Transcript Slide 1
Emergency Dermatology
Dr Melissa Barkham
Spotlight Seminar 30th September 2010
Why is this important?
Urgent recognition and
treatment of dermatologic
emergencies can be life saving
and prevent long term
morbidity
How do you differentiate rare
life threatening conditions from
the common skin complaints
that make up 10 - 20% of
consultations in primary care?
Skin structure and function
Protective barrier (toxins,
microbes, u.v. light,
physical injury)
Temperature regulation
Fluid homeostasis
Sensation
Immunological function
Synthetic
(e.g. Vitamin D)
Psycho-social
Consequences of Skin failure
Similar to patients
with extensive burns
Dehydration
Fluid and electrolyte imbalance
Hypo - albuminaemia
Hypotension
Hypothermia
Sepsis
Other organ failure
(e.g. renal, hepatic, CCF)
Emergency Dermatology Overview
Skin signs a diagnostic clue
(to serious underlying disorder)
Skin disease causing risk of vital
organ failure / death
Severe Infections
(e.g. meningococcaemia,
necrotising facsiitis,
staphylococcal scalded skin)
Severe adverse drug
reactions
(e.g. toxic epidermal
necrolysis)
Acute autoimmune disease
(e.g. SLE, systemic vasculitis)
Erythroderma
(e.g. due to extensive
inflammatory skin disease )
Paraneoplastic
(e.g. dermatomyositis)
Autoimmune Blistering
disorders
(e.g. pemphigus vulgaris)
Team approach
GP
Accident and emergency
On call medical
(or paediatric) team
Dermatology consultants and
specialist nurses
ITU
Histopathology
Microbiology
…..to name but a few
Cutaneous Adverse Drug Reactions
Common - severity variable
Can be life threatening
Potential long term sequelae
(e.g. blindness)
Think carefully before you
prescribe any medicine!
Yellow card reporting (MHRA)
Over the counter drugs and
supplements can be the culprit
Cutaneous Adverse Drug Reactions
History may not be
volunteered
Ask about all medications
taken in the last 3 months
Prescribed and non prescribed
(including household
remedies, herbal remedies,
vitamins and supplements)
Beware compound
preparations (e.g. cold and flu
remedies)
Severe Drug reaction - types
Exanthemous (morbilliform)
Stevens - Johnson Syndrome
(SJS) and Toxic Epidermal
Necrolysis (TEN)
Drug hypersensitivity syndrome
(DHS)
Urticaria +/- angioedema
Drug reaction - warning signs
Facial or mucous membrane
involvement
Widespread erythema
Skin pain
Blistering / skin necrosis
Fever
Lymphadenopathy / arthralgia
Features of anaphylaxis
Other organ involvement
(e.g. hepatic or renal dysfunction)
Exanthemous drug reaction - features
Commonest type
Onset 5-10 days after new drug
Morbilliform (measles like)
maculopapular rash
Usually itchy
Sometimes associated with fever / malaise
Commoner in patients with infectious
mononucleosis, leukaemia or HIV
Suspected drug (or drugs) should be
discontinued and rash subsides in 1-2 weeks
Exanthemous drug eruption - culprits
Penicillins
Carbamazepine
Allopurinol
Sulphonamides
NSAIDS
Phenytoin
Isoniazid
DHS - clinical features
Morbilliform rash with fever and
internal organ involvement
“Toxic erythema”
Mortality - about 10%
Later onset (2-6 weeks) after new drug
commenced
Fever, lymphadenopathy
Eosinophilia (DRESS) in some
Hepatic / renal failure
Treatment: withdrawal of offending
drug(s) and supportive care
DHS - culprits
Sulphonamides
Dapsone
Anticonvulsants
ACE inhibitors
Beta - blockers
Allopurinol
Minocycline
SSRI
TEN / SJS - clinical features
Rare drug reaction - presents with skin
and mucosal loss
Variants of the same condition
(differentiated by extent of skin involved TEN >30%, SJS <10%)
Mortality - 50%
Mucous membrane involvement (eyes,
mouth, genitalia) - can scar
Tender, blistering skin and necrotic
epidermis – areas of denuded skin
Positive Nikolsky sign (blisters extend
with skin pressure)
TEN / SJS - culprits
More than 100 drugs reported including ...
Penicillins
Sulfonamides
NSAIDS (including ibuprofen)
Anticonvulsants
Allopurinol
Antiretrovirals
.... and even paracetamol
Susceptibility factors HIV, genetic susceptibility
TEN / SJS - Differential diagnoses
Erythema Multiforme - self limiting
reaction triggered by infections e.g.
HSV. Typical target lesions especially on
acral sites. May involve mucosae.
Staphylococcal scalded skin
syndrome (SSSS) - a localised
infection with a toxigenic strain of S.
Aureus triggers fever, redness of skin
and easily ruptured blisters. Flexures
often affected and mucosae uninvolved.
Autoimmune blistering disorders
TEN / SJS - investigations
Skin biopsy for histology and
direct immunofluorescence (DIF)
H&E sections - basal or full
thickness epidermal keratinocyte
necrosis, supepidermal blistering
(SSSS - the split is higher)
DIF - negative (rules out
autoimmune disease)
TEN / SJS - management
Remove all possible culprit drugs
Supportive care in ITU or high
dependency setting (skin failure)
Careful fluid and electrolyte balance
Analgesia
Non - adherent dressings / sheets
Ophthalmology input
Prevention and treatment of secondary infections
Consider intravenous immunoglobulin
Future avoidance (including 1st degree relatives)
Drug induced Urticaria
Drug induced urticaria can occur with
or without angioedema
Up to 3 weeks after first exposure
(or minutes on re-challenge)
Types Type 1 hypersensitivity (e.g. penicillin) -
can be associated with anaphylaxis
Mast cell degranulation on first exposure
(e.g. NSAIDS, opiates)
Angioedema without urticaria
(e.g. ACE inhibitors)
Drug Induced Urticaria - culprits
NSAIDS
Penicillins
Cephalosporins
Sulphonamides
ACE inhibitors
Calcium channel
inhibitors
Vaccinations
What is Erythroderma?
Intense and widespread reddening of
the skin (more difficult to detect in
asian / black skin)
> 90% Body Surface area
involement
Often associated with exfoliation
(exoliative dermatitis / exfoliative
erythroderma)
Often results from exacerbation of a
pre-existing skin disorder
Causes of Erythroderma
Psoriasis
Dermatitis
Cutaneous T- Cell
lymphoma
Drugs
(red man syndrome)
Idiopathic
Paraneoplastic
Erythroderma - management
Identify underlying cause (biopsy)
Consider hospital admission
Supportive care (e.g. keep warm,
regular emollients, fluid balance, high
protein diet)
Treat underlying disease
(e.g. severe psoriasis - methotrexate or
other systemics, dermatitis - topical or oral
corticosteroids)
Avoid oral corticosteroids in severe
psoriasis
Generalised Pustular Psoriasis
Rare form of psoriasis (patient
presents with widespread sterile
pustules on a background of red and
tender skin)
Many have a background of chronic
plaque psoriasis
Trigger factors include sudden
withdrawal of oral (or potent topical)
corticosteroids, infections, irritating
topical preparations like tar or
dithranol, pregnancy and drugs
Generalised Pustular Psoriasis
Pustule swab (exclude infectious
causes)
Consider skin biopsy
Admission
Fluid balance and supportive
care
Bland emollients
May require systemic therapy
(e.g. oral retinoid such as
acitretin, Methotrexate or antiTNF therapy)
Pemphigus Vulgaris - clinical features
Rare autoimmune blistering
disorder
The blisters are intra-epidermal
(therefore easily ruptured)
IgG autoantibodies against a
desmosomal protein
Usually presents initially with
mucosal (oral, genital, conjunctival
erosions) - difficulty eating
+/- skin erosions / blisters (and
positive Nikolsky sign)
Pemphigus Vulgaris - treatment
Confirm diagnosis with skin biopsy
(including direct IF)
Fatal before advent of oral
corticosteroids
Likely to require admission for
supportive care
Non adherent dressings
High dose oral steroids initially
(1 mg/kg/day)
Prevention / treatment of infection
Additional steroid sparing agent
usually needed
Bullous Pemphigoid - clinical features
Autoimmune blistering disorder,
commoner in the elderly
Split is at the Basement Membrane
zone (deeper than in PV)
Crops of tense fluid filled blisters,
often with surrounding erythema
Itchy
Can be localised or widespread
Oral mucosal involvement less
frequent than PV
Usually less severe than PV
Bullous Pemphigoid -treatment
Confirm diagnosis with skin biopsy
(including direct and indirect IF)
Biopsy confirmation less probable if
patient already on oral
corticosteroids
Admission not always necessary
Treatment – usually oral +/- topical
corticosteroids (reducing course
commencing around 0.5 mg/kg/day)
Attention to dressings
May need steroid sparing agent
(e.g. dapsone, azathioprine)
Eczema herpeticum
Herpes simplex infections can
be more severe and extensive
in patients with underlying
skin disease (e.g. eczema)
Systemic antivirals +/antibiotics needed
May need admission
Ophthalmology input if eyelids
involved or eyes feel gritty
Learning points
Pause before you prescribe – is
this drug really necessary?
Warning signs in severe drug
reaction (e.g. fever, mucosal
involvement, blistering,
tenderness)
Caution with oral corticosteroids
in psoriasis (abrupt withdrawal
can precipitate generalised
pustular psoriasis)
When you need us.....
On call team (via switchboard on
01932 872000) if admission
needed
Call dermatology (particularly if
admission avoidable but urgent
treatment needed)
SPH
01932 723720
01932 722234
01932 722748
Ashford 01784 884352
…and a happy ending……
Any questions?