Hemangioma

Etiology • Benign developmental anomalies of blood vessels that may
be subclassified as congenital hemangiomas and vascular malformations
• “Congenital hemangioma” usually noted initially in infancy or childhood (hamartomatous proliferation)
• Congenital hemangioma due to proliferation of endothelial cells • “Vascular malformations” due to abnormal morphogenesis of
arterial and venous structures

Clinical Presentation • Congenital lesions usually arise around time of birth, grow
rapidly, and usually involute over several years. • Malformations generally are persistent, grow with the child,
and do not involute. • Color varies from red to blue depending on depth, degree of
congestion, and caliber of vessels • Range in size from few millimeters to massive with disfigurement • Most common on lips, tongue, buccal mucosa • Usually asymptomatic • Sturge-Weber syndrome (trigeminal encephaloangiomatosis)
includes cutaneous vascular malformations (port wine stains) along trigeminal nerve distribution, mental retardation, and seizures.
Diagnosis • Aspiration • Blanching under pressure (diascopy) • Imaging studies
Differential Diagnosis • Purpura • Telangiectasia • Kaposi’s sarcoma • Other vascular neoplasms
Treatment • Observation • Congenital hemangiomas typically involute, whereas vascular
malformations persist. • Surgery (scalpel, cryosurgery, laser [argon, copper])—congenital
hemangiomas usually are circumscribed and more easily removed than are vascular malformations, which are poorly defined. (Vascular malformations are associated with excessive bleeding and recurrence.)
• Sclerotherapy • Microembolization followed by resection for large malforma-
tions or if bleeding is problematic
Prognosis • Guarded