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Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
Pediatric Skin Diseases by Dr. Ramkesh Meena
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Pediatric Skin Diseases by Dr. Ramkesh Meena

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  • Human skin consists of three layers 1.Epidermis 2.Dermis & 3.Subcutaneous fatEpidermis consists of four layers(1)The first or basal layer consists of columnar cells that rest on the dermal-epidermal junction, serve as a continuing supply of keratinocytes for the normally differentiating epidermis as well as a reservoir of cells to repair epidermal damage. (2) The second, spinous cell layer consists of 3 to 4 rows of spinous cells. Their role is to begin formation of the epidermal barrier and to initiate vitamin D synthesis. (3)The third, Granular cell layer consists of 2 to 3 rows of granular appearing cells. Granular cells continue the process of epidermal barrier formation. (4)The fourth layer or stratum corneumcomposed of multiple layers of dead, highly compacted cells. The dead cells are composed mainly of disulfide-bonded keratins cross-linked by filaggrins.
  • Human skin consists of three layers 1.Epidermis 2.Dermis & 3.Subcutaneous fatEpidermis consists of four layers(1)The first or basal layer consists of columnar cells that rest on the dermal-epidermal junction, serve as a continuing supply of keratinocytes for the normally differentiating epidermis as well as a reservoir of cells to repair epidermal damage. (2) The second, spinous cell layer consists of 3 to 4 rows of spinous cells. Their role is to begin formation of the epidermal barrier and to initiate vitamin D synthesis. (3)The third, Granular cell layer consists of 2 to 3 rows of granular appearing cells. Granular cells continue the process of epidermal barrier formation. (4)The fourth layer or stratum corneumcomposed of multiple layers of dead, highly compacted cells. The dead cells are composed mainly of disulfide-bonded keratins cross-linked by filaggrins.
  • PEOTECTIO : from external environment, UV Rays, acts as a physical barrier.
  • Dermatology is a visual specility and some cases are diagnosed at a glance.
  • Begin at 24-48hrs of age.Individual lesion lasts for 4-5daysSmear of the central vesicle or pustule wil reveal numerous eosinophils on wright staining.Etiology-associated with normal bacterial flora in pilocebaceous orifice.D/D Miliariarubra, erythema in m. rubra is small i.e. ~1-2mm.
  • Lesions continue to recur until the age 2-3 years, treatment oral hydroxyzine 2mg/kg/day to decrease pruritusD/D Lesions of scabies can be vary similar to the lesions of ACROPUSTULOSIS OF INFANCY
  • lesions may be present over palms & soles disappear by 5 days of age.D/D
  • evolve into pustules over a few weeks , rarely present at birth.D/D Neonatal cephalic pustulosis, characterizedby erythematous papular/pustular lesions especially on theCheeks, develops in association with Malasseziasympodialisand Malasseziaglobosa
  • D/Dmolluscumcontageosum – does not usually appear in immediate neonatal period, Sebaceous gland hyperplasia-yellow rather than whitish
  • Cutis marmoratatelangiectaticacongenita is clinically similar, but the lesions are more intense, may be segmental, are persistent
  • d/d herpessimpiex infection, kerion- dermatophyte infection.
  • Cephalaxin 40-50mg/kg/day, dicloxacin 15-50mg/kg/day
  • 4 clinical forms , most common is chafing dermatitis-overconvaxicities, 7-12 months age.. 2nd limited to perianal area, observed in who have/had diarrhea. 3rd discrete shallow ulceration throught the diaper area. 4th beefy red confluent erythema-occurs after secondary c. albicans infection.
  • D/D-atopic or other forms of dermatitis , diaper change >_8 times /day-decrease incidence.
  • Interferon alfa-2a , 3 million unit/m2 BSA S/C injection for 12 months.PULSED DYE LASER-best for ulcerated lesions, 90% healing after 2 laser treatment.Heparin and FFP for bleeding.
  • Traces of Mongolian spots may persist into aolthood., Mongolian spots fade with time.
  • McCune-Albright:-giant café-au-lait spot, precocious puberty and polyostotic fibrous dysplasia.Proteus syn:-skeletal overgrowth+ large hamartomas+large café-au-lait spot.Patho melanocyte activity increased as is the melanin. Number remain normal.
  • Gingivostomatitis- in infants and children 60% of HSV infection appear as gingivostomatitis, almost all by HSV 1, erosions r extensive and painful. Primarily in infants <6 months age.
  • Rapid diagnostic test-fluorescent labelled monoclonal antibodies, PCR
  • Acyclovir therapy does not interfere with the induction of VZV immunityTretment indicated for:-nonpregnant female >13 yr of age and children >12 mo of age with chronic cutaneous or pulmonary disorders, Patients receiving short-term, intermittent, or aerosolized corticosteroid therapy, individuals receiving long-term salicylate therapy, and possibly secondary cases among household contacts. To be most effective, treatment should be initiated as early as possible, preferably within 24 hr of the onset of the exanthem
  • Acyclovir therapy does not interfere with the induction of VZV immunityTretment indicated for:-nonpregnant female >13 yr of age and children >12 mo of age with chronic cutaneous or pulmonary disorders, Patients receivingcorticosteroid therapy, and secondary cases among household contacts. To be most effective, treatment should be initiated as early as possible, preferably within 24 hr of the onset of the exanthem
  • Seroconversion 87% at 9 month, 95%at 1 yr, 98% at 15months.
  • Susceptible-presency of erythrocyte P antigen,Transient aplastic crisis or red cell aplasia in pt with chronic hemolytic anemia, immunocompromised.
  • Simillar illness by echovirus 16, febrile seizures r common, may mimic bacterial or viral meningitis.D/D rasha by drug taken for fever. t/t- ganciclovir is recommended in immunocompromised pt.
  • STAR compex by- rubella, human parvo virus B19, hepatitis B, adeno virus , echo virus,Contageous 2 days before to 7 days after rash.
  • D/Dpapular stage-rubella & morbiliform eruption,Vesicular – varicella but lesions acral distribution , few in no, non pruritic.Simillar illness by enterovirus 71. In severe illness by entero virus 71 , IVIG or Pleconaril may be effective.
  • For folliculitis mupirocin ointment topicaly.
  • Or ceftriaxone 100 mg/kg day for 7 days
  • Microsporumcanis
  • TREATMENT:-topical terbinafine twice a day 2-4 weeks, or clotrimazole 2-4 weeks Occasionally oral terbinafine or griseofulvin, fluconazole required.
  • 1% gamma banzeenhexachloride.Ivermectin 200microgram/kg single dose.
  • LONG-TERM THERAPY FOR PATIENTS WITH CORONARY ABNORMALITIES-Aspirin 3-5 mg/kg once daily orally, Clopidogrel 1 mg/kg/day (max 75 mg/day, ACUTE CORONARY THROMBOSIS-fibrinolytic therapy with tissue plasminogen activator or other thrombolytic agent under supervision of a pediatric cardiologistIVIG-resistant KD occurs in approximately 15% of patients and is defined by persistent or recrudescent fever 36 hr after completion of the initial IVIG infusionanother dose of IVIG at 2 g/kg is administered, or intravenous methylprednisolone
  • Etiology HSV antigen and DNA I n keratinocytesTo prevent recurrence-acyclovir 20mg/kg/day considered.
  • Transcript

    • 1. COMMON SKIN DISEASES IN PAEDIATRICS BY DR.RAMKESH MEENA
    • 2. INTRODUCTION • Skin is the largest and most superficial organ of the body. • Nearly one third(1/3rd) of the pediatric out patient visits involve a dermatology complaints. • In addition to wide variety of primary skin disorder seen during childhood, skin is a marker of underlying systemic disease and many hereditary syndrome.
    • 3. ANATOMY OF SKIN
    • 4. FUNCTIONS OF THE SKIN 1. PROTECTION 2. THERMOREGULATION 3. IMMUNOLOGIC RESPONSE 4. BARRIER TO WATER LOSS 5. SECRETION OF WASTES 6. SENSATION.
    • 5. NEONATAL SKIN IN COMPARISON WITH ADULT SKIN • Thinner, less hairy, weaker intercellular attachment • Fewer eccrine and sebaceous gland secretions • Increased susceptibility to external irritants • Increased susceptibility to micrococcal infection • Depressed contact allergen reactivity • Percutaneous permeability increased only in premature, damaged or scrotal skin.
    • 6. APPROACH TO THE CASE • HISTORY is important for diagnosing skin disease, may be crucial in complex cases. • EXAMINATION:- requires careful inspection of the entire cutaneous surface, many skin diseases are diagnosed only by their morphologic appearance. – identify the primary lesion, – the size in millimeters, – secondary changes, – color, – arrangement and distribution of the lesion. • The entire body surface, all mucous membranes, conjunctiva, hair, and nails should always be examined thoroughly under adequate illumination.
    • 7. MORPHOLOGY OF LESION • PRIMARY SKIN LESIONS: Initial pathologic change • SECONDARY SKIN LESIONS: Result from external forces such as scratching, picking, infection, or healing of primary lesions.
    • 8. MACULE: Color change in the skin that is flat to the surface of the skin and not palpable, <1cm in size. PATCH: If >1cm in size termed Patch. (café au lait spot,vitiligo,white macule) 9
    • 9. PAPULE: solid raised lesion with distinct borders 1 cm or less in diameter. (eg. Lichen planus, molluscum contagiosum) PLAQUE: solid, raised, flat topped lesion with distinct borders and an epidermal change larger than 1cm in diameter.(psoriasis) 10
    • 10. NODULE: A raised solid lesion with indistinct borders and a deep palpable portion.(rheumatoid nodule, neurofibrom a) WHEAL :Circumscribed, flattopped, firm elevation of skin with a well-demarcated and palpable margin Urticaria
    • 11. VESICLE: A raised lesion filled with clear fluid that is <1cm in diameter (varicella, herpes simplex) BULLA: A raised lesion filled with clear fluid, >1cm in diameter
    • 12. CYST: A raised lesion that contains a palpable sac filled with solid material.(epidermal cyst, dermoid cyst) PUSTULE: A raised lesion filled with a fluid exudate, giving it a yellow appearance. (acne, folliculitis)
    • 13. ATROPHY: The skin surface is depressed because of thinning or absence of the dermis or subcutaneous fat. (atrophic scar, fat necrosis) CRUSTING: Represents dried exudates of plasma combined with the blister roof, which sits on the surface of the skin after acute dermatitis. (impetigo , contact dermatitis) SCALING: Whitis plates present on the skin surface. (psoriasis, ichthyosis) {desquamation refers to peeling of sheets of scale after an acute injury to skin eg. Burn, toxic drug reaction}
    • 14. EXCORIATION: Oval to linear depressions in the skin with a complete removal of the epidermis , exposing a broad section of red dermis. (atopic dermatitis) FISSURE: Linear, wedge-shaped cracks in the epidermis extending down to the dermis and narrowing at the base. (warts) EROSIONS AND OOZING: Moist , circumscribed, slightly depressed areas representing a blister base with the roof of the blister removed. (burns , dermatitis)
    • 15. CLASSIFICATION OF DISORDERS OF INFANCY & CHILDHOOD 1. Transient Skin Disease/Neonatal 6. Genodermatosis dermatoses 7. Neurocutaneous disorders 2. Common Congenital 8. Metabolic & nutritional Malformations of Skin dermatoses 3. Birthmarks 9. Cutaneous manifestations of 4. Infections in infancy & systemic diseases Childhood 10. Miscellaneous conditions – Viral infections – Bacterial infections – Fungal infections 5. Infestations
    • 16. NEONATAL DERMATOSIS
    • 17. TOXIC ERYTHEMA OF NEWBORN (ERYTHEMA TOXICUM NEONATORUM) • Benign self–limiting eruption • Characterized by erythemaous macules and plaques, 2-3cm in size, with a tiny 1-3mm central vesicle or pustule. • Onset mostly during first week of life, rarely at birth. • Site – mostly on trunk and proximal extremeties. • Systemic symptoms are absent • Lesion spontaneously disappear in 3 to 7 days.
    • 18. MILIARIA RUBRA (PRICKLY HEAT) • Crops of superficial vesicles blockage of sweat ducts. resulting from • Tiny, papulo-vesicle are on erythematous base. • Site- flexural areas e.g. neck, groins, axilla and face, following excessive sweating. • Secondary infection by staphylococcus is common • TREATMENT  Avoidance of excessive heat and humidity.  Light clothing, cool bath and avoidance of heavy blankets
    • 19. ACROPUSTULOSIS OF INFANCY • Characterized by crops of intensely pruritic papulopustular or vesicopustular lesions appear for period of 7 to 10 days remits for 2 to 3 weeks prior to recurrence. • Etiology is unknown • Site - palm & soles, dorsal aspect hands, feet, wrists, ankles, face and scalp. of • Pustules are neutrophils & sterile and contain eosinophil • TREATMENT: Topical steroids to decrease the pruritus.
    • 20. TRANSIENT NEONATAL PUSTULAR MELANOSIS • Characterized by transient, benign, superficial, noninflammatory, vesicle-pustules that are extremely fragile last for 24-48 hrs. • Commonly present at birth. • Etiology - not known • Site – predominantly in clusters, under the chin, forehead, axilla and nape of the neck. • Lesions disappear spontaneously by Day 5 , No treatment required.
    • 21. NEONATAL ACNE • Child presents inflammatory with papules, multiple, pustules and discrete closed comedones (white heads). • Appear at 2-4 weeks of age as papules, evolve into pustules. Rarely present at birth. • Site – cheek, forehead, chest and back.
    • 22. NEONATAL ACNE • Exact cause is unknown, but has been attributed to placental transfer of maternal androgen. • Placental transfer of maternally ingested lithium and hydantoin may also cause acne in the neonates. • resolve spontaneously within 3 months. • Can be treated effectively with topical tretinoin and 2.5% benzoyl peroxide.
    • 23. CONGENITAL SYPHILS • Transplacental infection by Treponema pallidum • Characterized by reddish brown maculo-papular or papulo- squamous lesions • Site – Especially on palm and sole, face & around the mouth • Other features include anemia, fever, hepatosplenomegaly, lymphdenopathy, rhinitis, or “Snuffles” and osteochondritis etc. • TREATMENT -Penicillin is drug of choice.
    • 24. MILIA • Multiple, pearly- white papules, 1-2 mm in size particularly prominent on cheeks, nose, nasolabial fold and forehead. May be present in oral cavity – Epstein perls. • superficial epidermal inclusion cysts that contain laminated keratinized material. • Usually disappear spontaneously during first 3-4 weeks.
    • 25. CASE SCENARIO 1 A mother comes with a 4 day old baby to your OPD with c/o of generalised red rashes over body noticed since Day 1.
    • 26. ?HOW TO PROCEED FOR DIAGNOSIS • ?history -full term, stays comfortable, • ?any systemic symptoms- nil • ?systemic examination- normal • ?Type & size of lesion - numerous, 2-3cm,discrete,erythematous macules with a central vesicle or pustule. • ?Distribution- involving face, trunk and limbs , predominately over chest and proximal extremities with palmoplantar sparing. • ?CLINICAL DIAGNOSISErythema Toxicum Neonatorum Wright’s stained smears from a vesiclulo-pustule showed eosinophils predominately and investigation profile normal.
    • 27. WHY NOT OTHER DISORDERS (DIFFERENTIAL DIAGNOSIS) • MILIARIA RUBRA OR PUSTULAR MILIARIA: Lesions are usually small 23mm erythema predominating over flexures-neck, groin axilla. • TRANSIENT NEONATAL PUSTULAR MELANOSIS: lesions show predominance of neutrophils rather than eosinophils and resolve with residual pigmentation. • HERPES LESIONS: are usually painful, will coalesce and show multinucleated giant cells in Tzanck smears. • NEONATAL BACTERIAL/FUNGAL INFECTIONS: Negative culture for bacteria or fungus and KOH mounts from skin lesions reveals.
    • 28. CUTIS MARMORATA • Benign cutaneous vascular phenomena seen in neonates as an accentuated physiologic vasomotor response to the cold. • Reticulate, bluish mottling of skin on trunk and extremities. • Usually disappear as the infants is rewarmed. • It’s persistence is seen in syndrome, trisomy-18, hypothyrioidism. Downs
    • 29. INTERTRIGO • Superficial inflammatory dermatitis of apposed skin surface. • Heat, moisture, friction and sweat retention induce maceration and inflammation. • Secondarily infected by bacterial(s.aureus, group A streptococci) or fungal (candida) infection.
    • 30. INTERTRIGO • Initially skin is red and slightly macerated, when separated show erythema of contagious surface. • Itching, burning and offensive odour are common symptom. • TREATMENT – open wet compresses – Dusting powder – Antibiotics –cephalexin 40-50mg/kg/day or cloxacillin50100mg/kg/day for 10 days or fungicidal nystatin cream 4-5 times /day for 3-4 daysmay be used.
    • 31. DIAPER DERMATITIS (NAPPY RASH, NAPKIN DERMATITIS) • Acute inflammatory reaction of the skin associated with the wearing of napkins. • Irritant contact dermatitis – due to occlusive contact of urine and faeces with skin. • Rash is usually bounded by the margins of the nappy with sparing of the inguinal fold. • After prolonged contact, a papuloerosive eruption occurs with formation of multiple small ulcers, called Jacquet’s ulcers. • Secondary infection by candida is common.
    • 32. DIAPER DERMATITIS • MANAGEMENT -Remove the contactants, eliminate maceration, keep the diaper area dry. – Very frequent diaper change. – Contamination by Urine or Feces should be rinsed gently with warm water. – Zinc cream or petroleum jelly is useful . – Oil massage not allowed. – Topical antifungal if secondary infection present e.g. Clotrimazole or miconazole or nystatin.
    • 33. INFANTILE SEBORRHEIC DERMATITIS (Cradle Cap) • Characterized by erythematous, scaly or crusted eruption over the area rich in sebaceous gland. • Etiology - pityrosporum oval, hereditary (genetic) immuno- dysfunction, atmospheric humidity etc. • Site - Scalp, face, postauricular, presternal and intertriginous areas etc.
    • 34. INFANTILE SEBORRHEIC DERMATITIS (Cradle Cap) • Begins with a non-eczematous, erythematous, scaly dermatitis of the scalp (“Cradle cap”) and spread downward over the forehand, ears, eyebrows, nose and back of head. TREATMENT  selenium sulfide shampoo.  Topical weak corticosteroid -1% hydrocortisone
    • 35. Birthmarks • Birthmarks represent an excess of one or more of the normal components of skin per unit area: blood vessels, lymph vessel, pigment cells, sebaceous gland…… • Vascular birthmarks are most common. • Others :-.  Lymph vessel birthmarks  Pigment cell birth marks.  Hypopigmentation.  Epidermal birthmarks
    • 36. SALMON PATCH • Most common vascular lesion of infancy. • Appears as irregular dull, pinkish – red macular area often with fine linear telangiectasia. • Site – nape of neck (‘stork bite’) upper eyelid or the glabella. • Most of these lesions fade rapidly and disappear within a year.
    • 37. PORT WINE STAIN (NAEVUS FLAMMEUS) • Present at birth • Large, irregular, deep red or purple, flat area of skin, usually unilateral often on the face. • Represents a vascular malformation involving mature capillaries. • This birth mark persist throughout life • TREATMENT  Pulsed dye laser  Masking with cosmetic cryosurgery ,excision, grafting and tattooing.
    • 38. CUTIS MARMORATA TELANGIECTATICA CONGENITA • reticulated mottling of the skin. • present since birth. • does not disappear after warming • a few centimetres to a whole limb or hemitruncal involvement. • limbs are more commonly affected than other sites. • associated atrophy (more common) or hypertrophy of the underlying subcutaneous tissue
    • 39. CUTIS MARMORATA TELANGIECTATICA CONGENITA • TREATMENT• Most of the lesions improve in the first 2 years of life. Therapy should be deferred to await spontaneous improve. • For persistent reticulate erythema, pulsed dye laser may be used to further lighten the affected patches.
    • 40. STRAWBERRY MARK (CAPILLARY HAEMANGIOMA) • Appear in form of circumscribed oval or round, soft domed swelling of intense scarlet-red color. • Arise from immature angioblastic tissue. • Site – Head, neck region followed by trunk . • Usually not present at birth and develops during first few weeks of life. • Over 90 percent of these lesions disappear by age of 7 years. • Treatment:-First line Prednisolon 2mg/lg/day
    • 41. MONGOLIAN SPOTS • Mongolian blue spots black, are single flat, or slate gray multiple, to large macular lesion of various sizes. • Located over lumbosacral area, • Fade after first two years of life. • Occasionally persist into adulthood. • Represent collection of spindle-shape melanocyte located deep in the dermis
    • 42. CAFÉ-AU-LAIT SPOTS • Light, brown , oval macules. • Have distinct borders. • Rarely, present at birth, but increase in number with age. • Multiple café-au-lait spots occur in type one neurofibromatosis. • Large, solitary café-au-lait macule are usually isolated finding but may be seen in McCune-Albright and proteus syndrome.
    • 43. CONGENITAL MELANOCYTIC NEVI (CMN) • Dark brown or black solitary papule with smooth surface. • Lesions classified according to size small <1.5cm medium 1.5cm-20cm, large >20cm in greatest diametrer or covering >5% BSA. • Large CMN have risk for the development of melanoma. • naevi over the cranium or spine have association with Neurocutaneous melanosis which rarely may produce raised intracranial pressure, hydrocephalus or space-occupying spinal lesions.
    • 44. CONGENITAL MELANOCYTIC NEVI (CMN) An MRI scan should be considered in babies with naevi over the cranium or spine to exclude significant leptomeningeal melanocytosis.
    • 45. NEVUS OF OTA AND NEVUS OF ITO • Nevus of OTA (Nevus Fuscoceruleus Opthalmomaxillaris) represent usually unilateral, irregular, patchy discolouration of skin of face supplied by second division of the trigeminal nerve. • Site - Forehead, malar area, nose, sclera of ipsilateral eye etc. • Nevus of ITO (Nevus Fuscoceruleus acromiodeltoideus), have same feature
    • 46. APLASIA CUTIS CONGENITA • Oval,sharply marginated, depressed, hairless area covered by wrinkled epithelial membrane, or may appear as ulcer which heals with scar formation. • Primarily located in the midline of scalp. • Present since birth. • Represents a developmental failure of skin fusion. • Treatment:  small defect-Surgical excision with mobilization of scalp and closer.  Large defect-Hair transplantation
    • 47. COMMON SKIN DISEASES IN PAEDIATRICS - II BY DR.RAMKESH MEENA
    • 48. INFECTIONS IN INFANCY & CHILDHOOD
    • 49. HERPES SIMPLEX • On skin- in form of grouped vesicles on erythematous base. • On mucous membrane- blister base- erosion, is seen due to easy sheding of blister roof. • Site –60% of primary infection in oral cavity, Lips, nose, cheeks, fingers, eyes & scalp are common sites. • Caused by HSV 1
    • 50. HERPES SIMPLEX • Diagnosed by Tzanck smear preparation showing acantholytic cells and giants cells. • TREATMENT • Gingivostomatitis-Acyclovir ,15 mg/kg/dose 5 times a day PO for 7 days. • Herpes labialis-Valacyclovir -2,000 mg bid PO for 1 day, or acyclovir 200-400 mg 5 times daily PO for 5 days, or famciclovir 1,500 mg PO stat. • Eczema herpeticum oral acyclovir 200 mg 5 times a day PO for 5 days • Keratitis-eye drop 1% trifluridine, 3% Vidarabin
    • 51. NEONATAL HERPES SIMPLEX • Develop in~ 10% of infants of parents with active HSV2 infection. • grouped vesicles on erythematous base may appear upto 7th day after birth. • Disease may be mild with primary skin lesions. • Usually systemic illness with jaundice, progressive HSM, dyspnea, severe encephalitis. • Treatment:- Skin & mouth diseaseAcyclovir 20mg/kg-8hrly IV for 14 days • Encephalitis & systemic disease -21 days.
    • 52. CHICKEN POX • Caused by varicella-zoster virus (DNA - herpes virus group) • Fever, malaise, headache occur 24-48 hour before rash. • Eruption is characterized by the appearance of 'Tear drop ’ vesicles on an erythematous base. • A series of crops of papules, appear which become vesicular & later pustular and encrusted. • Typically lesions of different stage are present at same time. • Mucous membrane of the mouth & throat often involved
    • 53. CHICKEN POX • TREATMENT:- • Antiviral treatment modifies the course of both varicella and herpes zoster. • Acyclovir 20 mg/kg/dose, 4 doses/day for 5 days ,PO • Intravenous Acyclovir for severe disease and for varicella in immunocompromised patients -10mg/kg, 8 hourly for 5 days.
    • 54. MEASLES • Caused by RNA - paramyxovirus • Erythematous, maculopapular rash starts on 2-4 days after fever behind the ears & spreads over the face, trunk and limb. • Koplik's spots are diagnostic and are visible before onset of rash as ‘‘tiny white spots” like grains of sand on mucous membrane of the cheeks opposite the lower molars.
    • 55. MEASLES Diagnosis-almost always clinical & based on epidemiology. -Serologic confirmation by serum IgM antibody identification. -Viral RNA detection by PCR Treatment-only supportive -Maintenance of hydration, Antipyretics -Vitamin A supplementation. Prophylaxis -Measles or MMR vaccine . Postexposure prophylaxis – Measles vaccine within 72 hours of exposure Immunoglobulin within 6 days of exposure , in immunocompetent children 0.25ml/kg and in immunocompromised 0.5ml/kg
    • 56. ERYTHEMA INFECTIOSUM (FIFTH DISEASE) • Caused by human parvo B19virus • Erythematous, macular rash often begins on the face, giving the so called slapped cheek appearance. • Rash on extremities and trunk also present, with central fading of the eruption giving a reticular appearance. • Rash usually fades within a week but may reappear often several time, especially after bathing or exposure to sun up to 4 months. • Diagnosis-confirmed by s.IgM level within 30 days • Treatment –no specific treatment, nor prophylaxis.
    • 57. ROSEOLA INFANTUM(Exanthem subitum) • Caused by human herpes virus - 6 (HHV-6) • 2-3 days continuous fever followed by a pink morbilliform eruption appears transiently and fade within 24 hrs. • Predominantly occurs <2 years age. • Mild periorbital edema and lymphedenopathy are occasionally seen . • T/t- Tepid sponging and antipyretics for fever.
    • 58. RUBELLA (GERMAN MEASLES) • Characterized by innumerable, small discrete, rose – pink, macules first appear on face. • Becomes generalized and discrete on the first day, fade on face and coalesce over the trunk on second day, and usually disappear on third day . • Caused by RNA-togavirus • Little or no prodromal symptoms • A notable feature of rubella is the involvement of suboccipital, post auricular & cervical lymph nodes. • The pink lesion of rubella differs from the more vivid-red lesion of measles. • T/T- No specific treatment available, NSAIDS for
    • 59. HAND, FOOT & MOUTH DISEASE • Caused by Coxsackie A-16 virus (Occasionally A5A10) • Abrupt onset scattered papules that progress to oval or linear vesicle. • Distribution-Palms, fingertips, interdigital webs soles & buccal mucosa. • Pt is afebrile and not ill. • Clears spontaneously in about 7 days. • T/t- no treatment is required,
    • 60. STAPHYLOCOCCAL SCALDED SKIN SYNDROME (SSSS)(Ritter’s disease) • Caused by epidermolytic toxin A (exotoxin) produced by staphylococcus aureus. • start as a macular scarlatiniform eruption associated with conjunctivitis, or an upper respiratory infection. • First appear on face, axillae and groins then spread all over body.
    • 61. STAPHYLOCOCCAL SCALDED SKIN SYNDROME (SSSS) • Surface become wrinkled and then cracks leaving red raw erosions. • Baby may appear toxic and have bullae. • Nikolsky’s signs (i.e. separation of areas of epidermis in response to sheering pressure on the skin) is positive. • TREATMENT Parental antibiotics e.g. dicloxacillin 15-50 mg/kg/day. Clidamycin to inhibit bacterial protein(toxin) synthesis inhibition. Application of an emollient, clean with isotonic saline. Fluid and electrolyte balance.
    • 62. IMPETIGO • Superficial, contagious bacterial infection with brownish – yellow crust. • Cause by staphylococcus aureus, -hemolytic streptococcus or mixed infection. • Age – children between 4 to 7 years most commonly affected. • Most common site – face around nose, mouth and hand. • Superficial blister rupture easily, releasing a yellow exudates that dries and form a honey – colored crust.
    • 63. IMPETIGO • TREATMENT  Normal saline or potassium permanganate soaks will help to remove the crust.  Topical antibiotics – mupirocin or fusidic acid.  Systemic antibiotics–cephalexin 4050mg/kg/day for 10 days or  cloxacillin 50-100mg/kg/day for 10 days.
    • 64. FRUNCLES (BOILS) • Fruncles or boils are painful circumscribed perifollicular staphyloccocal abscess • Have tendency of central necrosis & suppuration with deeper extension in to dermis and subcutaneous tissue. • Site : face, back of neck, scalp, axilla, thigh etc. • Appear as red tender nodules which gradually become boggy and fluctuant and discharge pus. • Treatment-Dicloxacillin 20-50 mg/kg/day cephalexin 40-50 mg/kg/day oral for 10 days. • In MRSA-Rfampicin+ cotrimoxazole for 10 days or
    • 65. CARBUNCLE • Large deep seated staphylococal abscess composed of aggregates of interconnected furuncles that drain at multiple points on the skin. • Painful, tender, firm to hard, indurated lump with intense inflammatory changes in surrounding and underlying tissue. • Site : back of neck, shoulder, hip & thigh. • Treatment-Dicloxacillin 20-50 mg/kg/day cephalexin 40-50 mg/kg/day oral for 10 days. • In MRSA-Rfampicin+ cotrimoxazole for 10 days. or
    • 66. ERYSIPELAS • Superficial infection of skin involving upper subcutaneous tissue and lymphatic vessels. • Cause by group A β-hemolytic streptococcus. • Sharply marginated, red, tender edematous area associated with malaise and fever with impairment of lymphatic drainage. • Site – face and limb in children, Abdominal wall in infants. • TREATMENT  oral penicillin V 250mg/dose TID for 10 days.  or erythromycin.
    • 67. MENINGOCOCCAEMIA • Acute meningococcal meningitis may present with fever, malaise and purpuric eruptions. • Site – most commonly trunk and lower limbs. • More extensive haemorrhagic lesion with large ecchymotic areas are seen in fulminant meningococcaemia . • Lesions result from both intravascular coagulation and bacterial damage to blood vessels. • Treatment:Penicillin G 250000 U/kg/day IV for 7 day • Cefotaxime 200-300 mg/kg/day IV for 10 days.
    • 68. TINEA CAPITIS • Usual lesion is a patch of partial alopecia, • Circular in shape, with stumps of broken hair of different lengths . • Multiple affected sites produce a moth -eaten appearance of the hair. • Scaling and inflammation of scalp are variable. • Caused by Trichophyton tonsurans, M. canis • Infection of hair shaft with the animal ring worm' Trichophyton verrucosum (usually from infected cattle) cause a marked inflammatory reaction, called a kerion .
    • 69. TINEA CAPITIS DIAGNOSIS Skin scraping and KOH examination. Culture - For identifying the species of dermatophytes TREATMENT Systemic -Oral Griseofulvin 20 mg/kg/day for minimum 4 weeks is treatment of choice. Terbinafine 3mg/kg/day PO for for 2-4 weeks is alternative.
    • 70. TINEA CORPORIS • Characteristically appears as annular lesions with central clearing and an itchy, palpable erythematous advancing edge. • Active edge shows vesicles and pustules . • It is usually caught from pets. • Diagnosis – Skin scraping and KOH examination. Culture - For dermatophytes identifying the species of
    • 71. ORAL CANDIDIASIS (THRUSH) • Characterized by curdy or whitish gray, friable, cheesy pseudomembranous patches or plaques on markedly reddened mucosa. • Caused by yeast like fungi of genus candida - most common by candida albicans • Painful inflammation of tongue, soft and hard palate, buccal & gingival mucosa can extend to esophagus / pharynx. • Factor predisposing to candidiasis include diabetes mellitus, hypoparathyridism, addison disease, leukemia, prolonged antibiotic and corticosteroid therapy etc.
    • 72. ORAL CANDIDIASIS (THRUSH) • TREATMENT Clotrimazole 1% or hamycin 1% used as mouth paint 4 times ady for 3-5 days. Nystatin, amphotericin B or miconazole gel applied several time a day. Proper oral hygiene is maintained.
    • 73. INFESTATIONS
    • 74. SCABIES • Site – Wrists, border of the hand, sides of the fingers and finger web space. • In infants – palm, soles, and genitalia are also involved. • In children – head and neck may be involved. • Itching is worst at night when patient is warm. • TREATMENT 5% Permethrin to all household members Antihistamines to control itching Disinfection of recently used clothing, linens, stuffed animals
    • 75. PEDICULOSIS CAPITIS • Mainly confined to the sub-occipital region, with extension on to the posterior auricular and temporal region. • Over crowding, poor hygiene and low socio - economic status are associated factors. • Itching of the scalp is prominent symptom . • Oozing, crusting and eczematization of scalp with regional lymphadenopathy are also present. • TREATMENT  0.5% malathione left on the scalp for 12hr. Then washed off.  1% permethrin  1% Gamma benene hexachloride is also used  Maintain proper hygiene.
    • 76. CASE SCENARIO 2 One of the following 2-year-old boys has bullous impetigo, one has herpes zoster. Which patient has which condition?
    • 77. CASE SCENARIO 7 Patient A has • vesicles • follow the path of the S1 dermatome down the back of his leg hence HERPES ZOSTER
    • 78. CASE SCENARIO 7 Patient B has • many erosions, • few intact bullae, • over both buttocks; • not following the course of a dermatome hence BULLOUS IMPETIGO
    • 79. CASE SCENARIO 3 A 9 month old infant presents with numerous excoriated, erythematous papules and pustules on the wrists, abdomen, periaxillary skin, ankles, and feet. Some of the lesions appear to be infected secondarily. The patient appears uncomfortable. Mother reports that her other children only have a few pruritic lesions. Mother denies any lesions but habitually rubs the interdigital webs of her hand.
    • 80. ?HOW TO PROCEED FOR DIAGNOSIS • ?history –family history (+) • ?any systemic symptoms- nil • ?systemic examination- normal • ?Type & size of lesion - Pruritic papules, pustules, vesicles, and burrows • ?Distribution- Sides & webs of the fingers, lateral & posterior aspects of feet,axillary folds,genitalia • ?CLINICAL DIAGNOSIS- SCABIES Scraping of skin from an unscratched burrow-microscopy revealed female mite &/ her eggs.
    • 81. WHY NOT OTHER DISORDERS (DIFFERENTIAL DIAGNOSIS) • ATOPIC DEMATITIS:family h/o allergy,distribution mainly over face,trunk & extensors of extremities,presence of dry skin,severe itching,tendency to recur favours. • DERMATITIS HERPETIFORMIS: severe pruritic vesicles,usual onset in adolescence,grouped skin lesions involving elbow knee upper trunk & buttocks.associated with gluten sensitivity.Immunofluorescent of non involved adjacent to a blister biopsy being diagnostic.
    • 82. GENODERMATOSIS
    • 83. ICHTHYOSIS • Ichthyosis-excessive scaling of skin. • Four major hereditary types 1. Vulgaris 2. X-linked icthyosis. 3. Lamellar 4. Bullous
    • 84. ICHTHYOSIS • Ichthyosis Vulgaris: Fine scales, become prominent by 6 month to 1 year of age. Scales most prominent over lower legs trunk & buttocks. Inherited as semi dominant.
    • 85. ICHTHYOSIS • X-Linked ichthyosis- Usually present during infancy. Scales are thicker and brown color, present over back of neck, upper trunk & extensor surfaces of limbs. Sparing palms and soles.  Inherited as X-Linked recessive.
    • 86. ICHTHYOSIS • Lamellar Ictyosis: COLLODION BABY  Large, dark, platelike scales with erythematous skin.  Baby born with collodion membrane.  Ectropion and eclabium present at birth or appear after birth.  Inherited as AR trait.  Gene defect in Transglutaminase-1 gene.
    • 87. ICHTHYOSIS • Bullous icthyosis (epidermolytic hyperkeratosis)Inherited AD. Characterised by extensive scaling at birth, erythroderma, recurrent episodes of bullae formation. With child ages the lesions decrease in extension, by school agethick, warty, dirty-yellow scales on palms, soles, knee and elbow. Secondary S.aureus infection common.
    • 88. ICHTHYOSIS • TREATMENT: No satisfactory T/t available Hydration of skin and application of lubricants. Use A/b to treat sec. bacterial infections.
    • 89. BULLOUS DISORDERS
    • 90. EPIDERMOLYSIS BULLOSA • A group of inherited bullous disorders of the epithelial basement membrane zone characterized by blister formation in response to mechanical trauma. • Classification based on level of cleavage of the skin into three broad categories as follows
    • 91. EPIDERMOLYSIS BULLOSA • Epidermolysis bullosa simplex :– Blister develop intraepidermally, above the basement membrane. Usually confined to the hand & feet. • Junctional Epidermolysis bullosa :– Blister develop within the basement membrane, usually fatal involvement of the larynx and gastro intestinal tract occurs commonly • Dystrophic epidermolysis bullosa : – Blister develop below basement membrane ,tendency of blister to heal with scarring
    • 92. CHRONIC BULLOUS DERMATOSIS OF CHILDHOOD (CBDC) • Lesions comprise urticated papules and plaques, annular, polycyclic lesions often with blistering around the edge, the ‘string of pearl sign’ • Mucous membrane involvement is common in form of ulcers & erosions • Characterized by IgA basement membrane antibodies • Site – Face, perioral area, eyelids, ears, scalp, perineum, leg & feetSymptoms – mild pruritus to severe burning
    • 93. CHRONIC BULLOUS DERMATOSIS OF CHILDHOOD (CBDC) • TREATMENT Spontaneous remission after 3-6 yrs. Dapsone or sulphapyridine are also used
    • 94. XERODERMA PIGMENTOSUM (XP) • Autosomal recessive disease • Abnormal sensitivity to sun light, freckling & development of skin neoplasia • Fibroblast culture studies of patients with xeroderma pigmentosum show a defective excision repair of ultra violet damaged DNA, due to lack of a specific UV-endonuclease • Prenatal diagnosis by amniocentesis • MANAGEMENT • Protection from ultra violet rays • Sun screening (lotions or cream also useful)
    • 95. ERYTHROPOIETIC PROTOPORPHYRIA (EPP) • Autosomal dominant condition • Small pitted scars develop on the nose & cheeks • First evidence may be unexplained crying when the infants is outside in the sunlight • Complaints of a burning or stinging sensation on exposed skin • Hepatobiliary system may also be involved • Diagnosed by the presence of an excess of protoporphyrin in red cell & faeces. Urine is usually normal.
    • 96. NEUROCUTANEOUS DISORDERS
    • 97. NEUROFIBROMATOSIS • Autosomal dominant disease, • Characterized by cutaneous pigmentation and tumor of the nervous system which manifest by change in the skin, bones, endocrime system & muscle . • Six or more café-au-lait macules > 0.5 cm in diameter in prepubertal individuals and >1.5 cm in diameter in post purbertal individuals.
    • 98. NEUROFIBROMATOSIS • Axillary or inguinal freckling – consists of multiple hyperpigmented areas 2-3 mm in diameter • They are present at birth or may develop later • They are oval, pale brown patches scattered all over body surface with prediction for the trunk and extremities with sparing of face
    • 99. TUBEROUS SCLEROSIS • Classically defined by a triad of seizures, mental retardation and adenoma sabeceum • Autosomal dominant disorder • Periungual and gingival fibromas • Shagreen patch • Ash leaf spots
    • 100. METABOLIC AND NUTRITIONAL DISORDERS
    • 101. KWASHIORKOR • characterized by striking cutaneous and hair changes in association with developmental, mental and gastrointestinal features. • Cutaneous erythema develops first • progresses to fine desquamation along natural skin lines , on the shin, outer thighs & back • Circumoral pallor, cutaneous depigmentation, and purple patches are also present
    • 102. PHRYNODERMA • Manifestation of deficiency of vitamin A and essential fatty acids • Characterized by discrete, firm, horny, follicular, keratotic papules of various size. • Site – extensor aspect of extremities especially over the elbows, knees and thighs. • Bitot’s spots, xerophthalmia and keratomalacia may be associated.
    • 103. PHRYNODERMA • TREATMENT Topical application of linolenic acid, which is present in sunflower oils. Oral vit A (50,000 IU daily) till serum level of vit A normalized (Normal value > 20 g / dl) Appropriate nutrition containing essential fatty acids
    • 104. ACRODERMATITIS ENTEROPATHICA • Characterized by acral & periorificial vesiculobullous, pustular and eczematoid skin lesions • Blisters quickly collapse, begin to dry and crust • Secondary infection by candida is common • Triad of dermatitis, diarrhoea and alopecia • Related to zinc deficiency
    • 105. ACRODERMATITIS ENTEROPATHICA • Diagnosis by decrease in zinc level in plasma, red blood cell, hair & urine (Serum zinc level 70-110 mg / 100 ml – Normal, <50 mg /100 ml – diagnostic) • TREATMENT Zinc gluconate or sulfate (Dose is 5mg/kg/day with fruit juice)
    • 106. MISCELLANEOUS CONDITIONS
    • 107. PAPULAR URTICARIA • Chronic, recurrent, eruption of irritable urticarial papules, occurring in patients with an acquired sensitivity to insect bits. • The primary lesions are wheals or papules, wheals surmounted by papules often with a central hemorrhagic punctum • Age – children between 2-7 yrs.
    • 108. PAPULAR URTICARIA • Site - exposed parts of body • The lesions are grouped into clusters, markedly pruritic and top of lesions scratched off & crusted • TREATMENT – Antihistaminics, cool compresses and soothing lotions eg calamine lotion to which 0.25% menthol and 0.5% phenol also added – Short course of systemic steroids also helpful. – Dapsone 1-2 mg/kg/day for 6-12 weeks is helpful
    • 109. PERIORAL ECZEMA • Also known as lick eczema • Perioral eczema is attributed to habit of liplicking, lip-biting, thumb-sucking and dribbling. • It is common in association with atopic eczema.
    • 110. ATOPIC DERMATITIS • Atopic dermatitis is an eczema characterized by intense itching and a relapsing course in infants and children. • 70% children have positive family history of atopy. • Site – anticubital and popliteal fossa most commonly involved.
    • 111. ATOPIC DERMATITIS • Rubbing & scratching aggravate the eczema • As the child grows, affected skin becomes thickened with accentuation of normal skin creases known as lichenification. • Usually have dry flaky skin and this dryness tends to exacerbate the itching. • TREATMENT – Emollients – bath oil, soap substitute (emulsified ointment or aqueous cream), moisturizer – Topical steroids – 1% hydrocortisone – Antihistaminics
    • 112. PITYRIASIS ALBA • Seen as dry, slightly scaly, often hypopigmented area, predominantly on the face and upper trunk. • Peak age of onset is between 3 to 16 years. • Individual lesion is rounded, oval or irregular plaque which is red, pink and skin coloured and has fine lamellar or branny scaling. • Initially erythamatous scaly patch which subside to leave area of hypopigmentation. • MANAGEMENT Moisturizing cream and reassurance
    • 113. PITYRIASIS ROSEA • Characterized by single, oval or annular erythematus lesion called the ‘herald patch’ with a peripheral collarette of scale • Site – mainly on the trunk and spreading to upper arms & thighs • Typically, the distribution of these lesions is along the line of the ribs, giving a ‘Christmas tree’ appearance. • Rash clears spontaneously in about six weeks. • If irritation is present – 1% topical hydrocortisone cream is used.
    • 114. STEVENS-JOHNSON SYNDROME AND TOXIC EPIDERMAL NECROLYSIS • Large areas of epithelial necrosis. • SJS – Mucosal involvement is primary, severe, extensive and at least 2 mucosal surfaces involved. • Oral mucosa involved in all cases. • Epidermal necrosis progress rapidly over hours. • TEN-Similar cutaneous lesion like SJS but may occur in the absence of mucosal lesions.
    • 115. STEVENS-JOHNSON SYNDROME AND TOXIC EPIDERMAL NECROLYSIS Etiology- Most cases follws drug ingestion includingNSAIDS, Sulfonamides and anticonvulsants. Few cases following M. Pneumoniae infection. Diagnosis: History of drug ingestion Skin biopsy -full thickness epidermal necrosis and subepidermal blisters. Treatment: -Discontinue offending drug -maintenance of fluid and electrolyte balance. -Prevention of secondary bacterial infections -Prevent conjunctival scarring
    • 116. KAWASAKI DISEASE • FEVER for 5 or more days • High (>=101’ F), unremitting, unresponsive to antibiotics. • Presence of 4 or more of the following 1. Bilateral bulbar conjunctival injection without exudates. 2. Changes in the oropharyngeal mucus membranes-Erythema, lip cracking, strawberry tongue, diffuse injection of oral and pharyngeal mucosa
    • 117. KAWASAKI DISEASE 3. Changes in the extremities- • Acute: Erythema of palms, soles; edema of hands, feet. • Subacute: Periungual peeling of fingers, toes in weeks 2 and 3 4. Rash-Polymorphic 5. Cervical lymphadenopathy- >1.5 cm diameter ,usually unilateral • Illness can’t be explained by other diseases
    • 118. KAWASAKI DISEASE
    • 119. KAWASAKI DISEASE • DIAGNOSIS Clinical diagnosis No single test Diagnosis of exclusion Atypical Kawasaki disease -Do not fulfill all criteria -More common in <1 year and >8 years age
    • 120. KAWASAKI DISEASE • LABORATORY INVESTIGATIONS -Leukocytosis with neutrophilia and immature forms -Elevated erythrocyte sedimentation rate (ESR) -Elevated C-reactive protein (CRP) -Anemia -Thrombocytosis after week 1 -Sterile pyuria -Elevated serum transaminases
    • 121. KAWASAKI DISEASE • TREATMENT • ACUTE STAGE Admit to monitor cardiac function Complete cardiac evaluation Chest X-Ray, ECG, 2D ECHO. IV Ig 2gm/kg as single dose Aspirin 80-100 mg/kg/day until the patient has been afebrile for 48 hours. CONVALESCENT STAGE-Aspirin 3-5 mg/kg once daily orally until 6-8 wk after illness onset
    • 122. CASE SCENARIO 4 A mother brings her 4 year-old son to clinic due to a two day h/o high fever and refusal to eat or drink. Mother has also noted the development of “sores in and around his mouth” and copious drooling.
    • 123. ?HOW TO PROCEED FOR DIAGNOSIS • ?history –insignificant • ?any systemic symptoms- preceded by fever & malaise • ?systemic examination- normal • ?Type & size of lesion – erosions & ulcers are extensive • ?Distribution-characteristic grouped vesicles • ?CLINICAL DIAGNOSISHSV Gingivostomatitis Viral cultures and direct fluorescent antibody tests are positive
    • 124. WHY NOT OTHER DISORDERS (DIFFERENTIAL DIAGNOSIS) • APHTHOUS ULCER: usually 2-4 lesions,not extensive, • VARICELLA ZOSTER: unilateral involvement with pain along course of a nerve followed by grouped vesicular lesion,direct fluorescent antibody positive. • HAND FOOT MOUTH DISEASE: children not ill and characteristically afebrile,mainly acral distribution of lesion, oval to linear nature of individual vesicles or erosion. • Pemphigus vulgarish-lesions persists for months,
    • 125. • Identify the lesion – This is an iris or target lesion of erythema multiforme. -Acute onset erythematous, fixed, round/oval lesions Symmetrical distribution, progressive color changeCentral zone become dusky, blistered-target lesion no prodrome, no systemic symptom or sign Adolescents most commonly affected. T/T:-symptomatic- wet compresses, Antihistaminics for pruritus.
    • 126. CASE SCENARIO 5 A mother brings her infant in for evaluation of a diaper rash. Mother states that the patient suffered from diarrhea last week and then developed the rash. She has been treating him with over the counter Zinc oxide Paste with no improvement in the rash.
    • 127. DIAGNOSIS CANDIDA DERMATITIS
    • 128. CASE SCENARIO 5 A 3 year-old boy presents with recent history of URI symptoms followed by the rapid appearance of an “itchy” rash. The lesions appeared in groups, initially on the trunk and then spread peripherally.
    • 129. DIAGNOSIS CHICKEN POX
    • 130. REFERENCES • Colour Text Book Of Paediatric Dermatology- 4th edition by William L.Weston • Essential Paediatrics by O P Ghai • Nelson Textbook of Pediatrics-19th edition • Rooks Text Book Of Dermatology-8th edition • Basic Pediatric Dermatology, University of Wisconsin
    • 131. Based on the morphologic features of this photo, what is the most likely diagnosis? • A) Candida • B)Cellulitis • C)Herpes Simplex • D)Impetigo • E)Peri-oral dermatitis
    • 132. THANKS

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