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Oral Hemangiomas Treatment & Management

  • Author: Steven Brett Sloan, MD; Chief Editor: William D James, MD  more...
Updated: Feb 09, 2016

Medical Care

Diagnosis and management of oral vasoformative tumors and oral hemangiomas span a wide range of options. Treatment of oral vasoformative tumors can be divided into 2 broad categories: medical treatment and surgical or invasive treatment (see Surgical Care).

Management algorithm

Kane et al[25] developed a management algorithm that covers most of the current thinking regarding these tumors.

At initial presentation, a history and physical examination are performed, and an MRI is obtained to determine the extent of the lesion because extensive spread may not be evident on examination. Presence of bruits, pulsatility, or deep extent would also make angiography a useful adjunct.

From this database, whether the lesion in question is a vascular malformation or a hemangioma can be ascertained. If it is a hemangioma, then whether the lesion is proliferating needs to be ascertained. For proliferating lesions, either observation or steroids are options. In lesions that are not proliferating, whether the lesion is involuting needs to be determined. Involuting lesions can be managed by observation. If the involution is incomplete and arrested, then the lesion can be managed the same as a low-flow vascular malformation.

If the lesion in question is determined to be a vascular malformation rather than a hemangioma, then its flow characteristics must be gauged. High-flow lesions require presurgical embolization followed by aggressive ablative therapy. Low-flow vascular malformations can be managed in numerous ways. For the easily collapsible lesions that are accessible, sclerotherapy, laser therapy, or cryotherapy are alternatives. For those that are not accessible, do not have compressible components, or are functionally compromising, then ablative surgery is indicated. For lesions that are insufficiently ablated or sclerosed, other modalities can be used in a complementary fashion.


Treatment of vasoformative tumors represents a challenge because the morbidity can range from minor bleeding and swelling to life-threatening hemorrhage and airway embarrassment. Because of the propensity of hemangiomas to regress spontaneously, approaches to management depend on their size, their location, their behavior, and the age of the patient. Hemangiomas are usually managed conservatively, and vascular malformations in soft tissue are managed by a number of preferred methods, with special cases such as those in bone or muscle by other methods. The advent of technologic advances in interventional radiology and use of sclerosing and medical therapy has changed the management of these lesions considerably in the past few decades.

Most true hemangiomas require no intervention, but 10-20% require treatment because of their size, their location, or their behavior.[26] Individualized therapy depends on the age of the patient, the size and the exact location of the lesion, the stage of growth or regression, and the functional compromise. In general, the treatment of small hemangiomas that do not compromise function is observation. Conservative management consists of periodic visits, parental support, and photodocumentation. The ultimate result of involution for capillary hemangiomas is far superior to primary excisional therapy. Excision can be justified under certain conditions, especially when function is compromised.

For adults with oral vascular malformations, the treatment depends on the proliferative nature and the extent of the lesions and on the functional impairment, usually hemorrhage and airway problems. For limited lesions, treatment for cosmetic reasons may be an acceptable risk-benefit decision.

When lesions, especially those involving the oropharynx and the subglottic areas, are rapidly proliferative in children, urgent intervention is indicated. In adults, most of these lesions, if stable and not progressing, can be managed with conservative treatment. Treatment of the more extensive lesions can entail significant morbidity from the radical surgical treatment necessary to eradicate them. Many of the treatment alternatives have evolved to avoid the disfiguring and functionally debilitating standard treatments. Many of the treatments have resulted in recurrence or persistence of the lesions, and undergoing multiple procedures in an effort to eradicate disease is not unusual.

For high-flow vascular malformations, complete resection of extensive tumors can be a formidable task. Deep skull base extension and internal carotid artery or vertebral artery branch recruitment may preclude resectability. Embolization in this setting has not demonstrated significant palliative value. Kane has reported 3 deaths related to tumor extension and hemorrhage in this subset. With embolization, inadvertent passage of the agents to unwanted areas of the circulation is always a risk. Superselective catheterization and a careful choice of agents have minimized this complication.

Medical therapy

The 2 primary medical treatments are steroids and beta-blocker therapy.[27, 28, 29] Interferon is rarely used because of the risk of spastic diplegia. Vincristine has been reported to decrease the size of a large segmental mandibular hemangioma in the setting of PHACES syndrome.[30]

Steroids have become a mainstay in the treatment of proliferating hemangiomas in infants and children. High doses of systemic or intralesional steroids are the first-line treatment, and a dramatic response is observed in 30% of patients.[26]

Fost and Esterly[31] first reported the use of systemic steroids in the treatment of hemangiomas. Prednisone at a dose of 20-30 mg/d was given for 2 weeks to 4 months. Both of the patients with capillary hemangiomas had a definite response, and 3 of the 4 patients with mixed hemangiomas had a definite response. Fost proposed that therapy be discontinued if no response occurred after 2 weeks because of the multiple adverse effects of systemic steroids in infants. Edgerton[32] also proposed the use of systemic steroids in the treatment of hemangiomas. He followed 7 patients receiving 20-40 mg/d of prednisone for 30-90 days, with a definite response occurring in all of the patients.

Sasaki et al[3] used a tapering dose of steroids, starting with prednisone 3 mg/kg/d for 3 days, followed by 5 weeks of every other day dosing of prednisone at 1.5 mg/kg/d, and then by 1 week of every other day dosing of prednisone at 0.75 mg/kg/d. A response did not occur in any of the 13 patients with cavernous hemangiomas, and only 60% of the patients with capillary hemangiomas had a definite or probable response. Pope et al demonstrated in a randomized controlled trial that oral corticosteroids offered more clinical and biological benefit than pulse steroids, with a higher risk of adverse effects noted in 20 patients with problematic hemangiomas.[33]

Bartoshesky et al[34] had conflicting results with steroids, showing a definite response in only 2 of 17 patients with mixed hemangiomas. Hawkins et al[35] reported the use of steroids to control hemangiomas of the airway, and 8 of 9 patients showed improvement and avoided tracheotomy. Use of intralesional triamcinolone acetonide (4 mg/mL) led to a 4-fold increase in mast cells; a regression of the hemangioma; and a decrease of the cytokines platelet-derived growth factor-alpha (PDGF-alpha), platelet-derived growth factor beta (PDGF-beta), IL-6, TGF-beta1, and TGF-beta3 in one study.[36] bFGF and VEGF levels were unaltered by steroid therapy. Also, enhanced expression of the mitochondrial cytochrome b (CYTB) gene was noted following steroid therapy.

Of note, frequent monitoring of blood pressure should be performed using the appropriately sized blood pressure cuff during the administration of systemic corticosteroid therapy.

Although the effectiveness of interferon alfa in the treatment of hemangiomas has been documented in many reports, the risk of spastic diplegia generally favors an alternative agent. Blei et al[37] reported the use of interferon alfa-2a in parotid hemangiomas (13 females, 1 male) in which the response was poor. Greinwald et al[38] described a prospective randomized trial of interferon alfa-2a involving 24 patients with massive or life-threatening hemangiomas of the head and the neck. They were given daily subcutaneous injections for 4 months. Of those patients, 58% had a greater than 50% reduction in the size of the tumor and 42% had a complete response. Response rates were greater than those for corticosteroids (58% vs 30%). Another investigation found that interferon alfa-2b was effective in reducing the size of the tumor in more than two thirds of patients.

However, some concern exists regarding the toxicity of interferon alfa, especially in children. The most serious adverse effects include neurologic effects (eg, spastic paresis, seizures, coma), hematologic effects (eg, neutropenia, thrombocytopenia), and hepatic toxicity.

Spastic diplegia generally improves after discontinuation of the drug.[39]

Beta-blockers, most specifically propranolol, have been in use since mid 2008 for infants with severe or disfiguring hemangiomas. Beta-blockers can cause rapid involution of hemangiomas, but may be contraindicated in patients with malformations of the great vessels. Hypotension and bradycardia may occur.[27, 40] Most infants reported have been treated with propranolol at a dose of 2-3 mg/kg/d in 2-3 divided doses. Duration of therapy varies from 2-10 months. As early as 24 hours after the initiation of therapy, many infantile hemangiomas have begun to change from intense red to purple, with evidence of softening. Most continue to improve until nearly flat and with significantly diminished color.[29]

Leaute-Labreze et al conducted a randomized control trial to assess the safety and efficacy of oral propranolol. Of 460 infants who underwent randomization, 456 received treatment. On the basis of an interim analysis of the first 188 patients who completed 24 weeks of trial treatment, the regimen of 3 mg of propranolol per kilogram per day for 6 months was selected for the final efficacy analysis. The frequency of successful treatment was higher with this regimen than with placebo (60% vs 4%, P <.001). A total of 88% of patients who received the selected propranolol regimen showed improvement by week 5, versus 5% of patients who received placebo. A total of 10% of patients in whom treatment with propranolol was successful required systemic retreatment during follow-up. Known adverse events associated with propranolol (hypoglycemia, hypotension, bradycardia, and bronchospasm) occurred infrequently, with no significant difference in frequency between the placebo group and the groups receiving propranolol.[41]

The mechanism of action is unknown; however, some hypothesize that local vasoconstriction may be a factor, which is based on the early color change and softening of the lesion. One study has demonstrated that nonspecific and beta2-selective blockers (eg, propranolol) triggered apoptosis of capillary endothelial cells in adult rat lung tissue, suggesting a similar mechanism may be plausible for hemangioma endothelial cells.[42]

No protocol for initiating propranolol therapy in infants with hemangiomas is universally accepted. Therapy should be approached with extreme caution in neonates and infants who generally do not have preexisting venous hypertension or any other hemodynamic disorder. Of particular note, infants with hemangiomas associated with PHACES syndrome are at higher risk for cerebral vascular accidents secondary to cerebral vascular anomalies, and these infants should not receive beta-blockers.[29]

Ran et al reported six cases of infantile hemangiomas successfully treated with oral itraconazole at approximately 5 mg/kg/day. Since itraconazole has been shown to inhibit angiogenesis and tumor growth in vitro and in vivo associated with some cancers, they propose itraconazole may have a similar effect on infantile hemangiomas.[43]

Provisional guidelines for initiation of therapy


Exclude infants with evidence of the following:

  • Bronchospasm
  • Cardiac disease
  • CNS vascular anomalies (suspected PHACES syndrome, large cervicofacial hemangiomas [see Mortality/Morbidity for PHACES syndrome definition]

Baseline laboratory tests and evaluation include the following:

  • Blood glucose level
  • Blood pressure check
  • Electrocardiography
  • Echocardiogram (if considering PHACES syndrome or other clinical indications)
  • Pediatric cardiology consultation for evaluation and dosing recommendations


See below.


Initially in the hospital, especially if the patient is in a high-risk category (whether in or out of intensive care unit, cardiac care unit, or monitored bed), monitor for 24-72 hours; practices vary considerably.

Monitoring 1 hour after administration (dosing) includes the following:

  • Blood pressure check
  • Heart rate check (hold dose for heart rate at < 100 beats per min)
  • Blood glucose level
  • Temperature determination to evaluate for hypothermia
  • Observation for bronchospasm

At home, parents should observe for signs of lethargy, poor feeding, and/or bronchospasm.

Blood pressure and heart rate should be evaluated intermittently at the pediatrician's office.


Surgical Care

Surgical or invasive treatment of oral hemangiomas has evolved. Complete surgical excision of these lesions offers the best chance of cure, but, often, because of the extent of these benign lesions, significant sacrifice of tissue is necessary. For example, lesions of the tongue may require near-total glossectomy, which is followed by severe functional impairment to vital functions, such as swallowing, speech, and airway maintenance. As a result, multiple adjunctive procedures have been introduced to eradicate the disease, leaving less of a functional impairment. These adjunctive procedures have also been used to reduce both the blood loss and the morbidity of surgical procedures.


Embolotherapy is one of the more commonly used adjunctive procedures in the treatment of vascular tumors. Embolization literally means the occlusion of a vessel by the introduction of a foreign body. In a broader definition, it also means any other occlusion that is obtained with a proliferating reaction of the vessel wall. As technical expertise with interventional radiology advances, the options for treatment of vascular malformations and hemangiomas become broader. Vessels can be treated not only via superselective catheterization but also through permucosal and percutaneous techniques.

Although embolotherapy has attracted much interest in the last decade and a half, the principle of vascular embolization for head and neck tumors is not new. In 1904, Dawbain, Lussenhop, and Spence described the preoperative injection of melted paraffin-petrolatum into the external carotid arteries of patients with head and neck tumors. In 1930, Brooks introduced particulate embolization when he described the occlusion of a traumatic carotid-cavernous fistula by injecting a fragment of muscle attached to a silver clip into the internal carotid artery. The tremendous upsurge in interest in embolization came with the advent of advances in catheter technology to allow highly selective delivery of agents.

Agents for embolotherapy can be broadly divided into 2 groups: absorbable materials and nonabsorbable materials (see the List below). The nonabsorbable materials can be further subdivided into particulate, liquid, sclerosing, and nonparticulate agents. The Food and Drug Administration (FDA) status of the discussed materials should be investigated prior to their use; many are not FDA approved. A full discussion of the procedure for each use and the associated costs and complications is beyond this review. For a full discussion, individual references on each therapy should be consulted.

Embolotherapy agents

Absorbable materials are as follows:

  • Autologous blood clot
  • Modified blood clot
  • Gelfoam
  • Oxycel

Nonabsorbable materials are as follows:

  • Particulate agents are as follows:
    • Acrylic spheres
    • Autologous fat of muscle
    • Ferromagnetic microspheres
    • Methylmethacrylate spheres
    • Polyvinyl alcohol (Ivalon)
    • Silastic spheres
    • Stainless steel pellets
  • Injectable (fluids) are as follows:
    • Amino acid occlusion gel (Ethibloc)
    • Isobutyl 2-cyanoacrylate
    • Microfibrillar collagen (Avitene)
    • Silicone rubber
  • Sclerosing agents are as follows:
    • Absolute ethanol
    • Boiling contrast medium
    • Polidocanol
    • Sodium morrhuate
    • Sodium tetradecyl sulfate (Sotradecol)
  • Nonparticulate agents are as follows:
    • Stainless steel coils
    • Platinum coils
    • Silk streamers
    • Plastic brushes
    • Detachable balloons

In the treatment of vasoformative tumors, the resorbable materials are not particularly useful in the long term, except when they precede a surgical treatment and only short-term occlusion is required. They resorb over time, and the occluded vessel recanalizes, restoring flow to the occluded segment. Autologous clots produce a duration of vessel occlusion of only 48 hours, and, by 2 weeks, approximately one half of the vessels are recanalized. Gelfoam occlusion has a duration of 3-4 months, but recanalization usually follows. Gelfoam is occasionally used in combination with coils or other nonabsorbable substances (eg, tissue adhesive) for permanent occlusion.

Nonresorbable materials comprise the mainstay of embolotherapy for vasoformative tumors. Polyvinyl alcohol sponges (Ivalon) are obtained by reticulation of polyvinyl alcohol with formaldehyde. The sponge has the property of being compressible when wet and reexpanding to its original shape and size when a dried piece is placed in an aqueous solution, such as blood. These properties make Ivalon particularly well suited for large vessels, in which it produces a permanent occlusion. Histologically, Ivalon is initially invaded by fibroblasts, with subsequent dense, fibrous connective tissue around the sponge and a moderate inflammatory reaction around the area of thrombus that involves the artery wall. Then, organization of the thrombus occurs, with fibrosis of the arterial wall and disappearance of the inflammatory infiltrate.

Recanalization of the thrombus does not occur, and partial occlusion of the vessel wall by an organized thrombus is commonly found beyond the initial occlusion. Ivalon can be used in combination with stainless steel coils and other devices. Greene et al described 2 cases of embolization of maxillary hemangiomas with Ivalon followed by sclerotherapy with sodium morrhuate. No recurrence was reported at 2-year follow-up examinations in both cases.

Microspheres of stainless or ferromagnetic steel, acrylic, methylmethacrylate, silastic, and silicone are inert and available in a variety of sizes. They are rarely used when treating oral vascular formations.

Isobutyl-2-cyanoacrylate (IBCA) is a rapidly hardening plastic adhesive similar to superglue. The liquid plastic is readily injectable, even through very small catheters, and it polymerizes almost instantly upon contact with ionic fluids, such as blood or vascular endothelium. This polymerization leaves the plastic solid. Abroad, IBCA is the most popular tissue adhesive, but it is not available in the United States. N -butyl-2-cyanoacrylate, an adhesive with similar properties, is available in the United States.

Silicone rubber (Dow-Corning) is a convenient biocompatible material for vascular occlusion. A disadvantage of silicone rubber is that it does not have tissue adhesive properties; thus, the vascular bed must be completely filled to keep the substance in place. No tissue reaction between the elastomer and the vessel wall is apparent either macroscopically or microscopically.

Microfibrillar collagen (Avitene) is a hemostatic agent derived from bovine hide. Its mechanism of action is thought to involve platelet aggregation and activation. Two weeks after embolization, a severe granulomatous arteritis occurs, which subsides by 3 months, with fibrosis replacing inflammation.

Absolute ethanol is used as a sclerosing agent. Its presumed mechanism of action is a direct toxic effect on the vascular endothelium that activates the coagulation system on the dehydrated endothelium. Thus, the vascular occlusion is not achieved instantly but rather in days to weeks. The toxic effect extends to the perivascular tissue, and the use of absolute ethanol has led to perivascular necrosis. Absolute ethanol can be delivered through the tiniest of catheters. It is naturally sterile and is quickly diluted after injection, reducing its toxic effects. It is among the most popular of agents used in oral vascular malformations today; it is delivered permucosally, percutaneously, or through catheters. Ethyl alcohol (95%), which is percutaneously injected into the lesion, is similar to absolute ethanol.

When using absolute ethanol, approximately one third of the volume of the lesion can be injected.[44] Injection of alcohol into oral lesions is followed by marked swelling 6-8 hours later. By using small volumes and carefully avoiding direct deposition into the overlying mucosa, necrosis of the mucosa can usually be avoided. When necrosis does appear, it is usually present by 10 days[45] and heals with local care. Sclerosing solutions produce thrombosis of the vessels and a hard mass. The surrounding soft tissue becomes edematous, and ecchymosis, which increases in severity for 8-12 hours, is frequently present.[10]

Other agents used for sclerosis of oral vascular tumors include sodium morrhuate, sodium tetradecyl sulfate (STS), and hydroxypolyethoxydodecan (an agent that is a double hydrophilic and hydrophobic chain).

Gilbert et al[46] described their experience with 3 patients using intralesional sodium morrhuate for oral hemangiomas. Sodium morrhuate is used as a 5% solution of the sodium salts of cod liver oil. Multiple 0.05-mL injections are given by using a tuberculin syringe circumscribing the lesion, and a final injection is given into the center of the lesion. Aspiration is performed to avoid intervascular injection.[46] Repeat injections are performed at 4- to 7-day intervals. Morgan uses a similar scheme over a 12-year period with 5% sodium morrhuate, giving multiple 0.05-mL circumlesional injections and a final 0.5-mL injection into the center of the lesion. Repeat injections are given at 4-day intervals. Chin[47] used 5% sodium morrhuate in a maxillary hemangioma in an adult. The lesion shrank, and a repeat injection was given 3 weeks later. Five years later, no evidence of the lesion was present.

STS (Sotradecol) is another commonly used sclerosant for oral vascular tumors. STS causes intimal inflammation, thrombus formation, and often permanent obliteration of the veins.[48] In animal studies, STS produces long-term arterial thrombosis in large arteries and marked inflammatory reactions in small vessels, with eventual replacement by connective tissue. In an early report on the use of STS in oral hemangiomas, Baurmash and Mandel[49] used 1% STS. Later reports and more recent reports use a 3% solution.[50, 51, 52, 25, 48]

Minkow et al[50] used a technique of intralesionally injecting 0.1-0.5 mL of 3% STS into oral hemangiomas. Repeat injections were performed at 2-week intervals. He reported on 24 patients, ranging in age from 11-79 years and involving 15 females and 9 males. Satisfactory results were reported in all patients, with minimal adverse effects and disappearance of the lesions without scarring. O'Donovan et al[48] recommended 3% STS, using 0.5-2 mL volumes of sclerosants and manual compression of the lesions to ensure stasis.

Kane et al[25] recommended 3% STS used alone for oral hemangiomas but in combination with surgery for vascular malformations. Sclerotherapy was used as an adjunct, in which high-flow vascular malformations were first embolized with Ivalon sponges, Avitene, or Gelfoam. All sclerotherapy in vascular malformations was followed by surgery. Of the hemangiomas, 31% were treated by sclerotherapy alone.

Seccia and Salgarello[53] treated 18 patients over an 8-year period with hydroxypolyethoxydodecan. It acts as a detergent, attacking the lipids of the cell membrane. Multiple 0.5-mL injections were given. He reported that 90% of the oral lesions were controlled with sclerotherapy alone.

With many of the sclerosants, some precautions need to be heeded. Allergic reactions to sodium morrhuate, tetradecyl sulfate, and oleate[10] have been reported. Fatty acid and detergent sclerosants produce hemolysis, resulting in hemoglobinuria.[10] Sodium morrhuate was recommended to be limited to 90 mL.


Use of laser therapy for the treatment of hemangiomas has gained popularity. Lasers have evolved to where more selective photothermolysis can be attained rather than nonselective tissue destruction.

The yellow light lasers (578-585 nm) are selectively absorbed by hemoglobin. The only other competing chromophore with these lasers is melanin. Oral mucosa may be amenable to these lasers because little melanin is present in the mucosa. Little to no damage to the mucosa or the epithelium has been reported. In the macular stage of development, a 585-nm pulsed dye laser has been used to treat a capillary hemangioma.[54] The tunable dye laser can ablate superficial ecstatic blood vessels without significant epidermal damage or scarring. However, the 585-nm pulsed dye laser has limited penetration (1-2 mm). Waner described the use of pulsed dye lasers in the yellow light range on 11 cases of hemangioma, with 3 of them being in the oral cavity, with a successful outcome. Unfortunately, because of the minimal depth of penetration, in all but the thinnest lesions in the oral cavity, the usefulness of this laser is limited.

Apfelberg[55] reported using a neodymium:yttrium-aluminum-garnet (Nd:YAG) laser to treat massive hemangiomas and vascular malformations in the head and the neck via intralesional laser photocoagulation. A 600-µm bare fiber with 1-2 mm of the protective cladding removed was inserted several centimeters into the lesion. The laser is theorized to institute an initial thrombogenesis in many areas of the hemangioma or the vascular malformation, and this event initiates involution by normal body processes. The Nd:YAG laser emits beams in the near infrared region of the spectrum (1064 nm). This laser has deep penetration (1 cm) and an excellent hemostatic capability that makes it more suitable for thicker, larger, more developed hemangiomas.

Dixon believed that the Nd:YAG laser was the instrument of choice for debulking vascular malformations of the tongue. This laser has less selectivity for any particular chromophore, and use on nonmucosal surfaces is reported to result in more scarring.[2] Suen and Waner[56] reported satisfactory results with the use of the Nd:YAG laser for oral vascular malformations in 6 patients; however, 4 of the 6 patients required repeat treatments after the initial therapy.

Argon lasers emit beams in the blue-green part of the spectrum (488-514 nm), and the wavelengths are well absorbed by melanin and hemoglobin. Its depth of penetration is limited (about 1 mm). Reportedly, because of the strong absorption of the argon laser by melanin, a large proportion of patients have experienced scarring when it is used on the skin.[2] For laser photocoagulation of vascular malformations of the tongue, Dixon et al[57] believed that the argon laser was the instrument of choice for superficial bleeding.

The carbon dioxide laser emits light in the far infrared region, with a wavelength of 10,600 nm. This light is primarily absorbed by water molecules. Apfelberg[55] reported minimal-to-acceptable scarring in 17 of 21 patients with oral hemangiomas; 4 of the patients had fair results (poor scarring or minimal improvement in hemangioma deformity).


Cryosurgery for cutaneous lesions has been associated with scarring, but it may have a role in the treatment of oral mucosal lesions. Several authors have used cryosurgery for treating oral vascular tumors,[58, 59, 60, 61] although this technique has fallen into disfavor in recent years. Hartmann reported minimal scar contracture, good hemostasis, and little discomfort with the use of cryosurgery to remove a large oral hemangioma.

Combination surgical therapy

Complete surgical excision is a mainstay of treatment of vascular malformations if they are small and amenable to such therapy. However, for oral vascular tumors confined to the soft tissues, a combination of surgical therapies is often needed.

For central hemangiomas of the jaws, surgery is believed to offer the best chance of cure. Yih reported on 15 cases, where ligation of feeder vessels (and sometimes ipsilateral external carotid ligation) and resection or curettage were performed with no recurrences. Ligation alone of a single feeder vessel has been associated with recurrence of even larger arteriovenous malformations.

Surgery of intrabony lesions of the jaws is usually completed in combination with other procedures (eg, embolization, sclerotherapy) to reduce blood loss, but sclerotherapy alone for these lesions has been reported.[12, 62] No consensus exists on the best time interval between the embolization and the surgical treatment when embolization or sclerotherapy is used before surgery. Some clinicians advocate immediate surgery, while others suggest a delay of several days to a week. The decision on the timing needs to be individualized, depending on the goal of the embolotherapy. As the time between surgery and embolization progresses beyond 2-3 weeks, the embolization may prove to be of little development because of the development of collateral supply and recanalization of the vessels.



Treatment of these complex lesions often requires consultations with multiple specialties. In addition to surgeons, diagnostic and interventional radiologists, dermatologists, pediatricians, and internists are useful in treating these patients.

Contributor Information and Disclosures

Steven Brett Sloan, MD Associate Professor, Department of Dermatology, University of Connecticut School of Medicine; Residency Site Director, Connecticut Veterans Affairs Healthcare System; Assistant Clinical Professor, Yale University School of Medicine

Steven Brett Sloan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Connecticut State Medical Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Journal of the American Academy of Dermatology;Up to Date;Medical Review Institute of America.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Drore Eisen, MD, DDS Consulting Staff, Department of Dermatology, Dermatology Research Associates of Cincinnati

Drore Eisen, MD, DDS is a member of the following medical societies: American Academy of Dermatology, American Academy of Oral Medicine, American Dental Association

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Neil Shear, MD Professor and Chief of Dermatology, Professor of Medicine, Pediatrics and Pharmacology, University of Toronto Faculty of Medicine; Head of Dermatology, Sunnybrook Women's College Health Sciences Center and Women's College Hospital, Canada

Neil Shear, MD is a member of the following medical societies: Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, Canadian Dermatology Association, American Academy of Dermatology, American Society for Clinical Pharmacology and Therapeutics

Disclosure: Nothing to disclose.


Randall Wilk, MD, DDS, PhD Associate Professor, Department of Oral and Maxillofacial Surgery, Louisiana State University Health Science Center

Randall Wilk, MD, DDS, PhD is a member of the following medical societies: American Association of Oral and Maxillofacial Surgeons, American Dental Association, and American Medical Association

Disclosure: Nothing to disclose.

  1. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics. Plast Reconstr Surg. 1982 Mar. 69(3):412-22. [Medline].

  2. Waner M, Suen JY, Dinehart S. Treatment of hemangiomas of the head and neck. Laryngoscope. 1992 Oct. 102(10):1123-32. [Medline].

  3. Sasaki GH, Pang CY, Wittliff JL. Pathogenesis and treatment of infant skin strawberry hemangiomas: clinical and in vitro studies of hormonal effects. Plast Reconstr Surg. 1984 Mar. 73(3):359-70. [Medline].

  4. Folkman J, Klagsbrun M. Angiogenic factors. Science. 1987 Jan 23. 235(4787):442-7. [Medline].

  5. Takahashi K, Mulliken JB, Kozakewich HP, Rogers RA, Folkman J, Ezekowitz RA. Cellular markers that distinguish the phases of hemangioma during infancy and childhood. J Clin Invest. 1994 Jun. 93(6):2357-64. [Medline]. [Full Text].

  6. Christison-Lagay ER, Fishman SJ. Vascular anomalies. Surg Clin North Am. 2006 Apr. 86(2):393-425, x. [Medline].

  7. Stal S, Hamilton S, Spira M. Hemangiomas, lymphangiomas, and vascular malformations of the head and neck. Otolaryngol Clin North Am. 1986 Nov. 19(4):769-96. [Medline].

  8. Jacobs AH, Walton RG. The incidence of birthmarks in the neonate. Pediatrics. 1976 Aug. 58(2):218-22. [Medline].

  9. Amir J, Metzker A, Krikler R, Reisner SH. Strawberry hemangioma in preterm infants. Pediatr Dermatol. 1986 Sep. 3(4):331-2. [Medline].

  10. de Lorimier AA. Sclerotherapy for venous malformations. J Pediatr Surg. 1995 Feb. 30(2):188-93; discussion 194. [Medline].

  11. Dahlin DC, Unni KK. Bone Tumors: General Aspects and Data on 8,542 Cases. Springfield, Ill: Thomas. 1986.

  12. Hayward JR. Central cavernous hemangioma of the mandible: report of four cases. J Oral Surg. 1981 Jul. 39(7):526-32. [Medline].

  13. Cuesta Gil M, Navarro-Vila C. Intraosseous hemangioma of the zygomatic bone. A case report. Int J Oral Maxillofac Surg. 1992 Oct. 21(5):287-91. [Medline].

  14. Wolf GT, Daniel F, Krause CJ, Kaufman RS. Intramuscular hemangioma of the head and neck. Laryngoscope. 1985 Feb. 95(2):210-3. [Medline].

  15. Marchuk DA. Pathogenesis of hemangioma. J Clin Invest. 2001 Mar. 107(6):665-6. [Medline].

  16. Barrett AW, Speight PM. Superficial arteriovenous hemangioma of the oral cavity. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000 Dec. 90(6):731-8. [Medline].

  17. Yih WY, Ma GS, Merrill RG, Sperry DW. Central hemangioma of the jaws. J Oral Maxillofac Surg. 1989 Nov. 47(11):1154-60. [Medline].

  18. Bowers RE, Graham EA, Tomlinson KM. The natural history of the strawberry nevus. Arch Dermatol. 1960. 82:667-680.

  19. Lister WA. The natural history of strawberry nevi. Lancet. 1938. 1:1429-1434.

  20. Bivings L. Spontaneous regression of angiomas in children; twenty-two years' observation covering 236 cases. J Pediatr. 1954 Dec. 45(6):643-7. [Medline].

  21. Blackfield HM, Morris WJ, Torrey FA. Visible hemangiomas: a preliminary statistical report of a 10-year study. Plast Reconstr Surg. 1960. 26:326-329.

  22. Grabb WC, Dingman RO, Oneal RM, Dempsey PD. Facial hamartomas in children: neurofibroma, lymphangioma, and hemangioma. Plast Reconstr Surg. 1980 Oct. 66(4):509-27. [Medline].

  23. Yonetsu K, Nakayama E, Kawazu T, Kanda S, Ozeki S, Shinohara M. Value of contrast-enhanced magnetic resonance imaging in differentiation of hemangiomas from lymphangiomas in the oral and maxillofacial region. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1999 Oct. 88(4):496-500. [Medline].

  24. Johann AC, Salla JT, Gomez RS, de Aguiar MC, Gontijo B, Mesquita RA. GLUT-1 in oral benign vascular lesions. Oral Dis. 2007 Jan. 13(1):51-5. [Medline].

  25. Kane WJ, Morris S, Jackson IT, et al. Significant hemangiomas and vascular malformations of the head and neck: clinical management and treatment outcomes. Ann Plast Surg. 1995 Aug. 35(2):133-43. [Medline].

  26. Mulliken JB, Boon LM, Takahashi K, et al. Pharmacologic therapy for endangering hemangiomas. Curr Opin Dermatol. 1995. 109-113.

  27. Leaute-Labreze C, Dumas de la Roque E, Hubiche T, Boralevi F, Thambo JB, Taieb A. Propranolol for severe hemangiomas of infancy. N Engl J Med. 06/08. 358(24):2649-51.

  28. Siegfried EC, Keenan WJ, Al-Jureidini S. More on propranolol for hemangiomas of infancy. N Engl J Med. 12/08. 359(26):2846-7.

  29. Antaya RJ. Infantile Hemangioma. Medscape Reference. June 2010. [Full Text].

  30. Herrero Hernández A, Escobosa Sánchez O, Acha García T. Successful treatment with vincristine in PHACES syndrome. Clin Transl Oncol. April 2007. 9(4):262-3. [Medline].

  31. Fost NC, Esterly NB. Successful treatment of juvenile hemangiomas with prednisone. J Pediatr. 1968 Mar. 72(3):351-7. [Medline].

  32. Edgerton MT. The treatment of hemangiomas: with special reference to the role of steroid therapy. Ann Surg. 1976 May. 183(5):517-32. [Medline].

  33. Pope E, Krafchik BR, Macarthur C, Stempak D, Stephens D, Weinstein M, et al. Oral versus high-dose pulse corticosteroids for problematic infantile hemangiomas: a randomized, controlled trial. Pediatrics (Epub). May 2007. 119(6):e1239-47. [Medline].

  34. Bartoshesky LE, Bull M, Feingold M. Corticosteroid treatment of cutaneous hemangiomas: how effective? A report on 24 children. Clin Pediatr (Phila). 1978 Aug. 17(8):625, 629-38. [Medline].

  35. Hawkins DB, Crockett DM, Kahlstrom EJ, MacLaughlin EF. Corticosteroid management of airway hemangiomas: long-term follow-up. Laryngoscope. 1984 May. 94(5 Pt 1):633-7. [Medline].

  36. Hasan Q, Tan ST, Gush J, Peters SG, Davis PF. Steroid therapy of a proliferating hemangioma: histochemical and molecular changes. Pediatrics. 2000 Jan. 105(1 Pt 1):117-20. [Medline].

  37. Blei F, Isakoff M, Deb G. The response of parotid hemangiomas to the use of systemic interferon alfa-2a or corticosteroids. Arch Otolaryngol Head Neck Surg. 1997 Aug. 123(8):841-4. [Medline].

  38. Greinwald JH, Burke DK, Bonthius DJ, Bauman NM, Smith RJ. An update on the treatment of hemangiomas in children with interferon alfa-2a. Arch Otolaryngol Head Neck Surg. 1999 Jan. 125(1):21-7. [Medline].

  39. Barlow CF, Priebe CJ, Mulliken JB, Barnes PD, Mac Donald D, Folkman J. Spastic diplegia as a complication of interferon Alfa-2a treatment of hemangiomas of infancy. J Pediatr. 1998 Mar. 132(3 Pt 1):527-30. [Medline].

  40. Bigorre M, Van Kien AK, Valette H. Beta-blocking agent for treatment of infantile hemangioma. Plast Reconstr Surg. 2009 Jun. 123(6):195e-6e. [Medline].

  41. Léauté-Labrèze C, Hoeger P, Mazereeuw-Hautier J, et al. A randomized, controlled trial of oral propranolol in infantile hemangioma. N Engl J Med. 2015 Feb 19. 372 (8):735-46. [Medline].

  42. Sommers Smith SK, Smith DM. Beta blockade induces apoptosis in cultured capillary endothelial cells. In Vitro Cell Dev Biol Anim. 2002 May. 38(5):298-304. [Medline].

  43. Ran Y, Chen S, Dai Y, Kang D, Lama J, Ran X, et al. Successful treatment of oral itraconazole for infantile hemangiomas: a case series. J Dermatol. 2015 Feb. 42 (2):202-6. [Medline].

  44. Berenstein A, Lasjaunias P, Kricheff II. Functional anatomy of the facial vasculature in pathologic conditions and its therapeutic application. AJNR Am J Neuroradiol. 1983 Mar-Apr. 4(2):149-53. [Medline].

  45. Muto T, Kinehara M, Takahara M, Sato K. Therapeutic embolization of oral hemangiomas with absolute ethanol. J Oral Maxillofac Surg. 1990 Jan. 48(1):85-8. [Medline].

  46. Gilbert LD, Bakos LH, Graves RW. Sodium morrhuate--an alternative in the treatment of soft tissue hemangiomas. Review of the literature and case reports. W V Dent J. 1981 Apr. 55(2):11-5. [Medline].

  47. Chin DC. Treatment of maxillary hemangioma with a sclerosing agent. Oral Surg Oral Med Oral Pathol. 1983 Mar. 55(3):247-9. [Medline].

  48. O'Donovan JC, Donaldson JS, Morello FP, Pensler JM, Vogelzang RL, Bauer B. Symptomatic hemangiomas and venous malformations in infants, children, and young adults: treatment with percutaneous injection of sodium tetradecyl sulfate. AJR Am J Roentgenol. 1997 Sep. 169(3):723-9. [Medline].

  49. Baurmash H, Mandel L. The nonsurgical treatment of hemangioma with Sotradecol. Oral Surg Oral Med Oral Pathol. 1963 Jul. 16:777-82. [Medline].

  50. Minkow B, Laufer D, Gutman D. Treatment of oral hemangiomas with local sclerosing agents. Int J Oral Surg. 1979 Feb. 8(1):18-21. [Medline].

  51. Govrin-Yehudain J, Moscona AR, Calderon N, Hirshowitz B. Treatment of hemangiomas by sclerosing agents: an experimental and clinical study. Ann Plast Surg. 1987 Jun. 18(6):465-9. [Medline].

  52. Baurmash H, DeChiara S. A conservative approach to the management of orofacial vascular lesions in infants and children: report of cases. J Oral Maxillofac Surg. 1991 Nov. 49(11):1222-5. [Medline].

  53. Seccia A, Salgarello M. Treatment of angiomas with sclerosing injection of hydroxypolyethoxydodecan. Angiology. 1991 Jan. 42(1):23-9. [Medline].

  54. Glassberg E, Lask G, Rabinowitz LG, Tunnessen WW Jr. Capillary hemangiomas: case study of a novel laser treatment and a review of therapeutic options. J Dermatol Surg Oncol. 1989 Nov. 15(11):1214-23. [Medline].

  55. Apfelberg DB. Intralesional laser photocoagulation-steroids as an adjunct to surgery for massive hemangiomas and vascular malformations. Ann Plast Surg. 1995 Aug. 35(2):144-8; discussion 149. [Medline].

  56. Suen JY, Waner M. Treatment of oral cavity vascular malformations using the neodymium:YAG laser. Arch Otolaryngol Head Neck Surg. 1989 Nov. 115(11):1329-33. [Medline].

  57. Dixon JA, Davis RK, Gilbertson JJ. Laser photocoagulation of vascular malformations of the tongue. Laryngoscope. 1986 May. 96(5):537-41. [Medline].

  58. Goldwyn RM, Rosoff CB. Cryosurgery for large hemangiomas in adults. Plast Reconstr Surg. 1969 Jun. 43(6):605-11. [Medline].

  59. Murphy JB. The management of a large hemangioma of the oral cavity with cryotherapy. J Oral Med. 1978 Jul-Sep. 33(3):104-6. [Medline].

  60. Gongloff RK. Treatment of intraoral hemangiomas with nitrous oxide cryosurgery. Oral Surg Oral Med Oral Pathol. 1983 Jul. 56(1):20-4. [Medline].

  61. Hartmann PK, Verne D, Davis RG. Cryosurgical removal of a large oral hemangioma. Oral Surg Oral Med Oral Pathol. 1984 Sep. 58(3):280-2. [Medline].

  62. Greene LA, Freedman PD, Friedman JM, Wolf M. Capillary hemangioma of the maxilla. A report of two cases in which angiography and embolization were used. Oral Surg Oral Med Oral Pathol. 1990 Sep. 70(3):268-73. [Medline].

  63. Strand M, Smidt AC. Pain management for ulcerated infantile hemangiomas. Pediatr Dermatol. 2012 Jan-Feb. 29(1):124-6. [Medline].

Table 1. Classification of Vasoformative Tumors
Vasoformative Tumor New Nomenclature Old Nomenclature
  Capillary hemangioma Strawberry hemangioma
    Juvenile hemangioma
  Cavernous hemangioma  
  Mixed hemangioma Parotid hemangioma
Vascular malformations    
  Venous malformation Cavernous hemangioma
  Intramuscular venous malformation Intramuscular hemangioma
  Capillary malformation Capillary hemangioma
    Port-wine stain
  Arteriovenous malformation Arteriovenous hemangioma

Arterial angioma

Arteriovenous aneurysm

Cirsoid angioma

Red angioma

Serpentine aneurysm

  Lymphatic malformation Capillary lymphangioma

Cavernous lymphangioma


Cystic hygroma

Table 2. Complications From Ablative Surgery Following Embolotherapy or Sclerotherapy for Hemangiomas and Vascular Malformations
Complications Hemangiomas, % Vascular Malformations, %
Immediate Complications
Hemorrhage 27 60
Airway compromise 2 10
Hematoma 14 14-30
Skin necrosis 12 10-30
Coagulopathy 7 14-20
Late Complications
Restricted oral opening 8 27-40
Malocclusion 8 20-40
Drooling 23 40-47
Dysphagia 23 20-27
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