39. Skin rash/ eruptions
Clinical skills
Able to take focussed history in relation to rash/ eruptions
Specifically ask about:
 Duration of rash/ lesions
o Site of onset
o Spread
o Distribution
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Associated symptoms e.g. itch, pain
Aggravating factors e.g. sunlight, heat
Previous treatments
PMH of psoriasis/ atopy
DH including any previous treatment of current rash/ lesion
FH of psoriasis/ atopy
Occupation, especially if exposure to chemical irritants
SH including pets
Able to perform examination of skin and related structures
Skin
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Examine all the skin, hair and nails
Regarding rash/ lesions, consider:
o Distribution – flexures/ extensors, symmetrical?
o Are there grouped lesions?
o Are there crops of lesions?
o Are the lesions monomorphic (taking all one form) or polymorphic?
o Is there evidence of Kobners phenomenon (skin lesions which develop at site of
injury)?
o Pattern of lesions – ring/ linear/ targetoid (rounded lesion that is circumferentially
rimmed by >2 distinct densities or colours)?
Examine genitalia and mouth also for any lesions
Able to make clinical diagnosis of common skin rash/ eruptions
Symmetrical flexural distribution → atopic eczema
Symmetrical extensor surface distribution → psoriasis
Distribution at site of contact with jewellery or cosmetics → allergic contact dermatitis
Distribution in areas exposed to sun e.g. back of hands, face, neck → photosensitivity
Grouped lesions → herpes virus
 Ring pattern (active edge with healing centre) → fungal infection
 Linear pattern → Kobner’s phenomenon at sites of injury in psoriasis, lichen planus, plane
warts and vitiligo
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Targetoid pattern → erythema multiforme
Ring shaped lesions differentials
 Basal cell cancer - forms a ‘rodent ulcer’ i.e. pearly papule with central ulcer
 Tinea (ringworm)
 Granuloma annulare (benign, chronic inflammatory skin condition) – 1cm ring lesions seen
on hands
 Erythema multiforme – targetoid lesions commonly on extensor limb surfaces
 Rarely, leprosy
Brown pigmented lesions differentials
 Sun-related freckles
 Lentigos – persistent brown macules, often larger than freckles
 Café-au-lait spots – faint brown macules, if >5 consider neurofibromatosis
 Sebarrhoeic keratoses/ warts – benign greasy brown warty lesions usually on the face, back
and chest, very common in the elderly
 Malignant melanoma
 Chloasma (melasma) – brown patches on the face, related to pregnancy or Pill use, may
respond to topical azelaic acid
 Systemic diseases e.g.
o Addisons causing hyperpigmentation in the palmar creases, oral mucosa and scars
o Haemochromotosis
o Porphyria cutanea tarda (+skin fragility and blisters)
Round, oval or coin-shaped (discoid) lesions differentials
 Bowen’s disease – squamous cell carcinoma in situ, causing a well demarcated erythematous
plaque with an irregular border and surface crusting or scaling
 Discoid eczema – itchy/crusted/scaly eczema that is worsened by heat
 Psoriasis
 Pityriasis rosea – oval red lesions with scaly edge e.g. on trunk
 Erythema chronicum migrans
 Impetigo – well-defined red patches, covered with honey-coloured crust
Linear lesions differentials
 Kobner phenomenon – seen in psoriasis, lichen planus
 Dermatitis artefacta – lesions induced by patient, may be linear or bizarre-shaped
 Herpes zoster – polymorphous vesicles/pustules in a dermatomal distribution
 Scabies burrows – mite is visible as a speck just above a red linear lesion
Subcutaneous nodules differentials
 Rheumatoid nodule
 Rheumatic fever
 Polyarteritis nodosa (PAN)
 Xanthelasma
 Tuberous sclerosis
 Neurofibroma
 Sarcoid
 Granuloma annulare
Dermatology definitions
Alopecia
Hair loss
Atopy/ atopic Prone to allergic eczema, asthma or rhinitis. Typically affects city-based children
Atrophy
Thinning and loss of skin substance
Bulla
Blister >0.5cm in diameter
Vesicle
Blister <0.5cm in diameter
Crust
Dried brownish exudates
Erythema
Reddening of the skin which blanches on pressure
Purpura
Purplish lesion resulting from free RBCs in the skin – does not blanch on pressure,
may be nodular in vasculitis
Excoriation
A scratch which has broken the surface of the skin
Pustule
Well-defined pus filled lesion
Macule
Defined, flat area of altered pigmentation. Large macules are known as patches
Nodule
Solid lump >0.5cm in diameter, subcutaneous or intradermal
Papule
Raised, well-defined lesion <0.5cm in diameter
Weals/
Transient pale papules with pink margins (known as hives)
urticaria
Scale
Fragment of dry skin
Ulcer
Loss of epidermis and dermis which heals with scarring
Erosion
Superficial break in epidermal layer which heals without scarring
Underpinning sciences
Basic medical sciences
Structure and functions of the skin
 The skin consists of two layers – the epidermis and dermis
 Beneath the dermis is a layer of subcutaneous fat known as the hypodermis, and beneath
this layer lies muscle
Epidermis
 Relatively thin outer layer of the skin
 Most of the cells are keratinocytes, which originate from stem cells in the deepest basal
layer and migrate upwards to the surface of the skin undergoing maturation. Once
keratinocytes reach the skin surface, they are shed and replaced by newer cells
 Divided into five layers:
Layer of epidermis
Stratum corneum
Contents
Composed of 10-30 layers of
corneocytes (final stage of
keratinocyte differentiation); palms
and soles have the most layers
Function
Relatively waterproof
When undamaged, prevents most
bacteria, viruses, and other foreign
substances from entering the body
Stratum lucidum
Translucent layer of dead skin cells
that is only found in thick skin
Helps reduce friction and shear forces
between stratum corneum and
granulosum in areas of thick skin
Stratum
granulosum
Keratinocytes have lost their nuclei
and become granular in
appearance
Keratin proteins and water-proofing
lipids are produced and organised
Stratum spinosum
Contains columnar stem cells in the
first stage of differentiation
Langerhans cells are most
prominent in this layer
Stratum basale/
germinativum
Composed of one row of
undifferentiated columnar stem
cells that divide very frequently
Attached to the basement
membrane by hemidesmosomes
Melanocytes are also present in
this layer
Stem cells start to synthesise keratin
Langerhans cells are part of the skins
immune system; they take up microbial
antigens and become antigen-presenting
cells to T cells. Also have a role in skin
allergies
Half of the stem cells differentiate and
move to the next layer to begin
maturation. The other half stay in the
basal layer and divide to replenish the
layer
Melanocytes produce the pigment
melanin which contribute to skin colour
and filter out UV rays from sunlight
Dermis
 A thick layer of fibrous and
elastic tissue made mostly of
collagen, elastin and fibrillin –
giving the skin flexibility and
strength
 Contains nerve endings,
sweat glands, sebaceous
glands, hair follicles and blood
vessels
o Nerve endings sense
pain, tough, pressure
and temperature –
some areas contain
more nerve endings
that other e.g.
fingertips and toes
o Sweat glands produce
sweat in response to heat and stress – there are specialised apocrine sweat glands in
the armpits and genital regions that secrete a thick oily sweat which causes body
odour if digested by skin bacteria in those areas
o Sebaceous glands secrete sebum into hair follicles – this keeps the skin moist and
soft and acts as a barrier against foreign substances
o Hair follicles produce the various types of hair found throughout the body, which is
involved in regulating body temperature, providing protection from injury and
enhancing sensation
o Blood vessels of the dermis provide nutrients to the skin and help regulate body
temperature via vasodilation/ vasoconstriction
Subcutaneous fat layer
 Fat layer varies in thickness around the body
 Helps insulate the body, provides protective padding and serves as an energy storage area
Index conditions
EXANTHEMA SUBITUM (roseala infantum/ sixth disease)
Epidemiology
Most common in infants aged 6-18 months
Aetiology
Infection with human herpes virus 6 (HHV 6)
Clinical features
Incubation period of 10-15 days
Pyrexia
 Lasts for 3-4 days
 Uncommonly causes febrile convulsions
Macular exanthem (transient rash)
 Rose pink in colour
 Begins with pyrexia
 Initially involves the trunk, may spread to face and extremities
 Lasts for 2 days without desquamation or pigmentation
Mild pharyngitis and lymphadenopathy
Management
Mild and self-limiting condition; no treatment recommended
MENINGOCOCCAL DISEASE
Causative
organism
Neisseria meningitidis
Symptoms
General – in meningitis/ sepsis/ both
 Fever
 Lethargy
 Poor feeding/vomiting
 Irritability
 Drowsiness
 Loss of consciousness
 Seizures
Specific to meningitis
 Headache
 Photophobia
 In infants under 18 months, late signs include: bulging fontanelle, neck
stiffness and arched back
Specific to sepsis
 Non-blanching pupuric rash
Signs
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Pyrexial
Non-blanching purpuric rash may be present/ may develop
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Investigations
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Management
Positive Brudzinski’s sign i.e. flexion of the neck with the child supine
causes pain and resultant flexion of the knees and hips
Positive Kernig’s sign i.e. when the child is lying supine with the hips and
knees flexed, there is pain on extension of the knee
Signs of shock – capillary refill time over 2 seconds, tachycardia,
tachypnoea, pale, cold extremities
Focal neurological signs if meningitis
Altered conscious level – poor AVPU score
Papilloedema on funduscopy (rare)
FBC and CRP– shows raised white cell count and raised CRP
Coagulation screen – to see if there are lowered platelets, elevated
prothrombin time and elevated activated partial thromboplastin time
(aPPT), which would indicate DIC was occurring
U&Es, LFTs
BM
Arterial blood gas
Lumbar puncture + culture of CSF unless contraindicated
Blood cultures
Rapid antigen test for meninigitis organisms; can be done on blood, CSF
or urine
Cultures from throat swab and scrapings of purpuric lesion if present
Consider CT/MRI head and EEG
Resuscitation: ABCDE
Drug treatment
 In primary care: IM benzylpenicillin
 In hospital: cefotaxime or ceftriaxone (+ ampicillin in neonates to cover
possibility of Listeria monocytogenes) for 7 days in sepsis alone or 10-14
days with meningitis
 Dexamethasone (after the neonatal period) administered with antibiotics
reduces the risk of deafness
 Anticoagulants are frequently given if there is DIC although it is not
known whether this improves outcome
Other management
 IV fluids + fluid bolus if shocked - unless there is evidence of raised
intracranial pressure
 Dialysis or haemofiltration is usually required for fulminant (i.e. rapidly
spreading) meningococcal sepsis
DRUG ERUPTIONS
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Clear history of onset and duration of rash is essential
Record all drugs taken including herbal remedies
Stop likely offenders immediately
If clinical diagnosis is in doubt, prick test or skin biopsy may be useful
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Some advocate re-challenge with the suspected drug once the patient has recovered; not
often used in practice due to risk of erythoderma/ anaphylaxis and often against patient
wishes
Most are self-limiting; erythema multiforme and toxic epidermal necrolysis require referral
to a specialist
Type of
reaction
Muculopapular
Clinical features
Management
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Generalised erythematous macules and
papules particularly affecting the trunk +/fever and eosinophilia
Typically develops within 2 weeks after the
onset of drug therapy
Most common type of drug eruption
Causative drugs: penicillins,
cephalosporins, anti-epileptics
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Wheals +/- angioedema/ anaphylaxis
Rapid onset after taking drug
Can result from immunological and nonimmunological mechanisms
Causative drugs: morphine, codeine (direct
mast cell degranulation); penicillins,
cephalosporins (IgE responses); NSAIDs;
ACE-inhibitors
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Prompt antihistamine
+/- IV hydrocortisone/ IM
adrenaline if anaphylaxis
Widespread erythema and dermatitis +
erythoderma (scaling)
Causative drugs: sulphonamides,
allopurinol, carbamazepine, gold
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Emollients if dryness
Short course of topical
steroids if severe itch
Target lesions and polymorphic erythema
+ blistering mucosae (conjunctivae, oral,
labial, genital)
Causative drugs: sulphonamides,
anticonvulsants (phenytoin, barbiturates)
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Refer to dermatologist
Management options
include no treatment or use
of steroids
An extreme end of the erythema
multiforme spectrum
Widespread erythema and epidermal
necrosis with loss of large sheets of
epidermis
Mucosae severely affected
Increased risk in HIV patients
Mortality 30% - death usually due to
infection or ARDS
Causative drugs: sulfomamides,
anticonvulsants (phenytoin, phenobarbitol,
carbamazepine, valproic acid), penicillins,
allopurinol, NSAIDs
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Admit to hospital and
manage in a dermatology
or burns unit
Short term dexamethasone
pulse therapy
IVIG
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Utricaria
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Exfoliative
dermatitis
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Erythema
multiforme
major (StevenJohnsons
syndrome)
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Toxic epidermal
necrolysis
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Self-limiting, usually no
treatment required
Regular emollients if
dryness or itch
Lichenoid
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Well-defined purple papules distributed
symmetrically over trunk and limbs
Can be severely pruritic
May be scaly
Oral lesions uncommon
Causative drugs: beta blockers, thiazides,
gold, antimalarials
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Short course of topical
steroids if severe itch
LICHEN PLANUS
Clinical
features
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Lesions commonly seen on flexor aspects of wrists; forearms; ankles and
legs
Lesions are purple, polyangular, planar (flat-topped) papules
Associated pruritis
White lacy markings known as Wickham’s striae are also seen
Lesions often arise at sites of trauma
Other features:
 Scarring alopecia on the scalp
 Longitudinal ridges on nails
 Lacy white areas on inner cheeks of mouth and tongue
 Genital lesions
Management
Usually persists for 6-18 months
First line: Moderate to potent topical steroids e.g. betamethasone diproprionate
0.25%, fluocinonide 0.05%
+/- topical antifungals (used especially in oral disease e.g. fluticasone spray)
Severe disease: systemic steroids
PHOTOSENSITIVITY
Photosensitivity = skin conditions triggered by light i.e. solar urticaria, polymorphic light eruption,
poryphyria cutanea tarda and SLE. Can occur to visible light, UVA or UVB
Not to be confused with photoaggravation – disorders which are worsened by light but are not due
to abnormal sensitivity to light e.g. recurrent herpes labialis, rosacea
Polymorphic light eruption
Aetiology
 Thought to be an immunological reaction but the precise nature is
unknown
 Findings are consistent with a type IV delayed hypersensitivity reaction
Clinical features
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Common idiopathic disorder
Typically affects young fair skinned women in spring
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Management
Up to several days after light exposure, itchy red papules, vesicles and
plaques develop on exposed sites
Usually affects chest, arms or legs – face spared
Lesions often improve throughout the summer – due to the process of
‘hardening’ and tolerance to sunlight
Smoking and alcohol may trigger rash
Prevention
 Protection from sunlight with protective clothes and sunscreen (high
factor UVA and UVB sunscreen)
 Allow gradual exposure to sunlight to acclimatise the skin, may prevent
rash occurring
Treating the acute condition
 Potent topical steroids +/- short course of systemic steroids
 For severe cases: desensitisation with prophylactic light therapy before
sun exposure (photohardening) with UVB phototherapy or psoralen
combined with UVA (PUVA) treatment.
Porphyria cutanea tarda
Porphyrias are a group of inherited or acquired disorders of certain enzymes in the haem biosynthetic pathway. Haem is a component of haemoglobin and other haemoproteins
Aetiology
Clinical features
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Due to a defective liver enzyme (uroporphyrinogen decarboxylase)
Type 1 PCT generally begins in adulthood after exposure to certain
chemicals that increase the production of porphyrins (precursors of
haem) e.g.
o Alcohol
o Oestrogens – from OCP, hormone replacement or liver disease
o Polychlorinated aromatic hydrocarbons e.g. in pesticides
o Iron overload – due to excessive intake, viral infections esp hep C,
chronic blood disorders such as thalassamia or
haemochromotosis
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Type 2 PCT is familial and associated with abnormal genetic variants of
uroporphyrinogen decarboxylase, generally onsets at a younger age
Photosensitivity due to ↑poryphyrins in the skin: Increasingly fragile skin in areas
exposed to sun e.g. back of skin and forearms
 Sores and erosions following minor injuries
 Blisters – vesicles and bullae; milia arising as blisters heal
 Hyperpigmentation
 Occasionally, hardening of skin (sclerodermoid skin)
Alopecia
Dark urine
Investigations
Diagnostic:
 Skin biopsy
 Examination of the urine with a Wood's lamp: may reveal coral pink
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fluorescence due to excessive porphyrins
24 hour urine porphyrin profile: elevated total porphryins
Other tests:
 FBC and iron studies – ↑iron in 30% of patients, should prompt studies
for haemochromotosis
 LFTs – may be deranged
 Fasting blood sugar - ↑incidence of associated diabetes
 Antinuclear antibodies - ↑incidence of associated SLE
 Viral hepatitis studies – PCT may be associated with hep C
Management
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Avoid alcohol, oestrogens, iron and pesticides
Sun-cream and cover up when outside
Phlebotomy if ↑iron – 500ml every 1-2 weeks until iron drops, may then
be required yearly
Antimalarials e.g. low-dose chloroquine or hydroxychloroquine may be
recommended, but must be used cautiously - makes the porphyrins more
soluble so more are excreted in the urine
Autologous red cell transfusion – patient’s blood cells are washed of
plasma to remove circulating porphyrins and returned to the body
Treat Hep C if present
Solar urticaria = rare form of urticaria that occurs in response to sunlight or artificial light sourse
emitting UV radiation. May be due to an antibody-antigen reaction, causing allergic reaction and
urticaria
Epidemiology
 Rare
 M=F
 Mean age of onset 35 years
Clinical features
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Urticarial rash when exposed to sunlight/ UV radiation – may last minutes
– hours
If large areas of the body are affected, the loss of fluid into the skin may
result in light-headedness, headache, nausea and vomiting
Investigations
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Phototests to detect abnormal sensitivity to UVB radiation
Management
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Avoid or minimise sun exposure
Oral antihistamines may reduce urticaria but rarely prevent it altogether
Severe reactions: phototherapy or photochemotherapy may be
considered – desensitises patients to UV radiation but short-lived and
repeat treatment often required
ECZEMA= dermatitis i.e. inflammation of the dermis
Classification
 Atopic eczema – common in children, seen in many places on the body as opposed to
specific site in contact dermatitis
 Contact dermatitis – causes 70% of eczema, due to contact with a specific irritant/ allergen
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Seborrhaeic dermatitis – mainly affects the scalp (dandruff), nasolabial folds, cheeks and
flexures in adults, can occur as ‘cradle cap’ in neonates
Xerotic eczema – dry, itchy and cracked skin, commonly in older people in winter
Venous eczema – occurs where there is impaired circulation or varicose veins, most
commonly in the ankle area
Atopic eczema
Causes
Clinical features
Multifactorial
 Genetic: family history is common. Due to overactivity of Th2
lymphocytes, stimulating IgE production
 Infection: staphs can colonise eczema lesions and toxins act as a
superantigen
 Allergens: house dust mites and animals are common allergens
 Diet: food allergies e.g. eggs, dairy products may exacerbate eczema
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Pruritis
Redness and scaling of skin
May have widespread of localised blisters
Commonly affected areas: flexural surfaces of joints, face, groin
Children may also have rhinitis, asthma, hayfever, food allergies
Williams diagnostic criteria for atopic eczema – child must have itchy skin/
scratching + at least 3 of:
 Onset before 2 years
 History of skin crease involvement
 History of generally dry skin
 Personal history of other atopy or atopy in 1st degree relative
 Flexural dermatitis or involvement of cheeks/forehead and outer side of
limbs if <4 years old
Management
Emollients
 Should be used liberally 2x per day even if eczema not active
 Greasy emollients e.g. epaderm in severe eczema
 Less greasy e.g. E45, diprobase OK in moderate eczema
 Bath emollients such as Oilatum may be useful
Topical steroids for active sites
 Face, flexures and groin: 1% hydrocortisone/ 0.05% clobetasone
(Eumavate) if more potent steroids needed (<1 week on face)
 Elsewhere: higher potency 0.1% betamethasone (Betnovate)/ clobetasol
(Dermovate) is extremely potent, only for use on thick skin
 Haelan tape (fludroxycortide) is good at healing fissured digits
Topical immunomodulators – if topical steroids cannot be used/ have failed to
work
 E.g. tacrolimus, pimecrolimus
Antihistamines – may be used to prevent itching during a flare-up
Tar bandages containing itchthammol paste are used in lichenified eczema (skin
changes in response to repeated scratching)
If systemic treatments are required to control eczema: consider ciclosporing + get
help from dermatologist
Oral antibiotics if there are broken areas of skin – commonly Staph infections
therefore use flucloxacillin
Differentials
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Psoriasis – tends to occur on extensor rather than flexor surfaces
Urticaria – can look similar but there are usually raised red wheals as
opposed to flaking
CONTACT DERMATITIS
Pathophysiology Can be irritant or allergic
 Allergic contact dermatitis is a Type IV hypersensitivity reaction
Causative
agents
Irritants
 Detergents
 Soaps
 Oils
 Solvents
Allergens
 Nickel – in jewellery, watches, coins, keys
 Chromates – in cement, leather
 Lanolin – in creams, cosmetics
 Rubber - foam in furniture
 Plants (primulas)
 Topical antibiotics, antihistamines or anaesthetics
Clinical features
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Investigations
Pruritis
Redness and scaling of skin
Usually a sharp cut-off where contact ends but secondary spread is
common in allergic dermatitis due to auto-sensitisation
Hands most commonly affected in irritant dermatitis – weeping and dry
fissuring may occur
Irritant dermatitis often diagnosed on clinical grounds
Allergic dermatitis: patch testing (controlled exposure to common allergens) –
check for reaction 48 hours later
Management
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Remove contact with irritant/ allergen
Prevention: Emollient creams, soap substitutes if necessary, wearing
gloves if exposed to causative agent
Acute flare-ups: low potency topical steroids e.g. hydrocortisone,
alcometasone diproprionate (aclovate)
Moderate-severe: topical tacrolimus (immunosuppressant)
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Severe allergic dermatitis: systemic glucocorticoids/ immunomodulators
such as azathioprine may rarely be needed
PSORIASIS = chronic inflammatory skin condition
Classification
 Plaque/ discoid psoriasis – most common type,
plaques have a slivery-white scaly appearance
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Guttate psoriasis – eruption of small salmon-pink papules,
1-10mm in diameter, usually with a fine scale. URTI with
group A Strep e.g. Strep. pyogenes usually precedes the
eruption by 2-3 weeks
Pustular psoriasis – uncommon, widespread pustules occur on an
erythematous background. May have concurrent fever and toxicity with
↑WCC
Plaque/ discoid psoriasis
Epidemiology
 Affects 2% of Caucasians
 Peak incidence in the 20s and 50s
Pathology
Multifactorial
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Triggers
Symptoms
Triggers
 Stress
 Skin infections esp. Streptococcus
 Skin trauma (Kobner phenomenon)
 Drugs – lithium, beta blockers, antimalarials
 Alcohol
 Obesity
 Smoking
 Climate
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Signs
Inflammatory infiltration of epidermis by T cells – psoriasis is
commonly precede by a Strep infection, which initially activates T cells
Epidermal hyperplasia and improper cell maturation
Familial - 30% have a family member with psoriasis
Commonly affects extensor surface of knees and elbows, scalp,
sacrum, intergluteal clefts and penis
Tends to following a waxing and waning course related to exposure to
triggers
Skin lesions
 Symmetrical well-defined red oedematous plaques with silvery scale
on extensor surfaces
 Lesions frequently present in flexures also but these are non-scaly
Nail changes (occur in 50%)
 Pitting
 Oncholysis (separation from nail bed)
 Thickening
 Subungual hyperkeratosis
 ‘pepper pot nail pitting’
 ‘grease-spots’ underneath nails
Ocular features – tend to occur after skin symptoms have developed
 Tearing and redness of eyes due to conjunctivitis/ blepharitis
Other signs
 Aubitz sign – pinpoint bleeding on scale removal
 Kobner’s phenomenon – linear lesions at sites of injury
Systemic features
 7% develop a seronegative arthropathy (5 types –
mono/oligomonoarthritis, psoriatic spondylitis, asymmetrical
polyarthritis, arthritis mutilans, rheumatoid-like polyarthritis
Management
Education + remove triggers
Topical drugs – mainstay of treatment for mild disease
 First line: Combined vitamin D analogue calcipotriol + betamethasone
cream 0.05% (Dovobet) applied once daily
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Dithranol – must be washed off 30 mins after application, start at 0.1%
and consider 0.25-1%. SEs: burning and staining, avoid use in flexures/
on face
Tar may be used but messy
Tacalcitol (vitamin D analogue) may be used once per day for up to two
12 week courses per year
For flexural disease: Trimovate (topical steroid + antibiotic +
antifungal)
Moderate-severe psoriasis – refer to a dermatologist
 Goeckerman therapy – combination of coal tar applied to skin and
psoralen+UVA (PUVA) artificial radiation
 TNF inhibitors: Etanercept/ adalimumab
 Immunosuppression with methotrexate or ciclosporin may be
necessary
TINEA CORPORIS = dermatophyte (ringworm) fungal infection on the body
Risk factors
for infection
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Living in humid conditions
Wearing constrictive clothing
Participating in close contact sports e.g. rugby
Immunosuppresion e.g. HIV or taking immunosuppressants
Clinical
features


Round scaly itchy lesions
Edges of lesion are more inflamed than
centre
Investigations

Skin swabs – microscopy +/- culture
Management
First line: Topical antifungals at least twice a day for 2 weeks e.g. clotrimazole
If several lesions/ patient is immunocompromised: oral antifungals e.g. terbanifine,
itraconazole
BLISTERS
Causes of blisters
Widespread blisters
 Eczema
 Dermatitis hepetiformis
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Chickenpox
Erythema multiforme
Bullous pemphigoid
Pemphigus blisters
Drug eruptions
Locaslised blisters
 Eczema
 Psoriasis
 Impetigo
 Herpes simplex
Dermatitis hepetiformis = autoimmune blistering skin manifestation of Coeliac’s disease
Clinical
 Itchy bullous rash
features
 Characteristically affects extensor surfaces – scalp, buttocks, elbows, knees
 +/- symptoms of Coeliac disease
Investigations


Skin biopsy
Confirm celiac disease via autoantibody testing: IgA anti-tissue
transglutaminase or IgA endomysial antibodies
Management


Gluten-free diet
Dapsone (sulphone antibiotic)/ systemic steroids may be required to
reduce itch initially
Chicken pox
Cause
Clinical
features
Varicella zoster virus infection, airborne spread by respiratory droplets
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Management
Complications

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
Fever
Rash – begins initially as papules and develops vesicles. The rash typically
starts on the head and trunk and progresses to the peripheries – as
opposed to smallpox, which tend to start on peripheries. Lesions may
occur on the palate
Pruritus
Pustules (lumps filled with pus and necrotic fluid, as in acne) and crusting
may develop
Rash has usually gone within one week – new lesions appearing after 1days suggest defective cellular immunity
Other symptoms: myalgia (muscle pain), malaise, anorexia, vomiting, sore
throat, sore ears
Usually no treatment required
Paracetamol to ease symptoms
Aciclovir for severe chickenpox or in immunocompromised children
Secondary bacterial skin or lower respiratory tract infection
 Commonly with staphylococci or group A streptococcus

Can lead to further complications such as toxic shock syndrome or
necrotising fasciitits
Encephalitis
 Usually occurs early during the illness
 Prognosis is better than encephalitis caused by HSV
 Cerebillitis is characteristic – child develops ataxia and cerebellar signs
 Usually resolves within one month
Purpura fulminans
 Occurs as a consequence of vasculitis in the skin and subcutaneous tissues
 May rarely occur after VZV due to production of antiviral antibodies which
cross-react and inactivate coagulation factor protein S (more common after
meningococcal sepsis, causes the dark areas of rash seen in meningococcal
sepsis)
 Cutaneous haemorrhage and necrosis, low blood pressure, fever and DIC
occur – the condition can be life-threatening
In immunocompromised children:
 Lesions can become haemorrhagic
 Pneumonitis may occur
 Infection can become progressive and disseminated
 DIC can occur
 Mortality is up to 20%
Bullous pemphigoid = a rare, autoimmune skin disorder causing supepidermal blistering
Pathogenesis
Autoantigens against type XVII collagen which forms the junction between
epidermis and basement membrane of the dermis
Epidemiology
 Incidence 4.28 per 100,000 person years in the UK
 Most common in >70s
 M=F
Triggers
Symptoms
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Investigations
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Management

Lichen planus, psoriasis or any other chronic inflammatory skin
disease may precede development of bullous pemphigoid
Pruruitis may appear weeks-months before skin lesions
Blisters/ bullae typically in skin flexures
Skin may be normal/ erythematous
Mucous membranes involved in ¼ patients
Gold standard: Skin biopsy followed by direct immunofluorescence
Indirect immunofluourescence using fluid aspirated from a blister
may also be used
Histology reveals a supepidermal blister with inflammatory infiltrate
and eosinophilic predominance
First-line in localized disease: Strong topical steroids e.g. clobetasol
Prognosis

For severe/ extensive disease: oral steroids +/- immunosupressives.
Bisphosphonates, calcium + Vit D required in elderly patients taking
steroids for more than 1 month

Can persist with remissions and exacerbations for years although
normally remits completely within 5 years
Elderly patients are particularly at risk from steroid therapy, and
complications such as secondary infection, hypertension, diabetes,
osteoporosis, peptic ulcers and heart disease may occur from long
term steroid use

Pemphigus = a group of autoimmune disorders in which there is blistering of the epidermal layer of
the skin and/or mucous membranes
Three major variants:
 Pemphigus vulgaris – accounts for 70%, there is cutaneous blistering and oral lesions
 Pemphigus foliaceus - characterised by lesions which occur only in the skin
 Paraneoplastic pemphigus – presents in association with a tumour (may be occult)
Pathophysiology IgG autoantibodies (DSG 1 and DSG3) to antigens on keratocytes, causing
disruption of proteins and formation of superficial bullae in epidermal layer
Epidemiology


Rare: 0.68 per 100,000 person years in the UK
Incidence higher in women an older age groups
Triggers
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Drugs: penicillamine, captopril, rifampicin
Burns
Stress
Pregnancy
Vaccinations
UV light
Associations
Other autoimmune diseases; myasthenia gravis
Clinical features
Skin lesions
 Blisters: superficial, flaccid, rupture easily, may not be intact, may be
turbid
 Skin is normal/ erythematous and painful
 No pruritus
 Excess granulation and crusting of lesions may occur
 Nail lesions may occur - paronychias, nail dystrophies and subungal
haematomas
Mucous membranes
 Bullae in the oral cavity are most common: they are rarely intact, forming
irregular lesions which are painful and slow to heal
 Lesions may occur in genitalia, conjunctiva and oesophagus
Investigations

Skin/ mucosal biopsy from the edge of a blister – for histological

examination and immunofluorescence
ELISA for autoantibodies in serum
Other investigations necessary to assess if paraneoplastic pemphigus/ assess
suitability for different treatments
 Bloods: FBC, U&Es, LFTs, BM, antinuclear antibody
 CXR
 Urinalysis for protein, blood and sugar
 Blood pressure
 Bone densitometry
Management
Involves compression of the immune system in 3 phases: control, consolidation,
maintenance
Control
 Mild oral disease only: topical therapy alone e.g. beclometasone spray,
hydrocortisone lozenges
 First line for skin disease +/- oral disease: oral corticosteroids - 40-240mg
prednisolone per day depending on severity for 6-8 weeks to induce
remission
 If steroids fail: plasmapheresis to remove antibodies + cytotoxic drug e.g.
axathioprine, cyclophosphamide
 Resistant disease: IVIG + azathioprine
Once control is achieved, step-down regime is used to achieve lowest dose at
which control is maintained. Azathioprine, cyclophosphamide or methotrexate
may be used as maintenance to spare use of steroids
Complications
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Prognosis

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Secondary infection of skin lesions
Malignancies from immunosuppression especially leuakemias and
lymphomas
Growth impairment in children from corticosteroids
Osteoporosis and adrenal sufficiency from corticosteroids
Untreated pemphigus vulgaris mortality 75%
Mortality greatly reduced with treatment, but many suffer long term SEs
of treatment
Impetigo = localised, highly contagious staphylococcal and/ or beta-haemolytic streptococcal skin
infection
Epidemiology
Most common in Infants/ young children with pre-existing skin disease e.g. atopic
eczema
Clinical
 Lesions begin as erythematous macules which become vesicular/ bullous
features
blisters
 Ruptures of blisters causes honey-coloured crusted lesions
 Face, hands and neck usually affected
Investigations
Management
Clinical/ skin swab for culture + sensitivity
 Mild cases: topical antibiotics e.g. mupirocin


Severe cases: flucloxacillin / co-amoxiclav (easier regime so may be better
in children)
Affected children should not go to school until lesions are dry
OCCUPATIONAL SKIN ERUPTIONS
3 types:
 Irritant occupational contact dermatitis – commonest type, agents have a direct toxic effect
on the skin
 Allergic occupational contact dermatitis – type IV hypersensitivity reaction, worse prognosis
than irritant
 Occupational contact urticaria – may be immunological (type I hypersensitivity reaction and
release of IgE from mast cells) or non-immunological
Common
causative
agents
Irritant occupational contact dermatitis
 Alcohols
 Disinfectants
 Petroleum products
 Soaps
 Solvents
 Wet work
Allergic occupational contact dermatitis
 Cobalt
 Chromium
 Cosmetics and fragrances
 Nickel
 Plants
 Preservatives
Occupational contact dermatitis
 Cow dander
 Food and animal products
 Flour and grains
 Rubber and latex
At-risk
occupations
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Hairdressers and beauticians
Health care workers
Cleaners
Construction workers
Cooks and caterers
Mechanics
Metal workers
Chemical/ petroleum plant operatives
Agricultural workers
Bakers
Farmers
Prevention

Education for workers

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
Limit exposure to causative agents: Gloves (cotton-liner if allergic to latex)
After-work conditioning creams provided
Specific treatments via GP if necessary