This chapter covers the following topics:
- Describing skin lesions
- Autoimmune skin conditions
- Congenital skin conditions
- Hair conditions
- Trauma, drug reactions and bite reactions
- Dermatology cheat sheet
DESCRIBING SKIN LESIONS
Skin lesions may be primary or secondary. They may be further categorised according to the arrangement or distribution e.g. sun-exposed areas.
Primary Skin Lesions
They may be:
- Flat or raised
- Solid or fluid-filled (if raised)
Macules are well-circumscribed, flat, non-palpable lesions that are <1 cm in diameter. Patches are well-circumscribed, flat, non-palpable lesions that are >1 cm in diameter, see related image here.
They may be:
- Solid lesions (well-circumscribed, raised, palpable lesions which extend into the dermis or subcutaneous tissue)
- Papules – solid lesions <1 cm in diameter
- Plaques – flat-topped lesions >1cm diameter (see related image here.
- Nodules – dome-shaped lesions >1cm diameter (see related image here)
- Vesicles – well-circumscribed, raised lesions <1cm diameter which are filled with clear fluid (see related images here)
- Bullae – well circumscribed, raised lesions >1cm diameter which are filled with clear fluid
- Pustules – well-circumscribed, raised lesions <1cm diameter which are filled with pus
- Scale – accumulated fragments of stratum corneum produced from shed skin
- Crust – dried serum, blood or pus
- Erosion – open area of the skin which is the result epidermal loss
- Fissure – linear, open area of the skin which is the result epidermal loss
- Ulcer – irregular, open area of the skin which is the result epidermal loss and at least partial dermal loss
- Excoriation – superficial skin abrasion that usually results from scratching.
- Lichenification – dry, thickened, dark (hyperpigmented) skin with accentuated skin markings
Arrangement of Lesions
Lesions may be:
- Annular (ring-shaped) e.g. tinea corporis (ringworm), pityriasis rosea, syphilis, urticaria, lichen planus, psoriasis, seborrheic eczema
- Grouped e.g. herpes simplex (see related image here), insect bites, warts, molluscum contagiosum
- Linear e.g. scratch marks, scar, keloid, scabies, psoriasis, lichen planus, warts
Eczema is a chronic inflammatory skin disease which is common in children. It mainly affects the epidermis and may be complicated by secondary infection by bacteria (Staphylococcus aureus, Streptococcus pyogenes), viruses (HSV) or fungi (Candida albicans). Children may present with:
- Atopic eczema (see related image here and here)
- Nummular eczema
- Seborrhoeic eczema
- Napkin eczema
- Perioral eczema
This is a chronic condition that has acute exacerbations and which is often associated with asthma, allergic rhinitis and allergic conjunctivitis (see related image here).
The pathophysiology is poorly defined, but there are two hypotheses:
- Primary immune dysfunction leads to IgE sensitisation, allergic inflammation and secondary epithelial barrier disturbance.
- A primary epithelial barrier defect leads to secondary immunologic dysregulation and inflammation as bacteria are able to enter through the skin.
The child will present with:
- Acute eczema – red and swollen skin, weeping/oozing vesicles (clear, serous fluid), crusting (when the fluid dries up)
- Subacute eczema – mild erythema with or without oozing, scaling, early thickening
- Chronic eczema – lichenification (leathery, thickened skin, hyper/hypopigmentation, prominent skin markings)
The child’s presentation may vary depending on his/her age. Infants present with a red, wet and/or scaling eruption which involves the head, extensor areas and trunk. There is nasal sparing.
Older children usually have localized lesions in the flexures. They may have other signs which are pathognomonic of atopy (atopic diathesis):
- Allergic shiners (dark circles under the eyes which are the result of nasal or sinus congestion)
- Dennie-Morgan folds/infraorbital folds (lines on the skin below the lower eyelid)
- Muddy sclera (brown discolouration of the sclera)
- Infra-auricular fissures (fissures beneath the earlobes, which may be weeping)
- Headlamp sign (nasal/central face-sparing when there is eczema of the face).
- Nasal crease (produced because of chronic upward rubbing of the nose)
- Salute sign (action of rubbing the nose)
- Lip hyperlinearity
- Angular cheilitis (erythematous, swollen, and painful patches in the corners of the mouth
- Hyperlinearity of the palms and soles
- Keratosis pilaris (dry and rough patches on the skin of the upper arms, thighs, and cheeks)
The UK Working Party Diagnostic Criteria is used to diagnose atopic eczema. For the diagnosis to be made, the child must have 1 major and 3 minor criteria.
- Major criterion – pruritis
- Minor criteria:
- Family/personal history of atopy
- Onset <2 years old
- History of dry skin
- Visible flexural dermatitis
Atopic eczema is a clinical diagnosis, therefore no investigations are necessary. However, it may be helpful to do skin prick testing (SPT) to identify triggers.
The mnemonic ASSEBLIEF can be used to remember the approach to management for the child with atopic eczema (see related image here).
|A - Antihistamines||Oral antihistamines may be given to sedate the child and avoid nocturnal scratching. The child <2 years old may be given chlorphenamine (0.1 mg/kg/dose at night) and the child >2 years old may be given cetirizine (5-10 mg at night).|
|S – Steroids||Use potent topical steroids daily (initially and for flares). Use hydrocortisone 1% on the face or skin folds and use beclomethasone 0.1% on the rest of the body.|
|S - Scratching||An important aspect of treating eczema is avoiding scratching by keeping the skin moist (liberally use moisturisers). Explain the itch-scratch-itch cycle to the parents and child.|
|E - Education||Inform the parent and child that eczema is a chronic condition caused by barrier dysfunction. Provide support and counselling.|
|B – Bacteria||Eczema is vulnerable to bacterial/viral infection, especially S. aureus (impetiginised eczema) and HSV (eczema herpeticum). Keep the infected skin clean and moist. Treat with antibiotics if necessary.|
|L – Look||Look for associated atopic conditions and avoid triggers e.g. soaps, bubble bath, wool and other irritating fibres in clothing. Children with atopic eczema are more likely to have atopic rhinitis, conjunctivitis or asthma.|
|I – If||If severe, use wet wraps unless there is a secondary infection of that area.|
|E - Emollients||Use emollients as a soap substitutes (help remove crusts but is gentle on the skin) and moisturisers e.g. emulsifying ointment, cetomacrogol.|
|F – Forever||This condition is lifelong.|
Occlusive, wet dressings are to be used for severe or thick, lichenified skin. However, they must not be used if there is a sign of infection as it will promote spread of the infection.
It is superficial infection of eczematous skin with S. pyogenes or S. aureus. The affected skin will have yellow-brown crusting. If severe, there may be systemic signs (fever, malaise, lymphadenopathy). Impetiginised eczema is managed by:
Drugs Commonly Used in Dermatology
|Weak topical steroids (typically used on the face)||
||Moderate topical steroids||
|Potent topical steroids (typically used on the body)|
|Very potent topical steroids|
The cause and pathophysiology of nummular eczema are not known, but it may be associated with atopic eczema. Stress and bacterial infection can aggravate the condition.
The child will have well-rounded (discoid), discrete patches of eczema, usually with a crusted or weeping surface. They are most common on the limbs (especially on the legs) but may occur anywhere on the body.
Patients are managed with potent topical steroids (clioquinol where possible) and antibiotics (e.g. flucloxacillin 250 mg 6 hourly), if infected.
Seborrhoeic Eczema (‘Greasy Eczema’)
It is most common in children.
Aetiology and Pathophysiology
The cause and pathophysiology are unknown but it is associated with large sebaceous glands and is common in immunocompromised individuals. The condition may be aggravated by stress and yeast infection of the hair follicles.
The child will have erythematous, ill-defined lesions with greasy scale. Lesions are usually found in areas with many sebaceous glands e.g. flexural areas, scalp, face, scalp and nappy area.
The condition is usually self-limiting in infants. Skin lesions should be treated with hydrocortisone 1% cream, and scalp lesions treated with detergent shampoo (tar, detergent, selenium sulphide, ketoconazole or zinc pyrithione) and hydrocortisone 1% (if the scalp is inflamed). Oral antibiotics should be prescribed if the skin is infected.
This is a common form of irritant, contact eczema which may be due to soaps or prolonged exposure to urine and faeces in the diaper. Candidal infection may aggravate the condition.
The eczema ranges in severity from mild to severe:
- Mild napkin eczema:
- It is usually asymptomatic but the child may have some erythematous patches and papules. There is minimal maceration.
- Moderate napkin eczema:
- The child may have pain or discomfort.
- The skin will be shiny/glazed, red and macerated with superficial erosions.
- Severe napkin eczema:
- The child will have pain.
- There will be significant erythema, and glossy erosions, papules and nodules).
One must advise the parents to regularly change the child’s diapers and leave the child nappy-free for a few hours daily. Nappy cream should be applied (acts as a barrier). One should also apply a weak topical steroid (hydrocortisone 1%) mixed with aqueous cream twice daily. If candida is suspected, the child should be prescribed steroid 10% and nystatin 20% in zinc cream.
It is due to a skin irritation (irritant contact eczema) or an allergic reaction to substances in contact with the skin (allergic contact eczema). Common causes include cosmetics, creams, jewellery and detergents. The child will, therefore, present with a localised rash and compatible history.
Irritant Contact Eczema
There are two main types – napkin eczema (see above) and dry skin eczema. Dry skin dermatitis is usually due to excessive moisture exposure, such as soap or sweating. The child might experience burning, stinging and discomfort. On examination, the skin is dry and cracked with macular erythema. The mainstay of treatment is emollient therapy.
Allergic Contact Dermatitis
It is an inflammatory reaction of the skin secondary to exposure to an absorbed allergen or antigen. The child will present with itching and a rash. If acute, there will be oedema, erythema and vesicles that often rupture and form crusts. If subacute or chronic, there will be lichenification, erythema and scaling.
Its pathophysiology is not well understood but it is associated with prolonged topical corticosteroid use.
It most commonly affects young females. They present with small, inflammatory papules around the mouth and nose.
- Discontinuing topical corticosteroids
- Avoiding skin irritants
- Using topical calcineurin inhibitors
- Using oral tetracyclines
Pityriasis Sicca Alba
This is regarded as a mild phenotype of eczema due to unknown cause. It is thought to be caused by a genetic predisposition to impaired skin barrier function.
The child will have hypopigmented macules and patches with a fine scale (most common on the face). Central hyperpigmentation may also occur.
This is self-limiting condition but management may include:
- Allergen identification and avoidance
- Topical treatment
- Steroids (hydrocortisone 1%/LPC 5% in aqueous cream for the face, 10% steroid/ LPC 5% in emulsifying ointment for the body)
- Calcineurin inhibitors e.g. tacrolimus, pimecrolimus).
Antihistamines and wet dressings may also be employed.
AUTOIMMUNE SKIN CONDITIONS
This is a congenital skin condition.
The child will have diffuse depigmentation of the skin, hair and eyes. Chronic sun exposure can lead to premature aging, solar keratoses and sun-associated skin cancers.
Supportive measures include:
- Providing genetic counselling and emotional support
- Preventing the complications associated with sun exposure by encouraging sun avoidance, sunscreen use and wearing modest clothing
- Closely monitoring the child to detect skin cancers early
It is an autoimmune disorder in which there is melanocyte destruction, leading to depigmentation. Re-pigmentation may spontaneously occur and is often triggered by sun exposure.
The child will present with macular depigmentation that is often symmetrical but may be focal. Secondary sun damage (redness, thickening and scaling) and hair loss may also occur.
Re-pigmentation tends to start at the hair follicles. Acral areas (hands and feet), lips and genitalia seldom regain pigment.
Non-pharmacological management includes
- Counselling the child and family (must be informed that vitiligo is an autoimmune, lifelong condition with no definitive cure), see related image here.
- Encouraging moderate sun exposure but discouraging burning
- Camouflage cosmetics
- Vitamin C
- Oral antihistamines
- Potent topical steroids
This is a cell-mediated immune response of unknown origin. It is sometimes seen in sun-exposed areas and may be a response to drugs e.g. thiazide diuretics, hypoglycaemic agents, methyldopa and anti-TB treatment. Mucosal surfaces and skin are involved (wrists, forearms, palms, soles and nail folds).
Lichen planus is described using the six Ps – pruritic, purple, planar (flat-topped), polygonal, papules/plaques which can be polymorphous. Lesions may also have Wickham’s striae (white lacy network on the surface). The Koebner phenomenon may be present (appearance of new lesions at an area of injury).
Non-pharmacological management includes sunscreen use (if the rash is photo-distributed) and adjusting medication (if there is suspicion that it is drug-induced). Pharmacological management is with steroids (topical or systemic). Oral lesions may be treated with a steroid spray or gel.
This is an inflammatory immune-mediated condition which results in hyperkeratinisation.
Psoriasis usually starts in early adult life, see related image here. The patient has a genetic predisposition but the exact trigger is unknown.An immune response is activated by the presence of antigenic stimuli in the skin and results in T cell differentiation. These T cells release cytokines which cause keratinocyte hyperproliferation.
The child may present with:
- Skin involvement:
- There will be pink-to-red, well-demarcated, pruritic plaques with a silver scale. Pustules are occasionally seen
- Scratching the lesions may be associated with the Koebner phenomenon.
- Lesions are mostly seen on the scalp (crossing the hairline) and extensor surfaces (elbows and knees), but can occur anywhere on the body e.g. flexural areas, perineum.
- Nail signs e.g. pitting, onycholysis, opaque, deformed and crumbling nails
- Joint involvement (psoriatic arthritis)
Non-pharmacological management includes:
- Counselling and educating the patient and family
- Exposure to sunlight
- Avoidance of triggers like stress and streptococcal infection
Pharmacological management includes:
- For the skin:
- o LPC 10% or salicylic acid (to remove scales)
- Weak steroids for the face and potent steroids for the body
- For the scalp:
- LPC 10% or salicylic acid overnight
- Shampoo in the morning with a detergent or tar preparation
- Tar/dilute steroid lotion
- Systemic therapy (dermatologist-initiated)
It is caused by infection with a poxvirus.
The virus can be transmitted via direct skin contact or via contact with fomites e.g. bath towels, sponges, gymnasium equipment, shared bathwater. It may be inoculated into sites of minor skin trauma.The lesions usually undergo spontaneous resolution in 6 months to a year, but may take longer.
The child will have one or more round, dome-shaped, skin-coloured or pearly papule(s) which has an umbilicated centre and contains a caseous plug. Lesions can be anywhere in the body, but typically occur on the trunk, arms, legs, face or genitalia. See related image here.
There is no universally effective treatment. However, whatever the treatment, one must try to avoid scarring.The lesions may just be observed if they do not bother the child. Otherwise they may be treated with:
- Benzoyl peroxide cream (applied daily)
- Wart paint (applied to individual lesions)
- Liquid nitrogen (applied to individual lesions every 2-3 weeks)
- Tretinoin (applied to individual lesions)
- Imiquimod cream
- Surgical removal under local anaesthetic
Tinea is caused by fungal infection with dermatophytes. These fungi can be found on humans, animals or in the soil. Tinea of the nails may lead to recurrence.
Classification and Clinical Features
The child may have:
- Tinea capitis (scalp) – pruritic lesions with central scaling and patchy alopecia
- Tinea corporis/faciei (body/face) – erythematous, pruritic, scaly lesions (papules/pustules) with central clearing and raised, active edges (from which extension occurs)
- Tinea cruris (groin) – pruritic, inflamed, scaly lesions with well-defined edges and central clearing
- Tinea pedis/manuum (foot/hand) – grouped, pruritic blisters or scaly patches along the plantar line, on the sole, on the instep of the foot and/or involving the web spaces
The scale may be scraped and specimens sent for light microscopy or fungal culture.
Topical antifungals may be given e.g. Whitfield’s ointment, imidazole cream (such as clotrimazole 1%). However, these agents alone are not effective in tinea capitis. Oral antifungal agents (e.g. fluconazole) are given for tinea capitis or any other form of tinea which is extensive. A different diagnosis (e.g. psoriasis, eczema) must be considered if the rash is not resolving with adequate treatment.
Tinea Versicolor (Pityriasis Versicolor)
It is caused by infection with a yeast commensal (Pityrosporum orbiculare). Predisposing factors include high humidity and excessive sweating.
The child will have depigmented macules with or without fine scale, usually on the trunk. The presence of scale is indicative of active infection. The rash is sometimes hyperpigmented and may be pruritic.
One may examine skin scrapings under the microscope (will show short, unbranched hyphae and spores).
Topical treatment is with selenium sulphide shampoo (apply to the whole body once weekly for 3 weeks) or imidazole/terbinafine cream. The absence of scale means that there has been adequate treatment.
Its pathophysiology is unknown, but it is thought to be a response to viral infections
The child will have a herald patch (single lesion with an active edge) that usually precedes other lesions by a few days.It is often mistaken for tinea until the generalised eruption occurs.Lesions are oval, have a fringe of scale and are confined to the trunk.They can be pruritic.
The condition is self-limiting and resolves in 4-8 weeks. The child and family should be counselled and informed that the condition is not infectious and will spontaneously resolve. However, antihistamines can be given to help control itch and sedate e.g. chlorphenamine, cetirizine.
Pathophysiology and Aetiology
It is inflammation of the hair follicle and may be superficial or deep. The most common infective cause is S. aureus but may be due to other bacteria or fungi. The non-infective causes of folliculitis include follicular trauma and occlusion.
The child will have papules or pustules with an erythematous halo. These may occur in clusters.
Non-pharmacological management involves keeping the area dry and clean, removing predisposing factors and using antiseptic agents. Pharmacological management is with antibiotics (given if there is severe folliculitis e.g., flucloxacillin). The patient should be referred if there is no response to treatment.
Aetiology and Pathophysiology
It is caused by S. aureus infection of the hair follicle. The organism is carried in the nose or under the fingernails. Individuals are prone to recurrent attacks unless eradication therapy is given.
The patient will have a painful, firm, red swelling which eventually develops a necrotic centre and releases a pustular discharge. It is particularly common on the thighs or buttocks.
Treatment may include:
- Bathing with a povidone-iodine wash and shampoo
- Cutting the nails short and regularly scrubbing them
- Topical (apply antiseptic cream to the nostrils to eradicate S. aureus)
- Systemic (flucloxacillin)
They are caused by human papilloma virus (HPV) infection (spread via direct contact or inoculation).
The child will have flat, skin-coloured papules with smooth surfaces. The most common sites are the finger (especially around the nailfold), hands, arms and face.
The warts usually spontaneously resolve. They should not be excised. Keratolytics should be used instead e.g. tretinoin, salicylic acid, instead. Cryotherapy (with liquid nitrogen) is another option.
It is caused by infection with HSV 1 or HSV 2, which is transmitted by close physical contact with an infected individual. The virus remains latent in nearby nerve root ganglia and can reactivate and cause further active infections. See images related to herpes simplex here.
The child will have grouped, painful vesicles on an erythematous base. There may also be systemic signs.
The lesions resolve after 10 days. Thus, treatment is with analgesia. Oral acyclovir may be given for moderate or severe disease. The child and family must be counselled on how to prevent the spread of cold sores.
It is caused by mites, which are spread through close contact. The mites burrow into the upper layer of skin (see related images here).
Many members of the household may be affected. The child will present with an intensely pruritic, non-specific rash (papules, pustules, eczematous changes). Burrows help make the diagnosis of scabies. They are small, scaly, linear lesions with a white/black dot at the end (mite). Burrows are usually found in web spaces, and on the wrist, feet, axillae, umbilicus and palms.
All members of the household must be treated at the same time to prevent re-infection. All linen, towels and clothes should be washed in hot water and exposed to direct sunlight (to kill the mites). Children >2 years are treated with benzyl benzoate 25% lotion and those <2 years are treated with permethrin 5% lotion or diluted benzyl benzoate.
Erythematous Rash with Fever
Chicken Pox (Varicella Infection)
It is a highly infectious viral disease. The child will present with mild headache, fever, malaise and generalised, vesicular rash. There is permanent immunity once infected. It is treated with acyclovir, analgesia and calamine lotion.
It is caused by parvovirus B19 infection. The child will have arthropathy, “slapped cheek” appearance, perioral pallor, fever, coryza, headache and a lacy rash on the trunk. It is a self-limiting condition and does not require treatment.
The most important causes of erythema nodosum are S. pyogenes and TB. The child will have tender, red nodules, commonly on the anterior lower leg. The child should be investigated with tuberculin skin testing, ASOT and a CXR. The underlying cause must then be treated.
Hand, Foot and Mouth Disease
It is a viral illness caused by coxsackie virus. The child will present with:
- Abdominal pain
- Painful oral vesicles and erosions
- Sparse, small, grey vesicles on the hands or feet (see related image here)
Symptomatic treatment is given.
It is characterised by:
- Fever for >4 days
- Bilateral conjunctival injection
- Lip or oral cavity changes (strawberry tongue)
- Rash (mostly affecting the trunk)
Investigations should include:
- Blood tests – CRP, ESR and FBC
- Imaging – ECG, CXR and echocardiogram
Treatment is with aspirin and IVIG. Specialist referral is necessary.
It is a highly contagious virus which is characterised by:
- Koplik spots
Supportive treatment is given.
It is most commonly caused by HHV6. The patient will have a high fever, facial oedema and blanching rash. It is a self-limiting condition and is managed with supportive treatment.
It is a viral infection which causes skin disease that is less severe than measles. The child will have a discrete rash, palatal petechiae and occipital lymphadenopathy. Management is symptomatic, see related image here.
The child may have:
- Impetigo (characterised by crusting)
- Cellulitis (characterised by indistinct borders)
- Erysipelas (tender, warm, bright red, well-demarcated rash and swollen skin)
These infections are treated with penicillin.
CONGENITAL SKIN CONDITIONS
It is a congenital vascular malformation which may be part of a syndrome:
- Sturge-Weber syndrome – characterised by eye manifestations (glaucoma), skin manifestations (port-wine stain) and CNS manifestations (seizures)
- Klippel-Trenaunay syndrome – characterised by port-wine stain, varicose veins, and bony and soft tissue hypertrophy of the affected limb, see related image here.
The segmental, blanchable, erythematous patches are present from birth and persist for the rest of the child’s life.
The patient may need to be referred to the relevant specialist, depending on the site(s) involved. If the lesion involves the eye or upper third of face, refer to a neurologist.
Haemangioma (Strawberry Naevus)
This is a benign vascular tumour that is present at birth or develops in the first few weeks of life.
The naevus undergoes marked proliferation in the first year of life. This is followed by spontaneous involution/regression of the vascular component with replacement by fibrofatty tissue. Its exact cause is unknown but evidence suggests that hypoxia may play a key role in its development.
The child will have a red nodule or plaque which has been present from birth or developed in the first few weeks of life. Lesions may be multiple and can occur on internal organs.
One must reassure the patient and parents that treatment is not necessary, unless:
- The tumour obstructs a vital organ
- The tumour has the potential to impair function
- The tumour is on a site where life may be threatened, e.g. epiglottis (may obstruct the airway)
- There are multiple lesions (>5) on the skin (as that may imply internal organ involvement)
In these cases, the patient should be referred to a dermatologist for possible topical corticosteroids, oral propranolol or laser treatment.
Treponema pallidum can cross the placenta in an infected and untreated mother, and can infect the foetus. Foetal infection can occur at any stage of pregnancy. T. pallidum can also be transmitted to exposed neonates. Clinical manifestations may appear within the first 2 years of life (early disease) or after 2 years of life (late disease – not infectious). Untreated syphilis during pregnancy (especially early syphilis) can lead to miscarriage.Congenital syphilis has no primary stage (see images related to secondary syphilis here.
Early congenital syphilis can present with only a rash, which may delay diagnosis. The child may have vesicles and bullae or a maculopapular rash on the palms and soles. There may be associated desquamation. Other signs and symptoms include:
- Prematurity/low birth weight
- Neurological impairment
- Bone deformities
One should order:
- Maternal TPHA/RPR
- FBC (to identify anaemia and thrombocytopaenia)
- Chest X-ray
- Full body X-ray
One must try and prevent vertical transmission. Therefore, all pregnant patients with syphilis should be treated with 2.4 MU benzathine penicillin IM weekly for three weeks.
The symptomatic child with a positive syphilis test should be treated with penicillin G (50 000 IU/kg IVI twice daily for 10 days). Treatment must not be interrupted. The asymptomatic child with a positive test should be treated with penicillin G (50 000 IU IMI stat).
Its cause is unknown but it is the result of benign proliferation of melanocytes. One should be suspicious of malignancy if:
- A – there is asymmetry
- B – borders are poorly defined
- C – the colour is not uniform
- D – the lesion has a diameter > 6 mm
- E – the lesion is evolving (changes in shape, size or colour)
The child will have a well-circumscribed, brown/black papule or macule.
The benign acquired naevus does not require excision. The large congenital naevus (see related images here) should be regularly monitored. The child with an atypical naevus should be referred to a dermatologist.
It is common in Asian and Black neonates and less common in Caucasian neonates.
This lesion is benign and often fades. It is the result of the delayed disappearance of dermal melanocytes.
The child will have congenital, blue-grey patches with indefinite borders. These patches are most common in the sacral area.
It is a localised area of increased melanogenesis of unknown cause.
The child will have pigmented macules or patches which are present from birth or appear during early childhood. The colour of these lesions ranges from tan to dark brown.
Café-au-lait spots are associated with neurofibromatosis (the presence of six or more spots is a diagnostic criterion). Patients who meet this criterion should be referred to neurology.
The hair loss is possibly due to an autoimmune process. However, the exact mechanism remains unknown. The hair loss is sudden and occurs at any age without preceding inflammation. Spontaneous regrowth is expected in ~6-18 months in patients with mild disease. The more the hair loss, the worse the prognosis.
The child will have well-defined, patchy hair loss with normal underlying scalp.
The child and parents should be reassured if there is only a single patch. However, a potent topical steroid gel or lotion may still be applied.
Patients with extensive or recurrent hair loss should receive emotional support and can be encouraged to purchase a wig, as treatment might not work
This hair-loss (reflecting on images here) is as the result of bad hair-grooming practices which cause breaking of the hair e.g. trichotillomania (the patient pulls out his/her own hair. In children, this may signify family stress. There may be permanent hair loss in patients with traction alopecia if the damage is severe.
The child will present with hair loss at traction sites, commonly the scalp borders or vertex. At the site of alopecia, there will be damaged, brittle and broken off hair.
One must explain the likely cause to the patient and parents and give advice on hairdressing techniques.
This type of hair loss can follow a traumatic, inflammatory or neoplastic process. The loss of hair is usually permanent.
Affected scalp is bound down by fibrosis (see related images here). There is also a change in pigmentation.
One must explain that the hair loss is permanent. Chloroquine should be given if the child has discoid lupus. A dermatology referral should be made if the cause is unknown. Referral to a plastic surgeon may be considered.
Pediculosis (Lice Infestation)
It is common in children and is spread by close contacts. Therefore, there are often outbreaks at schools.
The child will present with intense scalp pruritus and white nits attached to the hairs. The constant scratching can lead to impetigo and secondary eczema.
Apply permethrin 5% topical lotion to kill the lice. The nits may be removed by going through the freshly-washed hair with a fine-toothed comb or shaving the head.Patients with lice-infested eyelashes should be referred as there might have been sexual abuse.
TRAUMA, DRUG REACTIONS AND BITE REACTIONS
It is an abnormal growth of scar tissue in individuals who are genetically predisposed. It may grow in response to trauma or spontaneously appear (see related imageshere).
The child will present with firm, rubbery nodules that vary in size. Keloid lesions tend to cross the scar borders and are less painful.
A zinc oxide (pressure) plaster and intralesional steroids should be applied. The patient should be referred to a plastic surgeon if the lesion is unresponsive or severe.
An excessive amount of collagen is deposited, producing a raised scar. It is similar to a keloid but the lesion is within the margins of the injury.
These lesions stay within the scar border, are inflamed and are very painful.
The patient should be treated with intralesional steroid injections or silicone gel compression.
Fixed Drug Eruption
This is a skin reaction that tends to appear following ingestion of certain medications or substances. Any drug has a potential to cause a fixed drug eruption, but it is most commonly seen with laxative, analgesic or sulphonamides use.
The patient will have round, sharply-demarcated, hyperpigmented macules. They are initially erythematous but go on to blister and then resolve (purple-grey colour). These lesions recur at the same spot every time the patient takes the offending medication/substance (see related images here).
Treat the patient with an alternative drug and order a MedicAlert bracelet.
It is a small, benign vascular tumour that develops in response to trauma (see related images here).
Pyogenic granulomata are common on the fingers. The child will have a nodule with a glistening, smooth and eroded surface. It easily bleeds on contact
Treatment may be with one of the options below:
Treatment may be with one of the options below:
- Excision or curettage removal followed by electrocautery of the base
- Application of very potent steroids
- Chemical cauterisation with a silver nitrate stick
It is a common, chronic pruritic condition which is caused by allergy to insect bites. It usually affects young children.
The lesions/bites occur in a line (“breakfast, lunch, dinner” distribution) or a group.
- Informing the patient and parents of the cause of the allergy
- Educating the family about chronicity
- Treating pets for fleas
- Checking mattresses for bed bugs
- Fumigating the home
- Applying topical corticosteroids
- Treating infected lesions with antibiotics
- Prescribing antihistamines for itch control and sedation
DERMATOLOGY SUMMARY (CHEAT SHEET)
Face or flexures
Area of contact
Perineum or thighs in infants
Scalp, face, chest or napkin area
|Scaly papules and plaques||Pink or red plaques with scale
Pink or red plaques on the trunkPurple/brown/silver papules
|Erythematous and purple lesions||Single red area
Flat and congenital
Raised and congenital
Several, raised and itchy
Raised, red and non-itchy
Tender nodulesWidespread, erythematous rash
Fixed drug eruption
Viral infection, streptococcal infection or drug reaction
|Papules and nodules||Red or pink
Brown or black
|Erythema nodosum, boil or acne
Pigmented naevus or wart
Wart, molluscum contagiosum or keloid
|Blistering diseases||Vesicles on erythematous skin
Vesicles on normal skin
Round, large and transparent
Concentric circles with a bullous centre
|Herpes simplex, chickenpox or acute eczema
Erythema multiforme, fixed drug eruption
Scabies, acne, boil or folliculitis
|Altered pigmentation||Smooth, depigmented skin
Scaly, hypopigmented skin
Smooth, hyperpigmented skin
Scaly, hyperpigmented skin
|Albinism or vitiligo
Pityriasis sicca alba or tinea versicolor