Neonatal Skin Findings & Vascular Birthmarks
Reassure the benign; act on marks that threaten sight, airway, or brain
Transient newborn eruptions
Reassurance is the usual treatment. Most rashes in the first weeks of life are physiologic and clear on their own. Suspect infection instead when the infant looks ill, vesicles are grouped, or a smear shows giant cells or bacteria.
| Condition | Timing | Appearance | Clue |
|---|---|---|---|
| Erythema toxicum | 24–72 h; gone in 1–2 weeks | Blotchy erythema with central yellow-white papules or pustules; spares palms and soles | Eosinophils on smear; rare in preterm infants |
| Transient neonatal pustular melanosis | Present at birth | Fragile pustules without erythema → collarette of scale → brown macules that fade over weeks to months; palms and soles possible | Neutrophils, sterile cultures; more common in Black infants |
| Milia | Birth; clear within weeks | 1–2 mm pearly white papules on nose, cheeks, chin | Keratin cysts; Epstein pearls on the palate |
| Miliaria | With overheating or swaddling | Crystallina: clear dewdrop vesicles; rubra: red papules in covered skin | Blocked eccrine ducts; cool the infant |
| Neonatal acne | Starts ~2–3 weeks; gone by ~3 months | Papules and pustules on cheeks, nose, forehead | Comedones few or absent; no scarring |
Erythema toxicum neonatorum. The most common newborn rash, seen in about half of term infants. The "flea-bitten" lesions cover the face, trunk and proximal limbs and need no treatment.
Miliaria and neonatal acne. Superficial sweat-duct obstruction gives clear vesicles (crystallina); deeper obstruction gives red "prickly heat" papules (rubra); cooling and loose clothing resolve both. Neonatal acne is driven by maternal and neonatal androgens (Malassezia is implicated in the pustular cephalic form); use gentle cleansing, avoid oils, and add ketoconazole cream if it persists. Infantile acne starts at 3–6 months, has comedones, can scar, and severe cases deserve an evaluation for hyperandrogenism.
Congenital dermal melanocytosis. Mongolian spots are blue-gray, poorly demarcated macules over the lumbosacral area and buttocks, present at birth, formed by dermal melanocytes arrested during neural crest migration. They are very common in Asian, Black, Hispanic and Native American infants, and most fade during early childhood.
Document dermal melanocytosis at birth. Unlike bruises, these patches are nontender and do not change color over days; bruises are rare in infants who are not yet cruising.
Infantile hemangioma
Tumor versus malformation. Vascular tumors proliferate after birth (infantile hemangioma, kaposiform hemangioendothelioma); vascular malformations are present at birth, grow in proportion with the child and never involute (capillary, venous, lymphatic, arteriovenous). Infantile hemangioma is GLUT-1 positive; malformations are not.
Life cycle. The most common tumor of infancy (about 4–5% of infants), more frequent in girls, preterm or low-birth-weight infants, White infants and multiple gestations. It is absent or a faint pale or telangiectatic patch at birth, becomes visible within weeks, grows fastest in the first 3 months with most growth complete by about 5 months, plateaus, then involutes slowly, mostly by age 4. Superficial lesions are bright red ("strawberry"); deep lesions are bluish. Involution may leave fibrofatty tissue or telangiectasia.
Who needs treatment. Most hemangiomas are observed, but high-risk lesions should reach a specialist by about 1 month of age, before peak growth:
- Periocular: amblyopia and astigmatism.
- "Beard" distribution (chin, jaw, lower lip, neck): subglottic hemangioma with stridor.
- Ulceration, the most common complication, typically on the lip or in the diaper area.
- Nasal tip, lip or large facial lesions that risk disfigurement, and large segmental lesions (PHACE, LUMBAR).
Propranolol. Oral propranolol is first-line systemic therapy. Give it with feeds and hold it when the infant is not eating, because it can cause hypoglycemia; other effects are bradycardia, hypotension, bronchospasm and sleep disturbance. Topical timolol suits small, thin superficial lesions.
PHACE and LUMBAR. A large segmental facial hemangioma (often >5 cm) prompts evaluation for PHACE: posterior fossa malformations (Dandy-Walker), hemangioma, arterial anomalies of the head and neck, cardiac defects (classically coarctation of the aorta), eye anomalies, and sometimes sternal defects. Obtain MRI/MRA of the head and neck, an echocardiogram and an eye exam before propranolol, since arterial anomalies raise stroke risk. LUMBAR, the lower-body analog, pairs a lumbosacral segmental hemangioma with spinal dysraphism (tethered cord) and urogenital, anorectal and renal anomalies; obtain spinal imaging.
Multiple hemangiomas. Five or more cutaneous lesions prompt abdominal ultrasound for hepatic hemangiomas. Multifocal or diffuse liver lesions can cause high-output heart failure and consumptive hypothyroidism (the tumor expresses type 3 iodothyronine deiodinase), so check TSH and free T4.
Capillary malformations and vascular tumors
| Feature | Nevus simplex | Port-wine stain | Kaposiform hemangioendothelioma |
|---|---|---|---|
| Look | Faint pink, midline (glabella, eyelids, nape) | Sharply demarcated, unilateral, dermatomal | Firm, violaceous, indurated mass |
| Course | Facial lesions fade by 1–2 years | Never regresses; darkens and thickens | Can enlarge rapidly |
| Association | None | Sturge-Weber when V1 | Kasabach-Merritt phenomenon |
| Treatment | None | Pulsed-dye laser | Sirolimus, vincristine or corticosteroids |
Port-wine stain. A capillary malformation caused by a somatic GNAQ mutation. It is present at birth as a flat pink-red patch, grows with the child, darkens to purple and may thicken and nodulate in adulthood. Pulsed-dye laser, ideally begun in infancy, lightens it.
Sturge-Weber syndrome. A forehead or upper-eyelid (V1) port-wine stain with ipsilateral leptomeningeal angiomatosis. Focal seizures often begin in the first year, with hemiparesis and developmental delay; glaucoma may be congenital (buphthalmos) or appear later, and choroidal hemangioma can occur. Imaging shows gyriform "tram-track" calcification. Evaluate with contrast brain MRI and an ophthalmology exam, and check intraocular pressure for life.
Salmon patch. Nevus simplex is the most common vascular birthmark: an "angel kiss" on the glabella or eyelids or a "stork bite" on the nape that darkens with crying. Nuchal lesions may persist.
Kasabach-Merritt phenomenon. Kaposiform hemangioendothelioma and tufted angioma, not ordinary infantile hemangiomas, trap platelets, causing profound thrombocytopenia, low fibrinogen and consumptive coagulopathy as the mass rapidly enlarges and becomes purpuric and painful. Platelet transfusion is reserved for bleeding or surgery because it can worsen tumor engorgement.
Diaper dermatitis
Irritant diaper dermatitis. The most common type. Prolonged contact with urine and stool, friction and moisture inflame the convex skin of the buttocks, genitalia and upper thighs, while the inguinal folds are spared. Treat with frequent changes, diaper-free time, gentle cleansing and a thick zinc oxide or petrolatum barrier; brief low-potency hydrocortisone helps severe inflammation.
Candidal diaper dermatitis. Beefy red, well-demarcated plaques involve the skin folds, with satellite papules and pustules. It often follows a rash lasting more than 3 days or a course of antibiotics; KOH shows budding yeast with pseudohyphae. Treat with topical nystatin or an azole plus barrier cream, and treat coexisting oral thrush.
Avoid high-potency steroids, including steroid–antifungal combination creams, under occlusive diapers: absorption is high and atrophy follows.
When it will not clear. Consider seborrheic dermatitis, psoriasis, zinc deficiency (acrodermatitis enteropathica) and Langerhans cell histiocytosis, whose petechial, eroded fold lesions warrant biopsy.