Eczema - Ipswich and East Suffolk CCG

Eczema
Dr Khalid Mahmood
Consultant Dermatologist
Definition
• Eczema is a pattern of inflammation of the
skin characterized clinically in the acute stage
by ill defined groups of erythematous vesicles
and/or papules andin the chronic stage by
scaling and Lichenification
• Eczema is usually associated with inflammation of
the skin and so the terms eczema and dermatitis
are often used interchangeably
• The condition may be induced by a wide range of
external and internal factors acting singly or in
combination
Classification Based On Aetiology
• Endogenous
• Exogenous
Endogenous
• Atopic
• Seborrhoeic dermatitis
• Asteatotic eczema
• Nummular eczema
• Dry discoid eczema
• Exudative discoid and
• lichenoid dermatitis
• Chronic superficial scaly dermatitis
• Pityriasis alba
• Gravitational (is patient on calcium channel blockers)
• Juvenile plantar dermatosis
• Pompholyx
• Hyperkeratotic palmar dermatitis
• Unusual patterns
Exogenous Eczema
• Irritant dermatitis (ordinary sopas,detergents,aqueous)
• Allergic contact dermatitis (Patch Test-not for food
allergens)
• Infective dermatitis (primary, secondary-e herpeticum)
• Photo-allergic contact dermatitis (drugs)
• Eczematous polymorphic light eruption
• Eczematous dermatophytosis (folds,nails)
• Dermatophytide (tinea pedis/cruris/nails)
ALL ENDOGENOUS ECZEMAS MAY HAVE AN
EXOGENOUS COMPONENT & NEEDS TO BE
IDENTIFIED & TREATED
Endogenous
Atopic Dermatitis
• Atopy is said to exist when there is a personal or family
history of eczema of a particular distribution, asthma
or hay fever (allergic rhinitis)
• A.D. is common affecting all races
• Usually starts at age 2 to 6 months
• Often starts on the face and spreads to trunk and limbs
• In infantile stage primarily involves chest, face, scalp,
neck and extensor extremities
• In childhood to adult phase often localized in flexor
folds of neck, elbows wrists and knees
MANAGEMENT
• Is it eczema?
• Rule out exogenous causes
• Assess severity
– Mild,mod,severe (inflammation & BSA)
– Psychological impact
• sleep,mood,work,school
• Psychosocial functioning
Identify & Manage Triggers
• CONTACT IRRITANTS
– soaps,
– shower gels,
– shampoos,
– aqueous cream,
– oilatum plus,
– temperature (water & room),
– sweating,
– Clothing (wool, synthetic)
Frictional/Pressure Effects
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Repeated rubbing/scratching
Tight clothes made up of synthetic material
Frictional folliculitis
Lichen simplex chronicus
Does not clear till rubbing/scratching stopped
Covering with ichthammol and zinc bandages
may be helpful
Controlling Inflammation
• Topical steroids
• Calcineurin inhibitors
(tacrolimus/pimecrolimus)
• Systemic corticosteroids
• Phototherapy
• Immunosuppressives
AIRBORNE ALLERGENS/INHALANTS
• Plants (allergic contact dermatitis in an
airborne distribution)
• Perfumes/deodrants/air
freshners/disinfectants
• Ask about symptoms around pets, pollen,
house-dust mites, pet dander, and moulds
especially in patients with seasonal flares,
asthma, rhinitis, or facial eczema. Sensitization
to inhaled allergens increase with age
DIET
• Ask about itch, redness after certain foods
(milk, eggs, nuts, soya, and wheat are
considered to be the most likely allergens).
• Sensitization to dietary allergens decreases
with age
• Needs Prick testing at allergy clinic in
ENT/Chest dept and NOT PATCH TESTING
EMMOLIENTS
• Frequently, liberally & regularly (optimum)
• Choice of moisturizer (lotions/gels, creams,
ointments, Oils)
• Avoid rubbing/scratching, use emollients
when itchy
• It is important to keep using the moisturizers
when skin is clear to prevent flares
THINK
IS IT ECZEMA?
NICE IOG MANAGEMENT OF SKIN
CANCER IN THE COMMUNITY
SKIN CANCER LESION RECOGNITION
NICE IOG ON SKIN CANCER 2010
http://www.nice.org.uk/nicemedia/liv
e/10901/48878/48878.pdf
ALL TYPES OF SKIN CANCER TO BE MANAGED
BY A MEMBER OF MDT EXCEPT LOW RISK
BCC’S WHICH CAN BE MANAGED BY
APPROPRIATELY TRAINED/ACCREDITED GP’S
IN THE CMMUNITY
Recognition of Clinical presentations
and histological variants of BCC
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NODULAR
SUPERFICIAL
MORPHOEIC
PIGMENTED
BASISQUAMOUS
Ability to decide appropriate
treatment options for a particular BCC
• monitoring – observation rather than immediate
treatment
• surgical excision
• curettage and cautery/electrodessication
• cryotherapy/cryosurgery
• topical treatment (for example, imiquimod)
• photodynamic therapy (PDT)
• Mohs micrographic surgery
• radiotherapy.
NICE IOG-PATIENT PERSPECTIVE
Patients want their BCC(s) to be treated
effectively the first time, with minimal risk of
recurrence and the best cosmetic result
possible. Should surgery be required, patients
want their healthcare professionals to ensure
that the risk of damaging important,
proximate anatomical features, such as
nerves, is kept to a minimum where possible.
MODELS OF CARE FOR LOW RISK
BCC’S
• MODEL 1:GPs performing skin surgery within
the framework of the Directed Enhanced
Services and Local Enhanced Services
• MODEL 2: ‘Group 3 GPwSI in dermatology and
skin surgery’ and include a new ‘GPwSI in skin
lesions and skin surgery’
• MODEL 3:outreach community skin cancer
services provided by acute trusts or LHBs
linked to the LSMDT
Low-risk BCCs for DES/LES
• The patient is not aged 24 years or younger
immunosuppressed or has Gorlin’s syndrome
• The lesion is located below the clavicle, is less than 1
cm in diameter with clearly defined margins, is not a
recurrent or previously incompletely excised, is not
morphoeic, infiltrative or basosquamous in appearance
• is not located over a major vessel or nerves, where
primary surgical closure may be difficult, where
difficult excision may lead to a poor cosmetic result
• A diagnostic doubt-refer
• If superficial-consider non surgical modalities
Criteria for accreditation of GPs within
the framework of the DES and LES
•
have specialist training in the recognition and diagnosis of skin
lesions appropriate to their role(for GPSI’s attachment to a
secondary care dermatology unit under the supervision of a
consultant dermatologist, for 50 clinics is recommended)
• demonstrate competency in performing local anaesthesia, punch
biopsy, shave excision, curettage and elliptical excision using the
direct observation of procedural skills (DOPS) assessment tool in
the Department Health Guidance for GPwSIs in dermatology and
skin surgery and then follow a program of revalidation
• maintain a ’fail-safe‘ log of all their procedures with histological
outcome to ensure that patients are informed of the final diagnosis,
and whether any further treatment or follow-up is required
• provide quarterly feedback to their PCT(CCG) or LHB on the
histology reported as required by the national skin cancer minimum
dataset, including details of all proven BCCs
Criteria for accreditation of GPs within
the framework of the DES and LES
• provide details to their CCG or LHB of all types of skin cancer
removed in their practice as described in the 2006 NICE guidance
on skin cancer services and should not knowingly remove skin
cancers other than low-risk BCCs
• provide evidence of an annual review of clinical compared with
histological accuracy in diagnosis for the low-risk BCCs they have
managed
• attend, at least annually, an educational meeting (organised by the
Skin Cancer Network Site Specific Group), which should:
– present the 6-monthly BCC network audit results, including a
breakdown of individual practitioner performance
– include one CPD session (a total of 4 hours) on skin lesion recognition
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and the diagnosis and management of low-risk BCCs
To be run at least twice a year.
New BCC ‘See and Treat’ service
in the community
BCC ‘See and treat’ service will include
confirmation of diagnosis so GP can still
refer if diagnosis uncertain
Suitable for most BCC’s but not all (see
details on referral proforma)
Based in the community (at Hadleigh
Health Centre)
Cost savings to CCG
GPSI Lead (Dr Jeremy Halfhide)
Fully supported by Dermatology MDT at
IHT
Will assist with ever increasing BCC
workload in Secondary Care
Open to referrals later in 2013 (details to
follow!)
LOW RISK BCC AND BENIGN SKIN LESION CLINIC
GP REFERRAL FORM
Dr:
REFERRING GP DETAILS
PATIENT DETAILS
Surname:
Surgery address:
Forename:
Date of Birth:
NHS No:
Patient's Address
Surgery phone number:
Patient's phone number::
1) Is lesion high risk, i.e. suspected melanoma or SCC? If yes please refer to secondary care
on usual 2 week wait fax proforma for SCC and Melanoma.
2) Is lesion a high risk BCC? Please complete table below and refer to Secondary Care by
routine letter if any answer is YES.
High Risk BCC
Nose, including nasofacial sulci / folds
Yes
No
Lips
Eyes ( periorbital areas)
Ears
Greater than 2cms in diameter below the clavicle
Greater than 1cm in diameter above the clavicle
Immunocompromised patient
Please state suspected diagnosis and management requested.
Significant past medical history. Please mention any past dermatology treatment.
Present medication and allergies. A printout or letter of this is an acceptable alternative.
If you do not answer yes to any question above please refer to:
Dr Jeremy Halfhide, The Low Risk BCC Service, Hadleigh Health Centre, (address below).
DOCTOR’S SIGNATURE:_____________________________________ DATE_______________
Please return the completed form to: Dr Jeremy Halfhide, The Low risk BCC Service, Hadleigh Health Centre, Hadleigh,
IP7 5DN; fax 01473 824895
Don’t refer BCC’s involving eyes, ears, nose or mouth!
But do refer all others 10mm or less in diameter above clavicle, or
20mm or less below clavicle (primary closure possible)
LESION RECOGNITION- MELANOMA
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Increase in size
Change in Color/shape
Bleeding
Asymmetry
Border
Color
Diameter
Dermoscopy
SSMM
Nodular Melanoma
Pyogenic granuloma like amelanotic
melanoma
Acral Lentiginous Melanoma
PG like ALM
LENTIGO MALIGNA
MELANOMA-DD
BENIGN ANGIOMAS
Pyogenic granuloma
PIGMENTED SK
SQUAMOUS CELL CARCINOMA
• A fleshy,
indurated,
scaly lesion,
which may
have an eroded
surface and
may ulcerate. It
should always
be referred
under the two
week wait rule
BOWENS +EARLY INVASION
BCC
Psoriasis
Debs Banerjee
The Norwich Road Surgery
Tutor Dept Of Dermatology Cardiff
University
Epidemiology
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Equal sex incidence
Mean age of onset 28 years
Affects 2-3 %
Family hx in 30%
72% concordance in monozygotic
twins
30% in dizygotic twins
Two types
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Type 1 : AD, age of onset 20 years,
85% HLA Cw6
Type 2 : sporadic , age of onset 60
years, 15 % HLA-Cw6
Shares chr 16q with Crohns therefore
more common in such pts.
Polygenic , can be expressed due to
environmental stimuli like strep.
What happens
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Inflammation
Vascular proliferation
Epidermal keratinocyte hyper-proliferation
Basalis to corneum  from 28 days to 4
days 7 times faster
Mostly TH1 lymphocyte.( Transplants)
Mostly accepted as a autoimmune disease
Did you know?
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Psoriasis (TH1) and Atopic Dermatitis (
TH2) therefore does not happen in the
same individual.
Psoriasis almost always never infects.
Flexural psoriasis has no scales due to
moist skin.
Seborrhoeic dermatitis is a spectrum
of similar condition ‘sebo-psoriasis’
Types of Psoriasis
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Stable plaque: 80%
Kobner
phenomenon
Auspitz sign
Palmoplantar Pustulosis
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Painful sterile pustules
Resolve with brown
PIH
? Separate condition
but assoc.
Common in smokers
and women
Treat with potent
topical steroids
Acitretin
Guttate Psoriasis
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Usually strep throat
2 weeks prior.
Self resolving in a
few weeks.
Trt Vit D3 and
topical steroids if
need be.
Psoriasis of Von
Zumbusch
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Severe psoriasis (
almost like
erythrodermic)
Life threatening
Plaques studded with
sterile pustules
? After usage of oral
steroids ( especially on
withdrawal)
? Also after widespread
use of topical steroids.
Psoriatic nails
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50% nail involvement
Pitting
Subungal ‘oildrop’
Dystrophic
Onycholysis
Subungal hyperkeratosis
Trt with topical Vit D3
analogues and topical
Steroids under occlusion.
Remember!!! Fungal nails
may co-exist.
Psoriatic arthritis
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10 % of pts with Psoriasis.
15% simultaneous
60% skin first
25% joint first
Asymmetrical sero-negative arthritis
Be-aware that oral steroids and NSAIDs can
worsen Psoriasis !!!
Trt with cyclosporin, MTX,
cyclophosphamide,Biologics.
Triggers
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Stress
Sterp throat
Lithium, antimalarials, B blockers,
NSAIDs
Sulight in 10%
Alcohol
Smoking
Myths dispelled
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Sun beds don’t help !!! (as mostly UVA, psoriasis
responds to UVB and PUVA)
Diet has no role.
Does not usually get infected.
Treatment does not affect the partners skin when
genital areas are treated.
Tar used for psoriasis does not cause cancer.
No role of alternate /Chinese herbal meds, no
reported benefits of hypnotherapy/aromatherapy
etc.
Treatment
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Emollients: all patients, has mild antipsoriatic effect.
Keratolytics: 5 % Salicylic acid, to descale
prior to active treatment.
First Line: Coal Tar0.5-5%. More
refined less active. Keratolytic and antiinflammatory/anti-proliferative. Compound
5% crude coal tar+ 5% SA+ potent topical
steroid 1:4 ointment.
First Line continued
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Dithranol (+UVB INGRAM regimen)
It the gold standard for day care treatment. Out pt
short contact 10-60min under observation. Clears
within 3 weeks.
Topical Steroids: for hands, feet ,flexures,
genitalia and scalp. Not more than 2-4 weeks
without review.
e.g. potent topical steroid BD for 2 weeks then
OD mane , Vit D3 analogue in evening for 2
weeks then Vit D3 analogue to cont.
For flexures use mild topical steroids !!
First line continued
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Vit D 3 analogues: calcipotriol, tocalcitol
etc.
Use 4 weeks then rest for 4 weeks then
again for 4 weeks and stop.
Be cautious on face and flexures.
Risk of hypercalcemia.
Calcipotriol (50mg/gm) use is limited to
100gm/week.
Anti-proliferative /anti-inflammatory and
stops differentiation.
First Line continued
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Topical retinoids:Tazarotene: once
daily gel. Can be used in conjunction
with topical steroids.
SCALP psoriasis: first line use tar+/antifungal shampoo ung cocois co
under occlusion on dry but damp
hair then application of topical Vit
D3 and steroids mane.
Second line : Hospital
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Narrow Band UVB ( but has higher risk
of no melanoma ca though lesser than
PUVA)
PUVA caution non melanoma ca and
cataracts.
Methotrexate
Ciclosporin
Acitertin: systemic retinoid.
biologics
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For failure to respond to standard
therapies including ciclosporin, MTX
and PUVA.
C.I to standard systemic trt.
Significant co-morbidity
biologics
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Anti-TNF : infliximab, etanercept ,
adalimumab.
Interleukin 12 & 23 : ustekinumab.
Etanercept is licensed for the
treatment of chronic severe plaque
psoriasis.