Acute and emergency dermatology Flashcards
Dermatology emergencies, oh no! what do we do?! in this we will find out
1
Q
What are the consequences of skin failure?
A
• Sepsis • Hypo- and Hyperthermia • Protein and fluid loss • Renal impairment • Peripheral vasodilation ○ Can occasionally lead to cardiac failure
2
Q
What is erythroderma?
A
- A descriptive term rather than a diagnosis
- “Any inflammatory skin disease affecting >90% of total skin surface”
3
Q
What are the causes of erythroderma?
A
- Psoriasis
- Eczema
- Drugs
- Cutaneous Lymphoma
- Hereditary disorders
4
Q
What are the principles of management of erythroderma?
A
- Appropriate setting - ?ITU or burns unit
- Remove any offending drugs
- Careful fluid balance
- Good nutrition (want avoid any low albumin)
- Temperature regulation
- Emollients – 50:50 Liquid Paraffin : White Soft Paraffin
- Oral and eye care
- Anticipate and treat infection
- Manage itch
- Disease specific therapy; treat underlying cause
5
Q
Explain Steven Johnson syndrome/ toxic epidermal necrolysis
A
- 2 conditions which are thought to form part of the same spectrum
- Rare
- 1-2/million/year (SJS)
- 0.4-1.2/million/year (TEN)
- Secondary to drugs
- Antibiotics
- Anticonvulsants
- Allopurinol
- NSAIDs
- Can be delayed onset
6
Q
What are the clinical features of Steven Johnson syndrome?
A
- Fever, malaise, arthralgia
- Rash
- Maculopapular, target lesions, blisters
- Erosions covering <10% of skin surface
- Mouth ulceration
- Greyish white membrane
- Hemorrhagic crusting
- Ulceration of other mucous membranes
7
Q
What are the clinical features of toxic epidermal necrolysis?
A
- Often presents with prodromal febrile illness
- Ulceration of mucous membranes
- Rash
- May start as macular, purpuric or blistering
- Rapidly becomes confluent
- Sloughing off of large areas of epidermis – ‘desquamation’ > 30% BSA
* Nikolsky’s sign may be positive
8
Q
What is the management of SJS and TEN?
A
- Identify and stop culprit drug as soon as possible
- Supportive therapy
- Don't know how effective but... ?High dose steroids ?IV immunoglobulins ?Anti-TNF therapy ?Ciclosporin
9
Q
What are the long term complications of SJS and TEN?
A
- Pigmentary skin changes
- Scarring
- Eye disease and blindness
- Nail and hair loss
- Joint contractures
10
Q
What is the aetiology of drug reaction with eosinophilia and systemic symptoms (DRESS)?
A
- Incidence estimated between 1 in 1000-10,000
- Mortality up to 10%
11
Q
What are the clinical signs of DRESS?
A
- Onset 2-8 weeks after drug exposure
- Fever and widespread rash
- Eosinophilia and deranged liver function
- Lymphadenopathy
- +/- other organ involvement
12
Q
What is the management of DRESS?
A
- Stop causative drug
- Symptomatic and supportive
- Systemic steroids (usually oral prednisolone)
- +/- Immunosuppression or immunoglobulins
13
Q
What are the clinical features of pemphigus?
A
- Antibodies targeted at desmosomes
- Skin: flaccid blisters, rupture very easily
- Intact blisters may not be seen
- Common sites: face, axillae, groins
- Nikolsky’s sign may be +ve
- Commonly affects mucous membranes
- Ill defined erosions in mouth
- Can also affect eyes, nose and genital areas
14
Q
Explain pemphygoid
A
- Antibodies directed at dermo-epidermal junction
- Intact epidermis forms roof of blister
- Blisters are usually tense and intact
15
Q
What’s the difference between pemphigus and pemphigoid?
A
Pemphigus
- Uncommon
- Middle aged patients
- Blisters very fragile (may not be seen intact)
- Mucous membranes usually affected
- Patients may be very unwell if extensive
- Treatment: systemic steroids, dress erosions, supportive therapies
Pemphigoid
- Common
- Elderly patients
- Blisters often intact and tense
- Even if extensive, patients are fairly well systemically
- Topical steroids may be sufficient if localised; systemic usually required if diffuse
16
Q
Explain Erythrodermic psoriasis and Pustular Psoriasis
A
- Can occur without previous history of psoriasis
- Common causes:
- Infection
- Sudden withdrawal of oral steroids or potent topical steroid
- Rapid development of generalised erythema, +/- clusters of pustules
- Fever, elevated WCC
- Exclude underlying infection, bland emollient, avoid steroids
- Often require initiation of systemic therapy
17
Q
Explain eczema herpeticum
A
- Disseminated herpes virus infection on a background of poorly controlled eczema
- Monomorphic blisters and “punched out” erosions
- Generally painful, not itchy
- Fever and lethargy
- Treatment dose Aciclovir
- Mild topical steroid if required to treat eczema
- Treat secondary infection
- Ophthalmology input if peri-ocular disease
- In adults consider underlying immunocompromise
18
Q
Explain staphylococcal scalded skin syndrome
A
- Common in children, can occur in immunocompromised adults
- Initial Staph. infection
- May be subclinical
- Diffuse erythematous rash with skin tenderness
- More prominent in flexures
- Blistering and desquamation follows
- Staphylococcus produces toxin which targets Desmoglein 1
- Fever and irritability
- Require admission for IV antibiotics initially and supportive care
- Generally resolves over 5-7 days with treatment
19
Q
Explain urticaria
A
- aka Weal or Hive:
- Central swelling of variable size, surrounded by erythema. Dermal oedema
- itching, sometimes burning
~ Histamine release into dermis
* fleeting nature, duration: 1- 24 hours
- Angioedema
- Deeper swelling of the skin or mucous membranes
20
Q
What is the etiology of acute urticaria
A
- Idiopathic
- Infection, usually viral
- DRugs, IgE mediated
- Food, IgE mediated
21
Q
What is the management of acute urticaria?
A
- Oral antihistamine
- Taken continuously
- Up to 4 x dose
- Short course of oral steroid may be of benefit if clear cause and this is removed
- Avoid opiates and NSAIDs if possible (exacerbate urticaria)
22
Q
What is the etiology of chronic urticaria?
A
- Autoimmune/ idiopathic
- Physical
- Vasculitic
- Rarely a type 1 hypersensitivity reaction
