Neonatal Skin Conditions

Presented by – Dr Srinadh Pragada

Moderator-Dr V.R. Sudha Reddy
 OBJECTIVES
• TO CLASSIFY THE NEONATAL SKIN
CONDITIONS
• TO DISCUSS THE CLINICAL FEATURES OF
NEONATAL SKIN CONDITIONS
• TO DISCUSS THE MANAGEMENT OF
NEONATAL SKIN CONDITIONS
 NEONATAL SKIN IN COMPARISON
WITH ADULT
• Thinner epidermis
• Higher epidermal proliferation and desquamation
rate
• Higher trans epidermal water loss
• Thinner, less hairy, weaker intercellular
attachments
• Fewer eccrine and sebaceous gland secretions
• Increased susceptibility to external irritants
• Increased susceptibility to microbial infections
 Classification
• Transient skin disorders
• Congenital disorders
• Acquired skin disorders
• Iatrogenic dermatologic complications
• 1) TRANSIENT SKIN DISORDERS
 VERNIX CASEOSA
• White creamy naturally
occurring biofilm
• Composed of
degenerated fetal
epidermis
• Functions – epidermal
barrier
– Antimicrobial cover
– Thermal regulation
– Anti-oxidant properties
SEBACEOUS HYPERPLASIA
• tiny monomorphous
pinhead-sized lesions,
white or yellow in color,
seen in abundance over
the nose, upper
lip,malar region, and
chin.
MILIA
• Benign keratinous cysts
– small firm pearly
white papules
predominantly
occurring over the face
• Treatment – usually
disappears within 3-4
weeks
• DD- sebaceous gland
hyperplasia – yellow
papules
MONGOLIAN SPOTS
• Blue gray poorly
circumscribed single or
multiple macular lesions
of varying size
• Due to entrapment of
melanocytes in dermis of
developing embryo
• Usually present at birth
• Most commonly over
lumbosacral region
• Resolve within first two
years of life
 CUTIS MARMORATA
• Benign cutaneous
vascular phenomena
due to accentuated
physiologic vasomotor
response to cold
• Reticulate bluish
mottling of skin
• Usually disappears as
the infant is re warmed
 CUTIS MARMORATA
• Its persistence is seen in
Down syndrome,
trisomy 18,
hypothyroidism, and
Cornelia de Lange
syndrome.
HARLEQUIN COLOR CHANGES
• More frequently seen in
low birth weight and
sick infants.
• When these infants are
placed on their sides, a
sharp longitudinal
midline bisects the
body into a pale upper
half and a deep-red
dependent half.
 HARLEQUIN COLOR CHANGES
• color change reverses if the infant is placed on
the opposite side
• The mucous membranes and genitals are not
involved.
• These changes are attributed to a temporary
imbalance in the autonomic regulatory
mechanism of the cutaneous vessels.
LAMELLAR DESQUAMATION
• Peeling of skin on hands,
ankles, and feet in term
infants. Postmature infants
have a more widespread
desquamation
• Rud’s syndrome, neutral
lipid storage disease,
essential fatty acid
deficiency, amino acid
deficiencies, and congenital
infections can also present
as desquamation at birth.
• Neonatal desquamation needs to be
differentiated from collodion baby, continued
peeling skin syndrome, and the different
forms of ichthyosis
LANUGO
• fine unmedullated vellus
hairs.
• prominent in preterm
neonates
• Neonatal hairs are
increased and widespread
in congenital
hypertrichosis lanuginosa,
congenital lipodystrophy,
leprechaunism, Cornelia
de Lange syndrome, and
mucopolysaccharidoses.
EYTHEMA TOXICUM
NEONATORUM
• Benign self limiting
disorder of unknown
etiology
• erythematous macules
or 1–3 mm sized pale
yellow to white papules
or pustules on an
erythematous base.
• ETIOLOGY-Sensitizing factors include late
toxicosis of pregnancy, and high level of
estrogen hormones.
• According to one study, erythema toxicum
neonatorum is an innate immune response of
a newborn infant to commensal microbes that
gain entry into the skin tissue, most probably
through the hair canal.
• PATHOLOGY-Erythematous macules show
edema of the upper dermis with a
perivascular inflammatory infiltrate consisting
of eosinophils.
• Papular lesions show an eosinophilic infiltrate
at the outer root sheath of the hair follicles.
• Pustules show intrafollicular accumulation of
eosinophils below the stratum corneum
• CLINICAL FEATURES-lesions consist of
erythematous macules up to 3 cm in diameter
scattered mostly on the trunk, especially the
back and buttocks. The palms and soles are
rarely affected
• DIAGNOSIS-Giemsa staining of the content
shows an eosinophilic concentrate.
• TREATMENT-Usually resolves within 6 to 8
days , reassurance
MILIARIA
• Its is as disorder due to
blockage of eccrine
sweat ducts
• common in neonates
probably because of
immaturity of the sweat
pores, warm and humid
environment
• 4 types
– Crystallina
– Rubra
– Pustulosa
– Profunda
MILIARIA CYSTALLINA
• Presents as crops of
clear thin walled
superficial vesicles
without erythema
• Rupture within 24 hrs-
bran like desquamation
• Seen on forehead scalp
neck and upper trunk
MILIARIA RUBRA
• Erythematous papules
1-4mm on background
of macular erythema
• Usually benign
• Lesions may be itchy
and hence child may be
irritabale
MILIARIA PUSTULOSA
• consists of
papulovesicles that
become pustular. The
lesions are not the
result of secondary
infection.
• Lesions rapidly enlarge
to form plaques.
• They may be a sweat-
related bromoderma
• DIAGNOSIS-The characteristic lesions with
absence of inflammation are seen in a warm,
humid climate and have a tendency to recur.
• Cytological examination reveals the absence
of inflammatory or giant cells
• TREATMENT-Since the lesions are transient
and asymptomatic, no treatment is needed.
SUCKING BLISTER
• A blister or denuded
area in neonates usually
seen on forearm, wrist
and fingers
• Due to vigorous suckling
in utero
• Treatment – heal
rapidly without
sequelae
ACROCYANOSIS
• Functional peripheral
vascular disorder – bluish
discoloration of skin –
vasospasm of small
vessels
• Involves palms and soles
• Absence of cyanosis of
warm central parts
• Resolves by itself or after
warming
TRANSIENT NEONATAL PUSTULAR
MELANOSIS
• Idiopathic pustular
eruptions that heals with
brown pigmented macules
• Usually present at birth – 1
to 3mm flaccid superficial
fragile pustules
• Absence of erythema and
association with pigmented
macules helps differentiate
this condition from other
pustules, and
staphylococcal and herpetic
infections
• Resolves within 24 to 48hrs
• Treatment – self resolving, reassurance
EPSTEIN PEARLS
• Yellowish white
keratinous cysts , 1-2mm
in diameter
• Seen in 85% of neonates
• Seen along the alveolar
ridge in the midline at
junction of hard and soft
palate
• Treatment – disappears
within few weeks
• 2)CONGENITAL SKIN DISORDERS
PORT WINE STAIN
• Vascular birth
mark(vascular
malformation)
• Large irregular deep red
or purple macule with
well defined borders
• Usually unilateral present
over the face
• Treatment – pulsed dye
laser & screening for CNS
malformations
SALMON PATCH
• Most common vascular
birth mark of infancy
• Area of superficial dilated
capillaries
• Appears as irregular
pinkish-red macules with
poorly defined borders
• Become more intense in
colour when child is crying
• Treatment – spontaneously
disappear within 1 yr
CAPILLARY HEMANGIOMA
• Localized superficial
hemangioma
• Usually present at birth
• Begin as small red
macules and have rapid
progression during first
five months of life
• Later disappear as scarlet
red color domed swelling
• Usually disappear by age
of 7 to 8 yrs
CUTIS MARMORATA TELANGIECTATCIA
CONGENITA
• Congenital vascular
malformation – fixed
patches of mottled skin
with reticulate blue to
pale purple patches
• Doesn’t disappear after
warming
• Localized or generalized
• Screen for congenital
abnormalities –
hypothyroidism,
craniofacial and skeletal
defects
CONGENITAL MELANOCYTIC NEVI
• Benign proliferation of cutaneous
melanocytes that arise as a result
of abnormal growth,
development or migration of
melanoblasts
• Present at birth , resolves by 1 yr
of age
• Naevi over cranium and spine –
rule out neurocutaneous
melanosis
• Treatment – cosmetic –
dermabrasion, laser, full thickness
excision and grafting
NEVUS OF OTA
• Extensive bluish patchy
unilateral dermal
melanocytosis that
affect the sclera and
skin adjacent to eye(
along 1st & 2nd branches
of trigeminal nerve)
• Treatment – cosmetic -
Q switched laser
INCONTINENTIA PIGMENTI(BLOCH
SULZBERGER SYNDROME)
• X linked dominant
ectodermal dysplasia
presenting within first
few days of birth
• Vesicles appear on
trunk and limbs
• Disappears after 1st
month of life and
followed by firm
papules and warty
plaques
CAFE-AU-LAIT PATCHES
• Hyperpigmented macules
with well defined borders
are usually of no
pathological significance
• Before puberty 5 or more
macules greater than
0.5cms diameter are
presumptive evidence of
neurofibromatosis
ICHTHYOSIS
• Excessive scaling of skin
• Autosomal recessive
congenital ichthyosis
– Harlequin ichthyosis,
bathing suit ichthyosis,
lamellar ichthyosis,
colloidon baby
HARLEQUIN ICHTHYOSIS
• Most devastating type of
congenital ichthyosis
• Mutation in ABCA12 gene
• Neonates are born like
armour like skin
• Characterized by impaired
movements, breathing
difficulties
• More prone for infections
COLLODION BABY
• Most common presentation of
congenital ichthyosis
• Baby encased in shiny
parchment like membrane
which may impair respiration
and sucking
• Usually peels off within 4
weeks of life
• Around 10-20% develop into
self improving congenital
ichthyosis
• Treatment – high humidity
incubator with close
monitoring of body
temperature
• In severe disease – oral
retinoids can be given
 EPIDERMOLYSIS BULLOSA(MECHANO
BULLOUS DISEASES)
• Group of inherited non inflammatory disorders in
which blisters and erosions occur with mechanical
,often minor trauma
• Prenatal diagnosis of mechano bullous diseases by
foetoscopy and skin biopsy can be done but risks
must always be evaluated.
 EPIDERMOLYSIS BULLOSA(EB)
• Mainly there are 3 types of EB
1. SIMPLE EPIDERMOLYSIS BULLOSA
2. JUNCTIONAL EPIDERMOLYSIS BULLOSA
3. DYSTROPHIC EPIDERMOLYSIS BULLOSA
SIMPLE EPIDERMOLYSIS BULLOSA

• Erosions at the time

birth due to skin
trauma can be present
• Blisters are formed by
the disintegration of
basal and suprabasal
cells. They become
rapidly tense with clear
fluid.
• Improveement occurs
with increasing age
JUNCTIONAL EPIDERMOLYSIS BULLOSA

• There is seperation between basement membrane

and basal cell plasma membrane
• Skin,mucosal membranes,teeth are affected
• Eroded areas heal slowly
• May be hemorrhagic and are frequently secondarily
infected.
DYSTROPHIC EPIDERMOLYSIS BULLOSA

• This severe scarring

form appears usually at
birth with minor trauma
producing blistering and
seperation of epidermis
• Mucous membranes are
affected
• Pharyngeal and
oesopageal involvement
produces strictures
• 3) ACQUIRED SKIN DISORDERS
DIAPER DERMATITIS
• Diaper dermatitis
(napkin dermatitis or
nappy rash) is one of
the most common skin
problems in the
newborn
• Friction between skin
and fabric plays some
part in the etiology
 DIAPER DERMATITIS
• Hydration of the skin increases the susceptibility to
frictional damage, which results in maceration of the
stratum corneum.
• also increases transepidermal permeability, making
the skin more susceptible to irritation.
• The urinary pH is also important as urine with a pH
of more than 8 applied to the infant’s skin induces
an inflammatory response.
• Feces contain a number of enzymes like proteases
and lipases, which have an irritant effect on the
infant’s skin
 DIAPER DERMATITIS
• Candida albicans has been isolated from the area in
many infants with napkin dermatitis
• Babies on broad-spectrum antibiotics have a higher
risk of developing diaper dermatitis.
• Soaps, detergents, and antiseptics that are used to
clean napkins have been incriminated as a cause of
dermatitis
• The rash appears after the third week of life.
• It is more common in the higher socioeconomic group
where napkins are used. It presents as a confluent
erythema on convex surfaces in close contact with
the napkin, i.e. buttocks, genitalia, lower abdomen,
pubic area, and upper thighs
• During the acute stage, the erythema has a glazed
appearance Later the skin peels off in sheets. Can also
present as erosive form as small vesicles, erosions,
and ulcers with crater like edges (Jacquet’s dermatitis)
 TREATMENT
• Plastic diapers are occlusive and should be avoided.
Oil massage should not be allowed. During the
inflammatory phase, lukewarm water or saline
solutions are helpful.
• The imidazoles are often useful because of their
antimicrobial and antifungal actions.
• Topical corticosteroids should be avoided in
mechanical and infective diaper dermatitis.
Hydrocortisone 1% is the ideal topical corticosteroid
for use in the diaper area,
 BACTERIAL INFECTIONS
• Bacterial infections are among the commonest skin
problems seen in neonates in India.
• Bacterial colonization of the skin and mucous
membranes occurs in the first few hours of life and is
due to organisms from the maternal vaginal canal or the
surrounding in which the baby is placed postnatally
• By six days of age, 30% of infants are colonized by
staphylococcal organisms
• pustules, paronychia, abscesses omphalitis, mastitis,
and conjunctivitis.
• Clinical disorders caused by an exotoxin produced by
Staphylococcus aureus include bullous impetigo and
staphylococcal scalded skin syndrome
PUSTULE
• Pustules are the
commonest sign of
staphylococcal infection
in neonates.
• Common sites of infection
are the neck folds, groin,
and the periumbilical
region.
• They can be differentiated
from erythema toxicum
neonatorum and pustular
melanosis by smear and
by culture.
OMPHALITIS
• Omphalitis, more
commonly called
umbilical sepsis, is
another common
manifestation.
• It may present as a
mucopurulent or
purulent discharge from
the umbilicus.
• Chronic infection may
be associated with an
umbilical granuloma.
 TREATMENT
• Babies with staphylococcal infections in the nursery
should be isolated. Oil application and massage
should be stopped.
• An antibiotic ointment should be rubbed into the
area when there are few lesions
• Systemic antibiotics should be administered to
preterm babies, babies at risk, or babies with
multiple lesions.
STAPHYLOCOCCAL SCALDED SKIN
SYNDROME (RITTER’S DIDEASE)
• syndrome of acute
exfoliation of skin caused by
epidermolytic toxin A
• Toxins act at zona granulosa
of epidermis causing
cleavage of desmoglein 1
complex
• Start as macular orange red
scarlantiniform eruptions
• Lesions usually become
more extensive and over
the next 24 hrs turns to
deep erythema with edema
• Surface then becomes
wrinkled before starting to
separate leaving raw red
erosions
• Nikolsky’s sign (i.e.
separation of areas of
epidermis in response
to shearing pressure on
the skin) is positive
• DIAGNOSIS-Cutaneous tenderness
differentiates SSSS from other causes of
erythroderma like epidermolysis bullosa,
epidermolytic hyperkeratosis, and boric acid
poisoning.
• Toxic epidermal necrolysis (TEN) is almost
identical in clinical presentation.
• Can be differentiated by the presence of
mucosal lesions and by the histopathology,
which reveals separation at the
dermoepidermal junction, unlike SSSS where
the separation is intraepidermal.
• TEN carries a poorer prognosis.
• TREATMENT-parenteral antibiotics to which
staphylococci are sensitive; cephalosporins or
cloxacillin may be used.
• The fluid and electrolyte balance must be
monitored as fluid may be lost from the
eroded surface.
• caused by Staphylococcus
aureus. The predisposing
factor in India is the wrong
Indian tradition of
squeezing out milk from
the infant’s breast
• affected breast is red,
swollen, tender, and warm
• Systemic antibiotics like
cephalosporins and other
penicillinase resistant
penicillins may be used.
The abscess requires
surgical drainage
BULLOUS IMPETIGO
• localized bullous skin
infection caused by
strains of Staphylococcus
aureus
• intraepidermal blisters
• bullous eruption starting
over the neck, perineum,
or periumbilical region
and may spread all over
the body. The bullae are
thin walled and filled with
a purulent fluid
• Should be differentiated from epidermolysis
bullosa, incontinentia pigmenti, bullous
ichthyosiform erythroderma, and
mastocytosis
• DIAGNOSIS-Impetigo can be differentiated by
the presence of gram-positive cocci in clusters
with numerous polymorphonuclear leukocytes
in smears from the bullous fluid. A culture of
the fluid shows gram-positive cocci
• TREATMENT-Bullae should be ruptured and an
antibiotic ointment rubbed into the area.
• The baby should be given a systemic antibiotic
that is penicillinase-resistant such as
cephalosporin or cloxacillin.
ECTHYMA GANGRENOSUM
• Caused by Pseudomonas
aeruginosa
• The condition develops as
vesiculopustules, which
may be hemorrhagic,
surrounded by edema
and erythema. The lesion
ruptures leaving a
necrotic base with an
elevated border
• Histology is characterized by vasculitis surrounded by
edema, hemorrhage, and necrosis of the surrounding
tissue, with minimal infiltration by neutrophils.
• TREATMENT-This is a serious infection in the neonate
and requires immediate treatment. Ceftazidime
should be given parenterally
 FUNGAL INFECTIONS
• CANDIDAL INFECTIONS IN THE NEWBORN
• These occur in two forms: congenital candidiasis and
neonatal candidiasis. Both are caused by Candida
albicans
CONGENITAL CUTANEOUS
CANDIDIASIS
• occurs in utero as a
result of ascending
infection from the
genital tract of the
mother causing
chorioamnionitis and
infection of the
placenta and cord
 CONGENITAL CUTANEOUS
CANDIDIASIS
• maculopapular rash often presenting within the first 12
hours. The lesions develop into vesicles, pustules, or
bullae in 1–3 days.
• The entire skin surface may be involved including the
palms and soles.
• Oral involvement is usually absent. The face is usually
spared
• A potassium hydroxide preparation of desquamating
skin demonstrates budding yeast and pseudomycelia
Differential Diagnosis
• Other vesiculopustular lesions of the newborn, e.g.
staphylococcal pustulosis, transient neonatal pustular
melanosis, and erythema toxicum, should be
considered.
Treatment
• Any topical anticandidal agent, e.g. nystatin,
clotrimazole, miconazole, or econazole, may be used.
NEONATAL CANDIDIASIS
• common disorder
occurs after the first
week of life but may
manifest at birth.
Infection is acquired
during delivery.
• White, “flaky,” creamy
patches are seen on the
tongue and mucous
membranes of the
mouth, gum, and palate
• Candida albicans is the commonest causative
organism
• Candida is most adherent to the human buccal
epithelial cells. This property, together with its
capacity to undergo filament formation, may
be responsible for its ability to colonize and
cause disease.
 MANAGEMENT
• DIAGNOSIS- made by the typical appearance of the
lesion. Curdled flakes of milk may be seen in the
baby’s mouth. These can be easily removed and
leave no erythematous base.
• TREATMENT- Clotrimazole (1%) may be applied to
the mouth 3 times a day for 5–7 days.
BLUE BERRY MUFFIN SPOTS
• Wide spread purple
eythematous oval circular
macules reflecting dermal
erythropoiesis
• Usually present over head
neck and face
• Present at birth and then
fade into light brown
macules by few weeks
• DD- rubella, CMV, syphilis,
toxoplasmosis, neonatal
lupus erythematosus
NEONATAL ACNE
• One of the types of
prepubertal acne
• Due to maternal and
infant androgens
• Seen in 20% of neonates
• Erythematous
papulopustular lesions
over the cheeks chin and
forehead
• Treatment – resolves
spontaneously
INTERTRIGO
• Superficial dermatosis
involving body folds that
develop through friction
• May be secondarily
infected by
bacteria(S.aureus, Grp A
Strept) fungal (candida)
• Initially skin is red and
slightly macerated with
erythema
• Treatment – open wet
compresses, Candid
dusting powder, if
required antibiotics
SEBORRHEIC DERMATITIS(Cradle Cap)
• Begins as non
eczematous,
erythematous, scaly
dermatitis of scalp
• Pityrosporum ovale has
been implicated as the
cause of seborrheic
dermatitis.
• erythematous or greasy, scaly
papulosquamous eruption of the scalp may
spread to affect the face, forehead, eyebrows,
and ears
• Extensive widespread cradle cap or
persistence of cradle cap beyond 3–4 months
is suggestive of atopic dermatitis.
• TREATMENT-Oil should be applied to the scalp
and left on for several hours to soften the
scales. The scalp should then be rinsed.
• One percent hydrocortisone cream may be
used for facial lesion.
• Applications containing salicylic acid should
be avoided for fear of percutaneous
absorption
NEONATAL LUPUS EYTHEMATOSUS
• Occurs in 1-2% of babies
born to mother with
clinical or subclinical
autoimmune connective
tissue disorder
• Pathogenesis –
transplacental passage of
antibodies
• Well defined areas of
macular or slightly
elevated erythema
• Site – face – forehead, temple and upper
cheeks
• Spectacle like distribution of lesions
• Treatment – sun protection
– Usually resolves within 6 to 12 months
CONGENITAL SYPHILIS
• Transplacental infection
• Lesions usually appear
between 3-8 weeks of age
• Lesions are reddish brown
in colour, macular or
papular
• Site – ano-genital area ,
face palms and soles
• Most common sign –
snuffles
• Erythema,scaling,fissuring
of plantar surfaces
• Other features – bone
abnormalities, anaemia,
hepatosplenomegaly,
lymphadenopathy, poor
feeding
• Treatment – Crystalline
penicillin
50000units/kg/dose BD
for 1st 7days and TID for
next 3 days
NEONATAL HERPES SIMPLEX
• Mostly from transmission
of HSV1(20%) and
HSV2(80%) during
delivery
• Transmission can occur
from infective lesions in
the genital tract during
delivery, as an ascending
infection82 when there is
prolonged rupture of
membranes
• can also occur postnatally by contact with non
genital sites
• Lesions are characterized by the presence of
intranuclear inclusion bodies.
• Ballooned epithelial cells containing
intranuclear inclusions can best be seen at the
margins of the vesicles.
• Common in premature and LBW babies
• Skin lesions appear between 2nd to 20th day
• Clustered red papules and vesicles – become
pustular -crusted and erosions by 3rd day
• scattered all over the body, but are more
commonly present on the face, scalp, and over
the presenting part.
• Neonatal HSV infection rates can be reduced
by preventing maternal acquisition of genital
HSV-1 and HSV-2 infection near term, by
cesarean delivery and by limiting the use of
invasive monitors among women shedding
HSV at the time of labor
• DIAGNOSIS-recovering the virus from tissue
cultures of clinical specimens such as CSF or
cutaneous, oral, or ocular lesions
• The optimal specimen is usually vesicle fluid
obtained within 3 days of its appearance
• The Tzanck smear is rapid and inexpensive,
but is only 60% sensitive
• Treatment – Acyclovir 20mg/kg 8th hourly IV
for 14-21 days depending upon the exttent of
disease
NEONATAL VARICELLA
• Most commonly caused
by maternal chickenpox
acquired during
pregnancy
• Lesions are
polymorphous – papules,
pustules and vesicles
• Rash appears towards the
end of 1st week
• Vesicles develop by 3 to
10 days
• Finally end up as scar
• If the infection in the mother is 5 or more days
prior to the delivery or in the newborn during
the first 4 days of life ,the infection is mild
• If the infection in the mother is within 5 days
to the delivery or in the newborn during the 5
to 10 days of life ,the infection is severe and
disseminated.
Period of gestation of infected mother Outcome in foetus

7-28weeks Fetal varicella syndrome

2 weeks before delivery Neonatal chicken pox
5 days before or after Neonatal disseminated
delivery chicken pox with
septicemia

TREATMENT – VZIG AND ACYCLOVIR

CONGENITAL RUBELLA
• Typically results from
maternal infection
• Skin lesions – discrete
round red or purple
infiltrated macules , 3-
8mm in diameter
• Site – scalp, face, back,
neck
• Blue berry muffin
lesions
• Classical triad – cataract , heart defects, SNHL
• Preconception – minimal risk
• 0-12 weeks – 100% risk of fetus being
Congenitally infected resulting in major
abnormalities
• 0-16 weeks – Congenital rubella syndrome
• After 16weeks – normal development,
minimal risk
• Extreme tenderness of skin is an early feature
• Child is pyrexial and distressed
• Nikolsky’s sign positive
• Treatment – IV oxacillin or nafcillin
– Other cephalosporin and clindamycin
– In case of community acquired MRSA- vancomycin
– Fluid and electrolyte balance
• IATROGENIC DERMATOLOGIC COMPLICATIONS
COMPLICATIONS OF PHOTOTHERAPY
• tanning, transient
erythematous macules,and
burns (due to the use of UVA
light without a Plexiglas shield
result into burns)
• The bronze baby syndrome is a
major complication that
occurs in infants with
underlying liver disease who
receive phototherapy for their
unconjugated
hyperbilirubinemia
 COMPLICATIONS OF PHOTOTHERAPY
• Its characteristic features are grayish brown
discoloration of the skin, plasma, and urine
• The color disappears spontaneously after
discontinuation of phototherapy.
• Hands and feet are particularly affected and
healing of these deeper blisters produce
syndactyly requiring plastic surgery
• Nails are dystrophic
• Systemic steroid therapy can be of help but
will affect growth
• Recently PHENYTOIN(as a collagenase
inhibitor ) has been found to be effective
• Cutaneous injuries or lacerations due to fetal
scalp electrodes and transcutaneous PO2
monitors
 RECENT ADVANCES
• Neonatal Phototherapy can be used as a novel
therapy to prevent allergic skin disease like
atopic dermatitis for at least 5 years1
• Ultraviolet (UV)-free blue light phototherapy has
been reported to treat atopic eczema
• A study had recruited 117,041 babies.

• 1. Ku M. Neonatal Phototherapy: A Novel Therapy to Prevent

Allergic Skin Disease for At Least 5 Years. Neonatology.
2018;114(3):235-241.
• METHODS-Those with neonatal jaundice and
receiving neonatal phototherapy were
classified as the icteric-phototherapy group (n
= 4,744), those with neonatal jaundice and
not receiving phototherapy were classified as
the icteric-non-phototherapy group (n =
5,003), and those without jaundice were
classified as the non-icteric group (n =
107,294).And the neonates were followed up
upto 5 years
• RESULTS-Atopic dermatitis prevalence was
lower in the icteric-phototherapy group than
in the icteric-non-phototherapy group.
• clinical visit times for allergic skin disease were
lower at age 1-4 years and topical agent
prescription for allergic skin disease were
lower at age 1-5 years in the icteric-
phototherapy group than in the icteric-non-
phototherapy group.
• CONCLUSIONS-this is the first study to report
on the effect of UV-free blue light therapy on
allergic skin disease in newborns. Blue light
therapy in newborns may be a novel method
to efficiently prevent allergic skin disease for
at least 5 years.
 REFERENCES
1) IADVL, Textbook of Dermatology. John Wiley
& Sons; 2013.
2) Paller A, Mancini A. Hurwitz clinical pediatric
dermatology. Edinburg : Elsevier; 2016.
3) Ku M. Neonatal Phototherapy: A Novel
Therapy to Prevent Allergic Skin Disease for
At Least 5 Years. Neonatology.
2018;114(3):235-241.
THANK YOU