Although hemangiomas are common in infancy and childhood, they are probably developmental

abnormalities rather than true neoplasms. Pathologists distinguish three classes: capillary,

cavernous, and mixed types. Cavernous hemangiomas are blue, soft, spongy masses that are not

encapsulated. Some hemangiomas of the tongue have a lymphangiomatous component, hence

the name hemangiolymphangiomas.

Although most hemangiomas of the tongue are asymptomatic, they could sometimes cause

significant bleeding, pain or difficulty in chewing, speaking, and  even swallowing, if they are

large enough. Small lesions can be excised with impunity.  Large lesions, if excised, could result

in significant functional  disability.  This is why several modalities of less invasive treatment

have recently been advocated (Argon laser, Nd:YAG laser, or both to avoid functional disability

caused by tissue loss). Also, there have been reports of treatment with superselective

embolization using polyvinyl alcohol foam (Ivalon) and absorbable gelatin sponge (Gelfoam)

particulates.

History

Hemangiomas and vascular malformations are diagnosed fairly easily with a careful history and

a physical examination.

Capillary hemangiomas are usually not present at birth but are antedated by a pale, well-

demarcated, flat area, most visible with agitation. These prodromal lesions may appear as a pale

halo surrounding an area of telangiectasis or as a very fine telangiectasia similar to the port-wine

stain.

Elevation occurs early during the first year of life and increases from the ages of 3-8 months,

with some growth continuing into the second year of life. A stable interval of 6-12 months often

follows the growth period. Then, a slow spontaneous involution, which usually begins in the

center of the lesion, takes place in most cases. Involution often begins as a darkening of color

followed by the appearance of numerous gray or pallid regions and fibrous septae within the

lesion. Historically, most lesions have reportedly involuted by the time the patient is aged 7

years, with 86% of those lesions regressing by the time the patient is aged 5 years.

The patient's sex and the size of the hemangioma do not influence the speed or the completeness

of resolution. The location of the lesion does not generally influence its behavior, but lesions of

the lower lip are less favorable. Patients with multiple lesions have rates of resolution similar to

those with single lesions; however, separate lesions in the same individual do not necessarily

grow or involute simultaneously. Lesions that have not improved after 3 years are unlikely to

resolve by age 7 years. Unfortunately, early improvement does not always lead to early

resolution. Involution may continue into the late teenage years.

Cavernous hemangiomas are composed of large, irregular, deep dermal and subcutaneous blood-

filled channels that impart a purplish discoloration to the overlying skin. They are typically soft,

poorly defined, and readily blanch with compression, giving them a characteristic "bag of

worms" feel. The lesion may expand and darken with crying, when agitated, or when placed in a

dependent position. Often, a capillary component overlies a cavernous component, and it may be

difficult to distinguish these components histologically. Cavernous and mixed hemangiomas

demonstrate the same patterns of proliferation as those of capillary lesions. However, involution

is often incomplete, depending on the location and the presence of associated arteriovenous

malformations.

Vascular malformations are present at birth and continue to grow with the child. The growth may

become accelerated when the patient undergoes puberty or pregnancy, with the attendant

hormonal changes.

On examination of the oral cavity, the vascular malformations of the mucosa and the adjacent

soft tissues are usually readily apparent. The tissues have a slightly bluish hue and are soft.

Venous channels become engorged when placed in a dependent position. They are readily

compressible and fill slowly when released. They lack a prominent pulsation; if they represent an

arteriovenous malformation, a thrill may be present.

Although the mucosal and soft tissue lesions are readily suspected by their appearance, the

intrabony lesions may be difficult to distinguish on sight alone. Central jaw lesions can show

hypermobility of the teeth and distortion of the arch form. Severe hemorrhage following dental

extraction is not an uncommon presentation of central hemangiomas of the maxilla and the

mandible. Common clinical findings in central hemangiomas of the jaws include gingival

bleeding, postextraction bleeding, swelling, pain, mobility of the teeth, and bony expansion. Root

resorption of the teeth has been reported in 30% of cases, but the vitality of the teeth is usually

not affected.

Intramuscular vascular malformations represent a challenge on diagnosis because they exhibit

few signs on clinical examination. Oftentimes, the extent of the lesion is not clinically apparent

on examination, and imaging studies frequently define more extensive lesions than suspected.

Causes

The causes of vasoformative tumors are unknown. One hypothesis postulates that placental cells,

such as the trophoblast, may be the cell of origin for hemangiomas. Therefore, hemangiomas

may arise secondary to some event in utero. However, conflicting evidence supports this

hypothesis. One study found placenta-associated vascular antigens to be expressed by

hemangiomas but not by other vascular malformations or tumors. On the other hand, a separate

investigation found immunohistochemical staining of certain trophoblastic markers to be

negative in all infantile hemangiomas that were examined. The relationship between

hemangiomas and placental tissues needs further investigation.

Imaging Studies

Workup of oral hemangiomas requires some form of imaging to determine their extent and flow

characteristics. The following modalities may be helpful:

Angiography is considered the most definitive of the studies, although the angiographic

appearance of intraosseous lesions is less well defined than that of soft tissue lesions.

Ultrasonography can be used to determine that a lesion is angiomatous in nature (ie,

hemangioma, lymphangioma), but it cannot be used to differentiate a hemangioma from a

lymphangioma.

Contrast-enhanced MRI can be used to differentiate a hemangioma from a lymphangioma

in the oral cavity. MRI appears to be highly reliable for lesions of either soft tissue or

bone.

On plain films or panoramic radiographs, a central vascular malformation of the bone

usually has a honeycombed appearance or cystic radiolucencies. Intraosseous vascular

malformations show a nonspecific reticulated or honeycombed pattern that is well

demarcated from normal bone. A sunburst effect, created by spicules radiating from the

center, is often present.

CT scans often show an expansile process with a high-density amorphous mass that may

be suggestive of fibrous dysplasia.

Procedures other than a clinical history or examination, including aspiration of intraosseous

lesions, that are used to diagnose oral hemangiomas readily produce frank blood. Performing a

biopsy of oral hemangiomas can be potentially dangerous.

Histologic Findings

Histopathologically, vasoformative tumors share many similar microscopic features, and overlap

between hemangiomas and vascular malformations exists. Hemangiomas are subclassified as

capillary or cavernous, depending on the size of the vascular channels. Vascular malformations,

as true structural anomalies, exhibit a normal rate of endothelial cell turnover. Spaces are lined

by endothelium without muscular support. An increase in normal- and abnormal appearing blood

vessels occurs. The endothelial cells of early lesions may be plump, obscuring the lumen of the

capillaries. Phleboliths may develop as a result of dystrophic calcification in thrombi. Intimal

thickening or diverse arteriovenous connections can sometimes be seen in serial sections. Johann

et al showed that histological diagnosis alone is not sufficient to correct diagnoses of oral

hemangioma. Moreover, immunohistochemistry to GLUT1 is a useful and easy diagnostic

method that may be used to avoid such misdiagnosis.

Salient histopathologic findings of vasoformative tumors that distinguish them are as follows:

Hemangiomas (proliferative phase):

o Endothelial cell hyperplasia forming syncytial masses

o Thickened (multilaminated) endothelial basement membrane

o Ready incorporation of tritiated thymidine in endothelial cells

o Presence of large numbers of mast cells

Hemangiomas (involuting phase):

o Less mitotic activity

o Little or no uptake of tritiated thymidine in endothelial cells

o Foci of fibrofatty infiltration

o Normal mast cell counts

Vascular malformations:

o No endothelial cell proliferation

o Contain large vascular channels lined by endothelium

o Unilamellar basement membrane

o Does not incorporate tritiated thymidine in endothelial cells

o Normal mast cell counts

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 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.

Intervention

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. 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. 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.

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.

Fost and Esterly 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 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 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.

Bartoshesky et al had conflicting results with steroids, showing a definite response in only 2 of

17 patients with mixed hemangiomas. Hawkins et al 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. 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 reported the use of interferon alfa-2a in parotid hemangiomas (13 females, 1 male) in

which the response was poor. Greinwald et al 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.

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. 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.

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.

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.

Provisional guidelines for initiation of therapy

Pretreatment

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

Monitoring

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

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:

o Acrylic spheres

o Autologous fat of muscle

o Ferromagnetic microspheres

o Methylmethacrylate spheres

o Polyvinyl alcohol (Ivalon)

o Silastic spheres

o Stainless steel pellets

Injectable (fluids) are as follows:

o Amino acid occlusion gel (Ethibloc)

o Isobutyl 2-cyanoacrylate

o Microfibrillar collagen (Avitene)

o Silicone rubber

Sclerosing agents are as follows:

o Absolute ethanol

o Boiling contrast medium

o Polidocanol

o Sodium morrhuate

o Sodium tetradecyl sulfate (Sotradecol)

Nonparticulate agents are as follows:

o Stainless steel coils

o Platinum coils

o Silk streamers

o Plastic brushes

o 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. 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 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.

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 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. 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 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. 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 used 1% STS. Later

reports and more recent reports use a 3% solution.

Minkow et al 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 recommended 3% STS, using 0.5-2 mL volumes of sclerosants and

manual compression of the lesions to ensure stasis.

Kane et al 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 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 have been reported. Fatty acid and detergent sclerosants

produce hemolysis, resulting in hemoglobinuria. Sodium morrhuate was recommended to be

limited to 90 mL.

Lasers

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. 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 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. Suen and Waner 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. For laser

photocoagulation of vascular malformations of the tongue, Dixon et al 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 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

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, 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. 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.