​Kembara Xtra - Medicine - Contact Dermatitis

​Kembara Xtra - Medicine - Contact Dermatitis 
Introduction 
A skin reaction to an external substance 
While the clinical appearance is the same, each kind has a unique mechanism.
Primary irritant dermatitis (ID) is a cutaneous inflammatory nonimmunologic reaction caused by direct chemical or physical injury to the stratum corneum that occurs more quickly than the skin can heal itself. There is no need for prior sensitization (2).
ID happens immediately after exposure or within 48 hours.
Allergic contact dermatitis (ACD) only affects people who have already been exposed to a chemical. It is an example of a postponed hypersensitivity reaction since it may take several hours or days for the cellular immunity cascade to become evident.
Skin/exocrine system impacted. Synonym(s): venenata dermatitis

Incidence and prevalence in Epidemiology 
Common Occurrence
According to one Australian study, occupational contact dermatitis affects 20.5/100,000 employees annually and can account for up to 70% of occupational skin disease cases.

Prevalence
The most common occupations include florists, hairdressers, cooks, beauticians, and metalworking machine operators.
Predominant sex: male = female - distinctions in exposure to harmful substances as well as typical cutaneous distinctions between sexes (function of the eccrine and sebaceous glands and hair distribution). Aspects of Geriatrics
ID incidence is rising as a result of skin dryness.
Child Safety Considerations
greater frequency of positive patch test results as a result of improved delayed hypersensitivity reactions


Pathophysiology and Etiology 

cellular immune response caused by an allergic reaction to a chemical
 Plants that contain the allergen urusiol include poison oak, sumac, and poison ivy.
- Plant contact (roots, stems, and leaves)
- Secondary contact: clothing or fingernails (not blister fluid, as the established eruption is not contagious or transmittable in and of itself).
 Chemicals - Nickel: Jewelry, hooks, zippers, and timepieces (4) - Potassium dichromate: a leather tanning agent
Hair dyes, fur dyes, and industrial chemicals all include paraphenylenediamine. - Turpentine: polishes, cleaners, and waxes
- Detergents & soaps

Neomycin is an example of a topical medication.
- The preservative thimerosal (merthiolate) is used in topical medicines. - Benzocaine is an anesthetic.
- Preservative used in topical medicines called parabens
- Formalin: shampoos, nail polish, and cosmetics
Genetics
ACD is more common in families with allergy sufferers.


Risk factors include: occupation, interests, travel, cosmetics, and jewelry.

Use of protective gloves (with cotton lining) may be useful. Avoidance of causative factors.

Assess for earlier exposure to irritant material when presenting history of itchy rash.

clinical assessment 
Acute: Papules, vesicles, and bullae with erythematous borders - Oozing and crunching - Chronic pruritus - Erythematous base
- Fissuring - Scaling - Thickening with lichenification
Distribution - Where the epidermis is thinner (eyelids, genitalia) - Sites of contact with the offending substance (such as nail polish) - The palms and soles, despite the prevalence of hand dermatitis, are significantly more resistant Lesions with strong boundaries and angles are pathognomonic, as are deeper skin folds that are spared.
- A clearly defined area covered in a papulovesicular rash

Differential diagnosis based on appearance, regularity, and localisation in the clinical impression

Herpes simplex clusters of vesicles
Bullous pemphigoid, diffuse bullous or vesicular lesions, photodistribution, and phototoxic/allergic response to a systemic allergen
Seborrheic dermatitis, Nummular eczema, Lichen simplex chronicus, Stasis dermatitis, Xerosis, and Id reaction are all skin conditions that can affect the eyelids. 

Laboratory Results 
Other/Diagnostic Procedures
For potential allergy triggers, think about using patch tests (systemic corticosteroids or recent, intense topical steroid usage may affect results).
Interpretation of the test: Intercellular edema 
The Bullae

Management: Recognize and get rid of the offending party. - Refrain
- Changes to the work
- Coverings for protection
Barrier creams, particularly moisturizing creams with a high lipid content (such as petrolatum, coconut oil, Keri lotion), topical soaks in lukewarm water, Aveeno oatmeal baths, Burow solution (1:40 dilution), and saline (1 tsp/pt water), and emollients (such as white petrolatum, Eucerin).

First Line of Medicine
Topical medicines include a lotion with talc, zinc oxide, menthol, and phenol (Gold Bond), as well as corticosteroids for both ACD and ID.
Fluocinonide (Lidex) 0.05% gel, cream, or ointment is a high-potency steroid. TID–QID
Use high-potency steroids for a brief period of time before switching to a cream or ointment with a low or medium potency. Avoid using for an extended period of time every day.
 Use caution around facial folds: Use less potent steroids, and limit your time with them. Once the acute phase has passed, switch to a topical steroid with a lesser potency.
Calamine lotion for symptomatic relief, topical antibiotics (bacitracin, erythromycin) for subsequent infections, and systemic antihistamines
 Hydroxyzine, which is particularly helpful for itching, 25 to 50 mg PO QID Cetirizine: 10 mg PO BID-TID and Diphenhydramine: 25 to 50 mg PO QID
Prednisone: taper commencing at 60 to 80 mg/day PO, lasting 10 to 14 days, occasionally 21 days, for corticosteroids.
- Applied to mild to severe instances, especially those involving the face or genitalia – There isn't much published research comparing the proper amount of treatment, but clinical experience suggests that short therapy courses (i.e., 5 to 7 days) are insufficient to stop rebound dermatitis.
- Although 14 days of treatment is usually sufficient, treatment for severe/extensive rash brought on by contact to strong allergens like urushiol (such as poison ivy) is typically advised for up to 21 days.
- For less severe dermatitis or less persistent immunogens, a burst dosage of steroids up to five days may be used. 
Drugs to treat secondary skin infections Erythromycin: 250 mg PO QID in penicillin-allergic patients; Dicloxacillin: 250 to 500 mg PO QID for 7 to 10 days; Amoxicillinclavulanate (Augmentin): 500 mg PO BID for 7 to 10 days; Trimethoprim-sulfamethoxazole (Bactrim DS): 160 mg/800 mg (1 tablet). (Suspected resistant Staphylococcus aureus) PO BID for 7–10 days Warning: Antihistamines may make you sleepy.
– Long-term usage of powerful topical steroids may result in local skin consequences (telangiectasia, atrophy, and stria).
– If taking oral steroids for more than five days, reduce the dose.
Next Line
Depending on the organisms and their sensitivity, additional topical or systemic antibiotics pregnant women's issues
drug with the usual prudence

Problems to Refer 

If standard treatment is ineffective, a dermatologist or allergist may need to be consulted. 

Further Treatments 
The use of complementary and alternative medicine is an addition to standard medical care, not a substitute for it.


Admission
Seldom requires hospital admission

Take Action 
Keep moving while avoiding getting too hot.
Patient monitoring, when needed for recurrence, and patch testing for the cause after the issue has been resolved
No particular diet, avoiding irritants, cleaning secondary sources (nails, clothes), and dispelling the myth that blister fluid spreads disease

Improvement in rash is less likely for people who stay in the same or comparable professions. Increased period of exposure and atopy are poor prognostic factors. 55% of patients still had contact dermatitis at 2 years following diagnosis.

Complications include subsequent bacterial infection and a generalized eruption brought on by autosensitization.

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