DERM - Acute and Emergency Conditions Flashcards
Acute Urticaria
Definition
Aetiology
Clinical Features
Management
1.) Definition - short-lived bouts of urticaria:
- transient eruption of erythematous or oedematous swellings of the dermis, often associated with itching
2.) Aetiology
- Abx: penicillin (main), cephalosporins, sulphonamides, aminoglycosides, tetracyclines
- other drugs: NSAIDs, opioids, ACEi, vaccines w/ egg protein
- food: nuts, white fish (cod), shellfish (prawn), eggs, milk, some fruits (strawberries, kiwis and citrus fruits)
- bee and wasp stings, idiopathic, exercise (v. rare)
3.) Clinical Features
- central, oedematous plaques (wheals) w/ redness (flares), annular lesions due to central clearing
- varying locations and sizes, itchy lesions last 30m to 4hrs, new lesions can come and go over days
- can be associated w/ angioedema or anaphylaxis
4.) Management
- avoid triggers
- non-sedating antihistamines (cetirizine, fexofenadine)
- may need a short course of PO steroids (pred)
- referral to immunologist: to identify allergies or in other cases of life-threatening reactions
Chronic (Spontaneous) Urticaria (CSU)
Definition/Pathophysiology
Clinical Features
Investigations
Management
1.) Definition/Pathophysiology - urticaria for >6wks
- can be autoimmune (have thyroid autoantibodies)
- can be autoallergic, however, it’s not allergy related
- triggers inc: heat, stress, NSAIDs, pseudoallergens
- often presents at 20-40s, F>M, atopic background
2.) Clinical Features - same as acute urticaria
- individual lesions last 30m to 4hrs but the condition may persist for several months (or years)
- can have elements of inducible urticaria such as dermographism or delayed pressure urticaria
3.) Investigations
- bloods: ↑thyroid autoantibodies (should check TFTs every 6 months due to ↑risk of thyroid disease)
- H.pylori status: in those who also have dyspepsia, urticaria may improve after H.pylori eradication
- no place for skin prick tests or patch testing as an allergic cause is highly unlikely
4.) Management
- avoid triggers, reduce stress, keep the skin cool
- 1°non-sedating antihistamines (loratadine, cetirizine): start on 1 dose a day going up to 4x a day (2x BD) for as long as needed
- 2°sedating antihistamines (chlorpheniramine): periodically at night if non-sedating is ineffective (avoid these long term)
- prednisolone for mod-severe flares
- referral: to consider treatment w/ omalizumab (monthly injections for 6 mths) or other DMARDs
Chronic Inducible Urticaria (Physical Urticaria)
Definition
Common Types of Physical Urticaria
Rare Types of Physical Urticaria
Management
1.) Definition - distinct subgroup of urticaria in which a specific stimulus is needed to induce the symptoms
- stimulus must be the main cause as patients w/ CSU may have features of inducible urticaria esp demographic and delayed pressure urticaria
- may last months or many years
2.) Common Types of Physical Urticaria
- dermographic: firm stroking of the skin produces an initial red line followed by a flare and linear wheal
- delayed pressure: sx at sites of sustained pressure several hours after contact, lasting 12-72 hours
- cholinergic: papules, triggers (heat, exercise, stress)
- contact: sx after direct contact w/ an offending substance e.g. latex or food allergy
3.) Rare Types of Physical Urticaria
- solar: sore, itchy rash w/in minutes of sun exposure
- cold: sx after cold exposure (wind, liquids), can develop life-threatening reactions if a sudden ↓temp
- aquagenic: wheals within 30mins of water exposure
4.) Management
- avoid triggers
- non-sedating antihistamines
- solar and cold urticaria is more complicated and should be referred to a dermatologist
Steven Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)
Differentiation
Associated Drugs
Clinical Features
Management
Differential Diagnoses
1.) Differentiation - variants of the same condition
- SJS: involves <10% of total body surface area
- TEN: involves >30% of the body surface area
- SJS/TEN overlap: 10-30% of body surface area
2.) Associated Drugs
- allopurinol, sulfa abx (co-trimoxazole (Septrin) inc trimethoprim), sulfa drugs (sulfasalazine, dapsone, SU, furosemide, hydrochlorothiazide, sumatriptan)
- penicillin antibiotics
- AEDs: lamotrigine, carba, phenytoin, phenobarbital
- oxicam NSAIDs: piroxicam and meloxicam
3.) Clinical Features
- sx onset within days of drug being commenced
- fever, malaise, myalgia and arthralgia
- tender erythema with local erosions and blisters progressing to confluent erythema with skin loss
- Nikolsky sign: gentle stroking of the skin causes the skin to separate at the epidermis
- mucosal: eyes, lips/mouth, oesophagus, URT (cough, resp distress), genitalia and GI (diarrhoea)
- complications: volume loss and deranged electrolytes
4.) Management
- stop the offending drug ASAP
- immediate assessment by dermatology
- patients best cared for in ICU or burns unit
- IVIG is often used first line, other options include: DMARDs e.g. ciclosporin and cyclophosphamide, plasmapheresis
5.) Differential Diagnoses
- erythema multiforme, staphylococcal scalded skin syndrome, pemphigus
Erythema Multiforme
Pathophysiology
Clinical Features
Management
1.) Pathophysiology - hypersensitivity reaction to numerous triggers (no provoking factor identified in up to 50% of cases), HSV-1 infection most common
- others: Mycoplasma pneumonia, parapoxvirus, varicella, hepB, rickettsia (bacterial), tinea (fungal), drugs (<10%) inc Abx, NSAIDs, sulphonamides
- most common in young adults
- distinct from SJS/TEN
2.) Clinical Features - of typical EM (EM minor)
- sudden development of up to 100s of red macules, beginning in hands and feet, spreads towards the trunk
- macules –> plaques –> typical target lesions with a red centre which may be crusted or blistered
- it can affect the face and is not usually itchy
- Koebner phenomenon (affects sites of trauma)
- HSV-1 infection precedes skin eruption by 3-14 days but prodromal sx are usually absent or mild
- mucosal involvement is mild or absent, if present, only affects one e.g. oropharynx, conjunctiva, genitalia, anus, URT, oesophagus, bowel
- EM major: more severe, more systemic upset
3.) Management
- self-limiting (lesions fade w/in 2wks), usually resolves without complications
- referral to ophthalmology if eye involvement
- mouthwash in mod-severe mucosal involvement
- hospital admission in severe cases (EM major)
- prophylactic aciclovir in recurrent EM due to HSV
Staphylococcal Scalded Skin Syndrome (SSSS)
Pathophysiology
Clinical Features
Management
1.) Pathophysiology - a superficial blistering skin condition caused by S. aureus exotoxins (toxin A/B)
- initial localised S. aureus infection of skin or URT
- mainly occurs in children <5 (esp neonates), adults who are immunocompromised or w/ CKD also at risk
- can occur individually or as outbreaks e.g. in nurseries (due to asymptomatic carriers)
- 15-40% of healthy humans are carriers of S. aureus
2.) Clinical Features
- fever and irritability but may not appear unwell
- macular erythema –> diffuse, confluent erythema with bullae that rupture easily –> sheet-like skin peeling leaving moist, bright red, tender areas
- Nikolsky sign: gentle stroking of the skin causes the skin to separate at the epidermis
- intraepidermal cleavage site (SJS/TEN involves necrosis of the entire epidermis)
3.) Management
- hospital admission w/ referral to dermatology
- IV abx for S. aureus and topical therapies (eg. fusidic acid or mupirocin) sometimes as an adjunct to abx
- children recover well (1-5% mortality) and healing is usually complete within 5-7d of starting treatment
- higher mortality in adults (50-60%) due to an underlying serious medical condition
- eradication therapy for exposed individuals in an outbreak e.g. either in a neonatal or childcare facility
Pemphigus Vulgaris (and Vegetans)
Pathophysiology
Clinical Features
Investigations and Management
1.) Pathophysiology - a rare immunobullous condition, characterised by suprabasal blisters and erosions
- IgG autoantibodies are directed to the pemphigus vulgaris antigen which is found in desmosomes in the keratinocytes near the bottom of the epidermis
- this leads to keratinocytes separating from each other, and they are replaced by fluid (the blister)
- vulgaris accounts for 70% of cases of pemphigus
2.) Clinical Features
- often presents as mucosal lesions (esp the mouth):
- slow healing, ill-defined, painful erosions mainly involving the lips, buccal mucosa and palate
- skin lesions: affect most patients, mainly affects the face, scalp, axilla, groin, pressure points
- fragile flaccid blister filled with clear fluid which may rupture to produce painful erosions
- Nikolsky sign is positive
- Pemphigus vegetans: a rare variant of vulgaris vegetating lesions are found in the flexures
3.) Investigations and Management
- blood test for skin antibodies
- 2 skin biopsies of blister and skin is required
- requires urgent referral to dermatology
- topical +/- systemic corticosteroids used
Erythroderma (Exfoliative Dermatitis)
Definition
Aetiology
Clinical Features
Investigations
Management
1.) Definition - erythema affecting > 90% of the body surface with exfoliation (skin peeling)
- the skin changes can obscure the primary lesion making it difficult to diagnose the underlying cause
- more common in males
2.) Aetiology
- exacerbation of eczema, psoriasis (most common)
- lymphoma and leukaemia (Sézary syndrome is one form of cutaneous T-cell lymphoma associated w/ it)
- drugs: >60 drugs implicated, the most common are:
- penicillin, sulphonamides, phenytoin, isoniazid, antimalarials, captopril and cimetidine
- idiopathic and some rare causes include pemphigus foliaceous, pityriasis rubra pilaris, dermatomyositis
3.) Clinical Features
- erythema spreads very quickly and there are varying degrees of itchiness (can become severe)
- scaling appears days 2-6 and after several weeks, scaling of the scalp can lead to hair loss
- thickening: skin, palms, soles (keratoderma), nails
- skin feels hot but patients feel cold due to heat and fluid loss –> hypothermia –> systemic compromise
- lymphadenopathy is common (esp in lymphoma or leukaemia) and secondary infection may arise
4.) Investigations - require a full workup
- FBC and peripheral blood film (↑Sezary cells is diagnostic of cutaneous T-cell lymphoma)
- multiple skin biopsies are also required
5.) Management - dermatological emergency
- admission if systemically compromised or high risk, otherwise an urgent out-patient appointment
- consider stopping all non-essential medication
- emollients required to improve skin barrier function
- topical steroids (will need larger amounts)
- if due to eczema or psoriasis, it usually clears with appropriate treatment but may recur anytime
Other Eczema and Psoriatic Complications
Eczema Herpeticum
Generalised Pustular Psoriasis
1.) Eczema Herpeticum - disseminated HSV1/2 infection due to impaired skin protection from eczema
- monomorphic punched-out erosions
- rapidly progressing painful vesicular rash which can ulcerate and crust with systemic effects, such as fever
- secondary bacterial infection with staphylococci or streptococci may lead to impetigo and/or cellulitis
- more common in infants/children w/ atopic eczema
- diagnosis confirmed w/ a viral swab + Tzanck test
- dermatological emergency, treat w/ IV aciclovir
2.) Generalised Pustular Psoriasis - rare form of psoriasis, don’t need to have chronic plaque psoriasis
- widespread pustules on red and tender skin (esp flexures, genitalia) w/ systemic upset, fever, malaise
- triggers: potent steroid withdrawal in psoriatic patients, lithium and salicylates, pregnancy
- dermatological emergency, need admission
