Acute and Emergency Dermatology Flashcards
(45 cards)
Name some functions of skin which may fail?
Barrier = Sepsis
Thermoregulation = Hyper or Hypothermia
Fluid/Electrolyte Balance = Loss of fluid, renal impairment, protein loss, vasodilation.
Can lead to Cardiac Failure.
What is Erythroderma?
Shows that skin failure has happened BUT IS NOT A DIAGNOSIS ITSELF - wouldnt diagnose someone with erythroderma.
Any inflamm condition which causes redness on >90% of the body = erythrodermic.
Very dangerous in elders.
What are the causes of Erythroderma?
Psoriasis
Eczema
Drugs
Cutaneous lymphoma
Hereditary disorders
What are the principles of management of Skin Failure/Erythroderma?
Admit to ICU/Burns Unit
Remove offending drugs
Maintain fluid balance
Good nutrition (losing lots of protein)
Ensure patient remains at suitable temperature (humidity and temp control)
Emollients - 50:50 liquid paraffin: white soft paraffin
Oral and eye care - to avoid long term effects
Anticipate and treat infection
Manage itch
Disease specific therapy; treat underlying cause (e.g - eczema, psoriasis, cutaneous lymphoma)
When do drug reactions resulting in skin symptoms often occur?
Commonly 1-2 weeks after drug - within 72 hours if re-challenged
What are the mild and severe forms of drug reactions?
Mild - morbilliform exanthem
Severe - Erythroderma, stevens johnson syndrome/toxic epidermal necrolysis, DRESS
What causes the onset of Stevens Johnson Syndrome and Toxic Epidermal Necrolysis?
Secondary to drugs -
–Antibiotics
–Anticonvulsants
–Allopurinol
–NSAIDs
Vital to recognise and treat - stop offending drugs.
What are the clinical features of SJS (Mild)?
Lost Epidermis and crusted erosions.
•Fever, malaise, arthralgia
•Rash
–Maculopapular, target lesions, blisters
–Erosions covering <10% of skin surface
•Mouth ulceration
–Greyish white membrane
–Haemorrhagic crusting
•Ulceration of other mucous membranes
Briefly describe TENS (Severe)?
Severe drug reaction with erythema/ulceration which covers >30% of body
Requires ITU setting, airway support, large haemorrhagic erosions, almost complete skin involvement
What is the clinical presentation of Toxic Epidermal Necrolysis?
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 - rub finger across skin and it comes off
What is the management for TEN?
Identify and stop culprit drug as soon as possible
Supportive therapy
- ?High dose steroids
- ?IV immunoglobulins
- ?Anti-TNF therapy
- ?Ciclosporin
What score is used to determine the prognosis of TEN?
SCORTEN
- Age >40
- Malignancy
- Heart rate >120
- Initial epidermal detachment >10%
- Serum urea >10
- Serum glucose >14
- Serum bicarbonate <20
Score 5 or more = >90% mortality
What are the long term complications of TEN?
–Pigmentary skin changes
–Scarring
–Eye disease and blindness
–Nail and hair loss
–Joint contactures
What is erythema multiform?
Abrupt onset of 100s of lesions over 24 hours - hypersensitivty reaction usually triggered by infection (HSV and mycoplasma pneumonia)
Think of as diff condition, similar rash to SJS but its due to viral trigger NOT DRUGS. These patients do much better than SJS and TEN patients.
Where are the lesions located in erythema multiforme?
Go from distal to proximal
Start at the palms and the soles
Includes mucosal surfaces
What happens to the lesions over time?
They evolve over 72 hours - pink macules become elevated and may blister in the centre
Resolves over 2 weeks - dont treat
What does DRESS stand for?
Drug reaction with eosinophilia and systemic symptoms
What is the onset of DRESS?
2-8 weeks after drug exposure
What are the clinical featrures of DRESS?
Fever and widespread rash
Eosiniphilia and deranged liver function
Lymphadenopathy
Possible involvement of other organs
What is the management for DRESS?
Stop causative drug
Treat symptoms
Systemic steroids
Possible immunosuppressants or immunoglobulins
Describe Pemphigus?
Split more superficial than in Pemphigoid. Split is in epidermis.
- 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
Describe Pemphigoid?
- Antibodies directed at dermo-epidermal junction
- Intact epidermis forms roof of blister
- Blisters are usually tense and intact – have to pop them to get rid of
- Usually older patients who get it
Where are antibodies directed in Pemphigoid?
•Antibodies directed at dermo-epidermal junction
What are the differences between Pemphigus and Pemphigoid?
