5. Common Skin Disorders edited.pptx

Common Skin Disorders In Pediatric age group Dr Sunil Jatana Prof Paediatrics Dr Tharam (2023) Introduction  Skin disorders are a common problem in children  Some of the skin infections spread from adults  Neonates & small infants – sometimes difficult to treat  May improve as child gr...

Common Skin Disorders In Pediatric age group Dr Sunil Jatana Prof Paediatrics Dr Tharam (2023) Introduction  Skin disorders are a common problem in children  Some of the skin infections spread from adults  Neonates & small infants – sometimes difficult to treat  May improve as child grows older Macule    Café au lait & axillary freckling Port wine stain Macule: an alteration in skin color but cannot be felt < 1 cm diameter. Lesion >1 cm diameter is called patch Change in colour due to melanin (lentigo, Café au lait, Mongolian spot and vitiligo), or blood or blood vessels (port wine stain and petechiae) Congenital dermal melanocytosis (Mongolian spots)  Flat blue or blue/grey spots with an irregular shape that commonly appear at birth or soon after  Most common at the base of the spine, on the buttocks, back and shoulders.  They are extremely common among Asian children, as well as children with dark skin, including people of Polynesian, Indian and African descent  The birthmarks have usually gone once the child reaches adolescence  <3 % will continue into adulthood, and these are usually the ones present in body sites other than the buttock and spine areas. Papules  Papules are palpable solid lesions raised and round-topped <0.5 cm, nodules 0.5-2 cm in diameter. Molluscum contagiosum Gottron papule Juvenile dematomyositis Rhumatic fever subcutaneous nodules Plaque    Plaque- raised flat topped and palpable with finger > 1 cm. There may be increase in the thickness of the epidermis and/or dermis/ subcutaneous fat due to underlying proliferative or inflammatory process Scaly plaque in psoriasis Wheals & urticaria  Palpable, non-scaly, flesh colored or erythematous papule or plaque  Each lesion is rapidly progressive, lasts <24 hours and resolves without residual pigmentation  Size varies few mm to few cm  Dermal edema secondary to mast cell degranulation e.g. urticaria Vesicle, bullae   Herpes simplex Bullous impetigo   Epidermolysis bullosa Herpes zoster Palpable ,fluid filled and together called blister Fluid is clear or pale yellow. Fluid blood or lymphatic accumulates in the epidermis or dermis separating the layers of skin from one another Vesicle <0.5 cm, bulla >0.5 cm Pustule  Palpable, filled with purulent fluid  Sub-classified into follicular and non-follicular Folliculitis Acne neonate Cysts  Cysts are circumscribed, thick-walled lesions located deep in the skin; covered by normal epidermis and contain fluid or semisolid material. Ganglion cyst Dermoid cyst Molluscum contagiosum Molluscum contagiosum  Caused by poxvirus, DNA virus.  3 types and type 1 most infectious  Acquired by direct contact with infected person or from fomites or autoinoculation  Well children age between 2-6 yrs  Immunosuppressed individuals are most commonly affected  The incubation period is estimated to be ≥ 2 weeks Clinical features Discrete, pearly, skin-colored, smooth, dome-shaped, papules vary in size from 1 to 5 mm. Have a central umbilication from which a plug of cheesy material can be expressed. Found mainly on the face, eyelids, neck, axillae and thighs Pustular erosion at the site of lesion may be seen and results in atrophic scars Molluscum contagiosum… Molluscum contagiosum.. Molluscum contagiosum: Treatment  Self limited disease. Average attack lasts for 6-9 months but can last for years  Cantharidin ointment locally (not for face)  Liquid nitrogen cryotherapy for independent lesions  Immunotherapy with Candida antigen Scabies Etiology  Caused by burrowing & release of toxic or antigenic substances by Sarcoptes scabiei var hominis – female mite  Spreads very fast in the household   Extent & duration of physical contact with infected person  Children & sexual partner most at risk Transmitted by fomites rarely as mite dies within 2-3 days Pathogenesis  Gravid female impregnates skin surface forms a shallow well within 30 min. Life span 1-2 months  Extends this tract & deposits 10-25 oval eggs and numerous brown fecal pellets (scybala) daily.  Egg laying is completed in 4-5 weeks, mite dies within the burrow. Pathogenesis..  Eggs hatch in 3-5 days, release larvae that move to skin surface  Maturity is achieved in about 2-3 wk.  Mating occurs, gravid female invades skin to complete the cycle. Clinical Manifestations  Intense pruritus – at night  Skin – 1-2 mm red papules, excoriated, crusted or scaling  Thread-like burrows are classic lesions  In infants – bullae and pustules are common  Palm, soles and scalp are affected Clinical manifestations…  In older children & adolescents – clinical pattern same as adults  Interdigital spaces, wrist flexors, anterior axillary folds, ankles, buttocks, umbilicus and belt line, groin, genital areas in males, breast areola in females  Head, neck, palms & soles generally spared  Nodular scabies-red brown nodule in covered areas axilla, groin and genitals Diagnosis  Type of lesions  Facial sparing  Affected family members  Poor response to topical antibiotics  Transient response to topical steroids  Confirmation – microscopic – mites, ova, scybala in skin scrapings Scabies Lesions Various sites On the skin Complications of Scabies Untreated  Eczematous dermatitis, impetigo, folliculitis, cellulitis, lymphangitis  Pyoderma followed by Glomerulonephritis after Streptococcal infection of scabies lesions Treatment   Permethrin 5% cream (Elimite)  Applied entire body, neck down & left for 8-12 hrs  Reapplied if necessary after 1 week Other therapies  Oral Ivermectin, Lindane 1% lotion or cream  Intense itching may persist – topical steroids  Whole family treated  Clothing, bed linen, towels thoroughly laundered Atopic Dermatitis Atopic dermatitis/Eczema  Most common chronic relapsing skin disease in infancy & childhood  10-30% children worldwide  Occurs in families with other atopic diseases – asthma, allergic rhinitis, food allergy  Infants with AD predisposed to allergic rhinitis and/or asthma – “the Atopic March” Etiology Complex genetic disorder  Defective skin barrier  Reduced skin innate immune response  Exaggerated T-cell responses to environmental allergens and microbes leads to chronic skin inflammation Clinical manifestations  Begins in infancy  50% symptomatic 1st year of life and  30% between 1- 5 years of age  Lesions intensely pruritic with erythematous papules  Pruritis more at night – itch-scratch-itch  Scratching & excoriation – increased skin inflammation – more pronounced skin lesions (cutaneous reactivity)  Dry, lack luster skin irrespective of stage of illness Atopic Dermatitis Atopic dermatitis Clinical manifestations…  In infants involves face, scalp and extensor surface of extremities  Diaper area usually spared  Older children – lichenification of skin in the flexural folds of extremities  AD goes into remission as child grows older  Prone to itching & inflammation when exposed to allergens Atopic Dermatitis Lichenification of skin Atopic Dermatitis  Acute AD skin lesions intensely pruritic and erythematous papules  Subacute AD erythematous, excoriated, scaling papules  Chronic AD lichenification or thickening of skin with accentuated surface markings and fibrotic papules (prurigo nodularis)  In chronic AD all 3 types of skin lesions may coexist  Most have dry lackluster skin irrespective of their stage of disease Skin areas affected by AD according to age Age group Area affected Infants 0-2 years • • • • Childhood 2 years to Puberty • Flexural surfaces of extremities • Neck • Wrist, ankles Adolescents/Adulthood Flexural surfaces of extremities Hands, feet Extensor surface of extremities Face, forehead, cheeks, chin Neck scalp Trunk Triggering factors  Infections-Bacterial, viral or fungal  Emotional stress  Allergens:  Food – cow’s milk, egg, peanut, wheat, fish, soy etc.  Aeroallergens- house dust mite, pollen, animal dander and moulds  Irritants-Hand washing soap or detergents, acrylic  Humidity, extremes of weathers  Excessive sweating Diagnostic criteria Major features (must have 3) Hanifin and Rajka criteria Pruritus Typical morphology and distribution • Facial and extensor involvement in infancy, early childhood • Flexural lichenification and linearity by adolescents Chronic or chronically relapsing dermatitis Personal or family history of atopy (asthma,allergic rhinoconjunctivitis, atopic dermatitis Minor / less specific features Xerosis Preauricular fissures Icthyosis/palmar hyperlinearity/keratosis pilaris IgE reactivity Hand/foot dermatitis Cheilitis Scalp dermatitis (cradle cap) Susceptibility to cutaneous infection Staph aureus and herpes simplex Perifollicular accentuation (esp. in pigmented races) Laboratory findings  No specific laboratory tests for diagnosis  Many patients have peripheral blood eosinophilia and increased serum IgE levels.  Prick skin testing can identify the allergens. Treatment Systematic multifaceted approach   Skin hydration – symptomatic relief  Lukewarm soaking baths  Application of emollient Topical anti-inflammatory therapy  Steroids  Use milder ones – hydrocortisone  Mometasone, fluticasone Steroid potency Potency of topical Topical steroids steroids Mild Hydrocortisone cream/oinment 1% Desonide Moderate Betamethasone valerate 0.025% (1:4) Eumovate (clobetasone butyrate) Potent Betamethasone valerate 0.05% Elomet (mometasone furoate 0.1%) Super potent Dermovate (clobetasol propionate 0.05%) Betamethasone dipropionate Treatment…  Calcineurin inhibitors > 2yrs age  Pimecrolimus cream 1%  Tar shampoos on scalp – anti-inflammatory & anti-pruritic  Anti-histamines at bedtime  Identification & elimination of triggers  If necessary – systemic steroids  Phototherapy  Cyclosporine Complications  Skin infection with Staphylococcus aureus  Viral and fungal skin infection  Exfoliative dermatitis, atopic kerato-conjunctivitis Prognosis  More severe & persistent in young children  Periods of remission more frequent as child grows  Spontaneous remission in 40-60% after age 5 yrs  Many become mild at adolescence Impetigo Etiology  Most common skin infection in children  2 classic forms:   Non-bullous impetigo   Non-bullous & Bullous Staphylococcus aureus, Group A β hemolytic Streptococcus (GABHS) Bullous impetigo  Staph aureus strains exfoliative toxins(ETA,ETB, ETD) Non-bullous Impetigo  >70% of cases are non-bullous  Staphylococcus spread from nose to the skin or on extremities that have been traumatized  Common lesions preceding  Insect bites, abrasions, lacerations, chicken pox, scabies, pediculosis & burns Non bullous impetigo  Begin on face/extremities that have been traumatized  Tiny pustule or vesicle initially  Develops into honey-colored crusted plaque < 2cm diameter  No pain, surrounding erythema or constitutional symptoms generally absent  Spread to other parts of body by fingers, clothing and towels Non-bullous Impetigo Non-bullous Impetigo Non-bullous Impetigo…  Occasionally pruritus  Regional lymphadenopathy in 90% cases  Leukocytosis may be present in 50% Bullous Impetigo  Infection of infants & young children  Flaccid, transparent bullae develop on face, buttocks, trunk, perineum & extremities  Neonates – diaper area  Rupture easily, leaving a narrow rim of scale at the edge of shallow moist erosion.  Develop on intact skin  No surrounding erythema or lymphadenopathy Bullous Impetigo Complications of Impetigo Potential but rare complications  Osteomyelitis  Septic arthritis  Pneumonia  Septicemia  Cellulitis in non-bullous impetigo 10% Complications of Impetigo…  Lymphangitis & suppurative lymphadenitis  Guttate psoriasis  Scarlet fever occasionally  Acute post streptococcal glomerulonephritis (M groups 2,49,53,55,56,57,60) Acute Rheumatic fever does not occur after Impetigo Treatment  Topical therapy with mupirocin 2%, fusidic acid, retapamulin 1% for localized disease  Oral antibiotics:  Widespread disease  Lesions near the mouth  Deep involvement like cellulitis, furunculosis, abscess formation and suppurative lymphadenitis  Cephalexin 25-50 mg/kg/day for 7 days  No improvement culture & ABST MRSA additional 7 days Staphylococcal Scalded Skin Syndrome Ritter disease Caused by Staphylococci phage group 2 strains 71 and 55 Foci of infection Etiology • • • • • • Nasopharynx Umbilicus Urinary tract Superficial abrasion Conjunctivae Blood Clinical Manifestation  Mediated by hematogenous spread of staphylococcal epidermolytic or exfoliative toxins A or B  Occurs predominantly in children < 5 years of age  Onset of rash preceded by malaise, fever, irritability, exquisite tenderness of skin  Scarlatiniform erythema develops diffusely and accentuated in flexural and periorificial areas  Conjunctiva inflamed, occasionally purulent  The brightly erythematous skin, rapidly acquire wrinkled appearance and in severe cases, sterile, flaccid blisters and erosions develop diffusely  Prominent circumoral erythema, radial crusting and fissuring around eyes, mouth and nose  Nikolsky sign epidermis may separate in response to gentle sheer force  Large sheets of epidermis peel away, moist, glistening, denuded areas, initially at flexures over much of body surface  Leads to secondary cutaneous infection, sepsis and fluid and electrolyte disturbances.  The desquamative phase begins after 2-5 days of cutaneous erythema  Healing without scarring in 10-14 days  Associated with pharyngitis, conjunctivitis and superficial erosions of lips, but intraoral mucosa is spared  Some appear ill, many comfortable except marked skin tenderness. Nikolsky sign Scalded skin syndrome Complications  Excessive fluid loss  Electrolyte imbalance  Faulty temperature regulation  Pneumonia  Septicemia  Cellulitis Treatment  Systemic therapy – oral (localized involvement) or parenteral antibiotics  Penicillinase resistant antibiotics – Cloxacillin, Vancomycin  Clindamycin (inhibits bacterial protein toxin synthesis)  Skin gently moistened & cleansed  Emollient application (lubrication and reduces discomfort)  Topical antibiotics not required  Fluid, electrolytes & nutrition Steven-Johnson syndrome (SJS) Mycoplasma pneumonia Etiology Drugs- sulphonamides, NSAIDs, antibiotics, anticonvulsants HLA-B*1502 and HLA-B*5801 in Han Chinese receiving carbamazepine and in Japanese receiving allopurinol Clinical manifestations 1-3  Lesions preceded by flu-like URI  Severe erosions of at least two mucosal surfaces with extensive necrosis of lips and mouth, and a purulent conjunctivitis  Upper airway and esophagus, gastrointestinal tract, anogenital mucosa  Presenting signs-burning sensation, edema and erythema of the lips and buccal mucosa  Followed by bullae, ulceration and hemorrhagic crusting Clinical manifestations 2-3  Pain:  Mucosal ulceration severe  Skin tenderness is minimal to absent  Corneal ulceration, anterior uveitis, panopthalmitis  Bronchitis, pneumonia, myocarditis  Hepatitis, enterocolitis, polyarthritis  Hematuria, ATN Clinical manifestations 3-3  Disseminated cutaneous bullae and erosions cause insensible fluid loss and bacterial superinfection and sepsis  New lesions in crops and complete healing in 4-6 weeks  Occular scaring, visual impairment  Strictures of esophagus, bronchi, vagina, urethra and anus  Nonspecific lab results: leukocytosis, raised ESR, increased transaminase levels and decreased serum albumin Toxic epidermal necrolysis (TEN)  More severe disorder  Constitutional toxicity  Extensive necrolysis of mucous membrane > 30% of body surface area Treatment 1-2  Supportive and symptomatic  Offending drug discontinued  Optho consult mandatory-application of cryopreserved amniotic membrane to the ocular surface during acute phase limits destructive long-term sequelae. Antiseptic eyecare, synechiea should be disrupted  Oral lesions – mouth washes and glycerin swabs, topical anaesthetics  Denuded skin cleansed with saline and Burrow solution compress, hydrogel  Antibiotic for secondary bacterial infection S.aureus and P. aeruginosa Treatment 2-2  May require ICU care  IV fluids and nutritional supports  Air-fluid bedding  Urinary catheterisation  IV immunoglobulin1.5-2g/kg/day x 3 days  Etanercept  Surgery for necrotic epidermis 6 Exanthems of childhood  First disease Measles,Rubeola Paramyxovirus  Second disease Scarlet fever  Third disease Rubella  Fourth disease SSD, Ritter’s  Fifth disease Erythema infectiosum Parvovirus B19  Sixth disease Streptococcus Rubella virus Staph aureus Roseola infantum (exanthem subitum) HHV 6B or HHV 7 The timing of rash in feverish children can predict likely aetiology  Very Sick Patients Must Take Double Tablets Varicella 1st day of fever Scarlet fever 2nd day of fever Small Pox 3rd day of fever Measles 4th day of fever Typhus 5th day of fever Dengue 6th day of fever Typhoid 7th day of fever Erythema infectiosum (Fifth disease)  Caused by Parvovirus B-19, DNA virus  Benign, self-limited exanthematous illness of childhood  IP 4-28 days (average 16-17)  Prodromal phase mild with low-grade fever (15-30%), headache and mild URI Fifth disease  Hallmark characteristic rash, which occurs in 3 stages  1st stage is an erythematous facial flushing, often described as a “slapped-cheek” appearance  2nd stage - spreads rapidly or concurrently to the trunk and proximal extremities as a diffuse macular erythema. More prominent on extensor surfaces, sparing palms and soles.  3rd stage - Central clearing, a lacy, reticulated appearance. They are afebrile and not ill  Resolves spontaneously  They are afebrile and not ill  Some have petechiae, older children and adults have mild pruritus  Rash resolves spontaneously without desquamation but wax and wane over 1-3 weeks  Recurs with exposure to sunlight, heat, exercise and stress  Lymphadenopathy and atypical papular, purpuric and vesicular rashes are seen Erythema infectiosum… Arthropathy  Arthritis and arthralgia may occur in isolation or with other symptoms  More common in adults, females and older adolescents  Diffuse polyarthralgia with morning stiffness to arthritis  Any joint, common hands, wrists, knees and ankles or any joint  Self-limited and resolve over 2-4 weeks  Some many months with transient RF+ve but no joint destruction Transient aplastic/aplastic crisis  Chronic hemolytic anemias- sickle-cell anaemia (sudden vasooclusive pain crisis), thalassemia, hereditary spherocytosis and pyruvate kinase deficiency (sudden fall of Hb. and reticulocytopenia).  Children will be ill with fever malaise and lethargy with S & S of profound anaemia, pallor, tachycardia and tachypnoea. Rash rarely present.  IP is short and coincident with viremia Immunocompromised persons  Impaired humoral immunity at risk of chronic parovirus B19 infection  Persons receiving chemotherapy, immunosuppressive therapy, congenital immunodeficiencies, AIDs and functional defect in IgG production  Chronic anemia with neutropenia, thrombocytopenia or complete marrow suppression Fetal infection  Parvovirus cytopathic effects primarily in erythroblasts bone marrow and extramedullary haematopoiesis in liver and spleen  Fetal infection as early as 6 week of gestation (erythroblasts in liver and after 4th month to bone marrow)  Profound fetal anaemia and high-output cardia failure  Nonimmune fetal hydrops, fetal demise and stillbirth in women with primary maternal infection (can cross placenta) 5%  Most infants infected in utero are born normally  US: Fetal measurement of peak systolic flow velocity of middle cerebral artery sensitive to diagnose fetal anemia and hydrops Myocarditis  Fetal myocardial cells express P-antigen, cell receptor for the virus (histology lymphocyte infiltrate)  In fetus, infants, children and few adults  Outcome varied complete recovery to chronic cardiomyopathy to fatal cardiac arrest  Rare potential cause of lymphocytic myocarditis in infants and immunocompromised persons Cutaneous manifestations  Variety of atypical skin eruptions  Petechial or purpuric with evidence of vasculitis in biopsy  Papular-purpuric “gloves and socks” syndrome (PPGSS)  PPGSS –fever, pruritus and painful edema and erythema localized to distal extremities “gloves and socks” followed by acral petechiae and oral lesions  Self limited and resolves in a few weeks usually young adults but also seen in children  Eruption associated with serological evidence of acute infection Erythema infectiosum..   Diagnosis  Clinical  Lab – B19 IgM (persists for 6-8 weeks), PCR viral DNA and nucleic acid hybridization  Viral DNA in fetal blood or amniotic fluid- fetal hydrops Treatment  Symptomatic  IVIG in immuno-compromised (200 mg/kg/day for 5-10 days and 1g/kg/day for 3 days). Not used for arthropathy  Fetus with anemia and hydrops treated with IU transfusions with risks Complications  Arthralgia and arthritis may persist after resolution of rash in adolescents and adults  Rarely cause thrombocytopenic purpura  Neurology: aseptic meningitis , encephalitis and peripheral neuropathy in in immunocompromised and healthy  Transient aplastic crisis in S-C disease, increased incidence of stroke  Haemophagocytic syndrome in immunocompromised Prevention  Children with RBC aplasia or Transient aplastic crisis are infectious requires treatment and isolated and for at least 1 week and until after resolution of fever. Roseola infantum  Exanthema subitum or 6th disease  Caused by human herpes virus (HHV) 6 & 7  Peak age 6-9 months  Abrupt onset of high fever. Seizure seen with fever. Fever usually resolves after 72 hours  Appearance of a faint pink or rose-colored, non-pruritic, 2-3 mm morbilliform rash on the trunk lasting for 1-3 days (blanching)  Spreading from trunk to face and extremities  Rash during fever or following defervescence Clinical features  Irritability  Inflammed tympanic membranes  Mild injection of pharynx, palpebral conjunctiva or tympanic membrane and enlarged suboccipital lymph nodes  Gastrointestinal complaints – diarrhoea, vomiting, pain abdomen Encephalopathy Ulcers at uvulapalatoglassal junction- Nagayama spots commonly in infants   Roseola infantum Roseola Infantum: Laboratory findings  Diagnosis  Clinical features  Primary HHV-6 lower mean numbers of TWBC (8900/mm3), lymphocytes (3400/mm3) and neutrophils (4500/mm3).  Thrombocytopenia, elevated serum transaminase and atypical lymphocytes  Mild CSF pleocytosis with slight elevations of protein  MRI T2 –weighted and FLAIR- areas of hyperintense signal in hippocampus, uncus and amygdala  PET scan increased metabolism within hippocampus Diagnosis  ELISA test  Viral DNA by PCR, RT-PCR from acellular fluid plasma  viral cultures (gold standard) Complication  Seizures most common in 1/3  Partial seizures, prolonged Sz, post-ictal paralysis and repeated seizures  Encephalitis, acute disseminate demyelination, acute cerebellitis, hepatitis and myocarditis  Late-developing long-term sequelae: developmental disabilities and autistic like features  Reactivation of HHV-6 in patients with human stem cell transplantation HSCT in 30-50%, 2-4 weeks after transplant; fever, rash, delayed engraftment of platelets and monocytes and GVH Complications  Post HSCT limbic encephalitis: short term memory dysfunction, confusion and insomnia with seizures clinically or on prolonged EEG monitoring Treatment and Prognosis  Treatment   Symptomatic – Paracetamol for fever Prognosis  Majority recover without sequelae  Risk of recurrent seizures not higher than other causes of febrile seizures Napkin/diaper dermatitis Fungal yeast infection Definition  Nappy rash is a reaction of the skin in the nappy area.  Nappy rash is often caused by prolonged skin. contact with baby's wee and poo, soaps, and. skincare preparations.  Urine is converted to ammonia by bacteria (urea splitting organism) alkaline irritant to the skin and fecal enzymes, proteases in the faeces Diaper dermatitis  Most common skin eruption in infants and toddlers  Occurs on convex skin surfaces that are in direct contact with the diaper, including the buttocks, lower abdomen, genitalia, and upper thighs  is a form of irritant contact dermatitis, eruptions in the diaper area may represent exacerbations of more diffuse skin diseases, such as seborrheic dermatitis or atopic dermatitis, or may be the manifestation of unrelated skin conditions that coincidently manifest in the diaper area  Rare differentials are acrodermatitis enteropathica (Zn deficiency) and Langerhan cell histiocytosis. Acrodermatitis enteropathica (Zn deficiency) Langerhan cell histiocytosis Symptoms of nappy rash • Red or raw patches on your baby’s bottom or the whole nappy area • Skin that looks sore and feels hot to touch • Scaly and dry skin • An itchy or painful bottom • Your baby seeming uncomfortable or distressed • Spots, pimples, or blisters on bottom (spots can appear red or brown, but may be less noticeable on brown and black skin) Do o • change wet or dirty nappies as soon as possible • keep the skin clean and dry – pat or rub the skin gently to dry it • leave nappies off when possible • use extra absorbent nappies • make sure your baby's nappies fit properly • clean your baby’s skin with water or fragrance-free and alcohol-free baby wipes • bath your baby daily (but not more than twice a day, as washing too much can make the skin dry out) • use olive oil to remove nappy rash ointment rather than water Don’t • do not use soaps, baby lotion or bubble bath as they can irritate the skin • do not use talcum powder or antiseptics on nappy rash • do not put nappies on too tightly as it can irritate the skin Treatment • thin layer of a barrier cream to protect the skin (Zn oxide) • paracetamol for pain relief (only suitable for babies over 2 months old). • a steroid cream or ointment to help with redness and soreness • an antifungal cream, if baby has a thrush infection • antibiotics, if baby has a bacterial infection Summary  Pediatric dermatology tender branch  Most disorders are treatable  Some resolve spontaneously with age  Some very irritating because of itchy nature  Child can only express by crying  Urgent resolution of symptoms required Thank You Nelson Textbook of Pediatrics 19th ed Pediatric protocol 4th ed https://www.nhs.uk/conditions/baby/caring-for-a-new born/nappy-rash Rash with fever in children: a clinical approach Paediatrics and Child Health 27:4, 2017