Vernix, derived from the same root as varnish, is the whitish-gray covering on newborn skin and is composed of degenerated fetal epidermis and sebaceous secretions.
AGE Newborns.
GENDER M = F.
PREVALENCE Seen in all infants.
The vernix caseosa is thought to play a protective role for the newborn skin with both water-barrier and antimicrobial properties.
TYPE OF LESION Adherent cheesy material which dries and desquamates after birth (Fig. 1-1).
COLOR Gray-to-white.
DISTRIBUTION Generalized.
The vernix caseosa is generally very distinctive but must be differentiated from other membranous coverings such as collodion baby and harlequin fetus. Both of these are much thicker, more rigid, and more dry.
In an otherwise healthy newborn, the vernix caseosa will fall off in 1 to 2 weeks.
No treatment is necessary. Much of the vernix caseosa is usually wiped from the skin at birth. The rest of the vernix is shed over the first few weeks of life.
Current newborn skin care recommendations are as follows:
Full immersion baths are not recommended until the umbilical stump is fully healed and detached.
At birth, blood and meconium can be gently removed with warm water and cotton balls.
Umbilical cord care and/or circumcision varies from hospital to hospital. Several methods include simply maintaining a dry cord environment, local application of alcohol (alcohol wipes), topical antibiotic (bacitracin, Polysporin, or neosporin), or silver sulfadiazine cream (Silvadene) to the area(s) with each diaper change. The umbilical cord typically falls off in 7 to 14 days.
Until the umbilical and/or circumcision sites are healed, spot cleaning the baby with cotton balls and warm water is recommended. After the open sites have healed, the baby can be gently immersed in lukewarm water and rinsed from head to toe.
Avoiding perfumed soaps and bubble baths is best. Fragrance-free, soap-free cleansers are the least irritating. Such cleansers should be used only on dirty areas and rinsed off immediately.
After bathing, newborn skin should be patted dry (not rubbed). The vernix caseosa may still be present and adherent for several weeks. Topical moisturizers are usually not recommended.
A physiologic red–blue reticulated mottling of the skin of newborn infants. It is seen as an immature physiologic response to cold with resultant dilatation of capillaries and small venules. Skin findings usually disappear with rewarming and the phenomenon resolves as the child gets older.
INSIGHT 
While cutis marmorata is essentially always normal, its analog in adults, livedo reticularis, can be associated with connective tissue disease and vasculopathies.
AGE Onset during first 2 to 4 weeks of life; associated with cold exposure.
GENDER M = F.
PREVALENCE More prevalent in premature infants.
Thought to be owing to the immaturity of the autonomic nervous system of newborns. Physiologically normal and resolves as child gets older.
Reticulated mottling of the skin resolves with warming.
TYPE Reticulated mottling (Fig. 1-2).
COLOR Reddish-blue.
DISTRIBUTION Diffuse, symmetric involvement of the trunk and extremities.
Cutis marmorata is benign and self-limited. It can be confused with cutis marmorata telangiectatica congenita (CMTC), a more severe condition that can also present as reticulated vascular changes at birth which do not ameliorate with warming the infant. CMTC is a rare, chronic, relapsing, severe form of vascular disease that can lead to permanent scarring skin changes.
Recurrence is unusual after 1 month of age. Persistence beyond neonatal period is a possible marker for trisomy 18, Down syndrome, Cornelia de Lange syndrome, hypothyroidism, or CMTC and children with such persistent presentations should be evaluated for additional workup.
Usually self-resolving.
Neonatal hair at birth is actively growing in the anagen phase, but within the first few days of life converts to telogen (the rest period before shedding hair). Consequently, there is normally significant hair shedding during the first 3 to 4 months of life.
INSIGHT 
Parents may complain that “back to sleep” is the cause of hair loss in their child; the sleep position only accentuates the normal loss and is not the cause.
SYNONYM Telogen effluvium of the newborn.
AGE Newborns, can be seen at 3 to 4 months of age.
GENDER M = F.
PREVALENCE Affects all infants to some degree.
There are three stages in the hair life cycle:
Anagen (the active growing phase that typically lasts from 2 to 6 years).
Catagen (a short-partial degeneration phase that lasts from 10 to 14 days).
Telogen (resting and shedding phase that lasts from 3 to 4 months).
At any given time in a normal scalp, approximately 89% of the hair are in anagen phase, 1% are in catagen phase, and 10% are in telogen phase. Neonatal hair loss occurs because most of the anagen hair at birth simultaneously converts to telogen phase in the first few days of life, resulting in whole-scalp shedding of the birth hair in 3 to 4 months.
During the first 3 to 6 months of life, there will be physiologic shedding of the newborn hair.
In some cases, the growth of new hair balances the shedding hair and the process is almost undetectable.
TYPE OF LESION Nonscarring alopecia (Fig. 1-3).
DISTRIBUTION Diffuse involving the entire scalp.
Neonatal hair loss is a normal physiologic process that is diagnosed clinically by history and physical examination. The alopecia may be accentuated on the occipital scalp because of friction and pressure from sleeping on the back. If associated with significant crusting, scale, or inflammation, other causes of hair loss should be excluded such as seborrheic dermatitis (cradle cap) and tinea capitis.
In an otherwise healthy newborn, the hair loss self-resolves by 6 to 12 months of age.
No treatment is necessary. The parents should be reassured that neonatal hair loss is a normal physiologic process and that the hair will grow back by 6 to 12 months of age without treatment. If hair regrowth does not occur or is irregular, structural disorders of the hair shaft, vitamin deficiencies, mineral deficiencies, and other processes such as alopecia areata should be ruled out.
Miliaria is a common neonatal dermatosis resulting from sweat retention caused by incomplete differentiation of the epidermis and its appendages. Obstruction and rupture of epidermal sweat ducts is manifested by a vesicular eruption.
INSIGHT 
In older children and adults, miliaria rubra is the most common form, usually seen in areas of moist occlusion, such as on the back of a bedridden patient with fever.
SYNONYMS Prickly heat, heat rash.
AGE Newborn.
GENDER M = F.
INCIDENCE Greatest in the first few weeks of life.
PREVALENCE Virtually, all infants develop miliaria. More common in warmer climates with greater proclivity for sweating.
ETIOLOGY Immature appendages and keratin plugging of eccrine duct lead to vesicular eruption.
Incomplete differentiation of the epidermis and its appendages at birth leads to keratinous plugging of eccrine ducts and subsequent leakage of eccrine sweat into the surrounding tissue. Staphylococci on the skin may play a role in the occlusion process as well.
TYPE Superficial pinpoint clear vesicles (Fig. 1-4). No surrounding inflammation.
COLOR Skin-colored, pink.
DISTRIBUTION Generalized in crops.
SITES OF PREDILECTION Intertriginous areas, commonly neck and axillae, or clothing- covered truncal areas.
TYPE Pinpoint papules/vesicles.
COLOR Erythematous.
SITES OF PREDILECTION Covered parts of the skin, forehead, upper trunk, volar aspects of the arms, and body folds.
The diagnosis of miliaria is made based on observation of characteristic lesions. Vesicles may be ruptured with a fine needle, yielding clear, entrapped sweat; infectious organisms are NOT present. Miliaria rubra—and particularly miliaria pustulosa (comprising pustular lesions)—requires close inspection to ascertain its nonfollicular nature to distinguish it from folliculitis. Miliaria can also be confused with candidiasis and acne.
In miliaria crystallina, vesicles are often found superficially in the stratum corneum and serial sectioning demonstrates direct communication with ruptured sweat ducts. Miliaria rubra histologically demonstrates degrees of spongiosis and vesicle formation within the epidermal sweat duct.
PREVENTION Avoid excessive heat and humidity. Lightweight and/or absorbent clothing, cool baths, and air conditioning help prevent sweat retention.
TREATMENT Preventative measures only for newborns; in older patients, cool moist dressings, antibacterial cleansers, and cream-based emollients may speed healing.
Multiple 1- to 2-mm milky-white/yellow superficial tiny cysts seen over the forehead, cheeks, and nose of infants. They may be present in the oral cavity (Epstein’s pearls).
INSIGHT 
So-called secondary milia (milia after trauma to the skin) can be seen in patients with blistering disorders such as epidermolysis bullosa.
AGE All ages, especially newborns.
GENDER M = F.
PREVALENCE Up to 40% of infants have milia on the skin, up to 85% of infants have the intraoral counterpart (Epstein’s pearls) on the palate.
ETIOLOGY May be related to trauma to the skin surface during delivery.
Milia and Epstein’s pearls are caused by the cystic retention of keratin in the superficial epidermis.
TYPE Few to numerous pinpoint white papules (Fig. 1-5).
SIZE 1 to 2 mm.
COLOR Yellow to pearly white.
DISTRIBUTION Forehead, nose, cheeks, gingiva, midline palate (Epstein’s pearls), rarely on the penis, and at sites of trauma.
Milia must be differentiated from molluscum contagiosum and sebaceous hyperplasia.
Molluscum contagiosum does not typically appear in the immediate neonatal period and is characterized by dome-shaped papules with central umbilication. Sebaceous hyperplasia is usually more yellow than white in color and, on close inspection, is found to be composed of tiny aggregates of micropapules with central umbilication. Epstein’s pearls can be differentiated from intraoral mucinous cysts by their typical midline palate location and spontaneous resolution.
DERMATOPATHOLOGY Superficial, tiny epithelial cysts containing keratin and developing in connection with the pilosebaceous follicle.
Milia and Epstein’s pearls should spontaneously exfoliate during the first few weeks of life. Unusually, persistent milia or widespread milia can be seen in conjunction with more severe developmental problems, namely, oral-facial-digital syndrome, steatocystoma multiplex, and hereditary trichodysplasia.
No treatment is necessary. Cosmetically, lesions may be incised and expressed. For long-standing or persistent lesions in older children, topical retinoids may be another useful treatment option.
Acne neonatorum is a benign, self-limited, acneiform eruption that develops within the first 30 days of life.
INSIGHT 
In severe cases that do not resolve, evaluation for underlying androgen excess is warranted.
SYNONYMS Transient cephalic neonatal pustulosis, neonatal cephalic pustulosis.
AGE Rare at birth, peaks between the age of 2 and 4 weeks of life.
GENDER M = F.
PREVALENCE Up to 50% of infants.
Some, perhaps most, of these cases are thought to be related to Malassezia yeasts on the skin. Transient increases in circulatory androgens may also contribute to neonatal acne.
Multiple discrete papules develop between the age of 2 and 4 weeks of life, evolve into pustules, and spontaneously resolve.
TYPE Inflammatory papules and pustules; comedones are rare (Fig. 1-6).
COLOR Erythematous.
DISTRIBUTION Face, scalp >> chest, back, and groin.
Erythema toxicum, candidiasis, and staphylococcal infection can be considered.
DERMATOPATHOLOGY Increased number of sebaceous glands and keratin-plugged pilosebaceous orifices lead to rupturing and neutrophilic or granulomatous inflammation.
Neonatal acne may persist up to 8 months of age. There is some suggestion that infants with extensive neonatal acne may experience severe acne as adults, though data are conflicting.
Neonatal acne typically resolves spontaneously. For severe involvement, 2% ketoconazole cream, 2.5% benzoyl peroxide gel applied twice daily, or a mild 1% hydrocortisone cream may be used.
Benign transient, blotchy erythema with central vesiculation is seen in newborns.
AGE Newborns.
GENDER M = F.
PREVALENCE Reports range from 4.5% to 70% of term infants. Less common in premature infants. May be slightly more common in infants delivered via cesarean section or from multiparous births.
The cause of erythema toxicum is unknown. The eosinophil response is suggestive of a hypersensitivity reaction, but specific allergens have not been identified.
Macular erythema with central vesicles and pustules appear between 24 and 48 hours of life.
TYPE Blotchy erythematous macules 2 to 3 cm in diameter with a central 1- to 4-mm central papule, vesicle, or pustule (Fig. 1-7).
COLOR Erythematous.
DISTRIBUTION Chest, back, face, and proximal extremities, sparing the palms and soles.
DIAGNOSIS Wright stain of a vesicle will reveal a predominance of eosinophils. Gram stain will be negative for bacteria.
DIFFERENTIAL DIAGNOSIS Erythema toxicum must be differentiated from miliaria rubra and transient neonatal pustular melanosis. The lesions of erythema toxicum are usually larger than those of miliaria rubra and have wider erythematous halos surrounding them. Transient neonatal pustular melanosis has a predominance of neutrophils rather than eosinophils in the vesicles and typically heals with residual pigmentation. Bacterial and fungal culture of erythema toxicum lesions will be negative differentiating it from neonatal bacterial infections and congenital candidiasis. More worrisome considerations include herpes infection and Langerhans cell histiocytosis. These entities may require virologic testing and skin biopsy for definitive diagnosis and must not be overlooked.
WRIGHT STAIN A smear of a vesicle with Wright stain reveals numerous eosinophils.
GRAM STAIN Negative.
DERMATOPATHOLOGY Intraepidermal vesicle filled with eosinophils.
HEMATOLOGIC EXAMINATION Peripheral eosinophilia of up to 20% may be seen in some cases.
Lesions may occur from birth to the 10th day of life and individual lesions clear spontaneously within 5 days. All lesions resolve by 2 weeks.
No treatment is necessary.
A benign and self-limited condition characterized by blotchy erythema and superficial vesicopustules of the newborn that heal with residual pigmentation.
INSIGHT 
Many times, particularly in postterm infants, no pustules or vesicles remain at birth and only pigmented macules are found.
AGE Newborns.
GENDER M = F.
RACE More common in black infants.
PREVALENCE 0.2% to 4% of newborns.
The pathophysiology is unknown.
Idiopathic, superficial, sterile vesicles and pustules that are present at birth rupture in 24 to 48 hours and heal with pigmented macules that slowly fade over several months.
TYPE Tiny vesicles, pustules (Fig. 1-8), or ruptured lesions with a collarette of scale. There is generally minimal or no surrounding erythema.
COLOR Hyperpigmented macules may develop at the site of resolving vesicles and pustules.
DISTRIBUTION Clusters on face, trunk, and proximal extremities, rarely palms and soles may be involved.
DIAGNOSIS Wright stain of a vesicle will reveal a predominance of neutrophils. Gram stain will be negative for bacteria.
DIFFERENTIAL DIAGNOSIS Includes erythema toxicum neonatorum, staphylococcal and other bacterial infections, candidiasis, herpes, and miliaria.
WRIGHT STAIN A smear of a vesicle with Wright stain reveals numerous neutrophils and an occasional eosinophil.
GRAM STAIN Negative.
DERMATOPATHOLOGY Vesicular lesions show intraepidermal vesicles filled with neutrophils. Macular hyperpigmented lesions show mild hyperkeratosis and basilar hyperpigmentation.
The vesicles and pustules usually disappear by 5 days of age and the pigmented macules fade over 3 to 6 months.
No treatment is necessary.
A benign vesicular and pustular pruritic eruption that begins in infancy and often has a waxing and waning course with recurrences every few months over the first years of life. Children with a prior exposure to scabies may be at a higher risk.
AGE Usually starts in first year of life; resolves over 2 years.
GENDER Male = Female.
RACE No clear racial predilection; Black race reported as having a higher incidence in some studies.
PREVALENCE Uncommon.
The exact pathophysiology of infantile acropustulosis is not known. One postulated mechanism is a persistent localized allergic hypersensitivity or inflammatory response to a foreign antigen. Reports suggest an increased prevalence of the eruption in children with a prior history of scabies, but no conclusive pathophysiologic link has been demonstrated. Other etiologic theories include an atypical infectious cause.
Lesions typically present during the first year of life. The skin eruption consists of crops of erythematous macules that evolve into vesicles and pustules predominantly on the palms and soles, as well as the dorsal hands and feet. The eruption is pruritic and infants may exhibit discomfort and irritability associated with the eruption. The lesions may spontaneously heal after 1 to 2 weeks and return periodically.
TYPE Vesicles, pustules.
COLOR Pink to whitish; tan brown residual hyperpigmentation after resolution (Fig. 1-9).
DISTRIBUTION Palms, soles > dorsal feet, dorsal hands, extremities.
DIAGNOSIS Clinical history and physical findings with vesicles and pustules confined to the feet and hands are sufficient to make the diagnosis. Skin scrapings of vesicles should be performed to rule out scabies infestation. Gram stain and KOH preparations should be negative in acropustulosis.
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