Eczema and Dermatitis Study Notes

Eczema and Dermatitis

Overview of Eczema and Dermatitis

• Eczema and dermatitis are a group of diseases categorized as papillosquamous disorders.
• Diagnosing eczema can be challenging due to the similar appearance of itchy rashes.
• Understanding the physical exam findings is crucial for accurate diagnosis.
• Considering the timeline of the skin disease helps identify primary and secondary lesions.
• Avoid simply treating symptoms with steroids without proper diagnosis.

Module Review

1. Diagnosis of Eczema: Defining what eczema is.
2. Physical Findings and Timeline: Identifying specific physical findings and understanding the timeline of presentation.
3. Classification System: Developing a meaningful classification system for eczemas for diagnosis and management.
4. ID Reaction: Reviewing the diagnosis and clarifying the ID reaction.
5. Clinical Scenarios: Highlighting presentations of eczema through clinical scenarios.

Specific Categories of Dermatitis

Nummular Dermatitis (Nummular Eczema)

• Definition: Coin-shaped lesions commonly found on the extremities.
• Characteristics:
  • Symmetrical with discrete edges.
  • Begin as small papules that become scratched plaques.
  • Lesions have defined edges, usually less than 3-4 cm in size.
  • Most lesions appear identical.
• Appearance: Discrete plaques with excoriations and dried crust indicating healing.
• Classification: Mostly subacute or chronic, with some cases showing post-inflammatory pigmentation changes.
• Cause: Unknown, but often seen with atypia or very dry skin. Associated with atopy characterized by allergies, hay fever, and asthma.
• Medication-Induced: Can be caused by drugs like ribavirin and interferon used to treat hepatitis C.
• Distribution: Typically involves extremities, legs, and distal arms; often associated with dry skin.
• Progression: May progress to become more generalized, associated with intense itching.
• Secondary Infection: Lesions can become secondarily infected, termed infected eczeminus dermatitis.
• Treatment: Similar to other eczemas (detailed later).

Infected Eczematous Dermatitis

• Appearance: Excoriated crusted plaque with erythema.
• Example: A patient with a rash of five months duration, treated unsuccessfully with topical steroids. Cultures grew staph.
• Treatment Outcome: Cleared with oral antibiotics and topical steroids.

Stasis Dermatitis

• History:
  • Stasis: Greek for "posture of standing."
  • Derived from "histimi" meaning "to stand still."
• Occurrence: Common in patients with chronic venous insufficiency of the lower extremities.
• Age of Onset: Rarely presents before age 50 unless predisposing conditions exist.
• Predisposing Factors:
  • Chronic venous insufficiency (acquired through injury or surgery).
  • Deep venous thrombosis.
  • Chronic lower extremity edema.
  • Venous valvular diseases.
• Appearance:
  • Symmetrical rash on lower extremities with plaque, scale, and erythema.
  • Crusting and excoriations.
  • Small raised plaques and nodules due to chronic rubbing.
• Development Causes:
  • Increased hydrostatic pressures in lower leg capillaries leading to changes in permeability and leakage of macromolecules.
  • Leakage of fibrinogen into tissue resulting in fibrin cuff surrounding dermal capillaries, reducing oxygen diffusion which leads to dermal fibrosis.
  • Leakage of leukocytes trapped in fibrin cuff releasing inflammatory cytokines contributing to further fibrosis.
  • Red blood cells leak out resulting in long-term hyperpigmentation.
• Physical Exam:
  • Begins distally on the lower extremity, especially the medial aspect of the ankle.
  • Rash moves cephalad toward the knees.
  • Post-inflammatory hyperpigmentation in skin of color.
• Timeline of Presentation:
  • Initial edema worsens throughout the day without acute dermatitis.
  • Repeated episodes leads to raised confluent plaques with lichenification and pigment changes.
  • Progressive fibrosis leads to lipodermatosclerosis (champagne glass deformity).
• Ulcerations:
  • Possible due to mild trauma or scratching.
  • Exudate causes irritation and maceration, worsening the ulcer.
  • Cultures needed to rule out secondary infection.
  • Associated allergic contact dermatitis from topical products (e.g., Neosporin containing neomycin).
• Hygiene Issues: Buildup of dead skin mixed with topical medications due to infrequent cleaning.
• ID Reaction: Generalized disseminated eczema or exfoliative erythroderma due to uncontrolled stasis dermatitis, characterized by progressive involvement of extremities and torso; resolves only when primary stasis dermatitis is improved.
• Management:
  • Address conditions contributing to chronic venous insufficiency or venous hypertension.
  • Detailed history of rash onset, swelling, leg pain to rule out deep venous thrombosis.
  • Evaluation by primary care physician or vascular surgeon.
  • Duplex ultrasound to rule out correctable venous conditions.
  • Improvement of lower extremity edema with leg elevation.
  • Compression hosiery (applied in morning, removed at night).
  • Weight reduction.
  • Assess workplace for aggravating factors.
  • Treat oozing areas with wet to dry compresses using dilute acetic acid solution or Domeboro compresses.
  • Apply mid-potent topical steroid ointments or sprays after compresses.
  • Identify and treat secondary infections with cultures and antibiotics.
  • Cover erosions with thin layer of Aquaphor or petrolatum.
  • Avoid creams with preservatives and home remedies.
  • For dilute acetic acid solution: Boil water, cool, add 1 tbsp distilled table vinegar, refrigerate.
• Chronic Stasis Dermatitis Management:
  • Topical corticosteroids (ointments preferred).
  • Apply 2-4 times daily as needed for itching.
  • Reduce potency with improvement to prevent atrophy.
  • Compression hosiery (thigh-high preferred).
  • Una Boots (zinc gelatin cast) for non-healing ulcers after excluding infection; changed every 5-7 days.
  • Evaluate for new lesions, considering look-alike conditions such as leukemic infiltrate or malignant growths (melanoma, basal cell or squamous cell carcinoma).
  • Biopsy any non-clearing nodular lesion in chronic ulcer area.

Lichen Simplex Chronicus (LSC)

• Definition: End-stage of any localized eczema.
• Characteristics:
  • Thickened skin.
  • Plaques with lichenification.
  • Accentuation of skin markings.
  • Changes in pigmentation (hyperpigmentation).
• Symptoms: Often worse at night, during idle times, and under stress.
• Progression: Localized lesions increase in number and thickness.
• Appearance: Lower extremity plaque with erythema, lichenification, fissures, and excoriations; or thickened hypertrophic plaques with lichenification and sharply marginated spared areas.
• Cause: Repeated vigorous rubbing and scratching, resulting from various dermatitides, insect bites, or stasis dermatitis.
• Mechanism: Scratching leads to healing and itching, perpetuating the cycle; simple rubbing is sufficient, but fingernail scratching accelerates plaque development.
• Typical Picture: Chronic plaque with linear parallel scratches, excoriations, and crusting superimposed on a background of stasis dermatitis.
• Distribution: Lower extremity, wrists, ankles, posterior neck, anal-genital areas.
• Primary Lesions: Plaques.
• Secondary Lesions: Lichenification, hyperpigmentation, excoriations.
• Treatment:
  • Reduce itching (main driver of prolonged lesions).
  • Consider secondary infection; culture and sensitivities; oral antibiotics for presumed MRSA, adjusting based on results.
  • Topical steroids (creams during the day, ointments at bedtime).
  • Plastic kitchen wraps over thick lichenified plaque to increase corticosteroid penetration.
  • Low potency non-fluorinated products for face, axilla, and groin.
  • Intermediate strength topical corticosteroids for other sites.
  • Ultra-potent topical steroids in a pulse pattern (2 weeks twice daily, 1 week off, repeated).
  • Mid-potency topical steroids during the rest week.
  • Mid-potency steroids for itching applied and massaged for 2-3 minutes.
  • Topical steroid-impregnated tape (Cordrin tape) for difficult plaques.
  • Intralesional Kenalog (10 mg/cc diluted to 2.5-3 mg/cc with saline or lidocaine) injected at least 1 cm apart, avoiding subcutaneous placement.

Dyshidrotic Eczema

• Definition: An eczematous disease of unknown cause.
• Characteristics: Characterized by extremely itchy papulovesicular lesions typically found on the palms and soles, fingers, and toes.
  • Chronic recurrent outbreaks, sometimes linked to increased stress.
  • Atopic history in approximately 50% of cases.
  • Hyperhidrosis (excessive sweating) in over one-third of cases.
  • Worsened by pressure or contact.
  • Higher incidence of allergic contact dermatitis (nickel, chromium, Balsam of Peru).
• Physical Exam:
  • Symmetrical distribution involving palms, volar aspect of fingers, lateral aspect of fingers, soles, and toes.
  • Primary lesions: deep-seated papular vesicles that may become pustular.
  • Secondary lesions: crust and scale.
  • Small pinhead-sized papular vesicles on palmar surface and volar aspect of digits.
  • Papulovesicular lesions may be sensitive, painful, and itchy.
  • Vesicles may rupture, producing a characteristic cholera of scale.
  • Lesions last for three or more weeks and gradually resolve.
  • Painful fissures, especially with chronic lesions under pressure.
  • Potential for secondary infection (cellulitis).
• Treatment:
  • Avoid known or suspected topical irritants and allergens.
  • Avoid excessive pressure on affected surfaces.
  • Potent topical corticosteroids for acute outbreaks (pulse for 2 weeks on, 1 week off).
  • Short courses of systemic steroids for disabling flare-ups.
  • Topical calcineurin inhibitors (Protopic or Elidel).
  • Wet compresses (potassium permanganate, aluminum acetate, or vinegar water solution) for oozy vesicles (20 minutes, three times a day), followed by potent topical steroids.
  • Oral antibiotics for secondary infection or cellulitis.

Asteatotic Eczema

• Also Known As: Winter itch, eczema craquele.
• Characteristics: Dull, dry skin with rough scale and cracked fissuring, resembling a dried riverbed or cracked mosaic glass appearance.
• Location: Typically found on the anterior aspect of the lower extremities.
• Cause: Dry skin with increased transepidermal water loss (TEWL), common in winter months with low humidity.
• Incidence: Increases in patients in their 50s and 60s.
• Association: Seen with other types of dermatitis; severe cases may become generalized.
• Exacerbating Factors: Elderly patients sitting in front of heaters.
• Management:
  • Moisturizers (urea, lactic acid, glycolic acid, salicylic acid, ceramide).
  • Topical steroid preparations for rapid improvement. Medium potency for early lesions, higher potency for chronic lichenified areas.
  • Reduce steroid strength as erythema and plaque improve, discontinue when nothing palpable remains.
  • Avoid topical corticosteroids as a preventative measure to prevent atrophy.
  • Avoid home remedies.

Contact Dermatitis

• Definition: Localized red rash or irritation caused by direct contact with a foreign chemical or substance (direct skin contact or airborne).
• Examples: Geometric areas of contact dermatitis after eyebrow waxing and linear distribution of allergic contact dermatitis due to poison ivy.
• Key Point: Rash develops at the exact point of contact; unusual geometric or linear patterns suggest contact dermatitis.
• Causes: Cleaning solutions, industrial chemicals, plant resins (poison ivy), topical medications (Neosporin), preservatives, cosmetics, and almost any other element.
• Subdivisions: Irritant contact dermatitis and allergic contact dermatitis.

Irritant Contact Dermatitis

• Characteristics: Direct toxic effect from a chemical (solvent, soap, alkali) on the skin.
• Severity: The stronger the substance and the longer the contact duration, the more severe the injury and intensity of the rash.
• Onset: Strong chemicals may elicit acute irritant contact dermatitis with initial contact; weaker irritants produce subacute or chronic dermatitis with repeated exposure.
• Transfer: Irritants can be transferred from fingers to the face or eyelid.

Allergic Contact Dermatitis

• Mechanism: Requires at least one skin exposure to the substance or chemical prior to the second exposure that triggers the immune response.
• Sensitization: After exposure to a strong contact allergen (poison ivy), the body's immune system processes memory T cells (generally takes two weeks to develop); re-exposure may cause inflammation in less than twelve hours.
• Low-Level Exposure: Sensitivity may develop after long-term chronic exposure to a low-grade contact allergen (may take years).
• Pathophysiology:
  • Small molecular weight chemicals latch onto a carrier protein on an antigen-presenting cell (Langerhans cell).
  • This results in the development of memory T cells that persist in the skin, dermis, and lymphatic system. Re-exposure causes an immune response and cytokine development.
• Common Causes:
  • Plant resins/saps (poison ivy) - allergen is urushiol.
  • Metals (nickel).
  • Preservatives and personal skin care items.
  • Fragrances.
  • Textiles (natural and synthetic fibers).
  • Topical medications (Neosporin containing neomycin).
  • Antiseptics (benzocaine).
• Diagnosis:
  • Positive contact history and physical exam (lesion distribution limited to contact site).
  • Patch testing (placing allergen on skin overnight; rash appears in location of allergen after a day or so).
  • Commercial patch test kit (TruTest - contains 29 of the most common allergens).
• TruTest Procedure:
  • Cleanse the back.
  • Apply patches containing allergens to the back for 48 hours.
  • Remove and inspect anywhere from two to seven days after disc removal. Positive test manifests in 48 hours and beyond (older patients may require longer times). Patients should not be patch tested while on prednisone, but may be patch-tested while on antihistamines.
• Treatment:
  • Identify the offending agent and avoid or decrease exposure (continued exposure prevents resolution).
  • Protective measures in clothing.
  • Material data safety sheets (MSDS) for review.
  • Rubber gloves for excessive hand washing (waitresses, dishwashers).
  • Barrier creams for plant exposure (poison ivy).
  • Systemic steroids (oral prednisone or intramuscular Kenalog), Topical Corticosteroid is mandatory for resolution after systemic effect.

General Principles for Treatment of Contact Dermatitis

• If it's wet, dry; if it's dry, wetten.
• Reduce symptoms and stop the itch. Topical corticosteroids are mandatory to reduce the inflammatory response. Antihistamines may help reduce the itching.
• Topical soaks with compresses to reduce oozing and weeping (cool water compresses, diluted Domeboro solution, vinegar water mixture).
• Apply topical steroids immediately after compresses.
• For chronic contact dermatitis: potent topical corticosteroids to reduce lichenified plaque; may apply under occlusion with plastic wrap at bedtime. Antihistamines (H1 and H2 type) to reduce itching; treat any evidence of secondary infection with appropriate oral antibiotics.
• Chronic contact dermatitis is a common problem in the workplace (frequent hand washings, alcohol gels). Use low potency, non preferred fluorinated to treat rash on the face, groin, or axilla with transition from mid potency fluorinated topical steroids to low potency topical fluorinated steroids to the lowest potency non fluorinated topical steroids.

Topical Steroid Use

• Principles are universal for any type of dermatitis or steroid-responsive dermatosis.
• Topical steroid creams, sprays, or foams typically stay on the skin better than thick ointments. Use Topical steroid creams, sprays or foams when treating acute contact dermatitis with vesicles, bully, and oozing. Selection of topical corticosteroid potency is based on the body site of the rash. Treat other sites with fluorinated topical corticosteroids.
• More potent topical corticosteroids should be used for the start to quickly reduce the inflammation and transition to weaker topical corticosteroids after. Topical steroids must be gradually reduced in a stair step fashion from mid potency fluorinated topical steroids to low potency topical fluorinated steroids to the lowest potency non fluorinated topical steroids to treat problems such as rebound flare of the dermatitis.
• Excessive topical corticosteroids can have adverse effects. Local adverse effects may be irreversible and are not reversible when the topical steroids are withdrawn. Educate patients, document in chart, and provide written instructions.
• Limit amount of topical corticosteroids used based upon the strength of the topical steroid selected. Example (No more than fifty grams per week should be used of a class one steroid such as clobetasol.) It is smart to avoid class one topical steroids for both infants and small children.

Prurigo Nodularis

• Definition: Multiple intensely pruritic bumps of unknown causes.
• History: Difficult to manage. Lesions are typically seen in adults and vary in number and size (pyragomitis for small bumps, prurigo nodularis for larger bumps).
• Cause: Repetitive scratching and rubbing, localized form of nodular lichen simplex chronicus; possible psychological disorders and emotional stress. Over 50% of patients have an atopic history.
• Clue: The chronic duration of a problem in the skin is the fact that one may see lesions next to scars and areas of dyspigmentation.
• Characteristics: Well-circumscribed bumps or nodules with scratched away tops, may have excoriations and crust. Prurigo Nodularis lesions of patients with skin of color take on a more dome shaped appearance.
• Distribution: Symmetrical lesions positioned over the extensor surface of extremities, sacral area, lower abdomen; rarely on the neck or face.
• Lesions: Brown and firm, often dome-shaped and smooth; excoriations are frequent; may be associated with crust and pigmentation, as well as hypopigmented scars; lesions in different stages of healing.
• Management:
  • Identify underlying cause of severe itching (internal disease investigation). Lab work may be necessary.
  • Interrupt the itch-scratch cycle. Sedative antihistamines can be beneficial. Topical corticosteroids should be applied each time the patient has the sensation to scratch Large, long standing lesions may be treated with steroid impregnated tape (Cordran tape) over the individual lesion (changed every 24 hours).
  • Intralesional Kenalog (no stronger than 5 mg/cc).
  • Topical corticosteroid and Una Boot wrap to prevent scratching (extremities only).
  • Psychiatric consultation may be suggested for anxiety or emotional upset. Larger, long standing lesions may be treated with steroid impregnated tape. Suggest psychiatric referral if the patient shows increased anxiety or emotional upset.

Autoexemitization or ID Reaction

• Definition: A secondary rash to an existing skin rash.
• Also known as: Disseminated dermatitis, autosynthesization eczema, generalized eczema.
• Mechanism: Spreading cutaneous eruption due to a primary cutaneous inflammatory condition (contact dermatitis, stasis dermatitis) or cutaneous infection.
• Cause: Patient with infected contact dermatitis due to poison ivy that spread rapidly to the trunk, the rash represents a patient with severe stasis with poor hygiene who developed a bacterial secondary infection.
• Examples include: Dermatophytid (follows dermatophyte infection), bactereb (follows bacterial infection), and eczematid reaction (follows non-infectious eczematid process).
• Onset: Typically follows the primary event by one to two weeks.
• Cause: Not completely known; may occur with immune system dysfunction with inflammation such as antigen stimulation and release of cytokines.
• Distribution: Symmetrically involves the extremities and/or torso.
• Primary Lesions: Often nummular in appearance, presenting round oval shaped plaques as well as papules, vesicles, pustules, and rarely presentation with a morbilliform pattern.
• Treatment: Directed at the primary skin problem; ID reaction should improve or disappear once the primary dermatologic problem is cleared; a short course of oral prednisone may be necessary.

Basic Eczema Management Principles

• Restoring and improving an intact skin barrier is key to retain moisture and prevent infection.
• Only water can hydrate the skin; moisturizers help hold the water in the skin.
• Avoid liquid soaps as they can be very drying; bath oils are of limited benefit due to fall risk.
• Moisturizers play a central role; select moisturizers with urea, salicylic acid, or alpha-hydroxy acids for moderate to severe dryness; ceramide-containing moisturizers are excellent for patients with a history of atopy.
• Apply moisturizers within three to five minutes after exiting the bath.