Acute & Emergency Dermatology Flashcards
List several general categories of A&E Dermatology conditions
Erythroderma and acute skin failure Severe drug reactions Blistering conditions Generalised pustular psoriasis Eczema herpeticum Staphylococcal scalded skin syndrome Urticaria
List 3 reasons for skin failure
Mechanical barrier to infection:
- Sepsis
Temperature regulation:
- Hypo- and Hyper- thermia
Fluid and electrolyte balance:
- Protein and fluid loss
- Renal impairment
- Peripheral vasodilation
What is meant by Erythroderma
A descriptive term rather than a diagnosis
“Any inflammatory skin disease affecting >90% of total skin surface”
List 5 conditions that cause Erythroderma
Causes:
- Psoriasis
- Eczema
- Drugs
- Cutaneous Lymphoma
- Hereditary disorders
+ Unknown
Principles of Management of A&E Dermatology conditions
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
Drug Reactions & A&E Dermatology conditions
Common 5% of inpatients Can occur to any drug Commonly 1-2 weeks after drug Within 72 hours if re-challenged Mild - Morbilliform exanthem Severe - Erythroderma - Stevens Johnson Syndrome/Toxic epidermal necrolysis - DRESS
Stevens Johnson Syndrome/ Toxic Epidermal Necrolysis - separate or same, which is most common?
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)
Casues:
Stevens Johnson Syndrome/ Toxic Epidermal Necrolysis
Secondary to drugs Antibiotics Anticonvulsants Allopurinol NSAIDs Can be delayed onset
Stevens Johnson Syndrome/ Toxic Epidermal Necrolysis
%
Stevens Johnson Syndrome <10%
Stevens Johnson Syndrome/ Toxic Epidermal Necrolysis 10-30%
Toxic Epidermal Necrolysis >30%
SJS – Clinical Features
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
Toxic Epidermal Necrolysis – Clinical Features
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
Management: Stevens Johnson Syndrome/ Toxic Epidermal Necrolysis
Identify and stop culprit drug as soon as possible
Supportive therapy
?High dose steroids
?IV immunoglobulins
?Anti-TNF therapy
?Ciclosporin
Stevens Johnson Syndrome/ Toxic Epidermal Necrolysis
Prognosis - scoring system
Prognosis Mortality up to 10% (SJS)/30% (TEN) SCORTEN Age >40 Malignancy Heart rate >120 Initial epidermal detachment >10% Serum urea >10 Serum glucose >14 Serum bicarbonate <20 SCORTEN Mortality 0-1 > 3.2% 2 > 12.1% 3 > 35.3% 4 > 58.3% 5 or more > 90%
Stevens Johnson Syndrome/ Toxic Epidermal Necrolysis
Long term complications
Pigmentary skin changes Scarring Eye disease and blindness Nail and hair loss Joint contactures
Erythema Multiforme
Hypersensitivity reaction usually triggered by infection
Erythema Multiforme causative agents
Most commonly HSV, then Mycoplasma pneumonia
Erythema Multiforme - clinical features
Abrupt onset of up to 100s of lesions over 24 hours Distal proximal Palms and soles Mucosal surfaces (EM major) Evolve over 72 hours Pink macules, become elevated and may blister in centre “Target” lesions Self limiting and resolves over 2 weeks Symptomatic and treat underlying cause
(DRESS) - expand on each letter
Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)
DRESS
Prevalence
Clinical features
Incidence estimated between 1 in 1000-10,000 Mortality up to 10% Onset 2-8 weeks after drug exposure Fever and widespread rash Eosinophilia and deranged liver function Lymphadenopathy \+/- other organ involvement
DRESS
Treatment
Stop causative drug
Symptomatic and supportive
Systemic steroids
+/- Immunosuppression or immunoglobulins
Pemphigus – Clinical features
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
Pemphigus – Clinical Features
Commonly affects mucous membranes
Ill defined erosions in mouth
Can also affect eyes, nose and genital areas
Pemphigus - Pathology/investigation
Histopathology
epidermal-dermal tears
Immunofluorescence - more widespread around cells
Pemphigoid - Pathology/investigation
Antibodies directed at dermo-epidermal junction
Intact epidermis forms roof of blister
Blisters are usually tense and intact
