Category Archives: Dermatology

Seborrheic dermatitis

Scaly skin condition in babies, particularly affecting scalp.

Oily, yellowish scales. Often nappy rash. Not usually very itchy.

In adults, affects face (esp around nose and ears) and can affect chest and upper back. Dandruff is a mild form. Can be itchy, can lead to hair loss but more usually cosmetic concerns.

Overgrowth of Malassezia fungus found, antifungals work well. Else topical steroids. In adults, anti -androgens.


= excessive sweating.

Primary usually develops in adolescence, usually focal esp palms, soles, axillae.  Often family history.

Secondary tends to be generalized but can be focal.  Long list of causes – endocrine, neurological, chronic infection, catecholamines etc.

Treatment in kids is limited to anti-perspirants and iontophoresis (devices available, administered via trays for feet and hands, via pads for body – do 3x per week).

For axillae – aluminium hydrochloride like Driclor. It causes irritation due to hydrochloride, so dry armpit carefully before use (blow dryer if required), and consider intermittent topical steroid to alleviate discomfort.

GPs can also prescribe 1% glycopyrrolate in cetomacrogol cream for topical use 2-4/d – this is obtainable from the Western Infirmary Production Unit (Pharmacy).

For generalised disease – probanthine or oxybutinin – dose titrated up slowly to point of efficacy and minimal side effects – works well.

Surgery – botox, or sympathectomy, eg if disabling i.e. constantly dripping hands,

Patient Support

Young person site although it is aimed at US families,


Or erythema subitum.  Dramatic viral rash.  Caused by Herpesvirus 6 and 7.

Classically high fever, URTI symptoms or no focus, potentially febrile convulsion!  Then rash appears as fever subsides, day 2-4.

Rash is widespread fine maculopapular, can be pale haloes around spots, mostly on trunk.  Can be in mouth!  Not itchy.


Congenital pigmented naevi

Particularly giant or multiple lesions usually present at birth but can be shortly after.

Number of naevi increases through childhood, but high volatility, eg over 3yr period, about a third change pattern, sun burn increases number. Halo pattern of disappearance  (with depigmentation) rare.

Can be associated with neurocutaneous melanosis; if suspected then neuroimaging is advisable, seeking evidence of leptomeningeal melanotic lesions.

Malignant change in childhood is possible, but only really in lesions greater than 1% BSA size.  Melanoma detection relies on morphology eg ABCDE criteria (asymmetry, border irregularity, color variegation, diameter (6 mm, and evolving).  ABCDE very low specificity in kids but melanoma does present in children (and pigmented naevi are risk factor).  Dermoscopic changes in blood vessels important.

Beckers naevus tends to present at puberty,  usually torso or upper arm, irregular, hairy.



  • Oculocutaneous Albinism is most common. Non-type 1more subtle – in fair skinned families, may only be obvious in comparison with family members.
  • Griscelli, Elejalde and Chediak–Higashi syndromes have been termed “silvery hair syndromes” – generalized, but eyes spared. Griscelli and Elejalde include severe neurological defects, as well as immunological. Immunodeficiency severe in Chediak-Higashi.
  • Menkes is X-linked copper defect, progressive CNS degeneration and death in early childhood.
  • Selenium deficiency? Only really in malnutrition.
  • In later life, homocystinuria.

Localized syndromes

  • Piebaldism looks like vitiligo but is congenital and permanent.
  • Waardenburg syndrome includes piebaldism, but also heterochromia irides and broad nasal root. Subtypes include limb defects, Hirschsprungs, deafness, dystopia canthorum (increased spacing of inner canthi, but without hypertelorism).
  • Single depigmented patch: naevus anemicus (vascular, Woods light neg), ash leaf macule of tuberosclerosis (usually multiple) or naevus depigmentosus (identical but single, less likely to be leaf like).
  • In later life, vitiligo (autoimmune), post inflammatory (eg eczema, pityriasis), lichen sclerosus and morphoea.

[Hong Liang Tey, Acta Dermato-Venereologica online]

Hair loss

  • Tinea capitis – “ringworm”, actually fungal.  Scalp abnormal.
  • Telogen effluvium – lots of hair shed all at the same time following some sort of trigger esp birth (both baby and mother can be affected!), infection.  Trigger usually 2-3 months preceding.  Clumps or general thinning.
  • Alopecia areata
  • Trichotillomania

On Examination

Exclamation mark hairs (thin proximally, at scalp, normal distally) suggest alopecia areata, but may be seen in trichotillomania, so not very predictive.

Pull test – gentle traction on about 20 hairs in 3 different locations.  Positive if more than 5 hairs extracted – suggests active alopecia areata.  You may miss dormant alopecia areata, but in that case hair regrowth should occur anyway.

Seborrhoeic dermatitis

Red (orange?), itchy, flaky skin problem.  Affects sebaceous (greasy) zones – face, scalp, centre of chest, skin folds (neck, groin).  V common (includes dandruff!).  Inside, outside and around ears can be affected.  Eyelids can be affected (blepharitis).

Babies get transient type – cradle cap (scalp) and nappy area, clears after a few months.

Thought to be caused by overgrowth of Malassezia yeast.  Can be severe in HIV.

Differential is psoriasis.  Scales in psoriasis are thicker and whiter – unusual for face to be affected.


For cradle cap in babies, usually enough just to use daily mild shampoo and gentle brushing.  Shampoo may make it worse if the diagnosis is actually atopic dermatitis!  Failing that, coconut oil (NOT olive oil, which has potential to damage skin, apparently) or other moisturizer left in overnight or applied just before bath.

For scalp, Zinc pyrithione, selenium or ketoconazole shampoo (but only licensed for older children).  Leave 5-10 mins before rinsing.  Descaling treatment available – coconut oil and salicylic acid, needs hours.

For body, moisturizer, antifungal eg Canesten HC, Trimovate.

For blepharitis, use baby shampoo to lift flakes.


Proliferation of mast cells.  Can be restricted to skin or be systemic, with infiltration of bone marrow, spleen, liver and lymph nodes.  Systemic involvement not always obvious in the skin! Messy though, since mast cell mediators might act systemically even if mast cells themselves not widespread.

Systemic mastocytosis can present with episodic symptoms of dyspnoea, collapse (hypotension), reflux, diarrhoea.  Rather non-specific, so easily missed.  May also have hepatosplenomegaly, lymphadenopathy, osteoporosis, bone abnormalities.

Skin lesions may be present but not always dramatic (might just look like freckles).  May be history of dermatographism, recurrent itching, flushing and/or urticaria.  Different skin patterns seen, but overlapping:

  • mastocytoma – slightly raised, can be slightly pigmented.  Physical irritation eg scratching causes flare and weal (Darier’s sign).  Can be present at birth, tend to be a good size eg 2-4cm nodule, may be blistering (in first 2 years of life only), else appear in first year of life.
  • Urticaria Pigmentosa – usually presents in first 2 years of life, freckles or larger nodules/papules/plaques.  Can be blistering.  Resolves if not improves at puberty.
  • Diffuse cutaneous mastocytosis (DCM) – no distinct lesions visible! Serious.
  • Telangiectasia macularis eruptiva perstans (TMEP) –  brownish small macules with telangiectasia, generally in adults.  Can be systemic.

So look at skin, try Darier’s sign (not v sensitive).  Feel for liver and spleen.  Check Tryptase level (rarely normal even in systemic – compare baseline to peak, rather than just absolute level). Consider bone marrow biopsy to look for mast cells. Consider bone scan to look for abnormalities.  PCR for the D816V mutation in KIT gene?


Control triggers (very individual):

  • Stress (emotional/physical), sleep deprivation, pain
  • Physical stimuation eg heat/cold, exercise/sex, sunlight, skin/scalp friction or trauma (tickling!)
  • Bee/wasp stings
  • Drugs esp aspirin/NSAIDs, opiates
  • Alcohol

60% of kids resolve during puberty!

In later life there is a slightly higher risk of haematological disorders including cancer. There is also an increased risk of osteoporosis.

Stabilize mast cells:

  • Anti-histamines, including H2 blockers.  Titrate dose to effect.
  • Cromoglycate
  • PUVA offers some temporary relief

Emergency treatment: Adrenaline auto-injectors for –

  • systemic
  • previous systemic reactions
  • Extensive blistering lesions?

UK support group at [Jess Hobart]

[Am Fam Physician. 1999 Jun 1;59(11):3047-3054.]