Skin in children and common paediatric rashes

• Most childhood rashes are benign and self-limited, but a few are early warnings of serious illness, so the first question is always "is this child well?"
• Common patterns are recognised by age, distribution, morphology and history rather than by tests; tests are usually unnecessary.
• Skin in children has its own problems that adults rarely get: nappy irritation, cradle cap, infantile haemangiomas, viral exanthems, birthmarks, impetigo, head lice and molluscum.
• Treatment should match the cause: barrier creams for nappy rash, emollients and mild steroids for dermatitis, propranolol for high-risk haemangiomas, antibiotics for impetigo, and usually observation for molluscum.
• Education, return-to-school advice and reassurance are as important as prescriptions; many of these rashes settle without any treatment at all.

By the end of this page you should be able to:

1. Assess a child with a skin rash, separating red flags from benign self-limited rashes.
2. Describe the presentation, cause and first-line management of nappy rash, cradle cap, infantile haemangioma, common viral exanthems, birthmarks, impetigo, head lice and molluscum.
3. Choose appropriate initial treatment, including doses and durations, and know when to refer.
4. Give practical advice on skin care, infection control and return to school or nursery.
5. Recognise age-related and resource-limited considerations in paediatric dermatology.

Skin disease is one of the commonest reasons a child sees a clinician. More than 70% of children with skin concerns, and 90% of those younger than 4 years, are assessed by a non-dermatologist.^[8] Most rashes are short-lived and harmless, and many clear without any treatment. The skill that matters most is pattern recognition combined with honest red-flag thinking: a child who is well and has a typical rash rarely needs tests, while a child who is unwell, or has a rash that does not fit a benign pattern, needs prompt and careful assessment. ^[10]

This page brings together the skin problems and rashes a medical student is most likely to meet in children. It deliberately groups them as a single approach rather than as eight separate diseases, because in clinic the question is usually "what is this rash?" rather than "tell me about nappy rash."

A note on wording: "paediatric" and "pediatric" are the same adjective. Drug names are given as generic (INN). Regional differences in first-line choices are marked as they arise.

• A non-blanching rash (purpura or petechiae), especially with fever, lethargy or neck stiffness: think meningococcal septicaemia, and treat as an emergency.
• A child who is systemically unwell with a rash: fever with toxicity, pain out of proportion, or rapid spread.
• Bullous or rapidly spreading infection in a neonate (aged 1 year or under): bullous impetigo in this group warrants referral and often hospital care.^[6]
• Mucosal involvement with widespread blistering (eyes, mouth, genitals) after a drug: possible Stevens-Johnson syndrome.
• A rapidly expanding, painful, hot lesion with fever: cellulitis or a deeper soft tissue infection, not a simple rash.
• A large lumbosacral birthmark cluster (haemangioma, hypertrichosis, subcutaneous mass, caudal appendage, or multiple abnormalities): occult spinal dysraphism is possible and needs imaging.^[7]
• A port-wine stain on the forehead (V1 distribution): associated with Sturge-Weber syndrome, requiring ophthalmology and neurology assessment.^[7]
• A solitary or multiple large congenital melanocytic naevus (projected size greater than 20 cm): melanoma risk; refer to paediatric dermatology.^[7]
• Five or more infantile haemangiomas: can signal hepatic haemangiomas with high-output cardiac failure and severe hyperthyroidism.^[2]
• A haemangioma threatening vision, airway, ulceration or scarring: refer promptly.^[2]
• Parvovirus B19 infection in pregnancy or in a child with sickle cell disease (aplastic crisis) needs specific management.^[10]

Ask about the following, in plain language. Each question has a reason.

• Age. Newborn rashes, infant rashes and toddler rashes have different common causes. Roseola, for example, classically occurs between 6 months and 2 years; cradle cap peaks at about 3 months.^[9][10]
• Onset and duration. Sudden onset with fever suggests a viral exanthem; weeks of greasy scale on the scalp suggests cradle cap; a lesion present since birth is a birthmark.
• Symptoms. Itch, pain, fever, malaise, poor feeding, disturbed sleep.
• Distribution. Does it follow the nappy area, a dermatome, the extensor surfaces, the flexures, or the limbs and buttocks? Distribution is often the most useful clue.
• Contacts and exposures. Household or school contacts with the same rash (head lice, impetigo, molluscum), new cosmetics or wipes, recent antibiotics, travel.
• Atopy and family history. Eczema, asthma, allergies in the child or family; atopic dermatitis affects 15 to 20% of children, usually starting before 2 years.^[8]
• Birth and neonatal history. Prematurity and low birth weight increase the risk of infantile haemangioma.^[2]
• Medication history. Recent drugs, and for older adolescents, sexual contact and new partners.
• Immunisation status. Falling vaccination rates mean vaccine-preventable rashes such as measles are reappearing.^[8]

Examine the whole child, not just the rash.

• General state: well or unwell; temperature, hydration, growth.
• Skin examination in good light: note morphology (macule, papule, plaque, vesicle, bulla, pustule, nodule, scale, crust), colour, size in millimetres, borders, and whether lesions are discrete or confluent.
• Distribution: symmetry, flexural vs extensor surfaces, exposed vs covered areas, mucous membranes, nails, scalp, nappy area.
• Signs of scratching or secondary infection: excoriation, honey-coloured crusting (impetigo), satellite pustules (Candida).
• Associated findings: lymphadenopathy, mucosal spots (Koplik spots in measles, Forchheimer spots in rubella), heart murmur or hepatomegaly with multiple haemangiomas, neurology and eye exam if port-wine stain on the forehead.
• Growth measurements when the rash is chronic or the child is failing to thrive.

Napkin dermatitis describes a group of conditions affecting skin under a nappy. The commonest is irritant contact dermatitis caused by urine and stool. It most often affects babies aged 3 to 15 months, and has been reported in up to 50% of babies in cloth nappies; it is much less common with modern multilayered breathable disposables.^[11] Nappy rash of any kind affects more than half of infants by 12 months.^[1]

Mechanism. Urine and occlusion over-hydrate and macerate the skin; faecal enzymes break down stratum corneum lipids and proteins; mixed urine and faeces form ammonium hydroxide, raising pH; the wet skin is colonised by microbes, particularly Candida; friction worsens it. Breastfed babies have a lower incidence, because their stools have a lower pH; once solid foods start, stool frequency and pH rise, and rash becomes more common.^[11]

Presentation. An erythematous, sometimes scaling rash on the convex surfaces in direct contact with the nappy, tending to spare the skin folds. Mild rash presents as macules and papules; severe rash can be erosive and distressing. Candida infection adds satellite pustules and involves the folds.^[1][11]

Other causes to consider. Seborrhoeic dermatitis, atopic dermatitis, psoriasis, perianal streptococcal cellulitis, threadworm, viral infection (hand, foot and mouth; herpes simplex), impetigo, and less commonly nutritional deficiency (zinc deficiency, acrodermatitis enteropathica), malabsorption, Langerhans cell histiocytosis and immunodeficiency.^[1]

Management.

• General skin care: change nappies as soon as wet or soiled; clean gently with water and a soft cloth (wipes are convenient but can irritate); pat dry; allow nappy-free time; use fragrance-free cleanser; avoid soaps, bubble baths and powders.^[1][11]
• Barrier cream with every change, containing zinc, white soft paraffin or petrolatum. Rash not responding to a low-zinc barrier may improve with a higher zinc concentration around 40%. Do not remove the barrier cream at every change: remove visible soiling and apply another layer over the top.^[1]
• For inflamed nappy rash not settling with simple measures, add a mild topical steroid such as hydrocortisone 1% cream once or twice daily for 1 to 2 weeks.^[1][11]
• If Candida is suspected (folds, satellite pustules), use an antifungal cream: clotrimazole 1% twice daily, or miconazole 2% twice daily, or combination preparations. Topical antifungal can be used together with 1% hydrocortisone.^[1]
• Strong steroid creams must not be applied to a baby's bottom, because of the risks of skin thinning, striae and tachyphylaxis.^[11]
• Treat bacterial infection (impetigo) with the appropriate topical or oral antibiotic (see impetigo below).

Persistent, severe or unusual nappy rash should prompt consideration of the less common causes above and referral.

Cradle cap is infantile seborrhoeic dermatitis of the scalp. It is very common, with an estimated prevalence of 9.5 to 10%, most often between 3 weeks and 12 months, peaking at about 3 months. There is no sex or racial difference.^[9]

Cause. Not fully understood. It may relate to heightened sebaceous gland activity in response to residual maternal androgens, with Malassezia playing an unclear role.^[9]

Presentation. Greasy yellow scales on the scalp, especially the vertex and frontal areas. It is usually not itchy and the infant is otherwise well. It can extend to the face, body and flexures as seborrhoeic dermatitis.^[9]

Differential diagnosis. Atopic dermatitis, impetigo, tinea capitis, contact irritant dermatitis and psoriasis.^[9]

Management. Start conservatively: emollient or repeated shampooing, then careful removal of scales with a soft toothbrush or comb. For more extensive or resistant disease, use a low-potency topical steroid such as hydrocortisone 1%, or an azole such as ketoconazole 2%, for 1 to 2 weeks, preferring a steroid if there is significant inflammation.^[9]

Course. Benign and self-limiting; usually resolves over weeks to several months without treatment. If it persists beyond 12 months, reconsider the diagnosis.^[9]

Infantile haemangiomas are the most common benign tumour of childhood, occurring in up to approximately 5% of infants. They are more common in girls, twins, preterm or low birth weight infants, and white infants.^[2]

Natural history. Most are small and self-resolving and need no treatment. Haemangiomas grow rapidly between 1 and 3 months of age and usually finish growing by about 5 months. Patients at greatest risk of permanent skin changes have larger lesions, lesions elevated more than 2 mm above the skin, or lesions that abruptly transition to normal skin.^[2]

High-risk features. Site (near the eye, ear or nose, breast, lip, neck, diaper area, axillae, beard area), large size by site, and five or more cutaneous lesions (which may signal hepatic haemangiomas, high-output heart failure and severe hyperthyroidism). High-risk lesions need prompt specialist referral.^[2]

Investigation. Imaging is not needed unless the diagnosis is uncertain, there are five or more lesions, or anatomic abnormalities are suspected. Ultrasonography is the first imaging modality when the diagnosis is uncertain; MRI when structural abnormalities are suspected.^[2]

Treatment. Oral propranolol at 2 to 3 mg per kg per day is the first-line medical therapy, given with or after feeding. Parents should be told about adverse effects such as sleep disturbance and bronchial irritation.^[2][7] Secondary options are oral corticosteroids (if propranolol is contraindicated or fails), intralesional triamcinolone and/or betamethasone for focal or bulky lesions, topical timolol for thin or superficial lesions, and surgery or laser mainly for residual skin changes after involution.^[2]

Early treatment matters. Beginning oral propranolol early improves success, and for high-risk haemangiomas it is the most effective treatment.^[2][7]

Viral exanthems are very common in children and most are benign and self-limited. They are usually diagnosed clinically by age, distribution and morphology, with investigations reserved for atypical cases. A clear history and examination are more useful than tests.^[10]

Cross-checking against paediatric sources, the following patterns are the ones most often met:

• Roseola infantum (human herpesvirus 6 or 7, spread by respiratory droplets). Primarily affects children aged 6 months to 2 years. There is a prodrome of high fever around 40 degrees C for 3 to 5 days, sometimes with febrile seizures, upper respiratory symptoms and lymphadenopathy. When the fever subsides, pink macules and papules start on the trunk and spread to the neck and extremities; the rash fades in a few days. Differential diagnoses not to be missed include Kawasaki disease and measles; measles starts on the face, not the trunk.^[10]
• Hand, foot and mouth disease (enterovirus, usually Coxsackie A16 or enterovirus 71). After a short prodrome of fever and a sore mouth, painful oral ulcers precede the rash. The rash consists of grey elliptical vesicles with an erythematous halo on the palms, soles, buttocks and sometimes the mouth. Lesions crust and disappear over 7 to 10 days. Nail changes (Beau lines, onychomadesis) may follow within 8 weeks. Differential diagnoses include bullous impetigo and eczema herpeticum.^[10]
• Erythema infectiosum (fifth disease) (parvovirus B19, respiratory droplets). Most common from 4 to 10 years. Stage 1: bright red slapped cheeks sparing the nasal ridge and perioral area. Stage 2, one to four days later: lacy reticular erythema on arms and legs, which may recur with sunlight, temperature changes or exercise. Serology (IgM) confirms if needed. Important: parvovirus can cause aplastic crisis in haemolytic anaemia (including sickle cell disease) and can cause hydrops fetalis in pregnancy.^[10]
• Gianotti-Crosti syndrome (papular acrodermatitis) (associated with many viruses and some bacteria; can follow vaccination). Ages 1 to 6 years. Prodrome of fever and upper respiratory symptoms, then a symmetrical papular or papulovesicular eruption on the extensor surfaces of limbs, buttocks and face, typically sparing the trunk. Usually not itchy; marked itch suggests scabies or papular urticaria. Consider liver function tests and hepatitis B serology. Self-limits over about 8 weeks.^[10]
• Varicella (chickenpox) (varicella zoster virus). Pruritic vesicular eruption on trunk, limbs and face: a red papule develops a thin-walled vesicle giving the "dewdrop on a rose petal", which umbilicates and crusts, with crops giving intermingled papules, vesicles, pustules and crusts. Individual lesions heal over 1 to 4 weeks. Diagnosis confirmed by PCR if needed. Atypical varicella can resemble impetigo or Stevens-Johnson syndrome.^[10]
• Measles and rubella. Measles is highly contagious with prodromal fever, cough, coryza and conjunctivitis, Koplik spots on the buccal mucosa, and a red maculopapular rash beginning on the head and spreading downwards. Rubella is usually mild, with a pink maculopapular rash starting on the face and spreading over 24 hours, tender lymphadenopathy and Forchheimer spots on the soft palate; congenital rubella syndrome is the major pregnancy concern.^[10]
• Non-specific viral exanthem associated with respiratory illness: a diffuse maculopapular rash in children that resolves within about five days.^[10]
• Hand, foot and mouth disease is common in outbreaks; standard supportive care. Topical analgesics in the mouth are not recommended (no benefit, theoretical toxicity).^[8]

General management of viral exanthems is supportive: antipyretics, fluids, and reassurance. Some, such as scarlet fever (a streptococcal infection with a sandpaper-like rash), are bacterial and need antibiotics within the recommended window to prevent rheumatic fever.^[8]

Birthmarks in newborns are usually grouped as vascular, melanocytic (pigmented), or markers of underlying developmental abnormalities of the nervous system. Most are benign. Parents' main concern is cosmetic, and reassurance plus explanation of expected natural history is central.^[7]

• Nevus simplex (salmon patch, stork mark). A benign capillary malformation. Common and usually fades. No treatment needed.
• Nevus flammeus (port-wine stain). A vascular stain that does not regress. A stain involving the forehead (trigeminal V1) warrants referral for ophthalmologic and neurologic evaluation because of Sturge-Weber syndrome. Treatment with a pulsed-dye laser before 1 year of age can reduce visibility.^[7]
• Infantile haemangioma (covered above). Treat with propranolol when high-risk features are present.
• Congenital melanocytic naevus. A pigmented naevus present at birth. A solitary lesion with a projected size of less than 20 cm can be observed in primary care. Lesions greater than 20 cm in any dimension, or multiple congenital melanocytic naevi of any size, should be referred to paediatric dermatology because of melanoma risk.^[7]
• Dermal melanocytosis (Mongolian spot). Blue-grey patches, usually over the lumbosacral area and buttocks. Benign, easily recognised, and they usually fade; no further evaluation is needed.^[7]
• Markers of occult spinal dysraphism. A lumbosacral haemangioma, hypertrichosis, subcutaneous mass or lipoma, caudal appendage, or multiple abnormalities, as well as an atypical solitary lumbosacral dimple, should be evaluated by ultrasound or MRI.^[7]

Impetigo is a common, highly contagious superficial bacterial skin infection, most often due to Staphylococcus aureus and/or Streptococcus pyogenes. It is most often non-bullous.

• Non-bullous impetigo: thin-walled vesicles or pustules that rupture quickly, leaving a golden-brown crust.^[6]
• Bullous impetigo: fluid-filled vesicles and blisters, often larger than 1 cm, that rupture to leave a thin, flat, yellow-brown crust. Caused by toxin-producing Staphylococcus aureus.^[6]

Management (NICE antimicrobial prescribing guidance).^[6]

• General advice: good hygiene to reduce spread to other body areas and to other people.
• Localised non-bullous impetigo (an area of less than 2% of body surface area is a useful primary-care rule of thumb^[8]) in a child who is not systemically unwell and not at high risk: consider hydrogen peroxide 1% cream applied 2 to 3 times a day for 5 days. ^[6]
• If hydrogen peroxide is unsuitable (for example, near the eyes) or ineffective, offer a short course (5 days, extendable to 7 on clinical judgement) of a topical antibiotic: fusidic acid 2% three times a day, or mupirocin 2% three times a day if fusidic acid resistance is suspected or confirmed. ^[6]
• Widespread non-bullous impetigo: offer a short course of topical or oral antibiotic, taking into account practicalities and resistance.
• Bullous impetigo, or any impetigo in a child who is systemically unwell or at high risk of complications: offer a short course of an oral antibiotic.
• Oral flucloxacillin (first choice): 1 month to 1 year 62.5 to 125 mg four times a day for 5 days; 2 to 9 years 125 to 250 mg four times a day; 10 to 17 years 250 to 500 mg four times a day. ^[6]
• Alternatives for penicillin allergy include clarithromycin by weight band; erythromycin in pregnancy (ages 8 to 17 years).
• Do not offer combined topical and oral antibiotics.
• If meticillin-resistant Staphylococcus aureus is suspected or confirmed, consult a local microbiologist.
• Refer to hospital if there are symptoms or signs of a more serious illness, or if impetigo is widespread in an immunocompromised child. Consider referral for bullous impetigo (particularly in babies aged 1 year or under), recurrent impetigo, systemic illness or high risk of complications.^[6]
• Recurrent impetigo: send a skin swab, consider a nasal swab and decolonisation. If a swab is sent, review the antibiotic choice when results are available and change if needed.^[6]

Good hand washing, not sharing towels and covering lesions reduce spread in households, schools and nurseries.

Head lice infestation is common in primary-school-aged children, most often between 4 and 11 years, and is more common in girls than boys. Lice are grey-brown insects up to 3 mm long that cannot fly, jump or burrow; transmission is mainly by head-to-head contact. Cleanliness is not a factor.^[3]

Diagnosis. Suspect in an itchy scalp or recurrent peri-scalp infections. Eggs (nits) are firmly fixed to the hair shaft near the scalp, take 7 to 10 days to hatch, and newly hatched lice lay more eggs 7 to 10 days later. Empty egg cases are white and shiny, further from the scalp. Repeated combing of wet and dry hair with a fine-toothed comb, in good light, confirms the diagnosis; styling products and dandruff wash off or slide, while real eggs are fixed.^[3]

Treatment. Treat only when an active infestation is confirmed (living, moving lice); itching alone or old empty egg cases are not reasons to treat.^[3]

• Three main options: a physical insecticide (dimeticone, isopropyl myristate with cyclomethicone, or isopropyl alcohol) that smothers lice, so resistance is unlikely; a chemical insecticide (malathion 0.5% aqueous liquid), to which resistance has been reported; or systematic wet combing with a fine-toothed comb.
• Wet combing is helped by conditioner; comb from roots to tips, cleaning the comb after each pass; repeat on days 1, 5, 9 and 13 to catch newly hatched lice.
• Head-lice shampoos are less effective than lotions because they are over-diluted and have insufficient contact time.
• Wet combing or dimeticone 4% lotion is generally recommended first line in pregnancy and breastfeeding, in children aged 6 months to 2 years, and in people with asthma or eczema. ^[3]
• Herbal and essential-oil preparations are not recommended (insufficient evidence).

Points for practice. All close contacts and household members should be checked; all affected members start treatment on the same day; wash combs and brushes in hot water daily; there is no need to exclude children from school while being treated. Chemicals should not be used regularly to prevent infestation.^[3]

Head lice can lead to secondary bacterial infection (impetigo) from scratching.

Molluscum contagiosum is a common, generally harmless poxviral skin infection, most common in children (typically 1 to 10 years) and young adults. It spreads by direct skin-to-skin contact or shared towels, flannels and bedding, and is seen more often in children with eczema, where dry cracked skin lets the virus enter.^{[4][5] [8]}

Presentation. Dome-shaped, pearly papules with a striking central dimple. They are usually 2 to 6 mm across (sometimes up to 20 mm), skin-coloured (may be pink or darker brown in darker skin), and number from one or two to fewer than 20, often clustered on the face, trunk and upper legs in children. They are usually not itchy; eczema-like patches may appear around them. Immunosuppressed children may have more and larger lesions.^[4][5]

Course. Self-limited: it usually clears in 6 to 18 months (BAD) or within 6 to 12 months (CDC), but can take up to 4 years. New bumps may appear while old ones clear. After healing, the skin may temporarily look white, pink or darker before normalising.^[4][5]

Management. Usually no treatment is needed, and most immunocompetent children can be observed. Procedural or topical therapy is offered for symptomatic or cosmetically worrying lesions.^[8]

• Squeezing is not recommended: it risks scarring and spread.^[4]
• Cryotherapy (liquid nitrogen), curettage after local anaesthetic, and in-office cantharidin are physical options; they can hurt and can scar.^[4][5]
• Topical options include salicylic acid and potassium hydroxide, applied carefully to irritate individual lesions.
• Oral cimetidine may gradually clear lesions and is often preferred for children because it is painless, can be given at home and is less likely to scar; facial lesions respond less well.^[5]
• Podophyllotoxin 0.5% cream is a home therapy for non-pregnant females, applied lesion by lesion; it is not recommended in pregnancy.^[5]
• Imiquimod is available for adults and has not been proven effective in children; it is not recommended in children because of possible adverse events.^[5]
• In immunocompromised children, the focus is on immune reconstitution; interferon and radiation have limited roles.^[5]
• Complications are mainly secondary bacterial infection.^[5]

General prevention: own towels and bedding, cover visible lesions, good hand hygiene. Children with molluscum do not need to be kept off school.^[4]

Most childhood rashes are diagnosed clinically. Tests are chosen sparingly.

• Skin swabs for bacterial culture when impetigo is worsening, not improving, recurrent, or when MRSA is suspected.^[6]
• Wood's lamp, scrapings for fungi or skin biopsy only in selected atypical cases; not usually needed for the rashes covered here.
• Serology (parvovirus B19 IgM, measles/rubella) for atypical suspected viral infection; pregnancy testing and obstetric referral when relevant.
• Ultrasound or MRI for haemangiomas when the diagnosis is uncertain or structural abnormalities are suspected, and for suspected occult spinal dysraphism.
• Blood tests for systemic illness, immunodeficiency or nutritional deficiency when clinically indicated.

General principles that apply to almost every child with a rash:

• Reassure when the diagnosis is benign; name the expected course.
• Advise simple skin care: regular emollients, avoid irritants and fragrances, short lukewarm baths, cotton clothing, do not scratch (cut nails, consider mittens in infants).
• Treat the identified cause with the appropriate agent and correct dose and duration.
• Give written or verbal advice on contagion, treatment application, and when to return.
• For viral and bacterial rashes, remind about good hand hygiene and not sharing towels or bedding.

When to refer:

• Red flags listed above, especially a non-blanching rash in an unwell child.
• Diagnostic uncertainty after careful re-examination.
• High-risk infantile haemangioma (site, size or number).
• Birthmarks needing specialist assessment (port-wine stain on forehead, congenital melanocytic naevus larger than 20 cm or multiple, occult spinal dysraphism markers).
• Severe, widespread, infected, or recurrent rash not responding to first-line treatment.
• Bullous impetigo in a baby aged 1 year or under, recurrent impetigo, or impetigo in a systemically unwell or immunocompromised child.
• Suspected MRSA or treatment failure.
• Any child with a rash and significant comorbidity or immunosuppression.

• Pattern recognition carries most of the diagnosis, since laboratory support may be limited.
• Emollients, zinc oxide/petrolatum barriers and soap substitutes are cheap and effective for nappy rash and dermatitis; avoid expensive or unproven products.
• Oral propranolol is affordable and effective for high-risk haemangiomas, but infants need safe assessment and monitoring during initiation.
• Where microbiology is unavailable, impetigo is usually treated empirically with the narrowest appropriate oral antibiotic available, following age bands, with referral for failure or recurrence.
• Ectoparasites and school nurses can coordinate head-lice management; visual diagnosis and wet combing avoid unnecessary insecticide use.

• Most childhood rashes are benign and self-limited; the priority is to recognise red flags.
• Age, distribution, morphology and history usually make the diagnosis; tests are rarely needed.
• Nappy rash is irritant contact dermatitis: barrier cream every change, mild steroid for inflammation, antifungal for Candida; avoid strong steroids on the nappy area.
• Cradle cap is self-limiting seborrhoeic dermatitis; emollients and gentle descaling first, then mild steroid or azole for 1 to 2 weeks.
• Infantile haemangiomas grow for up to about 5 months; high-risk features (site, size, number) warrant prompt referral and oral propranolol 2 to 3 mg per kg per day.
• Viral exanthems are diagnosed by pattern; classic examples include roseola (truncal rash as fever settles), hand, foot and mouth disease (grey vesicles on palms, soles and buttocks), and fifth disease (slapped cheeks then lacy rash).
• Birthmarks are usually benign; port-wine stain on the forehead and large or multiple congenital melanocytic naevi need specialist referral; Mongolian spots need only reassurance.
• Impetigo is treated by extent and risk: hydrogen peroxide for localised non-bullous, topical antibiotics if that fails, oral antibiotics for bullous, widespread or high-risk disease.
• Head lice: treat only confirmed infestation, use physical measures or dimeticone, repeat combing on days 1, 5, 9 and 13, check all contacts, no need to exclude from school.
• Molluscum is self-limited; observe usually, treat if symptomatic or cosmetically important, never squeeze.
• Parvovirus B19 can cause aplastic crisis in children with haemolytic anaemia and hydrops fetalis in pregnancy; measles is reappearing as vaccination rates fall.
• Reassurance, skin care and clear return advice are part of treatment, not an afterthought.

Skin conditions in children often overlap with adjacent MedGrasp topics: atopic dermatitis and other dermatitis, contact dermatitis, skin signs of systemic disease, cutaneous viral and fungal infections, scabies and other infestations, acne and adolescent skin, neonatal and infant conditions, childhood infections, travel and tropical skin disease, immunisation and vaccination, low-resource medicine, and psychosocial aspects of chronic skin disease. This page is a starting point; each condition above has a deeper topic of its own.