Paeds Dermatology Flashcards
Usually resolves by 16Y
Atopic Eczema Pathophysiology
onset in first year of life, uncommon in first 2m (seborheic dermatitis)
Family history of atopic disorder such as asthma, rhinitis, eczema
- Genetic deficency of skin barrier function - gaps leading to entrannce for irritants, microbes and allergens creating immune response -> inflammation.
Irritant:Soap, Detergents, skin infxs, contact allergens
Atopic Eczema Signs and Symptoms
- Itching
- Excoriated areas become erythematous, weeping and crusted
- skin is usally dry and prlonged scratching can lead to lichenification
- Inside elbows and knees common place in younger children
- Trunk and face affected in infants
- ## Older children: amore typical distribution: flexor surfaces, creases of face & neck.
Complications:
– eczema herpeticum (can also be caused by Varicella Zoster).
Regional lymphadenopathy is common and often marked in active eczema usually resolving when the skin improves
Atopic Eczema Investigations & Managment
clinical diagnosis
- Avoid irritants and exacerbating factors as much as possible.
- Emollients mainstay of treatment.
- Ointments preferrable if skin is really dry
- Hydrocortisone can be applied once ot twice daily - can cause thinning of skin and systemic S.E if used frequently
- Consider wet wrapping (large ammounts of emollient - sometimes steroid) applied under wet bandages.
- Severe cases ciclosporin should be used
if a topical steroid is also being used the emollient should be applied first followed by waiting at least 30 minutes before applying the topical steroid
- creams soak into the skin faster than ointments
Certain HLA genetic types are at higher risk.
Stevens-Johnson Syndrome Pathophysiology
Often a drug Rxn, or Infection
Drugs includ: Anti-epileptics, Antibiotics, Allopurinol, NSAIDs, sulphonamides, Oral contraceptive pill
Infection: HSV, mycoplasma pneumonia, CMV and HIV
- Severe systemic reaction affecting the skin and mucosa
- Disproportionate immune response causes epidermal necrosis leading to blistering and shedding of top layer of skin
- Less than 10% body affected: S-JS
- More than 10%: Toxic Epidermal Necrosis
Stevens-Johsnson Syndrome Signs & Symptoms
- Start with non-specific symptoms of Fever, cough, sore throat, mouth & eyes
- Purple/red rash developsthat spreads across skin and starts to blister
- Skin breaks away exposing raw tissue underneath
- +ve Nikolsky’s sign (Epidermal layer easily sloughs off when pressure applied)
- Pain and erythema can also occure on mucous membranes.
Complications
Morbidity, and mortality in some cases, may come from sepsis or electrolyte disturbances.
Dehydration may occur
Stevens-Johnson Syndrome Investigations and managmenet
- Definitive test: skin biopsy which should be done right away
- Pt admitted emergenccy burns or dermatology unit for treatment
- Good supportive care required
- Frequent emollient use
- first 2-3 days use systemic corticosteroids and Immunoglobulin which may be helpful in a life saving scenario.
Allergic Rhinitis Pathophysiology
Atopic individuals at greater risk
- IgE mediated Type 1 hypersensitivity rxn
- Environmental allergens lead to allergic inflammatory response in nasal mucosa
- Seasonal: tree pollen, grass allergens
- Perenial: House dust mites or pets can cause year round symptoms
- Occupational: school or work environment may cause this
Allergic Rhinitis Signs and Symptoms
- Runny, blocked and itchy nose
- bilateral nasal obstruction
- Sneezing
- Itchy, red and swollen eyes
Examination may reveal mouth breathing, postnasal drip, nose rubbing, reddened eyes.
There is evidence of an association with sinusitis.
Allergic Rhinitis Investigations and management.
Diagnosis usually clinical
- Skin prick test can be helpful especially when testing for specific allergens.
Managed using - Nasal Saline Irrigation
- Non-sedating antihistamines
- eye drops
- if the person has moderate-to-severe persistent symptoms, or initial drug treatment is ineffective intranasal corticosteroids
- short courses of topical nasal decongestants (e.g. oxymetazoline). They should not be used for prolonged periods as increasing doses are required to achieve the same effect (tachyphylaxis) and rebound hypertrophy of the nasal mucosa (rhinitis medicamentosa) may occur upon withdrawal
Referral to immunologist may be needed if symptoms are unmanageable.
s’green boy
Urticaria/angioedema pathophysiology
Acute urticaria is most common in children and adolescents.
described as ‘hives’, ‘wheals’, ‘nettle rash
- Urticaria describes a local or generalised superficial swelling of the skin. The most common cause of urticaria is allergy although non-allergic causes are seen.
- Release of histamine and other pro-inflammatory chemicals by mast cells in the skin. If the deeper tissues are involved there is swelling (angioedema), especially of the lips and soft tissues around the eyes.
- Acute urticaria is typically triggered by something stimulating the mast cells such as:
Food, medication or animal allergy
Contact with chemicals, latex, nettles
Chronic urticaria is an autoimmune condition, where autoantibodies target mast cells and trigger them to release histamines and other chemicals. - Acute <6wk.
- Chronic>6wks
Urticaria Signs And symptoms
- erythematous oedematous lesions that may be distributed on any part of the body
- Describe as burning
- pale, pink raised skin. Variously described as ‘hives’, ‘wheals’, ‘nettle rash’
pruritic
Up to 40% of cases have associated angioedema – typically presents as swelling of the face, tongue or lips. May lead to stridor if there is severe larynx affected.
Urticaria Management
- Inflammatory markers (CRP/ESR) elevated or normal.
- Skin prick testing may be positive with allergic cause.
- Antihistamines are the main treatment – fexofenadine is usually the antihistamine of choice for chronic urticaria.
- Oral steroids may be considered as a short course for severe flares.
If Suscpicious of Anaphylaxis then give IM Adrenaline
Anaphylaxis
causes: Food (nuts), Drugs, Venom(wasp sting)
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction.
Airway: swelling of throat and tongue- hoarse voice and stridor
Breathing: Resp wheeze, Dyspnoea
Circulation: hypotension, tachy cardia
Treat with IM adrenaline (antero-lateral middle third of thigh) - repeat every 5 mins if neccessary
Recover phase: chlorphenamine, may be given following initial stabilisation especially in patients with persisting skin symptoms
Serum tryptase levels are sometimes taken in such patients as they remain elevated for up to 12 hours following an acute episode of anaphylaxis
if no ABC problems then no anaphylaxis
Refractory anaphylaxis: persistence of issues after 2 doses of IM. IV fluids should be given for shock
Birthmarks
Port wine stains are vascular birthmarks that tend to be unilateral. They are deep red or purple in colour. Unlike other vascular birthmarks such as salmon patches and strawberry haemangiomas, they do not spontaneously resolve,
- Port wine often darken and become raised over time. Treatment is with cosmetic camouflage or laser therapy (multiple sessions are required).
Causes of napkin rashes
Nappy
- Irritant dermatitis - ammonia from faeces
- Candida dermatitis - Erythematous rash - satelite leisons
- Seborrhoeic Dermatitis - Erythematous rash with flakes. May be coexistent scalp rash
- Psoriasis: less common, also present elswewhere on body
- atopic eczema - Other areas of the skin will also be affected
Management
* disposable nappies are preferable to towel nappies
* expose napkin area to air when possible
* apply barrier cream (e.g. Zinc and castor oil)
* mild steroid cream (e.g. 1% hydrocortisone) in severe cases
* management of suspected candidal nappy rash is with a topical imidazole. Cease the use of a barrier cream until the candida has settled
