OVERVIEW: What every practitioner needs to know
Are you sure your patient has a transient neonatal skin lesion? What are the typical findings for this disease?
Newborns can present with several benign transient skin lesions and eruptions. They are diagnosed by their characteristic clinical appearance.
A sucking blister presents as a solitary, non-inflammatory, tense bulla without surrounding erythema or induration. It is most commonly seen on the hand, finger, or distal arm, reflecting anatomic locations most accessible to the fetal mouth. The blister may rupture in utero, leaving an erosion that is noted at birth.
Sebaceous gland hyperplasia is characterized by numerous tiny yellow-white papules at follicular openings of the face. They are most common in areas of numerous sebaceous glands, including the nose, forehead, and chin.
Milia present as discrete, shiny white, dome-shaped or slightly exophytic papules on the face. They may extrude central keratin. Like sebaceous gland hyperplasia, they are most common in areas of high sebaceous gland density.
Miliaria, to be distinguished from milia, presents as numerous discrete papules or vesicles, most common on the trunk of neonates. Miliaria crystallina (Figure 1) is characterized by small clear vesicles without surrounding erythema or induration. These superficial vesicles are easily ruptured. Lesions of miliaria rubra (Figure 2) are slightly larger and deeper, and have characteristic associated erythema.
Erythema toxicum usually presents on day 2 of life as discrete red papules, pustules, or papulovesicles with surrounding erythema and faintly edematous wheal. Any cutaneous site can be involved, although the face, trunk and proximal extremities are favored. Crops of lesions wax and wane until complete resolution.
Transient neonatal pustular dermatosis (Figure 3) is present at birth, and is characterized by solitary or aggregated pustules or vesicles that progress to crusty or scaly hyperpigmented macules or patches. Scaling and hypermelanosis are the most common findings. The hyperpigmentation is most notable in patients with dark skin, and dark skinned patients are most commonly affected. New lesions do not develop after birth, but the infant may be born with any stage of lesion, reflecting the in utero development of this eruption.
Neonatal acne/cephalic pustulosis (Figure 4) is generally not present at birth, but develops in the first weeks of life. It is characterized by numerous discrete erythematous papules and pustules in seborrheic areas (face, scalp, neck, upper chest). Comedones characteristic of classic acne may be present, but are rare.
What other disease/condition shares some of these symptoms?
Other non-inflammatory tense blisters can mimic sucking blister. Epidermolysis bullosa, perinatal trauma, bullous mastocytoma, thermal burn, and bullous impetigo should be excluded.
Sebaceous gland hyperplasia and milia may be difficult to distinguish. Milia are usually larger with a central white keratinaceous core.
Miliaria, erythema toxicum, transient neonatal pustular dermatosis, and neonatal acne share clinical features. Infectious causes of papular, pustular, or vesicular eruptions, such as herpes infection and candidiasis, can be considered as well.
What caused this disease to develop at this time?
Sucking blisters develop as a result of vigorous fetal sucking of the skin in utero.
Sebaceous gland hyperplasia is a manifestation of maternal androgen stimulation of neonatal sebaceous glands.
Milia represent small epidermal inclusion cysts of the pilosebaceous unit. They may also develop secondary to trauma, occlusion of the sweat duct, or in cutaneous diseases such as epidermolysis bullosa and pachyonychia congenita.
Miliaria occur as a result of eccrine sweat duct occlusion, with subsequent duct rupture and extrusion of sweat into the skin. When the occlusion is present within the stratum corneum, superficial vesicles (miliaria crystallina) result. When the obstruction is intra-epidermal, deeper inflammatory lesions (miliaria rubra) occur.
The cause of erythema toxicum and transient neonatal pustular dermatosis are unknown. No pre- or perinatal exposures or other factors have been identified.
The cause of neonatal acne/cephalic pustulosis is somewhat controversial. Many authors believe overgrowth of
Malassezia yeast species, perhaps in response to maternal androgens, is causative.
What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
Laboratory studies are generally not indicated.
In rare cases where a definitive diagnosis cannot be made clinically, erythema toxicum and transient neonatal pustular dermatosis can be distinguished by microscopic examination of pustule fluid stained with Wright or Giemsa stain.
Erythema toxicum will show numerous eosinophils, while transient neonatal pustular dermatosis demonstrates a neutrophilic infiltrate.
Neonatal acne lesions similarly stained may show small fungal yeast forms or spores.
Would imaging studies be helpful? If so, which ones?
Imaging studies are not indicated.
If you are able to confirm that the patient has a transient neonatal skin lesion, what treatment should be initiated?
No treatment is indicated for these cutaneous eruptions, as all are self-limited. Some cases of neonatal acne/cephalic pustulosis may respond to topical imidizole antifungal creams.
What are the adverse effects associated with each treatment option?
What are the possible outcomes of transient neonatal skin lesions?
Sucking blisters, sebaceous hyperplasia, milia, miliaria and neonatal acne resolve in the first few weeks of life with no treatment.
Erythema toxicum and transient neonatal pustular dermatosis resolve more quickly after birth, usually in several days.
What causes this disease and how frequent is it?
Sucking blisters are caused by trauma to the skin from fetal sucking. They are uncommon.
Sebaceous gland hyperplasia and milia are caused by androgen stimulation of neonatal sebaceous glands. Both are common.
Miliaria is caused by transient obstruction and rupture of superfical eccrine sweat ducts, and is exacerbated by heat and occlusion of the skin. It is relatively uncommon.
Erythema toxicum and transient neonatoal pustular dermatosis are very common, occurring in up to 10% and 4% of newborns respectively. The cause is unknown; maternal factors and exposures during pregnancy and the post-partum period do not appear to play a role. These eruptions affect males and females equally. Transient neonatal pustular dermatosis is more common in darker-skinned newborns.
Neonatal acne/cephalic pustulosis may be caused by
Malassezia infection, although conclusive studies are lacking.
There does not appear to be a genetic or familial predisposition to development of these transient neonatal eruptions.
How do these pathogens/genes/exposures cause the disease?
Other clinical manifestations that might help with diagnosis and management
What complications might you expect from the disease or treatment of the disease?
Complications are rare, and usually result from over-aggressive or unnecessary treatment of these benign conditions. Attempts at treatment are usually prompted by concern for cosmesis, or inappropriate diagnosis such as infection.
Are additional laboratory studies available; even some that are not widely available?
How can transient neonatal skin lesions be prevented?
There is no known preventive therapy for these conditions.
What is the evidence?
Alper, JC, Holmes, LB. “The incidence and significance of birthmarks in a cohort of 4,641 newborns”. Pediatr Dermatol. vol. 1. 1983. pp. 58-68. (This reference describes the incidence of birthmarks in a very large study population, and gives important information about the epidemiology of birthmarks.)
Eichenfield, L, Larralde, M, Schachner, LA, Hansen, RC. “Neonatal skin and skin disorders”. Pediatric dermatology. 2003. (This reference is a comprehensive textbook review of neonatal skin disorders.)
Lucky, AW, Eichenfield, LF, Frieden, IJ, Esterly, NB. “Transient benign cutaneous lesions in the newborn”. 2001. (This reference is a comprehensive textbook review of newborn skin lesions.)
Ongoing controversies regarding etiology, diagnosis, treatment
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- OVERVIEW: What every practitioner needs to know
- Are you sure your patient has a transient neonatal skin lesion? What are the typical findings for this disease?
- What other disease/condition shares some of these symptoms?
- What caused this disease to develop at this time?
- What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
- Would imaging studies be helpful? If so, which ones?
- If you are able to confirm that the patient has a transient neonatal skin lesion, what treatment should be initiated?
- What are the adverse effects associated with each treatment option?
- What are the possible outcomes of transient neonatal skin lesions?
- What causes this disease and how frequent is it?
- How do these pathogens/genes/exposures cause the disease?
- Other clinical manifestations that might help with diagnosis and management
- What complications might you expect from the disease or treatment of the disease?
- Are additional laboratory studies available; even some that are not widely available?
- How can transient neonatal skin lesions be prevented?
- What is the evidence?
- Ongoing controversies regarding etiology, diagnosis, treatment