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Skin lesions in the newborn and infant

Skin lesions in the newborn and infant
Literature review current through: Jan 2024.
This topic last updated: Dec 21, 2023.

INTRODUCTION — Benign skin and mucosal lesions seen in the newborn and infant are reviewed here. Vesicular, pustular, and bullous disorders; nodular lesions; cutaneous developmental anomalies; vascular lesions; and vascular tumors in the newborn and infant are discussed in more depth separately. Congenital nevi are also discussed separately.

(See "Vesicular, pustular, and bullous lesions in the newborn and infant".)

(See "Skin nodules in newborns and infants".)

(See "Cutaneous developmental anomalies in the newborn and infant".)

(See "Vascular lesions in the newborn".)

(See "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications".)

(See "Congenital hemangiomas: Rapidly involuting congenital hemangioma (RICH), noninvoluting congenital hemangioma (NICH), and partially involuting congenital hemangioma (PICH)".)

(See "Congenital melanocytic nevi".)

SKIN EXAMINATION OF THE NEWBORN AND INFANT — Newborn skin may display a variety of findings [1]. These may be physiologic and transient or may represent a sign of a more serious condition, such as a genetic or developmental anomaly. Careful examination not only of the skin and mucous membranes, but also of the entire body for any associated abnormalities, is of utmost importance. (See "Assessment of the newborn infant".)

TRANSIENT PAPULAR AND PUSTULAR LESIONS — Papules are palpable, discrete lesions measuring <1 cm in diameter that can occur as isolated or grouped lesions. Pustules are small skin papules containing purulent material.

Milia — Milia are white papules caused by retention of keratin and sebaceous material in the pilosebaceous follicles. They are frequently found on the nose and cheeks and resolve in the first few months of life [2].

Miliaria — Miliaria is a transient cutaneous eruption in newborns and infants due to obstruction of sweat ducts. Hot and humid environments are particularly common causes. There are three different presentations (ie, miliaria crystallina (picture 1), miliaria rubra (picture 2), and miliaria profunda), depending on the depth of the obstruction. Miliaria is discussed separately. (See "Miliaria".)

Sebaceous hyperplasia — Sebaceous hyperplasia presents with small (1 to 2 mm), white-yellow, smooth papules occurring most prominently on the face, particularly on the nose and upper lip, in up to one-half of normal newborns (picture 3) [1]. They gradually involute in the weeks after birth.

Erythema toxicum neonatorum — Erythema toxicum neonatorum is a common pustular eruption seen more commonly in term neonates within the first 72 hours of life that resolves spontaneously within one week (picture 4). It is discussed separately. (See "Vesicular, pustular, and bullous lesions in the newborn and infant", section on 'Erythema toxicum neonatorum'.)

Neonatal cephalic pustulosis (neonatal acne) — Neonatal cephalic pustulosis (previously called neonatal acne) is a pustular eruption on the head and neck of newborns with onset around three weeks of life (picture 5). Some studies have shown an association with Malassezia colonization. It resolves spontaneously without scarring in a few months but may be treated with topical azole antifungal preparations or mild topical steroids to speed clearance. (See "Vesicular, pustular, and bullous lesions in the newborn and infant", section on 'Neonatal cephalic pustulosis'.)

Benign cephalic histiocytosis — Benign cephalic histiocytosis (BCH), also called papular histiocytosis of the head, is a rare, self-healing type of non-Langerhans cell histiocytosis that typically occurs in infants and young children, with an average age of onset of 15 months [3,4]. BCH presents with small, yellow-red or yellow-brown, asymptomatic macules and/or papules located mostly on the head and neck (picture 6A-B). In some cases, lesions may extend to involve the trunk and upper and lower extremities. There is no visceral involvement.

The diagnosis is in most cases clinical. However, if the diagnosis is in doubt, a skin biopsy for histology and immunostaining should be performed. The histopathologic hallmark of BCH is a well-circumscribed, histiocytic infiltrate in the superficial and reticular dermis [4]. Immunohistochemical staining of lesional cells demonstrates positive staining for factor XIIIa, fascin, and CD68 but negative staining for CD1a, langerin, and S100 (table 1).

The differential diagnosis may include multiple Spitz nevi, juvenile xanthogranuloma, Langerhans cell histiocytosis, urticaria pigmentosa, and generalized eruptive histiocytosis. (See "Spitz nevus and atypical Spitz tumors" and "Juvenile xanthogranuloma (JXG)" and "Clinical manifestations, pathologic features, and diagnosis of Langerhans cell histiocytosis" and "Mastocytosis (cutaneous and systemic) in children: Epidemiology, clinical manifestations, evaluation, and diagnosis".)

Given the self-limiting nature of BCH, no treatment is needed. Lesions spontaneously regress over several months to years. Some resolve with superficial epidermal atrophy.

FOCAL PAPULES, VESICLES, AND BLISTERS

Sucking blisters — Sucking blisters are typically single, noninflammatory vesicles or bullae on the wrists, hands, or fingers of newborns due to vigorous sucking in utero (picture 7). Sucking blisters are discussed separately. (See "Vesicular, pustular, and bullous lesions in the newborn and infant", section on 'Sucking blisters'.)

Oral inclusion cysts — Intraoral inclusion cysts are small, keratin-filled cysts, analogous to milia, presenting on the oral mucosa of up to nearly 90 percent of newborns [5,6]. They are called Epstein pearls when located on the palate and Bohn nodules when on the vestibular or lingual surfaces of the alveolar ridge (picture 8) [7]. They resolve spontaneously within a few months after birth. (See "Congenital anomalies of the jaw, mouth, oral cavity, and pharynx".)

Occasionally, Epstein pearls can occur on the penile tip of male newborns (preputial Epstein pearls) [8,9].

Median raphe cysts — Median raphe cysts are uncommon epidermal inclusion cysts that occur on the foreskin and ventral surface of the penis and scrotum [10,11]. They may enlarge throughout infancy and may require surgical removal if large or if they become infected.

SKIN COLOR CHANGES — Benign causes of color changes in neonates include physiologic changes and vascular and melanocytic lesions.

Pigmentary anomalies

Melanin

Dermal melanocytosis — Congenital dermal melanocytosis, formerly called Mongolian spot, is the most frequently encountered pigmented lesion in newborns. There are marked ethnic differences in prevalence [12-15]:

85 to 100 percent in Asian neonates

>60 percent in Black neonates

46 to 70 percent in Hispanic neonates

<10 percent in White neonates

Congenital dermal melanocytosis typically appears as a blue-gray, pigmented patch with ill-defined borders, although it can also be greenish-blue or brown (picture 9). The diameter of the lesion may be 10 cm or more. The most common location is the sacral-gluteal region, followed by the shoulders [12]. They rarely occur on the head, face, or flexor surface of the extremities.

Congenital dermal melanocytosis is completely benign and usually fades during the first or second year of life [16]. By 6 to 10 years of age, the vast majority have disappeared. However, approximately 3 percent remain into adulthood, particularly those in extrasacral locations.

The lesions result from the delayed disappearance of dermal melanocytes. The sacral area and medial buttocks are the most common sites where active dermal melanocytes frequently remain at birth, but they can also be seen at extrasacral ("aberrant") sites (eg, the superior or anterior trunk and extremities). A biopsy, which is rarely indicated, shows the widely spaced dermal melanocytes in the deep dermis.

Although the distinctive clinical appearance of ill-defined, homogeneous, gray-blue patches is usually diagnostic, particularly when located in classic sites, dermal melanocytosis can be misinterpreted as bruises (which tend to change color and resolve more quickly), resulting in erroneous accusations of child abuse [12]. (See "Differential diagnosis of suspected child physical abuse", section on 'Bruises'.)

Congenital dermal melanocytosis should be distinguished from other forms of increased dermal melanocytes that do not fade, such as blue nevi, nevus of Ota, or nevus of Ito. Blue nevi present as blue to blue-black, dome-shaped papules with preserved skin markings that measure <1 cm in diameter. They are rare in children; appear mainly on the scalp, face, and dorsa of the hands and feet (picture 10); and have a raised, irregular surface with more discrete borders. Nevus of Ota and nevus of Ito have a specific distribution, occurring in the V1/V2 dermatomes of the face and on the neck and shoulders, respectively. Blue nevi [17] and nevus of Ota [18] are rarely associated with malignant changes, whereas congenital dermal melanocytosis spots are completely benign. (See "Acquired melanocytic nevi (moles)", section on 'Blue nevi' and "Benign pigmented skin lesions other than melanocytic nevi (moles)", section on 'Nevus of Ota' and "Benign pigmented skin lesions other than melanocytic nevi (moles)", section on 'Nevus of Ito'.)

Specific types of dermal melanocytosis have been associated with a number of pediatric disorders:

Extensive dermal melanocytosis with a ventral as well as dorsal distribution that is persistent and/or progressive in nature has been reported in at least 40 children with various lysosomal diseases [19-23]. (See "Inborn errors of metabolism: Classification", section on 'Lysosomal storage disorders'.)

Clinically apparent dermal pigmentation of the perioral area has been described in up to 20 to 50 percent of patients with cleft lip, implying a common pathogenic defect in migration of cells from the neural crest [24].

In phakomatosis pigmentovascularis type II, aberrant congenital dermal melanocytosis spots are seen in association with capillary malformations (port wine birthmarks); patients are further categorized based on the presence or absence of associated systemic features (eg, Sturge-Weber syndrome or glaucoma) [25,26]. (See "Vascular lesions in the newborn", section on 'Phakomatosis pigmentovascularis' and "Capillary malformations (port wine birthmarks) and associated syndromes" and "Sturge-Weber syndrome".)

Congenital dermal melanocytosis usually resolves spontaneously during the first decade of life. It is prudent to document these lesions at least upon initial physical examination; this will help to avoid confusion with bruises in the event that child abuse is suspected. (See "Differential diagnosis of suspected child physical abuse", section on 'Bruises'.)

Transient hyperpigmentation — In newborns with more darkly pigmented skin, very dark hyperpigmentation may be seen on the genitals, around the areolae, in the axillae, on the pinnae, at the base of the fingernails, and in a linear fashion on the lower abdomen [27]. There may also be horizontal bands of hyperpigmentation in abdominal or back creases as well as the knees [28].

Transient hypopigmentation — Children of parents with darker pigmentary phenotypes are generally born with a lighter pigmentation than what will be their adult pigmentary phenotype. Over months, their skin will darken. Several genetic disorders causing generalized hypopigmentation must be differentiated, including, but not limited to, oculocutaneous albinism, phenylketonuria, Griscelli syndrome, and Chediak-Higashi syndrome. (See "Oculocutaneous albinism" and "Overview of phenylketonuria".)

Nonmelanin color changes

Jaundice — Physiologic jaundice due to transient elevations of serum bilirubin causes a generalized yellow discoloration of skin and mucous membranes in the first few days of life. This fades with normalization of bilirubin levels. (See "Unconjugated hyperbilirubinemia in neonates: Etiology and pathogenesis", section on 'Benign neonatal hyperbilirubinemia'.)

Meconium stains — Meconium may stain the skin of newborns in yellow-brown patches that will fade as the skin desquamates.

Vascular changes

Increased hemoglobin levels

Rubor — Newborns have higher levels of hemoglobin in the first few weeks of life, resulting in generalized redness of the skin that fades as hemoglobin drops.

Twin transfusion — There may be major color differences between monochorionic twins at birth due to a discrepancy in the amount of blood shunted to one twin over the other and, therefore, resulting in a difference in hemoglobin levels. This is expected to improve with time.

Vasomotor instability

Cutis marmorata — Cutis marmorata is characterized by symmetric, reticular mottling of the skin of the extremities and trunk (picture 11) [29]. It is caused by a vascular response to cold and usually resolves with warming. No treatment is required.

Physiologic cutis marmorata must be distinguished from cutis marmorata telangiectatica congenita (CMTC), a vascular malformation in which the lesions do not resolve with warming [30]. CMTC predominantly affects the extremities (picture 12A-B) and may be associated with extracutaneous findings, including body and limb asymmetry, cleft palate, and glaucoma [31]. (See "Vascular lesions in the newborn", section on 'Cutis marmorata telangiectatica congenita'.)

Acrocyanosis — Peripheral cyanosis or acrocyanosis is a common finding in newborns. It presents as a blue-purple discoloration of acral surfaces, including the hands, feet, and lips, due to excess vasoconstriction in acral areas versus central areas of the body after exposure to colder temperatures. It is more common in premature infants, rapidly improves with rewarming, and resolves with age [2,5].

Harlequin color change — Harlequin color change (unilateral erythema) is observed when an infant is lying on his or her side [32]. It is characterized by intense reddening of the dependent side and blanching of the nondependent side, with a demarcation line along the midline. The duration ranges from a few seconds to 20 minutes. The etiology of harlequin color change is unknown. It may be related to the immaturity of the autonomic regulation of cutaneous blood vessel tone [33].

Harlequin color change occurs more often in preterm infants than in term infants. The frequency is greatest in the first few days of life, but it has been observed up to three weeks after birth.

Harlequin color change is entirely benign. The name should not be confused with the so-called "harlequin fetus," a severe congenital form of ichthyosis that can be lethal in the neonatal period. (See "Overview and classification of the inherited ichthyoses", section on 'Harlequin ichthyosis'.)

BIRTHMARKS

Vascular birthmarks — Vascular birthmarks include vascular tumors and vascular malformations. Some, such as nevus simplex or nevus anemicus, are clinically insignificant, but others may have associated abnormalities or develop complications. These lesions are discussed separately.

(See "Vascular lesions in the newborn".)

(See "Capillary malformations (port wine birthmarks) and associated syndromes".)

(See "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications".)

(See "Pyogenic granuloma (lobular capillary hemangioma)".)

(See "Congenital hemangiomas: Rapidly involuting congenital hemangioma (RICH), noninvoluting congenital hemangioma (NICH), and partially involuting congenital hemangioma (PICH)".)

(See "Tufted angioma, kaposiform hemangioendothelioma (KHE), and Kasabach-Merritt phenomenon (KMP)".)

(See "Sturge-Weber syndrome".)

(See "Klippel-Trenaunay syndrome: Clinical manifestations, diagnosis, and management".)

Transient capillary vascular malformations (nevus simplex/salmon patch) — Many infants of all ethnicities have pink to red or violaceous, smooth patches on the occiput, eyelids, glabella, nose, and upper lip that become more prominent with crying (picture 13 and picture 14). They typically fade with time, though some may persist. They must be distinguished from port wine birthmarks (capillary malformations) and early infantile hemangiomas, though generally this is possible clinically. (See "Vascular lesions in the newborn", section on 'Nevus simplex (macular stain)'.)

Nevus anemicus — Nevus anemicus is a vascular birthmark that may present at birth or may become more prominent with age (picture 15). It is caused by increased vascular reactivity to catecholamines in a localized area of skin, resulting in a patch of hypopigmentation that does not flush with scratching or stimulation. Although nevus anemicus is usually an isolated finding, it is seen with increased frequency in patients with neurofibromatosis type 1 and tuberous sclerosis complex. (See "Acquired hypopigmentation disorders other than vitiligo", section on 'Localized hypopigmentations due to vascular causes'.)

Pigmentary birthmarks

Congenital melanocytic nevi — Congenital melanocytic nevi are melanocytic neoplasms composed primarily of clonal proliferations of benign melanocytes that arise during embryogenesis and are present at birth. They are discussed separately. (See "Congenital melanocytic nevi".)

Café-au-lait macules — Café-au-lait macules are flat, brown macules or patches, typically present at birth in many neonates. They are commonly benign but may be associated with various syndromes, notably neurofibromatosis type 1. They are discussed separately. (See "Benign pigmented skin lesions other than melanocytic nevi (moles)", section on 'Café-au-lait macule'.)

Nevus depigmentosus — Nevus depigmentosus, also called nevus achromicus, is a birthmark that may be hypopigmented or lack pigment altogether and is typically present at birth (picture 16). They may be small or large and segmental but are usually an isolated finding. They must be differentiated from the ash-leaf macules of tuberous sclerosis. (See "Acquired hypopigmentation disorders other than vitiligo", section on 'Nevus depigmentosus'.)

Cutaneous hamartomas

Epidermal nevi — Epidermal nevi are benign, hamartomatous congenital skin lesions. They are discussed separately. (See "Epidermal nevus and epidermal nevus syndrome".)

Nevus sebaceous — Nevus sebaceous of Jadassohn is a congenital lesion that occurs primarily on the scalp or face (picture 17A-B). It is a hamartoma that combines epidermal, follicular, sebaceous, and apocrine gland abnormalities [34]. Nevus sebaceous and nevus sebaceous syndrome are discussed separately. (See "Nevus sebaceus and nevus sebaceus syndromes".)

Smooth muscle hamartoma — A smooth muscle hamartoma (also called arrector pili hamartoma) is a rare congenital lesion consisting of a collection of arrector pili muscles within the superficial dermis. It presents as a soft plaque, usually with overlying hypertrichosis, which may contract with rubbing (pseudo-Darier sign) (picture 18) [35]. Congenital smooth muscle hamartoma is most commonly seen on the trunk and proximal extremities. Biopsy may be undertaken for definitive diagnosis. Treatment is not needed. However, excision may be considered if desired and feasible.

Connective tissue nevus — A connective tissue nevus is a hamartoma composed of dermal tissue components. They may be sporadic or associated with genetic syndromes, notably tuberous sclerosis and Buschke-Ollendorff syndrome (see "Tuberous sclerosis complex: Clinical features" and "Buschke-Ollendorff syndrome"). They present as asymptomatic, firm, skin-colored to yellowish nodules or plaques, typically on the trunk or limbs, and may have a smooth or cobblestoned surface (picture 19) [36]. Diagnosis is made via biopsy, and excision is not necessary unless desired.

Medallion-like dermal dendrocyte hamartoma — Medallion-like dermal dendrocyte hamartoma (MLDDH), also known as plaque-like CD34+ dermal fibroma, is a rare, congenital, erythematous, and atrophic lesion most often located on the neck or upper chest (picture 20) [37-41]. Lesions are typically round or oval and 2 to 6 cm in diameter. In one report, MLDDH presented as a dermal nodule without epidermal changes [42]. Histologically, lesions consist of a benign dermal proliferation of dendrocytic cells that stain positive for CD34, factor XIIIa, and fascin, but negative for S100.

The differential diagnosis of MLDDH includes congenital atrophic dermatofibrosarcoma protuberans (DFSP), aplasia cutis congenita, and neurofibroma [43-46]. Congenital atrophic DFSP stains positive for CD34 but negative for factor XIIIa; the diagnosis can be confirmed by polymerase chain reaction or fluorescence in-situ hybridization of the tumor tissue showing COL1A1-PDGFB fusion gene [47,48]. (See "Dermatofibrosarcoma protuberans: Epidemiology, pathogenesis, clinical presentation, diagnosis, and staging" and "Aplasia cutis congenita".)

IATROGENIC AND TRAUMATIC INJURIES — Iatrogenic and traumatic injuries involving the skin and soft tissues in newborns may occur during pregnancy, labor, delivery, and after delivery. (See "Neonatal birth injuries".)

Puncture wounds — Depressed, dimple-like scars may occur in neonates after intrauterine procedures, such as amniocentesis [49,50]. Other injuries such as lacerations and ulcerations may occur, particularly on the scalp and face, due to intrauterine monitoring during labor and delivery.

Birth-related trauma

Caput succedaneum — Caput succedaneum is an edematous swelling of the scalp above the periosteum that can cross the midline and presents at birth after prolonged engagement of the fetal head in the birth canal or after vacuum extraction. Complications include halo scalp ring and erosive and necrotic lesions resulting in long-term scarring and alopecia. (See "Neonatal birth injuries", section on 'Caput succedaneum'.)

Halo scalp ring — Halo scalp ring describes a ring-shaped area of alopecia that develops in some infants with caput succedaneum or prolonged labor (picture 21) [51]. The alopecia usually resolves over a period of months to years but may be permanent [51,52].

Cephalohematoma — Cephalohematoma presents as a swelling of the scalp that does not cross suture lines due to a subperiosteal hematoma. It is more common after instrumented delivery. Most cases resolve spontaneously over weeks, but there can be complications, such as calcification or ossification, infection, and sepsis. (See "Neonatal birth injuries", section on 'Cephalohematoma'.)

Burns and thermal injuries — Newborn skin, and specifically the skin of very low birth weight infants, is particularly susceptible to outside insults. There have been reports of chemical burns in infants due to concentrated disinfectants, solvents, and isopropyl alcohol, as well as burn injuries due to contact with warming devices [53,54]. These types of injuries should be suspected when in an unusual or geometric pattern or shape or when clearly underneath or adjacent to instruments.

Calcinosis cutis — Deposition of calcium in the skin can be due to various causes and is classified as idiopathic (normal tissue and normal calcium to phosphorus ratio), dystrophic (damaged tissue and normal calcium to phosphorus ratio), metastatic (damaged tissue and a normal calcium to phosphorus ratio), or iatrogenic (most often due to extravasation of intravenous calcium). (See "Calcinosis cutis: Etiology and patient evaluation".)

In neonates, iatrogenic calcinosis cutis is usually due to infusion of calcium intravenously for treatment of neonatal hypocalcemia [55,56]. Soft tissue calcification may develop within days to weeks of calcium infusion and may present as white papules, nodules, or plaques with or without an intense inflammatory reaction surrounding it [55]. Lesions may be at or near the site of injection, more diffusely along fascial planes, or in vascular or perivascular patterns. Lesions generally resolve spontaneously with transepidermal elimination of calcified material.

Dystrophic calcinosis secondary to trauma may develop in infants who received multiple heel sticks during hospitalization. It presents as a benign, calcified papule or nodule on the heel that appears 4 to 12 months after birth and typically resolves spontaneously [57]. In most cases, no treatment is required. (See "Calcinosis cutis: Etiology and patient evaluation".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Heat rash (prickly heat) (The Basics)")

SUMMARY

Benign and transient lesions – Common, benign and transient, papular and pustular lesions include milia, sebaceous hyperplasia (picture 3), erythema toxicum neonatorum (picture 4), and neonatal cephalic pustulosis (neonatal acne (picture 5)). All of these lesions typically resolve in the first few weeks to months of life. (See 'Transient papular and pustular lesions' above.)

Skin color changes – Congenital dermal melanocytosis, also called Mongolian spot, is the most frequently encountered pigmented lesion in newborns, with high prevalence in neonates of Asian ancestry and in those with highly pigmented skin. It typically appears as a blue-gray, pigmented macule or patch with ill-defined borders, usually located on the sacral-gluteal region (picture 9). Extensive or multiple persistent spots may occur in association with several lysosomal diseases and in phacomatosis pigmentovascularis. (See 'Dermal melanocytosis' above.)

Color changes due to physiologic-increased hemoglobin levels and/or vasomotor instability include rubor, physiologic cutis marmorata (picture 22 and picture 12B), acrocyanosis, and harlequin color change. Cutis marmorata and acrocyanosis typically resolve with warming. (See 'Vascular changes' above.)

Birthmarks – Congenital skin lesions (birthmarks) include a wide range of common and rare lesions, such as vascular birthmarks (eg, nevus simplex/salmon patch (picture 13 and picture 14)), pigmentary birthmarks (eg, congenital melanocytic nevi, café-au-lait macules), and cutaneous hamartomas (eg, epidermal nevi, nevus sebaceous). Congenital melanocytic nevi and other pigmented skin lesions, epidermal nevi, and nevus sebaceous are discussed separately. (See 'Birthmarks' above and "Congenital melanocytic nevi" and "Benign pigmented skin lesions other than melanocytic nevi (moles)" and "Epidermal nevus and epidermal nevus syndrome" and "Nevus sebaceus and nevus sebaceus syndromes".)

Iatrogenic and traumatic injuries – Iatrogenic and traumatic injuries involving the skin and soft tissues in newborns may occur during pregnancy, labor, delivery, and after delivery. These include caput succedaneum and halo scalp ring (picture 21), cephalohematoma, burns and thermal injuries, and calcinosis cutis. The last is usually due to extravasation of calcium given intravenously for treatment of neonatal hypocalcemia or due to multiple heel sticks. (See 'Iatrogenic and traumatic injuries' above and "Neonatal birth injuries".)

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Topic 119230 Version 13.0

References

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