Haemangioma: clinical course, complications and management


  • Funding sources None.
  • Conflicts of interest I.J.F. is a consultant for Pierre Fabre Dermatology


Ilona J. Frieden.

E-mail: FriedenI@derm.ucsf.edu


Despite their high incidence, most infantile haemangiomas (IH) do not require treatment as they regress spontaneously and most do not leave significant sequelae. For the subset of haemangiomas that require treatment, indications for intervention can be divided into three main categories: ulceration, disfigurement and impairment of function or vital structures. In addition, certain IH have a risk of associated structural anomalies. Given the wide heterogeneity of haemangiomas, deciding which haemangiomas need intervention and when to intervene requires a detailed knowledge of natural history and clinical indicators of increased risk.

Infantile haemangiomas (IH) are the most common benign vascular tumour in infancy, occurring in approximately 4–5% of the population.[1] Higher risk is associated with several well-known factors, including female sex, white non-Hispanic background, prematurity and multiple gestation.[2] Despite their high incidence, most IH do not require treatment as they regress spontaneously and most do not leave significant sequelae. For the subset of haemangiomas that require treatment, indications for intervention can be divided into three main categories: ulceration, disfigurement and impairment of function or vital structures. In addition, certain IH have a risk of associated structural anomalies. Given the wide heterogeneity of haemangiomas, deciding which haemangiomas need intervention and when to intervene requires a detailed knowledge of natural history and clinical indicators of increased risk (Table 1).

Table 1. Risk features and rationale for intervention
Risk featureRationale for intervention
High risk
Segmental > 5 cm – faceAssociated structural anomalies (PHACE) scarring, visual/airway compromise
Segmental > 5 cm – lumbosacral/perineal areaAssociated structural anomalies (LUMBAR), ulceration
Bulky lesion – face (prominent dermal thickening, steep ascent from normal to involved skin)Tissue distortion with risk of permanent scarring/disfigurement
Early white discolorationMarker of ulceration
Central faceHigh risk of disfigurement
Periorbital, perinasal, perioralFunctional compromise, risk of disfigurement
Intermediate risk
Lateral face, scalp, hands, feetRisk of disfigurement; lower but possible risk of functional compromise
Body folds (neck, perineum, axillae)Higher risk of ulceration
Segmental > 5 cm – trunk, arms, legsRisk of ulceration and permanent residual skin changes
Low risk
Trunk, arms, legs (nonvisible)Low risk of disfigurement or functional compromise

Clinical course

Infantile haemangiomas (IH) have predictable growth characteristics, and an understanding of natural history is important for anticipatory guidance for parents and planning of management. At birth, IH are either absent or present as a precursor lesion. Premonitory marks usually consist of a vasoconstricted patch, a bruise-like macule, or an erythematous telangiectatic patch.[3, 4] After birth, there is often an early proliferative phase characterized by rapid growth. In the case of those IH with substantial superficial growth, serial photographs of newborns show that the most rapid growth actually occurs between 5·5 and 7·5 weeks of age.[5] A long-appreciated characteristic of haemangioma growth is its tendency to mark out its territory early on, with growth proceeding volumetrically rather than radially.[6] Prospective cohort studies have helped more precisely to characterize the proliferative phase, demonstrating that haemangiomas, irrespective of subtype or depth, reach 80% of their final size by 3 months.[6] The early proliferative phase is followed by a period of slower growth until age 6–9 months, the late proliferative phase, and finally by a period of involution that gradually takes place over years.

Exceptions to this growth pattern are not rare, however. A small but significant minority do not grow as expected. These haemangiomas, so-called IH with minimal or arrested growth, typically present as a patch of fine or coarsely reticulated telangiectasias, often within a zone of vasoconstriction.[7] By definition < 25% of their area proliferates. The growth trajectory of deep and segmental haemangiomas also tends to differ from that of localized superficial IH. Deep haemangiomas show delayed onset of growth by about 1 month and continue to grow about 1 month longer than their superficial counterparts.[6] Approximately 3% of haemangiomas have a distinctly prolonged growth phase beyond 9 months of age, and the majority of these are deep or mixed haemangiomas and segmental haemangiomas.[6, 8] This information on growth underscores the importance of age in decision-making. For high-risk IH, referral and consideration of treatment should be as early as possible – ideally at 4 weeks of age or younger, so that treatment, if undertaken, can have optimum impact.

Gradual involution of the IH takes place over the course of years but may leave permanent changes in the skin. The incidence of residual lesions varies widely depending on the study and has been reported in 25–69% of untreated haemangiomas[9, 10]; however, these estimates are in a referral population and thus do not reflect the rates of all haemangiomas. The most frequent residual lesions are telangiectasias, fibrofatty tissue, anetoderma, atrophy, erythema and hypopigmentation. When they occur, the residual lesions of deep nodular haemangiomas usually have a fibrofatty component. In addition, ulceration virtually always leads to atrophic scarring.[9] While previous studies predicted final involution at approximately 10% per year, more recent studies indicate that involution ends at a median age of 3 years, and that most haemangiomas cease to improve after 3·5 years of age.[11] Based on the above data, if reconstruction is required, this is often best initiated between the ages of 3 and 4 years as further involution is unlikely to occur beyond this time, and delay of treatment may lead to unnecessary psychosocial impact on the child.[11]

Complications and management

The majority of haemangiomas do not require treatment as there is spontaneous involution without complications or significant sequelae. For these, ‘active nonintervention’ is the gold standard and consists of close observation, education and anticipatory guidance. In today's age of technology, parents can easily find incorrect or alarming information, reinforcing the importance of parental education in the office. Serial photography provides objective data when monitoring course and is enormously helpful in monitoring growth and involution.

For the significant minority of haemangiomas requiring intervention, the rationale for treatment is divided into three main indications: ulceration, disfigurement or risk thereof, and functional impairment. The decision to initiate treatment is generally clear-cut when there is a primarily medical rationale, e.g. a threat to vision or airway. However, the decision-making process is often less straightforward if risk of permanent disfigurement is the major concern.


Ulceration, the most common complication of IH, occurs in approximately 15–25% of patients in a referral setting,[12, 13] with the highest risk between the ages of 4 and 6 months.[12] Ulceration is associated with large size, segmental morphology, mixed superficial and deep morphology, and location on the neck, anogenital area or lower lip.[12, 14] In addition, early appearance of grey-white colour on the haemangioma surface at age 2–3 months is a sensitive indicator of impending ulceration.[15] Other important factors are friction and moisture, resulting in a higher incidence on the lower lip and intertriginous sites. Ulceration virtually always results in scarring. In addition it can result in significant pain and functional impairment, e.g. difficulty moving an affected limb or pain with feeding if the lip is ulcerated. Bleeding occurs in 40% of ulcerations. Although sometimes a source of great parental anxiety, clinically significant bleeding is rare. Frank infection of the wound is uncommon but colonization with bacteria is not uncommon.[12]

Treatment of ulceration is outlined in Table 2. An effective wound care regimen with topical therapy is essential to encourage wound healing, prevent infection and decrease pain. Infection should be considered if there is purulent drainage, erythema, induration of surrounding skin, or malodour. For recalcitrant ulcerations, becaplermin (topical platelet-derived growth factor) gel was reported to be effective in expediting healing.[16, 17] Of note, the U.S. Food and Drug Administration has placed a boxed warning on becaplermin owing to reports of increased incidence of cancer-related deaths in adult patients with leg ulcer. The significance of this finding in the paediatric population is unclear but reinforces becaplermin's position as a second-line treatment.[18] Pulsed dye laser (PDL) can also be helpful for relieving pain and expediting healing in ulcerated haemangiomas.[19-21] In recent years, the application of oral propranolol has been expanded to treatment of ulcerated IH, and based on case series appears promising.[22-25] Rapid pain control within 2 weeks and complete healing within 2–6 weeks at doses of 1–3 mg kg−1 daily were observed in most cases.[22-24] Another retrospective case-controlled study found more rapid healing time with propranolol compared with historically matched controls (8·7 weeks vs. 22·4 weeks).[25] There has been little experience with topical β-blockers for ulceration, but timolol has recently been reported to be well tolerated and effective in treating two patients with ulcerated perineal IH.[26] Caution is advised given paucity of safety data and possibility of more systemic absorption in this setting.[27] Lastly, for ulcerated lesions likely to require eventual surgical correction for scarring, early excision can be considered.

Table 2. Treatment of ulcerated hemangioma
  1. a

    Telfa®, Covidien, Mansfield, MA, U.S.A.; DuoDERM®, ConvaTec, Skillman, NJ, U.S.A.; Aquaphor®, Eucerinus, Wilton, CT, U.S.A.; Regranex®, Novartis, Basel, Switzerland.

Wound care
Vaseline-impregnated gauzeCost-effective as it can be made at home by impregnating cotton gauze in petrolatum
Nonadherent dressing (e.g. Telfa®)Helpful for areas with oozing or as secondary dressing on top of occlusive ointment
Thin hydrocolloid dressing (e.g. DuoDERM®)Useful in areas of ulceration where the area can be adequately sealed to prevent contamination with faeces and urine
White petrolatum, Aquaphor® or zinc oxide pasteLiberal use of emollient can help wound healing and decrease pain
Antimicrobials for ulcerated haemangioma
Metronidazole gelAnecdotally effective for perioral, neck, perineal ulcerations
Mupirocin or bacitracin ointmentSometimes used to prevent bacterial overgrowth of Gram-positive organisms
CephalexinObserved by some authors to expedite healing even without clinically evident infection.[96] If infection is suspected, choice of oral antibiotic should be directed by culture results
Pain control
Lidocaine 2·5–5% ointmentPea size to the area of ulceration up to 4× daily for temporary relief, useful to ease bathing or diapering
Paracetamol (acetaminophen)For mild to moderate pain
Paracetamol (acetaminophen) with codeine or with hydrocodoneFor severe, recalcitrant pain
Expedite healing
Becaplermin gel (Regranex®)Second line due to expense, black box warning (in adults). Wound bed should be free of crusting for maximal efficacy
Pulsed dye laser (PDL)Several reports of accelerated healing – usually treated with low fluences (5–6 J cm−2). Response is not uniform. PDL can cause induction of new ulceration, especially in segmental facial lesions.[20, 82] Typically 1–2 treatments required
Early excisionReasonable option for ulcerated haemangiomas that are likely to require eventual surgical correction for scarring
PropranololAppears to shorten healing time and cause improvement in several reports[22-24]

Disfigurement and scarring

Over the past decade, the potential of permanent skin changes and psychosocial impact of haemangioma residua, particularly those located on the face, has been increasingly appreciated.[28] Disease-specific scores for haemangioma have been proposed.[29, 30] As noted in the discussion on clinical course, the risk of disfigurement depends on location, morphological subtype, size, shape and growth phase of the haemangioma. A lower threshold for treatment is indicated for haemangiomas located on the central face, nose and lips, sites which are not only readily visible, but have particular curves and textures that may be permanently distorted by IH growth. Even relatively small haemangiomas (e.g. ≤ 1 cm) can lead to stigmatizing and permanent skin changes if they involve the central face. The greatest risk of these changes is in those with marked dermal thickening, particularly thick superficial, sessile or pedunculated IH that have a steep ascent from normal to involved skin.

Once the risk for permanent disfigurement has been established, timing emerges as the single most important factor in deciding whether to intervene. Have permanent skin alterations already occurred at the time of presentation or will intervention have the potential to change the ultimate outcome? The answer will depend in large part on the patient's age and growth kinetics of the particular haemangioma. Treatment early in life (i.e. 0–8 weeks) has a greater chance of impacting outcome; however, for many localized haemangiomas, the risk for disfigurement is difficult to ascertain at this young age. In some cases the best strategy may be one of frequent visits or weekly review of photographs to assess the haemangioma behaviour. If the patient presents after the early proliferative phase, permanent skin changes may have already occurred. In all cases, the benefit of treatment must be weighed against the side-effect profile of treatment and the uncertainty that intervention will alter long-term outcome. Often, the parent's tolerance of risk associated with intervention helps decide whether or not treatment is initiated.

β-Blockers are now considered first-line treatment for high-risk lesions. Propranolol has largely replaced oral corticosteroids for those IH requiring systemic therapy (Fig. 1). Timolol solution (typically 0·5% gel-forming solution) may be useful in small superficial haemangiomas that do not warrant systemic treatment (Fig. 2). When a facial haemangioma presents early and the need for oral treatment is unclear, timolol solution may be started in conjunction with close follow-up, and therapy can be transitioned to oral propranolol if progression with high-risk features ensues. Intralesional corticosteroid is still useful in select localized lesions, for example small lip or nasal tip haemangiomas. If permanent scarring has ensued, referral for consideration of early surgical excision is a reasonable option. PDL can be helpful in lightening any superficial skin changes such as erythema or telangiectasias. Parents should always be offered the option of re-evaluation at age 3–4 years to assess whether permanent skin changes have occurred and if subsequent measures such as surgical correction or laser treatment are indicated.

Figure 1.

Thick sessile haemangioma on the face; this type of haemangioma has a high risk for leaving anetoderma-type skin changes. (a) Child at 6 months old, before propranolol treatment; (b) at 9 months old, after propranolol treatment for 3 months with partial response highlighting the limitations of treatment when started late.

Figure 2.

Small mixed superficial and deep haemangioma on the forehead. (a) Child at 2 months old, before timolol; (b) at 6 months old, after timolol treatment for 4 months with an excellent response to treatment. Haemangiomas with a more gradual slope from normal to involved skin are less likely to leave residual skin changes compared with those with steep ascent.

Impairment of function

Functional impairment may occur in a number of settings. The best described is periocular haemangioma, but there are other examples. A bulky haemangioma involving the neck can result in positional torticollis or plagiocephaly. Ulcerated lip haemangiomas, as mentioned above, can lead to poor oral intake. Intranasal haemangiomas can cause difficulties in nasal breathing.

Periorbital haemangiomas most often result in astigmatism due to the mass effect of the haemangioma on the cornea. Other less common sequelae include visual axis obstruction and strabismus. If uncorrected, any of these can result in amblyopia and the risk of permanent vision loss.[31, 32] Infants with periorbital haemangiomas should be referred for ophthalmological evaluation early, and examinations should occur frequently during the proliferative phase. If visual compromise is detected or suspected, therapy is indicated. Systemic and intralesional corticosteroids, surgical excision and laser have been used in the past,[33-36] but propranolol has now become a first-line treatment in this setting.[31, 32, 36-39] For small superficial haemangiomas of the eyelid without associated visual compromise, topical timolol maleate shows promise as a safe, new treatment based on case series and reports.[40-43] Patching of the good eye is often used as a way to diminish the risk of amblyopia.

Impairment of vital structures

IH affecting the airway and liver may result in life-threatening complications. Cutaneous haemangioma over the ‘beard distribution’ (facial segment S3), especially when bilateral, marks patients who are at high risk for airway involvement. Any patient with bilateral mandibular distribution, even in the absence of overt respiratory symptoms, should be referred to an otolaryngologist for airway evaluation. If airway haemangioma is visualized, prompt systemic therapy should be initiated. Again, oral propranolol is becoming a first-line treatment, although in some cases adjunctive treatment with other therapeutic modalities such as oral steroids,[44-48] surgical debulking and laser ablation are used.[49, 50] Parents should be educated on the signs and symptoms of airway haemangiomas such as hoarse cry, stridor or noisy breathing, which often develop between 4 and 12 weeks of age.

The liver is the most common extracutaneous site of involvement. A recent prospective study of infants with multiple cutaneous IH confirmed that patients with more than five skin lesions are at significantly higher risk for hepatic haemangiomas (HH)[51] and should be screened using abdominal ultrasound with Doppler flow.[52] One retrospective study has recently suggested that the risk may be more significant in patients with 10 or more lesions.[53] Most cases of HH are asymptomatic and do not require treatment, but if detected should be followed with serial ultrasounds to monitor for stabilization of growth.[54] Multifocal disease can result in high output congestive heart failure. Diffuse disease with virtual replacement of the liver by haemangiomas is very rare but can result in abdominal compartment syndrome and consumptive hypothyroidism.[55-57] All infants with hepatic disease should have thyroid function tests, and repeat studies are needed if the number of HH is increasing.

Associated structural anomalies

Segmental haemangiomas of the face and lumbosacral/perineal regions should alert the physician to the possibility of underlying structural anomalies (Figs 3-6). Large, facial segmental (> 5 cm) haemangiomas may be associated with PHACE(s) syndrome (posterior fossa malformations, haemangiomas, arterial anomalies, cardiac anomalies, eye abnormalities and sternal/supraumbilical raphe).[58, 59] Up to 30% of patients with large, facial segmental haemangiomas have PHACE. Haemangiomas involving the frontotemporal (S1) or mandibular (S3) segments are at particularly high risk, although any segment may be involved, and rare cases of PHACE have been reported with segmental haemangiomas of the torso and extremities in the absence of facial segmental IH.[60, 61] The most common extracutaneous findings are arterial anomalies of the cerebral vasculature followed by coarctation of the aorta.[60] Consensus criteria for PHACE have been proposed.[58] Patients with large, facial segmental haemangiomas should be evaluated with magnetic resonance imaging (MRI) and a magnetic resonance angiogram (MRA) of the head and neck, echocardiogram and ophthalmological examination.

Figure 3.

Evaluation of segmental haemangioma at risk for structural abnormalities. ENT, ear, nose, throat (otolaryngology); eval, evaluation; mo, months; MRA, magnetic resonance angiogram; MRI, magnetic resonance imaging; TFT, thyroid function tests; U/S, ultrasound.

Figure 4.

Multiple infantile haemangiomas on the back. This patient also had additional lesions on the face and extremities. A liver ultrasound at 2 months of age was negative for hepatic involvement.

Figure 5.

Severe perineal ulceration of a segmental infantile haemangioma: (a) at 2 months old, pretreatment; note the presence of early white discoloration at the periphery (‘white haemangioma sign’); (b) at 4 months old, healed ulcers treated with low-dose propranolol (1 mg kg−1 daily) and becaplermin gel.

Figure 6.

PHACE syndrome. This patient had (a) bilateral S3 (mandibular) segmental haemangioma with airway disease, (b) abdominal raphe. More widespread extrafacial haemangioma was present in this case extending down to the chest, back and right arm. Echocardiogram showed a tortuous aortic arch.

Because they are at high risk for haemangioma-related complications (e.g. disfigurement, ulceration, visual or airway compromise), most infants with PHACE require systemic therapy to treat their haemangioma(s).[62] Propranolol has become first-line therapy for IH (see discussion below) but in this setting carries a theoretical potential for causing stroke in patients with PHACE with significant arterial disease, as lowering of blood pressure could create demand-related ischaemia.[63] A recent, retrospective study of 32 patients with PHACE receiving propranolol found no patients with stroke or other catastrophic neurological event during treatment; however, worsened ulceration in the haemangioma and digital infarcts occurred in two patients. Caution is advised when using propranolol in this setting. Criteria for risk stratification of cerebrovascular findings have been proposed.[64] Ideally, patients at high risk for PHACE should have an MRI and MRA as well as echocardiogram prior to or at the inception of propranolol initiation. Propranolol in this setting should be dosed three times per day with slow upward titration, with the dosage kept at a minimum effective dose for the complications being treated.[64, 65]

Similarly, large segmental IH over the lumbosacral or perineal regions may be associated with underlying lipomyelomeningocele, tethered cord and other structural anomalies. Various names have been used to describe these associations, including LUMBAR (lower body haemangioma and other cutaneous defects, urogenital anomalies, ulceration, myelopathy, bony deformities, anorectal malformations, arterial anomalies and renal anomalies), PELVIS (perineal haemangioma, external genitalia malformations, lipomyelomeningocele, vesicorenal abnormalities, imperforate anus and skin tag syndrome) and SACRAL syndrome (spinal dysraphism, anogenital, cutaneous, renal and urological anomalies, associated with an angioma of lumbosacral localization), with all of these acronyms referring to the same group of associated anomalies.[66-68] MRI with contrast of the spine is the modality of choice for imaging at-risk infants. In patients with no evidence of sinus tract, ulceration of skin or neurological symptoms, this can be deferred until 4–6 months of age. For infants aged < 3 months, ultrasound may be used as an initial screening tool; however, for high-risk lesions, this should be followed by an MRI at 4–6 months of age as false negatives occur with ultrasound.[68, 69]


When treatment of IH is needed, the initial decision is whether to treat with topical/local or systemic therapy. Unfortunately, there has been a paucity of well-designed studies to provide evidence for the many proposed treatments of IH.[70] In general, topical/local agents are best employed for small, superficial and localized haemangiomas or during early proliferation when it may not be possible to determine whether a deeper component is present. Systemic therapy is reserved for larger IH, those with more aggressive growth characteristics or high threat of functional impairment, and those not responding to local measures where treatment is deemed necessary.

Topical/local therapies

Several topical agents have been proposed for use in IH. Since the first report in 2010, studies have supported the efficacy of timolol maleate 0·5% solution for treatment of small, superficial IH, including those of the periorbital region,[41, 42, 71, 72] although randomized placebo-controlled double-blind studies are lacking at this time. The gel-forming solution vehicle is preferred for haemangioma treatment as it has been shown to have less systemic bioavailability than solution form.[27] Theoretical complications may include hypoglycaemia, hypotension, wheezing and bradycardia secondary to systemic absorption. Thus far, such complications have not been reported in infants treated for IH. Until more is known, restricting use to 1–2 drops per application on intact (nonulcerated) skin has been advocated.[27] Clobetasol has also been shown to have some benefit in superficial IH, particularly in periorbital lesions.[73] Topical imiquimod cream may also be considered in early IH of the head and neck.[74-77] Possible complications include irritation, crusting and ulceration.

Intralesional steroids maintain a useful role as a local treatment for select cases, particularly for early, localized haemangiomas of the lip or nasal tip. Intralesional steroids may stabilize growth or decrease the size of the haemangioma, thus helping to avoid systemic therapy or surgery. Unlike topical therapies, intralesional injection is effective in deeper or bulkier lesions. Treatment should be initiated early for maximal efficacy and is usually repeated every 3–4 weeks until the growth phase is past. Usually, triamcinolone 10 mg mL−1 is employed, and doses should not exceed 1–2 mg kg−1 per injection. Possible side-effects include bleeding, skin atrophy and adrenal suppression from systemic absorption.

The flash lamp pumped PDL, usually at 595 nm, is the most common laser used for treatment of IH. PDL is generally accepted as being useful in lightening erythema and telangiectasias after involution and in accelerating healing of ulcerated PDL (see Table 2). Some authors also advocate using PDL to treat proliferating haemangiomas,[78, 79] but this strategy remains controversial.[80, 81] PDL can result in ulceration at fluences generally considered safe for port-wine stains so caution is recommended in treating IH with PDL.[82] Recently, ablative fractional carbon dioxide laser has been reported useful in ameliorating residual scarring.[83]

Systemic therapies


Since its efficacy in shrinking IH was first reported by Léauté-Labrèze et al.[84] 5 years ago, propranolol has dramatically altered the treatment landscape of haemangiomas. It is now considered by most experts to be the first-line therapy when systemic treatment is indicated. Over 200 articles including more than 1200 treated patients have since reported its efficacy, although the vast majority of these have been retrospective cohort studies.[85] Results from a large, international, randomized controlled trial should help to clarify further both the efficacy and toxicity of propranolol. Systematic reviews have shown response rates in approximately 97% of cases with better efficacy and less toxicity than the previous ‘gold standard’, systemic corticosteroids.[86] It seems to be effective in halting growth and diminishing size of haemangiomas not only during the proliferative phase but also, to a lesser extent, once growth has been completed.[87] Studies of propranolol use in ulcerated haemangiomas, periocular haemangiomas, airway haemangiomas and liver haemangiomas support its use in these specific clinical settings.[24, 38, 88, 89]

The majority of patients tolerate the doses used to treat IH (1–3 mg kg−1 daily) with minimal adverse events. In a recent systematic review, there were 371 total adverse events reported in 1189 patients. The most common adverse events are sleep disturbance and cold hands and feet. Hypotension was seen in 44 patients, although only five were reported symptomatic. Bradycardia occurred in nine patients, one of which was symptomatic, and respiratory events (infections, wheezing, stridor, etc.) in 35 patients. The most concerning side-effect of propranolol is symptomatic hypoglycaemia, which was noted in four patients, one of whom developed hypoglycaemic seizures.[90] Patients on propranolol are at risk for hypoglycaemia during prolonged periods of fasting or poor oral intake, e.g. during an acute illness. Frequent feedings, administration of the medication following feeds and avoidance of long periods of sleep help to minimize this risk.

Protocols for initiation and monitoring of propranolol may vary between centres. Consensus guidelines from a multidisciplinary expert panel have recently been published[65]; however, these are based on expert opinion rather than rigorous controlled studies, and as more data are rapidly accruing, these recommendations are likely to evolve over time. For infants younger than 2 months of age, these guidelines propose brief inpatient hospitalization for monitoring during induction of treatment. Initial dosing of propranolol starts at 0·5 mg kg−1 daily divided three times daily, increasing slowly to the desired dose.[65] Although protocols for administration vary widely, propranolol is usually administered at 1–3 mg kg−1 daily, with many practitioners favouring 2 mg kg−1 daily.[65, 91] Heart rate and blood pressure are monitored before treatment, at 1 and 2 h following the initial dose, and after any increased dose over 0·5 mg kg−1 daily. Infants should be fed every 4–6 h.[65]

There are no current guidelines on duration of therapy. Discontinuation of propranolol results in rebound growth in a subset of patients.[92] Therefore, many clinicians maintain treatment until the growth phase is completed, which can be up to 1 year of age in deep or large IH. Predictive factors that may predispose patients to rebound growth have yet to be identified. Currently, studies are under way to better characterize these factors, which may aid in determining which infants are at risk for recurrence.

Although most of the body of experience concerns propranolol, other β-blockers for the treatment of IH have been reported, including atenolol, acebutolol and nadolol.[93-95] Head-to-head trials comparing efficacy of these particular agents compared with propranolol have yet to be performed.

Systemic corticosteroids

Corticosteroids have traditionally been the mainstay of therapy for IH since the 1960s, but use as first-line treatment has largely been supplanted by propranolol. Prednisolone is usually administered at doses of 2–3 mg kg−1 daily as a single daily dose. It is usually effective in halting haemangioma growth during the proliferative phase. Side-effects are well documented and include gastrointestinal upset and irritability, weight gain, cushingoid appearance, hypertension, growth delay, adrenal suppression and immunosuppression. Height, weight and blood pressure should be monitored while on treatment.


IHs are common, and while most do not require treatment, a small minority do. Practitioners should be familiar with the natural history, specific growth characteristics and potential complications associated with IH, including ulceration, risk of disfigurement, functional impairment and potential association with structural anomalies. For high-risk lesions, referral or active invention is recommended, ideally as early as 4–6 weeks of age.


  • Image of creator

    Minnelly Luu, M.D. completed her undergraduate studies at Stanford University and subsequently attended medical school at Northwestern University in Chicago, IL, where she first developed an interest in pediatric dermatology. She trained in Dermatology at the State University of New York Downstate in Brooklyn, NY and is currently completing her pediatric dermatology fellowship at the University of California San Francisco under the mentorship of Dr. Ilona Frieden and her department. In fall 2013, Minnelly will start her career as Assistant Professor of Dermatology at the University of Southern California, where she will practice pediatric dermatology at the Children's Hospital Los Angeles. Her interests include atopic dermatitis and vascular birthmarks and anomalies.

  • Image of creator

    I.J. Frieden is a Professor of Pediatrics and Dermatology, Vice-Chair of Dermatology, and Chief of the Division of Pediatric Dermatology at the University of California, San Francisco. She received her medical degree from the University of California, San Francisco, where she also completed a paediatric internship and residency as well as a dermatology residency. She has been President of the Society for Pediatric Dermatology, President of the American Board of Dermatology and currently serves as a member of the Board of Directors of the American Academy of Dermatology. She is currently co-editor-in-chief of the journal Pediatric Dermatology and Secretary of the International Society for the Study of Vascular Anomalies. She is also on the steering committee of the Leadership Institute of the American Academy of Dermatology.

    Her particular interest in haemangiomas and other vascular birthmarks dates back to her dermatology residency at UCSF and to her “mini-fellowship” with Dr. Esterly in 1983. In 1991 she founded the Birthmarks and Vascular Anomalies Center at UCSF, which continues to meet on a monthly basis. In 2001 she helped found the Hemangioma Investigator group. She is the author of over 200 articles, numerous book chapters and is co-editor of the textbook, Neonatal Dermatology, now in its 2nd edition.