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?