Haemangioma

Overview

•Most common benign tumour of infancy; incidence ~10% by one year of age
•Female predominance (3:1); more common in premature/low-birthweight infants and multiple pregnancies
•Natural history: proliferative phase (peaks ~9-12 months) → plateau → spontaneous involution over years

Presentation

•Begins as faint red macule/telangiectatic patch in first 1-4 weeks of life, then rapid proliferation
•Superficial - bright red, raised, lobulated 'strawberry' plaque; sharply demarcated
•Deep - soft, bluish subcutaneous swelling; overlying skin may appear normal
•Mixed - combined superficial and deep components
•Ulceration - most common complication (~16%); especially in flexural areas (lip, perineum, neck)
•Periocular - risk of ptosis, visual axis distortion, and amblyopia
•Subglottic/airway - progressive biphasic stridor, worse when crying
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High-risk features requiring urgent treatment: periocular location (amblyopia risk), subglottic/airway involvement (respiratory compromise), large segmental facial haemangioma (PHACE syndrome), large ulcerated/bleeding lesion, large hepatic haemangioma causing high-output cardiac failure.

Investigations

•Clinical diagnosis in the vast majority - characteristic appearance, location, and age of onset are sufficient
•First-line imaging: ultrasound with Doppler - shows high-flow vascular lesion; distinguishes from vascular malformation (low/no flow)
•MRI - for large, deep, or segmental lesions; evaluate for PHACE or LUMBAR syndrome anomalies
•Ophthalmology review - first-line for any periocular lesion
•Bronchoscopy - gold standard for confirming subglottic haemangioma when stridor present

Differential Diagnosis

Key differentials from infantile haemangioma
ConditionKey distinguishing features
Vascular malformation (port wine stain)Present at birth, no proliferation or regression, proportionate growth, low-flow on Doppler
Kaposiform haemangioendotheliomaLocally aggressive; Kasabach-Merritt phenomenon (thrombocytopaenia, coagulopathy); GLUT-1 negative
Pyogenic granulomaAcquired; rapidly growing, friable, bleeds easily; often post-trauma; any age
Naevus flammeus (salmon patch)Flat, pale pink macule at birth (nape/glabella); fades within months; not a true haemangioma

Management

•Majority are low-risk - active observation and parental reassurance; explain natural history and expected involution
•High-risk lesions: treat promptly in proliferative phase (ideally before 5 months of age)
•First-line (high-risk): propranolol oral 1-3 mg/kg/day in divided doses - initiated under specialist supervision with cardiac and glucose monitoring; continued for at least 6 months or until involution complete

🥈 Second-line

•timolol maleate 0.5% topical gel - for small, superficial, low-risk lesions where treatment desired
•Pulsed dye laser - for superficial residual lesions, ulcerated haemangiomas, or telangiectatic residua post-involution
•Surgical excision - residual fibrofatty tissue post-involution or vision-threatening periocular lesion not responding to propranolol
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Propranolol is contraindicated in bronchospasm, heart block, decompensated heart failure, and PHACE syndrome with cerebrovascular anomalies (risk of stroke from reduced perfusion pressure). Always initiate under specialist supervision with pre-treatment ECG and blood glucose monitoring.
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Propranolol works via three mechanisms: immediate vasoconstriction (early blanching within days), inhibition of VEGF-driven angiogenesis, and promotion of endothelial cell apoptosis - explaining why treatment must continue for months despite early visible response.

Complications

•Ulceration - most common (~16%); pain, secondary infection, scarring
•Amblyopia - periocular lesions; irreversible if untreated within first 3 years of life
•Airway compromise - subglottic haemangioma; progressive stridor and respiratory distress
•High-output cardiac failure - large hepatic haemangiomas with arteriovenous shunting
•Residual skin changes - fibrofatty tissue, telangiectasia, or scarring after involution; up to 40% of lesions