Transient Cutaneous Alterations of the Newborn

Authors: Catarina Queirós,1 Mafalda Casinhas Santos,2 Rita Pimenta,1 Cristina Tapadinhas,1 Paulo Filipe1,3

1. Serviço de Dermatologia, Hospital de Santa Maria, Centro Hospitalar e Universitário de Lisboa Norte, Lisbon, Portugal 2. Serviço de Pediatria, Hospital de Vila Franca de Xira, Lisbon, Portugal 3. Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal *Correspondence to [email protected]

Disclosure: The authors have declared no conflicts of interest.

Received: 27.06.20

Accepted: 17.12.20

Keywords: Common rashes, cutaneous alterations, newborn, skin.

Citation: EMJ. 2021;6[1]:97-106.

Abstract Neonatal cutaneous alterations are common, usually appearing at birth or during the first few days of life. Most of these conditions are physiological, benign, and transient, arising from a combination of immaturity of the newborn skin with environmental factors. Nonetheless, some of them may eventually be a clue to underlying disorders. Physicians should therefore be aware of these clinical manifestations so that parents can be reassured and, when necessary, complementary investigations can be undertaken.

INTRODUCTION a cause of concern to parents, who need reassurance about its nature.

At birth, the skin of the newborn suddenly comes In this paper, several common cutaneous into contact with the extrauterine world: a dry and alterations observed in newborn skin are 1 aerobic environment. Newborn skin is 40–60% reviewed. In the first part, physiological changes thicker than adult skin, with weaker intercellular are covered, including traumatic, vascular, 2 attachment and decreased production of sweat. pigmentary, and hormonal conditions. In the Newborn skin is therefore more vulnerable, second part, a review of the most common rashes although structurally similar to adult skin, and of the newborn is undertaken. Although not trauma associated with delivery leaves its marks typically apparent during the neonatal period, 3 on it. Moreover, newborn skin must rapidly infantile acropustulosis and eosinophilic pustular adapt and mature to provide protection against are included as these are important in infection, toxins, changes in temperature, and the differential diagnosis of other conditions. transepidermal water loss, which poses an additional stress.1 PHYSIOLOGICAL ALTERATIONS Because of these factors, cutaneous alterations 3 are relatively common in the neonatal period. Vernix Caseosa Most of these conditions are physiological, benign, and transient, thus do not require The vernix caseosa is a protective layer which therapy.4 Nevertheless, they are frequently covers neonatal skin at birth (Figure 1). It is a

Creative Commons Attribution-Non Commercial 4.0 March 2021 • EMJ 97 complex membranous substance comprising easily, leading to linear or round erosions. Lesions 80% water, 10% protein, and 10% lipids, which are present at birth and are located mainly on the include barrier lipids such as ceramides, free forearm, wrist, and hand. Although frequently fatty acids, phospholipids, and cholesterol, partly solitary, blisters can be multiple and bilateral.6 synthesised by fetal sebaceous glands during the Diagnosis of congenital sucking blisters is one last trimester of .5 In its composition of exclusion. The absence of lesions in other there are also shed lanugo hair and desquamated body regions, the timing of onset, and the rapid cells. In utero, the vernix protects neonatal skin resolution of the blisters, in combination with the against amniotic fluid.1 During transition to an otherwise well appearance of the neonate, are extrauterine environment, the vernix has several highly suggestive of this condition.7 Differential important functions including lubrication of diagnosis of sucking blisters includes congenital the birth canal during parturition, prevention or neonatal virus infection, of water loss, and temperature regulation. fetal or neonatal varicella, bullous impetigo, It is also implicated in the development of epidermolysis bullosa, congenital , innate immunity and facilitates reduction of or congenital candidiasis, among other rarer skin pH to the ideal range for optimal skin entities.6 Sucking blisters resolve spontaneously 1,5 function; therefore, the vernix should be left as in days to weeks without sequelae, and therefore undisturbed as possible. Gentle bathing or dry no specific therapy is needed.6 wiping does not significantly disrupt this layer, and should therefore be the procedures of choice Caput Succedaneum and 1 for newborns’ hygiene. Cephalohaematoma

TRAUMATIC LESIONS Caput succedaneum refers to a collection of oedematous fluid above the periosteum, between the outermost layer of the scalp and Sucking Blisters the subcutaneous tissue. It is a common lesion Sucking blisters are estimated to occur in 1:250 seen at birth, and results from the high pressure live births and result from vigorous sucking by exerted on the ’s head by the vaginal walls the infant during fetal life. Clinically, flaccid bullae and uterus as the head passes through the on a noninflamed base are seen, which rupture narrowed cervix during labour.8

Figure 1: Vernix caseosa covering the skin of a newborn.

98 EMJ • March 2021 EMJ Although caput succedaneum may occur mouth and the extremities. It is caused by benign in the absence of risk factors, incidence vasomotor changes that result in peripheral increases in difficult or prolonged labours, with vasoconstriction and increased tissue oxygen premature rupture of the amniotic membranes, extraction, attributed to peripheral arteriole in primigravidae, and in instrument-assisted . Acrocyanosis is a benign condition deliveries. This condition is evident immediately and may persist for 24 to 48 hours. After this after delivery and gradually decreases in period, it may occasionally recur in the context size thereafter.9 On physical examination, it of cold exposure or crying.11 Acrocyanosis must is generally 1–2 cm in depth and has a soft, be distinguished from central cyanosis. This boggy feel with irregular margins. Petechiae, is defined as a dusky appearance of the body purpura, and an ecchymotic appearance may and the mucous membranes and is always 8 be present. concerning beyond the first 10 minutes of life. Cephalohaematoma is a subperiosteal Abnormalities in ventilation, congenital heart accumulation of blood, which occurs abnormalities, and haemoglobinopathies are 11 infrequently, with an incidence of 0.4–2.5% of all amongst the main causes of central cyanosis. live births. It is more common in primigravidae, Cutis Marmorata in with higher percentiles, and following instrument-assisted deliveries or prolonged, Cutis marmorata is a benign entity characterised difficult labour and, for unknown reasons, occurs by the appearance of a reticulated or livedoid twice as often in males as in females. Because purplish mottling of the skin, related to of the slow nature of subperiostial , physiological capillary and venular vasomotion cephalohaematomas are not usually present in the setting of cold exposure.12 Cutis at birth but develop hours or even days after marmorata seems to be associated with lower delivery.9 As the bleeding continues and blood gestational age and birth weight, which may occupies the subperiosteal space, pressure acts be associated with the greater vulnerability of as a tamponade to stop further bleeding. A firm, these neonates, who are therefore more likely enlarged unilateral or bilateral bump covering to present with vasomotor instability.3 This one or more bones of the scalp characterises condition must be distinguished from cutis this lesion. Unlike caput succedaneum, marmorata telangiectatica congenita, which 8 cephalohaematomas do not cross suture lines. is characterised by a fixed vascular change Cephalohaematoma and capput succedaneum associated with subtle dermal atrophy. This must be distinguished from subgaleal entity may be associated with limb length haematomas, which, unlike the former conditions, discrepancy, vascular, osseous, ocular, and can be life-threatening. Neonatal subgaleal neurologic malformations.12 haematomas are usually associated with vacuum extraction deliveries, although they have also Harlequin Colour Change been reported in deliveries without instrument Harlequin colour change presents as erythema 10 use. Observation is the primary treatment in one half (the dependent side) and pallor in for both uncomplicated caput succedaneum the other half of the body, usually lasting for and cephalohaematoma. Resolution of caput several minutes. This condition presents in the succedaneum is generally spontaneous and first 3 weeks of life, commonly between Day 2 occurs within the first few days following birth. A and Day 5.11,12 Although it has been observed in cephalohaematoma may take longer to resolve, neonates after the administration of anaesthetic 8 but most cases do so within 2 to 6 weeks of life. agents and alprostadil, harlequin colour change may also occur in healthy neonates in the VASCULAR PHENOMENON absence of medication. This phenomenon may occur as a result of changes in vascular tone, Acrocyanosis although it still remains unexplained. Harlequin color change is a benign and transient feature; Acrocyanosis is often seen in healthy newborns therefore, no treatment is necessary.13 during the first hours of life and refers to the occurrence of peripheral cyanosis around the

Creative Commons Attribution-Non Commercial 4.0 March 2021 • EMJ 99 Salmon Patch PIGMENTARY CHANGES Salmon patch, also known as naevus flammeus, naevus simplex, or unna naevus, is a common Mongolian Spot congenital capillary malformation that is usually Mongolian spot (MS) is a type of dermal found in the midline.14 It affects approximately melanocytosis, which presents at birth or soon 50% of newborns and is more frequent in thereafter as an ill-defined area of slate gray those born with greater weight, at term or to blue/black pigmentation, usually over the post-term. A slight female predominance has sacrococcygeal or lumbar area. Both sexes are been observed.15 Salmon patches arise from equally affected, and these lesions are more dilations of capillaries within the dermis, which common in newborns of Asian and/or African may result from persistent fetal circulation 16,17 in newborns.4 Clinically, they present as pink descent. MS arise from a defect in melanocyte or red irregular macules, which may become migration. Melanocytes are present in dermis of th confluent Figure( 2A). the embryos at the beginning of the 10 week of gestation, and they migrate to the epidermis Lesions tend to bleach with digital pressure, and between the 11th and the 14th week. After Week 20, are more apparent with crying, apnoeas, fever, no melanocytes are found in the dermis. Failure of and changes in ambient temperature. Salmon this migration results in the appearance of MS.16 patches occurr most frequently on the nape of Clinically, MS are round, oval, or irregular macules. the neck, the eyelids, and the glabella, and are The colour varies from blue to green, grey, black, usually transitory, disappearing during the first or a combination of any of these colours. Lesions 2 years of life. Nearly one-half of those located may be single or multiple, and their size ranges in the nape of the neck and in the sacral region, from <1 cm to >20 cm. Pigmentation is more and a small percentage of those located in the intense at the age of 1 year and gradually fades 14,15 glabellar zone, may persist. Salmon patches thereafter.16,17 MS must be differentiated from need to be distinguished from cutaneous other dermal melanocytoses like naevus of Ota, capillary malformation, formerly referred to as naevus of Ito, Hori naevus, and blue naevus. ‘port wine stain’, a potential marker of Sturge– Weber syndrome. The variant ‘en coup de sabre’ Onset at birth, disappearance with age, absence of congenital morphea is another differential of mucosal involvement, and no progression to diagnosis of this condition. malignancy favour the diagnosis of MS.

A B

Figure 2: Physiological alterations. A) Salmon patch in the upper eyelid of a 1-week-old female. B) Milia overlying the cheek of a 2-week-old newborn.

100 EMJ • March 2021 EMJ MS usually resolve by early childhood, hence, first few weeks of life, and therefore no treatment no treatment is needed if they are located in is required.19,20 the sacral area; nonetheless, it may be required 16 for extrasacral lesions due to cosmetic issues. OTHER PHYSIOLOGICAL LESIONS Although most MS are benign lesions, recent data suggested that MS may be associated with Epstein Pearls and Bohn’s Nodules inborn errors of metabolism such as lysosomal storage diseases. Therefore, extrasacral, Epstein pearls occur in 64–89% of neonates and extensive, persistent, and dark-coloured spots are more common in newborns of Caucasian should be looked upon with suspicion, especially descent. These lesions, also known as palatal in the presence of a consanguineous marriage or microkeratocysts of the newborn, are white- a strong family history of storage disorders.4 yellow cysts usually 1–3 mm in size. They are typically seen on the median palatal mouth raphe Epidermal Hyperpigmentation and represent epithelial tissue trapped during 20 Epidermal pigmentary changes are also the palatal fusion. Similar cysts on the alveolar common in newborns and include linea nigra ridges or in the periphery of the palate are called and hyperpigmentation of the knuckles, genital, Bohn’s nodules. These are keratin cysts derived axilla, or areolar regions. Hyperpigmentation of from the dental lamina, and they do not require the skin over the distal phalanges has also been treatment as they spontaneously resolve over the 20 described, particularly in newborns with higher first few months of life. 18 phototypes. This abnormal pigmentation is Milia Cysts transient and probably represents a response to maternal and placental hormones that enter the Milia cysts are small lesions resulting from newborn circulation. Among these hormones, retention of keratin within the dermis. They affect oestrogen and progesterone have been reported approximately 40–50% of newborns and may to exert a melanocytic stimulating effect, which be present at birth or appear later in infancy.19 is also responsible for the darkening of linea Milia cysts appear as tiny, white, or yellow alba in pregnant females. As these are transient smooth-surfaced 1–2 mm in diameter, and benign changes, no treatment is necessary.2 most commonly located over the cheeks, Abnormal hyperpigmentation may be a sign of forehead, nose, and nasolabial folds (Figure congenital adrenal hyperplasia; however, in this 2B).19,20 Lesions may be few or numerous and are condition, there are usually associated findings frequently grouped, with a tendency towards such as virilised external genitalia. disappearance during the first 3 to 4 weeks of life. The most important differential diagnosis HORMONAL CHANGES of milia cysts is , which tends to be slightly more yellow.20 No therapy hyperplasia is a common is required, as lesions tend to spontaneously physiological phenomenon in newborns, affecting resolve. However, it is important to note that mainly full-term infants.19,20 It is caused by high persistent and widespread milia may be a feature sebum secretion rates reflecting the stimulation of associated syndromes such as basal naevus by placentally transferred maternal , syndrome, Rombo syndrome, Brooke–Spiegler particularly .2,19 Clinically, syndrome, or Type sebaceous hyperplasia is characterised by II, and therefore complementary investigation multiple, yellow to flesh-coloured tiny papules should be conducted in these particular settings. on the nose, cheeks, and chin, where the density of sebaceous glands is highest.19,20 Sometimes the papules can coalesce into plaques without Koilonychia refers to nails with a transverse and/ surrounding erythema. The most important or longitudinal concave central depression. It differential diagnosis of this condition are milia can be hereditary, acquired, or idiopathic. In cysts, which are epidermal inclusion cysts, usually newborns, it is frequently idiopathic, affecting solitary and whiter in colour.20 Sebaceous gland particularly the hallux. In these circumstances, hyperplasia spontaneously resolves within the koilonychia tends to spontaneously regress

Creative Commons Attribution-Non Commercial 4.0 March 2021 • EMJ 101 with growth.21 Nonetheless, it is important to present in various combinations, which include remember that these changes, later in life, erythematous macules, wheals, papules, small may also be a manifestation of inflammatory pustules, and vesicles, usually measuring 1–2 mm. skin diseases such as , , or The eruption usually occurs throughout the body, secondary to systemic alterations, such as iron typically involving the trunk, face, buttocks, and deficiency or endocrine disorders.22 thighs; the palms, soles, and genitals are spared.24 Traumatic Punctate Diagnosis of ETN is usually clinical. A cytologic exam of pustule contents shows more than Punctate leukonychia is a true leukonychia caused 50% eosinophils, with or without a small by alterations or imperfections in the proximal number of neutrophils. Peripheral blood 21 nail matrix. As the nail plate has a very smooth eosinophilia up to 15% may frequently coexist. surface in newborns, these lesions can be easily Histopathologic examination is rarely necessary, 23 observed. No specific treatment is required, as but when performed it shows superficial dermal 21 they tend to resolve with nail growth. oedema with a mild diffuse and perivascular Beau’s Lines eosinophilic infiltrate. Pustules are subcorneal or intraepidermal and are associated with the Beau’s lines of the fingernails appear at 4 weeks pilosebaceous orifice in most cases.24 The of life in 92% of newborns and disappear with differential diagnoses of ETN include sepsis, growth, usually before 14 weeks.21 They result staphylococcal folliculitis, , congenital from intrauterine distress or physiological candidiasis, neonatorum, transient neonatal alterations during birth that cause mild trauma to pustular melanosis, infantile acropustulosis, the proximal nail matrix, with transiently reduced neonatal varicella, and occasionally nail growth.23 Clinically, one can observe linear incontinentia pigmenti.24 transverse nail plate surface depressions, which require no particular approach.21 It is important to educate parents about the transient nature of this eruption. Although antihistamines may alter the duration of ETN, COMMON RASHES their use is not necessary as the rash does not seem to bother the child. The most useful therapy Erythema Toxicum Neonatorum remains reassurance that the eruption is benign and will resolve without sequelae.24 Erythema toxicum neonatorum (ETN) is a common condition, affecting neonates of all races Transient Neonatal Pustular Melanosis and ethnicities worldwide. Its incidence ranges from as low as 3.7% to as high as 72%, affecting Transient neonatal pustular melanosis (TNPM) predominantly full-term neonates weighing is a benign condition most commonly affecting over 2,500 g.3,24,25 Although the pathogenesis infants who are black. It affects both sexes with of this condition is unknown, recent studies the same frequency and lesions are virtually suggest that ETN may represent a cutaneous always present at birth.26 So far, the aetiology immune reaction to an acute, transitory attack of TNPM remains unknown. Some authors of the commensal microflora that penetrate the consider it a variant of ETN, although this has not newborn skin via hair follicles, a condition which been confirmed.27 presupposes a certain degree of maturity of the TNPM features three different morphologies, immune system.3,24 which can coexist or occur sequentially. At ETN is a self-limited condition, usually beginning delivery, flaccid and superficial noninflammatory within the first 2 days of life and resolving entirely vesicopustules are usually present in the within 6 days. Recurrence occurs in up to 11% of chin, forehead, nape of the neck, lower back, neonates, usually between 5 and 11 days after the buttocks, and shins. These lesions are easily original eruption.24 This transient neonatal rash disrupted, leaving hyperpigmented macules is asymptomatic and resolves without sequelae, with fine collarettes of scale. Finally, residual with individual lesions rarely persisting for more hyperpigmented macules may persist for than 1 day.25 Five distinct components may be several months.27

102 EMJ • March 2021 EMJ Diagnosis of TNPM is generally clinical. accomplished by avoiding overheating and Cytological examination of the pustules shows excessive swaddling.27 polymorphonuclear neutrophils. Histological examination is rarely permorfed, but will show Neonatal Cephalic Pustulosis intra- or subcorneal pustules containing primarily Neonatal cephalic pustulosis (NCP) is a relatively neutrophils. Pigmented macules show increased common benign condition with prevalence melanin in basal . Differentialestimated between 10% and 66%.25 It usually diagnosis of this condition is similar to that of develops within the first 2–3 weeks of life, and is 26,27 ETN. As in ETN, no treatment is necessary for characterised by multiple inflammatory papules this condition. Parents’ reassurance of its benign and pustules mainly on the cheeks but also on and self-limited nature is all that is needed.27 the forehead, chin, neck, upper chest, and scalp (Figure 3B).27 Although an inflammatory response Miliaria to Malassezia spp. has been suggested to be Miliaria is a common condition affecting up to involved in the pathogenesis of NCP, this has not 15% of newborns, and is commonly observed in been confirmed.29 Diagnosis of NCP is usually summer months, febrile periods, or in newborns clinical. A Giemsa-stained smear of pustular with excess clothing.27 The most common type contents can show yeast forms, neutrophils, and 27 of miliaria in the immediate neonatal period is inflammatory cells. Although topical imidazole miliaria crystallina (MC), which is characterised or hydrocortisone are sometimes prescribed, no by small, clear, and flaccid vesicles over healthy treatment is needed for this condition as it has skin, especially on the face, neck, trunk, and a self-limited course with spontaneous involution occluded areas. MC is caused by obstruction of over weeks to months. the eccrine sweat duct as it courses through the stratum corneum.28 Neonatal acne occurs in up to 20% of newborns. Miliaria rubra (MR) is another type of miliaria, This condition may be evident at birth or appear also caused by obstruction of eccrine sweat during the first 4 weeks of life and is more gland ducts but deeper within the spinous layer. commonly seen in males.30 Several factors may Leakage of fluid into the lower epidermis and contribute to the development of neonatal acne, superficial dermis leads to local , including increased sebum excretion, stimulation characterised by numerous erythematous of the sebaceous glands by maternal or neonatal 28 papules, vesicles, and pustules (Figure 3A). MR androgens, and colonisation of sebaceous glands nd lesions usually begin after the 2 week of life and by Malassezia species.31 Neonatal acne typically predominate in the trunk and intertriginous areas, presents as small, closed comedones on the where occlusion by clothing is accentuated. In forehead, nose, and cheeks. Accompanying hot environments, lesions on the scalp, face, and sebaceous hyperplasia is often noted. Less 27 neck area may appear. Rarely, MR can progress frequently, open comedones, inflammatory to miliaria profunda, where the obstruction of the papules, and pustules may also develop. eccrine gland duct is even deeper.27 This type of Several eruptions should be considered in the miliaria is very rare in infants, usually occurring in differential diagnosis of neonatal acne, including older patients in tropical climates. erythema toxicum neonatorum, transient neonatal pustular melanosis, milia, and pustular Diagnosis of miliaria is clinical. Cytologic miliaria. Other entities to be considered include examination of vesicopustule material shows a bacterial folliculitis, secondary syphilis, herpes predominance of lymphocytes. Histologically, in simplex virus and varicella zoster virus, and skin MC, subcorneal or intracorneal vesicles centered colonisation by fungi of Malassezia species. Drug on the acrosyryngium are seen, with little eruptions associated with hydantoin, lithium, surrounding inflammation. In MR, intraepidermal or halogens should be considered in particular spongiosis and vesicles are found, along with a cases.30 Neonatal acne is usually mild and self- chronic inflammatory infiltrate in the dermis.27 limited, resolving spontaneously without scarring Lesions of milaria resolve without intervention, in approximately 1–3 months.31 but there is a proven benefit in lowering the environment temperature. Prevention may be

Creative Commons Attribution-Non Commercial 4.0 March 2021 • EMJ 103 A B

Figure 3: Common rashes. A) Miliaria rubra lesions on the back of a 2-week-old male. B) Neonatal cephalic pustulosis on the face of a 3-week-old female.

Therefore, in most cases no treatment is needed albeit rarely perfomed, demonstrates the except for reassurance. If necessary, comedones presence of subcorneal pustules filled primarily may be treated with azelaic acid cream 20% or with neutrophils. Scabies is the main differential cream 0.025–0.050%. For inflammatory diagnosis of this condition, and can usually lesions, solution 2.0% and benzoyl be excluded by skin scraping examination. peroxide gel 2.5% may be used. Severe or Incontinentia pigmenti is another condition in recalcitrant disease warrants a workup for the differential diagnosis of IA. Other clinically congenital adrenal hyperplasia, a virilising similar conditions, such as dyshidrotic eczema tumour, or underlying endocrinopathy.30 and palmoplantar pustulosis, are rare in infants. Treatment of IA is symptomatic, usually requiring Infantile Acropustulosis potent or superpotent topical 32 Infantile acropustulosis (IA) is an uncommon and oral antihistamines. condition, usually developing at approximately Eosinophilic Pustular Folliculitis 3–6 months of age, although it can begin earlier. It is more common in males and in infants of Eosinophilic pustular folliculitis (EPF) usually African descent.25 Clinically, IA is characterised affects infants between 5 and 10 months of by recurrent crops of pruritic vesicopustules life, with a male to female ratio of 4:1.33 EPF predominantly in the palms and soles, although it is a polymorphous eruption characterised by can also affect the back of the hands, feet, ankles, recurrent eruptions of pruritic papules, pustules, wrists, and scalp. Eruptions usually last between and vesicles. Pruritic vesicopustules may 7 and 14 days, recurring every 3–5 weeks. With coalesce, forming exudative and crusted plates time, episodes usually decrease in frequency and located mainly on the scalp, and less commonly severity, eventually resolving completely by 3 on the face and extremities. Eruptions are years of age.32 intermittent and self-limited, lasting from 1 to 4 weeks, and eventually resolving by 3 years of age. Diagnosis of IA is clinical. Cytological examination of pustular contents shows a Cytological examination of pustular contents predominance of neutrophils, with occasional reveals primarily eosinophils, without bacteria or eosinophils. Histopathological examination, other microorganisms. Histological examinations

104 EMJ • March 2021 EMJ show a dense eosinophilic infiltrate with a CONCLUSION predominant perifollicular distribution. Peripheral eosinophilia is observed in approximately 70% Neonatal cutaneous alterations are common, of cases.34 usually appearing at birth or during the first Differential diagnoses of EPF predominantly few days of life. Most of these conditions are include ETN, TNPM, IA, bacterial folliculitis, physiological and arise from a combination tinea capitis. and reactions to arthropod bites. of immaturity of the newborn skin with Other rarer conditions, such as Langerhans’ cell environmental factors. Although the majority histiocytosis and the vesicular-papulo-pustular of these conditions are benign and sponteously eruption associated with autosomal dominant reversible, some of them may eventually be hyper-IgE syndrome, should be considered in a clue to underlying disorders. Physicians the appropriate clinical settings. Treatment is should therefore be aware of these clinical primarily symptomatic and similar to that of IA, manifestations, so that parents can be including midpotency topical corticosteroids, reassured and, when necessary, complementary 33 topical tacrolimus, and oral antihistamines. In investigations undertaken. more recalcitrant cases, oral dapsone and other oral may be needed.34

References

1. Johnson E, Hunt R. Infant skin care: 11. Drapkin Z et al. Is my baby normal? 21. Starace M et al. Nail disorders in updates and recommendations. Curr A review of seemingly worrisome but children. Skin Appendage Disord. Opin Pedi-atr. 2019;31(4):476-81. normal newborn signs, symptoms 2018;4(4):217-29. and behaviors. Am J Emerg Med. 22. Walker J et al. Koilonychia: an update 2. Haveri F, Inamadar A. A cross- 2019;37(6):1153-9. sectional prospective study of on pathophysiology, differential cutaneous lesions in newborn. ISRN 12. Su J. Common rashes in neonates. diagnosis and clinical relevance. Dermatol. 2014;360590. Aust Fam Physician. 2012;41(5):280-6. J Eur Acad Dermatol Venereol. 2016;30(11):1985-91. 3. Ábrahám R et al. Cutaneous lesions 13. van den Berg G, Bakker H. Harlequin and disorders in healthy neonates color change in a neonate. N Engl J 23. Richert B, André J. Nail disorders in and their relationships with maternal- Med. 2020;382(5):456. children: diagnosis and management. neonatal factors: a cross-sectional Am J Clin Dermatol. 2011;12(2):101-12. study. World J Pediatr. 2017;13(6):571- 14. Redondo P. Classification of 24. Morgan AJ et al. Erythema toxicum 6. vascular anomalies (tumours and malformations). Clinical neonatorum revisited. Cutis. 4. Techasatian L et al. Neonatal characteristics and natural history. An 2009;83(1):13-6. birthmarks: a prospective survey in Sist Sanit Navar. 2004;27:Suppl 1:9- 25. Csoma Z et al. Overview of 1000 neonates. Glob Pediatr Heal. 25. (In Spanish). dermatologic disorders of neonates 2019;6:2333794X19835668. 15. Monteagudo B et al. Salmon in a central regional intensive care 5. Nishijima K et al. Biology of the vernix patch: a descriptive study. Actas unit in Hungary. Pediatr Dermatol. caseosa: a review. J Obs Gynaecol Dermosifiliogr. 2011;102(1):24-7. (In 2015;32(2):201-7. Res. 2019;45(11):2145-9. Spanish). 26. Nanda S et al. Analytical study of 6. Afsar F et al. Neonatal sucking blister. 16. Gupta D, Thappa DM. Mongolian pustular eruptions in neonates. Dermatol Online J. 2019;25(11):pii: spots. Indian J Dermatol Venereol Pediatr Dermatol. 2002;19(3):210-5. 13030/qt33b1w59j. Leprol. 2013;79(4):469-78. 27. Reginatto FP et al. Benign skin 7. Adam R, Schroten H. Picture of 17. Zagne V, Fernandes N. Dermatoses in disease with pustules in the newborn. the month. Congenital sucking the first 72 hours of life: a clinical and An Bras Dermatol. 2016;91(2):124-34. blisters. Arch Pediatr Adolesc Med. statistical survey. Indian J Dermatol 28. Antaya R, Robinson D. Blisters and 2007;161(6):607-8. Venereol Leprol. 2011;77(4):470-6. pustules in the newborn. Pediatr Ann. 2010;39(10):63-45. 8. Nicholson L. Caput succedaneum and 18. Pérez-Bescós L et al. Cutaneous : the cs that leave hyperpigmentation of the distal 29. Ayhan M et al. Colonization of bumps on the head. Neonatal Netw. phalanges in a newborn infant. An neonate skin by Malassezia species: 2007;26(5):277-81. Pediatr (Barc). 2006;65(4):390. relationship with neonatal cephalic pustulosis. J Am Acad Dermatol. 9. Petrikovsky BM et al. 19. Paller A, Mancini A, Hurwitz Clinical 2007;57(6):1012-8. Cephalhematoma and caput Pediatric . A Textbook succedaneum: do they always of Skin Disorders of Childhood 30. Serna-Tamayo C et al. Neonatal and occur in labor? Am J Obs Gynecol. and Adolescence (2011) 4th edition, vulgaris: an update. 1998;179(4):906-8. Chicago: Elsevier Health Sciences. Cutis. 2014;94(1):13-6. 10. Liu L, Antaya R. Neonatal subgaleal 20. Eichenfield L et al., Neonatal 31. Antoniou C et al. Clinical and from trauma during vaginal dermatology (2007) 2nd edition, therapeutic approach to childhood delivery without instrument use. Philadelphia: Saunders Elsevier Inc. acne: an update. Pediatr Dermatol. Pediatr Dermatol. 2017;34(1):e40-1. 2009;26(4):373-80.

Creative Commons Attribution-Non Commercial 4.0 March 2021 • EMJ 105 32. Mancini AJ et al. Infantile 33. Hernández-Martín Á et al. 34. Fukamachi S et al. Therapeutic acropustulosis revisited: history of Eosinophilic pustular folliculitis of effectiveness of various treatments for scabies and response to topical infancy: a series of 15 cases and eosinophilic pustular folliculitis. Acta corticosteroids. Pediatr Dermatol. review of the literature. J Am Acad Derm Venereol. 2009;89(2):155-9. 1998;15(5):337-41. Dermatol. 2013;68(1):150-5.

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