Vesicles and Pustules in the
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 reticulohistiocytosis Erythema toxicum neonatorum Vesicles and Pustules in the Newborn Represent 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 Neonatal candidiasis Staphylococcal scalded skin syndrome Herpes simplex Congenital varicella Congenital syphilis Erythema toxicum neonatorum DESCRIPTION INCIDENCE Types 20-60% of term infants 20 Less frequently in preterm neonates ~5% wide spectrum of disorders Several conditions presenting with these findings are truly lifelifethreatening Many conditions with these findings are innocuous and self self--limited of lesions: erythematous macules, wheals, papules and pustules Sites of predilection - face, trunk, proximal arms and buttocks Palms and soles almost never affected (due to lack of pilosebaceous units) Erythema toxicum neonatorum Erythema toxicum neonatorum ETIOLOGY Unknown Has been postulated to be hypersensitivity reaction based on eosinophilic response Erythema toxicum neonatorum Erythema toxicum neonatorum COURSE DIAGNOSIS Usually Most begin during second 24 hours of life Rarely present at birth May begin any time from birth to 2 weeks Exacerbations and remissions occur during first few weeks of life based on clinical appearance of the rash in an otherwise healthy term infant Atypical cases: Scraping of pustules stained with Wright’s stain demonstrate large number of eosinophils Peripheral Erythema toxicum neonatorum eosinophilia in 15% of cases Transient Neonatal Pustular Melanosis (TNPM) PROGNOSIS and TREATMENT INCIDENCE Self Self--limiting Requires no treatment Reassure parents as to benign/noninfectious nature of condition 2 to 5% of term black newborns of term Caucasian newborns Equal numbers of boys and girls affected 0.6% TNPM TNPM DESCRIPTION Pustules or pigmented macules, with/without a surrounding di collarette ll tt off scale l presentt singly i l or in i combination Located on forehead, chin, neck, back, hands and feet, including palms and soles TNPM TNPM ETIOLOGY COURSE Lesions present at birth and progress to a brownish crust or rupture leaving l i a fi fine white hi collarette ll off scale l Found in clusters or individually New lesions usually do not appear after birth Resolves in 24 to 48 hours Unknown TNPM TNPM DIAGNOSIS Usually made clinically based on lesion morphology, time of onset, onset and absence of other findings Gram stain - demonstrates neutrophils, rare eosinophils and absence of bacteria Wright and Giemsa stain - demonstrates neutrophils and rare eosinophils PROGNOSIS and TREATMENT Skin findings are not correlated with maternal infection or neonatal infection Prognosis is excellent with self self--resolution; however, hyperpigmented macules may last for several weeks to months before resolving Treatment is nonnon-essential Miliaria Miliaria DESCRIPTION INCIDENCE Vesicles, Occurs 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 pustules or papules in crops on the face, trunk and interiginous areas Usually presents in term and prepre-term neonates greater than ten days old Infrequently miliaria crystallina presents at birth; miliaria rubra more common after first week of life Miliaria ETIOLOGY Follows excessive warming in incubator, fever, occlusive l i dressings, d i or iinappropriately 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 Miliaria COURSE Miliaria crystallina is occasionally present at birth Miliaria Mili i rubra b more common after f first fi weekk off life lif 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 Acropustulosis of Infancy 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 INCIDENCE Seen in less than 1% of newborns Increased I d iin Af African Africani -American A i males l Association with atopy in some patients and families Acropustulosis of infancy DESCRIPTION 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 Intensely Usually follows scabies that has been severe or prolonged in duration Acropustulosis of infancy ETIOLOGY Unknown Acropustulosis of infancy COURSE may be present at birth, but more often d l iin the develop h fi first weeks k or months h off life lif The lesions appear in crops every 2 to 4 weeks; individual lesions last 55-10 days; course may last 1-2 years Lesions Acropustulosis of infancy DIAGNOSIS Must differentiate from scabies Giemsa, Gi W Wright i h and dG 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 be seen in up to 20% of newborns Acropustulosis of infancy PROGNOSIS and TREATMENT Usually remits spontaneously within 1 to 2 years treatment includes l d systemic antihistamines and potent topical steroids Severe disease may be treated with Dapsone 11- 2 mg/kg/day (requires laboratory evaluation for GG-6PD deficiency and frequent monitoring) Symptomatic Neonatal cephalic pustulosis DESCRIPTION Papulopsutular facial eruption usually concentrated on cheeks; also may involve forehead, chin, eyelids, neck, upper chest and scalp Comedones Neonatal cephalic pustulosis are absent Neonatal cephalic pustulosis ETIOLOGY Likely related to stimulation of sebaceous glands by maternal androgens or transient adrenal and gonadal androgen production Several authors have proposed Malassezia furfur and M. sympoidalis as causes of this condition Neonatal cephalic pustulosis COURSE May be present at birth Mean age of onset is 22-3 weeks Neonatal cephalic pustulosis DIAGNOSIS Usually made on clinical presentation Giemsa Giemsa--stained smears demonstrate fungal spores as well as neutrophils Condition remits spontaneously after several weeks Neonatal cephalic pustulosis TREATMENT Topical imidazole creams (e.g., ketoconazole) k l ) Low Low--potency topical steroids Condition remits spontaneously after several weeks Incontinentia Pigmenti DESCRIPTION Four Stages 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 Incontinentia Pigmenti INCIDENCE Over 700 cases reported 97% females due to XX-linked dominant inheritance Incontinentia Pigmenti- vesicular stage Incontinentia Pigmenti- hyperpigmented stage Incontinentia Pigmenti- hypopigmented stage Incontinentia Pigmenti Incontinentia Pigmenti ADDITIONAL FINDINGS Hair - scarring alopecia in 30% Nails - dystrophic changes in 5 to 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% Incontinentia Pigmenti ETIOLOGY dominant genodermatosis localized to gene locus l Xp11.21 X 11 21 or possibly ibl the h Xq28 X 28 region i NEMO gene (NFKB essential modulator) defect X-linked Incontinentia Pigmenti COURSE Skin lesions present at birth in 50%; occur within 2 weeks in 90% of cases Vesicular - birth to 2 weeks Verrucous - 2 to 6 weeks Hyperpigmentation - 3 to 6 months Hypopigmentation - 2nd to 3rd decades Incontinentia Pigmenti DIAGNOSIS Clinical and histologic correlation Detailed family history and complete skin exam of mother and female siblings Incontinentia Pigmenti PROGNOSIS and TREATMENT Normal life span Complete C l physical h i l exam Ophthalmology exam upon diagnosis Dental exam by 1 year Neurology exam upon diagnosis Genetic counseling for family
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