pediatric skin disease

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

5. FUNCTIONS OF THE SKIN
1. PROTECTION
2. THERMOREGULATION
3. IMMUNOLOGIC RESPONSE
4. BARRIER TO WATER LOSS
5. SECRETION OF WASTES
6. SENSATION.

6. 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.

7. 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.

8. 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.

9. 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

10. 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

11. 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

12. 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

13. 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)

14. 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}

15. 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)

17. 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

18. NEONATAL DERMATOSIS

19. 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.

20. 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

21. 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.

22. 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.

23. 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.

24. 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.

25. 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.

26. 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.

27. 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.

28. ?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.

29. 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.

30. 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

31. 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.

32. 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.

33. 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.

34. 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.

35. 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.

36. 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

37. 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

38. 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.

39. 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.

40. 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

41. 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.

42. 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

43. 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

44. 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.

45. 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.

46. CONGENITAL MELANOCYTIC NEVI (CMN)
An MRI scan should be considered in babies with
naevi over the cranium or spine to exclude
significant leptomeningeal melanocytosis.

47. 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

48. 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

49. COMMON SKIN
DISEASES IN
PAEDIATRICS - II
BY DR.RAMKESH MEENA

50. INFECTIONS IN INFANCY &
CHILDHOOD

51. 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

52. 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

53. 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.

54. 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

55. 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.

56. 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.

57. 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

58. 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.

59. 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.

60. 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

61. 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,

62. 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.

63. 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.

64. 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.

65. 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.

66. 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

67. 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

68. 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.

69. 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.

70. 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 .

71. 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.

72. 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

73. 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.

74. 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.

75. INFESTATIONS

76. 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

77. 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.

78. CASE SCENARIO
2
One of the following 2-year-old boys has bullous
impetigo, one has herpes zoster. Which patient has
which condition?

80. CASE SCENARIO
7
Patient A has
• vesicles
• follow the path of the S1
dermatome down the back of his
leg
hence HERPES ZOSTER

81. CASE SCENARIO
7
Patient B has
•
many erosions,
•
few intact bullae,
• over both buttocks;
•
not following the course of a
dermatome
hence BULLOUS IMPETIGO

82. 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.

84. ?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.

85. 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.

86. GENODERMATOSIS

87. ICHTHYOSIS
• Ichthyosis-excessive scaling of skin.
• Four major hereditary types
1. Vulgaris
2. X-linked icthyosis.
3. Lamellar
4. Bullous

88. 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.

89. 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.

90. 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.

91. 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.

92. ICHTHYOSIS
• TREATMENT:
No satisfactory T/t available
Hydration of skin and application of lubricants.
Use A/b to treat sec. bacterial infections.

93. BULLOUS DISORDERS

94. 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

95. 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

96. 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

97. CHRONIC BULLOUS DERMATOSIS OF CHILDHOOD
(CBDC)
• TREATMENT
Spontaneous remission after 3-6 yrs.
Dapsone or sulphapyridine are also used

98. 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)

99. 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.

100. NEUROCUTANEOUS
DISORDERS

101. 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.

102. 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

103. 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

104. METABOLIC AND NUTRITIONAL
DISORDERS

105. 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

106. 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.

107. 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

108. 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

109. 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)

110. MISCELLANEOUS CONDITIONS

111. 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.

112. 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

113. 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.

114. 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.

115. 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

116. 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

117. 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.

118. 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.

119. 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

120. 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

121. 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

122. KAWASAKI DISEASE

123. 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

124. 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

125. 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

126. 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.

128. ?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

129. 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,

130. • 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.

131. 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.

133. DIAGNOSIS
CANDIDA DERMATITIS

134. 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.

136. DIAGNOSIS
CHICKEN POX

137. 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

138. 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

139. THANKS