Infantile hemangioma

Prevalence ~4–5% of infants. Risk factors: premature birth, low birth weight, female sex (3–5:1), White non-Hispanic ancestry, multiple gestation, placental abnormalities (pre-eclampsia, placenta previa), advanced maternal age. Higher incidence in light-skinned infants, but IHs occur in all skin tones and are often recognized later in darker skin when the proliferative red appearance is attenuated.

Benign proliferation of endothelial cells expressing GLUT-1 — the key marker distinguishing IH from vascular malformations, other vascular tumors (congenital hemangiomas), and kaposiform hemangioendothelioma. Leading hypothesis: embolized placental endothelial cells or tissue hypoxia drives proliferation. Natural history is predictable:

• Proliferative phase (0–5 months most rapid; slower growth through ~9–12 months): enlargement, often disproportionate to the child's growth.
• Plateau (~12–18 months): stabilization.
• Involution (1–10 years): graying, flattening, regression. Rule of thumb: 50% involuted by 5 years, 90% by 9 years.
• Residuum: telangiectasias, fibrofatty residue, atrophic skin, scarring — varies; face and segmental lesions leave more residue.

Not usually present at birth — a precursor mark (pale macule, telangiectasias, ecchymotic patch) may precede the bright red lesion in the first 1–4 weeks of life. Morphology by location within the dermis:

• Superficial IH: bright red, dome-shaped or plaque — classic 'strawberry' appearance.
• Deep IH: bluish, soft, mass-like; overlying skin may appear normal or have subtle telangiectasias.
• Mixed IH: both components.

Configuration:

• Focal (localized): well-demarcated, discrete — most common.
• Segmental: plaque-like, follows a broad anatomic segment (e.g., S1 segment = beard distribution; S3 = midline chest/perineum). Segmental lesions have higher rates of complications (ulceration, associated syndromes, residual scarring).
• Indeterminate or multifocal.

Ulceration (most common complication, 10–15%) typically occurs in the proliferative phase at sites of friction/moisture — lip, perineum, intertriginous areas. Painful; can cause bleeding, infection, and scarring.

• Superficial IH appears violaceous, plum, or grey-blue rather than bright red on Fitzpatrick IV–VI. The 'strawberry' label is misleading in SoC.
• Precursor marks can be subtle — a pale or ecchymotic patch may be the earliest sign in darker skin; clinicians unfamiliar with this presentation may miss early lesions.
• Deep IHs look similar across skin tones (bluish, mass-like).
• Post-involution telangiectasias and fibrofatty residue are more cosmetically conspicuous on lighter skin; in SoC, the residual dyschromia (hypo- or hyperpigmentation) may dominate.
• Ulceration identification is harder in dark skin because erythematous rim is less visible — look for irritability, bleeding, odor, feeding refusal (perioral), and changes in parental report.

• PHACE syndrome — large (>5 cm) segmental facial IH + ≥1 of: Posterior fossa malformations, Hemangioma (large, facial), Arterial anomalies (cerebrovascular), Cardiac defects (coarctation of aorta), Eye anomalies. Rarely with sternal clefting/supraumbilical raphe (PHACES). Risk of stroke; evaluate MRI/MRA brain, echo, eye exam before starting propranolol.
• LUMBAR (SACRAL/PELVIS) syndrome — lumbosacral midline segmental IH (>2.5 cm) + ≥1 of: Lower-body IH, Urogenital anomalies, Ulceration, Myelopathy (tethered cord, spinal dysraphism), Bony deformities, Anorectal malformations, Renal anomalies. MRI lumbosacral spine.
• Diffuse neonatal hemangiomatosis (multifocal) — ≥5 cutaneous IHs → abdominal ultrasound for hepatic IHs. Monitor for high-output cardiac failure and consumptive hypothyroidism (large hepatic IHs express type 3 iodothyronine deiodinase, inactivating T4).

Refer to a hemangioma specialist / pediatric dermatology early, ideally before age 3 months, if any of:

• Periocular location (amblyopia risk within weeks)
• Beard distribution (airway risk)
• Large segmental facial (PHACE evaluation)
• Lumbosacral midline (LUMBAR evaluation)
• Multifocal (≥5) or hepatic
• Ulcerated or ulceration-prone sites (lip, perineum, intertriginous)
• Rapid proliferation affecting function or with high cosmetic-residue risk (nose, ear, breast in girls)

Early referral matters: the proliferative window (first 5 months) is when treatment has the largest effect on final outcome.

• Congenital hemangioma — fully formed at birth, GLUT-1 negative. RICH (rapidly involuting), NICH (non-involuting), PICH (partially involuting) variants.
• Vascular malformation (capillary — port wine stain, venous, lymphatic, arteriovenous) — present at birth, grows with child, no proliferative phase, GLUT-1 negative.
• Kaposiform hemangioendothelioma / tufted angioma — violaceous plaque, may be associated with Kasabach-Merritt phenomenon (consumptive coagulopathy — thrombocytopenia, DIC). Distinct biology; high mortality if untreated.
• Pyogenic granuloma — older children, friable, bleeds easily, often post-trauma.
• Dermoid cyst / nasal glioma / encephalocele — midline craniofacial; imaging before biopsy.

Most IHs diagnosed clinically. Imaging/labs driven by location and configuration:

• Periocular: ophthalmology exam for amblyopia, strabismus, globe distortion.
• Large facial segmental: MRI/MRA brain + neck, echocardiogram, ophthalmology (PHACE workup).
• Lumbosacral midline: MRI spine (LUMBAR).
• Multifocal (≥5): abdominal ultrasound; TFTs if hepatic involvement confirmed.
• Airway concern (beard distribution + stridor/biphasic breathing): bronchoscopy.
• Before propranolol: clinical exam for CV status; detailed pregnancy/birth history. Baseline HR/BP; screen for asthma, hypoglycemia risk, heart block. Echocardiogram not routinely required but obtained if cardiac anomaly is suspected or in PHACE.

Active non-intervention for small, non-functional, non-cosmetically-threatening IHs — most will involute.

Oral propranolol for complicated IH (first-line since 2008):

• Dosing: start 1 mg/kg/day divided, titrate to 2–3 mg/kg/day divided BID–TID over 1–2 weeks.
• Duration: through proliferative phase and into early involution, typically 6–12 months; many clinicians continue to age 12–15 months to reduce rebound growth.
• Outpatient initiation acceptable for most healthy term infants ≥5 weeks corrected age without comorbidities; inpatient monitoring for high-risk (PHACE, preterm, young age, cardiac comorbidity, multifocal).
• Monitoring: HR, BP, blood glucose. Feed every 4–6 hours; hold dose if NPO, febrile, or wheezing.
• Counsel parents on hypoglycemia signs (lethargy, poor feeding), bradycardia, bronchospasm, cold extremities, sleep disturbance.

Topical timolol 0.5% gel-forming solution (BID): first-line for small, superficial IH where systemic therapy is not indicated. Avoid on large or ulcerated lesions (systemic absorption).

• Pulsed dye laser (PDL, 595 nm) — for ulcerated IH (accelerates healing), residual telangiectasias after involution, or persistent erythema. Not typically first-line for proliferative IHs alone.
• Systemic corticosteroids (prednisolone 2–3 mg/kg/day) — historical first-line; reserved for propranolol contraindications or failure.
• Nd:YAG or Er:YAG laser — deeper targets, adjunct for selected cases.
• Surgical excision — residual fibrofatty tissue after involution; periorbital lesions causing amblyopia and not responding to medical therapy; discrete focal IHs in cosmetically sensitive areas (post-involution).
• Sirolimus / topical or oral mTOR inhibitors — emerging; more often for vascular malformations than classic IH.
• Ulcerated IH care: topical metronidazole, barrier ointments, PDL, pain control (acetaminophen; topical lidocaine sparingly — avoid large surface area), wound care.

Most IHs involute with minimal residua. Untreated lesions generally do well for small, non-segmental, non-facial locations. Residual changes are most notable with segmental, large, deep, ulcerated, or facial IHs — expect some combination of telangiectasias, fibrofatty tissue, pigmentary change, or scar. Early propranolol substantially reduces peak size, ulceration rate, and cosmetic residue when complicated IH is recognized in the proliferative phase.

• GLUT-1 positive = IH. Essential distinction when biopsy done; rules out vascular malformations and congenital hemangiomas.
• The proliferative phase is brief and critical. Most growth is in the first 5 months. Don't defer referral for a 'watch and wait' when the lesion is clearly problematic.
• Ulcerated lip IH feeds poorly — treat urgently; PDL + propranolol is synergistic.
• Segmental lesions > focal for syndromic risk. The size and configuration matter more than raw area.
• Do not inject intralesional steroids into periocular IH — historical practice with serious embolic risks; superseded by propranolol + ophtho.
• PHACE workup before propranolol in large facial segmental IH — untreated intracranial arteriopathy + propranolol can precipitate stroke. MRI/MRA first.
• Hepatic IHs can cause consumptive hypothyroidism — check TFTs in multifocal disease.
• Parental photos at every visit — the proliferation/involution arc is slow from week to week; photos make change objective.

Your baby has an infantile hemangioma — a benign 'birthmark' that proliferates for the first few months and then slowly regresses over years. Most will fade substantially without any treatment. Treatment is recommended when the location or size threatens function (eye, airway, feeding, urinating) or when we can prevent lasting scarring. Propranolol is a well-studied medication safely used for this purpose. Photographs at each visit help us track progress objectively. Some hemangiomas leave residual skin changes — extra tissue, small blood vessels, or pigment differences — which can be treated in childhood if they persist. Ask about anything new: bleeding, ulceration, feeding difficulty, vision changes, noisy breathing, or rapid growth.