BJD

S CH O L A R L Y R E V I E W British Journal of Dermatology

Haemangioma: clinical course, complications and

management
M. Luu and I.J. Frieden
Department of Dermatology, University of California San Francisco, 3rd floor, 1701 Divisidero Street, San Francisco, CA 94115,U.S.A.

Summary

Correspondence Despite their high incidence, most infantile haemangiomas (IH) do not require
Ilona J. Frieden. treatment as they regress spontaneously and most do not leave significant
E-mail: FriedenI@derm.ucsf.edu
sequelae. For the subset of haemangiomas that require treatment, indications
Accepted for publication for intervention can be divided into three main categories: ulceration, disfigure-
11 May 2013 ment and impairment of function or vital structures. In addition, certain IH
have a risk of associated structural anomalies. Given the wide heterogeneity of
Funding sources haemangiomas, deciding which haemangiomas need intervention and when to
None. intervene requires a detailed knowledge of natural history and clinical indicators
of increased risk.
Conflicts of interest
I.J.F. is a consultant for Pierre Fabre Dermatology

DOI 10.1111/bjd.12436

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 seque-
lae. For the subset of haemangiomas that require treatment,
indications for intervention can be divided into three main
categories: ulceration, disfigurement and impairment of func-
tion or vital structures. In addition, certain IH have a risk of
associated structural anomalies. Given the wide heterogeneity
of haemangiomas, deciding which haemangiomas need inter-
vention and when to intervene requires a detailed knowledge
of natural history and clinical indicators of increased risk
(Table 1).
Clinical course
Infantile haemangiomas (IH) have predictable growth charac-
teristics, and an understanding of natural history is important
for anticipatory guidance for parents and planning of manage-
ment. 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, demon-
strating 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 tel-
angiectasias, often within a zone of vasoconstriction.7 By defi-
nition < 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 con-
tinue to grow about 1 month longer than their superficial
counterparts.6 Approximately 3% of haemangiomas have a dis-
tinctly 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

20 British Journal of Dermatology (2013) 169, pp20–30 Ó 2013 British Association of Dermatologists
 Haemangioma: clinical course, complications and management, M. Luu and I.J. Frieden 21
Table 1 Risk features and rationale for intervention
Risk feature
High risk
Segmental > 5 cm – face
Segmental > 5 cm – lumbosacral/perineal area
Bulky lesion – face (prominent dermal thickening,
steep ascent from normal to involved skin)
Early white discoloration
Central face
Periorbital, perinasal, perioral
Intermediate risk
Lateral face, scalp, hands, feet
Body folds (neck, perineum, axillae)
Segmental > 5 cm – trunk, arms, legs
Low risk
Trunk, arms, legs (nonvisible)
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 hae-
mangiomas9,10; however, these estimates are in a referral
population and thus do not reflect the rates of all haeman-
giomas. The most frequent residual lesions are telangiectasias,
fibrofatty tissue, anetoderma, atrophy, erythema and hypo-
pigmentation. When they occur, the residual lesions of deep
nodular haemangiomas usually have a fibrofatty component.
In addition, ulceration virtually always leads to atrophic scar-
ring.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 sig-
nificant 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 pho-
tography 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,
Ó 2013 British Association of Dermatologists
Rationale for intervention
Associated structural anomalies (PHACE) scarring, visual/airway compromise
Associated structural anomalies (LUMBAR), ulceration
Tissue distortion with risk of permanent scarring/disfigurement
Marker of ulceration
High risk of disfigurement
Functional compromise, risk of disfigurement
Risk of disfigurement; lower but possible risk of functional compromise
Higher risk of ulceration
Risk of ulceration and permanent residual skin changes
Low risk of disfigurement or functional compromise
and functional impairment. The decision to initiate treatment
is generally clear-cut when there is a primarily medical ratio-
nale, e.g. a threat to vision or airway. However, the decision-
making process is often less straightforward if risk of perma-
nent disfigurement is the major concern.
Ulceration
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 morphol-
ogy, 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 ulcer-
ation.15 Other important factors are friction and moisture,
resulting in a higher incidence on the lower lip and intertrig-
inous sites. Ulceration virtually always results in scarring. In
addition it can result in significant pain and functional impair-
ment, 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 drain-
age, 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
British Journal of Dermatology (2013) 169, pp20–30
22 Haemangioma: clinical course, complications and management, M. Luu and I.J. Frieden

Table 2 Treatment of ulcerated hemangioma

Treatmenta Comment
Wound care
Dressing
Vaseline-impregnated gauze Cost-effective as it can be made at home by impregnating cotton gauze in petrolatum
Nonadherent dressing (e.g. Telfaâ) Helpful for areas with oozing or as secondary dressing on top of occlusive ointment
Thin hydrocolloid dressing (e.g. DuoDERMâ) Useful in areas of ulceration where the area can be adequately sealed to prevent
contamination with faeces and urine
Topical
White petrolatum, Aquaphorâ or zinc oxide paste Liberal use of emollient can help wound healing and decrease pain
Antimicrobials for ulcerated haemangioma
Topical
Metronidazole gel Anecdotally effective for perioral, neck, perineal ulcerations
Mupirocin or bacitracin ointment Sometimes used to prevent bacterial overgrowth of Gram-positive organisms
Oral
Cephalexin Observed 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
Topical
Lidocaine 2
5–5% ointment Pea size to the area of ulceration up to 49 daily for temporary relief, useful to ease
bathing or diapering
Oral
Paracetamol (acetaminophen) For mild to moderate pain
Paracetamol (acetaminophen) For severe, recalcitrant pain
with codeine or with hydrocodone
Expedite healing
Local
Becaplermin gel (Regranexâ) 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 excision Reasonable option for ulcerated haemangiomas that are likely to require eventual surgical
correction for scarring
Oral
Propranolol Appears to shorten healing time and cause improvement in several reports22–24
a
Telfaâ, Covidien, Mansfield, MA, U.S.A.; DuoDERMâ, ConvaTec, Skillman, NJ, U.S.A.; Aquaphorâ, Eucerinus, Wilton, CT, U.S.A.; Regra-
nexâ, Novartis, Basel, Switzerland.

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 com-
plete 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 propran-
olol compared with historically matched controls (8
7 weeks
vs. 22
4 weeks).25 There has been little experience with topi-
cal b-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 absorp-
tion in this setting.27 Lastly, for ulcerated lesions likely to
require eventual surgical correction for scarring, early excision
can be considered.
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 pro-
posed.29,30 As noted in the discussion on clinical course, the
risk of disfigurement depends on location, morphological sub-
type, 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

British Journal of Dermatology (2013) 169, pp20–30 Ó 2013 British Association of Dermatologists
 Haemangioma: clinical course, complications and management, M. Luu and I.J. Frieden 23
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 estab-
lished, timing emerges as the single most important factor in
deciding whether to intervene. Have permanent skin altera-
tions already occurred at the time of presentation or will
intervention have the potential to change the ultimate out-
come? The answer will depend in large part on the patient’s
age and growth kinetics of the particular haemangioma. Treat-
ment early in life (i.e. 0–8 weeks) has a greater chance of
impacting outcome; however, for many localized haemangio-
mas, the risk for disfigurement is difficult to ascertain at this
young age. In some cases the best strategy may be one of fre-
quent 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 interven-
tion helps decide whether or not treatment is initiated.
b-Blockers are now considered first-line treatment for high-
risk lesions. Propranolol has largely replaced oral corticoster-
oids 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 sys-
temic treatment (Fig. 2). When a facial haemangioma presents
early and the need for oral treatment is unclear, timolol solu-
tion 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
(a) (b)
Fig 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.
Ó 2013 British Association of Dermatologists
nasal tip haemangiomas. If permanent scarring has ensued,
referral for consideration of early surgical excision is a reason-
able 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 correc-
tion or laser treatment are indicated.
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 ophthal-
mological evaluation early, and examinations should occur fre-
quently during the proliferative phase. If visual compromise is
detected or suspected, therapy is indicated. Systemic and int-
ralesional 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 compro-
mise, 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.
(a) (b)
Fig 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.
British Journal of Dermatology (2013) 169, pp20–30
24 Haemangioma: clinical course, complications and management, M. Luu and I.J. Frieden
Impairment of vital structures
IH affecting the airway and liver may result in life-threatening
complications. Cutaneous haemangioma over the ‘beard distri-
bution’ (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 haemangi-
oma is visualized, prompt systemic therapy should be initi-
ated. 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 multi-
ple cutaneous IH confirmed that patients with more than five
skin lesions are at significantly higher risk for hepatic haeman-
giomas (HH)51 and should be screened using abdominal ultra-
sound 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
British Journal of Dermatology (2013) 169, pp20–30
asymptomatic and do not require treatment, but if detected
should be followed with serial ultrasounds to monitor for sta-
bilization 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 under-
lying 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. Haeman-
giomas 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 ex-
Fig 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.
Ó 2013 British Association of Dermatologists
 Haemangioma: clinical course, complications and management, M. Luu and I.J. Frieden 25

compromise), most infants with PHACE require systemic ther-

Fig 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.
tracutaneous findings are arterial anomalies of the cerebral vas-
culature followed by coarctation of the aorta.60 Consensus cri-
teria for PHACE have been proposed.58 Patients with large,
facial segmental haemangiomas should be evaluated with mag-
netic resonance imaging (MRI) and a magnetic resonance
angiogram (MRA) of the head and neck, echocardiogram and
ophthalmological examination.
Because they are at high risk for haemangioma-related com-
plications (e.g. disfigurement, ulceration, visual or airway
apy to treat their haemangioma(s).62 Propranolol has become
first-line therapy for IH (see discussion below) but in this set-
ting 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 receiv-
ing propranolol found no patients with stroke or other cata-
strophic neurological event during treatment; however,
worsened ulceration in the haemangioma and digital infarcts
occurred in two patients. Caution is advised when using pro-
pranolol in this setting. Criteria for risk stratification of cere-
brovascular 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 peri-
neal regions may be associated with underlying lipomyelom-
eningocele, 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, myelo-
pathy, bony deformities, anorectal malformations, arterial anom-

(a) (b)

Fig 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.

(a) (b)

Fig 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.

Ó 2013 British Association of Dermatologists British Journal of Dermatology (2013) 169, pp20–30
26 Haemangioma: clinical course, complications and management, M. Luu and I.J. Frieden
alies and renal anomalies), PELVIS (perineal haemangioma,
external genitalia malformations, lipomyelomeningocele, ve-
sicorenal abnormalities, imperforate anus and skin tag syn-
drome) and SACRAL syndrome (spinal dysraphism,
anogenital, cutaneous, renal and urological anomalies, associ-
ated 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 evi-
dence of sinus tract, ulceration of skin or neurological symp-
toms, 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
Treatment
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 stud-
ies 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, superfi-
cial 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 Theo-
retical complications may include hypoglycaemia, hypoten-
sion, 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 (nonul-
cerated) 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 treat-
ment for select cases, particularly for early, localized haeman-
giomas 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
British Journal of Dermatology (2013) 169, pp20–30
therapies, intralesional injection is effective in deeper or bulk-
ier 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 telangiec-
tasias 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 flu-
ences 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
b-Blockers
Since its efficacy in shrinking IH was first reported by Leaute-
Labreze 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 effi-
cacy, although the vast majority of these have been retrospec-
tive 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 feed-
Ó 2013 British Association of Dermatologists
 Haemangioma: clinical course, complications and management, M. Luu and I.J. Frieden 27
ings, 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 multidisci-
plinary expert panel have recently been published65; however,
these are based on expert opinion rather than rigorous con-
trolled 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 treat-
ment 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 charac-
terize these factors, which may aid in determining which
infants are at risk for recurrence.
Although most of the body of experience concerns propran-
olol, other b-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 lar-
gely 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 docu-
mented 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.
Conclusions
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
Ó 2013 British Association of Dermatologists
with structural anomalies. For high-risk lesions, referral or
active invention is recommended, ideally as early as 4–6 weeks
of age.
References
1 Kilcline C, Frieden IJ. Infantile hemangiomas: how common are
they? A systematic review of the medical literature. Pediatr Dermatol
2008; 25:168–73.
2 Haggstrom AN, Drolet BA, Baselga E et al. Prospective study of
infantile hemangiomas: demographic, prenatal, and perinatal char-
acteristics. J Pediatr 2007; 150:291–4.
3 Payne MM, Moyer F, Marcks KM et al. The precursor to the hem-
angioma. Plastic Reconstr Surg 1966; 38:64–7.
4 Hidano A, Nakajima S. Earliest features of the strawberry mark in
the newborn. Br J Dermatol 1972; 87:138–44.
5 Tollefson MM, Frieden IJ. Early growth of infantile hemangiomas:
what parents’ photographs tell us. Pediatrics 2012; 130:e314–20.
6 Chang LC, Haggstrom AN, Drolet BA et al. Growth characteristics
of infantile hemangiomas: implications for management. Pediatrics
2008; 122:360–7.
7 Suh KY, Frieden IJ. Infantile hemangiomas with minimal or
arrested growth: a retrospective case series. Arch Dermatol 2010;
146:971–6.
8 Brandling-Bennett HA, Metry DW, Baselga E et al. Infantile heman-
giomas with unusually prolonged growth phase: a case series. Arch
Dermatol 2008; 144:1632–7.
9 Bauland CG, Luning TH, Smit JM et al. Untreated hemangiomas:
growth pattern and residual lesions. Plastic Reconstr Surg 2011;
127:1643–8.
10 Bowers RE, Graham EA, Tomlinson KM. The natural history of the
strawberry nevus. Arch Dermatol 1960; 82:667–80.
11 Couto RA, Maclellan RA, Zurakowski D et al. Infantile hemangi-
oma: clinical assessment of the involuting phase and implications
for management. Plastic Reconstr Surg 2012; 130:619–24.
12 Chamlin SL, Haggstrom AN, Drolet BA et al. Multicenter prospec-
tive study of ulcerated hemangiomas. J Pediatr 2007; 151:684–9, 9
e1.
13 Hermans DJ, Boezeman JB, Van de Kerkhof PC et al. Differences
between ulcerated and non-ulcerated hemangiomas, a retrospective
study of 465 cases. Eur J Dermatol 2009; 19:152–6.
14 Shin HT, Orlow SJ, Chang MW. Ulcerated haemangioma of
infancy: a retrospective review of 47 patients. Br J Dermatol 2007;
156:1050–2.
15 Maguiness SM, Hoffman WY, McCalmont TH et al. Early white dis-
coloration of infantile hemangioma: a sign of impending ulcera-
tion. Arch Dermatol 2010; 146:1235–9.
16 Metz BJ, Rubenstein MC, Levy ML et al. Response of ulcerated peri-
neal hemangiomas of infancy to becaplermin gel, a recombinant
human platelet-derived growth factor. Arch Dermatol 2004;
140:867–70.
17 Sugarman JL, Mauro TM, Frieden IJ. Treatment of an ulcerated
hemangioma with recombinant platelet-derived growth factor. Arch
Dermatol 2002; 138:314–16.
18 Frieden IJ. Addendum: commentary on becaplermin gel (Regra-
nex) for hemangiomas. Pediatr Dermatol 2008; 25:590.
19 David LR, Malek MM, Argenta LC. Efficacy of pulse dye laser ther-
apy for the treatment of ulcerated haemangiomas: a review of 78
patients. Br J Plast Surg 2003; 56:317–27.
20 Kim HJ, Colombo M, Frieden IJ. Ulcerated hemangiomas: clinical
characteristics and response to therapy. J Am Acad Dermatol 2001;
44:962–72.
British Journal of Dermatology (2013) 169, pp20–30
28 Haemangioma: clinical course, complications and management, M. Luu and I.J. Frieden
21 Morelli JG, Tan OT, Weston WL. Treatment of ulcerated heman-
giomas with the pulsed tunable dye laser. Am J Dis Child 1991;
145:1062–4.
22 Hong E, Fischer G. Propranolol for recalcitrant ulcerated hemangi-
oma of infancy. Pediatr Dermatol 2012; 29:64–7.
23 Kim LH, Hogeling M, Wargon O et al. Propranolol: useful thera-
peutic agent for the treatment of ulcerated infantile hemangiomas.
J Pediatr Surg 2011; 46:759–63.
24 Saint-Jean M, Leaute-Labreze C, Mazereeuw-Hautier J et al. Pro-
pranolol for treatment of ulcerated infantile hemangiomas. J Am
Acad Dermatol 2011; 64:827–32.
25 Hermans DJ, van Beynum IM, Schultze Kool LJ et al. Propranolol, a
very promising treatment for ulceration in infantile hemangiomas:
a study of 20 cases with matched historical controls. J Am Acad Der-
matol 2011; 64:833–8.
26 Cante V, Pham-Ledard A, Imbert E et al. First report of topical
timolol treatment in primarily ulcerated perineal haemangioma.
Arch Dis Child Fetal Neonatal Ed 2012; 97:F155–6.
27 McMahon P, Oza V, Frieden IJ. Topical timolol for infantile he-
mangiomas: putting a note of caution in ‘cautiously optimistic’.
Pediatr Dermatol 2012; 29:127–30.
28 Tanner JL, Dechert MP, Frieden IJ. Growing up with a facial hem-
angioma: parent and child coping and adaptation. Pediatrics 1998;
101:446–52.
29 Janmohamed SR, de Waard-van der Spek FB, Madern GC et al.
Scoring the proliferative activity of haemangioma of infancy: the
Haemangioma Activity Score (HAS). Clin Exp Dermatol 2011;
36:715–23.
30 Haggstrom AN, Beaumont JL, Lai JS et al. Measuring the severity of
infantile hemangiomas: instrument development and reliability.
Arch Dermatol 2012; 148:197–202.
31 Ceisler EJ, Santos L, Blei F. Periocular hemangiomas: what every
physician should know. Pediatr Dermatol 2004; 21:1–9.
32 Bramhall RJ, Quaba A. A review of 58 patients with periorbital ha-
emangiomas to determine appropriate cases for intervention. J Plast
Reconstr Aesthet Surg 2008; 61:138–49.
33 Ranchod TM, Frieden IJ, Fredrick DR. Corticosteroid treatment of
periorbital haemangioma of infancy: a review of the evidence. Br J
Ophthalmol 2005; 89:1134–8.
34 Jalil A, Maino A, Bhojwani R et al. Clinical review of periorbital
capillary hemangioma of infancy. J Pediatr Ophthalmol Strabismus 2011;
48:218–25.
35 Schneider D, Lee MS, Harrison AR et al. Excision of periorbital he-
mangiomas to correct visual abnormalities. Arch Facial Plast Surg
2011; 13:195–8.
36 Ni N, Guo S, Langer P. Current concepts in the management of
periocular infantile (capillary) hemangioma. Curr Opin Ophthalmol
2011; 22:419–25.
37 El-Essawy R, Galal R, Abdelbaki S. Nonselective beta-blocker pro-
pranolol for orbital and periorbital hemangiomas in infants: a new
first-line of treatment? Clin Ophthalmol 2011; 5:1639–44.
38 Spiteri Cornish K, Reddy AR. The use of propranolol in the man-
agement of periocular capillary haemangioma – a systematic
review. Eye (Lond) 2011; 25:1277–83.
39 Cheng JF, Gole GA, Sullivan TJ. Propranolol in the management of
periorbital infantile haemangioma. Clin Exp Ophthalmol 2010;
38:547–53.
40 Xue K, Hildebrand GD. Topical timolol maleate 0.5% for infantile
capillary haemangioma of the eyelid. Br J Ophthalmol 2012;
96:1536–7.
41 Guo S, Ni N. Topical treatment for capillary hemangioma of the
eyelid using beta-blocker solution. Arch Ophthalmol 2010; 128:
255–6.
British Journal of Dermatology (2013) 169, pp20–30
42 Ni N, Langer P, Wagner R et al. Topical timolol for periocular
hemangioma: report of further study. Arch Ophthalmol 2011;
129:377–9.
43 Calvo M, Garcia-Millan C, Villegas C et al. Topical timolol for
infantile hemangioma of the eyelid. Int J Dermatol 2012; 52:603–
4.
44 Javia LR, Zur KB, Jacobs IN. Evolving treatments in the manage-
ment of laryngotracheal hemangiomas: will propranolol supplant
steroids and surgery? Int J Pediatr Otorhinolaryngol 2011; 75:1450–
4.
45 Denoyelle F, Leboulanger N, Enjolras O et al. Role of propranolol
in the therapeutic strategy of infantile laryngotracheal hemangi-
oma. Int J Pediatr Otorhinolaryngol 2009; 73:1168–72.
46 Buckmiller L, Dyamenahalli U, Richter GT. Propranolol for airway
hemangiomas: case report of novel treatment. Laryngoscope 2009;
119:2051–4.
47 Truong MT, Chang KW, Berk DR et al. Propranolol for the treat-
ment of a life-threatening subglottic and mediastinal infantile
hemangioma. J Pediatr 2010; 156:335–8.
48 Leboulanger N, Fayoux P, Teissier N et al. Propranolol in the thera-
peutic strategy of infantile laryngotracheal hemangioma: a preli-
minary retrospective study of French experience. Int J Pediatr
Otorhinolaryngol 2010; 74:1254–7.
49 Bitar MA, Moukarbel RV, Zalzal GH. Management of congenital
subglottic hemangioma: trends and success over the past 17 years.
Otolaryngol Head Neck Surg 2005; 132:226–31.
50 Vijayasekaran S, White DR, Hartley BE et al. Open excision of sub-
glottic hemangiomas to avoid tracheostomy. Arch Otolaryngol Head
Neck Surg 2006; 132:159–63.
51 Horii KA, Drolet BA, Frieden IJ et al. Prospective study of the fre-
quency of hepatic hemangiomas in infants with multiple cutane-
ous infantile hemangiomas. Pediatr Dermatol 2011; 28:245–53.
52 Dickie B, Dasgupta R, Nair R et al. Spectrum of hepatic heman-
giomas: management and outcome. J Pediatr Surg 2009; 44:125–
33.
53 Vredenborg AD, Janmohamed SR, de Laat PC et al. Multiple cutane-
ous infantile haemangioma and the risk of internal haemangioma.
Br J Dermatol 2013; 169:188–191.
54 Maguiness SM, Frieden IJ. Management of difficult infantile ha-
emangiomas. Arch Dis Child 2012; 97:266–71.
55 Christison-Lagay ER, Burrows PE, Alomari A et al. Hepatic heman-
giomas: subtype classification and development of a clinical prac-
tice algorithm and registry. J Pediatr Surg 2007; 42:62–7; discussion
7-8.
56 Kulungowski AM, Alomari AI, Chawla A et al. Lessons from a liver
hemangioma registry: subtype classification. J Pediatr Surg 2012;
47:165–70.
57 Bessho K, Etani Y, Ichimori H, et al. Increased type 3 iodothyro-
nine deiodinase activity in a regrown hepatic hemangioma with
consumptive hypothyroidism. Eur J Pediatr 2010; 169:215–21.
58 Metry D, Heyer G, Hess C et al. Consensus statement on diagnostic
criteria for PHACE syndrome. Pediatrics 2009; 124:1447–56.
59 Frieden IJ, Reese V, Cohen D. PHACE syndrome. The association
of posterior fossa brain malformations, hemangiomas, arterial
anomalies, coarctation of the aorta and cardiac defects, and eye
abnormalities. Arch Dermatol 1996; 132:307–11.
60 Haggstrom AN, Garzon MC, Baselga E et al. Risk for PHACE syn-
drome in infants with large facial hemangiomas. Pediatrics 2010;
126:e418–26.
61 Nabatian AS, Milgraum SS, Hess CP et al. PHACE without face?
Infantile hemangiomas of the upper body region with minimal or
absent facial hemangiomas and associated structural malformations.
Pediatr Dermatol 2011; 28:235–41.
Ó 2013 British Association of Dermatologists
 Haemangioma: clinical course, complications and management, M. Luu and I.J. Frieden 29
62 Haggstrom AN, Skillman S, Garzon MC et al. Clinical spectrum and
risk of PHACE syndrome in cutaneous and airway hemangiomas.
Arch Otolaryngol Head Neck Surg 2011; 137:680–7.
63 Siegel DH, Tefft KA, Kelly T et al. Stroke in children with posterior
fossa brain malformations, hemangiomas, arterial anomalies,
coarctation of the aorta and cardiac defects, and eye abnormalities
(PHACE) syndrome: a systematic review of the literature. Stroke
2012; 43:1672–4.
64 Metry D, Frieden IJ, Hess C et al. Propranolol use in PHACE syn-
drome with cervical and intracranial arterial anomalies: collective
experience in 32 infants. Pediatr Dermatol 2013; 30:71–89.
65 Drolet BA, Frommelt PC, Chamlin SL et al. Initiation and use of
propranolol for infantile hemangioma: report of a consensus con-
ference. Pediatrics 2013; 131:128–40.
66 Stockman A, Boralevi F, Taieb A et al. SACRAL syndrome: spinal
dysraphism, anogenital, cutaneous, renal and urologic anomalies,
associated with an angioma of lumbosacral localization. Dermatology
2007; 214:40–5.
67 Girard C, Bigorre M, Guillot B et al. PELVIS syndrome. Arch Dermatol
2006; 142:884–8.
68 Iacobas I, Burrows PE, Frieden IJ et al. LUMBAR: association
between cutaneous infantile hemangiomas of the lower body and
regional congenital anomalies. J Pediatr 2010; 157:795–801, e1-7.
69 Drolet BA, Chamlin SL, Garzon MC et al. Prospective study of
spinal anomalies in children with infantile hemangiomas of the
lumbosacral skin. J Pediatr 2010; 157:789–94.
70 Leonardi-Bee J, Batta K, O’Brien C et al. Interventions for infantile
haemangiomas (strawberry birthmarks) of the skin. Cochrane Database
Syst Rev 2011; 5:CD006545.
71 Chakkittakandiyil A, Phillips R, Frieden IJ et al. Timolol maleate
0.5% or 0.1% gel-forming solution for infantile hemangiomas: a
retrospective, multicenter, cohort study. Pediatr Dermatol 2012;
29:28–31.
72 Pope E, Chakkittakandiyil A. Topical timolol gel for infantile he-
mangiomas: a pilot study. Arch Dermatol 2010; 146:564–5.
73 Cruz OA, Zarnegar SR, Myers SE. Treatment of periocular capillary
hemangioma with topical clobetasol propionate. Ophthalmology
1995; 102:2012–15.
74 Senchak AJ, Dann M, Cable B et al. Successful treatment of cutane-
ous hemangioma of infancy with topical imiquimod 5%: a report
of 3 cases. Ear Nose Throat J 2010; 89:E21–5.
75 Hazen PG, Carney JF, Engstrom CW et al. Proliferating hemangi-
oma of infancy: successful treatment with topical 5% imiquimod
cream. Pediatr Dermatol 2005; 22:254–6.
76 Martinez MI, Sanchez-Carpintero I, North PE et al. Infantile heman-
gioma: clinical resolution with 5% imiquimod cream. Arch Dermatol
2002; 138:881–4; discussion 4.
77 McCuaig CC, Dubois J, Powell J et al. A phase II, open-label study
of the efficacy and safety of imiquimod in the treatment of super-
ficial and mixed infantile hemangioma. Pediatr Dermatol 2009;
26:203–12.
78 Hohenleutner S, Badur-Ganter E, Landthaler M et al. Long-term
results in the treatment of childhood hemangioma with the flash-
lamp-pumped pulsed dye laser: an evaluation of 617 cases. Lasers
Surg Med 2001; 28:273–7.
79 Rizzo C, Brightman L, Chapas AM et al. Outcomes of childhood
hemangiomas treated with the pulsed-dye laser with dynamic
Ó 2013 British Association of Dermatologists
cooling: a retrospective chart analysis. Dermatol Surg 2009;
35:1947–54.
80 Batta K, Goodyear HM, Moss C et al. Randomised controlled study
of early pulsed dye laser treatment of uncomplicated childhood
haemangiomas: results of a 1-year analysis. Lancet 2002; 360:521–
7.
81 Kessels JP, Hamers ET, Ostertag JU. Superficial hemangioma:
pulsed dye laser versus wait-and-see. Dermatol Surg 2013; 39:414–
21.
82 Witman PM, Wagner AM, Scherer K et al. Complications following
pulsed dye laser treatment of superficial hemangiomas. Lasers Surg
Med 2006; 38:116–23.
83 Brightman LA, Brauer JA, Terushkin V et al. Ablative fractional
resurfacing for involuted hemangioma residuum. Arch Dermatol
2012; 148:1294–8.
84 Leaute-Labreze C, Dumas de la Roque E, Hubiche T et al. Propran-
olol for severe hemangiomas of infancy. N Engl J Med 2008;
358:2649–51.
85 Hogeling M, Adams S, Wargon O. A randomized controlled trial
of propranolol for infantile hemangiomas. Pediatrics 2011; 128:
e259–66.
86 Izadpanah A, Izadpanah A, Kanevsky J et al. Propranolol versus cor-
ticosteroids in the treatment of infantile hemangioma: a systematic
review and meta-analysis. Plast Reconstr Surg 2013; 131:601–13.
87 Zvulunov A, McCuaig C, Frieden IJ et al. Oral propranolol therapy
for infantile hemangiomas beyond the proliferation phase: a multi-
center retrospective study. Pediatr Dermatol 2011; 28:94–8.
88 Peridis S, Pilgrim G, Athanasopoulos I et al. A meta-analysis on the
effectiveness of propranolol for the treatment of infantile airway
haemangiomas. Int J Pediatr Otorhinolaryngol 2011; 75:455–60.
89 Mazereeuw-Hautier J, Hoeger PH, Benlahrech S et al. Efficacy of
propranolol in hepatic infantile hemangiomas with diffuse neona-
tal hemangiomatosis. J Pediatr 2010; 157:340–2.
90 Marqueling AL, Oza V, Frieden IJ et al. Propranolol and infantile
hemangiomas four years later: a systematic review. Pediatr Dermatol
2013; 30:182–91.
91 Parikh SR, Darrow DH, Grimmer JF et al. Propranolol use for
infantile hemangiomas: American Society of Pediatric Otolaryngol-
ogy Vascular Anomalies Task Force practice patterns. JAMA Otolaryn-
gol Head Neck Surg 2013; 139:153–6.
92 Bagazgoitia L, Hernandez-Martin A, Torrelo A. Recurrence of
infantile hemangiomas treated with propranolol. Pediatr Dermatol
2011; 28:658–62.
93 Raphael MF, de Graaf M, Breugem CC et al. Atenolol: a promising
alternative to propranolol for the treatment of hemangiomas. J Am
Acad Dermatol 2011; 65:420–1.
94 Blanchet C, Nicollas R, Bigorre M et al. Management of infantile
subglottic hemangioma: acebutolol or propranolol? Int J Pediatr
Otorhinolaryngol 2010; 74:959–61.
95 Pope E, Chakkittakandiyil A, Lara-Corrales I et al. Expanding the ther-
apeutic repertoire of infantile haemangiomas: cohort-blinded study
of oral nadolol compared with propranolol. Br J Dermatol 2013;
168:222–4.
96 Yan AC. Pain management for ulcerated hemangiomas. Pediatr Der-
matol 2008; 25:586–9.
British Journal of Dermatology (2013) 169, pp20–30
30 Haemangioma: clinical course, complications and management, M. Luu and I.J. Frieden
Minnelly Luu, M.D. completed her undergraduate stu-
dies at Stanford University and subsequently attended medi-
cal school at Northwestern University in Chicago, IL,
where she first developed an interest in pediatric dermatol-
ogy. 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 Cali-
fornia San Francisco under the mentorship of Dr. Ilona Frieden and her
department. In fall 2013, Minnelly will start her career as Assistant Pro-
fessor 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.
British Journal of Dermatology (2013) 169, pp20–30
I.J. Frieden is a Professor of Pediatrics and Dermatol-
ogy, 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 Der-
matology 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 Vascu-
lar 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.
Ó 2013 British Association of Dermatologists