This document discusses common skin conditions seen in neonates. It describes the differences in neonatal skin compared to adult skin, including thinner epidermis and increased susceptibility to irritants and infection. Some conditions covered include vernix caseosa, cutis marmorata, milia, seborrheic dermatitis, neonatal erythema, and various birthmarks. Causes, presentations, treatments and distinguishing features are provided for each condition. The document serves as an overview of normal variations and abnormalities commonly encountered in neonatal dermatology.

1. COMMON SKIN CONDITIONS IN
NEONATES
Presenter – Dr Kezhaleto
Moderator – Dr Sushil Kakkar

2. • Neonatal period: first 4 weeks of extrauterine life
NEONATAL SKIN IN COMPARISON WITH ADULT
• Thinner epidermis
• Higher epidermal proliferation and desquamation rate
• Higher transepidermal water loss
• Thinner, less hairy, weaker intercellular attachment
• Fewer eccrine and sebaceous gland secretions
• Increased susceptibility to external irritants
• Increased susceptibility to microbial infection

3. CLASSIFICATION:
• Transient
• Birthmarks
• Infections
• Infestations
• Genodermatosis
• Neurocutaneous

4. VERNIX CASEOSA
• White, creamy, naturally occurring biofilm
covering the skin of the fetus during the last
trimester of pregnancy
• Composed of degenerated fetal epidermis
(Periderm) and sebaceous secretions
• Very low birth weight infants, i.e., <28 weeks'
gestation and < 1000g lack the protective
mantle of vernix caseosa
• At birth, vernix may cover the entire skin
surface or only confined to body folds.

5. Function:
• It performs an epidermal barrier function in utero to facilitate epidermal
growth underneath it
• Acts as an antimicrobial cover, protect against the bacteriologically rich
environment of the mother's genital tract
• Thermal regulation
• Antioxidant properties by virtue of the presence of antioxidants vitamin-E and
melanin in it
• Its color may reflect intra-uterine problems such as hemolytic disease of
newborn, post maturity, where it is of golden yellow color. Fetal distress in
utero may stain vernix by bile pigments present in meconium.

6. CUTIS MARMORATA
• Benign cutaneous vascular phenomena seen in
neonates as an accentuated physiologic vasomotor
response to cold.
• Reticulate, bluish mottling of skin on trunk and
extremities.
• Usually disappear as the infants is rewarmed.
• It’s persistence is seen in Downs syndrome, trisomy-18,
hypothyrioidism.

7. CUTIS MARMORATA
TELANGIECTATICA CONGENITA
• Congenital, vascular malformation, Present since
birth
• Characterised by fixed patches of mottled skin with
a marbled or reticulate blue to pale purple patches
• Does not disappear after warming (Unlike cutis
marmorata)
• Skin may appear indented due to dermal atrophy
• Localized or generalized. When localized, lesion
tends to remain unilateral, do not cross the midline,
and it may be sharply demarcated
• Limbs are more commonly affected

8. • Several congenital abnormalities associated –
Craniofacial, Neurological, Vascular, Skeletal,
Hypothyroidism
• Clinical Diagnosis
• TREATMENT-
• Most of the lesions improve in the first 2 years of
life. Therapy should be deferred to await
spontaneous improvement
• Monitor for development of associated
abnormalities

9. SUCKING BLISTER
• A blister or denuded area seen in neonates, usually seen
on the forearm, wrist and fingers
• Due to vigorous sucking in utero
• 0.5% of newborn
• One or two solitary clear bullous lesion with no
surrounding erythema. Can also present as an erosion or
a crusted lesion
Treatment:
• None, heal rapidly without sequelae
• Topical antibiotic/Dressing as needed if eroded

10. ACROCYANOSIS (PERIPHERAL CYANOSIS)
• Functional peripheral vascular disorder characterized by
bluish discoloration of skin
• Caused by vasospasm of the small vessels of the skin in
response to cold
• Usually particularly marked on the palms, soles and
around the mouth
• Absence of cyanosis of warm central parts
• Resolves with warming of the skin
• Recurrence unusual after 1 month of age

11. TOXIC ERYTHEMA OF NEWBORN
(ERYTHEMA TOXICUM NEONATORUM)
• Benign, self-limiting disorder of unknown etiology
• Most commonly, the eruption initially takes the form
of a blotchy, macular erythema
• Most commonly on the trunk, face and proximal parts
of the limbs (palms and soles not involved)
• In more severe cases, urticarial papules arise within
the erythematous areas, may be surmounted by small
pustules

12. • Onset rarely at birth, but in the first few days after birth
• Usually fade over 3-7 days, but recurrences may occur
for upto 6 weeks
• Systemic symptoms are absent
Investigations:
• Mostly a clinical diagnosis
• Smear of pustule contents will reveal numerous
eosinophils
• Negative bacterial and viral cultures

13. • Histologically
– the macular erythema shows oedema in the upper dermis, perivascular
inflammatory infiltrate comprising principally of eosinophils
– Papular lesions shows eosinophilic infiltration of the outer root sheath of one or
more hair follicles, above the point of entry of the sebaceous duct.
– Pustular lesions show intrafollicular accumulation of eosinophils immediately
below the stratum Corneum
• An associated blood eosinophilia of up to 20% of the white cell count
Treatment:
• No specific treatment
• Supportive

14. TRANSIENT NEONATAL PUSTULAR MELANOSIS
• Idiopathic pustular eruption that heals with brown
pigmented macules
• Usually present at birth, more common in black neonates
• Characterized by 1–3 mm, flaccid, superficial, fragile
pustules with no surrounding erythema
• Site – Any site, but predominantly in the chin, forehead,
axilla and nape of the neck.
• Eventually the pustules rupture and form brown crust
and finally a small collarette of scales

15. • Pustular lesions usually resolve within 24-48 hours
• Hyperpigmented macules may persist for about 3 months,
sometimes already present at birth
Investigation:
• Smear from pustules content reveals predominance of
neutrophils with occasional eosinophils
• Bacterial culture negative
• Biopsy shows intra or subcorneal collections of neutrophils
with a few eosinophils. Pigmented macules demonstrate
basal and supra-basal increase in pigmentation, without any
pigmentary incontinence
Treatment: No treatment, self resolving

16. ACROPUSTULOSIS OF INFANCY
• Condition of unknown etiology, characterized by
recurrent crops of pruritic, vesiculopustular lesions with
a predilection for the palms and soles
• Onset is usually in the first 3 months of life but lesions
may sometimes be present at birth
• Can also occur on the dorsa of the feet, hands, fingers,
ankles, and forearms
• Lesions appear to start as tiny, red papules, which evolve
into vesicles and then pustules over about 24 hr
• Each crop lasts for 7–14 days, and tend to occur at
intervals of 2–4 weeks

17. • Healing is succeeded by macular postinflammatory hyperpigmentation.
Investigations:
• Smears from the pustule content show predominance of eosinophils and later
neutrophils.
• Cultures are sterile
• Histopathology would reveal well-circumscribed subcorneal or intraepidermal
aggregations of neutrophils with a sparse lymphohistiocytic infiltrates in the
papillary dermis
Treatment:
• Potent topical corticosteroids

18. MILIA
• Benign, keratinous cysts, which affect about 40-50%
of newborn babies
• Small, firm, pearly- white papules, 1-2 mm in size
predominantly occurring on the face of newborn
babies
• Site - cheeks, nose, nasolabial fold and forehead
• Treatment - Usually disappear spontaneously during
first 3-4 weeks.
• D/D molluscum contageosum – does not usually
appear in immediate neonatal period, Sebaceous
gland hyperplasia-yellow rather than whitish

19. EPSTEIN PEARLS
• Yellowish white, keratinous cysts, 1–2 mm diameter,
• Seen in up to 85% of all neonates
• Site - Along the alveolar ridges and/or in the midline
at the junction of the hard and soft palate
• Treatment - Generally disappear without treatment
within a few weeks

20. SEBACEOUS GLAND HYPERPLASIA
• Common benign proliferation of the sebaceous glands
seen during the first weeks of life
• Result from maternal androgenic stimulation of
sebaceous gland
• Multiple, uniform, pinpoint, yellowish papules 1–3 mm in
diameter most prominent on the nose, cheeks, upper lip
and forehead
• Treatment - Resolves within few weeks

21. MILIARIA
• Miliaria is a disorder due to blockage of eccrine sweat
ducts
• Subdivided into three subtypes depending on the level of
blockage: miliaria crystallina (stratum corneum), miliaria
rubra (mid‐epidermal) and miliaria profunda (dermal–
epidermal junction)
• 3–8% of neonates
• Predisposing factors - Immature sweat ducts, Occlusive
clothing, high heat and humidity

22. Miliaria crystallina:
• Presents as crops of clear, thin‐walled, superficial vesicles
1–2 mm in diameter, without associated erythema.
• Generally rupture within 24 h, and are followed by bran-
like desquamation
• Presence of intracorneal or subcorneal vesicles in
communication with the sweat ducts
• Most frequently during the first 2 weeks of life, and are
particularly likely to be seen on the forehead, scalp, neck
and upper trunk

23. Miliaria rubra (prickly heat):
• Erythematous papules and papulovesicles about 1–4
mm in diameter, on a background of macular erythema
• Usually begin after second week of life and
predominate in the trunk and intertriginous areas
where occlusion by clothing is accentuated
• Lesions can be itchy or sore, child may be restless and
distressed
• Miliaria profunda is very uncommon in neonates as it
usually occurs in adults where there have been
repeated episodes of miliaria rubra.

24. Investigations:
• Clinical diagnosis
• Smear of a vesicle/pustule will show an absence of eosinophils
Treatment:
• Light clothing, cool bath and avoidance of heavy blankets
• Miliaria crystallina improves spontaneously as the sweat ducts mature
• Milaria rubra improves if the predisposing aetiological factors (high heat/humidity
and occlusion) are removed
• Antibiotics may be needed if staphylococcal infection occurs, but this is rare.

25. BIRTHMARKS (CONGENITAL NAEVI)
• Birthmarks are congenital, benign irregularity on the skin which is present at
birth or appears shortly after birth
• Represent an excess of one or more of the normal components of skin per
unit area: blood vessels, lymph vessel, pigment cells
• Vascular birthmarks are most common.

26. SALMON PATCH (NEVUS SIMPLEX)
• Most common vascular birthmark of infancy. Seen
in 40% of all newborns
• Cause: Area of superficially dilated capillaries
• Appears as irregular dull, pinkish – red macules with
poorly defined borders
• Site - On the face (angel kiss), nape of neck (stork
bite)
• Become more intense in colour when child is crying
• Most of these lesions spontaneously disappear
within a year.

27. PORT WINE STAIN (NAEVUS FLAMMEUS)
• Vascular birthmark, about 0.3% of newborns
• Large, irregular, deep red or purple macule with well
defined borders
• Usually unilateral, often on the face.
• Represents a vascular malformation involving mature
capillaries.
• Lesions do not enlarge but persist throughout life
Treatment:
• Pulsed dye laser
• Cosmetic masking, excision, grafting

28. STRAWBERRY MARK (CAPILLARY HAEMANGIOMA)
• Localised superficial haemangioma
• Usually not present at birth, develops during first few
weeks of life. Present in about 10% of infants
• Most of them start off as small red macules and usually
grow rapidly during the first four or five months of life
• Later appear as circumscribed oval or round, soft domed
swelling of intense scarlet-red color.
• Site – Head, neck region and trunk
• Over 90 percent disappear by the age of 7 years
• Treatment - Vascular specific Pulsed dye laser

29. MONGOLIAN SPOTS
• Blue-gray, poorly circumscribed, single or multiple,
macular lesion of various sizes
• Entrapment of melanocytes in dermis of developing
embryo, the cells fail to reach their proper location in
the epidermis
• Usually present at birth or appears within the first weeks
of life
• Most commonly over lumbosacral region
• Common in asian, black and hispanic infants
• Most fade during first two years of life
• Persist – Q switch laser, bleaching creams

30. CONGENITAL MELANOCYTIC NEVI (CMN)
• Benign proliferations of cutaneous melanocytes that arise
as a result of abnormal growth, development, or
migration of melanoblasts
• Affecting approximately 1% of newborns
• Present at birth or become apparent within the first year
of life
• Round or oval with smooth, well-defined borders, and the
surface texture can be papular, verrucous, or cerebriform
• Initially a nevus may be light in color, flat, or hairless, it
can become more pigmented, raised, and acquire long,
coarse hairs

31. • Lesions classified according to size - small <1.5cm, medium 1.5cm-20cm, large
>20cm in greatest diametrer or covering >2% BSA.
• Lifetime risk for malignant transformation depends largely on size, from 0-5% for
small CMN, and 5-10% for large CMN
• 70% of melanomas occur within the first decade of life
• Naevi over the cranium or spine have association with Neurocutaneous
melanosis
Treatment:
• Early treatment with full-thickness excision followed by grafting, otherwise
close observation
• Dermabrasion, chemical peels, and lasers improve cosmetic appearance

32. NEVUS OF OTA
• Extensive, bluish, patchy, unilateral dermal melanocytosis
that affects the sclera and the skin adjacent to the eye,
distributed along the first and the second branches of the
trigeminal nerve
• More common in Asians (0.014-0.034%) and blacks
• Most are present at birth or develop during first year of life
• Nevus of ITO – Same features as OTA, only distinguished by
location in the acromioclavicular region and the upper chest.
• Treatment - Q‐switched lasers, Cosmetic camouflage

33. BLUEBERRY MUFFIN BABY
• Widespread, purple, erythematous, oval or circular macules,
papules and nodules reflecting dermal erythropoiesis
• May be frank petechiae on the surface of some of the lesions
• Generalized distribution of 1 to 7 mm purpuric papules,
especially on head, neck, and trunk
• Generally fade into light brown macules within a few weeks
of birth
• This type of lesion has been recorded in a number of
congenital infections (Rubella, cytomegalovirus, Coxsackie
B2, syphilis, toxoplasmosis ) and a variety of disorders
(Rhesus haemolytic anaemia, ABO incompatibility, Neonatal
lupus erythematosus etc)

34. APLASIA CUTIS CONGENITA
• A rare disorder characterized by a focal absence of
epidermis, dermis, and in some cases subcutaneous
tissues – including bone and dura mater
• Most presentations (80–90%) involve the vertex of the
scalp
• Estimated rate of incidences is 1-3 in 10,000 births
• Oval, sharply marginated, depressed, hairless area
covered by wrinkled epithelial membrane, or may appear
as ulcer which heals with scar formation.
• A ring of hair around the defect, known as a ‘hair‐collar’
sign, is thought to be associated with an increased risk of
underlying defects

35. • Can occur in isolation or association with other types of disorders (limb
abnormalities, epidermal nevi, embryologic malformations, trisomy 13,
epidermolysis bullosa etc)
Treatment:
• Small defect- Surgical excision with mobilization of scalp and closer.
• Large defect- Hair transplantation
• Management of associated disorders accordingly, if present

36. NEONATAL ACNE
• Prepubertal acne can be divided into five subgroups:
neonatal, infantile, midchildhood, preadolescent and
adolescent
• Thought to be due to androgens (maternal & infant)
• May affect up to 20% of neonates, more common in boys
• Presents at or shortly after birth with erythematous
papulopustular lesions, and comedones
• Site - commonly on cheeks, chin and forehead

37. Treatment:
• Usually settles spontaneously and leaves little scarring.
• Gentle cleaners, oil‐free emollients
• If marked pustules - topical azole cream

38. NEONATAL CEPHALIC PUSTULOSIS
• Historically referred wrongly as neonatal acne because of
their clinical similarity
• Presents in the first 3 weeks of life
• Prevalence varies between 10 and 66% of newborns
• Postulated to develop in association with Malassezia
• Characterized by erythematous papulopustules,
surrounded by erythematous halo
• Site - cheeks, chin, eyelids, neck and upper chest

39. • Absence of comedones and presence of pustules surrounded by erythematous
halo help to differentiate this entity from neonatal acne
Investigation:
• Isolation of M. furfur in pustule content (50-60%)
Treatment:
• Self-limiting nature, heals in 1-3 months without scarring
• Persist/widespread – 2% ketoconazole cream for 15 days

40. INTERTRIGO
• Superficial inflammatory dermatosis involving body folds
that develops through friction
• Heat, moisture, friction and sweat retention induce
maceration and inflammation.
• Secondarily infected by bacterial (s.aureus, group A
streptococci) or fungal (candida) infection.

41. • Initially skin is red and slightly macerated, when separated show erythema of
contagious surface.
• Itching, burning and odour are common symptom.
• TREATMENT
– open wet compresses
– Dusting powder
– Antibiotics –cephalexin 40-50mg/kg/day or cloxacillin50-100mg/kg/day for 10
days or fungicidal nystatin cream 4-5 times /day for 3-4 days may be used.

42. DIAPER DERMATITIS (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 - the erythema
gets worse and there are satellite papular-pustulous lesions

43. Investigations: Skin swabs may be useful to confirm yeast or bacterial
infection.
Management:
• Remove the contactants, keep the diaper area dry.
• Frequent diaper change.
• Contamination by Urine or Feces should be rinsed gently with
warm water.
• Zinc cream or petroleum jelly is useful
• Mild topical steroid such as 1% hydrocortisone cream on inflamed
skin once or twice daily for 1–2 weeks
• Topical antifungal if secondary infection present e.g. ketoconazole,
nystatin at 100,000U/g or 1% miconazole nitrate
Jacquet’s ulcers
Candidosis

44. SEBORRHEIC DERMATITIS(CradleCap)
• Characterized by large flakes of yellowish scale on the
scalp, may become matted into large plaques of crust.
• Etiology - unknown
• Site - Scalp, face, postauricular, presternal and
intertriginous areas etc.
• Begins with a non-eczematous, erythematous, scaly
dermatitis of the scalp and spread downward
Treatment:
• Topical weak corticosteroid - 1% hydrocortisone
• Mild baby shampoo, ketoconazole 2% shampoo

45. NEONATAL LUPUS ERYTHEMATOSUS
• Occurs in about 1-2% of babies born to mothers with
clinical or subclinical autoimmune connective tissue
disease (primarily SLE and Sjögren's syndrome)
• Transplacental passage of maternal autoantibodies ssA-
Ro and ssB-La is thought to play role in pathogenesis
• Babies from subsequent pregnancies have a 20–25% risk
of skin or cardiac disease
• Present with either skin lesions (90%) or cardiac lesions
(1%)
• Well‐defined areas of macular or slightly elevated
erythema, frequently annular

46. • Site - face, particularly the forehead, temples and upper cheeks
• ‘Spectacle‐like’ distribution of lesions around the eyes is especially characteristic
• Congenital heart block (typically begins during the 2nd or 3rd trimester)
• Associated - hepatosplenomegaly, anemia, leukopenia, thrombocytopenia, and/or
lymphadenopathy
Investigation- skin biopsy, circulating autoantibodies in both the mother and the
child, ultrasound or electrocardiography
Treatment-
• Sunprotection
• Except for cardiac involvement, usually resolves in 6-12 months
• 50% with cardiac involvement will require a pacemaker

47. COLD PANNICULITIS
• Results from cold exposure to adipose tissue
• Fat of newborn are more highly saturated than that of older
children, with the effect that it solidifies at a higher
temperature
• Indurated, warm, red, subcutaneous plaques and nodules
appear within hours or days of appropriate cold exposure
• Skin biopsy shows a lymphohistiocytic infiltrate around blood
vessels at the junction of dermis and subcutaneous fat
• Induration resolves over a period of a week often leaving
some residual postinflammatory hyperpigmentation
• Self-limiting disorder and requires only symptomatic relief

49. CONGENITAL SYPHILS
• Transplacental infection by Treponema pallidum
• Lesions usually appear between 3-8 weeks of age
• 15% of children born to untreated mothers are infected
• Lesions are reddish brown in colour, may be macular or
papular
• Sites of predilection are the ano‐genital area, the face
and the palms and soles
• If ulcerative in nature, they are highly contagious
• Syphilis rhinitis (snuffles) most important and frequent
sign

50. • Other features include bone abnormalities, anemia, thrombocytopenia, fever,
hepatosplenomegaly, lymphdenopathy, and poor feeding
Investigations-
• X‐ray of long bones
• CSF examination
• Dark‐field microscopy and/or PCR from exudates
Treatment-
• Aqueous crystalline penicillin 50,000 units/kg/dose IV every 12 h during the first 7
days of life and every 8 h thereafter for a total of 10 days

51. NEONATAL HERPES SIMPLEX
• Incidence about 7/100 000 live births
• Mostly from transmission of HSV type 1 (20%) and HSV type 2
(80%) through the contact with an infected genital tract
during delivery. Intrauterine 5%
• Common in premature and low birth weight
• Of infected babies, 70% develop the skin/mucosal lesion, 90%
systemic
• Lesions appear between day 2 and 20
• Clustered red papules and vesicles, then become pustular,
crusted and erosion over the following 2-3 days

52. HSV infection in newborns usually develops in one of three patterns:
• Localized to the skin, eyes, and mouth (40%)
• Central nervous system (CNS) disease (35%)
• Disseminated disease involving multiple organs (25%)
Investigations: Serology, Viral culture, PCR
Treatment: Skin & mouth disease - Acyclovir 20mg/kg-8hrly IV for 14 days
Encephalitis & systemic disease -21 days.

53. NEONATAL VARICELLA
Neonatal varicella is mostly caused by maternal chickenpox
acquired during pregnancy (25% of cases)

54. FETAL VARICELLA SYNDROME

55. Cutaneous lesions:
• Lesions are polymorphous- papules, pustules and vesicles
• The infant's rash usually occurs toward the end of the 1st week to the early part of
the 2nd week of life
• Vesicles usually develop over 1st 3-10 days of life
• Localized scarring, most common cutaneous feature of FVS
• Localized absence of skin, usually on a limb
Investigations: PCR, Serology (IgM and IgG)

56. Treatment-
• Newborns whose mothers demonstrate varicella 5 days before to 2 days after
delivery should receive 1 vial of VZIG as soon as possible.
• All premature infants born <28 wk gestation to a mother with active varicella at
delivery (even if the maternal rash has been present for >1 wk) should receive
VZIG
• The infant should be treated with acyclovir (10 mg/kg every 8 hr IV) when lesions
develop

57. CONGENITAL RUBELLA
• Preconception minimal risk
• 0-12 weeks 100% risk of fetus being congenitally
infected resulting in major
congenital abnormalities.
Spontaneous abortion in 20% of cases.
• 0-16 weeks congenital rubella syndrome (85%)
• After 16 weeks normal development, slight risk
of deafness and retinopathy
Congenital rubella typically results from maternal infection

58. Congenital Rubella Syndrome
• Classical triad consists of cataracts, heart defects, and sensorineural deafness.
• Many other abnormalities, divided into transient, permanent and developmental.
• Transient low birth weight, hepatosplenomegaly, thrombocytopenic purpura
bone lesions, meningoencephalitis, hepatitis, haemolytic anemia
pneumonitis, lymphadenopathy
• Permanent Sensorineural deafness, Heart Defects (peripheral pulmonary stenosis,
pulmonary valvular stenosis, patent ductus arteriosus, ventricular
septal defect), Eye Defects (retinopathy, cataract, glaucoma, myopia)
Other Defects (microcephaly, diabetes mellitis, thyroid disorders)
• Developmental Sensorineural deafness, Mental retardation, Diabetes Mellitus,
thyroid disorder

59. • Discrete rounded, red or purple infiltrated macules, 3-8 mm in diameter
• Site – face, scalp, back of neck and trunk
• Blueberry muffin lesions
• Other skin manifestation – cutis mamorata, seborhoea and hyperpigmentation of
the forehead, cheeks, umbilical area and discrete deep dimples over bony
prominences, particularly the patellae
• Investigations: PCR - Rubella virus isolation
Rising titres of antibody (mainly IgG) - EIA
• Treatment: Supportive care

60. HAND, FOOT & MOUTH DISEASE
• Caused by Coxsackie A-16 virus (Occasionally A5-A10)
• Symptoms can develop within 2 weeks after birth.
• Abrupt onset scattered papules that progress to oval
or linear vesicle. Preceded by Fever
• Distribution- Palms, fingertips, interdigital webs soles
& buccal mucosa.
• Clears spontaneously in about 7 days.
• Treatment- Rest, fluids, Acetaminophen

61. BULLOUS IMPETIGO
• A contagious infection of the superficial epidermis
• Most often caused by phage group II strains of
staphylococcus aureus
• Due to staphylococcal exfoliative toxins (exfoliatin A–D),
which target desmoglein 1
• Lesions do not generally appear until the second week of life
• Superficial flaccid blister without erythema, initially clear,
yellow fluid that turns cloudy and dark yellow
• Rupture easily, dries and form a honey – colored crust
• Associated systemic symptoms - fever, malaise, generalized
weakness, and diarrhea

62. Investigations:
• Swab culture – bacteria
• Blood count may reveal neutrophil leucocytosis
• Biopsy - Acantholytic cells, Cleavage plane is subcorneal or upper granular layer,
Minimal inflammatory infiltrate in upper dermis
Treatment:
• Normal saline or potassium permanganate soaks to remove the crust.
• Topical antiseptic (povidone iodine, hydrogen peroxide cream, chlorhexidine)
or topical antibiotic (fusidic acid, mupirocin).
• Systemic antibiotics in extensive lesions

63. STAPHYLOCOCCAL SCALDED SKIN SYNDROME (SSSS)
(Ritter’s disease)
• Syndrome of acute exfoliation of the skin caused by
epidermolytic toxin A and/or B (exotoxin) produced by
staphylococcus aureus
• The toxins act at the zona granulosa of the epidermis,
causing cleavage of desmoglein 1 complex
• Greater incidence of this condition in neonates due to less
efficient metabolism and excretion of the toxin.
• These toxins reach the skin via the circulation from a
distant focus of infection, usually in the umbilicus, breast,
conjunctiva or site of circumcision or herniorrhaphy

64. • Start as a macular, orange‐red, scarlatiniform eruption
• Lesion generally becomes more extensive, and over the
next 24–48 h turns to a more confluent, deep erythema
with oedema
• Surface then becomes wrinkled before starting to
separate, leaving raw, red erosions.
• First appear on face, axillae and groins then spread all over
body.
• Extreme tenderness of the skin is an early feature
• Child is pyrexial and distressed

65. Investigations:
• Nikolsky’s signs - positive.
• Tzanck smear
• Skin biopsy, which shows intraepidermal cleavage at the granular layer
• Bacterial culture from skin, blood. The intact bullae are sterile
Treatment:
• Intravenous penicillinase-resistant penicillin, such as nafcillin or oxacillin
• Other antibiotics include cephalosporin and clindamycin
• Vancomycin should be considered in areas with a high prevalence of Community
Aquired-MRSA
• Fluid and electrolyte balance.

66. CANDIDIASIS
• Early weeks after birth, in the form of oral candidiasis.
• Acquired during delivery from the mother’s genital tract
(frequency of vaginal candidiasis 20% - 25%)
• Rash is usually focused in the perianal area, and is a deep
‘beefy’ red colour, with a moist appearance, often with
pustules at the periphery
• Pseudomembranous form is the most common and
appears as white plaques on the buccal mucosa, palate,
tongue, or the oropharynx
• Painful inflammation of tongue, soft and hard palate,
buccal & gingival mucosa can extend to esophagus/
pharynx.

67. • Congenital Candidiasis: A rare condition seen at birth, due to ascending
infection from the genital tract. Candida is able to find its way into the amniotic
fluid without prior rupture of membranes
• Two forms have been described:
1) Congenital cutaneous candidiasis: presents within 12 hours of birth. A macular
erythema that may evolve into a papular, vesicular or pustular phase over a
period of 1–3 days, finally results in extensive desquamation. Palmar and
plantar pustules are regarded as hallmark
2) Congenital systemic candidiasis: An invasive infection with a high mortality
rate, especially in VLBW infants. At least 50% do not have a cutaneous rash.
Presenting signs are pneumonia (most common), meningitis, candiduria
and/or candidemia.

68. Investigations:
• Skin/mucosa swab and scraping - candida
• Endoscopy in extensive oral candidiasis, to see the extent of the lesions
Treatment:
• Clotrimazole 1% used as mouth paint 4 times a day
• Nystatin, amphotericin B or miconazole gel applied several time a day.
• Systemic antifungal therapy for systemic infection (Amphotericin B drug of
choice - amphotericin B deoxycholate 0.5–1.0 mg/kg once daily)
• Maintain proper oral hygiene

69. SCABIES
• Scabies may present as early as three to four weeks of age
but is never present at birth
• Neonates do not itch, but present with extensive rashes,
irritability, poor feeding, and failure to thrive.
• Vesicles are common, leading to early pustulation,
crusting, and scaling.
• Eruption is generalized, including involvement of the head,
neck, face, palms, and soles, with an early tendency for
pustule formation

70. Investigations:
• Scraping of skin from an unscratched burrow- microscopy revealed female mite
&/or her eggs.
Treatment:
• Permethrin 5 % cream at bedtime to all skin surfaces in neonate and from the
neck down in older family members
• Disinfection of recently used clothing and linens

71. NEONATAL PURPURA FULMINANS
• Potentially lethal disorder characterized by progressive
haemorrhagic necrosis of the skin due to abnormal coagulation
and microvascular occlusion
• Usually due homozygous deficiency of protein C or, less
frequently, protein S
• Rarely, can occur due to infection, such as group B
Streptococcus , methicillin‐resistant Staphylococcus aureus
• Lesions most characteristically appear within first 12 h of life
• Symmetrical and well‐defined ‘lakes’ of confluent ecchymosis
• Patient is frequently febrile

72. • Onset is sudden, and the lesions enlarge rapidly, with coalescence and the
development of haemorrhagic bullae and central necrosis.
• There is surrounding erythema and the lesions are tender
• Site - Most often on the limbs, particularly at sites of pressure
Investigations: Thrombocytopenia, Polonged aPTT and PT
• Bacterial culture
• Histopath – cutaneous necrosis without evidence of inflammation, and occlusion
of blood vessels with platelet-fibrin thrombi
Treatment: Initially, fresh frozen plasma 10–15 mL/kg/12 h
• If protein C deficiency is confirmed, onward therapy with protein C concentrate
should continue until the skin lesions have healed
• Longer term treatment is with oral anticoagulants
• Any concomitant infection needs to be treated as well

73. ICHTHYOSIS
• Ichthyosis - excessive scaling of skin.
Major hereditary types
• Vulgaris, Recessive X-linked, Autosomal recessive,
Keratinopathic
Autosomal recessive congenital ichthyosis
• Includes all non‐syndromic autosomal recessive congenital
forms of ichthyosis without a tendency toward blistering
• Includes harlequin ichthyosis, bathing suit ichthyosis, lamellar
ichthyosis, self‐improving congenital ichthyosis, Colloidon
baby etc

74. Harlequin ichthyosis
• Most devastating type of ARCI. Often lethal in around 44% case
• Mutations in the ABCA12 gene
• Neonates are born with armour‐like skin (truncal plates with
fissuring)
• Impaired movement and the ability to drink and breath
• More prone to infection of the skin, as well as other organs such
as the lungs (major cause of death)
• Biopsy - enormous thickening of stratum corneum. Parakeratosis
and hypergranulosis and reduced non‐polar lipids
• Electron microscopy – numerous abnormal lamellar bodies in
stratum granulosum

75. Collodion baby
• Most autosomal recessive congenital ichthyosis (ARCI)
present at birth as collodion babies
• Baby encased in shiny parchement-like membrane which may
impair respiration and sucking .
• Usually peels off within the first 4 weeks of life.
• In 80% of cases, collodion baby is followed by the onset of an
ARCI subtype
• Around 10–20% develop into self‐improving congenital
ichthyosis

76. TREATMENT:
• High humidity incubator (60-80%) with close monitoring of body
temperature.
• Bland ointments two to four times a day
• In severe disease, the oral retinoids such as acitretin, isotretinoin at low
dosage, up to 0.5 mg/kg body weight

77. NEUROFIBROMATOSIS 1 (von Recklinghausen's disease)
• Autosomal dominant disease
• Due to mutation of NF1 gene in chromosome 17
• NF1 gene – neurofibronin (tumour suppressor)
• Most common type of Neurofibromatosis (90%), with a
prevalence of about 1 in 3,000 births
• Present at birth or shortly after
Characterised by the presence of:
• 6 or more café-au-lait spots (defined oval-shaped light
brown patches greater than 0.5cm in diameter)
• Multiple neurofibromas
• Freckling (under the armpits and areas of skin folds)
• Lisch nodules (tiny tumours on the iris of the eye)

78. INCONTINENTIA PIGMENTI
• X-linked dominant multisystem disease that is usually lethal in
males
The skin lesions develop in four stages:
• Erythematous papules and vesicles appear in crops in linear
streaks along the lines of Blaschko, usually at birth or within the
first few weeks of life, each crop lasting one to two weeks
• The verrucous stage follows, consisting of hyperkeratotic warty
papules or plaques in linear or swirling patterns
• The third pigmented stage presents as streaks of
hyperpigmentation in a swirled pattern
• The hyperpigmented streaks then may evolve into a final stage
of hypopigmentation and atrophic patches or streaks.

79. Associated Systemic abnormalities occur in nearly 80 percent of patients
• Teeth 80% - delay in eruption, unusually shaped, typically pegged or cone-shaped
• Nails 40% - nails may be ridged, pitted, thickened or completely disfigured
• Hair 50% - eyebrows and eyelashes, may be coarse, wiry and lack lustre
• Eyes 20-35% - Abnormal blood vessel growth resulting in scarring, blindness
• Central nervous system 30% - seizures
Treatment
• Prevent secondary bacterial infection of skin lesions
• Topical tacrolimus and topical corticosteroids has been reported to hasten the
resolution of the inflammatory stage.

80. THANK YOU