Keratosis pilaris is an extremely common skin condition seen mainly in teenagers and adults that is caused by accumulation of keratin in hair follicles. It is most commonly seen on the extensor surfaces of the upper arms and thighs, but can occur in other locations including the face, chest, buttocks and trunk. It is also sometimes associated with erythema (redness) and pigmentation of the skin on the cheeks of the face (keratosis pilaris rouge).

It is sometimes colloquially known as “Chicken skin” due to its appearance – which can also look a little bit like goosebumps. It occasionally can be itchy.

It often starts in childhood and peaks in adolescence. It is often better in summer and worse in winter.

The diagnosis is clinical and not investigations are required. Occasionally a skin biopsy may be performed if there is doubt about the diagnosis.

It is typically treated with exfoliation (such as a mildly abrasive sponge or scrub in the shower or bath), and if this is unsuccessful then moisturisers that contain urea, salicylic acid, lactic acid or alpha hydroxy acid can be used to break down the keratin. Rarely, topical retinoids may be used.

The condition is not serious and is not infections. It can occasionally lead to scarring and hair loss in the affected areas. It often resolves without treatment in adult life.

Epidemiology

• 80% of adolescents and 40% of adults
• Most patients are unaware or not bothered by the condition
• F > M

Differential diagnosis

• Acne vulgaris
• Atopic dermatitis
• Folliculitis
• Milia

Management

There is no cure. Management methods aim to reduce the symptoms, but are only temporary and it often returns when these methods are ceased.

• Avoid excessive dryness of the skin – use a regular emollient (moisturiser)
• Creams continuing urea, salicylic acid or hydroxy acids can reduce the bumps by breaking down the keratin
• Exfoliation with an abrasive sponge or other scrub can reduce the appearance of the bumps
• Laser treatment may be considered

Long term outcome is variable. About half of cases in adolescence will resolve in adult life.

References

• Keratosis Pilaris – dermnet NZ
• Keratosis pilaris – patient.info
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

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Chickenpox is a common, highly infectious, usually self-limiting viral illness caused by the varicella zoster virus. Varicella is a type of herpes virus – and like other herpes viruses – after the virus has been contracted it may remain dormant in the host for many years – and can sometimes reactivate. In the case of varicella – reactivation of the virus causes the illness shingles.

Although chickenpox is usually mild, it can cause pneumonia (more properly a pneumonitis) and in those who are immunocompromised and in neonates it can cause a serious disseminated (widespread to many organs) illness.

It is possible to be infected (including developing immunity) and never develop the clinical syndrome of chickenpox.

The virus is typically airborne and enters the body through the respiratory tract. Viraemia (virus in the blood) can be detected 4-6 days later, but the first symptoms don’t usually occur until 10-14 days after exposure and it can be as long as 21 days. There may be a short prodromal period of a few days before the rash develops. The rash is quite characteristic and can usually be diagnosed clinically.

Usually, no specific treatment is required and most cases resolved within about a week of the onset of the rash. A patient is considered no longer infectious once all of the lesions of the rash have crusted over.

Neonates and those who are immunocompromised, as well we pregnant women who are not immune may receive specific treatment such as IV immunoglobulin or the antiviral medication aciclovir.

In recent years, vaccines against varicella have been developed. In Australia it is now routine to vaccinate children against chickenpox – this comes in combination with the MMR vaccine – the MMRV vaccine – and is given with he third dose of the MMR at age 18 months. A single dose of varicella vaccine is required. Shingles is a significant cause of morbidity in older populations and vaccination is hoped will reduce the incidence of shingles in future, as well as the incidence of chickenpox and the risks of chickenpox in pregnancy.

Epidemiology and Aetiology

Varicella can be passed on by either an active case of chickenpox or an active case of shingles – however chickenpox is much more infectious than singles. Varicella is endemic in most countries and tends to occur in outbreaks. The peak time of year is in spring.

• Over 90% of the population have contracted the illness by the age of 15 in endemic areas (this stat is from the UK)
• Less common in tropical and subtropical regions
• Infection tends to occur before the age of 10 in most developed countries. An older age is more common in warmer climates
• Patients are infectious from a few days before the lesions show, until all the lesions have crusted over. Some sources suggest this is from day 8-21 after exposure
• Is it not possible to “catch shingles. Shingles is a reactivation of the varicella virus in a host who has previously had chickenpox. However it is possible to catch chickenpox from someone who has shingles – however this is rare. Covering up the lesions of shingles reduces the risk.

Presentation

The rash of chickenpox has a specific pattern and the diagnosis can usually be made clinically on the basis of this rash.

• The rash occurs in “crops”
• Each crop consists of a handful of spots
• The first crop is typically on the head, neck or torso
• Further crops follow several hours (up to 12 hours) later
• Over the course of 24-72 hours the rash becomes widespread on most of the body – the limbs are usually less severely affected
• The lesions at first are discreet red raised lesions
• These becomes fluid fills blisters, before crusting over and drying out
• There are usually patches in different places not he body going through a different part of this process
• The patient is considered to no longer be infectious once all the lesions have crusted and dried
• Marks are often visible for several weeks, but only rarely does it cause long term scarring
• The rash may be itchy bit isn’t always
• Females may have painful vulval lesions
• secondary bacterial infection of the lesions can occur – this is also more common in eczema

Other symptoms include:

• Fever – may be for up to 4 days
• Headache, myalgias – these can start several days before the rash begins
• In those two have been previously immunised a very mild form of the disease may develop
• Pneumonia is a rare but serious complication

Diagnosis

• Diagnosis is almost always clinical
• Swabs of the fluid from blister can be sent for laboratory confirmation but this is not usually necessary

Management

Most cases in previously well individuals do not require specific management. Children aged >1 week and <12 years do generally not require any specific treatment. The illness can be more severe in teenagers and adults. Advice should be given about:

• Avoiding scratching
  • Antihistamines and emollients (moisturises) are effective to reduce the itch
  • Calamine lotion is NOT recommended as the effect ceases as soon as it dried (which is usually very quickly)
• Avoid pregnant women, neonates and those who may be immunocompromised until all the lesions have dried and crusted over
  • Patients should isolate from school / work until no longer infectious
• Encourage adequate fluid intake
• Paracetamol may be given for fever and headache
  • 15mg/Kg QID in children
  • 1g QID in adults
• Avoid the use of ibuprofen and other NSAIDS
  • These can increase the risk of group A strep (GAS) infection when given with varicella virus
  • Aspirin should be avoided in children due to increase risk of Reye syndrome
• Aciclovir should be considered in those who are immunocompromised, pregnant or have serious illness. You may also consider prescribing it in those who present in the first 24 hours as it may reduce disease severity
  • Not recommended in children unless systemically unwell or immunocompromised. Specialist advise should be sought
  • Patients whom are considered at higher risk include:
    • HIV, organ transplant, haematological malignancy, on chemotherapy
    • Systemic disease
    • On long term steroids or other immunosuppressants
    • New lesions are appearing more than 8 days after the first

Contacts

Contacts who are at high risk of disease (See risk factors above) should be considered for prophylactic management

• VZIG can be given cup to 10 days after exposure as long as no rash has developed. More effective the earlier it is given
• Those who are known to not be immune can be vaccinated after exposure but before symptoms develop
• Early treatment with aciclovir may also be considered

Complications

• Secondary skin infection
  • Occurs in up to 20% of cases
  • More likely in patients who scratch a lot!
• Secondary bacterial infections – particularly groups A streptococcus (GAS)
  • This is a serious illness that can cause necrotising fasciitis and toxic shock syndrome
• Viral pneumonia
  • Can be fatal (very rare)
  • More common in older children and adults
  • Symptoms usually start within 4 days of onset of the rash
• Encephalitis

Varicella in pregnancy

Contracting varicella for the first time in pregnancy can cause serious and life-changing consequences. Varicella if contracted in the first 20 weeks of pregnancy can cause fetal varicella syndrome (FVS) – which can result in birth defects – of the skin, eyes, brain and gastrointestinal tract.

• This occurs in <1% of cases

Later in pregnancy there is a higher risk of stillbirth. Mothers than contact varicella in the last 4 weeks before birth can also pass on the virus to the child which can lead to the potentially life-threatening neonatal varicella. Varicella in pregnancy may also cause a serious illness in the mother – and can cause complications such as pneumonia.

• Primary varicella infection affects 3 in 1000 pregnancies in the UK
• Women from tropical and subtropical areas are at greater risk due to the reduced immunity in these areas

In Australia – all. mothers are screened for varicella immunity at the start of pregnancy. In the UK this is not routine but may be offered if there is no known previous history of infection or vaccination. If it is found that the mother is not immune:

• She should be advised about the risks of varicella in pregnancy and to avoid contact with anyone known to have chickenpox or shingles
• She should be advised to inform a healthcare worker immediately if she is known to be exposed to varicella
• She should be offered vaccination in the post-natal period (after the birth). Vaccination is not usually recommended during pregnancy. It is safe to breast-feed after vaccination

RCOG guidelines suggest the following for managing exposure and infection during pregnancy:

• Women with a known high risk exposure should be offered intravenous immunoglobulin (IV VZIG). This is effective for up to 10 days after exposure.
  • Note that if you receive VZIG then you are potentially infectious for longer than if you don’t (form 8-28 days after exposure as opposed to 8-21 days in people who don’t receive it
  • A second dose may be required if there is another exposure and more than 3 weeks has passed since the first dose was given
• Women who develop a rash need to be isolated form other pregnant women – this can have implications for their antenatal care
• Oral aciclovir can be given to women who develop a chickenpox rash
  • Before 20 weeks this is associated with teratogenic effects (but risk is probably lower than chickenpox risks)
  • After 20 weeks generally considered safe and should be offered to all women after this gestation
  • Course is usually 1 week long
• IV aciclovir should be given to all women with serious symptoms
• VZIG is of no benefit once the rash has developed and should not be given

References

• Chickenpox (varicella) – RCH
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy
• Chickenpox in pregnancy – RCOG
• NSW Health – Immunisation schedule – accessed on 25/06/2023
• NHS vaccines and when to have them
• Chickenpox vaccine – NHS

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Folliculitis is a common skin condition that describes inflammation of the hair follicles. It can be due to infection (bacterial or fungal), inflammation / irritation and / or a blockage of the pores. Common instances include:

• In children – more likely to be bacterial due to staphylococcus
• In shaved skin:
  • In adult men – common around the beard area
  • In those who shave their legs or arms (more commonly women)
  • These cases are typically sterile – and sometimes called pseudofolliculitis
• In teenagers and adults – may occur in sweaty areas – such as around the groin or the buttocks

Most cases are superficial and identify the cause may be difficult. Cases that are deeper in the skin are harder to treat and may result in scarring.

Management may involve:

• Topical agents – such as antiseptics, improve hygiene and occasionally antibiotics (tropical or oral) in more severe cases
• Removal of the irritant – in cases of irritant folliculitis
• Removal of hair – permanent options such as laser may be considered in difficult / recurrent cases

Epidemiology and Aetiology

• Bacterial causes
  • Staphylococcus Aureus – most common
  • Pseudomonas – associated with outbreaks that occur in public pools / baths / hot tubs. Can cause very intense itching – especially in the groin
  • Other Gram-negative organisms are associated with long-term antibiotics use – especially in acne – where tetracyclines (e.g. doxycycline or minocyline) are used long term.
• Fungal causes
  • More common in the beard area in men
  • May be associated with contact with animals
• Irritant causes
  • These will not grow any pathogens if cultured – they are sterile

Risk factors

• Sport participation
• Beard
  • Uncut beard
  • Shaving “against the grain”
• Clothing friction
  • Include tight clothes
  • Probably one of the reasons that sports participation is a factor
• Humid environment
• Sweating
  • Including not showering as soon as possible after sport – one of the most common presentations I see is in teenagers who are doing sports before or during school and not showering until the evening
• Use of topical steroids
• Reduced immunity
  • Diabetes
  • HIV
  • Cancer
  • Other chronic illness
  • Immunosupression by medication (e.g. to treat autoimmune disease)
• Skin abrasion
• Carrier of Staph. Aureus in the nose
• Occluded skin – e.g. wet wraps used in eczema
• Adolescent and you adult males have the highest incidence

Pathology

Folliculitis results from disruption of the normal activity of the pilosebacious glands in the skin – in particular it causes an obstruction that affects the flow of these glands.

Deeper infection int he hair follicle can form “furuncles” or “carbuncles” – i.e. bigger pimples!

Presentation

• Rash
  • May start of insidiously and become more pronounced
  • Raised red lumps on the skin
  • May become pustular – small pustules at the centre of the lesion – this does not necessarily indicate infection
  • Deeper infections may appear more like pimples or boils
  • Typically in hairy areas
  • May or may not be itchy
• Often if it not scratched or further irritated it will settle down by itself
• Deeper infections may be tender and painful
• It does not usually cause any systemic infection or systemic signs and symptoms

Differentials

• Acne vulgaris
  • Usually can be discerned by location
• Herpes simplex
• Keratosis pilaris
• Contact dermatitis
• Milia
• Periorifical dermatitis
• Insect bites

Investigations

Diagnosis is usually clinical and investigations are not typically required.

• If it is recurrent then swabs may be sent to identify an organism that is involved
• Consider de-roofing any of the pustules to get the contents on the swab
• Also consider testing for diabetes in those with recurrent episodes
• If the diagnosis is uncertain – then a punch biopsy may be taken and sent for histopathology to assist in the diagnosis

Management

General advice

• Ensure clothing not too tight
• Ensure adequate personal hygiene – e.g. washing or showering shortly after exercise
• Try to avoid a high humidity environment under clothing
• Consider use of chlorhexidine body wash
• Shaving advice – avoid going “against the grain”
• Avoid towel sharing within households
• Ensure adequate sterilisation of hot tubs!

Medical and surgical management

Most cases of superficial Folliculitis are mild and will resolve with the above measures an no other specific treatment is required. In more severe cases, consider:

• Topical (e.g. mupirocin BD-TDS, or clindamycin) or oral antibiotics (e.g. flucloxacillin or cephalexin 250-500mg QID). Antibiotic choice may also be based on culture results
• Gram-negative Folliculitis may be treated with isotretinoin (like acne) – but beware the side effects – especially the risk of brith defects in women of reproductive age
• Very rarely deep infections might require incision and drainage
• Consider laser hair removal in stubborn or recurrent cases

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy
• Folliculitis – patient.info
• Folliculitis – dermnet
• Bacterial Folliculitis – dermnet
• Therapeutic Guidelines – Folliculitis

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Hair on the scalp

• Grows in small clusters of 3-4 hairs per follicle unit

Hair growth

Hair follicles go through three growth phases

• Anagen – the main period of growth – lasts 3-6 years
• Catagen – slowing down (or starting up) – lasts 2-3 weeks
• Telogen – not currently growing – lasts 3-4 months

The follicle can move through this process and back again based on hormonal signalling

When anagen starts again, then the old hair is shed and a new hair starts to grow

92% of hairs are in anagen at any time.

Normally, an individual loses about 50-100 hairs per day

Signs of abnormal hair loss

• Hair on the pillow in the morning
• Clogged drain after a shower
• Hair stuck in a hair brush is NOT a significant sign and is impossible to quantify

Telogen effluvium

• Is where a greater proportion of hairs enter telogen
• Occurs after periods of stress (such as after childbirth, blood loss, high fevers, major bone fracture)
• At the time the hair loss is noted, patients are actually entering the recovery phase, as the hair follicles re-enter anagen growth phase and the old hair is being shed as a new one grows
• Can sometimes be chronic
  • Causes hairs to fall out sooner than usual (less than the normal 4 years or so)
  • Not commonly seen in men because they keep their hair short – more commonly seen in women – whereby they notice their hair is thinner as it gets longer (But hair is often thick at the scalp
• Management
  • Usually just time

Anagen effluvium

• Always abnormal. Can be caused by
  • Inflammation
  • Infection
  • Radiation

Alopecia Areata

• Non scarring
• Localised
• Often cause by tinea capitus – especially in children
  • Tinea capitus is rare in adults due to the way that adults sebaceous glands function
• Hair loss is not always complete
• Consider examining with a dermatoscope
  • Exclamation mark hairs – usually seen at the edge of an area of the alopecia. A sign of ongoing disease activity. The hair has started to grow, but this has set off inflammation around the follicle and as the hair grows, the inflammation continues and the hair becomes thinner and thinner until it falls out
  • Yellow dots (follicles without hairs) in the affected area
• May also affect the beard area
  • In men, this is a more common presentation than on the scalp. Sometimes mistaken for an area of depigmentation
• May involve the eyelashes
• Nail pits may be seen – much less obvious than those seen in psoriasis (not as deep, often from lines)
• Management
  • Topical corticosteroids
  • Corticosteroids sometimes injected intralesionally
  • Systemic corticosteroids (NOT long term) – hair often falls out again at the cessation of treatment
  • Topical immunotherapy (DCP – diphenylcyclopropenone) – is an irritant / allergen and it induces a mild contact dermatitis which stimulates hair regrowth
  • Phototherapy – PUVA
  • Laser

Diffuse, non-scaring alopecias

• No scarring – usually means that the hair follicles are not lost (initially)
  • In male pattern baldness hair follicles are lost eventually, but are often present for many years – producing fine vellum hairs before they finally die off
• Need to lose about 15% of hair until it is noticeable
• The most common cause is alopecia areata (again!)
  • Much more difficult to diagnose when it is diffuse
  • May required a biopsy
• Other causes include: telogen effluvium, anagen effluvium
• Androgenic alopecia
  • “baldness”!
  • Women actually lose hair at about the same rate as men – but they don’t lose it in a male pattern – but more generally – female pattern hairloss
  • About 25% of women have cosmetically significantandrogenetic alopecia by the age of 40
  • Hairs become thinner
  • Management of female pattern hairloss
    • No cure
    • Often just a case of slowing natural progression
    • Topical minoxidil +/- tretinoin
    • Oral antiandrogens (e.g. spironolactone e.g. 25mg – 100mg BD. Can cause menstrual irregularities at higher doses. Oral contraceptives may be an appropriate alternative. Can be used in combination with spironolactone)
    • Finasteride used occasionally but often not very effective in women
  • Management of male pattern hair loss
    • Finasteride is mainstay of treatment. Other anti-androgen are associated with a high risk of side effects
      • Need to use for 6-12 months to notice an improvement
      • 1% of patients will get gynaecomastia or impotence
      • Can be started as young as age 16
      • Be wary of FHx of early onset prostate cancer. Finasteride makes PSA unreliable
    • Minoxidil – orally 0.5mg – often compounded with spironolactone
      • Can cause excess hair growth at other sites (e.g. hairier arms and chests)
    • Topical minoxidil
      • 30% will have moderate re-growth
      • 30% will slow hair loss
      • 30% will not make any difference
      • Need to use it for more than 6 months
      • Mechanism – moves hair follicles into anagen. Follicles will only remain in anagen whilst on the minoxidil!
    • If doing a biopsy of the scalp – needs to be at least 4mm, and >1 biopsy is useful for the pathologist (and often may need >1 biopsy for a diagnosis)

Tinea Capitus

• Usually only seen in children
• Not seen in adults due to the difficult physiological functioning of the sebaceous glands in adults
• Diagnosed with a skin scraping
• Usually fairly acute onset
• Management
  • Intra-lesionsal steroid injection – very effective – but hard to perform in children
  • Topical corticosteroids and topical irritants are not very effective
  • Most cases resolve spontaneously within 6-18 months
  • Children often suffer bullying at school

Trichotillomania

• Patient pulling out own hairs
• Often unusual pattern of hair loss
• Short hairs – less than about 1cm – are very difficult to pull out, so these hairs often remain

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

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Impetigo is an infectious skin condition, usually caused by the bacteria Staphylococcus Aureus, and less commonly by Streptococcus pyogenes. 

It is highly infectious, and outbreaks often occurs in schools and within families. It causes pustules and a yellow / golden coloured crust, and is also sometimes referred to as “golden staph” or “school sores”.

It typically requires a skin defect to cause in infection – but this can something as minor as a scratch or abrasion, but it also means that it can cause secondary infections of other skin problems – such as eczema or herpes simplex.

Treatment is with topical antibiotics (in simple cases), or oral antibiotics in more complex cases.

Presentation

The presentation can be divided into two types:

• Bullous impetigo
  • Causes pustules and blisters
  • Always due to staphylococcus
  • Blisters due to toxins produced by the staphylococcus
  • Blisters are not often painful, but may be irritating
  • Blisters often leave a brown crust when they burst

• Non-bullous impetigo
  • Can be caused by staphylococcus aureus or streptococcus pyogenes
  • Not usually painful
  • May be itchy or irritating

Management

Medical management

• Topical antibiotics – e.g. mupirocin cream TDS for 7/7
• In severe or widespread infections – PO flucloxacillin 500mg QID (adults) or 12.5mg/Kg, max 250mg in children

Other factors

• Lesions should be covered to reduce the risk of transmission
• If lesions can’t be easily completely covered, then children should be off school until the lesions have dried, and adults should consider being off work
• It is recommended to use antiseptics to clean the wounds – e.g. iodine based solution
• Avoid sharing towels and clothes
• Frequent and diligent hand hygiene but the sufferer and their family until the lesions have resolved
• Avoid scratching or picking at lesions – the infection can easily be transferred from one site to another
• Be wary of nose-picking – a proportion of the population carry staphylococcus in the nose indefinitely, and this can be the source of infections
• Consider underlying factors affecting immune function in those with recurrent infection

Complications

Staphylococcus infections – whatever the source –  are associated with other diseases

• Post-streptococcal glomerulonephritis
• Rheumatic fever and rheumatic heart disease

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy
• Dermnet – Impetigo

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Skin ulcers are a common presentation to general practice – affecting 2-3 patients per 1000 per year, and can have several important causes:

• Venous ulcers
  • Due to venous blood stasis
• Arterial ulcers
  • A manifestation of peripheral vascular disease
• Mixed, venous and arterial ulcers
• Pressure sores and diabetic ulcers
  • Typically the result of excessive pressure to an area of skin, due to lack of sensation in this area from diabetic nephropathy
  • Also seen in immobile patients

Other rare causes can include:

• Autoimmune vasculitis – e.g. associated with rheumatoid arthritis, SLE
• Tropical disease
• TB
• Skin cancers
• Insect / spider bites

It is also important to differentiate between leg and foot ulcers as the causes are often very different:

• Leg ulcers
  • 65% are venous
  • 15% are arterial
  • 20% are other causes
• Foot ulcers
  • 70% are arterial
  • 5% are venous
  • 25% are other causes

Most ulcers are multifactorial, and important factors are obesity and sedentary life-style.

Treatment requires a multi-faceted approach. Regular wound dressings, and removal of dead sloughed tissues aids recovery. The use of moist dressings is important to create a physiological environment for healing. Wound swabs are often not useful as all chronic ulcers will become colonised with gram positive and gram negative bacteria.

Compression bandages are important in both treatment as prevention as they help to reduce venous stasis and promote blood flow.

Consider skin cancer, particularly SCC in any ulcer that fails to respond to treatment.

History

• Factors that make peripheral vascular disease (arterial ulcers) more likely:
  • Smoker or ex-smoker
  • Known cardiovascular disease (e.g. previous CVA or MI, history of coronary artery disease, angina)
  • History of claudication
• Past medical history
  • PVD
  • Diabetes
  • Rheumatoid arthritis, SLE or inflammatory bowel disease
• Drug history
  • Beta-blockers – can reduce peripheral blood flow
  • Steroids and NSAIDs – can reduce skin healing

Examination

• The most important part of the examination is checking the peripheral pulses!
  • Strong pulses throughout, indicate that arterial disease is unlikely
  • Absent pulses suggest arterial disease
• Ulcer location
  • Inside of the ankle and calf – likely venous ulcer
  • Areas of pressure – likely diabetic ulcer
  • Lateral foot and lower leg – likely arterial ulcer
  • Sun exposed areas – think about risk of skin cancers
• Appearance of the ulcer
  • Look at the wedge of the ulcer, and the base of the ulcer
  • A “punched out” ulcer refers to one that has clean straight edges and base – more likely arterial
  • An “undermined” lesion refers to a wide base of the ulcer, relative to the ulcer opening. Suggest pressure sores or diabetic ulcer
  • Lesions with raised edges suggest skin cancers (usually SCC or BCC)
  • Dry base of ulcer – suggests arterial disease
  • Moist base of ulcer – suggests venous disease

Venous vs arterial

Table adapted from a table in Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt

Pressure sores

Can be graded by severity:

• I – non-blanching erythema
• II – partial thickness ulceration
• III – full thickness ulceration
• IV – deel full thickness with extensive skin and tissue loss

Features:

• Slough at base
• Edges are “undermined” – i.e. the base is wider than the skin defect
• Can expand rapidly
• Often at sites of pressure – e.g. sacrum in bed bound patients, on sole of feet in mobile patients

Appearance

Arterial	“Punched out” Location: distal to ankle Surrounding skin often mottled to evidence of varicose veins and varicose eczema Painful – especially at night Associated PVD and / or risk factors
Venous	Location: proximal to ankle Surround skin might show haemosiderin deposition, varicose eczema or varicose veins May be infected (yellowish foul smelling discharge) Painless
Diabetic / neuropathic ulcer	Location: Pressure points – often on heel, tip of toes, between toes Painless Appearance often somewhat similar to arterial, but may lack other signs associated with PVD (e.g. pale cold foot, reduced pulses – may be normal)

Investigations

• Blood
  • FBC
  • U+Es
  • CRP
  • HbA1c or blood glucose
• Consider swab for MC+S
  • Useful in acute stages
  • In chronic ulcers – will often grow a variety of colonisation but not infective organisms
• Consider ABPI
  • ABPI – ankle-brachial pressure index
  • If <0.9 suggests arterial disease
• Doppler USS

Pathology

Arterial ulcers

• Insufficient arterial blood supply due to peripheral vascular disease
• Management is aimed at improving peripheral arterial blood supply

Venous disease

• Typically due to thrombophlebitis – venous inflammation and clots
• Associated with venous stasis – poor blood flow through the veins
• May have a history of DVT or varicose veins
• Causes chronic venous hypertension, which may lead to skin discolouration – dark, copper coloured skin – as a result of hyperpigmentation
• Often very slow to heal – especially if treated without compression
• Usually not painful
  • If they are associated with pain, this can often be relieved by raising the legs

Management

Arterial ulcers

• This should involve treating the underlying arterial insufficiency
• Usually this would be a referral to a vascular surgeon, for work-up for treatments to re-establish blood flow
• For more info, see management of peripheral vascular disease

Venous Ulcers

Ulcer heal better when occluded, and kept in a moist environment.

Principles of management

• Nursing care:
  • Regular dressing changes
  • Removal of slough and necrotic tissue
  • Keep wound moist
  • AVOID the use of anti-septics, which are toxic to cells and slow healing
    • Wash iff any antiseptics after 5 minutes
  • Cleaning should beamingly performed with saline
  • Dressings – are complicated – loads of different types, for slightly different purposes. Ask the nurse!
• Antibitoics
  • Are usually not indicated
  • Only useful if there is surrounding cellulitis
• Compression
  • Use a firm, elastic compression bandage
  • From the base of the toes to just below the knee
• Elevation
  • Elevate the affected limb
  • Aim for 60 minute BD, plus elevation overnight
  • Above the level of the heart
  • Aids venous drainage
• Medication review – avoid drugs that can affect healing
  • Steroids
  • NSAIDs
  • Beta-blockers
  • Smoking!
• Exercise
  • Encourage early ambulation and exercise
  • Helps to improve the pump action of the calf muscle which aids venous return
• Severe cases
  • May need surgery to treat varicose veins
• Prevention
  • Continue to use compression
  • Regular exercise
  • Use of emollients for varicose eczema
  • If BMI >25, then encourage weight loss
  • Smoking cessation

Pressure sores

• Management
  • Relieve the pressure!
  • Daily wound cleaning with saline and dressings
  • Vitamin C 500mg BD
  • Antibiotics
    • Are usually not indicated
    • Only useful if there is surrounding cellulitis
  • Negative pressure therapy
    • May be useful for non-healing wounds
  • Optimise nutritional status
  • Surgical wound debridement may be required in some cases
• Prevention
  • Particularly important in hospitals and residential care homes
  • Turning of patients every 2 hours
  • Daily skin checks for areas of pressure
  • Special mattresses – e.g. air filled – which may periodically change pressure in the mattress to change the areas of pressure on the patient
  • Control urinary and feral incontinence
  • Good general hygiene

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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Candida is the name of a group of yeast (fungal) species, which can cause skin and mucosal surface infections. It is one of three type of yeast that can infect humans:

• Tinea
  • Caused by dermatophyte fungus
• Candida
  • Caused by the candida fungus
• Pityriasis veriscolor
  • Caused by the malassezia fungus

Candida infection is sometimes called “candidiasis” and it is characterised by its white appearance. The most common species is candidiasis albicans. 

• Candida requires a host to survive
• It is a normal commensal organism of the digestive tract and is typically acquired soon after birth
• Candida infection is often associated with immunosuppression

Sites of infection include:

• Oral (oral thrush)
• Vaginal
  • Vaginal thrush is considered separately
• Nails
  • “Fungal nail infection”
• Skin
  • Particularly in skin folds – where it is sometimes called intertrigo
• Penis (balanitis)
• Nappy rash

Aetiology

Risk factors include:

• Extremes of age (babies, elderly)
• Warm climate
• Occlusion of skin – e.g. nappy rash
• Diabetes
• Iron deficiency
• Immunosuppresion
  • HIV
  • Chemotherapy
  • Other

Rarely, invasive candidiasis can occur – this refers to candidiasis in the bloodstream, leading to organ infection. It is typically associated with severe immunosuppression.

Diagnosis

Often a clinical diagnosis. Swabs can be taken for microscopy and culture, but be aware, that false positives are common – candidiasis often lives harmlessly on the skin. It can also cause secondary infection to an already existing skin condition (e.g. psoriasis or eczema).

Management

Oral candidiasis

• Often topical
• e.g. Nystatin liquid drops 100 000 units / ml QID for 7 to 14 days
  • OR miconazole 2% gel – applied orally and then swallowed QID for 7-14 days
  • Nystatin first line in babies,  miconazole in adults

Intertrigo (in skin folds)

• Miconazole or clotrimazole cream – typically applied BD

References

• Candida – Dermnet NZ
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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Tinea refers to a specific type of fungal infection, caused by dermatophyte fungus. Fungal infections are often divided into 3 different types:

• Tinea
  • Caused by dermatophyte fungus
• Candida
  • Caused by the candida fungus
• Pityriasis veriscolor
  • Caused by the malassezia fungus

Tinea is often given different names, depending on the location of the infection – for example tinea pedis affects the feet (athletes foot) and tinea corporirs affects the limbs (also sometimes referred to as “ringworm’ due to the ring-like nature of some of the lesions it causes).

Often, multiple locations of infection exists on the same patient, most commonly transferred from the foot. The exact species of tinea vary by geographical location. Some types are caught from pets or farm animals. Probably the most common form is Tinea rubrum. 

Aetiology

• Usually caught from another infected individual
  • e.g. shared towels, close skin contact, walking barefoot in shared changing rooms
• Tinea pedis
  • Occlusive footwear – e.g. heavy work boots
  • Excessive sweating, excessive exercise
  • Diabetes
  • Co-existing fungal nail infection
• Use of steroids
• Immunsuppression

Presentation

• May be acute or gradual onset
• Usually itchy and inflamed
  • Tinea pedis is often particularly itchy
• If widespread at presentation it can be particularly difficult to treat
• Tinea pedis
  • Usually asymmetrical pattern
  • Can be bilateral or unilateral
  • Most commonly affects the spaces between 4th and 5th toes
  • Scaly and may affect the whole of the sole of the foot

Diagnosis

• Diagnosis is usually clinical
• Skin scraping can be sent
  • Typical features can be seen on microscopy – which may negate the need for culture
  • Culture can take months

Differential diagnosis

Tinea pedis

• Eczema
• Psoriasis
• Contact dermatitis

Tinea corporis

• Impetigo
• Seborrheic dermatitis
• Psoriasis
• Eczema (especially discoid eczema)
• Lichen simplex
• Contact dermatitis
• Pityriasis rosea

Management

General advice

• Hygiene – dry thoroughly between feet after washing or showering
• Avoid use of occlusive footwear
• Use barrier protection – i.e. sandals – when using shared facilities

Topical anti-fungal agents

• OD or BD
• Examples include:
  • Terbinafine (Lamisil)
    • Some studies suggest this is the most effective agent
  • Clotrimazole (canesten)
  • Miconazole (Daktarin)

Oral anti-fungal agents

These may be indicated in severe or resistant cases. Options include:

• Terbinafine
  • 250mg OD for 2 weeks
  • In the case of fungal nail infection, long courses of up to 12 weeks, and frequent LFTs may be required
• Fluconazole
  • 150mg once weekly for 6 weeks
• Itraconazole

Prevention of recurrence

• Dry feet thoroughly after bathing
• Avoid occlusive footwear
• Thoroughly dry shoes and boots before wearing
• Clean shower and bathroom floors with bleach
• Treat shoes with anti-fungal powder

References

• Tines corporis – Dermnet NZ

Tinea pedis – Dermnet NZ

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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Rosacea is a common facial rash, of unknown aetiology. It is typically chronic and persistent.

It causes sterile inflammatory papules, pustule and nodes and it may sometimes be mistaken for acne, however it does not cause comedones.

There is an association between rosacea and a mite called demodex folliculorum. This mite usually lives on the skin of healthy individuals in hair follicles, and is not considered pathogenic. However it is found sin higher concentrations on the face of those with rosacea. It is not know if higher concentrations cause rosacea, or if the conditions created by rosacea lead to higher concentrations of the mite.

Epidemiology and Aetiology

• Typically affects patients aged 30-50
• Mainly females
• “Celtic” ethnic origin (Irish / Scottish)
  • Fair skin
  • Blue eyes

Presentation

• Red rash, often with inflammatory papules
  • May often begin as a increasing tendency for fascial flushing, before progressing to papules, pustules and nodules
• Patients often reports that their face feels hot or burns
• Typically rash on the cheeks, forehead, nose and chin
• Worse when flushed or blushing
• Usually peri-orbital and peri-oral areas are spared
• May also be associated with increased skin sensitivity, and stinging sensations
• May be accompanied by:
  • Telangectasia
  • Facial oedema
  • Seborrheic dermatitis
  • Sensitive skin – burning sensation to creams and other agents applied to face

Complications

• Blepharitis
• Conjunctivitis
  • About 50% of patients with suffer from belpharoconjunctivitis which typically causes dry and itchy eyes
  • Rarely – corneal ulceration
• Rhinohpyma
  • Development of a large, bulbous nose

Differential diagnosis

• Acne
• Seborrheic dermatitis
• SLE
• Periorifical dermatitis

Management

• Stringent sun protection
• Use gentle soap-free cleanser (e.g. emollient)
• Avoid oil based creams – use water-based make-up and sunscreen
• Avoidance of factors that cause facial flushing:
  • Heat, wind, sudden changes in environmental temperature
  • Alcohol
  • Excessive exercise
  • Hot baths
  • Spicy food
  • Hot drinks
• Cool packs
• Medication
  • Topical metronidazole cream 0.75% OD or BD
    • Use for 6-12 weeks
    • Long term maintenance therapy is often required
  • Oral Antibiotics – used when topical agents have not been successful – e.g. Doxycycline 100mg OD or erythromycin 250-500mg BD for 4-8 weeks
  • In women of menopausal age – consider menopausal related flushing as the cause which may respond to HRT
• Laser treatment for telangectasia
• Surgical correction of rhinophyma
• Avoid topical steroids

Flashcard

References

• Rosacea – Dermnet NZ
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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Seborrheic dermatitis, also sometimes called seborrheic eczema, is a common, chronic skin disorder, that typically affects the face, scalp and trunk. Some define it as a subtype of eczema.

Its pathology is poorly understood, but it is thought to be a inflammation of the skin, often associated with the presence of the malassezia fungus. Many people carry this fungus asymptomatically, and it is also known to cause pityriasis versicolor.

• “Dandruff” is a type of seborrheic dermatitis

It can be divided into two types – that affects children, and that affecting adults (often young adults).

Pathology

Associated with the malassezia fungus, although this is also found in many asymptomatic individuals. It is thought that there is some sort of inflammatory reaction induced by the waste products produced by the fungus. Individual variation in natural skin barrier and skin lipids may account for the condition.

Infantile seborrheic dermatitis

Presentation

If only the scalp is affected, it is often referred to as “cradle cap”

• Typically babies <3 months old
• Usually resolves by 12 months
• Non-itchy
• Affects:
  • Scalp, cheeks, folds of neck, nappy area, folds of elbows and knees
• Produces a yellow coloured greasy scale
• Commonly associated with a bad nappy rash, which is often co-infected with candida

Differentiating from atopic dermatitis (eczema)

Eczema typically:

• Onset after 3 months
• Very itchy
• Very dry cracked skin (not an oily yellow scale)
• Typically nappy area is spared

Management

Basic measures

• Keep areas clean and dry
• Wash with warm water and then pat dry
• Keep skin exposed to air as much as possible
• Avoid use of soap (use cetaphil or similar emollient)
• Cradle cap
  • Wash off flakes with baby oil or soft paraffin, then wash away loose scales
• Nappy rash
  • Change soiled nappies frequently – minimise time of waste matter in contact with the skin
• Zinc based cream (e.g. sudocreme) applied on affected areas (barrier cream)

Medical management

• Scalp
  • 1-2% sulphur + 1-2% salicylic acid cream
    • Apply overnight
    • Shampoo off the next day with baby shampoo
    • Use 3x/week until resolved
  • 6% salicylic acid lotion
  • In older children
    • Ketoconazole 1-2% shampoo
    • Miconazole 2% shampoo
• Face, limbs and trunk
  • 2% salicylate + 2% sulphur cream
  • Ketoconazole 2% cream applied OD or BD
  • If severe – used steroids
    • 1% hydrocortisone BD for up to 7 days
    • 0.05% betamethasone – if very severe
• Nappy area
  • 1% hydrocortisone cream with 2% ketaconazole OR 1% clotrimazole cream
  • May be available as combination cream – e.g. hydrozole cream

Adult seborrheic dermatitis

Presentation

• Presents from teenage years onwards throughout adulthood
• Often recurrent
  • Worse with stress and fatigue
• Typically affects the head – particularly around hair-growing regions – scalp eyebrows, eyelids (blepharitis), and the nasolabial folds
• May also affect the torso, groin and the perianal area
• Red rash, with a yellow greasy scale
• Secondary candidiasis infection is common – especially in flexures

Management

• Scalp
  • Salicylic acid 2% + sulphur 2% in aqueous cream – applied overnight
    • Wash off the following day with selenium sulphide shampoo
    • Apply 3x per week
  • Ketaconazole shampoo 2% (anti-yeast shampoo)
    • Use immediately after the medicated shampoo described above
  • If non-responsive – try steroids – betamethasone dipropionate 0.5% lotion
    • Apply once daily at night for 7 nights
  • If STILL non-responsive, add coal tar 1% applied overnight, and wash off the next morning with anti-yeast shampoo
• Face and body
  • Wash frequently with a plain soap and water
  • Hydrocortisone 1% + clotrimazole 1% cream (“Hydrozole”) applied BD for 1-2 weeks
  • If unsuccessful, use a stronger steroid cream and an anti-fungal cream separately, e.g.g :
    • Methylprednisolone aceponate 1% cream – daily for up to two weeks
    • Ketaconazole cream 2% – applied daily for up to 2 weeks

References

• Seborrheic Dermatitis – Dermnet NZ
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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