Vesicles and Pustules in the Newborn

Vesicles and Pustules
in the
Newborn
Julian Trevino, M.D.
Associate Professor
Boonshoft School of Medicine
Department of Dermatology
Vesiculobullous Diseases
Non-Infectious Etiology
Erythema toxicum neonatorum
Transient neonatal pustular melanosis
Miliaria crystallina and rubra
Acropustulosis of infancy
Neonatal cephalic pustulosis (neonatal “acne”)
Eosinophilic pustular folliculits
Incontinentia pigmenti
Neonatal herpes gestationis
Neonatal pemphigus
Epidermolysis bullosa
Congenital self self-healing healing reticulohistiocytosis
Erythema toxicum neonatorum
INCIDENCE
20 20-60% 60% of term infants
Less Less frequently in preterm neonates ~5%
Vesicles and Pustules in the
Newborn
Represent Represent wide spectrum of disorders
Several conditions presenting with these findings are truly life-
threatening
Many conditions with these findings are innocuous and self self-limited limited
All All newborns and infants with vesicles and
pustules should be evaluated with:
Thorough history and physical exam
Appropriate laboratory evaluation(s)
Vesiculobullous Diseases
Infectious Etiology
Scabies Scabies
Neonatal Neonatal candidiasis
Staphylococcal Staphylococcal scalded skin syndrome
Herpes Herpes simplex
Congenital Congenital varicella
Congenital Congenital syphilis
Erythema toxicum neonatorum
DESCRIPTION
Types of lesions: erythematous macules, wheals, papules
and pustules
Sites of predilection - face, trunk, proximal arms and
buttocks
Palms Palms and soles almost never affected (due to lack of
pilosebaceous units)

Erythema toxicum neonatorum Erythema toxicum neonatorum
Erythema toxicum neonatorum
COURSE
Most Most begin during second 24 hours of life
Rarely present at birth
May May begin any time from birth to 2 weeks
Exacerbations Exacerbations and remissions occur during first
few weeks of life
Erythema toxicum neonatorum
PROGNOSIS and TREATMENT
Self Self-limiting limiting
Requires Requires no treatment
Reassure Reassure parents as to benign/noninfectious
nature of condition
Unknown Unknown
ETIOLOGY
Has been postulated to be hypersensitivity reaction based on
eosinophilic response
Erythema toxicum neonatorum
DIAGNOSIS
Usually based on clinical appearance of the rash
in an otherwise healthy healthy term term infant
infant
Atypical cases:
Scraping of pustules stained with Wright’s stain demonstrate
large number of eosinophils
Peripheral eosinophilia in 15% of cases
Transient Neonatal Pustular Melanosis (TNPM)
INCIDENCE
2 2 to 5% of term black newborns
0.6% 0.6% of term Caucasian newborns
Equal Equal numbers of boys and girls affected

TNPM
DESCRIPTION
Pustules or pigmented macules, with/without a
surrounding di collarette ll tt of f scale l present t singly i l or in i
combination
Located on forehead, chin, neck, back, hands and
feet, including palms and soles
TNPM
Unknown Unknown
TNPM
ETIOLOGY
DIAGNOSIS
Usually made clinically based on lesion morphology,
time time of of onset, onset and and absence absence of of other other findings
findings
Gram stain - demonstrates neutrophils, rare
eosinophils and absence of bacteria
Wright and Giemsa stain - demonstrates
neutrophils and rare eosinophils
TNPM
TNPM
COURSE
Lesions present at birth and progress to a brownish crust
or rupture l leaving i a fi fine white hi collarette ll of f scale l
Found in clusters or individually
New lesions usually do not appear after birth
Resolves in 24 to 48 hours
TNPM
PROGNOSIS and TREATMENT
Skin Skin findings are not correlated with maternal
infection or neonatal infection
Prognosis Prognosis is excellent with self self-resolution; resolution;
however, hyperpigmented macules may last for
several weeks to months before resolving
Treatment Treatment is non non-essential essential

Miliaria
INCIDENCE
A common dermatosis of the neonate and infant
In warm climates, may be present in up to 15% of
newborns
Two types of miliaria occur in the newborn period -- --
milaria rubra (‘prickly heat”) and crystallina; miliaria rubra
is the most frequently seen
Equal among sexes and races
Miliaria
Miliaria Miliaria
Miliaria
COURSE
Miliaria Miliaria crystallina is occasionally present at birth
Mili Miliaria Mili Miliaria i rubra b more common after f first fi week k of f life lif
DESCRIPTION
Vesicles, pustules or papules in crops
Occurs on the face, trunk and interiginous areas
Usually presents in term and pre pre-term term neonates greater
than ten days old
Infrequently miliaria crystallina presents at birth;
miliaria rubra more common after first week of life
ETIOLOGY
Follows excessive warming in incubator, fever,
occlusive l i dressings, d i or i inappropriately i l warm clothing l hi
Obstruction of the eccrine duct, followed by leakage
of the eccrine sweat into the skin
Extracellular polysaccharide produced by some strains
of Staph epidermidis may obstruct sweat delivery
Miliaria
DIAGNOSIS
Usually based on lesion location, time of onset, and
history of excessive warming
In cases where diagnosis is uncertain a skin biopsy can
be performed

Miliaria
PROGNOSIS and TREATMENT
Resolves spontaneously, but may have recurrences with
rubra
The lesions resolve in 1 to 3 days with shedding of
keratinous plugs
Treatment involves cool baths and removal of excess
clothing
Acropustulosis of infancy
DESCRIPTION
Intensely pruritic vesicles and/or pustules on palms
and soles, dorsa of hands and feet, sides of fingers g
and toes, ankles, wrists, and occasionally the chest,
back, and abdomen
More common form occurs following scabies
infestation
Usually follows scabies that has been severe or prolonged
in duration
Acropustulosis of infancy
Unknown Unknown
ETIOLOGY
Acropustulosis of Infancy
INCIDENCE
Seen in less than 1% of newborns
I Increased di in Af African African-American i A AAmerican i males l
Association with atopy in some patients and families
Acropustulosis of infancy
Acropustulosis of infancy
COURSE
Lesions Lesions may be present at birth, but more often
d develop l i in the h fi first weeks k or months h of f life lif
The The lesions appear in crops every 2 to 4 weeks;
individual lesions last 55-10
10 days; course may last
1-2 2 years

Acropustulosis of infancy
DIAGNOSIS
Must differentiate from scabies
Gi Giemsa, W Wright i h and d G Gram stains i
Reveal numerous neutrophils, and occasional eosinophils
Bacteria, scabies mites/eggs/feces are absent
KOH - negative for hyphae
Neonatal cephalic pustulosis (neonatal “acne”)
INCIDENCE
May May be seen in up to 20% of newborns
Acropustulosis of infancy
PROGNOSIS and TREATMENT
Usually remits spontaneously within 1 to 2 years
Symptomatic treatment includes ld systemic
antihistamines and potent topical steroids
Severe disease may be treated with Dapsone 1-2 1 2
mg/kg/day (requires laboratory evaluation for G-6- G
PD deficiency and frequent monitoring)
Neonatal cephalic pustulosis
DESCRIPTION
Papulopsutular Papulopsutular facial eruption usually
concentrated on cheeks; also may involve
forehead, chin, eyelids, neck, upper chest
and scalp
Comedones Comedones are absent
Neonatal cephalic pustulosis Neonatal cephalic pustulosis
ETIOLOGY
Likely related to stimulation of sebaceous glands by
maternal androgens androgens or or transient transient adrenal adrenal and and gonadal
gonadal
androgen production
Several authors have proposed Malassezia furfur and M.
sympoidalis as causes of this condition

Neonatal cephalic pustulosis
COURSE
May May be present at birth
Mean Mean age of onset is 22-3
3 weeks
Condition Condition remits spontaneously after several
weeks
Neonatal cephalic pustulosis
TREATMENT
Topical Topical imidazole creams (e.g.,
ketoconazole)
k kketoconazole) l )
Low Low-potency potency topical steroids
Condition Condition remits spontaneously after
several weeks
Incontinentia Pigmenti
Four Four Stages
DESCRIPTION
Vesicular - erythematous macules, papules, vesicles and bullae
in a linear arrangement following the lines of Blaschko on extremities,
trunk and scalp
Verrucous - streaks of hyperkeratotic papules and pustules
Hyperpigmentation - hyperpigmented macules and patches along
Blaschko’s lines
Hypopigmentation - hypopigmentation of previously
hyperpigmented areas,with or without follicular atrophy
Neonatal cephalic pustulosis
DIAGNOSIS
Usually Usually made on clinical presentation
Giemsa Giemsa-stained stained smears demonstrate fungal spores
as well as neutrophils
Incontinentia Pigmenti
INCIDENCE
Over Over 700 cases reported
97% 97% females due to XX-linked
linked dominant
inheritance
Incontinentia Pigmenti- vesicular stage

Incontinentia Pigmenti- hyperpigmented stage Incontinentia Pigmenti- hypopigmented stage
Incontinentia Pigmenti
ADDITIONAL FINDINGS
Hair - scarring alopecia in 30%
Nails - dystrophic dystrophic changes changes in in 5 5 to to 10 10 %
%
Teeth - anodontia, peg/conical teeth in 66%
Eyes - strabismus, cataracts, optic atrophy, retinal vascular
changes and retrolental mass in 25 to 35 %
CNS - seizures, mental retardation and spastic paralysis in
30%
Hair
Nails
Teeth
Eyes
CNS
Incontinentia Pigmenti
ETIOLOGY
X-linked linked dominant genodermatosis localized to
gene l locus Xp11.21 X 11 21 or possibly ibl the h Xq28 X 28 region i
NEMO NEMO gene (NFKB essential modulator) defect
Incontinentia Pigmenti
Incontinentia Pigmenti
COURSE
Skin Skin lesions present at birth in 50%; occur within 2
weeks in in 90% 90% of of cases
cases
Vesicular Vesicular - birth to 2 weeks
Verrucous Verrucous - 2 to 6 weeks
Hyperpigmentation
Hyperpigmentation - 3 to 6 months
Hypopigmentation
Hypopigmentation - 2nd to 3rd decades

Incontinentia Pigmenti
DIAGNOSIS
Clinical Clinical and histologic correlation
Detailed Detailed family history and complete skin exam of
mother and female siblings
Incontinentia Pigmenti
PROGNOSIS and TREATMENT
Normal life span
C Complete l physical h i l exam
Ophthalmology exam upon diagnosis
Dental exam by 1 year
Neurology exam upon diagnosis
Genetic counseling for family