Skin and its Diseases

- Between body sites - e.g. eyelids highly permeable compared to palms
- By up to 40% between the same site on different people
- Pre-term infants (lack fully formed stratum corneum)
- Melanoma skin cancer

Racial skin types, gender, and on ageing.

measure a skin type's ability to tolerate sun exposure based on a persons characteristics; eye and hair colour, and skin colour.

Seaweed, oils, avocado, apricot kernel, carrot, tea tree, herbs like sage, and flowers like chamomile.

Can't easily be patented, company has to expense to prove natural product works, when competitors are making 'me too products' . Traditional use can be claimed, placebo effect can be useful.

Externally used in gels, creams. Used for inflammation; insect bites, bruises, arthritis, and oedema's due to fractures.

Main active constituents are sesquiterpene lactones and their esters. Sesquiterpene lactones affect inflammatory processes by inhibiting NF-kappaB and NF-AT at micro-molar concentrations. Also influence release of cytokines.

Nicotinic acid produces reddening of the skin (vasodilation), and is concentration dependent.
0.1% betamethasone shows a blanching effect (vaso-constriction)

After 3hr application, vasodilation apparent. Expected vast-constriction and possible inflammatory response. Very low amounts of activee phytochemical get across skin; very potent.

Arnica, circumin (turmeric), aloe vera, capsaicin. Natural products are complex mixtures that work synergistically.

- MUST place patients' safety first;
will it do them harm?
- Systemic or more likely local harm, e.g. irritation
- Will it interact with other medicines?
- Does it mean they won't use evidence based therapy?

Acne, cancers, psoriasis, eczema, rosacea, and fungal infections.

Least malignant and most common form of skin cancer
Most common skin types 1 & 2; rare in types 4 & 5
Common in later life on exposed sites.
• Lesions often on sun-exposed areas of face (rare on ear) and appear as shiny, dome-shaped nodules that later develop central ulcer with pearly, beaded edge.
• Can have small visible blood vessels (telangiectasia's)

Full cure in >99% of cases by surgical excision.
Radiotherapy can be useful for large superficial forms. Cryo-therapy also used for very superficial forms although follow up advised.
Fluorouracil
Imiquimod.

Arises from keratinocytes of stratified squamous epithelium.
Lesions are scaly red papules that can ulcerate and bleed.
Most often found on head (scalp, ears, lower lip) and hands, legs.
Grows rapidly and metastasises if not removed.
Multiple tumours can occur in those who've had long periods on immunosuppression; (e.g., renal transplant)
- Most common form of cancer on black skin

If caught early and removed surgically or by radiation therapy, chances of complete cure is good.

Urgent, wide surgical excision plus chemotherapy, possibly immunotherapy; IL2.
Depth of invasion and thickness of tumour predict prognosis and 5-yr survival rates.
Key to survival is early detection. Chance of survival is poor if lesion >4mm thick.

Most dangerous of all skin cancers; can occur in the eye. Increasing due to sun exposure & tanning.
History of childhood sun exposure (sun burn) important for MM development
+ve family history of MM also strong risk factor
Common on sun exposed areas. Highly metastatic and resistant to chemotherapy.
Occurs spontaneously in melanocytes and can begin wherever there is pigment.
Approx. 30% arise from pre-existing moles.

They advise the dangers of sunbathing, tanning beds and encourage appropriate use of sunscreens as being of utmost importance when trying to prevent skin cancer.
- Advice includes: avoiding sun exposure during hours of 11am-3pm, wear a sun hat, apply a high protection sunscreen and re-apply at regular intervals.

Melanomas in Blacks, Asians and native Hawaiians often occur on non-exposed skin with less pigment, majority with of tumours arising on the palms, soles, mucous membranes and nail regions.
In non-whites, the plantar portion of the foot is often most common site of skin cancer

A - asymmetry
B - border irregularity
C - colour not uniform; mole has more than one colour
D - diameter; >6mm
E - evolution; sudden changes in size, shape, and colour.

Major criteria = Change in size, shape, and colour
Minor criteria =
Diameter >6mm, inflammation, oozingleeding, mild itch/altered sensation.

NOT to diagnose or recommend therapy; unless as consultant oncology pharmacist.
Important to recognise suspicious lesions/moles
Advice to see GP; without terrifying patient.

Trichophyton, Microsporum, and Epidermophyton

Candida albicans

By microscopy and culture of skin, hair, or nail samples

The infecting organism, site of infection, and the host reaction.

Direct contact from other humans or infected animals
Use of communal showers, swimming pools, sharing of towels or sportswear aids infection transmission.

Tinea capitis: scalp
Tinea corporis: body
Tinea cruris: groin Tinea pedis: feet
Tinea manuum: hands

Fungal infection of the head; usually seen in children in the UK.
Caused by microsporum or Trichophyton species of human or animal; usually kitten.
Spread by close contact especially in schools and households; may be indirectly spread in hairdressers.
Fungus may confine itself within hair shaft or spread out over hair surface.
Patches of alopecia typically seen on head. Can be inflammatory.

Ringworm of the foot (athlete's foot); appears in toe clefts. Caused by Trichophyton species.
Presents as red, scaly eruption that itches.
Can develop into macerated and fissured area and
can spread to other parts.

Ringworm infection of trunk and/or limbs.
May be contracted from animals or humans; Usually due to Trichophyton species.
Isolated erythematous and scaly lesions or clusters of round or oval red patches.

"Jock itch"; "Gym itch"; "Crotch rot"
Very common, especially in warmer climates
Itching in groin, thigh skin folds, or anus.
Red, raised, scaly patches that may blister and ooze. Usually responds to self-care within a couple of weeks.

- Keep the skin clean and dry.
- Don't wear clothing that rubs and irritates the area.
- Apply topical over-the-counter antifungal or drying powders,
· If infections not responded in 2 weeks, see GP.

Fungal nail infections that are very difficult to treat. The nail plate is an excellent barrier to drug delivery.
Some lacquers and paints available; nail must be filed
before application.

Fungal skin infection modified by topical steroid treatment. Condition improves with steroid; reduces inflammation but worsens/spreads once treatment is stopped.

For localised ringworm use topical, broad spectrum antifungal creams e.g. imidazoles (e.g. clotrimazole, miconazole) or terbinafine.

Terbinafine 1% cream or spray / in situ film
- Cochrane review and trials show terbinafine better than imidazoles

Topical antifungals can't easily penetrate the follicle.
Due to the risk of scaring, alopecia treatment is usually systemic, normally terbinafine for 2-4 weeks.
Topical treatment; ketoconazole shampoo is recommended at least 2 times/week during the 1st 2 weeks of therapy
Treat all family members with ketoconazole shampoo
- More widespread infections require oral antifungal therapy e.g. terbinafine (250mg od), itraconazole (100mg od) are most effective used for 1-2 months, not currently licensed for use in children.

Advise on common tinea infections
If mild and localised; Athletes' foot, Jock itch, nail infections etc then OTC preparation available
If infection has spread and oral therapy is necessary, refer to GP; Tinea capitis

Barrier to ingress/egress
Regulates water loss - hydration gradient

Key role in barrier integrity
Mediates hydrolytic enzymes
- Health of the stratum corneum depends on maintaining optimal water content.
Skin 'feel' and texture, desquamation etc.
Stratum corneum described as having a ''biosensory function'', responding to external humidity to maintain optimal water output.

This is an endogenous breakdown product from filaggrin hydrolysis
Its a hygroscopic mixture including amino acids, pyrrolidone carboxylic acid (PCA), lactic acid and urea.

Maintains free water within the stratum corneum.
NMF generation together with other processes such as corneocyte maturation, desquamation and lipid biosynthesis regulate stratum corneum hydration. Gives SC flexibility, integrity, cohesion, and hydration. pH also increases when NMF decreases.

Profilaggrin is dephosphorylated to produce filaggrin. Hydrolysis then takes place to generate NMF.

10-12 filaggrin repeat units. Fewer than this causes drier skin.

Corneocyte deformation (flattening of surface skin cells); disrupts organisation of the extracellular lamellar lipid bilayers
A reduction in Natural Moisturising Factor (s), Including metabolites of pro-filaggrin
An increase in skin pH; which encourages serine protease activity.The enzymes which digest lipid- processing enzymes and desmosomes
Serine proteases also generate active cytokines; IL-1a and II - beta and promotes skin inflammation.

Loss of function mutations in the filaggrin gene

Eczema and allergy. Asthma, rhinitis, and genetic risk factor for peanut allergy.
More filaggrin prevents eczema.

Skin is erythematous, dry, flaky, oedematous and crusted (esp. if infected). Almost always itchy.

Skin is often thickened or lichenified (thickened epidermis, prominent normal skin markings). Almost always itchy

Most common form of eczema, especially in babies from 3 months. Occurs in 10-15% of all children
Appears as dry, scaly, erythematous and itchy rash particularly noticeable on face, scalp, neck, inside elbows, behind knees
Often resolves in childhood but can continue into adulthood

A typical sequence of immunoglobulin E (IgE) antibody responses
>50% of children with atopic dermatitis (eczema) develop asthma
~75% develop allergic rhinitis

''Internal'' inflammation, externally applied chemicals (e.g., soaps), environment; humidity. Probably all three
This leads to over production of a protease, breaks down corneodesmosomes, breaks epidermal cohesion and disrupts differentiation.

Results from skin damage from topically applied liquids/ chemicals in absence of an allergic mechanism.
Occurred shortly after patient had a baby; can be due to excess hand washing, chemical/irritant exposure; soaps, cleansers, or cold exposure, contact with certain vegetables; garlic, onions, and tomatoes.
Caused by frequent licking of lips (saliva- induced)

Mediated through an allergic mechanism, where patient is allergic to a specific allergen. Whenever skin contacts that allergen then get eczematous rash; nickel (jewellery, jean studs), leather (shoes, watch straps), dyes, plants.
Allergic contact in response to Rhus (poison oak) species. Not always blisters: allergy to nickel and potassium dichromate.

Emollients; aqueous cream, emulsifying ointment to maintain hydration of SC and reduce evaporation.
Helps avoid dryness and cracking of skin
· Topical steroids: e.g 1% hydrocortisone will reduce inflammation and itchiness.
· Sedating oral antihistamines: e.g. chlorpheniramine (Piriton) at night
Avoid soap (dries the skin/surfactants), wool fabrics and synthetic materials (irritate skin)

Is widely recommended
Contains 1% sodium lauryl sulphate (harsh anionic surfactant);
growing evidence of adverse reactions
''Itchy cream''
Aqueous cream BP reduces stratum corneum thickness, increases transepidermal water loss, affects stratum corneum pH and so enzyme activity and so NMF.
Shouldn't be used as a leave on emollient in AD (atopic dermatitis)
· Recommend emollient without SLS (sodium lauryl sulphate), e.g. E45 Cream (but lanolin may cause irritation), and only advise aqueous cream as a soap substitute.

Occlusion effects of emollient on top could increase drug delivery
Emollient on skin first could provide an additional barrier
Or excipients in emollient could act as permeation enhancer and increase subsequent steroid diffusion.
Or excipient could influence on the corticosteroid formulation, structure and release (increase or decrease)
· Unpredictable:
Corticosteroid cream or ointment can behave differently and different emollients have different effects on steroid delivery.
Generally advise corticosteroid first, leave an hour, then emollient.

common, harmless scaling rash affecting scalp, face, and other areas (eyebrows, ears, folds of underarms and groin)
Dandruff (pityriasis capitis) is seborrheic eczema of scalp Cradlecap in infants up to 6 months may be same condition
Related to proliferation of a normal skin yeast (Pityrosporum ovale)
Can be aggravated by illness, psychological stress, fatigue, change of season, and reduced general health Patients with neurological disorders; Parkinson's, stroke especially at risk. May predispose to psoriasis.

Reduce exposure to allergens; house dust mite, moulds, grass pollens, animal dander
Keep cool- wear loose cotton clothing, avoid wool and dusty conditions, wear gloves when handling chemicals, solvents, detergents.
Use soap- free cleansers.

Seborrhoeic eczema is very persistent in adults. Kept under control with regular use of antifungal agents and intermittent applications of topical steroids.
Infantile seborrhoiec eczema clears up completely before baby is 6 months old; rarely persists after one year.
If treatment is required, mild emollients, hydrocortisone cream and/ or topical ketoconazole are useful
Treatment depends on part of the body involved. It is likely to need repeating from time to time.

Cleanse affected skin thoroughly 1-2x each day.
· Ketoconazole cream once daily for 2-4 wks.
· Hydrocortisone cream can be used, applied up to 2x daily for 1-2 wks.
Severe cases may receive a course of UV radiation

Medicated shampoos containing ketoconazole, selenium disulphide, zinc pyrithione, coal tar, and salicylic acid, used 2x/ week for at least a month. Steroid scalp applications reduce symptoms, and should be applied daily for a few days every so often.
Tar creams can be applied to scaling areas and removed several hours later by shampooing.

Sometimes confused with eczema and mainly affects women between 35-45 yrs. Can be life threatening.
One symptom is classic "butterfly" rash on cheeks and nose. Can include trunk/extremities. Often exacerbated by sunlight/other stresses that increase skin circulation
· Other symptoms: non-specific joint pains (morning stiffness), fatigue,
rapid hair loss (re-grows during remission)
· Genetic origin (several loci involved)

Psoriasis is a common autoimmune disorder. It is a skin condition that causes skin redness, inflammation, and irritation. Most people with psoriasis have thick, red skin with flaky, silver-white patches called scales. Commonly eruption first appears back of elbows and front of knees (flexor surfaces). Patches can also be on other parts of body; scalp

Specific cause remains unknown Factors that may trigger psoriasis include:
1. Infection - some throat and upper respiratory tract infections lower threshold for psoriasis
2. Trauma - e.g. surgical incisions, burns, rubbing, scratching, picking, sunburn and/or local infection of skin
3. Emotional stress/anxiety
4. Climatic factors - Moderate sunlight is beneficial, but sunburn is detrimental. In some patients, any sunlight makes condition worse.
5. Certain drugs e.g. lithium, chloroquine, b-blockers, NSAIDs, ACE inhibitors, alcohol abuse (psoriasis can appear months after drug started)

Psoriatic epidermis shows marked elongation of rete ridges
Dilated and contorted dermal blood vessels reach into the tips of the dermal papillae.
A mixed inflammatory infiltrate with neutrophils accumulating within the epidermis is seen
By contrast with normal skin immunohistochemistry shows many T cells in the dermis and epidermis of lesional psoriatic skin.
Cell nuclei present in the stratum corneum characteristic for lesional psoriatic skin.

Plaque Psoriasis; most common form,
guttate (teardrop shaped) psoriasis,
flexural (inverse) psoriasis,
generalised pustular psoriasis, pustular psoriasis, and psoriatic arthritis

Manifests itself in form of scattered, raised, scaly patches, often on elbows, knees and scalp. Lesions can become itchy and sore.

Consists of numerous, small discrete patches scattered all over body. Commonly seen in the young and may follow throat infections in
predisposed individuals.
Up to 1/3 of patients will spontaneously
resolve.

Affects areas of skin-to-skin contact e.g. armpits, groin, buttocks. Tends to occur in later life

Acute, severe eruption of superficial pustules with reddening of the skin and high fever.
Pustules don't contain bacteria, and not caused by infection.
Can occur following use of large quantities of strong steroid creams or steroid tablets to treat psoriasis.
Uncommon.

Chronic, localised form on hands and feet occurring in middle age.

Inflammatory joint disease, usually affecting small joints of hands and feet.
In most patients, skin changes appear before onset of joint pain.

Occur in 25-50% of psoriasis patients
Very common in patients with psoriatic arthritis
Small indents (pitting) of nails are common as is lifting up of nails (onycholysis), discoloration, thickening and crumbling.

Control and management NOT cure; aims to make symptoms tolerable.

Emollients - always use for hydrating skin. May also have anti-proliferative effect in psoriasis; e.g. emulsifying ointment, aqueous cream. Esp. good for inflammatory psoriasis and plaque psoriasis on palms/soles
Topical corticosteroids - may see early improvement but not generally used as sole treatment. Can treat specific sites e.g. face, flexures (use mild corticosteroid e.g. hydrocortisone) or scalp, hands and feet (use strong steroid e.g. betamethasone, dermovate)
Calcipotriol (Dovonex) - synthetic vitamin D3 analogue that interferes with cell division and differentiation. Formulations are suitable alternatives for patients who have tried coal tar or dithranol
Each of above should be applied 1-2x a day to palpable lesions. Once lesions have flattened treatment can be stopped.

Emollient; Diprobase cream
- plus a steroid and vitamin D analogue - eg Dovobet ointment - or gel - (betamethasone dipropionate as the corticosteroid AND calcipotriol as the vitamin D analogue)

Cochrane review shows corticosteroids are as effective as calcipotriol, with fewer side effects than the vitamin D analogue. Some clinicians prefer to start with emollient and corticosteroid, then add in calcipotriol or similar
- Or for patients with sensitivity.

Anti-inflammatory and anti-scaling properties. Useful in chronic plaque psoriasis.
Most effective form (1-10% in soft paraffin base) but few patients tolerate smell/mess.
- Proprietary preps are cleaner but can take longer to work.

Used as a keratolytic in scalp psoriasis (in combination with emollient/other agents)

Most likely to induce remission c.f. other topical treatments. Esp. effective for chronic plaque psoriasis.
Apply to chronic extensor plaques only; avoid normal skin.
Problems with irritation of normal skin and stains skin and clothing.
Not generally suitable for widespread lesions. Don't use on face/flexures.
Start with low (0.1%) conc. then increase gradually up to 3%.
- Protect hands with gloves when applying.

0.05% tazarotene (vitamin A analogue).
- Recently used topically for mild - moderate plaque psoriasis affecting up to 10% of the skin

Effective for chronic stable psoriasis and guttate psoriasis.
- Consider in patients where topical treatment has failed. May irritate inflammatory psoriasis

Combination of long-wave UVA radiation with psoralen. Available in dermatology centres.
Psoralen (orally or topically) enhances effect of UVA, taken 2hrs before UVA exposure (allows drug time to reach skin).
Effective in most forms of psoriasis.
Early adverse effects include phototoxicity, pruritis.
High doses lead to skin ageing, risk of cataracts and skin cancer.

Integrates with DNA crosslinks as its very similar in structure to DNA bases.
Stops cell division, reduces cell turnonver, reducing psoriasis

Required for severe, resistant, unstable or complicated forms of psoriasis.
Should only be initiated under specialist supervision.

Acitretin, Cyclosporin, and Methotrexate

A retinoid often combined with other treatments.
- Therapeutic effect after 2-4 wks with maximum benefit 4-6 wks after.
Available only in hospital pharmacies and a small number of specified retail pharmacies.

By mouth, used for severe psoriasis and severe eczema.

For severe psoriasis.
- Usual dose is 10-25 mg weekly by mouth.
Folic acid sometimes given to reduce possibility of methotrexate toxicity (liver damageone marrow suppression)

Complex interplay of cutaneous cells with macrophages, dendritic cells, T cells, and other immune system cels
Involves many cytokines and chemokines that cause pathological changes in pre-psoriatic skin.
Adaptive (T cells) and innate immune cells (macrophages, mast cells, granulocytes) produce mediators that induce and maintain psoriasis and inflammatory response

Human monoclonal antibody in rheumatoid arthritis. Also treats; psoriatic arthritis, ankylosing spondylitis, Crohn's disease, ulcerative colitis, chronic psoriasis, etc.

TNF-inhibiting, anti-inflammatory. Binds to tumour necrosis factor-alpha (TNFα), which normally binds to TNFα receptors, leading to the inflammatory response of autoimmune diseases. By binding to TNFα, adalimumab reduces this inflammatory response. As TNFα is part of the immune system, treatment with adalimumab may increase risk of infections.

Used to treat Psoriasis. Designed to interfere with the triggering of the body's inflammatory response through suppression of certain cytokines.
Blocks interleukin IL-12 and IL-23 which helps activate certain T-cells, binds to the p-40 subunit of both IL-12 and IL-23 so they subsequently can't bind to their receptors.

For plaque psoriasis.
SC injection of 100mg given every 8 weeks (except for the 2nd dose, which is given 4 weeks after the 1st dose).
Targets the IL-23 subunit alpha (p19 subunit), preventing it from binding cell receptors that would otherwise be activated by its presence.
The drug showed superiority after 3 doses (16 weeks), and the response was maintained after treatment until week 48, with a comparable safety profile.

Achieved near complete skin clearance in 73% of plaque psoriasis patients against 66% for Humira. Only requires a dose every 8 weeks, instead of every week as in the case of Humira.

Dupilumab (Dupixent); eczema, moderate-severe atopic dermatitis, (& asthma?)
Brodalumab; moderate- severe plaque psoriasis in people who haven't improved with other treatment; use linked to increased risk of suicide. Binds to the IL-17 receptor and so prevents IL-17 from activating the receptor
Nemolizumab blocks the IL-31 receptor A; for itch in atopic dermatitis.
Siplizumab; selectively suppresses the function of T and NK cells, and is currently tested as a possible psoriasis treatment
Zanolimumab; developed for treatment of rheumatoid arthritis, psoriasis, melanoma,cutaneous and peripheral T-cell lymphoma; undergoing Phase II trials.
common side effects; suppress immune system, prone to infections (can be serious), hence search from more specific mabs

Eczema: Idiopathic, genetic; family history of atopy; Environmental triggers
Psoriasis: Idiopathic, genetic; triggered by trauma, stress, infection.
Contact dermatitis:
Contact leading to irritation; irritant (most people react to) or allergic (some people respond to)

Eczema: Abnormal IgE activity mediated by B lymphocytes
Psoriasis: Abnormal T cell activity; excess / hyperproliferation of skin cells
Contact dermatitis: Abnormal T cell activity mediated by T lymphocytes

Eczema: Dry scaly thickened skin often on flexural surfaces; common in children.
Psoriasis: Skin plaques "silvery" scales; rough red and raised skin; common on extensor surfaces.
Contact dermatitis: Red / burning itchy vesicles on skin surface. Irritant located at site of exposure (but may spread); allergic not localised to exposure site.

Eczema: Corticosteroid creams; emollients; wet dressing
Psoriasis: Emollients; Vitamin D analogues and corticosteroid; UV light; coal tar; monoclonal antibodies.
Contact dermatitis:
Avoid irritant; corticosteroid; calamine; antihistamine for itch

MHRA introduced labelling on all emollients, including paraffin- and non-paraffin-based products.
Emollients aren't flammable in themselves, or on the skin, bedding, clothing and dressings containing dried emollient residue catch fire, ignite and burn more quickly and intensely. Risk is low and emollients are essential for managing eczema, But advise patients to avoid naked flames & halogen heaters near clothing / bedding / dressings

Most emollients are plain (no API) but some contain:
Urea (a keratin softener and hydrating agent); Aquadrate®,Calmurid®, E45® Itch Relief Cream. Lauromacrogols (local anaesthetic properties, soothes itchy skin); Balneum® Plus, E45® Itch Relief Cream.
Lanolin or lanolin derivatives; hydrous ointment, E45® cream, Oilatum® emollient bath additive.
Antiseptic; Dermol® preparations (cream, lotion, shower, and bath emollient).
Emollients containing API's not recommended; increased risk of skin reactions, but useful for some people.

Prescribed according to skin dryness, and individual preference/tolerance.
Creams and lotions = Better for red, inflamed areas of skin. Evaporation of water-based products maybe cools the skin.
BUT DON'T ADVISE USE OF AQUEOUS CREAM
Ointments = Preferable for dry skin; (that isn't inflamed) as more effective than creams but, poorly tolerated; may affect their acceptability thus compliance.
Proprietary products often preferred to non-proprietary products
Several different emollients required for different areas of skin, stages of flare, or for different locations). Ideally, recommend an emollient with pump dispenser to minimise risk of.,,/,mm bacterial contamination and ease of use
For emollients that come in pots, advise using a clean spoon/spatula (rather than fingers) to remove the emollient helps minimize contamination, but most patients use a finger!

If bath emollients are used, its essential they DON'T replace standard emollients.
The effectiveness and acceptability of a particular emollient may vary with time.
If a person feels a particular product has become unsuitable for them (or have developed sensitivity to it), recommend an alternative emollient.
May be necessary to try a range of emollients before patient settles on the best combination.

Emollients are typically under-prescribed and under-used.
Results in suboptimal treatment of dry skin and eczema and may increase the occurrence of flares.
Dispense generous amounts; 500g to be used regularly often 4x daily.
Encourage appropriate usage
· The amount of emollient used should far exceed other topical treatments; corticosteroids by a factor of at least 10.

Skin reactions are the most common adverse effects of emollients. Due to skin sensitising additives; perfumes, preservatives, and biological components; lanolin (although newer hypoallergenic formulations of lanolin are less problematic).

If a skin reaction occurs, stop the emollient, and use alternative.
If the person has had previous skin reactions to emollients, consider testing a small quantity on the skin before widespread application.
If sensitivity to emollients is a known problem, prescribe a cream with few additives, or an ointment (ointments don't require preservatives and have less excipients), to reduce the chance of a further reaction.
The occlusive effect of ointments can cause folliculitis. If this occurs, stop the ointment (consider switching to a cream), and prescribe an antibiotic, if necessary.

Advise to use liberally and frequently, even when skin appears improved or is clear.
Recommended that 250-500 g of emollient be applied every week.
Frequency of application varies, but for very dry skin, application is every 2-3 hours is normal.
To facilitate frequent application, patient should consider keeping separate packs of emollients at work/school.
Important to use during or after washing.
Should be applied by smoothing them into skin along line of hair growth, rather than rubbing them in.
Can use better tolerated products; creams and lotions during the day, and ointments (which are usually poorly tolerated) at night.
Shouldn't be shared with others as they can become contaminated with bacteria.
Avoid use of soaps, detergents, and bubble bath when washing; use suitable soap substitute instead
(People who need to use large quantities (more than 100 g) of any paraffin-based product should regularly change clothing, bedding, or dressings which become impregnated with the product and keep away from naked flames, as there is a risk of fire)

Comedones (blackheads and whiteheads), papules (pinheads), skin elevation, no fluid 5-10 mm diameter Nodules (like a papule but bigger than 5-10 mm)
Cysts (cavity usually containing fluid)
Can be inflammatory or non-inflammatory
Appears on face, shoulders, may occur on trunk, arms and legs

When hair follicles and associated sebaceous gland become obstructed with sebum/dead keratinocytes.
Can become infected with normal skin anaerobe, Cutibacterium acnes leading to inflammation
Lipases from C. acnes metabolise triglycerides into free fatty acids, which irritate the follicular wall.
Pustules occur when active C. acnes infection causes inflammation within the follicle.
Nodules/cysts appear when inflamed follicles rupture.

Commonly occurs in adolescence but can arise at any age, including as an infant
Condition usually remits spontaneously by early 20s but can persist (usually women) until 40s
Tends to run in families
Most common trigger is puberty; surges in androgen that stimulates sebum production and hyperproliferation of keratinocytes.
Other triggers include:
Hormonal changes in pregnancy or menstrual cycle,
Occlusive cosmetics, cleansing agents and clothing,
Excessive humidity and sweating
Stress
Certain drugs; oral contraceptives, corticosteroids, testosterone, oestrogen, and phenytoin
No association between acne and diet; chocolate)

Visual examination of the affected areas by the physician.
Classification of Acne Severity
Mild
< 20 comedones, or < 15 inflammatory lesions, or < 30 total lesions
Moderate
20- 100 comedones, or 15- 50 inflammatory lesions, or 30- 125 total lesions
Severe
> 5 cysts, or total comedone count > 100, or total inflammatory count > 50, or > 125 total lesions

Main aim; reduce sebum production, comedone formation, inflammation and infection
Treatment depends on severity
cleanse affected areas daily. - extra washing, scrubbing, use of antibacterial soaps have no benefit
Changes in diet unnecessary
Mild- moderate usually treated topically
Moderate - severe usually systemic antibiotics (or when topicals failed)
Severe refer to dermatologist; may need aggressive therapy e.g. Isotretinoin

Comedones and inflamed lesions respond well to benzoyl peroxide; starting at a low dose and increased if necessary, 2.5-5%, then 10%
If no response in 2 months; consider topical anti-bacterial.
MoA =
As a peroxide is metabolised to benzoic acid and oxygen free radicals. Benzoic acid decreases pH.
Oxygen free radicals are bactericidal, and can also break down keratin so are comedolytic
Benzoyl peroxide also available with clindamycin (antimicrobial)

An alternative that has
anti-microbial and anti-comedonal properties. Less likely to cause local irritation than benzoyl peroxide. Patients may prefer, especially for face

Tretinoin/Adapalene) effective for comedones and inflamed lesions.
Can be irritant, initially giving redness/peeling
Avoid in pregnancy, avoid sun exposure.

Salicylic acid preparations are available; Keratolytic, and not suitable as other preparations
Sulphur/abrasive
Not considered beneficial
Topical corticosteroids should NOT be used (increase sebum secretions)

Responds best to oral systemic therapy with antibiotics; tetracycline, minocycline, doxycycline, erythromycin.
Tetracycline common 1st choice 500mg BD; between meals and at bedtime.
Expect maximum improvement after 4-6 months
If no benefits after 1st 3 months, consider swapping to doxycycline

Oral isotretinoin (1mg/kg daily for 16-20wks).
Almost always effective, but has serious side effects;
dryness of mucous membranes, depression, arthralgias, birth defects, elevated lipids.

Inflammatory skin disease affecting middle third of the face. Can be confused with acne, eczema or skin allergy.· No blackheads or whiteheads

Persistent redness over areas of face and nose that normally blush (fore-head, chin, lower half of nose).
Get dilatation of blood vessels under skin appearing as thread veins (telangiectasias)

Occurs in adults (30-60yrs), especially in those with skin types 1 &2. Affects both sexes; more common in females, but more severe in males.

Cyclical condition that can last for years and can progress to permanent disfigurement if not treated. Also can be progressive affecting the eyes (burning, gritty sensation viz. conjunctivitis), ears and nose that swells and grows (rhinophyma). Very disfiguring

Unknown cause (could be combination of genetic/ environmental factors)
Affects people who blush easily
Emotional factors: stress, fear, anxiety, embarrassment
Flare-ups can be caused by weather changes (strong winds, humidity). Sun exposure generally aggravates rosacea
Helicobacter pylori and certain medications e.g. vasodilators, corticosteroids linked with rosacea.
Tiny mites in human hair (Dermodex folliculorum) linked to clogging of sebaceous gland openings
Certain foodseverages:
alcohol, coffee, tea, spicy foods, hot soups can precipitate rosaea

Topical metronidazole. Rarely clears up without treatment. Skin treatments for acne (e.g. benzoyl peroxide) make rosacea worse.

Reduces inflammatory papules and pustules; has little/no effect on flushing or vascular component of the disease.
Reduces papules and pustules by ~65% over a 9-wk course.

Topical azelaic acid reduces redness/inflammation.
Oral antibiotics also used: tetracycline (1st line), minocycline, doxycycline and erythromycin
Commonly start with oral and topical formulations then move to maintenance with topical cream.
Depending on severity, camouflages may be used

More severe forms of rosacea treated with isotretinoin (Accutane).
Works by inhibiting sebaceous gland oil production. Possibility of serious side-effects (teratogenic)

In cases where blood vessels have become enlarged permanently and rhinophyma has begun, the only course of treatment available is surgery, including laser surgery and electrosurgery that'll reduce the visibility of blood vessels, remove tissue build up and improve appearance

Wear sunscreen with a sun protection factor (SPF) >30 to protect face from the sun
Protect your face in the winter (e.g. scarf)
Avoid irritating facial skin by rubbing/ touching too much
· Avoid facial products that contain alcohol/other skin irritants
When using moisturizer with a topical medication, apply the moisturizer after the medication has dried.
Use products that are labeled non-comedogenic; these won't clog oil and sweat gland pores as much
Avoid alcohol

Infestation of the skin with the mite, Sarcoptes scabiei
Obligate human parasite that lives in burrowed tunnels in stratum corneum. Burrows are a few mm - 1cm long.
Tiny black papules (the mite) often visible at one end
Human scabies often found between the fingers and on the wrist.
Easily transmitted from person-to-person through physical contact. Animal transmission also occurs

Primary risk factor is crowded conditions (schools, shelters, some households). No clear association with poor hygiene.

Causes intensely pruritic lesions, usually worse at night, with erythematous papules and burrows in web areas of hands, wrists, waistline and genitals
Severity related to patient's immune system, not geography

Diagnosis based on examination and skin scrapings
1st line treatment is with topical scabicides. Permethrin is drug of choice. Applied to entire body from neck down and wash it off after 8-14 h. Repeat treatment after 7d.
For infants and young children: applied to the head and neck, avoiding periorbital and perioral regions.
Special attention should be given to fingernails, toenails, and umbilicus. Mittens on infants keeps permethrin out of mouth.

Not recommended in children < 2 yr or in patients with a seizure disorder because of potential neurotoxicity

Precipitated sulphur 6 - 10% in petrolatum, applied for 24h for 3 days in a row, is safe and effective.
Close contacts should be treated too, personal items should be washed/isolated for at least 3 days (towels, clothing, and bedding)

Classic scabies,
Crusted (Norwegian) scabies, Nodular scabies,
Bullous scabies,
Scalp scabies,
Scabies incognito

erythematous papules first appear in finger web spaces, wrists, elbows, axillary folds, waistline. Face remains unaffected in adults.

Due to impaired immune system

More common in infants/young children. May be due to hypersensitivity to retained organisms

Children and elderly.

Occurs in infants and immuno- compromised patients. Can mimic seborrhoeic eczema

Widespread atypical form resulting from application of topical corticosteroids.

For patients who don't respond to topical treatment, unable to adhere to topical regimens, or are immunocompromised with Norwegian scabies.

Corticosteroid ointments and/or oral antihistamines
Symptoms and lesions take up to 3 wks to resolve despite killing off the mites.

Wingless, blood-sucking insects, 2-5mm in length, that can infest scalp (Pediculus humanus var. capitis), body (P. humanus var. corporis), pubis (crab lice; Phthirus pubis), eyelashes
All three kinds of lice differ substantially in morphology and clinical features. Can act as vectors for other diseases; typhus

Up to 30 days

Usually involves <20 live, causing severe pruritus.

By close contact; body lice in cramped, crowded conditions; pubic lice (crabs) by sexual contact.

Most common in girls aged 5-11, can affect almost everyone; rare in Afro-Caribbeans

hair. scalp, eyelashes, eyebrows, and beard.

By close contact (households, classrooms); may be ejected from hair by static electricity or wind.
Transmission also by sharing combs, brushes (hats unproven)
No association with poor hygiene/low socioeconomic status.

Detected by thorough combing-through of wet hair from scalp with fine-toothed "lice" comb; lice usually found at back of headehind ears. Can be difficult to see.
Nits are ovoid, greyish-white eggs fixed to the base of hair shafts

Each adult louse layer 3-5 eggs/day (nits vastly outnumber lice), hatch in 7 days.

Treat all family members.
Mechanical removal (wet combing) avoids resistance/irritation by chemicals. Use nit comb on wet hair ( conditioned may help). Comb whole scalp (esp. behind ears) at 4 day intervals for 2 weeks; eggs may hatch between combing.

Dimeticone (4%) - Apply to dry hair and scalp, allow to dry naturally, wash off after 8h. Repeat after 7 days.
Malathion (0.5%) - Apply to dry hair and scalp, allow to dry naturally, wash off after 12h. Repeat after 7 days. Unpleasant odour. Resistance reported
Permethrin - Active but not recommended for head lice.

Live on bedding/clothing primarily. Found in crowded conditions; barracks and in those of low socioeconomic status
Transmitted by sharing contaminated clothing and bedding

Intense pruritis
See small red puncta caused by bites. Esp. common on shoulders, buttocks and abdomen.
Diagnosis is by demonstration of nits/lice in clothing esp. at seams

Topical treatment of no use since body lice are found in clothing. Treat pruritus and secondary infection.

Malathion. Apply 0.5% aqueous preparation over whole body, dry naturally, wash off after 12h. Repeat application after 7 days
Permethrin. Apply 5% cream over whole body, dry naturally, leave 12h or overnight, wash off. Repeat after 7 days

Petrolatum ointment. Apply 3-4 times/day for 8-10 days.
Fluorescein drops 10-20%. Applied to the eyelids. Provides immediate pediculocidal effect.

Also called Furuncles and Carbuncles.
Tender nodules caused by Staphylococcal infection, often an infection of the hair follicle.

Appear as nodules or pustules. Common on neck, face, breasts, and buttocks. Can be very painful esp. if on nose, ears etc.

A cluster of furuncles connected subcutaneously, causing scarring. May be accompanied by fever.

Bacterial colonisation of skin, hot and humid climates, occlusion or abnormal follicular anatomy; comedones in acne, more common in obese, immunocompromised, elderly, and diabetic patients.

Diagnosis is by examination. Material for culture should be obtained from patients with single furuncles on nose/central face, from patients with multiple furuncles, and immunocompromised patients

Intermittent hot compresses to allow it to drain spontaneously.

For furuncle in the nose, central facial area, multiple furuncles, or carbuncles
penicillinase-resistant beta-lactam (S.aureus resistance)

For larger lesions, lesions that don't respond to topical care, evidence of expanding cellulitis, immune-compromised patients, or patients at risk of endocarditis. Incision and drainage occasionally necessary.

By application of liquid soap containing either chlorhexidine gluconate with isopropyl alcohol or 2-3% chloroxylenol, or by maintenance antibiotics over 1-2 mo.

Superficial skin infection with crusting caused by Streptococci, Staphylococci, or both.
Ecthyma is an ulcerative form of impetigo.
No predisposing lesion identified in most patients but can follow any break in skin

Moist environment, poor hygiene, chronic nasal carriage of staphylococci

Clusters of vesicles or pustules that rupture and develop "honey-coloured crust"

By small, purulent, shallow, punched-out ulcers with thick, brown-black crusts and surrounding erythema

Mild pain or discomfort. Pruritus is common, scratching can spread infection

Cultures of lesions indicated only when patient fails to respond to initial therapy. Patients with recurrent impetigo require nasal culture.
Localised disease treated with fusidic acid (2%, 3-4 times daily).
If MRSA, can use topical mupirocin, ( 2%, t.d.s. 10 days)
If extensive, refer for oral antibiotics:
Flucloxacillin ,
Clarithromycin
Prompt recovery usually follows timely treatment

Poorly understood reaction of skin to sunlight. Likely involving the immune system.

Redness, rash, urticaria. Within minutes of exposure to sunlight. In extreme cases can lead to dizziness, wheezing and other systemic problems.

Can occur after exposure to certain drugs or chemicals; phenothiazines
Treatment varies depending on cause:
Unusual reactions occur after brief sun exposure, suspect systemic disease or underlying skin disorder; lupus erythematosus.
If sunlight induces skin reaction following use of chemicals; in cosmetics, use topical corticosteroids and avoid causative agent.

Phototoxicity and Photoallergy.

Light-absorbing compounds directly generate free radicals and inflammatory mediators. Get tissue damage, pain and erythema (like sunburn).
Reaction doesn't require prior sun exposure, can appear in anyone and is highly variable.

Topical (e.g. perfumes, coal tar) or ingested (e.g. tetracyclines, psoralen-containing plants) agents.
Only on sun-exposed skin.

Type IV (cell-mediated) immune response; light absorption causes structural changes in drug/chemical, allowing it to bind to tissue protein and function as a hapten.
Prior exposure is required.

Aftershave lotions, sunscreens, and sulfonamides.
Reaction may extend to non-sun-exposed skin. Symptoms include: erythema, pruritus, and sometimes vesicles.

Burns are injuries of skin or other tissue caused by thermal, radiation, chemical or electrical contact.

Burns are classified according to their severity or depth. For example, in first-degree burns, only the epidermis is damaged; in second degree burns, the epidermis and upper dermis are damaged; in third degree burns, there is widespread damage of epidermis and dermis.

Burns caused from any external heat source; flame, liquids, solid objects, gases flash, or scald.

Burns that commonly result from prolonged exposure to solar UV radiation (sunburn). Can be from other sources; tanning beds, X-rays, non-solar radiation)

Strong acids or alkalis (e.g. cement), phenols, cresols. Skin/deeper tissue necrosis due to agents may progress over hrs

Burns that result from electrical generation of heat. Skin/deeper tissue damage may result despite minimal apparent cutaneous injury.

Protein denaturation and coagulation necrosis.
Platelet's aggregate, vessels constrict around coagulated burned tissue.
inflammation around damaged zone may get bacterial infection through damaged epidermal layer -> oedema and external fluid leakage.
Heat loss significant asg thermoregulation of damaged dermis is impaired and fluid leakage increases evaporative heat loss.

The greater the percentage of body mass surface (BSA) involved, the greater the risk of developing systemic complications.

>40% BSA, age >60 yrs or <2yrs, and presence of simultaneous major trauma or smoke inhalation.

Most common type of burn
Burns are red, blanch markedly with light pressure
Painful and tender
Limited to epidermis

(Partial thickness)
Involves part of dermis
Sub-divided into superficial and deep

Burns involve upper half of dermis; heal within 2-3 wks.
Rarely scar in this period unless become infected.
Skin is red/white, blanch with pressure
Intense pain and tender.
Vesicles develop within 24 hr.

Degree burns involve bottom half of dermis, take >3 wk to heal and scarring is common.
May be white, red, or mottled. Doesn't blanch and less painful/tender than more superficial burns.
Vesicles may develop.
Burns tend to be very dry.

Full thickness
Extend through entire dermis and into underlying fat

Examined/treated as soon as the patient is stable.
1st priorities, as for any injured patient, (airway, breathing, circulation).
Remove clothing covering burn, flush chemicals (except powders that are brushed off ) with water.
Burns caused by acids, alkalis flushed with lots of water for at least 20 mins.
Small burns immersed early in cold water until pain subsides (won't limit depth of injury)
IV fluids for patients in shock or with burns >15% BSA
Hypothermia/pain treated appropriately.
After cleaning wound, cover burn with topical antibacterial salve (e.g. 1% silver sulphadiazine) and sterile dressing.
Depending on severity, patient might need to be hospitalized.
Dressings are changed daily. Burn cleaned completely with water. Apply new layer of antibacterial salve and re-apply clean dressing

Indicated for all third degree burns and burns that don't heal within 3 wks (most deep 2nd degree burns)
Graft of a layer of healthy skin; 5cm2 from thigh.
Cut into a mesh - covers 10-20cm2

Physical break in the skin; tear, cut, erosion, puncture or ulcer.
Break in the skin barrier function
Loss of fluid, blood or heat; large burns
Allows invasion of microorganisms; e.g S. aureus, Cl. tetani)
Toxin ingress

Abrasion -
Graze, superficial epidermis scraped off
Laceration -
Irregular tear
Avulsion -
Removal of all skin layers by abrasion
Incision -
Regular slice with a clean sharp object, knife
Puncture -
e.g. nail or needle
Amputation
Cut off!

Necrotic
Dead (ischaemic) tissue, usually black and covered with dead epidermis
Hydrogels, hydrocolloids.
Sloughy
Yellow due to accumulation of cellular debris, fibrin, serum exudate, and bacteria
Hydrogels, alginates, spun hydrocolloids
Granulating
Deep pink/ red with a high vascularised irregular granular appearance
Alginates, hydrocolloids, foams
Epithelialising
Cells migrating from wound edges to start the process of re-epithelialisation.
Low and non-adherent dressings, knitted viscose, paraffin gauze, film dressings

1. An injury occurs
2. The platelets start to aggregate, RBC's lost, and presents the wound.
3. Neutrophils are attracted to wound by fibronectin and growth factor
4. Coagulation with fibrin, forms fibrin clots.
5. Early inflammation occurs as neutrophils are brought to clean and decontaminate.
6. Later inflammation stage = wound is essentially cleaned.
7. Body starts to proliferate re-epithelialized wound until it gets remodelled.

1. Haemostatic response - tries to stop blood loss
2. Inflammation - lasts 3 days, body cleans wound ready for self- repair
3. Proliferation -
- Granulation
- Epithelialisation
- Collagen Production
- Wound Contraction
4. Maturationemodelling

Process by which bleeding from an injured vessel is arrested or reduced. Vessel damage -> exposed collagen, platelet aggregation, vasoconstriction occurs, coagulation cascade, and then the haemostatic plug/clot that seals damaged vessel

Characterized by redness, heat, pain and swelling and typically lasts 4- 5 days
Initiates healing process by stabilizing wound through platelet activity ->stops bleeding and
triggers immune response.
Within 24 hours of initial injury, neutrophils, monocytes, and macrophages control bacterial growth and remove dead tissue.
Characteristic red colour and warmth caused by capillary blood system, increasing circulation & laying foundation for epithelial growth.

Begins within 24 hours of initial injury and can continue for up to 21 days
Characterised by 3 events:
Epithelialization
Granulation
Collagen synthesis

Formation of new capillaries that generate and feed new tissue; Angiogenesis
Granulation tissue is "beefy" red tissue that bleeds easily
Fibrous connective tissue replaces the fibrin clot
Grows from base of the wound

Formation of an epithelial layer that seals and protects wound from bacteria and fluid loss
Must have moist environment to foster growth of this layer. Initially very fragile, can easily destroy with aggressive wound irrigation or cleansing of. involved area.

Creates strength and a support matrix for new tissue
Oxygen, iron, vitamin C, zinc, magnesium & protein vital for collagen synthesis
This stage is the actual rebuilding of skin barrier
Influenced by overall patient condition (age, nutrition etc), and by wound bed condition.

Wounds contract ~ 1 week post injury
Fibroblasts differentiate into myofibroblasts
Cells mid-way between fibroblast and smooth muscle cell!
After healing, myofibroblasts lost by apoptosis. If not, can give keloid scars
Contraction can last for weeks and continues after wound is completely re-epithelialized.
Large wounds 40- 80% smaller after contraction.
Wounds contract at speed up to 0.75 mm/day, depending on how loose tissue in wounded area is
Contraction doesn't occur symmetrically; most wounds have an 'axis of contraction' to align cells with collagen.

Final stage of wound healing - begins ~day 21, could continue for ~2 years
Begins when collagen synthesis and degradation equalise.
Type III collagen produced during proliferation, gradually degraded and replaced with stronger type I collagen.
Originally disorganised collagen fibers are rearranged, cross-linked, and aligned along "tension lines"
Langer's lines = direction human cadaver's skin will split when struck with a spike. Corresponds to natural orientation of collagen fibres in the dermis.
- Termed re-modelling
During maturation, wounds tensile strength increases,
- ~50% that of normal tissue by three months after injury
- ~80% as strong as normal tissue when fully healed
As activity at wound site reduces, scar loses its red appearance as blood vessels no longer needed are removed by apoptosis.

Primary healing -
Healing by 1st intention, or primary wound closure.
Secondary healing -
Healing by secondary intention, or secondary wound closure.
Delayed primary healing -
May be called healing by 3rd intent/tertiary intention.

When wound edges brought together so they're both adjacent (re-approximated)
Most surgical wounds heal this way
Wound closure. performed with sutures (stitches), staples, or adhesive tape
Advantages:
- Minimizes scarring
- Lowers infection risk
- Usually faster than secondary

Wound allowed to granulate.
Surgeon may pack wound with gauze or use a drainage system.
Granulation causes broader scar than primary intent
Healing may be slow due to drainage from infection
Must perform wound care daily to encourage wound debris removal - allowing granulation tissue formation
Advantages:
- Allows removal of foreign bodies
- Prevents haematoma development (collection of blood outside of blood vessels that trap when wound closed immediately ;by stitches

Wound purposely left open, but
initially cleaned, debrided (remove dead, damaged or infected tissue) and observed.
By 4th day, phagocytosis of contaminated tissues, epithelisation, collagen deposition, and maturation occur.
Wound closed surgically after 4-5 days, but, if "cleansing" of the wound is incomplete, chronic inflammation can occur = significant scarring.

Areas of fibrous tissue. Natural part of the healing process, all wounds result in some degree of scarring (often not obvious)
Scar tissue- from collagen, but is highly orientated rather than as a "basket weave" So, weaker than random arrangement to future trauma, UV radiation.
Sweat glands and hair follicles don't grow back within scar tissue.

Myofibroblasts persist rather than cleared by apoptosis. May get keloid or hypertrophic scars

Over-production of collagen during healing causes raised scar above skin surface.
Typically, red raised lump on skin.
Less common following surgery ("closure by intention") more common for wounds closed by "secondary intention"
May seem camouflage

Overgrowth of collagen forming rubbery / shiny nodules that can be pink, red, brown. Often overgrow on area of initial trauma
Can continue to grow into large (benign) tumorous tissue
Keloid scars can be caused by surgery, accidents, acne or, from body piercings.
Inert collagen masses, thus harmless and non-cancerous, but cosmetically unacceptable to some patients.
Can be itchy or painful in some. Most common on shoulders and chest.

Sunken recess in skin with pitted appearance.
Caused when underlying structures supporting skin (fat / muscle) are lost.
Associated with acne, chickenpox, also found after some surgeries.

Form of scarring, caused when skin is stretched rapidly; during pregnancy, weight gain, adolescent growth spurts), and when skin is put under tension during healing process, (near joints).
Appearance improves over time (years)

Chemical peels
For superficial (e.g. acne) scars, not for keloids or with infections in scars
Filler injections
Helps appearance of atrophic scars (raise scar to skin level)
Dermabrasion
Removes top layer of scar tissue
Laser
Non-ablative can heat and redistribute collagen in keloids. Ablative lasers remove outer skin layers, not recommended for keloids
Radiotherapy
Low dose may help keloids. Not recommended due to adverse effects
Ointments and pressure dressings
No strong evidence of benefits
Steroids
Topical steroids ineffective. Can inject steroid directly into scar. Some evidence that it thins and softens the scar
Surgery
Cut out scar, let new wound heal by intention; scar may have come from accident / trauma)
But, keloid scars often recur (45%)