)[B]

–Prednisone 40 to 100 mg/day tapered after blister formation ceases (2)[B] Limited use due to significant side effects (4)[B]

–Psoralens plus ultraviolet (UV)-A(PUVA) therapy, either systemic/topical

or immersion in psoralens (2)[B] Recurrent cases (4)[B]

–Systemic steroids at onset of itching prodrome

–Prednisone 60 mg PO for 3 to 4 days

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Second Line

Topical calcineurin inhibitors (mitigate the long-term risks of topical steroid use)

–Topical tacrolimus (6)[B]

–Topical pimecrolimus (6)[B]

–May not be as effective on plantar surface

Other therapies (typically with dermatology consultation)

–Oral cyclosporine (4)[B]; monitor for hypertension and renal injury.

–Injections of botulinum toxin type A(BTXA) (6)[B]

Newer topical forms of BTXAcurrently being developed show promise.

Painful, requires nerve block

–Systemic alitretinoin (teratogenic) (5)[B]

–Topical bexarotene (a teratogenic retinoid X receptor agonist approved for use in cutaneous T-cell lymphoma) (6)[B]

–Methotrexate (6)[C] (significant side effects including GI intolerance and hepatotoxicity) (4)[B]

–Azathioprine (1)[C] (6 to 8 week onset of action; must monitor for GI side effects, liver toxicity, blood dyscrasia)

–Disulfiram or sodium cromoglycate in nickel-allergic patients (1)[C]

–Mycophenolate mofetil (2)[C] (GI side effects; benefit: no hepatotoxicity with long-term use) (4)[B]

–Tap water iontophoresis (2)[C]

ISSUES FOR REFERRAL

Allergist (if allergen testing required)

Psychologist (if stress modification needed)

ADDITIONALTHERAPIES

Other oral agents:

–Thalidomide (do not use in pregnancy/no available studies on efficacy)

–Dapsone 100 to 150 mg daily (also limited literature on efficacy; may be used in combination with steroids) both significant side effects; very

limited use (4)[B]

Radiation therapy (1)[C]

UV-free phototherapy (5)[C]

Treat underlying dermatophytosis (1).

BTXAin those in which excessive sweating is an exacerbating factor (4)[B]

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COMPLEMENTARY& ALTERNATIVE

MEDICINE

Conservative management:

–Antihistamines: hydroxyzine, cetirizine, loratadine

–Soaks/cold compresses of weak solutions of potassium permanganate,

Burow solution (aluminum acetate), or vinegar 15 minutes, 4 times daily (4)[C]

Exposure to sunlight as maintenance therapy, 12 minutes every other day, 10 to 15 exposures (5)[C]

Dandelion juice (avoid in atopic patients) (6)[C] Cognitive relaxation techniques (4)[B]

ONGOING CARE

FOLLOW-UPRECOMMENDATIONS

Patient Monitoring

Dyshidrotic Eczema Area and Severity Index (DASI) (1)

Parameters used in the DASI score

–Number of vesicles per square centimeter

–Erythema

–Desquamation

–Severity of itching

–Surface area affected

Grading: mild (0 to 15), moderate (16 to 30), severe (31 to 60)

Monitor BPand glucose in patients receiving systemic corticosteroids.

Monitor for adverse effects of medications.

DIET

Consider diet low in metal salts if there is history of nickel sensitivity (4)[B].

Updated recommendations for low-cobalt diet are available (1).

PATIENT EDUCATION

Instructions on self-care, complications, and avoidance of triggers/aggravating factors

PubMed Health: Dyshidrotic Eczema at: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001835/

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PROGNOSIS

Condition is benign.

Usually heals without scarring

Lesions may spontaneously resolve.

Recurrence is common.

COMPLICATIONS

Quality of life impact: skin tightening, pain, and decreased dexterity

Secondary bacterial infections (S. aureus most common)

Dystrophic nail changes

Fissures and ulcerations

Psychological distress

Lymphedema

REFERENCES

1.Veien NK. Acute and recurrent vesicular hand dermatitis. Dermatol Clin. 2009;27(3):337–353.

2.Wollina U. Pompholyx: a review of clinical features, differential diagnosis, and management. Am J Clin Dermatol. 2010;11(5):305–314.

3.Guillet MH, Wierzbicka E, Guillet S, et al. A3-year causative study of pompholyx in 120 patients. Arch Dermatol. 2007;143(12):1504–1508.

4.Lofgren SM, Warshaw EM. Dyshidrosis: epidemiology, clinical characteristics, and therapy. Dermatitis. 2006;17(4):165–181.

5.Letić M. Use of sunlight to treat dyshidrotic eczema. JAMA Dermatol. 2013;149(5):634–635.

6.Wollina U. Pompholyx: what’s new? Expert Opin Investig Drugs. 2008;17(6):897–904.

ADDITIONALREADING

Agner T, Aalto-Korte K, Andersen KE, et al; and European Environmental and Contact Dermatitis Research Group. Classification of hand eczema. J Eur Acad Dermatol Venereol. 2015;29(12):2417–2222.

Chen JJ, Liang YH, Zhou FS, et al. The gene for a rare autosomal dominant form of pompholyx maps to chromosome 18q22.1–18q22.3. J Invest Dermatol. 2006;126(2):300–304.

Gerstenblith MR, Antony AK, Junkins-Hopkins JM, et al. Pompholyx and

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eczematous reactions associated with intravenous immunoglobulin therapy. J

Am Acad Dermatol. 2012;66(2):312–316.

Molin S, Diepgen TL, Ruzicka T, et al. Diagnosing chronic hand eczema by an algorithm: a tool for classification in clinical practice. Clin Exp Dermatol. 2011;36(6):595–601.

Schuttelaar ML, Coenraads PJ, Huizinga J, et al. Increase in vesicular hand eczema after house dust mite inhalation provocation: a double-blind, placebocontrolled, cross-over study. Contact Dermatitis. 2013;68(2):76–85.

Soler DC, Bai X, Ortega L, et al. The key role of aquaporin 3 and aquaporin 10 in the pathogenesis of pompholyx. Med Hypotheses. 2015;84(5):498–503.

Stuckert J, Nedorost S. Low-cobalt diet for dyshidrotic eczema patients. Contact Dermatitis. 2008;59(6):361–365.

Sumila M, Notter M, Itin P, et al. Long-term results of radiotherapy in patients with chronic palmo-plantar eczema or psoriasis. Strahlenther Onkol. 2008;184(4):218–223.

Tzaneva S, Kittler H, Thallinger C, et al. Oral vs. bath PUVAusing 8- methoxypsoralen for chronic palmoplantar eczema. Photodermatol Photoimmunol Photomed. 2009;25(2):101–105.

SEE ALSO

Algorithm: Rash

CODES

ICD10

L30.1 Dyshidrosis [pompholyx]

CLINICALPEARLS

Dyshidrosis is a transient, recurrent, vesicular eruption, most commonly of the palms, soles, and interdigital areas.

Etiology and pathophysiology are unknown but are most likely related to a combination of genetic and environmental factors.

Best prevention is effective skin care and limiting exposure to irritating agents.

Treatments are based on disease severity; preferred treatments include topical

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steroids, oral steroids, and calcineurin inhibitors.

Condition, although benign and self-healing, can be chronic and debilitating with major concern for superimposed bacterial infection that may be avoided by preventative measures, early treatment, and recognition.

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DYSMENORRHEA

Taiwona Elliott, DO

BASICS

DESCRIPTION

Pelvic pain occurring at/around time of menses; a leading cause of absenteeism for women <30 years old

Primary dysmenorrhea: pelvic pain without pathologic physical findings Secondary dysmenorrhea: often more severe, results from specific pelvic pathology; severity based on activity impairment

–Mild: painful, rarely limits daily function, or requires analgesics

–Moderate: daily activity affected, rare absenteeism, requires analgesics

–Severe: daily activity affected, likelihood absenteeism, limited benefit from

analgesics

System affected: reproductive

Synonym(s): menstrual cramps

EPIDEMIOLOGY

Predominant age

–Primary: onset 6 to 12 months after the start of menarche, teens to early 20s

–Secondary: 20s to 30s

Predominant sex: women only

Prevalence

Up to 90% of menstruating females have experienced primary dysmenorrhea.

Up to 42% lose days of school/work monthly due to dysmenorrhea.

Up to 20% reported impairment in daily activities.

ETIOLOGYAND PATHOPHYSIOLOGY

Primary: Elevated prostaglandin (PGF2α) production through indirect hormonal control (stimulation of production by estrogen) causes nonrhythmic hypercontractility and increased uterine muscle tone with vasoconstriction and resultant uterine ischemia. Ischemia results in hypersensitization of type C pain nerve fibers; intensity of cramps directly proportional to amount of PGF2α released

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Secondary

–Endometriosis (most common cause)

–Congenital abnormalities of uterine/vaginal anatomy

–Cervical stenosis

–Pelvic inflammatory disease

–Adenomyosis

–Ovarian cysts

–Pelvic tumors, especially leiomyomata (fibroids) and uterine polyps

Genetics

Not well studied

RISK FACTORS

Primary (1)

–Cigarette smoking

–Alcohol use

–Early menarche (age <12 years)

–Age <30 years

–Irregular/heavy menstrual flow

–Nonuse of oral contraceptives

–Sexual abuse

–Psychological symptoms (depression, anxiety, increased stress, etc.)

–Nulliparity

Secondary

–Pelvic infection

–Use of intrauterine device (IUD)

–Structural pelvic malformations

–Family history of endometriosis in first-degree relative

GENERALPREVENTION

Primary: Choose a diet low in animal fats.

Secondary: Reduce risk of sexually transmitted infections (STIs).

Pediatric Considerations

Onset with first menses raises probability of genital tract anatomic abnormality (i.e., transverse vaginal septum, imperforate or minimally perforated hymen, uterine anomalies).

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