Dermatology Lesson Notes

Dermatology Skin Mean 2mm thick Epidermis = 0.2mm = cellular – from ectoderm Dermis = 1.8mm thick = vascular, collagen, elastic, glands, hair follicles – from mesoderm Then subcutaneous fat Keratinocytes – skin reproduction Melanocytes – pigmentation Langerhan’s cells – immune function Skin lesions Scales Papule Wheal Bulla – psoriasis, ringworm – wart – nettle sting, urticaria – 2nd degree burns Macule – freckles, measles Plaque – psoriasis Vesicle – chicken pox, herpes Ulcer – ruptured vesicle, injury Allergic reactions I – IgE immediate reaction e.g. acute urticaria à skin prick / serum Ab (RAST) tests II – Ab against cell bound antigens e.g. autoimmune blisters à immune-florescence / ELISA III – circulating immune complexes e.g. vasculitis à measure complex levels IV – T-cell mediated delayed hypersensitivity reaction e.g. allergic contact dermatitis à patch testing Sunlight Improves acne Worsens lupus, pellagra, porphyria & xeroderma pigmentosum Itching Local causes – tapework, hookwork, amoebiasis, allergic rhinitis, lichen simplex, vulvitis Systemic causes - Atopic eczema, Urticaria, Serum sickness, late pregnancy, parvovirus, drugs, vit A toxicity, conjugated jaundice, Hodgkin’s disease, renal osteodystrophy, dermatology problems e.g. icthyosis, pityriasis etc Urticaria (Hives) Itchy, erythematous eruption, flesh coloured wheals Due to local increased permeability of capillaries and small venules Can be associated with angioedema Papular Urticaria Hypersentivity to bite from flea/bed bug etc Urticaria pigmentosa Accumulation of mast cells in skin à orange / red maculo-papular rash. Urticariate with rubbing Can involve other tissue e.g. bone marrow Can be present in infancy Lesions become pigmented with time Rx with antihistamine + sodium chromoglicate (stabilises mast cells) Purpura Thrombocytopenic Decreased production – leukaemia, aplastic anaemia Increased destruction – ITP, SLE, Drugs, Alloimmune Consumptive – DIC, HUS, Thrombotic thrombocytopenic Purpura Congenital – giant haemangioma, wiskott-aldrich Vascular Congenital – e.g. connective tissue – OI, Elhers Danlos, Marfans Acquired – meningococcus Immune - HSP, SLE Drugs HSP Most common childhood vasculitis 1/3 proceeded by URTI Mainly extensor surface Can involve GI vessels à colic Renal involvement à glomerulonephritis Vascular lesions Stork mark (Capillary haemangioma) Fine non raised, pink macules on eyelids, mid forehead & nape of neck. On face fade over 1st year On neck become covered with hair Port wine stain (Naevus Flammeus) Present from birth Permanent vascular malformation of dermal vessels. Usually don’t cross midline Persists (don’t fade with age). Common on upper ½ of body If on CN V1 can have underlying eye / brain problems (Sturge-Weber syndrome) If around eye then increased risk of glaucoma Often darken with age and become more nodular Pulsed dye Laser Rx can help cosmetically Assoc with 2 syndromes: o Klippel Trenaunay Weber Syndrome § One or more distinctive port-wine stains with sharp borders WITH underlying … § Hypertrophy of bony and soft tissues, which may lead to local gigantism or shrinking. § Varicose veins § An improperly developed lymph system § IF NO PORT WINE STAIN = Klippel Trenaunay syndrome o Sturge Weber Syndrome § Port wine stain over 1st trigeminal distribution § Excess capillaries on pia à calcification à loss of nerve cells § Neurological Sx worsen with age à convulsions on contralateral side, muscle weakness, some have developmental delay & reduced IQ. § Can develop bulopthalmus and glaucoma Strawberry Naevus (cavernous Haemangioma) 5 x more common in girls Can affect up to 10% of children by age 1y Raised red haemangioma Usually appear 1-2 weeks after birth as plaque / nodule (can be present as telangectasia / bruise earlier) Increase in size until 6-9 months, then regress over 5 – 10 yrs Occasionally fully developed at birth and have rapid involution Best left untreated unless causing problems (e.g. over eye). Need close monitoring – steroids can be used if affecting hearing / vision Complications – ulceration, bleeding, function impairment (if blocks eye / ear), residual lesion (fibro-fatty lump / superficial haemangioma) Can have benign neonatal haemangiomatosis = multiple widespread haemangiomas or diffuse neonatal haemangiomatosis = above + organ involvement o Kasabach Merritt Syndrome § Large (<5cm) / rapidly growing § Trap platelets à thrombocytopenia & consumption of clotting factors § Can occur on any area of body Venous malformations Blue subcutaneous / mucosal nodules. Compressible. Enlarge on coughing / straining. Present at birth, enlarge with the child’s growth Possibility of sclerosing feeding vessels Lymphatic malformations Macrocystic – prev known as cystic hygroma – common in neck and axilla Microcystic – lymphangioma – fluid filled vesicles AV malformations Locally aggressive Can appear as port wine stain à increased flow with warmth and bruits HSP Can start as urticarial hives then progress to purpura Arthralgia and arthropathy (transient and remains within same joints (ankles, knees, hips)) Oedema of feet can be seen (transient) ITP Superficial bruising and petechiae (+/- mucosal bleeding from gums/nose) Often follows viral infection Immune destruction of platelets Can have intracranial haemorrhage Pertussis Periorbital petechiae after coughing spasm (also seen with NAI / cord around neck at birth) Naevi Epidermal Linear verrucous epidermal naevi (1/1000) Keratincyte naevi - present at birth as areas of light brown papules along Blasko lines Sebaceous Naevi Yellow plaques (oval / linear) mainly on head, cause alopecia if on scalp Can develop into neoplastic growths after puberty Dermal Congenital smooth muscle hamartoma (1/2500) Naevi on erector pilli muscles. Usually on trunk. Tan coloured, fade with time Connective tissue naevi Single / multiple skin coloured plaques with deposition of collagen and elastin Dermal melanocytes If trapped in dermis appear blue e.g. Mongolian blue spot (80% in dark skinned children), e.g. blue naevi (common in all races as dark papules in early childhood) Mongolian Blue-Spot o Blue / black discolouration to base of spine & buttocks o Mainly Afro-Caribbean / Asian infants. Can be up to 10% of white children o Fade over a few years o Document to exclude later child protection accusation Congenital Melanocytic naevi Melanocytes in epidermis / dermis Classified by size (small < 1.5cm, intermediate 1.5-20cm, giant > 20cm) 1% of children have at least one congenital naevus Small naevi à 10% of melanomas Giant naevi – 1 in 20,000 Mainly in trunk, low back & buttocks Grow in proportion to infant ½ of melanomas from these arise by 5 yrs Can affect meninges à hydrocephalus Giant naevi tend to be removed before 3/12 age Acquired melanocytic naevi = moles Congenital Hypopigmented patches Pale areas – reduced cutaneous melanin Vary in size from few cm to large areas covering trunk & limbs Can occur in Incontinentia Pigmenti Hypomelanosis of Ito Hypomelanotic macules along Blashkos lines Areas are present from birth and do not change Assoc with mental retardation, seizures, developmental delay and deafness Partial Albinism (piebaldism) AD Melanocytes absent from defined areas of skin NON progressive Waardenberg Syndrome AD Assoc with hypopigmented areas and white forelock ALSO high frequency sensorineural deafness, heterochromia, thin nose & squanre face Vitiligo Acquired hypopigmentation 50% of cases present before 20 years Can be assoc with IDDM, Pernicious anaemia & other endocrine disorders. Check skin carefully for malignant melanomas Occulo-cutaneous albinism type 1 Complete absence of melanin in hair, skin and eyes. Photophobia, mod-severe reduction in visual acuity & nystagmus OCA-1B = subgroup with some pigmentation in eyes & vision not as affected Occular Albinism Normal skin & hair colour (but lighter than siblings) Iris transillumination defects & congenital motor nystagmus Reduced visual acuity, refractive errors, fundus hypopigmentation, lack of foveal reflex and strabismus Other neonatal skin conditions Milia o White pimples on nose and cheeks o Aka milk spots Erythema toxicum neonatorum Common (up to ½ of mature neonates) in 1st few weeks Appears at 2-3 days Asymptomatic erythematous papulo-vesicles on face, trunk, nappy area, Resolves spontaneously in few days In dark skinned children = transient pustular melanosis à areas of hyperpigmentation which resolve in 2-3 months Neonatal acne (1% of children) Pustules of face & scalp in 1st month NO comedomes (black heads) Miliaria Occlusion of eccrine sweat glands assoc with overheating. 1st week = rare = miliaria crystallina – small vesicles on forehead. Rupture an heal within a week 1-4 weeks = miliaria rubra = red papules (+ pustules & vesicles) on neck = prickly heat Subcutaneous fat necrosis of the newborn Rare (more common in C-sect children). Occurs wks 0-4 Firm circumscribed flesh coloured / blue subcut nodules in fatty areas (buttocks, thighs) Assoc with hypercalcaemia. Resolves by 6m Neonatal lupus Transplacental transmission of anti Ro & anti La Ab 10% have congenital heart block ½ of neonatal lupus children have skin lesions Can be present at birth or develop a few weeks later (triggered by UV light). Red scaly patches, sometimes annular Mainly periorbital / malar May respond to topical corticosteroid, fades over a few months. Cutus Mamorata Physiological reaction to cold Mottling blue reticulated pattern Requires no treatment Seborrhoeic Dermatitis of infancy Well demarcated, erythematous, greasy scaly rash On scalp (cradle cap) OR nappy/axillary (glazed red eruption) à whole body Child is NEVER ill, not itchy Caused by yeasts Unlike eczema because not itchy & different distribution (confined to seborrhoeic areas) Spontaneously disappear (6-12 weeks) Rare after 9m Rx: usually self resolves. If severe à corticosteroid & antiseptic can improve recovery Irritant Napkin Dermatitis Irritant contact dermatitis from ammonia (alkali irritant) produced by bacteria from urine Very common after D&V Spares flexures as skin surfaces are opposed so no exposure Rx: change frequently, washing, often improves if left open to air, barrier cream If required can give topical steroid Candidiasis (monila) Satellite lesions + red background. Can be yellow, scaly plaques in nappy area May also have oral candidiasis Affects creases Swab then treat with topical nystatin Psoriasis Rare in infancy. If occurs is usually in nappy area Salmon pink, well demarcated, NOT scaly. Rx with steroids & tar Bullous impetigo Nappy and cord area, staph infection Discrete erythematous denuded areas – intact bullae rarely seen due to high friction area Rx with fluclox Aplasia cutis congenital (right) Focal absence of skin at birth Usually occurs to scalp in midline, can be on trunk / extremities Prevention of infection by grafting may be required Cutis Laxa Inherited disorder Skin hangs in folds Assoc with joint laxity & easy bruising e.g. connective tissue (NB not like elhers danlos where skin will spring back) Acrodermatitis Enteropathica Due to Inherited Zn deficiency Triad of: Dermatitis, diarrhoea & alopecia + Vesicular bullous rash around mouth & anus In infants à Persistent nappy rash with erosion of moist sites Fine sparse hair Failure to thrive & irritable Zn supplements à rapid improvement Atopic Eczema Incidence 15-20% (less common if breast fed for 1st 6m) Onset 12-18 months (90% present by 5 yrs) 70% resolve by 11yrs, 90% by 18y FH of asthma, hay-fever, asthma, skin prick tests can identify allergens No class preference Dx Itchy rash + 3 of the following Knees and elbows Personal / FH of atopy Dry skin for > 12 months Flexural involvement Onset < 2yrs old Dry, itchy, scratching, poor sleep à 2o S.Aureus infection In infants à dribble area (lick eczema) + extensor surfaces, usually spares nappy Older children à flexural - Dry, red, inflamed à scratching à thickening (lichenification) All ages à hands Rx Natural fibres, avoid biological washing powders Short nails & cotton gloves reduce scratching Ensure fully immunised Moisturise – oils / creams + bath oils (avoid soaps & detergents) Steroids – low dose regular or high dose intermittent Topical can à adrenal suppression Occlusion increases potency Tacrolimus (topical = calcineurin inhibitor) if failure of steroids and useful perioccular. Can à burning sensation and will photosensitise skin Bandaging – wet / dry over steroids to avoid scratching Oral sedating antihistamines to reduce itch and improve sleep Antibiotics as required for infection Avoid allergens – commonly foods, pollen and dust mites, Exclusion diets help in some cases Last lines – phototherapy, systemic steroids, ciclosporin, azathioprine Complications Secondary bacterial infections – most commonly S.Aureus HSV à eczema herpeticum (right) Allergic contact dermatitis Psoriasis g>b Uncommon < 10 yrs Incidence rises through teen years 50% have +ve FH (= more than in eczema) Assoc with HLA-DW6 T cell mediated, Immune driven disorder NOT as itchy as eczema Features Exacerbations with remissions Kobner Phenomenon Accelerated epidermal turnover Psoriasis Thick, silvery plaques – removal à pinpoint Epidermolysis bullosa simplex bleeding Rash of Systemic JCA New lesions on site of trauma = Koebner Warts Phenomenon Lichen planus, niditus & sclerosis Can occur to scalp, knees, elbows, umbilicus & genitalia Can à nail pitting Skin thickness (epidermis) is raised due to scaling Gentle trauma à pinpoint bleeds (Auspitz sign) Immune driven increased cell turnover à overactive keratinocytes Specific forms: Psoriatic erythroderma Local / general pustular psoriasis Linear psoriasis Guttate Psoriasis (droplets over trunk) Most common psoriasis in children typically initiated by streptococcus (exotoxin) in susceptible individuals (e.g. strep sore throat) à eruption of small red scaling lesions resolution within 2 months but liable to recur at any time Responds to Lassar’s Paste, Coal tar and topical corticosteroids More severe cases get PUVA and systemic treatments e.g. methotrexate & ciclosporin Treatment Emollients – minimises scaling Vit D Analogue – calcipotriol Coal tar – safe but messy Dithranol – effective but can burn UV light – for guttate flares. Risk of skin cancer Systemic – rarely used in children. Use methotrexate / ciclosporin Acne Infantile Acne Self limiting, effect of circulating maternal androgen More common in boys Can be with / without comedomes Rx of choice is erythromycin Acne Vulgaris Timing Rarely under 18 months If before puberty check adrenal pathology Common in puberty but still serious due to psych impact, Appearance Inflammation can be caused by proprionibacterium acnes Blockage of pilosebaceous units à comedomes & pustules Classically to face + back Treatment (aim to prevent permanent scaring) Good skin care to remove keratin plugs - Topical Benzyl peroxidase (use with Abx) Topical if focal Oral if widespread Topical Retinoids – if acne if comedogenic Oral tetracyclines are treatment of choice – but will stain adult teeth while forming & Teratogenic (stains teeth & bones of fetus) therefore need contraception Can predispose to Gr-ve and fungal infections Oral Erythromycin is an alternative If girls consider hormonal therapy (OCP) If severe à isotretinoin Indicated for moderate to severe acne with psychological distress Standard course is 4-5 months 30% cure 35% need subsequent topical / oral conventional 25% will relapse SE: Teratogenic – POP & barrier methods Inflammation – chelitis, cirrhosis (check LFTs), blepharoconjunctivitis, epistaxis Raised triglycerides & cholesterol Arthralgia, myalgia, depression, hair thinning, photosensitivity, staphylococcal infection DONT use with tetracycline as risk of Benign Intracranial Hypertension MUST check LFTs, Lipids (can increase lipids & derange LFTs) and B-HCG before starting Icthyotic disorders Skin resembles fish scales Ichthyosis Vulgaris Usually AD 1/250 of ppn Dry, finely scaling skin, spares flexures, face & palms 1st appears at approx 6 months Can complicate atopic dermatitis, Rx with E45 cream Recessive X-linked Ichthyosis Only affects males 1/2000 Scales are larger, darker and more adherent. Trunk & limbs affected, face usually spared Assoc with placental sulphatase deficiency à prolonged / difficult labour Collodion baby Autosomal recessive Baby at birth has skin which resembles dry plastic & cracks easily Blistering Diseases Neonates – most commonly infection à bullous impetigo Infants – infections, acute dermatitis, insect bites, erythema multiforme (target lesions common, blisters are rare) Chronic bullous disease of childhood – young children, small tense blisters in “string of pearls”, mainly perineal, usually spontaneous remission in a few yrs Infections e.g. impetigo, staph scaled skin syndrome, herpes simples, hand-foot & mouth disease Epidermolysis bullosa Inherited Non-inflammatory Blistering / bullous eruptions seen in 1st week of life in response to mechanical trauma Non scarring = epidermolysis bullosa simplex AD inheritance – ranges in severity Intra-epidermal Mild form, may not be recognised until later Blisters usually 1st noticed on hands & knees when becomes mobile (crawling) A more severe AR form may heal leaving atrophic areas Tend to improve by puberty Rx by puncturing blisters as they form Junctional Epidermolysis Bullosa – AR, blisters in lamina lucida. Scarring and affects hair and nails. Can à oesophageal strictures. Death by 3 years Scaring (dystrophic) forms Can be AD / AR Occur early & go deeper Scaring is destructive with loss of nails, ugly scars & contractures. Can get fusion of digits or result in amputations Immunobullous disorders e.g. dermatitis herpetiformis Rare in children Intensely itchy so blisters rarely seen (usually burst), extensor aspects (knees, sacrum, scalp) Can be assoc with coeliac e.g.pemphigus, phemphigoid Café-Au-Lait Patches NF1 TS Turners Russell-Silver McCune-Albright Fanconi’s anaemia Blooms syndrome Neurofibromatosis Type 1 = 1/5000 – error in neurofibromin AD inheritance – Chr 17 High penetrance, high rate of new mutations Clinical Diagnosis (need 2 criteria) • 6+ cafe au lait macules (may be present at birth) • Freckles in axillary / inguinal region (between 3 & 15 yrs) • 2 + iris hamartomas (occur 5-10yrs) = Lisch nodules (will be present in 90% of NF1 patients) • Optic glioma • Osseous lesions (thinning of long bone cortex, sphenoid wing hyperplasia) • 2 neurofibromas (occur after 10 yrs – soft pink lesion) or 1 plexiform neurofibroma (occur 1-2 yrs) • 1st degree relative with NF type 1 NB: cafe au lait macules also occur in type 2 NF and in McCune-Albright Syn, and in normal individuals Complications Neurological - low IQ, epilepsy, CNS tumours, optic / cord lesions Ortho – scoliosis, pseudoarthritis of tib & fib Opthal – congenital glaucoma Other – renal artery stenosis à high BP, phaeochromocytoma Type 2 (aka central neurofibromatosis) Chr 22 – mutation in tumour suppressor gene (Merlin) = AD Features: Bilateral acoustic neuromas à hearing loss at approx 20 yrs & tinnitus Cataracts Balance problems & vertigo (due to vestibular nerve branch affected) Headaches Facial nerve paralysis May develop other brain & spine tumours e.g. meningiomas / schawnnomas Tuberous Sclerosis AD TS1 = mutation in hamartin, TS2 = mutation in tuberin (both tumour suppressors) è Multisystem affecting ectoderm (+ eye & kidney & heart) è Non malignant tumours grow on brain, kidneys, heart, eyes, lungs & skin Triad of Skin lesions & epilepsy (70%) & mental retardation (70%) Skin lesions include: Ash leaf macule (a) – hypomelanotic - present from birth / early infancy, 0.5-3cm. see under wood’s light (b) Adenoma sebaceum (c) – Angiofibromatosis on nasolabial folds. Red macules & papules on nose & cheeks in butterfly distribution. Consist of blood vessels & fibrous tissue – occurs late childhood / puberty Shagreen patches (d) – thick leathery skin with orange-skin dimpling develop during adolescence as dermal plaque, usually in lumbar region Periungual fibromata (e) – aka Koenen’s tumours – small fleshy tumours around nails. Late childhood / puberty Forehead plaques: Raised, discoloured areas on the forehead. Can have cafe-au-lait macules Assoc with tumours – phakomata (flat grey lesions on macula (f)), malignant astrocytoma, rhabdomyoma (heart) à arrhythmias, & renal hamartoma Also renal, neuro and cardiac probs Incontinentia Pigmenti X linked dominant (female only –assumed lethal in males), NEMO gene. Usually obvious at birth Lesions follow blascko lines Stage 1 – vesicles + pustules - up to 6months (a) Stage 2 – linear verroucus plaques (b) Stage 3 – lineal whorled hyperpigmentation – can be different areas to stage 1&2 (c) Stage 4 – hypopigmentation atrophic lines (d) Also assoc with nail dystrophy, scarring alopecia, small teeth, unilateral breast aplasia. 10% have mental retardation & seizures Albinism Usually AR Inherited disorder of melanin production Congenital partial or complete absence of pigment from skin & hair & can involve iris Photophobia, nystagmus, decreased visual acuity Increased risk of cutaneous malignancy Pibaldism Symmetrical depigmentation, AD Ectodermal dysplasia Problems with hair, teeth, nail, sweat glands etc Hidrotic form Hyperkeratosis of hands & feet, sparse hair, hypoplastic nails, normal teeth Child is able to sweat Anhidrotic form Inability to sweat à hyperpyrexia Think skin, sparse hair, peg like teeth X-linked recessive, more severe in males Xeroderma Pigmentosum AR à defect in DNA repair ↑ photosensitivity & freckles keratoses à malignant skin tumours Infiltrations Cutaneous mastocytosis à Urticaria pigmentosa Presents at 0 - 2 yrs Yellow / brown macules / papules / plaques on trunk and proximal limb Rubbing à histamine release à wheal Tend to clear spontaneously NB: avoid aspirin and morphine If diffuse à blistering & thickening everywhere Cutaneous Histiocytosis Langerhans cell histiocytosis (1-4 yrs) 40% affects skin & is often the first diagnosis point Brown Papules & purpura à confluent erosions & crushing Mainly in scalp & flexures & nappy Often misdiagnosed a seborrhoeic dermatitis Assoc with DI Can be treated with topical steroids, nitrogen mustard / chemo Non Langerhans cell histiocytosis (0-1y) Juvenile xanthogranuloma = benign accumulation of lipid laden macrophage in dermis à red dome shaped nodules 2-20mm à yellow / brown & resolve spontaneously Erythema nodosum Painful, indurated, shiny, red, hot elevated (subcut / dermal) nodules of 1-3cm usually on shins Assoc with fever, malaise, Arthralgia Fade to purple then bruise & heal without scaring Uncommon under 6 years f>m Causes 30% are idiopathic Infection Bact – Strep, leptospirosis, cat-scratch, psittacosis, yersina Virus – EBV Others – TB, tularaemia, histoplasmosis, toxoplasmosis, coccidiomycosis Drugs – sulphonamides, OCP Systemic – SLE, Vasculitis, regional enteritis, UC, Bechets Can involve other sites e.f. thighs, arms, face Resolution in 5-6 weeks (turn blue during resolution) – can leave patches of hyperpigmentation Treatment is symptomatic Erythema Multiforme Local vascular reaction which can be triggered by viral infections (e.g. herpes), or mycoplasma or drugs Minor-symetrical shaped target lesions on hands, feet & extensor surfaces. NON pruritic Target lesions Can be caused by infections/ drugs / etc Affects limbs > trunk If involves mucous membranes = Steven’s Johnson Syndrome Erythema Marginatum Rheumatic fever = flat, non-painful, normal areas of skim surrounded by red rings with creeping borders Erythema Chronicum Migrans Lyme Disease – begins as annular lesions Stevens-Johnson Syndrome Severe bullous form of erythema multiforme involving mucous membranes e.g. mucositis, conjunctivitis, corneal ulceration, uveitis and genital ulceration Causes: Sulphonamides, HSV infections, Ibuprofen, Strep sore throat Assoc problems with pneumonia, polyarthritis, fluid & electrolyte imbalance, urine retention and inability to take oral nutrition Management = remove cause (drug etc), monitor electrolytes and treat 2o infections Pityriasis Rosea Increased in Nov-Feb Teens > infants Herald patch seen 3-4 days before the main eruption Acute, self-limiting erythematous scaling (brown/pink) macules, centrally distributed (trunk + proximal limbs = Victorian bathing costume distribution) Itching & fine scaling Rx: corticosteroids à resolution in 6-8 wks Granuloma annulare Asymptomatic dermal nodules Evolve into irregular annular lesions with raised borders Usually on elbows, back or fingers or dorsum of feet May take 1-2 years to resolve Can be assoc with DM Bacterial Infections (see also infection notes) Cellulitis Acute cellulitis (= erysipelas) is usually due to Grp A Haemolytic streps Rx ben-pen / pen-V (or erythromycin if allergy) Low grade cellulitis is more common & can recur Usually haemolytic streps, can also be S.aureus, S.Pneumonia or HiB Rx – Ben-Pen / Pen-V + fluclox Perianal cellulitis In young children – usually Grp A strep à itching, erythema, fissures, pus or PR bleed Rx – oral Pen V Impetigo S.aurus (S. Pyogenes) Can be recurrent if child is a carrier (usually nasal carriage) Usually enters via insect bite / dermatitis / scabies Short vesicular phase à Honey gold crusts (dried serum) on a red base Usually on the face / other local areas if scratch / bite Heals without scarring Usually treated with topical fuscidin in primary care à oral fluclox If bullae present = bullous impetigo Can have complications of pneumonia & osteomyelitis Staph scaled skin syndrome (Ritters disease) Due to exotoxin from some strains of staph Usually < 5 yrs Most of skin BUT not mucosa Bacteria (usually from nasopharynx, conjunctiva or umbilicus) release epidermolytic toxins à erythema in flexures à superficial erosions Preceded by conjunctivitis/otitis media/URTI Large blisters à red raw areas of underlying skin on bursting Nikolsky sign = gentle pressure à blister à layers of epidermis will separate Crusting and fissuring around eyes, nose & mouth Accompanied by fever & malaise Siblings may have impetigo Ix: Take blood cultures, Bullae are usually sterile but samples of fluid should be sent Rx: penicillinase resistant penicillins, fuscidic acid, erythromycin or cephalosporins Recovery in 5-7 days Non-scaring Complications: Secondary bacterial infection, generalised sepsis, fluid & electrolyte imbalance Toxic Shock syndrome High fever, macular rash à desquamation, hypotension, D&V, myalgia etc Erysipelas Superficial strep infection – well demarcated erythema, systemically unwell with febrile. Rx with penicillin Meningococcal disease Rapidly progressive life threatening condition Non blanching petechiae and purpura Scarlet fever Group A strep Diffuse erythema over abdomen, trunk and skin folds Sandpaper texture Pastia’s lines = red lines seen at skin creases Perioral pallor, strawberry tongue and can have desquamation of fingers & feet Viral Infections 1o herpes simplex Can cause gingivomastitis (fever, irritable, difficulty swallowing, ulcers on mucosa) Can get vulvovaginitis, keratoconjunctivitis or on rare occasions encephalitis. Rx: careful nursing to ensure fluids, oral acyclovir Varicella 10-14d incubation Then fever & malaise (mild systemic upset) Itchy erythematous vesicular rash Macules à vesicles à crust over (lesions at all stages seen together) Can involve mucous membranes 5-10% get secondary bacterial infection Other complications include pneumonitis, encephalitis, and cerebellar ataxia Can resemble eczema herpeticum Eczema Herpeticum Acute and can be disseminated Usually occurs over patches of eczema Sudden worsening of eczema à vesicles & oozing with systemic unwell Lesions may become haemorrhagic Can also get 2o bacterial infection Rx – IV acyclovir + swab to exclude secondary bacterial infection + broad spectrum Abx STOP topical steroids (these encourage spread) Complications: Encephalitis + ocular complications Viral Warts Usually HPV Harmless, self limiting Rx: only if discomfort, cryotherapy / salicylic acid Moluscum contagiosum Pox virus à small discrete pearly lesions with umbilication Affects covered areas of body Common in infants & young children Mildly itchy Can complicate atopic eczema. *** Steroids à worsen lesions so keep to emollients Self limiting - recovery in 6-12 months BUT are infectious therefore treatment can help reduce spread AND can get secondary infection requiring topical antiseptic / Abx Treatment = lance lesion with sharp instrument dipped in liquid phenol BUT can à scarring Measles Incubation 8-14 days Then coryza & koplik spots Rash starts behind ears then spreads = maculo-papular Complications include pneumonia, OM, encephalitis, myocarditis, lymphopenia. SSPE can occur 5-10 years after initial infection Fungal infection Ringworm (fungus) Can be hair/scalp/nails Can à pustules (kerion) Tinea Pedis - Uncommon in children, Rx: imidazole Tinea corporis – from cats & guinea pigs Tinea capitis – dermatopyte Highly contagious - Especially in afrocaribean children Usually Trichophyton tonsuratis, rarely microsporum canis Papule at base of hair follicle è Spreads peripherally è Scaly circular plaque = ringworm, with broken infected hairs = “exclamation mark hairs” è Pruritis & alopecia, rarely scars è Can à Kerion – boggy granulomatous mass with sterile pustules Dx – fungus on hair / scale Rx – griseofulvin for 3/12 / ketoconazole Infestations Scabies Sarcoptes scabiei (var. Hominis)= Mite spread by close contact Female burrows to lay eggs Mature to mate in 2 weeks Invades horny layer of skin to lay eggs Itching is due to allergic reaction to mites & products Occurs 6/52 after 1o infection, 48 hrs after reinfection Look for burrows (wavy dark lines with papule at one end) - Hands wrists, elbows, axillae, feet, genitals affected with intense itch & 2o erythematous popular rash More common in immunosuppression and downs Rx: Treat on suspicion - 5% permethrin (x2 at 1/52 apart) entire family Head lice (pediculosis capitis) Common in 4-11yrs 1-3mm long, live off host blood Females lay eggs close to scalp = light grey Nymphs hatch in 7d & mature in 10-14d à mate à lay eggs Scalp and nape of neck irritation Can get secondary bacterial infection “Nits” = empty egg cases Can also affect genitals & eyebrows Rx: ONLY Rx if seen to avoid resistance Leave lotion for 12 hours Permethrin / Pyrethrin / malathion Repeat in 7 days to kill hatchlings Kawasaki Clinical diagnosis High fever for 5 days + four out of: • Polymorphous rash (usually maculopapular) • Mucosal involvement (cracked lips, strawberry tongue) • Erythema & oedema of fingers & toes fb desquamation (after approx. 10 days) • Non-suppurative conjunctivitis (Only otherwise occurs in measles / TSS) • Cervical lymphadenopathy Differentials include • Strep (scarlet fever) • Staph (TSS / SSSS) • Measles, Rubella, Roseola infantum, EBV, Influ A / B, Adenovirus • Mycoplasma Pneumoniae • Stevens Johnson Syndrome • Systemic JIA Complications include: Aseptic meningitis, urethritis, sterile pyuria, arthritis, D&V, mild hepatitis, coronary artery aneurysms & thrombosis (2-4 weeks from onset) Treatment: high dose gamma-globulin + aspirin. Cardiology RV & echo Drug eruptions Uncommon in young children If seen = usually maculopapular eruption/ urticaria If severe can be Steven’s Johnson = mucosal involvement + skin loss (e.g. sulphonamides / anticonvulsants (carbemazepine / phenytoin)) Hair Alopecia areata Well circumscribe hair loss with normal underlying scalp (smooth, non scaly) Exclamation mark hairs seen Usually localised but can extend to total head and total body 5-25% have +ve FH Usually regrows white (within 6-9 months), then coloured Linked to autoimmune conditions / vitilgo Diffuse hair loss Can follow any serious illness or sign of thyroid / parathyroid problems Congenital Allopecia Can be due to incontinential pigmenti, hypomelanosis of ito or aplasia cutis (& others) Traumatic – e.g. tight ponytail / trichotillomaina Scaring – damage to hair follicle Systemic – e.g. low T4 / DM Cutaneous manifestation of systemic diseases Dermatomyositis – helitrope rash & Gottrons Papules Addisons – assoc with vitiligo Cutaenous T-cell lymphoma –mycosis fungoides = superficial patchy dermatitis à tumours Coeliac – dermatitis herpetiformis UC / Crohns – erythema nodosum DM – acanthosis nigricans Hep B – Gianotti-Crosti (right) = non pruritic erythematous papules on face, buttocks & extremities (also assoc with CMV) Zinc deficiency Can occur in prems after bowel resection for NEC Eczema (perioral, perineal, scalp) Diarrhoea Stomatitis Faltering growth Hair loss Acrodermatitis enteropathica = rare AR defective Zn absorption from gut = same manifestations Dx: low serum Zn levels + low ALP Rx: supplements Phyto-photodermatitis Combination of sunlight and certain plants (hogweed) Spares areas covered by clothes