Acute and Emergency Dermatology Flashcards
1
Q
What are the normal functions of the skin?
A
- Mechanical barrier to infection
- Temperature regulation
- Fluid and electrolyte balance
- Vitamin D synthesis
- Sensation
2
Q
What are the consequences of skin failure?
A
- Sepsis
- Hypo- and Hyper- thermia
- Protein and fluid loss
- Renal impairment
- Peripheral vasodilation (Can occasionally lead to cardiac failure)
3
Q
Erythroderma.
A
- A descriptive term rather than a diagnosis
- “Any inflammatory skin disease affecting >90% of total skin surface”
4
Q
What can cause erythroderma?
A
- Psoriasis
- Eczema
- Drugs
- Cutaneous Lymphoma
- Hereditary disorders
5
Q
What are the principles of management acute skin disease?
A
- Appropriate setting - ?ITU or burns unit
- Remove any offending drugs
- Careful fluid balance
- Good nutrition
- 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
6
Q
How common are drug reactions?
A
Common
-2-3% of inpatients
7
Q
What drugs can reactions occur with?
A
Any drug
8
Q
When do drug reactions usually occur?
A
- Commonly 1-2 weeks after drug
- Within 72 hours if re-challenged
9
Q
Give an example of a mild drug reaction.
A
Morbilliform exanthem
10
Q
Give examples of severe drugs reactions
A
- Erythroderma
- Stevens Johnson Syndrome
- Toxic epidermal necrolysis
- DRESS
11
Q
What 2 conditions are thought to form part of the same spectrum and can occur as a result of sever drug reactions?
A
- Stevens Johnson Syndrome
- Toxic Epidermal Necrolysis
12
Q
What drugs normally cause SJS/TEN?
A
- Antibiotics
- Anticonvulsants
- Allopurinol
- NSAIDs
13
Q
How rare are SJS/TEN?
A
- 1-2/million/year (SJS)
- 0.4-1.2/million/year (TEN)
14
Q
What is the difference between SJS and TEN?
A
-SJS affects <10% of body
TEN affects >30% of body
-Overlap between conditions 11-29%
15
Q
What are the clinical features of SJS?
A
- Fever, malaise, arthralgia
- Rash
- Mouth ulceration (Greyish white membrane, Haemorrhagic crusting)
- Ulceration of other mucous membranes
16
Q
Describe the rash present in SJS.
A
- Maculopapular, target lesions, blisters
- Erosions covering <10% of skin surface
17
Q
What does TEN often present with?
A
Prodromal febrile illness
18
Q
Describe the rash in TEN.
A
- 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
19
Q
How should drug reactions be managed?
A
- Identify and stop culprit drug as soon as possible
- Supportive therapy
- ?High dose steroids
- ?IV immunoglobulins
- ?Anti-TNF therapy
- ?Ciclosporin
20
Q
What system is used to identify prognosis of SJS/TEN?
A
SCORTEN
- Age >40
- Malignancy
- Heart rate >120
- Initial epidermal detachment >10%
- Serum urea >10
- Serum glucose >14
- Serum bicarbonate <20
21
Q
What is the mortality of SJS/TEN?
A
- SJS up to 10%
- TEN up to 30%
22
Q
What are the possible long term complications of SJS/TEN?
A
- Pigmentary skin changes
- Scarring
- Eye disease and blindness
- Nail and hair loss
- Joint contactures
23
Q
What is erythema multiforme?
A
- Hypersensitivity reaction usually triggered by infection
- Most commonly HSV, then Mycoplasma pneumonia
24
Q
How does erythema multiforme present?
A
- Abrupt onset of up to 100s of lesions over 24 hours
- Distal to proximal
- Palms and soles
- Mucosal surfaces (EM major)
- Evolve over 72 hours
- Pink macules, become elevated and may blister in centre
- “Target” lesions
25
How should erythema multiforme be managed?
- Self limiting and resolves over 2 weeks
| - Symptomatic and treat underlying cause
26
What does DRESS stand for?
Drug reaction with eosinophilia and systemic symptoms
27
What is the incidence of DRESS?
- Incidence estimated between 1 in 1000-10,000
| - Mortality up to 10%
28
How does DRESS present?
- Onset 2-8 weeks after drug exposure
- Fever and widespread rash
- Eosinophilia and deranged liver function
- Lymphadenopathy
- +/- other organ involvement
29
How is DRESS treated?
- Stop causative drug
- Symptomatic and supportive
- Systemic steroids
- +/- Immunosuppression or immunoglobulins
30
What causes pemphigus?
Antibodies targeted at desmosomes
31
How does pemphigus present?
- Skin – flaccid blisters, rupture very easily
| - Intact blisters may not be seen
32
What are the common sites of pemphigus?
- Face
- Axillae
- Groins
33
What sign be positive in pemphigus?
Nikolsky’s sign may be +ve
34
What is commonly affected in pemphigus?
- Commonly affects mucous membranes
- Ill defined erosions in mouth
- Can also affect eyes, nose and genital areas
35
What causes pemphigoid?
Antibodies directed at dermo-epidermal junction
36
How does pemphigoid present?
- Intact epidermis forms roof of blister
| - Blisters are usually tense and intact
37
Summarise pemphigus
- Uncommon
- Middle aged patients
- Blisters very fragile – may not be seen intact
- Mucous membranes usually affected
- Patients may be very unwell if extensive
- Treat with systemic steroids. Dress erosions. Supportive therapies
38
Summarise 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
39
What are common causes of erythrodermic and pustular psoriasis?
- Infection
| - Sudden withdrawal of oral steroids or potent topical steroid
40
How do erythrodermin and pustular psoriasis present?
- Rapid development of generalised erythema, +/- clusters of pustules
- Fever, elevated WCC
41
How is erythrodermic and pustular psoriasis treated?
- Exclude underlying infection, bland emollient, avoid steroids
- Often require initiation of systemic therapy
42
What is eczema herpeticum?
Disseminated herpes virus infection on a background of poorly controlled eczema
43
How does eczema herpeticum present?
- Monomorphic blisters and “punched out” erosions
- Generally painful, not itchy
- Fever and lethargy
44
How is eczema herpeticum treated?
- 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
45
Who is staphylococcal scalded skin syndrome common in?
Common in children, can occur in immunocommpromised adults
46
How does SSSS present?
- Diffuse erythematous rash with skin tenderness
- More prominent in flexures
- Blistering and desquamation follows
- Fever and irritability
47
How is SSSS treated?
Require admission for IV antibiotics initially and supportive care
Generally resolves over 5-7 days with treatment
48
What may SSSS follow?
Initial staph infection as Staphylococcus produces toxin which targets Desmoglein 1
49
What is urticarial?
Weal or hive
50
How does urticarial present?
- Central swelling of variable size, surrounded by erythema. Dermal oedema
- Itching, sometimes burning
51
How long does urticarial usually last?
Fleeting nature, duration: 1- 24 hours
52
What is angioedema?
Deeper swelling of the skin or mucous membranes
53
What causes urticarial?
Histamine released into dermis
54
What are the causes of acute urticaria (<6 week history)?
- Idiopathic (50%)
- Infection, usually viral (40%)
- Drugs, IgE mediated (9%)
- Food, IgE mediated (1%)
55
How is acute urticaria treated?
- 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)
56
What are the causes of chronical urticaria (>6 week history)?
- Autoimmune/Idiopathic (60%)
- Physical (35%)
- Vasculitic (5%)
- Rarely a Type 1 hypersensitivity reaction
57
How is chronic urticaria managed?
- Limited role for oral steroids. No good evidence base.
- Step up anti-histamine approach
- Consider anti-leukitrine
- Consider immunomodulant such as omalizumab (Monoclonal antibody to IgE, mechanism of action unknown)
