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Chapter 110: Infantile Hemangiomas

Kristin Khan; Clare Goggins; Annie Grossberg

INFANTILE HEMANGIOMAS

Therapeutic Approach

Infantile hemangiomas are common, benign tumors of infancy. They follow a predictable pattern of rapid proliferation during the first several months of life, cessation of growth typically by 12 months of age, and then slow involution for a variable number of years thereafter. Many infantile hemangiomas require no treatment given they are benign and tend to self-resolve; however, treatment is appropriate in certain clinical scenarios. Problematic infantile hemangiomas are those that may result in functional impairment due to location, permanent scarring in cosmetically sensitive areas, ulceration, and discomfort, or cause life-threatening complications (eg, airway, hepatic hemangiomas). Both pharmacologic and procedural interventions can be utilized, and therapeutic selection is based on myriad factors including the lesion location, clinical subtype, size, depth (superficial vs deep), ulceration, and potential for scarring/permanent skin changes. See Table 110-1.

Table 110-1Infantile Hemangioma Treatment Table
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Table 110-1 Infantile Hemangioma Treatment Table
MEDICATION NAME INDICATIONa MECHANISM OF ACTION DOSING ADVERSE EFFECTS SUGGESTED MONITORING LEVEL OF EVIDENCE (REFERENCE)
Topical Therapy
Timolol maleate IH (best response if thin, superficial) Nonselective beta-adrenergic receptor antagonist 0.25%-0.5% gel-forming solution;1-2 drops BID Local irritation; ulceration. Risk of systemic absorption (bradycardia, hypoglycemia, bronchospasm) Consider clinical monitoring to assess response every 2-3 mo, with consideration for closer follow-up during early proliferative phase IA1-3
High-potency corticosteroids IH Anti-inflammatory Clobetasol, halobetasol, betamethasone 1-2 times daily Dyspigmentation, atrophy, telangiectasias, acne, infection None IB4-5
Imiquimod IH Immunomodulatory; TLR7 agonist 5% ointment or cream; every other night Edema, crusting, ulceration, erythema, pain None III6-7
Intralesional corticosteroids IH Anti-inflammatory Intralesional triamcinolone 10-40 mg/mL, max recommended 3 mg/kg/dose; +/− intralesional betamethasone Dyspigmentation, atrophy, telangiectasia, injection site reaction, Cushingoid appearance, growth retardation None IB4,8,9
Intralesional bleomycin IH; may consider after propranolol non-response Local sclerosis; non-specific inflammation 15 IU/mL injection; 0.3-0.5 IU/kg/dose Ulceration, tissue necrosis, pain/swelling at injection site, atrophy None IB9-10
Systemic Therapy
Propranolola FDA-approved for proliferating IH Nonselective β-adrenergic antagonist; works via vasoconstriction, antiangiogenesis, inhibition of nitric oxide production, regulation of renin-angiotensin-aldosterone system 2-3 mg/kg/d; starting dose 0.6 mg/kg BID and titrate to 1.7 mg/kg BID Hypoglycemia, bradycardia, sleep disturbance, diarrhea, bronchospasm, peripheral vasoconstriction. HR, BP clinical evaluation every 1-3 mo while on therapy; based on patient history, consider blood glucose, EKG, echocardiography, MRA/MRI brain; in office or inpatient monitoring may be appropriate in certain cases 1A1,3
Atenolol IH Cardioselective β-adrenergic antagonist 1-2 mg/kg/d GI disturbance (nausea, vomiting, diarrhea, constipation), sleep disturbance, cool/sweaty extremities Can consider monitoring HR, BP, respiratory symptoms, cardiac failure symptoms); clinical follow-up every 1-3 mo while on therapy IB11,12
Nadolol IH Non-selective β-adrenergic antagonist 2-4 mg/kg/d Sleep disturbance, bronchospasm, hypotension HR, BP; monitor for regular stools III13,14
Oral corticosteroids IH; particularly if beta blockade poorly tolerated or contraindicated Anti-inflammatory Prednisolone or prednisone; 2-3 mg/kg/d Cushingoid appearance, infection, osteoporosis, ...

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