Version May 2024
INTRODUCTION — Vascular lesions of infants and children are classified into two major types: tumors and vascular malformations [1]. Infantile hemangiomas are the most common vascular tumors, followed by "congenital" hemangiomas, which include rapidly involuting congenital hemangioma (RICH), noninvoluting congenital hemangioma (NICH), and partially involuting congenital hemangioma (PICH) subtypes. Congenital infantile hemangiomas are clinically, genetically, and histopathologically distinct from infantile hemangiomas. One of the key clinical differences between the two is that congenital hemangiomas are fully developed at birth, often detected on prenatal ultrasound, whereas infantile hemangiomas, if detectable at birth, will present as a subtle "precursor" lesion with proliferation occurring over early infancy [2]. Other examples of vascular tumors include pyogenic granuloma, kaposiform hemangioendothelioma, and tufted angioma [3,4].
Infantile hemangiomas are characterized by a growth phase and an involution phase. In contrast, vascular malformations, which are structural anomalies derived from capillaries, arteries, veins, lymphatics, or a combination thereof, grow in proportion to the child but generally do not regress. Vascular malformations are discussed separately.
An overview of the epidemiology, pathogenesis, clinical features, and complications of infantile hemangiomas will be presented here. The evaluation and management are discussed separately. Congenital hemangiomas, PHACE (posterior fossa anomalies, hemangioma, arterial anomalies, cardiac anomalies, and eye anomalies) syndrome, and other vascular tumors are also discussed separately.
●(See "Infantile hemangiomas: Evaluation and diagnosis".)
●(See "Infantile hemangiomas: Management".)
●(See "PHACE syndrome".)
●(See "Tufted angioma, kaposiform hemangioendothelioma (KHE), and Kasabach-Merritt phenomenon (KMP)".)
●(See "Pyogenic granuloma (lobular capillary hemangioma)".)
EPIDEMIOLOGY AND RISK FACTORS — Hemangiomas are the most common tumors of infancy. The true incidence of infantile hemangiomas is unknown [5]. Although they are classically said to occur in up to 10 percent of White infants [6,7], 4 to 5 percent is probably a better estimate [5,8]. Infantile hemangiomas are generally noticed within the first few days to months of life [9,10]. Although most hemangiomas occur sporadically, familial transmission in an autosomal dominant fashion has been reported [11]. In one series of 136 patients/families, 34 percent had a family history of infantile hemangiomas, most often in first-degree relatives [12].
●Hemangiomas are two to three times more common among females than males [13-16]. Complicated hemangiomas are even more likely to occur among female infants, for reasons that are unknown [17].
●Hemangiomas are more common among White infants (Hispanic and non-Hispanic) than other racial groups [6,15,18].
●The incidence of hemangiomas is increased in preterm infants [15]; the most significant risk factor appears to be low birth weight [16].
●Multiple hemangiomas more commonly occur in products of multiple gestations [15].
●Prenatal associations include older maternal age, placenta previa, pre-eclampsia, and other placental anomalies [8,15].
●Chorionic villus sampling does not appear to play a significant role in the formation of most hemangiomas [15].
PATHOGENESIS — Hemangiomas are characterized by phases of proliferation and involution as defined by a rapid proliferation of blood vessels in the first year of life, followed by gradual regression of the vascular component with replacement by fibrofatty tissue. The exact mechanisms that govern these processes are incompletely understood but are beginning to be elucidated.
Multiple lines of evidence suggest that hypoxia may have a key role in the pathogenesis of hemangiomas [19,20]. They include epidemiologic data on the association of infantile hemangiomas with conditions related with placental hypoxia (eg, low birthweight, retinopathy of prematurity, multiple pregnancies, placental anomalies) [8,15] and the demonstration in proliferating hemangiomas of multiple targets of hypoxia inducible factor-1-alpha, such as vascular endothelial growth factor (VEGF)-A, glucose transporter isoform 1 (GLUT1), and insulin-like growth factor-2 (IGF-2) [21]. It has been proposed that in utero hypoxia or local hypoxia may be the initiating factor for the development of hemangiomas, with the proliferating phase being a homeostatic attempt to normalize the hypoxic tissue [22].
GLUT1 and placenta-associated vascular antigens (Fc-gamma-receptor II, merosin, and Lewis Y antigen) are highly expressed in the endothelial cells of infantile hemangiomas during both the proliferative and involution phase [23-25]. These markers are not expressed in normal dermal or subcutaneous capillaries, nor are they expressed in other types of vascular tumors. The only other vasculature known to share this constellation of markers is that of placental chorionic villi. The gene expression profiles of hemangiomas and placenta are very similar compared with other tissue, suggesting that they share a common genetic program [26]. However, the precise relationship between infantile hemangiomas and chorionic villi has yet to be explained.
Proliferation — Although biopsy of hemangiomas is not routinely necessary because the diagnosis can generally be made clinically, histologic examination during the proliferation stage demonstrates superficial proliferating angioblastic endothelial cells with few capillary lumina [27].
Current evidence suggests that hemangiomas are clonal proliferations of endothelial cells [28,29], resulting from vasculogenesis (the formation of primitive blood vessels from angioblasts), rather than angiogenesis (the growth of new vessels from pre-existing vessels) as traditionally thought [30]. This hypothesis is supported by a study in which implantation of multipotential stem cells from human hemangioma tissue (isolated based on expression of CD133, a stem cell population marker) gave rise to hemangioma-like lesions in immunodeficient mice that spontaneously regressed, similar to what occurs in infantile hemangiomas [31].
In addition, proliferating hemangiomas contain hematopoietic leukocytes of myeloid origin that may play a role in hemangioma growth. Hemangioma endothelial cell coexpression of myeloid markers CD83, CD32, CD14, and CD15 supports the concept that hemangioma endothelium is distinct from that of normal vasculature [32].
Hemangioma proliferation appears to result from an imbalance between positive and negative vasculogenic factors expressed by the hemangioma and adjacent normal tissue [33]. This is supported by the following observations:
●Increased expression of endothelial cell markers (eg, CD34 and CD31), primitive cell population markers (eg, CD133 and LYVE-1 [a marker for lymphatic vessels]), IGF-2, and certain integrins in proliferating hemangiomas [21,34-36].
●Overexpression of basic fibroblast growth factor (bFGF, FGF 2), VEGF, proliferating cell nuclear antigen, and type IV collagenase in proliferating hemangiomas [33,37,38].
●Infantile hemangioma has suppressed VEGF receptor 1 (VEGFR1) expression, but constitutive VEGF receptor 2 (VEGFR2) signaling, an effect mediated by nuclear factor of activated T cells (NFAT), and mutations in VEGFR2 or the integrin-like receptor TEM-8 have been found in some individuals with hemangiomas that inhibit the activity of NFAT pathway [39].
●Imbalance of two VEGF receptor tyrosine kinases (VEGFR1 and VEGFR2) affected availability of VEGF and endothelial cell proliferation in hemangioma-derived endothelial cells (figure 1) [39,40]. Treatment of the cell lines with VEGF neutralizing antibodies normalized the VEGF signaling profile.
●Increased quantities of bFGF and matrix metalloproteinases in the urine of patients with proliferating hemangiomas [37,41].
Involution — The spontaneous involution phase typically begins in the late part of the first year and continues over a variable number of years. Involution is characterized by histologic fibrosis of capillary lumina. Increased apoptosis during the second year appears to counteract proliferation and may be involved in initiating involution [42]. This is supported by the following observations:
●Increased numbers of mast cells and levels of tissue metalloproteinase (an inhibitor of new blood vessel formation) in involuting hemangiomas
●Upregulation of interferon-induced genes in involuting hemangiomas [32]
●Decreased quantities of bFGF in the urine of patients with involuting hemangiomas [37,43]
CLINICAL PRESENTATION
General features — The majority of hemangiomas are not clinically evident at birth but become apparent within the first days to months of life [14,44]. Some newborns have a premonitory cutaneous mark, such as a patch of telangiectasias with surrounding pallor (secondary to vasoconstriction) at the hemangioma site (picture 1). Early lesions may be so subtle as to go unrecognized and may be mistaken for a scratch or bruise. Less commonly, a hemangioma may appear initially as a bright red patch resembling a port wine birthmark.
The majority of lesions are solitary, but multiple lesions occur in up to 20 percent of infants and are especially common among multiple births [14]. Hemangiomas have a predilection for the head and neck, although they can occur anywhere in the skin, mucous membranes, or internal organs. Hemangiomas range in size from a few millimeters to many centimeters in diameter. They may be superficial, deep, or combined (compound hemangioma):
●The superficial presentation is most common [45] and consists of a bright red papule, nodule, or plaque raised above clinically normal skin (picture 2A-B). Superficial hemangiomas have been called "strawberry" or "capillary" hemangiomas, but superficial hemangioma is the preferred term [46], since not all superficial hemangiomas have the "strawberry" appearance, and not all strawberry-like lesions are hemangiomas [47,48].
●The deep, or subcutaneous, hemangioma is typically a raised, skin-colored nodule, which often has a bluish hue with or without central telangiectatic patch (picture 3). Purely deep hemangiomas are less common [45]. They have been called "cavernous" hemangiomas, a term that is also erroneously used to describe venous malformations and thus is best avoided.
●Combined hemangiomas are fairly common and contain both superficial and deep components [45].
Natural history
Proliferation and involution — Hemangiomas characteristically undergo a growth (proliferative) phase that is generally rapid for the first several months. Thus, early intervention before the completion of the rapid growth phase, ideally by four weeks of age, is recommended for infants with high-risk hemangiomas [49]. (See "Infantile hemangiomas: Management", section on 'When to start treatment'.)
Slow proliferation can continue for the first 6 to 12 months [50,51]. Proliferation after the first year can occur but is uncommon [3,51].
The growth characteristics of 526 infantile hemangiomas were described in a multicenter, longitudinal, cohort study of 433 children who were followed by pediatric dermatologists in tertiary care centers [51]. In this referral population:
●The largest increase in size occurred during the early proliferative stage; by three months of age, the average hemangioma had already achieved 80 percent of its final size. A large majority of hemangiomas have completed growth by five months of age.
●The late proliferative stage (ongoing, but less rapid growth) was usually complete by nine months of age; only 3 percent of lesions had documented growth after nine months of age. Deep hemangiomas tended to appear and grow later and longer than superficial hemangiomas.
●Hemangiomas proliferated within a defined anatomic area; increased volume was achieved without centrifugal spread.
In a small, prospective study including 30 infants, serial images were analyzed to evaluate the hemangioma growth rate. Photographs were taken at intervals of one to two weeks starting one to two weeks after birth [52]. The study found that hemangioma growth is nonlinear and that the most rapid growth takes place between 5.5 and 7.5 weeks of age.
The proliferative phase is followed by a spontaneous involution phase that typically begins after one year and lasts a variable number of years [51]. Superficial hemangiomas typically enter the involution stage earlier than deep hemangiomas [51].
The first clinical sign of involution within a superficial hemangioma is a color change from bright red or violaceous to dark red or from purple to gray, which often begins centrally as the tumor softens and flattens [14,51]. An early white discoloration of the hemangioma surface occurring in infants younger than three months may herald ulceration, not involution [53]. Deep lesions become less blue and warm. The rate and extent of hemangioma involution varies among affected children and may be proportional to size, with larger lesions exhibiting longer periods of growth and involution and smaller lesions exhibiting shorter periods of growth and involution [44].
Newer studies have demonstrated that 90 percent of hemangioma involution is complete by four years of age and that most hemangiomas do not improve significantly after three to four years of age [54,55]. It must also be emphasized that in many cases, complete involution does not result in normal-appearing skin. Up to one-half of children with hemangiomas experience residual changes such as scarring, atrophy, redundant skin, discoloration, and telangiectasias. Clinicians who evaluate children who have hemangiomas should be realistic with parents/caregivers about the potential outcomes:
●Superficial, very raised hemangiomas, especially those that exhibit a sharp, "cliff-like'" border (picture 2A, 2C), or pedunculated lesions (hemangiomas extending from a smaller base) are at risk for residual fibrofatty tissue, which may ultimately require surgical intervention.
●Hemangiomas of the lip that cross the vermillion border (picture 4) and large tumors of the nose ("Cyrano nose") and auricle are more prone to disfigurement.
●Large tumor or plaque-like lesions, especially when rapidly proliferating and/or in trauma-prone locations, show a tendency toward ulceration, which invariably leads to scarring.
Infantile hemangiomas with minimal or arrested growth — In a minority of cases, hemangiomas fail to proliferate beyond the telangiectatic patch associated with the premonitory stage, or only a small portion of the lesion proliferates (infantile hemangiomas with minimal or arrested growth) (picture 5) [56,57]. The majority of these hemangiomas occur on the lower body and also show a tendency toward acral locations. When extensive, infantile hemangiomas with minimal or arrested growth is the most common hemangioma morphology associated with LUMBAR (lower-body hemangioma and other cutaneous defects; urogenital anomalies, ulceration; myelopathy, bony deformities; anorectal malformations, arterial anomalies; and renal anomalies) syndrome. (See 'Acral lesions' below.)
Infantile hemangiomas with minimal or arrested growth are often confused with port wine birthmarks; a blotchy red-blue patch with perilesional blanching and both fine and coarse telangiectasias suggests a diagnosis of hemangioma [56]. A small proliferative component, often at the lesion periphery, is another useful diagnostic clue. However, a proliferative component is present in less than one-third of cases.
Additional studies are necessary to determine the natural history of this variant.
Localized lesions — Hemangioma morphology provides an important clue to potential complications [13]. Hemangiomas can be categorized as localized (or focal), segmental, or multiple. (See 'Complications' below.)
Localized hemangiomas, which constitute the majority of lesions, demonstrate clear, well-defined spatial containment, appear to arise from a single focus, and lack evidence of a linear or geometric pattern. Localized hemangiomas of the face appear to occur near lines of mesenchymal or mesenchymal-ectodermal embryonic fusion.
Segmental lesions — Segmental hemangiomas are usually patch- or plaque-like and demonstrate a linear and/or geographic presence over a specific cutaneous territory (picture 6) [13,58]. A mapping study of 549 facial infantile hemangiomas identified five distinct segmental patterns (figure 2) [59]:
●Frontotemporal, including the lateral forehead, anterior temporal and frontal scalp, and often the ipsilateral eyelid
●Maxillary, including the medial cheek and the ipsilateral upper lip but limited medially by the nasomedial sulcus
●Mandibular, including the preauricular cheek, mandible, chin, and lower lip
●Frontonasal, including medial frontal scalp and bridge, tip, ala, and philtrum of the nose
●C-shaped segment on the posterior auricular scalp
These observations suggest that neural crest derivatives may be involved in facial hemangioma development.
Segmental hemangiomas are more likely to occur among female infants and, compared with localized lesions, are much more likely to be associated with complications [13,60]. Children with segmental hemangiomas generally require more intensive and prolonged therapy and have a poorer overall outcome than children with hemangiomas of localized morphology [13].
PHACE syndrome — PHACE (posterior fossa anomalies, hemangioma, arterial anomalies, cardiac anomalies, and eye anomalies) syndrome (MIM #606519) is a neurovascular syndrome defined by the presence of a large, segmental hemangioma, usually on the face or head, in association with one or more congenital malformations, most commonly structural or cerebrovascular anomalies of the brain (table 1) [61-63]. The syndrome represents a spectrum of disease, with few infants manifesting the entire constellation of anomalies. The hallmark of PHACE syndrome, a large, segmental hemangioma usually on the face, may involve one to several facial dermatomes (picture 7) [62,64].
The clinical manifestations, diagnosis, and management of PHACE syndrome are discussed in detail separately. (See "PHACE syndrome".)
Lumbosacral lesions — Hemangiomas located over the lumbar or sacral spine may be associated with myelopathy, spinal bony, and/or genitourinary or anorectal anomalies [65-71]. The acronym "LUMBAR" is commonly used to describe the association of segmental lower-body hemangiomas with underlying developmental abnormalities [69]. This constellation of anomalies has been previously described under the acronyms "PELVIS" (perineal hemangioma, external genitalia malformations, lipomyelomeningocele, vesicorenal abnormalities, imperforate anus, and skin tag) and "SACRAL" (spinal dysraphism; anogenital, cutaneous, renal, and urologic anomalies, associated with an angioma of lumbosacral localization).
Localized lesions that are adjacent to but do not cross the midline usually do not warrant further evaluation [72]. In contrast, segmental lesions that span the midline over the gluteal cleft and lumbosacral spine (picture 8) are of greatest concern and should undergo MRI as part of their evaluation [70]. The evaluation of children with these lesions is discussed separately. (See "Infantile hemangiomas: Evaluation and diagnosis", section on 'LUMBAR syndrome'.)
Acral lesions — Approximately 18 percent of infantile hemangiomas occur on the extremities [73]. The majority of larger hemangiomas in this location exhibit a "biker-glove" distribution, which describes hemangiomas that extend on the digits, sparing the distal tips, and often maintain a contiguous border across digits when the fingers or toes are approximated (picture 9) [74]. These lesions often demonstrate a reticular morphology with minimal or arrested growth and may be complicated by ulceration.
Other associations — In addition to PHACE syndrome, spinal dysraphism, and genitourinary anomalies, solitary, segmental hemangiomas of the skin may be associated with visceral hemangiomas. Similar to the aforementioned associations, in such cases, visceral hemangiomas tend to be regional to their cutaneous counterparts [75].
Multiple lesions — In most children with multiple hemangiomas (arbitrarily defined as ≥5 generally small, localized hemangiomas), the hemangiomas are limited to the skin, and the condition is benign (benign neonatal hemangiomatosis). Visceral (particularly hepatic) hemangiomas that cause life-threatening complications (also known as diffuse neonatal hemangiomatosis) appear to be rare.
Hepatic hemangiomas — Multifocal hepatic hemangiomas most commonly occur in the presence of multiple (>5, with the risk increasing exponentially) skin hemangiomas and are probably most often asymptomatic, in which case they can be managed with observation with or without serial imaging [76].
Rarely, multifocal hepatic hemangiomas can have large vessel shunts that result in heart failure, which can be treated with pharmacotherapy or embolization if necessary. Diffuse liver hemangiomas, which may occur in the absence of skin hemangiomas, cause massive hepatomegaly with abdominal compartment syndrome, impaired ventilation, impaired venous return, and renal vein compression, and are associated with a high mortality rate [77]. An additional complication of diffuse liver hemangiomas is severe consumptive hypothyroidism due to increased production of the thyroid hormone inactivating enzyme type 3 iodothyronine deiodinase [78,79].
Other rare potential complications of visceral hemangiomas, dependent on specific organ involvement, include gastrointestinal hemorrhage, obstructive jaundice, and central nervous system sequelae due to mass effects [80-82].
COMPLICATIONS — Most cutaneous hemangiomas are uncomplicated and require no intervention. However, some lesions may ulcerate, leading to pain, bleeding, scarring, and/or infection. Other lesions may cause functional impairment during, and/or disfigurement after, the proliferative phase (table 2) [14].
Ulceration — Ulceration is the most common complication of hemangiomas [15]. In a prospective cohort of 1096 children (<12 years) with infantile hemangiomas, ulceration occurred in approximately 16 percent [83]. In a subsequent study performed after the advent of beta blocker treatment, the prevalence of ulceration was 11 percent [84].
Ulceration is particularly frequent when hemangiomas are rapidly proliferating and located in trauma- or pressure-prone locations (picture 10A-B) [83]. An early white discoloration of the hemangioma surface in infants younger than three months may herald ulceration [53]. The cause of ulcer formation is unknown, but given the typical locations, maceration and frictional stress are probable contributing factors [85]. Ulceration is often painful and may lead to bleeding, infection, and, invariably, scarring. The management of ulcerated hemangiomas is discussed separately.
Bleeding — Although a common concern among parents/caregivers, bleeding is rarely profuse and can generally be stopped with application of direct pressure.
Airway hemangiomas — Airway hemangiomas can develop in children who do not have cutaneous hemangiomas. However, the risk of airway hemangioma is higher with segmental hemangiomas located in a cervicofacial, mandibular, or "beard" distribution, which may include all or some of the following: the preauricular skin, mandible, lower lip, chin, or anterior neck (picture 11).
The possibility of airway hemangioma must be considered in any child who has a cutaneous hemangioma in a cervicofacial mandibular distribution and develops progressive hoarseness or stridor. Affected infants are most likely to experience symptoms between the ages of 6 and 12 weeks, when hemangioma proliferation is most rapid. Symptoms may progress from initial hoarseness or stridor to respiratory failure. Cough and cyanosis are other common manifestations. Airway involvement can be confirmed using endoscopic visualization [86]. The management of airway hemangiomas is discussed separately. (See "Infantile hemangiomas: Management".)
Periorbital hemangiomas — Periorbital hemangiomas may compromise normal visual development [87]. The majority of hemangiomas that lead to visual complications involve the upper medial eyelid. However, a hemangioma of any size or morphology in the periorbital location may pose a threat to vision (picture 12A-B). In a series of 89 patients with periocular hemangiomas, 60 percent had functional impairment of the eye, most frequently astigmatism and visual axis obstruction [88]. Subcutaneous periocular hemangiomas are of particular concern since they may extend deep into the orbit, causing exophthalmos or globe displacement with only subtle cutaneous manifestations [87]. Predictive factors for ocular complications, such as astigmatism and amblyopia, include size >1 cm in diameter, a deep component, and upper eyelid involvement [89].
Astigmatism, the most common complication, results from direct pressure of the growing hemangioma on the cornea. Other potential problems include ptosis, proptosis, and strabismus. Stimulus-deprivation amblyopia, a result of physical obstruction of the visual axis by a hemangioma, is one of the leading causes of preventable blindness in children. Astigmatism, strabismus, and amblyopia are discussed separately. (See "Evaluation and management of strabismus in children" and "Amblyopia in children: Classification, screening, and evaluation", section on 'Deprivation amblyopia'.)
Early examination by an ophthalmologist familiar with periorbital hemangiomas and their potential complications is mandatory, since prolonged, severe visual compromise can result in permanent damage, including blindness. The management of periorbital hemangiomas is discussed separately. (See "Infantile hemangiomas: Management".)
Other hemangiomas
●Hemangiomas of the ear may obstruct the auditory canal, leading to otitis externa [90]. Speech development is generally not affected except in the very rare case of bilateral obstruction.
●Hemangiomas of the tongue, oral cavity, or aerodigestive tract may rarely interfere with eating, swallowing, or speech [13,14,90]. Lesions in these locations that are significant enough to cause complications are much more often vascular malformations, not hemangiomas.
●Nuchal hemangiomas may temporarily impair range of motion of the neck. In some cases, consultation with physical therapy may be appropriate.
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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Hemangioma (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Epidemiology – Infantile hemangiomas are the most common vascular tumors in infants and children. They are more common in girls than boys and among White non-Hispanic infants than among those of other racial/ethnic groups. The incidence is increased in preterm infants. (See 'Epidemiology and risk factors' above.)
●Clinical presentation – The majority of hemangiomas are not clinically evident at birth but become apparent within the first days to months of life. Hemangiomas have a predilection for the head and neck, although they can occur anywhere in the skin, mucous membranes, or internal organs. They range in size from a few millimeters to many centimeters in diameter. They may be superficial, deep, or combined. (See 'Clinical presentation' above.)
●Natural history – Hemangiomas characteristically undergo a growth (proliferative) phase that is generally most rapid for the first several months. The proliferative phase is followed by a spontaneous involution phase that typically begins after one year and lasts a variable number of years. (See 'Natural history' above.)
●Clinical categories:
•Localized (focal) hemangiomas – Localized hemangiomas demonstrate clear, well-defined spatial containment, appear to arise from a single focus, and lack evidence of a linear or geometric pattern (picture 2A, 2C). (See 'Localized lesions' above.)
•Segmental hemangiomas – Segmental hemangiomas are usually plaque-like and demonstrate a linear and/or geographic presence over a specific cutaneous territory (picture 6). (See 'Segmental lesions' above.)
•Multiple hemangiomas – Multiple hemangiomas are arbitrarily defined as ≥5 generally small, localized hemangiomas. (See 'Multiple lesions' above.)
●Complications – Most cutaneous hemangiomas are uncomplicated and require no intervention. However, some lesions may ulcerate, leading to pain, bleeding, scarring, and/or infection. Other lesions may cause functional impairment and/or disfigurement during and after the proliferative phase (table 2). (See 'Complications' above.)
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