Dermatology Flashcards
What are 2 topical corticosteroids classified as “Very Potent” in Australian Classifications
Betamethasone dipropionate 0.05% in optimised ointment
Clobetasol propionate 0.05% ointment
What are 3 topical corticosteroids classified as “Potent” in Australian Classifications
Betamethasone dipropionate 0.05% in standard ointment
Betamethasone valerate 0.1% ointment
Mometasone furoate 0.1% ointment/cream
What are 5 topical corticosteroids classified as “moderate” in Australia
Betamethasone dipropionate 0.05% Cream/lotion
Betamethasone valerate 0.05% ointment and vream
Triamcinolone acetonide 0.1% cream
Methylprednisolone aceponate 0.1% ointment/cream/lotion
Clobetasone 0.05% cream
What are 2 topical corticosteroids classified as “Low potency” in Australia
Hydrocortisone or hydrocortisone acetate 0.5%, 1% (ointment/cream/lotion)
Desonide 0.05% (ointment/cream/lotion)
Features of different forms of topical corticosteroids
Ointments:
- improve drug absorption due to occluding skin and enhancing hydration
- greasy, difficult to spread, poor adherence
Creams:
- combo of 1 or more non-mixable liquids + emulsifying agent
- less greasy, easy to spread
- washable in water
Lotions:
- insoluble preparations dispersed into liquid
- may need shaking to prepare for use
- easy to apply
- can cover extensive areas
- preferred for children, and hairy skin
Local adverse effects of topical steroids
- Atrophy (skin transparency, brightness, telangiectasia, striae, easy bruising)
- Rosacea, acne or perioral dermatitis when used on face
Less common:
Hypopigmentation, delayed wound healing, glaucoma (when used around eye), rebound effect when ceased, loss of clinical improvement after period of use, masking or stimulation of cutaneous infections e.g. tinea incognito
Systemic adverse effects of topical corticosteroids
Uncommon, associated with prolonged use of high potency steroids in large or denuded areas
- reversible HPA axis suppression
- Addisonian crisis on ceasing
- Cushing’s syndrome
- DM
- hyperglycaemia
Diseases likely to be highly responsive to topical corticosteroids
Inflammatory conditions on thin skin;
e. g.
- intertriginous psoriasis
- Children’s atopic dermatitis
- other intertrigos
Diseases likely to be moderately responsive to topical corticosteroids
Psoriasis
Adult atopic dermatitis
Nummular eczema
Diseases likely to be least responsive to topical corticosteroids
Chronic, hyperkeratotis, lichenified or indurated lesions. e.g.
- palmo-plantar psoriasis
- lichen planus
- lichen simplex chronicus
Sites and absorption of topical corticosteroids
Palms, soles - poor absorption (0.1-0.8%)
Forearms - poor (1%)
Scalp and intertriginous areas - moderate (4%)
Face - moderate (10%)
Scrotum and eyelids - very high (40%)
Choice of topical corticosteroid vehicle for disesase
Ointments: thick, fissured lichenified lesions SHOULD NOT BE USED IN FLEXURAL OR INTERTRIGINOUS areas
Creams: most areas except scalp/hairy skin
Lotions: extensive areas
Solutions, gels, sprays, foams: scalp and hairy skin
Maximum doses of topical corticosteroids in adults
Potent: 45g/week
Moderately potent: 100g/week
Maximum duration of topical steroids
Face: 2 weeks
Rest of body: 3-4 weeks
Adjunctive treatments with topical corticosteroids
Skin care to improve skin’s overall integrity and improve clinical outcome
- soap-free cleansers
- moisturisers
Focused history for skin check
Presenting complaint - new, changing or concerned lesions
Occupation, sun exposure and sun protection
Personal and family history of NMSC and melanoma
General medical history (current and past)
Drug history (esp. anticoagulants, immunosuppressants)
High risk patients for skin cancer and how frequently should have skin check
3 monthly self examination, 12 monthly skin check
- red hair
- Type I skin >45y
- type II skin >65y
- Family history of melanoma in first degree relative in patients >15y
- > 100 naevi (>10 atypical)
- past history of melanoma
- Past history of NMSC or >20 solar keratoses
Medium risk patients for skin cancer and recommended frequency of skin checks
3-6 monthly self-check, 2-5 yearly skin check with doctor
- Blue eyes
- Type 1 skin 25-45y
- Type II skin 45-65y
- Type 3 skin >65
- Family history of NMSC
- Past history of solar keratosis
- multiple previous episodes of sunburn
Low risk patients for skin cancer and recommended frequency of skin checks
Annual self-check, one-off skin check with doctor for assessment of risk and advice regarding skin care
- Type I skin <25y
- Type II skin <45y
- Type III skin <65y
- Type 4 & 5 skin
Cure rate for solar keratoses with cryotherapy
86-99%
Contraindications for cryotherapy
- Lesions with poorly defined margins
- Lesions >2cm diameter
- Lesions >3mm deep
- lesions tethered to underlying structures
- lesions on ala nasi, eyelids, nasolabial fold and pre-auricular skin
- recurrent lesions
- agammaglobuliaemia cryoglobulinaemia
- blood dyscrasias of unknown origin
- cold urticaria
- Raynaud’s disease
- Pyoderma gangrenosum
- collagen and autoimmune disease
- avoid if histology is uncertain
- can be problematic for patients with Fitzpatrick III-V due to post inflammatory hyperpigmentation and hypopigmentation
- risk of alopecia on hair bearing skin e.g. beard area
Recommended technique for cryotherapy of solar keratosis
1x freeze cycle of 15 seconds, 1mm margin
Expected results after cryotherapy with liquid nitrogen
Day 1: red, swollen, blister may develop and may fill with blood - best to leave alone
Days 2-3: Treated area becomes weepy, leave skin open to air if mild and wash with soap and water, if excessive cover with dressing or topical antiseptic
Days 3-4: Area should stop weeping and form scab which usually spontaneously falls off within a week
Should then heal without a scar - may be slightly darker or lighter skin temporarily (may be permanent)
Indications to biopsy a clinical actinic keratosis
"Thickness" on palpation Pain - particularly on lateral pressure Bleeding Rapid growth Failure of standard topical treatments
recommended biopsy techniques for NMSC
Excisional
Punch from CENTRE of lesion if diagnosis required before management, unless ulcerated centre then use more distal site of lesion
- Incisional biopsy may be an option for ulcerated lesions including peripheral and central ulcerated components
Shave biopsy not advised
*BCC tends to be heterogenous and partial punch biopsy may fail to identify aggressive component in 15%
Recommended biopsy technique in pigmented lesions
If requires biopsy, excisional biopsy with 2mm clinical margins should be performed
EXCEPT:
- broad lesions on face may consider shave or incisional biopsy if no invasive component on palpation
- large lesions or lesions on functionally sensitive areas e.g. sole of foot - may consider punch or incisional biopsy to confirm diagnosis
Choosing inflammatory lesions to biopsy
Generally, choose estalbished lesions, not ones that are so old they have scarring or crust surface
In blistering, pustular or vasculitis conditions, early lesions within 48h of appearance are better
If other lesions available, avoid sites such as:
- cosmetically sensitive e.g. face
- areas prone to hypertrophic scarring e.g. shoulders, chest, breast
- legs as poor healing and venous stasis changes histo
- high risk areas for infection (axilla and groin)
- bony prominences or pressure bearing areas
Good areas: thighs, abdo, back, arms
Important info to include on request form for skin biopsy
Patient age and gender Precise anatomical site of biopsy morphological description of lesion(s) + any evolution Distribution of lesions Clinical impression and differentials Prior skin biopsy results or diagnoses Medications if drug eruption is a differential Other relevant patient clinical history
Specify if ancillary testing required
Provision of dermatoscopic and clinical photographs if possible
Post skin biopsy care
Dress with moist occlusive dressing and paraffin ointment and leave alone for 24-48h
After this, gently clean wound daily with warm water and reapply paraffin ointment with non-stick dressing until re-epithelialisation is complete
If sutures present, remove after:
- 5-7 days face
- 12-14 days back and legs
- 7-10 days other areas
Duration to leave sutures in for body sites
Face: 5-7 days
Back or legs: 12-14 days
Other areas: 7-10 days
Clinical features of cutaenous SCC
Enlarging scaly or crusted lumps (usually arise within pre-existing IEC or AK)
May ulcerate
Often tender or painful
Located on sun-exposed sites
Risk factors for cutaneous SCC
Older age, male gender Previous SCC or other skin cancer Actinic keratoses Outdoor occupation or recreation Smoking Fair skin, blue eyes, red/blond hair Previous cutaneous injury, burn, disease Inherited syndromes (albinism, xeroderma pigmentosum) Immune suppression/organ transplant
Features of high risk cutaneous SCC
Diameter 2cm or more
Location on ear, vermilion of lip, central face, hands, feet, genitalia
Arising in elderly or immune suppressed patient
Histological thickness >2mm, poorly differentiated histology or with invasion of subcut tissue, nerves and blood vessels
Margin for cutaneous SCC excision
3-10 mm
Risk factors for BCC
Elderly males Previous BCC or other skin cancer Sun damage Repeated prior episodes of sunburn Fair skin/blue eyes/ blond/red hair Previous cutaneous injury, thermal burn, skin disease Inherited syndromes - Xeroderma pigmentosum - Gorlin syndrome - Rombo syndrome - Oley syndrome
Clinical features of BCC
Slowly growing plaque or nodule
Skin coloured, pink OR pigmented
Spontaneous bleeding or ulceration
Clinical subtypes of BCC
Nodular:
- most common
- shiny/pearly nodule with smooth surface
- may have central depression/ulcerations/rolled edges
- blood vessels cross surface
Superficial BCC
- most common type in younger adults
- most common type on upper trunk and shoulders
- slightly scaly, irregular plaque
- think, translucent rolled border
- multiple microerosions
Morphoeic/sclerosing BCC:
- usually in mid-face
- waxy, scar-like plaque with indistinct borders
- may infiltrate cutaneous nerves
Basosquamous carcinoma
- mixed BCC and SCC
- infiltrative growth pattern
- potentially more aggressive than other forms of BCC
Treatment options for BCCs
Excision with 3-5mm margin: nodular, infiltrative or mrorphoeic
Moh’s surgery: high risk areas (face around eyes lips and nose)
Superficial skin surgery: shave, curettage and electrocautery
Cryotherapy: suitable for small superficial BCCs on covered areas of trunk and limbs (not head and neck or distal to knee
Photodynamic therapy: low-risk small superficial BCCs, not in sites of high risk of recurrence
Imiquimod: superficial BCCs <2cm
Fluorouracil: small superficial BCCs, high risk of recurrence
Radiotherapy: mainly used if surgery not suitable
Risk factors for melanoma
Increasing age
Previous melanoma or NMSC
Many melanocytic naevi
>5 atypical naevi (large or dysplastic on histo)
Strong family history of melanoma (2+ first degree relatives affected)
White skin that burns easily
Parkinson disease
Precursor lesions for melanomas
75% arise from otherwise normal-appearing skin
Benign melanocytic naevus
Atypical or dysplastic naevus
Atypical lentiginous junctional naevus or atyipcal solar lentigo
Large congenital melanocytic naevus
Most common sites for melanomas
Males: back
Females: legs
Dermoscopic signs of melanoma
Disorganised asymmetrical pigment network
Atypical vascular patterns
Blue-grey structures
Multiple colours
Clinical subtypes of melanoma
Flat/horizontal growth:
- superficial spreading
- lentigo maligna
- acral lentiginous melanoma
Vertical growth/deeper tissues:
- nodular
- mucosal
- desmoplastic/neurotropic
- Spitzoid
- spindle cell
- ocular
Diagnosis of melanoma
Elliptical excisional biopsy with 2mm margin for suspicious pigmented lesions
Special circumstances: deep shave biopsy or punch biopsy
Difference between ephelides and lentignes
Ephelides = freckles, inherited condition, not present at birth, no increase in melanocytes, fade in winter months
Lentignes: increased number of melanocytes, do not fade in winter months, may be precursor to other lesions e.g. seb K, naevi
What is solar elastosis
Yellow, thickened appearance of skin as a result of sun damage/photo-ageing (also result of smoking)
What is Leser-Trelat sign
Eruptive appearance of many seborrhoeic kerkatoses due to underlying malignancy (most commonly gastric adenocarcinoma)
Dermatoscopic clues of seborrhoeic keratosis
- Multiple orange or brown clods
- White “milia-like” clods
- Curved thick ridges or furrows forming brain-like (cerebriform) pattern
Treatment options for seborrhoeic keratosis
Cryotherapy Curettage/electrocauterisation Laser surgery Shave biopsy Chemical peel
Other names that may be used to describe skin tags
Papilloma
Acrochordon
Fibroepithelial polyp
Soft fibroma
Treatment options for skin tags
Cryotherapy
Excision (often with scissors)
Electrosurgery/diathermy
Ligation
Differentials for skin tags
Seborrhoeic keratoses
Viral warts
Molluscum contagiousum
Risk factors for worse/more skin tags
Obesity
T2DM
Clinical features of keratoacanthoma
Rapidly growing lesion over a few months, starts as small pimple/boil-like lesion but full of solid keratin then grows rapidly
May start at site of minor injury to sun damaged and hair-bearing skin
Cells from which keratoacanthoma arises
Hair follicle skin cells
Vascular birthmarks
Naevus simplex/Stork Mark: Pink-red on forehead/brow/upper eyelids or nape, self-resolve by 1-3 years
Naevus Flammeus/Port wine stain: If on face may indicate neuro or opthal structural abnormality and require investigations, otherwise darken and thicken overtime. Never fade
Infantile haemangioma/strawberry naevus:
- often unapparent at birth and grow rapidly for several months before gradual involution over several years, treat only if required for severe symptoms (e.g. eyes, airway etc.) with propanolol +/- prednisolone
Venous Malformations: skin coloured, blue or purple swellings anywhere on body, may become more obvious over time, grow in proportion to child’s general growth
Common isolated/local types of telangiectasia
Spider telangiectasia: central arteriole and radiating capillaries, arise more often in response to oestrogen (pregnancy, liver disease)
Venous lake: blue or purple compressible papule due to venous dilation, often on lower lip or ear, treat for cosmesis only (sclerotherapy, cryotherapy, IPL, laser)
Features of benign hereditary telangiectasia
Inherited autosomal dominant disease
Lesions appear in first years of life, rarely present at birth, more prominent in pregnancy
Widely distributed over face, neck, upper trunk, dorsal hands and knees
As age, increase in size and become paler
NO mucosal involvement
Asymptomatic and DO NOT bleed
Hereditary haemorrhagic telangiectasia
Rare inherited disorder presenting usually after 12y with recurrent nosebleeds, telangiectases that develop elsewhere after puberty, mostly on upper half of body INCLUDING MUCOSAL MEMBRANES. May have GI bleeding also
Diagnostic criteria for hereditary haemorrhagic telangiectasia
- Recurrent nosebleeds
- multiple telangiectases on skin and mucous membranes
- Involvement of internal organs
- affected parent, sibling or child
Malignant vascular tumours
Kaposi sarcoma
Angiosarcoma
Intravascular B-cell lymphoma
Risk of a single solar keratosis becoming malignant
1/1000 per annum
Treatment for tinea infections
anywhere EXCEPT scalp or nails: Topical treatment unless extensive (Canestan, Daktarin, terbinafine creams) until rash completely clears AND THEN FURTHER 2 WEEKS
For scalp or nails: oral terbinafine, fluconazole or itraconazole
+ for macerated lesions make sure kept dry
Clinical presentation of tinea capitis
Patchy alopecia
Scalp scaling
Broken hairs at scalp surface/black dots
Kerions (abscess-like lesions that are tender and fluctuant)
Favus (yellow crusts and matted hair)
Wood lamp examination may be useful in some cases
Most common organisms causing tinea
Trichophytum rubrum Microsporum canis (from cats and dogs) Trichophytum verrucosum (from farm cattle) Trichophytum interdigitales
Diagnosis of fungal infections
Fungal microscopy and culture PRIOR to antifungal treatment:
- skin scrapings
- subungual debris
- nail clipping
- plucked hairs
- scalp scales may be removed with a toothbrush
Predisposing factors to candidal infection
Infancy or elderly Warm climate Occlusion e.g. plastic pants, nylon pants, dentures Broad spectrum antibiotic treatment High oestrogen (OCP/pregnancy) Endocrine disorders (Cushing, DM) Iron or other nutritional deficiencies General debility e.g. cancer Immunodeficiency or suppression Underlying skin disease e.g. psoriasis, lichen planus
Risk factors for ORAL candidiasis specifically
Maternal vaginal yeast infection in newborns Dry mouth (e.g salivary disease or meds) Dentures Smoking Inhaled corticosteroids
Prevention of oral candidiasis
Good dental/oral hygiene
Warm saline as mouth wash, avoid antiseptic mouth washes
Rinse mouth after inhaled corticosteroids
Clean dentures with anti-candidals BD and store in dry place overnight
Treatment of oral candidiasis
Confirm candida before commencing treatment!
Denture-associated, managed with denture hygiene only
If antifungal therapy indicated:
amphotericin lozenges/miconazole gel/nystatin drops
Each is QID dosing for 7-14 days
Discuss with specialist if immunocompromised
Clinical features of CANDIDAL intertrigo
Erythematous and macerated plaques with peripheral scaling
+/- superficial satellite papules or pustules
Diagnosis usually clinical
Management of candidal intertrigo
Manage predisoposing factors
Topical antifungal e.g. clotrimazole for 2 weeks
If topical treatment impractical or response is poor, PO fluconazole as single dose
Treatment of nappy rash candidiasis
Keep child dry, change when wet
Wash hands before and after changing
Avoid plastic pants
Topical antifungal creams
Risk factors for pityriasis versicolor
Young adults most frequently M>F
More common in hot, humid climates
Heavy perspiration
May clear in winter months and recur each summer
Cause of pityriasis versicolor
Malassezia yeasts, most commonly:
- M globosa, M restrica, M sympodialis
Clinical features of pityriasis versicolor
Affects truck, neck and/or arms - uncommon elsewhere
Scaly patches coppery brown OR paler than surrounding skin OR pink
Treatment of pityriasis versicolor
Mild disease: topical antifungal creams (azoles or terbinafine creams or shampoos)
Oral antifungals if extensive or topical agents failed: itraconazole or fluconazole for few days oral terbinafine not useful for malassezia
note white marks may persist long after scaling and yeasts gone, further antifungal unhelpful in this case
Recurrent pityriasis versicolor treatment
Repeat antifungal treatment when scale recurs
If frequent: antifungal shampoo OR oral antifungal treatment 1-3 days each month
Prevalence of dermatitis
Will affect 1 in 5 people at some point in their lives
General treatments for dermatitis
- reduce frequency and duration of bathing (2-3 mins)
- use lukewarm/tepid water for bathing
- replace soap with mild soap-free cleanser from chemist
- wear soft, cool clothes e.g. cotton (avoid coarse fibres e.g. wool or synthetic)
- avoid irritants (chlorine, sand, grass, dust, detergents etc.) and wash immediately after coming into contact
- Liberal, regular use of non-perfumed emollients
- topical steroids
Usual age of atopic dermatitis
Most will develop before the age of 2, unusual before 4 months, symptoms worst 2-4y then tend to improve
Distribution of atopic dermatitis rash in infants
Often widely distributed, dry, scaly and red
Cheeks often first place affected
Nappy area often spared due to moisture retention
Clinical features of atopic dermatitis in toddlers and pre-schoolers
More localised and thickened
Vigorous itching
Extensor surfaces (esp wrists, elbows, ankles, knees)
Clinical features of atopic dermatitis in school-aged children
Flexural pattern - mostly elbow and knee creases
Other areas: eyelids, earlobes, neck and scalp
May develop pompholyx
May develop a nummular pattern
mostly improves during school years
Clinical features of atopic dermatitis in adults
Often drier and more lichenified than in children
Commonly persistent localised eczema in hands, eyelids, flexures, nipples
Contributes to occupational irritant contact dermatitis
Wet wraps for eczema
Layer of corticosteroid under wet layer of clothing or towel for 15-20 minutes
Bleach baths for eczema
Indicated to manage recurrent S. aureus infections
twice per week
Clinical features of periorifacial dermatitis
Clusters of small papules and surrounding erythema, may be scaly and occasionally vesicles or pustules develop
5-10mm skin adjacent to vermilion unaffected (contrast to contact dermatitis)
Precipitants of periorifacial dermatitis
Topical steroids (esp potent) Inhaled or intranasal steroids Thick moisturisers Sunscreen/cosmetics Inadequate face-washing Pregnancy or other hormonal change
Treatment of periorifacial dermatitis
- Avoid oil-based facial creams
- cleanse face twice daily with mild soap or non-soap cleanser
- Oral anti-inflammatory antibiotics for 4-8 weeks
- topical agents not effective and generally best avoided
- if already on topical steroid, possible flare up on stopping, if necessary continue with weaning onto milder product until weaned off
Age of onset of seborrhoeic dermatitis
Infantile: <3 months, resolves by 6-12 months
Adults; tends to begin in late adolescence, prevalence greatest in young adults and elderly
Risk factors for severe adult seborrhoeic dermatitis
Oily skin Familial tendency to seborrhoeic dermatitis Family history of psoriasis Immunosuppression Neurological and psychiatric disease Treatment for psoriasis Lack of sleep and stressful events
Clinical features of pompholyx/vesicular hand dermatitis
Intensely itchy crops of skin-coloured blisters on palms and sides of hands and fingers +/- feet
Common trigger of pompholyx
Emotional stress (which causes hyperhidrosis)
Cause of seborrhoeic dermatitis
Unclear, related to malassezia yeasts
Clinical features of infantile seborrhoeic dermatitis
Cradle cap/ armpit or groin fold rash
- Salmon-pink patches that may flake or peel
- not very itchy, baby often undisturbed
Clinical features of adult seborrhoeic dermatitis
Affects scalp, face (creases around nose, behind ears, within eyebrows) and upper trunk
- winter flares, improve after sun exposure
- minimal itch
- combo oily and dry mid-facial skin
- ill-defined localised scaly patches or diffuse scale in scalp
- blepharitis
- salmon-pink, thin, scaly, ill-defined plaques in skin folds on side of face
- rash in skin folds
- superficial folliculitis on cheeks and upper trunk
Treatment of infantile seborrhoeic dermatitis
Regular washing of scalp with baby shampoo followed by gentle brushing to clear scales
Treatment of adult seborrhoeic dermatitis
Scalp: medicated shampoos with ketoconazole and salicylic acid twice weekly for at least a month
+/- steroid scream applications to reduce itch
- Coal tar cream to scaling areas and remove several hours later with shampoo
Elsewhere: cleanse thoroughly 1-2 times per day using non-soap cleanser
Ketoconazole cream daily for 2-4 weeks
topical steroids or calcineurin inhibitor if required
Age of onset of psoriasis
Onset at any age
Bimodal peaks in late teenage years and 50-60yo
How common is psoriatic arthritis in patients with skin psoriasis
40% will have associated arthritis
What is Auspitz sign
Removal of thick psoriatic scale reveals pinpoint bleeding
Clinical features of chronic plaque psoriasis
Well defined, raised red patches with adherent silvery scale
Symmetrical rash
Not as itchy as eczema
Nail changes associated with psoriasis
Pitting, onycholysis, subungal hyperkeratosis
Less common forms of psoriasis (6)
Guttate psoriasis Psoriasis of palms and soles Pustular psoriasis Flexural psoriasis Erythrodermic psoriasis Infantile psoriasis
Clinical features of guttate psoriasis
Typically presents in teens or early 20s after a streptotoccal sore throat
May be florid outbreak of small plaques, especially on trunk and proximal limbs
Clinical features of psoriasis of palms and soles
Well defined edge of involved skin adjacent to normal skin
Back of the hands and web spaces unlikely to be involved
Clinical features of pustular psoriasis
Mostly on palms and soles (can occur on body)
Mix of new and old pustules (look like small brown dots)
HIGH CORRELATION WITH SMOKING
Clinical features of flexural psoriasis
Usually lacks scale due to moisture Well defined border (in contrast to intertrigo and eczema) No pustules (in contrast to thrush)
Clinical features of erythrodermic psoriasis
Appears rapidly when oral steroids have been stopped
Patient typically very unwell - unable to regular temperature or fluid
Entire skin surface red and scaly
Skin is hot, but patient often hypothermic
Clinical features of infantile psoriasis
May involve nappy area, axillae, neck, umbilicus
Child not distressed as little or no itch
Difficult to distinguish from seborrhoeic dermatitis
Common drug triggers for psoriasis
Lithium
Beta blockers
NSAIDs
Treatment of psoriasis
General health: - smoking cessation - diet - weight control - avoid excessive alcohol General skin measures: - avoid scratching/rubbing/picking - regular moisturiser - short tepid showers Specific treatments; - topical corticosteroids - topical calcipotriol - dithranol - tar cream Systemic treatments - phototherapy - MTX - cyclosporin - biological agents
Good initial management routine for psoriasis
- Quick tepid shower with soap substitute
- weekly bath with bath oil or oatmeal
- Sorbolene with 10% glycerine in the morning
- betamethasone 0.05% ointment at night
+/- short term intermittent treatment with ointment containing calcipotriol and betamethasone
Continue for 1 month, if good response continue with just moisturiser, if poor response consider adding further agents
Use of dithranol ointment
Used for psoriasis
Temporarily stains skin, permanently stains clothes
Apply carefully to plaque only and wash off after half an hour
avoid on face and flexures
Management of psoriasis on face or flexures
1% hydrocortisone (cream on moist areas, ointment on dry)
Calcipotriol may be used by more likely to cause irritation - may be appropriate to alternate with steroid
Management of infantile psoriasis
Usually responds well to bland emollients only (e.g. sorbolene)
Management of scalp psoriasis
Apply tar cream at night and wash out in morning 1-2x per week
Apply a steroid lotion on the other days
Management of nail psoriasis
Can be very resistant to treatment
Steroid lotion to cuticle and under the end of the nail each night
Apply moisturiser several times a day to nail
Slow response (months)
When to refer psoriasis to specialist
- extensive psoriasis (>10-20% BSA) that is not controlled
- diagnostic uncertainty
- significant associated arthritis
- rapidly progressive psoriasis, acute erythrodermic psoriasis or generalised pustular psoriasis (emergency)
- difficult to treat sites not responding to initial treatment (face, genitals, palms, soles)
- Psoriasis unresponsive to topical therapies
- major physical and/or psychological disability associated with the disease
Associated comorbidities of psoriasis
Hypertension Obesity Hyperlipidaemia Heart disease Diabetes Inflammatory bowel disease Lymphoma Depression
Epidemiology of rosacea
Most commonly affects fair skinned, blue eyed Europeans or Celtics
Symptoms typically peak 30-50y
More common in females, however phymatous rosacea more common in males
Clinical features of rosacea
Primary: persistent erythema of central face >3 months
Other findings:
- flushing
- telangiectasia
- oedema
- inflammatory papules
- pustules
- ocular symptms
- rhinophyma or hyperplasia of connective tissue
4 primary subtypes of rosacea
Erythrotelangiectactic (vascular) rosacea:
- flushing and vasodilation overtime leads to permanent erythema and telangiectasia
- central face most affected, ears, neck and upper chest can also be affected
Papulopustular rosacea
- persistent or episodic developement of inflammatory papules and pustules, often on central face +/- background ETR
- typically in middle-aged women
Phymatous rosacea
- hyperplasia of skin due to chronic inflammation
- nose most commonly affected (rhinophyma)
- most common in older men
- significant telangiectasia can be present over affected areas
Ocular rosacea:
- may precede skin symptoms
- blepharitis and conjunctivitis are most common findings
Common triggers for rosacea (12)
Emotional stress hot or cold weather Sun exposure Wind Exercise Hot drinks Alcohol Spicy foods Dairy products Hot baths or showers Certain skin care products/cosmetics Medications
Treatment of rosacea
General measures:
- identify triggers and avoid/keep journal to identify triggers
- sun protection
- soap-free and abrasive free cleansers
- moisturise if skin is dry
- avoid abrasive materials, pat dry with towel for better absorption of moisturiser
- cosmetics with green or yellow tint to conceal redness
First-line:
- metronidazole cream or gel + azelaic acid
- topical ivermectin can be added for inflammation +/- briminotide for erythema
If rhinophyma: isotretinoin (specialist)
+/- topical/oral antibiotics (doxycycline) for inflammatory lesions
What is acne conglobata and acne fulminans
Acne conglobata is a rare form of nodulocystic acne characterised by interconnecting abscesses and sinuses
Acne fulminans is a very rare and severe acute form of acne conglobata associated with systemic symptoms
Superficial lesions in acne
Open and closed uninflamed comedomes (whiteheads and blackheads)
Papules
Pustules
Deeper lesions in acne
Nodules (large painful red lumps)
Pseudocysts (cyst-like fluctuant swellings)
Secondary lesions in acne
Excoriations Erythematous macules (red marks from recently healed spots, mostly seen in fair skin) Pigmented macules (dark marks from old spots, mostly affecting dark skin)
How long do individual acne lesions last
<2 weeks for superficial lesions
Deeper papules and nodules may last several months
Grading severity of acne:
By total lesion count or inflammatory lesion count:
Mild: <30 total (<15 inflam)
Moderate: 30-125 total (15-50 inflam)
Severe: >125 total, >50 inflam OR >5 pseudocysts
Treatment of mild acne
Topical antiacne (benzoyl peroxide and/or tretinoin or adapalene gel)
Low dose COCP
Antiseptic or keratolytic washes containing salicylic acid
Light/laser therapy
Treatment of moderate acne
As for mild + doxycycline 50-200mg per day for 6 months (erythromycin or trimethoprim if doxycycline intolerant)
Anti-androgen therapy (cyproterone or spironolactone) for women not responding to low-dose COCP, esp if have PCOS
Isotretinoin if persistent or treatment resistant
Treatment of severe acne
Refer to dermatologist (urgently if systemic symptoms suggestive of acne fulminans)
Oral isotretinoin usually recommended
Oral antibiotics often used in higher than normal doses
General measures for acne control
Skin care: no picking/popping, no routine need for moisturiser, oil-free make up and sunscreen - ensure sun protection
Diet: balanced healthy diet, no evidence for specific diets
How long before a clinical effect will be apparent with acne management
Antibiotics: should see effect within 6 weeks
COCP: at least 3 months before any visible effect, peak effect after 6 months
Management of cellulitis
WITHOUT systemic features: oral antibiotics for 5-10 days, elevation, rest, and adequate fluid intake
WITH systemic illness: IV antibiotics, fluids
Change to orals once fever settles, rash regressing +/- CRP reducing
Risk factors for pitted keratolysis
moist skin
therefore occupational factors, hot humid weather, occlusive footwear, hyperhidrosis
Diabetes
advanced age
Immunodeficiency
thickened skin of palms and soles
Clinical features of pitted keratolysis
Smelly feet
White area on forefoot or heel with clusters of punched out pits that may coalesce to form crater-like lesions - more dramatic appearance when skin is wet
May cause itch or soreness when walking, usually asymptomatic
Treatment of pitted keratolysis
Clindamycin 1% lotion for 10 days
What is erythrasma
A common bacterial infection of skin folds under arms, in the groin and between the toes, caused by corynebacterium.
Clinical features of erythrasma
well-defined pink or brown patches with fine scaling and superficial fissures +/- mild itch
Occurring in skin folds, mostly groin, axillae or interdigital spaces
Management of erythrasma
Fusidate sodium 2% ointment topically BD for 14 days
OR
PO clarithromycin 1g PO as single dose
Usually self-limiting
Epidemiology of impetigo
Most common in children (boys>girls) with peak during summer Risk factors: - scabies - atopic dermatitis - skin trauma
Bacteria involved in impetigo
Most commonly staph aureus
In non-bullous impetigo and remote indigenous communities: usually strep pyogenes
Clinical features of impetigo
Usually affects exposed areas (face and hands)
Single or multiple irregular crops of irritable superficial plaques that extend as they heal, forming annular lesions
Bullous: small vesicles evolving into bullae with honey coloured fluid
Non-bullous impetigo: starts as pink macule -> vesicle or pustule then honey coloured cursted erosion
What is ecthyma
Punched out necrotic ulcerated lesion secondary to non-bullous impetigo
Management of impetigo in non-remote settings
Cleanse wound using moist soaks to gently remove crusts
Localised sores: mupirocin 2% to crusted areas TDS for 7days
Mulitple sores or recurrent infection:
- di/flucloxacillin 12.5mg/kg up to 500mg TDS for up to 10 days (stop earlier if infection resolved)
- cephalexin or bactrim if hypersensitive
Bactrim if non-responsive
Management of impetigo in remote/indigenous communities
As s. pyogenes more frequently the pathogen involved:
- benzathine penicillin IM stat
OR
- bactrim BD for 5 days (or higher dose daily for 5 days)
See guidelines for dosages
When should leprosy be considered as a differential
With any hypopigmented skin patches, particularly if altered sensation present, and in ATSI patients from Northern Australia, or migrants from higher risk countries (Brazil, India, Myanmar, Nigeria and Indonesia) - pacific islands and other developing countries are higher risk than most of Australia
Skin changes in syphilis
Primary: chancre on genitals, anus or mouth.
- non-tender, well defined margin with indurated base
- multiple chancres in 30%
- spontaneously heals within a few weeks even if untreated
Secondary:
- generalised rash over trunk (may only involve palms and soles)
- nonpruritic
- subtle OR rough, re-brown papules or patches appearing more obvious with physical activity or heat
- may have patchy alopecia
- may have condylomata lata (warthy growths) in ano-genital area
Management of viral warts
1/3 will spontaneously resolve within 3 months, 2/3 within 2 years
Initial treatment should be salicylic acid (best evidence)
Second line is cryotherapy with paring down of wart
Duration of exclusion for molluscum
No exclusion period required. Advise to avoid sharing towels or bathing together to reduce spread to siblings
Management of molluscum
Most children do not require treatment, complete resolution will occur when immune response develops in 3 months to 3 years (usually 6-9 months)
Secondary eczema may require treatment
Clinical features of molluscum
firm, pearly, dome-shaped papules with CENTRAL UMBILICATION
usually 1-3mm but up to 1-2cm
Presentation can often be propted by development of eczema in surrounding skin, obliterating the primary lesions
Clinical features of chicken pox.
Begins as itchy red papules progressing to vesicles -> crusted lesions
Begins on stomach, back and face then spreads to rest of body, can arise inside the mouth
Lesions at different stages present simultaneously
May have systemic symptoms (high fever, URTI symptoms, headahce, vomiting, diarrhoea)
Exclusion period for chicken pox
Until ALL blisters have formed scabs (usually 5-10 days)
Clinical features of measles
Prodromal phase: 10-12 days after exposure. Fever, malaise, anorexia, conjunctivitis, cough, coryza. Koplik spots (blue-white spots on inside of mouth opposite molars) Exanthem phase ( 24-48h after prodrome): red non-itchy maculopapular rash. Begins on face and behind ears with cephalocaudal spread to entire body within 24-36 hours). Associated high fever >40. Fades 3-4 days after onset.
Diagnosis of measles
In Australia as it is seen so infrequently, diagnosis required lab confirmation:
Viral NPS or blood serology
Clinical features of rubella
25-50% are so mild there are few or no signs or symptoms
Mild fever, URTI symptoms, malaise
Tender/swollen glands almost always accompany the rash (most commonly postauricular, occipital and posterior cervical chain)
Forchheimer sign: pinpoint or larger petechiar on soft palate and uvula during prodromal period
Rash: cephalocaudal spread from face, usually not as widespread as measles, pink/light red spots 2-3mm in size
Lasts up to 5 days (avg 3 days)
May or may not be itchy
As passes, affected skin may shed in flakes
Clinical features of roseola
Often few or no signs or symptoms Typically: - high fever (up to 40) for 3-5 days - URTI symptoms - Irritability, tiredness - Rash on day 3-5, as fever subsides : small, blanching rose-pink or red raised spots 2-5mm, mainly on trunk, non-itchy and painless. May fade within few hours or persist up to 2 days Main complication is febrile seizures
Clinical presentation of parvovirus B19
Non-specific viral prodrome (mild headache, fever)
Rash few days later: initially firm red cheeks feel burning hot for 2-4 days, then pink rash develops on limbs and sometimes trunk (lace-like or network pattern)
Most prominent in first few days, can persist for up to 6 weeks (at least intermittently) most obvious when warm
Other name for parvovirus B19 illness
erythema infectiosum
Epidemiology of roseola
Affects most children before the age of 1 (6m-3y)
Primary HSV1 infection presentation
most often gingivostomatitis in child 1-5yo Fevers, may be high Restlessness Excessive dribbling Foul breath Painful eating and drinking Red swollen gums, bleed easily Whitish vesicles -> yellow ulcers on tongue, throat , palate and inner cheeks Localised tender lymphadenopathy Recovery usually complete within 2 weeks
Common locations for HSV infections
(Face/lips, genitals)
Thumb sucker - thumb
Health care worker: herpetic whitlow (paronychia)
Rugby player: scrum pox (blisters on one cheek)
Most common sites for HSV2 infections
Males: glans, foreskin, shaft (anal in MSM)
Females: vulva and in vagina, painful to urinate. Infection of cervix may cause severe ulceration
Management of herpes simple infections
Mild primary infection: supportive +/- topical anaesthetic
Severe primary: oral antivirals
Mild recurrence: topical aciclovir 4 hourly for 5d from first sign of recurrence
Severe recurrence: oral antivirals
If immunocompromised or not tolerating oral, discuss with infectious disease specialist
Pregnancy specific pruritic diseases
Cholestasis of pregnancy
Prurigo of pregnancy (papular dermatitis of pregnancy)
Pruritic urticarial papules and plaques of pregnancy (AKA polymorphous eruption of pregnancy)
Pemphigoid gestationis
Clinical features of pemphigoid gesationis
(rare)
Onset at any stage of pregnancy/postpartum, most common in 2nd T
Itchy papules mainly affecting abdo, INCLUDING umbilicus. may appear as grouped or annular red papules, plaques and blisters
Clinical features of pruritic urticarial papules and plaques of pregnancy
Onset in 3rd T, more common in primips and multiple pregnancies
Itchy red papules and plaques first appearing in straie then spreading to trunk and proximal limbs, SPARING umbilicus
Management of pruritic urticarial papules and plaques of pregnancy
Emollients
Medium potency topical steroids
Sedative oral antihistamines for relief of symptoms
Systemic steroids if severe cases
Clinical presentation of prurigo of pregnancy
Scattered itchy papules developing at any stage of pregnancy
Should be managed with emollients (topical steroids may help INDIVIDUAL lesions but not the rash as a whole)
Clinical presentation of pruritus gravidarum/cholestasis of pregnancy
Unexplained itch in 2nd or 3rd T with no rash present.
Raised blood levels of bile acids and/or liver enzymes.
What is telogen effluvium and how does it present
Shedding of telogen hair - occurs 2-6 months after an event that stops active hair growth (childbirth, fever, weight loss, haemorrhage, surgery, illness or psychological stress, medications (OCP, anticoagulatns, anticonvulsants))
Normal hair growth cycle
Anagen: actively growing hair (most of them)
Catagen: in-between phase of 2-3 weeks when growth stops and follicle shrinks (1-3% of hairs at any time)
Telogen: resting phase for 1-4 months (up to 10% of hairs in a normal scalp at any one time)
What is anagen effluvium
Shedding of hair in anagen phase:
Caused but: autoimmune disease, mediations (e.g. CTx), inherited/congenital conditions)
If caused by a drug/toxin can return to normal within 3-6 months
Inflammatory skin conditions that can damage or destroy the hair bulb
Localised alopecia areata
Localised infection e.g. tinea capitis
Severe local skin disease (psoriasis, seborrhoeic dermatitis, eczema, lupus, T-cell lymphom)
Generalised skin disease e.g. erythroderma
Systemic causes of hair loss
Cause reversible patchy hair thinning, poor hair quality and bald patches.
Causes: Iron deficiency Hypothyroidism SLE Syphilis Severe acute or chronic illness
Risk factors for alopecia areata
Family history of same or other autoimmune conditions Personaly hsitory of thyroid disease, vitiligo or atopic dermatitis Chromosomal disorders (e.g. Down Syndrome)
Diagnosis of alopecia areata
Clinical
Should also be worked up for atopy, vitiligo, thyroid disease and other autoimmune conditions
Patterns of alopecia areata
Patchy:
- affects any hair-bearing area mostly scalp, brows, lashes and beard
- 3 stages: sudden loss of hair, enlargement of bald patch(es), regrowth of hair
- regrowing hairs often initially white or grey and may be curly when previously straight
Alopecia totalis:
- all or nearly all scalp hair is lost
Alopecia univeralis
- all hair on entire body is lost
Diffuse:
- sudden diffuse thinning of scalp hair
- positive hair pull test
- persisting hair turns grey (Turning white overnight)
- may be confused with telogen effluvium
Treatment of alopecia areata
If limited hair loss of recent onset:
- potent topical corticosteroid 3-4 months (betamethasone 0.05% cream/lotion/optimised vehicle 1-2x per day)
If extensive or topical treatment not successful within few weeks
Treatment of trichotillomania
In children: usually benign and self-limiting, will usually outgrow it. If response to significant stress at home or school may need to refer to psychologist/psychiatrist
In adults; usually psychopathological, refer to psychologist/psychiatrist
Definition of hirsutism
Male pattern of secondary or post-pubertal hair growth occurring in women (moustache and beard areas, + more hair on limbs and trunk)
Causes of hirsutism
Genetic (early onset)
Late onset may be due to hyperandrogenism:
- PCOS
- insulin resistance
- obesity
- androgenic medications
- Cushing syndrome
- Congenital adrenal hyperplasia
- tumour of adrenal gland or ovary
Assessing severity of hirsutism
Ferriman-Gallwey visual scale (score of 0-4 re: amount of hair present in different areas of body)
Investigations to perform for hirsutism
Free androgen index
- if high, DHEA (elevated if adrenal origin) and androstenedione (elevated if ovarian origin)
If premature adrenarche, early onset of family history of CAH: 17-OHP
If cushingoid: urine and serum cortisol
If menstrual disorder:
LH, FSH, prolactin
General: TFT, glucose, lipids, imaging if indicated by symtpoms
Treatment of hirsutism
Treatment of underlying cause (e.g. metformin if PCOS)
hormonal treatment: spironolactone, OCP, cyproterone
Definition of hypertrichosis
Excessive hair growth above normal for age, sex and race - can develop all over body or isolated to small patches
Causes of hypertrichosis
Generalised acquired causes:
- porphyria cutanea tarda
- malnutrition (e.g. .anorexia nervosa)
- malignancy
- drugs (ciclosporin, phenytoin, androgenic steroids, minoxidil)
Localised:
- increased vascularity
- repetitive rubbing or scratching (lichen simplex)
- application of plaster cast (temporary)
- repeated application of potent topical steroid, PUVA, iodine
- long eyelashes (trichomegaly) can arise from local bitanoprost
Treatment of hypertrichosis
Hair removal, treatment of underlying cause if identified
What is lichen simplex
AKA neurodermatitis, a localised area of chronic, lichenified eczema/dermatitis
Cause of lichen simplex
Not entirely understood
Follows repetitive scratching and rubbing secondary to chronic localised itch
(primary itch can be caused by all types of dermatitis, psoriasis, lichen planus, fungal infection, insect bite, neuropathy)
Clinical presentation of lichen simplex
Solitary plaque well circumscribed, linear or oval in shape and markedly thickened
Intensely itchy
Often unilateral, affecting patient’s dominant side (back of scalp/neck, scrotum or vulva, wrists and forearms, lower legs)
+/-: exagerrated skin markings, dry or scaly surface, leathery induration, broken-off hairs, pigmentation, scratch marks
Clinical appearance can be atypical - skin scrapings and biopsy may be necessary
If no known underlying skin problem/infection, consider neuropathy
treatment of lichen simplex
Treat symptoms and underlying cause
Potent tropical steroids until plaqu resolves (4-6 weeks), reduce potency or frequency once lichenification resolves
Moisturise, antihistamines PRN for itch
Treat underlying primary condition
Dermatological emergencies
Angioedema
Steven Johnson syndrome/ toxic epidermal necrolysis
Staphylococcal TSS
Necrotising fasciitis
Cause of staphylococcal toxic shock syndrome
Staph aureus produces exotoxins causing massive cytokine secretion by T cells -> fever, hypotension and multi-organ failure
Risk factors for staphylococcal TSS
Relatively rare as most adults have protective antibodies to exotoxin
- most common in healthy people 20-50y
- recent childbirth, miscarriage or abortion
- foreign bodies e.g. nasal packing for epistaxis or wound packing after surgery
- post surgical wound
Clinical presentation of staphylococcal TSS
2-3 day prodrome of malaise
Fever, chills, nausea, abdominal pain
Rapid onset generalised erythema with desquamation, fever, hypotension and multisystem failure
Rash begins on trunk and spreads peripherally to palms and soles
Management of staphylococcal TSS
Aggressive supportive management of hypotension
Obtain cultures
Treat with beta-lactamase resistant antibiotic (fluclox, benPen, cephazolin if non-immediate hypersensitivity or vancomycin if MRSA or immediate hypersensitivity)
Common causes of angioedema
Often idiopathic
Medications: especially ACE-i, NSAIDs, penicillins, radiographic contrast
Allergens
Physical agents (cold, vibration)
What is exfoliative erythroderma
AKA Red Man Syndrome
Generalised scaly erythematous skin eruption of >90% of skin surface
Causes of exfoliative erythroderma
Often idiopathic Can be related to underlying dermatoses Drug reaction (sulphonamides, penicillin, antimalarials, anticonvulsatns, allopurinol) Cutaneous T-cell lymphoma or leukaemia Paraneoplastic syndrome Dermatomyositis
Presentation of exfoliative erythroderma
Initially pruritus
Malaise and fever -> leading to excessive vasodilatation
Scaly erythematous rash covering >90% of skin surface
Management of exfoliative erythroderma
Determine cause and address, stop ALL unnecessary medications
Supportive therapy: hydration, nutrition, electrolyte monitoring and replacement, cardiac monitoring, temperature support
Skin care: emollients and compresses, topical corticosteroids
Antihistamines for pruritus
Antibiotics if signs of infection
Types of necrotising fasciitis
Type I: staph aureus, mixed anaerobes, gram neg bacilli, enterococci - most commonly seen in elderly or diabetics
Type II: Group A strep - affects all ages including healthy people
Type III: clostridia - follows significant injury or surgery, results in crepitus
Most common site for necrotising fasciitis
Lower leg
Risk factors for necrotising fasciitis
Diabetes
Peripheral vascular disease
Immunosuppression
Clinical presentation of necrotising fasciitis
Diffuse swelling of affected skin area -> developement of bullae which rapidly become burgundy in colour Severe pain indurated oedema Skin hyperaesthesia Crepitation Muscle weakness Foul-smelling exudate
Management of necrotising fasciitis
Aggressive management of sepsis
Surgical debridement of necrotic tissue
Broad spectrum antibiotics unless causative agent definitively identified
What are Stevens-Johnson Syndrome and Toxic epidermal necrolysis
Both represent a spectrum of drug-induced or idiopathic mucocutaneous reaction patterns characterised by skin tenderness, erythema, epidermal necrosis and desquamation
Common medications responsible for SJS/TEN
Sulfonamides
Anticonvulsants
Allopurinol
NSAIDs
Note drug administration typically precedes rash by 1-3 weeks
Clinical presentation of SJS/TEN
Prodrome: fever, stinging eyes, sore throat, odynophagia, coryza and cough, general aches and pains
Rash: development of dusky erythematous macules that progress to flaccid blisters, 2+ mucous membranes typically involved with erythema/erosions(buccal, genital, occular)
<10% of eridermis sloughs off in SJS
>30% in TEN
Mortality of TEN and SJS
TEN: 30%
SJS: 5%
Management of SJS/TEN
Identify and remove offending medication Admit to burn unit if necessary IV fluids Electrolyte and temperature maintenance Ophthal assessment Skin care: wound dressings oral hygiene (chlorhex rinses) Antihistamine Antibiotics in case of super infection
How does scabies spread?
Person-to-person only
20 minutes of close contact required (e.g. holding hands, sexual contact)
Household contacts highest risk of transmission
Note may be a delay of up to 6 weeks from first infestation to beginning of symptoms
Presentation of classical scabies
Often multiple household members have same
Papules/burrows in typical locations (web spaces, wrists, buttocks breasts, genitals)
Intensely itchy
Secondary bacterial infection in up to 90% (surrounding erythema, yellow crusting or pus)
Clinical presentation of Norwegian/crusted scabies
(hyperinfestation of millions of mites causing hyperkeratosis)
Plaques and extensive scale
Deep fissures in severe case
May not be itchy
Diagnosis of scabies
Usually clinical
If atypical appearance: ink from pen over burrow entrance will track along burrow
Or dermatoscope will show “delta sign”
Crusted scabies usually requires confirmation with skin scrapings
Management of scabies
ALL household contacts need to be treated at the same time
<2 months: crotamiton
> 2 months: permethrin 5% cream, apply to whole body and wash off after 8 hours, if symptoms persist, repeat in 7-14 days
Second line: benzyl benzoate 25% left for 24h then washed, diluted for children, repeat once after 7-14 days
Third line: oral ivermectin, 2 doses 7 days apart, if >5y, non-pregnant, not breastfeeding and failure to respond to topical treatment
Management of crusted scabies
Discuss with specialist
Combination of topical scabicides, oral ivermectin and topical keratolytics
LOTS OF SHEDDING SCABIES therefore very infectious
Treatment sometimes requires hospital admission for isolation and intensive treatment
Treatment of head lice
Children <2y: wet combing - put hair conditioner on, then comb sections with fine tooth comb and wipe conditioner + lice onto tissue. Daily for few days after last louse is found
Children >2y: pediculicides (OTC)
Exclusion from school only until appropriate treatment is commenced
Management of body lice
As live in clothing not body, only need treatment of body if infestation is widespread (same as headlice treatments)
Otherwise environmental measures only:
- laundering clothes and linen with hot washes and hot tumble-drying
- ironing with hot iron
- dry cleaning
- topical insecticide spray applied to clothing, especially seams
Treatment of pubic lice
Same treatments as head lice, apply to ALL hairy areas from neck to knees and repeat 7 days later
Sexual partners need to be treated, even if asymptomatic
What is latrodectism
Red back spider bite envenomation
Clinical presentation of red back spider bite envenomation (latrodectism)
Bite may not be felt, rarely leaves fang mark, erythema not always present
Localised sweating and piloerection (25% of patients) Pain typically increasing over about 1 hour - may radiate proximally along affected limb Systemic effects (uncommon) - hypertension - agitation/irritability - priapism - patchy paralysis - paraesthesia - fasciculations - cardiac effects
Management of red back spider envenomation
Antivenom if signs of systemic envenomation OR pain not controlled with simple analgesia/requiring repeated doses of opiates
Spiders which cause necrotising arachnidism
Recluse spider
NOT associated with white tailed spider (common myth)
In Australia necrotising arachnidism is very uncommon, there is more likely to be an underlying infective, inflammatory or traumatic cause that needs to be investigated
Skin conditions related to diabetes mellitus
Diabetic dermopathy/shin spots: pigmented, slightly indented scaly patches on shins often bilaterally
Diabetic bullae (rare) spontaneous, develop on hands and feet
Diabetic stiff skin/cheiroarthropathy: waxy, thickened, yellow skin - restricting mobility of joints of hands
Skin changes of hypothyroidism
Carotanaemia - yellowish hue to skin Eczema craquele Sparse and brittle hair Dry skin Loss of hair in outer third of eyebrows
Skin changes of hyperthyroidism
Nail changes: thyroid acropachy (distorted and overgrown nails) +/- onycholysis Generalised pruritus Urticaria Fine, soft and thinned scalp hair Flushing of face and hands
Grave’s only:
Pretibial myxoedema (reddish, tender swellings nodules and plaques on shins, calves and feet, prominent hair follicles give orange peel or warty appearance)
Exophthalmos
Skin changes of Cushing Syndrome
Purpura/easy bruising Purple Striae over abdomen Telangiectatic cheeks Fragile skin, poor wound healing Acne Hirsutism Clitoral hypertrophy Male-pattern baldness in females
Skin changes of Addison’s disease
Generalised hyperpigmentation
Women may have loss of androgen-stimulated hair (pubic and underarm hair)
Clinical features of mammary Paget’s disease
Chronic eczema-like rash of nipple and adjacent areolar skin Itchy, burning rash on and around nipple Skin may be broken and sore from scratching \+/-" - redness - swelling - oozing nipple - discharge - ulceration - inversion of the nipple
Usually only unilateral
Clinical features of extramammary Paget’s disease
Chronic eczema-like rash
Intense itching
pain and bleeding secondary to scratching
Thickened plaques may form
Most often occurs on vulva in middle aged women
(also occurs on axilla and anogenital area in males)
Skin changes associated with liver dsiease
Telangiectasia
Spider naevi
Palmar erythema
Terry nails (proximal leukonychia and pink distal nail plate)
haemochromatosis: bronze hyperpigmentation of skin
Wilson disease:
- Kayser-Fleisher rings
- pigmentation over skin
- blue lunulae (half-moons) on nails
Skin changes associated with coeliac disease
Dermatitis herpetiformis:
- intensely itchy herpetiform vesicles within erythematous or urticated plaques.
Symmetrical distribution over extensor surfaces and buttocks
Skin conditions associated with inflammatory bowel disease
Oral ulcers
Erythema nodosum (tender red subcutaneous nodules on shins)
Pyoderma gangrenosum (irregularly undermined necrotic ulcers on lower legs)
Swelling of oral cavity
Cutaneous polyarteritis notosa
Acute neutrophilic dermatosis/Sweet syndrome
Skin changes in vitamin B12 deficiency
Angular cheilitis
Hunter glossitis (atrophic, red, painful tongue)
Hair depigmentation
Hyperpimgenation
Skin changes in vitamin C deficiency
(Scurvy)
- enlarged hyperkeratotic hair follicles on posterolateral arms
- abnormal hair development
- swelling of gums, erythema
- splinter haemorrhages in nails
Skin changes secondary to vasculitides
Depends on size of inflamed blood vessel;
Capillaritis
- pigmented purpura
- petechiae resolving with haemosiderin staining
Small vessel vasculitis:
- palpable purpura
Medium vessel:
- nodules
- livedo reticularis
Large vessel infrequently results in cutaneous features
Epidemiology of lichen sclerosus
Most common in women >50y
10x more common in women than men
15% of patients have a family member with same condition
May follow or co-exist with another skin condition (e.g. lichen simplex, psoriasis etc. 0
Often personal or family history of other autoimmune conditions
Clinical features of lichen sclerosis
Mostly occurs on vulva
- non hair-bearing inner areas
- can be localised or extensively involve perineum, labia minora and clitoral head
- NEVER involves vaginal mucosa
- extremely itchy and/or sore
- may have painful fissuring of posterior fourchette
- can cause adhesions and scarring
Diagnosis of lichen sclerosus
Usually requires biopsy unless experienced physician
treatment of lichen sclerosus
General:
- wash 1-2 x per day with soap free (or no) cleanser)
- avoid tight clothing, rubbing or scratching
- manage incontinence
- emollients to relieve dryness and itch
Topical steroid ointment
- encourage to use mirror to apply directly to affected skin
- can take months for skin to return to normal
Other therapy:
- intravaginal oestrogen (reduces symptoms of atrophic vulvovaginitis)
- systemic treatments if severe or resistant
Complications of lichen sclerosus
Associated with increased risk of SCC and other cancers of vulva, penis and anus
Three principles to ulcer/wound management
- Define the aetiology
- Control modifiable factors affecting healing
- Select appropriate local environmental management
Most common chronic wounds seen in GP
Leg ulcers (venous, arterial, mixed)
Pressure wounds
Skin tears
Cause of venous leg ulcers
Breakdown of venous circulation -> increased venous pressure -> pitting oedema -> reduced perfusion to skin -> insufficient supply for healing to occur after trauma -> ulcer development
Clinical presentation of venous ulcers
- Commonly on gaiter area (lower 1/3 of leg)
- irregular shape
- pitting oedema
- haemosiderin staining of surrounding skin
- typical surrouding skin changes of venous eczema or atrophy blanche
Most common risk factors for venous ulcers
Obesity
Past DVT
Poor mobility
General treatment of venous ulcers
Graduated compression therapy (toe to knee) - ensure exclude arterial involvement first with ABI
Lower limb exercise
Address occupational factors (Rarely, surgery)
Clinical presentation of arterial ulcers
- commonly below ankles and foot/toes
- Punched out/sharply defined margins
- base covered in slough
- skin often shiny and friable
+/- other signs of ischaemia: - ischaemic pain esp at night
- intermittent claudication
- dusky/white foot on elevation
- sluggish capillary refill
- low ABI
- weak/absent pulses
- known peripheral vascular disease
Treatment of arterial ulcers
Surgical is mainstay: - angioplasty - stenting - bypass grafting - amputation Pain control! DO NOT APPLY COMPRESSION
Treatment of mixed leg ulcers
(15-25% of leg ulcers)
Determine if predominant cause is venous or arterial and treat it
**Depending on degree of arterial problem, graduated compression may be contraindicated, in this instance it is difficult to address the venous component of the problem and thus difficult to treat
How to simply reduce risk of skin tears
Applying moisturising lotion BD to patients in nursing homes
Treatment of skin tears
If possible, replace the flap, carefully holding in place with a few adhesive strips (no tension) and cover with silicone foam dressing and 1-2 layers of tubular compression to apply mild pressure
Review after 3 days and redress avery 5-7 days
General factors that affect wound healing
Arterial and venous circulation Anaemia Immune function Comorbidities (DM, RA) Age-related skin changes Balanced nutritious diet Mechanical stress (pressure, friction, shearing forces) Debris (slough, necrotic tissue, eschar, scab, sutures) Dessication Maceration Temperature (optimum 37 degrees) Infection Chemical stress (e.g. topical agents/antiseptics, smoking, steroids/NSAIDS, other drugs)
Principles of LOCAL wound management
Tissue (if non-viable, debride)
Inflamation/infection(only treat with Abx if signs of invasive infection)
Moisture (correct dressing for optimal environment)
Edge/epithelialisation (if advancing or undermining, reconsider diagnosis and use advanced therapies)
Correct dressings to use for very dry wounds/minor burns
Hydrogels
- increase wound moisture
- use for dry, scabbed, necrotic/escharotic wounds and minor burns
- usually require secondary dressings in form of foams
e. g. Aquaclear (sheet) or solosite (amorphous hydrogel comes in a tube)
Appropriate dressings for nil-to-low exudate wounds
Films
- neither absorb nor donate moisture
- semi-permeable, transparent and flexible
- maintains a moist environment and encourages sutolysis (keeps exudate within local environment)
e. g. Opsite, Tegaderm
Appropriate dressings for low-to-moderate exudate wounds and ulcers
Hydrocolloids:
- combine with exudate to form soft, moist gel that keeps wound bed hydrated
- encourage autolysis and aid removal of slough
E.g. duoderm (sheets, pastes), comfeel (sheets, pastes, powders)
Appropriate dressings for moderate-to-high exudate wounds
Foams:
- highly absorbent, non-adherent, insulating and cushioning
- used in exuding wounds to maintain moisture without maceration
e.g. Lyofoam, Mepilexx (foam sheet with soft silicone)
Absorbent fibre dressings
- absorbs exudate and maintains moist environment
- calcium alginates have haemostat properties
- need foams as secondary dressings
- e.g. Kaltostat (alginate sheet or rope) Melgisrob (alginate rope), Aquacel (hydrofirbe sheet, rope)
When to use activated charcoal as a dressing
(with or without silver)
On malodorous wounds to absorb odour and bacteria
What dressing to use on malodorous wounds
Activated charcoal +/- silver
When are non-adherent dressings used
Mainly as protective dressings for minor lacerations or healed wounds e.g. Mepitel (soft silicone mesh) or Jelonet (paraffin tulle)
When are negative pressure dressings required
Complicated exudating wounds (much more expensive than standard wound care
What is hidradenitis suppurativa?
AKA acne inversa, a chronic inflammatory disease of the skin in intertriginous areas characterised by multiple inflammatory nodules, abscesses, sinuses, fistulas and scarring. Related to follicular occlusion.
Prevalence of hidradenitis suppurativa
Approx 1%
F:M ratio 3:1
Inflammatory diseases associated with hidradenitis suppurativa
Pyoderma gangrenosum
Spondyloarthropathies
Crohn’s disease
Comorbidities associated with hidradenitis suppurativa
Obesity Acne hyperlipidaemia depression insulin resistance PCOS diabetes hypertension keratosis pilaris smoking
Follicular occlusion tetrad consists of:
Hidradenitis suppurativa
Dissecting cellulitis
Acne conglobata
Pilonidal sinus
Clinical presentation of hidradenitis suppurativa
Multiple (and often recurrent or chronic) lesions in intertriginous areas, including:
- Comedomes
- Painful nodules
- Abscesses
- Sinus tracks
- Fistulae
- Scarring
Lymphoedema can occur secondary to lymph node scarring and subsequent obstruction
Management of hidradenitis suppurativa`
General measures:
- loose fitting clothing
- smoking cessation
- healthy eating
- weight loss (if appropriate)
Topical therapy:
- topical antiseptic when bathing (benzoyl peroxide 5% wash, antibacterial soap)
- topical clindamycin 1% BD for up to 3 months
Oral therapy:
- antibiotics (doxy or mino 50-100mg daily, or erythromycin if tetracyclines contraindicated)
- COCP - ideally one containing cyproterone (i.e. Brenda, Dianne etc. ) OR desogestrel (Marvelon), drospiernone (Yaz) or gestodene (Minulet)
- spironolactone: severe disease only, start at 25-50mg daily
Biological agents:
- severe disease, refer to derm
Surgical:
- acute abscess I/D - likely to worsen scarring
- after review by derm ?wide local excision, deroofing etc.
